Dz of Stomach and Duodenum Flashcards
Dyspepsia
- sx
- degree of sx does not correlate with degree of mucosal abnormalities, T/F?
sx: indigestion, chronic/recurrent pain in upper abd, upper abd fullness, early satiety, bloating, belching, nausea, heartburn.
True!!!
Gastritis:
- what is this?
- types & common causes
- sx
What:
-inflammatory changes in the gastric mucosa
Types:
-erosive and hemorrhagic: stress, NSAIDS, and alcoholic gastritis, portal htn
-nonerosive, nonspecific gastritis: h. pylori, pernicious anemia, eosinophilic gastritis
Sx:
- asymptomatic
- anorezia, epigastric pain, n/v, upper GI bleeding
Erosive Hemorrhagic gastritis
- signs
- workk up
signs: –signs: melena (dark sticky feces), coffee ground emesis
Work uP: CBC, serum iron
*Go to test: upper endoscopy
Errosive Hemorrhagic: Stress Gastritis
- risk factors
- tx
Risk factors:
- INR greater than 1.5 and platelets less than 50,000
- need mechanical ventillation greater than 48hrs
- trauma, burns, shock
- sepsis, liver failure, kidney dz
- multiorgan failure
- CNS injury
Tx:
- enteral nutrition
- IV/PO PPI (omeprazole, pantoprazole) are best
- VI or PO H2 blockers (cimetidine, ranitidine); not as good as PPI.
- sucralfate PO (antacid)
- endoscopy
Errosive hemorrhagic: NSAID Gastritis:
- Is Cox1 or Cox2 most likely to cause gastritis?
- tx
- prevention of another ulcer after healing
- risk factors
Cox 2 inhibitors have a much lower incidence of significant ulcer formation, so Cox1 one is most likely to cause gastritis.
Tx:
- stop offending agent
- H2 blockers of PPI
Prevention:
- long term PPI therapy if NSAID must be continued
- prescribe NSAIDS at lowest dose and shortest duration possible
- use cox-2 inhibitor instead of a non-selective NSAID if no significant CV.
Risk factors:
- greater than 60YO
- hx of PUD
- aspirin or any other ASA or antiplatelet therapy
- oral glucocorticoid use
Errosive, hemorrhagic; NSAID Gastritis:
- red flag sx
- tx for red flag sx
- tx for non-red flag sx
Red flag;
- severe pain
- weight loss
- vomiting
- GI bleeding
- anemia
Tx: refer for upper endoscopy
Tx non-red flag:
- discontinue NSAIDS
- PPI 2-4wks
- if no improvement within 2 wks refer for endoscopay
Erosive Hemorrhagic: ETOH Gastritis:
- pathophysiology
- sx
- tx
Pathophys:
-alcohol disrupts the mucosal barrier, alcohol and aspirin together increase the permeaability of the gastric mucosal barrier and cellular damage occur
Sx:
-dyspepsia, n/v, minor hematemesis
Tx:
H2 blockers of PPIs
-and sucralfate 2-4 wks
-decrease ETOH consumption
Errosive hemorrhagic: Portal HTN Gastropathy
- what is this?
- tx
What: portal htn leads to congestion of gastric vessels
Tx: propranolol or nadolol to lower the portal pressures
Nonerosive, nonspecific Gastritis: H. Pylori
- gram+/-, shape?
- MOA
- transmission
- sx
Spiral gram negative rod
MOA:
- lives beneath the gastric mucous layer next to gastric epithelial cells. secretes urease and enables them to produce ammonia to buffer the acid. Cuases gastric mucosal inflamm.
- usually non-errosive but can cross the threshold and become errosive.
-fecal oral spread, contaminated water supply
sx:
- asymptomatic
- others may have alteration in acid production and increased gastrin leading to ulcers and CA.
Non-errosive gastritis:
H. Pylori
-dx testing
-tx
Dx:
- serology: IgG aby testing
- urea breath test* (tests for active infection)
- stool Ag teseting* (test for active infection)
- endoscopic bx
Tx:
-eradication therapy;
2-3 Abx + PPI
Non-errosive: Pernicious Anemia gastritis:
-MOA
MOA: autoabys to gastric gland parietal cells and intrinsic factor. Gastric gland and mucosal atrophy causes loss of acid production.
Non-errosive: Eosinophillic gastritis
- pathophys
- sx
- dx
- tx
pathophys: infiltration of eosinophils into GI tissue
sx: abdominal pain, n/v, early satiety, diarrhea
dx: bx
Tx: elimination diet, may need steroids.
Peptic Ulcer Dz
- what is this?
- cause
- MC in who?
- Duodenal and gastric ulcers MC in what ages?
What; break in the gastric or duodenal mucosa, must be greater than 5mm in diameter and extend through the muscularis mucosae. May be gastric or duodenal ulcer.
Cause: too much acid or pepsin
- NSAIDS
- H. pylori
- Zollinger-ellison syndrome
- CMV
- Crohns
- lymphoma
- idiopathic
PUD MC in smokers and NSAID users
Duodenal ulcers MC in 30-55yo
Gastric Ulcer MC 55-70YO
PUD:
- clinical presentation
- PE
Presentation:
- dyspepsia
- pain in epigastric area (gnawing, dull, aching, hunger like)
- nausea, anorexia
- pain may be relieved with food or antacids and returns 2-4hrs later
PE:
- often normal
- may have epigastric tenderness to deep palpation
- FOBT or FIT may be positive
PUD:
- work up
- tx
Work up:
- CBC, FOBT/FIT
- Upper endoscopy**(Test of choice)
- barium upper GI series
- abd CT if ulcer perforation suspected
- bx samples tested for H pylori infection and evaluated for malignancy
Tx:
- PPI***(faster sx relief and promotes fastest ulcer healing)
- H2 blockers (take at bedtime)
- 2nd line agents:
- -bismuth (pepto-bismol)
- -cytotec (prostaglandin e1 analog)
- -antacids
H. pylori
- tx
- how do we make sure the infection has cleared?
Tx: *combination therapy is necessary
- 2-3abx + PPI or bismuth
- if large or complicated ulcer continue for up to 6wks post completion of abx.
You retest; but it must be done greater than 4 weeks post abx therapy and greater than 2wks post discontinuation of PPI.
–Retest using Urea breath test, fecal ag, or endscopy w/ bx
Zollinger-Ellison Syndrome
- What is this?
- causes
- MC primary tumor site
- malignant or benign?
- Presentation
What: gastrin secreting gut neuroendocrine tumor
Causes:
-hypergastrinemia from increase acid secretion
Primary Tumors: MC is duodenal wall within the gastrinoma triangle.
2/3 are malignant, most are resectable.
Presentation:
- dyspepsia
- peptic ulcers
- doudenal ulcers
- diarrhea, steatorrhea, weight loss
Zollinger-ellison syndrome
- imaging studies
- tx
Imaging: SPECT Somatostatin receptor scintigraphy (SRS)*** (nuclear med study)
-CT and MRI for eval for hepatic metastases and primary lesions.
Tx:
- Metastatic dz: PPI’s to decrease acid hypersecretion
- localized dz: resection is only cure (15year survival rate)
Gastroparesis:
- what is this?
- causes
- sx
- PE
- work up
- tx
What: delayed gastric emptying in the absence of a mechanical obstruction
Causes:
-MC is idiopathic, diabetes, post surgical, viral, meds, neurologic dz, autoimmune
Sx:
-nausea, vomiting, early satiety, bloating, upper abd pain
PE:
- epigastric tenderness but no gaurding or rigidity
- abd distension
- scleroderma and DM
Work up:
- Upper endoscopy
- CT enterography or MRI
- assess gastric motility with scintigraphic gastric emptying
Tx:
- dietary modifications; small frequent meals, low fat, avoid insoluble fiber, etoh, tobacco.
- hydration
- vit supplementation
- optimize glycemic control
- prokinetics (reglan/metoclopramide & erythromyciin)
- anti-emetics; diphenhydramine, promethazine, can use 1st gen 5HT3 antagonist such as Zofran, kytril, anzemet
*refractory cases: surgical treatment; gastrostomy tube for decompression and jejunostomy for feeding.
Diabetic gastroparesis MC in Type 1 or 2?
Viral gastroparesis: sx duration, causes
Common medications that delay gastric emptying
Post-surgical gastroparesis: cause
MC in Type 1
Viral: sx duration is 1 year, cause:
- norwalk, rotavirus
- CMV, EBV, VZV
Common medications:
- narcotics
- TCA
- Ca 2+ blockers
- dopamine agonist
- Phenothiazines (antipsychotics, antiemetics)
Post-surgical gastroparesis causes:
- injury to vagus nerve
- gastrectomy
- fundoplication* MC cause*
- lung/heart transplant
- variceal scleropathy
- botuliunum toxin injection