GI & nutritional U-world journal

What is the most severely affected macronutrient in generalized malabsorption?

*Fats*--most complex digestive pathway -testing the stool for fat w/*Sudan III* stain is the most sensitive strategy for screening for malabsorptive disorders

Where does venous component of internal hemorrhoids drain into, lymphatics? External hemorrhoids?

*Internal hemorrhoids*: Venous: drains into middle & superior rectal veins, which communicated w/internal iliac & inferior mesenteric veins lymph: inferior mesenteric & internal iliac innervation: inferior hypogastric plexus; autonomic innervation; sensitive to stretch columnar epithelium *External hemorrhoids*: Venous: drain via inferior rectal vein into internal pudendal vein which communicates w/internal iliac veins lymph: superficial inguinal nodes innervation: inferior rectal nerve, branch of pudendal nerve ; cutaneous (somatic) nervous innervation sensitive to pain, touch, temp. modified squamous epithelium

What are the presenting clinical symptoms of other locations of colon cancer (adenocarcinoma)?

*LT-sided* - infiltrate intestinal wall & encircle the lumen, cause constipation & symptoms of intestinal obstruction--abdominal distension, nausea, vomiting Rectosigmoid: often causes hematochezia (blood in or w/stool) Liver & lungs are common sites of metastases in both RT & LT colon cancer

On histological path finding of abnormal islands of small cells of patient w/ a recent appendectomy, what might be origin of these small island of cells?

*Neuroendocrine Cells* *Carcinoid Tumors* composed of islands or sheets of uniform cells w/eosinophilic cytoplasm & oval-to-round stippled nuclei. -these tumors are often derived from neuroendocrine cells in GI tract -appendiceal carcinoids typically have benign course but may cause appendicitis, or rarely, carcinoid syndrome (eg, w/liver metastasis) -carcinoid syndrome (flushing, diarrhhea, bronchospasm)

What is the most common GI disorder in patients w/ Cystic fibrosis?

*Pancreatic insufficiency* (PI) mutations in in CF transmembrane conductance regulator gene prevents Chloride, Sodium & H20 to be secreted into respiratory & GI lumen--leads to thick, viscous secretions in lumens of pancreas, resulting in obstruction, inflammation, & subsequent fibrosis (develops in utero). *Loss of pancreatic tissue prevents pts. from developing pancreatitis.* clinical manifestations: steatorrhea, failure to thrive, & deficiency of fat-soluble vitamins (ADEK). PI is present at birth for most patients.

What are the initial clinical symptoms of colon cancer (adenomcarcinoma) based on the malignancy appearing on the RT side (Ascending colon)?

*RT-sided* - grow exophytic masses & present w/occult bleeding w/symptoms of anemia (fatigue, pallor); pts. generally do not develop intestinal obstruction b/c ascending colon has larger caliber lumen than descending colon & stool in proximal colon is more liquid. non-specific symptoms such as anorexia, malaise, & unintentional weight loss may occur Test positive for for fecal occult blood testing (guaiac-positive brown stool)

Describe *Chronic Mesenteric Ischemia* what pathogenesis is it similar to?

*Stable Angina* -characterized by atherosclerosis of mesenteric arteries, resulting in diminished blood flow to intestine after meals. -this causes postprandial epigastric pain ("intestinal angina") w/assoc. food aversion/weight loss -pathogenesis similar to angina pectoris

Describe hereditary hemochromatosis

*autosomal recessive*, most commonly in caucasians -most commonly caused by missense mutation in HFE gene, resulting in excessive intestinal iron absorption & organ damage (eg, cirhosis, diabetes mellitus, cardiomyopathy, arthropathy) due to iron accumulation w/in parenchymal tissues -presents w/ very high levels of ferritin & trasferrin saturation

Name specific laborartory finding that is specific for underlying cause of an *alcoholic patient's pancreatitis*

*macrocytosis, MCV >100 fl* -after gallstones, alcohol is the second most common cause of acute pancreatitis -macrocytosis & AST:ALT>2 in absence of gallstones; are pathognomic & indirect indicators of chronic alcohol consumption -alcohol-induced macrocytosis can occur in absence of anemia, & is likely due to poor nutrition, (eg, folate deficiency), liver disease, and/or direct toxicity of alcohol on bone marrow (note: it can occur independently of folae of deficiency)

Describe what effect can systemic mastocytosis have on the GI system

- characterized by abnormal proliferation of mast cells & increased histamine release -histamine causes hypersecretion of gastric acid by parietal cells in stomach as well as a variety of other symptoms (eg, hypotension, flushing, pruritis, syncope,urticaria) -increased gastric acid can lead to stomach ulceration; also in can inactivate pancreatic & intestinal enzymes, causing diarrhea; other GI symptoms include nausea, vomitting, & abdominal cramps Note: mast cell proliferation often assoc. w/mutations in KIT receptor tyrosine kinse--cells characterized by prominent expression of mast cell tryptase

What is the histological characteristic observered in T. whippelii when stained w/Periodic acid-Schiff (PAS)?

-*glycoprotein* in cell walls of actinomycete Tropheryma whippelii [gram positive] colors magenta w/PAS & is diastase-resistant, make this stain an excellent choice in evaluating tissue for whipple disease -bacteria proliferates only w/in macrophages of affected tissue -- *enlarged foamy macrophages* packed w/both rod-shaped bacilli & PAS-positive , diastase resistant granules (consist of lysosomes & partially digested bacteria)

what are the sources of the visceral & somatic pain in appendicitis?

-Appendicitis causes dull visceral pain at umbilicus due to afferent pain fibers entering at T10 level in spinal cord (SMA plexus) -progressive inflammation in appendix irritates parietal peritoneum & abdominal wall to cause severe somatic pain shifting from umbilicus to McBurney point (two-thirds of distance from umbilicus to anterior superior iliac spine)

Compared to sporadic colorectal carcinoma (CRC), colorectal malignancy would most likely exhibit what features?

-CRC most common type of malignancy in patients suffering inflammatory bowel disease (IBD), esp. ulcerative colitis -affect younger patients -progress from flat & non-polyploid dysplasia -histologically apprear mucinous and/or have signet ring morphology -develop early p53 mutations & late APC gene mutations; opposite that of sporadic disease -distributed w/in proximal colon (esp. w/Crohn's diease or concurrent primary sclerosing cholangitis) -multifocal in nature -higher histological grade, more likely to be anaplastic -duration & extent of colitis are most signif. risk factors typically develop after 10 years of colitis

What is a specific histological pathognomic for Chronic Hep B virus antigens in hepatocytes?

-Hep B infection causes hepatocellular cytoplasm to fill with hep surface antigen -these inclusions are highly specific for hep B infection & have finely granular, pale eosinophilic, ground glass appearance

Hepatic Encephalopathy

-Increased levels of ammonia & other neurotoxins in circulation lead to increased inhibitory neurotransmission & impaired excitatory neurotransmitter release -frequently precipitated by a stressors that alters ammonia balance (eg, GI bleeding, increased dietary protein)--increased load of nitrogenous substances absorbed by gut Note: BUN levels are actually lowered b/c hepatocytes are damage and unable to efficiently convert ammonia to urea

what clinical presentations are indicative of <adenocarcinoma of head of pancreas> compressing on common bile duct? what is the most important environmental risk predisposing patients to this cancer?

-Palpable but nontender gallbladder (*Courvoisier sign*), weight loss, obstructive jaundice (assoc. w/*pruritis, dark urine, & pale stools*) - smoking doubles the risk; other risks mentioned: patients age >50 yrs, chronic pancretitis, diabetes mellitus, & genetic predisposition (MEN syndromes, hereditary & nonhereditary non-polyposis)

Describe Clostridium difficle Colitis

-antibiotics ( also, PPIs) disturb normal intestinal flora-- lead to overgrowth of the gram (+) bacilli bacteria -leads to elaboration of enterotoxin A & cytotoxin B -disease may begin days or weeks following antibiotic therapy & can range in severity from mild, transient, watery diarrhea to pseudomembraneous colitis (epithelial cell necrosis & fibrin deposition) -white/yellow membrane-like plaques on colonoscopy are pathognomic

Sporadic colorectal carcinomas

-arise from polypoid lesions -molecular pathogenesis: APC mutation develop early & late p53 mutations -lower grade and less likely to anaplastic

Describe the pathophysiology and genetic mutation that results in Crohn's disease

-assoc. w/mutation in NOD2 (encodes an intracelluar microbial receptor), results in decreased activity of NF-kappaB (proinflammatory transcription factor) w/reduced cytokine production. -this impairs innate barrier function of intestinal mucosa & allows intestinal microbes to induce an exaggerated response by adaptive immune system, resulting in chronic GI inflammation

Describe Dubin-Johnson syndrome and explain why liver appears black in this pathology of the liver

-benign, autosomal recessive disorder -defective excretion of bilirubin glucuronides due to mutation in canalicular membrane transport protein -develop direct hyperbilirubinemia & intermittent episodes of jaundice Grossly, liver appears black b/c impaired excretion of epinephrine metabolites--histologically appear as dense pigments w/in lysosomes.

Resection of terminal ileum or extensive ileal involvement in setting of Chron disease can involve what type of malabsorptive complication?

-bile acid malabsorption--may lead to impaired absorption of fat-soluble vitamins (A, D, E, K) -Vit K deficiency can result in impaired coagulation w/easy bruising, large hamartoma formation in deep tissues & joints (hemarthrosis) after minor trauma, & prolonged bleeding after surgery note: Vit K cofactor for carboxylase enzymes for factors II, VII, IX, X

If appendix cannot be identified by palpation during appendectomy, what other way can it be located?

-by following the teniae coli to their origin at cecal base -teniae coli are 3 separate smooth muscle ribbons that travel longitudinally on outside of colon& converge at root of veriform appendix

Celiac disease

-caused by immune-mediated reaction to gluten (gliadin) & can present w/bloating, diarrhea, & flatulence, as well as short stature & weight loss due to malabsorption; extraintestinal symptoms: iron deficiency anemia, dermatitis herpetiformis -screening tests show elevated level of IgA against *tissue transglutaminase* (small intestinal enzyme required for approp. gluten metabolism) -gliadin triggers inflammatory reaction that causes small intestinal villus atrophy/flattening & lymphocyte infiltration of intraepithelial cells Duodenal biopsy of duodenum & jejunum (w/highest [gliadin] is confirmatory for diagnosis of celiac disease(sprue)

Describe the blood supply of the liver from celiac trunk

-celiac trunk is first main branch of abdominal aort--it provides oxygenated blood to spleen, stomach, liver, abdominal esophagus, & parts of duodenum & pancreas -the proper hepatic artery is distal branch of celiac trunk that supplies arterial blood to liver

What is a common cause for retroperitoneal hematoma?

-common complication of abdominal & pelvic trauma -pancreas is retroperitoneal organ & pancreatic injury is frequently source of retroperitoneal bleeding look up mneumonic: SAD PUCKER

Histology of Hep C virus?

-commonly has lymphoid aggregates w/in portal tracts & focal areas of macrovesicular steatosis other forms of histo findings of liver: hepatic steatosis-- large & small vesicles of fat in hepatocytes/commonly caused by excessive alcohol consump or obesity (nonalcoholic steatosis); Note: mallory bodies may be seen in alcoholic steaotitis-- charachterized by clumped, amporhous, eosinophilic intracytoplasmic inclusions made up of tangled intermediate filaments

What histological pattern is cirrhosis characterized by?

-diffuse hepatic fibrosis w/replacement of the normal lobular architecture by fibrous-lined parenchymal nodules -Portal HTN may develop from increased resistance to hepatic blood flow-- lead to esophageal varices and dangerous hemorrhage that can lead to death Chronic viral hepatitis (eg, hep B & C), alcohol, hemochromatosis, & nonalcoholic fatty liver disease are most common causes of cirrhosis in US

What are the different adenomatous polyps, name three types & describe the most dangerous type

-divided into tubular, villous, & tubulovillous -villous adenomas tend to be larger, sessile (velvety, cauliflower-like projections) & more severly dysplastic than tubular adenomas -villous adenomas can cause bleeding (eg, microcytic anemia), can secrete large amount of watery mucus leading to secretory diarrhea (eg,hypokalemia, hypovolemia, electrolyte imbalance) & partial intestinal obstruction w/pain constipation, & abnormal distension.

What is the cause of small intestinal bacterial overgrowth (SIBO) in gastric bypass?

-due to excessive bacterial proliferation in the blind-ended gastroduodenal segment (see pic) -SIBO results in deficiency of most vitamins (B12, A, D, E) and iron , but *increased production of folic acid & vitamin K (enteric organims produce these vitamins)* -this overproduction of Vit k & folate can result in nausea, bloating, abdominal discomfort, & malabsorption

Histologically, what does acute hepatitis cause?

-due to most hepatotropic viruses, it causes hepatocyte ballooning degeneration & apoptosis w/mononuclear cell infiltration ; both necrosis & apoptosis occur (see below) necrosis: cellular swelling & cytoplasmic emptying (ballooning)-- bridgeing necrosis apoptosis: cellular shrinkage, nuclear fragm., w/intense eosinophilia [acidophils (councilman bodies)] AKA: Eosinophilic apoptotic hepatocytes presence of virally infected & dying hepatocytes promotes mononuclear inflammation in sinusoids & portal tracts

Reflux esophagitis histo findings

-elongation of papillae, basal cell hypertrophy & intraepithelial eosinophils--repeat epithelial injury caused by reflux esophagitis lead to Barrett's esophagus

What are typical histological findings of squamous cell carcinoma in esophagus and what are the major risks associated?

-flattened polyhedral or ovoid epithelial cells w/eosinophilic cytoplasm -keratin nests or pearls w/in or in betwn cells -intercellular bridging -large hyperchromatic cells w/bizarre nuclei & atypical mitoses are commonly observed -middle aged Blacks & Asians w/ alcohol & cigarrette most common risk factor; Asians: chewing betel nuts & eating foods w/N-nitroso compounds

Where are the parietal cells found in the gastric wall?

-found primarily in superficial region of gastric glands (upper glandular layer--see pic) -parietal cells are oxyntic (pale pink), round, plate-like cells in gastric fundus & body

What does gallbladder hypomotility promote that results in gallstone formation?

-gallbladder functions to actively absorb water from bile -hypomotility causes bile concentration, which promotes *bile precipitation & accumulation of viscous biliary sludge* that predisposes to gallstone formation & bile duct obstruction.

What is Shigellosis, what is the most common form and how does it manifest/pathophysiology ?

-infectious disease that can be caused by variety of Shigella species; S sonnei is most common cause of shigellosis in industrialized nations Shigella invades GI mucosa by gaining access to microfold cells in ileal Peyer patches via endocytosis-subsequently, lyses endosome & spreads laterally into other epithelial cells, causing cell death & ulceration w/hemorrhage & diarrhea (blood & mucous)

Define the borders of the femoral hernia, clinical symptoms and complications

-inferior to inguinal ligament, lateral to pubic tubercle & lacunar ligament, medial to femoral artery/vein -present w/upper thigh, groin & pelvic discomfort or manifest w/bulge on upper thigh -complications: incarceration (bowel obstruction) and eventual strangulation (ischemia & necrosis)

Describe drug-induced liver injury/inhaled anesthetic hepatotoxicity

-inhaled anesthetics such as *halothane*, can be assoc. w/ lethal fulminant hepatitis--can't be distinguished from acute viral hepatitis -signif. elevated aminotransferase levels b/c of massive hepatocellular injury & *prolonged prothrombin time (PT)* due to failure of hetpatic synthetic fxn & deficiency of *factor VII* (shortest half life)

Typical patient presentation of gallston ileus patient

-intermittent abdominal pain & cholesterol-containing mass lodged at ileocecal valve; small bowel obstruction symptoms: abdominal pain/distension, nausea/vomitting, high-pitched (tinkling) bowel sounds & tenderness to palpation

What does new-onset odynophagia in setting of chronic gastroesophageal reflux disease indicate?

-presence of erosive esophagitis & formation of an ulcer -diagnosis is made by upper endoscopy

Describe "hyperestrenism in liver cirrhosis" & what is the possible pathophysiology?

-likely arises due to increase in androstenedione production, androgen aromatization, & sex-hormone binding globulin concentration (preferentially binds testosterone); impaired estrogen metabolism by liver may also be a contributing factor. -decreased free testosterone/estrogen ratio leads to gynecomastia, testicular atrophy, decreased body hair, & spider angiomata (increased estrogen may have vasodilatory effects on arterioles)

On CT scan, where is esophagus located?

-located btwn trachea & vertebral bodies in superior thorax -it's typically collapsed w/no visible lumen on CT images of chest note: to the RT of the esophagus is the arch of the azygous vein & to the LET is the Descending aorta (refer to pic)

Describe symptoms of acute hepatitis, which virus is it most common with and what age group?

-low grade fever, anorexia/nausea, dark-colored urine, & right upper quada abdominal tenderness--highly suggestive of acute viral hepatitis -Hep A is most likely responsible esp. with recent travel to endemic area; most common in young adults (travel)

What is the GI component of the CREST syndrome (systemic sclerosis)?

-may result in esophageal dysmotility & incompetence of lower esophageal sphincter due to atrophy & fibrous replacement of esophageal muscularis -this may cause gastroesophageal refulx w/an increased risk of Barrett's esophagus & stricture formation

Define gallstone ileus and a common radiographic finding

-mechanical bowel obstuction caused when gallstone erodes into intestinal lumen (usually duodenum) fistula between gallbladder & GI tract formed (cholecystoenteric fistula)--obstuction of ileocecal valve (ileum most narrow) stone get's stuck at this point; most common in elderly women -x-ray may reveal dilated bowel loops w/air fluid levels, & *pneumobilia (air in biliary trct)* due to retrograde passage of intestinal gas via fistula may be observed on X-ray

Describe the histological finding of the liver in Reyes syndrome

-microvesicular steatosis of hepatocytes w/out inflmmation & cerebral edema -occurs in children w/febrile illness treated w/salicylates (aspirin) -consists of hepatic failure & encephalopathy (hyperammonemia)--cerebral edema -vomitting, hematomegaly, jaundice rare liver function tests show elevated levels of AST, ALT, ammonia, & billirubin, & prolonged PT & PTT Avoid giving aspirin to children under age of 16, unless indicated for special diseases like Kawasaki

What is a typical presentation of patient with small bowel mucosa Whipple disease?

-middle aged caucasian males Systemic illness -abdominal discomfort -loose stool & recent weight loss, -involves small intestine, joints & central nervous, cardiac abnormalities may also be present

When ultrasound is inconclusive, what is another imaging test that may be utilized in acute cholecystitis?

-most often involves gallstones obstructing cyst duct; diagnosis can be made by identifying signs of gallbladder inflammation (eg, wall thickening, pericholecystic fluid) on ultrasonography -when ultrasound is inconclusive, *nuclear medicine hepatobiliary scanning* (ie, cholescintigraphy) can be used to assess cystic duct patency & make diagnosis

What histological pattern is seen on LM in Crohn's disease?

-noncaseating granulomas & resemble sarcoid granulomas -other classic findings: linear or serpiginous ulcerations, cobblestone appearance of mucosa, & transmural inflammatory infiltrate; fistulas & chronic intestinal obstruction (string sign) Crohn's = occult bleeding; non-caseating granulomas ulcerative colitis = gross bleeding, no granulomas

What are the environmental & lifestyle factors that may contributed to this colon cancer?

-obesity -cigarette smoking -consumption of red/processed meat, & low dietary intake of vegetables

What is biliary atresia & how does it present in a patient?

-obstruction of extrahepatic bile ducts -presents w/jaundice, *dark urine, & alcoholic stools (pale or clay colored)--due to excessive renal excretion of bilirubin & lack of intestinal bile, respectively* -occurs in first 2 months of life due to conjugated hyperbilirubinemia -Biopsy reveals intrahepatic bile duct proliferation, portal tract edema, & fibrosis Note: also present w/firm hepatomegaly due to inflammation

Describe Superior Mesenteric Artery syndrome

-occurs when transverse portion of duodenum is entrapped btwn SMA & aorta, causing symptoms of intestinal obstruction -this occurs when aortomesenteric angle critically decreases , secondary to diminished mesenteric fat(low BW, recent weight loss, severe burns) pronounced lordosis, or surgical correction of scoliosis, prolonged bed rest

Describe necrotizing enterocolitis & x-ray finding

-one of the most common GI emergencies affecting newborns -bacterial invasion & ischemic necrosis of bowel wall-- assoc. w/prematurity & enteral feeding (immunologic immaturity) of terminal ilium & colon --as disease progresses bowel congested & gangrenous w/formation of intramural gas collections -presents as abdominal distension, bloody stools & pneumatosis intestinalis -abdominal x-ray showing pneumatosis intestinalis (ie, air in the bowel wall) --curvilinear lucency that parallel the bowel wall lumen confirm diagnosis

What are VIPomas and how can it be treated?

-pancreatic islet cell tumors that hypersecrete vasoactive intestinal peptide (VIP)--increases intestinal chloride loss into stool & causes excess losses of accompanying water, sodium, & potassium VIP also inhibits gastric acid secretion Somatostatin (octreotide) inhibits secretion of VIP (also gastrin, glucagon, & CCK) & is used to treat symptoms of VIPoma WDHA (watery diarrhea, hypokalemia, & achlohydria) pancreatic cholera

What is the preferred diagnostic imaging study for toxic megacolon?

-plain abdominal x-ray -barium contrast studies & colonoscopy are contraindicated due to risk of perforation Note: toxic megacolon is a well-recognized complication of ulcerative colitis, C. difficile & other forms of infectious colitis can also cause toxic megacolon -patients typically present w/abdominal pain/distension, bloody diarrhea, fever, & signs of shock

Define porcelain gallbladder and the increased risk for associated condition

-porcelain gallbladder is potential manifestation of chronic cholecystitis & is often assoc. w/multiple gallstones -due to dystrophic intramural deposition of calcium salts in setting of chronic inflammation, "blusih, brittle, thickened gallbladder wall w/*crunchy texture* -associated w/increased risk of adenocarcinoma of gallbladder Note: mass or associated gallbladder issues localized to upper RT quadrant

What is a typical presentation of Crohn's disease?

-prolonged diarrhea & vague abdominal pain -constitutional symptoms (low grade fever, fatigue), malabsorption, and weight loss are also common. -transmural inflammation of bowel wall may result in formation of fistulas (eg, enteroenteric, enterocutaneous) abscesses, & fibrotic strictures

In patient with Crohn's disease affecting terminal ileum; what are gallbladder condition are they prone to develop and how?

-prone to developing gallbladder stones -decreased bile acid reabsorption promotes supersaturation of bile w/cholesterol, resulting in gallstone formation note: patients present w/upper right quadrant pain

Describe typical presentation of splenic laceration, what is a kehr sign?

-rigid abdomen assoc. w/left shoulder pain, hypotension, & tachycardia suggest possible splenic laceration & hemoperitoneum -any abdominal process (eg, ruptured spleen, peritonitis, hemoperitoneum) irritating phrenic nerve sensory fibers around diaphragm can cuse referred pain to the C3-C5 shoulder region (Kehr sign); phrenic nerve irritation can also cause hiccups due to spasmodic diaphragmatic contraction pulling air against closed pharynx

What are the histopathological features of esophageal squamous cell carcinoma?

-solid nests neoplastic squamous cells w/abundant eosinophilic cytoplasm & distinct borders -areas of keratinization (*keratin pearls*, see arrows) & presence of *intercellular bridges* -patients typically present w/progressive solid to liquid dysphagia, weight loss, retrosternal discomfort/burning chronic GI blood loss may lead to iron deficiency anemia & fatigue -usually in me age >50, history of prolonged smoking & alcohol use; prognosis not good

Describe the location of the third part of the duodenum in relation to SMA

-third part of duodenum courses horizontally across abdominal aorta & inferior vena cava at level of third lumbar vertebra -SMA vessels lie anterior to duodenum at this loction (tumors of duodenum in this location can compromise blood flow in this large vessel)

What is the possible pathophys bethind drug-induced liver & what is typical patient presenation & lab finding

-underlying mechanism might be due to hypersensitivity reaction to drug that causes an immune-mediated attack against hepatocytes Patient: fever, anorexia, nausea, myaligias, arthralgias, & rash -tender hepatomegaly (widespread live inflamm.) & jaundice may be seen on clinical presentation Labs: very high serum aminotransferase levels, prolonged prothrombin time, leukocytosis, eosinophilia

Describe stress-related mucosal disease

-usually caused by local ischemia in setting of severe physiological stress (eg, shock, extensive burns, sepsis, severe trauma)--systemic hypotension & splanchnic vasoconstriction main cause of ischemia -ulcers arising in setting of severe trauma/burns are called *Curling's ulcers* *(proximal duodenum)* -ulcers (esophagus, stomach, duodenum, arising from intracranial injury are caused by direct vagal stimulation & are called *Cushing's ulcers* (more likely to perforate )

Describe a typical symptoms of a pt w/RT-side colon cancer

-weight loss -iron deficiency anemia -guaiac-positive brown stool -colonoscopy shows mass in colon biopsy shows: pleomorphic cells w/large , dark nuclei forming irregular, crowded glands, some of which contain mucous

What is a common serum tumor marker for hepatocellular carcinoma(HCC)?

Alpha-fetoprotein (AFP) -often moderately elevated in patients w/chronic viral hepatitis -strikingly elevated in those w/hepatocellular carcinoma -sudden rise can be sign that patient w/chronic liver disease is harboring hepatocellular carcinoma note: AFP does not correlate w/size or stage of HCC

Describe the adenoma to carcinoma sequence, what is the final step in the sequence that leads to malignancy

Adenoma to carcinoma sequence: 1. progression from normal mucosa to small adenomatous polyp: mutation of *APC inactivation of tumor suppressor gene* (chrom. 5)--leads to Beta-catenin accumulation & uncontrolled cell proliferation 2. Increase in size of adenoma: mutation of *K-ras activation of protooncogene* facilitates this step by leading to a protein that also stimulates unregulated cell growth; DCC (Deleted Colon Cancer) (inactivated mutation)--avoid apoptosis 3. Malignant transformation of adenoma into carcinoma requires mutation of *TP53* (p53 inactivation); mutations found mostly in carcinomas & rarely in adenomas

In a young male patient w/acute pancreatitis that does not have gallstones or high alcohol intake, what other test can considered to find etiology of disease? Describe pathophys of why hypertriglyceridemia can cause acute pancreatitis

Inherited or acquired hypertriglyceridemia can cause acute pancreatitis if serum level of triglycerides exceeds 1000 mg/dL -concentration of free FA exceeds the binding capacity of albumin & leads to direct injury to pancreatic acinar cells--via direct tissue toxicity

What are clinical signs of a patient with portal vein thrombosis?

Portal vein thrombosis causes portal hypertension which results: esophageal varices, and other varicosities at portocaval anastomoses, splenic enlargement

Where is the greatest concentration of H. Pylori found in the GI system?

Prepyloric area of gastric antrum has fewer acid-secretory parietal cells & as a result, has the greatest yield of the organism

What are the anastomses btwn Superior Mesenteric Artery (SMA) & Inferior Mesenteric Artery (IMA)?

SMA & IMA are 2 main vessels supplying small & large intestines - they are connected via a pair of anastomoses: 1. Marginal artery of Drummond (marginal artery)-- principal anastomosis 2. inconsistently present arc of Riolan (mesenteric meandering artery)

What is the most common benign liver tumor?

Cavernous hemangioma -consist of cavernous , blood filled vascular spaces of variable size lined by single epithelial layer -biopsy of suspected hemangioma is not advisable-- may cause fatal hemorrhage & is of low diagnostic yield

What is an impt. factor in down-regulation of postprandial gastric secretion

Cephalic & gastric phases stimulate gastric acid secretion -while intestinal influences (intestinal phase) tend to reduce gastric acid secretion mechanism: ileum & colon release peptide YY, which binds to receptors on endocrine, histamine-containing cells described as enterchromaffin-like cells (ECLs) -such binding counteracts the cephalic & gastric phases of acid secretion by inibiting gastrin-stimulatd histamine release from ECLs, -other factors that inhibit acid secretion include somatostatin & prostaglandins

Describe Primary Biliary Cirrhosis

Chronic liver disease characterized by autoimmune destruction of intrahepatic, intralobulra bile ducts (florid duct lesion) & cholestasis (elveated alkaline phosphatse & cholesterol) assoc. w/other autoimmune diseases such as Sjorgen syndrom, celiac disease, etc. -the condition is most common in middle-aged women presents insidiously, w/severe *pruritis (esp. at night)* one of the first symptoms reported, fatigue, may eventually develop hepatosplenomegaly & signs of cholestasis (eg, jaundice, pale stool, dark urine) & hypercholesterolemia (eg, xanthelasma); Reduced bile flow to small intesitne may cause malabsorption for fat-solub. vitamins Late manifestation: cirrhosis & portal HTN

What type of ulcers in GI system are not related to cancer, what type of ulcers are related to cancer?

Duodenal cancers (even w/H. pylori) are not associ. w/ increased risk of carcinoma in same location -in contrast, esophageal, gastric, & colorectal cancers are frequently identified as ulcerative lesions on endoscopy

What should be checked next with moderately elevated alkaline phosphatase & unclear etiology?

Followed up w/glutamyl transpeptidase-- check whether the elevated alkaline phosphatase is of bony or hepatic origin

Gastric erosions vs ulcers & main pathophys of erosions

Gastric erosions are mucosal defects that do not fully extend through the mucosa - acute erosive gastropathy can be caused by a number of factors such as NSAIDs (inhibit prostaglanding synthesis), head trauma (cushing ulcers), burn trauma (curling ulcers), smoking, alcohol, surgical stress -symptoms: upper GI hemorrhage that leads to melena, epigastric pain/discomfort, nausea, & vomitting

Describe *Hereditary nonpolyposis colon cancer (HNPCC)* or *Lynch syndrome* and mutated genes involved that lead to this cancer

HNPCC or Lynch Syndrome leads to occurrence of *colonic adenocarcinoma* at young age (<50) along w/predisposition for extraintestinal malignancies (endometrial cancer in 1st degree relatives) -mutation of *DNA mismatch repair genes are responsible for HNPCC* MSH2 MSH6 MLH1 PMS2

Describe the different lab values in hepatic disease and its effect on hepatic disease and function; what laboratory finding is most indicative of poor prognosis in a patient w/cirrhosis?

Increased AST & ALT-- indicators of hepatocelluar disease/structural integrity of hepatocytes *Increased alkaline phosphatase & gamma-glutamyl transpeptidase indicate biliary injury* Serum albumin, bilirubin, & prothrombin time are reflective of the liver's biosynthetic function and of greatest prognostic significance in patients w/cirrhosis

What is the most common malignant hepatic lesion?

Metastasis from another primary site (breast, colon, lung), not hepatocellular carcinoma -presents with: non-tender hepatomegaly, weighloss (progressive anorexia), abdominal discomfort, *elevated alkaline phosphatase*, marginally elevated ALT

Why might a liver biopsy show no abnormalities in the liver in portal vein thrombosis?

Normal liver indicates that presinusoidal process is responsible for portal HTN portal vein thrombosis causes obstruction in portal venous flow upstream from liver--causing portal HTN while leaving liver unaffected. Ascites is uncommon w/portal vein thrombosis since sinusoidal HTN does not develop

Vitamin E deficiency

Occurs in individuals w/fat malabsorption -deficiency of this fat-soluble vit is assoc. w/increased susceptibilit of neuronal & erythrocyte membrane oxidative stress -clinical manifestation include ataxia, impaired proprioception & vibratory sesnation, & hemolytic anemia (*neuromuscular disease & *hemolytic anemia*) -Vit E primarily serves to protect fatty acids from oxidation; vit E deficiency predisposes cell membranes to oxidaative injury

Primary & secondary lactase deficiency

Primary - congenital(rare autosomal recessive) or acquired (common in Asian, Blacks, Hispanics, Native Americans)--lactase nonpersistance ceased production of the enzyme mid childhood -*mucosa is normal* Secondary- Celiac disease (atrophy of intestinal villi) or Crohn's disease (inflamm. w/non-caseating granulomas) *mucosa damaged* accompanied by other features of malabsorption (eg, iron deficiency, Vit D defic. )

When patient presents w/RT upper quad bleeding, if surgeon occuludes hepatoduodenal ligament to determine what?

Pringle Maneuver-- occlusion of portal triad (hepatic artery, portal vein, common bile duct) is a surgical techniquee use to distinguish source of RT upper quad bleeding -if hepatic bleeding persists after occlusion of portal triad, the inferior vena cava or hepatic veins are likely to be injured

What is abetalipoproteinia, and how does it present in an infant?

inherited (autosomal recessive), inbility to synthesize apolipoprotein B, an impt. component of chylomicrons & very low-density lipoprotein (VLDL) -mutation in loss of function MTP gene that incorporates lipids into VLDL & chylomicrons -lipids absorbed by small intestine can't be transported into blood & accumulate in intestinal epithelium--resulting in enterocytes w/clear or foamy cytoplasm Manifests in first year of life: abdominal distension , foul smelling stool, malabsorption of fat-soluble vitamins, (esp. Vit E),-- RBCs w/abnormal membranes & thorny projections (acanthocytes), & multiple neurologic abnormalities (progressive ataxia, retinitis pigmentosa)

Iron in breast milk

iron is low in breast milk but bioavailablity of iron in breastmilk is higher than supplemental iron & sufficient for infants until age 4 months -due to decreasing iron concentration in breast milk over time, supplementation is recommended for breastfed infants at age >4 months until solid food intake provides an adequate amount

What is the biopsy finding of kaposi sarcoma involvement of the GI that might cause profuse diarrhea?

kaposi sarcoma usually involves skin & GI tract & is common in HIV patients *not on retroviral therapy* endoscopy reveals characteristic lesions, which range from reddish/violet flat maculopapular lesions to raised hemorrhagic nodules or polypoid masses Biopsy can show spindle cells, neovascularization & extravasated red blood cells

Briefly describe pathogenesis of CREST syndrome

systemic sclerosis CREST syndrome (Calcinosis, Raynaud Phenomenon, Esophageal dysmotlity, Sclerodactyly, Telangiectasia)-- limited variant of systemic sclerosis w/skin disease that affects face, forearms, & fingers Pathogenesis: chronic autoimmune inflammation, *vascular endothelial injury* resulting in chronic ischemic tissue damage (fingertip ulcers) & *excessive activation of fibroblasts leading to progressive tissue fibrosis*.

Describe Zollinger-Ellison syndrome(ZES), where the tumors arise and what regions of the GI are effected by high leves of gastrin secretion

ZES is caused by gastrin-secreting tumors (gastrinomas) involving *small intestine or pancreas*. -Patients typically have peptic ulcers *(often beyond duodenal bulb)*; abdominal pain/acid reflux & diarrhea -diarrhea results b/c gastric acid damages intestinal epithelial cells & inactivates pancretic enzymes, preventing proper nutrient absorption note: often refractory to therapy This condition is frequently assoicated w/multiple endocrine neoplasia type 1.

Acute acalculous cholecystitis

acute inflammation of gallbladder in absence of gallstones -typically occurs in critically ill patients (ed, those w/sepsis, sever burns, trauma, immunosuppression) due to gallbladder stasis & ischemia -clinical finding: may be subtle--fever, right upper quad pain, leukocytosis -physical findings: may demonstrate jaundice & palpable right upper quad mass -ultrasound: no stones, edema & enlarged gallbladder

what supplementation is needed for infants that are exclusively breastfed?

Vit D Supplementation needed due to lack of sun exposure & prevent rickets note: Dark skin people in more need b/c melena in skin is natural sun block & prevents UV rays from reaching skin for Vit D synthesis, so need more sunlight exposure to produce adequate Vit D -breast milk content of Vit D & K insufficient for nutritional needs of newborn -Vit K is given parenterally to all newborns at birth to prevent hemorrhagic disease of newborn

What may be a cause of a Zenker (false) diverticulum in an elderly patient that presents w/oropharyngeal dysphagia, halitotosis, regurgitation, & recurrent aspiration (pneumonia)?

cricopharyngeal motor dysfunction--diminished relaxation of cricopharyngeal muscles during swallowing (deglutition) results in increased intraluminal pressure in oropharynx--may eventually cause mucosa to herniate through zone of muscle weakness in posterior hypopharynx, forming Zenker (false) diverticulum

What happens when lactose is not fully hydrolyzed due to lactase deficiency?

fermentation of undigested lactose by gut bacteria leads to increased production of short-chain fatty acids (eg, acetate, butyrate, proprionate) that acidify the stool (lower pH) -produce hydrogen gas (increased breath hydrogen contents), -high amounts of undigested lactose in gut leads to elevated stool osmolality--attracts excess H2O in bowel lumen--osmotic diarrhea

What disease does fungi Aspergillus aflatoxin in hight amounts?

high levels of dietary aflatoxin exposure is assoc. w/ G:C to T:A transversion in codon 249 of p53 gene , mutation thought to greatly increase hepatocellular carcinoma esp. in people w/Hep B inf.

Anal fissures

longitudinal tears in mucosa of anal canal distal to dentate line -- usually due to passage of hard stool in patients w/chronic constipation most fissures occur at posterior midline, likely due to decreased blood flow in this area

Describe pathyphys behind HFE gene in hereditary hemocromatosis

mutation of HFE protein leads to reduced iron uuptake & causes enterocytes and hepatocytes detect falsely low levels this causes following: - increase in enterocyte apical DMT1 expression causes more iron intestinal absorption from lumen -hepatocyte *decrease in hepcidin synthesis*, causes increase in basolater ferroportin expression on enterocytes causes massive realese of iron into circulation

What is the main or first event in pathogenesis of acute appendicitis?

obstruction of lumen of appendix-- acute appendicitis -fecaliths, hyperplastic lymphoid follicles, foreign bodies, or tumors may cause obstruction -periumbilical (visceral pain--dull pain) shifting to RT lower quad (severe/somatic, well-localized) nausea, vomitting, diarrhea, & fever are typical manifestations of acute appendicitis

where is portal vein located and how is it implicated in the liver cirrhosis, what is the treatment in ascites?

portal vein can be identified on x-sectional scans lying *medial to (or just w/in) the right lobe* of the liver anterior to inferior vena cava -pressure in portal system is elevated in liver cirrhosis -treatment: restrict sodium intake and take diuretics (furosemide, spirinolactone)

Which branch coming off of the splenic artery is vulnerable to ischemic injury due to poor anastomoses supplying the upper part of greater curvature of stomach?

short gastric branches

what is not retroperitoneal and what do these organs cause when ruptured?

spleen, liver, stomach, & transverse colon are intraperitoneal organs -rupture would lead to *hemoperitoneum (free blood in peritoneal space)*, not retroperitoneal hematoma

Describe the rapid urease test

used to diagnose helicobacter pylori infection -sample of gastric mucosa added to solution containing pH indicator & urea [H. pylori contains large amounts of extracellular urease] urease will convert urea to CO2 & ammonia & cause a pH increase & resultant color change of pH indicator, indicating alkalinaztion o f solution -observe solution for 24 hrs.

What is necessary to supplement to patients that undergo total gastrectomy?

very-high dose oral or parenteral Vit. B12 (water-soluble vitamin) IF is normally secreted by parietal cells in stomach & is necessary for absorption of Vit B12 in terminal ileum Patients who have undergone total gastrectomy require lifelong vit. B12 supplrementation due to inableity to produce IF