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Clinical Pharmacology > Hypertension and Heart Failure > Flashcards

Hypertension and Heart Failure Flashcards

1
Q

How do you calculate MAP?

A

MAP = CO x TPR

(CO= SV x HR)

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2
Q

What are the 2 key drivers to increase blood pressure when blood pressure drops?

A

Increased sympathetic activity and activation of RAAS

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3
Q

What end organ damage can result from hypetension?

A
  • Renal
  • Peripheral Vascular Resistance
  • Aneurysm
  • Vascular Dementia
  • Retinal Disease
  • Hypertensive heart disease → LVH causing cardiac failure
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4
Q

Why treat hypertension if it asymptomatic?

A

Early management slows down/ prevents progression to CVD

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5
Q

What is the NICE definition of hypertension?

A

Hypertension = 140/ 90 mmHg

(>40% of UK population)

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6
Q

What are the 2 main types of hypertension and what are their respective incidences?

A

1) Essential/ primary/ idiopathic - 90%
2) Secondary - related to other pathology (disease/ tumours)

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7
Q

What is the white coat/ clinic effect?

A

Elevated blood pressure when measured in the clinic vs a home

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8
Q

What is best practice for measuring BP?

A
  • Measure with patient sitting, arm supported and relaxed
  • Measure both arms - >15 mmHg difference repeat the measurement and use arm with highest reading
  • +/- ABPM / HBPM
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9
Q

what blood pressure would be considered a hypertensive emergency?

A

> 180 /120 mmHg

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10
Q

Define the stages of hypertension

A

Stage 1: 140/90 mmHg - 159/99 mmHg

Stage 2: 160/100 mmHg >

Stage 3: systolic blood pressure of 180mmHg or higher or diastolic 120mmHg or higher

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11
Q

What BP is defined as pre-hypertension?

A

>120/80 but <140/90 mmHg

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12
Q

What advice would you give to someone who is pre-hypertensive?

A
  • Promote regular exercise
  • Modified healthy/ balance diet
  • Reduction in stress and increased relaxation
  • Limit/ reduce alcohol intake
  • Discourage excessive caffeine consumption
  • Smoking cessation
  • Reduce dietary NaCl
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13
Q

What are the main actions of Angiotensin II?

A
  • Increase sympathetic activity
  • Tubular Na+/ Cl- reabsorption and K+ excretion → H2O retention
  • Aldosterone secretion from the adrenal gland
  • Increase arteriolar vasoconstriction
  • ADH secretion from pituitary → H2O absorption
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14
Q

Which receptor type does Angiotension II primarily exert its actions via?

A

AT1

(There are AT1 and AT2 receptors)

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15
Q

How does a reduction in Angiotensin II effects cause a reduced BP?

A
  • vasodilation
  • reduction in aldosterone release → increased Na+ and H2O excretion
  • reduced ADH release → increased H2O excretion
  • reduced cell growth and proliferation (vascular smooth muscle)
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16
Q

How is Angiotension II produced independently of ACE?

A

Chymases can convert angiotensin I → angiontensin II

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17
Q

What are the 2 major ACEi?

A

Lisinopril

Ramipril

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18
Q

What are the main side effects of ACEi?

A
  • hypotension
  • Dry cough
  • Hyperkalaemia (low aldosterone increases K+)
  • Renal failure (esp. in renal artery stenosis)
  • Angiodema (more common in black population)
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19
Q

Why do ACEi cause dry cough?

A

Bradykinin is a substrate for ACE too

Inhibiting ACE therefore builds up bradykinin which causes cough and vasodilation by NOS/NO and PGI2

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20
Q

In which patients are ACEi contraindicated in?

A
  • Renal Artery Stenosis
  • AKD
  • Pregnancy
  • Breastfeeding
  • CKD
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21
Q

In which patients should ACEi be prescribed with caution?

A
  • Other drugs that increase K+
  • NSAIDs
  • Other anti-hypertensives
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22
Q

Which receptor to Angiotensin II receptor blockers (ARBs) target?

A

AT1 receptor

More effective at inhibiting Ang II mediation vasoconstriction via chymase production

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23
Q

What are the 2 major ARBs used to treat hypertension?

A

Candesartan

Losartan

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24
Q

What are the benefits of ARBs over ACEi?

A

No effect on bradykinin so no dry cough and less angiodema

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25
Q

In which patients are ARBs contraindicated in?

A
  • Renal artery stenosis
  • AKD
  • Pregnancy
  • Breastfeeding
  • CKD
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26
Q

In which patients should ARBs be used with caution?

A
  • Other drugs that increase K+
  • NSAIDs
  • Other anti-hypertensives
27
Q

What is the normal function of calcium channels?

A
  • L type calcium channels found throughout the body (vascular smooth muscle and cardiac myocytes, AV/ SA node)
  • Allow inward Ca2+ influx into cells
  • Stimulates CICR from internal Ca2+ stores
  • Ca2+ release causes contraction
28
Q

Where do calcium channel blockers target VOCC?

A

3 classes of VOCC target different sites on the alpha 1 unit of VOCC

Selective for vascular smooth muscle/ myocardium

29
Q

What are the 3 classes of CCBs?

A
  1. Dihydropyridines
  2. Phenylalkylamines
  3. Benzothiazapines
30
Q

How do Dihydropyradines work?

A

Selectively target Calcium channels in peripheral vasculature

(little chronotropic or inotropic effect)

1st line CCB for hypertension

31
Q

How do Phenylaklyamines work?

A

Target Calcium channels depressing SA and AV node → slow conduction → negative inotropy

32
Q

How do benzothiazapines?

A

act on both myocardium and vascular smooth muscle

(sit in between benzothiazapines)

33
Q

In which patient groups are CCBs the primary choice of antihypertensive?

A

Patients with low renin e.g. black african patients

34
Q

What are the main dihydropyridines?

A
  • Amlodipine - long half life
  • Nifedipine
  • Nimodipine - selective for cerebral vasculature (useful in subarachnoid haemorrhage)
35
Q

What are some of the side effects of dihydropyridines?

A
  • Ankle swelling
  • Flushing
  • Headaches (due to vasodilatoin)
  • Palpitations (compensatory tachycardia)
36
Q

In which patients are dihydropyradines contraindicated in?

A
  • Unstable angina
  • Severe aortic stenosis
37
Q

In which patients should you use dihydropyradines with caution?

A
  • Amlodipine and simvastatin
  • Other anti-hypertensives
38
Q

What is the main phenylalkylamine?

A

Verapamil

39
Q

How do CCBs phenylalkylamines work? Which patients are they used to treat?

A

Class IV anti-arrhythmic agent prolongs the action potential / effective refractive period

Less peripheral vasodilation, negative chronotrophic and ionotropic effects

Used to treat: Arrhythmia, angina and hypertension

40
Q

What are some of the side effects of phenylalkylamines?

A
  • constipation
  • bradycardia
  • heart block
  • cardiac failure
41
Q

In which patients are phenylalkylamines contraindicated in?

A
  • Poor LV function
  • AV nodal conduction delay
42
Q

Which patients are phenylalkylamines to be used with caution?

A
  • Patients on Beta blockers
  • Other anti-hypertensives and antiarrhythmics
43
Q

What is the name of the main benzothiazapine?

A

Diltiazem

44
Q

What is the MoA of Thiazide and thiazide like diuretics?

A

Inhibit the N+/ Cl- co transporter in the distal convoluted tubule

Effect: increased Na+ and H2O excretion

45
Q

What are the 2 main thiazide and thiazide like diuretics?

A

Bendroflumethiazide

Indapamide

46
Q

What are some of the side effects of thiazide/ thiazide like diuretics?

A
  • Hypokalaemia
  • Hyponatraemia
  • Hyperuricemia
  • Arrhythmia
  • Increased glucose (esp. with beta blockers)
  • Increased cholesterol and triglyceride
47
Q

What patients should thiazide/ thiazide-like diuretics not be prescribed to?

A
  • Hypokalaemia
  • Hyponatraemia
  • Gout
48
Q

In what patients should thiazide/ thiazide like diuretics be used with caution?

A
  • NSAIDs
  • Other drugs that decrease K+
49
Q

Why are type II diabetics oftered ACEi/ ARB first line?

A

2 pronged approach

  • Decreased Peripheral Vascular Resistance which decreased BP
  • AND dilates the efferent glomerular arteriole→ decreased intraglomerular pressure
50
Q

If BP is not controlled after the 3rd step of treatment what can you add to the patients treatment?

Explain the MoA?

A

Spironolactone → aldosterone receptor antagonist

51
Q

Which patients should spironolactone be contraindicated / used with caution?

A

Contraindicated - hyperkalaemia, addison’s

Use with caution- other drugs that increase K+ , ACEi and ARBs

52
Q

Which drugs can you use to lower BP in pregnancy?

A

Labetalol (B blocker)

53
Q

How do Beta blockers work?

A
  • Block Beta adrenoreceptors
  • Decrease sympathetic tone by blocking action of NA and reducing myocardial contraction → decreased CO
  • Decreased renin secretion by B1
  • B1 are selective for the heart
  • B2 are selective for the lungs
54
Q

What are some of the side effects of Beta blockers?

A
  • Bronchospasm
  • Heart Block
  • Raynaud’s
  • Lethargy
  • Impotence
  • Can mask tachycardia
55
Q

Name 3 Beta blockers

A
  • Labetalol
  • Bisoprolol
  • Metoprolol
56
Q

Which patients should beta blockers not be prescribed to/ prescibred with caution?

A

Contraindicated: asthmatics, COPD, Haemodynamic instability, hepatic failure

Use with caution: non-dihydropyridine CCB (Verapamil and Diltiazem) can cause asystole

57
Q

Explain the MoA of alpha adrenoreceptors blockers

A
  • selective antagonist for alpha 1 adrenoreceptors
  • reduce peripheral vascular resistance
58
Q

What are some of the side effects of alpha adrenoreceptor blockers?

A
  • postural hypotension
  • dizziness
  • syncope
  • headache
  • fatigue
59
Q

Name 2 alpha adrenoreceptor blockers

A
  • Doxazosin
  • Tamsulosin (used to treat urinary tract problems: bladder, neck and prostate BPH)
60
Q

When should alpha adrenoreceptors be used with caution/ not used?

A

Contraindicated: Postural hypotension

Use with caution: dihydropyridine CCBs (can cause oedema)

61
Q

What are the aims when treating a patient with heart failure? (mechanism on the body)

A

Aim:

  • Dilate capacitance veins
  • Decrease preload
  • Reduced Sympathetic stimulation
  • Reduce blood volume
62
Q

What non-pharmacological methods can be used to manage heart failure?

A
  • reduce salt intake
  • reduce liquid intake ~1.5L
63
Q

What are the goals when treating heart failure?

A
  • reduce symptoms
  • manage increase in exercise tolerance
  • address arrhytmia, hyperlipidaemia, diabetes
  • decreased mortality

Clinical Pharmacology (25 decks)

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