Lower GI- PART III WK 7 Flashcards
definition of Acute Intestinal Peforation
EMERGENCY
Any part of GI tract can perforate, spilling gastric and intestinal contents into abd cacity
Causes of Acute Intestinal Peforation
Common causes: blunt or penetrating trauma, foreign bodies
Causes in SI: duodenal ulcer, corrosives, strangulation of bowel, acute appendicitis
Causes in colon: obstruction, diverticulitis, IBD, toxic megacolon
SSX of Acute Intestinal Peforation
sudden and catastrophic: severe generalized abd pain, tenderness, signs of shock, N/V, anorexia
In pts with underlying GI disorder, looks like “worsening” (more gradual and localized pain)
PE of Acute Intestinal Peforation
bowel sounds- quiet to absent
peritoneal signs - guarding and rigidity
work up for acute intestinal perforation
free air seen (usu in SI) on abdominal xray or abdominal CT
Gastroenteritits
Inflammation of lining of stomach, SI, and colon (from infections most commonly)
typically self-limiting, but can be serious in young, elderly, immunocompromised
Hx: ask re ingestion of potentially contaminated food or water, travel, contact with similarly ill person, medication use (recent antibiotic use)
Normal Intestinal Microflora
The typical GI tract is inhabited by 500 different bacterial species
Stomach and proximal small bowel: few bacteria because of acidity
Jejunum: lactobacilli, enterococci, gram pos aerobes, facultative anaerobes
Terminal ileum: enterobacteria, coliforms
Colon: anaerobes- bacteriodes, lactobacillus, clostridium, bifidobacterium
General SSX of Gastroenteritis
varies. sudden onset of N/V, anorexia, abdominal cramps and diarrhea
may be malaise and myalgia
PE & work-up for Gastroenteritis
PE: Distended abdomen, tenderness, borborymi
Work up: hemoccult, fecal WBCs, O&P, culture -> stool test
Rapid enzyme assays: viral antigens, Shiga toxin, CBC, CMP
factoids about Viral Gastroenteritis
comprises 30-40% of infectious diarrhea in US
viruses infect enterocytes in SI villi leading to transudate of fluid/salt into lumen, causes watery diarrhea, stools rarely contain blood or mucus
causes of Viral Gastroenteritis
Rotovirus Norovirus Astrovirus Enteric Adenovirus CMV and Enterovirus (in immunocompromised)
Rotovirus
most common cause of infectious diarrhea worldwide
highly contagious: fecal-oral route
prevalence throughout yr; peak incidence occurs in winter months
severe, dehydrating diarrhea in kids (can be deadly, peak incidence 3-15 mo), mild in adults
SSX: vomiting, fever >102, sx can last 5-7 days
Norovirus
older children and adults, year -round incidence
can be epidemic with water and food-borne outbreaks, highly contagious
SSX: acute onset vomiting, abdominal cramps, diarrhea, fever, HA, lasts 1-2 days
Astrovirus
infants and young kids, winter months, fecal-oral route
SSX: similar to rotavirus
Enteric Adenovirus
kids <2yo affected, year-round/summer, fecal-oral route
SSX: diarrhea followed by mild vomiting. Diarrhea lasts 1-2 weeks
CMV and enterovirus
can cause gastroenteritis in immunocompromised
causes of Bacterial gastroenteritis
Exotoxin Enterotoxin Parasitic infections Fungal overgrowth Drug and Chemical-related gastroenteritis
Exotoxin
toxin secreted by microorganism and released into the environment then pre-formed toxin ingested in contaminated food
causing nausea, vomiting, watery diarrhea within 12 hrs of ingestion
minimal systemic sx (except botulinum)
sx abate within 36 hrs
stools have NO blood or WBCs
Types of Exotoxin
Staphylococcus aureus
Bacillus cereus
Clostridium perfingens
Clostridium botulinum
Staphylococcus aureus (an Exotoxin, a cause of bact gastroenteritis)
Staphylococcus aureus- most common food poisoning, toxin introduced by food-handlers
common foods involved: custard, milk products, potato sald, coleslaw, processed meat/fish at room temp
SSX: sudden, abrupts, severe vomiting 2-6 hr after ingesting, explosive diarrhea, abd cramps, rarely fever
course: last 3-6 hrs, usu complete recovery
Bacillus cereus (an Exotoxin, a cause of bact gastroenteritis)
Bacillus cereus- spore-forming organism found in soil
contamination of food before cooking which survive high heat
common foods: contaminated rice or meat
SSX: 2 distinct syndromes: emesis- 2-6 hrs after ingestion severe vomiting, abd pain with or without diarrhea, no fever no systemic sxs OR diarrhea- h-16 hrs, foul smelling, profuse with nausea, abd pain, tenesmus
course: resolves in 12-24 hrs
Clostridium perfringens (an Exotoxin, a cause of bact gastroenteritis)
Clostridium perfringens - spore forming anaerobe widely distributed in feces, soil, air, water
most toxin synthesized before ingestion, additional produced in GI after ingestion of contaminated beef, beef products, poultry
food inadequately pre-cooked and then reheated before served
SSX- watery diarrhea, foul smelling with severe, crampy abd pain, 8-26 hr after ingestion
course: self-limited, resolves in 24-36 hrs
Clostridium botulinum (an Exotoxin, a cause of bact gastroenteritis)
Clostridium botulinum- (3 exotoxin types- A, B, E)
responsible for 1/3 of deaths from food borne dz
types A, B associated with improperly prepared home-canned non-acidic fruits & veg - string beans, corn, mushroom, spinach, olives, beets, asparagus
Type E assoc with smoked freshwater fish
boiling in water for 15 min can inactivate exotoxin
SSx- incubation 4 hr - 8 days after ingestin
phase 1- vague- short period of fatigue, N/V, abd cramps, darrhea
phase 2- visual- diplopia, decreased acuity, PERRLA, ptosis
phase 3- neurological- descending weakness or paralysis, dysarthria, dysphagia, weakness of trunk and extremities, sensorium unaffected, normal or low temp
blood, urine, CSF normal
Course: 65% mortality 2-9 days following ingestion
with tx < 10% supportive to prevent respiratory impairment
DDX: polio, encephalitis, M. gravis, curare, belladonna poisoining
Enterotoxin
Cytotoxin produced by bacteria, specific for the mucous membrane of the intestine (in vivo). The toxin impair intestinal absorption, increases secretion of water and electrolytes, causing watery diarrhea
Types of enterotoxin
Cholera and non-cholera vibrio (endemic in Asia)
Enterotoxigenic Escherichia coli
Clostridium difficile “C diff”
Cholera and non-cholera vibrio (an enterotoxin, a cause of bact gastroenteritis)
any fecal contaminated water or food may cause
in US from contaminated saltwater crabs and freshwater shrimp, incubation 1-3 days after ingestion
SSX: sudden, painless, profuse, large volume, water diarrhea, no blood or mucus
usu no fever, abd pain, vomiting, tenesmus
water and electrolyte loss leads to thirst, oliguria, muscle cramps, weakness, cold, cyanotic skin, dehydration, hypotension, tachycardia
course: recovery in 7-10 days if rehydration is adequate
fatal in over 50% of untreated severe cases
Enterotoxigenic E. coli (an enterotoxin, a cause of bact gastroenteritis)
diarrhea caused by tissue invasion or via its enterotoxin
fecal/oral route of contaminated water or food, traveler’s pathogen
incubation: 1-3 days
SSX: profuse, watery diarrhea, lasts 3-5 days
Clostridium difficile “C diff” (an enterotoxin, a cause of bact gastroenteritis)
overgrowth of intrinsic organisms (post antibiotic) or infection by external source (soil, water, household pets)
cytotoxin and enterotoxin cause pseudomembranous colitis
commonly nosocomial dz
SSX: watery diarrhea, cramping abd pain, N/V are rare
Complication: Toxic Megacolon - dilated colon with fever, abdominal pain, tachycardia
PE: tender abdomen, absent bowel sounds
Work-up: elevated WBC, distended bowel seen on xray, Colonoscopy is contraindicated
Risk of perforation, sepsis, septic shock
Other possible causes: UC, Crohn’s, Entamoeba histolytica, Yersinia infx
Mucosal invasion
mucosal invasion by ingested organism- cause microscopic ulceration, bleeding, exudates, secretion of electrolytes and water
Stool has WBCs, RBCs, possibly gross blood
fever and prostration are common
diarrhea may be watery or bloody: watery > 1 liter/day, usu no fever, h/a, myalgia, or arthralgia; bloody usu with abdominal pain, tenesmus, N/V, fever, malaise
Types of mucosal invasion
Salmonella Campylobacter jejuni and fetus Shigella Enterohemorrhagic E. coli Yersinia enterocolitica
Salmonella (a mucosal invasion, a cause of bact gastroenteritis)
ingestion of undercooked chicken or eggs, unpasteurized milk, contact with reptiles
requires large inoculum to produce infection
direct invasion of mucosa cause exudative diarrhea
SSX- watery diarrhea more common, bloody may occur, h/a, malaise, N/V, abd pain 6-48 hr after ingestion, may have fever
course: usu self-limited to 7 days
Campylobacter jejuni and fetus (a mucosal invasion, a cause of bact gastroenteritis)
most common bacterial cause of bloody diarrhea in US
from contaminated pork, lamb, beef, milk products, water, infected pets
incubation period 1-7 days
SSX: may be prodrome of h/a, malaise for 12-24 hrs (resembles flu), then severe abd pain, high fever, profuse watery diarrhea, then bloody diarrhea
course: usu self limited to 7-10 days
Shigella (a mucosal invasion, a cause of bact gastroenteritis)
most common in children 6 mos- 5 yrs
food, water, milk can be contaminated; person to person
highly contagious with very small inoculum
SSX: incubation 1-3 days
in most people starts as lower abdominal pain, diarrhea, fever in 50%, many pt have biphasic illness starting as fever, abd pain, diarrhea; then in 3-5 days rectal burning, tenesmus, small volume bloody diarrhea
course: variable - children- resolves in 1-3 days, adults- resolves in 1-7 days
Enterohemorrhagic E. coli (a mucosal invasion, a cause of bact gastroenteritis)
E. coli 0157:H7 strain, produces the Shiga toxin, bovine reservoir, follows ingestion of undercooked beef or unpasteurized milk, fecal-oral, esp toddlers in diapers (daycare), often affects several ppl, ask if anyone else sick
SSX: acute onset of severe abd cramps, watery diarrhea > 16 hr after ingestion, becoming bloody within 24 hrs
course: lasts 1- 8 days if uncomplicated
5% are complicated by: hemolytic-uremic syndrome (HUS) - hemolytic anemia, thrombocytopenia, acute renal failure
thrombotic thrombocytopenic purpura (TTP) - HUS, fever, neurological deficits
Yersinia enterocolitica (a mucosal invasion, a cause of bact gastroenteritis)
Undercooked pork, unpasteurized milk, contaminated water
SSX: watery or bloody diarrhea and fever. May mimic appendicitis (RLQ pain, fever, vomiting, leukocytosis) if infection in terminal ileum. AKA “acute ileitis”
Note: Traveler’s Diarrhea (Turista)
Gastroenteritis caused by contact with organism endemic to locale visited (contaminated water or food ingestion)
Enterotoxigenic E coli is most common organism, also norovirus
SSX: nausea, vomiting, borborygmi, abd pain/cramps, diarrhea—onset 12-72 hr after ingestion.
Usually self-limiting, fever and bloody diarrhea suggest more serious disease
Cause of parasitic infections
Giardia lamblia
Cryptosporidium parvum
Entamoeba histolytica
Giardia lamblia
fecal-oral from contaminated water, person to person (daycare), traveler’s pathogen, esp. in pt. with low IgA, hypochlorhydria, malnutrition, ingestion of cysts which break down releasing organism
SSX -incubation 7 days, may be asymptomatic, mild watery diarrhea, abd. bloating, cramps, flatulence for 1-3 wk, stools bulky, foul smelling
Course: may be self-limiting or infection may persist and produce chronic or recurrent dz. (may produce a celiac-like lesion causing lactose intolerance and malabsorption) fatigue, wt loss
Cryptosporidium parvum
high rate of infection in HIV, immune-compromised, daycare via contaminated water, food, pets (esp. cats
SSX- a. in non immune compromised pt: profuse, watery diarrhea, anorexia, low-grade fever 5 days after ingestion
Course: usu. self-limited, lasting ~2wks
b. in immune-compromised pt: may be chronic, watery diarrhea of up to 17/day, leads to dehydration
Entamoeba histolytica
endemic, travel associated, fecal-oral spread in institutionalized pt., HIV, AIDs, immune-compromised
cysts ingested, released leading to ulceration similar to IBD
SSX -if mild - crampy, abd. pain, intermittent diarrhea
if severe - bloody diarrhea, abd. pain, tenesmus, fever, toxic megacolon
INFLAMMATORY BOWEL DISEASE (IBD)
A loss of tolerance against indigenous enteric flora is believed to be the central event in the pathogenesis of inflammatory bowel disease (IBD).
May be triggered by:
Increased intestinal permeability or
Imbalanced microflora
Psychological stress exacerbates the conditions
Diseases that fall under IBD
Crohn’s disease
Ulcerative Colitis
Crohn’s disease
Chronic transmural inflammation of the colon involving mesentery as well as regional lymph nodes. May involve the entire GI tract with “skip lesions”
Early mucosal involvement consists of longitudinal and transverse aphthous ulcerations, which are responsible for cobblestone appearance. With progression, deep fissures, sinuses and fistulas develop.
Typical pattern is intermittent exacerbations and periods of remission, worse with stress
Etiology and risk factors for Crohn’s disease
Unknown; genetic, infectious, immunologic and psychological factors possible
smoking
use of oral contraceptives – 2:1 for women who use them
diet: diary, refined sugar, low fiber, high animal fat
dysbiosis, use of antibiotics
removal of inflamed appendix early in life
Epidemiology/incidence of Crohn’s
bimodal distribution: early peak age 15-25 yrs, smaller peak age 55-65 yrs. in patients 40 years.
ethnicity – 2-4X in Jewish population, also higher in Caucasians
inc in higher socioeconomic group, Type A personality
Slight predominance in females
Pathophysiology of Crohn’s
inflammation involves all layers of intestinal wall, which becomes thick patchy distribution with areas of normal bowel (skip areas) (normal tissue and inflamed)
May occur in any part of the GI from mouth to anus
rarely may also affect stomach, duodenum, esophagus
SSx of Crohn’s
Abd. pain, often steady and localized in RLQ, fatigue
Occult blood is common, blood in stool if colonic involvement (< common than UC)
Stool: usu. formed, may be loose if extensive colonic involvement or terminal ileum,
Fat malabsorption (steatorrhea seen) increases risk of gallstones, renal oxalate stones
1/3 of pt. have perianal dz. – fissures, fistulas, perianal abscess
Complications of Crohn’s
Intestinal obstruction is a frequent complication.
In the initial stage, obstruction from edema and inflammation commonly in the ileum are reversible. As disease progresses, fibrosis develops, leading to more constipation and intractable obstruction from fixed luminal narrowing.
Fistula formation is common and can cause indolent abscess, malabsorption, cutaneous fistula, persistent urinary tract infection, or pneumaturia.
Perforation and hemorrhage rare due to thickened mucosa
Increased risk of developing sqamous cell carcinoma
Work-up for Crohn’s
Lab
CBC: mild anemia, leukocytosis
Increased ESR, elevated CRP (higher than in UC)
Low serum iron, low vitamin B12
+ fecal lysozyme
Serology: ASCA (higher in Crohn’s), ANCA (higher in UC)
Imaging
plain radiography, double-contrast barium enema examination
single-contrast upper GI series with small-bowel follow-though barium x-ray shows irregularity, nodularity, stiffness, thickening of terminal ileum, narrowed ileum lumen. In advanced cases, string sign shows marked stricture of the ileum
CT and double-contrast evaluation of the small bowel. Ultrasonography and MRI can be used as adjuncts if radiation exposure is an issue in monitoring disease activity.
Colonoscopy - “skip areas”, “cobblestone appearance”, longitudinal ulcers, rectal sparing, narrowing, fistulas
1/2 of pt. have pathognomonic sarcoid-type epitheloid granulomas in the intestinal wall and occ in the involved mesenteric nodes
DDX for Crohn’s
IBS, lactose intolerance, Infectious colitis, UC, appendicitis, diverticulitis, Carcinoma
Ulcerative Colitis
chronic, recurrent inflammatory disease of the colon or rectal mucosal layer. superficial ulceration of the colon almost always involves rectum (95%) and continuous involvement with any other portion of the colon (NO skip areas)
Ulcerative proctitis–common, limited form of the dz., localized to the rectum
Etiology and Risk Factors assoc with UC
immune-mediated - abnormalities of humoral and cell-mediated immunity and/or generalized enhanced reactivity against intestinal bacterial antigens may cause. autoimmune - serum and mucosal autoantibodies vs intestinal epithelial cells
genetic susceptibility (chromosomes 12 and 16) is a factor. A positive family history (observed in 1 in 6 relatives) is associated with a higher risk for developing the disease.
smoking is negatively associated with ulcerative colitis (reversed in Crohn’s disease).
environmental factors may be involved.
dietary factors – dairy, refined sugar, low fiber, high animal fat
Epidemiology/Incidence of UC
2-4 times higher in Jewish people, also higher in Caucasians
Slight predominance in males
peaks ages 15-25 yrs and 55-65 yrs (can occur in people of any age).
SSX of UC
(severity of disease may range from mild to severe)
Cramping abdominal pain
Series of attacks of bloody diarrhea with asymptomatic intervals
begins insidiously, with increased urgency, lower abd. cramps, blood and mucus
if confined to recto-sigmoid area, stool may be normal, hard or dry with rectal d/c of mucus with RBC’s and WBC’s
if process extends proximally, stools become looser, 10-20/d with severe cramps, rectal tenesmus. Watery stools with pus, blood, mucus.
Systemic sxs: malaise, fever, anemia, wt. loss
Complications of UC
Hemorrhage most common
Toxic megacolon - markedly distended colon (ballooning, over 6 cm) with attenuated walls and IMMEDIATE DANGER OF PERFORATION may occur in severe colitis
(> 40% mortality)
Cells may become dysplastic with inc risk of colon cancer, adenocarcinoma
Work-up for UC
Lab
CBC – anemia, platelet count >350,000/mL
elevated ESR and elevated C-reactive protein
CMP – hypoalbuminemia, hypokalemia, hypomagnesemia, elevated alk phos
Stool analysis for organisms (clostridium, salmonella, shigella, E coli, yersinia)
Imaging
plain abdominal radiograph might show colonic dilatation in severe cases, suggesting toxic megacolon. Also, evidence of perforation, obstruction, or ileus can be observed.
Barium enemas can be performed safely in mild cases. They may show a narrow, tubular, shortened colon with loss of haustral folds, pseudopolyps, and small ulcers; “lead pipe” appearance (Used with caution as barium enemas may precipitate toxic megacolon in severe cases.)
flexible sigmoidoscopy can provide the diagnosis of colitis.
colonoscopy with biopsy confirms Dx. Also, useful for documenting the extent of the disease, for monitoring disease activity, and for surveillance for dysplasia or cancer. Used with caution because of risk of perforation with severe dz
Irritable bowel syndrome (IBS)
Diagnosis of exclusion—often too quickly used as diagnosis
Very common: most common of all GI disorders, up to 50% of pt. to gastroenterologist
Counseling is helpful because of pt. frustration with problem
Etiology of IBS
Etiology (postulated)
1. Changes in gastrointestinal motility (inc luminal contractions, inc motor activity)
2. Hypersensitivity of visceral afferent nerves of the gut
3. Increased mast cell in gut, releasing local histamine
4. Colonic muscle hyper-reactivity and neural and immunologic alterations of the colon and small bowel may persist after gastroenteritis.
5. abnormal glutamate activation of N-methyl-D-aspartate (NMDA) receptors, activation of nitric oxide synthetase, activation of neurokinin receptors, and induction of calcitonin gene-related peptide have been observed.
6. limbic system mediation of emotion and autonomic response enhances bowel motility and reduces gastric motility to a greater degree in patients who are affected than in controls.
7. hypothalamic-pituitary axis may be intimately involved in the origin. Motility disturbances correspond to an increase in hypothalamic corticotropin-releasing factor (CRF) production in response to stress. CRF antagonists eliminate these changes.
8. SIBO* provides a unifying mechanism for the common symptoms of bloating and gaseous distention. >50% of IBS cases have SIBO (see below)
9 Diet: low fiber, intolerance to lactose (diarrhea) and other sugars, (glucose intolerant, milk intolerant (casein) congestion, bronchitis, asthma, mucus; gluten
Red Flags that draw you away from IBS Dx
- symptom onset after age 50
- severe, unrelenting diarrhea
- nocturnal symptoms
- unintentional weight loss
- hematochezia
- family history of organic gastrointestinal diseases such as IBD, celiac sprue, or CA
- the absence of ‘red flags’ and/or any positive screening studies, additional diagnostic testing is not typically necessary.
Rome III criteria (2006) for the diagnosis of IBS
patients must have recurrent abdominal pain or discomfort at least 3 days/month during the previous 3 mos, associated with 2 or more of the following:
- relieved by defecation
- onset associated with a change in stool frequency
- onset associated with a change in stool form or appearance
SSX of IBS
- -crampy abdominal pain
- -constipation, diarrhea, both, or alternating
- -increased colonic mucus production
- flatulence, bloating/distention, nausea, anorexia
- -anxiety or depression
- -sxs related to stress
- -appearance of health
Work-up for IBS
PE
Diffuse abd. tenderness over colon- some areas worse, some areas of fullness
Lab (only to confirm other possible diagnosis)
CBC screen for anemia, inflammation, and infection
CMP - evaluate for metabolic disorders, R/O dehydration/ electrolyte abnormalities in patients with diarrhea
hemoccult test
stool examinations – complete GI health panel - lysozyme test normal
hydrogen breath tests - for lactose intolerance.
celiac testing
Imaging
x-ray may show altered GI motility (spasm)
sigmoidoscopy shows increased mucus & spasm (or often nothing)
IBS can be confidently diagnosed by identifying typical symptoms, performing a complete physical examination and excluding alarm features. The presence of alarm features should prompt a more detailed diagnostic evaluation directed by the patient's predominant symptoms. If, after appropriate tx interventions, the patient reports no significant improvement, follow-up must include more extensive diagnostic evaluation. Celiac disease may be more prevalent in patients with suspected IBS. Patients > 50 with IBS symptoms should undergo colonoscopy for colorectal cancer screening.
Small Intestine Bacterial Overgrowth (SIBO)
Increased number (>105/ml) or type of bacteria in small intestine, leading to fermentation, inflammation and malabsorption. Fermentation gases: hydrogen, methane.
Enteric toxins produced: ammonia, D-lactic acidosis, bacterial endotoxin stimulating cytokine release.
Carbohydrate, protein, fat, B12 malabsorption can all occur.
Organisms: Streptococci, Bacteriodes, Escherichia, Lactobacillus, Clostridium, Klebsiella
Overgrowth usually prevented by:
Antegrade peristalsis, gastric acid, bile, proteolytic enzymes, sIgA, intact ileocecal valve
Causes of overgrowth of SIBO
Anatomical anomalies: stricture, diverticula
Insufficient enzymes: hypochlorhydria, PPI use, low bile salts
Abnormal motility: obstruction, DM, scleroderma, Crohn’s, radiation damage, opiates
Abnormal communication b/w sm and large bowel: fistula, defective valve
Other: immunocompromised, alcoholism, cirrhosis, pancreatitis
History of SIBO
patient may report—
transient improvement in IBS after antibiotic treatment
Worsening of IBS on probiotic/prebiotic treatment
Worsening of IBS when eating more fiber
SSX of SIBO
abdominal pain/cramps, borborygmus, eructation, flatulence, bloating, watery diarrhea may alternate with constipation, dyspepsia, vomiting, heartburn, wt loss, steatorrhea, systemic symptoms (HA, joint pain, fatigue, rosacea)
PE & work-up for SIBO
PE: surgical scar? Abdominal distention, succussion splash
Work-up: CBC may show macroscopic (B12) or microscopic anemia, low ferritin, Glucose Breath Hydrogen analysis (H2)[14C]-d-xylose breath test (Methane)
Diverticular disease includes
Diverticulosis
Diverticulitis
Merckel’s Diverticulum
Diverticulosis
Sac-like outpouchings of colon mucosa and submucosa most commonly in the sigmoid
Due to factors that chronically increase intraluminal pressure: low fiber diet, high refined carbohydrates
SSX of Diverticulosis
usually asymptomatic (up to 70%)
may have recurrent LLQ tenderness, flatulence
may have history of painless rectal bleeding
Diverticulitis
(diverticulosis progresses to diverticulitis in 20%)
inflammation of 1 or more diverticula, potentially leading to obstruction, perforation and to abscess and fistula formation
may heal spontaneously or may enlarge and adhere to adjacent organs (bladder, vagina), fistula may form. Repeated inflammation may lead to obstruction and potentially dangerous perforation
SSX of Diverticulitis
abdominal pain - LLQ, tends to be steady, severe, and deep
fever/chills
previous episodes of dull, colicky, and diffuse abdominal pain accompanied with flatulence, distention, and change in bowel habits (initially diverticulosis)
altered bowel habits including diarrhea, increased
constipation, tenesmus
nausea and vomiting
Rectal bleeding: bright red-colored or wine-colored stools. onset of bleeding typically sudden, painless, and accompanied by an urge to defecate.
amount of bleeding typically massive and tends to stop spontaneously.
Concomitant ssx:
Dysuria, pyuria, and urinary frequency if bladder or ureter are irritated
Complications of Diverticulitis
Complication symptoms if perforation or fistula development
Pneumaturia or recurrent urinary tract infections (colovesicular fistulas)
Feculent vaginal discharge (fistulas with the uterus or vagina)
Severe and generalized abdominal pain, absent bowel sounds, fever (diffuse peritonitis)
Back or lower extremity pain (perforation)
PE for diverticulitis
Localized abdominal tenderness, rebound tenderness, may palpate mass
Assess vital signs to determine hemodynamic stability
Low-grade fever
Digital rectal examination identifies tenderness, establishes the color of stools, and determines the presence and extent of GI bleeding.
Proctoscopic exam may reveal a mass in the cul-de-sac.
DDX for diverticulitis
hemorrhoids or/ anal fissures (pain with defecation); UTI, nephrolithiasis, obstruction, colon cancer
history of weight loss and mucus in the stools indicates IBD
Imaging for diverticulitis
sigmoidoscopy shows narrowing and inflammation barium x-ray is hazardous in acute phase, may cause a perforation
Meckel’s diverticulum
Congenital bulge in distal ileum, remnant of the vitalline duct
2% of population, more common in males
Most are asymptomatic. Can produce bleeding, obstruction, volvulus, intussusception
Acute presentation may look like appendicitis
Malabsorption syndromes
Insufficient digestive elements
Carbohydrate intolerance/lactose intolerance
Tropical Sprue
Celiac disease
Malabsorption syndromes
General SSX of malabsorption: Chronic diarrhea, steatorrhea, abdominal bloating, weight loss, amenorrhea Macrocytic anemia (B12); microcytic anema (iron); easy bruising (Vit K and C); edema (protein); glossitis (B vits, iron); night blindness (vit A); bone pain/fractures (K, Mg, Ca, Vit D); muscle spasm (Ca, Mg); peripheral neuropathy (B1, B6, B12)
Insufficient digestive elements
Includes decreased pancreatic enzymes, liver enz, bile salts, HCl
post-surgical syndromes, biliary obstruction, cystic fibrosis, etc
Carbohydrate intolerance/Lactose intolerance
Disaccharides normally split to monosaccharides by duodenal enterocytes’ enzymes:
Disaccharidases– lactase, maltase, isomaltase, sucrase
Lack of splitting the molecules leads to inc osmotic load, then watery diarrhea; fermentation leads to gas (H2,CO2, and methane), flatulence, distention, abd pain
Enzyme deficiencies may be congenital (rare), primary or secondary
Epidemiology of enzyme deficiencies
Acquired lactase deficiency is most common form
In the US:
80% prevalence in blacks and Hispanics; ~100% of Asian American population; 25% prevalence in whites of NW European descent
Worldwide: >75% population is estimated to be lactose-deficient. Very common among Asian, South American, and African persons.
SSX of enzyme deficiencies
varies from minor abdominal discomfort and bloating to severe diarrhea in response to even small amounts of lactose
watery diarrhea, abdominal bloating and pain, flatulence, nausea, borborygmi
Lab for enzyme deficiencies
a. hydrogen breath test - test of choice
lactose administered after an overnight fast, after which expired air samples are collected before and at 30-minute intervals for 3 hours to assess hydrogen gas conc. A rise in breath hydrogen concentration > 20 ppm over the baseline after lactose ingestion suggests lactase deficiency.
b. dietary elimination: Resolution of symptoms with elimination of lactose-containing food products and resumption of symptoms with the reintroduction are findings suggestive of lactose intolerance
Etiology of Tropical Sprue
unknown, but thought to be from SI chronic infx by toxigenic coliform bacteria
Leads to malabsorption of folate, B12, iron
SSX of Tropical Sprue
a) acute phase: diarrhea with fever and malaise
b) chronic phase: diarrhea, nausea, anorexia, abd cramps, steatorrhea, paresthesias
Work-up for Tropical Sprue
CBC - megaloblastic anemia (60% of patients)
Stool analysis:
fecal fat - > 6 g in 24 hours is abnormal (positive for fat malabsorption). Fatty stools are usually observed when the stool fat content is 15 g or more.
CMP - decreased serum protein, calcium, phosphorus, cholesterol and prothrombin, hypochlorhydria, check pancreatic function
D-Xylose absorption test - 25 g D-xylose is administered orally. In well-hydrated patients with normal renal function, abnormal results (i.e., positive for mucosal malabsorption):
5-hour urine collection < 4 g
1-hour serum collection < 20 mg/dL.
Upper GI endoscopy will show characteristic histology
Celiac Disease
Immune-mediated enteropathy (reaction to gluten proteins leads to mucosal damage)
Autoimmune condition: Environmental trigger = gluten
Autoantigen = tissue transglutaminase
Elimination of the environmental trigger leads to a complete resolution
Epidemiology of Celiac disease
Highest incidence in Europe and US
Affects 0.5-1% of population. Prevalence rate high in those with GI symptoms (1/56) and in those with a first-degree relative with celiac disease (1/22).
Low rates in blacks and those of Hispanic or Asian ethnicity
Can occur at any age, but in adults the peak incidence is in the fifth decade.
Females are more commonly affected than males, 2: 1
Genetics: Most all patients express human leukocyte antigen (HLA-DQ2 or HLA DQ8), which facilitate the immune response against gluten proteins.
Pathophysiology of Celiac disease
Gliadins and glutenins (ingested proteins) in the presence of CD4+ T-cells with HLA-DQ genotypes activate cytokine production and clonal expansion of antibody-producing B-cells leading to lymphocyte-mediated destruction of the proximal small intestine mucosal villi.
When villi are damaged, vitamins, minerals, Ca+2, CHO, protein, and fats not well absorbed.
T cells may react with tissue transglutaminase (the principal component of the endomysium autoantigen), and set in motion a series of inflammatory events that result in the characteristic celiac mucosal lesion.
Risk factors for developing Celiac disease
heredity, early introduction of gluten in infant diet, absent breastfeeding, Crohn’s dz, Type 1 DM, Down syndrome, chronic fatigue syndrome, AI thyroid dz
Screen patients for the following who you suspect may have Celiac
Unexplained iron deficiency, early onset osteopenia, unexplained epilepsy, failure to thrive, poor glucose control, chronic diarrhea, infertility, miscarriages, elevated liver enz
SSX of Celiac dz
Classic symptoms: diarrhea, steatorrhea, bloating, flatulence, vit/min deficiencies
Atypical presentation may have extraintestinal signs: anemia, dermatitis herpetiformis, diabetes meletis, aphthous stomatitis, neurological symptoms, osteopathy
Work-up for Celiac dz
Lab: CBC: Anemia (microcytic, hypochromic/normocytic, normochromic w ↑RDW) Leukopenia
CMP: inc AST; low, Albumin/plasma protein; Low cholesterol (total, LDL, HDL)
Inc alkaline phosphatase
Procedure: Bone mineral density (low)
Specialized tests: - -Serology: 1) Serum IgA quantitation 2) Serum IgA anti-endomysial antibodies (IgA EMA) 3) IgA anti-tissue transglutaminase (IgA tTG) antibodies. Abnormal >100 units is highly specific. tTG antibody test is less costly because it uses an enzyme-linked immunosorbent assay; it is the recommended single serologic test for celiac disease screening in the primary care setting. 4) Deamidated gliadin peptide (DGP) IgA and IgG– high sensitivity and specificity, esp in elderly who have normal standard tests
