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Anaesthesiology > Pharmacology in Anaesthesia > Flashcards

Pharmacology in Anaesthesia Flashcards

1
Q

Name selective beta-1 antagonists

A

atenolol
metoprolol
bisoprolol
betaxolol
esmolol

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2
Q

Which drugs are safe to use in acute porphyrias

A

propofol
all neuromuscular blockers
all volatiles
opioids
local anaesthetics

?etomidate

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3
Q

Why do some anaesthetists avoid regional anaesthesia acute porphyrias?

A

In order to avoid confusion if neurological changes occur

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4
Q

Name dopamine antagonists

A

droperidol
promethazine
thiethylperazine
metoclopramide

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5
Q

Which disease causes increased resistance to depolarising neuromuscular blockers

A

myasthenia gravis

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6
Q

What is diazepam mixed with, and what is the result

A

Propylene glycol
Painful IV injection

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7
Q

What are the safe submucosal adrenaline doses for patients under anaesthesia

A

Anaesthesia with halothane: <2mcg/kg.
Arrhythmias occur in 50% of patients at doses >2.1mcg/kg

Anaesthesia with sevo/iso up to 1.2 MAC: 5mcg/kg
Arrhythmias occur in 33% of patients at doses 5-15mcg/kg

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8
Q

Side effects of propranolol

A

[propranolol is a non-selective B-blocker]
- blunted response to hypoglycaemia
- suppressed insulin secretion
- bronchoconstriction
- fatigue
- excessive myocardial suppression
- AV block
- rebound tachycardia after discontinuation
- accentuated response to potassium infusions

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9
Q

Effects of atropine

A
  1. reduced gastric acid secretion
  2. inhibition of salivary secretions
  3. tachycardia
  4. mydriasis
  5. decreased lower oesophageal sphincter tone
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10
Q

Which anticholinesterases can, and cannot, cross the blood brain barrier

A

Cannot cross:
neostigmine
pyridostigmine
edrophonium

Can cross:
physostigmine

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11
Q

Tell me about meperidine:
What is it,
What is important about its structure,
Metabolite,
Side effects

A

Opioid receptor agonist;
structurally similar to atropine;
metabolite normeperidine is renally excreted, causes delirium and seizures especially in patients with renal failure;
has local anaesthetic-like properties,
can impair myocardial contractility

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12
Q

Neuromuscular blockers that can cause histamine releast

A
  1. atracurium
  2. d-tubocurarine
  3. succinylcholine
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13
Q

Metoclopramide effects

A
  1. decreased secretions
  2. raised lower oesophageal tone
  3. increased gastric motility
  4. increased upper intestinal motility
  5. sedation
  6. dysphoria/agitation
  7. EPSEs
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14
Q

Causes of reduced sensitivity to non-depolarising neuromuscular blockers

A

hypercalcaemia
hyperparathyroidism

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15
Q

Drugs that enhance the effect of non-depolarising neuromuscular blockers

A
  1. aminoglycosides
  2. IV lignocaine
  3. magnesium
  4. volatiles
  5. dantrolene
  6. lithium
  7. furosemide
  8. calcium channel blockers
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16
Q

Laudanosine:
what is it,
how is it excreted,
what is its structure,
effect on CNS

A

Metabolite of atracurium and cisatracurium due to the effect of plasma cholinesterases;
renal and hepatic excretion;
tertiary amine;
crosses BBB and stimulates CNS

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17
Q

What are possible mechanisms for the cardiovascular effects of neuromuscular blockers

A

a. histamine release
b. effect on cardiac muscarinic receptors
c. effect on autonomic ganglia nicotinic receptors

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18
Q

Pre-curarisation attenuates which effects of succinylcholine

A

raised intraoccular pressure,
raised intracranial pressure,
myalgia,
bradycardia

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19
Q

What is the pH of thiopental and what is the relevance thereof

A

10.5
Highly alkaline, so high risk of tissue damage if injected arterial or subcutaneously;
bacteriostasis - stays sterile for 6 days at 22C;
is incompatible with most opioids, catecholamines, and neuromuscular blockers

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20
Q

Conditions where succinylcholine causes severe hyperkalaemia (only after a few days)

A
  1. severe burns
  2. severe abdominal infections
  3. stroke
  4. spinal cord transection
  5. myopathies
  6. muscular atrophy due to disease or disuse
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21
Q

Flumazenil:
what is it,
what are its side effects

A

specific antagonist to benzodiazepines;
nausea and vomiting
dizziness
tremors
hypertension

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22
Q

Triggers of acute intermittent porphyrias

A
  1. starvation
  2. dehydration
  3. stress
  4. sepsis
  5. certain drugs
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23
Q

Drugs that may trigger acute intermittent porphyrias

A

barbiturates
ketorolac
pentazocine
diazepam
phenytoin

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24
Q

Drugs that increase CSF production

A

enflurane
desflurane (only in setting of hypocapnoea)

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25
Q

Drugs that inhibit CSF production

A

halothane
furosemide
acetazolamide

(and hypothermia)

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26
Q

Drugs that can enhance conduction via accessory atrial pathways
(and are thus contraindicated in WPW syndrome)

A

pancuronium
ketamine
verapamil
meperidine

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27
Q

What does pseudocholinesterase metabolise

A

acetylcholine
succinylcholine
mivacurium
ester-type local anaesthetics

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28
Q

Ageing affects the recovery index of which non-depolarising muscle relaxants

A
  1. vecuronium
  2. d-tubocurarine
  3. pancuronium
  4. rocuronium
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29
Q

Side-effects of cyclosporine therapy

A
  1. limb parasthesias (50%)
  2. nephrotoxicity (25-38%)
  3. hypertension
  4. headache
  5. seizures
  6. somnolence/confusion
  7. elevated liver enzymes
  8. allergy
  9. gum hyperplasia
  10. hirsutism
  11. hyperglycaemia
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30
Q

Indications for cyclosporine therapy

A
  1. anti-rejection after organ transplant
  2. Crohn’s disease
  3. uveitis
  4. psoriasis
  5. rheumatoid arthritis
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31
Q

Side effects of dexmedetomidine

A
  1. hypertension initially, then hypotension after an hour
  2. bradycardia
  3. sinus arrest
  4. respiratory arrest
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32
Q

Tolerance develops eventually to which effects of morphine

A
  1. euphoria
  2. analgesia
  3. nausea
  4. respiratory depression
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33
Q

Tolerance DOES NOT develop to which effects of morphine

A

constipation
miosis

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34
Q

Cimetidine: side effects

A
  1. confusion/delayed emergence
  2. bradycardia
  3. elevated aminotransaminases
  4. CYP inhibition therefore impaired metabolism of:
    diazepam, lignocaine, propranolol
35
Q

Post anaesthetic shivering:
causes

A
  1. hypothermia
  2. pain
  3. anaesthetic
  4. transfusion reaction
36
Q

Post-anaesthetic shivering: drug treatment

A
  1. narcotics
  2. tramadol
  3. meperidine
  4. propofol
  5. cimetidine
  6. magnesium sulphate
  7. physostigmine
  8. dexmedetomidine
  9. ketanserin (5HT2-antagonist, anti-hypertensive)
37
Q

Treatment for accidental intra-arterial injection of thiopental

A
  1. blocks: stellate ganglion, brachial plexus
  2. antithrombotics: heparin, urokinase
  3. intra-arterial agents: lignocaine, papaverine
38
Q

Chlorpromazine:
What is it;
What are its effects/side-effects

A

D2-antagonist;
anti-emetic and antipsychotic;
potentiates narcotics;
interacts with guanethidine;
ECG changes;
lowers seizure threshold and causes EPSEs;
cholestatic jaundice;
impotence;
photosensitivity

39
Q

Chlorpromazine ECG changes

A

QT prolongation
PR prolongation
blunted T-waves
ST depression
PVCs
Torsades de pointes

40
Q

Drugs used in beta-blocker overdose

A
  1. GLUCAGON
  2. atropine
  3. dobutamine
  4. isoprotenerol (non-selective B-agonist, analog of adrenaline)
  5. aminophylline
  6. calcium chloride
41
Q

Signs and symptoms of opioid withdrawal

A

hyperthermia
raised blood pressure and heart rate
abdominal cramps
jerking legs
other signs of sympathetic stimulation

42
Q

Minoxidil: effects

A
  1. reduced blood pressure
  2. stimulates hair growth
  3. pericardial effusion
  4. cardiac tamponade
  5. pulmonary hypertension
43
Q

Thiocyanate:
what is it;
signs of toxicity

A

products of metabolism of sodium nitroprusside especially in renal failure;

tinnitus
abdominal pain
muscle weakness
confusion, seizures, coma

44
Q

Signs of cyanide toxicity

A

metabolic acidosis
resistance to antihypertensive effects of sodium nitroprusside
raised mixed venous partial pressure of oxygen

45
Q

Examples of monoamine neurotransmitters

A
  1. dopamine
  2. noradrenaline
  3. adrenaline
  4. histamine
  5. serotonin
  6. melatonin
46
Q

Primary precursor proteins of opioids

A

pro-opiomelanocortin
pro-enkephalin
pro-dynorphin

47
Q

Examples of
1. excitatory
2. inhibitory
amino acid neurotransmitters

A
  1. glutamate, aspartate
  2. glycine, GABA
48
Q

Acid drugs bind to:

Basic drugs bind to:

A
  1. albumin
  2. a1 acid glycoprotein (AGP)
49
Q

Examples of peptide neurotransmitters

A
  1. encephalins
  2. orexins
  3. substance P
50
Q

Name the neurotransmitter groups

A
  1. peptides
  2. excitatory amino acids
  3. inhibitory amino acids
  4. cholinergics
  5. monoamines
  6. nitric oxide
51
Q

Define: neurotransmitter

A

A substance that transmits
physiologic information
in the nervous system

52
Q

Which major channels do opioids affect, and how

A
  1. Calcium channels: inhibition, therefore inhibits release of substance P and glutamate
  2. Potassium channels: opens postsynaptic channels, causing hyperpolarisation and inhibiting the post-synaptic response
53
Q

Name locations of opioid receptors

A
  1. presynaptic terminals
  2. primary afferent neurons
  3. post-synaptic second-order pain transmission neurons
54
Q

Name the pain pathways

A
  1. Ascending
    peripheral nerves
    dorsal horn of spinal cord
    thalamus
  2. Descending
    midbrain
    periaqueductal grey matter
    rostral ventromedial medulla
    locus coeruleus
55
Q

Main effects of Substance P

A
  1. pain
  2. nausea and vomiting
56
Q

What is aprepitant,
and what does it act on

A
  1. antiemetic for chemotherapy and post-operative nausea and vomiting
  2. Neurokinin-1 receptor antagonist
57
Q

NMDA receptor antagonists

A
  1. ketamine
  2. dextromethorphan
  3. magnesium
  4. nitrous oxide
  5. xenon
58
Q

Receptors affected by ketamine

A
  1. NMDA
  2. AMPA
  3. opioid
  4. acetylcholine (nicotinic and muscarinic)
  5. GABA
  6. Monoaminergic
59
Q

Receptors in the cys-loop family

A
  1. GABA-A
  2. Glycine
  3. 5-HT
  4. Acetylcholine: nicotinic
60
Q

Agonists of GABA-A

A
  1. barbiturates
  2. etomidate
  3. propofol
  4. benzodiazepines
  5. volatile agents
61
Q

For gabapentin/pregabalin:
1. effect site
2. uses

A
  1. voltage-dependent calcium channels;
    post-synaptic dorsal horn
  2. relieving allodynia and hyperalgesia
62
Q

On what three segments of the kidney nephron do osmotic agents such as mannitol exert their diuretic effects?

A

proximal convoluted tubule
thin descending loop of Henle
collecting duct

63
Q

On what segment of the kidney nephron do loop agents such as furosemide exert their diuretic effects?

A

Ascending limb of loop of Henle

64
Q

On what segment of the kidney nephron do thiazides exert their diuretic effects?

A

distal convoluted tubule

65
Q

On what segment of the kidney nephron do potassium-sparing agents exert their diuretic effects?

A

collecting tubule

66
Q

On what segment of the kidney nephron do antidiuretic hormone antagonists exert their effects?

A

collecting duct

67
Q

In the proximal convoluted tubule, the filtrate is _____ (hypotonic/isotonic/hypertonic) to blood plasma.

A

isotonic

68
Q

In the thin descending limb of the loop of Henle, the filtrate is _____ (hypotonic/isotonic/hypertonic) to blood plasma.

A

hypertonic

69
Q

In the thick ascending limb of the loop of Henle and the distal convoluted tubule, the filtrate is _____ (hypotonic/isotonic/hypertonic) to blood plasma.

A

hypotonic

70
Q

On what segment of the kidney nephron does the diuretic acetazolamide exert its effects?

A

proximal convoluted tubule

71
Q

What are the clinical uses of mannitol?

A

treating:
shock
drug overdose
raised ICP/IOP

72
Q

What is the mechanism of action of mannitol?

A

osmotic diuretic
increasing osmolarity in the renal tubules;
producing increasing urine volume

73
Q

What side-effects are associated with mannitol?

A

pulmonary oedema
dehydration

74
Q

In what two conditions is mannitol contraindicated?

A

anuric renal failure
congestive cardiac failure

75
Q

What four side-effects are associated with acetazolamide?

A

hyperchloraemic metabolic acidosis;
neuropathy;
ammonia toxicity;
sulpha-like allergic reactions

76
Q

What is the mechanism of action of acetazolamide?

A

carbonic anhydrase inhibitor;
self-limited sodium bicarbonate diuresis;
reduction of total body bicarbonate stores

77
Q

What are the four clinical uses of acetazolamide?

A

Treating:
glaucoma;
altitude sickness;
metabolic alkalosis;
urinary alkalisation

78
Q

What are three (general) the clinical uses of furosemide?

A

Treating:
oedematous states;
hypertension;
hypercalcaemia

79
Q

What is the mechanism of action of furosemide?

A

inhibits sodium-potassium-chloride co-transport in thick ascending limb of loop of Henle;
abolishes hypertonic environment of renal medulla;
prevents ability to concentrate urine.

80
Q

What is the effect of the diuretic furosemide on calcium handling in the kidney nephron?

A

increases calcium excretion
(loops lose calcium)

81
Q

Name six toxicities associated with use of loop diuretics

A

ototoxicity;
hypokalaemia;
dehydration;
allergy (sulpha-like);
nephritis (interstitial);
gout

(OH DANG!)

82
Q

Ethacrynic acid has a mechanism of action similar to which other drug?

A

furosemide

83
Q

Which loop diuretic is used to diurese patients who are allergic to sulfa drugs?

A

ethacrynic acid

84
Q

Serum levels of which substances are increased as a result of the effects of hydrochlorothiazide?

A

hyperglycaemia;
hyperlipidaemia;
hyperuricaemia;
hypercalcaemia

Anaesthesiology (12 decks)

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