Disorders of the Stomach Flashcards

1
Q

Epigastric fullness or burning, early satiety, nausea, postprandial fullness; this is the hallmark of a stomach disorder

what is this sx?

A

dyspepsia

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2
Q

Retrosternal pain or burning, radiating to neck; this is the hallmark of GERD

what is this sx

A

heartburn

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3
Q

Conditions where there is epithelial or endothelial damage

A

Gastropathy

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4
Q

Denote conditions in which there is histological inflammation

A

Gastritis

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5
Q

EGD shows
Erythema
Red or black mucosal erosions
Petechial hemorrhages
Presence of blood vessels
Absence of rugal folds

what type of gastritis?

A

Erosive/Hemorrhagic

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6
Q

what category of gastritis is this

A

nonerosive

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7
Q

pathophys of erosive/hemorrhagic gastritis

A
  1. Recognized as acute
  2. hemorrhagic and erosive lesions develop shortly after exposure of gastric mucosa to injurious substances or reduction of mucosal blood flow= normal protective barrier disrupted
  3. acid and other substances penetrate into lamina propria
    - injury to vasculature, stimulate nerves
    - releasse histamine and other inflammatory mediators
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8
Q

causes of erosive gastritis

A
  1. Medications
  2. Alcohol
  3. Stress
    - Major risk factors:
    – Mechanical vent
    – Coagulopathy
    – Trauma
    – Burns
    – Shock/sepsis
    – CNS injury
    – Liver failure, kidney disease
    – Multiorgan failure
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9
Q

pt has
Anorexia
Epigastric pain
Heartburn
Nausea
Vomiting
Dyspepsia
hematemesis/“coffee ground”
Or melena

these s/s are for what dx?

A

erosive gastritis

can be asx
MC clinical manifestation is upper GI bleeding
Presents as hematemesis/“coffee ground”
Or melena

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10
Q

Erosive/Hemorrhagic gastritis Treatment

A
  1. Remove any causative agent
  2. limited course of acid suppression:
    - Proton Pump Inhibitor (PPI): Pantoprazole IV 80mg bolus, followed by 8mg/h continuous infusion
    — Add sucralfate suspension, 1g po q4-6h
  3. Endoscopy within 24 hours
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10
Q

work-up/diagnostics for erosive gastritis

A
  1. Upper Endoscopy (EGD) - most sensitive diagnosis
    - Have to distinguish between more serious lesions
  2. Done within 24 hrs of admission
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11
Q

management for NSAID gastritis

A
  1. Remove/Reduce exposure
    - Stop NSAID
    - Reduce to lowest possible dose
    - Take with meals
  2. Pharmacotherapy
    - PPI
    — Sucralfate (Carafate) as adjunct
    — Celecoxib (Celebrex) Cox-2 inh.
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12
Q

the most effective tx in healing and preention of NSAID related gastritis/ulcers is?

A

PPI
Omeprazole (Prilosec) 20 - 40mg po daily x 2-4 wks

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13
Q

Management: Stress related gastritis

A
  1. Stress-related mucosal erosions and subsequent hemorrhages may develop within 72 hours in critically ill patients
  2. Prophylaxis should be routinely administered to critically ill pt’s with risk factors for significant bleeding upon admission
    - Coagulopathy, sepsis, TBI, burns, liver disease
    - IV PPI’s: Pantoprazole 40mg/day or IV Omeprazole 60mg
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14
Q

cause of nonerosive gastritis

A
  1. H. pylori infection
  2. NSAIDS
  3. Systemic conditions
    - Autoimmune gastritis
    — Immune system attacks parietal cells in stomach, causing pernicious anemia
  4. Can be Acute or Chronic
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15
Q

Helicobacter Pylori is what type of bacteria? where does it live?

A

spiral gram-negative bacteria
lives in the outermost mucosal layer and invades the epithelial layer of the stomach mucosa

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16
Q

presentation of nonerosive gastritis

A

Dyspepsia/Epigastric Discomfort
N/V
Anorexia

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17
Q

complications with nonerosive gastritis

A
  1. patchy/diffuse atrophy of normal cardia, fundic, or antral mucosa
    - development of gastric intestinal metaplasia
    - dx histologically by presence of goblet cells/Paneth cells
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18
Q

Gastric intestinal metaplasia is believed to be an important precursor to ?

A

gastric cancer

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19
Q

PE for nonerosive gastritis

A

Unremarkable
Possible epigastric pain

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20
Q

work-up for nonerosive gastritis

A
  1. EGD - most accurate - bx confirms dx
  2. To help establish etiology
    - Urea Breath Test
    - Blood test
    - Stool test (fecal antigen test)
  3. <60 y/o with uncomplicated dyspepsia, initial noninvasive strategies
    - Noninvasive for H. Pylori
    — Urea breath test, fecal antigen test
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21
Q

what is the study of choice to diagnose nonerosive gastritis?

A

Upper endoscopy

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22
Q

indications for Upper endoscopy

A
  1. pts >60 with new onset dyspepsia
  2. younger pts with “alarm” sx (weight loss, rapidly progressive dysphagia, severe vomiting)
  3. sx fail to respond to initial therapy
  4. Family hx of GI cancer
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23
Q

H. Pylori produces an enzyme called _____, which breaks down urea into ammonia and Carbon dioxide

A

urease

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24
what is the urea breath test?
1. urea containing isotope tablet/solution is swallowed 2. If urease is present, breakdown into ammonia and CO2 will occur 3. As that passes through stomach = ammonium and bicarb = passed to bloodstream then lungs = pt expire CO2 4. Pt exhales into a scintillation fluid 5. If expiratory CO2 is “tagged” with urea isotope = H. Pylori Commonly used to sx and confirm if tx was successful
25
before a urea breath and fecal antigen test, what must be stopped beforehand?
Stop PPI’s, abx, bismuth 2 weeks prior
26
what type of antibodies are found in serologic testing for nonerosive gastritis?
IgG - most useful for monitoring treatment IgA - early infection do not have to discontinue PPI or abx prior to testing
27
tx for nonerosive gastritis
H. pylori 1. Omeprazole + Amoxicillin + Clarithromycin x 10-14 days 2. If allergies to amoxicillin, resistance to Clarithromycin, or tx failure: - Omeprazole + Bismuth + Tetracycline + Metronidazole
28
complications with gastritis
Ulceration GI Bleed Gastric Lymphoma (H. pylori)
29
A break in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall They develop and persist as a function of the acid-peptic activity in gastric juice
Peptic Ulcer Disease (PUD)
30
Peptic Ulcer Disease (PUD) occurs in what parts of the GI tract and at what ages?
1. Duodenum - 30-55 y/o 2. Stomach - Gastric ulcers 55-70 y/o
31
pathophys of PUD
A break in gastric or duodenal mucosa that arises when normal mucosal defensive factors are impaired or are overwhelmed by aggressive luminal factors such as acid or h.pylori Ulcers extend through muscularis mucosa and are >5mm in diameter
32
pathogenicity of PUD
1. H. pylori - M/C in duodenum 2. NSAIDS - M/C in stomach 3. Zollinger-Ellison
33
how do NSAIDs cause PUD?
block prostaglandin synthesis that helps protect mucosal layer of stomach lining
34
risk factors for PUD
1. NSAIDS - Long term use, combo with ASA, corticosteroids, or other drugs 2. Age > 60 3. Prior h/o PUD or H. Pylori infection 4. Smoking - Decreases healing rates - Impairs response to therapy - Increases chances to ulcer related complications
35
presentation of PUD
1. **_Epigastric Pain_** - **Hallmark** - Dull, gnawing, aching, “hunger-like” - 90 min - 3 hrs after eating - Relief with food or antacids - recurs in 2 - 4 hrs - Occur in intervals - for wks, then wks pain-free - **Nocturnal pain waking pt** - 11p-3am when circadian pattern of acid secretion is max 2. Nausea, Anorexia 3. Epigastric tenderness
36
PUD that is relieved with food or antacids is MC what type of ulcer?
duodenal ulcer
37
Procedure of Choice for PUD dx?
1. **_Upper Endoscopy_ w/ gastric mucosal bx** 2. H. pylori testing - fecal antigen assay or urea breath testing
38
indications for noninvasive assessment for H. pylori with fecal antigen assay or urea breath testing for PUD
- <60, no alarm features - With hx of peptic ulcer disease to diagnose active infections - pts following its tx to confirm eradication - bx not completed with EGD
39
tx for PUD
1. H. pylori - omeprazole + amoxicillin + clarithromycin x 10-14 d - alt: omeprazole + bismuth + tetracycline + metronidazole x 10-14 d - confirm eradication with urea breath test or EGD 4 wks after tx 2. NSAID-induced - PPI x 4-8 wks; DC NSAID
40
Once H. pylori eradication is confirmed, does the patient need continuous medication to prevent recurrence of PUD?
Do not need to continue meds to prevent recurrence Unless: 1. large (>2cm) ulcer 2. Failure to eradicate H. Pylori - Even after “salvage therapy” 3. Recurrent ulcers 4. Continued NSAID use MCC recurrence is unsuccessful eradication Should continue PPI for 4-6 wks after abx course
41
complications with PUD
1. GI bleed 2. perforation 3. penetration 4. gastric outlet obstruction
42
Pt that had PUD is now presenting with Melena - Dark, tarry, sticky stool containing partly digested blood Hematemesis - “Coffee grounds”’ or bright red blood upper gi tract source what is their complication?
GI bleed
43
work-up for GI bleed?
H/H
44
management for GI bleed?
1. Hospitalize, fluids 2. Hemodynamically stablity - Packed RBC 3. IV PPI - Protonix 4. Emergent EGD w/n 24 h - Render therapy - cautery, injection, endoclips, bands, EPI Recurrent bleeding may require surgery
45
pt with PUD is now experiencing _Sudden, severe abdominal pain_ Patients appear ill Rigid, Guarding & Rebound Tenderness on PE what is their complication
perforation
46
work-up for perforation (PUD)?
Hypotension develops later after bacterial peritonitis has developed CBC - leukocytosis Abdominal CT establishes diagnosis
47
management for perforation from PUD?
Surgery-laparoscopic perforation closure
48
where can PUD extend to if complications (penetration) happen
extends into contiguous structures - Pancreas, liver - From ulcers on posterior duodenum or stomach
49
pt with PUD is now experiencing Gradual increasing pain (radiates to back) Becomes severe and constant Unresponsive to antacids/food what is their complication?
penetration
50
work-up for PUD penetration?
EGD - reveal ulceration **CT - confirms penetration**
51
management for PUD penetration?
IV PPIs Surgery for those who do not improve
52
Due to edema or cicatricial narrowing of the pylorus or duodenal bulb Not as common what is this PUD complication?
Gastric Outlet Obstruction
53
pt with PUD is now experiencing Early satiety, vomiting, weight loss, epigastric fullness May develop dehydration what is this complication?
Gastric Outlet Obstruction
54
tx for Gastric Outlet Obstruction (PUD complication)
IV PPI, upper endoscopy, dilation of obstruction by hydrostatic balloons
55
indications for Misoprostol (Cytotec)
NSAID gastritis/ulcer prevention
56
MOA of Misoprostol (Cytotec)
Cytotec replaces protective prostaglandins that are consumed by NSAIDS inhibits gastric acid secretion and protects gastric mucosa
57
which med is used for pregnancy termination: used for labor induction
Misoprostol (Cytotec) Pregnancy, Women Desiring to Become Pregnant Pregnancy test: 2 wks prior to meds
58
SE of Misoprostol (Cytotec)
1. **Diarrhea** - Stimulates contraction of intestinal smooth muscle (abdominal pain) 2. Uterine contractions (abdominal pain/cramping)
59
indications for Sucralfate (Carafate)
NSAID induced gastritis/prophylaxis Stress gastritis/prophylaxis PUD
60
MOA of Sucralfate (Carafate)
Stimulates prostaglandin synthesis of mucous AND directly adheres to lining of stomach - forms mucoprotective barrier Adheres to ulcers, allowing them to heal
61
SE of Sucralfate (Carafate)
constipation
62
DDI of Sucralfate (Carafate)
Can alter the absorption of other drugs - do not take within 2 hrs of other meds Minimally systemically absorbed
63
causes of Gastric Outlet Obstruction
PUD Inflammatory bowel disease Malignancy m/c distal gastric adenocarcinoma Benign masses Polyps Pancreatitis Babies - Postnatal muscular hypertrophy of pylorus
64
presentation of Gastric Outlet Obstruction
1. Adults - Postprandial N/V - Epigastric Pain - Early Satiety - Abdominal Distention - Weight loss 2. Children - Postprandial vomiting ages 2-4 wks; can be as late as 12 wks - Infants hungry, fussy, nurse/feed avidly - “projectile vomiting” - Weight loss Both may show electrolyte abnormalities
65
PE of Gastric Outlet Obstruction
1. Adults - Abdominal Distention - Epigastric Tenderness - Succussion Splash (lay stethoscope over stomach, rock pt’s hips back and forth; if retained fluid has not passed through, will hear splashing sound) 2. Children - Upper abdomen distended with peristaltic waves - Palpable 5-15mm “**olive shaped mass**” present right upper abdomen; especially after vomiting - Dehydration
66
work-up for gastric outlet obstruction
1. Adults - Plain films will show enlarged gastric bubble and a dilated proximal duodenum - CT will confirm obstruction - **EGD to confirm dx and establish etiology** 2. Children - **Abd US imaging of choice** - Show hypoechoic muscle ring >4mm thickness with hyperdense center and pyloric channel length >15mm
67
Endoscopic features suggestive of GOO following nasogastric decompression include luminal narrowing of the stomach or duodenum what is this dx?
gastric outlet obstruction
68
Findings on abdominal CT scan include gastric distention, along with retained material within the gastric lumen and an associated air-fluid level what is this dx
gastric outlet obstruction
69
adult management for gastric outlet obstruction
1. NPO 2. IV fluids 3. NG tube - Remove any air/fluid before EGD 4. IV PPI 5. Tx of underlying cause - PUD - conservative treatment first, may need surgery - Mass - surgical removal
70
Longitudinal incision of the hypertrophic pylorus with blunt dissection to the level of the submucosa what is this intervention?
pyloromyotomy relieves constriction and allows normal passage of stomach contents into the duodenum Can be done laparoscopically
71
Delayed gastric emptying Food emptying from the stomach to small intestines what is this dx/term?
Gastroparesis
72
Gastroparesis is MC in who?
women and DM
73
causes of Gastroparesis
Idiopathic DM, Hypothyroidism Scleroderma Post-Viral Medications surgery /nerve injury
74
presentation of Gastroparesis
sx: Nausea Vomiting (1-3 hours after meals) Abdominal (Epigastric) Pain Early Satiety Bloating GERD/Regurgitation signs: epigastric distention or tenderness No guarding or rigidity +/- succussion splash
75
work-up for Gastroparesis
1. EGD - r/o mechanical obstruction 2. **Gastric emptying test - confirms dx** - Does not uncover CAUSE of gastroparesis - Blood tests as needed to look for CAUSE - ex. DM
76
management for Gastroparesis
1. Treat underlying cause - glycemic control - Avoid meds that decrease GI motility 2. Dietary Modification (low fat diet) 3. Pharmacotherapy - Prokinetic agents: Metoclopramide - Erythromycin - Induces high amplitude contractions
77
testing for Gastroparesis
Gastric Emptying test: 1. Documents presence of delayed gastric emptying and severity with scintigraphy 2. Pt given low-fat egg white meal tagged with radioactive material 3. scanner placed over abdomen 4. imaging immediately after ingestion: then again at 1, 2, and 4 hrs after ingestion - **Gastric retention >10% x 4 h**
78
causes of Zollinger-Ellison Syndrome
1. Gastrin-secreting neuroendocrine tumors (gastrinomas) - Hypergastrinemia/secretion of gastric acid 2. Arise in pancreas, duodenum, lymph nodes - Gastrinoma triangle: confluence of cystic and common bile ducts, neck of pancreas, and junction of 2nd and 3rd portion of duodenum) 3. ⅔ are malignant (carcinoid tumors) - Slow growing 4. MEN 1(25%) - Multiple small gastrinomas
79
work-up for Zollinger-Ellison Syndrome
1. **_Serum gastrin level (fasting)_** - **>10 x ULN + gastric pH <2** 2. +/- secretin stimulation test 3. CT, MRI - Identify tumor site/mets - Somatostatin Receptor Scintigraphy - Gastrinomas express somatostatin receptors that bind radiolabeled octreotide, which helps detects primary gastrinomas
79
presentation of Zollinger-Ellison Syndrome
1. PUD (90%) - **“Refractory” PUD** 2. Heartburn 3. wt loss - Gastric acid hypersecretion can cause direct intestinal mucosal injury and pancreatic enzyme inactivation, resulting in diarrhea, steatorrhea, and weight loss 4. Diarrhea sx are indistinguishable from other causes of PUD = May go undetected for years
80
indications for serum gastrin level (fasting) for Zollinger-Ellison Syndrome
1. Ulcers refractory to standard therapy 2. Large, atypical appearing ulcers (>2cm) 3. Multiple ulcers/frequent recurrences 4. Ulcers associated with diarrhea 5. Ulcers in pts who are H. pylori negative and who are not taking NSAIDS **Stop PPI’s 6 d prior to obtaining gastrin levels**
81
after a positive fasting gastrin level, what is the next step for Zollinger-Ellison Syndrome?
Confirm with _secretin stimulation test_ 1. Secretin administered IV 2. produces marked increase in gastrin in most with a gastrinoma 3. Samples of gastrin collected at -10, -1, 2, 5, 10, 15,20, and 30 minutes 4. The administration of secretin produces a marked increase in gastrin in most pts with a gastrinoma
82
management for Zollinger-Ellison Syndrome
1. Localized Disease - PPI’s - Surgical Resection 2. Metastatic Disease - The liver is the major metastatic site, bone is second - PPI’s - Surgical Resection/Ablation of Liver Mets - Prolong survival
83
benign Gastric Tumors
Polyps 1. Inflammatory epithelial polyps 2. Adenomatous polyps - premalignant potential
84
malignant Gastric Tumors
Gastric Adenocarcinoma Gastric Lymphoma Gastric Carcinoid Tumors (from Zollinger-Ellison)
85
causes/risk factors for gastric adenocarcinoma
1. **Adenocarcinomas** MC cancers of the stomach - Develop from the gland cells in the lining of the stomach 2. **_“Intestinal-type” MC_** - Chronic H. pylori infection - Smoking, high nitrate/salt diet - MC in advanced age 3. “Diffuse-type” - Genetic mutations/Hereditary - Spreads faster, difficult to treat
86
presentation of Gastric Adenocarcinoma
1. asx until advanced 2. Dyspepsia, vague epigastric pain 3. Anorexia, weight loss, early satiety 4. Hematemesis 5. Masses causing obstruction = postprandial vomiting 6. Palpable gastric mass (20%) 7. Signs of metastasis - Left supraclavicular lymph node (virchow’s node) - Umbilical nodule (Sister Mary Joseph nodule) - Rigid rectal shelf (Blumer shelf)
87
work-up for Gastric Adenocarcinoma
1. **EGD** - for >60 with new onset dyspepsia, anyone not responsive to ppi - Younger with “alarm” sx 2. Once diagnosed, CT of chest, abdomen, pelvis to delineate primary tumor/distal metastases
88
tx for Gastric Adenocarcinoma
Surgical Resection, Chemotherapy and or Radiation, Palliative Measures
89
how can gastric lymphomas be primary vs secondary?
primary - from gastric mucosa secondary - nodal spread Primary accounts for 3% of gastric cancers
90
MC risk factor for Gastric Lymphoma
Chronic H. pylori infection
91
presentation of Gastric Lymphoma
similar to gastric adenocarcinoma
92
dx and tx for gastric lymphoma
EGD with bx tx - radiation and/or chemotherapy