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CV Final Material > HTN Pathology > Flashcards

HTN Pathology Flashcards

1
Q

Morphology of HTN and associated risks in Large/medium arteries

A

 Accelerated atherogenesis  Degenerative changes in vascular walls  Increased risk of aortic dissection & cerebrovascular hemorrhage

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2
Q

Morphology of HTN in Small arteries/arterioles

A

 Hyaline arteriolosclerosis  Hyperplastic arteriolosclerosis

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3
Q

Hyaline arteriolosclerosis is seen in:

• Similar change in diabetics (microangiopathy) with _______nephrosclerosis

A

Elderly patients

“Benign”

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4
Q

What is the disease state below?

Descriptions?

A

Hyaline arterioloscloerosis

Homogeneous pink, thickening of vessels with narrowing of
lumen

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5
Q

In hyaline arteriolosclerosis we see Leakage of plasma across endothelium due to______

▫ Excess matrix production by the _________occurs secondarily

A

HTN

smooth muscle cells

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6
Q

You see Onion-skinning, concentric laminated
walls with luminal narrowing. This is characteristic of?

A

Hyperplastic arteriolosclerosis

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7
Q

What causes the onion skinning we see in hyperplastic arteriolosclerosis?

A

reduplicated basement membrane adn smooth muscle cells

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8
Q

Pt has malignant hypertenstion. On microscopy you see fibrinoid necrosis (seen below). What is this?

A

necrotizing arteriolitis

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9
Q

Hypertensive Heart Disease
• Systemic hypertensive heart disease
–
• Pulmonary hypertensive heart
disease –

A

left sided

right sided

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10
Q

Concentric left ventricular hypertrophy in
the absence of other cardiovascular pathology

A

Systemic Hypertensive Heart Disease

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11
Q

To be diagnosed with systemic hypertensive heart disease you must have a history or pathologic evidence of
hypertension >

*25% US diagnosed with this

A

140/90 mm Hg

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12
Q

systemic hypertensive disease morphology:

A

*Cardiomegaly: Concentric hypertrophy without
dilatation, >1.5 cm wall thickness, 500 – 600 g.
* Thickness of left ventricular wall impairs
diastolic filling and causes left atrial enlargement
*Myocyte hypertrophy
– Increased myocyte size & nuclear enlargement

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13
Q

What is going on with the image on the right?

A

myocyte hypertrophy

increase myocyte size and nuclear enlargement

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14
Q

What are possible clincial outcomes of systemic hypertensieve heart diease?

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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15
Q

Systemic Hypertensive heart disease causes cerebral damage: Cerebral vessels affected by arteriolosclerosis are

A

weakened and more likely to rupture, causing intracerebral
hemorrhage

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16
Q

Systemic Hypertensive heart disease causes cerebral damage such as

A
  • Lacunar infarcts
  • Hypertensive encephalopathy resluting in: Headaches, confusion, vomiting, convulsions and increased CSF pressure
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17
Q

What renal damage can result from systemic hypertensive heart disease?

A

Benign or malignant hypertenion

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18
Q

In Benign hypertension

kidneys are:

Hyaline arterioloscerlosis results in:

Glomeruli:

A

-Kidneys usually atrophic; granular, pitted surfaces
– Hyaline arteriolosclerosis of vessels results in ischemia and atrophy
– Glomeruli may become sclerosed

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19
Q

In Malignant hypertension we see
– these on the skin
– this type of damage to arterioles
– global ischemia as a result of

A

– Pinpoint petechial hemorrhages on surface
– Fibrinoid necrosis of arterioles
– Hyperplastic arteriolosclerosis and microthrombi lead to
global ischemia

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20
Q

Whats going on with this kidney?

A

Systemic Hypertensive Heart
Disease: Renal Damage

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21
Q

If you see this type of damage in the kidney, do you suspect benign or malignant hypertension?

A

This is showing hylaine arteriolosclerosis… this is found in benign HTN; results in ischemia and atrophy

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22
Q

If you see this from a kidney, what type of renal damag do you suspect?

A

This is hyperplastic ateriolosclerosis seen in malignant HTN

this leads to global ischemia

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23
Q

Right ventricular hypertrophy and/or dilatation and failure
secondary to pulmonary hypertension

A

Cor pulmonale

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24
Q

Causes and morphology of Cor pulmonale (Pulmonary hypertensive heart disease)

Acute:

A

– Acute: massive pulmonary embolism
• Dilatation of right ventricle without hypertrophy

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25
Q

Causes and morphology of Cor pulmonale (Pulmonary hypertensive heart disease)

Chronic

A

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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26
Q

Below we see RV hypertrophy which can result from what set of disease?

Has both acute and chronic causes?

A

Cor pulmonale or pulmonary hypertenisive heart disease

27
Q

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

A

Congestive Heart failure

28
Q

Common & recurrent condition with a poor prognosis
– Leading discharge diagnosis in hospitalized
patients over 65 years
– 1 million hospital admissions, 50,000 deaths/year
– Increasing prevalence

A

Congestive heart failure

29
Q

CHF pathogenesis

A

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

30
Q

Mechanisms of heart fail

A

Abnormal load presented to the heart

Impaired ventricle filling time

obstruciton dt valve stenosis

31
Q

In CHF pathogenesis

Abnormal load presented to heart
 Acutely we see :
 Chronically we see:

A

 Acutely: fluid overload, MI, valve dysfunction
 Chronically: ischemic heart disease, dilated cardiomyopathy,
hertension

32
Q

In heart failure we have impaired ventricular filling
 Acutely:
 Chronically:

A

Impaired ventricular filling
 Acutely: pericarditis or tamponade
 Chronically: restrictive cardiomyopathy, severe left ventricular
hypertrophy

33
Q

In CHF there can be obstruction due to valve stenosis
 Chronically:

A

rheumatic valve disease (usually mitral valve)

34
Q

Describe systolic dysfunction seen in CHF pathogenesis

A

– Systolic dysfunction: progressive deterioration of cardiac
(contractile) function
• Ischemic heart disease
• Pressure or volume overload
• Dilated cardiomyopathy

35
Q

Describe diastolic dysfunction seen in CHF:

A

inability of heart to relax, expand, and fill sufficiently during diastole
• Massive left ventricular hypertrophy
• Amyloidosis
• Myocardial fibrosis
• Constrictive pericarditis

36
Q

Describe the rapidly occuring compensatory mechanism for CHF

–involves Frank-Starling mech and is compensatory mech 1

A

– The 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

37
Q

Rapidly occurring compensatory mechanism for CHF we see activation of neurohumoral systems
• Release of norepinephrine by cardiac nerves:

A

increase heart rate, myocardial contractility, & vascular resistance

38
Q

Rapidly occurring compensatory mechanism for CHF we see activation of renin- angiotensin- aldosterone system:
increased Na and water resorption, increases cardiac
output and increased vasoconstriction

A

increased Na and water resorption, increases cardiac
output and increased vasoconstriction

39
Q

Rapidly occurring compensatory mechanism for CHF we see release of atrial natriuretic peptide:

A

secreted from atrial myocytes when atrium is dilated, causing vasodilation, diuresis

40
Q

Rapidly occurring compensatory mechanism for CHF we see

A
41
Q

Cardiac Hypertrophy is a compensatory mechanism to HTN…
– Compensatory response to ______occurring over weeks to months
– Increased numbers of sarcomeres makes fibers:

A

increased load

visibly bigger but no hyperplasia

42
Q

Extent of hypertrophy varies with underlying cause
– 600 g:
– 800 g:
– 1000 g:

A

600: pulmonary hypertension & ischemic heart disease

800: systemic hypertension, aortic stenosis, mitral
regurgitation, dilated cardiomyopathy

1000 :aortic regurgitation, hypertrophic cardiomyopathy

43
Q

There are different patterns of hypertrophy and they reflect the nature of the stimulus

Pressure overload:

Volume overload:

A

Pressure overload: concentric hypertrophy
• HTN, aortic stenosis
– Volume overload: hypertrophy accompanied by dilatation
• Mitral or aortic regurgitation

44
Q

Parellel sarcomeres result in _____ with venticular remodeling while sarcomeres in series result in ______ when remodeling

A

concentric hypertrophy (thicker walls from pressure)

Eccentric hypertrophy (dialated, from volume overload)

45
Q

Sustained cardiac hypertrophy often evolves to cardiac failure; we will see

A

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

46
Q

This is an independent risk factor for sudden death

A

LVH (left ventricular hypertrophy)

47
Q

Effects primarily due to progressive damming of
blood within the pulmonary circulation and
diminished peripheral blood pressure and flow

A

Left sided heart fail

48
Q

Causes of left sided heart failure

A

Ischemic heart disease
– Hypertension
– Aortic and mitral valve diseases
– Non-ischemic myocardial diseases
• Cardiomyopathies
• Myocarditis

49
Q

What morphology, in regards to the heart, do we see in left sided heart fail?

A

Heart:
– Left ventricular hypertrophy and often
dilation, often resulting in mitral valve insufficiency
– Secondary enlargement of left atrium

atrial fibrillation stagnant blood in
atrium thrombus, embolic stroke

50
Q

What clinical effects do we see in the lungs from Left sided heart failure?

A

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

51
Q

This is from the lungs… what’s going on?

A

pulmonary edema; we can see hemosiderine-laden macrophages = Heart fail cells

52
Q

What clinical effects do we see in the kidneys as a result of Left sided heart fail?

A

Kids have decreased renal perfusion–> activates RAAS–> then increases blood volume

*severe perfusion deficit–> prerenal azotomia (imparied kid fnx dt low perfusion)

53
Q

What clincal effects do we see in the brain as a result of both right and left sided heart fail?

A

cerebral hypoxia and encephalopathy

54
Q

Right-Sided Heart Failure
• Effects are primarily due to

A

engorgement of systemic and portal venous system:

55
Q

Causes of Right sided heart fail

A

– Secondary to left-sided failure, usually
– Pulmonary hypertension
– Primary myocardial disease
– Tricuspid or pulmonary valvular disease

56
Q

Clincal effects on the heart from right sided HF

A

Heart:
◦ Right ventricle responds to the increased workload with hypertrophy and often dilatation

57
Q

Effects to the liver and kidneys from right sided heart failure

A

 Liver and portal system:
◦ 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)

58
Q

In right sided heart fail, we see bad edema… describe

A

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

59
Q

These are symptoms of

Pulmonary congestion and edema prominent
– Kidneys: reduced perfusion, fluid retention, azotemia less prominent
– Brain: reduced perfusion, cerebral hypoxia and encephalopathy

A

Left sided heart fail

60
Q

These are symptoms of:
– Systemic and portal venous congestion
• Hepatosplenomegaly
• Peripheral edema
• Pleural effusion
• Ascites
– Kidneys: congestion, fluid retention and azotemia
more prominent
– Brain: venous congestion, hypoxia and
encephalopathy

A

Right Sided heart failure

61
Q

Whats going on with the kidneys in right sided heart failure?

A

Right sided heart failure causes venous congestion of kidneys
– More impairment of function than with left sided heart failure
– ? Secondary to lack of removal of metabolites in venous circulation (and, if congestion is severe, decrease and/or stasis on arterial side)

62
Q

Whats going on in kidneys in left sided heart failure?

A

Left sided heart failure causes low arterial flow to kidneys
– Usually less severe impairment than secondary to right sided heart failure
– ? Decrease and/or lack of nutrient supply to kidneys causes less damage than lack of metabolite removal

63
Q

In right sided heart fail we see ________ of the kidneys

In left sided heart fail we see _______ of the kidneys

A

venous congestion

low areterial flow

CV Final Material (16 decks)

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