Disorders of the stomach - Exam 3 Flashcards

1
Q

_____ cells secrete mucus

_____ cells secrete gastric acid

____ cells secrete pepinsogen

A

goblet secrete mucus

parietal secrete gastric acid

chief cells secrete pepsinogen

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2
Q

What are the 3 layers of the stomach mucosa?

A

epithelial layer

lamina propria

muscularis mucosa

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3
Q

What is dyspepsia? this symptom is the hallmark symptom of _______

A

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

hallmark symptom of a stomach disorder

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4
Q

What is the difference between gastropathy and gastritis?

A

Gastropathy: Conditions where there is epithelial or endothelial DAMAGE

gastritis: Denote conditions in which there is histological INFLAMMATION

but practically are used interchangably

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5
Q

What are the two categories of gastritis? What are the. major differences?

A

erosive/hemorrhagic: think acute and rugae are smooth

nonerosive: think chronic and rugae are more present

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6
Q

What is the pathophys behind erosive gastritis?

A

Characterized by hemorrhagic and erosive lesions that develop shortly after exposure of the gastric mucosa to injurious substances or reduction of mucosal blood flow resulting in a damaged normal protective barrier. Now other substances can penetrate into the lamina propria

causes injury to vasculature, nerves and causes a release of histamine and other inflammatory mediators

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7
Q

What are 3 major causes of erosive gastritis?

A

medications, alcohol and stress

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8
Q

What does “stress gastritis” mean? Which medication most commonly causes erosive gastritis?

A

Stress related mucosal erosions related to clinically ill patients: d/t inadequate gastric mucosal blood flow during periods of intense physiologic stress

NSAIDs due to the decrease in prostaglandins

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9
Q

NSAIDs are a ______ medication and cause a decrease in _________

A

COX 1 inhibitors and they decrease prostaglandins which is vital as part of the stomach’s natural defenses against acid

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10
Q

Anorexia
Epigastric pain
Heartburn
Nausea
Vomiting
Dyspepsia
upper GI bleed

What am I?
**What is the MC clinical manifestation?

A

erosive gastritis

upper GI bleed

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11
Q

What does an upper GI bleed commonly present as?

A

Presents as hematemesis/“coffee ground”
Or melena

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12
Q

**What is the most sensitive method of diagnosis for erosive gastritis? When does it need to be done? What will the results show?

A

EGD

Done within 24 hours of admission

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

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13
Q

What is the tx for generic erosive gastritis?

A
  1. Remove any causative agent
  2. Employ limited course of acid suppression with a
    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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14
Q

What is the tx of NSAID related gastritis?

A
  1. stop/reduce NSAID
  2. PPI with sucralfate: Omeprazole (Prilosec) 20 - 40mg po daily x 2-4 wks
  3. switch to COX 2 inhibitor (if possible)
    - celecoxib (celebrex)
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15
Q

What is the recommended COX -2 inhibitor as a option instead of taking NSAIDs?

A

Celecoxib (Celebrex) Cox-2 inh.

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16
Q

What is the most effective treatment in healing and preventing NSAID related gastritis/ulcers?

A

PPI!!

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17
Q

What is the tx for stress related gastritis? When does it tend to show up in critically ill pts?

A

IV PPI’s: Pantoprazole 40mg/day or IV Omeprazole 60mg to reduce risk for GI bleeding

may develop within 72 hours in critically ill patients

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18
Q

What are some common causes of nonerosive gastritis?

A

H. pylori infection
NSAIDS
Systemic conditions: autoimmune gastritis

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19
Q

What is happening in autoimmune gastritis?

A

Immune system attacks parietal cells in stomach, causing pernicious anemia

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20
Q

**Where is H pylori commonly found? What is the MC pt type?

A

H. Pylori is a spiral gram-negative bacteria that lives in the outermost mucosal layer

**most likely to occur in children who live in crowded conditions and areas with poor sanitation.

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21
Q

What does H. pylori cause?

A

It causes an inflammatory response, triggering the release of polymorphonuclear leukocytes (PMNs) and lymphocytes, which will = gastric mucosal inflammation. Pain usually subsides over a few days and then will progress to chronic

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22
Q

Dyspepsia/Epigastric Discomfort
N/V
Anorexia
can be asymptomatic
possible epigastric pain

What am I?
How is it diagnosed? Why is this important?

A

nonerosive gastritis

EGD with bx histologically by the presence of goblet cells/Paneth cells

Gastric intestinal metaplasia is believed to be an important precursor to gastric cancer

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23
Q

What are 3 tests that be helpful when trying to determine etiology of nonerosive gastritis?

A

Urea Breath Test
Blood test
Stool test (fecal antigen test)

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24
Q

In patients younger than age 60 with uncomplicated dyspepsia, what should you order first?

A

Urea breath test, fecal antigen test to look for noninvasive H. Pylori before ordering EGD

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25
Q

When would you want to order an EGD if concerned about nonerosive gastritis?

A

Upper endoscopy reserved for pts over 60 with new onset dyspepsia

Selected younger pts with “alarm” symptoms (weight loss, rapidly progressive dysphagia, severe vomiting)

When symptoms fail to respond to initial therapy

Family hx of GI cancer

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26
Q

How does the urea breath test work? When do you use it?

A

used as to dx H. Pylori

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27
Q

**What is the urea breath test pt education before the pt has the test?

A

**Stop PPI’s, abx, bismuth 2 weeks prior

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28
Q

besides the urea breath test, what is an additional non-evasive test used to dx H. pylori? **What is the pt education prior to this test?

A

fecal antigen test

**No PPI or abx 2 weeks prior to testing

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29
Q

What is the 3rd option for noninvasive testing for H. pylori? What is the pro and con?

A

serologic testing

pro: do not have to stop abx or PPI prior to testing

con: expensive!!

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30
Q

**What is first line H. pylori treatment?

A
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31
Q

**What is the tx for H. Pylori If allergies to amoxicillin, resistance to Clarithromycin, or triple therapy treatment failure?

A
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32
Q

What are the pt criteria to start quadruple therapy instead of triple therapy in H. Pylori? IN what circumstances should you treat with IV therapy?

A

If allergies to amoxicillin, resistance to Clarithromycin, or treatment failure

patients with bleeding ulcers can be given IV treatment

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33
Q

What are 3 complications from chronic gastritis?

A

Ulceration
GI Bleed
Gastric Lymphoma (H. pylori)

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34
Q

______ is the MC cause of gastric lymphoma?

A

H. Pylori

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35
Q

How does the natural protection of stomach mucosa work?

A

mucous cells secrete a combination of mucus and bicarb to protect the mucosa from autodigestion by HCl

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36
Q

What is happening in PUD? If your patient is between 30-55, where is the most common place? If your patient is between 55-70, where is the most common place?

A

A break in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall

**30-55: duodenum

**55-70: stomach

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37
Q

**In PUD, by definition ulcers extend through the _____ and are usually _____ in diameter

A

muscularis mucosa

over 5mm

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38
Q

What are the 3 common causes of PUD? Which one is MC in the duodenum? MC in the stomach?

A

H. pylori infection: M/C in duodenum

NSAIDS: M/C in stomach

Zollinger-Ellison

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39
Q

______ block prostaglandin synthesis that helps protect mucosal layer of stomach lining. What does it lead to?

A

NSAIDS

peptic ulcer disease

40
Q

What are the 4 risk factors for PUD?

A

NSAIDs

older than 60

Prior h/o PUD or H. Pylori infection

smoking

41
Q

** What is the hallmark presentation for PUD? Describe the pattern. When does it occur?

A

Dull, gnawing, aching, “hunger-like” that starts approx 1.5-3 hours after eating

cyclical presentation: Symptoms for weeks, then weeks pain free

nocturnal pain waking the pt

42
Q

What is the diagnostic of choice for PUD? What may also be done?

A

EGD with bx establishes dx

Noninvasive assessment for H. pylori with fecal antigen assay or urea breath testing may be done in patients

43
Q

What is the tx for PUD? What is PUD is H.pylori?

A

Different Treatments Depending on Cause of PUD

triple therapy: omeprazole, amoxicillin and clarithromycin for 10-14 days

44
Q

When do you need to avoid giving Clarithromycin as part of triple therapy for H. Pylori?

A

***avoid in settings where h.pylori resistance to Clarithromycin is > 15%

45
Q

What do you need to do once the pt has completed H. pylori therapy for PUD?

A

Confirm eradication with urea breath test or EGD 4 weeks after therapy

46
Q

Under what circumstances does the pt need to continue therapy for PUD? How long do pts need to continue _____?

A

Pt was diagnosed with large (>2cm) ulcer

Failure to eradicate H. Pylori: Even after “salvage therapy”

Recurrent ulcers

Continued NSAID use

Should continue PPI for 4-6 weeks after antibiotic course

47
Q

What is the MC cause of H. Pylori PUD recurrence?

A

The most common cause of recurrence is unsuccessful eradication

48
Q

What is the tx for NSAID induced PUD?

A

4-8 week course PPI
Remove offending agent if possible

if the pt cannot stop NSAID: PPI is recommended for as long as the NSAID is being used

49
Q

up to 50% of GI bleeds are due to ______. What is the clinical presentation? What lab study do you need to order?

A

Up to 50% of all UGI bleeds d/t PUD

**melena and hematemsis

hemoglobin and HCT to check RBC

50
Q

** What is the tx for a GI bleed?

A
51
Q

What is a VERY severe complication of PUD? How do they present? What will you expect to find on PE?

A

perforation

sudden and severe abdominal pain!!!

Rigid, Guarding & Rebound Tenderness on PE

52
Q

What need to be part of your work up for a pt with stomach perforation? ____ establishes diagnosis. What is the management?

A

CBC

Abdominal CT establishes diagnosis

Surgery-laparoscopic perforation closure

53
Q

What will the diagnostic tool of choice show for a pt with stomach perforation?

A

abdominal CT will show free air in the anterior peritoneal space indicating some sort of perforation

54
Q

What are 3 complications of PUD?

A

perforation

penetration to other organs

gastric outlet obstruction

55
Q

What will penetration due to PUD present like? How do you dx? What is the management?

A

Gradual increasing pain (radiates to back)
Becomes severe and constant
Unresponsive to antacids/food

EGD to reveal ulceration and CT will CONFIRM penetration

management:
IV PPIs
Surgery for those who do not improve

56
Q

Early satiety, vomiting, weight loss, epigastric fullness
May develop dehydration

What am I?
What is the underlying cause?
What is the tx?

A

gastric outlet obstruction

Due to edema or cicatricial (scarring) narrowing of the pylorus or duodenal bulb

tx: IV PPI, upper endoscopy, dilation of obstruction by hydrostatic balloons- depends on how sick the pt presents

57
Q

______ MOA replaces protective prostaglandins that are consumed by NSAIDS. Also inhibits gastric acid secretion and protects gastric mucosa. What are the indications?

A

Misoprostol (Cytotec)

NSAID gastritis/ulcer prevention

58
Q

** What is the BBW for Misoprostol (Cytotec)?

A

Pregnancy!! Women Desiring to Become Pregnant because it is used in pregnancy termination and used in labor induction

59
Q

What are the SE of Misoprostol (Cytotec)? What test do you need to order 2 weeks before?

A

diarrhea and abdominal pain/cramping

need to order pregnancy test 2 weeks before

60
Q

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

A

Sucralfate (Carafate)

61
Q

What is the MC SE of sucralfate? What is the pt education point?

A

Constipation

Can alter the absorption of other drugs - do not take within 2 hours of other medications

62
Q

What is the MC malignanct cause of gastric outlet obstruction? What is it called in babies?

A

distal gastric adenocarcinoma

pyloric stenosis due to hypertrophy muscle

63
Q

Postprandial N/V
Epigastric Pain
Early Satiety
Abdominal Distention
Weight loss

What am I?
**What is the highlighted s/s?

A

Gastric Outlet Obstruction in adults

**Postprandial N/V

64
Q

Postprandial vomiting between ages 2 and 4 weeks; can be as late as 12 weeks
Infants hungry, fussy, nurse/feed avidly
Often “projectile vomiting”
Weight loss

What am I?
**What is the highlighted s/s?

A

pyloric stenosis in children

**Often “projectile vomiting”

65
Q

What are both children and adults at high risk for if they have a gastric outlet obstruction?

A

Both children and adults may show electrolyte abnormalities d/t persistent vomiting

66
Q

What will the PE of adults with gastric outlet obstruction present like? **What is a common PE finding in children with pyloric stenosis?

A

Abdominal Distention
Epigastric Tenderness
Succussion Splash

**Palpable 5-15mm “olive shaped mass” present in RIGHT upper abdomen, especially after vomiting

67
Q

adults with gastric outlet obstruction what need to be part of their diagnostic work-up? **What confirms dx? What will each show?

A

Plain films: enlarged gastric bubble and a dilated proximal duodenum

CT will confirm obstruction: gastric distention, along with retained material within the gastric lumen and an associated air-fluid level

**EGD to CONFIRM diagnosis and establish etiology

luminal narrowing of the stomach or duodenum

68
Q

** What is the imaging of choice for a child with pyloric stenosis? What will it show?

A

Abdominal ultrasound imaging of choice

Show hypoechoic muscle ring greater than 4mm thickness with hyperdense center and pyloric channel length greater than 15mm

69
Q

What is the management for a gastric outlet obstruction in an adult?

A
70
Q

What is the tx for a child with pyloric stenosis?

A
71
Q

What is gastroparesis? What is the MC pt?

A

Delayed gastric emptying
Food emptying from the stomach to small intestines

M/C in women & DM

72
Q

Nausea
Vomiting (1-3 hours after meals)
Abdominal (Epigastric) Pain
Early Satiety
Bloating
GERD/Regurgitation

What am I?
What will the PE show?

A

gastroparesis

May reveal epigastric distention or tenderness but NO GUARDING or rigidity, may have succussion splash

73
Q

What needs to be including as part of the pt w/o for gastroparesis? What confirms the diagnosis?

A

EGD to r/o mechanical obstruction

Gastric emptying test - confirms the diagnosis

blood tests to look for the cause!

74
Q

What does the gastric emptying test NOT tell you in a pt with gastroparesis? What else do you need to order?

A

Does not uncover CAUSE of gastroparesis

Blood tests as needed to look for CAUSE

75
Q

Describe the gastric emptying test. ** What confirms the dx of gastroparesis?

A

** Gastric retention >than 10% at 4 hours is diagnosed delayed gastric emptying

76
Q

What is the management for gastroparesis? What is the tx for severe refractory gastroparesis? What can be used as a short term tx?

A

Severe Refractory cases - may require PEG or jejunostomy tube for enteral feedings

Erythromycin for a short term tx

77
Q

**What is Zollinger-Ellison Syndrome? ** What are the 3 underlying pathologies?

A

rare endocrine disorder

  1. gastrinoma: gastrin secreting tumor large amounts of gastrin lead to excess HCL acid and ulcer formation
  2. increased gastric acid secretion by the parietal cells
  3. peptic ulcer

all leads to excessive amounts of HCL and can perforate stomach, invade tissues and spread through lymph

78
Q

Where do the gastrinomas present as part of Zollinger-Ellison Syndrome? What are the components of the triangle?

A

Arise in pancreas, duodenum, lymph nodes

confluence of cystic and common bile ducts, neck of pancreas, and junction of 2nd and 3rd portion of duodenum

79
Q

the majority of gastrinomas present in Zollinger-Ellison Syndrome are ____ and _______. 25% are associated with ______

A

2/3 are malignant and SLOW growing

MEN1

80
Q

How does Zollinger-Ellison Syndrome present?

A

**refractory PUD: that often goes undetected for years
hearburn
weight loss
diarrhea

81
Q

** How do you dx Zollinger-Ellison Syndrome? What is the pt education point? What test results are considered diagnostic?

A

**Dx with fasting serum gastrin level

Stop PPI’s 6 days prior to obtaining gastrin levels

A serum gastric value greater than 10 times the upper limit of normal in the presence of a gastric pH below 2 is diagnostic

82
Q

What characteristics would make you think to look for Zollinger-Ellison Syndrome and order serum gastrin levels?

A

Ulcers refractory to standard therapy

Large, atypical appearing ulcers (>2cm)

Multiple ulcers/frequent recurrences

Ulcers associated with diarrhea

Ulcers in patients who are H. pylori negative and who are not taking NSAIDS

83
Q

If your pt’s fasting serum gastrin is positive, what do you do next? Describe it. What would you expect the result to be if the pt has ZES?

A

Secretin stimulation test

Secretin (digestive hormone) is administered IV.
Secretin produces a marked increase in gastrin in most patients with a gastrinoma.
Samples of gastrin collected at -10, -1, 2, 5, 10, 15,20, and 30 minutes

The administration of secretin produces a marked increase in gastrin in most pts with a gastrinoma

84
Q

Both the fasting serum gastrin and secretin stimulation test are positive, what do you do next? What is the Somatostatin Receptor Scintigraphy?

A

imaging!! CT or MRI to location other sites/mets

Gastrinomas express somatostatin receptors that bind radiolabeled octreotide, which helps detects primary gastrinomas

85
Q

What is the management for ZES? The ____ is the major metastatic site, ____ is second MC metastatic site

A

PPI and surgical resection

liver

bone

86
Q

What are the 2 kinds of benign gastric tumors? Which one has premalignant potential?

A

Inflammatory epithelial polyps

Adenomatous polyps - premalignant potential

87
Q

What are the 3 kinds of malignant gastric tumors? Which one is MC with H. Pylori?

A

Gastric Adenocarcinoma

Gastric Lymphoma- MC with H. Pylori

Gastric Carcinoid Tumors (from Zollinger-Ellison)

88
Q

**_____ are most common cancers of the stomach. What do they develop from?

A

Adenocarcinomas

Develop from the gland cells in the lining of the stomach

89
Q

What are the 2 difference “types” of gastric adenocarcinoma? Which one is MC? What are features of each?

A

“Intestinal-type”: MC
Chronic H. pylori infection
Smoking, high nitrate/salt diet
More common in advanced age

“Diffuse-type”:
Genetic mutations/Hereditary
Spreads faster, difficult to treat

90
Q

What are the different stages of stomach cancer? What layers are involved in each?

A

Stage 0: mucosa layer only

Stage 1: mucosa and submucosa only

Stage 2: mucosa, submucosa and muscle layer

Stage 3: mucosa, submucosa, muscle layer and serosa

Stage 4: mucosa, submucosa, muscle layer, serosa that has spread outside of the stomach

91
Q

Asymptomatic until advanced
Dyspepsia, vague epigastric pain
Anorexia, weight loss, early satiety
Hematemesis
Masses causing obstruction = postprandial vomiting

What am I?
**What are 3 signs of metastasis? Which one is MC?

A

Gastric Adenocarcinoma

Left supraclavicular lymph node (virchow’s node) -MC
Umbilical nodule (Sister Mary Joseph nodule)
Rigid rectal shelf (Blumer shelf)

92
Q

Left supraclavicular lymph node is known as ______

Umbilical nodule is known as ______

Rigid rectal shelf is known as ______

Which one is MC presented in gastric adenocarcinoma?

A

(virchow’s node)** MC

(Sister Mary Joseph nodule)

(Blumer shelf)

93
Q

What is part of the diagnostic work up for gastric adenocarciomas? What is the tx?

A

EGD is procedure of choice

CT of chest, abdomen, pelvis to delineate primary tumor/distal metastases

Surgical Resection, Chemotherapy and or Radiation, Palliative Measures

94
Q

How common is gastric lymphoma? **What is the MC risk factor? How do you make dx? What is the tx?

A

Primary accounts for 3% of gastric cancer

M/C Risk Factor - Chronic H. pylori infection

Dx - made by EGD with bx

Treatment - radiation and/or chemotherapy

95
Q
A