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

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

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seesaw

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gift

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shark

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banana

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thief

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rocket

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gift

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thief

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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

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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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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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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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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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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

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heart

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rocket

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fairy

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banana

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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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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

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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

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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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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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