Reference

Illness scripts

Compact disease representations in one fixed frame, because diagnosis is matching the patient's story against these. The frame is the point: who, tempo, symptoms, findings, investigations, differentiators.

Heart failure with reduced ejection fraction

Cardiology

Who?: Older adults with prior infarction, hypertension, or cardiomyopathy.
Time course?: Chronic with acute decompensations over days.
Key symptoms?: Exertional dyspnea, orthopnea, PND, edema, fatigue.
Key findings?: Raised JVP, displaced apex, S3, crackles, peripheral edema.
Key investigations?: Echo shows EF below 40 percent; NT-proBNP elevated; CXR congestion.
What differentiates it?: The S3 and displaced apex point at a dilated, failing pump; preserved-EF disease shares the congestion but not the systolic signature.

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CompareHFrEF vs HFpEF

Heart failure with preserved ejection fraction

Cardiology

Who?: Older, often hypertensive patients, frequently with obesity, diabetes, or AF.
Time course?: Chronic; exertional intolerance dominant, decompensating with volume or AF.
Key symptoms?: Exertional dyspnea and intolerance; edema; symptoms flare with tachycardia.
Key findings?: Hypertension, S4 more than S3, congestion without a displaced apex.
Key investigations?: Echo: EF at or above 50 percent with diastolic dysfunction and atrial enlargement; NT-proBNP raised (less than HFrEF, and blunted by obesity).
What differentiates it?: Same congestion, stiff rather than weak ventricle; diagnosis leans on echo indices and the company it keeps (age, hypertension, AF).

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CompareHFrEF vs HFpEF

Nephritic syndrome

Nephrology

Who?: Any age; post-infectious in the young, vasculitis and IgA across adults.
Time course?: Days to weeks.
Key symptoms?: Dark (tea or cola) urine, edema, headache from hypertension, oliguria.
Key findings?: Hypertension, edema, hematuria.
Key investigations?: Dysmorphic red cells and red cell casts; subnephrotic proteinuria; complement pattern and serologies steer the cause.
What differentiates it?: Inflammation leaks cells: blood and casts dominate over protein. The nephrotic pattern is the mirror image.

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UrineRead the sediment

Nephrotic syndrome

Nephrology

Who?: Children (minimal change) through older adults (membranous, diabetes, amyloid).
Time course?: Weeks to months, often insidious.
Key symptoms?: Progressive edema, frothy urine, weight gain.
Key findings?: Marked edema, sometimes periorbital; blood pressure variable.
Key investigations?: Proteinuria above 3.5 g/day, hypoalbuminemia, hyperlipidemia; bland sediment.
What differentiates it?: A podocyte leak, not inflammation: protein without cells. Companions include thrombosis (renal vein), infection, and lipiduria.

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CompareNephritic vs nephrotic

Diabetic ketoacidosis

Endocrinology

Who?: Type 1 diabetes (new or established); increasingly type 2 under stress or SGLT2 inhibitors.
Time course?: Hours to two days.
Key symptoms?: Thirst, polyuria, vomiting, abdominal pain, air hunger.
Key findings?: Kussmaul respiration, dehydration, ketotic breath, tachycardia.
Key investigations?: Glucose high (or near-normal in euglycemic DKA), ketones, high anion gap metabolic acidosis.
What differentiates it?: The gap acidosis plus ketones is the identity; HHS shares the sugar but not the acid.

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Blood gasThe DKA gas

Pulmonary embolism

Respirology

Who?: Immobilization, surgery, malignancy, estrogen, prior VTE; often nobody obvious.
Time course?: Sudden to hours.
Key symptoms?: Pleuritic chest pain, dyspnea out of proportion, syncope in large emboli, hemoptysis occasionally.
Key findings?: Tachycardia, tachypnea, clear lungs despite hypoxia; unilateral leg swelling sometimes.
Key investigations?: Wells score gates D-dimer versus CTPA; ECG shows sinus tachycardia most often, S1Q3T3 rarely.
What differentiates it?: Hypoxia with a clear chest film and a clear chest exam is the classic dissonance.

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CalculatorWells score

Anaphylaxis

Allergy & Clinical Immunology

Who?: Any age; foods, stings, drugs (antibiotics, contrast), latex; sometimes no identified trigger.
Time course?: Minutes; biphasic recurrence hours later in a minority.
Key symptoms?: Urticaria and flushing with airway (throat tightness, stridor), respiratory (wheeze), GI (cramping, vomiting), or circulatory (presyncope) involvement.
Key findings?: Hives, angioedema, hypotension, wheeze; skin findings absent in up to a fifth.
Key investigations?: Clinical diagnosis; serum tryptase drawn early supports it retrospectively.
What differentiates it?: Two or more organ systems after a plausible exposure. Epinephrine early is both treatment and, in effect, the diagnostic commitment; there is no lab to wait for.

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drugSteroids' supporting role

Delirium

Geriatric Medicine

Who?: Older, frail, cognitively vulnerable, or acutely ill inpatients; postoperative and ICU settings.
Time course?: Hours to days, fluctuating through the day; worse at night.
Key symptoms?: Acute inattention with disorganized thinking; hyperactive, hypoactive (most missed), or mixed.
Key findings?: Failure of attention tasks (months backwards); altered arousal; a cause elsewhere: infection, retention, impaction, drugs, pain, metabolic upset.
Key investigations?: Directed by the suspected driver: glucose, electrolytes, cultures with a symptom anchor, medication review always.
What differentiates it?: Acuity and fluctuation separate it from dementia; attention is the axis. Delirium is a syndrome pointing at a cause list, never a stopping point.

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ApproachApproach to confusion

Febrile neutropenia

Medical Oncology

Who?: Patients on cytotoxic chemotherapy, typically 7 to 14 days after a cycle.
Time course?: Hours; can collapse quickly despite looking well early.
Key symptoms?: Fever, sometimes nothing else: neutropenia mutes every localizing sign.
Key findings?: Often unremarkable; examine lines, perineum (no rectal exams), mouth, skin. Absence of findings excludes nothing.
Key investigations?: CBC with differential (the defining count), cultures from every lumen before antibiotics, directed imaging.
What differentiates it?: Fever plus an absolute neutrophil count below 0.5: empiric broad antibiotics within the hour, no waiting for localization. The classic oncologic emergency of omission.

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CaseThe sepsis clock, same rules

Hypercalcemia of malignancy

Medical Oncology

Who?: Known or occult malignancy: lung, breast, myeloma, renal cell.
Time course?: Days to weeks; faster and higher than primary hyperparathyroidism.
Key symptoms?: Polyuria and thirst, constipation, nausea, lethargy through confusion ('groans, stones, moans').
Key findings?: Volume depletion, altered mentation at higher levels; short QT on ECG.
Key investigations?: Corrected calcium, PTH (suppressed), PTHrP and vitamin D metabolites by mechanism hunt.
What differentiates it?: A suppressed PTH divides it from primary hyperparathyroidism, the other common cause. Treatment starts with volume, then antiresorptives; the cancer is the diagnosis.

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CalculatorCorrected calcium

Acute gout

Rheumatology

Who?: Middle-aged and older adults; diuretics, alcohol, renal disease, metabolic syndrome.
Time course?: Hours; often overnight onset.
Key symptoms?: Abrupt monoarticular agony, classically first MTP; exquisite touch sensitivity.
Key findings?: A red, hot, swollen joint; tophi in chronic disease.
Key investigations?: Synovial fluid: needle-shaped, negatively birefringent crystals, inflammatory cell counts.
What differentiates it?: Only aspiration separates it definitively from its dangerous mimic, the septic joint, and the two can coexist.

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FluidThe crystal tap

Septic arthritis

Rheumatology

Who?: Prosthetic or damaged joints, immunosuppression, diabetes, injection drug use, recent bacteremia; any age.
Time course?: Hours to a day or two; the joint is destroyed within days if untreated.
Key symptoms?: A single hot, swollen, exquisitely painful joint held still; fever and rigors, though the elderly may have neither.
Key findings?: Warm effusion, pain on the slightest passive movement, refusal to bear weight; a portal of entry sometimes found on the skin.
Key investigations?: Aspiration before antibiotics: turbid fluid, white cells typically above 50,000 with neutrophils dominant (lower counts do not exclude it), Gram stain and culture; blood cultures; inflammatory markers support and never exclude.
What differentiates it?: Gout and pseudogout look identical at the bedside and can coexist with infection; the Gram stain and culture are the only arbiter, and a positive crystal result does not close the question.

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FluidThe hot joint tap

Decompensated cirrhosis

Gastroenterology

Who?: Established cirrhosis from alcohol, viral hepatitis or fatty liver disease; a trigger is found in most admissions.
Time course?: Days; each decompensation (ascites, encephalopathy, variceal bleeding, jaundice) marks a step down in prognosis.
Key symptoms?: Abdominal swelling, confusion or reversed sleep, hematemesis or melena, deepening jaundice, fever.
Key findings?: Ascites with shifting dullness, asterixis, spider nevi, palmar erythema, gynecomastia, a small hard liver, splenomegaly.
Key investigations?: Diagnostic paracentesis on every admission with ascites (cell count for SBP, SAAG), INR, albumin, bilirubin and creatinine for the Child-Pugh and MELD scores, a search for the trigger: infection, bleeding, drugs, alcohol, thrombosis.
What differentiates it?: The precipitant is the diagnosis: spontaneous bacterial peritonitis, a bleed, a new nephrotoxin or a portal vein thrombosis sits behind almost every decompensation, and treating the ascites without finding it misses the point.

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FluidThe ascitic tap that grows bacteria CaseCirrhosis on the ward

Upper gastrointestinal bleeding

Gastroenterology

Who?: NSAID and anticoagulant users, Helicobacter pylori carriers, heavy drinkers and cirrhotics with varices, older adults.
Time course?: Minutes to hours; hemodynamic collapse can precede the first visible blood.
Key symptoms?: Hematemesis or coffee-ground vomiting, melena, presyncope; epigastric pain in ulcer disease, painless in varices.
Key findings?: Tachycardia and a postural drop before hypotension; melena on rectal examination; stigmata of chronic liver disease steer the cause.
Key investigations?: Hemoglobin (initially misleading), urea raised out of proportion to creatinine, INR and platelets, group and crossmatch; endoscopy within 24 hours, sooner if unstable; the Glasgow-Blatchford score decides who can wait.
What differentiates it?: Melena with a raised urea to creatinine ratio places the source above the ligament of Treitz; the liver stigmata decide whether terlipressin and antibiotics join the proton pump inhibitor before the scope.

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ApproachApproach to GI bleeding CaseThe melena admission

Iron deficiency anemia

Hematology

Who?: Menstruating and pregnant women, older adults with occult gastrointestinal loss, vegetarians, malabsorption (celiac disease, bariatric surgery).
Time course?: Months; symptoms lag the fall in hemoglobin because the body adapts.
Key symptoms?: Fatigue, exertional breathlessness, restless legs, pica and ice craving, hair loss; often none.
Key findings?: Pallor of the conjunctivae and palmar creases, koilonychia and angular cheilitis in long-standing disease, a flow murmur; the examination hunts the source as much as the anemia.
Key investigations?: Microcytic hypochromic indices with a raised red cell distribution width, low ferritin (the defining test, but falsely normal in inflammation), low transferrin saturation; in men and postmenopausal women, endoscopy of both ends of the gut unless a cause is obvious.
What differentiates it?: Thalassemia trait is microcytic with a normal ferritin and a raised red cell count; anemia of chronic disease has a normal or high ferritin. Iron deficiency is a finding, and in the wrong patient it is a colon cancer until proven otherwise.

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LabsRead the iron studies CompareIron deficiency vs thalassemia trait

Immune thrombocytopenia

Hematology

Who?: Children after a viral illness (acute, self-limiting) and adults of any age (often chronic); more women in the adult form.
Time course?: Days to weeks in children; insidious and relapsing in adults.
Key symptoms?: Petechiae, easy bruising, gum and nose bleeding, heavy periods; serious bleeding is uncommon above 20 to 30 thousand platelets.
Key findings?: Petechiae over dependent areas and pressure points, mucosal blood blisters; no splenomegaly, no lymphadenopathy, and a well patient, which is the point.
Key investigations?: An isolated thrombocytopenia with a normal film apart from large platelets; the diagnosis is one of exclusion, so HIV and hepatitis C serology, a medication review and a pregnancy test come before the label.
What differentiates it?: Isolated and well separates it from the thrombocytopenias that are not: schistocytes and hemolysis point to a microangiopathy that is an emergency, and other cytopenias or a spleen point to marrow disease or hypersplenism.

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ApproachApproach to thrombocytopenia LabsThe consumptive alternative

Bacterial meningitis

Infectious Diseases

Who?: Infants, adolescents in shared housing, older adults, the asplenic, the immunosuppressed and anyone with a skull base defect or a recent neurosurgical procedure.
Time course?: Hours; a well patient in the morning can be obtunded by evening.
Key symptoms?: Headache, fever, neck stiffness and photophobia; vomiting, confusion, a non-blanching rash with meningococcal disease.
Key findings?: Fever and meningism (neck stiffness, Kernig and Brudzinski signs), altered consciousness; petechiae or purpura; the classic triad is complete in under half.
Key investigations?: Blood cultures then antibiotics without waiting; lumbar puncture when safe (CT first only for focal deficits, seizures, papilledema or reduced consciousness): a raised opening pressure, neutrophils in the thousands, low glucose ratio, high protein, organisms on Gram stain.
What differentiates it?: The CSF glucose and the cell type separate it from viral meningitis, which has lymphocytes and a normal glucose; the rash and the speed separate meningococcus from the rest. Antibiotics are never delayed for the tap.

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FluidBacterial CSF FluidViral CSF, for contrast

Infective endocarditis

Infectious Diseases

Who?: Prosthetic valves and devices, injection drug use (right-sided), rheumatic and degenerative valve disease, hemodialysis, recent dental or invasive procedures.
Time course?: Days (acute, staphylococcal) to weeks and months (subacute, streptococcal).
Key symptoms?: Fever with sweats, malaise and weight loss; breathlessness from valve failure; the complications present first in some: stroke, back pain, a cold limb.
Key findings?: A new or changed regurgitant murmur, splenomegaly, the peripheral stigmata (splinter hemorrhages, Janeway lesions, Osler nodes, Roth spots), heart failure, embolic phenomena.
Key investigations?: Three sets of blood cultures from separate sites before antibiotics, echocardiography (transthoracic first, transesophageal for prosthetic valves and negative studies with high suspicion), the modified Duke criteria to assemble the diagnosis.
What differentiates it?: Persistent bacteremia with a typical organism (Staphylococcus aureus, viridans streptococci, enterococci) plus endocardial involvement on echo makes the diagnosis; a fever that keeps producing positive cultures despite a plausible other source is endocarditis until the echo says otherwise.

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ApproachApproach to fever CaseFever and hypotension on the ward

Community-acquired pneumonia

Respirology

Who?: Older adults, smokers, chronic lung disease, alcohol use, immunosuppression, after influenza; anyone.
Time course?: Days; abrupt with rigors in pneumococcal disease, more gradual with the atypicals.
Key symptoms?: Cough with purulent sputum, fever, pleuritic chest pain, breathlessness; confusion or a fall as the only complaint in the old.
Key findings?: Fever, tachypnea, focal crackles, bronchial breathing and dullness over consolidation, reduced saturations; a pleural rub.
Key investigations?: Chest radiograph for the consolidation, CRP and white count, blood and sputum cultures before antibiotics in the admitted, urinary antigens where available, and the CURB-65 score to decide the setting of care.
What differentiates it?: A new infiltrate with fever and a productive cough separates it from bronchitis and from the heart failure that mimics it on the film; the severity score, not the organism, decides the first hours.

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CalculatorCURB-65 ApproachApproach to dyspnea

Syndrome of inappropriate antidiuresis

Nephrology

Who?: Older adults on SSRIs, carbamazepine or thiazides, patients with lung or brain disease, malignancy (small cell lung cancer), pain, nausea and the postoperative state.
Time course?: Days to weeks; acute falls (under 48 hours) are the dangerous ones.
Key symptoms?: Nausea, headache, confusion, gait instability and falls; seizures and coma when the sodium falls fast or far.
Key findings?: Clinically euvolemic: no edema, no orthostasis, moist mucous membranes; the examination's job is to exclude the hypovolemic and hypervolemic alternatives.
Key investigations?: Low serum osmolality with an inappropriately concentrated urine (osmolality above 100), urine sodium above 30 on a normal salt intake, normal thyroid and adrenal function, a review of the drug chart.
What differentiates it?: Euvolemia with a concentrated urine and a urine sodium above 30 is the signature; hypovolemic hyponatremia has a low urine sodium and a patient who is dry, and both improve with different fluids. Correct the sodium slowly unless there are seizures.

See it in action

UrineThe SIADH urine AlgorithmHyponatremia pathway

Adrenal crisis

Endocrinology

Who?: Known adrenal insufficiency (Addison disease, hypopituitarism) under stress, and anyone on long-term steroids who stops them or falls ill; occasionally the first presentation of the disease.
Time course?: Hours; precipitated by infection, surgery, vomiting or a missed dose.
Key symptoms?: Profound weakness, nausea and vomiting, abdominal pain, dizziness on standing, confusion; in Addison disease, a history of salt craving, weight loss and darkening skin.
Key findings?: Hypotension refractory to fluids, tachycardia, fever, dehydration; hyperpigmentation of creases and mucosa in primary disease, and its absence in secondary.
Key investigations?: Hyponatremia with hyperkalemia (primary disease), hypoglycemia, a raised urea; a random cortisol drawn before the first dose of hydrocortisone, but treatment never waits for it.
What differentiates it?: Shock with hyponatremia, hyperkalemia and hypoglycemia in the right story is adrenal until proven otherwise; septic shock shares the hypotension but not the electrolytes, and the response to hydrocortisone is both treatment and confirmation.

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LabsThe adrenal crisis panel

Acetaminophen overdose

Clinical Pharmacology & Toxicology

Who?: Deliberate self-poisoning in adolescents and adults, and the unintentional staggered overdose of the person treating pain with too many combination products.
Time course?: Silent for the first day; liver injury peaks at 72 to 96 hours; the window for the antidote is the first 8 hours.
Key symptoms?: Nothing, or nausea and vomiting early; right upper quadrant pain, jaundice and confusion as the liver fails on day two to three.
Key findings?: A normal examination early, which is the trap; later, tender hepatomegaly, jaundice, asterixis.
Key investigations?: A level timed from ingestion plotted on the nomogram for a single acute ingestion; for staggered or unknown-time ingestions the nomogram does not apply and treatment is started on any detectable level with a raised ALT; INR, ALT, creatinine and a gas track the injury.
What differentiates it?: The absence of symptoms in the first hours distinguishes nothing and reassures nobody: the timed level decides. Acetylcysteine within eight hours prevents almost all serious injury, and the staggered overdose is treated on suspicion.

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CaseThe staggered overdose LabsHepatocellular injury on the panel

Opioid toxicity

Clinical Pharmacology & Toxicology

Who?: Illicit and prescribed opioid use, especially with a new supply or after a period of abstinence; the ward patient with renal failure on morphine; combinations with benzodiazepines or alcohol.
Time course?: Minutes with intravenous use; hours with oral and long-acting preparations, and recurring as naloxone wears off.
Key symptoms?: Drowsiness through unresponsiveness; the patient rarely complains of anything.
Key findings?: The triad: depressed consciousness, respiratory rate under 12 with shallow breaths, pinpoint pupils; hypoxia, bradycardia and hypothermia follow; track marks or a fentanyl patch found on examination.
Key investigations?: A clinical diagnosis: the response to naloxone confirms it; a blood gas shows the respiratory acidosis, and the glucose is checked in every unresponsive patient.
What differentiates it?: Pinpoint pupils with a slow respiratory rate separate it from the other causes of coma; the reversal with naloxone is diagnostic, and its short half-life means the patient is watched for the toxicity to return, especially after long-acting opioids.

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Blood gasThe opioid gas drugOpioids on the ward

Uncontrolled cancer pain

Palliative Medicine

Who?: Advanced cancer, particularly bone metastases, pancreatic and head and neck disease; any patient whose analgesia has not kept pace with the disease.
Time course?: Days to weeks of escalation, with breakthrough episodes over minutes; a crisis when the patient can no longer function or rest.
Key symptoms?: Constant background pain with breakthrough peaks; the type matters: aching bone pain worse on movement, burning or shooting neuropathic pain, colicky visceral pain.
Key findings?: Guarding and reduced movement, allodynia or altered sensation in neuropathic pain, focal bony tenderness; look for the complication behind a new pain: a fracture, cord compression, obstruction.
Key investigations?: Directed at the cause of a new or changed pain (a film for a fracture, MRI spine for cord compression, calcium) and at safe dosing (renal function before opioid titration); the pain assessment itself is the investigation.
What differentiates it?: A new pain in a patient with cancer is a new event until proven otherwise; back pain with any neurological change is cord compression until the MRI is done. The analgesic ladder is climbed by the mechanism of the pain, with adjuvants for bone and nerve pain, and the regular dose is titrated against the breakthrough use.

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drugOpioids: titration and safety ApproachApproach to back pain

Vasovagal syncope

General Internal Medicine

Who?: Young and otherwise well people, with a prodrome and a trigger: standing, heat, pain, blood, emotion; recurring across a lifetime.
Time course?: Seconds of prodrome, seconds of unconsciousness, minutes of fatigue after.
Key symptoms?: Warmth, nausea, tunnelling vision and sweating before the collapse; a witness describes pallor and a brief loss of tone, occasionally a few jerks.
Key findings?: A normal examination; a normal lying and standing blood pressure once recovered; no injury pattern of an unheralded fall.
Key investigations?: An ECG in everyone, looking for the things that kill (conduction disease, long QT, pre-excitation, hypertrophic cardiomyopathy); no further testing when the story is classic and the ECG normal.
What differentiates it?: The prodrome and the trigger are the diagnosis. Syncope during exertion, while supine, without warning, with palpitations, or with a family history of sudden death is cardiac until proven otherwise, and a bitten tongue with prolonged confusion after is a seizure.

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ApproachApproach to syncope AlgorithmSyncope pathway