Uw Set 1

Front 1

Nitroprusside toxicity related confusion and disorentation. What is the "elemental" antidote?

Back 1

Sulfur.

Nitroprusside cause mix vaso/venodilation with onset ~30sec, but met. into CYANIDE and nitric-oxide. Cyanide met by liver Rhodanase to thiocyanate (in urine). Tx with SODIUM THIOSULFATE to enhance rhodanase act.

Front 2

What is the lipid metabolism pathway?

Back 2

Dietary lipid transported to peripheral tissue as CHYLOMICRONS, which hydrolyzed by lipoprotein lipase (LPL) releasing TRIGLYCERIDE (TG).

I.e. LPL hydrolizes TG in chylo and periphery.

Front 3

Turbid plasma with creamy spernatant. Lipoprotein lipase (LPL) is low. What is the problem and presentation?

Back 3

PT cannot clear dietary lipid in chylomicrons. Often has marked HLD, pancreatitis (abdo pain), lipemia retinalis, skin xathomas, and hepatosplenomegaly. Risk of pancreatitis incr in TG conc above 1000mg/dL.

Front 4

Besides anti-clotting, how does Heparin affect lipid metabolism?

Back 4

Heparin releases endothelim-bound (marginated) lipases, which encourages clearance of TG from the circulation.

Front 5

Patient with exertional angina, decrease sexual performance, and h/o MI. What causes present symptoms of leg muscle cramps?

Back 5

CLAUDICATION due to atherosclerosis resulting from stenotic atheromatous lesions. Atheromas are lipid-filled INTIMAL PLAQUE that bulges into the arterial lumen.

Front 6

Patient with orange-yellow discoloration (jaudice) of palmar creases and yellow papules (xanthomas) on elbow, knee, and buttock. Lab shows LACK of ApoE3/E4 in curc lipoprotein. What is impaired?

Back 6

Chylomicron remnant uptake by LIVER CELLS (familial dys-beta-lipoprotein-emia, type III). Apolipoprotein found on chylomicrons and VLDL binds to hepatic apolipoprotein receptors, which removes them from circulation.

Front 7

What are the derivatives of common cardinal vein?

Back 7

SVC (and maybe IVC)

Front 8

What are the stop-codons on mRNA? And what is its tRNA correspondant?

Back 8

mRNA: 5'--UAG/UAA/UGA--3'
tRNA: 3'--AUC/AUU/ACU--5'

Front 9

At the L1 level CT, what structure lies anterior to the right renal artery? How is this position related to the aorta? And what two structures are connected to form this one?

Back 9

At L1 abdo CT, the IVC lies anterior to the right renal artery and to the right of the aorta. The IVC is formed by the union of the RIGHT and LEFT common iliac veins at the L4-L5 level.

Front 10

What is the best site for harvesting saphenous vein?

Back 10

- Saphenous vein (superficial system) in inner thigh
- Femoral vein (deep)

Front 11

What is the ABG in metabolic acidosis?

Back 11

pH: low (duhhh)
pCO2: low (lungs comp)
HCO3: low (kidney wasting)

Front 12

What is the ABG in metabolic alkalosis?

Back 12

pH: high (duhhh)
pCO2: high (lungs comp)
HCO3: high (kidney retaining)

Front 13

What is the ABG in respiratory acidosis?

Back 13

pH: low (duhhh)
pCO2: high (lungs cant breathe)
HCO3: high (kidney comp)

Front 14

What is the ABG in respiratory alkalosis?

Back 14

pH: high (duhhh)
pCO2: low (lungs lose acid)
HCO3: low (kidney comp)

Front 15

What is the ABG in ASA toxicity?

Back 15

Dont know

Front 16

What are the causes of Anion-gap metabolic acidosis?

Back 16

MUD-PILES

Methanol
Uremia
DKA

Propylene glycol
Infection
Lactic acidosis
Ethylene glycol (anti-freeze)
Salicyclates (ASA)/Starvation

Front 17

What are the causes of non-gap acidosis?

Back 17

HARD-UPS

Hyper-alimentation
Acetazolamide (CA inhibitor)
RTA
Diarrhea

Uterosignoidostomy
Pancreatic fistula
Spironolactone

Front 18

What are the effects of EPI on HR and BP? Also which receptor is involved with each effect?

Back 18

HR - tachy (B1)
Systolic - HTN (B1, A1)
Diatolic - low dose: hypo (B2>A1), high dose: hyper (A1>B2)

Front 19

Which drug, when coupled with EPI, could increase the diastolic BP and stablize HR?

Back 19

Incr dias BP could mean either (1) inhibit B2 effect, or (2) enhance A1 effect.

However, associated maintenance of HR suggests inhibition of B1 receptor, which hints toward a B-blocker (PROPRANOLOL)

Front 20

Right DVT with h/o HTN, DM2, AF, and stable angina. Why is there increase serum creatine kinase (CK) level after surgery?

Back 20

Reperfusion injury.

1. O2 radical generation by prenchymal cells, endothel, and leuks.
2. Severe irreversible mito damage
3. inflammation attract PMN's.
4. Complement activation
5. Cell wall damage release CK

Front 21

Puritus and flushing s/p cholesterol-lowering med. What is the effect of this drug on chol metabolism?

Back 21

Nicotinic acid (vit-B3 Niacin) is used to Tx HLD by decrease synthesis of hepatic TG and VLDL by suppressing FA release in periphery. Also decr VLDL conversion to LDL (lower LDL). Also incr HDL by 25-30%.

ADR = flushing (tx c ASA), hapatotoxic

Front 22

Exertional CP with h/o HTN, DM, HLD. Stress test (+)ischemia. Cardiac cath 80% occlusion of RCA, 60% LCA. What is the first cell type injured in this PT?

Back 22

Endothelial cells FIRST, which causes incr permeability and monocyte/lymphocyte adhesion into the intima.

Front 23

Recent-onset oliguria, high serium creatinine, and persistent intra-nasal ulcer. Which is the most prominent AB against?

Back 23

Neutrophils (PMN's).

Nasal mucosa ulcer and glomerulonephritis are pathomnemonic for Wegener's (Granulomatosis with polyangiitis) -- dx with c-ANCA against neutrophils.

Front 24

What are the derivative of the pharyngeal arches? (i.e. aortic arch and nerve)

Back 24

1st - 1st aortic (gone), trigeminal nn
2nd - 2nd aortic (gone), facial nn, muscle of facial expression
3rd - 3rd aortic (common & prox internal carotid), glossopharyngeal nn.
4th - 4th aortic (true arch and subclavian), superior laryngeal br of Vagus nn.
5th - gone in utero
6th - 6th aortic (pulmonary rr, ductus arteriosus), recurrent laryngeal br of Vagus.

Front 25

Persistent HA and dysphagia. Aterial BX shows multinuclear giant cells and internal elastic membrane fragmentation. Why is initial PREDNISONE so important?

Back 25

Prevent blindness (ophthalmic artery occlusion)

Multinucleated giant cells (granulocytes) are indication of granulomatous inflammation, which are pathomnemonic for giant cell arteritis (TEMPORAL arteritis) - MC vasculitis in adult. GCA usually in adult >50yo causing HA, face pain, jaw claudication, vision loss, and high EST.

Front 26

Skin BX shows IgA and C3 deposition. What is the disease and presentation?

Back 26

IC vasculitis with IgA and C3 deposition is HSP (henoch-schonlein purpura) -- aka "Butt Man" rash. Present with NORMAL platelet, gastroenteritis, and intersusception. MC in male, 3-11yo, and self limiting.

Front 27

Bluish lesion under nail, extremely tender to touch. If lesion is a tumor, what is the cell-of-origin? And what is its function?

Back 27

Maybe Glomangioma (glomus tumor) or subungual melanoma (melanocytes).

Melanoma should be pigmented (not this case), so Glomus tumor is more likely. Glomus are encapsulated organ in the dermis responsible for thermoregulation (shunting blood away from periphery in cold condition)

Front 28

Dysphagia, HA, and temporal tenderness. What will arterial BX shows? Which disease present similar to this?

Back 28

Dx most likely GCA, a/w HA, facial pain, vision loss. Arterial BX most likely shows granulocytes (giant cells) inflammation of the MEDIA. Affect older >50 males.

TAKAYASU vasculitis (pulseless) affect the aortic arch similarly. Affect younger <40yo female.

Front 29

Some stupid protein. 72kD, inflammatory cells only (incl macrophages) but not in other normal tissue. What drug bind to this enzyme?

Back 29

Cyclooxygenase-2 (COX-2) is the enzyme. COX-1 is expressed in all tissue, while COX-2 is only in inflammatory. ASA irreversibly binds COX-1/2 which require new synthesis to restore enzymatic activity.

Front 30

What is the BX finding in PT with diastolic BP of 120-130's?

Back 30

120-130: hypertensive crisis - hyperplastic arteriolosclerosis diastolic (onion-skinning)

* Hyaline-arteriosclerosis (homogenous acellular deposition) present in less severe HTN

Front 31

A drug designed to inhibit a step in FA oxidation, which aim to tx stable angina. What is the mechanism of this drug?

Back 31

Less oxygen used per one ATP synthesized.

Myocardial cell energy is from 3 source: glycolysis (5%), glucose oxidation (30%), and FA oxidation (50%, require the most ATP).

Front 32

Fever, wt loss, myalgia, abdo pain, BP of 150/90, HR 90 -- DX with polyarteritis nodosa (PAN). Which organ is spared?

Back 32

Pulmonary.

PAN is segmental, transmural, necrotizing inflammation of small-med arteries in ANY organ but spare the bronchial arteries.

Front 33

HTN patient tx with ramipril (ACE-I) that result in incr serum creatinine. Which part of the kidney does ACE-I affect the most?

Back 33

Afferent arteriole.

ACE-I could acutely reduce GFR by altering autoregulation in kidney -- causing a rise in serum creatinine. Inhibition of AT-2 decr efferent arterial tone.

Front 34

BP 120/80 supine, 90/60 standing (orthostatic hypo). Which receptor is under stimulated in this PT?

Back 34

A1-adrenergic

Orthostatic hypo is a fall >20mm syst or >10mm dias.

Front 35

What are the effect of the A1-adrenergic receptor?

Back 35

A-1 "constrictor"

a. vasoconstriction
b. sm muscle constriction
c. glucose met (-neogen, -lysis)

Front 36

What are the effect of the A2-adrenergic receptor?

Back 36

A-2 "constrictor"

a. anal sphincter constriction
b. glucose met (+glucagon, (-) insulin)
c. inh NE release (no insulin)

Front 37

What are the effect of the B1-adrenergic receptor?

Back 37

B-1 "heart"

a. incr HR
b. incr contract
c. incr conduction

Front 38

What are the effect of the B2-adrenergic receptor?

Back 38

B-2 "dilation"

a. broncho-dilation
b. vaso-dilation
c. sm muscle relaxation

Front 39

Patient with HA and vomiting, then slip into coma and dies. Autopsy shows ruptured cerebral aneurysm and ICH. What is this associated with?

Back 39

Coarctation (causing HTN proximally)

Front 40

Which drug inhibit platelet aggregation (anti-clotting) AND directly dilate arteries?

Back 40

Cilostazol (Pletal)

1. inh PDE-3 (phosphodiesterase) -- antiplatelet
2. suppress cAMP degradation -- vasodilation

Front 41

A medication antagonize the effect of NE (i.e decr NE's ability of maximially vasoconstrict). What is the medication?

Back 41

Phenoxybenzamine (tx of pheo)

NE is a potent agonist of A1 and B1 receptors, which causes vasoconstriction and tachycardia.

Front 42

Female with HLD and acute cholecystitis. Dad died of MI, mom has DM. Which med combination likely cause her gallstone?

Back 42

Gemfibrozil (fibrates) and Cholestyramine (bile-acid binding resin)

Front 43

What are the bile-acid binding resins?

Back 43

"CHOLES-" Choles-tyramine, choles-tipol, chole-sevelam.

Reduce enterohepatic circulation -- decr LDL -- incr bile acid production (and cholesterol content of bile, causing stone).