PBL 2 Flashcards
Sympathetic cardiac response NT and receptor?
NE
alpha-1
Main use of BNP lab value?
rule OUT acute heart failure
SENSITIVE but no specific
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
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
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)
LDL role in CAD?
↑LDL in intima→inflammation→macrophage recruitment→foam cells = fatty streak
foam cell accumulation→necrosis→↑inflammation→fibrous tissue forms cap–>stenosis
First grossly visible fatty arterial lesions? What are they comprised of?
fatty streaks
Foam cells
Anelgesic acts on mu receptors to reduce pain?
morphine
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
Irreversibly blocks ADP receptors→ blocks platelet activation?
Clopidogrel
Potentiates activity of antithrombin III → inactivates thrombin → prevents conversion of fibrinogen to fibrin?
Heparin
Binds to GPIIb/IIIa receptor on activated platelets → prevents fibrinogen from binding → prevents aggregation.
Eptifibatide
Directly or indirectly aid conversion of plasminogen → plasmin, which cleaves thrombin and fibrin clots.
Alteplase (tPA), reteplase, tenecteplase
MOA of statins?
inhibition of cholesterol synthesis
HMG-CoA reductase inhibitors decrease mortality post-MI
reducing plaque formation in the vessels
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.
Two possible complications of fibrinolysis or angioplasty?
- Reperfusion of irreversibly damaged cells results in calcium influx, leading to hypercontraction of myofibrils → contraction band necrosis!
- Return of oxygen and inflammatory cells may lead to free radical generation → further damaging mycocytes → reperfusion injury
Contraindications for use of drug-eluting stents:
- bleeding risk or chance of surgery in the following 12 months
- risk of non-compliance with anti platelet therapy
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.
Inheritance pattern of familial hypercholesterolemia?
autosomal dominant
homozygotes have severe CV disease
heterozygotes less severe
