Choledochal cyst

Choledochal cyst

Choledochal cyst

¤Congenital cyst occuring in CBD
¤ manifest by 1 - 2 yrs of age
¤ TODANI classification
 type 1 - fusiform dilatation of              CBD
  type 2- lateral saccular                   diverticuli of CBD
  type 3 - Dilatation of intraduodenal segment of CBD
 type4-   Dilatation of CBD + intrahepatic biliary dilatation.
 type5 multiple intrahepatic cyst
CLINICAL FEATURES -
1. Age - children within 1-2 yrs of age
2. Common in females
3. Abdominal distention due to large cyst & cyst palpated.
4. Slow progressive laundice, recurrent attacks with abdominal pain.

INVESTIGATION -
1.USG - confirm presence of abnormal cyst
2. MRI - reveal relation between bile duct & pancreatic duct.
3. ERCP

¤TREATMENT -
  -premalignant anomaly
excision of cyst & reconstruction is treatment of choice
Type1- excision of cyst followed by Roux-en-y-hepaticojejunostomy.
 Type 2- excision of diverticulum wit suturing of CBD.
 Type 3 - endoscopic sphincterntomy is adequate
  Type 4- difficult to treat. Treated by Lilly's technique. In this technique posterior wall of byst can be left, after removal of mucosa
COMPLICATIONS -
1. Recurrent cholangitis wit high grade fever
2. Rupture of cyst
3. CBD  stones
4. Carcinoma in cyst

Cf of ca tongue

Cf of ca tongue

Cf of ca tongue

Clinical presentation_

1 bleeding ulcer.
2 pain in the tongue is due to involvent of lingual nerve.In such case,pain frm the tongue can b referred to the ear n lower temporal region.
3 Anlyloglossia is restricted mobility of tongue.It is due to infiltration of the floor of the mouth or mandible.
4 dysarticulation_ difficulty in talking is due inability to move the tongue freely.
5 dysphasia is a common presentation frm ca of post 1/3 rd .
6 foetor oris is due to infected necrotic growth.
7 bilateral massive enlargement of lower deep cervical nodes in an elderly pt is suggestive of ca of post 1/3 rd of the tongue.

Premalignant condition of ca tongue_

1 leuknplakia_causes of leukoplakia r smoking,spices,spirits,sharp tooth,sepsis,sunlight,syphilis etc.
2 erythroplakia
3 submucous fibrosis
4 papilloma of the tongue or cheek
5 chronic hyperplastic candidiasis.
6 syphilic glossitis
7 discoid lupus erythematosis
8 dyskeratosis congenita

Choleteatoma

Choleteatoma

Choleteatoma

Cholestesteatoma="Skin hn d wrong place"

it has 2 parts

a=matrgx
-made of keratinised squamous epithlm resting on d thin stroma of fibrous tissue

b=central white mass
-consisting of keratin debris produced by matrix
also caled epidermosis/keratoma

* Origin of cholestma

1=presence of congenital cell rests

2=invagination of tympanic membrne 4m d attic in form of retraction pocket=Wittmaacks theory

3=basal cell hyperplasia. The basal cels of germinal layer of skin proliferate due 2 infection=Ruedis theory

4=epithelial invasion. The epithelium 4m d meatus grows in2 middle ear through a pre-existing perforation=Habermans theory

5=metaplasia. Middle ear mucosa undergoes metaplasia due 2 repeated perforation and convert in2 squamous type=Sades theory

* Classification

1. Congenital

- arises 4m d embryonic epidermal cell
- sites: middle ear,petrous apex,cerebellopontine angle
- presents as white mass behind d intact tympanic membrane and causes conductive hearing loss

2. Acquired primary

- there is primary bcos there no history of previous otitis media/perforation
- theories :

a. invagimation of pars flaccida
- persistent -ve pressure in d attic causes a retraction pocket which accumulate keratin debris
b. basal cell hyperplasia
c. squamous metaplasia

3. Acquired secondary

- there is already pre-exisisting perforation in d pars tensa
- always asociated with d posterosuperior marginal or sometimes central perforation

- theories :

a. migration of squamous epithelium
b. metaplsia

* Expansion of cholestoma

- 4m d middle ear invade d surrounding structure and follows d path of least resistance and then enzymatic bone distruction
- attic cholstoma may extends backwards 2 aditus,antrum,mastoid, downward in2 mesotympanum and medialy surrounds d incus

* Distruction of bone

- cholstoma has d property 2 distroy bone e.g. ear occicles, bony labyrinth, canal of facial nerve, sinus plate, tegman tympani

Cervical Rib

Cervical Rib

Cervical Rib

This is an extra rib present in d neck in about 1 to 2% subject
unilateral
mostly on Rt side
it is d ant tubercle of d transverse proces of d 7th cervical vertebra whch atains excesive devlopment and result in cervical rib

¤ Types

1. Free end of d rib is expanded in2 a hard, bony mass whch can b felt in d neck
2. Complete cervical rib extend 4m c7 vertebra posteriorly 2 d manubrium ant
3. Incomplte cervical rb ir partly bony partly fibrous
4. A complete fibrous band whch gives rise 2 symptms but cant be diagnosed by x ray

¤ Clinicl features

1. Common in young females, it is congenital but symptoms apears only aftr puberty
2. Dull aching pain in d neck is causd by expanded bony emd of cervicl rib
3. Features of uper limb ishaemia
_claudication pain
_low temperature, palor, sweating, splinter hemorrhage, ischemic ulcers in finger and gangrene of d skin
4. Featurs of ulnar nerve paralysis
_paralysis of intercostal muscles, wasting of hypothenar muscles, tinglin, numbness
_it is tested by card test and froments sign
5. A hard mass may be visible or palpable in d root

¤D/D

1. Cervical spondylosis
2. Cervical disc protrusion and spinal cord tumour
3. Carpal tunnel syndrome
4. Raynauds phenomen
5. Pancost tumour

¤ Investigations

1. X ray neck

¤ Treatment

1. conservative
shouldr girdle exercises and correction of favlty posture

Ca head of pancreas

Ca head of pancreas

Ca head of pancreas

70% of the cases occurs in the head of the pancreas including periampullary region

AETIOLOGY:-

1. Tropical pancreatitis and hereditary pancreatitis r associated with pancreatic cancer such malignancies can be multifocal
2. Haemochromatosis:-produces extensive calcification of pancreas.Also a precancerous condition
3. Diabetes:-diabetic patients r 10 times more vulnerable for carcinoma of pancreas
4. Other possible aetiological factors:-alcohol and smoking:-it is related to tobacoo specific nitrosamines
 -westernization of diet:-fatty food,rich in animal proteins can cause pancreatic cancer
 -indusrial carcinogens:-B11-naphthylamine,benzidine,gasoline r the possible agents

PATHOLOGY

 -Periampullary refers to carcinoma arising from ampulla of vater,the duodenal mucosa or the lower end of the common bile duct
 -microscopically,types are:
1. Mucus secreting carcinoma of ductal origin
2. Non mucus secreting carcinoma of acinar origin
3. Anaplastic carcinoma are poorly differentiated and tend to arise from the body of the pancreas
4. Cystadenocarcinomas are rare,slow growing and tend to attain a large size

CLINICAL FEATURES

1. Age: 50-70 years
2. Sex: comon in both sexes equally
3. Duration of symptoms: short duration( 1-3 months)
4. Symptoms:
 -pain: there may be some discomfort in abdomen but colicky pain is not a feature.Pain is relatively rare in carcinoma head of pancreas
 -fever: when obstruction becomes severe,there is bile stasis.Cholangitis,fever with cills and rigors can occur
 -jaundice: as a result of slow developing obstruction at periampullary region,jaundice is persistent,progressive,painless,pruritic,in 5% of cases growh may ulberate into the duodenum.It can cause melaena and jaundice may temporarily subside.
 -stools: clay coloured stools are common and when mixed with blood it is called silvery stools or aluminium paint stools
 -pruritus: severe due to bile salts in the circulation
 -loss of appetite: significant
 -loss of weight
5. Signs
 -jaundice: sometimes greenish yellow
 -anaemia: it is usually present
6. Per abdomen
 -liver can be enlarged due to back pressure.If it is nodular,with sharp border,hard in consistency,it is due to secondaries in liver
7. Gall bladder
 -gall bladder is palpable in 70-75% cases
8. Metastasis
 -left supraclauicular node,ascites etc.

D/d:

1. Carcinoma stomach
 such mass may not be mobile.It does not move with respiration because it is fixed to pancreas
 -these patients will have vomiting first followed by backache at a later date
2. Ca transverse colon
 -produces constipation and bleeding per rectum.Vertical mobility may be present.
 -right to left peristalsis may be present
3. Para aortic lymph mass may be due to
 -intra abdominal malignancies,lymphoma,testicular tumor etc

invest

1. Hb% is low in malignancy
2. BT,CT,PT r altered
3. Urine for urobilinogen is negative
4. Serum alkaline phosphatase: increased >500 units
5. Abdominal usg: it is most useful,noninvasive,reliable and quick investigation for obstructive jaundice
 -dilated biliary radicles,both intrahepatic n extrahepatic can be demonstrated
 -stones can be diagnosed with their postier acoustic shadow
 -mass lesion in the head region can be made out in cases of chronic pancreatis or ca head of the pancreas causing obstructive jaundice
7. CT scan:-
8. Endoscopy:-useful to diagose a periampullary carcinoma which may be seen as an ulcerative lesion in the 2nd part of the duodenum,biopsy can also be taken which shows adenocarcinoma
9. Barium meal:
 distortion of the medial border of the duodenum giving rise to inverted 3 sign
 -in ca head of the pancreas there may be widening of C loop of deodenum -Pad sign
10. ERCP ( Endoscopic Retrograde Cholangio Pancreatography)

TREATMENT

surgical treatment

 1. Radical pancreaticoduodenectomy -"whipple's operation"
 -in this operation growth along with 'C' loop of duodenum upto DJ flexure,removal of the head of pancreas upto the neck n partial gastrectomy is done followed by
-pancreaticojejunal anastomosis,gastrojejunostomy n choledochojejunostomy
 2. Pylous preserving pancreaticoduodenectomy PPPD
 in this operation,pylorus is preserved. Thus ,gastric motility is not disturbed
 3. Triple bypass: cholecystojejunostomy +enteroenterostomy +gastrojejunostomy
 this is a palliative surgery in which distended gall bladder is anastomosed to a long loop of jejunum to relieve jaundice.To prevent food particles entering into the gall bladder,enteroenterostomy is done.

Non surgical treatment

 -very elderly patients who r not fit candidates for surgery n patents who have metastasis can be treated by palliative stenting.Howerver,results of a surgical bypass is superor to stenting

Caldwel luc operation

Caldwel luc operation

Caldwel luc operation

Caldwel luc operation is .process of opening maxillary antrum through canine fossa by sublabial approach and dealing with the pathalogy inside antrum

indications  

1. Chronic maxillary sinusitis with changes in sinus mucosa
2.Removal of foreign bodies or root of tooth
3.Dental cyst
4 oroantral fistula
5. Suspected neoplasm
6  recurrent antrochoanal polyp
7 fracture of maxilla
8 approach to ethmoids
9 approach to pterigopalatine fossa

contraindications

patient below 17 yrs age

Anasthesia

general anasthesia with cuffed endotracheal tube and  a pharyngeal pack
local anasthesia can be done

position

reclining with head end of tabel raised . Patient lies supine with  face turned

Technique

1. Incisison
a horizontal incision with its end upward is made below gingivolabial sulcus from lateral incisor to 2nd molar it cuts through mucous membrane and periosteum

2 .Elevation of flap
mucoperiosteal flap is raised from the canines fossa to infraorbital nerve

3. Opening the antrum
using cutting burr hole is in antrum

4 Dealing with pathology
after opening maxillary antrum pathology is removed with elavator and foreceps

5 Making nasoantral window
a curved haemostat is pushed into antrum from inferior meatus
and then opening enlarged with kerrisons and sidebiting foreceps

6. Packing the antrum
ribbon guaze impregnated with liqid parrafin can be packed in antrum and its end brought out from nasoantral window into nose  Intrasinus packing is done if there is severe bleeding

7. Closure of wound
sublabial incision is closed with  catgut sutures

post operative care

1 . Ice packs over cheek in first 24 hours prevent odema haematoma
2  packing in sinus and nose can be removed in 24 to 48 hrs
3antibiotics are given for 5 tn 7 days
4  patient should avoid blowing his nose to avoid surgical emphyesema

complications

1 Post operative bleeding
2 injury to nasolacrimal duct
3 sublabial fistula
4 osteomylitis of maxilla
5 anasthesia of teeth
6 anasthesia of cheek due stretching  of  infraorbital nerve

Caput succedaneum

Caput succedaneum

Caput succedaneum

It is the formation of swelling due to stagnation of fluids in the layers of scalp beneath the girdle of contact.
  Girdle of contact may be bony or dilating cervix or vulval ring.
Swelling is diffuse baggy & not limited by the suture lines
mechanism-when head descend to press over the dilating cervix the overlying scalp is free of pressure  but the tissue in contact with the full circumference of the girdle of contact is compressed.This interference with the venous return & lymphatic drainage from unsupported area of scalp leads to stagnation of fluid & appearance of swelling in the scalp .
 It usually occurs after the rupture of membranes.

Importance=

1>it signifies static position of head for a long period of time.
2>location of it gives idea about position of head occupied in the pelvis & the degree of flexion achieved.With increasing flexion caput is placed more posteriorly.      

Candidiasis

Candidiasis

Candidiasis

CANDIDIASIS= 

1- candida albicans is causative organism. It causes following conditions=   1- oral thrush- condition tht favour oral candida infection.. 2-cutaneous candidiasis..3- chr. mucocutaneous candidiasis..4-oesophageal candidiasis...5-candidiasis of urinary tract.,6-hametogenous dissemination...

TREATMENT=

 1- topical application antifungal agents like nystatin, clotrimazole.. 2- swallowing nystatin suspension or sucking on clotrimazole torches for oesophageal candidiasis.. 3-systemical antifungal agent ketoconazole 200-400 mg/day, fluconazole 200 mg/day.  4-for oesophageal candidiasis therapy expended for 3 wks to 2wks aftes symptoms suaside..5-severe systemic infection require amphotericin B. 

Ca rectum treatment

Ca rectum treatment

# Carcinoma upper 1/3rd of rectum

@  High anterior resection includes removal growth with nodes followed by colorectal anastomosis
@ treatment of choice when growth is situated between 11 to 15cm from anal verge
@ this is sphincter saving surgery

# ca of lower 1/3 of rectum

@ growth within 7cm 4o anal verge
@ abdomino perineal resection
- pt put in Lloyd Davis position [supine with lithotomy]
- 2 surgeons operate simultaneously 1 from abd m one 4m perineum
- abdomen opened 1st growth mobilised 4m sacrum n bladder
- at this stage anus is kept close by perineal surgeon
- rectum n anal canal mobilised
- following structures removed
1 entire rectum m anal canal , 2 fascia propria with papa rectal nodes
3  2/3rd of sigmoid colon n mesocolon with lymphatic n LN
4. Muscle n peritoneum of pelvic floor
5. Wide area of perianal skin with part of ischiorectaj fossa
- this followed by permanent do colostomy by bringing out sigmoid colon outside in left iliac fossa
- it is sphincter sacrificing surgery

@ local excision

mobile tumors < 4cm, less than 40% of rectal wall involvement , located within 6cm of anal verge, lesion should be T1 or T2, no vascular or lymphatic or nodal invasion

# ca middle 1/3rd rectum

@ refers to growth between 7to 11 cm from anal verge
@ APR or low anterior resection can be done
@ in cases of well diff ca 2cm margin n in anaplastic ca 5cm margin clearance necessary

# Hartmann's operation

#Radiotherapy

@ rectal cancers r more radiosensitive  and colonic r more chemo sensitive
@ neutron beam radiation 4000-5000 cGy units
@ pre op radiotherapy when tumor extended thro wall
@ post op 2 reduce recurrence
@ Papillon's intra cavity radiation indicated 4 small localised n exophytic ca as curative therapy

# Chemotherapy

1] inj 5 FU 475mg/m2/daw IV into 5 dayp with inj leucovorhn 30mg/day for 5 days. 3 such courses
2] inj 5 FU with levamisole 150 mg BD for 3 days once in 15 days for 1 yr

Ca rectum

Ca rectum

Ca rectum

Aetiipahogenesis:

- SAD factors
    Smoking
    Alcohol
    Dietary
- diet rich in red meat has high aminal fat which is responsible for formn of carcinogenic polycyclic aromatic compounds
- colecystectomy- increase in free bile acid conc
- genetic factors

Prrcancerous condns:

- polyps in FAP
- villous adenoma
- ulcerative colitis and cohns dis

Pathological types

- annular-- common at the rectosigmoid jucn, presents with constipation and obstruction, takes abt 12 months for grow to encircle the lumen (napkin ring)
- polypoidal-- common in ampula
- ulcerative-- occures nywhere, hs raised edges and growth occures in transverse direcn
- diffuse-- similar to lininis plastica, develops frm ulcerative colitis, worst prognosis
- colloid-- contents r gelatenous, seen in youngs

C/f

1) constipation requiring incresed dose of pergatives
2) bleeding per rectum--frank blood or mixed with stool, it is never massive, is painless, and is the earliest symptom
3) early morning spurious diarrhoa due to accumulation of mucus overnight ina the ampulla, causes an urgency to pass stools bt results in onlly mucus with minimum stools, thr is always a sence  of incomplete defication
4) tenesmus-- painful incomplete defication asso with bleeding
5) bloody slime-- attempt at defecation results in mucucs mixd with blood
6) loss of apetite, loss of wt due to liver secondaries and abdominal disyension r late features

On exam:

- done in every case of bleeding per rectum
- indurated colinflower like growth or infiltrative ulcer cn b felt
- finger stained with blood
- rectal ca presenting as fistula in ano is equivalent to perforated colon ca, is a bad prognostic sign

DDs

- proctitis
- solitary rectal ulcer syndrome

Spread:

1) local:
    Involves muscle coat and spreads into extrarectal tissue, anteriorly involves prostate seminal vessicals and bladder base in males, and vagina nd uterus in females. Posteriorly sacral plexus
2) lymphatic:
   Frm the upper and middle onethird, spreads upwards first to pararecatl nodes of gerota.
  Frm lowe 1/3 spreads laterally and can involve internal illiac nodes
3) blood spread
 - occures in lung and liver
4) peritoneal spread
 - results in ascitis, malignant nodules

Investigations

-proctoscopy
- signoidoscopy
- barium enema
- colonoscopy
- carcino embryonic antigen levels
- ultrasound for sec
- endorectal ultrasonography
-CT scan

Treatment

# Carcinoma upper 1/3rd of rectum

@  High anterior resection includes removal growth with nodes followed by colorectal anastomosis
@ treatment of choice when growth is situated between 11 to 15cm from anal verge
@ this is sphincter saving surgery

# ca of lower 1/3 of rectum

@ growth within 7cm 4o anal verge
@ abdomino perineal resection
- pt put in Lloyd Davis position [supine with lithotomy]
- 2 surgeons operate simultaneously 1 from abd m one 4m perineum
- abdomen opened 1st growth mobilised 4m sacrum n bladder
- at this stage anus is kept close by perineal surgeon
- rectum n anal canal mobilised
- following structures removed
1 entire rectum m anal canal , 2 fascia propria with papa rectal nodes
3  2/3rd of sigmoid colon n mesocolon with lymphatic n LN
4. Muscle n peritoneum of pelvic floor
5. Wide area of perianal skin with part of ischiorectaj fossa
- this followed by permanent do colostomy by bringing out sigmoid colon outside in left iliac fossa
- it is sphincter sacrificing surgery

@ local excision

mobile tumors < 4cm, less than 40% of rectal wall involvement , located within 6cm of anal verge, lesion should be T1 or T2, no vascular or lymphatic or nodal invasion

# ca middle 1/3rd rectum

@ refers to growth between 7to 11 cm from anal verge
@ APR or low anterior resection can be done
@ in cases of well diff ca 2cm margin n in anaplastic ca 5cm margin clearance necessary

# Hartmann's operation

#Radiotherapy

@ rectal cancers r more radiosensitive  and colonic r more chemo sensitive
@ neutron beam radiation 4000-5000 cGy units
@ pre op radiotherapy when tumor extended thro wall
@ post op 2 reduce recurrence
@ Papillon's intra cavity radiation indicated 4 small localised n exophytic ca as curative therapy

# Chemotherapy

1] inj 5 FU 475mg/m2/daw IV into 5 dayp with inj leucovorhn 30mg/day for 5 days. 3 such courses
2] inj 5 FU with levamisole 150 mg BD for 3 days once in 15 days for 1 yr

Ca penis

Ca penis

Ca penis

Etiology

Circumcision soon after birth confess almost complete immunity against carcinoma of the penis.later circum. does not seem to have d same effect.chronic balanoposthitis is known to b a contributory factor,there r different precarcinomatous states-
-leucoplakia of d glans
-long standing genital warts
-pagets disease of penis is persistent rawness of the glans lik a longstanding balinitis followed by cancer of penis.

Pathology

Carcinoma of the penis may be flat and infiltrating or papillary.it can start as leukoplakia.d earliest lymphatic spread is to the inguinal and then to iliac nodes.once the growth breaches the partial barrier formed by fascial sheath of Corpora cavernosa it spreads rapidly and iliac lymph node involvement is common

C/f

-forty percent patients are under 40 years of age.
-initially discomfort and light discharge
-foul bloody discharge and little or on pain.
-sixty percent have inguinal lymph node enlargement when they present
-prepuce is non retractile
-untreated the whole glans may b replaced by a fungating offensive mass.

Treatment

-radiotherapy is effective (60-70% survival at 5years) if the growth is small.circumcision precedes treatment which may b delivered by implanted radioactive tantalum wires,external beam radiation or by means of radio.mould applicator applied to penis

-surgery is needed if there is infiltration of shaft n when radiotherapy fails.partial amputation used for distal growths.when an advanced infijtrating or anaplastic lesion present total ampu is necessary.

-block dissection of enlarged lymph nodes.  

Ca stomach

Ca stomach

Ca stomach

Etio

1) Environmntl & dietary factrs

-incidnc incresd in persons who consum red meat, cabbage, spices, spirits, saltfish etc
-smoked salmon fish ws rsponsbl for incresd incidnc, probably relatd 2 releas of polycyclic hydrocarbons & aromatic amino acids
-smoking, spicy food & alcohol takn ovr a period of many yrs produc chronic gastritis whch may change in2 Ca stomch

2) Precancerous conditions

i)Atrophic gastritis
due 2 smoking, continuos ingestion of drugs, reflux of bile in2 stomach etc
ii)Pernicious anaemia
incresd risk 4to6 tims more
it caures atrophic gastritis & precipitats Ca stomach fundus
iii)pts wid hypogamaglobulinemia 50fold r @ risk
iv) H. pylori infn results in atrophic gastritis, folowd by intestinal typ of gastric mucosa, den metaplasia, den dysplasia. Eventuly leads 2 intestinl typ of gastric cancer
v)TypeA gastritis predispos 2 proximl Ca stomach
TypeB gastritis predispos 2 distl Ca stomach
vi)Adenomatous polyps whch ocur in antrum hav highest risk of malignant transformation
vii)Menetrier's diseas is protein losing enteropathy, along wid giant hypertrophy of gastric mucosal folds. It is a precancerous condition
viii)Gastric ulcer benign
ix)Previous GJ / gastric resection predisposes aftr a period of 15-20yrs

3)Genetic & familial factors

-can run in families, hwevr only 10% of pts giv family H/O Ca stomach
-Ca stomch more comon in bld grup A pts

PATHOLOGY & PATHO TYPE

A) Gross types

i. Cauliflowr like growth wid friable tisue
ii. Infiltrativ lesion wid dense submucosal fibrosis whch convert stomach in2 a small, contracted, functionless stomch i.e Linitis Plastica / Leather Bottle Stomach
iii. Ulcerativ wid clasicl evrted edges wid central slough
iv. Ulcer cancer refers 2 carcinoma arising in a pre-existing gastric ulcer
v. Colloid carcinoma- malignant cels sepratd by colloid material

B) Depending on depth of invasion

1)Early Gastric Cancer- Cancer limitd 2 mucosa & submucosa wid/widout lymph node invo(T1 & N) represented as Japanese Clasificn
Type I protruding
Type IIa elevated superficial
Type IIb flat superfial
Type IIc depressd superficial
Type III & IIc excavated

Criticism for early gastric cancer- node negativ early gastic cancer is more dan 95%

2)Advancd gastric cancer
refers 2 involv of muscularis mucosa &/or serosa wid/widout invo of lymph nodes
Borrmann's classn
Type I single polypoidal Ca
Type II uleroproliferativ
Type III ulcerativ
Type IV difuse Ca

C/F

very often pts wud hav vague symptoms- early satiety, flaulence, discomfort, pain upper abdo
1)Silent growth but manifests as secondaries in liver, ascites, Virchow's node etc
2)Obstructn @ pyloric antrum wid featurs of vomiting wid/widout bld
3)Lump in abdo whch is hard & iregular
4)Insidious in onset- anaemia, anorexia, asthenia of short duration
5)Dyspepsia in man ovr age of 40
Featurs of stomch mass
i)stomch moves wid respi
ii)upper border of stomach mass cn b mad out
iii)anatomicl location of mass- rt hypochondrium in a pyloric mass, epigastrium & lt hypochondrium in a mass arising 4m body of stomch
iv)knee elbow position- mass does fall forwards unles fixd
v)mass may hav intrinsic mobility

SPREAD

1)Penetration of gastric serosa- dis is d most imp prognostic indicator. Wen serosa is not penetrated 50% surviv for 5yr aftr resectn
2)Lymphatic spread
lymph nod invo is a poor progno indicator
invo of 4/more nodes is less favourabl
**Lymphatic Zones
lymphatic drainag 4m stomch clasified in2 4 zones
Zone1- in gastrocolic omentum along rt gastroepiploic vessels, dis drains pyloric antrum & lowr half of greater curvature
Zone2- lies in gastroepiploic omentum & gastrosplenic ligament along lt gastroepiploic vessels. Dis drains uper half of greater curvature
Zone3- lies in lesser omentum draining proximl 2/3rd of stomch. 4m here lymph drains in2 perioesophageal LN
Zone4- 4m distal portion of lesser curve & pylorus along hepatic artery & rt gastric artery in2 para aortic nodes
3)Bld spread
most comon sites r liver & lungs, produces extensiv secondaries. Dey r signs of inoperability
4)Transcoelomic spread
results in ascites, Krukenberg Tumor-bilat bulky ovarian deposits & rectovesicl deposits

INVEST

1)complete bld pictur
20% pts of early gastric Ca hav anaemia, iron defi- microcytic
2)routine examn, fasting & postprandial sugars, ECG, renal function for fitness b4 surgry
3)Videoendoscopy
to knw extent of lesion
to confirm diagno
to take 6 quadrant biopsy
4)Ultrasound, CT, MRI
to rule out secöndaries in liver
to look for enlargd coeliac nodes
ascites can b demonstrtd
to detect Krukenberg tumor
useful to detect metastasis
5)Endoscopic USG
differentiat early gastric Ca 4m advncd tumors in 80% of pts
6)Barium meal may show intrinsic, persistent, iregulr, filling defect. Useful in Linitis Plastica study

TNM STAGING

T : Primary tumor
T0 : no evidence of prim tumor
Tis : Ca in situ
T1 : invasion of lamina propria / submucosa
T2 : invasion of muscularis propria / subserosa
T3 : penetration of serosa
T4 : invasion of adjacent structurs

N : Lymph nodes
N0 : no regionl LN
N1 : 1-6 LN positiv for maligncy
N2 : 7-15 LN positiv
N3 : more dan 15 LN

M : Metastasis
M0 : no distant metastasis
M1 : distant metastasis presnt

HISTOPATH

it is an adenoCa of stomch. Basicly 2 typs of gastric Ca as per Lauren's classn, also calld D.I.O. classn
D- Difuse more comon in young, females, & poor prognosis
I- Intestinl more comon in eldrly males, shows areas of intestinl metaplasia, better prognosis
O- Others mixd lesions leather bottle stomch or linitis plastica is poorly diffrentiatd wid anaplastic cels

Rx

Surgery is main modality of Rx

1)Curative resections

i)Ca of pyloric antrum & body of stomch
radical subtotal gastrectomy whch includs removl of 60-70% of stomch wid greater omentum along wid enlargd LN folowd by GJ anastomo
ii)Ca of fundus
oesophago-gastrectomy, in whch removl of uper part of stomch, lowr end of osophagus, wid regionl LN, spleen, folowd by oesophagogastric anasto or oesophagojejunl anasto
iii)difuse grwth(linitis plastica)
radicl total gastrectomy folowd by oesophagojejunostomy

2)Palliativ surgery

i)Ca pyloric antrum inoperable- palliativ ant GJ is done 2 relieve vomiting, by anastomosing a jejunal loop 2 stomch in prepyloric region
ii)Palliativ gastrectomy to get rid of ulceratd, necrotic / bleeding lesion

3)Chemotherapy

partialy responds
in abt 30% cases givn @ advncd stage
Inj. 5-FU(Flurouracil) 500mg IV daily for 5 days evry 28 days
*Mech of action- it is an antimetabolite & acts by interfering wid DNA synthesis
-Combn of 5FU wid adriamycin, mitomycin, cisplastin tried but more toxic
FAM & ECF r popular drugs
-Intraperitöneal mitomycin & mitomycin C-impregnated charcol also usd

Ca larynx

Ca larynx

Ca larynx

Aetiology:

@ male preprondrance (10:1)
@ age: 40 to 70 yrs
@ tobacco alcohol: cigarrette smoke contains benzopyrine and other hydrocarbons
@ previous radiation to neck for benign lesions or laryngeal papilloma
@ genetic factor: familial laryngeal malignancy
@ occupational exposure to asbestose, mustard gas and petrolium products

CLASSIFICATION OF SITE AND VARIOUS SUBSITES UNDER EACH SITE IN LARYNX

A) SUPRAGLOTIS:
i) lingual and laryngeal surfaces of suprahyoid epiglottis
ii) infrahyoid epiglottis
iii) aryepiglottic folds
iv) arytenoids
v) ventricular bands
B) GLOTTIS
   true vocal chords (ant and post. commissure)
C) SUBGLOTTIS
   upto lower border of cricoid cartilage

TNM CLASSIFICATION

A) Supraglottis:

T1: tumour limited to one subsite with normal vocal chord mobility
T2: Tumour invades mucosa more than one adjuscent subsite of supraglottis or glottis or region outside sgtis (mucosa of base of tounge vallecula medial wall of pyriform sinus) without fixation of larynx
T3: Limited to larynx with vocal chord fixation and or invades- portcricoid area, preepiglottic tissues paraglottic space and minor thyroid cartilage.
T4a: Invades through thyroid cartilage and or invades tissue beyond larynx (trachea strap muscles thyroid or oesophagus)
T4b: Invades prevertibral space encases carotid artery or mediastenal structures

B) GLOTTIS

T1: limited to vocal chord with normal mobility
T1a: limited to 1 vocal chord
T1b: both
T2: extends to supraglottis and or subglottis and or with vocal chord mobility
T3: lmtd to lx with vocal chord fixation and or invades paraglottic space and or minor thyoid cart. erosion
T4a: invds thyroid cart. and or invds tissues beyond lx
T4b: Invades prevertibral space encases carotid artery or mediastenal structures

C) SUBGLOTTIS

T1: lmtd to subglottis
T2: extends to vocal chord with normal mobility
T3: lmtd to lx with vocal cord fixn
T4a: invds cricoid or thyroid cart. and or invds tissues beyond lx
T4b: Invades prevertibral space encases carotid artery or mediastenal structures

Regional lymph nodes(LN)

Nx: LN cnt b assessed
No: no regional LN metastasis
N1: metastasis in single epsilateral LN. 3 cm or less in greatest dimension
N2a: metastasis in single epsilateral LN. more than 3 cm bt less than 6 cm in greatest dimension
N2b: metastasis in multiple epsilateral LN. none more than 6 cm in greatest dimension
N2c: metastasis in bilateral or quantralateral LNs. none more than 6 cm in greatest dimension
N3: metastasis in LN more than 6 cm in greatest dimension

Distant metastasis:(M)

Mx: distant metastasis cnt b assessed
Mo: no distant metastasis
M1: distant metastasis

VOCAL REHABILITATION AFTER TOTAL LARYNGECTOMY

i) oesoqhageal speach:
   pt. taught 2 swallow air and hold it in upper oesophagus and then slowly ejject it into pharyx
ii) artificial laryx:
  a) electrolarynx
  b) transoral pneumatic device
iii) tracheo-oesophageal speach
    an attepmt is made to carry air frm trachea to oesoqgus or hypopharynx by d creation of skin lined fistula or by basement of an artificial prosthesis
    artificial prosthesis:
a) Blom-Singer prosthesis
b) Panje prosthesis

Ca cervix

Ca cervix

Ca cervix:

    Most common genital ca.

AETIOLOGY:

1) Age 35-45 yrs
2) sexual intercourse b4 18 yrs of age.
3) multiple sexual partners
4) 1st baby b4 age of 20 yrs
5) multiparity
6) poor personal hygiene
7) poor socio-economic status
8) exposure to smegma from uncircumcised partner.
9) smoking
10) infections like STD, HIV infection, herpes, HPV
11) immunosuppresion
12) preinvasive lesions
13) COC and progesteron use over 8 yrs or more
14) diethylstilboesterol exposure

PATHOLOGY:

 Two types of cancer of cx.

  1) epidermoid ca (80%): arises frm stratified squamous epithelium
  2) endocervical ca (20%): arises frm mucous membrane of endocervical canal.
95% ca are squmous Ca only 5% are adenocarcinomas.

CLINICAL FEATURES:

Symptoms:

1) irregular menses
2) menometrorrhagia
3) continuous bleeding, postcoital bleeding
4) leucorrhoea, blood stained discharge

Signs:

1) cx reveals growth or ulceration which bleeds on touch
2) bulky uterus due to pyometra in adv stage
3) rectal examination reveals induration of uterosacral ligaments
4) biopsy reveals:
    A) alterd morphology
    B) nuclear: cytoplamic ratio is increased
    C) hyperchromatism
    D) thickening of nuclear memb
    E) clumping of cromatin material
    F) leaking of cancer cells into stroma (evident of cellular infiltration)

DDs:

*tubercular or syphilitic ulcer
*polypus
*sarcoma of cx

STAGING:

STAGE 1~~CA CONFINED TO CX
 * 1A ~ microinvasive ca
 * 1A1 ~ measured stromal invasion of less than 3.0mm in depth and less than 7.0 mm in horizontal spred
 * 1A2 ~ measured stromal invasion bet. 3 and 5 mm in depth and not exceeding 7 mm in horizontal spred
 * 1B ~ clinically visible lesion
 * 1B1 ~ clinically visible lesion 4cmor less in size
 * 1B2 ~ clinically visible lesion more than 4 cm in size

STAGE 2~~cancer spred beyond the cervix but not to pelvic wall or third of the vagina
  2A ~~tumour without parametrial invasion
  2B~~tumour with parametrial invasion

STAGE 3~~tumour exceeds lateral pelvic wall . Involves lower third of vagina
 3A ~~tumour involves the lower third of the vagina  no extention to lateral wall
 3B ~~tumour extends to the pelvic wall and or involves kidney

STAGE 4 tumour spreds ty the pelvic organ or distal metastatis
 4A ~~tumour involves bladder or rectum or spreds beyond the true pelvis
 4B ~~widespred tumour with distal metastatis

Δ DIAGNOSIS:

Investigations:

 * routine investigations like,
Haemogram, urine analysis, blood sugar, LFT, RFT, serum electrolytes, ABO and Rh grouping, pylography, cystography, ECG etc.
* CT and MRI : these techniqes offer imroved imaging and staging and ca can be detected in early stages
* positron emission tomography (PET): detects tissue biochemical changes
*FDG-PET using F-18 fluro-2-deoxy-D-glucose:
  Useful in determination of primary rx, lymph node detection and local reccurence detection.

TREATMENT:

Stage IA1:
* conization with clear margin is adequate.
* Hysterectomy may be suggested in elderly or parous women.
* lymphadenectomy is not required
* lifelong follow up is necessary

Stage IA2:
* extended hysterectomy and lymph node sampling (if growth < 2cm)
* postoperative radiotherapy is required in nodal involvement
* conservative rx comprises of laproscopic lymphadenectomy followed by vaginal trachelectomy-- consist of 80% removal of cx, upper vagina and Mackenrodt's ligaments. Done in women desirous of childbearing. 30-40% success.

Stage IB and IIA:
* Wertheim's hysterectomy:  comprises of removal of entire uterus, both adnexa,pelvic LNs, medial one-third of parametrium, upper one-third of vagina, sacral glands r spared. Overies may be retaind.
* Schauta's operation: consists of removal of entire uterus, adnexa, most of vagina, medial part of parametrium. Later it is followed by extraperitoneal lymphadenectomy. PO radiotherapy may b given.
* Radiotheray: surgical and radiotherapy combined incrases the morbidity in the woman. It consists of brachytherapy followed external radiation
* Combined therapy: required in,
   Postoperative radiotherapy in LN metastasis
   Preoperative chemoradiotherapy in endocevical ca.--- Neoadjuvant paclitaxel 90 mg and inj ifosfamide 2000 plus mesna 400 mg wkly for 3 cycles.
Cisplatine 50 mg wkly aft surgery

Stages IIB, III and IV:

Chenoradiotherapy to extend life.

Ca breast etiology

Ca breast etiology

Ca breast etiology

Atiologcal factor_

1 it is rare below the age of20.The highest incidence is found bet 40-60 yrs of age.
2 breast ca. N syndrme-
a Li-fraumeni syndrome
b cowden disease
c ataxia telangiectasia.
3 chromosomal abnormalities hv been found in short arm of chromosome 17 in women with a family history of ca breast.BRCA-1 n BRCA-2 r the genes associated increased risk.
4 Diet-increased risk has bee found in postmenopausal wome n is due to increase synthesis of oestrogen in the body fat.Alcohol intake is associated with 1.5 increased risk of ca breast.Vit C may hv protective value.Increase intake of saturated fats n reuduce intake of phytooestroge increases risk.
5 endocrine cause_
a longer the cumulative period of menstruation more the risk
b more the cumulative period of lactation better the protection.
C  more abortions n each occurin later increases risk.
D more oestrogen content in OCP n OCP taken early in the reproductive life increases risk.
E  HRT increases risk if the oestrogen content is higher n if taken for more than 5 yrs.
6 female sex itself is a risk factor .
7 Geogrophical_
ca breast is a disease of white,western women. It is rare in Japan n Taiwan.
Structure remove in patey mastectomy_
entire breast including areaola n nipple r removed with pectoralis minor followed by axillary block dissection.

Ca bladder

Ca bladder

Ca bladder

Aetiology

@  occupation : anniline dye workers leather industry worker, paint industry n rubber industry workers
@ bilharziasis or schistosomiasis - squamous cell ca
@ chronic irritation by stones catheter : 95% of tumors originate in mucus membrane
@ chronic smoking
@ cyclophosphamide

# Pathology

1 Malignant villous tumors
@ they r transitional cell type
- villi r stunted swollen n resemble cauliflower
- can b sessile - high grade
- bladder wall more vascular
2 solid tumors are always malignant
3 carcinomatous ulcer arises in leukoplakia

# Histological types

@ transitional - 90%
@ squamous cell
@ adenocarcinoma arises 4m urachal remnants n urethral  glands
@ mixed variety
@ undifferentiated

C/F

1 painless intermittent haematuria
2 severe cystitis like symp occur in carcinomatous ulcer
3 later painful micturition
4 strangury painful micturition with bleeding n incomplete emptying of bladder
5 loin pain due 2 ureteric obstruction with hydronephrosis
6 surpapubic pain n groin pain n perineal pain due 2 nerve infiltration

Investigations

1 urine: cytology  of 3hour specimen

2 IVP: filling defect in bladder dilataton of ureter

3 USG : can detect blades ca n liver metastasis

4 CT : investigation of choice to know spread of disease - to know infiltration of muscle, perivesical tissue, n prostate n pelvic wall

5 cystoscopy : indications
haematuria with normal IVP and howes urinary tract symptom and malignant cells in urine cytology

6 Bimanual palpation rectoabdominally  in males n vaginoabdominally in females under GA

Staging

TNM
 Tis tumor insitu
 Ta - involving mucosa without invading lamina propria
 T1 - involving mucosa lamina propria n sub mucosa
 T2 - muscle layer
 T3a - muscle layer total thickness
 T3b - extendin 2 perivesical eat / peritoneum n adjacent organs
 T4 - rectum n prostate inv
 N0 - no lymph nodes
 N1 - nodal metastasis
 M0 - no distant metastasis
 M1 - distant met

Jewett Strong n Marshall staging

1 superficial/ non invasive
2 infiltrating / invasive
3 ca in situ

Rx

1 Tis Ta T1
a) transurethral resection of tumor
b) post operative intra vesical chemotherapy with thiotepa adriamycin n mitomycin retained inside bladder 4 1hour such 6 to 8 courses at weekly
c) BCG / interferon immunotherapy intravesically

2) T2 to T4
 Radical cystectomy : [removal of bladder with pericystic eat n prostate n seminal vesicles in both plus
 urethra in men n cervix uterus n ant vaginal vault n ovaries in women]
 followed by systemic chemotherapy
MVAC - Mtx, vinblastin, adriamycin, cisplatin

3] any T N1 M0 / any T N0 M1
systemic chemotherapy MVAC

4] small lesion involving muscle in vault of bladder partial cystectomy with growth margin 2 to 3 cm  followed  by intra vesical chemoth

5] radiotherapy
@ local
if lesion not anaplastic is 4cm / less after open diathermy excision  radio therapy given
@ deep x ray therapy
in un differentiated ca by using cobalt 60 / linear accelarator

Ca Maxilla

Ca Maxilla

Ca Maxilla

AETIOLOGY

1.Worker in hardwood  furniture industry nickel refining, leather work and manufacture of mustard gas have shown higher incidence of sinunasal cancer
2.Commn in bantus of south africa where locally made snuff is used which is rich in nickel and chromium .
3. Worker of furniture industry

Disease is common in 40-60 age group with preponderance in male .

CLINICAL FEATURES

early features of maxillary sinus malignancy are
1. nasal stiffiness
2.Blood stained nasal discharge
3.Facial paraesthesias or pain and epiphora

DIRECTIN OF SPREAD AND EXTENT OF GROWTH

1.Medial spread to nasal cavity gives rise to nasal obstruction, discharge and epistaxis.
2.Anterior spread  cause swelling of the cheek and later invasion of the facial skin.
3.Inferior spread causes expansion of alveolus with dental pain ,loosening of teeth ,poor fitting of dentures. Ulceration of gingiva  and swelling in the hard palate .
4.Superior spread : invades the orbit causing proptosis ,diplopia,occular pain and epiphora.
5.Posterior spread ir into pterygomaxhllary fossa ,pterygoid plates and the musckes causing trismus. Growth may also spread to the nasopharynx,sphenoid sinus and base of skull
6.Intracranial spread
to ethmoid ,cribriform plate or foramen or foramen lacerum
7.Lymphatic spread  occur in the late stage of disease .
Submandibular and upper jugular nodes are enlarged .Maxillary and ethmoid sinuses drain primarily into retropharyngeal nodes, but these nodes are inaccessible to palpation.
8.Systemic metastases
 may be seen in the lungs and occasionally in bone

CLASSIFICATION

A] Ohngren's clas.
An imaginary line is drawn extending between medial canthus of eye & angle of mandible.
Growths situated above this plane have a poorer prognosis.

B] Lederman's clas.

It uses two lines horizontal lines of Sebileau one passing through the floors of orbits & d other through floors of antra. There r 3 parts.
1. Suprastructure. Ethmoid, sphenoid & frontal sinuses & olfactory area
2. Mesostructure. Maxillary sinus & respiratory part of nose.
3. Infrastructure. Containing alveolar process.
Vertical lines extending down d medial walls of orbit to separate ethmoid sinuses & nasal fossa fm d maxillary sinuses.

C] American Joint Committee on Cancer(AJCC) clas.

Used only 4 squamous cell carcinoma. Histopathologically it is graded as
1. Well differentiated
2. Moderately diff.
3. Poorly diff.

D] TNM Clas. & staging system.

Maxillary sinus
T1
tumor limited to maxillary sinus mucosa with no erosion or destruction of bone.
T2
tumor cousing bone erosion or destruction including extension into d hard palate & or middle nasal meatus, except extension to post. wall of maxillary sinus and pterygoid plates
T3
tumor invades any one of following. Bone of post. wall of maxillary sinus, subcutaneous tissues, floor or medial wall of orbit, pterygoid fossa & ethmoid sinuses
T4a
tumor invades ant. orbital contents, skin of cheek, pterygoid plates, infratemporal fossa, cribriform plate, sphenoid or frontal sinuses
T4b
tumor invades any of d following: orbital apex, dura, brain, middle cranial fossa, brain, cranial nerves other than maxillary division of trigeminal, nasopharynx or clivus.

Regional Lymph nodes( N )
Nx
minimum criteria of assessment cannot be met with.
No
No regional LN metastasis
N1
Metastasis in a single ipsilateral LN, 3cm or less in greatest dimension
N2a
Metastasis in a single ipsilateral LN more than 3cm but not more than 6cm in greatest dimenson
N2b
Metastasis in multiple ipsilateral LN none more than 6cm in greatest dimension
N2c
metastasis in bilateral or contralateral LN none more than 6cm in greatest dimension.
N3
Metastasis in a LN more than 6cm in greatest dimension

Distant Metastasis ( M )
Mx Distant metastasis cannot be assessed.
M0 No distant metastasis
M1 distant metastasis

STAGE GROUPING OF CANCER OF MAXILLARY SINUS

StageI. T1 N0 M0
StageII. T2 NO MO
StageIII. T3 N0 M0
          T1 orT2 orT3 with N1 M0
StageIV A. T4 N0 M0
             T4 N1 M0
StageIV B. Any T N2 M0
              Any T N3 M0
StageIV C. Any T Any N M1

DIAGNOSIS

A)Investigations
 Non Invasion
1. x rays water's view,max sinus partly
2. usg
3.CT SCAN with contrast
B)Invasive
1.Antral puncture
2.Biopsy
3.ECG

1.Radiograph of sinuses

opacity of the involved sinus with expansion and destruction  of the bony walls
2.CT scan if available this is the best non invasive method to find the extent of disease . CT scan done both in axial and coronal planes .It also helps in staging of disease.
3.BIOPSY :if growth presents in the more or mouth .Biopsy can be easily taken . In early cases ,with suspicion of malignacy ,sinus should be explored by caldwell luc operatiom .Direct visualisation  of the site of tumour in the sinus also helps in staging of the tumour .0
4.ENDOSCOPY of the nose and maxillary sinus will provide detailed examination ..

TREAMENT.

1.Surgery
2.Radiology
3.Chemotheraphy

1 .SURGERY

Maxillectomy
 two types
PARTIAL  Maxillectomy
1)vertical partial
2)horizontal partial Maxillectomy
TOTAL Maxillectomy
INCISION. 2 to 3 mm below lid margin not too far or not too close.

2. RADIOTHERAPY

a. External beam. X ray, beta rays or gamma rays using elements like co 60 and radium using proper precaution.
b. Interstitial. Beads or needle with radioactive material implanted in tumor by caldwell luc op.

3. CHEMOTHERAPY

a. Local. Through feeding vessels
b. Systemic. Used if there is distant metastasis or radio resistant or palliative care.
EG. Methotrexate, 5 fluro niacin, bleomycin

DIFFERENTIAL DIAGNOSIS

1. Malignant tumors
@lymphoreticular system tumors like lymphoma, extramedullary plasmocytosis
@olfactory neurofibroblastoma
@salivary gland malignant tumors like  adenoidcystic ca, adenocarcinoma etc.
@melanoma
@sarcomas like rhabdomyosarcoma, kaposi

2. Benign tumors
hemangioma, meningioma, chondroma, angiofibroma, amyloblastoma

3. Cherubism

Causes of leg ulcer Rx of varicose ulcer

Causes of leg ulcer Rx of varicose ulcer

Causes of leg ulcer Rx of varicose ulcer

Rx of varicose ulcer

A)Conservative Rx

1)elevation of affected limb.
2)vertical leg drainage to reduce n eliminate leg edema
3)passive movements maintain mobility of ankle n foot
4)active movements of calf muscles
5)blue line bandage is applied spirally from toes to knee.
6)antibiotics n analgesics
7)ulcer with yellow base n poor granulation tissue recquire daily dressing.
8)absorbant adherent dressing with spirit application to promote drying n scaling
9)once ulcer is clean Orahesive powder may b applied on surface of ulcer.

B)Surgical Rx

1)incompetent perforators n varicose veins r treated by surgery or sclerotherapy.
2)larger needs split skin graft
3)ascending phlebograph is done to detect incompetent calf perforating veins
4)subfascial ligation of Cocket n Dodd
*incision is made in lower half of leg 2.5 cm behind posterior border of tibia.
*incision deepened till deep fascia is reached n margins r undermined
*deep fascia is incised n lifted up.
*perforating veins r ligated n devided.
5)radical surgical approach
*superfascial varicosities r ligated n stripped with subfascial ligation of perforating veins.
6)by-pass operation
*for iliofemoral occlusion contralateral saphenous vein is passed suprapubically n anastomosed to affected side distal to occlusion
7)excision n skin grafting.

Carpal tunnel syndrom

Carpal tunnel syndrom

Carpal tunnel syndrom

Charctrsd by comresion of median nerve as it passes beneath flxr retinaculum.

Causes:-

Any space ocupying lesion of carpal tunel may b rsponsbl
i) Inflamtry-rheumatoid arthritis,wrist osteoarthritis
ii) Posttraumatic-bone thickning aftr Colle's#
iii) Endocrine- myxoedma,acromgaly
iv)Idiopathic-commonest cause

C/F

Pt is genrly midle aged woman complaining of tingling, numbnes or discomfort in thumb & radial one & half fingers i.e in median distri.
Tingling more prominent during sleep. Feeling of clumsiness in carying out fine movts.
*On exam.
features of low median nerve compresion r found. Nerve conduction studies show dlayed/absent conductn of impulses in median nerve acros wrist

Rx

dividing flxr retinaculum & thus decompres nerve

Cardiac arrest

Cardiac arrest

Cardiac arrest

Definition:-
An abrupt loss of cardiac pump function which may b reversible by a prompt intervention, but will lead 2 death in its absence.

Cardiac arrest may result 4m 1 of 4 mechanisms-
1)Ventricular fibrillation
2)Pulseless ventricular tachycardia
3)Ventricular asystole
4)Pulseless electrical activity

**Causes**

§Ventricular fibrillation
  -myocardial ischaemia or infarction
  -Electrocution
  -Hypokalaemia & hyperkalaemia
  -Drugs
§Ventricular asystole
  -Localised failure of conducting tissue
  -Massive myocardial infarction
§Pulseless electrical activity
  -Cardiac rupture
  -Massive pulmo embolism

**Management**

Cardiopulmonary resuscitation (CPR):-
Provides artificial ventilation & perfusion 2 vital organs i.e heart & brain until spontaneous cardiopulm function is restored
It encompasses both basic life support & advanced life support
1)Basic life support
indicates manoeuvres which, widout special equipment either prevent circulatory & respi arrest or externally support circulation & venti of victim in arrest
 i)Airway
 ii)Breathing
 iii)Circulation
 iv)Defibrillation
2)Advanced life support
Consists of basic life support & use of special equipment & drugs for establishing & maintaining effective venti & circu
 i)Advanced airway
 ii)Advanced breathing
 iii)Advanced circulation