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SURGERY > Surgical scenarios + Wrap up > Flashcards

Surgical scenarios + Wrap up Flashcards

1
Q

Describe the different fluid compartments

A

INTRAcellular ~60% High K+ and Mg2+

EXTRAcellular ~40% High Na+ and Cl- 
Plasma 
Interstitial (includes lymph) 
Dense connective tissue and bone 
Transcellular (fluid involved in transport)
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2
Q

How long does VTE prophylaxis continue?

A

Until resolution of acute medical illness or hospital discharge

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3
Q

How long should VTE pharmacological prophylactic treatment continue after total knee replacement?

A

14 days

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4
Q

How long should VTE pharmacological prophylaxis continue following total hip replacement?

A

35 days

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5
Q

What IV fluids are used for fluid resuscitation?

A

0.9% saline (or ‘normal saline’) and colloid

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6
Q

What are some patient risk factors for VTE?

A

Age, obesity, long travel/immobility, previous DVT/PE, varicose veins, pregnancy, thrombophilia, deficiency of antithrombin, protein C/S Estrogen therapy (OCP, HRT)

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7
Q

What are the 5 steps for VTE risk assessment?

A
  1. Assess pt baseline risk of VTE
  2. Assess pt additional risk of VTE (e.g. surgical procedure, trauma, etc.)
  3. Assess pt risk of bleeding or contraindications to VTE prophylaxis
  4. Formulate overall risk assessment (risk vs. benefits)
  5. Select appropriate method of prophylaxis based on risk assessment and consultation with pt
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8
Q

What are the benefits and disadvantages of intermittent pneumatic compression?

A

Prevent venous stasis and promote fibrinolysis

Poor patient compliance, discomfort, risk of skin erosion

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9
Q

What are the different types of IV fluids?

A

5% glucose (dextrose) +/- KCl

  • Isotonic
  • Used for maintenance hydration
  1. 9% saline (normal saline)
    - Similar Na content to plasma
    - Used for initial fluid resusc, replacement fluids, and maintenance hydration

Colloids

  • High osmotic content
  • Fluid resusc but NOT hydration

Hypertonic glucose

  • Treat hypoglycaemia
  • Irritant

Hartmann’s solution

  • Isotonic
  • Post-op
  • Replacement of deficit (esp upper GIT losses)
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10
Q

What are the mechanical options for VTE prophylaxis?

A

Graduated compression stockings, intermittent pneumatic compression, venous foot pumps

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11
Q

What are the pharmacological options for VTE prophylaxis?

A 
Subcut LMWH 
UV unfractionated heparin 
NOACs
Oral aspirin (prevents platelet aggregation) 
Oral warfarin (Vit K antagonist)
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12
Q

What are the symptoms of under-filled and over-filled fluid patient?

A

UNDER - Tachycardia, dry mucus membranes, decreased urine output, postural BP drop, decreased skin turgor and sunken eyes, cool peripheries

OVER - Tachypnoea, bibasal creps, pulmonary oedema on CXR, oedema (peripherally and centrally if severe)

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13
Q

What are the two different receptors controlling fluid balance?

A

Osmoreceptors

  • In hypothalamus
  • Sense increased [Na+] or increased ECF osmolarity –> increase ADH synthesis

Baroreceptors

  • less sensitive but more potent than osmoreceptors (response to hypovolaemia more potent than to hyperosmolarity)
  • Low pressure (in RA and great veins)
  • High pressure (in aortic arch and carotid sinus)
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14
Q

What disease or surgical procedures put patients at increased risk of VTE?

A

Cancer, trauma or surgery (especially of hip, lower leg), heart failure, recent MI, IBD, infection, nephrotic syndrome

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15
Q

What is Virchow’s triad?

A
  1. Hypercoagulability
  2. Endothelial damage
  3. Haemostasis/immobility
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16
Q

What is the function of the OVLT and SFO?

A

Vascular organ of lamina terminalis and subfornical organ

Sense Ang II –> promote thirst and ADH release

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17
Q

What is the pharmacological prophylaxis treatment for VTE in high risk patients?

A

Enoxaparin 40mg daily (LMWH accelerates action of antithrombin –> increased inactivation of Factor V –> decreased thrombin formation)

OR Daltaparin 5000U daily

OR LDH 5000U twice or three times daily

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18
Q

Where is ADH produced and how does it function to increased fluid?

A

Produced in supraoptic and paraventricular nuclei Acts on V2 receptors in CD –> increases aquaporin 2 channels –> increase H2O reabsorption
Acts on V1, 2, 3 to promote vasoconstriction

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19
Q

What 4 issues need to be considered for consent to be valid?

A
  1. Capacity
  2. Freely given - no time constraints, pressures, duress
  3. Adequately informed of risks, benefits, alternative treatments, cost
  4. Specific to the procedure
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20
Q

Who else can give consent

A

Spouse
Care giver
Close relative
Friend

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21
Q

Describe the AMPLE history method

A 
Allergies
Medication
Past medical history
Last meal
Events leading
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22
Q

What are the different ways to reverse warfarin?

A
  • Pro-thrombinex (not a ‘blood product’, works in 15mins and lasts 2 days, doesn’t require ABO matching)
  • Fresh frozen plasma (‘blood product’, needs to be unfrozen, takes longer)
  • Vitamin K (takes 6hrs IV, 24hrs oral, lasts a long time)
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23
Q

What investigations need to be performed in someone with sepsis?

A

2 x blood cultures from 2 different sites
FBC, LFTs, EUCs, coags, glucose
Add culture from urine/sputum/wound/faeces
Add ECG, CXR, Abdo CT if necessary

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24
Q

What is the criteria for diagnosing SIRS? Sepsis? Severe sepsis? Septic shock?

A 
SIRS = 2 or more of the following:
1. Temp <36 or >38
2. HR >90
3. RR >20
4. WCC >12
Sepsis = SIRS + proveable infection
Severe sepsis = Sepsis + signs of end organ dysfunction and hypoperfusion
Septic shock = severe sepsis with hypotension not responding to fluid resusc
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25
Q

What are the important criteria when deciding which conditions to screen for?

A
  1. Disease or condition - must have significant burden of suffering, adequate disease prevalence and severity
  2. Screening test - must be simple to administer and interpret, be cost effective, tolerable
  3. Treatment - safe and effective, evidence that preventative intervention / treatment reduces morbidity or mortality and community accepts that cost of intervention is worthwhile
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26
Q

Draw the sensitivity / specificity table

A

cond pos| cond neg
Test +ive: true +ive| false +ive | PPV (true +ive/both row)
Test _ive: false -ive| true -ive | NPV (true -ive/both row)
Sensitivity| Specificity
Sensitivity (true +ive/both col)
Specificity (true -ive/both col)

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27
Q

What is the definition of a SSI?

A

Infection related to operative procedure that occurs at or near the surgical incision within 30 days of surgery, 90 days if prosthetics

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28
Q

What are some risk factors for SSI?

A

Patient-related: obesity, smoking, diabetes, immunosuppression, age, renal failure, malnutrion
Pre-operative: shaving skin, inadequate prophylactic antibiotics, inadequate skin prep
Intra-operative: surgical technique, length of procedure, inadequate oxygenation, wound classification
Bacteria virulence factors: size and site of surgery

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29
Q

What is the best way to skin prep before surgery?

A

Alcoholic chlorhexidine

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30
Q

What are the indications for prophylactic antibiotics in surgery?

A

If procedure carries HIGH risk of infection OR the occurrence of post-op infection carries serious consequences (e.g. prosthesis)

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31
Q

When is the best time to give surgical prophylactic antibiotics?

A

Within 60 minutes of beginning procedure, preferably within 30 minutes

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32
Q

How long does post-operative antibiotic prophylaxis continue?

A

Up to 24hrs only required in defined circumstances (e.g. lower limb amputation)

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33
Q

What are the first line and second line prophylactic antibiotic therapies for abdominal surgery?

A

First line: Cephazolin 2g and Metronidazole 500mg

Second line: Vancomycin and Gentamicin

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34
Q

When would you add gentamicin to your prophylactic antibiotic treatment?

A

When there is a risk for contamination with gram negative bacteria
OR when cephazolin is contraindicated

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35
Q

What are the complications of gentamicin use?

A

Nephrotoxicity - usually reversible
Ototoxicity
* Not predicted by dose

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36
Q

Why is cancer staging important?

A
  • Planning treatment – surgical and oncological
  • Prognosis
  • Systematic collection of data for research
  • Allows like with like comparison nationally and internationally
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37
Q

What is the difference between hyperplastic and adenomatous polyps?

A

Hyperplastic are benign tumours with no malignant potential
- Most polyps found on colonoscopy are of this kind
Adenomatous polyps are turmours with malignant potential

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38
Q

What are the three recognised types of adenomas with increased malignant potential?

A

Tubular adenoma
Tubulovillous adenoma
Villous adenoma
- Diagnosed on histology

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39
Q

Describe the epidemiology of CRC

A
  • Sporadic is most common 75%
  • Positive family history 10-30%
  • HNPCC / Lynch syndrome 2-3%
  • FAP <1% (both autosomal dom)
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40
Q

Describe the features of FAP

A

APC gene mutation (TSG)
- Disrupted Wnt signalling pathway –> no destruction of b-catenin –> stimulation of cell division
Hundreds of adenomatous polyps in colon and rectum
Develops at a young age, high risk of developing CRC
Supernumary teeth, epidermoid cysts

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41
Q

Describe the features of HNPCC / Lynch syndrome

A

Mutation in DNA MMR genes (MLH1, MSH2)
- Microsatellite instability
Less polyps but with greater malignant potential

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42
Q

What are the other primary malignancies associated with Lynch syndrome?

A

Endometrial cancer is most common

Cancer of small bowel, urogenital, ovary, stomach, hepatobilliary, skin

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43
Q

What is the Amsterdam criteria and how is it relevant in CRC?

A

Amsterdam criteria are a set of diagnostic criteria used by doctors to help identify families which are likely to have Lynch syndrome (must fulfil each criteria)

  1. 1 x family member dx with CRC <50
  2. 2 affected generations
  3. 3 x affected relatives, 1 of whom is 1st degree relative
  4. FAP excluded
  5. Tumours reported by pathological examination
  6. Tumours of endometrium, small bowel, ureter, renal pelvis
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44
Q

What are some of the procedures with HIGH risk of bleeding?

A 
TURP
Cholectomy
Vascular
CABG
AAA repair
Bilateral knee replacement
45
Q

What are some of the procedures with LOW risk of bleeding?

A 
Cholecystectomy
Abdo hysterectomy
GI endoscopy
Carpel tunnel
D&amp;C
Skin cancer excision
46
Q

Draw coagulation cascade - where does heparin work?

A

Draw
12, 11, 9, X, thrombin
Increases antithrombin

47
Q

What is the mechanism of action heparin?

A

Activates antithrombin III (natural inhibitor of coag cascade - prevents spontaneous coag)
- Neutralises 12, 11, 9, X, thrombin (last 2 especially)

48
Q

What is the mechanism of action of warfarin?

A

Inhibits hepatic production of of Vit K-dependent coagulation factors (2 (thrombin), 7, 9, 10)
- Also blocks protein C and S function (paradoxical pro-coagulant effect)

49
Q

How is UFH reversed?

A

Protamine sulphate from fish sperm

50
Q

What is the half life of heparin? Compare UFH and LMWH

A

30-150mins
UFH
- Usually administered as continuous IV infusion
- Very short half life - have to stop 6hrs before surgery
- Good for tight anticoag control
- Requires monitoring

LMWH (enoxaparin - clexane)

  • Subcut
  • Longer half life - have to stop 12hrs before surgery
  • No monitoring required
  • Significant renal excretion
51
Q

What is the mechanism of action of aspirin?

A

Anti-platelet agent
Irreversible inhibition of COX-1 –> blocks conversion of AA –> prevents formation of TXA2
- Prevents recruitment, activation and aggregation of platelets for lifespan of platelet (7-10 days)

52
Q

What is the half life of aspirin? How long does it take to achieve safe levels of normally functioning platelets?

A

Half life is 6hrs
Aspirin is non-reversible
Takes 7 days to achieve safe levels of normally functioning platelets

53
Q

What is the mechanism of action of clopidogrel?

A

Antiplatelet agent
Irreversibly inhibits P2Y ADP-receptor on platelet cell membrane –> prevents platelet activation and aggregation and eventual cross linking of fibrin
Half life ~1hr

54
Q

What is the half life of warfarin? How many days does it take to become therapeutic?

A

Half life ~36 hrs (1.5 days)

Takes 5 days to become therapeutic

55
Q

What are the conditions of warfarin therapy for surgery?

A

INR must be <1.5 on day of surgery
Cease warfarin 5 days before surgery to allow time for warfarin to be metabolised and new clotting factors to be synthesised

56
Q

What is the mechanism of action of dabigatran? When does it reach peak concentration?

A 
Direct thrombin inhibitor 
Pro-drug
Peak concentration in 2hrs
Excreted in bile and kidneys
Irreversible
57
Q

What is the mechanism of action of rivaroxaban? When does it reach peak concentration?

A

Direct Xa inhibitor
Peak concentration 4hrs
Excreted in bile and kidneys
Irreversible

58
Q

What is the mechanism of action of apixaban? When does it reach peak concentration?

A 
Direct Xa inhibitor
Half life 12hrs
- Needs to be stopped 2 days before surgery
Renal clearance
Irreversible
59
Q

Describe the CHA2DS2VAS score

A 
CCF (1)
HTN (1)
Age >75 (2)
Diabetes
Stroke/TIA (2)
Vascular disease (1) - CAD, MI, PAD, aortic plaque
Age >65 (1)
Sex female (1)
60
Q

List some causes of post-operative confusion

A

Pain
Full bladder
Hypoxia (PE, fat embolism lung collapse, oversedation)
Drug effect or withdrawl
Elderly - change in environment
Sepsis
Metabolic - BSLs, acidotic, dehydration, Na

61
Q

What are some causes of low urine output?

A

Pre-renal: hypovolaemia, sepsis, hypoperfusion due to RAS, pump failure (CCF, MI)
Intra-renal: ATN (ABx, hypotension)
Post-renal: blocked catheter, ureteric obstruction

62
Q

What are the maintenance fluid and electrolyte requirements for a 70kg male?

A

Basal fluid requirements (4:2:1) = 110ml/kg/hr water, average about 2.5L/day
Na+: 2 mmol/kg/day = 150mmolL/day
K+: 1mmol/kg/day = 70 mmol/day
Cl-: 1mmol/kg/day = 70 mmol/day

Daily needs can be met, for example, with 1L NS and 2L of 5% Dextrose with premixed 30mmol KCL at 120mls/hr

63
Q

What is the MINIMUM urine output per hour?

A

0.5mL/kg/hr

Aim for 40mL/hr

64
Q

What are the different kinds of wounds and give an example of each

A

Clean: uninfected operative wound, did not enter viscus, no inflammation, primary wound closure
e.g. hernia repair
Clean contaminated: controlled viscus entered, no inflammation, primary wound closure
e.g. elective cholecystectomy
Contaminated: fresh accidental wounds, break in sterile technique, gross spillage from viscus, inflammation apparent
e.g. emergency appendicectomy
Dirty: traumatic wounds, foreign bodies, inflammation and infection ++

65
Q

What is the class and coverage of amoxycillin?

A

Penicillin - beta-lactam
Mostly strep
Gram pos with some gram neg

66
Q

What is the class and coverage of ceftriaxone?

A

3rd generation cephalosporin

Strep, enterobacteria (E.coli, Klebsiella), haemophilus influenzae

67
Q

What is the class and coverage of gentamycin?

A 
Aminoglycoside
Gram negatives
Pseudomonas
ESC(A)PMM
Good for urosepsis
68
Q

What is the class and coverage of metronidazole?

A

Anaerobes

69
Q

What is the class and coverage of doxycycline?

A

Tetracycline
Staph, strep, some negs (broad spec)
- Also anti protozoal and worms

70
Q

What is the class and coverage of azithromycin?

A 
Macrolide
Staph, strep, Gram negs
Good for atypical pneumonia
Chlamydia and gonorrhoea
Pertussis!
71
Q

What is the class and coverage of cephazolin?

A

1st generation cephalosporin

Staph, strep, enterobacteria (E.coli, Klebsiella)

72
Q

What is the class and coverage of vancomycin?

A

Glycopeptide
Staph, strep
MRSA

73
Q

Give examples of gram pos and gram neg cocci and rods

A

Gram pos cocci - Staph (grapes), strep (chains)
Gram neg cocci - Meningococcal
Gram pos rods - Bacillus
Gram neg rods - Klebsiella, E.coli

74
Q

Give an example of a 1st, 2nd, 3rd and 4th generation cephalosporin

A

1st: cephalexin, cephazolin (IV)
2nd: cephuroxime
3rd: cetriaxone, cefetaxime
4th: cefepime

75
Q

What’s the difference between amoxicillin and ampicillin?

A

oral

IV

76
Q

What is the best antibiotic to cover strep?

A

Penicillin

- Rarely resistant

77
Q

What’s the most common cause of a sore throat? What is the best treatment?

A

Strep pyogenes

Penicillin

78
Q

What are the most common causes of otitis externa?

A

Pseudomonas and staph aureus

79
Q

What are the most common causes of otitis media?

A

Strep, h.influenza, moraxella

80
Q

What is Augementin? What does it cover?

A

Bactrim
Amoxycillin + beta lactamase inhibitor (clavulanate)
Gram pos, gram neg, some anaerobes

81
Q

When are carbapenems used?

A

When suspect multi-drug resistant bacteria

82
Q

Someone with infectious mononucleosis develops a rash after taking amoxycillin - are you concerned? Why not?

A

Unlikely to be allergy unless signs of anaphylaxis
Post-mononucleosis amoxil rash 85% of the time
Diffuse, maculopapular, erythematous rash

83
Q

What is the best treatment for candida albicans?

A

Fluconazole

84
Q

What is the best treatment for cellulitis? What if it starts to get worse?

A

Cephazolin IV
Worsening after cefazolin 2 days
- Give vancomycin (probably MRSA)

85
Q

What is the treatment for C.diff associated diarrhoea?

A

Metronidazole

86
Q

What is the therapeutic INR for a metallic heart valve?

A

2.5-3.5

87
Q

What is a co-analgesic you can use for neuropathic pain?

A

Pregabalin or gabapentin

- Anti-epileptics (inhibit Ca2+ channels on post-synaptic membrane)

88
Q

What are the features of steroid toxicity?

A

Gastric ulceration, psychosis in elderly, immunosuppression, osteoporosis

89
Q

Explain the drug metabolism of codeine and why it is ineffective for pain relief in some people

A

Codeine is a pro-drug converted to morphine at 1:4 conversion
○ 20-25% of caucasians don’t have the enzyme to convert it

90
Q

What is the conversion ratio of morphine to hydromorphine?

A

5: 1

i. e. Oral Morphine 5mg = Oral Hydromorphone 1mg

91
Q

When can you give activated charcoal?

A

Panadol overdose

Within 4 hours of intoxication

92
Q

How does N-acetyl cysteine aid in the treatment of panadol overdose?

A

Panadol in excess overwhelms the glucurodination and sulphation pathways –> creates toxic NAPQI
NAC add glutathione to NAPQI creating non-toxic conjugates

93
Q

How do you manage a panadol overdose?

A
  1. Check when ingestion was (if >8hours ago give NAC immediately anyway)
  2. Check blood paracetamol concentration
  3. Plot on normogram
  4. If above the line, start treatment with NAC
  5. Do LFT, INR/PT, EUC, lactate, ABG
94
Q

What is the treatment for digoxin overdose?

A

Digibind - very expensive
Also treat hyperkalaemia
- Insulin, glucose, bicarb, beta blockers (all draw K into the cell)

95
Q

What is the treatment for hyperkalaemia?

A
  1. Rapidly stabilise cardiac membrane: calcium gluconate
  2. Redistribute K back into cells: beta-blockers, bicarbonate, insulins
  3. Increase K excretion: Resin - binds to and draws potassium into gut to be excreted
96
Q

What drugs cause anticholinergic toxidrome?

A 
Results in too much SNS
	○ Anti-histamines
	○ Anti-psychotics
	○ Anti-depressants
	○ Anti-parkinsons
97
Q

What are the signs and symptoms of anticholinergic syndrome?

A

“Blind as a bat, mad as a hatter, red as a beet, hot as hades”
“Dry as a bone, bowel and bladder lose their tone, heart runs alone”
Dilated pupils, confused, flushed skin, tachycardic, hyperthermic, dry mouth and eyes, urinary retention and constipation

98
Q

What drugs cause a cholinergic syndrome?

A

Results in too much PSNS

- Organophosphates (pesticides)

99
Q

What are the signs and symptoms of cholinergic syndrome?

A 
Defecation
Urination
Miosis
Bronchospasm, bradycardia
Emesis
Lacrimation
Salivation, sweating
100
Q

What do you see with opiate overdose? What is the treatment?

A
  1. Coma
  2. Pinpoint pupils
  3. Respiratory depression
    - Naloxone is reversal agent
    - May require ventilation
101
Q

What is the difference between pharmacodynamics and pharmacokinetics?

A

Pharmacodynamic - drugs action on the body

Pharmakokinetic - body’s action on the drug

102
Q

Which drugs have a low therapeutic to toxic ratio?

A

Lithium
Gentamycin
Digoxin
Theophylline

103
Q

What are the signs/symptoms of local anaesthetic toxicity?

A

Arrythmias (HTN / tachycardia –> peripheral vasodilation –> profound hypotension and bradycardia)
Neurotoxicity (vertigo / twitching / seizures –> decreased LOC / apnoea)

104
Q

What are the common side effects of a steroid injection?

A

Pain at site of injection
Flare up of pain over next 24hrs
Can induce a hot flush, will subside

105
Q

What is your system for describing wounds?

A 
Site
Size
Shape
Edges, base
Smooth
Surrounding skin
Pain? Signs of infection
106
Q

What is the purpose of a FAST scan? What are the indications?

A

To identify free fluid (usually blood) in the peritoneum, percardium, pleural spaces, identifies pneumothorax
Indications: blunt / penetrating trauma, unexplained hypotension, trauma in pregnancy

107
Q

What are some contraindications for catheterisation?

A

ABSOLUTE = Known or suspected urethral injury

  • Blood at urethral meatus
  • Gross haematuria
  • Perineal haematoma

RELATIVE = urethral stricture, recent surgery, difficult patient

108
Q

What are the principles of intravenous fluid therapy?

A 
Correct deficits:
- Fluid deficit (mL) = wt (kg) x percent (%) dehydration x 10
e.g. 20kg = 20 x 5 x 10 = 1000mL
Maintenance:
4:2:1 rule x 10mL per kg 
Replace ongoing losses 
- ADD TO THE VOLUME GIVEN DAILY
- For upper GIT losses use 0.9% NS + 5% glucose + KCl 20mmol/1000mL
109
Q

How do you describe and examine a lump?

A

Site
Size
Shape, is it well circumscribed
Surface - appearance and colour
Consistency (firm (fluid filled or hard - cancer), soft)
Pulsatility
Compressable / reducible
Fluctuant (indicates a fluid- or fat-filled lump)
http://www.oxfordmedicaleducation.com/clinical-examinations/lump-bump-examination/

SURGERY (5 decks)

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