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14 Cards in this Set

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  • Back
What is the molecular process in genetic imprinting?
Transfer of a methyl group.
What is the "double-barrel" sign? And what is the #1 risk factor?
"Double-barrel" refers to the division of the Aorta by a membrane, which is indicative of an aortic dissection creating an intramural hematoma. The RF is hypertension.
Which treatment of high cholesterol lead to incr TG as an ADR?
Cholestyramine (bile-acid binding resins).

This causes the liver to incr bile-acid secretion (lowering chol) but also incr VLDL and TG as a co-product.
Which enzymatic activity causes rupture of a thrombus creating an emboli? Where does this enzyme come from?
Metalloproteinases, from activated macrophages.
Patient with HLD with h/o angina and HTN. Which treatment will have skin flushing and warmth as an ADR?
Prostaglandin, from Niacin B3.

325mg ASA given 30-60min prior help reduces these cutaneous ADR's.
Patient with severe HTN shows low serum potassium [K], depressed renin activity, and right-sided adrenal mass. What does this patient has and what is the DOC for treating this pt?
This patient has ALD-secreting tumor causing CONN's syndrome (primary hyperALD).

He should be treated with Eplerenone. We used Spironolactone before. MC ADR is gynecomastia.
What is the different pathophysical process of Aortic dissection vs. AAA?
Dissection: Vasa-vasorum obliteration. Present with wide mediastinum and AR.

AAA: atherosclerosis from intimal streak. Present with pulsating abdomen.
What are the cellular effect of NE?
Incr cAMP in cardiac cells.

NE is an adrenergic agonist the affect A1 and B1 receptors, causing vasoconstrict (a1) via IP3/DAG pathway and incr HR/CO/CONTR (b1) via GPCR. Beta-1 incr HR is compensated by baro-mediated reflex brady maintaining normal HR.
How does B12 help in decr thrombosis?
Folic acid (B9) and B12 help decreases Homocysteine, which leads to a decr in Methionine.

Methionine and THF are formed when methyl-THF donate a methyl group to homocysteine.
Are the the step-wise treatment for high LDL, high TG, and low HDL?
High-LDL (chol): lifestyle, statin, ezetimibe.
High-TG: lifestyle, fibrates, niacin
Low-HDL: lifestyle, niacin
Patient with hypersen to tobacco develops exertional calf pain and foot ulcers. What is this condition and mechanism?
Buerger's (thromboangiitis obliterans), which affect medium-to-small arteries.

There's a chronic inflam of arterial wall, which thrombose the lumen, which undergo recanalization affecting adjacent veins and nerves.
A patient with HTN and DM-2 is now placed on Niacin for HLD. How would you adjust his previous HTN and DM meds?
Decrease HTN med (because niacin's vasodilatory effect) and increase DM med (because incr insulin resistance).
Severe HTN (170/70) elderly patient received an unknown therapy. Later c/o bilateral ankle swelling and flushing but BP is controlled. What is the most likely therapy used?
Amlodipine

Isolated HTN is common in elderly. 1st line tx includes (1) thiazide diuretics and dihydropyradine CCB.
A mystery drug has andrenergic agonist property and no antagonistic property. Trial shows incr systolic/diastolic, and decr HR. What is the physiologic effect of this drug?
alpha-1 adrenergic (A1) is consistent with the BP/HR physiologic changes (i.e. phenylephrine, methoxamine).

A1 stimulation causes vasoconstriction, leading to incr TPR and BP. This stim the barocereptor, turning on vaso-vagal reflex which decr HR.