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Definition Deck > Drug Properties > Flashcards

Drug Properties Flashcards

1
Q

Dantrolene presentation

A

20mg dantrolene sodium, orange powder
3g mannitol
recon with 60ml of sterile water
alkaline, highly irritant when extravasated

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2
Q

Dantrolene dose

A

2.5mg/kg IV up to 10mg/kg

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3
Q

Dantrolene protein binding

A

85%

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4
Q

Dantrolene metabolism

A

hepatic -> 5-hydroxy-dantrolene
50% active
Renal excretion

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5
Q

Dantrolene T1/2B

A

12 hours

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6
Q

Porphyria pathophysiology

A

defect in first step of haem synthesis + partial deficiency of enzymes subsequent to this process.

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7
Q

Drugs to trigger porphyria

A

barbiturates
ketamine
clonidine
ketorolac
phenytoin

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8
Q

plasma pseudocholinesterase deficiency

A

Genetic
Acquired - pregnancy, liver failure, renal failure, malignancy, malnutrition, burns, thyrotoxicosis

Post plasmapheresis

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9
Q

Excretion vs. elimination?

A

excretion is the removal of drugs from the body
elimination is removal of drugs from the plasma
- Can occur via distribution, metabolism, excretion

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10
Q

CSHT Remi

A

5 mins

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11
Q

CSHT Propofol

A

8 mins after 1 hour
40 mins after 8 hours

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12
Q

CSHT Fentanyl

A

at 2 hours = alfentanil at 50mins

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13
Q

CSHT Alfentanil

A

50 mins post 2 hours -> context insensitive

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14
Q

CSHT thiopental

A

150 mins post 8 hours (active pentobarbital, zero order kinetic)

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15
Q

Difference between iso and enflurane structures

A

positional isomers
3F on terminal carbon for iso, Cl + H on C2
End 2F on C2

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16
Q

changes to neonatal drug response - PO absorption

A

delayed GI emptying, prolonged contact with small bowel wall -> increased absorption of drugs

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17
Q

Neonatal NMJ changes

A

immature until 2 months of age
small reserve of Ach, more sensitive to NDMRs

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18
Q

Define shelf-life

A

length of time a drug can stay on the shelf without degrading to unacceptable level (minimum 90%)

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19
Q

What is sulphite addictive?

A

found in adrenaline (sodium meta-bisulfites)
antioxidants
can cause hypersensitivity, neurological damage from intrathecal administration

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20
Q

preservative in ketamine?

A

benzalkonium chloride

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21
Q

Side effect of benzalkonium?

A

histamine release -> hypotension

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22
Q

Class of agent - sevo

A

halogenated compound
poly-fluorinated isopropyl methyl ethers

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23
Q

Class of agent - des

A

halogenated, methyl ethyl ether

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24
Q

Difference between sevo and des structures?

A

2x CF3 on sevo while des has a fluoride instead.

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25
Q

Structure-relationship of volatiles - purpose of low MW

A

reduce boiling point, increase SVP

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26
Q

Structure-relationship of volatiles - H+ vs F- side chain

A

H+ - increase flammability, increase potency
F- - decrease flammability, C-F bond strong and resistant to oxidative metabolism, decrease potency

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27
Q

Structure-relationship of volatiles - CHF2 (di-fluor-methyl group)

A

interacts with soda lime to form CO -> increase carboxyhb

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28
Q

Metabolite of des / iso / halothane

A

TFA - trifluroacetate

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29
Q

Types of halothane hepatic toxicity

A

reversible - increase transaminase
fulminant necrosis - TFA chloride + hepatic proteins -> antibody formation

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30
Q

pathophys of nephrotoxicity from methoxyflurane

A

extensive metabolism into inorganic fluoride -> accumulation

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31
Q

Factors to increase MAC

A

Children
Hyperthermia
Hyperthyroid
Hypernatraemia
Catecholamines
Chronic opioid use, acute amphetamine use
anxiety

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32
Q

Factors to decrease MAC

A

Elderly, pregnancy
hypothermia
hyponatraemia
shocked state
A2 agonist, acute opioid use
Hypercapnic, hypoxia

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33
Q

MW of N2O

A

44g/mol

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34
Q

MW of O2

A

32

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35
Q

MW of sevo

A

200

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36
Q

MW of des

A

168

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37
Q

MW of xenon

A

130

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38
Q

Boiling point of des

A

23.5

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39
Q

Boiling point of sevo

A

60

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40
Q

Boiling point of N2O

A

-88

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41
Q

SVP at 20 degrees of N2O

A

50 bar

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42
Q

SVP at 20 degrees of des

A

600mmHg

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43
Q

SVP at 20 degrees of sevo

A

160mmHg

44
Q

MAC of xenon

A

70%

45
Q

Blood gas coefficient of xenon

A

0.14

46
Q

Ranking of oil/gas coefficient of different agents

A

Halothane > iso > sevo > des > xenon > N2O

47
Q

Resp effect of N2O

A

no blunting of laryngeal reflex.
no change to minute ventilation
increase pulmonary vascular resistance

48
Q

Haem effect of N2O

A

oxidation of cobalt ion in B12 -> interferes with DNA synthesis -> megaloblastic anaemia, agranulocytosis, peripheral neuropathy, teratogenic

49
Q

Cylinder pressure of O2

A

137 bar, white cylinder

50
Q

How do volatiles cause tachycardia?

A

vagal inhibition

51
Q

Indication of nitric oxide

A

severe ARDS
pulmonary HTN
severe right-sided heart failure

52
Q

Effects of nitric oxide

A

reduce HPV -> reduce V/Q mismatch in ARDS
increase cerebral blood flow
inhibit PLT aggregation
Methb

53
Q

pKa of ketamine

A

7.5

54
Q

Protein binding of thiopental

A

80%

55
Q

Protein binding of propofol

A

> 99%

56
Q

Protein binding of ketamine

A

25%

57
Q

Clearance of thiopental

A

3.5ml/kg/min

58
Q

Clearance of propofol

A

30-60ml/kg/min

59
Q

Clearance of ketamine

A

15ml/kg/min

60
Q

Structure relationship Barbiturates - keto vs enol

A

keto active, lipid soluble
enrol water soluble

61
Q

Structure relationship Barbiturates - methohexital

A

methylation of nitrogen atom -R3
increase onset time, shorten duration
increase excitatory phenomena

62
Q

Content of thiopental

A

500mg sodium thiopental
6% sodium carbonate -> to make pH 10.5
fixed in nitrogen to prevent reaction with CO2 to reduce pH and reduce water solubility

reconstitute in 20ml of H2O to make 2.5% solution

63
Q

Metabolite of thio + fate

A

pentobarbital, active 30-50%
hepatic saturable kinetics
renally excreted

64
Q

Propofol action aside from GABA A

A

glycine receptors
nAchR
D2 receptors

65
Q

Characteristic of propofol infusion syndrome

A

in prolonged sedation in ICU, critically ill patients.
metabolic acidosis
rhabdomyolysis
cardiac and renal failure

66
Q

Benefit of S-ketamine

A

better analgesia
more rapid metabolism
better bronchodilator
less intense emergence phenomena

67
Q

Metabolite of ketamine

A

norketamine, 30% activity

68
Q

Receptors ketamine acts on

A

NMDA
mu and keppa
Muscarinic Ach receptor antagonist
Increase DA and Na release

69
Q

Midaz PO bioavailability of

A

50%

70
Q

Midaz pKa

A

6.5

71
Q

Midaz protein binding

A

95%

72
Q

Midaz Vd

A

1.5L/kg

73
Q

Midaz Cl

A

5-10ml/kg/min

74
Q

Midaz metabolite

A

1-a-hydroxy-midazolam, 50% activity
Oxazepam

75
Q

Flumazenil effect

A

competitive antagonist at the a/y interface receptor, competitively reverses effect of benzodiazepines

76
Q

Flumazenil onset time

A

2 mins

77
Q

Flumazenil dose

A

0.1mg increments up to 2mg

78
Q

Flumazenil t1/2b

A

<1 hour, shorter than benzo

79
Q

Flumazenil side effects

A

lower seizure threshold -> seizure
N/V
withdrawal symptoms if dependent on BDZ

80
Q

A2 agonists - indications

A

HTN, sedation, premed, anxiolytics, intra-op haemodynamic stability, analgesia, post-op shivering

81
Q

Protein binding clonidine

A

20%

82
Q

Protein binding dexmedetomidine

A

90%

83
Q

Metabolism of clonidine

A

50% metabolised, inactive metabolite
50% excreted unchanged

84
Q

Metabolism of dexmed

A

almost complete metabolism to inactive compounds

85
Q

T1/2b of dexmed

A

2 hours

86
Q

Effect of A-agonist on coronary blood flow

A

direct vasoconstriction, offset by reduced SNS tone and local release of NO

87
Q

Metabolic effect of A-agonist

A

Reduce ADH, reduce insulin from b-islet cells

88
Q

Effect of A1 receptors

A

Gq GPCR -> increase [Ca]
contraction of vascular SM, eye radial muscle, vas deferent, GIT sphincter

Gluconeogenesis

89
Q

Effect of B1 receptors - hormonal / renal

A

increase renin release from kidneys

90
Q

Effect of B2 receptors

A

reduce histamine release from mask cells
vascular smooth muscle relaxation
Liver - glycogenolysis, gluconeogenesis

91
Q

How is sedation / hypnosis mediated by dexmet

A

A2, Gi GPCR at locus cerulean in the medial dorsal pons

92
Q

Dexmet analgesic mechanism

A

Reduce NA release -> reduce inhibition on the descending pathway

At dorsal horn, inhibit release of substance P

93
Q

Clinical uses of dexmed

A

Sedation, anxiolytics, reduced salivary secretion
Maintain stable HD to stimulation
Analgesia
MAC sparring
Prevents shivering
Smooth induction and emergence, reduce delirium
Reduce withdrawal Sx

94
Q

Adult dose of dexmed

A

Loading 1microg/kg over 10mins then 0.6microg/kg/hr
Reduced to 50% dose in elderly

95
Q

CSHT of dexmed

A

stable at 2 hours, 70 mins

96
Q

Contraindications of A2 agonist

A

Shock, bradycardia / heart block, allergy

IHD, autonomic neuropathy

97
Q

What are the components of accelero-myography?

A

Piezoelectric crystal attached to thumb
measurement of acceleration of the crystal

98
Q

Sux protein binding

A

30%

99
Q

Sux Vd

A

0.2L/kg

100
Q

Sux metabolites

A

succinyl-mono-choline + choline
Succinct acid

101
Q

Vec metabolism

A

hepatic de-acetylation, 60% activity, renal excreted

102
Q

Roc metabolism

A

Minimally metabolised, mainly excreted unchanged in bile and less extent in urine

103
Q

Intubating dose atracurium

A

0.5mg/kg

104
Q

What physiological states affect Hoffman elimination

A

acidosis, hypothermia -> reduced reaction -> increase [atracurium]

105
Q

ID cisatracurium

A

0.15mg/kg

106
Q

ID mivacurium

A

0.2mg/kg

107
Q

Neostigmine distribution facts

A

Low Vd
Low protein binding

Definition Deck (5 decks)

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