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SA Clinical Pharmacology & Therapeutics > S4) Hypertension and Heart Failure > Flashcards

S4) Hypertension and Heart Failure Flashcards

1
Q

What is the 1st line pharmacological therapy for treating hypertension in the UK?

A
  • ACE inhibitors / ARBs
  • Calcium channel blockers
  • Diuretics
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2
Q

Which drug would one prescribe for the following patients presenting with hypertension:

  • <55 y/o and not Afro-Caribbean
  • > 55 y/o or any age Afro-Carribean
A
  • < 55 y/o and not Afro-Caribbean – ACE inhibitor
  • > 55 y/o or any age Afro-Carribean – Ca2+ channel blocker

(they have reduced renin

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3
Q

Describe the action of ACE inhibitors

A

Competitive inhibitors of Angiotensin Converting Enzyme:

  • Reduce formation of angiotensin II
  • Arteriole vasodilation → reduce peripheral resistance
  • Reduce circulating aldosterone so less Na and K reabsorbed and urinate more
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4
Q

Provide two examples of ACE inhibitors

A
  • Lisinopril
  • Ramipril
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5
Q

Identify some important side effects of ACE inhibitors

A
  • Dry cough (main) → unable to break down bradykinin
  • Angio-oedema (rare, common in black patients)
  • Renal failure (incl. renal artery stenosis)
  • Hyperkalaemia as K isn’t excreted
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6
Q

Describe the action of ARBs

A

Bind to angiotensin AT1 receptor: (so inhibit angiotensin 11 at receptor)

  • Inhibit vasoconstriction better than ACEi as they directly target the receptor
  • Inhibit aldosterone stimulation
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7
Q

Provide two examples of ARBs

A
  • Losartan
  • Candesartan
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8
Q

Identify two important side effects of ARBs

A
  • Renal failure
  • Hyperkalaemia

they don’t cause dry cough as they don’t have any effect on bradykinin

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9
Q

Describe the action of CCBs

A

Bind to alpha subunit of L-type calcium channel, reducing cellular calcium entry into the heart and arteries :

- Ca causes heart to pump harder and faster - blocking means they can relax

- Vasodilates peripheral, coronary and pulmonary arteries

  • No significant effect on veins
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10
Q

Identify the three main groups of CCBs and provide an example for each

A
  • Dihydropyridines e.g. nifedipine, amlodipine
  • Benzothiazepines e.g. diltiazem
  • Phenylalkylamines e.g. verapamil
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11
Q

Describe the properties and adverse effects of Dihydropyridines (calcium channel blockers) e.g. amlodipine

A
  • Properties: good oral absorption, protein bound > 90%, metabolised by the liver, good half life
  • Adverse effects: oedema, SNS activation – tachycardia and palpitations, flushing, sweating

they

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12
Q

Describe the properties and adverse effects of Phenylalkylamines (calcium channel blockers) e.g. verapamil

A
  • Properties: impedes calcium transport across the myocardial and vascular smooth muscle cell membrane, peripheral vasodilation, ↓ myocardial contractility
  • Adverse effects: constipation, bradycardia, can worsen heart failure
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13
Q

Describe the properties and adverse effects of Benzothiazepines (calcium channel blockers) e.g. diltiazem

A
  • Properties: impedes calcium transport across the myocardial and vascular smooth muscle cell membrane, peripheral vasodilation, ↓ myocardial contractility
  • Adverse effects: bradycardia, can worsen heart failure
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14
Q

Describe the action of thiazide diuretics

A

Reduce distal tubular sodium reabsorption:

  • Initial blood volume decrease
  • Later, total peripheral resistance falls
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15
Q

Identify four adverse effects of thiazide diuretics

A
  • Hypokalaemia (Na/K pump)
  • Increased urea and uric acid levels
  • Impaired glucose tolerance
  • Increased cholesterol and triglyceride levels
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16
Q

Describe the actions of alpha blockers

A

Selective antagonism at post-synaptic α-1 adrenoceptors:

  • Antagonise contractile effects of NA on vascular smooth muscle
  • Reduce peripheral vascular resistance
  • Benign effect on plasma lipids / glucose
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17
Q

Provide an example of an alpha blocker

A

Doxazosin

18
Q

Identify 3 adverse effects of alpha blockers

A
  • Postural hypotension
  • Headache and fatigue
  • Oedema
19
Q

Describe the action of beta blockers

A
  • Reduce HR and CO
  • Inhibit renin release
  • Initially TPR increases later falls to normal
20
Q

Provide three examples of beta blockers

A
  • Bisoprolol
  • Atenolol
  • Nebivolol
21
Q

Identify five adverse effects of beta blockers

A
  • Lethargy
  • Reduced exercise tolerance
  • Bradycardia
  • Impaired glucose tolerance
  • Contraindication – asthma
22
Q

Provide three examples of centrally acting agents

A
  • Methydopa
  • Clonidine
  • Moxonidine
23
Q

Describe the action of the following centrally acting agents:

  • Methydopa
  • Clonidine
  • Moxonidine
A
  • Methydopa: converted to α-methyl-noradrenaline – a potent α2 adrenoceptor agonist
  • Clonidine: direct pre-synaptic α2 adrenoceptor agonist
  • Moxonidine: imidazoline I1 receptor agonist and some α2 agonist effect
24
Q

Identify 2 adverse effects of centrally acting agents

A
  • Tiredness/lethargy
  • Depression
25
Q

In four steps, describe the clinical management of heart failure

A

⇒ Correct underlying cause

⇒ Non-pharmacological measures

⇒ Pharmacological therapy – symptomatic improvement, delay progression of HF, reduce mortality

⇒ Treat complications / associated conditions / CV risk factors e.g. arrhythmias

26
Q

What are the five main drugs used in the pharmacological management of heart failure?

A
  • Diuretics
  • ACE inhibitor
  • ARB
  • β-blocker
  • Spironolactone
27
Q

Describe the effects of beta blockers on heart failure

A
  • Reduce HR (cardiac beta receptor + myocardial oxygen demand)
  • Reduce BP (reduced CO + myocardial oxygen demand)
  • Reduce mobilisation of glycogen
  • Negate unwanted effects of catecholamines
28
Q

what conditions that patients have mean they shouldn’t be prescribed ACEi and ARB

A
  • renal artery stenosis (kidney already low perfused, ACE inhibitor will prevent more blood entering kidney)
  • AKD
  • Pregnancy
  • idiopathic angioedema (ACIi)
29
Q

who should you not prescribe Dilydropyridine to?

A

unstable angina, severe aortic stenosis

30
Q

who should you not prescribe Phenylalkylamines to?

A

poor LV function and AV conduction delay as it prolongs the action potential

31
Q

staging of hypertension

A
  • STAGE 1: bp ranging from 140/90 to 159/99
  • STAGE 2: 160/100 to 180/120
  • STAGE 3: 180 or higher
32
Q

what is the order of treatment for treating hypertension

A
33
Q

how do ACEi help diabetes

A
  • reduces diabetic neuropathy and CKD
  • it dilates the efferent arteriole of the glomerulus so reduces proteinuria
  • two pronged approach: reduces peripheral vascular resistance → vasodilation → reduced intraglomerular pressure
34
Q

what to do if blood pressure isn’t controlled after prescribing both ACEi, ARB and CCB and thiazide like diuretic

A
  • spironolactone - aldosterone receptor antagonist
  • adverse effects: hyperkalemia, gynaecomastia (men grow breast)
  • people to avoid: hyperkalemia, Addisons

if someone has high K then you can give them a and b blockers

34
Q

what to do if blood pressure isn’t controlled after prescribing both ACEi, ARB and CCB and thiazide like diuretic

A
  • spironolactone - aldosterone receptor antagonist
  • adverse effects: hyperkalemia, gynaecomastia (men grow breast)
  • people to avoid: hyperkalemia, Addisons

if someone has high K then you can give them a and b blockers

35
Q

what is the last resort to treating someone with high blood pressure

A

B-adrenoceptor blockers

  • decrease sympathetic tone so reduce myocardial contractility, also reduce renin secretion
  • adverse effects: bronchospasm, heart block, cold hands, lethargy
  • people to avoid: asthma, haemodynamic instability, hepatic failure
36
Q

non pharmaceutical things to do to reduce blood pressure

A
  • regular exercise
  • balanced diet
  • reduced stress
  • reduce alcohol
  • stop smoking
37
Q

diagnosis of hypertension

A
  • take blood pressure when sitting and standing
  • AMBP - Ambulatory blood pressure (device you attach to measure Bp regularly)
  • HBPM - home blood pressure is where you measure bp frequently
38
Q

what is the pathophysiology of hypertension

A
  • high Bp
  • vascular changes / remodelling, thickening and hypertrophy
  • increased vasoactive substances
  • vascular remodelling due to salt sensitivity
  • endothelial dysfunction and increased ROS

CAN lead to:

→ permanent and maintained hypertrophy

→ end organ damage

→ hypertensive heart disease (dilated cardiac failure)

39
Q

what is the white coat effect

A
  • when someone visits the doctor their Bp rises
40
Q

what is the white coat effect

A
  • when someone visits the doctor their Bp rises
41
Q

target blood pressure

A
  • <140/90 for under 80 including type 2 diabetes
  • <150/90 over an including 80 yrs
  • <135/85 type 1 diabetes

SA Clinical Pharmacology & Therapeutics (36 decks)

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