Exam 6: GI Disorders Flashcards
gastric parietal cells
secrete hydrochloric acid and intrinsic factor -> necessary for the absorption of vitamin B12 in the small intestine
gastric goblet cells
secrete mucus and prostaglandin E2 (PGE2), a lipid-rich molecule, which exerts a strong protective effect. PGE2 stimulates gastric mucus production and bicarbonate secretion, which reduce the effects of HCL
GERD
Epi: most common GI disorder
Patho: Decreased closure of the LES, which allows acidic gastric contents to reflux up into the esophagus. Acid of the stomach damages the esophageal epithelium.
Two types: erosive or non-erosive (difference in damage to esophageal mucosa)
CM: Frequent heartburn = pyrosis, reflux (regurgitation) with bitter taste gastric contents into mouth, dysphagia, chest pain, chronic cough, hoarseness, wheezing
Complication: metaplasia of cells at the gastroesophageal junction = Barrett’s esophagus = can lead to esophageal cancer
Diagnosis: S/S, endoscopy, pH testing, biopsy
Hiatal hernia
Protrusion or herniation of the stomach through the esophageal hiatus of the diaphragm
Sliding hiatal hernia is common, non-significant in asymptomatic people
With GERD and large hiatal hernia can cause further irritation/pain requiring intervention
Peptic ulcer disease (PUD)
Inflammatory erosion in the stomach or duodenal lining. Ulceration occurs four times more often in the duodenum than in the stomach.
Etiology: H. Pylori & NSAIDS. Advanced age, prior PUD
Patho: exact process not clearly known. H. Pylori induce inflammation release cytokines to continue to mucosal damage. NSAIDS like aspirin thought to inhibit prostaglandin synthesis.
CM: epigastric pain, burning/gnawing, b/t meals, comes and goes
Diagnosis: endoscopy, biopsy for H. Pylori
Complications: Can lead to perforation (peritonitis), hemorrhage (acute abdominal pain), penetration
Upper GI bleed
bleeding in the esophagus, stomach, or duodenum (from lesion, erosion, ulceration, varicosed vein)
CM: Hematemesis, coffee ground emesis, melena
Slow chronic bleed -> iron deficiency anemia, fatigue, lethargy
Acute large GI bleed -> anxiety, dizziness, weakness, shortness of breath, tachycardia, tachypnea, pallor
Diagnostic: CBC, Endoscopy, positive FOBT
Pyloric stenosis
Constriction of the pyloric sphincter that impairs the movement of gastric contents into the small intestines
Etiology: build up of thick muscularis layer or fibrous tissue from PUD
CM: Delayed emptying of the gastric contents causes distension, can develop into pyloric obstruction
Bowel obstruction
Etiology: mechanical physical obstruction (adhesions, hernia, neoplasms) or nonmechanical which is reduced or absent peristalsis. (Paralytic ileus, Crohn’s, gallstones, intussusception, volvulus)
CM: vary depending on severity -> Abdominal pain, distention distal to site, N/V, hyperactive bowel sounds. Pain occurs in waves with peristalsis. partial = liquid diarrhea.
Diagnosis: Abdominal X-Ray -> excessive gas proximal to obstruction, CT & US
Complications: ischemic bowel, perforation, shock, infection, death. Can have fluid and electrolyte imbalances *small bowel absorbs a lot of water
Small bowel obstruction
post-surgery adhesions (bond sections of intestine together) -> typically requires surg intervention
Large bowel obstruction
colon cancer, diverticular disease, volvulus
generally in the stigmoid colon
high mortality if not caught early
Celiac disease
autoimmune disease w/ genetic component triggered from environmental (gluten)
patho: destroys intestinal villi from inflammation, flattens intestinal wall and reduces absorption
CM: excessive gas, muscle wasting, steatorrhea, weight loss, concern for anemias from lack of absorption of protein
diagnosis: serology celiac panel (immune) -> positive antibody titer of IgA, upper endoscopy
Irritable bowel syndrome (IBS)
Altered bowel activity and S/S w/ no pathological change
Experience periods of frequent abdominal pain, bloating, constipation/diarrhea, mucus in stools
Inflammatory bowel disease (IBD)
Pathological changes to the GI track
Failure of immune regulation
Ulcerative colitis
Crohn’s disease
Crohn’s disease
unclear etiology (genetics, autoimmune, environment)
entire bowel wall and all layers affected - any area of GI tract, chronic inflammation -> large immune response,
**skip lesions (patchy through small & large). risk for fistulas or abscesses
CM: abdominal pain, diarrhea, fatigue, weight loss
Diagnosis: colonscopy/endoscopy, biopsy, anemia labs
Ulcerative colitis
unclear etiology
episodes of inflammation in colon and rectum (inc in T, B, plasma IgG & IgE)
**continuous inflammation large bowel only
risk for colorectal cancer
CM: diarrhea, abd pain, melena
Diagnosis: scopy (psuedopolyps seen)
Appendicitis
Children/YA more common; can be caused by trauma
Patho: narrowing of the lumen from obstruction (build up of bacteria/inflammation) leads to ischemia
CM: starts vague abd pain -> RLQ, radiates from umblicus to RLQ (Psoas, Rovsing’s, & Obturator’s signs)
Needs surgical treatment or could rupture
HCG to r/o ectopic, UA to r/o stone or pylo
Diverticulitis
Patho: weakened bowel wall muscles -> protrusion of diverticula which can fill with intestinal content and become inflammed -> can lead to a mass/obstruction
CM: LLQ abd pain, N/V, fever, constipation/diarrhea
Diagnosis: ^ CRP (>50), ^ WBCs, abd imaging
Peritonitis
inflammation of peritoneum
can happen after perforation (trauma, ulcer, appendix, diverticula) surgery, or ectopic preg
CM: rebound tenderness, distention/rigid abd, fever
Bilirubin metabolism
bilirubin from RBC breakdown (unconjugated)
Liver converts to water soluble form (conjugated)
conjugated excreted in bile -> feces
Protein metabolism
Liver synthesizes and breaks down protein -> creates ammonia to be able to break down
ammonia (NH3) is integrated into urea and excreted through kidneys
Stages of hepatitis
Prodromal (preicterus period)
Icterus period
7-14 days
Recovery period
1-4 months
Carrier state: infection with HBV and HCV no symptoms but can transmit
*no carrier state for HAV
Hep A
fecal-oral route
Diagnosis: elevated IgM and antibodies to A (IgG anti HAV)
self-limiting
no carrier state
Hep B
blood/sexual contact
most don’t recover entirely -> can lead to cirrhosis or failure or cancer
Diagnosis: HBsAg antigen and antibodies, best indicator is HBV DNA in serum (HBcAg)
Hep C
blood (IV use)
lots of carriers and asymptomatic
AST, ALT, HCV antibody testing
alcoholic liver disease
pts w/ 30 or more grams of ETOH
broken into 3 stages
Fatty liver: accumulation of fat in hepatocytes (steatosis) liver yellow and enlarged
Alcoholic hepatitis: increase in alcohol intake leads to inflammation and necrosis of liver cells. Hepatic tenderness, pain, anorexia, nausea, fever, jaundice, ascites or liver failure can be fatal
Alcoholic cirrhosis: continued drinking leads to fibrotic liver and end stage liver diseases
Non-alcoholic fatty liver disease
liver has fat tissue in the cells in many cases from type II diabetes, metabolic syndrome or hyperlipidemia
asymptomatic, need biopsy.
NASH or nonalcoholic steatohepatitis same idea.
Cirrhosis
Functional liver w/ fibrous tissue and nodules -> vascular disruption and blockages
CM: RUQ tender, jaundice (hyperbilirubinemia), spider angioma, caput medusa, steatorrhea, dark urine, hepatic encephalopathy, **portal HTN, ascites, esophageal varices
Diagnosis: ^ AST and ALT, hypertriglyceridemia, hypercholesterolemia, hyperbilirubinemia, hypoalbuminemia, coag disturbances
US & biopsy
Portal hypertension
Fibrotic liver pushing on the hepatic portal vein.
build up of fluid and this fluid has to go somewhere so it builds up in other veins and out into the peritoneal cavity -> ascites
Collateral veins also develop to take off pressure, but these vessels are weak and easily rupture. -> esophageal varices which are prone to rupture and cause an upper GI bleed
Pancreatitis
Etiology: gallstones (blockage) or ETOH abuse
Digestive enzymes perform autodigestion and damage pancreatic cells -> edema, vascular insufficiency, ischemia
CM: epigastric pain, N/V, Cullen or Grey Turner signs (bleeding)
Diagnosis: ^ amylase & lipase & BGL, leukocytosis, hypocalcemia, abd US, CT
Cholelithiasis
Gallstones
F’s: forty, female, fat, fair, and fertile
lodge in cystic duct and cause backup/pain -> can cause necrosis
