PRACTICE MAKES PERFECTPom – Jin – FYK – MHR - Crabball

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

Café au Lait spot cafe-au-lait spots: are

not necessarily a diagnostic sign of NF

Multiple lesions occur in a variety of syndromes:N

• Neurofibromatosis

V• Von Hippel – Lindau

disease

A• Fanconi anemia• Ataxia Telangiectasia

T• Tuberous sclerosis

S• Silver-Russell dwarfism

B• Bloom syndrome• Basal cell nevus syndrome• Gaucher disease

H• Chédiak-Higashi syndrome• Hunter syndrome

M• Marfan's syndrome• Maffucci syndrome• McCune-Albright syndrome• Multiple endocrine

neoplasia type 2

P• Peutz-Jeghers Syndrome

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

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.

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.

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%)

NeurofibromatosisAxillary 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

NeurofibromatosisLisch Nodules

a pigmented hamartomatous nevus (a type of benign tumor) affecting the iris

Neurofibromatosis

Multiple cutaneous and subcutaneous neurofibromas

NeurofibromatosisAcoustic NeuromaIn NF2

NeurofibromatosisSpinal Neurofibroma

Neurofibromatosis

Scoliosis

NeurofibromatosisIntraspi

nal tumors

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

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

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.

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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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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Presented with:- LOA, LOW, Right upper quadrant pain, Vomitting

Diagnosis?

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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What abnormality? Why? Causes?

Gynaecomastia Abnormal development of large

mammary gland in males resulting in breast enlargement

Causes:- Estrogen Androgen Imbalance (Kidney &

Liver problems) Drugs (cimetidine, spironolactone,

omeprazole, imatinib mesylate,finasteride, and also some antipsychotics)

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Click icon to add pictureWhat abnormality can you see?Diagnosis?Complications?

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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What abnormality? Diagnosis?

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

Sturge-Weber SyndromeClinical 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.

Sturge-Weber SyndromeClinical 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.

Sturge-Weber SyndromeClinical 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.

Sturge-Weber SyndromeDiagnosis.

The CT scan highlights the extent of the calcification that is usually associated with unilateral cortical atrophy and ipsilateral dilatation of the lateral ventricle.

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.

Port-Wine Stain Reddish/ purplish discoloration of skin Naevus flammeus a.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

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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What abnormality? Diagnosis?

Diffuse neck swelling over anterior triangle… (???)

Multinodular Goitera/w Grave’s disease. Pt presented with symptoms of hyperthyroidism; tremor, sweating, palpitation, Grave’s eye disease etc

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.

Tuberous SclerosisETIOLOGY 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.

Tuberous SclerosisClinical Manifestationsash-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.

Tuberous SclerosisClinical ManifestationsShagreen 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

Tuberous SclerosisClinical Manifestations

Café-au-lait spots occur with increased

frequency but are not as numerous as in neurofibromatosis

Tuberous SclerosisClinical ManifestationsAdenoma 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

Tuberous SclerosisClinical ManifestationsSubungual fibromas arise from the stratum

lucidum of the finger and toe in many patients with TS during adolescence.

Tuberous SclerosisClinical ManifestationsPeriungual Fibroma Also called Koenen

tumors

Generally do not manifest until puberty

May involve and eventually destroy the entire nail

Tuberous SclerosisClinical 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

Tuberous Sclerosis two astrocytic

hamartomas. One is calcified.

Tuberous Sclerosis Renal

Angiomyolipomas

Tuberous SclerosisDiagnosis

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.

Tuberous Sclerosis CT of the brain

revealed ventriculomegaly and multiple calcified subependymal nodules in the lateral ventricles

Tuberous Sclerosis periventricular

tubers

Tuberous SclerosisDiagnosis 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

Tuberous SclerosisManagement 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.

Tuberous SclerosisPrognosis: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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Multinodular goitre

Neck swelling?

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

HYPERTHYROIDISMAnxiety, restlessnessFine alopeciaHeat intolerance, excessive sweating

Increased appetite, low of weight, diarrhoea

Palpitation, tachycardia, atrial fibrillation

Exophthalmos, lid lag, lid retraction, oculomotor palsies

HyperreflexiaPretibial myxoedema

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PHYSICAL EXAMINATION CAN YOU GET ABOVE THE SWELLING?

YES NO

CAN THE TESTIS BE FELT SEPARATELY FROM THE SWELLING?

IS THERE A COUGH IMPULSE?

YES NO

TRANSILLUMINATION

YES•Hydrocele

NO•Testicular tumour•Tender swelling

YES•Epididymal cyst

SOMETIMES•Spermatocele

YES•Indirect inguinal hernia

NO•Infantile hydrocele

Indirect inguinal hernia Abdominal content slides in to the

scrotum via deep inguinal ring---inguinal canal---superficial inguinal ring--- spermatic cord--- testicular swelling

Clinical featuresIndirect inguinal hernia Direct inguinal hernia

Can descend into scrotum Cannot descend into scrotum

Reduces upward, then laterally and backward

Reduces upwards and then straight backwards

Controlled, after reduction by pressure over internal inguinal ring

Not controlled, after reduction by pressure over internal inguinal ring

After reduction, bulge reappears in middle eg inguinal region and then follows medially b4 turning down to neck of scrotum

After reduction, bulge reappears exactly where it was before

Defect is not palpable, as it behind the fibres of external oblique muscle

Defect may be felt in the abdominal wall above pubic tubercle

Common in children and young age Common in elderly

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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.

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:

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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Arterial ulcer. 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.

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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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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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,smooth surface,soft in consistency,mobile vertically and horizontally,fluctuant,not transluminate

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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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Curbuncle swelling behind the neck,irregular

shape,multiple sinuses seen,erythematous skin overlying the swelling

Warm,tender

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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,regular border,smooth surface,soft,mobile,reducible

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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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Multinodular goitre Multinodular anterior neck swelling Size- 6cm x 7cm bysize No skin changes,no dilated vein Move up with swallowing Palpation-no tenderne,not warmth,irregular

border,nodular surface,consistency Percussion-retrosternal Auscultation-bruit

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Squamous cell carcinoma Large sun-induced squamous cell

carcinoma on the forehead/temple

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• Physical Examination :1. Ant. & Post Triangle?2. Moves on swallowing/ tongue

protrusion?3. Single or Multiple?4. Cystic or solid?

Types of swelling in the:Ant. triangle Post. triangle

•Thyroid•Lymph nodes•Brachial cyst•Cold abscess•Thyroglossal cyst

•Lymph nodes•Cystic hygroma•Pharyngeal pouch•Subclavian Aneurysm•Ocassionally a 2nd deposit of papillary thyroid CA.

Moves On Swallowing or Moves on Tongue Protrusion

yes no

Thyroid Midline=Thyroglossal Cyst Lateral = Thyroid Mass

Many / Multiple

No

Cystic

yes

CystCystic HygromaBranchial Cyst

yes

Lymph Nodes

no

Solid Mass

TB AbscessSubclavian Artery 1.Aneurysm2.Ectasia

no yes

Tumors Sternocleidomastoid tumors (torticollis) Carotid Body Tumors

1. Causes 1. Simple Goiter develops into Multinodular Goiter 2. Types 1. Non-Toxic Multinodular Goiter 2. Toxic Multinodular Goiter (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

6. Complications 1. Toxic Multinodular Goiter (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 Multinodular Goiter 1. Superior Vena Cava Syndrome 1. Results from thoracic outlet obstruction

Features Favour Benign nodule/goitre

Features increase the suspicion of a malignant nodule

Family history – Hashimoto’s thyroiditis

Age <20 or >70 y/o

Family history – benign nodule/goitre

Male gender

Soft, smooth, mobile Swallowing difficulties

Multinodular goitre without a predominant nodule (lots of nodule)

New onset of hoarseness of voice

‘warm’ nodule on thyroid scan (produce normal amount of hormone)

H/o external neck irradiation

Simple cyst on US Firm, irregular and fixed

Presence of hard,swollen cervical LN

Previous history of thyroid Ca

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 hormonedarker image ‘hot’ Cannot truly differentiate benign/malignant

Differentiating features between benign and malignant lesions on diagnostic tests

Features Benign Malignant

Thyroid function tests Maybe abnormal Normal

Antithyroid antibodies Maybe raised in thyroiditis

Normal

Calcitonin levels High in thyroid cell hyperplasia

Raised in Medullary Ca

Serum Carcinogenic Embryonic Antigen (CEA)

Normal High in Medullary Ca

Colour doppler in US No vascular flow in a cystic lesion

Increased Vascularity in a cystic lesion

PAPILLARY THYROID CA(MOST COMMON->70%)

FOLLICULAR THYROID CA(2ND MOST COMMON-~15%)

MEDULLARY THYROID CA3RD MOST COMMON

30-50y/o 40-60 y/o-more malignant than papillary Ca

Occurs in 4 clinical settings:1.Sporadic – 80% cases2.MEN-II (Sipple syndrome)3. MEN II-B4. Inherited malig without associated endocrinopathies

F:M = 3:1 F:M = 3:1 F>M

Prognosis related to tumour size(<1.5cm– good)

< 1cm – good prognosis Regional metastases (neck LN) occurs early in the ds

85% - radiation exposure Rarely a/w radiation exposure Not associated with radiation

50% - spread to cervical LN ~10% spread to LN (rare) Origin- upper central lobe of thyroid

Distant spread - rare(common site:lung,bone)

Invasion into vascular structure(veins/arteries) within gland – characteristicDistant spread common- lung,bone,brain,liver,bladder,skin

Spread to distant organs – late- liver, bone, brain, adrenal medulla

Cure rate high (near 100% for small lesions in young patients)

Cure rate high(near 95% for small lesion in young pt)

Poor prognostic factor-Age >50-Distant spread-a/w endocrinopathies

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Sebaceous cysts (epidermal cysts) may be a foreign term

to you, but many women have indeed experienced them -- perhaps without really knowing what they

were at the time.

Sebaceous cysts are small lumps or bumps just under the skin. To be more

specific, they are closed sacs that contain keratin -- a "pasty" or "cheesy"

looking protein that often has a foul odor. Although they are usually found on the face, neck, and trunk, they also occur in the vaginal area or other parts

of the genitalia.

In cases of the latter, it is not uncommon for women to fear

that they are the result of genital herpes. But genital herpes create a blister-type sore that eventually becomes crusty, not just a bump

or lump under the skin.

What Causes Sebaceous Cysts?

• Sebaceous cysts are often the result of swollen hair follicles or skin trauma.

Symptoms and Signs/Symptoms of Infection

• Sebaceous cysts are usually painless, slow-growing, small bumps or lumps that move freely under the skin. It's important not to touch or try to remove the substance inside to prevent tenderness, swelling, and infection of a sebaceous cyst.• Occasionally, infections may occur. Signs or symptoms that may indicate infection of sebaceous cysts include:

• * redness• * tenderness• * increased temperature of the skin over the bumps or lumps• * greyish white, cheesy, foul-smelling material draining from the bump or lump

How Are Sebaceous Cysts Diagnosed ?

• Sebaceous cysts, to the trained eye, are usually easily diagnosed by their appearance. In some cases, a biopsy may be necessary to rule out other conditions with a similar appearance. You should see your doctor to get a formal diagnosis if you suspect that you have a sebaceous cyst.

Treatments for Sebaceous Cysts

• Sebaceous cysts most often disappear on their own and are not dangerous. As stated, however, they may become inflamed and tender. Sometimes sebaceous cysts grow large enough that they may interfere with your everyday life. When this happens, surgical removal may be necessary, and this procedure can be done at your doctor's office. Small inflamed cysts can often be treated with an injection of steroid medications or with antibiotics.

Complications of Sebaceous Cysts

• If sebaceous cysts become infected, they can form into painful abscesses.• The surgical removal of a sebaceous cyst that does not involve the excision of the entire sac may cause the cyst to come back (although, recurrence is not usual).• Remember to consult your healthcare provider anytime you notice any type of growth, bump, or lump on your body. Although sebaceous cysts are not dangerous, your

doctor should examine you to ensure that another more dangerous concern is not present.

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DERMOID CYSTS.

Dermoid cyst is a cyst, deep to the skin & lined by skin.They are congenital / acquired.

CONGENITAL DERMOID CYSTS.HISTORY.

1. DURATION.-may be noticed at birth but oftena few years later when it begins to

distend

2. SYMPTOMS - parental distress.It rarely becomes big / infected

3. MULTIPLICITY.-Not usually multiple.

.

EXAMINATION

1. 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.

2. SHAPE & SIZE Ovoid/ spherical & 1-2 cm in diam.

3. SURFACE Smooth.

4. 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.

ACQUIRED “IMPLANTATION” DERMOID CYSTS.

HISTORY.Cyst follows the survival of a piece of skin forcibly implanted into the

subcutaneous tissues by an injury-often a small deep cut / stab injury.Symptoms.-usually small and tense.

EXAMINATION.1. SITE.

Found beneath skin liable to injury,e.g. fingers.2. SHAPE & SIZE.

Spherical, smooth and small, 0.5-1.0 cm in diam.3. COMPOSITION.

Hard and tense, sometimes stony hard.4. DIFFERENTIAL DIAGNOSIS.

Commonly confused with sebaceous cyst.History of an old injury and scar closely related are the most significant diag.

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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.1. AGE.

Occurs in all age group but rarely present before adolescentMostly present in early adulthood & middle age.

2. DURATION. Slow growing and have usually been present for some years.

3. 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.

EXAMINATION.

1. SITE Most are found in the hairy parts of body.They can occur

wherever there are sebaceous glands.2. SHAPE & COLOUR

Most are tense & spherical.Skin over the cysts are normal.3. SIZE

Vary,few mm to 4-5 cm in diam.4. SURFACE.

Surface is smooth5. EDGE.

Is well defined & easy to feel as it is usually lying in subc. tissue

6. TENDERNESS. Not tender unless infected..

7. TEMPERATURE. Normal except when inflamed.

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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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.

1. AGE. Majority btw age 20 and 60 years old.Rare in children.

2. DURATION. Grows slowly.

3. SYMPTOMS.- not painful

EXAMINATION.

1. SITE. Most found near capsule of jointat least 90% on the dorsal &

ventral surface of the wrist joint and hand.2. SHAPE & SURFACE.

-spherical and has smooth surface.Some are multilocular3. SIZE.

Small:0.5-1.0 cm, tense , spherical.Large, 5-6 cm across,flattened and soft

4. COMPOSITION. -Most fluctuate,provided not very small and tense.

5. REDUCIBILITY. May slip away btw deep structures when pressed , giving

false impression that its contenthave reducedinto the joints.

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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PHYSICAL EXAMINATION? 6S 2T 2C R

INGUINAL•SITE: just above the pubic crest and the pubic tubercle and is widest medial to the pubic tubercle•SIZE:1-2cm in diameter/extend down to the knee joint•SHAPE: pear-shaped or hour-glass appearance•SKIN:normal as the surrounding skin. But if strangulated, the skin ,may be a little reddened•SURFACE:usually smooth•SURROUNDING: Normal•TEMPERATURE: normal but if strangulated or infected, it become hot•TENDERNESS: discomfort. If strangulated, it can be very tender•COMPOSITION: gut (soft, resonant, fluctuant, bowel sounds), omentum (firm, dull, non-fluctuant)•COUGH IMPULSE: positive•REDUCIBILITY: positive

FEMORAL CANAL

•SITE: below and lateral to the pubic tubercle•SIZE: small•SHAPE: flattened•SKIN: normal as the surrounding skin. But if strangulated, the skin ,may be a little reddened•SURFACE: smooth•SURROUNDING: Normal•TEMPERATURE: normal but if strangulated or infected, it become hot•TENDERNESS: discomfort. If strangulated, it can be very tender•COMPOSITION: depend on content•COUGH IMPULSE: many femoral hernia do not have a positive cough impulse•REDUCIBILITY: reduced incompletely

TERMS: INGUINALOGY?

Incarcerated

•irreducible hernia where the irreducibility is due to adhesions within the sac in the absence of obstruction or strangulation. •OR hypotheses - because of faeces within the large bowel. •SIMPLY: a hernia as being irreducible but not obstructed or strangulated.

Obstructed

•The bowel within the hernia is obstructed. The patient may have the four cardinal signs of obstruction (pain, vomiting, distention and constipation).

Strangulated

•occluded blood supply by pressure at the neck of the hernia. •Viability of bowell will impaired [except if contain omentum only]•1st veins are occluded P 2nd arterial occlusion gangrene developing.

HOW DO YOU DIFFERENTIATE IT ANATOMYCALLY?

DIRECT INGUINAL HERNIA

•Hernia pushes its way directly forward through posterior wall of inguinal canal.•Does not go down into the scrotum

INDIRECT INGUINAL HERNIA

•Pass through internal ring, along the canal in front of spermatic cord, within layers of spermatic fascia and cremasteric fascia,•If large enough, descend into the scrotum

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LEFT INGUINAL HERNIA

STRANGULATED HERNIAPatient 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?

FEMORAL HERNIAFemoral 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.

WHAT IS THIS HERNIA?

UMBILICAL HERNIAThey 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.

WHAT IS THIS HERNIA?

INCISIONAL HERNIAAn 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.

WHAT IS THIS HERNIA?

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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

Severity of LymphedemaMild 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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Factors predisposing to rupture of abdominal aorticaneurysmsx Diameter of aneurysmx Diastolic blood pressurex Chronic obstructive pulmonary diseasex Smokingx Family history of ruptured aneurysmx Expansion ratex Intrinsic biology—inflammation within the aortic wallx Thrombus free surface area of aneurysm sac

The cause of aneurysms is unclear, but the majority (90%) arethought to be due to degenerative process. Abdominal aorticaneurysms show familial clustering in 15–25% of cases. It isinferred that susceptibility to the development of abdominal aorticaneurysms is a multifactorial process with multiple genetic andenvironmental 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 ofan existing aortic graft.

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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)”

Causes of vocal cord paralysis Malignant : This accounts for 25% of

cases, one half being caused by carcinoma of lung

Causes of vocal cord paralysis

Surgical/Traumatic: (20% cases)ThyroidectomyPneumonectomyCABG Penetrating neck or chest trauma.Post intubationWhiplash injuriesPosterior fossa surgery

Causes of vocal cord paralysis Neurulogical (5-10%)

Wallenberg syndrome (lateral medullary stroke) Syringomyelia Encephalitis Parkinsons, Poliomyelitis Multiple Sclerosis Myasthenia Gravis, Guillian-Barre Diabetes

Causes of vocal cord paralysis Inflammatory:

Rheumatoid arthritis ,( really a "fixed" cord here)

Infectious: Syphilis Tuberculosis Thyroiditis Viral

Causes of vocal cord paralysis Idiopathic (20-25%):

Sarcoidosis, Lupus Polyarteritis nodosa Ortner's syndrome (left atrial hypertrophy).

Intracranial causesHead injuryCVABulbar poliomyelitis

Distinctive features

Other neurological signs and symptoms due to combined paralysis of soft palate, pharynx and larynx

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IndicationsAirway

obstruction

•eg. Tumour, bilateral vocal cord palsy

Ventilation

•long term intubation

Dead space and secretions

•weaning from ventilator, chronic lung disease

Protection of airway

•eg. Chronic aspiration

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

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