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Flashcards in GIT Deck (104):

Oral Leukoplakia

Morphology- white patch or plaque caused by epidermal thickening or hyperkeratosisi
-not removed with scraping
- can be benign to highly dysplastic.(3-7% malignant
-precancerous until proven otherwise

clinical feature
-common in older men
white patch in buccal mucosa, tongue, floor of mouth

associations- tobacco, dentures, HPV infection.



Less common

Morphology: red velvety eroded area that is poorly circumscribed
more atypical epithelial changes and typically marked as dysplasia

MALIGNANT transformation in more than 50%


Hairy luekoplakia

Almost always seen in HIV,
EBV in majoriy

Morphological: White, confluent, fluffy or hairy hyperkeratotic thickenings layers of keratotic squames on underlying mucosal acanthosis(hyperkeratotic.)


congenital stenosis/atresia

elongation and separation of esophagus and trachea during embryogenesis

assocaited tracheal lesions-tracheo-esophogeal fistulas
---most common subtype is blind upper esophagus with lower esophagus connected to trachea

associated with maternal polyhydramnios and single umbilicle artere or other congenital abnormalities, cyanosis. gastric dilation due to swallowed air

clinical features, excessive drooling in new born, choking and cyanosis with first feed.


hiatal hernia

Morphology- enlarged esophageal hiatus in diaphragm.

incompetance of the lower esophageal sphincter

sliding- gastic lining slips up past the diaphragm.
para-gastric lining stays trapped above the diaphragm

Clinical presentation
Sliding-95%-incomeptance of lower esophageal sphincter.
epigastric pain, heart burn in sliding type

complications- volvulus, strangulation, and perforation(paraesophageal type.



Morphology- , dilatation of esophagaus, loss of ganglion cells in myenteric plexus, barium swallow- Bird beak sign.

Etiology-failure of distal esophageal inhibitory neurons,- iditopathic. chagas disease, trypanosoma cruzi causes destruction of myenteric plexus.
-diabetic autonomic neuropathy,
-infiltrative disorders like malignancy, amyloidosis, sarcoidosis, lesions of dorsal motor nuclei, polio, surgical ablation.

Pathogenesis-dilatation of esophagus above lower esophageal sphincter, increased tone of LES, esophageal, aperistalsis
- destruction of myenteric plexus, causes failure of LES to relax and esophageal dilatation.
Progressive dysphage.

Clinical presentation
-dysphagia, odynophagia, reflus of contents, vomiting,
-manometry is diagnostic.

complications- risk of developing squamous cell carcinoma
and Aspiration pnumonia


mallory-weiss syndrome

Morphology-longitudinal tears of esophagogastric junction tear may be mucosal or transmural

Etiology- alcoholics after a sever bout of retchin

Pathogenesis- inadequate relaxation of LES during vomiting

Clinical presentation- PAINFUL hematemesis.

complications- usually heals but sometimes fatal due to hypovolemic shock- this happens in Boerhaave syndrome.(transmural tears that cross the gastroesophageal junction


Reflux esopohagitis GERD

Morphology- hyperemia, inflammatory cells, eosinophils, neutrophils, lymphocytes, elongation of lamina propria, basal zone hyperplasia

Etiology- decreased LES tone, delayed esophageal clearance, decrease in reparative capacity of esophagus, increased gastric volume

Clinical presentation- heartburn and regurg, espeically on lying down, dyspepsia, Water brash, nocturnal cough

complications- bleeding, stricture, bronchospasm, aspiration pneumonia, asthma, barret's esophagus, adenocarcinoma.


Barret's esophagus

More common in men and whites.

Morphology- tongues of red granular mucosa(salmon pink patch extending up into esophagus, intestinal or gastri ype epithelium in esophagus,

Etiology- chronic exposure to gastric secretions, GERD

Pathogenesis- metaplasia of squmous mucosa for columnar epitheliam

Clinical features
-heart burn, dyspepsia, epigastric pain, substernal discomfort, relieved with antacids.

30-40 fold risk of dysplasia and adenocarcinoma do a serial endocopic biopsy to screen.


Esophageal varices

Morpholgoy- dilated mucosal veins in lower third of esophagus overlying mucsoa normal inflamed or ulcerated.

etiology- occurs in 2/3 of patients with cirrhosis and portal hypertension- this causes blood shunting

clinical presentation- usually asymptoatic, but will have massive PAINLESS hematemesis when ruptured.

Associations- decompensated cirrhosis and HCC

Complications, fatal hemorrhage.cause of death in 50% of patients with advanced cirrhosis.


Squamous cell carcinoma

-UPPER and MIDDLE Esoph-most common type of esophogaeal carcinoma in the world. Adults over 50 more common in males, blacks more than whites.

Risk factors:ABCDEF
Alcohol and achalasia
Barrett's esophagus (adeno)
Celiac disease
DIET( vitamin A, C riboflavine, pyroxidine deficiency, high nitrite))
Esophageal web
Ectodermal dysplasia.
Fungal contamination

polypoid exophytic masses, diffusely infiltrative neoplasm, will see carcinoma, insitu, invasive.


clinical presentation-
asymptomatic, weight loss, anorexia, bleeding, hoarsenss or cough.

Route of metastasis-
direct to adjacent trachea and heart or lymphatic to the cervical, mediastinal(paratracheal, tracheobronchial, or gastric celiac nodes


Pyloric stenosis

incidence- occurs more commonly in male infants 3-1 ratio

morphology- muscular hypertrophy of the pyloric sphincter secondary to hypetrophy of pyloric muscularis mucosae.

clinical presentation- regurgitation and projectile vomiting in second week of life. wave peristalsis visible in abdomen, palpable oval abdominal mass (olive)

course- chronic antral gastritis, peptic ulcers, malignancy, treated by surgery(myotomy)

associated with Turner and Edward's syndrome


acute gastric ulcers

Etiopathogenesis- severe trauma, major surgeries, extensive burns (curling ulcers) head injuries/intracranial lesions (cushing ulcers), systemic acidosis and hypoxia due to severe trauma and burns, vagal stimulation(intracranial lesions.

clinical features- massive upper GIT bleed, usually multiple and asymptomatic. 5-10% admitted to ICU

Morphology- multiple small and circular ulcerations, gastric rugae are normal, base usually not indurated. Adjacent gastric mucosa is normal or with reactive changes.



peptic ulcers

Etiopathogenesis- exposure to aggressive actin of acidic peptic juices H. pylori, NSAIDS, Smoking, Alcohol, Psychological stress, Sollinger ellison syndrome.

Locations in desceding order
-Duodenum, stomach, GE junction, Margins of Gastrojejunostomy, Meckel's diverticulum, Zollinger Ellison syndrome.

clinical features,
- burning epigastric pain 1-3 hours after meals, relieved by food and alkali, worse at night, associated weight loss, gastric outlet obstruction

Morphology- round oval punche dout with relatively straight walls, sharp and raised margins but not everted. depth varies but may penetrate entire wall. Smooth and clean base, radiating surroudning mucosal fold.
-active ulcer has 4 zones, Necrotic fibrinoid debris, non specific inflammator infilatrates(PMN), granulation tissue, fibrosis and collagenous scar
- features of chronic gastritis in adjacent mucosa

complications- bleeding perforation, gastric outlet obstruction, malignant transforamtion (rare)possibly malignant intially. Iron deficiency anemia, pyloric obstruction


Gastrointestinal stromal tumors (GIST)

Histogenesis- mesenchymal tummmor, cells of cajal or pacemaker cells. may be misdiagnosed as leiomyomata

common sites- anywhere in the GIT, Esophagus, STOMACH, small intestine, large intestine.

benign or malignant based on size and mitoses.

morphology- usually submucosal with whorls and bundles of spindle shaped cells

CKIT CD117 is the tumor marker.


Gastric carcinoma


risk factors,

classification:based on depth, early and advanced, early confiened to mucos and submucosa regardless of involvement of regional lymph nodes.

Sites: pylorus/antrum, Cardia, Body and fundus


clinical features: most asymptomatic in early stages. non specific weight loss, anorexia, ab pain, pyloric outlet obstruction, KRUKENBERG TUMOR, VIRCHOW LYMPH NODE

prognosis- depends on depth of invasion and nodal status. growth patern is exophytic, flat or excavated, spreads regionally, transcelomicly, lymphaticly, hematogenously


Celiac Spure

Epidemiology- common in whites, age presentations typically 1-10 years, more common in females with familial clustering, HLA B8, DR3 and DRq

Morphology- atrophy and loss of vili, increased intraepithelial lymphocytes, elongated and hyperplastic crypts, increased lymphocytes, macrophages and plasma cells in lamina propria. villous atrophy with hyperpasia of crypts, increased intraepithelial lymphocytes, increased plasma cells in lamina propria.

Etology- hypersensitivity to gluten and gliaden

sensitivey causes loss of small bowel filli and malabsorption

Clinical features. - iron deficiency syndrome, take a biopsy and reversal of signs and symptoms after gluten free diet, abdominal distension, bloating and flatulence, diarrhea and steatorrhea, with weightloss, dermiatits herpetiformis

Diagnosis: can do anti gliadin and anti endomysial antibodies, , or anti tissue transglutaminase tTG antibodies which is a specific endomysial antigen.

complications- long term risk of intestinal T-cell lymphomas.

associated with infection of type 12 adenovirus.


Tropical sprue

Epidemiology- peopel living in or visiting tropics, appear after months or years of visit.

Morphology- all parts of small intestine equally involved, small may appear near normal. difficult to differentiate from celiac disease, villous atrophy with hyperpasia of crypts, increased intraepithelial lymphocytes, increased plasma cells in lamina propria.


Pathogenesis- affects travellers to tropical regions. related to bacterial infection superimposed on pre-existing small intestine injury

Clinical features. malabsorption, ab distension, bloating flatulence, diarrhea steatorrhea and wight loss. megaloblastic anemia, responds to antibiotics.


Whipple disease

Epidemiology- men 10:1,

Morphology- mucos laden distended macrophages in lamina propria- conatin PAS POSITIVE GRANULES, may have granulomatous inflammation, rod shaped bacilli can be seen on EM

EtologyTrophera whippelii- gram positive sickle shcaped actinomycete


Clinical features. involves many organs including small intestines joints, heart liver spleen and CNS, presents with malabsorption weight loss, diarrhea, skin hyperpigmentation, lymphadenopathy, arthritis


Chronic pancreatitis





Clinical features.



eitology- underlying obstruciton of the lume in 50-80% of caseses

pathogenesis- unclear in non obstructive cases, in obstructive- obstrction--> continued secretion of mucinous fluid--> increased intraluminal pressure--> collapse of draining veins--> ischemic injuy--> bacterial proliferation--> inflammation of edema


clinical presentation- mild fever, nausea, vomiting, tenderness at mcburneys point, neutrophilia.(leukocytosis.

common complications- perforation, peritonitis, periappendiceal abscess, liver abscess, bacteremia


Mucocele of the appendix

Dilation of lumen due to mucinous secretion

-lining epithelium may be adenomatous(mucinous cystadenoma) or carcinomatous(cystadenocarcinoma)
-Rupture may lead to pseudomyxoma peritonei

pseudomyxoma peritonei- peritoneal studding by mucinous implants-

range- entirely mucnous with no epithelieum
abudant mucin- scant low grade neoplastic epithelium,
- abundant malignant epithelial cells- signet ring cells, infiltrating column epithelium


Hirischprung disease

age predilection- moct common cause of congenital intestinal obstruction- incidence is 1-5000 M4:1. In 10% of down syndrome

Morphology-dilatation and hypertrophy proximal to aganglionic segmment

etiology absence of ganglion cells in meissner and auerback's plexus. rectum is always affected

pathogenesis- defect in migration of survival of neuroblasts, functional obstruction, dilatation proximal to obstruction.

clincal features- delayed passage of meconium, constipation, abdominal distension, diagnosed by rectal biopsy,

complications-enterocolitis, perforation and peritonitis.


Pseudomembranous colitis

morphology- colon (rectosigmoid, has raised yellow plaques.
- fibrinopurulent necrotic debris
-- durface epithelium denudesd
-- supeficially damaged crypts distended by mucopurulent exudate which erupts to form a muschrooming cloud
-- coalescence of these clouds leads to pseudomembrane formation.

Etiology- associated with broad spectrum antibiotic used, caused by clostridium dificile

pathogenesis- toxin mediated damage.

clinical features- diarrhea, abpain, usually below umbilicus, abdominal cramps, tenesmus- painful defecation.




age predilection- 50% older than 50

Morphology- aquired outpouching of bowel wall characterised by herniation of the mucosa and submucosa through the muscularis propria. - found in double row along the antimesenteric tenai coli.
-aquire outpatchings since only two layers of the bowel wall ar involved. flask like structures (95% sigmoid colon) mucosal outpouchings from lumen through muscular layer.


pathogenesis- lack of dietary fiber leads to sustained bowel contraction and increased intraluminal pressure, herniation of colonic wall at sites of focal defects

clincal feature- asymptomatic, constipation alternating wiht diarrhea, left lower quadrant, ab cramping and discomfort, occult bleeding and an iron deficiency anemia, lower GI hemorrhage

complications- diverticulitis, fistuals, performation.



age predilection-50% older than 50

Morphology- flask like structures (95% sigmoid colon) mucosal outpouchings from lumen through muscular layer.

low fiber.
pathogenesis- lack of dietary fiber leads to sustained bowel contraction and increased intraluminal pressure, herniation of colonic wall at sites of focal defects

clincal features- lower ab pain, constipation, diarrhea, flatulence, fever

complications- can be complicated by perforation- fistula lead to peritonitis, abscess formation or bowel stenosis. give antibiotics.


Ischemic colitis


Etiology- venous, arterial insufficiency, occusive or non occlusive
--occlusive- arterial thrombosis, systemic atherosclerossi, vasculitis, hypercoaguable states, angiographic procedures
---- arterial embolism from cardiac vegetations, atherothromboembolism and angiographic procedures
---- venous thrombosis- hpyercoabulable tates, oral contraceptives, intraperitoneal, sepsis, post operative.
-- non occlusive- cardiac faiulre, shock dehydration,
-- miscelanesu, radiation, volvulus, hernation.


clinical features-diarrhea, abpain, usually below umbilicus, abdominal cramps, tenesmus- painful defecation.
- nausea, vomiting blood stools,
- transmural invovlement, severe ab pain/tenderness, gangrene, perforation, peritonitis, shock, and vascular collapse, mortality is very high

course- can become chronic which is insidiuous, chornic inflammation and fibrosis, stricture formation, common at water shed areas, and splenic flexure. Intermittent attacks of pain, intestinal angina. can mimic inflammatory bowel disease.


Amebic colitis

morphology -chronic destructive colitis with flask shaped ulcers.

Etiology- entamoeva histolytical


clinical features-diarrhea, abpain, usually below umbilicus, abdominal cramps, tenesmus- painful defecation.
may resemble IBD on biopsy.


Ulcerative colitis

Idiopathic inflammatory bowel disease, non granulmoatous ulcerative inflammation limited to large bowel.

epidemiology- peak between 20 and 25 years, more common in whites.

assocation- primary sclerosing cholangitis, HLA DRB1 assocation.

morphology - serosa is normal, mucosa is red, granular and friable, broad based ulcers, involves the mucosa/submucosa, not muscularis. isolated islands of interevening regenerating mucosa bulge create pseudopolyps.
-distance between bottom of crypt and submucosa is increased there is branching in the crypts and distortion of the crypts. branching in the crypt, and distortion of the crypts, cryptitis if in the wall, cryptabscess in the lumen
- thin wall apperance, superficial ulcers,

pathogenesis- starts in rectum and then extends in a continuous fashion proximally to involve the whole of the colon.

clinical featuers- no fat vitamin malabosorption, good response to surgery.

complications- back wash ileitis

malignant potential- yes


Crohn disease

is an idiotpathc inflammatory bowel disease, a systemic with predominant GIT involvement, often granulomatous which can affect any part of the GIT from mout to anus. also called, terminal ileitis, regional ileitis and granumoatous colitis.

epidemiology- common in US, adolescents and young adults, F 1.6:1, more common in jews. associated with HLS DR7 and DQ4

morphology- sharply delimited and transmural invovlement by an inflammtory process, presence of non-caseating granulomas, mucosal fissuring with formation of fistulas.
-mesentery thickened and fibrotic, wall thickened
-long thickened segments of small intestine(unlik TB strictures which are short.
- skip lesions, colon thin wall, SI, thick wall.
- transmural inflammation, deep ulcers, SI no pseudopolyps,marked fibrosis, serosistis, granulomas, fistulas.


clinical featuers- edema, hypertrophy of wall, fibrosis and inflammation Xray- string sign.

complications- creeping fat- mesenteri fat wraps around bowel serosa.

malignant potential- yes.


Lesions that can produce small intestinal obstruction

congenital malformations like atresias, intussception, adhesions, bands, volvulous, tumors, stricture formation due to RB and radation.


hyperplastic polyps(inflammatory)

Incidence- people age 50-60 years old

morphology- multiple and ovoid in shape, less than 1 cm in diamter. smooth surface. irregular cystically dilated and elongated foveolar glands. lamina propria is edematous with variable degrees of acute and chornic inflamamtion.

pathogenesis- happen with chronic gastritits that initiates the injury and reactive hyperpasia that cause the polyp growth. If assocatied with H.Pyloir, may regress with antibiotics.

clinical features

malignant potential- correlats with the size with an increased reisk greater than 1.5 cm


Juvenile polyps- AKA retention polyp- n

Incidence- common in children under 5, also seen in adults

morphology-rectum is a comon site, sporadic single polyps,usually 1.-3 cm lobulated with stalk. may have inflammatory cells.

pathogenesis- lamina propria forms the bulk and encloses abundant cystically dilated galnds

clinical features

malignant potential- sporadic single- none juvenile polyposis syndrome: increased risk, also seen in cowden and bannayan-ruvacalba-riley syndromes(PTEN mutations.)


tubular adenomas

Incidence- usualy solitary and 90% in colon.

morphology- small pedunculated polyps composed of small , rounded tubular glands.

malignant potential- precursor to adenomas. risk increaesed with size and dysplasia, invasion of submucosal stalk constitutes invasive carcinomas.


villous adenomas

morphology- larger and covered by slender villi

malignant potential precursor to adenomas. risk increaesed with size and dysplasia, invasion of submucosal stalk constitutes invasive carcinomas.

Clinical features- loss of fluid, proteins and electrolytes, hypoproteinemia, hypokalemia, loss of blood will show iron anemia.


Tubulovillous adenomas

morphology- tubular and villous elements

malignant potential precursor to adenomas. risk increaesed with size and dysplasia


Peutz Jegher syndrome (Hamartomatous polyp)

genetics- AD,

morphology- multiple polyps in whole of GIT,
-arborizing network of smooth muscle extending into the polyp and surrounds glands
- glands are lined by non-dysplastic epihelium rich in goblet cells.

clinical features -Melanotic pigmentation in mucocutaneous areas, lips, perioral areas, face, genetalia palms.

malignant potential- no malignant potential in the colon, at risk of carcinomas in pancrease, breast, lung, ovary and uterus


Familial adenomatous polyposis

genetics- APC gene- 5q21

morphology- usually tubular, in small intestine and stomach,Tons of adenomas, min 100

clinical features- iron anemia, asymptomatic.

malignatn potential- carcinoma in young individuals,

complications: Gardner Syndrome- tubular adenomas with multiple osteomas, desmoid tumors and epidermal cysts.
Turcot syndrome- adenomas and CNS gliomas.


Hereditary nonpolyposis colorectal cancer Lynch syndrome (HNPCC)

AKA walrthin lynch syndrome

genetics- defective DNA repair genes MLH1, MSH 2 and Microsatetllite instability

morphology- less polyps than AP but can be multiple, precursor- none, sessile serrated adenoma, large hyperplastic polyps. more common on right side.
- mucinous histology, increased number of tumor infiltrating lymphocytes.

clinical features

malignant potential

association with carcinomas in endometrium, ovaries, stomach, small intestine, biliary tract.


colorectal carcinoma

occurs in elderly, in young with UC or polyposis

etiology- risk factors- obesity, inactivity, low fiber, animal fat. no fruits and veggies(atntioxidants protective)

-Chromosomal instability, MSI pathway. APC GENE- FAP, Gardner, Turcot
- MSI- may arise from adenomas or other lesions. mismatch repair genes, MLH1 MSH2 MSH6 PMS- sporadic, 15% familial- HNPCC/ Lynch syndrome.
-neoplastic glands invading submucosa and beyond, may produce extensive mucin, spread to lymph nodes i frequent, systemic to liver, lung and bones.
morphology- usually solitary, multiple cancers, proximal colon- exophytic polypoidal lesions and obstruction is common, disttal colon- annular, encircling napkin ring constrictions.

well : 1-glands in 95%,
moderate: 2- 50-95 % glands
poor and undifferentiated 3 less than 5% glands

staging critera
T- 1. invasion of submucosa 2. invasion of muscularis propria 3. invasion through muscularis propria into subserosa or nonperitonealized pericolic tissue 4. direc invasion of other organs or structures or perforates visceral peritoneum

N- 1. 1-3 positive, 2, 4 or more positive

M- 1 any metastasis..

clinical features- asymptomatic Right sided- fatigue weakness, iron deficiency anemia
- left sided- altered bowel habits
-tumor marker- CEA

course- iron deficiency anemia in old men unless proven otherwise.


right vs left colon carcinoma

Distal colon(left)- annular, encircling napking ring constrictions- can cause obstruction

Proximal(right)- exophytic polyploidal lesions and obstructions is uncommon. - HNPCC- uncommon but may grow to large size and metastsize. extend along one wall of the cecum and ascending colon

clinical features: are insicious and may not be discovered for a long time.
right sided- fatigue and weakness due to iron deficiency anemia. (assume colon cancer in older men and postmenopausal women if iron deficiency.
left sided- occult bleeding, changes in bowel habits, cramping, left lower quadrant discomfort.


Carcinoid tumor

origin- derived from endocrine cells.(they generate bioactive compounds, it is rare in esophagus, and uccurs in the stomic in three settings.

-Esophagus rare
--Type 1 gastric atrophy and achlorhydria- hypergastrinemia leads to ECL cell hyperplasia, there may be multiple carcinoids usually follows a bengn course
--Type 2 Gastrinoma (ZE syndrome) usually in MEN2 sundrome, hypergastrinemia
--Type 3 sporadic, usually aggressive tumor with metastasis.
-Small intestine and appendix- most common site in TI tract, often small, occult primary turmors, can metastisize widely leading to carcinoid syndrome when liver involved.
-Rectum- often small and benign

clinical features

common sites


Carcinoid syndrome

Wheezing diarrhea and flushing. rare because it has to involve the liver


Gastrointestinal lymphoma

epidemiology- gut most common site of extrandoal lymphomas and incedence i increasing



Assocations. B- Cell also called mucosa associated lymphoid tissue or MALT- type. low grade and indolent. High grade DLBCL also common.
- mantle cell, Burkitt and Burkitt like lymphoma, follicular lymphomas and other nodal types of lymphoma
immunodeficiency related, Post transplant, acquired AIDS, congenital immunodefciency syndrome, IBD asst, Methotrexat therapy assocaiated

T- cell- Enteropathy assocaited EATL including ulcerative jejunitis, gamma delta hepatosplenic T-cell lymphoma, Angioimmunoblastic type T-cell lymphoma, Estranasal NK cell and NK cell like T-cell lymphoma.
Anaplastic large cell Ki-1 lympohma, true histiocytic lymphoma, Hodkin's disease, leukemic infiltration of GI tract.

Extranodal marginal zone lympohma of malt type- MALT lympohma, Maltoma, recapitulates histology of mucosa associated lymphoid tissue (peyer patches- MALT- cells die in absence of H-pylori, and when only chemical mitogens are used, they also die when T-cells are removed from the culture, you can treat this if you treat H. Pylori.


common sites- stomach more than small intestine more than colon and rectum.

clinical features- 27-84 with mean at 60 males more than females, Non specific symptoms of Dyspepsia, pain abodmen, nausea vomting, weight loss, on examination therer will be abdominal mass and blood loss,

course, eradicate Hpylori, 67-90% remission with 10% relapse, slow growing and remain localized, 5 y is 90% and 10y is 65-75% unresponsive case treated wtih chemo- the anti CD 20 agent Rituximab


prehepatic jaundice

Predominantly unconjugated
hemolytic anemias,
Increased blood resorption from homorrhage
inneffective erythropoiesis


hepatic jaundice

viral hepatitis, cirrhosis, drugs and hereditary hyperbilirubinemias
-reduced uptake- drugs interfere with membrane carrier system diffuse liver disease- unconjugated
-impaired conjugation- in newborn- unconjugated
-decreased excretion- drugs, transporter deficiency- conjugated
-impaired bile flow- bile duct destrutction. -conjugated


post hepatic jaundice

Predominantly conjugated
Gall stones, Ca head of pancrease, stones in the CBD and Calcium of the extra hepatic bile ducts.
- biliary atresia common in neonates- partial or complete destruction or absence of extrahepatic bile ducts.



morphology- bridging fibrous septa, parenchymal nodules created by regeneration, architectural disruption

etiology- alcoholic liver disease(most common), viral hepatitis, NASH, biliary tract diseases, hereditary hemochromatosis, wilson disease, alpha 1 antitrypsin deficiency, cryptogenic cirrhosis.

pathogenesis- diffuse liver process with fibrosis and conversion of normal architecture into structurally abnormal nodules, stage in evolution of many chronic liver diseases with consequences unrelated to primary etiology
- Chornic inflammation of TNF alpha, TGF beta, IL10, disrution of ECM, cytokine production by kupffer cells and hepatocytes, and direct stimulation of Itocells by toxins stimulate the Ito cells- this causes deposition of colalgen I and II in the space of disse
- collagen deposition causes
--loss of fenestrations in endothelial cell--> impaired hepatocellular secretion of proteins like albumina nd clotting factords
-- new vascular channels in fibrous septa==> shunting of blood
-- obstruction of biliary channels- jaundice

Clinical- may be silent, non specific signs and symptoms- usually features of portal hypertension and liver failure, increased risk of HCC


Portal hypertension

etiologic factors- increased resistance to portal blood flow, other disorders other than cirrhosis

clinical feactures and complications
- ascites
-portosystemic shunts- esophageal , gastric varices, rectum retroperitoneum, abdominal wall- caput medusae.
-congestive splenomegaly- thrombocytopenia
-hepatic encephalopathy


Hepatitis A

•Nomenclature of antigens and antibodies- IgM apper at the onset of sign and symptoms after a few months IgG, anti HAV figured out this way.

•Epidemiology- common in children, people who live in crowded areas.

•Modes of transmission- feco oral route

•Incubation period- 2-6 weeks

•Morphologic findings (from Pathology)
•Clinical features- usually mild self limited disease, fatigue, and loss of appetite and often develop jaundice.
•Does not cause a carrier state
•Complications - doesn't cause chronic hepatitis, rarely causes fulminat hepatitis.


Hepatitis B- serum hepatitis.

•Nomenclature of antigens and antibodies- HBsAG or antibody to HBcAG(core protein)- dane particle

•Epidemiology- big global health problem. live in asia or pacific rim. high in africa as well.

•Modes of transmission- parenteral, sexual contact, perinatal, blood transfustion and blood products, IV drug abuse, homosexuals, needle stick injuries. - present in all pathological and physiological fluids.

•Incubation period-1-4 months

•Laboratory findings- elevated HBeAg, HBV DNA HBsAg in acute, also elevated IgM and anti HBc, anti HBe, anti HBc, all start after incubation period. in chronic they persist.

•Serologic findings at various stages in course of disease

•Clinical features and course, - sometimes causes chronic liver disease. acute hepatitis with recovery and clearance of virus, nonprogressive chronic hepaitits(rare), progressive chornic disease ending in cirrhosis, fulminant hepatitis with massive liver necrosis(rare), an asymptomatic carrier state.
-anorexia, fever, jaundice, and upper right quadrant pain. self limited resolves without treatemnt.

carrier state dictated by age at infection, highest when infection occurs in children perinatally and lowes when adults are infected.


Heptatits C

•Nomenclature of antigens and antibodies

•Epidemiology- most important cause of transfusion associated hepatits and chronic liver disease

•Modes of transmission
•Incubation period- 1-3 weeks.

•Serologic findings at various stages in course of disease
•Clinical features and course- persistent infetion and chronicity are hall mark.
- acute infection can resolve, cause chornic hep (85%) or rarely cause fulminant hep. if chornic 80% become a stable disease, 20% cause cirrhosis and increased risk of HCC, 50% of cirrhosis are stable, and 50% death.



replication defective RNa virus,
infective only when encapsulated by HBsAG,
- either coinfection or established HBV infection before super infection
Super infection is more dangerous.


hepatits E

Enterially transmitted as endemics
-uneveloped SS RNA
NO CHRONICITY- immunosuppresed post liver transplatn patients
-usually a self limited disease but high mortialty in pregnant females.
-ever cholestasis which persists for longer period


Alcoholic liver disease

morphology of steatosisstarts out initally as enalrged yellow fatty liver wich progresses to fibrotic and fatty shrunken liver.

morphology of alcoholic hepatitis
- Mallory hyaline bodies- tangled skeins of intermediate filaments,
-seen as eosinophilic cytoplasmic inclusion.
morphology of cirrhosis
- mainly micronodular, macronodules may be formed at a later stage.

clinical features


Hepatocellular carcinoma

frequency- commonest malignant tumor world wide, 16,000 cases in USa, Male predominance usually in adults. Children with metabolic liver disease

risk factors
cirrhosis, Hep B and C, hemochromatosis, alcoholic cirrhosis, A1AT deficiency, alfatoxin, non alcoholic fatty liver disease.

morphology- unifocal or multifocal with diffuse infiltrate, usually paler than surrounding hepatic parenchyma, likely to invade vascular channels. can be well-poorly differnetiated, trabeular , sinusoidal psuedoacinar pattern. Bile production by tumor cells, cytoplasmic inclusions, usually cirrhosis in adjacent liver parenchyma.

etiology- strongly related to prevalence of HBV

pathogenesis- Young person gets HBV through fetal route and have the virus since infancy so they are at high risk.

realtion to cirrhosis- majority related but not reuqired.

Diagnosis (AFP)- raised in 60-75%. FNAC biopsy

Clinical findings- not uniform, usually masked by underlying liver disease, ill defined upper abdominal pain, fatigue cachexia, majority are not surgical candidates due to multicentricity, parenchymal dysfunction.



frequency-most common in liver tumor in neonatesusually occurs at 18months (0-40 months) with slight male predmoniance

morphology- fetal- small uniform cells in cords
-embyronal and fetal- fetal components with sheets of round, usiform cells
-arranged in rosettes, cords and ribbons.
-combined epithelial mesenchymal components
--epithelial with mesenchymal elements (fibrous tissue or osteoid or cartilaginous differentiation.


pathogenesisrapid growth spreads to lungs LN and peritoneum, poor prognosis, transplant considered if no metastais.

realtion to cirrhosis

Diagnosis (AFP)- elevated in 80-90%

Clinical findings-hepatomegaly, abdominal mass, jaundice is rare.

Associations- beckwith weidermann syndrome, down syndrome, familial polyposis coli, hemihypertrophy, renal malformation, cytogenetic abnormalities


Fibrolamellar variant of HCC

frequency- males equal to females,

morphology- usually a single hard tumor with fibrous bands traversing through it. well differentiated polygonal cells in cords, nests, separated by fibrous septa. very fibrotic

etiology- no association with HBV or cirrhosis

pathogenesis-better prognosis.

realtion to cirrhosis- none

Diagnosis (AFP)
better prognosis than HCC
Clinical findings
can be resected




morphology-cut surfaces, firm and grity, adenocarcinoma with extensive fibrosis(markedly desmoplastic.)

etiology- majority have no well known risk factors
Sclerosing cholangitis, cystic dilatations, malformation of biliary system, gallstones, Benzidene, nitrosamines, Parasite clonorchis sinensis and opisthorchis viverini

pathogenesis- can be intra or extra hepatic. most common at the hilu of the liver, most in upper third of the hilum

realtion to cirrhosis

Diagnosis (AFP)- normal levels

Clinical findings- malaise, weight loss, jaundice, cholangitis, Charcot triad(Jaundice, fever, chills). Raynaud pentad(charcot triad with hypotension and mental status changes-poor prognosis)
- clinically silent for long periods

complications- more likely to spread beyond liver than HCC, prognosis is poor usually death within 6 months.


metastatic carcinoma of the liver

frequency- second most commonly involved organ by metastatic disease after lymph nodes. multiple lesions are more likely metastatic than primary- most common 1. Colon, Stomach, pancreas, breast, lung, eye, childrenneuroblastoma, wilms tumor, leukemia

morphology- Multifocal,

etiology- metastasis from other parts of the body

Diagnosis (AFP)- usually normal

Clinical findings



risk factors -
Cholesterol Stones
-western developed countries
-advancing adge
-OCP, Pregnancy(women)
-obesity, rapid weight reduction, gall bladder stasis, inborn error of bile salt metabolism, hyperlipidemia syndromes
Pigment stones
-common in asians
-rural more than urbanchronic hemolytic syndromes, biliary infections, GI disorders like crohn's or ileal resection or bypass, cystic fibrosis of pancreas.

mechanism of stone formation- bile is supersatured with cholesterol, GB hypomotility promotes precipitation of cholseterol from bile into vesicles(necluation.) Cholesterol nucleation is accelerated, Mucus hypersecretion traps the crystals, permitting aggregation into stones (acts like glue)

composition of stones- cholesterol or pigemented.

morphology of stones- yellow or green pigmented.

clinical features -70-80% asymptomatic, may present with pain constant or colicky

complications- empyema, perforation, fistulas, cholangitis, pancreatitis, gallstone ileus, increased risk of carcinoma


Acute vs Cholecystitis


Acute- chemical irritation and inflammation in setting of obstruction of flow, mucosal phospholipase is converted to lysolecithin, damage to glycoprotein layer of mucosa, further release of prstaglandins from mucosa, cumulatively leads to mucosal and mural inflammation, gall bladder dysmotility and increased intraluminal pressure, superimposed bacterial contamination.
Chronic- repeated episodes of acute, or no attacks of acute. role of gall baldder not clear. 1/3 can be cultured from bile in 1/3 of patients.

associated diseases-
Chronic- increased assocation with cancer.

Chronic- rarely extensive dystrophic calcification (porcelain gall bladder

clinical findings-
Acute:-pain right hypochondrium or epigastrium, may be surgical emergency, assocaited with fever nausea, vomiting



Carcinoma of the gall bladder

epidemiology-most common in seventh decade of life. slightly more common in females. Gallstones in 60-90% of patients. risk factors of pyogentic or parasitic infections.

relationship to cholelithiasis- carcinogenic derivatives fo bile may play a role

morphology- mostly adenocarcinoma

clinical findings-most have invaded or spread to liver at diagnosis.



Exocrine pancreatic insufficiency


etiology-poor digestion of complex foods and digestion of breakdown products, pancreatitis and cystic fibrosis most common causes.

clinical manifestations- malabsorbtion syndrome, usually significant with 90% function of loss, fat malabsorption, loose greasy foul smelling stool. fat soluble vitamins not absorbed lipolytic activity decreases faster than proteolysis. , glucose intolerance due to diabetes mellitus.

laboratory abnormalities


Cystic fibrosis

AR disease, CFTR gene mutation, 1 in 3200 live births. most common in whites, most common fatal AR disease

primary defect- defective chloride ion transport- h

morphologic findings in
thick luminal secretions in GIT
-pancreas- affected 85-90% eosinopihli scretions or concretions the secretions represent mucoprotein fat necrosis is present.
-lung- most seirous, thick secretions
-liver disease later in course
-salivary glands
-male genital tract- bilateral absence of vas deference, infertility

clinical findings - gene sequencing whill show it. symptoms varied, cardiorespiratory complications are most common cause for death.

course- life expentancy is about 30 years


acute vs chronic pancreatitis

etiologic/predisposing factors
-Acute -proenzymes become active and causes enzymatic necrosis and infllamtion of pancrease. assocaited with gallstones and acoholisms(80%). infections- mumps, cocksackie, mycoplasma, acute ischemeia due to shock trauma, vascular thrombosis, embolism, vasculutits, hyperlipoproteinemias, drugs like diuretics, azothioprine, estrogens.
-chronic: middle aged alcoholics(Most common cause, Pacreatitc divusm. Tropical pnacreatitis, Hereditary pancreatitis, CFTR mutation assoicated, 40%idiopathic

-Acutefocal fat necrosis in pancreas and peripancreatic tissues and abdominal cavity. Calcium deposits, severe cases you will have necrosis and hemorrhage.
-Chronic- bouts of mild to moderate inflammation withloss of pancreatic parenchyma with fibrosis- this is irreversible

-Acute- release of enzymes, toxins and cytokines in circulation leads to activation of systemic inflammatory response.

laboratory manifestations-
-Acute- elevated pancreatic enzymes in serum
-Chronic-Xray and CT show calcifications, 10% have pseudocyts.

clinical findings
Acute- ab pain epigastric with nausea and vomiting, constant intense and referred to upper back. , acute inflammation
- leucocytosis, DIC, heolysis, peripheral vascular collapse, shock with ATN, ARDs, Hypocalcemia, tetany, raised amylase levels in first 24 hours, followed by lipase within 72-96 hours,
Chronic: Chronic abdominal pain, Chronic inflammaion, progressive loss of pancreatic endo/exocrine function
-repeated attacks of severe or persistant pain and back pain.

-Acute- ARDS, ATN, pacreatic abscess
-Chronic: pancreatic insufficiency leading to chronic malabsorption(can be given supplements to help. , diabetes, moderate increase risk of carcinoma(particularly by alcohol)


differental diagnosis of epigastric and chest pain caused by lesions of GIT

peptic ulcers
acute pancreatitis


adenocarcinoma of pancreatic head vs body/ tail

morphology- head, calcium of head of pancreas/ampulla obstructs bile flow , dense stronal fibrosis, propensity for perinueral invasion. majority are ductal type adenocarcinomas.

incidence 60-70% head, 5-10% body, 10-15 % tail.

risk factors-only convincing one is smoking, alcohol, and diet rich in fats. strong association with familial relapsing pancreatits.

Clinical presnetation- pain usually first symptom, most silent until late, treousseaus sign, sometimes raised CA 19-9

complications- obstructive jaundice.

prognosis- obstructive jaundice.




morphology- usually solitary

benignity vs. malignancy- usually benign

immunohistochemical charicteristics

endocrine function- insulin levels are increased.

clinical features- show signs and symptoms of hypoglycemia, hypoglycemia accentuated by fasting and relieved with intake of glucose. May clinically mainfest as whipple triad. (ow blood sugar, presence of symptoms, reversal of symptoms when the blood sugar normalized.





morphology- multiple ulcers- esophagus, stomach, duodenum, jejunum which are refractory to conventional treatment.

benignity vs. malignancy- many are locally invasive or metastatic at diagonsis.

immunohistochemical charicteristics associated with MEN I

endocrine function-Gastrin producing endocrine tumors.

clinical features- hypergastrinemia.

course- can arise in duodenum with similar frequency a in pancreas or in the peripancreatic tissues.
- can result in zollinger ellison syndromes which is multiple deodenal peptic ulcers, prominent gastric rugal folds due to increased oxyntic gland mass


acinar cell carcinoma

rare1-2% of all exocrine neoplasm, older aged white men, subcutaenous fat necrosis and panniculitis due to overactive secretion of lipase.


IPM intraductal papillary mucinous neoplasm

arise within the ductal system, majority in the head, more common in men than in women, dilated duct filled with mucin, small risk of malignancy, cysts can be multiloculated, lined by tall columnar secreting cells, Cytology benign, low grade/boderline, malignant, invasive, lacks ovarian type stroma.


MCN Mucinous ystic neoplasms

2-5% of all exocrine neoplasms, almost exclusively in women, mostly in tail, not connected to the ductal system, tall columnar mucin secreting cell. Cytology, Benign borderline malignant invasion.


carcinoma of the tongue

Risk factors- leukoplakia, erythroplakia(50% CA)
-tobacco use
HPB 16,18
alcohol abuse
Protracted irrigation

morphology- may be exophytic or endophytic. moderately to well differentiated keratinised squamous carcinomas

Spread- lymph nodes, extensive regional spread.


oesophageal webs

web-like protrusions of esophageal mucosa into lumen

Schatzki ring- web narrowing at GE junction

ET: plummer vinson syndrome

clinical triad- dysphagia , iron deficiency anemia, glossits
increased risk of carcinoma.


Adenocarcinoma of the Esophagus

-lower- esophagus Adenocarcinoma- most common in US- associated wtih precursor is barrett's esophogaus, multistep dysplasia
median age is 50 years and most comon in white males, signs and symptoms similar to squamous cell. Prognosis is por.


Acute gastritis( erosive or shallow ulcer.)

erosion without inflammation. High incidence in ICU patients.

Morphology- loss of surface epithelium, erosions and hemorrhage, hyperemia, edema and congestion of lamina propria, neutrophils in surface epithelium and lumina of the glands.

etiology factors
NSAIDS, Excessive alcohol, smoking, ischemia and shock, severe stress, burns surgery, chemo, systemic infections, uremia. oral iron,

clinical features- asymptomatic, epigastric pain, nausea, vomiting, Hematemesis and melena, bleeding can be fatal.


Chronic gastritis

Chronic mucosal inflammatory changes leading to mucosal atrophy and epithelial metaplasia, Antral type is most common gastritis in USA

Morphology- normal to patchy/diffuse erythema with hemorrhage to boggy with thick mucosal folds- inflammatory infiltrate in the lamina proprai,
PMN's n surface epithelium and glandular lumen, reactive lymphoid aggregates that are mainly superficial
- intestinal metaplasia and glandular and parietal cell atrophy sometimes dysplasia.

-Chronic H. Pylori(angtral type Type B)
-autoimmune atrophic.(fundic type A)
-alcohol and smoking
post surgical after antretomy
-granulomatous conditions. (crohn's disease and sarcoidosis.

Clinical features- Asymptomatic
-nausea, vomiting, epigastric discomfort, Dyspepsia indigestion
complications- hypochlorrhydria or acholorrhydria which leads to increased serum gastrin, and perincious anemia



two patterns of gastritis, superficial antral inflammation and multifocal leading to multifocal gastric atrophy

proteases, ureases, phospholipases to cause mucosal damage and attracts PMNS and other inflammatory cells to cause damage. this can also lead to uncontrolled proliferation of B cells and lymphoma.

Diagnosis- Endoscopy based invasivie, Rapid urease test, culture, PCR, NON-invasive, urea breath test, serology, PCR in saliva and feces.

associated with Chronic gastritits, duodenal and gastric peptic ulcers, gastric carcinoma, MALT tumors


Autoimmune gastritits

anti parietal cell with anti intrinsic fator antibodies leads to gland destruction/atrophy which leads to loss of acid production and loss of intrinsic factor which causes B 12 deficiency and pernicisous anemia.

Achloryhydria, increased gastrin levels, long term risk of GASTRIC CARCINOMA, also risk factor for CARCINOID TUMORS


Hypertrophic gastropathy zollinger ellison syndrome

Stomach- enlarged rugal folds
- distal duodenum and jejunum have multiple intractable peptic ulcers(non responsive to normal therapies)

etiology- duodenal or pancreatic gastrinoma

Pathogenesis- Gastrinoma causes increased gastrin, which causes increased acid secretion, which causes multiple duodenal and jejunal ulcers, enlarged rugal folds 2/3 of the gastrinomas are malignant


Meckel's Diveticulum

incomplete of involution of vitelline duct

on antimesenteric border, all layers of GIT is a true diverticulum, some times lined by gastric mucosa or pancreatic tissue.


Complications- hemorrhage and peptic ulcer, intestinal obstruction, diverticuluitis, perforation, fistula.


Malabsorption syndrome

clinically present with chronic diarrhea and fatty fees, defective apsorption of fats, fat soluble and other vitamins, proteins, carbs, electrolytes, minerals and waters.



twisting of a segment of bowel on its vascular mesentary resulting in intestinal obstruction and infarction, sigmoid colon.



telscoping of a proximal segment of the bowel into the distal segment, comon in infants and children, may be because of exposure of new antigens causing hypertrophy of the lymphoid follicles.

presentation with classic triad of sudden colicky ab pain, ab distension and currant jelly stools.
complications are infarction of the intussuscepted segementL.


Luminal small bowel obstrucion

-Food bolus, fruit or vegetable, persimmon, macaroni, sauerkraut
-predisposing factors- false teeth, gastrectomy, intestinal adhesions, inadequate mastication and large amounts of food.
therapeutic agents like barium sulphate and atacid gels, ingested hair, (bezoars) mass of round worms, and tumors.
-swallowed foreign bodies, endogenous origin like meconium ileus in infants with cystic fibrosis, and gallstone ileus where the stone is bigger than 2.5 cm long and lodges in the terminal ileum usually through a cholecystoduodenal fistual.


intramural bowel obstruction

congenital atresias or inflammatory conditions- crohn, TB, drug induced stenosis, ischemic strictures, radiation damage, polypoid or infiltratie neoplasms.


Extramural bowel obstruction.

generally peritoneum diseases, mesenteric omental bands, peritoneal tumors or adhesion. (follwoing infection or endometriosus that forms fibrous bridges within which bowel trapped.

Intussuscception, volvulus.



clinical features- relapsing disorder, attacks of bloody mucoid diarrhea, lower abdominal pain, abdominal cramps, tenesmus, flareups with phsyical and mental stress, fever and wieght loss in severe cases. features of malabsorption
smallintestine- features of subacute intestinal obstruciton

Extraintestinal manifestations- seen in both CD and UC more common in UC
- can develop even before the onset of GI sign symptoms- migratory polyarthritis, sacroileitis, ankylosing spondylitis, erythema nodosum, clubbing of ingers, sclerosing cholangitis. Increased risk of developing malignancy, CD less than UC. .


Intestinal ulcers

UC- intermittent rectal bleeding, bloody diarrhea, and ab pain. typically continuous colonic involvment
CD- more variable symptoms than UC that include ab pain, fatigue, weight loss and fever, typically patchy transmural involvment
Infective colitis- bloody diarrhea, nausea, vomiting, fever, lamina propria hemorrhage, erosion, and neutrophils. infiltrate lamina propria and glands.


Infectious colitis

amebic colitis- gradula dysentery, flask shaped ulcer with organisms englufing red cells

typohid, fever headache, abdominal pain, rash and diarrhea.
- longitudinal ulcers, typically over peyer patches

-chronic abdominal pain- multifocal invovlemnt, jejunum to ileum- TI most common
- annular circular or oval ulcers, lying transversely,
- single ulcers large, multiple ulcers smaller
- garnulomatous inflammation, often necrotizing.


Lab investigations for liver disease

-decreased serum ablumin- chronic liver disease
-increased prothrombin time,- acute and chronic liver diseases
-AFP- increased in HCC
-increased serum ammonia- hepatic failure
-anti nuclear, mitochondrial and smooth muscle antibodies are immunological and viral markers
-decreased ceruplasmin in wilson disease


viral infection so f the liver

infectious mononucleosis (EBV) , CMV, yellow fever.


other cuases of chornic hepatitis

alcohol use, metabolic and genetic liver diseasem wilson disease, A1AT deficiency, hemochromatosis, Dugs, autoimmune


Fulminant hepatitis

denotes clinical hepatic insufficiency, that progresses rapidly to hepatic encephalopathy within 2-3 weeks
viral hep most common- but drug and chemical toxicity as well
-rare cases, ischemic necrosis, acute fatty liver of pregnancy, wilson disease.


Autoimmune hepatitis

common in females- prominent interface plasma cell hepatitis, high titers of IgG, anti nuclear and anit smooth muscle antibodies. anti LKM (liver kidney microsomal) antibodies
respond to immunosuppressive therapy.


Primary biliary cirrhosis

disease of middle aged women, immune mediated: anti mitochondrial antibodies in 90%
chronic, progressive and can progress to cirrhosis
- non suppurative, granulamtous destruction of medium sized bile ducts
death usually occurs becaue of liver failure


secondary biliary cirrhosis

due to partial or total bile duct obstruction, tumors, strictures, gallstones implicated.


primary sclerosing cholangitis

inflamamtion, fibrosis and dilatation of intra and extra hepatic ducts, ERCP beading of the biliary tree, P-ANCA in bout 80% of cases, associated with chornic ulcerative colitis.



excessive accumulation of iron- HFE gene increased iron absorption
common in males, rarely manifests before 40, characterized by micronodular cirrhosis, diabetes mellitis, skin pigmentation,

- involved in pancrease, heart skin,


causes of secondary iron overload

-parenteral iron overload, repeated blood transfusion, iron dextran injections
-inefective erythropoiesis, Beta thalassemias, other chornic hemolytic anemias
-increased oral intake- bantu disease,
-chronic liver disease


wilson diseasse

AR disease of gene on ch13, presentation before 6 years, accumuation of copper in liver brain and eyes
brain-basal ganglia
eyes- kayser fleisher ring in corneal limbus, sunflower cataracts
blood- hemolysis.
-liver- fatty change, acute hepatitis, chronic hepatitis, cirrhosis, rarely massive necrosis.

decreased ceruloplamsmin levels, increased hepatic copper, more than 250 micrograms per gram of dry weight
increased urinary copper excretion.


A1AT dsiease

autosomal recessive, encoded by PiMM gene on Chr 14, synthesized mainly by hepatocytes, most allelic variants have slightly reduced levels, deficient variants have retntion of mutant polypeptided
PIZZ -markedly decreased levels and have emphysema, forms numerous inclusins and have liver disease.
- associated hepatic syndromes variable. - neonatal hepatitis with or without cholestasis, smoldering chronic inflammation, cirrhosis at early age,
-hepatocellular carcinoma
-liver transplantation is only treatment


Non alcoholic fatty liver disease

changes like ALD in non drinkers, steatosis with or without hepatitis,
- risk factors, obesity, insulin resistance, hyperlipidemias,
-usually asymptomatic, wiht mild elevation in serum transferases but may lead to cirrhosis.