Uworld

Cardiac impulses conduction pathway

AV note to common bundle, then bundle branches..... then Purkinje, then the ventricle myocardium Purkinje system is fastest, AV node is the SLOWEST. Atrial system is higher then ventricle system. Purkinje>atria>ventricle>AV node

carboxyl tails to plasma membrane

Accomplished by palmitoylation, which increases protein hydrophobicity by anchorin receptor carboxyl tails to plasma membrane.

fourth heart sound

A low frequency, late diastolic atrial gollop sound that occurs *BEFORE S1* AFTER the onset of P wave (coincides with ventricular filling). (de-Lub-dub!!!) Sign of *diastolic dysfunction*. It occurs when there is a *rise in end-diastolic ventricular pressure* caused by *atrial contraction against a STIFFENED LEFT VENTRICLE*. (so it occurs IMMEDIATELY after atrial contraction) Best heard with bell over cardiac apex with patient in left lateral position. Occurs in conditions such as: Ventricular hypertrophy, acute MI, long standing HTN, aortic stenosis,

Scopolamine

A muscarinic antagonist. • Treats motion sickness. Might be able to inhibit other cholinergic effects like diarrhea, cramping, sweating, nauaea. • Causes mydriasis and cycloplegia. Can also cross blood brain barrier and result in CNS manifestations of anticholinergic toxidrome. Also causes dry mouth, palpitations, urinary retention.

Kussmaul's sign

Paradoxical increase in JVP with inspiration. Found in chromic constrctive pericarditis, and other heart problems.

anabolic steroids and acne

Test to DHT promotes both: 1) Follicular epidermal hyperproliferation 2) excessive sebum production

What 2 ways can intracerebral neoplasms raise ICP?

1) Obstruction of normal CSF flow - 2) disruption of blood brain barrier causing increased permeability and blood vessel leak into the interstitium. (called Vasogenic edema!!)

valproic acid

Used as anticonvulsant AND a mood stabilizer!!! Used in Mania!!! It blocks voltage gated sodium channels, and enhances GABA. Used mostly for myoclonic seizures, and tonic-clonic seizures!!!! Valproate increases the risk of neural tube defects!!!!!!!!!!!

bile salt function

emulsifying fats for digestion Destroy gram negative bacteria by disrupting bacterial outer membranes. Cholestasis permits bacterial overgrowth.

cavernous sinus

structures that pass through it include: -internal carotid artery - CN's III, IV, V1/V2, VI... so infection is a risk to all of these.

oculomotor nerve lesion and vision (CN III)

"Out and down" eye .....due to the unopposed actions of the superior oblique and lateral rectus muscles.) Mydriasis (fixed-dilated pupil)- Enlarged pupil, nonreactive pupil (blurry vision) ptosis (CN III also innervates the levator palpebrae superioris, which serves to elevate the upper eyelid. A lesion would thus result in ptosis (droopy upper eyelid) Vertical AND horizontal diplopia Blurry vision- *lack of accommodation*. # what is the feared cause of CN III palsy ? • Uncal (transtentorial) herniation • Aneurysms of the posterior communicating artery!!!

If a screening test is positive in 250 of 1000 affected patients..... and positive in 100 of 1000 healthy controls. .....How many false positives would be expected in a population of 100,000, with disease prevalence of 10%??

+ - + 250 100 - 750 900 Sensitivity= 250/1000= 0.25 Specificity= 900/1000= 0.9 Disease prevalence= 10% , this means that 10,000 people have the disease 90,000 do NOT have disease Sensitivity = 25%, so 25% will be diagnosed correctly..... so TP = 250 Specifity= 90%... so there are 90,000 x 0.9 TN's = 81,000 + - + 250 - 81,000 Next, fill in the rest. + - + 2,500 9,000 - 7,500 81,000

fluid compartments

60-40-20 rule 60% of body is water. 2/3 of that (40% total body) is intracellular 1/3 of that (20% total body) is extracellular ECF is further divided into: ¾ of the 20% is interstitial ¼ of the 20% is plasma

transcription factors

All nucleated cells in the body possess the entire genome. Transcription factors specific for each individual tissue allow only those genes relevant to a cell's specific type and function to be expressed. Transcription factors dictate differentiation.

staph vs strep

All staph are gram positive cocci that form clusters. Staph are catalase positive!!! Strep are catalase negative !!! Coagulase positive staph= staph aures Coagulase negative staph= the other kinds of staph

Primidone

An anti-epileptic that is metabolized to* phenobarbital* and phenyl-ethy-lmalonamide (PEMA). It is first line (or propranolol) for *BENIGN essential tremor*!!!!!

# what drugs cause Torsades de pointes

Anti arhythmics, phenothiazides, and TCA's. Sotalol

superior orbital fissue

Area where all of the following enter the orbit CN III CN IV V1 CN VI

Carbamazepine sides

BONE MARROW suppression (leading to anemia, agranulocytosis, thrombocytopenia) - it is HEPATOTOXIC - can cause SIADH

complete central vs partial central diabetes insipidus

Complete central diabetes insipidus increases urine osmolality over 50% in response to administration of desmopressim. Partial only increases it around 10%. This is because in partial central, there is some vasopressin already present.

stroke volume depends on

Contractibility Preload (linear relationship)... Preload approximated by ventricular EDV Afterload (opposite) ... approximated by MAP and arteriole resistance

cardiac output

Either HR X stroke volume OR O2 consumption/ arteriovenous O2 difference

club aka clara cells

Found in the ciliated epithelium, may secrete GAGs. Degrade toxins via cytochrome P450 pathway. Act as stem cells as well. Secrete club cell secretory protein - a surfactant-like molecule.

cough syncope

Generally occurs in overweight patients with COPD. Increased intrathoracic pressure during coughing decreases venous return to the heart, thus decreasing CO and cerebral perfusion. (basically the same as Valsalva)

# dress syndrome

Reaction to drugs, typically 2-8 weeks after starting anticonvulsants (phenytonin, carbamazepine!!!), allopurinol, or antibiotics. Patients develop: - fever - generalized lymphadenopathy - facial edema - diffuse skin rash!!! (eosinophilia!!)

treat nephrogenic diabetes insipidus

Treatment involves adequate hydration, hydrochlorothiazide (thiazide diuretic), indomethacin, or Amiloride (potassium sparing diuretic). Treat with hydrochlorothiazide (paradoxical, but it increases renal Na excretion, → ECF volume contraction → This decreased volume will decrease GFR, and increase proximal tubular reabsorption of water and Na. Therefore, ultimately less water and Na are lost as urine.

osteoclast activity markers !!)

Urinary deoxypyridinoline is the most reliable. It is released into circulation when bone is absorbed by osteoclasts.

third heart sound (S3)

Ventricular gallop which occurs AFTER S2. (Lub-dub-by!!) Heard because of *rapid filling of ventricles in diastole*. It is commonly associated with *increased left ventricular end-systolic volume* because of *left ventricular systolic failure* !!!!! Can be heard by listening at the END of expiration and lieing in the left lateral postion, with the BELL over the apex!!!

# fetal erythropoiesis location

Yolk sac (3-8 weeks) During yolk sac fetal hematopoiesis, the hemoglobin formed is embryonic hemoglobin, subunits ζ2ε2. Liver ( 6 weeks-birth) Spleen (10-28 weeks) Bone Marrow (18 weeks - adult)

# what muscles attach to lateral clavicle??

deltoid, traps Deltoid pulls the lateral clavicle inferiolaterally Traps pull the lateral clavicle superiomedially Clavical fracture tends for the distal fragment to be pulled inferiolateral by deltoid. The "medial" aspect of the clavicle in a fracture is pulled UPWARD by the sternocleidomastoid !!! (SCM)

Roc curve

plots true positive rate (sensitivity) against the false positive rate (1-specificity) for different cutoffs of a diagnostic test

anaesthetics general side effects on the body

1. Increase cerebral blood flow and ICP (decrease vascular resistance) 2. ALL are respiratory depressant 3. Decrease GFR and RPF 4. Decrease hepatic flow 5. Decrease cardiac output

paclitaxel coating in stents

2 complications of stents: - acute silent thrombosis - Restenosis due to intimal hyperplasia paclitaxel is a antineoplasmic agent that binds b-tubulin and PREVENTS microtubule breakdown... thus, the cell cycle is arrested in the M-phase, and intimal hyperplasia cannot occur.

Ethosuxamide

Blocks T-type calcium channels which trigger/sustain rhythmical burst in thalamic neurons! it is used for ABSENCE seizures!!!!!!!

Mean arterial pressure

CO X TPR MAP= 2/3 diastolic pressure + 1/3 systolic pressure

hemorrhagic cystitis

Common effect of cyclophosphamide and ifosfamide use, because a metabolite of those called *acrolein* irritates the bladder mucosa and causes hematuria, dysuria, urinary frequency/urgency. Acrolein is the cyclophosphamide metabolite responsible for hemorrhagic cystitis Prevention can be accomplished via co-administration of MESNA (sodium-2-mercaptoethane sulfonate), which binds to and inactivates acrolein. !!!!!!!

cortisol and catecholamine effects

Cortisol itself does NOT affect vascular reactivity, however, it DOES augment the vasoconstrictive effects of catecholamines. This is an example of a *permissive* effect, because cortisol itself does NOT have any effect on vascular reactivity.

CN III palsy and light reflex in diabetes

Diabetic mononeuropathy often involves cranial nerve III, BUT, it *spares* peripheral parasympathetic fibers, so it does NOT impair light reflex OR accommodation. Note: *medical causes* (diabetes)often SPARE the pupil... while surgical causes usually *involve the pupil early*.

anaesthetic arteriovenous concentration gradient (!!)

Difference between concentration of a gas anesthetic in arterial and venous blood. It is a measure of SOLUBILITY. If tissue solubility of drug is high, a large amount is taken up from arterial blood (low venous concentration)... this means it has a slower onset of action because *a lot of it is absorbed by peripheral tissues*, and *slower equilibrium with the brain*. Anaesthetics with low peripheral tissue solubility have smaller arteriovenous gradients, and thus they act faster because there is *less peripheral tissue update*..... so here, *concentrations in the brain are reached faster*.

# Staph aures food poisoning

Due to ingestion of preformed *enterotoxins* from staph aures, which makes it very rapid onset (2-6 hours). Foods classically associated with S. aureus enterotoxin-mediated food poisoning: - mayonnaise-containing foods (especially salads—potato salad, macaroni salad, tuna salad) !!!! - meat - poultry - milk/egg/dairy products - cream-filled pastries (eg, custards)

insulin resistance indication

Elevated BASELINE insulin during fasting is highly suggest insulin resistance. insulin resistance may occur due to: high FFA's and TAG's. Serine and threonine residue phosphorylation by serine kinases !! (note: TNF-a, catecholamines, glucocorticoids and glucagon increase insulin resistance this way!!!)

why do prolactin levels rise with pregnancy, but pregnant women do not lactate?

Estrogen and progesterone prevent prolactin from causing lactogenesis. Once they drop with birth, lactation begins

abducens nerve palsy ( CN VI)

Eye is deviated *medially* Palsy here causes HORIZONTAL diplopia

# drug bioavailability

Fraction of drug administered that reaches circulation unchanged. Oral bioavailability is *area under the oral curve* divided by *area under the IV curve*... so it is ALWAYS less than 1 !!!

fetal circulation

From the placenta, it uses the *left umbilical vein* and then goes through the *ductus venosus* to avoid hitting the liver, and then into the IVC, and then the heart. From the *IVC*, most of the blood is diverted from the right atria to the left atria through the *foramen ovale*, where it then circulates out of the aorta and into systemic circumation. Blood that escapes the *foramen ovale* and ends up in the right ventricle, is then diverted from the *pulmonary artery* to the *DESCENDING aorta* through the *ductus arteriosum*.

sweating

Function of the cholinergic postganglionic neurons of SNS *thoracic sympathetic trunk*. SNS postganglionic nerve innervate: - eccrine glands - apocrine glands. Eccrine glands is responsible for hyperhidrosis. The postganglionic sympathetic neurons that synapse on eccrine glands are cholingergic!! Eccrine (sweat) glands contain a secretory coil and a straight duct. • Eccrine glands are composed of three cell types: • Clear cells • Dark cells • Myoepithelial cells • Autonomic stimulation via acetylcholine (ACh) stimulates the eccrine glands to form an isotonic solution in the gland lumen. • Due to the active resorption of electrolytes by the sweat gland, sweat secreted by eccrine glands is a hypotonic solution. • Eccrine glands also excrete heavy metals, drugs, and organic molecul Apocrine sweat glands are glands that secrete a milky viscous fluid into the hair follicle, rather than directly to the surface of skin !!! Apocrine sweat glands are inactive until puberty !!!! • Apocrine sweat glands are found in or around the: o Axillae o Areola o Perianal region o External genitalia • Apocrine sweat is initially odorless, and starts to sting with breakdown by bacteria (!!!!)

Staph aures microbio

Gram +, cocci in clusters, catalase +, coagulase +, β-hemolytic, forms yellow/golden colonies (aurei="golden"). Produces Protein A which binds to Fc portion of IgG activating complement!!!

migratory thrombophlebitis , aka Trousseau syndrome!!!

Ie, phlebitis in ams AND legs. Should ALWAYS make you think of "cancer". Hypercoagulability is a very common paraneoplastic syndrome seen most commonly in *adenocarcinomas* of the pancreas, colon or lung. Hypercoagulability occurs because adenocarcinomas produce a *thromboplastin-like substance* that is capable of causing chronic intravascular coagulations which are disseminated and migrate.

Nephrogenic diabetes insipidius

Impaired renal response to ADH due to inherited mutations in the V2 receptor, or secondary to - drugs (lithium)!! • demeclocycline, • hypercalcemia or • sickle cell disease. - amyloidosis In nephrogenic diabetes insipidus, hyperosmolality and hypernatremia occur despite a high plasma concentration of ADH. Similar to central diabetes Insipidus, but does NOT respond to desmopressin !!!! (b/c kidney cannot respond) to it.

# cholinergic agonists!!!

Increase GI motility (nausea, vomiting, abdominal craps and diarrhea). Decrease HR, cause bradycardia, hypotension. increase sweating, salivation, lacrimation.

Carbamazepine

It is a *voltage gated sodium* channel antagonist. Used for Simple partial seizures, complex partial seizures, trigeminal neuralgia!!!!!!!!

# pulmonary capillary wedge pressure

It measures left atrial end diastolic pressure (LA-EDP) !! Normally, the LA-EDP is nearly equal to the LV-EDP (both less than 12!!!) *Mitral stenosis* elevates both LA-EDP, and thus, PCWP.... While LV-EDP is unaffected. This implies there is a resistance to flow between the left atrium, and left ventricle (ie, mitral stenosis).

Posterior inferior cerebellar artery stroke

Leads to WALLENBERG syndrome. contralateral loss of pain, temp ipsilateral deficits of CN V, VIII, IX, X, XI... and Horner's syndrome.

Minimal alveolar concentration

Measure of the POTENCY. It refers to the *concentration of anesthetic in the alveoli that renders 50% of the patients unresponsibe to painful stimuli*. MAC and potency are INVERSELY related!!! (higher MAC, lower potency)!!!! Is does not depend on the type of surgery, sex, weight, height, etc....

what is the most common enzyme deficiency in beta oxidation ??

Medium chain acyl CoA dehydrogenase deficiency. (note, could also be short and long chain Acyl CoA dehydrogenase). Shows hypoglycemia after prolonged fasting with LOW ketones.

phenytonin

Metabolized by CYP450 !!! (it is an ACTIVATOR) Anti-convulsant used in grand mal (tonic clonic) seizures, SECOND LINE for status epilepticus (after benzos!!!!) . It BLOCKS voltage gated sodium channels in cortical neurons, and increases the refractory period. It *affects the CNS* and can cause ataxia and nystagmus. Main side effect is *gingival hyperplasia* after 3-4 months, due to increased expression of PDGF. Also: corse facial features.

muscarinic agonist actions

Muscarinic receptors are located on the ENDOTHELIAL surface, and binding of cholinomimetric agents promotes release of NO and *endothelium-derived relaxing factor*. NO then activates guanylate cyclase which increases cGMP, and cGMP then causes *calcium efflux* from the cells, which relaxes ENDOTHELIAL smooth muscle.

if in a disease of breast cancer mutations, of those with the mutations, 30 get the disease and 65 do not...... and in those WITHOUT the mutations, 20 get the disease and 75 do not..... what is the relative risk of the mutation???

Mutation: 30/ 30+65 = 30/95 = 0.32 No- mute: 20/ 20+75= 20/95 = 0.21 Relative risk = 0.32/ 0.21 = 1.5

injury and hepatic acute phase reactants and ESR

Neutrophils and macrophages release TNF-a, IL-1, IL-6 (!!!) They stimulate hepatic reactants: fibrinogen, ferritin, CRP, amyloid, complement. Fibrinogen coats erythrocytes to form *rouleau stacks* that sediment faster than individual erythrocytes... this is ESR !!! Negative consequences to the production (or downregulation) of acute phase reactants include: • Fever • Anemia of chronic disease • Behavioral changes (anorexia, somnolence, lethargy) • Muscle wasting • Cachexia Acute phase reactants that are downregulated during periods of inflammation include: • Albumin • Transferrin Downregulation of albumin production conserves amino acids for positively upregulated acute phase reactants. • Transferrin is a protein that is internalized by macrophages in order to sequester iron. This inhibits microbial iron scavenging.

PE

PE is often silent!! (b/c lung has dual blood supply, pulmonary artery and bronchial artery... also because most emboli are small, and they usually self resolve) most common source is DVT of femoral, iliac, or popliteal veins. PE causes VQ mismatch by affecting PERFUSION!!!!

cervical sympathetic ganglion

Provides sympathetic innervation to tarsal muscle, lacrimal gland, salivary glands, radial muscles of eye

alkaline phosphatase kinds

Released by osteoblasts and liver mostly. Also placenta and intestine. Bone alkaline phosphatase is easy denatured by heat (bone=boil), while liver is NOT.

staph epidermis

S. epidermidis, which is novobiocin sensitive. Contrast this with S. saprophyticus is novobiocin resistant. S. epidermidis is capable of generating a sticky, protective biofilm, facilitating colonization and infection of prosthetic devices including prosthetic heart valves and indwelling urinary catheters. Prosthetic valve endocarditis during the initial year after surgery is almost exclusively caused by S. epidermidis.

general anaesthetic liver complications (!!!)

Sometimes, inhaled halogenated anaesthetics (halothane, enflueane) can cause severe liver damage and *fulmanent hepatic failue* as it is metabolized there. Causes massive hepatic necrosis, liver tenderness, increased ALT, AST, bilirubin. !! There is a PROLONGED PT !!! NOTE: Most of the S:Sx of liver failure (decreased albumin, ascites, palmar erythema, gyno) are due to CHRONIC liver failure!! They are NOT seen in acute!

serotonin syndrome drugs

St John's Wort (Sinners and Saints!) SELlective Serotonin Reuptake Inhibitors Dextromethorphan TCAs MAO inhibitors MEperidine TRIPtans (anti-migrane medications) ONdansetron (anti-epetic) TRAMadol (analgesic) LINEzolid (antibiotic)

restless leg syndrome

Strange sensation in legs and uncontrollable urge to move them. Associated with inactivity and relieved by movement. restless leg syndrome occurs in: Middle/older age patients. Iron deficiency Chronic kidney disease Diabetes (esp neuropathy) # treat restless legs Avoid aggravating factors (ie alcohol, sleep deprivation) Supportive measures (exercise, leg massage, heating pads) Dopamine agonists (!!)

IVC obstruction

Suspect in any patient with new, unexplained and severe lower extremity edema in the absence of an explanation for it (RHF, severe hepatic cirrhosis, nephrotic syndrome). Can occur with renal tumor !!

systemic mastocytosis

Systemic mastocytosis, often termed systemic mast cell disease (SMCD), is a myeloproliferative neoplasm characterized by infiltration of clonally derived mast cells in different tissues, including bone marrow (see the image below), skin, the gastrointestinal tract, the liver, and the spleen. The mast cells secrete excess histamine. Histamine in turn, causes gastric hypersecretion. Because gastric acid secretion increases, *this inactivates pancreatic and intestinal enzymes, causing diarrhea. * Often also presents with histamine mediated symptoms: syncope flushing hypotension, tcycardia Skin manifestations (pruitis, urticarial)

# essential tremor

The MOST commonly diagnosed movement disorder. It is often AD inherited. It WORSENS when a posture is being maintained, ie, holding a cup of tea. Symptoms actually improve with alcohol.

infant first breath

The foramen ovale closes as the result of: • Decreased pulmonary vasculature resistance following neonatal breathing, leading to an increase in left atrial pressure compared to the right. • Reduced blood flow and pressure in the right atrium following placental circulation occlusion. 2. The ductus arteriosus closure is mediated by elevated oxygen levels and decreased prostaglandins. 3. Ductus venosus closes within a week. Note, The foramen ovale is actually patent in 20-30% of adults.!!!!

Respiratory cell histology layers

Trachea to a main bronchus, then segmental bronchus, then terminal bronchiole, then respiratory bronchiole, then alveoli. Ciliated cells go all the way down to the terminal portion of the respiratory bronchioles!!! (not in alveoli themselves).... Anything below this relies on *alveolar macrophages*. Goblet cells go down as far as the segmental bronchus, they are NOT found in the terminal bronchioles or below. The epithelium is initially pseudostratified ciliated columnar epithelium ..... but by the terminal bronchioles, it is ciliated simple cuboidal.

coronary steal syndrome

What happens is that in coronary artery disease, collateral vesicles are formed which allow coronary blood flow to occluded areas. But, with a drug such as *dipyridamole* and *adenosine* which are *coronary vasodilators*, decrease flow through the collateral areas, because the ischemic areas are already maximally dilated. So there is LESS blood to ischemic areas, more blood to normal areas.

PE and DVT and blood gasses

With risk factors for DVT like prolonged immobility and advancing age, a PE is suspected with things like swollen calf, acute dyspnea. PE causes hypoxemia secondary to a VENTILATION PERFUSION (V/Q) mismatch (redistribution of pulmonary flow). *Hypoxemia* leads to *hyperventilation* and *respiratory ALKALOSIS*!!!! PaO2 will be low PaCO2 will be low (hyperventilation) pH will be high (respiratory alkalosis from hyperventilation)

# torsades de pointes

an ECG finding during arrhythmia, where there are prolonged QRS complezes that change in amplitude and cycle length during the attacks. It is ALWAYS associated with a prolonged QT interval (due to *decreased K+ efflux!!) which predisposes to torsades de pointes. Thus, treat with magnesium sulfate!!!!

function of type II pneumocytes

cuboidal and clustered. 2 important functions: 1) regeneration of alveolar lining after injury, and can regenerate themselves and also type I pneumocytes 2) surfactant production

cheyne-stokes breathing

cyclic breathing in which apnea is followed by gradually increasing tidal volumes, then gradually decreasing tidal volumes commonly seen in cardiac disease (congestive heart failure) and neurological disease (stroke, injury, tumors). It indicates a poor prognosis. During start of apnea, PaCO2 levels at lowest (suppressing respiration)... then because of apnea they tend to rise. However, slowed respiratory feedback delays the respiratory response, and PaCO2 rises higher than it should. Basically a period of apnea, followed by hyperventilation (occurs when PaCO2 at highest)

phenytonin teratogen

digital hypoplasia and cleft lip/palate

homeobox HOX genes

highly conserved genes found in animals, fungi, plants. They modulate *transcription regulators* which control the expression of other genes in the cell. They guide development from earliest stages of embryogenesis to the final differentiation of cells. HoxA-13 is mutated in hand foot genital syndrome clinodactyly, shortened thumbs, small feet, short toes genito-urinary abnormalities.

Physical exam findings associated with constrictive pericarditis

include elevated jugular venous pressure, which is almost a universal finding. Kussmaul sign, the paradoxical rise in jugular venous pressure (JVP) on inspiration, is another common, but nonspecific finding. • The most common worldwide cause of constrictive pericarditis is tuberculosis. The majority of cases in the US are idiopathic or due to scarring from previous open heart surgery. • Classic image findings associated with constrictive pericarditis include dystrophic calcification on chest x ray in the parietal pericardium.

# Bethanechol !!!!

is a direct cholinergic agonist that stimulates both M2 and M3 receptors. It especially favors M3 activation. • Bethanechol has the following physiologic effects. o Through stimulation of the M3 receptor, bladder detrusor contraction increases with concurrent bladder sphincter relaxation, which promotes urination. o Gut motility also increases as a result of M3 activation. • Bethanechol is usually used to treat postoperative/neurogenic ileus and *bladder atony (urinary retention). * Bethanechol has the following side effects. • Bradycardia • Hypotension • Sweating/flushing • Salivation • Diarrhea • However, there are no effects on the CNS as bethanechol cannot cross the blood-brain-barrier.

Pericarditis

is inflammation of any of the layers of the pericardium. It often presents with the presence of fluid in the pericardial space. The fluid can be composed of blood, serous fluid, or transudate. Severe and constant middle/left chest pain that radiates to neck/shoulders. Pain increases on inspiration, relieved by sitting up and leaning forward. !!!!!! Physical symptoms of acute pericarditis include a friction rub on auscultation!!! This can best be auscultated with the diaphragm of the stethoscope over the left lower sternal edge or apex during end expiration with the patient sitting up and leaning forward . It may be accompanied by dyspnea/tachypnea in patients with sizable effusions. The pericardial friction rub can be distinguished from a pleural friction rub in that it does not disappear when the patient holds their breath. Pericarditis is worsened by swallowing!!!! Rember, there is a major link with it and SLE!!!!!!

Serotonin Syndrome

occurs when SSRIs are co-administered with any drug that can increase serotonin levels (e.g. MAOIs, meperidine, stimulants) • Serotonin Syndrome consists of the following triad: 1. Cognitive effects - mental confusion, agitation - hypomania, hallucinations, headache, coma 2. Autonomic effects - shivering, sweating - hyperthermia, hypertension, tachycardia - dilated pupils 3. Somatic effects - myoclonus !!! - hyperreflexia - tremor

# RAS gene mutation

point mutation commonly mutated in MANY cancers. Seen in many carcinomas, lung, colon, pancreas, leukemias ras normally associated with GDP where is is inactive).... but is active when associated with GTP!! Activated Ras then activates MAPk. There is a protein called GAP (GTPase associated protein), this helps ras cleave GTP and turn it off.... GAP mutation causes excess ras cell signalling

paroxysmal supraventricular tachycardia (PSVT)

rapid palpitations due to stimulation of atria/AV node. Treat with ADENOSINE to very rapidly slow conduction through the AV node. Side effects of adenosine: - flushing chest burning AV block

Trochlear nerve palsy (CN IV)

results in the eye being pointed superomedially (up and in) Associated with VERTICAL diplopia (happens when eye looks down at nose, ie, walking down stairs, reading a paper)!!! Compensatory head tilting to the opposite shoulder (Bielschowsky sign) is common for these lesions. Most palsies here are idiopathic OR traumatic.

# *paradoxical embolus*

where an embolus that originates on the right side and would normally lodge in pulmonary vasculature, instead it goes a intracardiac or intrapulmonary shunt (patent foramen ovale, ASD, VSD, pulmonary malformation). It occurs commonly when cerebrovascular events (ie stroke, TIA) occur in setting of known thromboembolic disease.!!!

Status epilepticus

• Life threatening, persistent seizure activity in the brain • Treatment: First line anti-seizure drugs are benzodiazepines, such as diazepam. First line drug for prophylaxis is phenytoin to increase seizure threshold

staph aures causes

• S. aureus is the most common cause of: • Hospital-acquired bacterial pneumonia • Ventilator-associated bacterial pneumonia (Pseudomonas aeruginosa is the 2nd most common cause) • Cellulitis • Osteomyelitis • Impetigo • Acute infective endocarditis POSE w/ your staff Pneumonia (bacterial in hospital) Osteomyelitis Skin -impetigo (bullous) cellulitis Endocarditis -acute infective

staph saprophyticus

• S. saprophyticus is novobiocin resistant. Contrast this with S. epidermidis, which is novobiocin sensitive. • S. saprophyticus causes urinary tract infections and cystitis. S. saprophyticus infections spread via bodily fluids and often occurs in sexually active young women. S. saprophyticus is nitrate reductase negative, so a dipstick test will produce a false-negative result.