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
Adult-type coarctation of aorta
Aortic narrowing is post ductal (no need for PDA). Notching of ribs, hypertension of upper extremities, weak/delayed pulses in lower extremities.
25
What is adult coarctation of aorta associated with?
Other congenital cardiac abnormalities, Berry aneurysm. These patients die of HTN causes.
26
Lipoprotein lipase
hydrolyzes chylomicrons to triglycerides
27
Lipoprotein lipase deficiency
Results in increased concentrations of serum chylomicrons. Body cannot clear dietary lipid loads. Presents as hyperlipidemia and pancreatitis (abdominal pain)
28
How does heparin affect triglycerides?
Releases lipases from endothelium, increasing clearance of triglycerides from circulation
29
What does frothy foamy urine suggest?
Proteinuria or bile salts in urine
30
Churg-Strauss syndrome
Small vessel vasculitis, granulomatous necrotizing vasculitis with eosinophilia, MPO-ANCA and/or p-ANCA, increased IgE
31
Churg-Strauss presentation
Asthma, sinusitis, palpable purpura, peripheral neuropathy May involve heart, GI, kidneys
32
Prevention of DVT in high risk pts (eg about to have hip surgery)
Heparine Note: aspirin isn't enough!
33
Saphenous vein graft - where do you get it?
Medial leg, inferolateral to the pubic tubercle
34
Phenoxybenzamine
Irreversible alpha blocker --> vasodilation. Major use is pheochromocytoma
35
Lymphangiosarcoma
Lymphatic malignancy associated with persistent lymphedema (e.g. several years post radical mastectomy)
36
Side effects of niacin, mediator
Mediated by prostaglandin. Skin flushing and warmth. Preventable with pre-treatment aspirin
37
"Red man syndrome"
Vancomycin side effect mediated by histamine
38
How does capsaicin reduce pain?
Decreases levels of substance P in PNS.
39
Energy for myocardial cellular function comes from: (3)
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
Fatty acid oxidation inhibitors
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
ACE-I first dose concern
First-dose hypotension from reduced venous return to heart. Worse if pt is already hypovolemic/hyponatremic from diuretics.
42
Syphilis vascular compliations
Begins with vasa vasorum endarteritis and obliteration. Causes weakening of adventitia --> ascending aortic aneurysm --> aortic regurg. Test for syphilis with FTA-ABS
43
Tx for BPH and hypertension
Alpha-1 blockers (doxazosin, prazosin, terazosin)
44
Tx for hypertension and heart failure
beta blockers
45
What drug increases serum CK?
Statins - myopathy
46
How do fibrates interact with statins?
Increase concentration of statins, and also causes myopathy on its own --> increased risk of mysitis
47
Fibrates plus bile resins - main side effect
gallstones
48
One-sided kidney atrophy in elderly pt with atherosclerosis
Renal artery stenosis
49
Volume of distribution
= amt of drug given / plasma concentration in body
50
Total body water? ECF? Plasma volume?
41 L, 14 L, 3L
51
Low Vd (3-5)
Drug stays in plasma. Bound to plasma proteins, high MW, or very polar
52
Medium Vd (around 15L)
Plasma plus interstitial volume (ECF). Drug is small and hydrophilic, so it can go to interstitial fluid.
53
Large Vd (around 40L)
Can cross membranes, reach intracellular compartments. Small MW and lipophilic.
54
Huge Vd (larger than total body water)
Avidly bound in tissues, accumulate in cells and keep low plasma concentrations.
55
Polyarteritis nodosa presentation, associated with
Fever, weight loss, malaise, headach. GI symptoms like abdominal pain, melena. Hep B infection
56
What causes intermittent claudication?
Atherosclerosis of larger arteries