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Flashcards in PBL 2 Deck (19):
1

Sympathetic cardiac response NT and receptor?

NE

alpha-1

2

Main use of BNP lab value?

rule OUT acute heart failure

SENSITIVE but no specific

3

When would you start to see elevated troponin?

Peak?

Return to normal?

-begins to rise 2-4 hours after myocyte death/damage

-peaks at 24 after infarction

-returns to normal 7-10 days after infarction

4

Mechanism for elevated D-Dimer:

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

negative rules out thrombogenic process

positive is not specific

elevated in:
PE
DVT
DIC

5

Usefullness of CK levels?

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)

6

LDL role in CAD?

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

7

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

fatty streaks

Foam cells

8

Anelgesic acts on mu receptors to reduce pain?

morphine

9

MOA of NTG?

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

10

Irreversibly blocks ADP receptors→ blocks platelet activation?

Clopidogrel

11

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

Heparin

12

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

Eptifibatide

13

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

Alteplase (tPA), reteplase, tenecteplase

14

MOA of statins?

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

15

Pathological timeline of MI?

- 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.

16

Two possible complications of fibrinolysis or angioplasty?

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*****

17

Contraindications for use of drug-eluting stents:

1. bleeding risk or chance of surgery in the following 12 months

2. risk of non-compliance with anti platelet therapy

18

MOA and role of ASA in MI:

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.

19

Inheritance pattern of familial hypercholesterolemia?

autosomal dominant

homozygotes have severe CV disease

heterozygotes less severe