short cases for final year mbbs medical student in sri lanka
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Short cases for Final MBBS
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Dr Rasnayaka M MudiyanseDepartment of Paediatrics,
Faculty of Medicine,University of Peradeniya
Possible short cases
• Examine a system– CVS– RS– Abdomen
• Examine CNS– Lower limbs– Cranial nerves
• Examine a child
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• Development assessment• Evaluate growth• Examine
– Face– Leg– Limbs
• Observe walking
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CVS
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Examine CVSCommon cases
• VSD• Fallots tetrology• PDA• Complex heart diseases • PS• AS
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Objectives of Examining CVS
1. Recognize the anomaly ( structural or functional) 2. Size/extent of the structural anomaly3. Complications
1. Evidence of pulmonary hypertension 2. Cardiomegaly3. Evidence of heart failure4. Effect on growth and development
4. Associations 5. Cause of the CHD (etiology) 6. Evidence of interventions
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Recognize the anomaly ( structural or functional)
• Cyanotic heart disease– T– T– T– T– T– Critical pulmonary
stenosis – Complex heart disease– Shunt reversal
• Acyanotic Heart disease– ASD– VSD– PDA– PS– AS– Coarctation– Peripheral pulmonary
artery stenosis
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How to recognize the structural anomaly
• VSD – PSM +/- palpable thrill at lower left sternal edge
• Fallot’s tetralogy – Cyanotic heart disease– Ht Murmur over the pulmonary area– No cardiomegaly– P2 not loud – Oligaemic lung field
• PS– ESM murmur over the pulmonary area– Soft P2
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How to recognize the structural anomaly
• ASD– Split second sound ( fixed) – SM over the PA
• PDA– Machinery M or a long SM slightly lateral to PA– Radiate to back– Bounding pulse
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Complications
• Pulmonary hypertension• Cardiomegaly• Ventricular hypertrophy (R & L) • Heart failure• Failure to Thrive • Growth failure• Shunt reversal• Bacterial endocarditis • Embolic phenomena
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Evidence of Pulmonary Hypertension
• Loud P2• Palpable P2• Evidence of RVH
– Para sternal heave ( RVH)– ECG
• Prominent R in R chest leads• Deep S in L chest leads • RAD• Peaked P waves ( R Atrial hypertrophy)
• CXR – Peripherals pruning
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Evidence of Heart Failure
• Tachycardia• Gallop rhythm• Tachypnea• Cradiomegaly• Hepatomegaly• Rapid weight gain• Lung crepitations
• FTT• Edema • Sweating while
feeding• SOB on feeding
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Effect on Growth
• FTT– Current weight centile– Growth pattern
• Flattening• Crossing centile
• Growth failure – short stature - Chronic disease • Why do they get FTT
– Increased BMR due to sympathetic over activity– Difficulties in feeding and frequent vomiting – Recurrent chest infections– Associated conditions
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Cause of the CHD• Syndrome
– Downs– Turners/Noonas– Digeorge syndrome/ Velocardio facial syndrome – Others
• Associations– VACTARAL– CATCH– ..
• Congenital infections– Rubella– Toxoplasma
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Reason for Tachypnea? HF or RTI
• HF– Rapid shallow breathing– Not much effort of breathing– Fine crepitation ( not course) – Other evidence of HF
• RTI – Effort of breathing – recessions and noises – Fever– Corse creps
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Reason for FTT
• Feeding• Recurrent RTI• HF ( sympathetic over activity Increased BMR)
• Other
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Size and extend of the lesion
• Any complications suggest large lesion • Apical mid diastolic murmur in VSD or ASD
Intensity of the Heart murmur does not correlate with size of the lesion. Loud murmur does not
mean that the lesion is small or large
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Try to give a comprehensive diagnosis
• Large VSD or AV canal defect with pulmonary hypertension and failure to thrive in a child with trisomy 21, probably he has LRTI also.
• Complex cyanotic heart disease with growth failure probably has had an embolism in the brain.
• This syndromic child has tetrolgy of fallout seems to be uncomplicated. Growth and development seem satisfactory.
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What investigations
• ECG – Axis– Ventricular hypertrophy
• CXR• Echo• Catheterization• Angiography
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How do you manage
• Treat the acute problem• Plan for surgery• Attend to nutrition• Provide routine care • Follow up and monitoring• Social, economical and psychological support • Attend to dental caries
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Presentation of the case
1. This 3 year old boy with trisomy 21 has a large VSD complicated by pulmonary hypertension and heat failure. His growth seem inadequate and currently he has a chest infection.
2. This 8 year old girl has a cyanotic heart disease with evidence of cardiomegaly. Her P2 is loud, growth is inadequate. She has some dimorphic feature that does not fit in to a diagnosis.
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RS
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Examine the Respiratory SystemCommon cases
• Bronchial asthma• LRTI• Bronchiolitis • Pneumonia• Pleural effusion• Upper airway obstructions ( Croup, Congenital
laryngomalacia)
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Objectives
• What is the pathology/diagnosis• What is the severity• Acute or chronic • Associated problems
– FTT– CHD– Other
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What is the Pathology
• Upper air way – Stridor• Lower airway – inspection, palpation, percussion, auscultation
– Diffuse – Bilateral signs– Localized – Lobar pneumonia
• Pleural effusions• Pus or other effusions
• Systemic pathology
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What is the diagnosis
• Bronchiolitis– Infant or young child– Bilateral diffuse crepes +/- rhonchi– Hyperinflation– Look for associated CHD,FTT
• LRTI • Bronchial Asthma • Pneumonia• Pleural effusions
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Lobar Pneumonia or Pleural effusion
• Pleural effusion– Stony dull on percussion– Reduced breath sounds– Tracheal deviation to opposite side – Evidence of aspirations
• Lobar pneumonia– Dull on percussion– BB– No tracheal deviations
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What is the severity• Effort
– RR– Recessions– Accessory muscles– Noises – grunting, rhonchi, creps and striodr
• Efficacy– Chest expansion– Saturation
• Effects– CNS – drowsiness– CVS – Cyanosis/pallor
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How to recognize sever asthma
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How to recognize life threatening asthma
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Try to give a comprehensive diagnosis
• Moderately severe bronchiolitis in a child with failure to thrive.
• Bronchial asthma – with mild distress in a child with persistent asthma who has an eczema as well
• Pleural effusion with some respiratory distress probably a child recovering from DHF
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Investigations
• CXR – only when indicated• US scan – For effusions• FBC• CRP• Sputum
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How do you manage?
• Acute problem– Depends on severity
• Long term care
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Abdomen
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Examine the abdomenpossible cases
• Massive hepatospleenomegaly ( ? Thal)• Small hepatospleenomegaly• Only liver or spleen• Ascites• Renal lumps• Pelvic lumps
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Massive hepato-spleenomegaly• Transfusion dependent anemia
– Thalassemia – beta or E beta– Aplastic anemia– Heraditory spherocytosis– Dyserythropoitic anemia
• Gouaches disease• Osteopetrosis• .• .
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Massive hepato-spleenomegaly? Transfusion dependent anemia
• Objectives to achieve are to assess – Adequacy of blood transfusions– Type of chelation – Injection marks– Adequacy of chelation– ? Spleenectomy– Complications
• Cardiac• Endocrine• Hepatic• Other
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Adequacy of Blood Transfusion
• Inadequate blood transfusion result in – Growth failure – Bony deformities– Spleenomegaly or early spleenectomy
• Transfusion records will confirm it – Pre transfusion will be below Hb 9-10 gr/dl
frequently
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Chelation – Adequacy • Inadequate chelation is suggested by
– Pigmentations– Complications
• Cardiac• Growth• Pubertal delay• Diabetes Mellitus • Hypocalcaemia• Hypothyroidism
• Treatment history – dose and frequency and duration of infusion
• Serum ferritin level
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Complications of transfusion dependent anemia
• HF– Early heat failure may be asymptomatic– MRI t2*/Muga scan
• Short stature• FTT• Sexual maturity - Tanner stage• Diabetes mellitus• Phypoparathyroidism
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Reasons for Short Stature
• Chronic anaemia• Nutritional• Poor socioeconomic conditions • Endocrine – Growth, thyroid, adrenal, gonadal
hormone function • Recurrent infections• Chelaters• Zinc deficiency
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Reasons for jaundice in thalassemia patients
• Hemolysis• Liver involvement – iron toxicity or infections• Gallstones • Coinheritance of Gilberts
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What investigations
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How are going to manage
• Evaluate the current management• Find out the problems
– Blood transfusion– Chelation– Psychosocial problems– Complications
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Small liver +/- spleenBe able to demonstrate
• DD– Viral fever/IMN – Fever, skin rashes, palatal
hemorrhages – Hepatitis– Early hemolytic anaemia – Pallor, jaundice – Typhoid– Leukemia – pallor, pateche, LN, bone tenderness
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Spleen or Kidney
• Spleen – Has its shape and notch– Can not feel the upper border– Direction of enlargement is towrads RIF – No band of resonance over the lump – Lump is not balatoble
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Ascites
• What clinical features – Flank dullness– Shifting dullness – be able to demonstrate
• Causes – Nephrotic syndrome– CRF– Liver failure– Malnutrition
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Ascites – how to investigate
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Examine Lower Limb
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Examine lower limb Possible short cases
• Duchene muscular dystrophy• CP – Diplegia, hemiplegia, quadriplegia • Gullian barre• Rickets • Other deformities
Adequate exposure and get the child to walk
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Approach to ‘examination of lower limb’
• Functional of structural – inspection while walking
• If functional– UMN – hypertonia, clonus, hyper reflexia, up
going plantor– LMN- hypotonia, hypo-reflexia, fasciculation – Due to structural
• If structural – Bone, muscle or skin
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DMD
• Calf muscle hyper trophy • Demonstrate the weakness • Look for cardiac involvement
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Guillain-Barre
• Grade muscle power• Hypotonic• Areflaxia• No sensory level• Bladder not involved• Check upper limb• Check cranial nerves
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CP
• Grade the severity • Anatomical diagnosis
– Quadriplegic– Hemiplegic– Monoplagic– Ataxic– Chorio athetoid
• Complications• Associated problems • Cause
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Development delay
• Describe the best ability and least disability• Global or specific delay• The cause
– CNS – Peripheral nerves– Muscles– Other
• Complications – FTT, contractures, care …
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Objectives
• What is the diagnosis/ likely diagnoses • Impact on the child• Complications
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Examine a region
• Inspection• Palpation• Percussion• Auscultation • What is the
– anatomical diagnosis– Pathological diagnosis
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Child with Petechial Hemorrhages
• ITP• Leukemia• Aplastic anaemia • Thrombocytopenia
– Dengue
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Child with Echymosis
• Bleeding disorders• ITP• Leukemia• Aplastic anaemia • Thrombocytopenia
– Dengue
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Could this be ALL
• Ill looking • Bony tenderness• Pallor• Lymphadenopathy• Splenomegaly• FBC
– Abnormal cells
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New Born Baby
• Good bed side manners• Confirm normal – Wt, OFC, length• Head to toe examination (total examination)
– Hips– Spine– Perineum
• Detect minor anomalies
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Down syndrome
• Comment about mothers age• Establish it is downs syndrome• Assess
– Development & IQ (give a positive comment) – Growth– Cardiac involvement – Hypothyroidism– Evidence of gut surgery
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Place for chromosomal analysis
• Non dysjunction• Translocation
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Examine the Face
• Facial palsy• Cranial nerve palsy• Dysmorphic features
– Downs syndrome– Sturge weber– Other syndrome
• Don’t miss obvious micro/macro-cephaly
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Facial Palsy
• Observe all the clinical features• Is it upper motor or lower motor • Severity and complications• What is the cause
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Facial Palsy
• Observe all the clinical features– Absent or asymatrical naso-labial folds– Mouth Deviation– Closing eyes– Blowing the mouth– Drooling saliva – Bells sign
• Is it upper motor or lower motor – Upper motor – only the lower half is affected– Lower motor – both upper and lower half affected
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Facial Palsy
• Severity and complications– Exposure keratitis– Drooling of saliva– Depression
• What is the cause– Bells palsy– Ramsey-hunt – blisters in the external ear – Brain stem tumors
• Cerebeller signs• Other cranial nerves• Long tract signs
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Rickets
• Observe all the clinical features of rickets– Head – fontal bossing, cross bun appearance– Chest – rickety rosary, Harrison sulcus– Limbs – widening of wrists and ankle, bowing – General - hypotonia
• Anthropometric measurements• What is the cause
– Nutritional– Renal– Hypophospatemic
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Comment about the X ray
• Widening• Fraying• Splaying• Cupping• Osteopenia• Micro fractures
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Investigations for rickets
• Alkaline phosphate – Increase in all forms of rickets + some forms of metaphysial dysplasia)
• Serum calcium – low in hypocalceamic rickets ( but can be normal deu to PHT activity they will have increased aa in urine)
• Serum phosphate – Low in hypophosphatemicrickets ( increased 24 hr PO4 excretion)
• Renal functions – Renal rickets• Urinary aa and sugar – Fanconi associated rickets• Hypo K hyper Cl acidosis - RTA
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