Osce Sample: DR Bashir Bnyunus

OSCE SAMPLE
Dr Bashir BnYunus
Surgery Resident
AKTH
bbinyunus2002@gmail.com 1
Picture 1
Questions
 Describe and give differential diagnose

 Classify and treat if the swelling brilliantly
transilluminate and cannot be felt separate from the
testis
Answers
 Steps in describing an inguinoscrotal swelling

 Differential
 Hernia
 Hydrocele
 Other differentials;
 Lipoma of the cord
 Lymphangiectasis of the cord
 Varicocele
 Funiculitis
 Hydrocele
 Abnormal collection of fluid within the tunica vaginalis of
the testis.
 Classification as;
Communicating and non-communicating
Or
Congenital
acquired; primary or secondary
 Primary/idiopathic
 Congenital
 Infantile
 Funicular
 Encysted hydrocele of the cord
 Hydrocele of canal of nuck
 Vaginal hydrocele
 Secondary
 Trauma
 Inflammation- epididymoorchitis
 Lymphatic obstruction-filariasis
 Tumour
 Treatment
 Paeditrics ; herniotomy
 Adult; hydrocelectomy
Picture 2
Questions
 Describe the pathology

 What are the types
 What is the timetable of testicular descent
 What factor affect testicular descent
 How is it treated
 What are the complications
Answers
 Left undescended testes

 True undescended or retractile
 Timetable;
 3rd month intrauterine- iliac fossa
 7th month of fetal life- deep inguinal ring
 Later part of 7th month travels down the inguinal canal
 8th month IU- superficial ring
 9th month shortly before birth drop into the scrotum
 Right testis descends before left
Factors affecting descent
 Favours;
 Shorting of gubernaculum
 Differential body growth in relation to gubernaculum
 Raise intraabdoinal pressure
 Higher body temperature inside the abdomen
 Development and maturation of epididymis
 Hormones; hCG, testosterone and DHT
 Factors interfering
 Retroperitoneal adhesion
 Obstruction at the deep ring
 Short vas deferens
 Short testicular vessels
 Short pampiniform plexus
 Insufficient pull by the gubernaculum testis
 Deficient hormonal stimulation
 Prune belly
 External exposure to estrogen during the 1st trimester
 Treatment
 Orchidopexy ;before 2year
 Orchiectomy ;
 Atrophic testis
 Adolescence and adult ; risk of malignant transformation
 Intra-abdominal that cannot be brought down
 Complication
 Infertility
 Trauma/torsion/tomour
 Hernia
 inflammation
1. identify this pathology
2. how is it classify
3. mention two diagnostic clinical features in this
photo.
4. what could be two major problems if unrepaired?
5. what will you advise the parents against?
6. list three components of surgical repair.
1. hypospadias
2. Classify as; glandular, coronal, penile,
penoscrotal, scrotal, perineal.
3. ventral urethral meatus, hoody, chordee,median
grooving of the glans, spatulation of the glans
4. (a) body wetting during urination, (b)
psychological problems, (c) sexual problems, (d)
social stigmatization
5. advise against circumcision
6. (a) orthoplasty, (b) urethroplasty, (c)
glanduloplasty (d) meatoplasty, (e) scrotoplasy,
(f) skin cover
 Identify and give differentials
 How is it classified
 What are the complication
 What syndromes could be associated with it
 Capillary hemangioma
 Strawberry hemangioma
 Portwine stain(naevus flammeus)
 Salmon patch
 Hemangioma are classified as
 Capillary, cavernous or mixed
 Treatment
 Reassure and observe lesion regresses spontaneously (during
this period, cosmetic creams can be used to camoflage)
 Corticosteroids; intralesional triamsinolone or oral
prednisolone
 Sclerotherapy
 Embolization
 Laser therapy
 Surgical excision
 Radiotherapy
 Complications of hemangioma
 Atrophy of overlying skin
 Ulceration
 Haemorrhage
 Calcification
 Thrombosis
 Infection
 Recurrence
 Pressure effect especially in skeletal hemangioma;
osteoporosis or bony erosion
 Limb overgrowth
 Huge hemangioma can cause congestive cardiac failure
 Complications related to syndromes
 Syndromes associated with hemangioma;
 Kassabach Merritt syndrome; haemangioma assiociated with
thrombocytopenia
 Maffucci’s syndrome; haemangioma associated with
dyschondroplasia
 Von Hippel-Ladau syndrome; hemangioma of the face associated
with cerebellar hemangioma, glaucoma and pancreatic disease
 Sturge-Weber syndrome; hemangioma associated with ipsilateral
glaucoma, intracranial hemangioma and focal epilepsy
 Osler Rendu-Weber syndrome; hemangioma of GI, Urinary tract,
liver, spleen and brain
 Klippel Trenauny- Weber syndrome ; associated osteohypertrophy
of the extremities and AV fistula
 What is the common name of this lesion?
 What is the other name that it is also called that depicts its
pathogenesis?
 What is the pathogenesis?
 List two (2) other sites of occurrence, though less frequent
 Name a striking lesion, though infrequent, that may be associated
 List 2 diagnostic clinical signs of this lesion.
 List two (2) effective modalities of treatment.
 Complications
 Cystic hygroma
 Lymphangioma or hydrocele of the neck
 Types; capillary, cavernous lymphangioma and cystic hygroma
 Pathogenesis; benign proliferation of the lymphatic tissue that donot
communicates freely with the lymphatic system.
 Sites
 1. Posterior triangle of the neck—75%—most common site.
 Eventually may extend upwards in the neck
 2. Axilla—20%
 3. Cheek
 4. Tongue—lymphangiogenetic macroglossia
 5. Groin
 6. Mediastinum
 7. Often multiple sites
 May be associated with macroglosia
 Swelling is smooth, soft, fluctuant (cystic), not
compressible, brilliantly transilluminant. It is not
reducible completely.
 Treatment
 Sclerotherapy ; for recurrent lesion. Scelosant ;
bleomycin,sodium tetradecyl sulphate and glucose, Ok-432
 External beam radiation
 Complications ;
 Airway obstruction, infection, hemorrhage into cyst,
insinuation into major structures, obstructed labour
• Identify this abnormality
• How is it classified
• What is the aetio-pathology?
• List 2 clinical conditions that may be associated.
• List 3 complications of this condition.
• State the timing and type of a corrective operative
technique for this condition.
• State another specialist, apart from a plastic surgeon,
that should be involved in management of this boy
 Cleft lip
 Classification;
 Central cleft- rare
 Lateral cleft
 Unilateral or bilateral
 Complete(extend into the nostril) or incomplete
 Simple or compound(associated with cleft of alveolus)
 Complicated(associated with cleft palate) or uncomplicated
 Aetio-pathology
 Both genetic and environmental factor
 15% are familial through male sex-linked recessive gene
 Nutritional deficiency; Vit B, Vit A folic acid.
 Rubella infection
 Drugs; steroid, phenytoin,diazepam
 Anoxia
 Radiation
 Stress
 Advance maternal age
 Diabetic
 Consanguineous marriage
 In association with other syndrome;
 Cleft palate and VACTARL abnormality
 Complications of cleft lip;
 Cosmetically ugly
 Defective suction during breast feeding
 Dental irregularity
 Defective speech with particularly with labial letters ;
B,F,M,P,V,W
 Timing for corrective operation
 Millard rule of 10; child should fulfil
 ≥ 10weeks
 10lbs (4.6kg)
 Hb 10g
 So the operation is performed when the child is 2.5-
3month
 Patient’s nutrition is accepted for GA and operation
 Lips element are larger and repair is precise and easy
 Dropper feed is easier post operatively to facilitate
healing
 Operative technique
 Millard’s rotation advancement flap
 Tennison- Randall triangular flap
 Multidisiplinary ; plastic surgeon, orthodontist, paedo-
dentist, paediatrcian, speech therapist, ENT surgeons
 Identify the pathology
 Classify
 What are problems associated with it
 How is it corrected
 What is the optimum time for repair
 Cleft lip and palate
 Classification of cleft palate
Incomplete
 Bifida uvula
 Cleft of soft palate along its entire length
 Cleft of the whole length of the soft palate and the
posterior part of the hard palate.(intra-maxillary)
Complete
 Cleft soft palate and whole length of the had palate
 Problems associated with cleft palate;
 Defective suction
 Defective speech consonant like; B,D,K,P,T
 Defective smell
 Defective hearing and chronic otitis media
 Repeated respiratory tract infection
 Chances of aspiration bronchopneumonia
 Defective dentition because of irregular development of
alveolus
 Cosmetically ugly look particularly when associated with
cleft lip
 Treatment of cleft palate
 Von Langenbeck palatoplasty
 V-Y pushback palatoplasty
 Furlow
 Others
 The optimum time for repair
 14-18month ie before the child can speak (however
current trend 9month -1year because child start making
effort to produce understandable sounds )
 List there (3) differential diagnosis of this lesion
 What is the definitive diagnosis of these swellings that are soft (but not
cystic) and tender on examination ?
 What is the other name the condition is known as which is based on its
features?
 How is it classify
 Complications
 Differentials;
 Lipoma
 Neurofibroma
 Cystic swellings
 Dercum’s disease(adipose dolorosa) – multiple
neurolipomatosis
 Lipoma
 Classification of lipoma;
 Encapsulated or diffuse (in relation to capsule)
 Fibrolipoma, neavolipoma or neurolipoma (histological)
 Classification
 Solitary or multiple (number)
 Sessile or pednculated (shape)
 Anatomical
 Subcuteneous
 Sub-fascial
 Intermuscular
 Intramuscular
 Subperisteal
 Subsynovial
 Intra-articular
 Submucous
 Subserosal
 Subdural or extradural
 Complications of lipoma;
 Cosmetically urgly
 Necrosis due to repeated trauma
 Calcification
 Haemorrhage
 Infection
 Lipomatosis may cause huge enlarment and deformity
 Liposarcoma
 Myxomatous degeneration
 Ulceration
 What investigation is shown
 What are the indications
 How is it reported
 What are mammographic findings of malignancy
 Mammography
 Indications;
 Screening ; women >50year or >35years with risk factors
 Diagnostic mammography to evaluate existing feature of
breast disease
 Obese patient
 Whenever breast conservation is planned
 To rule out tumour in the contralateral breast
 Mammography guided biopsy
 Follow up of benign breast disease with malignant potential
 Follow up after conservative breast surgery
 mastalgia
 BIRADS- breast imaging reporting and data system
 Grade - features
 0- need for further imaging
 1- negative
 2- benign (repeat mammography in 1year)
 3- probably benign (mammography in 6month)
 4- suspicious as carcinoma (biopsy)
 5- highly suggestive of carcinoma(biopsy)
 6- known carcinoma
 Mammographic findings of malignancy;
 Microcalcification
 Branching calcification
 Spiculations
 Ductal distortion
 Mass effect
 Loss of symmetry
 Clustering
 Spot diagnosis
 How is pathology classified
 How would this patient be treated
Ans;
 Double-bubble sign- duodenal atresia
 Types of atresia;
 Type1-mucosal defect with continuity of the wall-20%
 Type 2- lumen atretic with fibrous cord btw proximal and distal lumen
 Type 3a – complete atresia with V shape mesenteric defect
 Type 3b- apple peel or chrismas tree deformity
 Type 4 – multiple atresia
 Adequate resuscitation
 N-G tube decompression
 Iv fluid, fluid and electrolyte correction
 Antibiotic prophylaxis
 Vit K prophylaxis
 Doudenoduodenostomy
a) What is the spot diagnosis
(b) State 3 other parts of the body that may

have this type of abnormality.
(c)List 4 Aetiologic/Risk factors that may

predispose to this condition.
(d)List 4 complications of this condition.
(e)List 2 surgical treatment options.
Answers
(a) Varicose veins

(b) Oesophageal varices; haemorrhoidal venous plexus;
pampiniform venous plexus,
(c) Occupation (Prolonged standing), congenital absence or
incompetence of valves, obstruction to venous return eg
intra abdominal tumour or pregnancy, recurrent
thrombophlebitis, A-V malformations, iliac vein thrombosis
(d) lipodermatosclerosis, venous ulcer, eczema and dermatitis,
haemorrhage; periostitis, ankylosis of joints,
thrombophlebitis, calcification, equinovarus deformity.
(e) Tredenlenberg operation, Venous stripping, Subfascial
ligation of Cocket and Dodd, Subfascial endoscopic
perforator ligation surgery, Endoluminal laser ablation
(a)What is the condition in this picture called?
(b)Mention 4 deformities present?
(c)What are the pathological lesions causing these
deformities ?
(d)Mention 2 congenital conditions that may be associated
with this condition.
(e)Mention 2 acquired causes of the condition.
(f)What are the treatment modalities
Answers
a)Congenital talipes equinovarus deformity
(
(b)-Fore foot adduction and supination (varus)

-Hind foot adduction and supination(inversion)
-Equinus deformity.
-High arched dorsal surface of the foot
-Plantar cavus
(c)-Dorsolateral subluxation of the navicular
-Medial displacement at the subtalar joint
-Soft tissue contractures
(d)-Congenital constriction band syndrome
-Spinal dysraphism
-Myelodylpasia
-Arthrogryposis
(e)-Post polio paralysis
-Cerebral palsy
TREATMENT OF TALIPIS
EQUINOVARUS
 Goals
 To correct early
 To correct fully
 To maintain in the corrected position until growth stops
 Timing
 Within 1st week of birth
 Non-operative
 Steps
 First correct the forefoot adduction
 Secondly correct the inversion
 Finally the equinus
 Operative treatment;
 Indications;
 when plateau have reach in non operative treatment
 Response not obtained after 6month
 Resistant cases declares themselves after 8-12weeks of serial
manipulation and strpping
 Relapsed cases
 Rigid club foot
 Late presentation after 6months of age
 Complementary to conservative treatment
 Treatment is soft tissue release on the medial side of the
foot and lenghting of tendoachillis
 How age roughly guide the choice of treatment;
 Less than 5years; soft tissue release(posterior medial).
Incisions; Cincinatti, Turco and Caroll
 More than 5years; requires bone releasing e.g dorso-
lateral wedge excision of the calcaneo cuboid joint(Evans
procedure). Osteotomy of the calcaneum to correct the
varus (Dwyer)
 More than 10years ; lateral wedge tarsectomy or triple
arthrodesis recommended after skeletal maturity
 Ilizarov method can be used as a primary procedure but is
normally reserved for recurrent CTEV
 Defined the above image
 Classify
 What are the indications
 Colostomy; an artificial colo-cutaneous fistula on the
anterior abdominal wall for the purpose of discharging
faeces and flatus.
 Types;
 According to duration
 Temporal
 Permanent
 According to anatomical location;
 Sigmoid colostomy
 Transverse colostomy
 Caecostomy
 Desending colostomy
 According to appearance;
 End colostomy
 Loop colostomy
 Double- barreled colostomy
 According to function
 Diverting or defuntioning
 Decompression colostomy
Indications for colostomy
Congenital malformations
 Anal atresia
 Hirschsprung’s disease
Neoplasm
 Colon carcinoma
 Rectal carcinoma
Inflammatory - intrinsic and extrinsic
 Chronic diverticular disease
 Crohn’s disease
 Lymphogranuoma venesum
 Radiation injury to colon
 Endometriosis of the colon or rectum
Colorectal Fistulas
 Colocutaneous
 Rectovaginal
 Vesicocolic
Trauma
 Large colonic injuries with faecal contamination
 Rectal injury
Surgical Operation
 Distal anastomosis (FAP)
 Low rectal excision
Miscellaneous
 Volvulus of sigmoid colon or caecum
 Severe or persistent colonic hypomotility
 Anal incontinence from repeated operation for
inflammatory perianal disease
 Paraplegia, extensive decubitus ulcer/severe burns or
infection of the perineum.
complications
 Immediates
 Bleeding
 Necrosis of distal end of stoma
 Electrolyte derangement
 Intermediate
 Retraction
 Prolapse
 Stenosis
 Intestinal obstruction
 Fistula
 Abscess
 Stricture
 Parastomal cellulitis- skin excoriation
 Intraperitoneal abscess
 Late
 Colostomy hernia
 Colostomy diarrhea
 Recurrence of malignancy
 Psychological trauma
 a)What is the function of this tube in this picture?
 (b)State 3 indications
 (c)State 4 complications/problems associated with the
use
 (d)State 2 contraindications to use of this tube
 Gastrostomy feeding tube
 Severe malnutrition, major surgeries, severe sepsis,
trauma, head and neck surgeries, oesophageal
obstruction. It is done if feeding is required for more
than one month.
 Leak-gastric fistula, displacement, blockage of tube,
tube migration, diarrhea, bloating, abdominal cramp,
wound infection.
 Previous gastric surgeries, intestinal obstruction, gastric
outlet obstruction.
Types of gastrostomy
 Base on technique;
 Stamm temporary gastrostomy
 Kader-Senn temporary gastrostomy
 Percutaneous endoscopic gastrostomy
 Janeway’s mucus lined permanent gastrostomy
 Base on duration;
 Temporal
 Permanent
 Base on lining;
 Mucus lined (permanent )
 Serosal lined (temporal)
 Give differential diagnosis
 What are the risk factors for breast ca
 Mention 2 syndromes associated with breast ca
 What are the pathological types
 What are the prognostic factors
 Differential diagnosis;
 Carcinoma of the breast
 Tuberculosis of the breast
 Traumatic fat necrosis
 Chronic breast abscess
 Risk factors for breast ca;
Very high risk;
 Therapeutic radiation
 Family history in two 1st degree relative
 Family history of breast and ovarian cancer
 BRAC 1 and BRAC 2 mutation carrier or first degree relatives
with mutation
 Moderate to high risk;
 Age > 60years
 History of DCIS,LCIS
 Cancer of the contralateral breast
 Slight to moderate risk
 Nulliparity
 Early menarchy, late menarchy
 HRT
 Obesity
 Alcohol
 Benign breast disease
 Syndromes associated with breast ca;
 Li Fraumeni syndrome
 Cowden’s syndrome
 Ataxia telangiectasia
 Pathological types
 Non invasive
 a) Ductalcarcinoma-in-situ
 b) Lobularcarcinoma-in-situ
Invasive
a) Invasive ductal carcinoma
b) Invasive ductal carcinoma with a predominant
intraductal componenl
c) Invasive lobular carcinoma
d} Mucinou scarcinoma
c) Medullary carcinoma
f) Papillary carcinoma
g) Tubular carcinoma
 h) Adenoid cystic carcinoma
 i) Secretory (juvenile) carcinoma
 j) Apocrine ca
 k) Carcinoma with metaplasia
 i) Squamous type
 ii) Spindle - cell type
 iii) Cartilaginous and osseous Iype
 iv) Mixed type
 l) Inflammatory carcinoma
 m) Others
 Prognostic factors
 I. Absence or presence of axillary node metastases.
 2 Presence or absence of systemic dissemination.
 3. Menstrual status of the patient.
 4. Biological propensity and grade of the tumour.
 5. Size of the tumour at the time of diagnosis.
 6. Hormone dependence.
PREDICTIVE FACTORS;
 these predicts the probability of a tumour to respond to
certain drugs
 ER, PR positive tumours have a good response to hormonal
manipulation.
 HER-2/neu overexpression. They do not respond to hormonal
manipulaton, are resistant to CMF and show partial resistance
to anthracyclines. However, they respond to trastuzumab
(herceptin)
 p53 mutation also shows resistance to anthracyclines but have
greater sensitivity to taxanes.
 Age below 35 years tend to have high grade tumours with poor
response to treatment.
 Identify
 Classify
 Aetiology
 What is thyroid storm and how is it managed
Ans
 Thyrotoxicosis
 Types
 Primary (graves disease)
 Secondary
 Aetiology;
 Auto- immune
 Genetic – autosomal dominant non-autoimmune hereditary
familial thyrotoxicosis
 Iodine induce – Jod Basedow thyrotoxicosis
 Treatment; 3 forms
 Antithyroid drug therapy
 Radioactive iodine
 Surgery
 Drud therapy;
 Indications;
 Children
 Adolescents
 Female patient who is reliable to take drugs and attend
follow up
 Impalpable thyroid
 Heart failure
 Recurrence after subtotal thyroidectomy
 Drugs
1. Carbimazole or metimazole 10-15mg tds. They prevent
binding of iodine to tyrosine and MIT and DIT to T3 and T4
2. Proply or methyl- thiouracil 100-200mg tds acts like
carbimazole
3. Sodium or potassium perchlorate 800mg daily. They prevent
trapping of iodine. Maintenance is 100-200mg daily
 Propranolol, a B- adrenergic blocker is added 40mg tds
to relieve palpitations
 Phenobarbitone or diazepam are give to reduce anxiety
 Symptoms improve in 7-14days and when patient
becomes euthyroid usually in 4weeks, the antithyroids
are reduce to maintenance for 12-18months and then
stopped. 50% of patients relapse in 1-6months.
 Drug toxicity;
 Skin rashes, arthralgia, agranulocytosis, and rarely
aplastic anaemia. Monthly white cell and red cell counts
are done and treatments stopped if leucopenia or sore
throat occurs.
 Radio- active iodine
 I¹³¹ taken up irradiates and destroys the thyroid gland.
 Patient should be made euthyroid before giving the
radioactive iodine since only 50% becomes euthyroid
 Not given below 45years for fear of malignancy later
and pregnant women
 Problems ;
 Ophthalmoplegia 15%
 Hypothyroidism 10% in one year and at 5years 40-50%
 Surgery;
 Subtotal thyroidectomy is performed after patient is made euthyroid
 Leaving about 4g (2g on each lobe), or 1/8 of the gland by visual estimation or
by comparative weighing of tissue remove and tissue left behind
 Complications;
 Early
 Respiratory obstruction; hemorrhage, bilateral abductor paralysis of the
vocal cord from damage of recurrent laryngeal nerve, tracheal collapse,
oedema from intubation
 Hypothyroidism
 Recurrent laryngeal nerve paralysis
 Thyrotoxic crisis
 Wound infection
 Late ; hypothyroidism, recurrence, keloid
 Thyroid storm (thyrotoxic crisis);
 Acute exacerbation of thyrotoxicosis and occurs in patient who is not
euthyroid at the time of operation.
 Occurs 6-24hours post surgery, patient is restless, maniacal with profuse
sweating, severe dehydration, circulatory collapse, hypotension,
hyperpyrexia(40°C), tarchycardia, hyperventilation, tremours, vomiting
and diarrhea.
 Treatment;
 Iv hydrocortisone
 Propranolol 20mg 6hourly
 Proplythiouracil via N-G tube
 Diazepam or phenobarbitone
 Lugol’s iodine
 IV fluids to correct dehydration
 Tepid sponging
 IV PCM
 Oxygen may also be given
 Identify
 What are the sites of predilection
 Types
 complications
 How does it differs from hypertrophic scar
 Keloid
 Genetic predisposition
 Preponderance in Africans
 Commoner in adolescence, highest incidence is btw 10-
30years
 Commoner in females
 Persons suffering from TB are more prone
 Most common site is the sternum
 Does not occur in palms or sole
 Area of predilection; sternum, earlobe, face, neck,
lower extremities, breast, chest, back and abdomen.
 Types
 Progressive(claw-like processes) and non-progressive
 Acquired and spontenous
 Complications
 Ulceration
 Infection
 Malignant transformation; fibrosarcoma
 Itching and tenderness
 Treatment ; very difficult
 Multimodality; occlusive dressing, compression therapy,
intralesional steroid injection, cryosurgery, excision,
radiotherapy and leser surgery
 Excision and radiotherapy
 Excision and triamcinolone injection
 Triple therapy; surgery, radiotherapy and triamcinolone
injection
 Compression therapy
 Recent involution; intralesional interferon, 5FU,
doxorubicine, bleomycin, verapamil,retinoic acid etc
DIFFERENCE BETWEEN KELOID AND HYPERTROPHIC SCAR
KELOID HYPRETROPHIC SCARS
Genetic predisposition yes no
Site of occurrence chest wall, upper arm anywhere in the body,

ears, lower neck common in flexure areas
Growth continues to grow without growth limits for 6 month

time limit, goes beyond scar limit to scar tissue only.
and extends to normal skin.
Treatment poor response good response to steroid
Recurrence very high uncommon
Collagen synthesis 20 times more than normal 6 times than normal skin
skin,(type III thick ) (type III fine collagen)
Age adolescence and middle children

age
Sex commoner in females equal in both sex
Race more in blacks (15 times) no racial relation
Structure Thick collagen with increased Fine collagen with

epidermal hyaluronic acid increased alpha actin
Size of injury no relation, small healed scar related to size of injury and
can form large keloid duration of healing.
 Identify and how is it prevented
 Complications;
 Keloid or hypertrophic scar
 Deformity and limitation of movement
 False ankylosis
 Marjolin’s ulcer
 Cosmetically ugly
 Treatment;
 Timing ; 6month -1year when scar has matured
 Contracture release and grafting
 Method of release; single or multiple Z-plasty at the point
of maximum tension
 Post burns contracture
 From full thickness burns
 Neglected Superficial burns which undergoes infection and
ulceration
 Prevention
 Proper treatment of superficial burns
 Adequate splintage of part in extension during healing
 Prevention of infection
 Early skin grafting
 Early physiotherapy
 Differential diagnosis
 What are the various types of malignant melanoma
 Which has the worst prognosis
 What are other site lesion could be found
 What features make a lesion suspicious
 How is it staged
 Treatment options
 Prognosis
 Malignant melanoma
 Squamous cell ca
 Basal cell ca
 Seborrhoeic keratosis
 Cuteneous agiomata
 Pyogenic granuloma
 Kaposi sarcoma
Types of malignant melanoma
 Superficial spreading (55%)

 Nodular (15-30%)
 Lentigo maligna(10%)
 Acral lentiginous (29-72% in blacks and 2-8% in
whites)
 The nodular melanoma has the worse prognosis, then

the acral lentigenous type. The lentigo maligna has the
best prognosis
 Common sites; skin, uveal coat of the eye, GI tract,
leptomeninges, perianal skin.
 Origin
 De novo 10%
 Pre-existing naevus 90%
 Signs of malignant changes in a benign naevus;
 Pain
 Itching
 Satellitism
 >6mm
 Deepening of pigmentation
 Crust formation
 Inflammatory changes
 ulceration
 Bleeding
 Irregularities of edges
 Lymph node metastesis
 Staging
 TNM – see text
 Treatment;
 Excision
 Excision + elective lymph node dissection (ELND)
 ELND is recommended only in patient with palpable or proven
lymphadenopathy
 Immunotherapy; cytokine and interferon as adjuvant

 New immune and gene therapies; vaccine and gene
therapy
 Melanoma are radio and chemo- resistant
Prognosis
 Clinical indicators
 Sex ; better in females
 Age ; better in younger < 60years
 Site; worse in scalp, feet, hands and trunk
 Pre-existing naevus ; better prognosis
 Skin colour ; non- white poorer prognosis
 Pathological indicators;
 Tumour thickness (Breslow’s level); < 0.7mm good,>1.5mm
likelihood to metastesis, >3.5mm greater tendency to met.
 Ulceration; poor prognosis
 Nodular, acral lentigenous and genital; unfavorable prognosis
 Clark’s level (invasion)
 Size of tumour; <2cm without spread good
 Type of melanoma; lentigo maligna good prognosis
Breslow’s classification (1970): Based on thickness of invasion
measured by optical micrometer—most important prognostic
indicator until nodal spread
 I: Less than 0.75 mm
 II: Between 0.76 to 1.5 mm
 III: 1.51 mm to 4 mm
 IV: more than 4 mm
Clark’s levels
 Level 1: Only in epidermis
 Level 2: Extension into papillary dermis
 Level 3: Filling of papillary dermis completely
 Level 4: Extension into reticular dermis
 Level 5: Extension into subcutaneous tissue
 Relation of Tumour Thickness to Nodal Spread—Based on
AJCC Classification
 Lesion Tumour thickness Nodal spread
 Thin < 1 mm < 10%
 Intermediate 1-4 mm 20-25%
 Thick > 4 mm 60%
 Defined
 Classify
 What are the causes
 What abnormalities may be associated with it
 How does OFC changes with age
 Excessive accumulation of cerebrospinal fluid (CSF) in the ventricles
and subarachnoid spaces due to disturbance in its formation, flow or
absorption
 Classification;
1. Communicating(non-obstructive) or non-communicating(obstructive)
2. Congenital or acquired
3. Hydrocephalus with increased ICP or Normal pressure Hydrocephalus
 Causes ;
 Increase CSF production; choroid plexus papilloma and choroid plexus
carcinoma
 CSF flow obstruction; aqueductal stenosis, brain lesion and tumour,
infections, intraventricular bleeds, Dandy Walker cyst
 Reduce CSF absorption; obstruction at the arachnoid granulations, otitic
hydrocephalus, sinus thrombosis, arachnoiditis
 Familial causes; Bicker’s Adam syndrome, an X-linked recessive
abnormality
Associated abnormalities
 Dandy-Walker syndrome
 Arnold-Chiari malformation
 Spina bifida
 Aqueductal stenosis
 Treatment;
 Medical; pre-operatively is commenced;
 Acetazolamide- a carbonic anhydrase inhibitor
 Furosemide- has synergistic action with acetazolamide
 Surgery
Shunting procedure ;
 Ventriculo-peritonel
 Ventriculo-pleural
 Ventriculo-atrial
 Lumboperitoneal
 Torchedsen shunt
 Hydrocephalus ex-vacuo
 Hydrancephaly
 Familial big head
 OFC- occipito-frontal circumference
 At birth average 35cm
 1st year it increase by 12cm to 47cm
 In the 1st 3months, increase by 2cm/month (gain of 6cm)
 In the next 3months increase by 1cm/month (gain of 3cm)
 In the last 6months increase by 0.5cm/month (gain of 3cm)
 What are the type
 Risk factors
 Prenatal diagnosis
 What problems may be associated with it
Types ;
 Spinal bifida occulta
 Spinal bifida aperta (cystica)
Risks factors;
 Pre-conception maternal folic acid deficiency
 Maternal exposure to excessive heat during time of fetal
embryogenesis
 Use of valproic acid (an anticonvulsant) during
pregnancy
 Previous birth of a child with NTD
 Maternal cocaine abuse
 Prenatal diagnosis;
 Maternal serum alpha-fetoprotein at 15-20weeks is more than
twice for that gestational age
 Prenatal ultrasound detects 90-95% of spinal bifida
 Amniotic fluid alpha-fetoprotein is very high
 Extreme maternal age
 Complicated pregnancies e.g toxemia, hydramnois,
malpresentations
 Associated anomalies
 Hydrocephalus
 Club foot
 Fecal incontinence
 Urine incontinence
 Treatment;
 Multidisiplinary
 Myelomeningocele excision and repair
 Serial manipulation of club foot
 Incontinence at an older age
 Complications of surgery
 Wound infection and meningitis
 CSF leak
 Hydrocephalus
 Nerve or spinal cord injury
(a)State 3 descriptive features of the bowel in this picture
(b) What is the likely diagnosis
(c) State 3 investigation necessary to confirm this diagnosis
(d) What surgery was being carried out
(e) State 2 complications of this surgery
(a)Megacolon, transition zone and collapsed bowel
segament
(b)Hirschsprung’s disease
(c)Unprepared Barium enema, rectal biopsy, anorectal
manometry
(d)Pull through surgery
(e)Rectal prolapsed/retraction, gangrene, bowel
perforation
PIX 4
(a)What is the spot diagnosis?
(b)State 2 differential diagnosis
(c)What is the embryologic origin of this condition?
(d)State 3 possible complications
(e)Classify this condition
(a)Sacrococcygeal teratoma
(b)Spinal bifida; Lipoma
(c)Primitive streak
(d)Infection, Ulceration, malignant transformation
(e) -Type I predominantly external with minimal presacral
component
-Type II external with a significant intrapelvic component
-Type III external with predominant pelvic mass with intra
abdominal extension
-Type IV entirely presacral without external or pelvic
extension
 Defined
 Classify
 Modalities of treatment
 Lymphoedema; is interstitial oedema of lymphatic origin

resulting in protein-rich fluid accumulation in the
interstitial compartment.
 Classification ;
 Primary
 Secondary
 Primary ; developmental defects of subcutaneous
lymphatic channels. There are 3 types;
 Lymphoedema congenital(10%) ; aplasia
 < 2year of age
 10-25% of all primary lymphedema
 When Sporadic or familial (Milroy's disease)
 More common in males
 Lower extremity is involved 2 times more frequently than the
upper extremity
 2/3 patients have bilateral lymphedema
 Lymphedema praecox (75%) : hypoplasia (reduced
number and caliber)
 Evident after birth and before age 35 years
 Most often arises during puberty
 65-80% of all primary lymphedema cases
 Females are affected 4 times
 70% of cases are unilateral, with the left lower extremity
being involved
 Lymphoedema tarda (15%);
 not evident until 35 years or older
 Rarest form of primary lymphedema
 Only 10-15% of cases
 Hyperplasic pattern, with tortuous lymphatics increased in
caliber and number
 Absent or incompetent valves
Secondary lymphedema;
 Trauma
 Surgery—inguinal block or axillary block dissection/postmastectomy
with axillary clearance
 Filarial lymphoedema due to Wuchereria bancrofti—common cause
in coastal region
 Tuberculosis
 Syphilis
 Fungal infection
 Advanced malignancy—hard, fixed lymph nodes in axilla orin
inguinal region
 Postradiotherapy lymphoedema
 Bacterial infection
 Rare causes: Rheumatoid arthritis, snake, and insect bite, DVT,
chronic venous insufficiency
Brunner’s grading
Treatment Modalities
 Conservative;
 Hygiene of affected limb
 Limb elevation
 Compression stockings once swelling is reduced
 Physiotherapy
 External pneumatic compression
 Surgery
Debulking operations ;
 Homan’s procedure
 Charlse procedure
 Sistrunk procedure
 Thompson’s procedure
 Bypass surgery
 Lymphaticovenous anastomosis
 Lymphaticolyphatic anastomosis
 Enteromesenteric bridges
 Omental bridges
 Skin and muscle flap
Identify and how is it treated
Polydactyly
Excision and wound closure
 Identify the lesion in this 24year man
 How is it classified
 What are the differential diagnosis if unilateral
 What are relevant investigation
 What are the modalities of treatment
 Gynaecomastia
 Grade;
 1- minor breast enlargement with no redundant skin
 2a- moderate breast enlargement with no redundant skin
 2b-moderate breast enlargement with redundant skin
 3- grossly enlarged breast
 Unilateral enlargement;
 Breast cancer
 Fibroadenoma
 Fibrocystic changes
 Phylloides tumour
 Investigations
 Hormonal assay; testosterone, estrogen, LH, FSH, prolactin,
TFT
 LFT
 Abdominal USS, testicular USS, CXR
 Biopsy; FNAC
 Treatment; over 80% regress spontenously ;
 If the cause found and treated
 Subcutenous mastectomy; via an infra-mammary incision or
endoscopic with small distant incision to prevent breast scar
 Danazol 200mg bd for 3month reduces breast in 50%
 Tamoxifen 20mg od cause complete regression in 80% of
middle aged
 List 3 differential diagnosis
 If the swelling moves with tongue protrusion how is it
treated
Differential diagnosis;
 Thyroglossal cyst
 Ectopic thyroid
 Pretracheal lymph node
 Dermoid cyst
 Solitary nodule of thyroid—isthmus
 Submental lymph node
 collar stud abscess
 Subhyoid bursa
Treatment of thyroglossal
cyst
Sistrunk operation:
 Excision of cyst and also full tract upto the foramen
caecum is done along with removal of central part of
the hyoid bone, as the tract passes through it.
 Identify
 What is the incidence
 How is the spectrum of the disease
Bladder extrophy (ectopia vesicae)
Incidence;1/10,000-50,000. M:F is 2:1
Other associated pathology; widely separated pubic rami,
externally rotated femora, epispadia. May be associated with
other genital, neuronal or anorectal anomalies,undescended
testes, inguinal hernia.
Cause of death; ascending pyelonephritis
200 time risks of carcinoma.-adenocarcinoma
Treatment
 Defect is repaired early to prevent metaplasia and

malignant changes
 Bladder is closed or augumented by ileum
 Bladder neck reconstruction
 Pubic rami is approximated
 Anterior abdominal wall closed
 At times, the bladder is excised and continent urinary
diversion done and later epispadia repair
 Spectrum
 Covered extrophy (only apical portion of the bladder is
involved the anterior abdominal wall muscle is intact)
 Epispedia
 Ectopia vesicae
 Cloacal extrophy
 Spot diagnosis
 What side is commoner and why
 Important signs
 How is it graded
 How are the types differentiated
 An important complication
 What are the modalities of treatment
 Varicocele; dilatation, elongation and tortusity of the
vein draining the testis (pampiniform venous plexus)
 Types;
 Primary or idiopathic
 Secondary
 Signs; bag of worm feel, cough impulse, disappears on
lying, reappears from bottom to top on standing, bow
sign.
 Grade; 1- are palpable only on valsava maneuver
2- palpable without any maneuver
3- visible to the exerminer’s eye
 Commoner on the left side because;
 Left spermatic vein drains into the left renal vein at rigth
angle
 Left testicular vein is longer
 Absent valve at the termination of left spermatic vein
 Left renal vein is crossed by and may be compressed by
left colon, may also be obstructed by left renal artery
 Metastatic renal tumour may cause obstruction of the vein
 Primary varicocele empties as the scrotum is elevated
when patient is lying while secondary does not.
 Complication
 Infertility
 Treatment
 Conservative
 Surgery
open
Open ligation of varicocele – scrotal, inguinal
approach(ivanissevitch procedure) and suprainguinal
extraperitoneal approach (Palomo approach)
Laparoscopic
embolisation
 Generalised neurofibromatosis or Von Recklinghausen’s
disease
 Neurofibroma; a benign tumour containing a mixture of
neural(ectodermal) and fibrous(mesodermal) element.
It arise not from the nerve proper but from
endoneurium which is a supporting connective nerve
tissue
 Types;
 Type 1 and type 2
 Type 1
 Autosomal dominant with defective gene on chromosome 17
 Diagnostic criteria; two or more of;
 six or more cafe-au -lait > 5mm in diameter if prepubertal
individuals and> 15mm in postpubertal individuals,
 Two or more neurofibroma or one plexiform neurofibroma,
 freckles in the axilla or groin,
 optic glioma,
 Two or more iris hamartomas,
 a distinctive osseous lesion such as sphenoid dysplasia or
thing of long bone cortex with or without pseudoarthrosis ,
 A first degree relative with NF-l.
 Complications of type 1;
 Hypertension (6%). Due to renal artey stenosis
 scoliosis, bowing of the legs, impaired vision, ptosis,
optic atrophy, language or learning disorders , mental
retardation, precocious puberty or hypogonadism, GI
hemorrhage,
 Malignancy(5%)
 Type 2
 Autosomal dominant with defect on chromosome 22
 Diagnostic criteria are;
 Bilateral 8th nerve masses seen with appropriate
imaging techniques (e.g. CT, MRl) or One 8th nerve mass
With two of the following: neurofibroma, meningioma.,
glioma, Schwannomas or posterior lenticular opacity.
 Complications;
 hearing loss. tinnitus, dizziness, loss of balance,
headaches, fits.
 There may be a first-degree relative with NF-2.
treatment
 All patients must be reviewed yearly .
 Surgery is employed only when there is severe cosmetic
deformity , increase in. size, Evidence of malignant
change, functional disturbance or pain
 A progressive 8th nerve tumour that causes tinnitus or
vertigo is removed while bilateral hearing remains.
 Any signs of epilepsy should be investigated and
responsible tumours removed.
 Genetic counselling should also be given
 If histology shows cell-nest,
 what is the likely diagnosis
 what are likely pre-existing skin lesions
 Risk factors
 What are the modalities of treatments
 Differentials;
 Squamous cell carcinoma
 Basal cell carcinoma
 Keratoacantoma
 Amelanotic melanoma
 Nest cells is characteristic of squamous cell ca
 Pre-existing lesions;
 Senile(or solar) keratosis
 Bowen’s disease- erythroplasia of Queyrat
 Leukoplekia
 Lupus vulgaris
 Xeroderma pigmentosis
 Radiodermatitis
 Chronic ulcer
 Chronic skin irritation; ‘chimney sweep ca’- scrotal, kangri ca of
Kashmir, etc
 Types;
 Proliferative or cauliflower
 Ulcerative - common
 Risk factors;
 UV light exposure
 Ionizing radiation
 Immunosuppression
 Chronic inflammation
 Arsenic exposure
 Inherited disorders; albinism, xerodma pigmentosis
 Smoking
 Treatment options;
 Radiotherapy
 Topical treatment(5-FU, phytodynamic therapy)
 Electrosurgery (curettage and electrodessication)
 Cryotherapy
 Moh’s surgery
 Identify
 What are radiological findings in infantile blount’s
disease and angles of radiological importance
 Treatment
 Genu varum
Differential diagnosis;
 Physiologic genu varum
 Pathologic conditions
 Metabolic bone disease – rickets, hypophosphatemia
 Asymmetrical bone arrest or retardation- blount disease,
trauma near the growth epiphysis of femur, osteomyelitis,
tumour affecting the lower end of femur and upper tibia.
 Bone dysplasia; metaphysical chrondrodysplasia
 Congenital; deficient tibia relative to long fibula
 Neuromuscular; in adult, degenerative
disorders(osteoarthritis of the knee) and paget’s disease are
important causes.
 AP and lateral Xray ;
 Flattening or disappearance of the medial aspect of the
epiphysis and apparent increase in the height of the
lateral aspect of the epiphyseal plate
 Breaking of the proximal medial tibial metaphysis
 Fragmentation with a protuberant step deformity
 Angles of radiological importance;
 Metaphysial- diaphyseal angle
 Tibiofemoral angle
 Metaphyseal- epiphyseal angle
 Metaphyseal-diaphyseal angle is important in
differentiating Blount’s disease from physiological
bowing in a child less than 2years
 MDA< 11° normalphysiologic bowing
 MDA 11-15° equivocal
 MDA> 15° blount disease
Treatment
Non-surgical;
 Observation and trial of bracing (2-5years)
Surgical
 Corrective osteotomy aiming at 6-10° of valgus
 Others;
 Hemiepiphysiodesis
 Asymmetric physeal extraction
 External fixation with distraction osteogenesis
 Identify
 What are the causes
 Treatment
Genu valgum (knock knee)
Causes;
 Idiopathic
 Bone softening; rickets, osteomalecia, paget disease
 Laxity of ligament; medial collateral ligament
 Trauma; lateral tibial condyle
 Ostheoathritis
 Muscle weakness
NB; intermalleola distance > 10cm
Treatment
Non-operative
 Idopathic- ignored <7years
 Raising inner side of the heel by 3-4mm
 Using splint
Operative;
 For > 10years
 Risk factor corrected
 Stapling innerside of epiphysis to stop growing
 Supracondylar osteotomy, after growth is completed
 State two (2) differential diagnoses.
 Give one major reason why Burkitt’s tumour is not a
likely differential diagnosis of this particular lesion.
 State (a) types of Surgical treatment that may be
offered and (b) for which types of cases?
 List two major complications that may follow surgical
treatment in this specific case.
 Differentials
 1. Benign Parotid tumour
 a. Pleomorphic adenoma (mixed parotid tumour) – 60%
 b. Monomorphic adenoma (Adenolymphoma - Warthin's Tumour) – 10%
 2. Malignant Parotid tumour
 a. Mucoepidermoid tumour )
 b.Acinic cell tumour ) – 4%
 c. Adenoid cystic carcinoma )
 Investigations
 1. FNAC helps to diagnose most cases of malignancies but it is not always reliable. Frozen section also
gives some false-positive results.
 2. CT is the most accurate investigation. It helps to determine the local and regional extent of the disease.
 Treatment
 Superficial/total Parotidectomy
 1. Benign mixed tumors arising in the lateral lobe. Wide excision to prevent recurrence.
 a. Identify the facial nerve and branches
 b. Facial nerve may be excised if involved in malignancy
 c. Medial lobe involvement may require a total parotidectomy
 BARAKALLAHU FI
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Osce Sample: DR Bashir Bnyunus

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OSCE SAMPLE

 Describe and give differential diagnose

 Steps in describing an inguinoscrotal swelling

 Describe the pathology

 Left undescended testes

(b) State 3 other parts of the body that may

(c)List 4 Aetiologic/Risk factors that may

(d)List 4 complications of this condition.

(e)List 2 surgical treatment options.

(a) Varicose veins

(b)-Fore foot adduction and supination (varus)

KELOID HYPRETROPHIC SCARS

Genetic predisposition yes no

Site of occurrence chest wall, upper arm anywhere in the body,

Growth continues to grow without growth limits for 6 month

Treatment poor response good response to steroid

Recurrence very high uncommon

Age adolescence and middle children

Sex commoner in females equal in both sex

Race more in blacks (15 times) no racial relation

Structure Thick collagen with increased Fine collagen with

 Superficial spreading (55%)

 The nodular melanoma has the worse prognosis, then

 Immunotherapy; cytokine and interferon as adjuvant

 Lymphoedema; is interstitial oedema of lymphatic origin

 Defect is repaired early to prevent metaplasia and

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