General Anaesthetic Pharmacology - Pre-med, inhalation, intravenous, muscle relaxants, opioids, interactions Flashcards

1
Q

OBJECTIVES OF PRE-MEDICATION

A
  1. reduction of sensory input
  2. improving emotional state (+amnesia)
  3. reduction of metabolic rate
  4. reduction of autonomic nervous system activity
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2
Q

EFFECTS OF ANXIETY

A
  • psychological trauma
  • activation of sympato-adrenal exis
  • activation of pituitary-hypothalamic-adrenal cortical system
  • increased gastric juice secretion
  • increased gastric volume
  • delayed gastric emptying
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3
Q

POPULATIONS TO BE CAREFUL OF WITH PRE-MEDICATION

A
  • infants and the elderly
  • debilitated patients
  • altered LOC
  • intracranial pathology
  • upper airway obstruction
  • respiratory distress
  • severe obstructive/restrictive lung disease
  • hypovolemia/shock
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4
Q

EFFECTS OF PARASYMPATHETIC SYSTEM BLOCKADE

A
  1. reduced vagal tone
  2. reduced secretions
  3. reduced gastric fluid volume and acidity
  4. reduced gastrointestinal tone and motility
  5. reduced nausea/vomiting
  6. reduced hypersensitivity
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5
Q

EFFECTS OF SYMPATHETIC SYSTEM BLOCKADE

A
  1. reduced catecholamine release
  2. reduced nausea
  3. depressed central noradrenergic outflow
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6
Q

EFFECTS OF OPIATES AS PRE-MED

A
  • analgesia
  • reduced IV induction dosage needed
  • reduced inhaled MAC needed
  • reduced surgical stress response
  • blunted intubation reflexes
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7
Q

ADVANTAGES OF BENZODIAZEPINE AS PRE-MED

A
  • anxiolysis
  • sedation
  • anterograde amnesia
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8
Q

DISADVANTAGES OF BENZODIAZEPINE AS PRE-MED

A
  • respiratory depression
  • declined cognitive function
  • declined fine motor function
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9
Q

A BENZODIAZEPINE WITH SHORT HALF LIFE

A

midazolam

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10
Q

A BENZODIAZEPINE WITH LONG HALF LIFE

A

diazepam

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11
Q

A BENZODIAZEPINE WITH LITTLE MYOCARDIAL DEPRESSION

A

lorazepam

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12
Q

A BENZODIAZEPINE WITH PSYCHOMOTOR AGITATION AND CONFUSTION IN THE ELDERLY

A

lorazepam

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13
Q

DRUG USED TO COUNTER NAUSEA ASSOCIATED WITH OPIATES

A

phenothiazine

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14
Q

ANTICHOLINERGICS USED

A
  • atropine
  • scopolamine
  • glycopyrrolate
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15
Q

ANTICHOLINERGIC THAT DOES NOT CROSS THE BBB

A

glycopyrrolate

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16
Q

REASONS FOR USING ANTICHOLINERGICS

A
  1. dry secretions
  2. reduce bronchomotor tone
  3. prevent bradycardia from laryngeal stimulation
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17
Q

SIDE EFFECTS OF ANTICHOLINERGICS

A
  1. central anticholinergic syndrome
  2. reduced tone of LES
  3. mydriasis
  4. raised body temp
  5. increased physiological dead space
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18
Q

SIGNS OF CENTRAL ANTICHOLINERGIC SYNDROME

A
  • restlessness, drowsiness
  • prolonged anaesthesia
  • coma
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19
Q

TREATMENT: CENTRAL ANTICHOLINERGIC SYNDROME

A

IV physostigmine

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20
Q

HEALTH STATUS GRADINGS

A
  1. healthy patient
  2. mild systemic illness
  3. significant systemic illness but not incapacitated
  4. significant systemic illness, constant threat
  5. very ill, unlikely to survive 24 hours
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21
Q

SITES OF ACETYLCHOLINE

A
  • neuromuscular junction, nicotinic receptors
  • autonomic ganglia
  • post-ganglionic parasympathetic nerve endings
  • sympathetic nerve endings of sweat glands
  • CNS
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22
Q

TWO FORMS OF CHOLINESTERASE

A
  1. acetylcholine esterase

2. pseudocholine esterase

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23
Q

SHORT, MEDIUM AND LONG-ACTING ANTICHOLINE ESTERASES

A

SHORT: edrophonium
MEDIUM: neostigmine, pyridostigmine, physostigmine
LONG: organophosphates

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24
Q

EFFECTS: MUSCARINIC AGONISTS

A
  • smooth muscle contraction
  • pupillary contraction
  • decreased rate/force of heart
  • glandular secreations (salivary, sweat, pancreas)
  • gastric acid secretion
  • vasodilation
  • inhibit neurotransmitter release
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25
Q

EFFECTS: MUSCARINIC ANTAGONISTS

A
  • inhibit secretions
  • tachycardia
  • pupillary dilatation
  • relaxation of smooth muscles
  • inhibition of gastric secretions
  • antiemesis
  • inhibit tremor
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26
Q

COMMON MUSCARINIC ANTAGONISTS

A
atropine
hyoscine
tropicamide
cyclopentolate
ipratropium
benztropine
pilocarpine
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27
Q

CLINICAL USES: ANTICHOLINESTERASES

A
  1. glaucoma treatment
  2. myasthenia gravis treatment
  3. reversal of non-depolarising neuromuscular blockers
  4. Alzheimer’s dementia
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28
Q

CLINICAL USES: ADRENERGIC AGONISTS

A
  1. cardiac arrest
  2. cardiac failure
  3. heart block
  4. anaphylaxis
  5. asthma
  6. nasal decongestion
  7. inhibition of premature labour
  8. prolong effects of local anaesthesia
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29
Q

BE CAREFUL IN THESE PATIENTS WITH BETA BLOCKERS

A
  1. asthma/ obstructive lung disease
  2. diabetics
  3. poor cardiac function
  4. cardiac conduction disturbances
  5. peripheral vascular disease
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30
Q

EFFECTS OF THIOPENTAL INDUCTION

A
  • pleasant induction
  • reduced cerebral blood flow
  • reduced ICP
  • anticonvulsant
  • reduced nausea
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31
Q

SIDE-EFFECTS: THIOPENTAL INDUCTION

A
  • urticarial rash
  • anaphylactoid reactions
  • coughing/hiccups/irregular respiration
  • venodilation
  • negative inotropy
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32
Q

CONTRAINDICTATIONS: THIOPENTAL INDUCTION

A
  • porphyria
  • cardiac tamponade
  • hypovolaemia
  • cardiac failure
  • IHD
  • condiction defects
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33
Q

PREVENTING ARTERIAL INJECTION OF THIOPENTAL

A
  • dilute it to 2.5%

- use an established IV line

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34
Q

MX: ARTERIAL THIOPENTAL

A
  1. papaverine 40-80 mg
  2. lignocaine 25-50 mg
  3. diluted heparin
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35
Q

BENEFITS: ETOMIDATE

A
  • high safety margin
  • safe in epilepsy
  • minimal circulatory effects
  • no myocardial effects
  • minimal acumulation
36
Q

SIDE-EFFECTS: ETOMIDATE

A
  • myoclonic movements
  • respiratory depression
  • histamine release
  • post-op N&V
  • thrombophlebitis
  • depressed adreno-cortical fx
37
Q

BENEFITS: PROPOFOL

A
  • short awake/recovery time
  • amnesia, anxiolysis, sedation
  • safe in MH
  • antiemetic
38
Q

SIDE-EFFECTS: PROPOFOL

A
  1. grand mal seizures
  2. abuse potential
  3. respiratory depression
  4. bradycardia
  5. severe hypotension
  6. anaphylactoid reactions
  7. culture growth
  8. metabolic acidosis
  9. adverse neurological outcome
  10. pain on injection
39
Q

CONTRA-INDICATIONS: PROPFOL

A
  • sepsis
  • hypotension
  • hypovolaemia
40
Q

BENEFITS: KETAMINE

A
  • amnesia
  • anticonvulsant
  • bronchial smooth muscle dilatation
  • sedation
  • safe in MH
41
Q

SIDE-EFFECTS: KETAMINE

A
  • raised ICP
  • increased salivation
  • hypertension
  • tachycardia
  • raised cardiac output
42
Q

CONTRA-INDICATIONS: KETAMINE

A
  • porphyria
  • raised ICP/IOP
  • psych problems
43
Q

INDICATIONS: KETAMINE

A
  • lung disease
  • hypovolaemia
  • cardiac tamponade
44
Q

DEFINE MAC

A

percentage of one atmosphere required to prevent purposeful response to noxious stimuli in 50% of patients

45
Q

PROPERTIES: IDEAL INHALED ANAESTHETIC

A
  1. pleasant inhalation
  2. potent
  3. rapid emergence
  4. depth adjustable
  5. easily measured
  6. inexpensive
  7. stable outside body
  8. specific for CNS unconsciousness
  9. no CVS/respiratory side-effects
  10. post-operative analgesia
46
Q

FACTORS AFFECTING MAC

A
  1. age
  2. body temperature
  3. pregancy
  4. physiological alterations
  5. anaesthetic adjuvants
47
Q

SIDE-EFFECTS: HALOTHANE

A
  1. ventricular extrasystoles in response to adrenaline/hypercarbia
  2. mild hepatic reactions
  3. severe hepatic necrosis
48
Q

SIDE-EFFECTS: DESFLURANE

A
  1. CVS stimulation, tachycardia
  2. increased airway resistance
  3. laryngospasm, coughing
  4. increased carbon monoxide poisoning
49
Q

SIDE-EFFECTS: ISOFLURANE

A
  1. cross-sensitivity to halothane

2. increased carbon monoxide production

50
Q

AGENTS THAT WORK ON NMDA RECEPTORS

A

ketamine

nitrous oxide

51
Q

SIDE EFFECTS: NITROUS OXIDE

A
  1. raised systemic vascular resistance
  2. raised ICP
  3. post-op nausea, vomiting
  4. increased size of air-filled spaces
  5. oxidation of vitamin B12
52
Q

CONTRA-INDICATIONS: NITROUS OXIDE

A
  1. raised ICP
  2. pneumothorax
  3. eustachian tube pathology
  4. bowel obstruction
  5. abnormalities of folate metabolism
53
Q

WHAT IS COMPOUND A

A

a vinyl ether

degradation product of sevoflurane

54
Q

COMPOUND A LIKELIKHOOD INCREASED BY

A
  1. sevoflurane
  2. carbon dioxide
  3. low fresh gas flow
  4. raised temperature
  5. dehydration
  6. potassium
  7. sodium hydroxide
55
Q

CLASSIFY NEUROMUSCULAR BLOCKERS

A

a. depolarising (suxamethonium)
b. non-depolarising: benzylisoquinolines (-curium)
c. non-depolarising: steroidals (-curonium)

56
Q

SUBJECTIVE TESTS FOR MUSCLE FUNCTION POST-RELAXATION

A
  • head lift

- hand grip

57
Q

PERCENTAGE BLOCKADE WITH FOURTH/THIRD/SECOND TWITCH ABSENT

A

FOURTH: 75%
THIRD: 80%
SECOND: 90%

58
Q

BLOCKAGE REQUIRED FOR SURGERY

A

75-90%

59
Q

TOF REQUIRED FOR RESPIRATORY MUSCLE FUNCTION

A

0.8

60
Q

WHAT IS FADE AND WHAT DOES IT INDICATE

A

FADE: gradual dimunition of evoked response during prolonged/repeated nerve stimulation
INDICATES: non-depolarising block of at least 75%

61
Q

CORRELATION BETWEEN TOF AND CLINICAL SIGNS

A
    1. unable to lift hand/arm
    1. 3s head lift, eyes open
    1. 5s head lift, cough, 60% grip
    1. normal vital capacity and inspiratory force
62
Q

SIDE-EFFECTS: SUXAMETHONIUM

A
  1. malignant hyperthermia
  2. fasciculations, muscle pain
  3. hyperkalaemia (especially in burns)
  4. bradycardia
  5. raised IOP
  6. raised intra-gastric pressure and LES pressure
  7. raised ICP
  8. masseter muscle rigidity
  9. anaphylactic reactions
  10. scoline apnoea
63
Q

LONG-ACTING NDMR

A

pancuronium

64
Q

MUSCLE RELAXANT SUITABLE IN IHD

A

vecuronium

65
Q

MUSCLE RELAXANT APPROPRIATE IN KIDNEY DISEASE

A

rocuronium

66
Q

NDMR ALTERNATIVE TO SUX

A

rocuronium

rapacuronium

67
Q

MUSCLE RELAXANTS WITH HISTAMINE RELEASE

A
  • atracurium
  • mivacurium
  • suxamethonium
68
Q

NDMR METABOLISED BY PLASMA CHOLINESTERASE

A

mivacurium

69
Q

REVERSAL OF NDMR BLOCKADE

A
  1. cholinesterase inhibitors

2. anticholinergic agent e.g. atropine, glycopyrrolate

70
Q

EFFECTS OF UP/DOWN REGULATION OF RECEPTORS ON MEDICINE CHOICES

A

UP REGULATION:
higher sux affinity
lower NDMR affinity

DOWN REGULATION:
lower sux affinity
higher NDMR affinity

71
Q

CONDITIONS RESULTING IN UP-REGULATION OF ACH RECEPTORS

A
  • UMN lesions
  • LMN lesions
  • muscle trauma
  • burns
  • immobilisation
  • sepsis/infection
72
Q

CONDITIONS RESULTING IN DOWN-REGULATION OF ACH RECEPTORS

A
  • myasthenia gravis

- organoposphate poisoning

73
Q

EXAMPLES: ENDOGENOUS OPIOIDS

A

enkephalins

endorphins

74
Q

OPIOID RECEPTORS

A

mu
kappa (1-3)
delta

75
Q

EFFECTS OF OPIOIDS

A
CENTRAL
- analgesia (spinal, supraspinal, peripheral)
- anaesthesia (reduce MAC/induction dose)
- miosis
- euphoria
RESPIRATORY
- resp depression
- anti-tussive
- blunted upper airway reflexes
CVS
- hypotension
- bradycardia
GIT
- nausea & vomiting
- constipation
- increase tone of gut sphincters, also of Oddi
HISTAMINE RELEASE
76
Q

OPIOID ANTAGONISTS

A

naloxone

nalorphine

77
Q

OPIATE POTENCIES, FROM WEAK TO STRONG

A
  1. codeine
  2. pethidine
  3. morphine
  4. alfentanil
  5. fentanyl
  6. sulfentanyl
78
Q

OPIATE GIVING CHEST WALL RIGIDITY

A

fentanyl

79
Q

OPIATE CROSSING BBB RAPIDLY

A

alfentanyl

80
Q

OPIATE USEFUL IN CHOLINESTERASE DEFICIENCIES

A

remifentanyl

81
Q

OPIATE WITH SIMILARITY TO ATROPINE

A

pethidine

82
Q

ACTION OF TRAMADOL

A
  1. acts on opioid receptors
  2. inhibits noradrenaline uptake
  3. enhances serotonin release
83
Q

OPIOID DESIGNED TO REDUCE ABUSE

A

pentazocine

84
Q

DEFINE PHARMACEUTICAL INTERACTIONS AND GIVE GOOD/BAD EXAMPLES

A

reactions between two drug alters chemical properties such that they cannot be absorbed/utilised
GOOD: protamine reverses action of heparin
BAD: insulin adheres to glass/plastic containers
thiopentone and adrenalin cause a precipitate

85
Q

DEFINE PHARMACOKINETIC INTERACTIONS AND GIVE GOOD/BAD EXAMPLES

A

a drug alters degree of absorption/distribution/clearance of another
GOOD: second gas effect
IV opioid reduce MAC/induction dose
BAD: Rifampicin with halothane = hepatitis

86
Q

DEFINE PHARMACODYNAMIC INTERACTIONS AND GIVE GOOD/BAD EXAMPLES

A

interactions at effector site, often by means of receptor competition
GOOD: nitrous oxide added to halothane requires less halothane
BAD: NSAIDs increase warfarin free portion