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MPharm2 SL22108 > Surgery > Flashcards

Surgery Flashcards

1
Q

What are the 7 steps of a pre-op assessment?

A
  • patient ‘clerked’
  • physical exam
  • procedure explained, consent forms signed
  • opportunity for questions
  • discuss post-op care
  • meds rec
  • peri-operative medicines management
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2
Q

What are the 8 steps of the elective surgical pathway?

A

Patient sees GP
Referred to specialist
Diagnosis
Adjunct treatment (e.g. chemotherapy)
Decision made for surgery
Patient usually seen at pre-operative assessment clinic a few weeks pre-op
Patient arrives in Admission Suite 07:30 – morning of surgery

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3
Q

What are the 8 checks for pre-op fitness?

A
  • Blood tests – eGFR, Hb, Crossmatch
  • Weight – important for medication doses
  • MRSA screen and eradication
  • BP – may need treatment
  • Cardiac function: ECG / ECHO
  • HbA1c – optimise diabetes management pre-op
  • Medication history
  • Prescribing e.g. anticoagulant bridging therapy
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4
Q

What does NBM pre-op mean?

A

Technically nil-by-mouth, but small sips of water and usual medications are okay (if given go-ahead)
6 hours fasted for food, up to 170ml/hr non-milky fluids

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5
Q

Why is the meds rec done pre-op?

A

If not performed, no accurate source of medication to inform prescribing
Potential for critical missed doses
Pre-op patient is alert, with family / carer, medication is available
Post-op patient is drowsy, family not available, medication may have been sent home

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6
Q

Why are there specialist pre-op pharmacists?

A

In pre-op assessment clinics

Medication experts that can ensure appropriate advice given on management of long terms conditions

Minimise post-op complications

Prepare patient for discharge

Stable workforce compared to rotating junior doctors

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7
Q

What is the procedure on the morning of surgery?

A

Patients arrive 07:30
First operation scheduled for 08:00
Surgeon finalises operation detail and consents patient
Anaesthetist ensures fit to proceed
Nurse gives pre-meds, TED stockings, takes observations
Re-check of medicines reconciliation

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8
Q

What is the procedure during and after surgery?

A

Operation takes place in theatre (intra-operative period)
Recovery – woken up, orientated, pain relief, PONV prophylaxis
Patient sent to ward (post-operative period)
Duration of stay depends on:
Surgical procedure
Previous co-morbidities
Need for IV medication (pain relief, antibiotics)
Post op complications
Enhanced recovery pathway

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9
Q

What are the pre-op considerations for Warfarin?

A
  • it has a long half life, so stop 5 days before surgery
  • INR must be under 1.5 to proceed with surgery
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10
Q

What are the post-op considerations for Warfarin?

A
  • usually restart asap after surgery depending on bleed risk
  • consider all bleeding risks (wound, internal, epidural)
  • can use LMWH as prophylaxis/bridging therapy if bleeding risk is high
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11
Q

What are the considerations for Warfarin for emergency surgery?

A
  • give vitamin K within 4-24 hours, best if surgery can be delayed 4 hours
  • not always best as you can go too far with it
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12
Q

What are the main reasons for anti-coagulant therapy?

A

Mechanical Heart Valves:
- Depends on type of valve
- Generally considered high risk of thrombosis if anticoagulation held
- “Bridging” usually needed

Deep Vein Thrombosis or PE:
- Risk is very high in first 3 months post thrombosis
- If >3 months: Most patients can receive just prophylactic dose LMWH post procedure
- “Bridging” may be needed if recurrent DVTs/PEs or in last 3 months

Atrial Fibrillation:
- Depends on thrombosis risk: previous TIAs and CHADS2 score

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13
Q

What are the considerations for DOACs for elective surgery?

A
  • short acting so wear off, bridging not usually required
  • stopping time varies as clearance rate varies (renal function, drug half-life)
  • Bridging not usually required as can usually stop prior to surgery
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14
Q

What are the consideration for anti-platelets?

A
  • aspirin: if under 150mg, continue, if over 150mg, reduce until under
  • clopidogrel: stop 7 days pre op, sub for aspirin if possible
  • however different considerations for cardiac surgery and dual antiplatelet
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15
Q

What are the considerations for restarting antiplatelets and DOACs?

A
  • usually restart DOACs within 24-72 hrs, with considering all bleeding risks
  • DOACs can be covered with LMWH prophylactic dose
  • antiplatelets can be continued from morning after
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16
Q

What are the considerations for cardiac medications?

A
  • surgery can increase HR and BP so meds continued
  • ACEi/ARB + diuretics may be omitted due to risk of hypotension
  • always continue beta blockers, digoxin, anti-arrhythmics
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17
Q

What are the considerations for long term steroid therapy?

A
  • patients on steroids may have pituitary-adrenal suppression and natural stress response impairment which leads to circulatory collapse
  • stress from surgery causes plasma adrenocorticotrophic hormone and cortisol levels to rise
  • all oral steroids considered, other routes sometimes
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18
Q

What are the steroid replacements for minor surgeries?

A
  • usual dose in morning
  • or hydrocortisone 25-50mg IV
  • recommence after surgery
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19
Q

What are the steroid replacements for moderate/major surgeries?

A
  • usual dose morning of, + hydrocortisone 100mg IV
  • hydrocortisone 25-50mg IV TDS between 24-72 hrs post-op
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20
Q

What are the considerations for non-insulin hypoglycaemics?

A
  • continue metformin, pioglitazone, DDP4 inhibitors, GLP-1 analogues, restart when eating and drinking normally
  • omit SGLT2 inhibitors 24-72 hrs pre-op and restart once E+D restarted and VRII stopped
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21
Q

What are the considerations for short-acting insulins?

A
  • omit doses for meals skipped while NBM
  • restart when VRIII stopped and eating post-op
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22
Q

What are the considerations for long/intermediate insulins?

A
  • continue at 80% of usual dose throughout surgery
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23
Q

What are the considerations for mixed insulins?

A
  • halve usual morning dose
  • restart post-op if adequate oral intake
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24
Q

What is VRIII?

A
  • two IV lines
    • line 1: 50 units actrapid in 50ml saline
    • line 2: 500ml 5% dextrose over 5 hrs
  • aim for 6-10 mmol L-1 for VRIII
  • continue long acting and GLP-1 analogues
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25
Q

What are the considerations for HRT?

A
  • Oestrogen containing birth control caries 3x risk of VTE
  • mini pill carries no extra risk
  • suggest stopping COCs 4-6 weeks prior to major surgery
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26
Q

What must be done for a patient on HRT needing emergency surgery?

A

Thromboprophylaxis

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27
Q

What are the considerations for Tamoxifen?

A
  • carries increased VTE risk
  • consider stopping 4 weeks before surgery
  • always discuss with oncologists
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28
Q

What are the considerations for MAIOs?

A
  • potentially fatal interactions
  • reduce and stop 2 weeks before or
  • switch to reversible MAIO or
  • choose MAIO-safe anaesthetic
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29
Q

What are the potential interactions for MAIOs?

A
  • analgesics - CNS toxicity or increased convulsant risk
  • sympathomimetics - increased risk of hypertensive crisis
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30
Q

What are the considerations for Lithium?

A
  • fluid imbalance can precipitate toxicity
  • preferably stop 1-2 days before surgery
  • if continued
    • monitor lithium levels and fluid
    • avoids NSAIDs
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31
Q

What are the considerations for anti-convulsants?

A
  • continuation is essential
  • consider by alternative routes if NBM
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32
Q

What is an ‘-ectomy’?

A

removal of

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33
Q

What is an ‘-otomy’?

A

opening of

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34
Q

What is an ‘-ostomy’?

A

bring to surface

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35
Q

What is an ‘-scopy/scopic’?

A

looking into

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36
Q

How can you check the status of your post-op patient?

A

General appearance
Signs e.g. NBM, free-fluids (FF), E&D
Fluids, drains, NG tubes
TPN, enteral feeds
Pumps e.g. PCA, epidural, heparin, Sliding scale
Mobility
Vomit bowl
Oxygen requirement
Dressings

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37
Q

What are the considerations for antibiotic prophylaxis?

A
  • type of surgery
  • duration depends on degree of contamination
  • drug depends on causative organism
  • IV route preferred
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38
Q

What are the three degrees of contamination?

A

Clean
- non-traumatic, no inflammation, no break in technique

Clean-contaminated
- non-traumatic but breach in technique or unsantiary area

Contaminated
- major break in technique
- gross spillage
- traumatic wounds

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39
Q

What is virchow’s triad of VTE risk?

A
  • prothrombotic change
  • vascular wall injury
  • circulatory stasis
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40
Q

What are the 3 actions of VTE prophylaxis?

A
  • mobilise patient asap
  • avoid dehydration
  • stop meds that increase risk
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41
Q

What are the 2 mechanical ways of VTE prophylaxis?

A
  • stockings
  • intermittant pneumatic compression devices
42
Q

What are the 4 pharmalogical solutions of VTE prophylaxis?

A
  • LMWH
  • UFH
  • DOACs
  • fondaparinux
43
Q

What is the reccomended VTE prophylaxis for a hip replacement?

A
  • LMWH for 10 days, aspirin for next 28 days or
  • LMWH + AES for 28 days or
  • DOAC OD for 35 days
44
Q

What is the reccomended VTE prophylaxis for a knee replacement?

A
  • aspirin 75-150mg OD for 14 days or
  • LMWH + AES for 14 days or
  • Rivaroxaban 10mg for 14 days
45
Q

Why must pain be well managed?

A

↓ Recovery & ↑ length of stay
↓ Mobility & ↑ VTE risk
↓ wound healing
↑ BP & Pulse
↑ Anxiety & disturbed sleep

46
Q

What does WHO recommend for mild pain?

A
  • regular
    • paracetamol
    • +/- NSAIDs
  • PRN
    • Tramadol
    • Codeine
47
Q

What does WHO recommend for moderate pain?

A
  • regular
    • paracetamol + tramadol or codeine
    • +/- NSAIDs
  • PRN
    • Oxycodone
    • Morphine
48
Q

What does WHO recommend for severe pain?

A
  • regular
    • paracetamol + morphine or oxycodone
    • +/- NSAIDs/tramadol
  • PRN
    • short acting strong opioid
    • codeine
49
Q

What are epidurals?

A
  • Analgesia localised to chest, pelvis, lower limb depending on catheter site
  • Can provide better pain relief than other methods
  • Usually local anaesthetic +/- opiate (e.g. Levobupivacaine and Fentanyl)
50
Q

What are the risks associated with epidurals?

A
  • motor neurone block
  • haematoma
  • infection
  • dural puncture
51
Q

What is patient controlled analgesia?

A
  • strong opioid (fentanyl, oxycodone, morphine)
  • bolus dose when button pressed with 5 min lock time
52
Q

What are the risk factors for PONV?

A
  • female
  • history of motion sickness
  • non-smoker
53
Q

What causes PON+V?

A

Anaesthetic agents
Opioid analgesia
Bowel surgery
Antibiotics
U&E disturbances
Bowel obstruction

54
Q

Why are some patients NBM post op?

A

After most surgical procedures, patients can eat and drink the same day
Post major GI surgery may be NBM for several days or have impaired absorption e.g. oesophagectomy, Whipple’s

55
Q

How must medicines be managed post op?

A
  • surgical procedures take away need for certain meds
  • new medicines may be needed to replace certain organ functions
  • medicines may be altered by different organ function
56
Q

What 3 things are required of an anaesthetic?

A
  • abolition of sensation
  • abolition of pain
  • triad of GA
    • unconciousness
    • analgesia
    • muscle relaxation
57
Q

What are the 3 routes of administration of anaesthetics?

A
  • inhalation (gases or vapours)
  • IV
  • intradermal
58
Q

What are the 4 advantages of inhaled anaesthesia?

A
  • controllable
  • rapid
  • stable
  • potent
59
Q

What are the 4 stages of anaesthesia?

A

Stage 1: analgesia
- conscious, drowsy, amnesia

Stage 2: excitement
- loss of consciousness, delirium, apnoea, gagging

Stage 3: anaesthetic
- regular respiration, loss of reflex + muscle tone

Stage 4: medullary paralysis
- depression of cardio-respiration, death

60
Q

What are the 7 inhaled anaesthetics and their properties?

A
  • chloroform (obsolete)
  • desflurane (fast on and off)
  • halothane (vets use, dev countries)
  • isoflurane (non-epileptogenic)
  • enflurane (fast, potent, hepatotoxic)
  • sevaflurane (fast, potent, hepatotoxic)
  • NO
61
Q

What are the 6 IV anaesthetics and their properties?

A
  • propofol (rapid metabolism, induction + maintenance)
  • fospropofol (water soluble, prodrug)
  • barbiturates (pre-op)
  • opioids (provides analgesia + supplemental sedation)
  • ketamine (slow onset, dissociative, analgesic)
  • etomidate (rapid metabolism, muscle jerks)
62
Q

What is the lipid theory of GA?

A
  • potency is proportional to lipid solubility
63
Q

What is the protein theory of GA?

A
  • Luciferase inhibition correlates with anaesthetic potency
  • anaesthetics interact with membrane proteins
  • receptors + ligand gated ion channels
64
Q

What is the MoA of GA?

A
  • anaesthetics don’t belong to any particular drug class
  • affect different types of ion channels
  • block excitatory ligand-gated ion channels
  • enhance activity of inhibitory ion channels
  • reduce neuronal excitability through effects on K channels
65
Q

What are the 5 types of local anaesthetics?

A
  • topical
  • infiltration
  • nerve block
  • spinal
  • epidural
66
Q

What are topical anaesthetics?

A
  • applied directly to the skin or mucous membranes
  • top 3, benzocaine, lidocaine + tetracaine
  • used to relieve or prevent pain from minor burns, irritation or itching
  • can numb before an injection
  • adverse effects involve skin irritations + hypersensitivity
67
Q

What are infiltration anaesthetics?

A
  • produce loss-of-sensation restricted to a superficial, localised area
  • injection of anaesthetic solution directly into area of terminal nerve endings
  • used for minor surgical + dental procedures
68
Q

What are nerve block anaesthetics?

A
  • regional anaesthetics
  • injection of a local anaesthetic to numb the nerves supplying a particular part of the body
69
Q

What are spinal anaesthetics?

A
  • a single injection with a thin needle that puts the local anaesthetic close the nerves
  • used to numb the lower body
  • rapid onset, only lasts a few hours
  • side fx - low BP, headache, back pain
  • provides pain relief post surgery
70
Q

What is epidural anaesthesia?

A
  • injection into space outside sac
  • tube left in epidural space, anaesthetic pumped continously
  • slow onset, long duration
  • side fx - heart rhythm problems, seizures, hematoma in epidural space
71
Q

What is the MoA of LA?

A
  • block voltage-gated Na+ channels
  • no entry of Na+ ions into cell
  • no depolarisation
  • no generalisation of action potential
  • no generation + conduction of impulse to CNS
72
Q

What are the 5 combined approaches in surgical anaesthesia?

A

Pre-op (sedation, anxiolysis, amnesia)
- midazolam and other benzodiazepines

Rapid unconsciousness
- i.v. of rapid short acting agent eg. thiopental

Maintain unconsciousness
- inhalation agents eg.nitrous oxide, halothane

Supplement analgesia
- i.v. agents eg.fentanyl

Paralysis
- neuromuscular block eg.suxamethonium

73
Q

What are the 6 types of imaging?

A

Plain film (x-ray)
Ultrasound
CT
Fluoroscopy
MRI
Nuclear medicine imaging

74
Q

What are the 3 types of contrast media used for scans?

A

Iodine based Contrast Media
Gadolinium based Contrast Media
Barium Sulphate

75
Q

What are the 4 types of CVADs?

A

Acute Central Catheter
Hickman/Apheresis -Tunnelled
PICCs/Acute – Non Tunnelled
Implanted Ports – Chest & Arm

76
Q

What are the 5 advantages of CVADs?

A
  • Provides reliable long-term venous access
  • Multiple blood sampling
  • Administration of blood products, medication, PN, fluids, chemotherapy, contrast media
  • Removes the need for constant venepuncture and/or peripheral cannulation
  • Outpatient / ambulatory Antibiotic Therapy, chemotherapy
77
Q

What are the 5 disadvantages of CVADs?

A
  • Pneumothorax, haemothorax, air/catheter embolus, haemorrhage, haematoma, malposition, nerve damage,
  • Infection risk
  • Thrombosis risk – new Endexo technology now available
  • Hospital / community nursing and medical staff knowledge / skill in caring for the device
  • Implications related to body image and daily living – external catheters, scarring, children, physical activities, seat belt use
78
Q

What are the 5 steps to care for and maintain a CVAD?

A

Site Inspection – signs of infection

Securement – Type of dressing

Dressing change & type - ANTT

Cleaning solution – ChloraPrep

Flushing – Positive pressure

79
Q

What 4 complications can arise from a CVAD?

A
  • Infection – systemic/local
  • Thrombus
  • Catheter Fracture
  • Extravasation
80
Q

Why must muscle reflexes be supressed during anaesthesia?

A
  • During induction of anaesthesia reflexes mayhamper intubation
  • Often important to immobilize the area underinvestigation
  • Muscle spasms can occur due to mechanicalmanipulation of limbs and nerves
  • Reflexes not suppressed until deep anaesthesia
81
Q

How is ACh released at the NMJ?

A
  • Action potential conducted along the motor nerve
    depolarisation
  • Influx of calcium at nerve terminal
  • ACh released from storage vesicles into the synapse
  • High density of nicotinic receptors (nAChR)
  • ACh metabolised by acetylcholine esterases
82
Q

What is the NMJ end plate?

A
  • ACh binding to nicotinic receptors leads to Na+ influx
  • Initiates opening of voltage-gated Na+ channels
  • Action potential in muscle cell membrane
83
Q

What are the two types of neuromuscular-blocking agents?

A

Non-depolarising agents:nicotinic antagonists
Depolarising blocking agents:weak nicotinic agonists

84
Q

What are non-depolarising agents?

A
  • Competitiveantagonists of ACh receptors at the endplate
  • Curare is a mixture of alkaloids found in South American plants including d-tubocurarine
  • Causes paralysis by blocking neuromuscular transmission but not nerve conduction or muscle contractility
  • Used by Indigenous South Americans in poison arrows
  • Poor oral absorption – safe to eat
85
Q

What is d-Tubocurarine

A
  • Binds to nicotinic receptor at NMJ as an antagonist
  • Much more ACh than needed is released when NMJ activated, so need to block about 90% of receptors to have any effect
  • Blocking receptors causes a decrease in end-plate potential
  • Synthetic derivatives now used clinically:gallamine, rocuronium,pancuronium,vecuronium
86
Q

What is the effect of tubocurarine on neuromuscular transmission?

A
  • Nerve stimulation initiates end-plate potential (epp)
  • Initiates action potential
  • Tubocurarine reduces the epp amplitude so that no action potential is generated
87
Q

How do you recover from non-polarising NMBA?

A
  • Rocuronium – fast onset, intermediate duration
  • Determined by susceptibility to cholinesterases and clearance
  • Newer non-depolarising blockers have shorter duration of action
  • Safer
  • Paralysis fades after surgery
88
Q

What are the 6 side effects of non-depolarising blockers?

A

Hypotension due to ganglion blockade

M2blockade(gallamine,pancuronium) (tachycardia

Histamine release from mast cells

Bronchospasm in sensitive individuals

Respiratory failure (assisted ventilation used)

Autonomic ganglion block at high doses

89
Q

What are depolarising NMBAs?

A
  • Initially bind and activate nicotinic receptor
  • Opens end-plate voltage-sensitive Na+ channels
  • Depolarises muscle
  • Slowly hydrolysed by cholinesterases
  • Depolarisation maintained at the end-plate
  • Lossof electrical excitability
  • Produces initial twitching of skeletal muscleprior to block
  • Decamethonium,suxamethonium(succinylcholine)
90
Q

What is phase 1 block?

A
  • Depolarising block
  • Bind to nicotinic receptors
  • Prolong ion conductance & depolarisation
  • No repolarisation
  • Potentiation by AChE inhibitor
91
Q

What is phase 2 block?

A
  • Desensitisation block
  • Persistent stimulation ofnicotinic receptors leads to desensitisation
  • Channel no longer open inresponse totransmitterbinding tonicotinic receptor
  • Muscle becomes flaccidas Ca2+taken intostores
92
Q

What are the 4 advantages of depolarising NMBA?

A
  • Rapid onset, short duration of action
  • Useful for intubation (paralyse larynx)
  • Surgery during pregnancy/caesarean section
  • Suxamethonium ionised so crosses blood-placenta barrier poorly and does not affect newborn respiration
93
Q

What are the 6 side effects of depolarising NMBA?

A
  • Bradycardiadue to direct muscarinic action
  • Hyperkalaemia which can cause ventricular dysrhythmia
  • Prolonged paralysis incholinesterasedeficient individuals
  • Increased intraocular pressure
  • Contraction of extra-ocular muscles
  • Post-operative pain
94
Q

What are the 3 differences between depolarising and non-depolarising NMBA?

A

Non-depolarising blockers work by competing with acetylcholine for receptors, reversed by increasign ACh concentration

Depolarising agents cause prolonged stimulation and subsequent desensitisation of the receptors, producing initial small involuntary twitches

95
Q

How are NMBAs reversed?

A

Neostigmine
- Acetylcholinesterase inhibitor
- Raises ACh in synapse
- Reverses non-depolarising block
- Potentiates depolarising block

Sugammadex
- Chelates aminosteroid non-depolarising blockers
- reverses steroidal non-depolarizing neuromuscular blocking drugs (rocuronium and vecuronium)

96
Q

What is neostigmine?

A
  • Quaternary ammonium compound
  • Competes with ACh on cholinesterase
  • Lipid insoluble, does not cross blood–brain barrier
  • Onset (i.v.) within 1 min, peak effect in 10 min
  • Duration of action 20–30 min
  • Slowly metabolised by plasma esterases
  • Increases postoperative nausea and vomiting, GI disturbance
  • Anti-muscarinic usually co-administered
97
Q

What are general anaesthetics?

A

Sedative-hypnotics act by enhancing the inhibitory actions of GABAA receptors

98
Q

What are the 3 ideal properties of GA?

A

Fast onset and recovery (titratable)

Few side effects/high therapeutic index

Aqueous solubility for easy formulation

99
Q

How was propofol improved?

A
  • it was insoluble as an o/w emulsion
  • was transformed in water soluble fospropofol
100
Q

What are benzodiazepines?

A
  • Widely used as anxiolytics, amnestics and sedative-hypnotics
  • Less used as anaesthetic induction agents due to cv depression and prolonged recovery times

MPharm2 SL22108 (7 decks)

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