Unit 6A Sigs | Baamboozle - Baamboozle | The Most Fun Classroom Games!

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Explain the role of metoprolol in the management of HCM.(Sigs Case 6.3b)

antagonizes catecholamine binding at Beta1 adren. receptors (card. nodal cells)-> decrease HR; antagonize B1-adren. recept. on card. myocytes-> decr. contract

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

Contrast normal systolic and diastolic function in a healthy heart with the systolic and diastolic function of HCM.(Sigs Case 6.3b)

may have average systolic funct. but poor diastolic funct.; diastolic dysf. will have preserved EF; systolic dysf will have reduced EF

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.

Describe the alterations in vascular reactivity that result from endothelial damage. (SIGS 6.3a)

damage to endothelium--> dysfunction (inability to react to vasodilation)--> structural remodeling--> alters function

Characterize specific dietary modifications, medicinal foods, and lifestyle modifications for ASCVD.  (SIGS 6.3a)

Med. diet, Ornish Undo It, DASH, olive oil, nuts, cocoa, red wine, whole grains, fiber, B vitamins

Correlate hyperlipidemia with the development of atherosclerotic plaques in blood vessels. (SIGS 6.3a) 

lipids/lipoproteins->cross endothelial barrier to artery intima-> retention & endo.dysfunct.-> inflam.-> macroph-> foam cells-> calcification-> rupture

Contrast how the distal arterioles compensate for the stenosis in their respective coronary arteries.(Sigs 6.3a)

MILD: dilation --> meet met. need; MOD: dil.--> meet met. need @ rest; exertion: max blood flow low despite dil. --> can't meet met. need;COMPLETE OCCUL: unable

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

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

Describe how ventricular preload and contractility are altered in DCM and their effects on cardiac output. (SIGS 6.2b)

myocyte damage-> enlargement of chamber-> incr. preload (filing); enlarged chamber w/ decr. contract. d/t eccentric fibrosis

Discuss the effects of alcohol on the heart. How can alcoholism lead to thiamine deficiency and exacerbate DCM? (SIGS 6.2b)

myocyte damage/necrosis, mitochon. degeneration, fibrosis, chamber dilation; deficiency d/t poor nutrition & poor vitamin absorption

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

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

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

Discuss the use of ACE-inhibitors and beta-blockers to slow or reverse cardiac remodeling. (Sigs Case 6.2a)

ACE-inh.: allows heart to get more blood flow & decrease LV filing & decreases peripheral resistance; BB: decreases demand on heart and lowers BP

Describe integrative approaches to atrial fibrillation. (SIGS 6.1b)

Med. diet, stress reduction, no alcohol or caffeine, diet high in magnesium, fish oil, CoQ10

Explain how atropine alters conduction. (SIGS 6.1b)

M2 muscarinic antagonist--> block muscarinic receptor--> decrease parasympathetic response--> increase HR, decrease phase 4 of nodal cells

Distinguish between cardiac conduction blocks (sinus block; bundle branch block; hemiblock) on an EKG. (SIGS 6.1b)

A: Sinus block; B: LBBB; C: RBBB; D: Hemi/fascicular (Left posterior hemiblock is associated with a frontal plane QRS axis more positive than +120°)

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

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 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

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

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

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