Kora Study Hub

📖 Rheumatology Orthopaedics
& Pathophysiology

A complete interactive study companion for exam revision.

96
Pages
35+
Conditions
7
Body Systems
5
DD Charts
30
Quiz Qs

🎯 Quick Links

🔥 Rheumatoid Arthritis
1% prevalence, HLA DR4, seropositive, pannus formation, swan neck deformity
🦴 Ankylosing Spondylitis
HLA B27 90%, bamboo spine, syndesmophytes, Schober's test
💥 Disc Prolapse
L4/L5 vs L5/S1, nerve root table, cauda equina emergency
🧠 Multiple Sclerosis
Demyelination, 2 episodes distinct in time & site, Beta Interferon
⚠️ Cauda Equina Syndrome
MEDICAL EMERGENCY — bladder/bowel loss, saddle anaesthesia
🫁 Pink Puffers vs Blue Bloaters
COPD: emphysema vs chronic bronchitis, alpha-1 antitrypsin

📋 What's Inside

This study guide covers all conditions from the Rheumatology textbook, organised into Rheumatology & Orthopaedics (pages 1–32), Pathophysiology (pages 33–56), and Letter Writing (pages 69–96). Each condition includes: definition, epidemiology, aetiology, pathology, symptoms, signs, investigations, treatment, prognosis, and exam tips. Use the sidebar to navigate, take the quiz to test yourself, and use search to find any term instantly.

🏛️ Rheumatology Study Resource

Exam revision companion for osteopathic students.

📑 Table of Contents

Click any topic to jump to its study page.

🦴 Rheumatology & Orthopaedics

🧬 Pathophysiology

📊 DD Charts

🎯 Study Tools

🦴 Arthritis & Osteoarthritis

Osteoarthritis (Osteoarthrosis) — "Wearing out" of the joint +
DefDegenerative joint disease — progressive "wearing out" of articular cartilage
IncidenceCommon — present to some degree in every elderly person
AgeIncreases with age. Secondary OA can develop at any age
SexF > M
GeneticsPrimary OA has genetic link; family history is a strong risk factor
AetiologyPrimary OA: No apparent cause, family history. Affects large joints (knee, elbow) + IP joints.
Secondary OA: Uneven load bearing from trauma, malalignment, unequal leg lengths, occupational wear
SymptomsPain worsened by use, eased by rest. Stiffness. Functional impairment.
SignsSwelling, muscle wasting, tenderness, reduced movement, crepitus, deformity.
Heberden's nodes at DIPJ · Bouchard's nodes at PIPJ
Common sites: hips, knees, spine, 1st MTPJ, PIPJ, DIPJ
X-rayReduced joint space · Osteophytes · Periarticular sclerosis · Subchondral cysts · Irregular margins
TreatmentEducation · NSAIDs & analgesics · OT & appliances · Physiotherapy/mobilisation · Steroid injections · Joint replacement, osteotomy, fusion · Treat exacerbating factors
PrognosisProgressive but symptoms can be relieved — quality of life improved by maintaining mobility
📌 Exam Key: Primary OA → Heberden's (DIPJ) & Bouchard's (PIPJ) nodes. X-ray: reduced joint space + osteophytes + sclerosis + cysts. Secondary OA → asymmetrical wear from trauma/alignment.
💥 Disc Prolapse — Nerve Root Guide +
LevelNerve RootPower LossMovement WeakReflex ↓Sensory Loss
L3/L4L4Tibialis AnteriorAnkle InversionKneeMedial foot & leg
L4/L5L5Extensor Hallucis LongusBig toe dorsiflexionNoneDorsum of foot
L5/S1S1Peroneus Longus & BrevisAnkle dorsiflexion & eversionAnkleLateral foot
L4/L5 prolapse → L5 nerve affected → weak big toe extension (EHL). L5/S1 prolapse → S1 nerve affected → absent ankle reflex + lateral foot sensory loss. SLR positive on affected side.
ACUTE SPINAL CORD / CAUDA EQUINA COMPRESSION IS A MEDICAL EMERGENCY! Bladder/bowel loss, saddle anaesthesia, loss of anal tone — send to Casualty IMMEDIATELY.
🛠️ OA Treatment Summary +
ConservativeEducation · NSAIDs & analgesics · OT & appliances · Physiotherapy & mobilisation
InjectionsSteroid injections into affected joints
SurgicalJoint replacement (hip/knee) · Osteotomy · Fusion (arthrodesis)
OtherTreat exacerbating factors (obesity, alignment, leg length discrepancy)

🔥 Rheumatoid Arthritis — The Full Picture

📋 Epidemiology & Aetiology+
DefProgressive chronic inflammatory disorder of unknown aetiology — primarily affects synovium, but can affect many tissues
Prevalence1% of population
AgePeak 35–55
SexF > M
GeneticsHLA DR4 & DR3 linked
Theory 1Hormonal: Symptoms reduced in pregnancy
Theory 2Infective: Reaction to viral infection
Theory 3Genetic: HLA links as above
Theory 4Immunological: Possibly in reaction to infective agent. Evidence: rheumatoid factor in blood/synovium correlates with severity; synovial membranes show immunological mediated damage
Rheumatoid factor is NOT specific to RA. If present, patient is called "SEROPOSITIVE". High RF correlates with: severe disease, nodules & vasculitis, Sjögren's, neuropathy, lung involvement, Felty's syndrome. It is a predictor of severity, not a cause.
🔬 Pathology — What Happens Inside the Joint+

RA synovial fluid contains immune complexes + WBCs → reduce Tsuppressor activity, increase macrophage activity. Tissue damage is via inflammatory response.

EarlyBlood vessels dilate + thrombase · Synovium swells & thickens (hyperplasia) · WBCs infiltrate → inflammation, oedema, fibrosis
LaterArticular cartilage invaded by synovium (Pannus formation) · Cartilage destroyed by proteolytic enzymes · Pain + swelling from prostaglandins & lymphokines · Immunoglobulins produced
SevereIntra-articular pressure ↑ · Ligaments weaken & become lax · Capsule weakens · Joint subluxes due to abnormal muscle/tendon pull · Eroded bone + malalignment + fibrosis + destruction
Pannus formation = synovium invading & destroying cartilage. This is THE hallmark pathological process of RA joint destruction.
🖐️ Joint Distribution & Deformities+
Joint patternPolyarticular · Symmetrical · Small joints of hands & feet primarily · PIPJ, DIPJ, MTPJ, wrist in 80%
OnsetInsidious in most cases

Hand Deformities:

  • MCP subluxation
  • Ulnar deviation (especially at MCPJ)
  • Swan neck deformity
  • Z deformity of thumb
  • Extensor tendon rupture
  • Ulnar styloid prominence

Foot Deformities:

  • MTPJ subluxation with callus formation
  • Prominent metatarsal heads ("walking on marbles")
  • Hallux valgus
  • Valgus mid-foot deformity
🩺 Symptoms, Signs & Investigations+

Symptoms:

  • Pain, tenderness & swelling of joints
  • Functional impairment
  • Constitutional symptoms (fatigue, fever, malaise)
  • Carpal tunnel syndrome — 50% of patients
  • Stiffness after inactivity, especially mornings — at least 20–30 mins

Signs:

Early: Swelling, effusion, tenderness, reduced movement, warmth, muscle wasting, oedema

Late: Symmetrical joint involvement, deformity, swelling, wasting, extra-articular manifestations

Investigations:

  • Rheumatoid factor latex agglutination test (80% positive)
  • FBC — anaemia + raised WBCs
  • ESR raised in inflammation
  • Synovial fluid shows WBCs
  • Biopsy — characteristic histology
  • Arthroscopy & arthrograms

X-ray Changes:

Early: Soft tissue swelling · Periarticular osteoporosis · Marginal bone erosions

Late: REDUCED joint space · Erosive changes & bone destruction · Subluxed/dislocated joints · Ankylosis · Secondary degeneration

💊 Treatment & Prognosis+
MedicationsNSAIDs · Disease-modifying drugs (Gold, Penicillamine) · Immunosuppressants (Azathioprine) · Steroids
PhysicalEducation · Physical therapies · OT & special appliances
InjectionsSteroid injections into affected joints
SurgeryJoint replacements · Synovectomy · Plastic surgery

Prognosis — Worse if:

  • Insidious onset
  • Young patient
  • Rheumatoid factor positive
  • Early erosions
  • Marked systemic disease

3 Disease Patterns:

  • Persistent (75%): If lasts >3 years, remission is rare
  • Intermittent (25%): Episodes 6–12 months with remissions months to years
  • Monoarticular: Progresses to polyarticular within 10 years in 40%

50% have little disability · 40% moderate to severe · 10% severe. Some die directly from disease.

🦋 Systemic Lupus Erythematosus (SLE)

📋 Epidemiology & Aetiology+
DefMultisystem disorder with widespread organ involvement
IncidenceCommon — one of major causes of inflammatory arthritis
AgePeak early 20s, onset 10–35
SexF:M = 9:1
GeneticsHLA A1, B8, DR3, C4. Familial tendency

Aetiology Theories:

  1. Hormonal: Women more affected; worse in pregnancy & before menstruation
  2. Genetic: Familial tendency, twin studies show increased risk
  3. Infective: Acute stage resembles viral illness (fever, lymphadenopathy)
  4. UV light: Disease flares up in UV exposure
  5. Drugs: Some drugs can cause similar reaction
  6. Immunological: Major role — Tsuppressor cells impaired, B cells produce more antibodies, direct immune damage to RBCs, indirect damage via immune complexes (e.g. kidney)
🔬 Pathology — 3 Major Components+
  1. Fibrinoid necrosis — mostly in small blood vessels, surrounded by inflammation (vasculitis)
  2. Haematoxylin bodies — altered DNA
  3. Immune complex deposition — Type 3 reaction in kidney & skin especially
📊 Organ Involvement — By Frequency+
Organ System%Manifestation
Musculo-articular95%Arthralgia, myositis, avascular necrosis (steroid-induced)
Cutaneous (skin)81%Butterfly rash on face
Fever77%Swinging pyrexia
Neuro (CNS)59%Infarcts & thrombosis
Renal (kidneys)53%Glomerulonephritis — leading cause of death
Pulmonary (lungs)48%Pleural effusion, infections
Cardiac (heart)38%Pericarditis, endocarditis
Butterfly rash = classical sign across cheeks & nose. Anti-dsDNA assay +ve in 100% of cases. Erosive arthritis is rare in SLE (unlike RA).
💊 Treatment & Prognosis+
NSAIDsFor joint symptoms
HydroxychloroquinAntimalarial — disease-modifying for SLE
SteroidsFor acute flares & organ involvement
ImmunosuppressivesFor severe/refractory disease
PlasmapheresisIn severe cases

Prognosis: 10-year survival now >90%. Death occurs from renal disease & vasculitis. Some patients have only one severe flare then are virtually symptom-free forever.

🦴 Seronegative Arthropathies

Group of inflammatory arthritides with similar histology to RA but Rheumatoid Factor ABSENT. Includes: Ankylosing Spondylitis, Reiter's Syndrome, Psoriatic Arthritis, Enteropathic Arthritis, Juvenile Chronic Arthritis.

1️⃣ Ankylosing Spondylitis — The Full Breakdown+
DefChronic inflammatory arthritis principally affecting the axial skeleton
Incidence0.5–2% of Caucasians. Incomplete forms more common
Age20–40, peak at 17–25
SexM > F 5:1
GeneticsHLA B27 in >90% of cases. 7% of 1° relatives affected
AetiologyGenetic (HLA B27) + environmental (Klebsiella bacteria in gut linked in some studies)

Pathology — 2 Processes:

  1. Synovitis: Identical to RA
  2. Enthesopathy: Inflammatory reaction at ligamentous attachment → calcification

Sites: Sacroiliac joints, spinal apophyseal, costovertebral. Enthesopathy at annulus fibrosus insertion → syndesmophytes (bony bridges) → bamboo spine. Symphysis pubis & manubriosternal joints also involved. Peripheral joints may show synovitis with rapid ankylosis.

Extra-articular: Iritis (25%), cardiac (2–8% — arrhythmia/valve disease), pulmonary fibrosis, cauda equina lesions. Complications: Spinal fractures, amyloidosis, reduced vital capacity.

Symptoms:

Low back pain (thoraco-lumbar junction), radiates to buttocks, at night. Not relieved by rest, relieved by moderate activity. Stiffness & poor posture.

Signs:

  • Loss of lumbar lordosis
  • SI tenderness
  • Restricted movement in all 3 planes
  • Later: Kyphosis + rigidity
  • Chest expansion <5cm at 4th intercostal space
  • Schober's test — reduced lumbar flexion
  • Tragus test — distance from earlobe to wall increases as posture deteriorates

Investigations & Treatment:

X-ray: SI sclerosis → ankylosis → bamboo spine. ESR raised. RF ABSENT.

Tx: Indomethacin (NSAIDs) · Sulphasalazine (peripheral) · Physiotherapy · Exercises · Surgery for positioning. Radiotherapy as last resort.

Prognosis: Wide range. Many get severe kyphosis. Hip involvement = poor prognosis.

Bamboo spine = hallmark radiological sign. Schober's & Tragus tests = the clinical exams you MUST know for the practical.
2️⃣ Reiter's Syndrome — "Can't see, can't pee, can't climb a tree"+
Triad1. Non-specific urethritis · 2. Conjunctivitis · 3. Arthritis
TypeReactive arthritis
AgePeak 16–35
SexVenereal M:F 20:1 · Post-dysenteric 10:1 · Childhood 5:1
GeneticsHLA B27 in 60–80%
TriggersSexually acquired urethritis (Chlamydia, Ureaplasma) OR Enteric infections (Shigella, Yersinia, Salmonella)
PathologySynovitis with lymphocyte & leukocyte infiltration (like RA). Periostitis on sole of foot. Sacroiliitis & spondylitis.
JointsAsymmetrical, mainly lower limb. Sausage digits (swollen toes). Achilles tendonitis & plantar fasciitis.

Prognosis: Exacerbations 2–4 months with remissions up to years. 50% have recurrences. 30% permanent disability (usually feet). 20–40% go on to sacroiliitis, 20% develop full AS.

The mnemonic: "Can't see" (conjunctivitis) · "Can't pee" (urethritis) · "Can't climb a tree" (arthritis — lower limb). Remember: the gut infection agents can cause transient arthritis in ANYONE.
3️⃣ Bechet's Syndrome & Variations+

Uncommon. Characterised by:

  • Oral & genital ulcers
  • Uveitis
  • Skin lesions
  • Vascular lesions including thrombophlebitis
  • Arthritis
  • CNS or gut involvement

🦴 Osteoporosis, Osteomyelitis & More

🦴 Osteoporosis — The Silent Thief+
DefReduced bone mass per unit volume vs normal for age, sex & race. No change in bone volume!
AgeMostly women >60, men >70
SexF > M

3 Types:

  • Primary: Ageing + post-menopause
  • Secondary: Endocrine (Cushing's), chronic disease (alcoholism, malabsorption), malignancy, myeloma, RA, steroids, heparin, immobilisation
  • Juvenile: Spine & long bone ends. Self-limiting.

Key Physiology:

Oestrogen stimulates osteoblasts & reduces osteoclasts. Weight-bearing also stimulates bone laying. Bone mass peaks at 35–49 (some say late 20s). After menopause: 5% loss/year for 5 years, then 1%/year. Early menopause = higher risk.

3 Main Fractures:

  1. Fractured Neck of Femur — 10–20% mortality at 3 years (treated), untreated few survive a year
  2. Vertebral fracture — Crush/wedge → loss of height + kyphosis. Often first sign is painless thoracic kyphosis
  3. Colles' fracture of wrist — Fall on outstretched arm → "dinner fork deformity" (radial dorsal angulation, impaction, radial deviation)

X-ray:

Reduced bone density — >30% of bone must be lost before visible on X-ray

Treatment:

  • Prevention is key: Exercise (jumping!), Vitamin D + Calcium
  • HRT — delays post-menopause 5% loss until stopped
  • Bisphosphonates (e.g. Etridonate) — increase bone mass
  • Calcitonin injections · Prophylactic Etridonate with steroids · Surgery

Prognosis: Once a fracture occurs, another is likely. Directly or indirectly, osteoporosis is life-threatening.

On X-ray: you need >30% bone loss before it shows. That's why DEXA scans (bone densitometry) are essential for early diagnosis. Prevention > cure!
🦠 Osteomyelitis — Bone Infection+

Bone infection — usually chronic except immediately post-op or post-trauma. Can be due to haematogenous spread.

PresentationPain, redness, discharging sinus (to outside). Systemic unwell.
PathologyCavities within bone (involucrum) + dead bone pieces (sequestra) act as infection focus
X-rayInvolucrum + sequestra visible
TreatmentConservative — antibiotics. Surgery to remove sequestra if needed

NB: Bone abscess = small abscess at end of long bone. May lie dormant for years.

💥 Spine: Disc, Stenosis, Scoliosis & More

📋 Disc Prolapse — Complete Details+

Disc herniation is a common cause of back pain & sciatica. Often precipitated by injury on a background of age-related degeneration. Common sites: L5/S1 and L4/L5.

Mechanism:

Rent in annulus fibrosus → nucleus protrudes → impinges nerve root (postero-lateral) or cauda equina/spinal cord (posterior). Small bulge → stretches longitudinal ligament → back pain. Larger → pressure on nerve root → sciatica. Severe → extrusion into canal → loose fragment (sequestration). Healing by shrinkage & fibrosis.

Clinical Picture:

Sudden severe back pain → dies down over days → sciatic pain in buttock, down back of leg to foot. May have sciatic scoliosis. Restricted forward flexion. SLR positive.

Treatment:

Conservative (most cases): Analgesia, gentle mobilisation, physiotherapy/osteopathy. Surgery (rarely warranted): decompression, laminectomy, fusion — variable success. Chemonucleolysis in some centres.

⚠️ Cauda Equina Syndrome — EMERGENCY+
ACUTE SPINAL CORD COMPRESSION IS A MEDICAL EMERGENCY! If untreated within ~6 hours, permanent damage can occur.

Diagnosis:

  • Bladder or bowel loss of control (incontinence or retention)
  • Loss of saddle sensation (perineum)
  • Loss of anal tone

Action: Patient needs to go to Casualty IMMEDIATELY for urgent spinal decompression and/or laminectomy.

📐 Scoliosis — All Types+

Scoliosis = lateral angulation >5°. Can be accompanied by vertebral rotation.

Idiopathic Structural Scoliosis (3 subgroups):

  • Infantile (0–3 yrs): Left curve, M>F. Two types — resolving & progressive. Most resolve. Brace/fusion if needed.
  • Juvenile (4–9 yrs): Before 6 M>F, after 6 F>M. Mostly thoracic right curves. Most progressive.
  • Adolescent (puberty): Thoracic curve to right with rotation. Surgery for curves >40°.

Secondary Structural Scoliosis:

Congenital (hemivertebra, OI, Marfan's), Polio, Neurofibromatosis

Other Types:

  • Compensatory: Lumbar, compensates for pelvic tilt (short limb, hip deformity)
  • Postural: Adolescent girls, mild left curve, resolves on bending. Spontaneous recovery
  • Sciatic: Temporary, muscle pull protecting spine (e.g. disc prolapse)
🦴 Other Spinal Conditions+
SpondylolysisNeural arch defect in L5 (or L4) — loss of bone between facets, replaced by fibrous tissue. Congenital or post-trauma. Usually asymptomatic. Makes spondylolisthesis more likely. Treatment: surgical.
SpondylosisDisc degeneration → no disc space reduction + facet joint displacement. Recurrent backache, hard work/sitting aggravates, lying relieves. Pain referred to buttocks/greater trochanter. Acute locking/giving way.
SpondylolisthesisSpontaneous forward displacement of lumbar vertebra upon vertebra below. Causes: congenital, spondylolysis, OA of facet joints. Usually L4/L5 or L5/S1. Mostly symptom-free.
Spinal StenosisCongenital narrow spinal canal → pain in gluteal region & lower limb on standing/walking. Nerves & vessels compressed in narrow canal after minor disc prolapse or osteophytes. More common in middle-aged men.
Scheuermann's DiseaseCause of kyphosis. Intrusion of IV disc into vertebral end plate at multiple levels in thoracic spine. 13–16 year olds. Active stage → pain.

🔌 Nerve Injuries & Cervical Conditions

💪 Brachial Plexus Injuries+

Caused by severe traction with arm in abduction (motorcycle accident, forceps delivery, shoulder dislocation, stab/gunshot). Tethering from fibrosis adds to symptoms later.

Differentiating Brachial Plexus vs Nerve Root:

Brachial PlexusNerve Root
↑ by side bend away from affected side↑ by side bend toward affected side
Unaffected by compression/distraction↑ by compression, ↓ by distraction

Differentiate from shoulder pain: shoulder pain only extends to elbow; brachial plexus extends to hand.

Severe Injuries — 3 Categories:

  • Erb's Palsy (C5, C6): Shoulder abductors & external rotators paralysed → arm hangs close to body, inwardly rotated — "Waiter's Tip"
  • Klumpke's Palsy (C8, T1): Intrinsic hand muscles paralysed → claw hand + ulnar sensory loss
  • Entire plexus: Whole arm paralysed & numb

Axillary Nerve Palsy:

Injured by shoulder dislocation or fractured humeral neck. Supplies deltoid → abduction weak at shoulder + "regimental badge" numbness over lower deltoid.

🦒 Cervical Conditions — Spondylosis, Rib, Neuritis+
Cervical SpondylosisMost common C-spine disorder. Degeneration & flattening of IV discs + bone spurs at vertebral margins → encroach on nerve foramina. Middle-old age. Neck pain & stiffness, worse on rising, may radiate to scapulae & occiput. X-ray: disc space narrowing + spurs. Later facet joints involved. Differentiate from cervical rib, carpal tunnel, cervical tumours. Tx: heat + massage + maintain mobility.
The Rheumatoid Neck30–40% of RA patients. 1) Erosion of atlanto-axial joints & transverse ligaments. 2) Erosion of atlanto-occipital articulation → odontoid rises into foramen magnum (danger of peg fracture). 3) Mid-cervical facet erosion.
Acute Brachial NeuritisNeuralgic amyotrophy — thought to be viral. Severe shoulder pain from nerve root infection → may extend to hand. Wasting of deltoid & hand. Tx: Pain control. Recovery months to years.
Cervical SpondylolisthesisRare. Anterior displacement from: 1) Congenital failure of odontoid fusion. 2) Inflammatory pathology in transverse ligament of Axis. 3) Previous RA instability.
Cervical RibCongenital over-development of C7 transverse process (bony or fibrous). Can be asymptomatic or cause neurovascular complications. Diagnosis: Adson's test + X-ray. Also positive in Thoracic Outlet Syndrome / Scalenus Syndrome.

🩻 Other Orthopaedic Conditions

🦵 Chronic Lumbar Ligamentous Strain+

"Simple back pain" — backache with no discernible pathology. Failure of spinal muscles to protect ligaments from overstretching. Associated with obesity, poor fitness, chronic illness. More common in females. Diagnosis of exclusion — all investigations normal. Chronic course regardless of treatment. Osteopathic treatment far better than most.

🦴 Coccydynia+

Pain in coccyx region. Usually chronic, after fall → strain at sacro-coccygeal joint or fracture. Pain when sitting, disappears on standing. Localised tenderness. Self-limiting — treatment usually not needed. Rare: excision or manipulation.

🧬 Spina Bifida+

Congenital malformation — failure of folding of neural tube in developing embryo. 4 grades:

  1. Spina bifida occulta: Failure of fusion of vertebral arch. Most common. Usually asymptomatic. Faun's beard in some. Symptoms from dural tethering.
  2. Meningocele: Meninges expand beyond vertebrae
  3. Myelomeningocoele: Meninges + cauda equina expand beyond
  4. Rachischisis: Complete failure of fusion — opening posteriorly

Frequency decreases with severity — mainly due to antenatal screening & folic acid in pregnancy. Varying motor/sensory loss in lower limbs for aperta types.

🧬 Pathophysiology: Cancers

🥩 Oesophageal & Gastric Cancer+
OesophagealGastric
IncidenceVery rareRare
AgeIncreases with age. 65+ main riskIncreases with age
SexF > M slightly (men >3x in US)M > F
GeographyHighest Africa & USSRHighest Japan
AetiologyHot foods, smoking, heavy drinking (>3/day), obesity, acid reflux, Barrett's oesophagusH. pylori infection (main cause), diet, blood group A, chronic gastritis, polyps >2cm
PathologyPolyp and/or wall invasion. Local spread. Adenocarcinoma (lower, US most common) vs Squamous cell (upper, worldwide most common)95% adenocarcinoma. Invades locally through stomach wall → early lymphatic spread. Late symptoms
SymptomsDysphagia, food stuck, pain on swallowing, chest/back pain, weight loss, hoarse voice/coughEarly satiety, vague abdominal pain (mimics PUD), weight loss, anaemia, haematemesis, melena
TreatmentUsually palliative. Radiotherapy, dilation ± stents. Surgery (mortality ~50%)Usually palliative. Surgery ineffective for cure
Prognosis5% cure10% cure — spreads early, <15% survive >5 years
Barrett's oesophagus = acid reflux damage → increased risk of adenocarcinoma. H. pylori = #1 cause of gastric cancer. Both have vague early symptoms → late presentation = poor prognosis.
🔴 Colorectal Cancer — Dukes Staging+
DefCarcinoma of the colon/rectum. Most common GI cancer
IncidenceCommon
AetiologyWestern diet, carcinogens + increased gut transit time (low fibre) → malignant change. Most are adenocarcinomas forming polyps → malignant transformation → invade wall → lymphatics → liver
Location80% within 30cm of anus

Dukes Staging System — 5-Year Survival:

StageDescription5-Year Survival
Dukes AInvasive no deeper than muscularis layer98%
Dukes BBelow muscularis but not through gut wall80%
Dukes CInvaded through wall40%
Dukes DDistant metastases5%

Symptoms: Bleeding PR, mucous, tenesmus, dissatisfaction passing stool, weight loss, cachexia
Signs: Often none. Mass may be felt PR
Treatment: Surgery ± chemotherapy

🫁 Lung Carcinoma+
IncidenceOne of commonest cancers (19% of all cancers)
AgeIncreases with age
SexM > F (changing)
AetiologySmoking, asbestos, iron oxides → chronic inflammation → increased cell turnover → DNA damage → mutation in cell division regulation → cancer
PathologyTumour in large airways. Most common: Squamous cell carcinoma from bronchi. Mesothelioma from asbestos. Spread: local → metastases (brain, bone, liver, adrenals)

Symptoms by Site:

  • Tumour: Haemoptysis, cough, SOB, chest pain
  • Local spread: SOB, hoarse voice (recurrent laryngeal n.), chest pain (pericarditis/rib mets), SVC obstruction, nerve palsies
  • Metastases: Brain, bone, liver, adrenal symptoms
  • Constitutional: Weight loss, fatigue. Endocrine effects e.g. SIADH

Signs: SOB, stridor, cyanosis, clubbing, nicotine stains, mediastinal shift, Horner's, SVC obstruction

Treatment: Surgery if small + no mets. Otherwise palliative radiotherapy/chemo.

Prognosis: Very poor.

👩 Female Reproductive Cancers+
TypeKey Features
OvarianWomen >50, often presents late. Multiple types. Usually asymptomatic except abdominal distension & ascites. Has often metastasised by presentation → poor prognosis.
EndometrialWomen 40–60. Post-menopausal bleeding or abnormal bleeding. Uncommon but early detection allows treatment. Spread: pelvic organs → liver. Unopposed oestrogen post-menopause is important cause.
CervicalYoung women. Uncommon. Risk factors: unprotected sex with multiple partners. Caused by HPV. Detected by cervical smears (CIN). Treatment: radical surgery + chemotherapy.
🎀 Breast Cancer+
Incidence~1 in 35 women. 99% are women, 1% men
AgeMore common with age
AetiologyUnknown. Most common is invasive carcinoma (usually one breast; lobular form is bilateral)
PathologyDevelops in one breast. Spreads EARLY via lymphatics to axillary nodes and beyond
SymptomsBreast lump, occasionally nipple discharge, blood, skin changes
TreatmentElderly: Tamoxifen (oestrogen-dependent). Younger (= more aggressive): Lumpectomy/mastectomy + axillary node dissection ± adjuvant chemo
PrognosisElderly: often slow. Younger: can recur 10 years after treatment. Only 25–30% actually die of cancer. Many are young.

🫁 Respiratory Pathophysiology

🌬️ Asthma — Reversible Airways Disease+
DefReversible airways disease, often with inflammatory component
IncidenceCommon — up to 20% of population
AgeMost common in children; second peak 50–60
SexM = F

Two Types:

  • Extrinsic: Type 1 hypersensitivity (e.g. house dust mite). IgE on mast cells → allergen activates → histamine, bradykinin release → bronchoconstriction in large airways + mucosal inflammation
  • Intrinsic: Hyper-reactive airways (e.g. winter asthma). Bronchoconstriction ± inflammation. May be due to beta blockers

Clinical:

Symptoms: SOB, chest tightness, nocturnal cough ± waking, wheeze

Signs: Tachypnoea, peripheral cyanosis, audible wheeze, use of accessory muscles, barrel chest

Investigations: Allergen testing, reversibility studies with bronchodilators

Treatment: β2 agonists (e.g. salbutamol) for smooth muscle relaxation. Inhaled steroids for inflammatory component

Prognosis: Childhood asthma — many grow out of it, may recur later. Maturity-onset tends to remain.

🫁 COPD — Pink Puffers vs Blue Bloaters+

COPD = Emphysema + Chronic Bronchitis. Common. Elderly. M=F. More in Western societies.

Definitions:

  • Emphysema: Permanent increase in alveolar air spaces due to destructive changes
  • Chronic Bronchitis: Repeated sputum production on most days in 3 consecutive months over 2 years

Aetiology:

  • Emphysema: Alveolar walls destroyed by smoking → chronic irritation + inflammation. α1-antitrypsin deficiency → unopposed proteolysis → severe early emphysema
  • Chronic Bronchitis: Smoking destroys microvilli → retention of secretions → bacteria thrive → repeated infections → more lung damage

Key Pathology & Types:

Pink Puffers (Emphysema dominant)Blue Bloaters (Bronchitis dominant)
PathologyAlveoli destroyed → large air sacs (bullae) → ↓ surface area. Lung volume ↑ but vital capacity ↓. Elastic tissue destroyed → difficult to ventilate.Chronic inflammation → ↑ secretions + ↓ clearance. Repeated infections.
CO₂Initially normal/low (puffing to keep CO₂ down)CO₂ creeps up → loss of respiratory drive → cyanosis → respiratory failure
AppearancePink, thin, use accessory musclesBlue (cyanosed), oedematous

X-ray: Hyperexpanded "black" lungs ± signs of infection. LFTs: Reduced vital capacity, increased total lung volume.

Treatment: Bronchodilator + steroid inhalers · Antibiotics for exacerbations · Oral steroids · Nebulisers · Oxygen for respiratory failure.

Prognosis: It gets worse! Deterioration reduced by stopping smoking but destroyed lung can never be repaired.

Pink Puffers (emphysema) — pink skin, puffing to breathe, CO₂ normal. Blue Bloaters (bronchitis) — cyanosed, oedematous, high CO₂, loss of respiratory drive. α1-antitrypsin deficiency = severe early emphysema.
🦠 Pneumonia & Pulmonary Embolism+

Pneumonia

DefLung infection → acute inflammation of alveolar tissue
TypesBronchopneumonia: Spreading throughout lung. Risk of death → fibrosis on resolution.
Lobar pneumonia: Confined to 1–2 lobes. Usually S. pneumoniae. Younger patients.
AetiologyBacterial infection in immunosuppressed host (elderly, infant, chronic disease, viral infection)
SymptomsTemperature, SOB, productive cough, general unwell
Signs↑ RR + pyrexia, confusion, cyanosis, accessory muscles, asymmetrical chest expansion, dullness to percussion, ↑ breath sounds ± crackles
X-rayConsolidation
TxAntibiotics
PrognosisOften terminal for elderly/COPD → septicaemia. Younger: some permanent damage but usually no functional impact.

Pulmonary Embolism

DefClot from elsewhere lodged in pulmonary vasculature
Risk factorsVirchow's Triad: 1) Stasis (long flight, post-op, pregnancy) · 2) Vessel damage (surgery, orthopaedic) · 3) Hypercoagulability (familial, post-op, pregnancy, antithrombin 3 deficiency)
Small clotPart of lung not perfused → eventually dies. Rest of lung works harder → ↑ RR + ↑ HR + cyanosis
Large clotBlocks pulmonary trunk/major vessel → inadequate perfusion → right heart strain + ↓ O₂ + ↓ flow to left heart → coronary ischaemia → cardiac arrest
V/Q scanAreas ventilated but NOT perfused
TxWarfarin
PrognosisAlways increased risk of recurrence

🧠 Neurological Conditions

🧠 Multiple Sclerosis — "Lesions scattered in time & space"+
DefAcute episodes of neurological deficit from demyelination — sporadic in time & place, spontaneous but partial remission
Prevalence50–80/100,000
AgeYoung adulthood
SexF > M 3:2
GeneticsIncreased incidence in families
AetiologyUnknown. Theories: slow virus (like CJD), genetic factor
PathologyCNS white matter demyelinated in patches with inflammation. Spontaneous recovery occurs slowly. Demyelinated nerves conduct more slowly → severe functional impairment
Common 1st siteOptic nerve → sudden vision loss
Other sitesBrainstem, cerebellar peduncles, motor tracts — any part of brain

Symptoms & Signs:

  • UMN motor deficit (paraparesis, hemiparesis, monoparesis)
  • Retrobulbar neuritis — vision loss
  • Sensory deficit · Cerebellar signs · Diplopia (internuclear ophthalmoplegia)
  • Vertigo · Urinary incontinence · Frontal lobe lesions · Dementia

NB. IQ & language skills often unaffected until late.

Diagnosis: 2 episodes distinct in time AND site. MRI, LP, VEP

Treatment: Steroids (acute) · Psychological support · Beta Interferon "Avonex, Betaferon" (neurologist-prescribed, ~£50,000/year)

Prognosis: Average duration 20 years. 80% have progressive disability. 5% die in 5 years. May have 30-year latent period after first attack of retrobulbar neuritis.

⚡ Motor Neurone Disease+
DefProgressive degeneration of: Anterior Horn Cells (spinal cord) · Lower Cranial Motor Nerves · Neurones of Motor Cortex
Incidence1.5/100,000 (rare)
Age50–70
SexM > F 1.5:1

3 Forms:

  1. Progressive Muscle Atrophy: LMN weakness — wasting, reduced tone, fasciculation, absent reflexes. Starts in hands → limbs
  2. Progressive Bulbar Palsy: LMN of lower cranial motor nuclei → fasciculation & wasting of tongue, absent swallow
  3. Amyotrophic Lateral Sclerosis (ALS): UMN — spastic weakness starting in legs

Any combination. Some say all 3 must be present. No sensory/cognitive deficit. No real treatment. Death from aspiration within 2 years.

🎯 Parkinson's Disease — Tremor, Rigidity, Bradykinesia+
DefDisturbance of voluntary motor function: rest tremor + bradykinesia + rigidity
Prevalence1–1.5/1,000 (common). Over 70: 1/200
AgeIncreases with age (usually >60)
SexM > F
AetiologyIdiopathic: Dopamine deficiency in Substantia Nigra + relative excess of Acetylcholine in Corpus Striatum
Atherosclerotic: Damage to Substantia Nigra from atheroma/stroke (often less tremor)
Drugs: Neuroleptics · Poisoning: Manganese, Copper · Postencephalitic · Boxing
Core triad: Rest tremor (pill-rolling) + Bradykinesia (slow movement) + Rigidity (cogwheel/lead pipe). Dopamine ↓, Acetylcholine ↑ → imbalance.
⚡ Epilepsy & Increased Intracranial Pressure+

Increased Intracranial Pressure:

Causes: Bleed, tumour, abscess, hydrocephalus, oedema (CVA/infection).

Mechanism: Direct pressure → midline shift → optic nerve stretched → pupil dilates then fixed. Pressure pushes brainstem → ↑BP + ↓pulse. Eventually "coning" → respiratory arrest.

Chronic raised pressure: Headache worse in morning & sitting up, worsened by Valsalva. Optic disc cupping.

Epilepsy:

Often idiopathic. Grand Mal: aura (strange taste/smell) → generalised fit → loss of consciousness ~½ hour post-fit → headache. May have incontinence + tongue bitten.

Investigations: EEG, CT. Treatment: Carbamazepine, Phenytoin, Valproate. Surgery.

📊 Differential Diagnosis Charts

Clinical DD grids from the textbook — organised by body region. Perfect quick revision.

🤕 HEADACHE — DD by Category

TRAUMATIC

  • CSF Shunts
  • Blows to head
  • CVA/TIA
  • Epidurals/myelograms
  • RTA (concussion, whiplash)
  • Birth trauma

METABOLIC

  • ↑BP
  • Vit A toxicity
  • Anorexia/Bulimia
  • Paget's
  • Acromegaly
  • Excessive alcohol/drugs

FUNCTIONAL

  • Visual impairment
  • Postural (bad ergonomics)
  • RSI
  • Previous trauma/loss of motion
  • Muscle spasm
  • Somatic Dysfunction C.Sp/TMJ
  • Dehydration
  • Depression/PMT
  • Tension/Stress
  • Drugs
  • Fatigue/lack of sleep

INFLAMMATORY

  • RA
  • PMR
  • Vasculitis

DEGENERATIVE

  • OA
  • Degenerative disc disease
  • Neurological disease
  • ↑BP

VASCULAR

  • CVA (subdural, subarachnoid, intracerebral, thrombo-embolic)
  • Hypertension
  • Anaemia
  • Migraine
  • Aneurysm

CONGENITAL

  • Apical ligament instability (Downs)
  • Abnormal Foramen Magnum
  • Vertebral abnormalities
  • Vascular anomalies
  • ↑CSF production
  • Sutural fusion
  • Budd-Chiari malformation

INFECTIVE

  • Viral/Bacterial toxic headache
  • Trigeminal neuralgia
  • Otitis externa/media
  • Cholesteatoma
  • Dental abscess
  • TMJ discitis

NEOPLASTIC

  • Space occupying lesions
  • Pituitary tumours
  • Cranial nerve tumours
  • Meningeal tumours
  • Metastatic
  • Bone cancer
  • Multiple Myeloma

🦵 KNEE PAIN — Full DD

TRAUMATIC

  • Muscle strain
  • # Patella/femur/tib/fib
  • Dislocation
  • Ligament rupture/sprain
  • Meniscal tears (bucket handle, pedunculated)
  • Recurrent dislocating patella

FUNCTIONAL

  • RSI
  • Osgood Schlatters
  • LLI
  • Bursitis
  • Somatic dysfunction

REFERRED

  • OA hip
  • Shin splints
  • Neurological
  • Pelvis/foot/ankle

DEGENERATIVE

  • OA/RA
  • AS
  • Retropatella wear
  • Bucket handle tear
  • Baker's cyst
  • Discoid lateral meniscus
  • Loose bodies (OA 1–10, chip # 1–3)
  • Synovial chondromatosis

INFLAMMATORY

  • RA/AS/Reiters
  • Bursitis
  • Arthritis with GIT disturbance
  • SLE
  • Gout

METABOLIC

  • Vit C/D deficiency
  • Rickets
  • Hyperparathyroidism

NEUROLOGICAL

  • Neurovascular bundle compression
  • Compartment syndrome
  • L234 somatic dysfunction
  • Charcot joints (tabes dorsalis)
  • Neuroma

CONGENITAL

  • Flabella
  • Genu Varum (bow legs)
  • Genu Valgus (knock knee)
  • Osteogenesis imperfecta
  • Diaphysial aclasis
  • Absent patella

INFECTIVE

  • Rheumatic Fever
  • Pyogenic Arthritis
  • TB
  • Osteomyelitis
  • Herpes

NEOPLASTIC

  • Primary bone (osteosarcoma)
  • Soft tissue
  • Metastatic
  • Ewing's (onion peel)
  • Giant cell tumour

🦶 ANKLE/FOOT PAIN — Full DD

TRAUMATIC

  • Ligament tear/rupture/sprain
  • Muscle tear/rupture/strain
  • #/dislocation
  • March # (2/3 neck of met)
  • Pilot's #
  • Laxity
  • Haglund's Deformity

INFLAMMATORY

  • RA/OA/Bursitis
  • Gout

METABOLIC

  • DM (Charcot's)
  • Crystal Deposition
  • Osteoporosis

DEGENERATIVE

  • OADJ disease
  • Psoriatic arthritis
  • Reiters (fluffy heel spurs)
  • AS (Achilles tendonitis, plantar fasciitis, sausage digits)

NEUROLOGICAL

  • Tarsal Tunnel Syndrome
  • Foot Drop
  • Charcot Marie Tooth (Pes Cavus)
  • Friedreich's ataxia
  • Spastic Flat Foot
  • Polio
  • Morton's neuroma

🦿 HIP PAIN — Full DD

TRAUMATIC

  • # Femur/acetabulum/head
  • #/dislocation head of femur
  • # pubic ramus
  • Dislocated pubis symphysis
  • Pelvic floor tears
  • Slipped upper femoral epiphysis

INFLAMMATORY

  • RA/OA
  • Bursitis
  • Irritable hip (synovitis)

METABOLIC

  • Gout (uric acid)
  • Pseudogout (calcium pyrophosphate)
  • Rickets

DEGENERATIVE

  • OA/RA
  • Perthes disease
  • Intermittent claudication
  • Paget's

CONGENITAL

  • Congenital dislocation of hip
  • Coxa vara
  • OI

INFECTIVE

  • TB
  • Bursitis
  • GIT disturbance
  • Pyogenic
  • Osteomyelitis

NEOPLASTIC

  • Primary bone
  • Metastatic
  • Soft tissue

💪 SHOULDER PAIN — Full DD

TRAUMATIC

  • Biceps tendon rupture
  • # clavicle/humerus/scapulae
  • AC & CC ligaments
  • Rotator cuff rupture
  • Recurrent dislocation
  • Long thoracic N. palsy

INFLAMMATORY

  • RA
  • Gout
  • Tendonitis (biceps, rotator cuff)
  • Brachial neuritis
  • PMR
  • Bursitis · SLE

DEGENERATIVE

  • Tendonitis
  • Cuff tears (partial/complete)
  • OA

NEUROLOGICAL

  • Peripheral nerve palsy
  • Discus
  • Foramina (spondylosis)
  • Syringomyelia
  • Pancoast (apical lung)

🧠 Exam Quiz

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