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

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

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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

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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.

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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

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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

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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

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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

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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

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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

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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

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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

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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

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