Latihan membawa ke arah kesempurnaan

1. PRACTICE MAKES PERFECT Pom – Jin – FYK – MHR - Crabball

2. Neurofibromatosis Café au Lait spot Discrete, well-circumscribed uniformly brown lesions with irregular border 2 - 20 mm Isolated lesions occur in 10 - 20% of population; 98% of normal individuals have less than three lesions

3. Café au Lait spot cafe-au-lait spots: are not necessarily a diagnostic sign of NF Multiple lesions occur in a variety of syndromes:

4. Neurofibromatosis NF1 and NF2 are autosomal dominant, with approximately 50% of cases having no family history NF1 is also called von Recklinghausen disease NF2 is also called bilateral acoustic neurofibromatosis

5. Neurofibromatosis ETIOLOGY NF1 is caused by DNA mutations located on the long arm of chromosome 17 responsible for encoding the protein neurofibromin. NF2 is caused by DNA mutations located in the middle of the long arm of chromosome 22 responsible for encoding the protein merlin.

6. Neurofibromatosis EPIDEMIOLOGY & DEMOGRAPHICS NF1 is the most common neurocutaneous syndrome, affecting approximately 1/3000 persons NF2 occurs in about 1/50,000 Equally affects males and females.

7. Neurofibromatosis PHYSICAL FINDINGS & CLINICAL PRESENTATION Common features of NF1 include: Café-au-lait macules (100% of children by age 2) Hyperpigmented skin lesions occurring anywhere on the body except the face, palms, and soles Appear early in life and increase in size and number during puberty Focal or diffuse Axillary and inguinal freckling (70%) Multiple cutaneous and subcutaneous neurofibromas (95%) Firm, varying in size from mm to cm Vary in number from a few to thousands May be sessile, pedunculated, regular or irregular in shape Lisch nodule (small hamartoma of the iris) found in >90% of adult cases Visual defects possibly related to optic gliomas (2% to 5%) Neurodevelopment problems (30% to 40%) Common features of NF2 include: Hearing loss and tinnitus related to bilateral acoustic neuromas (>90% of adults) Cataracts (81%) Headache Unsteady gait Cutaneous neurofibromas but less than NF1 Café-au-lait macules (1%)

8. Neurofibromatosis Axillary freckles Small (0.5cm) brown, well-circumscribed macules Generally go unnoticed High correlation with neurofibromatosis when six or more freckles are present in the axilla

9. Neurofibromatosis Lisch Nodules a pigmented hamartomatous nevus (a type of benign tumor) affecting the iris

10. Neurofibromatosis Multiple cutaneous and subcutaneous neurofibromas

11. Neurofibromatosis Acoustic Neuroma In NF2

12. Neurofibromatosis Spinal Neurofibroma

13. Neurofibromatosis Scoliosis

14. Neurofibromatosis Intraspinal tumors

15. Neurofibromatosis DIAGNOSIS NF1 is diagnosed if the person has two or more of the following features: Six or more café-au-lait macules >5 mm in prepubertal patients and >15 mm in postpubertal patients Two or more neurofibromas of any type or one plexiform neurofibroma Axillary or inguinal freckling Optic glioma Two or more Lisch nodules (iris hamartomas) Sphenoid wing dysplasia or cortical thinning of long bones, with or without pseudarthrosis A first-degree relative (parent, sibling, or child) with NF1 based on the previous criteria

16. Neurofibromatosis DIAGNOSIS NF2 is diagnosed if the person has either of the following two criteria: Bilateral eighth nerve masses seen by appropriate imaging studies OR a unilateral eighth nerve mass A first-degree relative with NF2 and either or two of the following: neurofibroma, meningioma, glioma, schwannoma, or juvenile posterior subcapsular lenticular opacity

17. Neurofibromatosis WORKUP LABORATORY TESTS Genetic testing is available. Results can only tell if an individual is affected but cannot predict the severity of the disease. In NF2, linkage analysis testing provides a >99% certainty the individual has NF2. IMAGING STUDIES MRI with gadolinium is the imaging study of choice in both NF1 and NF2 patients. MRI increases detection of optic gliomas, tumors of the spine, acoustic neuromas, and “bright spots” thought to represent hamartomas.

18. Neurofibromatosis TREATMENT Primarily supportive AEDs for seizures Surgery for for accessible tumors Orthopedic procedures for bony deformities Routine MRI studies to screen for optic gliomas in nonsymptomatic children

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21. Incisional Hernia Descriptions Midline scar extending from epigastric to paraumbilical region Bulging over the midline scar What type of scar? Laparotomy scar What is the bulging consist of? Small intestine

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23. Presented with:- LOA, LOW, Right upper quadrant pain, Vomitting Diagnosis?

24. Obstructive Jaundice Gallbladder ca Pancreatic ca Ductal ca Choledocholithiasis Biliary atresia Fluke worm Pancreatitis Pancreatic pseudocyst Malignancy a/w with LOA, LOW

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26. What abnormality? Why? Causes?

27. Gynaecomastia Abnormal development of large mammary gland in males resulting in breast enlargement Causes:- Estrogen Androgen Imbalance (Kidney & Liver problems) Drugs (cimetidine, spironolactone, omeprazole, imatinibmesylate,finasteride, and also some antipsychotics)

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29. What abnormality can you see? Diagnosis? Complications?

30. Facial Asymmetry Facial asymmetry, lower half is underdeveloped Hemifacial microsomia (congenital disorder that affects the development of the lower half of the face, most commonly the ears, the mouth and the mandible. It can occur on one side of the face or both) difficulties in breathing, obstructing the trachea and requiring a tracheotomy

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32. What abnormality? Diagnosis?

33. Sturge-Weber Syndrome It occurs sporadically, with a frequency of approximately 1/50,000 and consists of: Facial nevus (port-wine stain) Seizures Hemiparesis Intracranial calcifications Mental retardation

34. Sturge-Weber Syndrome Clinical Manifestations The facial nevus is present at birth and tends to be unilateral and always involves the upper face and eyelid. The nevus may also be evident over the lower face, trunk, and in the mucosa of the mouth and pharynx. Unilateral in 70% and ipsilateral to the venous angioma of the pia Even when the facial nevus is bilateral,the pial angioma is usually unilateral. The size of the cutaneous angioma does not predict the size of the intracranial angioma. Not all children with facial nevi have Sturge-Weber disease. Buphthalmos and glaucoma of the ipsilateral eye are a common complication.

35. Sturge-Weber Syndrome Clinical Manifestations Seizures develop in most patients during the 1st year of life typically focal tonic-clonic and contralateral to the side of the facial nevus seizures tend to become refractory to AEDs and are associated with a slowly progressive hemiparesis in many cases.

36. Sturge-Weber Syndrome Clinical Manifestations Although neurodevelopment appears to be normal during the 1st year of life, mental retardation or severe learning disabilities are present in at least 50% during later childhood.

37. Sturge-Weber Syndrome Diagnosis. The CT scan highlights the extent of the calcification that is usually associated with unilateral cortical atrophy and ipsilateral dilatation of the lateral ventricle.

38. Sturge-Weber disease Axial CT without and with contrast in a one-year-old boy with seizures. In (a) no calcifications have yet formed; cortical atrophy is seen on the left. In (b) marked cortical enhancement following contrast injection.

39. Port-Wine Stain Reddish/ purplish discoloration of skin Naevusflammeusa.k.a Port Wine stain Port-wine stains are present at birth and persist throughout life. The area of skin affected grows in proportion to general growth. Port-wine stains occur most often on the face but can appear anywhere on the body. Early stains are usually flat and pink in appearance. As the child matures, the color may deepen to a dark red or purplish colour. In adulthood, thickening of the lesion or the development of small lumps may occur

40. Sturge-Weber Syndrome Treatment Treat seizure hemispherectomy or lobectomy may be needed Because of the risk of glaucoma, regular measurements of intraocular pressure with a tenonometer is indicated. Flashlamp-pulsed laser therapy holds considerable promise for clearing of the port-wine stain. because of the high frequency of developmental disabilities, special educational facilities are frequently required.

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42. What abnormality? Diagnosis?

43. Diffuse neck swelling over anterior triangle… (???) Multinodular Goiter a/w Grave’s disease. Pt presented with symptoms of hyperthyroidism; tremor, sweating, palpitation, Grave’s eye disease etc

45. Tuberous Sclerosis The classic clinical triad is skin lesions in association with epilepsy and mental retardation. Multisystemic disorder affecting primarily tissues derived from ectoderm but also involving organs of mesodermal and endodermal origin, particularly the eyes, kidneys, and heart.

46. Tuberous Sclerosis ETIOLOGY AND EPIDEMIOLOGY Autosomal dominant condition with variable expression and an estimated frequency of 1/6,000 . Mutations have been mapped to chromosome 9q34 (TSC1) and 16p13.3 (TSC2). The TSC2 product is tuberin, which has sequence homology with a GTPase-activating protein and may have a role in regulating cellular growth by acting as a growth suppressor gene. TSC1 also is postulated to act as a growth suppressor. Approximately half of cases are due to new mutations.

47. Tuberous Sclerosis Clinical Manifestations ash-leaf macule the most reliable early cutaneous sign. presents at birth or in early infancy, often years before other signs of the disease. seen in more than 90% of cases in this age group. also appear in 2–3/1,000 normal newborns. they are sharply demarcated, pale, 0.5–3cm lesions that often assume the shape of a mountain ash leaflet.

48. Tuberous Sclerosis Clinical Manifestations Shagreen patch Is present by 15 years in 50% of affected children Most often occurs on trunk or in lumbosacral area but can occur on any glabrous skin Discrete, usually flesh-colored, flat to slightly elevated lesions with a “pig-skin” or “orange-peel” appearance Highly variable in size Are plaques of subepidermal fibrosis

49. Tuberous Sclerosis Clinical Manifestations Café-au-lait spots occur with increased frequency but are not as numerous as in neurofibromatosis

50. Tuberous Sclerosis Clinical Manifestations Adenoma sebaceum Present in approximately 50%of patients who are > four years old; unusual before 4 years of age Earliest manifestations are erythema that slowly progresses to flesh-colored to pink lesions at nasolabial folds, malar region, chin, forehead and, sometimes, the scalp Often confused with acne Are actually angiofibromas

51. Tuberous Sclerosis Clinical Manifestations Subungualfibromas arise from the stratum lucidum of the finger and toe in many patients with TS during adolescence.

52. Tuberous Sclerosis Clinical Manifestations Periungual Fibroma Also called Koenen tumors Generally do not manifest until puberty May involve and eventually destroy the entire nail

53. Tuberous Sclerosis Clinical Manifestations Mental deficiency occurs in 60–70%; nearly all have epilepsy. Epilepsy is also present in approximately 70% of those patients without mental retardation. Epilepsy begins in infancy (IS) or early childhood and is often progressively more severe. Clinical Manifestations Retinal tumors Rhabdomyoma of the heart Renal tumors Cysts of the kidney,bones and lungs

54. Tuberous Sclerosis two astrocytic hamartomas. One is calcified.

55. Tuberous Sclerosis Renal Angiomyolipomas

56. Tuberous Sclerosis Diagnosis Diagnosis of TS relies on a high index of suspicion when assessing a child with infantile spasms. A careful search for the typical skin and retinal lesions should be completed in all patients with a seizure disorder. Head CT scan or MRI confirms the diagnosis in most cases. The CT scan typically shows calcified tubers in the periventricular area, but these may not be apparent until 3–4 yr of age.

57. Tuberous Sclerosis CT of the brain revealed ventriculomegaly and multiple calcified subependymal nodules in the lateral ventricles

58. Tuberous Sclerosis periventricular tubers

59. Tuberous Sclerosis Diagnosis Molecular genetic testing of the TSC1 and TSC2 genes is complicated by the large size of the two genes, the large number of disease-causing mutations, and a 10% to 25% rate of somatic mosaicism However, the molecular testing for both genes is available

60. Tuberous Sclerosis Management consists of : seizure control baseline studies, including brain CT/MRI renal ultrasonography echocardiogram chest X-ray In Europe and Canada, infantile spasms associated with TS are often treated with vigabatrin (rather than ACTH), with good results. Vigabatrin is not available in the United States.

61. Tuberous Sclerosis Prognosis: 75% of patients with tuberous sclerosis die before the age of 25 yr, most commonly as a complication of: Epilepsy intercurrent infection cardiac failure pulmonary fibrosis

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63. Multinodulargoitre

64. Neck swelling?

65. SIMPLE MULTINODULAR GOITRE Rare before middle age Slowly increasing in size Nodular/lobulated May extend retrosternally Nodules may be colloid or cellular, and cystic degeneration and haemorrhage are common Mediastinal compression with stridor, dysphagia and obstruction of the superior vena cava Recurrent laryngeal palsy

66. HYPERTHYROIDISM Anxiety, restlessness Fine alopecia Heat intolerance, excessive sweating Increased appetite, low of weight, diarrhoea Palpitation, tachycardia, atrial fibrillation Exophthalmos, lid lag, lid retraction, oculomotor palsies Hyperreflexia Pretibial myxoedema

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72. Clinical features

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76. INSTRUCTION: EXAMINE THIS GENTLEMANS ABDOMEN. TO PATIENT: HELLO MR.SAM. MY NAME IS DR. NAZISH GHAZANFAR. HOW ARE YOU FEELING TODAY? REPLY ACCORDINGLY. MAY I PLEASE EXAMINE YOUR TUMMY? THANK YOU. LET ME JUST DRAW THE CURTAINS TO ENSURE PRIVACY. I HAVE ALREADY WASHED MY HANDS. COULD YOU PLEASE LIE DOWN FLAT ON THIS COUCH WITH MAXIMUM ONE PILLOW BEHIND YOUR HEAD, WITH YOUR ARMS BY YOUR SIDE AND YOUR LEGS UNCROSSED TO RELAX YOUR ABDOMINAL MUSCLES? CAN I PLEASE EXPOSE YOU FROM YOUR LOWER CHEST TO GROIN.I WILL COVER YOUR PRIVATE PARTS SIR. ARE YOU COMFORTABLE SIR? DO YOU MIND IF I TALK ABOUT YOU TO THE EXAMINERS AS I GO ALONG? I AM JUST GOING TO HAVE A LOOK FIRST OF ALL. ACT: STAND BACK AND LOOK GENERALLY AT THE PATIENT AND AT THE ABDOMEN FROM THE FOOT END OF BED AND FROM THE RIGHT SIDE OF BED. TO EXAMINER: ON GENERAL INSPECTION THIS GENTLEMAN LOOKS WELL AND IS COMFORTABLY LYING ON COUCH WITH NO EVDIENCE OF SYSTEMIC DISEASE AS PALLOR, JAUNDICE, WEIGHT LOSS OR SHORTNESS OF BREATH. HIS ABDOMEN IS ROUNDED/ PROTUBERANT AND IS MOVING WITH RESPIRATION. THERE IS A SMALL LUMP BESIDES/ADJACENT TO THE UMBILICUS WHICH IS ABOUT 2 BY 3 CMS IN SIZE. THE UMBILICUS IS PUSHED TO ONE SIDE AND STRETCHED INTO A CRESCENT SHAPE. THERE IS NO EVIDENCE OF ANY REDNESS, DISCOLOURATION, VISIBLE VEINS, PERISTALSIS, DISCHARGE, DRIED SEBACEOUS SECRETIONS OR SCAR IN THE OVERLYING SKIN. THE SURROUNDING SKIN IS THIN WITH NO EVIDENCE OF SCARS OF PREVIOUS DRAIN SITES OR STOMAS. THERE IS GENERALIZED ABDOMINAL WALL LAXITY WITH AN APRON OF PENDULOUS FAT ACROSS THE LOWER ABDOMEN. TO PATIENT: I AM NOW GOING TO TEST FOR A COUGH IMPULSE. SIR COULD YOU PLEASE TURN YOUR HEAD TO THE OTHER SIDE AND COUGH? TO EXAMINER: THE LUMP SHOWS AN EXPANSILE COUGH IMPULSE. TO PATIENT: I AM NOW GOING TO FEEL YOUR TUMMY. PLEASE LET ME KNOW IF IT IS TENDER ANYWHERE. I WILL BE VERY GENTLE. ACT: KNEEL ON RIGHT SIDE OF PATIENT SO THAT YOUR ARM AND FOREARM ARE AT SAME LEVEL. RUB YOUR HANDS TOGETHER TO MAKE THEM A BIT WARM BEFORE TOUCHING PATIENT. LOOK AT PATIENTS FACE AND START PALPATION FURTHEST AWAY FROM THE LUMP. BEFORE TOUCHING LUMP, CHECK TEMPERATURE AND COMPARE WITH SURROUNDINGS, THEN LIGHTLY PALPATE OVER IT FOR TENDERNESS LOOKING AT PATIENTS FACE. THEN PALPATE DEEPLY IN ALL QUADRANTS COMING TO THE LUMP.

77. TO EXAMINER: THE OVERLYING SKIN IS NOT WARM. IT IS A NON TENDER LUMP WITH SMOOTH SURFACE AND WELL DEFINED EDGES. IT IS SOFT(BOWEL)/FIRM(OMENTUM) IN CONSISTENCY AND IS NON COMPRESSIBLE. TO PATIENT: I AM JUST GOING TO TEST FOR A COUGH IMPULE. SIR COULD YOU PLEASE TURN YOUR HEAD TO THE OTHER SIDE AND COUGH? TO EXAMINER: THE LUMP HAS AN EXPANSILE COUGH IMPULSE. TO PATIENT: I AM JUST GOING TO PINCH THE OVERLYING SKIN. TO EXAMINER: THE SKIN IS FREELY MOVEABLE OVER THE LUMP. TO PATIENT: I AM NOW GOING TO MOVE THE LUMP. TO EXAMINER: THE SKIN AT THE CENTRE OF THE UMBILICUS IS NOT ATTACHED TO CENTRE OF LUMP BUT THE UMBILICAL SKIN IS FIRMLY APPLIED TO THE SIDE OF THE LUMP. TO PATIENT: I WOULD LIKE TO SEE THE ACTUAL EXTENT OF THE LUMP AND THE PRESENCE OF ANY CO EXISTENT HERNIA. SIR COULD YOU PLEASE RAISE BOTH YOUR HEAD AND SHOULDERS OFF THE COUCH WITH YOUR HANDS FOLDED ACROSS YOUR CHEST? THANK YOU. YOU MAY REST YOUR HEAD BACK NOW. TO EXAMINER: THE EXTENT OF THE LUMP CAN BE SEEN MORE CLOSELY WHEN THE PATIENT RAISES HEAD AND SHOULDERS OFF THE COUCH. THE ACTUAL SIZE OF THE LUMP IS ABOUT 3 BY 3 CMS IN SIZE AND THERE IS NO EVIDENCE OF ANY CO EXISTENT HERNIA. NOW I WOULD LIKE TO DETERMINE THE DEFECT IN THE ABDOMINAL WALL IN THE LINEA ALBA. TO PATIENT: BEFORE I DO THAT SIR, COULD YOU PLEASE TELL ME WHETHER THE LUMP GOES BACK IN? CAN YOU GET IT BACK IN YOURSELF? WILL YOU DO THAT PLEASE, I DON’T WANT TO HURT YOU. THAT’S GREAT. THANK YOU. NOW I WILL TAKE IT. ACT: FEEL FOR THE DEFECT IN THE ABDOMINAL WALL IN LINEA ALBA AND DETERMINE ITS SIZE. TO EXAMINER:

78. THERE IS A FINGER TIP SIZED DEFECT IN THE LINEA ALBA AFTER IT IS REDUCED. ALTERNATIVELY IF THE PATIENT SAYS IT DOES NOT GO BACK IN, TAKE HIS WORD FOR IT AND SAY, THE PATIENT CANNOT REDUCE THE LUMP. AS I DO NOT WANT TO CAUSE PAIN TO THE PATIENT I WOULD NOT FEEL FOR THE DEFECT IN THE LINEA ALBA. TO PATIENT; I AM JUST GOING TO GENTLY TAP OVER IT. TO EXAMINER: THE PERCUSSION NOTE IS DULL/RESONANT. DULL….OMENTUM RESONANT…BOWEL. TO PATIENT: I AM JUST GOING TO LISTEN OVER THE LUMP. TO EXAMINER: BOWEL SOUNDS ARE/ ARE NOT PRESENT/AUDIBLE. TO PATIENT: THANK YOU VERY MUCH SIR. LET ME COVER YOU UP. YOU MAY SIT DOWN AND RELAX. THANK YOU AGAIN. TO EXAMINER: I WOULD LIKE TO COMPLETE THE REST OF THE ABDOMINAL EXAMINATION. THS IS A PARAUMBILICAL HERNIA. I WOULD LIKE TO WASH MY HANDS.

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81. Arterialulcer. Arterial ulcer on a 80 year old female patient's foot, exuding pus and surrounded by bruised and inflamed tissue. The ulcer shows a "punched out" appearance typical of arterial ulcers. Arterial ulcers are infected open sores caused by inadequate blood supply. They are often painful and inflamed, and are more difficult to cure than to prevent. The usual treatment is application of a wet dressing.

82. Characteristics * Present almost anywhere on the leg; usually distal to impaired arterial supply, between toes or tips of toes, over phalangeal heads, around lateral malleolus, or at sites subjected to trauma or rubbing of footwear. * Wound margins are even, sharply demarcated, and punched out. * Wound may be superficial or deep. * Wound beds may be pale, gray or yellow with no evidence of new tissue growth; necrosis or cellulitis may be present; commonly accompanied by dry necrotic eschar and exposed tendons. * Have minimum exudate. * Periwound tissue may appear blanched or purpuric and is often shiny and tight; loss of hair at ankle or foot. * Usually very painful; pain is often relieved by dependent leg position and aggravated by elevation.

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85. Venous Ulcer Venous ulcers result from valve incompetence in perforating veins, a history of deep vein thrombophlebitis and thrombosis, a failed calf pump, obesity, age, or pregnancy in women with a family history of venous ulcers. Healing is best expedited by increasing venous return, decreasing edema, appropriate compression, and proper skin and wound management. Characteristics of venous ulcers * Occur anywhere between the knee and the ankle, with medial and lateral malleolus the most common sites. * Usually are superficial. * Wound beds vary in appearance, frequently ruddy, beefy red, granular tissue; calcification in wound base is common; a superficial fibrinous gelatinous necrosis may occur suddenly with healthy appearing granulation tissue underneath. * Have moderate to heavy exudate. * Tend to be large with irregular margins. * Surrounding skin is characterized by hyperpigmentation, dermatitis, and lipodermatosclerosis. * May be painless; however, pain varies unpredictably and often is relieved with leg elevation.

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89. Ganglion There is a single spherical shape swelling at the dorsal part of the wrist . It is 3cm times 3 cm by size Regular border No skin changes Palpation-no incerase in warmth and non tender regular border,smoothsurface,soft in consistency,mobile vertically and horizontally,fluctuant,nottransluminate

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92. Inguinal Hernia Swelling over the inguinal area,size 6cm x 10 cm by size,no skin changes Reducible,prominent on cough Palpation-non tender,no increase in warmness,border-cannot get above it,surface,reducibility,cough reflex,

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95. Curbuncle swelling behind the neck,irregularshape,multiple sinuses seen,erythematous skin overlying the swelling Warm,tender

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98. Incisional Hernia Irregular shape swelling over the central of abdomen,size 15cm x 10 cm by size ,10 cm vertical surgical scar seen over the swelling,well heal Non tender,not increase in warmth,regularborder,smoothsurface,soft,mobile,reducible

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101. Venous Ulcer Ulcer seen at the gaiter area Irregular shape Redness and hyperpigmented skin Irregular border Edge- Base- granulation tissue,exposed muscle/tendon?,bleeding,pus

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104. Multinodulargoitre Multinodular anterior neck swelling Size- 6cm x 7cm bysize No skin changes,no dilated vein Move up with swallowing Palpation-no tenderne,notwarmth,irregularborder,nodularsurface,consistency Percussion-retrosternal Auscultation-bruit

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107. Squamous cell carcinoma Large sun-induced squamous cell carcinoma on the forehead/temple

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111. Moves On Swallowing or Moves on Tongue Protrusion yes no Many / Multiple Thyroid Midline=Thyroglossal Cyst Lateral = Thyroid Mass No yes Cystic Lymph Nodes yes no TB Abscess Subclavian Artery 1.Aneurysm 2.Ectasia Cyst Cystic Hygroma Branchial Cyst Solid Mass no yes Tumors Sternocleidomastoid tumors (torticollis) Carotid Body Tumors

113. 6. Complications 1. Toxic MultinodularGoiter (Thyrotoxicosis) 1. Cardiovascular complications 1. Atrial Fibrillation 2. Tachycardia 3. Congestive Heart Failure 2. No Ophthalmopathy (Proptosis and stare) 3. No Dermopathy 2. Both Toxic and Non-Toxic MultinodularGoiter 1. Superior Vena Cava Syndrome 1. Results from thoracic outlet obstruction 1. Causes 1. Simple Goiter develops into MultinodularGoiter 2. Types 1. Non-Toxic MultinodularGoiter 2. Toxic MultinodularGoiter (50%) 1. Results in Thyrotoxicosis 3. Differential Diagnosis 1. Thyroid Cancer 4. Symptoms 1. Dysphagia 2. Choking sensation 5. Signs 1. Markedly enlarged nodular Thyroid 2. Stridor

115. investigations Thyroid scans: Classified: cold, hot, warm Thyroid cells absorb iodine(radioactive) to make thyroid hormone ‘butterfly image’ If nodule/ goitre is composed of cells that do not make thyroid hormone don’t absorb iodine  ‘cold’ nodule Make too much hormonedarker image ‘hot’ Cannot truly differentiate benign/malignant

116. Differentiating features between benign and malignant lesions on diagnostic tests

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126. EXAMINATION SITE. Can occur at any point in the mid-line of trunk, but common in the face and neck., along the lines of fusion of the ophthalmic & the maxillary facial processes, & at the inner & outer end of the upper eyebrow. SHAPE & SIZE Ovoid/ spherical & 1-2 cm in diam. SURFACE Smooth. COMPOSITION. Cysts on the face often feels soft,not tense.They fluctuate but only transilluminate if got clear fluid.Large cysts will conduct a fluid thill and are dull to percussionThey are not pulsatile, compressible/ reducible.

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130. SEBACEOUS CYSTS. When mouth of a sebaceous gland becomes blocked ,the gland becomes distended by its own secretion and ultimately becomes a sebaceous cyst. HISTORY. AGE. Occurs in all age group but rarely present before adolescentMostly present in early adulthood & middle age. DURATION. Slow growing and have usually been present for some years. SYMPTOMS. Most frequently found on scalp.As lump that gets stretched when the patient is combing hair.If infected, it enlarges and becomes acutely painful.A slow discharge of sebum fr a wide punctum sometimes harden to become a sebaceous horn.Infection of the cyst wall & the surrounding tissues produces a boggy, painful,discharging swelling known as Cock’s Peculiar Tumour.This only happens if an infected cyst is neglected.

131. EXAMINATION. SITE Most are found in the hairy parts of body.They can occur wherever there are sebaceous glands. SHAPE & COLOUR Most are tense & spherical.Skin over the cysts are normal. SIZE Vary,few mm to 4-5 cm in diam. SURFACE. Surface is smooth EDGE. Is well defined & easy to feel as it is usually lying in subc. tissue TENDERNESS. Not tender unless infected.. TEMPERATURE. Normal except when inflamed.

132. 8.COMPOSITION. -Most cysts feel hard & solid.On scalp the resistance of underlying skull enables one to fix the cyst & press it firmly:fluctuation.They are dull to percussion & don’t have a fluid thrill even when large because their contents are like thick cream.They are not compressible / pulsatile. 9.LYMPH DRAINAGE. -Not enlarged.

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135. GANGLIONS. A ganglion is a cystic, myxomatous degeneration of fibrous tissue.It can occur anywhere in the body, but common where there is a lot of fibrous tissue esp, around the joints. HISTORY. AGE. Majority btw age 20 and 60 years old.Rare in children. DURATION. Grows slowly. SYMPTOMS. - not painful

136. EXAMINATION. SITE. Most found near capsule of jointat least 90% on the dorsal & ventral surface of the wrist joint and hand. SHAPE & SURFACE. -spherical and has smooth surface.Some are multilocular SIZE. Small:0.5-1.0 cm, tense , spherical.Large, 5-6 cm across,flattened and soft COMPOSITION. -Most fluctuate,provided not very small and tense. REDUCIBILITY. May slip away btw deep structures when pressed , giving false impression that its contenthave reducedinto the joints.

137. 7.RELATIONS -Usually attached to the fibrous tissue they originate from.Not attached to overlying skin. surrounding tissues should be normal. 8.DIFFERENTIAL DIAGNOSIS. -Bursae and cystic protrusion of the synovial cavity of arthritic joints-soft .Ganglion is tense .In bursae and ganglion,joint is normal.

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140. PHYSICAL EXAMINATION? 6S 2T 2C R

141. TERMS: INGUINALOGY?

142. HOW DO YOU DIFFERENTIATE IT ANATOMYCALLY?

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144. LEFT INGUINAL HERNIA

145. STRANGULATED HERNIA Patient presented with acute, painful, non-reducible inguinal hernia. It's worthmentioning that in spite of rapid diagnosis and prompt surgical exploration, gangrenous bowel was identified. This highlights the potential seriousness of this condition What is this hernia?

146. FEMORAL HERNIA What is this hernia? Femoral hernias occur just below the inguinal ligament, when abdominal contents pass into the weak area at the posterior wall of the femoral canal. They can be hard to distinguish from the inguinal type (especially when ascending cephalad): however, they generally appear more rounded, and, in contrast to inguinal hernias, there is a strong female preponderance in femoral hernias. The incidence of strangulation in femoral hernias is high. Repair techniques are similar for femoral and inguinal hernia.

147. What is this hernia? UMBILICAL HERNIA They involve protrusion of intraabdominal contents through a weakness at the site of passage of the umbilical cord through the abdominal wall. These hernias often resolve spontaneously. Umbilical hernias in adults are largely acquired, and are more frequent in obese or pregnant women. Abnormal decussation of fibers at the linea alba may contribute.

148. INCISIONAL HERNIA What is this hernia? An incisional hernia occurs when the defect is the result of an incompletely healed surgical wound. When these occur in median laparotomy incisions in the linea alba, they are termed ventral hernias. These can be the most frustrating and difficult to treat, as the repair utilizes already attenuated tissue.

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153. What is lymphedema? Lymphedema is an abnormal accumulation of high-protein concentrated fluid, usually in the arms and legs. Dell & Doll, 2006 Image reproduced with permission from vascularsociety.org

154. Severity of Lymphedema Mild lymphedema: One to two cm increase in girth measurements between the involved and non-involved limb Moderate lymphedema: Two to five cm increase in girth measurement Severe lymphedema: Greater than five cm increase

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160. Factors predisposing to rupture of abdominal aortic aneurysms x Diameter of aneurysm x Diastolic blood pressure x Chronic obstructive pulmonary disease x Smoking x Family history of ruptured aneurysm x Expansion rate x Intrinsic biology—inflammation within the aortic wall x Thrombus­free surface area of aneurysm sac

161. The cause of aneurysms is unclear, but the majority (90%) are thought to be due to degenerative process. Abdominal aortic aneurysms show familial clustering in 15–25% of cases. It is inferred that susceptibility to the development of abdominal aortic aneurysms is a multifactorial process with multiple genetic and environmental risk factors. Other causes of aortic aneurysm are: • infection (mycotic aneurysms) • cystic medial necrosis • arteritis • trauma • disorders of connective tissue • pseudoaneurysm caused by disruption at the anastomosis of an existing aortic graft.

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163. Wegner and Grossman Theory “In the absence of cricoarytenoid joint fixation, an immobile vocal cord in paramedian position has total pure unilateral recurrent nerve paralysis, and an immobile vocal cord in lateral position has a combined paralysis of superior and recurrent nerves (the adductive action of cricothyroid muscle is lost)”

164. Causes of vocal cord paralysis Malignant : This accounts for 25% of cases, one half being caused by carcinoma of lung

165. Causes of vocal cord paralysis Surgical/Traumatic: (20% cases) Thyroidectomy Pneumonectomy CABG Penetrating neck or chest trauma. Post intubation Whiplash injuries Posterior fossa surgery

166. Causes of vocal cord paralysis Neurulogical (5-10%) Wallenberg syndrome (lateral medullary stroke) Syringomyelia Encephalitis Parkinsons, Poliomyelitis Multiple Sclerosis Myasthenia Gravis, Guillian-Barre Diabetes

167. Causes of vocal cord paralysis Inflammatory: Rheumatoid arthritis ,( really a "fixed" cord here) Infectious: Syphilis Tuberculosis Thyroiditis Viral

168. Causes of vocal cord paralysis Idiopathic (20-25%): Sarcoidosis, Lupus Polyarteritis nodosa Ortner's syndrome (left atrial hypertrophy).

169. Intracranial causes Head injury CVA Bulbar poliomyelitis Distinctive features Other neurological signs and symptoms due to combined paralysis of soft palate, pharynx and larynx

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172. Indications

173. Complications of Tracheostomy Intraopertaive Complications. Bleeding and injury to big vessels Injury to tracheoesophageal wall Pneumothorex Early Complications Bleeding Tracheostomy tube obstruction Tracheostomy tube displacement Infection Late Complications Tracheal Stenosis Granulation tissue Tracheocutaneus fistula Tracheo - inominate fistula

174. TERIMA KASIH KEPADA SEMUA PEMBUAT SLIDES… POM-POM CRABBALL FYK MHR@LOVE