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Anaesthetic & Pre-medications Drugs > Anaesthetic and Pre-med Drugs > Flashcards

Anaesthetic and Pre-med Drugs Flashcards

1
Q

What is analgesia?

A

Drugs that allows the reduction of pain. “pain-relief”

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2
Q

Describe some negative effects associated with pain?

A
  • Reduced food intake, shift to catabolic state.
  • Delayed anaesthetic recovery.
  • Prolonged wound healing
  • Central sensitisation and hyperalgesic states (being in pain makes you more in pain).
  • Ethical reasons!
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3
Q

How does Analgesia work?

A

Analgesia work by interrupting the ascending pain pathway at various levels and suppressing the sensation of pain.

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4
Q

What does “Balanced Analgesia” mean?

A

Groups of drugs that act on different levels of the pathway, some block pain at several levels.

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5
Q

When do we use analgesia?

A
  • Control acute pain
  • Control chronic pain
  • Balanced anaesthesia
  • pre-emptive analgesia
  • Neuroleptanalgesia (premed).
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6
Q

What are Opioid analgesia?

A
  • Potent analgesia
  • Act at the spinal cord and brain to decrease perception of painful stimuli.
  • Act on opioid receptor: = agonist, partial agonists, antagonist.
  • Used for severe pain (pure agonists ).
  • Many are controlled drugs.
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7
Q

What do the receptors do when opioid drugs are administered?

A

Receptors are protein molecules on surface of cell that respond to chemical/drug in some way.
- Drugs tend to be specific in terms of which receptors they will bind to.

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8
Q

What do the Opioid Drugs mimic?

A

Opioid drugs mimic the actions of endogenous opioids (endorphins) at opioid receptors.

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9
Q

How does an Agonist work with Opioids?

A

Drugs that bind to receptors on a cell and trigger a response by a cell.
often mimic the action of a naturally occurring substance.
-agonist produce an action.

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10
Q

How does an Antagonist work with Opioids?

A

Drugs that bind to receptors on a cell but fails to activate the receptor.
blocks receptor from activation from agonists.

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11
Q

How does a Partial agonist work with Opioids?

A

activates a receptor but cannot elicit the same max response as full agonist even if they have the same affinity for the receptors.

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12
Q

Receptor for Mu

(MOR) where does this effect and what occurs at this site?

A 
Pain pathways throughout brain and spinal cord. respiratory centre. 
Action at this site: 
Analgesia
Sedation/narcosis
Respiratory Depression
Euphoria (Hallucinogen) 
Hypothermia
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13
Q

Receptor Kappa (KOR), where does it effect and what occurs at this site?

A

The Brain
Actions at this site:
Dysphoria (unpleasant hallucinogen effects)
Sedation without respiratory depression.

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14
Q

Receptor Delta (DOR), what does it effect and what occurs at this site?

A 
Spinal Cord. 
Action at this site: 
Spinal Analgesia
Possibly Cardiac
Stimulation/Dysphoria.
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15
Q

What are the effects of Opioid Analgesia?

A
  • Profound analgesia - drug and dose dependent.
  • Respiratory depression
  • Sedation OR excitation
  • Nausea, vomiting, defecation.
  • Depression of cough reflex
  • Tolerance/dependence with prolonged use.
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16
Q

What is Premedication?

A

Administration of a drug/combination of drugs as the inital part of GA.
- Sedatives and tranquillisers commonly used in conjunction with analgesia.

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17
Q

Why might we use premedication?

A
  • Calm and control patient
  • Relieve pain
  • Reduce the amount of anaesthetic agents used
  • Reduce side effects
  • Smooth recovery from GA
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18
Q

When patients are calm and controlled, why do we want this?

A
  • easier handling
  • smooth induction
  • reduce circulating “catecholamines” - arrythmias.
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19
Q

Why do we want pain to be relieved, when given a premed?

A
  • decreased central nervous system activity -> enhanced effects of anaesthetic.
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20
Q

What drug reduces unwanted side effects?

A

Atropine!

  • widely used when ether was maintenance agent.
  • Reduces salivation and bronchial secretions.
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21
Q

What are the disadvantages of atropine?

A
  • Increases metabolic rate
  • increase HR
  • myocardial oxygen consumption
  • May cause Illeus,
  • Arrhythmia
  • Mydriasis
  • Does not work on RABBITS
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22
Q

What are the disadvantages of using a premed ?

A
  • Side effects
  • Prolong recovery
  • Contraindicated in some patients
  • Timings.
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23
Q

When do you specify, what premed to give to a patient?

A
  • SPECIES/BREED
  • AGE
  • PHYSICAL CONDITION
  • TEMPERAMENT
24
Q

With species/breed what to consider?

A

some breeds may experience adverse effects.

Syncope (collapse) in boxers with full doses of ACP.

25
Q

With age, what to consider?

A
  • age related illnesses meaning animals less able to metabolic certain drugs
  • young patient with immature livers
26
Q

With physical condition, what to consider?

A
  • Obese
  • Dehydrated
  • Malnourished
  • Epileptic
  • Diabetic
  • Depressed
27
Q

With temperament, what to consider?

A
  • highly excitable or aggressive patients.
    may be resistant to some drugs
    -e.g. use Medetomidine rather than ACP
28
Q

When selecting a premed what other things to consider?

A

Presence of pain
- most suitable analgesic
Subsequent anaesthesia
- any prev hx of anaesthesia/reaction to anaesthetic drugs.
Post op considerations:
- calm and pain-free during recovery period
-Caesarian - need to recover quickly to feed neonates.

29
Q

What are three types of premedicants?

A
  • Sedative/Tranquillisers
  • Parasympathetic agents
  • Analgesics
30
Q

Name 4 types of sedatives/tranquillisers.

A
  • Phenothiazines
  • Butyrophenones
  • Hypnotics
  • Alpha-2 agonists.
31
Q

Name a parasympathetic agent?

A

Anti-muscarinics (atropine)

32
Q

Name 2 Analgesics?

A
  • Opiates

- NSAIDs

33
Q

When do you inject anaesthetics?

A
  • Induction of anaesthesia
  • As a supplement to inhalation anaesthesia when additional rapid control is required.
  • As the sole anaesthetic agent for short periods (TIVA).
34
Q

What is the pharmacology of injectable anaesthetics?

A
  • Intravenous agents
  • Pass rapidly to the brain as it has a rich blood supply.
  • Once conc are high enogh, there is a loss of consciousness.
  • The drug then travels to other organs
  • When levels in the brain fall, consciousness returns.
35
Q

Why are most anaesthetics are metabolised in the liver?

A
  • convert lipids into water soluble molecules.
  • excreted easily in bile
  • exit the body via urine and faeces.
36
Q

what advantage when administering injectable anaesthetics?

A

Injectable anaesthesia provides rapid onset and good conditions for intubation.

37
Q

Name 4 types of injectable anaesthetics.

A
  • Barbituates
  • Steroids
  • Phenols
  • Dissociative agents
38
Q

What are Barbituates?

A
  • Hypnotics that cause unconsciousness but poor analgesia.
  • Adequate muscle relaxation.
  • Highly lipid soluble - redistribution
  • Extravasation causes sloughing.
39
Q

What drugs are in the Barbituate anaesthetics group?

A
  • Thiopentone sodium
  • Methotrexate sodium
  • Pentobarbitone sodium
40
Q

Name two steroid anaesthetics drugs?

A
  • Saffan (Alphaxalone/Alphadolone)

- Alfaxalone (Alfaxan)

41
Q

What is Saffan?

steroid drugs

A

Insoluble in water, dissolved in the solvent Cremephor EL.

The Cremephor EL causes histamine release in dogs causing severe hypotension.

42
Q

What is Alfaxalone?

Steroid anaesthetics

A
  • Licensed for use in dogs, cats and rabbits.
  • Does NOT cause histamine release.
  • Administer IV or deep IM.
  • May cause apnoea on induction and excitation on recovery.
43
Q

What are Phenol Anaesthetics?

A

Examples: Propofol
- Lipid soluble and highly protein bond.
Rapid onset of anaesthesia, should be administered in incremental boluses to effect.
-Fetal depression minimal so good for caesarians.
- Short acting and fast recovery.

44
Q

Give an example of dissociative anaesthetics?

A

KETAMINE

45
Q

What does dissociative anaesthetics do?

A

Induces a state of almost total analgesia combined with superficial sleep.

46
Q

What are the side effects from using dissociative anaesthetics?

A
  • causes muscle rigidity, so combine with alpha2 agonist or benzodiazepine.
  • Slow acting, 1-2 MINS after IV or IM injection.
  • Cardiovascular effects - direct myocardial depression and indirect stimulation sympathetic nervous system - latter normally dominates so get increased HR and BP.

DO NOT USE IN HYPERTHYROID CATS!

  • Schedule 2, controlled drug.
47
Q

What is inhalation anaesthetics?

A
  • Anaesthetics agents provided as a gas or vapourised into a carrier gas.
  • Generally used to maintain anaesthesia (induction stressful/slow).
  • The animal usually intubated.
48
Q

Name 2 types of inhalational anesthetics?

A

Gases

Volatile agents

49
Q

Name 2 types of Gases?

A

Nitrous Oxide

Cyclopropane

50
Q

Name 5 types of volatile agents?

A
  • Halothane
  • Isoflurane
  • Sevoflurane
  • Methoxyflurane
  • Ether
51
Q

What is the pharmacokinetics of anaesthetics gases?

A

The gases pass into the lung then diffuse into the pulmonary circulation.
Travels around the body and is distributed to the tissues.
Will diffuse back into the bloodstream, eliminated via lungs
Onset and elimination depend on the solubility.
Partition coefficients.

52
Q

Other notes on Pharmacokinetics.

A

Used to describe the solubility of inhalation anaesthetics in blood, gas, oil.
Blood: gas coefficient - alveolar gas to blood
- if highly soluble, takes a long time to reach equilibrium, therefore, slower effect/longer duration.
- low solubility - reaches equilibrium faster therefore rapid effect/short duration.

53
Q

What is nitrous oxide?

A 
Good analgesic properties, weak anaesthetics effect - use as adjunct. 
Stores as liquid - weight cylinder
DO NOT USE WITH
- closed breathing systems
- charcoal scavengers
54
Q

How is Nitrous Oxide eliminated?

A

By the lungs.

55
Q

What is the process of Nitrous Oxide?

A

When the N20 is turned off, blood levels are higher than in alveolus.
N20 returns to the alveolus quickly and “dilutes” the oxygen -> patient inspires hypoxic gas.
To counteract this, administer 100% O2 for 10 MINS after the N20 is turned off.

56
Q

What are the contraindications?

A
  • Pregnancy - N20 may be teratogenic, causes impairment of folate synthesises, fetal abnormalities.
  • Raised intracranial pressure - increases cerebral blood flow
  • Diffusion hypoxia worsened where there are large areas of gas e.g. GDV, intestinal obstruction, pneumothorax.
  • Anaemia - due to diffusion hypoxia

Anaesthetic & Pre-medications Drugs (1 decks)

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