MRCS B: Previous Q – 2019

MRCS B-2019 Q

MRCS B: Q-2019


  1. Station 1: History of PR bleeding
    58 year old lady With 6 months history of PR bleeding, blood mixed stool, dull abdominal pain. No history of other Type B symptoms- weight lost, appetite change etc. She has strong family history (brother has colorectal ca).
    Further questions: Differentials- colorectal malignancy, inflammatory bowel disease, haemorrhoids, diverticular disease…
    Investigations: blood test, colonoscopy with biopsy
  2. Station 2: Clinical Examination-
    Day 5 post-op left hemicolectomy peritonitic abdomen.
    -Acute assessment 6 minutes(combine ABCDE with abdominal examination & assessment of wound)
    -Later given: ECG(tachycardia- AF), vital sign(septic trending) & Blood results(raised inflammatory markers),
    What is immediate management: fluid resuscitation + monitor input/output, commence antibiotic as per protocol, possible blood transfusion as required, request to preform CT scan!
    What’s differentials: Anastomotic leak, Internal bleeding, Hospital acquired infection( pneumonia or uti) & PE (do ABG analysis)
    What is definite management: depends on ct result- if localized infective collection then can perform ir drainage or not then reoperate
  3. Station 3: Pathology-
    Patient with bicuspid aortic valve…
    What’s pathogenesis of the risk of aortic stenosis in patient (higher pressure outflow causing turbulence and progressively leading to chronic inflammation/fibrosis of valve thus stiffen the valve!)
    What’s other possible risk due to bicusp valve-higher risk of infective endocarditis,
    How does the disease spread-from blood stream?
    What common organism causing endocarditis- group a staph aureus…….
    Patient progressive require TAVI-Transcatheter aortic valve implantation (TAVI) why? As the infection cause vegetation at difficult to eradicate.
    Why patient need to be on warfarin and nothing else, as need to archive higher level of anticoagulation
    What is the pharmacodynamics of warfarin , prevent activation of extrinsic and common pathway clotting factor via vitamin k.
  4. Station 4: Anatomy-
    Three pictures of anterior thigh, posterior hip and popliteal fossa,
    asked me to identify muscle under ileotibial band( I said vastus lateralis but not the Answer he wanted, may be he was asking about Tensor fascia lata & Gluteus maximus)
    What’s the action of ileotibial band- to secure help to stabilise knee joint,(Functionally, the iliotibial tract extends the tensor fascia latae muscle into the lower thigh and leg, allowing it to function as an abductor, medial rotator and flexor of the thigh. It also allows the tensor fascia latae and gluteus maximus muscles to support the extension of the knee while standing, walking, running and biking).
    -moved to second picture & asked me to identify gluteus medius, it’s nerve supply (superior gluteal nerve) and it primary action while walking (to prevent tilting of other side of the hip during stance phase of the limb).
    -moved to third picture, asked me to identify biceps Femoris it’s nerve supply, how many heads(two) and it’s action while walking(extend hip and flex knee,rotate the leg laterally)
    What’s the nerve run across fibulae head-common peroneal nerve,
    What is the sensory supply via common peroneal nerve( it supplies dorsum of the foot via superficial peroneal nerve, first web space/first interdigital cleft of toe via deep peroneal nerve-medial terminal branch & lateral cutaneous branch of supercficial peroneal nerve communicating with sural nerve.
    What muscle it supply- lateral compartment(Superficial peroneal nerve): Peroneus longus & brevis; anterior compartment(deep peroneal nerve): the extensors muscles: tibialis anterior, EHL, EDL & Peroneus tertius; Foot: EDB
    What is the presentation when the nerve is damaged- foot drop, loss of eversion & sensory loss of dorsum of foot.
  5. Station 5: Procedural skill-
    Asked to select instruments including needles(choose ethelon), toothed forceps, needle holder & suture scissors, need to check expiry date. Pinch patient with forceps to assess effect of analgesia. Perform 4 interrupted sutures with instrument tie, & need to handle sharps safely.
    Pt will ask question: is it painful- explain the local will work for a few hours after that can take some paracetamol & ibuprofen if necessary. Explain as this is non-absorbable suture thus need to be removed after 10 days either by gp/ district nurse, however if notice redness, bleeding, infective looking it may require to reopen suture earlier.
    Examiner asked about the local anesthesia to be used- lignocaine, why for both adrenaline and without adrenaline, use lignocaine because quick onset of effect, use adrenaline because vasoconstriction reduce bleeding and localised effect. Calculate the dosage to be given.
  6. Station 6: Anatomy- Skull
    -Identify optic nerve, exit point of the nerve(optic canal),
    -Identify the dural layer overlying middle & posterior cranial fossa,
    -Identify internal carotid artery( this is tricky as it only a luminal structure appear next to optic chiasma, rule out other answer eg middle cerebral artery, cavernous sinus etc.)
    Identify oculomotor nerve, where is it’s origin( I said piercing out from pons but i think he wants where the nucleus of the nerve is), where is it exiting cranial fossa (via superior orbital fissure), what muscle does it supply, superior inferior medial rectus & levetor palpabrae superioris and pupillary muscle via parasympathetic supply.
    -What is the prominent sign when it is compressed by SOL( blow out pupil),
    -What is the type of aggressive form of SOL-Glioblatoma multiforme
    -What is the other presentation of oculomotor nerve palsy-ptosis and laterally deviated(abducent nerve) and downward looking(by trochlear nerve)
    -Definition of false localising sign……
  7. Station 7: Anatomy-
    -Identify external carotid artery and ascending pharyngeal artery,
    -Identify facial artery, if transected is it detrimental to its supply(no as it has cross tributaries from opposite facial artery and lingual artery as well).
    -At what level common carotid bifurcate (c4,c5) -What is carotid body (presence of chemoreceptor detect ph paO2 level for changes).
    -Identify submandibular gland?
    -Where is the duct opening (into at next to frenulum floor of mouth via duct of Wharton),
    -Identify parotid gland, what type of secretion it produces(serous),
    -Where is it’s duct opening( at opposite of second upper molar; examiner wants specifically the space between the teeth and buccal mucosa)