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130 Cards in this Set
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definition of peptic ulcers
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cellular destruction with loss of mucosal, submucosal and sometimes muscular layer of GI tract
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where do ulcers form?
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anywhere along the gi tract.
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where do duodenal ulcers form?
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– 95% occur in the duodenal bulb
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where do gastric ulcers form?
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located primarily in the antrum.
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Incidence and prevalence of peptic ulcer disease?
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• Affects 10% of all Americans
• Gender: similar between men and women • No correlation – race, occupation and socioeconomic class |
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tell use about the number of hospitalizations of gastric ulcer?
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it's in overall decline.
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tell us about the overall decline of hospitalizations of gastric ulcer?
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• More effective treatments
• Hospitalization criteria • Declining smoking rates • Shift to ambulatory care |
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tell us about the hospitalizations of gastric ulcers?
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less dramatic decline than gu
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the overall mortality of ulcers (men and women)...
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is in decline.
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mortality of men due to ulcers is...
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in decline
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mortality of women is in ...
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overall increasing.
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the mortality of women b/c of ulcers is increasing due to ...2
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develop arthritis when aging, taking NSAIDs – induce ulcer)
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the esophagus parts
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• Tube from pharynx to stomach
• Innermost layer provides lubricating mucous • Mucus layer • Lower esophageal sphincter |
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each cell secretes:
Parietal cells: Chief cells Mast cells: G cells: |
hcl
pepsinogen histamine gastrin |
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normal ph of the duodenum
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5 - 8
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the duodenum receives alkaline salts and enyzmes from...
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alkaline salts... gallbladder
enzyme...pancreas/ bile |
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what are the aggressive factors.
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Bile acids
Gastrin Pepsinogen Acid |
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what are the Mucosal Protective Factors.
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Mucus, Blood flow
Bicarbonate Cell regeneration Prostaglandins |
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what is the pathogenesis of peptic ulcer disease.
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an imbalance of intraluminal aggressive and mucosal protective factors.
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what are the three causes of ulcers?
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drugs
h.pylori zes |
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what drugs cause ulcers?
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nsaids, adrenocorticosteroids, chemo
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drugs cause more gastric or duodenal ulcers?
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gastric
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h. pylori causes ?% of duodenal and gastric ulcers?
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92% duodenal
70% gastric |
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how do adrenocorticosteroids promote gi injury?
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increase gastric acid. secretion
inhibit prostaglandin synthesis |
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what has been isolated from GU patients receiving immunosuppressive agents post renal transplant
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CMV
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what are the risk factors of ulcer formation?
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smoking, alcohol, caffeine, spicy foods, genetics, psychological stress.
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the cigarette smoking risk factor to ulcers?
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• Not a direct cause of PUD, but there is an association
• The risk is proportional to the amount smoked (>10/day) • Associated with increased incidence of PUD • Decreases response to H2RAs • Contributes to ulcer recurrence |
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the alcohol risk factor to ulcers?
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• Gastric mucosal irritant
• May cause bleeding |
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what are the two major etiologies of peptic ulcers?
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nsaids, and h. pylori
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about the caffeine risk factor to peptic ulcers?
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• Gastric acid stimulant
• May cause dyspepsia |
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spicy food to peptic ulcers?
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• May cause dyspepsia
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genetics risk factor to peptic ulcers?
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• Familial factors associated with DU
• Patients with blood type O have a 30% increased incidence of DU |
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Psychological stress to peptic ulcers.
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• Does not cause PUD
• May contribute to ulcer pain and disability |
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what are the four clinical presentation signs of peptic ulcers?
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Epigastric pain
Bleeding Decreased intravascular volume Other: • Heartburn • Bloating • Belching • GU: anorexia, nausea, vomiting, weight loss |
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epigastric pain clinical presentation?
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•Frequently nocturnal
•DU tend to be episodic and occur in clusters •Pain may radiate to the back •Antacids provide relief •Food may relieve or increase pain |
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bleeding clinical presentation?
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•Hematemesis: vomiting of blood
•Melena: dark stool (blood) •Occult: old blood •Monitor efficacy and adverse effects of drugs |
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other gi symptoms clinical presentation?
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•Heartburn
•Bloating •Belching •GU: anorexia, nausea, vomiting, weight loss |
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Decreased intravascular volume (monitoring parameters) clinical presentation
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•Decreased BP
•Increased HR •Decreased Hgb and Hct |
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what don't cause pud, but worsen the symptoms.
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the risk factors.
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go over the signs and symptoms table.
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later
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what is the differential diagnosis of non-ulcer dyspepsia?
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Vague symptom complex characterized by abdominal discomfort & epigastric pain in the ABSENCE of an ulcer or other structural disease
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pathogenesis of nud.
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unknown; may be related to H.pylori and/or alternations in gastric motility
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2. Clinical features of pud
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symptoms similar to PUD
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3. Management of nud.
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questionable efficacy of anti-ulcer medications, possible use of prokinetic agents if it is related to motility
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Gastritis – definition. acute/ chronic
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inflammation of gastric mucosa without ulceration; acute gastritis is usually self-limiting whereas chronic gastritis persists for long periods with some forms resulting in destruction of parietal and chief cells (gastric atrophy)
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1. Pathogenesis of gastritis (mostly drugs)
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asa, nsaids, iron, chemotherapeutics, ethanol, radiation, ischemia, healthy aging, pernicious anemia, infections
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2. Clinical features of gastritis
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acute symptoms include epigastric pain, nausea and bleeding or asymptomatic
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3. Management of gastritis
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treat symptoms with antacids
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hiatus hernia pathogenesis
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stomach passes through the esophageal hiatus into chest above the diaphragm
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ZES (Zolligner Ellison Syndrome
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hypersecretion of HCl, need higher dose PPI than to treat PU
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what are the two imaging and endoscopy diagnostic tests for ulcers?
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1.Radiography (upper GI)
2.Esophagealgastroduodenography (EGD) |
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Radiography (upper GI)
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•Visualization of ulcer crater using radiopaque barium and x-ray examination
•May result in false negative of small ulcers •Shows 30-60% of actual ulcers |
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Esophagealgastroduodenography (EGD)
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•Procedure, which permits direct visualization of GI mucosa through lighted endoscope
•Allows for photography •Allows for histologic sampling •Most accurate and conclusive |
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what is the gold standard of h. pylori testing?
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1. Histology (microbiologic exam of various stains)
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what is the problem with a histologic sampling of h. pylori?
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• Patchy distribution of HP can cause false negatives
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what are the five tests for h. pylori?
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Histology
Culture Urease Urea breath test Serology |
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a culture of h. pylori
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• Used to test for antibiotic resistance
• Results are not immediate • False negatives are common |
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a urease biopsy of h. pylori
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• Campylobacter-like organism (“CLO” test)
• HP ammonia causes color change • Test of choice at time of endoscopy • Rapid results – tests for active infection |
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Urea breath test of h. pylori.
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• C13 – nonradioactive
• C14 – radioactive • HP urease breaks down ingested C-labeled urea • Patient exhales labeled CO2 • Avoids sampling error • Can be used to confirm HP eradication • |
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serology test of h. pylori.
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• Laboratory based test quantitates IgG or IgA antibody titers to HP
• Does not differentiate active from previous infection as the antibody persists after treatment and slowly falls (over period of 6-12 months) |
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h. pylori tests cost higher with? h
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endoscopy which are the histology, culture, and urease test.
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4 chronic complications of pud.
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A.Gastrointestinal bleeding
B.Perforation and penetration C.Gastric outlet obstruction D.Gastric cancer |
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gastrointestinal bleeding complications.
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• Most frequent complication
• Occurs in about 20% of patients • Cause by erosion of ulcer into wall of blood vessel • s/s include melena, hematenesis, weakness, shock (SBP<90) and death |
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B. Perforation and penetration complications.
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• Life threatening
• Occurs in about 5-10% of patients • Caused by erosion of ulcer through all layers of stomach or duodenal wall or into a solid organ • s/s include intense abdominal pain, peritonitits, systemic infection |
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C. Gastric outlet obstruction complications.
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• Caused by scarring of pylorus
• Occurs in <5% of patients • s/s include increased abdominal discomfort, N/V, loss of appetite and weight loss |
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D. Gastric cancer complications.
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• Not a direct complication of PUD
• Gastric cancer may present itself as an ulcer • Long-standing HP is associated with various types of gastric cancer |
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A. Characteristics of H. pylori
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• Gram negative spiral bacterium
• Flagella • Mucopolysaccharide coat • Acid labile – requires pH >4 to survive • Secretes urease to form NH3 and CO2 • Infects the gastric antrum under the mucus layer • Carried into the duodenum by peristalsis • Class I carcinogen |
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B. Epidemiology of h. pylori
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• >40% of world population infected
• Prevalence higher in developing countries • Prevalent in lower socioeconomic classes • Prevalent in AA and Hispanics • Infected pt usually asymptomatic |
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routes of transmission of h.pylori
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• Oral-oral
• Fecal-oral • Intrafamilial clustering • Instrumentation – endoscopes |
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what is the association btw. hp and pud?
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there are positive and negative arguments. can you remember what they are?
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positive:
•Increased prevalence of HP in PUD •Eradication promotes ulcer healing •Eradication decreases ulcer recurrence Negative: •Most people with HP are asymptomatic •HP persists but ulcers come and go •Drugs with no effect on HP heal ulcers |
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what are the non-pharmacologic measures of managing hp-pud?
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• Avoid irritating foods: spicy foods, fried food
• Avoid caffeine and alcohol • Stop smoking • Stress management |
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what are some factors to consider when giving agents to heal h. pylori?
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Efficacy: eradication rate, ulcer healing
Tolerability Drug interaction potential Antibiotic resistance Compliance: number of drugs, tolerability, duration Cost: medication cost, cost-effectiveness of treatment |
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what is the goal of healing h. pylori
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90% eradication with 1 week of therapy.
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what are the reinfection rates of h. pylori?
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adult (1% per year),
children (18% per year) |
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what are the drug regimens like for h. pylori?
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dual and triple.
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what's the problem with one drug regimens?
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no one drug gives 90% cure rate.
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describe the adv. and dsadv. of one drug regimens.
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-1 antibiotic with an antisecretory agent
̶Fewer adverse effects ̶Less drug doses/day ̶̶Since only one antibiotic, increases chance for resistance to occur |
2-4 week regimen
̶PPI > 2 weeks is recommended, but unnecessary unless complicated ulcer or GERD |
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describe the 3 drug regimen.
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̶ 10-14 days of therapy
̶ Shorter duration of therapy under investigation ̶ Less antibiotic resistance |
̶2 antibiotics with an antisecretory agent
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what are the two 3 drug regimens for h. pylori?
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Clarithromycin + omeprazole + amoxicillin (COA)
Metronidazole + omeprazole + clarithromycin (MOC) |
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when are only 4 drug regimens used?
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for pt failed 3drug regimen (MOC or COA) or pts with PCN allergy
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what are the dsadv. of 4 drug regimens?
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̶Increased incidence of adverse effects
̶Multiple drug doses per day ̶Non-compliance |
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don't interchange these antibiotics.
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Ampicillin and amoxicillin
Doxycycline and tetracycline Azithromycin and clarithromycin |
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you may interchange ppi's.
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true
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DO NOT interchange ranitidine bismuth citrate & bismuth subsalicylate.
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yes
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PPIs vs. H2RAs
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can't substitute h2ra's for ppi's. you know what i mean. ppi's are better than h2ra's so you can do that. but h2ras aren't better than ppi's so you can't do that.
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probiotics in h. pylori healing.
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̶Used to control H. pylori colonization in patients at risk
̶May play a role in decreasing mucosal inflammation and healing gastric ulcers ̶Low cost alternative that may increase eradication rates |
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describe tolerability of bismuth preparations.
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Black stools and tongue
Salicylate sensitivity and bleeding Constipation |
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tolerability of antibiotics.
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Diarrhea
C. difficile colitis Unpleasant taste (metronidazole, clarithromycin) Disulfiram-like reaction (metronidazole) Hypersensitivity reactions Drug interactions (clarithromycin, metronidazole) Use in pregnancy (avoid tetracycline, clarithromycin and metronidazole in the first trimester) Use in children (avoid tetracycline – stain teeth) |
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patient education of h. pylori drug regimens.
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•Cause – ulcers associated with bacteria
•Treatment – antibiotics and ulcer drugs •Administration – take PPI ½ hour before meals and all others with meals •Adverse effects – report intolerable effects •Complete treatment – even if feeling better •Compliance – increases effectiveness •Alarm symptoms – report bleeding, vomiting, and severe pain |
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NSAID use in the United States
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1.17 million people take NSAIDs regularly
3.73 million prescriptions per year for rheumatoid arthritis 4.13% of people 65 years or older use prescription NSAIDs regularly 5.Prescriptions cost about $1.7 billion annually 6.Widespread use of nonprescription NSAIDs |
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NSAID induced mucosal damage
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1.Total hospitalizations per year = 107,000
2.Deaths per year = 16,500 3.Total cost per year ($5,000 per hospitalization) = $535 million |
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Pattern of gastroduodenal injury due to injury.
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• Disruption of surface epithelium (almost everyone)
• Petechial hemorrhage (most people) • Adaptation and spontaneous resolution (most people) • Erosions and ulcers (small number) |
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what are the local and systemic effects of nsaid induced ulcers?
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local; direct damage of the mucosa
systemic; inhibition of prostaglandin synthesis |
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nsaids inhibit the cox enzyme, 1 and 2, of prostaglandin synthesis.
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yes
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• CLASS Trial
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long term data showed no difference between NSAID and Celecoxib rate of ulcer complications
•CV effects also shown no difference between NSAID and colecoxib |
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what's the dosing of cox-2 inhibitors?
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• !!!Use lowest dose possible for the shortest amount of time!!!
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clinical presentation of nsaid induced ulcers.
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•Often the typical symptoms of PUD do not occur
•Asymptomatic bleeding or perforation (especially in the elderly) •Poor correlation between symptoms and endoscopic findings |
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Risk factors for serious NSAID-induced GI complications
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•History of PUD or upper GI bleed
•Concomitant corticosteroid therapy •Anticoagulant treatment •High dose and/or long duration NSAID use •Older aged patient > 65 years •smoking •Poor general health (e.g. chronic major organ impairment) |
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how do you treat nsaid induced ulcers?
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stop the nsaid, treat with h2ra or ppi, large ulcers should be treated with a ppi and may require higher doses. if nsaid s can't be stopped definitely use a ppi.
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Strategies to minimize NSAID-induced injury
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•Discontinue or decrease NSAID dose
•Take NSAID with food or antacid •Switch to a less potent NSAID •Use enteric-coated aspirin or non-acetylated salicylate •Use acetaminophen (max 4g, exp pt on warfarin – 2g) |
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what are the two adjuncts to use to prevent nsaid induced injury?
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misoprostol and ppi's.
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this drug prevents NSAID-induced DU and GU
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misoprostol
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dose of misoprostol?
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200mcg TID or QID with food
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adverse effects of misoprostol?
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Diarrhea
Abdominal cramping Nausea All resolve with continued use Cut dose by half, titrate up again |
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CIs and warnings of misoprostol.
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Pregnant women – causes stimulation of uterus, causes miscarriage
Women of child-bearing age are required to take a pregnancy test before use and use contraception while on the medication Do not give with Mg-containing antacids – will cause worsening of diarrhea |
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cytotec
arthrotec |
misoprostol
misoprostol and diclofenac. |
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why are ppi's used over misoprostol in nsaid prevention of ulcers?
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due to misoprostols adverse effects.
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go over the risk level and guidelines table.
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ok
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Low risk of ulcers; definition/ guidelines
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No risk factors or age < 65 & no ASA, no prior ulcer, no hx of ulcer related GI complication
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Non selective NSAID or partially selective NSAID
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moderate risk of ulcers; definition/ guidelines
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1-2 risk factors (age > 65, low dose ASA, high dose NSAID)
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Non selective NSAIS or partially selective NSAID plus PPI or misoprostaol cotherapy; selective COX-2 inhibitor
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high risk of ulcers; definition/ guidelines
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≥ 3 risk factors or concomitant use of low dose ASA and either corticosteroids, warfarin or clopidogrel
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Non selective NSAIDS or partially selective NSAID plus PPI or misoprostol cotherapy
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very high risk of ulcers; definition/ guidelines
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Prior ulcer or ulcer related complication plus additional risk factors (eg age > 65, concomitant use of low dose ASA, corticosteroids, warfarin or clopidogrel
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Non selective NSAIS or partially selective NSAID plus PPI or misoprostaol cotherapy; selective COX-2 inhibitor plus PPI or misoprostol cotherapy; consider NSAID or COX-2 inhibitor if available plus PPI and misoprostol cotherapy
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• When taking misoprostol, explain warnings and cautions to women like what?
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Pregnant women – causes stimulation of uterus, causes miscarriage
Women of child-bearing age are required to take a pregnancy test before use and use contraception while on the medication |
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patient education of nsaids.
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• Advise patient to report alarm symptoms such as bleeding or vomiting
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Bleeding Peptic Ulcers; Approximately 80% of patients will stop bleeding spontaneously without recurrence.
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yes, Most morbidity and mortality occur among the remaining 20% who have continued or recurrent bleeding.
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1. Clinical predictors of increased risk for rebleeding included
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• age older than 65 years
• shock (BP<90) • poor overall health status/ comorbid illnesses • low initial hemoglobin level • melena (black tarry stools) • transfusion requirement • fresh red blood on rectal examination, in the emesis, or in the nasogastric aspirate |
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2. An increased risk for death due to rebleeding was associated with
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age older than 60 years
• continued bleeding or rebleeding (hemodynamically unstable) • or elevated urea, creatinine, or serum aminotransferase levels. |
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3. Rationale for acid-suppressant therapy
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they're bleeding in the stomach, and the high acid inhibits clot formation to stop the bleeding and the pepsin causes clot lysis.
platelet aggregation and coagulation optimal at pH 7.4 platelet aggregation impaired at pH<5.9 • gastric acid impairs ulcer healing • hypersecretion of gastric acid occurs in pt with bleeding ulcers |
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what to use in bleeding (20%) peptic ulcers? optimal dose?
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PPIs, 80mg bolus IVP followed by 8mg/h be used to reduce the risk of rebleeding in high-risk patients who have undergone endoscopy hemostasis
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H2RAs are competitive, reversible inhibitors of the histamine receptor, increasing doses are needed to maintain activity. PPIs, on the other hand, will not be affected by increased histamine release, as they inhibit acid secretion in its final pathway. The theoretical possibility of PPI-induced tolerance has been suggested although tolerance has not been demonstrated in clinical studies.
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yes
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the dose with the longest % of time above.
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80mg bolus IVP followed by 8mg/h
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what is Zollinger-Ellison Syndrome (ZES) ?
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A. Uncommon disease (<1%) characterized by gastric acid hypersecretion and formation of multiple, severe DUs and GUs
B. Related to a gastrin-producing tumor (gastrinoma) located most frequently in the duodenum or pancreas |
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what are the three treatments of ZES?
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PPIs (omeprozole), octreotide, tumor resection
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ppi used to treat zes?
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• Any PPI can be used at equipotent doses
• Starting dose of omeprazole is 60mg/day and should be adjusted to individual patient response • Doses should be divided and given every 8 to 12 hours • Doses as high as 360mg/day of omeprazole have been administered |
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octreotide used to treat ZES?
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•Directly inhibits acid secretion
•Inhibits the release of gastrin •100-250mcg SQ TID |
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two h. pylori tests that do not require endoscopy.
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serology and urea breath test.
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the three tests that require endoscopy.
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histology, culture, and urease (biopsy).
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cost of h. pylori tests are more with...
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endoscopy.
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Patient education on ulcers.
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•Cause – ulcers associated with bacteria
•Treatment – antibiotics and ulcer drugs •Administration – take PPI ½ hour before meals and all others with meals •Adverse effects – report intolerable effects •Complete treatment – even if feeling better •Compliance – increases effectiveness •Alarm symptoms – report bleeding, vomiting, and severe pain |
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patient education of nsaid induced ulcers.
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• Instruct on NSAID use to relieve arthritis
• Explain possible GI effects associated with NSAID use • Discuss ways to minimize or prevent NSAID-induced injury • Instruct when and how to take medications • Advise patient to report intolerable side effects • Discuss importance of compliance • Advise patient to report alarm symptoms such as bleeding or vomiting • When taking misoprostol, explain warnings and cautions to women |
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