GIT Flashcards
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.
Erythroplasia
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.)
NO MALIGNANCY
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.
Etiology
incompetance of the lower esophageal sphincter
Pathogenesis
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.
Paraesophoageal-5%
epigastric pain, heart burn in sliding type
complications- volvulus, strangulation, and perforation(paraesophageal type.
achalasia/cardiospasm
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
Etiology
-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) Cigarrettes Celiac disease Diverticuli(zenker's DIET( vitamin A, C riboflavine, pyroxidine deficiency, high nitrite)) Esophageal web Esophogitis Ectodermal dysplasia. Familial Fungal contamination
Morphology
polypoid exophytic masses, diffusely infiltrative neoplasm, will see carcinoma, insitu, invasive.
Pathogenesis
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.
complications.
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
epidemiology-
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
morphology
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
Pathogenesis
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.
Etology-unkown
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
Pathogenesis
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
Epidemiology
Morphology
Etology
Pathogenesis
Clinical features.
appendicitis
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
morphology
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.
course
Diverticulosis
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.
etiology
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.
Diverticulitis
age predilection-50% older than 50
Morphology- flask like structures (95% sigmoid colon) mucosal outpouchings from lumen through muscular layer.
etiology- INFLAMMATION OF DIVERTICULI.
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
morphology
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.
pathogenesis
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
pathogenesis
clinical features-diarrhea, abpain, usually below umbilicus, abdominal cramps, tenesmus- painful defecation.
may resemble IBD on biopsy.
course
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.
pathogenesis
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)
pathogenesis-
-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.
grading:
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.
