Week 3/4 - A - Hypertension - Diagnosis/Stages/Monitoring - Clinic BP/A.B.P.M/H.B.P.M, A.C.E.I/A.R.B/C.C.B/Thiazide, a/b blocker) Flashcards
What is hypertension defined as?
Hypertension is defined as a raised blood prssure >/= 140/90 mmHg
What is the most common type of hypertension? What causes the other type?
Primary hypertension or essential hypertension accounts for the majority of cases - cause is unkown but there are risk factors Other type is secondary hypertension
Secondary hypertension causes include * Renal disease * Endocrine disease * Others What are renal causes of hypertension?
Renal disease * Eg renal artery stensois * Glomerululonephritis * Polycystic kidneys
Where are different endocrine causes of secondary hypertension eg * Phaeochromocytoma * Conn’s syndrome * Cushing’s syndrome What happens in these?
Phaeochromcytoma - tumours producing excess adrenaline - leads to vasoconstriction via alpha-1 adrenoreceptors Conn’s syndrome - excess production of aldosterone - causing increase Na+ and Water retention Cushing’s syndrome - excess corticosteroid release - causes increased BP (can’t remember pathway)
Hypertension is defined as a blood pressure >/= 140/90 mmHg What may cause this however is only due to the BP being measured in the clinic? How is this identified?
If clinic BP greater than or equal to 140/90 mmHg, then ambulatory blood pressure monitoring should be carried out (if ABPM cannot be carried out, then do HBPM) This is due to some patient’s experiencing white coat syndrome - where the clinic BP is raised but the blood pressure outside of the clinic is actually normal * Therefore clinic BP >/= 140/90 * however ABPM (or HBPM)
What is the opposite of white coat hypertension?
The opposite of white coat hypertension is masked hypertension - * where the clinical reading shows a normotensive patient (BP /=135/85 * unsure of reason - more common in smokers/drinkers
How are both ABPM and HBPM carrid out?
ABPM - device records BP * at least two blood pressure measurements are taken per hour during the person’s normal waking hours * Use the average of at least 14 measurements HBPM - self recorded BP (use if ABPM unsuitable) * BP recorded twice per day (morning/night) and each recording is carried out twice, when seated and one minute apart. Record for 4-7 days * First day measurement discarded, take average of remaining results
What is stage 1,2 and 3 hypertension?
Stage 1 hypertension * Clinic BP >/=140/90 AND * ABPM or HBPM >/=135/85 Stage 2 hypertension * Clinic BP >160/100 AND * ABPM or HBPM >/=150/95 Stage 3 hypertension * Clinic systolic BP is 180 mmHg or higher OR * Clinic diastolic BP is 120 mmHg or higher.
Hypertension is usually asymptomatic and is diagnosed on routine screening However, in patients with malignant (aka accelerated) hypertension, symptoms can persist What is malignant (or accelerated) hypertension?
Accelerated (or malignant) hypertension is a severe increase in blood pressure to 180/120 mmHg or higher (and often over 220/120 mmHg) leading to vascular damage - there are signs of retinal haemorrhages +/- papilloedema (swelling of the optic nerve)
What are the symptoms seen in hypertension? What do the blood vessels show if biopsied in malignant hyeprtension?
Symptoms seen in mmalignant hypertension include * Headache * Visual disturbance * Cerebral infactions common * Also heart failure Fibrinod necrosis is seen in vessels (arterioles)
What tests are offered to all patients with hypertension to assess for end-organ damage?
Urine analysis - looking for protein or blood - kidney damage Fasting glucose - evidence of diabetes U&Es - help to exclude other causes usch as Conn’s 12 lead ECG - LV hypertrophy, past MI Examine fundi for hypertensive retinopathy
Lifestyle advice should be given to all patients with hypertension regardless of the stage What lifestyle advice can be given to help reduce hypertension?
Stop smoking Low fat diet (increases unsaturated fats, decrease saturated) Reduce alcohol and salt intake Increase exercise and reduce weight if obese
When should treatments with drugs be initiated in a patient with hypertension?
Treatment with drugs for hypertension should begin if Stage 2 hypertension * Clinic BP >/=160/100 AND ABPM/HBPM >/=150/95 Treat if stage 3 hypertension * Clinic BP >/=180/120
When is treatment started in patients with stage 1 hypertension? When are statins started for primary prevention against cardiovascular disease?
If there is end (target) organ damage or the patient has a calculated 10-year cardiovascular risk 10%, start antihypertensive drug treatment Offer atorvastatin 20 mg a day (unless contraindicated) for the primary prevention of cardiovascular disease (CVD) to people with an estimated CVD risk of 10% or more
It is important to monitor response to lifestyle changes or drug treatment in people with hypertension What are the BP targets? * Clinic BP targets * ABPM/HBPM targets for those identified whit white-coat or masked hypertension
Clinic BP targets Aim for BP <140/90 in people aged under 80 Aim for BP <150/90 in people aged 80 and over ABPM/HBPM targets Aim for BP <135/85 in people aged under 80 Aim for BP <145/85 in people aged 80 and over Ie in patients under 80, want them to be less than stage 1
What is the initial treatment of essential hypertension? * Step 1, 2 and 3
For Afro-Carribean family origin or age >55 * Step 1 - Calcium channel blocker (CCB) * Step 2 - ADD Angiotensin converting enzyme inhibitor (ACEi) or Angiotensin receptor blocker (ARB) * Step 3 - CCB + ACEi/ARB + Thiazide diuretic Patient under 55 and not Afro-Carribean family origin * Step 1 - ACEi or ARB * Step 2 - CCB or Thiazide diuretic * Step 3 - ACEi/ARB + CCB + Thiazide diuretic
What helps make the choice between CCB and thiazide diuretic for step 2 management of hypertension in patients under 55 or Caucasian?
Do not give CCB if the patient has oedema as this may worsen it
What is it known as when triple drug therapy fails? What tests are carried out here?
If hypertension is not controlled in people taking the optimal tolerated doses of an ACE inhibitor or an ARB plus a CCB and a thiazide-like diuretic, regard them as having resistant hypertension. Confirm the resistant hypertension by ABPM or HBPM Also check the patient for postural hypotension
What is the next treatment step for patients with resistant hypertension?
For people with confirmed resistant hypertension, seek specialist advice or add a fourth antihypertensive drug. * For people with a blood potassium level of 4.5 mmol/l or less, consider further diuretic therapy with low-dose spironolactone. * For people with blood potassium level of more than 4.5 mmol/l, consider a beta blocker or an alpha-blocker
What is the mechanism of action ACE inhibitors? Give examples? State side effects
MOA in ACEI is that they inhibit the angiotensin converting enzyme therefore preventing angiotensin 1 being converted to angiotensin II - prevents angiotensin II effects (vasoconstriction, stimulating thirst/adh release, stimulating aldosterone production) Examples - lisinopril (drugs ending in pril) Side effects - dry cough , renal dysfunction, hyperkalaemia
If patients experience dry cough with ACEi, switch to ARB What is the mechanism of action ARBs? Give examples? State side effects
Angiotensin receptor blockers are angiotensin receptor type 1 inhibitors - AT receptor type 1 are the receptors for angiotensin II Examples - losartan, candesartan (drugs ending in sartan) Side effects - renal dysfunction, no cough, hyperkalaemia
When are ACEi and ARBs contraindicated? How can ACEs and ARBs cause hyperkaelaemia?
Both are contraindicated in pregnancy Can cause hyperkalaemia due to decreasing aldosterone production. Potassium rises due to aldosterone inhibition cause K+ to be retained by kidneys/
What are the two types of CCB? When is each used? Give drug examples?
CCB Dihydropyridines eg amlodopine - hypertension and angina Rate limiting CCB - eg verapamil or diltiazem - for Supraventricular arrhythmias and angina
What is the mechanism of action CCB? Which type has a higher affinity for the calcium channels of the heart? Which type has a higher affinity for the calcium channels of the blood vessels?
Dihydropyridines eg amlodopine (drugs end in pine) * Calcium channels block the L-type calcium channels -decreasing Calcium entry - * decreases heart rate * reduces contraction force in the heart * causes vasodilation decreasing SVR and BP Rate limiting have a higher affinity for the CA+ channels in the myocardium Dihydropyridines have a higher affinity for the blood vessels
Name side effects of calcium channel blockers?
Ankle oedema Hypotension Constipation
Thiazides are usually added to ACEi and CCBs in step 3 of hypertension management Which type are added here? What are the different main two types? and how do they work?
Thiazide diuretics are the type added in step 3 of HBP management Main two diuretic types Thiazide diuretics - inhibit the Na+/Cl- symporter in the distal convoulted tubule Loop diuretics- inhibit the Na+/K+/2Cl- co transporter in the thick ascending loop of Henle
What are thiazides and loop diuretics used in? What are the side effects?
Thiazide diuretics are used in hypertension Loop diuretics are used in heart failure Side effects * Hypokalaemai - tired and arrythmia * Hyperglycaemia - diabetes * Hyperuricaemia - Gout * Metabolic alkalosis * Impotence OTHER SIDE EFFECTS DISUCSSED IN RENAL LECTURES
How can diuretics cause hyperuricaemia?
Hyperuricaemia - diuretics are secreted into the proximal tubule lumen via transport processes - they compete with uric acid for this transporter and therefore increase this level in the blood
How can diuretics cause hypokaelaemia / metabolic alkalosis?
Hypokaelaemia/Metabolic alkalosis - because diuretics reduce sodium absorption in thick ascending loop of henle or distal convoluted tubule, at the collecting duct K+ and H+ ion transporters cause loss of these ions in an attempt to retain sodium
Give examples of thiazide and loop diuretics?
Thiazide diruetics used in hypertension - indapamide (becoming favorable) or bendroflumethiazide Loop diuretics - frosemide
How do beta blockers work? Give examples?
Cardioselectve BBlockers - B1-antagonists eg atenolol and bisoprolol (reduces heart rate (negative chronotrope) and contractility (negative inotrope)) Non-cardioselective block both B1 and B2 receptors - B2 ADR cause airway smooth muscle relaxation eg propranolol
State the side effects of beta blockers? When should they definitely not be used?
Beta blockers - Tiredness Cold peripheries Can worsen heart failure in short term DO NOT USE IN ASTHMA - can cause bronchospasm
What is the mechanism of action of alpha blockers? Give examples? State the side effects?
Selective alpha-1 adrenoreceptor blockers are used - A1-adr cause vasocontriction of vascular smooth muscle, therefore Alpha blockers cause vasodilation Examples - doxazosin, prazosin (drugs ending in zosin) Side effects Postural hypotension and dizziness
Spironolactone is a thiazide like diuretic usually given in step 4 of hypertension treatment if potassium levels <4.5mmol/l What is the mechanism of action? What are the side effects?
Spironolactone is an aldosterone antagonist This drug inhibits the action of aldosterone in the distal collecting duct - * inhibits the aldosterone mediate sodium reabsorption and potassium excretion * Therefore known as a potassium sparing diuretic * These agents prevent loss of K+ that occurs with thiazide/loop Aide effects - hyperkalaemia, gynaecomastio, renal failure
