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)
