What is the MOA of Colchicine and how does it relate to the management of pericarditis?(Sigs Case 6.2a)
used as a theoretical anti-inflamm. agent; inhibits IL-1 from cascading, interferes w/ NFK-B; binds to microtubular tubulin in neutrophils-> inhibits mitosis
Identify the AV blocks, rhythm, and atrial and ventricular rates on the ECGs.(SIGS 6.1b)
1st: Prolonged PR; 2nd Type I: Prolong PR, drop P; 2nd Type II: Drop QRS w/out PR prolong; 3rd: No association between P and QRS constant R-R interval
Describe the potential benefits and precautions for the use of CoQ10 and L-carnitine for cardiac function. (SIGS 6.3b)
CoQ10: facilitates ATP production via ETC in mitochondria; body can become dependant- do not stop abruptly; L-Carn.: "shuttle" for FA to mitochondria in L vent.
Explain the mechanism of action of amiodarone and the rationale for its use in dysrhythmias. (SIGS 6.2b)
Class III anti-arryth; MOA: blocks VG K+ channels --> inhibit Phase 3 repol--> prolong cardiac action potential & refractoriness--> decr. SA node firing rate
Explain how multiple wandering re-entrance circuits can result in atrial fibrillation. (SIGS 6.1a)
Wandering re-entrance circuits able to continuously find excitable tissue--> depolarization of atria--> fibrillatory contractions in atrial myocytes
Describe the pathogenesis of coxsackievirus type B and how it relates to viral myocarditis. (Sigs Case 6.2a)
GI tract (stable at low gI pH)→infects mucosal epithelial cells→viremia→infects + lyse heart/pleural surfaces
Explain the relationship of HCM and heart failure with preserved ejection fraction (HFpEF)(Sigs Case 6.3b)
diastolic dysfunction (early diastolic relaxation) + LV hypertrophy (concentric)- thick wall = pressure overload + less volume (EDV-ESV/EDV) = up EF
Describe how cardiac chamber dilation results in global hypokinesis and systolic dysfunction.(Sigs Case 6.2b)
constant backup fluid-> dilation chambers-> decrease ability to contract & overstretching-> impaired contraction-> less EF-> systolic dysfunct-> systolic fail
Define the characteristic histopathologic features of acute viral myocarditis.(Sigs Case 6.2a)
lymphohistocytic; infiltration of lymphocytes that bring about T lymphocytes; myocyte is elongated w/ nuclei
Contrast how the distal arterioles compensate for the stenosis in their respective coronary arteries.(Sigs 6.3a)
Explain the effects of electrolyte imbalance on cardiac conduction and the impact erythromycin would have. (SIGS 6.1a)
alter depol/ pol/ repol; macrolide antibiotic w/ AE prolonged QT intv. d/t blockage of K+ channels--> delays phase 3 repolariz.--> more intracellular K+--> EADs
Describe the mechanism(s) of action of diltiazem and its effect on cardiac conductivity (SIGS 6.1a)
MOA: inhibits inflow Ca2+ ions into cardiac smooth muscle (SM) during depolarization; Decr. intracellular Ca2+ --> incr. SM relaxation/vasodilation--> decr. BP
Describe the role of INR monitoring in anticoagulation therapy and explain the need for bridge therapy with warfarin. (SIGS 6.1a)
monitor coagulability (maintain optimal level- not too low or too high); Bridge therapy for warfarin due to taking several days to achieve therapeutic effects
Correlate hyperlipidemia with the development of atherosclerotic plaques in blood vessels. (SIGS 6.3a)