Medicine Cases

SPECIALITY : GENERAL MEDICINE
CASE : NEPHROTIC SYNDROME

NAME OF THE EXPERT : PROF. P.V. BHASKAR REDDY,
PROF & HOD MEDICINE, SRMC & RI, PORUR,
CHENNAI-600 116
HISTORY
Swelling of face, hands and legs

Frothy urine
Diabetes mellitus
History towards Syhilis, Malaria, Tuberculosis and HIV
History of Cancers- Breast cancer, Lung cancer and Hodgekin’s
lymphoma
Collagen vascular diseases( Lupus)- skin lesions, oral ulcers, joint
pains, prolonged fever
Blood transfusion- Hepaitis B Hepatitis C and HIV
Drug history-NSAIDs, D Pencillamine, heroin, Alternative and
complimentary medicines (Heavy metals)
Personal history- STD- Syphilis, HIV and Hepatitis
Family History- Renal diseases
CLINICAL EXAMINATION
General Exam-Anasarca, Malar Rash
Swelling of tissues around the eyes (periobital edema 0
Swelling of feet and ankles
Scrotal edema
Dysnoea ( fluid overload- pulmonary edema)
Dry Skin
CVS- Pericardial effusion
RS- Pleural effusion
ABD- Ascites, genital edema
CNS- Diabetic retinopathy and neuropathy
INVESTIGATIONS
Baseline-
Blood sugar
Urinanalysis- protein cast, lipid cast
24 hour urinary protein ->3.5gm/day
LFT- Serum albumin< 3.0 gm/dl
RFT
Lipid Profile(increased cholesterol and TGL)
Low Iron and Vitamin-D levels
Special-ANA,Anti dsDNA, Hbsag, HCV, Serum protein electrophoresis
ASO titre
USG-Enlarged kidneys- Dimensions
Renal vein thrombosis
Renal biopsy
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National Board of Examinations, cases Medicine
COMPLICATIONS
Infections- Peritonitis, Cellulitis and Sepis

Hypercoagubality- DVT, Pulmonary Embolism and Renal Vein
Thrombosis
Hyperlipedemia
Chronic Kidney disease
Growth delay in children
DIFFERENTIAL DIAGNOSIS
Nephritic syndrome
Cardiac Failure
Hepatic Failure
Hypothyroidism
Cushings syndrome
In children Fluid overload mistaken as lung allergic conditions
TREATMENT
If systemic causes of nephtric syndrome is present therapy should be

instituted for the systemic disease
Diet
Low Protein
Low Salt-1-2 gms
Resticted fluid
Corticosteroids to reduce the proteinurea and edema
Salt free Albumin- to restore the blood volume
Diuretics- to maintain fluid balance and caution to avoid hypovolemia
Cyclophosphamide when bot responding to steroids
ACE inhibitors, ARB reduce the rate of progression of the renal disease
COMPLICATIONS
Edema- Diuretics
Dyslipedemia- statins
Thromboembolic phenomena- If renal vein thrombosis- Heparin
Vitamin-D supplementation
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SPECIALITY :- GENERAL MEDICINE
CASE :- EXTRA PYRAMMODAL DISORDER
NAME OF THE EXPERT :- DR GEETHA K.SUBRAMANYAM
M.D. (MEDICINE-DELHI), SENIOR CONSULTING PHYSICIAN, HEAD OF
MEDICAL UNIT III, ST. MARTHA’S HOSPITAL, BANGALORE
Extra Pyramidal disorders are
Associated with abnormalities in basal ganglia constituted by five

paired nuclei namely candate nucleus, putamen , globus pallidus , sub-thalmic
nuclei and substantia nigra.
The common movement disorders are:
1.Parkinsonism
2.Tremors
3. Chorea
4. Athetosis
5. Dystonia
6. Hemi ballismus
HISTORY
1. H/O of Rheumatic fever, past H/o encephalitis (viral), H/o epilepsy.
2. H/o drug intake (methyldopa, phenothiazines, O.C. pills etc.)
3. Family history of similar complaints
4. Psychological history
5. H/o exposure to toxics like carbon monoxide, manganese etc.
6. Duration and progress of the disease.
7. H/o associated Jaundice or any evidence of Chronic Liver disorder (for
Wilson’s disease).
8. H/o vasculitis, arthralgia, low grade fever(for S.I.E.)
9. Any aggravating or relieving factors.
CLINICAL EXAMINATIONS
Most important
In a case of Parkinsonism, look for the following features:
1. Lack of facial expression( Mask-like)
2. On the face
Note tremors, absence of blinking, dribbling of salvia, glabellar- tap,
ocular movements , for supra nuclear gaze palasy, feel for a greasy or
sweaty blow ( due to autonomic dysfunction)
2 Speech:- Monotonus, soft , poorly articulated and faint.
3 Ask the patient to write
( Look for micrographia)
4 Paucity of movements
5 Ask the patient to walk, turn quickly and stop and restart. ( Note the
difficulty in starting, stuffing ,freezing and festination)
3
6 Look for propulsion and retropulsion ( with care)
7 Resting tremors with the arms relaxed (“pill rolling” movement)- on
finger- nose testing, the resting tremors disappears.
8 Test for wrist tone , for cog-wheel or lead- pipe rigidity.
EXAMINATION OF A PATIENT WITH WITH OTHER EXTRA PYRAMIDAL

MOVEMENT DISORDERS
1. Higher mental functions
2. Chorea- gremacing of face, jerking of head.
3. Examination of the patient’s arms for chorei from movement, Athetosis
And hemi –bellimus and tremors ( description of the movements of the
arms is very important.
4. Shake hands with the patient “Milk-maid grip”- lack of sustained grip.
5. Ask the patient to hold hands out and look for the classical choreic
posture. (Finger and thumb hyper restricted and wrist flexed due to
hypotonia)
6. Reflexes
7. Conjuctival injection (ataxia telengec tasia)
8. K.F. ring (wilson’s disease)
9. Examination of cardio-vascular system
INVESTIGATIONS
1. Complete Haemogram
2. L.F.T.
3. Detailed Opthalmic examination
4. ASLO titres
5. Work up for SLE
6. Thyroid function tests if autoimmune thyroidities is suspected
7. Serum copper and ceruloplasmin levels.
8. L.P.
9. CT Scan Brain
10. MRI S can of Brain
11. EEG if required
12. Estimation of drug levels( if required)
13. ECHO
TREATMENT
Parkinsonism
1. Symptomatic, supportive and palliative.
2. Physical therapy and psycho-therapy
3. Requirement of lifelong medications
4. Treatment programme to be personalized
5. Medical treatment for compensated phase and decompensated phase.
6. Medications under evaluation
7. Role of surgery
TREATMENT OF OTHER MOVEMENT DISORDERS

1. Drug treatment of Tremors
2. treatment of Dystonia
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3. Role of surgery
4. Use of botulinum toxin
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CASE :- RHEUMATOLOGICAL DISEASES
NAME OF THE EXPERT :- Dr. N. KARUNANIDHI
INSTITUTE OF INTERNAL MEDICINE, MADRAS MEDICAL COLLEGE,
GOVT. GENERAL HOSPITAL, CHENNAI-600 003
MUST BE COVERED POINTS IN RHEUMETOLOGICAL DISEASES
INTRODUCTION
The diagnosis and assessment of articular disease are based on the clinical
processes of history- taking and examination. Blood tests and radiological
investigations are often useful, and may be essential , but they cannot replace careful
history- taking and examination of the patient. Unnecessary investigations are
expensive , may cause anxiety to patients, and if taken out of clinical context, lead to
over-diagnosisand over-treatment. The initial history and examination may lead
immediately to the diagnosis of a specific disorder, such as rheumatoid arthritis, or
may indicate a pathological process such as vas ulitisor synovitis, or may suggest
that the condition is self-limiting or non- pathological.
Appropriate assessing the patient and the results of the investigations, the physician
should be able to offer the patient an explanation of his symptoms in terms the
patients can understand and formulate with the patient a plan for treatment.
THE HISTORY
The patient should be asked first about the nature of the main problem
and it’s impact on their daily life. Factor’s such as the patient’s age, sex, race and
employment are often relevant. The mode of the onset of the symptoms and any
precipitating factors such as trauma should be asked about. The development of
symptoms, their evolution over time, and pattern of remission and relapse are also
important. The effect of previous therapies, the patient’s compliance with them and
any adverse reaction are important in planning future treatment.
Pain
Pain is a cardinal symptom of rheumatic disease and should be enquired about

in detail.
Site
It is important, and sometimes surprisingly difficult, to establish whether the
pain arises from a joint, muscle, bone or other tissue, in general, pain arising in a
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joint is worse when the joint is moved, whereas pain arising elsewhere will not be
affected by joint movement. Associated symptoms such as joint swelling suggesting
inflammatory joint disease or paraesthesiae and weakness, suggesting a
neurological cause for the pain, may also help. It is helpful to ask patients to
demonstrate on their own bodies the site where pain is felt.
Quality or character
Pain is notoriously difficult to describe in words, but some features are very
useful. Pain, which is worse at night, disturbs sleep and is unrelenting and
unaffected by position, is strongly suggestive of serious disease such as malignancy
and requires urgent investigation. The pain of malignancy is usually less acutely
severe than the pain of an acute inflammatory condition such as gout. The severe
shooting pain of nerve root entrapment, which travels down a limb or around the
trunk, is often characteristic enough to be diagnostically useful
iii. Relieving and exacerbating factors

Joint pain due to mechanical problems without inflammation is typically
worsened by movement and rapidly relived by rest. Inflamed joints are
often painful at rest and somewhat better after a few minutes of use.
Patients with active inflammatory joint disease are often troubled by
severe night pain and stiffness.
Stiffness and restriction of movement
Stiffness is highly subjective and variable sensation of tightness and

resistance to movement. Patients may equate stiffness with fatigue, pain, weakness,
loss of range of movement or swelling. Most patients with joint pain experience an
initial, shot-lived sensation of stiffness after immobility. This needs to be
differentiated from the severe stiffness experienced with patients with inflamed joints
when they begin to move after sleep or rest. This stiffness typically “ wears off”after
minutes or hours, and patient can often quantify this time quite accurately. The
duration of “early morning stiffness” on first arising after the night’s sleep may be
used to assess the changing severity of inflammatory disease. A duration of more
than 30 minutes of morning stiffness remains one of the American Rheumatism
Association criteria for rheumatoid arthritis.
Swelling
Patients may notice swelling, but it is unwise to assume that what the
patient is describing is synovial swelling or joint infection unless the description is
very clear, or there is evidence of synovitis or effusion on examination. Stiffness ,
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paraesthesiae from nerve entrapment, malallignment, discolouration or pain itself
may lead the patient to a perception of swelling which is not confirmed by
examination. If swelling or deformity is present, it is necessary to determine whether
it is due to fluid, soft-tissue or bone.
Family History
The family history may be useful; a history of similar problems in other

family members may give a clue to HLA B27- related arthropathies, psoriatic arthritis,
gout or some autoimmune rheumatic diseases.
Systemic symptoms
Symptoms of systemic illness such as fever, weight loss and malaise may be
due to active inflammatory joint disease, but should also alert the doctor to the
possibility of an underlying infection, malignancy or tuberculosis, may be relevant.
Non- articular symptoms associated with joint disease such as ankylosing spondylitis
should be specifically asked for ; patients will seldom associate a history of a painful
red eye; skin rash or urethral discharge with their painful swollen knee. Tact, and
appropriate explanation, are needed when enquiring about sexually transmitted
diseaseand genital symptoms, but failure to ask the relevant questions may result in
misdiagnosis.
Essential points in the history
* Pain Onset
site and radiation; referred pain
character
effect of movement and rest
night pain and unremitting pain
* Stiffness morning- duration
Immobility stiffness and gelling

o Swelling and deformity
o Disability and handicap
o Systemic illness, extra-articular features, sleep and
depression
o Social and family history
Patients should be asked specifically about sleep disturbance depression,

which are commonly features of chronic painful conditions. Fatigue is a
characteristic symptoms of autoimmune disease such as reheumatoid arthritis and
systemic lupus erythematosus.
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Examination of the locomotor system
Swelling
Swelling around a joint may be cause by fluid, as in an intra-articular
effusion or effusion into an inflamed bursa, by soft tissues such as synovium or extra-
articular fat pads, or by bony enlargement as in the osteoarthritis. Subluxation, as
the metacarpophalangeal joint, may also give an impression of swelling. Intra-
articular fluid produces a swelling defined by the margins of the joint capsule. The
synovial lining layer is normally too thin to be palapable but the thickened inflamed
synovium in chronic synovitis such as rheumatoid arthritis may have a “boggy”
consistency and be easily felt. Effusion without synovial thickening, where the joint
line can be clearly felt , is usually due to trauma or osteoarthritis. Fluid can often be
shifted from one area of the joint to another by compressing one side of the swollen
joint.
Tenderness, redness and warmth
Inflammed joints are tender along the joint line. Paplation may also
localize tenderness to the sites of attachment of tendons or ligaments, bursae,
muscles or fat pads . Inflammed joints are usually warmer than the surrounding
tissues. Redness over the joint is a sign of intense inflammation, usually due to gout,
pseudogout or infection.
Limitation of movement, deformity and instability
Limitation of a movement is a common symptom of joint disease. Older

people have less mobile joints than the young, women are generally more flexible
than men and joint mobilityis greater in some races than others. It is important to
develop a feeling for the normal for a particular race, age and sex so that generalized
hypermobility, as well as restriction of movement at specific joints may be detected.
Limitation of movement of a joint may be due to swelling, soft-tissue contracture,
tendon rupture, muscle weakness, joint subluxation or dislocation as well as pain ,
the commonest cause. The extent of loss of function resulting from limitation of
movement should be assessed. The pattern of loss of movement may indicate
whether it is due to inflammation of the joint itself or to another cause such as rupture
of tendon. There may be a greater range of passive than active movement. This is
commonly due to pain but may be due to muscular weakness or tendon rupture.
Deformity of a joint may result from contracture of the capsule or

surrounding soft tissue , subluxation, ankylosis in an abnormal position or bony or
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soft tissue swelling. Deformity usually results in some loss of function and placing of
the abnormal stresses on the joint. A joint is said to be unstable if a greater than
normal range of passive movement is possible. If there is partial loss of congruity of
the joint surfaces the joint is subluxed; if there is complete loss of cartilage-to-
cartilage contact the jont is located.
1. Look Position in which the joint is held

Swelling
Deformity
Associated tissues-skin changes, muscle wasting nails.
2. Feel Warmth
Tenderness
swelling; bone, soft-tissue(synovium or other 0 or fluid?
Crepitus; soft-tissue(synovial) or bony?
3.Move ACTIVE MOVEMENT
assess the range, rhythm and ease of movement the patient
can achieve.
PASSIVE movement
Compare the range of movement when you move the joint
Assess the stability of the joint.
4. Function Assess the degree (or loss) of useful function eg; of the hand
or arm.
Extra-articular manifestations of common rheumatic diseases
Skin
Nodules Rehematic fever, rheumatoid arthritis, gout,
Hyperlipidaemias
Rash Systemic lupus erythematosus, rheumatic fever,

Still’s ,
Disease, psoriasis, Reiter’s dermatomyositis,
cutaneous
Vasculitides, drugs Lyme arthritis, viral infection,
Kawasaki’s disease, HIV – related arthritis.
Erythema nodosum TB, drugs, streptococcoal sore throat, Behcets,

sarcoidosis, fungal infections, idiopathic, inflammatory
bowel disease, leprosy ( erythema nodosum leprosum)
Other panniculitis Inflammatory bowel disease, SLE, Weber-Christian

Disease, malignancy.
Raynaud’s Progressive systemic scelrosis, polymyositis –

dermatomyositis, SLE , rheumatoid arthritis, vasculitis.
Sclerodactyly Progressive systemic sclerosis, CREST, overlap.

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syndromes
Leg ulcers Fetly’s syndrome, behcet’s systemic vasculitis,

inflammatory bowel disease.
Livedo reticularis SLE, polyarteritis nodosa
Hairloss SLE, drugs (cytotoxic) hupothyroidism
Ski pustules Gonococcaemia, Behcet’s
Heberden’s nodes Primary osteoarthritis
Bouchard’s nodes Primary osteoarthritis
Oral cavity
Aptheous ulcers Behcet’s inflammatory bowel disease

Superficial painless
Ulcers Reactive arthritis
Dry mouth Sjogren’s syndrome – primary, secondary
Ocular
Conjunctivitis reactive arthritis, relapsing polychondritis
Scleritis- episcleritis Rheumatoid arthritis, relapsing polychondritis
Anterior uveitis Juvenile chronic arthritis, seronegative spondyloarthritis
Iritis Spondylarthritis, Behcet’s
Dry eyes Sjogren’s syndrome
Summary of the Screening Examination of the Joints
1. Gait
Watch the patient as he stands, walks and sits.
Pain, stiffnessor deformity of the lower limb joints or back may lead to a limp.
An abnormal gait, a limp, or abnormal posture may indicate disease in the
spine, hip, knees or feet.
2 With the patient sitting, examine

neck- range of movement and lymph nodes
elbow- range of movement And swelling
wrist-range of movement and swelling
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hands- for skin, nails, joint swelling, deformity, pinch and power grips
3. With the patient lying, examine

hip- rotation
knees- for effusion, range of movement
feet- for deformity and MTPJ squeeze pain
4. With the patient lying, examine
Spine- for abnormal contour and range of lumbar movement.
INVESTIGATIONS
Nonspecific Tests
The tests included are completed blood counts and ESR, routine
urinalysis, total proteins with albumin and globulin levels, C-reactive protein (CRP)
and a host of acute-phase rectant (APR). The time profile of each APR is different,
e.g. CRP values can change within 24 hours while ESR takes a few days. This
difference allows judicious use of the tests. Their serial estimation helps to monitor
disease activity between clinical activity and ESR.
ESR should be measured by the Westergren method. High ESR is a
feature of inflammatory rheumatic disorders. Very high ESR(>100mm in 1 st hour) is
commonly seen in infections (TB), rhematic diseases (SLE, Still’s disease) and
malignancies (myeloma, leukaemias, lymphomas). CRP estimation is not required
routinely. In normal healthy persons the levels are complement pathway is activated.
Normal C4 and lowered C3 levels indicate activation of the alternate pathway.
Genetically determined low levels of individual complement components are
sometimes seen. These individuals may develop SLE or other rheumatic diseases.
Immunoglobulins
Rise in immunoglobulin levels is a nonspecific findings and hence is the

routine estimation is not essential. Multiple myeloma and agammaglobulinaemia are
the two main indications fro estimation of individual immunoglobulins. The same can
be said of routine protein electrophoresis.
Other immunological tests

Circulating immune complexes are of research interest. However, in
routine practice their detection has not been found to be of great help. Further, no
single method has found universal acceptance. Cryoglobulins, PEG precipitation,
Clq binding and Raji cell assay are some of the better known.
Non- Surgical Management

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1. Non –steoridal anti-inflammatory drugs.
2. Reconstructive hand surgery
3. Arthoplasty
4. Anti-cytokine agents
5. Immunosuppressive therapy
Surgical management
1. Open on arthroscopic synovectomy

2. Reconstructive hand surgery
3. Arthroplasty
4. Total Joint Replacement
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CASE :- THYROTOXICOSIS
NAME OF THE EXPERT :- DR A.V. GODBOLE
K.E.M. HOSPITAL
489, RASTA PETH,
SARDAR MOODLIAR ROAD,
PUNE-411 011
What is the difference between the terms thyrotoxicosis and hyperthyroidism?
Points in the history
1. Male: Female
2. Age
3. Stress?
4. Smoking
5. Pregnancy
6. Hyperactivity/ irritability
7. Heat intolerance/ Sweating
8. Palpitations
9. Weight loss with increased appetite
10. Diarrhoea
11. Polyuria
12. Loss of libido
Points to be covered in clinical examinations

1. Tachycardia, AF
2. Tremor
3. Goiter
4. Muscles wasting, proximal myopathy without fasciculation,chorea
5. HPP
6. Eye signs
7. Gynaecomastia
8. Skin ‘changes’/Thyroid dermopathy.
9. Scoring of orbital changes.
NO SPECS scheme
Points in investigations
1. TSH, uncombined TSH, uncombined T3

2. TPO antibiotics
3. TBll or TSI measurement
4. Radionuclide scar.
5. Liver function tests
6. S. Ferritin levels
7. Haemogram/ PBS for microcytic anaemia & thrombocytopenia
Points in Differential Diagnosis

1) Nodular thyroid disease
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2) Destructive thyroiditis
3) Ectopic thyroid tissue
4) Factitious thyrotoxicosis
5) TSH-secreting pituitary tumor.
6) Panic attacks, mania
7) Phaeochromocytoma
Points in Management
1. Antithyroid drugs
2. Surgery-subtotal thyroidectomy
a. Thyrotoxic crisis
b. Complications of surgery
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Specialty :- Medicine
Case :- Diabetes Mellitus
Name of the expert:- Dr. Gurcharan Avasthi
Sherpur Chowk, G.T. Road ,
Ludhiana
Definition:- The national diabetes data group &WHO have issued diagnostic
Criteria
for D.M.
 Symptoms of Diabetes plus random blood glucose concentration
> 200mg/dL or
 Fasting plasma or glucose>126mg/dL or
 Two hour plasma Glucose> 200mg/dL during an oral glucose
tolerance test.
History:-
 Polyuria, Polydipsia, Polyphagia, weight loss.
 Blurred vision, lower extremity paresthesias, yeast infection,
particularly Voluovaginitis in women, balanitis in men.
 Obese patients,
 Patient first degree relative with type 2 diabetes mellitus.
 Patients with hypertension,
 Patients with high triglyceride or HDL- Cholesterol <35mg/dL.
 Polycystic ovary disease
Examination:-
 Obesity
 Anthropometric data
-Height
-Weight
-Waist-hip ratio
-Fat fold thickness
 Skin Changes
 Hair loss
 Prominent veins
 Callus formation
 Crackers and fissures
 Ulcers in the foot and deformities
 Peripheral pulses
 Blood pressure recording (both recumbent and standing)
 Auscultations for bruits over carotid and femoral arteries
 Neurological examination
- cranial nerves
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- Deep tendon reflexes
- Autonomic function
Differentials:-
 Diabetes incipidus
 Insulin resistance
 Obesity
 Maturity onset diabetes mellitus
 Latent autoimmune diabetes of adults(LADA)
 Stein- Leventhal syndrome
Investigation:-
 Fasting plasma glucose (fpg) greater than or equal to 126MG/dL or
random glucose greater than or equal to 200mg/dL and classic
symptoms polyuria, polydipisia, polyphagia, weight loss
 Hemoglobin Alc (HbAlc or Alc) or glycosylated hemoglobin (GHb)

 Screening urine microralbumin measurements is recommended
 Measuring insulin or C-Peptide Concentrations
 Antibodies to insulin, islet cells, or glutmatic acid decarboxylase (GDA)
- Non- Sulfonylurea
- Repaglinide
- Nateglinide
(B) Biguanides
- Metformin
(C) L.glucosidace inhibitor

-Acarose
- Meglitol
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(D) Thiazolidinedione
- Rosiglilatazone
- Pioglitazone
 Ii1sulin:-
(A) Short Acting

- Lispro
- Insulin Aspart
- Regular
(B) Intermediate acting

- NPH
- Lente
-
(C) Long Acting
- Ultralente
- Glargine
 Complication monitoring
 SMBG
 Surgery:-
- Whole pancreas transplantation
Diet:-
- Weight reduction (in obese)
-Hypocaloric Diet
- Total calories between 1000-1200 kcal/ day
- For obese- 20 kcal/kg ideal weight ~
- For normal adults (sedentary)- 30 kcal/kg ideal body weight
- for normal adults( manual worker) and growing children 40kcal /kg
ideal
body weight.
- Carbohydrate- 50-60 % of total calories.
- Fibers - 25 gm of fibres per 1000 kcal
- Proteins- 25-30% of total calories.
- Fats - 25-30% of total calories
 Exercise:-
- Isotonic exercise like brisk walking, swimming or cycling are
recommended.
- Aerobic exercise for 30-45 minutes/ day, 5 times per week should be
advocated.
- Exercise regimen should start with warm up stretching for 10 minutes,
aerobic exercise for 30- 45 mintues, and cool down streching for
5-10 minutes.
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Hypoglycemia
1. History:-
- Tremor
- Sweating
- Anxiety
- Pallor -Nausea
- Shivering
- Palpitation
- Impaired concentration
- Confusion
- Inappropriate behavior
- Difficulty in speaking
- Aggression or non- cooperation
- Focal/generalized seizure
-Hunger
- Weakness
- Epigastric discomfort
- Blurred Vision .
2. Examination:-
-Tachycardia
-Increased Pulse pressure
- Focal neurological deficit including transient nemiplegia.
- Drowsiness progressing to coma
- Permanent neurological change, if prolonged hypoglycemia.
- Grading: - Clinically, hypoglycemia may be usefully graded
as follows :-
Grade 1:- Biochemical hypoglycemia in the absence of symptoms
Grade 2:- Mild symptomatic- treated successfully by the patient.
Grade 3:- Severe- assistance required from another person.
Grade 4:- Very severe- causing coma or convulsion.
3. Differential:-
* Nonketotic Hypersomolar State
* Diabetic Ketoacidosis
* Metabolic encephalopathy
4. Invetigation:-
*Random blood sugar
*ABG
* Chest x rays
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5. Management:-
In type 1 OM
Grade 1-2 Hypoglycemia:-
 2-4 Dextrose tablets
 2 tsfSugar (10 gm), honey or jam (ideally in water)
 A small glass of carbonated sugar- containing soft drink.
Grade 3-4 Hypoglycemia:-

 Buccal glucose gel:-Proprietary thick glucose gel (e.g.
Hypostop) Or honey, can be smeared on the buccal
mucosa (variable efficacy)
 Intravenous glucose:- Administer 25ml of 50% glucose
(or 10Oml Of 20%Dextrose) into a large vein, ideally after
cannulation.
 Glucagon: - 1 mg can be given I. V , SIC or I.M
In type 2 DM:-
 Intravenous dextrose :- Mandatory continuous infusion of

5% or 10% may be required for several days.
 Diaz oxide
 Hydrocortisone
 Glucagon
 Mannitol :- to reduce cerebral odema
 Octriotide: - for prevention of sulphonylurea - induced
hypoglycemia. However, clinical
experience is very limited.
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Diabetic Ketoacidosis
1. History:-
* Nausea, Vomiting
* Thirst, Polyurea
* Abdominal Pain.
* Shortness of breath.
* Confusion, Drowsiness, Coma.
* Acute weight Loss.
* Generalized muscular weakness.
* Visual Disturbances.
* Muscular Cramps.
2. Physical Examination:-
* Tachycardia.
* Dry Mucous Membranes, Reduced Skin turgor
* Dehydration, Hypotension.
* Tachypnoea, Kussmaul Respiration/Respiratory distress.
* Abdominal Tenderness.
* Lethargy, Obtundation, Cerebral Odema, Coma.
3. Differential Diagnosis:-
 Alcoholic Ketoacidosis.
 Acute Appendicitis
 Hyperosmolar Hyperglycemic Nonketotic coma
 Salicylate Toxicity.
 Hyponatremia
 Hypothermia.
 Lactic Acidosis.
 Metabo1ic Acidosis.
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4. Investigation:-
* Random Blood Sugar.
* Urine for Ketones.
* ABG.
* S. Electrolytes (K+, Na+, Mg++, CI-, Bicarbonate, Phosphate)
* Acid-base status-PH, Hco3-, Pco2, β-Hydroxybutyrate.
* Renal Function test.
* Blood Culture.
* Chest X-Rays.
* ECG.
5. Management:-
- Fluids and Electrolytes
* Volumes: - lL/h X 3, thereafter adjust according to requirements.
* Fluids: - Normal Saline (150mmol/L) is routine.
- Hypotonic ("Half- normal") Saline (75 mmol/L), if serum
Sodium exceeds 150mmol/L.
- 5% Dextrose 1 L 4-6 hrly when blood glucose has fallen
to
15mmol/L.
* Potassium: - No potassium in first 1L unless initial plasma

potassium
<3.5 mmo1/L.Thereafter, add 40mmol/L KCL
- 3.5-5.5 mmo1/L, add 20mmol KCL
- > 5.5 mmo1/L, 40mmol KCL
- severe hypo kalemia may require more aggressive
KCL
replacement
*lnsulin:-1. By continuous intravenous infusion: - regular insulin is
administrated as I.V(0.1 U/Kg) or 1.M (0.4U/Kg), then 0.1
U/Kg/hr continuous I. V infusion; increase 2-10 fold if no
response
by 2-4hour.
2. Administer intennediate or long acting insulin as soon as

patient is eating. Allow for over lap in insulin infusion
and subcutaneous insulin injection.
22
5. Other Points:-
* Search for and treat precipitating cause (e.g. infection, MI)
* Hypotension usually responds to adequate fluid replacement.
* CVP monitoring in elderly patients or if cardiac disease present.
* NG tube, if conscious level impaired to avoid aspiration of gastric
content.
*Urinary Catheter.
* Continuous ECG monitoring may warn of hyper or hypokalemia
* ARDS mechanical ventilation (100% 02; IPPV) avoid fluid overload.
* Mannitol (up to 1 gm /kg I. V) if cerebral odema suspected.
* Meticulously updated clinical & biochemical record using a purpose
designed flow chart.
23
Hyperosmalar Coma
1. History:-
* Elderly with known history of type 2 DM
* Polyuria
* Weight loss
* Diminished oral intake that culminates in mental confusion, lethargy,
and coma.
* Prior hospitalization for hyperglycemia
* Increasing thirst with polyuria, polydipsia, and weight loss
* Drowsiness and lethary
- Delirium
-Coma
- Seizuers
- Visual/Disturbance
* Clues to underlying DM:-
- Needle pricks or calluses on finger tips.
- Obesity
- Aonthosis nigricans
* Diabetic dermopathy
* Necrobiosis on the pretibial surface
* lower extremety infections,(e.g. cellulites , carbuncles)
* Balanities
* Valvovaginitis
* Thrush
* Gingivitis
* Tachycardia
* Hypotension
* Seizures, Hemiparesis
* A positive Babinski sign
* Myoclonic jerks
* Change in muscle tone
* Nystagmus, diplopia and altered mental status
2 Differentials:-
* Diabetes insipidus
*Diabetic Ketoacidosis
* Myocardial Infarction
* Aphasia
* Pulmonary Embolism
24
3. Investigation:-
* Plasma glucose
* Arterial blood gases (pH,Pco2,Hco3-,K+,Na+)
* Plasma ketones
* Serum osmolality and calculated serum osmolality
* Urinalysis
* Plasma Electrolytes
* Calculated Anion Gap
* Creatinine and BUN
* Complete blood count and differential
* Creatine Kinase (Rhabdomyolysis)
* Chest radiograph
* CT scan of the head
* Electrocardiogram
4. Treatment:-
* Intravenous fluid hydration and electrolyte hemoeostasis
* Corrections of hyperglycemia
* Treatment of underlying diseases
* Cardiopulmonary monitoring
 Neurological Monitoring
25
DIABETIC NEUROPATHY
1. History:-
* Sensory Symptoms:-
- Negative or Positive
- Diffuse or Focal
*Negative Sensory Symptoms are feelings of numbness or deadness.
Loss of Balance
Especially with eyes closed.
Painless injuries
* Positive Sensory Symptoms may be describe as Burning
Pricking pain
Tingling Sensation
Pins & Needles Feeling
Aching, tightness
Hypersensitivity to touch
* Motor Prombles:-
- Distal, proximal
- More focal weakness .
- Fine hand coordination and difficulty with tasks
- Foot slapping and toe scuffing or frequent tripping
- Weakness
- Limb weakness
- Difficulty climbing up the stairs and getting up from a seated or supine
position, falls.
* Autonomic Symptoms:-
-Dry skin due to lack of sweating or excess defined areas
-Poor dark adaptation, sensitivity to bright light
-Cardiovascular postural hypotension lightheadedness, fainting.
-Urinary (Urgency, incontinence, dribbling)
-Gastrointestinal (nocturnal diarrhea, constipation, nausea, or vomiting)
-Sexual (Erectile impotence and ejaculatory ability to reach sexual
climax in woman)
* Examination:-
- Symmetrical or Asymmetric neuropathies involved.
* Symmetric polyneuropathies: - multiple nerves diffusely and symmetrically
involved.
- Distal symmetric polyneuropathy
- Small Fiber neuropathy
- Diabetic autonomic neuropathy
- Diabetic neturonathic cachexia
26
 Asymmetric neuropathy: - Single or multiple cranial mononeuropathies
- Cranial Mononeuropathy
- Somatic Mononeuropathy
- Diabetic Polyradiculopathy
-Diabetic radiculoplexopathy
-Chronic inflammatory dymyelinating polyneuropathy.
2. Physical:-
- Loss of ankle jerks or loss of vibratory sensation over the
great toes.
- Weakness of small foot muscles.
3. Differentials:-
- Alcohol ( Ethanol) related neuropathy
- Chronic Inflammatory Dymyelinating Polyradiculoneuropathy -
Nutritional Neuropathy
- Sarcoidosis and Neuropathy
- Thyroid Disease
- Toxic Neuropathy
- Uremia Neuropathy
- Vasculitic Neuropathy
4. Investigation:-
- Complete blood count (CBC) .
- Complete metabolic panel (Electrolytes and liver function panel)
- Vitamin B-12 and folate levels
- Thyroid-stimulating hormone and thyroxine
- Erythrocyte sedimentation rate
- Serum protein electrophoresis with immunofixation
electrophoresis.
- Antinuclear antibody
- Rheumatoid factor
- Paraneplastic antibodies
- Elevated hemoglobin Alc levels>8%
- MRI of the cervical, thoracic, and lumbar regions
- Electro physiologic studies(Electromyography and nerve
conduction studies).
5. Treatment:-
27
 Medical care :- General aspects of treatment
- Education on foot care
- regular foot examinations
* Current treatments for pain:-
- Tight and stable glycemic control is probably the most important
- Gabapentin, Pregabalin, Topical lidocaine, and duloxetine
- Phenytoin, lamotrigine, and opioids
- Topical therapy with capsaicin
 Treatments for autonomic dysfunction
- For Erectile impotence
- Papaverine
- Sildenafil
 Glycopyrrolate
 Aldose reductase inhibitors (e.g., Alrestatin, sorbinil, tolrestat)
 Alpha-lipoic acid
 Gamma- Linolenic acid
 Nerve growth factor(NGF)
28
Diabetic nephropathy
History
* History of Diabetes:-
* Passing of foamy urine
* Otherwise unexplained proteinuria in a patient with diabetes
Examination:-
* Foot edema secondary to hypoalbumineia
* other associated disorders such as peripheral vascular disease
* Hypertension
* Evidence of diabetic retinopathy after funduscopy or fluorescein
angiography
* Peripheral vascular occlusive disease * Evidence for diabetic neuropathy
* Evidence for fourth heart sound during cardiac auscultation * Nonhealing
skin ulcers/osteomyelitis
Differentials:-
*Multiple Myeloma
*Nephritis, interstitial
*Nephrosclerosis
*Nephrotic Syndrome
*Renal artery stenosis
* Renal Vein Thrombosis
* Renovascular Hypertension
Investigations:-
* Urinalysis
* Microalbuminuria
* 24- hour urinalysis for urea
* Microscopic urinalysis
29
*Renal ultrasound
- Kidney size
- Obstruction
- Echogenicity studies
* Serum and urinary electrophoresis

* Renal biopsy
Treatment:-
*Medical care:- Glycemic control
* Antihypertensive treatment
* RAS inhibition -ACE..I & ARB
* Specific therapies: - includes modification &/or to treatment of risk
factors
- Peritoneal dialysis
- Hemdialysis
- CAPD
- Continuous Renal Replacement therapy
(A) Continuous arteriovenous hemodiafittration with or without
dialysis
(B) Continuous veno-venous hemodaifiltration with or without
dialysis.
* Surgical
-Renal replacement therapies
- Kidney pancreas transplantation
- A. V fistula
Diet:-
* ADA suggests diets of various energy intake (caloric values).
* With advancing renal diseases, protein restriction of as much
as 0.8- 1 gm/kg/day may retard the progression of nephropathy.
Activity:-
No restriction in activity, unless associated complication of diabetes like
coronary artery disease or
peripheral vascular disease.
30
OPHTHALMOLOGIC COMPLICATIONS
1. History:-
* Transient disturbance of refraction.
* Gradual loss of vision - suggestive of maculopathy or cataract.
* Sudden painless loss of vision-vitreous hemorrhage. Retinal
arterial & venous thrombosis may also occur in diabetic patients.
* Appearance of 'floaters'- possible small/recurrent vitreous hemorrhage.
* Chronic pair & redness- rubeosis & secondary glaucoma.
* Field defects and impaired night vision.
2. Examination:-
* Visual acuity, maculopathy, cataract, glaucoma.
* Fundus Examination
- Background retinopathy
- Pre-proliferative retinopathy
- Proliferative retinopathy
- Advanced diabetic eye disease
- Maculopathy
* Branch retinal vein occlusion
* Central retinal vein occlusion
* Ocular ischemia syndrome .
* Retinopathy, haemoglobinopathy
* Sickle cell disease.
4. Investigation:-
*Blood sugar
*Fundus, Slit -Lamp Examination
*Ultrasound Eye, Flurescein angiography (for macular edema)
5. Management:-
*Background retinopathy
-Explanation
-Search for other complication
-Review of glycemia control
* Proliferative retinopathy
- Laser Photocoagulation (pan-retinal photocoagulation)
* Advanced diabetic eye ds (Retinal detachment owing to fibrin traction,
Rubeosis iridis (new vessels on the iris)
- Pan- retinal photocoagulation
31
- Surgical vasectomy –
- Enucleation
* Maculopathy
- Photocoagulation
- Control of hypertension
* Cataract
-Surgical extraction with IOL implantation, once the cataract has
matured.
DIABETIC FOOT DISEASE & PEREPHERAL VASCULAR DISEASE
1. History:-
* Intermittent claudication
* Rest pain
* Leriche Syndrome (buttock & leg claudatcation, erectile impotence as a
result of major stenosis of the
aortofemoral vessels).
* Foot ulceration- past or present
* Smoking habits.
* Family history of atherosclerotic disease.
* Other manifestations of atherosclerosis- i.e of MI, TIA, stroke and lipid
status.
2. Examination:-
* Palpation of peripheral pulses .
* Auscultation for bruits.
* Trophic changes in skin
* Limb temperature (Limb is pale & cold in the presence of significant
ischemia but may appear red with critical
impairment of blood flow ('Sunset Foot').
* Buerger's Sign
* Examination of ulcer- Base, Edge, painful or Painless
* Dry and warm
* Callus formation
* Gangrene
* Cellulites
* Deep skin and soft tissue infections-Gangrene
* Acute Osteomyditis
* Chronic Osteomyelites.
4. Investigation:-
* Complete Haemogram
* Blood Sugar
* Pus culture & Sensitivity
* X-rays feet & joints.
* Doppler Studies
* Duplex scanning
* Oxygen tension
32
* Angiography
* Nuclear medicine bone scans
* MRI of foot, Bone biopsy Culture
5. Management:-
(A) Peripheral Vascular ds
* Aspirin
* Foot care:-
- Inspect feet daily
- Check foot wear for forigen objects before wearing
- Have feet measured carefully when purchasing shoes
- Keep feet away from heaters, Fires and hot water bottles.
- Check feet temperature of bathwater before bathing
- Avoid walking barefoot especially outdoors.
- Avoid unaccustomed lengthy walks when on holiday.
* Vasodilators
* Surgical Sympatheotomy- Lumbar sympathecto
* Reconstructive surgery.
* Angioplasty.
* Amputation. .
* Rehabitation:-
(B) Diabetic Foot:-
* High risk patients should be identified during routine foot
examination
performed on all patients with DM.
*Patient Education:-
1. Carefull selection of foot wears.
2. Daily inspection of feet to detect early sign of poor fitting
..
foot wears/ minors trauma.
3. Daily foot hygine to keep the skin clean and moist.
risk 4. Avoidance of self treatment of foot abnormalities and high
behavior (e.g. Walking barefoot)
5. Prompt consultation with a health care provider if an
abnormalities
arise.
*Risk factor modification:-
1. Orthotic shoes and devices.
2. Callus management
3. Nail Care.
4. Proplylactic measures to reduce increased skin pressure
from abnormal bony architecturesmoking, dyslipidemia,
hypertension.
33
5 Antibiotic (IV & oral):- According to culture sentivity report.
Wound debridement.
6 Osteomyelitis is best treated by a combination of prolonged
antibiotic (IV & Oral) and Possible debridement of infected
bone.
7 A recent consensus statement from ADA identified six
interventions with demonstrated efficacy in diabetic foot
wound:-.
1. Off- loading
2. Debridement.
3. Wound dressings.
4. Appropriate Use of antibiotics.
5. Revascularization
6. Limited amputation
* Hyperbaric oxygen.
34
Erectile Dysfunction
1. History:-
* Through sexual medical and psychosocial history * Difficulty obtaining
erection
* Rapid (premature) ejaculation
* Obtain information about current medications and prior surgeries,
*Any h/o of pelvic surgery, trauma, prior prostate surgery, or radiation to
the prostate.
* Tobacco use, alcohol intake, caffeine intake, and illicit drug
* Stress factors and tension at work and at home
* Indication of depression,
* loss of libido
* Problems and tension in the sexual relationship lethargy, moodiness
 Stress from work or other sources.
2. Examination:-
*Penile plaques
* Small tsetse
* Evidence of possible prostate cancer
* Prostatitis, vascular disorder
* Benign prostatic hyperplasia
*Status of the genitalia and prostate
* Size and texture of the testes
*Abnormalities of the penis such as hypospadias and peyronie plagues.
3. Differentials:-
 Abdominal trauma
 Atherosclerosis
 Cirrhosis liver
 Depression
 Haemo chromatosis
 Hypertension
 Hyperthyroidism
 Hypopituitarism (Panhypopituitarisum)
35
 Hypothyroidism
 Non bacterial prostatitis
 Peripheral arterial occlusive disease
 Peyronie Disease
 Priapism
 Prostate Cancer
 Prostatitis
 Endovascular Hypertension
 Sclerodema
 Sickle Cell Anemia.
* Antidepressant medication
* Antipsychotic
* Antihypertensive
* Hyperlipidemia medications
4. Investigation:-
* Evaluation of the patient's hormone status
* Measuring morning serum testosterone level, total and free
* Measurement of luteinizing hormone, prolactin
* Evaluating the patient for diabetes with a hemoglobin Alc
measurement
* Lipid profile, and prostate specific antigen
* Investigate the hypothalamic-pituitary- gonadal axis by
evaluating testosterone
level
* Serum thyroid- stimulating hormone evaluation
* Urinalysis looking for RBCs, WBCs, protein and glucose
* Nocturnal penile tumescence testing, testing for penile blood
flow studies
* Angiography
* Duplex ultraSonography
* Ultrasonography of testes
5. Treatment:-
* Medical care:- .
-Use of oral PDE-5 inhibitor - most common practice
-Combination therapy with one of the PDE-% Inhibitors plus
Yohimbine,
MUSE or intracavemosal injection, in selected cases
* Drugs are PDE-5 inhibitors
- Sildenafil (Viagra)
- Vardenafil (Levitra)
- Tadalafil (Clalis)
- Vasodilators (nitroglycerine)
36
- Pentoxifylline (trental)
* Yohimbine
* Apomorphine (Uprima)
* Phentolamine (Vasomax)
* Androgens
- Alprostaladill, POE 1 - small supossity that can be introduced in to
the uretha.
* Intraurethral therapy (MUSE)
* Hormonal (testosterone) therapy
- Hypogonadotrophic hyponganadism- parenteral testosterone
200mg I.M
6. Surgical :-
* Penile implants
- Semirigid or malleable rod implants
-Fully inflatable implants
- Self- contained inflatable unitary implants
- Vascular Reconstructive surgery

- Microvascular arterial bypass surgery
7. Others
* Psychological care.
* Vaccume devices- to draw blood in to penis
* Penile injection therapy
37
Dermatologic Manifestations
(1) Diabetic dermopathy-( pigmented pretibial papules)- erythematous

area and evolves in to an area of circular hyperpigmentation, more
common in elderly men with DM.
(2) Nerobiosis lipoidica diabeticorum: - young women with type IDM.

Usually begins in the pretibial region as an erthemations plaque or
Papules that gradually enlarge darkeen and develop irregular margins,
with atrophic centers and ulceration.
(3) Acanthosis nigricans- (hyper pigmented velvety plaques seen on the

neck,
axilla or extrensor surfaces)- features of severe insulin resistance and
accompanying diabetes
(4) Gramuloma annulare- erthematous plaques on the extremities or trunk.
(5) Sclerdema- areas of skin thickening on the back or neck at the site of ,
previous
superficial infections.
(6) Lipoatrophy and Lipohypertrophy at insulin injection sities but are

unusual with use of human insulin.
(7) -Xerosis & pruritus.
38
Infections
* Pneumonia
* Urinary Tract infection
* Skin and soft tissue infection

- Furuncles
- Carbuncles
- Cellu1ites
- Gas gangrene
* Emphysematous pyelonephrities
* Emphysematous cystitis
* Superficial and deep candidial infection
* Vulvovaginitis, Balanitis
* Post operative wound infection
* Rhino cerebral mucormycosis
* Emphysematous infection of gallbladder
* "Malignant" or invasive otitis extema, osteomyelitis and meningitis
* Pulmonary tuberculosis
39
Macrovascular Complications
(A)Coronary artery disease:- (Silent ischemia, myocardial infarction)
History:-
* Chest pain! chest discomfort
- Retrostemal
- Radiating to back left arm, neck, jaw
- Heavy, squeezing, Crushing, Stabbing or burning.
* Epigastric discomfort
* Weakness
* Fatigue
* Breathlessness
* Nausea, Vomiting
* Anxiety
* Sweating
* Sudden loss of consciousness
* Confusional state
* Palpitation
* Risk factor (Hypertension, cigarette smoking, alcohol, family
history etc)
Examination:-
* Anxious
* Restless
* Pallor
* Perspiration
* Coolness of extremities
* Tachycardia! Bradycardia, Arrhythmia 'I
40
* Hypertension! hypotension
* Precordium quiet
* Apical impulse difficult to palpate
* Fourth heart sound and third heart sound
* Decrease intensity of first heart sound
* Paradoxical splitting of second heart sound
* Transient midsystolic or late systolic apical systolic murmur
* Pericardial friction rub
* Carotid pulse
* Elevated temperature (up to 38°c)
* Arterial pulse
Differential Diagnosis:-
* Gastro-Esophageal reflux disease
* Pneumonitis, Asthma.
* Mediastinitis
* Dissection of aorta
* Pericarditis
* Myocarditis
* Oesophageal rupture
* Cafe coronary
* Pulmonary embolism
Investigations:-
(1) ECG
(2) Cardiac Biomarkers
* Myoglobin
* Creatine phosphokinase (ck) - CKMB
* Cardiac specific troponin- T and I
* Lactate Detrydrogenase
* AST (SOOT)
* Leukocytosis
* ESR
(3) Cardiac Imaging
* Two- dimensional echocardiography
* Radionuclide imaging techniques
- Myocardial perfusion imaging with 201 TI or 99m
Tc- sestamibi.
- Radionuclide ventriculography
(4) Angiography
41
Management:-
* Medical
- Oxygen
- Aspirin
- Clopedogerel, Heparin/low molecular weight Heparin
(LMMH)
- Morphine
-Nitroglycerine
- Beta blockers
- ACE Inhibitor
- Calcium Channel Blocker
- Statins
- Thrombolysis (streptokinase, Urokinase, tenecteplase and

reteplase)
- GP nb/liJ,a inhibitor
- Glycemia control (insulin)
Surgical:-
* CABG (Coronary artery bypass Grafting)
Others:-
- Diet
- Exercise/activity
- Bowel (constipation)
- Sedation
42
Macrovascular Complications
(B) Cerebrovascular accidents: - (Occlusive stroke and transient ischemic

attacks)
History:-
* Sudden onset of loss of sensation (one side of body)
* Sudden onset weakness (one side of body)
* Change in vision
* Gait disturbance
* Inability to speak/understand
* Sudden, severe headache
* Seizure
* Fever/sepsis
* Risk factors (hypertension, cigarette, smoking, alcohol, family
history etc)
Examination:-
* High motor function
* Cranial nerves
* Motor examination
* Sensory tests
* Gait
* Coordination
* Carotid bruit
Differential Diagnosis:-
* Intracranial hemorrhage
43
* Subarachnoid hemorrhage
* Migrane
* Meningitis
* Metabolic Encephalopathy
* Cerebal Venous thrombosis
* Subdural Hematoma, Neoplasm
* Head Injury
* Todd's paralysis
* Multiple Scletosis
* Vestibular disorder
* Hysteria
Investigation:-
* Complete haemogram with platlet count
* ESR
* Bleeding time, clotting time and prothrombin time

* Sickle cell test
* Anticardioplipin antibodies
* C-reactive protein
* Lipid profile
* Uric acid and electrolytes
* Serum protein C and S level
* Homocystein level in blood
* Chest x Rays
* ECG, Hotler monitoring
* 2D Echocardiography
* CSF
* VDRL of blood and CSF
* Fluorescent treponemal antibody absorption test (FTA- ABS)
*HIV
*Computed tomography
*Carotid Doppler
* MRI of Brain
*MRA or digital subtraction angiography
*SPECT of brain
Management: -
* Medical
44
* Maintenance of vitals
- Temperature
- Pulse
- Respiration (ventilation)
- Blood pressure
- Fluid and electrolytes
* Prevention of complications like pulmonary aspiration,
seizures, thromboplebitis and bedsores.
* Glycemic control
* Mannitol, Dexamethasone
* Aspirin
* Clopidogreal
* Heparin / low molecular weight heparin (LMWH)
* Thrombolytic therapy (RT -P A- Recombinant tissue plasminogen

activator)
* Neuroprotective agents
Surgical:-
* Carotid endarterectomy
* Extracranial to intracranial bypass surgery * Angioplasty and stenting
Others:-
* Diet
* Exercise! activity
* Stroke prevention (modification of risk factors)
45
SPECIALITY :- Medicine
CASE :- Jaundice
NAME OF THE EXPERT :- Dr Geetha K. Subramanyam
M.D. (Medicine- Delhi)
Senior Consulting Physician
Head of Medical Unit 111rd
St. Martha’s Hospital,
Bangalore
History :-
1. Alcohol intake ( quantity and duration)
2. Length of history of liver disease (P/H Hepatitis, Jaundice including
contact, H/o during addiction (i/V), Tatoos, transfusions. H/o drug
intake, overseas travel, H/o fever).
3. H/o D.M, Cardiac failure, arthropathy.
4. Treatment history
5. History suggestive of complication, (e.g.) any P/H encephalopathy, G.I.
bleeding, abdominal pain, distention of abdomen secondary to ascites.
6. P/H any operations.
7. H/o travel to endemic areas ( for malaria, leptospirosisLook for signs
of )
EXAMINATION:
1. Note the patient’s racial origin (for Hepatitis B and Hepatitis c)
2. chronic liver disease( Spider Neave, Gynaecomasia, Palmar erythema,
petichae, etc.)
3. Look for signs of Liver failure, flapping , breath, confusion , stupor,
4. Small of alcohol
5. Anaemia/ WT loss/Tatoos/ body piercing, needle pricks/scratch
marks/oedema xanthelesma/ K.F. rings/ Duputren’s contractures/
lymphode lubbing.
6. Examination of the Abdomen
7. Exclude severe Rt. Heart failure, Tricuspid Regurgitation, Constrictive
Pericarditis.
8. Rectal Examination.
INVESTIGATIONS :-
The following list covers all the causes for Jaundice. One could narrow it
down to the selected one’s depending on the provisional diagnosis made.
1. Full Haemogram including peripherial smear and reticulocyte count.
2. L.F.T. including P.T/INR
3. Auto immune workup
4. Ascitic Tap
5. Abdomino-Pelvic U/S Scan
6. Hepatitis-B and Hepatitis-C
7. Abdominal Doppler Studies- Arterial
8. CT scan Abdomen
9. Barium Series
10. Endoscopy
46
11. Alpha Feto Protein
12. FNAC and Liver biopsy if indicated
13. ERCP/MRCP (Diagnostic and Thearapetic)
14. Serum Ammonia levels and copper levels.
15. Serum Electrolyte
DIFFERENTIAL DIAGNOSIS (FEW OF THEM)
1. Haemolytic Disease
2. Hepatitis/ Cirrhosis of Liver
3. G.I . Malignancy with Metastastasis
4. Primary biliary cirohosis
5. Wilson’s disease
6. Obstructive Jaundice
7. Hemolysis due to infection
NON SURGICAL MANAGEMENT
(Conservative )-) ( Depends on the diagnosis made)
1.Diuretics
2.Salt restriction
3.Removal of precipitating causes
4. Treatment of infections
5. Treatment of Haemolysis
6 Treatment of chronic Hepato cellular failure
7. Treatment of G.I. Bleeding
8. Steroids in specific auto immune hepatitis.
9.i/v Octreoatide, Beta Blockers
SURGICAL TREATMENT
1.Sclerotherapy
2.Esophageal banding (Superior to Sclerotherapy)
3.Peritoneal shunts
4.Various specific surgical procedures for obstructive jaundice.
5.Splenectomy.
47
Specialty :- Medicine
Case :- Diabetes Mellitus
Name of the expert:- Dr. Gurcharan Avasthi
Sherpur Chowk, G.T. Road ,
Ludhiana
Definition:- The national diabetes data group &WHO have issued diagnostic
Criteria for D.M.
Symptoms of Diabetes plus random blood glucose concentration >
126mg/dL during on oral glucose tolerance test.
History:-
 Polyuria, Polydipsia, Polyphagia, weight loss.
 Blurred vision, lower extremity paresthesias, yeast infection,
particularly Voluovaginitis in women, balanitis in men.
 Obese patients,
 Patient first degree relative with type 2 diabetes mellitus.
 Patients with hypertension,
 Patients with high triglyceride or HDL- Cholesterol <35mg/dL.
 Polycystic ovary disease
Examination:-
 Obesity
 Anthropometric data
-Height
-Weight
-Waist-hip ratio
-Fat fold thickness
 Skin Changes
 Hair loss
 Prominent veins
 Callus formation
 Crackers and fissures
 Ulcers in the foot and deformities
 Peripheral pulses
 Blood pressure recording (both recumbent and standing)
 Auscultations for bruits over carotid and femoral arteries
 Neurological examination
- cranial nerves
- Deep tendon reflexes
- Autonomic function
Differentials:-
 Diabetes incipidus
 Insulin resistance
 Obesity
 Maturity onset diabetes mellitus
 Latent autoimmune diabetes of adults(LADA)
 Stein- Leventhal syndrome
Investigation:-
48
Fasting plasma glucose (fpg) greater than or equal to 126MG/dL or
random glucose greater than or equal to 200mg/dL and classic
symptoms polyuria, polydipisia, polyphagia, weight loss
49
SPECIALTY :- MEDICINE
CASE :- HYPOTHYROIDISM
NAMES OF THE EXPERTS :- PROF. DR. MATHEW THOMAS, SENIOR
CONSULTANT, DR. ROSHNA RAMACHANDRAN, 2ND YEAR DNB
RESIDENT, DR. EUNICE. S,2ND YEAR DNB RESIDENT, DR. PRAKASH S.
GUDSOORKAR, 1ST YEAR DNB RESIDENT,DEPT. OF INTERNAL
MEDICINE, KIMS TRIVANDRUM
History:
1. Age : Simple Goitre: is commonly seen in girls approaching pubertal
age. Hashimoto’s thyroiditis: middle aged human.
Autoimmune Hypothyroidism 4/1000 women: 1/1000men.
2. Sex: majority of thyroid disorder common in females>men.

3. Place: endemic area for goiter.
4. Any history of swelling in neck.
- When was the swelling 1st sighted?
- Has the size of swelling remained same/gradually increasing?
- Any pain at the sight of swelling?
(In Hasimoto’s thyroiditis there will be some discomfort in the

neck)
4 Any history of painful enlargement of thyroid gland with fever?

(Thyroiditis)
[ Initially there will be thyrotoxic state-> Hypothyroid state]
5. History of symptoms S/o Hypothyroidism
a) History of tiredness, weakness
b) History of loss of appetite with weight gain
c) History of cold intolerance
d) Recent excessive loss of hair
e) History of any change in voice(hoarseness of voice)
f) History of parasthesia suggested by tingling numbness in
limb, any loss of sensations suggested by inability to feel foot
wear (this complication/symptom is very rare/late)
g) Any history of dysponea on exertion and effort angina
h) History s/o constipation
6. Personal History:-
i) Decrease in appetite
ii)History of constipation
iii)History of loss of libido
7. Menstrual history/ Obstetric history:
Complete obstetric history- GPL status
Ask specifically for history of any congenital Hypothyroidism in
baby.
Suggested by:
a. Prolonged jaundice
b. Feeding problem
c. Flaccidity
50
d. Macroglossia
e. Delayed bone maturation
f. Umbilical hernia
g. Permanent neurological deficits in the child.
Menstrual history:
History of increase flow (menorrhagia) followed by
decrease flow.
(oligomenorrhea) and then amenorrhoea.
History of recurrent abortions.
8 Drug/ Treatment history:
A] H/o recent thyroid surgery or treatment with radio iodine in
recent past.
B] iodine excess {eg: contrast imaging}
C} Drug history:
-Amiodarone
-lithium
-Antithyroid drugs
- Para amino salicyclic acid.
- Interferon alfa
9. Family History:
H/o similar illness in the family.
Past history of snake bite ( causing pan hypopitutariam)
pituitary disease or surgery,
Excessive post partum hemorrhage.
CLINICAL EXAMINATION
1. General examination:
A} Build and nourishment:
Patient is obese and overweight. Patient appears
lethargic & tired.
B} Facies: Dull expressionless facies, periorbital puffiness with
boggy eyelid.
Coarse hair, patchy alopecia
Dry and rough skin.
Facial pallor.
C} Pulse: Sinus bradycardia.
D} Blood pressure: Diastolic pressure may be high due to
hypercholesterolemia & artherosclerosis.
E} Pallor: Moderate to severe. Usually a normocytic
normochromic anemia.
F} Sclera may be lemon yellow tinged s/o carotenemia.
G} Edema of feet: Non pitting edema. Puffiness of face,
supraclavicular fossa, neck. [ due to deposition of mucinuous
material,
Mucopolysacharides hyaluronic acid & chondroitin sulphate]
SYSTEMIC EXAMINATION
1] Cardiovascular system:
51
a) Pulse: Sinus bradycardia. [ mention rate, volume,
character, peripherial
pulses condition of vessel wall ]
b) Blood pressure:
Mention in which limb& which position.
Diastolic hyperten
c) Heart sounds, may be muffled , features due to pericardial
effusion. (30%)
2] Central nervous system:
A] Higher mental function: Shows memory impairment &
mental slowing.
Depression
Myxedema coma
Slow and sluggish speech [bradylalia] with hoarse voice.

B] Carnial nerve:8thnerve deafness. There may be
conductive deafness due to fluid accumulation in middle ear
cavity. [serious cavity]
C] Tone : Hypotonia
D] Power : usually normally.
E] Reflexes : Sluggish.
F] Sensory- Entrapment syndromes. Eg: carpal tunnel
syndrome- tingling numbness in the distribution of the median
nerve.
G] Myopathy : Painful muscles cramps [ Hoffman’s
syndrome}
Calf muscle hypertrophy
H] Cerebellar ataxia
3. GIT : Macroglossia:
Decreased bowel sounds
Presence of free fluid
4. Respiratory system: Vocal cord edema- hoarseness of
voice
Pleural effusion
Respiratory muscle fatigue
5. Examination of thyroid:
a] Inspection:
Pizzilo’s method: Ask patient to keep patients
behind head and to press head against
clasped hand. Ask patient to swallow-thyroid
swelling moves with degulgition.
Look for any dilated veins over swelling.
Look for any scar over the anterior part of neck s/o any previous
thyroid surgery.
B] Palpation:
- Always palpate with patient’s head flexed
- Gland is palpated from behind by four fingers with thumb at nape
- Palpate for any swelling.
If present- note for

52
-Local/entire gland involved
- position
- size
- shape
- extent consistency
- mobile/fixed
- Palpate individual lobe-lahey’s method
- Place thumb on the thyroid &ask patient to swallow [rile’s
method] To palpate whether swelling moves with deglutition.
6) Other associate conditions: autoimmune conditions like
 Vitiligo
 Pernicious anaemia
 Addison’s disease
 Type 1 DM
 Alopecia areata
Differential Diagnosis
Differential diagnosis will depend on what symptom is
presenting with and accordingly the discussion will go on
pertaining to the evaluation of that particular symptom.
INVESTIGATIONS
1. Complete hemogram:
Low Hb- Anaemia usually normocytic anaemia
[Anaemia may be due to menorrhagia]
2. Serum electrolytes- Hyponatremia
3. Serum cholesterol- Total cholesterol usually> 250mg
-High triglycerides
4. ECG- Sinus Bradycardia
- Low voltage complexes [height of R waves in limb leads<5mm&
that of precordial leads<10mm]
- Non specific ST-T wave changes
5. Thyroid function test:
-TSH usually>20mu/1
CLINCAL SUSPICION OF HYPOTHYROIDISM
DETERMINE TSH & free T4
FreeT4 &TSH Free T4low FreeT4low FreeT4High

Normal TSH High TSH normal or low TSH high
Euthyroid Primary Secondary Thyroidhormone
Hypothyroidism Hypothyroidism resistance [defect

InTHBR]
53
NB: During early stages of hypothyroidism T$ &FT4 lie just below the normal
range. T3 is normal & TSH is barely elevated. This is sub clinical
hypothyroidism or failing thyroid syndrome.
Normal hyperthyroid Hyperthyroid
T$[ug/dl] 4.5-12.5 >12.5 <4.5
FT4[ng/dl 0.9-2.0 >2.0 <0.9
Ts[ng/dl] 80-220 >220 <80
TSH[uU/mml] 0.3-6.0 <0.3 >6.0
5. Demonstration of autoantibodies:
Antimicrosomal antibody for which Thyroid Peroxidase
antigen is positive in 80%cases of Hashimoto’s thyroiditis.
Antithyroglobuin antibodies positive in 60% cases of
Hashimoto’s thyroiditis.
6. Radio Iodine uptake scan: Decrease uptake of radio iodine.

7. FNAC and usage of thyroid: Evidence of inflammatory infiltrate &in
Hashimoto helps to differentiate a thyroid mass suspected of
Hashimoto’s& e/o Hurthle cells.
FNAC helps to differentiate a thyroid mass suspected of Hashimoto’s
from lymphoma.
8.Others:
- Increase in creatine kinase
- Increase in LDH
- Increase in AST
9.Chest X-Ray &ECHO
Increase in cardiac silhouette s/o pericardial effusion.
10. investigations for other associated endocrine disorders lide
addison’s disease etc.
TREATMENT
1. If there is no thyroid residual thyroid function the daily replacement
dose of levothyroxine is 1.6 ug/kg/body wt[100-150 ug/day]
2. If there is underlying autonomous function [eg: developing
hypothyroidism or after treatment of Grave’s disease] the dose will be
75-125ug/day
Special consideration:
A] In elderly patient> 60 years esp with CAD starting dose is 12,5-25
ug/day [angina may develop]
B] Adults under 60years without e/o CAD starting dose is
50-100ug/day.
C] In the pregnancy the dose may be increased >50% during
pregnancy & returned to previous levels after delivery.
D] There are no universally accepted guidelines for the management
of mild or subclinical hypothyroidism which is defined as biochemical
evidence of thyroid hormone deficiency in patients without any clinical
features/o hypothyroidism. In patients with subclinical or mild
54
hypothyroidism esp. if TSH> 6mu/L & TPO antibodies are increased
the starting dose will be 25-50 ug/day.
NB:
- The tablets to be taken in the morning in empty stomach with
water.
- Patient who miss doses can be advised to take up 3 doses of the
skipped doses at once because T4 has along life [7days]
FOLLOW-UP:
TSH response is gradual & should be measured about 2 months after
instituting the therapy. Adjustment of the dose is made in 12.5 or 25
ug increments if TSH is high
every 2-3 weeks.
NB: In patients with pituitary hypothyroidism replacement should be
made only after replacement of hydrocortisone has been initiated. [as it
may result in adrenal crisis]
MYXOEDEMA COMA:-
1. Levothyroxine- 500ug iv bolus followed by50-100 ug/day. [ It can
be given through NGT if iv preparation not available]
2. An alternative is to give Liothyronine [T3] in the dose of 10-15ug iv
Q8thor Q12th.
OR
3. Combination of L-thyroxine [200ug] & Liothyronine [25ug] single iv
bolus followed by daily treatment with levothyroxine 50-100ug/day &
T3 10 ug Q8th.
4. Inj. Hydrocortisone 500mg iv 6th or 8th hrly as there is concomitant
impairment of adrenal reserve.
SUPPORTIVE MEASURES:
1. External warming with space blankets if temprature,30dC
2. Precipitating factors should be corrected.
3. Hypertonic saline for hyponatremia.
4. iv glucose for hypoglycemia
5. Sedatives should be avoided if possible or sused in reduced doses.
6. Ventilatory support with regular ABG may be needed in the initial 48
hrs.
7. Medication should be continued lifelong.
8. If patients with a dose of> 200ug/ day & still elevated TSH, other
causes must be excluded. Eg. Malabsorption, estrogen therapy &
drugs that interfere with T4 absorption or clearance such as
cholestyramine, ferrous sulphate, calcium supplements, lovastain,
aluminium hydroxide, rifampicin, amiodarone, carbamazepine
phenyotin.
SURGICAL TREATMENT:-
Not indicated unless there is tracheo esophageal compression
or for cosmetic purpose. [Goitre]
55
NEONATAL SCREENING AND PREVENTION
Neonatal screening by measurement of TSH or T$ levels in heel prick
blood sample . when diagnosis is confirmed thyroid supplements are
given. Iodine supplements to prevent iodine deficiency.
REFERENCES:
1) Harissons principles of internal medicine 16 ed.
2) Current Medical Diagnosis And Treatment 2005:
Hypothyroidism pg no: 1098-1102.
3) Cecil text book of Internal Medicine 21st ed: The thyroid gland
pgno: 1231-1244.
4) Davidson’s Textbook of medicine.
5) S.Das: clinical methods in surgery.
6) Internet ref. www. Nejm.org
www . Emedicine.com
www. Medscape.com
56

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SPECIALITY : GENERAL MEDICINE

CASE : NEPHROTIC SYNDROME

Swelling of face, hands and legs

Infections- Peritonitis, Cellulitis and Sepis

If systemic causes of nephtric syndrome is present therapy should be

Extra Pyramidal disorders are

Associated with abnormalities in basal ganglia constituted by five

EXAMINATION OF A PATIENT WITH WITH OTHER EXTRA PYRAMIDAL

TREATMENT OF OTHER MOVEMENT DISORDERS

MUST BE COVERED POINTS IN RHEUMETOLOGICAL DISEASES

Pain is a cardinal symptom of rheumatic disease and should be enquired about

iii. Relieving and exacerbating factors

Stiffness is highly subjective and variable sensation of tightness and

The family history may be useful; a history of similar problems in other

Essential points in the history

* Stiffness morning- duration

Immobility stiffness and gelling

Patients should be asked specifically about sleep disturbance depression,

Tenderness, redness and warmth

Limitation of movement, deformity and instability

Limitation of a movement is a common symptom of joint disease. Older

Deformity of a joint may result from contracture of the capsule or

1. Look Position in which the joint is held

Extra-articular manifestations of common rheumatic diseases

Rash Systemic lupus erythematosus, rheumatic fever,

Erythema nodosum TB, drugs, streptococcoal sore throat, Behcets,

Other panniculitis Inflammatory bowel disease, SLE, Weber-Christian

Raynaud’s Progressive systemic scelrosis, polymyositis –

Sclerodactyly Progressive systemic sclerosis, CREST, overlap.

Leg ulcers Fetly’s syndrome, behcet’s systemic vasculitis,

Livedo reticularis SLE, polyarteritis nodosa

Hairloss SLE, drugs (cytotoxic) hupothyroidism

Ski pustules Gonococcaemia, Behcet’s

Heberden’s nodes Primary osteoarthritis

Bouchard’s nodes Primary osteoarthritis

Aptheous ulcers Behcet’s inflammatory bowel disease

Ulcers Reactive arthritis

Dry mouth Sjogren’s syndrome – primary, secondary

Iritis Spondylarthritis, Behcet’s

Dry eyes Sjogren’s syndrome

Summary of the Screening Examination of the Joints

2 With the patient sitting, examine

elbow- range of movement And swelling

wrist-range of movement and swelling

3. With the patient lying, examine

4. With the patient lying, examine

Spine- for abnormal contour and range of lumbar movement.

Rise in immunoglobulin levels is a nonspecific findings and hence is the

Other immunological tests

Non- Surgical Management

1. Open on arthroscopic synovectomy

What is the difference between the terms thyrotoxicosis and hyperthyroidism?

Points in the history

Points to be covered in clinical examinations

1. TSH, uncombined TSH, uncombined T3

Points in Differential Diagnosis

 Hemoglobin Alc (HbAlc or Alc) or glycosylated hemoglobin (GHb)

(C) L.glucosidace inhibitor

(A) Short Acting

(B) Intermediate acting