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

1
Q

What is hypertension defined as?

A

Hypertension is defined as a raised blood prssure >/= 140/90 mmHg

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2
Q

What is the most common type of hypertension? What causes the other type?

A

Primary hypertension or essential hypertension accounts for the majority of cases - cause is unkown but there are risk factors Other type is secondary hypertension

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3
Q

Secondary hypertension causes include * Renal disease * Endocrine disease * Others What are renal causes of hypertension?

A

Renal disease * Eg renal artery stensois * Glomerululonephritis * Polycystic kidneys

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4
Q

Where are different endocrine causes of secondary hypertension eg * Phaeochromocytoma * Conn’s syndrome * Cushing’s syndrome What happens in these?

A

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)

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5
Q

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?

A

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)

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6
Q

What is the opposite of white coat hypertension?

A

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

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7
Q

How are both ABPM and HBPM carrid out?

A

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

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8
Q

What is stage 1,2 and 3 hypertension?

A

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.

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9
Q

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?

A

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)

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10
Q

What are the symptoms seen in hypertension? What do the blood vessels show if biopsied in malignant hyeprtension?

A

Symptoms seen in mmalignant hypertension include * Headache * Visual disturbance * Cerebral infactions common * Also heart failure Fibrinod necrosis is seen in vessels (arterioles)

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11
Q

What tests are offered to all patients with hypertension to assess for end-organ damage?

A

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

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12
Q

Lifestyle advice should be given to all patients with hypertension regardless of the stage What lifestyle advice can be given to help reduce hypertension?

A

Stop smoking Low fat diet (increases unsaturated fats, decrease saturated) Reduce alcohol and salt intake Increase exercise and reduce weight if obese

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13
Q

When should treatments with drugs be initiated in a patient with hypertension?

A

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

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14
Q

When is treatment started in patients with stage 1 hypertension? When are statins started for primary prevention against cardiovascular disease?

A

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

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15
Q

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

A

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

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16
Q

What is the initial treatment of essential hypertension? * Step 1, 2 and 3

A

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

17
Q

What helps make the choice between CCB and thiazide diuretic for step 2 management of hypertension in patients under 55 or Caucasian?

A

Do not give CCB if the patient has oedema as this may worsen it

18
Q

What is it known as when triple drug therapy fails? What tests are carried out here?

A

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

19
Q

What is the next treatment step for patients with resistant hypertension?

A

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

20
Q

What is the mechanism of action ACE inhibitors? Give examples? State side effects

A

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

21
Q

If patients experience dry cough with ACEi, switch to ARB What is the mechanism of action ARBs? Give examples? State side effects

A

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

22
Q

When are ACEi and ARBs contraindicated? How can ACEs and ARBs cause hyperkaelaemia?

A

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/

23
Q

What are the two types of CCB? When is each used? Give drug examples?

A

CCB Dihydropyridines eg amlodopine - hypertension and angina Rate limiting CCB - eg verapamil or diltiazem - for Supraventricular arrhythmias and angina

24
Q

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?

A

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

25
Q

Name side effects of calcium channel blockers?

A

Ankle oedema Hypotension Constipation

26
Q

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?

A

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

27
Q

What are thiazides and loop diuretics used in? What are the side effects?

A

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

28
Q

How can diuretics cause hyperuricaemia?

A

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

29
Q

How can diuretics cause hypokaelaemia / metabolic alkalosis?

A

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

30
Q

Give examples of thiazide and loop diuretics?

A

Thiazide diruetics used in hypertension - indapamide (becoming favorable) or bendroflumethiazide Loop diuretics - frosemide

31
Q

How do beta blockers work? Give examples?

A

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

32
Q

State the side effects of beta blockers? When should they definitely not be used?

A

Beta blockers - Tiredness Cold peripheries Can worsen heart failure in short term DO NOT USE IN ASTHMA - can cause bronchospasm

33
Q

What is the mechanism of action of alpha blockers? Give examples? State the side effects?

A

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

34
Q

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?

A

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