MRCS PART B 2014

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Contents
Coventry May 2014 .................................................... 5
CRITICAL CARE ........................................................................ 5
1. Pancreatitis................................................................... 5
2. Splenic Haematoma ..................................................... 5
PATHOLOGY .............................................................................. 6
3. Malignant melanoma on left arm .................................. 6
4. Testicular tumours with metastasis ............................... 7
5. Rhabdomyolysis .......................................................... 7
COMMUNICATION .................................................................... 8
6. Book ICU Bed ............................................................. 8
PROCEDURAL SKILLS ............................................................. 8
7. Sutures: choices of material .......................................... 8
8. Procedure: Giving LA .................................................. 9
ANATOMY ................................................................................... 9
9. Head & Neck ............................................................... 9
10. Lumbar spine model................................................... 11
11. Lower Limb ............................................................... 11
PHYSICAL EXMATIONATION .............................................. 11
12. CVS system ............................................................... 11
13. Cranial nerve.............................................................. 13
14. Knee exam ................................................................. 13
15. Lipoma ...................................................................... 13
HISTORY TAKING ................................................................... 13
16. Epigastric pain ........................................................... 13
17. PVD........................................................................... 13
Coventry May 2014 (2) ............................................. 13
PATHOLOGY ............................................................................ 13
1. FAP ........................................................................... 13
2. Tubercuosis................................................................ 13
ANATOMY ................................................................................. 13
3. Cervical spine ............................................................ 13
4. Thorax & Abdomen ................................................... 13
5. Lower Limb ............................................................... 13
CRITICAL CARE ...................................................................... 14
6. Epidural Anaesthesia.................................................. 14
7. Gastric Outlet Obstruction .......................................... 14
8. Ischaemic Colitis........................................................ 14
PHYSICAL EXAMINATION .................................................... 14
9. PVD........................................................................... 14
10. Stoma......................................................................... 14
11. LHC pain ................................................................... 14
12. Parotid lump .............................................................. 14
HISTORY .................................................................................... 14
13. Depression ................................................................. 14
14. Dysphagia .................................................................. 14
PROCEDURAL SKILLS ........................................................... 15
15. IV Cannulation........................................................... 15
16. Sutures ....................................................................... 15
COMMUNICATIONS ................................................................ 15
17. Transfer Patient .......................................................... 15
18. OGD consent ............................................................. 15
Kula Lumpur Feb 2014 ............................................ 15
ANATOMY ................................................................................. 15
1. Thorax & Neck .......................................................... 15
2. Base of Skull .............................................................. 17
3. Foot & Ankle ............................................................. 21
PATHOLOGY ............................................................................ 22
4. Melanoma .................................................................. 22
5. Neck lumps ................................................................ 23
CRITICAL CARE ...................................................................... 23
6. Burns management..................................................... 23
7. Opioid overdose ......................................................... 26
8. RTA........................................................................... 26
Liver laceration & Pneumothorax ........................................ 26
PROCEDURAL SKILLS ........................................................... 27
9. Closing wounds ......................................................... 27
10. OT Management ........................................................ 28
PHYSICAL EXAMINATION .................................................... 29
11. CVS exam.................................................................. 29
12. Knee exam ................................................................. 29
13. Cranial nerve exam .................................................... 29
14. Hernia exam ............................................................... 30
HISTORY TAKING.................................................................... 30
15. Abdominal pain .......................................................... 30
16. AMT .......................................................................... 30
COMMUNICATION .................................................................. 30
17. Book ICU bed ............................................................ 30
18. Talk to family regarding ascites .................................. 30
Kula Lumpur Feb 2014 (2) ...................................... 30
PROCEDURAL SKILL .............................................................. 30
1. T&S ........................................................................... 30
2. OT listing ................................................................... 30
ANATOMY.................................................................................. 30
3. Head & Neck .............................................................. 30
4. Middle Cranial Fossa .................................................. 31
5. Foot & Ankle ............................................................. 32
PATHOLOGY ............................................................................. 32
6. Melanoma .................................................................. 32
7. Enlarged lymph node .................................................. 33
CRITICAL CARE ....................................................................... 35
8. Burns.......................................................................... 35
9. Multiple trauma .......................................................... 35
10. Type 1 Respiratory Failure ......................................... 35
COMMUNICATIONS ................................................................ 35
11. Book ICU bed ............................................................ 35
12. Counselling angry patient ........................................... 35
HISTORY TAKING.................................................................... 35
13. AMT .......................................................................... 35
14. Gallstone disease ........................................................ 35
PHYSICAL EXAMINATION .................................................... 35
15. CVS exam .................................................................. 35
16. CNS exam .................................................................. 35
17. Indirect hernia ............................................................ 35
18. Knee exam ................................................................. 36
Kula Lumpur Feb 2014 (3) ...................................... 36
ANATOMY.................................................................................. 36
1. Thorax & Abdomen.................................................... 36
2. Lower Limb ............................................................... 36
3. Genitourinary Tract .................................................... 38
PATHOLOGY ............................................................................. 38
4. Rheumatic heart disease.............................................. 38
5. PUD and PTH ............................................................ 40
CRITICAL CARE ....................................................................... 41
6. Massive transfusion .................................................... 41
7. Obstructive jaundice ................................................... 41
8. Fluid overload ............................................................ 42
PROCEDURAL SKILLS ............................................................ 42
9. FNAC......................................................................... 42
10. Suturing...................................................................... 42
PHYSICAL EXAMINATION .................................................... 43
11. Respi exam (COPD) ................................................... 43
12. Arterial exam.............................................................. 43
13. Neuro exam (LL) ........................................................ 43
14. Scrotal exam ............................................................... 43
COMMUNICATIONS ................................................................ 43
15. Angry patient.............................................................. 43
16. Update trauma consultant ........................................... 43
HISTORY TAKING.................................................................... 43
17. SOB ........................................................................... 43
18. PR bleeding ................................................................ 43
Sheffield Feb 2014 .................................................... 44
PROCEDURAL SKILLS ............................................................ 44
1. FNAC......................................................................... 44
2. Surgical ties ................................................................ 44
PHYSICAL EXAMINATION .................................................... 44
3. Cranial Nerves ............................................................ 44
4. Parastomal hernia ....................................................... 44
5. Submandibular gland swelling .................................... 44
6. Abdominal exam ........................................................ 45
COMMUNICATIONS ................................................................ 45
7. Crying mother ............................................................ 45
8. Call for Transfer of Care ............................................. 45
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ANATOMY ................................................................................. 45
9. Lower Limb ............................................................... 45
10. H&N .......................................................................... 46
11. Thorax & Thyroid ...................................................... 46
CRITICAL CARE ...................................................................... 47
12. Respiratory failure...................................................... 47
13. Pneumoperitoneum .................................................... 47
14. Ruptured AAA ........................................................... 47
HISTORY TAKING ................................................................... 48
15. Thyroid swelling ........................................................ 48
16. Abdominal pain ......................................................... 48
PATHOLOGY ............................................................................ 48
17. Rheumatic heart disease ............................................. 48
18. PVD........................................................................... 48
Sheffield Feb 2014 (2) ............................................... 48
COMMUNICATIONS ................................................................ 48
1. OGD & Barium swallow ............................................ 48
2. Inform consultant about AOR .................................... 48
HISTORY TAKING ................................................................... 49
3. PR bleeding ............................................................... 49
4. Groin lump................................................................. 49
5. Knee Pain .................................................................. 49
PATHOLOGY ............................................................................ 49
6. Gallbladder cancer ..................................................... 49
7. Medullary thyroid CA ................................................ 50
CRITICAL CARE ...................................................................... 50
8. Fluid overload ............................................................ 50
9. Post-thyroidectomy hypocalcaemia ............................ 51
10. Ischaemic Bowel ........................................................ 52
PROCEDURAL SKILLS ........................................................... 52
11. IDC insertion ............................................................. 52
PHYSICAL EXAMINATION .................................................... 52
12. Submandibular gland ................................................. 52
13. Abdominal exam (Appendicitis)................................. 53
14. CVS exam.................................................................. 53
15. Thyroid exam ............................................................. 53
ANATOMY ................................................................................. 53
16. Hand .......................................................................... 53
17. H&N .......................................................................... 54
18. Shoulder & Hip .......................................................... 56
TEST ............................................................................................ 57
19. Trauma activation ...................................................... 57
Glasgow May 2014 .................................................... 57
CRITICAL CARE ...................................................................... 57
1. Acute Pancreatitis ...................................................... 57
2. Pre-Op Aortic Stenosis ............................................... 59
PHYSICAL EXAMINATION .................................................... 59
3. Lipoma ...................................................................... 59
4. Submandibular gland ................................................. 59
5. PVD........................................................................... 59
6. Pulmonary Embolism................................................. 59
PROCEDURAL SKILLS ........................................................... 60
7. OT Listing ................................................................. 60
8. Turkey Leg ................................................................ 60
PATHOLOGY ............................................................................ 60
9. Ulcerative Colitis ....................................................... 60
10. Gallbladder Cancer .................................................... 61
11. Enterocutaneous fistula .............................................. 62
HISTORY TAKING ................................................................... 62
12. Thyroid Goitre ........................................................... 62
13. Pre-op Confusion ....................................................... 63
ANATOMY ................................................................................. 64
14. Trunk & Thorax ......................................................... 64
15. Parotid Gland ............................................................. 65
16. Shoulder..................................................................... 66
COMMUNICATIONS ................................................................ 66
17. CTVS transfer ............................................................ 66
18. Angry patient ............................................................. 67
Glasgow May 2014 (2) .............................................. 67
HISTORY .................................................................................... 67
1. Progressive dysphagia ................................................ 67
2. Post-op Depression .................................................... 67
COMMUNICATION .................................................................. 67
3. OGD Counselling ....................................................... 67
4. Transfer (Post-op Complication) ................................. 67
PROCEDURAL SKILLS ............................................................ 68
5. IV Cannulation ........................................................... 68
6. Sutures ....................................................................... 68
PHYSICAL EXAMINATION .................................................... 68
7. Inguinal Hernia ........................................................... 68
8. PVD ........................................................................... 68
9. Goitre ......................................................................... 68
10. Post-op Abdominal Pain ............................................. 68
PATHOLOGY ............................................................................. 68
11. Tuberculosis ............................................................... 68
12. Pathological Fracture .................................................. 69
ANATOMY.................................................................................. 69
13. Thorax & Abdomen.................................................... 69
14. Lower Limb ............................................................... 70
15. Cervical Spine ............................................................ 70
CRITICAL CARE ....................................................................... 71
16. Acid base & Electrolytes ............................................ 71
17. Epidural...................................................................... 71
18. Perforated Viscus ....................................................... 72
Edinburgh 2014 ........................................................ 72
CRITICAL CARE ....................................................................... 72
1. Variceal bleeding ........................................................ 72
2. Pneumothorax ............................................................ 73
3. Pain Management ....................................................... 74
PATHOLOGY ............................................................................. 74
4. PUD ........................................................................... 74
5. Gallbladder cancer ...................................................... 75
PROCEDURAL SKILL .............................................................. 75
6. IDC insertion .............................................................. 75
7. Chest Tube Insertion ................................................... 75
ANATOMY.................................................................................. 75
8. Thorax & Upper limb ................................................. 75
9. Skull & Lateral Spine X-ray ....................................... 75
10. Ankle ......................................................................... 76
PHYSICAL EXAMINATION .................................................... 76
11. CVS ........................................................................... 76
12. PVD ........................................................................... 76
13. RHC Pain ................................................................... 76
14. Bilateral hemianopia ................................................... 77
COMMUNICATIONS ................................................................ 77
15. Call trauma consultant ................................................ 77
16. Angry patient.............................................................. 77
HISTORY TAKING.................................................................... 77
17. LBP ............................................................................ 77
18. Diarrhoea.................................................................... 77
Singapore Aug 2014.................................................. 77
HISTORY TAKING.................................................................... 77
1. Altered Mental State ................................................... 77
2. PR Bleeding ............................................................... 77
PROCEDURAL SKILLS ............................................................ 77
3. OT listing ................................................................... 77
4. Excision of lump ........................................................ 78
PHYSICAL EXAMINATION .................................................... 78
5. Cranial nerves............................................................. 78
6. Inguinal hernia............................................................ 78
7. CVS ........................................................................... 79
8. OA knee ..................................................................... 79
COMMUNICATIONS ................................................................ 79
9. Update Consultant ...................................................... 79
10. Patient AOR ............................................................... 79
ANATOMY.................................................................................. 79
11. Shoulder ..................................................................... 79
12. Cervical spine ............................................................. 80
13. Abdominal aorta ......................................................... 80
PATHOLOGY ............................................................................. 81
14. Ulcerative colitis......................................................... 81
15. Rheumatic heart disease.............................................. 81
CRITICAL CARE ....................................................................... 81
16. Acute Pancreatits ........................................................ 81
17. Nutrition ..................................................................... 82
18. Epidural anaesthesia ................................................... 82
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Cairo Oct 2014 .......................................................... 83
ANATOMY ................................................................................. 83
1. Mandible.................................................................... 83
2. Thorax ....................................................................... 83
3. Femoral Triangle........................................................ 83
PATHOLOGY ............................................................................ 83
4. Infective Endocarditis ................................................ 83
5. Gangrene & Lung CA ................................................ 83
CRITICAL CARE ...................................................................... 84
6. Hypothermia .............................................................. 84
7. Acid Base .................................................................. 84
8. AF & Pneumoperitoneum .......................................... 84
PHYSICAL EXAMINATION ................................................... 84
9. Cranial nerves ............................................................ 84
10. Lipoma ....................................................................... 84
11. Submandibular Gland ................................................. 84
12. Inguinoscrotal hernia .................................................. 84
HISTORY .................................................................................... 84
13. Thyroid goitre............................................................. 84
14. IBS ............................................................................. 84
COMMUNICATIONS ................................................................ 84
15. Counselling for appendicectomy ................................. 84
16. Refer CTVS ............................................................... 85
PROCEDURAL SKILLS ............................................................ 85
17. Sutures ....................................................................... 85
18. FNAC......................................................................... 85
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Coventry May 2014
CRITICAL CARE
1. Pancreatitis
2. Splenic Haematoma
a. Preparatory station: Convincing a patient with splenic haematoma to stay at the hospital.
b. Giving information to a patient with splenic haematoma insisting to be discharged.
Splenic trauma can occur after: 1) blunt trauma or 2) penetrating injury, it can also be secondary to medical intervention i.e. iatrogenic.
Signs/Symptoms
- LUQ pain (stretching of the splenic capsule)
- Peritonitis
- Kehr’s sign – referred pain to the left shoulder worse with inspiration due to irritation of the phrenic nerve from blood adjacent to the left
hemidiaphragm

Associated injuries
- Left hemidiaphragm
- Left lobe of the liver
- Left kidney
- Left adrenal gland
- Pancreatic tail

Radiological investigation
Ultrasound e.g. FAST scan: determine the presence of free fluids
CT: imaging of choice
- Splenic parenchyma should be assessed in portal venous phase as the heterogeneous contrast-enhancement seen on arterial phase can mimic
splenic laceration/contusion
- Arterial phase scans can be useful in detecting vascular injuries such as pseudoaneurysm and AV fistula
- Grading (I-V): American Association for the Surgery of Trauma (AAST) splenic injury grading
 Grade I-III classified according to the extent of parenchymal injury and associated haematoma
 Grade Iv-V classified according to the parenchymal injury only

Management approach
Non-operative management:
- In minor injuries (grade I-III) and evidence hemodynamic stability
- Encompasses both observation and embolization
- Rationale is based upon the assumption that salvaging functional splenic tissue avoids the surgical and anaesthetic risks and complications a/w
laparotomy and abrogates the risk of early infectious complications, and postsplenectomy sepsis.
- Immune function depends on residual splenic tissue and is not grade specific
- Keep NBM, vitals monitoring, serial abdominal examination, Hb trend
- Duration of observation should be individualized based upon the grade of splenic injury, nature and severity of other injuries, and the patient's
clinical status. (rule of thumb: grade + 1 day)
- 86% who failed non-operative management did so ≤96hr, 61% of failures occurred in ≤24 hours

Operative management:
- Indications
 Hemodynamic instability/peritonitis
 Persistent coagulopathy/bleeding
 Intra-abdominal injury requiring surgery
 Confounding injuries that interferes with monitoring e.g. pelvic # with continuous bleeding
 Worsening pain
 ± severe splenic injury
- Options: splenorrhaphy, partial splenectomy, splenectomy
- Complications of splenectomy:
 General:
 General anaesthesia  Specific
 Bleeding  Injury to adj. organ: stomach, splenic flexure, diaphragm, pancreas (fistula)
 Chest infection  Subphrenic abscess
 Ileus  Thrombocytosis usual occurs in the 1st 48hrs  vascular thrombosis
 OPSS
 Development of splenunculi – splenic tissue shed during surgery undergoes
hypertrophy

Overwhelming post-splenectomy sepsis (OPSS)

- Rare but fatal infection following splenectomy due to encapsulated bacterium, which usually occurs within 2 years of surgery.
- Mechanism: loss of the ability for opsonisation mediated phagocytosis of encapsulated bacterium
- Prevented by administering vaccines 14 days PRIOR or 14 days following surgery
- Penicillin prophylaxis, duration of prophylaxis is debatable: 2 years vs. lifelong prophylaxis; infants are recommended to continue till
adulthood.

Follow Up
- Ultrasound at day 5 for non-operative management to document non-progression
- Repeat CT is not routinely required:

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  Eastern Association for the Surgery of Trauma (EAST) concluded that there are insufficient data to determine whether routine follow-up
imaging is necessary
 May be used to lift activity restriction, or for patients whose work requirements or lifestyles place them at higher risk for re-injury
- Restriction from high-risk activities for 3 months (not EBM)

PATHOLOGY
3. Malignant melanoma on left arm
a. Post-operative complications
b. Axillary vein thrombosis
Melanoma is a malignant neoplasm of epithelial melanocytes primarily arising in skin, it can also occur in the leptomeninges, eyes, GIT, oral and
genital mucous membranes.
Predisposing factors
Congenital/Non-modifiable
- Xeroderma pigmentosum (AR disorder of DNA repair deficient in the ability to repair damage caused by UV light)
- Filtz Patrick Skin Type 1
- Dysplastic naevus syndrome
- Family history (1st degree relative)

Acquired/Modifiable
- Sunlight exposure: intermittent high-energy exposure
- Immunosuppression

Tools to evaluate suspicious lesion: Glasgow 7 point checklist or ABCDE’s of melanoma

Glasgow 7 point checklist (high risk if >3 points)
Major (2 points) Minor (1 point)
Change in size/shape/colour Diameter >7mm
Inflammation
Oozing/bleeding
Itch/Altered sensation

ABCDE
Asymmetry
Border irregularity
Colour variation (especially if >3 colours)
Diameter over 6 mm
Evolving (any changes in colour, size, shape, surface or symptoms)

Types of Malignant Melanoma

Superficial spreading
Nodular
Lentigo maligna melanoma
Acral lentiginous melanoma (70% of these are in dark skin individuals)
Amelanocytic melanoma

Prognostic Factors:
Breslow thickness (currently replaced by AJCC depth )
Presence of ulceration
Stage (TMN)
LN involvement
Distant metastasis

Breslow thickness: measured from the stratum granulosum to the deepest part; one of the most important prognostic histological factors
(Stage I – ≤0.75mm, Stage II – 0.76 to 1.5mm, Stage III – 1.51 to 2.25mm, Stage IV – 2.26 to 3.0mm, Stage V – >3mm)

Clark’s level: describes the anatomical of myeloma invasion, low predictive values, used mainly in thin myeloma (<1mm)
Level I: confined to epidermis
Level II: invasion into papillary dermis
Level III: invasion to the junction of papillary dermis and reticular dermis
Level IV: invasion into reticular dermis
Level V: invasion into subcutaneous tissue

Management (gold standard les in the surgical excision with tumour negative margins followed by adjuvant chemo/interferon therapy)
Surgical excision
- Excision biopsy with 2mm margin for diagnosis and confirm Breslow thickness
 Melanoma in-situ: 0.5cm
 Thickness ≤2mm: 1cm
 Thickness ≥2mm: 2cm
- Wide excision with adequate margins based on Breslow thickness
- Consider Moh’s micrographic margin controlled surgery for excision of thin melanoma in area where tissue sparing is required e.g. face
- ± SLNB, consider if
 Thick melanomas
 Adverse features: ulceration, lymphovascular invasion, mitotic rate ≥ 1mm2

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Adjuvant: chemotherapy and biologics (IFN-α)
Palliation: RT

4. Testicular tumours with metastasis

a. Types of testicular cancer
b. Tumour markers
c. Histological report
Types of Testicular cancers
Primary Testicular Tumours
Germ Cell Tumours (90-95%)
- Seminanoma: originates in the germinal epithelium of the seminiferous tubules (refers to CLASSICAL seminoma)
- Non-seminoma (NSGCT):
 Embryonal carcinoma
 Teratoma: dermoid cyst, monodermal teratoma, teratoma with somatic type malignancy
 Yolk sac tumour – most common testis cancer in infants/children
 Choriocarcinoma (Trophoblastic tumours)
 Mixed germ cell tumour
Stromal tumours (Non-germ cell tumours: 5-10%): Arises from the stromal component of the ovary/testis
- Leydig cell tumour – most common non-germ cell tumour
- Sertoli cell tumour
- Granulosa cell tumour
Other: Gonadoblastoma – contains germ cells, immature sertoli cells or granulosa cells, and gonadal stromal cells.

Secondary Testicular Tumours: Lymphoma, leukaemia, metastatic

Age Most Common Testicular Cancer AFP Β-hCG Random Facts

0-10 Yolk Sac Tumour ± ± - Classical seminomas is
20-30 Choriocarcinoma (NSGCT) - ++  most common testicular tumour in adults
25-35 Embryonal (NSGCT) ± ±  most common tumour in undescended testis
Teratoma (NSGCT) - - - Malignant lymphoma
30-40 Classical seminoma - ±  Most commonly bilateral
>50 Malignant lymphoma NA NA  Most common metastatic tumour of the testis
 Most common testicular tumour in men > 50 y/o

Presentation
- Most commonly on the right (cryptorchidism R>L)
- Painless testicular mass/swelling
- Testicular pain (10%): usually due to infarct/haemorrhage
- Hydrocele (5-10%)
- Gynaecomastia in germ cell tumours (5%) and Sertoli/Leydig
tumours (30-50%)
- Back pain from retroperitoneal metastasis: non-seminoma >
seminoma
- Bilateral testicular cancer: lymphoma most likely cause
Investigations
- Blood investigations
 Tumour markers (AFP/β-hCG/LDH), LFT, FBC, UE
(retroperitoneal mets can obstruct ureter)
 N.B. the S category in TNM staging is the nadir value of
the post-orchidectomy tumour markers
- Radiological
 US Scrotum: intra-testicular lesion is highly suspicious
 CT AP: 30% false negative rate (i.e. up to 30% with normal CT
may have retroperitoneal LN)
 CXR ± CT Thorax

Management
Surveillance
- For Seminoma Stage 1 (recommended for men with prior XRT, IBD, kidney in radiation field e.g. horseshoe/ectopic)
 Protocol: PE + CXR + CT AP + tumour markers every 3-4 months for 1-3 years, then every 6 months for 4-7 years, then every 12 months
 Relapse rate 15-20%
- For NSGCT Stage 1: relapse rate 30%
 Protocol (more stringent)
 CXR + tumour marker every 1-2 months for 1st year, every 2 month for 2nd year, every months for 3rd year, every 4 month for 4th
year, every 6 month for 5th year, every 12 month thereafter
 CT AP every 2-3 month 1st year, every 3-4 month 2nd year, every 4 month 3rd year, every 6 month 4th year, every 12 months
thereafter
 Periodic PE

Curative
- Radical inguinal orchidectomy ± retroperitoneal lymph node dissection
- Chemotherapy/XRT/ RPLND
 For seminoma stage 1: surveillance vs. chemotherapy vs. XRT
 For NSGCT stage 1: surveillance vs. RPLND vs. chemotherapy

Adjuvant: XRT and chemo

Fertility and Sperm banking

5. Rhabdomyolysis
a. Patient with LL injury for 3-4 hours then brought to the hospital. Discuss

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COMMUNICATION
6. Book ICU Bed
b. Call ICU registrar to book a bed for an old lady going for laparotomy with renal impairment and
electrolyte disturbances
The ICU is the main place in the hospital for invasive ventilatiory support and the support of ≥2 failing organs (including respiratory system).
Criteria for admission
- Requiring or likely to require advance respiratory support
- Require ≥2 organ support
 Respiratory: ETT/CPAP
 Renal: haemodialysis
 Cardiac: continuous ECG monitoring and inotropic support
 Hepatic: blood transfusion
 Neurological: ICP monitoring
- Chronic impairment of ≥1 system restricting daily activities (≥ASA III) who require support for acute, reversible failure of another organ
system
- Require one-to-one nursing care

PROCEDURAL SKILLS
7. Sutures: choices of material
Types of Sutures
Absorbable vs. non-absorbable
Monofilament vs. braided
Natural vs. synthetic

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Commonly used suture size
Bowel 2/0 – 3/0
Fascia 1–0
Ligatures 0 – 3/0
Pedicles 2–0
Skin 2/0 – 5/0
Arteries 2/0 – 8/0
Microsurgery 9/0 – 10/0
Corneal surgery 9/0 – 10/0

Abdominal wall closure

Mass closure the preferred method

8. Procedure: Giving LA
MOA of LA
- Amines (lidocaine, bupivacaine, prilocaine) and esters (cocaine, procaine)
- Reversible inhibition of cell membrane Na+ channels, preventing the generation and propagation of action potential
- LA with greater lipid solubility have a more potent and longer duration of action
- LA penetrate the cell membrane in an uncharged form, hence in an acidic environment (e.g. infection) it becomes charged and is unable to exert
it’s effect
- NAHCO3- may be added to increase pH and increase efficacy (keeping it in an uncharged form)
- Adding adrenaline to LA
 Produces local vasoconstriction, decreases absorption of LA from the site of infiltration and increase duration
 Should not be used in tissues with end-arteries e.g. digits & penis

Drug Onset Maximum Dose Duration

(with Epinephrine) (with Epinephrine)
Lidocaine Rapid 4.5 mg/kg (7 mg/kg) 120 min (240 min)
Mepivacaine Rapid 5 mg/kg (7 mg/kg) 180 min (360 min)
Bupivacaine Slow 2.5 mg/kg (3 mg/kg) 4 hours (8 h)
Ropivacaine Medium 2-3 mg/kg 3 hours (6 h)
Levobupivacaine Medium 2.0 mg/kg or 400mg in 24 hrs 4-6 hours (8-12 h)
Procaine Slow 8 mg/kg (10 mg/kg) 45 min (90 min)
Chloroprocaine Rapid 10 mg/kg (15 mg/kg) 30 min (90 min)
Etidocaine Rapid 2.5 mg/kg (4 mg/kg) 4 hours (8 h)
Prilocaine Medium 5 mg/kg (7.5 mg/kg) 90 min (360 min)
Tetracaine Slow 1.5 mg/kg (2.5 mg/kg) 3 hours (10 h)

How much LA is in a 1% solution?

- 1ml of 1% solution contains 10mg of LA (i.e. 100% is 1kg)

Complications of LA
They are associated to membrane destabilisation, primarily affecting the neurological system and the CVS at higher doses.
- Neurological: perioral and glossitic paraesthesia, dizziness, drowsiness, seizures, tinnitus, tremors, coma
- Cardiovascular: bradycardia, hypotension, arrhythmia (VF/asytole)
- Hypersensitivity/Allergy

Management of LA Toxicity
- ACLS principles: ABC
- Seizure control with diazepam/midazolam (N.B. phenytoin is ineffective)
- ECG and cardiac monitoring KIV defibrillation
- Infusion of 20% lipid emulsion solution e.g. Intralipid
 Lipid soluble fraction of LA is sequestered in the lipid emulsion and removed from plasma
 Bolus 1.5 ml/kg then 0.25 ml/kg/min for 30-60min

ANATOMY
9. Head & Neck
a. Thyroid vessels, strap muscles, nerve supply
Thyroid anatomy
Butterfly shape gland with 2 lobes (left and right) connected via the isthmus. The isthmus overlies the 2nd and 3rd tracheal rings, the lateral lobes
overlies the thyroid cartilage to 6th tracheal ring. An inconstant pyramidal lobe projects from the isthmus, usually on the left site (remnant descent of
embryological descent of thyroid).

Envelopes by the pretracheal fascia, covered anteriorly by the strap muscles and laterally by the SCM.

Thyroid Blood supply Strap Muscles (infra-hyoid muscles)

Arterial supply Muscle Innervation
- Superior thyroid artery (branch of ECA) Sternohyoid Ansa cervicalis (C1-3)
- Inferior thyroid artery (branch of thyrocervical trunk, 1st part of subclavian) Sternothyroid Ansa cervicalis
- Thyroid ima artery (brachiocephalic trunk, present in 10%) Thyrohyoid C1 spinal nerve
Venous drainage Omohyoid Ansa cervicalis
9
- Superior and middle thyroid veins  IJV
- Inferior thyroid veins  brachiocephalic vein
N.B. the inferior thyroid artery lies posterior to the thyroid gland

Thyroid Innervation
Derived from the autonomic system:
- Sympathetic fibres from superior, middle and inferior ganglia
- Parasympathetic fibres from vagus nerve

Thyroid Embryology
- At 3-4 weeks of gestation, starts developing at the foramen caecum (junction of middle and posterior third of tongue)
- The gland then descends inferiorly passing anterior to the hyoid bone via the thyroglossal duct

Thyroidectomy
Layers approached during thyroidectomy
- Skin  subcutaneous fat  superficial cervical fascia  deep investing layer of cervical fascia  strap muscles  pertracheal fascia 
isthmus of thyroid gland
- Ligate and divide superior thyroid artery & vein medially
 Ext. branch of superior larygenal nerve runs with the superior thyroid artery before turning medially to supply the cricothyroid muscle
- Ligate and divide inferior thyroid artery inferiorly
 Inferior thyroid artery and the RLN has a variable relationship thyroid gland
 RLN lies deep to inferior thyroid artery (40%)
 RLN lies superficial to inferior thyroid artery (20%)
 RLN lies between branches of inferior thyroid artery (35%)
 Zuckerkandl's tubercle marks the posterolateral aspect of the thyroid lobe and is most often found lateral to RLN

10
10. Lumbar spine model
a. Foramina, contents
b. Anatomy of disc, disc herniation
c. MRI interpretation
Vertebrae Body Vertebral Transverse Process Spinous Process Others Movements
Canal
Cervical Small, Large Small with foramen Short & bifid Flexion, Extension, Lat.
broad triangular Flexion
Thoracic Heart shape Small & long & angles posteriorly Long & angles Costal demi- Lateral rotation
circular inferiorly facets*
Lumbar Kidney Small Massive, no foramen, no Quadrangular Large pedicles Flexion, Extension, Lat.
shaped costal facets Massive Flexion

Anatomy of disc herniation

- Vertebral bodies joined by intervertebral disc which are secondary cartilaginous joints
- The disc contains the annulus fibrosis on its periphery, and the nucleus pulposus in the center
- Torsional strain weakens the annulus fibrosis and causes a tear which leads to herniation of the nucleus pulposus
- 95% involves L4/5 or L5/S1

11. Lower Limb

a. LL muscles, movement, nerve supply
b. Knee and ankle jerk: how to perform and root value
Gluteal Region:
- Superficial abductors: gluteal maximus, medius and minimus
- Deep lateral rotators: Piriformis, obturator internus, superior and inferior gemelli, quadratus femoris

Thigh Region:
- Anterior compartment: iliacus, psaos, quadriceps (vastus medialis, intermedius, lateralis & rectus femoris), satorius
- Medial compartment: adductor magnus, longus & brevis, gracilis, obturator externus, pectinueus
- Posterior compartment: Biceps femoris, semimembranosus, semitendinosus

Leg Region:
- Anterior compartment: TA, FHL, FDL, PT
- Lateral compartment: PL, PB
- Posterior compartment: Gastrocnemius, soleus, plantaris; popliteus, TP, EHL, EDL

PHYSICAL EXMATIONATION
12. CVS system
a. Midline sternotomy scar with left lower para-sternal scar

11
 b. Prosthetic heart valve going for hernia repair on warfarin: pre-op optimisation
Principles of perioperative anticoagulation
Work closely with the anaesthetist and cardiologist/haematologist
- Determine the indication of anti-coagulation to determine the estimated thromboembolic risk
 If thromboembolic risk is transiently increased, delay surgery until the risk returns to baseline
- Estimated bleeding risk depends on the type of surgery
- Determine the timing of anticoagulation interruption – dependent on the renal function and risk of bleeding**
 Warfarin half-life: 20-60 hours (about 40 hours)
 For the short acting newer anticoagulants e.g. stop between 3-5 days before op and resume on POD1-3 depending on bleeding risk
- Determine whether to use bridging anticoagulation

Anticoagulant Renal Interval between last dose and procedure Resumption after procedure
function & NOTE: No anticoagulant is administered the day of the procedure
dose High bleeding risk Low bleeding risk High bleeding Low bleeding
risk risk
Dabigatran CrCl >50 Give last dose 3 days before Give last dose two days before Resume 48 to Resume 24
mL/minute procedure (i.e. skip 4 doses on the procedure (i.e. skip 2 doses on the 72 hours after hours after
150 mg BD two days before the procedure) day before the procedure) surgery surgery
CrCl 30 to 50 Give last dose five days before Give last dose three days before (i.e. POD 2-3) (i.e. POD 1)
mL/minute procedure (i.e. skip 8 doses on the procedure (i.e. skip 4 doses on the
150 mg BD four days before the procedure) two days before the procedure)
Rivaroxaban CrCl >50 Give last dose three days before Give last dose two days before
mL/minute procedure (i.e. skip 2 doses on the procedure (i.e. skip 1 dose on the
20 mg OM two days before the procedure) day before the procedure)
CrCl 30 to 50
mL/minute
15 mg OM
Apixaban CrCl >50 Give last dose three days before Give last dose two days before
mL/minute procedure (i.e. skip 4 doses on the procedure (i.e. skip 2 doses on the
5 mg BD two days before the procedure) day before the procedure)
CrCl 30 to 50
mL/minute
2.5 mg BD

12
13. Cranial nerve
a. Head injury with left hearing impairment, what investigations would you do?

14. Knee exam

15. Lipoma

HISTORY TAKING
16. Epigastric pain
17. PVD

Coventry May 2014 (2)

PATHOLOGY
1. FAP
Shows picture of numerous colonic polyps
a. Diagnosis & Surgical options
b. Ulcer def, PUS def An ulcer is a breach in the epithelial/mucosal surface, accompanied by disintegration of tissue; Pus is a thick
yellowish or greenish opaque liquid produced in infected tissue, it contains dead WBC, bacteria with cellular debris & serum.
c. Extracolonic manifestations. Other tumours: desmoid, PTC, periampullary CA, hepatoblastoma
d. APC gene is a tumour suppressor gene
e. Why must take out in 22yo? Adenoma-dysplasia sequence
f. Inheritance pattern – AD
FAP HNPCC
Diagnosis for FAP Diagnosis: Amsterdam II criteria (3211)
- colonoscopy ≥10 colonic adenomas (can have >100 adenomas seen) - ≥3 other associated cancer
- ≥10-20 cumulative colorectal adenomas (suspected attenuated FAP) - ≥2 successful generations affected
- Genetic testing for germline mutation in the APC gene - 1 should be a 1st degree relative of the other two
- 1 diagnosed before 50 years old
Extracolonic manifestation - Exclusion of FAP
- Endodermal (digestive/respiratory tract): GI polyps e.g. gastric/duodenal,
endocrine tumours e.g. PTC Associated tumours
- Mesodermal (connective tissues): skeletal abnormalities e.g. osteoma of - Pelvis – endometrial, ovarian & prostate
skull/jaw, desmoid tumour - Upper tract TCC – renal pelvis, ureter
- Ectodermal: cutaneous e.g. sebaceous cyst, CNS tumours e.g. astrocytoma, - Upper GI – gastric CA, small bowel CA
medulloblastoma; eye e.g. CHRPE (congenital hypertrophy of retinal - CNS tumour – glioblastoma
epithelium)
Management
Management - Colonoscopy offered at 20-25 years or 5-10 years before
- Endoscopic surveillance every 1-2 years starting age on 10-12 years the earliest diagnosis (whichever comes 1st)
- Surgical options (generally deferred until the patient has reached an - Surgical treatment for CRC
appropriate physiological age)  Subtotal colectomy with ileorectal anastomosis
 proctocolectomy with IPAA  Proctocolectomy with IPAA
 total colectomy with ileoanal anastomosis  Total proctocolectomy with ileostomy
 total proctocolectomy with ileostomy - Consider prophylactic hysterectomy

2. Tubercuosis
Stem: Indian lady with anterior triangle lump + LOW
Differentials – Infection, neoplasm (1° vs. 2°), inflammation
Stains – Ziehl Neelsen stain

ANATOMY
3. Cervical spine
Cervical spine XR, model spine, as well as actress around – (Glasgow May 2014, 2, Q15)

4. Thorax & Abdomen

a. Identify tricuspid valve, chordate tendinae, papillary muscle, pulmonary artery and vein
b. Name azygos vein and tributaries (2) (KL Feb 2014, 3, Q1)
c. Spleen supply, ribs (behind 9-11th), structures to be wary when splenectomy – pancreas tail
d. Duodenum – how many parts, gastroduodenal artery behind D1 (Glasgow May 2014, 2, Q13)
e. Referred pain mechanism Referred pain occurs when visceral organs transmits pain to a particular skin area which shares the
same dermatomal innervation. Visceral afferent fibres which runs with the sympathetic nerve, synapses with the DRG in the spinal cord,
these signals are interpreted as pain arising from the corresponding dermatomal level on the skin.

5. Lower Limb
Repeat of lady fallen of horse

13
CRITICAL CARE
6. Epidural Anaesthesia
Epidural anaesthesia, patient post lobectomy, c/o dyspnea, SpO2 90%, oliguria10ml over 6h
a. Differentials – should have spammed cause of SOB, AKI
b. Advantages
c. Why test pain temperature and not dorsal column in checking levels? (Glasgow May 2014, 2, Q17)
d. Why might epidural be dangerous at T4? (Glasgow May 2014, 2, Q17) cardiac sympathetics at level of T2-4
e. What would you do if suspect overanaes/toxicity, how to check? Check for symptoms of LA toxicity
f. Level of block depends on ___ (dose, duration, position)
Level of block in SPINAL anaesthesia: position of patient, baricity of solution (density compared to CSF e.g. hyperbaric solution floats
downwards in CSF)
Duration of block in SPINAL anaesthesia: increased with vasoconstriction e.g. epinephrine

7. Gastric Outlet Obstruction

Standard UEC disorder hypo Na, Hypo K, Hypo Cl, metabolic alkalosis (Glasgow May 2014, 2, Q16)
a. Why bicarbonate increased? Loss of H+
b. Why paradoxical aciduria?
c. What other adjuncts you wanna consider – NBM,IV fluid, NGT, catheter
d. Who do you wanna call? Renal? DIM? Fk, dunno who to call… cannot manage yourself meh?

8. Ischaemic Colitis
Ischemic colitis, perf viscus, CXR : free air under diaphragm, AF elderly, c/o ado pain
Common causes of AF: metabolic (↓ K/Mg/Ca, thyroid), infection, trauma, sepsis, stress, underlying heart disease, pulmonary embolism,
anastamotic leak, ischaemic bowel
How to optimise for surgery? Rate control, monitor BP, treat underlying aetiology

PHYSICAL EXAMINATION
9. PVD
Ischemic limb with claudication
Patient has murmur, MR damn loud. But examiner didn’t look impressed.
Some atrophic skin changes – dry, loss of hair, nail. No ulcers. Feel all the pulse
Got Doppler by bedside – but no time
What other inx – assess severity ABPI, contrast angio, assess risk factors, LDL, BP, DM, IHD

10. Stoma
Poor stoma output in patient s/p APER (Can offer to examiner its likely an end colostomy, and perineum will have scar.)
Pt got Kocher incision, midline lap, SPC, incisional hernia, stoma – end colostomy LIF
Why got NO output – OBSTRUCTION, ILEUS (op was 18 mo ago, say Adhesion pls), recurrence
Management – What scan – CT AP , PET? no time

11. LHC pain

Colectomy POD1 with LHC pain
Actress – fake peritonitic signs – rebound, guarding, cross tenderness, got TEDS on stem not specified, so just do cursory chest and abdo exam, and
inspect plug site got MEWS (HD chart) – T 38, HR tachy, BP dropping, ECG tachycardia
a. Differential diagnosis
b. Management – NBM, iv drip, abx, analgesia, CT AP, prep for drainage, or repair (abscess or anastomotic leak, but it’s POD1)

12. Parotid lump

Parotid lump without facial nerve involvement
Differentials – include malignant
Management – US, FNAC

HISTORY
13. Depression
Patient weary teary, post gastrectomy – almost time to dc, and CTSP patient not wanting to go home
Let the pt talk about how sad he is. ‘I got time, take your time,’
Do you think is depression
What would you do. But I think examiner failed me, just told me answer – you will reassure him. I got the story he not sleeping well, worried about
recurrence, follow up, why his op was put on a Saturday, is it that his case not important. Lol. Yeah I lo at him. And reassure him
Then present like a MSE?? and then the examiner ask what is it? He will insist it’s depression (but off the top of my head, bloody DSM criteria say
must be more than few months right, so now only a few days duration post op, ITS ACUTE ADJUSTMENT DISORDER)

14. Dysphagia
Pt pub owner, drinks, tells you got vomit blood x1/7. But actually dysphagia x6/12, solid>liquid, LoW+, DRINK 5u/d, Smoke since teenager, no
fhx, takes nsaids for hip replacement pain
14
Differentials – esophageal adenocarcinoma (from barretts esophagus), benign stricture, PUD (lol, during hx taking, I told pt it is likely PUD?!? then
the examiner come round and ask whats my top differentials, I had to backpaddle like shid.) this examiner is cfm laughing executioner type !! still
say well done at the end. Confirm GG

PROCEDURAL SKILLS
15. IV Cannulation
Pt got into some accident, HD unstable, do usual pt details, chat a bit on allergy, needle phobia, why put needle
Later she will say wanna go home tonight during your first attempt, but generally cooperative
I too distracted to read the stem properly, I think she was HD unstable needed large amount of fluid. No touch technique
and alcohol wipe, normal gloves, no need clean petri dish too. aim median cubital, but previous candidates made a hole
elsewhere, and I follow suit, only got on 2nd try, anyhow plaster the tegaderm too.
Q. What fluid, how much, how fast?

16. Sutures
Handtie rubberband with non-absorb braided(silk knot 3x), handtie deep cavity hook absorb braided Vicryl- knot3x)-
advice – wear SMALL GLOVES. Their medium size very big underrun vessel with figure of 8 knot with non absorb
mono fil – prolene knot 6x
Q. property of each one, tensile strength, why tie more knot

COMMUNICATIONS
17. Transfer Patient
Phone call to transfer bile leak case
Q. Why bile leak – clips slipped, CBD injury, interval stones
Q. What to do – nbm, iv fluid, abx, what else what else? The stem says no ERCP available, so I didn’t say, quite silly,
they just want to hear you say it. Plan decompress – ERCP not available on site (LOL I offer octreotide) wah examiner
tell me not medical exam here lol. Anw offer MRCP/PTC

18. OGD consent

Case file stem: guy had dysphagia, middle age, smoker, ETOH use +, went on to have Ba swallow, looks benign so here
at clinic to be consented for OGD, Dilatation and BIOPSY.
Tests show : ALP raised, Bil slightly, Hb LOW. NCNC pic.
Risk/ Indication/ asked if will be done under GA hm.. I dunno maybe coz more painful?
The stem didn’t say but a bit weird thinks there is more than meets the eye.

Kula Lumpur Feb 2014

ANATOMY
1. Thorax & Neck
a. Branches of the aortic arch
b. Arterial supply, venous drainage and lymphatic drainage of thyroid (Coventry May 2014)
c. Nerve supply to thyroid (Coventry May 2014)
d. Vagus & Phrenic nerve

Branches of aortic arch

- Brachiocephalic trunk, left subclavian artery and left common carotid artery
Subclavian artery (divided into 3 parts by the scalenus anterior)
- 1st part (medial border of scalenus anterior)
 On the right the vagus nerve gives of the recurrent laryngel branch
 On the left the thoracic duct opens into the commencement of the left brachiocephalic vein
 Branches:
 vertebral artery
 thyrocervical trunk (inferior thyroid artery, transverse cervical artery & suprascapular artery)
 internal thoracic artery
- 2nd part (lies behind the scalenus anterior, separating it from the subclavian vein)
 Branches: costocervical trunk
- 3rd part (lateral margin of scalenus anterior to outer border of 1st rib – responsible for subclavian groove on 1st rib)
 No constant branch (±dorsal scapular artery)

15
Common carotid artery
- Ascends in the carotid fascia sheath containing the IJV laterally and vagus nerve posteriorly
- The cervical sympathetic chain ascends immediately posterior to the carotid sheath
- In the neck the CCA lies on the cervical transverse process
- Bifurcates at the level of the upper border of thyroid cartilage (at C4 vertebral level)

External Carotid Artery

- Terminates within the parotid
gland at the neck of mandibular
dividing into the superficial
temporal artery and maxillary
artery
- Branches (Some Anatomists Like
F-ing, Others Prefer S&M)
 Superior thyroid artery (Ant)
 Ascending pharyngeal artery
(Post)
 Lingual artery (Ant)
 Facial artery (Ant)
 Occipital artery (Post)
Running along the inferior
border of the digastric
muscle’s posterior belly,
grooving the inferior aspect
of the temporal bone, to the
back of the scalp, where its
pulse is often palpable.
 Posterior auricular artery
 Superficial temporal artery
 Maxillary artery

Internal carotid artery

- Is dilated at its origin into the carotid sinus  baroreceptor supplied by CN XI  controls BP/HR
- Deep to the bifurcation of CCA lies the carotid body, a chemoreceptor also supplied by CN XI  controls respiration
- No branches in the neck
- Enters the cranial cavity via the carotid canal in the petrous part of the temporal bone
- Branches:
 Opthalmic artery
 Middle and anterior cerebral artery

Thyroid Lymphatic Drainage

The lymphatic drainage of the thyroid gland courses the periglandular LN, to the prelaryngeal, pretracheal and paratracheal LN along the recurrent
laryngeal nerve. Then drains to the mediastinal LN.

Lymph node involvement is in thyroid cancer

- Most commonly involving the central compartment (level 6) located medial to the carotid sheaths on both sides, with extension from the
hyoid bone superiorly to the sternal notch inferiorly.
- The jugular lymph node chains (levels 2-4) are the next most common sites of cervical node involvement.
- Lymph nodes in the posterior triangle of the neck (level 5) may also develop metastases.

Phrenic Nerve
Provides motor and sensory supply to the diaphragm (N.B. the phrenic nerve only supplies the sensory component for the central portion of the
diaphragm, the peripheral portions are supplied via T5-11 intercostal nerve & T12 subcostal nerves)

16
 Right Left
Neck Arises from the anterior rami of C3-5 between the scalenus anterior and medius.
Runs on the scalenus anterior
Thorax Enters the thorax posterior to the subclavian veins (anterior to the subclavian artery)
Enters lateral to the right brachiocephalic vein Crosses anterior to aortic arch and left pulmonary artery
Descends lateral to SVC, RA and IVC. Descends lateral to LV
Travels in front of the root of lung
Leaves via the IVC opening (at T8 vertebral level) Pierces the diaphragm to enter the abdominal cavity

Vagus Nerve (CN X)

- Branches in the neck
 Pharyngeal branches
 Superior laryngeal nerve:
 External laryngeal nerve supplies the cricothyroid msucles
 Internal laryngeal nerve provides sensory innervation to the larynx above the vocal folds
 Recurrent laryngeal nerve:
 right branch hooks under the right subclavian, left branch loops around aortic arch distal to ligamentum arteriosus
 both courses superiorly in the TEG to enter the larynx
 Beahr’s triangle: bounded by the CCA laterally, inferior thyroid artery superiorly and RLN inferiorly
 Supplies all the laryngeal muscles except cricothyroid; sensory innervation to laryngeal mucosa below the vocal folds
 Superior cardiac nerve
- Branches in the thorax: inferior cardiac branches, anterior pulmonary plexus, esophageal branches
- Branches in the abdomen: gastric branches, celiac branches, hepatic branches

Right Left
Head Originates from the medulla oblongata
Exits the skull through the jugular foramen (middle compartment) with inferior petrosal sinus, CN IX and XI, sigmoid sinus.
Neck Descends within the carotid sheath posterolateral to ICA and CCA. Medial to IJV at the root of neck.
Gives off superior laryngeal nerve (internal and external branches) in the neck
Passes into the thoracic cavity via thoracic inlet behind the lung
Thorax Anterior to 1st part of subclavian artery Anterior to subclavian artery between left subclavian artery and
common carotid artery
Descends lateral to trachea, inclines behind the hilum Descend lateral to aortic arch, courses behind the hilum
Becomes the posterior vagal trunk Becomes the anterior vagal trunk

2. Base of Skull
a. Optic canal
17
 b. Foramen Rotundum/Ovale/Spinosum
c. Boundary of Middle cranial fossa
d. Spread of infection through middle ear cavity
e. Cavernous sinus
f. Spread of infection from face

Orbit
Bones that articulate to form the orbit (7): frontal, sphenoid, zygoma, maxilla, lacrimal, ethmoid, palatine
Optic canal: transmits the optic nerve and ophthalmic artery, central retinal vein
Superior orbital fissure: Spread of infection from the middle ear
- Superior & inferior division of oculomotor nerve (III) - Direct extension through the bone e.g. in cholesteatoma
- Trochlear nerve (IV) - Spread from the oval/round window into the IAM
- Lacrimal, frontal and nasociliary branch of ophthalmic nerve (V1) - Spread through the venous channels into dural venous sinuses
- Abducens nerve (VI)
- Ophthalmic vein
- Orbital branch of middle meningeal artery
Inferior orbital fissure:
- Branches from maxillary nerve (V3) – zygomatic nerve, infraorbital nerve
- Infraorbital artery and vein
- Inferior ophthalmic vein

18
Cranial fossa
CRANIAL BONE FORAMINA VESSELS NERVE
FOSSA
- Fontal Supraorbital Supraorbital artery & vein Supraorbital nerve (terminal br. of
frontal nerve V1)
Anterior Frontal Foramen caecum Emissary veinsup. sagittal sinus -
Ethimoid Cribiform plate foramina - Olfactory nerve
Middle Sphenoid Optic canal Ophthalmic artery, central retinal Optic nerve
vein
Superior orbital fissure Superior ophthalmic vein, occipital Oculomotor nerve (III), trochlear
branch of middle meningeal artery nerve (IV), lacrimal, frontal &
nasociliary br. of ophthalmic nerve
(V1), abducens nerve (VI)
Foramen rotundum - Maxillary nerve (V2)
Foramen ovale Accessory meningeal artery Mandibular nerve (V3) ± lesser
petrosal nerve (IX)
Foramen spinosum Middle meningeal artery & vein Meningeal branch of mandibular
nerve (V3)
Foramen lacerum Internal carotid artery, emissary Greater petrosal nerve (VII)
veins
- Sphenoid/Maxilla Inferior orbital fissure Inferior ophthalmic vein, infra- Zygomatic & infra-orbital br. of
orbital artery & vein maxillary nerve (V2)
Posterior Temporal Internal acoustic meatus Labyrinth artery Facial nerve (VII), vestibulotrochlear
nerve (VIII)
Jugular foramen Posterior meningeal artery, internal Glossopharyngeal nerve (IX), vagus
jugular vein, inferior petrosal nerve (X), accessory nerve (XI)
sinus, sigmoid sinus
Occipital Hypoglossal canal - Hypoglossal nerve (XII)
Foramen magnum Anterior & posterior spinal Medulla obloganta
arteries, vertebral arteries

19
Cranial fossa and their boundaries
Anterior Cranial Fossa Middle Cranial Fossa Posterior Cranial Fossa
Anterior Inner surface of frontal bone Lesser wing of sphenoid Petrosal temporal bone
(with falx cerebri in midline)
Posterior Lesser wing of sphenoid Petrous part of temporal bone Occipital bone
Lateral - Squamous temporal bone; greater wing of Squamous & mastoid part of temporal
sphenoid & parietal bone bone
Midline Cribiform plate (ethmoid bone) Body of sphenoid Sphenoid & basilar occipital bone
Contains Frontal lobe Temporal lobe, pituitary gland Brainstem, cerebellum

20
Carvenous Sinus
The cavernous sinus lies on either side of the
sella tunica; it is a complex web of veins that do
not contain valves, allowing blood flow in any
direction depending on the prevailing pressure
gradient.
Tributaries
- Facial vein (via superior & inferior
ophthalmic venis)
- Sphenoid vein
- Middle cerebral vein
Drainage
- Inferior petrosal sinus  IJV
- Superior petrosal sinus  sigmoid sinus
 IJV

Cavernous sinus thrombosis

Signs & Symptoms
- Previous sinusitis/mid face infection e.g. furuncle 5-10 days ago
- Headache followed by fever, periorbital oedema & CN signs
 The headache is usually sharp, increasingly progressive and localized to regions inverted by V1 and V2
- Clinical features
 Periorbital oedema
 Chemosis from occlusion of ophthalmic veins
 Lateral gaze palsy  isolated CN VI palsy as it lies freely within the sinus
 Ptois, mydriasis & ophthalmoplegia  CN III palsy
 Raised retrobulbar pressure: exophthalmos & ophthalmoplegia
 Raised ICP: sluggish pupils, decreased VA (traction of optic nerve & central retinal artery)
 Meningeal signs

3. Foot & Ankle

a. Name bones of foot
b. Deltoid ligament
c. Which position is the ankle most stable: dorsiflexion
d. Put tibia and fibula together
e. Tendons of foot
f. Arterial supply of foot
g. Inversion – what muscles/nerve
h. Actions of ankle joint

Bones of the foot (from distal to proximal)

- Distal/middle/proximal phalanges
- Metatarsal
- Medial, intermediate and lateral cuneiforms medially; cuboid laterally
- Navicular
- Calcaneus and talus

Ankle ligaments
- Tibia-fibula: anterior & posterior tibiofibular, inferior transverse ligaments
- Medial ligaments
 Deltoid ligament (4): Posterior tibiotalar, anterior tibiotalar, tibionavicular and tiboicalcaneal ligaments
 Spring ligament (calcaneonavicular ligament)
- Lateral ligaments (3): anterior talofibular ligament, posterior talofibular ligament, calcaneal fibular ligament
- Medial arch: plantar calcaneonavicular ligament (spring ligament) + TP + TA + PL + plantar aponeurosis
- Lateral arch: long & short plantar ligament, extensor tendons

In general the plantar arches are maintained by: shape of interlocking bones, ligaments and muscles

Ankle most stable in dorsiflexion as the wider anterior portion of the talus fills the mortise more completely; hence the contact between the articular
surfaces is maximal.

Tendons of the foot

Anterior ankle tendons: Tom Hates Dick (medial to lateral) – TA, EHL, EDL
Posterior ankle tendons: Tom Dick And Very Nervous Harry – TP, FDL, post. tibial artery, post. tibial vein, post. tibial nerve, FHL

Arterial supply of the LL

Femoral artery
- Distal continuation of the EIA beyond the inguinal ligament  enters the femoral triangle with the femoral vein in the femoral sheath

21
- Transverses the femoral triangle, through the adductor canal, leaving the
canal via the adductor hiatus in the adductor magnus to become the
popliteal artery
- Branches in the groin
 Superficial circumflex iliac artery
 Superficial epigastric artery
 Superficial & deep external pudendal artery
- Branch in the thigh: profunda femoris  medial & lateral circumflex
Popliteal artery
- Continuation of the femoral artery from the adductor hiatus and
terminates at the lower border of the popliteus muscle
- Gives of the branches to the knee joint and terminal branches, anterior &
posterior tibial artery
Posterior tibial artery
- Descend deep to the soleus, becomes superficial in the lower third of the
leg, passes behind the medial malleolus between FDL and FHL
- Accompanied by its corresponding veins and nerve
- Gives off the peroneal artery about 4cm from its origin which runs down
the posterior aspect of the fibula
- Enters the sole of the foot through the tarsal tunnel, which then splits into
the medial and lateral plantar arteries  deep plantar arch
Anterior tibial artery
- Arises at the bifurcation of the popliteal artery, passes forward between
the tibia and fibula through the aperture in the upper part of the
interosseous membrane and descends on the membrane in the anterior
compartment
Dorsalis pedis (branch of the anterior tibial artery)
- The anterior tibial artery becomes the dorsalis pedis as it continues over
the dorsum of the foot
- Passes over the dorsal aspect of the tarsal bones, then plunges deeply
between the 1st and 2nd MT bone
- It then anastomoses with lateral plantar artery to form deep plantar arch

Ankle joint movements

Dorisflexion: anterior compartment – TA, EHL, EDL, peroneus tertius
Plantarflexion: posterior compartment – gastrocnemius, soleus, TP, FHL, FDL
Inversion: TA, TP aided by EHL/FHL
Eversion: PL + PB
Inversion and eversion occurs at the subtalar joint

PATHOLOGY
4. Melanoma
a. Risk factors (Coventry May 2014)
b. Macroscopic and microscopic features of malignant lesions
c. Histology vs. cytology
d. Axillary vein thrombosis – management
Macroscopic features: Glasgow 7 point checklist or ABCDE ± palpable lymph nodes
Microscopic features:
- Pleomorphism (variation in cell size & shape)
- Frequent mitosis
- High nucleus/cytoplasmic ratio
- Increased nuclear DNA content (hyperchromatism)
- Prominent nucleoli or irregular chromatin distribution within nuclei
- Invasion to surround tissue

Histology is the microscopic study of tissue architecture

Cytology is the microscopic study of cells itself

Axillary vein thrombosis (Paget–von Schrötter disease)

A form of upper extremity DVT
Aetiology
- Primary:
 Effort related (Paget-Schrotter syndrome)
 Idiopathic
- Secondary:
 Catheter associated,
 Hypercoagulability e.g. factor V leiden, protein C/S deficiency, antithrombin III deficiency, pregnancy, OCP
Investigations: Duplex US, contrast venography, MRA
Management
- Medical:
 Oral anticoagulation
22
  Heparin followed by warfarin for 6-9 months (keep INR 2-3)
 May require long term anticoagulation in the presence of hypercoagulable disorders
 Prophylactic warfarin against catheter related thrombolysis for patient undergoing chemotherapy
- Interventional: catheter directed thrombolysis
- Surgical
 Indication
 Presence of an anatomic anomaly such as anomalous subclavius or anterior scalene muscle, congenital fibromuscular bands
 Rethrombosis of the vein after previous thrombolytic treatment
 Surgical options:
 Embolectomy
 Bypass
 First rib resection via axilla/supraclavicular approach
 Medial subtotal claviculectomy

5. Neck lumps
a. Anterior neck lumps – TB lymphoma
b. What information would you need on the request form
c. Granuloma – 3 examples
d. Giant cell of Langerhans
e. Name one other mycobacterium
f. Culture medium for mycobacterium
g. Rapid detection of mycobacterium

Anterior triangle of the neck

Boundaries: midline, anterior border of SCM, ramus of mandible
Sub-triangles
- Submental triangle
 Boundaries: midline, hyoid bone, anterior belly of digastric muscle
 Key contents: anterior jugular veins
- Submandibular triangle
 Boundaries: anterior and posterior belly of digastric muscle, body of mandible
 Contents: submandibular gland
- Carotid triangle
 Boundaries: SCM, posterior belly of digastric muscle, superior belly of omohyoid muscle
 Contents: CCA and ECA
- Muscular triangle
 Boundaries: hyoid bone, midline, superior belly of omohyoid, SCM
 Contents: larynx & trachea, thyroid and parathyroid gland
Contents
- Muscles: suprahyoid muscles & infrahyoid muscles
- Nerves: recurrent & external laryngeal nerve, vagus nerve (in carotid sheath), ansa cervicalis, hypoglossal nerve
- Vessels: CCA and bifurcation, branches of ECA, IJV
- Others: thyroid and parathyroid gland; submandibular gland, trachea and oesophagus

Granuloma
Granulomatous inflammation is a form of chronic inflammation characterized by aggregates of activated macrophages that assume an epitheloid
appearance. Granulomas are characterized by epitheloid cells, multinucleated giant cells (Langerhan cells) and lymphocytes which may surround a
central zone of caseating necrosis as in TB.

Mutlinucleated giant cells are derived from the fusion on ≥20 macrophages, and contain nuclei arranged in a horseshoe-shaped pattern
Epitheloid cells are macrophages but they resemble epithelial cells, as they have elongated nuclei

Aetiology
- TB (Mycobacterium tuberculosis)
- Leprosy (Mycobacterium leprae)
- Sarcoidosis
- Syphilis
- Cat-scratch disease
- Crohn disease (IBD)
- RA
- Foreign body

Mycobacterium
Types of mycobacterium: mycobacterium lepare, marium, avium, tuberculosis
Culture medium: Lowenstein-Jensen medium (requires 3-4 weeks)
Rapid detection: Ziehl-Neelsen staining, PCR (24 hours), ELISpot (enzyme-linked immunospot)
- Mycobacterium resistant to Gram staining due to the presence of mycolic acid

CRITICAL CARE
6. Burns management

23
 a. Initial management
b. Calculation of TBSA
c. Fluid resuscitation – Parkland formula & type of fluids given
d. Interpret CXR of ARDS
e. Definition of ARDS
f. Management of ARDS
g. Complications of ARDS

Assessment of thermal burns

Extent of burns:
- Wallace rule of 9: Head 9%, UL 9%, LL 18%, anterior trunk 18%, posterior trunk 18%, genitalia 1%
- Lund & Browder charts
- Patient’s hand – area of closed palm ~1% of TBSA

Depth: maybe superficial, partial or full thickness and this can be determined by the appearance, the texture & sensation to pain
Burn thickness Layers involved Colour/Texture Capillary refill Sensation
Superficial partial thickness Superficial (papillary) Pink soft skin, moist, Blanches and refills rapidly, Very painful
dermis blistering no fixed staining
Deep partial thickness Deep (reticular) dermis Yellow/white soft skin, Blanches and refills, some Painful
fairly dry, ±blistering fixed staining in tissue
Full thickness Through entire dermis White/brown skin, leathery Skin does not change colour Painless
with pressure

Initial management (ABC)

The initial management involves adherence to the ATLS protocol and identifying injuries & complications specific to burns patient
Airway
- Check for airway burns/inhalational injury  mucosal oedema (can occur up to 8 hours after burns) upper airway obstruction
- Low threshold for anaesthetic review
- Risk factors:
 History of fire in enclosed space
 Soot around nostrils, nose or mouth
 Singeing of nasal hair
 Carbonaceous sputum
 Hoarseness, stridor, wheeze
 COHb > 10%

Breathing
- Start high flow oxygen with SpO2 monitoring
- Assess for full-thickness chest burns which can impede chest expansion

Circulation
- Continuous vitals monitoring and strict I/O charting (insert urinary catheter)
- Early fluid resuscitation according to Parkland’s formula
- KIV insert CVP line

Other common complications

- Analgesia e.g. IV opioids
- Prevention of hypothermia
- Stress ulcer prophylaxis with IV PPI
- Broad spectrum IV antibiotics in the presence of sepsis
- Surgical intervention of circumferential burns and chest burns
- Early nutritional supplementation – enteral nutrition required

Parkland Formula
Fluid requirement = 4 x % burn x weight (kg)
- 1st half within 8 hours from burn incident, 2nd half in the subsequent 16 hours
- Watch for BOTH adequacy of resuscitation and fluid overload
- Indication for fluid resuscitation
 Burns > 15% in adults OR burns > 10% in children

Need for fluid resuscitation

- Hypotension from
 Hypovolaemia  increased insensible loss due the loss of epithelial layer
 Distributive shock  SIRS and sepsis
- Limit progression of burns  Jackson’s burn model
 Zone of stasis has compromised tissue perfusion due to damaged microcirculation

Complications of burns
Early
- Localised
 Localised infection

24
 Increased risk of renal failure
 Compartment syndrome - Hypovolaemia  ↓ perfusion  ATN
- Systemic - Rhabdomylolysis  ATN
 Sepsis - Sepsis & SIRS
 ARDS
 Renal failure Increased risk of respiratory compromise
 Electrolyte disturbances (hypo/hypernatremia, hyperkalaemia, hypocalcaemia) - Upper airway oedema from burns in
 Respiratory failure nose/nasopharynx
- Hypoxia from smoke inhalation
 Stress gastric ulcer (Curling’s ulcer)
- ARDS
 DIVC  coagulopathy and haemolytic anaemia
- CO or other toxic gases
 Death
- Chest burns
Late
- Pulmonary oedema from fluid overload
- Limb loss
- Pneumonia
- Contracture & scarring  functional disability & cosmesis
- Chronic regional pain syndrome

ARDS Definition
ARDS is a clinical syndrome of acute respiratory failure with non-cardiogenic pulmonary oedema leading to decreased lung compliancy and
hypoxaemia refractory to oxygen therapy.

Berlin criteria 2012

- Acute onset of ≤1 week
- bilateral opacities consistent with pulmonary oedema on CXR or CT
- PF ratio <300mmHg
- Must not be fully explained by cardiac failure or fluid overload, can be assessed objectively by 2DE
- Old criteria include PAWP<18mmHg

Causes of ARDS
- Pulmonary: pneumonia, aspiration, smoke inhalation, fat embolism
- Multiple trauma
- Sepsis
- Others: massive transfusion, DIVC, acute pancreatitis, CABG, burns

Pathology in ARDS
ARDS can be considered a respiratory component of the multiorgan effects of SIRS
Phase Onset Pathology
Inflammatory/ 1-2 days Activated neutrophils & macrophages secrete cytokines  complement cascade and clotting cascade
Exudative Endothelial injury increases capillary permeability  pulmonary oedema
Endothelial injury manifest as a decrease in Type II penumocytes  reduced surfactant production
Proliferative 5-10 days Hyperplasia of type II pneumocytes and fibroblast  interstitial fibrosis
Fibrosis 2-4 weeks Significant pulmonary fibrosis

Consequence of pathological changes

- Decreased lung compliance  increased work of breathing
- Increased secretion  local atelectasis  reduced functional residual capacity  increased V/Q mismatch
- Increased pulmonary vascular resistance  pulmonary hypertension  right heart failure
 Pulmonary oedema compressing vessels
 Hypoxic pulmonary vasoconstriction

Principles of Management
- Management in ICU
- Treat causative factor
- Early and adequate nutritional support (ideally enteral nutrition)
- Mechanical ventilation with high level of positive end expiratory pressure (PEEP)
 Positive PEEP splints open the stiff alveoli and improves alveolar recruitment throughout the respiratory cycle
 Positive PEEP increases risk of barotrauma
- Low tidal volume ventilation
- Reversed I:E ratios to allow increased inspiratory phase (allow a moderate degree of hypercapnia)
- Prone ventilation with frequent turning to redistribute secretions and minimize basal atelectasis
- Strict fluid management
- Inhaled NO: local pulmonary vasodilator, reducing pulmonary hypertension and improving perfusion to better ventilated areas.

Complications of ARDS
Acute
- Ventilator associated pneumonia, line sepsis
- Pneumothorax, pneumomediastinum
- Prolonged bed rest  DVT, UTI, bedsores
- MODS  renal failure, DIVC, left/right heart failure
- Death
Chronic
- Severe pulmonary restrictive disease
- Cognitive impairment

25
7. Opioid overdose
a. How is CO2 transported in blood
b. Write formula for CO2 transport in blood, which part of the formula does carbonic anhydrase act on
c. Interpret ABG – types of respiratory failure
d. Where does opioid act on
e. Respiratory drive – chemoreceptors
CO2 Transportation
- Carbamino groups (20-30%)
 CO2 binds to amine groups e.g Hb to form carbaminohaemoglobin
 Haldane effect: dexoygenation of blood promotes its ability to transport CO2 as more Hb is available for the formation of carbamino
- Dissolved CO2 (10%)
- HCO3- (60-70%)

O2 Transportation
- Via haemoglobin which consist of 4 peptide chains; 2α and 2β. Each peptide Factors Decrease Increase
can carry four O2 molecules Temperature Left shift Right shift
- Oxygen dissociation curve 2,3 DPG Left shift Right shift
 Left shift: increases Hb affinity to oxygen pCO2 Left shift Right shift
 Right shift: decreases Hb affinity to oxygen (increases oxygen extraction) [H+] Left shift (alkalosis) Right shift (acidosis)

Formula for CO2 transportation

CO2 + H2O  H2CO3  HCO3- + H+
Carbonic anhydrase catalyses the 1st reaction

Respiratory Failure
Respiratory failure occurs when pulmonary gas exchange is impaired causing hypoxaemia ± hypercapnia

Type 1 respiratory failure (PaO2 < 60mmHg or 8kPa)

A failure of oxygenation where PaO2 is low but PaCO2 remains normal
- V/Q mismatch: Pneumonia, PE, bronchiectasis, asthma, ARDS, ILD, pulmonary oedema
- Right-to-left shunt: cyanotic heart disease

Type 2 respiratory failure (PaO2 < 60mmHg + PaCO2 > 50mmHg or 6.7kPA)
A failure of ventilation where both PaO2 and PaCO2
- COPD
- Chronic emphysema
- Chest wall deformities and fail chest
- Respiratory muscle weakness e.g. GBS, myasthenia gravis
- Respiratory depression e.g. opioids, head injury

Feedback control of respiration

- Central chemoreceptor
 Situated in the CNS close to the respiratory centre in the medulla
 Sensitive to changes in PaCO2
 CO2 diffuses into the brain and reacts with water to form H+ causing central acidosis  stimulates an ↑ in RR
- Peripheral chemoreceptors
 Located in the carotid bodies close to the bifurcation of the CCA
 Respond to changes in arterial pH & PaO2

Opioids
Mu (µ) receptor: analgesia, euphoria, respiratory depression, and miosis
Kappa (κ) receptor: analgesia, miosis, respiratory depression, and sedation
Delta (δ) receptor: euphoria, analgesia, and seizures
Nociceptin receptor: dysphoria, hallucinations, and psychosis

Effects of opioids
- CNS: analgesia, sedation, mood changes
- CVS: mild bradycardia, peripheral vasodilation
- Respiratory depression
- GI: NV, decrease motility  constipation
- Pruritus (histamine release)
- ARU
- Opioid-induced hyperalgesia

Opioid toxicity: CNS depression + respiratory depression + miosis

- Naloxone 0.1-2mg/dose Q2min titrated to effect (max dose 10mg)
- Followed by naloxone drip, administering 2/3 of the initial successful dose over 1 hour in a continuous infusion

8. RTA
Liver laceration & Pneumothorax

26
 a. Initial management at A&E
b. Type of airway management
c. How would you manage “circulation”
d. Trauma series X-rays
e. Interpret CXR – subcutaneous emphysema
f. Interpret CTAP – liver laceration
g. How would you manage liver laceration
Airway management
Head tilt chin lift with C-spine stabilisation
Adjuncts: oropharyngeal airway, nasopharyngeal airway, LMA
Definitive: orotracheal/nasotracheal intubation
Surgical: needle vs. surgical cricothyroidotomy, tracheostomy

Liver laceration
Mechanism of injury: blunt trauma and penetrating injury
Trauma evaluation
- FAST: hypoechoic rim of subcapsular fluid, intraperitoneal fluid around the liver, fluid in the Morrison’s pouch (hepatorenal)
- DPL
- CT: pooling of fluid IV contrast in or around the liver; able assess for associated intra-abdominal and thoracic injury
Associated injuries
- MSK: chest wall, lower ribs, spinal cord and pelvic #
- Thoracic: diaphragm, right lung
- Intra-abdominal: spleen, duodenum, colon, right kidney, vena cava

Hepatic injury grading (AAST)

- VI grades (in contrast to splenic injury V grades)
- Based on haematoma size (% of surface area), laceration size, vessel involvement, integrity of liver, vascular status

Grade Description of injury

I small (<10%, < 1cm)
II moderate (10-50%, < 10cm)
III large (>50%, > 10cm or expanding)
IV large with parenchymal disruption (>25% of a hepatic lobe)
V large with parenchymal disruption (> 75% of a hepatic lobe) or juxtahepatic venous injury
VI hepatic avulsion

Management
Initial management would involve strict adherence to the principles of the ATLS protocol
- Non-operative management consists of observation and supportive care with adjunctive use of arteriography & hepatic embolization
 Suitable for patient who are haemodynamically stable and low grade injury (≤grade III)
 Contraindications: haemodynamic instability, other indications for abdominal surgery, gunshot injury
 N.B. missed GI hollow viscus injury generally present by post-injury day 4
 Observation
 Monitored in the hospital with bed rest + monitoring of Hb trend
 Mechanical and chemical thromboprophylaxis if not contraindicated (i.e. Hb has stabilized and <1g/dL decrement over 24hr)
 Hepatic embolization
 May be used in patients who failed observation e.g. downward trend of Hb; or rebleeding after initial surgical intervention
 Ideal choice in patients with liver injury demonstrating pooling of IV contrast on CT
- Surgical intervention
 Exploratory laparotomy followed by four-quadrant abdominal packing  systematic inspection of all intraabdominal organs, and
exploration of the retroperitoneum
 Control of bleeding: manual compression, portal clamping (Pringle manoeuver), perihepatic packing
 Damage control surgery vs. primary definitive control of bleeding e.g. topical haemostatic agent, ligation of parenchymal vessels,
direct liver suturing
 High grade injury may involve hepatic artery ligation or debridement of the liver ± hepatectomy ± liver transplant

Complications
- General and specific
- Specific: perihepatic abscess, bile collection (biloma), perioperative fluid collection

PROCEDURAL SKILLS
9. Closing wounds
a. Prepare your own tray – suture/instruments
b. Answer questions from patient – Painful? Antibiotics? STO? Scar?
c. Types of LA and maximal safe does (Coventry May 2014)

27
Prepare suture tray/instruments
Surgical drapes
Gauze (count before and after)
Suture material
Antiseptic solution and saline
Scalpel
Haemostat (curved and straight)
Forceps (Tooth and non-tooth)
Needle driver and scissors
General principles for STO
Facial wounds 3-5 days
Scalp wounds 7-10 days
Limbs 10-14 days
Joints 10-14 days
Trunk 7-10 days

10. OT Management
a. Re-arrange OT list
b. Warfarin pre-op management (Coventry May 2014)
c. DM pre-op management
d. COPD pre-op management
e. Penicillin allergy, what alternative prophylactic antibiotics for laparotomy?
f. Show on mannequin the extent of cleaning for each surgery: laparotomy, BKA, hernia repair
g. Types of diathermy esp. for patients with pacemaker
h. Show on mannequin the location of electrode plate placement
DM pre-op management
Identification of high risk patient i.e. poorly controlled diabetes and diabetic complications
Early pre-operative assessment
- Assess glycaemia control, consider referral if HbA1C > 8.5% and/or hypoglycaemia unawareness
- Identify other co-morbidities
- Clear and written instructions with the changes to their medication prior to admission
 Discontinuation of oral hypoglycaemic agents on the day of surgery
 Reduction of ON insulin dose
Reduce starvation time – prioritise patients on OT list (aim for only 1 missed meal)
Optimization of diabetes control and complication prior to surgery

Hospital admission
- IV fluids: use of 0.45% NaCl and 5% Dextrose ± 0.15% or 0.3% KCl as appropriate
- Monitor CBG regularly with target of 6-10 mmol/L (10-14 mmol/L is acceptable)
- Start on variable rate IV insulin infusion OR subcutaneous sliding scale
- Consider continuing LONG ACTING insulin on top of variable rate insulin infusion

Early post-op mobilization, resumption of normal diet and usual DM management

COPD Pre-op management

Per-operative assessment + anaesthesia review
- Smoking history, exercise intolerance
- Evidence of active COPD
- Pulmonary function test + CXR
- Smoking cessation at least 4-8 weeks preoperatively is optimal
- Optimisation of lung function using inhaled bronchodilators in patients with severe COPD can decrease postoperative complications
- Although oral corticosteroids are not recommended for chronic disease management in the patient with COPD, those who are taking these
agents chronically should be treated with systemic steroids in the perioperative period to minimise the risk of adrenal insufficiency
- Pulmonary rehabilitation should be considered in high-risk patients undergoing elective procedures. Pre- and postoperative pulmonary
rehabilitation

http://www.thoracic.org/clinical/copd-guidelines/for-health-professionals/management-of-stable-copd/surgery-in-and-for-copd/perioperative-
management.php

Risk of surgical site infection (SSI)

Patient factor: age, nutrition, obesity, DM, smoking, co-existing infection, bacterial colonization, immunosuppression, prolong hospital stay
Surgical factor: pre-operative skin preparation, duration of surgery, antimicrobial prophylaxis, OT ventilation, foreign material, surgical drains,
surgical technique e.g. haemostasis, closure, tissues trauma; post-op hypothermia

Wound class
Class Definition
Clean Operations in which no inflammation is encountered and the respiratory, alimentary or genitourinary tracts are not entered. There
is no break in aseptic operating theatre technique
Clean Operations in which the respiratory, alimentary or genitourinary tracts are entered but without significant spillage.
contaminated
Contaminated Operations where acute inflammation (without pus) is encountered, or where there is visible contamination of the wound.
Examples include gross spillage from a hollow viscus during the operation or compound/open injuries operated on within four
hours
Dirty Operations in the presence of pus, where there is a previously perforated hollow viscus, or compound/open injuries more than
four hours old.

28
Pre-op Antibiotics
Nature of procedure Common pathogens Recommended IV antimicrobials
Cardiac Procedures Staphylococcus aureus, S. epidermidis Cefazolin 1g
Vancomycin 15mg/kg (max 2g)
Clindamycin 900mg
Gastroduodenal Surgery Enteric Gram-negative bacilli, Gram-positive cocci Cefazolin 1g
Open (Biliary Tract) Enteric Gram-negative bacilli, enterococci, clostridia Cefazolin 1g
Laparoscopic (Biliary Tract) NA None
Appendectomy Enteric Gram-negative bacilli, anaerobes, enterococci Cefazolin 1g + Metronidazole 500mg
Small Bowel Surgery Enteric Gram-negative bacilli, anaerobes, enterococci Cefazolin 1g + Metronidazole 500mg
Hernia Repair Aerobic Gram-positive organisms Cefazolin 1g
Colorectal Surgery Enteric Gram-negative bacilli, anaerobes, enterococci Cefazolin 1g + Metronidazole 500mg
Cefazolin 1g + Unasyn 3g
Rigid cystoscopy (Urology) Enteric gram-negative bacilli, enterococci Ciprofloxacin 400mg
Open or Laparoscopic (Urology) Enteric gram-negative bacilli, enterococci Cefazolin 1g
Hysterectomy (O&G) Staph epi, Staph aureus, Group B Strep, Enterococcus Cefazolin 1g
Caesarean section (O&G) Enteric Gram(-) bacilli, Group B Strep, Enterococcus Cefazolin 1g
Head & Neck Surgery Anaerobes, enteric gram-negative bacilli, S. aureus Cefazolin 1g + Metronidazole 500mg
Neurosurgery Staphylococcus aureus, S. epidermidis Cefazolin 1g
Orthopaedics (with implants) Staphylococcus aureus, S. epidermidis Cefazolin 1g
Vascular Surgery Staphylococcus aureus, S. epidermidis, enteric gram- Cefazolin 1g
negative bacilli

For patients allergic to penicillins and cephalosporins, clindamycin (900 mg) or vancomycin (15 mg/kg IV; not to exceed 2 g) with either gentamicin
(5 mg/kg IV), ciprofloxacin (400 mg IV), levofloxacin (500 mg IV), or aztreonam (2 g IV) is a reasonable alternative. Metronidazole (500 mg IV)
plus an aminoglycoside or fluoroquinolone are also acceptable alternative regimens, although metronidazole plus aztreonam should not be used since
this regimen does not have aerobic gram-positive activity.

Recommended re-dosing interval for surgeries ≥ 4 hours

Drug Recommended Re-dosing interval
Cefazolin, Cefuroxime, Cefotetan, Cefoxitin, Ampicillin/sulbactam, Clindamycin 4 hours
Ciprofloxacin 6 hours
Gentamicin, Metronidazole 8 hours
Vancomycin 12 hours

Extent of cleaning
- Laparotomy: nipple to pubic symphysis
- BKA:
- Inguinal hernia repair:

Diathermy
Surgical diathermy involves the usage of high-frequency alternating current between 2 electrodes and through tissues. This produces high heat to
allow for cutting and coagulation

Monopolar Diathermy Bipolar Diathermy

High power required (400W)
Current is delivered from a generator to an active electrode and spreads
throughout the body, returning to the generator via a patient plate
electrode
Patient electrode plate required with good skin contact of ≥70cm2
Can touch other instruments to pass current through
Low power required (50W)
Current passes from a generator to a pair of forceps and passes from 1
limb of the forceps, through tissues, to the other limb of the forceps
No patient plate electrode required
Safer for use on end arteries, structure with narrow pedicles & patients
with pacemakersSafer for use on end arteries, structure with narrow
pedicles & patients with pacemakers

Diathermy & Pacemaker

Potential problems
- High frequency of the monopolar diathermy may induced currents in the circuits of the pacemaker  arrhythmias
- Diathermy close to the pacemaker may result in currents travelling down the pacemaker wires  myocardial burns
Pacemaker management for surgery
- Pre-op: CVM to evaluate/reprogram pacemaker for surgery, ICD to be programmed OFF just before op and ON post-op
- Intra-op
 Continuous ECG, SpO2, vitals monitoring ± IA line
 Avoid diathermy if possible  consider bipolar
 If monopolar must be used
 Use only for short burst (prevent long periods of asytole)
 Ensure that the return electrode is placed such that the pathway between the diathermy and return is far away from the ICD

PHYSICAL EXAMINATION
11. CVS exam
12. Knee exam
13. Cranial nerve exam

29
14. Hernia exam

HISTORY TAKING
15. Abdominal pain
16. AMT
Assess AMT for consent taking
AMT
1. How old are you?
2. Date of birth
3. What is the year
4. What is the time
5. Date WWII began? 1939
6. Ask the patient to remember an address and will ask them again (42 West Street)
7. What is the name of this hospital/place
8. Can you identify 2 ppl
9. Who is the current monarch? Queen Elizabeth
10. Count back from 20 to 1

COMMUNICATION
17. Book ICU bed
18. Talk to family regarding ascites

Kula Lumpur Feb 2014 (2)

PROCEDURAL SKILL
1. T&S
a. Introduction, consent taking and patient advice
b. LA dosing

2. OT listing
a. Prioritize between
i. COPD with strangulated hernia
ii. Diverticular abscess with penicillin allergy & iodine allergy
iii. MRSA DM foot for BKA
b. Pre-op orders for each case in OT i.e. what anaesthesia, cleaning solution
c. Where to place diathermy pads
Hernia first because emergency and best done without prior contamination. DM foot last case by doing spinal or RA.
Types of anaesthesia
- Inguinal hernia: GA, spinal, LA  for strangulated ideally GA
 GA for laproscopic hernia repair
 RA for most cases of hernia repair
 LA for patients of average weight with a primary unilateral hernia (recurrent hernias, bilateral hernias, and hernias in obese patients are
generally performed with regional anaesthesia)
- Diverticular abscess: GA
- MRSA DM foot: Spinal vs. nerve block

Cleaning solution: iodine vs. chlorhexidine wash

Then examiner asked what pre op orders u want for each case. What anaesthesia, what cleaning solution (choose between iodine and chlorhex) and
where to place diathermy pads for each case.

ANATOMY
3. Head & Neck
a. Identify aortic arch, vagus nerve and recurrent laryngeal nerve (Coventry 2014)
b. Thyroid anatomy, blood supply and its origins/drainage (Coventry 2014)
c. Brachial plexus: upper & lower palsy, posterior cord (from which root level)
Drawing the brachial plexus:
https://www.youtube.com/watch?v=9gPsHCflFfA

30
Posterior Cord: consist of all root levels from the brachial plexus (C5-T1)
- Branches include:
 Upper subscapular (C5-6)
 Lower subscapular (C5-6)
 Thoracodorsal (C6-8)
 Axillary (C5-6)
 Radial (C5-T1)

Erb palsy (C5,6)

- Presentation: “waiter’s tip” position with the arm hanging limply by the side, forearm pronated and palm facing backwards
- Muscle affected:
 C5 weakness: axillary nerve (deltoids, teres minor), suprascapular nerve (supra/infraspinatus), musculocutaneous nerve (biceps)
 C6 weakness: radial nerve (brachioradialis, supinator)
- Causes: dystocia, forceps delivery, fall on side of head & shoulder forcing the 2 apart

Klumpke’s palsy (C8, T1)

- Presentation:
 Clawed hand ± numbness along inner and upper arm/forearm centred on elbow joint level
 ± Horner’s syndrome with involvement of the sympathetic chain
- Muscles affected:
 All intrinsic muscles of the hand (both ulnar and median nerve)
 “clawed” hand
 Wrist in extreme extension due to unopposed action of extensors
 Hyperextension of MCPJ – loss of lumbricals
 Flexion at IP joints – loss of lumbricals
 Causes: breech delivery, sudden upward traction on arm, cervical rib, Pancoast’s tumour

4. Middle Cranial Fossa

a. Bones that make up the middle cranial fossa
b. All the foramina within it (Coventry 2014)
c. Cavernous sinus and contents (Coventry 2014)
d. Optic canal:
i. Surrounding sheath of optic nerve and clinical
significance
ii. What other structure: ophthalmic artery and
its significance (it’s an end artery)
Anterior cranial fossa: frontal bone + ethmoid bone + sphenoid bone
Middle cranial fossa: sphenoid + temporal + parietal bone
Posterior cranial fossa: temporal + occipital bone

Optic nerve is ensheathed in all 3 meningeal layers as embryologically it is

derived from an out-pouching of the diencephalon.

Ophthalmic artery is the 1st branch of the ICA, its most important branch is CRA
31
- Orbital group (orbital structures)
 Lacrimal artery
 Supra-orbital artery
 Posterior and anterior ethmoidal artery
 Supratrochlear artery
 Dorsal nasal artery
- Ocular group (eyes and its muscle)
 Long & short posterior ciliary arteries
 Anterior ciliary artery
 Central retinal artery

5. Foot & Ankle

a. How to put a tibia and fibula together – its superior and inferior articulations (KL 2014)
b. Identify sustentaculum tali
c. Bones that make up medial and lateral arch
d. Medial and lateral collateral ligaments (KL 2014)
e. Identify extensor tendons in dorsum of foot from medial to lateral (KL 2014)
f. Which muscles invert/evert foot, most stable position of ankle (KL 2014)
Sustentaculum tali is a shelf like projection from the calcaneus which gives attachment to the plantar calcaneo-navicular ligament, tibiocalcaneal
ligament and medial talocalcaneal ligament.

Medial arch: calcaneus + talus + 3 cuneiforms + 1-3th MT

Lateral arch: calcaneus + cuboid + 4-5th MT

PATHOLOGY
6. Melanoma
a. Significance of full pathology report (remember size and breslow thickness)
b. Surgical treatment
c. Complications of axillary vein thrombosis
d. Pulmonary embolism management + complications
Information in pathology report
- Macroscopic appearance
- Breslow thickness + size of tumour
- Clark’s level (level of invasion)
- Circumferential margins
- Lymphovascular invasion
- Satellite lesions
- Histology subtype
- Microscopic appearance e.g. mitosis
- TMN staging and grade

Deep Vein Thrombosis

Causes of DVT
Endothelial Dysfunction Stasis/Turbulence Hypercoagulable State
Atheroma Previous DVT Increased clotting factor Decreased clotting factor
Radiotherapy Poor outflow: SLE, APLS Anti-thrombin III deficiency
Trauma e.g. IVDA - sepsis, polycythaemia OCP/Pregnancy/HRT Protein C/S deficiency
- immobilization, major surgery, Factor V Leiden
Poor inflow: Malignancy, sepsis
- AMI, CCF, AF
Nephrotic syndrome*
*
Due to urinary loss of antithrombin III + increased hepatic production of clotting factors

32
Presentation
- Painless/painful LL swelling, warmth/erythema over areas of thrombosis
- Phlegmasia cerulean dolens: acute ischaemic and cyanotic leg following a massive ileo-femoral venous thrombosis
- Phlegmasia alba dolens: acute ischaemic, swollen and white leg following massive ileo-femoral venous thrombosis with arterial spasm
- Pulmonary emoblism

Pulmonary Embolism
Causes of PE: similar to DVT (note DVT is also a cause)
Presentation:
- Tachycardia, tachypnoea ± pleuritic chest pain ± haemoptysis
- Fever
- Signs/symptoms suggestive of thrombophlebitis e.g. DVT
- Hypotension in massive PE  RVOTO presenting as systemic hypotension with cool, pale peripheries
- Sudden cardiac death, arrhythmias, PEA

Wells’ Criteria for PE (Don’t die tell the team to calculate criteria!) – <2 points low risk, 2-6 moderate risk, >6 high risk
DVT – 3 points
Diagnosis most likely PE – 3 points
Tachycardia>100 – 1.5 points
Three days of immobilization OR surgery in the past Thirty days – 1.5 points
Thromboembolism in the past – 1.5 points
Coughing blood – 1 point
Cancer – 1 point

Investigations
The diagnostic investigation of choice is a CT pulmonary angiogram; other investigation aids the initial workup & identification of risk factors
- Initial investigation
 ABG: presence of hypoxia and hypocarbia
 D-dimer: elevated (not useful if patient is at moderate-high risk of PE
 ECG
 sinus tachycardia, non-specific ST segment & T wave changes
 RV strain pattern (T wave inversion in right pericardial leads V1-4 ± inferior leads)
 SIQIIITIII pattern – deep S wave in lead I, Q wave in lead III & T wave inversion in lead III
 CXR (to exclude differential diagnosis)
- Aetiology
 Coagulation studies (aPTT & PT)  hypercoagulation workup
 LL Doppler US
- Diagnostic: CTPA, VQ scan (not routinely done)

Management
Involves initial resuscitation with respiratory support and haemodynamic support following which the initiation of empirical anticoagulation if the
patient is haemodynamically stable.
- Haemodynamically stable
 Anticoagulation: LMWH (Enoxaparin/Clexane) at 1mg/kg Q12H then warfarin aim INR 2-3 for at least 3 months
 IVC filter: for patients who failed anticoagulation, developed complications or has unacceptable bleeding risk
- Haemodynamically unstable
 IV Thrombolysis
 Embolectomy (catheter vs. open): for patients whom thrombolysis is unsuccessful or contraindicated

MOA of warfarin: inhibits vitamin K epoxide reductase, preventing the reduction of vitamin K epoxide to vitamin K; thereby inhibiting the vitamin
K dependent carboxylation of the glutamic acid of the precursor clotting factors 2, 7, 9 & 10.

MOA of heparin: augments the activity of antithrombin III (AT), inactivating thrombin (factor II) and factor X

7. Enlarged lymph node

a. TB and lymphoma
b. Most common lymphoma in young Caucasian lady Primary mediastinal large B cell lymphoma?
c. Impact of TB on the community (2 major impacts)
d. What other pathological test will you do for the lymph node (histology, culture, staining?)
Lymphoma
It is malignancy of the lymphoid system which produces mass in involved lymph nodes or other tissues.
WHO Classification of Lymphoma
Lymphoma
Hodgkin Lymphoma (HL)* Non-Hodgkin Lymphoma (NHL)
- Nodular sclerosis (NSHL) B-cell Lymphomas T-cell & NK cell Lymphomas
- Mixed cellularity (MCHL)
- Lymphocyte rich (LRHL)
- Lymphocyte depleted (LDHL)
- Nodular lymphocytic predominant (NLPHL)
*
The 1st 4 types of HL are referred to as classical HL, with the 5th being termed as non-classical HL due to its unique clinical features & treatment

33
Clinical differences between HL & NHL
Feature HL NHL
Pattern of spread Orderly spread by anatomical contiguity Non-contiguous spread
Distribution of nodes involved Often localised to a single axial group of nodes e.g. Often involves multiple peripheral nodes
cervical, mediastinal, para-aortic
Nodes involved Mesenteric nodes & Waldeyer’s ring rarely involved Mesenteric nodes & Waldeyer’s ring commonly involved
Extranodal presentation Uncommon Common

Hodgkin Lymphoma
Epidemiology
- Bimodal distribution with initial peak in young adults (15-34) & older adults (>55)
- Males > Females, gender predilection is more pronounced in children
- NSHL more common in young adults, MCHL more common in older adults

Presentation: Asymptomatic lymphadenopathy, B symptoms ± local symptoms e.g. CP/SOB for large mediastinal masses
Investigation:
- Blood: FBC, ESR, LFT (LDH and ALP), HIV screening, Hepatitis screening (before starting chemotherapy)
- Radiological: CT TAP, bone scan
- Histological (usually excisional biopsy but for H&N cancer consider FNAC 1st to exclude squamous cell histology)
 Classical Reed-Sternberg cells in a non-neoplastic inflammatory background
 RS cells are cells with 2 mirror-image nuclei, each containing an inclusion like nucleolus surround by a distinctive clear zone,
imparting an owl like appearance.

The Ann Arbor classification

Stage I: A single lymph node area or single extranodal site
Stage II: 2 or more lymph node areas on the same side of the diaphragm
Stage III: Lymph node areas on both sides of the diaphragm
Stage IV: Disseminated or multiple involvement of the extranodal organs

Management: RT, induction/salvage chemotherapy, haematopoietic stem cell transplant

Prognosis (in terms of 5 year survival)
- Local disease 90%
- Regional disease (spread to regional LN) 92%
- Distant spread 76%

Non-Hodgkin Lymphoma
Epidemiology:
- Most common haematological malignancy (5 times more common than HL)
- Whites > Blacks, males > females (1:1.4)
- Primary mediastinal large B cell lymphoma are more common in YOUNG WOMEN
- Median age of presentation >50 years old

Presentation:
- Painless peripheral adenopathy
- Extranodal involvement – GI (which include Waldeyer ring), GU (e.g. testicular mass), skin, bone marrow, sinuses, thyroid & CNS
- B symptoms (late stage)
- Bone marrow involvement (frequent)

Investigation (similar to HL)

- Blood: FBC, ESR, LFT, HIV, hepatitis
- Radiological: CT Neck + TAP, bone scan, US Scrotum, MRI brain/spinal cord (for 1° CNS lymphoma)
- Endoscopic: upper GI series + small bowel follow through for H&N lesions or GI primaries
- Histological: excisional biopsy, BMA

Management: chemotherapy, pharmacotherapy, surgery

Prognosis: in general about 63%, use of International Prognostic Index (IPI)

Most common type of lymphoma in young Caucasian woman: Primary mediastinal large B-cell lymphoma (NHL)
Impact of TB on the community:
- Population health burden  spread of TB by asymptomatic/inadequately treated patients (Less than half of all TB cases world-wide are ever
diagnosed, and fewer than 60% of those diagnosed are cured)
- Social burden  affecting woman during their reproductive years (Among women aged 15 to 44 years, TB accounts for the annual loss of an
estimated 8.7 million years of life.)
- Economic burden  TB halts work in the formal and informal economies, as well as within households. Country studies document between
three and four months work time lost annually to the disease, and lost earnings of 20 to 30% of household income. Families of persons who die
from the disease lose about 15 years of income.

Pathological test for LN

Immunohistochemistry staining to determine the type of cell involved
Immunophenotyping
Cytogenetics
Molecular genetic analysis to look for specific genetic mutations

34
Viral studies
Cancer genetics
Culture

CRITICAL CARE
8. Burns
a. Estimation of burns (give the exact numbers) – (KL Feb 2014)
b. Parkland formula (KL Feb 2014)
c. Recognition of the types of burns (KL Feb 2014)
d. Choice of fluids (KL Feb 2014)
e. Recognition, definition and management of ARDS (KL Feb 2014)

9. Multiple trauma
a. CXR with pneumothorax, subcutaneous emphysema and rib fractures
b. Management: according to ATLS principles
c. Read CT coronal slice: liver laceration and management (KL Feb 2014)

10. Type 1 Respiratory Failure

a. Illustrate CO2 and H2O equation (KL Feb 2014)
b. How is CO2 transported – 3 ways (KL Feb 2014)
c. Which part of blood does the reaction occur? (KL Feb 2014)
d. Explain the metabolic compensation mechanism in respiratory acidosis
e. Explain chloride shift
Metabolic compensation in respiratory acidosis
The kidney controls the [HCO3-] to compensate acid-base disturbances; it increases HCO3- via 3 mechanisms
- Reabsorption of filtered HCO3- in the PCT
- Reabsorption of HCO3- in the PCT via buffering of H+ with urinary buffer e.g. phosphate (titratable acid)
- Generation of new HCO3- from the formation of ammonium in the PCT via glutamine metabolism

Chloride Shift
Also known as the Hamburger shift, it refers to the exchange of HCO3- for Cl- across the membranes of RBCs.
- RBC cell membranes are impermeable to H+ ions; however; the presence of carbonic anhydrase in RBCs allow the conversion of dissolved
CO2 and H2O to form HCO3- and H+ ions
- The rise in intracellular HCO3- causes exchange of extracellular Cl- for intracellular HCO3-

COMMUNICATIONS
11. Book ICU bed
a. Speak to ICU registrar for reservation of ICU bed for exploratory laparotomy
b. Discussion on ACLS and secondary resuscitation of patient
c. Offer to discuss with your consultant and call back if the registrar refuses

12. Counselling angry patient

Counselling for patient whose husband’s scan got postponed and consultant too busy to talk to them (refer to DrExam counselling )

HISTORY TAKING
13. AMT
a. Assessing confused patient coming for elective surgery
b. Plan for the patient: postpone surgery, involve the family etc.

14. Gallstone disease

a. Questions including differential diagnosis, investigation and management

PHYSICAL EXAMINATION
15. CVS exam
a. EDM with collapsing pulse: AR differentials, management, investigation
b. Pre-op precautions with hernia repair (Coventry 2014)
i. Discussion regarding IE and anticoagulation (For IE see KL 2014, 3)
16. CNS exam
a. Pituitary adenoma
17. Indirect hernia
a. Hernia management
b. Special consideration in respiratory patients consider spinal anaesthesia
35
 c. Advice post-op
18. Knee exam

Kula Lumpur Feb 2014 (3)

ANATOMY
1. Thorax & Abdomen
a. Identify pulmonary trunk, ascending aorta
b. Branches of ascending aorta
c. Right and left coronary arteries
d. Identify sympathetic trunk: sources of trunk (originates from T1 – L2)
e. Tributaries of azygos vein: hemiazygos, right post. IC vein, right superior phrenic vein, bronchial/pericardial/oesophageal vein
f. Identify papillary muscles & chordae tendinae: both prevents regurgitation during ventricular systole
g. Identify the spleen
h. Course of splenic artery
i. Structures damaged during splenectomy? stomach, splenic flexure, diaphragm, tail of pancreas (fistula)
Coronary arteries
Right coronary artery
- Arises from the anterior aortic sinus, passes forward between RA and pulmonary trunk into the AV groove, continues along the right part of
the AV groove to anastomose with the left coronary artery in the posterior interventricular groove
- Gives off the marginal branch & the posterior interventricular branch which runs forward to anastomose with the LAD at the apex

Left coronary artery

- Arises from the left posterior aortic sinus which passes posterior and to the left of the pulmonary trunk
- Gives off left anterior descending/anterior interventricular branch 2cm from its origin (most important branch)
- The left coronary runs laterally around the left border as the left circumflex artery

Variations
- Left coronary may give off the posterior interventricular branch (known as left dominance occurring in 10%)
- Right and left coronary having equal contribution to the posterior interventricular branch in 10%
- 60% of the SA node supplied by RCA, 40% by the left circumflex, 3% has dual supply
- AV node supplied by RCA in 90%, circumflex in 10%

Coronary veins
Bulk of the venous drainage is achieved by veins accompanying the coronary arteries ultimately emptying into the RA, most veins drains into the
coronary sinus before emptying into RA except anterior cardiac vein
- Great cardiac vein in the anterior ventricular groove (next to LAD)
- Middle cardiac vein in the inferior AV groove (next to posterior ventricular branch)
- Small cardiac vein accompanies the marginal artery
- Oblique vein descends obliquely on the posterior aspect of LA

Splenic artery arises from the coeliac trunk (T12) and runs laterally along the superior border of the pancreas within the splenorenal ligament. Gives
off the following branches: branch to pancreas, short gastric & left gastro-omental artery
Splenorenal ligament – splenic vessels & pancreatic tail; gastrosplenic ligament – short gastric and left gastro-omental artery

2. Lower Limb
a. Identify the sciatic nerve
i. What are the nerve roots? L4,5, S1,2,3
ii. Bony landmark; variations of its normal course in the buttock
b. Identify gluteal medius
i. Nerve supply, muscle action and consequence of weakness, causes of weakness
ii. Describe Trendelenburg test
c. Popliteal fossa
i. Contents and boundaries, identify popliteal artery, common peroneal nerve, tibial nerve
ii. Causes of popliteal fossa swelling
iii. Where does the lymph node from the popliteal fossa drain from? Lateral aspect of the leg and foot
following the course of the short saphenous vein
iv. Structure that maybe damaged in supracondylar fracture of tibia? Popliteal artery

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Nerves of the LL
Lumbar plexus Sacral Plexus
- Formed by anterior rami of L1-4 + T12 - Originates from the anterior rami of L4-5, S1-4
- Formed in the substance of psoas major, all branches emerges - Sacral nerves emerge from the ant. sacral foramina & unites in
from the lateral border of the psoas except obturator nerve (medial front of the piriformis where they are joined by lumbosacral trunk
border) & gentiofemoral nerve (anterior aspect) (L4-5)
Iliohypogastric nerve (T12, L1) Superior gluteal nerve (L4-S1)
Ilioinguinal nerve (L1) Inferior gluteal nerve (L5-S2)
Genitofemoral nerve (L1, L2) Nerve to quadratus femoris (L4-5, S1)
Lateral cutaneous nerve of thigh (L2, L3) – meralgia paraesthesia Nerve to obutrator internus (L5, S1-2)
Obturator nerve (L2-4) Nerve to piriformis (S1-2)
Femoral nerve (L2-4) Sciatic nerve (L4-5, S1-3)
Posterior cutaneous nerve of thigh (S1-3)
Pudendal nerve (S2-4)

Femoral nerve
- Passes through the psoas major, emerging on the lateral aspect  passes under the inguinal ligament into the femoral triangle
- About 5 cm below the inguinal ligament terminates into its terminal branches
 Muscular: anterior compartment of thigh
 Cutaneous branches: medial and intermediate cutaneous of thigh  medial and anterior aspect of thigh; Saphenous nerve  medial
aspect of leg and foot
 Articular branches to hip and knee

Obturator nerve
- Emerges from medial border of psaos  runs downwards posterior to the iliac artery to reach the upper lateral border of obturator foramen 
enters the thigh through the obturator canal  splits into anterior and posterior branches
 Anterior branch descends between adductor longus and brevis  branches to gracilis, adductor longus & brevis + skin over medial aspect
of thigh and hip joint
 Posterior branch descends behind the adductor brevis  supplies adductor magnus, obturator externus

Sciatic nerve
- Emerges from greater sciatic foramen below piriformis & descends between superficial and deep gluteal muscles
- Descends on posterior surface of adductor magnus, crossed by long head of bicep femoris
- Divides into terminal branches at the apex of the popliteal fossa (variable)
- Branches: supplies the hamstring portion of adductor magnus, hamstring muscles. All the branches except to the short head of biceps arises on
the medial side of the nerve  lateral side is relatively safe for surgery
- Bony landmarks: superiorly midway between PSIS and ischial tuberosity; inferiorly midway between ischial tuberosity and GT
- Variations: below piriformis, peroneal division between piriformis, peroneal division over piriformis, entire nerve through piriformis

Pudendal nerve
- Emerges from the greater sciatic foramen below piriformis, medial to sciatic nerve
- Winds over scarospinous ligament  re-enters pelvis via lesser sciatic foramen  enters pudendal canal (Aclock’s canal) in the obturator
fascia on the lateral wall of the ischiorectal fossa together with the int. pudendal vessels  gives of 3 branches
 Inferior rectal nerve
 Perineal nerve
 Dorsal nerve of penis

Gluteal medius
- Supplied by superior gluteal nerve, causes abduction and medial rotation of hip joint
- Causes of weakness: Nerve (sup. gluteal neuropathy, L5 radiculopathy), muscle (myopathy, tendon rupture), bone (AVN, NOF#, coxa vara)

Popliteal fossa
- Boundaries: superiorly by the tendons of the biceps femoris laterally, semi-membranosus/tendinosus medially; inferiorly by the 2 heads of the
gastrocnemius
- Roof is by skin and superficial fascia; the floor is covered by the popliteus muscle covering the tibia
- Contents: sciatic nerve dividing into the tibial and common peroneal nerve, popliteal vein & artery, lymph nodes (drains lateral aspect of the leg
& foot)  Popliteal artery the deepest structure & the nerves are the most superficial
- Causes of swelling:
 Skin & subcutaneous tissue: sebaceous cyst & lipoma
37
  Vessels: popliteal aneurysm, dilated veins at saphenopopliteal junction, DVT
 Cyst: popliteal cyst (enlargement of bursa), baker’s cyst (below knee joint, deep to gastrocnemius a/w degenerative changes)

3. Genitourinary Tract
a. Identify the bladder
i. blood supply, identify the iliac artery superior & inferior vesical artery (br. of int. iliac artery)
ii. muscles of the bladder detrusor muscles
iii. innervation of the detrusor muscle: hypogastric nerve (T10-L2) & pelvic splanchnic (S2-4)
iv. Most common cancer (2 types): TCC, SCC
v. What is transitional epithelium and where can it be found?
vi. Orientate the bladder, identify posterior structure
vii. Relations of the peritoneum to bladder
b. Identify the ureter
i. How does it enter the bladder
ii. Identify the opening of the ureter on the inner surface of the bladder
c. Layers encountered when performing SPC

Internal iliac artery

The common iliac artery bifurcates to its terminal branches when it is
crossed anteriorly by the ureters.
Posterior division
- Iliolumbar artery, lateral sacral artery, superior gluteal artery
Anterior division
- Obturator artery, inferior gluteal artery, umbilical artery (gives artery
to vas deferens & superior vesical artery), uterine & vaginal artery,
inferior vesical artery, middle rectal artery, internal pudendal artery

Transitional epithelium are epithelial cells that varies with stretching; at

rest they are cuboidal and flatten outs when stretched. They can be found
in the renal pelvis, ureters, urinary bladder and the superior urethra

Ureters
Blood supply: superior: ureteric branch of renal artery; middle: aorta,
gonadal & iliac vessels; inferior: superior vesical & gonadal artery
Course: arises from the renal pelvis  descends on the psoas adj. to tip
of transverse processes  passes over genitofemoral nerve & gonadal
vessels  crosses the pelvic brim and descends into pelvis  turns
medially at level of ischial spine  enters bladder inferiolaterally

PATHOLOGY
4. Rheumatic heart disease
a. Diagnosis from the clinical vignette? – previous rheumatic fever with rheumatic heart disease
b. Pathophysiology of rheumatic heart disease
c. What do you expect to see macroscopically
d. Post valve replacement – anticoagulation used
e. Types of common anticoagulation & their MOA
f. Clotting factors that are vitamin K dependent? Factor II, VII, IX, X & Protein C and S
g. Reversal of warfarin? Vitamin K
h. Urgent reversal of warfarin toxicity? FFP
i. Now patient presents with fever, likely cause? Infective endocarditis
j. Signs in the hands? Pathophysiology of Osler nodes & Janeway lesions
k. Why are patients with rheumatic heart disease or valvular replacement more susceptible to IE?
l. Features to look for in 2DE?
m. If you see right sided vegetations, what aspect of history do you need to ask the patient?
n. Treatment of IE
Rheumatic heart disease
It is a form of cardiac inflammation and scarring triggered by an autoimmune reaction to infection with Group A streptococci.
Pathophysiology:
- Rheumatic fever is a late inflammatory, non-suppurative complication of pharyngitis that is caused by group A-haemolytic streptococci
- Molecular mimicry, a Type II hypersensitivity reaction occurs in RHD, where antibodies cross react with bacterial M proteins
- Symptom onset is usually 1-3 weeks after the onset of streptococcal pharyngitis.

Gross findings
- Acute phase: valvular vegetations (verrucae) along the lines of closure, having little effect on cardiac function
- Chronic phase: commissural fibrosis, valve thickening, and calcification + shortened and fused chordae tendinae  fish mouth deformity

38
Microscopic findings
- Aschoff bodies, a form of granulomatous inflammation which consists of a central zone of degenerating extracellular matrix infiltrated by
lymphocytes, plasma cells and Anitschkow cells (activated macrophages also termed as caterpillar cells due to wavy nuclear outlines)
- These Aschoff bodies can be found in all 3 layers of the heart – pericardium, myocardium or endocardium

Modified Jones Criteria

Used for the diagnosis of rheumatic fever, the diagnosis can be made with 2 major criteria or 1 major + 2 minor criteria in presence of evidence of
streptococcal infection: elevated/rising Antistreptolysin O or DNAse, Strep group A throat culture
- Major criteria (JONES)
 Joints – polyarthritis usually involving large joints starting in the legs and migrating upwards
 Carditis
 Subcutaneous Nodules – painless, firm nodules over bones/tendons on the wrist, elbows and knees
 Erythema marginatum – nonpruritic, painless, serpiginous, erythematous eruption on the trunk.
 Syndenham’s chorea
- Minor criteria (5 criteria but 6 P’s)
 Pyrexia, Past history, Polyarthralgia, Phase reactant *, PR prolongation
*
Acute phase reactants include that of ESR/CRP/leuckocytosis

MOA of Anticoagulation
Warfarin: inhibits vitamin K epoxide reductase, preventing the reduction of vitamin K epoxide to vitamin K; thereby inhibiting the vitamin K
dependent carboxylation of the glutamic acid of the precursor clotting factors 2, 7, 9 & 10.
Heparin: augments the activity of antithrombin III (AT), inactivating thrombin (factor II) and factor X
Rivaroxaban: Factor Xa inhibitor preventing the formation of thrombin
Dabigatran: direct thrombin inhibitor

Warfarin Reversal
- Assess bleeding risk/active bleeding
- Determine cause of raised INR
- Reversal agents:
 Vitamin K1
 Immediate reversal with PCC is preferred over FFP
 PCC (Prothrombin complex concentrates): factor II, IX, X and low levels of VI
 FFP: all clotting factors, fibrinogen, protein C & S, antithrombin III
 Cryoprecipitate: factor VIII, XIII, fibrinogen, vWF

Infective Endocarditis
Types of IE
- Native valve endocarditis (NVE)
 Subacute: α-hemolytic streptococci or enterococci
 Acute: S aureus and group B streptococci
- Prosthetic valve endocarditis (PVE)
 Early (≤60 days): S. aureus and coagulase-negative staphylococci
 Late (>60 days): Streptococci and S. aureus, followed by coagulase negative staphylococci and enterococci
- IVDA

Diagnosis (Modified Duke Criteria)

Involves fulfilling 2 major criteria, 1 major + 3 minor criteria, 5 minor criteria
- Major criteria
 Positive blood cultures with typical microorganism consistent with IE: 2 separate cultures, or 2 cultures drawn >12 hours apart, all of 3 or
a majority of 4 (with 1st and last sample drawn 1 hour apart)
 Typical organism: S. viridians, S. bovis, S. aureus, enterococci, HACEK group
 Evidence of endocardial involvement on 2DE
 Oscillating intra-cardiac mass on valve/supporting mass, or in the path of regurgitant jets OR
 Myocardial abscess OR new partial dehiscence of prosthetic valve OR new-onset valvular regurgitation
- Minor criteria (5 P’s)
 Predisposing risk factor
 Pyrexia
 Vascular Phenomenon: emboli, pulmonary infarcts, mycotic aneurysm, intracranial/conjunctival haemorrhage, Janeway lesion
 Immunological Phenomenon: GN, Osler nodes, Roth spot
 Positive culture not meeting major criteria with organism consistent with IE

Janeway lesions arises from septic microembolism

Osler nodes are caused by deposition of immune complexes
Splinter haemorrhages are caused by engorgement of capillaries under the nail, potential mechanism include vasospam & embolic events
Features in 2DE: vegetation, myocardial abscess, valve perforation, valve dehiscence

Management of IE
- General measures e.g. oxygen therapy, heart failure management
- Antimicrobial therapy
 IV Penicillin G 12-18 million U/day Q4H for 4 weeks OR IV Ceftriaxone 2g/day + IV Gentamicin 1mg/kg Q8H for 1st 2 weeks
 For penicillin allergy, IV Vancomycin 30mg/kg/day in 2 divided doses  for vancomycin check trough keep levels 15-20 mcg/ml
 PVE: Vancomycin 30mg/kg/day OR gentamicin + Rifampicin for 4-6 weeks

39
  Rifampin is necessary in treating individuals with PVE or other foreign bodies as it can penetrate the most biofilm
- Surgical intervention
 CCF refractory to medical therapy
 Fungal IE
 Failed medical therapy
 Persistent sepsis after 72hrs of appropriate antibiotics
 Recurrent septic emboli after 2 weeks of antibiotic treatment
 Valvular complications e.g. valvular abscess, valvular obstruction
 Ruptured aneurysm of the sinus of Valsalva

5. PUD and PTH

a. Review history & lab results, what do you think caused the patient’s PUD? H pylori infection (CLO test +ve)
b. Other contributory factors? Hypercalcaemia
c. What is CLO test?
d. What is an ulcer? An erosion/breach on epithelial surface such as skin or mucous membranes
e. Treatment for H pylori infection?
f. Review laboratory results, what is the cause of this patient’s hypercalcaemia? 1° hyperparathyroidism
g. Most likely cause?
h. What investigation would you do? Bloods, Sestamibi scan
i. You see a prominent spot on the Sestamibi scan, what would you do? Offer parathyroidectomy
j. Where do you expect to find the parathyroid glands
k. Why can the inferior parathyroid gland be found near/with the thymus?
l. FS report: hypertrophy of one parathyroid gland with primarily chief cells, others show involution
m. What is a frozen section and how is the specimen fixed on a FS? Frozen section is a pathological laboratory procedure
used to perform rapid microscopic analysis of specimens. It is fixed in a gel like medium OCT (optimal cutting temperature compound)

CLO test (Campylobacter-like Organism Test) is a rapid diagnostic test for the diagnosis of H. pylori infection. Antral biopsies are obtained, and
based on the ability of H. pylori to secrete urease which catalyses the conversion of urea to ammonia, the mucosa obtained is placed into a medium
containing urea and a medium e.g. phenol red, which changes from yellow to red in an alkali environment.

Triple Therapy: Amoxicillin 1g BD + Clarithromycin 500mg BD + PPI (omeprazole 20mg BD OR esomeprazole 40mg OM) x 10-14 days
followed by PPI for 6 weeks (Metronidazole 500mg BD can be substituted for amoxicillin in penicillin allergy)

Quadruple Therapy: PPI + Bismuth (525mg QDS) + Metronidazole 250mg QDS + Tetracycline 500mg QDS; it is an appropriate initial treatment
in areas with metronidazole/clarithromycin resistance of ≥15%

Endocrine disorders in H. pylori infection

Autoimmune thyroid diseases, Autoimmune atrophic thyroiditis. Hashimoto’s thyroiditis
Thyroid mucosal associated lymphocyte tissue (MALT) lymphoma
Diabetes mellitus, Dyslipidemia, Obesity
Osteoporosis, Primary hyperparathyroidism

Hyperparathyroidism
Hyperparathyroidism Primary Secondary Tertiary
Serum Calcium ↑ ↓/Normal ↑
Serum Phosphate ↓ ↑/Normal ↑
PTH ↑ ↑ ↑↑

Primary hyperparathyroidism
Causes: 85% are caused by solitary adenoma, 15% are due to multiple glands i.e. multiple adenoma OR hyperplasia; rarely due to parathyroid
carcinoma. Consider MEN I & IIA syndrome.
Presentation
- Skeletal: bone/joint pain, pseudogout and chondrocalcinosis
- GI: anorexia, abdominal pain, PUD, pancreatitis, constipation
- Renal: polyuria, renal stones
- Neuro: myopathy, fatigability, mood changes (depression)
- CVS: bradycardia, shortened QT interval

Diagnosis: bloods (UE, phosphate, intact PTH), urine calcium (to ddx 1° hyperparathyroid from FHH (familial hypocalciuric hypercalcemia)
Localization: Technetium-99m Sestamibi scan, intra-operative PTH monitoring

Parathyroid gland
The superior parathyroid usually lies at the posterolateral aspect of the superior pole of the thyroid, above the level at which the inferior thyroid
artery crosses the RLN. The inferior parathyroid has a more variable location, most commonly below the inferior thyroid artery near the lower pole
of the thyroid OR within 1cm of the lower pole of the thyroid gland

Embryologically, the superior parathyroid arises from the 4th pharyngeal pouch; where else the inferior parathyroid gland develops from the 3rd
pharyngeal pouch together with the thymus. As the thymus descends, the parathyroid is dragged down towards the mediastinum; hence they inferior
parathyroid can be found anywhere along the thyrothymic tract.

40
(N.B. thymus develops from ventral part of the 3rd pharyngeal pouch; the inf. parathyroid develops from the dorsal part)

CRITICAL CARE
6. Massive transfusion
a. Patient in ED with suspected leaking AAA s/p emergency repair, post-op Hb 6, temperature 35°c
b. What is hypothermia? Core temperature <35°c – best measured with rectal/bladder probe
c. What are the contributions to hypothermia in this case?
d. What are the mechanisms by which you can lose heat?
e. Complications of massive transfusion
f. How would you correct coagulopathy? Platelets and FFP in 1:1:1 ratio, tranexamic acid
Contributions to hypothermia in this patient
- Circulatory shock: reduced tissue perfusion  reduced cellular metabolism
- Massive transfusion and resuscitation with unwarmed fluids
- Prolonged open surgery and blunting of thermoregulatory response due to anaesthetic agents

Mechanism of heat loss from the body:

- Evaporation and conduction from the skin
- Convection from skin due to air movement & from the lungs
- Radiation from naked skin

Transfusion reaction
IMMUNE-MEDIATED MASSIVE TRANSFUSION GENERAL
Acute haemolytic reaction Citrate toxicity DIC
- Signs: fever, hypotension, flushing, Dilutional coagulopathy Infection, bacterial sepsis
wheezing, red-coloured urine Hyperkalaemia Thrombophlebitis
- Antibody mediated: discontinue Hypocalcaemia (from citrate binding)
transfusion, prophylactic dopamine + Fe2+ overload
vigorous fluid resuscitation, osmotic Hypothermia
diuresis with 20% mannitol, treat DIVC Thrombocytopaenia
- Non-antibody mediated: diuresis with Metabolic acidosis
NaCl until the intense red colour of Fluid overload & CCF
haemoglobinuria ceases
Non-haemolytic febrile reaction
Delayed haemolytic febrile reaction
GVHD
TRALI
- Signs: SOB, hypoxemia, rales without
signs of cardiogenic pulmonary oedema
- Discontinue transfusion, supportive
measures, diuresis not indicated, no
evidence exists that steroids/anti-
histamines are beneficial
Allergic reaction
- Diphenyhydramine to relieve pruritus +
steroids (IV/oral depending on severity of
reaction)
Anaphylaxis
- SC epinephrine (N.B. no evidence for the
use of steroids in acute anaphylaxis)

7. Obstructive jaundice
a. Read and interpret the lab results: obstructive jaundice
b. What is bilirubin conjugated to? Bilirubin is conjugated with glucuronic acid by the enzyme glucuronyltransferase
c. What is urobilinogen? Colourless by-product of bilirubin, formed by the metabolism of bilirubin by colonic bacteria
d. Explain the enterohepatic circulation of bile salts
e. Explain the function of bile salts in the digestion of fats. Emulsification of lipid droplets via the formation of micelles
which increases the surface area for pancreatic lipases to act on.
f. What investigation would you do for this patient? Blood, US HBS
g. If US HBS shows stones  ERCP
h. If this patient has fever and pain, what would your concerns be? Ascending cholangitis

Heme metabolism

41
Unconjugated bilirubin
Haemoglobin is broken down to heme and globin parts. The
heme is then turned into unconjugated bilirubin in the spleen.
Unconjugated bilirubin is not soluble in water, and is bound to
albumin to be transported to the liver.

Conjugated bilirubin
Bilirubin is conjugated with glucuronic acid by the enzyme
glucuronyltransferase, in the liver. It goes to the bile and out
into the small intestine. 95% of the secreted bilirubin is
reabsorbed by in the terminal Ileum, reaches the liver by portal
circulation and then resecreted.

About half of the conjugated bilirubin remaining in the large

intestine (about 5% of what was originally secreted) is
metabolised by colonic bacteria to form urobilinogen, which
may be further oxidized to urobilin and stercobilin which give
faeces its brown colour. Some of the urobilinogen is reabsorbed
and 95% of what is reabsorbed is resecreted in the bile which is
also part of enterohepatic circulation. A small amount of the
reabsorbed urobilinogen (about 5%) is excreted in the urine
following further oxidation to urobilin which gives urine its
characteristic yellow colour. This whole process results in only
1–20% of secreted bile being lost in the feces. The amount lost
depends on the secretion rate of bile.

Urine
When biliary drainage is blocked, some conjugated bilirubin leaks out of the hepatocytes and appears in the urine, turning it dark amber.
However, in disorders involving haemolytic anaemia, there is an increase in the amount of unconjugated bilirubin in the blood. Because the
unconjugated bilirubin is not water-soluble, one will not see an increase in bilirubin in the urine. As there is no problem with the liver or bile
systems, this excess unconjugated bilirubin will go through all of the normal processing mechanisms that occur and will show up as an increase in
urine urobilinogen.

Enterohepatic circulation of bile

The enterohepatic refers to the recirculation of bile acid. Primary conjugated bile or “bile salt” travels to the gallbladder during the interdigestive
phase for storage and to the duodenum via the CBD during digestion. 95% of the secreted bile acids are reabsorbed predominantly in the terminal
ileum, and transported back to the liver via the portal circulation. The remaining 5% of bile acids are altered by bacterial flora and become insoluble,
and thus excreted. The net effect of this recycling process is that each bile salt molecule gets reused about 20 times.

8. Fluid overload
a. Read and interpret the anaesthetic records, what can you tell when about the patient when he was
discharged from anaesthesia recover? still hypertensive and tachycardic
b. Comment on the fluid status: received 5 unit NaCl and 2 unit colloid in 12 hrs with poor urine output, likely fluid overload, too
much electrolytes (sodium) given as well (all crystalloids were normal saline)
c. Comment on the CXR: fluid overload with bilateral congestion in all lung fields and pleural effusion
d. Management of this condition? ABC, lasix, asked for another drug besides Lasix
e. How do you think you can prevent this poor management from occurring again? Report to hospital incident
reporting system, better training of junior staff

Management of cardiogenic pulmonary oedema

Address ABCs of resuscitation
Ventilatory support: consider non-invasive ventilation in severe APO (CPAP preferred for cardiogenic pulmonary oedema)
Medical management:
1) Preload reduction – nitrates e.g. GTN (caution in hypotension), diuretic, IV morphine sulphate
2) After load reduction – ACE inhibitor e.g. enalapril 1.25mg IV or captopril 25mg sublingual; ARB
3) Ionotropic support – Dobutamine ideal for cardiogenic shock; Dopamine (5-10mcg/kg/min for stimulation of β-receptors)

PROCEDURAL SKILLS
9. FNAC
a. Greet intro explain reconfirm indication and consent, site and side
b. Steps: sharps handling, fix specimen onto slide, put the rest into cytospin bottle; explain to patient follow up plan
c. Patient asks if this is likely to be cancer (has previous history of melanoma in the same limb)

10. Suturing
a. Tie with non-absorbable braided suture (hand tie); what are the types of knots you know?
b. What are the advantages of a braided suture?
c. Tie a hook in a cavity with absorbable braided suture (hand tie); what are the potential complications
when tying a knot in a cavity?

42
 d. Overrun a bleeding spot with a figure of 8 suture with a non-absorbable monofilament (instrument tie);
why do you have to tie prolene so many times?

PHYSICAL EXAMINATION
11. Respi exam (COPD)
a. For elective hernia repair now for pre-op review, chronic smoker
i. Findings: mild clubbing, palmar erythema, barrel chested chest, with scatter coarse crepitations, no rhonchi  diagnosis COPD
b. Operative considerations? Refer Anaesthesia, Respiratory, manage COPD first, advise smoking cessation, consider further
investigations, cannot do laparoscopic hernia repair

12. Arterial exam

a. LL vascular exam: left foot previous 2nd rays, 4/5th toe dry gangrene, absent DP/TP, Buerger's +ve
b. What else would you like to do? ABPI, Doppler of LL pulses, examine abdomen and CVS
c. What are you looking for when examining the abdomen and CVS systems?
d. Diagnosis? Critical limb ischaemia (c/o pain at rest when I asked before examining + tissue loss)
e. Basis of Buerger’s test: holding up the leg for a minute induces an ischaemic environment, when the patient hangs the leg over the
side of the bed, there is dependent rubor secondary to reactive hyperaemia as result of autonomic stimulation due to the increased acidity
in an ischaemic environment

13. Neuro exam (LL)

a. LBP radiating down bilateral LL + numbness
i.Tenderness over L4/5 L5/S1 region with para vertebral spasm, no other signs, sensation normal
ii.Differential diagnosis: spinal stenosis vs. vascular claudication
b. Pathophysiology of pain in spinal tenderness? Stenosis causing ischemia of the cord
c. Investigations & Management

14. Scrotal exam

a. Left hydrocele with enlarged testis
i. What else would you like to examine? Abdomen looking for enlarged masses e.g. renal mass
ii. Other differentials? Hernia, varicocele
b. Investigations
i. US shows hydrocele & enlarged testis, differentials? Testicular tumour
ii. US only shows hydrocele, management? Jaboulay’s procedure or Lord’s plication

COMMUNICATIONS
15. Angry patient
a. Son bib father earlier with fall from height resulting in splenic rupture now in ot for splenectomy, now
speak to angry mother who just arrived
b. Why no consent from mother, what are the complications of splenectomy, deal with complaint about
incompetent husband, 'was he drunk???', future considerations of splenectomy

16. Update trauma consultant

a. Young gentleman RTA with right tib/fib open fracture now right LL pulseless and cold, FAST for
abdomen ?some collection but otherwise stable, left hand metacarpal fractures: Basically just update on issues,
prioritize and give your plan

HISTORY TAKING
17. SOB
a. POD5 THR now complaining of SOB, take full SOB history
i. Acute onset with haemoptysis and pleuritic chest pain
b. Differentials? PE, Pneumonia, TRO ACS
c. Investigation & Management

18. PR bleeding
a. PR bleeding (?melenic stools) x many months
b. Differential diagnosis
c. Investigation  colonoscopy showed sigmoid CA, management

43
Sheffield Feb 2014
PROCEDURAL SKILLS
1. FNAC
a. History of excision for melanoma; patient asked if it is a recurrence?
Minimal fluid from 'cystic lesion' on aspiration, did all I could to smear on slides and tell the examiner to cytospin the others.

2. Surgical ties
a. Hand tie to oppose rubber bands with nonabsorbable braided
b. Hand tie hook in 'cavity' with absorbable braided, what hand tie method you just used? (told examiner my
'granny knot' cause I feel that it holds better, but alternatively I can surgeon's knot)
c. What to do so that you will not damage deep structures on tying knots?
d. Stitch fake skin/sponge with nonabsorbable monofilament. How many throws did you do?

PHYSICAL EXAMINATION
3. Cranial Nerves
Cranial nerves (anosmia) stem: NOT required to test visual acuity or smell. Turns out bitemporal hemianopia
a. Causes, Ix (bld, scans), Mx

Causes: pituitary adenoma, craniopharyngioma (brain tumour derived from the pituitary stalk)
Investigations
- Laboratory (Anterior Pit. – GH, TSH, ACTH, FH/LH, PRL; Posterior Pit. – ADH, oxytocin)
 Prolactin
 GH abnormalities: GH, IGF-1, OGTT
 Cushing’s disease: 24h urine cortisol, 8am serum cortisol, dexamethasone suppression test, serum ACTH
 TSH, T3/4, LH/FSH
- Imaging: MRI pituitary gland
Management
- Medical: dopamine agonist for prolactinoma e.g. bromocriptine, cabergoline; somatostatin analogue for acromegaly e.g. octreotide;
replacement therapy
- Surgery via transsphenoidal vs. transnasal endoscopic approach

4. Parastomal hernia
a. Short history of T3N2 low rectal CA s/p APR years ago now presenting with abdominal pain (Do not open the
stoma bag – asked by patient and examiner)
b. How to treat parastomal hernia, what are the principles of repair? Why is mesh not encouraged here?
c. Investigations: Need TRO recurrence, tumor marker trend, colonoscope, CT scan
d. Whether will recommend surgical resection (depends on staging if really recurrence)

Parastomal hernia
It is a type of incisional hernia that occurs at the site of the stoma or immediately adjacent to the stoma.
Risk factors
- Patient: age, wound infection, ↑ intra-abdominal pressure, COPD, obesity, weight gain after ostomy construction, malnutrition, glucocorticoids,
immunosuppression, malignancy, and IBD
- Technical: emergency stoma creation, surgical technique for ostomy construction, abdominal wall strength

Management
- Conservative management e.g. with stoma belt (surgical repair is avoided due to the high rates of recurrences)
- Indications for repair: IO 2° incarcerated hernia
 Relocation of stoma
 Primary repair of fascia defect – generally avoided as it creates tension on the repair, which leads to a high rate of recurrence
 Onlay mesh repair – technically straightforward, slightly higher recurrence rates compared to sublay approach, increased risk of wound
and mesh infection
 Sublay mesh repair (intra-abdominal repair)
 Reduction of hernia contents into the abdominal cavity
 Closure of fascial defect by securing a piece of mesh under the defect with wide overlap onto the normal abdominal wall

5. Submandibular gland swelling

a. Asked the patient whether there was pain over the swelling? He answered: no swelling
b. Examined, bimanual palpation, frenulum checked, cervical nodes, nothing felt
c. Examiner looked puzzled but proceed with DDX, Ix and Mx (tricked me, keep asking what other XR, I asked for other
than sialography, but the answer she wanted was CT SCAN)
d. If painful, need TRO malignancy
e. Need full ENT examination if suspected lymphadenopathy

44
DDX: Parenchymal vs. non-parenchymal swelling
Parenchymal Non-parenchymal
Neoplastic (Benign vs. Malignant) Lymph node
Pleomorphic adenoma, adenoid cystic carcinoma, lymphoma, Skin & soft tissue swelling: lipoma, sebaceous cyst
leukaemia, metastasis
Stones: Sialolithiasis
Infection: Sialadenitis
Infiltrative: Sarcoidosis
Systemic Disease: acromegaly, DM
Imaging: can consider CT scan with simultaneous sialography

6. Abdominal exam
POD6 elective left hemicolectomy for CA, now has abdominal pain & BNO 1day (actor actually looked septic!)
Given charts: rising temperature, rising PR, BP sliding down slowly, O2 requirements rising to maintain SpO2
Given blds: TW raised, Hb normal, CRP raised, Urea Creatinine on the rise; Given ECG: AF
Physical findings: left sided tenderness, localized guarding and rebound, otherwise soft, no generalized peritonism, not distended, BS present, radial
pulse not in AF (haha.. examiner ask to ignore radial pulse), pt in TEDS stockings
Diagnosis & management: anastomotic leak; NBM, abx, drip, IDC, KIV NG tube if starts vomiting, CXR, CT AP with contrast, CT PA
(TRO PE as cause for AF and increasing O2 requirements)

Signs of anastomotic leak:

- Usually presents on POD 7-10
- Low grade fever usually the first sign
- New onset tachycardia or arrhythmia (usu. AF)
- Signs of sepsis e.g. raised inflammatory markers
- Abdominal pain (can be localized in a contained leak); or peritonism
- Cardiac, respiratory and renal impairment/failure

Factors contributing to anastomotic leakage

- Systemic factors: anaemia, DM, malnutrition (hypoalbuminemia), vitamin deficiencies, steroids
- Localized factors: irradiated bowel, diseased bowel, poor surgical technique, haematoma formation at anastomotic site

COMMUNICATIONS
7. Crying mother
11 y/o perforated appendicitis, severely dehydrated, resuscitating now (anaesthesia/paeds on board), consultant coming back to do the surgery
a. Mother concerned about surgery and risks
i. Apparently the father/husband, had oesophagectomy 2yrs ago by Mr Mann, post-op leak, and died
ii. Started blaming herself for working extra-time and leaving kid to neighbour, think she could had brought kid in earlier

8. Call for Transfer of Care

RTA, young man, widened mediastinum on CXR and bilateral hemothorax, right femur #, GCS 14 BP 100/60 PR 102 SpO2 stable.
- Call CTS consultant for transfer
- Called misleading written phone number, nonstop blowing history and presentation for 1min before the girl on the phone asked: 'Are u ok, this
is the HR dept..' Ran out to seek help STAT
- CTS consultant: OK, can transfer, who will be accompanying pt? I said, 'Me'.
- Consultant asked: 'You sure you OK? What if need to intubate the pt? You comfortable?'
- Naturally, I went, 'No problem, I can intubate the pt if necessary.' The consultant, 'You sound very experienced!'
- No shit... I immediately, 'I will ask anesthesia colleagues to come along with me.....'

ANATOMY
9. Lower Limb
a. Femoral triangle: Boundaries, contents, identify muscles and femoral vessels
b. Boundaries of femoral canal, what's the importance (lymphatics)
c. Branches of femoral nerve? Identify L1, L2, L3 dematomes (KL 2014, 3)
d. Look at the provided LL angiogram, which one is SFA? What are the 3 branches?
Femoral triangle
- Boundaries: inguinal ligament superiorly, adductor longus medially and sartorius laterally
- Floor: iliacus, psoas major, pectineus & adductor longus
- Roof: Skin, superficial fascia, superficial inguinal LN, deep fascia of thigh (fascia lata), pierced by GSV & lymphatics at saphenous opening
- Contents (NAVEL)
 Femoral nerve
 Femoral artery – gives off the profunda femoris laterally The femoral sheath, a prolongation of the fascia derived from the
 Femoral vein – GSV drains into the vein within the triangle transversus fascia anteriorly & fascia over the iliacus posteriorly,
contains ONLY femoral artery + vein + femoral canal
 Femoral canal with deep inguinal LN

Femoral canal:
- Boundaries: anteriorly inguinal ligament, posteriorly pectineal ligament, medially lacunar ligament (±abnormal obturator artery), laterally the
femoral vein

45
- Contents: Cloquet’s node which serves as a lymphatic pathway for the LL to external iliac nodes
- Clinical significant: dead space allows for expansion of distended femoral veins & contains the intra-abdominal contents in femoral hernia

10. H&N
a. Identify mandible + muscles of mastication
b. C-spine lateral XR shown: Identify C1 structure
c. Skull, foramen ovale and structures, Stylomastoid foramen and structure (what happens if cut)
d. At what age is the mastoid developed?
e. Pterion and bones that form it, why EDH with trauma
f. Skull XR: identify coronoid suture, what condition gives lytic skull lesions? Point to pituitary fossa

Muscles of mastication – supplied by mandibular nerve V3

Muscle Attachments Actions
Masseter Superficial & deep origination from the zygomatic arch & Elevates the mandible and protrudes mandible
inserts into ramus of mandible
Temporalis Originates from temporal fossa and inserts into coronoid Elevates and retracts the mandible
process of mandible
Medial pterygoid Deep head from lateral pterygoid plate, supf. head from Bilaterally: elevates and protrudes the jaw
maxillary tuberosity & pyramidal process of palantine Unilateral and alternate movement: side to side movement
bone; inserts into the ramus of the mandible near the angle
of mandible
Lateral pterygoid Sup. head from the greater wing of sphenoid, inf. head Bilaterally: protrudes the jaw
from the lat. pterygoid plate; inserts to neck of mandible Unilateral and alternate movement: side to side movement

Stylomastoid foramen: transmits the facial nerve &

stylomastoid artery
Facial nerve branches
- Intra-cranial: Greater petrosal nerve, Nerve to stapedius,
chorda tympani
- Extra-cranial: Posterior auricular, nerve to posterior
belly of digastric & stylohyoid, major facial branches
Course of facial nerve
- Arises from the pons and travels through the IAM
(petrous part of temporal bone)
- The nerve leaves the IAM and enters the facial canal
where the nerve forms the geniculate ganglion and then
gives rise to its intracranial branches.
- It exits the facial canal via the stylomastoid foramen
- After exiting the skull it gives off the posterior auricular
nerve, then the nerve to digastric and stylohyoid
muscles before piercing the parotid gland to give off the
facial branches

Mastoid air cell development:

- Pneumatized cells are believed to appear on 22-24th
week of foetal life
- Pneumatization of the mastoid cells occurs at the 33rd
week and reaches adult size on the 35th week
- This continues up to 8-9 years old

EDH
Occur at the pterion comprising of frontal, parietal, temporal and sphenoid bone. It is the weakest part of the skull where the middle meningeal artery
runs underneath.

Lytic bone lesion in the skull: Paget disease, multiple myeloma, metastasis, OM

11. Thorax & Thyroid

a. Prosection of thorax to jaw; show aortic arch, brachiocephalic art/L common carotid/L subclavian, vagus,
recurrent laryngeal (KL Feb 2014)
b. Thyroid, blood supply, nerves damaged (Coventry May 2014 Q8), physiological response to thyroidectomy
c. Embrylogy of thyroid, formation of thyroglossal cyst
d. Parathyroids and PTH function
e. Brachial plexus, Erb and Klumpke's palsy (KL Feb 2014, 2 Q3)
Thyroid embryology
- Appears as epithelial proliferation at the base of the tongue at the foramen caecum at 3-4 weeks of gestation
- It then descends in front of the pharyngeal gut via the thyroglossal duct
- It eventually migrates to the base of the neck, anterior to the hyoid bone
- Thyroglossal cyst occurs due to the failure of the thyroglossal to involute

46
Parathyroid
Location & embryology (see KL Feb 2014, 3 Q5)
Arterial supply: both inferior and superior parathyroid are supplied by the inferior thyroid artery
Venous drainage: superior, middle &inferior thyroid veins
Histology: chief cells which secretes PTH and oxyphil cells are of unknown function

Calcium haemostasis
Hormone Function Stimulators Inhibitors
Parathyroid Overall ↑ Ca2+ and ↓PO43- Decreased Ca2+ Increased Ca2+
Bone: increases bone resorption by stimulating osteoclast Increased PO43- Severe decrease in Mg2+
Kidney: Increases reabsorption of Ca2+ and Mg2+, increases excretion Activated Vitamin D
of PO43- in the PCT. Increase production of activated vitamin D in the (calcitriol)
kidneys, PTH upregulates the enzyme 1-α-hydroxylase
Vitamin D Overall ↑Ca2+ and ↑PO43— PTH
Bone: increases bone resorption by stimulating osteoclast Decreased PO43-
Gut: increases absorption of Ca2+ and PO43-
Kidney: increase reabsorption of Ca2+ and PO43-
N.B. Vit D inhibits PTH production via negative feedback
Calcitonin Not physiologically significant except in hypercalcaemia Increased Ca2+
Bone: decreases bone resorption by inhibiting osteoclastic activity

CRITICAL CARE
12. Respiratory failure
Post-op given morphine, now in respiratory failure, RR 5/min, ABG hypercarbia, PaO2 normal (FiO2 0.6)
a. Respi drive, Mu receptors, Naloxone (KL Feb 2014, Q7)
b. Central and peripheral chemoreceptors for respi control (KL Feb 2014, Q7)
c. CO2 transport, carbonic anhydrase, place of conversion, Chloride shift (KL Feb 2014, 2, Q10)
d. Why respiratory acidosis but bicarb still normal? Kidneys take time to compensate
e. Further Mx: to HD, close monitor, KIV further doses of naloxone

13. Pneumoperitoneum
70+ presents with peritonism, confusion. Given: CXR pneumoperitoneum, ECG AF (need to say check name, IC, time and date of XR and ECG)
a. Causes of the above
b. Consent in confused patient: speak to family about pre-morbid wishes regarding surgery, any NOK
c. Consultant sign consent

Causes of pneumoperitoneum: perforated viscus, ischaemic bowel, after laparotomy/laparoscopy, peritoneal dialysis, Chilaiditi syndrome

14. Ruptured AAA

Ruptured AAA, lost 4L, hypothermic, in OT now
a. Why hypothermia, how to prevent? (KL Feb 2014, 3, Q6)
b. Why coagulopathy?
c. DIVC and blood products?
d. Early/Immediate complications of massive transfusion
e. Who to involve in care of pt? Hematologist (they're in charge of blood bank!)
DIVC
Characterized by activation of the coagulation pathway  consumptive coagulopathy, microvascular thrombi in various organs  MODS
Aetiology
- Infection
- Malignancy – lymphoproliferative and myeloproliferative cancers, adenocarcinoma
- Obstetric – Placenta abruption, amniotic fluid embolism, eclampsia
- Trauma – burns, MVA
- Transfusion – haemolytic reaction
- Others – liver disease, acute hepatic failure

Pathophysiology
- Pathological activation of the coagulation pathway due to cytokine release by damaged tissues
- This is followed by a pathological activation of the fibrinolytic pathway causing
 Diffuse intravascular thrombosis  small & large vessel occlusion by fibrin
 Vascular occlusion  shock  end organ dysfunction
 Bleeding  mucosal surfaces, petechial rash
 AKI, ARDS, hepatic dysfunction

Haematological findings: ↑D-dimer (fibrinogen degradation product), ↓ PLT, ↓ fibrinogen, prolonged aPTT/PT, reduction in clotting factors
Management
- Treat underlying cause
- Vitamin K for all cases

47
- Consider heparin if anti-thrombin ↓ (indicates on-going coagulation)
- Blood products to be given as below

Administration of blood products

- Platelets: indicated if <20 x 109 or if active bleeding with levels 20 – 50 x 100/L
- Coagulation factors: usage of FFP (cryoprecipitate/factor concentrates can worsen the coagulopathy)
- RBC: PCT may be used in severe haemolytic anaemia

Acute complications of massive transfusion

- Immune related: febrile non-haemolytic reaction, acute haemolytic reaction, allergy/anaphylaxis, TRALI, GVHD
- Specific to massive transfusion: coagulopathy, ↑K+, ↓Ca2+, fluid overload
- Others: bacterial septicaemia, air embolism

HISTORY TAKING
15. Thyroid swelling
Presents with thyroid swelling for 8 years now enlarging with toxic symptoms, what further investigations?

16. Abdominal pain

Abdominal pain, US at GP showed gallstones. Also c/o alternating BO habits, more diarrhoea (pt volunteered related to stress), no other red flags.
Prompted and prompted, the pt said husband lost job, now no $$
Examiner: further Ix?

PATHOLOGY
17. Rheumatic heart disease
Pt with aortic stenosis with history of joint pains at young age; has RHD, now replaced mechanical valve
a. Why on warfarin, mechanism of action, how to monitor (KL Feb 2014, 3, Q4)
b. Now prolonged fever likely IE; what stigmata on hands and what's the pathophysiology
c. Why abx not very effective, what micro-organisms, if tricuspid valve whether IVDU
d. What surgery may be performed? Valve replacement, valve repair, TAVI (transcatheter aortic valve implantation)
For prosthetic valve endocarditis, the organism involves forms biofilm on the infected device, which antibiotics have difficulty penetrating (noted
Rifampin is necessary to treat PVE as it can penetrate the biofilm of most organism)

Challenges in treating IE
Eradicating bacteria from fibrin-platelet thrombus is extremely difficult as
- There is a high concentration of organism present within the vegetation
- The organisms are located DEEP within the thrombus
- Interference of fibrin and white cells with antimicrobial action

18. PVD
Patient has history of DM, PVD, now came with black toe, shipyard worker
a. Risk factors of PVD? DM, HTN, HLD, CVA, smoking
b. Dry gangrene vs wet, what determines level of amputation
c. Patient returned with pleural effusion? Perform diagnostic pleural tap, examiner: mesothelioma (work exposure)
d. Then returned again with SOB, cough, LOW, said need TRO malignancy

Sheffield Feb 2014 (2)

COMMUNICATIONS
1. OGD & Barium swallow
Explain barium swallow result, address concerns; talk about the indications and risks of OGD, biopsy & dilatation.

2. Inform consultant about AOR

Some damn long history…i think like 10 pages of info. On top of that, your stem is like a FULL A4 sized page.
Anyway is POD 2 s/p R SMAC, patients daughter wants to AOR because she doesn't want to travel to and fro between the hospital and her own
house. Environment is not ideal because her husband and herself work as school teachers, and she stays with 2 teenage daughters. I think also got a
dog. She has convinced the mother to go home, although prior to this the mother was more keen to recover in hospital before going back home.

4 pages of labs are all normal -- but note these are all preop
Call your consultant to tell her about the situation.

Salient points -- 58 yr old Caucasia lady who is POD 2 R sentinel lymph node biopsy, then continued to perform SMAC. No intraop complications,
blood loss minimal. Postop D1 well, POD 2 developed SOB, mild tachycardia HR 95 and BP holding 135/90. Drain output 410mls (bloody) <-
30mls (serous). Axilla is also puffy.

Use the standard SBAR format, and update consultant as per how u would on a normal ward round.
Form to sign for AOR, offer to update the team's primary consultant.

"Is there any policy in the hospital that we can force her to stay in for treatment?"

48
Hmm. I said if she is mentally competent can sign AOR and we can't keep her unfortunately ( i dunno whether this is right). Then she asked, so is
the pt mentally competent? I said that i hadn't assessed formally, but noted from the notes that it seemed that she was.

HISTORY TAKING
3. PR bleeding
Lady comes in with 6/12 of PR bleed and change in bowel habits.
Examiner did not let me get past the differential diagnosis  DDX malignancy, polyps, diverticular disease, and haemorrhoids. I think they were
looking for IBD. Sigh.

4. Groin lump
Male patient presenting with right groin lump, symptomatic & affecting work (likely hernia); have been drinking some tonic thingy. Had previous
GU problem (think it's gonorrhea). Asked if he had slow stream but didn't have (was worried about urethral stricture)
a. How would you manage hernia?
b. What are your differentials: inguinal, femoral hernia, saphena varix, LN, femoral aneurysm. Examiner satisfied.
c. Approaches for repair of inguinal hernia? lap vs open.
d. Which would you recommend? Open: unilateral
e. Are you worried about the tonic Yes, I would like to know if these are steroid containing
f. Good, so he goes hypotensive after the op -- explain Addisonian crisis.
g. What is your management -- ABC, Fluids, hydrocortisone

5. Knee Pain
Patient presents with R knee pain for many years, recently has increasing pain.
A/w pain that wakes him up from sleep. Otherwise very mechanical. I asked if he had any previous medical issues -- He denied. But, if you elicit
enough history, then he will tell u he had injured his ligament before and had a washout done. Now affecting his work. Summarize your findings
a. What is your diagnosis?
b. What signs in the PE will you be looking for? FFD, swelling (bulge test), crepitations, intact collateral ligament
c. What other differentials? RA knee, gout flare, ligamentous instability.
d. Why do you say that secondary OA is your top differential?
e. How to investigate? Xrays (skyline, weight bearing AP/Lat), FBC, ESR, CRP. What else? MRI knee, uric acid.
f. Management?

PATHOLOGY
6. Gallbladder cancer
a. What is the most common histology for GB CA? adenocarcinoma (80-85%), SCC, sarcomas, lymphoma, melanoma
b. What are the risk factors? What is the most common risk factor in the UK? Usually arises from a setting of
chronic inflammation: cholesterol gallstones (75%), porcelain GB (10-25%), PSC, UC, liver flukes, chronic Salmonella typhi & paratyphi
(obesity contributing to gallstones most common cause in the UK)
c. What are the common routes of spread? Local invasion, lymphatics, haematological
d. Patient went for op, develops infection on POD2. What is the most likely offending organism? S. aureus
e. If there is minimal cellulitis, what is your management? Cover with antibiotics with regular wound dressing
f. Patient deteriorates and the wound is necrotic, what is your diagnosis? Necrotizing fasciitis
g. What is your treatment for that? Broad spectrum antibiotics (i said fortum, he seemed to agree), fluids and debridement
h. What are some the organisms responsible?
i. Postoperatively she recovers, but develops PR bleed. What are your 4 differential diagnoses? C diff,
ischemic bowel, stress ulcers. Really dunno, DIVC and coagulopathy is not correct. Infective colitis (Translocation of bacteria)
j. Look at the colonoscopy picture -- what do you see? Pseudomembranes
k. Mechanism of how C diff causes pseudomembranes? Exudative fibrin deposition as the bacteria secretes proteases to
damage the bowel mucosa.

Necrotizing Fasciitis
It is a rapid progressive infection of the fascia with necrosis of the subcutaneous tissues
Necrotizing fasciitis syndromes:
- Type I: Polymicrobial
- Type II: group A streptococcal
- Type III: gas gangrene, clostridial myonecrosis

Bacteria involved: Group A streptococcus (S. pyogenes), S. aureus, Clostridium, Bacteroides, E. coli, Pseudomonas, Proteus, Klebsiella
(variant of NF type I is saltwater necrotizing fasciitis caused by Vibrio species)

Presentation
Very atypical presentation
- Early: pain, cellulitis like picture, pyrexia, swelling/induration, ±skin anaesthesia, tachycardia
- Late: severe pain, purple/black discolouration, blistering, haemorrhagic bullae, crepitus, discharge of “dishwater” fluid

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Diagnostic tool (LRINEC – Laboratory Risk Indicator for Necrotizing Fasciitis)
3 groups: low risk (score low ≤ 5, <50% risk), moderate (score 6-7, 50-75% risk), and high risk (≥ 8, > 75% risk)
Parameters: CRP, WBC, Hb, Sodium, Creatinine, Glucose

Investigation
Laboratory: FBC, CRP, Procalcitonin, renal panel, ABG, urinanylsis, blood & tissue cultures
Imaging:
- Ultrasound – subcutaneous emphysema spreading along deep fascia, swelling, & increased echogenicity of the overlying fatty tissue with
interlacing fluid collections
- MRI – evidence of an inflammatory process infiltrating the fascial planes.
Finger test & biopsy: LA over suspected area  2cm incision down to deep fascia (can be done in A&E, ward or OT)
- Absence of blood flow
- Dirty “dishwater” fluid
- Discolouration of fat
- Minimal resistance on rapid finger sweep at the level of the fascia

Management
- Antibiotics: carbapenem/β-lactam-lactamase inhibitor PLUS clindamycin PLUS agent with activity to MRSA (e.g. vancomycin, daptomycin,
linezolid)
- Surgery: extensive wound debridement
 Surgical incisions should be deep and extend beyond the areas of necrosis until viable tissue is reached
 The entire necrotic area should be excised
 The wound should be well irrigated
 Haemostasis should be maintained, and the wound should be kept open
 Surgical debridement and evaluations should be repeated almost on a daily basis
 The wound should be inspected in the operating room

PR Bleed: Ischaemic colitis, infective colitis (C. difficile), stress ulcer (Curling’s ulcer), coagulopathy, other common causes of PR bleed

Mechanism of pseudomembrane formation: antibiotic usage alters gut flora allowing the proliferation of C. difficile, the pathogenic strain
produces toxins – Toxin A an enterotoxin & Toxin B a cytotoxin. These toxins bind to intestinal mucosa causing the formation of
pseudomembranes, a plaque-like adhesion of fibrinopurulent debris and muscus on damaged intestinal epithelium.

7. Medullary thyroid CA
Medullary thyroid CA: stains calcitonin +.
a. Asked you to fill up the pathology report.
b. What is it associated with? MEN2A and MEN2B
c. What are the other features, oncogene mutation and the mode of inheritance of MEN 2?
d. What would you like to exclude before operation? Phaeochromocytoma. Why? Labile BP, dangerous.
e. How do you do so? Urine VMA, Metanephrines. What else? I want a blood test.
f. Explain in layman terms what immunohisto chemical staining is.
MEN1 is autosomal dominant, mutation of MEN1 gene (menin) a tumour suppressor gene on chromosome 11 (11q3)
- Pituitary, parathyroid and pancreas (gastrinoma, insulinoma, vipoma, glucagonoma)
MEN2 is autosomal dominant, mutation of RET proto-oncogene on chromosome 10 (10q11.2)
- MEN2A: parathyroid, pheochromoytoma, medullary thyroid
- MEN2B: pheochromocytoma, medullary thyroid, mucosal neuroma, marfanoid

Pheochromocytoma (Rule of 10: 10% extra-renal/bilateral/malignant/in children/familial/not associated with HTN)

Clinical presentation: headache, sweating, palpitations
Laboratory test: 24h urinary creatinine, total catecholamines, vanillylmandelic acid, and metanephrines; fractionated plasma free metanephrine
Medical preparation pre-op:
- Required to prevent intra-operative hypertensive crisis, arrhythmias, multi-organ failure
- Combined α and β blockage – α blocker given 10-14 days before surgery, β blocker given 2-3 days before surgery

CRITICAL CARE
8. Fluid overload
Post-op hypertension, with desaturation and low urine output. (Asked to interpret the vitals chart and I/O chart).
Explained fluid overloaded cos net 5L + input.
a. What are your expected physical exam findings?
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 b. What investigations would you want to do? What are your expected findings? CXR, cardiac enzymes, ECG
c. Interpret this CXR: pulmonary edema ++, loss of cardiophrenic angle, cardiomegaly.
d. How will you manage this pt? (KL Feb 2014, 3, Q8)
e. Can you explain the patient's low urine output? What is the minimum urinary output?
f. What are some physiological causes for his low urine output postop?
g. Explain what are the fluids that have been given? Which are crystalloids, colloids.
h. What are the Na requirements in a patient? 1-1.5 mmol/kg/day
i. What are the K requirements in a patient? 1 mmol/kg/day
j. Can you give a few suggestions on how this situation can be prevented or detected earlier? Put patient in
HD?? (the examiner laughed). Times up. In retrospect -- maybe the answer he was looking for was CVP line insertion postop.

Low urine output in fluid overload:

- Low CO  decreased renal perfusion  decreased urine output (target is ≥0.5ml/kg/hr)
- During fluid overload, the LVEDV is high, this causes the interdigitation of actin and myosin in cardiac muscles to no longer overlap  further
worsening of the fluid status decreases SV and hence CO.
- ↓ in the renal perfusion is detected by the juxtaglomerular apparatus, this activates the RAAS, hence increasing fluid conservation
- Acute tubular necrosis 2° ischaemia
- Post-op fluid conservation:
 Increased secretion of cortisol and aldosterone (both have mineralocorticoid activity)
 ADH secretion from posterior pituitary

9. Post-thyroidectomy hypocalcaemia
Post total thyroidectomy with low Ca. All other bloods normal
a. Explain how Ca is carried in the body and which part is active (bound to albumin, ionized fraction is active)
b. Which hormones are involved in Ca regulation (name 3). What are their actions? (examiner asked the exact mechanism
of how parathyroid hormone causes phosphate excretion in the kidneys. wtf.
c. How is active vit D3 formed? See below
d. What are the physiological roles of Ca in the body? Name 4. Cardiac, nervous, haemostasis and bone.
e. Why does this lady have hypoparathyroidism? Removal of parathyroid, ischemia to parathyroid glands.
f. Concerns? Respiratory depression 2° laryngospasm
g. How does hypocalcaemia cause SOB? Laryngospasm causing upper airway obstruction
h. What other signs of HypoCa do you know of? Chovsteks and Trousseaus sign. Can you describe them?
i. So what would you want to do for her? Give Ca replacement -- IV Ca gluconate. What is the exact dose that you and the
concentration? What would you ink up in the IMR? 10mls 10% Ca gluconate
j. What other management? Said A, B, C…examiner not interested. Monitoring -- ECG, SaO2 monitoring. What else? Regular
Ca monitoring? Digoxin? HD? bell ring. Sigh.

Calcium
99% of calcium is stored in bone, only 1% is free. Of this 1%, 40% is bound to albumin and 60% is free.
Acidosis increases the amount of ionized calcium via osteoclastic activity on bone
Function of Calcium
- Propagation of cardiac action potential
- Constituent of bones and teeth
- Excitability of nerves and muscle
- Muscle contraction
- Enzymatic co-factor
- Co-factor in the coagulation cascade

Vitamin D activation
Vitamin D is obtained from diet or dermal synthesis from UV light. It is first metabolized in the liver to 25-hydroxycholecalciferol. Activated
Vitamin D (1,25-dihydrxyocholecalciferol OR calcitriol) is produced in the proximal tubules in the kidneys catalysed by the enzyme 1-α-
hydroxylase. The enzyme’s activity is up regulated by PTH.

Signs of Hypercalcaemia
- Chovstek sign: contraction of muscles innervated by the facial nerve by striking about 2cm in front of the ear lobe
- Trousseau sign: carpopedal spasm (flexion at wrist/MCPJ, extension of IPJ, adduction of digits) when BP cuff is inflated to ≥20mmHg above
systolic BP for 3-5 minutes

Management of hypercalcaemia
- IV calcium replacement: 10m 10% calcium gluconate in 50ml of D5 given over 10min (90 mg of elemental calcium per 10 mL) with ECG
monitoring, repeat till patient is asymptomatic. Followed by calcium gluconate infusion – dilute 100ml of 10% calcium gulconate in 1L of
NaCl and infuse at 50-100ml/h, titrate to achieve normocalcaemia
- Concurrent hypomagnesemia: 2g of 10% magnesium sulphate over 10-20min
- Oral calcium replacement
- Vitamin D analogues: calcitriol 0.25mcg/day (Vit D metabolite of choice as it does not need renal activation), ergocalciferol/cholecalciferol
- Check 2 hours post-replacement

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10. Ischaemic Bowel
Previously well 53 year old admitted for 1/52 duration of bloody diarrhea, suddenly stopped having any more episodes of diarrhoea and now has
abdominal distension.
a. What are your differentials: Enterocolitis, IBD, colon CA, C. diff, ischaemic colitis, diverticular bleed, haemorrhoids
b. Interpret & explain all the abnormalities: Na128 K3.1 Cr109 U9 Hb8 (MCHC) TW12 PLT666
c. Do you think he has chronic or acute anaemia? Chronic? Why? MCHC anaemia. NCNC in acute bleed
d. Why are the platelets high? Dehydration, acute bleed, acute phase reactant.
e. What do you see on the AXR? Thumbprinting is suggestive of ischaemic colitis
f. Besides all these investigations, how else would you investigate this patient? (FBC, UECr, AXR done)
CRP, ESR, stool c/s + OCP, Stool C diff, CEA, specific antibodies for Crohns and UC (only at a later date right?) How else will u
investigate the patient? Colonoscopy at later date (doesn't seem like the answer)
g. How will you monitor the progress? Clinically: fever/ diarrhoea settle. Biochemical: TW, CRP decreases.
h. What would you do for this patient?
i. What are the indications for operative management?
j. What surgery will you perform for him?

Investigation for ischaemic colitis

- Laboratory: FBC, UE, CRP, ABG, aPTT/PT/INR, amylase/lactate/LDH
- Cardiac: ECG, 2DE
- CTAP & CT angiography

Management
- NBM and NGT
- Vitals monitoring + IDC insertion for strict I/O monitoring
- Broad spectrum antibiotics: IV ceftriaxone and metronidazole (protect against bacterial translocation)
- Surgery for ischaemic colitis:
 Right sided – right hemicolectomy ± primary anastomosis; consider right colectomy with end ileostomy if gross spillage
 Left sided – sigmoid resection OR left hemicolectomy with proximal stoma creation ± distal muscous fistula

Indications of surgery for IBD:

- Failure/Complications from medical therapy
- Extracolonic manifestation
- Toxic megacolon
- Perforation
- Severe bleeding
- Malignancy
- Fistula
- Intestinal obstruction

PROCEDURAL SKILLS
11. IDC insertion
a. What will you do if there is no urine? Aspirate the urine. If still no urine? Flush and aspirate.
b. What is your logic for flushing and aspirating?
c. If still no urine and no good flow what will you do? Take out the IDC
d. Why? What are your differentials? False passage, catheter tip in urethra instead of bladder, not a true
palpable bladder i.e. a suprapubic mass
e. What are differentials for a suprapubic mass? Pt was male. Malignancy from bladder, prostate, CLR CA,
pelvic collections, abscesses, mesenteric cysts.
f. Layers through SPC insertion: skin, subcutaneous fat, superficial fascia, ant. rectus sheath, rectus muscle, transversalis fascia,
extraperitoneal fat

PHYSICAL EXAMINATION
12. Submandibular gland
Small swelling about 2cm, quite deep not easily felt
a. Questions asked: what are your differentials for the swelling?
b. What are the causes of each differential? Enlarged cervical LN and submandibular gland enlargement
c. How to differentiate Submandibular gland and cervical LN? And which is your top differential and why?
d. What is the management of this swelling?
Differentiate submandibular gland from cervical LN
- History
- Clinical: LN rubbery sensation, movable under skin; submandibular gland has a more fixed position
- Investigation: radiological & FNAC

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13. Abdominal exam (Appendicitis)
a. How would you perform an appendicectomy? Open vs laparoscopic
b. What are the advantages of lap? less scarring, can perform diagnostic lap
c. What will you be looking at in the lap?
d. How do you do the diagnostic lap and where do you insert the ports?
Laparoscopic appendicectomy
- Port placement:
 2cm supraumbilical curvilinear incision, directly above the umbilicus for the placement of 12mm Hasson trochar
 Position patient into a Trendelenburg position for placement of two 5mm trochar
 1st trochar to the left of midline, 1cm above pubic ramus (suprapubic area)
 2nd trochar place 2cm above and medial to left ASIS

14. CVS exam

Pacemaker with aortic valve replacement

15. Thyroid exam

ANATOMY
16. Hand
a. Name all the bones of the carpus and show them on the Xray given. (AP and Lat view)
b. Name all the movements of the thumb and demonstrate it to me.
c. Show me which muscles control these movements and what is their innervation?
d. Show me the median nerve distribution of the hand. They ask for the extent of the dorsum also.
e. What muscles make up the thenar eminence. What is the nerve supply of thenar eminence?
f. What are the boundaries and contents of the anatomical snuffbox? Demonstrate to me where it is.
g. What is the significance of snuffbox tenderness in the anatomical snuffbox? Scaphoid #
h. Why do you get AVN in scaphoid #?
i. How do you test for collateral circulation of the hand? Describe the test for me. Allen’s test
j. Identify the superficial palmar arch (on prosection). What is the supply?
k. What are the roots of the ulnar nerve? What does it supply in the hand?

Movements of the thumb: Flexion, extension, adduction, abduction, opposition

- Flexion: FPL & FPB (median nerve)
- Extension: EPL & EPB (PIN)
- Abduction: Abductor pollicis longus (PIN) & brevis (median nerve)
- Adduction: Adductor pollicis (ulnar nerve)
- Opposition: Opponens pollicis (median nerve)

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Median nerve sensory distribution on the hand: medial 3.5 fingers on the palmar aspect & the fingertips of thumb – middle finger

Median Nerve
(Palmar branch) Ulnar
Nerve

Ulnar
Nerve
Radial Nerve

Anatomical snuff box

Boundaries Contents
Ulna border: EPL Radial artery
Radial border: APL + EPB (brevis btw 2 longus) Branch of radial nerve
Prox. border: radial styloid Cephalic vein
Floor: trapezium and scaphoid

AVN in scaphoid #
- The major blood supply for the scaphoid is via the dorsal carpal branch which supplies 80% of the scaphoid via retrograde flow
- A distal fracture, especially with displacement causes the blood supply to be disrupted, hence proximal scaphoid is devoid of blood supply

Superficial palmar arch: predominantly formed by ulnar artery

Deep palmar arch: predominantly formed by radial artery
Ulnar nerve (C8, T1) muscles in the hand:
- Hypothenar muscles: opponens digiti minimi, abductor digiti minimi, flexor digiti minimi brevis
- Others: 3rd and 4th lumbricals, dorsal and palmar interossei, adductor pollicis, flexor pollicus brevis (deep head)

17. H&N
a. Identify the pterion. Show the 4 bones that converge? Its clinical significance? (Sheffield Feb 2014, Q10)
b. Identify this bone – atlas (N.B. Axis is C2 vertebrae)
c. What part is this? Anterior tubercle of atlas
d. Show me the foramen lacerum (contains internal carotid, emissary veins & greater petrosal nerve (VII)
e. What is posterior cranial fossa formed by? Anteriorly by petrous temporal, lateral by mastoid and squamous temporal bone,
posteriorly by the occiput
f. Identify this part: petrous temporal bone
g. Given lateral X-Ray of skull – show me the sella turcica.
h. What is this: ethmoid sinus
i. On prosection: What is this muscle -- temporalis
j. What is its blood supply? Deep temporal artery, from maxillary artery (see below)
k. What supplies the scalp over the temporalis muscle? Superficial temporal artery. Where is it from?
l. On prosection: This is the optic chiasma. What nerve is this? Occulomotor nerve.
m. What are the autonomic innervation to the pupil? What does sympathetic do and what does
parasympathetic do? Sympathetic via cervical ganglion; parasympathetic via oculomotor nerve (ciliary ganglion)
n. What do you get in raised ICP? Why? Fixed dilated pupils (non-reactive to light); due to uncal herniation
o. What exact structure is CNIII pressed against? Show me on the prosection.

54
Maxillary artery (3 parts)
The larger of the 2 terminal arteries of the ECA (the ECA ends within the parotid gland at the angle of mandible)
1st Part 2nd Part 3rd Part
Deep auricular artery Masseteric artery Sphenopalatine artery (Nasopalatine artery is
Anterior tympanic artery Pterygoid branches the terminal branch of the Maxillary artery)
Middle meningeal artery Deep temporal arteries (anterior and posterior) Descending palatine artery
Inferior alveolar artery (gives off its mylohyoid Buccal artery Infraorbital artery
branch just prior to entering the mandibular Posterior superior alveolar artery
foramen) Artery of pterygoid canal
Accessory meningeal artery Pharyngeal artery

55
18. Shoulder & Hip
There is a skeletal model and you are given a pointer.
a. Show me the attachments and origins of the rotator cuff muscles
b. Show me the spiral groove. What nerve runs in it? Radial nerve
c. Identify the medial epicondyle. What will deficits will you get in fractures there? Ulnar nerve palsy
d. Show me on your hand what is the area supplied by the ulnar nerve (show both palmar and dorsum)
e. What is the principle flexor of the hip? Show me the insertion. Iliopsoas inserts into the lesser trochanter
f. What muscle has its origin at the ASIS? What is its nerve supply? Sartorius, supplied by femoral nerve
g. What nerve runs under the inguinal ligament? What syndrome happens if this nerve is caught? Lateral
cutaneous nerve of thigh, its entrapment give rise to Meralgia paresthesia (pain on the lateral aspect of thigh)
h. Show me the origin and insertion of the gluteus medius and minimus
i. Show me the origin and insertion of the quadratus femoris

Hip Joint
Ball & socket joint
Hip Flexion: iliacus, psoas major, rectus femoris, sartorius, pectineus (medial compartment)
Hip Extension: gluteus maximus & posterior compartment (biceps femoris, semimembranosus, semitendinosus)
Hip Abduction: gluteus medius & minimus, tensor fasciae latae
Hip Adduction: medial compartment (adductor magnus, longus & brevis, gracilis, pectineus except obturator externus)
Lateral rotation: Gluteus maximus, deep gluteal muscles (piriformis, obturator internus, gemelli, quadratus femoris)
Medial rotation: gluteus medius & minimus, tensor fasciae latae

56
TEST
19. Trauma activation
You have a motorcyclist who is now GCS 3, cyanosed and not breathing. Has cardiac output.
Examiner and mannequin. Gel and glove up. Has no C collar on. Testing ATLS.
- I said would ask the nurse to hold the head or put sandbags
- Secure airway -- jaw thrust: sweep foreign bodies. What foreign bodies could these be? Patient's vomitus, dentures, loose teeth etc.
- Patient is still cyanotic. What will your next step be? Guedel airway.
- Sats still not picking up. Offered intubation -- "you mean you can intubate?" I said i will ask an A&E colleague haha. " Well, that is not
wrong."
- But what else can you do?
- Bag valve mask the patient. Show me.
- Now the sats have started to pick up.. what else do you want to do?
- Put on the C collar. "OK, show me."
- What if sats still not picking up. What will you do? If upper airway obstruction.. offered needle cricothyroidotomy  formal
cricothyroidotomy. Asked on how to do it.
- And how long can a cricothyroidotomy last? Is it permanent? How to perform a tracheostomy?
- And why is it performed at the level of the 2nd and 3rd rings of the trachea? I said lower risk of tracheal stenosis but this is wrong :(

Damage to the 1st tracheal ring causes subglottic stenosis & lower placement increases the risk of trachea-inominate fistula.

Glasgow May 2014

CRITICAL CARE
1. Acute Pancreatitis
Guy went out partying, drank alcohol, has epigastric pain radiating to back. Showed some bloods outside the station for you to read in 1 minute
before entering. Basically amylase 2100, and out of Glasgow score, glucose, albumin, calcium, urea, total whites were deranged
N.B Just give one-word/short answers to allow examiner to tick the box. They are not interested in anything else.
a. What is the diagnosis, differentials surgical (PUD, perforated viscus, hepatitis, GB/CBD disease) vs. non-surgical (DKA, AMI)
b. What in the investigations led you to your diagnosis (amylase)
c. Name me one scoring system for severity, no need the values, just components Ranson
d. For your scoring system, what is the time interval to do the tests? 48 hours after admission
e. Causes of normal amylase in pancreatitis? (too early, too late)
f. How do you manage the pain? Opioids (usually in the form of PCA)
g. Why cannot give NSAIDS? (afraid of renal injury & potentially worsen pancreatitis)
57
 h. What other option if opioids not enough? (epidural)
i. What is pseudocyst? Localized fluid collection rich in amylase and pancreatic enzymes, that has a non-epithelializing wall
consisting of fibrosis and granulation tissue, which usually appears several weeks after the onset of pancreatitis.
j. Why hypocalcaemia? Fat saponficaiton, glucagon and AKI (causing hypocalcaemia)
k. Complications of pseudocyst? BGIT (erosion into adj. vessels), infected, IO, rupture (into enteric organ vs. peritoneal cavity)
l. What in blood results leads you to suspect pseudocyst? Persistently raised amylase despite resolution of pancreatitis
m. Is amylase a marker of severity? Serum amylase & lipase DOES NOT indicate disease severity
n. Where would you manage the patient? (ITU)
PANCREATITIS
It is an acute inflammatory process in which pancreatic enzymes autodigest the gland
Aetiology
- Metabolic: alcohol, hypertriglyceridemia, hypercalcaemia, hypothermia, drugs*, genetics (CF), scorpion venom
- Mechanical: cholelithiasis, ERCP, pancreatic duct obstruction, duodenal obstruction, HOP cancer
- Vascular: atherosclerosis, vasculitis (e.g. SLE), PAN, haemodialysis
- Infection: Mumps, Coxsackie B, CMV, Cryptococcus
*
drugs causing pancreatitis SAND – sulphonamides, azathioprine, NSAIDs, diuretics

Amylase vs. Lipase

Amylase level ↑ rapidly over 3 to 6 hours, with a half-life of 10-12 hours; it remains elevated for 3 to 5 days and is excreted by the kidney. Serum
amylase can be normal in acute on chronic pancreatitis (loss of acinar cells), hypertriglyceridemia-induced pancreatitis or in late presentations,
severe pancreatitis with extensive pancreatic necrosis.

Serum lipase level increases in 3 to 6 hours, peaks in 24 hours and remains elevated for one to two weeks, it is reabsorbed by the kidney tubules and
hence remains elevated for prolonged period.

Investigation
Diagnostic: amylase & lipase (>3 times of normal limit)
Prognostic/Supportive/Aetiology:
- Laboratory
 Severity: FBC, UE, Glucose, LFT (AST & albumin), LDH, CRP, ABG, Ca2+
 Aetiology: Ca/Mg/PO4, fasting lipids, CE & ECG (exclude AMI)
- Imaging:
 US (identification of gallstones  early ERCP can improve gallstone pancreatitis)
 CTAP – usually after 72 hours to look for complications
 AXR limited usage, may identify sentinel loop, pancreatic calcification in acute-on-chronic pancreatitis
 CXR to exclude ARDS

Severity classification
Glasglow criteria: PANCREAS – PaO2, Age, Neutrophils, Ca2+, Renal, Enzymes (LDH & AST), Albumin, Sugar
Ranson criteria: WALLS FOr CHUB – WBC, Age, Liver enzymes, LDH, Sugar; Fluid deficit, Oxygen, Ca2+, Hct, Urea, Base excess

Management
1. Initial resuscitation
2. Monitoring in ICU (if severe pancreatitis)
3. NBM & IV fluid replacement
- Bowel rest for at least 2 days, start feeds early in severe pancreatitis (enteral nutrition preferred over parenteral)
- NGT insertion if persistent vomiting, ileus, gastroparesis
- Acid suppression primarily to prevent stress ulcer formation
4. Analgesia: opioids usually in the form of PCA (fentanyl is preferred due to its safety profile in renal impairment)
5. Treat fluid & electrolyte abnormalities: watch for hypocalcaemia
6. Antibiotics should not be given prophylactically. Imipenem is used in pancreatic necrosis.
7. Supportive management of other organs
8. ERCP + Cholecystectomy for gallstone pancreatitis (cholecystectomy as an elective surgery)

Complications
Local complications:
- Peripancreatic fluid collection
- Pseudocyst – fluid collection encased by granulation tissue which presents as abdominal pain, GOO, persistently ↑ amylase
- Abscess
- Pancreatic necrosis
- Infected necrosis
- Chronic pancreatitis, endocrine/exocrine insufficiency
- BGIT – autodigestion of adjacent arteries e.g GDA
- Splenic artery pseudoaneurysm

Systemic complications:
- Sepsis, MODS (ARDS, AKI, DIVC)
- Pancreatic ascites, pancreatic-pleural effusion
- Hypocalcaemia – laryngospasm, arrhythmias, seizures

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2. Pre-Op Aortic Stenosis
Patient planned for elective transurethral resection of bladder tumour was found to have aortic stenosis.
a. What is the pathophysiology of aortic stenosis? Narrowing of the aortic valve
b. What are the symptoms of aortic stenosis? Classic triad of angina, syncope & dyspnoea
c. What are the signs of aortic stenosis, where do you hear the murmur
d. What are the complications of aortic stenosis? Heart failure, conduction defects e.g. LBBB; arrhythmias
e. Read this ECG, what does it show? (LVH) other common changes e.g. LBBB, 1st degree heart block
f. How do you calculate the heart rate from the ECG?
g. Would you still let him go for op? What would you do? (contact consultant, anaesthesia, CVM, explain to patient, call OT
to cancel listing, MDT, etc)
h. If cancel the op, what are you worried about? (that is is a cancer and it should be done the sooner the better)
i. What investigation would you do for him? (2DE)
j. Need antibiotics for him? (yes, NICE guidelines) – No??
Signs of AS
- ESM best heard at the aortic area (upper right sternal edge) which radiates to the carotids ± palpable thrill
- Heaving and displaced apex beat
- Sign of CCF
- Pulsus parvus et tardus: slow rising, low volume pulse
- Signs of anaemia e.g. conjunctival pallor and sclera icterus (2° MAHA from severely calcified valve)

NICE guideline for prophylaxis against IE (2008)

- Patients at risk of IE are defined as:
 Acquired valvular heart disease with stenosis or regurgitation
 Valve replacement
 Structural congenital heart disease, including surgically corrected, but excluding isolated ASD, fully repaired VSD/PDA
 Previous IE
 HOCM
- Antibiotics prophylaxis not recommended for: UGIT/LGIT, GU & upper/lower respiratory tract procedures
- If a person at risk of infective endocarditis is receiving antibiotics because they are undergoing a GI/GU procedure at a site where there is a
suspected infection, the person should receive an antibiotic that covers organisms that cause infective endocarditis.

PHYSICAL EXAMINATION
3. Lipoma
Referred from GP for a lump over the upper back
Asked pt whether the lump is painful. Assured patient I will not hurt u and will stop immediately if pain.
Pt says pain on flexion of neck to study.
10x15cm soft oval lump over the C7 vertebrae, no skin changes, deep to skin, But not attached to the back muscles.
Questions
a. Present your findings – as above
b. Differential diagnosis – Lipoma most likely, Sebaceous cyst, Muscular haematoma, Neurofibroma
c. Invx – US lump
d. Mx - In view of functional symptoms and impairment, recommend operative removal
e. Complications and risks of surgery - GA, Surgery. Bleeding, infection, recurrence

4. Submandibular gland
Take short history and perform physical exam then discuss
History
Patient noticed swelling below tongue for few days, Swelling worsen and pain on ingesting of food. No discharge, no fever, no LOW, no LOA.
Physical exam
No distinct lump felt. No LN palpable. Slight swelling over right floor of mouth on bimanual palpation. No discharge from opening of wharton’s
duct. No tongue deviation, able to depress mandible
Differential? Sialolithiasis, Infection, tumour (benign vs. malignant)
Investigation? Sialogram. Examiner asked for something non-invasive. XR KIV U/S
Management? Conservative. Some stones can pass out or can be milked out. If not, surgery.

5. PVD
This gentleman has calf pain on walking for 100m, please examine his lower limb vascular system.
No ulcers present, small scar on medial aspect of left knee but unrelated.
a. What do you think this patient had?
b. What investigations would you do and in what order?
c. How would you manage this patient? – conservative vs surgical

6. Pulmonary Embolism
Right sided chest pain s/p cholecystectomy POD8 Sees patient (actor) with oxygen mask.
Asked patient where the pain is and assured patient i will not hurt u, will stop immediately if pain.
Started with respiratory examination on the posterior chest - chest expansion, percussion, auscultation.
Patient cringed in pain when taking deep breath - told patient to normal breaths
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CVS examination - just ascultated aortic, pulmonary, tried to ask pt to lift up left breast to listen to mitral but stopped by examiner.
Tried to position patient to examine Abd but stopped by examiner
Went to the calves, squeeze left calf and patient nearly jumped
Shown vitals chart: HR100-130, RR 20-30, 92% on room air over the last 1hr
Questions (KL Feb 2014, 2, Q6)
a. Findings – Pleuritic chest pain on deep inspiration with no wheeze/dullness to percussion, patient speaking full sentences. Tender
left calf.
b. Differential diagnosis – Pulmonary embolism from deep vein thrombosis
c. Investigation – FBC, coagulation profile, d-dimer, fibrinogen. Definitive: CT pulmonary angio
d. Mx – ABC, anticoagulate with IV heparin. If haemodynamically unstable, for embolectomy

PROCEDURAL SKILLS
7. OT Listing
55yo Mrs Thompson with penicillin and iodine allergy has diverticular abscess for sigmoid colectomy
Mr Philip with IDDM, AF (warfarin but converted to LMWH) has MRSA left foot ulcer for BKA
Mr McPhee with pacemaker and severe COPD has strangulated hernia
Question
a. Arrange the op in order: Strangulated hernia, then Sigmoid colectomy, then BKA
b. Reason for order
c. Important things to note for each patient
i. Strangulated hernia: in view of severe COPD, should attempt RA rather than GA. in view of pacemaker, should use
bipolar. What prophylactic antibiotics? Cefazolin
ii. Pencillin and iodine allergy: Iodine allergy, can use alcohol/chlorhexidine based antiseptic. Pencillin allergy, can use
clindamycin or vancomycin. You are not sure? Consult the hospital bacteriogram and the infectious disease physicians
iii. BKA with IDDM: need sliding scale. warfarin, need to make sure INR<1.5 and LMWH stopped in the morning. MRSA,
vancomycin for prophylactic abx another abx: bactrim, clindamycin? If you are not sure, what can you do? refer to ID physician
for antibiotics guidance. Have you heard of “tigermycin”? (some T drug which i didnt recognise)

MRSA surgical site prophylaxis: vancomycin, teicoplannin

(vancomycin, linezolid, daptomycin, telavancin, clindamycin, ceftaroline )

8. Turkey Leg
Young man who crashed into glass window, debridement of giant turkey leg with a wound laden with pepper and pebbles
1 assistant and 1 examiner, given large syringe, NS, curette, scalpel (10 and ?14 blade), tooth forceps
a. What instruments would you use
b. Asked what I would do – went on to flush copiously, tried to refashion wound edges and pick out the pebbles with the forceps
c. What invx would I do? I said the usual blood invx and IV abx. Got prompted for xr when I forgot
d. How would you know if a blood vessel was cut – said might see spurting if arterial injury, he seemed satisfied with that
e. What would you do if you saw a radial artery cut?
f. What would you do if a nerve was cut
g. What will you do with the wound

PATHOLOGY
9. Ulcerative Colitis
a. What is UC? Inflammatory bowel disease
b. Pathophysiology? Just need to say unknown/idiopathic and u get the mark. Added that studies show immunogenetics link (HLADR
2) but not needed (wasted my time).
c. On histo, how to tell if it is Crohn’s?
d. Why need to scope?
e. Recent colono histo result: Tubular dysplasia in one part, adenocarcinoma in one part
f. Picture of cancer eroding through muscularis layer. Name one tumor staging classification and stage
tumor. Duke’s. So tumor is Duke A.
g. Describe APC pathway. APC tumor suppressor gene damage leading to hyperproliferation. Mutation to Oncogene KRAS leading
to dysplasia. Loss of p53 causing adenocarcinoma.
h. Surgical Mx: Colectomy. Asked examiner which part CA is in colon. Examiner asked if I wanted to do partial colectomy in a very
shock manner. Got the hint and said total colectomy since patient has UC.

Pathophysiology of IBD
It is an idiopathic disease caused by dysregulated immune response to intestinal microflora, the pathogenesis of IBD involves genetic susceptibility
& failure of immune regulation.
- CD is associated with HLA-DR7 and HLA-DQ4
- UC is associated with HLA-DRB1

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Difference between CD & UD
Crohn’s Disease Ulcerative Colitis
Distribution Can affect any part of GI tract – from mouth to anus, Affects large bowel only, occasionally involves terminal
frequently terminal ileum ileum (‘backwash ileitis’)
Endoscopy Rectum frequently spared Rectum always affected
Findings Healthy bowel btw diseased segments (skip lesions) Continuous inflammation
Bowel wall is thickened and has ‘cobblestone’ appearance Bowel wall is thin and featureless in severe disease
due to deep ulceration
Histology Granuloma is characteristic finding Crypt abscesses & pseudopolyps
Fissure like transmural inflammation Inflammation usually confined to mucosa
Thickening of muscularis mucosae & propria Granular and friable mucosa
Fibrosis of all tissue layers
Radiology Strictures, fissures and fistulae are common Less common in ulcerative colitis
Asymmetric inflammation Symmetrical inflammation
Smoking Strongly associated with smoking Associated with non-smokers or ex-smokers
Predicts a worse course of disease – Increased risk of surgery Appears to protect against disease
and further surgery
Clinical Common: Diarrhoea, abdominal pain, fever, LOW Gross bleeding more common
Presentation Faecal occult blood positive, but seldom gross bleeding
unless Crohn colitis present

Cancer screening for IBD (British Society for Gastroenterology)

- 10 years after disease onset to assess extent of disease and risk factors (high/intermediate/low risk)
- Frequency of surveillance: low risk Q5 yearly, intermediate risk Q3 yearly, high risk Q1 yearly
- Low risk: no active endoscopic or histologic inflammation, left-sided colitis, Crohn colitis involving <50% of the colon
- Intermediate risk: mildly active endoscopic/histologic inflammation, post-inflammatory polyps, 1st degree family with CRC ≥ 50 y/o
- High risk: moderate inflammation, stricture ≥ 5 years, dysplasia ≥ 5 years not treated, PSC, 1st relative with CRC < 50 y/o
- Method: pancolonic dye spraying with target biopsies vs. 2-4 random biopsies every 10cm of the entire colon and suspicious area

CRC Staging (Duke vs. TNM staging)

Duke staging
Stage Description Prognosis
A Confined to bowel wall 90%
B Invasion beyond the muscularis propria, not involving LN 80-70%
C Lymph node metastasis 50%
D Distant metastasis 2%

TMN staging Comparison between TMN & Duke Staging

T staging Stage T N M Duke
T1 Limited to mucosa & submucosa I T1 N0 M0 A
T2 Invades muscularis propria but not beyond T2 N0 M0 A
T3 Invade through muscularis propria involving paracolic tissue II T3 N0 M0 B
T4 Invasion of adjacent structure T4 N0 M0 B
N staging III T1-4 N1-2 M0 C
N1 1-3 regional lymph nodes involved IV Any T Any N M1 D
N2 4 or more regional lymph nodes involved N.B. Stage II, III & IV can be further broken down
M staging
M1 Distant metastasis

Genetic pathway in CRC

APC pathway (APC = adenomatous polyposis coli)
- The adenomatous polyposis pathway accounts for 80% of the sporadic CRC, which involves mutation of the APC tumour suppressor gene at
5q21; hence, multiple stepwise mutations of other oncogenes & tumour suppressor genes.
 APC  accumulation of β-catenin  promotes cellular proliferation  Mutation of proto-oncogene KRAS (12p12)  mutation of p53
tumour suppressor gene
- Morphologically a stepwise progression from localised epithelial proliferation  small adenoma  dysplastic adenoma  CIS  invasive
cancer can be observed. The APC pathway is involved in FAP.

DNA mismatch repair

- Involved in 10-15% of the sporadic CRC due to mutations of DNA mismatch repair genes (e.g. MSH 2/6, MLH1, PMS1/2) resulting in
microsatellite instability affecting the genes involved in tumour growth (BAX gene & type II TGF-β receptor)
- Morphologically, there are no clear identifiable lesions (e.g. adenoma) however; sessile serrated polyps on the ascending colon can suggest a
precancerous stage.
- Tumours that arise from this pathway is associated with a better prognosis than tumour arising from the APC pathway

10. Gallbladder Cancer

Patient has gallbladder CA s/p op (KL Feb 2014, 3, Q6)
a. What causes gallbladder CA? Chronic inflammation (gallstone, polyps..etc)
b. What kind of CA? Adenocarcinoma most common (others include SCC, adenosquamous, carcinoid)
c. First area that it spreads to? Most likely LN (common areas of spread: liver, cystic duct, CBD, portal hepatic LN)
d. Post op had localised collection. What to do? I said Abx with drainage (open vs percutaneous).

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 e. Examiner asked, do we give Abx for abscess? Told him drainage most impt as Abx do not penetrate abscess well.
f. Now there is pain, swelling over surgical site, septic. Why? Told him wound dehiscence TRO necrotising faciitis
g. What organisms? Staph Aureus, Strep pyogenes, Clostiridium perfigens (gas gangrene)
h. Patient started having bloody diarrhoea. Name 4 differentialss. GE, IBD, Opsite bleeding, PMC.
i. Showed colonoscopy pic of PMC (as expected). What is this?
j. Cause? Use broad spectrum Abx, normal flora destroyed. Overgrowth of C. difficle that produce Enterotoxin A,B leading to PMC.

11. Enterocutaneous fistula

a. What is a fistula? Abnormal connection between 2 epithelial or endothelial surfaces. An ECF is an abnormal connection between
the GIT and the skin.
b. The risk factors for enterocutaneous fistula? Divided into patient, surgeon and other factors
c. What are the factors that predispose non closure of a fistula? FRIENDS
d. If the patient is for conservative Tx, what would your management be? SNAP but no P
e. What other complications will the fistula have besides metabolic disturbances? Dehydration, wound infection
f. Why would the patient be acidotic? Where is HCO3- mainly produced? Due to bicarbonate secretion especially in
pancreatic fistula and bile secretion

Enterocutaneous fistula
High output stomas is defined as greater 500ml of effluent/day, low output is define as less than 200ml of effluent/day
Risk factor of ECF
- Patient/Disease factor: IBD, tuberculosis, diverticular disease, malignancy (following rupture/abscess formation), malnutrition
- Surgical factor: anastomotic breakdown, emergency surgery, inadvertent enterotomy/small bowel injury
- Others: radiotherapy, sepsis (esp. intra-abdominal sepsis), distal bowel obstruction

Factors that predispose to non-closure of ECF (FRIENDS)

Foreign body, Radiation, Inflammation/Infection/IBD, Epithelisation of fistula tract, Neoplasm, Distal obstruction, Steroids

Complications
- Early: hypovolaemia, electrolyte imbalance, malnutrition, sepsis, skin excoriation
- Late: short bowel syndrome (multiple repairs), stricture & obstruction at fistula site, oesophageal stricture from prolonged NGT

Investigation
Laboratory investigation: FBC (anaemia), blood cultures, UE, inflammatory markers (CRP/ESR), LFT (albumin)
Radiological: CT with oral contrast imaging of choice, barium follow through, fistulogram

Management of ECF
Early intervention to close fistula should be avoided due to high mortality 2° sepsis, electrolyte imbalances and malnutrition. In the absence of
diseased bowel or distal obstruction, majority of the ECF closes spontaneously within 6 weeks. If not closed by 12 weeks, plan for definitive surgery.
Principles of conservative management (SNAPP):
- Sepsis elimination & effluent reduction
 open or percutaneous drainage of collections, appropriate antimicrobials
 Reduce effluent via NGT suction, NBM, early TPN, somatostatin, PPI & H2 antagonist
- Nutritional resuscitation/optimization – enteral nutrition whenever possible (needs at least 120cm of small bowel) ± supplementation with
parenteral nutrition; also involves the correction of electrolyte imbalances
- Anatomy – defined using radiological investigations
- P – protect surround skin from intestinal enzymes with stoma appliances/skin barriers, VAC dressing
- Plan for definitive surgery if non-healing

Nutritional requirement:
Low output: 30-35kcal/kg/day, 1-2g/kg/day of protein
High output: 40-45 kcal/kg/day, 1.5-2.5g/kg/day of protein

Anatomical location Volume secreted (ml/day) Na mEq/L K mEq/L Cl mEq/L HCO3- mEq/L
Stomach 1500 60 10 130 -
Duodenum No active secretion 140 5 80 -
Ileum 3000 140 5 100 30
Colon - 60 30 40 -
Pancreas 100-800 140 5 75 115
Bile 50-800 145 5 100 35

HISTORY TAKING
12. Thyroid Goitre
Middle aged lady, with longstanding history of goiter, but has sudden increase in R side.
Thyroid function: hyperthyroidism – LOW, heat intolerance, anxiety, palpitations, tachycardia, diarrhea, irregular menses.
Symptoms of compression – dysphagia with solids worse than liquids
Nil other family hx, nil hoarseness of voice, nil SOB
a. What investigation would you do on this patient? U/S and FNAC
b. What other investigations would you do? Radioisotope scan

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 c. What are the possible causes of the sudden enlargement? – Benign (Toxic adenoma, part of MNG) Malignant
(Papillary follicular medullary, less likely anaplastic) N.B. long standing goitre is a risk factor for anaplastic carcinoma
d. What are the possible treatments? Surgical intervention is required (compressive symptoms). Spoke about hemi vs total
thyroidectomy
e. Possible surgical complications that you would advise this patient? RLN injury, hypocalcemia, thyroxine replacement

PRINCIPLES OF MANAGEMENT: 1) Surgery 2) RAI 3) TSH suppression

BRITISH THORACIC ASSOCIATION JUL 2014

Risk factors: Age > 45 y/o, widely invasive, LN/distant metastasis, angioinvasion Lateral neck dissection: level III & IV
SURGICAL MANAGEMENT Central neck dissection: level VI & VII
Surgery for Papillary Carcinoma (PTC)
- Tumours >4cm OR multifocal/bilateral/extra-thyroidal spread require TT
- Tumour 1-4cm WITHOUT risk factors can be treated with hemithryoidectomy (insufficient evidence to recommend HT vs. TT for radiation
induced tumours)
- Prophylactic central neck dissection is NOT recommended
- Prophylactic lateral neck dissection is NOT recommended (insufficient evidence to recommend lateral neck dissection in patient with central
compartment disease)
- Central compartment disease  central neck dissection; lateral compartment disease  central & selective lateral neck dissection

Surgery for Follicular Carcinoma (FC)

- Tumours >4cm OR WITH risk factors require TT
- Tumours ≤4cm WITHOUT risk factors can be treated with hemithyroidectomy
- Pre-op OR intra-op suspicion of nodal disease REQUIRE FNAC or FS prior to therapeutic node dissection

Surgery for Papillary Microcarcinoma (subset of PTC which is defined as ≤1cm)

- Thyroid lobectomy in UNIFOCAL microPTC
- TT for microPTC with FNMTC, multifocal disease involving both lobes
- Prophylactic central neck dissection in multifocal disease, pT3 and with extra-thyroidal spread

RADIOACTIVE IODINE
Only for patient with total/near total thyroidectomy
No indication for RAI (all criteria below should be met)
- Tumour ≤ 1cm
- Histology: classical PTC, follicular variant of PTC or follicular cancer
- Minimally invasive without angioinvasion
- No extra-thyroidal extension

Indication for RAI (any one)

- Tumour >4cm, extrathyroidal extension, distant metastasis
Sample regimen -28 days -14 days Day of RAI
TT/Near TT Levothyroxine Liothryonine Low iodine diet
>4 weeks before RAI (short-acting T3) (1-2 weeks before RAI)

TSH SUPPRESSION
Recommended for ALL patients to prevent hypothyroidism & minimise potential TSH stimulation of tumour growth
- Low risk: 0.1 – 0.5 mU/L
- Intermediate or high risk: <0.1 mU/L

EXTERNAL BEAM RT (limited usage)

- metastatic thyroid CA refractory to RAI OR incomplete resection margins OR region control in local recurrence OR palliative therapy

13. Pre-op Confusion

You are the MO, patient was acting weirdly. Due for surgery tomorrow, you are supposed to take consent. (For non-urgent benign surgery)
I just did AMT scored 1/10 – patient had to purposely think before answering so he could answer wrongly.
Don’t forget to ask family for collaborative history – apparently AMS is longstanding
a. What test did you just do and why did you do it?
b. What are the causes of AMS in a patient like this?
c. Will he be able to give consent? Why? No! Cannot retain information, cannot make an informed decision etc.
d. Should the surgery proceed? Only if patient has lasting powers of attorney
e. Family does not have lasting power of attorney but wants surgery to proceed. Can they? Refer for work up
f. If this was an emergency can the surgery proceed? Yes, with 2 consultants signatures, in the best interest of the patient.
Cause of AMS: Delirium, dementia, amnesia

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ANATOMY
14. Trunk & Thorax
Prosection of heart, mediastinum
a. Identify the right atrium, left ventricle, and pulmonary trunk
b. Identify the pulmonary valve. How many cusps are there in the valve? All the valves have 3 cusps except mitral
valve which has 2 cusps
c. Identify this triangular structure (auricle of right atrium)
d. Name the structures that pass through the hilum of the lung? Which is the most anterior? Pulmonary vein
e. What are the branches of the pulmonary trunk? Left & right pulmonary arteries
f. What are the first 2 organs injured in a stab wound to the epigastrium? liver, small bowel, colon & stomach
g. What demarcates the left and right lobes of the liver? Anatomically: Falciform ligament; Physiological: IVC
h. What is the venous drainage of the liver? Via the right, middle and left hepatic veins into IVC
i. What branch of the celiac trunk supplies both the stomach and the liver? Common hepatic artery
j. In what structure does it run to reach the porta hepatis? Portal vein posteriorly, common hepatic duct anterior to the
right, hepatic artery anterior to the left AND lymph nodes
k. Point out the quadrate lobe. What are the boundaries of the quadrate lobe?

The transverse plane is at divided by the main branches of

the portal vein. The sagittal planes are divided by the right,
middle and left hepatic vein

Boundaries of quadrate lobe (segment IV):

- Anteriorly: anterior margin of the liver
- Posteriorly: porta hepatis
- Right (laterally): fossa for FB
- Left (medially) fissure for ligamentum teres

Boundaries of caudate lobe (segment I):

- Right (laterally): fossa for IVC
- Left (medially): ligamentum venosus

Celiac Trunk (level of T12)

- Left gastric artery – oesophageal & gastric branches
- Common hepatic artery – hepatic artery proper, right
gastric artery & GDA
 GDA branches to right gastro-omental &
superior pancreaticoduodenal artery
- Splenic artery – dorsal pancreatic, short gastric, left
gastro-omental artery, greater pancreatic artery

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 Right Lung
Hilum of the lung (RAILS)
Right pulmonary artery anterior to bronchus
Left pulmonary artery superior to bronchus

Left Lung

15. Parotid Gland

Prosection of parotid, base of skull, patient
a. Show me the surface landmark of the parotid gland on the patient
b. Show me the surface landmark of the parotid duct mid-point of intertragic notch of ear and philtrum
c. What are the differential diagnoses if the patient has a lump in the parotid gland?
d. Other than parotid gland, what else could the lump arise from?
e. What are the structures that lie within the parotid gland? From lateral to medial: facial nerve, retromandibular vein
(junction of superior temporal & maxillary veins), ECA (divides into terminal branches at neck of mandible)
f. Which parasympathetic ganglion supplies the parotid gland? Otic ganglion (from the glossopharyngeal nerve)
g. Which region of the body does the pre auricular lymph node drain?
h. On the prosection, show me the parotid duct
i. Show me the branches of the facial nerve
j. On the base of skull, show me where the facial nerve exits. Stylomastoid foramen
k. Nerve involved in gustatory sweating (Frey’s syndrome)? Auriculotemporal nerve (V3)

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Relations of the parotid gland
- Superiorly – TMJ and external acoustic meatus
- Inferiorly – posterior belly of digastric muscle
- Anteriorly – angle mandible and masseter
- Posteriorly – mastoid process & SCM

Parasympathetic ganglia in H&N

Ganglia Pre-sympathetic fibres Post-sympathetic fibres Innervation
Otic ganglion Glossopharyngeal nerve (IX) via Travels with sympathetic fibres of Parotid gland
lesser petrosal nerve auriculotemporal nerve (br. of V3)
Submandibular ganglion Superior salivatory nucleus via Submandibular & sublingual
chorda tympani & lingual nerve gland + glands in tongue & floor
(br, of V3) or mouth
Ciliary ganglion Sphincter pupillae, ciliary muscles
Pterygopalatine ganglion Facial nerve through greater Via trigeminal nerve Lacrimal gland & glands in the
petrosal nerve nasal cavity/palate
All postsynaptic parasympathetics will use some branch of the Trigeminal Nerve to get from one of four parasympatheic ganglia (Otic, Ciliary,
Submandibular, and Pterygopalatine) to their destinations in either smooth muscle or glandular tissue (secretomotor).

16. Shoulder
Prosection: chest wall, shoulder girdle. Bones: clavicle, humerus, scapula
a. Identify this bone (clavicle). Which side is it from? Name the parts of the clavicle
b. Identify this bone (scapula). Which side is it from? Name the parts of the scapula
c. Identify this bone (humerus). Which side is it from? Name the parts of the superior aspect of the bone.
Where is the surgical neck? Where is the anatomical neck?
d. Please articulate the scapula and humerus
e. Please articulate the clavicle and scapula
f. What movements take place at the shoulder joint? Show me using the scapula and humerus
g. What contributes to the stability of the shoulder joint? Of these, which is the most important?
h. What are the components of the rotator cuff?
i. Identify these muscles please (points to supraspinatus, infraspinatus, teres minor, subscapularis). What
innervates them?
j. Identify this muscle (pectoralis major). What innervates it? Medial and lateral pectoral nerve
k. What is this structure? (Cephalic vein in arm piercing clavipectoral fascia)
l. What is this structure? (Long head of biceps). From where does it originate? Supraglenoid tubercle
m. What attaches to the humerus medially and laterally to it? Triceps (see below)
n. What are these structures? (Long and lateral head of triceps). What innervates them?
o. What passes through this space? (Quadrangular space)
p. What does the axillary nerve supply? Motor: deltoid, teres minor, LONG head of triceps. Sensory: regimental badge
q. Identify the structures you see on the MRI of the shoulder
Shoulder stabilizer
- Soft tissue & bone: glenoid labrum, joint capsule
- Ligament: superior, middle & inferior glenohumeral ligament, coracohumeral ligament, coracoacromial ligament
- Muscle: Rotator cuff muscles
 Suprascapular nerve – supraspinatous (abduction), infaspinatous (lateral rotation)
 Upper & lower subscapular nerve – subscapularis (medial rotation)
 Axillary nerve – teres minor (lateral rotation)

Quadrangular space
- Boundary – superior: teres minor, inferior: teres major, medial: long head of biceps, lateral: surgical neck of humerus
- Contents: axillary nerve and posterior circumflex humeral artery

Triceps brachii (long, lateral & medial head)

- Origin: long head – infraglenoid tubercle, lateral head – above radial groove, medial head – below radial groove
- Inserts: olecranon process of ulnar
- Innervation: radial nerve & axillary nerve (long head)

COMMUNICATIONS
17. CTVS transfer
Young motorcyclist involved in RTA, wearing full leathers and helmet at time of injury
Quite a few pages of info from patients notes:
- Documented by reg that ST1 should call for transfer to CTVS before going to see the patient
- Noted in patients bag an appointment card for a diabetic clinic this coming Tuesday
- GCS 14, PR 120, HR 100/80, T 37, complaining of right sides chest pain, 4L crystalloids given so far, requested 6 units of blood for standby
- Noted left thigh swollen, no open wounds, ?fracture - no Thomas' traction yet
- CXR: widened mediastinum, bilat pleural effusions
- AXR: psoas shadow not seen, dilated small bowel loops

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- Left femur XR: shaft fracture
- CT not available for next 3 hours as it is being serviced
- Registrar also documented insertion of chest tube on the right. Swinging fluid with 200mls of blood stained fluid
- Hb 8, otherwise FBC normal, UECr/LFT normal, CRP raised very minimally
- pH 7.32, PaO2 10kPa, PaCO2 6.0kPa, HCO3 19
Wanted to give SBAR but examiner kept interrupting to ask questions
a. What is the issue?
b. Will you do CT scan?
c. What will you do for his C-spine?
d. What are you going to do for his leg?
e. Is there any abdominal issue?
f. What are you going to do about the blood pressure?
g. Why should you not increase the BP? - prevent further bleeding (permissive hypotension)
h. What are his blood abnormalities?
i. Why do you say metab acidosis?
j. Who will accompany the patient?

18. Angry patient

Previously arthroscopy cancelled. Symptomatic. Now here for arthroscopy again. Op cancelled due to emergency case. Patient frustrated.
Went in preparation bay to find a stack of about 10+ pages of notes ranging from patient details to patient's GP letter to blood results.
- Take note of all the dates, as they may not run in order
- You have 9 minutes to write down all the information that you will need, before going to the next station to talk to the patient
- The story: this guy has left knee pain, and his GP has assessed him to have possible meniscal tear. Wrote referral to Ortho. Ortho assessed him,
recommended him for arthroscopy for diagnosis KIV repair. Op was scheduled last month, but got cancelled due to some reason. Also noted
CRP at that time to be high, possibly related to sinusitis. Rescheduled for operation. GP wrote another letter urging Ortho to expedite operation,
as his work as postman is affected, and he has been putting on weight. Also, he is in pain.
- Knee xray shows joint space narrowing. However, this operation will have to be postponed again as consultant has to attend to E-trauma.
- It helps to write a numbered list of the issues you need to address with the patient.
 Knee pain – he would tell you his ibuprofen has been causing him gastric pain. Give him alternatives
 Weight loss – swimming, physio, etc with analgesia cover
 Work as postman – offer to write to employer to explain situation and cover with MC
 Sinusitis - must get GP to sort it out to prevent operation being cancelled a 3rd time
 Offer avenue to complain – PALS
 Offer to talk to wife & assure him his operation will be placed on priority list, etc etc
It helps to just keep quiet and let him talk, so that you can understand his issues that need addressing. Of course with the usual cues of listening in
conversations like nodding etc

Glasgow May 2014 (2)

HISTORY
1. Progressive dysphagia
Progressive dysphagia 6mth with odynophagia, LOW 2 stones (= 20lb), drinker. Diagnosis & differentials? (Oesophageal CA) Management?

2. Post-op Depression
Patient post op after gastrectomy for cancer, physically well and due for discharge today but nurses think he is depressed. Interview patient and
assess. Patient makes no eye contact and gives monosyllabic answers, looks down and shakes his head says "I don't know" to everything. Asked why
he is upset? Cancer may come back, there's nothing I can do. Asked if we can help in anyway – no.
Present your findings. What is the cause of his depression? Management plan? Who should see patient? Would
you discharge this patient today?

COMMUNICATION
3. OGD Counselling
Patient referred from GP after dysphagia, barium swallow shows stricture likely benign. Counsel for OGD, biopsy and dilatation, in particular the
risks. Smokes 40 sticks/day & drinks 20 units a week. Labs show bilirubin a bit high, low Hb 10.0.
Is it my fault? Is it cancerous? Will it go away if I just stop smoking? Can I go home today?

4. Transfer (Post-op Complication)

Interval cholecystectomy POD2. Op uneventful, 2 clips to CBD 2 clips to cystic artery, but since yesterday worsening abdominal pain with
tachycardia, US shows free fluid in abdomen no CBD dilatation. Labs show TW 18 and CRP 50, bilirubin raised (something like that). Your
consultant thinks there is bile leak from CBD injury, wants you to transfer to HPB consultant Prof Archibald Rose at regional centre.
His reg picks up. Reg not too happy that your labs are from yesterday and nothing was done now you are calling
at 4pm on a Friday. What do you think he has? Where is the source of the bile leak? Do you have any evidence
where it's coming from? Could you arrange ERCP to confirm the source of the bile leak? Is it urgent? Will you
need to speak to anyone? (Bed manager)

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PROCEDURAL SKILLS
5. IV Cannulation
Set IV plug on hypotensive trauma patient possible pelvic and lower limb fracture. Don't need to wear gloves or gown. Insert into dummy arm, blood
splatters all over the shop, draw blood. Connect the IV tubing (unfamiliar equipment), secure plug with transpore tape (struggle cos blood all over
the place, no tegaderm).
What blood tests would you send for? FBC, UE, aPTT/PT, GXM, CE + ECG, ± ABG & lactate
Write fluid order.
What else would you do? Trauma series, relevant X-rays, traction + inform orthopaedics team for LL fracture, vitals + GCS monitoring

6. Sutures
Given silk, vicryl, prolene. Hand-tie 2 rubber bands together with braided non-absorbable. Hand tie deep hook in cylinder with braided absorbable.
Overrun bleeder with figure of 8 using monofilament non-absorbable and instrument tie. Wear gloves and throw away your sharps.
a. What knot did you use for your rubber bands? Why did you use a square knot?
b. What other knots could you use?
c. What are advantages of braided sutures? Easier handling,
d. What is vicryl made of? How long does vicryl last? Polyglactin, last for about 30 days
e. What's the difficulty with deep tying and how to overcome it?

PHYSICAL EXAMINATION
7. Inguinal Hernia
Indirect inguinal hernia with previous appendicectomy scar.
a. Why do you transilluminate?
b. Present your findings.
c. How to differentiate from femoral hernia? Inguinal hernia above and medial to pubic tubercle
d. Have you seen femoral hernias above pubic tubercle? (Examiner has, they can extend above. but they are lateral).
e. Is there any relationship between open appendicectomy and hernia?
f. How else can you test the ilioinguinal nerve? Upper medial thigh, anterior 1/3 scrotum, labia majora, root of penis
g. What types of repair are there? When would laparoscopic repair be favoured? (Bilateral hernia)
h. What types of anaesthesia? When would you use RA/local anaesthesia? LA, RA, GA

8. PVD
Smoker claudication distance 50-100m. Plump gentleman, difficult to palpate pulses except femoral and DP; no time to do Doppler and ABPI.
a. How long must you wait in Buerger's test? Hold for about 1 minute
b. What other examination would you do? CVS & palpate all peripheral pulses
c. What's the cause of his peripheral arterial disease based on his history? (Smoking.)
d. What tests can you do in clinic since you can't palpate pulses? (Doppler.)
e. What would you expect his ABPI to be? How to manage? Conservative vs. surgical

9. Goitre
Neck lump, examine. Glass of water available but no tendon tapper. Examine and present.
a. What else do you want to examine? Assess the patient’s thyroid function clinically + palpate LN
b. What's your diagnosis? Grave’s disease.
c. What differentials? What tests to do? Thyroid panel, US thyroid, FNAC of palpable nodes
d. What management? Conservative
e. If patient comes back with pain on swallowing, difficulty breathing, does it change your management?

10. Post-op Abdominal Pain

Post-op patient after colectomy or something, midline laparatomy wound covered up by a dressing. (No need to take it
off.) Tenderness at LUQ and LLQ radiating to left shoulder. T 39°; PR 150, BP normal, TW 15 and CRP high. Examine
and present. Why is there shoulder pain? How to manage?
Differentials: anastamotic leakage, cholecystitis, IO
Irriation of diaphragm which is innervated by C3, 4, 5 causing referred pain to the shoulders
Management: NBM, IV antibiotics, blood c/s, LFT, amylase, CE + ECG (tachycardia), AXR/CXR, CTAP

PATHOLOGY
11. Tuberculosis
23yo lady just came back from Bangladesh, has anterior neck lump night sweats.
a. What are your top differentials? Infection, neoplasm (1° vs. 2°), inflammation
b. What two broad categories of tests can you do from the FNAC? (Microbiology, cytology.)
c. How do you label the specimen? (Category 3 hazard) Biosafety level 1, 2, 3 & 4
d. What tests for TB? What stains can be done for TB? (Ziehl Neelsen or auramine.)
e. How long to culture TB? Medium (Lowenstein-Jensen or Middlebrook 7H10), 3-4 weeks (doubling time of TB is 22 hours)

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 f. What is the public health concern?
g. Whom to notify? Consultant in Communicable Disease Control
h. What is the histological appearance of TB? What is a giant cell?
i. What other granulomatous diseases do you know of? (Leprosy, Crohn's, Wegener's, sarcoidosis.)
j. What type of protein deposition occurs? (Amyloid.)
k. What other mycobacterium causes enlarged lymph nodes abscesses in immunosuppressed? (Prefers the term
MAI rather than MAC; MAI – Mycobacterium avium-intracellulare OR MAC – Mycobacterium avium-complex

12. Pathological Fracture

40yo lady got pathological fracture of femur shaft while cycling. Examiner is a poker-faced dude who just says "Thank you" to all your answers.
a. What is a pathological fracture? It is a bone fracture caused by a disease that led to weakness of the bone
b. What could be the causes? What 5 cancers classically metastasise to bone?
c. Fixation done, how to check what malignancy? Histo shows follicular cells, where is it from?
d. Cannot find anything wrong with thyroid, where could the cancer be?
e. Pathologist wants to confirm it’s from the thyroid, how? What epithelial malignancy of thyroid cannot be
found on radionuclide scan and why?

Causes of pathological fracture

- Metabolic bone disease: osteoporosis, osteomalacia, Paget’s disease, renal osteodystrophy
- Benign neoplasm: simple bone cyst, brown tumour (Osteitis fibrosa cystica), GCT (usually benign)
- Malignant neoplasm: multiple myeloma, metastatic bone disease, osteosarcoma
- Infection: osteomyelitis

ANATOMY
13. Thorax & Abdomen
Thorax and upper abdo prosections (specimens all hard as wax).
Posterior view coronal section of heart and mediastinum.
a. What is this? (Pulmonary trunk.) What structure here? (Pulmonary valve.)
b. What branches does the pulmonary trunk have? Right and left pulmonary artery
c. Identify this. (Papillary muscles.) What structure are they attached to in this specimen? (Tricuspid valve.)
d. What connects them to atrioventricular valves? What is their function? Chordae tendineae connects the AV valve to
the papillary muscles, prevents regurgitation during ventricular systole.

Saggital section thorax and mediastinum.

a. Identify azygos vein. Name 2 tributaries or structures that drain into the azygos vein.
b. Where does azygos vein drain into? SVC
c. What is this? (Thoracic sympathetic trunk.) Where do the preganglionic fibres that supply sympathetic trunk
come from? Lateral horn of grey matter of the spinal cord from T1-L2. What connects the sympathetic trunk to the
spinal nerves? The pre-ganglionic fibres enters the anterior rami of spinal nerves through the anterior root

Azygos system
Collective term for the H-shaped configuration of azygos, hemiazygos, accessory hemiazygos veins and left superior intercostal vein that drain much
of the posterior thoracic wall and some mediastinal structures. Provides an alternate pathway for venous return in IVC/SVC obstruction.

Azygos vein
Formed by the union of ascending lumbar veins and right subcostal vein at T12. Ascends in the post. mediastinum before arching over the right main
bronchus posterior at the root of right lung (level of T5-6) where it joins the SVC.
Tributaries: hemiazygos, post. right IC vein, right superior phrenic vein, bronchial vein, pericardial vein, oesophageal vein

Anatomy of Sympathetic Nervous System

- Cell bodies are found within the lateral horn of grey matter of the spinal cord from T1-L2
- Preganglionic fibres passes through the anterior horn to enter the anterior rami of spinal nerve
- Leaves the spinal nerve via white rami communicantes to enter the sympathetic chain where they synapse
- The synapses can occur at the level of the nerve root OR the preganglionic fibres ascend/descend a level
- Post-ganglionic fibres return to the anterior rami via the grey rami communicantes for distribution to target organs

Anterior view of thorax and upper abdo.

a. Identify the spleen. What is the blood supply? Describe course of splenic artery. (KL Feb, 3, Q1)
b. What structure must be preserved in splenectomy? Splenic artery?
c. What 2 other structures does it supply? Pancreas and stomach via left gastro-omental
d. Identify this structure. (Duodenum.) How many parts does it have? 4 parts (superior L1, descending L1-3, inferior
L3, ascending L3-2)
e. Where does ampulla of vater open into? Posterior medial aspect of D2
f. Which structures open into the duodenal papilllae? What do they drain? CBD (bile) & Pancreatic duct (pancreatic
enzymes)

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 g. What blood vessel runs posterior to D1? Gastroduodenal artery

14. Lower Limb

Anterior thigh
a. Identify femoral vein. What structure is medial? (Femoral canal.) Sheffield Feb 2014, 2, Q9
b. What structures are found in femoral sheath? Femoral artery & vein + femoral canal
c. Is femoral nerve inside femoral sheath? No
d. What structure is this? (Rectus femoris.) Function? AIIS to patella tendon, hip flexion and knee extension
e. Point out ITB. What inserts into ITB? What does the ITB do when I'm standing at attention?

Iliotibial Band
The gluteus maximus and tensor fascia latae inserts into the ITB.
Originates from anterolateral iliac tubercle and inserts at the lateral condyle of the tibia at Gerdy’s tubercle.
During knee extension  ITB moves anterior stabilising the knee in extension & prevents lateral displacement of the proximal end of the femur
During knee flexion  ITB moves posterior

Posterior gluteal region, reflected gluteus maximus

a. What is this structure? (Gluteus medius.) Nerve supply? What is its function when I'm marching? Superior
gluteal nerve (L4,5 S1), hip abduction prevents tilting of the pelvis during marching

Posterior thigh
a. Identify biceps femoris. How many heads? Nerve supply? Long & short head, supplied by sciatic nerve (tibia)
b. Identify common peroneal nerve. What muscles does it supply? What sensory supply?
c. What happens in common peroneal nerve transection?
d. What is this? (Gastrocnemius.) Affected if I cut the common peroneal nerve? No, gastroc supplied by tibial nerve
e. If no trauma, got loss of dorsiflexion and numbness of dorsum of foot, where do I look for the lesion?
External compression at fibular head from habitual crossing?

Common peroneal nerve

Motor: lateral compartment of leg (superficial branch) & anterior compartment of leg (deep branch)
Sensory: lateral cutaneous nerve of calf – upper lateral leg, superficial peroneal – anterolateral leg & dorsum of foot except 1st dorsal web space,
deep peroneal nerve – 1st dorsal web space

15. Cervical Spine

a. How many cervical vertebrae are there? 7
b. How many cervical nerve roots are there? C1-8
c. Which vertebrae are atypical? What are the atypical features?
d. Gives you bone - what is this vertebra? (C1 atlas.) Show me the features.
e. What runs through foramen transversarium? What level do they first enter? Vertebral usually enters the
transverse foramen at C6, 7.5% of the cases enter at C7
f. On patient, landmark the hyoid bone. What level is it? Hyoid (C3) thyroid cartilage (C4-5) cricoid (C6)
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 g. What structure is found at C6? What part of GI tract is found at C6? Where does oesophagus end?
Structure at C6 – superior limit of trachea & oesophagus; oesophagus starts at C6 behind cricoid, enters diaphragm at T10 and ends at the
cardia of stomach at T11.
h. I feel down the C-spine; what's the first process I feel? C7 vertebra prominens (N.B. T1 is the most prominent)
i. Why can't I feel the upper spinous processes? (Bifid and attached to nuchal ligament)
j. Landmark the brachial plexus on this patient. What muscles does the brachial plexus run between? The
clavicle can be used for the landmark of the brachial plexus, is runs between the scalene anterior and medius

Atypical cervical vertebrae (C1 – atlas, C2 – axis see Sheffield Feb 2014, 2, Q17 for pictures)
Atlas has no body, kidney shaped superior articular facet on the lateral mass which articulates with the occipital condyle, the posterior arch is
grooved by the vertebral artery.
Atlas bears the dens (odontoid process) on the superior aspect of its body.
Atlanto-occipital joint – flexion and extension; atlanto-axial joint – rotation

Important vertebral levels (C3/4 & C5/6): C3/4 demarcates the superior border of the thyroid cartilage and is where the CCA bifurcates; C5/6
marks the lower limit of pharynx and larynx & the superior limit of oesophagus and trachea,

Lat C spine X-ray and open mouth odontoid - Identify cervical vertebrae on lat x-ray. (Count C1 down to C7.)
a. What's this? (Body of C2) What's this? (Hyoid)
b. Apart from fracture, what other signs of c-spine injury can be seen on lateral x-ray? (Abnormal alignment,
prevertebral soft tissue swelling)
c. How this view taken? (Open mouth odontoid)
d. What features can you see? (Odontoid process, lateral masses of C1, C2 spinous process)
e. What ligaments are attached to odontoid process? Alar ligaments and transverse ligaments of atlas

CRITICAL CARE
16. Acid base & Electrolytes
Crit care: Lady vomiting, epigastric fullness. Labs show Na 125, K 1.9, Cl 59, pH 7.2 etc.
a. What does she have? Why got hypochloremic alkalosis? Why got hyponatremia?
b. How to classify hyponatremia and what examples? Hypovolaemia, euvolaemia, hypervolaemia
c. What are the complications of hyponatremia? Neurological symptoms: confusion, lethargy, muscle weakness, cramps,
seizures, LOC. Complications – seizures, respiratory depression, cerebral oedema (if ↓↓ quickly), CPM (rapid correction)
d. Why got hypokalemia (the simple answer)? (Loss in vomitus)
e. Why got aciduria? What is the key element in these exchanges? (Sodium)
f. How would you treat? Who else should be involved in management? Correct fluid deficit with IV hydration, add K+
supplementation in the fluid regimen, keep NBM, strict I/O charting, IDC insertion
g. When would this lady be fit for surgery?
Hypokalaemia: 1) vomiting 2) intracellular shift of K+ due to metabolic alkalosis 3) urinary loses (see below)

Pathophysiology of hypochloraemia hypokalaemic metabolic alkalosis with paradoxical aciduria

- GI loss causes volume contraction and activation of RAAS
- GI losses are associated with chloride depletion, the usual maintenance of electrical neutrality with reabsorption of both NaCl for fluid
conservation by the kidney is disrupted
- Therefore, the lumen’s negative gradient with sodium reabsorption, causes obligate cation excretion i.e. H+ & K+
- This causes worsening of metabolic alkalosis & hypokalaemia, together with the phenomenon of paradoxical aciduria

17. Epidural
S/p lobectomy and epidural T3 T4 level, now has hypotension bradycardia SpO2 92%.
a. What causes of this clinical picture? An epidural blocks both somatic and sympathetic nervous system OR accidental dural
puncture converting epidural to a high spinal block, blocking the the cardioaccelerator fibres which originates at T1-4
b. What's so good about epidural in this patient?
c. Why do we use temperature sensation to check? Type C fibres which are blocked transmit pain and temperature. (Type A
largest fibres transmit pressure & motor, Type B are moderately sized & myelinated fibres transmit preganglionic fibres, Type C are
unmyelinated and the smallest transmit pain & temperature.)
d. How would you do it in real life?
e. How to manage? Fluid resuscitation and vasopressor e.g. atropine, ephedrine
Spinal vs. Epidural
Spinal (Subarachnoid) Anaesthesia Epidural Anaesthesia
Volume of drug given Small Large
Onset Fast Slow
Density of blockade Usually dense Potential for patchy sensory blockade
Opportunity for redosing No Yes, as catheter routinely inserted
Systemic blood levels of injected medication Negligible May be significant
Anatomic region L3-4 Any vertebral level
Ability to augment post-op analgesia <24 hours Days

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Benefits of spinal/epidural
- Epidural has the benefit of redosing and it is able to augment post-op analgesia
- Has been shown to reduce post-op mortality and morbidity: ↓ in PE, DVT, transfusion requirement, pneumonia, MI & renal failure

Epidural technique
- Midline or paramedian approach
- Identification of epidural space: US guided, loss of resistance technique, hanging-drop technique
- Layers penetrated: skin, subcutaneous fat, supraspinous ligament, interspinous ligament, ligamentum flavum
- Contraindications: infection in the area, ↑ICP, uncontrolled coagulopathy, allergy, patient refusal

Types of peripheral nerve fibres (N.B. the diameter of the fibre decreases with each order)
- Motor: A alpha fibres (myelinated) – controls muscles
- Sensory: A alpha & beta (myelinated) – proprioception and vibration
- Sensory: A delta fibres (thinly myelinated) – pain and cold perception
- Sensory: C fibres (unmyelinated) – pain & warmth perception
Hence due to differential blockade, sympathetic nerves are typically blocked first followed by sensory blockade and finally motor blockade.

18. Perforated Viscus

Elderly gentleman has abdo pain, looks confused. CXR showing free air under diaphragm, ECG showing AF.
a. What must you confirm on CXR and ECG? CXR - air under diaphragm, ECG – arrhythmia & ST changes
b. What is the problem with taking consent from this dude?
c. What do you call all this stuff about how patient must understand information be able to repeat?
d. Who should make decision? Lasting power of attorney vs. 2 consultant
e. What's the significant finding on this CXR? What is differential diagnosis of perforated viscus?
f. What pathologies in the large bowel could cause it?
g. Tell me about this ECG. (Irregularly irregular.) What is the rate? How come different from my automatic
reading?
h. What are the causes of AF in a SURGICAL population? Ischaemic bowel, anastamotic leakage, hypovolaemic shock,
electrolyte abnormalities, Type II STEMI
i. What broad principles to manage AF? If stable how to manage? What 1st line drug? What dose?
Causes of pneumoperitoneum: perforated viscus, ischaemic bowel, after laparotomy/laparoscopy, peritoneal dialysis, Chilaiditi syndrome
Causes of perforated viscus: Perf ulcer, obstructed bowel, intestinal conditions like crohn’s, diverticulitis, appendicitis, mesenteric ischaemia 
bowel infarction
Management of AF: stable vs. unstable AF
- Rate control (Goal HR of 60-80, 90-115 with exertion)
 Amiodarone: IV 150mg over 10min  0.5 to 1 mg/min
 Beta blockers:
 PO bisoprolol 1.25mg, PO atenolol 25mg
 IV propranolol 1mg over 1min Q2min for up to 3 doses (if no cardiac failure OR severe respiratory airway disease)
 Calcium channel blocker:
 IV verapamil 5-10mg over 2min, very 30min
 IV diltiazem 0.25mg/kg over 2min, start infusion at 5-15mg/h 15 minutes later
 Digoxin: IV 250mcg review 4-6 hours later, KIV add 125mcg
- Rhythm control
- Cadioversion

Edinburgh 2014
CRITICAL CARE
1. Variceal bleeding
45 yr old chronic alcoholic, p/w haematemesis, low BP, tachycardic
a. Differential – oesophageal varices
b. FBC picture shows low Hb and platelets
i. Reasons for low platelets – DIVC, liver dysfunction
ii. If you call haematologist, will you ask for platelets? Yes
c. Sengstaken Blakemore tube
i. Describe usage. Used in oesophageal varicies that does not respond to medical therapy (which includes endoscopic
hemostasis and vasoconstrictor therapy) OR when endoscopic intervention is unavailable
ii. Contraindications: recent oesophagogastric surgery, oesophageal stricture, oesophageal tear
iii. 3 ports – what are they for and where do the balloon sits. Gastric balloon port, gastric aspiration port,
oesophageal balloon port. Gastric balloon sits at the GEJ and is usually filled with 100-150ml of air/water, oesophageal ballon is
inflated up to 30-45mmHg (above portal pressure).
iv. What is the modification – port anterior to oesophagus?
v. If there is no modification, what do you do? (insert NGT)
vi. Problems associated aspiration pneumonia, airway obstruction (proximal migration of the SB tube compressing upper
airway), oesophageal perforation/ulceration,

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Indications for platelet transfusion:
- Actively bleeding – threshold is <50,000/microL & <100,000/microL in DIVC patients
- Prevention of spontaneous bleeding – threshold is <10,000/microL in general, <30,000/microL in septic and febrile patients

Placement of SB tube
- Patient should be intubated and the head of the bed up at 45 degrees.
- Test balloons on Blakemore and fully deflate.
- Insert the Blakemore tube through the mouth just like an NGT
- Stop at 50 cm. Test with slip syringe while auscaltating over stomach and lungs. Inflate gastric port with 50 ml of air or saline.
- Get a chest x-ray to confirm placement of gastric balloon in stomach.
- Inflate with additional 200 ml of air (250 ml total)
- Apply 1 kg of traction using roller bandage and 1 liter IV fluid bag hung over IV pole. Mark the depth at the mouth. The tube will stretch
slightly over the next 10 minutes as it warms to body temperature.
- After stretching, the tube may be secured.
- If bleeding continues, you will need to inflate esophageal balloon.
- Attach a manometer to the second 3-way stopcock on the esophageal port of the Blakemore. Inflate to 30-45mm Hg
- Deflate the oesophageal balloon for 5min Q6H to prevent oesophageal necrosis

Management of variceal bleeding

- Resuscitation (ABC)
- Adjuncts – NBM, IDC insertion with strict I/O charting, KIV intubation
- Medications – IV omeprazole 80mg bolus  8mg/hr infusion for 3 days, IV somatostatin, IV antibiotics, stops NSAIDs/anti-coagulation
- Close monitoring
- Emergency OGD
- Surgical – TIPPS (Transjugular intrahepatic porto-systemic shunt), shunt surgery e.g. portocaval (portal vein to IVC)

2. Pneumothorax
Insertion of central line  patient became breathless  CXR shows left sided pneumothorax
a. Initial Management: ABC, inspect/percuss/palpate, O2
b. Before looking at CXR what to do – check pt identifiers, date etc.
c. How to look at CXR – check view, exposure, rotation, well inspired? Patient details, film details (e.g. AP erect fulm),
penetration, rotation, inhalation, lungs + trachea, heart, hilar, skeletal & soft tissue, external devices (e.g. CVP line, NGT)
d. Types of pneumothorax – closed, open, tension; primary vs. secondary (aetiology)
e. Management – insertion of chest tube
Pneumothorax aetiology
- Primary (iatrogenic)
- Secondary – airway disease (COPD, asthma, CF), infection (TB, PCP), ILD, CTD (RA, AS, Marfan, Ehlers-Danlos), cancer (lung CA)

Management of Pneumothorax

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Indications for surgery (VATS, pleurodesis – with talc OR doxycycline/minocycline)
- Persistent air leak (>7 days)
- Recurrent, ipsilateral pneumothorax
- 1st presentation in high risk occupation e.g. pilot, diver

3. Pain Management
70yr old man 9h post laparotomy, c/o lower abdominal pain. Vitals stable, slightly tachycardic, apyrexic. Drug chart given.
a. How do you assess pain Wong-Baker FACES Pain Rating Scale, Numeric pain rating scale
b. How do you assess pt History & PE
c. Drug chart shows IV paracetamol and IV diclofenac, s/c morphine with cinnarizine
d. WHO pain ladder stepwise progression of escalation of analgesia (mild pain – NSAIDs ± adjuvant, moderate pain – weak opioid e.g.
tramadol ± adjuvant, severe pain – strong opioid e.g. morphine, fentanyl ± adjuvant
e. Side effects of morphine (KL Feb 2014, Q7)
f. PCA – what is it? Patient controlled analgesia
i. Problems – pt has to be alert and orientated to be able to
ii. Machine can break down/run out of battery use it

PATHOLOGY
4. PUD
Elderly lady with b/g gastric ulcer, now p/w haematemesis, OGD done, shows peptic ulcer - biopsied. Pt now in clinic to trace report of biopsy.
Report of biopsy – clo test +ve. FBC shows anaemia, Ca raised. Pt taking long term abx.
a. What is an ulcer – breech in epithelium
b. What is CLO test (campylobacter like organism), exact mechanism of CLO test (The basis of the test is the
ability of H. pylori to secrete the urease enzyme, which catalyzes the conversion of urea to ammonia and carbon dioxide. A biopsy of
mucosa is taken from the antrum of the stomach, and is placed into a medium containing urea and an indicator such as phenol red. The
urease produced by H. pylori hydrolyzes urea to ammonia, which raises the pH of the medium, and changes the color of the specimen
from yellow (NEGATIVE) to red (POSITIVE).
c. Treatment – triple therapy (amoxicillin 1g BD, klacid 500mg BD, PPI)
d. Another reason for haemetemsis – hypercalcaemia  increased gastrin release  increased HCl production
e. 2 common causes for hypercalcaemia – parathyroid adenoma, renal failure
f. shown pathology report with chief cells: parathyroid adenoma
g. where are parathyroid glands located
h. management of parathyroid – sestamibi scan, parathyroidectomy
Glands in the stomach
Type of gland Secretion Region
Mucous neck cells Mucus gel layer Fundus, cardia, pylous
Parietal (oxyntic) cells Gastric acid & intrinsic factor Fundus
Chief (zygomatic) cells Pepsinogen & lipase Fundus
Enteroendocrine cells Gastrin, histamine, endorphins, serotonin, cholecystokinin and somatostatin Fundus, cardia, pylorus

Regulation of gastric acid

- Histamine produced by enterochromaffine-like cells (ECL)
- Acetylcholine from parasympathetic activity of vagus nerve
- Gastrin works by binding to cholecystokinin B receptors (CCK) on ECL cells stimulating histamine release

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5. Gallbladder cancer
50 yr old lady gone for elective lap cholecystectomy converted to open, histo: gallbladder CA
a. Commonest histo of gallbladder CA - adenoCA
b. Commonest cause of gallbladder CA in UK – stones causing chronic inflammation
c. Site where gallbladder CA commonly spreads to – liver segment V (the gallbladder straddles the intersegment plane
between liver segment IVb & V, tumours of the fundus and body may invade these segment)
d. POD 3 pt has pain at wound site, redness, what do you suspect? Wound site infection
i. Mgt: abx, take swab for c/s
ii. Commonest organism – staph
e. Inflammation seen at wound, no cellulitis, what else can you do?
f. Wound worsens – develops necrotizing fasciitis
i. Mgt – ABC, abx, debridement
ii. Commonest organisms: staph, streptococcus,
g. Pt develops bloody diarrhea – shown picture of pseudomembranous colitis
h. Why does pseudomembrane happen – biofilm formation clostridium (broad spectrum abx  normal gut flora destroyed  C
diff produces enterotoxin A& B  damages bowel mucosa  exudative fibrin deposition  pseudomembranes)

PROCEDURAL SKILL
6. IDC insertion
a. Commonest causes of anuria – blocked catheter
b. Commonest causes of blocked catheter – gel
c. If obstruction – flush catheter and aspirate
d. Flushed and aspirated, still no urine shown temperature and vitals chart – consider hypovol shock

7. Chest Tube Insertion

a. Select equipment – chest tube (size 10)
b. Margins of triangle of safety – lateral border of pectoralis major, anterior border of latissimus dorsi, 5th intercostal space
c. Connect to underwater seal
d. Complications of chest tube insertion
Complications: improper placement, bleeding, organ penetration (GIT/liver/spleen/lung), dislodge, empyema, re-expansion pulmonary oedema
Equipment
- LA (10ml 1% Lignocaine)
- 10ml syringe, green and blue needles
- Sterile gloves and apron; sterile drapes
- Antiseptic solution
- Dressing, sleek, tegaderm
- Cotton gauze swabs
- Scalpel and blade
- Suture (e.g. 1/0 silk)
- Instrument for blunt dissection (e.g. a curved clamp)
- Chest tube (small bore 10-14; large bore 26-32F)
- Connection tubing and connectors
- Sealed underwater drainage system with 500ml of sterile water
- Suction available

ANATOMY
8. Thorax & Upper limb
a. Arch of aorta – brachiocephalic trunk, left CCA, left subclavian
b. Vagus nerve (Preganglionic parasympathetic fibres travel in it)
c. Recurrent laryngeal nerve (Muscles that it supplies) all the laryngeal muscle except cricothyroid (posterior & lateral
cricoartytenoid, transverse & oblique arytenoid, thryoarytenoid
d. Thyroid – parts of thyroid, blood supply, nerves associated, embryology (Coventry May 2014, Q9)
e. Parathyroid – location, why do inferior thyroid go down into the thymus (KL Feb 2014, 3, Q5)
f. UL brachial plexus injury (KL Feb 2014, 2, Q3)
i. Erb’s palsy – nerve roots, asked to show upper & lower roots
ii. Klumpke’s palsy – muscles involved all the intrinsic muscles of the hand – thenar (APB, FPB, OP), hypothenar
(Adductor pollicis, FDM, ODM, ADM), lumbricals, interossei muscles (N.B. thenar + hypothener = A OF A OF A)

9. Skull & Lateral Spine X-ray

a. Temporomandibular joint
i. What joint is it: synovial joint with a fibrocartilaginous articular cartilage dividing the joint cavity
ii. In a living person what do you find???
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 iii. Movements of the TMJ: elevation, depression, protrusion, retraction, side to side movement
iv. Muscles acting on joint: temporalis, masseter, medial and lateral pterygoid, digastric, mylohyoid, geniohyoid
b. Shown pituitary fossa
c. Coronoid suture
d. What are diploic veins? Diploic veins are thin-walled valveless which runs between the internal and external tables of the skull, it
communicates with the meningeal vein, sinuses of dura and veins of the pericranium. (N.B. emissary veins connects the extracanial venous
system i.e. scalp, face, neck, with the intracranial venous system)
e. Foramens on base of skull – name them foramen spinosum, foramen ovale, styolmastoid foramen
f. Pterion – significance and bones that make it up
g. Muscles attached to styloid process: stylohyoid muscle (VII), styloglossus muscle (XII), stylopharyngeus muscles (IX)
h. Show cervical vertebrae on Cspine xray
i. What is odontoid process. It is a distinctive characteristic of C2, its is a protuberance of C2 which arises from the
superior surfaces of the body
ii. What is the joint between odontoid and atlas – pivot joint (synovial joint)
iii. What type of joint is atlanto-occipital joint – condyloid joint (synovial joint)
Muscles affecting TMJ movement
- Elevation: masseter, temporalis & medial pterygoid
- Depression: lateral pterygoid with digastric, mylohyoid, geniohyoid, gravity
- Retraction: posterior fibres of temporalis
- Protraction: lateral pterygoid
- Side-to-side: lateral & medial pterygoid alternating on each side

10. Ankle
(KL Feb 2014, 2, Q5)
a. Orientate the tibia/fibula
b. Name each bone of the foot
c. Subtalar joint – talonavicular and calcaneocuboid
d. Name bones that form medial and lateral arches of foot
e. Sustentaculum tali – attachment to the plantar calcaneo-navicular (spring), tibiocalcaneal, and medial talocalcaneal ligament.
f. Medial ankle collateral ligament
g. Lateral ankle collateral ligament
h. Which position is the ankle most stable
i. Movements of ankle
j. Show tendons and name muscles of all compartments of LL
k. Landmarks of dorsalis pedis and posterior tibial artery
l. Blood supply of foot (KL Feb 2014, Q3)
m. Muscles responsible for inversion of foot & eversion of foot (KL Feb 2014, Q3)

PHYSICAL EXAMINATION
11. CVS
CVS examination with murmur of mitral regurgitation, asked to check BP & give diagnosis

12. PVD
Patient p/w claudication, routine examination
Offered to do ABPI, asked about LL arterial supply

13. RHC Pain

a. Differentials for RHC pain: cholecystitis, PUD, cholangitis, lower lobe pneumonia, pancreatitis, renal
pathology
b. Bedside tests you can do to help in your diagnosis – blood tests, UFEME, US abdomen
c. US shows gallstones – cholecystitis
d. Management of cholecystitis – abx (3rd gen cephalosporin + metronidazole)
e. Surgical options: early vs. interval cholecystectomy OR cholecystostomy with T-tube decompression
Cholecystectomy (Early vs. Late) – N.B. early surgery has been found to be more beneficial
Early Late
Advantage: one admission, easier to operate as the GB is oedematous Advantage: better laparoscopic success

Disadvantage: Disadvantage:
Ongoing inflammation  increased risk of bleeding Fibrosis  difficulty mobilising FB
Higher risk of surround injury due to difficulty visualising Require readmission
Higher conversion to open surgery Chance of recurrence/acute pancreatitis during the wait for surgery
Increased risk of post-op infection

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14. Bilateral hemianopia
Elderly guy p/w headache, do cranial nerves examination – bitemporal heminanopia (Sheffield Feb 2014, Q3)
a. Differential: pituitary adenoma
b. Management: CT brain/MRI, blood test/hormone test, surgical/medical txt (bromocrpitine)

COMMUNICATIONS
15. Call trauma consultant
21 yr old male RTA victim with LOC 15min during incident. Reg in OT, please call trauma consultant.
Pt GCS15 initially, lucid, vitals stable initially, blood test ok, has pain over right UL (XR shows metacarpal #), open tibia # over left LL. FAST
shows small amt of free fluid in abdomen. Later left LL no distal pulses.
a. What is most urgent – open #, arterial damage OR compartment syndrome
b. What do you do
i. Immobilize and reduce the fracture
ii. CT abdo/pelvis to rule out injury & CT head
c. Plan for next 12hr

16. Angry patient

Pt p/w abdominal swelling – ascites. Pt had tap done, shown malignant cells. Scheduled for CT scan but was cancelled because scan machine broke
down. Given options – either do US or t/f to other hospital for CT scan. Wife has arrived and is angry wants to s/t consultant but he is in emergency
surgery. To s/t wife.

HISTORY TAKING
17. LBP
40 yr old lady with generalized back pain X 5 yrs
Red flags of back pain, differentials, what examination will you perform?

18. Diarrhoea
25 yr old girl p/w diarrhea, blood stains
a. Differentials – inflammatory bowel disease, IBS, cancer
b. Investigations – FBC, UECr, Stool c/s, colonoscopy
c. Features seen on colonoscopy

Singapore Aug 2014

HISTORY TAKING
1. Altered Mental State
Patient came for elective THR. Nurses are concerned that pt is confused and the consent is not valid. Please assess pt.
Did AMT scoring, offered MMSE. pt got 0 out of 10 pts for AMT (they gave the pts details on a piece of paper)
Patient did not even know why she was in hospital (i did not bother gg on to ask pt if she knew the risks of op, or the alternatives available)
- Discussed with examiner: said that pt definitely not fit for op.
- Offered to speak to pts daughter to see if confusion was acute or chronic, to speak to doctor who took the consent. If acute, offered various ix
for workup: hypocount, bloods, vitals, neuro exam; if chronic, offered geriatric review KIV scan head
- To reschedule another appt to assess fitness for consent as OA hip replacement was nonurgent examiners didnt really ask any questions for this
case, so i just kept talking. Frankly, im not sure whether i headed in the right direction.

2. PR Bleeding
Middle age lady, alternating bowel habits, family hx of cancer. pr bleed for 6/12
Conversation was totally not guided by examiners. had to time my own history taking, move on to differentials and investigations. Didn’t manage to
move on to management; on hindsight, shouldn’t have spent so much time on taking an extensive history.

PROCEDURAL SKILLS
3. OT listing
Man with strangulated hernia. b/g of severe copd, has pacemaker
Lady with perforated diverticular abscess for Hartmanns operation, has penicillin and iodine allergy
Man with LL ulcer for BKA. background DM on insulin and AF on warfarin, mrsa positive
Prioritizing should be in the order above, based on urgency of op.
a. Why the order above?
b. How long will you expect each operation to last? How extensive will you clean and drape the patient?
c. What to worry about for copd? (may not be suitable for GA)
d. Question on monopolar and bipolar diathermy
e. How to manage the pacemaker
f. What to give if has iodine allergy
g. How to manage DM and AF pre-op (for DM start SCSI & arrange for 1st case if possible, for AF see below)
h. When to give spinal or epidural anaesthesia

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Led on to mannequin on the bed
a. Where will you place the diathermy pad for monopolar/bipolar (trick question) Why that spot?
b. If you have to use monopolar for the pacemaker pt, where will you place the pad?

The above patient is high risk with significant bleeding risk

4. Excision of lump
Consultant was in the process of excising a benign nevus on pts left thigh, but was called away after giving the LA.
- Expected to check consent again (was hidden away at a corner in a room)
- Pick the instruments you require, pick the stitch you want. Need to mount your own scalpel blade, otherwise quite straightforward
- Stem offered chance to draw out margins if required, but I feel it just wastes time
- The sponge used was quite stiff and hard to close. a lot of the candidates ended up tearing through the sponge, myself included. My advice is
that since they probably don’t judge your suturing skills, just throw very big bites to minimise the risk of tearing through
- Remember to throw your sharps, including the scalpel blade tip and give quick advice on TCU plans and how to keep the would clean

PHYSICAL EXAMINATION
5. Cranial nerves
Lady had a fall 2 days ago sec to alcohol intoxication. now has left sided hearing loss. Perform examination of her hearing, and other cranial nerves
as necessary. No otoscopy required. Performed webers, rinnes, and a full CN examination anyway because there was time.
a. What are your findings?
b. Causes for conductive hearing loss - ear wax, infection, hemotympanium sec to trauma
c. Which CN is the most important to examine together? CN7. Exits together at IAM AND the facial canal lies near to the
medial wall of the middle ear, and the chorda tympani enters the middle ear via the posterior wall
d. How will you fix the otoscope? How to perform? How will you position the pts ear to make otoscopy
easier? Pull the patient’s external ear in a posterior superior fashion
e. Showed picture of hemotympanium. What is this?
f. What investigation to do? CT head, audiogram, ENT review

Cause of CHL
- External ear: impacted ear wax, otitis externa, FB
- Middle ear: AOM, OME, TM perforation, otosclerosis, cholesteatoma, haemotympanium
Base of Skull Fracture
- Sign/Symptoms: hearing loss (can be CHL or SNHL), vestibular symptoms (vertigo, nystagmus), bleeding from EAC, CSF otorrhea &
rhinorrhea, haemotympanium, battle sign (mastoid ecchymoses), raccon eye (periorbital ecchymoses), halo sign (double ring of CSF fluid on
filter paper as it separates from blood)
- Diagnosis: otoscopy, CT head, audiogram, CSF leak – check halo sign OR send fluid for β-2-transferrin

6. Inguinal hernia
a. Where is the deep ring? Where are the inguinal ligament landmarks? Deep ring – midpoint of inguinal ligament,
defect in the transversalis fascia; superficial ring – immediately above the pubic crest, triangular defect in aponeurosis of ext. oblique
b. What are your differentials? Examiner looking for lipoma of cord
c. What ix will you do? I offered US of contralateral side because I thought there might also be a contralateral hernia
d. Lap or open?
e. Mesh repair or primary repair? Is it proven that one has better results than the other? Yes, tension free mesh
repair has reduced recurrence rates (Cochrane Database Syst Rev. 2002 AND EU Hernia Trialists Collaboration)
f. Pt doesn’t want operation because his job requires heavy lifting, has no money, cannot take MC. I offered
to discharge pt with advice, but apparently examiner was looking for a second TCU with patient to let
patient reconsider
g. How long must patient avoid heavy lifting for after hernia repair? Light work can be resumed after 1 week, heavier
jobs after 6 weeks

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7. CVS
Mitral valve replacement, mid sternotomy scar, audible metallic click even at bedside. no other complications.
a. What is the diagnosis?
b. What are your concerns for operation? Anticoagulation, current cardiac function, risk of IE
c. On mention of anticoagulation, examiner pulls out a ACC warfarin chart of pt. Asked qns abt warfarin
mechanism of action, how to bridge with clexane, when to resume warfarin
d. What preop ix : ECG, 2DE
e. NICE guidelines for IE prophylaxis (Glasgow May 2014, Q2)
f. Patient presents with fever 5 days postop. what are ur concerns

8. OA knee
OA knee. examination largely unremarkable except for mild crepitus over knee joints
a. Expected to perform hip and ankle examination
b. Expected to offer neurovascular examination
c. Asked for dermatomes
d. Asked for differentials

COMMUNICATIONS
9. Update Consultant
Expected to read through 'case notes' and piece the story together within ten mins prep station.
Scenario was an elective left hemicolectomy for caecal tumor, with liver biopsy for suspected mets. Currently postop D1, having persistent
tachycardia 120 and hypotension SBP 90-100 post op, temp 37.5. postop bloods unremarkable except drop in Hb from 12 to 10, Cr 116, Urea 16.
ECG normal - no MI/PE. CXR clear. pt documented as having benign abdomen, appears dehydrated. I/O in negative 150mls balance, GW nurses
said theres no urine output in IDC. asked to call consultant on call, as consultant incharge is on leave.
- Asked who the consultant of the case was (need to pick up this info, some candidates didn’t realise leading to some confusion)
- Asked to summarize the case
- Asked 'so what do you think it is?' (offered dehydration, need to check whether catheter is blocked'
- Asked for plans of action, whether patient need to be brought down to H
- Asked whether candidate feels the consultant on call needs to come back (I said no, but will call him again if patient does not respond to fluid
resuscitation or the repeat set of bloods shows any worsening. Offered to proceed with CTPA if has desaturation, but will keep on clexane and
TED stockings for now)
- Asked whether it is possibly an anastamotic leak? (I offered that as pt is non-toxic, it is very unlikely. But i'll do serial abdo exam, and let
consultant know again if pt becomes peritonitic)

10. Patient AOR

Counselling: Pt wants to AOR. please advise patient
Preceded by a prep station. Given information that patient suffered a splenic hematoma after an accidental fall, seen on CT scan, sec to rib fractures.
No evidence of lung injury. Hb dropped by 1g/dl, bloods otherwise stable. (Nothing much to prepare for this. Just sat around and stoned)
- Counselling pt was easy. pt offered all the information required.
- Explored pts concern: some story abt how pt has job interview the next day. When offered to speak to family, said that he doesn’t want wife to
know, and that she had breast cancer
- Offered options to excuse patient from job interview.
- Patiet insisted on AOR in the end. Advised patient to return by giving him warning symptoms
- Not much knowledge required at this station. Pt kept the conversation gg 90% of the time.

ANATOMY
11. Shoulder
a. Piece the clavicle scapula and humerus
b. What’s the surgical and anatomical neck
c. Parts of the scapula
d. Greater and lesser tuberosity
e. Range of motion of shoulder joint abduction (0-180° N.B. scapulothoracic takes over after 90°), adduction (0-45°), flexion (0-
180°), extension (??), external rotation (0-45°), internal rotation (thumb reaching T7 i.e. inferior angle of scapula)
f. Factors affecting stability of a shoulder joint (Glasgow May 2014, Q16)
g. What does shoulder joint need to do to complete abduction? Requires depression of the sternoclavicular joint AND
scapula rotation
h. Muscle that stabilises shoulder joint (Glasgow May 2014, Q16)
i. Identify supraspinatus infraspinatus teres minor and subscapularis. whats the nerve supply
j. Identify functional parts of the pec major clavicular head (C5-7) & sternocostal head (C8-T1)
k. Nerve root supply of pec major. Supplied by lateral (C5-7) and medial (C8-T1) pectoral nerves (N.B. medial pectoral nerve
supplies the pectoralis minor)
l. Actions of deltoid – shoulder abduction, flexion & extension
m. Axillary nerve dmg, whats the consequence (Glasgow May 2014, Q16)
n. Where does the brachial plexus run? (posterior triangle of neck)
o. MRI shoulder photos

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12. Cervical spine
a. Number of C-spine, number of C-spine nerve roots – (Glasgow May 2014, 2, Q15)
b. Which are atypical C-spine processes – (Glasgow May 2014, 2, Q15)
c. Parts of the C2 spine (lamina, dens, foramina transversalis, verterbrae body, articulation areas)
d. Where do nerves exits – spinal nerves exit the vertebral column via the intervertebral foramen (N.B. all cervical nerves emerges
ABOVE the corresponding vertebrae except C8, subsequently all spinal nerve emerge below their corresponding vertebrae)
e. Ligaments between C1 and C2
f. Shown Xrays of C spine (odontoid open mouth and lateral view): identify various parts of various
g. Bones on both views (C1 C2 hyoid)
h. In traumatic rugby injury, what are the abnormalities you’ll expect to see on the xray besides
i. Fractures? (soft tissue swelling, dislocation)

13. Abdominal aorta

a. Point out the aorta/ IVC
b. Branches of aorta (specifically which are the posterior branches, which branches supply the GI tract and
at what level does it exit)
c. Which level does the aorta enter the abdominal cavity, what level does it bifurcates? Enter abdomen at T12 via
aortic hiatus in the diaphragm, bifurcates at L4
d. What structures overlie the aorta: duodenum 1 and 4, head of pancreas, liver
e. Point out the tributaries of the IVC
f. Identify the left and right gonadal vein (the left couldn’t be seen actually, was hidden between all the other structures)
g. Shown mesenteric angiogram. Asked the identify the branches
h. Shown CT angiogram of AAA. asked to identify it (saccular, infrarenal AAA)
i. What is a dissecting aneurysm? What is the pathogenesis? A dissecting aneurysm is a false aneurysm as it does not
involve all 3 layers of the aortic wall. An intimal tear creates a direct communication between the tunica media and the aortic lumen, this
allows the splaying of the laminar layer forming a blood filled lumen within the aortic wall.
j. What are the causes? Which is the most common cause worldwide (hypertensive, atherosclerosis, smoking)

Relations of abdominal aorta

- Anterior: lesser omentum, stomach, uncinated process, splenic vein, left renal vein, 3rd part of duodenum
- Posterior: bodies of L1-4 vertebra, left lumbar veins, cisterna chyli
- Right side: IVC, thoracic duct, azygos vein
- Left side: left sympathetic trunk

Branches of abdominal aorta Branches of coeliac artery

- Single ventral branches (3): coeliac artery (T12), SMA (L1), IMA (L3) - Left gastric artery
- Paired branches (5): inferior phrenic artery (T12), adrenal artery (T12), - Splenic artery
renal artery (L2), gonadal artery (L2-3), 4 paired lumbar arteries  Short gastric artery
- Single terminal branch (1): median sacral artery (L4)  Splenic branches
 Left gastro-omental arteries
Tributaries of IVC (formed by the confluence of CIV at L5) - Common hepatic artery
- Common iliac vein (L5)  Cystic artery
- Lumbar veins (L1-5)  Right gastric artery
- Right gonadal vein (L2) – the left gonadal vein drains into the left renal vein  Gastroduodenal (right gastro-omental,
- Renal veins (L1) superior pancreaticoduodenal)
- Right suprarenal vein (L1) – left suprarenal vein drains into left renal vein  Hepatic artery proper
- Hepatic veins (T8)
- Paired inferior phrenic veins (T8)

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PATHOLOGY
14. Ulcerative colitis
a. What is pathogenesis of ulcerative colitis (Glasgow May 2014 Q9)
b. If it is Crohns, what will the microscopic features be?
c. What is a proto-oncogene. Proto-oncogene is a normal gene that codes for protein that regulate cell growth and differentiation, it
can become an oncogene due to mutation and leads to unregulated cellular growth and differentiation
d. Why will the patient require colonoscopic surveillance? Cancer
e. Colono done shows TA with LGD and evidence of invasive adenoCa. What surgery will you offer the
patient? (total colectomy)
f. Identify the duke or TNM staging (schematic diagram given, showing invasion into propria and 1/4 LN
affected)
g. If there was liver mets, how will it affect the TNM staging?
h. How will you manage the patient preoperatively in view of long term steroids
i. Questions on HPAA axis. How will the cortisol affect the adrenal gland? Will it cause both the cortex and
medulla to atrophy? Long term steroid usage causes adrenal cortex atrophy
j. Postoperatively, pt was found to be unconscious and hypotensive. ABG and bloods were normal.
k. What is the cause? (addisonian crisis)
l. Pathogenesis of addisonian crisis? In SECONDARY adrenal insufficiency, exogenous steroids suppresses the HPA axis, a
sudden withdrawal of steroids and the stress of surgery induces a cortisol requirement in excess of the adrenal gland’s ability to respond
immediately
m. How will it affect the glycemic control of the patient? Causes hypoglycaemia (metabolic derangements: ↓Na+, ↑K+,
metabolic acidosis and hypoglycaemia)

15. Rheumatic heart disease

Stem on man with aortic valve failure, with history of joint pains when young. (KL Feb 104, 3, Q4)
a. What is the likely cause?
b. How did rheumatic heart disease cause the aortic stenosis? (examiner wanted answers on inflammation of the valve)
c. If the patient is having fever now, what is the like cause?
d. What are the common organisms in IE?
e. What are three signs you find on the hands in IE? What is the pathogenesis?
f. What antibiotics will to you give? Why is it difficult to treat IE?
g. If it occurs on the tricuspid valve in a younger person, what will you be worried about? ASD (patent foramen
ovale) vs. IVDA
h. If the pt suddenly develops renal impairment, whats the cause? Immune complex glomerulonephritis
i. What blood test will you use to monitor progress of disease? Blood cultures to document eradication of bacteraemia
j. If the pt does not respond to antibiotics, what options are there? (I gave aortic valve replacement, but I think examiner
was looking for heart transplant)
k. What kind of matching do you need before transplant? (HLA antigen)
l. What kind of immunologic reaction will occur if not matched? What is the consequence?
m. How do you prevent transplant rejection?
n. What is the consequence of long term steroids? (looking for lymphoma/leukaemia as malignancy)
Challenges in treating IE
Eradicating bacteria from fibrin-platelet thrombus is extremely difficult as
- There is a high concentration of organism present within the vegetation
- The organisms are located DEEP within the thrombus
- Interference of fibrin and white cells with antimicrobial action

CRITICAL CARE
16. Acute Pancreatits
Glasgow May 2014, Q1
a. What is the likely diagnosis? (based on stem and blood results)
b. What causes normal amylase level in pancreatitis? Does amylase correlate with severity of pancreatitis?
c. What causes the hypocalcemia?
d. What are the consequences of severe pancreatitis?
e. What radiological investigations will you do? (CT scan and US HBS)
f. What is a pancreatic pseudocyst?
g. What are the symptoms to suggest a pancreatic pseudocyst?
h. Name two forms of scoring and explain one of them.
i. What glasgow score breakdown is? What score will be considered as severe?
j. What analgesia will you give the patient?
k. What is the WHO analgesia ladder?

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 l. Is morphines effect on the sphincter spasm real or theoretical? Studies have shown that morphine an increase in
sphincter of Oddi pressure; however, there is no clinical studies to demonstrate that morphine can aggravate pancreatitis

17. Nutrition
a. What does X-ray show? (small bowel I/O)
b. What is the likely cause? ( SB stricture sec to Crohn’s)
c. What are the feeding options? (parenteral vs non parenteral)
d. What are types of non-parenteral feeding options? NGT, NJT, PEG, PEJ (gastric vs. post-pyloric feeding)
e. What are the complications of non-parenteral feeding?
f. What are constituents of TPN? Sugars, water, fat emulsions, nitrogen, electrolytes, vitamins and trace elements
g. What is the main source of carbohydrate in TPN? Dextrose/Glucose
h. What is the consequence of using glucose only as the main form of carbohydrate source?
i. What are the complications of parenteral feeding? Catheter related vs. metabolic
j. How do you give parenteral feeding? Via central indwelling central venous access OR PICC
k. What are the indications for parenteral feeding?
l. What are the consequences of bowel mucosa atrophy? Translocation of bacteria
Complication of enteral feeding
- Aspiration with gastric feeding: decrease risk with 45°, post pyloric feeding
- Diarrhoea: concentrated feeds less likely to induce diarrhoea, fibre helps significantly but CI in patients with impaired peristalsis & on pressors
- Metabolic derangements: refeeding syndrome, hyperglycaemia, micronutrient deficiencies
- Constipation
- GERD  oesophagitis, oesophageal stricture, aspiration pneumonia

Complications of TPN
- Mechanical (venous assess)
 Line sepsis, venous thrombosis, air embolism
 Pneumothorax, neurovascular injury during insertion
- Metabolic derangements
 Fluid overload: large sodium load is osmotically active
 Hyperglycaemia from large carbohydrate load  HHNK, dehydration, fatty liver
 Refeeding syndrome
- Gut atrophy with bacterial translocation: loss of barrier function due to lack of direct contract with nutrients (esp. glutamine)

Constituents of TPN
- Carbohydrate 50%
- Fat emulsions 30-40%
- Fat: 1-2g/kg/day
- Nitrogen
- Water: 30-35ml/kg/day
- Electrolytes: Na+, K+, Cl-, Ca2+, Mg2+, PO43-
- Vitamins: A, D, E and K (fat soluble); B and C

Indications of TPN
- Critical illness: severe malnourishment (>10% LOW), multiple trauma, severe burns/sepsis, MODS
- GIT abnormalities: ECF, short gut, IBD, radiation enteritis, pancreatitis (enteral feeding mandates a functional GIT – ≥100cm of SB, no IO)

Problems with glucose as the main form of energy

- As part of the stress response, the critically ill patients are often hyperglycaemic & glucose intolerant. Therefore, using glucose as the primary
source of energy, patients will not receive their daily required amount due to poor utilisation of gluose
- Excess glucose will be converted to lipids in the liver, these can lead to derangements in the LFT
- Extra CO2 produced upon oxidation of glucose may lead to respiratory failure and increase ventilatory requirements
- Relying solely on glucose may lead to deficiencies of essential fatty acids

18. Epidural anaesthesia

Post lower lobectomy, pt now is hypotensive, bradycardic and desaturation. Patient had spinal anaesthesia at T4/T5, and had epidural catheter
a. What are your differentials? (hemopneumothorax, paralysis of diaphragm, paralysis of intercostal)
b. What is the management plan? (for all the different scenarios. remember to call consultant of op as well
as anaesthetist to review)
c. What factors affect the epidural efficacy?
d. Why do you test for temperature sensation rather than pain?
e. How do they test for temperature sensation in the OT?
f. How does epidural cause the hypotension and bradycardia?
Efficacy of epidural anaesthesia
- NOT affected by baricity or position of patient unlike spinal anaesthesia
- Type of LA used: e.g. fast onset with short duration medication like lidocaine vs. slower onset and longer duration medications such as
bupivacaine and ropivacaine

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- Addition of opioids enhances pain control
- Duration increased with addition of vasoconstrictors e.g. epinephrine
- Addition of bicarbonate to epidural increases the penetration of LA through the dura layer (bicarbonate keeps the LA in the non-ionized form)

Cairo Oct 2014

ANATOMY
1. Mandible
a. Identify the condyle, TMJ and articulate the mandible with the skull
b. TMJ ligaments: major ligament – temopromandibular ligament; minor ligament – stylomandibular and sphenomandibular
c. What happens when opening the mouth?
d. Identify pterion, diploic veins.
e. Lateral x ray spine id. Odotoid process, post. arch of atlas, type of ligament between axis and atlas
f. Foramen spinosum, styloid process ligaments attached, stylomastoid foramed,
g. Layers encountered when making a burrhole
Temporal styloid process
Serves as an anchor point for several muscles associated with the tongue
- Muscles: styloglossus, stylohyoid, stylopharyngeus
- Ligaments: stylohyoid and stylomandibular ligament

Layers encounter in burrhole (SCALP)

- Skin, Connective tissue, Aponeurosis (dense fibrous tissue), Loose areolar tissue, Periosteum

2. Thorax
a. Identify right & left subclavian artery, right & left CCA, right & left RLN
b. Parts of the thyroid, blood supply &venous drainage
c. Embryology of thyroid, thyroglossal cyst
d. Identify trunks of brachial plexus, erb'palsy motor and sensory, klumbek's palsy

3. Femoral Triangle
a. Boundaries of femoral triangle
b. Identify femoral artery & vein, femoral nerve and muscles supplied by femoral nerve
c. Subsartorial canal and boundaries, contents
d. Surface anatomy of femoral art, surface anatomy of saphenofemoral junction
e. Boundaries of femoral ring , contents of femoral sheath
Subsartorial canal
- Boundaries: anteriorly – sartorius, posterior medial – adductor longus and mangus, laterally – vastus medialis
- Contents: femoral artery, vein and branches of the femoral nerve (specifically the saphenous nerve and nerve to vastus medialis)

Femoral artery: mid-inguinal point; Saphenofemoral junction: 4cm below and lateral to the pubic tubercle

PATHOLOGY
4. Infective Endocarditis
a. Definition of infective endocarditis
b. Organisms, 3hand signs, rheumatic fever , young patient with IE involving TV
c. Endocarditits risk factors, failure of treatment, complications, types of matching in heart transplantation
d. Complications of immunosupressive therapy
Risk factors for IE
- Acquired valvular heart disease with stenosis or regurgitation
- Valve replacement
- Structural congenital heart disease, including surgically corrected, but excluding isolated ASD, fully repaired VSD/PDA
- Previous IE
- HOCM

Complications of IE
- Cardiac – AMI, pericarditis, arrhythmia, valvular insufficiency, CCF, sinus of Valsava aneuryms, intra-cardiac abscess, arterial emboli
- Non-cardiac – GN, AKI, Stroke, mesenteric/splenic abscess or infart

5. Gangrene & Lung CA

a. Definition of gangrene It is a potentially life threatening condition that arises when there is considerable amount of necrotic tissue
b. Difference between dry and wet gangrene
c. Athersclerosis, risk factors, types of cell death
d. Difference between mesothelioma and bronchogenic caricinoma,

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 e. Signficance of pleural plaques
f. Risk factors of mesothelioma
Dry gangrene is a form of coagulative necrosis that develop in ischaemic tissue
Wet gangrene occurs when the tissue that undergoes ischaemic necrosis becomes infected

Bronchogenic carcinoma vs. mesothelioma

Mesothelioma Bronchogenic carcinoma
Risk Factors Asbestos (mining, shipyard, ceramics, paper Smoking, asbestos, COPD/ILD, TB, radiation,
milling, railroad repair) halogen exposure
Histology Epithelial, sacromatoid, mixed NSCLC – adenomcarcinoma, SCC, large cell
SCLC (strongly associated with smoking)
Prognosis Poor Poor

Pleural plaques
- Most common manifestation of asbestos related disease
- Patients are usually asymptomatic and the plaques are incidentally found on chest radiographs
- These plaques are benign and require no treatment or follow up

CRITICAL CARE
6. Hypothermia
a. Definition of hypothermia, risk factors, ways of heat loss
b. Why is there coagulopathy in hypothermia? Reduced platelet function, impaired activation of coagulation cascade
c. Complications of massive transfusion?
d. DIV and treatment, who to involve in care?
e. Ruptured AAA, organs to be ischemic if AAA ruptures

Organs affected: cardiopulmonary, renal ischaemia, intestinal ischaemia (predominantly colonic due to extension into IMA), extremity ischaemia
(LL), pelvic ischaemia ± spinal ischaemia

7. Acid Base
a. Ways of CO2 transport, draw equation, where does it occur, chloride shift
b. Why does morphine cause respiratory depression
c. When to treat respiratory acidosis and why, how to treat?
d. Why PaO2 is still normal despite on 60% O2, why bicarbonate still low

8. AF & Pneumoperitoneum
CXR (air under diaphragm) and ECG (AF)
a. Causes of air under diaphragm? Sheffield Feb 2014, Q13. Causes of AF? Coventry May 2014, 2, Q8
b. Calcuate heart rate from ECG, why different from the one measured by the machine?
c. How to treat AF?
The difference occurs when a given electrical depolarization and systolic contraction does not generate a palpable peripheral arterial
pulsation. The ECG measures heart rate via the R-R interval, in patient with short R-R interval e.g. AF, the increased heart rate impairs
diastolic filling and these reduced SV causing imperceptible arterial pulsation.

As the pulse oximeter and automatic non-invasive BP monitoring depend on arterial pulsation to determine the HR, pulse deficits due to
poor CO causes a discrepancy with the heart rate measured by the ECG.

PHYSICAL EXAMINATION
9. Cranial nerves
10. Lipoma
11. Submandibular Gland
12. Inguinoscrotal hernia

HISTORY
13. Thyroid goitre
A woman with a 10 history of goiter recently turned to be toxic

14. IBS
A woman referred from her GP for calcular cholecystits and on history taking discovers to be an IBS?

COMMUNICATIONS
15. Counselling for appendicectomy
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Anxious mother about her 10 y old daughter going to have appendectomy, questions about confirming diagnosis, how
big is the scar, any harm to reproductive tubes.

16. Refer CTVS

Phone cardiothoracic consultant to make a refer of polytrauma patient with aortic rupture, never lie if you are not sure of
any thing

PROCEDURAL SKILLS
17. Sutures
Hand tie 2 rubber bands, deep tying in a hock, figure of eight a bleeding point
Name of knot, why, other knots, how to protect deep structure when tying at depth, material of vicryl, how much it keeps
tensile strength, advantages of braided sutures.

18. FNAC
FNAC of cystic lesion suspicious to be a recurrence of malignant melanoma
Assistant offers you many types of syringes and needles to choose, offers LA, 2slides to put on and a cytospine
container, patient ask is it malignant, where to know pathology report?

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