Cardio I Flashcards

1
Q

describe hypertrophy

A
  • increase in size of the cardiac myocytes
  • induction of genes coding for proteins:
    • actin, myosin (fetal isoforms of proteins) → increased sarcomers
  • usually not accompanied by increase in vascularization → relative decrease in capillary density → ischemia → fibrosis → reduced diastolic relaxation
  • coupled with increased metabolic and O2 need → cardiac decompensation
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2
Q

describe concentric hypertrophy

A
  • occurs in pressure overload on ventricles
    • e.g. HTN, aortic stenosis → new sarcomeres are added in parallel to existing sarcomeres → increased wall thickness and decreased diameter of cavity
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3
Q

describe eccentric hypertrophy

A
  • occurs in volume overload on ventricles
    • e.g. aortic regurgitation → new sarcomeres are added in series with existing sarcomeres → muscle mass increases proportional to chamber dilatation; there can be significant hypertrophy without any increase in thickness of the walls
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4
Q
A
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5
Q
A
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6
Q

describe systolic dysfunction and examples of when it occurs

A

systolic dysfunction = inability to contract properly

  • myocyte loss, e.g. MI
  • pressure overload, e.g. hypertension
  • volume overload, e.g. valvular regurgitation
  • decreased contractility e.g. myocarditis, DCM
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7
Q

describe diastolic dysfunction

A

diastolic dysfunction = inability of the heart to relax and fill

  • massive ventricular hypertrophy
  • myocardial fibrosis
  • amyloidosis
  • constrictive pericarditis
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8
Q

describe high output failure vs. low output failure

A
  • high output failure:
    • occurs due to increased tissue demands e.g. anemia, hyperthyroidism, pregnancy
    • symptoms of heart failure occur in spite of well-functioning heart (high cardiac output)
    • is a systolic dysfunction
  • low output failure:
    • heart failure with decreased cardiac output
    • majority of cardiac disease causes low output HF
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9
Q

describe forward vs. backward heart failure

A
  • forward failure:
    • decreased output to the systemic circulation
    • leads to renal hypoperfusion → activation of renin-angiotensin system → sodium and water retention → edema
    • patient would have low BP, fatigue, syncope, shock
  • backward failure:
    • pulm. congestion → pulm. edema → pulm. HT → RHF → systemic venous congestion → edema, ascites, raised JVP, congested liver
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10
Q

describe compensatory mechanisms found in heart failure

A
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11
Q

describe how LHF affects the brain, kidney and lungs

A
  • brain: hypoxic encephalopathy
  • kidney: acute tubular necrosis
  • lungs:
    • gross:
      • heavy & wet lungs, cut surface → exudes a frothy mixture of surfactant-rich fluid and blood
    • histo:
      • congestion of pulm. alveolar capillaries
      • edema fluid in alveolar spaces
      • persistent cases → brown induration of lungs
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12
Q

describe how RHF affects the liver and spleen

A
  • liver:
    • chronic passive congestion
    • nutmeg liver
  • spleen:
    • enlargement and congestion of spleen
  • soft tissue edema
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