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Clinical Pharmacology > 3.1 Hypertension And Heart Failure > Flashcards

3.1 Hypertension And Heart Failure Flashcards

1
Q

How do you calculate mean arterial pressure?.

A

CO x TPR.

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2
Q

What is resistance to flow inversely proportional to?

A

Inversely proportional to the radius (to the 4th power)

So, Vacoconstiction = increased peripheral resistance = increased BP

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3
Q

What can hyperinsulinemia and hyperglycaemia lead to?

A

Endothelial dysfunction and reactive oxygen species, decreased NO

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4
Q

Why do you need to treat Hypertension?

A

Precursor to cardiovascular disease

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5
Q

Define hypertension

A

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

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6
Q

What are some causes of hypertension?

A

White coat/clinic
Isolated systolic/diastolic (only one is raised)
Prehypertensive
Secondary

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7
Q

How do you diagnose and treat hypertension?

A
  • screening sessions
  • increase public awareness of risk factors
  • reliable diagnoses based on clinical guidelines
  • promote appropriate lifestyle changes to limit risk
  • regulate monitoring and refinement of medication.
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8
Q

What are the clinical methods of diagnoses of hypertension?

A

Measure BP with patient sat relaxed with a supported arm

Measurements in both arms should be similar, within 20mmHg

Severe = medical emergency, send to A&E

Patient management follows diagnoses

Cardiovascular risk and wend organ damage should be assessed whilst waiting for HT conformation

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9
Q

Normal BP?

A

<120/80 mmHg

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10
Q

Stage 1 hypertension measuring ?

A

140/90 mmHg or higher

Home - 135/80 mmHg

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11
Q

Stage 2 hypertension BP?

A

160/100 mmHg or higher

Home 150/95

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12
Q

Severe hypertension bp?

A

SYSTOLIC IS 180 mmHg or higher or diastolic is 110 mmHg or higher

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13
Q

What is prehypertension?

A

Elevated BP below stage 1 diagnoses with no end organ damage that can be treated in the first instance with lifestyle changes

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14
Q

What can lifestyle changes can treat elevated bp in prehypertension?

A

Regular exercise
Modified health/balanced diet
Reduction in stress and increased relaxation
Limited/reduced alcohol intake
Discourage excessive caffeine consumption
Smoking cessation
Reduction in dietary sodium

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15
Q

What are some primary HT therapeutic agents?

A

ACE inhibitors
Angiotensin receptor blockers
Calcium channel blockers
Diuretics

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16
Q

Where does ACE and Ang 2 act?

A

Luminal surface of capillary endothelial cells, predominantly in the lungs

Catalysts conversion of Ang 1 to And 2 which is a vasoconstrictor

Ang 2 acts through AT1 and AT2 receptors

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17
Q

Name 4 ACE inhibitors.

A

Captopril
Enalapril
Lisinopril
Ramipril

18
Q

Why do ace inhibitors cause a dry cough?

A

ACE substrate = bradykinin

If ACE is inhibited, get a build up of bradykinin = dry cough

19
Q

What side affects are associated with ACE inhibitors?

A

Dry cough
Angioedema
Renal failure
Hyperkalaemia

20
Q

How do angiotensin 2 receptor blockers work?

A

Block AT1 receptors which carry out majority of angiotensin 2 functions (unlike AT2 receptor)

Directly targeting AT1 receptors means they’re more effective at inhibiting Ang 2 mediated vasoconstriction

21
Q

What side effects do you get with ang 2 receptor antagonists?

A

Renal failure and hyperkalaemia

No dry cough as no effect on bradykinin

22
Q

Name 4 ang 2 receptor antagonists

A

Losartan
Candesartan
Eprosartan
Irbesartan

23
Q

What do calcium channel blockers target?

A

Calcium inhibiated smooth muscle contraction

There are three classes that interact with different sites on a1 subunit of VOCC selectivity for vascular smooth muscle cells or myocardium

24
Q

What are the three classes of calcium channel blockers?

A
  • Dihydropyridine

Non dihydropyridine
- Phenylalkamines and benzothiazapines

25
Q

How do dihydropyridine CCB work and what are their properties?

A

More selective for peripheral vasculature, show little chronological or inotropic effect

  • first line CBB for HT
  • good oral absorption
  • protein bound
  • metabolised by liver
26
Q

Name an example of a dihydropyridine CBB and name its adverse effects.

A

Amolodipine is an example

Adverse effects

  • sympathetic NS activation = tachycardia (rare)
  • palpitation
  • flushing/sweating/throbbing headache
  • oedema
27
Q

What is the mode of phenylalkylamines CBB?

A

Depresses SA node and slows AV conduction, negative inotropy

Prolongs the AP and effective refractory period

Impede ca transport across myocardial and vascular smooth muscle cell membrane

28
Q

Give an example of a phenylalkylamine and give it’s adverse effects

A

Verapamil

Effects include

  • constipation
  • bradycardia
  • negative inotrope = can worsen heart failure, especially with a beta blocker
29
Q

What are the properties of benzothiazapines CBB ?

A

Impede ca transport across ca and smooth muscle cell membrane

Prolong AP

30
Q

Name a benzothiazapines CCB and give its adverse effects

A

Diltiazem

Effects

  • risk of bradycardia
  • negative inotropic effect less than verapamil = can worsen heart failure
31
Q

What are some adverse effects of thiazides? Name an example

A

Example = bendroflumethiazide

Effects

  • hypokalaemia
  • increased urea and Uris acid levels
  • impaired glucose tolerance especially with beta blockers
  • cholesterol and triglycerides levels increase
  • activates RAAS
32
Q

Why is there no point in giving ARBs to a low renin patient?

A

Low activity in RAAS system anyway so no point in targeting it for treatment.

33
Q

In pregnancy or a hypertensive emergency, what centrally acting drugs would you use?

A

Labetalol reduced sympathetic outflow

34
Q

What is spironolactone?

A

Mineralocorticoid/ aldosterone receptor antagonists

35
Q

What is amiloride?

A

A K+ sparing diuretic acting on distal tubule

36
Q

What is the effect of alpha adrenoreceptors blocking agents? Name an example.

A

Doxazosin is an example

They antagonise the contractile effects of noradrenaline on vascular smooth muscle

Reduced peripheral vascular resistance

Benign effect on plasma lipids/glucose

Safe in renal disease

Adverse effects

  • postural hypotension
  • headache and fatigue
  • oedema
37
Q

What is the effect of beta adrenoreceptors blockers? Name an example

A

Bisoprolol is an example

Decreased sympathetic tone by blocking Nad and reducing myocardial contraction = decreased CO = decreased renin secretion

38
Q

What are the adverse effects of beta adrenoreceptors blockers?

A

Adverse effects

  • bronchoconstriction so don’t give in asthma, COPD and 2nd/3rd degree heart block
  • mask tachycardia = sign of insulin induced hyperglycaemia = caution in diabeties
  • lethargy and impaired concentration
  • reduced excersise tolerance
  • bradycardia
  • raynauds

E.g bisoprolol

39
Q

What are the aims of heart failure treatment?

A

Manage symptoms
Increase exercise tolerance
Decreased mortality
Address arrhythmia

NB: furosemide is typically used in most patients for symptoms but has little impact on survival

40
Q

How can ace inhibitors and ARBs treat heart failure?

A

In LV dysfunction

Low initial dose reduces risk of sudden rapid fall in BP, especially in patients already taking diuretics

If ACE inhibitors not tolerated, use ARB as alternative

If not working can use both together

Make sure you monitor renal function

41
Q

Why may a patient be given spironolactone with a ACE inhibitor or diuretic?

A

It maximises their effects.

NB: spironolactone is a aldosterone/mineralocorticoid receptor antagonist

42
Q

What is the role of B adrenoreceptors antagonists?

A

Recommended for all patients with stable clinical heart failure

Introduced once ACE inhibitor or ARB therapy is initiated
Blunts sympathetic influences especially on HR = slower HR = longer diastolic filling period = better filling = more output

May stabilise electrical conduction reducing arrhythmia

May also blunt circulating RAAS by working on renin but probably minor since already on ACE

Low initial dose which may cause transient worsening of symptoms

Clinical Pharmacology (27 decks)

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