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

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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

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

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

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

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

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

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 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

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 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

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

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 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

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

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

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

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) 

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

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

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

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°)

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 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