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Flashcards in Nervous 4 Deck (48)
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1
Q

What is MAC with drugs how used

A
  • Minimal alveolar concentration of anaesthetic to prevent movement to surgical incision in 50% of healthy (patients)
  • Use to compare potency of different agents
2
Q

List the 5 main individual inhalation agents

A

1) Nitrous Oxide
2) Halothane
3) Isoflurane
4) sevoflurane
5) methoxyflurane

3
Q

Nitrous oxide what type of agent, potency, uses, solubility

A
  • individual inhalation agents
  • Low potency (MAC 100%) - unlikely to become unconsciousness
  • Increases flow rates and decreases oxygen availability
  • Good analgesic, but are better analgesics available now
  • Low solubility–> rapid onset and offset -> short acting
  • not use as sole anaesthetic
4
Q

Halothane what type of agent, how soluble, main toxicity issues and side effects

A
  • Relatively Soluble in blood and lipid
  • Toxicity issues
    ○ Sensitizes myocardium to catecholamines -> high risk arrhythmias
    ○ Halothane hepatitis (rare)
    ○ Spontaneous abortion (OHS issue)
  • Decreases CO, BP and organ perfusion
5
Q

What are the 2 main side effects of halothane and describe

A

1) Arrythmia - major problem in small animals, generally adrenaline + halothane -> cause ventricular fibrillation/cardiac arrest
2) Malignant hyperpyrexia - especially in pigs, very rare condition, likely to be fatal -> been breed out
- uncontrolled hyperthermia, acidosis leading to death

6
Q

Isoflurane what type of agent, how common, soluble, how cardidepressive

A

Individual inhalation agents - anesthetic

  • Most common used at the moment
  • Less soluble than halothane
  • Less cardiodepressive
7
Q

Sevoflurane what type of agent, how fast, what similar too and how compare

A

Individual inhalation agents - anesthetic

  • Rapid onset and offset - Not gentle! Will go down very fast -> dramatic effect
  • Very similar to isoflurane
  • Less soluble
  • Less irritant to airways
  • Less smell (Mask inductions)
8
Q

Methoxyflurane what type of agent, how fast is induction, what else used by and main clinical use

A

Individual inhalation agents - anesthetic

  • Slow induction and recovery
  • Up to 50% metabolised
  • Good analgesia
  • Used by paramedics - the green whistle for initial management
9
Q

List 3 advantages and disadvantages of injectable anaesthetics

A
ADVANTAGES 
- Rapid induction through excitement phase 
- Need little equipment 
- Lend themselves to combination use 
DISADVANTAGES 
- Once administered can't be withdrawn -> pharmacokinetics is very important 
- Elimination can be more prolonged 
Require access to a vein
10
Q

How does distribution and redistribution work in terms of injectable anaesthetics

A
  • Same as inhalation however ventilation does not contribute to the amount given
  • Head is the active site
  • Tissues with high blood flow receive a greater proportion of drug initially, but equally lose it rapidly
  • Animals wake up from the anaesthetic because it redistributes away from the brain
    ○ Into the muscle then fat group (due to blood supply)
    ○ If large amount of fat may get large amount of drug distributed there
  • The blood flow to the brain is autoregulated (fixed)
11
Q

what are the 3 important characteristics in pregnant animals in terms of injectable anaesthetics

A

1) High cardiac output
2) reduced plasma protein binding
3) all anaesthetics cross the placenta

12
Q

what are the 4 important characteristics in neonates in terms of injectable anaesthetics

A

1) proprtion of blood fow to the brain is much higher
2) immature liver and idneys - metabolism can be depressed
3) immature sympathetic NS: less cardiovascular reserve
4) much more senstive to opiates

13
Q

List the 5 classes of injectable anaesthetics

A

1) Barbiturates (oxy and thio barbiturates)
2) Propofol
3) Dissociative anaesthetics eg ketamine
4) Steroid anaesthetics - alphaxalone/alphadalone
5) Benzodiazapines

14
Q

Barbiturates what type of drug and mechanism of action

A

injectable anaesthetics
The GABA receptor - Mechanism of action
- GABA-mimetic
- Allosteric modulation - change the shape of the GABA receptor so that GABA binds better
○ GABA is inhibitory neurotransmitter -> therefore CNS depression
§ Binding GABA -> open CL- channels -> hypo polarise

15
Q

Give an example of a barbiturate that is ultra-short acting, short acting and long acting

A
- Ultra-short acting 
○ Thiopentone - only one using 
- Short acting 
○ Pentobarbitone 
- Long acting 
○ Phenobaritone 
	§ Slow onset of action and long duration 
	§ Sedative 
	§ Seizure control
16
Q

Barbiturates what are the 3 main CNS effects and is it a analgesic

A

CNS
Decrease
- cerebral blood flow, cerebral oxygen consumption, medullary centers
-> thermoregulation, respiratory, vasomotor, vagus
- NOT analgesic

17
Q

What are the cardiovascular and respiratory effects of barbiturates

A
Cardiovascular effects - depressant 
- Heart rate increase
- Stroke volume decrease
- High dose or rapid injection 
-> peripheral vasodilation/hypotension 
Respiratory effects 
- Potent respiratory depressants
18
Q

Thiobarbiturates and Oxybarbiturates how does termination occur

A

Thiobarbiturates
- Termination of effect is due to redistribution
- Metabolised to active metabolites
- Patient wakes up because the concentration has redistributed away from the brain towards the viscera -> muscle and then finally in fat
Oxybarbiturates
- Termination of effects depends on hepatic metabolism
○ Hepatic enzyme induction -> metabolise more quickly overtime therefore may need to increase dose overtime due to adaption
Elimination (metabolism + excretion) is species dependent

19
Q

Thiobarbiturates what type of drug, how administered and the 4 precautions and contraindications

A

Injectable anaesthetic - IV injection ONLY

  1. thin patients - less redistrubution into fat so long lasting
  2. obese patients - may require overdose
  3. hepatic dysfunction (metabolised in the liver)
  4. respiratory depression
20
Q

Dissociative anaesthetics what type of drug, how different from others and the main drug name

A

Injectable anaesthetic
- Dissociates higher and lower brain centres
○ Separation from higher and lower brain centres -> decrease respiratory effects
- KETAMINE

21
Q

Ketamine what type of drug and the mechanism of action

A

Injectable anaesthetic - Dissociative anaesthetics
Mechanism of action
- Specific antagonist at glutamate NMDA receptor
- Antagonist at ACh muscarinic receptor
- Agonist at opioid receptor
- A SCHEDUE 8 drug (restricted) - control highly regulated

22
Q

Ketamine what type of drug, CNS effects and is it a analgesic or muscle relaxant

A

Injectable anaesthetic - Dissociative anaesthetics

  • Anaesthesia induced by functional dissociation between thalamus and cortex
  • Central stimulation of sympathetic nervous system
  • > increase sympathetic tone
  • Cataleptic state
  • Potent cerebral vasodilator
  • > increased cerebral blood flow
  • > increased intracranial pressure
  • Hallucinations and emergence reaction
  • GOOD ANALGESIC
  • Poor muscle relaxant
23
Q

Ketamine what type of drug and cardiovascular and respiratory effects

A

Injectable anaesthetic - Dissociative anaesthetics
- Resembles sympathetic n.s.stimulation
○ Increase HR, increase CO
Increased myocardial oxygen consumption
○ Increased blood pressure
- Respiratory depression rarely occurs

24
Q

Propofol what type of drug, major advantage, how different and metabolism

A

Injectable anaesthetic
- Major advantage: short duration of action and rapid recovery
- Useful for induction/short procedures or outpatient cases
- Formulated as emulsion (not a solution) (with soya bean oil and glyceral) exists as an oil at room temperature
Rapidly metabolised

25
Q

Propofol what type of drug, mechanism of action, comparison with thiopentone in terms of cardiovascular and respiratory effects

A

Injectable anaesthetic
- GABA-mimetic
- Equivalent to thiopentone in cardiovascular and respiratory effects:
○ Apnoea following rapid injection
○ Myocardial depression, vasodilation and hypotension - still side effects
Rapid metabolism means little accumulation of drug (thiopentone)

26
Q

Steroid anaesthetics what type of drug, main example, mechanism of action and main effects

A

Injectable anaesthetic s -> Alphaxalone

  • Act by modulation of GABA activity
  • gold standard -> expensive
  • Less C/Vasc and respiratory depression than other anaesthetic agents
  • Reduces cerebral O2-consumption more than reduced blood flow should indicate
27
Q

Steroid anaesthetics what is the major problem, how fixed and problem with that

A

Injectable anaesthetic
- Solubility is a major problem
○ Supplied in cremaphor vehicle
§ Cremaphor -> histamine release and anaphylactic deaths in humans
§ Peanut cremaphor -> resulted in death of humans due to allergic response
- Withdrawn from human market
- Registered for cats “Saffan”- still had allerigic reactions
- Now available in veterinary medicine in cyclodextrin vehicle “Alfaxan CD”

28
Q

Benzodiazepines what type of drug, main example, mechanism of action and effects of skeletal muscle

A

Injectable anaesthetic
- Diazepam (valium)
mechanism of action - allosteric effect on GABA receptor - increase permeability of CL-
- Skeletal muscle - relaxation
○ So used with ketamine to provide muscle relaxation

29
Q

Benzodiazepines what type of drug what are the 6 main clinical uses

A

Injectable anaesthetic

  1. Anxiolytic - behaviour modifiers
  2. Hypnotics
  3. Premedicants
  4. Anaesthesia induction
  5. Antibconvulsants (status epilepticus)
  6. Appetite stimulation (cats)
30
Q

List the 3 anaesthetics provide analgesia

A
  1. Ketamine
    1. Nitrous oxide
    2. Methoxyflurane
31
Q

Local anaesthetics and nerve fibres what are 3 important factors

A

§ Smaller/unmyelinated PAIN fibres blocked at lower dose
§ Myelinated MOTOR fibres are blocked at higher doses
§ To increase drug effect, infiltrate greater length of nerve fibre rather than increasing local dose

32
Q

pharmacokinetics of local anaesthetics what occurs with ester and amide linked

A
  • Ester linked: metabolised fast by esterase in tissue and plasma - short duration eg procaine, cocaine
  • Amide linked: metabolised in liver-medium to long lasting eg lignocaine, bupivicaine
33
Q

What are the 4 factors that influence absorption and potential toxicity of anaesthetics

A
  • Site of injection
  • Total dose
  • Addition of vasoconstrictor (adrenalin)
  • The pharmacodynamics of the particular local anaesthetic
34
Q

What is the cause of hepatic and renal encephalopathy and brain lesions

A
  • auto-intoxication due to failure of hepatic detoxification functions or circulatory bypass of the liver
  • dogs with portosystemic shunting and (to a lesser extent) chronic hepatitis
    Lesions - extensive spongy vacuolation (status spongiosus) of CNS white matter (with intra-myelinic oedema
  • identical lesions to HE may occasionally be found in animals in renal failure
35
Q

What is the cause of thiamine deficiency and brain lesions

A

thiamine deficiency -> CNS depletion of high energy phosphates (e.g. ATP) and decreased glucose utilisation by neurons
1. adrupt alteration of ruminal microflora - most common cause
2. destruction of thiamine within GIT
Lesion - acute diffuse cerebral oedema -> brain enlargement, flattening of cerebrocortical gyri +/- yellow discolouration of grey matter of the dorsal cerebral hemispheres +/- caudal displacement of the brain (coning - death)

36
Q

pathogenesis of thiamine deficiency and what occurs with swayback and enzootic ataxia

A
  • copper deficiency can be primary (e.g. due to copper-deficient soils and inadequate intake from forage) or secondary (e.g. interference with absorption due to antagonism by dietary molybdenum, zinc, cadmium, iron or inorganic sulphates)
  • neurological signs may be present at birth (swayback in lambs, rarely in kids) or their onset may be delayed up to 6 months of age (enzootic ataxia in lambs and kids)
  • in swayback, affected lambs (and rarely kids) may be blind, deaf and apathetic, lie prostrate with flaccid paralysis or, if able to stand, will fall when attempting to move
    ○ some may be stillborn
    ○ gross brain lesions of hydranencephaly or porencephaly or may be present
37
Q

what is believed to be the cause of equine degenerative myeloencephalopathy

A

Vit E deficiency

38
Q

what do most neurotoxins produce in terms of brain lesions

A

no significant gross or microscopic CNS lesions

39
Q

What occurs with lead posioning in dogs and cats

A

○ poisoning is usually via ingestion (rarely by inhalation or via the skin) and can be peracute, acute, subacute or chronic
○ only a small proportion of ingested lead is absorbed because of formation of insoluble salts in the alimentary tract
○ in acute poisoning, absorbed lead is deposited especially in the liver and kidneys
○ in chronic poisoning, lead deposition in bone is important, with slow continuous turnover and gradual elimination in bile and urine

40
Q

Indicate the causes of nigropallidal encephalomalacia and mycotoxic leukoencephalomalacia in horses

A
  • caused by prolonged ingestion (> 1 month) of yellow star thistle (Centaurea solstitialis) or Russian knapweed (Centaurea repens)
    poisoning typically occurs during hot dry summers when the thistles remain green whilst other forage is dry and unpalatable
  • ingesting (usually for a month or more) mouldy feed (especially corn or corn by-products) contaminated by the fungus, Fusariummoniliforme
41
Q

What occurs with Phalaris toxicity and the 3 distinct clinical syndromes in sheep

A

Contain 4 types of toxic indole alkaloids

  1. sudden death cardiac syndrome
  2. polioencephalomalacia-like sudden death syndrome
  3. subacute to chrornc staggers syndrome
42
Q

What are the typical CNS lesions seen in phalaris staggers in sheep

A
  • characteristic of the staggers syndrome is grey-green-brown discolouration of brainstemnuclei, spinal grey matter, dorsal root ganglia +/- renal cortex due to accumulation of indole pigments within lysosomes of nerve cell bodies at sites of action of the toxic alkaloids
    ○ the discolouration is usually grossly obvious
43
Q

list the malignant tumousr that are most likely to metastasise to the brain in dogs and cats

A

most common metastatic tumour in dogs is mammary carcinoma but others include lymphoma, haemangiosarcoma, fibrosarcoma and malignant melanoma
○ the most common metastatic tumours in cats are mammary carcinoma and lymphoma

44
Q

what is the most common primary tumour of the brain of cats and expected behaviour

A

meningioma

  • usually older cats
  • well circumscribed, smooth-surface
  • most intra-cranial meningiomas are benign and do not invade the CNS or metastasise
  • expansile growth may nevertheless cause significant CNS dysfunction due to compression of the brain
  • foci of necrosis, haemorrhage and low-grade inflammation are commonly found in meningiomas
45
Q

what is the most common primary tumour of the brain of dogs and expected behaviour

A

most common type being an astrocytoma
- rarely metastasise within or beyond the cranial cavity but may be classified as malignant if there is cytological evidence of anaplasia, evidence of local infiltrative growth or compression of vital brain centres

46
Q

List 3 main degenerative lesions of the brain with age

A

1) brain and spinal cord reduced in weight and volume
2) grossly discoloured grey-yellow and palpably firmer
3) cerebral gyri become narrow and wrinkled and the sulci become broad and shallow

47
Q

What are the 4 reflexes wtihin the forelimb and the nerves involved

A
  1. Extensor carpi radialis reflex
    ○ Afferent and efferent arms are radial nerve
  2. Biceps tendon reflex
    ○ Afferent and efferent arms are musculocutaneous nerve - C6,7,8
  3. Triceps tendon reflex
    ○ Afferent and efferent arms are radial nerve - C7,8,T1,2
  4. Withdrawal - pinch the webbing between the toes
    ○ Involves the axillary, musculocutaneous, ulna and median nerve
48
Q

What are the 4 reflexes within the hindlimb and the nerves involved

A
  1. Patellar reflex
    ○ Afferent and efferent via femoral nerve - L3-L4
  2. Gastrocnemius reflex
    ○ Afferent and efferent arms are tibial nerve - L5,6,7
  3. Cranial tibial
    ○ Afferent and efferent arms are peroneal nerve - L5,6,7
  4. Withdrawal - pinch the webbing between the digits
    ○ Afferent and efferent is the sciatic nerve