immunodeficiency and vasculitis level one

sulfonyureas are special because they are the only drugs that can

cause increased c peptide of all the type two diabetes drugs it is the largest risk of causing HYPOGLYCEMIA

thromboangitis obliterates

distal digital thrombosis in men 30-50 associated with smoking

DDP4 inhibitors

glipping Da PP DDP4 is inhibited from breaking down glucagon

what does glucagon do ?

glycogenolysis in muscles and liver and in FAT it does fat break down and ketone synthesis

proteus mirabilis

gram negative swarming motility when plated may form stag horn calculi and struvite calculi UREASE positive helps it form stag horn calculi fishy odor give sulfonamide

testricular torsion

spermatic cord twisting decreased blood flow on doppler *cremater reflex is absent* *high riding testes*

epididmitis

testicular pain + cremaster +prehn sign..relief with testes

what is the short acting insulin?

regular insulin 3 hours

large vessel vasculitis

'GIANT SAMURAI'

vasculitis disease (small)

*small German men who cry-* all the vasculitis here are german

vibrio cholera

ALL VIBRIO comma shaped bacteria, gram negative grows on alkaline, acid labile, oxidase positive vibrio cholera: causes watery diarrhea choler toxin increases cAMP by binding to and constitutively activating the Gs pathway TX: supportive vibrio vulnificas and parahemolyticus: contaminates oysters

alpha glycosides inhibitors is

Acarbose SE: is diarrhea GI upset flatulence alpha glucosidase inhibition causes glucose absorption decrease

leukocyte adhesion deficiency

CD 18- responsible for adhesion and chemotaxis CD 18 will be missing elevated neutrophil count but signs of acute infection because the CD18 knocked out L A D late separation of the umbilical cord A: absent pus D: dysfunctional neutrophils

Chronic granulomatous disease pneumonic

CGD catalase granuloma disease aka chronic granulomatous disease

anti centromere antibody is associated with ?

CREST syndrome *use CREST tooth paste to clean *central teeth*

e. coli Etech

ETECH: travelers diarrhea via water sources esp in mexico heat LABILE toxin which increased cAMP (el Agua) and a heat stable toxin cGMP (San Gabriel) WATERY DIARRHEA NOT bloody

GLP1 is

EXANTIDE an GLUCAGON LIKE Protein incretin that binds in the pancreas the pancreas thinks this is glucagon the pancreas COUNTERACTS this but realizing the opposing factor INSULIN (pancreas thinks there is a lot of glucose because there is a lot of glucagon that goes in and stimulates all the glycogenolysis etc) Goey like pod tide pod exnatide

antibody associated with drug induced: SLE

anti histone his-stoned- on drugs

Pseudomonas

Gram negative ROD, OBLIGATE AEROBE thrives in water hot tub folliculitis oxidase positive and catalase positive (CGD patients as risk) produces blue green pigment (pyoverdin and cydanin) fruity odor toxin: exotoxin A- riboslyates elongation factor 2 causing inhibition of protein synthesis and cell death (JUST THE DIPHTHERIA) ECTHYMA GANGRENOSUM: black necrotic lesions on skin OTITIS EXTERNA (CGD patients as risk) #1 cause of gram negative nosocomial pneumonia and respiratory failure in CF patients can cause osteomyelitis in diabetes and IV drug users and indwelling catheters

INSULIN timing pneumonic

I-n-s-u-lin I- immediate 1 hour s- short 3 hours u-U remember intermediate right? - 5 hours lin- Long insulin - 24 hours

all the sulfonylureas end in ?

IDE SulFONDLEurea Ide hit it tolbutamide glybruode glypizide

type 1 DM drugs are all

INSULIN in some form remember insulin in the liver and muscle it will stimulate glycogenesis in the muscle and liver in fat is makes triglycerides

chediak Higashi syndrom LMNOP pneumonia

LMNOP lymphohysticytosis M: microtubule dysfunction (the basis of all the symptoms) N: neurological Sxs. O: phagOOOOlysosome formation Pancytopenia

chediak higashi syndrome what gene is dysfunctional?

LYST gene is dysfunction

Chronic granulomatous disease pathophysiology

NADPH + O2 ---> superoxide --->H2O2 you use the enzyme NADPH oxidase for the first step and superoxide dismutase for the second enzyme in patients with this disease you are missing NADPH which is okay in bacteria who are catalase negative because you still can use hydrogen peroxide by stealing it from the bacterias metabolism but in CATALASE POSITIVE organism you cannot do that because they keep breaking it down so you have NO oxidative burst SO your bodies only defense mechanism is building a wall around it (GRANULOMA) and keeping it secluded

what do you have a deficiency of in CGD

NADPH oxidase defieicny which hurts you in the presence of catalase positive organism that infect you

intermediate insulin is?

NPH

dermatomyositis antibody ?

anti-Jo-1 *dermatologists can sip their cup of JO*

Wiskott Aldrich Syndrome

Wiskott Al-DRINK- syndrome WATER Was gene is dysfunctional )WASp protein Antigen presenting cells (due to the was gene not being present) Thrombocytopenia Eczema Recurrent infections

yersinia enteroliticis and pestis

YERSINIA Enterocolitica: the dog in the picture: puppy feces transmission-> children most common demographic can also be transmitted through contaminated milk also restraint to cold temperature ( like l monocytogenes) gram negative /BIPOLAR STAINING most heavily on two ends-> safety pin encapsulated invasive bloody diarrhea//can mimic appendicitis Yersinia Pestis: black plague main reservoir is prairie dogs, transmitted by FLEAS causes boboes swollen tender lymph nodes-> abcesses blackening and death of tissues DIC is caused by endotoxin exotoxin too YERSINIA ASSOCIATED OUTER PROTEINS cause macrophage and neutrophil dgysfunctio by inhibiting phagocytosis and cytokine production allowing the organism to invade rapidly and spread (TYPE THREE SECRETION SYSTEM) TX: ahminoglycosides in combination with tetracycline

Metformin MOA

acts in the liver to decrease hepatic gluconeogensis

anti smooth muscle antibody is associated with

autoimmune hepatitis *AH! a smooth criminal*

SGLT-2 inhibitors work at the proximal renal tubule

blocks SGLT2 causing the glucose to be pissed out patients will get dehydrated-> more glucose will be peed out causing water to follow also will have UTI canagliFLOZINS gliFLOWZINS canagliflozin and empagliflozin some glucose is lost to the tinkle SGLT2

Wegners Granulomatosis

c-ANCA Lungs Kidneys Nasopharynx W-Cner draw a C over the stick figure

e. coli EHEC

catalase positive fimbria/pili green on EMB agar lactose fermenter #1 cause of e. Coli #1 cause of gram negative sepsis due to its LPS endotoxin causes meningitis in neonates (if it has the K capsular antigen) EHEC: most commonly transmitted by eating undercooked meat-> bloody diarrhea EHEC is the *ONLY e.coli that doesn't ferment sorbitol* shiga like toxin- targets the 60s subunit of ribosomes HUS esp in children under ten: HUS pathogenesis: shiga like toxin damages endothelial cells in the glomerulus-> the damaged lining becomes thrombogenic causing platelets to adhere and causing platelet decrease as it cuts them and causing spherocytes EHEC:*O157H7* the serotype that causes massive outbreaks

what are the three rapid acting insulins?

insulin lispro aspart or glulsine 1 hour

Scrotal Fullness symptom

causes: hydrocele or varicocele hydrocele will transilluminate varicocele will NOT translumminate

anti endomysial antibody

celiacs disease

epididmytitis

chlamydia/neisseria if they are UNDER 35 E. COLI if they are over 35 +cremaster reflex is intact (when you stroke the medial portion of the thigh the testciles retract) +prehnsign (relief with lifting up the testes) pneumonic: epididymitis think epididy-MIDAS got the MIDAS touch if you lift it you feel better

2 types of hydrocele

communicating and noncommunicating communicating- you have probably had it since birth noncummnicating- your an adult probably remember this is TRANSILLUMINATING

varicocele

dilated panpiniform plexus NO transillumination bag of worms (these are usually on the the left side, the venous outflow goes up through the kidney and then into the IVC: things that could cause this is RENAL CELL CARCINOMA)

cryglobulinemic vasculitis & HSP vasculitis both have what

hematuria palpable purpura arthralgia ONLY HSP has GI pain ONLY HSP has Iga Deposition ONLY HSO follows a recent URI (B19 and GaS) HSP has stomach pain CRYGLOBUNEMIC VACULITIS HAS HEP C as n underlying issue HEP C and cryoglobulin deposition must treat hep C to get better C gets viral

a decrease in insulin means?

high level glucagon

thiazolidinediones everything you need to work

increase PPARgamma receptors causing more insulin sensitivy three adverse reactions: CV toxicity edema and weight gain pneumonic is PAR3 (3 in greek is gamma) 2 ADRS Cv toxicity, edema and w/g 3 mechanism: PPAR gamma 3 letters: TZD

what is the long acting insulin ?

insulin glargine and detrmire

Giant cell temporal arteritis

intimal thickening and fragmentation of lamina elevated ESR Jaw claudication and temporal headaches polymyalgia rheumatica visual problems (ophthalmic artery) : diplopia must give patients HIGH DOSE CORTICOSTEROIDS BEFORE BIOPSY so you don't cause the patient to go blind

metromin accumulates in what state?

kidney damage making it more likely to cause lactic acidosis contrast especially can temporarly injury the kidneys

Microscopic polyangitis onlu involves the>

lungs and the kidneys p ANCA

metformin is the BIG ONE

metformin is a beiguanide it has the most severe SE lactic acidosis everyone gets started on metformin

MOA of sulfonurea

mimic glucose causes hyper polarization of K channels increasing intracellular calcium and release of insulin

anti-U1-RNP antibody is associated with what disease

mixed connective tissue disorder

CHURG Strauss syndrom aka eosinophilic granulomatosis with polyangitis

necrotizing eosinophilic granulomatous infiltration P-ANCA Asthma/Allergic Rhinitis Balls in the nose sensory deficits anTIbodies chug struass

kawasaki dz

necrotizing vasculitis involving coronary arteries occurs in children can cause MI in children IV immunoglobulins plus ASPIRIN the cow that MOO'D MI in children adenOpathy OROPHARYNGEAL tongue Desquamation (rash)

how do you confirm a CGD diagnosis

nitroblue tetrazolium test would turn blue which would mean there is no NADPH

medium vessel vasculitis

obliterating your cow in a medium pan *kaw*asacki thromboangilitis *obliterans* *pan*polyarteritis nodosa

what is the adverse drug reaction for GLP1 and DDP4 inhibitors

pancreatitis

campylobacter

thermogenic intrinsically linked to heat esp common in chicken bloody diarrhea CURVED gram negative ROD oxidase positive can get bacteria from campy invasive reactive arthritis (reiters syndrome can occur) Gillian Barre can occur which is an autoimmune destruction of myelin *ASCENDING* paralysis opposite of botulism which is DESCENDING

TZDS- thiazolidinediones how do they work?

they work at the nucleus activating PPARgamma receptor causing an increased insulin sensitivity these drugs are the glitazones

PAN polyarteritis nodosa

transmural arteritis with fibrinoid necrosis renal, coronar and mesenteric strong of pearls appearance on Bx fibrinoid necrosis-> fibrosis-> necrosis-> fibrosis 30% have Hep B

takayasu arteritis

transmural fibrous thickening of aortic branches japans women under 40 *pulseless disease* uneven BP in upper extremities subclavian artery may degenerate elevated esr