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By Dr Sonam Tshering

High yield notes for Paces St 2 & 5
2nd Edition
Complied by Paces network team
© Copyrights with dr Sonam Tshering. All rights reserved
By Dr Sonam Tshering
High yield notes for Paces
St 2 & 5
Complied by Paces network team
© Copyrights with dr Sonam Tshering. All rights

Can present as:

 Carpal tunnel syndrome

 Headaches
 Bitemporal hemianopia/vision problem

Clinical communication skills :

Focused presenting history:
 Carpal tunnel syndrome- tingling of lateral 3 and half fingers,
pain more at night, look for scars at wrist for carpal tunnel
release surgery, wasting of thenar muscle
 Change in appearance over time? Change in shoe and ring
size? Old photographs?
 Headaches, sweating
 Bumping into objects, decreased vision
 DM-increased thirst
 Joint pains
 OSA-daytime somnolence, early morning headaches, snoring
 CCF features
 Proximal myopathy
 Alarm symptoms( change in bowel habit, rectal bleeding,
severe headache with double vision with ptosis(pituitary

Past medical and surgical history:

 DM, HTN, OSA, arthopathy, CCF, CTS
 Transphenoidal surgery, carpal tunnel release

Drug history:
Social history
Family history
Personal history-?smoker
Occupational history: ?taxi driver
Physical examination:
 Hands- large and doughy (spade like) hand, look for CTS,
sweaty? BM testing marks
 Face- prominent supraorbital ridges, enlarged nose and lips,
prognathism, bitemporal hemianopia, visual acuity and
othalmoscopy for optic atrophy, macroglossia, interdental
separation, look for surgical scars (transphenoidal surgery
inside the nose, underside of upper lips,
transcranial(forehead or side of head)
 Neck-?goiter
 Chest and axilla-gynaecomastia, hyperpigmentation, skin
tags, acanthosis nigricans, hirsuitism
 Heart- ?ccf
 Check for proximal myopathy
 Features of hypopituitarism
 Ask to measure BP, dip urine for glycosuria, any old

Concerns and questions? And addressing it

 Your symptoms are due to a benign growth in the pituitary

gland that produces too much of growth hormone. For your
headaches, I am going to give pain killers as a temporary
measure however, it is very important to establish the cause
with urgent investigations.
 As your vision is impaired, I am afraid you will have to inform
DVLA and stop driving immediately.
 I am going to do some urgent blood tests and urgent
scan(mri) of brain and ask the eye specialists to see you to
assess what extent the growth has affected vision.
 Most physical features do not regress after treatment(if

 Failure of GH to suppress to <2nmol/l following OGTT.
 IGF1
 MRI of pituitary
 Test anterior pituitary function(TFT, LH, FSH, Testosterone,
short synacthen test, cortisol levels)
 Test for complications- fasting blood glucose, measure BP ,
ECG, ECHO, Nerve conduction studies for CTS, sleep studies
for OSA, visual perimetry, colonoscopy

Treatment :
 Surgery-transphenoidal hypophysectomy
 Radiotherapy
 Medical-somatostatin analogues(octreotride and
lancreotide), dopamine agonists, GH receptor

Active disease
 Sweating
 Skin tags
 Peripheral oedema
Acute Kidney Injury


 Pre renal- hypovolumia (diuretics, vomiting, diarrhoea,

haemorrage, pancreatitis,burns, decreased renal perfusion
due to sepsis, anaphylaxis, heart failure, ACEi and ARB in
volume depleted patients, hepatorenal syndrome)

 Renal- ATN, Tubulo interstitial nephritis, GN

1. Vascular( renal vein/artery obstruction with thrombosis
and emboli, microangiopathy(TTP, HUS, DIC), scleroderma
renal crisis, malignant HTN
2. Glomerular causes (anti-GBM disease/goodpsature
syndrome, ANCA-associated glomerulonephritis,
postinfectious GN)
3. Tubular-rhabdomyolysis, tumour lysis syndrome,
aminoglycoside, contrast agents, lithium
4. Interstitial causes- Drugs such as penicillins,
cephalosporins, NSAIDs, PPI…, pyelonephritis, lupus,

 Post renal-renal outflow tract oubstruction-stone disease,

stricture, tumours, thrombosis, fibrosis

Presenting illness:

 Reduction in urine output, dysuria, frequency, haematuria

 Uraemia?- restlessness, confusion(encephalopathy), chest
 Fluid overload( dyspnea, oedema) or hypovolumia( thirsty ,
 Look for the causes as above

Past medical history- DM, HTN, connective tissue diseases,

vasculitis, PKD, renal stone,
Drug history*

Physical examination:

 Observation chart-Pulse, BP, urine output

 Examine fluid status- hypervolumia or hypovolumia
 Uraemia- flapping tremor, confusion
 Abdomen-palpable PKD, palpable bladder in obstruction


 S.Electrolytes
 Urine microscopy
 ECG(hyperkalaemia)
 USG renal tract
 Cxr(fliud overload)
 Look for the causes


 Stop nephrotoxic medications

 i/v fluids to optimize volume status
 adjust antibiotic doses for renal dysfunction
 management of hyperkalaemia
 haemodialysis may be needed
Addisons disease

Can present as:

 Tiredness and fatigue

 Postural hypotension
 Skin pigmentation

DD for tiredness
 Addisons disease
 Anaemia( blood loss?
 Hypothyroidsm
 DM
DD of postural hypotension:
 Addisons disease
 DM
 Fluid loss
 Drugs
 parkinsons

Focused history:
Presenting illness:
 Tiredness-duration, variation during day, ?effect on quality of
 Postural hypo-dizzy while standing, any collapse?
 Skin changes
 Loss of appetite, weight loss
 GIT-vomiting,diarrhoea , abdominal pain
 Look for causes of addisons( features of TB, cancer
 Exclude DDs such as hypothyroidsm, OSA, DM, Anaemia
 Other autoimmune diseases(graves,DM, connective tissue
diseases, celiac disease, pernicious anaemia)

Past medical and surgical history: TB? DM, Vitiligo, previous

pituitary surgery
Drug history: ?steroid use
Personal history: smoker?
Social, family and occupational history:
Menstrual history: amenorrhoea/oligo
Travel history: contact with TB

Physical examination:
 Hands-pigmentation of palmer creases, pulse, ask to
measure lying and standing BP
 Face-pallor, oral cavity for pigmentation, ?cushingoid
 Neck- any goiter?
 Chest-?vitiligo, TB? Loss of hair esp in females
 Abdomen: scars for adrenalectomy
 Visual field defects(nelsons syndrome)

Addressing concerns :
 I think your symptoms are caused by a condition called
addisons disease where your body is not able to produce
enough natural steroids from a gland called adrenal gland
located above kidneys.
 we will have to admit you to confirm investigations and also
to exclude other causes such as anaemia, DM. if we start
treatment without confirmation, it will interfere with the
 the treatment is lifelong replacement of steroids, need to
increase dose in physiological stress
 steroid alert card/medic alert bracelet,

 FBC(lymphocytosis, eosinophilia, anaemia)
 S.electrolytes(hyponatraemia, hyperkalaemia)
 RBS-Hypoglycemia
 Short synacthen test( if after injection of synacthen, cortisol
level increases >550nmol/l, then addisions can be excluded)
 9 am cortisol
 Adrenal autoantibodies
 ACTH (raised in primary hypoadrenalism)
 Imaging-CXR(TB), CT adrenal glands

Treatment :
 If in adrenal crisis-fluid resuscitation, i/v hydrocortisone
 Chronic case:
Glucocorticoid replacement(hydro or prednisolone)
Mineralocorticoid replacement(fludrocortisones for postural
Androgen replacement

DX: primary hypoadrenalism(addisons disease) likely

cause is autoimmune/tb

Nelson’s syndrome: bilateral adrenalectomy done for

cushings syn resulting in loss of negative feedback loop , so
high ACTH levels causing enlarged pituitary glands and
hence diffuse skin pigmentation(MSH), look for bitemporal

Polyglandular autoimmune syndrome:

 Type 1: addisons, hypoparathyroidism, chronic
mucocutaneous candidiasis
 Type 2: addisons, Type 1 DM, thyroid disease(hypo or hyper)
Ankylosing spondylitis

Can present as:

 Low back pain and stiffness

 Exertional dyspnea(pulmonary fibrosis)

DD of low back pain and stiffness:

 Ankylosing spondylitis
 Other seronegative arthritis(psoriatic, enteropathic, reactive)
 Rheumatoid arthritis
 Osteoarthritis

Focused history of presenting illness:

 Low back pain-onset, duration, severity, variation,
exacerbating and relieving factors, radiation, morning
stiffness, effect on life? ( pain is worse at night and morning
with stiffness, exercise helps it)
 Any other joints involved?
 Heel pain?
 Red eyes
 Sob(pulmonary fibrosis)
 AR(palpitations, sob, leg swelling)
 IBD-Bowel habits, mouth ulcers?
 Skin rash(psoriasis)
 Any trauma? Fever?
 Alarm symptoms- spinal cord compression?

Past medical and surgical history: IBD? Psoriasis?

Medication history: NSAIDs? Any side effects?
Family history? *
Personal history
Occupational history?
Social history? Living alone?
Physical examination:
 Ask to walk- question mark, Stooped posture? Loss of
lumber lordosis and exaggerated thoracic kyphosis and neck
hyperextension, protuberant abdomen
 Check cervical movements
 Check low back movements(fix the patients pelvis before the
 auscultate lung apex for pulmonary fibrosis
 heart for AR, pacemakers(conduction blocks)?
 Eyes for anterior uveitis
 Ask to perform modified schober’s test
 occiput wall distance test
 ask to check chest expansibility
 Urine dip for proteinuria( amyloidosis , NSAID induced

Addressing concerns and questions:

 You might have a condition called ankylosing spondylitis
where your own immune system is mistakenly attacking the
spine and other joints leading to pain and stiffness
 For your pain, we will start with pain killers/anti-inflammatory
agents and will ask physiotherapists to see you
 We will do some blood tests(inflammatory markers) and
obtain an X ray of your back and also MRI scan of your back
 I will refer to AS clinics for detailed measurements and also
Rheumatologist who can start you with medication to
dampen down the immune system if not responding to initial
 ?help of occupational therapists if needed
 Inform the employer about diagnosis for work adjustments
 15-20% chance to get it if 1st degree relative has it, 2%
chance if HLA B27 positive
 Info about support groups

 Inflammatory markers-ESR, CRP, CBC(anaemia)
 HLA B27
 RFT and URE(for Amyloidosis)
 X ray of LS spine and sacroiliac joint
 MRI of LS spine and sacroiliac joint
 CXR, Pulmonary function tests, HRCT for Pul fibrosis
 ECHO for AR

Treatment : MDT approach

 Exercise, physiotherapy, occupational therapy
 NSAIDs(1st line), intraarticular steroids
 DMARDs (sulphasalazine) may be effective in peripheral
 Biological agents -Anti-TNF alpha therapy(etanercept,
 Surgical-hip replacement

Extra-articular features:
 Anterior uveitis
 Apical pul fibrosis
 AR, Aortic conduction blocks
 Atlanto-axial subluxation
 Achilles tendinitis
 Amyloidosis, IgA nephropathy
Avascular necrosis of femoral head/osteonecrosis

*results from interruption of blood supply to the bone

Clinical features: non-specific symptoms and signs

 Painless in early stage

 Pain and limitation of motion-pain mostly localized to groin
area, sometimes in ispilateral buttock, greater trochanteric
region, and knee. Exacerbated with weight bearing and
relieved by rest

 Traumatic, displaced femoral neck fracture, hip dislocation,
 Atraumatic- steroid , alcohol abuse,
DIC/coagulopathies/thrombophilias, chemotherapy,
radiation, sickle cell disease, vasculitis, SLE


 Imaging- x ray hip, MRI hip(choice), bone scan

 Lab- CBC, Clotting profile, HB electrophoresis(sickle cell)
 Angiography(invasive means of confirmation)

X ray features- subcondral sclerosis, increased lucency, flattening

of femoral head, joint space narrowing, collapse of femoral head

MRI –low signal intensity band (indicate necrotic femoral head)


 Address risk factors if any

 Analgesics for pain
 Restricted weight bearing with use of a cane or crutches
 Surgical intervention
1. Prophylactic measures- core decompression( necrotic
femoral head is removed in order to stimulate repair),
often supplemented with bone grafting
2. Reconstruction procedures- hip replacement
Behcet’s disease

Stem-painful red and blurring of vision in one eye (anterior


Anterior uveitis associations:

 Rheumatological-Behcet’s disease, seronegative arthritis, RA

 Infection-TB, Syphilis,herpes, lyme disease
 Sarcoidosis


 Conjunctivitis(gritty, itchy red eye, sticky in the morning,

purulent discharge)
 Scleritis-red eye, pain on eye movement, injected sclera
 Episcleritis- less painful than scleritis
 Acute ACG- Painful red eye, nausea, vomiting
 Trauma

Presenting illness:

 Painful red eye, photophobia, blurring

 Exclude above DDs
 Look for associations:
 Behcet’s disease- recurrent oral ulcers, recurrent painful
genital ulcers, skin lesions, multi-organ involvement-
vasculitis, thrombosis, N/S-seizures, lungs-pul vasculitis,
HTN, pulmonary artery aneurysm, MSK-arthritis, GIT-
bleeding, abdominal pain, GU-urethritis, epididymitis, renal-
GN, Heart-pericarditis, endo and myocarditis

Past medical history: behcet’s disease, seronegative arthritis,

IBD, sarcoidosis
Physical examination:
 Eye-circumlimbial injection, visual acuity-may be decreased,
pupil-small, irregular and non-reactive pupil, fundoscopy-
keratitic precipitates, hypopyon
 Look for causes-oral ulcers, arthopathy etc…



To look for causes
 Pathergy test
 Biopsy from affected site-eg skin, joint, kidneys, lungs etc
 Imaging of joints/chest/brain


Anterior uveitis

 Steroid eye drops

 Mydiatrics
 Systemic steroids and immunosuppressants in severe cases

Treatment of cause:
Behcet’s disease-organ based(MDT approach)
 Oral and genital lesions-topical steroids, sucralfate solution.
Colchicine to prevent relapse. for severe mucocutaneous
lesions-systemic steroids and immunosuppressants
 Ocular disease-azathioprine, steroids, interferon alpha
 GI lesions-sulfasalazine, steroids, azathioprine
Benign essential Tremor:


 Parkinson’s disease
 Thyrotoxicosis
 Cerebellar tremor
 Alcohol and drug withdrawal tremor
 Anxiety disorder
 Drugs: salbutamol, theophylline,sodium valproate, lithium,
 Wilsons disease

Presenting illness:
 Tremor- at rest/postural/related to action, which part
affected? Unilateral/bilateral, exacerbating and relieving
factors(?alcohol), effect on hand writing(becomes poorly
legible in BET) and hand functions
 DD-Parkinsons disease(unilateral tremor, rigidity,
bradykinesia, micrographia, slurring of speech) ,
cerebellar(action tremor, uncoordinated movements, look for
causes), thyrotoxicosis

Past medical history: Parkinsons disease , thyroid disorder,

anxiety disorder,
Drug history-above list, recreational drug use
Family history*
Personal- alcohol*
Social, occupational- impact on driving?

Physical examination:
 Mainly postural tremor
 Exclude parkinson’s disease(rest tremor), thyrotoxicosis,
cerebellar syndrome(action tremor)
Addressing concerns:

 I think your tremor and difficulty writing may be due to a

condition called benign essential tremor. I don’t think it is
parkinson’s disease as there are no other features.
 Although, I am sure about the diagnosis, I would like to check
your thyroid function with a blood test as it can cause tremor
as well. It would be good if you reduce your alcohol now as I
will be giving you medication which will help with the
 The medication that can treat is called b-blocker
 Physio, occupational support
 Inform DVLA about diagnosis


Clinical diagnosis, however do exclude DD

 Plasma glucose(hypoglycemia)

 B blocker(1st line)
 Primidone(2nd line)-anticonvulsant
 Physio, occupational and psychological support

*Lithium toxicity tremor- action tremor(cerebellar dysfunction-

check for other cerebellar signs), potentiated by use of
diuretics(dehydration), ACEi, NSAIDs, other features-nausea,
vomiting,abdominal pain, diarrhoea, confusion, seizures
Black outs/collapse


With complete or partial LOC

 Syncope
 Epilepsy
 Hypoglycemia
 Vertibrobasilar TIA

Without affecting consciousness:

 Falls
 Psychogenic pseudosyncope

*Presyncope- prodromal symptoms(dizziness) prior to fainting


1. Reflex syncope
 Vasovagal syncope(emotion,fear, pain, orthostatic
 Situational syncope(cough, micturation, post-exercise)
 Carotid sinus syncope
2. Cardiac syncope
 Arrhythmias-bradycardia and tachycardia(svt, vt)
 Structural heart disease-HOCM, valvular heart disease,
 Pulmonary embolism
3. Syncope due to orthostatic hypotension
 Primary autonomic failure(MSA,Parkinson’s)
 Secondary autonomic failure(DM, amyloidosis)
 Drug induced hypotension-vasodilators, diuretics
 Volume depletion-diarrhoea, vomiting
Presenting illness: did you lose consciousness? Do you
remember falling?

Symptoms preceding , during and after the event

 Vasovagal syncope : Before: Prodromal symptoms

such as flushing, light-headedness, nausea and
blurring of vision. Precipitated by hot environment,
prolonged standing, anxiety.
During: Transient LOC, collateral history: pallor as
observed by others, lasting few seconds
After: rapid recovery, any injury?
 Carotid sinus syncope- during neck movements,
shaving, wearing a tight collar
 Situational-during coughing, defecation, micturation
 Cardiac syncope- Before: chest pain, SOB,
palpitations. During: exertion(HOCM, AS,
arrhythmias), After: rapid recovery. h/o cardiac
 Syncope due to postural hypotension: during
standing or change in posture, ask about causes.
 Seizure- BEFORE- aura, precipitated by flashing
lights, sleep deprivation, alcohol, DURING: Collateral
history-LOC,Jerking of limbs, tongue biting, frothing
at the mouth, rolling of the eyes, loss of control of
urine and faeces, repeated head turning to one side.
Absent seizure-repeated eye blinking. Any injury?
How long? Colour change(cyanosis)
AFTER: delayed recovery, post ictal headache,
confusion, drowsiness, limb weakness.
 Vertebrobasilar ischaemia-raising the arms above
head may precipitate collapse by sub-clavian steal
 Hypoglycemia-
Past medical history: past collapse, heart disease, epilepsy,
DM(autonomic failure, orthostatic hypotension, hypoglycemia),
anxiety disorder

Drug history: B-blockers,CCB, ACEi, ARB, insulin, OHA etc….

Family history- sudden death?(HOCM, long QT syndrome)

Social and occupational: driver? Risk while falling? Alcohol?

Physical examination:

 Pulse
 Ask to measure postural drop of BP
 Anaemia
 Carotid bruit
 Heart

Addressing concerns:

 Syncope is caused by a temporary reduction in

blood flow to the brain due to number of reasons
and in your case it was due to sudden pain(glitch in
the mechanism of autonomic nervous system)
 But we will investigate to see any problems in heart
beginning with heart tracing as it can cause the
same problem as well(though unlikely) and also
would like to measure your standing and lying
blood pressure
 Treatment is avoiding any possible triggers and
treating the cause if any and putting in recovery
position after collapse

 Resting ECG, 24 hour ECG
 CBC(anemia), Blood glucose, s.electrolytes
 Echocardiography

Based on suspected cause:

 Tilt table test(reflex syncope)

 Event recorders or implant recorders
 Carotid sinus massage(carotid sinus
 EEG(seizure)
 Carotid Doppler(carotid stenosis)
 MRA of vertebral vessels(for suspected
vertebrobasilar ischaemia)
 Electrophysiological studies for arryhthmias

Treatment : according to underlying cause

Tilt table test is done for:

 Reflex syncope(fall of BP and heart rate on
when tilted to 60 degrees from supine
 Postural hypotension(with no drop in heart
 Postural orthostatic tachycardia
syndrome(POTS)-hypotension with tachycardia
Bloody diarrhoea:


 Infective dirrhoea(shigella, pseudomembranous colitis(CD),

CMV colitis)
 Bowel malignancy
 Behcet’s disease( GI symptoms like IBD, anterior uveitis,
saggital sinus thrombosis, cranial nerve palsies, ulcers and
pathergy, arthritis)
 Radiation colitis
 Ischaemic colitis

Focused history:
Presenting illness:
 Diarrhoea-duration, frequency, blood/mucus
 Associated symptoms-abdominal pain, fever
 Mouth ulcers, perianal symptoms
 Alarm symptoms- features of malignancy(extreme weight
loss, anorexia, anaemia), features of intestinal obstruction,
sepsis(fever, rigors)
 Extraintestinal features of IBD-eye redness, joint pain, skin

Past medical and surgical history:

 PSC?, pyodermagangreonosum, any past colectomy?
Drug history:?
Family, social , occupational history
Travel history*
Physical examination:
 Hands-clubbing, leukonychia
 eyes-anaemia, anterior uveitis, jaundice
 mouth ulcers
 abdomen-laparotomy scars, sites of previous ileostomy and
colostomy, abdominal masses
 skin-EN, PG
 would perform DRE

Addressing concerns:
 I think your symptoms are related to a condition called IBD,
which is caused due to overactive immune system leading to
inflammation of bowels
 First, we need to exclude bug infection as the cause of your
diarrhea by taking stool samples and start treatment right
 We need to perform a test from back passage with a tube
with camera in it and take tissues from the bowel for
confirmation , for which I will refer to my bowel consultant
 It is usually managed with medications and sometimes
surgery is occasionally needed to remove the affected bowel.

 CBC(anaemia), ESR, CRP
 S. Albumin
 Stool for microscopy and c/s
 Sigmoidoscopy/colonoscopy and biopsy
Carpal tunnel syndrome

Presenting illness:

 Numbess, tingling and pain in lateral 3 and half fingers.

Night time symptoms that awake the patients, patient
relieves the symptoms by shaking the hand or wrist.
Unilateral or both hands?
 Weakness/clumsiness-Ask about hand functions-loss of grip,
dropping things
 Autonomic symptoms-tight/swollen feeling of fingers/hands,
temperature changes(cold/hot), changes in sweating
 Look for underlying causes-ask for features of
hypothyroidism, Acromegaly, RA, DM, obesity

Past medical history-Acromegaly, hypothyroidism, RA , dialysis,

amyloidosis, DM, colles fracture, wrist trauma


Occupation-using vibrating tools?

Addressing concerns:

 CTS is a pressure on a nerve in your wrist causing the

symptoms that you have
 In your case it is related to the underlying condition that you
are suffering from called acromegaly
 I am sure about the diagnosis and I will recommend you with
wrist splints initially for 4 weeks. If that doesn’t work, might
have to try steroid injections in the wrist and if not working, I
will refer to surgeons for a minor surgery.
 Also , we have to make sure your acromegaly is well
Physical exam:

 Confirm carpal tunnel syndrome

 Examine to look for causes


 Ultrasound scan
 Look for causes


 Physio , occupational therapy

 Wrist splints-(1)st line
 Steroid injections into the carpal tunnel
 Surgical decompression
Chest pain:


 Cardiac- stable or unstable angina, MI, Pericarditis, aortic

dissection, AS
 Pulmonary embolism
 Lungs-pleurisy(pneumonia, pleural effusion, pneumothorax,
 GIT- GERD, esophageal spasm
 MSK-Costochondritis
 Herpes zoster
 Anxiety

GERD-heartburn, regurgitation, dysphagia, cough, wheeze, chest

pain more on lying down

Esophageal spasm-chest pain, dysphagia, regurgitation

Costochondritis-chest wall pain with history of repeated minor

trauma, exacerbated by movement and even in deep inspiration
Chronic diarrhoea


 Infective diarrhoea/small bowel overgrowth
 Celiac disease
 Thyrotoxicosis
 HIV infection
 Colorectal cancer
 Chronic pancreatitis
 Lactose intolerance
 Bile salt malabsoption
 Carcinoid

Presenting illness:

 Diarrhoea-focus on above DDs

Past medical history: Thyroid problem, systemic sclerosis,

Chronic pancreatitis, celiac disease, dermatitis herpetiformis
Past surgical history-bowel resection?
Past investigations?
Drug history-laxative abuse?
Family history-colon cancer
Personal-smoking and alcohol
Social history-does diarrhoea interfere with work?
Travel history*, sexual history*
Menstrual history

Physical examination: depends on cause from history

 IBD-clubbing,leukocychia, mouth ulcers, abdomen(stomas,
surgical scars, iliac fossa mass), erythema
nodusum/pyoderma gangreonosum
 Celiac disease-dermatitis herpetiformis, anaemia
 Malignancy-anaemia, cachexia, abdominal mass
 Thyrotoxicosis-hand , eye and heart signs
Investigations: according to cause

 Stool microscopy and culture

 CBC, S.Electrolytes, RFT, Blood sugar
 TFTs
 Anti-HIV
 Colonoscopy and biopsy
 Celiac serology


According to cause
Coeliac disease

Can present as:

 Dermatitis herpetiformis
 Diarrhoea, abdominal pain, weight loss
 Anaemia

 Infective diarrhoea
 Bowel malignancy
 Chronic pancreatitis
 Lactose intolerance
 Bacterial overgrowth

Focussed history:
 Diarrhoea-consistency, frequency , duration, any mucus, any
blood, any tenesmus, exacerbating factors(gluten, lactose),
associated with fever? steatorrhea
 Abdominal pain, mouth ulcers,
 Alarm symptoms(weight loss, maelaena, haematemesis,
symptoms of lymphoma)
 Dermatitis herpetiformis-blistering itchy rash in extensor
surfaces, aggravated with gluten
 Malabsorption- bleeding? Osteomalacia(proximal myopathy),

Past medical history:

 Autoimmune diseases-DM, Thyroid disorders, pernicious
anemia, CTD
Drug history
Personal, social and family history
Dietary history

Physical examination:
 ?cachectic
 Koilonychias, anaemia
 Rash-pruritic vesicular rash on extensor aspects
 Neck-?goiter
 Abdomen-normal, to exclude IBD.

Addressing concerns:
 Your symptoms are suggestive of a condition called celiac
disease. It is the inflammation of lining of gut caused by
allergy to gluten containing foods. However we need to
exclude other inflammatory conditions as well
 We will do some blood tests and confirm by taking a piece of
tissue from the small gut with the help of a tube with
camera in it, which is a safe procedure
 It responds to exclusion of gluten from the diet. Gluten is
found in anything containing wheat(pasta, bread etc)
 Will ask dietician to see you for the diet, GP can prescribe
special prescription diet
 Speak to the occupational therapist/employer for different
job in the same company(if pasta chef)
 Celiac support groups

 CBC-anaemia
 Stool RE and culture(to exclude infective dirrhoea)
 S.albumin, s.calcium, vit D
 Serological tests- IgA Tissue transglutaminase antibodies,
anti-endomysial antibodies, IgA gliadin,reticulin
 Upper GI endoscopy and duodenal biopsy
 Skin biopsy-immunoflorescence will show IgA deposition in
dermoepidermal junction
 Baseline DEXA scan

Management :
 Strictly gluten free diet
 Correct nutritional deficiencies
 Immunosuppresants(prednisolone and azathioprine) if not
responding to diet exclusion
 Dapsone for DH
Cushings syndrome

Can present as: DM+HTN+Weight gain+leg weakness

DDs of weight gain:

 DM
 Hypothyroidism
 Pseudo-cushings

Presenting illness:

 Weight gain- distribution(does the patient feel that it has

particulary affected face, neck and torso?), duration, how
much kg gain?
 Diabetic symptoms
 Proximal myopathy-difficulty getting up, raising arms
 HTN-how long?
 Skin changes-easy bruising, skin thinning, stretch marks*
 Any depressive symptoms?
 Broken bones(osteoporosis)
 Alarm symptoms- lung cancer(ectopic ACTH), Pituitary
adenoma(visual field loss)

Past medical history: DM, HTN, depression, any chronic

inflammatory condition requiring steroids

Drug history with drug allergy: Steroids*(previous or


Social /occupational /family/personal

Menstrual history*
Physical examination:
 Face-cushingoid facies, plethoric, acne
 Arms-check for proximal myopathy
 Back and chest- acne, supraclavicular and interscapular fat
pads, kyphoscoliosis, hirsuitism
 Chest and abdomen- striae, purpuric rashes, truncal obesity,
atrophy of skin, acanthosis nigricans, scars for bilateral
adrenalectomy for cushings disease(before advent of
transphenoidal surgery, in which case there will be
 Lower limbs-proximal myopathy
 Ask to measure BP, test visual fields, dip urine for Glycosuria.

Addressing concern:
 I think your symptoms may be due to a condition called
cushing’s syndrome. In your case, it is due to the steroids
tablets you have been taking(iatrogenic) in which case I will
get an opinion from the respective consultant regarding
further management or due to overproduction of steroids by
your body(we need to find the underlying cause and treat it)
 we need to collect your urine for 24 hours and see the
cortisol(steroid) level in it and some imaging tests as well.
 Offer Support groups, physio , occupational therapy

 screen with 24 hour urinary free cortisol, overnight
dexamethasone suppression test( to suppress ACTH and
cortisol production , which won’t happen in Cushings)
 confirm with-low dose dexamethasone suppression
test(differentiate cushings from pseudocushing), also
midnight cortisol level will be raised
 to establish the aetiology:
Suspected ACTH-Independent cushing
syndrome( suppressed ACTH levels)-CT or MRI adrenal
Suspected ACTH-dependent syndrome(high ACTH levels)-
high dose dexamethasone suppression test(partial
suppression in cushings disease, no change in ectopic), CRH
test( no increase in cortisol in ectopic), inferior petrosal
sinus sampling, MRI of pituitary, CT chest(ectopic ACTH)

 fasting blood glucose, DEXA scan, lipid profile, ecg, echo

Treatment :Depends on cause

 Iatrogenic-reducing the dose or replace with steroid sparing
 Adrenal tumour-surgical resection
 Cushings disease-transphenoidal hypophysectomy
 Management of DM, HTN , osteoporosis

Causes :
1. ACTH independent
 Iatrogenic (steroids)
 Adrenal adenoma/carcinoma
 Adrenal nodular hyperplasia
2. ACTH dependent:
 Cushings disease(pituitary adenoma)
 Ectopic ACTH production(lung cancer, carcinoids)
Deep vein thrombosis


 Cellulitis
 Compartment syndrome(h/o trauma, on anticoagulants)
 Ruptured baker’s cyst(h/o RA)

Presenting illness

 Painful calf swelling- one or both legs? Extent of swelling,

redness, warmth
 DD- fever, h/o trauma, h/o joint pain/RA
 Exclude PUL embolism- Shortness of breath, haemoptysis,
chest pain
 Asses risk factors-

Past medical history: Cancer, thrombophilias, previous

thromboembolic diseases, CCF, Nephrotic syndrome

Past surgical history-prolonged immobilization, major

surgeries, fractures

Drug history- OCP

Personal history- smoker?*

Travel history- recent long haul flight?

Family history/social/occupational history

Pregnancy? *

Physical examination:

 Unilateral leg swelling , knee joint, pulses

 Pul embolism- tachycardia, JVP, loud p2? Lungs-
consolidation/pleural rub
 Look at observation chart
Addressing concerns:

 You may be suffering from a condition called DVT. It is

development of clots in veins of the leg
 If left untreated, the clot may break and impact in the blood
vessels of lungs which can be fatal
 I will arrange a Doppler USG scan of the leg to confirm it and
meanwhile as the suspicion of DVT is high, you will have to
commence the treatment immediately-blood thinning
agent(LMWH). Once confirmed you will be given blood
thinning agent called warfarin to be taken for 3-6 months
(decision will be taken by blood doctor). Give info about
warfarin if time permits


 Doppler USG of leg

 CBC-Thrombophilic (polycythaemia, thrombocythaemia)
 D-dimer
 Look for causes- thrombophilia screen, cancer screen
 If suspected pul Embolism-ECG, CXR, CT Pulmonary


 LMWH followed by warfarin (3 months for those with

temporary risk factors, 6 months for those with idiopathic
DVT and permanent risk factors)

 Can present as difficulty climbing stairs and rash around


DD: of proximal myopathy:

 Myositis-Dermatomyositis, polymyositis, inclusion body
 Polymyalgenia rheumatic
 Endocrine-hypo/hyperthyroidism , cushing’s syn
 Drugs-statins
 Myasthenia gravis
 osteomalacia

Presenting illness:

 Proximal myopathy-difficulty standing up, raising arms.

Painful( myositis)or not(endocrine causes)? Any difficulty
with fine movements(distal myopathy), effect on daily life?
 Skin changes -heliotrope rash(violet colour, symmetrical
distribution in periorbital areas), gottrons papule
 Shortness of breath( ILD or respiratory muscle weakness)
 Dysphagia
 Alarm symptoms- features of malignancy(lung, breast , GI,
 Exclude endocrine causes

Past medical history- malignancy,

Drug history*(statins, hydroxyurea,chloroquine)
Occupational history*, social and family history

Physical examinations:

 Eyes -Heliotrope rash over eyes associated with mild

periorbital oedema
 Hand-violaceous , scaly , papular rash on knuckles, elbows,
knees called gottron’s papules
 Arms-proximal myopathy
 Neck and chest- V shaped photosensitive rash(shawl sign).
Lung bases to exclude ILD
 Lower limbs-proximal muscle weakness with tenderness
 ? malignancies
Addressing concerns:
 I think the cause of your symptoms may be due to a
condition called dermatomyositis. It is inflammation of the
muscles and skin due to overactive immune system
 We will do some blood tests and do some specific tests to
see electrical conduction of your muscles(EMG) and possibly
a muscle biopsy. We may have to do other tests which may
precipitate this condition(malignancy)
 We can address the pain with anti-inflammatory medications
and start specific management (steroids) one the diagnosis
is confirmed.

 CK
 ANA, anti-Jo 1 antibodies
 EMG(Spontaneous fibrillation)
 Muscle biopsy, skin lesion biopsy
 HRCT, lung function tests-ILD
 Malignancy screen

Treatment :

 Avoid sun exposure, use of sunscreen

 Physiotherapy
 Specific-steroids, methotrexate, azathioprine, IV Ig may be
considered in refractory condition
Diabetes insipidus

Stem: history of head injury, polyuria


 Diabetic insipidus(central)-decreased secretion of ADH

 Nephrogenic DI(resistance to ADH action in the kidney)
 DM
 primary polydipsia

Presenting illness:

 polyuria
 polydipsia
 nocturia
 history of trauma
 weight loss, fatigue

Past medical/surgical history: head trauma/surgery, DM,

psychological disorder

Drug history

Physical examination:

 Dehydration?
 Scars in head

Addressing concerns:

 DI is a rare condition where you produce large amount of

urine and often feel thirsty. It is not related to DM.
 It is caused due to a lack of hormone(vasopressin) or when
hormone doesn’t function in the kidneys
 Treatment is replacement of the hormone and correction of
fluid balance
 Will do some blood tests and refer to endocrinologist who will
be doing more tests and give you the treatment.


 Simultaneous urine and plasma osmolarity( low urine

osmolarity(<200mosm/kg), high plasma osmolarity)
 Blood glucose, s.electrolytes
 Plasma ADH level(low in central DI)
 24 hour urine collection for urine volume
 Urine specific gravity
 Water deprivation test followed by administration of
vasopressin- in central and nephrogenic DI , urine
osmolality will be less than 300mosm/kg after water
deprivation. After ADH administration, the osmolality will rise
to more than 750mosm/kg in central DI but will not rise at all
in nephrogenic DI
 MRI pituitary gland


 Fluid replacement
 Desmopressin(drug of choice) in central DI, others are
synthetic vasopressin, chlorpropamide, thiazides, NSAIDs
Diabetic retinopathy:

DD for gradual loss of vision:

 Diabetic retinopathy
 Hypertensive retinopathy
 Chronic glaucoma
 Cataract
 Retinitis pigmentosa

Presenting illness:

 Vision-gradual deterioration, diurnal variation? Double

vision? Pain? One eye or both? Floaters, flashes or perception
of curtain over vision(RD or retinal tear)
 DM-duration, how well controlled? Latest HBA1C? any other
complications such as nephropathy, p.neuropathy?
frequency of hyper or hypoglycemia? When was last
opthalmological check up?

Past medical history and surgical history: DM, HTN, high

cholesterol levels, MI, stroke , any laser surgery?

Drug history and allergy: insulin or oral HGA, compliance?


Family history

Occupational : driver?

Social history

Physical examination:
 Visual acuity- drop in vision usu. Suggests maculopathy
 Fundoscopy- look in anterior eye for cataracts, retina for
diabetic changes, photocoagulation scars
 Check visual fields and eye movements
 Ask to check BP, dip urine for glycosuria

Addressing concerns:
 I think the reason why your eyesight has deteriorated is
because , diabetes has affected the blood vessels in the
back part of eye called macula, which is important for vision
 I will ask eye doctor to see you urgently to confirm the
diagnosis. Meanwhile, I will help your blood glucose level to
keep under control. And it is essential that you stop driving
and inform DVLA until we know how severely your eyesight
has been impaired.
 The eye doctor will most likely need to perform a laser
treatment on the blood vessels on the back of your eye. It is
usually painless.

 Fasting blood glucose, HbA1c, lipid profile, urine for albumin,
 Eye-fluroscence angiography, OCT, B scan ultrasonography

Treatment :
 Good glycemic and hypertensive control-diet, exercise, drugs
 Pan-retinal photocoagulation for severe pre-proliferative and
proliferative retinopathy
 Focal laser photocoagulation for maculopathy
 Novel therapies- intra-vitreal Anti VEGF monoclonal
antibodies, intravitreal corticosteroids

Classification of diabetic retinopathy:

 Non proliferative diabetic retinopathy
1) Mild: atleast one microaneurysm
2) Moderate: haemorrhages, microaneurysms, hard
3) severe- haemorrhages and microaneurysms in four
quadrants, venous beading, intraretinal microvascular

 Proliferative diabetic retinopathy:

Neovascularizaion, macular oedema, RD, vitreous

Previous classification :
 Background diabetic retinopathy: microaneurysms, dot and
blot haemorrhages, hard exudates(well defined outline,
 Pre-proliferative: background changes plus cotton wool
stops(poorly defined borders), IRMA, venous looping and
 Proliferative-neovascularization
 Maculopathy(at any stage of retinopathy)-hard exudates
within 500um of macula in a circinate pattern
 Advanced diabetic eye disease-RD, vitreous haemorrhage


 Scleroderma*(esophageal dysmotility , stricture)

 Muscular disorders*-Dermatomyositis, polymyositis,
muscular dystrophies
 Motility disorders*- achalasia, scleroderma, diffuse
esophageal spasm
 Esophatitis*-GERD, Infectious(HIV, candidiasis), radiation,
 Malignancy-esophageal, oral*
 Structural- esophageal stricture, webs, rings
 Central-MS, MND, CP, stroke, GBS, Brain trauma, brain
 Endocrine-secondary myopathies in cushings, thyroid
 Psychogenic

Presenting illness:

 Dysphagia- onset, duration, progression, solid or liquid or

both, pain? Where the food gets stuck?
Haematemesis,malaena, weight loss, change in bowel habit,
 Ask about DDs

Past medical history* as above

Drug history- steroids? NSAIDs

Physical examination:

 Look for causes

 Examine mouth, neck
Ehlers-Danlos syndrome

Defect in collagen and connective tissue synthesis, 11 variants,

AD or AR Inheritance pattern.

Presenting illness:

 Skin changes-lax, easily extensible, skin fragility-purpura

 poor wound healing
 Eyes-myopia, glaucoma, retinal haemorrhage/detachment
 CVS- MVP, AR, MR, aortic dissection
 Lungs- pneumothorax
 GIT-bleeding, features of anaemia
 MSK-Osteoarthritis

Past medical history- Poor wound healing, heart diseases,


Surgical history*

Physical examination:

 Skin- thin (visible vessels), hyperextensible and elastic.

Impaired wound healing, cigarette paper scars. Purpura,
 Joints-hyperextensible
 MSK-kyphoscoliosis
 Examine other system manifestations as above.

Addressing concerns:

 It is group of inherited disorder affecting connective tissues

that support the skin, bones, blood vessels and many
 I will refer to joint specialist for confirmation and geneticist
 Unfortunately, there is no specific treatment , but with
advice and support it is possible to manage many symptoms
 Advise to avoid contact sports and heavy lifting
 Physio and occupational therapist support
 Genetic counselling


 Genetic testing
 CBC-anaemia


 VIT C/ascorbic acid-cofactor of collagen synthesis

 Organ based
 Physio, occupational therapy
 Genetic counselling
Epilepsy, 1st episode of seizure

*recurrent unprovoked seizures

1. Generalized (primary Vs secondary)

 Tonic-clonic seizure(stiffening followed by jerking of limbs,

rolling of eyes, cyanosis and frothing at mouth, LOC, urinary
or faecal incontinence)
 Absence seizure-vacant stare and eye blinking
 Myoclonic seizure-sudden onset involuntary movements of
body parts, usually in morning
 Atonic seizures-brief loss of postural tone

2. Partial(simple vs complex(impairment of consciousness))

 Temporal lobe seizures-lip smacking, chewing, grimacing

 Frontal lobe seizures- jacksonian seizure(convulsion
beginning in one body part and spreading to adjacent
ipsilateral body parts), violent movements
 Parietal lobe seizure-positive sensory symptoms and pain
 Occipital lobe-visual hallucinations

Causes of seizure:

1. Primary/unprovoked
2. Secondary/provoked seizure
 Infection-meningitis, encephalitis, TB cerebral malaria
 Neoplastic-primary or metastases
 Vascular-stroke,
 Trauma
 Metabolic-hypoglycemia, hyponatraemia
 Drugs-lithium toxicity, benzodiazepine withdrawal,
ciprofloxacin, imipenem, phenothiazines
 Alcohol withdrawal
 Epileptic syndromes-tuberous sclerosis, sturge-weber
History of presenting illness:

 Record the events before, during and after the seizure

 Events before(aura)-strange smells/tastes/sensations, rising
sensation in epigastrium, autonomic(sweating, pallor,
nausea, vomiting)
 During— did you lose consciousness?*
 1st attack or repeated
 Precipitants-flashing lights, sleep deprivation, alcohol, recent
illness, non-compliance with medication
 Exclude meningitis-fever, headache, neck stiffness, skin
rash, photophobia….recent ENT infections(spread to CNS),
exclude stroke, space occupying lesion

Past medical history-storke, meningitis/encephalitis, trauma to

head, cerebral metastases, tuberous sclerosis

Drug history-compliance, lithium toxicity?

Family history?

Occupational history?..driver? swimmer?


Physical examination:

To exclude epileptic syndromes

 Tuberous sclerosis-skin changes

 Sturge –Weber syndrome
 Full neurological exam
 Cardiac exam
Addressing concerns:

 Epilepsy is a condition that affects brain and causes

repeated seizures due to overfiring of electrical impulses in
brain cells
 Often the cause is not found
 Will do some blood tests and refer to specialist doctor for
further tests and treatment
 Life style modification
 Stop driving and inform DVLA
 Pregnancy? Increase dose of OCP, Folic acid, counsel about
possible birth defects


 Electrolytes
 Blood sugar
 LFTs
 Drug levels-lithium, and anti-epileptic levels
 ECG to exclude cardiac cause of syncope
 MRI brain
 EEG-Inter-inctal EEG, ambulatory EEG


 General-life style measures-avoidance of precipitants,

driving, recreation(avoid swimming, cycling)
 Generalized tonic clonic- sodisum valproate (1 st
line)carbamazepine and lamotrigine
 Partial/secondary generalized- carbamazepine and
lamotrigine(1st line)
When to give AED?

 Usually after second seizure

 1st unprovoked seizure with neurological deficit, abnormal
EEG, Structural abnormality on brain Imaging, family/carers
consider the risk of having a further seizure unacceptable


1. Epilepsy
 Group 1- must notify DVLA, Must stop driving. Duration-
5 years(with or without epilepsy medication)
 Group 2-must not drive and must notify DVLA. Duration-
10 years(without epilepsy medication)
2. 1 unprovoked epileptic seizure/isolated seizure

 Group 1-must not drive and must notify DVLA. Duration-

6 months(12 months if increased risk of seizure)
 Group 2- duration-5 years
3. Secondary causes of seizure-apply above rules, except in
case of seizure at the time of acute head
injury/intracranial surgery, rules are different
Fever in returning traveller


1. Short incubation(less than 10 days)

 Dengue fever
 Typhoid
 legionnaire’s disease
 Meningococcal infections
 Acute HIV infection
 Influenza
 Rickettsial infections
2. Medium incubation(less than 1 month)
 Hepatitis A
 Amoebic liver abscess
 Shistosomiasis
3. Long incubation
 Malaria
 Tuberculosis
 Lyme disease
 Brucellosis
 Histoplasmosis

Presenting illness:

 Fever-onset, duration, pattern, chills and rigors, night

 Neuro-headache, neck stiffness, photophobia, rash,
altered consciousness, weakness, seizure
 ENT-sorethroat, ear ache,facial pain, voice change,
runny nose
 Respiratory- cough, sob, pleuritic chest pain, purulent
 CVS-Palpitations, dyspnea, chest pain
 Abdomen-abdominal pain, nausea, vomiting, diarrhoea,
distension, constipation, haematochezia, maelaena,
haematemesis, jaundice
 Genitourinary- dysuria, increased frequency, genital
 MSK-joint pain, stiffness, swelling
 Skin-rash, oral ulcers

*make sure to document whether symptoms started before ,

during or after return form travel

Travel history: dates of travel, duration of stay in each region,

urban/rural, accommodation (camping, hotel,rural dwelling,
guesthouse), means of transportation

Exposure history:

 Sexual history(homo/heterosexual, no.of partners,

barrier protection)
 Animal contact-birds, rodents
 Insect exposure-bites of mosquitoes, ticks
 Needle and blood exposure-shared needle, tattoes,
 Food and drink-
 Soil or water contacts-freshwater lakes

Medical and family history- pevious HIV test, splenectomy?

Medications- immunosuppressive?

Vaccinations? Hep A, B, meningococcus, influenza, yellow fever,


Chemoprophylaxis?....malaria prophylaxis(regimen, compliance,

duration before and after travel)

Addressing concerns:
 Explain the likely cause of fever
 Explain about investigations
 Give info about travel clinics, safe sexual practice,
malaria prophylaxis, insect avoidance, food and water
 Obtain help from infectious disease specialist and

Physical examination:

 Pulse, temperature
 Anemia, jaundice, neck stiffness
 lymphadenopathy
 skin rashes
 lungs
 abdomen-hepatosplenomegaly



 LFT, RFT, S.Electrolytes
Specific to diseases:
 Thick and thin film for malaria
 CXR, Sputum for AFB…TB
 Anti HIV
 Dengue serology
 Urinary legionella antigen
 Blood /urine/stool culture for typhoid


According to the cause

Frozen shoulder/adhesive capsulitis

 Uncertain etiology of significant restriction of both active and

passive shoulder motion in the absence of known intrinsic
shoulder disorder


 Polymyalgia rheumatic with GCA

 Polymyositis
 Rotator cuff tendinopathy
 Osteoarthritis
 Calcific tendinitis, subacromial bursitis
 Cervical spondylosis


1. Idiopathic
2. Secondary FSS- trauma, shoulder surgery, DM,
IHD,stroke,hopo and hyperthyroidism, parkinson’s disease,
HTN, drugs(Protease inhibitors, antiretrovirals), malignancy

Presenting illness:

 Initial freezing stage(painful)-dull pain at deltoid insertion,

pain on shoulder movement, inability to sleep on affected
side, nagging pain at night causing sleep disturbance,
marked limitation of active and passive shoulder rotation
 Frozen stage (stiffness)-stiffness and severe loss of shoulder
motion. Less pain

Past medical and surgical above

Drug history*

Occupational history, handedness?

Physical examination:
 Limitation of shoulder movement-active and passive
 Tenderness at deltoid insertion

Addressing concerns:

 It is a condition when the tissue around the shoulder joint

becomes inflamed making the tissue tighter and shrink
,causing pain and stiffness of shoulder joint , limiting the
movement of shoulder
 It is usually a self limiting condition over 1-2 years
 Treatment is with pain killers and physiotherapy

Investigations: clinical diagnosis


 Blood glucose
 X-ray of shoulder joint
 MRI to rule out rotator cuff tear


 Physiotherapy
 NSAIDs, oral steroids, intra-articular steroids
 Surgery –only in refractory cases
Gout :

Can present as:

 Acute –monoarthritis/oligoarthitis
 Chronic tophaceous gout

DD of monoarthritis:
 Gout
 Septic arthritis
 Pseudogout
 Osteoarthritis
 Spondyloarthritis
 Tubercular arthritis

Presenting illness:
 Joint pain- distribution, severity, more at night?, swelling?
Colour changes? Relieving and aggravating factors, duration,
associated with low grade fever, functional status
 Exclude septic arthritis(high grade fever , rigors, foci of
 Risk factors( obesity, cancer, chemotherapy, CKD, alcohol
 Exclude seronegative arthritis- bowel changes, urethritis,
 History of trauma

Past medical history: cancer(lymphoma), PRV, CKD, HTN

Drug history: thiazides, chemotherapy
Personal- alcohol? Smoker
Dietary history- diet rich in purine?
Family, social and occupational history
Travel history

Physical examination:
Joint exam: look for swelling,redness, warmth
Check movement if no pain.
Look for tophi, functional status
Look for causes such as RRT for CKD, Lymphadenopathy etc
Ask to measure BP, dip urine for glycosuria(metabolic

Addressing concerns:
 I think your joint pain is due to a condition called gout. It is
deposition of a chemical called uric acid in the joints leading
to inflammation
 We will do some blood tests, and draw a fluid from the joint
for confirmation and exclude infection in the joint, which is
crucial as infection can destroy the joint.
 We will address your pain with strong painkillers and anti-
inflammatory medications. You may have to take another
medication after few weeks to reduce the frequency of
 Dietary referral, reduce alcohol

 S.uric acid
 Aspiration of synovial fluid for analysis
 Blood culture if septic arthritis is suspected
 X ray of the joint.

Treatment :
 Acute – NSAIDs, Colchicine, steroids
 Chronic/recurrent- allopurinol , febuxostat, probenecid
 Dietary changes, reduce risk factors
 Physiotherapy, occupational therapy

Risk factors for gout:

1. Increased uric acid production
 High purine diet –meat, sea food, beer
 Lymphoproliferative and myeloproliferative disorders
 Psoriasis
 Obesity
 Chemotherapy
2. reduced uric acid excretion
 Drugs-diuretics, ACEi, low dose aspirin, pyrizinamide,
 Dehydration
 ketoacidosis
Grave’s disease

Can present as: hyperthyroid/euthyroid/hypothyroid

 Palpitations
 Diplopia
 Anxiety and sweating

 Thyrotoxicosis
 Pheochromocytoma
 Anxiety disorder
 Cardiac causes of palpitations

Presenting illness:
 Palpitations
 Sweating, heart intolerance, weight loss despite good
appetite, irritability, diarrhoea, oiligomenorrhoea( also ask
features of hypothyroidsm)
 Eye changes-double vision, dry eyes
 Proximal myopathy
 Phreochromocytoma(intermittent symptoms of headache,
flushing, palpitaitons)
 Alarm symptoms-cardiac disease? Chest pain, SOB

Past medical history: autoimmune diseases

Past surgical history- thyroid operation?
Drug history with allergy history: amiodarone, B-
blocker(mask tachycardia)
Personal- smoker?
Family, social and occupational history

Physical examination:
 Hands- tremor, tachycardia/AF
 Eyes- exopthalmos(visible lower sclera), lid lag, lid retraction,
conjunctival chemosis, complex opthalmoplegia(eye
movement exam)
 Neck exam-diffuse neck swelling, bruit?
 Proximal myopathy?
 Pretibial myxoedema

Addressing the concerns:

 I think the cause of your palpitations is an overactive thyroid
gland. Probably the underlying thyroid problem is because of
a condition called graves disease( overactive immune
system), which may also affect the eyes
 We will perform TFT today to confirm it and obtain heart
tracing as well. We may have to perform ultrasound scan of
the neck
 Treatment can be done in three ways: medications, surgery,
radioiodine. We will talk to you about it once the diagnosis is
confirmed to see which one is appropriate for you.
 Warn of agranulocytosis

 TSH receptor stimulating antibodies, anti-thyroid peroxidase
 Radioisotope uptake scan
 Usg neck

 Anti-thyroid medications
 B-blockers
 Radio-iodine therapy
 surgery


 Pulmonary embolism*
 Infection-pneumonia, TB*, lung abcess, bronchiectasis,
bronichitis, aspergillosis
 Bronchial malignancy*, metastases
 Cardiac-mitral stenosis, Acute LVF
 Vasculitis-wegener’s , goodpasture’s, HHT
 Bleeding disorders, anticoagulants

Presenting illness:
 Haemoptysis- onset, frequency, amount, colour-fresh blood,
pink(Pul oedema and MS), Brown/rusty(indicates
mucopurulent sputum)
 Associated symptoms- to exclude DD.
 Features of malignancy , tuberculosis and pulmonary
 Rash , arthralgia, myalgia, epistaxis, rhinosinusitis(wegener’s
 Ask about DVT(leading to PE)

Past medical history*

Drug history-anticoagulants, antiplatelets, OCP(P.E)


Occupational-exposure to asbestos

Travel history-contact with TB patient


 Sputum for c/s, AFB stain, Malignant cell
 LFT, RFT, Electrolytes
 Clotting profile
 D-Dimer, CT pulmonary angiogram
 CT chest
 Bronchoscopy
 Echo if MS, LVF
 Auto-antibody screen-ANCA, anti –GBM antibodies
 Urine analysis(GN-Wegener’s, good pasture)


1. Primary headaches
 Migraine
 Tension- type headache
 Trigeminal autonomic cephalgias(TAC)- cluster headache,
paroxysmal hemicranias, short lasting unilateral
neuralgiform headache attacks with conjunctival injection
and tearing (SUNCT), hemicrania continua
 Other primary headaches- primary cough headache, primary
exercise headache, primary headache associated with sexual
activity, primary thunder clap headache, primary stabbing
headache etc…..
2. Secondary headaches
 Headache attributed to trauma/injury to head and neck
 Due to cranial or cervical vascular disorder
 Non vascular intracranial disorder
 Due to substance or its withdrawal
 Due to infection
 Due to disorders of ENT
 Due to psychiatric disorder

3. Painful cranial neuropathies


 Migraine without aura- headache(unilateral location in

frontotemporal region, pulsating quality, moderate or severe
in intensity, aggravated by routine physical activity,
associated with nausea, photophobia, phonophobia, usu
lasting 4-72 hours, at least 5 such attacks, may have
menstrual relationship
 Migraine with aura- reversible aura symptoms such as
visual( zig zag flashes), sensory(pins and needles,
numbness) , speech(aphasia, dysarthia), motor(hemiplegic
migraine-sporadic or familial hemiplegic migraine),
brainstem( dysarthia, vertigo, tinnitus, ataxia, diplopia,
decreased level of consciousness but without motor
weakness), retinal(reversible monocular visual disturbance
such as blindness, scintillations), the aura is followed by

Tension-type headache: subtypes: episodic and chronic

 Headache-typically bilateral, pressing or tightening in

quality, mild to moderate in severity, lasting minutes to days
Note: medication over use headache will come in all

Cluster headache:

 Headache- severe, unilateral orbital/supraorbital/temporal

pain, lasting 15mins to 3 hours, once to 8 times a day,
associated with ipsilateral conjunctival congestion,
lacrimation,nasal congestion,rhinorrhea, facial sweating,
miosis,ptosis, restlessness/agitation

Paroxysmal hemicranias:

 Same as above but lasting 2-30 mins, occurring several

times a day, responds to indomethacin.


 Same as above but lasting seconds to minutes, at least once

a day, prominent redness and lacrimation

SAH- Sudden onset, severe thunder clap headache peaking in

seconds or minutes , associated with focal neurological deficits
RED FLAG SIGNS in headache:

 Thunder clap headache

 Inability to move a limb
 Recent trauma
 Being woken from sleep
 Confusion
 Headache worsens with coughing, sneezing, exertion,
changing posture, (raised ICP)
 GCA-jaw claudication, vision loss
 Neck stiffness, fever, rash
 h/o cancer, thrombosis

Physical examination

 Raised ICP-Dilated pupil? 6 the nerve palsy by checking eye

movements, fundoscopy for papilloedema
 neurological exam of limbs

Investigations: Clinical diagnosis

 brain imaging for red flag features(otherwise no need of



Cluster headache- nasal/subcutaneous triptans, oxygen

Henoch schonlein purpura:


 Vasculitis(small vessel vasculitis, including

cryoglobulinemia), vasculitis due to RA, SLE, Bechcets syn,
 Thrombocytopenia, DIC, Haemophilia
 Drugs-penicillin, sulphonamides
 Infection –meningococcus, hep B, C

Presenting illness:

 Rash : location: lower limbs and buttocks, itchy? Blanch

able? Duration? Pain? What precipitated?
 Abdominal pain, bloody motion
 Joint pain
 Precipitant- recent upper RTI
 Alarm signs- reduced urine output, haematuria, leg swelling?
 Exclude other vasculitis-respiratory symptoms?
Fever(meningococcal), connective tissue diseases ? bleeding

Past medical history- CTD, vasculitis, ITP

Drug history with allergy history: penicillins, sulphonamides,
ACEi, thiazides
Personal, social, occupational, family history

Physical examination:
 Skin survery- non blanching palpable purpuric rash esp. on
extensor aspects of lower limbs and buttocks
 Joints- swelling?
 Check pedal oedema(nephrotic syn)
 Ask to measure BP, dip urine for haematuria
Addressing concerns:
 I think the cause of your symptoms and rash may be due to
a condition called HSP. It is caused by inflammation of small
blood vessels.
 We will do some blood tests and urine tests and refer to skin
doctor for skin biopsy. Sometimes, it can affect kidneys as
well, we need to ensure that it is not affected as well and
needs follow up for the same reason.
 I will give painkillers and NSAIDs for your joint pain and the
condition should resolve by its own. Rarely, we may have to
give steroids for this condition.

 Urine dipstick and microspopy
 Coagulation profile
 Abdominal imaging if severe abdominal pain
 Skin biopsy( IgA and C3 deposition seen under
immunoflorescence), renal biopsy(IGA nephropathy)

Management :
 Spontaneous resolution
 Analgesics(NSAIDs may be avoided in active phase of
disease )
 Immunosuppressive therapy on severe renal involvement
 Follow up to see renal involvement
Hep C with skin rash

Dermatologic manifestations:

 Lichen planus-pruritic, papular lesions involving skin, scalp,

nails, oral mucosa, genitalia
 Acral necrolytic erythema-hyperkeratotic plaques with
erythema in acral parts(esp dorsum of the feet and ankles)

 Cryoglobulinemia-leukocytoclastic vasculitis-palpable
purpura in the legs, livido reticularis, urticaria. Ask about
pain,pruritus, raynaud’s phenomenon

 Sicca syndrome-dry eye, dry mouth

 Porphyria cutanea tarda-blisters, vesicles esp on sun

exposed surfaces

 Non-Hodgkin lymphoma, MALT syndrome

 Erythema nodusum

 Erythema multiforme

Presenting illness:

 Rash- distribution, pruritus, pain, photosensitivity

 Features of CLD due to Hep C- ascites, hep encephalopathy,
SBP, variceal bleeding
 Other extrahepatic manifestations-myalgias, arthralgias,
sicca syndrome, sensory neuropathy, pruritus

Past medical history: blood transfusion,organ transplants,

Drug history-I/V drug abuse
Sexual history*
Occupational history*
Family history

Physical examination:
 Rash
 Stigmata of CLD
 Tattoos, injection marks

Addressing concerns:

 Your rash may be related to the bug infection called Hep C .

 I will do some blood tests to confirm it and refer to skin
doctor, bowel doctor and liver doctor for further
management of the condition.


 Anti-HCV antibody
 Skin biopsy
 Investigations to see liver involment-LFT, USG HBS, a-

Treatment :

 DAA-interferon, ribavirin
 Biological agents-rituximab
Hereditary hemorrhagic telangiectasia/ Osler-Weber-

Presents with anaemia , recurrent epistaxis and vascular lesions

in mucous membrane

Presenting illness:

 Epistaxis- frequency ,severity

 GI bleeding
 Anaemia-exertional dyspnea
 Red spots in mouths and lips
 SAH or recurrent headache(cerebral AVMs
 Pulmonary AVM-SOB
 AVM in liver-? CLD?
 Look for other causes of anaemia, other causes of

Medical history- anaemia

Medication history- iron tablets, blood transfusion
Family history* A.D
Personal , occupational , social history

Physical examination:
 Pallor
 Telangiectasias of face, lips, tongue,oral cavity
 Bruit in the lung?
 ?stroke

Addressing concerns:
 I think your symptoms are due to a condition called HHT,
where blood vessels bleed without any warning and it can
make you anaemic leading to tiredness
 I will have to check your blood to see how anaemic you are
and refer for further tests to see any abnormal blood vessels
in different organs or not( CT angiogram)
 The treatment involves treating the anaemia with iron
tablets, or blood transfusion and also trying to stop the blood
vessels from bleeding
 This is an inherited condition, I will refer to geneticist if you
are thinking of having children.

Investigations: it is a clinical diagnosis

 CBC-anaemia, platelet count
 Clotting profile
 Screening of AVMs with CT/MR angiography

 Oral or i/v iron
 BT
 To reduce bleed-tranexamic acid, aminocaproic acid,
estrogen therapy, cauterization, laser, AVMs-embolisation,
surgical resection
 Genetic counselling
Hoarseness of voice


 Hypothyroidism*, Goiter
 Laryngeal malignancy*
 Acute laryngitis(mostly viral)
 chronic laryngitis( fungal- steroid inhaler use)
 Reflux laryngitis-GERD*
 Vocal fold-polyp, nodule, cyst
 Bilateral vocal cord paralysis
 Overuse of voice(singer)


1. Primary
2. Secondary
 Endocrine-primary hyperaldosteronism(conn’s
syndrome), cushing syndrome, pheochromocytoma,
thyroid dysfunction, acromegaly, congenital adrenal
 Renal- renal artery stenosis, PKD, CKD, GN
 Vascular-coartation of aorta, vasculitis, connective
tissue disease(SLE, scleroderma)
 Drugs-cocaine, amphetamines
 Pregnancy induced pre-eclampsia/eclampsia

Presenting illness:

 Ask about above causes

 Target organ damage-heart failure, CKD, stroke,
retinopathy, encephalopathy
 Primary-usually asymptomatic
 Uncontrolled HTN-headache, visual problem
 Conn syndrome- features of
hypokalaemia(weakness,muscle cramps,
 Cushing-weight gain, proximal muscle weakness, skin
changes, depression, new onset DM
 Pheochromocytoma- triad of episodic headache,
sweating, palpitations. Tremor, weight loss, flank pain.
 Renovascular HTN-sudden onset, resistant to
antihypertensives, sudden onset SOB(flash pulmonary
 Co-arctation of aorta-palpitations, cold feet, leg pain,
muscle cramps
 Ask about connective tissue diseases
 White coat HTN

Past medical history : as above

Drug history-steroids, OCP? NSAIDs, steroids, ciclosporin

Side effects of antihypertensives: bendroflumethiazide(impotence

and gout)

Recreational-cocaine, amphetamine

Family history*

Personal-alcohol, smoking

Menstrual history

Physical examination:

To look for causes:

 Pulse-radio radial and radio femoral delay, unequal

radial pulses, surgical scar for coarctation repair
 Cushingoid facies
 Renal bruit
 Evidence of connective tissue disease?

Look for target organ damage

 Ask for fundoscopy

 Heart failure, LVH
 NS-for stroke
 Features of CKD
 Ask for urine dipstick for proteinuria and haematuria

Baseline lab work up and also to see target organ damage

 Urine microscopy
 S.Electrolytes
 Lipid profile
 Blood glucose
To look for causes:
 Coartation of aorta- CXR, CT angiography, echo
 Conn syndrome-
1. screening tests-hypokalaemia, bicarbonate
level(metabolic alkalosis), plasma aldosterone to rennin
activity ratio(ARR) when greater than 20-25 is highly
suggestive, kaliuresis(urinary K excretion more than 30
2. confirmatory- urinary aldosterone level,s.aldosterone
level , salt loading test
3. CT scan adrenal gland
 Renovascular HTN-doppler flow USG , CT/MR angiography

Life style modification
Treatment of HTN and its cause
Treat target organ damage

Presenting illness:

 GH deficiency- short stature(if in children), diminished sense

of well being(fatigue and weakness)
 MSH deficiency- pale, dry and wrinkled skin
 Gonadotrophin deficiency –loss of secondary sexual
characteristics(loss of axillary, facial and pubic hair) , erectile
dysfunction and infertility, amenorrhea, hot flushes
 ACTH deficiency- glucocorticoid deficiency leading to
hypotension, no minerolocorticoid deficiency due to intact
Renin-angiotensin system( so no hyponatraemia,
hyperkaemia unlike addisions disease), lack of pigmentation
 TSH deficiency- signs and symptoms similar to primary
 Prolactin deficiency- inability to lactate following delivery
 ADH deficiency-DI(in panhypopituitarism)
 Local effects of pituitary disease-headaches, visual

Past medical history- pituitary tumours, pituitary

surgery/radiotherapy, infiltrative diseases such as sarcoidosis and
haemochromatosis, sheehan’s syndrome(pituitary infarction),
pituitary apoplexy(haemorrhage into pituitary gland),

Pregnancy- blood loss?

Physical examinations:

 Pallor
 Skin-dry , pale and wrinkled
 Pulse-bradycardia(hypothyroidism)
 Check eyes-pallor, eye movements, Visual fields
 Look for axillary, facial hair
 Gynaecomastia?(mostly found in primary hypogonadism due
to elevated LH levels but can be found in hypopituitarism
with hormone replacement therapy)
 Ask to measure Postural drop of BP, palpate testes for
testicular atrophy


 CBC-anaemia?
 TSH, T4
 Morning cortisol and ACTH
 Testosterone, oestradiol, LH, FSH
 Prolactin
 GH levels
 Water deprivation test and vasopressin stimulation test
 MRI pituitary

Treatment : hormone replacement and treatment of underlying


 Glucocorticoids
 Thyroxine
 Testosterone, HCG injection(if fertility is desired), estrogen
 GH- if symptomatic
 Treatment of cause such as pituitary tumour by surgery.

Stem- Lethargy and weight gain


 Hypothyroidism
1. Primary hypothyroidism
*prior treatment for hyperthyroidism-previous thyroid
surgery, radioiodine therapy, excessive use of carbimazole
*iodine deficiency
*autoimmune disease-hashomoto’s thyroiditis,
*post partum thyroiditis
*subacute/D-quervain’s thyroiditis
*drugs-amiodarone, lithium

2. secondary hypothyroidism- hypothalamic and pituitary

disease(tumours, amyloidosis, sarcoidosis)

 Cushing’s syndrome
 Addisions disease
 Type 2 DM

Presenting illness:

 Lethargy
 GIT-constipation, weight gain
 Metabolic-cold intolerance, menorrhagia
 N/S-fatigue, depression, cognitive impairment, psychosis
 Hoarse of voice
 Neck lump
 Coarsening of hands

Past medical history- thyroid surgery, radioiodine, autoimmune


Drug history-amiodarone, carbimazole, lithium

Family history* Pregnancy*

Physical examination:

 Elevated BMI
 Hand-pulse(bradycardia), dry skin, nail changes(onycholysis,
ridging), carpal tunnel syndrome
 Face-periorbital puffiness, xanthelesma
 Neck-goiter, thyroidectomy scars
 Proximal myopathy
 Lower limbs- non pitting oedema, Slow relaxing tendon
 Look at eyes for grave’s disease
 Look for autoimmune diseases-vitilgo, pernicious anemia, DM
 Ask for postural drop of BP(to exclude coexisting addisons)
 Look for carpal tunnel syndrome, cerebellar features

Addressing concerns :

 You have a condition called hypothyroidism which means an

underactive thyroid gland which is not producing enough of
thyroid hormone
 I will confirm with a blood tests today and the treatment if
replacement of the hormone


 TFT-TSH, T4 , t3
 Anti-TPO(Thyroid peroxidase antibodies) , anti-thyroglobulin
 FBC-macrocytic anaemia
 Lipid profile
 9 am cortisol
 USG of neck


 Levothyroxine replacement

*disorder of keratinization-abnormal epidermal differentiation


 Inherited –ichthyosis vulgaris, lamellar ichthyosis, x-linked

ichthyosis, epidermolytic hyperkeratosis
 Acquired –autoimmune disorders, malignancy, HIV infection

Presenting illness:

 Onset in early childhood

 Dry skin with scales most prominent over trunk, abdomen,
buttocks and legs
 May be associated with atopic dermatitis
 Eye-corneal ulcers, opacities

Past medical history-atopic dermatitis, autoimmune disorders,

malignancy-mostly haematological, HIV

Drug history*

Family history*

Sexual history

Physical examination:

 Skin-dry, scaly skin

 Eyes- eye lids(ectropion,trichiasis, madarosis), corneal ulcer,

Addressing concerns:

 It is a condition that causes widespread and persistent dry,

fish scale skin
 Some types are inherited and some acquired
 Refer to skin doctor for skin biopsy and management
 Treatment involves skin emollients, topical creams and oral
drugs as well
 There is no cure, but manageable with the medication
 Psychological therapy?


 Skin biopsy
 Genetic testing
 CBC with PBF
 Autoimmune screen-ANA, anti-dsDNA(SLE), anti-centromere
 Tests for sarcoidosis


 Oral retinoids-isotretinoin, etretinate

 Ocular therapy-artificial tears
 Topical therapy-topical cyclosporine A, petroleum ointments,
10% urea ointment, topical tazarotene, salicylic acid
 Treatment of secondary bacterial infections
Idiopathic intracranial hypertension

*headache with history of isotretinoin intake for Acne

Presenting illness:

 Obese female
 Increased ICP- non-specific headache ,nausea and vomiting
 Papilloedema-leading to secondary progressive optic
atrophy-visual loss
 Diplopia-on lateral gaze(false localizing sign-6 th nerve palsy)
 tinnitus
 Exclude DD—migraine, tension, ICSOL

Past medical history: HTN, hypothyroidism, cushing’s

Drug history*-isotretinoin,steroids, tetracycline,OCP

thyroxine,nitrofurantion, lithium, SLE, Sarcoidosis


Physical examination:

 Visual acuity-usu. Intact

 Visual fields- peripheral visual field constriction due to
 Eye movements- check for 6th nerve palsy, lateral gaze palsy
 Fundoscopy-bilateral papilloedema*

Addressing concerns :

 The brain and the spinal cord are bathed by a clear watery
fluid called CSF within the skull.
 IIH is raised pressure within the skull which puts pressure on
the brain. The exact cause is not known. The raised pressure
will give pressure to back of the eye where the nerve
responsible for vision called optic nerve is situated. It gets
swollen and if not treated, might lead to blindness.
 I will give medications to relieve your headache and ask eye
doctor to see you and refer to brain doctor.

 MRI/CT Brain(to rule out intracranial lesion)
 LP
 Bed side USG-measure diameter of optic nerve sheath
 Detailed ophthalmic assessment(formal perimetry, OCT)


 General- treat obesity -weight loss, diet , exercise*

 Medical therapy-acetazolamide, furosemide,steroids ,
NSAIDs and paracetamol for headache(amytryptylline,
propanolol, topiramate-prophylaxis)
 Surgery-optic nerve sheath fenestration, LP or VP shunt
 Serial LP
Klinefelter’s syndrome


 kallman’s syndrome
 other causes of primary hypogonadism

DD of tall stature:

 klinefelter
 familial
 marfan’s
 homocystinuria

Presenting illness:

 Infertility, tall stature, Men

 Gynaecomastia
 Other symptoms of hypogonadism- erectile
dysfunction,fatigue, low shaving frequency, high pitched
 Academic difficulties and behavioural problems
 DD… kallman’s syn(smell difficulty)

Past medical history- increased evidence of autoimmune

diseases(SLE, RA, DM, hashimoto’s thyroiditis), mitral valve

Social history?*

Physical exam:

 Tall stature
 Gynaecomastia
 Paucity of facial and axillary hair
 Auscultate precordium for mitral valve prolapsed
 Ask to palpate testes-small and firm


 Primary gonadal failure- low testosterone, high FSH, LH

 Karyotyping( 47xxy)
 Echo for MVP
 Dexa scan for osteoporosis

Treatment :

 Testosterone replacement therapy

 Fertility assessment and assistance
 Surgery for gynaecomastia
Lower GI bleed


 Anatomic-diverticulosis/diverticulitis of colon or small

 Inflammatory- IBD
 Infectious-salmonella, shigella, pseudomembranous colitis
 Neoplasm-colonic, rectal, anal malignancy, rectal polyps,
small intestinal malignancy
 Haemorrhoids , anal fissures
 Vascular-angiodysplasia, ischaemic colitis,radiation induced
 AV malformations
 Coagulopathy

Presenting illness:

 Stool-bright red blood(left side of colon), maroon stool(right

side of colon), 1st or recurrent episode?
 Features of shock
Look for causes:
 Infectious and IBD-fever, abdominal pain, mucus, oral
ulcers, joint pain, eye redness
 Diverticular - older patient, painless bleed, mild
abdominal cramp
 Ischaemic colitis-abdominal pain, diarrhoea, bleeding,
may have cardiovascular diseases
 Haemorrhoids-blood drops on toilet paper or toilet bowl,
stools streaked blood,
 Angiodysplasia-painless bleed, repeated bleed, iron
deficiency anaemia, syncope

Past medical history- as above

Family history-colon cancer

Physical examination:

 Pulse, BP
 Anaemia
 Abdomen-?mass, features of IBD
 Perform DRE


 FBC, LFT, RFT, S.elctrolytes, clotting profile

 Blood grouping and cross match
 Colonoscopy, capsule endoscopy, double ballon
enteroscopy,push enteroscopy, OGD
 Helical CT scan
 Radionuclide scanning
 Mesenteric angiography, Meckel scan


 Stabilize the patient with ABCDE approach

 Treat according to cause –localize the site of bleeding with
colonoscopy-coagulation and injection with
vasoconstrictors(vasopressin, epinephrine) or sclerosing
agents(absolute alcohol) , embolization with gelatin sponge,
polyvinyl alcohol…., surgery
Lower motor neuron facial nerve palsy

Causes : unilateral causes

 bells palsy
 ramsay hunt syndrome –vesicles
 parotid tumour/surgery/parotitis, middle ear infections,
 trauma-base of skull fracture, temporal bone fracture
 brain stem MS, Brain stem stroke(nuclear lesion)-check for
 CPA tumour
 mononeuritis multiplex

Bilateral LMN FN palsy:

 sarcoidosis
 lyme disease
 myasthenia gravis,
 myotonic dystrophy-frontal balding, myotonic facies,
myotonic grip, percussion myotonia,
 fascioscapulohumeral dystrophy-winging of scapula,
proximal myopathy with wasting
 bilateral bells palsy

Presenting illness:

 Bell’s palsy-acute sudden onset facial paralysis, posterior

auricular pain, decreased tearing, hyperacusis, taste
disturbances, earache, poor eyelid closure, tingling or
numbness of the cheek/mouth. Associated with HSV
 Ramsay-hunt syndrome-vesicular rash on ear canal, auricle,
mouth, otalgia/hearing loss,vertigo,tinnitus. Associated with
 Ear discharge(CSOM)
 Parotid region swelling
 CPA tumour-headaches, gait problem, hearing loss
 Exclude stroke-hemiparesis? Speech?

Past medical and surgical history- HTN, DM, parotid tumour,

CSOM, parotid surgery, trauma

Physical examination:

 Examine 7th CN, 5TH CN, 8TH CN, look for vesicles in ear and
oral cavity, look for scars in mastoid and parotid region, look
for hemiparesis
 Ask about taste sensation and lacrimation

Addressing concerns:

 Bell’s palsy is a condition that causes paralysis of the

muscles in one side of face. It is due to swelling of the nerve
that supplies muscles of face called facial nerve. The exact
cause is unknown , possibly due to viral infection called
 It is a clinical diagnosis, but I would like to measure BP and
check glucose level, coz it is commonly associated with high
blood pressure and Diabetes
 7 out of 10 people recover completely with or without
 Treatment is with a steroid which can reduce the swelling of
facial nerve, eye care….


 CBC with ESR

 Blood glucose
 Nerve conduction studies
 audiometry
To look for the cause
 Infection screen-anti-HIV,RPR/TPHA
 MRI of brain stem
 Lyme serology
 VZV isolation in conventional cell culture, PCR , Tzanck test
(RH syndrome)
 Serum ACE, CXR(sarcoidosis)


General- eye care, face physiotherapy

Specific treatments: based on cause

Bell’s palsy- steroid

Ramsay-Hunt syndrome- oral steroids, oral acyclovir


 80% recover completely within 6 weeks to 3 months


*black tarry stool


 Upper GI bleeding due to any cause-PUD, variceal bleed,

erosion, Mallory weiss tear, malignancy, drugs(warfarin),
thrombocytopenia, haemophilia, vascular malformation
 Bleeding from ascending colon, small intestine

Presenting illness:

 Stool-jet black, tar like, and sticky, duration

 Ask for haematemesis, abdominal pain, dyspepsia,
dysphagia, odynophagia, abdominal distension(CLD)
 Features of shock

Past medical history- PUD,CLD, IBD, GI malignancy

Drug history-NSAIDs, steroids, anticoagulants, iron tablets

Personal-alcohol , smoking

Physical examination

 Pulse, ask to measure BP

 Stigmata of CLD
 Anaemia
 Ask to perform DRE to confirm malaena


 FBC, UnE, LFT,RFT, clotting profile, PT, INR

 Blood grouping and crossmatching
 USG whole abdomen
 Capsule endoscopy and colonoscopy may be required

Note: fall in haemoglobin and rise in urea:creatinine ratio is an

indicator of Upper GI bleed


 ABCDE approach to stabilize the patient

 OGD –and treat based on the underlying cause
Marfan syndrome

Can present as:

 Tall stature
 H/O Spontaneous pneumothorax
 Chest pain, palpitations, sob(AR)

Presenting illness:
 Pneumothorax-when? Frequency? How treated?
 Syncope,chest pain, sob, palpitations( aortic dissection, AR)
 Eye- vision problem?
 Joints-hypermobility?
 Joint pain/back pain?
 Learning difficulties, epilepsy, developmental

Past medical history: penumothorax(collapsed lung), AR,

Surgical history-chest drain?
Drug history-
Social, occupational, family

Physical examination:
 Tall with disproportionately long limbs compared to trunk
 Hands- thumb sign(steinberg sign)), wrist sign,
arachnodactyly, joint hyperextensibility of joints
 Kyphoscoliosis
 Eyes-lens displaced upward, heterochromia? Blue sclera?
Myopia, RD, Iridodenesis(inspect closely)
 Mouth-high arched palate, crowding of teeth
 Heart- AR? MVP?
 Lungs-pectus excavatum or carinatum, chest drain scars, ?
 Pes planus
Addressing concerns:
 Your symptoms may be due to a condition called marfan
syndrome . it is inherited condition affecting muscles, joints
and sometimes can affect heart and eyes.
 We will do tests to exclude problem with the heart and refer
to eye doctor for assessment for any eye problem
 Treatment is symptomatic with treatment of underlying
condition associated with it
 Support groups

Investigations: clinical diagnosis based on revised Ghents

 Back pain(dural ectasia)-MRI
 Genetic testing- fibrillin 1 gene

 Genetic counseling
 Cardiac- lifelong B-blockade, elective aortic root replacement
when diameter is >50mm or if dilatation is occurring at
>5mm/year or if there is family history of dissection
 Opthalmological follow up
 Physio and occupational therapy
MEN type 1 syndrome

3Ps-parathyroid tumours,pituitary tumours, pancreatic islet cell


AD and can be sporadic as well

Presenting illness:

 Parathyroid tumours(primary hyperparathyroidism)-

hypercalcemia(polydipsia, polyuria, constipation, malaise),
 Pancreatic islet cell tumours- gastrinomas(diarrhoea,
recurrent peptic ulcer disease), insulinomas(hypoglycemias),
glucagonomas(hyperglycemia,necrolytic migratory
erythema), VIPomas(watery diarrhoea, hypokalaemia,
 Pituitary tumours- headaches, visual field defects.
Prolactinomas(decreased libido and erectile dysfunction in
men,amenorrhea and galactorrhoea in women), GH-
 Carcinoid tumours-flushing, diarrhoea, bronchospasm

Past medical and surgical history- renal stone, peptic ulcer,

headaches, parathyroid surgery

Family history*

Physical examination:
 Visual acuity, visual field defects, fundoscopy
 Parathyroidectomy scar in neck, thymectomy scar
 Ask to measure BP

Addressing concerns:
 MEN type 1 syndrome is a rare hereditary disorder that
causes tumours in the glands that produces hormones, such
as parathyroids, pancreas and pituitary. It produces
excessive hormones that can lead to disease.
 However the tumours are usually non-cancerous(benign)
 Although it can’t be cured, regular testing is needed to
detect problems
 Will refer to gland doctor, bowel doctor, and surgeons……
 Genetic counselling


 Hyperparathyroidism- calcium and parathyroid hormone

levels, USG of neck , DEXA scan for bone abnormalities
 Pituitary- MRI, S.Prolactin, GH levels
 Gastrinomas-fasting gastrin level, secreting stimulation test,
endoscopic USG, Scintigraphy(choice)
 Insulinomas-supervised 72 hour fast, CT/MRI , scintigraphy,
SPECT scan
 Glucagonomas- hyperglycemia, glucagon levels
 Carcinoids- plasma chromogranin A, urinary 5-
hydroxyindoleacetic acid, CT/MRI chest
 Genetic testing


 Hyperparathyroidism-subtotal or total parathyroidectomy

with forearm autotransplantation
 Gastrinoma- PPI, Surgical removal, somatostatin analogues
 Insulinoma-surgical removal, octreotide
 Pituitary tumours- transphenoidal surgery, radiotherapy,
octreotide, bromocriptine
 Carcinoid-surgery, radiotherapy, octreotide
MEN type 2A syndrome

*mutation in RET proto-oncogene

Presenting illness:

 Medullary thyroid carcinoma- neck mass, diarrhoea due to

elevated calcitonin levels
 Pheochromocytoma(benign tumour of adrenal medulla)-
hypertension , episodic sweating, headaches
 Parathyroid hyperplasia-features of hypercalcemia

Past medical and surgical history-thyroidectomy surgery, HTN,

renal stones

Physical examination:

 Pulse, BP
 Neck mass/thyroid nodule, neck scar
 Fundoscopy-hypertensive retinopathy

Addressing concerns:

 Is a rare hereditary condition that causes tumours in thyroid,

parathyroid and adrenal glands
 Will do blood tests, scans of neck and refer to gland doctor
for further investigations and management
 Genetic counselling, family screening

 MTC-calcitonin levels, USG neck, carcinoembryonic antigen,

CT chest and abdomen for metastatic disease, radionuclide
scanning to see extent of metastases, tumour removal and
 Parathyroid hyperplasia-calcium and parathyroid hormone
levels, USG neck
 Pheochromocytoma-urinary catecholamines and
metanephrine, plasma metanephrine, CT/MRI of adrenal
glands, MIBG(metaiodobenzylguanidine) scan


 Pheochromocytoma- alpha blocker followed by b-blocker ,

then surgery
 MTC-surgery(thyroidectomy)
 Hyperparathyroidism-management of hypercalcemia,

Long term monitoring: yearly

 24 hour urinary catecholamines, metanephrine

 Calcitonin, CEA levels
 S.calcium, PTH levels

Hereditary pheochromocytomas:

 MEN 2 syndrome
 Von-Hippel-Lindau Syndrome
 Neurofibromatosis
 Tuberous sclerosis
Meralgia paraesthetica

*it is an entrapment neuropathy of a lateral femoral cutaneous


*the segmental origin is L2 and L3 and it is purely sensory with no

motor fibers(so no motor involvement)

*more common in males


 Idiopathic entrapment under inguinal ligament just medial to

Anterosuperior iliac spine
 Injury –traumatic(pelvic fracture, seat belt injury), following
 Mononeuritis multiplex-diabetes
 Pelvic-pregnancy, tensed ascites, pelvic tumours,
retroperitoneal haemorrhage(on anticoagulants)
 Obesity, tight fitting garments, belts
 Malignant infiltration of the nerve
 Lumbar disc-L2,3 root compressions

Clinical features

 Burning or numbness, pain down the upper lateral aspect of

the thigh, may be bilateral, symptoms are usually
aggravated by standing and relieved by sitting
 Ask about injury, surgeries, diabetes, pregnancy, pelvic
tumours etc
 Ask about danger signs-spinal cord compression
 Examination of lower limbs-motor(normal), sensory(loss in
anterolateral aspect of the thigh),
 pelvic compression test( the pain can be reproduced by
deep palpation just below the anterior superior iliac spine
and also by extension of the hip
 Look for causes as per history

 Lumbosacral plexopathy-diabetic, neoplastic)

 Mononeuritis multiplex
 Lumber degenerative disc disease
 Lumber spondylosis
 Pelvic neoplasm
 Retroperitoneal haemorrhage


 Bed side: Pelvic compression test, lidocaine injection of the

nerve will abolish the pain
 Blood sugar
 USG of nerve
 Nerve conduction studies and EMG may be useful
 MRI neurography, MRI to investigate lumber plexus
 Ultrasound pelvic region
 X ray pelvis to look for fracture

Management :

Conservative initially

General :

 Physical therapy-TENS, Heat application

 Reduce weight if obese
 Avoid wearing constrictive garments/belts

Medical :

 NSAIDs, antricyclics, pregabalin for pain,

 Local steroid injections
 Treatment of underlying cause if any
Surgery: nerve decompression surgery

Prognosis: mostly self limiting

Myasthenia gravis

Stem- blurring of vision

Presenting illness:

 Double vision, droopy eye lids

 Proximal myopathy-worsens as the day progress
 Dysphagia, shortness of breath, slurring of speech
 Triggering/exacerbating factors-stress, surgery, viral
infection, medications(aminoglycosides, lithium, chloroquine,
b-blockers, phenytoin)

Past medical history: autoimmune diseases, thymectomy


Drug history*

Personal-smoker, alcohol?

Physical examination

 Face- bilateral facial weakness, ptosis

 Eye-ptosis, complex opthalmoplegia, fatiguability
 Chest-sternotomy scars
 Proximal myopathy

Addressing concerns:

 MG is a rare condition that causes muscle weakness that

comes and goes. It commonly affects the muscles that
control eyes, face, swallowing and arms
 Will refer to the specialists doctor for further tests to see how
well your nerves are working and also blood tests
 Treatment involves avoiding the triggers, medication to
improve the weakness
 If you develop severe breathing or swallowing difficulties,
you may need urgent treatment in the hospital…medic alert


 Bedside-ice pack and tensilon test

 Serology- anti-AchR antibodies, anti-MUSK antibodies
 EMG, repetitive nerve stimulation
 CT chest
 Spirometry
 Screen for autoimmune diseases

Management: MDT approach

General-avoid precipitant drugs


 cholinesterase inhibitors-pyridostigmine
 immunosuppresants-steroids, azathioprine, cyclosporine,
 I/V IG


Surgical: Thymectomy if thymoma, thymic hyperplasia and

generalized MG with age 55 or less.

Medic alert bracelets

Necrobiosis Lipoidica Diabeticorum


 Diabetic dermopathy
 Cutaneous sarcoidosis
 Granuloma annulare

Presenting illness:

 Skin lesion- located mostly in shins, usually painless, can be

painful, often bilateral
 History DM
 Other skin manifestations-diabetic dermopathy

Past medical history: DM(duration, latest HBA1c, complications)

Drug history

Physical examination:

 Skin lesion- well-circumscribed oval plaques on the anterior

surface of lower legs with shiny surface, yellow, waxy and
atrophic center and telangiectasias with red-brown margins.
Check peripheral pulses
 Features of DM-finger prick marks, urine dipstick,
fundoscopy, examine for peripheral neuropathy

Addressing concerns:

 Your skin lesion may be due to a condition called NLD

 It is a rare condition of skin associated with DM or Pre-
diabetes or sometimes in normal people
 Occurs due to abnormal deposition of fat and thickening of
blood vessels wall
 I will check blood glucose and refer to skin doctor for biopsy
and confirmation


 Fasting blood glucose, post prandial, HBA1c

 Skin biopsy


 Skin protection from trauma

 Topical or intralesional steroids
 Good diabetic control
 Surgery-laser, excision and skin grafting in severe cases

Presenting illness

 Skin-neurofibromas, skin colour changes

 Neurological- hearing problems(acoustic neuroma), visual
problems(optic gliomas), epilepsy, learning difficulties(CNS
tumours), radicular pain(nerve compression), Spinal cord
 MSK-back pain, fractures
 CVS- hypertension( pheochromocytoma, RAS, coarctation of
aorta), restrictive cardiomyopathy
 Lungs- pulmonary fibrosis, pneumothorax

Past medical history- HTN, brain tumours, pulmonary fibrosis,

Drug history
Family history*

Physical examination:
 Skin-neurofibromas, café-au-lait spots, axillary freckling,
scars from previous surgery, plexiform neuromas
 Arm- ask for blood pressure

 Eye-look for Lish nodules on iris (small brown dots) with

torch light. If not visible, to see in slit lamp examination,
visual acuity, fundoscopy(optic glioma)
 Ears- hearing aids? If so, look for Features of CPA angle
tumour signs
 MSK- Kyphosis, bowing of long bones, charcot joints
Addressing concerns:

 It seems that you are suffering from neurofibromatosis type

 It is a genetic disorder, that causes tumours to form on nerve
tissue which is present anywhere in nervous system
 The tumours are usually benign
 Genetic counselling

Clinical diagnosis

 MRI brain to exclude tumours

 Biopsy of tumour if malignancy is suspected
 Doppler USG renal tract to exclude RAS
 Investigate for pheochromocytoma if suspected
 Echo to exclude MVP


2 or more:

 6 or more café-au-lait spots(>15mm in postpubertal and

>5mm in prepubertal children)
 2 or more neurofibromas or 1 plexiform neuroma
 Freckling in axillary and inguinal regions
 2 or more lish nodules
 Optic glioma
 Sphenoid dysplasia and thinning of long bones
 1st degree relative with NF

NF type 2(if either of the following)

 Bilateral 8th cranial nerve masses(on CT or MRI)
 1ST degree relative with NF 2 and either a unilateral 8 th nerve
mass or 2 of:neurofibroma, meningioma, glioma,


 Patient edu and genetic counselling

 Treatment of HTN
 Hearing aids
 Surgery to remove tumours
Obstructive sleep Apnea

*OSA that is associated with excessive daytime sleepiness is

called OSA syndrome.


 Asthma
 Narcolepsy
 Central sleep apnea syndrome( due to stroke and heart
failure…no airway collapse)

Presenting illness:

 Nocturnal symptoms-snoring, witnessed apneas, gasping

and choking sensations, nocturia, insomnia, restless sleep
 Daytime symptoms-excessive day time sleepiness(EDS),
tiredness, waking up tired, morning headache, memory and
intellectual impairment, mood changes such as depression
and anxiety, decreased libido, impotence, HTN, GERD
 Alarm features-ankle swelling, blue lips
 Ask for causes- ?obesity, acromegaly, hypothyroidism,
 Exclude DD

Past medical history- HTN(Systemic , pulmonary arterial), DM,

Hypothyriodism, acromegaly

Drug history-sedatives?



Social? How is it affecting daily life, occupational dysfunction?

Physical examination:

 Obese
 Dyspneic or sleepy at rest, on oxygen therapy , CPAP
machine nearby
 Face-facial plethora, central cyanosis, conjuctival
congestion(secondary polycythaemia), macroglossia,
tonsillar enlargement?
 Neck-ask to measure neck circumference(>17 inch in men
and >15 inch in women)
 Examine Respiratory system
 Look for signs of Pulmonary HTN, CCF
 Ask to measure BP, dip urine for glucose

Addressing concerns:

 OSA is a condition where the walls of the throat relax and

narrow during sleep, interrupting normal breathing and
hence disturbing sleep.


 Overnight polysomnography/sleep study

 Lipid profile, blood glucose, s.uric acid(metabolic syn)
Treatment of OSA:

 General- weight loss-(diet, exercise, orlistat), smoking and

alcohol cessation
 Drug-modafinil
 mandibular advancement devices
 surgery

Risk factors of OSA

 Overweight or obese
 Male
 Large neck, narrow airway(tonsils, adenoids,small lower jaw)
 Alcohol,smoking
 Acromegaly, hypothyroidism
 Sedatives
 Family history
Optic Atrophy


1. sudden loss of vision- ischaemic cause

 non arteritic-thromboembolism(HTN, DM,IHD,
 arteritic-GCA

2. Sub acute loss-demyelination(MS and NMO)

3. Gradual loss

 compressive –optic nerve glioma/meninigioma, frontal

meningioma, pituitary tumour
 nutritional-VIT B 1,6,12 deficiency
 toxic- ethambutol, methanol, tobacco, Lead
 glaucoma

4. Inherited- Leber’s optic neuropathy, DIDMOAD(DI, DM, Optic

atrophy, deafness), friedreich’s ataxia

Presenting illness

 deterioration in vision- unilateral/bilateral, onset and

progression, usually painless
 DD: sudden vision loss with headache-exclude GCA(jaw
claudication, weight loss), pain on eye movement(optic
neuritis-MS), features of pituitary tumour?

Past medical history: DM, HTN, MS, tuberculosis,

Drug history-ethambutol?


Family history*

Occupational –lead? Methanol?

Physical examinations:
 Visual acuity- reduced
 Light reflex- RAPD may be there
 Fundoscopy-optic disc may look total pallor, temporal pallor,
 Colour vision
 Visual fields
 Eye movement-INO in MS, Nystagmus
 Look for causes- such as cerebellar signs if MS

Addressing concerns:

 Optic atrophy is the condition that affects optic nerve at the

back of the eye which carries impulses of vision from the
eye to brain
 There are several causes which can damage the optic nerve
and in your case, it seems like due to a condition called MS
 Referral to eye doc
 Starting steroid


 Formal perimetry, ERG, OCT

 Based on suspected cause- Blood glucose, lipid profile, ECG,
 ESR, Temporal artery biopsy(GCA)
 CT/MRI brain and orbit
 VIT B12 levels
 Heavy metal screen
 Infection screen-TORCH panel

Treatment: depends on cause

 Steroids in optic neuritis

 Steroids in Arteritic AION(GCA)
 VIT b12 replacement
Osteogenesis imperfecta

 Can present as history of fracture with blue sclera

 Marfan syndrome
 Ehlers danlos syndrome
 Pseudoxanthoma elasticum

Presenting illness:

 Fractures- where? Frequency? Cause(low impact)

 Chest pain, syncope, sob(AR)
 Hearing loss
 Hypermobility of joints

Past medical and surgical history: fracture, AR

Drug history: steroid use?
Occupational , social and family history*

Physical examination:
 Short stature as opposed to Marfan’s, kyphoscoliosis
 Face- blue sclera, hearing aids?, dentinogenesis imperfecta,
 Locomotor-evidence of previous multiple fractures, bowing of
long bones, joint hypermobility,
 Heart-AR/surgical scars
 Skin-hyperlaxity

Addressing concerns:
 I think your fractures and the problem with the eyes are
connected and may be due to a condition called
osteogenesis imperfecta. It is a condition where there is
rapid formation and destruction of bone leading to weakened
 We need to do some tests to confirm it and tests to see the
thickness of your bone.
 Treatment involves preventing fractures by giving
medications to strengthen the bone
 It is inherited condition, and will refer to geneticist as there
will be implication if you want to have children in the future

Investigations: clinical diagnosis

 Genetic testing
 DEXA scan
 Echocardiography

 Patient edu and genetic counselling
 Calcium, vit D, bisphosphonates
 Orthopaedic interventions for fracture, hearing aids
 Physio, occupational therapy


Paget’s disease

Bone pain and raised ALP

 Pagets disease
 Osteomalacia
 metastases

Presenting illness:

 Bony pain
 Fractures
 Increasing hat size
 Hearing loss
 Alarm symptoms-high output cardiac failure, cord
 Features of OA and gout associated with it

Past medical history:

Drug history: Bisphosphonates?
Occupational, social , family history*

Physical examination:
 Collapsing pulse(hyperdynamic)
 Enlargement of the skull-frontal bossing, enlarged maxilla
 Deformities of long bones- bowing of tibia, previous fractures
 Kyphosis
 Hearing aid?(CN 8TH nerve), other CN nerves may be affected
 Exclude osteomalacia- proximal myopathy
 Heart –CCF?

Addressing concerns:
 Pagets disease –due to high turnover of the bones
 We will do x rays and blood test(ALP), also check vit D and
calcium levels as it can cause similar symptoms
 We will address your pain with analgesia

 ALP(raised), calcium and phosphorus levels are often normal
 VIT D(normal)
 Imaging- x ray and bone scintigraphy/isotope bone
scan(areas of increased uptake in pagetic bone)

 Medical-NSAIDs, Bisphosphonates, cal and vit D supplements
 Physio, occupational therapy
 Orthopaedic interventions



 AF
 SVT( A.flutter, AV nodal reentrant tachycardia-rapid and
regular pounding in the neck),
 Atrial/ventricular extrasystoles(typically a missed beat
followed by strong beat, improves on exercise)
 Ventricular arrhythmias-VT(presyncope/syncope)
 Causes of AF(Rheumatic heart diease, IHD, HTN,
(rapid and regular palpitations are due to sinus tachycardia,
SVT, VT,,,,, Irregular palpitations-AF and extrasystoles)

*Non cardiac:

Panic attacks, anxiety disorder,

Focused history:
 Palpitations-regular/irregular, nature of onset , duration, how
fast, have you counted your pulse?, how frequently? Ask to
tap the rhythm, any triggers such as caffeine, alcohol,
exercise(precipitates VT)?, how does it terminate?(SVT
terminate by holding breath/straining-valsalva, extra systoles
terminate with exercise), associated symptoms such as
chest pain, SOB, collapse? Presyncope? Anxiety?(perioral
and finger tip paraesthesias.
 Look for causes-features of thyrotoxicosis, rheumatic heart
disease,pheochromocytoma(headaches, flusing, sweating)
 Alarm symptoms-angina, syncope, stroke signs, CCF
Past medical history:
 Rheumatic heart disease, IHD, HTN, hyperthyroidism,
stoke/TIA, DM, Vascular disease( CHADS2-VAS)

Medication history:
 Thyroxine? Salbutamol? Recreational drugs-cocaine,
 Drugs that prolong QT segment may precipitate polymorphic
VT( Macrolides, quinidine , amiodarone, ssri, TCA)

Personal history-smoker? Alcohol, caffeine

Family, social and occupational history

Physical examinations:
 Pulse-irregularly irregular
 Ask to measure BP
 Eyes and face-thyroid eye signs, malar rash
 Neck-goiter, carotid bruits
 Heart-any murmur?
 Lung bases-fine crepts for heart failure

Addressing concerns:
 I think the cause of your palpitation is an irregular heart
beat called atrial fibrillation. The cause is often not found but
we will look for underlying problems if any and treat them
 The fact that you complain of chest pain and sob may mean
a reduced blood supply to your heart
 We will need to confirm with ECG and investigate further
with ultrasound scan of your heart(echo), may need 24 hour
measurement of your heart rhythm, and dye test to see
blood supply in your heart.
 We can treat AF by getting the heart back to normal rhythm
or try stopping beating it fast. We may have to use blood
thinning agents as AF is a risk factor for formation of blood
clots esp in heart.
 Resting ECG, 24 hr ECG monitoring(holter monitor)
 Echocardiogram
 Coronary angiogram, stress echo, myocardial perfusion scan
 Implantable loop recorders, electrophysiological studies
 CBC-anaemia
 S.electrolytes

Treatment :
Paroxysmal AF:
 Rhythm control strategy is preferred: best achieved by DC
cardioversion following several weeks of anticoagulation,
and followed by B-blockers/amiodarone
 Rate control-B-blockers, calcium channel
blockers(verapemil),amiodarone, digoxin(ABCD)

Persistent and permanent AF:

 Rate control strategy is preferred
 Anticoagulation with warfarin/ novel anticoagulants
according to CHADS2-VASC score
Other therapies-radiofrequency ablation
Treatment of risk factors

CHADS2-VASC score(score of 2 or more-

A-age 75 or more(2)
S-Stroke/TIA/previous thromboembolic disease(2)
V-vascular disease(MI,PVD)-1
SC-Sex Category(female)-1
Papilloedema(Usu bilateral , can be unilateral)

Due to raised ICP.

Can present as headache and blurring of vision:


 ICSOL-tumour , haemorrhage
 IIH( OCP, Tetracycline)-female, obese,hypothyroidism
 Malignant hypertension
 Excessive CSF production-choroid plexus papilloma
 Decreased CSF resorption-meningitis, SAH, Venous sinus
 CO and lead poisoning
 Graves opthalmopathy(usu unilateral)

Presenting illness:

 Headache-worse in morning and lying down, nausea and

 Blurring of vision, double vision on outward gaze(6 th nerve
palsy), loss of visual acuity(late cases), Painless
 Features of primary tumor(metastases)

Past medical history: Meningitis, cancer, HTN(that has been

difficult to treat), SAH
Drug history: OCP, tetracycline, isotretinion, steroids
Social- gas heaters, CO poisoning
occupational –lead poisoning

Physical examination:
 Eye exam- visual acuity(usu. Normal), fields-tunnel vision if
severe, eye movement( 6th nerve palsy), fundoscopy-
 ask for BP and urine dipstick(accelerated HTN)
 fundoscopic findings- venous engorgement and tortuosity
with loss of venous pulsation, optic discs appears blurred
and hyperemic, haemorrhages, exudates, cotton wool spots
around the disc.

Addressing the concerns:

 I think your symptoms of headache and blurring of vision are
related to a raised pressure within the skull. It can lead to
swelling of the optic nerve head at the back of the eye
leading to blurring of vision which is called papilloedema
 We will have to investigate urgently with scans of brain and
further investigations will depend upon the results of initial
 For your pain, I will give you pain killers and treatment will
be based upon the cause.
 Referral to eye doctor.
 Inform DVLA

 CT or MRI brain
 Lumber puncture

Treatment :
Based on underlying cause:
Idiopathic intracranial hypertension:
 life style changes-losing weight, stopping precipitant drugs
 medical-diuretics , carbonic anhydrase inhibitors, steriods
 interventional-serial lumber puncture, lumboperitoneal
shunts, optic nerve sheath fenestration
Paroxysmal Nocturnal Haemoglobinuria

*50% die of thrombotic complications

*break down of RBC(believed to be triggered by acidosis
during sleep)-release of haemoglobin into urine-dark
coloured urine in the morning
*triad of haemolytic anaemia, thrombosis and

 Aplastic anaemia
 Haemolytic anemias
 Paroxysmal cold haemoglobulinemia

Presenting illness:

 Passage of dark urine during night and morning with

partial clearing during the day
 Haemolytic anaemia-look for symptoms of anaemia
 Thrombosis-hepatic vein(Budd-chiari syndrome),
cerebral(stroke, cavernous sinus thrombosis), renal vein
thrombosis, mesenteric vein thrombosis(abdominal pain,
may lead to bowel infarction). Dermal vein
thrombosis(raised , painful nodules in the skin-necrosis),
portal vein thrombosis, splenic vein thrombosis
 Pancytopenia-bleeding,infections
 Erectile dysfunction
 Features of reduced NO levels(Hb combines with NO and
depletes NO)- leading to vasoconstriction-abdominal
pain,bloating, headaches, fatigue, esophageal spasms,
erectile dysfunction, pulmonary hypertension
 Renal failure-pigment(heme and iron) nephropathy, renal
vein thrombosis, tubular obstruction with pigment casts
 Triggers-infections,alcohol, exercise, stress
Past medical history-thrombosis

Drug history-OCP? Advise not to use OCP(risk of thrombosis)

Physical examination:

 Anaemia/pallor
 Skin ecchymoses
 Fever?
 Abdomen-hepatomegaly, ascites(Budd-Chiari syndrome),
absent bowel sounds(bowel necrosis)
 Papilledema in presence of cerebral vein thrombosis
 Tender skin nodules

Addressing concerns:

 PNH is a rare, acquired life threatening disease of the

blood, characterized by breakdown of RBC leading to
anaemia, blood clots and impaired bone marrow function.
 We will do some blood tests today and refer to blood
doctor for confirmation
 The disease may vary from simple anaemia to life-
threatening problems


 CBC and peripheral blood film

 Tests for intravascular haemolysis- elevated LDH,
elevated reticulocyte count, low/absent haptoglobin,
haemoglobinuria and haemosiderinuria
 Flow cytometry of peripheral blood( measures % of cells
that are deficient in glycosyl phosphatidylinositol –
anchored proteins(GPI-APs))
 Bone marrow analysis: erythroid or hyperplastic bone
marrow during hemolytic phase and hypoplastic bone
marrow in the aplastic phase
 Imaging studies for thrombosis


 Stem cell transplantation only curative therapy

 eculizumab(monoclonal antibody)-reduces intravascular
haemolysis(mainstay of treatment)
 Bone marrow hypoplasia - bone marrow transplant, anti-
thymocyte globulin
 Anaemia-leuko-depleted packed RBCs, iron, folic acid
 Treatment of thrombosis
 Corticosteroids during haemolysis


 Thrombosis
 Complications of pancytopenia-infections, anaemia
 Leukaemic transformation

Can present as blistering rash and mouth lesions


 Bullous pemphigoid
 pemphigus
 Dermatitis herpetiformis
 Drug eruption
 Herpes gestationis
 Liner IgA disease
 impetigo

Presenting illness:
 Mucous membrane lesions develop initially by months (50%)
-mouth lesions/vaginal
 Cutaneous blisters- tensed (pemphigoid) or flaccid? Pain?
Distribution? Itchy?
 Alarm symptoms- features of secondary infection/septic

Past medical history: Autoimmune diseases( hypothyroidism,

myasthenia gravis)
Drug history*(it can precipitate Pemphigus)-penicillins, ACEI,
NSAIDs, phenobaribitone

Drug allergies

Occupational ,social, family history

Physical examination:
 See the location of rash, see inside mouth
 Skin blisters are flaccid blister filled with clear fluid located
on normal skin or erythematous base and easily broken
down, leaving red denuded skin and crusted erosions
 Nikolsky sign(not to be performed in exam)
 Ask to look at TPR chart
Addressing concerns:

 I think your skin and mouth blisters are due to a condition

called pemphigus, which occurs due to an overactive
immune system
 To make the diagnosis, I will refer to skin doctor who will take
a skin biopsy from the blister and perform a special test
called immunofluorescence
 Treatment will include steroids and other drugs which will
dampen down inflammation


 Confirm with skin biopsy (direct immunofluorescence of the

specimen shows IgG deposition in epidermis)
 CBC, S.electrolytes

Treatment :
 General-nutrition, hydration, emollients for skin, barrier
nursing, treat secondary infection
 Specific-immunosuppressants, IV IG, Bilogic therapies
Peripheral neuropathy: mixed /sensory neuropathy

Causes to look for:

 DM
 Alcohol
 Drug induced
 Nutritional-vit B12 deficiency
 Hypothyroidism
 Vasculitis
 Infection-HIV, leprosy

Presenting illness:

 Sensory-Positive symptoms(pins and needles or tingling,

pain(burning, shooting , electric shock like),
allodynia(abnormally painful or unpleasant sensation to fine
touch). Negative symptoms-numbness to touch, cold or
warmth. Distribution of sensory loss or symptoms-stocking
and glove?
 Motor-distal weakness-dropping things
 Autonomic-postural hupotension, sexual dysfunction,
excessive sweating
 Ask for features of underlying causes -DM-Duration,
admission for DKA/hypoglycemias, latest HBA1c, other
complications such as nephropathy, retinopathy

Past medical history-DM, CLD, hypothyroidism, vasculitis, CKD

Drug history- INH, phenytoin,nitrofurantoin, amiodarone,



Family history*
Physical examination-Lower limbs exam, look for charcot
arthopathy in DM

Addressing concerns:

 It seems that you are suffering from peripheral neuropathy

 PN is a disorder when the nerves located in the periphery
(which carries sensation from periphery to brain) are
damaged. The damaged nerves might not send a pain signal
even if something is harming you
 It is commonly associated with DM, due to high sugar levels
destroying small vessels supplying the nerves
 I will arrange some blood tests looking for causes esp
Diabetes and treatment will focus on treatment of the
underlying cause. For the pain, I will give you neuropathic
pain killers
 Referral to foot specialists, diabetic nurse, nutritionist, physio
and occupational therapist


 NCS to confirm it
 Look for causes- CBC, fasting blood glucose, LFT, gamma
GGT, TFT, VIT b12, B1 assays, infection screen, vasculitis

Treatment: MDT approach

 Physio, occupational therapy

 Neuropathic pain killers
 Treatment of underlying cause
 Foot care-special foot wears, splints etc
Polycythaemia rubra vera

Stem: history of itching for 10 months. Ankle joints pain (on and
off). Father died of blood cancer.

Provisional diagnosis: PRV with gout due to hyperurecemia


 autoimmune liver disease

 IBD associated arthritis with PSC/PBC

Presenting illness:

 Blood hyperviscosity- headache, dizziness, vertigo, tinnitus,

visual disturbances, angina, intermittent claudication
 Pruritus exacerbated by warm bath-histamine release
 Bleeding complications-epistaxis, gum bleeding,
ecchymoses, GI bleed
 Thrombotic complications-DVT, thromboembolism, stroke,
budd chiari syndrome
 Abdominal pain due to mesenteric vein thrombosis, peptic
ulcer disease
 Hyperuricemia-increasd cell turn over-gout

Past medical history-thrombosis, embolism, stroke, gout


Family history*

Physical examination:

 Evidence of venesection
 Plethoric face
 Polycythaemia/injected conjunctival vessels
 Splenomegaly/hepatosplenomegaly
 Ask to measure BP

Addressing concerns:

 Your symptoms are likely due to a condition called PRV

 PRV is a rare bone marrow disorder in which your body
produces too much of RBCs. When there are too many RBCs
in the blood, it becomes thicker and flows more slowly and
begin to form clots in the vessels cutting down blood supply
reaching to vital organs such as brain, heart
 I will do some simple blood tests today and refer to blood
doctor for further confirmation
 Treatment involves routine drawing of excess blood and
medications to prevent blood clot. It is an incurable
condition, but treatments are available to prevent

 Pulse oximetry to measure arterial oxygen saturation(to rule
out hypoxia as a secondary cause of erythrocytosis)
 CBC,,,increased three cell lines, Increased Hb, increased
 Red blood cell mass
 JAK2 mutation and serum erythropoietin level( positive JAK2
mutation and low Epo level confirms diagnosis)
 Bone marrow biopsy(not usually necessary)
 S.uric acid
 USG abdomen to look for hepatosplenomegaly

 Phlebotomy(to keep haematocrit level below 45%)

 Aspirin 81 mg daily if no contraindications
 Hydroxyurea(cytoreductive agent) for those at high risk of
thrombosis. Others are interferon alpha, busalphan, JAK
Inhibitors ruxolitinib


 Thrombosis-DVT, stroke, Embolism

 MI
 Bleeding
 Leukaemic transformation(AML)
 Myelofibrosis
 Hyperuricemia-gout
Proximal myopathy


 Endocrine : hypothyroidism, hyperthyroidism, cushing’s

syndrome,parathyroid disorders
 Drug induced-statins, steroids, zidovudine, amiodarone,
 Inflammatory-dermatomyositis, polymyositis, PMR(with GCA)
 Alcohol
 osteomalacia
 NM junction disorder-Myasthenia gravis, LEMS
 Muscular dystrophies –FSHD, DMD,BMD
 Periodic paralysis
 Diabetic amyotrophy-very painful, sensory loss on thigh
 Systemic –Sarcoidosis, SLE, RA
 Infection-lyme disease, HIV, EBV
 Metabolic-Glgycogen storage diseases

Presenting illness:

 Symmetric proximal muscle weakness, onset , progression

 Look for underlying causes as above

Past medical history: as above

Drug history*
Family history-perdiodic paralysis, muscular dystrophies
Personal-alcohol? Smoker?
Occupational: housewife, muslim?-osteomalacia

Physical examination:
 Test for proximal myopathy
 Tone, reflexes and sensory may be normal on limb exam
 Look for causes- thyroid(hand signs, eye signs, neck, deep
tendon reflex), Myositits(rash,gottron’s papules), MG(partial
ptosis, complex opthalmoplegia, fatiguability, facial muscle
weakness), Cushing’s syndrome

To confirm muscle disease

 CK(creatine phosphokinase), LDH, LFT, Aldolase

To look for causes:

 VIT D levels
 LFT(Alcohol)
 Urinalysis- myoglobulinemia
 S.electolytes
 PTH level
 Muscle biopsy, anti-Ro, anti La antibodies , anti RNP
antibodies -Myositis
 EMG- MG, Myositis
 Genetic testing-muscular dystrophies

Treatment: according to cause, physiotherapy, counselling

Pseudoxanthoma elasticum

Mostly AD, sometimes Autosomal recessive inheritance

Presenting illness: a systemic disease

 Skin changes on neck and flexural areas-lax, wrinkled and

hanging in folds
 Eyes- decreased vision, angioid streaks, blue sclera
 Heart- HTN, AR, MR, MVP, CAD, Cardiomyopathy
 GIT- haemorrhage
 Peripheral pulses-diminished or absent due to arterial wall
thickening and narrowing(features of PVD)
 Joints-hyperextensible
 CNS- cerebral infarction /haemorrhages
 Kideys- renovascular HTN

Past medical history- HTN, Heart disease

Physical examination-

 Skin survey- folds of loose skin over neck, axillae , groin,

periumbilical region, antecubital fossa. There are areas of
yellow coloured papules coalescing to form larger
pseudoxanthomatous plaques giving ‘pucked in chicken’
 Eyes- blue sclera, visual acuity, fundoscopy
 Heart-AR/MR/MVP
 Pulse and BP

Addressing concerns:

 I think you have a condition called pseudoxanthoma

 It is genetic disorder affecting connective tissue , specifically
called elastic fibers. There is degeneration of elastic fibers
leading to fragmentation with calcification in different parts
of the body
 Referral to eye doctor, check up if heart is involved or not,
measure BP

Investigations: diagnosed based on criteria

 Genetic testing
 Skin biopsy
 CBC-anaemia
 Fecal occult blood test-to see GI bleed
 Lipid profile(associated with atherosclerosis)
 Imaging-Echocardiography

Treatment: no specific therapy

 General –smoking cessation, moderate exercise

 Skin lesions- surgical excision
 Treat CVS conditions

Can present as itchy scaly plaques


 Psoriasis
 Eczema
 Discoid lupus

Presenting illness
 Rash-nature, distribution, scaly? Precipitating factors
(alcohol, streptococcal throat infection, stress, drugs,
sunlight), itchy?
 Joint pain?

Past medical history: arthritis?

Drug history: B-blockers, lithium, ACEi, Antimalarials,
Family history*

Physical examination:
 Rash- well circumscribed erythematous plaque with silvery
white scales in extensor surfaces, scalp
 Nails-pitting, ridging, onycholysis, subungual hyperkeratosis
 Joints-asymmetrical arthritis?

Addressing concerns
 Your itchy rash is due to a condition called psoriasis
 I will give some emollients and creams containing steroids
and vit D. if that doesn’t improve, I will refer to skin doctor
for further treatment.
 Support groups

It is a clinical diagnosis, if in doubt, skin biopsy
 General – avoid precipitating factors, emollients,
 Topical therapy- steroids, Vit
analogues(calcipotriol),retinoids(tazarotene), coal tar,
 Systemic therapy- retinoids(acitretin), MTX and other
immunosuppresants, biologics
 PUVA therapy

Variants of psoriasis:
 Chronic plaque
 Pustular
 Guttate
 Erythrodermic
 Palmoplanter
Psoriatic arthropathy:


 Rheumatoid arthritis
 Seronegative arthropathy(enteropathic, reactive, ankylosing

Presenting illness:
 Joint pain- pattern/which joints? , swelling? Stiffness and its
duration? More at rest or activity? Functional status
 Skin rash, bowel symptoms, urinary symptoms, back
pain/neck pain
 Nail changes
 Extra-articular- apical pulmonary fibrosis, anterior uveitis,
Achilles tendinitis

Past medical history: IBD, Psoriasis, RA

Drug history: NSAIDs? Side effects?
Occupational * social and family history

Physical examination:
 Pattern of joint involvement: asymmetrical oligoarthritis,
symmetrical rheumatoid like pattern, DIP arthopathy,
spondylitis, arthritis mutilans
 Nail changes?
 Finger-dactylitis
 Skin-psoriasis
 Lungs-apical fibrosis,
 Heart –AR?

Addressing concerns:

 You have a condition called psoriatic arthopathy

 I will do some blood tests to see how active it is and also
obtain x rays of the joints.
 I will prescribe you anti-inflammatory painkillers and refer to
physio and occupational therapist.
 If symptoms don’t control with that, then will refer to joint
 Support groups


Clinical diagnosis


 X RAY of joints
 MRI sacroiliac joint

Treatment: MDT approach

 Physio, occupational therapy

 Medical-analgesia, NSAIDs , intra-articular steroid,
DMARDs(MTX, Sulphasalazine) , anti-TNF alpha
therapy(etanercept, infliximab, adalimumab)
Pyoderma gangrenosum

DD of chronic non healing ulcer:

 Pyoderma gangrenosum
 Malignant ulcer
 Infective-tubercular
 Venous ulcer/arterial ulcer
 Neuropathic ulcer
 Vasculitis
 Trauma

Presenting illness

 Ulcer- pain? Site? Progression? How it started? Trauma?

Pus/bloody discharge?
 Look for features of IBD, haematological
malignancies(lymphoma), autoimmune liver disease, RA

Past medical and surgical history: IBD, lymphoma, behcets

disease, RA
Drug history-
Social, occupational and family history

Physical examination:
 Ulcer- edge (purplish, necrotic, overhanging), floor-may be
purulent, surrounding erythema, tender
 Abdomen-IBD
 Lymph nodes(lymphoma)

Addressing concerns:

 I think the painful ulcer in your leg is due to a condition

called P.G
 It is sometimes related to other conditions and in your case,
the blood in your stool is likely to be caused by IBD
 I will do some blood tests and swabbing the ulcer for culture
to see any bugs in it to exclude infection. Then, I will refer to
skin doctor for confirmation by skin biopsy, and for your
bowel problem, I will refer to bowel doctor
 For your pain, I will give you some painkillers, and ulcer
needs to be cleaned regularly


 Wound swab for gram stain and C/S
 Skin biopsy
 Bowel-endoscopy and biopsy


 Topical steroids(for mild cases)

 Immunosuppressive therapy-steroids, ciclosporin, MMF,
azathioprine, anti-TNF alpha therapies
 Paracetamol/NSAIDs for pain
 Dressing
Raynaud’s disease

Presenting illness-

 Hands- on exposure to cold, colour changes (white, blue and

red after warm exposure), pain, symmetrical? What relieves?
Duration? Effect on daily activities?
 Exclude raynaud’s phenomenon( systemic disease such as
SS, SLE, RA, Sjogren’s syndrome…..joint pain, skin tightness,
rashes, dysphagia, muscle aches and pains
 Other sites-tip of nose, ear lobes, toes

Past medical disease- SS, SLE, RA, Hypothyroidism,


Drug history- B-blockers, OCP, Bromocriptine, ergot

Personal history- smoker?*

Occupational –vibration injury?

Physical examination:

 Examine hands-symmetrical involvement , sclerodactyly,

check hand functions
 Check pulse
 Look for associated conditions

Addressing concerns:

 You may have a condition called raynaud’s disease. It is due

to poor circulation in the hands as the vessels supplying the
hands constrict abnormally in response to cold exposure. It
seems an isolated condition however we will have to exclude
any conditions which might associate with it
 B-blockers have worsened your condition, I will stop it and
substitute with CCB
 Cessation of smoking and OCP is recommended
 Avoiding cold by using gloves and keeping warm can help.
There are tablets available which helps to open up the

Investigations: to exclude systemic diseases

 RF
 Anti-centromere antibodies, anti-scl70 antibodies
 ANA, Anti dsDNA
 CXR-cervical rib


 Keeping warm, use gloves, smoking cessation

 Stop precipitating drugs-OCP, b-blocker
 Medical- CCB, ACEi/ARB, iloprost(prostacyline analogue)
Reactive arthritis

Stem-acute ankle joint pain with urinary problem


 Enteropathic arthritis
 Psoriatic arthritis
 Ankylosing arthritis
 Septic arthritis

Presenting illness:

 painful inflammatory arthritis(Usu. After 1-4 weeks of

infection with Chlamydia, salmonella, shigella,
 malaise, fatigue, fever
 heel pain
 Low back pain
 History of Urethritis/ diarrhoea
 Conjunctivitis-irritation and redness
 Keratoderma blenorrhagicum-rash on palms and soles
 Exclude DD

Physical exam-joints (asymmetrical oligoarthritis),fingers(sausage

shaped finger-dactylitis), soles- Keratoderma blenorrhagicum,

Past medical history-urethritis, dirrhoea/dysentery, psoriasis

Family history

Occupational history

Sexual history*

Travel history*
Addressing concerns:

 Reactive arthritis is inflammation affecting mainly the joints,

eyes. It usually occurs following infection in the bowels or in
the urine (following sexual exposure). May be genetically
 Diagnosis is based on clinical features , will do some blood
tests today and if the joint is swollen, will aspirate fluid for
 Majority of the cases(70%) clears up in few months without
causing long term problems
 Will give you NSAIDs for the pain and if that doesn’t work,
will refer to joint doctor.
 Prevention-avoid STI and bowel infections- use condom,

Investigations: clinical diagnosis

 Urine microscopy
 Serology and culture for Chlamydia(urine, blood, stool,
 HLA B27
 Plain x ray on joints
 Synovial fluid analysis to rule out infectious process

 Medical- NSAIDs, steroids(systemic , intraarticular),
tetracycline if Chlamydia is positive, DMARDs,
 physiotherapy
Retinal vein occlusion

Central(Ischaemic and non ischaemic) and peripheral RVO

Presenting illness

 Sudden unilateral painless blurred vision. Impending CRVO

presents with mild blurring of vision worse on waking and
improves towards the day

Past medical history: Look for risk factors*

Personal history- smoker?

Physical examination:

 Visual acuity
 Papillary reflex-normal or RAPD
 Visual field
 Fundoscopy- tortuosity and dilatation of all branches of
central retinal veins, widespread dot/blot/flame shaped
haemorrhages in all quadrants , optic disc and macular
edema may be present, cotton wool spots may be present.
 Look for risk factors-plethoric face(PCRV), dm
 Ask to measure BP


 Fluorescein angiography
 Look for risk factors: FBC, ESR, blood glucose,lipid profile,
plasma protein electrophoresis

No effective medical therapy available

 Identify and Treat the risk factors

 Macular oedema can be treated with intravitreal
corticosteroid therapy
 Panretinal photocoagulation if there is neovascular

Risk factors

 AGE(old age)
 DM, HTN, hyperlipidaemia,smoking
 glaucoma,
 myeloproliferative disorders(polycythaemia, MM,
waldenstrom macroglobulinemia)
 acquired hypercoagulable states(APS)
 Inherited hypercoagulable states(protein C deficiency,
protein S deficiency, antithrombin deficiency, Activated
protein c resistance
 Inflammatory diseases- bechcet’s syndrome, sarcoidosis
Retinitis pigmentosa

DD of gradual loss of vision

 Diabetic /hypertensive retinopathy

 RP
 Cataract
 Glaucoma
 Laser photocoagulation(DD for RP)

Presenting illness:

 Vision impairment: one or both eyes, duration, progression,

variation during day, painless or painful, peripheral or central
vision? Double vision? Colour vision?( In RP-mostly night
vision affected, tunneling of vision, colour vision affected,
flashes of light(photopsia) )
 Bardet-Biedl syndrome-obesity, polydactyly , learning
disability, subfertility/hypogonadism, DM, renal
disease(interstitial nephritis)
 Kearns –sayre syndrome- syncope(heart block),
diplopia(opthalmoplegia), SN deafness
 Abetalipoproteinemia-learning disability, steatorrhea,
peripheral neuropathy, cerebellar ataxia
 Deafness( usher, refsums, KS syndrome)

Medical history- DM/HTN(retinopathy)

Surgical history-laser surgery

Family history* of blindness

Physical examination:

1. visual acuity-impaired if it involves macula
2. fields: peripheral vision loss/constriction of visual field
3. eye movement-opthalmoplegia in KS syndrome
4. fundoscopy-peripheral spiculated black pigments in both
retinas, pale optic disc/optic atrophy, attenuated retinal
5. Look for cataract(50%)
 Any hearing aids? Polydactyly? DM?

Addressing concerns

 Your vision impairment is due to a condition called RP, it is

an inherited disorder
 I will refer to eye doctor for confirmation and refer for
genetic counselling
 Unfortunately, there is no cure for this condition but we can
do to help you
 Inform DVLA
 Support groups

Investigations: clinical plus

 Genetic testing
 Electroretinogram (objective measure of rod and cone

Treatment :

 Genetic counseling
 Supportive-visual aids
Rheumatoid arthritis


 Psoriatic, enteropathic, ankylosing spondylitis, reactive

 Crystal arthritis
 Osteoarthritis

Presenting illness (New or Old case)

 Joint pain- pattern, duration, stiffness, swelling, functional

 Nail changes?
 Colour changes? Raynaud’s phenomenon
 DD- skin rash? Bowel symptoms, urinary symptoms, heel
 Extra-articular- red and painful eyes? Cardio-respiratory
symptoms, dry eye/dry mouth(sjogrens syndrome),
peripheral neuropathy

Past medical history- HTN

Drug history- NSAIDs?

Occupational history? Caplan’s syn
Family history*
Social history*

Physical examination:
 Joints- symmetrical deforming polyarthopathy affecting
MCPs, PIPs and classically sparing DIPs
 Deformities- swan neck(flexion of DIP), boutonniere’s
deformities, Z deformity of thumb, ulnar deviation of
fingers, subluxation at MCPs
 Palmer erythema, wasting of small muscles of hand
 Look for rheumatoid nodules
 Check for hand function
 Eyes
 Lungs
 Abdomen-splenomegaly in felty’s syn
 Check BP, urine dipstick for GN

Addressing concerns:

 I think the cause of your symptoms is due to rheumatoid

arthritis. However, number of conditions look similar, we
need to do tests to confirm it
 I will request some blood tests and x rays of your hands and
then refer to rheumatologist(joint doctor)
 For your pain, I will start with NSAIDs and if the diagnosis is
confirmed, you will be given specific medication by the joint
 Physio and occupational therapy
 Support groups


Dx based on ACR/EULAR criteria

 CBC(neutropenia, anaemia)
 RF
 Anti-CCP
 X-ray of hands
 RFT, urine dipstick
DX: RA, active or not? Functional status, ? look for mixed
connective tissue diseases, look for systemic manifestations


 General-edu, physio, occupational therapy

 Pharmacological- NSAIDs, steroids(intra-articular/pulse),
DMARDs, biologic agents(etanercept, infliximab)
Severe back pain in 73/f:


She lives alone, struggling at home. Known to have osteoporosis.

GP is concerned of another vertebral fracture.

RR-18,Pulse-90, bp-150/85, temp-38, spo2-98

*the patient has fever from above info.

DD to think of:

 Vertebral fracture due to osteoporosis

 Secondary metastases
 Discitis(coz of fever)
 Potts disease/tuberculosis of spine(fever)

Clinical communication skills:

 Presenting illness-
Establish nature of back pain(onset-gradual or rapid,
severity(disturbs sleep or not, daily activities?), exacerbating
and relieving factors, radiation, what precipitated? Any

Fever, sweating (discitis)

Features of primary malignancies-lung, GI tract, breast,


Exclude cord compression (leg weakness, bowel and

bladder control)

History of contact with TB patient

 Past medical and surgical history- patient will give history of

cut injury in toe 1 month back, history of vertebral fracture in
the past.
 Medication history-
Past- history of incomplete antibiotic course for the cut injury
1 month back
Present-alendronate 70mg once a week, calcium
supplements. Ask for any side effects?
 Personal history-smoking, alcohol
 Family history- mother had fracture at hip
 Social history-widowed,living alone
 Occupational history-retired school teacher

Physical examination:
 Ask for pain and feel for the spine
 Examine lower limbs for tone, power, reflexes and check
sensation if time and also indicate the need to check
perianal tone and sensation
 Look at observation chart
 Indicates the need to look for signs of endocarditis( heart

Concerns and questions? Is it another fracture? Why I am

generally feeling unwell?

Addressing concerns:
It is not likely a case of another fracture (but would do x ray
to exclude it). It is likely the part of adjacent vertebral bones
known as disc might be infected with a bug, and probably
the bug entered from the cut injury travelling in the blood
stream (due to incomplete antibiotic course) and finally
reaching the vertebra where the bone was previously broken
(as broken bones act as a favourable place for bugs to grow).
Because of the infection, you are feeling generally unwell.

Clinical judgement:
 Immediate management- admit in hospital, asses for signs of
sepsis syndrome, fluid balance
 Commence empirical antibiotic after taking blood sample for
culture( i/v flucloxacillin)
 Immediate tests- CBC, Blood culture, urea and electrolytes,
CRP, x ray spine and MR spine looking for evidence of
discitis/cord compression
 The need to discuss with the senior/consultant and liaison
with microbiologist and surgeon
 Recognizes the abnormal bone(previous bone fracture as
nidus for infection)

Physical signs:
 Pyrexia( from the info)
 Excludes septic shock
 Identifies spinal tenderness and excludes cord compression

Probable diagnosis:
 Infective discitis presumed secondary to bacteremia
following incompletely treated soft tissue infection
 Osteoporotic fracture
Sheehan’s syndrome

Infarction/necrosis of pituitary gland following postpartum

haemorrhage and hypovolumic shock leading to hypopituitarism
ranging from selective hormonal deficiencies to

Presenting illness:

 Prolactin deficiency-failure to lactate/difficulties with

lactation(common initial symptom
 Gonadotrophin deficiency- amenorrhea, oligomenorrhea, hot
flashes, decreased libido after delivery
 TSH deficiency-secondary hypothyroidism(later part)
 ACTH deficiency-secondary adrenal insufficiency(later part)-
weakness, fatigue, dizziness, hypoglycemia
 Hyponatraemia-acute presentation
 GH deficiency-decreased muscle mass, fatigue

Past medical history: PPH, hypovolumic shock

Physical examination:
 Pallor
 Pulse-brady(Hypothyroidism)
 Postural drop of BP
 Skin-dry, wrinkled
 Eye movements and visual fields
 Reduced axillary hair

Addressing concerns:

 It seems that you are suffering from a condition called

sheehan’s syndrome
 It is due to severe blood loss during and after child birth,
leading to less blood supply to different parts of body and
hence lack of oxygen damaging pituitary gland responsible
for producing so many hormones
 I will do some blood tests and refer to hormone doctor who
will confirm and treat you by hormone replacement


 TSH, T4
 S.Electrolytes(hyponatraemia, normal K)
 S.cortisol, ACTH
 LH, FSH, S.estradiol
 GH levels
 Prolactin levels
 Insulin tolerance test ( induces hypoglycemia and as a result
leading to increased cortisol levels in normal person, in this
case, the cortisol level will not rise)
 MRI of pituitary-?emty sella

Treatment: hormone replacement

 Hydrocortisone replacement initially, then thyroid hormone

and estrogen with or without progesterone. GH replacement
in adults is controversial
Shortness of breath/CCF


 Acute cases- acute severe asthma, pulmonary embolism,

acute heart failure/pulmonary oedema, pneumothorax
 Gradual- CCF, COPD, ILD, bronchiectasis, pleural effusion

Congestive cardiac failure: New or Old case

Focused history:
 Shortness of breath: onset, frequency, on exertion or at rest,
functional status(MRC dyspnea scale), orthopnea, PND,
exacerbating(activity) and relieving factors(rest, GTN),
 Associated symptoms- chest pain, palpitations,
 Ankle swelling
 To exclude DD( respiratory symptoms cough, wheeze,
sputum production, haemoptysis, chest pain,fever, chest

Past medical history and surgical history

 Cardiac-Previous MI,HTN, DM, Hyperlipedemia, any CABG ?
any PCI?
 Lungs-asthma, copd, ild, pulmonary embolism

Drug history: any OCP? Compliance? allergy?

Personal history

Family history
Social , occupational history

Physical examination:
 Dyspnea at rest
 Pulse, ask to measure BP
 Cyanosis
 Precordium exam
 Lungs-fine crepts
 Pedal oedema

Addressing concerns:
 I think the cause of your shortness of breath and swollen
ankles is heart failure. It means that your heart muscle is not
effectively pumping as it should, so fluid collects in lungs and
 I would like to obtain Heart tracing(ECG) and confirm with
ultrasound of heart(echo), also some blood tests to exclude
 We can start treatment right away and one of which is water
tablets to remove fluid collection and other tablets as well

 CBC(anaemia), s.electrolytes, TFT, BNP
 Cxr

Treatment :
 General-no added salt, restricted fluid intake, influenza
vaccination, cardiac rehab
 Medical- diuretics, ACEi or ARB, B-blockers, spironolactone,
 Interventional/surgical-ICD, CRT, CABG, Heart transplant
 Manage risk factors-smoking, hyperlipedemia, DM
Sickle cell anaemia

Due to mutated form of haemoglobin, HbS

Autosomal recessive disorder

Clinical features

Vaso-occlusive crisis (occurs when microcirculation is

obstructed by sickled RBCs causing ischaemic injury to the
organ. Present as pain crisis and can affect any part of
body. Pain is accompanied by fever, malaise

 Abdomen-resemble acute abdomen, reactive ileus, solid

organ infarctions(splenic infarction and autosplenectomy,
papillary necrosis of kidneys)
 Bones- severe deep pain in bones due to bone marrow
infarction, avascular necrosis
 joints and soft tissues: dactylitis, arthritis(hand foot
 Facial pain
 Anaemia-haemolytic, chronic
 Aplastic crisis- due to infection with parvovirus B19(fever,
rash, malaise )
 Splenic sequestration-rapid enlargement of spleen with life
threatening anemia, with high reticulocyte count
 Lungs : Acute chest syndrome(chest pain, fever , cough,
tachypnea, leukocytosis, pulmonary infiltrates in upper
lobes). Pulmonary hypertension
 CNS-stroke, seizures
 Heart- due to microinfarcts and chronic anaemia,
hemosiderin deposition(hemolysis and BT) in myocardium
 Gall stones-due to hemolysis
 Eye-retinitis
 Leg ulcers
 priapism
 Infection with encapsulated bacteria
 Growth retardation, delayed sexual maturation


Anemia, jaundice, abdomen (cholecystectomy scar, splenectomy

scar/splenomegaly), heart- heart failure? Lungs-pulmonary HTN,
acute chest syn, leg ulcers, neurological exam to look for deficicts

Triggers for vaso-occlusive crisis

 Hypoxemia
 Dehydration
 Cold temperature(vasoconstriction)


 Confirm with Hb electrophoresis-HbS

 CBC , Reticulocyte count, PBF-haemolytic anaemia
 RFT, LFT, S.electroltes, urine analysis
 Iron prolife-iron overload
 Imaging-based on organ involvement

Screening of HbS at birth , prenatal testing via CVS



 Hydroxyurea- increases total and fetal Hb

 Management of vaso-occlusive crisis- for acute chest
syn(oxygen, antibiotics, analgesics,hydration, blood
transfusion, bronchodilators)
 Management of chronic pain syndromes-NSAIDs, opioids,
 Management of chronic hemolytic anaemia-folic acid
 Prevention and treatment of infections-
vaccination(pneumococcal, meningococcal , influenza)
 Management of various organ damages
 Prevention of stroke-long term transfusion therapy,


 Stem cell transplant-can be curative

 Blood transfusions, erythocytapheresis/automated red cell
exchange procedure
Systemic lupus erythematosus

Presents with rash on face

DD of rash on face

 Dermatomyositis
 Eczema
 Rosacea
 Mitral stenosis
 Carcinoid syndrome

Presenting illness:
 Facial rash- photosensitive
 Hair loss(alopecia)
 Mouth ulcers
 Lungs-Pleurisy and effusion
 Heart-Pericarditis/myocarditis/endocarditis
 Easy bruising(thrombocytopenia)
 Renal involvement –reduced urine output, ankle and facial
swelling, high blood pressure
 MSK-arthritis, raynaud’s phenomenon
 CNS-psychosis, seizures, depression, weakness/paraesthesia
 DD: MS(palpitations, sob, chest pain), acne rosacea(pustules,
flushing), carcinoid(flushing, diarrhoea, wheeze)
 Features of mixed connective tissue disorder

Past medical history: HTN, CKD, History of thrombosis, recurrent


Drug history-drug induced lupus-INH , hydralazine, phenytoin,


Social, occupational and family history

Physical examination:

 scalp and face-alopecia, erythematous maculopapular malar

rash in butterfly distribution sparing nasolabial folds with
scaling, anaemia, oral ulcers.
 Hands- arthopathy(may be symmetrical) , raynaud’s
phenomenon, nail fold infarcts, palmer erythema
 Skin-purpura, livedoreticularis, vasculitic lesions,
 Chest-pleural effusion, ILD, pul HTN
 Heart- pericarditis(rub), cardiac murmurs due to libman-
sacks endocarditis
 CNS-polyneuropathy/mononeuritis multiplex, hemiparesis
 Renal - ask to measure BP and urine dipstick

Addressing patient’s concerns:

 I think the cause of your symptoms is called SLE due to

overactive immune system
 Unfortunately it can affect different organs, we will do blood
tests to confirm it and tests to exclude involvement of
different organs
 For your rash, we will prescribe sun block and once we
confirm diagnosis, our joint doctor might start you on
steroids and other immunosuppressants
 Support groups


ACR criteria(4 of 11 needed)

 CBC-pancytopenia?
 ESR(Raised in active disease), CRP
 Urine dipstick
 Immunology- ANA, anti-dsDNA antibody, anti-smith antibody,
anti-Ro and anti La antibodies, anti-RNP antibody(mixed
CTD), anti-phospholipid antibodies(anti-cardiolipin antibodies
and lupus anticoagulant), C3 AND C4 decreased in active
 Organ based:
1. Kidney- kidney biopsy
2. Lngs-CXR, CT chest
3. Heart-ECG, echo
4. CNS-MRI brain(neuropsychiatric manifestations)
5. Skin-skin biopsy

Treatment: MDT approach

1. General measures
 Patient education and counselling
 Avoid excessive sunlight-sunscreens, hats
 Removal of offending drug
 Physio and occupational therapy
 Management of cardiovascular risk factors
2. Medical
 Analgesics, NSAIDs for arthritis (may worsen renal
involvement )
 Hydroxychloroquine, topical steroids for Skin disease
 In severe systemic disease-systemic steroids,
cyclophosphamide, azathioprine, MMF, monoclonal
antibodies(rituximab), IV Ig
 Autologous stem cell transplantation(for severe disease)
 RRT for end stage RF due to lupus nephritis
Drug induced lupus:

 H/O oF drug intake

 Rare CNS and renal manifestations
 Positive anti-histone antibodies, negative dsDNA antibodies
 Resolution of clinical manifestations after discontinuation of
 Male:female(1:1)

WHO lupus nephritis

Class I-normal

Class II-Mesangial GN-Consider steroids

Class III-Focal proliferative GN (AZA, MMF, CYCLO)

Class IV-diffuse proliferative GN-

Class V-membranous GN-Steroid therapy, if proliferative

component (treat as above)

Class VI-sclerosing GN- Consider RRT

Systemic sclerosis

Presenting illness:

 Raynaud’s phenomenon- colour changes(pale, blue , red),

cold aggravates, relieving factors, duration, ulcers in finger
tips, amputation
 Joint pain
 Skin tightening –extent
 Respiratory symtoms (ILD, pul HTN)
 Ankle swelling( heart failure, pul htn, renal involvement)
 Dysphagia, diarrhoea(bacterial overgrowth), Primary biliary
 Cardio(pericarditis, cardiomyopathy)
 Mixed connective tissue disease( Features of RA,

Past medical history: HTN, CKD, PUL fibrosis, PUL HTN, IHD,
autoimmune diseases (thyroid disorders)

Drug history:


Occupational, social and family history

Physical examination:

 Hands- sclerodactyly(shiny, smooth and tight skin),

raynaud’s phenomenon, atrophy of finger tips, digital
ulceration/gangrene, calcinosis, amputated digits, arthritis,
dystrophic nails, dilated nail-fold capillaries
 Face-pinched
mouth opening, tight and shiny face
 Lungs-fibrosis and pul HTN
 Ask to measure BP and urine dipstick
Addressing concerns:

 You have a condition called systemic sclerosis due to

overactive immune system

 We will do some blood tests to confirm it and also obtain x

ray of your chest as it can involve lungs, tests function of
kidneys as well

 I will refer to joint doctor for treatment of the condition.

 Support groups


 Inflammatory markers-ESR, CRP

 Urine dipstick
 Anti-centromere antibody(limited SS)
 Anti-Scl 70 antibody(anti DNA topoisomerase 1), anti RNA
polymerase antibody I, II, III-diffuse SS,
 To see organ involvement:
1. Lungs-CXR, pulmonary function tests, HRCT
2. Heart-ECG, echo
3. Renal-renal biopsy
4. GIT-glucose breath test for bacterial overgrowth
Treatment of SS:

 General- edu and counselling, physiotherapy

 Treatment of raynaud’s phenomenon
1. General-smoking cessation, hand warmers, avoid cold
2. Medical-calcium channel blocker, ACEi/ARB, Prostacyline
analogues(iloprost), sympathectomy in severe cases
 Based on organ involvement
1. Renal involvement- ACEi
2. Respiratory disease-prednisolone, cyclophosphamide,
Bosentan(endothelin recep antagonist)
3. GI disease- PPI(for reflux symptoms), Metoclopramide for
bowel dysmotility, antibiotics for small bacterial
4. Skin sclerosis-methotrexate

Scleroderma- localised (morphea) and systemic(limited

and diffuse)

Diffuse-skin involvement in trunk and extremeties

Limited SS- only extremities and face

Limited SS is previously called CREST syndrome

Takayasu Arteritis

*large vessel vasculitis, affects women of child bearing age


 Giant cell arteritis

 atherosclerosis

Presenting illness:

 Asymptomatic (10%)
 Constitutional symptoms-headache, malaise, arthralgias,
fever, weight loss
 CVS-HTN, CCF, AR, Pericarditis, MI, raynaud’s phenomenon,
 N/S-headache, stroke, TIA,seizures, visual disturbance
 Skin lesions-erythema nodosum

Past medical history: HTN(Renal artery stenosis), heart

failure, stroke
Past surgical history*

Physical examination:
 Peripheral pulses-decreased pulsation in brachial
arteries(one or both arm)
 Blood pressure-difference of at least 10mmhg of systolic BP
between arms*
 Neck-carotid bruit*, subclavian bruit, neck scars for previous
 Abdomen-renal bruit
 Heart- AR*, CCF, pulmonary hypertension
 Fundoscopy for hypertensive changes
Addressing concerns:

 Your symptoms may be related to a condition called TA

 It is due to inflammation of the large arteries mainly
affecting the aorta(the main artery carrying blood from heart
to rest of the body) leading to narrowing of the artery and
hence when the organs don’t get the sufficient blood supply,
and symptoms occur
 I will arrange some blood tests today and obtain some tests
to scan the vessels
 Treatment is controlling your blood pressure and controlling
the inflammation initially with steroids


Diagnosis based on ACR criteria

 CBC-normocytic anemia, ESR, CRP may be high

 RFT, urine analysis to see renal involvement-HTN
 CT angiography or MRA to see stenosis or aneurysms,
carotid Doppler USG
 PET scanning
 Tissue biopsy-little role
 Echocardiogram

ACR diagnostic criteria(3 of 6 are necessary):

 Onset of disease 40 years of age or below

 Claudication of an extremity
 Reduced brachial artery pulsation
 Difference in Systolic pressure of more than 10mmhg in arms
 Aortic or subclavian artery bruit
 Angiographic abnormality

 Controlling hypertension, treating CVS risk factors

 Controlling inflammatory process- corticosteroids*,
cytotoxics-azathioprine, MTX, Cyclophosphamide,,, biological
agents-rituximab, infliximab
 Surgical-angioplasty and stenting, CABG
 Low dose aspirin

Prognosis: usually good, may follow relapsing and remitting


 25% unaffected by the disease(self limiting )

 25% are able to perform normal daily activity in remission
 50% are unable to consistently perform normal daily
 25% will not able to do their work
Transient global amnesia


 TIA/stroke
 Temporal lobe seizure
 Hypoglycemia
 Migraine variant
 Dementia

Presenting illness:
 Paroxysmal, transient loss of memory function verified by a
witness. Remote memory is preserved (remember who you
are, recognize the people you know well). Striking loss of
memory for recent events(can’t remember where you are or
how you got there) and impaired ability to retain new
information(registration of information is intact)
 Anxious and agitated, may repeatedly ask questions
concerning the events.
 Symptoms lasts typically less than 24 hours
 Precipitants-stress, pain, exertion, sexual intercourse
 Exclude DD
 Any head injury
 Annual Recurrence (4-5%)

Past medical history: past attack of TGA, migraine, risk factors of

TIA(DM, HTN, hyperlipidemia

Drug history-sedatives

Alcohol*, smoker*

Physical examination:

 Limbs- tone, power, reflexes, gait

 Pulse, BP, Carotid bruit, heart murmur

Addressing concerns:

 TGA is a sudden temporary loss of memory, inability to

recollect recent events. The cause is not known.
 I will do some blood tests today and obtain ECG tracing of
your heart. Although, there are no tests to diagnose this
condition, I will refer to nerve doctor for further tests to
exclude serious condition which can present in similar ways
such as stroke/mini-stroke
 It is harmless and there is no need of treatment as well. If
anxious, referral to psychiatry/counsellers.


 Electrolytes, RBS
 MRI/CT scan to rule out stroke
 EEG to rule out seizure


 reassurance
Transient ischaemic attack

Neurological deficit<24 hours is key

Sudden onset, focal neurological symptoms, symptoms maximal

at onset rather than progressing, negative symptoms

DD of TIA:

 Migraine
 Focal epilepsy
 Hypoglycemia
 MS

DD of amaurosis fugax:
 Central retinal vein or branch occlusion
 Diabetic maculopathy
 Vitreous haemorrhage
 hypoglycemia

Presenting illness:

 TIA affecting anterior cerebral artery-dysphasia, contralateral

weakness, emotional changes
 TIA affecting MCA-dysphasia, contralateral weakness, visual
field loss, sensory loss
 TIA affecting PCA- contralateral visual field loss, neglect,
weakness, sensory loss
 TIA affecting Vertebrobasilar artery-nausea, vomiting,
vertigo, visual disturbance, dysarthia, ataxia, weakness +_
sensory disturbance
 Amaurosis fugax(transient monocular blindness)- curtain
coming down vertically in the field of vision in one eye/
dimming or fogging of vision
 Exclude DD
 Look for underlying cause of TIA-? Palpitations, chest pain,

Past medical history: Risks of TIA)( Past stroke/TIA, HTN, DM,

Hyperlipidemia, cardiac disease

Drug history- recreational drug use?

Personal history-smoker? Alcohol?

Family, social and occupational history

Physical examination (there should not be residual neurological


 Amaurosis fugax- visual acuity, field, eye movement,

 Pulse for AF
 Ask for BP
 Listen to carotid bruits and cardiac murmurs
 Limbs for power, and reflexes or ask to perform complete
neurological examinations including cranial nerves

Addressing concerns:

 It seems that your symptoms are related to a condition

called TIA/mini-stroke. This means, you lost your vision
temporarily due to blockage of the vessels supplying the
back of the eye responsible for vision.
 Fortunately, it was temporary and your symptoms resolved,
but it is a warning sign that you may get a serious form of
attack called stroke.
 There are certain risk factors for it, I will investigate with
blood tests and obtain tracing of your heart and a special
jelly scan of your neck vessels as well and treat the risk
factors accordingly and refer to TIA clinic and probable
imaging of brain.
 Meanwhile, I will start you with a medication called aspirin
300mg, which will reduce the frequency of such attacks


 Blood glucose, HbAIc

 Lipid profile
 colour Doppler scan of carotid
 MRI of brain/CT brain


Asses ABCD2 score:

Age : 60 or more(1)
Blood pressure- 140/90mmg or more(1)
Clinical features-unilateral weakness(2), speech impairement
without weakness(1)
Duration of symptoms: 60 mins or more(2), 10-59(1), <10(0)

ABCD2 score 4 or above (high risk for stroke) or

people with crescendo TIA(2 or more TIA in one week)
 Aspirin 300mg immediately
 Admit in ward
 Specialist assessment within 24 hours,
 Measures of secondary prevention(addressing individual risk
1. Treat HTN
2. Treat DM
3. Treat hyperlipedemia
4. Stop smoking, reduce alcohol
5. Symptomatic carotid stenosis of 50-99% according to
NASCET(North American symptomatic carotid
endarterectomy trial)- urgent carotid endarterectomy and
stenting within 2 weeks of TIA or non-disabling stroke
6. AF- anti-coagulate if no contraindications
7. Diet and exercise

Note: TIA patient on warfarin needs admission to exclude ICH


ABCD2 score 3 or less

 Aspirin 300mg immediately

 Refer to TIA clinic
 Specialist assessment within one week
 Measures of secondary prevention as above

2 day risk of stroke:

 1% if score 0-3
 4% if score 4-5
 8% if score 6-7
Tuberous sclerosis

Presenting illness

 Skin- adenoma sebaceum/angiofibromata, colour changes

Due to hamartomas in different organs
 Brain- seizure, mental retardation (Epiloia- epilepsy, low
intelligenence and adenoma sebaceum)
 Heart- cardiac rhabdomyoma(heart block, arrhythmias)
 Lungs- peumothorax, LAM
 Kidneys- renal hamartoma or angiomyolipoma, renal failure,
 GIT-harmartomous rectal polyps

Past medical history: epilepsy, CKD, neprectomy

Drug history-anti-epileptics

Social history-low intelligence

Physical examination:

 Face- adenoma sebaceum/angiofibromata(salmon coloured

papulo-nodular lesions in butterfly distribution particularly in
nasolabial folds, it can be macules as well)
 Hand fingers and toes- periungual and subungual fibromas
 Ash leaf macules(hypopigmented macules)
 Shagreen patches( thickened plaques, green to brown in
colour over buttocks)
 Look for gums-gingival hypertrophy (phenytoin use)
 Ask to look for other systems …. Fundoscopy for retinal
hamartoma, oral(gingival hamartoma, dental pitting, high
arched palate), abdomen-Renal cysts, complete neurological
exam to look for deficits
Addressing concerns:

 I think your symptoms are due to a condition called tuberous

 It is a rare genetic disease that causes tumours to grow in
different parts of the body
 Unfortunately , there is no cure for this condition, but there
are treatments available for the associated conditions
 Referral to geneticist

Investigations: clinical diagnostic criteria is used

 Genetic testing (in uncertain cases)

 Imaging- CT or MRI brain, renal ultrasounds,
echocardiogram, EEG


 Rapamycin(immunosuppressant)
 Treatment of organ based involvement:
Antileptic medications, surgery
Turner syndrome


 Noonan syndrome (A.D disorder, Learning disability, short

stature, hypertelorism, low set ears, epicanthal folds,
webbed neck, cardiac disease(pulmonary stenosis, ASD,

 Down syndrome(short stature, single palmer crease, low set

ears, epicanthal folds, flattened nasal bridge, short neck,
learning disability, heart(VSD, ASD, TOF), endocrine(DM,

 Fragile x syndrome(learning disability, ADHD, face(enlarged

ears, elongated face, high arch palate), macro-orchidism,
hyperextensible joints)

Presenting illness:

 Female patient with short stature, amenorrhea and HTN

 Lack of secondary sexual characteristics( defective breast
 Heart- bicuspid aortic valve, coarctation of aorta, HTN, Aortic
 Endocrine-DM, hypothyroidism
 Renal-horseshoe kidneys
 Learning disability?
 Limbs swelling (congenital lymphedema?)

Past medical/surgical history: HTN, coartation repair surgery,

hypothyroidism, DM, renal disease

Drug history: hormone replacement?

Social /occupational/family history

Physical examination:

 Short stature
 Limbs-wide carrying angle/cubitus valgus at elbow, short
fourth and fifth metacarpal/metatarsal bones,
lymphoedema(puffiness over fingers and toes)
 Face-high arch palate, inner canthal folds, ptosis, cataracts
 Ear- hearing loss (ottitis media and otosclerosis), anomalous
 Neck-short neck, webbed posterior neck, low posterior hair
line*, goiter?
 Chest-shield chest with widely spaced nipples, pectus
excavatum may be present
 Heart- biscuspid aortic valve, coartation of aorta(?repaired)
 Skin-excessive pigmented naevi
 Ask to measure BP

Addressing concerns:

 I think you have a condition called turner’s syndrome. It is a

problem with the chromosome where you lack one x
 I will refer to geneticist for confirmation with a blood test
called karyotyping. Meanwhile, I will do some tests to check
sugar levels, thyroid functions, scan your heart and kidneys
as it can affect them.
 I will also refer you to hormone specialist because you will
require hormone replacement.
 Psychological supports

 Karyotyping -45XO karyotype in peripheral blood
 Exclude organ involvement:
1. Heart- ECHO
2. Endocrine-blood glucose, TFT, Low plasma estradiol with
raised LH, FSH(Hypergonadotrophic hypogonadism), vit D
levels/bone prolife(risk of osteoporosis)
3. Renal- USG(horseshoe kidneys)

Treatment : MDT approach

 Recombinant growth hormone to increase height
 Genetic counseling
 Pregnancy-specialist fertility clinic input, very few may
conceive but will have major risk of severe congenital
 Treatment of associated conditions
 Prophylactic gonadectomy in case of mosaicism as there is
chance of gonadoblastoma
 Psychological therapy
Uncomplicated MI 5 weeks ago, now presents with fatigue:

Patient Information:

AGE-45/F, RR-22, pulse-56, Bp-105/65, Spo2-96

DD to think of:
 Anaemia(GI bleed)
 Postural hypotension
 Fatigue due to b-blocker(if given)
 Dehydration secondary to AKI by ACE inhibitor
 Electrolyte imbalance

Clinical communication skills

 Obtain detail of recent MI-how it happened? How
investigated? How treated? Cardiac rehab?
 Establish nature of lethargy( ?generalised weakness, dizzy
while standing,
 Ask about chest pain(recurrence)
 Exclude heart failure
 Look for features of anemia( any bleeding?)
Past medical and surgical history- about MI, PCI
Drug history:
 current medication (aspirin 75mg od, ramipril 10mg od,
bisoprolol 5mg od, clopidrogrel 75mg od, atorvastatin 80mg
hs, GTN spray sos).
Ask about any side effects from it? Headache due to use of
GTN, Bleeding, postural hypo due to ramipril
Any recent change in dosage? (ramipril increased by gp from
5 to 10mg od 2 weeks ago)
No regular past medication
Allergy ?
 Relevant personal history-smoking, alcohol
 Social history
 Occupational history
 Relevant family history

Physical examination:
 Check pulse, offer to examine lying and standing BP
 Check anemia
 Listen to heart and lung bases
 Asks for/look at observation charts

Any concerns or questions?( is it a heart attack again? Is

it due to drugs?
Clinical judgement
Offer Immediate Investigations :
 FBC(Anaemia)
 Urea and electrolytes
 RFT (to exclude AKI)
 Ecg(to exclude MI)
Explaining that it could be coz of ACEi leading to drop in BP
while standing up. Unlikely to be MI, but will exclude with
Would advise withholding ACEI and restarting at lower dose.
Probably does not need to stay in hospital once AKI and GI
bleed is excluded, could go home for instructions for GP
follow up.

*Physical signs: identifies that patient is not in shock but

only postural hypotension
 Postural hypotension due to increased dose of ramipril(main)
 Lethargy induced by b-blocker
 Dehydration secondary to AKI due to ACEi
Uncomplicated MI 5 weeks ago, now presents with fatigue:

Patient Information:

AGE-45/F, RR-22, pulse-56, Bp-105/65, Spo2-96

DD to think of:
 Anaemia(GI bleed)
 Postural hypotension
 Fatigue due to b-blocker(if given)
 Dehydration secondary to AKI by ACE inhibitor
 Electrolyte imbalance

Clinical communication skills

 Obtain detail of recent MI-how it happened? How
investigated? How treated? Cardiac rehab?
 Establish nature of lethargy( ?generalised weakness, dizzy
while standing,
 Ask about chest pain(recurrence)
 Exclude heart failure
 Look for features of anemia( any bleeding?)
Past medical and surgical history- about MI, PCI
Drug history:
 current medication (aspirin 75mg od, ramipril 10mg od,
bisoprolol 5mg od, clopidrogrel 75mg od, atorvastatin 80mg
hs, GTN spray sos).
Ask about any side effects from it? Headache due to use of
GTN, Bleeding, postural hypo due to ramipril
Any recent change in dosage? (ramipril increased by gp from
5 to 10mg od 2 weeks ago)
No regular past medication
Allergy ?
 Relevant personal history-smoking, alcohol
 Social history
 Occupational history
 Relevant family history

Physical examination:
 Check pulse, offer to examine lying and standing BP
 Check anemia
 Listen to heart and lung bases
 Asks for/look at observation charts

Any concerns or questions?( is it a heart attack again? Is

it due to drugs?
Clinical judgement
Offer Immediate Investigations :
 FBC(Anaemia)
 Urea and electrolytes
 RFT (to exclude AKI)
 Ecg(to exclude MI)
Explaining that it could be coz of ACEi leading to drop in BP
while standing up. Unlikely to be MI, but will exclude with
Would advise withholding ACEI and restarting at lower dose.
Probably does not need to stay in hospital once AKI and GI
bleed is excluded, could go home for instructions for GP
follow up.

*Physical signs: identifies that patient is not in shock but

only postural hypotension
 Postural hypotension due to increased dose of ramipril(main)
 Lethargy induced by b-blocker
 Dehydration secondary to AKI due to ACEi

DD of hypopigmentation:

 Vitiligo
 Pityriasis versicolor
 Leprosy
 Post inflammatory-chemical exposure
 Morphea
 Discoid lupus
 Tuberous sclerosis(ash leaf macules)

Presenting illness:

 White patches- duration, location, number, hypopigmented

hairs, itchy? Progression
 Other autoimmune diseases- alopecia, features of thyroid
disorder, DM , addision’s disease(weakness, postural drop,
nausea, vomiting, pigmentation), pernicious anaemia

Past medical history- DM, thyroid disorders, addisons disease,

percicious anaemia,alopecia areata, PBC, celiac disease

Family history*

Social history*- embarrassment or distress?

Physical examinations:

 Description-symmetrical hypopigmented macules or patches

often with hyperpigmented borders(well-demarcated) and
hypopigmented hair
 Look for autoimmune diseases- scalp for alopecia, anaemia,
buccal pigmentation and postural drop of BP for addisions,
neck for goiter/thyroidectomy scars of grave’s/hashimoto
 Ask to measure postural drop of BP, urine dipstick for

Addressing concerns:

 I think you have a condition called vitiligo. It is related to

immune system
 I will refer to skin doctor for treatment options
 It is associated with some other conditions, I will do some
blood tests to look for it
 Unfortunately, it is very difficult to treat; one option is to use
special make up to conceal the patches.
 Support groups


Clinical diagnosis, however in doubt-skin biopsy will confirm.

Other tests to exclude autoimmune diseases are

 FBC(anaemia)
 Blood glucose
 9 am cortisol (addison’s disease)

Treatment :

 General- and counseling, sunscreen, cosmetic

 Medical – topical potent steroid(mometasone), topical
 Phototherapy
 Surgery-mini-grafting

*lipid laden macrophages

Presenting illness:

 Cutaneous xanthomas(xanthelesma palpebrarum, tuberous

xanthoma, tendinous xanthoma, eruptive xanthoma, planar
 History of MI, atherosclerosis, AR, pancreatitis

Past medical history: IHD, pancreatitis, DM

Family history* of xanthomas, IHD

Smoker? Alcohol?

Physical examination:

 Xanthelesma(eye)
 Tuberous xanthomas-firm, painless red –yellow nodules,
usually in extensor surfaces such as knee, elbow and
buttocks (pressure areas)
 Tendinous xanthomas-nodules related to tendons and
ligaments(Achilles tendon mostly)
 Eruptive xanthomas-crops of small red to yellow papules,
 Look for features of atherosclerosis(unequal and weak pulse,
Features CCF due to MI)

Addressing concerns:

 Xanthomas is a condition in which fatty growths develop

underneath the skin
 Associated with high fat levels in the body which can be
dangerous for the heart(heart attack) due to narrowing of
 We will do blood tests to measure the fat level and start
treatment right away.
 The growths usually takes months or years and sometimes
may not disappear , so surgical excision may be advised


 Fasting lipid profile

 Biopsy
 Asses cardiovascular status
 Exclude secondary causes of hyperlipaedemia such as
hypothyroidism, nephrotic syndrome

Treatment: if associated with hyperlipaedemia

 Diet-low cholesterol diet

 Statins, fibrates, nicotinic acid, bile-acid binding resins
 Surgical-excision, laser

Frederickson classification of lipid disorders

1. Type 1(chylomicrons)-lipoprotein lipase deficieny

2. Type IIa(LDL)-Familial hypercholesterolemia, hypothyroidism,
nephrotic syndrome
3. Type IIb(LDL, VLDL)-Familial combined hyperlipidemia
4. Type III(IDL)-dysbetalipoproteinemia
5. Type IV(VLDL)-Familial hypertriglyceridemia,DM
6. Type V(chylomicrons, VLDL)-DM
Acute intermittent porphyria

*defects in heme metabolism and result in excessive secretion of

porphyrins and porphyrin precursors

*autosomal dominant, due to defects in enzyme porphobilinogen-

deaminase leading to accumulation of porphobilinogen

Presenting illness: episodes of neurovisceral symptoms

 Autonomic neuropathies- abdominal pain, constipation ,

vomiting, hypertension, tachycardia
 Abdominal pain-often epigastric pain and colicky in nature
 Peripheral neuropathies-mainly motor neuropathies
resembling GBS
 CNS-psychiatric symptoms(depression), seizures, delirium,
cortical blindness, coma
 Skin-usually no rash
 Fever in some cases

Family history*


 Spot urine test for porphobilinogen during acute attack

 S.electrolytes-Hyponatraemia(SIADH)
 CBC-mild leukocytosis
 Abdominal imaging to exclude DD
 Genetic testing for family can be done

Treatment: goal of treatment in acute attacks is to decrease heme


 Diet-high carbohydrate diet during the attack

 High dose glucose 5% in NACL
 Hematin infusions usually in recurrent attacks
 Liver transplantation(rarely required)
 Symptomatic- pain control with narcotics, seizures with
gabapentine, treatment of HTN

Acute porphyrias-AIP

Cutaneous-PCT, erythopoietic porphyria

Acute and cutaneous-variegate porphyria, hereditary




Heriditary angioedema


 Hereditary –
1. Type 1-low C1 Inhibitor
2. type 2-C1 inhibitor doesn’t function properly
3. with Normal C1 Inhibitor(formerly Type 3)
 Acquired –Type 1 and type 2
 Idiopathic
 Allergic
 ACE-inhibitor induced
 Non-histaminergic

Notes: the presence of urticaria in presence of

angioedema usually suggests a diagnosis other than
HAE and acquired angioedema

Presenting illness:

 Swelling of lips, eyelids, tongue, hands, feet, scrotum/vulva

 Larynx-throat tightness, SOB, Stridor
 Abdomen-abdominal pain, nausea, vomiting
 Ask about urticaria
 Determine types of angioedema
 Hereditary-family history may be there
 Allergic- in response to food, insect stings,
drug(NSAIDs), Latex
 Idiopathic
 ACEI- History of ACEI.

Past medical history: past attack of angioedema, urticaria

Drug history-ACEI, NSAIDs

Family history..HAE is autosomal dominant

Occupational history*

Addressing concerns:

 Angioedema is a swelling underneath the skin, usually a

reaction to a trigger such as medication, sometimes
cause can’t be found
 It can be life threatening if it involves the larynx
 Dial for ambulance if sudden SOB, swelling of lips and
tongue. Use adrenaline auto-injector .


 Hereditary-C1 Inhibitor , C4 is low, C1q, C1 and C3 are

 Allergy testing- RASTs(radioallergosorbent tests)-to identify
 Idiopathic angioedema-normal complements


ABCD approach:

 Airway protection- intubation , cricothyotomy, tracheostomy

may be required
 Antihistamines
 Steroids
 Adrenaline(if larynx is involved )
 Based on underlying type….
1. HAE- C1 Inhibitor concentrate, plasma kalikrein inhibitor,
bradykinin receptor antagonist, anabolic steroids-danazol
2. ACEI- stop the drug
Churg-Strauss Syndrome/eosinophilic granulomatosis with

Three phases

 Allergic stage-asthma, allergic rhinitis,sinusitis

 Eosinophilic stage-
 Vasculitic stage

Presenting illness

 Allergic rhinitis and asthma, sinusitis, haemoptysis,

eosinophilic pneumonia
 Constitutional-malaise, weight loss, fatigue, flu like
 GIT-GI vasculitis, eosinophilic gastritis/colitis-abdominal pain,
diarrhoea, vomiting
 NS- mononeuritis multiplex*, stroke
 MSK-arthralgias
 Skin-nodules, urticaria, palpable purpura
 Heart-heart failure, carditis ,MI
 Renal- GN, renal failure, HTN

Past medical history-asthma


Occupational history*

Physical exam

 Skin-palpable purpura, livedo reticularis

 Lungs-asthma, pneumonitis
 Urine dipstick

Plan of action
 It is inflammation of the small blood vessels
 The exact cause is not known, likely due to overactive
immune system targeting healthy blood vessels
 Will do blood tests and refer to different doctors depending
on the organ involvement
 Treatment is to dampen down inflammation initially with
steroids and based on organ damage


 FBC with differential-eosinophilia, ESR, CRP

 Urine microscopy
 RFT, s.electrolytes
 CXR, CT chest
 Lung function tests


 p-ANCA
 biopsy-skin , lung, kidney

Treatment: MDT approach

 Steroids
 Rituximab, cyclophosphamide,azathioprine, MTX
 Treatment of asthma

*delirium- is sudden onset and fluctuating impairment in cognitive

and consciousness

*dementia-progressive and irreversible decline in global cognitive

function (without impairment in consciousness)

Causes of confusion:

 Elderly
1. Infections-UTI, RTI
2. Electrolyte imbalance
3. Polypharmacy/recent change in medications
4. Stroke/subdural haematoma
5. Metabolic disturbance-hepatic, uraemic encephalopathy
6. Hypo or hyperglycemia
7. Cerebral metastases, tumours
8. Alcohol withdrawal syn
 Young
1. Recreational drug use and withdrawal
2. Alcohol withdrawal syn
3. Meningitis
4. Infections as above
5. Metabolic disturbances

Presenting illness:

 Confusion-sudden onset, short duration, may fluctuate

during the day, is this a dramatic change in behavior from
baseline?, any previous episodes? Altered consciousness
(episodes of drowsiness and agitation), inattention (difficulty
focusing) , disorganized thinking(do you have difficulty
following his/her conversation?)
*systems review to look for the causes
 N/S
1. Meningitis/encephalitis-headache , fever, neck
stiffness ,seizure, photophobia, rash, behavior change
2. Stroke-
3. Subdural haematoma- recent head injury/falls
 Respiratory system- RTI and pulmonary embolism
 Cardiac-CCF, MI
 GIT-hepatic encephalopathy, C.difficle diarrhoea
 GU-UTI, urinary retention
 Psychiatric-visual hallucinations and delusions can occur

Past medical history: as above

* In Parkinson’s disease (confusion is common due to side-effects

of dopaminergic medications)

Drug history- current drug regimen( dose change,new

medication, abrupt withdrawal of benzodiazepines and opiates)


*drugs causing confusion- levodopa, procyclidine for Parkinson,

TCA, SSRI, Opiates, steroids

*recreational drug use?

Social *

Personal-alcohol(delirium tremens,wernickes encephalopathy)

Plan of action:

 To determine the cause of confusion, thorough examination

and investigations are required
 It is usually reversible when the cause is treated
 Treatment is by treating the cause but if patient becomes
violent or is in danger to himself, sedation is required

 Blood glucose
 S.electrolytes
 Urine microscopy and c/s
 Urine toxicology screen
 Blood culture
 CT scan of head if needed


 General-nursing in quiet room with adequate lighting, clear

communication, reminders of time, place and person, have
familiar objects from home around the patient
 Specific- identify and treat the cause, haloperidol is used for
sedation, also olanzapine
Cystic fibrosis

*disease of exocrine gland function

Presenting illness

Long history of symptoms

 Lung-bronchiectasis, COPD, recurrent pneumonia,
wheezing, haemoptysis, pneumothorax
 GIT- pancreatitis, steatorrhoea,
 DM
 Poor growth and weight gain
 Infertility/subfertility

Past medical history-bowel obstruction, recurrent chest infection

Family history*

Social history- infertility may be an issue

Plan of action:

 CF is an inherited disorder that causes damage to the

lungs and digestive systems in body
 CF affects cells that produce mucus, sweat and digestive
 Will do some blood tests and obtain x ray of chest and
also special scans of chest
 There is no cure but it can be managed with MDT
approach…treating lung problems, taking care of nutrition
 Since it is inherited condition, will refer for genetic
 Males may be infertile, females might be able to conceive
 Screened at birth: low immunoreactive trypsin (heel prick)
 Sweat test: Na+ > 60 mmol/L (false‐positive in
hypothyroidism and Addison’s) or chloride
 Genetic screening
 Sputum for gram stain/CS
 CXR, CT chest, lung function tests
 ViT D, calcium, clotting profile

Treatment: MDT approach

General: education, counseling, nutrition, immunizations
 Chest Physiotherapy: postural drainage and active
cycle breathing techniques
 Prompt antibiotics for infections
 Mucolytics (DNAse)
 Inhaled bronchodilators
 Anti-inflammatory agents
 Double lung transplant (50% survival at 5 years)

 Pancreatic enzyme supplements
 Fat soluble vitamins
Hypersensitivity pneumonitis /Extrinsic allergic alveolitis

*inflammatory syndrome of lung caused by repetitive inhalation of

antigenic agents in a susceptible host


 Acute-type III hypersensitivity

 Subacute and chronic-Type IV

 Pneumonia
 Asthma
 Pulmonary fibrosis

Presenting illness:


 Flulike symptoms-fever, chills, cough, malaise,chest

tightness, headache, sob( develop within hours of exposure
and symptoms usually resolve)


 Insidious onset of productive cough, Sob, fatigue over



 Progressive symptoms as above, weight loss

Ask for exposure:

 Farmer’s lung-moldy hay

 Bird breeder’s lung-pigeons, fowl
 Malt worker’s lung-
 Chemical worker’s lung-
 Humidifier/air conditioner lung and etc…….
Past medical history

Occupational history**



Addressing concerns:

 HP happens when your lung develops immune response

(inflammation) to something you breathe in resulting in
inflammation of lung tissue. One example is bird fancier’s
lung caused by breathing in particles of bird droppings or
from feather
 Symptoms occur usually after exposure and resolve without
any sequele but repeated exposure may lead to lung
 Consult with resp medicine specialist, occupational medicine



 Precipitating antibodies against antigens
 Lung function tests
 BAL for lymphocytes and antibodies
 Lung biopsy


 Avoidance of antigen if possible

 Exposure minimization with protective
equipment(respirators) or environmental control
 corticosteroids


 Gastritis
 Gastric malignancy
 Pancreatitis
 Cholilithiasis/cholecystitis
 Esophagitis, barret’s esophagus
 achalasia
 Functional dyspepsia

Presenting illness:

 Typical(esophageal) symptoms-heart burn(retrosternal,

occurs after eating or when lying supine or bending over),
regurgitation, dysphagia
 Atypical-cough, chest pain, wheezing, aspiration pneumonia,
 Exclude above DDs

Past medical history- PUD, gastritis

Surgical history-hiatus hernia repair, gastric surgery
Drug history-NSAIDs, steroids, bisphosphonates ,,,, drugs
such as nitrates , calcium ch antagonists, theophyllines
precipitate reflux
Personal-smoking , alcohol
Dietary /life styles/obesity?-when do you sleep after eating?
How many pillows?
Family history –of gastric cancer

Plan of action:
 GERD is a condition where the acid from the stomach leaks
up into the gullet (esophagus). It usually occurs due to the
weakened ring of muscles at the bottom of gullet
 Your symptoms are consistent with GERD and there are no
danger symptoms such as unexplained weight loss and
difficulty swallowing which would need further tests.
 So, I will prescribe you some medications to lower down the
acid level in your tummy for 4-8 weeks and review the
response. You also need to change your lifestyle-need to lose
weight, avoid smoking, alcohol, avoid large meals, and avoid
immediately sleeping after meals and need to elevate the
head end while sleeping.
 If it doesn’t respond to the medication and lifestyle
changes..Will refer to bowel doctor for further tests such as
breath tests and endoscopy tests

 Endoscopy- to look for complications of reflux such as
esophagitis, , strictures, barret’s esophagus) and to see
anatomy(hiatal herinia, strictures, masses)
 Manometry-determine lower esophageal sphincter pressure
 Ambulatory 24 hour PH studies/testing
 Test for H pylori-carbon-13 urea breath test/ stool antigen
test(keep 2 weeks wash out period of PPI)


1. General-lifestyle modifications
 Losing weight
 Avoid alcohol, smoking, citrus fruits, tomato based products
 Avoiding large meals
 Waiting 3 hours after a meal before lying down
 Elevating the head of bed by 8 inches
2. Pharmacologic- trial of PPI initially
3. Surgery-laparoscopic fundoplication, sleeve gastrectomy
Giant cell arteritis/temporal arteritis and PMR

*systemic inflammatory vasculitis, typically affects superficial

temporal arteries, also affects ophthalmic , occipital,
vertebral,proximal vertebral arteries

Presenting illness:

 Usually age more than 50 years

 Female to male-3.7:1
 Constitutional-fever, anorexia, malaise, myalgia, weight loss,
night sweats
 Headache-new onset headache, or new type of headache in
chronic headache, usu. Localized to temporal and occipital
area, throbbing/dull/boring/burning pain, scalp tenderness
while combing
 Neck, torso, shoulder, pelvic girdle pain and stiffness
consistent with PMR
 Jaw claudication
 Eye- blurring or vision loss, visual hallucinations, amaurosis
 Others-limb claudication,TIA, stroke, tongue claudication,
multi- dementia etc….

Past medical history-

Personal-smoking increases risk

Physical examination

 Pulse
 Measure bp in both arms
 Visual acuity, visual field, fundoscopy- mainly anterior
ischaemic optic neuropathy(optic disc may be chalky white
and oedematous), also central and branch retinal artery
 Scalp tenderness
 Proximal myopathy
 Auscultate carotid artery for bruit

Addressing concerns:

 GCA is a condition in which medium and large arteries

usually in the head and neck, become inflamed.
 Will do some blood tests and
 Will start on high dose steroids to dampen down the
inflammation by consulting rheumatologist . It might lead to
blindness, so starting steroids at the earliest is crucial. Will
ask eye doctor to see you urgently, refer to surgeon to take
a tissue from the artery in the temple and study under
microscope for confirmation
 Steroids can weaken bones and for that, will start
prophylactic bone protection drugs, calcium and VIT D, GI
protection with PPI


 CBC-mild normocytic normochromic anaemia
 Colour duplex USG of temporal artery-wall oedema
 Temporal artery biopsy
 Screening of large vessel aneurysm with CT scan


 High dose steroids as soon as on suspicion for 4 weeks, then

taper.( prophylactic PPI, bisphosphonates, calcium, vit D, low
dose aspirin)
 Steroid sparing- cyclosporine, azathioprine, MTX


 Septic arthritis
 Crystal arthritis
 OA
 Gout

Presenting illness:

 Joint –pain, swelling, warmth, decreased range of motion

 Ask for causes-trauma, bleeding disorder,
 Exclude DDs

Past medical history- haemophilia

Past surgical history-surgery in knee joint

Drug history-warfarin


 Aspiration of synovial fluid and study/arthocentesis

 X-ray of the joint
 USG of joint
 Look for causes- haemophilia, PT, INR(warfarin)


 Drainage of blood from the joint

 PRICE strategy
 Treatment of cause- replacement of clotting factors in
 If severe arthritis-synovectomy and joint replacement

Causes: local and systemic

 Renal stone
 Renal tract malignancy
 GN-IgA nephropathy, post-infectious GN, Alport syndrome,
sickle cell nephropathy
 Pulmonary-renal syndromes-goodpasture syndrome,
wegener’s syndrome, microscopic polyangitis
 Other VasculItis-PAN, HSP
 Connective tissue diseases- SLE, Slceroderma
 Radio/chemotherapy
 Drugs-anticoagulants
 Bleeding disorders

Presenting illness:

 Haematuria-onset, number of episodes, any clots?, do you

notice blood at the beginning(prostrate and uretha) or
throughout(bladder and above) or at the end of
urination( bladder base, prostrate)?
 Frothy urine-proteinuria
 Look for causes
1. UTI-dysuria, frequency,urgency
2. BPH-obstructive symptoms
3. Renal calculi-renal colic, calcuria
4. IgA nephropathy-RTI followed by haematuria
5. Pulmonary-renal syndromes- haemoptysis, RTI, sinusitis
6. Connective tissue diseases-SLE, Scleroderma
7. Vasculitis- HSP(Rash, arthralgia, abdominal pain)
8. Renal tract malignancy-weight loss, anorexia
9. Post exercise? Post trauma?

Past medical history –bleeding disorders and above

Drug history-oral anticoagulants, cychophosphamide,
Recreational drug use-estacy, heroin(rhabdomyolysis)
Family history-
Occupational- work in dye, rubber industry?
Travel history-fresh water swimming(schistosomiasis-

Physical examination
 Puffy face?
 Measure BP
 Abdomen- PKD
 Features of SLE, Scleroderma, vasculitis

Plan of action:

 You have a condition called haematuria-blood in urine

 It needs to be investigated initially with urine analysis and
simple blood tests and USG of renal tract. Further
investigations will depend on the initial results, may need
kidney biopsy
 Will refer to kidney doctor after the results of the initial tests,
treatment will be according to the cause


 Urinalysis for blood , protein, leukocytes, casts. Mid stream

urine for c/s
 RFT, s .electrolytes
 24 hour urinary protein, urine albumin creatinine ratio
 Clotting screen(bleeding disorder)
 USG renal tract, plain x ray KUB, CT KUB
 Autoantibody screen-SLE-ANA, anti ds-DNA,
Canca(wegener’s), Panca(microscopic polyangitis), anti-
GBM(Good Pasture)
 CXR(Pulmonary haemorrhage
 Renal biopsy

Treatment: according to cause


 Non-PTH mediated hypercalcemia-malignancy, tamoxifen

linked hypercalcemia, sarcoidosis, iatgrogenic(Vit D ,
 PTH mediated hypercalcemia-Hyperparathyroidism

Presenting illness:

 Nausea, vomiting, constipation

 Polyuria, polydipsia, nocturia
 Alteration of mental status, confusion, coma
 Headache
 Depression
 Abdominal pain
 Renal colic

Past medical history-malignancy

Drug history-thiazides, tamoxifen


 S.calcium
 S.albumin to calculate total corrected calcium level
 PTH level
 Investigations for malignancy


 Hydration
 Loop diuretics
 Bisphosphonates
 Patients with malignancy may require chemo, radio and

*normal calcium value-2.1-2.6mmol/L


*deficiencies of humoral immunity (b-lymphocytes), infection with

encapsulated bacteria

Common types of primary immunodeficiency:

 Hypogammaglobulinemia(Common variable
 IgA deficiency
 X-linked agamamglobulinemia/Bruton’s


 Cystic fibrosis
 AIDS, lymphoproliferative disorders(secondary

Presenting illness:

 History of recurrent infections-

o RTI including chronic OM,sinusitis, bronchitis,
o GI-bacterial or parasitic gastroenteritis, malabsoption
o skin infections
o meningitis
o joints-arthritis
o lymphadenopathy
o associated with autoimmune disorders
o increased risk of malignancies
 age of onset*

Past medical history-recurrent RTI, GI infections, autoimmune

diseases, malignancies? past history of Blood transfusion
Sexual history*-risk factor for HIV
Family history*

Addressing concerns:
 hypogammaglobulinemia –is a condition due to deficiency of
antibody..that can fight infections.
 Referral to immunologist
 MDT approach
 Avoid life vaccines
 CVID-can be autosomal recessive

BASIC and to see manifestations of disease
 CBC with differential, ESR, CRP
 Sputum for gram stain/c/s, AFB
 Stool RE
 S. albumin, s.calcium, vit D, clotting profile (malabsorption)
 Anti-HIV
 HRCT, Lung function tests

 Levels of serum immunoglobulin-total IgG, IgA, IgM
Common variable immunodeficiency-IgG levels less than 2
SD below the mean, also low levels of IgA and Ig M
Selective IgA deficiency
Hyper-IgM syndrome-IgM markedly increased, others are
 Flow cytometric analysis-Peripheral blood lymphocyte
phenotyping- absent or less B-lymohocytes
 Checking antibodies to vaccines the child
received..antibodies will be absent(antibody response to
 Absence of antibodies to blood group A and B antigens
 Complement levels
 Serum electrophoresis
 Replacement of Ig G(i/v or S/C) for primary
 Treatment of secondary hypogammaglobulinemia –according
to underlying cause
 Stem cell transplantation for severe combined
 Treatment of infections-lungs and GI
 Avoid life vaccines
Lithium toxicity

Stem…38/M with DM, HTN, asthmatic, smoker with tremors.

Tremors for last 20 years back due to salbutamol inhaler but changed its character
in two weeks. Mainly intentional (while holding objects). Started on lithium for mood
change 6 months back. On lisinopril, HCT, metformin. Has been suffering from
traveller’s diarrhoea.

Dx: lithium toxicity precipitated by diarrhoea, diuretics and ACEi

DD: cerebellar syndrome due to other causes, thyrotoxicosis


Three categories of toxicity

 Acute-mainly GI
 Acute on chronic-both GI and neurological involvement
 Chronic-only neurological manifestations.

Desired serum level: 0.6-1.2mEq/L

Lithium clearance is mainly through kidneys, minimally protein bound so it is
filtered at a rate that depends on GFR

Acute lithium toxicity

 GI-nausea, vomiting, cramping, diarrhea.
 CNS involvement in some cases-tremor,ataxia
 Cardiac dysrrythmias(rare)- t wave flattening

Chronic :
 CNS- tremor, seizures, altered mental status, coma. SILENT syndrome-
syndrome of irreversible lithium effectuated neurotoxicity(cognitive
impairment, cerebellar dysfunction,peripheral neuropathy)
 Renal toxicity-nephrogenic DI, neprhotic syn, chronic TIN, renal tubular
 Endocrine-hypothyroidism
 Aplastic anaemia

Precipitants of lithium toxicity:

 Diuretics-promotes renal sodium wasting

 ACEi-reduce GFR and enhance tubular resorption of lithium
 NSAIDs-reduces GFR
 Diarrhoea/dehydration

 Blood lithium level

 S.electrolytes, RFTs, urine analysis
 TFTs
 ECG- Non specific and diffuse ST segment depression, T wave inversion,


Supportive therapy(mainstay of treatment)

 GI decontamination if presented within 1 hour of ingestion. Activated charcoal
has no role
 Enhanced elimination:
1. fluid therapy(Normal saline)
2. hemodialysis- for those with renal failure and unable to eliminate lithium,
for those who cannot tolerate hydration(CCF, Liver disease), consider for
those with severe signs of neurotoxicity(seizures, profound altered mental
status), consider if chronic toxicity with symptoms plus lithium level of
more than 2.5 or acute with symptoms plus lithium level 4 or more
 stop precipitant drugs


 mostly favorable outcome

 10% develop chronic neurological sequele
Multiple Myeloma

*proliferative of malignant plasma cells and a subsequent

overabundance of monoclonal protein(M protein)


 Metastatic bone disease


Presenting illness

1. bone pain(most common) mostly in lumbar spine
2. pathologic fractures-mostly vertebral
 spinal cord compression-back pain, weakness and numbness
in extremities
 bleeding-thrombocytopenia
 infections-due to leucopenia
 Aaemia-weakness
 hypercalcemia-confusion, somnolence, bone pain,
constipation, polyuria, thirst
 hyperviscosity-malaise, fever, paresthesia, sluggish
mentation,headache, sensory loss, blurring of vision,
epistaxis, stroke, MI
 N/S-Carpal tunnel syndrome, peripheral neuropathies
 Renal failure
 Amyloidosis
 Soft tissue masses-plasmacytomas
 Cryoglobulinemia, raynauds phenomenon

Past medical –pathological fracture, renal failure, Stroke, CTS

Plan of action

 Multiple myeloma is a type of bone marrow cancer( bone

marrow is the spongy tissue found at the center of bones, it
produces the body’s cells. MM affects the plasma cells(a type
of blood cell) inside the bone marrow
 The myeloma cells divide and expand in the bone marrow
damaging the bone and production of other healthy blood
 Will do some blood tests and x rays of your spine and then
refer to haematologist for further tests and scan
 There is no cure for MM but treatment can help control over
many years
 Managed by MDT-oncologists, haematologists, radiologists,
experts in stem cell transplants, orthopaedic surgeons


 CBC(pancytopenia)
 Peripheral blood film-Rouleau formation
 Total protein, albumin, globulin
 S.calcium and electrolytes
 24 hour urine for quantification of Bence Jones protein,
protein, creatinine clearance
 Serum protein electrophoresis
 Urine protein electrophoresis-to identify bence jones protein
 B2 microglobulin is a prognosticator in MM
 Serum viscosity
 Skeletal survey-plain x rays(osteolytic lesions), MRI, PET scan
 Bone marrow studies-more than 10% plasma cells


1. Transplant candidates
 Induction therapy followed by autologous stem cell
Induction therapy, bortezomib based (bortezomib,
cyclophosphamide, dexamethasone or bortezomib,
doxurobicin, dexamethasone, or bortezomib, lenalidomide,
2. Non transplant candidates
Bortezomib, melphalan, prednisolone,,,, lenalidomide,
doxurobicin, vincristine

 Bone fracture
 Spinal cord compression
 Renal failure
 Infections , bleeding , anaemia
 Hyperviscosity-stroke, MI
 Amyloidosis

Cause of Renal failure

 Direct tubular injury-light chain nephropathy

 Amyloidosis
 Hypercalcemic nephropathy

MGUS-monoclonal gammopathy of undetermined significance

 Serum monoclonal M protein <3g/dl

 Bone marrow plasma cell <10%
 No evidence of end organ damage

Smoldering MM- values above above levels plus no evidence of

end organ damage

*rare catecholamine secreting tumour..only 10% is malignant

 Isolated
 Associated with 3 syndromes- MEN 2, Von-Hippel-Lindau
syndrome, NF type 1


 Anxiety disorder
 Insulinoma-hypoglycemia
 Hyperthyroidism
 Paroxysmal SVT

Presenting illness:

 Episodic spells –headaches, palpitations, sweating

 Others are-tremor, nausea, weakness, anxiety, sense of
doom, epigastric pain, constipation, flank pain, weight loss
 Hypertension-encephalopathy, heart failure, nephropathy,
 Dizzy-Postural hypotension from volume contraction
 Look for associated syndromes-MEN 2-medullary thyroid
carcinoma, hyperparathyroidism features,,, NF-
neurofibromas, skin changes, VHL-kindey cancer

Past medical history- Uncontrolled HTN, MTC, NF, kidney cancer

Surgical history- MTC removal, neprectomy

Family history* of kidney cancer

Personal-smoking, alcohol

Plan of action:

 It is a are tumour of the adrenal glands, which sit above the

 They are usually benign/non-cancerous, although around 1 in
10 are cancerous
 The adrenal glands produce a number of hormones, and in
this case, they produce excessive fight or flight hormones
called adrenaline and noradrenaline. This hormone control
heart rate, blood pressure and metabolism and because of
excess hormone, it will cause palpitations and high blood
 Will do some blood tests and special urine tests and special
scans for the diagnosis
 Treatment of choice is removal of the tumour by surgery-
keyhole surgery/open surgery , managed by MDT approach.
And need to control blood pressure before surgery.



 Plasma metanephrine
 24 urinary collection for catecholamines and metanephrines
 Imaging-abdominal CT scan, MRI, scintigraphy, PET scan

Note: scintigraphy/MIBG(metaiodobenzylguanidine ) scan is

reserved for biochemically proven pheochromocytoma which
is not visible with CT or MRI abdomen

To rule out syndromes:

 Intact PTH, s.calcium levels

 genetic testing
To see target organ damage by HTN:

 RFT, Urine for albumin
 Blood glucose
 Fundoscopy


 Surgical resection of tumour is treatment of choice

Pre-operative medical stabilization:

 Alpha-blockade(phenoxybenzanamine) 7-10 days before
 Provide volume expansion with isotonic NACL
 Initiate B-blocker only after adequate alpha blockade, usually
after 2 days
Polyglandular autoimmune syndrome (PGA syndrome) or autoimmune
polyendocrine syndrome(APS)

Three types

Type 1: mainly 3 components ( at least 2 needed for diagnosis). Usually inherited in

autosomal recessive pattern

 Chronic mucocutaneous candidiasis

 Hypoparathyroidism
 Autoimmune adrenal insufficiency
 Others-autoimmune Type 1 DM, Pernicious anaemia, autoimmune hepatitis,
alopecia, vitiligo

Type II: usually inherited in autosomal dominant pattern. Occurs in 3 rd or 4th decade
of life

 Autoimmune Addison disease plus either

 Autoimmune thyroid disease(mainly Hashimoto’s thyroiditis) or
 Type 1 DM
 Others-hypogonadism, pernicious anaemia, celiac diasese, PBC


 CBC, blood glucose, s.electrolytes, TFTs, LFTs

 Serum autoantibodies screen:
1. Autoantibodies to 21 hydroxylase and 17 hydroxylase for addision,
2. thyroid peroxidase antibodies (TPO) for hashimoto’s
3. TSH receptor stimulating antibodies for Grave’s disease
4. glutamic acid decarboxylase-65 and islet cells antibodies for Type 1 DM
5. tissue transglutaminase antibodies for celiac disease
6. parietal cell and anti-intrinsic factor antibodies for pernicious anemia
 evaluation of end organ function
1. addisons-plasma cortisol, acth level, synacthen test, CT adrenal gland
2. autoimmune thyroiditis- TFTs, USG neck, thyroid isotope uptake scan
3. type 1 DM-fasting blood glucose
4. FSH, LH, Testosterone, estradiol


Organ based: hormone replacement therapy

Family member screening with serum autoantibodies

Porphyria cutanea tarda

80% are acquired(sporadic) and 20% are familial(autosomal


*heme synthetic enzyme uroporphyrinogen decarboxylase(UROD)

is deficient

Presenting illness

 Skin- blistering of mostly sun exposed areas, photosensitive,

skin fragility, followed by scarring, milia(tiny white spots),
occasionally skin becomes thickened and hard
 Discoloured urine may be there (tea coloured?)
 Changes in hair growth(hypertrichosis) and
 Precipitating factors-alcohol, OCP,Hepatitis
 Features of HCC?
 Commonly associated with haemochromatosis

Family history*

Alcohol history*

History of hepatitis

Plan of action:

 PCT is a condition due to deficiency of an enzyme in liver

and sometimes in RBCS. This enzyme deficiency leads to
build up of chemicals called porphyrins , which in the skin
interacts with light
 It is normally inherited or precipitated by alcohol, viral
hepatitis, haemochromatosis(build up of iron in liver)
 The skin features are usually a nuisance rather than serious.
Most people with PCT will have too much of iron in the body,
with removal of iron, the skin often improves


 Urinary porphyrins-pink fluorescence under wood lamp

 UROD enzyme activity assay in RBC
 LFT, alpha fetoprotein, iron profile, viral hepatitis screen
 Skin biopsy, liver biopsy
 Imaging-USG HBS


 General-avoidance of sunlight, alcohol, tobacco cessation,

treatment of hepatitis(hep C)
 Venesection reduces iron stores and hence improves heme
synthesis. Use iron cheletors if venesectio is not applicable
 Hydroxycloroquine in low dose
Primary sclerosing cholangitis with IBD

Presenting illness:

 asymptomatic
 Jaundice, pruritus, fatigue,right upper quadrant pain
 Might present as acute hepatitis
 Bacterial cholangitis-recurrent febrile episodes
 CLD-Ascites, variceal bleeding, hepatic encephalopathy
 IBD-mostly ulcerative colitis, also chron’s disease

Past medical history-IBD, cholangitis

Personal history-alcohol, smoker

Physical examination:
 Stigmata of CLD
 Features of IBD

Plan of action:
 PSC is a disease of the bile ducts, which carry the digestive
liquid bile from the liver to your small instestine
 In PSC, inflammation causes scars within the bile ducts,
leading to narrow bile duct and damaging liver
 It is commonly associated with bowel condition called IBD
 Will do blood tests to check the liver function and then refer
to liver specialist for further investigations and management

 LFT-raised ALP, gamma glutamyl transpeptidase,
aminotransferases and bilirubin
 PT, INR, S.Albumin
 ERCP* OR MRCP*(preferred)
 Liver Biopsy-staging and prognosis, shows onion skin
fibrosis/periductal fibrosis
 Percutaneous Transhepatic cholangiography if ERCP fails
 UGIE for varices

 Immunosuppresants-steroids
 Bile salts-ursodeoxycholic acid
 Cholestyramine for itching
 Liver transplantation
 Replacement of vit A, D, E, K

*multisystem inflammatory disease of unknown aetiology,

manifests as non-caseasting gralulomas


 Tuberculosis

Presenting illness

 Aymptomatic
 Fever, anorexia, arthralgia, fatigue
 Lungs-cough, chest pain, sob on exertion
 Lofgren’s syndrome-fever, polyarthralgias, bilateral hilar
 Eye-uveitis
 Heart-heart block, sudden death,arrhythmias,
 Skin-erythema nodusum , lupus pernio,
 Lumps and bumps-lymphadenopathy
 NS-Hypothalamic pituitary sarcoidosis-DI and hypoginadism,
cranial nerve palsies, lymphocytic meningitis

Past medical history- TB? Drug history, Travel history, smoking?

Plan of action

 Sarcoidosis is a rare condition which causes inflammation in

organs mainly lungs and skin
 The exact cause is not known, thought to be auto-immune
 Will do some blood tests and obtain x ray of chest and
special scans of chest
 will consult with lung doctor and rheumatologist( based on
organ involvement)
 Most people don’t need treatment as the condition often
goes away on its own, usually within a few months or years.
Simple measures such as over the counter pain relievers are
required for flare ups
 but if critical organs are involved-then, treatment is usually a



 S.calcium
 S. ACE levels
 Imaging-CXR, HRCT chest
 Lung function tests, transfer factor of CO
 Transbronchial biopsy
 Lymph node biopsy
 Gallium scan(used infrequently)

 Symptomatic therapy with NSAIDs
 Steroid and steroid sparing agent(MTX, Azathioprine),
 Surgery-lung transplantation(stage 1v sarcoidosis)

Indications of steroid:

 Significant lung symptoms

 Involvement of heart, liver, eyes, kidneys, CNS

Staging of sarcoidosis:

 Stage 0-normal CXR

 Stage 1-BHL
 Stage 2-BHL with infiltrates
 Stage 3-infiltrates alone
 Stage 4-fibrosis
Sub acute intestinal obstruction

Stem: recurrent vomiting and abdominal pain

*intestinal obstruction for short duration in a patient who has

previously undergone abdominal surgery, often incomplete
obstruction and often will settle with conservative

 Adhesions-post surgery, tuberculosis
 Stricture of small bowel-chron’s , tuberculosis
 Bowel malignancy
 hernias

Presenting illness:

 Recurrent vomiting
 Recurrent crampy abdominal pain
 Abdominal distension
 Visible/palpable bowel loops
 Gargling noises
 constipation
 Features of Tuberculosis?

Past medical and surgical history-abdominal surgery*,

previous radiation, IBD, malignancy

Plan of action:
 Seems like your bowels have difficulty moving the
contents due to narrowing and bends in the bowel
because of adhesions. It can happen following abdominal
 Will do some blood tests and obtain x-ray, usg scan and
special scan called CT scan after drinking some contrast
liquid to see the affected bowel
 Will get an opinion from surgical team
 Treatment is laxatives, anti-sickness medication, pain
 But if the bout of SABO is bad, need to rest bowel
completely without taking anything from mouth
 Surgery is usually not helpful as obstruction can be at
multiple levels , but obviously will get an opinion from the
 Give tips about diet-low fiber diet, eat small servings, 5/6
times a day, softer foods, drink fluids,

 RFT, S.electrolytes
 IMAGING- plain x ray, USG, contrast CT scan abdomen
 Diagnostic laparoscopy

Treatment: MDT approach-surgical team consultation

Can be managed with:

 Laxatives-lactulose, laxido
 Anti-emetics
 Pain relievers-
 Short course of steroids

If bad bout of SABO,then


 Frequent mouth care

 Rest the bowel-Nil by mouth with or without NG tube
 IV hydration
 Introducing liquids

Surgery may be required

Treatment of cause- TB, chron’s


 Small vessel
1. Wegener’s granunomatosis/granunomatosis with
2. Churg-strauss syndrome
3. Microscopic polyangitis
 Medium vessel- PAN, Kawasaki disease
 Large vessel-Giant cell arteritis, Takayasu’s arteritis
 Variable vessel-Behcet’s disease
 Associated with connective tissue disease-SLE, RA
 Cryoglobulinemia

Wegener’s granulomatosis:

Presenting illness:

 Recurrent upper and lower RTI

 Non-specific-fever, weight loss, fatigue
 Eye-uveitis,conjunctivitis , scleritis
 ENT-chronic sinusitis, rhinitis, epistaxis, serous ottitis media
 Lungs-pulmonary infiltrates, haemorrhage, haemoptysis,sob,
 Heart-MI,pericarditis
 GIT-abdominal pain due to splanchnic vasculitis
 Renal-crescenteric necrotizing GN, renal failure
 MSK-myalgias, arthralgia/arthritis
 Skin-palpable purpura,skin ulcers, livedo reticularis
 NS-mononeuritis multiplex, sensorimotor polyneuropathy,
cranial nerve palsies

Past medical history: RTI, rhinitis, hearing loss, renal failure

Drug history
Plan of action:

 It is a rare disease which causes walls of the blood vessels to

become inflamed
 The exact cause is not unknown, thought to be an
autoimmune disease
 It is a serious condition affecting multiple organs and tissues
 Will do blood tests and may need a biopsy
 Will refer to different disciplines of doctor- rheumatologists,
pulmonologists, nephrologists, ENT specialists
 Treatment will be to dampen down inflammation


Routine blood tests:

 CBC, ESR , CRP- normocytic normochromic anaemia,
 Urine microscopy
 RFT, S.Electrolytes
 CXR, CT chest
 C-ANCA-Cytoplasmic antineutrophil cytoplasmic antibody
 Renal or lung biopsy

Treatment: MDT approach

 Induction of remission-cyclophosphamide with steroid, MTX

with steroid, rituximab with steroid, plasma exchange
 Maintenance of remission-azathioprine, MTX

Polyarteritis nodusa
 Lungs are usually spared
 ANCA is usually negative
 Rx is steroids
Von-Hippel-Lindau(VHL) disease

*rare genetic disorder characterized by visceral cysts and benign

tumors in different organs that have potential for malignant

*autosomal dominant

Presenting features

 Pheochromocytomas
 Eye-retinal haemangiomas/haemangioblastoma, retinal
detachment, vision loss
 CNS(brain and spinal cord)-haemangioblastoma-usually arise
from cerebellum
 Kidney-renal cysts, renal cell carcinoma(common cause
of mortality)
 ear-endolymphatic sac tumours of middle ear-hearing loss,
tinnitus, vertigo
 pancreas-cysts, pancreatic cancer
 ovarian cyst in women, epididymal cyst in men

Past medical history-HTN, RCC

Surgical history-nephrectomy

Family history*

Plan of action:

 is a rare inherited disorder caused by faulty gene causing

cysts and tumors in different organs mostly eyes,
cerebellum, spinal cord, kidneys, and pancreas
 most tumours are benign but with subsequent malignant
 genetic counselling-each of the children will have 50%
chance of inheriting the disease
 will do some blood tests and scans all over the body
 management is done based on organ involvement by
respective doctors in the area
 needs screening of family
 needs annual screening to see organ involvement


 CBC-Polycythaemia(due to EPO secretion from renal cysts

and CNS haemangioblastoma)
 RFT, Electrolytes
 Pheochromocytoma investigation
 Imaging-
1. USG abdomen-renal cysts, RCC, pancreatic cysts
2. CT scan abdomen
3. MRI abdomen
4. Brain CT/MRI
5. Ocular colour Doppler USG
 Genetic testing for VHL gene

Treatment: MDT approach based on organs involved

 General-genetic counselling, education
 Depends on specific complications/organs involved- Surgical
excision of tumours/cysts
 Ophthalmic surgery-laser photocoagulation, cryotherapy,
vitreous surgery, radiation

Screening/follow up
 Yearly eye examination
 Yearly physical exam
 Yearly 24 urine test to screen for elevated catecholamines
 Yearly abdominal USG In teenage, CT abdomen in adulthood
 MRI of brain and spinal cord 2 yearly