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Y2 Pharmaco > General Anaesthetics > Flashcards

General Anaesthetics Flashcards

1
Q

What are good properties of an ideal General Anaesthetic?

A
  • induction of smooth & rapid loss of consciousness
  • allow prompt recovery of consciousness after discontinuation
  • wide safety margin & no adverse effects
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2
Q

Why do we use a combination of GAs instead of monotherapy?

A
  • all desirable effects of GA cannot be achieved via monotherapy
  • thus, use ** balanced anaesthesia** for favourable properties & minimal risks
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3
Q

What are the aims of GA?

A
  1. Unconsciousness
  2. Amnesia
  3. Analgesia
  4. Relaxation of skeletal muscles
  5. Loss of autonomic nervous system reflexes

UAARL

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4
Q

Name some Inhaled Anaesthetics:

A
  1. Halothane
  2. Nitrous oxide
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5
Q

List out the IV anaesthetics:

A
  1. Barbiturates (thiopentone)
  2. Benzodiazepines (not a GA! It’s a pre-anaesthetic sedative)
    - diazepam, lorazepam, midazolam
  3. Propofol
  4. Ketamine
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6
Q

List the stages of anaesthesia:

A
  1. Analgesia
    - initial analgesia w/o amnesia, then both are achieved
  2. Excitement
    - amnestic but appears delirious, irregular respiration, may retch or vomit if stimulated
  3. Surgical anaesthesia
    - regular respiration recurs followed by apnea. Loss of eye movements, eye reflexes as depth of anaesthesia increases
  4. Medullary depression
    - severe depression of brain stem and medullary function
    (Medulla helps control heart rate, breathing & blood pressure)
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7
Q

What is the most reliable sign of surgical anaesthesia?

A

Loss of motor & autonomic response to noxious stimuli
- basically u pinch the person n see if they respond

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8
Q

List the factors that determine the rate of onset of inhaled anaesthetics:

A

absorption & distribution ‘SCRAP’

  1. Solubility in blood
  2. Conc. in inspired air
  3. Rate & depth of pulmonary ventilation
  4. Pulmonary blood flow
  5. Arteriovenous conc gradient
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9
Q

Nitrous oxide has a _____ solubility in the blood, reaches ____ arterial tension rapidly, resulting in ______ equilibration w the brain and a _____ onset of action.

A

Low solubility in blood => high arterial tension rapidly => rapid equilibration => fast onset of action

Basically itll precipitate out into the brain faster cuz it doesnt wanna stay in the blood.

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10
Q

CVS effect of inhaled anaesthetics:

A
  1. Decreased mean arterial pressure
    - decreased cardiac output (halothane, enflurane)
    - decreased systemic resistance (isoflurane, sevoflurane)
  2. Depression of myocardial function

^ bad for ppl w heart problems..
* postural hypotension

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11
Q

What is malignant hyperthermia?

A
  • autosomal dominant skeletal muscle disorder
  • GA in susceptible px trigger hyperthermia, hypertension, tachycardia, severe muscle rigidity & acidosis
  • increased muscle cell Ca2+ ions
  • treat w dantrolene => release of Ca2+

^ what killed the 24 yr old who went for wisdom tooth extraction
- shd have been given dantrolene (inhibits Ca2+ ions)

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12
Q

Pros of intravenous anaesthetics over inhaled anaesthetics

A
  1. Faster onset than inhaled => commonly used for induction
  2. Recovery is sufficiently rapid => good for short outpatient procedures
  3. Do not require specialised vapouriser equipment & facilities for disposal of exhaled gases
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13
Q

Cons of intravenous anaesthetics over inhaled anaesthetics

A

Most intravenous anaesthetics lack analgesic properties => combine w inhaled/LA for short procedures

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14
Q

What is monitored anaesthetic care?

A
  • IV + LA/regional anaesthesia
  • good for minor procedures
  • patent airway maintained
  • able to respond to commands
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15
Q

Name the types of General anaesthesia a px can be put under:

A
  1. Balanced anaesthesia
    - combination of inhaled and intravenous anaesthetics
    - intravenous for induction
    - inhaled for maintainence
    - for major procedures, done by anaesthesiologists
  2. Monitored anaesthesia care
    - using local anaesthesia supplemented by intravenous anaesthetics
    - need anaesthesiologists for possible ventilatory support
    - airway is still patent and px can respond to commands
  3. Conscious sedation
    - used primarily by non-anaesthesiologists (aka dentists)
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16
Q

Definition of General Anaesthesia:

A
  • medically induced coma and loss of protective reflexes resulting from the administration of one or more general anaesthetic agents
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17
Q

Which intravenous anaesthetic is not considered a proper general anaesthetic?

A

Benzodiazepine. It’s a pre-anaesthetic sedative.

Since it’s not a GA, can be and is most frequently used by dentists. No need for anaesthesiologist to be present.

18
Q

List out the Benzodiazepine drugs.

A

Diazepam, Lorazepam, Midazolam

19
Q

What is Benzodiazepine used for?

A

pre-anaesthetic sedative w GA/adjuvant during LA procedures
1. Sedative
2. Anxiolytic
3. Amnestic

=> thats why its good as a pre-anaesthetic sedative, makes u sleep, less anxious & forget the trauma

20
Q

How do Benzodiazepines work? (MOA)

A
  1. Binds to specific benzodiazepine sites in CNS
  2. Potentiates GABA by increasing frequency of GABA gated Cl- channel opening
  • GABA-dependent
21
Q

What is Flumanezil?

A

Antagonist against Benzodiazepines
- to accelerate recovery after procedure w benzodiazepine, esp after high doses/elderly patients
- however, it has short duration of action (<90mins), may require multiple doses

22
Q

Onset & Recovery of benzodiazepines is _____ and dose required for sedation is _______.

A

Onset & recovery: slow
- slower onset of CNS depression than barbiturates => inadequate for surgical anaesthesia

Dose: high dose required for deep sedation
- but will lead to slower recovery (CNS & respiratory depression)
- may cause anterograde amnesia

23
Q

How do Barbiturates work? (MOA)

A
  1. Binds to GABA receptors => facilitate its action by increasing DURATION of GABA gated Cl- channel opening
  2. Act on AMPA receptor => depress glutamate mediated excitation
24
Q

Onset & Recovery of Barbiturates is..

A

Fast.
- so it is usually used for induction
- los of consciousness happens quickly w sufficient dosage

25
Q

How does Propofol work? (MOA)

A
  1. potentiate GABA by slowing down channel-closing time
  2. Na+ channel blocker
26
Q

Thiopentone is a..

A

Barbiturate

27
Q

Onset & recovery of Propofol is..

A

Fast. (like thiopentone)
- but even faster recovery than thiopentone

Thus: used for induction & maintenance of anaesthesia (part of balanced anaesthesia)

28
Q

Uses of Propofol:

A
  1. induction & maintenance of balanced anaesthesia
  2. monitored anaesthesia
  3. Sedation
29
Q

IV anaesthetics lack what property? So what are they usually used for?

A
  • most lack analgesic properties, except ketamine
    => must combine w inhaled or LA
  • usually used for induction, cuz of its fast onset (make patient fall asleep
30
Q

What is special about Ketamine!!

A

IV anaesthetic that has both analgesic & anaesthetic properties

31
Q

What drugs are used for conscious sedation?

A
  • Midazolam/Diazepam (reversible using flumanezil)
  • propofol: sedation
  • opioid analgesic (reversible using Nalaxone)

Conscious sedation is when px maintains airway & responds to commands, used by non-anaesthesiologists

32
Q

Mechanism of action for inhaled anaesthetics (list):

A
  1. Interact w members of ligand gated ion channel family => modify ion currents
    - GABA, nicotinic, glycine
    - direct activation
    - indirect activation via increase in Cl- flux
  2. Act at multiple levels of CNS
    - spino-thalamic tract (pain)
    - reticular activating system (consciousness)
33
Q

What are the notable adverse effects inhaled anaesthetics has on our organ systems?

A
  1. CVS:
    - decreased mean arterial pressure
    - decreased cardiac output
    - decreased systemic resistance
  2. Respiratory:
    - decreased minute ventilation
    - increased apneic threshold (arterial Co2 tension)
    - bronchodilation
    - depression of muco-ciliary function
  3. Brain:
    - increased cerebral blood flow via decreased vascular resistance => undesirable in px w high intracranial pressure => use NO instead
  4. Liver:
    - decreased hepatic blood flow
    - repeated exposure to halothane => liver damage
34
Q

Which GA drug causes hepatic toxicity?

A

Halothane

  • small no. of pxs previously exposed to halothane develop hepatitis (1:30000) => sudden & severe liver necrosis
  • reactive metabolites may directly damage liver/initiate immune mediated responses
35
Q

Which GA drug causes renal toxicity?

A

Methoxyflurane (inhaled anaesthetic)
- causes renal dysfunction
- metabolism of methoxyflurane => releases F- ions

36
Q

Nitrous oxide is commonly used as

A

Analgesic agent for labour pain

37
Q

Potency, rate of onset & recovery of Halothane? What does it do?

A

Potent, medium rate of onset & recovery => used to maintain anaesthesia + for induction(commonly in children)

Uses: Relaxes skeletal muscles & potentiates skeletal muscle relaxants

38
Q

Potency, rate of onset n recovery of nitrous oxide (NO)? What is it used for?

A
  • rapid onset & recovery, lacks potency
  • used as adjunct w other inhaled anaesthetics
    -> 20%: significant analgesia
    -> 30-80%: sedation
    -> maximum dose (80%): cannot give complete unconsciousness/surgical anaesthesia alone
  • used as analgesic agent for labour pain
39
Q

What is nalaxone?

A
  • used to reverse opioid analgesic (in conscious sedation procedures)
40
Q

Factors determining rate of recovery - metabolism & excretion:

A
  1. Solubility in blood:
    - low solubility => fast recovery
  2. Duration of exposure:
    - increased duration=> more soluble anaesthetic accumulation in muscle, skin, fat => slow recovery
  3. Rate of pulmonary ventilation & blood flow:
    - increased ventilation/flow => faster recovery
  4. Hepatic metabolism:
    - clearance of halothane
  5. Bacteria in GIT:
    - ** break down NO**
41
Q

What is Fentanyl?

A
  • synthetic opioid
  • widely used in induction and maintenance of general anaesthesia
  • could prolly also be used for conscious sedation

Y2 Pharmaco (22 decks)

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