Avishek Recent Recalls

2021
MRCS OSCE PART B

NEW STATIONS - 2021
All the stations are collected and edited by Dr Avishek and Dr Kazi Sadman
Contents
Gallbladder stones - ASSCC...................................................................................................................................... 2
Pulmonary Embolism (PE – ASSCC) ......................................................................................................................... 6
Sigmoid Volvulus + Metabolic Alkalosis (ASSCC) .................................................................................................... 9
Renal Cell carcinoma (Pathology) ......................................................................................................................... 13
Squamous Cell Carcinoma (SCC) On Arm - Pathology .......................................................................................... 17
Post-tonsillectomy Bleeding (ASSCC) .................................................................................................................... 20
Extra Questions from DO-HNS .............................................................................................................................. 21
Bleeding Pseudoaneurysm - Pathology ................................................................................................................ 24
Lung Cancer (PATHOLOGY) .................................................................................................................................... 26
Breast Cancer (PATHOLOGY) ................................................................................................................................. 29
HCV (PATHOLOGY) ................................................................................................................................................. 33
Acute Pancreatitis (PATHOLOGY) .......................................................................................................................... 39
Hip Pain (History Taking) ....................................................................................................................................... 41
MRCS OSCE B NEW STATIONS 2021

1
Gallbladder stones - ASSCC
SCENARIO:
Young patient with right upper quadrant pain aggravated by a fatty meal. Observation chart (BP, HR and temp
– all normal
D/D:
Common:
• Cholelithiasis, cholecystitis
• Appendicitis
• Perforated peptic ulcer
• Acute pancreatitis
Rare:
• Acute pyelonephritis
• MI
• Pneumonia – right lower lobe
Most probable Dx?

Gall stones (Cholelithiasis)
Pathology of gall stones?

Cholesterol stones: (Most common in western
countries): When cholesterol concentrations
exceed the solubilizing capacity of bile
(supersaturation), cholesterol can no longer
remain dispersed and nucleates into solid
cholesterol monohydrate crystals. Four conditions
appear to contribute to formation of cholesterol
gall stones:
• Supersaturation of bile with cholesterol
• Hypomobility of GB
• Accelerated cholesterol crystal nucleation
• Hypersecretion of mucus in the GB
Pigment stones: Disorders that are associated
with elevated levels of unconjugated bilirubin in
bile increase the risk of developing pigment
stones. These include:
• Chronic hemolytic anemia
Factors associated with gallstone formation
• Severe ileal dysfunction or bypass
• Bacterial contamination of biliary tree

2
Causes and risk factors of gall stones?
Cholesterol stones Pigment stones
• Demography: Northern Europeans, North and • Demography: Asian more than western, rural
south Americans, native Americans, Mexican more than urban
Americans • Chronic hemolytic anemia
• Advancing age • Biliary infection
• Female sex hormones • Gastrointestinal disorder:
o Female Gender o Ileal disease (e.g., Crohn’s disease)
o Oral contraceptives o Ileal resection or bypass
o Pregnancy o Cystic fibrosis with pancreatic
• Obesity and metabolic syndrome insufficiency
• Rapid weight reduction
• GB stasis
• Inborn disorders of bile acid metabolism
• Hyperlipidemia syndromes
Patient is young, no fever, what investigations are required?

• LFT
• US Scan
• Consider MRCP (If US has not detected stones in CBD but bile duct is dilated or LFT abnormal
Management of GB stones? (See NICE CG188)

• Reassurance for asymptomatic GB stones in normal GB and normal biliary tree (No treatment required
unless symptomatic)
• Offer laparoscopic cholecystectomy for symptomatic patients (elective day care procedure)
o Early surgery (within 1 week) of acute cholecystitis
• Offer percutaneous cholecystostomy to manage gall bladder empyema when
o Surgery is contra-indicated
o Conservative management is unsuccessful
Management of CBD stones?

• Bile duct clearance and laparoscopic cholecystectomy in symptomatic or asymptomatic patients
• Clear the bile duct
o Surgically at the time of laparoscopy
o Or with ERCP
• If bile duct can’t be cleared with ERCP, then use biliary stenting to achieve biliary drainage as
temporarily
What is MRCP and what’s its indications?

Magnetic resonance cholangiopancreatography is a special type of MRI exam that produces detailed images of
the hepatobiliary and pancreatic system (non-invasive procedure)
Indication
Can be used to evaluate various conditions, for e.g.:
• Identification of congenital anomalies of the cystic and hepatic ducts
• Post-surgical biliary anatomy and complications

3
• Anomalous pancreaticobiliary junction
• Choledocholithiasis
• Biliary stricture
• Chronic pancreatitis
• Pancreatic cystic lesions
• Trauma to biliary system
If patient has fever, what could it be?

• Acute cholecystitis
• Ascending cholangitis
• Empyema
What surgery will you do for acute cholecystitis?

• Early cholecystectomy
• Emergency cholecystectomy if patient is deteriorating
If patient not fit for surgery, what will you do?

Percutaneous cholecystostomy
A cholecystostomy or cholecystotomy is a procedure
What other options? where a stoma is created in the GB, which can facilitate
Percutaneous cholecystostomy placement of a tube for drainage
Risk or possible complications of laparoscopic cholecystectomy?

• Bleeding
• Injury to bile duct, liver or intestine
• Bile leaking in the body
• Post cholecystectomy syndrome (abdominal pain, diarrhea, indigestion, fever)
• Hernia
• Peritonitis
• Small scars, small risk of wound infection
• Numbness in surgical area
• DVT
• Complications from anesthesia
Complications of Gallstones:
• Biliary colic
• Acute and chronic cholecystitis
• Empyema of GB
• Mucocele
• Perforation
• Biliary obstruction
• Acute cholangitis
• Acute pancreatitis
• Intestinal obstruction (gallstone ileus)

4
If GB infected, what is this? How will you manage?
May be acute cholecystitis or Empyema
(Management as above)
If patient refused surgery, what will you do?

• IV fluids
• Antibiotics
• Analgesics
• Discuss with patient about the benefits of surgery
• Explain to patient regarding complications of untreated cholecystitis such gangrenous cholecystitis,
perforation, biliary peritonitis, abscess, fistula, jaundice and sepsis
• Consider other medications such as ursodiol or chenodiol which have been shown to dissolve some gall
stones, these are available in oral bile acid pills. These medications work by thinning the bile, which
allow gall stones to dissolve.

5
Pulmonary Embolism (PE – ASSCC)
SCENARIO:
Male patient POD 3 post sigmoid colectomy has tachycardia, tachypnea and fever. Obs chart: pulse 110, O2 sat
90% at room air, RR 24, BP 110/70
What is your differential diagnosis?

• Pulmonary embolism
• Chest infection
• Basal atelectasis
• Abdominal sepsis
• Intra-abdominal hemorrhage
• Fluid overload
Why suspected PE?

• Hypercoagulability state as he has cancer
• Clinical symptoms: tachypnea, tachycardia, decreased PO2
• Post – operative
How to approach the patient?

1. I will manage the patient according to CCrISP protocol
a. Starting the airway: If patient is talking, so patent airway
b. Breathing: oxygen via a tight-fitting non-rebreather mask then assess oxygen saturation. If not
improving, will inform anesthesia or ITU for intubation of the patient.
c. Then I will assess and manage circulation: 2 wide bore cannula and start fluid and assess the
circulation by the pulse, BP, UOP and capillary refill time
2. Inform my senior
3. Then order investigations including: ABG, ECG, CXR, CTPA
• If patient is stable and non-massive PE: Start treatment with LMWH according to trust protocol
• If moderate PE, unstable patient: LMWH, catheter directed surgical embolectomy
• Massive PE:
o If low bleeding risk: surgical embolectomy, full dose TPA
o If high risk of bleeding: surgical embolectomy, catheter directed lysis
ABG
PH: 7.49
PO2: 8
PCO2: 3.8
HCO2: 24
Base excess: 1.2
The examiner will show this ABG, what is your diagnosis?

6
Respiratory Alkalosis
Why do you think the patient has respiratory alkailosis?

Because of hyperventilation with elimination of CO2
The examiner will show ECG and ask you the findings:
Tachycardia with sinus rhythm
What is the gold standard investigation? CTPA
The examiner will show you CTPA, comment?

Filling defect in pulmonary vessels suggesting large PE
CTPA – Saddle pulmonary emboli

7
PE- adherent to vessel wall
Pathogenesis of clot formation?

See pathology – bleeding pseudoaneurysm station
• Epithelial injury
• Blood stasis
• Platelet aggregation
• Platelet activation
• Intrinsic pathway activation

8
Sigmoid Volvulus + Metabolic Alkalosis (ASSCC)
SCENARIO:
Vomiting, abdominal pain and distension, Constipation. Decreased Na+, ABG: pH 7.5. Patient clinically
dehydrated, AXR: Volvulus
Causes of the clinical picture?

Sigmoid volvulus (AXR showing coffee-bean shape)
What does the ABG indicate?

Metabolic alkalosis
Also see “Gastric Outlet Obstruction” station
How would you manage this patient?

• I would manage the patient according to CCrISP
protocol (ABC)
• Keep NBM, NG tube
• Catheter and fluid balance chart
• IV access Plain radiograph showing “coffee bean” sign of
• Start IV fluid (Normal saline + Kcl) cecal volvulus with apices pointing to the left
• Monitor vital signs

• Early detorsion with rigid sigmoidoscopy +/- insertion of flatus tube (rectal tube)
• Followed by elective surgery to correct underlying cause
Explain the biochemical abnormalities (metabolic alkailosis, Hyponatremia, Hypokalemia, Hypochloremia,

increased bicarbonate, Aciduria)?
Also see “GOO” section

• Alkalosis, due to
o Loss of H+ ions in the vomitus
• Hyponatremia, due to
o Na+ loss in the vomitus
o Metabolic alkalosis stimulating renal excretion of NAHCO3
to decrease blood alkalinity
• Hypokalemia, due to
o Renal K+ loss in exchange with Na+ reabsorption because
of RAAS action (which is stimulated by decreased
intravascular volume and Na+)
• Hypochloremia, due to
o Loss in the vomitus
• Increased Bicarbonate, due to
o Renal re-uptake of bicarbonate stimulated by
hypochloremia, to maintain electrochemical neutrality
Plain radiograph showing “bent inner tube” – sign

of sigmoid volvulus with apex pointing to the right
9
o Decreased acid load in the duodenum causing retention of bicarbonate rich pancreatic juice
• Aciduria, due to
o Loss of H+ in urine in exchange for Na+ and water renal retention (RAAS action)
Vomiting + Loss of
Na+ Cl+ H+ Fluid
Hyponatremia Hypochloremia Metabolic Alkalosis Decreased Intravascular

volume and dehydration
Re-uptake of HCO3 in renal Loss of acid load Kidneys excretes the

tubules to maintain bicarb (In the form of
in the duodenum
NAHCO3) to decrease
electrochemical neutrality
blood alkalinity
Decreased pancreatic
Increased juice secretion and
Bicarbonate retention of bicarbonate
rich pancreatic juice)
RAAS System
Na+ and water retention

K+ and H+ excretion
Hypokalemia Aciduria
A volvulus is a twisting or axial rotation of a portion of bowel about/around

its mesentery. The rotation causes obstruction of the lumens (>180-degree
torsion) and if tight enough also causes vascular occlusion in the mesentery
(>360-degree torsion)

10
Clinical picture of sigmoid volvulus?
• Constipation
• Abdominal distension
• Abdominal pain
• Late vomiting (Feculent vomiting)
• Dehydration, secondary to fluid third spacing + vomiting →
tachycardia, hypotension, oliguria
Complications of sigmoid volvulus?
• Bowel ischemia and gangrene

Causes predisposing to sigmoid colon volvulus. Idiopathic
• Perforation megacolon usually precedes the volvulus in African people
• Peritonitis and sepsis
Gastrografin enema showing “bird beak” sign

Sigmoid volvulus
Who are you going to involve in the patients care?

• General Surgeon/Colorectal Surgeon
• Anesthetist
• ITU
Surgical options for a patient with sigmoid volvulus?

• Sigmoid resection with primary anastomosis
• Hartmann’s procedure with end colostomy or Paul-
Mikulicz procedure
Clinical picture of hyponatremia?

• Confusion
• Agitation
• Fits
• Reduced GCS

The paul-Mikulicz operation applied to
volvulus of pelvic colon 11
Causes of hyponatremia?
• Depletional:
o Diarrhea
o Diuretics
o Burns
• Dilutional:
o Heart failure
o Post-operative over administration of 5%
glucose
• Endocrine:
o Addison's disease
o Hypothyroidism Surgical finding of sigmoid volvulus
• Pseudohyponatremia:
o Multiple myeloma
• SIADH

12
Renal Cell carcinoma (Pathology)
SCENARIO:
Young patient with a background of hyperparathyroidism, has now developed secondary renal failure. He also
has renal stones. Blood results available.
How hyperparathyroidism caused renal failure?

Abnormalities in renal tubular absorption of phosphate → Secondary hyperparathyroidism is
Hyperphosphatemia → acts on parathyroid cells (++ PTH defined as a derangement in Calcium
secretion). hemostasis, which leads to
compensatory increase in PTH secretion.
It occurs primarily as a result of chronic
kidney disease and therefore sometimes
Chronic Kidney
referred to as renal hyperparathyroidism
Disease (↓GFR)
1,25-dihydroxy Phosphate
vitamin D retention
↓ Intestinal High serum

Calcium absorption
phosphorus
Low serum
Calcium
↑ PTH
Synthesis
Secondary
hyperparathyroidism
RCC. Typical cross-section of yellowish, spherical

neoplasm in mid-polar region of kidney. Note
13
the tumor in the dilated thrombosed renal vein

What is the lining epithelium of urinary tract?
Stratified, transitional epithelium
What are the genitourinary complications of stones?

• Deterioration of renal functions
• Obstruction
• Pyelonephritis, pyelonephrosis
• Rupture
• Fistula
• Infection, sepsis
• Carcinoma
Types and Treatment of urinary stones?

Types:
• Calcium oxalate – 85% (second most radio-opaque)
• Cystine – 1% (radio-dense)
• Uric Acid – 5-10% (radio-lucent)
• Calcium Phosphate – 10% (Most radio-opaque)
• Struvite – 2-20% (mostly associated with infection)
Treatment:
• Less than 5mm – Expectant management
• Less than 2cm - Lithotripsy (or URS if pregnant)
• Complex renal calculi and staghorn calculi – PCNL
• Stone any size + obstructed, infected system – Urgent decompression (URS or nephrostomy)
Most common type of Renal Cell Carcinoma?

Clear cell carcinoma is the most common type, accounting for 70-80% of renal cell carcinoma. The tumors are
made up of cells with clear or granular cytoplasm and are non-papillary.
Secon most common renal cell carcinoma?

Papillary carcinoma accounts for 10-15% of renal cancers.
Its is characterized by a papillary growth pattern and occurs in both familial and sporadic form
Risk factors of RCC?

• Tobacco
• Obesity
• Hypertension
• Unopposed estrogen therapy
• Exposure to asbestos, petroleum products and heavy metals
• ESRD, CKD, acquired cystic disease and tuberous sclerosis

14
Macroscopic and microscopic findings in RCC? (Reference to pathology report)
Clear cell cancer (ccRCC) Papillary Carcinoma (pRCC)

Macroscopic • Arises from proximal convoluted • Arises from distal convoluted tubules
tubules • Bilateral and multiple
• Solitary, unilateral • Less vibrantly orange yellow because of
• Bright yellow-grey-white spherical their lower lipid content
masses • Papilla formation with fibrovascular cores
• Margins are sharply defined and • Necrosis, hemorrhage and cystic
confined within the renal capsule degeneration
• Prominent areas of cystic softening or
of hemorrhage
Microscopic • Rounded or polygonal shape and • Cuboidal or low columnar cells arranged
abundant clear or granular cytoplasm, in papillary formations
which contains glycogen and lipid • Interstitial foam cells
• Psammoma bodies may be present
• Stroma is usually empty
What is R1?
• R0 – No residual tumor When dysplasia is severe and involves
• R1 – microscopic residual tumor the full thickness of the epithelium, but
• R2 – macroscopic residual tumor the lesion does not penetrate the
basement membrane, it is referred to as
carcinoma in situ.
How can stones cause cancer?

Stones → Chronic inflammation and infections → altered proliferation in urothelial cells → development of a
tumor
How can irritation lead to neoplasia?

Chronic inflammation → Dysplasia and DNA damage → Cancer

15
Staging?
CT imaging with contrast enhancement of the chest, abdomen and pelvis is required for optimal staging
Staging of RCC based on size, position and lymph node involvement:
• Stage I: Tumor < 7cm is largest dimension, limited to
kidney
• Stage II: Tumor > 7cm in largest dimension, limited to
kidney
• Stage III: Tumor in the major vein or adrenal gland with
intact Gerota’s fascia or regional LN involved
• Stage IV: Tumor beyond gerota’s fascia

16
Squamous Cell Carcinoma (SCC) On Arm - Pathology
SCENARIO:
Venous ulcer in forearm, not healed, biopsy taken.
PLEASE READ “BCC” SECTION TOO
From biopsy report, what are the criteria of malignancy?

• Invasion: Malignant cells do not respect tissue
boundaries, and can be seen infiltrating or invading
into surrounding structures
• Increased mitotic rate: Malignant cells will often
have increased numbers of mitoses.
• Differentiation and anaplasia: Normal cells are
usually structured in a particular way that
corresponds with their function. This is known as
differentiation. Malignant cells may become less
A
differentiated as part of their path to malignancy.
This is known as anaplasia. Well-differentiated
malignant cells show features similar to the parent
tissue. For example, well differentiated
adenocarcinoma cells will tend to form gland-like
structures; well differentiated squamous cell
carcinomas may show intercellular bridging or
keratin formation. Poorly differentiated cells have
lost most of their resemblance to the parent tissue,
which may be difficult to identify without special
staining techniques. Anaplastic cells have no
resemblance to their parent tissue, and usually B
indicate a very aggressive malignancy.
Invasive SCC
A – A nodule, hyperkeratotic lesion on the ear, associated with
Anaplastic Features: metastasis to a prominent post auricular LN (arrow)
• Loss of normal tissue architecture: Normal B – Tumor invades the dermal soft tissue as irregular
projections of atypical squamous cells exhibiting acantholysis
cells are usually arranged in an orderly
fashion. Epithelial cells often have polarity,
with their nuclei at a specific location. Malignant cells lose this architecture and are arranged
haphazardly
• Pleomorphism: Malignant cells may show a range of shapes and sizes, in contrast to regularly
sized normal cells. The nuclei of malignant cells are often very large (often larger than the
entirety of a normal cell) and may contain prominent nucleoli.
• Hyperchromatic nuclei: The nuclei of malignant cells typically stain a much darker color than
their normal counterparts.
• High nuclear-cytoplasmic ratio: The nuclei of malignant cells often take up a large part of the cell
compared with normal cell nuclei

17
• Giant cells: Some malignant cells may coalesce into so-called giant cells, which might contain the
genetic material of several smaller cells.
Six months later, patent developed cervical lymphadenopathy. How does cancer spread to lymph nodes?
Malignant tumors release growth factors such as VEGF-C to induce lymphatic vessel expansion (lymph
angiogenesis) in primary tumors and in draining sentinel LNs, thereby promoting LN metastasis.
• Permeation
• Embolization
Excision done but not enough, what will you do?

Re-excision
What is frozen section?

It’s a pathological laboratory procedure to perform rapid microscopic analysis of a specimen.
How the specimen is fixed?

The surgical specimen is placed on a metal tissue disc which is then secured in a chuck and frozen rapidly to
about -20 to -30 °C. The specimen is embedded in a gel like medium called OCT and consisting of poly ethylene
glycol and polyvinyl alcohol. Subsequently, it is cut frozen with the microtome portion of the cryostat, the
section is picked up on a glass slide and stained (usually with hematoxylin and eosin, the H&E stain).
What is the advantage of frozen section?

Frozen section technique shortens the time to make a preliminary diagnosis significantly from traditional tissue
biopsy preparation.
What other alternatives to frozen section?

• FNAC
• Imprint Cytology
After excision and grafting, graft became infected and sloughed. Swab shows MRSA. What will you do?
• Inform infection control team/microbiologist
• Follow, infection control protocol
• Wound debridement and regular dressing, If abscess, I&D
• Give antibiotics according to trust/local protocol
Outpatient:
o Oral Antibiotics as clindamycin, amoxicillin plus tetracycline or tmp/smx, linezolid*
Inpatient:
o Vancomycin Dose to target trough level 7-14days
o Linezolid 600 mg twice daily, PO or IV 7-14
o Daptomycin 4 mg/kg once daily 7-14
o Telavancin 10 mg/kg once daily 7-14
o Clindamycin 600 mg IV or 300 mg PO 3times daily
Decolonization with mupirocin nasal or chlorhexidine for body decolonization

18
Define granulation tissue?
Combination of proliferating fibroblast, loose
connective tissue, new blood vessels and scattered
chronic inflammatory cells. Forms a type of tissue
that is unique to healing wounds and is called
granulation tissue.
Fate of granulation tissue?

Remodeling – the connective tissue that has been
deposited by fibroblasts is recognized to produce the
stable fibrous scar. This process begins 2-3 weeks
following injury.
Granulation tissue showing numerous blood vessels,

edema and a loose extracellular matrix containing
associated inflammatory cells. Collagen is stained blue by
the trichrome stain, minimal mature collagen can be seen
at this point

19
Post-tonsillectomy Bleeding (ASSCC)
SCENARIO:
6-year-old Jehovah’s witness with secondary hemorrhage (POD6) after tonsillectomy. HR 120. Patient is stable
now.
If Hb is 74, how will you manage? Will you give blood?

Since Hb is 4 and is acute bleeding, transfusion starts at less than 90, but the patient is stable and Jehovah’s
witness, I will start resuscitation with colloids and crystalloids other than blood until I get consent from parents.
If they refuse, I will inform my consultant and legal team to get a court order to start blood transfusion
How will you manage the airway?

• I will start by assessing the airway “look, feel, listen” and call for help from ENT.
• If foreign body/blood clots are found, I will try to remove by suction to open the airway
• Chin lift and jaw thrust if needed to maintain an open airway.
• If failed and airway not patient, oropharyngeal or nasopharyngeal airway and oxygenation
• If failed intubation by expert(anesthetist)
How to stop bleeding in theatre?

• Packing with adrenaline-soaked gauze/surgical
• Bipolar cautery, underrunning sutures, gel foam
• Medication
• Last option, external carotid ligation if bleeding can’t be controlled
Type of diathermy?
Bipolar diathermy
Which medications will help? Dose?

Tranexamic acid, 10-15mg/kg
What will you look for when the patient is in recovery?

Hb level
Calculate bolus dose?

Use glucose-free crystalloids that contain sodium in the range 131-154 mmol/liter, with a bolus of 20ml/kg over
less than 10 minutes for children and young people.
Calculate maintenance dose?

Using Holiday-Segar formula
• 100ml/kg/day for the first 10kg of weight
• 50ml/kg/day for second 10kg of weight
• 20ml/kg/day for the weight over 20kg

20
• Be aware that over a 24-hour period, males rarely need more than 2500ml and females rarely
need more than 2000ml
Using surface area
• Range 300-400ml/m2/24 hours
How will you make sure you are operating on the correct patient?
WHO check list
Extra Questions from DO-HNS

SCENARIO:
You are called to see a 5-year-old boy, who underwent an elective adenotonsillectomy for an obstructive sleep
apnea several hours ago. He is now sweaty, tachycardiac and there is an active blood ooze in his oropharynx.
What is the diagnosis?

Primary post (adeno) tonsillectomy bleed.
This is a pediatric medical emergency, which requires urgent assessment and management.

21
What is your management plan?
• Promptly assess the child and then follow the pediatric life support (PLS) protocol in the initial
resuscitation of the patient. There is an active bleeding in oropharynx, sitting patient upright improves
airway and breathing. Encourage the patient to spit the blood out rather than swallowing it.
• Ensure intravenous access, send bloods for FBC, Urea and electrolytes (U&E), clotting, group and save
and start fluid boluses of 20ml/kg.
• Contact the senior ENT colleagues, anesthetist, theatre stuff to arrange taking patient to theatre
What is the circulating blood volume in a child?

80ml/kg
Mention three surgical options to stop bleeding?

• Use of bi-polar diathermy
• Application of linen ties to directly treat an obvious source of bleeding
• Underrunning suture to the tonsillar fossa (with a rounded bodied needle to avoid traumatizing the
fragile tissue)
• Stitching tonsillar pillars with surgical between them
• Packing the postnasal space with postnasal packs and keeping the child intubated if difficult to control
post adenoidectomy bleed
What is packing, explain it?

Using gauze or sponges to pack the tonsillar fossa, the pressure from which stops the bleeding
What does this picture illustrate?
Packing of the postnasal space and keeping the child intubated is sometimes required in cases of difficulty to control post-
adenoidectomy bleeds
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What is the blood supply to the palatine tonsil?
The palatine tonsils are supplied by branches of the external carotid artery:
• The inferior tonsillar artery via the facial artery
• The anterior tonsillar artery from the dorsal lingual artery
• The superior tonsillar artery via the greater palatine branch of the maxillary artery
• The posterior tonsillar artery from the ascending pharyngeal arteries and the facial artery
The venous drainage is via the peritonsillar plexus, which drain to the pharyngeal plexus or facial vein and into
the IJV.

23
Bleeding Pseudoaneurysm - Pathology
SCENARIO:
Male patient known case of HIV, HBV, HCV presented with red groin mass after injection in groin.
Type of HIV virus? Subtypes of HIV

Single-stranded RNA Retrovirus HIV 1 (more common - 95% of all infection
HIV 2 (less common, less infectious and progresses
more slowly, mainly found in west Africa)
Characteristics of HIV?
Human immunodeficiency virus (HIV) is a retrovirus
transmitted through body fluids
In most cases, HIV is sexually transmitted and occurs by
contact with or transfer of blood, pre-ejaculate, semen and
vaginal fluids
Non-sexual transmission can occur from an infected

mother to her infant during pregnancy, during childbirth by
exposure to her blood or vaginal fluid, and through breast
milk.
Causes of true and false pseudoaneurysm?

True:
• Congenital: Marfan’s, Ehlers-Danlos
• Acquired: atherosclerosis The structure of HIV 1 virion, the viral particle is covered by
• Infection: Syphilis a lipid bilayer derived from the host cell and studded with
viral glycoproteins gp 41 and gp 120
False:
• Trauma: IV Injections, horse rides “popliteal
aneurysm”
• Surgery
Which layer is affected in pseudoaneurysm?

24
Sub-intimal layer
Why does he have bleeding?

• From the trauma
• Liver involvement (HCV and HBV) affecting coagulation
You keep pressure on wound, but bleeding has not stopped, why?
Because there is liver involvement and affection of VIT K dependent clotting factors 2,7,9,10 and
thrombocytopenia
Precaution when stop bleeding?

Apron, eye protection, double gloves,
cap, mask
Sequence of clotting?
Injury to blood vessels → Platelets
aggregation → Platelet plug →
activation of intrinsic pathway
Why are clotting factors not working

properly?
• Due to liver affection where Injury to a blood vessel exposes collagen and thromboplastin, recruiting platelets to the
most of the factors are site of injury to form a temporary plug. Platelets release 5-hydroxytryptamine, among
manufactured (2,7,9,10 – VIT other factors, resulting in smooth muscle contraction and vasoconstriction. Activation of
the clotting cascade in response to collagen and thromboplastin activates thrombin,
K dependent) which converts circulating fibrinogen to fibrin monomers. Fibrin monomers polymerize
• Lower CD4 count, damage to and are cross-linked and accumulate with platelets at the site of injury to form the
the bone marrow where blood definitive clot.
cells are produced.

25
Lung Cancer (PATHOLOGY)
SCENARIO:
70-year-old male smoker, COPD with small cell lung cancer. Histology report saying carcinoid invading pleura
and lymph nodes
What other lung cancers do you know?

Small cell and non-small cell See previous station (Gangrene + Mesothelioma)
What are the signs of aggressiveness on the report?

• Invading pleura
• Lymph nodes involved
Pathogenesis of clubbing?
Various hypotheses have been proposed over the years to explain the pathophysiology of digital clubbing.
• Some research found significantly higher plasma growth hormone levels in patients with lung carcinoma
and clubbing than patients without clubbing.
• Megakaryocyte or platelet clusters, lodged in the peripheral vasculature of the digits, release platelet-
derived growth factor (PDGF) and lead to the increased vascularity, permeability, and connective tissue
changes that are the hallmark of clubbing
Pancoast paraneoplastic syndrome, what hormones?

ACTH causing Cushing syndrome
Now the patient presents with metastasis, poorly differentiated, how to tell its epithelial origin?
Immunohistochemistry
FISH technique?
Fluorescence in situ hybridization (FISH) is a kind of cytogenetic technique which uses fluorescent probes
binding parts of the chromosome to show a high degree of sequence complementarity. Fluorescence
microscopy can be used to find out where the fluorescent probe bound to the chromosome See Breast Cancer
station
If the tumor was epidermal growth factor positive, what will be the chemotherapeutic agent?
Tyrosine kinase inhibitor (imatinib)
6 months later he came with back pain. Why?

Bone metastasis
What other tumor metastasis to bone?

Breast, Bronchus, Renal, Thyroid, Prostate
Define adenocarcinoma

26
Adenocarcinoma is cancer that forms in mucus-secreting glands throughout the body. The disease may develop
in many different places, but it is most prevalent in the following cancer
Define emphysema
Emphysema is a lung condition that causes shortness of breath. In people with emphysema, the air sacs in the
lungs (alveoli) are damaged. Over time, the inner walls of the air sacs weaken and rupture — creating larger air
spaces instead of many small ones.
Paraneoplastic syndromes? Give examples?

Definition: Symptom complexes that occur in patients with cancer and that cannot be readily explained by local
or distant spread of the tumor or by the elaboration of hormones indigenous to the tissue of origin of the
tumor are referred to as paraneoplastic syndromes.
• The most common paraneoplastic syndromes are hypercalcemia, Cushing syndrome, and nonbacterial
thrombotic endocarditis, and the neoplasms most often associated with these and other syndromes are
lung and breast cancers and hematologic malignancies.
• Paraneoplastic syndromes also may manifest as hypercoagulability, leading to venous thrombosis and
nonbacterial thrombotic endocarditis.
• Other manifestations are clubbing of the fingers and hypertrophic osteoarthropathy in patients with lung
carcinomas

27
28
Breast Cancer (PATHOLOGY)
SCENARIO:
mammogram+ pathology report
What can you recognize in mammogram?

Speculated mass + microcalcifications
What other tests to do?

Tissue biopsy (TRU-cut, FNAC)
FNAC done showed C4 lesion what this mean?

• C1 – inadequate sample
• C2 – benign
• C3 – equivocal
• C4 – suspicious
• C5 – malignant
Excision, you are given a pathology report. What to

report/look for?
• Type of cancer
• Number of positive lymph nodes
• Margins status
• HER2 receptors status – poor prognosis
• ER/PR receptor status – good prognosis
• Ki 67 proliferation index – how progressive the cancer is? i.e.
the higher its % the higher the progression of the cancer
What is the most common site of breast cancer?

Most common site is upper outer quadrant as it has more
glandular tissue
What’s the most common type of breast cancer?

Invasive duct carcinoma

29
HER2?
Oncogene, biomarker, transmembrane Human Epidermal growth factor Receptor 2 and it is overexpressed in
15% of breast cancer cases and associated with bad prognosis.
Test: IHC, FISH.
How to test for HER2

Immunohistochemistry (IHC) measures the amount of HER2 protein in the cancer cells. Fluorescence in situ
hybridization (FISH) looks at the number of copies of the HER2 gene in the cancer cells.
Identification of HER2-positive breast cancer. HER2 protein overexpression is virtually always caused by amplification
of the region of chromosome 17q that contains the HER2 gene. The increase in HER2 gene copy number is detected
by fluorescence in situ hybridization (FISH) using a HER2-specific probe (red signal), which is typically co-hybridized
to tumor cell nuclei with a second probe specific for the centromeric region of chromosome 17 (green signal),
allowing the chromosome 17 copy number to be determined. Alternatively, HER2 protein overexpression in tumor
cells can be detected by immunohistochemical staining with antibodies specific for HER2.
What is HER positive?

HER2-positive breast cancer is a breast cancer that tests positive for a protein called human epidermal growth
factor receptor 2 (HER2), which promotes the growth of cancer cells. They're less likely to be sensitive to
hormone therapy HER2-positive breast cancers tend to grow faster and are more likely to spread and come
back. Treatments that specifically target HER2 are very effective. (e.g. Lapatinib, Neratinib, Pertuzumab,
Trastuzumab)

30
Why is it important to know if HER positive or negative?
For treatment choice (see above) and for prognosis
Herceptin (trastuzumab) and how it works at cellular level?

Trastuzumab, (Herceptin) is a monoclonal antibody that interferes with the HER2/neu receptor, which are
embedded in the cell membrane and communicate molecular signals from outside the cell to inside the cell and
turn genes on and off. The HER (human epidermal growth factor receptor) protein, binds to human EGF and
stimulates cell proliferation, leading to inhibition of MAPK and PI3K-Akt.
Herceptin: (trastuzumab) mode of action?

Causes antibody mediated destruction of cells overproducing HER2, taken 3 times weekly for 12
months.
What else in management?

• Radiotherapy
• Chemotherapy
• Hormonal therapy:
o Premenopausal: Tamoxifen (20mg /d) for 5 years – blocks estrogen receptor
o Postmenopausal: Aromatase inhibitors (anastrozole) to prevent peripheral conversion to estrogen
Who should be involved in care of this patient?

Radiologist, surgeon, oncologist, pathologist.
Patient going for an implant and flap, what single microbiological screening test would you do for this
patient? MRSA screen
What if positive?
Patient is a carrier and will require decolonization – According to trust Please note the difference
protocol in treatment between
Nose: Mupirocin 2% (Bactroban Nasal®) nasal ointment TDS for 5 days MRSA infection and MRSA
Skin: Once daily wash with Chlorhexidine 4% (Hibiscrub®) for 5 days carrier
Hair: Wash with Chlorhexidine 4% (Hibiscrub®) on day 1 and day 5
Now has breast erythema and discharge from nipple, what single microbiological test would you do now?
Cultures and sensitivity
What is the causative organism?

Staph. aureus
How would you treat her?

• Broad spectrum antibiotic (after discussion with microbiologist and according to trust policy) most likely
Flucloxacillin
• Wound care
Patient has redness around nipple, why?

• Eczema
• Paget disease

31
Pathophysiology of Paget disease?
It is caused by the extension of DCIS (ductal
carcinoma in situ) up the lactiferous ducts and
into the contiguous skin of the nipple, producing
a unilateral crusting exudate over the nipple and
areolar skin.
Unlike Paget disease of the vulva, Paget disease
of the nipple stems from in situ extension of an
underlying carcinoma.
Paget disease of the nipple. Ductal carcinoma in situ arising within the
ductal system of the breast can extend up the lactiferous ducts and into
the skin of the nipple without crossing the basement membrane. The
malignant cells disrupt the normally tight squamous epithelial cell
barrier, allowing extracellular fluid to seep out and form an oozing scaly
crust.

32
HCV (PATHOLOGY)
SCENARIO:
55-year-old lady, IVDU with left lower limb venous ulcer
Hepatitis C?
Is inflammation that disrupts hepatocytes and small bile ductules that is caused by virus C via parenteral
transmission (e.g., IVDA, unprotected intercourse, needle stick) risk from transfusion is almost nonexistent due
to screening of blood
The leading causes of chronic liver failure
Hepatitis C virus? worldwide include chronic hepatitis B, chronic
Is a single-stranded RNA virus from family flaviviruses hepatitis C, nonalcoholic fatty liver disease, and
Hepatitis virus causes acute hepatitis, which may progress to alcoholic liver disease
chronic hepatitis
• Acute hepatitis presents as jaundice (mixed CB and UCB) with dark urine (due to CB), fever, malaise,
nausea, and elevated liver enzymes (ALT > AST)
• Chronic hepatitis is characterized by symptoms that last > 6 months. With a risk of progression to cirrhosis
& HCC
What is the pathological sequence in HCV?

1. Acute Hepatitis
2. Chronic Hepatitis
3. Liver cirrhosis & portal hypertension
4. Liver cell failure
5. HCC
Most common risk factors for HCV infection?

• Intravenous drug abuse
• Multiple sex partners
• Having had surgery within the last 6 months
• Needle stick injury
• Multiple contacts with an HCV-infected
individual
• Employment in the medical or dental field
Cirrhosis
End-stage liver damage characterized by
disruption of the normal hepatic parenchyma by
bands of fibrosis and regenerative nodules of
hepatocytes
Clinical features & Pathological sequence?

• Portal hypertension
o Ascites
o Congestive
splenomegaly/hypersplenism
o Portosystemic shunts (esophageal
Major clinical consequences of portal hypertension in the

setting of cirrhosis, shown for the male. In women,
oligomenorrhea, amenorrhea, and sterility as a result of
hypogonadism are frequent.
33
varices, hemorrhoids, and caput medusae)
o Hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)
• Decreased detoxification
o Mental status changes, asterixis, and eventual coma (due to raised serum ammonia)
o Gynecomastia, spider angiomas and palmar erythema due to hyperestrinism
o Jaundice
• Decreased protein synthesis
o Hypoalbuminemia and edema
o Coagulopathy due to decreased synthesis of clotting factors.
• Hepatocellular carcinoma
The most common cause of cirrhosis in the UK?

Chronic Alcoholism
Alcoholic liver disease. The

interrelationships among hepatic steatosis,
alcoholic hepatitis, and alcoholic cirrhosis
are shown, along with depictions of key
morphologic features. It should be noted
that steatosis, alcoholic hepatitis, and
steatofibrosis may also develop
independently. In particular some patients
present initially with cirrhosis without any
of the other forms of alcoholic liver disease.
The most common cause of death in cirrhosis?

Rupture esophageal varices
Necrosis:
Necrosis is a form of cell death in which cellular membranes fall apart, and cellular enzymes leak out and
ultimately digest the cell
Divided into several types based on gross features
• Coagulative necrosis: ischemic infarction of any organ except the brain

34
• Liquefactive necrosis: Brain infarction, Abscess,
Pancreatitis
• Gangrenous necrosis: dry gangrene, wet gangrene
• Caseous necrosis: TB
• Fat necrosis: Traumatic in breast, Enzymatic in
Pancreatitis
• Fibrinoid necrosis: Hypertension
See Gangrene + Mesothelioma station
What is the type of necrosis in HCV?

Coagulative
Mechanisms of fibrosis. Persistent tissue injury leads to

chronic inflammation and loss of tissue architecture.
Cytokines produced by macrophages and other
leukocytes stimulate the migration and proliferation of
fibroblasts and myofibroblasts and the deposition of
collagen and other extracellular matrix proteins. The net
result is replacement of normal tissue by fibrosis.

35
Types of Candida? Candida albicans is the most
• Oral
common disease-causing fungus.
• Vaginal
It is a normal inhabitant of the
• Cutaneous
• Invasive oral cavity, gastrointestinal tract,
Oral candida albicans is the most common type (oral thrush) it can grow as and vagina in many individuals.
yeast, pseudohyphae, or true hyphae Systemic candidiasis (with
associated pneumonia) is a
disease restricted to
immunocompromised patients
that has protean manifestations.
In tissue sections, C. albicans

demonstrates yeastlike forms
(blastoconidia), pseudohyphae,
and true hyphae
Pseudohyphae
Are an important diagnostic clue
and represent budding yeast cells
joined end to end at
constrictions, thus simulating true
fungal hyphae. The organisms
may be visible with routine H&E
stains, but a variety of special
“fungal” stains (Gomori
The morphology of fungal infections. (A) Candida organism has methenamine-silver, periodic
pseudohyphae and budding yeasts (silver stain). (B) Invasive aspergillosis acid–Schiff) commonly are used to
(gross appearance) of the lung in a hematopoietic stem cell transplant better highlight the pathogens.
recipient. (C) Gomori methenamine-silver (GMS) stain shows septate
hyphae with acute-angle branching, consistent with Aspergillus. (D)
Cryptococcosis of the lung in a patient with AIDS. The organisms are
somewhat variable in size.
What are the stages and classification of venous leg ulcers?

CEAP classification
• C0 – No visible or palpable signs of venous disease
• C1 – Telangiectasias or reticular veins
• C2 – Varicose veins
• C3 – Edema
• C4a – Milder skin changes due to venous disorder (pigmentation, eczema)
• C4b – Severe skin changes due to venous disorder (dermatosclerosis, atrophie blanche)
• C5 – Healed ulcers
• C6 – Skin changes with active ulcer

36
Causes of inguinal lymphadenopathy?
Systemic
• Neoplastic
o Hodgkin’s and non-Hodgkin’s
lymphoma (common)
o Leukemia (uncommon)
• Inflammatory
o Tuberculosis (uncommon)
o Sarcoid (uncommon)
Local causes
• Infective
o Non-specific reactive lymphadenopathy
form infection in groin or lower limb
(very common)
• Specific infections
o Cat scratch fever (very rare)
o Lymphogranuloma venereum (very
rare)
• Neoplastic
o Metastatic disease (from primary lesion I lower limb, external Follicular hyperplasia
genitalia, perianal region) is caused by stimuli that
o Malignant melanoma activate B cell follicles, e.g.
RA, HIV
What you will see microscopically in inguinal LN cut section in this patient?
Chronic non-specific reactive lymphadenopathy (One of the three patterns Paracortical hyperplasia
depending on the causative agents) caused by stimuli that trigger
• Follicular hyperplasia T-cell–mediated immune
Predominantly B-cells response with germinal center hyperplasia which may responses, e.g. EBV
be associated with marginal zone hyperplasia. Follicles vary in size and shape
(vs lymphoma). Sinus histiocytosis
o collagen vascular disease refers to an ↑ in the no. and
o systemic toxoplasmosis size of the cells that line
o syphilis lymphatic sinusoids. It is
• Paracortical (interfollicular) hyperplasia nonspecific but may be
prominent in LNs draining

cancers
37
Reactive changes within the T-cell region of LN with paracortical expansion caused by
o viral infection e.g. infectious mononucleosis (EBV)
o certain vaccination (e.g., smallpox)
o immune reaction induced by certain drugs
• Sinus histiocytosis (reticular hyperplasia)
Distension and prominence of lymphatic sinusoids, due to marked hypertrophy of lining endothelial cells
and an infiltrate of macrophages (histocytes). It is often encountered in
o LN draining cancers
o Immune response to tumor or its products
Paracortical hyperplasia, identified by

the prominence of postcapillary venules
Follicular Hyperplasia.
A, Low-power view showing marked differences in
size of germinal centers, their well-circumscribed
character, and the fact that they are surrounded
by a well-defined mantle.
B, High-power view showing numerous “tingible
body” macrophages.
Sinus Hyperplasia. The cells present in the sinus
represent an admixture of histiocytes and sinus
lining cells.

38
Acute Pancreatitis (PATHOLOGY)
SCENARIO:
50-year-old patient complaining of epigastric pain. Recent history of hospitalization for acute pancreatitis 3 weeks
ago
What is amylase and what is its function?

• Group of proteins (digestive enzymes) found in saliva and pancreatic juice
• All are glycoside hydrolases and act on α 1,4-glygoside bond to convert starch into smaller
carbohydrate molecules (oligosaccharides and disaccharides)
What is CRP and from where it produced?

• C-reactive protein (CRP) is a substance produced by the liver early in response to inflammation
(acute phase reactant)
• It is not very specific, it isn’t unique to one disease
• Can help to monitor disease progress and flares.
What is blood test to do in acute pancreatitis?

• Serum amylase
• Serum lipase (preferred over the amylase due to higher sensitivity)
• LDH
• CRP
• FBC
What biochemical test to do?

• Electrolytes
• ABG
• Ca+2
• Albumin
The patient having a compression over stomach, what is that?

Pseudocyst
What non-bacterial organism can cause infection in this patient?

• Viruses (e.g. Mumps, Coxsackie B and hepatitis)
• Parasites (e.g. ascaris lumbricoides, fasciola hepatica, and hydatid disease)
• Bacteria (mycoplasma pneumonia and leptospirosis)
Patient’s haemoglobin is dropped, why?

• Rupture of splenic artery (GDA, PDA) pseudoaneurysm
• Haemorrhage
What non-surgical option to stop bleeding?

Interventional radiology

39
How does it work?
Using real-time imaging, the physician guides a catheter
through the artery and then releases clotting agents
(coils, particles, gel, or foam) into the blood vessel
slowing the blood flow and causing an internal injury to
activate the coagulation cascade
Which part of coagulation will be activated?

Intrinsic pathway
What factors involved in intrinsic pathway?

(Factors XII, XI, IX, X)

40
Hip Pain (History Taking)
SCENARIO:
Old male with hip pain, needs an operation but refused. Now presenting to pre-operative assessment clinic.
Hello. I am Dr X one of the exam candidates

May I confirm your name and age please?
Nice to meet you Mr. .... Today I’ve been asked to ask you few questions regarding your condition, are you OK
with this?
How can I help you today?

I am so sorry to hear that.
(Site, Onset, course, duration, character, radiation, timing, severity, aggravating and relieving factors and
associated factors)
• Where did you feel that pain?
• Could please point to the site?
• Does it move anywhere?
• When did you first notice that pain?
• Did it start suddenly or gradually?
• Did it come and go?
• Has this changed recently?
• Is there any specific time during the day that the pain increase?
• Is there anything makes this pain stops?
• Is there anything makes that pain increases?
• Could please describe that pain for me?
• Is it colicky, cramping, or stabbing?
• How badly is this affecting your day-to-day life?
• If you had to rate the pain from 1 to 10, with 10 being the worst pain you can imagine, how would you
rate it?
(Associated factors for differential diagnosis)

1. Osteoarthritis/trauma/AVN/fracture NOF
• Does the pain present all the day and increase at night?
• Did you notice any shortening of your leg or difficulties in walking?
• Was there any history of trauma, slipped recently?
2. Rheumatoid arthritis
• Have you noticed any stiffness in your joint(s) when you wake up in the morning?
• How long does that last for?
3. Septic arthritis
• Have you noticed swelling of your Hip? Or redness?
• Is there any discharge?
4. Neoplasm
• Have you noticed any significant weight loss over the past few months?
• How is your appetite?

41
5. Referred pain from back
• Have you noticed an Have you noticed weak or numb legs?
• Do you have back pain?
(Past medical or surgical history, Drug history, Family history, Ideas, concerns and expectations, other system
review)
Do you have any other medical conditions, see your GP for anything, ever had surgeries? (DM, ASTHMA, HTN,
IHD)
Do you take any medications? Dose? (Warfarin)
Do you have any allergy against any drug?
Do you mind if I ask personal questions?
What is your occupation?
Who is at home with you?
Do you have any difficulty with the stairs?
Do you smoke? How many packs/ days?
Do you drink alcohol? How many units/ weeks?
Is there anyone else in the family has had a similar problem?
Before I go any further, could I ask?
What do you think the cause is?
What are you the most concerned about?
What are you hoping us to do for you?
Urogenital Abdominal pain, micturition, dysuria, urgency, polyuria, hematuria
Rheumatic: any muscle or joint pain?
Anything else you want to add?
Thank you
Summarize
D/D?
Osteoarthritis
RA
Trauma, fracture, muscle strain/tear
Septic arthritis
Neoplasm
Could this patient go for surgery today?

No, patient has many co-morbidities, will need pre-op anesthetic revies and optimization. Patient is also on
warfarin which will be needed bridging with heparin
What is pre-operative work up?

A history and physical examination, focusing on risk factors for cardiac, pulmonary and infectious
complications, and a determination of patient’s functional capacity. Also includes pre-operative investigations.
Thank You

42

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2021

MRCS OSCE PART B

MRCS OSCE B NEW STATIONS 2021

Most probable Dx?

Pathology of gall stones?

MRCS OSCE B NEW STATIONS 2021

Patient is young, no fever, what investigations are required?

Management of GB stones? (See NICE CG188)

Management of CBD stones?

What is MRCP and what’s its indications?

MRCS OSCE B NEW STATIONS 2021

If patient has fever, what could it be?

What surgery will you do for acute cholecystitis?

If patient not fit for surgery, what will you do?

Risk or possible complications of laparoscopic cholecystectomy?

MRCS OSCE B NEW STATIONS 2021

If patient refused surgery, what will you do?

MRCS OSCE B NEW STATIONS 2021

What is your differential diagnosis?

Why suspected PE?

How to approach the patient?

The examiner will show this ABG, what is your diagnosis?

MRCS OSCE B NEW STATIONS 2021

Why do you think the patient has respiratory alkailosis?

Tachycardia with sinus rhythm

What is the gold standard investigation? CTPA

The examiner will show you CTPA, comment?

CTPA – Saddle pulmonary emboli

MRCS OSCE B NEW STATIONS 2021

Pathogenesis of clot formation?

MRCS OSCE B NEW STATIONS 2021

Causes of the clinical picture?

What does the ABG indicate?

How would you manage this patient?

• Monitor vital signs

Explain the biochemical abnormalities (metabolic alkailosis, Hyponatremia, Hypokalemia, Hypochloremia,

Also see “GOO” section

MRCS OSCE B NEW STATIONS 2021

Na+ Cl+ H+ Fluid

Hyponatremia Hypochloremia Metabolic Alkalosis Decreased Intravascular

Re-uptake of HCO3 in renal Loss of acid load Kidneys excretes the

Na+ and water retention

A volvulus is a twisting or axial rotation of a portion of bowel about/around

MRCS OSCE B NEW STATIONS 2021

Complications of sigmoid volvulus?

• Bowel ischemia and gangrene

Gastrografin enema showing “bird beak” sign

Who are you going to involve in the patients care?

Surgical options for a patient with sigmoid volvulus?

Clinical picture of hyponatremia?

MRCS OSCE B NEW STATIONS 2021

MRCS OSCE B NEW STATIONS 2021

How hyperparathyroidism caused renal failure?

↓ Intestinal High serum

RCC. Typical cross-section of yellowish, spherical

MRCS OSCE B NEW STATIONS 2021

What are the genitourinary complications of stones?

Types and Treatment of urinary stones?

Most common type of Renal Cell Carcinoma?

Secon most common renal cell carcinoma?

Risk factors of RCC?

MRCS OSCE B NEW STATIONS 2021

Clear cell cancer (ccRCC) Papillary Carcinoma (pRCC)