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Pathoma LAH > Cardiology: 8.2: CHF > Flashcards

Cardiology: 8.2: CHF Flashcards

1
Q

Name 5 causes of L-sided heart failure.

A
  1. ischemia
  2. HTN
  3. dilated cardiomyopathy
  4. MI
  5. restrictive cardiomyopathy
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2
Q

What is congestive heart failure?

A

failure of the heart to pump appropriately

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3
Q

Why does HTN cause CHF?

A

HTN –> LV hypertrophy = more muscle = harder to oxygenate –> ischemic damage –> pump failure

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4
Q

What is dilated cardiomyopathy?

A

dilation of all 4 chambers of the heart

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5
Q

Why does dilated cardiomyopathy cause CHF?

A

systolic dysfunction (ventricles cannot pump) –> biventricular CHF

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6
Q

What are the causes of dilated cardiomyopathy?

A
  • most common = idiopathic
  • others:
    • Genetic mutation (usually autosomal dominant- ex: Duchenne muscular dystrophy, hemochromatosis, sarcoidosis)
    • Myocarditis- usually due to Coxsackie A or B
    • Alcohol abuse –> Wet Beriberi (vitamin B1/thiamine deficiency)
    • Drugs (e.g., Doxorubicin, Cocaine)
    • Pregnancy—seen during late pregnancy or soon (weeks to months) afterchildbirth
    • Chagas disease
    • *** ABCCCD
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7
Q

What is the tx for dilated cardiomyopathy?

A
  • Na+ restriction
  • ACE inhibitors
  • β-blockers
  • diuretics
  • digoxin
  • implantable cardioverter defibrillator (ICD)
  • heart transplant
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8
Q

What are the complications of dilated cardiomyopathy?

A
  • mitral and tricuspid valve regurgitation
  • arrhythmia
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9
Q

What is the inheritance of Duchenne muscular dystrophy?

A

X linked auto dominant

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10
Q

What causes Duchenne muscular dystrophy?

A
  • frameshift or nonsense mutations —> Ž truncated dystrophin protein Ž–> inhibited muscle regeneration
  • “Duchenne = Deleted Dystrophin”
  • Loss of dystrophin = myonecrosis
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11
Q

Name the largest protein-encoding human gene.

A

Dystrophin gene (DMD)

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12
Q

Why do the calf muscles hypertrophy in Duchenne muscular dystrophy?

A

fibrofatty replacement of muscle

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13
Q

What is the most common cause of death in Duchenne muscular dystrophy?

A

Dilated cardiomyopathy

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14
Q

What lab findings are seen in Duchenne muscular dystrophy?

A
  • increased CK
  • increased aldolase (part of glycolysis)
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15
Q

What does dystrophin do?

A
  • helps anchor skeletal and cardiac muscle fibers
  • connects the actin to the transmembrane proteins α- and β-dystroglycan, which are connected to the extracellular matrix (ECM)
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16
Q

Does hypertrophic cardiomyopathy result in increased, normal, or decreased force of contraction?

A

decreased

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17
Q

If ventricular end diastolic volume (preload) is on the x-axis and stroke volume (or CO) is on the y-axis, how will a Starling curve change in heart failure?

A
  • very increased ventricular end diastolic volume (preload)
  • very decreased stroke volume (CO)
  • –> curve is shifted down and to the right
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18
Q

What is the most common cardiomyopathy?

A

dilated

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19
Q

What are the s/s of dilated cardiomyopathy?

A
  • HF
  • S3
  • systolic regurgitant murmur
  • dilated heart on echocardiogram
  • balloon appearance of heart on CXR
20
Q

Why does restrictive cardiomyopathy cause HF?

A

can’t fill heart appropriately –> can’t pump blood –> LV HF

21
Q

What are the s/s of L-sided HF?

A
  • pulmonary congestion –> increased hydrostatic pressure in pulmonary vessels –> pulmonary edema (dyspnea, paroxysmal nocturnal dyspnea, orthopnea, crackles)
  • heart-failure cells
22
Q

What are heart-failure cells?

A
  • macs that ingest blood and iron from ruptured pulmonary vessels in heart failure
  • iron accumulates –> hemosiderin-laden macs
23
Q

What do heart failure cells look like? Where are they found?

A
  • they’re brown macs (hemosiderin-laden)
  • in the alveolar air spaces
24
Q

Left-sided heart failure also causes decreased forward perfusion. What does this cause? What is the tx?

A
  • decreased blood flow to the kidneys –> activation of RAAS
  • tx = ACE-inhibitors (end in ‘-pril’)
25
Q

ACE-inhibitors are contraindicated in what complement disorder?

A

C1 esterase inhibitor deficiency

26
Q

What are the most common SEs to ACE-inhibitors?

A
  • dry cough
  • angioedema
  • teratogen
  • increased Cr (decreased GFR)
  • Hyperkalemia
  • Hypotension
27
Q

Do ACE-inhibitors change the preload, afterload, or both? How?

A
  • decrease BOTH preload and afterload
  • inhibit RAAS (decrease blood volume and pressures)
  • inactivate bradykinin (a vasodilator)
28
Q

Where in the nephron do ACE-inhibitors act?

A

the efferent arteriole

29
Q

What kind of ABG changes can be seen when taking ACE-inhibitors?

A
  • normal anion gap (hyperchloremic) metabolic acidosis
    • from Hyperkalemic renal tubular acidosis (type 4)
30
Q

What is the tx for AD PKD?

A

ACE-inhibitors or ARBs

31
Q

How do ACE-inhibitors protect a diabetic’s kidneys?

A

decrease intraglomerular pressure –> slows GBM thickening

32
Q

Can ACE-inhibitors be given in pregnancy?

A

no - teratogenic- causes fetal kidney damage

33
Q

Other than L-sided heart failure, what are the causes of R-sided heart failure?

A
  • L-to-R shunt
  • chronic lung disease (cor pulmonale)
34
Q

What do BVs in the lungs do in response to hypoxia?

A

constrict

35
Q

What is cor pulmonale?

A

isolated R-sided heart failure from a pulmonary cause

36
Q

What can pulmonary HTN do to the heart?

A

cause cor pulmonale (isolated R-sided heart failure)

37
Q

What are the s/s of R-sided heart failure?

A
  • blood back up into areas that feed the right heart, seen as:
    • JVD
    • painful HSM (–> cirrhosis)
    • dependent pitting edema
38
Q

What does a nutmeg liver look like? What causes this?

A
  • liver full of red spots venous
  • congestion in the liver (from R-sided heart failure)
39
Q

What is the most common causative infectious agent of dilated cardiomyopathy? How will this appear on microscopy? How will this present clinically?

A
  • Coxsackie A or B
  • characterized by a lymphocytic infiltrate in the myocardium
  • results in chest pain, arrhythmia with sudden death, or heart failure
40
Q

What is doxorubicin? How does it work?

A
  • a cancer Abx
  • intercalates DNA –> DNA breaks –> decreased replication
  • causes free radical damage
41
Q

What are the SEs for Doxorubicin? How are these prevented?

A
  • dilated cardiomyopathy
  • myelosuppression
  • alopecia
  • prevent with Dexrazoxane (an iron chelating agent)
42
Q

What is Doxorubicin used for?

A
  • tx of cancer, including:
    • solid tumors
    • leukmias
    • lymphomas
43
Q

What is an S3 heart sound? Is it normal or abnormal? What causes it?

A
  • extra heart sound in early diastole (after S2)
  • only normal in children and young adults
  • increased ventricular filling pressure from:
    • mitral regurg
    • heart failure
    • dilated ventricles
44
Q

What is orthopnea?

A

SOB when supine

45
Q

What is paroxysmal nocturnal dyspnea?

A
  • breathless awakening from sleep

Pathoma LAH (77 decks)

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