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Anaesthetic FRCA Primary - eLFH Pharmacology > eLFH - Vasodilators and Antihypertensives > Flashcards

eLFH - Vasodilators and Antihypertensives Flashcards

1
Q

Methods of reducing MAP

A

Reduce SVR

Reduce HR

Reduce SV

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2
Q

Methods of reducing SVR

A

Vasodilatation

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3
Q

Methods of reducing SV

A

Reduce preload - venodilatation or reduce circulating volume

Reduce contractility

Reduce afterload - arteriolar vasodilatation

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4
Q

Pathway of adreno-receptor intracellular action

A

Adrenaline binds to e.g. beta 2 receptor

GDP replaces GTP in Gs protein causing conformational change

Alpha subunit of Gs protein activates Adenylate cyclase

Magnesium binds to Adenylate cyclase as co-factor

AC converts ATP to cAMP

cAMP activate Protein Kinase A

PKA inhibits myosin light chain kinase

Therefore unable to phosphorylate myosin light chain and results in smooth muscle relaxation

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5
Q

Gs protein structure

A

Alpha subunit with GDP/GTP binding site

Beta subunit

Gamma subunit

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6
Q

Action of Atrial Natriuretic peptide

A

ANP stimulates membrane bound cGMP

Guanylyl cyclase on smooth muscle membrane converts GTP to cGMP intracellularly (cyclic Guanosine monophosphate)

cGMP activates Protein Kinase G

PKG activates Myosin phosphatase and potassium channels (hyperpolarisation of cell) but inhibits calcium entry into cell

Results in smooth muscle relaxation

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7
Q

Classification of antihypertensives by site of action

A

Central nervous system

Peripheral autonomic nervous system

Direct action on vascular smooth muscle

Reducing blood volume (and direct action on smooth muscle)

Renin-angiotensin system

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8
Q

Antihypertensives which act via Central nervous system

A

Alpha 2 agonists

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9
Q

Examples of alpha 2 adrenergic receptor agonists (which also have some minimal alpha 1 agonism)

A

Clonidine

Methyldopa

Dexmedetomidine - more selective alpha 2 agonist

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10
Q

Routes of administration of clonidine

A

Epidural

Subarachnoid

IV

PO

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11
Q

Routes of administration of Methyldopa

A

PO

IV (rarely)

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12
Q

Mechanism of action of alpha 2 adrenergic receptor agonists

A

Alpha 2 receptor stimulation

Decreased noradrenaline release

Reduced alpha 1 receptor stimulation

Reduced sympathetic tone

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13
Q

Side effects of clonidine

A

Diuresis via inhibition of ADH release

Inhibits insulin release

Rebound hypertension post abrupt cessation

Sedation

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14
Q

Side effects of methyldopa

A

Sedation

Positive direct Coombs test in 10-20% cases

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15
Q

Antihypertensives which act on peripheral autonomic nervous system

A

Ganglion blocking agents

Adrenergic neurone blocking agents

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16
Q

Mechanism of action of Ganglion blocking agents

A

Non-depolarising competitive antagonist at ganglion type of nicotinic receptor of autonomic ganglia

Reduced sympathetic input to peripheral vasculature

Vasodilatation

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17
Q

Side effects of Ganglion blocking agents

A

Associated histamine release

Side effects mostly due to parasympathetic antagonism

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18
Q

Example of Ganglion blocking agent

A

Trimetaphan

Generally these agents aren’t used anymore

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19
Q

Mechanism of action of adrenergic neurone blocking agents

A

Enters adrenergic neurone via uptake 1 noradrenaline pathway

Displaces noradrenaline and prevents further norad release

Reduced alpha 1 receptor stimulation

Vasodilatation

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20
Q

Example of adrenergic neurone blocking agent

A

Gaunethidine

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21
Q

Route of administration of Guanethidine

A

PO

IV

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22
Q

Side effects of adrenergic neurone blocking agents

A

Diarrhoea

Postural hypotension

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23
Q

Use of adrenergic neurone blocking agents

A

Now only commonly used in chronic pain management

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24
Q

Antihypertensives which have direct action on vascular smooth muscle

A

Hydralazine

Nitrates

Sodium nitroprusside

Magnesium

Calcium channel blocking agents

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25
Q

Hydralazine mechanism of action

A

Hydralazine activates Guanylyl cyclase on smooth muscle cell membrane
(Also possible nitric oxide donor which also activates GC)

GC converts GTP to cGMP

cGMP decreases sensitivity to calcium and decreases calcium entry into cells

Vasodilatation - mainly acts on arterioles

26
Q

Bioavailability of hydralazine

A

Affected by acetylator status

27
Q

Side effects of hydralazine

A

Reflex tachycardia

Fluid retention

Increases cerebral blood flow

Nausea / Vomiting

Long term oral use can cause lupus like syndrome

28
Q

Nitrates mechanism of action

A

Nitrate converts to Nitric Oxide (NO)

NO activates Guanylyl cyclase on smooth muscle cell membrane

GC converts GTP to cGMP

cGMP decreases sensitivity to calcium and decreases calcium entry into cells

Vasodilatation

29
Q

Pharmacokinetics and pharmacodynamics of nitrates

A

Lower doses act on veins
Higher doses can act on arterioles

GTN (glyceryl trinitrate) highly lipid soluble so can be given transdermal route

30
Q

Side effects of nitrates

A

Headache

Flushing

Postural hypotension

Tachycardia

Tolerance

Methemoglobinemia

GTN is absorbed by PVC plastic

31
Q

Mechanism of tolerance to nitrates

A

Depletion of sulphydryl groups

32
Q

Sodium Nitroprusside mechanism of action

A

Sodium Nitroprusside converts to Nitric Oxide (NO)

NO activates Guanylyl cyclase on smooth muscle cell membrane

GC converts GTP to cGMP

cGMP decreases sensitivity to calcium and decreases calcium entry into cells

Vasodilatation

33
Q

Routes of administration of sodium nitroprusside

A

Only parenteral

Must cover syringes as can breakdown to form cyanide on light exposure

34
Q

Pharmacokinetics and pharmacodynamics of sodium nitroprusside

A

Rapid onset and offset

Acts on arterioles and venules

Increases ICP but autoregulation maintained

35
Q

Cautions with use of sodium nitroprusside

A

Can cause rebound hypertension if stopped abruptly as activates RAAS and increases plasma catecholamines

Inhibits hypoxic pulmonary vasoconstriction so can result in shunt

36
Q

Side effects of sodium nitroprusside

A

Reacts with oxyhaemoglobin to form cyanide, nitric oxide and methaemoglobin

High infusion rates can cause cyanide accumulation

Methaemoglobin can react with cyanide to form cyanmethaemoglobin

37
Q

How many cyanide ions form per molecule of sodium nitroprusside

A

5

38
Q

Cyanide overdose treatment

A

Dicobalt edetate - chelates cyanide so can be excreted

39
Q

Magnesium mechanism of action

A

1) Blocks alpha 1 receptors so less stimulation by catecholamines

2) Blocks L type calcium channels so less Ca2+ influx into smooth muscle cells

3) Generation of cAMP is magnesium dependent

40
Q

Uses of magnesium

A

Severe pre-eclampsia - unknown mechanism but may prevent cerebral vasospasm

Acute asthma

41
Q

Calcium channel blocking agents mechanism of action

A

Block L type Ca2+ channels, reducing Ca2+ influx into smooth muscle cells

Results in:
- Vasodilatation
- Reduced cardiac contractility
- Reduced propagation of cardiac depolarisation

42
Q

Subgroups of calcium channel blockers

A

Phenylalkylamines

Dihydropyridines

Benzothiazepines

43
Q

Examples of Phenylalkylamine calcium channel blockers

A

Verapamil

44
Q

Examples of Dihydropyridine calcium channel blockers

A

Nifedipine

Amlodipine

45
Q

Examples of Benzothiazepine calcium channel blockers

A

Diltiazem

46
Q

Uses of Phenylalkylamine calcium channel blockers

A

Anti-arrhythmia

47
Q

Uses of Dihydropyridine calcium channel blockers

A

Mainly cause arteriolar vasodilatation

Therefore used as antihypertensive and anti-anginal

48
Q

Uses of Benzothiazepine calcium channel blockers

A

Affect peripheral and myocardial Ca2+ channels

Used more as anti-anginal

49
Q

Side effects of calcium channel blockers

A

Headache

Flushing

Tachycardia

Postural hypotension

Ankle oedema

50
Q

Antihypertensives which reduce blood volume (and have direct action on smooth muscle)

A

Diuretics - commonly thiazide diuretics

51
Q

Thiazide diuretic mechanism of action

A

Lower dose - Activate potassium channels which cause hyperpolarisation and relaxation of smooth muscle cell

Higher dose - Inhibits Na+ and Cl- reabsorption in distal tubule of kidney

Initially CO drops but then recovers and SVR is reduced (possible due to low intracellular Na+)

52
Q

Side effects of diuretics

A

Potassium depletion

Adverse effects on lipid metabolism

53
Q

Antihypertensives affecting RAAS

A

ACE inhibitors

Angiotensin II receptor blockers

54
Q

ACEi and ARB mechanism of action

A
55
Q

Subgroups of ACEi / ARB and examples of each

A

Active drug - metabolised to active metabolites, e.g. Captopril

Pro drugs - activated in liver, e.g. Ramipril

Active drugs - excreted unchanged in urine, e.g. Lisinopril

56
Q

Side effects of ACEi / ARB

A

Transient hypotension on initiation

Renal failure with renal artery stenosis +/- NSAIDs

Hyperkalaemia / Hyponatraemia with reduced aldosterone

Dry cough

Proteinuria

Angio-oedema

Bone marrow suppression - rare

57
Q

Cause of dry cough with ACEi

A

Accumulation of bradykinin

58
Q

Antihypertensives used for deliberate perioperative hypotension

A

GTN

Alpha 1 adrenoreceptor blockers

Beta adrenoreceptor blockers

Sodium nitroprusside - rare

Hydralazine - rare

59
Q

Antihypertensives used for moderate hypertension in pregnancy

A

Oral treatment

Methyldopa
Labetalol
Nifedipine

60
Q

Antihypertensives used for severe hypertension in pregnancy

A

Labetalol PO / IV
Nifedipine PO
Magnesium IV
Hydralazine IV

61
Q

Antihypertensives used for essential hypertension

A
62
Q

Potential anaesthetic side effect of nifedipine

A

Can reduce the MAC of volatile agents

Anaesthetic FRCA Primary - eLFH Pharmacology (11 decks)

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