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43 Cards in this Set
- Front
- Back
Do all myocardial adaptations results in structural changes?
What are examples non-pathological structural remodeling? |
No, some changes may merely be physiological, such as changes in rate, resistance, output
Normal structural changes = postnatal remodeling, adaptation to an exercise program |
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What results in abnormally high preload?
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Preload = volume of blood in ventricle and wall stress during diastole
Anormal preload = volume overload due to valve incompetence or loss of contractility Ventricle doesn't empty properly during systole or received blood from great artery during diastole |
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What results in an abnormally high afterload?
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Pressure overload such as in systemic or pulmonary hypertension, valve stenosis, coarctation of aorta
Myocardium may be intact, but must adapt to meet prolonged increase in work demands |
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What is myocardial hypertrophy an adaptation to?
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Response to increase in work
Results in increased size of myocytes and interstitial tissue Not all bad, e.g., fitness programs Note dilation occurs before hypertrophy |
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What changes occur in myocardial hypertrophy?
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Increased myocyte diameter, length
Additional sarcomeres Inc'd contractile proteins Inc'd mitochondria (for ATP) Inc'd collagen |
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What are the mechanical and trophic triggers of myocardial hypertrophy?
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Mechanical: Stretching
Trophic: IGF-1 (polypeptide GF) Ag-II, Endothelin I, alpha agents (Vasoactive) |
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What genes are induced in myocardial hypertrophy?
What do these genes allow for? |
c-fos
egr-1 c-jun These are early genes that reactivate embryonal/fetal gene programming: Expression of Atrial Natriuretic Factor (ANF) Change from a-myosin heavy chain to b-myosin heavy chain (more energetically-economic contraction) |
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What is cor pulmonale?
Causes? |
Hypertrophy of RV
Can be due to COPD, recurrent pulm emboli, MS (anything that increases Pulm Artery pressure) Leads to tricuspid regurg |
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When does heart failure occur?
Define: Congestive Failure Forward Failure |
Heart unable to maintain output sufficient for metabolic requirements
Congestive: congestion present in lungs Forward: dec'd output Backward: Inc'd EDP and inc'd venous pressure |
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Heart Failure:
Systolic vs Diastolic Causes |
Systolic: loss of contractility
Diastolic: inadequate inflow into ventricle |
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Effect of heart failure on:
beta-adrenergic receptor density cAMP endothelin-1 |
ALL DECREASE
(these things tend to increase with hypertrophy) |
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B-type Netriuretic Peptide (BNP):
Role Diagnostic Use |
Peptides which regulate fluid homeostasis and vascular tone
Secreted by ventricular myocardium when volume expanded or pressure overloaded; it's a measure of myocardial stretching Can be used to diagnose CHF! |
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Signs of Left Heart Failure
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Left:
Pulm congestions, edema: Congested capillaries, veins Edema in septa and alveoli Hemosiderin-laden macs (if long-term) Renal effects: Azotemia (not getting rid of waste products) Tubular Necrosis Renin Activation Brain effects: Hypoxic encephalopathy |
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Signs of Right Heart Failure
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Congestion in systemic organs
Liver (hepatomegaly, nutmeg liver, centrilobular necrosis) Splenomegaly Edema Effusions in pleural, peritoneal, and pericardial cavities |
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Aging heart changes
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Formerly known as brown atrophy due to presence of LIPOFUSCIN
Bphil degeneration due to accumulation of glycogen metabolism byproducts Hypertrophy due to inc'd wall stress from inc'd resistance (from arterial wall stiffness) Inc in collagen Fewer myocytes (due to apoptosis) Amyloidosis (from tranthyretin): can be cardiac or systemic LV cavity decreases in size, upper septum bulges into LV Outflow Tract Calcification Lambl's excrescences |
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Eccentric Hypertrophy:
Causes |
Eccentric: RV and LV hypertrophy; causes: volume overload (mitral regurg)
Don't get LV dilation with mitral stenosis |
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