Module 4 EB #2 Flashcards
S/S associated with constipation
-physical exam
-additional dx tests
-digital rectal exam w/ assessment for anatomic abnormalities (anal stricture, rectocele, rectal prolapse, or perineal descent during straining) and assessment of pelvic floor motion during stimulated defecation (the patient’s ability to “expel the examiner’s finger)
-CBC, serum electrolytes, glucose, TSH, colonoscopy or flexible sigmoidoscopy –> MUST be performed in patients w/ any of the following: >equal 50 yrs old, severe constipation, signs of an organic disorders, alarm sx (hematochezia, wt loss, positive FOBT or FIT), or family hx of colon cancer or inflammatory bowel disease
Chronic constipation treatment - dietary and lifestyle measures (5)
- establish regular bowel regimen (regular timing, proper positioning, and abdominal pressure)
- ensure adequate fluid and fiber intake
-prescribe fiber supplements
-SE: distention; flatulence (diminished over several days; may take 7-10d for full effect); best in patients with normal colonic transit
-Fiber will EXACERBATE SYMPTOMS: colonic inertia, defecatory disorders, opioid-induced constipation, or IBS - regular exercise
- D/C meds that may be causing or contributing to constipation
- Probiotics: improves stool frequency and consistency (low efficacy)
Fecal impaction
-def
-predisposing factors
-clinical presentation
-severe impaction of stool in the rectal vault may result in obstruction to further fecal flow, leading to partial or complete large bowel obstruction
-medications (opioids), severe psychiatric disease, prolonged bed rest, neurologic disorders of the colon, and spinal cord disorders
-decreased appetite, nausea and vomiting, and abdominal pain and distention; may be paradoxical “diarrhea” as liquid stool leaks around the impacted feces
fecal impaction
-digital rectal exam
-initial treatment
-long-term care
-firm feces are palpable on digital exam of the rectal vault
-relieve the impaction w/ enemas (saline, mineral oil, or diatrizoate) or digital disruption of the impacted fecal material
-maintain soft stools and regular BMs
Chronic constipation treatment
-laxatives: who to give it to; types of laxatives
-ONLY give an intermittent or chronic basis for constipation that does not respond to dietary and lifestyle changes
-Osmotic laxatives: initiated w/ regular (daily) use of an osmotic laxative
*MOA: increase secretion o water into the intestinal lumen, thereby softening stools and promoting defecation
*Polyethylene glycol 3350 (MiraLAX) is a component of solutions traditionally used for colonic lavage prior to colonoscopy and does not cause flatulence
*Onset: generally w/i 24 hr
-Purgative laxative: rapid tx of acute constipation - magnesium citrate
*magnesium citrate may cause hypermagnesemia
-Stimulant laxatives: pt w/ incomplete response to osmotic agents; “rescue” agent or on a regular basis 3-4x/wk
*MOA: stimulate fluid secretion and colonic contraction
*Onset: 6-12 hours after oral ingestion (@bedtime) or 15-60 minutes after rectal admin
*Meds: bisacodyl, Senna, and cascara
Gastrointestinal gas: belching
-def
-prevalence
-etiology
-involuntary or voluntary release of gas from the stomach or esophagus
-occurs most frequently after meals
-normal reflex and does not itself mean GI dysfunction
*virtually all stomach gas comes from swallowed air
*excessive amounts - distention, flatulence, and abdominal pain
*occurs with rapid eating, gum chewing, smoking, and the ingestion of carbonated beverages
Gastrointestinal gas: belching
-restrict eval to pt with other complaints
-chronic excessive belching
-dysphagia, heartburn, early satiety, or vomiting
-supragastric belching or true air swallowing (aerophagia) = BEHAVIORAL D/O seen in pt with anxiety or psych disorders
*REFER TO BEHAVIORAL/SPEECH THERAPIST
Gastrointestinal gas: flatus
-derived from two sources
-etiology (abnormal gas production)
-swallowed air (primarily nitrogen) and bacterial fermentation of undigested carbohydrate
-increased ingestion of lactose (dairy products); fructose (fruits, corn syrups, and some sweeteners); polyols (stone-fruits, mushrooms, and some sweeteners); and fructans (legumes, cruciferous vegetables, pasta, and whole grains) or disorders of malabsorption
Gastrointestinal gas: flatus
-education
-treatment
-provide patient with a list of foods containing FODMAPS + REFER to dietician
-activated charcoal (may afford relief, but simethicone is of no proved benefit)
*long-history of flatulence w/ no other sx: treated conservatively
*AVOID gum chewing and carbonated beverages; assess lactose intolerance (2 week trial of a lactose-free diet or by a hydrogen breath test)
Gastrointestinal gas: bloating
-cause
-treatment
-production of excess gas or impaired gas propulsion –> bloating
*underlying functional GI disorder (IBS or functional dyspepsia)
-reduce fermentable sugars w/ a FODMAP-restricted diet
*reduce intake of dietary fat (delays intestinal gas clearance)
*tx constipation
*encourage exercise
Gastrointestinal gas: bloating
-medication
rifaximin, 400mg twice daily
-MOA: a nonabsorbable oral abx; reduces abd bloating and flatulence in approx 40% of treated pt
-SE: relapse (bloating) commonly occurs w/i days after stopping the abx
Diarrhea
-def
-important to distinguish what?
-increased stool frequency >3BMs/day or liquidity of feces
-distinguish acute vs chronic diarrhea, as the evaluation and tx are entirely different
Diarrhea: acute diarrhea
-def
-acute noninflammatory diarrhea vs acute inflammatory diarrhea
-diarrhea of >2 weeks’ duration is most commonly caused by invasive or noninvasive pathogens and their enterotoxins
-acute noninflammatory diarrhea: watery, nonbloody; usually mild, self-limiting; virus or noninvasive bacteria
*diagnostic evaluation: limited to patient’s w/ diarrhea that is severe or persists beyond 7 days
-acute inflammatory diarrhea: blood or pus, fever; invasive or toxin-producing bacterium
*diagnostic evaluation: requires routine stool bacterial cultures in all and testing as clinically indicated for Clostridium difficile toxin, and ova and parasites
Diarrhea
-etiology
-clinical findings (6)
-acute diarrhea that persists for <2wks due to infectious agents, bacterial toxins, or meds
*community outbreaks (nursing homes, schools, cruise ships): viral etiology or common food source
*Similar recent illnesses in family members: infectious origin
*ingestion of improperly stored/prepared food: food poisoning
*Day care attendance or exposure to unpurified water (camping, swimming): Giardia or Cryptosporidium
*recent travel abroad: “traveler’s diarrhea”
*abx administration w/i the preceding several weeks: C difficile colitis
Acute inflammatory diarrhea
-def
-patho
-S/S
-fever and bloody diarrhea (dysentery)
-colonic tissue damage r/t by invasion (shigellosis, salmonellosis, Campylobacter or Yersinia infection, amebiasis) or toxin (C difficile, Shiga-toxin-producing E coli)
-SMALL VOLUME of DIARRHEA + LEFT LOWER QUADRANT CRAMPS, urgency, and tenesmus
Acute inflammatory diarrhea
-labs
-impact of: E coli; CMV
-infectious dysentery must be distinguished from what?
-fecal leukocytes or lactoferrin (usually are present in infectious w/ invasive organisms)
-E coli: shiga-toxin - producing noninvasive organism; contaminated meat = severe hemorrhagic colitis
-CMV: immunocompromised & HIV-infected pt = intestinal ulceration w/ watery or bloody diarrhea
-infectious dysentery must be distinguished from acute ulcerative colitis: BOTH can be present acutely with fever, abd pain, and bloody diarrhea
how is diarrhea categorized if it lasts longer than 14 days?
diarrhea that persists longer than 14 days is not attributable to bacterial pathogens (except for C difficile) and should be evaluated as chronic diarrhea
acute noninflammatory diarrhea
-def
-patho
-S/S
-watery, nonbloody diarrhea associated w/ periumbilical cramps, bloating, nausea or vomiting
-suggests small bowel source r/t a toxin-producing bacterium (enterotoxigenic E coli, staphylococcus aureus, bacillus cereus, clostridium perfringens) or other agents (viruses, Giardia)
-VOLUMINOUS AMOUNTS OF DIARRHEA = dehydration w/ hypokalemia and metabolic acidosis (cholera)
Acute noninflammatory diarrhea
-labs
-what bacteria causes food poisoning sx prominent vomiting?
-NO tissue invasion = NO fecal leukocytes
-S aureus food poisoning: prominent vomiting (viral enteritis)
Diarrhea
-what does 90% of patients with diarrhea illness respond to for treatment?
-responds w/i 5 days to simple rehydration therapy or antidiarrheal agents
-diagnostic investigation is unnecessary except in suspected outbreaks or in patients at high risk for spreading infection to others
Diarrhea
-what is the goal of initial evaluation
distinguish patients w/ mild disease from those w/ more serious illness
-if diarrhea worsens or persists >7-14 days, send stool for analysis for viral, protozoan, and bacterial pathogens
Diarrhea
-when is prompt medical evaluation required? (8)
*inflammatory diarrhea signs: fever >38.5C, WBC>15000, bloody diarrhea, severe abd pain
*6+ unformed stools in 24 hours
*profuse water diarrhea and dehydration
*frail older patients or nursing home residents
*immunocompromised patients (AIDS, post-transplant)
*exposure to abx
*hospital-acquired diarrhea (onset following at least 3 days of hospitalization)
*systemic illness
Diarrhea
-physical exam
-labs
-assess patient’s level of hydration, mental status, presence of abd tenderness or peritonitis
*peritoneal findings may be present in infection w/ C difficile or STEC
*Hospitalization: required in patient w/ severe dehyration, organ failure, marked abd pain, AMS
-stool specimen should be collected in patient’s w/ dysentery (blood stools), severe illness, or persistent diarrhea to assess for fecal WBC and protozoa
*blood stools: perform serotyping for Shiga-toxin-producing E coli (STEC)
*Hospitalized patients w/ abx exposure: test for C difficile toxin
Diarrhea
-treatment options
-Diet
-Antidiarrheals
-Antibiotic therapy
Diarrhea: treatment options
-diet
adequate oral fluids (w/ carbohydrates and electrolytes); rest the bowel (avoid high-fiber foods, fats, milk products, caffeine, and alcohol
-frequent feedings of tea, “flat” carbonated beverages, and soft, easily digested foods (e.g. soups, crackers, bananas, applesauce, rice, toast
Diarrhea: treatment options
-antidiarrheal agents
-may be used safely in pts w/ mild to moderate diarrheal illnesses to improve patient comfort
*opioid agents: do not use in pt w/ bloody diarrhea, high fever, or systemic toxicity; d/c in pt if diarrhea is worsening despite tx
*loperamide: preferred; take after each loose stool
*bismuth subsalicylate (pepto bismol): give for pts with traveler’s diarrhea and reduce vomiting associated w/ viral enteritis
*anticholinergic agents: CONTRAINDICATED in acute diarrhea because of rare precipitation of toxic megacolon
Diarrhea: treatment
-antibiotic therapy
-empiric tx: not indicated in acute, community-acquired diarrhea; most sx will resolve w/i several days w/o antimicrobials
-Consider in pts with non-hospital-acquired diarrhea; those w/ moderate to severe fever, tenesmus, or bloody stools; and those w/ no suspicion of infection w/ STEC; immunocompromised and those with significant dehydration
*drug of choice: fluoroquinolones (ciprofloxacin, ofloxacin, levofloxacin)
*alternative drugs: trimethoprim-sulfamethoxazole or doxycycline
*DO NOT GIVE: Macrolides and PCN (widespread microbial resistance)
Empiric tx of non-inflammatory diarrhea: rifaximin and azithromycin
Chronic diarrhea
-def
-what must be excluded before workup?
-present for longer than 4 weeks
-exclude common causes BEFORE conducting extensive workup: meds, chronic infections, IBS
Chronic Diarrhea
-common causes (9)
- medications
- osmotic diarrheas
- secretory conditions
- inflammatory conditions
- malabsorptive conditions
- motility disorders
- chronic infections
- systemic conditions
Chronic diarrhea
-medications that may cause chronic diarrhea
-cholinesterase inhibitors
-SSRIs
-angiotensin II receptor blockers
-PPIs
-NSAIDs
-metformin
-allopurinol
-orlistat
Chronic diarrhea: osmotic diarrheas
-causes
-how to differentiate: carbohydrate malabsorption/dx
-carbohydrate malabsorption (lactose, fructose, sorbitol), laxative abuse, and malabsorption syndromes
-osmotic diarrheas resolve during fasting
*carbohydrate malabsorption: COMMON; consider in ALL patients w/ chronic diarrhea; ask patient about their dairy intake (lactose), fruits and artificial sweeteners (fructose and sorbitol), processed foods and soft drinks (high-fructose corn syrup), and ETOH
*elimination trial for 2-3 weeks or by hydrogen breath tests
Chronic diarrhea: secretory conditions
-etiology
-causes
-increased intestinal secretion or decreased absorption –> high-volume watery diarrhea w/ a normal osmotic gap
-endocrine tumors (stimulating intestinal or pancreatic secretion), bile salt malabsorption (stimulating colonic secretion), and microscopic colitis (common cause of watery diarrhea in older adults)
Chronic diarrhea: inflammatory conditions
-etiology
-other sx
-IBS, UC, Crohn disease
-abdominal pain, fever, weight loss, and hematochezia
Chronic diarrhea: malabsorptive conditions
-MAJOR CAUSE
-characterized by
-small mucosal intestinal diseases, intestinal resections, lymphatic obstruction, small intestinal bacterial overgrowth, and pancreatic insufficiency
-weight loss, osmotic diarrhea, steatorrhea, and nutritional deficiencies
**significant diarrhea in the absence of weight loss is not likely to be d/t malabsorption!
Chronic diarrhea: motility disorders
-MOST COMMON CAUSE
-consider in
-irritable bowel syndrome (young adults)
-lower abdominal pain + altered bowel habits WITH NO OTHER EVIDENCE OF serious organic disease (weight loss, nocturnal diarrhea, anemia, or GI bleeding)
Chronic diarrhea: chronic infections
-etiology
-MUST EXCLUDE
-Bacterial infections
-immunocompromised pt
-protozoans (Giardia, Entamoeba histolytica, Cyclospora) and intestinal nematodes
-strongyloidiasis and capillariasis (pt from endemic regions - esp when eosinophilia is present)
-C difficile
-Microsporidia, cryptosporidium, CMV, isospora belli, cyclospora, and mycobacterium avium complex
Chronic diarrhea: systemic conditions
thyroid disease, DM, and collagen vascular disorders (r/t alterations in motility or intestinal absorption)
Chronic diarrhea: things to ask pt regarding diarrhea
-continuous or intermittent
-occurs at night or during day
-stool appearance
*malabsorption disorder = greasy or malodorous)
*inflammatory disorder = containing blood or pus
*secretory process = watery
-abdominal pain? IBS or IBD
Chronic diarrhea:
-what warrants further evaluation?
presence of nocturnal diarrhea, weight loss, anemia, or positive results on FOBT (fecal occult blood test) are inconsistent w/ these disorders and warrant further evaluation!
Chronic diarrhea:
-labs (routine)
CBC, serum electrolytes, liver chemistries, Ca, Phos, albumin, TSH, vitamin A/D, INR, ESR, and C-reactive protein should be obtained in most patients
Chronic diarrhea:
-what does anemia, folate, iron deficiency, vit B16 issues indicate?
-Malabsorption syndromes
-Inflammatory conditions
Chronic diarrhea:
-what does hypoalbuminemia indicate?
-malabsorption
-protein-losing enteropathies
-inflammatory conditions
Chronic diarrhea:
-what does hyponatremia, nonanion gap metabolic acidosis indicate?
-secretory diarrheas
Chronic diarrhea:
-what does increased ESR/C-reactive protein indicate?
inflammatory bowel disease
Chronic diarrhea: treatment
-med options
-opioids?
-Loperamide
-Diphenoxylate w/ atropine
-Clonidine
-Octreotide
-opioids are safe in most patients w/ chronic, stable sx
Chronic diarrhea: serologic testing (tTg test)
-what is this test for?
celiac disease
Chronic diarrhea: routine stool studies
-what do you analyze it for? (6)
-ova/parasites
-electrolytes (to calculate osmotic gap)
-qualitative straining for fat (Sudan stain)
-occult blood
-leukocytes
-lactoferrin
Chronic diarrhea: what do these positive tests indicate?
-stool antigen assays OR microscopy w/ special stains
parasitic infections
-giardia, E histolytica, cryptosporidia, cyclospora
Chronic diarrhea: what do these positive tests indicate?
-increased osmotic gap
-osmotic diarrhea
-malabsorption condition
Chronic diarrhea: what do these positive tests indicate?
-+ fecal fat stain
malabsorption condition
Chronic diarrhea: what do these positive tests indicate?
fecal leukocytes or lactoferrin
IBD
Chronic diarrhea:
-what does an endoscopic exam and mucosal biopsy exclude?
IBD (Crohn disease and UC), microscopic colitis, colonic neoplasia
Chronic constipation
-what is an upper endoscopy w/ small bowel biopsy used to dx?
small intestinal malabsorptive disorder is suspected (celiac disease, Whipple disease) from abnormal laboratory studies or a positive fecal fat stain
Acute UPPER GI Bleeding
-essentials of dx
-hematemesis (bright red blood or “coffee grounds”)
-Melena (most cases)
-Hematochezia: massive upper GI bleed
-Assess volume status to determine severity of blood loss: Hct is a poor early indicator of blood loss
-Endoscopy (diagnostic)
Acute UPPER GI Bleeding: general info
-mortality
-most common
-self-limited in 80% of cases
-etiology
-higher if >60yr and those who develop bleeding while hospitalized
-Hematemesis or melena
-bleeding >48h prior to presentation have a LOW RISK of recurrent bleeding
-PUD; portal HTN, Mallory-weiss tears; vascular anomalies; gastric neoplasms; erosive gastritis; erosive esophagitis; trauma
Acute UPPER GI Bleeding: initial evaluation (5)
REFER TO HOSPITAL
1. Abx (prior to scope)
2. maintain hemodynamic status w/LR
3. eval for blood replacement
4. insert NG tube
5. Upper endoscopy: ALL patients w/ upper tract bleeding should undergo upper endoscopy w/i 24 hours of arriving in the ED
*Done to identify source of bleeding, determine risk of rebleeding, guide triage
Acute UPPER GI Bleeding: treatment (acute meds)
-acid inhibitory therapy
-intravenous PPIs
-MOA: reduce the risk of rebleeding in patients w/ peptic ulcers w/ high-risk features (active bleeding, visible vessel, or adherent clot) after endoscopic treatment)
Acute UPPER GI Bleeding: treatment (acute meds)
-oral PPIs
omeprazole, esomeprazole, or pantoprazole; lansoprazole or dexlansoprazole
-MOA: lesions at low-risk for rebleeding (esophagitis, gastritis, clean-based ulcers, and Mallory-Weiss tears)
**continuous IV PPI before endoscopy results in fewer ulcers w/ lesions that require endoscopic therapy
Acute UPPER GI Bleeding: treatment (acute meds)
-octreotide
continuous IV infusion
-MOA: reduces splanchnic blood flow and portal blood pressures; effective in the initial control of bleeding related to portal HTN
-Give to those w/ active upper GI bleeding + evidence of liver disease or portal HTN until the source of bleeding can be determined by endoscopy
Acute LOWER GI Bleeding: essential of dx (2)
-hematochezia: usually present
-colonoscopy: perform stable pt
-massive active bleeding: evaluation w/ sigmoidoscopy, upper endoscopy, angiography, or nuclear bleeding scan
Acute LOWER GI Bleeding: general info
-severity
-when to eval in outpatient setting
-etiology
-mild anorectal bleeding to massive large volume hematochezia
-bright red blood dripping into bowl after BM or mixed with solid brown stool = mild bleeding (anorectosigmoid source); evaluate in OUTPATIENT SETTING
-(depends on age and severity of bleeding): <50y (infectious colitis, anorectal disease, IBD); >50y (diverticulosis, angioectasia, malignancy, ischemia)
Acute LOWER GI Bleeding: S/S
-color of stool
*Brown stools mixed or streaked w/ blood
*Large volumes of bright red blood
*Maroon stools
*black stools
*Painless large volume bleeding
*Bloody diarrhea + cramping abd pain, urgency, or tenesmus
-Brown stools mixed or streaked w/ blood: rectosigmoid or anus
-Large volumes of bright red blood: colonic source
-Maroon stools: lesions in the right colon or small intestine
-Black stools (melena): proximal to the ligament of Treitz
-Painless large volume bleeding: diverticular
-Bloody diarrhea + cramping abd pain, urgency, or tenesmus: IBS, infectious colitis, or ischemic colitis
Acute LOWER GI Bleeding: initial treatment (2)
**SAME AS UPPER GI BLEEDING = SEND TO THE HOSPITAL
-therapeutic colonoscopy: high-risk lesions (e.g. angioectasia or diverticulum, rectal ulcer w/ active bleeding, or a visible vessel) may be treated endoscopically w/ epinephrine injection, cautery (bipolar or heater probe), or application of metallic endoclips or brands
-surgical tx: emergency surgery is required in <5% of patients w/ acute lower GI bleeding d/t the efficacy of colonoscopic and angiographic therapies
*it is indicated in pts w/ ongoing bleeding that requires more than 6 units of blood w/i 24 hours or more than 10 total units in whom attempts at endoscopic or angiographic therapy failed
*most such hemorrhages are caused by a bleeding diverticulum or angioectasia
GERD: essentials of dx
-heartburn exacerbated by?
-do typical uncomplicated cases require diagnostic studies?
-what diagnostic tool used to dx?
-exacerbated by meals, bending, recumbency
-typical uncomplicated cases do not require diagnostic studies
-endoscopy: abnormalities in 1/3 of pt
When does GERD develop?
develops when reflux of stomach contents causes troublesome sx of complications
Most common sx of GERD
heartburn, regurgitation
Other sx (besides heartburn and regurgitation) of GERD
dyspepsia, dysphagia, belching, chest pain, cough, hoarseness
GERD causes damage to what?
esophageal mucosal damage
-reflux esophagitis
-up to 1/3 of pt; more serious complications develop in a few others
GERD: dysfunction of the Gastroesophageal Junction
-when do most reflux episodes occur?
-what causes GERD (anatomically)?
-occurs during transient relaxations of the LES - triggered by gastric distention by a vasovagal reflex
*incompetent LES: increased acid reflux esp when supine or when intraabdominal pressures are increased by lifting or bending
*Hypotensive sphincter: >equal 50% of pt w/ severe erosive GERD
*Hiatal hernias: 1/4 of pt w/ nonerosive GERD, 3/4 w/ severe erosive esophagitis, >90% of pt w/ Barrett esophagus. Inc reflux episodes occur during normal swallowing - induced relaxation, transient LES relaxations, and straining d/t reflux of acid from the hiatal hernia sac into the esophagus
*truncal obesity may contribute to GERD: increased intra-abd pressure = dysfunction of the gastroesophageal junction and increased likelihood of hiatal hernia
GERD: Etiology (4)
- dysfunction of the gastroesophageal junction
- abnormal esophageal clearance
- Irritant effects of refluxate
- delayed gastric emptying
GERD: abnormal esophageal clearance
-what happens normally in esophageal clearance
-things that impact esophageal clearance
-acid refluxate normally is cleared and neutralized by esophageal peristalsis and salivary bicarbonate
-diminished clearance: 1/2 pts w/ severe GERD; r/t hypotensive peristaltic contractions of intermittent failed peristalsis after swallowing
-medical conditions: scleroderma = diminished peristalsis
-Sjogren syndrome, anticholinergic medications, and oral radiation therapy: exacerbate GERD d/t impaired salivation
GERD:
-irritant effects of refluxate
-pH of gastric fluid
-esophageal mucosal damage r/t potency of the refluxate + amount of time it is in contact w/ the mucosa
-acidic gastric fluid (pH >4.0): extremely caustic to esophageal mucosa; major injurious agent in most cases
GERD: delayed gastric emptying
impaired gastric emptying r/t gastroparesis or partial gastric outlet obstruction
GERD: special exams and tx
-bothersome vs not bothersome sx
-heartburn + regurgitation should be treated empirically w/ a twice-daily H2 receptor antagonist or a once daily PPI for 4-8 wks
-initial dx studies and treatment not warranted for pts w/ typical GERD sx suggesting uncomplicated reflux disease
GERD
-when is further investigation required?
-what is used for further investigation?
-in patients w/ sx persistent despite empiric acid inhibitory therapy to identify complications of reflux disease and to diagnose other conditions, particularly in pts w/ “alarm features” (troublesome dysphagia, odynophagia, wt loss, iron deficiency anemia)
-Upper endoscopy
-Esophageal pH or combined esophageal pH-impedance testing
*establish temporal relationship between reflux events and sx
GERD
-sx
heartburn = most common
*severity is not correlated w/ degree of tissue damage
GERD
-onset
-relief
-30-60 min after meals & upon reclining
-taking antacids or baking soda
GERD
-regurgitation
-dysphagia
-“atypical” or “extraesophageal” S/S of GERD
-spontaneous reflux of sour or bitter gastric contents into mouth
-d/t erosive esophagitis, abnormal esophageal peristalsis, development of esophageal stricture
-asthma, chronic cough, chronic laryngitis, sore throat, noncardiac chest pain, OSA
GERD: treatment
-mild sx
-lifestyle modifications/medical interventions
*eat smaller meals and eliminate acidic foods
*consider wt loss
*avoid lying down w/i 3 hours after meals
*nocturnal sx: elevate the HOB
*infrequent heartburn (<once weekly): tx on demand w/ antacids or oral H2-receptor antagonists
*antacids (H2-receptor antagonists); cimetidine, ranitidine, nizatidine, famotidine
-try to take before meals known to provoke heartburn, these agents reduce sx
GERD: treatment
-initial therapy
once-daily oral PPI
-take 30 min before breakfast for 4-8 weeks
-PPIs are preferred to H2-receptor antagonists for tx of acute and chronic GERD
GERD: treatment
-long-term therapy
pt who have sx relief w/ course of empiric once-daily PPI –> d/c therapy after 8-12 weeks
-relapsed sx: tx with either continuous PPI therapy, intermittent 2- to 4-week courses, or “on demand” therapy (drug taken until sx abate) or twice daily H2-receptor antagonists may be used to control sx in pts w/o erosive esophagitis
**patients who require twice-daily PPI therapy for initial sx control and patients’ w/ complications of GERD, including severe erosive esophagitis, Barrett esophagus, or peptic stricture, should be maintained on long-term therapy w/ a once- or twice-daily PPI titrated to the lowest effective dose to achieve satisfactory sx control
SE of PPI
uncommon
risk of long-term use of PPIs
-used with GERD long-term therapy
-infectious gastroenteritis (c-diff), iron/vit B12 def, hypomagnesemia, pneumonia, hip fx (possibly d/t impaired calcium absorption)
what do you do if GERD is unresponsive to tx?
undergo endoscopy for detection of severe, inadequately treated reflux esophagitis AND other gastroesophageal lesions (eosinophilic esophagitis)
treatment for GERD (chest pain of undetermined origin)
empiric 4-week trial of acid-suppressive therapy w/ a high-dose PPI is recommended
-persistent sx: obtain ambulatory esophageal pH or impedance and pH study
Gastritis/Gastropathy
-def
-gastropathy: conditions w/ epithelial or endothelial damage w/o inflammation
-gastritis: conditions w/ histologic evidence of inflammation
3 categories of gastritis
-erosive and hemorrhagic “gastritis” (gastropathy)
-nonerosive, nonspecific (histologic) gastritis
-specific types of gastritis (distinctive histologic and endoscopic features diagnostic of specific disorders)
erosive/hemorrhagic gastritis (gastropathy)
-who tends to have this dx?
-most common causes
-sx
-alcoholics, critically ill patients, patients taking NSAIDs (often asymptomatic; may cause epigastric pain, N/V)
-meds (NSAIDs), ETOH, stress (severe medical/surgical illness); portal HTN (portal gastropathy)
*major RF for stress gastritis: mechanical ventilation, coagulopathy, trauma, burns, shock, sepsis, CNS injury, liver/kidney disease, and MODs –> use of enteral nutrition reduces the risk of stress-related bleeding
-anorexia, epigastric pain, N/V
*most common clinical manifestation: upper GI bleeding (hematemesis, “coffee grounds” emesis, bloody aspirate; melena)
Erosive/Hemorrhagic Gastritis (Gastropathy)
-labs
-special test
-diff dx
-nonspecific; LOW Hct (if significant bleeding has occurred)
-upper endoscopy (MOST SENSITIVE METHOD OF DX)
*performed w/i 24 hours in pt w/ upper GI bleeding to ID source
-epigastric pain: peptic ulcer, GERD, gastric cancer, biliary tract disease, food poisoning, viral gastroenteritis, and functional dyspepsia
-SEVERE PAIN: CONSIDER perforated or penetrating ulcer, pancreatic disease, esophageal rupture, ruptured aortic aneurysm, gastric volvulus, GI ischemia, and myocardial ischemia
Stress gastritis (erosive/hemorrhagic gastritis (gastropathy))
-two of the most RF for bleeding
-other RF
- coagulopathy (platelets < 50,000 or INR >1.5)
- respiratory failure
-TBI, severe burns, sepsis, vasopressor therapy, corticosteroid tx, Hx of PUD and GI bleeding
Stress gastritis (erosive/hemorrhagic gastritis (gastropathy))
-treatment
once bleeding occurs, admin continuous infusions of a PPI
NSAID gastritis (erosive/hemorrhagic gastritis (gastropathy))
-when is there less incidence of endoscopically visible ulcers?
if pt uses more selective COS-2 enzyme drugs (celecoxib, etodolac, and meloxicam)
NSAID gastritis (erosive/hemorrhagic gastritis (gastropathy))
-COX-2 selective drugs –> what do they increase the risk of?
increase risk of MI, CVA, Death
NSAID gastritis (erosive/hemorrhagic gastritis (gastropathy))
-if patient has alarm sx or signs, what diagnostic test should be done?
diagnostic upper endoscopy
NSAID gastritis (erosive/hemorrhagic gastritis (gastropathy))
-treatment
d/c NSAIDs, reduce to lowest effective dose, or admin with meals
NSAID gastritis (erosive/hemorrhagic gastritis (gastropathy))
-empiric tx
2-4 wk trial of a PO PPI (same drugs as GERD)
-get diagnostic upper endoscopy if s/s don’t improve!
Alcoholic gastritis (erosive/hemorrhagic gastritis (gastropathy))
-etiology
-tx
-excessive alcohol consumption = dyspepsia, nausea, emesis, and minor hematemesis
-tx: H2-receptor antagonists, PPIs, or sucralfate for 2-4wks
portal hypertensive gastropathy (erosive/hemorrhagic gastritis (gastropathy))
-patho
-S/S
-Tx
-gastric mucosal and submucosal congestion of capillaries and venules (correlates w/ severity of portal HTN and underlying liver disease)
-asymptomatic (may cause chronic GI bleeding - 10% of pt)
-propranolol or nadolol (reduces incidence of recurrent acute bleeding via lowering portal pressures)
Non-erosive non-specific gastritis
-dx
-main types
-based on histologic assessment of mucosal biopsies (endoscopic findings are normal in many cases and do not reliably predict the presence of histologic inflammation)
-H pylori infection, those associated w/ pernicious anemia, eosinophilic gastritis
Helicobacter pylori gastritis (non-erosive non-specific gastritis)
-etiology
-patho
-prevalence
-transmission
-acute infection
-spiral gram-negative rod resides beneath gastric mucous layer adjacent to gastric epithelial cells
-gastric mucosal inflammation w/PMNs and lymphocytes
-higher in non-whites + immigrants from developing countries
-person to person (during infancy and childhood)
-characterized by: transient clinical illness of nausea + abdominal pain (last for several days) + associated w/a acute histologic gastritis w/ PMNs
*when sx resolve - majority of pt progress to chronic, diffuse mucosal inflammation (gastritis) characterized by PNMs and lymphocytes
Non-erosive non-specific gastritis: Helicobacter pylori gastritis
-3 gastric phenotypes determine clinical outcomes
-mild, diffuse gastritis: MOST COMMON; does NOT disrupt acid secretion
*this phenotype causes increased gastrin, increased acid production; increased risk of developing peptic ulcers (duodenal ulcers)
-inflammation that predominates in the gastric body: destruction of acid-secreting glands –> resultant mucosal atrophy, dec acid secretion, intestinal metaplasia
*this phenotype is associated w/ an inc risk of gastric ulcers and gastric CA
Long-term tx w/ PPI can potentiate the development of???
H pylori-associated atrophic gastritis
-chronic H pylori gastritis –> duodenal or gastric ulcers, gastric cancer, low-grade B cell gastric lymphoma
Non-erosive non-specific gastritis: helicobacter pylori gastritis
-tx
-labs
-testing/empiric tx (if positive)
-antibiotics
-pt w/ active or hx of documented PUD, gastric MALToma, and personal or family hx of gastric carcinoma
-young patients <60yrs old w/ uncomplicated dyspepsia prior to further med evaluation; functional dyspepsia; patients taking low-dose aspirin or NSAIDs long-term to reduce the risk of ulcer-related bleeding
Non-erosive non-specific gastritis: helicobacter pylori gastritis
-noninvasive testing for H pylori
-endoscopic testing for H pylori
-fecal antigen immunoassay and (13C) urea breath test
*excellend sensitivity and specificity (>95%); cost: <$60
*recent PPIs or abx significantly reduce sensitivity of urea breath tests and fecal antigen assays
*prior to testing: d/c PPIs 7-14d and abx for at least 28 days
-NOT indicated to dx H pylori infection
Non-erosive nonspecific gastritis
-types
- helicobacter pylori gastritis
- pernicious anemia gastritis
Non-erosive non-specific gastritis: pernicious anemia gastritis
-etiology
-labs
-metastatic spread is UNCOMMON in lesions <2cm
-rare autoimmune disorder; involves fundic glands w/ resultant achlorhydria, decreased intrinsic factor secretion, vitB12 malabsorption (small # pts w/ B12 deficiency have pernicious anemia)
-anti-intrinsic factor antibodies are present in 70% of patients
-risk of gastric adenocarcinoma is increased threefold, w/ a prevalence of 1-3%
*endoscopy w/ biopsy is indicated in patients with pernicious anemia at the time of dx
*pts with extensive atrophy and metaplasia involving the antrum and body, dysplasia or small carcinoids require periodic endoscopic surveillance
what is indicated at the time of diagnosis for pernicious anemia?
endoscopy with biopsy
Peptic Ulcer Disease: generally
-essentials of dx
- hx of dyspepsia (variable relationship to meals)
- ulcer sx characterized by rhythmicity and periodicity
- ulcer complications
- most NSAID-induced ulcers are asymptomatic
- upper endoscopy w/ gastric biopsy for H pylori
**diagnostic procedure of choice - gastric ulcer biopsy or documentation of complete healing
**required to exclude gastric malignancy
what is required to exclude gastric malignancy in PUD?
gastric ulcer biopsy or documentation of complete healing
what is the diagnostic procedure of choice for PUD?
upper endoscopy w/ gastric biopsy for H pylori
etiology of PUD
NSAIDs and chronic H pylori infection
what does not cause PUD?
alcohol, dietary factors, stress
other conditions that cause PUD (besides NSAIDs and chronic H pylori) (8)
- acid hypersecretory states (zollinger-ellison syndrome or systemic mastocytosis)
- CMV (esp in transplant recipients)
- Crohn disease
- lymphoma
- medications
- cirrhosis
- CKD
- idiopathic
general considerations of PUD
-def
-etiology
-break in the gastric or duodenal mucosa that arises
-normal mucosal defensive factors are impaired or overwhelmed by aggressive luminal factors (acid and pepsin)
PUD patho
ulcers extend through muscularis mucosae (usually >5mm in diameter)
-occur either in duodenum (95% in bulb or pyloric channel) or in the stomach (benign ulcers in the antrum - 60%)) or at junction of antrum and body on the lesser curvature (25%)
-duodenal ulcers: common in ages 30-55yrs
-gastric ulcers: common in ages 55-70yrs
in what age range are duodenal ulcers common?
-30-55yrs
in what age range are gastric ulcers common?
-55-70yrs
PUD: H pylori associated ulcers
-what are duodenal ulcers due to?
h pylori
PUD: H pylori associated ulcers
-how often is recurrence?
85% of pt will have endoscopically visible recurrence w/i 1 yr
PUD: H pylori associated ulcers
-after successful eradication of H pylori w/ abx, what are ulcer recurrence rates?
-reduced dramatically to 5-20% at 1 year
PUD: H pylori associated ulcers
-dx
dx by endoscopy w/ biopsy
PUD: H pylori associated ulcers
-noninvasive was to test for H pylori presence?
fecal antigen assay
urea breath testing
PUD: H pylori associated ulcers
-tx of uncomplicated H pylori-associated ulcers
-PPI-based H pylori regimen x14d
PUD: H pylori associated ulcers
-large or complicated ulcers: tx
continue antisecretory agent for additional 2-4wk (duodenal ulcer) or 4-6wk (gastric ulcer) after completion of the abx regimen to ensure complete ulcer healing with once-daily oral PPI
how long after stopping abx and PPI therapy can H pylori eradication be tested?
> 4wk after completion of abx therapy; >2wk after d/c PPI therapy
PUD: NSAID-association ulcers (gastric ulcers d/t NSAIDS)
-when is the risk of NSAID complications greater?
-tx of active ulcers
-greater w/i the first 3MO of tx in pt >60yr, those w/ prior hx of ulcer disease, those who take NSAIDs + aspirin, corticosteroids, anticolgulants
-STOP offending agent
*H2-receptor antagonists or PPIs: gastric/duodenal ulcers respond rapidly once NSAIDs are eliminated
*Undergo H pylori testing: ALL PTS w/ NSAID associated ulcers
*antibiotic eradication tx: given if H pylori POSITIVE
PUD: NSAID-associated ulcers
-tx
oral PPI given once daily
-PPIs are not fully protective in high-risk pts in preventing NSAID-related complications
-PPIs are HIGHLY effective in PREVENTING complications related to low-dose aspirin, even in high-risk patients
PUD
-s/s
-physical exam (what is abnormal?)
-epigastric pain (dyspepsia): hallmark of PUD; well localized to epigastrium; not severe
*characterized as gnawing, dull, aching, or “hunger-like”
relieved w/ food or antacids
-recurrence of pain 2-4hr later
*periodicity (symptomatic periods lasting up to several weeks’ w/ intervals of months to years in which they are pain free
-normal exam for uncomplicated PUD
PUD
-labs
-uncomplicated PUD: normal labs; order to exclude ulcer complications or confounding disease entities
PUD
-diagnostic tests
upper endoscopy: procedure of choice for dx of duodenal and gastric ulcers
-duodenal ulcers are virtually never malignant; do not require biopsy
-if endoscopy abnormal, F/U endoscopy should be performed 12 wk after start of therapy to document complete healing
**nonhealing ulcers are suspicious for malignancy
PUD: tx
-acid-antisecretory agents (oral PPI) *preferred agents
-H2-receptor antagonists *administer once daily bedtime
-agents enhancing mucosal defenses
-H pylori eradication therapy
PUD: tx
-acid-antisecretory agents
-PPIs: PO agents inhibit over 90% of 24hf acid secretion
-tx w/ oral PPIs: >90% healing of duodenal ulcers after 4 wk and 90% gastric ulcers after 8 wk when given once daily
what does long-term PPI use cause?
dec vitB12, iron, mag, Ca absorption; inc risk of enteric infections (cdiff and bacterial gastroenteritis); pneumonia, hip fx , acute and CKD and dementia
PUD: tx
-H2-receptor antagonists
-effective in tx of peptic ulcer disease (but PPIs are preferred)
-give once daily at bedtime; used for uncomplicated peptic ulcers
PUD: tx
-Agents enhancing mucosal defenses
bismuth sucralfate, misoprostol, antacids
PUD: tx
-h pylori eradication therapy
-combo regiments (abx + PPI)
-first line therapy: 14 day bismuth-based or nonbismuth-based regimen of so-called quadruple therapy
Zollinger-Ellison Syndrome (gastrinoma): essentials of dx
-common or rare?
-2 components
-rare
- peptic ulcer disease: severe and atypical; gastric acid, hypersecretion
- diarrhea: common, relieved by NG suction. Most cases are sporadic.
*25% w/ multiple endocrine neoplasia type 1 (MEN1)
Zollinger-Ellison Syndrome (gastrinoma)
-etiology
-gastrin-secreting gut tumors (endocrine cells of the pancreas, or less frequently, the duodenal wall) –> excess acid production by GI tract
Zollinger-Ellison Syndrome (gastrinoma)
-where do a majority of gastrinoma arise?
Gastrinoma triangle
-porta hepatis
-neck of pancreas
-3rd portion of duodenum
Zollinger-Ellison Syndrome (gastrinoma)
-complications
perforation, hemorrhage, obstruction
Zollinger-Ellison Syndrome (gastrinoma)
-S/S
-90% of pts develop PEPTIC ULCERS: indistinguishable from peptic ulcer disease and therefore goes undetected for many years
-GERD sx
-Diarrhea (occurs in 1/3 of pts)
Zollinger-Ellison Syndrome (gastrinoma)
-why do patients suffer from diarrhea?
direct intestinal mucosal injury/pancreatic enzyme inactivation from gastric acid hypersecretion leads to diarrhea, steatorrhea, and wt loss
*NG aspiration of stomach acid stops the diarrhea
Zollinger-Ellison Syndrome (gastrinoma)
-screening for Zollinger-Ellison Syndrome (gastrinoma)
obtain fasting gastrin levels in pts with:
REFRACTORY TO STANDARD TX; giant ulcers; ulcers located distal to duodenal bulb; multiple duodenal ulcers; frequent ulcer recurrences; ulcers associated w/ diarrhea, ulcers occurring after ulcer sx; patients w/ ulcer complications
who should also be screened for Zollinger-Ellison Syndrome (gastrinoma)?
-pt with peptic ulcers who are H pylori-negative and not taking NSAIDS; ulcer hx w/ hypercalcemia or family hix of ulcers (suggests MEN1)
Zollinger-Ellison Syndrome (gastrinoma)
-what is the most sensitive and specific method for identifying Zollinger-Ellison syndrome?
-increased fasting serum gastrin concentration (>150pg/mL)
*take levels when pt hasn’t taken H2-receptor antagonists for 24hrs of PPIs for 6d
Zollinger-Ellison Syndrome (gastrinoma)
-what type of study is used to identify tumors of SRS?
80% sensitivity for tumor detection of SRS exceeds all other imaging studies
Zollinger-Ellison Syndrome (gastrinoma): treatment
-metastatic disease
*what is the MOST important predictor of survival?
*what is initial tx drected at?
-prognosis
-MOST important predictor of survival is presence of hepatic metastases
-patients w/ multiple hepatic metastases, direct initial tx at controlling hypersecretion
*oral PPIs (omeprazole, etc)
-slow growth of tumors = 30% of pt w/ hepatic metastases have a survival of 10 years
Zollinger-Ellison Syndrome (gastrinoma): localized disease
-tx (cure)
-prognosis
-surgery?
-cure can be achieved ONLY if gastrinoma is resected BEFORE hepatic metastatic spread occurs (lymph node metastases do not adversely affect prognosis)
-15 year survival of pt who DO NOT have liver mets at initial presentation is over 95%
-surgery NOT recommended in pts w/ MEN1 d/t presence of multifocal tumors and long-term survival in the absence of surgery in most pts
Celiac Disease: essentials of dx
-typical sx
-atypical sx
-weight loss, chronic diarrhea, abd distention, growth retardation
-dermatitis herpetiformis, IDA, osteoporosis
Celiac Disease: essentials of dx
-dx
-tx
-abnormal serologic test + small bowel biopsy
-clinical improvement on gluten-free diet
Celiac Disease: general info
-def
-etiology
-patho
-permanent dietary disorder
-immunologic response to glute (storage protein found in certain grains)
-ingestion of gluten –> diffuse damage to proximal small intestinal mucosa + malabsorption of nutrients
Celiac Disease: general info
-manifestation of sx
-prevalence
-between 6-24MO after introduction of weaning foods, most cases present in childhood or adulthood
-whites of Northern European ancestry
*celiac disease develops only in people w/ the HLA-DO2 (95%) or DQ8 (5%) class II molecules (40%)
Celiac Disease
-labs (what arises suspicion)
nonspecific lab abnormalities may be present that may raise the suspicion of malabsorption and celiac disease
Celiac Disease
-recommended test
-test used to confirm dx
-Sero test: IgA tissue transglutaminase (IgA tTG) antibody
98% sensitivity and 98% specificity for the dx of celiac dx
-mucosal biopsy of proximal duodenum (bulb) and distal duodenum
An adequate normal biopsy excludes the dx
Celiac Disease
-S/S
-GI sx: depend on length of small intestine involved + pt age when the disease presents
*classic sx of malabsorption
..<2yrs old: diarrhea, steatorrhea, wt loss, abd distention, weakness, muscle wasting, growth retardation
..Older children/adults: chronic diarrhea, dyspepsia, flatulence (colonic bacterial digestion of malabsorbed nutrients); variable wt loss; extraintestinal “atypical” manifestations - fatigue, depression, IDA, osteoporosis, short stature, delayed puberty, amenorrhea, reduced fertility
Celiac Disease
-physical exam
-abd exam
-dermatotits -herpetiformis
-normal (mild cases): may reveal signs of malabsorption
*loss of muscle mass or subcutaneous fat, pallor d/t anemia, easy bruising d/t vitamin K deficiency, hyperkeratosis d/t vitamin A deficiency, bone pain d/t osteomalacia, or neurologic signs (peripheral neuropathy, ataxia) d/t vit B12 or vit E deficiency
-distention w/ hyperactive bowel sounds
-cutaneous variant of celiac disease
Celiac Disease
-tx
-relationship between glucose and lactose intolerance
-remove gluten from diet (wheat, rye, barley)
-most pts w/ celiac diseae also have lactose intolerance: AVOID DAIRY products until intestinal sx have improved on gluten-free diet
Celiac Disease
-most common reasion for tx failure
-incomplete removal of gluten
Lactase Deficiency
-essentials of dx (common sx)
diarrhea, bloating, flatulence, and abd pain after ingestion of milk-containing products
Lactase Deficiency
-dx
-dx confirmed
-supported by symptomatic improvement on lactose-free diet
-hydrogen breath test
Lactase Deficiency: general info
-patho
-lactase enzyme level at birth
-lactase is the brush border enzyme (hydrolyzes the disaccharide lactose) into glucose and galactose)
-high but declines steadily in MOST people of non-European ancestry during childhood and adolescence and into adulthood
*90% Asian Americans
*70% African Americans
*95% Native Americans
*50% Mexican Americans
*60% Jewish Americans
= are lactose intolerant compared with <25 of white adults
Lactase deficiency
can arise from GI disorders that affect proximal small intestinal mucosa (Crohn disease, celiac disease, viral gastroenteritis, giardiasis, short bowel syndrome, and malnutrition)
Lactase Deficiency
-labs (what test is used to dx)
MOST widely available test for dx of lactase deficiency: hydrogen breath test
*positive test: after ingestion of 50g of lactose, a rise in breath hydrogen of more than 20ppm w/i 90min indicates bacterial carb metabolism
Lactase Deficiency
-what do clinicians prescribe?
empiric trial of lactose-free diet for 2 weeks
-resolution of sx (bloating, flatulence, diarrhea) is suggestive of lactase deficiency and may be confirmed, if necessary w/ a breath hydrogen study
*though a placebo response cannot be excluded
Lactase Deficiency
-S/S (mild-mod; higher)
-clinical sx vary - depending both on severity of lactase deficiency and the amount of lactose ingested
-most patients with lactose intolerance can drink at least one 8oz serving of mild daily (12g of lactose) w/o sx, though rare pts have almost complete intolerance
-mild-mod amounts of lactose malabsorption: bloating, abd cramps, flatulence
-higher lactose ingestions: osmotic diarrhea
Lactase Deficiency
-treatment
*goal
*find threshold
-Lactase enzyme replacement (lactaid, lactase, dairy ease)
-caplets or drops of lactase: taken w/ milk products, improving lactose absorption and eliminating sx
-goal of tx is to achieve patient comfort
-patients usually find their threshold of intake at which sx will occur
-spread out dairy produce intake through the day: most pts can take dairy products w/o sx and DO NOT require lactase supplements
Lactase Deficiency
-what are patients at increased risk of when eliminating/restricting milk products?
osteoporosis
**supplement with 500mg orally 2x/3x dailiy
Appendicitis: essentials of dx
-early sx
-later sx
-periumbilical pain
-RLQ pain + tenderness. Anorexia, N/V, constipation.
*McBurney point: tenderness or localized rigidity
*low-grade fever + leukocytosis
Appendicitis: general info
-prevalence
-patho
-between ages 10-30yrs
-initiated by obstruction of appendix by a fecalith, inflammation, foreign body, or neoplasm –> increased intraluminal pressure, venous congestion, infection, thrombosis or intramural vessels
What is the MOST COMMON abdominal surgical emergency?
-what occurs if left untreated?
appendicitis
-gangrene and perforation develop w/i 36 hours
Appendicitis
-labs (what is elevated?)
WBC
-moderate leukocytosis (10,000-20,000) + neutrophilia common
-microscopoic hematuria + pyuria: present in 25% of pts
Appendicitis
-diagnostic tests
-abdominal US: useful in dx appendicitis _ excluding other diseases with similar sx (adrenal disease in younger women)
-CT scanning appears to be MORE accurate = GOLD STANDARD
Appendicitis
-S/S (beginning, w/i 12 hrs)
-vague, often colicky periumbilical or epigastric pain
-pain shifts to RLQ, manifested as a steady ache that is worsened by walking or coughing
*ALMOST ALL patients have nausea w/ one or two episodes of vomiting
-Feeling constipated
-low-grade fever
Appendicitis
-is protracted vomiting or vomiting that begins BEFORE onset of pain suggests another dx?
YES
Appendicitis
-does high fever or rigors suggest another dx or appendiceal perforation?
YES
Appendicitis
-physical exam
-localized tenderness + guarding RLQ elicited w/ gentle palpation w/ one finger
-coughing: able to precisely localize painful area = sign of peritoneal irritation
Appendicitis
-signs of adjacent inflammation
-what are these signs strongly suggestive of?
-Psoas sign: pain on passive extension of the right hip
-Obturator sign: pain w/ passive flexion and internal rotation of the right hip
-signs of adjacent inflammation - strongly suggestive of appendicitis
Appendicitis
-tx
surgery
-prior to surgical appendectomy, admin broad-spectrum antibiotics w/ gram-negative and anaerobic coverage
-surgery for early, uncomplicated appendicitis
-surgery if pt appendix has RUPTURED + generalized peritonitis
Appendicitis
-complications (what do you suspect if pain persists >36hr, high fever, diffuse abd tenderness or peritoneal findings, palpable abd mass, marked leukocytosis)
-PERFORATION!
Appendicitis
-prognosis
-extremely low 0.2% (higher in older adults 15%)
Irritable Bowel Syndrome: essentials of dx
-characterized by?
-onset of sx?
-more common in which sex?
*chronic functional disorders
-abd pain w/ alterations in bowel habits
-late teens to early twenties
-more common in women
Irritable Bowel Syndrome: general info
-def
-characterized by
-other sx
-idiopathic clinical entity
-chronic (>6MO) abd pain that occurs in association with altered bowel habits; sx may be continuous or intermittent
*2016 Rome IV Def of IBS: abd pain + 2 of the 3 following sx (present avg at least 1d/wk)
..associated w/ change in freq of stool
..related to defecation
..associated w/ change in form (appearance of stool)
Irritable Bowel Syndrome
-other sx
-other somatic/psychological complaints
-abnormal stool frequency; abnormal stool form (lumpy or hard; loose or watery); abnormal stool passage (straining, urgency, or feeling of incomplete evacuation); and abd bloating or a feeling of abd distention
-dyspepsia, heartburn, chest pain, headaches, fatigue, myalgias, urologic dysfunction, gynecologic sx, anxiety or depression
Irritable Bowel Syndrome
-Labs/Diagnostics
in patients with sx that fulfill diagnostic criteria for IBS and who have no other alarm sx = DO NOT SUPPORT FURTHER DX TESTING
*Routine sigmoidoscopy or colonoscopy NOT RECOMMENDED in young pts w/ sx of IBS w/o alarm sx
-in patients >equal 50yrs who have not have previous eval: colonoscopy should be obtained to exclude malignancy
Irritable Bowel Syndrome
-S/S
sx should be present at least 6MO before dx can be considered
-abd pain: intermittent, crampy, and in lower abd region
*associated with change in stool frequency or form and may be improved or worsened by defecation
**DOES NOT USUALLY OCCUR at night or interfere w/ sleep
Irritable Bowel Syndrome
-4 categories
-IBS Diarrhea: loose or watery stools, frequent stools (>3 per day), urgency, or fecal incontinence
-IBS Constipation: <3BMs per week, hard or lumpy stools, straining
-IBS mixed constipation + diarrhea: firm stool in the morning followed by progressively looser movements
-IBS Not subtyped: ask pt about alarm sx suggestive of dx other than IBS and warrant further investigation
Irritable Bowel Syndrome
-most important interventions
-mind-gut interaction
-education
-clinicians should offer reassurance, education, and support
-things that impact gut: foods, meds, hormones, stress
-IBS is a chronic disorder characterized by periods of exacerbation and quiescence
*shift emphasis on finding cause of sx to HOW TO COPE WITH SX
..resist repeated dx studies
-moderate exercise is beneficial
Irritable Bowel Syndrome
-what foods should be avoided?
fatty foods, alc, caffeine, spicy foods, grains
-must exclude lactose intolerance (hydrogen breath test or trial of lactose-free diet in pts w/ diarrhea, bloating, and flatulence
Irritable Bowel Syndrome
-six food groups that exacerbate bloating, flatulence, and diarrhea
- fructose (corn syrups, apples, pears, honey, watermelon, raisins)
- lactose
- fructans (garlic, onions, leeks, asparagus, artichokes
- wheat-based products
- sorbitol (stone fruits)
- raffinose (legumes, lentils, Brussel sprouts, soybeans, cabbage)
Inflammatory Bowel Disease
-types
- UC
- Crohn’s disease
Inflammatory Bowel Disease: UC
-essentials of dx (sx, key to dx)
-more common in what population?
-bloody diarrhea, lower abd cramp, fecal urgency, anemia, low albumin, neg stool cs, sigmoidoscopy = key to DX
-non-smokers and former smokers
*disease severity may be lower in active smokers and worsen in pt who stop smoking
-appendectomy <20yrs fora cute appendicitis is associated w/ reduced risk of developing UC
Ulcerative Colitis:
-physical exam
*what is the hallmark sx
*what should you ask pts about?
*focus exam on what?
-hallmark sx: bloody diarrhea
-stool frequency, presence + amount of rectal bleeding, cramps, abd pain, fecal urgency, tenesmus
-volume status (orthostatic BP + pulse & nutritional status); abdominal exam: look for tenderness + evidence of peritoneal inflammation. Red blood may be present on digital rectal exam.
UC
-mild disease
<4BMs per day + intermittent rectal bleeding and mucus
-stools: loose in consistency
-urgency/tenesmus: rectal inflammation
-left lower quadrant cramps: relieved by defecation
-NO SIGNIFICANT ABDOMINAL TENDERNESS!
UC
-moderate disease
-more severe diarrhea (4-6 BMs per day) + frequent bleeding
-mild abd pain + tenderness
-mild fever, anemia, and hypoalbuminemia
UC
-severe disease
> 6 bloody BMs per day
-severe anemia, hypovolemia, impaired nutrition w/ hypoalbuminemia
-+abdominal pain and tenderness
-fulminant colitis: subset of severe disease characterized by rapidly worsening sx w/ signs of toxicity
UC
-labs
-dx
-goal of tx
-obtain Hct, sed rate, serum albumin
-sigmoidoscopy with mucosal appearance characterized by edema, friability, mucous, and erosion
*colonoscopy should not be performed in pts w/ fulminant disease because of risk of perforation (once pt has improvement w/ tx, perform colonoscopy to determine extent of disease
-terminate the acute, symptomatic attack and prevent recurrence of attacks
UC
-antidiarrheal agents?
DO NOT GIVE ANTIDIARRHEAL AGENTS during acute phase of illness
Crohn Disease
-sx
-cigarette smoking
-insidious onset; intermittent bouts of low-grade fever, diarrhea, RLQ pain
*RLQ mass/tenderness
-STRONGLY associated with development of Crohn disease, resistance of medical tx, and early disease relapse
Crohn Disease
-physical exam
-types
-not pts temp, weight, nutritional status, presence of abd tenderness or mass, rectal exam, extraintestinal manifestations
*most commonly, there is one or a combo of the following clinical constellations:
..chronic inflammatory disease
..intestinal obstruction
..penetrating disease and fistulae
..perianal disease
..extraintestinal manifestations
Crohn Disease
-***chronic inflammatory disease
-intestinal obstruction
-penetrating disease and fistulae
-perianal disease
-extraintestinal manifestations
-MOST COMMON presentation in pts w/ ileitis or ileocolitis
-report malaise, wt loss, diarrhea, and loss of energy
-may be blood diarrhea and fecal urgency (left colon/ rectal involvement) mimicking sx of UC
-cramping or steady RLQ or periumbilical pain is common
-physical exam reveals RLQ focal tenderness; palpable, tender mass in lower abd (represents thickened or matted loops of inflamed intestine)
Crohn Disease
-chronic inflammatory disease
-***intestinal obstruction
-penetrating disease and fistulae
-perianal disease
-extraintestinal manifestations
-narrowing of small bowel (may occur r/t inflammation, spasm, or fibrotic stenosis)
-pt report postprandial bloating, cramping pains, and loud borborygmi
-may occur w/ active inflammatory sx (as above) or later in the disease w/o other systemic sx or signs of inflammation
Crohn Disease
-chronic inflammatory disease
-intestinal obstruction
-***penetrating disease and fistulae
-perianal disease
-extraintestinal manifestations
-sinus tracts that penetrate through bowel (form fistulas to adjacent structures): intra-abdominal or retroperitoneal abscess - fevers, chills, a tender abd mass, and leukocytosis
-fistulas between small intestine and colon: asymptomatic; can see diarrhea, wt loss, bacterial overgrowth, malnutrition
-fistulas to the bladder: recurrent infections
-fistulas to vagina: malodorous drainage, problems w/ personal hygiene
Crohn Disease
-chronic inflammatory disease
-intestinal obstruction
-penetrating disease and fistulae
-***perianal disease
-extraintestinal manifestations
1/3 of pt; large painful skin tags, anal fissures, perianal abscesses, and fistulas
Crohn Disease
-chronic inflammatory disease
-intestinal obstruction
-penetrating disease and fistulae
-perianal disease
-***extraintestinal manifestations
seen w/ both Crohn disease and UC
-arthralgias, arthritis, iritis or uveitis, pyoderma gangrenosum, or erythema nodosum
-oral aphthous lesions are common
-there is an increased prevalence of gallstones d/t malabsorption of bile salts from the terminal ileum
-nephrolithiasis w/ urate or calcium oxalate stones may occur
Crohn disease
-labs
-dx
-tx
-CBC and serum albumin in ALL pts; send stool specimens for culture for routine pathogens, microscopy for ova and parasites, and conventional or rapid PCR diagnostic assessment for C difficile toxin
*fecal calprotectin: excellent noninvasive test. elevated levels correlate w/ active inflammation as demonstrated by ileocolonoscopy or radiologic CT or MR enterography
-clinical picture w/ supporting endoscopic pathologic, and radiographic findings
*colonoscopy
-diet, d/c smoking, drink fluids, avoid lactose, avoid raw fruits/veggies/popcorns/nuts
*parenteral vitB12 + vitD supplementation
How common is it for Crohn’s patients to need a surgical procedure?
over 50% of pt require at least 1 surgical procedure.
is toxic megacolon more common in crohns disease or UC?
UC
location
-UC
-Crohns
-anywhere from mouth to anus; frequently affects the terminal ileum; most cases (70-80%) have small bowel involvement and sparing of the rectum
-always affects rectum extending to varying degrees around the large bowel
inflammation
-UC
-Crohns
-Continuous, diffuse mucosal inflammation (inflammation limited to the mucosa); sharp transition between diseased and normal colon
-“patchy (skip areas), transmural inflammation”; locality in the setting of relatively normal intervening mucosa, segmental; asymmetric involvement of different parts of the wall w/i given segments of bowel
hematochezia (common or rare)
-UC
-crohns
-common
-rare
mucus/pus (common or rare)
-UC
-Crohns
-common
-rare
small bowel disease (no or yes)
-UC
-Crohns
-no
-yes
UGI tract involvement (no or yes)
-UC
-Crohns
-no
-yes
abdominal mass present?
-UC
-Crohns
-rare
-RLQ
extra intestinal involvement (common or rare)
-UC
-Crohns
-common
-common
small bowel obstruction (yes, no, common, or rare)
-UC
-Crohns
-no
-common
colonic obstruction (rare or common)
-UC
-Crohns
-rare
-common
perianal disease
-UC
-Crohns
-no
-common
strictures and fistulas (no or yes)
-US
-Crohns
-no
-yes
