Basic Science/Embryology Flashcards

1
Q

When does vasculogenesis start

A

Yolk sac day 17

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2
Q

Which embryologic structure and arch becomes ligamentum arteriosum?

A

Ductus arteriosus (6th arch)

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3
Q

Which aortic arch do the subclavians come from?

A

Seventh

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4
Q

Which aortic arch do the common and internal carotids come from?

A

Third

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5
Q

What is a bovine arch? How frequent?

A

Left CCA originates from the brachiocephalic trunk - 22%

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6
Q

What normally inhibits platelets from aggregating and adhering to the vessel wall?

A

Endothelium secretes NO, prostacyclin and ADPase

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7
Q

What is a platelets life span

A

8-10 days

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8
Q

When vessel wall is injured and subendothelium exposed, which molecules interact with platelet surface?

A

tissue factor, von willebrand, collagen, fibronectin

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9
Q

When vessel wall is injured and subendothelium exposed, which platelet surface molecules interact with vessel wall?

A

a2b1, glycoprotein 1b/9, a5b1

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10
Q

When vessel wall is injured and subendothelium exposed to platelet surface molecule, a conformational change happens to platelets and what do they release?

A

ADP and thromboxane A2

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11
Q

What does thromboxane A2 do?

A

Vasoconstricts and recruits platelets to site of injury

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12
Q

What do GP 2b3a do?

A

Bridges platelets together - fibrinogen cleaved by thrombin makes fibrin and then platelet plug made by mesh of fibrin

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13
Q

How does aspirin work?

A

Irreversible COX 1 inhibitor, interrupts thromboxane A2 production. At higher doses ASA also COX 2 inhibitor and antiinflammatory

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14
Q

How quickly does EC ASA work? What about if you chew it?

A

3-4 hours, 20 min if chewed

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15
Q

Clopidogrel is a prodrug - what cytochrome acitivates it?

A

CYP 450

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16
Q

How does clopidogrel inhibit platelet aggregation?

A

Irreversibly blocks P2Y12 a key ADP receptor on platelet surface

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17
Q

What dose of clopidogrel do you bolus to activate it within 2 hours

A

300-600 mg

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18
Q

Which medications may interact with clopidogrel?

A

PPI

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19
Q

What does ticlopodine do?

A

Like clopidogrel, irreversibly binds P2Y12 ADP receptor on platelet surface. No longer available because associated with TTP, neutropenia and aplastic anemia.

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20
Q

What does ticagrelor do?

A

Direct inhibitor - Reversibly binds P2Y12 ADP receptor on platelet surface (vs. plavix is irreversible binding and 30% of patients dont show platelet inhibition)

21
Q

What class of medications are: abciximab, eptifibatide, and tirofiban?

A

Antiplatelet - GP2a3b inhibitors. IV drugs

22
Q

What did the CAPRIE trial show?

A

Compared ASA vs plavix for ischemic events. Slight benefit for plavix for stroke/MI/death - 8% RRR

23
Q

What are the 2 zones of the basal lamina? What is its function?

A

1 - clear inner zone (glycoprotein laminin)

2 - dense fibrillar zone (type 4 collagen)

Gives vessel wall strength and ability to change conformation with pulsation/torsion/flexion

24
Q

What size arteries have vasa vasorum?

A

Over 200 micron

25
Q

What is the shear stress equation?

A

tau = 4 x viscosity x flow/ (pie x radius^3)

26
Q

How do endothelial cells respond to high shear stress (3)?

A
  1. More elongated cells
  2. Higher amounts of stress fibers (actin, myosin)
  3. Release vasoactive substances (enhances NO pathway)
27
Q

What is the most common vascular anomaly?

A

Patent ductus arteriosus. 6th arch should obliterate by 1 month old and become the ligamentum arteriosum. When this remains patent, high pressure blood is shunted from thoracic aorta to pulmonary system and causes pulmonary hypertension

28
Q

How long does intimal hyperplasia occur after vein grafts are inserted into the arterial circulation?

A

Self limiting process, 2 weeks

29
Q

What is the difference between vasculogenesis, arteriogenesis, angiogenesis?

A

Vasculogenesis - de novo formation of embryonic blood vessels from progenitor cells

Arteriogenesis - forming collateral circulation to bypass obstructed vessels

Angiogenesis - increasing capillary density to deliver oxygen and nutrients to ischemic tissue

30
Q

What does hypoxia induce - angiogenesis, arteriogenesis, or vasculogenesis? Via which transcription factor?

A

Angiogenesis via hypoxia inducible factor 1 (HIF 1)

31
Q

What does flow shear stress induce - angiogenesis, arteriogenesis, or vasculogenesis?

A

Arteriorgenesis (growth of collateral vessels)

32
Q

What are the 3 components of intra-arterial pressure?

A

1) hydrostatic
2) static filling pressure
3) dynamic pressure produced by cardiac contraction

33
Q

What is Bernoulli’s law in words?

A

Fluid flowing from one point to another, the total fluid energy stays constant (if there are no frictional losses)

34
Q

What is Pouiselle’s law? What assumptions are made?

A

Steady (non pulsatile) laminar flow in a straight rigid cylinder

35
Q

What is being demonstrated in this image?

A

Flow separation. Central rapid flow in common carotid gets compressed to inner wall of the bulb producing area of high shear stress. Outer wall has helical flow patterns with slower flow, lower shear stress and flow reversal.

36
Q

What 3 ways does antithrombin act as a central anticoagulant?

A

1) Inihibition of thrombin prevents removal of fibronopeptide A and B from fibrinogen, limiting fibrin formation
2) thrombin becomes unavailable for activation of factors 5 and 8 thus slowing coagulation cascade
3) thrombin mediated platelet activation and aggregation are inhibited

37
Q

Which coagulation factors does antithrombin inhibit?

A

7a, 9a, 10a, 11a, 12a

38
Q

Which factors does activated protein C inhibit?

A

5a and 8a

39
Q

Name 3 mechanisms of plasminogen activation

A

1) fibrin bound tpa
2) upa
3) factor 12, kallikrein, 11 - each indipendently convert plasminogen to plasmin

40
Q

What is the mode of genetic transmission of varicose veins?

A

Autosomal dominant with variable penetrance

41
Q

What is the risk of having varicose veins if both parents were affected? What about one parent affected? Neither parent affected?

A

Both - 90%

One parent: females 60%, males 25%

Neither: 20%

42
Q

What is the vascular resistance in lymph, veins and arteries?

A

Lymph: relatively high

Veins: low

Arteries: high

43
Q

What is the secondary propulsive force for lymph, veins and arteries?

A

Lymph: haphazard - breathing, yawning, peristalsis

Veins: skeletal muscle

Arteries: vasomotion

44
Q

What is the primary propulsive unit for lymph, veins and arteries?

A

Lymph: lymphangion

Veins: heart

Arteries: heart

45
Q

What is dysphagia lusoria

A

Difficulty swallowing associated with impingement of aberrant right subclavian artery on the esophagus

46
Q

What are the 4 segments of the IVC and what primitive veins did they develop from

A
  1. Postrenal (from supracardinal vein - also gives rise to hemiazygous and azygous vein)
  2. Prerenal (subcardinal vein)
  3. Renal collar (subcardinal and supracardinal segments)
  4. Hepatic (hepatic sinusoids)
47
Q

What are the most common types of IVC abnormalities?

A
  1. Isolated left IVC
  2. Double IVC
  3. Atresia or agenesis of a segment or total IVC
  4. Azygous or hemiazygous continuation of the IVC.
48
Q

Embryologically - how does a doublt IVC develop?

A

Persistence of both the right supracardinal and left supracardinal veins

49
Q

Embryologically - how does a left IVC develop?

A

Regression of the right supracardinal vein with persistence of the left supracardinal vein