Gastro

• 1. Ach - gastrin - makes acid.
• 2. Prostaglandins that make mucus

Both are protective for the stomach

• Stimulated by SNS and PNS (SNS makes thick secretions and PNS makes increased volume)
• Has a Cl-pump in the acinus
• Hypotonic so we can taste food
• Amylase but not essential like pancreatic lipase
• No protein digestion enzymes (therefore, tofu tastes like nothing)

Opiod agonist that binds to mu receptors in GI tract and slows motility. High doses combined with atropine to decrease physical dependance and euphoria

Bismuth sulfate and ocreotide

• Urea is converted to CO2 and NH3 and causes a pH increase - causing alkalinization of the urine.
• CO2 measured in a breath test.

Intestinal stenosis and atresia: absence of part of the bowel (e.g. formation of blind-ending proximal jejunem) and terminal ileum wraps around an ileocolic vessel.

• Glycosylase cleaves the misplaced uracil
• Endonuclease cleaves the 5' end and lyase cleaves the 3' end
• DNA polymerase and ligase fill in the single nt gaps

• Increased intraluminal pressure causes mucosa and submucosa to herniate through weak spots in the muscular layer.
• sigmoid colon
• Risk factor: chronic constipation

Malabsorption (fatty stools) due to failure to secrete adequate amylases, proteases, lipases. 

Biliary colic, jaaundice, cholangitis: fever, RUQ pain, + Murphy's sign. 

Gallstone ileus: Cholecystenteric fistula forms --> allows stone to go into the small bowel and dislodge in the ileum. Intestinal gas enters the gallbladder and biliary tree. 

AA, IVC

Pancreas (except the tail), kidneys, adrenal glands

2nd and 3rd part of the duodenum, ascending and descending colon, rectum, ureters, bladder

• Increased osmotic stool gap (osmolarity increases due to decreased absorption of substances)
• Increased breath H+ content (osmotic diarrhea)
• Decreased stool pH

• PPV
• NPV (inverse relationship with prevalence)

• Abnormal development of anorectal structures (small dimpling instead of an anus opening)
• Inability to pass meconium
• Meconium can exit from urethra if fistula present = GU problems
• Associations: VACTERL (less common than GU sx)
• vertebral defects
• anal atresia
• cardiac problems
• TE fistula
• esophageal atresia
• renal problems
• limb defects

CD4 accumulation, increased tissue fibrosis due to collagen deposition

• Absence of ova and parasites
• Inflammatory: watery and then bloody

• Toxin A (enterotoxin): mucosal inflammation, loss of water with diarrhea, mucosal death
• Toxin B (cytotoxin): actin depolymerization, loss of cytoskeleton integrity, mucosal necrosis

• 1. NRTIs
• 2. cyanide

• Normal: bile acids are produced in liver, excreted with bile and reach terminal ileum become micelles with fat and reabsorbed in the liver again. 
• Crohn's: damaged terminal ileum - no bile acid reabsorption = gallstones

Dimercaprol

Mucosal IgA (immune protection)

• Hyperglycemia
• Cushing's (lipodystrophy = redistribution of fat)
• P450 inhibition

Hep A and E (fecal-oral)

Injury to the duodenal and jejunal mucosa by adhering to the intestinal brush border, severe IgA deficiency predisposes (no adaptive immunity)

Mixed aerobic and anaerobic bacteria

• Ballooning degeneration (hepatocyte swelling)
• Councilman bodies (eosinophilic apoptotic hepatocytes)
• Hep A and E

• Nodular regeneration
• Hep B and C

Increased venous pressure associated with cirrhosis

• Increased intraluminal/abdominal pressure caused by vomiting, retching. 
• Hiatal hernias also a cause

• Increases NH3 deposition due to waste products (GI bleeding, hypovolemia, hypokalemia, metabolic alkalosis, infection, hypoglycemia)
• Lactulose

• Cricopharyngeal muscle dysfunction (decreased relaxation of pharyngeal muscles during swallowing). 
• Increased intraluminal pressure causes mucosa to herniate through

• DNA binding proteins (c-jun and c-fos)
• dsDNA probe

• Proto-oncogene: codes for a membrane-G protein which activates MAP kinase pathway and activates transcription.
• Doesnt directly bind to DNA

• 1. Glycolysis/Gluconeogenesis
• 2. B-oxidation
• 3. TCA
• 4. Urea cycle (OTC)

• 1. RBCs have no mitochondria
• 2. Hepatocytes have mitochondria, but lack succinyl-coA enzyme

• 1. irradiation
• 2. water chlorination
• 3. boiling for 1 min
• 4. bleach
• 5. autoclaving (120C) for 20 mins

1 

• <1
• Area under oral curve x IV dose/Area under IV curve x oral dose

• 1. Estrogen upregulates HMG-CoA reductase increasing cholestrol synthesis
• 2. Progesterone-induced gallbladder hypomotility and decreases bile secretion

Biliary stones (decrease in bile reabsorption)

• Cholinergic and vagal stimulation
• Presence of thought, sight, smell, food

Gastrin stimulation and stomach distention increases acid release

• Inhibits gastrin release
• Ileum and colon release peptide YY, which binds to ECLs

COX-2 overexpression

Antibiotics

• Chr 6.
• HFE gene encodes a HLA-class I transporter that affects Fe absorption in the duodenum

NF-kB causes cytokine production

Transcription regulators encoding morphogenesis.

• 1. Intestinal obstruction
• 2. Midgut volvulus (intestinal ischemia

• 1. Duodenal atresia (ischemia)
• 2. Intestinal obstruction distal to duodenum (ampulla of Vater)

• Peristalsis waves from the stomach to the small intestine when food is not present. 
• Sweeps undigested food and maintains low bacterial counts in the SI.

• Increased intestinal bacteria
• Decreased gastric emptying
• Slows duodenal motility

Identifies C.diptheria from other oropharynx flora

CAMP factor produced by S.agalactaie - used to distinguish between Group A and B strep

GIP

• 1. 5HT3 antagonists (Ondasteron)
• 2. Cental dopamine antagonists (Metachlopromide)

Necrosis and hemorrhage --> Septic shock

• NK-1 antagonist and block susbtance P
• (NK receptors present in the brainstem and control the emetic reflex)
• Treats nausea and vomiting with moderate anti-neoplastic agents

• Accumulation of acylcarinitines in the urine
• B-oxidation impairment - low ATP levels
• Low ATP = deficiency of urea cycle
• Urea cycle def = hyperammonia
• Fasting hypoglycemia (low glucagon)
• No ketone bodies

• Inhibits gastric acid secretion via somatostain
• Inhibits gastric emptying
• Contraction of gallbladder and relaxation of sphincter of Oddi
• Digestion in the duodenum
• Increases production of hepatic bile 

n.b. CCK antagonist can also increase CCK levels

• Encephalopathy and hepatic failure
• Mitochondrial dysfunction: impairs B-oxidation and oxidative phosphorylation (glycolysis)

• Ascaris infection
• Hernias
• Adhesions 
• Tumors - intessuception
• Midgut volvulus

• Mucus (impedes H+ ion flow)
• Gastrin (mucosal growth)

Mucus

Serous 

Serous + Mucus

• 1. Gastrin 
• 2. Ach (vagal stimulation)
• 3. Histamine

• Secretin
• VIP

• Increased AST and ALT
• Normal amylase (no pancreatitis)
• Normal ALP (no injury to the bile ducts or biliary tree)

• Short gastric
• (left gastroepiploic anastomoses with right gastroepiploic)

• Mainly by conversion from NH3 to urea by the urea cycle in the liver
• (Liver disease inhibits this causing encephalopathy)
• Excreted as free acid (NH4+) by the kidney (minimally)

• Urease causes breakdown of urea into NH4+ increasing acidity, and feedback inhibition onto gastrin. 
• Bacteria can survive acid environment of stomach
• Damage to mucosa causes ulcer formation

Increased fibrosis causes thickening of skin in esophagus, making it difficult to swallow, causes heartburn, absence of persistalsis and LES

• Increased conjugative bilirubin
• Increased urine bilirubin (colour of urine darkens)
• Decreased urobilinogen (therefore, clay coloured stools)

• Hemolytic anemias
• Cirrhosis
• Clonorchis sinesis (liver fluke)

• Focal nodular hyperplasia 
• (variant of HCC)

Sliding hiatal hernia

• Part of gastric cardia slides up into the thorax, alongside the esophagus. 
• GE junction is at the esophageal hiatus (not displaced)

Fluoroquinolones (mostly for gram negatives)

• Failure of recanalization of the embryonic duct = intestinal obstruction
• Bilous vomiting after feeding
• Two air-filled structures in the stomach
• No distal air bowel gas

• Occurs when oral foods are introduced in preemies mostly
• Ischemic injury of the gut leading to septic shock
• Affected mostly with giving formula rather than breastmilk - lack of maternal antibodies. 
• Do pass meconium on 1st day

• Osmotic diarrhea 
• (unabsorbed solutes draw water in)

• Meperidine: M3 antagonist so it causes relaxation of the spincter 
• (Morphine causes contraction of the sphincter, even though a good pain reliever)

Reduced secretions causes thickened mucus plugs = accumulation of pancreatic enzymes

Can occur in the SI and produce enough acid to cause peptic ulcers and then bleeding

Cori's disease: debranching enzyme defect = incomplete glycogen degradation (a,1,6 glucosidic bonds cannot be broken)

Doesn't have 3'-5' exonuclease activity

• Arises from dysplastic flat lesions (no polyps)
• Early p53 mutations and late APC gene mutations
• Multifocal in nature
• Histo: mucinous and/or signet ring morphology

• Hirschrpung's dz: Rectum
• Vagal stimulated: NC cells give rise to Meissner's (submucosal) and Auberbach plexi (myenteric)
• NC cell migration moves caudally

• Complication of pancreatitis
• Fluid-filled with enzymes and inflammatory debris
• Walls have granulation tissue and fibrosis, no epithelium

• Candida
• Herpes simplex - small vesicles with punched out lesions, eosinophilic intranuclear inclusions
• CMV - linear ulceration, intranuclear and intracytoplasmic inclusion bodies

• Toxic megacolon - supportive treatment
• (barium enema and colonscopy can cause perforation)

Mast cell proliferation in multiple organs. Massive release of histamine - acts on parietal cells to stimulate gastric acid - inactivates pancreatic and intestinal enzymes - diarrhea, etc.

• Toxin mediated watery diarrhea (increased cAMP)
• Not invasive 
• No blood or pus (leukocytes) on stool microscopy

• Enzyme: B-galactosidase
• Galactosyl-B-1,4glucose --> Galactose

Contraction of smooth muscle cells of the sphicter of Oddi, increasing pressure in bile duct and gallbladder (biliary colic)

• Located on posterior midline distal to the dentate line
• Severe tearing pain when needed to pass stool
• Due to low fibre diets and constipation

• 1. APC gene mutation causes adenomatous polyps to form from normal colonic mucosa
• 2. K-ras mutation = cell proliferation (size increase in polyps)
• 3. p53 mutation - last step from adenoma to carcinoma

Duodenum and jejunem

• Type III H.S.
• 5-10 days after drug given
• Sx: arthralgias, utricaria, proteinuria, lymphadenopathy

Increased TH1 helper cells = increases IFN-gamma, IL-2, and TNF causing intestinal injury.

• Wilson's dz
• Chr 13
• AR

25-70 bp upstream from its associated gene

Variable: upstream, downstream, or within the transcribed gene

• Mucosal invasion by entering M cells via Peyer's patches
• Escapes phagosome and enters epithelial cells to release shiga toxin

• Chloroquine has no effect against latent hepatic infections (P.vivax and P.ovale)
• Primaquine used to treat these and prevent relapse

• Cause: E.granulosus (tapeworm)
• Aspiration of cyst leads to anaphylactic shock

• Aflatoxin
• Gene mutation in p53
• Prone to HCC

• Mucoid, secretory diarrhea
• Mass found in sigmoid colon (obstruction)
• Lower intestinal bleeding
• Progresses to adenocarcinoma

• Antral gastritis: decreased # of somatostatin-antral producing cells
• High gastrin causes high acidity 

• Dont need an increase level of acid
• Normal acid levels are sufficient as in the stomach
• Destruction of mucosal barrier due to bacteria

• G cells of the gastric antrum
• Fundus

• Receptive relaxation is inhibited (cannot relax when food enters the stomach from the esophagus)
• Peristalsis can still occur

Activates AC increasing cAMP in the intestinal crypt cells activating Cl- secretory channels

Fat soluble vitamins

• n.b. Bile acids have a co-dependent Na+ transport in ileum
• Glycerol is a water soluble molecule of lipid digestion and doesnt need micelles

• Major anion is HCO3 in pancreatic secretions (higher than plasma)
• Cl- is lower than plasma
• Stimulated by presence of fatty acids in the duodenum

• Secretin stimulates pancreatic HCO3 secretions
• CCK stimulates pancreatic enzyme secretions

Releases GIP which causes release of insulin from endocrine pancreas

• Hypotonic
• High HCO3- relative to plasma
• Presence of a-amylase and lingual lipase
• No proteases

• Campylobacter (take couple of days to develop)
• Salmonella non-typhi
• S.aureus (immediate, within hours)

All over the body, including skin and GI tract mucosa

• Seen in 10% of patients who have cirrhosis with ascites
• Ascites: culture medium for bacteria that invade the bowel wall or spread to serosa
• E.coli

Signet cell adenocarcinoma

Intussusception

Hirshprung's disease

• HCO3 secretion into the mucus
• Rapid gastric epithelial regeneration
• Epithelial cell mucus secretion
• Increased mucosal blood flow

n.b delayed gastric emptying promotes ulcers by keeping acid in there

Rotavirus

Diverticulitis producing an abscess, peritonitis or both. 

• B cell neoplasms:
• a) Kaposi's sarcoma
• b) non-Hodgkin's lymphoma
• c) anorectal SCC

Non-AIDS: MALT lymphomas with sprue, H.pylori infection