Pathology of Hypertension

Question 1

Hypertension – morphology

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

Answer 1

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

Question 2

Which age group is hyaline arteriolosclerosis usually seen in?

Answer 2

Elderly patients

Question 3

What is the morphology of hyaline arteriolosclerosis?

Answer 3

• 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

Question 4

What does hyaline arteriolosclerosis typically characterize?

Answer 4

“Benign” nephrosclerosis

Question 5

What does hyperplastic arteriolosclerosis typically characterize?

Answer 5

Characteristic of malignant hypertension

Question 6

What is the morphology of hyperplastic arteriolosclerosis?

Answer 6

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

Question 7

Malignant hypertension – morphology:

Answer 7

Necrotizing arteriolitis:

• term used when these changes are associated with fibrinoid necrosis

Question 8

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

Answer 8

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

Question 9

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

Answer 9

• 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

Question 10

Systemic Hypertensive Heart Disease: morphology

Answer 10

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

Question 11

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

Answer 11

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

Question 12

What causes Cerebral Damage in systemic hypertensive heart disease?

Answer 12

• 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

Question 13

How can Renal Damage differ in systemic hypertensive heart disease?

Answer 13

• 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

Question 14

How does pulmonary hypertension affect the ventricles?

Answer 14

Cor pumonale:

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

Question 15

Causes and morphology of acute vs. chronic pulmonary hypertension:

Answer 15

• 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

Question 16

What is congestive heart failure?

Answer 16

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

Question 17

What does CHF usually result from?

Answer 17

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

Question 18

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

Answer 18

• 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)

Question 19

CHF – Systolic vs. diastolic dysfunction:

Answer 19

• 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

Question 20

Describe the Frank-Starling compensatory mechanism in CHF:

Answer 20

• 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

Question 21

Describe the activation of neurohumoral systems in CHF:

Answer 21

• 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

Question 22

What is cardiac hypertrophy a response to?

Answer 22

Compensatory response to increased load occurring over weeks to months

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

Question 23

How can the extent of hypertrophy determine the underlying cause?

Answer 23

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

Question 24

Pressure overload vs. volume overload hypertrophy:

Answer 24

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

Question 25

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

Answer 25

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

Question 26

How does sustained cardiac hypertrophy often evolve to cardiac failure?

Answer 26

* _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_

Question 27

What is **LVH an independent risk factor** for?

Answer 27

**sudden death**

Question 28

What is **left-sided heart failure primarily due to**?

Answer 28

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

Question 29

What are causes of left-sided heart failure?

Answer 29

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

Question 30

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

Answer 30

**mitral valve insufficiency**

Question 31

What can **enlargement of the left atrium** result in?

Answer 31

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

Question 32

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

Answer 32

**↑ 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

Question 33

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

Answer 33

**↓ renal perfusion activates renin-angiotensin-aldosterone system → increased blood volume** * If perfusion deficit is severe → _prerenal azotemia_ (impaired kidney function due to low perfusion)

Question 34

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

Answer 34

**cerebral hypoxia and encephalopathy**

Question 35

What is **right-sided heart failure primarily due to**?

Answer 35

**engorgement of systemic and portal venous systems**

Question 36

What are causes of right-sided heart failure?

Answer 36

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

Question 37

Right-sided heart failure: **Clinical effects and morphology** * Heart * Liver and portal systems * Kidneys * Brain

Answer 37

* **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_

Question 38

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

Answer 38

* _Pleural and pericardial effusion_, atelectasis * _Peripheral edema_ * At ankle (pedal) * Presacral * Eventual _anasarca_ (generalized massive edema)

Question 39

**Azotemia in Right vs. Left sided heart failure:**

Answer 39

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