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Semester 4 - Clinical Pharmacology And Therapeutics > Hypertension And Heart Failure > Flashcards

Hypertension And Heart Failure Flashcards

1
Q

What is blood pressure?

A

Blood pressure provides a driving force to defuse organs with blood - it determines the tissue perfusion pressure.

It is not uniform throughout the body and, as result of the cardiac cycle, is cyclical.

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2
Q

What is mean arterial pressure equal to?

A

MAP = CO X TPT

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3
Q

What is CO equal to?

A

CO = SV x HR

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4
Q

Describe the relationship between resistance and increased maBP

A

Smooth muscle tome changes TPR.

Vasoconstriction causes an increase in TPR and therefore an increase in BP.

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5
Q

Why does elevated BP cause an increase in morbidity and mortality?

A

Leads to vascular changes inc. remodelling and thickening and hypertrophy.

Increase vasoactive substances inc. ET-1, NAD, angII

Vascular remodelling as direct result of local salt sensitivity

Hyperinsulinemia and hyperglycaemia - endothelial dysfunction and ROS cause decreased NO. Resulting in permanent and maintained medial hypertrophy of vasculature causing increased TPR and decreased compliance.

End organ damage (renal, peripheral vascular disease, aneurysm, vascular dementia, retinal disease)

LVH - dilated cardiac failure

All causing increasing morbidity and mortality.

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6
Q

Why is the incidence of hypertension lower in women?

A

As they are protected until menopause (not sure why)

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7
Q

Why do you treat HT even when it presents asymptoatically?

A

Because the risk of CHD and stroke increases.

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8
Q

Define Hypertension

A

An elevation in blood pressure that is associated with an increase in risk of harm. .

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9
Q

What level of BP defines hypertension?

A

Over 140/90

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10
Q

How do you diagnose and treat HT?

A

Screen those at risk

Increase public awareness of risk factors.

Reliable diagnoses based on clinical guidelines.

Promote appropriate lifestyle changes to limit risk - no immediate gain.

Regular monitoring and refinement of medication.

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11
Q

What is the best practise for clinically diagnosing BP?

A

Measure BP while patient is sitting, relaxed and arm is supported.

Measure in both arms and if there is >20mmHg difference then repeat and use higher reading.

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12
Q

What is stage 1 hypertension?

A

> 140/90 mmHg

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13
Q

What is stage 2 hypertension?

A

> 160/100 mmHg

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14
Q

What is severe hypertension?

A

> 180 mmHg systolic or > 100 mmgHg diastolic

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15
Q

How does diabetes and renal change BP criteria?

A

Stage 1 = > 130/80

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16
Q

What is prehypertension?

A

Elevated BP below stage 1 diagnoses with no end organ damage.

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17
Q

What do you recommend for people in a prehypetensive stage?

A

Lifestyle changes:

Regular exercise

Healthy / balanced diet

Reduce stress and relaxation

Limit / reduce alcohol intake

Discourage excessive caffeine consumption

Smoking cessation

Reduction in dietary sodium

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18
Q

What are the primary HT therapeutic agents?

A

Angiotensin converting enzyme (ACE) inhibitors
Angiotensin (AT1) receptor blockers (ARBs)
Calcium channel blockers (CCBs)
Diuretics
Others in specific circumstances

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19
Q

How does ACE work?

A

ACE is present on the luminal surface of capillary endothelial cells, predominantly in the lungs.
ACE catalyses the conversion of Ang-I to Ang-II, a potent active vasoconstrictor.

Ang-II works through AT1 and AT2 receptors.

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20
Q

How do ACE inhibitors work?

A

Limit conversion of AngI-AngII by inhibiting circulating and tissue ACE

So:
Vasodilation
Reduced aldosterone release
Reduced ADH release
Reduced cell growth and proliferation

All can contribute to antihypertensive effects.

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21
Q

Give exampleof ACE inhibitors

A

Ramipril
Lisinopril
Enalapril
Captopril

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22
Q

What are some common side effects of ACE inhibitors?

A

Dry cough (bradykinin)

Angiodema (more common in black people)

Renal failure (inc. renal artery stenosis)

Hyperkalaemia

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23
Q

What is losartan?

A

An ARB (angiotensin receptor blocker)

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24
Q

Describe how ARBs work

A

They directly target AT1 receptors so are more effective than ACEi at inhibiting Ang-II mediated vasoconstriction.

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25
Q

Why no cough on ARBs?

A

As don’t make bradykinin because directly act onAT1 receptor. But, means less effective in low-renin hypertensives.

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26
Q

What are the side effects of ARBs?

A

Renal failure

Hyperkalaemia

27
Q

Where are L-type calcium channels?

A

They are expressed through the body including:
Vascular smooth muscle cells
Cardiac myocytes

28
Q

How do CCBs work (broadly)?

A

LTCCs allow inward Ca2+ influx into cells via VOCCs.

Large Ca flux into cell, further Ca from ST and activation of contractile proteins (actin and myosin).

CCBs target Ca initiated smooth muscle contraction.

29
Q

What are the classes of CCBs?

A

Dihydropyridine

Phenylalkylamines (non-dihydropyridine)

Benzothiazapines (non-dihydropyridine)

30
Q

What are dihydropyridies class selective for?

A

Selective for vascular smooth muscle.

They show little chronotropic or inotropic effects (first line CCB for HT)

31
Q

What do phenylalkamines do?

A

They depress SA node and slow AV conduction, they express negative inotropy.

32
Q

When are CCBs used?

A

They are the primary choice in low-renin hypertensives.

33
Q

What is amlodipine?

A

CCB (dihydropyridine)

Nifedipine and nicardipine are also CCBs.

34
Q

What are the properties of dihydropyridines

A

Good oral absorption

Protein bound >90%

Metabolised by the liver

Few have active metabolites

35
Q

What are the adverse effects of dihydropyridines?

A

Sympathetic nervous system activation -tachycardia (rare)

Palpitations

Flushing, sweating, throwing headache

Oedema

Amlodipine and simvastatin react.

36
Q

What is verapamil?

A

A phenylalkylamine

37
Q

Describe the action of phenylalkylamines

A

Impedes calcium transport across the myocardial and vascular smooth muscle cell membrane.

Classic IV anti-arrhythmic agent / prolongs the AP / effective refractory period.

Less peripheral vasodilation, negative chronotropic and inotropic effects.

Arrhythmia, angina (hypertension)

38
Q

What are the adverse effects of phenylkylamines?

A

Constipation
Risk of bradycardia
Negative inotrope -can worse HF -additive with B blocker.

39
Q

What is diltiazem?

A

Benzothiazapine

40
Q

Describe the properties of benzothiazapines (diltiazem)

A

Impedes Ca transport across the myocardial and vascular smooth muscle cell membrane.

Prolongs the action potential / effective refractory period

Sits between amlodipine and verapamil in vascular and cardiac effects.

Angina (hypertension)

41
Q

What are the adverse effects of diltiazem?

A

Risk of Bradycardia

Negative inotropic effect (but less than verapamil). Can worsen HF

42
Q

How do thiazide diuretics work?

A

Moderately potent, inhibit Na+ reabsorption in DCT.

Diuresis resulting in lower blood and extracellular volume - low TPR

Useful over CCBs in oedema.

Long term effects mediated by sensitivity of VSM to vasoconstrictors Ca2+ - we think

43
Q

What are the adverse effects of thiazide diuretics?

A

Hypokalaemia

Increased urea and uric acid levels

Impaired glucose tolerance

Cholesterol and triglyceride levels increased

Activates RAAS

44
Q

What other therapeutic agents can treat hypertension?

A

alpha-adrenoreceptor blockers
beta-adrenoreceptor blockers
Spironolactone
Amiloride (K+ sparing diuretic on DCT)
Direct renin inhibitor (aliskirin)
Other direct vasodilators e.g. nitrates (hypertensive emergency - I.V.)
Centrally acting drugs - labetalol - reduce sympathetic outflow.

45
Q

What is spironolactone

A

Mineralcorticoid / aldosterone receptor antagonist

46
Q

What is labetalol?

A

A centrally acting drug that reduces sympathetic outflow.

47
Q

What is doxazosin?

A

alpha-adrenoreceptor antagonist.

48
Q

How do alpha-adrenoreceptors work?

A

Selective antagonism at post-synaptic a-1 adrenoreceptors and antagonise the contractile effects of noradrenaline on vascular smooth muscle.

Reduces peripheral vascular resistance

Benign effect on plasma lipids / glucose

Safe in renal disease

49
Q

What a re the adverse effects of a-adrenoreceptor blockers?

A

Postural hypertension

Headache and fatigue

Oedema (especially if combined with dihydropyridine)

50
Q

What is bisoprolol?

A

Beta-adrenoreceptor blocker

51
Q

How do B blockers work?

A

Decrease sympathetic tone by blocking Nad and reducing myocardial contraction - Decrease CO (decrease renin secretion) affording antihypertensive effects.

52
Q

What are the adverse effects of B blockers?

A 
Bronchoconstriction 
Tachycardia 
Lethargy and impaired concentration 
Reduced exercise tolerance 
Bradycardia 
Raynaud’s syndrome (cold hands)
53
Q

What is heart failure?

A

Abnormality in cardiac function which is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of metabolising tissues.

54
Q

What ate the symptoms of heart failure?

A

Firstly asymptomatic

Exercise intolerance, breathlessness, fatigue

55
Q

Describe the aetiology of Herat failure

A

Usually cardiomyopathy

Inherited:
Congenital hypertrophic CM
Arrhythmogenic RV CM

Acquired:
Ischaemic cardiomyopathy
Pressure overload 
Valve disease 
Infection / inflammation / alcohol
56
Q

Why is heart failure a self perpetuating spiral?

A

Because the physiological neurohormonal response in its attempt to compensate will eventually lead to further pathology.

57
Q

How do you manage HF?

A

Usually dealing with LV systolic dysfunction associated with reduced LV ejection fraction (<45%).

Where there is preserved ejection fraction the optimal treatment is not clearly defined.

Correct underlying cause (e.g. valve replacement)

Non pharmacological - reduce salt, liquid reduction

58
Q

What are the aims of the treatment of heart failure?

A

Reduction in symptoms

Managed increase in exercise tolerance

Decreased mortality

Address arrhythmias, hyperlipodaemia, diabetes

59
Q

What is almost always ued to treat HF?

A

Diuretics - furosemide

This reduces symptoms but has almost no impact on survival.

60
Q

How are ACEi and ARBs used to treat HF?

A

Used in all grades of LV dysfunction.

Low initial dose to reduce the risk a sudden rapid fall in BP, especially if already on diuretics.

If ACEi not tolerated,ARBs may be used as they have a similar benefit.

61
Q

How is spironolactone used to treat HF?

A

Amazing benefits, used in all later stage HF patients.

Use alongside ACEi and diuretic.

62
Q

When are B-blockers used to treat HF?

A

Recommended for all patients with CHF unless contraindicated or not tolerated.

Introduced once ACEi or AT1 antagonists is initiated.

63
Q

How do B blockers work to treat HF?

A

Benefit is related to blunting of sympathetic influences especially on heart rate.

Slower HR = longer diastolic filling period = better filling = more output.

May also stabilise electrical condition - reducing arrhythmias.

May blunt circulating RAAS directly inhibiting renin, but properly minor effect as already on ACEi

Low initial dose which may cause transient worsening of symptoms.

64
Q

Why is a persistent dry cough a common side effect fo ACEi?

A

Bradykinin is a substate for ACE.

ACE is kininase-II -breaks down kinins inc. BK.

ACEi therefore make more bradykinin.

So, it causes vasodilation via NOS/NO and PGI2

Causing a persistent dry cough.

Semester 4 - Clinical Pharmacology And Therapeutics (26 decks)

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