Pathology 3 - Hypertension Flashcards

1
Q

What proportion of Australians Australians aged 18 and over are estimated to have high blood pressure or are on medication for that condition?

A

30%

More common as you get older

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2
Q

What is currently considered to be hypertension?

A

Systemic blood pressure above 90 mmHg diastolic and/or 140 mmHg systolic is generally regarded as too high

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3
Q

What is the most common type of hypertension?

A

Primary or ess

ential: no specific identifiable cause (90-95%

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4
Q

What is secondary hypertension?

A

Secondary (5-10%): identifiable cause

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5
Q

What are benign and malignant hypertension?

A

Benign = rises gradually
Malignant = BP gets to very high levels and rises rapidly
(both have significant complications)

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6
Q

What damage does high BP cause to the large arteries?

A

Arteriosclerosis (loss of elasticity and hardening)
–Media: fragmentation of elastin, increased collagen
–Intima: increased collagen

The aorta is a bit dilated with age

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7
Q

What damage does high BP cause to the small and medium arteries?

A

–Media: fragmentation of elastin, increased collagen, sometimes calcification

–Intima: increased collagen -> thickening

Can get narrowing of the lumen and damage
- Hyaline arteriolosclerosis

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8
Q

What happens in hyaline arteriolosclerosis?

A

– 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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9
Q

What are the causes of primary or essential hypertension?

A

Multifactorial: genetic and lifestyle influences

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10
Q

What are some lifestyle factors which influence hypertension?

A
  • Amount of salt in diet
  • Alcohol intake
  • Levels of physical activity
  • Abdominal obesity and metabolic syndrome
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11
Q

What is the role of age, gender and race in hypertension?

A
  • Prevalence lower in premenopausal females than in age-matched males and in postmenopausal women
  • Higher in blacks
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12
Q

What is the suggested role of inflammation in hypertension?

A
  • Elevated circulating inflammatory molecules

* Cause or effect?

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13
Q

What is the relationship between renin levels and essential hypertension?

A

High and low plasma renin activity forms: possibly correlate with vasoconstrictor and volume dependent forms of HT

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14
Q

Pathogenesis of Systolic hypertension with wide pulse pressure?

A

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

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15
Q

What are some causes of secondary hypertension?

A
Renal
Endocrine
Vascular 
Medications
Other
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16
Q

What are the renal causes of hypertension?

A

Mechanisms include decreased capacity to excrete sodium, excessive renin secretion in relation to volume, excessive sympathetic activity

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17
Q

Does aortic atherosclerosis cause hypertension?

18
Q

When does atherosclerosis cause hypertension?

A

Renal atherosclerosis

19
Q

Why is hypertension important?

A

On its own it is asymptomatic but is causes a variety of other organs

20
Q

What is most likely to cause an aneurysm?

A

Weakening of the media

21
Q

Where does an aortic dissection take place?

22
Q

Where does aortic dissection take place?

A

The ascending aorta

23
Q

What are some complications of aortic dissection?

A

Haemopericardium
Extension of dissection
Rupture

24
Q

What is a chronic aortic dissection?

A

Where blood re-enters the aorta

25
What can concentric hypertrophy cause?
Impairing diastolic filling Increasing the myocardial oxygen demand Reducing the coronary perfusion pressure gradient (ischemia)
26
Why is hypertension a risk factor for renal injury?
• Transmission of elevated pressures to glomeruli -> sclerosis • Hyaline arteriolosclserosis -> chronic ischaemia
27
What does proteinuria measure?
Proteinuria is a marker of the severity of chronic kidney disease and is a predictor of its progression
28
What is benign nephrosclerosis?
a
29
What happens to athero-sclerotic plaque?
It can embolise
30
What is the usual cuase of renal infarction?
Athero-embolism
31
What is the most common cause of stroke?
Cerebral infarct
32
What is a risk factor for cerebral infarct?
Hyaline arteriolosclerosis
33
What are lacunar infarct?
Infarct (a couple of mm across caused by small vessels)
34
What are berrry aneurysm?
Cause subarachnoid haemorrhage
35
How does hyaline arterioloscerlosis affect the retina?
AV nipping, exudates, ischaemia, haemorrhages and other changes
36
What are the consequences of long standing hypertension on the retina?
Can cause visual disturbances
37
How doe we assess a patient for hypertension?
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
38
What are lab tests for evaluation of hypertension?
–Diagnosis of potential secondary causes –Evaluation of risk factors –Detect end organ damage
39
How is hypertension managed?
``` details determined by absolute risk and presence of end organ damage –Treat any secondary cause –Lifestyle intervention: for all –Pharmacologic therapy –Follow-up ```
40
What is Malignant hypertension or hypertensive emergency?
* Syndrome associated with abrupt, severe increase in BP * May develop de novo in those with normal BP or in those with pre-existing essential HT * Uncommon * Full blown syndrome is a medical emergency * Complications related to changes in small arteries and arterioles
41
What does Malignant hypertension cause?
Hyperplastic arteriolosclerosis (hyperplasia of the media cells) Fibrinoid necrosis and thrombosis
42
What are the progressive effects of malignant hypertension?
* Retinopathy (arteriolar spasm, hemorrhages, exudates, papilledema) * Deteriorating renal function * Microangiopathic hemolytic anemia * Encephalopathy: failure of autoregulation of cerebral blood flow, hyperperfusion and cerebral oedema