splenomegaly causes

A>mild splenomegaly
1>infective-typhoid infective endocarditis septicemia
2>hematological-early stages of hemolytic anaemia
3>malignancy-early stages of lukemia
B>moderate-massive splenomegaly
1>infective-chornic malaria kala azar toxoplamosis
2>hematological-hemolytic anaemia thalasemia major/intermedia
3>malignancy-chronic myeloid leukemia hodgkins disease
4>congestive-portal HTN
5>metabolic-gauchers disease

JAUNDICE

Definition=jaundice defined as yellowish pigmentatn of skin,mucous membrane nd sclera by bilirubin ,rusulting frm elevated levels of bilirubin in blood.
Clinical jaundice occurs when serum bilirun is more than 2.5 mg %.
Latent jaundice is when serum bilirubin is more than 1 mg % but than 2.5 mg %
Classification=
1..Based on underlying derangement of bilirubin metabolism
a..Predominantly unconjugated hyperbilirubinaemia
b..Predo conjugated hyperbilirubinaemia
2..Based on pathology
a..Haemolytic jaundice
b..Hepatocellular jaundice
c..Cholestatic jaundice
A..HEMOLYTIC jaundice=
it results frm increased distructn of red cells resulting in increased bilirubin production
Unconjugated bilirubin accumulates in plasma.
Causes=
1..Intraerythocytic-
spherocytosis,sickle cell disease ,thalassaemia ,g6pd defi
2..Extraerythocytic_
autoimmune haemolytic anemia ,malaria ,prosthetic valves ,PND..
Clinical feature=

.Pallor
.Mild jaundice
.Hepatosplenomegaly
.Dark stool
Investigatn=
.No bilirubin in urine
.Urobilinogen increased
.Serum bilirubin incr
.Unconjugated bilirubinemia
.Normal liver functn test
B..Hepatocellular jaundice
.Results frm inability of liver to transport bilirubin into bile leading to liver cell damage..
Here both conjugated nd unconjugated bilirubin level rises.
Causes=
.Viral hepatitis
.Alcoholic hepatitis
.Chr hepatitis
.Cirrhosis
C..Cholestatic jaundice
.Means failure of bile flow ,coz may lie anywhere btw hepatocytes nd duodenum
.It is usually a surgical jaundice.
Causes=
1.Small duct obstructn due to=
drugs ,alcohol ,viral hepatitis ,cirrhosis ,chr hepatitis ,hodgkins disease
2..Large duct obstructn duue to=
gall stone ,carcinoma head of pancrease ,ca of ampulla of vater ,stricture bile ducts ,ca of bile ducts
.C/F=
symptoms=
.Jaundice
.Pruritus
.Dark urine
.Fever with chils nd rigors
.Wt loss
.Haemorrhagic tendency
.Bone pains
.Signs=
.Deep jaundice
.Xanthelasmas on eyelids
.Xanthomas
.Palpable gall bladder
.Hepatomegaly
.Signs of liver cell failure
.Investigatn=
.Bilirubin in urine
.Urobilinogen absent in urine
.Ser bilirubin raised
.Conjugated hyperbilirubinemia
.Ser alkaline phosphates rised
.Ultrasonography
.Liver biopsy

GERD

The reflux of gastric contents into the lower esophagus is called GERD.

Causes
1.sliding hiatus hernia-in this type of hernia the esophagogastric junction slides up through the diaphragm.this results in....a. Loss of obliquity of entry of eso into stomach.b.loss of reinforcing effect of intra abdo. pressure on d lower eso. sphincter.these 2 factors facilitates reflux.
2. Cardiomyopathy and vagotomy
3. Pregnancy,obesity,ascites,wt lifting,straining.
4. Cig smoking,alcohol,fatty foods,caffeine
5. Large volume meals.
6. Systemic sclerosis.
7. Drugs lik aminophylline,beta agonist,nitrates,ca channel blockers.
8. H.pylori.

C/f
-heart burn is deply placed burning pain behind the sternum radiating to the throat.it occurs after meals brought on by bending lifting weight and straining. It occurs on lying down in bed at night and relieved by sitting up.
-regurgitation of contents into mouth.
-aspiration pneumonia
-odynophagia
-persistant n transient dysphagia
-anemia due to bld loss
-hoarseness,sore throat,cough,laryngitis,otitis media.



Investigations
-endoscopy
-barium swallow and meal for hiatus hernia
-eso. pH
-bernstein test
-resting ECG n stress ECG
-eso motility studies.

Treatment
General
-weight reduction. Cessation of smoking
-small volume feeds.
-avoid alcohol.fatty food.weight lifting.
-avoid late night meals

Medical
-liquid antacid 10 to 15ml, 1 and 3 hrs. After meals.
-H2 antagonists lik cimetidine 400mg or ranitidine 150mg twice daily
-proton pump inhibitors lik omeprazole 20-40mg/day,lanso 15-30,panto 40,esomeprazole 40
-metoclopramide/domperidone 10mg thrice daily.
-h.pylori Rx regime
-oral iron for anemia

Surgical
-resection of strictures
-surgical return of lower eso sphincter to abdo.
-fundoplication

BLIND LOOP SYNDROME

Also called small bowel bacterial ovnrgrowth..
Disorders which impair normal physiological mechanisms controlling bacterial overgrowth.
.Most imp coz r 1. loss of gastric acidity
.2.Impaired intestinal motility
.3..Structural abnormalites
.C/F=
.Pt present with watery diarrhoea nd steatorrhoea with anemia due to b12 vitamin defi.
.INVESTIGATion =
.Serum vitamin b12 conc low
.Barium study or small bowel enema reveal blind loops or fistulae
.Endoscopic duodenal biopsies exclude mucosal disease
.Endoscopic aspiratn of jejunal contents
.MANAGEMENT =
.Tetracycline 250 mg 6 hry for 7 days
.Metronidazole 400 mg 8 hrly
.Intramuscular vita.B12 supplementatn

SCEROSING CHOLANGITIS

Def...it is characterisd by development of multiple stricture, dilatation of CBD with features of fibrous thickening of CBD

¤ Types
1. Primary
no cause is found but occurs with folowing conditions
e.g. Ulcerative colitis, crohns dis,graves dis, sjogrens syndrom
2. Secondary
due to stones or injuries

¤Complications
due 2 long standing obstruction biliary cirrhosis and cholaniocarcinoma develop

¤Diagnosis
1. Ultrasound 4 intrahepatic dialation
2. MRCP shows multiple strictures and dilatation
3. ERCP is d invst. of choice shows strictures in d CBD and dilation whch described as beaded appearance



¤Rx.
Stenting is the choice

irritable bowel syndrome

Def
  a functional disordepr of git it is one for which no infective structural or biochemical cause can be found

  irritable bowel syndrome
is benign chronic symtom complex of altered bowel habits and abdominal pain

aetiology
no organic cause
altered gi motility gastric emtying increased bowel contractions
serotonin an important factor
psycho disturbances

clinical features
abdominal pain
diarrhoea
stools pallet like
post prandial tenesmus



investigations
aim  to exclude organic bowel disease
sigmoidoscopy
barium enema

treatment

reassurance of patint

for pain predominant ibs
bulk luxative like methylcellulose
diclomine
psychotropic agent amitriptyptyline

for dirrhoea predominant ibs
loperamide
cholestyramine
alosetron

for constipations predominant ibs
  fibre supplementation
lectulose milk of magnesia can be given

DYSPAGIA

Def...it is dificulty in swallowing

# Causes
1) congenital
_congenital stenosis of oesophagus
_TEF
_congn. Web

2)Acquired
¤ in oesophgeal lumen_foreign body
¤in oeso. wall_strictvre, ca. Oeso., reflux eso., achalasia cardia, PV syndrome, oesophagitis, oeso. Spasm
¤outside wall_thyroid swelling, secondaries in neck, medistinal abscess and nodes, aortic aneurysm
¤dises. Of mouth and pharynx_stomatitis, tonsilitis, pharyngitis, retropharyngeal absces
¤neurological dis._polio, bulbar paralysis, myasthenia gravis

Other causes r tetanus, rabies

Biliary cirrhosis

Biliary cirrhosis is the cirrhosis of the liver secondary to prolonged obstruction of biliary system, anywhere between the interlobular bile ducts and the papilla of Vater. Obstruction results in progressive destruction of bile ducts.

Primary biliary cirrhosis.
Occurs in chronic inflammation and obliteration of intrahepatic bike ducts.
Aetiology.
Mac predominantly in females in the middle age.
Due to immune reactions resulting in liver damage.

Pathology.
Chronic granulomatous inflammation destroying the interlobular ducts, Resulting in fibrosis and later cirrhosis of the livers and its complications.



Clinical features.
1. Cardinal features are pruritis, hyperpigmentation, and jaundice.
2. Liver involvement.
 Progressive jaundice, later becomes intense.
 Patients acquires a ' bottle green colour'.
 Scratch marks, froger clubbing.
 Hepatospleenomegaly.
 Hepatocellular failure, portal hypertension and ascitis.
3. Hypercholesterolaemia.
 Xanthelasmas around the eyes.
 Xanthomas over joints, tendons, hand creases, elbows and knees.
 Pain, tingling and numbness over feet and hands due to peripheral neuropathy resulting from lip infiltration of peripheral nerves.
4. Malabsorption
 steatorrhoea and diarrhoea  from malabsorption of fat.
 Easy bruising and ecchymosis from vitamin K deficiency.
 Hepatic osteodystrophy -
 might blindness due to vitamin A deficiency.

Investigations.
 Hyperbilirubinaemia of conjugated type.
 Mile elevation of transaminases.
 Two to five dole rise of serum alkaline phosphatase.
 Marked rise of serum 5'- nucleotidase activity
 hyperlipidaemia.
 More than 90% of the patients have antimitochondrial antibodies and increased levels of cryoproteins consisting of immune complexes.
 Antinuclear, antismooth muscle antibodies.
 Lives biopsy confirms the diagnosis.

Management.
Ursodeoxycholic acid(10-15mg/kg) improves bilirubin and aminotransferase values.
 Steroids may improve biochemical and histological disease but may lead to osteoporosis.
 Other therapies azathioprine, colchicine, methottrexate.
 Steatorrhoea is treated by limiting eat intake and substituting long chain triglycerides with medium chain triglycerides in the diet.
 Monthly injections of vitamin K.
 Vitamin D 1mg/day.
 Calcium supplementation in the form of calcium gluconate 2-4 g/day.
 Airpinsignocter to reduce osteoporosis.
 Lives transplantation.
 Management of pruritis.
 *cholestyramine 4-16 g/day.
 *Rifampicin, ondansetron and opiate antagonists.

Secondary biliary cirrhosis.
*results from prolonged obstruction to large bike duct by ;
 stones.
 Bile duct strictures.
 Sclerosing cholangitis.

Clinical features
1. Recurrent abdominal pain in stones.
2. Fluctuating jaundice in stones.3. Previous history of abdominal surgery in strictures.
4. Chronic cholestasis with episodes of ascending cholangitis and even lives abscess.
5. Right upper quadrant pain due to cholangitis or biliary colic
6. Cirrhosis, ascites and portal hypertension are late features.
Investigations.
1 hyperbilirubinaemia of the conjugated type.
2. Markedly elevated serum alkaline phosphatase activity.
3. Ultrasound and CT of abdomen.
4 .ERCP.
5. Lives biopsy.

Treatment.
1. Relief of obstruction to bike flow by ERCP or surgery.
2. Antibiotics in sclerosing cholangitis.

WHIPPLES DISEASE

1 it is chronic multisystem disease associated with malabsorbtion
2 it is caused by gram positive bacteria   - Tropheryma whippelii
3 there is characteristic PAS positive macrophages in the small intestine causing malabsorbtion

## clinical features

1 symptoms are steatorrhoea , polyarthritis , weight  loss and abdominal pain
2 other features are migratory arthralgias ,fever,ophthalmological features and nurological fea. Including dementia in late stager
3 signs include generalised l n pathy ,Arthopathy ,skin pigmentation ,abdominal disten. And tenderness

## investigations

jejunal biopsy and biopsy of other tissue shows plenty of PAS positive macrophages which contain small bacilli

## treatment

trimethoprin-sulpmethoxazole (double strength) twice a day for 1 year

Portal HTN

Portal HTN is characterised by prolonged elevation of portal venous pressure .
   Normal portal venous pressure = 2-5mm Hg
   In Portal  HTN portal venous pressure > 12mm Hg
    *AETIOLOGY
1. Extrahepatic post - sinusoidal     -Budd-Chiari syndrome
2. Intrahepatic post - sinusoidal     -Veno - occlusive disease
3. Sinusoidal
    -Cirrhosis (most common )
    -Cystic liver disease
    -Partial nodular transformation of liver
    -Metastatic malignant disease 4. Intrahepatic pre - sinusoidal      -Schistosomiasis (common)
    -Sarcoidosis        
    -Congenital hepatic fibrosis
    -Vinyl chloride
    -drugs
5. Extrahepatic presinusoidal
    -Portal vein thrombosis
    -Abdominal trauma ,including surgery
    -Malignant disease of pancrease  or liver
    -pancreatitis
    -Congenital
   
*PATHOGENESIS
  Extrahepatic postal vein obstruction common cause in childhood & adolescence while cirrhosis in adults.
  Schistosomiasis common cause of portal HTN  world wide.
  Portal venous pressure determined by
    -Portal blood flow
    -portal vascular resistance    Increased portal vascular resistance is main factor produsing portal HTN .
     Increased portal vascular resistance - < flow of portal blood to liver  - development of collateral vessels - portal blood enters the systemic circulation directly.
     Collateral vessels formation sites :- oesophagus , stomach, rectum & anterior abdominal wall.
     Increased portal blood flow contributing to HTN is not dominating factor
     *C/f
1. Splenomegaly is cardinal feature. Usually less than 5cm below costal margin. Manifesting as thrombocytopenia & leucopenia
2. Collateral vessels visible as caput medusae
3. Haematemesis & melaena
4. Fetor hepaticus due to portosystemic shunting of blood 5. Cruveilhier-Baumgarten syndrome association of dilated abdominal wall veins & loud venous hum at umbilicus.  
6. Liver may be enlarged or shrunken
  a)small, contracted, fibrotic liver - very high portal HTN
  b)soft liver - extrahepatic portal vein obstruction
  c)firm liver - cirrhosis
7. Haemorrhoids may occur
8. Ascites occurs partly
    *IINVESTIGATIONS
1. Barium swallow -varices as feeling defect
2. Upper GIT Endoscopy
3. USG :- detects size of liver & spleen
4. Portal venography :- demonstrates site & cause of portal venous obstruction
5. Portal venous pressure measurement :- wedge hepatic venous pressure (WHVP) - free hepatic venous pressure (FHVP)= hepatic venous pressure gradient (HUPG).
 Low HUPG indicates pre-sinusoidal portal pressure.
     *COMPLICATIONS
 1. Variceal bleeding :- oesophageal, gastric, other (rare ).
2. Congestive gastropathy    
3. Hypersplenism
4. Ascites
5. Renal failure
6. Hepatic encephalopathy
     *TREATMENT
1. Absolute bed rest
2. Salt free high protein diet. Protein restricted at onset of encephalopathy
3. Rx of infections by proper AMA
4. Rx of variceal haemorrhage by
    - blood transfusion
   - vasopressin , octreotide or  infusion of somatostatin
    - Sengstaken tube
    - Endoscopic sclerotherapy
    - TIPSS
5. Rx of hepatic encephalopathy  

Inflammatory bowel disease

Inflammatory bowel disease include several condition most commonly being
1. Ulcerative colitis.
2. Crohn's disease .
Other uncommon inflammatory bowel disease include
1 microscopic ulcerative colitis
2microscopic lymphocytic colitis
3.microscopic collagenous colitis

ULCERATIVE COLITIS
DEF.
    #ulcerative colitis is an inflammatory disease affecting mainly the large intestine characterised clinicaly by recurrent attack of bloody diarrhoea and pathologically diffuse inflammation of colonic mucosa.
 # Disease extent can be broadly divide into distal and more extensive disease
 -distal disease refer to colitis confined  to rectum or rectum or sigmoid colon.
 -more extensive disease include "left side colitis" (up to the splenic flexure). Extensive colitis (upto the hepatia flexor ) and pancolitis)
.
AETIOLOGY
1. Familial or genetic
  a. Strong family history
  b. Occupance in monozygotic twins
2.infection
 a. Mycobacterium
 b. Measles virus
 c. Listeria monocytogens  .
 d yeast
 e. Endogenous bacteria
  bacteroides
  E-coli.
3. DIETARY FACTORS
 Deficiency of certain nutrients (butyric  
 acid. Sulphides. L - arginine glutamine.)
4.SMOKING
 -Can exacerbate Crohn's disease
 -increased risk of ulcerative colitis in non smokers
5.PSYCHOLOGICAL
 Characterised personality and major psychologica stresses are related to flare ups and ppt symptoms 6.DEFECTIVE IMMUNE REGULATION
 MANY Immunological ABNORMALITIES LIKE punt of macrophages leading to excessive production of cytokine (interlukin.1 interlukin 6 and tunn necrosis factor alpha ) also activation of other cells like eosinophills mast cells fibroblast
-immune complexes  are responsible for extra intestinal menifestatiom.
-

PATHOLOGY
1. Primarily involves the colonic mucosa
2. Mucosa involvement is uniform and continuous  with no intervening areas of normal mucosa
3.rectum is involved in 95 percent cases 4. From the rectum the disease extend proximally into the colon in a continuous fashion
5.Back wash ileitis in involvement of a few centimeter of ileum when the entire colon is involved
6. Macroscopically the mucosa appears hyperaemic haemorrhagic of ulcerated. Ulcer do not usually extend deeper beyond the sub mucosa .
7.Pseudopolyps are regenerationi island of mucosa surrounde by areas of ulcerative and denuded mucosa .they protrude into the lumen of colon like polyps.
8.microscopically the lamina propria is infiltered with lymphocytes and plasma cells . There is loss of goblet cell also .
9.crypts absess are characterised wits infiltration with neutrophills.
10. In toxic meghacolon , transverse colon is dilated ,walls are thin , mucosa denuded and inflammation extend to serosa. It may rupture.
11. In the chronic variety there is fibrosis and shortening of colon with loss of normal haustral pattern . The surface epithelium may show features and coal abscesses are uncommon.
,
CLINICAL FEATURES
A. General
 1.severity of symptoms reflects the extent the extent of colonic involvement and the intensity of inflammation .
2.Exacerbation and remission are characteristic.    
.3. Bloody diarrhoea with mucosa  and pus .
4 abdominal pain ,especially lower abdominal .
5.fever ,weight loss , loss of apetite.
6.symptoms and signs of dehydration and anemia
7. Extraintestinal manifestation
8.tenderness on palpation over the left iliac fossa .
9. Incidence of carcinoma
,
B. Acute variety
1. Systemic symptoms like fever ,weight loss and loss of apetite .
2. Diarrhoea and dehydration
3. Tachycardia and postural hypotentsion
4. Tenesmus .lower abdominal . Pain , left iliac fossa
5.rupture of colon ,,
,
CHRONIC VARIETY ,
1. Bowel is damaged  by fibrosis . It behaves like rigid tube incapable of absorbing fluids action like faecal reserviour
2.chronic diarrhoea
,
DISEASE CONFINED TO RECTUM
1.SYSTEMIC SYMPTOMS ARE ABSENT.
2. Loose motions and blood streaking of stools
3.bleeding and ovat per rectum
,,
Distal colitis
1. Constipation rather than diarrhoea
2 Retention of faeces in the proximal colon and small hard stools.
,
INVESTIGATION
1. Anaemia ,raised ESR AND leucocytosis
2.electrolyte imbalance
3hypoproteinaemia
4.abnormal liver function
5.blood culture in septicaemia
6.stool examination and culture
7.plain radiography abdomen
8.Barium enema
_irritability and incomplete filling
_ulceration
_pseudopolyps and strictures.
_bowel has assymetrica ,ahustral, tubular(pipe stem appearance).
9.sigmoidoscopy
_uniform continuous involvement of mucosa
_loss of mucosal vascularity
_diffuse hyperaemia
_exudate of mucus, pus and blood.
_,shallow but small or confluent ulcer .
_pseudopolyps
11. Colonoscopy
ht is preferable to flexible sigmoidscopy,
since there is high risk of bowel perforatin and flexible sigmoidoscopy .
12. Rectal biopsy shows mucosal inflammation.
13Serogical markers
_ pANCA :Perinuclear anti neutrophilc cytoplasmic antibody
_ASCA ANti-Saccharomyces cerevisiae antibody.
_ANTI-GOBLET cell auto antibodies in 30-40percent . Cases of ulcerative
--
TREATMENT
GENERAL MEASURES
1.Parental nutrition
2. High protein diet, low residue diet.
3.blood and plasma infusion .
4. Correction of dehydration and electrolyte imbalance .
5. Codeine phosphate and loperamide for diarrhoea .

CORTICOSTEROIDS
local treatment
_HYDROCORTISONE or PREDNISOLONE enemas, suppositors or foam.
_duration of treatment is 3to 6 weeks.
SYSTEMIC TREATMENT
_Prednisolone 40 to 60 mg orally daily for 3 to 6 weeks
_increase hydrocortisone 100-200 Mg.
-steroids  are gradually tapered and withdrawn.
-
AMINOSALICYLATES
-it includes 5aminosalicylic acid or mesalazin alone os combination of 5ASA carrier which release 5-ASA after splitting an bacteria in colon (sulphasalazine,osalazine, basalazide).
Side effect include nausea ,headache ,rashes,sterility in males ,haemolytic anaemia ,steven johnsen syndrome and agranulocytosis.
DOSE : 2 to 4 gm/day in mile to moderate attack and 0.5gm QID to prevent relapse .

IMMUNOSUPPRESSIVE AGENTS
-Azathioprine and 6-mercartopurine both are useful in inducing and maintaining remission and have steroid sparing activities
-useful in patient who require two or more corticosteroid within a balcodes year .
-methotrexate
-cyclosporine- an inhibitor of calcineurin- preventing expansion of T cell subset .
-Surgical management
emergency surgical procedure is colectomy with ileostomy, the rectum and distal colon being removed at a later stage.

Indication of emergency surgeries
severe forms of disease
toxic dilation of colon
perforatin
severe haemorrhage
--
indication of elective surgeries
acute disease which fails to respond to medical treatment
-frequent relapse in spite of adequate treatment
-chronic disease with permancouly damaged bowel.

DYSPEPSIA

 it is a collective description of variety of GIT symp.
 - upper abdo. Pain
 - gastro oesophageal reflux n heart burn.
 - anorexia, nausea n vomiting
 - flatulence n areograpy

ulcer dyspepsia includes d dyspeptic symptoms associated wit peptic ulcer.
Flatulent dyspepsia is usually due to functional disorder.
H. Pylori inf. Seen in many as 30% cases of dyspepsia.

CAUSES
1 FUNCTIONAL DYSPEPSIA
2 DYSPEPSIA ASSOCIATED WIT ORGANIC DISEASE OF UPPER GIT
 - peptic ulcer
 - peptic oesophagitis n gastroesophageal reflux disease.
 - gastric carcinoma
 - lactose intolerance
3 ASSOCIATED WIT OTHER CONDITION
 - pancreatic disease
 - crohns disease
 - colon maligancy
 - ca lung
 - drugs, alcohol
 - pregnancy



COMMON DRUG COUSING DYSPEPSIA
 - Acarbose
 - antibiotibs eg erythromyicin
 - corticosteroid
 - irom
 - theophyllin
 - Bisphosphates

D/D
 - GERD
 - Peptic ulcer disease
 - Gastric malignancy.

Diagnostic criteria
 Rome ||| criteria 4 functional dyspepsia
at least 3 mnt, wit onset at 6 mnt previously, of one or more of the folloing
 - bothersome postprandial fullness
 - early satiation
 - epigastic pain
 - epigastic burning
 - no evidence of structural disease.

Ascites

DEFINATION.:
Ascites is defined as collection of excess of fluid within the peritoneal cavity.

MECHANISM-
1. Inflammation of peritoneum-->increased capillary permeability-->transudation of fluid into peritoneal cavity. Eg. Bacterial and T.B  peritonitis,
2. Venous obstruction -->transudation of fluid into peritoneal cavity. Eg. I.V.C  obstruction.
3. Lympathic obstruction -->chylous ascites.
4. Rupture of viscus-->outpouring of blood and cystic fluid -->ascites.
5. Mechanism in liver cirrhosis.
A. Liver failure -->redistribution of blood -->reduced G.F.R  -->salt and water retension. -->Ascites.
B. Failure of liver to metabolise vasopressin -->reduce renal water clearance.
C. Portol hypertension-->raised hydrostatic pressure -->extravasation of fluid from plasma into peritoneal cavity.
D.Hypoalbuminaemia--> reduced oncotic pressure -->extravasation of fluid.
E.Secondary hyperaldosternism-->salt and water retension.

CAUSES :-

TRANSUDATE.
1.cirrhosis and portal hypertension.
2. Congestive cardiac failure. .
3. Nephrotic syodrome.
4. Constrictive pericarditis.
5.Beri beri.
6. I.V.C obstruction.

EXUDATIVE.
1. T.B peritonitis.
2. Malignant peritonitis.
3. Bacterial peritonitis.
4. Pancreatic peritonitis.

MISCELLANEOUS :
1. Meigs syodrome.
2. Chylous ascites.
3.Budd  chairi syodrome.



CLINICAL FEATURE-
SYMPTOMS=
- Abdominal distension.
- bloated feeling in abdomen.
-dyspnoea nd orthopnoea.
- indigestion and heart burns

SIGNS=
-abdomen distension and fullness in flanks.
-skin over abdo stretched and shiny.
- umbilicus may be flat or everted.
-divartication of recti and herni.
-Abdo wall may show distende veins.caput medusae-->veins radiating out with flow away from umbilicus. Prominent veins in flanks with upward flow of blood ->I.V.C obstruction.
-large amount of fluid -->horse shoe shaped dullness. Epigastric and umbilical region remain resonant due to floating intestine.
- shifting dullness if fluid >1000  ml.
-fluid thrill positive in tense ascitis.
- puddle sign can detect as low as 120 ml. Of fluid.

SECONDARY EFFECTS
-Scrotal oedema.
-pleural effusion ,right sided.
-cardiac apex sifted upward due to raised diaphragm.
-Neck veins distended.

INVESTIGATION
1.Ultra sonograph.
2.Diagnostic paracentesis.
3.Lararoscopy.
4.Peritoneal biopsy.

EXAMINATION OF ASCITIC FLUID.
INVESTIGATION
1. Gross appearance.
A. Clear, straw colored -> cirrihosis, congestive cardiac failure.
B. Haemorrhagic.->T.B., malignancy.
C. Cloudy ->bacterial peritonitis.
D. Milky white -> lympathic obstruction.
2. Specific gravity,
transudate <1.016;
exudate >1.016.
3. Protein ,
transudate  <2.5g /dl.
Exudate >2.5g /dl.
4. Glucose->low in malignancy ,tuberculosis.
5. Amylase activity  >1000units/ lit
6.Microscopy,for ziehl neelsen staining.cytological examiniation.
7.Culture.
8.S.A.A.G_1.1g/dl in portal hypertension.And <1.1 g/dl. Other causes.


TREATMENT
Treatment depends on the cause .
1.Tuberculosis peritonitis.
-Anti tuberculosis chemotheraphy.
2. Malignant peritonitis
-repeated paracentesis.
-Intra peritoneal instillation of methotrexate,nitrogen or chloroqvine slows down rate of accumulation.
3.Pancreatic ascites.
-nasogastric station.
-Ascitic tap.
-octretide inhibits pancreatic recreation.
4.Bacterial peritonitis.
-surgical emergencyi
-correction of fluid and electrolyte disturbance.
-broad spectrum antibiotic.
-treat shock.
5.Chylous ascites.
-surgical treatment.
-ascitic fluid tapping.
6.Meigs syndrome
-removal of pelvic tumour.

Upper GIT bleeding

 Upper GIT bleeding indicates bleding proximal to duodeno-jejunal  junction
    * AETIOLOGY
     1. Oesophageal causes
  - oesophageal variaes :-occur from lower 5cm of oesophagus
 - Oesophagitis
 - Oesophageal carcinoma
 - Mallory -Weiss syndrome :- results from linear tear in the distal oesophagus & proximal stomach. Episode of forceful retching precedes the bleeding.
      2. Gastro-duodenal causes   - Erosive gastritis :- occur after ingestion of NSAIDs & alcohol
 - Stress ulcers
 - Peptic ulcers
 - Gastric carcinoma
      3. Miscellaneous causes
 - Rupture of aortic aneurysm
 - Coagulation defects
       *C/f
 1. Haematemesis &/or melaena
 2. Colour of vomitus  depends on time for which blood was in stomach .
  Bright red - rapid & siseable haemorrhage
  Coffee ground - small bleed
 3. Melaena occurs when > 60ml blood is lost in upper GIT
 4. Haematochezia:- Frank blood per - rectum occurs in massive bleed
 5. Symptoms of blood loss :-         - dizziness ,pallor & shock
   - hypotension & tachycardia
 6. Features suggesting of severe bleeding
    - presence of clots in vomitus
    - fall in SBP > 10mm Hg & rise of pulse rate of > 20 beats /mins on change of posture from lying to sitting position
 
 *DIAGNOSIS
 1. H/o alcohol or drug (NSAIDs) ingestion , trauma , burns or sepsis  -  gastric erosion
 2. H/o peptic ulcer
 3. H /o jaundice ,pedal oedema, ascites , splenomegaly or other features of liver cell failure - variceal bleed
 4. Retching followed  by  Haematemesis  - Mallory - Weiss tear
  5. H/o dysphagia  & wt loss - malignancy
    *MANAGEMENT
  A) massive bleeding :- resuscitate & give IV fluids immediatety
  B) Monitor
    BP
    pulse
    urine output
  C) Blood for grouping cross matching
  D) Gastric Lavage
    Performed by instilling 500ml of ice cold water every 30-60min . Leads to temporary cessation of bleeding
   E) Gastric aspiration
  helps to  1) asses rate of bleeding.  2) Clear the stomach for endoscopy . 3)remove blood from stomach
   F) Endoscopy
  Helps in
1. Early diagnosis
2. Identify rebleed
3. Rx
    - by use lasers, electro-coagulation & heater probe
     -Endoscopic sclerotherapy       G) Balloon tamponade, vasopressin, octreotide
      H) Embolisation of bleeding artery
       I) H2 blocker & proton pump inhibitors
       J) Surgical
   Required when bleeding continues despite medical Rx
    - oesophageal varices.:- shunt surgery
     - gastric erosions :- total gastrectomy or vagotomy with drainage

Peptic ulcer

Peptic ulcer refers to an ulcer in the lower oesophagus,stomoch or duodenum,in the jejunum after surgical anastomosis to stomoch n in ileum adjecent to a meckels divirticulum.
Atiopathogenesis-
1 heredity
2 acid pepsin vesus mucosal resistance_cause of peptic ulceration is digestion of the mucosa with acid plus pepsin of gastric juice.
3 gastric hypersecretion is more important in etiology of duodenal ulcer.
4 other risk factor include smoking n alcohol consuption
clinical features_
it is chronic condition with natural history relapse n remission lasting for decade even life long.
The most common presentation is that of recurrent abdominal pain which has three notable characters_1 localisation to epigastrium  2 relation to food
3 periodicity.
Epigastric pain,burning in character.
Hunger pain,night pain r other features.

Complication-
1 upper gastrointestinal bleed
2 perforation
3 gastric outlet obstruction
4 gastric malignancy
5 pancreatitis
Investigation_
1 double contrast barium meal may shows ulcer as crater or as deformed duodonal cap.
2 endoscopy can visualise the ulcer.A biopsy can b taken frm gastric ulcer to rule ot malignancy n H pylori infection.
3 test for H.Pylori.
A on endoscopic biopy_rapid urease test,histoly n culture.
B non invasive_serology for IgG,urea breath test.,H.Pylori stool antigen test.
4 serum gastrin n gastric acid analysis.
Treatment_
short term management-
1 general care_avoid smoking.,avoid aspirin n NSAIDs drugs.
Alcohol to b moderated,No spicy dietory advice.
2 Antacids-mainly prescribe for symptomatic relief.Sodium biocarbonate is the quickest acting antacid
3 histamine H2 receptor antagonist-includes Cimetidine,ranitidine,famotidine,n nizatidine
mechanism of action is inhibition of acid n pepsin secretion by blockhning H2 receptor.
Ranitidine 150mg BD,cimetidine 400mg BD.Duration of treatment for duodenal ulcer is 4wks n in gastric ulcer 6-8wks.
4 Proton pump inhibitors_
these includes Omeprazole,lansoprazole,pantoprazole n esmoprazole.
Mechanism of action is irriversible inhibitio of acid secretion by the proton pump.
Omeprazole_20mg BD daily for 4_8wks.
Indication_reflux oesophagitis n GERD.,peptic ulcer unresponsive to other medical measures.,zollingor ellison syndrome.
5 Prostaglandin analogues_ misoprostole 200microgram 4 times daily,useful in preventing NSAIDS induce mucosal injury.
6 colloidal bismuth subcitrate
7 Sucralphate 2g BD.
8 carbenoxolon sodium
9 treatment of H.Pylory_triple therapy omez,clarithromycine,metronidazole.
LONG TERM MANAGEMENT_
itermittent treatment for sympotomatic relapse.
Maintainanance treatment.
Surgical treatment-
for gastric ulcer_partial gastrectomy with Billroth1 anastomosis..
For duodenal ulcer_selective vagotmy with pyloroplasy,highly selective vagotomy.

Peptic ulcer

Peptic ulcer refers to an ulcer in the lower oesophagus,stomoch or duodenum,in the jejunum after surgical anastomosis to stomoch n in ileum adjecent to a meckels divirticulum.
Atiopathogenesis-
1 heredity
2 acid pepsin vesus mucosal resistance_cause of peptic ulceration is digestion of the mucosa with acid plus pepsin of gastric juice.
3 gastric hypersecretion is more important in etiology of duodenal ulcer.
4 other risk factor include smoking n alcohol consuption
clinical features_
it is chronic condition with natural history relapse n remission lasting for decade even life long.
The most common presentation is that of recurrent abdominal pain which has three notable characters_1 localisation to epigastrium  2 relation to food
3 periodicity.
Epigastric pain,burning in character.
Hunger pain,night pain r other features.

Complication-
1 upper gastrointestinal bleed
2 perforation
3 gastric outlet obstruction
4 gastric malignancy
5 pancreatitis
Investigation_
1 double contrast barium meal may shows ulcer as crater or as deformed duodonal cap.
2 endoscopy can visualise the ulcer.A biopsy can b taken frm gastric ulcer to rule ot malignancy n H pylori infection.
3 test for H.Pylori.
A on endoscopic biopy_rapid urease test,histoly n culture.
B non invasive_serology for IgG,urea breath test.,H.Pylori stool antigen test.
4 serum gastrin n gastric acid analysis.
Treatment_
short term management-
1 general care_avoid smoking.,avoid aspirin n NSAIDs drugs.
Alcohol to b moderated,No spicy dietory advice.
2 Antacids-mainly prescribe for symptomatic relief.Sodium biocarbonate is the quickest acting antacid
3 histamine H2 receptor antagonist-includes Cimetidine,ranitidine,famotidine,n nizatidine
mechanism of action is inhibition of acid n pepsin secretion by blockhning H2 receptor.
Ranitidine 150mg BD,cimetidine 400mg BD.Duration of treatment for duodenal ulcer is 4wks n in gastric ulcer 6-8wks.
4 Proton pump inhibitors_
these includes Omeprazole,lansoprazole,pantoprazole n esmoprazole.
Mechanism of action is irriversible inhibitio of acid secretion by the proton pump.
Omeprazole_20mg BD daily for 4_8wks.
Indication_reflux oesophagitis n GERD.,peptic ulcer unresponsive to other medical measures.,zollingor ellison syndrome.
5 Prostaglandin analogues_ misoprostole 200microgram 4 times daily,useful in preventing NSAIDS induce mucosal injury.
6 colloidal bismuth subcitrate
7 Sucralphate 2g BD.
8 carbenoxolon sodium
9 treatment of H.Pylory_triple therapy omez,clarithromycine,metronidazole.
LONG TERM MANAGEMENT_
itermittent treatment for sympotomatic relapse.
Maintainanance treatment.
Surgical treatment-
for gastric ulcer_partial gastrectomy with Billroth1 anastomosis..
For duodenal ulcer_selective vagotmy with pyloroplasy,highly selective vagotomy.

hepatic failure

Fulminant hepatic failure_
a syndrome is characterised by hepatic encephalopathy resuling frm sudden severe impairement of hepatic function,occuring within 4 wks of onset of symptoms in a absence of any evidence of pre existing liver disease.
Onset of encephalopathy within 7 days of symptoms is known as hyperacute hepatic failure.
Atiology-
1 acute viral hepatitis B n E
2 hepatotoxic drugs like cyclosporhin,methotrexate,valproic acid.
3 pregnancy
4 autoimmune hepatitis
5 wilson's disease
6 shock 7 poisoing.
Pathogenesis_elevated ammonia in the blood apparently play a role in the pathogenesis of hepatic encephalopathy.

Clinical features_
general features-weakness,nausea vomitting.Jaundice,rt hypochondriac pain.
Liver may enlarge initially but later shrinks.
Live dullness absent on percussion.Ascites n oedema develop later.
Featurs of hepatic encepalopathy_ reduce alertness,poor cöncentration,restlessness,manic episode,drausiness n coma.
Confusion,disoriantation,inversion of sleep rhythm,slurred speech,convulsion,foetor hepaticus n flapping tremor.
Featurs of cerebral oedema_bradycardia,hypertensiön,irregular respiration.
Unequal or abnormally reacting pupil,fixed pupil n spontaneous respiration.
Investigation_
1 urine contains proteion,bilirubin n urobilirubin.
2 leucocytosis
3 serum bilirubin is raised
4 hypoalbumineamia
5 prothrombin time is prolonged
6blood ammonia level r elevated.
7 plasma n urine amino acid increased
8 USG-shrunken liver 9 ICT raisd.
Complication_
encephalopathy,cerebral oedema,respiratory failure,bleeding n hypotension,hypothermia,ifections,pancreatitis,renal failure.
Management_
general-
monitor vital signs,hrly urine output.,central venous pressure,renal functions n electrolytes.
Fluid n electrolyte therapy.
Calories r supplied as glucose 300g/day orally or by nesogastric tube.
Ventilatory support for respiratory failure..
Cefotaxime iv plus metronidazole for infection.
Ranitidine 50mg IV 8hrly to prvent gastrointestinal beed.
Renal failure is treated with dialysis..Fresh frozen plasma if PT is more than 1.5 times normal.
Treatment of encephalopathy_
head elevation at 30degree n elective ventilation in pt with grade 3  n 4 encephalopathy.
Mannitol 20% 1g/ke body wt iv over half an hr.Dose may b repeted every 6 hr with serum osmolality kept below 310mosmol/L. Sodium thiopental bolus dose 2-4 mg/kg over 15 min is followed by iv infusion of 1_2 mg/kg/hr in resistant cases.

COELIAC DISEASE

Defination=a chronic intestinal disease producing malabsorptn nd caused by intolerance to gluten,characterised by immune mediated enteropathy ,nd improve after withdrawl of gluten.
ETIOLOGY= 1.Immunological damage to mucosa due to gluten protein of wheat.Toxic component in gluten is gliadin
2.High assoc with HLA DQ2
Pathology=1.Mucosa of duodenojejunal flexure shows partial villous atrophy or subtotal villous atrophy.
2. Lamina propria demonstrate cellular infiltrates of plasma cells nd lymphocytes.
CLINICAL features=
1.Range frm mild anemia to florid malabsorption.Most common coz of anemia is iron def,it may b due to folate nd vit.B12 defi.
2.Diarrhoea ,weight loss
3.Peripheral neuropathy,hypoproteinemia,oedema,bone pain ,tetany
4..Features of vitamin defi
5..Clubbing,glossitis,angular stomatitis,skin pigmentatn
6..Amenorrhoea ,infertility
7..Other autoimmune disease assoc with coeliac disease r type 1 diabetes,rheumatoid arthritis,SLE,Addison disease
8..Other extraintestinal fetures include IgA nephropathy,elevated liver enzymes nd liver failure,myocarditis

Complication=
1..Dermatitis herpetiformis
2..Intestinal lymphoma involving jejunum
3..Peripheral neuropathy
4..Epilepsy
5..Osteomalacia
6..Amyloidosis
INVESTIGATIONS=
1..Serologic tests
IgA antiendomysial antibodies
IgG nd IgA antigliadin antibodies
Antitransglutaminase antibodies
2..Abnormal jejunal biopsy
3..Tests indicating malabsorption of proteins,carbohydrate,fat nd vitamins
TEATMENT =
1..Strict gluten free diet,.Avoid wheat nd wheat products,oats,rye nd barley
2..Rice,corn,soyabean,potato,nuts nd beans ,meat r safe
3..Beer must b avoided.Same is true for all kinds of whisky
4..Corticosteroids may given in ill pt who present with acute coeliac crisis with severe diarrhoea,dehydration,weght loss,acidosis,hopocalcaemia
5..Vitamin nd mineral supplemention including iron therapy for anemia
6..Diary products avoided as secondary lactase deficiecy is often assoc with coeliac disease..

ALCOHALIC LIVER DISEASE

Etiopathogenesis=
.Alcohol intake..
Alcohol is metabolised by liver to acetaldehyde by mitochondrial enzyme,ADH.
Acetaldehyde forms adducts with cellular proteins in hepatocytes which activate immune system,leading to cell injury.
Acetaldehyde then metabolised to acetyl coA nd acetate by ALD,this generate NADH,which changes redox pontential of cell
 Cytochrome CYP2E1 is induced by alcohol,which generates microsomal peroxidation leading to oxygen free radicals formatn leading to mitochondrial damage
.PATHOLOGY=
.Alcoholic hepatitis
.Lipogranuloma
.Neutrophil infiltratn
.Mallory hyaline
.Pericellular fibrosis
.Macrovesicular steatosis
.Fibrosis nd cirrhosis
.Central hyaline sclerosis

.C/F=
.Clinical syndrome of alcoholic liver disease=
.1..Fatty liver=
abnormal liver biochemistry ,normal/large liver
.2..Alcoholic hepatitis=
.Jaundice
.Malnutritn
.Hepatomegaly
.Portal hypertension features like ascites ,encephalopathy
.3..Cirrhosis=
.Stigmata of chr liver disease
.Large/normal liver
.Ascites
.Encephalopathy
.Hepatocellular carcinoma
INVESTIGATION =
.Clinical history frm pt abt alcohol misuse,duratn ,severity
.Biological markers in absense of anemia
.Raised GGT wil b elevated in hepatic steatosis nd fibrosis
.Unexplained rib fracture on chest x ray suggest alcohol misuse
.Presence jaundice suggest alcoholic hepatitis
.Liver biopsy
.Maddreys score by prothrombin time nd bilirubin give discriminant function
.MANAGEMENT=
.Cessatn of alcohol consumptn.Life long abstinence is best advice
.Treatment of complicatn of cirrhosis such as variceal bleeding ,ecephalopathy nd ascites
.Nutrition is imp nd enteral feeding via fine bore nasogastric tube needed.
.Corticosteroids r of valve in pt with severe alcoholic hepatitis
.Pentoxifylline,a weak anti TNFaction beneficial in sever alcoholic hepatitis
.Liver transplantation.

TROPICAL SPRUE

Def-malabsorption in pt of tropics in absence of other intestinal diseses
etiology-a>E.Coli,klebsiela,enterobactor b>folic acid def
pathology-a>jejunal biopsy show partial villous atrophy b>abnormal jejunal biopsy rule out tropical sprue
C/F-a>3 phases:1>initial phase of acute diarrhoea 2>intermediate phase 3>late phase b>spontaneous remmisios n relapses c>diarrhoea,abdominal distention,anorexia,wt loss,fatigue d>mdgaloblastic anaemia,edema,glositis
investigation-a>stool exam 4 giardia,entamoeba histolytica,cryptosporidium b>megaloblastic anaemia
c>hypoalbuminemia d>abnormal test 4 fat absorption e>D-xylose test abnormal f>vit B 12 malabsorption g>partial villous atrophy on jejunal biopsy
TREATMENT-a>tetracycline 1g daily in 4 divided doses 4 6 mths b>folic acid 5mg daily c>correction of def of fluids,electrolyte,vit,iron d>symptomatic treatment 4 diarrhoea