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GI Pathophysiology

Western Path - ONeill

A broad spectrum of processes that induce inflammatory changes in the gastric mucosa that may involve the entire stomach or a region of the stomach Acute Gastritis
What are the two categories of Acute Gastritis? Erosive (w/ superficial, deep, or hemorrhagic erosions) and Nonerosive (generally caused by Heliobacter pylori)
What are some causes of Acute Gastritis? Drugs (NSAIDS, cocaine, iron), ETOH, bacterial infections (H. pylori), viral infections (CMV), acute stress/shock, radiation, allergy, food poisoning, bile reflux, ischemia
A common cause of gastritis and complications can result from a chronic infection rather than from an acute infection H pylori (bacterial acute gastritis)
How does an H pylori mobilize? has flagella that enable it to move and penetrate the mucus layer so that it comes into contact with gastric epithelian cells, producing inflammation by activating a number of toxins and enzymes
an intense inflammation from H Pylori can result in what? Atrophic Gastritis - loss of gastric glands responsible for the production of HCl, Intrinsic Factor, Pepsin, etc
how does h pylori gastritis evolve? starts as an acute gastritis in the antrum, causing asymptomatic inflammation and may extend to involve the entire gastric mucosa resulting chronic gastritis
what is the physical examination findings for acute gastritis? normal to mild epigastric tenderness to palpation
Differential Diagnosis for Acute Gastritis cholecystitis, cholelithiasis (gallstones -> biliary colic), viral gastroenteritis, crohn disease, peptic ulcer disease, gastric cancer, pancreatitis
what is the treatment for acute gastritis usually clears normally, discontinue use of drugs causing gastritis, antacids, h2 blockers to supress basal gastric acid output, PPIs can inhibit acid secretion
how does a practitioner eradicate h pylori PPI (proton pump inhibitor), clarithromycin, amoxicillin or metronidazole
what are the consequences of h pylori chronic gastritis peptic ulcers (associated with antral predominant gastritis) and gastric adenocarcinomas (multifocal atrophic gastritis)
What is a peptic ulcer disease? defects in the gastric or duodenal mucosa that extend through the muscularis mucosa (h pylori - 60% gastric ulcers, 80% duodenal ulcers)
less common cause of peptic ulcer disease in which a gastrinoma tumor of the pancreas which stimulates parietal cells of the stomach to maximal activity, with consequent GI mucosal ulceration Zollinger-Ellison Syndrome
describe the symptoms experiencing a gastric ulcer may be asymptomatic or have vague epigastric pain and nausea, may present with iron-deficiency anemia or acute life-threatening hemorrhage
define important history taking for gastric ulcer disease pain occurring shortly after meals, antacide form minimal relief, epigatric pain or right upper quadrant pain, may have history or hematemesis, melena or episodes of presyncope
gastric ulcer physical examination may or may not have epigastric tenderness, involuntary guarding - peritonitis secondary to gastric perforation, should be checked for melena via DRE
gastric ulcer differential diagnosis crohns disease, duodenal ulcer, gastric cancer, chronic pancreatitis, zollinger-ellison syndrome
gastric ulcer work up labs (cbc and iron studies to detect anemia andh pylori studies), EGD - multiple mucosal biopsies to check for h pylori and rule out malignancies
history of duodenal ulcer sharp, dull or burning epigastric pain that radiates to the back, relieved by food, nightly pain, history of fullness and bloating associated with nausea and emesis after food intake, GI bleeding, melena, tar emesis or hematemesis
what does presence of frank blood in the stool or maroon colored stool suggest? precipitous GI bleeding
physical examination for duodenal ulcer epigastric tenderness, abdominal rigidity, guarding, and rebound tenderness indicating perforation in diffuse peritonitis
how do you treat duodenal ulcer? H pylori eradication, PPI, endoscopic intervention, elective vagotomy
a primary mode of treating bleeding ulcers in which a bipolar cautery or hemoclips with local injection of epinephrine is done endoscopic intervention
resection of the vagus nerve which eliminates the autonomic stimulation of the parietal cell elective vagotomy, though a truncal vagotomy led to gastric atony (flaccidity), but selective vagotomies w/c preserve celiac and hepatic branches of the vagus nerve and decrease gastric atony is chosen
where is the anatomic cut-off for upper GI bleed ligament of Treitz, w/c connects the 4th portion of the duodenum (ascending) to the diaphragm near the splenic flexure of the colon
what is the underlying mechanism of nonvariceal upper GI bleeding? either arterial hemorrhage (peptic ulcer disease or mucosal tears) or low pressure venous hemorrhage (angioectasia and telangiectasias)
non-variceal upper GI bleed causes duodenal ulcer hemorrhage, gastric ulcer hemorrhage, mucosal tears of the esophagus, erosive esophagitis or gastritis, gastric cancer, dieulafoy's lesion
history of upper GI bleed weakness, dizziness, syncope with hematemesis, melena, hematochezia, hx of previous dyspepsia, ulcer disease and NSAID use
physical exam findings for an upper GI bleed acute blood loss >20%, shock (cool extremities, chest pain, presyncope, confusion, delirium), hematemesis, melena, chronic liver disease signs (spider angiomata, gynecomastia, splenomegaly, ascites, pedal edema), hx of alcohol use or hepatitos B/C
UGIB workup Labs (CBC level of blood loss/platelet level, coagulation studies, liver function tests, gastric level, BMP) and Imaging (CXR, ab xray, Ct scan, ultrasonography)
treatment for UGIB emergent therapy (stabilize RBC with IV fluids), endoscopic techniques (heater probe, epi injection), medical therap
bleeding of recent duration that originates beyond the ligament of Treitz and results in instability of vital signs and signs of anemia Lower GI bleed
causes of LGIB diverticulosis, angiodysplasia & arteriovenous malformations, infectious colitis, non-infectious colitis, neoplasm, anorectal etiology (hemorrhoideee, fistula), drug induced (anticoagulant tx), HIV
pocket of tissue bulging out from the colonic walls due to pressure (more common near the end of the left colon and the sigmoid colon) diverticulosis
Diverticulosis and LGIB - most pts with diverticular disease have no sx but some may bleed without concurrent diverticulitis and it does not increase the risk of bleeding
where does a diverticula develop at a small point of weakness where penetrating vessels perforated though colonic circular muscle fibers. These vessels become draped over the dome of the diverticulum and are separated from the bowel lumen by the mucosa.
what leads to erosion of the vessel and bleeding chronic trauma to the luminal aspect of the vasa recta
responsible for 50-90% of the bleeding in diverticulosis and LGIB right sided diverticula - due to wider necks and domes, which expose the vasa raecta to injury over a greater length
risk factors for diverticular bleeding lack of dietary fiber, constipation, advanced age, NSAID /aspirin use
what is angiodysplasia a degenerative dilation of the venules and arteriolar capillaries (when vessel walls become thing, lacking in smooth muscle and dilated)
characteristics of angiodysplasia - asymptomatic, bleeding is self-limited but can be chronic, recurrent, or life-threatening, increases with age, associated with aortic stenosis, von Willebrand disease, and chronic renal failure
What is an AVM defects of the circulatory system comprised of snarled tangles of arteries and veins that arise during emryonic or fetal devt, it can thicken, expand or multiply in time (hemodynamically active)
why is AVM an active, fast-flow vascular malformation? arterial feeders and enlarged draining veins directly connect through micro- and macro-arteriovenouus fistulas that create the epicenter of the AVM
LGIB history first/recurrent, hx of NSAID use, present systemic disease, hx of radiation or coagulopathies
difference b/w infectious/noninfectious colitis and right/left side bleeding in LGIB young pt - fever, dehydration, abdominal cramps, hematochezia - infectious/non-infectious colitis; right side LGIB - melena, left side LGIB - bright red blood by rectum; UGIB or right sided bleed - brisk, massive bright red blood
Diverticular/Angiodysplasia LGIB hx older pts experience painless bleeding and minimal bleeding and sx but diverticular - mild ab cramps from colonic spasms and self limited bleeding, angiodysplasia - hematoccult+ stools, anemia, syncope (d/t bleeding)
clinical presentation of ulcerative colitis bleeding can be minimal but severe ones present with bloody diarrhea w/ pus, abdominal cramps, dehydration, weight loss, fever
clinical presentation of Crohns disease fever, nonbloody diarrhea, abdominal pain but crohns colitis can have bloody diarrhea
clinical presentation of colon cancer right sided bleeding, iron deficiency anemia, right sided - melena, left sided - bright red blood
clinical presentation of ischemic colitis may or may not have abdominal pain, bloody diarrhea, usually happen in older patients with cardiovascular comorbidities, fulminant (sudden/severe), with acute abdominal pain, rectal bleeding, hypotension or insidious with pain and rectal bleeding
physical examination for LGIB pulse & bp taken in supine & upright positions - changes in vital signs indicate blood loss of 20% or >; look for signs of shock, hematemesis, melena, signs of chronic liver disease, hx of alcohol use or hep b/c (incr risk of variceal hemorrhage)
what are some signs of shock cool extremities, oliguria, chest pain, presyncope, confusion, delirium
how does hematemesis and melena important in LGIB PE the more red the stool the more rapid the transit, larger lower tract hemorrhage
what are signs of chronic liver disease spider angiomata, gynecomastia, splenomegaly, ascites, pedal edema, asterixis
LGIB work up colonoscopy, radionuclide scans, angiography
what is hemoglobin (Hb) protein contained in red blood cells responsible for delivery of oxygen to the tissues (male 14-18g/dl; female 12-16 g/dl)
what is hematocrit (Hc) proportion, expressed as a percentage of the volume of blood that consists of RBC (male 40-54%; female 36-48%)
what is a peritoneum (parietal and visceral) thin membrane that lines the abdominal/pelvic cavities & covers most of the intraabdominal organs; parietal - lines the abdominal/pelvic cavities, visceral - covers the external surfaces of most abdominal organs; space b/w these layers - peritoneal cavity
describe the pathophysiology of mesenteric ischemia can be acute/chronic, decreased intestinal blood flow results in ischemia at the cellular level that may progress to devt of mucosal injury, tissue necrosis, metabolic acidosis (usually 2ndary to arterial causes - atherosclerosis, arterities, aneurysms..)
epidemiology of mesenteric ischemia older population >60 but can be seen in younger population too
3 causes of AMI (acute mesenteric ischemia) embolic, arterial thrombosis (acute worsening of ischemia from preexisting atherosclerosis), nonocculive etiologies (intestinal vasoconstriction from systemic shock)
condition where tissues dont receive enough O2 and nutrients to allow cells to function; progression can lead to organ failure and systemic failure shock (cells malfx, waste products build up, increase acidosis, worsening systemic environment)
describe the different etiologies of shock hypovolemic - lack of fluid w/in the body preventing maintenance of blood pressure and cardiac output, hemorrhagic, cardiogenic shock - end stage heart failure, neurogenic shock - sympathetic trunk stop working and blood vessels dilate and blood pools
AMI history severe abdominal pain, visceral and localized pain, acute if embolic disease, often related to meals, nausea, vomiting, diarrhea
what is often the cause of chronic mesenteric ischemia diffuse atherosclerotic disease (usually all 3 mahor mesenteric arteries are occluded)
physical exam findings of chronic mesenteric ischemia signs of malnutrition, disproportionate pain (diffuse mild ab tenderness or no rebound or guarding), abdominal bruits, signs of peripheral vascular disease such as carotid bruits, decreased pulses, poorly perfused extremities
an abnormal twisting of the intestine impairing blood flow to the intestine from a malrotation of the bowel during fetal devt volvulus (can lead to gangrene and death of that segment of the GI tract)
s/s of volvulus sudden onset, abdominal pain, nausea, vomiting, blood in stools
condition in which a body orifice or passage in the body is abnormally close or absent atresia
describe the pathophysiology of a small bowel obstruction SBO leads to proximal dilation ot the intestine d/t accumulation of GI secretions and swallowed air increasing peristalsis (freq loose stools, flatus, vomit), increased intraluminal pressure leading to bowel wall lymphedema, resulting in 3rd spacing
small bowel obstruction Hx simple - abdominal pain (crampy, intermittent), proximal - nausea/vomiting, early - diarrhea, late (strangulation) - constipation, fever, tachycardia, medical hx may expose previous ab or pelvic surgery
SBO physical examination abdominal distension, hyperactive bowel sounds (early), hypoactive (late), gross or occult blood during rectal exam, fever, tachycardia, peritoneal signs
SBO work up BMP (BUN/Creatinine levels increased), CBC (wbc elevated, increased hematocrit), increase in Lactate dehydrogenate, type and crossmatch (for surgery), abdominal xray (dilated small bowel loops w/ air)
what are causes of large bowel obstruction mechanical - flow of intestinal contents, or pseudo-obstruction - dilation of the colon in the absence of an anatomic lesion
what causes a mechanical LBO malignancies (tumor growth), diverticular disease (repetitive inflammation causes fibrosis), colonic volvulus (twisting)
what causes an acute colonic pseudo-obstruction Ogilvie syndrome (ACPO) - loss of peristalsis, accumulation of gas and fluid in colon, from an autonomic imbalance from decreased parasympathetic tone or excessive sympathetic output
LBO hx obstipation (no gas or bm), ab distension, nausea, vomiting, crampy ab pain, abrupt onset (volvulus), change in stool or constipation (diverticulitis/carcinoma), lesion devt
physical examination for LBO abdominal distension, bowel sounds, hyperresonant abdomen, tender abdomen (fever and sever tenderness, ab rigidity - peritonitis), Guaiac+ stools, rectal or sigmoidal mass
DDx for LBO diverticular disease, colorectal carcinoma, cecal volvulus, intussusception, ogilvie syndrome, sigmoid volvulus
describe the pathophysiology of diverticulitis fecal material or undigested stool may accumulate in the diverticulum causing inflammation leading to obstruction and mucus secretion and overgrowth of colonic bacteria
Diverticulitis hx left lower quadrant pain, crampy, associated with change in bowel habits, nausea, vomiting, constipation, diarrhea, flatulence, bloating, right colon (mistaken for appendicitis), transverse (mimic PUD, pancreatitis or cholecystitis)
diverticulitis physical examination localized ab tenderness in area of affected diverticula, LLQ, may have tender palpable mass, distended or tympanic upon percussion, bowel sounds may be absent
Tx for diverticulitis maintain lifelong high-fiber diet, colonoscopy to rule out other dx
Infectitious Enterocolitis Pathophysiology diarrheal illnesses can be classified into (osmotic d/t diminished absorption, inflammatory, secretory, motile)
Gastroenteritis hx diarrhea >month, fever, vomiting, pain
how do you gauge dehydration? diminished skin turgor, acute weight loss, resting hypotension, tachycardia, dry mucus membraines, decreased frequency of urination, changes in mental status, orthostasis, children: absence of tears, poor capillary refill, sunken eyes, depressed fontanels
how do you gauge nutritional status muscle wasting, signs of neural dysfunction
defects occurring in digestion and absorption of food nutrients malabsorption syndrome
malabsorption hx diarrhea, steatorrhea, weight loss and fatigue, flatulence and abdominal distension, edema, anemia, bleeding disorders, metabolic disorders
physical examination for malabsorption orthostatic hypotension, fatigue, weight loss, muscle wasting, loss of subcutaneous fat, distended abdomen, hyperactive bowel sounds, ascites, glossitis, mouth ulcers
malabsorption work up CBC - anemia d/t iron deficiency or b12 malabsorption, prothrombin time increased
chronic disease of the digestive tract that interferes with the digestion and absorption of food nutrients (inability to tolerate gliadin - gluten) celiac disease
pathophysiology of celiac disease mucosa of the intestines is damaged by an immunologicallu mediated inflammatory response to gliadin. there is also an absence of intestinal villi & lengthening of intestinal crypts
epidimiology of celiac disease 8-12 months, 3rd/4th decades, usually diminish in adolescence
celiac disease GI symptoms diarrhea, steatorrhea, flatulence, borborygmus, severe abdominal pain,
celiac disease extraintestinal symptoms weight loss, weakness, fatigue, anemia, osteopenia and osteoporosis, neurological symptoms, skin disorders
celiac physical examination protuberant and tympanic abdomen from fluids and gas, ascites, weight loss, muscle wasting, hypoproteinemia, orthostatic hypotension, peripheral edema, ecchymosis, glossitis, peripheral neuropathy, trousseau sign or chvostek sign
celiac work up IgA confirmation
celiac treatment removal of gluten from diet, corticosteroids
an idiopathic chronic inflammatory disorder in the colon, extending proximally from the anal verge in an uninterrupted pattern to involve part or all of the colon ulcerative colitis
ulcerative colitis pathophysiology anti-neutrophil antibodies, loss of tolerance against enteric flora, genetic susceptibility, smoking, appendectomies, milk consumption
ulcerative colitis hx frequent rectal bleeding w/ or w/o mucus, urgency, tenesmus, abdominal cramps, weight loss, synovitis, ankylosing spondylitis, erythema nodosum, apthous stomatitis, uveitis, primary sclerosing cholangitis, uric acid renal stones
ulcerative colitis physical examination findings mild tenderness in the LLQ, volum depletion, toxicity, fever, tachycardia, abdominal tenderness, weight loss
ulcerative colitis work up anemia, thrombocytosis, elevated sedimentation rate and elevated C-reactive protein, hypoalbuminemia, hypokalemia, hypomagnesemia, elevated alkaline phosphatase
ulcerative colitis therapy anti-inflammatory agents - corticosteroids ot 5-aminosalicylic acid derivatives, TNF inhibitors, immunodilators
an idiopathic, chronic, transmural, inflammatory process of the bowek that leads to fibrosis and obstructive symptoms crohns disease
pathophysiology of crohns disease abdominal pain, diarrhea from genetic, microbial, immunologic, environmental, dietary, vascular, psychosocial factors
crohns disease hx involves the ileocolic region - low grade fever, prolonged diarrhea with ab pain, weight loss, fatigue, RLQ or periumbilical pain relieved by defacation
crohns disease physical examination tachycardia, pale mucosa, abdominal muscle sounds, RLQ tenderness, skin tags, fistulae, abscesses, scarring in the perianal region, uveitis, peripheral arthritis,
CD therapy antidiarrheal agents (loperamide), abdominal cramps relieved by dicyclomine (Bentyl), antiinflammatory (Sulfasalazine), Mesalamine, steroid therapy, immunosuppresants
obstruction of the appendiceal lumen leading to distension of the appendix d/t accumulated intraluminal fluid acute appendicitis (ineffective lymphatic & venous, drainage, allows bacterial invasion of the appendiceal wall and perforation of pus into the peritoneal cavity
appendicitis hx anorexia, periumbilical pain with nausea, RLQ pain, vomiting, rebound tenderness, pain in percussion, rigidity, guarding
mantrels criteria migration of pain to the RLQ=1A, anorexia=1, n/v=1, rebound pain=1, elevated temp=1, shift og wbc to left=1, tenderness in RLQ=2, leukocytosis=2, total=10
Created by: dmgrace
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