PBL 2

Question 1

Sympathetic cardiac response NT and receptor?

Answer 1

NE

alpha-1

Question 2

Main use of BNP lab value?

Answer 2

rule OUT acute heart failure

SENSITIVE but no specific

Question 3

When would you start to see elevated troponin?

Peak?

Return to normal?

Answer 3

• begins to rise 2-4 hours after myocyte death/damage
• peaks at 24 after infarction
• returns to normal 7-10 days after infarction

Question 4

Mechanism for elevated D-Dimer:

Answer 4

plasmin acts on cross-linked fibrin to form d-dimers

negative rules out thrombogenic process

positive is not specific

elevated in:
PE
DVT
DIC

Question 5

Usefullness of CK levels?

Answer 5

Dx reinfarction

begins to rises 4-6 hours post infarction

peaks 24 hours post infarction

normalizes in 48-72 hours (when trop is still elevated from initial infarction)

Question 6

LDL role in CAD?

Answer 6

↑LDL in intima→inflammation→macrophage recruitment→foam cells = fatty streak
foam cell accumulation→necrosis→↑inflammation→fibrous tissue forms cap–>stenosis

Question 7

First grossly visible fatty arterial lesions? What are they comprised of?

Answer 7

fatty streaks

Foam cells

Question 8

Anelgesic acts on mu receptors to reduce pain?

Answer 8

morphine

Question 9

MOA of NTG?

Answer 9

forms free radical NO → activates guanylyl cyclase → increases cGMP → activates MLC phosphatase → dephosphorylation of MLC → smooth muscle relaxation → vasodilation (mostly veins) → decrease blood returning to heart → decrease preload → decrease stress on myocardium

Question 10

Irreversibly blocks ADP receptors→ blocks platelet activation?

Answer 10

Clopidogrel

Question 11

Potentiates activity of antithrombin III → inactivates thrombin → prevents conversion of fibrinogen to fibrin?

Answer 11

Heparin

Question 12

Binds to GPIIb/IIIa receptor on activated platelets → prevents fibrinogen from binding → prevents aggregation.

Answer 12

Eptifibatide

Question 13

Directly or indirectly aid conversion of plasminogen → plasmin, which cleaves thrombin and fibrin clots.

Answer 13

Alteplase (tPA), reteplase, tenecteplase

Question 14

MOA of statins?

Answer 14

inhibition of cholesterol synthesis
HMG-CoA reductase inhibitors decrease mortality post-MI
reducing plaque formation in the vessels

Question 15

Pathological timeline of MI?

Answer 15

• Under 4 hours, no changes are seen, micro or macro
• 4-24 hours, coagulative necrosis and a darker discoloration of the tissue is seen
• > 24 hours Neutrophils followed by macrophages are seen.

Question 16

Two possible complications of fibrinolysis or angioplasty?

Answer 16

1. Reperfusion of irreversibly damaged cells results in calcium influx, leading to hypercontraction of myofibrils → contraction band necrosis!
2. Return of oxygen and inflammatory cells may lead to free radical generation → further damaging mycocytes → reperfusion injury

Question 17

Contraindications for use of drug-eluting stents:

Answer 17

1. bleeding risk or chance of surgery in the following 12 months
2. risk of non-compliance with anti platelet therapy

Question 18

MOA and role of ASA in MI:

Answer 18

Irreversibly inhibits COX1 & COX2 → inhibits TXA2→ inhibits platelet aggregation. Taking aspirin during a MI will slow the clotting and decrease the size of the clot that is forming.

Question 19

Inheritance pattern of familial hypercholesterolemia?

Answer 19

autosomal dominant

homozygotes have severe CV disease

heterozygotes less severe