Hypertension Flashcards
Pathophysiology of atherosclerosis
1) Dysfunctional epithelial cells + high circulating LDLs
2) LDLs move into tunica intima
3) Endothelial cells release ROS and oxidise the LDLs, trapping them
4) Triggers endothelial cells to express adhesion molecules for WBCs
5) Monocytes move into intima and become macrophages
6) Macrophages take up LDLs and become foam cells
7) Foam cells release chemokines and IGF-1 and also die
8) Attraction of more macrophages, smooth muscle cell migration and proliferation, production of more collagen, and release of lipid contents/ROS/cytokines
9) Increased inflammation in area (plaque)
10) Plaque grows and can rupture
Mechanisms of hypertension
Atherosclerosis - increases SVR
Low renal blood flow - kidneys secrete renin which helps kidneys retain water, leading to higher pressure
Pathology in RAAS system seems to be main mechanism, rather than baroreceptor pathology
Symptoms and signs
Usually asymptomatic
Secondary causes of hypertension
1) Renal disorders - chronic pyelonephritis, diabetic nephropathy, glomerulonephritis, PKD, obstructive uropathy, renal cell carcinoma
2) Vascular disorders - coarctation of aorta, renal artery stenosis
3) Endocrine disorders - primary aldosteronism, phaeochromocytoma, Cushing’s, acromegaly, hypo or hyperthyroidism
4) Drugs - alcohol, ciclosporin, cocaine, COCP, steroids, EPO, leflunomide, liquorice, NSAIDs, sympathomimetics, venlafaxine
5) Others = CTDs, retroperitoneal fibrosis, OSA
Normal blood pressure
<120/80
Categorisation of hypertension (clinic BPs)
Stage 1 = 140/90 - 159/99 AND ABPM >=135/85
Stage 2 = 160/100 - 180/120
AND ABPM >=150/95
Stage 3 = 180 or higher/120 or higher (either diastolic or systolic)
Risk factors for primary hypertension
Old age, obesity, salt-heavy diet, sedentary lifestyle, black people, genetics, social deprivation, smoking, alcohol, anxiety and stress
Hypertensive crisis symptoms
Confusion, drowsiness, chest pain, breathlessness
How to confirm hypertension
BP in clinic - 3 readings
Confirmed by ambulatory BP monitoring or home BP monitoring (if clinic BP 140/90-180/120)
Accelerated (or malignant) hypertension definition
Severe increase in blood pressure to 180/120 mmHg or higher (and often over 220/120 mmHg) with signs of retinal haemorrhage and/or papilloedema. It is usually associated with new or progressive target organ damage.
If BP is 180/20 or higher?
Refer for same day specialist assessment if signs of retinal haemorrhage and/or papilloedema, life-threatning symptoms e.g. confusion, chest pain, heart failure, AKI
If no symptoms/signs –> carry out investigations for target organ damage ASAP
Investigations for target organ damage/cardiovascular risk
Urine dip - haematuria
Urine ACR (protein in the urine)
HbA1C
Electrolytes, creatinine, and EGFR (for CKD)
Fundoscopy (for hypertensive retinopathy)
ECG (for cardiac function/LVH)
Serum total cholesterol and HDL cholesterol
QRISK assessment
Symptoms/signs of renal causes of secondary hypertension
Chronic pyelonephritis - usually detected unexpectedly on USS
Diabetic nephropathy — microalbuminuria or proteinuria
Glomerulonephritis — microscopic haematuria.
Polycystic kidney disease — abdominal or flank mass, microscopic haematuria, or family history.
Obstructive uropathy — abdominal or flank mass.
Renal cell carcinoma — haematuria, loin pain and a loin mass
Symptoms/signs of coarctation of aorta
Upper-limb hypertension. Significant difference in BP between arms.
Absent or weak femoral pulses, radio-femoral delay, palpable collateral blood vessels in the back muscles, and a suprasternal murmur radiating through to the back.
Symptoms/signs of renal artery stenosis
Peripheral vascular disease Abdominal bruit
BP resistant to treatment Raised plasma renin
Primary hyperaldosteronism signs/symptoms
Hypokalaemia, alkalosis, and plasma sodium level greater than 140 mmol/L,
Tetany, muscle weakness, nocturia, or polyuria.
Symptoms/signs phaeochromocytoma
Intermittently high or labile blood pressure, or postural hypotension, headaches, sweating attacks, palpitations, or unexplained fever and abdominal pains.
Hyperthyroidism signs/symptoms
tremor, anxiety, sweating, weight loss, diarrhoea, and heat intolerance.
Hypothyroidism signs/symptoms
fatigue, weight gain, dry skin and hair loss, constipation, and muscle weakness.
Cushing’s signs/symptoms
Truncal obesity and striae
Acromegaly signs/symptoms
Enlargement of hands and feet, facial changes, sweating
BP target for non-diabetics etc.
Adults aged under 80 years — clinic blood pressure below 140/90 mmHg.
Adults aged 80 years and over — clinic blood pressure below 150/90 mmHg.
BP targets for diabetics
If end-organ damage (e.g. renal disease, retinopathy) < 130/80 mmHg
otherwise < 140/80 mmHg
Investigations for secondary causes
- U&E + estimated GFR (renal disease)
- Renal ultrasound/arteriography (renal artery stenosis)
- 24h urinary meta-adrenaline (raised in pheochromocytoma)
- Urinary free cortisol (raised in Cushing’s)
- Renin aldosterone ratio (aldosterone high in Conn’s)
- MR aorta (coarctation)
Non-pharm managament of cardiovascular risk factors
Healthy diet + regular exercise Weight loss Reduce caffeine Low dietary sodium Smoking cessation Reduce alcohol
Step 1 in pharm treatment
If <55 or T2DM = ACE inhibitor (or ARB)
If >=55 or black = calcium channel blocker
Step 2 in pharm treatment
A + C
Step 3 in pharm treatment
A + C + D (thiazide-like diuretic)
Step 4 in pharm treatment
A + C + D
+ spironolactone if potassium =<4.5
+ alpha or beta blocker if potassium >4.5
Step 5 in pharm treatment
Refer for specialist review if on 4 drugs and not controlled
ACE inhibitors
- mechanism, SEs
Inhibit the conversion angiotensin I to angiotensin II
S/Es - cough, angioedema, hyperkalaemia, can worsen renal function
ARB
- mechanism, SEs
Block effects of angiotensin II at the AT1 receptor
S/E - hyperkalaemia
Calcium channel blockers
- mechanism, SEs
Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction
S/Es - flushing, ankle swelling, headache
Thiazide like diuretics
- mechanism, SEs
Inhibit sodium absorption at the beginning of the distal convoluted tubule
S/Es - hyponatraemia, hypokalaemia, dehydration
Spironolactone
- mechanism, SEs
Aldosterone antagonist which acts in the cortical collecting duct
S/E - hyperkalaemia, gynaecomastia
Alpha blockers SEs
postural hypotension
drowsiness
dyspnoea
cough
Beta blockers
Reduce cardiac output, alter baroceptor reflex sensitivity, and block peripheral adrenoceptors. Some beta-blockers depress plasma renin secretion. May have central effect.
S/Es - abdo discomfort, bradycardia, peripheral coldness, dizziness, can cause AV block and bronchospasm (uncommon)
Management of hypertensive emergency
IV antihypertensive therapy - reduce BP by 20-25% within 2 hours
e.g. with labetalol, GTN, nitroprusside, hydralazine…
Management of hypertensive urgency
Gradually reduce BP over 24-48 hours with oral antihypertensive therapy e.g. labetalol or amlodipine or felodipine
In hypertensive crisis, why should BP be reduced gradually?
If reduced too quickly, there is a risk of reduced organ perfusion leading to cerebral infarction, blindness, deterioration in renal function, and myocardial ischaemia.
What is BP determined by? (2)
Cardiac output x systemic vascular resistance
Stages of hypertensive retinopathy
1 = arteriolar narrowing and tortuosity, silver wiring 2 = AV nipping 3 = cotton wool exudates, flame and blot haemorrhages 4 = papilloedema
Pathology of target organ damage caused by accelerated hypertension
A rise in systemic vascular resistance starts the cycle
- -> increase in BP
- -> mechanical stress and endothelial injury
- -> increased permeability
- -> activation of the coagulation cascade and platelets, and deposition of fibrin
- -> ischaemia and release of vasoactive mediators, generating ongoing injury
