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1
Q

What are local anaesthetics

A

Drugs that block pain sensation in region administered

2
Q

How do local anaesthetics work

A

Reversibly block fast VGSCs of nerve fibres reversibly inhibiting conduction of nerve impulses and pain within a limited area

3
Q

Nerve fibres are affected by LA in what order

A

Nerve fibres that carrypain sensation have the smallest diameter and are first to be blocked by LAs

Loss of motor function and sensation of touch and pressure follow, depending on duration of action and dose of the LA used

4
Q

When is combining adrenaline with local anaesthetic CI?

A

Pts with CVD
Pts taking TCAs or MAO-Is
End-arterial locations

5
Q

Why is adrenaline used with local anaesthetic

A

LAs have vasodilatory effect –> increases absorption into systemic circulation increasing toxicity risk/systemic SEs + reducing local anaesthetic action

Adrenaline is a vasoconstrictor so increases duration of action and permits a higher upper dose limit

6
Q

Types of local anaesthesia

A

Surface/topical anaesthesia
Infiltration anaesthesia
IV regional anaesthesia
Nerve block anaesthesia
Epidural anaesthesia
Spinal anaesthesia

7
Q

Describe surface anaesthesia

A

Used for mucous membranes (nose, mouth, bronchial tree, urinary tract, uterus)

e.g., lidocaine
e.g., EMLA = eutectic mixture of LAs: mixture of lignocaine and prilocaine for application to skin for venepuncture in children

8
Q

What is a risk of surface anaestheia

A

Risk of systemic toxicity when high concentrations and large areas are involved

9
Q

Describe infiltration anaesthesia and it’s use

A

Direct injection into tissues to reach nerve branches and terminals

Used in minor surgery: suitable for small ares only otherwise serious risk of systemic toxicity

10
Q

Describe intravenous regional anaesthesia

A

LA injected distal to a pressure cuff to arrest blood flow –> remains effective until circulation restored

e.g., lidocaine in Bier’s block for limb surgery

11
Q

What are the risks of IV regional anaesthesia

A

Systemic toxicity if cuff released prematurely but risk is small if cuff remains inflated for at least 20mins

12
Q

Describe nerve block anaesthesia and uses

A

LA is injected close to nerve trunks (e.g., brachial plexus, intercostal nerves, dental nerves) to produce a loss of sensation peripherally

Used for surgery, dentistry, analgesia
May be slower onset

13
Q

Describe spinal anaesthesia and uses

A

LA is injected into the subarachnoid or intrathecal space containing CSF to act on spinal roots and spinal cord.

Used in surgery to abdomen, pelvis, leg
Post-operative pain relief: addition of opioids provides prolonged postoperative analgesia, but risk of late respiratory depression

e.g., lidocaine

14
Q

Why is spinal anaesthesia sometimes combined with glucose

A

Hyperbaricity so spread of LA can be controlled by tilting patient

14
Q

Describe epidural anaesthesia

A

LA injected into epidural space blocking spinal roots

Used for abdominal/pelvic/leg surgery
Used as postoperative pain relief
Used for painless childbirth

e.g., lidocaine

14
Q

Risks and adverse effects of spinal anaesthesia

A

Autonomic sympathetic block: bradycardia, hypotension, post-operative urinary retention
- esp. if block is above T10

Phrenic nerve/respiratory centre effects: respiratory depression

Dural puncture headache

NB. epidural anaesthesia has similar risks but less probably due to reduced longitudinal spread of LA

15
Q

Examples of nerve block anaesthaesia

A

Interscalene block for shoulder surgery
Axillary brachial plexus for upper limb surgery
Femoral and sciatic nerve blocks for lower limb surgery
Transversus abdominis plane block for abdominal surgery

16
Q

Explain TAP local anaesthesia

A

Transversus abdominis plane block (nerve block LA)

T6-L1 segmental nerves enter Triangle of petit just medial to anterior axillary line

Injection of LA into fascial plane b/w internal oblique and transversus abdominis muscles allows a block of all these nerves, and excellent anaesthesia of anterior abdominal wall

17
Q

Describe a Bier’s Block

A

Form of IV regional anaesthesia

Excellent anaesthesia for short surgery esp. for the upper limb (e.g. carpal tunnel release)

Exsanguination using Esmarch bandage → inflation of proximal cuff of double tourniquet is followed by IV injection of prilocaine into vein on back of hand that is being operated on → after 5–10mins, distal cuff of tourniquet is inflated and proximal one deflated

Even if surgery is finished, tourniquet should be left inflated until LA has bound to tissues (20 minutes) so that release of local anaesthetic into systemic circulation does not occur
- Lignocaine can be used with caution (consider safe dose and time of tourniquet inflation), but bupivacaine should never be used for Bier’s block

18
Q

What are the pros and cons of using epidural anaesthesia vs spinal and GA

A

Slower in onset than spinal but this allows better control of hypotension

Advantage of prolonged analgesia by multiple dosing or continuous infusion through a catheter placed in the epidural space

Early mobilisation and reduced respiratory complications compared to GA

Technically more difficult than spinal anaesthesia
- higher failure rate
- risk of nerve damage and spinal injuries
- accidental spinal injection of large volume of LAs - infection
- epidural haematoma

19
Q

What method of local anaesthesia is frequently used for PCA

A

Patient controlled analgesia

Epidural:
Continuous infusion with a patient-controlled bolus of weak local anaesthetic combined with opioids (e.g., fentanyl) is routinely used for postoperative analgesia.

20
Q

Side effects of local anaesthesia

A

Complications uncommon

Local infection
Haematoma

Systemic toxicity 2˚ to OD or injection directly into BV (dose dependent)

Allergy
- acute: anaphylaxis (rare)
- delayed: pruritic rash with blisters at site within 72hrs of admin

Vasovagal syncope

Prilocaine OD → methaemoglobinaemia

Bupivacaine OD → treatment-resistant ventricular arrhythmia and cardiac arrest

21
Q

What are the features of systemic toxicity 2˚ to local anaesthetic

A

CNS: tinnitus, metallic taste, perioral paraesthesia, seizures, CNS depression/depressed consciousness (somnolence, coma)

CVS (esp. bupivacaine): bradycardia, decreased cardiac contractility, AV block, ventricular arrhythmis (esp. cocaine), HTN/hypotension, cardiac arrest, cardiogenic shock

Haematological: methemoglobinemia (LAs esp. benzocaine may oxidate Hb) → cyanosis, gray skin, fatigue

22
Q

How does inflammation/infected tissue affect local anaesthetic?

A

Decreasesefficacyof LAs

Inflamed tissue has an acidic environment
LAs are composed of alipophilic and hydrophilic group → permeability depends on which group is predominant

Alkalineanaestheticsare chargedand hydrophilicgrouppredominates →↓ abilityto penetrate nerve cellmembranes →↓efficacy

23
Q

Indications for peri-operative prophylactic antibiotics

A

Significant risk of postoperative infection (e.g., colonic resection)

Postoperative infection would have serious consequences (e.g., infection associated with prosthetic implant), even when such infection is uncommon

24
Q

Peri-operative prophylactic ABx for gastric/oesophageal/duodenal surgery

A

IV cefazolin 2g administered ~ 60mins or less before incision

25
Q

Peri-operative prophylactic ABx for SBO or appendectomy surgery

A

IV cefazolin 2g administered ~ 60mins or less before incision

IV metronidazole 500mg ~ 2hours or less before incision

- + IV metronidazole and gentamicin 2 mg/kg intravenously over 3 to 5 minutes, within the 120 minutes before colorectal surgery - Gentamicin is recommended for the few procedures requiring a broader spectrum of Gram-negative activity and is also used as an alternative when cefazolin is contraindicated.
26
Q

Peri-operative prophylactic ABx for colorectal surgery

A

IV cefazolin 2g administered ~ 60mins or less before incision

IV metronidazole 500mg ~ 2hours or less before incision

IV gentamicin 2 mg/kg over 3 to 5 minutes ~ 2hours or less before incision

27
Q

Discuss principles of antimicrobial stewardship

A
28
Q

Tetanus prophylaxis

A

Standard: DTP vaccination

After injury: wound cleaning and debridement, DTP vaccination +/- IVIg

29
Q

Antibiotic prophylaxis for traumatic wounds

A

Prophylaxis for wounds requiring surgical management
- IV cefazolin 2g +/- IV metronidazole 500mg if heavily contaminated severe injury

Prophylaxis for wounds that are significantly contaminated (e.g., penetrating injuries through footwear, stab wounds)
- oral dicloxacillin or flucloxacillin 500mg

Bites and open # should also receive prophylaxis

30
Q

What pathogens are most likely to contaminate traumatic wounds

A

S. aureus, S. pyogenes (GAS)

Anaerobic infection (c. perfringens) rare but may follow severe injuries if wound heavily contaminated

Broader range of pathogens in wounds that have been immersed in water

31
Q

When is tetanus vaccine and IVIg indicated after a traumatic wound

A

Pt has received 3+ doses of tetanus toxoid vaccine and last dose was < 5 years ago: vaccination is not indicated

Pt has received 3+ doses of tetanus toxoid vaccine and last dose was 5-10 years ago:
- Clean minor wound: tetanus toxoid vaccination is not indicated
- All other wounds: tetanus toxoid vaccination

Pt has received 3+ doses of tetanus toxoid vaccine and last dose was >10 years ago: tetanus toxoid vaccination

Pt has received < 3 doses of tetanus toxoid vaccine or vaccination Hx unknown:
- Clean minor wounds: tetanus toxoid vaccination
- All other wounds: tetanus toxoid vaccination + tetanus IVIg

32
Q

Use of unfractionated heparin

A

Used in renal failure patients/situations with high risk of bleeding such that anticoagulation may need to quickly be reversed

33
Q

MOA of unfractionated heparin

A

Heparin activates antithrombin III which inhibits thrombin, factor Xa, and other serine proteases by binding to the active site

34
Q

MOA of LMWH

A

Increase action of antithrombin III on factor Xa but not its action on thrombin

  • to inhibit thrombin heparin must bind to thrombin and antithrombin III
  • to inhibit factor Xa heparin must only bind to antithrombin III
  • LMWH molecules are too small to bind to both enzyme and inhibitor so cannot inhibit thrombin
35
Q

Direct oral anticoagulants examples and MOA

A

Dabigatran: Direct thrombin and IIa inhibitor
Rivaroxaban/apixaban: Direct factor Xa inhibitors

36
Q

What are the benefits of DOACs compared to warfarin

A

Reduced bleeding risk
Does not require frequent INR checks and dose titrations
Stable dosing and wider therapeutic index/safety margin

37
Q

Warfarin MOA

A

Vitamin K antagonist –> inhibits hepatic synthesis of vitamin-K dependent clotting factors (II, VII, IX, X)

38
Q

Warfarin drawbacks

A

Requires frequent INR testing and dose individualisation

Easily affected by diet and medications

Low margin of safety

Takes several days for anticoagulant effect and has initial procoagulant effect (start with parenteral anticoagulant to bridge)

39
Q

Advantage of LMWH over UFH

A

Longer elimination half-life than unfractionated heparin independent of dose (first-order kinetics) →effects more predictable and dosing less frequent (once or twice a day)

Monitoring not required routinely (due to predictability)

NB. UFH prolongs APTT but LMWH does not
- target APTT for UFH is 1.5-2.5x ULN

40
Q

Why is LMWH contraindicated in renal failure pts

A

Is mainly renally excreted

41
Q

Why is warfarin contraindicated in pregnancy

A

Crosses placenta

Teratogenic in first trimester
Risk of neonatal ICH during delivery

42
Q

Can warfarin be given to breastfeeding pts

A

Appears in milk but newborns are vitamin K deficiency and routinely prescribed vit K to prevent haemorrhagic disease so warfarin Tx of mother does not generally pose risk to breastfed infant

43
Q

SEs of heparin

A
  • Haemorrhage
  • Thrombosis (associated with heparin-induced thrombocytopenia (HIT))
  • Osteoporosis & spontaneous fracture with long-term (6 months+) Tx
  • Hypoaldosteronism (with consequent hyperkalaemia) is uncommon but increases with prolonged treatment (check plasma K+ concentration if Tx continued for >7 days)
  • Hypersensitivity reactions are rare with heparin but more common with protamine sulfate
44
Q

How should heparin induced haemorrhage be Tx

A

Stop therapy
If necessary give IV protamine sulfate (heparin antagonist that forms an inactive complex with heparin)

45
Q

Describe Heparin Induced Thrombocytopaenia

A

A transitory early decrease in platelet numbers is not uncommon after initiating heparin Tx → not clinically important

More serious thrombocytopenia ~ 2–14 days after start of therapy (uncommon; type II HIT): IgM or IgG antibodies against complexes of heparin and platelet factor 4 attached to surface of endothelial cells (platelet-derived chemokine)
→ CICs bind to circulating platelets, and cause thrombocytopenia
→ Immune injury of the vessel wall, thrombosis and DIC

LMWHs are less likely than unfractionated heparin to cause thrombocytopenia and thrombosis by this mechanism

46
Q

SEs of warfarin

A

Haemorrhage (esp. into bowel or brain)

Teratogenic → disordered bone development (binding to vitamin K-dependent protein osteocalcin)

Hepatotoxicity occurs but is uncommon

Necrosis of soft tissues (e.g., breast, buttock) due to thrombosis in venules = rare but serious: occurs shortly after starting Tx and is attributed to inhibition of biosynthesis of protein C → procoagulant state soon after starting treatment (prevent by starting with LMWH concurrently)

47
Q

Tx of warfarin induced haemorrhage

A

Withhold warfarin
Life-threatening bleeding: administer vitamin K, FFP or prothrombin concentrates

48
Q

Clinically important warfarin interactions

A

Factors that potentiate warfarin → increased risk of haemorrhage
- Liver disease interferes with synthesis of clotting factors
- High metabolic rate (fever and thyrotoxicosis) → increased degradation of clotting factors
- Agents that inhibit hepatic drug metabolism e.g., co-trimoxazole, ciprofloxacin, metronidazole, amiodarone, many antifungal azoles
- Drugs that inhibit platelet function e.g., aspirin, NSAIDs, some antibiotics e.g., moxalactam and carbenicillin

Factors that lessen effect of warfarin
- Conditions (e.g., pregnancy) → increased coagulation factor synthesis
- Hypothyroidism → reduced degradation of coagulation factors
- Vitamin K = component of some parenteral feeds and vitamin preparations
- Drugs that induce hepatic P450 enzymes (e.g., rifampicin, carbamazepine) → increases rate of degradation of warfarin
- Drugs that reduce absorption e.g., colestyramine binds warfarin in gut

49
Q

MOA of PPIs

A

IrreversibleinhibitionofH+/K+-ATPase (proton pump) inparietalcells (last stage in gastric acid secretion = H+ secretion into gastric lumen via pump)→reduced basal and stimulated gastric acid secretion → increasedstomachpH

  • Given in inactive form → activated and takes effect in an acidic environment (e.g., the canaliculi of apical parietal cells)
  • The lower thepHlevel is, the higher the enrichment of PPIs inthe parietal cells
  • The highest levels ofH+/K+-ATPase enzyme activity are reached in parietal cell after period of prolongedfasting → PPIs before first meal of day achieves highestefficacy

E.g., omeprazole, esomeprazole

50
Q

SEs of PPIs

A
  • Nausea, diarrhoea, abdominal pain, flatulence
  • Increased risk of clostridium difficile diarrhoea esp. in pts who are immunosuppressed or have been receiving antibiotics
  • Reactive hypergastrinemia → increased incidence of carcinoid tumours
  • Reduced iron, vitamin B12, calcium, and magnesium absorption
  • →increased osteoporosis risk in long-term use → increased risk of fractures in elderly
  • Use of these drugs may ‘mask’ the symptoms of gastric cancer
51
Q

PPI mitigation policy

A
52
Q

Describe mild acute pain

A

Low pain score and minimal difficulty carrying out activities despite pain e.g., superficial wound, mind sprain, sinus headache

53
Q

Describe moderate acute pain

A

Some difficulty carrying out activities e.g., uncomplicated appendicitis, laparoscopic/minimally invasive surgery, minor fracture

54
Q

Describe severe acute pain

A

High pain score and considerable difficulty carrying out activities e.g., major burns, renal colic, long bone fracture, total joint replacement

55
Q

What is acute pain

A

Acute pain usually occurs due to an acute illness (eg appendicitis), or following surgery or trauma. It lasts less than 3 months, and there is an expectation of recovery and return to usual function.

56
Q

Using the analgesic ladder explain the Mx of mild pain

A

Foundation: Non-pharmacological strategies
If needed: Add paracetamol and/or an NSAID

Use adjuvants e.g., antiemetics, anticonvulsants etc. depending on patient needs

In certain situations consider local anaesthetic e.g., EMLA for venepuncture in children

57
Q

Using the analgesic ladder explain the Mx of moderate pain

A

Foundation: Non-pharmacological strategies, paracetamol and/or an NSAID
If needed: Low dose/weak opioid e.g., tramadol/tapentadol/codeine

Use adjuvants e.g., antiemetics for nausea, anticonvulsants/gabapentin/TCAs for neuropathic pain

In certain situations consider inhaled analgesics e.g., for prompt time limited analgesia (trauma) or before opioid analgesia can be established

58
Q

Using the analgesic ladder explain the Mx of severe pain

A

Foundation: Non-pharmacological strategies, paracetamol and/or an NSAID, weak opioid, strong opioid (e.g., morphine/fentanyl)

Use adjuvants e.g., antiemetics, anticonvulsants etc. depending on patient needs, gabapentinoids for neuropathic pain.

59
Q

Paracetamol MOA

A

Reversiblyinhibitscycloxygenase mainly in CNS → reduced prostaglandin-mediated pain and pyrexia (not anti-inflammatory)

60
Q

NSAID MOA

A

Reversible inhibition of COX-1 and COX-2 enzymes→decreasedprostaglandin synthesis and prostaglandin-mediated pain (antiinflammatory, antipyrexial, anti-platelet)

(Aspirin irreversibly inhibits)

61
Q

Opioid MOA

A

Bind to opioid receptors to reduce synaptic neurotransmisison:

Presynaptic inhibition: closing of presynaptic Ca2+ channels → hyperpolarisation→ ↓ docking of vesicles and ↓NT release
Postsynaptic inhibition: opening of postsynaptic K+ channels → hyperpolarisation

  • μ1 → supraspinal analgesia, bradycardia, sedation
  • μ2 → respiratory depression, euphoria, physical dependence
  • δ → spinal analgesia, respiratory depression,
  • κ → spinal analgesia, respiratory depression, sedation
62
Q

How does a paracetamol OD occur and what is the consequence

A

Paracetamol normally metabolised to non-toxic products but exhaustion of metabolic pathways in liver with high dose results inincreased formation of toxic metabolite NAPQI

Glutathione usually inactivates NAPQI but its reserves are eventually depleted → irreversible oxidativehepatocyte injury

Hepatotoxicity/drug-induced hepatitis
Minimum toxic dose = 7.5 g/dayin adults

63
Q

Clinical features of paracetamol OD

A

Asymptomatic in the first24 hoursafter ingestion → progressive liver impairment

Nonspecific symptoms: nausea, vomiting,pallor, lethargy

Liver specific: RUQ pain, hepatomegaly, liver tenderness, abnormal LFT → acute liver failure/recovery

64
Q

Mx of paracetamol OD

A

Measure levels 4hrs after ingestion
Administer activated charcoal if < 4hrs after
Antidote = N-acetylcysteine (NAC) replenishes glutathione stores in liver

65
Q

NSAID complications

A

Peptic ulcer → risk of GI bleeding and perforation(COX inhibition disrupts production of protective gastricmucosal prostaglandins)
- Prophylactic PPIs if longterm NSAIDs needed

Increased risk of MI and stroke (except aspirin and naproxen)

Renal function impairment:Prostaglandins normally maintainRBF by inducingafferent arteriole vasodilation → NSAIDS inhibitprostaglandin production → harmful hypoperfusion of kidneys and reduced GFR → electrolyte and fluid abnormalities (hyperkalaemia, hyponatraemia, oedema), worsening HTN)
- ARF (rare) → tubulointerstitial nephritisandpapillarynecrosis

Aplastic anaemia

Pseudoallergic reaction: urticaria, angio-oedema, asthma

66
Q

Opioid SEs

A

Confusion, delirium, agitation
Dependence

Respiratory depression
Sedation

Nausea
Vomiting
Constipation
Urinary retention

Itching
Xerostomia

Hyperprolactinaemia

67
Q

Contraindications of opioids

A

Absolute contraindications: lung disease (acute/severe bronchial asthma, COPD), alcohol or sedative intoxication, paralytic ileus, IBD, suicidality, concomitant substance use that could lead tolife-threateningdrug interactions (e.g., heroin), hypersensitivity

Relative contraindications: pregnancy and breastfeeding (can lead to resp depression andwithdrawal Sx in newborns but short-termusually safe), renal failure, liver failure, concurrent SSRI use (increased risk of serotonin syndromewhen combined with opioids that also inhibit5HTreuptake) acute pancreatitis, biliary tract impairment (use with caution)

68
Q

Non-pharmacological pain Mx

A
  • Calm atmosphere
  • Distraction  TV, games, talking, music, reading
  • Relaxation techniques  deep breathing
  • Humour
  • Counting
  • Heat or cold packs
  • Warm soak
  • Heat or cold cream rubs or vibration devices