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Vessels > Vessels UWorld 1 (All) > Flashcards

Vessels UWorld 1 (All) Flashcards

0
Q

Expression of COX enzymes

A

COX-1 is constitutively expressed, but COX-2 is only seen where inflammatory cells are activated. Thus COX-2 is an inducible enzyme.

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1
Q

V/Q studies show large perfusion defect, no ventilation defect.

A

Specific for pulmonary embolism

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2
Q

Colchicine

A

Binds to tubulin to inhibit microtubule formation, results in impaired neutrophil mitosis and decreased motility

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3
Q

Infliximab

A

Monoclonal antibody that irreversibly binds and inhibits TNF-a. Inhibits inflammatory response, used for autoimmune diseases (IBD, RA, psoriasis, ankylosing spondylitis)

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4
Q

First line tx of isolated systolic HTN

A

Thiazides and DHP CCBs

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5
Q

Doxazosin prazosin, terazosin: class, use, side effects

A

Alpha-1 blockers. Treat HTN and BPH. Cause first-dose effect, cause hypotension on initiation.

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6
Q

Eplerenone

A

Aldosterone antagonist

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7
Q

Aldosterone antagonist most common side effect

A

Gynecomastia

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8
Q

Homocysteine + methylcobalamin –>

A

Methionine

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9
Q

Temporal arteritis: therapy? Trying to prevent?

A

Steroids (prednisone) to prevent blindness

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10
Q

Embryologic origin of PDA

A

Pulmonary arteries and ductus arteriosus from the 6th aortic arch

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11
Q

What is used to close a PDA? Keep it open?

A

Close: indomethecin
Open: PGE2

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12
Q

What arteries are associated with embryonic aortic arches?

A

1) Maxillary 2) None 3) ICA 4) Arch of aorta, subclavian 5) none 6) Pulmonary arteries, ductus arteriosus

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13
Q

What cranial nerves are associated with the embryonic aortic arches?

A

1) Trigeminal (5) 2) Facial (7) 3) Glossopharyngeal (9) 4) Superior laryngeal of vagus (10) 5) none 6) Recurrent branch of laryngeal (10)

5-7-9-10-0-10

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14
Q

-sartan suffix

A

ARB = angiotensin receptor blocker

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15
Q

ARB mechanism, effects

A

Block effects of angiotensin II by blocking AT-1 receptors. Decrease aldosterone, reflex increase in renin, ATI, and ATII. No change on bradykinin.

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16
Q

ACE-I and ARB effects on bradykinin

A

Bradykinin is broken down by ACE, so ACE inhibitors increase levels of bradykinin, causing cough. ARBs do not have this effect.

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17
Q

How do metalloproteases affect atherosclerotic plaques?

A

involved in remodeling, instability and risk of rupture

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18
Q

Common side effects of statin therapy

A

Hepatotoxicity and myopathy. Myositis can lead to elevated serum creatinine kinase

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19
Q

Effect modification

A

occurs when the effect of a main exposure on an outcome is modified by another variale. E.g. likelihood that asbestos exposure will result in lung cancer impacted by smoking status

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20
Q

Transmural inflammation of arterial wall with fibrinoid necrosis

A

polyarteritis nodosa

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21
Q

Dopamine effects at low, med, high dose

A 
Low = D1, increases GFR, vasodilation
Med = D1+B1 = also increases HR, contractility, SBP
High = D1+B1+a1 = generalized systemic vasoconstriction, decreased CO
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22
Q

Isolated systolic hypertension

A

After age 50, becomes common. Caused by decreased compliance in aorta

23
Q

Causes of spontaneous intracranial hemorrhage in young adults

A

1) AVMs
2) Ruptured cerebral aneurysms
3) Drugs, such as cocaine

24
Q

Adult-type coarctation of aorta

A

Aortic narrowing is post ductal (no need for PDA). Notching of ribs, hypertension of upper extremities, weak/delayed pulses in lower extremities.

25
Q

What is adult coarctation of aorta associated with?

A

Other congenital cardiac abnormalities, Berry aneurysm. These patients die of HTN causes.

26
Q

Lipoprotein lipase

A

hydrolyzes chylomicrons to triglycerides

27
Q

Lipoprotein lipase deficiency

A

Results in increased concentrations of serum chylomicrons. Body cannot clear dietary lipid loads. Presents as hyperlipidemia and pancreatitis (abdominal pain)

28
Q

How does heparin affect triglycerides?

A

Releases lipases from endothelium, increasing clearance of triglycerides from circulation

29
Q

What does frothy foamy urine suggest?

A

Proteinuria or bile salts in urine

30
Q

Churg-Strauss syndrome

A

Small vessel vasculitis, granulomatous necrotizing vasculitis with eosinophilia, MPO-ANCA and/or p-ANCA, increased IgE

31
Q

Churg-Strauss presentation

A

Asthma, sinusitis, palpable purpura, peripheral neuropathy

May involve heart, GI, kidneys

32
Q

Prevention of DVT in high risk pts (eg about to have hip surgery)

A

Heparine

Note: aspirin isn’t enough!

33
Q

Saphenous vein graft - where do you get it?

A

Medial leg, inferolateral to the pubic tubercle

34
Q

Phenoxybenzamine

A

Irreversible alpha blocker –> vasodilation. Major use is pheochromocytoma

35
Q

Lymphangiosarcoma

A

Lymphatic malignancy associated with persistent lymphedema (e.g. several years post radical mastectomy)

36
Q

Side effects of niacin, mediator

A

Mediated by prostaglandin. Skin flushing and warmth. Preventable with pre-treatment aspirin

37
Q

“Red man syndrome”

A

Vancomycin side effect mediated by histamine

38
Q

How does capsaicin reduce pain?

A

Decreases levels of substance P in PNS.

39
Q

Energy for myocardial cellular function comes from: (3)

A

1) Fatty acid oxidation (60%, requires most oxygen)
2) Glucose oxidation (30%)
3) Glycolysis

Shifting this balance away from FA oxidation may help in angina, to decrease oxygen requirements

40
Q

Fatty acid oxidation inhibitors

A

Inhibit fatty acid oxidation, which makes energy but requires a bunch of oxygen. Potential treatment for angina. Also may prevent buildup of toxic metabolites

41
Q

ACE-I first dose concern

A

First-dose hypotension from reduced venous return to heart. Worse if pt is already hypovolemic/hyponatremic from diuretics.

42
Q

Syphilis vascular compliations

A

Begins with vasa vasorum endarteritis and obliteration. Causes weakening of adventitia –> ascending aortic aneurysm –> aortic regurg.

Test for syphilis with FTA-ABS

43
Q

Tx for BPH and hypertension

A

Alpha-1 blockers (doxazosin, prazosin, terazosin)

44
Q

Tx for hypertension and heart failure

A

beta blockers

45
Q

What drug increases serum CK?

A

Statins - myopathy

46
Q

How do fibrates interact with statins?

A

Increase concentration of statins, and also causes myopathy on its own –> increased risk of mysitis

47
Q

Fibrates plus bile resins - main side effect

A

gallstones

48
Q

One-sided kidney atrophy in elderly pt with atherosclerosis

A

Renal artery stenosis

49
Q

Volume of distribution

A

= amt of drug given / plasma concentration in body

50
Q

Total body water? ECF? Plasma volume?

A

41 L, 14 L, 3L

51
Q

Low Vd (3-5)

A

Drug stays in plasma. Bound to plasma proteins, high MW, or very polar

52
Q

Medium Vd (around 15L)

A

Plasma plus interstitial volume (ECF). Drug is small and hydrophilic, so it can go to interstitial fluid.

53
Q

Large Vd (around 40L)

A

Can cross membranes, reach intracellular compartments. Small MW and lipophilic.

54
Q

Huge Vd (larger than total body water)

A

Avidly bound in tissues, accumulate in cells and keep low plasma concentrations.

55
Q

Polyarteritis nodosa presentation, associated with

A

Fever, weight loss, malaise, headach. GI symptoms like abdominal pain, melena.

Hep B infection

56
Q

What causes intermittent claudication?

A

Atherosclerosis of larger arteries

Vessels (3 decks)

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