Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Morphology of HTN in Small arteries/arterioles

A

 Hyaline arteriolosclerosis  Hyperplastic arteriolosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hyaline arteriolosclerosis is seen in:

• Similar change in diabetics (microangiopathy) with _______nephrosclerosis

A

Elderly patients

“Benign”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the disease state below?

Descriptions?

A

Hyaline arterioloscloerosis

Homogeneous pink, thickening of vessels with narrowing of
lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Hyperplastic arteriolosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes the onion skinning we see in hyperplastic arteriolosclerosis?

A

reduplicated basement membrane adn smooth muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

necrotizing arteriolitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

left sided

right sided

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Concentric left ventricular hypertrophy in
the absence of other cardiovascular pathology

A

Systemic Hypertensive Heart Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is going on with the image on the right?

A

myocyte hypertrophy

increase myocyte size and nuclear enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What renal damage can result from systemic hypertensive heart disease?

A

Benign or malignant hypertenion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Whats going on with this kidney?

A

Systemic Hypertensive Heart
Disease: Renal Damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

Cor pulmonale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

Acute:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Causes and morphology of Cor pulmonale (Pulmonary hypertensive heart disease) 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
26
Below we see RV hypertrophy which can result from what set of disease? Has both acute and chronic causes?
Cor pulmonale or pulmonary hypertenisive heart disease
27
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
Congestive Heart failure
28
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
Congestive heart failure
29
CHF pathogenesis
Usually results from a slowly developing intrinsic deficit in contraction, (but occasionally occurs acutely)
30
Mechanisms of heart fail
Abnormal load presented to the heart Impaired ventricle filling time obstruciton dt valve stenosis
31
In CHF pathogenesis Abnormal load presented to heart  Acutely we see :  Chronically we see:
 Acutely: fluid overload, MI, valve dysfunction  Chronically: ischemic heart disease, dilated cardiomyopathy, hertension
32
In heart failure we have impaired ventricular filling  Acutely:  Chronically:
Impaired ventricular filling  Acutely: pericarditis or tamponade  Chronically: restrictive cardiomyopathy, severe left ventricular hypertrophy
33
In CHF there can be obstruction due to valve stenosis  Chronically:
rheumatic valve disease (usually mitral valve)
34
Describe systolic dysfunction seen in CHF pathogenesis
– Systolic dysfunction: progressive deterioration of cardiac (contractile) function • Ischemic heart disease • Pressure or volume overload • Dilated cardiomyopathy
35
Describe diastolic dysfunction seen in CHF:
inability of heart to relax, expand, and fill sufficiently during diastole • Massive left ventricular hypertrophy • Amyloidosis • Myocardial fibrosis • Constrictive pericarditis
36
Describe the rapidly occuring compensatory mechanism for CHF --involves Frank-Starling mech and is compensatory mech 1
– 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
Rapidly occurring compensatory mechanism for CHF we see activation of neurohumoral systems • Release of norepinephrine by cardiac nerves:
increase heart rate, myocardial contractility, & vascular resistance
38
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
increased Na and water resorption, increases cardiac output and increased vasoconstriction
39
Rapidly occurring compensatory mechanism for CHF we see release of atrial natriuretic peptide:
secreted from atrial myocytes when atrium is dilated, causing vasodilation, diuresis
40
Rapidly occurring compensatory mechanism for CHF we see
41
Cardiac Hypertrophy is a compensatory mechanism to HTN... – Compensatory response to \_\_\_\_\_\_occurring over weeks to months – Increased numbers of sarcomeres makes fibers:
increased load visibly bigger but no hyperplasia
42
Extent of hypertrophy varies with underlying cause – 600 g: – 800 g: – 1000 g:
600: pulmonary hypertension & ischemic heart disease 800: systemic hypertension, aortic stenosis, mitral regurgitation, dilated cardiomyopathy 1000 :aortic regurgitation, hypertrophic cardiomyopathy
43
There are different patterns of hypertrophy and they reflect the nature of the stimulus Pressure overload: Volume overload:
Pressure overload: concentric hypertrophy • HTN, aortic stenosis – Volume overload: hypertrophy accompanied by dilatation • Mitral or aortic regurgitation
44
Parellel sarcomeres result in _____ with venticular remodeling while sarcomeres in series result in ______ when remodeling
concentric hypertrophy (thicker walls from pressure) Eccentric hypertrophy (dialated, from volume overload)
45
Sustained cardiac hypertrophy often evolves to cardiac failure; we will see
– 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
This is an independent risk factor for sudden death
LVH (left ventricular hypertrophy)
47
Effects primarily due to progressive damming of blood within the pulmonary circulation and diminished peripheral blood pressure and flow
Left sided heart fail
48
Causes of left sided heart failure
Ischemic heart disease – Hypertension – Aortic and mitral valve diseases – Non-ischemic myocardial diseases • Cardiomyopathies • Myocarditis
49
What morphology, in regards to the heart, do we see in left sided heart fail?
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
What clinical effects do we see in the lungs from Left sided heart failure?
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
This is from the lungs... what's going on?
pulmonary edema; we can see hemosiderine-laden macrophages = Heart fail cells
52
What clinical effects do we see in the kidneys as a result of Left sided heart fail?
Kids have decreased renal perfusion--\> activates RAAS--\> then increases blood volume \*severe perfusion deficit--\> prerenal azotomia (imparied kid fnx dt low perfusion)
53
What clincal effects do we see in the brain as a result of both right and left sided heart fail?
cerebral hypoxia and encephalopathy
54
Right-Sided Heart Failure • Effects are primarily due to
engorgement of systemic and portal venous system:
55
Causes of Right sided heart fail
– Secondary to left-sided failure, usually – Pulmonary hypertension – Primary myocardial disease – Tricuspid or pulmonary valvular disease
56
Clincal effects on the heart from right sided HF
Heart: ◦ Right ventricle responds to the increased workload with hypertrophy and often dilatation
57
Effects to the liver and kidneys from right sided heart failure
 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
In right sided heart fail, we see bad edema... describe
 Pleural and pericardial effusion, atelectasis  Peripheral edema ◦ At ankle (pedal) and Presacral  Eventual anasarca (generalized massive edema)
59
These are symptoms of Pulmonary congestion and edema prominent – Kidneys: reduced perfusion, fluid retention, azotemia less prominent – Brain: reduced perfusion, cerebral hypoxia and encephalopathy
Left sided heart fail
60
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
Right Sided heart failure
61
Whats going on with the kidneys in right sided heart failure?
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
Whats going on in kidneys in left sided heart failure?
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
In right sided heart fail we see ________ of the kidneys In left sided heart fail we see _______ of the kidneys
venous congestion low areterial flow

CV Final Material (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions