MAAS-MI Prep Small Physiology

These exercises rehearse the reasoning of A Small Physiology of the Noticed Body: how a complaint is generated from a mechanism and a region, and how to read a complaint through to the mechanism and the diagnosis. Read the chapter, reason each task out in your own words, then reveal the worked reasoning. No scores — the aim is to make the mechanism visible and the reasoning yours.

How to use these exercises

  • Read the matching chapter of A Small Physiology first, then work through its exercises.
  • Commit before you reveal — reason the task out, then compare. The comparison is the learning, not the reading.
  • Each answer gives more than the right reading: it shows why the tempting wrong one fails, and links to the chapter and family behind it.
  • Work in a small group when you can, and bring your reasoning to a tutor. Prep builds what you can do alone; real patients and supervision do the rest.

What this is — and isn’t. The cases here are classic teaching examples, chosen to make the reasoning visible. They are a way to rehearse the method, not a clinical protocol — the real diagnosis is always the patient in front of you. These exercises build the framework; applying it well grows with clinical experience.

Five ideas run through every chapter. Hold them, and the rest is practice.

Five Threads of Medical Problem-Solving

1. The list is generated, not memorised. Fifty-five complaints are one equation: grammar × mechanism × region. Learn how a complaint is produced, and you can read most of the review of systems rather than remember it.

2. Reasoning follows the feel to its mechanism. The patient hands you the grammar; you read it for the mechanism and the region that produced it, and the diagnosis follows.

3. The feel carries the mechanism. The quality-word names an insult, the timing a mode of failure, the companions a family. The body’s grammar is small — four dimensions — and it points.

4. Danger is built into the presentation. For a cross-cutting complaint the catastrophic mechanism is a member of the set, not a coincidence. Chest pain always carries dissection, pulmonary embolism and tamponade; the rule-out runs every time, before the likely answer settles.

5. The diagnosis is a prediction. The right mechanism predicts the right relief and the right complication. Follow-up is the experiment that confirms the reasoning, or tells you the mechanism was wrong.

Prep-Medical Problem-Solving

1The Noticed Body

What a sensation actually reports, and the moment it crosses from unnoticed into a complaint.

  • 1.1Name the regulatory failure a sensation reports

    A patient says: “I get short of breath climbing the stairs, and it has been getting worse over a month.” In one sentence, name the regulatory failure the sensation reports — and the one feature of the story that tells you.

    Reveal answer

    A failure to match oxygen delivery to demand on exertion — the body can no longer keep tissue oxygenation defended when metabolic demand rises. The tell is that it appears on exertion and eases at rest. Contrast: breathlessness that is worse lying flat points instead at a cardiac/fluid mechanism (orthopnoea); breathlessness at rest with tingling points at a metabolic or anxiety driver. (Small Physiology, Ch 1; Family II.)

  • 1.2Mark the moment a sensation crosses into notice

    A patient with long-standing knee osteoarthritis says it was “a bit stiff for years, but three days ago it became hot, swollen, and I cannot weight-bear.” When did it cross from unnoticed to noticed, and what tipped it?

    Reveal answer

    The crossing is three days ago — heat, swelling, loss of weight-bearing. A new process (acute inflammation: an effusion, or a septic joint) was added on top of the chronic mechanical background; the change in tempo is the tell that a second process has joined the first. Contrast: had the same joint slowly grown stiffer over months, that would be the old process progressing, not a new one. Because a hot single joint can be septic, the danger is built in — aspirate. (Small Physiology, Ch 1; the safety principle, Ch 4.)

  • 1.3Read one process in health and in disease

    Take coronary perfusion. Describe the quiet (physiological) version and the disturbed (pathological) version, and name what tips one into the other.

    Reveal answer

    Quiet: coronary flow rises to meet myocardial demand — the vessels dilate on exertion, delivery keeps pace, and no sensation is produced. Disturbed: a fixed stenosis caps the rise, so on exertion demand outstrips supply and ischaemia is felt as pressure (angina); at rest supply again suffices and it fades. What tips it is demand exceeding the now-limited reserve — the same process read at two moments, not two different diseases. (Small Physiology, Ch 1; Family II.)

  • 1.4The Top-7 — quality-word to mechanism, confirmed by one question

    A patient calls chest discomfort “a heavy pressure, like a weight.” Which mechanism does it most point at — and which single question best confirms it?

    • A) Inflammation — confirm by asking about tenderness
    • B) Ischaemia — confirm by asking whether exertion brings it on and rest eases it
    • C) Reflux — confirm by asking about a sour taste after meals
    • D) Anxiety — confirm by asking about life stress
    Reveal answer

    B. “Heavy pressure” is the grammar of ischaemia (Family II); the confirming H3 is the exertion-and-relief pattern. A would read as sharp and tender, not pressure. C burns and follows meals, not exertion. D is possible but is a diagnosis of exclusion — pressure with an exertional trigger must not be closed on anxiety first. Naming a plausible mechanism is not the same as confirming it — the discriminating question is what tests it. (Small Physiology, Ch 1; App 1, the Top-7.)

2The Quiet Body

How a healthy body stays silent as an active achievement, and the ways that quiet is overrun.

  • 2.1Name the achievements that keep a system quiet

    A patient with compensated heart failure still walks his dog and sits down saying nothing is wrong. Which of the six achievements — negative feedback, reserve, redundancy, adaptation, anticipation, perceptual filtering — are keeping him quiet, and how?

    Reveal answer

    All six run. Negative feedback: baroreceptors raise the heart rate to correct the falling stroke volume. Reserve: the margin he still holds above resting need. Redundancy: collateral circulation as a second route. Adaptation: the hypertrophied ventricle, remodelled to the load. Anticipation: the sympathetic ramp that lets him start walking without complaint. Perceptual filtering: the brain explaining away the small breathlessness of early exertion. Each runs invisibly, and each costs something to run — which is why the sign appears before the symptom. (Small Physiology, Ch 2.)

  • 2.2Read the compensation gap — the sign before the symptom

    A young trauma patient has lost significant blood but “feels fine.” Predict the sign the body is already showing that the symptom has not yet reported.

    Reveal answer

    Compensated hypovolaemia: vasoconstriction and tachycardia still defend the blood pressure, so the patient feels fine — but the signs precede the symptom: a raised heart rate, cool peripheries, a narrowed pulse pressure, delayed capillary refill, with a still-normal blood pressure. Contrast: a falling blood pressure is a late sign — waiting for it is waiting for decompensation. The dangerous reassurance is the normal symptom — read the sign the reserve is spending. (Small Physiology, Ch 2.)

  • 2.3Three modes of failure — reserve, rate, regulator

    An elderly patient with stable COPD becomes rapidly more breathless over two days, with fever and green sputum. By which mode did the illness arrive?

    • A) Reserve exhaustion — the slow using-up of a margin
    • B) Rate outpacing adaptation — a demand faster than the system can adapt to
    • C) Regulator breakdown — the control system itself fails
    • D) None — this is just baseline COPD
    Reveal answer

    B. A new infection (H4: fever, purulent sputum) imposed an acute demand faster than the already-thin respiratory reserve could adapt; the H2 tempo — two days, not the usual slow decline — is the tell. A is the slow background COPD trajectory, not this acute change. C would be a failure of a control system (e.g. endocrine), not an added demand. D ignores the tempo change. (Small Physiology, Ch 2.)

  • 2.4Congruent sensation versus a complaint

    Breathlessness after sprinting for a bus, versus breathlessness walking to the kitchen. Which is congruent, which is a complaint, and what makes the difference?

    Reveal answer

    Sprinting → congruent: the sensation matches the demand — the body reporting appropriate effort. Kitchen → complaint: the sensation is out of proportion to a trivial demand, so it reports a failure to meet an easy load. The difference is congruence with context — the same sensation is normal or pathological depending on whether it fits the demand that produced it. (Small Physiology, Ch 2.)

3The Grammar of the Sensation

The four dimensions of every complaint, quality, location, companions and timing, read together as one signature.

  • 3.1Separate the four dimensions into a coherent signature

    “A burning pain behind the breastbone, comes after meals, worse lying down, with a sour taste.” Split it into quality, location, companions, and timing, and say whether they cohere into one signature.

    Reveal answer

    Quality burning; Location retrosternal; Companions sour regurgitation (acid); Timing post-meal, worse recumbent. They cohere into one signature — acid mucosal irritation (reflux): the burning fits a mucosal/chemical insult, the location fits the oesophagus, and the acid companion with the post-meal/postural timing all point the same way. Contrast: if the “burning” came with exertional pressure and radiation to the arm, the four would not cohere — and a mixed signature is a warning to reconsider cardiac. (Small Physiology, Ch 3.)

  • 3.2Quality — the reporter and the insult

    A patient calls a pain “burning.” Name the reporter and the insult it implies — then predict the quality-word if the reporter changed but the insult stayed the same.

    Reveal answer

    “Burning” is reported by nociceptors sensing a chemical/mucosal or neuropathic insult (acid, inflammation, an irritated nerve). Change the reporter — a well-innervated somatic surface instead of mucosa or nerve — and the same irritation reads as “sharp” or “raw.” The quality-word is set by the reporter as much as by the insult. (Small Physiology, Ch 3.)

  • 3.3Location — referral and migration

    (a) A heart attack is felt in the left arm and jaw — name the shared source. (b) Appendicitis pain began peri-umbilical and moved to the right iliac fossa — what does the migration report?

    Reveal answer

    (a) The heart and those dermatomes share spinal cord segments (~T1–T4); the cord cannot separate visceral from somatic afferents converging on the same neurons, so the pain is referred. (b) The migration marks a change of reporter: the early peri-umbilical pain is visceral (midgut, referred to T10) from the distended appendix; the shift to the right iliac fossa is the moment the inflamed appendix touches the parietal peritoneum, which is precisely localised. The migration reports the disease advancing from visceral to parietal. (Small Physiology, Ch 3.)

  • 3.4Companions and timing — which halo, which tempo

    A headache is “like being hit on the back of the head,” maximal within seconds. Which reading fits best?

    • A) Tension-type — gradual, band-like
    • B) A vascular catastrophe (subarachnoid haemorrhage) — the instant onset is decisive
    • C) Migraine — builds over an hour, often with aura
    • D) Sinus — worse on bending, with congestion
    Reveal answer

    B. Timing is the decisive dimension: only a vascular rupture reaches maximal intensity within seconds (thunderclap). Companions to seek: neck stiffness, photophobia, reduced consciousness. A, C and D all describe slower builds and cannot produce an instant maximum. Tempo alone reclassifies this headache from benign to emergency. (Small Physiology, Ch 3; the safety principle, Ch 4.)

  • 3.5The swap — reading a negative-departure complaint

    An older patient’s family reports he “cannot follow conversations and turns the TV up.” Give the pattern of the deficit, the functional probe, and whose report is doing the sensing.

    Reveal answer

    This is a lost function, read on the negative-departure track. Pattern: reduced hearing, likely high-frequency and gradual (presbyacusis) — asymmetry would raise concern. Probe: audiometry, with Weber and Rinne to localise conductive versus sensorineural. Sensor: the informant is primary — the patient may not notice a slow, symmetrical loss, so the family’s observation is the presenting signal. Same grammar, read with three swaps: sensation→lost function, patient→informant, complaint→observed change. (Small Physiology, Ch 3; developed in Ch 7.)

4The Complaint Equation

How every complaint is generated from three factors: grammar, mechanism, and region.

  • 4.1Decompose a complaint into its three factors

    Take “biliary colic.” Break it into its three factors — grammar, mechanism, region — and show the three together generate the name.

    Reveal answer

    Grammar: cramping in waves, right-upper-quadrant with shoulder-tip radiation, autonomic halo, post-fatty-meal timing. Mechanism: obstruction (a stone intermittently blocking the cystic duct, smooth muscle contracting against it). Region: the biliary lumen (a hollow, distensible tube). Obstruction × hollow lumen produces cramping-in-waves; the biliary region gives the RUQ location and its referral; the fatty-meal trigger names the provocation. Grammar × mechanism × region = biliary colic. (Small Physiology, Ch 4.)

  • 4.2Region-types and the grammar they carry

    Take a vascular territory (a coronary artery). Name its region-type and two or three grammar-values you would expect its complaints to take — and two it would not take.

    Reveal answer

    A vascular territory is a deep, poorly-somatically-innervated region reporting via visceral afferents. Expect: pressure / heaviness / tightness (not sharp), poorly localised, with an exertion-and-relief timing when the mechanism is ischaemia. It would not take a precise pin-pointable location, or reproducible-on-palpation tenderness — a vessel wall has no rich somatic afferents to generate those. Region constrains the grammar before mechanism is even considered. (Small Physiology, Ch 4.)

  • 4.3Hold two factors, vary the third

    Hold the mechanism at ischaemia and vary the region. List the review-of-systems complaints that result.

    Reveal answer

    Ischaemia × coronary → angina / chest pain; × cerebral → TIA / stroke symptoms; × mesenteric → post-prandial abdominal pain (“intestinal angina”); × limb → claudication; × retinal → amaurosis fugax. One mechanism, five regions, five complaints — each with the same demand-led or loss grammar, shifted by its region. (Small Physiology, Ch 4.)

  • 4.4Recognise the exception class

    A patient presents with “fatigue” and nothing else. Which class is this, and which factor of the equation carries the most diagnostic weight?

    • A) Cross-cutting — many mechanisms at one signature
    • B) Branching — one word splitting into sub-qualities
    • C) Systemic-companion — no localised signature; the companions carry the weight
    • D) Mechanical edge — no active process to disturb
    Reveal answer

    C. Fatigue is systemic-companion: the signature is degenerate at H1 (no quality-word, no location), so the companions (H4) across systems become the presenting axis — you reason from the companions inward. A still has a localised signature (e.g. chest pain). B needs a quality-word that splits (e.g. dizziness). D is a structural, reproducible-on-movement complaint. (Small Physiology, Ch 4; the sweep / H4-driven pattern, Ch 6.)

  • 4.5The safety principle — name the catastrophic alternative

    A patient has a headache you think is migraine. Name the catastrophic alternative and the single question or test that separates them.

    Reveal answer

    The catastrophic alternative is subarachnoid haemorrhage. The separator is onset speed: “Did it come on instantly — worst headache of your life, maximal within seconds — or build over minutes to hours?” A thunderclap onset mandates imaging (CT, then LP if needed) before migraine is accepted. Run the rule-out even when the benign diagnosis is more likely: for a cross-cutting complaint the catastrophic mechanism is a structural member of the set, and the clean answer is the one that invites premature closure. (Small Physiology, Ch 4; App 3.)

5The Five Families

The seventeen mechanisms grouped into five families by shared logic, and the seven aetiologies beneath them.

  • 5.1Identify the family from its signature

    “Symmetric small-joint pain, tenderness, morning stiffness, a low fever.” Which family, and the signature that decided it?

    • A) Family I — Tissue Insult & Response (inflammation)
    • B) Family II — Perfusion & Oxygenation
    • C) Family IV — Luminal & Pressure Dynamics
    • D) Mechanical edge — a structural fault
    Reveal answer

    A. The signature: tenderness, symmetrical small-joint involvement, morning stiffness, a stable-to-crescendo course, and a systemic halo (low fever). The Family I move — “is there tenderness, and does anything systemic go with it?” — is yes to both. B would be demand-led pressure, not tender joints. C cramps in waves. D is reproducible on movement with no systemic halo. (This picture is inflammatory synovitis; e.g. rheumatoid arthritis.) (Small Physiology, Ch 5.)

  • 5.2Match the signature to the family

    Five patients, five sentences. For each, name the family the complaint belongs to and the failure at its centre.

    The five families are: I Tissue Insult and Response, II Perfusion and Oxygenation, III Vessel and Fluid Balance, IV Luminal and Pressure Dynamics, V Signal and Regulation.

    1. A burning behind the breastbone after meals, eased by an antacid.
    2. A pressure across the chest on walking uphill, gone within a minute of sitting down.
    3. One calf swollen, warm and tender over a single day.
    4. Cramping abdominal pain coming in waves, with vomiting and no wind or stool.
    5. Burning, tingling numbness in both feet, worse at night.
    Reveal answer
    1. Family I — Tissue Insult and Response. Acid meeting an unprotected mucosa: chemical irritation of the tissue.
    2. Family II — Perfusion and Oxygenation. Demand outrunning supply: ischaemia in coronary territory.
    3. Family III — Vessel and Fluid Balance. A vessel failing to keep blood moving: venous thrombosis.
    4. Family IV — Luminal and Pressure Dynamics. A blocked lumen with pressure rising behind it: obstruction.
    5. Family V — Signal and Regulation. Disordered nerve signalling: a peripheral neuropathy.

    Notice that the family fell out of the failure, not the organ — the same reasoning places chest pressure in Family II whether it strikes the heart, the leg, or the gut.

  • 5.3Reconcile the stack — complaint to mechanism to family to aetiology

    Take “acute coronary syndrome.” Name its family, dominant mechanism, and driving aetiology — then trace the stack forward from aetiology to complaint.

    Reveal answer

    Family II (Perfusion & Oxygenation); mechanism ischaemia; aetiology degenerative (atherosclerosis), usually with an acute thrombotic (physical/vascular) trigger. Forward: a degenerative aetiology narrows a coronary vessel → ischaemia in coronary territory → grammar of exertional or rest pressure with an autonomic halo → the complaint “chest pain” → the diagnosis ACS. Aetiology drives mechanism drives grammar drives complaint. (Small Physiology, Ch 5; App 4, the stack.)

  • 5.4The mechanical edge

    The Mechanical edge is where a structural finding sits outside physiology — and where an image can mislead.

    Two patients with low back pain, each with a scan. For each, decide whether the imaging finding is the mechanism of the complaint or an incidental finding — and say what settles it.

    1. Back pain radiating down one leg to the outer foot, worse on coughing, with numbness along the same line. MRI: a disc herniation compressing the S1 nerve root.
    2. Aching pain across the low back after a day in the garden, no radiation, eased by moving about. MRI: a mild disc bulge at L4–L5.
    Reveal answer

    Case 1 — the finding is the mechanism. The grammar matches what an S1 compression produces: pain in the root’s distribution, radiating to the outer foot, provoked by the cough that raises pressure on the root, with numbness along the same dermatome. Finding and complaint fit.

    Case 2 — the finding is almost certainly incidental. Disc bulges are common in people with no pain at all. The grammar here is mechanical and axial — no radiation, no dermatome, eased by movement — which points at a soft-tissue mechanism, not root compression. The bulge is a bystander.

    What settles it: an imaging finding earns the name mechanism only when the complaint’s grammar matches the syndrome that finding would produce. The scan does not diagnose; the fit between grammar and finding does.

  • 5.5Sort Family III by onset speed

    Three patients, one family — Vessel and Fluid Balance. Before any test, let onset speed do the first sorting: decide for each which of the three sub-mechanisms is in play — vascular leak or rupture, Starling-force oedema, or haemostatic disturbance — and name the grammar that told you.

    1. A sudden, tearing pain between the shoulder blades, maximal the instant it began.
    2. Both ankles swelling over three weeks, worse by evening, painless, the rings still fitting.
    3. Bruising after the lightest knocks, and gums that bleed when brushing.
    Reveal answer
    1. Vascular leak or rupture. Instant, tearing, maximal at onset — the temporal signature of a wall that failed all at once.
    2. Starling-force oedema. Gradual, gravity-dependent, painless accumulation — the capillary exchanging more fluid than the lymphatics can return.
    3. Haemostatic disturbance. Bleeding and bruising out of proportion to the trauma — the cascade that patches microtrauma has failed.

    Onset speed did the sorting before anything was sent to the lab: instant points at a wall that gave way and takes precedence over everything; gradual painless growth points at Starling; bleeding out of proportion points at haemostasis. Only after that sort do the aetiology, the treatment, and the safety-net open properly.

6The Interview as Machinery

Clinical reasoning as the equation run backwards, reading the grammar back to the mechanism through five patterns.

  • 6.1Follow the feel to the mechanism, heuristic by heuristic

    A patient reports cramping right-upper-quadrant pain after a fatty meal. Take the four heuristics in order and name the factor each solves for.

    Reveal answer

    H1 (nature): cramping, RUQ → the grammar signature → sets Family IV (luminal / obstruction) in a hollow region. H2 (time): waves, post-meal → mode of failure and tempo → intermittent obstruction. H3 (modifying): worse after fatty food, eased when the stone passes → the specific mechanism (biliary obstruction). H4 (companions): nausea, sweating → the autonomic halo, confirming a visceral source. Each heuristic solves one factor; together they follow the feel to biliary colic. (Small Physiology, Ch 6.)

  • 6.2Choose which of the four patterns is called for

    A 55-year-old presents with acute central chest pain, sweating, at rest. Which of the four patterns is called for?

    • A) Pattern recognition — the fast whole read (the destination)
    • B) Branching — one signature splitting into sub-qualities
    • C) Rule-out, in parallel — several mechanisms held at once, each excluded
    • D) Schema-based, entered at H4 — a degenerate signature, read through the companions
    Reveal answer

    C. Chest pain is cross-cutting: the same signature admits several mechanisms at once (ischaemia, aortic dissection, PE, tamponade, oesophageal rupture). The feature is that a catastrophic alternative is a structural member of the set — none is safe to prefer without excluding the others in parallel. A would be premature closure — a fast read that skips the danger. B needs a splitting quality-word. D needs a degenerate signature (fatigue, fever), which this is not. Naming the leading hypothesis is necessary but not sufficient — the move is to actively test the alternatives before settling. (Small Physiology, Ch 6; App 3.)

  • 6.3Walk the sweep — schema-based, entered at H4

    A patient presents with unexplained weight loss and nothing else. Walk the traversal: where do you start, which companions do you ask about and roughly in what order, and where do H2 and H3 come in?

    Reveal answer

    H1 is empty — no quality-word, no address — so you cannot start there; enter at H4, the companions across systems, which are the presenting axis. Sweep the systems for that axis: appetite and bowels (malignancy, malabsorption); fever and night sweats (infection, lymphoma); heat intolerance and tremor (thyroid); thirst and polyuria (diabetes); mood and sleep (depression). H2 (the tempo — weeks versus months) narrows the class; H3 and investigations then confirm. H1 remains only as a rule-out check for a hidden localised complaint the patient did not name. This is the systematic sweep (the interview handbook’s schema-based pass), entered through the one door the complaint leaves open. Cannot-miss: malignancy. (Small Physiology, Ch 6; App 3; the systemic-companion class, Ch 4.)

  • 6.4Pattern selection under time pressure

    Busy clinic; a patient with a classic migraine history says today’s headache feels the same. Name the pattern, its shortest safe run, and the questions you cannot skip.

    Reveal answer

    Pattern: rule-out (one likely benign, one cannot-miss). Shortest safe run: confirm the headache matches the prior migraine pattern (same quality, tempo, triggers, aura) and actively exclude the red flags. Cannot skip: onset speed (thunderclap → SAH); fever with neck stiffness (meningitis); new neurology or “worst ever”; posture and wake-time pattern (raised ICP). If every red-flag is negative and the pattern matches, migraine settles. The gap to guard is the one where the pattern matched but a red-flag was skipped — that is where missed diagnoses hide. (Small Physiology, Ch 6; App 3.)

  • 6.5Close the loop — predict relief and complication

    You diagnose GERD and start a proton-pump inhibitor. Name the relief and the complication it predicts, and what you would revise if the prediction fails.

    Reveal answer

    Predicted relief: the burning eases within days to a couple of weeks on acid suppression — the mechanism (acid mucosal irritation) predicts a response to removing acid. Predicted complication if untreated: oesophagitis, stricture, bleeding. If the predicted relief does not appear, the mechanism was likely wrong — return to the H3 branch point (cardiac pain mimicking reflux, or a motility or malignant cause) and look for red-flag features warranting endoscopy. A wrong prediction is the most useful result — it names exactly which branch to revisit. (Small Physiology, Ch 6; Ch 8.)

  • 6.6When the reversal fails

    A patient returns repeatedly. The pain shifts location and quality between visits, the companions fit no single family, and two treatments that each predicted relief brought none. What regime are you in, and how should the reasoning change?

    Reveal answer

    The warning signs — a grammar that will not cohere across its four dimensions, companions and timing that fit no family, a story that shifts between visits, and repeated readings that predict a relief which never comes — signal the uncoupled regime: the reporter is sensitised, not the tissue, so the founding assumption (the feel carries the mechanism) no longer holds. This is not a rare edge — functional and medically-unexplained presentations, now often grouped as persistent physical symptoms, are a large fraction of primary-care contacts — so the move is to suspect it rather than be ambushed by it. Stop forcing the equation; name the uncertainty honestly, cover any dangerous branch that remains open, and shift toward the interview’s process skills (Scales A, B, C) and shared decision-making (Scale 3). Forcing a mechanism onto a body that is not producing one is the error to avoid. (Small Physiology, Ch 6 §5; App 3, “When the grammar does not resolve.” On the persistent-symptom regime and its management: Löwe et al., Lancet 2024;403:2649.)

7mechanism-Cause

  • 7.1The second half — what H5 to H7 recover

    A patient’s mechanism is settled — say, coronary ischaemia behind stable angina.

    There is a mechanism now, but not yet a cause or a plan. Name what each of the three extended heuristics still has to recover — H7, H6 and H5 — and why the plan cannot be built until they have.

    Reveal answer

    H7 — the aetiology. Why the mechanism arose at all: here, the atherosclerotic substrate and the risk factors that built it.

    H6 — the substrate and what has been tried. The stage of the disease, the prior treatments, and the current medicines — some of which can themselves be part of the cause.

    H5 — the person. The life the disease sits in: function, meaning, what “better” would look like, what the patient can actually carry.

    The mechanism says what is happening. H5–H7 say why, in whom, and what can be done — and the plan is composed from all three, never from the mechanism alone.

  • 7.2H6 — a current medicine as the cause

    A patient’s blood pressure stays high despite treatment. H6 asks what medicines they take and what has already been tried.

    Name one current medication that could itself be raising the pressure — and explain how a prior treatment that failed can be read as diagnostic data rather than a dead end.

    Reveal answer

    A regular non-steroidal anti-inflammatory — ibuprofen taken two or three days a week for arthritic knees — can raise blood pressure and blunt the drugs meant to lower it. It is a current medication that is part of the cause, not just background: an H6 finding you can act on by removing it.

    A prior antihypertensive that did not work is not a wasted step. It is an H3 test whose answer was “no” — it narrows the mechanism by ruling out the target that drug addressed, and it points the next choice. H6 turns the medicine list into both a cause to remove and a set of experiments already run.

  • 7.3The life-course question

    H5 sometimes needs the longer question — what a person’s earlier life was like — the kind you would not ask on a first visit.

    For a patient whose recovery keeps stalling, write how you would open that question so it invites the context without reducing the person to it. Then note what you would do with what you hear.

    Write a few lines — there is no answer key.

    Reveal a note to compare

    A good opening is open and permissioned — “Can I ask what life was like for you, growing up?” — offered, not demanded, and left for the patient to fill or to decline.

    The discipline is in what you do next. The childhood household that drank, the smoking that started at fifteen, the loss that changed the daily walk — these are life-course context that shapes the present, not a label that explains the illness away. You are trying to understand the person the disease sits in, not to reduce the disease to a story. The evidence that early adversity tracks with later disease is real, but it is a lens for understanding, not a verdict.

    How to ask it warmly is the interview handbook’s craft; that it is worth asking is the point here.

  • 7.4Split the treatment — relief and cure

    Take a diagnosis with both a mechanism and an aetiology — stable angina on atherosclerotic disease.

    Name what treats the mechanism (relief) and what treats the aetiology (cure); and where the aetiology has two arms, name both.

    Reveal answer

    Relief — aimed at the mechanism. A nitrate dilates the under-supplied coronary vessel and the pressure eases. The symptom stops; the disease beneath it is untouched.

    Cure — aimed at the aetiology. The atherosclerotic substrate, addressed on two arms: a pharmacological one (a statin, blood-pressure control, an antiplatelet) and a behavioural one (walking, diet, stopping smoking).

    Relief without cure leaves the disease running quietly under an eased symptom. For a disease whose aetiology has both arms, the plan that addresses both is what the evidence supports — and the behavioural arm is where H5, the person, decides what can actually be carried.

  • 7.5The same H3 across three visits

    A patient is seen across three visits for the same problem. Each time, the same heuristic — H3, what makes it better or worse — is being asked, but it is testing something different each time.

    Name what H3 is testing at the first visit, at the second, and at a third where the treatment has failed.

    Reveal answer

    Visit one — recovering the mechanism. “What makes it better or worse?” separates the candidate mechanisms and confirms which one is at work.

    Visit two — testing the treatment. The same question, now asked of the treatment: did the predicted relief appear? If it did, the mechanism is confirmed by outcome, not just by reasoning.

    Visit three — a treatment that failed. An H3 “no.” The failure is purposeful data: it sends you back to the branch point to reconsider the mechanism. A failed treatment is not a defeat but a test result — and the interview structure carries the thread between visits.

  • 7.6When the aetiology will not resolve

    Sometimes the second half does not narrow the plan: the aetiology will not resolve.

    Name the three things this can mean — an idiopathic case, an uncoupled (persistent-symptom) regime, or a case that simply needs more time — and how you would tell them apart.

    Reveal answer

    Idiopathic. The cause is genuinely not found after an adequate search. The honest move: name the uncertainty, cover the dangerous branch, and follow up.

    Uncoupled. The complaint has decoupled from a tissue mechanism — the persistent-symptom regime. More tests will not resolve it; it needs its own approach, and often a bridge to the mental-health handbook.

    Needs more time. The process is still evolving; the next visit will show what this one could not.

    You tell them apart by three things: how complete the search has been, whether the grammar still coheres, and how the picture answers to time. Not every hard case is psychosocial, and not every unresolved one is idiopathic — the boundary itself is the clinical judgement.

8When the Patient Is Not the One Who Notices

The complaints noticed by someone else first: lost function, the informant as sensor, and the functional probe.

  • 8.1Who noticed — patient, informant, or both

    A wife brings her husband: he has become withdrawn and repeats himself; he says nothing is wrong. Who is the primary noticer?

    • A) The patient — he is the one experiencing it
    • B) The informant (the wife) — the change is a lost function the patient cannot see
    • C) Both equally
    • D) Neither — this needs a test first
    Reveal answer

    B. The mismatch between a reported change (withdrawal, repetition — a lost cognitive function) and the patient’s own non-report (“nothing is wrong”) is the tell. Negative-departure complaints, especially cognitive ones, are often invisible to the affected faculty itself, so the sensor shifts to the informant. A over-trusts a patient who lacks insight; C misses the asymmetry; D delays — you interview both first, and the gap between them is itself diagnostic. (Small Physiology, Ch 7.)

  • 8.2The collateral interview

    For the same presentation (possible cognitive decline), list the H1–H4 questions you would ask the informant, and how you would arrange the encounter.

    Reveal answer

    H1 (nature): what exactly changed — memory, language, personality? H2 (time): sudden or gradual; stepwise or steady? H3 (modifying): better or worse at times of day; triggers or new medications? H4 (companions): gait, continence, mood, sleep, weight? Arrange it so you hear each source separately — interview the patient alone (their account and their insight) and the informant alone (their observations) — because each carries a different sensor, and the gap between them is itself diagnostic. (Small Physiology, Ch 7.)

  • 8.3Functional probes, level by level

    A patient has hearing loss. Name the probe that tests each level of the pathway, and interpret the results.

    Reveal answer

    Whispered-voice testing (or audiometry) establishes the deficit; Rinne and Weber localise the level. Rinne (tuning fork mastoid vs ear): air > bone is normal or sensorineural, bone > air is conductive. Weber (fork on the forehead): lateralises to the affected ear in conductive loss, to the better ear in sensorineural. Each probe isolates one level — outer/middle (conductive) versus cochlea/nerve (sensorineural) — so the pattern of results names the level of the lesion. (Small Physiology, Ch 7.)

  • 8.4Read the gap across the four configurations

    Name the four configurations of patient-versus-informant report, and how the diagnostic direction changes across them.

    Reveal answer

    (1) Patient reports, informant confirms → both agree, straightforward. (2) Patient reports, informant does not → a sensation invisible to others (e.g. pain), or amplification — weigh the patient’s interior access. (3) Informant reports, patient does not → the classic insight-loss / negative-departure case — trust the informant; suspect the faculty is itself the noticer. (4) Neither reports but signs are present → screening or compensated disease — the body shows a sign before either senses it. The direction of trust shifts with the configuration. (Small Physiology, Ch 7.)

  • 8.5The bridge to the mental-health framework

    A patient with possible psychosis has no insight that anything is wrong. Recognise the handover moment, and name what the mental-health framework adds that somatic reasoning cannot.

    Reveal answer

    The handover is when insight itself is the faculty at stake — the somatic reversal (“the feel carries the mechanism”) no longer holds, because the patient cannot report the disturbance and the disturbance is of thought or perception, not tissue. The mental-health framework adds the parallel machinery: the mental-state examination, collateral history weighted heavily, and a phenomenological rather than somatic-mechanism reading. Somatic reasoning hands over; it does not stretch to cover insight. (Small Physiology, Ch 7; and the mental-health handbook.)

9The Loop Closes

Follow-up as the experiment that checks the reasoning: the right mechanism predicts the right relief and the right complication.

  • 9.1State the relief you expect at follow-up

    You diagnose bacterial community-acquired pneumonia and start antibiotics. State the relief you expect at follow-up, and what you would revise if it does not appear.

    Reveal answer

    Expected relief: the fever settling within 48–72 hours and symptomatic improvement over days as the treated organism clears — the mechanism (bacterial infection) predicts a response to the right antibiotic. If it does not appear, reconsider: wrong organism or resistance, a complication (empyema, abscess), or a wrong mechanism entirely (PE, or malignancy with post-obstructive change). The failed prediction refutes the working diagnosis — treat it as data that names the next step, not a treatment failure to wait out. (Small Physiology, Ch 8.)

  • 9.2Name the earliest complication to watch for

    You diagnose a first deep-vein thrombosis. Name the earliest specific complication to watch for, and the safety-net advice you would give at the end of the visit.

    Reveal answer

    Earliest specific complication: pulmonary embolism — a clot embolising — because the mechanism (a venous thrombus) predicts it directly. Safety-net advice: seek urgent care for sudden breathlessness, pleuritic chest pain, coughing up blood, or collapse; and cover the bleeding risks of anticoagulation. The complication you name is the one the mechanism most directly produces, and the advice arms the patient to catch it early. (Small Physiology, Ch 8.)

  • 9.3Present the solution, grounded in the mechanism

    You have reasoned to tension-type headache. Walk the five Scale-3 (Presenting Solutions) moves in your own words, and check each is grounded in the mechanism.

    Reveal answer

    (1) Explain the diagnosis: a muscle-tension / central-sensitisation headache, not a dangerous cause — grounded in the benign grammar and the negative red flags. (2) Explain the mechanism plainly: tight, sensitised pain pathways, not brain damage. (3) Share the plan: simple analgesia used sparingly, and address the triggers (stress, posture, sleep) — grounded in the mechanism’s drivers. (4) Safety-net: return if the pattern changes, or with thunderclap onset, fever, or new neurology — the rule-out mechanisms. (5) Check understanding and agreement. Each move is anchored in the mechanism reasoned to, not generic advice. (Small Physiology, Ch 8; interview handbook, Scale 3.)

  • 9.4The explanation the patient came for

    Many patients come to be told what is going on, not to be treated.

    Take a benign complaint — a burning behind the breastbone, or a tension headache. In three plain sentences the patient would understand, say what the mechanism is, why it produces this exact feel, and why it is not dangerous.

    Write it out in your own words, then compare.

    Reveal a note to compare

    A good explanation does three things in plain words. For the burning behind the breastbone: “The burning is acid from your stomach rising into your gullet. Your gullet has none of the thick lining your stomach has, so the acid stings it — that is the burning, and it is worse after meals and lying down, when acid rises most easily. It is uncomfortable and worth treating, but it is not your heart, and once we settle the acid the lining heals and the burning stops.”

    Notice what carries it: a mechanism named without jargon (acid on an unprotected lining), the feel tied to the mechanism (why it burns, why after meals), and reassurance made honest and specific (not the heart; heals with treatment) — with the safety-net kept ready for the follow-up (come back if swallowing becomes difficult, or there is blood or weight loss). The content is the mechanism this book recovers; how you say it warmly at the bedside is the interview handbook’s craft.

  • 9.5The end-state — grounded recognition

    Think of a diagnosis you now recognise almost instantly. Can you still take it apart into grammar → mechanism → region? Where in your own practice should that fast recognition be trusted, and where should you deliberately slow down and walk the reasoning through again? Write a few lines for yourself — there is no answer key.

    Reveal a note to compare your thinking

    With repetition the reasoning becomes automatic — the expert does not walk the equation each time; the pattern fires as a whole (an illness script). The aim of this book is that when that automatic recognition forms, it is grounded in mechanism rather than in surface appearance: a grounded script is one you could still take apart and justify if asked; a surface one fires on look-alikes and mis-fires on the atypical. Trust the fast read on the ordinary and the classic; deliberately slow down and walk the reasoning through again when the case is atypical, high-stakes, or when the pattern fires too easily. (Small Physiology, Ch 8; Ch 6 §5, encapsulation.)

10How to Proceed

You have now rehearsed the reasoning of the whole book, chapter by chapter: reading a sensation, decomposing a complaint, naming the mechanism, running the reversal, and closing the loop. What follows is how to keep that reasoning alive and turn it into competence.

Keep it alive. Come back to these exercises after a gap rather than all at once — spacing strengthens what you can recall — and revisit them in a mixed order, jumping between complaints and chapters rather than working straight through one chapter at a time, so each time you have to recognise afresh which reasoning applies. Pay special attention to any case where your first answer was wrong: that is where the reasoning grows.

Take it to patients. The framework is built here; diagnosis itself grows with real and simulated encounters, under supervision. Carry each exercise’s reasoning into MAAS Practice and into the clinic, and check whether the mechanism you reasoned to predicted the relief and the complication you expected.

Build the skill deliberately. To grow the reasoning from the ground up — simple cases first, then complex — follow the companion path, Learn to Reason, which re-sequences these exercises as a spiral and adds whole-case practice.

Keep a record. Note your reasoning as you go, and bring it to a tutor or study group. A worked reasoning you can take apart and justify is worth more than a remembered answer.

The equation is the ground your intuition will stand on. With practice, the walked reasoning becomes automatic — and because it is grounded in mechanism, it holds when a patient does not fit the pattern.