Show the model answerAttempt it first — that is what makes it stick
(a) Receptor to effector muscle 4 marks
The flexor withdrawal reflex: polysynaptic, multisegmental, and complete within the spinal cord.
What earns the marks4 marks
| Receptor | Nociceptor — free nerve ending in forearm skin |
|---|---|
| Afferent | Aδ and C fibres; cell body in the dorsal root ganglion; synapse in the dorsal horn |
| Integration | Interneuron pools, polysynaptic, spread over several segments |
| Reciprocal innervation | Flexors excited, extensors inhibited |
| Efferent | α motor neuron → ventral root → Aα fibre → neuromuscular junction |
| Effector | Flexor contraction withdraws the arm |
Commonly lost: The majority wrote only the ascending pain pathway and stopped. The efferent limb to the effector is half the marks.
| Step | Structure | Detail |
|---|---|---|
| 1 · Receptor | Nociceptor (free nerve ending) | Activated by incision directly and by inflammatory mediators from damaged tissue |
| 2 · First order neuron | Aδ and C fibres; cell body in the dorsal root ganglion | Aδ thinly myelinated, ~12-30 m/s; C unmyelinated, ~0.5-2 m/s. Central process enters via the lateral division of the dorsal root |
| 3 · Synapse | Dorsal horn | Glutamate and substance P released onto interneurons and projection neurons |
| 4 · Integration | Interneuron pools, dorsal horn and intermediate grey | Polysynaptic. Propriospinal fibres spread the signal over C5-T1 — a single-segment reflex could not withdraw the arm |
| 5 · Reciprocal innervation | Excitatory and inhibitory interneurons | Flexor α motor neurons excited; extensor α motor neurons inhibited. Without it the limb co-contracts instead of moving |
| 6 · Efferent neuron | α motor neuron, anterior horn (laminae VIII, IX) | The final common pathway. Aα fibres, ~70-120 m/s, leaving in the ventral root |
| 7 · Neuromuscular junction | Acetylcholine on nicotinic (N-M) receptors | End-plate potential → propagated muscle action potential |
| 8 · Effector | Flexors of elbow and shoulder | Contraction withdraws the arm from the stimulus |
Two additions worth a clause each
- Crossed extensor reflex — with a strong stimulus, commissural interneurons cross the cord and excite the contralateral extensors, so the opposite limb takes the weight.
- The ascending limb runs in parallel — the second order neuron crosses and ascends in the spinothalamic tract to thalamus and cortex, where pain is perceived. It is not part of the reflex: withdrawal happens before, and independently of, perception, which is why an anaesthetised patient still withdraws.
Commonly lost: The cardiac sympathetic response to the raised blood pressure was not required here and earned no mark. Save it for part (b), where it is the point.
(b) The change in cerebral blood flow 4 marks
What earns the marks4 marks
| Calculate | MAP ≈ 123 mmHg from 160/105; CPP ≈ 113 mmHg |
|---|---|
| State the answer | CBF essentially unchanged, or only modestly raised: the pressure is inside the autoregulatory range |
| Name the mechanism | Myogenic (Bayliss) vasoconstriction, raising CVR |
| Link to the scenario | Pain → sympathetic activation → raised MAP, while cerebral sympathetic nerves limit the rise in flow |
Commonly lost: No candidate related autoregulated cerebral blood flow to the sympathetic activation caused by the pain. That link is the question.
Step 1 · Put the numbers in
- MAP = DBP + ⅓(SBP − DBP) = 105 + ⅓(55) ≈ 123 mmHg
- With a normal ICP of about 10 mmHg, CPP = MAP − ICP ≈ 113 mmHg.
- The MAP lies within the autoregulatory range, a mean arterial pressure of about 70-150 mmHg in most adults.
Step 2 · State the answer
Cerebral blood flow is essentially unchanged, or rises only modestly, held near 50 mL/100 g/min. It is not pressure-passive: the rise has not exceeded the upper limit.
Cerebral blood flow against mean arterial pressure: autoregulation
Step 3 · Name the mechanism that is actually operating
- Against a rise in transmural pressure, the mechanism is myogenic: the Bayliss effect.
- The rise in pressure depolarises arteriolar smooth muscle, calcium enters through voltage-gated channels and is released from intracellular stores, and the muscle contracts: vasoconstriction.
- CVR rises with CPP, so by CBF = CPP / CVR flow is held relatively constant.
Commonly lost: Listing all mechanisms of autoregulation showed a lack of understanding in relation to the scenario. With CMRO₂ unchanged and the pressure rise acute, the myogenic mechanism is the one operating. Say which, and why.
Step 4 · The link nobody made
| Effect of the sympathetic response | Consequence for CBF |
|---|---|
| Raises MAP, and therefore CPP | This is the change autoregulation is now buffering: the hypertension and the reflex movement have the same cause |
| Increases activity in the sympathetic fibres to the cerebral arteries, from the superior cervical ganglion | Limits the rise in downstream microvascular pressure and flow that the surge would otherwise produce |
| Net | CBF is maintained and the blood-brain barrier is protected against hypertensive breakthrough. The sympathetic brake is more effective against a rising pressure than a falling one |
- If chronically hypertensive: traditionally the curve is already shifted right, so this pressure is tolerated but a large fall would not be; more recent studies find autoregulation preserved in hypertensive patients.
- If the upper limit were exceeded: autoregulation is overwhelmed, flow rises passively, and the blood-brain barrier is at risk of breakthrough.
Commonly lost: Writing the determinants of cerebral blood flow earned nothing — that is a different question.
(c) How the muscle cell membrane initiates contraction 2 marks
What earns the marks2 marks
| Sarcolemma | Conducts the action potential over the whole fibre |
|---|---|
| T tubules | Carry the depolarisation into the depth of the fibre |
| Triad | T tubule flanked by two terminal cisternae of sarcoplasmic reticulum |
| DHPR | Voltage sensor in the T-tubule membrane; changes conformation |
| RyR1 | Mechanically coupled; opens, releasing Ca²⁺ from the SR |
Commonly lost: Three well-known answers earned nothing here: the action potential at the synaptic cleft, the ionic changes creating the muscle action potential, and actin-myosin coupling. The question is about the membrane, after the junction has depolarised.
| Structure | What it does | Why it matters |
|---|---|---|
| Sarcolemma | Propagates the muscle action potential from the end-plate in both directions | Spreads excitation over the surface of the whole fibre |
| Transverse (T) tubules | Invaginations of the sarcolemma running transversely into the depth of the fibre | The key structure. Depolarisation reaches the centre of the fibre essentially at the same time as the surface — without them, activation would spread inward by diffusion, far too slowly and unevenly |
| The triad | Each T tubule flanked by two terminal cisternae of sarcoplasmic reticulum | Puts the T-tubule membrane and the SR membrane in close apposition |
| Dihydropyridine receptor (DHPR) | An L-type calcium channel in the T-tubule membrane acting as a voltage sensor | Depolarisation of the T tubule produces a conformational change in it |
| Ryanodine receptor (RyR1) | Calcium release channel in the SR membrane, physically coupled to DHPR | The conformational change opens it directly; Ca²⁺ floods into the cytosol, rising roughly a hundredfold, and binds troponin C |