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Flashcards in Anaesthesia Deck (24)
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a) Triad
b) Phases (general)
c) 3 stages of hypnosis

a) Unconsciousness, muscle relaxation and analgesia (local/systemic)
b) Induction, maintenance, emergence
c) Awake, sedated, asleep


Pre-operative medication.
a) Omit what medications? (ensure others taken as normal)
b) Add in what medications? (3 classes)

a) ACE inhibitors/sartans (24 - 72 hours)
Anti-TNFs (2 weeks)
Platelet inhibitors - aspirin, clopidogrel (7 - 10 days)
b) Analgesia, antiemetics, sedatives


a) Block what enzyme?
b) Hence, prevent conversion of arachidonic acid into what 3 things?
c) Block effects with what drug?
d) Asthma use
e) Renal effects
f) Give 4 contraindications
g) NSAID given IV in anaesthetics

a) Cyclo-oxygenase (COX). COX-1 more involved in stomach, COX-2 more important for inflammation and nociception
b) Thromboxanes (platelet aggregation, vasoconstriction), prostacyclin (vasodilation, anticoagulation), prostaglandins (inflammation, pain, gastric protection)
c) Misoprostol (synthetic prostaglandin), or PPI/H2RA
d) Do not use in aspirin-sensitive asthma, use with caution in other asthmatics (20% have asthma attack, due to increased leukotriene synthesis)
e) PGs dilate afferent arteriole. NSAIDs therefore constrict afferent arteriole, causing reduced renal blood flow. May also lead to fluid overload and hyperkalaemia
f) Renal failure, hyperkalaemia, hypotension, circulatory failure, pre-eclampsia, liver failure
g) Parecoxib


Induction agents.
a) Inhalational - examples
b) IV - examples
c) Rapid (RSI) vs. standard induction
d) Induction agents used in 'classic' and 'modified' RSI
e) Consciousness centre

a) Fluranes (isoflurane, sevoflurane, desflurane) - may irritate airway, usually keep breathing spontaneously
b) Propofol, thiopental sodium, ketamine - require IV access, depress airway reflexes, usually causes apnoea so require ventilation
c) Standard (assess ability to ventilate before muscle relaxant given), Rapid (give muscle relaxant without first assessing ventilation)
d) Classic (thiopentone - allegedly has a 'more defined clinical endpoint') vs. modified (propofol)
e) Reticular activating system (RAS) in medulla


Neuromuscular junction.
a) Neurotransmitter
b) Receptors
c) Mechanism of action

a) ACh
b) Nicotinic AChR (2 binding sites)
c) ACh released from pre-synaptic membrane binds to NAChR on the post-synaptic membrane, causing influx of Ca2+ ions, depolarisation (Na+ entry) and action potential propagation


Neuromuscular blockade.
a) Depolarising - explain, example
b) Non-depolarising - explain, example. Which is the quickest onset for a non-depolarising agent?
c) Specific reversal agent for rocuronium/vecuronium
d) Reversal agent that works for most non-depolarising agents
e) Can suxamethonium be reversed?
f) Indications for muscle relaxants
g) If muscle relaxants used, the patient must be...?
h) Only 2 agents may be used in RSI - what are they?
i) Metabolism of atracurium vs. rocuronium

a) Two ACh molecules bolted together that stimulate both ACh binding sites causing contraction and preventing further contraction. They are not broken down by AChE so cause paralysis (e.g. Suxamethonium) - must anaesthetise first as can cause pain before paralysis
b) Competitive antagonists at NAChR (e.g. rocuronium, atracurium, vecuronium) - more commonly used. Roc has the quickest onset, hence it can be used in RSI.
c) Sugammadex
d) AChE inhibitors (e.g. neostigmine +/- glycopyrronium bromide) - caution: these potentiate the effects of suxamethonium.
e) No, but is short-acting
f) Most surgery, passing artificial airway, status epilepticus
g) Ventilated. Some patients may be under GA but breathe spontaneously if not under a NMB
h) Sux / Roc
i) Atracurium: Hofmann (heat) degradation whereas rocuronium metabolised by Hofmann degradation AND P450 liver metabolism


Post-operative care.
a) 5 standard procedures
b) Other management as necessary
c) Analgesic ladder

a) Analgesia, antiemetics, antibiotics, anticoagulants, fluids
b) +/- blood products, oxygen, inotropes
c) Step 1 (paracetamol, NSAIDs), Step 2 (weak opioids: codeine, tramadol), Step 3 (stronger opioids: morphine, oxycodone, methadone, buprenorphine)


Local anaesthesia: types and indications.
a) Local nerve blocks - how they work
b) Regional
c) Neuraxial

a) Minor surgery, wound repair. MoA: reversible Na+ channel blockade, inhibit action potentials
b) Generally post-op analgesia: e.g. brachial plexus, sciatic, transversus abdominus plane (TAP) block
c) Intraoperative and post-operative: Spinal (subarachnoid), epidural


Cardio-stimulant 'rescue' drugs.
a) Main one to raise BP intra-operatively. - how do you know it's working?
b) Alternative used (in what cases?). Receptors activated. - how do you know it's working?
c) Main one to raise HR intra-operatively.
d) ITU drug used to raise BP in heart failure

a) IV Metaraminol: alpha-adrenoreceptor agonists, causes vasoconstriction, raising BP but causing reflex bradycardia. (NAD-lite, note: NAD can only be given through large central vein due to its necrotic effects if extravasation occurs). You know it's working as HR drops (often by around 5bpm)
b) IV Ephedrine: alpha- and beta-adrenoreceptor agonist, hence raises BP and HR - useful in bradycardic patients. (Adrenaline-lite. note: adrenaline only used in arrests/ITU/anaphylaxis). You know it's working as etCO2 goes up (due to increased CO).
c) IV Glycopyrronium (anticholinergic, inhibits the vagus nerve, atropine-lite, slower acting than atropine and doesn't cross BBB)
d) Dobutamine (beta-agonist)


Patient with low BP.
a) Induction method
b) Why not standard propofol/thiopentone or gas?
c) Maintenance

a) Fentanyl and midazolam (+/- small amount of propofol)
b) These depress CVS and lower BP, whereas fentanyl and midazolam just depress the RS.
c) Ketamine


Flurane gases.
a) Name 3 (most to least common)
b) Give the lipophilia of each
c) Explain the resultant speed of onset and offset
d) Give the financial cost and environmental impact of each
e) Who should Des be used in?

a) Sevoflurane, desflurane, isoflurane
b) Lipophilia: Iso > Sevo > Des
c) Speed of onset/offset: Des > Sevo > Iso
d) Cost and environmental damage: Des highest
e) Fat people (quicker wake-up than with Sevo, which would stay in their fat stores longer) and those with liver damage


a) Stands for...?
b) MAC of 1.0 means what?
c) Why is it flawed? (>50% people in theatre with MAC of 1.0 will be deeply anaesthetised, and most with MAC >0.7
d) How is it increased/decreased?
e) Why might it need to be increased/decreased?

a) Minimum alveolar concentration
b) 50% people will be anaesthetised to a painful stimulus at a MAC of 1.0 (based on anaesthetic gas alone)
c) Based on anaesthetic gas alone, also in days gone by people were generally overly anaesthetised. In theatre, co-induction agents like fentanyl and other analgesics are used, which increase the threshold necessary for a painful stimulus
d) Increasing/decreasing anaesthetic gas or TIVA
e) According to how painful the operation is likely to be (abdominal > peripheral vascular), also if patient's vital signs show pain is experienced (e.g. tachycardic)


Spinal anaesthesia.
a) Surface landmarks
b) Barriers from skin to CSF
c) vs. epidural
d) When might you use a combined spinal-epidural (CSE)
e) Region affected. How long does it last?
f) Risks of spinal anaesthesia
g) How is dural puncture CSF leak repaired?

a) Iliac crests (inter-cristal line) at L4/L5, go between bony prominences (spinous processes)
b) Pierce skin with introducer, stay in supraspinous ligament then put stilette in (resistance, through), ligamentum flavum (resistance, through), then pierce dura mater (pop), CSF should start flowing (if not, may have kebabbed it, so withdraw)
c) Location: subarachnoid vs epidural space. Administration: bolus vs. catheter infusion (note: epidurals often having opiates in infusion as well so don't prescribe additional opiates)
d) Longer operations (spinal would wear off, so can be topped up with epidural for analgesia, or possibly even anaesthesia)
e) Start distally and works up to around T10 (umbilicus) - incisions above this region will require GA. Anaesthesia lasts around 2h and completely wears off after ~6h.
f) Inefficacy, Infection, bleeding, low BP, nerve damage, CSF leak and low CSF headache
g) Epidural blood patch (autologous blood intrathecal injection)


Local anaesthesia
a) Channels affected
b) Fibres affected in what order?
c) Why often combined with adrenaline?
d) What arteries should adrenaline not be used in?
e) Types used

a) Na+ channels (reversible blockade)
b) Smallest to largest: B-fibres (autonomic - vasodilation), C- and A-alpha (pain and temp), A-beta (light touch and pressure), A-alpha and A-gamma (motor and proprioception)
c) Causes vasoconstriction - reduced bleeding and prolonged effect (due to reduced tissue absorption)
d) End arteries
e) Lidocaine (minor procedures: immediate onset, 15 mins duration), bupvicaine (regional, spinal and epidural: 10 minute onset, 2 hours anaesthesia and 12-24 hours analgesia)


a) 4 effects
b) Short-term drug
c) Long-term

a) Reduce anxiety, reduce consciousness, reduce airway irritability, induce amnesia
b) IV midazolam
c) IV Propofol +/- fentanyl


a) MoA
b) Be cautious in who?

a) Unknown, Theories: COX-inhibition, cannabinoid receptors
b) Liver failure, low weight (children, elderly, cachexia)


Pain vs. nociception

Pain is subjective and cannot be experience if unconscious
Nociception is objective and can be experienced irrespective of conscious level


a) vs. opioids
b) Side effects
c) Pre-operative
d) Intra-operative
e) Post-operative

a) Opioid (drug with morphine-like qualities), opiate (natural opioids)
b) CNS (sedation, miosis), CVS (bradycardia, hypotension), resp (bradypnoea, apnoea), GI (nausea, vomiting, constipation), urinary retention, itching
c) Weak (codeine, tramadol), strong (morphine, oxycodone, methadone, buprenorphine)
d) IV fentanyl or alfentanil (more rapid onset/offset). remifentanil (very rapid onset/offset)
e) Codeine, tramadol, morphine (may be given as PCA)


a) Vomiting mechanism
b) Receptors involved and example for each receptor antagonist
c) Intra-operative use
d) Post-operative N/V (PONV) use
e) Risk factors for PONV

a) Blood-borne stimulus - chemoreceptor trigger zone in area postrema of medulla - solitary tract nucleus. Other stimuli that go to higher centres include the inner ear, emotion, pharyngeal stimulation and GI tract

b) H1 (histamine) antagonist - cyclizine
5HT-3 (serotonin) antagonist - ondansetron
D2 (dopamine) antagonist - metoclopramide

c) IV dexamethasone, IV ondansetron
d) Ondansetron, cyclizine
e) Patient (female, previous PONV, non-smoker), surgical factors (ENT, Gynae, GI), anaesthetic factors (peri-operative opioids, gastric insufflation during intubation, long duration of anaesthesia)


Sympathetic 'fight or flight' response.
a) Alpha receptors - explain main response and the rationale.
b) Beta-1 receptors - explain 2 main sites with response and rationale
c) Beta-2 receptors - explain 3 main sites with response and rationale
d) Why are alpha-receptor agonists (vasopressors) useful in sepsis?

a) Alpha-receptors: found in blood vessels, activation causes peripheral vasoconstriction (rationale: don't need blood flow peripherally, need increased venous return to increase CO to vital organs)
b) Heart: increase inotropy (SV) and chronotropy (HR) to increase CO.
Kidney: renin release, activating RAAS and causing fluid retention an increased BP (maintain perfusion to vital organs)
c) Lungs: bronchodilation (increase oxygen delivery to alveoli and tissues in response to higher cellular metabolic demands)
Liver: glycogenolysis (increased glucose availability for cellular respiration)
Skeletal muscle: increased blood flow to meet increased metabolic demands
d) Sepsis causes peripheral vasodilatation - vasopressors combat this and increase venous return


Cellular respiration.
a) What is the equation for aerobic respiration?
b) What is the equation for anaerobic respiration?
c) Why is aerobic respiration preferable?

a) Glucose + oxygen >>> CO2 + H2O + ATP
b) Glucose >>> Lactate + ATP
c) Anaerobic respiration produces about 20x less ATP and lactate, which is acidic.


Explain Frank-Starling curve

- Increased venous return leads to increased EDV (preload)
- This leads to stretching of the cardiac myocytes
- Subsequently, cardiac output increases
- In heart failure, increased venous return (preload) leads to falling cardiac output


a) What is it?
b) What drugs are particularly associated with it?

a) Acute, sudden decrease in response to a drug after its administration, i.e. a rapid and short-term onset of drug tolerance. It can occur after an initial dose or after a series of small doses
b) Dobutamine, salbutamol, local anaesthetics,


Cardiac arrest.
a) VF/VT - usual cause
b) PEA/asystole - possible causes

a) Cardiac (e.g. MI, arrhythmia), electrolytes, electrocution (rare)
b) 4Hs (hypoxia, hypovolaemia, hypothermia, hypo/hyperkalaemia/hypoglycaemia, etc.) 4Ts (thrombosis, tamponade, tension pneumo, toxins)