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Human Diseases Yr3 > Analgesia and Anaesthesia > Flashcards

Analgesia and Anaesthesia Flashcards

1
Q

Pain in the orofacial region is transmitted mainly by trigeminal nerve. What is the exception to this?

A

Angle of the jaw supplied by upper cervical nerves

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2
Q

What algogenic substances (pain signals) can be inhibited by analgesics?

A

Substance P and Prostaglandins

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3
Q

What are the 2 main types of nociceptive axons?

A

a) A delta - fast and myelinated. Respond to high intensity mechanical stimuli
b) C polymodal - unmyelinated and slower. Mechanical thermal and chemical stimuli

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4
Q

What do the nociceptors in the a delta and c fibres send signals to?

A

Trigeminal ganglion and onto the brainstem

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5
Q

In the trigeminal nucleus caudalis, what are the following responsible for?

a) Mesencephalic nucleus
b) Principle nucleus
c) Spinal nucleus

A

a) Proprioception from PDL and muscle fibres in jaw close reflex
b) Proprioception for oral facial behaviour except jaw close reflex
c) Nociception (pain) from primary afferents of trigeminal nerve

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6
Q

Where do third order neurones synapse?

A

In the thalamus

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7
Q

What are the 2 mechanisms of pain modulation?

A

Descending impulses e.g. gate control

Sensitisation

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8
Q

In the process of sensitization, what is the definition of

a) Hyperalgesia
b) Allodenia

A

a) Increase in painful signal

b) A signal that isn’t usually painful now is

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9
Q

What is peripheral sensitisation?

A
  • Nociceptors have increased responsiveness to lower thresholds and recruits sleeping nociceptors
  • More persistent and intense = hyperalgesia
  • Caused by chronic tissue damage so releases continual allogenic substances
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10
Q

What is central sensitisation?

A
  • Second order neurones recieve prolonged stimulus so become sensitized - allodenia
  • May occur as a result of nerve trauma, genetic and environmental factors
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11
Q

What does convergence present as?

What does divergence present as?

A
  • Referred pain - brain can’t tell where pain is coming from
  • Radiation of pain
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12
Q

What are the warning signs of persistent pain?

A
  • Coming from multiple teeth
  • No obvious pathology
  • Numbness and tingling or burning sensation
  • LA doesn’t provide pain reduction
  • Pain has abnormal triggers
  • Doesn’t disturb sleep
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13
Q

What do peripherally acting analgesics mainly target? E.g. parecetamol, NSAIDS, COX 2 inhibitors

A

Inflammatory cascade by inhibiting algogenic substances

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14
Q

For paracetamol

a) What are its properties?
b) What is the adult dose?
c) What pts should you avoid giving it to?
d) Where is it metabolised

A

a) Analgesic, anti-pyretic, weakly anti-inflammatory
b) 500mg-1g qds
c) Liver disease
d) Liver - NAPQI

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15
Q

What is the treatment for paracetamol overdose?

A

4hrs = activated charcoal
12hr = N-acetylcycteine

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16
Q

What is the MOA of NSAIDS e.g. ibuprofen, aspiring, diclofenac and mefenamic acid?

A

Non-selective block of COX enzyme

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17
Q

What are the properties of aspirin?

A
  • Analgesic
  • Anti-platelet
  • Anti-inflammatory
  • Anti-pyretic
  • Rapid absorption GI
  • 300mg can be used in suspected MI
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18
Q

What are the properties of ibruprofen?

A
  • Low GI and CVS risk
  • Analgesic
  • Anti-pyretic
  • Anti-inflammatory
  • 1.2-2.4g total daily dose - for dentistry 400mg po tds
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19
Q

What are the adverse effects of NSAIDS?

A
  • Gastric ulceration - avoid in liver disease pts
  • Anti-platelet - don’t use in other coagulopathies as increased risk of bleed
  • Can induce asthma attack, especially ibuprofen
  • Non-selective Pg block leads to renal toxicity - avoid in kidney patients
  • Reyes syndrome - no aspirin for under 16s
  • Extensively protein bound so drug interactions
  • CVS risk with Diclofenac and Indomethacin
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20
Q

What are COX2 inhibitors known by? Why are they different to aspirin?

A
  • oxib e.g. Celecoxib
  • Safe aspirin as selective block so decreased gastric side effects but increased Pg block so prothrombotic effect and increased risk of MI
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21
Q

What are centrally acting analgesias (opioids) antagonised by?

A

Naloxone

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22
Q

What receptor do opioids mainly work on and what effects does it cause?

A
  • u

- Analgesia, respiratory depression, pupil constriction, euphoria, decreased GIT motility, dependence

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23
Q

What is the MOA of opioids?

A
  • Descending inhibitory control of nociception through PAGM

- Peripheral afferent hyperpolarisation

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24
Q

What are the unwanted effects of opioid use?

A
  • Respiratory depression
  • Nausea
  • Pupillary effects so dont use with head injuries
  • Decreased urinary flow
  • Dependence - tolerance - increased receptor number and sensitivity
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25
Q

What drug helps manage opioid addiction?

A

Methadone

26
Q

What are the risks of Tramadol?

A

Seizure threshold and seretonin syndrome

27
Q

What is the MOA of Benzodiazepines?

A
  • Enhance effects of GABA which inhibits neurotransmission

- Mimics effects of glycine which is a inhibitory NT

28
Q

What are the effects of Benzodiazepines?

A
  • Muscle relaxation
  • Sedative
  • Anxiolytic
  • Disinhibition
  • Anticonvulant
  • Anaethesia
  • Amnesia
29
Q

What is the drug of choice for sedation?

A

Midazolam: 5mg in 5ml ph3.5

30
Q

What drugs do benzodiazepines have a synergistic effect with?

A

Opiates

31
Q

What are the side effects of benzodiazepines/ midazolam?

A
  • Respiratory depression - decreases response to CO2
  • Reduced BP
  • Heart rate increases
  • Synergistic with other CNS depressants e.g. opiates, alcohol, antihistamines
32
Q

What drugs inhibit midazolam?

A

Erythromycin and cimetidine

33
Q

What are the effects of nitric oxide?

A
  • Depressive and euphoriant effects
  • Myocardial depressant at high dose
  • Mild depression of alveolar ventilation
  • Analgesia
  • Relaxation
  • Paraesthesia
  • Amnesia
34
Q

What is the maximum N20?

A

100ppm over 8hrs

35
Q

What are the side effects of chronic nitric oxide exposure?

A
  • Pernicious like anaemia (impaired DNA synthesis and bone marrow depression)
  • Peripheral neuropathy (paraesthesia)
  • Liver disease
  • Increased miscarriage and decreased fertility
36
Q

What are the theories of the MOA of local anaesthesia?

A
  • Membrane expansion

- Specific receptor - LA binds to h gate on sodium channel holding gate closed and the cell in refractory period

37
Q

What 3 parts is an LA molecule made up of?

A
  • Aromatic group (lipophilic)
  • Intermediate chain (ester or amide link)
  • Substituted amino terminal (hydrophilic)
38
Q

Which of the LAs are

a) Amides
b) Esters (more allergies)

A

a) - Lidocaine
- Articaine
- Bupivacaine
- Prilocaine
- Mepivacaine
- Ropivacaine
- Levobupivacaine

b) - Benzocaine (topical)
- Procaine
- Amethocaine

39
Q

Why is an LA with a higher proportion of uncharged molecules after injection most effective?

A

Enters the cell quicker (has to be uncharged to enter cells)

40
Q

What does a a) low pH and b) low pka mean for number of uncharged molecules

A

a) Less uncharged molecules e.g. infected tissues

b) More uncharged molecules so quicker onset of action

41
Q

What is partition coefficient of LA and which ahs a higher partition coefficient, lidocaine or procaine?

A

Measure of lipid solubility, so higher partition coefficient means more lipid soluble so enters cell quicker
Lidocaine

42
Q

Lidocaine is 64% protein bound and bupivacaine is 96% protein bound. Which has a longer half life?

A 
Lidocaine = 90 mins 
Bupivacaine = 160 mins
43
Q

What is the only LA that is not a vasodilator?

A

Cocaine

44
Q

What are the vascular effects of adrenaline?

A
  • Alpha adrenoreceptors : skin and mucous membrane vasoconstriction
  • Beta adrenoreceptors : skeletal muscle and liver vasodilation
45
Q

What are the metabolic effects of adrenaline?

A
  • Alpha : inhibiton of insulin release so increased blood glucose
  • Beta : activates sodium potassium pumps
46
Q

What are the cardiac and pulmonary effects of adrenaline?

A
  • Cardiac: activation of beta, increases rate and force of contraction
  • Pulmonary: activation of beta, bronchodilator
47
Q

How does adrenaline affect wound healing?

A
  • Decreased O2 tension in tissues

- Increased fibrinolysis - decreased stability of blood clots

48
Q

What is the amount of adrenaline in an LA cartridge?

A

1:80000 so 2.2ml contains 27.5ug/ml

49
Q

What are the effects of felypressin? How much is in a cartridge of LA?

A
  • Coronary artery vasoconstriction
  • Oxytoxix action on uterus (induce labour)
  • 2.2ml contains 1.2ug
50
Q

What does the rate of LA entering the bloodstream depend on?

A
  • Vasodilatory ability
  • Protein binding
  • Presence of vasoconstrictor
  • Route of administration
  • Dose volume and concentration
51
Q

What LA is partly metabolised in the lung?

A

Prilocaine

52
Q

What is the metabolism of

a) Esters
b) Amides

A

a) In blood by pseudocholinesterase and some in liver. Non active metabolites

b) In liver. Metabolites possess LA and sedative properties
NB articaine also pseudocholinesterase

53
Q

What is the amount of LA that causes CNS toxixity?

A

5mg/L

54
Q

What is the rule of thumb for lidocaine dose per kg?

A

1/10 cartridge per kg or 1 cartridge per kg

55
Q

Why can liver disease cause overdose with LA?

A
  • Major site of metabolism and pseudocholinesterase produced in liver
  • Reduce dose
56
Q

In LA Toxicity what is the effects on

a) CNS
b) CVS

A

a) At low dose = excitatory. At high dose = inhibitory, depressant effect (confusion, drowsiness, shivering) and then unconsciousness and respiratory arrest
b) Depressant action of heart

57
Q

What is different in the positioning of a patient for LA overdose and adrenaline overdose?

A

LA = Lie pt flat and maintain airway
Adrenaline = patient semi-supine to minimise increase in cerebral BP

58
Q

What is the difference between afferent and efferent neurons?

A

Afferent = sensory nerve passing impulses from receptors to the CNS
Efferent = motor nerve conveying information from CNS to muscles/glands

59
Q

What is the management of an opiod overdose?

A

ABC 100% high flow O2
Naloxone 0.2-0.4mg IV
Repeat every 3 mins up to 10mg

60
Q

What is the dosing regimen of codeine?

A

30-60mg

Human Diseases Yr3 (6 decks)

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