GI Flashcards
Pleomorphic adenoma (gland)
Mixed epithelial and stroma tumor usually in parotid; benign but has high rate of recurrence and is associated with radiation
Warthin’s tumor
Benign heterotopic salivary gland tissue trapped ina lymph node, surrounded by lymphatic tissue
Mucoepidermoid carcinoma
Most common malignant tumor of salivary glands; usually located in the sublingual gland (most parotid tumors are benign while most sublingual are malignant)
Zenker diverticulum
Above upper esophogeal sphincter; risk for adenocarcionma
Traction diverticulum
midpoint of esophagus; risk for adenocarcinoma
Epiphrenic diverticulum
immediately above lower esophageal sphincter
Acute gastritis histology
neutrophils above BM, loss of surface epithelium, fibrin-containing purulent exudate
Chronic gastritis histology
lymphoid cell aggregates in lamina proria, columnar absorptive cells, atrophy of glandular structures
Zollinger ellison syndrome histology
Thickening of gastric folds, elevated gastrin levels, glandular hyperplasia
Drugs promoting gastric motility
Cholinergic agonists (bethanechol), acetylcholinesterase inhibitor like neostigmine, Metoclopramide (5HT agonist and Dopamine antagonist - potential for seizures), Macrolides (stimulate smooth muscle receptors)
tubular adenomas
pedunculated and smaller; dysplastic colonic mucosal cells that form tubular-shaped glands
Villous adenomas
cauliflower or fingerlike projections; dysplastic epithelial cells forming villi-like projections; can cause bleeding, secretory diarrhea and partial intestinal obstruction. Are larger sessile and more severely dysplastic than tubular; high risk of progression to adenocarcinoma
Tubulovillous adenoma
mixture of villous and tubular histology
Hamartomatous polyp
can occur sporadically or as part of Peutz-Jeghers syndome and Juvenile polyps. Can cause bleeding and intussusception but not diarrhea.
Peutz-Jeghers syndrome
associated with multpiple hamartomatous polyps and black spots on skin and mucosa of young patients. Secretory diarrhea is not common in this condition. Rare compared to adenomatous polyps; increased risk of CRC
Signet ring cell carcinoma can be found here
stomach, breast, ovary, colorectal area.
Treatment for acute arsenic poisoning
Dimercaprol - displaces arsenic from sulfydryl groups
Treatment of choice for Mercury and lead poisoning
EDTA which complexes with mono-, di- and trivalent ions
Secretin
Duodenal S cells release secretin in response to H+; stimulates pancreatic cells to increase bicarb secretion; As pancreatic juice flow rates and secretin stimulation increase the bicarb concentration increases and Cl concentration decreases
Curling ulcer
ulcers arising in proximal duodenum assoc with severe trauma or burns.
Cushing ulcer
esophageal, stomach, or duodenal ulcers associated with high intracranial pressure. Due to to impaired oxygenation of tissues, induced by vagus stimulation from brain resulting in hypersecretion.
Two subtypes of gastric adenocarcinoma
Intestinal: intestinal glands similar to colonic adenocarcinoma; Diffuse: signet-ring cells. Gastritis, barrett esophagus, H pylori, nitrate consumption, diet lacking in fruit and vegetables, cigarette smoking are risk factors
Opioid side effects on GI system
Constriction of sphincter of Oddi which can cause increase in common bile duct pressure. Cause histamine release leading to vasodilation and itching. Cause constipation by slowing motility, decrease parietal cell acid secretion, can indirectly increase somatostain secretion.
Duodenal ulcer associateions
pain decreased with meals. Almost always H pylori. Some have increased gastric acid secretion as in ZE syndrome. Hypertrophy of Brunner’s glands. NOT assoc w risk of carcinoma (esophageal, gastric and colonic ulcers are)
Duodenal ulcer location
Most occur in duodenal bulb; when found in distal duodenum or other atypical locations Zollinger-Ellison syndrome is suspected. Multiple ulcers, ones refractory to therapy also.
Midgut embryology; timing and potential problems
6th week midgut herniates (allows for rapid growth of intestine and liver despite slower growth of abdominal cavity). 10th week 270degree turn counterclockwise around SMA. If this is abnormal, malrotation occurs and cecum is found in RUQ, fixed fibrous bands to second portion of duodenum. Obstruction occurs dt bands which compress duodenum which results with bilious vomiting. Twisting around SMA can also cause midgut volvulus with intestinal gangerene.
VIP
produced by pancreatc islet cells and neurons in GI mucosa. Relaxes smooth m, inhibits H+ secretion, stimulates pancreatic bicarb and chloride secretion.
CCK
increases secretion of Pancreatic enzymes and contraction of gall bladder, inhibits gastric emptying. Produced by I-cells of proximal small bowel mucosa in response to fatty acids and monoglycerides
Secretin
produced by S-cells in respnse to duodenal acidity and fatty acids. Increases pancreatic and biliary bicarb secretion and decreases gastric acid secretion
Gastrin
G-cells in stomach mucosa. Stimulates gastric acid production and growth of gastric mucosa, gastrinomas classically cause intractable peptic ulcer disease
Glucagonoma
pancreatic alpha-cell tumor that hypersecretes glucagon. Secondary diabetes mellitus and necrolytic migratory erythema of the skin
Ulcerative colitis associated carcinoma differs from sporadic how
affects younger patients; progresses from flat non-polypoid dysplasia; appears mucius or has signet ring morphology; early p53 but late APC gene mutation, opposite of sporadic; distributed within proximal colon; multifocal in nature.
Amatoxins (death cap mushroom toxins)
Bind to DNA-dependent RNA polymerase II and halt mRNA synthesis. Results in apoptosis of hepatic cells.
Modes of transmission of campylobacter versus shigella
Both are fecal-oral but campylobacter is carried by domestic animals where shigella is not. Campylobacter is mostly acquired from animals or undercooked poultry or unpasteurized milk.
Somatostatin
made in a bunch of different locations such as hypothalamus, stomach, intestine, and pancreas. It inhibits GH, TSH, and suppresses all other GI hormones
Why is shigella’s Infective dose so low?
it is resistiant to acid and bile, it also binds to intestinal mucosal M cells on peyer’s patches. Other organisms with small infective inoculum are Campylobacter, Entamoeba histolytica (it takes only 1), Giardia (only 1 needed)
GERDs typical cause
LES transient relaxation. Acidic gastric contents reflux back into esophagus and irritate mucosa leading to inflammation. Presents with nocturnal cough many times. Biopsy shows basal cell hyperplasia, elongation of lamina propria and inflammatory cells (eosiniphils, neutrophils, lymph)
Anal fissure
tear in the lining of anal canal distal to the dentate line that occurs most often on the posterior midline (this area is poorly perfused making it sensitive to trauma by hard fecal mass). Patients complain of severe tearing pain with passage of bowel movements. Assoc w low fiber and constipation.
Typical signs of lead poisoning
Colicky abdominal pain “lead colic”, constipation, headaches, impaired short-term memory, blue pigmentation at gum-tooth line “lead lines”; wrist drow or foot drop due to peripheral neuropathy; microcytic hypochromic anemia and basophilic stippling
CEA
serum carcinoembryonic antigen, marker for colon cancer. It is a glycoprotein involved in cell adhesion. Produced in the embryonic pancreas.
Leptin action
produced in adipocytes; decreases food intake by decreasing production of neuropeptide Y (an appetite stimulant in arcuate nucleus); stimulates POMC in arcuate nucleas which is cleaved to MSH which inhibits food intake.
Erosions versus ulcers
erosive gastritis: caused by NSAID use, trauma, burns, alcohol or tobacco, stress, bacteria. Defined as mucosal defects that don’t penetrate the muscularis mucosa. Ulcers extend into submucosal inner muscular and outer muscular layers.
hyperplastic polyp
well-differentiated mucosal cells that form glands and crypts
Hamartomatous polyp
mucosal glands, smooth muscle and CT. May be sporadic or in Peutz-Jeghers or juvenile polyposis.
Inflammatory polyps
seen in IBD. Composed of regenerating intestinal mucosa
Lymphoid polyps
found in children and consist of intestinal mucosa infiltrated with lymphocytes
Malignant potential of adenomatous polyps (adenomatous polyps are the ones that contain dysplastic cells that can transform into carcinoma)
Degree of dysplasia, villous histology, size >1cm
Imperforate anus
abnormal development of anorectal structures; most often associated with urorectal, urovesical, or urovaginal fistulas. When a fistula is present, meconium may discharge from the urethra or the vagina. Associated findings are renal agenesis, hypospadias, epispadias, and bladder extrophy.
Intestinal atresia
occurs due to vascular accidents in utero. If the SMA is obstructed the “apple-peel” atresia occurs. It manifests as blind-ending proximal jejunum with absence of a long length of small bowel and dorsal mesentery. The terminal ileum distal to the atresia assumes a spiral configuration around an ileocolic vessel.
Crohn’s disease molecular pathogenesis
NF-kB is responsible for the cytokine production seen. NOD2 gene (expressed in epithelial cells and leukocytes) appears to act as microbial receptor that triggers NF-kB. NF-kB induces cytokines in response to infectious pathogens. The NOD2 mutation increases NF-kB allowing intracellular microbes persisting and inducing chronic inflammation within GI tract
Fibrosis of islets of pancreas
DM type I
pacnreatic ducts filled with mucus plugs
Cystic fibrosis
Lymphocytic infiltration of islets of langerhans
DM type 1
Lipid digestion
occurs in duodenum and is ABSORBED in the Jejunum.
Complications of Ulcerative colitis
Sclerosing cholangitis, CRC, Toxic Megacolon (presents with bloody diarrhea, fever, signs of shock; perforation is a life-threatening complication of megacolon, do not do any barium or contrast studies for fear of perforation)
Complications of Crohn’s
Strictures, fistulas, perianal disease, CRC
Esophageal squamous carcinoma risk factors
alcohol, tobacco smoking, nitroso containing foods; asian and african descent
Esophageal adenocarcinoma risk factors
Barrett esophagus, obesity, GERD, tobacco use
Vitelline duct abnormalities
Persistent vitelline duc, meckel diverticulum, viteline sinus, and vitelline duct cyst. This normally obliterates during week 7. Also called omphalomesenteric duct
esophageal varices
shunt involving Left gastric vein and esophageal vein
Caput medusae
Paraumbilical veins to superficial and inferior epigastric
Hemorrhoids in ascites
Superior rectal veins to middle and inferior rectal veins which drain into interna linguinal vein
acute interstitial pancreatitis pathyphys
stasis of secretions leads to lipase autodigestion and calcium doposition onto free FA’s. Pancreas looks edematous with focal fat necrosis and calcium. If the inflammatory process continues it can lead to necrosis.
Acute Necrotic pancreatitis
If inflammation from acute interstitial pancreatitis continues the edema cuts off blood supply rendering ischemic damage to acinar cells leading to inappropriate trypsin activation. The trpsin ten activates other proteoltic enmes and initiates autodigestion. The areas of white chaly fat necrosis can spread onto mesentery, omentum etc.
Chronic Gastritis Types A and B
Type A is Autoimmune etiology and is found in the body (pernicious anemia); Type B is bacterial in nature (h pylori) and is found in the Antrum
adenocarcinoma biopsy and colonoscopy findings
protuberant mass on scope; mucosal cells with gland formation on biopsy
colonic CMV scope and biopsy
ulcers and mucosal erosions on scope; Inclusion bodies on micro
Colonic cryptosporidium scope and microscopy
scope shows generalized inflammation; basophilic clusters are seen on surface of intestinal mucosal cells
Entamoeba histolytica scope and microscopy
scope shows flask shatped ulcers; trophozoites have red blood cells
Kaposi’s sarcoma scope and microscopy
Reddish violet flat maculopapular lesions or hemorrhagic nodules; the microscopy shows spindle-shaped tumor cells with small-vessel proliferation
MSH2 gene
mutated in HNPCC and is responsible for DNA mismatch repair
APC gene
located on Chromosome 5 responsible for regulation of growth and cell adhesion
Systemic mastocytosis
abnormal proliferation of mast cells and increased histamine secretion. This causes many systemic effects mediated by histamine. In the GI system it leads to increased secretion of Gastric acid
Histamine action on parietal cells
H2 receptor stimulates cAMP and PKA
Acetylcholine action on parietal cells
M3 receptors leads to increased calcium via IP3
Gastrin action on parietal cells
increase of intracellular calcium. It stimulates histamine synthesis and release by enterochromaffin-like cells which is most potent mechanism
Risk factor for gallstone ileus
usually in patients with long history of gallstones, a long standing stone creates a fistula between gallbladder and adjoining gut tissue which allows passage into small bowel. This allows for gas to be let into the gallbladder. The gallstone blocks the ileocecal valve and you can see air in the biliary tree
CREST
Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactyly, Telangiectasia
Factors recucing gastric secretion after a meal
peptide YY to block histamine release, Somatostatin, and prostaglandins
Vitamins deficient after gastrojejunostomy
B12, Iron, folate, and fat-soluble vitamins
Most common locations of colonic masses
rectosigmoid colon > Ascending colon > Left sided tumors (infiltrate wall of colon and narrow lumen)
Causes of acute pancreatitis
Gallstones and alcohol are most common; less common are ERCP procedure, drugs, infection, hypertriglyceridemia, structural abnormalities, surgery, hypercalcemia
Spcific antibodies for celiacs
anti-tissue transglutaminase; IgA endomysial antibody
Gastric adenocarcinoma, two types
Signet-ring carcinoma: cells don’t form glands, diffuse involvement of stomach wall, have plaque appearance, infiltrate large areas of stomach creating leather-bottle stomach (linitis plastica). Intestinal-type adenocarcinoma: resmbles colon cancer, grows nodular polypoid and well-demarcated masses. Most important prognostic factors is depth of invasion and regional lymph. Nitrosamines, achlorhydria, chronic gastritis are risk factors so is type A blood
Retroperitoneal Structures
Abdominal Aorta, Pancreas, Descending and ascending colon, Spleen, Ureters, Suprarenal gland, kidney, IVC, deodenum (2nd 3rd and 4th parts), esophagus, rectum
Falciform ligament
Attaches liver to anterior abdominal wall
Hepatoduodenal ligament
Contains portal triad. Connects greater and lesser sacs
Gastrohepatic ligament
Lesser curvature to liver. Contains R and L gastric artery, separates greater and lesser sacs.
Gastrocolic ligament
Contains gastroepiploic arteries, part of greater omentum. Attaches to greater curvature.
Gastrosplenic ligament
contains short gastric arteries, separates left greater and lesser sac
Splenorenal ligament
Connects spleen to posteriosterior abdominal wall, holds splenic artery and vein
Normal epithelium of esophagus
stratified squamous nonkeratinized
Stomach epithelium
gastric glands
Duodenal histology
Villi and microvilli. Brunner’s glands, Crypts of Leiberkuhn
Jejunum histology
plicae circulares and crypts of lieberkuhn
Ileum histology
Peyer’s patches, plicae circulares, crypts. Largest number of goblet cells (goblet cells increase density as you mover farther down the ileum)
Colon Histology
Crypts but NO villi
Layers of digestive tract anatomy
Epithelium (columnar), lamina propria, muscularis mucosa, submucosa with glands and meissner’s plexus, Muscularis externa with auerbach’s plexus then serosa
Name branches and location of branches of abdominal aorta descending order
Inferior phrenic aa., Celiac trunk (T12), SMA (L1), L suprarenal a. (L1), R and L renal aa. (L1-L2), R and L testicular (ovarian) aa. (L2/3), IMA (L3), Bifurcation of aorta L4.
Branches of the celiac trunk
L gastric, Spleenic, Common hepatic.
Rectum above pectinate line, pathology and venous drainage
Adenocarcinoma, supplied from Superior rectal artery (IMA). Drains to Superior rectal vein and to IMA, then to portal system
Rectum below pectinate line
Somatic innervation so hemorrhoids are painful. Drains to inferior rectal vein to internal pudendal then internal iliac to IVC. Squamous cell carcinoma and supplied arterially from Internal pudendal.
Indirect Inguinal hernia
More common in males, happens in infants owing to failure of processus vaginalis to close (can form hydrocele). Covered by all 3 layers of spermatic fascia
Direct inguinal hernia
Through hesselbach’s triangle (inferior epigastric, lateral rectus abdominis, inguinal ligament). Goes through superficial inguinal ring only covered by external spermatic fascia and is seen in older men.
Femoral hernia
Protrudes below inguinal ligament, is a common cause of bowel strangulation. Through the femoral canal below and lateral to pubic tubercle. More common in women
Gastrin
G cells (antrum); gastric mucosa growth, motility, H+; stomach distention or pH increase, amino acids, peptides, vagal.
CCK
I cells (duodenum jejunum) stimulated by FA’s and Protein, increases pancreas secretion (via stimulation of parasympathetics), gallbladder contraction, increased sphincter of oddi relaxation, decrease emptying
Secretin
S cells (duodenum) increases HCO3 from pancreas, decreases gastric acid secretion, increased by acid and fatty acids.
Somatostatin
D cells (pancreas, GI mucosa); decreases all GI hormones, inhibits release of GH and TSH. Increased by acid and decreased by vagal stimulation.
GIP
K cells (duodenum jejunum) increases insulin release and decreases H+ secretion. Stimulated by oral glucose (more rapid than glucose given IV)
VIP
Parasympathetic ganglia increases secretions and relaxes intestinal smooth m. adecreased by adrenergic input
Motilin
Small intestine Produces migrating motor complexes, increased in fasting state
Glucose and galactose absorption
SGLT1 (Na dependent)
GLUT-5
Fructose transporter in intestine
D-xylose test
distinguishes GI mucosal damage from other causes of malabsorption
Peyer’s patches
Small intestin lamina propria and submucosa. M cells take up antigen. B cells stimulate germinal centers and IgA-secreting plasma cells are created. IgA receives protective secretory component and is then transported across epithelium to gut to deal with antigen.
nocturnal couph and dyspnea
GERD or Barrett’s
Diffuse esophageal spasm (DES)
esophageal motility disorder presenting with severe non-cardiac chest pain due to uncoordinated contractions of esophageal body, mimics angina
Symptoms of whipple’s disease
cardiac, arthralgias, and neurological
Celiac sprue antibodies and genetic association
HLA-B8, occurs primarily in jejunum, Anti-gliadin, anti-endomyseal, anti-reticulin,anti-transglutaminase
Acute gastritis etiology
decreased protection of mucosa, dt stress, NSAIDS, alcohol, uremia, burns (curling), head trauma (cushings),
Menetrier’s disease
gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucous cells. Precancerous. Rugae of stomach look like brain gyri
Virchow’s node
supraclavicular node on left side (drains lower GI) and is a place of mets from stomach
Sister Mary Joseph’s nodule
Perimbilical gastric metastasis
Familial adenomatous Polyposis (FAP)
AD; APC gene on chromosome 5q. Thousands of polyps.
Gardner’s syndrome
FAP + osseous tumors and retinal hyperplasia with other soft tissue
Turcot’s syndrome
FAP + CNS tumors
HNPCC
MSH2 gene mutaiton in DNA mismatch repair. Proximal colon is most common location (R-sided)
Carcinoid and B3 deficiency
Makes Serotonin which is synthsized by tryptophan so it can cause a secondary tryptophan deficiency leading to niacin deficiency
Alcoholic hepatitis
destruction via acetaldehyde which stimulates cells that used to store vitamin A to change and make collagen and fibrous tissue instead. There is a neutrophilic infiltration. Formation of mallory bodies which are ubiquinated keratin microfilaments.
Hepatocellular carcinoma risk factors
HBV HCV, alcohol, wilson’s disease, hemachromatosis, alpha-1-AT, carcinogens, Aspergillus toxins.
Cavernous hemangioma
biopsy contraindicated due to risk of bleeding. Congenital malformations that enlarge by ectasia not hyperplasia. Common benign liver tumor; typically occurs at age 40.
primary sclerosing cholangitis
associated with ulcerative colitis. Etiology unknown. It looks like a beaded structure with onion skin lesions. Mostly occurs in men, pANCA, risk for cholangiocarcinoma. Hyper IgM.
Primary biliary sclerosis
autoimmune disease, histologically is granulomatous inflammation of INTRAhepatic bile ducts. Starts off variably throughout liver progresses to a diffuse green stained liver that is uniformly micronodular. + anti-mitochondrial antibodies. Associated with other autoimmune diseases especially women
