PathoPhys Week 1 and 2

ANS innervate GI tract. in general, what impact do sympathetics and parasympathetics have on GI motility?

parasympathetics- stimulate GI motility
sympathetics- inhibit GI motility

The enteric nervous system is located in the gut. what are the 2 functional components and where are they located?

Submucosal/Meissner plexus- located between musculares mucosa and circular muscle in the submucosa
Myenteric/Auerbach plexus- located between circular and longitudinal muscle

what are the pacemaker cells of GI tract that lead to peristalsis via the generation of slow waves?

Interstitial cells of Cajal

enteric motor neurons can be influenced by neurocrines such as VIP, NO, Ach, Substance P. which are excitatory and which are inhibitory toward gastric motility?

Ach/Substance P = excitatory
VIP/NO = inhibitory

Esophagus = conduit for solids and liquids to the stomach. the UES = striated muscle, body = mix, LES = smooth muscle. what controls LES relaxation?

vago-vagal reflex via enteric nervous system and NO

what is primary peristalsis in the esophagus? what about secondary persitalsis?

1- peristaltic wave associated with swallowing
2- unnoticed clearing of residual food in esophagus

in response to peristalsis in the esophagus, the fundus undergoes receptive relaxation. where are liquids vs. solids handled?

liquids- upper
solids- lower near antrum where pulverized

the small intestine is primarily important for absorption of nutrients. what is the motor pattern in the small intestine during fasting state?

MMC extending from stomach (every 90 min)
has four phases- sweeping function

what is achalasia? what is cause?

when LES fails to relax on swallow
lose post ganglionic inhibitory neurons (NO) in myenteric plexus of esophagus

what is the pathology of achalasia?

lymphocyte infiltrate in myenteric plexus/loss of ganglion cells

what are the manometry findings of achalasia?

high LES resting pressure and poor peristalsis in body of esophagus

what are symptoms of achalasia?

dysphagia solid and liquids, malnourishment/weight loss, heartburn/chest pain, regurgitation
(failure of LES to relax due to loss of post ganglionic inhibitory neurons containing NO in myenteric plexus)

endoscopy is performed in pts who present with symptoms of achalasia. what will it show?

dilated esophagus with food
LES = tight

barium swallow can be used as a primary screening test for achalasia. what will it show?

dilated esophagus with bird beak appearance of distal stenosis

what is another name for severe dilation of esophagus that can be seen in achalasia?

sigmoid esophagus

how is achalasia defined diagnostically?

aperistalsis and abnormal LES relaxation with an integrated relaxation pressure >15mmHg

achalasia can be defined by aperistalsis and abnormal LES relaxation with an integrated relaxation pressure >15mmHg. there are 3 classifications of achalasia. what determines them?

manometry (pressure test)

what is tx for achalasia?

1. endoscopic- balloon dilation, POEM, botox
2. sx (hellers myotomy)
3. medical- Ca2+ channel blocker/nitrates

what is a major complication of untreated achalasia?

malignancy- increased risk of squamous cell esophageal carcinoma

what are causes of secondary achalasia aka pseudoachalasia? (3)

1. Chagas disease from T cruzi infection
2. gastric carcinoma/malignancy
3. sarcoidosis/amyloidosis

GERD is the MC esophageal disorder, characterized by excessive reflux of gastric juice into the esophagus. what are reflux symptoms?

heartburn, regurgitation, dysphagia, chest pain, water brash (salivation)

what is definition of heartburn?

burning retrosternal discomfort worse after eating, exercise, or lying down

what are the esophageal defense mxns? (4)

1. competent gastroesophageal junction
2. effective esophageal emptying of refluxed material
3. neutralization of gastric acid via salivary bicarb
4. intact mucosa

what are the 2 broad categories of GERD esophageal syndromes?

1. non erosive reflux disease
2. erosive esophagitis

can you dx and tx GERD in the setting of typical symptoms of heartburn and regurgitation?

yes- tx empirically with PPI

what is the clinical standard for determining the extent of esophagitis and excluding other causes of patient's acid reflux symptoms?

upper endoscopy (90-95% specific)
however note that not a sensitive test bc a lot of patients DO NOT have any endoscopic findings

LA grading can be used to determine extent of erosive esophagitis in setting of GERD. what are the different grades ?

A/B = mild
C/D = severe

what life style modifications is recommended for patients with GERD?

1. losing weight in patients who ARE overweight or have recent weight gain (moderate)
2. head of bed elevation and avoid meals 2-3 hrs before bed in patients with nocturnal GERD (low evidence)

is routine global elimination of food that can trigger reflux (chocolate, caffeine, alcohol, spicy food) recommended in tx of GERD?


what is medication used to tx GERD? when and how should it be taken?

PPI- regular, once a day basis before food

who should be referred to Gastroenterologist with GERD?

1. atypical symptoms
2. alarm symptoms (vomit, weight loss, fam hx cancer, anemia)
3. unresponsive symptoms
4. typical symptoms but no endoscopy

what is complication of erosive esophagitis?

intestinal metaplasia = Barrett's esophagus = pre malignant for esophageal adenocarcinoma

if patient presents with typical symptoms of GERD (heartburn/regurgitation) do you need endoscopy to begin tx?

no- start PPI in primary care setting

what should be on differential when a patient presents with heartburn, dysphagia, chest discomfort?

GERD/ eosinophilic esophagitis

What is eosiniophilic esophagitis? Who is it MC seen in? What are features endoscopically and clinically?

immune mediated esophageal disease characterized by eosinophilic inflammation in pts with genetic predisposition/atopy
young, M>F
atypical heartburn, chest discomfort, hx of food impaction/dysphagia not responsive to PPI completely
endoscopy- ringed appea

what is Barretts esophagus? what is demographic for Barretts esophagus?

intestinal metaplasia of distal esophagus in response to GERD
male, white, obese pt

what is classic endoscopic finding for Barrett's esophagus?

salmon pink mucosa in distal esophagus

gastric emptying is controlled by PSM, SYM, ICC, and regulated by the physical and chemical composition of food. describe the difference between solids/liquids and different food content.

liquids- empty fast (first order kinetics)
solids- 2 phases- lag (trituration where particles = broken up) and linear
high calorie content, acids, and deviation from iso-osmolar delay emptying

where is the pacemaker region of stomach?

not a distinct anatomical entity
on greater curve of stomach (accumulation of ICC)

relaxation of proximal stomach and accommodation of meal volume are controlled by?

vagal mediated relaxation

what is gastroparesis? who is it most common in? what are clinical symptoms?

delayed gastric emptying in the absence of mechanical gastric outlet obstruction
F>M, ~35 yo
N, V, abdominal pain, bloating, early satiety, bezoars = large accumulation of food stuck in stomach

gastroparesis = delayed gastric emptying in the absence of mechanical gastric outlet obstruction. what are causes?

MC- idiopathic, DM, post sx
other- post inf., autoimmune, neurologic dx

what is required to dx gastroparesis? what is the most valid measurement of this test?

gastric emptying test
give radiolabeled eggs, determine extent of meal in stomach 1, 2, and 4 hours later
most valid measurement = % retention solids after 4 hours (>10% = definite, >5% = probable)
(make sure off all meds that have influence on gastric em

is all delayed gastric emptying due to gastroparesis?

no- eating disorders, rumination syndrome can lead to delayed gastric emptying

diabetic gastroparesis is seen in DM 1 and 2, usually 5+ yrs after diabetic state. what is it the result of?

autonomic neuropathy and loss of ICS + hyperglycemia

what cause of gastroparesis = good prognosis with most improving in 1 year?

post inf- can be bacterial, viral, protozoal
(may be after certain vaccinations- tetanus, HPV, Hep B, anthrax)

what is tx of gastroparesis?

1. DM- control DM
2. lifestyle- consume small, frequent meals, low fat, avoid fruits and veggies (fiber), soft particle (mashed up)
3. prokinetic agents = metoclopramide, erythromycin

what is the only medication available for gastroparesis? what is its MOA? what are ADE?

central and peripheral D2 antagonist, 5HT3 antagonist, 5HT4 agonist
ADE- hyperprolactinemia, acute CNS effets, chronic dyskinesia

what drug = motilin agonist that promotes MMC and can be used for acute episodes of gastroparesis (not long term bc tolerance)?


gastric electrical stimulation can be used in patients with refractory N/V with gastroparesis. what patients may see improvement in symptoms and gastric emptying?

diabetic GP

what is difference between ulcer and erosion? can width/lesion size indicate difference?

ulcer has more depth
erosion does not penetrate muscularis mucosa while ulcer does
width cannot discriminate

what are causes of peptic ulcers?

1. H. pylori (single MCC, 60-70%)
2. NSAID/aspirin use
3. acid hypersecretion

when are most H pylori infections acquired?


most H pylori infections are acquired in childhood. chronic gastritis develops in almost all individuals, but the majority will not be symptomatic.
what is difference in disease course for patients with higher acid output vs. lower acid output?

higher acid- antral gastritis, duodenal ulcers
lower acid- gastritis in body of stomach, gastric ulcer, gastric carcinoma

can H pylori infection lead to peptic ulcer and gastric cancer in the same person?

NO- it can lead to a peptic ulcer OR gastric cancer but never both in same person

H pylori can cause peptic ulcers. what type is most common? what are consequences on cellular level?

duodenal ulcer > gastric ulcer
antral gastritis --> hypergastrinemia --> increased parietal cell mass --> increase acid secretion --> duodenal gastric metaplasia

how do NSAIDs and aspirin cause peptic ulcer disease?

alter mucosal defense against acid
by blocking prostaglandin facilitated bicarb/mucus/ blood flow protection

what is clinical presentation of peptic ulcer disease?

chronic intermittent (not daily) epigastric pain helped with food, antacids
(can't distinguish gastric from duodenal ulcer)

how is peptic ulcer disease dx?

endoscopy- rules out other causes and can distinguish gastric vs duodenal ulcer

if a ulcer is seen on endoscopy, should the ulcer be biopsied what about gastric mucosa? why?

always biopsy the gastric mucosa if gastric or duodenal ulcer present to check H pylori infection

how do you distinguish PUD from functional dyspepsia?

both present with epigastric pain but PUD pain = intermittent, long pain free spells while functional dyspepsia = pain every day
PUD = pain gets better with eating
FD = pain worse with eating
PUD- pain at night, antacids helpful
FD- bloating, fullness, na

what is the prevalence of H pylori in US vs outside?

higher prevalence in pts born outside US (remember it is acquired in childhood so where grew up = important )

what if a serologic test comes back + for H pylori? do you need endoscopy and biopsy?

only means patient was at some point infected (IgG based test)
yes- still need endoscopy and biopsy

if a patient takes a full course of abx for H pylori PUD do they need a post tx endoscopy to confirm eradication of H pylori? can we assume the patient has been successfully cured? can serology be used to determine if pt is cured?

can't assume pts have been cured bc H pylori = hard infection to eradicate (resistant abx)
every pt needs to be rechecked to see if infection = cured BUT NOT W ENDOSCOPY
recheck with urea breath test
don't use serology bc will always be +

what test is used to check if H pylori PUD has been cured after tx?

urea breath test
(give carbon labeled urea orally and see if labeled CO2 is expired from breath --> if it is, means that urease still present)
it is important that patients are NOT on acid suppressing, bismuth, or abx drugs bc FN possible

can H pylori infections recur and cause PUD?

probability is low- so if cured pt = at average risk for future PUD of any cause

how does PUD present in patients who are elderly/on NSAIDs?


how do gastric ulcers typically present on endoscopy? when and when shouldn't they be biopsied?

large, well circumscribed, symmetrical
should always be biopsied to check for gastric carcinoma
and H pylori infection
if patient had gastric bleeding (black tarry stool/anemia) should wait to biopsy the ulcer

in pts with hx of PUD caused by NSAID/aspirin, should these medications be avoided?

NO- if stable and tx with PPI, reintroduce low dose aspirin and switch to COX2 inhibitor celecoxib bc require it for other medical conditions
also keep on PPI

what is the mxn of NSAID/Aspirin mucosal injury? what COX is responsible for producing protective PGs?

inhibition of protective prostaglandins (reduce blood flow, mucin, bicarbonate)
others- microvascular injury bc reduced NO
COX1 = important, want to block COX2

if a patient has been tx with PPI for NSAID/aspirin related PUD do they need a post tx endoscopy to confirm ulcer healing? do they need to stay on PPI?

yes need a post tx endoscopy to confirm ulcer has healed and check for gastric cancer
need to stay on PPI for a long time/at least as long as still taking aspirin/NSAIDs

what are the protective mxns that prevent against premature activation of pancreatic enzymes? (4)

1. enzymes = synthesized as inactivate pro-enzymes
2. enzymes = in protective membranes
3. trypsin inhibitors present in cell
4. separate pathways for protease activation

what are the 3 main ways that secretion of pancreatic enzymes from acinar cells is stimulated?

1. secretin- cAMP- PKA- exocytosis of granules
2. vagus nerve- Ach- increase intracellular Ca2+- exocytosis of granules
3. CCK- PLC- IP3- increase intracellular Ca2+- exocytosis of granules

what is the earliest event in the pathogenesis of acute pancreatitis?

conversion of pancreatic zymogens to active forms in the acinar cells

In general acute pancreatitis = Inflammatory response secondary to premature and exaggerated activation of digestive enzymes within pancreas itself via localization of zymogens and granules, thought to be initiated by Ca2+.
describe the pathogenesis of ac

alcohol- sensitization to CCK- CCK induced premature activation of zymogens
coxsackie- oxidative stress, increased production of matrix proteins
biliary obstruction- blockage of secretion
hereditary pancreatitis- early activation of trypsin/pancreatic enz

how do pancreatic proteases cause inflammatory response in pancreatitis?

proteases activate complement
C3a and C5a recruit PMNs and macrophages
release of cytokines --> inflammation and vascular injury

what are the local effects of pancreatitis? systemic effects?

local- autodigestion of pancreas --> edema, fat necrosis, hemorrhage
systemic- circulating TNF a can lead to fever, malaise, confusion, kallikrein activation- hypotension, thrombin activation- DIC, phospholipase A2 activation- hypoxemia

what are the proteases that circulate and inactivate pancreatic enzymes to contain the response of pancreatitis?

1. a1 antitrypsin - inactivate proteases
2. a macroglobulin - inactive trypsin

a1 antitrypsin and a macroglobulin = circulating proteases that inactivate pancreatic enzymes to contain the response of pancreatitis?
if there is failure in containment- severe pancreatitis ensues.
what are the inflammatory, vascular, respiratory, and me

inflammatory- TNF a- fever, malaise, confusion
vascular- thrombin- DIC, hemorrhage; kallikrein- hypotension
respiratory- phospholipase A2- hypoxemia
metabolic- hypocalcemia- fat saponification

what are the main causes of acute pancreatitis? what are symptoms? what is management?

gallstones; alcohol = main
autoimmune IgG4 mediated
abdominal pain that radiates to back/worse when supine, N, V
aggressive IV fluid!!!!, pain meds, remove stones

what is cause of hereditary pancreatitis?

AD- trypsinogen mutation in degradation site that prevents inactivation
mutation of serine protease 1 = MC

CF can lead to pancreatitis. describe how?

decrease in pancreatic bicarbonate secretion by ductal cell--> thick acidic secretions can lead to duct obstruction
(multiple mutations in CFTR = req)

what is diagnostic criteria for acute pancreatitis?

need 2/3
1. clinical- abdominal pain, N/V
2. labs- elevated amylase/ lipase (3x normal)
3. CT- pancreatic inflammation/extent of necrosis

gallstone as cause of acute pancreatitis is most commonly seen in what pt demographic?

F, >50yo

what is tx of pancreatitis? when are abx indicated?

AGGRESSIVE IV FLUIDS- prevents ischemia of other tissues and decrease hypoxemia/hypotension
relief of pain
abx- if biliary pancreatitis

what is the pathophysiology of chronic pancreatitis?

recurrent injury with tissue destruction and fibrosis

chronic pancreatitis is caused by recurrent injury with tissue destruction and fibrosis due to alcohol use most commonly. Other causes = CF, hereditary, and autoimmune IgG4. what are the symptoms

abdominal pain, steatorrhea, DM

describe the pathophysiology of chronic pancreatitis

chronic alcohol ingestion or genetic defects --> abnormal secretion--> protein plug/ductal obstruction --> pancreatitis and injury --> cell death and stellate cell activation --> fibrosis and malabsorption/diabetes

what is the most important enzyme that needs to be replaced in chronic pancreatitis?

lipase --> fat malabsorption and steatorrhea

why does severe chronic pancreatitis (80% of gland destroyed) lead to DM?

loss of insulin and glucagon (endocrine pancreas) due to tissue damage and fibrosis

CF is a AR genetic disorder of defective chloride and bicarbonate secretion. when does it present? what are common symptoms?

pediatric patient
lung infections, pancreatitis, hypertonic sweat, meconium ileus, infertility

why does CF lead to infertility in Males?

congenital bilateral absence of vas deferens

how is CF dx? treated ?

sweat chloride test, pulmonary function test, genetic test
tx- replace pancreatic enzymes, abx for pseudomonas infections, possible genetic transfer

vast majority of pancreatic cancer = adenocarcinoma of ductal origin. how do they present? (4) what is prognosis?

present with abdominal pain radiating to back, weight loss due to malabsorption, jaundice due to obstruction, migratory thrombophlebitis = Trousseau sign
poor prognosis bc very aggressive and metastasis = common at time dx

what are risk factors for pancreatic adenocarcinoma?

1. smoking and tobacco use
2. chronic pancreatitis (alcohol use) or hereditary pancreatitis
3. fam hx

vast majority of pancreatic cancer = adenocarcinoma of ductal origin. what serum marker is elevated?


what will CT of pancreatic adenocarcinoma show?

hypodense mass (usually in head)

how are pancreatic adenocarcinomas tx?

chemo and radiation are limited in effect- most have metastatic disease
sx- whipple procedure = pancreaticoduodenectomy for head lesion; distal pancreatectomy for tail lesion

gastrointestinal motility in colon = regulated by enteric nervous system modulated by parasympathetic vagal and sacral nerves and sympathetic lumbar nerves. what is the function of the large intestine?

1. mix contents/reabsorption of water and electrolytes (segmentation)
2. storage until evacuation is convenient (compliance)
3. mass movement- (peristalsis)

neurohumormal influences can affect gastric motility. what affect does CCK have on segmental contractions in intestine? what about serotonin?

CCK- increases freq/amplitude segmental contractions
serotonin- intestinal peristalsis, secretion, and pain perception

when does colonic motility peak in 24 hr period?

in the day
"sleeps when you sleep

what affect does food intake (especial calorie/fat) have on colonic motility?

stimulant of colonic motility

what are risk factors for constipation?

-African American
-Sedentary lifestyle
- Advanced age
- low education/SES

is having fewer than 3 defecations per week = dx of constipation?

need at least 2 criteria
straining, lumpy/hard stool, sensation of incomplete evacuation/obstruction, use of manual maneuvers to evacuate

T or F: the majority of constipated person have <3 bowel movements/week


what are primary causes of constipation? what is MCC constipation?

drugs- analgesic, opiate, anticholinergic, cation supplement

what is MCC constipation in pediatrics? how can it present?

functional (95%)- meaning that there is no known anatomic/physiologic cause and due to functional retention (learned behavior fear of painful bowel movement)
can present as involuntary fecal leakage (encopresis)

alarm symptoms of constipation include hematochezia, anemia, weight loss, fam hx colon cancer or IBD, acute onset.
what should next steps be?

rule out electrolyte/thyroid problems
colonoscopy or barium edema
anorectal manometry

what is the approach to patient with chronic constipation without alarm signs or symptoms?

empiric tx- educate to increase fluid/fiber; give laxatives and dietary fiber

what are the different agents that can be used to tx constipation? (3 categories)

bulk agents- psyllium, methylcellulose that = soluble and draw water into lumen
osmotic agents that are not soluble- magnesium salt, polyethylene glycol, lactulose
stimulants- senna that stimulate enteric nerves to contract

is chronic use of laxatives harmful?


colonic transit studies can be used to evaluate intractable (hard to tx) constipation. In these studies, a patient swallows capsule filled with radio-opaque markers and passage through colon is monitored via radiographs on day 5.
what is considered normal

normal- 80% passed day 5 (5 or fewer left)
colonic inertia- delayed passage of markers in proximal colon (see capsules throughout colon)
outlet delay- markers are stagnate in rectum (see markers in rectum)

what is tx of intractable (hard to tx) constipation?

1. behavioral approach to relax muscles
2. sx colectomy only if unresponsive to medical tx, colonic inertia pattern, no intestinal dysmotility

who is at risk for developing a megarectum/megacolon?

children- retentive soiling
institutionalized elderly
psychiatric disorders (schizophrenia)
neurologic disorders (parkinson)

who is at risk for developing a toxic megacolon?

C dif patients
inflammatory bowel disease (crohn/ulcerative colitis)

What is Hirschsprung's disease?

congenital megacolon characterized by lack of ganglion cells and enteric nerve plexuses in distal segment of colon leading to functional obstruction and proximal dilation
(constipation since birth)

in Hirschsprung dx there is lack of ganglion cells and enteric nerve plexuses in distal segment of colon leading to functional obstruction and proximal dilation. the internal anal sphincter is inhibited. what is rectal distention?

absent- rectum = collapsed

what is gold standard for dx Hirschsprung?

rectal biopsy- no myenteric neurons

what is tx of Hirschsprung?

resect aganglionic segment of bowel and anastomose normal ganglionic bowel to anas

What is dyssynergic defecation?

ineffective defecation due to failure of EAS/puborectalis muscle to relax

dyssynergic defecation = ineffective defecation due to failure of EAS/puborectalis muscle to relax. how is dx made?

1. anorectal manometry
2. defecography
3. inability to expel water filled balloon from rectum in 1 min

what is clinical definition of diarrhea? physiologic?

increase in frequency, urgency, or volume of defecation (can have changes in consistency)
>200 gm stool output per day

where does the majority of fluid input to GI come from?


where does the majority of fluid absorption by gut take place? what region of gut is most efficient at absorbing fluid?

majority of fluid absorption occur in small intestine
but large intestine = most efficient at absorbing fluid

what drives normal fluid absorption in GI tract?
specifically in small intestine and large intestine

small intestine- villi- Na+ solute transporters and Na+ H+ exchange
large intestine- crypts- enac channels

the pathophysiology of diarrhea involves increased intraluminal fluid and more rapid transit through GI tract. what are the 3 main causes of increased intraluminal fluid?

1. decreased absorption of fluid (ingest unabsorbable solute)
2. increased secretion (active secretion of electrolytes into lumen)
3 inflammation leading to compromise of epithelial barrier

the pathophysiology of diarrhea involves increased intraluminal fluid and more rapid transit through GI tract.
increased intraluminal volume can be due to ingestion of insoluble solute (osmotic), secretion of electrolytes (secretory), or compromise of epi

can tell difference between osmotic and inflammatory from secretory bc secretory has large amount of fluid

what is MCC of osmotic diarrhea?

non absorbable carbs (lactose)

what is physiology behind secretory diarrhea?

increased Cl- secretion into gut via secondary messengers
(cAMP and Ca2+)

what are the 3 categories of secretory diarrhea mediators?

1. bacterial enterotoxins (E coli and cholera)
2. neurohumoral agent (VIP, Ach, serotonin)
3. immune mediators (histamine, PGs)

how can you tell difference between osmotic and secretory diarrhea on basis of:
1. volume
2. fasting
3. flatulence
4. pH
5. osmolar gap

osmotic- low volume
secretory- high volume, watery
osmotic- resolves
secretory- doesn't resolve
osmotic- present
secretory- not present
osmotic-pH <5
secretory- 6-7
osmolar gap
osmotic- >125
secretory- <50

acute diarrhea = <3 weeks. what is the etiology/pathophysiology?

secretory/inflammatory diarrhea that is self limited and tx = supportive

what is MCC infectious diarrhea?

viral both in US and developing country

What is the MCC of traveler's diarrhea?

Enterotoxigenic E. coli

what are risk factors for Clostridium difficile colitis? what causes colitis? what will endoscopy show?

abx use
extreme of age
cytotoxin A and B
pseudomembranes on endoscopy

the dx of c difficile colitis can be made with the endoscopy showing pseudomembranes and stool assay + for toxin A.
what is tx?

if on abx tx STOP
give metronidazole, vancomycin, and cholestyramine (binds to toxins)

chronic diarrhea is diarrhea >3weeks. it can be characterized by mucosal injury or no mucosal injury.
what are causes of no mucosal injury?

due to osmotic/secretory cause
maldigestion- lactose intolerance, pancreatic insufficiency, hx of resection sx, bacterial overgrowth
hypermotility- IBS, diabetic neuropathy, hyperthyroidism, alcoholism
malignancy/factitious- VIPoma, carcinoma, laxative ab

Irritable bowel syndrome is a disorder of motility and pain perception. how does it present?

symptoms related to bowel movements- abdominal pain and bloating
cause of constipation/chronic diarrhea WITHOUT red flag symptoms of anemia, bleeding, weight loss, malnutrition

chronic diarrhea is diarrhea >3weeks. it can be characterized by mucosal injury or no mucosal injury.
what are causes of mucosal injury?

chronic infections- HIV, tropical sprue, whipple dx, parasites
allergic/immune mediated- celiac sprue, crohn's, ulcerative colitis, microscopic colitis
malignancy- colon cancer and lymphoma

the initial approach to patients with chronic diarrhea = assess for unintentional weight loss, nocturnal diarrhea, malnutrition, and rectal bleeding.
how would irritable bowel disease, HTH, infection, malabsorption, and malignancy present?

IBD- bleeding, pain, weight loss
HTH- weight loss
Infection- bleeding, cramps
Malabsorption- weight loss, anemia
Malignancy- weight loss, bleeding