Hypertension Flashcards
Certain genetic loci have been associated with hypertension risk
Variations in the genes encoding the renin-angiotensin system.
Particularly mutations in the genes of the angiotensinogen and angiotensin receptor locus
Risk factors in hypertension
Stress
Obesity/sedentary lifestyle
Smoking
High salt intake
How common is secondary hypertension?
Rare - 5%, due to:
Adrenocortical hyperfunction (Cushing’s etc)
Exogenous hormones (glucocorticoids, etc)
Phaeochromocytoma
Renal artery stenosis
Hyaline arteriosclerosis
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
Hyaline arteriosclerosis mainly affects
Retina
Kidney
Heart
Hyaline arteriosclerosis also occurs as part of another condition
Diabetic microangiopathy
The major complications of hypertension are
Cardiac hypertrophy and heart failure Multi-infarct dementia (Lacunar infarcts) Aortic dissection Renal failure Major risk factor for atherosclerosis
Accelerated (Malignant) hypertension
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)
Hyperplastic arteriosclerosis (Onion-skinning)
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)
Which organ are most effected by necrotising arteriolitis?
The kidney
The difference between accelerated and malignant hypertension
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
End organ damage in malignant hypertension
Hypertensive encephalopathy/Intracerebral haemorrhage/acute thrombotic stroke
IHD/ACS/LVF with pulmonary oedema/Aortic dissection
Renal impairment
Eclampsia
Causes of malignant hypertension
Majority chronic essential hypertension with rapid rise, sometimes no reason, often due to discontinuation of medications
Also - Renal/renovascular disease, SLE, Cushing’s
The majority of hypertension is
Essential (idiopathic) hypertension - 95%
This is a multifactorial disease with multiple genetic and environmental factors feeding into it
Hypertensive encephalopathy
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
Treating severe hypertension
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
BP should not be lowered too rapidly in severe hypertension because
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
Agents used to acutely treat severe hypertension
Sodium nitroprusside - long term use can cause cyanide poisoning
Glyceryl trinitrate, Labatelol, Hydralazine
Don’t use sublingual nifedipine - dangerous
Drugs used for the initial treatment of hypertension
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
Stages of HTN
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
Postural hypotension
Is a drop in systolic BP of 20> when standing with symptoms
Treatment Step 1
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
Treatment step 2
Add CCB to ACEi/ARB or thiazide if intolerant of CCB
Add ACEi/ARB to CCB or thiazide (ARB if black)
Treatment step 3
ACEi/ARB + CCB + Thiazide
Resistant HTN
remains above 140/90 after step 3 treatment. If renal function is good add spirolactone (K+<4.5) or increase thiazide
ACEi contraindications
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
Asthmatics
Careful with ACEis and B-blockers, as can trigger attacks
CCB Contraindications
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
ARB contraindications
Contraindicated in pregnancy & pts with bilateral renal artery stenosis
Thiazide diuretic contraindications
Increase triglycerides, cholesterol, glucose, LDL
and decreases volume, sodium, potassium.
decreased efficacy NSAIDs, corticosteroids increasehypokalaemia, B-blockers potentiate hyperglyaemia/hyperlipidaemia
Risk of gout
Gestational Hypertension
Treat with MethylDOPA
