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CPT > L3 Hypertensive Drugs > Flashcards

L3 Hypertensive Drugs Flashcards

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1
Q

Hypertension

A

Elevation of blood pressure that is associated with an increased risk of harm

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2
Q

Essential hypertension

A

90%

Idiopathic

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3
Q

White coat effect

A

Spike in pulse and increase in blood pressure transiently when visiting the GP or hospital

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4
Q

Causes of secondary hypertension

A 
Pre hypertensive drugs 
Tumours e.g. pheochromocytoma
Diabetes
Hyperthyroidism 
Pre-eclampsia
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5
Q

When to offer hypertension treatment

A

140/90 - under 80yrs old + T2DM
150/90 - over 80 yrs old
135/85 - T1DM

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6
Q

Stages of hypertension

A

Stage 1 - 140/90
Stage 2 - 160/ 100
Stage 3 - 180/120

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7
Q

How to treat pre-hypertension

A
  • promote regular exercise
  • decrease cholesterol and healthier diet
  • reduced stress
  • limit alcohol intake
  • reduced excessive caffeine intake
  • stop smoking
  • decrease salt intake
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8
Q

Angiotensin converting enzyme

A
  • Released from the luminal surface of capillary endothelial cells especially in the lungs
  • catalysed the conversion of ang I to ang II
  • breakdown bradykinin
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9
Q

Angiotensin II receptors

A

AT1 - predominant
AT2 - higher concentrations in the brain

Also released from ang I independent of ACE via chymases

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10
Q

Ang II functions via AT1

A
  • increased sympathetic activity
  • increased Na+ and water reabsorption
  • stimulates release of ADH from the posterior pituitary gland
  • stimulates the release of aldosterone
  • vasoconstriction
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11
Q

ACE inhibitors

A

Inhibit the conversion of Ang I to Ang II by inhibiting circulation and tissue ACE

Therefore:

  • vasodilation
  • less ADH and aldosterone release
  • less salt and water reuptake - decreasing stroke volume and preload
  • reduced cell growth and proliferation of SMC (lesser extent)
  • decrease breakdown of bradykinin
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12
Q

Bradykinin

A

Vasodilation via nitric oxide and prostaglandins

Can cause dry cough

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13
Q

Side effects of ACE inhibitors

A

Hypotension
Dry cough
Hyperkalaemia - reduced aldosterone release
Renal failure - vasodilation of efferent arterioles decreases GFR
Angioedema - via bradkinin and more common in black people

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14
Q

Contraindications and important interactions of ACE inhibitors

A

Contraindications:

  • Renal artery stenosis
  • AKD
  • Pregnancy
  • Breastfeeding

Interactions:

  • potassium sparing drugs
  • NSAIDs - inhibit prostaglandins which causes vasodilation of the afferent arterioles
  • other antihypertensives
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15
Q

Examples of ACE inhibitors

A

Ramipril

Lisinopril

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16
Q

Angiotensin II receptor blocker (ARBs) examples

A

Candesartan

Losartan

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17
Q

ARB mechanism of action

A

Directly targets AT1 receptors therefore more effective at inhibiting Ang II mediated vasoconstriction

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18
Q

Benefits of ARBs

A

Does not cause dry cough or angioedema

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19
Q

Disadvantages of ARBs

A

Less effective in hypertensive patients with low renin e.g. black population

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20
Q

Contraindications and interactions of ARBs

A

Contraindications

  • renal artery stenosis
  • AKD
  • pregnancy
  • breast feeding

Interactions:

  • K+ sparring drugs
  • NSAIDs
  • other antihypertensives
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21
Q

L- type calcium channels

A
  • Allow influx of calcium into cells via voltage operated Ca2+ channels (VOCC)
  • Expressed throughout the body e.g. SAN, AVN, cardiac myocytes and vascular SMC
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22
Q

Classes of calcium channel blocker

A

Dihydropyridines
Phenylalkylamines
Benzothiaziapines

Interact with different sites on the alpha 1 sub unit of VOCC

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23
Q

Dihydropyridines

A

Selective for peripheral vasculature
First line CCB for hypertension
Can be selective for cerebral or peripheral smooth muscle

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24
Q

Mechanism of action of CCB

A

Decreased influx of calcium into a cell therefore less smooth muscle contraction occurs

Used as first line hypertensive in patients with low renin levels

25
Q

When are cerebral CCBs used?

A

If a patient has had a subarachnoid haemorrhage

26
Q

Phenylalkylamine mechanism of action

A

Selective for cardiomyocytes, SAN and AVN

  • decreases SAN impulses - negative chronotropy
  • decreased strength of contraction of cardiomyocytes - negative inotropy
  • decreased peripheral vasodilation
  • class IV antihypertensive drug which inhibits calcium influx therefore prolonging action potentials for a longer refractory period
  • decrease upstroke + longer plateau
27
Q

Benzothiazapines

A

Affect peripheral SMCs and heart

28
Q

Examples of dihydropyridines

A

Amlodipine
Nifedipine
Nimodipine - cerebral vasculature

29
Q

Side effects of dihydropyridines

A

Ankle swelling
Flushing
Headaches - vasodilation
Palpitations - compensatory tachycardia can occur therefore not useful in angina

30
Q

Contraindications and interaction of dihydropyridines

A

Contraindications

  • unstable angina
  • severe aortic stenosis

Interactions

  • when amlopdipine is used with simvastatin, the effect of simvastatin increases therefore may need a lower simvastatin dose
  • other hypertensives
31
Q

When are phenylalkylamines used?

A

Patients with:

  • arrhythmia
  • angina
  • hypertension (lesser extent)
32
Q

Side effects of phenylalkylamines

A

Constipation
Bradycardia - IV
Heart block
Cardiac failure

33
Q

Contraindications and interactions of phenylalkylamines

A

Contraindications:

  • poor LV contractility and function
  • AV nodal conduction delay

Interactions:

  • Beta blockers
  • Other antihypertensives
  • other antiarrhythmic agents
34
Q

Example of phenylalkylamines

A

Verapamil

35
Q

Benzothiazapine example

A

Diltiazem

36
Q

Examples of thiazides and thiazides like diuretics

A

Bendroflumethiazide

Indapamide

37
Q

Mechanism of action of thiazides diuretics

A

Inhibit the Na+/Cl- cotransporter in the DCT
Therefore decreasing sodium and water reabsorption

  • can activate RAAS
  • useful over CCB in oedema
38
Q

Side effects of thiazides diuretics

A

Hypokalaemia
Hyponatraemia
Hyperuricaemia
Arrhythmia

Increased glucose - especially with beta blockers
Increased cholesterol and triglycerides

39
Q

Contraindications and interactions of thiazides diuretics

A

Contraindications:
Hypokalaemia
Hyponatraemia
Gout - due to hyperuricaemia

Interactions:

  • NSAIDs
  • K+ secreting drugs e.g. furosemide
40
Q

First line treatments of hypertension

A

Black Africa or 55 yrs old or over:
- CCB

T2DM or under 55 yrs old
- ACEi or ARB

41
Q

Step 4 in treating hypertension

A

Confirm elevated BP with ABPM or HBPM
Discuss adherence
Check for postural hypotension

  • low dose spironolactone if blood potassium is less than 4.5 mmol/l
  • alpha or beta blocker if blood K+ is higher
42
Q

Two pronged approach to treating primary hypertension

A
  • decreases diabetic nephropathy and CKD with proteinuria by dilating the efferent arteriole
  • therefore GFR decreases decreasing intraglomerular oressure therefore the load on the kidneys decreases and good for T2DM
  • also peripheral vascular resistance decreases which decreases BP
43
Q

Spironolactone

A

Aldosterone receptor antagonist

44
Q

Contraindications and interactions of spironolactone

A

Contraindications:

  • Hyperkalaemia
  • Addison’s disease - decreased aldosterone release due to destruction of the adrenal cortex

Interactions:
- K+ sparring drugs including ACEi and ARBs

45
Q

Beta adrenoceptor blocker examples

A

Labetalol
Bisoprolol
Metoprolol

46
Q

Mechanism of action of beta adrenoreceptor blockers

A

Decreased sympathetic tone
Blocks noradrenaline receptors
Reduces myocardial contraction - decreasing CO and HR
Decreased renin secretion

47
Q

Side effects of B Blockers

A 
Bronchospasm 
Heart block
Raynaud’s - cold hands 
Lethargy 
Impotence
48
Q

Contraindications and interactions of beta blockers

A

Contraindications:

  • asthma
  • COPD
  • haemodynamic instability
  • hepatic failure - dose monitoring

Interactions:
- non dihydropyridine CCB - similar mechanisms of action therefore can go into asystole

49
Q

Alpha adrenoreceptor blocker example

A

Doxazosin

50
Q

Mechanism of action of alpha adrenoreceptor blockers

A
  • Selective antagonism of alpha 1 adrenoreceptors
  • Reduces peripheral vascular resistance
  • in urinary tract, bladder neck and prostate
51
Q

Tamsulosin

A

Treats BPH by acting on alpha 1 adrenoreceptor a causing decreased peripheral vascular resistance

52
Q

Side effects of alpha adrenoreceptor blockers

A 
Postural hypotension 
Dizziness
Syncope 
Head ache 
Fatigue
53
Q

Contraindications and interactions of alpha adrenoreceptor blockers

A

Contraindications:
- postural hypotension

Interactions:
- dihydropyridine CCB - cause oedematous effects

54
Q

Heart failure drug administration

A
  1. Offer furosemide diuretic for symptoms and fluid retention
  2. HFpEF - manage comorbidities e.g. hypertension and atrial fibrillation
  3. HFrEF - ACEi (consider ARB if intolerant) and Beta blocker
  4. If symptoms continue - spironolactone
55
Q

If resistance to ACEi and ARB

A

Hydralazine and nitrate

56
Q

Reduced ejection fraction

A

Below 45%

57
Q

Non pharmological treatment of HF

A
  • reduced salt intake

- liquid reduction to 1.5 L

58
Q

Symptoms of heart failure

A

Exercise intolerance
Dyspnoea
Fatigue
Oedema

59
Q

Aims in treating heart failure

A

Reduce symptoms
Increase exercise tolerance
Address arrhythmias, hyperlipidaemia and diabetes
Decrease mortality

CPT (23 decks)

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