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

eLFH - Vasodilators and Antihypertensives Flashcards

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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
Hydralazine mechanism of action
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
Bioavailability of hydralazine
Affected by acetylator status
27
Side effects of hydralazine
Reflex tachycardia Fluid retention Increases cerebral blood flow Nausea / Vomiting Long term oral use can cause lupus like syndrome
28
Nitrates mechanism of action
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
Pharmacokinetics and pharmacodynamics of nitrates
Lower doses act on veins Higher doses can act on arterioles GTN (glyceryl trinitrate) highly lipid soluble so can be given transdermal route
30
Side effects of nitrates
Headache Flushing Postural hypotension Tachycardia Tolerance Methemoglobinemia GTN is absorbed by PVC plastic
31
Mechanism of tolerance to nitrates
Depletion of sulphydryl groups
32
Sodium Nitroprusside mechanism of action
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
Routes of administration of sodium nitroprusside
Only parenteral Must cover syringes as can breakdown to form cyanide on light exposure
34
Pharmacokinetics and pharmacodynamics of sodium nitroprusside
Rapid onset and offset Acts on arterioles and venules Increases ICP but autoregulation maintained
35
Cautions with use of sodium nitroprusside
Can cause rebound hypertension if stopped abruptly as activates RAAS and increases plasma catecholamines Inhibits hypoxic pulmonary vasoconstriction so can result in shunt
36
Side effects of sodium nitroprusside
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
How many cyanide ions form per molecule of sodium nitroprusside
5
38
Cyanide overdose treatment
Dicobalt edetate - chelates cyanide so can be excreted
39
Magnesium mechanism of action
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
Uses of magnesium
Severe pre-eclampsia - unknown mechanism but may prevent cerebral vasospasm Acute asthma
41
Calcium channel blocking agents mechanism of action
Block L type Ca2+ channels, reducing Ca2+ influx into smooth muscle cells Results in: - Vasodilatation - Reduced cardiac contractility - Reduced propagation of cardiac depolarisation
42
Subgroups of calcium channel blockers
Phenylalkylamines Dihydropyridines Benzothiazepines
43
Examples of Phenylalkylamine calcium channel blockers
Verapamil
44
Examples of Dihydropyridine calcium channel blockers
Nifedipine Amlodipine
45
Examples of Benzothiazepine calcium channel blockers
Diltiazem
46
Uses of Phenylalkylamine calcium channel blockers
Anti-arrhythmia
47
Uses of Dihydropyridine calcium channel blockers
Mainly cause arteriolar vasodilatation Therefore used as antihypertensive and anti-anginal
48
Uses of Benzothiazepine calcium channel blockers
Affect peripheral and myocardial Ca2+ channels Used more as anti-anginal
49
Side effects of calcium channel blockers
Headache Flushing Tachycardia Postural hypotension Ankle oedema
50
Antihypertensives which reduce blood volume (and have direct action on smooth muscle)
Diuretics - commonly thiazide diuretics
51
Thiazide diuretic mechanism of action
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
Side effects of diuretics
Potassium depletion Adverse effects on lipid metabolism
53
Antihypertensives affecting RAAS
ACE inhibitors Angiotensin II receptor blockers
54
ACEi and ARB mechanism of action
55
Subgroups of ACEi / ARB and examples of each
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
Side effects of ACEi / ARB
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
Cause of dry cough with ACEi
Accumulation of bradykinin
58
Antihypertensives used for deliberate perioperative hypotension
GTN Alpha 1 adrenoreceptor blockers Beta adrenoreceptor blockers Sodium nitroprusside - rare Hydralazine - rare
59
Antihypertensives used for moderate hypertension in pregnancy
Oral treatment Methyldopa Labetalol Nifedipine
60
Antihypertensives used for severe hypertension in pregnancy
Labetalol PO / IV Nifedipine PO Magnesium IV Hydralazine IV
61
Antihypertensives used for essential hypertension
62
Potential anaesthetic side effect of nifedipine
Can reduce the MAC of volatile agents

Anaesthetic FRCA Primary - eLFH Pharmacology (11 decks)

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