TOP 70 PACES CASES SUMMARISED SUMMARIES BY DR SUJIT VASANTH

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DIABETIC RETINOPATHY (41) microaneurysms, blot haemorrhages,

hard exudates (Background), circinates of hard exudate near macula, poor acuity
(Macular oedema), cotton wool spots, flame haemmorhages, leashes of new vessels,
photocoagulation scars (proliferative), vitreous haemorrhage/scars, retinal
detachment (advanced diabetic eye dx). may be bp, cateract. indications for referral:
all except background, refer background involving macula. indications for
photocoagulation: pre-proliferative (cotton wool spots, multiple blots, venous
beeding) or proliferative retinopathy.
RHEUMATOID ARTHRITIS (31) symetrical deforming arthropathy,
spindling of fingers. PIP, MCP swelling, DIP spared, muscle wasting, deformity, pain.
nodules at elbow/dorsum hand, ulnar deviation, nail fold infarcts, arteric lesions.
warmth and swelling sugests active inflam. swan neck, boutonnire deformity, Z
thumb, palmer erythema, anaemia, episcleritis, CVS/RESP signs. causes of anaemia:
chronic dx, nsaids, myelosupressive drugs, feltys, assoc pernicious
anemia. treatment: general (education, excercise, physio - thermal, splinting, diet),
NSAIDs, DMARDs (1st line: methotrexate, sulphasalazine, gold, penicillamine,
(hydroxy)chloroquin, 2nd line: azathioprine, cyclophosphamide, chlorambucil),
corticosteroids (7.5 mg/day with calcium, bisphophanates), biological agents.
EXOPTHALMOS (26) (protrusion of eye revealing sclera above lower lid on
forward gaze). bilateral asymetrical swelling of medial caruncle, congestion of lateral
canthus, and exopthalmos. look for pretibial myxoedema, thyoid acropachy. graves
malignant exopthalmos: may be eu/hypo/hyperthyroid with severe exopthalmos,
chemosis, exposure keratitis, corneal ulceration, painful opthalmoplegia (lateral,
upward and convergent). due to muscle infiltration, oedema, fibrosis. sight
threatening due to optic nerve pressure. Rx: steroids, tarsoraphy (scar), orbital
decompression, radiotherapy. Causes: hyperthyroid graves dx, euthyroid graves dx,
hypothyroid graves. asymetrical: cavernous sinus thrombosis, carticocavernous fistula
(pusatile), unilat: retroorbital tumour, orbital celulitis (Hertel
exopthalmometer) Treatment: lubricant eye drops, avoid smoking, wrap around
glasses, optimize thyroid status. radioiodine may worsen exopthalmos.
ACROMEGALLY (24) prominent supraobital ridges, large lower jaw,
exagerated wrinkles, full lips, malocclusion/prognathism, interdental spaces,
nose/tongue/ears enlarged, kyphosis, large doughy spade hands, thick skin, carpal
tunnel syndrome, excesive sweating, 1/3 hersuit, husky, cavernous voice, bitemporal
hemianopia. Others: shoe/hat size, bowed legs, rolling gait, gynaecomatia,
gallactorhoea, large/small testes, acne, greasy skin, skin tags (colonic polyps),
acanthosis nigricans, osteoarthrosis, prox muscle weakness, cardiomegally (bp,
cardiomyopathy), CN3 palsy. Associations: DM, bp, hyercaliuria, hypercalcemia (if
MEN1=pipa=pituitry, islet cell, parathyroid, adrenal), urolithiasis, hyperTG, diabetes
insipidus, hypopituitrism. Inv: IGF1, GTT absent GH supression, MRI pituitry, visual
fields, old photos, SXR, ant pit tests (short synACTHen, ITT, TSH, T4, oestadiol,
LH/FSH, testosterone, prolactin). Rx: trnasphenoidal/transfrontal hypophysectomy,
external irradiation, gold/yttrium implants, bromocriptine (no shrinkage),
somatostatin analogues (shink). cause:99% pit adenoma, 1% gangliocytoma
CHRONIC LIVER DISEASE (21) icterus, pigmentation, clubbing,
leuconychia, palmer erythema, Dupytrens, spider naevi, flapping tremor, scratch
marks, purpura, gynaecomastia, scanty body hair, small testes, hepatomegally,
splenomegally, ascites, ankle oedema, distended abdo veins flow away +/- cyanosis
from pulm-venous shunts. consider transplantation. causes alcohol, viral hepatitis,
autoimmune CAH, haemochromtosis, cryptogenic. other: cardiac failure, constrictive
pericarditis, Budd Chiari, 2ry billiary cirrhsis, drugs (methotrexate, mehydopa,
isoniazid, CCl4, amiodarone, aspirin, phenytoin, propylthiouracil, sulphonamides),
Wilsons dx, alpha1antitrypsin def, metabolic (galactosemia, tyrosinemia,
glycogenosis4)

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FIBROSING ALVEOLITIS (21) sob, clubbing, steroid purpura, reduced

symetrical expansion, fine inspiratory crackles (+/- cyanosis, dullnes lung base,
LTOT) causes cryptogenic, rheumatoid, conn tissue disorders (systemic sclerosis,
SLE, polymyositis, dermatomyositis, Sjorgens), ankylosing spondylitis, extrinsic
allergic alveolitis, asbestosis, silicosis, drugs (bleomycin,buslphan, nitrofurantoin,
amiodarone), radiation fibrosis, chemicals (Berylium, mercury), poisons (paraquet),
ARDS.
PROSTHETIC VALVES (17) Mitral valve prosthesis midline sternotomy, S1
prosthetic click, diastolic opening click +/- mid diastolic flow murmur, pansystolic
murmur/failure suggests leak. Aortic valve replacement midline sternotomy, normal
S1, systolic opening click, prosthetic S2 +/- systolic flow murmur, early diastolic
murmur/collapsing pulse suggests leak Complictions thromboemolism, haemorhage,
endocarditis, valve leak, dehiscence, Starr-Edwards ball embolus, valve obstruction
(thrombus/fibrosis), haemolysis.
HEPATOSPLENOMEGALLY (17) spleen enlarged..cm below costal
margin. Liver palpable ... cm below right costal margin. Check for anemia,
lymphadenopathy, chronic liver disease and renal enlargement. Causes:
myeloproliferative,lymphoproliferative (CLL, lymphoma), liver cirrhosis with portal
hyperension, infections (hepB/C, EBV, CMV), zoonoses (brucella,weils, toxplasma),
megaloblastic anemia, storge dx (gauchers, glycogen storage), amyloidosis,
sarcoidosis,budd chiari=hep vein thrombosis, infantile PKD. worldwide causes:
malaria, kala azar, schistosomiasis, TB. Bruit suggests hepatoma.
PNEUMONECTOMY (16) chest wall deformity, with flattened L side
associated ith L thoracotomy scar, L tracheal deviation, L expansion reduced,
percussion dull, breath sounds diminished. Bronchial breathing L upper zone due to
tracheal deviation. L lower lobctomy deformity chest, L lower ribs pulled in, L
thoracotomy scar, trachea central, apex displaced L, percussion dull L lower zone,
breath sounds diminished.Indications for pnumonectomy 25% non small cell ca (26% mort), solitary pulm nodule of uncertain cause, treatment unresponsive
bronchiectasis, TB in preantibioic era.
RETINITIS PIGMENTOSA (16) widespread scattering of black pigment
resembling bone spicules, the macula spared. There is tunnel vision and night
blindness. Associaions: cateracts, deaf mutism, mental deficiency. Other causes of
pigmentary degeneration Laurence Moon Biedl, Refsums dx, hereditary ataxia,
familial nuropathy, neuronal lipidoses (ceroid lipofuscinosis).
SYSTEMIC SCLEROSIS (15) middle aged female, skin smooth, shiny, tight
fingers and face. Raynaulds, atrophy of finger tips, telangectasias face, pigmentation,
nodules of calcinosis palpable on some fingers. other: skin ulcers, vitiligo, Sjorgens,
diffuse intersitial fibrosis (leading cause of death) Rx vasoilators. other systems:
CREST, renal (bp, failure), CVS (cardiomyopathy, effusion), muscle (myositis,
arthritis), intestinal hypermotility, PBC. Treatment: general (education, exercise,
lubricants), Raynauds (calcium ch blockers, ACEi, proscycline, calcitonin GRP),
oesophagus (PPI, prokinetics=cisapride), malabsoption (low residue diet,
supplements, rotational abx), renal (ACEi, steroids), pulm vasc dx
(vasodilators),fibrosis (dpenicillamine, corticosteroids).
POLYCYSTIC KIDNEY DISEASE (14) bilateral flank masses, bilaterally
ballotable, can get above them, percussion resonant, abdominal scars from
CAPD/cyst aspiration, AV fistula, uremic facies, hypertension, renal transplant,
parathyroidectomy. Complications: flank pain, bleeding, uti, nephrolithiasis,
obstrucive uropathy. Other features: berry aneurysm, mitral valve prolapse, renal cell
carcinoma. Genetics: PKD1 (Ch16, 85%, renal failure), PKD2 (Chr4, 15%), PKD3
rare. Liver cysts: rare in adult AD-PKD, common in infantile AR-PKD. Screening:
U/S and genetic testing at 20 years (inconclusive before 20), earlier if FH aneurysm,
signs renal dx. Bilateral renal enlargement: polycystic kidney dx, bilateral
hydronephrosis, amyliodosis, tuberous sclerosis, von Hippel Lindau disease.
MITRAL REGURGITATION (13) pulse regular, JVP not raised, no
ankle/sacral oedem unless cardiac failure, thrusting apex suggestng volume overload

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in 6 ICS, ant axilliary lne, possible systolic thrill, left parasternal heave, Soft S1, S3
suggests severe MR. Loud pansystolic murmur at apex radiates to axilla. MR with
pulm bp. Causes: degenerative, rheumatic heart dx, severe LV dilatation, MV
prolapse, papillairy muscle dysfunction, previous valvotomy for mitral stenosis,
infective endocarditis, annular calcification, hypertrophic cardiomyopathy, chodrae
rupture, congenital (marfans, erhler danlos, pseudxanthoma elasticum), endocardial
fibrosis. Indications surgry: SOBOE despite ACEI,/diuretics, increased end systolic
volume (> 30 ml/m2), serial echo progressive LV dilatation, valvuloplasty +/annuloplasty preferable due to dec mort/no anticoagulation. Mitral vave prolapse:
post leaflet LSE, ant eaflet over spine.
SPLENOMEGALLY (13) mass left hypochondrium, cnnot get above it, there
is a notch. It moves diagonally cross abdomen, percussion is dull over left lower chest
and mass. I think this is a spleen enlarged at..cm. Causes: v.large: CML (Ph chr
t9;22), myelofibrosis, makaria/kala arar. Large (4-8cm):myeloproliferaive (CML,
myelofibrosis), lymphoproliferative (lymphoma, CLL), cirrhosis with portal
hypertension.Small (2-4 cm): myeloproliferative, lymphoproliferative, cirrhosis with
portal hypertension, infections (EBV, hepatitis,SBE)
NEUROFIBROMATOSIS (13) multiple (5+) neurofibromas, sessile
pedunculated fibromata some soft others firm, some single others lobulated, some
mobile subcutaneously lumps others nodules along peripheral nerves, cafe au lait
spots, 2/3 axilliary freckling, Lisch nodules=iris harmatomas, retinal harmatomas, rib
nochiing, mental retardation, epilepsy, renal art stenosis. complications:
kyphoscoliosis, pressure effect (acoustic neuromas CN5-8, cerebellar signs), CN5
neuroma, spinal nerve root, sarcomatous change, lung cysts (honeycomb lung),
pseudoarthrosis, plexiform neuroma. Can also have: glioma, meningioma,
medulloblastoma. Genetics: aut dominant , NFT1=von Ricklenhausen (chr 17), NFT2
(chr 22) bilateral acoustic neuroma
BRONCHIECTASIS (12) underweight, cyanosed, sob, finger clubbing,
frequent productive cough, sputum pot, inspiratory clicks heard with unaided ear,
localised crepitations, may be widespread ronchi.. causes: childhood infections
(whooping cough, measels, TB), cystic fibrosis, bronchial obstruction (foreign body,
carcinoma, sarcoid, lymphadenopathy and fibrosis), hypogammaglobulibemiam,
allergic bronchpulmonary aspergillosis, Marfans, yellow nail, congenital (defomity,
Kartageners) , smoking related copd (common)
PSORIASIS (12) (11) Asymetrical arthropathy involving mainly TIP, pitting
of fingernails, onycholysis, some nail plates thickened, hypetkeratosis under
them.Patches of psoriasis over bony prominemces particularly elbows, knees, trunk,
scalp, intragluteal cleft, behind ears, in navel. Plaques circular, well difined edges, red,
silvery scaly surface. Other arthropathy: arthritis mutilans, Rheumatoid-like,
oligo/mono artthropathy, ank spond treatment local sunlight, uv light, coal tar,
dithranol, local steroids, calipotriol, PUVA (psoralen and uv light). Treatment
systemic: acitretin (retinoid), antimetabolites (sulphasalazine, methotrexate,
azathioprine, hydroxyurea). Analgesic anti inflam for arthropathy, intraarticular
steroids. Chloroquin contraindicated worsens skin. Incidence 5% Caucasian, NW
europe, USA. Uncommon in Japanese, N American Indians, Japanese.
OSLER WEBER RENDU (11) (heridatary haemmorhagic telangectasias)
Telangectasias on face, around mouth, on lips, tongue, buccal and nasal mucosa and
fingers. Anemia but no features of systemic sclerosis .complications: GI
haemorhhage, epistaxis, hemoptysis 2ry to pulm AV aneurysms, conjunctival
telagactesias (bloody tears), retinal detachment/haemorrhage, cirrhosis
(telangectasias/transfusion), massive intrahepatic shunting Treatment: chronic oral
Fe therapy, oestrogens to induce squamous metaplasia of nasal mucosa, low dose
finbrinolytic agents (aminocaproic acid), pulse dye laser NOT cautery. Genetics:
Autosomal dominant, several gene defects possible.. non contractile capillaries cause
prologed bleeding.
PLEURAL EFFUSION (10) Pulse regular, JVP normal, trachea usually
central,expansion normal, percussion stony dull at R/L base, diminished TVF, VR and

diminished breath sounds. May be bronchial breathing over effusion. Causes Exudate
(>30 g/l, LDH >200) bronchial carcinoma, secondary malignancy, PE with infarction,
pneumonia, TB, mesothelioma, rheumatoid arthritis, SLE, lymphoma. Transudate
(<30 g/l) cardiac failure, nephrotic syndrome, cirrhosis. Other causes of dullness at
lung bases raised hemidiaphragm, basal collapse, collapse/consolidation totally
occluding distal airways, pleural thickening. (TB, asbestos, empeyema) Pleural bx:
Abram's needle for tb/malignancy place in normal saline. Thoracoscopy for either
diagnosis and pleurodesis
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PERIPHERAL NEUROPATHY (9) impaired light touch, vibration, joint
position and pinprick in a stocking +/- glove distribution. causes: DM, carcinomatous
neuropathy, vitB12 def, vit B def (alcoholics, poor nutrition, dialysis), drugs
(isoniazid, vincristine, nitrofurantoin, gold, ethanbutol, phenytoin, hydralazine,
metronidazole, amiodarone, chloramphenicol, cyclosporin), idiopathic, leprosy, other
(guillin barre, PAN, amyloidosis, AIDS), rare (myxoedema, acromegaly, sarcoidosis,
uremia, Lyme dx, tetanus, botulism, paraprotein, hereditary ataxia, Refsum's dx,
arsenic posoning, POEM syndrome) Motor causes: carcinomatous, lead, porphyria,
diptheria, Charcot Marrie Tooth.
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MIXED AORTIC VALVE DISEASE (9) Predominant AS Regular slow
rising pulse (possibly bisferens). JVP not elevated. Apex palpable 1 cm left of MCL,
forcefull sustained heave (pressure overload). Systolic thrill apex, aortic area and
carotid. Harsh ejection systolic murmur aortic area radiating to neck, soft A2, early
diastolic murmur LSE loudest on leaning forward, in inspiration. BP low with low
pulse pressure.Predominant AR regular pulse, large volume and collapsing (possibly
bisferens). JVP not raised. Apex in ant ax line 6ICS thrusting (volume overload).
Harsh systolic murmur aortic area radiating to neck, early diastolic murmur LSE
loudest on leaning forward, in inspiration. BP.Management: Cardiac cath is gold
standard, gradient on echo is unreliable in severe AR. Best treatment AV repair,
surgery indicated for stenotic symptoms, lv compromise in regurgitation. Ex testing
can be used except for severe AS.
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MIXED MITRAL VALVE DISEASE (9) Predominant MS malar flush, left
thoracotomy scar. Pulse irregularly irregular, JVP not raised. Tapping Apex, not
displaced. Left parasternal heave. Loud S1, pansystolic murmur radiating axilla, loud
P2, opening snap, mid dialstolic rumbling localised to apex. Predominant MR with
pulm hypertension left thoracotomy scar, pulse irregular. Apex thrusting (volume
pverload), apex 6 IC ant ax line, soft S1loud pansystolic murmur LSE and or apex.
Loud P3, in left lateral posn mid diastolic low rumble followed by opening
snap. Management: Cardiac catheter study gold standard.
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TRANSPLANTED KIDNEY (9) Usually assoc APKD. Fullness in flanks,
swelling under scar RIF. Bilateral flank masses bimanually ballotable (or 1 mass and 1
nephrectomy scar). Palpable rounded mass under the scar in RIF feels like
kidney. Diseases leading to transplantation: DM nephropathy, hypertensive renal dx,
glomerulonephritis. Difficult to transplant: HUS (recurrence possible, esp if on
cyclosporin), sickle cell (increased crisis), systemic sclerosis (chornic vasular/gi
problems), focal glomerulosclerosis (recurrence in graft common), oxalosis (severe
recurrence of stone dx), cystinosis and Farby's dx (continued dx activity). 5, 10 yr
outcome: HLA identicle living (88, 73), other living (74, 56), HLA matched cadaver
(70, 56).
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GRAVES DISEASE (9) M:5F, hyperthyroid graves usually female, thin,
sweaty palms, fine tremor of outstretched hands, tachycardia, fidgety and nervous,
small diffuse goitre with bruit, exophalmos (?chemosis, opthalmoplegia, lateral
tasoraphy), lid lag. Euthyroid Graves:exopthalmos, thyroid acropachy, pretibial
myxoedema, pulse regular with normal rate, palms not sweaty, no hand tremor, no lid
lag. Previous thyroidectomy scar. Hypothyroid Graves: exopthalmos, goitre,
thyroidectomy scar, pretibial myxoedema, thyroid acropachy, hypothyroid facies,
hoarse voice, slow pulse, slowly reacting reflexes.. It is likely that she has
hyperthyroidism treated in the past (?thyroidectomy or radioactive iodine) now on
inadequate throxine replacement alternatively Graves occasionally develops

autoimmune hypthyroidism. Ask some questions: heat intolerence, weight loss,

increased apetite, diarhhoea, exertional dyspnoea, fatiguability, can't keep still,
irritability, nervousness, menstrual symptoms., other signs: fever, systolic
hypertension, vasodilation, flow murmur, proximal myopathy, hyperactive reflexes,
childhood choreoathetosis, fine thin hair with temporal recession, onycholysis
(Plummer's nails esp 4[SUP]th[/SUP] finger), palmer erythema, spider naevi,
minimal hepatosplenomegally, axillary lymph nodes, osteoperosis, regardless of
thyroid statud pulse may be regular or irregular. Graves can occur without eye signs
and in elderly males. Graves exopthalmos due to retrorbital fat, enlarged intraorbital
muscles, lymphocytic infiltration inc water and mucopolysacharide. Can develop
without hyperthyroidism , course not linked to thyroid status. Pretib
mxyoedema develops usually after hyperthyroidosm treated esp with
radioiodine. Investigations: thyrotrophin receptor Abs, even radioiodine uptake with
exception of nodules, new bone formation (acropachy) on xray = soap bubbles, coarse
spicules cf HPOA(=linear new bone formation). Organ specific autoimmune
dx thyroid, pernicious anemia, atrophic gastritis, DM, Addisons, hypoparathyroidism,
premature ovarian failure, renal tubular acidosis, fibrosing alveolitis, chronic active
hepatitis, primary biliary cirrhosis. Female propenderence assoc premature hair
greying, alopecia areata, vitiligo. Autoimmune thyroiditis also assoc with Sjorgens,
myasthenia gravis, systemic sclerosis, mixed conn tissue dx, cranial arteritis,
polymyalgia rheumatica. Autoimmune thyroid dx's: Grave's, Hashimotos thyroiditis,
atrophic myxoedema, usually FH of other 2. all 3 fall under hashitoxicosis.
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RHEUMATOID LUNG (8) possibly cyanosis and dyspnoea. Fine inspiratory
crackles aka crepitations on auscultation both bases. In view of rheumatoid changes
in the hands the likely diagnosis is fibrosing alveolitis associated wirg rheumatoid
disease. Comments: Develops overtly in 2% RA, subclinical in 50%, poor prognosis,
progessing to honeycomb CXR, bronchiectasis, chronic cough, progressive dyspnoea.
PFT reduced diffusion capacity and compliance, restrictive pattern. Gold can induce
same interstitial lung dx but reverses on discontinuing drug.Pulm Rheumatoid
dx: pleural disease (exudate, Rh F +ve, low glucose, WCC <5), intrapulmonary
nodules (can become infected/cavitate/haemoptysis/rupture -> pneumothorax,
massive confluent nodules in assoc with pneumoconiosis=Caplan syndrome),
obliterative bronchiolitis (classucally dyspnoea, high pitched wheeze=squawk,
hyperinflation), pulmonary arteritis, apical fibrobulous dx.
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MIXED MITRAL AND AORTIC DISEASE (8) If 1 murmur found LOOK
FOR 2ND MURMUR e.g .Mixed aortic and mitral valve diseaseLeft thoracotomy
scar, malar flush, pulse irregularly irregular, slow rising, jvp not elevated, apex is
heaving/lifting, etc in the abt ax line, parasternal heave, systolic thrill at apex, aortic
area and neck. S1 loud, harsh ejection systolic murmuraortic area radiating to neck,
pansystolic murmur LLSE radiating to apex and axilla, early diastoli mumur just
audible in aortic area and down LSE with patient sitting forward in expiration and
opening snap followed by mid diastolic rumbing murmur localised to apex. Which
lesion is dominant? Slow rising pulse suggests AS is the dominant aortic valve lesion,
it is not possible to determine major mitral valve lesion. Further investigation with
echo leading to TOE +/- cardiac catheterisation with LV angiography would be
required to assess heamodynamic signifance of each lesion.
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MYOTONIC DYSTROPHY (8) Myopathic facies (drooping mouth, long
lean, lifeless, sad, sleepy expression), male frontal balding, ptosis (may be unilateral),
wasting of facial muscles (temporalis, masseter, sternomastoid, shoulder girdle,
quadreiceps. When making a fist unable to open it quickly especially repeatively.
Worsen in cold and excitement, difficulty opening eyes after firm closure. When
shaking hands difficulty releasing grip (feature of myotonia). dimples/depressions
induced by percussion fill slowly (percussion myotonia of tongue/thenar
eminence). Genetics: Aut dom, expanded trinucleotine repeats Chr 19 myotonin
protein kinas gene, shows anticipation (ancestors presenile cateracts), diagnosis by
genetic test, M>F. Other features: cardiomyopathy, intellect/personality
deterioration, slurred speech combined with tongue/pharyngeal myotonia, testicula

atrophy, diabetes mellitus (end organ unresponsiveness to insulin). myotonia

congenita (Rhomsens's dx) myotonia without other features of dyotonic dystrophy.
Normal refkexes, possible Herculean appearance ?involuntary isometric exercise. Aut
dom/recessive ion channelopathies.
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CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (8) Emphysema thin man pink puffer appearance, nicotine staining
of fingers. Tachypnoeic at rest, lip pursing, prolonged expiration, suprasternal notch
to cricoid distance reduced suggesting hyperinflation (normally >3 finger breaths).
Chest hyperinflated, expansion mainly verticle, tracheal tug. Accessory muscles
respiration, indrawing of lower ribs on inspiration due to flattened diaphragm.
Percussion hypersonant obliterating cardiac and hepatic dullness, breath sounds
quiet in classical emphyema, wheezes are often heard if associated bronchial dx.
SOMETIMES decreased breath sounds over the upper/middle/lower zoneof R/L lung
raises possibility of emphysematous bulla. Chronic Bronchitis male smoker, foggy
city, dust/fumes, frequent respiratory infection, classical blue bloater. Nicotine
staining, stocky, centrally cyanosed, suffused conjuntivae. Hyperinflated ches
evidenced by use of accessory muscles on inspiration and tracheal tug, pulse 80 bpm,
venous pressure not elevated (ankle oedema, hepatomegally if cor pulmanal present),
trachea central, suprasternal notch to cricoid distance reduced. Expansion equal but
reduced to 2 cm, percussion note resonant, auscultation: expiratory phase prolonged,
widespread expiratory ronchi (and may be coarse crepitations). Forced expiratory
time 8 seconds, no flapping tremor (unless severe hypercapnoea in which case fundi
papilloedema). Possibly cor pulmanale if ankle oedema.Definitions: Emphysema
= pathological diagnosis, chronic bronchitis = cough productive of sputum on 3
months of the year in 2 consequtive years. COPD = obstructive spirometry. Causes of
empysema: smoking (assoc with chronic bronchitis mixed centrilobular and
panacinar), alpha1atitrypsin deficiency (young, lower zone, panacinar ?iceterus,
hepatomegally), coal dust (centrilobular emphysema simple coal dust
pneumoconiosis only minor abnormalities of gas exchange), Macloed's syndrome
(Swyer-James rare unilateral emphysema following childhood bronchiolitis and
subsequent impaired alveolar growth.
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CARCINOMA BRONCHUS (0,8) LOOK FOR RADIOTHERAPY
TATOES Carcinoma bronchus with pleural effusion: Clubbing, nicotine staining,
hard lymph node in R/L supraclaviculare fossa, pulse regular, JVP not elevated,
trachea central, chest expansion normal, persussion stony dull at R/L base, tactile
fremitus, vocal resonance and breath sounds all diminished over area of
dullness. Carcinoma of bronchus with radiation therapy : cachectic, radiation burn
R/L upper chest, clubbing, noctine staining, pulse regular, JVP nor elevated, no
lymph nodes. Trachea deviated to R/L, expansion diminished R/L upper chest, TVF
and resonance increased over upper chest, dull percussion note, area of bronchial
breathing. Likely radiotherapy for carcinoma bronchus causing collapse and
consolidation of /L upper lung. Pancoast's syndrome:radiation burn to chest, lymph
nodes palpable in R/L axilla, trachea central, chest signs normal, wasting of small
muscles of R/L hand, sensory loss +/- pain over T1 dermatome (can be C8-T2), R/L
Horner's syndrome (ptosis, myosis, anhydrosis, enopthalmos). This is pancoast's
syndrome due to apical carcinoma involving the lower brachial plexus and cervical
sympathetic nerves. Lobectomy: R/L thoracotomy scar, trachea deviated R/L/ R/L
chest expansion diminished, percussion resonant, breath sounds harsher. R/L
lobectomy for removal of tumour, resistant lung abscess or localised
bronchiectasis. Complications : local effects: SVC obstruction (?oeema face/upper
extremities, suffusion eyes, fixed engorgement of neck veins, dilataio superficial
veins), stridor (SVC obstruction, dysphagia). Metastases and their effects (pain, ?
hepatomegally, neurological signs). Non metastatic effects: HPOA wrists/ankles,
peripheral neuropathy, cerebellar degeneration, encephalopathy, priximal myopathy,
polymyosistis, dermatomyositis, Eaton Lambert syndrome), SIADH, ectopic ACTH,
PTH,PTHrP, carcinoid), gynaecomastia (?HCG secreting tumour?), thrombophlebitia
migrans, non bacterual thrombotic endocarditis, anemia (usually normoblastic,

occasionally leucoerythroblastic), pruritis, Herpes zoster, acanthosis nigricans,

arythema gyratum repens (irregular wavy bands with marginal desquamation on
trunk, neck and extremities).
30.
HYPERTENSIVE RETINOPATHY (0, 8) Narrow retinal arterioles
(normal AV ratio 1:1), may be tortuous, varying calibre, increased light reflex
(copper/silver wiring), AV nipping (all occur in aging, arteriosclerosis, hypertension).
Flame haemmorhages and blot haemorrhage , cotton wool exudates (this constitutes
grade 3 retinopathy and a diagnosis of malignant (accelerated) hypertension even
without papilloedema), there is papilloedema (cerebral oedema or malignant
hypertension haemorrhages and exudates not necessary). This is grade 4
retinopathy. Causes of hypertension: essential (94%), renal (4% - ?RAS, acute
nephritis, PKD), endocrine 1% (cushing's, conn's, phaechromocytoma, acromegaly,
hyperPTH, hypothyroidism, OCP), miscellaneous <1% (caorctation, polycythemia,
acute porphyria, pre-eclampsia). cerebral tumour or raised ICP from any cause can
cause 2ry hypertension (Cushing's reflex). If phaeochromocytoma screen for MEN2
and von Hippel-Lindau in patient AND families.
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AORTIC STENOSIS (7) Aortic stenosis: Pulse regular, small volume and
slow rising, JVP not raised (unless cardiac failure), apex 1cm left of MCL 5ICS (i.e.
Apex Normal or Slightly displaced unless cardiac failure) with forcefull sustained
heave (pressure overload). Sysolic thrill aortic area, carotids +/- apices. Harsh
ejection systolic murmur aortic area radiating to neck., soft A2 (or absent). Associated
ejection click if valve bicuspid). Blood pressure low normal with decreased pulse
pressure. Murmur quietens as dx progresse/cardiac failure. Look careflully for MS as
both conditions obscure eachother. (MS missed AS severity unerestimated) need
echo. Aortic sclerosis: normal pulse, apex undiplaced, barely palpable, no thrills,
ejection systolic murmur not harsh or loud, only radiates faintly to neck. A2 normal
+/- ejection click. This is aortic sclerosis (assoc with 50% inc death CVS risk, no
significant gradient on echo). Causes: 1. Rheumatic heart disease (often associated
mitral valve dx or aortic regurg), 2. Bicuspid aortic valve (M 60's), 3. Degenerative
calicification (in elderly, stenosis usually mild), 4. Congenital (worsen during
childhood and adolescence due to calification). Indications for surgery: symptoms,
pressure gradient 50-60 mmHg lower if EF low, may need simultaneous CABG, ,
consider valvotomy in young. Beta blockers as temporising measure. Av block in
calcific aortic stenosis/post aortic valve operation/pacemaker insertion..Other causes
of short systolic murmur: prolapsed mitral valve, trivial MR, hypertrophic
cardiomyopathy.
32.
OCCULAR PALSY (3, 7) 6[SUP]th[/SUP] nerve palsy: convjivergent
strabismus, impairment lateral movement R/L eye, diplopia worse on looking R/L.
(outermost image comes from affected eye). Causes mononeuritis multiplex,
demyleinating dx, raised ICP false localising sign due to long course, neoplasm (assoc
ipsilateral facial palsy if pontine tumour, myasthenia gravis, vascular lesions,
compression by aneurysm (ectatic basilar artery uncommon), subacute
meningitis (carcinomatous, lymphomatous, fungal (AIDS), TB, meningovascular
syphilis) 3[SUP]rd[/SUP] nerve palsy.: ptosis, lifting lids reveals divergent
strabismus, dilated pupil, eye fixed in down and out position (and there is angulated
dipliopia. This is complete (NB often partial) causes unruptured aneurysm of Post
comm art (or int carotid) artery painful, mononeuritis multiplex, vascular lesion
(contralateral hemiplegia = Webers synddrome, opthalmoplegia
predominant=vascular if ptosis/pupil changes prominent extriinsic compression), 4.
midbrain demyelinating lesion (intranuclear opthalmoplegia commoner), myasthenia
gravis, other (sabacute meningitis, opthalmoplegic migraine, paraseller neoplasm,
sphenoidal wing meningioma, carcinomatous lesions skull
base) 4[SUP]th[/SUP] nerve palsy adducted eye cannoot look downwards causing
one above the other diplopia, angulated diplopia on looking down and out,
worse on reading or going down stairs, SKEW deviation (sometimes also seen in
brainstem lesions). Cavernous sinus (Sup orb fiss) total or subtotal
opthalmoplegia often painful, sensory loss in CN5i (absent corneal reflex) due to

tumor compressing 3, 4, 5, 6 as travel from cavernous sinus to SOF. Causes of

Mononeuritis multiplex: DM, PAN, Churg Strauss, Rheumatoid, SLE, Wegeners,
sarcoidosis, carcinoma, amyloidosis, leprosy, Sjorgens, Lyme dx). Other causes
ocular palsy: 1. intranuclear opthalmoplegia (abduction impaired bilaterally,
normal adduction or vice versa, no strabismus, ataxic nystagmus distguishes from
bilat CN6 palsy), 2. Exopthalmic opthalmoplegia (upward and outward gaze most
often reduced), 3. Myasthenia gravis (?ptosis, variable strabismus, facial weakness,
snarling smile, proximal muscle weakness, weak nasal voice, WORSENS ON
REPITITION, FATIGUABILITY test eye movements wuth eyes held 1 position
between movements, count to 50 may superficially resemble 3[SUP]rd[/SUP] of
6[SUP]th[/SUP] nerve palsy.,4. Cavernous sunus syndrome, 5. 4[SUP]th[/SUP] n
palsy, 6. Ocular myopathy
33.
MITRAL STENOSIS (7) Malar flush, left thoracotomy scar, irregularly
irregular pulse in rate and volume OR sinus rythm small volume pulse. JVP not
raised, no ankle or sacral oedema (unless in heart failure). Tapping cardiac impulse
(S1), apex indisplaced, left parasternal heave, loud S1, loud P2, opening snap, middiastolic low rumbling murmur (with presystolic accentuation if NSR), localised to
the apex heard loudest in left lateral position, diagnosis is mitrak stenosis with
previous valvotomy. There are signs of pulmonary hypertension. Opening snap:
nearer S2 = tighter stenosis, absent=calcified mitral valve, s1 will be soft) Other signs:
giant v waves (tricuspid incompitence), Graham Steele murmur (rare 2ry pulmary
incompetence. Brief high pitched early diastolic whiff). Indications for surgery/
valvuloplasty:symptoms limiting normal activity, pulmonary iedena without cause,
recurrent emboli (anticoagulate most MS's even if sinus rhythm), pulm oedema in
pregnancy (emergency valvotomy), deterioration due to AF unresponsive to med rx),
haemoptysis. valvotomy criteria: mobile valve: louds S1, opening snap absence of
calcium in submitral apparatus on TOE, absence of MR. Esp in young female desiring
later pregnancy. MS accentuated by exercise.
34.
GOITRE (7) 1) multinodlar goitre: multinodular goitre, R/L lobe more
enlrged cf L/R. No lymph nodes, no retrosternal extension, no bruit, clinically
euthyroid (check pulse, palms, tremor lid lag, tendon reflexes). Diagnosis in middle
aged/elderlyy patient is likely to be simple multinodular goitre which is due to relative
iodine deficiency in suscetible person. Multinodular suggests longstanding. If no
recent change asymptomatic observe 6-12 months otherwise FNAC.. Diffuse
goitre firm, diffusely enlarged goitre, without retrosternal extension (check for bruit,
feel pulse to assess thyroid status) Causes of diffuse goitre: 1. simple goitre
(euthyroid, no bruit, relative iodine deficiency, esp females ?puberty, pregnancy), 2.
treated Grave's dx (?exopthalmos +/- bruit, eu or hypothyroid), 3. hyperthyroid
Graves (?bruit, tachycardia, exopthalmos, tremor, sweating, 3. Hashimito's dx
(usually micronodular, symetrical, ?hypthyroid facies, bradycardia, jerks, 4. de
Quervain's viral throiditis (tender, contitutional upset, absent radioiodine uptake , inc
T4, supressed TSH), 5. goitrogens (e.g. Lithium, iodine xs, phenylbutazoned, paraaminosalysilic acid), 6. dyshormonogenesis (6 congenital enzyme defects all
rare) solitary thyroid nodule check for lymphadenopathy. Causes solitary
nodule: 1. palpable nodule in multinodular goitre, 2. thyroid adenoma (variable
radioiodine uptake), 3. toxic adenoma (hot nodule, tacy, sweaty palms, lid lag), 4.
thyroid cysts, 5. thyroid carcinoma (?hard, lymph nodes, recent change, cold on scan).
check TFT's, FNAC, radioiodine scan (cold = possible malignancy), possible subtotal
lobectomy. thyroid carcinoma: 1. papilliary carcinoma (commonest,
children/middle aged. Regional lymph node spread, often resectable, good prognosis,
often TSH dependent so responds to thyroxine. 2. follicular carconimoa
(2[SUP]nd[/SUP] commonest, later life, blood borne mets, rx surgery, supressive
thyroxine, fair prognosis, take up/respond to radioiodine therapy. 3. anaplastic
carcinoma (elderly, highly malignant), 4. medullary ca (rare, young adults, secretes
calcitonin, sometimes ACTH, usually good prognosis), 5. usually previous
Hashimoto's, large rapidly expanding mass. MEN2a(sipple's) med ca thyroid,
phaeochromocytoma, parathyroid hyperlasia (50%) MEN 2b(aka 3) med ca thyroid ,

phaeochromocyto,a, nuro abnormalties (mucosal neuromas, marfanoid,

pigmentation, proximal myopathy, megacolon, intestinal ganglioneuromatosis. Both
aut dom, RET oncogene, genetic screening prophylactic thyroidectomy or annual
calcitonin check, urine catecholamines, serum calcium)
35.
DIABETIC FOOT/CHARCOT JOINT (7) Diabetic foot ulcer on sole R/L
foot (most commonly under head of 1st metatarsal), 2 toes previously amputated.
Thick callous over pressure points of feet, normal concavity of transverse arch at head
of metatarsals is lost. Loss of sensation to light touch, vibration and pinprick in glove
and stocking distribution. Feet cold, foot pulses not palpable, loss of hair lower legs
which are shiny. Peripheral neuropathy, neuropathic ulcer, evidence periph vasc dx, it
is likely underlying diabetes (?fundi). Charcot joint:relevent above plus ankle joint
greatly deformed and swollen, loud crepitus accompanying movement which is of
abnormal range. Charcot joint (neuropathic arthropathy gross osteoarthrosis and
new bone formation from repeated minor trauma without normal protective pain
response causing painless joint destruction). Contributing factors to DM foot: injury,
neuropathy (calluses), small vessel dx, large vessel dx (ischemia, gangrene), inc
susceptibility to infection, maldistributed pressure and foot deformity. causes of
neuropathic ulcers: tabes dorsalis, leprosy, porphyria, amyloidosis, progressive
sensory neuropathy (familial, cryptogenic), rare late manifestation of Charcot-MarieTooth dxCauses of Charcot joint: DM, tabes dorsalis, syringomyelia, leprosy
(worldwide), other (yaws, progressive sensory neuropathy, hereditory neuropathy,
neurofibromatosis)
36.
OLD TUBERCULOSIS (6) Thoracoplasty: Trachea deviated R/L. R/L
upper chest shows deformity with decreased expansion, dull percussion note.
Bronchial breathing and crepitations. Apex beat may be displaced to R/L.
Thoracotomy scar posteriorly with evidence of rib resections. This patient has had
R/L thoracoplasty for Rx of TB in pre-chemotherapy era. Apical TB trachea deviated
R/L. Diminished expansion, crackles at R/L apex suggesting R/L apical fibrosis. Old
TB is likely cause. Phrenic crush: Expansion diminished on R/L, dullness,
reduced/absent breath sounds at R/L base. R/L supraclavicular scar (+/crepitations). Patient has had phrenic crush for TB before the days of chemotherapy.
37.
HEMIPLEGIA (6) R/L UMN facial weakness, R/L arm and leg weak
(without wasting), increased tone, hyperreflexia. R/L plantar is extensor, abdominal
reflex diminisghed on R/L side. This is R/L hemiplegia. May be also R/L hemisensory
loss, visual field testing may reveal R/L homonymous hemianopia. causes:-CVA
(thrombosis, haemorrhage - check bp, embolism AF, murmurs, bruits), Brain
tomour (?insidious onset, papiklloedema, headache, ?evidence of 1ry e.g.
Clubbing). posterior circulation nystagmus, ocular palsy, dysphagia, cerebellar
signs. Parietal lobe signs: agnosia (inattention) e.g. tactile (astereognosis=cant
recognise by feel), visual, auditory (only recognises voice if can see/touch),
autotopognosia (parts of own body), apraxia (cannot execute despite normal
power/coord) e.g. dressing apraxia (usually r parietooccipital|), gait apraxia, trunk,
facial movements.( Corpus collosum, parietal, premotor) Constructional apraxia
(hepatic encephalopathy), dyslexia (reading), dysgraphia (writing), dyscalculia
(calculating) post parietal lobe.
38.
CEREBELLAR SYNDROME (6) unilateral cerebellar lesion: Nystagmus to
R/L, ataxia with eyes open evidenced by rapid alternating movements
(dysdiadokinesia). Finger-nose test impaired on R/L.with past-pointing, intention
tremor (increased on approaching target), heel-shin tetst impaired on R/L, gait ataxic
with tendency to fall R/L. Ataxic dysarthria with explosive staccato speech. Patient
has a R/L cerebellar lesion. Other cerebellar sugns: ipsilateral hypotonia, reduced
power, pedular jerks, skew deviation eyes, pendular arm drift rebound. Cerebellar
vermis lesion: widebased cerebellar ataxia and robergism same eyes open and closed
(cf sensory ataxia which is wirse eyes closed). Little or no abnormality in limbs when
tested on bed. Causes: 1. mutiple sclerosis (?internuclear opthalmoplegia, optic
neuritis, atrophy, etc), 2. brainstem vascular lesion, 3. posterior fossa SOL
(papilloedema e.g. tumor, abscess e.g. 2Ry to otitis media), 4. paraneoplastic

cerebellar syndrome (clubbing, cachexia, 5. alcoholic cerebellar degeneration

(nutritional), Freidrich's ataxia (?scoliosis, pes cavus, pyrimadal and dorsal colum
signs, absent ankle jerks). Other causes of cerebellar ataxia: hypothyroidism (?facies,
pulse, reflexes), anticonvulsant toxicity (esp phenytoin nystagmus), ataxia
telangactasia (recessive progressive ataxia, choreoathetosis, ocular apraxia,
telangectasia conjunctivae, face, skin, low IgA infections, lymphoreticular
malignancy).
39.
TOPHACEOUS GOUT (6) Asymetrical swelling small joints of hands and
feet, tophi formation in perarticular tissues. Occasional severe deformity. Tophi on
helix of ear and some of the tendon sheaths (esp ulnar surface forearm, olecranon
bursa, achiles tendon and pressure points). treatment: avoid aspirin causes uric acid
retention unless v high doses. Rx 1[SUP]st[/SUP] line NSAIDs (except if CRF, GI
ulcer, severe heart failure), colchicine (SE: nausea, diarrhoea, abdo pain),
2[SUP]nd[/SUP] line: intrarticular/systemic steroids. Allopurinol or uricosuric
(probenecid, sulphinpyrazone) drugs started 2-3 weeks after acute episode (otherwise
prolong acute attack, trigger further episides). Indictations for prophylaxis if:
recurrent, tophi, chronic arthritis, renal dx, young with hyperuricemia FH renal/heart
dx, normo-uricaemia not achieved by lifestyle i.e. wt loss, decease alcohol, food
and high purines). Significance of tophi Tophus proportional severity and duration.
Paradoxically tophi indicate dec frequency, severity cf non tophacouus. Large tophi
may have area of necrosis exuding pasty/chalky monosodium urate crystals. Sinuses
possible.Complications: renal dx, carpal tunnel syndrome. Associations: obesity,
hyperlipidemia, hypertension these cause an association with DM and IHD.causes of
2ry uricemia: drugs (esp thiazides, also ethanbutol, nicotinic acid, cyclosporin),
myeloproliferative and lymphoproliferative disorders (cell tunover preformed
purines), chronic renal failure, alcoholism, obesity.
40.
RASH OF UNCERTAIN CAUSE (6) Rash description routine. Visual
survey, distribution, surrounding skin (scratch marks, radiotherapy field marks,
paper thin skin). Adequate exposure. Monomorphic or pleomorphic. 6 features. 1.
colour (erythema, pigment), 2. size, 3. shape (oval, circular, annulaar), 4. surface
(scaling or eroded), 5. character (papule, macule, vesicle, etc), 6. secondary features
(lichenification, crusting, etc). Discussion: DD, how you would differentiate, mention
drug hx. Emolients, abx for infection. Consider biopsy. Dermatology terms:
macule=flat curcumscribed, not raised, papule=raised, circumscribed, <1cm,
nodule=larger papules, weals=circumscibed elevations itchy, tingly, vesicles=small
well defined fluid collections (bullae=large vesicles), scales, crusts , scars, pustules
(contain puss),
ulcers have: shape, edge, floor, base and secretion.
41.
HYPOTHYROIDISM (6) myxoedema Overweight, myxoedematous facies
(thickened and coarse facial features, periorbital puffiness and pallor). Skin rough,
dry and inelastic with distinct yellowish tint (carotenemia), generalised non pitting
swelling subcutaneous tissues, hoarse voice, croaking, hard of hearing, slow
movements, thinning of hair which is dry and brittle, may be loss of outer third of
eyebrow (not reliable). Slow pulse (give rate), no palpable goitre, relaxation of ankle
jerks (and other reflexes) is delayed and slow. Patient has myxoedema (look for assoc
autoimmune dx). Other symptoms: CNS disorders: peripheral neuropathy, cerebellar
ataxia, pseudodementia, drop attacks, epipepsy. myxoedema=accumulation
hyaluronic acid binding water in dermis Hasimoto's thyroiditis. as above +
symmetrical firm, fine micornodular goitre, likely diagnosis is Hasimotos thyroiditis
(assoc autoimmine dx). Hypothyroid Grave's dx as above + exopthalmos, patient
likely to have Grave's dx treated with radioiodine or thyroidectomy (scar) and is now
hypthyroid (occasionally Grave's sponteously progresses to hypothroidism). ask
patient some questions: deafness and hoarse voice, cold intolerence, tiredness and
depression, constipation (occasionally presents to surgeons), angina unmasked once
rx started, menhorhagia (middle aged), 1ry/2ry amennorhea (younger). Other
feature: anemia (normochromic Fe deficient due to atrophic gastritis, magaloblastic
pernicious anemia, mild form in siimple hypothyroidism), carpal tunnel,

preipheral cyanosis (+/- malar flush), Raynaud's phenomenon, hypertension,

accident prone, hypothermia, Hoffman's syndrome (pain, ache, swellin muscles after
exertion and myotonia), pychosis (myxoedema madness), hypothyroid coma. Assoc
autoimmune dx: pernicious anemia (?spleen, SACDC), Addisons dx (?buccal + scar
pigmentation), vitiligo, Rheumatoid arthritis (?hands, nodules), Sjorgens (?dry eyes
and mouth), ulcerative colitis, idiopathoc (presumed autoimmune ?CAH with icterus
etc), SLE (?rash), haemolytic anemia, diabetes mellitus (?fundi), Grave's dx,
hypoparathyroidism, premature ovarian failure. Comments: should check B12, fasting
sugar. Autoimmune thyroiditis presents as case 1 or 2.
42.
OPTIC ATROPHY (6) Disc pale, clearly delineated, pupil reacts
consensually to light but not directly. Field testing with head of hat pin reveals central
scotoma. Well defined disc edge suggests not 2ry to papilloedema (yellow grey disc
blurred margins). V early optic neruritis direct pupil reflex sluggish not absent
check Marcus Gunn phenomenon (diret reflex, then rapidly alternate pupil and will
slowly dilate).Causes: 1. mutiple sclerosis (temporal pallor only ?nystagmus, scanning
speech, cerebellar ataxia, etc), 2. compression of optic nerve by a) tumour (pituitry ?
bitemporal heminaopsia)) b) aneurysm. 3. Glaucoma (?pathological cupping), 4.
Optic atrophy in DM assoc with DID-MOAD (Diabetes insipidus, DM, deafness rare
recessive inheritence), 5. Other causes: ischemic optic atrophy (abrupt visual loss in
elderly +/- pain; thrombosis or embolus of post ciliary art; temporal arteritis), Lebers
optic atrophy (6M:1F), retinal artery occlusion, toxic ambylopia (lead, methyl alcohol,
arsenic, insecticides, quinine), nutritional ambylopia (famine, etc, tobacco-alcohol
ambylopia, B12 deficiency, DM), Freidrichs ataxia, tabes dorsalis, Pagets dx ,
consecutive optic atrophy (2ry to ganglion cell destruction)
43.
AORTIC REGURGITATION (5) Regular pulse, large volume, collapsing in
character. JVP not raised, vigourous arterial pulsations in neck (Corrigan's sign), apex
thrusting (volume overload) in ant axilliary line, 6 ICS, high pitched early diastolic
murmur audible down LSE and aortic area, louder on expiration, sitting forward.
Wide pulse pressure e.g. 250-300/30-50). Look for cause: high arched palate, aryl
robertson pupils, arthropathy/ank spond, if none then Rheumatic/IE likely. Other
signs: de Mussett sign (head nods), Quinkes signs (visible cap pulsation), Duroziez's
sign (fem art auscultated when compressed distally, diastolic murmur = retrograde
flow). Austin flint murmur=severe aortic incompetence (regurgitant jet interefes with
mitral valve). Causes: Rheumatic fever, Infective endocarditis, longstanding
hypertension (aortic dilatation, aneurysm), Marfans syndrome (tall extermities,
arachnodactyly, high arched pakate), Ank spond (male, fixed kyphosis, question
mark), Rheumatoid arthritis, coarctation of aorta (inn assoc with biscupid aortic
valve), associated with mermemranous VSD, syphilitic aortitis (argyll robertson
pupils, asc aortic anerysm), Hurlers syndrome. Indication surgery: aim to replace
valve before serious LV dysfunction occurs. Serial echoes, radionuclear angiography,
mild/moderate dx: ACEinhibitors, calcium antagonists decrease rate of deterioration.
Replace valve urgently for infective endocarditis.
44.
HEPATOMEGALLY (5) Liver palpable at x cm below right costal margin (?
icterus, ascites, signs of cirrhosis esp gynaecomastia, pigmentation, lymph
nodes). Common causes: cirrhosis usually alcohol (?spide naevi, gynaecomastia,
etc.), secondary carcinoma (?hard nobly, cachexia, evidence of primary), congestive
cardiac failure (?raised JVP, ankle oedema, S3/murmur, tender pulsatille liver wiith
giant v waves in tricuspid incompetence) Causes of hard, nobbly
hepatomegally Malignancy 1ry or 2ry, polycstic kidneydx (?kidneys?),
macronodular cirrhosis (after hep B with widespread necrosis), hydatid cysts
(eosinophylia, rupture -> anaphylaxis), syphilitic gummas (late benign syphilis
usually hepatosplenomeggaly and anemia, rapid response to penicillin). Other causes
of hepatomegally: infection (hep A/B, glandular fever, Weils dx), primary tumours
(hepatoma, adenoma), lymphoproliferative (?lymph nodes), PBC (?middle aged
female, scratch marks, xanthelasma), haemochromatosis (male, slate grey),
sarcoidosis (?erythema nodosum, lupus pernio, chest signs), amyloidosis (?
rheumatoid artritis or other chronic dx), hydatid cyst (?welsh connection Nb

patients name), amoebic abscess (?tropical connection ?name ?appeaance), budd

chiari syndrome (?icterus, ascites, tenser hepatomegally), Reidels lobe, emphysema
(apparent hepatomegally).
45.
CHARCOT MARIE TOOTH DISEASE (5) Distal wasting of lower limbs,
relatively preserved thighs. Pes cavus, clawing of toes, weakness of extensors of toes
and feet. Ankle jerks are absent, plantars no response. Only slight distal sensory
sensoty loss, lateral popliteal ?and ulnar nerves palpable (in some families only),
steppage gait due to bilateral foot drop. May be wasting of small muscles of
hand. Commentry:Variable inheritance. deformity>>disability. Rarely: Talipes
eqionovarus, toe retraction, fasciculation. Mainly motor nerves, also dorsal
roots/columns, pyramidal tracts slightly effected. Condition becomes arrested in
midlife. FH: formes fruste (minor changes e,g, pes cavus, absent ankle jerks only).
Inverted champagne botle legs is more neuromythology.There is slow progression up
the limbs.
46.
MOTOR NEURONE DISEASE (5) Weakness, wasting, fasciculation of
hand, arms, shoulder, but upper limb reflexes are exagerated (Progressive muscular
atrophy minimal pyramidal signs can be inc, dec, absent). There is upper motor
neurone spastic weakness with exagerated reflexes in the legs. (amyptrophic lateral
sclerosis). Ankle clonus, bilateral extensor plantars, may have indistinct nasal speech,
fasciculating tongue and palatal paralysis (progressive bulbar palsy). There are no
sensory signs. Other causes of fasciculations: cervical spondylosis, syringomyelia
(dissoc sensory loss), Charcot Marie Tooth (champagne bottles, pes cavus, palpable
nerves), acute stages of poliomyelitis rarely in old polio, neuralgic amyotrophy (eg.
Following viral infection), thyrotoxic myopathy, syphilitic amyotrophy, chronic
symetrical spinal muscular atrophy, after exercise in fit adults, benign giant
fasciculations. DD of MND: cervical cord compression (Cx MRI), syphilitic myopathy,
occasionally old polio, spinal muscular atrophy juvenile onset type 3 (Kugelberg
Welander dx) survival motor neurone gene defect.
47.
ULNAR PALSY (5) Generalised muscle wasting of hands (dorsal guttering,
loss hypothenar eminence), weakness sparing the thenar eminence. Sensory loss over
5[SUP]th[/SUP] finger, adjacent half of 4[SUP]th[/SUP] finger, darsal and palmer
aspects of medial hand. (hyperextension at MCP joints, flexion interphalyngeal joints
in 4[SUP]th[/SUP] and 5[SUP]th[/SUP] fingers ulnar claw hand). Patient has
ulnare nerve lesion, now look at elbow for cause. Causes: 1. fracture dislocation of
elbow (?scar deformity, hx injury), 2. osteoarthrosis elbow with osteophytic
encroachment of ulnar nerve in cubital tunnel -> limited elbow movement, 3.
occupational with leaning on elbow (clerks, secretaries on telephone), 4. constant
flexion/extension elbow (bricklayer, painter/decorater, carpenter, roofer)
predisposed by shallow ulnar groove, 5. excessive carrying angle (malunion), 6.
injuries at wrist/elbow, 7. mononeuritis multiplex (DM, polyarteritis nodosa, Churg
Strauss, Rheumatoid, SLE, Wegeners, sarcoid, carcinoma, amyliod, leprosy, Sjorgens
syndrome, Lyme dx). Commentry: Wasting of small muscles pf hands due to other
causes does not preserve thenar eminence. (syringomyelia, C8 lesion (Pancoasts
tumor ?Horners), cervical rib (sensory disturbance v light).
48.
VISUAL FIELD DEFECT (5) homonymous hemianopia homonymous
hemianopia, optic tract lesion behind chiasma. Macular sparing therefore normal
acuity. Causes CVA (?ipsilateral hemiplegia, AF, heart murmur, briuts, hypertension),
2. tumour (?ipsilateral pyramidal signs, papillloedema). Bitemperal
hemianopia bitemporal field defect worse on R/L.suggesting lesion in optic chiasm.
Sometimes scotoma 2ry to compression of optic nerve causing optic atrophy. causes 1.
pituitry tumour (?acromeg
sujitvasanth10, Jun 13, 2007
#1

sujitvasanth10Guest

SUMMARIES CONTINUED
1.

VISUAL FIELD DEFECT (5) homonymous hemianopia homonymous

hemianopia, optic tract lesion behind chiasma. Macular sparing therefore normal
acuity. Causes CVA (?ipsilateral hemiplegia, AF, heart murmur, briuts, hypertension),
2. tumour (?ipsilateral pyramidal signs, papillloedema). Bitemperal
hemianopia bitemporal field defect worse on R/L.suggesting lesion in optic chiasm.
Sometimes scotoma 2ry to compression of optic nerve causing optic atrophy. causes 1.
pituitry tumour (?acromegally, hypopituitrism, gnaecomastia, galactorrhoea,
menstrual irreg), 2. carniopharygioma (calcification on skull xray), 3. supraseller
meningioma, 4. aneurysm (glioma, granuloma, mets). Funnel/tunnel vision:
visual fields constricted with central vision presevered, tunnel vision. Examine fundi
for retinitis pigmentisa, glaucoma (pathological cupping), widespread
choroidoretinitis. (occasionally seen in hysteria, papilloedema causes enlarged blind
spot and peripheral constriction). Scotoma: central scotoma. disc is pale (atrophy),
swollen and pink (papillitis), or normal (retrobulbar neuritis) causes: consider
demyelinating dx (?nystagmus, cerebellar signs, etc but MS frequently causes
retrobulbar neuritis without other signs), compression, ischaemia, Lebers optic
atrophy (6M:1F), toxins (methyl alcohol), mescular dx, nutritional (famine, tobaccoalcohol ambylopia, B12 def, DM). homonymous upper
quadrantanopia. Suggests lesion in contralateral temporal cortex. Field defects
occasionally due to retinal damage.
2.
SPINAL CORD COMPRESSION (5) Brown sequard
syndrome:difficulty walking, monoparesis R/L leg, hypertonia, muscular weakness
without wasting, hyperreflexia, extensor plantars, lossof joint position/vibration
senses on side of monoparesis, loss of pain and temp on opposite side below the level
of e.g. T8/9 segments. Theses features suugest Brown Sequard syndrome
(hemisection of spinal cord from injury, tumour, late myelopathy from radiation,
multiple sclerosis). Spinal cord compression: muscular weakness both legs, more
on R/L with hypertonia, hyperreflrxia (?clonus), bilateral extensor plantars. Soft
touch, pinprick diminished both legs up to level of e.g. T8 segment. Joinf position and
vibration in tact. No neuological abnormality in upper limbs. RECENT ONSET back
pain suggests spinal cord compression requires urgent investigation. Nat hx: midline
pain, , radiular pain, weakness, sensory loss, sphincter disturbance. Immedate
dexamethasone, X ray, CT, MRI (preferred over myelograpphy) Disc herniation:
R/L buttock is loose and droopy due to wasting of unerlying glutei, cirresponding calf
muscles flabby with weakness of extension and abduction at hip. And plantar flexion
at ankle. Pt unable to stand on toes, ankle jerk absent on effected side. Sensation
impaired on outer border of foot, outer half of sole. Walks with trendelenburg lilmp as
pelvis shifts to normal side due to weak abductors on affected side. Spinal disc
problem due to herniation of L5 disc compressing S1 root. Causes: vertebrae/discs:
fracture/dislocation, disc prolapse, spondylosis, osteoperotic vertebral collapses,
Pagets, atlanto axial dislocation )trauma, RA), ank spond, sickle cell, tumours:
epidural (mets, lymphoma, 1ry tumor), intradural extramedullary (neurofibroma,
meningioma, sarcoma, etc), intramedullary (ependymoma, astrocytoma,
2rys), haemorhage/haematomomyeloma trauma, spinal vasc malformation,
intradural spinal neoplasm, coarctation aorta, ruptures spinal cord anerysm, blood

dyscrasia, anticoagulants, inflamatoryspinal osteomyelitis, TB/Potts dx spine, spinal

arachnoiditis, intoduce blood / foreign sustances intrathecally, acute disseminated
encephalomyelitis, MS, Devic's dx, progressive necrotising myelopathy (young adults
with acute illness/malignancy), transverse myelitis.
3.
CUSHING'S SYNDROME (5) Moon face, acne, truncal obesity, buffalo
hump, thin skin (skin fold on back of hand), excessive bruising, purple striae on
abdomen (cf pale pink in obesity, stretch marks pregnancy), she is hersuite, with deep
voice, proximal muscke weakness, difficult rising normally from squatting. Best signs:
easy bruising, proximal muscle weakness. Look for underlying steroid resoinsive
inflam/autoimmune disorder. other features: hypertension, peripheral oedema (salt
retention), irregullar menses, impotence, back pain (osteoperosis, vertebral collapse,
kyphosis, loss of height), diabetes mellitus, pigmentation (esp ectopic/exogenous
ACTH), pychiatric disorder (commonly depression). Causes of Cushings: 1.
therapeutic corticosteroids, 2. therapeuric ACTH, 3. Cushing's dx (pituitry adenoma
(basophilic or chromophobe) or hypothalamic lesion leading to XS ACTH, Rare
causes 4. adrenocortical adenoma (MEA1 = 1ry parathyroidism, islet cell tumor e.f.
Zollinger Ellison, pituity tumour), 5. adrenocortical carcinoma, 6. ectopic ACTH
secreting non endocrine tumour (oat cell ca of bronchus (wt los, pigmentation, low K
alkalosis, oedema), bronchial adenoma, carcinoid tumour (usually bronchial), ca
pancreas, non teratomatous ovarian tumour. Diagnosis: 1. 24hr urinary cortisol,
overnight/low dose dexamethasone suppression test, loss of circadian rhythm, 2.
establish cause. Dex supression test, MRI. Normal response is supression with low
dose 2mg/day 2days or overnight DST 1mg night before, high dose DST 8 mg/day 2
days supresses in Cushings Dx (pit) but not extopic ACTH or adrenal tumour. CRH
test cushings dx 50% inc cortisol. 20% of FalsePos. Treatment: transpheniodal
hypophysectomy (usually microadenoma) 80% cured, medical Rx (metyrapone) with
radiotherapy. Last resort bilateral adrenalectomy risks Nelson's syndrome
(unsupressed pit tumour mass effect, often pigmented due to ACTH, visual field
defect), treat with pre-adrenalectomy radiation. prophylaxis for osteoperosis: HRT
women, testosterone men, bisphosphonates, cmmalcitriol. For all patients >7.5
mg/day prednisolone for >3 months or immediately if >15mg/day. RF: longterm
steroids, 65+, premature menopause <45, low trauma fracture, amenorrohea, slender
build, immobility, endocrine disorders (Cushings, thyrotoxicosis)
4.
ASCITES (4) Generalised swelling abdomen, everted umbilicus, flanks stony
dull on precussion , central resonance, shifting dullness, fluid thrill. Causes: 1.
cirrhosis and portal hypertension (?hypatomegally icterus, spider naevi, leuconychia
Rx diuretics spirinolactone, aioride, parascentesis, 2. intrabdominal malignancy
(esp. ovarian and gastrointestinal hard nobbly liver, mass, cachexia, nodes, e.g.
Trosier's sign), 3. Congestive cardiac failure (??raised JVP, ankle/sacral oedema,
hepatomegally pulsatile if TR, cardiomegally, tachycardia, S3, murmur) Other:
neprotic syndrome (?young, diabetes (fundi), chronic dx, amyloid, collagen dx),
hypoalbuminemia (e.g. Malabsorption), TB peritonitis (?ethnic origin, chest signs,
cirrhotics), constructive pericarditis ((JVP, abrupt xy descent, loud early S3
(pericardial knock), paradoxical pulse, clear lungs, CXR calcified pericardium), Budd
Chiarri (rapid ascites, icterus, ,smooth hepatomegally no chronic signs, underlying
tumor, OCP, polycythemia rubra vera, UC, severe dehydration), myxoedema (?facies,
ankle jereks v rare), Meigs syndrome (ovarian fibroma surgically treatable),
pancreatic dx, , chylous dx (lymphatic obstrction)
5.
SPASTIC PARAPARESIS (4) Increased tone legs, weak (if chronic
contractures, disuse atrophy), ankle clonus, petallar clonus, extensor plantars (?
abdominal reflexes, gait). Causes: 1. MS (nystagmus, stocatto speech, ataxia,
dysdiadokinesia), 2. cord compression (?sensory level, back/neck pain, no signs above
level, cx spondylosis), 3. trauma (?scar, deformity of back), 4. Birth injury (cerebral
palsy, Little's dx), 5. Motor neurone dx (?no sensory signs,
fasciculations). Other: syringpmyelia (kyphoscoliosis, wasted hands, dissociated
sensory loss, Horners syndrome), ant spinal art thrombosis (sudden onset,
dissociated sensory loss yp to level), Freidrichs ataxia (?pes cavus, cerebellar signs,

kyphoscoliosis), hereditary spastic paraplegia, SACDC (?post column loss, absent

ankle jerks, peripheral neuropathy, anemia), parasagital cranial meningioma, HTLV1
(afrocarribean pops tropical spastic paraperesis), AIDS myelopathy (late phase
direct HIV CNS involvement), general paralysis of the insane (?dementia, vacant
expression, trombone tremor of tongue), taboparesis (?Argyll Robertson pupils, post
column loss) .
6.
ABNORMAL GAIT (4) Cerebellar ataxia wide based gait, arms held wide
(upper and lower limbs tend to shake). Ataxic, tends to fall to R/L, esp during heel to
toe test which he fails. Rombers test negative. suggests cerellar dx predom R/L (finger
nose, dysdiadokinesia, nystag, stocatto dysarthria). Causes: demylinating dx, tumour,
non metastatic sydrome of malignancy (esp bronchus), alcoholic cerebellar
deterioration, other cerebellar degenerations (?Freidrichs ataxia pres cavus,
kyphoscoliosis, absent ankle jerks, extensor plantars).Spastic gait stiff, awkward
sissors or wading through mud gait suggesting spastic paraplegia. (examine tone,
reflexes, plantars, sensation to confirm) Causes of spastic paraplegia: demyelinating
disease, 2. cord compression, 3. Hereditary spastic paraplegia (rare), 4. cerebral
diplegia (rare). Sensory ataxia taxic and stamping (feet tend to throw; both heels
and toes slap on the ground). Walks on a wide base, watching his feet and the ground.
Difficulty walking heel to toe, ataxia worse on closing eyes. Rombergs positive.
Suggests sensory ataxia (look for argyl robertson pupils, anemia). Causes: 1. SACDC
(?pyramidal signs, absent ankle jerks and peripheral neuropathy, anemia, spleen, no
argyl robertson pupils), 2. Tabes dorsalis (?facies, pupils, pyramidal signs if
taboparesis present), 3. cervical myelopathy (?mid cervical reflex pattern in arms,
pyramidal signs in legs), 4. Diabetic pseudotabes (?fundi), 5. Freidrichs ataxia (pes
cavus, scoliosis, cerebllar signs), 6. demylinating dx (ataxia in MS is usually mainly
cerebellar). Parkinsonian gait: face depressed, expressionless, unblinking and
stiff, stooping gait, initially hesitent, shuffling and lost its spring. Arms held flexed
and do not swing. Hands show pill rolling tremor, gait festinant (i.e. About to fall
forward. He has Parkinsons dx. (wrists cog-wheel rigidity, elbows lead piping,
glabellar tap sign) in milder cases lessor swing of arm, tremor often
unilateral. Steppage gait: steppage gait, lifts right foot to avoid scraping toe
because he has R/L foot drop. Unable to walk on his R/L heel. Causes of foot
drop lateral popliteal n palsy (?injury below and lateral to knee), 2. Charcot Marrie
Tooth dx (?pes cavus, distal leg atrophy, hand muscles wasted, palpable lat pop +/ulnar neerve), 3. Old polio (?effected leg short due to polio as child), 4. Heavy metal
poisoning e.g. Lead. (rare). Hemiplegic gait: R/L leg stiff, with each step tilts pelvis
to other side to keep toe off ground, R leg describes semicircle, toe scraping floor,
forefoot flops to ground before heel. R/L arm flexed, held tightly to side, fist clenched.
This is hemiplegic gait. Waddling gait: lumbar lordosis, wide based waddling gait,
trunk moves side to side, pelvis dropping on each side as foot leaves ground. Toes
reach ground before heel. This suggests weakness of proximal lower limbs and pelvic
girdle. Commest causes Duchenne muscular dystrophy, polymyositis,
rickets/osteomalacia. Gait apraxia (magnetic gait) elderly person with briad
based gait, takes short steps, placing feet flat on the ground like walking on ice (sticky
feet, magnetic gait), neither turning or straight walking is fluent, tendecny to
retropulsion (therefore inc risk falls), cannot hop on 1 foot. This is gait apraxia. (look
for frontal lobe signs dementia, suck and grasp reflexes). Causes/l degen dx similar to
Alzheimers, subdural hematoma, tumour, normal pressure hydrocephalus, lacunar
state.
7.
ANKYLOSING SPONDYLITIS (4) Male, loss lumbar lordosis, fixed
kyphosis compensatory extension cervical spine to keep visual axis horizontal,
stooped question mark posture. when asked to turn to side whole body turns as a
block (rigid spine), chest expansion reduced, increased diaphragmatic excursion
causing prominent abdomen. Look at eyes for iritis, aortic incompetence, chest for
apical fibrosis. Tests:Fails Heel, hip, occiput test (against wall). Schobers test
sacral dimples , 2 marks 5 cm above and below. Distance normally increases >5cm on
flexion. Discussion: 8M:F, 87% HLA B27 positive (50% 1[SUP]st[/SUP] deg relatives

HLAB27, 9% sacroilitis). Starts <45yrs, initially asymetrical peripheral arthritis large

joints, low back pain worse on waking, better on exercise, enthesitis (plantar fascitis,
achiles tendinitis). extrarticular manifestaations: 1. iritis (acute, deep aching pain,
redness, photophobia, sluggish pupils, circumcorneal conjuctival injection causing
synechiae, cateracts), 2. aortiitis, 3. apical fibrosis, 4. cardiac conduction defects, 5.
traumatic fracture/atlantoaxial subluxation, sacroiliitis, 6. secondary amyloidosis.
8.
POLYCYTHEMIA RUBRA VERA (4) Facial plethora, dusky cyanosis face,
hands and feet (lips, tongue, musous membranes). Echymosis (spontaneous
bruising), scatch marks (pruritis), with permission pull down lower lid
conjunctival vessels engorged, fundi dilated retinal veins, splenomegally (70%),
hepatomegally (40%), blood pressure raised. 1ry polycythemia: raised red cell mass,
exlude 2ry causes including psuedopolycythemia dehydration), rbc, wcc, plt, b and
HCTall elevated. Low MCV (iron stores depleted). 2ry polycythemia: Phyiologically
apropriate: arterial hypoxemia (COPD, RtoLshunt, pickwickian syndrome), abnormal
O2 release (2,3 DPG deficiency, smokers COHb), interfence tissue O2 metab (cobalt
poisoning). Phys inappropriate neoplasm (renal, hepatocellular, ovarian, cerebellar,
hemangioblastoma, phaeochromocytoma), non neoplastic dx cysts, hydronephrosis).
9.
STRIDOR (4) Comfortable at rest, from bedside noisy high pitched sound
with each inspiration. Resp rate 12, chest expansion normal, resonance
normal,auscultation normal breath sounds, no added sounds, healed tracheostomy
scar. Likely tracheal stenosis following prologed ventilatory
support. Inspiratpry stridor: upper airway obstruction, tracheal narrowing
(extrathoracic): acute (infective epiglottitis, croup), trauma (FB, smoke inhilation),
chronic (neoplastic, tracheal stenosis). Expiratory stridor (lower intrathoracic
obstruction: FB, intralluminal mass/neoplasm, lower tracheal stenosis, bronchial
stenosis. Management: refer for rigid bronchoscopy to thoracic surgeon for dilatation
and/or stent insertion or primary reconstruction. Tracheal stenosis
causes: congenital (webs, tracheomalacia), aquired (tracheostomy or intubation),
post trauma, post infection (e.g. TB), neoplasia.
10.
PARKINSONS DISEASE (3) Expressionless, unblinking face, slurred low
volume monotonous speech, drroling (hypersalivation, dysphagia), titubation.
Difficulty starting walking (freezing), once startedshows quick shuffling steps trying
to keep up with centre of gravity, stooped, does not swing arms, continous pill rolling
tremor, poor balance, tends to fall, lead pipe rigidity at elbow, cogwheeling at wrist.
Positive glabellar tap, signs generally asymetric (decreased by intention,) handwriting
small, treulous untidy, blephroclonus (eyeslid tremor when gently
closed). Discussion: 3M:1F. Features: tremor, rigidity, bradykinesia (touch thumb
with each finger slow initiation, fatiguability), cannot perform 2 motor tasks
simultaneously. PD often misdiagnosed as benign essential tremor (aut dom,
intention tremor worsened by stress, no other focal abnormality, improves with
alcohol, sometimes diazepam, propranolol). Causes of Parkinsonism: drug induced,
postencephalopathic, axonal brain damage (cardiac arrest, carbon monoxide,
Manganeses poisoning), neurosyphilis, cerebral tumours affecting basal
ganglia. Stiff-Man syndrome: rare disease severe progressive muscle stiffness,
spine lower extremities superimposed muscle spasms trigerred by ext
stimulus/emotion falls like tin soldier. Age 30-50 respons to bdz. EMG
characyeristic, 60% anti GAD ab positive. Also seen in aotuimmune condition DM,
thyroid, vitiligo, pernicous anemia). Diseases with Extrapyramidalfeatures:
1. arterioscclerotic Parkinsons, 2. normal pressure hydrocephalus (head injury,
meningitis, SAH, idiopathic triad: urinary incontinence, gait apraxia, dementia
CT/MRI diagnosis consider ventriculosystemic shunt), 3. Steele-RichardsonOlszewski syndrome(supranuclear gaze palsy, axial rigidity,tendency to fall
backwards, pyramidal signs, subtle dementia/frontal lobe syndrome), 4. stratonigral
degeneration: part of mutisystem atrophy (autonomic failure, olivopontocerebellar
atrophy), 5. Alzheimers dx (severe dementia, mild extrapyramidal), 6. Wilsons dx
(Kyser-Fleisher rings, cirrhosis, chorea, psychotic behaviour, dysarthria, dystonic
spasms/posturing, dementia if untreated), 7. Jakob-Creutzfeldt dx (prion

11.

12.

13.

14.

encephalopathy, rapidly progressive dementia, myoclonus, multifocal neuro signs

aphasia, cerebellat ataxia, cortical blindness, spasticity), 8. hypoparathroidism (basal
ganglia calcification).
MULTIPLE SCLEROSIS (3) Cerebellar syndrome: ?young adult, ataxic
nystagmus, ionternuclear opthalmoplegia, temporal pallor of discs, slurred speech
with ataxia and widespread cerebellar signs. Pyramidal and dorsal column signs. Most
likely diagnosis is demyelinating dx (useful euphamism) Spastic paraparesis: ?
middle aged, increased tone, bilateral spasticity, weakness, bilateral clonus, petellar
clonus, extensor plantars. Abdominal reflexes absent, heel-shin test suggests some
ataxia in legs, slight upper limb dysdiadokinesia. Suggests spastic paraplegia due to
demyelinating dx. Fundi may show involvement. Discussion: 2M:3F, rare in tropics,
usually euphoria despite disability, unpredictable course (acute, subacute, remitting
(66%), insidious), worsens with temp, fatigue, paroxysmal symptoms may respond to
carbemazepine, Lhermitte's phenomenon (Tingling down spine on bending
neck). Benign course: if pure sensory presentation, long remissions, infrequent
relapses, onest with optic/sensorimotor (i.e. NOT cerebellar/brainstem), benign
condition after 5 years.).Investigations: Check VEP's (delayed), CSF oligoclonal bands
in CSF but not in serrum, <1g/l protein,lymphocytosis up to 50 cells/mm3.
Oligoclonal bands also in infection, stroke, brain tumour. MRI scan best imaging
modality.
VENTRICULAR SEPTAL DEFECT (3) Often young patient, regular pulse,
normal JVP. Apex displaced half way bttween mid clavicular and ant ax line. Left
parasternal heave, possible thrill. Pansystolic murmur LSE, also aidible at apex. Loud
p2 if pulm hypertension, possible pulmonary regurgitation. Other features of
VSD Maladie de Roger, Eisenmengers complex, acute SBE, 5% assoc AR, mitral middiastolic flow murmur in large shunt. Associations acute MI with septal rupture,
downs, turners. Percutaneous transcatheter closure. Conxlude with heamodynamic
significance. Muscular septum defects close spotaneously duting childhood.
DERMATOMYSOSITIS (3) Heliotrope rash, over eyelids and periorbital
areas, back of hands especially knuckles (Gottron's papules=flat topped violaceous
papules), and fingernails (prominent nail-fold telangectasias), extensor sirfaces
elbows/knees. Subcutaneous oedema (mainly eyes) proximal muscle weakness +/tenderness.(heliotropum=fragrent purple flowers). Other features like polymyosistis,
associated malinancy (current recommendation 40+ yrs investigate for breast, ovary,
lung, GI tract), overlap with Rheumatic fever, rheumatoid arthritis, scleroderma,
lupus, other conn tissue dx steroid responsiveness more likely),dysphagia due to
upper oesophagus involvement, Raynaud's, arthralgia, subcutaneous/ intramuscular
calcification. Investigations: muscle enzymes (aldolase, CPU), urine creatine, EMG
(fibrillation, polyphasic action potentials, high freq bizare discharges), muscle biopsy.
ESR often normal. Treatment: steroids (initially high dose), high dose iv
immunoglobculins if refractory, azathioprine. Discussion: 2M:F May present with
pseudohematuria (myoglobinemia). Juvenile form occurs 1st decade, myopathy,
contractures, skin/muscle calcification, raynauds rare, not assoc malignancy.
ADDISONS DISEASE (3) Generalised pigmentation due to ACTH
increasing melanin, more marked in skin creases (e.g. Palmer), in scars (esp recent
ones), buccal mucosa, in nipples and pressure points (also periorbital). Diagnosis
Addisons or Nelsons (?temporal field defect, ?abdominal scar for bilateral
adrenalectomy). may have associated premature ovarian failure and vitiligo (also
associated with thyroiditis, DM, pernicious ane,ia, hypoparathyroidism). Causes of
1ry hypoadrenalism: autoimmune adrenalitis, TB (?lung signs), bilateral
adrebalectomy, secondary deposits, amyloidosis (hypoaadenalism preceded by
nephrotic syndrome), haemochromatosis, granulomatous dx (rarley sarcoidosis),
fungal dx (histoplasmosis), comgenital adrenal hyperplasia (inherited defects e.g. 21OH def -> neonatal salt wasting, low bp, ambiguous genitalia in females),
meningococcal and pseudomonal sepsis. AIDS related hypoadrenalism: adrenal
haemorrhage (newborns esp breech, anticoagulants), adrenal vein thrombosis after
trauma/venography). Causes of Skin pigmentation: racial including skin

pigment, sun tanning, endocrine (ACTH therapy (e.g. Asthma), Cushings dx,
thyrotoxicosis, extopic ACTH), chronic debilitation (malignancy, malabsorption,
chronic infection esp TB, cirrhosis, uremia), pigments (haemochromatosis slate
grey, hepatosplenomegally, arhyria, chronic arsenic poisoning), drugs
(phenothiazines (blue-grey), antimalarials (blue grey), amiodarone (grey), cytotoxics,
minocycline (purple-blue bone and blue oral discoloration).
15.
ABDOMINAL MASS (2, 4) Mass RIF: young, somewhat pale adult, freely
mobile 5x4 cm (measure) firm non-tender mass RIF. No abdominal organs enlarged,
no fitulae. This is Crohn's disease. Causes: illiocecal TB (?asian ?chest signs),
carcinoma caecum (?older person, non tender hard mass, lymph nodes, colonoscopy),
amoebic abscess (?travel), lymphoma (?hepatosplenomegally, lymph nodes
eksewhere, investigate CT), appendix abscess (investigate with US), ovarian tumour
(US, CT), ileal carcinoid (rare) Mass LIF: ekderly patient with freely mobile
6x5 mass in LIF, no organomegally. This is probably a diverticular
abscess usually tender. Investe with: US/CT. Causes: carcinoma colon
(non tender, hepatomegally, colonoscopy), ovarian tumour (US/CT),
faecal mass, amoebic abscess. Epigastric mass: round hard non tender mass
8x6 cm with ill defined edges in epigastrium. Does not move with respiration, no
hepatosplenomegally. Check for cervical lymph nodes ?Troisiers sign. Causes:
carcinoma stomach, (Troisier's sign, OGD), carcinoma pancreas (?icterus, ?
courvoisier's sign palpable gall bladder unlikely stones, needs CT), lymphoma
(generalised lymphadenopathy, splenomegally, needs CT). Pulsatile mass: vulsatile
abdominal mass (anterior and transverse) 6x4 cm palpable 2 cm above umbilicus
reaching to epigastrium. Femoral pulses palpable just before radials (i.e no
dissection), no bruits over mass or femorals., look for PVD in feet. Likely AAA
commonest cause atherosclerosis. Mass in upper abdomen: define size, shape,
consistency, get above?, bimanually ballotable?, moves with respiration?, tender?.
Must differentiate from renal mass, spleen or liver. Causes: carcinoma colon,
retroperitoneal sarcoma, lymphoma (generalised lymphadenopathy, spleen),
diverticular abscess (?tender),
16.
MARFAN'S SYNDROME (2) Tall with disproprtionatley long extremities
(pubis-sole > pubis-vertex), elongated fingers and toes (arachnodactyly), high arched
palate, long narrow face, span greater then height. Underdeveloped musculature,
hypotonia (+/- funnel/pigeon chest, pectus excavatum, kyphoscoliosis, flat feet, genu
recurvatum, hypertextendable joints, recurrent dislocations). Tremor of the iris
(iridodenesis) often only visible on slit lamp suggesting lens dislocation. May have
collapsing pulse, auscultate for AR (cystic necrosis of aortic media, disscetion can
occur) Other signs: heterochromia of iris, myopia, retinal detachment, cystic lung
disease (pnemothorax, bullae, apical fibrosis, aspergilloma, bronchiectasis), mitral
valve prolapse, aortic coarctation, bacterial endocarditis, inguinal/femoral hernia,
decreased subcutaneous fat, Meischer's elastoma (smooth nodules/papules in neck
skin). Discussion: Life expectency 40 years. beta blockade decreases development of
aortic complications in some patients. Aut dominant, fibrillin defect Chr
15q. Homocystinuria can appear similar (other abnormalities mental retardation,
malar flusj, osteoperosis, DOWNWARD lens dislocation (Marfans upgoing). Urine
cyanide-nitrprusside test positive).
17.
LMN FACIAL PALSY (2) On the R/L side there is paralysis of upper and
lower face, so the eye cannot be closed (or can be easily opened by examiner; cannot
bury eyelashes), the ee turns up on attempted closure (Bell's phenomenon) and
unable to to raise R/L eyebrow. Corner of mouth droops, nasolabial fold smoothed
out, volunatary and involunatey movements of mouth paralysed on R/L.(lips and
tongue drawn opposite side). Look for heerpes in ear/on neck (trigeminal, cervical,
occipital). Causes: 1. Bells palsy, 2. Ramsay Hunt syndrome (herpes zoster on ext
aud meatus and geniculate ganglion taste ant 2/3 tongue lost +/- palatal lesions)
Facial weakness includes frontalis (raise eyebrows), corrugator superficialis (frown),
orbicularis oculi (close your eyes tight). Taste preserved in mild Bell's palsy (swelling
nerve in facial canal), more severe taste lost, stapedius paralysis causes

hyperacusis). Differential diagnosis:cerebellopntine angle compression (acoustic

neuroma or meningioma 5,6,7,8 palsy, cerebellar signs, tast loss ant 2/3/ tingue),
parotid tunour (?palpable, taste not affected.), trauma, pontine lesion (MS, tumour,
vascular lesion), middle ear dx (deafness), mononeuritis multiplex (DM,PAN, Churg
Strauss, Rheumatoid, SLE, Wegeners, sarcoid, carcinoma. Amyloid,
leprosy). bilateral LMN CN7 palsy easily missed as no asymettry. Casues: Guillain
Barre, sarcoidosis, bilateral Bell's, myasthenia gravis (?ptosis, variable strabismus,
proximal muscle weakness), cingenital facial diplegia, some muscular dystrophies,
MND (rarely), Lyme dx (classic bilateral CN7+/- meningoencephalitis, peripheral
radiculopathy, peripheral radiculopathy, knee effusion, ruptured Baker's cyst, heart
block). Discussion: chorda typani:leavesfacial nerve in middle to supply ant 2/3
tongue. Sup petrosal branch leaves before this to supply lacrymal gland and stepdius.
18.
CARPAL TUNNEL (2) Stout middle aged lady, complaining of pain,
numbness or paresthesia in palm and fingers, particularly bad at night. Sensory loss
over palmer three and a half fingers and wasting of thenar eminence. Weakness of
abduction, flexion and opposition of thumb.Non invlovement of forearm flexors
i.e. Can flex DIP thumb) suggests carpal tunnel syndrome. Check for facies
(acromegally, myxoedema) and rheumatoid arthritis. Tennels sign to confirm
(percussion paraesthesia), Phallens sign (flex wrists 1 minute), torniquet test (2
minutes above systolic -> parethesia). Investigation: nerve conduction
studies Treatment: intrcarpal steroid injections, surgical
decompression. Causes: idiopathic (females, middle aged obese, younger women
excessive hand use, males with unaccustomed hand use), pregnancy, OCP.
Myxoedema (?facies, hoarse voice, pulse, ankle jerks), acromegally (?facies, large
spade-like hands, hemianopia), Rheumatoid arthritis (?spindling of fingers, ulnar
deviation, nodules), osteoarthrosis (?related to old fracture), tuberculous
tenosynovitis, primary amyliodosis (?peripheral neuropathy, thick nerves, autonomic
neuropathy, heart, joint, gut (rectal bx), tophacous gout.
19.
ATRIAL FIBRILLATION (2) Pulse is ..../min and irregularly irregular in
rate and volume suggesting atrial fibrillation with a controlled ventricular response
(uncontrolled if >90). look at neck (goitre), eyes (exopthalmos), face (mitral faces,
hypothyroidism, hemiplegia), chest (thoracotomy scar). Differetial
Diagnosis: mutiple extrasystoles (only 1 pause at a time, may be abolished with
exercise cf AF which is worsened), A flutter with variable block, multiple atrial
ectopics with shifting pacemaker, paroxysmal atrial tachycaria with block. Causes of
AF: 1. ischaemic heart disease (esp MI), sinoatrial (sick sinus syndrome) disease with
primay involvement of conduction tissue, rheumatic heart disease, hypertensive heart
disease, thyrotoxicosis, cardiomyopathy (idiopathic i.e. -ve angiogram, viral, dilative
often 2ry to IHD), acute infection esp lung, constrictive pericarditis, local neoplastic
infiltration (paricularly lymphoma). Treatment: anticoagulation (see latest
guidelines), role of cardioversion, treatment aim (rate control vs
cardioversion). Causes of cardiomyopathy: 1. Toxic (alcohol, adriamycin,
cyclophosohamide, emetine, corticosteroids, lithium, phenothiazines), 2. metabolic
(thiamine deficiency, kwashiokor, pallegra, obesity, prophyria, uremia, electrolyte
imbalance), 3. endocrine (thyrotoxicosis, acromegally, myxoedema, |Cushings, DM),
4. Colleagen dx (SLE, pAN, etc), 5. infiltrative (myloidosis, heamochromatosis,
neoplastic, glycogen storage dx, sarcoidosis, mucopolysaccharideosis, gaucher's,
Whipples dx), 6. infective (viral, rickettsial, mycobacterial), genetic (HOCM, muscular
dystrophies) , 7. fibroplastic (endomyocardial fibrosis, Lofflers endocarditis,
carcinoid), 9. misc (postpartum, icessent atrial tachycardia).
20.
HYPERTROPHIC CARDIOMYOPATHY (2) Regular or irregular pulse,
normal volume (jerky if very severe(, JVP not elevate (may show a wave), forcefull
apex 5ICS, just lateral to MCL, may be double apical impulse caused by a strong
presysolic impulse of atrial systole), thrill at left sternal border, 4[SUP]th[/SUP] heart
sound, ejection systolic murmur (may be harsh) over left 3[SUP]rd[/SUP] interspace,
radiates WIDELY to base and axilla. There may be mitral regurgitation. Intensity
enhamced by minimal exercise. Discussion: symptoms: asymptomatic, sob,

palpitations, angina, dizziness, syncope often after cessation after exercise (decreased
CO or VT) cf aortic stenosis DURING exercise. ECG normal in 25%, tall QRS midprecordial leads, septal hypertrophy (Q inf and lat precordia; ;eads), LAD. CXR
normal or left atrial enlargement. Echo: asymetrical septal hypertrophy, systolic
anterior motion of mitral valve leaflet. HCM = aut dom various myosin genes, often
de novo, variable penetrance, offer 1[SUP]st[/SUP] deg relarives screening. Risk
factors of poor outcome: syncope, FH sudden death, poor bp response to exercise,
ventricular arrythmiad, outflow tract gradient >40 mmHg, septal thickness >18 mm.
Treatment: beta blockers, rate limiting calcium antags, septal ablation, myomectomy,
pacing (ICD for high risk individuals).
21.
TARDIVE DYSKINESIA (2) Elderly patient with chronic schizophrenia
with stereotyped tic-like orofacial dyskinetic (involuntary movements) including lip
smaking, chewing, pouting and grimacing. There may be choreoathetoosis of limbs
and trunk. It is likely patient on sustained phenothiazine treatment for at least 6
months. tardive = not occuring till 3 months. Discussion: Condition often persists
even after drug withdrawn. Neuroleptics that ihibit dopamine: phenothiazines
(chlorpromazine), butyrophenones (haloperidol), substituted benzamides
(metoclopromide), reserpine, tetrabenazine. other neuoleptic induced
extrapyramidal reactions: acute dystonia (soon after starting drug e.g. oculogyric
crisis), akathasia (restlessness, unease), Parkinson's syndrome (tremor less common,
responds to anticholinergics rather than Ldopa)
22.
LUNG TRANSPLANT (2) Successful lung transplant: young man
(major operative procedure for severe chronic respiratory problem) not breathless at
rest, RR=12, bilateral clubbing, midline sternotomy, equal expansion bilaterally,
precussion and breath sounds normal. I suspect cystic fribrosis with successful double
lung transplant. Bronchiolitis obliterans syndrome: middle aged woman with
right lung transplant increasingly breathless over last few months. RR=18. Oxygen
2l.min nasal cannulae, bilateral clubbing, features of Cushing's syndrome, right
thoracotomy scar, reduced exapnsion both lungs, left base dull to precussion, fine
inspiratory crackles to mid zones left lung, few scattered inspiratory squeeks right
lung. Suggest lung transplant for pulmonary fibrosis, there may have been recurrent
episodes of acute rejection now developed borchiolitis obliterans syndrome requiring
large doses of steroids and continuous oxygen therapy. Spirometry recording book,
may be on active transplantation list llok for a bleeper.Inidcations for Lung
transplant: pulmonary hypertension:primary, or secondary to systemic disease
and Eisenmengers syndrome. Restrictive lung disease: pulmonary fibrosis
(idiopathic, secondary to connective tissue disease, sarcoidosis, chronic allergic
alveolitis), Obstructive lung disease (emphysema, alpha1antitrypsin deficuency,
Langerhans cell granulomatosis, lymphagioleiomyomatosis. Suppurative lung
disease includes cystic fibrosis, bronchiectasis.Complications: perioperative (e.g.
Graft dehiscence), infection: viral (CMV, HSV, bacterial, fungal Candida,
Aspergillus, other pneumocystis), rejection hyperacute (within hours), acute
(common 1-2 episodes in first 6 months\0, bronchiolitis obliterans syndrome
progressive obstruction rapid progression, poor survival. Acute rejectiion=non
productuve cough, dyspnoea, malaise, irreversible airflow obstruction, reduced TLC
and gas transfer. No effective treatment immuosuppressives commonly tried.
Consider retrasplantation, drug side effects azathioprine, cyclosporin,
corticosteroids.
23.
CHOREOATHETOSIS (2) Brief, jerky, abrupt, quasi purposeful involuntary
movements (do not integrate into a coordinated act). Movements flit to dofferent
parts of body randomly, present at rest, accentuated by activity preventing relaxation
and distorting movement, general air of restlessness, unable to protrude tongue (darts
in and out), abnormal posturing of hands (wristr flexed, fingers hyperextended at
MCP joints). When the upper limbs are raised there is pronation of the forearm. This
is chorea. Causes: sydenham chorea (5-15 yrs old, ?heart murmur, 1/3 Hx
Rheumatic fever, may occur during preg or OCP), huntingtons chorea (often lower
limbs, dancing gait, dementia, age 30-40, family history), drug induced chorea

(neuroleptics, L-dopa), senile chorea (idiopathic orofacial dyskinesia no

dementia), other(epidemic encephalitis, assoc exanthem, idiopathic hypocalcemia,
throtoxicosis, SLE, carbon monoxide, Wilsons).Hemichorea/hemibalism: CVA (?
hemiplegia, hemianopia), intracerebral tumour (?pyramidal, chorea, papiloedema),
trauma, post-thlamectomy. Other dyskinesias: athetosis (slow coarse irregular
writhing muscular distortion hands, feet, digits, occasionally face,
tongue), dystonia (sustained deforming spasm e.g. torticollis, some may result on
lordosis, scoliosis)., myoclonus (shock-like jerks e.g. Epilepsy, essential familial,
physiologic (sleep, exrecise, anxiety), metabolic (renal, resp, hepatic), subacute
encephalitis), tremors (PD, thhyrotoxicosis, drugs (alcohol, caffein, salbutamol), MS,
spinocerebellar degeneration, CVA, essential/familial), tics.