Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI: Clin Med IIA > Disorders of the Stomach > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

what is this sx

A

heartburn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Conditions where there is epithelial or endothelial damage

A

Gastropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Denote conditions in which there is histological inflammation

A

Gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what category of gastritis is this

A

nonerosive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

presentation of nonerosive gastritis

A

Dyspepsia/Epigastric Discomfort
N/V
Anorexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

gastric cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

PE for nonerosive gastritis

A

Unremarkable
Possible epigastric pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the study of choice to diagnose nonerosive gastritis?

A

Upper endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

urease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the urea breath test?

A
  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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

before a urea breath and fecal antigen test, what must be stopped beforehand?

A

Stop PPI’s, abx, bismuth 2 weeks prior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what type of antibodies are found in serologic testing for nonerosive gastritis?

A

IgG - most useful for monitoring treatment
IgA - early infection

do not have to discontinue PPI or abx prior to testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

tx for nonerosive gastritis

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

complications with gastritis

A

Ulceration
GI Bleed
Gastric Lymphoma (H. pylori)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

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

A

Peptic Ulcer Disease (PUD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Peptic Ulcer Disease (PUD) occurs in what parts of the GI tract and at what ages?

A
  1. Duodenum - 30-55 y/o
  2. Stomach - Gastric ulcers 55-70 y/o
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

pathophys of PUD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

pathogenicity of PUD

A
  1. H. pylori - M/C in duodenum
  2. NSAIDS - M/C in stomach
  3. Zollinger-Ellison
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how do NSAIDs cause PUD?

A

block prostaglandin synthesis that helps protect mucosal layer of stomach lining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

risk factors for PUD

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

presentation of PUD

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

PUD that is relieved with food or antacids is MC what type of ulcer?

A

duodenal ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Procedure of Choice for PUD dx?

A
  1. Upper Endoscopy w/ gastric mucosal bx
  2. H. pylori testing - fecal antigen assay or urea breath testing
38
Q

indications for noninvasive assessment for H. pylori with fecal antigen assay or urea breath testing for PUD

A
  • <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
Q

tx for PUD

A
  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
Q

Once H. pylori eradication is confirmed, does the patient need continuous medication to prevent recurrence of PUD?

A

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
Q

complications with PUD

A
  1. GI bleed
  2. perforation
  3. penetration
  4. gastric outlet obstruction
42
Q

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?

A

GI bleed

43
Q

work-up for GI bleed?

A

H/H

44
Q

management for GI bleed?

A
  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
Q

pt with PUD is now experiencing
Sudden, severe abdominal pain
Patients appear ill
Rigid, Guarding & Rebound Tenderness on PE

what is their complication

A

perforation

46
Q

work-up for perforation (PUD)?

A

Hypotension develops later after bacterial peritonitis has developed
CBC - leukocytosis
Abdominal CT establishes diagnosis

47
Q

management for perforation from PUD?

A

Surgery-laparoscopic perforation closure

48
Q

where can PUD extend to if complications (penetration) happen

A

extends into contiguous structures
- Pancreas, liver
- From ulcers on posterior duodenum or stomach

49
Q

pt with PUD is now experiencing
Gradual increasing pain (radiates to back)
Becomes severe and constant
Unresponsive to antacids/food

what is their complication?

A

penetration

50
Q

work-up for PUD penetration?

A

EGD - reveal ulceration
CT - confirms penetration

51
Q

management for PUD penetration?

A

IV PPIs
Surgery for those who do not improve

52
Q

Due to edema or cicatricial narrowing of the pylorus or duodenal bulb
Not as common

what is this PUD complication?

A

Gastric Outlet Obstruction

53
Q

pt with PUD is now experiencing
Early satiety, vomiting, weight loss, epigastric fullness
May develop dehydration

what is this complication?

A

Gastric Outlet Obstruction

54
Q

tx for Gastric Outlet Obstruction (PUD complication)

A

IV PPI, upper endoscopy, dilation of obstruction by hydrostatic balloons

55
Q

indications for Misoprostol (Cytotec)

A

NSAID gastritis/ulcer prevention

56
Q

MOA of Misoprostol (Cytotec)

A

Cytotec replaces protective prostaglandins that are consumed by NSAIDS
inhibits gastric acid secretion and protects gastric mucosa

57
Q

which med is used for pregnancy termination: used for labor induction

A

Misoprostol (Cytotec)

Pregnancy, Women Desiring to Become Pregnant

Pregnancy test: 2 wks prior to meds

58
Q

SE of Misoprostol (Cytotec)

A
  1. Diarrhea - Stimulates contraction of intestinal smooth muscle (abdominal pain)
  2. Uterine contractions (abdominal pain/cramping)
59
Q

indications for Sucralfate (Carafate)

A

NSAID induced gastritis/prophylaxis
Stress gastritis/prophylaxis
PUD

60
Q

MOA of Sucralfate (Carafate)

A

Stimulates prostaglandin synthesis of mucous AND directly adheres to lining of stomach - forms mucoprotective barrier
Adheres to ulcers, allowing them to heal

61
Q

SE of Sucralfate (Carafate)

A

constipation

62
Q

DDI of Sucralfate (Carafate)

A

Can alter the absorption of other drugs - do not take within 2 hrs of other meds
Minimally systemically absorbed

63
Q

causes of Gastric Outlet Obstruction

A

PUD
Inflammatory bowel disease
Malignancy
m/c distal gastric adenocarcinoma
Benign masses
Polyps
Pancreatitis

Babies - Postnatal muscular hypertrophy of pylorus

64
Q

presentation of Gastric Outlet Obstruction

A
  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
Q

PE of Gastric Outlet Obstruction

A
  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
Q

work-up for gastric outlet obstruction

A
  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
Q

Endoscopic features suggestive of GOO following nasogastric decompression include luminal narrowing of the stomach or duodenum

what is this dx?

A

gastric outlet obstruction

68
Q

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

A

gastric outlet obstruction

69
Q

adult management for gastric outlet obstruction

A
  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
Q

Longitudinal incision of the hypertrophic pylorus with blunt dissection to the level of the submucosa

what is this intervention?

A

pyloromyotomy

relieves constriction and allows normal passage of stomach contents into the duodenum
Can be done laparoscopically

71
Q

Delayed gastric emptying
Food emptying from the stomach to small intestines

what is this dx/term?

A

Gastroparesis

72
Q

Gastroparesis is MC in who?

A

women and DM

73
Q

causes of Gastroparesis

A

Idiopathic
DM, Hypothyroidism
Scleroderma
Post-Viral
Medications
surgery /nerve injury

74
Q

presentation of Gastroparesis

A

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
Q

work-up for Gastroparesis

A
  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
Q

management for Gastroparesis

A
  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
Q

testing for Gastroparesis

A

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
Q

causes of Zollinger-Ellison Syndrome

A
  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
Q

work-up for Zollinger-Ellison Syndrome

A
  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
Q

presentation of Zollinger-Ellison Syndrome

A
  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
Q

indications for serum gastrin level (fasting) for Zollinger-Ellison Syndrome

A
  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
Q

after a positive fasting gastrin level, what is the next step for Zollinger-Ellison Syndrome?

A

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
Q

management for Zollinger-Ellison Syndrome

A
  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
Q

benign Gastric Tumors

A

Polyps

  1. Inflammatory epithelial polyps
  2. Adenomatous polyps - premalignant potential
84
Q

malignant Gastric Tumors

A

Gastric Adenocarcinoma
Gastric Lymphoma
Gastric Carcinoid Tumors (from Zollinger-Ellison)

85
Q

causes/risk factors for gastric adenocarcinoma

A
  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
Q

presentation of Gastric Adenocarcinoma

A
  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
Q

work-up for Gastric Adenocarcinoma

A
  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
Q

tx for Gastric Adenocarcinoma

A

Surgical Resection, Chemotherapy and or Radiation, Palliative Measures

89
Q

how can gastric lymphomas be primary vs secondary?

A

primary - from gastric mucosa
secondary - nodal spread
Primary accounts for 3% of gastric cancers

90
Q

MC risk factor for Gastric Lymphoma

A

Chronic H. pylori infection

91
Q

presentation of Gastric Lymphoma

A

similar to gastric adenocarcinoma

92
Q

dx and tx for gastric lymphoma

A

EGD with bx
tx - radiation and/or chemotherapy

GI: Clin Med IIA (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions