Pathology of Hypertension Flashcards Preview

Cardiovascular System > Pathology of Hypertension > Flashcards

Flashcards in Pathology of Hypertension Deck (39):
1

Hypertension – morphology

  • Large/medium arteries:
  • Small arteries/arterioles:

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

2

Which age group is hyaline arteriolosclerosis usually seen in?

Elderly patients

3

What is the morphology of hyaline arteriolosclerosis?

  • 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

A image thumb
4

What does hyaline arteriolosclerosis typically characterize?

“Benign” nephrosclerosis

5

What does hyperplastic arteriolosclerosis typically characterize?

Characteristic of malignant hypertension
 

6

What is the morphology of hyperplastic arteriolosclerosis?

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

A image thumb
7

Malignant hypertension – morphology:

Necrotizing arteriolitis:

  • term used when these changes are associated with fibrinoid necrosis

8

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

  • Systemic hypertensive heart disease ⇒ left sided
  • Pulmonary hypertensive heart disease ⇒ right sided

9

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

  • 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

10

Systemic Hypertensive Heart Disease: morphology

  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

11

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

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

12

What causes Cerebral Damage in systemic hypertensive heart disease?

  • 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

13

How can Renal Damage differ in systemic hypertensive heart disease?

  • 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

14

How does pulmonary hypertension affect the ventricles?

Cor pumonale:

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

15

Causes and morphology of acute vs. chronic pulmonary hypertension:

  • 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

16

What is congestive heart failure?

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

What does CHF usually result from?

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

18

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

  • 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

CHF – Systolic vs. diastolic dysfunction:

  • 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

Describe the Frank-Starling compensatory mechanism in CHF:

  • 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

Describe the activation of neurohumoral systems in CHF:

  • 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

What is cardiac hypertrophy a response to?

Compensatory response to increased load occurring over weeks to months

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

23

How can the extent of hypertrophy determine the underlying cause?

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

24

Pressure overload vs. volume overload hypertrophy:

  1. Pressure overload: concentric hypertrophy
    •  HTN, aortic stenosis
  2. Volume overload: hypertrophy accompanied by dilatation (eccentric hypertrophy)
    • Mitral or aortic regurgitation

25

  1. What will pressure overload increase? 
  2. What will volume overload increase?

  1. Pressure overload → ↑ systolic wall stress
  2. Volume overload → ↑ diastolic wall stress

26

How does sustained cardiac hypertrophy often evolve to cardiac failure?

  • 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

What is LVH an independent risk factor for?

sudden death

28

What is left-sided heart failure primarily due to?

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

29

What are causes of left-sided heart failure?

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

30

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

mitral valve insufficiency

31

What can enlargement of the left atrium result in?

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

32

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

↑ 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

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

↓ 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

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

cerebral hypoxia and encephalopathy

35

What is right-sided heart failure primarily due to?

engorgement of systemic and portal venous systems

36

What are causes of right-sided heart failure?

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

37

Right-sided heart failure: Clinical effects and morphology

  • Heart
  • Liver and portal systems
  • Kidneys
  • Brain

  • 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

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

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

39

Azotemia in Right vs. Left sided heart failure:

  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