153 - Hypertension Flashcards

1
Q

Proportion of Australians over 18 who are hypertensive

A

~30%

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2
Q

Arbitrary definition of hypertension

A

Systolic over 140mmHg and diastolic over 90mmHg

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3
Q

Primary/essential hypertension

A

No specific identifiable cause.

Responsible for 90-95% of hypertension

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4
Q

Secondary hypertension

A

Identifiable pathology that is causing hypertension

5-10% of hypertension

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5
Q

Benign hypertension

A

Blood pressure rises gradually, over a long period.

Majority of cases.

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6
Q

Malignant hypertension

A

Blood pressure rises rapidly, over a short period.

Minority of cases.

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7
Q

Two forces that leads to blood pressure

A

Cardiac output (stroke volume, heart rate, blood volume) and resistance in arteiroles.

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8
Q

Aortic changes from age
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3

A

Aorta: loss of elasticity, hardening i.e. ‘arteriosclerosis’
Media: fragmentation of elastin, increased collagen
Intima: increased collagen

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9
Q

What effect does hypertension have on blood vessels?

A

Exacerbates age-related changes.
Aorta: loss of elasticity, hardening i.e. ‘arteriosclerosis’
Media: fragmentation of elastin, increased collagen
Intima: increased collagen

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10
Q

Age-related arterial changes in small and medium arteries
1
2

A

– Media: fragmentation of elastin, increased collagen, sometimes calcification
– Intima: increased collagen -> thickening

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11
Q
Age-related arteriolar changes 
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A

Arteriolar hyalinosis/hyaline arteriolosclerosis
– Deposition of plasma proteins in wall
– Increased collagen
– Smooth muscle atrophy
–Arteriole wall becomes thickened by homogenous eosinophilic glassy material (‘hyaline’) and the lumen narrowed

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12
Q

Arteriolar change in hypertension, or with age

A

Arteriolar hyalinosis/hyaline arteriosclerosis

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13
Q

What can hyaline arteirolosclerosis lead to?

A

Can slightly increase diastolic blood pressure with age.

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14
Q
Genetic predispositions to primary hypertension 
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A

– Polygenic genetic influences. Genetic polymorphisms may influence for example
• Sympathetic responses
• Transport of ions across cell membranes in vessels or kidney
• Arteriolar responses to local regulatory factors
• Activity of components of the renin-angiotensin-aldosterone system and secretion of renin
• Genetic determinants may also influence target organ damage

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15
Q
Lifestyle factors contributing to primary hypertension
1
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3
4
A
  • Amount of salt in diet
  • Alcohol intake
  • Levels of physical activity
  • Abdominal obesity and metabolic syndrome (can influence e.g. renal sodium retention, increased sympathetic activity, ion transport across cell membranes)
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16
Q

Age, gener, race predispositions to primary hypertension
1
2

A
  • Prevalence lower in premenopausal females than in age-matched males and in postmenopausal women
  • Higher in those of African descent
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17
Q

Broad divisions of primary hypertension

A

High plasma renin and low plasma renin.

Possibly correlate with vasoconstrictor and volume-dependent forms of hypertension.

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18
Q

Systolic hypertension with wide pulse pressure
1
2

A

Several groups:
• Decreased compliance of aorta (arteriosclerosis).
Age related changes –> loss of elasticity -> elevation of the systolic pressure and widening of the pulse pressure. If excessive -> isolated systolic hypertension

• Increased stroke volume e.g. aortic regurgitation, hyperthyroidism, fever (can treat some of these causes)

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19
Q

Most common pathology leading to secondary hypertension

A

Renal disease

EG: diabetic glomerulosclerosis, certain glomerulonephritides, polycystic renal disease, chronic renal diseas

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20
Q
Examples of non-renal causes of secondary hypertension 
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A

– Endocrine e.g. adrenocortical adenoma producing cortisol or aldosterone, phaeochromocytoma, pituitary adenoma producing ACTH

– Vascular e.g. coarctation of aorta, renal artery stenosis

– Medications e.g. corticosteroids, oestrogen

– Other e.g. neurogenic/cerebral, hypercalcemia, toxaemia of pregnancy, obstructive sleep apnoea, cocaine use

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21
Q

Coarctation of the aorta

A

Congenital narrowing of aorta

22
Q

Does atherosclerosis cause hypertension

A

Under certain circumstances.

EG when it is stenosing renal arteries.

23
Q

Effects of essential hypertension

A

Causes complications by causing concentric left ventricular hypertrophy and by predisposing to pathology in arteries and arterioles.

24
Q

Examples of arterial and arteriolar effects of hypertension
1
2
3

A

• Large and medium sized arteries
- Atherosclerosis
- Aortic dissection
•Medium arteries: berry aneurysm (Circle of Willis)
•Arterioles: hyaline arteriolosclerosis/arteriolar hyalinosis

25
Q

What is an aneurysm most directly related to?

A

Weakening of media.

Arterial wall can normally withstand increased pressure from hypertension, but will only dilate if media is weakened.

26
Q

Where is the blood in an aortic dissection?

A

Between inner 2/3 and outer 1/3 of media

27
Q

What causes the majority of myocardial infarcts?

A

Atherosclerosis with thrombosis of a coronary vessel

28
Q

Effect of hypertension on heart function

A

Can predispose to myocardial infarcts from coronary vessel atherosclerosis

29
Q

Effect of concentric hypertrophy on LV chamber size

A

Doesn’t actually change it that much. The chamber walls can stretch to accommodate blood.

30
Q

Effects of concentric hypertrophy on LV
1
2
3

A

1) Impairing diastolic filling (pressure is too high)
2) Increasing the myocardial oxygen demand
3) Reducing the coronary perfusion (increased pressure in wall increases capillary pressure, which reduces the pressure gradient between coronary arteries and capillaries

31
Q
What are individuals with concentric hypertrophy at increased risk of?
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A

1) Angina
2) Myocardial infarction
3) Congestive cardiac failure
4) Atrial fibrillation
5) Sudden cardiac death

32
Q

How is hypertension a risk factor for renal injury?
1
2

A

Two theories (neither might be the case):

• Transmission of elevated pressures to glomeruli –> sclerosis

•Hyaline arteriolosclserosis -> chronic ischaemia
Proteinuria is a marker of the severity of chronic kidney disease and is a predictor of its progression

33
Q
Benign nephrosclerosis
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3
4
A

Age-related.
Rough surface of kidney.
Atrophy of nephrons.
Because of arteriolosclerosis

34
Q

How can hypertension exacerbate age-related benign nephrosclerosis?

A

Can lead to arteriolosclerosis.

35
Q

Histological features of benign nephrosclerosis
1
2
3

A

1) Interstitial scarring
2) Chronic inflammation
3) Atrophic glomeruli and tubules
4) Sclerosed glomeruli

36
Q

What does chronic injury of a glomerulus lead to?

A

Sclerosis of the glomerulus

37
Q

Characteristic histological feature of thrombo-emoli

A

Cholesterol crystal plaques

38
Q

Most common cause of cerebral infarctions

A

Thrombo-emboli

39
Q

Biggest risk factor for cerebral haemorrhages

A

Hypertension (leads to arteriolosclerosis)

40
Q

Lacunar infarctions

A

Small infarctions in the brain, from hyalinised vessels occluding flow.

41
Q

Effects of hypertension on the retina

A

AV nipping.
Exudates.
Haemorrhages.
These changes are caused by hyaline arteriolosclerosis

42
Q
How to assess a hypertensive patient 
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A

• Complete history and physical examination to:
– Confirm diagnosis: guidelines for measuring BP and confirming diagnosis
– Seek other cardiovascular risk factors and assess absolute cardiovascular risk (risk of a cardiovascular event occurring within the next 5 years)
– Seek secondary causes of HT
– Identify end-organ damage
– Seek comorbidities
– Determine the potential for intervention, including lifestyle modification

43
Q

Malignant hypertension or hypertensive emergency development

A

May develop de novo in those with normal BP or in those with pre-existing essential HT

44
Q

Complications of malignant hypertension
1
2

A
  • Hyperplastic arteriolosclerosis

* Fibrinoid necrosis and thrombosis

45
Q

Differences in vascular changes between benign and malignant hypertension

A

Benign has hyaline arteriolosclerosis.

Malignant has hyperplastic arteriolosclerosis

46
Q

Hyperplastic arteriolosclerosis

A

Onion-skin appearance, with increased layers of media.

Can have fibrinoid necrosis

47
Q

Effect of hyperplastic arteirolosclerosis on kidney

A

Deteriorating renal function

48
Q

Effect of hyperplastic arteirolosclerosis on the retina

A

Retinopathy (arteriolar spasm, haemorrhages, exudates, papilledema)

49
Q

Effect of hyperplastic arteirolosclerosis on brain

A

Encephalopathy. Failure of autoregulation of cerebral blood flow, hyperperfusion and cerebral oedema

50
Q

Effect of hyperplastic arteirolosclerosis on blood

A

Microangiopathic haemolytic anaemia