Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Vessels > Vessels UWorld 2 > Flashcards

Vessels UWorld 2 Flashcards

0
Q

ApoA-1

A

LCAT acivation, cholesterol esterification

Chylomicrons and HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Defect in ApoE3 and ApoE4

A

Familial dysbetalipoproteinemia. Liver cannot remove chylomicrons and VLDL remnants from cirulation –> serum cholesterol and triglyceride elevation. Xanthomas and premature heart and vessel disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ApoB-48

A

Chylomicron assembly and secretion by intestine

Chylomicron and remnants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ApoB-100

A

Binds LDL receptor, LDL uptake by extrahepatic cells

VLDL, IDL, LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ApoC-II

A

Lipoprotein lipase activation

Chylomicron, HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ApoE

A

VLDL, chylomicron uptake by liver

Chylomicron, remnant, VLDL, IDL, HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dilated tortuous veins: risk factors, complications

A

Varicose veins. Long periods of standing, age, obesity, multiple pregnancies, genetic defects.

Complications include painful thromboses, skin ulcerations, dermatitis, infection, poor wound healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Embryonic vein derivatives: vitelline, umbilical, cardinal

A

Vitelline –> portal
Umbilical degenerate
Cardial –> systemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Atherosclerosis begins with injury to which cell type?

A

Repetitive endothelial injury, leads to chronic inflammatory state in the intima

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What meds cause hyperkalemia

A

Things that interfere with aldosterone (ACE-I, ARBs, K-sparing diuretics, NSAIDs)

Cardiac glycosides

Non-selective beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

After endothelial injury, what causes intimal thickening?

A

Smooth muscle cells, collagen deposition. Intimal hyperplasia and fibrosis results.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Earliest lesion of atherosclerosis

A

Intimal fatty streaks of intimal lipid-filled foam cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What makes up foam cells?

A

Macrophages and smooth muscle cells that have engulfed LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Equation for net filtration pressure

A

Hydrostatic pressure gradient - oncotic pressure gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Side effects of niacin (B3)

A

Exacerbates gout, acanthosis nigricans (hyperglycemia), red flushed face/vasodilation, hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What meds increase serum uric acid levels?

A

Niacin, hctz, cyclosporine, pyrazinamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Most important risk factor for aortic dissection

A

hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why do ACE inhibitors increase serum creatinine? What affect does this have in pts with renal artery stenosis?

A

Reduce ATII, causing decreased efferent arterial tone –> efferent dilation. Decreases glomerular pressure and renal perfusion. Pts with renal artery stenosis are dependent on efferent constriction to keep perfusion high, so this can cause renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Statins decrease cholesterol synthesis. What is the LDL receptor response?

A

Increased receptor density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is abnormal in varicose veins?

A

Incompetent venous valves –> venous hypertension, retrograde flow from deep to superficial veins in extremities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What tissue extracts the most oxygen from blood?

A

Heart. 75-80% at rest, up to 90% with exercise

21
Q

What 2 lipid lowering agents can cause gallstones?

A

Fibrates and bile acid resins

22
Q

Genomic imprinting

A

An offspring’s genes are expressed in a parent specific manner. Produced by methylation (epigenetics)

23
Q

Alpha 1 agonist: effects on heart

A

Directly increases contractility, but that is usually overridden by reflex decreases in rate, conduction, and contractility due to contraction of vascular smooth muscle

24
Q

Cystic medial degeneration

A

Myxomatous changes in large arteries. Fragmentation of elastic tissue, separation of elastic and fibromuscular components of media by small spaces filled with extracellular matrix.

Seen in Marfan syndrome

25
Q

Hyaline arteriolosclerosis: describe it, and who does it happen to

A

Homogenous deposition of eosinophilic hyaline material in intima and media of small arteries/arterioles. Lumen is narrowed.

Seen in non-malignant hypertension and diabetes

26
Q

Compare and contrast giant cell arteritis and Takayasu arteritis

A

Both have granulomatous inflammation of media

GC affects branches of carotid artery, older patients.
T affects arch of aorta and proximal great vessels

27
Q

What vessels are spared in polyarteritis nodosa?

A

Pulmonary

28
Q

Norepinephrine extravasation

A

NE leak causes a1 vasoconstriction which can lead to local necrosis. Presents as cold, hard, pale local tissue. Can be prevented with an alpha blocker, such as phentolamine (must be done within 12 hr)

29
Q

Alpha blockers (2 non selective, 2 a1, 1 a2)

A

Nonselective: Phenoxyenzamine (irreversible), phentolamine (reversible)

a1: Prazosin (other -zosins), tamsulosin
a2: Mirtazapine

30
Q

Buerger disease aka thromboangiitis obliterans

A

Seen in heavy smokers (tobacco hypersensitivity) with early onset
Segmental thrombosing vasculitis, intermittent claudication. Found in medium vessels, seen often in calf, foot, hand. May extend into contiguous veins and nerves

31
Q

Platelet involvement in atherscerosis

A

Endothelial dysfunction promotes platelet adhesion, aggregation, and release of GF and cytokines. PDGF is released by platelets as well as endothelial cells and macrophages. It promotes proliferation and migration of smooth muscles cells into intima. Platelets also secret TGF-b, which calls in smooth muscles cells and collagen production

32
Q

Tx of anaphylactic shock

A

Epinephrine
Stimulates a1 - counteracts vasodilation, increases BP
B1 effects also raise BP and improve perfusion
B2 - bronchdilation

33
Q

ACE-I causes facial swelling and difficulty breathing. What happened?

A

Angioedema - swelling of tongue, lips, eyelids, laryngeal edema, difficulty breathing. Due to bradykinin accumulation. Rare.

34
Q

What prevents cerebral hypoperfusion upon standing?

A

a1-vasoconstriction

35
Q

Anti- glomerular basement membrane antibodes

A

Goodpasture’s

36
Q

Anti-neutrophil antibodies and URI

A

Wegener’s granulomatosis with polyangiitis

37
Q

Migratory thrombophlebitis

A

Trousseau’s syndrome. Think visceral cancer! Hypercoaguability is a common paraneoplastic syndrome, especially in pancreas, colon, lung

38
Q

Niacin effects on hypertension, diabetes

A

Potentiates anti-hypertensives via vasodilation

Increased insulin resistance and acanthsis nigricans

39
Q

Effects of epinephrine

A

a1, b1, b2 agonist, a1 predominates at high dose

Raises HR (b1)
Raises systolic BP (b1 and a1)
Low dose decreases diastolic BP (b2)
High dose increases diastolic BP (a1)
40
Q

What receptors does phentolamine hit?

A

Non specific alpha blocker –> decrease in diastolic BP and reflex tachycardia

41
Q

What receptors does phenylephrine hit?

A

Selective a1 agonist –> vasoconstrictor

42
Q

What receptors does propanolol hit?

A

Nonselective beta blocker

43
Q

What receptors does isoproterenol hit?

A

Non-selective beta agonist –> increases HR and contractility, vasodilation

44
Q

What receptors does atropine hit?

A

Muscarinic antagonist. Increases HR by blocking vagal stimulation

45
Q

Treatment of high LDL

A

Diet exercise, statin, ezetimibe

46
Q

Tx of high triglycerides

A

Diet exercise, fibrate, niacin

47
Q

Tx of low HDL

A

Diet/exercise, niacin

48
Q

Timeline for strawberry heangioma

A

Present at birth, initially grow with child, and fade after a few years. Most are gone by age 7

49
Q

Dipyridamole, cilostazol: mechanism, use, toxicity

A

Inhibit phosphodiesterase, which leads to increased cAMP and decreased aggregation. Cilostazol is also a direct vasodilator. Can be used for intermittent claudication, peripheral artery disease, prevention of stroke, angina prophylaxis. Toxicity includes nausea, headache, flushing, hypotension, abdominal pain

50
Q

Ticlopidine, clopidogrel, prasugrel, ticagrelor

A

ADP receptor inhibitors, prevent GP2b3a from binding fibrinogen

Used for acute coronary syndrome, coronary stenting. Ticlopidine causes neutropenia.

Can cause TTP/HUS

51
Q

Nitroprusside altered mental status, lactic acidosis

A

Cyanide toxicity. Treat with sodium thiosulfate. Sulfur helps the liver metabolize and detox cyanide to thiocyanate

Vessels (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions