(a) Describe the hip joint under the following headings : (i) Factors responsible for its stability (ii) Arterial supply of upper…

(a)(i) Factors responsible for the stability of the hip joint (5 marks)

The hip is a ball-and-socket synovial joint, and it is the most stable large joint in the body because of its bony, ligamentous and muscular arrangements.

• Bony: the femoral head (about two-thirds of a sphere) sits deeply in the acetabulum, which is deepened by the fibrocartilaginous labrum that grips the head beyond its equator. The transverse acetabular ligament closes the acetabular notch.
• Capsule and ligaments: the strong fibrous capsule is reinforced by three ligaments that twist and tighten in extension. The iliofemoral (Y-shaped ligament of Bigelow) is the strongest ligament in the body and prevents hyperextension and holds the trunk erect in standing, the pubofemoral limits abduction and extension, and the ischiofemoral limits extension and medial rotation. The ligament of the head of the femur is only a minor stabiliser.
• Atmospheric pressure and synovial fluid: the negative intra-articular pressure and the cohesion of the fluid film form a suction seal.
• Muscles: the surrounding muscles give dynamic stability, especially gluteus medius and minimus, which hold the pelvis level in single-leg stance, with the short lateral rotators posteriorly and iliopsoas anteriorly.

(a)(ii) Arterial supply of the upper end of the femur and avascular necrosis of the head (5 marks)

Arterial supply. The upper end of the femur has three sources.

• The retinacular arteries from the trochanteric (cruciate) anastomosis, formed by the medial and lateral circumflex femoral arteries (branches of the profunda femoris) with the superior and inferior gluteal arteries. The medial circumflex femoral supplies the largest share, through the posterosuperior and posteroinferior retinacular branches. These run upwards along the neck, under the reflected synovium and within the capsule, to enter the head near the articular margin. The lateral circumflex supplies the anterior retinacular vessels.
• The artery of the ligament of the head (from the acetabular branch of the obturator artery), which supplies only a small area around the fovea and is inadequate in adults.
• The nutrient (metaphyseal) artery to the shaft, which reaches the neck only in part.

Mechanism of avascular necrosis. In the adult, the epiphyseal plate is closed and the metaphyseal supply does not reach the head. So the head depends mainly on the retinacular vessels. An intracapsular fracture of the neck (subcapital), or a dislocation, tears or kinks these vessels, or the vessels are occluded (by steroids, alcohol, sickle-cell disease, or decompression). The result is:

• Ischaemia and death of bone and marrow in the head, with the articular cartilage surviving for a time on synovial fluid.
• Weak, revascularising bone, since new bone is laid down on dead trabeculae (creeping substitution), which then collapses under load, giving a subchondral fracture (crescent sign) and flattening of the head.
• Secondary osteoarthritis, pain and limitation of movement.

(b) Paradoxical right hemidiaphragm after lung surgery (10 marks)

(i) Anatomical basis. The right phrenic nerve (C3, C4, C5, mainly C4) supplies the motor and sensory innervation of the right hemidiaphragm. In the thorax it runs down on the right side of the mediastinum along the superior vena cava and right atrium, in front of the root of the lung, over the pericardium. In this patient it has probably been injured during hilar and mediastinal dissection for the lung tumour (or by tumour infiltration). The right dome is then paralysed. In a normal inspiration, the left dome contracts and descends, creating negative intrathoracic pressure, and the paralysed dome, being flaccid, is passively pulled upwards into the chest, so it moves paradoxically, up on inspiration and down on expiration. This gives less effective ventilation, basal collapse and shortness of breath, and it shows on a sniff test on fluoroscopy, ultrasound and dynamic MR imaging.

(ii) Openings of the diaphragm.

• Caval opening, T8 (in the central tendon, to the right of the midline): the inferior vena cava and the branches of the right phrenic nerve.
• Oesophageal opening, T10 (in the muscle of the right crus): the oesophagus, the anterior and posterior vagal trunks, the oesophageal branches of the left gastric vessels, and lymphatics.
• Aortic opening, T12 (behind the median arcuate ligament): the aorta, the thoracic duct, and often the azygos vein.
• Other openings: the greater, lesser and least splanchnic nerves pierce the crura; the sympathetic trunk passes behind the medial arcuate ligament (with psoas); the subcostal nerve and vessels pass behind the lateral arcuate ligament (with quadratus lumborum); the hemiazygos vein pierces the left crus; and the superior epigastric vessels and lymphatics pass between the sternal and costal slips (foramen of Morgagni). The left phrenic nerve pierces the left dome of the muscle.

(c) Carcinoma of the head of the pancreas with obstructive jaundice (10 marks)

The tumour compresses the common bile duct where it runs through the pancreatic head, and it may also block the pancreatic duct. Bile cannot reach the gut, so the picture is that of post-hepatic (obstructive) jaundice with steatorrhoea.

(i) Serum markers of cholestasis.

• Raised conjugated (direct) bilirubin, so the jaundice is yellow-green.
• Markedly raised alkaline phosphatase (from the biliary canaliculi) and gamma-glutamyl transferase (GGT), with raised 5′-nucleotidase to show the hepatic origin of the ALP.
• Raised bile salts and cholesterol (lipoprotein X), and a mild rise in transaminases, which is a late and small change.
• Prolonged prothrombin time from vitamin K malabsorption, which is corrected by parenteral vitamin K. CA 19-9 is raised as a tumour marker.

(ii) Biochemical findings.

• Serum: conjugated hyperbilirubinaemia, with high ALP, GGT and bile salts, and raised cholesterol.
• Urine: bilirubin present (dark, frothy urine), since conjugated bilirubin is water-soluble and is filtered. Urobilinogen is absent or greatly reduced, since bile does not reach the gut where bacteria form it. Bile salts are present in the urine.
• Stool: pale, clay-coloured because of the absence of stercobilin, and bulky, offensive, and greasy with a high fat content. Stool urobilinogen (stercobilinogen) is absent.

(iii) Cause of the greasy stools (steatorrhoea). Fat is not digested and absorbed properly, for two reasons. Bile salts do not reach the duodenum, so fat is not emulsified and mixed micelles cannot form, and lipase action and absorption fall. If the pancreatic duct is blocked as well, pancreatic lipase and colipase are also missing, and fat stays undigested. The unabsorbed fat (more than 7 g/day) appears in the stool, which is pale, bulky, foul-smelling and floats. There is also malabsorption of the fat-soluble vitamins A, D, E and K.

(d) Action potential in a neuron and conduction in myelinated and unmyelinated fibres (10 marks)

The graph shows the phases. The resting membrane potential is about −70 mV, maintained by K+ leak channels and the Na+/K+ pump (3 Na+ out, 2 K+ in).

• Depolarisation: a stimulus opens a few voltage-gated Na+ channels. When the membrane reaches the threshold (about −55 mV), more open in a positive-feedback (Hodgkin) cycle, and the rapid Na+ influx drives the potential upwards.
• Overshoot: the potential reaches about +30 to +35 mV, near the Na+ equilibrium potential (about +60 mV).
• Repolarisation: the Na+ channels are inactivated (inactivation gate closes) and the voltage-gated K+ channels open, so K+ leaves the cell and the potential falls.
• After-hyperpolarisation: the K+ channels close slowly, and the potential dips towards the K+ equilibrium potential (about −80 to −90 mV), before it returns to rest through the pump and leak channels.
• Refractory periods: during the absolute refractory period, from depolarisation to about the middle of repolarisation, no stimulus can trigger a second spike since Na+ channels are inactivated; in the relative refractory period a stronger stimulus is needed. This makes the spike all-or-none and one-directional. The whole spike lasts 1–2 ms.

Conduction.

• Unmyelinated fibres: the impulse spreads continuously along the membrane, each patch depolarising the next through local currents. The velocity is slow (0.5–2 m/s), it rises with the square root of the fibre diameter, and the process uses much energy, since ions cross the whole membrane and the pump must restore them.
• Myelinated fibres: the myelin sheath insulates the axon and increases membrane resistance and lowers capacitance, and the voltage-gated Na+ channels are concentrated at the nodes of Ranvier (about 1 mm apart). The impulse jumps from node to node (saltatory conduction). Velocity is much higher (up to 120 m/s), rising in proportion to the fibre diameter, and less energy is used since only the nodes depolarise. Loss of myelin (multiple sclerosis, Guillain–Barré syndrome) slows or blocks conduction.

(e) Principal connections of the basal ganglia (10 marks)

The basal ganglia are the striatum (caudate nucleus and putamen), globus pallidus (external, GPe, and internal, GPi), the subthalamic nucleus (STN), and the substantia nigra (pars compacta, SNc, and pars reticulata, SNr). They modulate movement through loops with the cortex and the thalamus. The diagram shows the main connections.

Afferents. The striatum, the input nucleus, receives an excitatory glutamatergic projection from the whole cerebral cortex (corticostriatal, mainly the motor, premotor and prefrontal areas), from the intralaminar thalamic nuclei, and a dopaminergic projection from the substantia nigra pars compacta (nigrostriatal).

Efferents. The output nuclei, GPi and SNr, send inhibitory GABAergic fibres to the ventral anterior and ventral lateral nuclei of the thalamus, which project back to the premotor and motor cortex (the cortico-striato-pallido-thalamo-cortical loop), and to the brainstem (pedunculopontine nucleus and superior colliculus).

Pathways.

• Direct pathway: cortex excites striatal neurons that carry D1 receptors (GABA and substance P), which inhibit GPi and SNr. This releases the thalamus from inhibition, so the thalamus excites the cortex and movement is facilitated.
• Indirect pathway: cortex excites striatal neurons that carry D2 receptors (GABA and enkephalin), which inhibit GPe. GPe therefore stops inhibiting the STN, which excites GPi and SNr, and so the thalamus is inhibited more and movement is suppressed.
• Hyperdirect pathway: the cortex drives the STN directly, providing a fast brake.
• Dopamine from the SNc excites D1 neurons and inhibits D2 neurons, so both actions favour movement.

Clinical relevance. In Parkinson's disease the loss of nigral dopamine reduces the direct and enhances the indirect pathway, causing bradykinesia and rigidity. Degeneration of striatal neurons in Huntington's disease causes chorea, and a lesion of the STN causes hemiballismus.