LITERALLY RANDOM FINALS

Describe infection on HIV

gp120 (HIV surf) connected to viral memb prot (gp41)--> gp120 binds CD4 & chemokine recep CCR5--> Gp41 pierces memb of targ cell.

what arteries provide blood to the erectile tissue of the penis?

helicine arteries

how does *high altitude* affect PIO2?

high altitude → *decreased barometric pressure → decreased PIO2*

spermatogenesis is remarkable for what hormone?

high testosterone levels

You administer supplemental O2 to a pt w/ COPD & the pt stops breathing. Offer a possible explanation.

his PaO2 is >60 so carotid body stops b/c no 02 drive to breath

what is the long-loop feedback?

hormones produced at target gland feedback to inhibit production of both hypothalamic and pituitary hormones

A lightly anesthetized pt is removed from a ventilator after surgery & the pt fails to breath for 1 minute. offer a possible explanation for this observation?

how long it took his PO2 to fall below 60 since central chemoreceptors are still knock out & can't respond

How is the ventilatory response to hyercapnia altered by hypoxia?

hypercapnia (kicks in central chemoreceptors) & hypoxia kicks in carotid body (peripheral chemoreceptors) ie. Kussmaul breathing

16 yo female with short stature, prepubertal genital exam, primary amenorrhea. elevated FSH/LH, and low estradiol. Dx and additional testing?

hypergonadotrophic hypogonadism karotype would show 45 XO.

MCC of gastric outlet obstruction in infants

hypertrophic pyloric stenosis

Hemoptysis is commonly seen in patients with Cystic Fibrosis, and when massive, this condition can be life threatening. What mechanism causes this increased bleeding potential in CF patients when hemoptysis is present?

hypervascularity of the airway

MCC 2ndary hyperparathyroidism

hypocalcemia of chronic renal disease

What are concerning findings on a thyroid nodule US?

hypoechoic, microcalcifaction without shadowing, increased intranodular vascular flow, irregular border

Lab result indicating SIADH over DI

hyponatremia DI is hypernatremic

what is the ultrashort-loop feedback?

hypothalamic hormone repressing its own synthesis

what thyroid issue is a possible cause of osteoporosis?

hypothyroidism

3 Important Events assoc. w/changes in puberty due to estrogen...

i. a. Estrogen ind leptic sec from adipocyt b. Leptin stim GnRH prod & pulsatility c. Leads to inc gonadotropins in blood ii. Growth spurt med by GH & IGF-1--> inc bone mass/maturity, IGF-1 inc GnRH secretion/pulsatility & leads to EVEN MORE LH & FSH in blood iii. Combo of leptin & IGF-1 effects signals menarche/ovulation to begin

LAMAs- Tiotropium

improve sx; do not speed resolution, no MACE risk

where are the rete testis?

in the mediastinum testis

Lung volume in children/adolescents increase due to...

increase # of respiratory bronchioles, not alveoli? (check on this)

what hormone changes in hyperphosphotemia?

increase PTH increase FGF-23 decrease Vit D3 decrease Klotho protein decrease absorption in kidney and gut = decrease in P to normal

what hormone changes happens in a hypocalcemic state?

increase PTH decrease calcitonin secretion NET: increase calcium + decrease P

If a lung disease were to cause an increased non-uniformity of ventilation but not blood flow, what would happen to PAO2, PaO2, & %SaO2?

increase in PAO2 but decrease in PaO2 & %SaO2

If the distribution of VA/Q ratios become more non-uniform due to lung disease, how would physiological dead space change? How would venous admixture change?

increase in physiological dead space increase in venous admixture

Adiponectin action and source

increase insulin sensitivity adipocytes

How does PVR change if a patient is put on a ventilator w/ (+) end-expiratory P to elevate end expiratory lung volume? Under what conditions could this be detrimental? Under what conditions could this be beneficial?

increase is PVR b/c more particles (intrinsic P increased) -detrimental w/ HTN, HF, Pul edema -beneficial for hypotension, hypoxia

How does O2 loading in lungs affect CO2 release from blood?

increase release of CO2

What is the hallmark of CF -

increased trans epithelial electric potential difference b/c Cl- is not absorbed (Done with Nasal biopsy)

how does the TH affect catecholamine function?

increases beta receptors thus sensitizing tissue to catecholamines (permissive action of TH)

List the 4 factors which will increase the P50 for Hbg. What is the functional significance of an increase P50 (rightward shift in the O2 dissociation curve)?

increases in [H+], BPG, T, [CO2] -increase O2 delivery of O2 affinity for Hb

List 3 physiologically significant consequences of having surfactant present.

increases lung compliance, prevents alveolar collapse, promotes dry alveoli

what is the difference from ACTH indep from dep?

indep = primary adrenal hypersecretion as the adrenals are the source (ACTH will be low here b/c pituitary is acting normally while adrenal is the problem) dept = secondary adrenal hypersecretion (ACTH will be high despite the negative feedback from cortisol; issue lies in the pituitary NOT the adrenals. usually a pituitary adenoma or ectopic neoplasm)

HbA1c reflects what?

indicator of the mean glucose over the past 2-3 months. percentage of the glycation (coating) of hemoglobin in RBCs

has does TNGalpha action work on adipose?

induces lipolysis inhibits TAG formation induces insulin resistance in adipocytes suprresses PPARg activity which thus inhibits recruitment of preadipocytes into ature adipocytes

When should you suspect TB-associated lung disease?

infiltrates in apices use negative pressure isolation, if suspected

How does Cushing's affect Ca homeostasis?

inhibits ca absorption to extent that excess PTH is secreted which in turn stimulates osteoclastic bone resorption

leptin action and source

inhibits food intake and stimulates overall energy consumption (hypothalamus) stimulates lipolysis white adipocytes (and some other places to a much lesser extent)

what does cortisol antagonize?

insulin

what hormone opposes TAG breakdown? what inhibits this hormone?

insulin GH inhibits insulins inhibition so allows for TAG breakdown

what hormones promote storage of excess glucose?

insulin IGF

half life of GHRH

intermediate (50min)

24 hr urine Ca results measure what physiological process in the body?

intestinal absorption of Ca. Order in the workup of hyperparathyroidism. Will be elevated (make sure not on diuretic). low urine Ca suggestive of inefficient intestinal absorption

how does estrogen affect thyroid hormone binding?

it increases thyroid binding

why is somatostatin important for glucose regulation?

it modulates via inhibition various fnx so that we don't get one big dump of glucose all at once

What can cause physiological enlargement of the pituitary?

lactotroph hyperplasia during pregnancy primary gland failure d/t thyrotroph, gonadotroph hyperplasia

what is the preferred orientation of collagen in bone? less stable orientation?

lamellar/layered/concentric = preferred random/woven = not

alveolar air has _________ O2 and __________ CO2, when compared to inspired air

less O2; more CO2

The diabetes prevention program indicates

lifestyle changes are more effective than drugs in the prevention of progression from IRS to DM if done correctly

what are the key features of leydig cells?

like other steroid producing cells -well developed SER -mito with tubular cristae -numerous lipid droplets in cyto

2 missions of GH and how they work

liniear growth via IGF regulation of serum glucose and lipid metabolism via GH itself (done to preserve lean body mass and pref use lipids as energy source)

what produces thryoid binding globulin (TBG)?

liver (liver basically does all proteins, bro)

half life of CRH

long

half life of TH

long

half life of TSH

long

half life of cortisol

long

what 2 triggers are there for increasing thyroid axis activity? how?

low BMR (low body temp) stress (alpha adrenergic agonists) stimulates hypothalamus to release TRH

what happens during a hypocalcemic state that induces the stimulation of renal 1alpha hydroxylase to form more VitD3/calcitriol/1,25(OH)D? *(THIS WILL probs BE A Q)*

low serum phosphate + elevated PTH work in concert to stimulate this change subsequent increase in Vit D3 neither alone suffice to accomplish this

what happens during a hypocalcemic state that induces the stimulation of renal 1alpha hydroxylase to form more VitD3/calcitriol/1,25(OH)D? *(THIS WILL BE A Q)*

low serum phosphate + elevated PTH work in concert to stimulate this change subsequent increase in Vit D3 neither alone suffice to accomplish this

what does calcitonin do? and when is it stimulated?

lowers blood Ca levels regulated by blood calcium; high levels of Ca stim secretion it TONES DOWN the CALCIUM.

at steady state, how are lung O2 uptake rate and cell O2 utilization rate related?

lung O2 uptake rate = cell O2 utilization rate

TdT and CD34

lymphoblast markers (acute lymphoblastic neoplasms)

PAS(+) Dutcher body

lymphoplasmacytic lymphoma (LPL)

regulated release hormone (meaning and path to release)

made continuously storage of premade hormone anticipating release 1. trigger 2. receptor 3. 2nd messenger system 4. synthesize enzymes to make hormones 5. 2nd trigger 6. 2nd receptor 7. secretory protein (usually do to Ca2+)

constitutive hormone (meaning and path to release)

made on demand no storage 1. trigger 2. receptor 3. 2nd messenger system 4. synthesize enzymes to make hormones

what are the 2 missions of the thyroid?

maintain basal metabolic rate increase protein synthesis for growth and metabolism

What role does the Cl- shift play in CO2 transport by blood?

maintain electroneutrality

t(11;14) CCND1 w/ immunoglobulin heavy chain over-expression of cyclin-D1

mantle cell lymphoma

what 3 factors stop uncontrolled osteoblast activity during formation?

maturation of osteoblast to osteocyte PTH bax activation (apoptosis)

what does thyroid resin uptake test measure?

measures number of unoccupied binding sites on TBG

what is produced in the pineal gland and what does this affect?

melatonin circadian rhythem

action of PTH

mobilize Ca from bone inhibit renal excretion of Ca increase renal excretion of P NET: increase Ca and decrease P

3 part mission of glucagon

mobilize glucose and FA from storage promote gluconeogenesis modulate glucose transport into tissues

half life of aldosterone

moderate

purpose of pancreatic polypeptide

modulatory (esp with heavy protein meals) again so we don't get a big dump of glucose all at once

Key about mets from lungs

more than 50% go BILATERAL ADRENALS

Cavitation on chest radiograph makes pt? AIDS or IC pts have more or less cavitation?

much MORE infectious! IC patients have less cavitation, making them less contagious

(+) CD4 (-) CD8, CD7 tumor form is strongly positive for CD30

mycosis fungoides

Sézary cells (cerebriform nuclei)

mycosis fungoides Sézary syndrome

histo of paraganlioma

nests (zellballen) of round to oval chief cells (neuroectodermal in origin) surrounded by deliate vascular septae bound by sustentatcular cells neurosecretory graunlues on EM ******* Test question? stain + for neuroendocrine lineage immunohistochemistry

what is the most common gas present in atmospheric air?

nitrogen

how does changes in Thyroid binding affect thyroid panel results?

no affect on free TH will affect total

If there were similar decrease in ventilation & blood flow to every alveolus in the lung, how would PaO2 change? (assume no change in the composition of mixed venous blood.)

no change in PaO2

popcorn cells/LP cells/L-H cells

nodular lymphocyte predominant hodgkin lymphoma (NLPHL) - non-classical

(+) CD45, CD20 (-) CD15, CD30

nodular lymphocytic predominant hodgkin lymphoma (NLPHL) - non-classical

lacunar cells

nodular sclerosis - CHL

Assume a normal value for pulmonary artery pressure a PAWP=5mmHg, & CO=5L/min. What is pulmonary vascular resistance?

normal Ppa=15mmHg PVR= (Ppa-Pla)/CO PVR=(15-5)/5= 2mmHgmin/L

fnx of sertoli cells

nourishing germ cells participate in germ cell movement and differenetiation structural support blood-testis barrier actively secrete androgen-binding protein AND inhibin phagocytize residual bodies and degenerated germ cells

what receptor binds Vit D3 at target tissue?

nuclear recetor

PFT normal Values

o FEV1 > 80% o FVC > 80% o FEV1/FVC > 0.7

Equation for Anion Gap? Normal Values? Causes of elevated AG

o Plasma anion gap = Na - (Cl + HCO3) ▪ Normal ~ 12 (3x normal albumin level) *causes of elevated AG metabolic acidosis*: MUDPALES - Methanol, Uremia, DKA, Paraldehyde, Alcoholic ketoacidosis, Lactic acidosis, Ethylene glycol (antifreeze), Salicylates (*ASA, pepto-bismol, alka-seltzer)

What is the principal difference b/n obstructive disease & restrictive disease?

obstructive dx: increased RV restrictive dx: decreased RV

when do we use ATPS?

only exists in equipment *NEVER use an ATPS on a patient's chart*

embryonic origin of adenohypophysis of pituitary

oral ectoderm (glandular epithelial tissue)

Gold standard in diagnosing acromegaly?

oral glucose tolerance testing. giving glucose should decrease GH. won't do this is pt's with acromegaly

what marker is used to determine total bone turnover?

osteocalcin

what 4 factors stop uncontrolled osteoclast activity during remodeling?

osteoprotegerin estrogen calcitonin bcl-2 activation (apoptosis)

what are the 2 layers of the capsule of the testis?

outer dense CT = tunica albuginea inner loose CT = tunica vasculosa

how does *oxygen therapy* affect PIO2?

oxygen therapy → *increased FIO2 → increased PIO2*

***Churg-Strauss vaculitis (emphasized in class) Microscopic polyangiitis Idiopathic crescenteric GN

p-ANCA + MPO-ANCA

Major concern in all HYPERtriglyceridemia disorders?

pancreatitis*

what cells are P-sensitive?

parathyroid cells thyroid c-cells osteocytes

what cells are Ca-sensitive?

parathyroid cells Thyroid C-cells

what are the cells of the parathyroid gland? what do they do?

parathyroid chief cells - produce PTH (opp of calcitonin) oxyphil cells - not well understood

MEN2 and multiple parathyroid glands...what could it be?

parathyroid hyperplasia

mutations in PIGA gene

paroxysmal nocturnal hemoglobinuria

RBCs and WBCs (-) for CD55 and CD59

paroxysmal noturnal hemoglobinuria (DAF & MIRL)

regions of the adenohypophysis?

pars distalis (bulk) pars intermedia (thin remnant of wall of Rathke's pouch with lumen known as Rathke's cyst) pars tuberalis (collar/sheath around infundibular stalk)

where does the inferior hypophyseal a. go?

pars nervosa

regions of the neurohypophysis

pars nervosa infundibulum

where does the superior hypophyseal a. go?

pars tuberalis, infundibulum, median eminence

What is the single most important factor in chronic care management?

physicians must empower their patients to help themselves with their own disease process

Single most important factor in chronic care management

physicians must empower their patients to help themselves with their own disease process.

capsule of the pineal gland is...

pia mater

what cells are found within the pineal gland? and what do they do?

pinealocytes - principle cells - modified neurons that secrete melatonin glial cells (interstitial cells) - support cells

what is short-loop feedback?

pituitary hormones inhibiting further production of hormone from hypothalamus

What does hypoglycemia with low levels of GH represent?

pituitary insufficiency GH levels should rise with hypoglycemia

MC salivary gland tumor (adults & children)

pleomorphic adenoma--benign mixed tumor

Spirometry findings to diagnose asthma:

post-SABA FEV1 ↑ by ≥ 12% & ≥ 200 mL

MCC of lactotroph hyperplasia? MCC of Thyrotroph hyperplasia?

pregnancy (pt will have amenorrhea and enlarged thyroid) Hashimoto thyroiditis DON'T image early in dx process!!

what are the actions of vit D3?

primarily: intestine - promotes absorption of Ca and P to restore deficient state secondary: bone - activates bone resorption (this is why you don't want it in excess as this will be damaging in the long term; more PTH's game anyway) tertiary: kidney - promote renal resorption of both Ca and P [thus self corrects PTH induced reduction]

what is the difference btw primary, permissive, synergistic, and antagonistic effects when it comes to hormone action?

primary = independent permissive, synergistic, antaongistic = combination action primary = hormone binds to target cell and produces response permissive = hormone binds to target cell but produces no overt response; instead, sensitizes cell to 2nd agent/hormone synergistic = 2+ hormones complement each others' actions (either cause response but together get full response) antagonistic = one hormone action is opposed by another (e.g. insulin vs glucagon)

Labs with a low sodium, high potassium are indicative of?

primary adrenal insufficiency. secondary may have nml K. low glucose. Sx: n/v, weakness, fatigue, confusion. hyperpigmentation, wt. loss in chronic.

2 causes of hyperthryoidism. explain

primary hypothyroidism - disease of thyroid (this is source) that can't produce enough TH despite proper stimulation from TSH secondary hypothyroidism - pituitary lesion that produces inadequate amounts of TSH

Complication of cholesteatoma?

progressive enlargement can ERODE into ossicles, labyrinth, adjacent bone

what is the lining for the ductus epididymidis?

pseudostratified columnar epithelium with STEREOCILIA

What is the Somogyi effect?

pt's blood glucose decreases in the middle of the night from too much insulin then peaks in the morning making pt's think they need more insulin when they actually need less. Have pt's check blood sugar 3-4 hours prior to eating breakfast to try to confirm this

Legionella Characteristic features:

relative bradycardia, hyponatremia

MCC death in SLE

renal failure or intercurrent infection *Coronary artery dz is becoming an increasing cause of morbidity/mortality

what does Klotho protein do?

responsible for calcium homeostasis negatively reg Vit D3

2 missions of cortisol

restore liver glycogen after a fast regulate serum glucose so that glycogen synth in liver is promoted

MCC of mitral stenosis

rheumatic heart disease

MCC of subarachnoid hemorrhage

rupture of berry aneurysm

what sperm line cells quickly go through meiosis II to produce spermatids?

secondary spermatocytes

small granule cells (nose)

secretory cells homologous to enteroendocrine from GI --was on quiz control overall rate of secretion *membrane-bound, dense core granules @ BASE of cell Develop from evagination of primitive foregut--one of these is a prediction

location of pituitary gland

sella turcica of the sphenoid bone

order of tubules in the male repro

seminiferous tubules (germ cells and sertoli) tubule recti (sertoli w/o germ) rete testis (simple cuboidal) epidymis -ductuli efferentes (*low pseudostrat columnar with CILIATED and nonciliated --> saw tooth look*) -ductus epididymidis (tall pseudostrat columnar with STEREOCILIA) ductus deferens (pseudostrat columnar with long MICROVILLI)

what tubules are found in the testis?

seminiferous tubules with straight tubule that turns into the rete testis at the mediustinum testis

what is the name for the support cells of the seminiferous tubule?

sertoli cells

what cells are in the seminiferous tubules?

sertoli cells - support cells spermatogenic cells - become sperm

what are inhibin and activin involved in? how do they work? where are they produced? what about follistatin?

sertoli cells, granulosa cells, placenta, some pit/adren involved in gonadal productions inhibin INHIBITS FSH production activin STIMULATES FSH production follistatin binds both but pref activin so skews equilibrium of circulating activity twd inhibin to decrease FSH

half life of ACTH

short

half life of IGF

short

half life of TRH

short

half life of androgens

short

Women with 45XO would have what clinical appearance/hx?

short webbing of neck 1° amenorrhea *Turners syndrome --hypergonadotrophic hypogonadism

half life of GH

short (20 min)

ringed sideroblasts

sideroblastic anemia dyserythropoiesis refractory anemia w/ ringed sideroblasts refractory cytopenia w/ multilineage dysplasia

describe the regulation of GH release

similar to TSH, it is released in pulses due to the combined efforts of GHRH and SST

lining of rathke's cyst and filling

simple cuboid epithelium colloid

describe the cells lining the inside of a thyroid follicle

simple cuboidal follicular epithelium

What is the most common cause of hyperparathyroidism and what would the labs look like?

solitary parathyroid neoplasm Ca and PTH elevated

most abundant endocrine cells of the adenohypophysis?

somatotropes (>50%)

low glycemic index meals (protein) lead to what hormone production?

some insulin but also counterregulatory glucagon so that gluconeogenesis can occur to prevent hypoglycemia

what is the first sperm cell precursor that is haploid?

spermatid

describe the phases of spermatogenesis

spermatogonial phase -type A dark spermatogonia --> type A pale and type B spermatognia -type A pale --> type B spermatognia -type B --> NEXT stage primary spermatocytes spermatocyte phase -primary spermatocytes (at prophase I of meiosis) --> secondary spermatocytes -secondary spermatocytes (go through meiosis II) --> NEXT stage spermatids spermatid phase -spermatid remodeled --> mature sperm mature sperm

what is another name for the adrenocortical cells of the zona fasciculata?

spongiocytes b/c spongy looking due to numerous lipid droplets in cyto

2 missions of insulin

stimulate transport of glucose into tissues sequester glucose into storage forms like glycogen

how does *suffocation* affect PIO2?

suffocation → *increased FICO2 → decreased PIO2*

what forms the primary capillary plexus? explain its development and content from here

superior hypophyseal a. ---> primary capillary plexus (picks up hormones from the hypothalumus at the infundibulum and median eminence) --> hypophyseal portal vein to pars distalis --> secondary capillary plexus (hypothal hormones delivered to A pituitary and hormones produced here are picked up--> collecting vein

2 part mission of catecholamines

support basal metabolic rate provide necessary metabolic support for the body in times of stress

What is meant by the term apneuses? Experimental brainstem section in what 2 places would combine to produce it? Input from what respiratory centers or pulmonary receptors is being removed & what fx do they normally serve?

sustained inspiratory efforts, if you cut the pneumotaxic center & vagi you would stop breathing so you lose all response of chemoreceptors

Diagnosing DM requires

symptoms + one of the following (all serum levels): RPG > 200mg/dL FPG > 126 mg/dL 2-h PPG > 200 mg/dL A1c > 6.5

what factor does the *partial pressure of H2O* depend on?

temperature in general a *higher temperature → higher water vapor air can hold*

Which portion of the lung is pulmonary blood flow the greatest when a pt stands on his head?

the apex b/c of gravity, normally blood flow is the greatest at the base

What relationship exists b/n the volume of an elastic structure & its transmural P?

the elastic recoil of a structure is its transmural P

what does the mucosa of the seminal vesciles do?

the epithelial cells produce viscous fluid that contains spermatozoa activating substances and composes about 70% of human ejaculate

seminal vesicles produce what?

the epithelium produces spermatozoa activting substance in the viscous fluid it secretes (carbs, prostoglandins, protein, fructose)

what does the ductus deferens look similar too?

the female urethra both look star shaped on slides

what part of the epididymis contains mostly efferent ductules?

the head

what is the major regulator of phosphate?

the kidneys with a balance of filtration and reabsorption

When evaluating DXA what needs to be considered for the results to be valid?

the least significant change needs to be >/= 3=5% or could be due to lab error

what is the difference btw cells of the cortex and cells of the medulla in the adrenal gland?

the medullary chromaffin cells can store their hormone while the cortex cells cannot

what does melatonin inhibit?

the steroidogenic activity of the gonads

where do you find benign prostatic hyperplasia?

the transitional zone of the prostate

what are gluco-incretins? what do they do?

they are GI hormones released by food ingestion stim Beta-cells to promote release of insulin

Thiazolidinediones...

think--THIGHazolidinediones make your THIGHS bigger and other --aZONES (ending of drug names) of your body. If your tummy (the NUCLEUS of your body) gets too fat it might peep (PPAR) out from under your shirt. If you are SENSITIVE (increases insulin sensitivity) if may hurt your feelings (heart problems) when someone points it out. It causes you to get fat cause it inhibits leptin--> suppresses your satiety center. *Thiazolidinediones--PPAR-gamma-->goes to nucleus--> increase insulin sensitivity-- PAR-3 (3 is 3rd letter of greek alph) 3-ADRs: CV toxicity, edema, weight gain

how does the pulsatile release of GH important for its action of target cells?

this limits exposure of the target cells to GH as overexposure rapidly down-reg GH receptors on target tissue

Hemothorax > 200 cc/hr, how should you treat?:

thoracotomy

what can cause hyperthyroidism that isn't an autoimmune disorder (aka graves)? what they do?

thyroid adenoma --increase TH production pituitary tumor --excess TSH production despite feedback selective pituitary resistance to TH -- feedback inhibition unable to work do to faulty receptor

***find slide about GSD)

too lazy right meow

where do we measure the *partial pressure of inspired air*?

trachea

what is the main and powerful amplifier of insulin release?

truncated GLP-1 (main gluco-incretin)

what type of glands are in the prostate? their lining?

tubuloalveolar glands low col or cuboidal pseudostrat

Define "health risk behaviors"? What four behaviors are responsible for the majority of chronic disease?

unhealthy behaviors that can be changed • lack of exercise or physical activity • poor nutrition • tobacco use • high alcohol consumption

what marker is used to determine resorption of bone (ARF)? 1 urine marker and 1 serum marker

urine = hydroxyproline serum - tartrate-resistant acid phosphatase (TRAP)

What do you do if history is unclear in a patient w/low uptake?

urine iodine testing

when do we use BTPS?

used to chart almost all volumes & flows *except O2 uptake (VO2), CO2 production (VCO2), and diffusing capacity (DLCO)*

when do we use STPD?

used to chart: *O2 uptake (VO2)* *CO2 production (VCO2)* *diffusing capacity (DLCO)*

equation: *Fick's Law of Diffusion*

used to determine the *rate of uptake of a gas* across a membrane A = diffusion membrane area D = diffusivity T = diffusion membrane thickness P1/P2 = pressures on opposing sides of the diffusion membrane

Heerfordt syndrome

uveoparotid fever - fever, parotid gland enlargment, anterior uveitis and facial nerve palsy--associated w/sarcoidosis! Tx with steroids

Tx for presbylaryngis-aging larynx

voice therapy

What is meant by unstressed volume? At what lung volume is the chest wall at its unstressed volume? At what lung volumes are the lungs at their unstressed volume? At what lung volume is the total respiratory system at its unstressed volume?

volume at which a structure no longer has elastic recoil force. chest wall @ 65%TLC lungs @ 10% total @ 45%

ATP III Diagnostic Criteria for Metabolic Syndrome - IRS

waist circumference - males > 40 in; females > 35 in TG > or = 150 mmol/L HDL - men < 40; women < 50 BP - > or = 130/85

What is the criteria to use supplemental O2 for dyspnea: Dx test of choice:

when *O2 Sat < 90%* or if PaO2 is *<60mmHg* Dx: Chest Xray

what is the importance of AMP-activated protein kinase (AMPK)?

when AMP is high (aka ATP low) it is phosphorylated (active) the active enzyme mediates phosphoylation events which switch cellular metabolic poise from ATP consumption to ATP production this resets the metabolic poise so that energetic status is improved (ATP generated)

though GH can act independently, how does it act as a trophic hormone?

when it stimulates the liver to produce IGF IGF negatively feedbacks to decrease GH producion (inhib GHRH and stim SST)

Of what significance is the fact that the CO2 dissociation curve is linear over the normal range? Hint: how does this affect mixing of blood?

you can average 2 pCO2 values b/c linear (constant slope) but you can't pO2 b/c curve

describe the progression of cells/zones in the cortex of the adrenal glands

zona glomerulosa = pyramidal/cuboid cells following arched capillaries zona fasciculata = long cords of cells following straight capillaries zona reticularis = small dirty looking cells following loops of capillaries that form a network ("reticulum")

Health Care associated pneumonia Mortality rates increase w/:

• Bacteremia (Pseudomonas or Actinobacter) • Medical (vs. surgical) illness • *Tx with ineffective intial abx therapy increases mortality dramatically * o Empiric Abx Tx: *Minimum of 5 Days*

What are the Symptoms of acute exacerbation bronchiectasis?

• Change in sputum production (typically a decrease in sputum, can't get it out) • Increased dyspnea, cough, or wheezing • Fever • Malaise, fatigue, lethargy, exercise intolerance • Reduced pulmonary function • Radiographic changes • Changes in chest sounds

A tall, long-limbed, 25 y/o male with a previous diagnosis of Marfan Syndrome presents to the ED with sudden onset dyspnea and pleuritic chest pain, with decreased lung sounds on the left. Based on this information, what is the most likely diagnosis for this patient's current clinical condition, and what is the next best step in this patient's management?

• Dx: *Primary Spontaneous Pneumothroax* (PSP) • Next best step: *CXR* - plain film, upright and lateral decubitus

Classic Tetrad of Narcolepsy:

• Excessive daytime sleepiness - chronic: 3+ weeks • Cataplexy: sudden loss of muscle tone • Hypnagogic hallucinations: as you're falling asleep • Sleep paralysis

Define the lights criteria?

• Pleural Fluid : Serum Protein ≥ 0.5 • Pleural Fluid : Serum LDH ≥ 0.6 • Pleural Fluid LDH > ⅔ the upper limits of normal serum LDH • *if 1 of 3 is present* → EXUDATE

Latent TB: + Skin or Blood Test, - CXR or Sputum Description:

• Pts are *ASYMPTOMATIC* (Only ID'd by screening test) • Pts *Do have M. Tuberculosis in body* • Pts DO *NOT have TB Disease* • Pts *CANNOT* spread disease to others

Signs of clinical stability post-pneumonia

• Temp ≤ 37*F • HR ≤ 100 bpm • Resp. rate ≤ 24 bpm • SBP ≥ 90 mmHg • SpO2 ≥90% or PaO2 ≥ 60 mmHg on RA • Ability to maintain oral intake • Normal mental status

Define the conditions of the CURB-65 severity scale for community-acquired pneumonia (CAP)

• if score ≤ 1 → outpatient • if score = 2 → inpatient • if score ≥ 3 → ICU • Confusion → 1 pt • Urea > 7 mmol/L → 1 pt • RR ≥ 30 bpm → 1 pt • BP - SBP ≤ 90 or DBP ≤ 60 → 1 pt • Age ≥ 65 → 1 p

What's the benefit of a diabetic patient eating a protein meal?

↑Insulin response w/o ↑plasma glucose

Patient presents with bradycardia, constipation, pseudomyotonia, cold, course skin. What does the thyroid panel show for 1° and 2°?

↑TSH ↓T4 normal TSH ↓T4

What is the thyroid panel for patient w/ tach, thyroid bruit, goiter, warm damp skin, vitiligo, proptosis, nervous, insomnia, palpitation, loose stool, wt loss?

↓TSH ↑T4 High aby: TSH, TPO, TG

Why should we keep A1c under 7%

↓microvascular complications, sometimes macro Really competent patient= encourage stringent goals <6.5%

Pt. presents w/ coughing & production of purulent sputum. If you suspected bronchiectasis, what would you expect to see on CXr?

"tram-tracks" or "ring-shadows"

MCC of cardiac hypertrophy and/or Vent dysfuncgtion

#1 HTN #2 Aortic Stenosis

Obstructive parameters: PFT

(COPD, asthma) Flow-volume loop is caved in *FEV1/FVC ratio < 0.7* decreased VC, *increased TLC*, RV, FRC, increased (RV/TLC), disproportionate

You are highly suspicious that your patient has pneumonia. What is the best FIRST test you should order to aid in diagnosing this patient? If these results return as "inconclusive", what should you consider next?

*1st test = CXR*, IF inconclusive = Chest CT

What test (and results) can be utilized to establish the clinical progression of Interstitial Lung Disease?

*6 Minute Walk Test*; progression is assoc. with a decreased distance walked and an increased degree of oxygen desaturation

High risk characteristics of thyroid neoplasia

*AMES * -Age- males 41+, females 51+ -Metastasis: presence suggest malig. -Extend: extrathryroidal, major capsular involvement -Size: 5 cm

Upon Bronchoalveolar Lavage (BAL) you find milky fluid, foamy macrophages, and *PAS+ lipo-proteinaceous* material in the alveoli. What is the diagnosis? *Other BAL Findings?* bierbeck granules ferruginous bodies non-caseating granulomas on lumen

*Alveolar Proteinosis* • Other BAL findings a. Langerhans histiocytosis - bierbeck granules b. Asbestosis - ferruginous bodies c. Sarcoidosis - -non-caseating granulomas on lumen

Shipyard, Insulation, Lenoleum - What inorganic pneumoconioses is most associated with the following image? Describe the structure of the prominent structure within this image:

*Asbestos* - Ferruginouus body - needlepoint fibers coated with an iron-containing proteinaceous material

A retired fluorescent light bulb factory worker presents to your office with a chronic cough. Upon physical exam, you noticed granulomatous lesions on the skin. CXr reveals bilateral interstitial fibrosis changes. What is the most likely diagnosis of this patient's condition?

*Berylliosis - also associated w/ rockets*

Indications/Contraindications for Mech Vent

*Bipap reduces risk of intubation and mortality* Non-invasive Ventilation - BIPAP or CPAP *Indications* for mechanical ventilation 1. Moderate to sever dyspnea 2. Moderate to severe acidosis 3. Respiratory Freq > 25 bpm *Contraindications* - Respiratory arrest, CN instability, high aspiration risk)

Indications/Contraindications for Mechanical Ventilation

*Bipap reduces risk of intubation and mortality* Non-invasive Ventilation - BIPAP or CPAP *Indications* for mechanical ventilation 1. Moderate to sever dyspnea 2. Moderate to severe acidosis 3. Respiratory Freq > 25 bpm *Contraindications* - Respiratory arrest, CN instability, high aspiration risk)

Symptoms: very COPD-like o Cough + chronic sputum production (thick and string-like) o Both have airflow obstruction and hyperresponsiveness o No smoking Hx o It's the primary infection that they never get over. o Pseudomonas o *Purulent sputum, stringy, thick viscous, hemoptysis (instead of clear with COPD)* Dx: Definition: Pathophys: Mediated by what cell?

*Bronchiectasis* Definition: abnormal permanent dilation of bronchi *neutrophil* (↑ elastase) - Destruction/inflammatory changes of medium-sized airways -↑ elastase --> replaced by fibrous tissue - thick purulent material pools in dilated airways - *bronchial wall vascularity increases

Things to consider in pharmacotherapy of DM

*Certain drugs' impact on wt *Pick glucose-lowering meds not assoc w/wt gain *BMI >35 and DM qualifies for bariatric surgery --helps achieve near normalization of glycemia --requires support and monitoring

During a Bronchodilator Reversibility testing, what is necessary to diagnosis Asthma:

*FEV1* increases more than *200ml and 12%* above pre-bronchodilator FEV1

A patient presents with hemoptysis, SOB, and multiple recent bone fractures. CBC reveals the patient is hypercalcemic and CXr reveals a mass in the lungs. What paraneoplastic syndrome might this patient have, and what is the most likely type of lung mass to cause this condition?

*Hypercalcemia* (of malignancy) - MCC = *Squamous Cell Lung CA (NSCLC)*

Name two types of Granulomatous Reactions associated with interstitial lung disease?

*Hypersensitivity Pneumonitis* - Farmers lung, Ground Glass Opacities *Sarcoidosis* - Sudden substernal CP, elevated ACE + Ca, non-caseating granulomas

Types of Hypoxia

*Hypoxic* hypoxia: From high altitude, recreational use of NO, sleep apnea, COPD or respiratory arrest (decreased ventilation) *Hypemic* (anemic) hypoxia: PaO2 is normal but the oxygen content of blood is reduced ▪ Abnormal Hgb - sickle cell disease, *CO poisoning* *methemoglobinemia* *Histotoxic hypoxia*: O2 delivery is normal but something on the cellular level prevents utilization due to various enzyme deficiencies - *cyanide poisoning* *Ischemic hypoxia*: oxygen content of blood is normal but delivery is decreased due to restricted blood flow (*CAD) - Ischemic heart* CVA

A premenopausal woman presents with a history of frequent pneumothorax, and empysema. Upon questioning, it is revealed she is taking *estrogen*. Based on these symptoms/history, what should you immediately include in your diagnosis? Pathophys? Tx? Cure?

*Lymphangioleiomyomatosis (LAM)* Pathophys: Abnormal muscle cells invade cells to disrupt blood flow and disturbs lymph Tx: Progesterone, & Leutenizing hormone to releasing analogs & discontinue estrogen drugs Cure: Lung Transplant **(LAM) is an indolent, progressive growth of smooth muscle cells throughout the lungs, pulmonary blood vessels, lymphatics, and pleurae. It is rare and occurs exclusively in young women. Symptoms are dyspnea, cough, chest pain, and hemoptysis; spontaneous pneumothorax is common.

A patient presents with a Pulmonary Embolism. What would you expect to see physiologically and diagnostically?

*Physiology* - causes hypoxemia, leads to V/Q mismatching, increases physiological dead space *Diagnostic Test*: D-Dimer (+), EKG - *S1Q3T3*, Wells criteria > 4 (high probability) >/= 3 points: High Risk 1 to 2 Points: Moderate Risk <1 Point: Low Risk

Diagnostic Criteria for Sleep Apnea and scale?

*Polysomnography = sleep study* *Apnea-Hypopnea Index (AHI)* - average number of apneas & hypopneas per hour o Mild OSA - 5-15/hr AHI o Moderate OSA - AHI 15-30/hr o Severe OSA - AHI >30/hr o *RDI: respiratory disturbance index: total # of events (apneas, hypopneas, or RERAs (respiratory effort related arousals)) per hour of sleep Most other labs not useful, except *TSH*

How do you treat amenorrhea in patients who do not improve with estrogen replacement?

*Progesterone withdrawal/challenge*: begin with estrogen balance (replacement) followed by brief treatment with progesterone then removal of progresterone and estrogen tx. menses should begin after progesterone is stopped bc adequate estrogen is on board. don't continue to give estrogen and progesterone

What are the major complications of *OSA*?

*Pulmonary HTN*, ↑ incidence of MVAs, ↑ risk of perioperative complications

Prevention of Future Exacerbation/readmission and improving functional capacity after COPD exacerbation

*Pulmonary Rehab* The single best thing for preventing hospital readmission and improving functional capacity after COPD exacerbation 2nd choice - Methylxanthanes (PDE inhibitor) - Roflumilast - risk reduction of 17%

What therapies have been shown to *decrease mortality* in patients with COPD?

*Smoking Cessation, O2 Therapy, Lung Volume reduction surgery*

Requirement to diagnosis COPD:

*Spirometry* - should not do spirometry in absence of respiratory symptoms (no screening) • Performed *after bronchodilator*, FEV1 determines severity • Obstructive disease: post-bronchodilator *FEV1/FVC <0.7*

A 60 pack-year smoker presents to your office with cough and hemoptysis. CT reveals a centrally-located mass in a patient's left lung. There is no evidence of lymphatic spread, and the mass appears to be contained within the lung parenchyma. Based on this description, What is the most likely type of tumor present? How would stage this tumor? How would you treat this tumor?

*Squamous Cell Lung CA* • How would stage this tumor? Stage I NSCLC • How would you treat this tumor: Surgical Removal

Standard therapies employed in the treatment of Non-Small Cell Lung CA (NSCLC)? Staging Tx

*Stage* • Stage 1 → In lung parenchyma only, NOT lymph nodes • Stage 2 → Spread to local lymph nodes or chest wall • Stage 3a → Spread to mediastinal lymph nodes • Stage 3b → Spread mediastinal structures (Heart, Vessels, Esophagus) • Stage 4 → Distant metastasis to bone, brain, liver *Tx:* • Stage 1 → surgery • Stage 2 → surgery + chemo & rad • Stage 3a → chemo+rad; maybe surgery • Stage 3b → chemo; sometimes rad • Stage 4 → chemo, target drug therapies, clinical trials + supportive/palliative care

Standard therapies for SCLC

*Staging:* Limited: Lung cancer in one lung, and its local lymph nodes Extensive: Cancer extends to both lungs, more distant lymph nodes, or other organs *Tx* Limited: Combined chemo and radiation, rarely surg Extensive: Chemo, Clinical Trials, Supportive/Palliative Care

What is the ONLY pharmacological therapy demonstrated to unequivocally decrease mortality rates in patients with COPD? Indications?

*Supplemental O2* Indications for supplemental O2: o Resting SpO2 of 88% or less o PHTN or RHF <90% o Nocturnal oximetry showing 88% for >5min o 6 min walk test - Desaturations w/ exercise that recovers w/ supplemental O2

list the basophils and acidophils of the adenohypophysis

*acidophils* [these are the ones that have both + and - stimulation from the hypothalamus] -somatotropes -lactotropes *basophils* [these are the ones with only + stim from hypothalamus] -corticotropes -gonadotropes -thyrotropes

A 72 y/o male has COPD as a result of smoking. Laboratory tests would most likely reveal?

*elevated 2,3-BPG* [2,3-BPG] increases in response to chronic hypoxia. Elevated [2,3-BPG] decreases the affinity of Hb for O2 → permitting greater unloading of O2

what gases (present in atmospheric air) are *most soluble*?

*most soluble = CO2 (0.075)* next most soluble = O2 (0.003) *nitrogen & helium are relatively INSOLUBLE gases*

as diffusion occurs across the alveolar membrane, O2 & CO2 move in the (same/opposite) directions

*opposite* O2 moves from within the alveoli, INTO the pulmonary capillaries CO2 moves from within the pulmonary capillaries, OUT into the alveolar air space (for expiration)

where is prostate cancer often found?

*peripheral zone* of the prostate

Spiro w/methacholine challenge is positive...what do you do? Negative?

+ Bronchodilators - Check sputum for eosinophils PPIs for GERD

NEF gene

+ regulatory factor--> increases infectivity In cytosol & works via kinases Down-reg CD4 recept level (prevents tox superinfection of cell)

Describe the theca externa in the secondary follicle?

- CT layer - bundles of collagen fibers and fibroblasts

Psittacosis

- Chlamydophila Psittaci Macrophages have inclusion bodies - Levinthal-Coles-Lillie Bodies

What are features of luteal cells?

- abundant SER (cause steroid producing cells) - lipid droplets - mitochondria with tubular cristae - blood vessels will grow into corpus luteum

The ooplasm (cytoplasm of an oocyte) contains what?

- accumulations of Golgi membranes and vesicles - endoplasmic reticulum - mitochondria - lysosomes

what does the prostate secrete? and one important action

- acid phosphatase, citric acid, fibrinolysin - serve to liquefy the semen - contraction of fibromuscular tissue of the prostate pumps the secretions into the urethra during ejaculation

What are the two cell types in the epithelium of the uterine tube?

- ciliated cells - peg cells

What is a cystic teratoma?

- cystic teratoma - usually benign - contains odd tissues like bone, cartilage, thyroid follicles, hair, etc

What happens to the corpus luteum if fertilization does not occur?

- degenerates - cells undergo autolysis

What happens to the released oocyte if not fertilized?

- degenerates as it passes through the uterine tube

What triggers the release of the oocyte from the mature follicle?

- enzymatic proteolysis of the follicular wall by plasminogen - macula pellucida stops receiving blood and becomes elevated, and ruptures - oocyte surrounded by corona radiata is released from ovary into the peritoneal cavity - oocyte is picked by the extended ostium of the uterine tube

What happens to the follicle after ovulation?

- follicle collapses - bleeding of capillaries in the theca interna into the follicular lumen causes the formation of corpus hemorrhagicum

What is the infundibulum part of the uterine tube?

- funnel like part of the tube - fimbriae (finger-like projections) - traps ovum as it is expelled from follicle

What forms the corpus luteum?

- granulosa and theca interna cells - turn into luteal cells - CT from the stroma invades the antral cavity

What distinguishes a secondary follicle?

- granulosa layer reaches thickness of 6-12 cells - antrum is formed and filled with hyaluronic acid-rich fluid called the liquor folliculi

What are the two types of luteal cells?

- granulosa lutein cells - large, produce progesterone and *convert androgens into estrogen* - theca lutein cells - small, produce progesterone and androgens

what inhibits the follicular development in the ovaries during pregnancy>

- high levels of progesterone produced by corpus luteum

What are the regions of the uterine tube?

- infundibulum - ampulla - isthmus - intramural part

What are the two laters of the muscularis of the uterine tube?

- inner circular layer - thick - outer longitudinal layer - thinner **muscularis is thicker in the isthmus and helps move egg along by peristaltic contractions

Describe the theca interna in the secondary follicle?

- inner highly vascular layer - cells have characteristics of steroid-secreting cells (lipid droplets, mitochondria, well-developed SER, tubular cristae) - cells have LH receptors that when bind stimulate androgens secretion - secrete androgens that are converted into estrogen within granulosa cells

What are changes that occurs in the mature (Graafian) follicle?

- larger cell - theca folliculi becomes more prominent - membrane granulosa becomes thinner as the antrum increases - granulosa cells form a thickened mound called the cumulus oophorus which the oocyte is embedded - corona radiate present

Describe ovarian follicular atresia?

- most follicles go through this - atresia is stimulated by granulosa cells that stop dividing, detach from b.m. And undergo apoptosis - oocyte becomes smaller and degenerates - granulosa is invaded by neutrophils and macrophages to clean up debria - stromal cells fill in with scar tissue

What are ciliated cells in the epithelium of the uterine tube?

- most numerous esp in infunfibulum and ampulla - beating of cilia directs egg toward uterus

What are the three layers of the uterine wall?

- mucosa - musclularis - serosa

Describe multilaminar primary growing follicles?

- multi-layered stratified epithelium around oocyte - follicular cells become granulosa cells - forms stratum granulosum - oocyte cytoplasm contents increase - cortical granules are seen beneath the plasma membrane of an oocyte

What are the peg cells in the epithelium of the uterine tubes?

- non-ciliated secretory cells - produce nutritive material for egg

Where do the uterine tubes open?

- one end in the peritoneal cavity next to the ovary - into the uterus

Describe unilaminar primary growing follicles?

- only one layer of follicular cells - oocyte secretes a protein "shell" (zona pellucida) around itself to separate it from follicular cells - oocyte microvilli project into zona pellucida - follicular cells form microvilli that project into oocyte

What are found in primordial follicles?

- oocyte - large, round, euchromatic - single layer of squamous follicular cells on top of basal lamina

What are the functions of the ovary?

- oogenesis - steroidogenesis - estrogens/progesterones

What is in the cortex of the ovary?

- ovarian follicles embedded into a highly cellular stroma - interstitial glands

What are the parts of the female reproductive system?

- paired ovaries - uterine tubes - uterus - vagina - external genitalia - mons pubis; labia majora/minora; clitoris, and the vestibule

What are the types of growing follicles?

- primary - secondary

The ovarian cortex contains what three types of follicles?

- primordial (earliest stage) - growing - mature (Graafian)

What does the functioning of the corpus lutuem depend on?

- production of human chorionic gonadotropin (Hcg)

What do estrogens/progesterones do?

- promote growth and maturation of the sex organs - form sex characters - prepare sex organs (uterus) for future implantation and pregnancy - prepare mammary gland for lactation

What is the role of cortical granules?

- released after fertilization of the oocyte - make zona pellucida impermeable for other spermatozoa in order to prevent polyspermy

Describe the interstitial glands of the ovarian cortex?

- remnant of atretic follicles - composed of luteal cells - produce hormones - estrogen mainly - more prominent in 1st year of life - then decrease - more abundant in mammals with large litters

What is in the ovarian medulla?

- rich vascular bed and nerves - loose CT

Describe the corona radiata in the mature follicle?

- single cell thick layer of granulosa cells that surround the oocyte - microvilli form gap junctions with those of the oocyte - stays attached to oocyte during ovulation

What is the role of hormones secreted by the corpus luteum?

- stimulate growth and secretory activity of the uterine endometrium in preparation of implantation

What are the two layers of the theca folliculi in the secondary follicle?

- theca interna - theca externa

What are the types of primary growing follicles?

- unilaminar (early) - multilaminar (late)

Usual ductal hyperplasia

-*Increased # of luminal and myoepithelial cells* - > 4 cell layers lining ducts/lobules: mod to florid hyperplasia -Usually incidental -May be assoc with microcalcifications seen on mammogram

Embryologic Derivative Of: --Adenohypophysis --Neurohypophysis --Medullary (chromaffin) Adrenal Cells --Cortical Adrenal Cells --Parathyroid Cells --Thyroid Cells

--Adenohypophysis--Oral Ectoderm --Neurohypophysis--Neural Tube/Ectoderm --Medullary (chromaffin) Adrenal Cells--Neural Crest (ectoderm)--CHROMAFFIN CRESTS --Cortical Adrenal Cells--Mesoderm --Parathyroid Cells--Endoderm --Thyroid Cells--Endoderm

Alveolar macrophages are derived from? Where are they located?

--BLOOD MONOCYTES --SEPTAL WALLS & ALVEOLAR SPACES

How to remember reactions vitamin B1 is involved in?

--Co-factor for TPP (think Trans Pikachu Patient)...he did not look like a female but wanted to B1 --He was a TransKet (trans kid) Transketolase rx (HMP shunt) --Escorted by the PD (Pyruvate dehydrogenase--links glycolysis to TCA cycle) --surprised by the BRANCHED CHAIN Ketoacid dehydrogenase (kid had Down under) --a-ketoglutarate dehydrogenase (A Kig Got Ditched) by his own escape vehicle Tried to act all sweet in the beginning which made the problem worse (Give thiamine BEFORE Dextrose to dec risk of wernicke)

Key Risk factors for Squamous Cell Carcinoma

--EtOH --Smoking --HPV-16 Note: HPV for squamous papilloma & papillomatosis are associated with 6 & 11, not 16.

Where did small granule cells come from? Characteristics? Homologous to (quiz)?

--Evagination of PRIMITIVE forgut --MEMBRANE-BOUNDED, dense core granules at the BASE of the CELL --Homologous to enteroendocrine cells

Tetrad of Narcolepsy

--Excessive daytime sleepiness (chronic 3+ weeks) --Cataplexy (sudden loss of muscle tone) --Hypnagogic hallucinations (as you are falling asleep) --Sleep paralysis

How to remember 5a-reducatse inhibitors

--Finasteride & Dutasteride --Five-a-naster-RED inh.--> inhib type II (sex one--> 2 testicles)--blocks conv. of testosterone to DHT@ male ext genilatia--> dec prostate vol & riks of cancer. AND dec prolif of prostatic epi cells--> dec size of prostate gland --Dutasteride is the SAME but it inhibs DUAL--> both type II & type II. Tx: BPH, Male pattern baldness, hirsutism--makes prostate FINER (smaller) --treats FINE(asteride) hair as well as makes hair FINER on women. Combined w/Tamsulosin AE: impotence, orthostatic hypotension, gyneocomastia --Fi-NASTY-ride or DisASTERIDE (dutasteride)--> LIMP DICK --may faint at said limp dick --they can give a dude some FINEAS$ tiddies, a fine DUO (dutasteride) Tamsulosin w/dutasteride!

MCC of blindness in the world?

--Glaucoma & Diabetic retinopathy your dumba$$ probably thought it was CHlamydia but that is the leading INFECTIOUS cause of blindness in the world.

How to remember androgen receptor antagonists

--Guys don't normally play the flute cause it is seemingly antagonistic to being a man and it is not received well --think Skin flute--> FLUTAMIDE (& Bicalutamide, Nilutamide, Enzalutamide) --we would always compete in band (flute) each year (competitive against our opponents--> antagonists) --Skin flute--> prostate cancer & excess androgen effects in women. AE: Hepatic injury, Hot flashes, diarrhea --FLASHamide, FLUKEamide (flukes can injur liver), TOOTamide--> diarrhea.

How would you treat Hypogonadotrophic hypogonadism if fertility is in question? Restoring male horm level w/o fertility? What acts as a form of birth control?

--HCG or GnRH administration --Testosterone IM, transdermal patch/ gel (Stand. of Care!!) --Testosterone **ORAL T NOT USED

What's the tx of choice for Type 2 Hyperlipoproteinemia? Most important organ for cholesterol removal?

--LDL aphoresis, LDL particle removal --Liver Tx w/meds: statins+chol absoprtive drugs/bile acid sequest. 2a=LDL accum 2b= LDL and VLDL accumulation

What is deficient in Type 1 hyperlipoproteinemia (part of familial chylomicronemia syndrome)? What is elevated? Tx?

--LPL and ApoC-2 --TG >>1000 mg/dl --Dietary fat restriction Childhood w/pancreatitis

Histology of paraganglioma (emphasized a lot so maybe test Q)--also enjoy a nice story...

--NESTS (ZELLBALLEN) of round-oval chief cells (neuroectodermal in origin) --surrounded by delicate vascular septae BOUND by SUSTENTACULAR CELLS --neurosecretory granules on EM Tumor of parasymp (& symp) ganglia. --Carotid body tumor--LOCATION --Since carotid body sense oxygen--> HIGH ALTITUDES contribute to this tumor --LOF mutation in genes for succinate dehydrogenase subunits (remember succinate dehydrogenase is Complex II)--aka conezyme Q --think of 2 MEN (middle aged--50s/60s) climbing mount everest. They are a PAIR/GANG *SLOWLY* traversing the mountain. They require a lot of oxygen (sensed by CAROTID BODY--location of the TUMOR) and the low O2 content is doing them in. --Think of the meme of the guy with NO LEGS climbing mount everest--> What's your excuse? His legs DON'T HURT (this is a slow growing PAINLESS mass).--can also think para cause it is next to the nerve and it is SO SLOW, not compressing it. --the dude also LOST FUNCTION of his legs, which really SUCKS...(LOF mutation)-->2 legs--> COMPLEX II (conezyme Q--SUCKsinate dehydrogenase) --on EM shows nuerosecretory granules --histo--NESTS--ZELLBALLEN of round-oval chief cells. -surrounded by delicate vascular septae bound to SUSTENTACULAR cells --if the pair/gang of dudes get stranded on the mountain, they will have to form a little NEST in the snow....maybe freeballin, maybe ZELLBALLIN, & cuddling--(naked & afraid)

MC pattern of growth for invasive serous carcinoma? What is special about this??

--PAPILLARY growth pattern is MC --MC one sees irregular branching papillae w/cellular budding *Note: precursor to invasive serous carcinoma = SEROUS endometrial INTRAEPITHELIAL CARCINOMA -ALL type II tumors are considered HIGH GRADE (FIGO grade 3)

trachea pulled toward affected side

--SPONTANEOUS pneumothorax--think SUCKED to the SIDE --pneumonectomy --Atalectasis --Agenesis/hypoplasia --Fibrosis

Sarcoidosis story

--Systemic disease, non-caseating granulomas, --African American females --likely CD4 T Helper cells --Smoking does NOT increase risk --3-4th decade --Uveitis --associated w/diabetes insipidous (granulomatous infiltration of posterior pituitary) --↑ serum ACE (not uniformly) --HYPERcalcemia ( ↑ 1-α-hydroxylase → hypervitaminosis D--> can cause hypercalemia and renal failure chronically think- of single BM who is like a loan SHARK--SHARKoidosis--trying to get her child support from all her baby daddies for her 3-4 kids (3-4th decade). --She is on ChilD#4 (CD4), she SMOKES while pregnant because the other kids were NOT AFFECTED. (so she says) --she buys knock off Mac n Cheese (NON-CASEATING sarcoidosis) --Also gets HI(lar lymphnodes) in front of her kids but she thinks she is a good mother who ACEd parenting. --She offered her infant a SIP of her soda, it refused and she told it to DIE (Diabetes insipidous) --she thinks she looks good, but is actually rough on the eyes due to all her pregnancies (UVEITIS)--she looks like a COW--> HYPERcalcemia --She also keeps all of her children in one crowded RHEUM & they feel very RESTRICTED. --At the rate she is reproducing, it would take an ASTEROID (asteroid bodies) to restore the population to normal. --she asks for money online for SHAUS for her kids (SHAUMAN bodies)

What is the Friedewald Formula? What is typically calculated?

--Total Cholesterol= LDL + Trglycerides/5 + HDL --LDL

Which type of familial dysbetalipoproteinemia has accumulation of remannt liproprotien particles and has genetic variation in APO E? Tx?

--Type 3 Hyperlipoproteinemia --Diet responsive; statins, niacins, fibrates More periph vascular dz, premature ASCVD, adult presentation

If VLDL production is increased or degradation is impaired leading to TG between 250-1000. What does the pt have? Tx?

--Type 4 hyperlipoproteinemia (Familial hypertriglyceridemia) --Diet, fibrates, fish oil, niacin (aggressive to avoid pancreatitis) Type 5 is more severe; VLDL and chylomicrons are competing for same degradation path

Most salivary tumors are unilateral EXCEPT

--Warthrin tumors (think both sides go to war) --some pleomorphic adenoma & acinic cell carcinomas

ER+, Her2- Pathway?

--arises by MC pathway --low-proliferation index (luminal A) --high-proliferation index (luminal B) -MC TYPE associated w/BRCA2 germline mutation

What do/don't bronchioles contain?

--basically same morphology as bronchi (but remember NOT CARTILAGE since the lack of cartilage plates is WHEN the bronchi become bronchioles --NO GLANDS (on quiz so probs not on test)

Description and special fact about Sertoli cells

--large, irregular very, light staining, Euchromatic nucelus w/a well expressed nucleolus. -Cellular junctions/occluding/adhrens can DISASSEMBLE & REASSEMBLE **Maybe too obvious of a test Q tho...

What is important about the basement membrane of the TRACHEA? What is important about the LP of the TRACHEA? What happens in smokers?

--resp epi of TRACH (comprised of ciliated pseudo columnar epi) + LP rest on a THICK BM. --BM has WELL-DEVELOPED RETICULAR LAMINA comprised of COLLAGEN! --LP has FIBER RICH ELASTIC LAMINA propria (well developed)--sep from submuc by elastic memb. --SMOKERS--> THICK BM 2/2 irritation.

Formed elements -Leukocytes; basophils

-0.4-1.4% of WBCs -8-10 micron -Lobed nucleus -Basophilic granules containing histamine and herparin

Formed elements -Leukocytes

-1 WBC per 600 RBC -5000-9000/mm^3 Infection - > 12000 (leukocytosis) - < 5000 (leukopenia) -Use blood as transport system via ameboid movement to move thru tissues -Two types: granulocytes, agranulocytes

Path of Sperm

-1.seminiferous tubules (germ cells and sertoli) -A. tubule recti (sertoli w/o germ) -B. rete testis (simple cuboidal) 4. epidymis a. ductuli efferentes (low pseudostrat columnar with CILIATED and nonciliated --> saw tooth look) b. ductus epididymidis (tall pseudostrat columnar with STEREOCILIA) 5. Ductus (vas) Deferens (pseudostrat columnar with long MICROVILLI)--complete w/ ampulla + seminal vesicles = ejaculatory duct (term portion of DD) 7. Prostatic urethra

Anti-RNP

-100% of Mixed Connective Tissue Disorder pts (SLE, systemic sclerosis, polymyositis)

Formed elements -Leukocytes; eosinophils

-2-4% of all WBC; rare -Slightly larger than neutrophils (11-14 micron) -Bilobed nucleus -Granules: cytotoxins, neurotoxin, histaminase

Anti-Centromere Antibodies

-22-36% of pts with scleroderma (usually lcSSC) Correlation with -Raynaud's -CREST syndrome -Primary biliary cirrhosis

Hereditary breast cancer -Li-Fraumeni Syndrome

-3% -TP53 tumor suppressor gene mutation -Sarcoma, leukemia, brain tumors

Hereditary breast cancer -BRCA2

-32% -Less common -Tumor suppressor gene -Breast and ovarian cancer

Formed elements -Leukocytes; monocytes

-4-6% of WBC -Large cells 12-20 micron -Bean/kidney shaped nucleus -Cytoplasm contains many lysosomes and small mito

Hereditary breast cancer -BRCA1

-52% -More common -Tumor suppressor gene -Breast and ovarian cancers -Basal subtype (triple negative)

HLA-B27

-90% ankylosing spondylitis* -80% reactive arthritis -80% Yersinia, Shigella, Salmonella -50% uveitis -8-10% normal population

ds-DNA

-95% specific for SLE -If negative, don't r/o SLE

Vestibular Neuronitis....Symptoms? Longevity?

-A few days-weeks, VIRAL INFECTION -NO HEARING LOSS, vertigo real bad, nystagmus

Angioedema -Source

-ACE-I

Clinical comment -Neutropenia

-Abnormal decrease in # of neutrophils in peripheral blood -Often assoc with autoimmune diseases and is common feature of AIDs -Pts with this condition suffer from bacterial infections more often

Endometrial polyp -Presentation

-Abnormal uterine bleeding -Poss side effect of tamoxifen

Chronic endometritis -Presentation

-Abnormal uterine bleeding, pain -Infertility -*Plasma cells (clock face)*

Anti-SSa, Anti-SSb Antibodies

-Absence of nephritis (lupus) Sjogrens -SSA (40-95%) -SSB (15-85%) -SLE -Neonatal SLE

CRP

-Acute phase protein produced by liver Pros -Rises and falls more rapidly -Not affected by gender, age, pregnancy, temp, drugs, smoking as ESR

Anti-Topoisomerase Antibody

-Aka SLE-70 test -High specificity for scleroderma (22-40%)

Plasma -Proteins

-Albumin (MC) -Globulins: gamma (immuno), alpha and beta globulins (non-immune) -Clotting factors (prothrombin, fibrinogen)

Breast carcinoma

-Almost all breast malignancies are adenocarcinomas and based on expression of estrogen receptor and HER2, divided into 3 maor biologic groups 1- Estrogen receptor pos, HER2-neg (50-60% of tumors) 2- HER2-pos (10-20% of tumors, may be either ER-pos or ER-neg) 3- ER-neg, HER2-neg (10-20% tumors)

Formed elements -Platelets, structure, zones, central, vesicles

-Alpha-granules contain adhesion proteins and clotting factors (such as von Willebrand factor, fibrinogen) -Dense granules contain factors involved in platelet adhesion (serotonin, ADP; serotinin is vasoconstrictor)

Scleroderma -Dx

-Anti-topoisomerase (Scl-70) = diffuse -Posiitve anti-centromere ab = limited

Allergic rhinitis -MOA

-Antiallergy: TH1 (IFN-gamma) -Allergy producting: TH2 (IL-4, 5, 13)

Antinuclear antibody (ANA)

-Antibodies directed against numerous macromolecules seen in cell nucleus -Many AI diseases assoc with + value -Ordre this when CT disease like SLE is suspected due to hx/physical -Specific findings include: photosensitivity, malar rash, alopecia, mouth ulcers, sicca symptoms, Raynaud's phenomenon, inflammatory arthritis or pleuropericarditis

Formed elements -Leukocytes; lymphocytes, B cells, activation

-Antigen exposure -Small lymphocytes (programming), mature -Large lymphocytes -Mitotic divisions (cloning) -Lymphocyte to plasma cell -Plasma cells make antibodies -Humoral immunity

Drug-induced SLE

-Antihistone antibodies

Formed elements -Erythrocytes; characteristics

-Anucleate -8 x 2.5 microns -Biconcave disk (more surface area) -No organelles -Hemoglobin -Transport of O2 -Cell membrane: braced, flexible

Formed elements -Platelets

-Anucleate -Abundant (200k-300k/mm^3) -8-10 day lifespan

Formed elements -Leukocytes; lymphocytes, B cells

-Arise from bone marrow -Reside in lymphoid tissues Programming of lymphocytes (spleen, etc) for -Virus -Bacteria -Foreign proteins -Surface Ig

Formed elements -Leukocytes; lymphocytes, T cells

-Arise from bone marrow and embryonic hemopoietic organs; travel in blood to thymus, where they mature and multiply -After entering blood as mature, characterized by presence of T cell receptor (TCR) and CD3 on the surface

Proliferative breast disease with atypia

-Atypical ductal hyperplasia -Atypical lobular hyperplasia

Clinical comment -Coagulation disorders, thrombocytopenia

-Autoimmune disease caused by deficiency of platelets (< 150k/mm^3) -Antibodies coat platelets -Lifespan 1 day -"Stress" platelets produced by bone marrow in response (large) -Spontaneous hemorrhages (beneath skin and mucous membranes) -Steroid hormone tx

Formed elements -Leukocytes; granulocytes, stains

-Azurophilic granules stain purple (lysosomes) -Specific granules stain dark Blue (Basophilic), orange (eOsinophilic), or no stain (neutrophilic)

Acute endometritis

-Bacterial infection of endometrium; due to retained products of conception

Serum sickness -SSx

-Begin 1-3 weeks after last dose

Sex cord stromal tumors -Fibroma

-Benign fibroblast tumor -*Assoc with pleural effusions and ascites (Meigs syndrome)*

Leiomyoma

-Benign neoplastic proliferation of myometrium due to estrogen -MC female tumor -Grossly well defined, white whorled; multiple often

Drug/latex allergy -MCC

-Beta-lactams (penicillin) -IV route (severe rxns)

Formed elements -Platelets, structure

-Biconvex discoid particles with diameter 2-4 micron -Contain few mito; many granules -Two major parts: peripheral zone, central zone

Formed elements

-Blood cells (RBC, WBC or erythrocyte, leukocyte) -Cell fragments (platelets)

Inflammatory carcinoma

-Breast swelling, hot, tender, with skin thickening -Dermal lymphatic involvement by tumor -Poor prognosis

Complement levels

-C3 and C4 -Looking for consumption of complement (indicates immune complexes have activated complement pathways and use them up)

Formed elements -Leukocytes; lymphocytes, T cells, TH

-CD4+ -Secrete cytokines -Cause change in B-lymphocytes to plasma cells -Promote cell-mediated immunity (activate macrophages and Tc)

Formed elements -Leukocytes; lymphocytes, T cells, Treg

-CD4+, CD25+ -Secrete cytokines -Inhibit other leukocytes -Inhibit autoimmunity

Formed elements -Leukocytes; lymphocytes, T cells, Tc

-CD8+ -Destroy cells carrying the antigen -Release cytotoxins and proteolytic enzymes (causes swelling, lysis, and death of target cell) Ex -Destroy malignant cells; cells carrying virus -Rejection of body transplants

Molecular classes of breast ca by gene expression -HER2 +

-Cancers (amplification and overexpression), 20%

Inflammatory carcinoma

-Carcinoma in dermal lymphatics -Inflamed, swollen breast (like acute mastitis, but abx don't resolve issue)

Invasive ductal carcinoma

-Carcinoma of breast forming duct like structures -MC invasive carcinoma of breast -Tubular, mucinous, medullary, inflammatory

Infectious arthritis -Tx; chlamydia

-Ceftriaxone

Formed elements -Leukocytes; eosinophils, function

-Chemotactic movement to get to area of inflammation or allergic rxn -MC found for parasitic infections and allergic rxns (responsible for modulating allergic response breaking down histamine and inhibiting mast cell degranulation; phagocytize antigen-antibody complexes)

Chronic endometritis

-Chronic inflammation of endometrium due to retained products of conception -Chronic PID, IUD, TB

Formed elements -Leukocytes; monocytes, function

-Circulate thru peripheral blood, adhere to walls of blood vessels, ameboid movement, target object -Become macrophages at tissue

Atypical ductal hyperplasia

-Clonal proliferation having some but not all histologic features of DCIS -Proliferation of monomorphic, evenly placed epithelial cells involving terminal lobular unnits -Partially fill involved duct -1 or 2 completely involved ducts < 2 mm in aggregate dimension -Close follow-upand tamoxifen

Ovarian tumors -Epithelial, malignant (cystadenocarcinoma)

-Complex cysts, thick shaggy lining -Post-menopausal (60-70 yo)

Radial scar

-Complex sclerosing lesion -Stellate lesio of entrapped glands within hyalinized stroma -Can mimic invasive cancer on clinical exam by mammography -Retains myoepithelial layer

Ovarian tumors -Germ cell, cystic teratoma

-Comprised of fetal tissue from 2-3 embryologic origins (skin, hair, bone, gut, etc) -MC germ cell tumor -Benign unless immature neural tissue or somatic malignancy present

Formed elements -Platelets, blood clotting process

-Damage -Platelets adhere to exposed collagen of vessel damaged -Platelets release thromboxane, serotonin, ADP (promote adhesion, vasoconstriction) -Actin/myosin forming platelets slide along each other; cause clot to contract -After adhere, platelets release alpha-granules containing platelet thromboplastic factor (PTF) -PTF converts prothrombin to thrombin -Thrombin converts fibrinogen to fibrin -Fibrin forms meshwork of fibers in area of damage; act as skeleton for clot -Platelets provide sticky surface for clot assembly

Angioedema -Acquired; Dx

-Decreased C1q

Angioedema -Hereditary; Dx

-Decreased C4

Formed elements -Erythrocytes; hemoglobin, pathologies, hypochromic anemia

-Decreased amount of hemoglobin in RBCs -Can be due to trauma and blood loss, or can be caused by genetic disorders that have to do with iron utilization by RBCs in bone marrow (atransferrinemia), or can be caused by iron deficiency

Platelet count

-Decreased from anti-platelet antibodies in SLE -Increased secondary to inflammation

WBC count

-Decreased if anti-WBC antibodies in SLE or from immunosuppression therapy

Hgb/Hct

-Decreased in anemia of inflammatory disease (chronic) -Hemolytic anemia in SLE

Formed elements -Erythrocytes; formation

-Depends on utilization of iron, recycled from RBCs destroyed in the spleen and liver -Average lifespan 120 days; senile ones become phagocytized by macrophages in spleen/liver -Heme is broken down to bilirubin

HPV -E7 protein

-Destroys Rb (removes antiproliferative effect)

HPV -E6 protein

-Destroys p53 (G1-S phase tumor suppressor)

Endometriosis

-Displaced endometrial glands and stroma (outside uterine endometrial lining)

Plasma -Inorganic components

-Dissolved gases -Electrolytes, etc.

Carcinoma in situ

-Ductal -Lobular -Malignant clonal cell population limited to ducts and lobules by basement membrane -8-10x risk of breast cancer

Invasive breast carcinomas -Histologic types

-Ductal (no special type) 80% -Lobular 10% Other -Medullary -Mucinous/colloid -Tubular -Papillary -Metaplastic

BUN/Cr

-Elevated from renal disease; drug toxicity

Creatine kinase, aldolase, LDH, AST/ALt

-Elevated in inflammatory muscle disease (polymyositis, dermatomyositis, inclusion body myositis, juvenile dermatomyositis)

Adenomyosis

-Endometriosis involving uterine myometrium

Extramammary Paget disease -Presentation

-Erythematous -Pruritic, ulcerated vulvar skin

Paget disease of breast

-Extension of DCIS into lactiferous ducts and into nipple skin = unilateral red crusted lesions of nipple/areolar skin

Acute endometritis -Presentation

-FEVER -Pelvic pain -Abnormal uterine bleeding after deliver or miscarriage

Rh blood group system -Erythroblastosis fetalis

-Fetal hemolytic disease, occurring when Rh+ newborns delivered by Rh- mothers and results in immune rxn of anti-Rh IgG passed across the placenta from mother -Anti-Rh antibodies produced by mom in response to Rh antigen expressed on fetal RBCs that can leak into her circulation during pregnancy -Administer anti-Rh antibodies (RhoGAM) to mother during pregnancy and after parturition destroys any circulating Rh(D)+ fetal RBCs that persist in mothers blood, thus preventing Rh-incompatibility rxn in future pregnancies

Stromal tumors, breast

-Fibroadenoma (common) -Phyllodes tumor (rare)

Phyllodes tumor

-Fibroadenoma-like tumor with overgrowth of fibrous component -Post-menopausal; leaf-like projections on biopsy

MCC of palpable breast mass in pts betw 25-50? Under 25?

-Fibrocystic changes of breast -fibroadenoma

Pap smear recommendations

-Fist at age 21, or within 3 years of onset of sexual activity; every 3 years thereafter After age 30 -Neg for high risk HPV: 5 years -Pos for high risk HPV: 6-12 mos

Embryonal rhabdomyosarcoma -Presentation

-Grape-like mass protruding from vagina or penis < 5 yo -Stains + for desmin, myogenin

Endometrial hyperplasia -Categorization

-Growth pattern (simple, complex) -Presence of cellular atypia (important predictor for carcinoma progression)

Urticaria -Tx

-H1 antihistamines; H2

Formed elements -Erythrocytes; formation, process

-Heme broken down to bilirubin; RBCs phagocytized -Iron is bound to Ferritin (iron-protein complex, aka hemosiderin) which is reincorporated into erythroblasts in bone marrow by endocytosis -Process depends on B12; B12 absorption depends on intrinsic factor in stomach (deficiency results in anemia)

Blood -Characteristics

-Human adults have ~6 L -Formed elements (RBC, WBC, platelets); plasma

Endometrial polyp

-Hyperplastic endometrium

ABO system -Blood transfusion

-If transfused with blood of an incompatible type, recipients antibodies will attack donor erythrocytes, causing hemolytic transfusion rxn destroying RBCs

Allergic rhiniits

-IgE mediated

Major prognostic factors in breast cancer

-In situ tumor > 95% surival Axillary lymph node metastases -No + nodes 70-80% 10-yr -1-3 + nodes 35-40% - > 10 + nodes 10-15% -Distant metasasis -Tumor size -Local involvement -Dermal lymphatic involvement -Estro/prog receptor status -HER2/neu statis -Proliferative rate

Endometrial hyperplasia

-Increased # of glands relative to stroma due to unopposed estrogen (obesity, PCOS)

Breast carcinoma -Established high risk factors

-Increasing age; women > 50 peaking 75-80 -Female gender -BMI > 30 -First-degree relative with breast ca -Previous breast biopsy showing proliferative disease with atypical hyperplasia -White rate -Estrogen levels

Metabolism of: -Indacterol (ultra LABA) -Dapsone (folic acid synth inhib)

-Indacterol CYP3A4 -Acetylation & glucuronidation

ESR

-Inflammatory marker -Not specific -Measures acute phase proteins -Higher with age, women

Hereditary breast cancer

-Inheritance gene or gene is primary cause of 12% breast ca -3% attributed to BRCA1, BRCA2 -9% familial ca though to be due to inheritance of multiple genes with weak effects Hereditary etiology probability increases with risk of -Multiple first-degree rel -Tumor before menopause -Male breast ca (BRCA2) -Fam members also develop ovarian ca (BRCA1 and 2)

Phyllodes tumor

-Intralobular stromal orgin -Fast-growing, usually > 40 yo -Small to massive size -Distinguished from fibroadenoma by stromal cellularity, mitoses, nuclear pleiomorphism, and infiltrating borders -No excision with wide margins -No nodal mets, but rarely hematogenous metastasis

Invasive lobular carcinoma

-Invasive carcinoma growing in single file pattern, due to lack of E-cadherin -Cells may have signet ring morphology

Cervical intraepithelial neoplasia (CIN)

-Koliocytic change -Disordered cell maturation -Nuclear atypia -Increased mitotic activity within cervical epithelium

Formed elements -Leukocytes; lymphocytes, NK cells

-Large lymphocytes -Innate immunity Programmed during development to -Kill certain virus-infected cells -Some tumor cells -Some degree of body transplant rejection

Formed elements -Leukocytes; lymphocytes, morphology, small

-Large spherical or slightly indented heterochromatic nucleus surrounded by tiny rim of cytoplasm -Cytoplasm contains ribosomes, few mito, inactive RER and Golgi -Circulate thru blood and internal organs, mature, divide

Lichen sclerosis chronicus -Presentation

-Leukoplakia -Thick, leathery vulvar skin; chronic irritation and scratching

Molecular classes of breast ca by gene expression -ER+, HER2 -

-Luminal; MC 40-45%

Formed elements -Leukocytes; neutrophils

-MC WBC; 55-70% of all -3000-6000/mm^3 -Fairly large (10-12 microns) -Multilobed nuclei (2-4 lobes); 2nd X-chromosome on females creates Barr body/drumstick-shape

Fibroadenoma

-MC bening tumor of breast -3rd decade -Discrete, movable, painless mass -Size < 1 cm to large tumors -Grossly well-circumscribed, rubbery nodule -Tx: shelled out, no need for wide excision

Invasive breast carcinomas -Ductal

-MC breast malignancy -Desmoplastic fibrous stromal response typical -Heterogenous microsopic patterns, with tumor grading based on tubular formation, nuclear pleiomorphism, mitotic rate -2/3 espress E or progesterone receptors -1/3 overexpress HER2 protein

Breast cancer

-MC non-skin malignancy in women -Second only to lung cancer -Invasive breast carcinoma 70-85% -In situ carcinomas 15-30% of which 80% are ductal carcinoma in situ

Ovarian tumors -Epithelial

-MC ovarian tumor (70%) -Serous, mucinous types -Benign, borderline or malignant classes of each type -BRCA1 increases risk for serous -Poor prognosis

Anaphylaxis -Triggers

-MCC: food

Ectopic pregnancy

-Main risk factor: scarring due to PID, endometriosis -Lower quadrant abdominal pain a few weeks after missed period

RF

-Major marker of RA -Not + in all RA pts; approx 80% of RA are + -False + in 5-10% of population

Sex cord stromal tumors -Granulosa-theca cell tumor

-Malignant -Presents with signs of estrogen excess

Invasive breast carcinomas -Ductal, micro; and CIS

-Malignant cells infiltrating surroudning area -CIS inside

Extramammary Paget disease

-Malignant epithelial cells in epidermis (cercinoma in situ) of vulva; no underlying carcinoma

Lobular carcinoma in situ

-Malignant proliferation of cells with no invasion of basement membrane -Does not produce mass or calcifications

Ductal carcinoma in situ

-Malignant proliferation of duct cells (ducts connect lobules with nipples) without basement membrane invasion -Does not produce mass -Calcifications seen on mammogram (cells within duct die due to lack of blood, calcification results)

Endometrial carcinoma

-Malignant proliferation of endometrial glands -MC invasive carcinoma of female GU tract

Leiomyosarcoma

-Malignant proliferation of smooth muscle from myometrium

Embryonal rhabdomyosarcoma

-Malignant tumor of skeletal muscle -Rare malignant proliferation of immature skeletal muscle

Ovarian tumors -Germ cell, yolk sac (endodermal sinus)

-Malignant tumor, mimics yolk sac -MC germ cell tumor in children -Elevated alpha-fetoprotein -Schiller-Duval bodies (glomerulus-like structure)

Invasive ductal carcinoma -Presentation

-Mass; dimpling of skin or retraction of nipple -Biopsy shows structures in desmoplastic stroma

OA -Presentation

-Matrix metalloproteases (inflammatory mediator)

Sclerosing adenosis

-May mimic breast cancer -Firm, rubbery consistency -Morph: increased # of acini per terminal duct and architectural distortion due to fibrosis -Relatively well circumscribed (non-infiltrative) margins -Presence of myoepithelial layer

Intraductal papilloma

-May occur as single lesion or multiple foci -Large duct pailloma occurs within lactiferous duct, often subareolar -Clinical: unilateral serous or bloody discharge -Multiple small duct papillomas assoc with slightly increased risk of breast cancer

Sex cord stromal tumors -Sertoli-Leydig

-May produce androgens, sertoli cells from tubules; Leydig cells from Reinke crystals -Masculinization or defeminization

Krukenberg tumor

-Metastatic mucinous tumor -Involves both ovaries -Commonly due to gastric carcinoma (signet cells)

RA -Tx

-Methotrexate (1st line)

Cervical carcinoma -Presentation

-Middle aged (40-50) -Vaginal bleeding (esp post-coital) -Cervical discharge

Ovarian tumors -Germ cell, choriocarcinoma

-Mimics placental tissue; malignant tumor comprised of cyto- and syncytiotrophoblasts, no villi -Small hemorrhagic tumor -beta-HCG (produced by syncytioblasts)

Formed elements -Leukocytes; agranulocytes

-Mononuclear -Granules: azurophilic (few), NO specific granules -Types: lymphocytes, monocytes -*Capable of mitosis* -Longer lifespan

Gout -Dx

-Monosodium urate crystal

Paget disease of breast -Micro

-Mucin stains purple; melanoma will not produce mucin

Lobular carcinoma in situ -Presentation

-Multifocal, bilateral, cells lack E-cadherin adhesion protein -Pre-menopausal

Criteria to use anti-IgE (3)

-Must be 6 years or older -Elevated IgE -evidence of sensitivity to PERENNIAL AEROALLERGEN

Scleroderma -Tx

-Nifedipim (CCB) -> Raynaud's -HTN/renal -> ACE-I

Perennial non-allergic rhiniits

-No IgE

Lobular carcinoma in situ

-No mass lesion clinically/no mammographic density -1/3 develop invasive ca -Often multifocal, bilaterla, so increased risk of invasive ca in either breast -Not assoc with calcifications -Prior to menopause -Typically ER/PR +; HER2/neu - -Lack expression of E-cadherin (DCIS is +)

Antinuclear antibody (ANA) -If negative

-No need to check ANA "panel"

Anti-Smith Antibodies

-Nuclear protein -3-10% of white pts with SLE; 30% in black and Chinese

Breast carcinoma clinical features

-Occult -Palpable mass lesion or prominent nodes -Skin dimpling -Nipple retraction -Nipple discharge -Dermal edema -Mass with overlying skin ulceration

Carcinoma in situ -Ductal

-Often identified by calcifications on mamogram Subtypes -Comedo and noncomedo Comedo DCIS -Lesions show high grade cytology are frequently negative for estrogen receptor expression; show frequent amplification of HER2/neu gene aneuploid; tp53 mutations Noncomedo DCIS -Wide variety of patterns

Oral manifestation of infectious mononucleosis?

-PALATAL PETECHIAE ** -acute pharyngitits/tonsillitis -enlarged lymph nodes in neck

Gout -Tx

-Pain: Colchicine -Control: allopurinol -Don't eat tuna, herring; alcohol, red meats sparingly

Lichen sclerosis

-Paper like skin -Thinning of epidermis and thickening/fibrosis of dermis -Benign; slight increase in SCC risk

Intraductal papilloma

-Papillary growth into large duct; fibrovascular projections Presentation -Nipple discharge-bloody -Pre-menopausla women

Formed elements -Leukocytes; neutrophils, functions

-Perform selective phagocytosis of bacteria and are part of cell-mediated immunity -Binding of chemotactic agents causes release of *tertiary and neutrophilic granules* -"Kamizake" cells -Form the pus (dead cells, bacteria) -Produce IL-1; induces increased body temp

OA -Tx

-Physical therapy, weight loss (1st line)

Formed elements -Erythrocytes; hemoglobin, pathologies, Sickle cell

-Point mutation in beta-globin chain of HbA producing abnormal type (HbS) -HbS tends to aggregate under conditions of reduced oxygen causing erythrocytes to fold and become sickle-shaped

Formed elements -Leukocytes; granulocytes

-Polymorphonuclear (nucleus divided into lobes) -Granules: azurophilic (primary lysosomes) and specific -Types neutrophils, eosinophils, basophils -Amitotic -Short lifespan of few days -Die via apoptosis if not activated

Lichen sclerosis -Presentation

-Post-menopausal -White patch (leukoplakia); parchment like vulvar skin

Endometrial hyperplasia -Presentation

-Post-menopausal bleeding -Need to r/o cancer

Leiomyoma -Presentation

-Pre-menopausal (50 yo) -Abnormal uterine bleeding, pelvic mass, infertility possible

Anti-Histone Antibodies

-Present in 95% of drug-induced SLE; 50% of idopathic SLE -Not correlated with disease activity, but may reflect possible joint disease prevalence -Seen in RA: 14% low titer

Ovarian tumors -Epithelial, presentation

-Present late with vague abdominal sx (pain fullness) -Can spread to peritoneum

Formed elements -Leukocytes; neutrophils, life cycle

-Produced in bone marrow, released into blood -Spend ~7 hrs in blood -Triggered by cytokines produced by endothelial cells, they adhere to walls and form marginating pool -Then migrate into tissue thru endothelium of post-capillary venules and become tissue neutrophils

Clinical comment -WBC cancers, chronic lymphocytic leukemia

-Progresses slowly -Involves partially differentiated cells -MC in adults -Responds poorly to tx, but in many cases is rather indolent

Atypical lobular hyperplasia

-Proliferation of cells identical to those of lobular carcinoma in situ, but cells do NOT fill or distend more than 50% of the acini within a lobule -Incidental finding

Formed elements -Erythrocytes; hemoglobin

-Protein specialized for transport of O2, CO2 -Consists of 4 protein subunits, each bound to a heme (iron containing portion) 3 types -HbA (MC, 96%; 2 alpha, 2 beta chains) -HbA2 (1.5-3%; 2 alpha, 2 delta chains) -HbF (< 1%; 2 apha, 2 gamma chains)

Scleroderma -MCC death

-Pulmonary interstitial disease

Where in the respiratory system do we find Goblet cells?

-RESPIRATORY SEGMENT (epithelium) -TRACHEAL MUCOSA -BRONCHI-- MUCOSA

Clinical comment -WBC cancers, acute lymphocytic leukemia

-Rapidly progressive blood cancer -Involves undifferentiated precursor cells -MC in children -Responds well to tx

Male breast cancer

-Rare Risk factors -First degree -BRCA2 -Klinefelter -Hyperestrinism *Gynecomastic not risk factor

Paget disease of breast

-Rare manifestation of breast 1-4% -Extension of DCIS into lactiferous ducts and into nipple skin -Underlying invasive carcinoma 50-60% -Clinical: unilateral red crusted lesion of nipple/areolar skin -Micro: epidermis permeated by malignant cells with clear cytoplasm, often mucin +

Ovarian tumors -Germ cell, dysgerminoma

-Resembles oocytes, tumor of large cells with clear cytoplasm, central nuclei -*MC malignant germ cell tumor* -Elevated serum LDH

Sex cord stromal tumors

-Resembles sex cord stroma of ovary Types -Granulosa-theca cell -Sertoli-leydig -Fibroma

Clinical comment -Hereditary spherocytosis

-Result of spectrin mutations -Membrane not properly braced and RBCs are not able to sustain the biconcave shape and become spherical -RBCs are fragile and are easily destroyed

Endometriosis -Presentation

-Retrograde menstruation; dysmenorrhea, pelvic pain which is cyclic with menstrual cycle

Cervical carcinoma -MC

-SCC (80%) -Adenocarcinoma (15%)

Antinuclear antibody (ANA) -R/o

-SLE r/o if negative -Test not useful for monitoring disease -1:40 titer is cutoff; 32% of general population have + value, 12% are + at 1:80

Lupus -Dx

-SOAP BRAIN MD (4/11; simultaneous or at different times)

HIV -MC skin manifestation

-Seborrheic dermatitis

Formed elements -Leukocytes; lymphocytes

-Second MC WBC at 20-30%; *MC agranulocytes* Vary in size (6-14 micron), depends on stage of development -Small 6-8 micron -Med 8-10 micron -Large 10-14 micron

Ovarian tumors -Germ cell

-Second MC ovarian tumor (15%), reproductive age Tumor subtypes resemble tissues normally produced by germ cells: -Cystic teratoma -Dysgerminoma -Endodermal sinus tumor -Choriocarcinoma -Embryonal carcinoma

Ovarian tumors -Epithelial, benign (cystadenoma)

-Single cyst with flat lining -Pre-menopausal (30-40 yo)

Formed elements -Leukocytes; basophils, function

-Slightly phagocytic; major function to produce histamine -Similar to mast cells; when exposed to antigen they degranulate -Release of basophilic granules results in allergic rxn causing vasodilation, bronchoconstriction -Most commonly found in peripheral blood during chronic granulocytic leukemia and chicken pox Basophils Bronchoconstriction, Chronic Granulocytic Leukemia, Chicken pox

Anti-citrullinated cyclic peptide (Anti-CCP)

-Specificity for RA: 97% -Assoc with erosive RA

Formed elements -Leukocytes; lymphocytes, T cells, types

-T helpers (TH) -T regulatory (Treg) -Cytotoxic (Tc)

Signs of clinical stability post-pneumonia

-Temp<37 -HR <100 -SBP >90 -SpO2 >90% or PaO2 >60 on RA -Ability to maintain oral intake -normal mental status

Lichen sclerosis chronicus

-Thickening of skin, hyperplasia (increased cell number) of vulvar squamous epithelium -Benign with no increased risk of SCC

Blood -Functions

-Transport for O2, CO2, nutrients, waste -Acts as buffer -Regulates temp, hormone levels, pH, osmotic pressure -Clots if exposed to air

Molecular classes of breast ca by gene expression -ER -, PR - , HER2 -

-Triple negative; basal like

Hydatiform mole

-Trophoblast proliferation characterized by swollen and edematous villi -Snowstorm appearance and absent heart sounds on US -Grape-like mass in vaginal canal

Allergic rhinitis -Tx

-Tx for 3-5 years -Shift TH2 to TH1

Adenomyosis -Presentation

-Uniformly enlarged uterus -Menometorrhagia -Colicky dysmenorrhea; dyspareunia/pelvic pain

Anaphylaxis -SSx

-Urticaria, angioedema (MC) -Laryngeal edema (2nd)

Proliferative breast disease without atypia

-Usual ductal epithelial hyperplasia (mod or fibroid) -Sclerosis adenosis -Intraductal papilloma -Radial scar -1.5-2x risk of breast cancer; fam hx increases risk

Invasive breast carcinomas -Lobular

-Usually presnet as palpable mass or mammographic densities -Small monotonous cells, linear infiltrative pattern (lack expression of E-cadherin); loss CDH1, gene -Almost all express hormone receptors -HER2/neu exprssion unusual

Anaphylactoid -In kids

-Viurs + beta lactam = rash

Blood -Hematocrit

-Volume of blood which is composed of cells relative to total volume -Healthy individuals have about 47-48% value; plasma value about 52%

c-ANCA, PR3-ANCA

-Wegener granulomatosis

6 aspects of the Chronic Disease Model of Care

-an organizing framework for improving chronic illness care (and care in general) at both the individual and population level 1. Health System 2. Self-management support 3. Delivery System design 4. Decision support 5. Clinical information Systems 6. Community-resources & policies

Leiomyosarcoma -Presentation

-de novo origin -Post-menopausal (70-80 yo) -Singular lesion with necrosis and hemorrhage

what happens to these hormones during: SHORT TERM FAST -insulin -glucagon -GH -Catecholamines -cortisol

-insulin DOWN -glucagon UP -GH +- -Catecholamines +- -cortisol DOWN

what happens to these hormones during: INDUCED HYPOGLYCEMIA -insulin -glucagon -GH -Catecholamines -cortisol

-insulin DOWN -glucagon UP -GH UP -Catecholamines UP -cortisol UP

what happens to these hormones during: LONG TERM FAST -insulin -glucagon -GH -Catecholamines -cortisol

-insulin DOWN -glucagon UP -GH UP -Catecholamines UP/+- -cortisol +-

what happens to these hormones during: EXERCISE -insulin -glucagon -GH -Catecholamines -cortisol

-insulin DOWN -glucagon UP/+- -GH UP -Catecholamines UP -cortisol UP

How does maximum forced expiratory flow change w/ lung volume? Why? How does maximum expiratory flow change w/ obstructive disease? Why?

-it's proportional to lung volume b/c of elasticity -it decreases b/c decrease in elastins

Epithelium of the larynx? (any importance?)

-larynx supp by Hyaline & Elastic cart. --lined w/CILIATED PSEUDOSTRATIFIED COLUMNAR EPITHELIUM that changes to STRATIFIED SQUAMOUS (in areas of high abrasion like EPIGLOTTIS & VOCAL CORDS)

Tracheotomy care

-maintain/secure airway for 48-72 hrs, wait 3-5 days before any trach changes -Change inner cannula q shift/day -HUMIDIFY, provide skin care, -cuff pressure needs to be LESS THAN 25 cm HG (to decrease scarring)

(+) for Auer rods

-refractory anemia w/ excess blasts-2 -acute myeloid leukemias (in myeloblasts) -acute promyelocytic leukemia (hypergranular form) however, NOT seen in: -microgranular form of APL -isolated del(5q) -refractory cytopenia w/ multilineage dysplasia -refractory anemia w/ excess blasts-1 -AML M0

How is synthesis of TH related to its release? What are the steps in synthesis of T3 & T4?

-synthesis is INDEPENDENT of release -Thyroglobulin-synth in RER/Gogli of follicular cells--> sec to lumen of follicle --Iodide transport from blood--> cytoplasm. --on *apical membrane* iodide is oxidized--> iodine & immediately rel. to colloid (TEST Q prediction) --Iodination of thyroglobulin--> T3 or T4 stored in lumen (still linked to thryo) --TSH causes follicular cells to *reabsorb the colloid* --Thyroglobulin destroyed by lysosomes. --T3 & T4 released (1:20)--> cross plasma membrane---> blood

Type 1 hyperproteinlipenemia

1 LP, ApoC (2), high TG, achilees Diet

What GPCR do the following adrenergic R coupled with? 1) alpha-1 2) alpha-2 3) beta 1 & 2

1) Gq - Ca release, smooth m. contraction--think there is only ONE Alpha snake and that is the king Qobra (ik its wrong)--they also contrict things--think of a giant snake so this is the PENIS way of remembering things...Giant PrettyLargeC0ck Does Infact PromoteKinkyC0ck touching. 2) Gi - decreases neurotransmitter release & decreased cAMP (smooth m. relaxation)--Think Gi's think they are the alpha top dog when really their wife has a 2nd guy back home. A2--> remember Giant A$$es Can PromoteKinkyA$$ Touching 3) Gs - increases intracellular cAMP *enhancing smooth m. contraction *smooth muscle relaxation *glycogenolysis remember B1 & 2 is considered "everything else"

what are the primary and secondary missions of IGF?

1- growth 2-metabolic (long term carb metabolism reg)

House-Brackmann Facial Nerve Grading System

1- normal 2-SLIGHT weakness, slight asymmetry 3. Clear difference between hemifaces, but not total asymmetry, can CLOSE EYES with EFFORT 4. INCOMPLETE CLOSURE of EYES, NO MOVEMENT of forehead 5. Asymmetry at rest 6. no movement in any part of the face

Histological Buzzwords for: 1. Nasopharyngeal Angiofibroma 2. Fibroblast plugs withIN alveolar spaces 3. Exophytic/fungiform pattern 4. Asthma 5. Warthrin tumors (gross) 6. Kuttner Tumor 7. LAM

1. "Staghorn appearance," (looks like erectile tissue w/resp epi) 2. COP (formerly BOOP--think you BOOP the snoot which are AIR HOLES) 3. Sinonasal papilloma 4. Smooth muscle hyperplasia, excess mucus/inflammation 5. Motor oil--> if yo man can't change yo motor oil he is warthless 6. Kuttner--Chronic Sclerosing Sialadenitis* *firm enlargement of submand gland mistaken for maligancy. Cirrhotic changes w/destruction of acinar cells. 7. Benign lesions derived from PERIVASCULAR EPITHELIOD CELLS

Explain how (and the conditions) at which GH affects... 1. Glucose 2. Adipose 3. Amino Acids 4. Protein synthesis

1. & 2.--DECREASES glucose & adipose UPTAKE in muscle ONLY @ PHARMACOLOGIC doses of GH 2.--STIMULATES LIPOLYSIS in adipose ONLY @ PHYSIOLOGICAL GH doses. 3. STIMULATES AA UPTAKE & PROTEIN SYNTHESIS in MUSCLE & LIVER.

rule of 10's for pheochromocytoma

1. 10% extra-adrenal (more likely to be malignant) 2. 10% of sporadic adrenal pheochromocytomas are bilateral 3. 10% arise in setting of MEN-2A, or 2B 4. 10% of adrenal pheochromocytomas are biologically malignant (w/mets) 5. 10% are NOT associated w/HTN

Describe HIVs: 1. genome 2. Envelope proteins 3. Other protein? 4. lipids

1. 2 strands of RNA, 9749 nucleotides 2. gp120 (heavily glycosylated protein) is bound to gp41 (integral memb protein) 3. Inner memb prot P17 (attached to inner surf of viral envelope via fatty acid acylation) &Core protein 4. lipid in viral envelope are from T4 lymphocytes' plasma memb

1. Ras genes encode __________ and they show similarity to _________ because _______ 2. Mutations in Ras __________

1. 21 kDa proteins, similar to G proteins cause they BIND & HYDROLYZE GTP 2. Mutations in Ras: a. inc or dec PKC activity b. altered PKC activity--> phosphorylation of effector genes, which are vital for control of *cell proliferation*

1. Primary sermatocytes that enter meiosis are.... 2. Cells after 1st mitotic division are... 3. Cells after 2nd mitotic division are... 4. What types of cells have golgi phase, cap phase, acrosome phase, & maturation phase? 5. Order of Types of Cells starting at spermatogonia

1. 2N/4C 2. N/2C 3. N/C 4. Spermatids! 5. Spermatogonia, Spermatocyte, Spermatid, Spermatazoan

Explain steps of vitamin D formation and where they occur What regulates metabolism of Vit D

1. 7-dehydrocholesterol--> Vitamin D3 (skin) via photolysis rxn 2. Vitamin D3 (delivered to liver)--> 25(OH)-D3 via 25 hydroxylation in the ENDOPLASMIC RETICULUM via NADPH-dependent cytochrome P450 reductase & cytochrome P450 3. 25(OH)-D3 enters circulation & transported via vit D binding protein to Kidney 4. In Proximal renal tubule 25(OH)-D3--> 1, 25(OH)D3 via NADPH, Mg++, molecular oxygen and *1-alpha hydroxylase* Soooo...Low Ca++ diet and hypocalcemia--> INCREASE in 1-a-hydroxylase activity High levels of 1,25(OH)2-D3 inhibit renal 1 a-hydroxylase and INCREASE activity of 24-hydroxylase producing INACTIVE 24,25(OH)2-D3 analog (PREDICTION)

1. Causes of Primary osteoporosis 2. Causes of secondary osteoporosis

1. A. Decreased GH/IGF and gonadotropin/sex steroid hormones w/age. B. Juvenile C. Idiopathic (young/middle aged) 2. A. CT disease B. Immobilization C. Endocrine--hypogonadism, hypercortisolism, hyperthyroidism, hyperparathyroidism, cancer

BUZZWORDS: What (in respiratory system) contains: 1. larger blood/lymphatic vessels, & nerves 2. fiber-rich, elastic, well-developed lamina propria 3. Loose CT w/glands & Adipose tissue 4. Ducts of glands that extend THRU LP on open surface--> secrete glycoproteins 5. Contains BALT 6. loose connective tissue & seromucous glands 7. Moderately dense CT (adjacent to pulmonary artery & lung parenchyma)

1. ADVENTITIA of the TRACHEA 2. LP of the TRACHEA 3. SUBMUCOSA of BRONCHI--bodacious bronchi be FAT 4. SUBMUCOSA of TRACHEA 5. SUBMUCOSA of BRONCHI (it's in the name) 6. SUBMUCOSA of TRACHEA 7. ADVENTITIA of BRONCHI

1. Gold Standard for Tb 2. How to rule out?

1. AFB 2. 3 negative sputum cultures 6 mos Tx --> culture - OR culture +, CXR-, HIV- 9 mos Tx-- Culture + & CXR cavitation + Culture + & CXR -, HIV +

Exam finding of PTA

1. ANTERIOR PILLAR fullness (actually peritonsillar space) 2. Uvula shifts away (obviously cause the fluid is building up)

4 statin benefit groups

1. ASCVD score of over 7.5% 10 yr risk and age 40-75--NO DIABETES 2. Diabetes: age 40-75 and LDL 70-189 3. Age 21+ AND LDL>190 4. Clinical ASCVD NOTE: if pt is NOT diabetic but they give age and LDL is NOT above 190--THEY MUST GIVE ME ASCVD % or else unable to answer Qs If pt needs high intensity--> Atorvostatin 80, Rosuvastatin 20 If they need low--> Pravastatin 10-20 or Lovastatin 20

1. MC tumor of the palate 2. 2nd MC tumor of the palate 3. 2nd MCC of hoarseness in children 4. MCC of recurrent respiratory papillomatosis

1. Adenoid cystic carcinoma (minor salivary glands) 2. Polymorphous low grade adenocarcinoma (located in minor salivary glands) 3. Recurrent respiratory papillomatosis 4. HPV 6 & 11

1. When can eclampsia/HTN be diagnosed? When does it most commonly begin? 2. Biggest risk factor for this? 3. MCC surgical emergency is appendicitis but what is the MC perinatal complication? 4. 2nd MC surgery in pregnancy

1. After 20 weeks--can diagnose, most often dx after week 32 2. Biggest risk factor is 1st pregnancy 3. MC perinatal complication--> Pre-term labor 4. Gallbladder

Adverse prognostic factors of Papillary Thyroid Carcinoma

1. Age >40 2. Extra-thyroidal extension 3. Distant metastases to lungs/other organs METS TO CERVICAL LYMPH NODES DOES NOT worsen prognosis

1. Laminin receptors ______ 2. Integrins bind to _____ 3. the main serine protease produced by tumor cells

1. Aid in attaching cells to BM 2. bind to variety of adhesion mol aiding tumor cells in binding to ENDOTHELIUM BEGINNING process of extravasation (*RGD sequence*) 3. Plasminogen activator (Urokinase type)--> mice w/o uPA can't get mets.

1. Origin of ameloblastoma? 2. MC submandibular & minor salivary gland malignancy 3. Develops from long-standing pyogenic granuloma or de novo from cells of periodontal lig

1. Ameloblastoma--From Odontogenic epithelium, commonly cystic, slow, invasive 2. Adenoid Cystic Carcinoma 3. Peripheral ossifying fibroma

Classification of Hormones: Derivatives and examples... 1. Amino acid derivative 2. Tripeptide 3. Small peptide 4. Intermediate peptides 5. Cholseterol derivative 6. FA derivative 7. Phospholipid derivatives 8. Purine derivative 9. How big is calcitonin?

1. Amino acid derivative- Catecholamines, 5-HT, thyroxine 2. Tripeptide- TRH 3. Small peptide-- Vasopressin & Somatostatin (think- Very Smol) 4. Intermediate peptides-- Insulin & PTH (I & P for intermediate peps) 5. Cholesterol derivative-Glucocort. mineralcort. androgens, estrogens, vit D. 6. FA derivative--Prostaglandins, Leukotrienes 7. Phospholipid derivatives--Platelet-activating factor 8. Purine derivative-adenosine 9. Calcitonin is 32-AAs- has cute little ring on end.

What do the following mean: 1. +Progesterone test (bleeding) 2. -Progesterone test (no bleeding) 3. Estrogen withdrawal test (if progesterone test neg.)--if bleeding +

1. Annovulation OR PCOS 2. LOW estrogen OR outflow tract defect 3. Low estrogen confirmed

1. Apical surfaces of follicular epithelial cells (of the thyroid) are in contact with _______________ and basal surfaces rest on ___________. 2. More active thyroid follicles __________ 3. How does iodide get from blood to follicular cytoplasm and where is iodide oxidized to iodine?

1. Apical--Colloid, Basement--Basal lamina 2. have TALLER EPITHELIUM (typically cuboidal) 3. Iodide from blood--> cytoplasm of follicular cells--ACTIVE TRANSPORT, Iodide & is converted --> Iodine--IMMEDIATELY on APICAL MEMBRANE--> released into colloid then once thyroglobulin broken down by lysosomes--> T3 & T4 DIFFUSE into blood

1. MCC of otomycosis? Tx? 2. MC benign adenoma

1. Aspergilliosis...Frequent and meticulous debridement 2. Follicular adenoma

3 causes of Pulmonary Alveolar Proteinosis

1. Autoimmune (#1 cause) 2. 2ndary (infection) 3. Hereditary--rare defect in GM-CSF --PATCHY bilateral ASYMMETRIC pulmonary opacifications--PAP is PATCHY --inc. size/weight of lung -CHUNKS of GELATINOUS MATERIAL in sputum

2 important placental features

1. Avascular septa project from basal plate--> intervillous zone 2. Fibrinoid deposits form in both basal & chorionic plates but MORESO in basal plate where they form RUPTURE ZONE

Tx for Bordatella Pertussis infection

1. Azithromycin/Clarithromycin 2. 2nd line is Sulfa/trim

Risk factors for Ovarian Cancer

1. BRCA1/BRCA2 2. *CLOMIPHENE USE* 3. Childhood gonadal dysgenesis 4. Hereditary nonpolyposis colon cancer (HNPCC, Lynch syndrome) 5. Long term Estrogen RT 6. Nulliparity 7. Older age Think--NULL is a big goose egg O, Older, childhOOd gOnadal dys, nOnpOlypOsis cOlOn cancer, clOmiphene, BRA--> BRO--> Brovaries, have 1 ovary & another (2nd) ovary. BRCA1 & 2

Effects of GH/IGF on... 1. Bone 2. Adipose 3. Liver 4. Kidney 5. Reproductive Note: has effects on Endocrine Axis but different card

1. Bone: GH: clonal expansion of prog cells--> differentiation IGF: GH-stim stem cells responsive to IGF--> cells prod. IGF--> IGF autocrine/paracrine--> clonal exp. of diff cells--> growth 2. Adipose: ONLY GH--> Preadipocyt--> adipocytes ALSO GH--> LYPOLYSIS in mature adipocytes 3. Liver: GH/IGF--> CYP450 enzym prod, prod of LIPOPROTEINS & LDL receptors, ALSO inc. LIPOPROTEIN A & serum TAG 4. Kidney: ONLY GH: antiNATRIuretic (high HG = Na+ & H20 retention) 5. Reproductive: GH--> gonad dev/puberty IGF--> Sensitives gonads to FSH/LH and inc # of rec. Remember Kidneys & Adipose are GH only! FAT KIDS have a LOT OF GH cause they are so fat.

Match the Condition: 1. Hyperinflation of lungs & depression of diaphragm 2. Intercostal retractions 3. Associated w/nasopharyngeal angiofibroma 4. Persistent fever, AMS, diplopia, infraorbital hyesthesia

1. Bronchiolitis 2. Bronchiolitis AND viral croup 3. Familial adenomatous polyposis 4. Severe bacterial rhinosinusitis

Bolded from respiratory lecture 1. MC age group of bronchiolitis 2. Therapy for flu A & B 3. Pertussis lab value 4. MCC death from diphtheria

1. Bronchiolitis <1 year of age 2. Therapy--Neuraminidase inhibitors & Viral cap-dependent endonuclease protein inhibitor 3. LYMPHOCYTOSIS-pertussis 4. Myocarditis

1. Carcinosarcomas (MMMT) genetically resemble...

1. CARCINOMAS (not sarcomas)

Diseases Associated w/Bronchiectasis...What is NOT associated?

1. CF 2. Primary Ciliary Dyskinesia 3. Necrotizing PNA 4. Bronchiole obstruction/FB aspiration 5. Infectious/inflammatory dz 6. *Ig deficiency* 7. Allergic bronchopulmonary Aspergillosis 8. A1AT deficiency!! NOT SMOKING! I REPEAT, NOT SMOKING

1. Never use as monotherapy in COPD 2. Never use as monotherapy in asthma

1. COPD--> NEVER ICS alone 2. Asthma--> NEVER LABA alone

1. Gold standard for acute/chronic rhinosinusitis 2. Gold standard for bronchiecTASIS 3. 1st step in treatment for bronchiectasis 4. Tx for M. Kansasii associated bronchiectasis

1. CORONAL CT 2. High-resolution CT 3. empiric ABX (amoxicillin, TMP-SMX, levofloxacin) 4. Rif, Iso, Ethamb X12 mos

Ways to remember how things go across placenta....

1. Ca++--*Actively sequestered* much like it is inside muscle cell...but also Phosphate & Ascorbate also (Actively Piles up) 2. Na+ & Cl- diffusion via channels (just like gradients/sweat) 3. AAs sequestered by placenta but diff possible in both dir--> initially they were sequestered by PEOPLE but now they are free to leave or stay... 4. FAs--Non-facilitated diffusion--> FAsses may not fit in the facilities but it makes no DIFF to me cause I'm not one. 5. Glucose- facilitated diff via insulin sens. translocase (makes sense since big diff between mom's sugar & fetus') 6. Iron--> captured transferrin, which is absorbed by placenta.

State how/if the following cross placenta: 1. Ca++ 2. AAs 3. O2 & CO2 4. Proteins/Large Molecules 5.Iron 6. K+ 7. Glucose 8. Phosphate & ascorbate 9. Cl- 10. Wastes (urea, Cr, uric acid) 11. FAs 12. Na+ 13. Xenobiotic compounds

1. Ca++: actively sequestered 2. AAs: sequestered by placenta w/diffusion possible bidirectionally 3. O2 & CO2: freely diffuse 4. Proteins/Large Molecules: slowly transferred (IgG may use this) 5.Iron: taken from transferrin (which is absorbed by placenta) 6. K+: actively 7. Glucose: facilitated diffusion via insulin-sensitive translocase 8. Phosphate & ascorbate: actively sequestered 9. Cl- : diffusion via channels 10. Wastes (urea, Cr, uric acid): freely diffuse or facilitated out of fetal comp. 11. FAs: NON-facilitated diff. 12. Na+: Diffusion via channels 13. Xenobiotic compounds: caught by placenta & met to protect fetus

Blood Supply of Adrenals & where they branch/drain: 1. Capsular arteries 2. Cortical Arteries 3. Medullary arteries 4. Adrenomedullary collecting veins 5. Central adrenomedullary vein

1. Capsular art--didn't say where 2. Cortical-branch in cortex--form dense network of fenestrated sinusoidal cap--drain to medullary art 3. Medullary art--pass thru cortex--form dense network of fenestrated sinusoidal cap-->drains oxygenated medullary capillary blood & glucocorticoid blood (from cortical caps) 4. Adrenomedullary collecting veins--receive from medulla, drain to LARGE central adrenomedullary vein 5. *Central adrenomed vein--> drains to IVF on the R and L renal vein (on left)*

1. 3rd most common cancer in women worldwide 2. #5 leading cause of CA death in women

1. Cervical Carcinoma--(C is the 3rd letter of alphabet. C for cancer.) 2. OVARY has 5 letters. Ovarian.

Chromophiles vs crhomophobes

1. Chromophiles--secretory granules that pick up dye 2.Chromophobes--stromal cells & degranulated chromophiles: A. Acidophiles-Somatropes & lactotropes (S & L--sour lingual) B. Basophiles- Corticotropes, Gonadotropes, thyrotropes SOMATOROPES are MOST ABUNDANT ENDOCRINE CELLS in ADENOHYPOPHYSIS

1. Anatomical borders of mastectomy 2. Level I axillary nodes lie 3. 42 yo palp right breast mass (non-tender). Mammorgram & US findings consistent w/simple cyst. Next best step? 4. 38 yo female gets US of left breast & has BiRADS class 2 lesion. Does it require immediate biopsy? 5. Given above info, what is most likely diagnosis?

1. Clavicle, sternum, lat dorsi, inframmamary fold, pec major 2. Lateral to pec minor muscles 3. Routine screening & observation 4. NO (Benign lesion, f/u w/yearly routine screening) 5. Fibroadenoma

1. What results,anatomically, from bacterial inf of mastoid process? 2. Cornerstone of therapy for acute otitis externa

1. Coalescence of mastoid air cells 2. thorough cleaning

1. Only __________ & ____________ can secrete matrix proteins 2. Marker of bone turnover 3. Marker for bone formation? 4. Markers for Resorption 5. Promotes expression of RANKL on osteoblasts

1. Committed preosteoblasts & mature osteoblasts 2. Osteocalcin 3. Bone-specific Alkaline phosphatase (BSAP) 4. Urine- hydroxyproline, Serum- Tartrate-resistant acid phosphatse 5. *Parathyroid hormone & 1, 25-hydroxyl-vitamin D*-> OSTEOCLAST ACTIVATION

1. Meconium ileus 2. most common thyroid carcinoma--what is seen on histo?

1. Concern for CF--Check CFTR mutation on chromosome 7 2. Papillary carcinoma--Psammoma bodies (tx: full thryoidectomy, radioactive ablation w/iodine)

1. Adduction of vocal cords...pitch in singers 2. Neurogenic voice 3. MC cause of vocal cord paralysis

1. Cricothyroid---Superior Laryngeal nerve 2. Spasmodic dysphonia--more commonly adductor 3. Neoplasm

Smoking-related interstitial lung diseases

1. DIP 2. PAP 3. Langerhans Cell Histiocytosis If you use DIP (or smoke) for too LANG, may be in trouble and end up on the PAP (biPAP)

1. Genital excurrent ducts A. Accessory sex glands

1. Ductuli efferentes 2. Ductus epididymidis 3. Ductus (vas) deferens A. Seminal vesicle B. Prostate 3. Bulbourethral glands

Matching: 1. low pseudostratified columnar-ciliated and non-ciliated 2. Sertoli cells initially & __________ cells distally? 3. Simple cuboidal (literally could be anything but...) 4. pseudostratified columnar w/LONG microvilli 5. Epithelium w/rich secretory granules 6. Lines the prostate glands? 7. Lines the spongy urethra...what else is found 8. Distal urethra lined by

1. Ductuli efferentes--E turned looks like a saw--> see-saw--need EFFRIEND to see-saw w/ (it requires LOW EFFORT, and LOW amount of MUSCLE--Thin smooth muscle around terminal part 2. Straight tubules (connected to sem tub)--Distally cells are SIMPLY CUBOIDAL (remember your left overs in cube tupperware 3. Rete testis--I RETE hope dis TESTIS SIMPLE, something a SQUARE could do, but they could ask ANASTY questions 4. Ductus vas deferens--VAST microvilil, & VAST (DEEP longitudinal folds) 5. Epithelium of semial vesicle mucosa 6. Columnar/cuboidal PSEUDOstratified epi lines the COMPOUND TUBOALVEOLAR GLANDS --like when a dumba*ss w/prostate says he's gonna take you to comPOUND TOWN w/his TUBE sock a*ss looking penis--but is just another FAKE (PSEUDOSTRATIFIED) SQUARE/column 7. Pseudostratified columnar epithelium (think of similar to lining prostate gland) 8. Distal- non-keratinized stratified squamous epi (GLANS is ALSO THIS)

1. MC invasive carcinoma of female genital tract? 2. MC type of Endometrial Carcinoma? 3. MC type of Type II endometrial carcinoma? 4. 2nd MC malignancy of female genital tract?

1. Endometrial carcinoma 2. TYPE I--> Endometrioid carcinoma! (80% of cases) 3. TYPE II--> serous carcinoma 4. Ovarian cancer (2nd mcc gyne malignancy)

Difference between epinephrine & norepinephrine secreting cells

1. Epinephrine--smaller secreotyr granules (but more abundant) 2. NE--LARGER secretory granules (but fewer)

4 health risk behaviors resp for majority of chronic illness

1. EtOH 2. Smoking 3. Inactivity/no physical activity 4. Poor nutrition

Malignant cells in the vulva....name of disease? What must be determined and how?

1. Extramammory Paget's disease (of vulva) 2. R/o melanoma vs carcinoma 3. Melanoma vs Carcinoma Melanoma--PAS- Keratin -, S100+ Think you POSITIVELY must wear Sunblock w/100% coverage to not get melanoma Carcinoma (Paget's disease)--PAS+, Keratin +, S100- Pagets--PAS (ps), Ceratin+ (carcinoma-pagets)

1. Flattened inspiratory portion 2. Flattened expiratory portion

1. Extrathoracic obstruction 2. Intrathoracic obstruction

1. MCC exudative pleural effusion 2. MCC of non-iatrogenic causes of transudative pleural effusions

1. Exudative--Parapneumonic--tube thoracotomy + stain & culture 2. Transudative--CHF--diuretics

1. Iron deficiency increases risk of..... 2. Ionizing radiation increases risk of.... 3. Associated w/inherited tumor syndrome

1. FOLLICULAR CARCINOMA (over papillary)--Iron Fe--> Follicular 2. PAPILLARY CARCINOMA (over follicular carcinoma)--all the psych pts thought my PC (computer) was RADIATING them. --this does NOT mean follicular is not, it is just moreso. 3. FOLLICULAR carcinoma of the thyroid

Label 1. Impaired Fasting Glucose: 2. Impaired Glucose Tolerance 3. DM

1. FPG: 100-125 2. 2H Postglucose: >140-199 3. FPG: >126 or 2H Postgluc >200 Or random gluce >200 w/sx 1 and 2 are pre-diabetes

1. MC benign tumor of female breast 2. MC tumor in women 3. MC SOLID benign tumor 4. MC cystadenoma 5. 2nd MC cystadenoma

1. Fibroadenoma 2. Leiomyoma 3. Ovarian fibroma (Meigs syndrome uncommon)--> Overly Full (solid) 4. Serous type-cystadenoma 5. Mucinous type-cystadenoma

Important functions of pulmonary circulation (besides the obvious)

1. Filter blood 2. Reservoir for L ventricle 3. ACE 4. Supply nutrients to lung itself 5. Exchange fluid

1. What regulates SECRETION of PTH?

1. G-protein Ca++ receptor stimulated by increase in Ca++--> activates PLC--> inhib AC--> rise in IP3 and decrease in cAMP--> DECREASED PTH release. So decrease in IP3 and increase in cAMP = increase PTH secretion

________ Codes for: 1. GAG 2. POL 3. ENV

1. GAG- CORE proteins 2. POL-Enzymes 3. ENV-envelope These are all structural genes

GH effect on bone?

1. GH induces clonal expansion of osteoblast-type cells 2. GH induces osteoblastic cells to produce IGF 3. IGF promotes proliferation of osteoblast-lineage cells 4. WORKS SYNERGISTICALLY W/ THYROID HORMONE (especially @ growth plates, which is why hypothryoidism causes short stature in children)

Buzzwords: 1. Stimulates linear growth 2. Upregulates GH receptors @ target organs 3. Puberty causes stimulation/synthesis/secretion of... 4. a. What stimulates GHRH while suppressing SST? What just suppresses SST? 5. Release is proportional to exercise intensity? 6. GHBP that has higher affinity for GH? Which one has higher capacity? 7. Inhibits dimerization of receptors decreasing effects of GH

1. GH via IGF release from kidney 2. Estrogen 3. GH caused by estradiol 4. a. Dopamine AND Galanin b. Opioids, ACh, Arginine 5. GH--exercise if MOST EFFECTIVE release stimulus 6. GHBP1- HIGHER AFFINITY, GHBP2--HIGHER CAPACITY 7. Too high [GH] will bind all spare receptors in their SINGLE SUBUNIT form

1. the Natural ligand of GHS-R 2. Where is the GHS-R expressed 3. What hormones STIMULATE GHRH but SUPPRESS SOMATOSTATIN 4. What hormones suppress SOMATOSTATIN 5. Which GH-BP has HIGH Affinity & LOW capacity? 6. Which GH-BP has LOW affinity and HIGH capacity? 7. Half-life of GHRH vs GH? 8. Randle Effect?

1. GHRELIN is the ONLY one 2. Anterior pituitary and Hypothalamus 3. Dopamine & Galanine STIMULATE GHRH but suppress SOMATOSTATIN 4. DA, galanine, arginine, ACh, Opioids 5. GH-BP-1 HIGH AFFINITY (low capacity) 6. GH-BP-2- LOW AFFINITY (high capacity) 7. GHRH 50 minutes! GH only 20 mins 8. Randle Effect--inc FFA decrease glucose uptake by cells that preferentially use fat (muscle)..thus decreasing use of protein for gluconeogenesis--GH STIMULATED LIPOLYSIS *Randle Effect--mediated by glucagon--> it INHIBITS activity via phosphorylation of pyruvate dehydrogenase

1. Symptoms/signs of Laryngopharyngeal reflux--GOLD STANDARD? 2. What should we associate with expiratory stridor? 3. Recurring chills rather than shaking chills. 4. Air-filled dilation of appendix of ventricle 5. Blunted alveolar septa

1. GLOBUS SENSATION, NOCTURNAL COUGH, throat mucus, post nasal drainage, dry cough, choking spells, ear pressure. GOLD STANDARD- 24 hr pH probe (not practical) 2. Expiratory Stridor--> trachEomalacia 3. Aspiration PNA 4. Laryngocele 5. Emphysema

Genetic factors of follicular carcinoma....which ones are unique?

1. GOF of RAS & P13KCA 2. LOF of PTEN (tumor suppressor) 3. UNIQUE--> t(2;3)(q13;q25) creating PAX8-PPARG fusion-ONLY FOLLICULAR CA of THYROID note: RET/PTC and BRAF NOT SEEN HERE.

How to remember G-protein coupled receptor cascade

1. Giant A$$ PromotesKinkyA$$ Touching (G--> AC--> cAMP--> PKA--> Transcription) Gs---everything else Gi--if someone INHIBITS you from touching 2 great A$$ cheeks you say "DAM"---D2, A2, M2 (2 for 2 cheeks) 2. Giant PrettyLargeC0ck (PLC) Does Infact PromoteKinkyC0ck Touching (G-->PLC--> DAG/IP3-->PKC--> Transcription) Gq--> H1, A1, V1, M1, M3 HAV a (1) 13-inch Manpart

GH & IGF Levels & GH & IGF Receptors in (ONLY abnormalities of receptors noted... 1. Gigantism 2. Acromegaly 3. Dwarfism 4. Pygmyism 5. Laron-Type GH Insensitivity

1. Gigantism-- Serum GH & IGF both HIGH. 2. Acromegaly--Serum GH & IGF both HIGH, (repressed IGF rec) 3. Dwarfsim--Serum GH & IGF both LOW (dwarf, duo) 4. Pgymyism--Serum IGF LOW (everything else normal)--Pigmy's Pick one abnormality (think P IG(females) are Less than) 5. Laron-Type Insensitivity--serum GH HIGH, serum IGF LOW, MUTATED GH receptors (appears low)

1. CML is treated w/________, which targets ________. 2. Activated oncogenes usually affect __________. 3. the Ras genes found in all eukaryotes

1. Glivec, which targets BCR-ABL fusion kinase 2. Receptor-mediated signal transduction 3. Harvey (cH-ras), Kirsten (cK-ras), N-ras (cN-ras)

Quick and dirty phases of spermatids

1. Golgi phase- PAS+, proacrosomal granules form acrosomal vesicle @ anterior pole of nuc. Centrioles go posterior (diff into axoneme of flagellum) 2. Cap phase- acrosomal ves wraps anterior surf of nuc, thickens, non-porous, chromatin condense 3. Acrosome phase-ant pole reduced, cap abuts plasma memb, microtubs form manachette--> makes more ovoid forms head, centrioles diff into neck--links dev flag--> posterior pole of nuc Think- AXosome phase--> Machettes to cut off someone's head--group of people watch person in center get neck cut...now neck is with posterior part of body is flailing (flagellum) and now majority of neck is connected to post part. 4. Maturation phase- residual body phag by sertoli (excess cytoplasm excocytosed), mitochond surround flag distal to neck (middle piece)

1. MCC of aquired Laryngeal stenosis? What type of stenosis? 2. 3rd MC laryngeal anomaly. Sx? Tx? 3. 2nd MCC of epiglottitis? 4. MC spot for Wegner's Granulomatosis? 5. MC spot for Sarcoidosis?

1. Granulomatous-->TB--SUBGLOTTIC stenosis 2. Congenital subglottic stenosis--biphasic stridor, reflux management, Open surgery Grades 3-4 3. S. pyogenes 4. SUBGLOTTIS (c-ANCA--remember the C that goes thru drawing of guy and it affects the nares/oropharynx unlike Goodpasture's) 5. Epiglottis

1. MC STI 2. MCC genital ulcers 3. MCC of death from gynecological cancer

1. HPV--Type 16>Type 18 (more prevalent among the high risk ones) 2. HSV2 3. Ovarian (serous cystadenoma are MC>mucinous cystadenoma)

Sites of hematopoiesis....Correlate this w/stages from histology & what cells are present 1. 2-3 months--> 6-7 months 2. 3rd week of gestation 3. from (5)-7 months--> 4. a "few weeks" after 3rd week

1. Hepatic & splenic phase-->we see NUCLEATED erythrocytes @ 6th week, which is beginning of hepatic phase...(also WBCs start @ 8 weeks) Also, splenic phase starts around 12th week 2. yolk sac-erythroblasts present (Mesoblastic phase) 3. Bone marrow (Myeloid phase) 4. AGM region (intraembryonic aorta/gonad/mesonephros)--note beginning of Hepatic phase (week 6 per histo)

1. Improves with removal of irritating agent? (And 3 key forms of this) 2. Does NOT improve when exposure ceases? 3. Multiple lesions that do not progress (but does not regress) when exposure stops

1. Hypersensitivity pneumonitis--loosely formed interstitial granulomas & chronic inflammation a. Pigeon breeder's lung b. Farmer's lung c. Humidifier/air conditioner 2. Silicosis--he don't give a f*ck 3. Caplan's syndrome--> any inorganic pneumoconiosis + Auto immune disease (lupus, RA)--multiple lesions, coal macules

1. How is IGF stored/released/produced? 2. Dominant form of IGF-BP found in INTERSTITIAL FLUID? 3. Dominant form of IGF-BP found in CSF 4. Dominant form of IGF-BP found in SERUM 5. IGF-BP formation INVERSELY related to INSULIN LEVELS.

1. IGF is NOT STORED. Released CONSTITUTIVELY and is INDUCIBLE...Think--Inducible, Given Freely (constitutive)-IGF 2. Interstitium-IGF-BP1 --> 1 = I for interstitium 3. Serum- IGF-BP3 4. CSF - IGF-BP2--> cerebrospinal"TWO"id.... 5. IGF-BP1 & IGF-BP2 formation INVERSELY to INSULIN

During ovulation what 4 factors cause physical rupture of mature follicle?

1. Inc. amount of liquor folliculi 2. Glycosaminoglycans disrup CUMULUS OOPHORUS (severs tethers of 2/2 oocyte) 3. Proteolysis degrades thecal wall immediately over 2/2 oocyte 4. SM of tehca externa contracts= inc intra-thecal pressure

Pseudohypoparathyroidism...labs and sysmptoms?

1. Inherited disorder-biologically active PTH BUT end organs cannot respond. LOW Ca++, HIGH PO4- (cause it ain't responding) Symptoms-short metacarpal bones, MR, short stature

Glucocorticoid effect on bone...how?

1. Inhibits osteoblast formation and collagen deposition by osteoblasts 2. Inhibits Ca++ absorption from gut to the point where PTH cannot increase Ca++ without stimulating osteoclastic resorption

1. What cells make renin? 2. What do these cells respond to? 3. What effect does this have on (specifically)--next questions about same organ 4. Describe the histo of this other organ... 5. Describe the capillaries supplying this organ

1. JG cells 2. Sensitive to BP changes & Na+ & Cl- concentration in renal tubular fluid 3. JG cells produce renin--> ACE I--> ACE II--> simulates Zona glomerulosa (of the adrenal cortex) to produce aldosterone (mineralocorticoids) 4. *Zona glomerulosa--closely packed cuboidal/pyramidal, arranged in ARCHED cords, or curved columns.* 5. *Arched cords/curved columns of ZONA GLOMERULOSA surrounded by FENESTRATED SINUSOIDAL CAPILLARIES.* Think Zona GEMerulosa...gems/minerals..are cuboidal/pyramidal shaped...think of jewel box in stl...ARCHED cords (stl ARCH).

1. Bulging fissure on chest XR? 2. Pneumatocele on CXR think?

1. K. pneumoniae 2.S. aureus (in kids), can also result from pulmonary trauma during mech vent.

Most common organisms to infect COPD pts?

1. Klebsiella pneumoniae 2. H. Influenza Makes sense since Alcoholics AND old people are susceptible to aspiration.

1. Langerhan's Histiocytoses Markers 2. a. SqCC Markers, SqCC-mutations 3. AdenoC Markers

1. Lang: + S100, CD1a, Langerin (CD207) & NEG for CD68 2. SqCC: P40, P63, Mutations: HIGHEST TP53 mutations of ALL histologic types 3. AdenoC: TTF-2, Napsin A

Breast carcinoma is...

1. MC non-skin malignancy in women 2. 2nd MC cause of cancer deaths (#1 lung cancer)

1. MC metastatic tumors of ovary are derived from? 2. MC Extra-mullerian?

1. MULLERIAN origin--> Uterus, fallopian tube, CONTRALATERAL ovary, or pelvic peritoneum 2. CA of BREAST & GI tract (colon, stomach, biliary tract, & pancreas)

Matching: 1. When middle piece is formed (also describe) 2. Nuclea membrane thickens becoming non-porous & chromatin condenses 3. Acrosomal vesicle moves to anterior pole of nucleus 4. Anterior pole of cell is reduced leaving acrosomal cap abutting plasma membrane. 5. Centrioles migrate to posterior pole of spermatid and begin to differentiate into axoneme of flagellum 6. Microtubules adjacent to nucleus form Manachette, which reshapes nucleus into more elongate ovoid. 7. PAS+ granules accumulate and combine to form acrosomal vesicle 8. Group of centrioles differentiate into NECK, which links ________ & ___________ 9. Excess cytoplasm pushed out of spermatid via exocytosis 10. Residual body is _________ and it is phagocytized by __________ 11. B1-integrins that link spermatozoans to sertoli cells are disrupted 12. Head of sperm dec in size and additional cytoplasm lost...what next?

1. Maturation phase- mitochondria surround flagellum just DISTAL to neck (forming middle piece) 2. Cap phase (also anterior surface of nucleus forms acrosomal cap) 3. Golgi phase 4. Acrosome phase 5. Golgi phase 6. Acrosome phase 7. Goglie phase--the PAS+ granules (proacrosomal granules accumulate in GOLGI 8. Group of centrioles differentiate into NECK, which links DEVELOPING FLAGELLUM & POSTERIOR POLE of nucleus 9. Maturation phase 10. Maturation phase--the lost vesicle cytoplasm (residual body) is phagocytized by SERTOLI CELLS 11. Spermiation--after this, spermatozaoans are loose in lumen of SEMINIFEROUS TUBULE (liberation) 12. this is called MATURATION...after dec in size and cytoplasm loss, sperm plasm undergoes changes in anticipation of membrane fusion

Predictions... 1. What marks transition to Mature Follicle? 2. What defines a Secondary Follicle? 3. When is the oogonia formed? 4. Distinction of outer cortex & inner medulla? 5. When do we get follicular cells? 6. Primordial follicle? 7. Primary ooctye? When does it become granulosa cells? 8. Primary follicle?

1. Mature follicle = DIFFERENTIATION of GRANULOSA CELLS $ 2. 2/2 Follicle--Presence of ANTRUM $ 3. OOGONIA--once the germ cells are in the OVARIAN CORTEX. 4. Outer cortex & inner medulla formed when EXTRAEMBRYONIC GERM CELLS preferentially settle in the PERIPHERY 5. Follicular cells--Single layer of squamous stroma cells surround each oogonia, which are surrounded by a basal lamina 6. Single layer of follicular cells + the oogonium = primordial follicle 7. Primary oocyte--when primary follicle resums meiosis I... granulosa cells when they prolif & become more cuboidal. 8. Primary oocyte surrounded by granulosa cells surrounded by thecal cells --> primary follicle $ OGT--> primary

1. Interacts w/FGF23 and causes.... 2. Interacts w/TRPV5 (transient receptor potential cation channel)...Location of channel & effect?

1. Membrane Klotho protein-coreceptor--> Klotho-FGF-FGFR complex NEGATIVELY regulates synth of active vit D (1, 25(OH2)vit-D by suppressing synth of 1-alpha-hydroxylase --> net effect dec Ca++ absorption in gut & slows bone resorption 2. Soluble protein-Beta-glucuronidase (Klotho protein) interacts w/ 5TRPV5 in DISTAL CONVOLUTED TUBULES...Deglucuronidates the TRPV5 recep. to TRAP them in cell membranes & INCREASE Ca++ reab in kidney.

What kind of protease and what do they degrade... 1. Interstitial collagenases degrade... 2. Type IV & V collagenases degrade... 3. Secreted......correlates with metastatic potential 4. Describe steps of formation of invadopodia

1. Metalloprotease--> degrades collagen I, II, & III 2. Metalloprotease--> BM, which are found in highly metastatic variants of certain cell lines. 3. Cysteine proteases--> CATHESPIN B activity can degrade type IV collagen (high met pot). 4. Tyrosine kinase--> act src--> act cortactin--> actin assembly--> forms invadopodia, which secrete proteases

1. Location of polymorphous low grade adenocarcinoma 2. MC head & neck neoplasm in children--present by 6 mos 3. Epithelium on top of LYMPHOID tissue (classic presentation) 4. Infiltrating SHEETS/NESTS of cells w/granular cytoplasm

1. Minor salivary glands 2. Hemangioma 3. Warthrin tumor--cystic spaces lined by double layered eosinophilic epithelium (embedded in lymph stroma) 4. Acinic Cell Carcinoma

1. Most important part of Local Anesthesia? Less important? 2. Most common form of hermaphroditism

1. Most important -- pt position Less important--needle size 2. Female pseudohermaphrodite--> 46 XX (usually CAH)

MC epithelial tumor of ovary? 2nd most?

1. Mucinous 2. Serous Remember this is EPITHELIAL NOT Cystadenoma

1. For pharm when controlling DM what is never the answer? 2. When growth on growth curve is below parent's.... 3. GH deficiciency causes what features to develop? 4. Endocrine growth failure causes

1. NPH/human insulin--> give LONG ACTING insulin instead 2. pick TURNER SYNDROME 3. Midline defects assoc w/cleft lip/palate, chiari malformation, & septo Optic dysplasia 4. GH RECEPTOR DEFECT These were apparently hints from another year...said they were on the "test"

Match the Mutation game: 1. NTRK1 2. Inactivation of p53 (just MORE of these mutations) 3. RET/PTC fusion 4. germline RET mutations 5. PAX9/PPARG 6. AOF of BRAF 7. Beta-catenin 8. GOF RAS 9. PI3K activation

1. NTRK1-papillary carcinoma 2. Inactivation of p53-anaplastic carcinoma 3. RET/PTC-- Papillary carcinoma (its in the name) 4. Germline RET--Medullary carcinoma 5. PAX9/PPARG--Follicular carcinoma 6. AOF of BRAF--Papillary carcinoma 7. Beta-catenin--anaplastic carcinoma 8. GOF RAS--follicular carcinoma 9. P13K activation-follicular carcinoma

2 fun unique facts about GH? Because of one of these facts, explain how our our body releases it...How does it occur? When is GH release stimulated?

1. Only hormone that *causes growth dose-dependently* 2. Only hormone that causes PATHOLOGIC growth in tissues when chronically elevated GH --Pulsatile release helps prevent overexposure of cells to GH--prevents down-regulation of GH receptors on those cells. --Because GHRH causes RELEASE of SST (seems counter-intuitive) to make sure "on switch" is only on for a short period of time. --GHRH stimulates GH when SST levels are LOW.

Ahmed hint Drug and Action: 1. Orlistat 2. Phentermine, diethylpropion, phendimetrazine & TOPIRIMATE 3. Lorcaserin hydrochloride

1. Orlistat--inhib pancreatic lipase activity in GI tract, thus blocking digestion/absorption of dietary fat 2. Phentermine & TOPIRIMATE: enhances release of NT NE, which suppresses appetite. 3. Lorcaserin hydrochloride--Interacts w/brain serotonin receptors to increase satiety & reduce food intake

1. MC aspirate 2. 2nd MC aspirate 3. What phase?

1. Oropharyngeal secretions 2. Gastric acid 3. Pharyngeal phase

How to remember these glycoproteins: 1. Osteonectin 2. Ostocalcin 3. Osteoponin

1. Osteonectin-involved in mineralization (think of mineral oil applied to the neck) 2. Osteocalcin-- regulates osteoblast differentiation/proliferation (think- osteaCLASScin--differentiation)--serum lev els = total level of turnover!! 3. Osteoponin--binding site or activator for osteoclasts--Ponin--pontiac--park the pontiac or turn it on (activation)

DDx of 2/2 amenorrhea

1. PCOS (have adequate estrogen but inc androgen) 2. Uterine defects/trauma 3. Pregnancy/profound stress

1. Most important factor in aldosterone release 2. Where is Preproinsulin synthesized 3. Whipple's Triad

1. POTASSIUM LEVELS (not Na+ or Ang II) 2. RER 3. A. Sx of hypoglycemia B. Plasma glucose <50 C. Amelioration of sx w/restoration of normal BG

Prediction 1. PTH is secreted ______ to serum ca++ conc...Set point for PTH? Max rate of secretion? 2. Why must PTH be continously synthesized? 3. Most rapid change in Ca++ accomplished by? Largest change in Ca++ caused by?

1. PTH inversely proportional to Ca++ conc. Secretion starts at 1.3 mmol/L and is MAX at 1.1 mmol/L 2. Parathyroid glands have few storage granules...can only continuously secrete for 1.5 hrs 3. Rapid-kidneys, largest-bones

What exam finding w/ paget's consistent w/underlying invasive carcinoma, what is it usually and what is the prognosis?

1. Paget's--> if PALPABLE mass more likely invasive carcinoma--> ER - & Her2+ (POORER PROGNOSIS) So, Paget's Palpable, Poor, Think- for (a fat Pig-Paget's) Her it will POSITIVELY End Real Negatively. --w/o palpable mass--> DCIS--> better prognosis

Most common locations for salivary neoplasms (most to least)

1. Parotid 2. Submandibular 3. Sublingual/minor-least PML-to remember

1. Superior hypophyseal artery supplies? 2. Carries? 3. Inferior hypophyseal artery

1. Pars Tuberalis, Infundibulum, Median eminence, & Pars distalis--hypophyseal portal system runs through infundibulum & median eminence--> pars distalis--> 2ndary cap plexus 2. Carries GHRH,TRH, GnRH 3. Pars nervosa

Buzzwords: 1. Rathke's cysts & cell type? 2. Pituicytes 3. Long axons of neurohypophysis have terminals located in the ________. 4. Herring bodies, how do they stain? Location? 5. Copora arenacea 6. Spongiocytes

1. Part of Pars intermedia (of adenohypophysis) lined w/ cuboidal epithelium 2. Glial cells of the nuerohypophysis 3. Pars nervosa 4. Large distended axon terminals (from the hypothal)--stain pink, located in the PARS NERVOSA 5. aka "brain sand"--aggregates of CaPO4 found in pineal gland 6. Spongiocytes--zona fasiculata

DM care concepts

1. Patient centeredness 2. Diabetes across the lifespan 3. Advocacy for Patients w/diabetes

Prostate zones/facts: 1. Contains main prostatic glands 2. Located near prostatic urethra 3. Makes up 70% of glandular tissue 4. Stroma contains... 5. GLand lumina in older men contained in the lumen of TUBOALVEOLAR GLANDS.... 6. Secretions of prostate... 7. Contraction of _____ causes secretions to _______ 8. Role of testosterone? If too low? 9. Cancer of prostate...what type? 10. Posterior thickening of tunica albuginea--what is this called? What runs through it?

1. Peripheral zone-- (equiv to post/lat lobes) 2. transitional zone (ant/middle lobes) 3. Peripheral zone 4. fibroblasts, collagen fibers, SM 5. spherical concentrations of glycoprotein--CORPORA AMYLACEA 6. acid phosphatase, citric acid, fibrinolyisn--> liquefy semen 7. Contraction of fibromusc tissue of prostate--> secretions into urethra 8. Maintain struc & func integrity of prostate...too low = reduced secretory activity 9. main glands of peripheral zone--> adenocarcinoma (surg, radio,)-hormone tx used for mets but poor prog 10. Medaistinum testis--blood vessels, lymphatic vessels, rete testis pass thru

Buzzword matching: Endocrine histo 1. Large,euchromatic nuelei w/prominent nucleolus 2. Small, heterochromatic neclei 3. Lipid droplets, mitochondira w/tubular cristae, & abundant SER 4. Microtubule-containing processes extended from cell body 5. Melatonin inhibits... 6. Adrenal cortex color vs Medulla color 7. Contains lipufucin granules 8. Polyhedral cells in clumps/cords 9. Modified postsynaptic neurons 10. Accumulate & store hormones 11. Distinctive feature of oxyphil cells

1. Pinealocytes--inpoorly-defined clumps/clusters 2. Glial cells (interstitial cells) of pineal 3. Adrenal cortical cells (since they produce steroids) 4. Pinealocytes 5. Steroidogenic activity of gonads 6. Think- cortex produces steroids so it is yellow! Medulla-reddish/brown layer 7. Zona Reticularis--*androgens* & glucocorticoids--think ReticuLIPOFUCIN 8. Adrenal medulla 9. Chromaffin cells--neural crest cell origin 10.Chromaffin cells---chromstuffin cells store 11. Large # of mitochondria in cytoplasm

1. Primary hyperparathryoidism-cause 2. Secondary hyperparathyroidism--explain it?

1. Pituitary adenoma 2. HYPERPLASIA of parathyroid glands and hypersecretion of PTH (renal failure 2/2 lack of vitamin D synthesis) Decreased conversion of 25(OH)D3 to 1,25(OH)2-D3 in diseased parenchyma = inefficient absoprtion in gut & secondary rel of PTH in compensatory effort to maintain Ca++ levels

1. MC benign tumor of each salivary gland? 2. Derivation of Small Cell Carcinoma 3. MC esophageal malignancy 4. MC finding in primary cholesteatoma 5. Rough skin lesion from what type of PNA

1. Pleomorphic adenoma, slow, painless, unilateral, firm toward tail of parotid 2. Neuroendocrine progenitor cells 3. SCC--middle 1/3 of esophagus 4. Pars flaccida packets & white pearly mass in middle ear 5. Blastomyces dermatitis

1. Cause of Polymenorrhea? 2. Cause of Hypermenorrhea

1. Poly--Short follicular phase OR luteal insufficiency 2. Hyper--Tumor OR tissue hyperplasia

MCC chronic cough (probably on test)

1. Postnasal Drip 2. Asthma (2nd MCC: adults, 1st MCC in kids) 3. GERD

1. MOA of PDE inhibitor 2. AE of PDE inhibitor 3. AE Buproprion 4. AE of Ultra-LABA

1. Prevents PDE from degrading cAMP to 5'AMP thus allowing more cAMP to stay in cell & fuel Ca++ sequestration--> relaxation of smooth muscle AND Inhibits mast cell degranulation (somehow) 2. PDE inhibitors-- Gi, psychiatric, weight loss, back pain 3. Buprioprion--BLACK BOX WARNING for SI, also dec seizure threshold, insomnia, tremor, diff conc. , GI sx 4.- local-cough, oropharyngeal pain systemic-DOSE RELATED-similar to other beta agonists, PROLONGED QT

1. Nasal obstruction, epistaxis...what tumor and where met? 2. loss of right heart border on CXR 3. MC characterization of Eczematoid Otitis Externa 4. MC presentation of olfactory neuroblastoma? 5. MC vascular anomaly to cause stridor 6. MCC congenital laryngeal anomaly 7. MCC stridor in neonate & chronic pediatric

1. Primary nasopharyngeal carcinoma--> mets to cervical lymph nodes 2. Right middle lobe infiltrate 3. Pruritis, spectrum of scaling, edema & otorrhea (tx w/baby oil or steroid cream) 4. Nasal obstruction and/or epistaxis 5. Double aortic arch--Right dorsal aorta persists & 2 arches form vascular ring around trachea & esophagus 6. Laryngomalacia 7. Also laryngomalacia--stridor worse w/feeding/crying

Name the following cells of hematopoiesis... 1. Express CD34 & HLA-DR 2. Give rise to a single or limited lineage of progenitor cells 3. First recognizable cell in given lineage 4. Irreversibly committed to a certain lineage 5. last cell to express CD34

1. Progenitor cells 2. Multilineage (multipotent) progenitor cells 3. Blast cell 4. Progenitor cells 5. Blast cell

Matching Granulopoiesis style: 1. Basophilic cytoplasm w/azurophilic granules, +mitotic activity 2. Abundant free ribosomes & rER, NO granules, delicate chromatin strands 3. Indicative of _________ if seen in >3% 4. First cell to NOT exhibit mitotic activity. 5. Indented nuclei & nucleoli are NOT seen 6. First cell to show specific granules 7. Largest of the cells 8. Contains perinuclear clear zone that is formed by _________. 9. Bean shaped nucleus 10. What can we see in some myeloid neoplasms

1. Promyelocyte (when we FIRST see granules--azurophilic b/c lysosomes) 2. Myeloblast 3. Band form--> GRANULOCYTIC LEUKEMIA 4. Metamyelocyte 5. Metamyelocyte 6. Myelocyte--gonna Live My life & do my own SPECIFIC thing 7. Promyelocyte 8. Myelocyte--perinuclear zone formed by GOLGI complex. 9. Metamyelocyte--remember- NO mitotic activity 10. Monoblasts & promocytes

1. Levinthal-Coles-Lillie Bodies 2. 2nd MC thyroid cancer (particularly elderly females) 3. Soft, raspberry-like proliferations & location 4. MC mets to lungs 5. MC in submandibular gland (90% radiopaque)--Tx?

1. Psittacosis from Chlamydia Psittaci 2. Follicular Carcinoma (1st is papillary carcinoma)--FC is hematogenous spread 3. .Squamous papilloma & papillomatosis--on TRUE VOCAL CORDS 4. Prostate, Breast, colon 5. Acute silolithiasis--salivary stones (CT, MRI, Tx w/gland massage or transoral incision)

CT disease that have pulmonary involvement

1. RA (cricoarytenoid joint) 2. Systemic Sclerosis (scleroderma) 3. SLE *Scleroderma-->anti-centromere CREST-calcinosis (deposits in skin) R-Raynaud's E-Esophageal problems S-Sclerodactyly Telangiectasis

Effects of stimulating lipolysis at PHYSIOLOGICAL GH doses?

1. Randal Effect- HIGH serum FFA red glucose transport & oxidation in lipid-preferring tissues. 2. Spares GLUCOSE so it can be used by muscle. 3. Spares PROTEIN--Reduces need for gluconeogenesis Also remember---that since GH simulates LIPOLYSIS, decreased GH (w/age) causes OBESITY!

1. Painful rock hard fibrotic thyroid 2. MCC of hypoparathyroidism 3. What is the ONLY vocal fold abductor? Innervation? 4. Location of Cricoid in peds airway 5. Location of larynx in peds airway

1. Reidel Thyroiditis 2. Iatrogenic (surgery) 3. POSTERIOR CRICOARYTENOID--inn by RLN 4. C4-cricoid 5. C1-larynx

1. Biological activity of PTH 2. Length? 3. Where is PTH processing carried out? Fates? 4. What decreases expression of PTH? 5. What increases expression of PTH?

1. Resides in the N-terminal of molecule (PTH 1-34).--Region primarily responsible for RECEPTOR BINDING is 25-34 2. PTH is 84 amino acid peptide--Chief cells & precursor is 115 3. Processing in ER & golgi complex of chief cells--> secretory vesicles w/3 fates: a. transport into storage pool b. degradation c. immediate secretion 4. PTH expression dec when 1, 25(OH)2-D3 increases and binds to VDREs, which dec expression of PTH. 5. Hypocalcemia OR 1,25(OH)2-D3 deficiency--> inc size & of chief cells = inc PTH synthesis

1. Oral/nasal speech balance-talking through nose 2. ENOG test of 90% or greater 3. MC type of hyperthyroidism 4. MCC of 2ndary hyperthyroidism 5. MCC of hypothyroidism

1. Resonation 2. Warrants surgery--paresis doesn't warrant elctrophys test (only House Brackman Grade 6 does) 3. Primary 4. Chronic renal failure 5. Hashimoto thryoiditis

1. MC vascular anomoly to compress aerodigestive tract 2. MCC of esophageal rupture 3. What should we know about the lungs (unique feature) 4. Associated with impacted wisdom tooth. 5. Results from longstanding inflammation of tooth pulpitis/tooth trauma

1. Retroesophageal Right subclavian artery (must repair) 2. Instrumentation 3. Over 50% go to bilateral adrenals 4. Dentigerous cyst--around CROWN of UNERUPTED tooth, UNILOCULAR LESIONS on XR 5. Periapical cyst

Most importants: 1. Factor in prognosis of endometrial carcinomas

1. STAGE is most important in endo carc.

Quick and dirty breakdown of steroid synthesis

1. STAR (rate-limiting step of cholesterol transfer into mitochondria to begin steroid synth)--ACTH dependent in ADRENAL 2. Cholesterol --> pregnenolone via P450 SCC or Cholesterol-20-22-desmolase (RATE LIMITING STEP of cholesterol proceeding to steroid hormone) 3. A. Zona Glomerulosa (18-hydroxylase & 18-hydroxydehydrogrogenase-aka aldosterone synthase) B. Zona Fasciculata- 17-a-hydroxylase (part of protein P450c17)--to make cortisol (think F$ck @ 17 on prom night- prom night has prom court. C. Zona Reticularis- 17, 20 lyase, or 17, 20-desmolase (also part of P450c17) --think the laws where a 17 yo has sex w/20 year old (lyase with them) are a bit reticulous but horny boys full of androgens & DHEA will do it anyway.

Bold in handout so must be important... 1. Heinz bodies are only seen on.... 2. Deficiency of G6PD results in anemia...

1. SUPRAVITAL STAINS (NEW METHYLENE BLUE)...NOT on Wright-stains. BITE CELLS are seen on PERIPHERAL BLOOD SMEARS. 2. ONLY if person is exposed to oxidant stress (dapsone, fava beans)--X-linked

Flow of fluid...technically...?

1. Seminiferous tubules 2. Straight tubules 3. Rete testis 4. Ductuli efferentes 5. Ductus Epidiymidis 6. Ductus (vas) Deferens 7. Ampulla (plus semi tub) 8. Ejaculatory duct 9. Prostatic urethra Sem Straight Re*tards Definitely Epitomize DumDums, Amping rEJECTS Problematically

1. Sertoli tumors, benign or malignant? 2. Reinke crystals 3. Hydrocele causes fluid in... 4. Schiller-Duval body...tumor and marker 5. Verrucus Carcinoma...malignant? Associated with? 6. Parathyroid adenoma vs primary hyperplasia? (how many glands enlarged? 7. Markers of Embryonal cell tumor 8. MC extracranial solid tumor of children 9. MCC of primary hyperaldosteronism

1. Sertoli-RARE-- Sertoli--Bertoli--Benign 2. Leydig tumors 3. Tunica vaginalis 4. yolk-sac tumor-ENDODERMAL SINUS TUMOR--increased AFP 5. Verrucus--LOW malignant potention, HPV association 6. Parathyroid adenoma ONE gland, primary hyperplasia ALL 4 glands 7. Embryonal cell tumor +for CYTOKERATIN & CD30 and NEGATIVE for cKIT (seminomas have + c-KIT) 8. Neuroblastoma 9. Idiopathic--bilateral adrenal hyperplasia

Causes of hypemic hypoxia?

1. Sickle cell disease 2. CO poisoning 3. Methoglobinemia 4. Anemia

1. Simple PTX pressures 2. Tension PTX pressures

1. Simple--> Pleural P < atm P (trach shifts toward side) 2. Tension--> Pleural P > atm P (trach shifts away)--> needle decompression

Matching of sperm dev phases 1. Results in extensive cell remodeling 2. Undergo meiosis 3. Spermatocytes in meiosis II derived from primary spermatocytes are called... 5. Initial stage in sperm dev 6. Location of spermatogonia 7. Get arrested in the first division of meiosis...What phase? What cell? Derivation? 8. Nucleus is round or oval... 9. 2nd mitotic division results in... 10. Nucleus of spermatids

1. Spermatid phase (or spermiogenesis)--they DIFFERENTIATE INTO MATURE SPERM HERE 2. Spermatocyte phase 3. Secondary speratocytes (QUICKLY go into meiosis II) 5. Spermatogonial phase 6. Basal compartment of seminiferous epithel (since immature and start there) 7. Primary spermatocytes (der from B spermatogonia) arrested in PROPHASE I (first division of meiosis) 8. Spermatogonia 9. Haploid spermatids 10. Early- round nucleus, Later spermatids--elongated/flattened nuc.

Match these exam findings... 1. Stertor 2. Gurgly 3. Inspiratory stridor & feeding problems 4. Inspiratory OR biphasic stridor + hoarsness 5. Biphasic stridor + barking cough 6. Expiratory stridor

1. Stertor--nasopharyngeal 2. Gurgly--oropharynx (think of gurgly bubbles when trying to intubate oropharynx) 3. Inspiratory stridor & feeding problems--Supraglottic 4. Inspiratory OR biphasic stridor + hoarsness--Glottic 5. Biphasic stridor + barking cough--Subglottic 6. Expiratory stridor---trachEomalacia

1. Cell type shape commonly seen in alcoholics/alcoholic liver dz 2. Hemoglobin C dz mutation

1. Stomatocytes (mouth cells)--can also be seen in hydroxyurea therapy or myelodysplastic syndromes 2. POINT mut 6 in B-globin, glu-->lys

1. MCC of PAINFUL thyroiditis 2. MC site of otosclerosis 3. MCC of mucoepidermoid CA

1. Subacute granulomatous thyroiditis (de Quervain) 2. Otosclerosis--ANTERIOR to oval window 3. Radiation

Genes associated with: 1. Idiopathic pulmonary fibrosis 2. Adenocarcinoma (and what is a poor prognostic factor?) 3. Markers--Melanocytic & muscle markers

1. TERT and TERC genes (think people who use the word "TERF" are IDIOpaths) 2. EGFR (on quiz so probs not on test), ALK KRAS--poor prognosis 3. Lymphangiomyomatosis

Ductus (vas) deferens spans from what to what?

1. Tail of EPIDIDYMIS --> URETHRA -think--I epiDID this to Myself (or epiDID I MISS) by posting something on FB--> but now I found URETHRA the A*RSHOLE (You're the arsshole)--> now I am going to DIRTY DELETE (DD) Also remember--it has a VAST amount of muscle --Distal Dilates--> AMPULLA (like ANNOUNCING to the world you are TRASH)-->maybe you said some anti-semetic (seminal vessels dump here) remarks and they EJECTED (ejaculated you)-ejaculatory duct.--> so URTHRA as*shole

1. What could indicate a testicular or adrenal neoplasm? 2. What could indicate a testicular or pulmonary neoplasm? 3. MCC of hyperprolactinemia

1. Test and adren--> high estradiol 2. Test or pulm---> HCG 3. Hypothyroidism 4. Systemic illness

MCC midline neck masses

1. Thyroglossal duct cyst 2. Dermoid cyst

1. Lower 2/3 of vagina derived from? 2. Upper 1/3 of vagina derived from? 3. Tumors from lower 2/3 of vagina tend to spread to? 4. Tumors from the upper 1/3 of the vagina tend to spread to?

1. Urogenital sinus--squamous cell epithelium 2. Mullerian ducts---columnar epithelium 3. Inguinal nodes 4. Iliac nodes Lower 2/3-->Urogenital sinus (squam)--> inguinal nodes Upper 1/3--> Mullerian duct (colum epi)--> iliac nodes

Classic pimping question (maybe not test Q)....signs of placental separation

1. Uterus rises high in abdomen--> becomes globular 2. Cord lengthens 3. Gush of blood

Effects of ___________ on IGF & GH.... 1. Vasopressin 2. Acute (increase) Cortisol 3. Chronic (increase) cortisol 4. Which Sex hormones & thyroid hormones affect GH and which IGF? 5. Prolactin

1. Vasopressin--> stimulates ONLY GH 2. Acute (increase) Cortisol--> inc both IGF & GH 3. Chronic (increase) cortisol--> GH actions reduced 4. GnRH/LH/FSH/Estrogen/Test--> INC. IGF rel from gonads low TRH/TSH/T4/T3--> Low IGF & GH 5. Trick Q--> HIGH GH binds to prolactin recept--> lactation

GSDs 1. Deficiency of glucose-6-phosphatase 2. Lysosomal a 1, 4 glucosidase 3. debranching enzyme def 4. Branching Enzyme 5. Muscle Phophorylase 6. Liver Phosphorylase 7. Muscle phosphfructokinase 8. Liver Phosphorylase Kinase

1. Von Gierke's aka Type 1 2. Pompe's disease-Type II--Lame A$$ Girl is 2 pompus 3. Cori's disease Type III-duh 4. Anderson's disease, Type IV-he always reaches out to me (like branches) but I think him 4 the netflix subscription 5. McArdle's- Type V--MP--most people who eat at McDonald's or Arby's and get their $5 deals, don't have much Muscle... 6. Her's--VI--6 for the soccer chicks (I was also #6)-->destroying the liver was always fun on Sundays after soccer 7. Type VII--> Tarui's--> muscle phosphfructokinase-->MPFK--Many People F$ck/Kiss, while playing VII mins in heaven. 8. LPK--Let the Gr8est take the PK (in soccer)

1. Deletions in this lead to nephoblastoma in childhood 2. Mutations in Rb causes loss of ________ 3. Func of p53

1. WT1-Wilm's tumor (on chromosome 11) 2. Normal cell differentiation for most cells (rel to osteosarcoma, retinoblastoma) 3. DNA repair (DNA-binding phosphoprotein), growth arrest (neg reg of cell growth), apoptosis, complees w/viral prot prod by viruses (strongly assoc. w/tumors)--> loss of apoptosis. p53--> hepatocellular CA, Li-Fraumeni synd.

NHLBI rules for metabolic syndrome

1. Waist circ (40+ men, 35+ women--think- of course women are held to different lower weight standards lol) 2. Triglycerides- 150+ 3. HDL- <40 HDL men, <50 HDL women OR on drug for tx low HDL 4. BP- 130/85 5. FBG- 100+ OR drug tx for blood glucose

1. Axonotmesis **

1. Wallerian degeneration w/preservation of ENDONEURAL sheath.

BIOCHEM ENDOCRINE 1. Aldosterone synthase found in... 2. What enzyme is found in ZG but NOT ZF 3. Rate limiting enzyme in testosterone synth and function

1. ZG...aka 18-hydroxydehydrogenase 2. 18-hydroxylase 3. STAR is rate limiting--stimulated by LH--star transports chol--> mitochondria (ACTH-esterase from medullar req.). Star also removes side chain from chol--> PREGNENOLONE (This is IRREVERSIBLE & happens in mito)-P450

Buzzwords: 1. Acrosome of head of sperm degrades the _________. 2. Where centrioles are located on the sperm 3. Part of sperm that contains axoneme covered w/outer dense fibers 4. Part of sperm not covered w/outer dense fibers 5. Contains spiral mitochondria wrapped around outer dense fibers that surround the axoneme 6. Structure w/smooth mucosa? Without smooth mucosa? 7. Compound tuboalveolar glands of prostate lined with... 8. Organized into poorly defined layers w/i sem epi w/ most immature stages closer to ________ and most mature stages closer to......(what cell and location) 9. Principal cells that absorb luminal fluid & secrete substances to the lumen that aid in ___________. Location?

1. ZONA PELLUCIDA of the OVUM 2. Neck of sperm 3. Principal piece of sperm--LONGEST segment of sperm 4. End piece of tail 5. Middle piece of tail (which is actually attached to neck of sperm) 6. Smooth mucosa--ductus deferens (ducks definitely want smooth water), non-smooth mucosa--epididymis 7. Low columnar/cuboid pseudostratified epithelium 8. *Speramtogenic (germ) cells--Immature-Tunica Propria (basal comp) and mature--adluminal comp. 9. Aid in maturation of sperm--located in DUCTUS EPIDIDYMIDIS

healthy 200 lb man is producing 300ml/min of CO2 (STPD) at sea level (Pb=760mmHg). His minute ventilation (Ve) is 7.8L/min at a RR 12. Assume RQ is 0.8. 1. est. anatomic dead space. Are anatomic & physiologic dead space likely to be similar? 2. What is his alveolar ventilation? 3. What is his estimated dead space ventilation? What percentage of his ventilation is his wasted ventilation? 4. What is his mean alveolar PCO2 (PACO2)? His mean arterial PCO2 (PaCO2)? 5. Is he hypo-ventilating or hyperventilating? 6. calculate est. alveolar PO2 (PAO2). 7. Calculate his est. O2 consumption (VO2) 8. PaO2=83mmHg. What is his A-a gradient? a/A ratio? What does this tell us about gas exchange?

1. anatomical dead space: est. as numerically = to ideal body wt measured in Ibs. Since he is healthy, anatomical & physiological dead space are likely to be similar b/c anatomical dead space is negligible unless disease alters V/Q. 2. VA= VE -Vdf =7.8L/min - 200mlx12/min(L/1000ml)= 5.4L/min 3. VD= Vdf= 200x12(L/1000ml)=2.4L/min -what %: 2.4/7.8= ~30% 4. PaCO2=PACO2 so PaCO2=863 (VCO2/VA) PaCO2= 863 (300ml/min)(L/1000ml)/(5.4L/min) PaCO2=47mmHg 5. hypoventilating 6. PIO2= (760-47)x.209=149mmHg PAO2=PIO2 - PaCO2/R PAO2= 149- 47/0.8 = 90mmHg 7. VO2= VCO2/R = 300/.8 =375ml/min 8. PAO2=90mmHg (see #6), given PaO2=83mmHg =90-83= 7mmHg a/A= 83/90= 0.92, normal is > or = to0.8 so gas exchange is ideal

1. Enzyme that converts testosterone to estradiol 2. Enzyme that converts testosterone to dihydrotestosterone

1. aromatase (after you use the bathroom after a guy you need to aromatize it--> maybe DIOL the spray) 2. 5 alpha reductase (remember five-nasty-RED--finasteride)n

what factors determine the partial pressure of inspired oxygen?

1. barometric pressure 2. fractional concentration of inspired O2 the *partial pressure of inspired oxygen is inversely proportional to barometric pressure & fractional concentration of inspired O2*

1. Growth Factor Receptors (oncogene) 2. Protein kinases (esp tyrosine kinase)-oncogene 3. GTP binding proteins 4. Nuclear proteins acting as transc. fact.

1. c-erB, c-fms ("enlarge really big" & f&cking massive size) 2. c-src, c-fes 3. cH-ras, cN-ras, cK-ras 4. c-myc, c-fos, c-jun

Match the following 1. hyperglycemia/nl glucose tolerance 2. impaired glucose tolerance 3. T2DM a. 2x ↑ CV mortality b. 3x ↑CV mortality c. endothelial dysfxn

1. c. 2. a 3. b

Describe the organization of: 1. Adenohypophysis 2. Pineal gland 3. ZG 4. ZF 5. ZR 6. Adrenal medulla

1. clumps/cords around fenestrated capillaries 2. Poorly-defined clumps/clusters w/axons, pinealocyte cell processes, BV, & corpora arenacea in the spaces. 3. ZG--cuboidal/pyramidal cells in ARCHED/CURVED cords/colums-think of nephronglomeruli...they are curvy/arched 4. ZF: Straight cords that run at a RIGHT ANGLE and have fenestrated SINUSOIDAL capillaries between them. 5. ZR-irregular cords that anastomose to form a network 6. AM-polyhedral cells in clumps/cords

Penis: 1. Smaller ventral cylinder 2. 2 large dorsal cylinders 3. Which contains glands of Littre? What are they? 4. Proximal vs distal portions of corpus spongiosum 5. Which one ends distally with the glans penis? 6. What is the prepuce rich in 7. Arteries of penis? What does one form? 8. Supply of the corpus spongiosum?

1. corpus spongiosum 2. corpora cavernosa 3. Corpus spongiosum--glands of Littre (sponges soak up litter SORTA-pseudo stratified)--spongy urethra PROXIMAL PORTION 4. Proximal-pseudostratified, Distal-non-keratinized strat sqam epi (makes sense since about to leave 5. Corpus spongiosum--overlap of penile skin called prepuce 6. Prepuce-elastic fibers 7.- Deep arteries, dorsal arteries, artery of bulb, urethral arteries Deep form nutritive HELICINE arteries (helical while flaccid--straighten while errect) 8. Well since it forms the bulb--artery of the bulb

how do we calculate the *inspired partial pressures* for a given gas?

1. determine barometric pressure 2. subtract the vapor pressure of H2O at body temp (47 mmHg) 3. multiply this value by the dry air fraction of the given gas

MC manifestation of: 1. Primary hyperaldosteronism

1. elevated BP

Steps of knockout

1. gen of mouse germ-line chimeras from embryo-derived cells (ES), which cont. targeted gene disruption 2. transfect w/targeting vector (ES cell cultur w/rare targeted cell) 3. Pure population of targeted ES cells 4. Injection of ES cells into blastocyst 5. Implantation into foster mother 6. chimeric mouse breeds w/ +/+ animals 7. Germ-line transmission of ES cell genome containing targeted modification.

Functions of Sertoli cells

1. interact w/ spermatogenic cells during dev 2. Nourish germ cells by secreting fructose 3. Germ cell movement & differentiation-move from basal to adluminal comp (elongate spermatids via "passive stretch") 4. Structural support of sem tub-->well-dev cytoskeleton (allows for shape, transport organelles, and stabilize plasma memb. 5. Form tight junction w/ other sertoli & germ cells-->divide seminiferous epi into *BASAL* and *ADLUMINAL* compartments 6. Secrete enzymes (diff card) 7. Phagocytize residual bodies & degenerated germ cells --Active cells, w/Large, irregular, very-light staining, EUCHROMATIC nucleus, well-expressed nucleolus Think- Bertoli spaghetti... YOU (EUCHROMATIC-me) eat IRREGULAR meals, but when I do they are LARGE meals. I am also an active person (sometimes). My hunger is WELL-EXPRESSED so I NUCH some food (well expressed nucleoli)...if i spill something on my shirt i might get a LIGHT STAIN. -Tight/occluding junctions that can dissassemble/reassemble (tuperware). -SECRETE ABP- My boyfriend, Always Be Peter trynna take over the kitchen (cause he wants to maintain his high levels of TESTOSTERONE--leydig.) --he is always INHIBINing me from tryna cook-->cause he a Food Stealing Hoe (inhibits FSH) -- -then you eat residual bodies

Which one is microvascular complications & which one is macro? 1. During prediabetic phase 2. Onset of hyperglycemia

1. macro 2. micro

What are the four benefit groups for statin therapy?

1. pt's with clinical ASCVD 2 Pt's with primary elevation of LDL C >189 3. Pt's 40-75 yo with DM and LDL C 70-189 without clinical ASCVD 4. Pt's without clinical ASCVD or DM between 40-75 with LDL C 70-189 with estimated 10 year ASCVD risk 7.5 or greater

List 2 important surface tension properties of surfactant.

1. surface tension is proportional to area 2. average ST is low

Buzzwords: 1. Location of rete testis 2. contain the ductus epididymidis 3. Contain mostly efferent ductules 4. Formed by anastomosing system of ducts lined w/simple cudoidal epithelium 5. Opens into bulb of spongy (penile urethra) 6. Contains numerous wide, irregularly shaped vascular spaces lined w/epithel 7. Vascular spaces filled with blood during erection, what forms these? 8. What weird trend happens in ductus epididymidis?

1. within connective tissue that forms the MEDIASTINUM--call respiratory if mediastinum in wrong pl (not really doe) 2. Body & Tail of ductus epidiymidis 3. Head of epididymidis--BEGINNING of ductus epididymidis 4. Rete testis--I Rete (hope dis) TESTIS SIMPLE--so a SQUARE can get it (cuboidal epi)...but they could be really ANASTY w/Qs. 5. Bulbourethral glands 6. Corpora cavernosa 7. In the corpora cav or copus spongiosum--> Thin layers of smooth muscle forms TRABECULAE 8. *Height of epithelium & length of Stereocillia decrease distally...but thickness of Smooth muscle coat INCREASES distally*

1. Histological description of pituitary gland capsule 2. Pineal gland capsule?

1.Pituitary--Dense irregular (since it is dura mater) 2. Pineal--pia mater capsule w/septa/with blood vessels

What is meant by P50?

1/2 of Hb binding sites are filled PO2 27mmHg at 50% sat

What should Plasma Glucose be if A1c is 6? 12?

126 298 7=154 8=183 9=212 10=240 11= 269

What is best in diffuse small thyroid w/o nodule? What do you avoid it in?

131-iodine; highly effective avoid in thyroid eye disease

1st MCC of hereditary thrombophilia 2nd MCC of hereditary thrombophilia

1st- Factor V Leiden 2nd- Prothrombin 20210A transition

Patient presents with nausea, weakness, confusion, hyperpigmentation, abdominal tenderness and postural hypotension. What do they have? What do their electrolytes look like? What test do we need to do? Should we operate?

1° AI Hyperkalemia and Hyponatremia Cosyntropin stim test (goal of cortisol= >20mcg/dl) NO! could precipitate an adrenal crisis (w/o proper steroids) Hypoglycemia (rare Longer AI might see electrolyte imbalance and wt loss

Patient presents with hypokalemia, HTN and metabolic alkalosis. What do they have? Is renin high or low?

1° Hyperaldosteronism Renin is low (would be high in 2°)

Major & minor criteria for rhinosinusitis...how many do you need of each?

2 major or 1 + 2 minor Major: facial pain, nasal obstruction, hyposmia, purulence on exam, fever Minor: Ha, fatigue, dental pain, cough

2. Spermatazoa-activating substances ________ produces by _________ in the _________. 3. seminal vesicles enter into ampulla becoming... 4. Muscular coat of ampulla is..... 5. Connects rete testis to ductus epididymidis 6. Contains pseudostratified columnar epi w/ sterocilia 7. Contains low pseudostratified columnar--both cil & non-cil = saw-tooth pattern 8. Contains smooth muscle & CT w/associated vessels in its walls, what does it receive fluid from? 9. Contains inner longitudinal, middle circular, & outer longitudinal layer 10. Runs thru prostate & connects to prostatic urethra

2. Muscosa-sec granules of seminal vesicles--> carbohydrates (fructose), prostaglandins, & proteins 3. Ejaculatory duct 4. Thinner than rest of vas deferens 5. Ductuli efferentes 6. Ductus epidydmidis--pseudostrat columnar w/stereo--ducts on EPInephrine are SORTA (PSEUDO) crazy...and they STARE a lot 7. Ductuli Efferentes-turn E on its side and SORTA (PSEUDO)--looks like a saw --> see-saw---see saw w/EFFRIEND (efferentes)-can't do it alone 8. Ductus epididymidis (receives fluid from ductus efferentes) 9. Muscularis of ductus vas deferens--to shoot it far (VAST) you gotta have a LOT more muscle than before- 3 layers 10. Ejaculatory duct

Presents with adrenal crisis with ambiguous genitalia. What enzyme deficiency do they have? What sex? How would it present if they were older?

21 hydroxylase def (congenital adrenal hyperplasia) Female (infant) Adult=hirsutism

If you can't use free cortisol levels (in blood) in a pt taking estrogen how can you check them? *From review of cases

24 hr urine cortisol

BAL in bronchioalveolar lavage in eosinophilic lung disease shows how many eosinophils?

25%

Terminal Sac phase

26 W-birth -Simple squamous epithelium forms -Terminal sacs become alveolar sacs -pneumocytes I & II form -ALVEOLI form

Patient presents with fatigue, weakness and no change in skin color. Labs show ↓Na, and normal K Does this patient have 1° or 2° AI? What imaging should be done for both kinds of AI?

2° Typically steroid dependent (hx of longterm use) CT= 1° MRI= 2°

Pt has ↑PTH and normal or low Ca. What do they have?

2° HyperPTH Causes: hypercalciuria, hypo VitD→renal failure, intestinal surg w/malabsorption, low PO4, insuff sunlight, loop diuretics

VitD deficiency provokes 1° or 2° hyperPTH?

2° HyperPTH VitD def→↓U(Ca) Tx: OTC/Tx VitD (can be measured as storage form) Tx: may resolve what may appear to be oseopenia/porosis

Formed elements -Leukocytes; lymphocytes, populations

3 main populations -T cells (80%) -B cells (15% -NK cells (< 5%)

Patient with HIV is pre-diabetic when should you check them next?

3-6 months later

Buzzwords: 3. Fibrocollagenous capsule that surrounds ________ which sends septa part-way into its body (ill-def lobes) 4. Contraction of ______ during ejaculation secretes ________ 5. Contains deep longitudinal folds 6. Testicular temperature due to the ___________ that _________. 7. Principle site of sperm maturation 8. When spermatozoa become motile 9. Straight tube that continues from epididymis--> prostatic urethra (emptying into it) 10. Smooth muscle coat that inc distally--> 3 layered in tail 11. Pseudostratified columnar epitelhium w/LONG microvilli/stereocilia

3. Prostate--capsule also cont smooth muscle fib 4. Muscularis of seminal vesicles secretes into ejaculatory ducts 5. Mucosa of ductus vas deferens 6. 35 degrees...due to PAMPINIFORM PLEXUS around spermatic artery that acts as COUNTER-CURRENT heat exchange system 7. *Epididymis* 8. *When they pass thru ductus epididymidis* --DUCKs on EPInephrine do more work!! 9. Ductus (vas) deferens 10. Ductus epididymidis 11.Mucosa of ductus vas deferens (think ductus VAST deferens--their microvilli/stereocilia-think I have AVATAR on DVD and it was LONG--it was like pseudoscience (pseudostratified epi)

Active hormone testing should be considered when testosterone falls below what number? What's the best time of day to check?

300 peak is at 8am screen total testosterone goal 300-400 highest T value= true value if it's nl @ 4pm

Body of larynx forms from what pharyngeal arches

4 & 6

4. Mucus secreting glands that produce watery/slightly mucous fluid w/abundant sugars....where is this and what is the purpose? 5. Dilation of vas deferens prior to prostatic urethra--description of this structure? 6. Seminal vesicle gland activity controlled by.... 7. Forms primary, secondary, tertiary folds... 8. Largest accessory sex gland in male--what kind of glands does it contain? 9. Binds seminal vesicle to the surrounding structure 10. Compound tubuloalveolar glands...

4. Bulbourethral glands--Fluid PRECEDES the thicker semen and is thought to have a LUBRICATING effect 5. Ampulla--HIGHLY FOLDED 6. Testosterone 7. Mucosa of seminal vesicles 8. Prostate--BRANCHED TUBOALVEOLAR GLANDS embedded in sup stroma 9. A fibrous coat--Adventitia of seminal vesicle 10. Bulbourethral glands (Cowper's glands)--Compound Cowper--cows eat daisy bulbs

In a normal person what would the O2 saturation at a PO2 of 40 mmHg? At 27 mmHg? At 60mmHg?

40-->75% 27-->50% 60-->90%

ACS recommendations for breast cancer screening

40-44 yo-annual mam if they want 45-54- annual 55+= every 2 years or continue annually --stop when no longer in good health and life expec is <10 yrs

in a normal person, what would be the O2 saturation at a PO2 of 40mmHg? At 27mmHg? At 60mmHg?

40mmHg=75% 27mmHg=50% 60mmHg=90%

what is the vapor pressure of H2O at body temperature?

47 mmHg

What's the karyotype for Klinefelter? Turner? nl male?

47XXY (hypergonadotrophic hypogonadism) 45XO (hypergonadotrophic hypogonadism) 46XY

What converts T4 to T3?

5'-deiodinase

Estimated average glucose (prediction?) 5 6 7 8 9 10 11 12

5-97 6-126 7-154 (7x8 = 54) 8-183 9-212 10-240 (most people A-TEN-D medical school @ 24) 11-269 (11 heaven--> 2 people 69) 12-298 (basically 300) 6&8 have a number mate

Who needs to be screened for Lung CA? How often?

55-80 yo w/ 30 pk/yr hx and currently smoking or quit in last 15 years, LOW DOSE CT, ANNUALLY

Pseudoglandular phase of lung development

6-16 weeks--> between that time you're pseudo--almost a teenager -Columnar epithelium--cause it makes up big ole glandy bois. -highly vascular but isolated from epithelium -lung is MORE GLANDULAR (hence the name) than respiratory --TERMINAL BRONCIOLE is MOST DISTAL

p-ANCA, MPO-ANCA

98% specific for -Microscopic polyangiitis -Churg-Strauss vasculitis -Idopathic crescentic GN

HIV -Dx

< 200 CD4 T cell count = AIDS Once progressed in stage, never go back

PG value for HYPOglycemia?

< or = 70 mg/dL*

What's the recommended A1c for a nonpregnant adult w/DM? Peak postprandial capillary plasma glucose?

<7% <180mg/dl

What are the diagnostic criteria for DM type 2? FPG 2 hour plasma glucose during OGTT A1c Random plasma glucose

>126 mg/dl >200 mg/dl >6.5% >200 mg/dl (w/sx of hyperglycemia)

How much will FEV1 drop after Methacholine Challenge (bronchoprovacation) in asthma pt?

>20%

Suitable culture from sputum or blood must have:

>25 neutrophils,< 10 Squamous epithelial cells

What's the goal for 25 (OH)2 Vit D

>30 Calcitriol is endo of the line prod of VitD in kidney

Where are the following found? A. Motile cilia B. Immotile Cilia C. Immotile microvilli D. Microvilli (handout did not specify)* (in olfactory epithelium) *what do these cells do?

A. Motile Cilia--> *Respiratory segment (on the TALL COLUMNAR CELLS)*--think--need to move mucous along surface B. Immotilie Cilia--OLFACTORY CELLS (specifically on the APICAL surface of the) C. Immotile Microvilli BRUSH CELLS (short blunt, immotile MICROVILLI) D. Sustentacular cells!--Produce ODORANT-BINDING proteins (ie METABOLIC support) & provide mechanical support TL;DR: Motile Cilia--> RESPIRATORY EPITHELIUM Immotile Cilia-->OLFACTORY CELLS Immotile Microvilli--> BRUSH CELLS Microvilli--> SUSTENTACULAR CELLS

Evidence grades?

A: meta-analysis of randomized controlled trials B: non-randomized or case-controlled trials, prospective cohort studies, retrospective case-control studies C: cross-sectional studies, surveillance studies, consecutive case series, single case reports D: no evidence, just theory and opinion

what hormone promotes melanocytes to produce melanin other than MSH?

ACTH

Cushing disease?

ACTH-dependent Cushing syndrome. usually d/t pituitary adenoma causing increased secretion of ACTH leading to increased cortisol secretion

Predicted normal values for PFTs depend on:

AGE, Height, Sex, Ethnicity

How are pregnant women screened for gestational DM and what results confirm dx?

ALL pregnant women screening 2 hour OGTT at 24-28 weeks FPG >92 1 hr > 180 2 hr >153 If any are positive, she has GDM

gingival hyperplasia

AML

t(16;16)

AML w/ inv(16)

t(8;21) ETO

AML w/ t(8;21) younger patients

strongly MPO positive (spikey sea urchin)

APL

what is the key model for bone turnover?

ARF activation resorption formation

Adult w/nasal polyps & bronchospasm

ASA-intolerant asthma (in Children test for CF)

MCC of acute renal failure

ATN

What factors are evaluated according to ATP III in diagnosing Insulin Resistance Syndrome

Abdominal obesity (waist > 40 in men, 35 in women) Hypertriglyceridemia (>150 mg/dL) Low HDL (men <40, women <50) Elevated BP (>130/85) Hyperglycemia (serum random glucose >110) 3/5 considered IRS.

A-glucosidase inhibitor

Acarbose (and miglitol)--inhib a-glucosidase & delay absorption of carbs from intestines --AVOID METFORMIN....think of acarbose--> a carpet in aladdin--aladdin was FORBIDDEN---> met FORBIDDEN... -obvi diarrhea & cramps/flatulence

MCC of dwarfism

Achondroplasia

2nd most common MALIGNANT salivary gland tumor in CHILDREN...Where is it almost ALWAYS located? What other tumors are almost always located here too?

Acinic Cell Carcinoma (2nd most in children, *1st is mucoepidermoid carcinoma*) Located in the PAROTID GLAND: -Salivary Duct Carcinoma (remember the parotstitute) -Mucoepidermoid carcinoma (#1 in children) -Warthrin tumor (motor oil) -Oncocytoma -Pleomorphic Adenoma (but sometimes other glands) mnemonic--Parostitutes (gland) Accept (in the accinic region) Old Warthless Mucky PeonisAnd (pleomorphic aden) SD (salivary duct)

*Sulfur granules on sinus tracts* in microscopic eval from pus/tissue CXR pneumonia will cross fissures Tx

Actinomyces - indolent progressive infection that colonies mouth, colon or vagina prolonged: IV PCN for 2-6 weeks, followed by PO Amoxicillin for 6-12 months

Cough Work up #1 Nasal Antihistamine-Decongestant #2 ???

Add nasal steroid or anticholinergic

Cough workup #1 Nasal Antihistamine-decongestant #2 ???

Add nasal steroid or anticholinergic

Infiltrates perineural spaces surrounding nerves

Adenoid Cystic Carcinoma--> PAINFUL (malignancy w/late mets)

What is metastatic at dx, presents w/wt loss and is rapid onset?

Adrenal Carcinoma

What's the difference between ACTH independent and ACTH dependent Cushing disease?

Adrenal dz (low ACTH and high cortisol) vs Cushing Dz: Pituitary= source (high ACTH high cortisol) Cushing sydrome: ectopic source (MCC=Small cell_)

What is the gold standard for dx of 1° hyperaldo? Treatment options?

Adrenal venous sampling Unilateral adrenal (aldo) adenoma (conn synd)= surgery IHA w/bilat dz = no surg, spironolactone, restrict Na

Components of Cumulus mass

After thecal wall ruptures and rel liquor folliculi, cumulus mass left over & contains... 1. 2/2 oocyte 2. Zona pellucida 3. Corona radiata 4. Remnants of oophorus (still attached to corona radiata)

List some things important in Medical history of DM eval

Age and characteristics of onset of DM Eating patterns, nutritional status, wt history, activity level common comorbidities, psychosocial dz screen depression, diabetes smoking, alcohol, substance abuse DM education, self-management previous treatment regimens and response results of glucose monitoring History of ↑BP, lipids, tobacco use Micro vs Macro problems **hopefully this is a common sense slide

What are the variables considered in the WHO Frax program model?

Age, sex, weight, height, previous fx, fmhx of hip fx, current smoker, glucocorticoids, RA, secondary osteoporosis, 3 or more units of ETOH/day, femoral neck BMD Modifiable RF: smoking, ETOH, weight

What is the part os the uterine tube where the egg is fertilized?

Ampulla

Systemic Anterior Subglottic mass

Amyloidosis

Most aggressive cancer with poor prognosis

Anaplastic no response to RAI or surgery

How often should you monitor for a prediabetic patient?

Annually (also can receive DSME/DSMS) promote diet and exercise Metformin for BMI >35 , <60yoa, and women w/GDM

Antibody SPECIFIC for RA

Anti-CCP antibody

splicing precursor mRNA aka "anti-U1-RNP" Commonly seen with anti-sm seen in all Mixed connective tissue disorder cases

Anti-RNP

highly SPECIFIC for scleroderma aka "anti-Scl-70"

Anti-Topoisomerase I antibody

antibody found in DRUG induced (95%) cases **Hydralazine, Procainamide, Isoniazid **Common board question

Anti-histone antibodies

MC culprit in DILE

Anti-hypertensives & anti-fungals Hydralazine, procainamide, isoniazid, D-penicillamine * high freq of anti-histones

What is the prep for a thyroidectomy?

Anti-thyroid meds and beta blocker Thyroid fxn: pre-op= surgery day

Antibody NON-specific for lots of stuff Directed against nuclear macromolecules Order when SLE suspected dt Hx and PE can R/O SLE when negative Will indicate pts with arthritis

Antinuclear Antibody (ANA) *ANA panel NOT necessary when ANA is negative

Superior mediastinal widening >9cm supine suggestive of what?

Aortic Disease

Superior mediastinal widening >9 cm supine suggestive of what

Aortic disease

MCC of death in first few hours after MI

Arrythmia

Arthralgia vs arthritis

Arthralgia -Joint pain (may not be inflammation) Arthritis -Inflammation of joint -Redness, pain, swelling, warmth, fluid accumulation, stiffness (esp in AM)

What structure forms from neural crest cells and develops into arytenoid cartilages and reshape the laryngotracheal groove into the glottis?

Arytenoid swelling

If I take a Bronchodilatory reversibility test and my FEV1 increases more than 200ml and 12% above pre-dil FEV1 what do I have?

Asthma

When do you give DSME/DSMS?

At diagnosis Annually (assessment of education, nutrition and emotional support) When new complicating factors arise that influence self-management Transitions in care

Proper degree of inspiration in an Adult CXR:

At least 9 or 10 Posterior Ribs & 5-6 anterior Ribs

Proper degree of inspiration in adult CXR

At least 9-10 posterior ribs -5-6 anterior ribs

Where is decompression for Bell's palsy directed?

At the narrowest part, Labyrinth portion. Middle fossa decompression of nerve performed within 14 days of paralysis significantly improves outcome

If my patient needs a high intensity statin what are my options?

Atorvastatin (80mg) Rosuvastatin (20 mg)

High dose statins

Atorvastatin 40-80 (think 8-torvostatin) Rosuvastatin 20-40

MC cytology abnormality on PAP

Atypical Squamous Cells of Undertermined Significance (ASC-US) Comprise 1/2 pts w/CIN2 or CIN3

Describe Grave's disease

Autoimmune dz autoab (TSI-Ab) attack TSH receptor stimulating it to overproduce TH --> thyroid hypertrophy --> goiter

(+) for CD34, TdT, CD19, CD20

B-ALL or B-LBL

Causes for a post-infectious cough?

B. pertussis, M pneumo, C. pneumo also consider ACE-i use and psychogenic

US shows hypoechoic microcalcification, not shadowing ↑intranodular vascular flow irregular border Bad or Good

BAD! Good: hyperechoic, lg, course calcification w/shadowing, peripheral vascularity, comet tail, egg shell calcification

What thalassemia can present 2/2 cryptic splice site? And what is a Cryptic splice site?

BETA!! Remember COLTEEEE is a beta and Larissa SPLICED his dumb little heart. Cryptic splice site is ALMOST a splice site and has variable interpretation during transcription so sometimes read, sometime not. --Can change reading frame--> can cause no Hb

Who has continuous smooth muscle? Who has discontinuous cartilage? What is the cartilage surrounded by? Who has discontinuous smooth muscle?

BOTH of the first 2 apply to the BRONCHI: --*Continuous SMOOTH MUSCLE in the MUSCULARIS--makes sense since it needs to constrict the whole vessel* --DISCONTINUOUS CARTILAGINOUS PLATES (hyaline) (betw. submucosa & adventitia) ^Perichondrium surrounds it and descends ALL the way into MINOR BRONCHI--> when they disappear--> it is now a bronchiole! TRACHEA--> smooth muscle betw submuc & adventitia) is DISCONTINUOUS (only found on POSTERIOR side of TRACHEA)

Bowman's gland is what type of gland? Other name? Where is it found? What else is found in this location?

BOWMAN'S GLAND = OLFACTORY GLAND --BRANCHED TUBOALVEOLAR, SEROUS SECRETING GLANDS. --short ducts bring WATERY secretion to surface--> washing of olfactory surface --Found in LAMINA PROPRIA of olfactory epithelium (reminder--> the LP here is Thicccc) --unmyelinated axons & VENOUS SINUSES are NUMEROUS here.

Where is the order of layers screwy/confusing?

BRONCHI!--they be crazy 1. mucosa (balt is here) 2. MUSCULARIS 3. submucosa 4. discontinuous cartilaginous plates 5. Adventitia

Use of PDE inhibitor in CODP

BRONCHODILATOR in COPD

Other diseases and infections that may have RF ***(he said we don't need to memorize these, but they are starred in the lecture, so they get a note card): Infections: (5) Pulm diseases: (1) Misc: (2)

Bacterial endocarditis Hep B or C Syphilis Leprosy Viral Infx Sarcoidosis Primary Biliary Sclerosis Malignancy

MC type of vulvular cyst

Bartholin cyst -MC in 3rd decade

Basal cell vs Squamous cell Carcinoma of the pinna? (sun exposure? men/women?)

Basal cell--elderly men, YES SUN Sq Cell--older women, NO SUN

Base Excess equation? Interpretation of value

Base excess = [HCO3 Observed] - [HCO3 Predicted] Positive value: accumulation of bicarb (uncompensated alkalosis) *Negative value*: accumulation of acids (*uncompensated acidosis*)

In the upright normal lung: 1. Ventilation is greatest at _________. 2. Blood flow is the greatest at _________. 3. V/Q ration is greatest at the __________.

Base, base apex

Change the Care system CCM: Decision support

Basing care on EBM Expand role of team Redesign care process implement EHRs activate and educate patient remove financial barriers ID community resources Coordinated primary care changes to reimbursement

What happens to the epithelium when the primordial follicle changes to a primary follicle?

Becomes cuboidal/columnar

Out of the two cells produced as the result of meiosis 1 of the primary oocyte only one will continue as the secondary oocyte. What happens to the other cell?

Becomes first polar body - receives little cytoplasm and will go through apoptosis

2 newest TB drugs

Bedaquiline--inhibits proton pump for ATP synthase (bactericidal) Delamanid-inhibits mycolic acid synthesis both can cause QT Prolongation

MC FNA result

Benign

Ovarian tumor 30+ yo

Benign surface epithelial tumor

Pediatric salivary tumors--MC benign and MC malignant

Benign: MC--Hemangioma & pleomorphic adenoma Malignancy: Mucoepidermoid tumors

GPIb gene mutations

Bernard-Soulier syndrome

Hemoglobin D mutation

Beta chain Glutamate 121 --> Glutamine

Targeted Drug Therapies: monoclonal Antibodies

Bevacizumab - monoclonal antibody therapy that prevents neo-vascularization by inhibiting blood vessel growth Erlotinib - blocks chemical that cause CA cell to grow & divide

MCC of cholestatic jaundice in newborn

Biliary atresia

Traditional first choice in treatment of osteoporosis?

Bisphoshphonates. poorly absorbed and need to be taken on an empty stomach. pt can't lay for 1 hour after.

Patient takes medicine on empty stomach with full glass of water and is NPO for one hour. What med did they take?

Bisphosphonate (1st choice for osteoporosis tx) Also don't lay down; ↓fx risk ADVERSE: osteonecrosis of jaw and joint aches

How does O2 unloading in tissues affect CO2 uptake by blood?

Bohr: decreases CO2

Patient presents with ↓PO4, ↑Ca (24hr) & ↑PTH/inappropriately nl PTH. What do they complain of in the clinic?

Bones (osteoporosis), groans (kidney stones), and psychic moans

Q fever presents how

Bradycardia Hepatomegaly Endocarditis Abnormal LFTs

Difference between branchial cleft cyst & thyroglossal duct cyst

Branchial cleft cyst--LATERAL NECK, does NOT MOVE when pt swallows --big branches of a tree stick out laterally and dont move when swallows land on them Thyroglossal duct cyst--MIDLINE, DOES MOVE when patient swallows.

What does it mean if pt has Pagets carcinoma of the breast vs vulva?

Breast--CANCER in the BREAST--Breast--Bad Vulva--NO underlying Cancer (big important)

You decide to utilize Coumadin as prophylactic therapy for a DVT. What must you do to ensure that this therapy is successful?

Bridge Coumadin therapy with *LMWH/Heparin until INR reaches 2.0-3.0*

Blastomycosis - Features

Broad Base budding - SE, south central states, MW, Canadian provinces by great lakes

Tram tracks or ring-shadows?

BronchiecTASIS

t(8;14) c-myc w/ immunoglobulin heavy chain mostly (also IGK, IGL)

Burkitt lymphoma

"starry-sky" appearance of tissues or lymph nodes

Burkitt lymphoma blastoid mantle cell lymphoma acute lymphoblastic lymphoma others

Ki-67 (+) almost 100% TdT and CD34 (-) deeply basophilic cytoplasm w/ lipid vacuoles

Burkitt lymphoma (look like blast but aren't b/c they are negative for TdT and CD34 which are markers of immaturity)

A textile-worker presents to your office with complaints of asthma-like symptoms that are worst on Mondays, and diminish throughout the week. PFT shows obstructive changes. What is their diagnosis?

Byssinosis Back to work on Monday--> Back to Byssinosis as usual

Acute phase protein produced by the liver

C reactive protein

Angioedema -Tx

C1 esterase inhibitor

Treatment for all the pneumonias under all the conditions

CAP Outpatient--DOXY or Azithromycin CAP-inpatient-- Ceftriaxone +Azith or DOXY CAP-ICU------Ceftriaxone + Azitrhomycin OR levofloxacin

Criteria for bone marrow and the ONLY contraindication?

CI: not meeting one of the following: 1. fever unknown origin 2. Blood abnormality w/o known cause 3. monitoring response to therapy 4. Diagnosis of neoplasms 5. Staging/management 6. Atypical but nondiagnostic lymphoid process in other sites 7. Eval for inf disease when other tests non-informative 8. unexplained radiographic lesions 9. Eval of pt who does not follow predicted course of initial diagnosis 10. Bone marrow eval prior to transplant

If patient complains of severe muscle sx or fatigue while taking statins what 3 labs would you check? and for what reason?

CK Creatinine UA for myoglobinuria --check for Rhabdo *Possible test Q?*

"soccer ball" lymphocytes and smudge cells

CLL/SLL

Role of Lipoproteins in respiratory system? Produced by what?

CLUB CELLS produce SURFACE-ACTIVE AGENTS that prevent luminal adhesion in case of airway collapse. --club promotors prevent the FAT PEEPS from crowd SURF(acing)...cause they may cause COLLAPSE and that would be a STICKY (adhesion) situation.

Well-developed RER,SER, and Golgi...what cells in respitratory system? What do these cells have?

CLUB CELLS--bulging surface cytoplasm --since they secrete protein they obviously have well-developed RER, SER, Golgi --Vesicles contain CLUB CELL PROTEINS & LIPOPROTEINS that are SURFACE-ACTIVE agents that prevent luminal adhesion in case of airway collapse. -

dwarf (monolobulated) megakaryocytes and pseudo-gaucher cells

CML

MC congenital viral infection

CMV--> Common Mom Vector

Name the single most important blood gas value determining the level of central chemoreceptor stimulation? Peripheral chemoreceptor stimulation?

CO2 O2

In what form is CO2 carried in blood? What is the % contribution of each?

CO2 is carried in the blood: (90%)HCO3-, dissovled in plasma (5%), bound to Hb (5%)

Pt has an O2 consumptions of 500ml/min. if his arterial-venous O2 difference is 5ml/dl, what is his CO?

CO=Q Q=VO2/(CaO2-CvO2) Q=(500ml/min)/(5ml/dl)=100dl/min(L/10dl) =10L/min

-Risk of ICS in COPD pts -AE effects of ICS in general

COPD--PNA --oral candidiasis, dysphonia --high dose, HPA axis suppression, CATARACTS, GLAUCOMA, bone demineralization

OSA treatment?

CPAP

ANCA -Drugs

Can be + with drugs -Hydralazine -Minocycline -PTU

SGTL2 Inhibitors

Canagliflozin, Dapagliflozin, Empagliflozin --Some Glucose Lost 2 Tinkle (GLUT2 mostly) --10% kidney & gut (SLGT1) --90% PCT (SGLT2) --DM II--dec risk of CV death, CVD (Empagliflozine & Canagliflozin) --Significantly Gain (of) Total Life! --Rifampin INDUCES UGT1A9--> DECREASES CANAGLIFLOZIN--> Rifampin causes Canagliflozin to RIP through you canal (excrete fast basically) --inc risk for UTI (glucose excretion-duh)

Multiple lesions, coal macules do not grow/progress after exposure. What disease can this associated with?

Caplan's Syndrome - Any inorganic pneumoconiosis + Autoimmune disease (Lupus, RA)

What should pradial insulin dose match in T1DM?

Carb intake, premeal blood glucose, anticipated activity

MCC of breast mass in post-menopausal pts

Carcinoma of the breast: Invasive ductal, invasive lobular, medullary carcinomas, mucinous carcinomas

MCC of hydrothorax

Cardiac failure (Either uni or bilateral)

Where is each type of emphysema located in the lungs?

Centroacinar--> Apex (since caused by smoking/smoke rises) Panacinar--Lower lungs/ant margins Paraseptal--mostly upper half of lungs Irregular--small foci anywhere

What MUST you do if pt has acute cervicitis

Cervical CULTURE is MANDATORY Also get: Gram stain, PAP (to R/O CIN), Dx by: Vaginal pH>4.7, Cervix Friable to touch, Wet mount = Multiple PMNs

What is the "gold standard" for diagnosing a PE? Tx?

Chest CT with Contrast (CTA) Treatment of PE: Fibrinolysis

Explain synthesis & post-translational process of PTH protein

Chief Cells in PT gland work on *N-terminal* Prepro-PTH processing in *ER & Golgi* then released to: -transp to storage -degrade -immediate secretion

The exception to fever in neonatal PNA?

Chlamydia trachomatis

When is it indicated to get an CXR for a pt w/ cough?

Chronic Cough or Smoker

MC chronic form of cutaneous lupus erythematosus

Chronic discoid erythematosus (DLE) *systemic manifestations rare, dsDNA RARELY present

I tap the cheek and the mouth and eyes twitch. What's this called? What's causing it?

Chvostek Sign ↓Ca ↓PO4

Patient presents with pleural effusion, from a traumatic injury. Fluid is Milky fluid w/ high TAGS. Dx:

Chylothorax - thoracic duct leaks lymph fluid, usually due to trauma

What is the epithelium of the uterine tube?

Ciliated simple columnar

Terminal bronchioles lined with?

Ciliated simple cuboidal epithelium AND Club Cells CLIATED CELLS outnumber all other cell types

Reed-Sternberg cell

Classical Hodgkin lymphoma (must have at least two nucleoli in two separate nuclear lobes)

Grading system A

Clear evidence from RCT includes evidence from multicenter trial/meta analysis compelling nonexperimental evidence supportive evidence from RCT

CI for thyroidectomy/adenoidectomy

Cleft palate, leukemia, hemophilia, systemic disease

MCC of painless jaundice

Common bile duct strictures caused by carcinomas of the pancreatic head

Besides checking height, wt, BMI, BP what other important exam did he mention was important for a diabetic eval?

Comprehensive foot exam

Where are type II pneumocytes concentrated and what do they contain? How do they release substances? More or less than type I pneumocytes?

Concentrated at the SEPTAL JUNCTIONS --they contain MULILAMELLAR BODIES (surf) --EXOCYTOSIS -- type I & type II pneumocytes are EQUAL in #

Where are primordial follicles found?

Concentrated in the outer cortex close to the tunica albuginea

CURB65....what does it tell us?

Confusion Urea >7 mmol RR >30 BP- <90 or <60 65-yo All 1 point if <1--> outpatient if 2 --> inpatient if 3 --> ICU Hospitalization for CAP

Function of the alveolar pores

Connect neighboring alveoli and EQUALIZE AIR PRESSURE & PROVIDE COLLATERAL AIR CIRCULATION

Criteria for screening for T2D/pre-diabetes in asx adults

Consider in: -anyone with a BMI >24 or Asian Americas >23 with a RF -test everyone starting at 45. repeat testing every 3 years. can perform: FPG, 2hr serum after OGTT, or A1c.

What's the most important recommendation regarding nutrition for a patient on a fixed insulin program?

Consistent pattern of carb intake w/respect to time & amount **result in improved glycemic control and ↓risk of hypoglycemia **this better be on the exam

Aspiration pneumonia usually shows up on CXR as?

Consolidations in the dependent lung segments

Type of Respiratory Dyspnea that involves brain and chest wall Sx: air hunger, chest tightness

Controller hypervent d/t hypoxia and hypercapnia

Type of respiratory dyspnea that involves brain/chest wall. Sx: air hunger, chest tightness

Controller, hypervent d/t hypoxia & hypercapnia

MCC of acquired heart disease in children younger than 5

Coronary artery dilation (2ndary to Kawasaki disease) *Nearly a quarter of untreated children will develop coronary artery dilation)

If you have an adrenal tumor producing causing leg cramps what hormone is high which electrolyte is low? *From review of cases

Cortisol K+

Diagnosing Adrenal Insufficiency?

Cosyntropin stimulation test. Draw baseline serum cortisol then give Cosyntrophin. Re-check cortisol 30-60 minutes then ACTH Primary adrenal insufficiency: ACTH will increase but cortisol production will not increase more than 20 mcg/dL Secondary adrenal insufficiency: cortisol will increase greater than 20 mcg/dL.

3 Symptoms of COPD:

Cough, Sputum production, or exertional dyspnea AND must have *hx of exposure to risk factors* • Risk factors: *Smoking*, occupational hazards, air pollution

-AE of Cycloserine -Use caution prescribing these TB meds to gout pts -warning for Aclindium (LAMA) -Dapsone toxicities

Cycloserine- (2nd line TB drug) CNS toxicity--> seizures Ethambutol and Pyrazinamide inc plasma urate levels Aclindium--Category C Dapsone-- hemolysis & METHEMOGLOBINEMIA, skin rashes, GI probs, MUSCLE PARALYSIS

1A newborn presents with *Meconium Ileus*. What genetic condition must you now include on your differential diagnosis? What is the causative mutation of this condition?

Cystic Fibrosis; CFTR protein mutation on Chromosome 7

Formed elements -Leukocytes; eosinophils, granules

Cytotoxins -Destroy protozoan and helminthic parasites -Major basic protein (MBP), eosinophil cationic protein (ECP) and eosinophil peroxidase Neurotoxin -Causes parasite CNS dysfunction Histaminase -Present in specific granules breaks down histamine

Pt has hypernatremia, dehydration, ↑serum osmolality and ↓ urine osmolality. What do they have and what test did you do to confirm this? What caused their hypernatremia?

DI (loss of ADH) (high dilute urine volume) Water deprivation Dehydration (think nursing home patient)

How might hypoxemia due to diffusion abnormalities be distinguished clinically from that due to non-uniform VA/Q ratios?

DLCO

How is diffusing Capacity of the lung measured? What is the basis for using CO in making the assessment?

DLco=Vco/PAco -easy measurement b/c any CO in your blood must have been from the breath you took in

MOA of 1,25(OH)2-D3 (prediction)

DNA binding domain that contains the ZINC FINGER MOTIF characteristic of other steroid receptors.

Strongly hinted at test question....DPP4 inhibitor what can it be used with? What can't it be used with?

DPP4 inhibitor--think about it..it BLOCKS GLP-1 catabolism and GLP-1 agonists obviously increase the effect of GLP-1--> HYPOGLYCEMIA--cannot use!! DPP4-inhibitor CAN be used w/Metformen and TZDs

Markers for RA

DR4, DR1, DR10, DR14

What is a t score? What is considered osteoporosis? What is a z score? What is considered Osteoporosis?

DXA compared to young adult -2.5 or worse DXA compared to same age -2.0 or worse Precision: ↓ of less than 3%= not mathematically true

1. Which drug this unit can inadvertently cause adrenal insufficiency?

Danazol (inhibits gonadotropin secretion)--progestin used to help tx endometriosis.

Describe hormone spikes during menses

Day 0-7--FSH & LH secreted (fairly evenly)--> follicle is maturing and FSH causes follicle to gradually secrete 17B-estradiol. So ESTROGEN gradually climbs as well. Day 7-17- LH surge and just after surge, ovulation begins! (FSH had a small surge around this point). Now enters LUTEAL PHASE. Progesterone starts rapidly climbing as estrogen starts to decline. Progesteron peaks around DAY 19.

Causes of hypogonadotrophic hypogonism

Decreased Hormone Production--Kills Pituitary And Naughtybits D- Delayed puberty H-Hemocrhomatosis (or other infiltrative) P-Prolactinemia (hyper!) K-Kallman syndrome (anosmia) & low GnRH P-Pituitary (hypo) A-Anorexia/excessive exercise N-Neoplasm (brain)

The mucosa of the uterine tubes form _____________________ best expressed in the ampulla?

Deep longitudinal folds

Inflammation, hyper responsiveness, and reversible obstruction. Predominant cell triggering pathology Symptoms: Wheezing, Cough, Dyspnea, Chest Tightness Typical lavage microscopy?

Definition of Asthma: Eosinophils (Activated and directed by IL-5) *Lavage microscopy:* Charcot-leyden crystals - lysophopholipases form eosinophils Curschmann sprials - mucus plugs Creola bodies - desquamated epithelial cells

A young patient presents with COPD. On CXr it becomes apparent that the entire lung is affected. What is a possible genetic cause of this patient's COPD?

Degradation of elastin due to --> Alpha-1 Antitrypsin Deficiency (Panacinar)

How do you treat IRS?

Diet (wt. managemen=3500 cal/lb loss) Exercise LIFESTYLE>>>DRUGS

Definition of Sleep Apnea:

Disorder in which individual may have irregular breathing/stop breathing while asleep. When airflow is <10% of baseline for at least 10 sec • Symptoms: 3 S's: *Snoring, Sleepiness (daytime), Significant*

What is the Clinical Approach for bronchiectasis? What should be provided for adequate nutrition?

Do CXR, PFT & Sputum analysis - match findings w/ bronchiectasis o Thick Sputum = + Pseudomonas 3 Layered purulent o PFT = Obstructive --> If HRCT is normal - close observation, maybe bronchoscopy or GERD/aspiration evaluation (possible infection) -->If HRCT is abnormal o Focal bronchiectasis: bronchoscopy or induced sputum for AFB (Acid fast bacillus) o Diffuse bronchiectasis: *CF genotyping/Cl-sweat test* or semen analysis or a1antitrypsin level or quantitative Ig analysis, etc Adequate Nutrition: • Replace pancreatic enzymes • Replace fat-soluble vitamins - E & K • Insulin therapy for hyperglycemia

What are 3 principles of statin therapy?

Don't focus on LDL-C or non-HDL-C as tx goals Use meds proven to ↓ASCVD risk Clinician-patient discussion to eval benefits and harms for pt (optimal lifestyle emphasized)

After development, dorsal edge of transverse septum is at _____________ and ventral edge is at __________.

Dorsal T12 Ventral T7 (TEST PREDICTION)--no reason to believe that tho

When is the corpus luteum most active?

During first 8 weeks

Tb Confirmatory Test: Tx: How long

Dx: Sputum AFB GOLD Standard Need *3 negative* sputum cultures to *rule out* active TB (Latent TB wont cough up) Tx: Isoniazid (side effects: hepatotoxicity and peripheral neuropathy) *6 Months* Culture - or Culture +, CXR - , HIV - *9 Months* Culture + & CXR Cavitation+ Culture + & CXR -, HIV +

Extramammary Paget disease vs. vulvar melanoma

EP -PAS + -Keratin + -S100 - Mel -PAS - -Keratin - -S100 +

Inflammatory marker correlates with disease activity measures acute phase proteins (APP) generally higher in women rises with age NON-specific

ESR (Erythrocyte sedimentation rate)

What should I do before I biopsy an adrenal gland?

EXCLUDE PHEO Don't want to precip a pheo crisis by putting a needle in it

Lamina propria of the nares contains...

EXTENSIVE VENOUS PLEXUS--> INFERIOR & MEDIAL NASAL CONCHAE --it swells during hayfever

Your colleague recently diagnosed one of his patients with small cell lung carcinoma (SCLCA). Despite this diagnosis, he cannot explain why his patient is experiencing weakness & tingling of his extremities. Using your MEDI knowledge, what condition would you include in your DDx?

Eaton-Lambert Syndrome

Differentiate between Eaton-lambert + Myasthenia Gravis:

Eaton-Lambert Syndrome gets *BETTER with exercise* (due to ↑ NT levels) Myasthenia Gravis tends to get *WORSE* with repeated/ongoing activity

Components of knock out genes

Embryonic stem cells Mutated gene Transfection Homologous recombination Mosaic or chimeric mouse

What's the most important recommendation regarding nutrition for a type 2 diabetic patient?

Emphasize healthy food choices and portion control Modest weight loss has huge benefits *suggested calorie intake= 10 cal/lb/day (150lb person should take in 1500 calories)

Coccidiomycosis - Location

Endemic in San Joaquin Valley, South central Arizona, Rio Grande Valley (SW United States)

The corpus luteum acts as an ___________ gland?

Endocrine

where are parafollicular cells derived from?

Endoderm

What does elevated insulin level with normal or elevated blood glucose define? Causes?

Endogenous Insulin Resistance (res to gluc disposal) Measure w/HOMA (Fasting) (Insulin x Glucose X 0.055)/22.5 Know this graph Cause: obesity, pregnancy, stress, infection, glucocorticoid excess, acromegaly Variables: genetic, lifestyle, ethnicity (↑risk: mexican-americans)

Most important factor in determining birth weight?

Energy--Increase daily intake by 300kcal/day Also avoid mercury (just good advice)

What is the patient taking if TT4/TT3/TBG is high but TSH and FT4 are normal?

Estrogen

Stimulate prolactin release

Estrogen & dopamine antagonists (since DA inhibits prolactin release)

normal TSH, high TT4, normal FT4, high TBG

Estrogen -- BIRTH CONTROL

Estrogen effect on bone?

Estrogen promotes Growth & receptor development in replicating osteoblasts. -Promotes maturation/closure of grwoth plates during puberty

Somogyi effect...how to treat?

Excess insulin production at night leading to rebound hyperglycemia in the morning. The answer is to actually decrease insulin dose, not increase.

Ptyalism

Excessive salivation Tx: anticholinergics

MCC Cushing syndrome?

Exogenous steroids Dex test doesn't suppress cortisol

Cause if chronic Laryngitis

Extraesophageal reflux

MC vulvular adnexal malignancy

Extramammary paget disease (Intraepidermal Adenocarcinoma)

Males in 50s/60s, mostly of Asian or Latin American descent. What tumor? What is it associated with?

Extranodal NK/T cell lymphoma EBV inside the tumor cells

What is TG w/in VLDL composed of?

FA +glycerol synthesized in liver

What is indicative of obstructive disease with spirometry?

FEV1/FVC < 0.7

In determining the RV of the lung, what volume or capacity is actually measured? Using what technique or techniques? How is residual volume calculated from this measure?

FRC is actually measured (FRC=ERV + RV) Techniques: N2 washout, He dilution, plethysmography, CXR -subtract ERV from FRC -> RV measure

Hormones secreted by Sertoli cells and their functions...and what stimulates their release?

FSH-->from Anterior pituitary--> sertoli cell-->ABP--Androgen-binding protein which helps increase conc. of test in seminiferous tubules & excurrent ducts for prop dev spermatogenic cells/sperm maturation FSH--> Anterior pituitary--> sertoli cell--> INHIBIN, which inhibits rel of FSH

What diseases cause low uptake?

Factitious (exogenous source; doc gave too much iodine) Struma ovarii (uptake is elsewhere---not thyroid) Iodine-induced (contrast for CT or amiodarone) Thyroiditis (↑↑TG) (poor visualization)

True/False? The abdominal & internal intercostal muscles drive expiratory flow during normal breathing.

False

True/False? An increase is CSF [H+] will suppress ventilatory drive.

False this will immediately stimulate the central chemoreceptors

True or False. When a pt's VC is reduced there is a primary problem involving the lung?

False. Any restrictive disease would do it & those aren't necessarily primary lung problems.

What is the disorder characterized by elevated triglycerides d/t lipoprotein lipase and ApoC-II deficiency?

Familial Chylomicronemia syndrome: Type I hyperlipoproteinemia deficiency prevents hydrolysis of TGs so TG will be >1000 mg/dL usually presents in childhood with pancreatitis. ts with dietary fat restriction

If a family member has hyperCa what should you consider?

Familial Hypocalciuric Hypercalcemia (FHH) surgery not helpful set pt for serum Ca is higher

What is the lipid disorder associated with elevated LDL and nml TG d/t genetic variations in APO E?

Familial dysbetalipoproteinemia: Type III hyperlipoproteinemia Mixed hyperlipidemia b/c variations in APO E interfere with clearance of remnant lipoprotein particles leading to buildup. Clinical development usually contributed to by diet, diabetes, hypothyroidism, obesity. premature ASCVD (usually in adults tho not nuggets) and higher incidence of PVD than FH. Tx with *diet.* can add statins, fibrates, niacin

What is the lipid disorder associated with elevated LDL and normal triglycerides d/t mutations in the LDL receptors?

Familial hypercholesterolemia: Type II hyperlipoproteinemia (IIa: LDL accumulation, IIb: LDL + VLDL accumulation) mutations in the LDL receptors allowing LDL build up. causes tendon xanthomas and premature CAD d/t plaque (7 y.o. with MI) tx with LDL apheresis + statins + cholesterol absorptive drug

What is the name of the disorder characterized by elevated triglycerides, elevated VLDL, low HDL, and mildly elevated total cholesterol?

Familial hypertiglyceridemia: Type IV hyperlipoproteinemia

What is the disorder characterized by elevated TG and chylomicrons?

Familial hypertiglyceridemia: Type V hyperlipoproteinemia VLDL and chylomicrons compete for same degredation pathway HDL is low tx with dietary restriction, fibrates, Niacin, fish oil

What's an important factor in discharge criteria for patient with COPD exacerbations? TEST

Family are confident patient can manage successfully at home. TEST

A farmer presents to your office with bronchospasms and wheezing. Two years later, follow up reveals the presence of granulomas, IPF, and necrosis. What condition does this patient have? How could the progression of this disease have been avoided? Stages? Spirometric Changes?

Farmer's Lung- Creates vasculitis that causes necrotizing granulomas & pulmonary fibrosis *Stages* Early stage: IgE - mediated, Type I Sensitivty Later Stage: IgG-mediated, Type III *Spirometric Changes* in Hypersensitivity Pneumonitis (Farmers Lung) Acute phase - restrictive physiology, but may present like asthma Chronic - pt develops severe restriction and/or mixed restrictive/obstructive pattern DLCO - is decreasing in all stages

Non-proliferative breast changes

Fibrocystic changes (3% lifetime risk) -Cysts -Fibrosis -Apocrine metaplasia -Adenosis

Triggered by a surge in FSH and LH 24 hours before ovulation the primary oocyte will complete what?

First meiotic division - enters meiosis 2 but gets arrested in metaphase 2

Allergic rhinitis -Tx; 1st line

Fluticasone

Formed elements -Erythrocytes; plasma membrane, bracing

Formed by several components -Spectrin: meshwork of fibers on cytoplasmic side; spectrin filaments bind actin to ankyrin -Ankyrin: binding b/w spectrin filaments and integral membrane proteins (such as band 3 protein)

COP and how to remember it

Formerly BOOP--think BOOP the SNOOT --> cop a boop on the snoot of an unsuspecting dog. -loose organizing fibrosis --2 snoot holes so can be bilateral --snoot holes are AIR HOLES--this affects the ALVEOLI--fibroblast plugs in bronchioles, alveoli, ducts. (sometimes you plug a dogs snoot) --NOTE: ALL DOGS ARE PUPPIES! (all lesions are SAME AGE). --puppies lower my cort levels--> improve w/corticosteroids. --NO ARCHITECTURAL CHANGES, NO HONEYCOMBING etc.--> think you let your dog live in YOUR house, you don't build separate architecture for it. SAME ARCHITECTURE. Dx: Moo is a terrible guard dog and he would OPEN the door for a stranger (OPEN BIOPSY) --also think of GRAFT vs HOST--bad guard dog, & autoimmune disorders

What is ionized calcium and how do you calculate it?

Free calcium Corrected Ca= [(4-albumin) x 0.8] + serum Ca

What Testosterone value is most important in the overweight pt?

Free or physiologic

Compared to adenomas, adrenoicortical carcinomas are _______ likely to be functional.... When an adrenal cortical neoplasm causes virilizing features it is most likely.....

Functional Carcinoma

Etiologic agents of protracted mastoiditis?

GAS (S. pyogenes), Pseudomonas, S. aureus, Fusobacterium necrophorum Pyogenes, Pseudo-Protracted

Label what the glucose levels are for Carpenter/Coustan Step 2 100g OGTT test. Fasting 1 hr 2 hr 3 hr

GDM dx made if 2 + of glucose levels are met/exceeded 95mg/dl 180 mg/dl 155 mg/dl 140 mg/dl

Octreotide

GH Antagonist--Synthetic somatostatin analog --SSTRs agonists @ pituitary, panc, GI tract, immune cells--> INHIBITS GH rel from pit & rel of TSH, glucagon, & insulin Tx: Acromegaly, Carcinoid Syndrome, gastrinoma, glucagonoma, insulinoma, diarrhea, Esophageal varice bleeding -AE--Sinus brady, CP, HYPERglycemia, hypothyroidism --since it inhibs insulin (i think to a greater extent)--> increase blood sugars

Pegvisomant

GH antagonist Polyethylene glycol (PEG) is a derivative of MUTANT GH...People w/acromegaly look like MUTANTS PEG binds to GHr--> dimerization--> block conformational change for signal transduction Pirates w/peglegs block (conformational change) for SIGNAL TRANSDUCTION so victims cannot cry out for help.

why is GH excess bad for GH receptor binding?

GH binds one half of the 2 part receptor and recruits the other half to dimerize and JAK/STAT this bitch BUT too much GH leads to excess hormone binding a single receptor subunit thus producing a shortage of "second halves" needed to dimerize and fnx this decreases activity despite excess

what are the levels of GH and IGF during anorexia/starvation? what other important dz state does this happen in?

GH elevates IGF depresses this interrupts the normal system btw these two this also happens in diabetes

how does the GH short loop differ slightly from normal?

GH inhibits GHRH but stim SST net = decrease GH production

Mescasermin/IGF-1

GH- agonist---Recombinant Human IGF-1 (rhIGF1) --IGF-1 (ligand for IGF1r-tyrosine kinase receptor) @ target tissues--> simulates systemic body growth @ skeletal/muscles/bone/cartilage --IGF- deficiency in kids w/short stature UNRESPONSIVE to EXOGENOUS GH due to mutations in: GHr, GH sig pathway, GH neutralizing ab, IGF-1gene defect PK-Mecasermin rinfabate mixture increases 1/2 life AE- can cause hypoglycemia so MUST take carbs 20 mins before, Intracranial HT, Adenotonsillar hypertrophy? --children are recombinant-- Impish Goblin F$cktrophies --think of a child's birthday party...meCASTLEmin (like a bouncy castle) when short kids are unresponsive to Gentle Hands (growth hormone---lack of discipline) and continue to scream and be obnoxious. --you can rinfa (rufee) them to increase effectiveness of parenting AE: --Then they eat cake at the Bday party like 20 mins before jumping in the bounce house (or heaven forbid they get hypoglyemic and pass out) --the parent's intracranial pressure raises as they continue to scream --The kids scream until there Adenoids/tonsils hypertrophy.

bone synthesis (modeling) is affected by what 3 factors?

GH/IGF TH gonadotropin/sex steroids

You've given metformin. What's your second med option?

GLP1 NOT Sulfonylureas

What can potentiate effects of B2 agonists? What else do these drugs do?

GLUCO/CORTICOsteroids --suppress mucus secretion --dec pro-inflam cells/proteins

How do you assess the degree of airflow limitation for a COPD Patient?

GOLD Grading Criteria

Type of Resp Dyspnea that involves O2/CO2 transport

Gas exchanger PNA, pulm edema, aspiration

What should a child diagnosed with diabetes in the first 6 months of life receive?

Genetic testing (consider MODY in patient w/mild stable fasting hyperglycemia and multiple family members w/DM not characteristic of type 1 or 2)

Hydatiform mole -Complete

Genetics -Empty ovum, two sperm, 46 chromosomes Fetal tissue -Absent Choriocarcinoma risk -Higher

Hydatiform mole -Partial

Genetics -Normal ovum, two sperm 69 chromosomes Fetal tissue -Present Choriocarcinoma risk -Minimal

Genetics of anaplastic (undifferentiated) carcinoma of the thyroid.... Environmental risk factors...

Genetics: 1. Alterations seen in other thyroid CA, just higher rate 2. Inactivation of p53 3. Activating mutations of beta-catenin Environmental 1. radiation exposure 2. long-standing iodine deficiency 3. Pre-existing thyroid disease

Ovarian tumor 15-40 yo

Germ cell tumor

Use caution in using muscarinic antagonists with...

Glaucoma Prostatic hyperplasia Bladder neck obstruction b/c of muscarinic effect on eye & urine retention

If a patient is at significant risk of severe hypoglycemia what should you prescribe? Who else needs to be involved in this process?

Glucagon instruct caregivers in administration Glycemic targets should be raised to avoid further hypoglycemi in insulin-treated patients w/hypoglycemia unawareness or episodes of severe hypoglycemia

Under hormonal regulation ___________________ are deposited between the cumulus oophorus-oocyte complex and the membrana granulosa in the mature follicle?

Glucosaminoglycans

Optimize provider and team behavior CCM: Delivery System design

Goal setting ID language, numeracy, cultural barriers integrated EBM incorporate care management teams

What is a sign of inadequately controlled asthma?

Going through > 1 cannister/month of SABA

How to assess degree of airflow limitation for COPD pt (hospitalization risk)

Gold 1: mild FEV1>80% predicted Gold2: Moderate FEV1 50%-80% Gold3: Severe FEV1 30%-50% Gold 4: Very Severe FEV1 <30% Risk of Exacerbation: 2+ exacerbations in last year OR FEV1 < 50% predicted value *CHOOSE HIGHEST RISK CATEGORY*

MC malignant sex cord-stromal tumor?

Granulosa cell tumor

MCC of thyrotoxicosis

Grave's

What does a nuclear thyroid scan help distinguish between?

Graves from thryoiditis. determines if the elevated TSH is due to overproduction of thyroid hormone (Graves) or inflammation of the gland causing contents to "leak out" (thyroiditis)

What are findings on thyroid nuclear scan for Graves and thyroiditis?

Graves will have high uptake thyroiditis will have low uptake

CXR of chronic interstitial lung disease may show BILATERAL infiltrative lesions described as?:

Ground Glass Opacity - Honeycombing in severe cases

Ankylosing spondylitis Reactive arthritis (Reiter's syndrome) Yersinia, Shigella, Salmonella arthropathy

HLA-B27`

MCC of acquired renal failure in children

HUS (typically E. coli O157/H7)

Hemoptysis in CF patients could be life threatening...what is the reason for this?

HYPERVASCULARITY of the AIRWAY--> hemorrhage

Triggers HYPERsecretion of GH? Triggers HYPOsecretion of GH? Which glucose transporter is insulin sensitive? How is AMPK activated?

HYPERsecretion--> pregnancy, anorexia, gigantism, acromegaly, diabetes, HYPOsecretion--> dwarfism, lOw cOrtisol, Obesity, hypOthryroidism GLUT-4 AMPK is ACTIVE when PHOSPHORYLATED

what 2 things cause thryoiditis? how?

Hashimoto's thryoiditis (autoimmune - antithryoid microsomal Ab) post-partum thyroiditis (partly autoimmune, partly collapse of tissue overdevelopment b/c of estrogen of preg)

80 year male, no sputum production, no fever, hypercapnic, on BiPAP. What's the best reason why this patient would need antibiotics (Doxy)? TEST

He requires mechanical ventilation TEST Abx: early treatment, reduce Tx failure, reduce ICU mortality, doesn't increase risk of ventilation, decrease readmission --viral exacerbations=longer and more severe --bacterial= MC in smokers and severe COPD

80 yo male, no sputum production, no fever, hypercapnic, on BiPAP...best reason for doxy?

He will require mechanical ventilation (possibly on test)

Support Patient behavior change CCM: Self-management support

Healthy lifestyle Disease self management Prevention of DM complications

Patient presents with pleural effusion, from a traumatic injury. Fluid is mainly blood w/ Pt hct 46%. The fluid in the pleural space hct is 23%. Dx: Tx:

Hemothorax - blood effusion w/ HCT of pleural space >50% of pts venipuncture hct (usually due to trauma) a. Eg: Pt hct 46%, there pleural space hct must be at least 23% b. Tx w/ tube thoracotomy if > 200 cc/hr

MCC of spuriously elevated activated partial thromboplastin time (aPPPT) values

Heparin contamination

MC liver cancer in kids

Hepatoblastoma

Which tumors are spread hematogenously

Hepatocellular Carcinoma Papillary Carcinoma of the Thyroid Renal Cell Carcinoma Choriocarcinoma Carcinomas Prefer Riding Heme (the four that spread via blood)

2nd MC molecular subtype of invasive breast cancer

Her2+, ER +/-

what is in the pars nervosa?

Herring bodies (large distended axon terminals of neurons from the hypothalamus which stain pink and secrete *oxytocin and ADH*) numerous axons of hypothalamic neurons pituicytes (glial cells)

Type of CV dyspnea that includes anemia, LR shunt, PHTN, obesity

High CO

Dx of DKA?

High glucose, low bicarb Anion gap elevation [Na-(Cl+bicarb)] pseudohyponatremia. to find correct value add 1.6 mEq of Na to every 100 mg/dL of glucose above normal. "I couldn't actually find this in the handout so idk if he talked about it this year*

"gold standard" for diagnosing bronchiectasis.

High-resolution CT

MCC of congenital intestinal obstruction

Hirschprung disease--dilation of bowel PROXIMAL to aganglionic segment...Rectum ALWAYS involved Agagnglionic segment looks grossly normal

What kind of hypoxia do I have if I have normal O2 delivery but abnormal utilization d/t enzyme deficiency? Cyanide poisoning

Histotoxic

What should be considered for a pt w/ ovarian failure (insuff E) or severe post-menopausal sx? What's the goal of this treatment?

Hormone replacement (Progesterone) **need to know reason for insuff E Tx should be brief

A pt presents with drooping of the eyelid, marked ipsilateral pupillary contraction, and decreased sweat production. CXr reveals an apical lung mass. Dx?

Horner's Syndrome - paraneoplastic syndrome, disruption of the sympathetic chain network by an apical lung cancer

Subtype of follicular carcinoma...more aggressive

Hurthle cell

Treatment of Primary adrenal Insufficiency?

Hydrocortisone. Start Iv in the hospital. PO 25 mg/d outpt. make sure to double if acutely ill.

What can induce HbF in sickle cell pt to take over HbS

Hydroxyurea

*CO poisoning* causes what type of hypoxia?

Hypemic (Anemic) Hypoxia PaO2 is normal but the oxygen content of blood is reduced Abnormal Hgb - sickle cell disease, CO poisoning, methemoglobinemia

What kind of hypoxia do I have if I'm anemic, have sickle cell, CO poisoning, methemoglobinemia?

Hypemic (anemic) hypoxia; low CaO2

What's the cause of elevated PTHrP?

Hypercalcemia of malignancy discovered inpatient ↑Ca ↓PTH tx: IV saline, Loop diuretic (hydrate 1st), IV bisphosphonate (only w/severe hyperCa)

Indication for non-invasive ventilation in COPD exacerbation

Hypercapnia- PaCo2 > 6.0 kPa OR 45 mmHg Acidosis pH <7.35

Gynecomastia, male

Hyperestrinism due to -Liver cirrhosis -Klinefelter -Estrogen-secreting tumor -Adverse drug rxn: marijuana, antiretroviral, anabolic steroids

24 yoa male presents w/ female body habitus, no 2° sex characteristics or facial hair, infertile. PE= sm. testicles & Tanner1 What are the LH/FSH levels? T levels?

Hypergonadotrophic (high LH/FSH) hypogonadism (low T)

20 y.o. male presents with female body habitus, lack of secondary sex characteristics, absent facial hair, infertility, with small testicles. Lab shows elevated LH and FSH with low testosterone. Dx and additional testing?

Hypergonadotrophic hypogonadism (elevated gonadotropins with low gonadal hormones) If karyotype showed 47 XXY, Klinefelter syndrome

Patient has osteoporosis, nephrogenic Diabetes insipidus and has a peptic ulcer. What do they have? Is Ca high or low?

Hyperparathyroidism HyperCa→ can cause hypercalciuria→prevents ADH MCC: solitary parathyroid neoplasm

Medical (bromocriptine or cabergoline) is the treatment of choice for what condition?

Hyperprolactinemia -causes galactorrhea, infertility, amenorrhea, ↓libido Causes: HypoTH, pit neoplasm, non-fasting, meds, **Dopamine antagonist

MCC of sudden death in athletic adolescents

Hypertrophic cardiomyopathy ...followed by coronary artery abnormalities

What hormone def can also cause ↑PRL, suppression of gonadotropins, ↓male horm, infertility, gynecomastia

HypoTH Gynecomastia also in elderly, obese (fat has aromatase enzyme which converts androgens →E), puberty (E→promotes; androgen suppress)

In patient with poor cognitive function when should glucose therapy be utilized/tailored for patient? Hypoglycemia or hyperglycemic patient

Hypoglycemic patient Statin therapy >>>risk of cognitive dysfxn Monitor wt change, glucose in pt on anti-psychotic

14 yoa male has lack of 2° sex characteristics and gynecomastia. What are his LH and FSH?

Hypogonadotrophic (low LH/FSH) hypogonadism

What condition might you see in an olympic gymnast?

Hypogonadotrophic hypogonadism d/t excess exercise (↓LH/FSH; ↓estradiol) Also seen in 16 yoa w/ no hx of menses (1° amenorrhea)

Hypomenorrhea...what is it and what causes it?

Hypomenorrhea--Normal periods w/Abnormally SMALL amounts of bleeding....ALWAYS (and I mean F$cking ALWAYS) due to.... OUTFLOW TRACT DEFECTS

Patient has low Ca and low PTH (or normal PTH). What do they have and where is the problem?

Hypoparathyroidism Parathyroid *glands should respond d/t low Ca MCC: surgery "dectomy"

A mountain climber presents with low PaO2. What is the diagnosis?

Hypoxic Hypoxia From *high altitude*, recreational use of NO, sleep apnea, COPD or respiratory arrest (decreased ventilation)

If I'm at high altitude, use NO, have sleep apnea, COPD, or physiologic shunts what kind of hypoxia might I have?

Hypoxic: low PaO2

Did you look at the CT image of a pituitary adenoma on slide 9 of the first pituitary lecture? Bc you should know the anatomy.

I think the sphenoidal sinus, stalk, hypothalamus, optic chiasm are probs the important part

Don't do electrophysiologic testing on paresis grades....

I-V, ONLY VI is eligible (which makes sense)

Long-term 1st line asthma control`

ICS

Most important & effective long-term controller for persistent asthma?:

ICS

what buffers IGF activity?

IGF-BP (3 is dominant) tightly binds IGF to store it in the blood for when it is needed and protects it from degredation

Characteristics of Invasive Lobular Carcinoma

ILC--> In Line Carcinoma (linear infiltrative pattern) --I Lack Cadherin (ductal has it but not lobular) -- --Spiculated masses, multicentric/BILATERAL.

Most important risk factor for NAFLD?

IRS (hepatic manifestation) ↑FA oxid → oxidative stress on liver Random: IRS = ↑risk of breast cancer

When will the secondary oocyte go through meiosis 2?

If penetrated by spermatozoon

Define the conditions of the SMART-COP severity scale for community-acquired pneumonia (CAP).

If score of ≥ 3 → *admit to ICU* (Low BP, Poor O2, Low pH are 2pts each) o Low *S*ystollic BP - 2 pts o *M*ulti-lober CXR involvement - 1 pt o low *A*lbumin level → 1 p o high *R*espiratory rate → 1 pt o *T*achycardia → 1 p o *C*onfusion → 1 p o poor *O*xygenation → 2 pts o low arterial *pH* → 2 pts SOH2--these are the 2 pointers

pCO2 = 1.5(HCO3-) + 8 +/- 2

If serum pCO2 is within calc, there is CORRECT compensation and NOT a 2nd met disorder

Antineutrophil Cytoplasmic Antibodies

Immunofluoresence 1-c-ANCA 2-p-ANCA ELISA 1-PR3-ANCA 2-MPO-ANCA 1-2 matching in relation

Pathogenesis of bronchiectasis from *non-infectious causes*: What are the Non-infectious possibilities of Bronchiectasis?

Impairment of pulmonary defense mechanism. o *Ig deficiency* - recurrent respiratory infections o Primary ciliary disorder o CF o Inhalation of toxic gases: ammonia or gastric acid aspiration o *a1-antitrypsin deficiency* - panacinar emphysema - @ presentation possible liver dys cirrhosis = ZZmutant o RA o IBD (most commonly seen with chronic UC) o Yellow Nail Syndrome - due to hypoplastic lymphatics

What happens to the oocyte if fertilized in the oviduct?

Implants in uterine endometrium

When to use BTPS

In the chart EXCEPT: V02, Vc02, & DLCO

What is osteomalacia and what causes it?

Inadequate Ca++ Uptake 1. Vitamin-D dependent (low intake/skin synthesis-extrinsic depletion, intenstinal malabsorption/loss/poor vit stoarage or celiac disease, impaired hydroxylation) 2. Hypophophatemia--Defect in renal tubular resorption of phosphate-> defect in transporter, tumor-induced (hyper PTH, or PTHrP, prolonged use of aluminum containing antacids) 3. Ca++ deficiency--insufficient mineralization (and dec dietary intake obvi)

What stimulates the development from primordial follicles into growing follicles?

Increase in FSH at the beginning of the menstrual cycle

Anthonisen Criteria Type 1

Increased dyspnea, sputum volume and purulence

Anthonisen Criteria Type 2

Increased sputum volume and purulence

How do you treat high U (Ca) w/renal Ca leak that's provoking hyperPTH

Indapamide (Thiazide diuretic)

MCC of anorectal fistula and abscess

Infection of anal glands that empty into anal canal @ level of DETATE LINE.

MCC of LATE fatalities in burn pts

Infection--pseudo (I think dehydration is #1 for early?)

Most likely markers of Inflammatory carcinoma? Prognosis? What determines this?

Inflammatory Carcinoma--> most likely ER/PR- & Her2+ Poor prognosis (<5 years)... As STAGE INCREASES, life expectancy DECREASES...since stage is dependent on SIZE, accurate measurement is crucial

Straight tubule (tubuli recti) lined w/? Describe these cells

Initial part--SERTOLI cells (no sem cells) Distal Part- SIMPLE CUBOIDAL EPITHELIUM Think- Sertoli- Bertoli-- I only like STRAIGHT TUBES of pasta (like long cylinders)-- Initially....my LEFT OVERS (later--> Distal) I SIMPLY put it in my CUBE tupperware. But now I am in a food coma so I am NOT MOTILE--neither are the sperm Straight--> Sertoli--> Simp Cub

Frey Syndrome

Injury to auriculotemporal nerve--> abberant innervation of cutaneous sweat glands SSx: sweating/reddening w/meals

If T2DM pt is not achieving glycemic goals what shouldn't you delay?

Insulin (also newly dx'ed pt w/sx and ↑glucose or A1c) Metformin is initial tx Consider adding 2nd oral agen (GLP1 or Insulin)

Pt Presentation: Progressive exertional dyspnea, persistent non-productive cough, Hemoptysis, wheezing. DLCO - decreased

Interstitial Lung Disease Definition: diseases that involve the parenchyma of the lung (Alveoli, alveolar epithelium, capillary endothelium) DLCO - decreased in most ILDz, nonspecific finding, degree of reduction doesn't correlate to severity *If CO2 retention is present, this is suggestive of advanced or end-stages of ILDs (poor prognosis)

What constitutes the interstitium? What is present within alveolar septum? What represents Air/blood barrier?

Interstitium = CT + Capillaries (the RICHEST CAPILLARY NETWORK in the BODY) --Numerous elastic fibers (duh) --Air blood Barrier = Type I pneumocytes + endothelial cells + fused basal laminae (this is where gas Xchange occurs)--> quiz question so prolly not on test

What's components are in exogenous path? endogenous?

Intestine→chylomicrons (TG from intestines→tissue and liver) VLDL (new TG →fatty tissue) IDL LDL Liver (kind of both though) extrahepatic tissues HDL

Intraductal papilloma vs carcinoma

Intraductal -Projections lined with epithelial and myoepithelial cells Carcinoma -Projections line with epithelial cells, WITHOUT myoepithelial cells

MCC of nipple discharge

Intraductal papilloma (if no mass)

What part of the uterine tube opens into the lumen of the uterus>

Intramural part

How to remember Tyrosine Kinase

Intrinsic--think of the GOONIES and their MAP! (They were also a close circle of friends--intrinsic. Think of deformed guy--had a problem with GROWTH FACTOR-not hormone- (FGF, EGF, IGF, AND INSULIN)-- again for insulin think inside group of friends. they were TRYING (tyrosine) to find the Gold First--GROWTH FACTOR Receptor-Associated--JAK-STAT--when you ******** tyrone STAT--you touch the TIP and see GROWTH (while making that HOR-MOAN--growth hormone) of you EPO TIP-->Thrombopoietin, immunomudulators, PROLACTIN

Size is important for staging in _______ so accurate measurement is essential

Invasive Ductal Carcinoma Think--Inches Do Count! (size matters)

MC breast malignancy

Invasive Ductal Carcinoma--> -- Is Dominant Carcinoma --Is Desmoplastic Carcinoma (Desmoplastic fibrous stromal response)

MCC goiter and hypothyroidism in 3rd world? 1st world?

Iodine Deficiency Auto-immune disease

HYPERthyroid + LOW radioactive iodine uptake + LOW TBG

Iodine contamination

TRIAD Processes of Care

Iperiodic testing of A1c, lipids, urine albumin examine retina and feet advise on ASA use smoking cessation performance feedback, reminders address barriers (patient, meds, system)

MCC of hypochromic microcytic anemia

Iron deficiency anemia GI bleed is MC cause of iron def anemia in adults

What kind of hypoxia do I have due to restricted blood flow, ischemic heart dz?

Ischemic (decreased O2 delivery)

How to remember Isoniazid

Isoniazid (9 months)--Iso-NINe-azid --Isoniazid can work ISOLATED--> isoLATE (latent) --trump wants to build a WALL to ISOLATE us, (also think LATE--> LATENT)--nhibits MYCOLIC ACID SYNTHESIS --he wants to keep people IN and keep people OUT (Works INTRACELLULARLY & EXTRCELLULARLY) --can cause numbness/tingling--> give pyridoxine (B6) --Acetylated: trump is a big Actyl-hole --causes hepatotoxicity, neurotox, allergies

Risk factors for Carcinoid tumors Markers for carcinoid tumors

Jokes on you idiot, there are no risk factors Markers--serotonin, chromogranin, synaptophysin (do the last 2 sound like the same ones for small cell? ;)

If patient has def in GnRH and anosmia what do they have?

Kallman syndrome (true cause?) *Differential for 2° hypogonadotropic hypogonadism

Primary Ciliary Dyskinesia is associated with what two conditions?

Kartagener's Syndrome, Situs Inversus

Adrenocortical Antagonists

Ketoconazole, Metyrapone, Mitotane -Metyrapone--think me-TERROR-prone, or Martyr-prone--> pregnant mombies are terrors but they think they are martys. Can be used in pregnancy. --Selectively inhibit 11-hydroxylation (which inhibits cortisol & corticosteron synthesis)--> me-TERROR-prone--> terrorist attack--> twin towers--9/11. --would cause your ADRENALS to kick in if terror attack occured.--> but this decreases Corticosterone synth and cort. --treats CUSHING syndrome--watch the terror attack from your CUSHY house and didn't have to worry about being injured. -H20 retention & Hirsutism--pregnant women retain H20, maybe they get hairy

Food allergies -MC

Kids: milk, soy, eggs, wheat Adults: nuts (peanuts), fish (shellfish)

Trachea to opposite side of problem

L-Large pulmonary mass E-Effusion (so you don't confuse the "E" for edema) D- Diaphragmatic hernia away cause there was too much TENSION (tension PNEUMO)--cause air enters pleural space but is unable to exit....TENSION is a TRUE medical emergency

What class of drug should never be used as monotherapy for asthma?

LABA (salmeterol = advair, formoterol)

Most interstitial lung diseases cause a restrictive pattern on PFT. Name two exceptions to this "rule."

LAM & Tuberous Sclerosis - Obstructive Tuberous sclerosis---a rare disease that causes tumors, or growths, in the brain and other organs. These growths can occur in the skin, kidneys, eyes, heart, or lungs. They are usually benign. The first signs of tuberous sclerosis may occur at birth

The 2 interstitial lung diseases that are actually OBSTRUCTIVE

LAM & Tuberous sclerosis

In elderly, why might _______ be better bronchodilators?

LAMAs--since LABAs could interfere with their BP meds (b-blockers) Could inc risk of tachycardia, skel musc remors, etc.

What takes cholesterol to cells? What collects cholesterol to return it to the liver? Which one is good? bad?

LDL (BAD) HDL (GOOD) ↑fat ↓protein = lg and dense

What is the goal in the management of diabetic dyslipidemia?

LDL < 100 mg/dL

ASCVD risk factors:

LDL > 100, smoking, HTN or on HTN meds, overweight/obesity, fmhx of premature ASCVD

What are the main drugs used for the treatment of high LDL and high TG's?

LDL: statin TG: fibrates

_________ must be ________ in order for ovulation to occur

LH SURGE MUST be pulsatile in order for ovulation to occur

What hormones regulate follicular growth?

LH and FSH

What stimulates Leydig cells? and to do what?

LH from the gonadotropes of the anterior pituitary stimulates testosterone secretion from the leydig cells

what does LH and FSH do to the male repro?

LH stimulates leydig cells to produce testosterone FSH stimulates secretion of androgen-binding protein from the sertoli cells and spermatogenesis

Pregnant patient protocol for DVT prophylaxis:

LMWH Fonidarinux --> switch to UFH 2 wks prior to delivery, Warfarin 4-6 wks post delivery

LOOK at cases in PPT

LOOK at cases in PPT

What's the most important enzyme in lipoprotein metabolism? What clears VLDL remnants, IDL and LDL?

LPL LDL receptors

Angioedema -Hereditary; MCC death

Laryngeal edema

Starts as strep throat, progresses to deep pharyngeal tissue--> drains to lateral pharyngeal space (containing carotid artery & IJV). Septic thrombosis of IJV causes pain, dysphagia, neck swelling/stiffness. Sepsis occurs & infection spreads--> fatality 50% of time

Lemierre's disease (postanginal septicemia)

Tx for long-term aspirin-sensitive asthma -

Leukotriene modifier (Montelukast, Zileuton

How do you treat 1° hypothyroidism? 2°? Myxedema coma?

Levothyroxine (synthroid...USE BRAND NAMES!) for both Can't use TSH as f/u for pt w/2 ° 1. Hydrocortisone (give 1st to avoid adrenal crisis) 2. T4 3. Fluids 4. Resp support if needed

Well-developed SER, mitochondria w/tubular cristae, & numerous lipid droplets What other special feature?

Leydig cells-- Crystals of Reinke (acc of protein) Think- well-developed SER (sir) Might stick his TUbe in critae even though she is FAT. (Lipid droplets) Leydig--> sometimes when Crystal spreads her leydigs...it's REINKE..>BUT guys with a lot of TESTOSTERONE will do it anyway (they produce this in response to GnRH from hypo--> LH in ant pit --> Leydig cells --> Testosterone

What's #1 on T2DM management algorithm? From principles of AACE/ACE 13 total items

Lifestyle tx (medically supervised wt loss) #2: A1c target #3 Glycemic control targets fasting and postprandial gluc

GLP-1 agonists

Liraglutide, Exantide, Dulaglutide (think of tide pods--Gooey Laundry Pods)--eating tide pods could also stimulate gluc dep insulin --Stimulates Glucose-dependent insulin & INHIBITS POSTPRANDIAL GLUCAGON RELEASE (think--inhibits someone from eating f$cking tide pods) --DMII--dec risk for major CV, MI, stroke, CVD (because if you die of tide pods first you won't have the chance to develop this)--causes WEIGHT LOSS (if you die your weight is lost...useless) --DDI: delays gastric emptying so it decreases absorption of other drugs...Gastric Lethargy Problems --can cause hypoglycemia

What is the Silhouette sign?

Loss of the interface btw air density of lungs vs soft tissue density of surrounding (Ex: Pneumonia)

What would thyroglobulin be in a patient who takes thyroid hormone w/o doctor's knowledge and no known thyroid disease?

Low thyroid fxn is high in lab and clinical exam Iodine (supplement) contamination also causes low uptake

Type of CV dyspnea that includes systolic pump failure (CAD, nonischemic cardiomyopathies)

Low CO

A patient will be undergoing a hip replacement tomorrow. To decrease the risk of DVT, what pharmacological agent should be used?

Low Molecular Weight Heparin (LMWH) or Fondaparinux

Treatment method for DVT

Low dose heparin - 5000 units subQ every 8-12 hrs (Need PTT) *LMWH* better Warfarin (Contraindicated in pregnant, and Inhibits vitamin K-dependent factors (II, VII, IX, X) (Need INR) Intermittent compression stocking around the calves for low-risk patients *Duration:* 1st DVT, either time-limited(pregnancy) or reversible risk factors - 3 months min 1st idiopathic DVT - 6 months to 1 year Recurrent DVT - Possibly Indefinitely

Lab results in primary hyperaldosteronism?

Low renin and high aldosterone. Low renin/aldosterone ratio

MC sx of Ovarian Epithelial tumor

Lower abd pain & abd enlargement

What is the only DEFINITIVE treatment for respiratory failure in patients with Cystic Fibrosis?

Lung Transplant

What is the difference b/n a lung volume & lung capacity?

Lung Volumes: RV, TV, ERV, IRV Lung Capacity: sum of 2 or more lung volumes -TLC=TV, IRV, ERV, RV -VC=TV + IRV + ERV= TLC-RV -FRC= ERV + RV -IC= TV + IRV

what are the 2 proteins that osteoblast express when triggered for bone turnover? do each do?

M-CSF (MO colony stim factor) - osteoclast proliferation and expression of RANK + RANKL Receptor Activator of Nuclear factor Kappa b Ligand) - cause expression of osteoclast markers and with enough exposure to RANKL and IL-1 there will be ruffled border formation (the mark of activated osteoclasts)

MCC of non-tuberculous Mycobacterium (NTM) associated bronchiectasis? Tx:

M. avium complex (MAC) organisms: M. intracellulare; M. avium Tx MAC-associated bronchiectasis: clarithromycin/azithromycin + ethambutol for 18 months (or 12 months after negative sputum sample)

1. Genetic factors involved in papillary carcinoma

MAP for pap! Abberant act of MAP Kinase pathway via 3 mechanisms: Major 1: rearrangements of RET (RET/PTC fusion genes--irradiation) OR NTRK1 Think--> assoc. w/ irRETiation Major 2: Activating gain-of-function point mutations of BRAF (not spec to ptc. also found in MELANOMA & others.)---BRAFs are NOT found in the above listed mutations (mutally exclusive) Minor 3: activating RAS mutations (follicular variant of PTC) Note: RAS>RET frequency in FOLLICULAR, +/- BRAF

Common causes of Pleural Effusions (Transudative + Exudative)

MCC of transudative effusions (Clear, Low protein, pH 7.4-7.55) *Heart Failure (CHF)*, followed by hepatic hydrothorax, nephrotic syndrome, cirrhosis MCC of exudative effusions: (Cloudy, high Protein, pH 7.3-7.45) -Hospitalized --> *Parapneumonic (empyema)* - followed by drug induced -Non Hospitalized --> Malignant

MCC of pleural effusion (transudative & exudative)

MCC of transudative effusions (Clear, Low protein, pH 7.4-7.55) *Heart Failure (CHF)*, followed by hepatic hydrothorax, nephrotic syndrome, cirrhosis MCC of exudative effusions: (Cloudy, high Protein, pH 7.3-7.45) -Hospitalized --> *Parapneumonic (empyema)* - followed by drug induced -Non Hospitalized --> Malignant

MCC of fetal tachycardia in fetal monitoring

MCC- Maternal fever But also caused by fetal compromise, arrhythmias, certain meds etc.

Failure of epithelium of larynx to clear the glottal opening...

MEDICAL EMERGENCY--Emergency trach -Laryngeal atresia--> baby unable to ventilate or cry

MCC of death in the US

MI

How do you image Cushing disease?

MRI of pit ACTH indep= CT/MRI of adrenals Ectopic: CT chest/localize source

Keys about asbestosis...Clinically rel diseases?

MUST DOCUMENT EVERYTHING due to potential for suing. -MC manifestation is localized FIBROUS PLAQUES -pulm eff, parenchymal IF, other carcinomas, meso

When do microvascular/macrovascular complications begin to have an impact in pt's?

Macro: effects begin when glucose starts increasing Micro: much later onset of effect. usually not until well after diabetes dx. a before i

What are we concerned about if female patient demonstrates virilization rather than classic feminine phenotype?

Malignancy Check DHEAS of adrenal origin (malig @ 2x nl) check Total T of ovarian origin (malig @ >200 ng/dl)

Ovarian tumor 60-70 yo

Malignant surface epithelial tumor

Screening Tests for Latent TB: How is it performed?

Mantoux tuberculin skin test (PPD test causes type 4 hypersensitivity to Tb infection Measure the size of *INDURATION*, not erythema a. 5mm - positive in IC patients close contact with known b. *10mm - Positive in high risk groups (Doctors, hospital employees)* c. 15mm - Positive in people w/o known risk factors for TB

Net increase in bone mass due to osteoclast hypofunction...name of disease? Associated w/?

Marble bone disease (OSTEOPETROSIS) -"banding on XR" -Carbonic Anhydrase deficiency can cause this (plus metabolic acidosis)

MYH-9 mutations

May-Hegglin anomaly

Medications to avoid in pregnancy.... Anti-biotics/Anti-microbials to avoid in pregnancy...

Medications--Statins, Warfarin, ACEi, Methotrexate (duh) ABX: 1. Tetra/tigecycline 2. Aminoglycosides 3. Voriconazole 4. Miltefosine 5. Quinine 6. Thalidomide (duh) 7. Ribavirin 8. Efavirenz Avoid: 9. Metro in 1st semester 10. Nitro in 3rd semester 11. SXM-TMP- in 1st & 3rd semester

Aggressive, sporadic or genetic, markers are calcitonin/CEA

Medullary No response to RAI Surgical tumor

Which cells between cortical and medullary adrenal cells release/store?

Medullary (Chromaffin) Cells-- Accumulate & Store Hormone--Meds--ChromSTUFF their cells Cortical Cells--> Release STEROID hormones IMMEDIATELY

MCC of aneuploidy

Meiotic Non-disjunction

What shows a base excess of >2?

Metab Alkalosis loss org acids, gain bicarb

What compensation is d/t changes in proton excretion or bicarb reabsorption and takes hours

Metab compensation

If ph and plasma HCO3 change in the same direction

Metabolic

What shows a base excess of <2?

Metabolic Acidosis accumulation of org acids, loss bicarb nl/increased anion gap MUDPALES

A patient presents with a chief complaint of vomiting. ABG reveals an acid-base disorder. Based on these symptoms and results, how would you classify this patient's current state?

Metabolic Alkalosis

In what stage is the primary oocyte arrested after meiosis 1?

Metaphase 2 - becomes the secondary oocyte

Which drug promotes wt loss? TZDs or Metformin Which one is not safe for liver? Which one is not safe for kidney, active liver dz, pulm dz?

Metformin (TZD promote wt gain) TZD Metformin

First line treatment for T2D and main contraindication?

Metformin but can't use in kidney failure

Metformin/GLP-1 vs. Glinides/Sulfonylureas in T2DM management?

Metformin/GLP-1 slower onset of action (long-acting) with low risk of hypoglycemia Glinides/Sulfonylureas: rapid-acting. indicated after meals. High risk of hypoglycemia. Apparently not supposed to use glyburide

Bronchoprovocation will utilize what drug, and what outcome for Asthma Dx?

Methacholine, FEV1 will Drop 20%

Paradise criteria for tonsillectomy

Minimum Frequency of Sore Throat episodes: --7 or more episodes in the preceding year OR 5 or more episodes in each of the preceding 2 y OR 3 or more episodes in each of the preceding 3 y --Temp >38.3 OR cervical lymphadenopathy OR tonsillar exudate OR + culture for group A B-hemolytic streptococcus Tx: ABX Documentation: is key, but if not fully documented--subsequent observance by the clinician of 2 episodes of throat inf w/patterns of freq and clinical features cons. w/initial history

U1 ribonucleoprotein antibody

Mixed connective tissue disease

Most common malignancy of salivary glands (most to least)

Most Sublingual>minor>submandibular> parotid Licking Minors Mandates Parole (malignant predatory behavior)

Patient w/ cystitis has leukocytesterase and in urine but negative nitrates. What is the likely cause? A. E. fecalis B. E. coli C. Proteus mirabilis D. S. saprophyticus E. K. pneumoniae

Most likely S. Saprophyticus. Remember that Enterococcus, S. Saprophyticus, & Acinetobacter do NOT produce nitrite & results in false-negative results. All the others listed DO produce nitrates.

Histoplasmosis - location?

Most prevalent in US (ohio and MS river valleys)

What if your patient can't tolerate high intensity statins? What might indicate that they don't tolerate statins?

Move to moderate intensity --Impaired renal or hepatic fxn --Hx of statin intolerance/muscle disorder --ALT elevation >3 x ULN --Patient characteristics or drugs affect statin metab --Age >75 yoa

MCC cause of cognitive decline w/stepwise drop in function of prior cerebrovascular disease & stroke

Multi-infarct dementia

What's a classic cause of Hypergonadotrophic hypogonadism?

Mumps also germ cell arrest surgery,chemo, alcohol, immune, intra-abdominal testicles

Mutation in 21-hydroxylase deficiency

Mutations of CYP21A2

Expression of this oncogene is mutated in Burkitt's as well as __________ & __________. It contains what type of region?

Myc--> crucial to cell proliferation (nuc prot that acts like transc fact. Mutated in Small Cell Lung CA & Neuroblastoma *contains basic DNA binding region & leucine zipper dimerization region* --prediction

Patient presents w/hypothermia, hypoventilation, hyponatremia, hypotension, seizers, bradycardia and hypoglycemia. What do they have?

Myxedema coma --associated adrenal insufficiency -extreme hypothyroidism ***intestinal malabsorption

ATPIII IRS Criteria: List important numbers for the following Abdominal obesity (insulin sensitivity better w/less fat) HyperTG Low HDL ↑BP Hyperglycemia

NEED 3 out of 5 **men: >40 women >35 **150 mg/dl **men <40 women <50 **>130/85 **110mg/dl **HDL and TG more reliable

Do I do a total thyroidectomy for solitary or dominant nodule?

NO only for cancer or bilateral nodules CAN'T JUST REMOVE NODULE

Can patient have iodized salt before RAI? What's the TSH number supposed to be? What's the goal of RAI? What are the precautions?

NO: pt should be on low I diet TSH needs to be >30 (can use recomb. thyrotropin) tissue starved of I to cause increased uptake on imaging Don't give to pregnant women, kids; sleep alone, keep dist.

Formed elements -Leukocytes; neutrophils, granules

Neutrophilic granules -Specific or primary; contains bactericidal proteins; these small granules don't stain with regular dyes Azurophilic granules -Non-specific / secondary; represent lysosomes Tertiary -Contain gelatinase and glycoproteins

Can you use free cortisol levels (in blood) in a patient who is taking estrogen? *From review of cases

No

Can I treat diabetes with vitamins, minerals, herbs or spices? Can my female diabetic patient drink 2 alcoholic beverages every day?

No No, (unless they're in med school according to Dr Sutton)

Hertel instrument measures pupillary arc is 18mm out of the socket. Does patient have exopthalmos? If they do what do you advise them not to do.

No (needs to be 20mm) Tell pt to STOP SMOKING, avoid RAI Tx: steroids, radiation, surgery (Severe)

Patient has postphlebitic syndrome (complication of DVT) Tx:

No effective therapy - leg elevation and compression socks (The key is prevention)

Should an overweight 44 yoa be tested for diabetes (no other risk factors)?

No, age 45 Normal test: check min of 3 yr intervals also test: **asx adult of any age w/BMI >25 (23 in asian americans) w/ 1+ risk factors for diabetes (for kids they have to have 2+risk factors) **ID CVD risk factors

Do you give statins to a 30 yoa w/ LDL-C of 180mg/dl? What intensity level?

No, needs to be >190 High

Do you give statins to a 50 yoa non-diabetic patient w/LDL of 160 and a 10 year ASCVD risk of 6.5%? What intensity level?

No, risk needs to be >7.5% Moderate if no 10 year risk >7.5% IF QUESTION DOESN'T STATE 10 YEAR ASCVD RISK THEN THERE'S NOT ENOUGH INFO TO ANSWER THE QUESTION!!!! (mentioned in class)

A patient presents with a chief complaint of diarrhea. ABG reveals an acid-base disorder. Based on these symptoms and results, how would you classify this patient's current state?

Non-Anion Gap Metabolic Acidosis

Chronic cough: idiopathic with sputum eosinophils

Non-asthmatic eosinophilic bronchitis

How is a selective PDE inhibitor different from a non-selective

Non-selective CAN bronchodilate via increasing cAMP--theophylline is non-selective Selective CANNOT bronchodilate (only works to decrease inflammation) --Roflumilast is PDE4 inhibitor

Major Types of Lung Cancer: Descriptions

Non-small cell lung carcinoma—adenocarcinoma, SCCA, large cell CA, mixed tumors, carcinoids of lung *Small cell lung carcinoma*—one of the little blue cell cancers, exclusive to heavy smokers *Metastatic*- Lung tumors from another primary type of cancer— MC=prostate, *breast*, or colon, etc

Which type of Idiopathic pulmonary fibrosis morphology is related to CT diseases (like sarcoidosis)?

Non-specific Interstitial Pneumonia--also note TEMPORALLY HOMOGENOUS (& architecture preserved) -can have CELLULAR (lymphcytes) or FIBROSING (collagenous) pattern (or both in same biopsy)--> hence non-specific -DRAMATIC RESPONSE to CORTICOSTEROIDS

Type of CV dyspnea that includes diastolic dysfunction, pericardial dz

Normal CO

What are labs for thyroid nodules?

Normal thyroid fxn, normal TSH and T4 ↑↑TSH=suspicious →→get FNA thyroid scan

What is the goal for corrected Ca? Is 10 good?

Normal total Ca Yes, Goal in post op pt >8 <8=oral Ca and VitD; acute? = IV Ca

Calculate the O2 carrying capacity of a person w/ [Hbg] 18g/dl. What is the approx. arterial saturation if his CaO2 is 17ml/dl

O2 carrying capacity: 18x1.36 sat= O2cont/o2 carrying capacity sat= 17/(18x1.36) think the numbers are flipped?

When do you treat with O2 supplementation

O2 sat <90% SpO2 <60 correct underlying conditions

What effect does O2 uptake in the lungs have on the buffering capacity of blood/ What does O2 unloading in tissues have?

O2 uptake in lungs-Haldene: decreases buffering O2 unloading in tissues-Bohr: increases buffering

LPR

OCCURS WHILE UPRIGHT 35% heartburn dysphonia/hoarseness chronic cough non-productive throat clearning

Which one (obst vs rest) has FEV1/FVC ratio <0.7

Obstructive reduced peak flow, scooped out mid-curve--> steeple pattern and rapid fall off in severe cases no change/increase TLC

Types of Sleep Apnea

Obstructive (OSA) - no airflow is detected despite respiratory effort (effort to breath) (MC sleep disorder breathing) Central Sleep Apnea - respiratory interruption without respiratory effort (no effort to breath) CSA - O2 Drops (Cheyne-Stokes Breathing)

Types of Sleep Apnea

Obstructive (OSA) - no airflow is detected despite respiratory effort (effort to breath) (MC sleep disorder breathing) Central Sleep Apnea - respiratory interruption without respiratory effort (no effort to breath) CSA - O2 Drops (Cheyne-Stokes Breathing) CENTRAL--CHEYNE --when airflow is <10% of baseline for at least 10 sec--Snoring, sleepiness, significant --USE PSG and EPWORTH SLEEPINESS SCALE

How do we identify olfactory cells on slides? What are the other cells and where are their nuclei located?

Olfactory cell--> nuclei in the MIDDLE of the epithelial lay Basal cells-->basally located--duh Supporting/Sustentacular cells--> APICAL nuclei (they are supportive so they are holding their nuclei up high!)

Anthonisen Criteria Type 3

One of previous sx and coughing, wheezing, URI sx

What do the ovaries produce?

Oocytes and sex hormones

Food allergies -Dx

Oral challenge test -Double blind placebo controlled*

Both ears are affected, usually familial. Autosomal dominant mostly --transmission w/variable inheritance pattern --What determines severity of hearing loss in this disease?

Otosclerosis --Degree of Immobilization

MCC of death from gynecological malignancy

Ovarian

What diseases cause high uptake?

Overproduction of TH Graves hCG Hashimoto

What are the normal values for PAO2, PACO2, PaO2, PaCO2, PvCO2?

PAO2 =100mmHg, PACO2=40mmHg, PaO2=80-95mmHg, PaCO2=40mmHg, PvCO2=45mmHg

If a lung disease were to cause an increased non-uniformity of blood flow but not ventilation, what would happen to PAO2, PaO2, & %SaO2?

PAO2 increases but decrease in PaO2 & %SaO2

Papillary carcinoma vs follicular carcinoma....who likes to invade what?

PAPILLARY----> LYMPHATICS FOLLICULAR---> VASCULAR

What results from a methacholine challenge are diagnostic for asthma?

PC20 (positive test): provocative concentration of methacholine → ≥ 20 ↓ FEV1

What is the gonadal manifestation of IRS?

PCOS -chronic anovulation -hyperandrogenism -infertility -found in obese and lean PCOS pt

What syndrome has adequate estrogen but excess androgen? Does it have 1 ° or 2° amenorrhea

PCOS 2°

What presents with oligomenorrhea and androgen excess? What's the Tx?

PCOS E-containing oral contraceptives also could see hirsutism, ↑predisposition to gluc intolerance

How to remember PDE5 inhibitors...Treatment?

PDE5-I inhibs PED5--> inhibits cGMP hydrolysis--> enhances NO effect--> prolonged erection Think- Penis Doesn't Erect (for more than) 5 Minutes--> can't Get My Penis hard (hydrolyzed)---> NOOOO!!! Enhances loudness of NO. Tx: Raynaud's, severe altitude sickness, ED, RAY can NOT get his dick to HIGH ALTITUDES Sildenafil--additionally can treat PAH Tadalafil--> BPH (think the bladder is toTALLY FUL--> bph) -Penis Doesn't Erect in 5...4...3... (so remember CYP3A4 metabolism) -Ketoconazole inhibs CYP3A4--> may hit the floor cause of syncope.--> Penis Doesn't Erect 5--> isn't my main concern...it's not KEY (important) --CYP3A4--> Rifampin can induce it so will dec levels of PDE5 inhib--> RIFAMPIN can DAMPIN your sex life. --AE: If you masturbate too much you will go BLINE & DEAF (blurry vision/blindness). If you get caught masturbating you will FLUSH in embarassment. --can also have HA, nasal congestion, dyspepsia diarrhea

MC genetic abberations of Clear Cell CA of Ovary

PIK3CA, ARID1a, KRAS, PTEN, & TP53 NOTE: TP53 mutation is MOST COMMONLY mutated gene in SPORADIC CANCERS

How do PIO2 & PaCO2 change during exercise?

PIO2 doesn't change w/ exercise. It changes w/ humidity & change in Pb. PaCO2 increases b/c blowing off more CO2.

Idiopathic inflammatory myopathy of STRIATED muscle (so dysmotility of prox 1/3 of esoph), PROXIMAL muscle wasting....What condition and what lab value would we expect to be elevated?

POLIOMYOSITIS Elevated CPK

Key about Hypersensitivity Pneumonitis

POORLY FORMED, LOOSELY ORGANIZED granulomas, intense Ag exposure

Med management for LPR

PPI as 1st line therapy (1/d for GERD, 2/d (maybe 3) for LPR) Lifestyle: no eating 3-4 hrs before lying down

What hormone alone can contribute to low libido?

PRL

44 yoa male w/breast tenderness and enlargement, ↓sex drive, nl genitals. What lab is elevated?

PRL (tx is same as hyperprolactinemia) Hypogonadotrophic d/t HyperPRL nl TH, estradiol, ß-HCG, low active TTestosterone Nl gonadotropin (inappropriate!!)

What should be included for testing hypercalcemia?

PTH also calcium, albumin, phosphorus, BUN, Cr, 25(OH)-vitamin D

what 2 hormones promote expression of RANKL?

PTH vit D3

how do the following affect P? -PTH -VitD3 -calcitonin -FGF-23

PTH - increase urinary P excretion (decrease) vit D3 - tertiary action of increasing P resorption in kidney (increase) calcitonin - debated but maybe decreases FGF-23 = inhibits renal reabsorption of phosphate in the kidney (mostly prox tubule) (decrease?)

What drug can I give a woman in her 1st trimester?

PTU (hepatotoxic) Methimazole: #1 choice outside of pregnancy Anti-thyroids: check CBC, LFT, fever/sore throat better in kids/pregnant women NOT DEFINITIVE in nodular thyroid disease

equation: *ideal gas law*

PV = nRT *V = nR(T/P)*

Pt has CO=6L/min, Ppa=30mmHg, PAWP=20mmHg. What is the pt's pulmonary vascular resistance? Is the pulmonary circulation abnormal? What primary type of problem might the patient have? What secondary effects might occur in the lungs?

PVR=(Ppa-Pla)/CO Pla=PAWP PVR=(30-20)/6= 1.6mmHgmin/L -pt's PVR is normal but pressures & CO are all elevated -pt might have pul HTN -pt may have pulmonary edema (increased interstitial fluid in the lungs) assoc. w/ HF or pleural effusion (increased fluid b/n lung & chest wall)

How will each of the following impact PaO2, arterial %SaO2, & O2 content of art blood. 1. Anemia 2. Polycythemia 3. low PO2-inspired air 4. 2,3 BPG 5. Increased PaCO2 6. Fever 7. CO poisoning 8. Methoglobinemia

PaO2 %SaO2 O2 cont 1. Anemia N N down 2. Polycythemia N N up 3. low PO2-inspired air----down across the board 4. 2,3 BPG------------------down across the board 5. Increased PaCO2-------down across the board 6. Fever---------------------down across the board 7. CO poisoning N down down 8. Methohemoglobinemia UP N/low UP

How would PaO2 & PaCO2 be affected if the diffusion of these gases across the alveolar-capillary membrane became limited?

PaO2 would do down (O2 can't diffuse in) & PaCO2 would go up (CO2 can't diffuse out)

What T1DM treatment requires lifelong immunosuppression?

Pancreas and Islet cell transplantation Pt undergoing renal transplant, following renal transplant, recurrent ketoacidosis

Psammoma Bodies are found in....

Papaillary carcinoma of thyroid Somatostatinoma a Meningioma Mesothelioma Ovarian serous papillary cystadenocarcinoma Milk (prolactinoma) a

MC cancer

Papillary best prognosis least aggressive total thyroidectomy ablative Tx w/RAI

What hormone activates bone turnover osteoclasts and coverts 25-OH→ 1,25 (OH)2 VitD?

Parathyroid hormone Kidney: Ca retentive; PO4 loss in urine Gut: Calcium resorptive Normal: ↑Ca ↓PTH

Patient with decreased DLCO...What else would be super bad to see in this patient?

Patient has interstitial lung dx but it does NOT CORRELATE w/severity. BAD---> CO2 retention = poor prognosis

Discharge criteria for patients w/ COPD

Patient, *family*, and physician are confident patient can manage successfully at home

Key recommendations

Patient-centered communication (B) Timely and EBM based treatments Aligned w/ CCM (proactive team and informed patient) (A) Support team based care, community involvement, patient registries and decision support tools to meet pt needs (B_

RLS has an opposite, but similar condition called...

Periodic Limb Movement disorder that gets WORSE with rest

Petrous apicitis/Gradenigo's syndrome Tetrad

Periorbital unilateral pain diploplia otorrhea

Formed elements -Platelets, structure, zones

Peripheral (hyalomere)--think "halo-mere"--periphery -Made of cytoskeletal elements including spiral of microtubules; important for shape -G and F-actin Central (granulomere) -Three vesicle types: lysosomes, alpha-granules, dense granules

Where is T3 made?

Peripheral tissues T4→T3 d/t RT3 -recognized by feedback reg (do you know your phys?!) Give T4 as replacement

Which chemoreceptors show some responsiveness to arterial O2 content?

Peripherals especially carotid bodies

MCC of cobalamin deficiency

Pernicious anemia

Inspiratory sound at end of coughing spell *Paroxysmal phase* Tx:

Pertussis • Paroxysmal phase: post-tussive vomiting, post-tensive syncope, fatigue • *Abx Erythromycin* + Place all hospitalized patients on *droplet isolation*

Young, lean patient, unusual HTN, diaphoretic and complains of headaches. What's this disease called? Treatment?

Pheochromocytoma Catecholamines from adrenal medulla; reg by ANS MRI usually Phenoxybenzamine NO BETA BLOCKERS!! (precip crisis)

t(9;22) BCR-ABL1 fusion gene

Philadelphia chromosome - abnormal tyrosine kinase chronic myelogenous leukemia (CML) most commonly also seen in ALL and myeloid leukemias

Active form of phophoprotein phosphatase? Active form of glycogen synthase?

Phosphoprotein phosphatase-->ACTIVATED by +P via phophorylase kinase A Glycogen synthase ACTIVATED when -P (glucagon--> cAMP--> inhib -P via glycogen synthase)

How do you treat pituitary Cushings? Ectopic? Adrenal?

Pit: Surgery, Rad, anti-adrenal Ectopic & Adrenal: Surg, Rad

Patient presents with abrupt blurring of vision with tunnel vision, decreased peripheral vision and bitemporal hemianopsia. What do they have? What do you do?

Pituitary Apoplexy Call 911 and go to ED

Patient has Low K, high glucose, striae and wt gain. What's the next step imaging? *From review of cases

Pituitary MRI (Cushing Dz) **Don't do shotgun approach

What do you need to warn all patient with pituitary neoplasms about?

Pituitary apoplexy Tumor abruptly bleeds or swells compressing optic chiasm compromising pituitary function and vision. neurosurgical emergency

Patient is a young athlete, with a traumatic injury. Dx: Simple Tension

Pneumo Thorax - young athlete Simple - pleural P < atm P (trachea shift to side of collapse) Tension - pleural P> atm P (Trachea shifts away from injury d/t) Medical emergency --> *Use needle decompression*

Empyema:

Pockets of pus in the pleural cavity - manifestations of long-standing anaerobic infection • Drainage is required

If Spiro w/methacholine challenge is positive what do you do? If negative what do you do?

Positive--> check sputum for eosinophils Negative--> PPIs for GERD

When might you see ↑FSH? If testosterone is low what should be elevated?

Post menopausal women (↓Estradiol) LH Think hypopit patient: What should their normal response be (↓ cortisol? then ↑ACTH...if not then it's a pituitary prob)

A patient presents with cough + nasal drainage. On exam, you recognize the appearance of what is known as "cobblestone throat." What is the diagnosis?:

Post-Nasal Drip

Most common causes of Subacute or Chronic Cough (3-8wks): Work-up:

Post-nasal Drip, Asthma (MC in children), GERD 1) Attempt medication challenge empirically with *nasal antihistamine-decongestant combo* ▪ If partial relief - Adding nasal steroid or anticholinergic. 2. If no relief, try *spirometry with methacholine challenge*. ▪ If positive - Treat with bronchodilators if positive result. ▪ Consider checking sputum for eosinophilia 3. Empiric Tx with *PPI for GERD*, w/lifestyle and dietary changes

MC age & location of Lichen Sclerosis

Postmenopausal women in anogenital region

MCC Chronic Cough (>8w)

Postnasal Drip Asthma (2nd MCC: adults, 1st MCC: kids) GERD

True/False? Diastolic bp is similar in the pulmonary artery & R ventricle?

Ppa=8 & R ventricle=0, so difference of 8 during diastolic, but during *systolic* they are =

A portion of lung has Ppa=10mmHg, an alveolar P= 5mmHg & pulmonary venous P=0mmHg. Which zone of the lung is this? What is the pressure gradient driving flow? What portion of the normal lung might be in this condition?

Ppa>PA>Pv = 10>5>0 This is zone 2 Pressure Gradient =5mmHg (10-5) -upper lung (above base) would be in this condition

Amyline mimetic

Pramlintide--> Post prandial glucose! (kinda in the name)...decreases gastric emptying & suppresses glucagon...think of PRAMCAKES...enjoy them and don't eat them so fast. Also don't put too much sugar on them--suppress the glucagon.... Both type Is and type IIs like pancakes. --eat too many and you will be nauseous, can cause hypoglycemia and INJECTION site rxn

If my patient needs a low intensity statin what are my options?

Pravastatin 10-20 mg Lovastatin 20 mg

What's stage 1 tanner? 5?

Prepubertal Adult genitalia

Formed elements -Erythrocytes; pathologies, anisocytosis

Presence of RBCs of different size in the peripheral blood -Megalocytes (macrocytes): abnormally large RBC; > 9 micron -Microcytes: abnormally small; < 6 micron

What two values should you make sure are normal before you diagnose Hypergonadotrophic/hypo hypogonadism

Prolactin Thyroid fxn

Pt presents with galactorrhea, infertility, amenorrhea and decreased libido? PRL >200mcg/L. What do they have? How do you treat it?

Prolactinoma (PRL elevation prop to size of tumor) MC: functional pit neoplasm Tx: Dopamine agonist: Bromocriptine, Cabergoline Other causes: pregnancy, pit stalk compression, anti-pscychotics, dopamine antagonists Note: any pit tumor large enough to cause stalk compression can increase PRL (also eval for visual changes)

The oocyte remains as a primary oocyte arrested in ______________ until just before ovulation?

Prophase 1

Pt w/ persistence of fluid in middle ear w/o evidence of infection and PAINLESS hearing loss...what should you do??

Pt has Recurrent Serous Otitis Media...However if this is UNILATERAL persistent middle ear fluid you MUST INSPECT NASOPHARYNX *Sometimes the only sign of laryngeal lymphoma or Nasopharyngeal carcinoma!!! You will get sued if you f*ck this up

MCC of pulmonary regurgitation

Pulmonary HTN (or dilation 2/2 CT disorder)

What's the best way to prevent hospital readmission and increase functional capacity? TEST

Pulmonary Rehab -BiPAP decreases mortality, shortens hospital stay TEST

What is the best way to prevent hospital readmission & increase functional capacity (HIGHLY EMPHASIZED)

Pulmonary Rehab, BiPAP decreases mortality & shortens hospital stay!! (probs test Q)

Takayasu arteritis

Pulseless disease; difficult to control HTN

Calculate the partial pressure of O2 in dry air at the following locations, assuming that PH20=0 & dry air is 20.93% O2 (V/V) independent of Pressure. Calculate for humidified inspired air at the locations. Barometric P: -honolulu=760mmHg -denver=635mmHg -Mt. Everest=234mmHg

Px=Pb x Fx -> PO2 =760x(0.2093)=159mmHg =635x(0.2093)=132.0mmHg =234x(0.2093)=49mmHg PIO2=(Pb-47)xFIO2 PIO2=(760-47)x(0.2093)=149mmHg PIO2=(635-47)x(0.2093)= 123mmHg PIO2=(234-47)x(0.2093)=39mmHg

GLucose can be formed from...

Pyruvate Lactate Alanine Glycerol Amino Acids Propionyl-CoA

Pt has CO=8L/min, a CaO2=20ml/dl & Cvo2=14ml/dl. What is his VO2 (O2 consumption)?

Q=VO2/(CaO2-CvO2), so... VO2=Q(CaO2-CvO2) VO2=(8L/min)(20-14ml/dl)(dl/100ml) =0.48L/min

Analysis of the alveolar air equation for a patient shows that PA02=100mmHg which corresponds on the O2 dissociation curve to a content of 20ml/dl. CaO2=19.5ml/dl & Cvo2=13ml/dl. Right to Left shunt represents what % of pulmonary blood flow?

Qs/QT= (Cc'O2-CaO2)/(Cc'O2-CvO2) =(20-19.5)/(20-13) = 1/14 x 100% =7%

How many times should you perform an A1C test in patients whose therapy has changed or who are not meeting glycemic goals?

Quarterly Meeting tx goals= 2x annually

MC Rheumatic dx with RF

RA Sjogrens Syndrome Mixed Connective Tissue

Pt has ↑TSH ↑FT4 ↑FT3 (thyrotoxicosis) Feels nervous and anxious What do they have?

RARE DON't ASSUME THAT IT's a TSH secreting tumor TSH is most accurate lab Think: undertreated hypothyroidism pt took levo too close to lab Most patients w/hypoTH don't have goiters

Formed elements -Erythrocytes; pathologies, poikilocytosis

RBCs are irregularly shaped -Vermiform -Elongated -Spindle-shaped

Right common cardinal vein will form _____________ Left common cardinal vein will form _________

RCCV-Proximal end of SVC LCCV--portion of Coronary sinus & oblique vein of left atrium

Elderly person with lung abscess...what must we do?

RULE OUT CARCINOMA

How much air is in the lung at the end of normal expiration? How much is this expressed as a % of TLC?

RV + ERV = FRC ~50% of TLC

Explain effects of loss of renal parenchyma? Cause of osteomalacia?

Reduced 1,25(OH)D2-D3--> red absorption of Ca++--> PTH elevates--> bones rel Ca++--> INCREASED ECF Ca++ -->extensive bone turnover--> renal osteodystrophy Osteomalacia--Ca++ & phosphorous absorption & DECREASED ECF conc of these ions...mineralization of osteoid to form bone is unimpaired. Undermineralized--> weak bone Renal Osteodystophy--> INCREASED ECF ion conc Osteomalacia---> DECREASED ECF ion conc.

Hypopnea defined as:

Reduction of airflow - decreases at least 30% from baseline - accompanied by 3%+ oxyhemoglobin desat (4% for Medicaid)

Hypopnea is defined as....(also medicaid qualifications?)

Reduction of airflow decreases at least 30% Accompanied by 3% oxyhemoglobin desat (4% for Medicaid)

REV gene...

Reg of virion prot exp (selective reg +) Protein product allows virus to prod differing amounts of reg or structural components Controls extend to of viral mRNA splicing & exportation (from nuc)

Pars intermedia

Region of the adenohypophysis that is the remnant of RATHKE'S pouch....contains rathke's cysts lined w/*cuboidal epithelium*

MCC of 2ndary hypertension

Renal disease Next MC are pheocytoma, conn syndrome, & acromegaly

Meglitinides

Repaglinide--meg from family guy is REPULsive --induces res by blocking ATP sensitive K+ channels (depolarizing membrane)--> Ca++ influx--> insulin release--SAME MOA for SULFONYLUREAS. --CYYP3A4 & CYP2C8--Meg from family guy ATE too much--she is NOT a GEM (do not use w/gemfibrozil) --Hypoglycemia

Rh blood group system

Represents transmembrane polypeptide that is part of an erythrocyte integral membrane protein complex that may express 3 clinically significant rhesus antigens -D, C and E -A person with at least 1 of the antigens is Rh+ -All 3 antigens stim production of anti-Rh antibodies in individuals w/o same antigens

What is the mission of AMPK?

Reset metabolic poise so energetic status is improved aka INCREASE ATP GENERATION

What compensation is d/t changes in CO2 by RR that takes minutes

Resp Compensation

If ph and PaCO2 change in opposite directions

Respiratory

Upon physical exam, it is noted that your patient experiences unpleasant paresthesias during voluntary leg movements. What should you automatically include in this patient's DDx?

Restless-Leg Syndrome (RLS) RLS gets *worse* with rest *DDx: Involuntary leg movements - Periodic Limb Movement Disorder

Which one (obst vs rest) has FEV1/FVC >0.7?

Restrictive decrease TLC Normal peak flow, reduced volume (tall and peaked)

MC risk factor of acute endometritis

Retained POC

An Auto-antibody to Self IgG Fc Major laboratory hallmark of RA NOT + in all patients (severe/erosive manifestations) 80% RA patients have this marker

Rheumatoid Factor

Loss of *right heart border* on CXr is consistent with the presence of an infiltrate in what lobe of the lung?

Right Middle Lob

What does water deprivation show in patient w/central DI? How do you differentiate between central and nephro DI?

Rising serum Na w/ rising serum osmolality and BUN --can't dilute urine Desmopressin given: central: urine concentrates nephro: no response (ADH is actually elevated) --Cause: Lithium

Thiazolidinediones

Rosiglitazone Pioglitazone --activate PPAR-gamma--> inc cellular response to insulin--> increased sensitivity --cause weight gain!--Thiazes increase in certain ZONES--> if you gain enough weight, your stomach will PPAR out from under your shirt and you may be sensitive... AE for both: CHF risk, fluid retention/edema PK: Rosiglitazone--> CYP3A4 & CYP2C8-- Rosie o'donell ATE too much (got fat) and is NOT a GEM (DO NOT use with GEMFIBROZIL cause it is potentn inhibitor of CYP2C8)--use fenofibrate AE Rosiglitazone-->she is at risk for MI

How to remember small cell carcinoma

S--Smoking, Sentrally located, small chance of living --if you're CUSHING on someone and have a SMALL CRUSH (crush artifact) at the party AZZOPARDI (the azzopardi effect), you're gonna be a little salty (salt & pepper chromatin & SIADH & CUSHING) if someone else steals your man and you see them NECKING (very necrotic). --It would be even worse if you saw them banging like rabbits (BRISK MITOTIC ACTIVITY)--rabbits also love carrots ("Carrot-shaped). It may cause you to SYNAPT (synaptophysin positive & chromogranin + --due to the mitotic activity) --So you go outside or a smoke. You're so sick you don't even want to EAT (lambert-eaton)...Your best bet is that the W*HORE suffers an ECTOPIC (ectopic neuroendocrine hormone production--ENOLASE or PARATHYROID hormone)... it makes your core SUPER DARK (dense core neurosecretory granules) --now you have a SMALL set of options (staging is only LIMITED or EXTENSIVE--no other classification)

MCC of lobar PNA world-wide

S. Pneumoniae

Etiologic agents for otitis media with EFFUSION

S. pneumo, non-typable H. influenzae, M. catarhalis & H. PYLORI that mutherfecker

What do you withhold before Spiro?

SABA, LABA, Ipratropium, Tiotropium, caffeine, smoking

What is the Hering-Breurer reflex, what is its physiological role, & what receptors are involved?

SARS (slowly adapting stretch receptors) important in adults during exercise, COPD pts, & help terminate inspiration in babies

Hering-Breurer reflex (role) and what receptors are involved?

SARS--slowly adapting stretch receptors --important during EXERCISE in adults, COPD pts, & help TERMINATE INSPIRATION in babies. Think the Herring Bringeth & the Herring taketh (away your baby)

SCC in the parotid lymph nodes....

SCC of head/neck usually met to these lymph nodes so it is a 2ndary SCC of the parotid (primary is NOT common)

Patient with esophageal dysmotility of the lower 2/3. Autoimmune disorder, atrophy of smooth muscle and collagen deposition. Dx?

SCLERODERMA! CREST Syndrome

Patient presents with hyponatremia, low serum osmolality and high urine osmolality. What do they have? How do you treat?

SIADH (excessive fluid volume) Fluid restriction --can use aquaresis w/Vaptan to correct hypoNa MCC: Small cell

What's the speed of my titration for someone with CAD, elderly or kids?

SLOW rapid for very low thyroid fx, or pregnancy No T4 day of TFT

Sjogrens antibodies

SS-A (Anti-Ro) SS-B (Anti-La)

what lab finding makes a thyroid nodule less suspicious? what is the next step in treatment?

SUPPRESSED TSH next step = thyroid scan

Pt presents w/ compression of Superior vena cava, swelling of face, neck, and UEs with neuro symptoms:

SVC Syndrome

How do hormones from pars distalis enter blood stream?

Secondary capillary plexus--fenestrated sinusoidal capillaries.

DNA topoisomerase 1

Seen in diffuse scleroderma while anti-centromere is in limited (CREST) scleroderma

What's the #1 step of Foundations of Care (holistic approach; facilitates comprehensive assessment)?

Self-Management Education (DSME) ---Self- Management Support (DMMS) 2= Nutrition 3= Counseling 4= Physical Activity 5= Smoking cessation

What are the two methods to assess effectiveness of management plan on glycemic control?

Self-monitoring of blood glucose (SMBG) A1c SMBG requires ongoing instruction and regular eval of technique use it before meals, bedtime, exercise, hypoglycemic events

What's the gold standard for diagnosing acromegaly?

Serial GH values during OGTT **GH is not suppressed Tx: Trans-sphenoidal surg, ocreotide/pegvisomant, rad tx

SMART-COP is used for what? List them.

Severity scale for CAP S-Systolic < 90 M-Multi-lobular A-Albumin (low) R-RR high T-Tachycardia C-Confusion O-Oxygenation (poor) P-pH low HOS--> 2 Pointers (all the others 1 pt), Think HOS are more likely to put you in HOSPITAL Score < or = 3 --> ICU

What is the thyroid panel after a hard labor involving severe blood loss and LOF @ pituitary?

Sheehan syndrome ↓TH; TSH would NOT RESPOND not autoimmune

Shift vs drift influenza...

Shift--causes EVERYTHING to go to SHIFT--PANDEMIC---> both H & N replaced through RECOMBINATION w/animal influenza viruses (bird flu) Drift--small changes that cause epidemics. Reminder: Influenza are SINGLE-STRANDED RNA viruses When you are single you can SHIFT and DRIFT wherever you want

Insulin duration...

Short D, Rapid A---guys w/ SHORT Ds are lustful (LISPRO) & they release their GLULisine B4 (GLUT4) you ASTART (ASPART) and it's AFRRENzy (AFREZZA) Short D, Slow A--Reg insulin Intermediate D--NPH & insulin Detemir (can't determine so it is in the middle), No Preference Here (neither long, nor short) Long D--Insulin glargine--> gLARGEine amount of time

Sandblasting, mining, Sandstone assoc w/ what disease/etiology?

Silicosis - Higher risk for Myco Kansasii infection (Atypical Mycobacterial Infection)

MOA of silicosis and other important things?

Silicosis - Higher risk for Myco Kansasii infection (Atypical Mycobacterial Infection)--the ONLY ONE that inc. RISK OF TUBERCULOSIS due to INHIBITION of PHAGOLYSOSOME FORMATION -most prevalent chronic occupational disease in the world. --Fibrotic nodules in the UPPER LOBES of the LUNG --associated w/Sandblasting, mining, Sandstone -Eggshell calcification --*progresses even after exposure STOPS* Sidenote: Bronchogenic carcinoma from ASBESTOS ALSO WORSENS after exposure stops!!

What is the epithelium of the ovary?

Simple cuboidal epithelium covers the ovary (instead of mesothelium) - germinal epithelium

MCC of congenital abnormalities

Since CMV is the most common congenital (microbial) disease, it is the MCC of congenital abnormalities)

What is the progression of thyroiditis? What treatments do you use?

Sine wave fxn Outset=hyperTH (tx=propanolol)→→Normal (TH is spent) TH leaks out→hypoTH (tx=levothyroxine)→recovery Hashimoto discovered in hypoTH

MCC of aortic valve insufficiency world-wide? What would we hear?

Siphilis--combo of diastolic murmur, "water hammer" pulse, and wide pulse pressure!

DPP-4 inhibitors

Sitagliptin, Saxagliptin, Linagliptin, Alogliptin --Dat P&ssy Packs 4 INside (DPP-4 inhibitors)--Inhib activation of INCRETIN--> blocks GLP-1 CATABOLISM--> INC insulin secretion & response to inc glucose. --Guys Like P4ssy...Guys Like P$ssy so you don't turn them away (you don't catabolize them)---since you can fit 4. --combine w/ METFORMIN or TZDs.-->think FOUR MEN (metformin)--> DPP4 dicks on TZDs (on tuesdays). --if you messing w/4 dudes, you going to prolly have KID problems (renal probs) & hypoglycemia

40 fold increased risk for lymphoma?

Sjogren (MALT type of lymphoma)

Treatment of Insomnia:

Sleep Hygiene - Actions that tend to improve and maintain good sleep

In patients with insulin resistance (like that seen in metabolic syndrome) what would their plasma insulin vs. glucose lowering ability graph look like?

Slide 3 of the metabolic syndrome. Insulin resistance would shift the graph down and to the right a lil. Basically pt's resistant to insulin have a decreased drop in blood glucose than normal individuals at a certain insulin level.

A smoker presents to your office with bilateral lung masses and distant metastases to the brain and liver. Biopsy reveals the presence of small, blue cells with scant cytoplasm. Based on this description: What is the most likely type of tumor present? How would stage this tumor? How would you treat this tumor?

Small Cell Lung CA • How would you stage this tumor? Extensive SCLC • How would you treat this tumor? Chemotherapy + Supportive/Palliative Care Small cell cancer o Local/limited disease—affects 1 lung & local lymph nodes- single lesion w/no mets o Extensive—cancer affects both lungs, distant lymph nodes &/or other organs

What can be used to decrease potential for adverse effects of inhaled drugs?

Spacer

What are spironolactone bodies and where are they found?

Spironolactone bodies are concentric, laminated eosinophilic structures found in ALDOSTERONE secreting tumors (ADRENOCORTICOTROPIN ADENOMA)

Carincoma of the larynx

Squamous cell carcinoma

What is the ONLY major form of lung CA for which surg removal is indicated as a curative therapy?

Stage 1 NSCLC

What is the ONLY major form of lung cancer for which surgical removal is indicated as a curative therapy?

Stage 1 NSCLC

Patient has a severe asthma attack that doesn't respond to Beta2-agonists Tx:

Status Asthmaticus - High Dose Corticosteroids, hydration, O2, Beta2-agonists q4h

Dx of CF

Step 1- clinical indication (presence of 1+) -Characteristic phenotypes -hx of CF in sibling - + newborn screening test Step 2- abnormal Cl- sweat test

Women with no previous DM diagnosis does a 50g GLT (nonfasting) and her 1 hour plasma glucose level is >140. What is next?

Step 2: 100g OGTT while patient is fasting

Prednisone 20 mg PO daily (<2w)

Steroid that you give if NO respiratory failure

Solumedrol 20 mg IV (<2w)

Steroid that you give if respiratory failure

Pt w/ Increasing dyspnea and change in sputum Tx: Which COPD patients do you give antibiotics?

Steroids and Abx - Give to patients w/ Type 1, Type 3 exacerbation, or *pt on ventilator (Eg: BIPAP, intubation)* *Anthonisen Pathophys: o Type I: increased dyspnea, sputum volume and purulence o Type II: increased sputum vol and purulence o Type III: just 1 of the above & cough/wheeze/URI symptoms • Example: Corticosteroids: <2w, oral > IV, low dose > high dose o Prednisone 20mg PO daily (if NO respiratory failure) o Solumedrol 20mg IV q12h (if respiratory failure)

MOA of B2 agonists...

Stimulate Gs to AC--> inc cAMP--> act. PKA to K+ channels then membrane hyperpolarization--> closes voltage dep Ca++ channels, which sequesters Ca++ -Induces airway smooth m relaxation -inhibits mass cell degranulation

According to FRAX name 3 examples of what a patient can do to reduce fracture risk

Stop smoking Reduce Alcohol intake Reduce or stop using glucocorticoids

Easiest thing to do when Dx of Cough?

Stop smoking and ACE-i Get CXR

MC types of monodermal Teratoma

Stuma ovarii & carcinoid (ALWAYS UNILATERAL)

Grading system C

Supportive evidence from poor controlled/uncontrolled study/evidence from observational studies w/high potential for bias evidence from case series/reports conflicting evidence w/wt of evidence supporting recommendation

Grading system B

Supportive evidence from well-conducted cohort/case control study

What is the primary treatment for hyperPTH? Who is it preferred in?

Surgery younger, higher Ca >12, renal insuff or lithiasis, osteoporosis, PUD, urine freq, mental status change,

What is best with cold nodules and large thyroids?

Surgery requires pre-treatment w/antit-thyroid and beta blocker

Tx of choice for Cushing? *From review of cases

Surgery- transphenoidal

Which of the following procedures would NOT be considered an appropriate therapy for the treatment of small cell lung carcinoma?

Surgical Removal

Tunica lamina propria of male....

Surrounds seminiferous epithelium TLP contains fibroblasts & collagen fibrils

(+) CD4 (-) CD7 CD4:CD8 ratio >10

Sézary syndrome

(+) for TdT, CD34, CD2, CD5, CD7

T-ALL or T-LBL

abundant pale cytoplasm w/ distinct pink cytoplasmic granules

T-cell large granular lymphocytic leukemia

STAT3 mutation

T-cell large granular lymphocytic leukemia (also hyper-IgE syndrome)

anthonisen classification of COPD exacerbation:

T1 (severe) = increased dyspnoea, sputum volume, sputum purulence T2 (mod) = any 2 of the above T3 (mild) = any 1 of the above symptoms, and 1 or more of the following: - cough - wheeze - PUO - URTI in past 5 days Corticosteroids: <2w, oral> IV, low dose>high dose Prednisone if NO resp failure Solumedrol if resp failure

After development the dorsal edge of the trasverse septum is at what level? ventral edge is at what level still?

T12 T7 test prediction (prolly not though)

How does estrogen aka BCP alter thyroid tests?

T3 resin uptake will be decreased because estrogens increase TBG production. (greater number of unbound binding sites). Total T4 is elevated

This TFT falls if patient is on Estrogen

T3RU inversely related to TBG *don't order this test

TAT gene...

TAT- large amount of viral protein made when activated- (TAT activated by antigen stimulation of inf T4 cell) TAT is rel from inf CD4 T lymph & can inhibit prolif of uninfected T-cells

What TFT is high if patient is on birth control, pregnant or has liver disease?

TBG low in malnutrition (example: nursing home patient)

Key about UIP (was on quiz so maybe not on test)

TEMPORAL HETEROGENEITY!--Old and New, if one lesion's time is UP (UIP), the next one will take over. -Patchy fibrosis w/fibroblast foci -MOST OFTEN associated with IPF

what stimulates synthesis (not release) of GH?

TH cortisol GHRH

how does a sudden increase in TBG affect serum TH?

TH gets bound by the increased TBG to produce a transient hypothyroid pt even though total serum is not changed this situation is usually transient as axis kicks in to restore steady-state

how do TRH and somatostatin work together in the production of TSH?

TRH is stim for TSH + released first SST is inhib for TSH + released later due to TRH being the trigger to stimulate production from the hypothalamus as these 2 hormones are out of phase with each other it produces a "pulse" of TSH release called the PULSE GENERATOR pulse height, number, and duration are what determine level of hormone released

What are the actions of TRH?

TRH stimulates synthesis and secretion of PROLACTIN and TSH (so both lactotropes and thyrotropes)

guide to diagnosis in thyroid disorders?

TSH

What is the first choice TFT?

TSH used for screening inversely related to TH production

What is normal in patient with pit dysfxn? Where do you check?

TSH, ACTH (e.g.= nl ACTH but ↓cortisol), LH, FSH **malnourished patient=↓cortisol **Estrogen= ↑CBG→↑cortisol End organ testing

What is the main screening test for thyroid function?

TSH/Thyrotropin

ADAMTS13 deficiency

TTP

#1 & #2 & #3 AI associated w/T1 diabetes? #1 disease associated w/hypothyroidism? #1 association w/vitiligo?

TYpe I Diabetes: 1. Hypothyroidism, 2. Celiacs, 3. RA Hypothyroidism:. Celiac Vitiligo: Hypothyroidism--CHECK thyroid Ab

Conditions of PSI (PNA Severity Index)

Takes into account: -Age -Physical Exam -Comorbidities -Lab findings Class III (71-90)-> admit for OBS Class IV (91-130) or Class V (>130)--> admit to hospital

Define the conditions of the Pneumonia Severity Index (PSI) for community-acquired pneumonia (CAP)

Takes into account: *age, physical exam, comorbidities, lab findings* • if Class III (71-90) → admit for observation • if Class IV (91-130) or Class V (>130) → admit to hospital

MCC of talar fracture? MCC of central cord syndrome MCC of pathologic fx in children MCC osteoarthritis in ankle

Talar-Automobile accident CCS--Falls then motor accidents Path fx child: Solitary bone cyst Ankle OA-Trauma

What's the only anabolic agent used for osteoporosis treatment?

Teriparatide *severe osteoporosis only ↑bone quality more than bisphosphonates Non Rx= diet, exercise, fall prevention

Anabolic agent for osteoporosis treatment?

Teriparatide (PTH). used in pt's with severe osteoporosis. increased BMD.

MCC of cyanosis within first few weeks of life

Tetralogy of Fallot Caused by ANTERIOR SUPERIOR displacement of INFUNDIBULAR SEPTUM

What is the embyrologic hx of the epiglottis?

The hypopharyngeal eminence forms from the 3rd and 4th pharyngeal arches, then the caudal portion of the eminence forms into the epiglottis

Important feature of the immotile cilia on the apical surface of the dendrite of the olfactory cell....

The plasma membrane of the Immotile Cilia of the olfactory cell contains: OLFACTORY RECEPTORS (G-protein coupled receptors)

What is ovulation?

The process of releasing the oocyte from the Graafian follicle

Connective tissue around the late (multilaminar) primary follicle forms a sheath and becomes what?

Theca folliculi

What differentiates Megakaryocyte maturation from maturation of erythroid & myeloid cells?

They GET BIGGER and they are polypLoid!! (NOT polyPoid)

Low urine Ca suggests malabsorption but what drug could make urine Ca unhelpful?

Thiazide diuretics ↑Urine Ca= ↑Ca loss, ↑intake, renal leak

how to remember 17a-alkylated androgens

Think of a 17 year old abusing anabolic steroids. --Methyltestosterone, Oxandrolone, Fluoxymesterone --Bind testosterone & DHT to androgen receptor--> transactivation of target genes --Ligand-androgen rec interacts w/other co-activators--> transactivates/tansexpression of target gene expression. --Commonly abused, OXANDROLONE has more ANABOLIC > ANDROGEN effects. Indication--hypogonadal men w/dec androgen sec, Protein met agents--reverse protein loss after TRAUMA, SURGERY, MUSCLE WASTING in AIDS patients, Prolonged immobilization, Growth stimulator in boys w/delayed puberty, Slows loss of lean muscle mass (aging)-NOTE these are also same indications for natural testosterone, testosterone cypionate, and testosterone ananthate CI: PREGNANCY, (17 year old boys should NOT be getting people pregnant), Carcinoma of breast/prostate--> interest of 17 yo boys, never us in infants/young children--> CNS effects PK: Inc oral availability (wink), AE: Sports enhancement--think of LIVE(r) strong when lance armstrong enhanced himself--> yellow band--> yellow person (jaundice), PELIOSIS, Atherosclerosis: dec HDL, inc LDL, Prostatic hyperplasia & prostate cancer (These AE only apply to Methyltestosterone and oxandrolone?)

List 2 factors which can influence the diffusivity (D) of a gas. List 3 factors that influence the diffusing capacity (DL) of a gas.

Think of the equations: Diffusivity is influenced by the solubility of the gas and molecular weight. Diffusing Capacity is influenced by membrane area & thickness, and diffusivity DL=(AxD)/T=Vgas/(Palveolus-Pcapillary)

How to remember ethambutol

Think of xmas cause of Red-green dyschromatotopsia Inhibits cell wall synthesis by inhibiting polymerization reactions--polymerization reminds us of a STRING of LIGHTS -- Clark W. Griswold Jr. was ECSTATIC for the lights--Ethambutol is the only RIPE drug that is bacterioSTATIC --Ethambutol only active INTRACELLULARLY--remember when he got stuck in the attic --distrubutes everywhere in the body, including CNS--> he put XMAS lights EVERYWHERE!

How to remember causes of hypergonadotrophic hypogonadism

Think- If Someone Can Make Appropriate Gonado Trophins I- Immune S-Surgery C-Chemotheraphy M-Mumps A-Alcohol G-germ cell arrest T-Testes (intra-abdominal)/ TURNER SYNDROME FOR EXAMPLE, if pt has had hysterectomy where OVARIES have been removed (or MENOPAUSE)!!--> hypertrophic hypogonadism

Centrally located trachea

Think- M^2EC --> the TRECH to MECCA is the CENTRAL meeting place for them. --M-mass of pleura or CW --> mass amount of people (church also has mass) --E-Pulmonary edema--> after a long trech to mecca, your feet are sure to be swollen --It's a LARGE CONSOLIDATION of people.

How to remember Angiomyolipoma

Think- The FAKE abbreviation for this would be AML (just like that FAKE water bucket challenge for the REAL AML) We did this outside of the TSC--so remember it is associated w/tublosclerosis (Loss of function mutations in TSC1 & TSC2) -It is composed of abnormal vessels, smooth muscle, and adipose tissue. -Think, when waiting for the water to be dumped, it was like a SPONTANEOUS HEMORRHAGE (kinda a surprise-which could kill)--> otherwise benign though cause it is just water --> so basically BENIGN

Cannalicular phase and how to remember

Think--16 yos think they CAN do whatever they want, then they realize they need their parent's health insurance until age 26. (16-26 weeks) --their parents try to put a CAP (illary) on their behavior and they begin to (a)BUT heads.--> capillaries start to abut respiratory epithelium --this is when you CAN technically start breathing (at the end of this phase) --Columnar--> ciliated cuboidal--> all about the Cs. --the respiratory bronchioles & alveolar ducts CANALICULIZE

Biguanide...

This is the BIG ONE always prescribed--METFORMIN --suppresses Gluconeogenesis @ liver & enhances glucose uptake in muscle--suppresses the BIG G (gluconeogenesis) --no hypoglycemia (possible weight loss but im not sure on that...) ---not for pre-diabetes---since this is the BIG ONE you gotta be BIG sure you have diabetes --CI: GFR <30, d/c metformin in hospital cause of possible contrast... --AE: MC n/d/abd pain, LACTIC ACIDOSIS

What is the preferred treatment in T4 deficiency?

Thyroxine (Levothyroxine). Brand name (synthroid, levoxyl, tirosint) are preferred.

Sulfonylureas

Tolbutamide & Glyburide (-ride, -mide, -zide) induces res by blocking ATP sensitive K+ channels (depolarizing membrane)--> Ca++ influx--> insulin release--SAME MOA for Meglitinides Think--SulFONDLEurea---> IDE hit that! IN All The PLaces (especially that potASSium) --more potent than megs. --peter griffin works in brewery--> EtOH--> disulfiram reaction--drinks a lot and gets LIVER PROBLEMS (CI in liver disease) --BBs block B2 receptors and decreases glucose lowering effect --can cause HYPOglycemia --however, must d/c INSULIN prior to starting this medication

Calculate LDL

Total Cholesterol = LDL + Triglycerides/5 + HDL*

What's 1st step in osteoporosis treatment?

Treat underlying lab abnormality (normalize Ca balance) Rx: must ↓fracture risk

How do you treat hypogonadism?

Treat with hCG of GnRH for fertility issues or replace testosterone. doesn't matter if hypogonadism is hypogonadotrophic or hypergonadotrophic

MC sexually transmitted form of vaginitis

Trichomnoniasis

The hand cramps with use of BP cuff. What's this called?

Trousseau sign ↓Ca

True or False. The pulmonary arterioles vasoconstrict in response to an arterial PaO2 below about 60mmHg

True, 60mmHg is the critical Po2

What is directly under the germinal epithelium of the ovary and separates the epithelium from the cortex?

Tunica albuginea

MCC of primary amenorrhea

Turner syndrome

ABO system

Two antigens -A, B Four blood groups -A, B, AB, O -Universal donor: O -Universal acceptor: AB

What disease has fasting with hyperglycemia?

Type 1 DM because glucagon is predominant always to always adding more glucose into the mix

Type of Familial Hyperchol. ↑LDL nl TG LDL rec mutation Tendon Xanthoma

Type 2 Hyperlipoproteinemia premature CAD

Endometrial carcinoma -Development

Type I Hyperplasia (75%) -Due to estrogen exposure, early menarche, late menopause, nulliparity, infertility, obesity -50-60 yo -NORMAL histology Type II Sporadic (25%) -Atropic endometrium, no precursor lesions -Serous or papillary type w/ psammoma bodies -p53 mutations -70+ yo -ABNORMAL histology

What did the DCCT trial indicate?

Type I DM pt's with tight control of their A1c had decreased risk of CVD events/retinopathy/microalbuminuria

Types of Rickets and special facts about them (also prediction) Associated disorders?

Type I--AR- defect in conversion of 25(OH)-D3 --> 1,25(OH)2-D3 (remember this step is completed by 1 a-hydroxylase but never said this was the reason) Type II (prediction)--AR, SINGLE AA change in ONE of ZINC FINGERS of DNA-binding domain of VDR--> non-fucntional receptor. Associated diseases w/specific polymorphisms of Vitamin D receptor gene---colorectal adenoma, Type I & Type II diabetes

MC pattern of renal injury in SLE

Type IV--> Diffuse "wire-loop" appearance on light microscopy, pts symptomatic (hematuria & proteinuria)

MCC Acute Cough (<3w)

URI

Patient presents with cough lasting for 2 weeks, what is the most likely cause?

URT Infection (Common cold, sinusitis, pertussis)

--DDI of Umecflidinium --DDI of PDE inhibitors --DDI of Ultra-LABAs

Umecflidium--it's a LAMA--CYP2D6 PDE inhibitors--CYP1A2--cimetidine, erythromycin Ultra-LABAs (formeterol, salmeterol)-->CYP3A4, PGP

What is associated with lack of treatment intensification? What is associated w/ treatment intensification?

Uncontrolled A1c, lipids, BP Improved A1c, BP, lipids

Where are vocal polyps found?

Unilateral at free edge of middle to anterior third of vocal fold Polyps PICK a side --Nodules are bilateral @ junc of middle/anterior 3rd of vocal cords

In ACUTE respiratory acidosis, every time pCO2 increases by 10 what happens to HCO3 & pH -In Chronic respiratory acidosis?

Use these equations... Acute resp acid---> pH = 0.008X(PCO2 - 40) Chronic resp acid->pH = 0.003X(PCO2 - 40) Acute resp alk----> pH = 0.008 X (40 -PCO2) Chronic resp alk--> pH = 0.003 X (40 - PCO2 ) For Acute use 0.008 For chronic use 0.003 For Acid PCO2 - 40 For Alk 40 - PCO2

Assume that an alveolus is ventilated w/ room air at sea level & gets venous blood w/ PVO2=43 & PVCO2=38? What values would paO2 & PaCO2 approach if ventilation but not blood flow were stopped?

V/Q is going to 0 so approaching venous if Q is stopped approach affinity

What is meant by vital capacity? Is vital capacity increased or decreased in restrictive disease? In obstructive disease?

VC= max expiration after max inspiration VC is decreased in BOTH restrictive & obstructive disease.

Normal value of CO2 production Normal value of O2 Consumption

VCO2--> 200 ml/min VO2----> 250 ml/min

Innervation of 4th & 6th pharyngeal arches

Vagus

What test is considered the "gold standard" for diagnosis of a DVT?

Venography (invasive)

Type of Resp Dyspnea that involves muscles of chest wall sensation of increased work of breathing

Ventilator Pump disorders that weaken muscle/change chest wall dynamics

Genital warts (from HPV) in children are most commonly....

Verruca vulgaris caused by HPV type 2 -if you see condylmona acuminatum in peds pop (HPV6 or 11) it is SEXUAL ABUSE UNTIL PROVEN OTHERWISE

Fick's Law

Vgas = A x D x (P1-P2) /T Determines rate of uptake of a gas across a membrane

Causes of COPD Exacerbation?

Viral 50% - Rhinovirus *Bacterial MCC*: S. Pneumo, H. Flu, Moraxalla Caterhallis (Same 3 mcc of Otitis Media)

Dx of influenza

Viral antigen detection tests- RIDT-point of care 30 min testing. --culture & isolate the virus

Virchow Triad of Venous Thromboembolism

Virchow's Triad a. Endothelial Cell Injury b. Venous Stasis c. Hypercoagulable State AT3 Deficiency, *Protein C & S Deficiency, Factor V Leiden*, Homocysteinemia, HIT, Prothrombin Gene Mutation

When is a transphenoidal resection required for a pit tumor (most are benign)?

Visual field defects (compression of optic chiasm) Growth of tumor (macroadenoma= >1cm) Non-functional adenomas can be observed

what happens to Vit D3 production during high cortisol times? what does this result in?

Vit D3 synthesis is dominantly suppressed leading to bone resorption versus the IL-1 suppression which promotes bone formation thus the net result is bone resoprtion osteoporosis

13. Aspergillosis Tx:

Voriconazole & Itraconazole IV

What type of vulvar SCC is MC associated w/HPV

Vulvar--> HPV-Non-keratinizing, basaloid, & warty (keratinizing is NON-HPV related)

Drug/latex allergy -Dx

Wait 1-3 weeks post-anaphylaxis before skin testing

Tumor with upper layer of cells called oncocytic?

Warthrin tumor Funfact: this is also the 2nd MC salivary gland tumor!

2nd MC salivary tumor

Warthrin tumor--think peter is my SO (#2 in the relationship)--he pronounces WAR incorrectly, men are also "warthless." --he loves teefers (oncocytic). --he plays both sides (BILATERAL)--acts differently around his parents --changes his motor oil -smokers 8X more likely

Diagnosing Diabetes Insipidus?

Water deprivation testing complete H2O restriction with hourly intervals of weight and labs for Na. DI dx confirmed with weight loss, increasing serum Na+/serum osmol/BUN, decreasing urine osmol -once confirmed give desmopressin If urine concentrates= central DI If urine doesn't concentrate=nephrogenic DI

Tx of Sleep Apnea

Weight loss & Exercise *Positive Airway Pressure (PAP)* CPAP - continuous PAP (MC) First Line Medication are *not* indicated as first line therapy

Family are confident patient can manage successfully at home.

What's an important factor in discharge criteria for patient with COPD exacerbations? TEST

When does a bronchi transition to a bronchiole?

When the DISCONTINUOUS CARTILAGINOUS plates of the BRONCHI disappear!

MC genitourinary CA in children

Wilms tumor

Is a neoplasm of 6cm more likely to develop "function"

Yes Benign adenomas are common 70% are non-functioning in pt w/o endo sx 25% lesions >6cm= adrenal cancer 20% can develop functional component

Patient has nodule that is 2cm. Do I do a biopsy? Patient has nodule that is 0.5 cm. Biopsy? What if the 0.5cm nodule is hot?

Yes (anything >1.5) No (<1cm =observe) No (don't biopsy hot nodules or those assoc w/hyperTH) If you can palpate it=biopsy it If it's firm/hard (R/o Reidel and Hashimoto)

Do you give statins to a patient with clinical ASCVD? What intensity level?

Yes, one of 4 statin benefit groups High

If I'm uncertain if my patient needs a statin will an ABI of 0.5, an- CRP of 3 mg/L and a CAC score of 400 agaston units help sway my decision?

Yes, the following might sway your choice to give statins --FHx of premature ASCVD --↑ lifetime risk of ASCVD --LDL-C >160 mg/dL --hs-CRP >2.0 mg/L --CAC score >300 Agaston units ABI <0.9

should you check for T2DM at 1st prenatal visit if they have risk factors? should you check for GDM at 24-28 weeks gestation (no diabetes prior)? should you use OGTT to check women w/GDM for persistent DM @ 6-12 postpartum?

Yes, yes and yes Also: women w/GDM hx should have lifelong screening every 3 yrs Women w/GDM and prediabetes should receive lifestyle intervention/metformin to prevent diabetes (A) !!

Do you give statins to a 50 yoa diabetic with an LDL-C of 160 mg/dl? What intensity level?

Yes: 1° Prevention if LDL is btwn 70-189 Moderate High if 10 year risk is >7.5%

what stimulates each adrenal cortex zone and to produce what that cause what?

ZG - AngII --> mineralcorticoids (aldosterone) - reabsorption of Na ZF - ACTH --> glucocorticoids (cortisol) - increase metabolism and depress immun/inflam response ZR - ACTH --> androgen,glucocorticoids

How do you calculate corrected Ca?

[(4-albumin) x 0.8] + serum calcium. Nml: 8.5-10.2. measure of ionized/free Ca

If PaO2=50mmHg & PaCO2=40mmHg calculate the concentrations of dissolved O2 & CO2 in arterial blood units of ml gas/100ml plasma. Use given solubility coeficients:

[gas]dissolved=solubility coefficient(a) x Pgas [O2]dissolved=0.003x50mmHg=0.15mlO2/dl blood [CO2]dissolved=0.075x40=3mlO2/dl blood

what doe the a, b, d, and f cells of the endocrine pancreas produce?

a = glucogon b = insulin d = somaDOstatin f = pancreatic polypeptides

How will each of the following affect PaO2 & arterial %SaO2, & O2 content of arterial blood (CaO2)? a)anemia b)polycythemia c)low PO2 in inspired air d) 2,3 BPG e) increased PaCO2 f) fever g) CO poisoning h) methehomoglobinemia

a) anemia: only change is O2 content will go down b) polycythemia: O2 content increases, nothing else changes c) low PO2: lowers all of them d) 2, 3 BPD-lowers all e) Increased PaCo2-lowers all f) Fever-lowers all g) CO poisoning-decrease all EXCEPT PaO2 is normal because the amount of CO is so small it does not alter amount of O2 dissolved in the plasma. h) Methohemoglobinemia--increase PaO2, increase total O2 content, (possibly low/normal O2 sat)

What transmural P difference = the recoil P of the lung? The chest wall? The whole respiratory system?

a) transpulmonary b) transthoracic c) transthoracic - transpulmonary= PA-Pbs

MCC of hypoparathyroidism

accidental parathyroidectomy

resistan action and source

acts mainly on the liver to oppose action of insulin and thus promote insulin resistance adipocytes

t(15;17) PML-RARA fusion gene

acute promyelocytic leukemia (APL) hematologic emergency tx w/ ATRA and chemo

high risk of DIC = hematologic emergency

acute promyelocytic leukemia (APL) tx w/ ATRA and chemo

two parts of the pituiary and what they correspond to

adenohypophysis (anterior lobe) neurohypophysis (posterior lobe)

what other axes feed into proper GH axis fnx?

adrenal gonad thyroid prolactin

what are the key findings of adrenal insufficiency?

adrenal atrophy hypoglycemia altered pigmentation (darker with 1* and paler with 2* due to ACTH low) hypotension

sx in Cushing's syndrome

adrenal hypertrophy hyperglycemia protein wasting altered pigmentation (dep. on ACTH-indep or dep) HTN regional obesity striae

Gold standard for localized testing of primary hyperaldosteronism?

adrenal venous sampling. evaluate both sides for hormone level, side with higher venous content likely has tumor. Done d/t high rate of adrenal incidentalomas on CT/MRI

flower cells

adult T-cell leukemia/lymphoma

(+) for HTLV-1

adult T-cell leukemia/lymphoma (presents almost like multiple myeloma, but also has rash and pt in question stem is from Japan or Caribbean)

what does the inferior hypophyseal a. contain?

after going through the pars nervosa it picks up ADH and oxytocin

what does pathologically high levels of cortisol inappropriately stimulate? what does this result in?

aldosterone receptors --> increase water retention (HTN)

CD30 (+) CD20, CD45 (-)

all types of Classical hodgkin lymphoma

Treatment of pheochromocytomas

alpha-blockers (phenoxybenzamine) DO NOT TREAT WITH B-BLOCKERS

Define the Chronic Care Model (CCM): What six aspects make up the Chronic Disease Model of Care?

an organizing framework for improving chronic illness care (and care in general) at both the individual and population level • Health System • Self-Management Support • Delivery System Design • Decision Support • Clinical Information Systems • *Community - Resources and Polices*

hallmark cell (horseshoe-shaped nuclei)

anaplastic large cell lymphoma, alk positive (ALK(+) ALCL)

t(2;5) fusion protein NPM-ALK

anaplastic large cell lymphoma, alk positive (ALK(+) ALCL)

what is a sx that is seen in both GH/IGF insuff. and excess?

anovulatory amenorrhea (insuff = low hormones; excess = receptor down reg?)

nuclear protein seen with RA seen in Lupus antibody is higher in African American and Chinese patients with SLE

anti-Sm (Anti-Smith antibody)

Define chronic disease:

any disease that does NOT get better, requires frequent follow up, medication adjustment, & change, and will be present for the remainder of the patient's life

At FRC which portion of the lungs is most inflated? During inspiration from FRC, which portion of the lung is best ventilated?

apex, the dependent portion of the lung is best ventilated

JAK2 mutations

associated w/ many things -polycythemia vera -essential thrombocytosis

What is the basal-bolus insulin concept?

attempts to imitate body's normal insulin release. can be used in both type I and 2 50% of insulin is basal (glargine-long acting) other 50% is bolus (short acting) given at mealtime 10-20% of total daily insulin is given at each meal. best if combined with carb counting

MCC of AI What is the treatment?

autoimmune adrenalitis= Addison Dz Hydrocortisone (glucocort) (always wean pt off steroids) **Acute?= Double dose Fludrocortisone (mineralcort) aldo replacement **Goal=high renin

In which part of the normal, upright lung is ventilation greatest? Blood flow greatest? VA/Q ratio greatest?

base, base, apex

Hemoglobin E mutation

beta 26 glutamate --> lysine low hgb b/c mutation activates cryptic splice site --> decreases synthesis Hemoglobin E--> think of COLTEEE-- he is a BETA male, he is no longer 26 (on his mom's insurace) but sure acts like it. He fell in love with Larissa's GLUTES, thinking they would get to MATE. Da bish be LY(s)INE doe cause she is CRYPTIC. She SPLICED his dumb little heart--> decreased synthesis. He was LOW HEME-ing fruit so she went for it (low Hgb) Maybe his next mail order bride with be from a TRIANGLE in SOUTHEAST ASIA.

what marker is used to determine bone formation (ARF)?

bone-sepcific alkaline phosphatase (BSAP)

what 2 components are required to get the maximum effect from insulin?

both gluco-incretins AND glucose this is seen in the diagram his said would be a QUESTION where IV admin of glucose does not produce as much insulin as intrajejeunal glucose as there are the gluco-incretins that are needed to get the large insulin effect

What is the most common malignancy caused by asbestos?

bronchogenic carcinoma • Worsens after exposure stops

Wegener granulomatosis

c-ANCA + PR3-ANCA

What test do you order for pheo Don't image early but if you do need to pick one what do you do? What meds for tx? *From review of cases

catecholamines metanephrines VMA Urine --needs to be VERY above normal --MRI --Phenoxybenzamine

what cells are found in the adrenal medulla?

chromaffin cells - neural crest cells that are modified postsynaptic neurons that lack axons - secrete catecholamines (E and NE) ganglion cells - modulate activity of chromaffin cells and innervate the blood vessels within the medula

how are the cells of the adenohypophysis organized?

clumps and cord around fenestrated capillaries

What is a T-score for osteoporosis measuring and what values are concerning?

compares bone density to *normal young adult with DXA* -1 - -2.5= osteopenia less than -2.5= osteoporosis

equation: *Henry's Law*

concentration of a dissolved gas is directly proportional to the partial pressure of that gas in the gas phase

under what conditions is *ambient temperature & pressure saturated (ATPS)* measured?

conditions: - room temperature - ambient pressure, corrected for room vapor pressure (PB - 47 mmHg) - saturated @ room temperature

under what conditions is *body temperature & pressure saturated (BTPS)* measured?

conditions: - temperature = 37 °C or 310 °K (body temperature) - ambient pressure, corrected for room vapor pressure (PB - 47 mmHg) - saturated with water vapor = 47 mmHg

under what conditions is *standard temperature & pressure dry (STPD)* measured?

conditions: - temperature = 0 °C or 273 °K - pressure = 760 mmHg - no water vapor

1st step in a complete medical eval at initial visit is:

confirm and classify diagnosis (ask patient why they're here) then Detect complications and potential comorbidities review prior treatment and risk factor control begin & develop care management & continuing care plan

describe the ductuli efferentes

connect rete testis to ductus epididymidis low pseudostrat columnar with ciliated and nonciliated cells --> saw tooth appearance

Lining of the respiratory bronchiles...describe them

contain CILIATED CUBOIDAL CELLS w/Large number of CLUB CELLS--> CLUB CELLS increase DISTALLY (obviously ciliated decrease) --Getting turnt in the BACK of the RB CLUB!--also getting CILLY @ the club CUBE

nutritional overload leads to increase # and size of adipocytes, what happens in the state of CONTINUED nutrtional overload?

continued preadipocyte recruitment leads to increas secretion of MO chemoattractants MO infiltrate to promote chronic infalamm in the adipose --> TNF-alpha secreted --> reduces insulin signaling, suppresses differentiation of peadipocytes, promotes leptin release, suppresses adiponectin release, inhibits muscle AMPK (will lead to steatosis eventually) TAG deposition is impaired and lipolyisis promoted --> elevates serum TAG and FFA all of this leads to onset of leptin resistance if not stopped

in older men, what can be found in the lumen of the tubuloalveolar glands of the prostate?

corpora amylacea

notable structure in the pineal gland

corpora arenacea (brain sand) which are aggregates of clacium phophate which also increase with age

what is the origin of the adrenal cortex vs medulla?

cortex = mesenchymal (mesodermal) medulla = neural crest cells (ectodermal)

what is the name for compact bone vs spongy? prominence of each? turnover?

cortical = compact (80%) slow turnover cancellous (trabecular) bone = spongy (20%) faster turnover

Pt's on metformin with T2D need to have what re-evaluated every year?

creatinine, urine albumin, potassium. GFR has to stay normal for pt's to continue on metformin. If pt's have decreasing GFR, refer to nephrologist and increase GFR screenings.

how does addison's and cushing's affect GH?

crosstalk leads to reduced GH and IGH in both excess and insufficient cortisol leading to SHORT STATURE in both cases

Nasal polyps in children?

cystic fibrosis until proven otherwise → chloride sweat test

describe compensatory hypothyroidism

damaged thyroid gland is able to meet needs for TH ONLY with excess stimulation of gland thus everything is normal EXCEPT high TSH

what hormones change in hypophosphatemia?

decrease PTH decrease FGF-23 increase vit D3 (via suppressed FGF-23) increase klotho protein NET: increase kidney reab + increase dietary absorption = increase P to normal overshoot of correction prevented by Klotho-FGF-FGFR complex

what hormone changes occur during hypercalcemia?

decreased PTH (Ca blocks Mg to suppressed) increased calcitonin (Ca mediated) subsequent decrease in Vit D3 NET: decrease Ca and P

Restrictive parameters: PFT

decreased TLC (scoliosis, neuromuscular stuff, MD) o Flow-volume loop is tall & peaked o *FEV1/FVC ratio is normal or increased * o FEV1 and FVC *< 80%* (opp of normal) but FEV1/FVC ratio >0.7 Decreased VC; decreased TLC, RV, FRC, no change or decrease (RV/TLC) proportionate

MCC of aortic stenosis in people >60

degenerative calcific aortic stenosis

*this will be a question* describe the dexamethasone supression test

dexamethasone mimics cortisol and acts as it in the regulatory loop give this for an overnight test and serum cortisol is measured afterward NORMAL = decreased cortisol (as dex. acts as neg feedback for axis) Cushing's (either ACTH dep or indep) = plasma cortisol is > or = 200nM (b/c normal regulation is not occuring)

this will be a question describe the dexamethasone supression test

dexamethasone mimics cortisol and acts as it in the regulatory loop give this for an overnight test and serum cortisol is measured afterward NORMAL = decreased cortisol (as dex. acts as neg feedback for axis) Cushing's (either ACTH dep or indep) = plasma cortisol is > or = 200nM (b/c normal regulation is not occuring)

what agents stimulate GHRH? what inhibit SST?

dopamine and galanin do both opioids, ach, arg do just inhibiting of SST

embryonic origin of neurohypophysis of pituitary

downgrowth of neuroectoderm of diencephalon (neural secretory tissue)

very SPECIFIC (95%) for SLE (-) does NOT R/O SLE Order when SLE suspected and ANA is (+) Reflects dx activity associated with nephritis

dsDNA

where do the spermatozoa pass when they become motile?

ductus epididymidis

What is the Bohr Effect? The Haldane Effect?

due to high PCO2 in the tissues O2 will dissociate (in tissues) Haldane: increased PO2 decreases the CO2 bound to your Hb (in lungs)

what is the capsule of the pituitary gland?

dura mater

When is Ca liberated during the bone turnover model?

during resorption in the dissolution stage

Key about Farmer's lung

dust from warm/humid/newly harvested hay --> rapid proliferation of spores of THERMOPHILIC ACTINOMYCETES

what is the key factor that influences hormoal response?

effective receptor occupancy -how many receptors are bound by hormone and for how long HIGHER effective receptor occupancy means GREATER hormone effect

What are 4 key outcomes of DSME (DM Mngmt Education)

effective self management ↑ clinical outcomes ↑ health status ↑ quality of life *should be patient centered, respectful, responsive

what is the terminal portion of the ductus deferens that travels through the prostate and cnx to the prostatic urethra?

ejaculatory duct

What 2 forces contribute to lung compliance & must be overcome to inflate a lung? For each force, name a common lung disorder in which it is altered?

elastic forces & surface tension elastic force: emphysema surface tension= IRDS

During forced expiration flow becomes limited. What 2 pressures add together to make alveolar P? What P determines pressures at the equal pressure point?

elastic recoil (transmural P) + pleural P= alveolar P -just pleural P determines P at = Pressure

what triggers aldosterone release? (3)

elevated EC K levels AngII pathologically high levels of ACTH

what are the origins of insulin resistance?

elevated TNF-alpha suppressed adiponectin elevated cytokines(SOCS-rich tissue is going to be insulin-resistant)

First step in the treatment algorithm for bronchiectasis? Tx M. kansasii-associated bronchiectasis?

empiric Abx (amoxicillin, TMP-SMX, levofloxacin) rifampin + isoniazid + ethambutol for 12 months

2 important fnx of testosterone?

enter seminiferous tubules to stimulate spermatogenesis enter capillaries to maintain male repro organs (like prostate)

How does TH affect growth?

essential for proper activity of growth hormone axis

how is estrogen related to the thyroid axis?

estrogen promotes axis activity (permissive) by: -increasing number of TRH receptors to enhances its effect -increase synthesis of thyroglobulin and TPO complex

what 2 hormone excesses leads to amenorrhea?

excess TH leads to overpro of SHBP leading to depressed free estrogen excess prolactin inhibits GnRH leading to decreased LH/FSH

how does a change in the thyroid axis affect menstruation?

excess TH overproduces steroid hormone binding globulin which then depresses estrogen levels --> presents as amenorrhea ALSO, excess TSH can cause oversecretion of prolactin which in turn inhibits GnRH leading to galactorrhea/amenorrhea syndrome

describe an endemic nontoxic goiter

excessive TSH stimulation under conditions of TH underproduction due to missing/inhibited component of production unrelated to hormones (e.g. iodine deficiency) (thyroglobuin is not inhibited just that final step to TH) thus gland hypertrophies

Grading system D

expert consensus or clinical experience

what is the action of FGF-23 (fibroblast growth factor #23)? where does it come from?

expressed mostly in bone and CT inhibits renal reabsorption of phosphate in kidney (prox tubule mostly)

the connective tissue of teh lamina propria contains (nares)

extensive venous plexus --> INFERIOR & MEDIAL nasal CONCHAE (prediction) warm the air up --swelling of these during hayfever

3 important fx of pulmonary circulation besides gas exchange?

filter, blood reservoir for L ventricle, ACE, supply nutrients to the lung itself, fluid exchange

Why do we have patients perform self-monitoring of their blood glucose thru fingerstick testing?

fingerstick values are not used for dx purposes but important for medication dosing, especially insulin dosing. -nml daytime readings with high fasting glucose: give galrgine -nml fasting glucose with high A1c and high mealtime readings: give meal-time insulin

Important step before performing adrenal gland biopsy?

first exclude pheochromocytoma. DONT STICK A NEEDLE IN A PHEO

What would a flow volume loop look like with vocal cord dysfunction?

flattened inspiratory portion Extrathoracic obstruction

Treatment of SIADH?

fluid restriction to normalize intravascular fluid volumes

describe the cells of the thryoid...origin of these cells? Origin of follicular cells?

follicular cells - synthesize TH (T3 and T4)---Endoderm parafollicular cells - synthesize calcitonin--neural crest cells

"buttock cells" - indented nuclei

follicular lymphoma

t(14;18) BCL2 w/ immunoglobulin heavy chain

follicular lymphoma

Anion gap equation Causes of ANION GAP

gap = Na+ - (Cl- + HCO3)--> normal is 12 (3x normal albumin) MUDPALES Methanol, Uremia, DKA, Paraldehyde, Alcoholic Ketoacidosis, Lactic acidosis, Ethylene glycol, Salicylates

Positive Test for PPD ALWAYS do what next step?

get a *CXR/CT* • Tb is AEROBIC, more likely to be in the *apex* of the lungs

what is the only known natural ligand for GH secretogogue receptor (GHS-R)? what does this do?

ghrelin -stim GH secretion (also increases appetite)

How might hypoxemia due to a true shunt be distinguished clinically from that due to non-uniform VA/Q ratios?

give them O2

what is the name for the mucous secreting glands in the spongy urethra of the penis?

glands of Littre

what hormones prevent hypoglycemia?

glucagon Epi GH cortisol

what hormones promote TAG breakdown?

glucagon epi ne

what happens in long term fasting?

glucagon predominatees Arg and lys --> GH release --GH inhibits proteolysis (mostly in muscles) BBB becomes leaky and the brain begins to use ketones/FA though still uses glucose most

what happens in short term fasting?

glucagon predominates -promotes mobilization of foodstuffs: gluconeogenesis -inhibits storage pathways the body spares glucose by inhibiting glycolysis and reducing demand for glucose by the tissues (this is RANDLE effect)

what nutritional status inhibits GH? which stim?

glucose and FA decrease a.a. increase, esp arginine