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Pharmacology RCOA > Anaesthetic Drugs > Flashcards

Anaesthetic Drugs Flashcards

1
Q

What are the pKa values of the induction agents?

A

Thio: 7.6
Prop: 11
Etom: 4.2
Ket: 7.5

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2
Q

Are the different induction agents weak acids or bases?

A

Thio: Acid
Prop: Acid
Etom: Base
Ket: Base

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3
Q

How does Suggamadex work?

A
  • Modified gamma-cyclodextrin
  • Encapsulating agent
  • Binds free NMB molecules
  • Creates Conc gradient between IV compartment and NM junction
  • Drug moves down Conc gradient away from NM junction terminating its effects
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4
Q

Give an example of short, medium & long-acting anticholinesterases

A

Short: Tensilon - used to diagnose myasthenia
Med: Neostigmine/ Pyridostigmine
Long: Echothiophate - used in Sarin/nerve gases, last weeks due to covalent bonding

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5
Q

What are the Sx of an anti cholinesterase overdose?

A

SLUDGE
S: Salivation
L: Lacrimation
U: Urination
D: Defecation
G: GI upset
E: Emesis
Death by paralysis & resp depression
Tx: Atropine/ Pralidoxime

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6
Q

How does Neostigmine work?

A
  • Carbamylates active site of enzyme
  • Once bonded hydrolyses ACh
  • Inhibits action of plasma pseudocholinesterase so prolongs effects of Sux & Miva
  • Reverses competitive NMB
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7
Q

What is Thiopentone made from?

A

-Sulphur analogue of pentobarbitone
- Formulated as sodium salt (yellow powder)
- Highly insoluble in neutral pH so need transforming from kept to enol form (alkaline)
- Stored in glass vials containing Nitrogen

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8
Q

What’s an absolute contraindication for Thiopentone?

A

Acute porphyria

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9
Q

How much Thiopentone is in the active form at normal pH?

A

-12%
-60% free drug = unionised
- Non-protein bound & unionised
- Rapid onset due to high lipid solubility
- Emergence due to rapid redistribution

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10
Q

What are the 2 types of local anaesthetic drug groups?

A
  • Esters: Contain COO link, hydrolysed in plasma
  • Amides: Contain NHCO link, hepatic metabolism
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11
Q

What are the types of LA esters?

A
  • Amethocaine
  • Cocaine
  • Procaine
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12
Q

What are the types of LA amides?

A
  • Bupivacaine
  • Etidocaine
  • Lignocaine
  • Ropivacaine
  • Prilocaine
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13
Q

In what way is systemic absorption of LA greater than epidural administration?

A
  • Caudal injection
  • Intercostal injection
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14
Q

What drugs bind to the b subunit on GABA?

A

Propofol
Volatiles
Etomidate
Barbituates

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15
Q

What are the uses of Thio?

A
  • GA
  • Status epilepticus - produces isoelectric EEG = max reduction of cerebral O2 requirements (may need inotropes)
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15
Q

What are the SE of Thio?

A
  • Dose-dependent reduced CO/SV/SVR
  • Resp: broncho/laryngospasm, resp depression
  • Anaphylaxis
  • Renal: Reduced UO due to inc ADH release
16
Q

Why do acidotic patients require less Thio?

A
  • Reduced plasma-protein binding
  • Greater fraction of drug in unionised form
  • Fewer plasma protein binding sites
17
Q

Why does Thio infusion lead to linear metabolism?

A

Zero order: Saturation of hepatic enzymes (P450)

18
Q

Is intra-arterial injection of Thio bad?

A
  • More Keto formation than Enol
  • Less water-soluble solution
  • Precipitation of Thio crystals which wedge in small blood vessels
  • Tx: Procaine, Papaverine, analgesia
19
Q

What are the effects of Propofol?

A
  • Reduced SVR/BP/contractility, Brady,
  • Resp depression
  • Antiemetic (Dopamine antagonist)
  • Propofol syndrome
  • CNS excitatory effects
20
Q

What is Propofol bound to?

A

98% protein bound to Albumin

21
Q

How is Propofol metabolised?

A
  • Hepatic
  • 40% Conjugation to glucuronide
  • 60% metabolised to Quinol excreted as Sulfate & Glucuronide
22
Q

What is Ketamine derived from?

A

Phencyclidine

23
Q

How is Ketamine presented?

A
  • Racemic mixture
    or
  • Single S enantiomer (2-3 times as potent as R enantiomer)
24
Q

What are the effects of Ketamine?

A
  • Sympathetic NS stimulation
  • Inc circulating NorA/adrenaline
  • Inc HR/CO/BP/Myocardial O2 requirements
  • Inc RR, preserved airway reflexes, BronchoD
  • Dissociation
  • Salivation
  • Severe interstitial cystitis (high does)
  • Inc cerebral blood flow/ICP/O2 consumption
25
Q

Which type of Ketamine produces less cardiac depression?

A

S(+) Ketamine
Better for IHD (doesn’t block ATP sensitivity K+ channels)

26
Q

What happens in Ketamine dissociation?

A
  • Dissociation between thalamocrtical & limbic systems
  • a rhythm replaced by 0 & d wave activity
  • Takes 90secs rather than 1 arm-brain cycle to work
27
Q

How do Ketamine levels fall?

A
  • Conc falls in bi-exponential fashion
  • Initial fall = lipid membrane distribution
  • Slower fall = hepatic metabolism
28
Q

How is Ketamine metabolised?

A
  • Least protein bound of all GAs
  • Demethylated to active metabolite norKetamine by P450
  • Then metabolised to inactive glucuronide excreted in urine
29
Q

What is Etomidate?

A

Imidazole derivative & ester

30
Q

What are the effects of Etomidate?

A
  • Fall in PVR
  • Adrenocortical suppression
  • Precipitate porphyric crisis
31
Q

How does Etomidate cause adrenal suppression?

A
  • Inhibits enzyme 11B-hydroxylase & 17a-hydroxylase
  • Inhibits cortisol & aldosterone synthesis
32
Q

What are the kinetics of Etomidate?

A
  • 75% bound to Albumin
  • Action determined by rapid distribution into tissues
  • Elimination based on hepatic metabolism (hepatic esterase, plasma cholinesterase)
33
Q

What are the effects of N2O?

A
  • Fall in TV, inc in RR
  • Inc sympathetic activity
  • Mild cardiac depression
  • Inc cerebral blood flow
34
Q

How is Sux broken down?

A

Hydrolysed by plasma cholinesterase to choline & succinylmonocholine (weakly active)

35
Q

What type of block does Sux produce?

A

Phase 1 block: Train of 4 >0.7
Repeated administration = phase 2 block like Non-depolarising NMB

36
Q

What is the MOA of Sux?

A

Binds to nicotinic Ach receptors
Depolarises membrane
Lack of plasma cholinesterase at NMJ
Sux remains attached to receptor blocking its action

Pharmacology RCOA (12 decks)

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