Disorders of the stomach Flashcards
(35 cards)
1
Q
- What is the primary symptom indicating a stomach disorder
- What is dyspepsia?
- What is heartburn?
A
- Dyspepsia
- Epigastric pain or burning, early satiety, postprandial fullness
- Retrosternal pain or burning
2
Q
-What are possible differential diagnoses for dyspepsia?
A
-Gastritis Peptic Ulcer Disease (PUD) Food/Drug Intolerance/Allergy Idiopathic (Functional) GERD Pancreatic Disease Biliary Tract Disease Gastric or Esophageal Cancer Systemic Conditions
3
Q
- What is the etiology of gastritis?
- How does H. pylori cause gastritis?
A
-Erosive: medications, alcohol, stress
Non-erosive: H. pylori infection, systemic conditions
Gastritis can be acute or chronic
-It lives in outermost mucosal layer and invades epithelial layer. Causes an inflammatory response, triggering the releases of PMN’s and lymphocytes.
4
Q
- What are risk factors for erosive gastritis?
- Non-erosive?
- What is the clinical presentation of gastritis?
A
- NSAID use; alcohol use; hospitalized, critically ill patients (post-operative, mechanical ventilation, trauma)
- H. pylori present in 30-50% of population
- Dyspepsia, epigastric discomfort, N/V, anorexia, asymptomatic, hematemesis (with erosive type only, but not hemodynamically significant)
5
Q
- What will you find upon physical exam?
- What is the diagnostic work-up?
- How is the urea breath test administered?
A
-Unremarkable, possibly epigastric pain
-H. pylori: urea breath test, blood test, stool test; EGD: most accurate - biopsy confirms the diagnosis
-Urea Breath Test
Stop PPI’s, abx, bismuth 2 weeks prior
Ingests radioactive isotope urea solution
H. pylori converts urea into CO2 (tagged with isotope)
The patient exhales into “scintillation” fluid
Fluid is measured for tagged CO2
Commonly used to diagnose and confirm if treatment was successful
6
Q
-Potential complication of chronic gastritis?
A
-Ulceration, GI bleed, gastric lymphoma (H. pylori, small risk of this happening)
7
Q
-How do you manage NSAID gastritis?
-What is the most effective treatment in healing and prevention of NSAID related gastritis?
-What is the usual dose?
-
A
- Remove/reduce exposure: stop NSAID, reduce to lowest possible dose, take with meals
- Pharmacotherapy: PPI, Misoprostol, Sucralfate
- PPI’s
- 20-40 mg po daily x 2-4 weeks
8
Q
-How do you manage H. pylori associated gastritis?
A
-H. pylori eradication protocol
9
Q
-What other drug can be used in NSAID related gastritis and ulcer prevention?
A
-Misoprostol
10
Q
- What is the MOA of misoprostal?
- What are the dosage forms?
- What are the black box warning contraindications?
- What are the side effects?
- What kind of lab work must you obtain before prescribing this medication?
A
- Prostaglandin analog which inhibits gastric acid secretion and protects the GI mucosa
- Oral tabled (TID/QID dosing); combo form with NSAID
- Pregnancy, women desiring to become pregnant
- Most common it diarrhea, abdominal pain (stims contraction of intestinal smooth muscle); uterine contractions
- Pregnancy test on females
11
Q
- What is the MOA of sucralfate?
- What is it indicated for?
- How is it dosed?
- What are the adverse effects?
- Drug interactions?
A
- Stimulates PG synthesis of mucous and directly adheres to lining of stomach and forms a mucoprotective barrier adhering to ulcer and allowing them to heal
- NSAID induced gastritis/prophylaxis; stress gastritis/prophylaxis; PUD
- Tablet, oral suspension (1gm/10 mL), 1 gm QID
- Constipation is most common, hyperglycemia
- Can alter absorption of other drugs, do not take within 2 hours of other meds
12
Q
- What are the possible etiologies of PUD?
- What are the risk factors?
A
- H. pylori infection (m/c in duodenum), NSAIDS (m/c in stomach), Zollinger-Ellison
- NSAIDS (in combo with aspirin, corticosteroids and other drugs); age 60+; prior h/o PUD
13
Q
-What is the clinical presentation of someone with PUD?
A
- Epigastric Pain - Hallmark
- –Dull, aching, “hunger-like”
- —-Relief with food (duodenal) - recurs in 2 - 4 hrs
- ——-Highly variable
- —-Occur in intervals
- Nausea, Anorexia
- GI Bleed
- –May be asymptomatic until signs of bleeding
- —-Esp. with NSAID induced ulcers
- –Melena, Heme + stool,Coffee Ground Emesis
14
Q
- What is the procedure of choice for diagnosis of PUD?
- What are potential complication of PUD?
A
- EGD (also H. pylori testing)
- Bleeding, perforation, obstruction, malignancy (gastric ulcers)
15
Q
- What is the standard first line therapy for H. pylori eradication?
- If the patient has a PCN allergy, what should be substituted for the amoxicillin?
- What is the problem with standard therapy?
- What is the 2nd line treatment?
A
- Triple therapy: Omeprazol 20 mg BID (PPI), Clarithromycin 500mg BID, Amoxicillin 1 gm BID
- Metronidazole 500mg BID
- Clarithromycin resistance
- Quadruple therapy: PPI, Bismuth, Tetracycline, Metronidazole; also sequential therapy
16
Q
- How do you confirm eradication of H. pylori in a person with PUD?
- If triple therapy failed to eradicate the infection, what should you do?
- How do you confirm H. pylori eradication in a patient with PUD but without ulceration and H. pylori was the only cause?
A
- Urea breath test, or EGD
- Initiate quadruple therapy
- No need to confirm
17
Q
-How do you manage NSAID induced PUD ?
A
-PPI, misoprostol (same as for NSAID induced gastritis)
18
Q
- What can cause refractory ulcers in PUD?
- What must you remember to counsel patients on during treatment for PUD?
A
- Persistant H. pylori infection; continued NSAID use; hypersecretion disorders (Zollinger-Ellison); malignancy; they may require surgery
- Dietary modifications and side effects of pharmacotherapy
19
Q
- What are potential complications of PUD?
- What is the clinical presentation of a GI bleed?
- What lab studies would you do?
A
- GI bleed (50% of all UGI bleeds are due to PUD, 80% stop spontaneously, 7% mortality rate); Perforation; Penetration
- Dark stools, throwing up blood
- H/H
20
Q
How would you manage a GI bleed?
A
Hospitalize
- Hemodynamically stable (RBC’s if needed)
- IV High Dose PPI
- Emergent EGD - diagnostic & therapeutic
- –epinephrine injection
- –cauterization
- –clipping
- Remain hospitalized for at least 72 hrs
- –Reduces risk of rebleeding
21
Q
- How common are perforations in PUD patients?
- What is their clinical presentation?
- Diagnostic work-up?
- Management?
A
- <5%
- Sudden, severe abdominal pain; guarding and rebound tenderness on PE
- CBC (leukocytosis); abdominal x-ray
- Surgery
22
Q
- What is ulcerative penetration?
- Which other organs are most likely to be involved with a penetration?
- Clinical presentation?
- How do you make the diagnosis?
- Management?
A
- Ulcer extends into contiguous structures
- Pancreas, liver (from ulcers on the posterior duodenum or stomach)
- Gradual increasing pain that radiates to the back
- EGD to reveal ulceration, CT confirms penetration
- Surgery
23
Q
-What are possible etiologies of gastric outlet obstruction?
-Clinical presentation?
-PE findings?
Diagnostic work-up?
A
- PUD (less common now); Malignancy (most common distal gastric adenocarcinoma), benign masses (polyps)
- Postprandial N/V, epigastric pain, early satiety, abdominal distention
- Abdominal distention, epigastric tenderness, succussion splash
- Imaging studies; EGD to confirm cause of obstruction
24
Q
How would you manage a gastric outlet obstruction?
A
- NPO
- IV fluids
- –Parenteral nutrition if definitive treatment not imminent
- NG tube
- IV PPI
- Treatment of underlying cause
- –PUD - conservative treatment first, may need surgery
- –Mass - surgical removal
25
- What is delayed gastric emptying called?
- Epidemiology?
- Etiology?
- What are your differential diagnosis?
- Gastroparesis
- Most common in women and DM
- Idiopathic, DM, meds, surgery/nerve injury, scleroderma, post-viral
- Nausea, abdominal (epigastric) pain, early satiety, bloating, vomiting
- Obstruction, PUD
26
- What is the diagnostic work-up for gastroparesis?
| - How do you manage it?
- EGD to r/o mechanical obstruction; scintigraphic gastric emptying test to confirm diagnosis (but does not uncover the cause); blood tests as needed to look for cause
- Treat underlying cause (good glycemic control), dietary modification, pharmacotherapy
27
-What is the etiology of Zollinger-Ellison syndrome?
- Gastrin-secreting neuroendocrine tumors (gastrinomas)
- --Hypergastrinemia
- --Hypersecretion of gastric acid
- Arise in pancreas, duodenum, lymph nodes
- ⅔rds are malignant (carcinoid tumors)
- --Slow growing
- Most are solitary
- --Often associated with liver mets
- Can be associated with MEN 1(25%)
28
What is the clinical presentation of ZE syndrome?
-PUD (90% of patients with ZE, account for ,1% of patients with PUD, refractory PUD); GERD; diarrhea; weight loss
29
- What is the diagnostic work-up for patients with ZES?
- When would obtain a fasting serum gastrin level?
- Can an EGD make the diagnosis?
- How do you confirm the diagnosis?
- How long before taking serum gastrin levels must the patient stop taking PPI's?
- Diagnose with a fasting serum gastrin level
- Ulcers are refractory to standard therapy; large atypical appearing ulcers (>2 cm); multiple ulcers/frequent recurrences; ulcers associated with diarrhea, ulcers in patients who are H. pylori negative and not taking NSAIDS
- NO!!
- Secretin stimulation test
- 6 days
30
- What imaging studies would you use for work-up of ZES?
- How would you manage localized disease?
- Metastatic disease?
- CT, MRI, SPECT (to id tumor site/mets)
- Surgical resection (not effective in MEN 1
- PPI's, surgical resection/ablation of liver mets (prolong survival)
31
- What types of gastric tumors are benign?
| - Malignant types?
- Polyps
- --Inflammatory epithelial polyps
- --Adenomatous polyps (pre-malignant potential)
- Gastric adenocarcinoma; gastric lymphoma; gastric carcinoid tumors (from ZES)
32
- What are the etiology and risk factors for the intestinal type of gastric adenocarcinoma?
- What are the etiology and risk factors for the diffuse type of gastric adenocarcinoma?
- Most common; chronic H. pylori infection; smoking and high nitrate/salt diet; more common in advanced age
- Genetic mutations/hereditary
33
- What is the clinical presentation of gastric adenocarcinoma?
- PE findings?
-Asymptomatic until advanced, Dyspepsia, vague epigastric pain, Anorexia, weight loss, early satiety, Hematemesis, Masses causing obstruction (postprandial vomiting)
-Palpable gastric mass (20%)
Signs of metastasis
----Left supraclavicular lymph node
----Umbilical nodule (Sister Mary Joseph nodule)
----Rigid rectal shelf (Blumer shelf)
34
- What is the diagnostic work-up?
- Treatment?
- How do you know when to obtain an EGD?
- EGD is procedure of choice
- Surgical resection, chemotherapy and or radiation, palliative measures
- Over age 55 with new onset dyspepsia, anyone not responsive to PPI's
35
- What are primary and secondary gastric lymphoma?
- What is the most common risk factor for gastric lymphoma?
- Clinical presentation?
- How do you diagnose it?
- How do you treat it?
- Primary is from the gastric mucosa; secondary is nodal spread
- Chronic H. pylori infection
- Similar to gastric adenocarcinoma
- EGD with biopsy
- Radiation and/or chemo
