Gastrointestinal Flashcards

Question

Gastric Adenocarcinoma

Answer 1

* ETIOLOGY: highest occurrence in Japan and South Korea * Pylorus/Antrum: 50-60% * TYPES: * Intestinal: chronic gastritis due to H.pylori → metaplasia is precursor * Older patients * Sister Mary Joseph nodule * Diffuse: E-cadherin mutation → no gland formation or metaplasia * Young females * Signet ring cells * Leather-bag appearance (linitis plastic appearance) * GROWTH PATTERNS: * Exophytic * Flat * Endophytic (Excavated) • SYMPTOMS: • Early Carcinoma: confined to mucosa and submucosa • Advanced Carcinoma: Krukenberg tumor, Virchow’s lymph node (left supraclavicular lymph node)

Answer 2

* ETIOLOGY: previously misdiagnosed as leiomyomata * Submucosal * PATHOGENESIS: Cells of Cajal (pacemaker cells of enteric plexus) * CD117 tumor marker • c-Kit mutation in exon 11 * MORPHOLOGY: whorls and bundles of spindle shaped cells * Kit mutations (Imatinib = Kit inhibitor)

Answer 3

* ETIOLOGY: Rule of 2’s * 2% of normal population * First 2 years of life * 2 feet from ileo-cecal valve * 2 inches long * 2 types of tissue: gastric + pancreatic * PATHOGENESIS: incomplete involution of the vitelline duct * True diverticulum: includes all layers of the GIT • LOCATION: anti-mesenteric border * SYMPTOMS: asymptomatic * Painless rectal bleeding * Meckel’s Diverticulitis (mimic’s appendicitis) * Perforation * Fistula * Peptic ulver * Hemorrhage

Answer 4

* ETIOLOGY: common in whites, 1-10 years old * HLA DQ2/DQ8 * PATHOGENESIS: atrophy and loss of villi (reduced SA) * Proximal part of intestine * MORPHOLOGY: * Increased intraepithelial lymphocytes – Typical: Villous atrophy • Elongated and hyperplastic crypts (for compensation) • Increased immune cells in lamina propria * SYMPTOMS: chronic diarrhea (w/ steatorrhea) * Iron deficiency anemia * Long-term risk of T-cell lymphomas * DIAGNOSIS: * Anti-gliadin / Anti-endomysial antibodies * Anti-tissue transglutaminase (tTG) antibodies • TREATMENT: reversal of epithelium changes after gluten-free diet

Answer 5

• ETIOLOGY: people living or visiting tropical areas → contract diarrheal illness • PATHOGENESIS: bacterial infection superimposed on pre-existing small intestine injury • Diffuse throughout intestine * Damage to brush border→ failure of reabsoprtion of micelles * secondary folate + Vit B12 deficiency * SYMPTOMS: appear months or years after visit * TREAMENT: responds to antibiotics + Supplemental Folate

Answer 6

* ETIOLOGY: systemic → intestines, joints, CNS * Males \> females * PATHOGENESIS: gram positive actinomycete → Tropheryma whippelii * Macrophages try to digest bacteria * Accumulation of macrophages causes congestion in lamina propria * Compression of lacteals (→ abnormal fat absorption) * MORPHOLOGY: distended macrophages in lamina propria * Possible granulomatous inflammation * SYMPTOMS: malabsorption and steatorrhea * DIAGNOSIS: PAS–positive granules containing bacteria * Mucosa laden with distended macrophages in lamina propria-contain PAS positive granules * TREATMENT: responds to antibiotics

Answer 7

• Protozoan gut pathogen with flagellum – Trophozoites and cysts are shed • Usually acquired from drinking water contaminated with cysts – Poor sanitation and crowded living conditions predispose to infection • Immunosuppression increases risk

Answer 8

* Self-limited infection in a normal host * Chronic diarrhea in AIDS * Intracellular but appears at top of cell microscopically

Answer 9

* Food bolus: macaroni, sauerkraut, fruit or vegetable * Therapeutic agents: barium sulfate, antacid gels * Bezoars: ingested hair * Parasite: Ascaris lumbricoides (round worms) * Tumors * Swallowed foreign bodies: dentures, bones, pins, coins, screws, nails * Endogenous origin: * Meconium ileus in infants (Cystic Fibrosis) * Gallstone ileus: stone \>2.5cm

Answer 10

• Congenital atresias * Inflammatory conditions: * Crohn’s Disease * Tuberculosis - causes transmural granulomatous inflammation of intestine with makred congestion, edema + fibrinoud adhesions → eventually replaced with scar tissue * Drug-induced stenosis * Ischemic strictures * Radiation damage * Polypoid neoplasms

Answer 11

•Mechanical→ involement of entire segment * Diseases of peritoneum: * Congenital mesenteric/omental bands * Peritoneal tumors * Peritoneal adhesions - bands of adhesion tissue→ fibrinious bridges within which bowels are trapped * Hernias * Intussusception: telescoping of proximal bowel segment into distal * Often in adults due to tumor lymphoid hyperplasia in children→ strong association with adenovirus infections • Volvulus: twisting of bowel loop

Answer 12

* Enteric Fever * Salmonella typhi → lymphoid aggregates → ulceration → perforation * Longitudinal ulcers * Tuberculosis * Caseation → necrosis → ulceration → healing → fibrosis → obstruction * Terminal ilium most common * Annular, circular or oval ulcers lying transversely Ischemia of the Small Intestine Acute - villi become tin and detach from basement membrane Chronic - crypt atrophy and lamina propria fibrosis • Volvulus * Strangulated hernia * Gangrene

Answer 13

* ETIOLOGY: inflammation of the appendix * Underlying obstruction of the lumen in 50-80% of cases • PATHOGENESIS: • Obstruction → continued secretion → increased intraluminal pressure → collapse of draining veins → ischemia → bacterial proliferation → inflammation + edema * SYMPTOMS: * Periumbilical pain → RLQ * Nausea, vomiting, anorexia, fever * McBurney’s Point tenderness * Complications: perforation, peritonitis, abscess * INVESTIGATION * CBC→ Increased Nuetrophils * DDX * Meckels Diverticulitis * Ectopic Pregnancy * Chron's Disease

Answer 14

• ETIOLOGY: peritoneal studding by mucinous implants * MORPHOLOGY * Entirely mucinous: no epithelium * Abundant mucin: scant low grade neoplastic epithelium * Abundant malignant cells: Signet ring cells, infiltrating columnar epithelium

Answer 15

* ETIOLOGY: most common cause of congenital intestinal obstruction * Congenital megacolon: dilation and hypertrophy proximal to aganglionic segment * Association with Down Syndrome * M:F is 4:1 * Rectum is always affected ``` • Dilatation and hypertrophy proximal to aganglionic segment (congenital megacolon) ``` • PATHOGENESIS: absence of ganglion cell migration to Meissner/Aurbach’s plexus * SYMPTOMS: * Delayed passage of meconium * Constipation * Abdominal distention * Enterocolitis * Perforation / peritonitis

Answer 16

* ETIOLOGY: diverticulosis * Western world * Most common: sigmoid colon * \>60 years * Diverticulosis = false diverticulum • PATHOGENESIS: lack of dietary fiber leads to sustained bowel contractions and increased intraluminal pressure • Herniation of colonic wall at sites of focal defects • decreased fiber→ sustained bowel contraction & increased intraluminal pressure→ herniation of the colonic wall ``` • MORPHOLOGY: flask-like structures of mucosal outpouchings from lumen through the muscular layer (95% sigmoid colon) ``` * SYMPTOMS: lower abdominal pain, constipation, fever, painless bleeding * Usually asymptomatic, can cause painless bleeding * Diverticulitis – Lower abdominal pain – Constipation, diarrhea, flatulence – Fever * Can be complicated by perforation – Fistula

Answer 17

* ETIOLOGY: ulcero-inflammatory disease limited to colon * White people * 20-25 years old * HLA-DRB1 association * MORPHOLOGY: mucosa is red, granular and friable * No skipped lesions → continuous → curable by surgery * Broad based ulcers * Regenerating mucosal bulges create pseudopolyps * Lead-pipe appearance on barium enema (loss of haustra) * Crypt Abscess + cryptitis • No Granulomas * SYMPTOMS: begins in rectum and extends proximally to involve whole colon * Inflammatory diarrhea * 10% of cases → backwash ileitis * Associated with Primary Sclerosing Cholangitis → p-ANCA PRESENTATION: LLQ abdominal Pain

Answer 18

* ETIOLOGY: terminal ileitis, regional ileitis, granulomatous colitis * Adolescents / young adults * Females \> males * Jews * HLA-DR7, DQ4 • PATHOGENESIS: mesenteric fat wraps around bowel serosa (creeping fat) •Bacteria in lamina propria→ dendritic cells presentation to TH1→ release of TNFa & INF-Y→ activates macrophages→ Transmural inflammation * MORPHOLOGY: mesentery thickened and fibrotic (transmural) * Cobblestone appearance (gross morphology) * Intestinal wall thickened: edema, hypertrophy, fibrosis, inflammation * Transmural fibrosis = (String Sign) * Non-caseating granulomas * Mucosal fissuring with fistula formation * Skip-lesions (not continuous) * Linear Ulcers * SYMPTOMS: malabsorption ( Vit B12 + Bile Salts), fever, weight loss, diarrhea * Migratory polyarthritis * Ankylosing spondylitis * Erythema nodosum

Answer 19

• ETIOLOGY: following travel to the tropics * PATHOGENESIS: Entamoeba histolytica * Cyst → 4 nuclei * Trophozoite → 1 nuclei w/ RBCs inside • MORPHOLOGY: flask-shaped ulcer * SYMPTOMS: abdominal pain, mucoid/bloody diarrhea * Hypoalbuminemia * Hypokalemia * Perforation * Liver abscess * DIAGNOSIS: stool assay for cysts * Complications * perforation→ peritonitis→ E.coli sepsis→ DIC * Abscesses→ liver,lungs, brain

Answer 20

* ETIOLOGY: Clostridium difficile infection secondary to chronic antibiotic treatment * PATHOGENESIS: exotoxin * MORPHOLOGY: raised yellowish / grey membrane * Fibropurulent-necrotic debris – Surface epithelium denuded – Superficially damaged crypts distended by mucopurulent exudate which erupts to form a mushrooming cloud – Coalescence of these clouds leads to pseudo membrane formation • SYMPTOMS: diarrhea, fever, abdominal pain • DIAGNOSIS: exotoxin in stool assay • NO COLONOSCOPY → will perforate the membrane and bowel

Answer 21

* ETIOLOGY: venous or arterial insufficiency * Common in elderly • PATHOGENESIS: transmural • Occlusive (Arterial thrombosis, arterial embolism, venous thrombosis) • Non-occlusive (cardiac failure, shock, dehydration) * SYMPTOMS: * Absent bowel sounds * Severe abdominal pain * Gangrene, perforation, peritonitis * Shock / vascular collapse * High mortality

Answer 22

* ETIOLOGY: stricture formation * Common at watershed areas * Splenic flexure • MORPHOLOGY: chronic inflammation and fibrosis * SYMPTOMS: can mimic inflammatory bowel disease * Intestinal angina • Intermittent attacks of pain

Answer 23

* Allergy: ow’s milk protein allergy * Parasites • Iatrogenic Drugs, radiation • Collagen vascular diseases Rheumatoid arthritis, Churg-Strauss syndrome • Inflammatory bowel disease • Tumor or tumor-like conditions - Leukemia/lymphoma - Hypereosinophilic syndrome

Answer 24

* ETIOLOGY: common in children \<5 years * Rectum is most common site * No malignant potential if single polyp * MORPHOLOGY: 1-3cm, lobulated with stalk * Lamina propria forms the bulk * Dilated glands * PTEN mutation Histologically: • Expanded lamina propria • Abundant cystically dilated glands • Inflammatory cells may be present * Usually 1-3 cm, lobulated with stalk * Juvenile polyposis syndrome→ leads to increased risk of malignancy •associated: Cowden and Bannayan-Ruvacalba-Riley syndromes

Answer 25

• ETIOLOGY: hamartomatous polyp • MORPHOLOGY: arborizing network of smooth muscle extending into the polyp and surrounds glands • Glands are lined by non-dysplastic epithelium rich in goblet cells • SYMPTOMS: no malignant potential * Peutz-Jegher Syndrome: autosomal dominant * Multiple polyps * Melanotic (black) pigmentation in lips, face, genitalia

Answer 26

* ETIOLOGY: epithelial proliferative dysplasia * 90% in the colon * Precursor lesions of carcinomas * Malignant risk increases with: polyp size, Severity of dysplasia ,Villous architecture, 3 or more adenomas • MORPHOLOGY: adenomatous epithelium is severity of dysplasia tall, hyperchromatic and disordered • Tubular • Villous • Tubulovillous * SYMPTOMS: asymptomatic * Anemia (occult blood loss) * Villous adenoma → dehydration, hypoproteinemia, hypokalemia • Intussusception

Answer 27

* ETIOLOGY: genetic defect in APC gene (5q21) - requires 2 hits plus p53 and KRAS * Young people • Bright, red bloody, & mucoid diarrhea * MORPHOLOGY: tubular type in left (descending colon) * Typically 500-2500 mucosal adenomas * Minimum required for diagnosis is 100 * SYMPTOMS: * Gardener Syndrome: tubular adenomas with multiple osteomas, desmoid tumors, and epidermal cysts • Turcot Syndrome: adenomas and CNS gliomas

Answer 28

* ETIOLOGY: elderly individuals * Young individuals if history of ulcerative colitis and polyposis syndromes • RISK FACTORS: obesity, low fiber diet, diet rich in animal fat • PATHOGENESIS: Iron deficiency, Blood in stool • Chromosomal Instabilities (90%): APC, p53, KRAS • MSI Pathway (10%) : MLH1/MSH2 * MORPHOLOGY: neoplastic glands invading submucosa and beyond * Proximal Colon: exophytic polypoidal lesions * Distal Colon: annular, encircling napkin ring constrictions * SYMPTOMS: asymptomatic * Right Sided: fatigue, weakness, iron deficiency anemia * Left Sided: altered bowel habits * Spread to liver, lung, and bones • DIAGNOSIS: CEA

Answer 29

• Warthin-Lynch Syndrome * ETIOLOGY: MLH1/MSH2 mutation - DNA repair Gene * Microsatellite instability * MORPHOLOGY: ascending colon more common * Large, sessile - Villious Adenocarcinoma ( no benign polyps) * Less polyps than FAP * SYMPTOMS: occult bleeding - Fatigue and Iron deficiency , anemias due to blood loss * Associated with carcinomas of other abdominal sites

Answer 30

* ETIOLOGY: derived from endocrine cells * MORPHOLOGY: nested and organized - Salt pepper appearance • STOMACH: • Type 1: gastric atrophy and achlorhydria → hypergastrinemia leads to ECL cell hyperplasia • Type 2: Gastrinoma (Zollinger-Ellison Syndrome) → MEN1 syndrome, hypergastrinemia • Type 3: Sporadic (most aggressive) * SMALL INTESTINE + APPENDIX: most common site * Carcinoid syndrome → wheezing, diarrhea, flushing • DIAGNOSIS: 5HT elevated→ may lead to right sided heart failure

Answer 31

* ETIOLOGY: lymphoma presenting with the main bulk of disease in the GI tract * SITES: stomach \> small intestine \> colon/rectum * B-CELL: * MALT-type * High grade DLBCL * Mantle Cell lymphoma * Burkitt Lymphoma * Follicular lymphoma * T-CELL: * Enteropathy Associated (EATL) * Hepatosplenic T-cell lymphoma * Angioimmunoblastic-type T cell lymphoma

Answer 32

* ETIOLOGY: 60 years (mean) * MALToma cell proliferates in-vitro with heat killed H.pylori • SYMPTOMS: dyspepsia, abdominal pain, nausea, vomiting, weight loss * TREATMENT: * Antibiotic treatment for H.pylori

Answer 33

* DEGENERATION: * Ballooning: irregularly clumped cytoplasm * Feathery: fine foamy cytoplasm → detergent action of bile salts • STEATOSIS * MACROVESICULAR: single fat vacuole displaces nucleus to periphery * Alcohol * MICROVESICULAR: multiple vacuoles, central nucleus * Acute fatty liver of pregnancy * Reye’s Syndrome * Drugs * NECROSIS: focal, bridging, or massive/sub-massive * APOPTOSIS: Councilman’s Bodies, Acidophil Bodies • REGENERATION: Thickening of hepatocyte cords, mitosis, and some disorganization • FIBROSIS

Answer 34

* ETIOLOGY: diffuse liver process with fibrosis and conversion of normal architecture into structurally abnormal nodules * Alcoholic liver disease * Viral hepatitis * Hemochromatosis * A1AT Deficiency * Wilson’s Disease * Budd-Chiari Syndrome * MORPHOLOGY: * Bridging fibrous septa • Parenchymal nodules created by regeneration – Diffuse involvement of liver • Architectural disruption Based on nodule sized, often classified as: – Micronodular \< 3mm nodules – Macronodular \> 3 mm nodules * PATHOGENESIS: * Chronic inflammation + cytokines + toxins stimulate Ito cells * Deposition of collagen I and III in Space of Disse * Loss of fenestrations, new vascular channels in septa, obstruction of biliary channels * Impaired hepatic secretions, shunting of blood, jaundice * SYMPTOMS: * Portal hypertension • Liver failure • Increased risk for HCC

Answer 35

• PATHOGENESIS: increased resistance to portal blood flow • SYMPTOMS: • Ascites • Portosystemic shunts: esophageal varices, gastric varices, hemorrhoids, caput medusae * Congestive splenomegaly * Hepatic encephalopathy

Answer 36

• ETIOLOGY: most common infectious disease of the liver • HEPATITIS A -- SsRNA • Does not cause chronic hepatitis • Common in children • Fecal-oral route • Diagnosis- IgM anti-HAV at onset of disease • HEPATITIS B: Enveloped DNA Virus • Propensity for chronicity • Transfusion of blood, sexual intercourse, IV drug abuse, homosexuals, needle sticks • HEPATITIS C: SsRNA • Most important cause of transfusion-associated hepatitis • Inherently unstable → no vaccine • Persistent infection + chronicity • HEPATITIS D: Replication Defective RNA Virus • Infective only when encapsulated by HBsAg • Co-infection of super-infection • HEPATITIS E: Unenveloped single stranded RNA virus • Transmitted as endemics • No chronicity • Self-limited • Severe cholestasis • High mortality in pregnant females

Answer 37

• ETIOLOGY: common in females * PATHOGENESIS: * Type I: Anti-nuclear antibodies (ANA), Anti-smooth muscle antibodies (ASMA) * Type II: Anti LKM antibodies (liver kidney microsomal) * DIAGNOSIS: high IgG titers * TREATMENT: immunosuppressive therapy HISTOLOGY - clusters of lymphocytes and plasma cells in the interface of portal tracts and hepatic lobules COMPLICATIONS - liver cirrohsis

Answer 38

* ETIOLOGY: * Hepatic steatosis * Alcoholic hepatitis * Fibrosis → cirrhosis • MORPHOLOGY: initially enlarged fatty liver with progresses to fibrotic, fatty, and shrunken • Mallory Hyaline Bodies: tangled intermediate filaments (eosinophilic inclusions) INVESTIGATIONS : AST \> ALT & increased GGT

Answer 39

* ETIOLOGY: disease of middle aged women * PATHOGENESIS: anti-mitochondrial antibodies * MORPHOLOGY: granulomatous destruction of medium sized (intrahepatic) bile ducts * Dense lymphoid infiltration with florid duct lesion * SYMPTOMS: death occurs due to liver failure * Secondary Biliary Cirrhosis: due to partial or total bile duct obstruction * Tumors, strictures, gallstones

Answer 40

• ETIOLOGY: inflammation, fibrosis, and dilation of intra and extra hepatic ducts Median age is 30 years and most commonly in male * Inflammatory destruction of Extrahepatic and large intrahepatic ducts * Periductal inflammation and fibrosis – “onion skin” lesions * P-ANCA (80%) * SYMPTOMS: associated with chronic ulcerative colitis * DIAGNOSIS: ERCP → dilating and beading of the biliary tree • Associated with ulcerative colitis

Answer 41

* ETIOLOGY: excessive accumulation of iron * Males \<40yrs. * Liver fibrosis, eventually cirrhosis (micronodular) * PATHOGENESIS: HFE gene * Increased Fe absorption • Parenteral iron overload – Repeated blood transfusions – Iron dextran injections • Ineffective erythropoiesis – β thalassemia – Other chronic hemolytic anemias • Increased oral intake – Bantu disease • Chronic liver disease – Alcohol, hepatitis C * Common in males * Rarely manifests before 40 * SYMPTOMS: * Micronodular cirrhosis * Diabetes mellitus * Skin pigmentation * Cardiomyopathy • PANCREAS – Hemosiderin in both acinar and Islet cells → Diabetes mellitus • HEART – Hemosiderin in myocardial fibers (cardiomyopathy) • SKIN – Iron in dermal melanophages – Increased melanin production

Answer 42

• ETIOLOGY: accumulation of toxic levels of copper in liver, brain, eyes • MORPHOLOGY: • Fatty change in liver • Acute hepatitis PATHOGENESIS - due to lack of Cu transporters into bile - Defective Cu incorporation into Ceruloplasm Carrier→ Cu into the Blood - Copper is toxic via Fenton Reaction→ Free Radical Damage to Hepatocytes * SYMPTOMS: * Deposition of copper in basal ganglia * Kayser-Fleischer rings * DIAGNOSIS: * Decreased serum ceruloplasmin levels * Increased hepatic Cu * Increased urinary copper excretion

Answer 43

* Autosomal recessive disorder * Markedly low levels of α 1 AT (protease inhibitor that is a glycoprotein encoded by the PiMM gene on Chr14) * Synthesized mainly by hepatocytes • Homozygosity for mutant variant (PiZZ) leads to retention of mutant protein in cells * Cytoplasmic globules in hepatocytes * Lung disease (emphysema) can be present → Liver transplantation is the only treatment • Clinical presentation – Neonatal hepatitis with or without cholestasis – Chronic hepatitis – Cirrhosis • Hepatocellular carcinoma

Answer 44

• ETIOLOGY: changes like in alcoholic liver disease in non-drinkers * RISK FACTORS: * Obesity * Insulin resistance * Hyperlipidemias • MORPHOLOGY: steatosis with or without hepatitis * SYMPTOMS: usually asymptomatic * Mild elevation of serum transferases * May lead to cirrhosis

Answer 45

Tumor composed of vascular space often filled with thrombus * ETIOLOGY: commonest liver tumor * Females \> males • DIAGNOSIS: incidental on CT scan * TREATMENT: depends on the following factors * Bleeding * Location * Size * Platelet consumption

Answer 46

Benign tumor of hepatocytes • ETIOLOGY: associated with oral contraceptive pill or anabolic steroids * SYMPTOMS: * Abdominal pain * Shock/hemorrhage * May be fatal during pregnancy * DIAGNOSIS: normal serum AFP * TREATMENT: stop causative medication

Answer 47

* ETIOLOGY: females \> males * DIAGNOSIS: central scar on CT, MRI HISTOLOGY - Composed of multiple spherical aggregates of hepatocytes held together in a fibrosis meshwork + central stellate Scar - NON- Neoplastic - localized vascular abnormalities - Normal Liver and Spleen Scan

Answer 48

* ETIOLOGY: most common liver tumor in neonates and children * ~18 month * Associated with Down Syndrome, Beckwith-Wiedemann syndrome * MORPHOLOGY: * Small uniform cells in cords with rapid growth * SYMPTOMS: * Hepatomegaly * Abdominal mass * Spread to lungs and peritoneum • DIAGNOSIS: AFP elevated

Answer 49

* ETIOLOGY: global distribution strongly related to prevalence of HBV * Highest frequencies in Taiwan, Mozambique and China * Hepatitis B+C * Hemochromatosis * Alcoholic cirrhosis * Alpha-1-antitrypsin deficiency * Aflatoxin * MORPHOLOGY: unifocal or multifocal * Paler than surrounding hepatic parenchyma * Propensity for invading vascular channels (portal vein/IVC) * Trabecular, sinusoidal or pseudoacinar pattern – Bile production by tumor cells, cytoplasmic inclusions – Usually cirrhosis in adjacent liver parenchyma * SYMPTOMS: * RUQ pain * Fatigue * Cachexia * Masked by underlying liver disease • DIAGNOSIS: AFP, FNAC, biopsy

Answer 50

• ETIOLOGY: no association with HBV or cirrhosis - chimeric Proteins • MORPHOLOGY: single hard tumor with fibrous bands traversing through • Well-differentiated polygonal cells in cords or nests, separted by fibrous septa • SYMPTOMS: better prognosis - INVESTIGATION → Normal AFP

Answer 51

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Answer 52

• Acute Inflammation of gallbladder wall resulting in ischemia and • Pathogenesis: – Chemical irritant and inflammation in the setting of obstruction to flow → mucosal phoshpholipase convert lecithin to lysolecithin which causes → Damage to glycoprotein layer of the mucosa which results in → increased release of prostaglandin from the mucosa. – Cumulatively leads to mucosal and mural inflammation → Gall bladder dysmotility and increased intraluminal pressure →superimposed bacterial contamination • Presentation: – Pain in the right hypochondrium/ epigastrium – May become surgical emergency – Associated fever, nausea, vomiting --\> Most patients recover – Positive Murphy's sign: • Examiner presses on RUQ and asks patient to deeply inspire --\> patient stops inspiration d/t to pain * Will be negative if there is only bile duct obstruction and not inflammation (cystitis) * Complications: rupture and perforation • Chronic Cholecystitis – Sequelae of repeated acute cholecystitis – More common: no antecedent attacks of acute cholecystitis → Starts off as chronic! – HALL MARK: PORCELAIN GALL BLADDER Appearance →high association with carcinoma due to the extensive dystrophic calcfication – The role of gallstones with chronic cholecystitis is unclear – Micro-organism can be cultured from bile in 1/3rd of patients – Rokitanksy Aschoff Sinus : increased pressure in I the gall bladder causing diverticuli (dilated cysts) • Herniation of gall bladder mucosa in to the muscularis

Answer 53

* ETIOLOGY: carcinoma of bile duct origin * Normal serum AFP RISK FACTORS: Sclorising cholangitis, parastic infection, cyctic dilation, gall stones * PATHOGENESIS: * Gallstones * Chemicals: benzamine, nitrosamines * Parasites: Clonorchis sinesis, Opisthorchis viverini * MORPHOLOGY: adenocarcinoma with extensive fibrosis (desmoplastic) * Most commonly at hilum of liver * Upper 1/3 → 60% * Middle 1/3→ 20% * SYMPTOMS: * Malaise * Weight loss * Jaundice * Charcot Triad: jaundice, fever, chills * Raynaud Pentad: Charcot triad + hypotension + mental changes * Poor prognosis

Answer 54

* ETIOLOGY: * Cholesterol stones → cholesterol monohydrate (80%) (obesity) → Yellow • Pigment stones → bilirubin calcium salts (20%) (chronic hemolytic anemia) → Black * RISK FACTORS: * Cholesterol stones: advancing age, female, OCP, obesity, hyperlipidemia • Pigment stones: Asians, hemolytic syndromes, biliary infections * PATHOGENESIS: * Mucosal phospholipase convert lecithin to lysolecithin • GB hypomotility promotes precipitation of cholesterol from bile • Mucus hypersecretion traps crystals and promotes aggregation * SYMPTOMS: * Empyema • Perforation • Cholecystitis • Pancreatitis • Porcelain gall bladder (rarely dystrophic calcification, high association w/ cancer) * DIAGNOSIS: * Cholesterol Stones = radiolucent on Ultrasound, X-ray • Pigment Stones = radio-opaque on Ultrasound, X-ray

Answer 55

Chronic inflammation of the gall bladder * ETIOLOGY: females \> males, 7th decade * MORPHOLOGY: exophytic - growin into lumen at irregular cauliflower mass invading underlying wall * PATHOGENESIS: * Squamous: p53 * Adenocarcinoma: KRAS + Cholelithiasis * COMPLICATIONS: metastasis to the liver by the time of diagnosis * Poor prognosis

Answer 56

* ETIOLOGY: 80% cases associated with gallstones and alcoholism → causes contraction of the sphincter of Oddi → damage to pancrease→premature activation of enzymes * Infections: Mumps, Coxsackie, Mycoplasma * Acute ischemia * Hyperlipoproteinemias * Drugs: diuretic, azathioprine, estrogens * MORPHOLOGY: * Focal fat necrosis in pancreas and peripancreatic tissues * Ca2+ deposition * SYMPTOMS: * Abdominal (epigastric pain) - upper back * Elevated pancreatic enzymes → amylase (24-48hrs) then lipase (72-96hrs) * Leukocytosis * Hypocalcemia (due to saponification), tetany * Complications: ARDS, ATN, pancreatic abscess → DIC

Answer 57

• ETIOLOGY: repeated bouts of mild to moderate pancreatic inflammation with loss of pancreatic parenchyma and its replacement by fibrosis – Progressive loss of pancreatic endocrine and exocrine function • Middle aged alcoholics * SYMPTOMS: * Back pain * Persistent abdominal pain * Malabsorption * Pancreatic pseudocyst: enzymes + fibrous scar + dystrophic calcifications * Diabetes (if islet is damaged) * Pleural effusion * DIAGNOSIS: X-Ray or CT → calcifications

Answer 58

• ETIOLOGY: association with smoking * LOCATION: * Head (60-70%) * Tail (10-15%) * Body (5-10%) * MORPHOLOGY: * Ductal-type adenocarcinomas * Dense stromal fibrosis (desmoplasia) * Perineural invasion • SYMPTOMS: pain usually first symptom (invasion of posterior abdominal wall) • Trousseau’s Sign (migratory thrombophlebitis) → PAF + procoagulants + mucin • Obstructive jaundice (if in head of pancreas) * DIAGNOSIS: CA19-9 * GOLD STANDARD = biopsy

Answer 59

* ETIOLOGY: usually benign, solitary * PATHOGENESIS: arise from beta-cells • SYMPTOMS: • Hypoglycemia (especially by fasting) • May manifest as Whipple triad (low blood glucose, presence of symptoms, resolution when blood glucose is normalized) • Increased insulin

Answer 60

* ETIOLOGY: gastrin-producing endocrine tumors * Associated with MEN-1 mutation • PATHOGENESIS: hypergastrinemia * SYMPTOMS: multiple ulcers * Results in Zollinger-Ellison Syndrome * Multiple duodenal peptic ulcers * Prominent gastric rugal golds due to increased oxyntic gland mass * Steatorrhea

Answer 61

* 1-2% of all exocrine neoplasms * 40-81 Y (62Y) * M:F = 2:1 * Whites \> Blacks * Subcutaneous fat necrosis and panniculitis (16%) due to lipase * Aggressive tumors, can metastasize to liver

Answer 62

* Arise within the ductal system * Majority in the head * Dilated duct filled with mucin • Cysts can be multiloculated; lined by tall columnar mucin secreting cells (papillary/pseudopapillary/flat) • Histologic features – Noninvasive: Low-Grade/High-Grade tumor cells confined to duct lumen – Invasive: extension of tumor cells beyond the pancreatic duct into stroma – Lacks ovarian type stroma

Answer 63

* 2-5% of all exocrine neoplasms, mostly tail * 20-82 Y (49Y) * Almost exclusively in women * Not connected to the ductal system • Histologic features -Tall columnar mucin secreting cells - Noninvasive with low grade/high grade cytology - Invasive component can be present - Characteristic feature: ovarian-type stroma

Answer 64

• Islet cell tumors, make islet cell type hormones – Functional (Insulinomas, Gastrinoma, Glucagonoma) – Non-functional • Behavior difficult to predict reliably – All are potentially malignant – NET Grading based on size and mitotic activity – Less common: neuroendocine carcinoma, small cell or large cell

Gastrointestinal Flashcards

(92 cards)