Hypertension Flashcards

1
Q

Certain genetic loci have been associated with hypertension risk

A

Variations in the genes encoding the renin-angiotensin system.

Particularly mutations in the genes of the angiotensinogen and angiotensin receptor locus

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2
Q

Risk factors in hypertension

A

Stress
Obesity/sedentary lifestyle
Smoking
High salt intake

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3
Q

How common is secondary hypertension?

A

Rare - 5%, due to:
Adrenocortical hyperfunction (Cushing’s etc)
Exogenous hormones (glucocorticoids, etc)
Phaeochromocytoma
Renal artery stenosis

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4
Q

Hyaline arteriosclerosis

A

Arteriolar wall is thickened due to increased protein deposition narrowing the lumen
This is due to plasma proteins leaking across injured endothelial cells and increased smooth muscle matrix deposition in response to raised haemodynamic stress

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5
Q

Hyaline arteriosclerosis mainly affects

A

Retina
Kidney
Heart

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6
Q

Hyaline arteriosclerosis also occurs as part of another condition

A

Diabetic microangiopathy

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7
Q

The major complications of hypertension are

A
Cardiac hypertrophy and heart failure
Multi-infarct dementia (Lacunar infarcts)
Aortic dissection
Renal failure
Major risk factor for atherosclerosis
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8
Q

Accelerated (Malignant) hypertension

A

A rapid rising blood pressure that if untreated leads to death with two years
High pressure causes hyperplastic (onion skinning) arteriosclerosis which obliterates the lumen
Mainly affects the kidney (AKI) or the brain (cerebral haemorrhage)

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9
Q

Hyperplastic arteriosclerosis (Onion-skinning)

A

Occurs in accelerated hypertension
High pressure causes intimal hyperplasia and necrosis.
Produces concentric laminations of VSMCs with thickened and duplicated basement membranes
Accompanied by fibrinoid deposits and vessel wall death (necrotising arteriolitis)

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10
Q

Which organ are most effected by necrotising arteriolitis?

A

The kidney

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11
Q

The difference between accelerated and malignant hypertension

A

Accelerated - Hypertensive urgency, severe hypertension associated with grade 2/3 KWB retinopathy
Malignant - Hypertensive crisis, severe hypertension associated with grade 4 KWB retinopathy with papilloedema +- impending or progressive end organ damage - 90% untreated 1year mortality

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12
Q

End organ damage in malignant hypertension

A

Hypertensive encephalopathy/Intracerebral haemorrhage/acute thrombotic stroke
IHD/ACS/LVF with pulmonary oedema/Aortic dissection
Renal impairment
Eclampsia

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13
Q

Causes of malignant hypertension

A

Majority chronic essential hypertension with rapid rise, sometimes no reason, often due to discontinuation of medications
Also - Renal/renovascular disease, SLE, Cushing’s

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14
Q

The majority of hypertension is

A

Essential (idiopathic) hypertension - 95%

This is a multifactorial disease with multiple genetic and environmental factors feeding into it

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15
Q

Hypertensive encephalopathy

A

Caused by cerebral oedema and haemorrhage after failure of auto regulation in the context of hypertension
Causes severe headache, nausea, vomiting, confusion, visual disturbances, nystagmus, seizures and focal neurological signs

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16
Q

Treating severe hypertension

A

If no sign of end organ damage then can be treated in high intensity out patient basis
If evidence of end organ damage then ITU admission required
Arterial line to monitor BP and rapid gradual reduction in BP
Reversible if treated but can be fatal

17
Q

BP should not be lowered too rapidly in severe hypertension because

A

Rapid reduction below the autoregulatory range gives a risk of end organ ischaemia
Aim to reduce BP by 20% in the first hour/to 160/100 in first 6hrs
IV infusion of short acting titratable anti-hypertensive

18
Q

Agents used to acutely treat severe hypertension

A

Sodium nitroprusside - long term use can cause cyanide poisoning
Glyceryl trinitrate, Labatelol, Hydralazine
Don’t use sublingual nifedipine - dangerous

19
Q

Drugs used for the initial treatment of hypertension

A

A (55yrs or black) –> A + C –> A + C + D —> resistant hypertension A + C + D + B
A - ACEi C - calcium channel antagonists
B - Beta-blockers D - thiazide diuretics

20
Q

Stages of HTN

A

stage 1 –> 140/90> & ambulatory/home average BP >135/85
Stage 2 –> 160/100> & ambulatory/home average BP 150/95>
stage 3/severe –> clinical systolic >180 or diastolic >110

21
Q

Postural hypotension

A

Is a drop in systolic BP of 20> when standing with symptoms

22
Q

Treatment Step 1

A

ACEi (enalapril, etc) if 55 or black
ARB (Lorsartan, Candasartan) if ACE not tolerated, if neither then B-blocker
Atypical Thiazide (chlortadidone, indapamide) if CCB not tolerated

23
Q

Treatment step 2

A

Add CCB to ACEi/ARB or thiazide if intolerant of CCB

Add ACEi/ARB to CCB or thiazide (ARB if black)

24
Q

Treatment step 3

A

ACEi/ARB + CCB + Thiazide

25
Q

Resistant HTN

A

remains above 140/90 after step 3 treatment. If renal function is good add spirolactone (K+<4.5) or increase thiazide

26
Q

ACEi contraindications

A

Dont use for pts with previous angiooedema/ hypersensitivity or with renal artery stenosis
Caution should be taken with pts with Aortic or pulmonary stenosis/outflow obstruction, dehydrated/hypovolaemia or haemodialysis
Sig. pregnancy risk in 2nd or 3rd trimester and shouldnt be taken by women at risk of pregnancy
Risk of hyperkalaemia, cough and angioedema

27
Q

Asthmatics

A

Careful with ACEis and B-blockers, as can trigger attacks

28
Q

CCB Contraindications

A

Can cause flushing, headache, hypotension and oedema
Should not be given to pts at risk or bradycardia, conduction defects or heart failure.
Should not combine with a B-blockers

29
Q

ARB contraindications

A

Contraindicated in pregnancy & pts with bilateral renal artery stenosis

30
Q

Thiazide diuretic contraindications

A

Increase triglycerides, cholesterol, glucose, LDL
and decreases volume, sodium, potassium.
decreased efficacy NSAIDs, corticosteroids increasehypokalaemia, B-blockers potentiate hyperglyaemia/hyperlipidaemia
Risk of gout

31
Q

Gestational Hypertension

A

Treat with MethylDOPA