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Cardiovascular System > Pathology of Hypertension > Flashcards

Pathology of Hypertension Flashcards

1
Q

Hypertension – morphology

  • Large/medium arteries:
  • Small arteries/arterioles:
A
  • Large/medium arteries:
    • Accelerated atherogenesis
    • Degenerative changes in vascular walls
    • Increased risk of aortic dissection & cerebrovascular hemorrhage
  • Small arteries/arterioles:
    • Hyaline arteriolosclerosis
    • Hyperplastic arteriolosclerosis
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2
Q

Which age group is hyaline arteriolosclerosis usually seen in?

A

Elderly patients

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3
Q

What is the morphology of hyaline arteriolosclerosis?

A
  • Similar change in diabetics (microangiopathy)
  • Homogeneous pink, thickening of vessels with narrowing of lumen
    • Leakage of plasma across endothelium due to HTN
    • Excess matrix production by the smooth muscle cells occurs secondarily
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4
Q

What does hyaline arteriolosclerosis typically characterize?

A

“Benign” nephrosclerosis

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5
Q

What does hyperplastic arteriolosclerosis typically characterize?

A

Characteristic of malignant hypertension

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6
Q

What is the morphology of hyperplastic arteriolosclerosis?

A
  • Onion-skinning
    • ​concentric laminated walls with luminal narrowing
  • Due to reduplicated basement membrane and smooth muscle cells
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7
Q

Malignant hypertension – morphology:

A

Necrotizing arteriolitis:

  • term used when these changes are associated with fibrinoid necrosis
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8
Q

What sides of the heart does systemic and pulmonary hypertensive heart disease affect?

A
  • Systemic hypertensive heart disease ⇒ left sided
  • Pulmonary hypertensive heart disease ⇒ right sided
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9
Q

What type of hypertrophy is typically seen in systemic hypertensive heart disease?

A
  • Concentric left ventricular hypertrophy in the absence of other cardiovascular pathology
  • History or pathologic evidence of hypertension >140/90 mm Hg
  • 25% of US population
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10
Q

Systemic Hypertensive Heart Disease: morphology

A
  1. Cardiomegaly:
    • Concentric hypertrophy without dilatation
    • >1.5 cm wall thickness
    • 500 – 600 g
  2. Thickness of left ventricular wall impairs diastolic filling and causes left atrial enlargement
  3. Myocyte hypertrophy:
    • Increased myocyte size & nuclear enlargement
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11
Q

What are the possible clinical outcomes for systemic hypertensive heart disease?

A
  • Normal longevity
  • Progressive ischemic heart disease
    • HTN potentiates ischemic heart disease
  • Progressive renal damage or stroke
  • Progressive heart failure
  • Sudden cardiac death
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12
Q

What causes Cerebral Damage in systemic hypertensive heart disease?

A
  • Cerebral vessels affected by arteriolosclerosis are weakened and more likely to rupture, causing intracerebral hemorrhage
  • Lacunar infarcts
  • Hypertensive encephalopathy
    • Headaches, confusion, vomiting, convulsions
    • Increased CSF pressure
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13
Q

How can Renal Damage differ in systemic hypertensive heart disease?

A
  • Benign hypertension
    • Kidneys usually atrophic; granular, pitted surfaces
    • Hyaline arteriolosclerosis of vessels results in ischemia and atrophy
    • Glomeruli may become sclerosed
  • Malignant hypertension
    • Pinpoint petechial hemorrhages on surface
    • Fibrinoid necrosis of arterioles
    • Hyperplastic arteriolosclerosis and microthrombi lead to global ischemia
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14
Q

How does pulmonary hypertension affect the ventricles?

A

Cor pumonale:

  • right ventricular hypertrophy and/or dilatation
  • failure secondary to pulmonary hypertension
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15
Q

Causes and morphology of acute vs. chronic pulmonary hypertension:

A
  • Acute: massive pulmonary embolism
    • Dilatation of right ventricle without hypertrophy
  • Chronic: primary pulmonary hypertension or secondary pulmonary hypertension due to chronic lung diseases
    • Right ventricular hypertrophy, up to 1 cm in thickness, secondary to pressure overload
    • Obstruction of pulmonary arteries/arterioles/septal capillaries
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16
Q

What is congestive heart failure?

A

Inability of the heart to pump blood at a rate to meet the needs of active tissues

  • Or can do so only from an elevated filling pressure
  • poor prognosis
17
Q

What does CHF usually result from?

A

Usually results from a slowly developing intrinsic deficit in contraction, (but occasionally occurs acutely)

18
Q

What are the possible mechanisms of CHF (acute vs. chronic)?

A
  • Abnormal load presented to heart
    • Acutely: fluid overload, MI, valve dysfunction
    • Chronically: ischemic heart disease, dilated cardiomyopathy, hypertension
  • Impaired ventricular filling
    • Acutely: pericarditis or tamponade
    • Chronically: restrictive cardiomyopathy, severe left ventricular hypertrophy
  • Obstruction due to valve stenosis
    • Chronically: rheumatic valve disease (usually mitral valve)
19
Q

CHF – Systolic vs. diastolic dysfunction:

A
  • Systolic dysfunction: progressive deterioration of cardiac (contractile) function
    1. Ischemic heart disease
    2. Pressure or volume overload
    3. Dilated cardiomyopathy
  • Diastolic dysfunction: inability of heart to relax, expand, and fill sufficiently during diastole
    1. Massive left ventricular hypertrophy
    2. Amyloidosis
    3. Myocardial fibrosis
    4. Constrictive pericarditis
20
Q

Describe the Frank-Starling compensatory mechanism in CHF:

A
  • Frank-Starling mechanism
    • increased preload dilation (increased end diastolic filling volume) helps to sustain cardiac performance by enhancing contractility (lengthened fibers contract more forcibly)
  • Does result in increased wall tension & oxygen requirements
21
Q

Describe the activation of neurohumoral systems in CHF:

A
  • Release of norepinephrine by cardiac nerves:
    • increase heart rate, myocardial contractility, & vascular resistance
  • Activation of RAA system:
    • increased Na and water resorption, increases cardiac output and increased vasoconstriction
  • Release of atrial natriuretic peptide:
    • secreted from atrial myocytes when atrium is dilated, causing vasodilation, diuresis
22
Q

What is cardiac hypertrophy a response to?

A

Compensatory response to increased load occurring over weeks to months

  • Increased numbers of sarcomeres makes fibers visibly bigger
  • No hyperplasia
23
Q

How can the extent of hypertrophy determine the underlying cause?

A
  • 600 g:
    • pulmonary hypertension & ischemic heart disease
  • 800 g:
    • systemic hypertension, aortic stenosis, mitral regurgitation, dilated cardiomyopathy
  • 1000 g:
    • aortic regurgitation, hypertrophic cardiomyopathy
24
Q

Pressure overload vs. volume overload hypertrophy:

A
  1. Pressure overload: concentric hypertrophy
    • HTN, aortic stenosis
  2. Volume overload: hypertrophy accompanied by dilatation (eccentric hypertrophy)
    • Mitral or aortic regurgitation
25
Q
  1. What will pressure overload increase?
  2. What will volume overload increase?
A
  1. Pressure overload → ↑ systolic wall stress
  2. Volume overload → ↑ diastolic wall stress
26
Q

How does sustained cardiac hypertrophy often evolve to cardiac failure?

A
  • Increased myocyte size results in:
    • decreased capillary density
    • increased intercapillary distance
    • increased fibrous tissue
  • Higher cardiac oxygen consumption
  • Altered gene expression and proteins
  • Loss of myocytes due to apoptosis
27
Q

What is LVH an independent risk factor for?

A

sudden death

28
Q

What is left-sided heart failure primarily due to?

A
  1. progressive damming of blood within the pulmonary circulation
  2. diminished peripheral blood pressure and flow
29
Q

What are causes of left-sided heart failure?

A
  1. Ischemic heart disease
  2. Hypertension
  3. Aortic and mitral valve diseases
  4. Non-ischemic myocardial diseases
    • Cardiomyopathies
    • Myocarditis
30
Q

Besides sudden death, what can LVH (and sometimes dilation) result in?

A

mitral valve insufficiency

31
Q

What can enlargement of the left atrium result in?

A

Secondary enlargement of left atrium → atrial fibrillation → stagnant blood in atrium → thrombus, embolic stroke

32
Q

What are the effects of left-sided heart failure on the lung?

A

↑ pressure in pulmonary veins which is transmitted to capillaries and arteries

  • Pulmonary congestion and edema
  • Heart failure cells
  • Dyspnea (shortness of breath), orthopnea (dyspnea when recumbent) and paroxysmal nocturnal dyspnea
    • When supine, venous return increases & diaphragms elevate
  • Rales on exam
33
Q

What are the effects of left-sided heart failure on the kidneys?

A

↓ renal perfusion activates renin-angiotensin-aldosterone system → increased blood volume

  • If perfusion deficit is severe → prerenal azotemia (impaired kidney function due to low perfusion)
34
Q

What are the effects of left-sided heart failure on the brain?

A

cerebral hypoxia and encephalopathy

35
Q

What is right-sided heart failure primarily due to?

A

engorgement of systemic and portal venous systems

36
Q

What are causes of right-sided heart failure?

A
  1. Secondary to left-sided failure, usually
  2. Pulmonary hypertension
  3. Primary myocardial disease
  4. Tricuspid or pulmonary valvular disease
37
Q

Right-sided heart failure: Clinical effects and morphology

  • Heart
  • Liver and portal systems
  • Kidneys
  • Brain
A
  • Heart
    • Right ventricle responds to the increased workload with hypertrophy and often dilatation
  • Liver and portal systems
    • Elevated pressure in the portal vein leads to congestive hepatosplenomegaly, cardiac cirrhosis, ascites
  • Kidneys
    • congestion, fluid retention, peripheral edema, azotemia (more marked with right heart failure than left)
  • Brain
    • venous congestion and hypoxic encephalopathy
38
Q

What can be seen systemically in right-sided heart failure?

A
  • Pleural and pericardial effusion, atelectasis
  • Peripheral edema
    • At ankle (pedal)
    • Presacral
  • Eventual anasarca (generalized massive edema)
39
Q

Azotemia in Right vs. Left sided heart failure:

A
  1. Right sided heart failure causes venous congestion of kidneys
    • More impairment of function than with left sided heart failure
  2. Left sided heart failure causes low arterial flow to kidneys
    • Usually less severe impairment than secondary to right sided heart failure

Cardiovascular System (35 decks)

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