Pathology of Hypertension Flashcards

1
Q

Definition of hypertension

A

Disorder in which the level of sustained arterial pressure is higher than expected for the age, sex, and race of the individual

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2
Q

Accepted value of hypertension and flaw?

A

Greater than 140/90 mmHg

But there is normal variation in BP and around 25% of the population have unknown hypertension

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3
Q

Cautions when taking and interpreting BP readings?

A

Normal variation in individuals at different times of day - REPEAT measurements

WHITE COAT hypertension - nervousness of having BP reading taken

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4
Q

Two types of BP, in relation to variation?

A

Stable - not much variation (more effective remodelling than in labile)

Labile - great variation in readings at different times (likely to be worse in terms of complications)

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5
Q

What does hypertension CAUSE?

A

Cardiac failure

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6
Q

Hypertension is a risk factor for?

A

Cerebral haemorrhage
Atheroma; also, increased rate of progression of that atheroma
Renal failure
Sudden cardiac death

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7
Q

Where are when is hypertension more common?

A

Higher in Black populations
If there is a familial tendency
Rises with age

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8
Q

Types of classification of hypertension?

A

According to cause (aetiological):
Primary
Secondary

According to consequences (clinicopathological):
Benign
Malignant

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9
Q

How can BP change?

A

Changes in CO due to changes in:
HR
Contractility (SV)
Blood volume (SV)

Changes in TPR due to:
Vasoconstrictors, e.g: Ang. II and catecholamines (adrenaline, noradrenaline)
Vasodilators, e.g: NO, certain prostaglandins

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10
Q

What do SBP and DBP mean?

A

SBP - peak BP that coincides with left ventricular ejection

DBP - baseline below which BP does not fall and coincides with left ventricular relaxation

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11
Q

What are the resistance arteries?

A

Arterioles contribute most to TPR

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12
Q

Main regulation of the RAAS system?

A

Mainly, renal blood flow (kidneys and brain auto-regulate blood flow)
If BP decreases, renin is released

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13
Q

Function of Ang. II?

A

First bio-active component of the RAAS system:
Vasoconstrictor

Aldosterone (mineralocorticosteroid) release causes Na+ and water retention to increase blood volume

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14
Q

Reason for which RAAS system activity may be high?

A

Due to polymorphisms in renin, etc

May contribute to familial hypertension

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15
Q

What is primary hypertension?

A

Majority (90%) of cases have NO OBVIOUS CAUSE

Genetic factors are strongly implicated - from twin studies

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16
Q

How can protein intake affect BP?

A

Increased protein intake, increases renal blood flow so more RAAS activity

17
Q

What is salt-sensitive hypertension?

A

Where an increase in dietary salt increases BP (controlled by a reduced salt diet) - due to genetic polymorphisms

NOT ALL PRIMARY HYPERTENSIVES ARE SALT-SENSITIVE

18
Q

What type of hypertension is normally salt-sensitive?

A

Hypertension secondary to renal disease

19
Q

What is secondary hypertension?

A
Underlying disease is implicated, e.g:
Renal disease (most common secondary cause)
Endocrine disease
Aortic disease
Renal artery stenosis
Drug therapy
20
Q

Renal causes of secondary hypertension?

A
Any renal disease, e.g: diabetic renal disease (almost all diabetics become hypertensive)
Renal artery stenosis
Acute/chronic glomerulonephritis
Chronic pyelonephritis
Cystic diseases
Interstitial nephritis
21
Q

How do renal disease cause hypertension?

A

Reduced renal blood flow so excess renin release

Salt and water overload increase blood volume

22
Q

Endorcrine causes of hypertension?

A

Adrenal gland hyperfunction/tumours:

Conn’s Syndrome (primary aldosteronism) - excess aldosterone
Cushing’s syndrome - excess corticosteroid
…adrenal cortex responsible for these two

Phaeochromocytoma - tumour of adrenal medulla leading to excess noradrenaline

23
Q

How does coarctation of the aorta cause hypertension?

A

Congenital narrowing of segments of the aorta (increase in resistance)

24
Q

Example of drugs which cause hypertension?

A

Corticosteroids

25
Q

What is benign hypertension?

A

Remains a cause of serious life-threatening mortality

ASYMPTOMATIC - incidental findings often in health checks

26
Q

Benign hypertension is a risk factor for?

A

Left ventricular hypertrophy (increased left ventricular load as pumping into a greater resistance)

Congestive cardiac failure

Increases atheroma

Increases aneurysm (sacular dilatations) rupture - aortic dissection, Berry aneurysms (within brain circulation)

Renal disease

Stroke

27
Q

Consequences of left ventricular hypertrophy?

A

Increased left ventricular load
Poor perfusion (due to thickening, particularly to subendocardial part of the heart)
Interstitial fibrosis
Micro-infarcts (causes small areas of scarring)
Diastolic dysfunction (left ventricle unable to dilate properly, so filling of left ventricle is impaired)

28
Q

Left venticular hypertrophy increases risk of?

A

Sudden cardiac death - due to arrhythmias and poor perfusion

Cardiac failure

Affects outcomes of other diseases

29
Q

How can hypertrophy due to hypertension be distinguished from hypertrophy due to other causes?

A

Hypertensive hypertrophy tends to be concentric

30
Q

Consequences of fibrosis in hypertension?

A

Lots of collagen laid down

Contraction becomes ineffective (as fibrous tissue is not contractile) leading to cardiac failure

31
Q

What are microvascular changes?

A

Blood vessel wall changes - small arteries and arterioles
Can occur in the retina and kidney

Thickening of media

HYALINE ARTERIOSCLEROSIS - plasma proteins are forced into the vessel walls (thickening)

32
Q

What is malignant hypertension?

A

Serious life-threatening condition (diastolic 130-140 mmHg)

Can develop from either benign primary or secondary hypertension (“accelerated” hypertension), or arise (rarely) de-novo

Requires urgent treatment to prevent death

33
Q

What does malignant hypertension cause?

A

Causes cerebral oedema - seen as papilloedema (swelling of optic disc)

Acute renal failure

Acute heart failure

Headache and cerebral haemorrhage

Blood vessels show fibrinoid necrosis (accumulation of amorphous, basic, proteinaceous material in the tissue matrix with a staining pattern reminiscent of fibrin); fibrin is deposited and there is endarteritis proliferans of their walls (marked increased in the fibrous tissue of the intima)

34
Q

Consequences of pregnancy-associated hypertension?

A

Increased maternal and fetal morbidity and mortality

Can be pre-eclampsia - hypertension associated with protein urea, which resolves following birth
Can sometimes progress to eclampsia (obstetric emergency) - onset of seizures in a women with pre-eclampsia

35
Q

Other causes of hypertension during pregnancy?

A

Occasionally, in mothers, hypertension secondary to silent renal or systemic disease may be encountered