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OSCE SAMPLE Dr Bashir BnYunus Surgery Resident
AKTH
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1
Picture 1
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Questions
Describe and give differential diagnose
Classify and treat if the swelling brilliantly transilluminate and cannot be felt separate from the testis
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Answers
Steps in describing an inguinoscrotal swelling
Differential
Hernia
Hydrocele
Other differentials;
Lipoma of the cord
Lymphangiectasis of the cord
Varicocele
Funiculitis
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Hydrocele
Abnormal collection of fluid within the tunica vaginalis of the testis.
Classification as; Communicating and non-communicating Or Congenital acquired; primary or secondary
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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
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Treatment
Paeditrics ; herniotomy
Adult; hydrocelectomy
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Picture 2
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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
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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
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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
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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
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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
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1. 2. 3. 4. 5. 6.
identify this pathology how is it classify mention two diagnostic clinical features in this photo. what could be two major problems if unrepaired? what will you advise the parents against? list three components of surgical repair.
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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
(a) orthoplasty, (b) urethroplasty, (c) glanduloplasty (d) meatoplasty, (e) scrotoplasy, [email protected] (f) skin cover 6.
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Identify and give differentials
How is it classified
How is it treated
What are the complication
What syndromes could be associated with it
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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
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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
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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
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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 [email protected]
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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
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May be associated with macroglosia
Swelling is smooth, soft, fluctuant (cystic), not compressible, brilliantly transilluminant. It is not reducible completely.
Treatment
Surgical excision
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
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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 • • • • • •
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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
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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;
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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
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So the operation is performed when the child is 2.53month
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, paedodentist, paediatrcian, speech therapist, ENT surgeons
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Identify the pathology
Classify
What are problems associated with it
How is it corrected
What is the optimum time for repair
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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
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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
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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 )
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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
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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)
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Classification
Solitary or multiple (number)
Sessile or pednculated (shape)
Anatomical
Subcuteneous
Sub-fascial
Intermuscular
Intramuscular
Subperisteal
Subsynovial
Intra-articular
Submucous
Subserosal
Subdural or extradural
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Complications of lipoma;
Cosmetically urgly
Necrosis due to repeated trauma
Calcification
Haemorrhage
Infection
Lipomatosis may cause huge enlarment and deformity
Liposarcoma
Myxomatous degeneration
Ulceration
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What investigation is shown
What are the indications
How is it reported
What are mammographic findings of malignancy
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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
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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
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Mammographic findings of malignancy;
Microcalcification
Branching calcification
Spiculations
Ductal distortion
Mass effect
Loss of symmetry
Clustering
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Spot diagnosis
How is pathology classified
How would this patient be treated
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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
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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.
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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
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(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
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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
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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
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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
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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 dorsolateral 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
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Defined the above image
Classify
What are the indications
What are the complications
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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
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According to appearance;
End colostomy
Loop colostomy
Double- barreled colostomy
According to function
Diverting or defuntioning
Decompression colostomy
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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
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Colorectal Fistulas
Colocutaneous
Rectovaginal
Vesicocolic
Trauma
Large colonic injuries with faecal contamination
Rectal injury
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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.
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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
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Late
Colostomy hernia
Colostomy diarrhea
Recurrence of malignancy
Psychological trauma
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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
What are the types
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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.
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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)
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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
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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
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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
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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
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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
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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
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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.
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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.
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Identify
Classify
Aetiology
How is it treated
What is thyroid storm and how is it managed
Ans
Thyrotoxicosis
Types
Primary (graves disease)
Secondary
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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
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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
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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
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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.
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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%
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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
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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
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Identify
What are the sites of predilection
Types
complications
How is it treated
How does it differs from hypertrophic scar
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Keloid
Genetic predisposition
Preponderance in Africans
Commoner in adolescence, highest incidence is btw 1030years
Commoner in females
Persons suffering from TB are more prone
Most common site is the sternum
Does not occur in palms or sole
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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
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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
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DIFFERENCE BETWEEN KELOID AND HYPERTROPHIC SCAR KELOID
HYPRETROPHIC SCARS
Genetic predisposition
yes
no
Site of occurrence
chest wall, upper arm ears, lower neck
anywhere in the body, common in flexure areas
Growth
continues to grow without time limit, goes beyond scar and extends to normal skin.
growth limits for 6 month limit to scar tissue only.
Treatment
poor response
good response to steroid
Recurrence
very high
uncommon
Collagen synthesis
20 times more than normal skin,(type III thick )
6 times than normal skin (type III fine collagen)
Age
adolescence and middle age
children
Sex
commoner in females
equal in both sex
Race
more in blacks (15 times)
no racial relation
Structure
Thick collagen with increased epidermal hyaluronic acid
Fine collagen with increased alpha actin
Size of injury
no relation, small healed scar can form large keloid
related to size of injury and duration of healing.
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Identify and how is it prevented
What are the complications
How is it treated
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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
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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
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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
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Differential diagnosis;
Malignant melanoma
Squamous cell ca
Basal cell ca
Seborrhoeic keratosis
Cuteneous agiomata
Pyogenic granuloma
Kaposi sarcoma
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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.
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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
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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
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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
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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
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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
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Relation of Tumour Thickness to Nodal Spread—Based on AJCC Classification
Lesion
Thin
< 1 mm
< 10%
Intermediate
1-4 mm
20-25%
Thick
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Tumour thickness
> 4 mm
Nodal spread
60%
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Defined
Classify
What are the causes
What abnormalities may be associated with it
How is it treated
Differential diagnosis
How does OFC changes with age
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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
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Associated abnormalities
Dandy-Walker syndrome
Arnold-Chiari malformation
Spina bifida
Aqueductal stenosis
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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
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Differential diagnosis;
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)
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What are the type
Risk factors
Prenatal diagnosis
What problems may be associated with it
How is it treated
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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
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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
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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
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(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
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(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
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PIX 4
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(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
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(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 [email protected]
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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
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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
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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
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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
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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
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Brunner’s grading
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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
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Bypass surgery
Lymphaticovenous anastomosis
Lymphaticolyphatic anastomosis
Enteromesenteric bridges
Omental bridges
Skin and muscle flap
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Identify and how is it treated
Polydactyly Excision and wound closure
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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
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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
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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
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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
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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.
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Identify
What is the incidence
How is the spectrum of the disease
How is it treated
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 [email protected]
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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
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Spectrum
Covered extrophy (only apical portion of the bladder is involved the anterior abdominal wall muscle is intact)
Epispedia
Ectopia vesicae
Cloacal extrophy
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Spot diagnosis
What are the types
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
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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
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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.
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Complication
Infertility
Treatment
Conservative
Surgery
open Open ligation of varicocele – scrotal, inguinal approach(ivanissevitch procedure) and suprainguinal extraperitoneal approach (Palomo approach) Laparoscopic
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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
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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.
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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%)
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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.
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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
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Differential diagnosis
If histology shows cell-nest,
what is the likely diagnosis what are likely pre-existing skin lesions
What are the types
Risk factors
What are the modalities of treatments
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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
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Types;
Proliferative or cauliflower
Ulcerative - common
Risk factors;
UV light exposure
Ionizing radiation
Immunosuppression
Chronic inflammation
Arsenic exposure
Inherited disorders; albinism, xerodma pigmentosis
Smoking
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Treatment options;
Surgical excision
Radiotherapy
Topical treatment(5-FU, phytodynamic therapy)
Electrosurgery (curettage and electrodessication)
Cryotherapy
Moh’s surgery
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Identify
Differential diagnosis
What are radiological findings in infantile blount’s disease and angles of radiological importance
Treatment
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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.
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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
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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
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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
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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 [email protected]
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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
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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.
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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
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BARAKALLAHU FI
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Test questions
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AKTH
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Picture 1
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Questions
Describe and give differential diagnose
Classify and treat if the swelling brilliantly transilluminate and cannot be felt separate from the testis
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Answers
Steps in describing an inguinoscrotal swelling
Differential
Hernia
Hydrocele
Other differentials;
Lipoma of the cord
Lymphangiectasis of the cord
Varicocele
Funiculitis
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Hydrocele
Abnormal collection of fluid within the tunica vaginalis of the testis.
Classification as; Communicating and non-communicating Or Congenital acquired; primary or secondary
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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
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Treatment
Paeditrics ; herniotomy
Adult; hydrocelectomy
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Picture 2
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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
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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
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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
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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
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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
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1. 2. 3. 4. 5. 6.
identify this pathology how is it classify mention two diagnostic clinical features in this photo. what could be two major problems if unrepaired? what will you advise the parents against? list three components of surgical repair.
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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
(a) orthoplasty, (b) urethroplasty, (c) glanduloplasty (d) meatoplasty, (e) scrotoplasy, [email protected] (f) skin cover 6.
16
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Identify and give differentials
How is it classified
How is it treated
What are the complication
What syndromes could be associated with it
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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
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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
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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
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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 [email protected]
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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
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May be associated with macroglosia
Swelling is smooth, soft, fluctuant (cystic), not compressible, brilliantly transilluminant. It is not reducible completely.
Treatment
Surgical excision
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
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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 • • • • • •
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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
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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;
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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
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So the operation is performed when the child is 2.53month
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, paedodentist, paediatrcian, speech therapist, ENT surgeons
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Identify the pathology
Classify
What are problems associated with it
How is it corrected
What is the optimum time for repair
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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
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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
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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 )
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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
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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)
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Classification
Solitary or multiple (number)
Sessile or pednculated (shape)
Anatomical
Subcuteneous
Sub-fascial
Intermuscular
Intramuscular
Subperisteal
Subsynovial
Intra-articular
Submucous
Subserosal
Subdural or extradural
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Complications of lipoma;
Cosmetically urgly
Necrosis due to repeated trauma
Calcification
Haemorrhage
Infection
Lipomatosis may cause huge enlarment and deformity
Liposarcoma
Myxomatous degeneration
Ulceration
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What investigation is shown
What are the indications
How is it reported
What are mammographic findings of malignancy
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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
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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
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Mammographic findings of malignancy;
Microcalcification
Branching calcification
Spiculations
Ductal distortion
Mass effect
Loss of symmetry
Clustering
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Spot diagnosis
How is pathology classified
How would this patient be treated
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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
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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.
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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
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(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
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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
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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
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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
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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 dorsolateral 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
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Defined the above image
Classify
What are the indications
What are the complications
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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
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According to appearance;
End colostomy
Loop colostomy
Double- barreled colostomy
According to function
Diverting or defuntioning
Decompression colostomy
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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
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Colorectal Fistulas
Colocutaneous
Rectovaginal
Vesicocolic
Trauma
Large colonic injuries with faecal contamination
Rectal injury
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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.
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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
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Late
Colostomy hernia
Colostomy diarrhea
Recurrence of malignancy
Psychological trauma
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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
What are the types
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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.
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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)
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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
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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
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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
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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
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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
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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
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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.
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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.
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Identify
Classify
Aetiology
How is it treated
What is thyroid storm and how is it managed
Ans
Thyrotoxicosis
Types
Primary (graves disease)
Secondary
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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
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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
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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
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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.
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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%
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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
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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
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Identify
What are the sites of predilection
Types
complications
How is it treated
How does it differs from hypertrophic scar
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Keloid
Genetic predisposition
Preponderance in Africans
Commoner in adolescence, highest incidence is btw 1030years
Commoner in females
Persons suffering from TB are more prone
Most common site is the sternum
Does not occur in palms or sole
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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
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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
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DIFFERENCE BETWEEN KELOID AND HYPERTROPHIC SCAR KELOID
HYPRETROPHIC SCARS
Genetic predisposition
yes
no
Site of occurrence
chest wall, upper arm ears, lower neck
anywhere in the body, common in flexure areas
Growth
continues to grow without time limit, goes beyond scar and extends to normal skin.
growth limits for 6 month limit to scar tissue only.
Treatment
poor response
good response to steroid
Recurrence
very high
uncommon
Collagen synthesis
20 times more than normal skin,(type III thick )
6 times than normal skin (type III fine collagen)
Age
adolescence and middle age
children
Sex
commoner in females
equal in both sex
Race
more in blacks (15 times)
no racial relation
Structure
Thick collagen with increased epidermal hyaluronic acid
Fine collagen with increased alpha actin
Size of injury
no relation, small healed scar can form large keloid
related to size of injury and duration of healing.
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Identify and how is it prevented
What are the complications
How is it treated
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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
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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
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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
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Differential diagnosis;
Malignant melanoma
Squamous cell ca
Basal cell ca
Seborrhoeic keratosis
Cuteneous agiomata
Pyogenic granuloma
Kaposi sarcoma
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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.
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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
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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
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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
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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
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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
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Relation of Tumour Thickness to Nodal Spread—Based on AJCC Classification
Lesion
Thin
< 1 mm
< 10%
Intermediate
1-4 mm
20-25%
Thick
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Tumour thickness
> 4 mm
Nodal spread
60%
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Defined
Classify
What are the causes
What abnormalities may be associated with it
How is it treated
Differential diagnosis
How does OFC changes with age
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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
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Associated abnormalities
Dandy-Walker syndrome
Arnold-Chiari malformation
Spina bifida
Aqueductal stenosis
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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
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Differential diagnosis;
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)
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What are the type
Risk factors
Prenatal diagnosis
What problems may be associated with it
How is it treated
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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
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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
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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
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(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
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(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
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PIX 4
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(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
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(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 [email protected]
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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
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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
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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
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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
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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
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Brunner’s grading
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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
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Bypass surgery
Lymphaticovenous anastomosis
Lymphaticolyphatic anastomosis
Enteromesenteric bridges
Omental bridges
Skin and muscle flap
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Identify and how is it treated
Polydactyly Excision and wound closure
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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
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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
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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
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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
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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.
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Identify
What is the incidence
How is the spectrum of the disease
How is it treated
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 [email protected]
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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
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Spectrum
Covered extrophy (only apical portion of the bladder is involved the anterior abdominal wall muscle is intact)
Epispedia
Ectopia vesicae
Cloacal extrophy
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Spot diagnosis
What are the types
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
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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
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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.
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Complication
Infertility
Treatment
Conservative
Surgery
open Open ligation of varicocele – scrotal, inguinal approach(ivanissevitch procedure) and suprainguinal extraperitoneal approach (Palomo approach) Laparoscopic
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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
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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.
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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%)
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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.
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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
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Differential diagnosis
If histology shows cell-nest,
what is the likely diagnosis what are likely pre-existing skin lesions
What are the types
Risk factors
What are the modalities of treatments
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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
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Types;
Proliferative or cauliflower
Ulcerative - common
Risk factors;
UV light exposure
Ionizing radiation
Immunosuppression
Chronic inflammation
Arsenic exposure
Inherited disorders; albinism, xerodma pigmentosis
Smoking
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Treatment options;
Surgical excision
Radiotherapy
Topical treatment(5-FU, phytodynamic therapy)
Electrosurgery (curettage and electrodessication)
Cryotherapy
Moh’s surgery
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Identify
Differential diagnosis
What are radiological findings in infantile blount’s disease and angles of radiological importance
Treatment
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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.
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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
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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
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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
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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 [email protected]
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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
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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.
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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
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BARAKALLAHU FI
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Test questions
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