Free MRCS Part A practice questions

A positive lift-off test with increased passive external rotation indicates rupture of subscapularis, the only rotator cuff muscle that inserts on the lesser tuberosity and the main medial rotator of the shoulder. Subscapularis tears often follow a fall or an anterior dislocation and may allow the long head of biceps to sublux medially, but the biceps tendon itself does not produce the lift-off sign. A supraspinatus tear weakens abduction and gives a painful arc. An infraspinatus tear weakens external rotation, producing the opposite picture of reduced active external rotation. The coracohumeral ligament reinforces the rotator interval and restrains external rotation in adduction; its injury does not abolish active medial rotation. Reference: Last's Anatomy 12e.

In the adult the femoral head is supplied almost entirely by the retinacular (lateral epiphyseal) vessels, which arise from the deep branch of the medial circumflex femoral artery, run beneath the capsular reflection along the neck and enter the head at the margin of the articular cartilage. A displaced intracapsular fracture tears these vessels, so avascular necrosis and non-union are common after fixation and arthroplasty is preferred in the older patient. The lateral circumflex femoral artery supplies the anterior neck and the greater trochanter but contributes little to the head. The artery of the ligamentum teres, a branch of the obturator artery, is an important source only in childhood and is negligible in the elderly. The superior and inferior gluteal arteries supply the gluteal muscles and the trochanteric anastomosis, not the head itself. Reference: Last's Anatomy 12e; Apley & Solomon's System of Orthopaedics 10e.

Along the midaxillary line the chest wall is covered by the fleshy digitations of serratus anterior, which arise from the outer surfaces of the upper eight or nine ribs, so a lateral drain passes through serratus anterior (or between its digitations) before reaching the intercostal muscles. Deep to serratus the track crosses the external intercostal, then the internal intercostal, then the innermost intercostal and endothoracic fascia before the parietal pleura. Pectoralis major lies anterior to the safe triangle and latissimus dorsi posterior to it, which is precisely why the triangle is defined between their borders; neither is traversed by a correctly placed drain. The internal intercostal is encountered only after the external layer. Reference: Gray's Anatomy for Students 4e.

A mass that persists and becomes more tender on tensing the abdominal wall (positive Fothergill's and Carnett's signs) in an anticoagulated patient is a rectus sheath haematoma. Most arise below the arcuate line, where branches of the inferior epigastric artery enter the sheath on the deep surface of the muscle and where, lacking a posterior sheath, bleeding can spread widely into the extraperitoneal and prevesical tissues. The superior epigastric artery supplies the upper rectus above the umbilicus, where haematomas are small and confined between tendinous intersections. The deep circumflex iliac artery runs along the iliac crest in the lateral wall, and the superficial epigastric artery lies in the subcutaneous fat. External iliac bleeding would produce a retroperitoneal haematoma with haemodynamic collapse rather than a wall mass. Reference: Bailey & Love 28e; Last's Anatomy 12e.

Internal haemorrhoids are enlargements of the anal cushions, vascular plexuses in the submucosa above the dentate line at the left lateral, right anterior and right posterior positions (3, 7 and 11 o'clock in the lithotomy position). They are fed by terminal branches of the superior rectal artery and drain through the superior rectal vein to the inferior mesenteric vein and so to the portal system, which is why the anal canal is a site of portosystemic anastomosis. The middle rectal veins drain the muscular wall of the lower rectum to the internal iliac veins, and the inferior rectal veins drain the canal below the dentate line to the internal pudendal veins, both systemic. The median sacral vein drains the back of the rectum and sacrum. Reference: Last's Anatomy 12e.

This is a subgaleal haematoma tracking forward into the eyelids. The fourth layer of the scalp, the loose areolar tissue, is the plane of movement of the scalp over the skull and is continuous anteriorly with the eyelids because the aponeurosis has no bony attachment at the front; frontalis inserts into the skin of the brow. Blood or pus in this layer therefore spreads freely from the occiput to the orbital margins and appears as periorbital bruising a day or two after injury. A subperiosteal haematoma (cephalhaematoma) is limited by the sutures to a single bone because the pericranium is adherent at the suture lines, so it cannot reach the eyelids. The dense connective tissue layer is bound by septa and does not allow spread; the aponeurosis is a sheet, not a space. Reference: Last's Anatomy 12e.

This is a Jefferson burst fracture of the atlas from axial loading. The atlas is a ring with no body, so the load splits the ring at its weakest points and the lateral masses spread apart. The transverse ligament of the atlas runs between the tubercles on the medial aspects of the lateral masses and holds the dens against the anterior arch; combined lateral mass overhang of more than about 7 mm implies that it has ruptured, allowing anterior translation of the atlas on the axis and threatening the cord. The alar ligaments run from the dens to the occipital condyles and check rotation; the apical ligament is a small vestigial band from the tip of the dens to the basion; the tectorial membrane is the upward continuation of the posterior longitudinal ligament; the ligamentum nuchae is a posterior midline raphe of no stabilising importance here. Reference: Last's Anatomy 12e; Apley and Solomon's System of Orthopaedics and Trauma 10e.

The indicator-dilution principle gives a compartment volume from the dose of marker divided by its equilibrium concentration, provided the marker distributes only within that compartment. Inulin (like mannitol, sucrose, thiosulphate or radiolabelled bromide) crosses capillary walls freely but cannot enter cells, so it measures the extracellular fluid. Deuterium oxide and antipyrine, like tritiated water, cross all membranes and measure total body water. Evans blue dye and radiolabelled albumin bind to or are plasma proteins that remain within the vasculature and so measure plasma volume. The intracellular volume cannot be measured directly and is calculated as total body water minus extracellular fluid; interstitial volume is extracellular fluid minus plasma volume. Reference: Ganong 26e.

The loop shows the response to an isolated rise in afterload. The ventricle must reach a higher pressure before the aortic valve opens, so ejection starts later and ends earlier on the same end-systolic pressure–volume line: end-systolic volume rises, stroke volume (the width of the loop) falls, and the loop becomes taller and narrower. A lower end-systolic volume with a larger stroke volume is the response to reduced afterload or to a rise in contractility. The slope of the end-systolic pressure–volume relation is an index of contractility and is not altered by an α1-agonist. Over subsequent beats the retained volume raises end-diastolic volume and the Frank–Starling mechanism partially restores stroke volume, but that is a secondary adjustment, not the immediate change. Peak systolic pressure rises, not falls, with increased resistance. Reference: Ganong 26e; Guyton & Hall 14e.

This is the immediate transient response of acute inflammation. Histamine released from mast cells (with bradykinin and leukotrienes) causes endothelial cells of post-capillary venules to contract, opening inter-endothelial gaps; protein-rich fluid escapes within minutes and the leak is short-lived, lasting 15–30 minutes. Direct endothelial necrosis follows severe injury such as burns and produces an immediate sustained leak. Leucocyte-mediated injury is a later event, appearing hours after neutrophils arrive. Increased transcytosis contributes chiefly to the leakiness of new vessels driven by VEGF. Lymphatic obstruction causes protein-rich oedema over days to weeks, not a weal that resolves within the hour. Reference: Robbins Basic Pathology 10e.

The picture is perioperative anaphylaxis, an IgE-mediated type I hypersensitivity reaction in which allergen cross-links IgE on mast cells and basophils, releasing histamine, tryptase and leukotrienes; neuromuscular blocking agents, antibiotics and chlorhexidine are the usual culprits. Mast cell tryptase peaks about one hour after onset and has a half-life of around two hours, so samples are taken as soon as feasible after resuscitation, at 1–2 hours and at 24 hours or later as a baseline; a transient rise confirms mast cell degranulation. Total IgE does not identify an acute reaction. Complement levels help in immune-complex disease. Skin testing is done by an allergy clinic four to six weeks later, not acutely. Histamine is cleared within minutes, so a next-day level is useless. Reference: NAP6, Royal College of Anaesthetists (2018); Robbins Basic Pathology 10e.

In a shocked trauma patient the induction agent should least depress the circulation, and ketamine is the usual choice. As an NMDA receptor antagonist it produces dissociative anaesthesia while central sympathetic stimulation and reduced catecholamine reuptake tend to preserve heart rate, vascular tone and blood pressure; it also maintains airway reflexes better than other agents. Propofol and thiopental both cause dose-dependent vasodilatation and myocardial depression, so they can precipitate profound hypotension or arrest in the hypovolaemic patient unless the dose is greatly reduced. Midazolam has too slow an onset for a rapid sequence induction and also lowers blood pressure. Inhalational induction with sevoflurane is slow, leaves the full-stomach airway unprotected and vasodilates. Even ketamine is given in a reduced dose because a catecholamine-depleted myocardium may be depressed by it. Reference: BNF; Smith & Aitkenhead's Textbook of Anaesthesia 7e.

This is Fournier's gangrene, a type I (polymicrobial) necrotising fasciitis of the perineum. It typically follows anorectal or urogenital sepsis or surgery in diabetic, obese or immunocompromised patients, and cultures grow a synergistic mixture of facultative Gram-negative bacilli (such as Escherichia coli), streptococci, enterococci and anaerobes such as Bacteroides; crepitus reflects gas from anaerobic metabolism. A pure group A streptococcal growth defines type II necrotising fasciitis, usually of a limb in a previously healthy person. Clostridial myonecrosis follows deep contaminated wounds and involves muscle rather than fascia. Vibrio vulnificus causes a marine-associated monomicrobial type III infection. MRSA alone is an uncommon cause. Reference: Bailey & Love 28e.

Severe epigastric pain, unproductive retching and inability to pass a nasogastric tube form Borchardt's triad of acute gastric volvulus, typically organoaxial rotation of a stomach that has herniated through a para-oesophageal defect. Strangulation and gastric necrosis follow if it is not decompressed and reduced urgently, after CT confirmation. Spontaneous oesophageal rupture follows forceful vomiting rather than unproductive retching and produces chest pain and surgical emphysema. Gastric outlet obstruction causes large-volume vomiting of undigested food, and a tube passes easily. Pancreatitis and myocardial infarction may cause epigastric pain and nausea but do not obstruct passage of a nasogastric tube. Reference: Bailey & Love 28e.

NICE NG12 separates breast lumps by age. A suspected cancer pathway referral is made for people aged 30 and over with an unexplained breast lump, with or without pain; for those under 30 with an unexplained lump, a non-urgent referral should be considered, because cancer is uncommon and most lumps in this group are fibroadenomas or cysts. A two-week suspected cancer referral would be correct were she 30 or older. Mammography is not the first imaging test in a young woman, whose dense breasts make it insensitive, and it should be part of triple assessment in clinic rather than arranged in primary care. Dismissing a persistent new lump without assessment is unsafe. Genetic referral depends on family history, which is not described. Reference: NICE NG12.

A myocardial infarction, stroke, transient ischaemic attack or coronary stent within the last three months is one of the ASA's examples of severe systemic disease that is a constant threat to life, so he is ASA IV despite being symptom-free. Once more than three months have passed the same history is graded ASA III, which is the closest wrong answer. ASA II would describe mild controlled disease such as treated hypertension. ASA V is a moribund patient not expected to survive without surgery. Grading him correctly matters because it feeds into risk tools such as P-POSSUM and the NELA model and into the consent discussion. Reference: ASA Physical Status Classification System (2020).

This is aspiration pneumonitis (Mendelson's syndrome): a chemical injury from acidic gastric contents, which are normally sterile in an otherwise well patient. Treatment is supportive with oxygen, physiotherapy and observation; most patients improve within 24–48 hours, and antibiotics are reserved for those who fail to improve, develop features of infection, or have aspirated colonised material as in bowel obstruction. Empirical antibiotics from the outset select resistant organisms without improving outcome. Corticosteroids have not been shown to help. Bronchoscopy is for aspirated solid particles causing lobar collapse, not liquid; saline lavage spreads the injury. Nebulised alkali does not neutralise acid that has already damaged the alveolar epithelium. Reference: Mandell LA, Niederman MS. Aspiration pneumonia. N Engl J Med 2019.

Continued arterial bleeding despite a fully tightened tourniquet means arterial inflow has not been occluded, most often because the thigh is large and a single narrow band cannot generate enough pressure. ATLS 10e advises a second tourniquet placed immediately proximal to the first, which widens the compression zone and usually achieves control. Releasing the tourniquet risks further exsanguination while it is moved, and the lower leg's paired bones make tourniquets below the knee less effective. A pressure bandage over a failing tourniquet adds little. Removing it in favour of packing abandons control of a limb wound that is suitable for a tourniquet. Blind clamping wastes time and injures adjacent nerves and veins. Reference: ATLS 10e.

Older patients have reduced physiological reserve, and beta-blockers prevent the compensatory tachycardia of haemorrhage, so a normal heart rate offers false reassurance. A systolic pressure of 116 mmHg is a substantial fall from his usual value, and ATLS 10e notes that in older adults a systolic pressure below about 110 mmHg may represent shock. Cool peripheries and a raised lactate confirm tissue hypoperfusion, so haemorrhage must be presumed and sought. This is not a normal response to injury. Neurogenic shock causes warm peripheries and needs a cord injury. Blunt cardiac injury is possible but haemorrhage is far more common and is assumed first. A vasovagal episode is transient and does not raise lactate. Reference: ATLS 10e.

Bilious vomiting in a neonate is malrotation with volvulus until proven otherwise, even in a well baby with a soft abdomen — the bowel can infarct within hours. The pathway is to decompress the stomach, start intravenous fluids and discuss with and transfer to a paediatric surgical centre the same day for an upper gastrointestinal contrast study to define the position of the duodenojejunal flexure. Pyloric stenosis causes non-bilious vomiting at a few weeks of age. A formula change and overnight review lose the window to save the midgut. A normal plain film does not exclude volvulus, so it cannot justify observation. Hirschsprung's disease is suggested by delayed meconium and distension, which are absent here. Reference: Bailey & Love 28e.