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Pharmacology > General Anaesthetics: Revised > Flashcards

General Anaesthetics: Revised Flashcards

1
Q

GA MOA?

A
  1. GA increase the sensitivity of GABA(A) receptors to the inhibitory neurotransmitter GABA=increases chloride ion influx hyperpolarisation of neurons
  2. Blockade of NMDA(Inhibt Glutamate)
  3. Blockade of ext post synaptic nicotinic receptors
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2
Q

Which GA is the execpetion when it comes to MOA?

A

Nitrous oxide & Ketamine

They work by inhibiting NMDA receptors. Selectively inhibit NMDA receptor to increase glutamate from increasing Calcium influx.

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3
Q

Inhaled volatile GA drugs?

A

SHINE

  1. Sevoflurane
  2. Halothane
  3. Isoflurane
  4. Nitrous Oxide
  5. Enflurane
  6. Desflurane
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4
Q

Halothane:

  1. MOA
  2. Admin.
    3.Odour
  3. Targert group in why?
  4. Hepatoxicity
  5. A/E
A
  1. Increases sensitivity to GABA(A) & Increases hyperpolarisation
  2. Inhaled or IM
  3. Pleasant odour therefore it does not induce respiratory reflexes
  4. Best in children because it is not hepatotoxic
  5. Not hepatotoxic
  6. A/E:

-Cardiotoxic: Bradycardia, Cardiac arrhythmias & concentration-dependent hypotension

-Malignant Hyperthermia
>Indiced by malignant hyperthermia or uncontrolled increased skeletal msucle oxidative metabolism

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5
Q

Why is halothane a drug of choice?

A

It has rapid induction and quick recovery

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6
Q

How do you avoid the toxic reaction of halothane?

A

Halothane is not administered at intervals of less than 2 to 3 weeks

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7
Q

Which property of halothane is responsible for some toxic reactions women develop post halothane anesthesia?

A

Halothane is metabolised in the body to tissue-toxic hydrocarbons and bromide ion and this makes it responsible for toxic reactions that some females develop after Halothane anaesthesia

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8
Q

What are the toxic reactions that people have post halothane?

A

Fever
Anorexia
Nausea
Vommiting
Hepatitis

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9
Q

Which patients are susceptible to Halothane-induced malignant hyperthermia?

A

Burn victims and individuals with muscular dystrophy, myopathy and osteogenesis imperfecta

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10
Q

What is the Tx Halothane-induced malignant hyperthermia?

A

Dantrolene (blocks release of Ca2+) from the sarcoplasmic reticulum of muscle cells,
reducing heat production and relaxing muscle tone. Monitored and supported
respiratory, circulatory, and renal systems

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11
Q

Stages of anaesthesia?

A
  1. Induction
  2. Maintenance
  3. Recovery
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12
Q

Depths of anaesthesia?

A

AESM

Stage I: Analgesia
Stage II: Excitement/Delirium
Stage III: Surgical Anaesthesia
Stage IV: Medullary Paralysis

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13
Q

Sevoflurane:

  1. Odour
  2. Target patients & their admin
  3. DOA & why
  4. Metabolised
  5. MOA
A
  1. Low pungency, allowing rapid induction without irritating the airways
  2. Suitable for inhalation induction in paediatric patients
  3. Has a rapid onset and recovery due to low blood solubility
  4. Metabolised by the liver → metabolites can be nephrotoxic
  5. Increases sensitivity of GABA(A) to Cl- & inhibit excitatory synaptic channel activity by binding nicotinic acetylcholine, serotonin, and glutamate receptors.
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14
Q

Isoflurane:

  1. MOA
  2. Odour
  3. Effect of kidney/liver/heart & why
  4. Admin
    5.
A
  1. Increases sensitivity to GABA(A) & Increases hyperpolarisation
  2. It has a pungent odor and stimulates respiratory reflexes (irritation,
    salivation, coughing, laryngospasm), therefore not used for inhalation
    induction
  3. This agent undergoes little metabolism and is, therefore, not toxic to
    the liver or kidney, also, it does not induce cardiac arrhythmias
  4. Inhalation but Not inhalation because of the pungent smell
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15
Q

Desflurane

  1. Onset of action & why?
  2. Frequency of use in patients?
    3
A
  1. Provides very rapid onset and recovery due to low blood solubility
  2. A popular anesthetic for outpatient procedures
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16
Q

Why is desflurane administered via a special heated vaporizer?

A

It has a low volatility, requiring administration via a special heated
vaporizer

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17
Q

Desflurane relationship with vascular resistance and tissues?

A

It decreases vascular resistance and perfuses all major tissues very
well

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18
Q

Why is Desflurane not used for inhalation

A

It stimulates respiratory reflexes, not used for inhalation induction

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19
Q

Sevoflurane

  1. Odour
  2. Admin
  3. Use in pediatric patients
  4. Onset and recovery
  5. Metabolism
A
  1. Has low pungency, allowing rapid induction without irritating the
    airways
  2. Inhalation
  3. Suitable for inhalation induction in paediatric patients
  4. Has a rapid onset and recovery due to low blood solubility
  5. Metabolised by the liver → metabolites can be nephrotoxic
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20
Q

Nitrous oxide?

A

“laughing gas” is a non‐irritating potent analgesic but a weak general anaesthetic

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21
Q

How do we counter the effects of diffusion-hypoxia when administering nitrous oxide?

A

We administer with Oxygen

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22
Q

What allows nitrous oxide to move quickly in and out of the body?

A

Poorly soluble in blood and other tissues, allowing it to move very rapidly
in and out of the body

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23
Q

How does nitrous oxide cause pnemothroax?

A

Can increase the volume (pneumothorax) or pressure (sinuses), because it
replaces nitrogen in various air spaces faster than the nitrogen leaves

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24
Q

Nitrous oxide effects on:

  1. The respiratory system
  2. Muscle Relaxation
  3. CVS
  4. Cerebral
A

Does not depress respiration

Does not produce muscle relaxation.

When co‐administered with other anaesthetics, it has moderate to no effect on the CVS

Increasing cerebral blood flow, and it is the least hepatotoxic of the inhalation agents

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25
Q

Intravenous anaesthetic drugs?

A

KEPTD For in VEIN

Ketamine
Etomidate
Propofol
Thiopentone
Diazepam

Fospropofol

26
Q

Ketamine

-Duration
-Liphophillic/phobic
-CI

A

-A short‐acting, non‐barbiturate anaesthetic

Lipophillic

Contraindicated in hypertensive or stroke patients

27
Q

Ketamine & dissociated state?

A

Induces a dissociated state in
which the patient is unconscious (but may appear to be awake) and does
not feel pain

28
Q

Ketamine effects on brain, heart and bronchus?

A

It stimulates central sympathetic outflow, causing stimulation of the heart
with ⬆️ blood pressure and CO. It is also a potent bronchodilator (used in
hypovolemic or cardiogenic shock and in asthmatics)

29
Q

Ketamine limited use?

A

⬆️cerebral blood flow and may induce hallucinations,
particularly in young adults

30
Q

Why is ketamine used illicitly?

A

Ketamine may be used illicitly, since it causes a dream‐like state and
hallucinations similar to phencyclidine (PCP)

31
Q

Ketamine effects?

A

This dissociative anaesthesia provides sedation, amnesia, and immobility

32
Q

Etomidate?

A

A hypnotic agent used to induce anaesthesia, it lacks analgesic activity

33
Q

Etomidate and analgesic activity?

A

It lacks analgesic
activity

34
Q

Etomidate solubility and solution?

A

Poorly water soluble, formulated in a propylene glycol solution

35
Q

Etomidate onset of action and duration of drug?

A

Induction is rapid, and the drug is short‐acting

36
Q

Etomidate effect on the heart and lungs

A

Little to no effect on the heart and circulation

37
Q

Etomidate target patient?

A

Only used for patients with CVS dysfunction

38
Q

Etomidate S/E?

A

⬇️ plasma cortisol and aldosterone levels (up to 8 hours), injection site reaction, and involuntary skeletal muscle movements

39
Q

Propofol?

A

An I.V sedative/hypnotic used for induction and/or maintenance of anesthesia

40
Q

Propofol solubility?

A

Poorly water soluble, and supplied as an emulsion containing soybean
oil and egg phospholipid, giving it a milk‐like appearance

41
Q

Propofol induction?

A

Induction is smooth and occurs 30 ‐ 40 seconds after administration

42
Q

Propofol plasma and highly perfused tissue?

A

Following an I.V bolus, there is rapid equilibration between the plasma and the highly perfused tissue of the brain

43
Q

Why does plasma level declines post administration of propofol?

A

Plasma levels decline rapidly as a result of redistribution, followed by
a more prolonged period of hepatic metabolism and renal clearance

44
Q

Propofol pharmacokinetics change?

A

The pharmacokinetics of Propofol are not altered by moderate hepatic or renal failure

45
Q

Propofol pharmacological CNS effects?

A

Depresses the CNS, accompanied by excitatory phenomena (muscle
twitching, spontaneous movement, yawning, and hiccups)

46
Q

Propol and pain at site?

A

Transient pain at the injection site is common

47
Q

What is Propofol useful in CNS?

A

Less CNS depressant effect: useful neurosurgeries

48
Q

Propofol effects on pain and vomiting?

A

It does not provide analgesia, has some antiemetic effects

49
Q

How is propofol administered to provide sedation

A

Propofol is commonly infused in lower doses to provide sedation

50
Q

Propofol S/E?

A

tremor, urine retention, green urine, flushing

51
Q

Thiopental duration?

A

Ultra-short acting barbiturate with high lipid solubility

52
Q

Thiopental anaesthetic and analgesic effects?

A

A potent anaesthetic but a weak analgesic

53
Q

Thiopental explanation on the quick loss of the drug in the CNS and body?

A

When given I.V, quickly enter the CNS and depress function, often in less than 1 minute, and diffusion out of the brain can also occur very rapidly
because of redistribution to other tissues

54
Q

Thiopental effects on the CVS?

A

Has minor effects on the normal CVS, may contribute to severe hypotension
in patients with hypovolemia or shock

55
Q

Thiopental S/E?

A

apnoea
coughing
chest wall spasm laryngospasm
bronchospasm

56
Q

Diazepam used in conjunction with what and for what?

A

The BDZ are used in conjunction with anaesthetics for sedation

57
Q

What are the most commonly used diazepam’s?

A

Diazepam, Midazolam and Lorazepam

58
Q

Diazepam Cv and respiratory effects?

A

Minimal CV depressant effects, with potential respiratory depressants

59
Q

Diazepam metabolism?

A

Metabolised by liver

60
Q

What do we do to prolong the effects of Diazepam?

A

Erythromycin may prolong their effects

61
Q

BDZ effect on amnesia and memory?

A

BDZ can induce a temporary anterograde amnesia in which the patient retains memory of past events, but new information is not transferred into
long‐term memory

Pharmacology (44 decks)

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