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GI block > GI Goljan stomach disorders > Flashcards

GI Goljan stomach disorders Flashcards

1
Q

What are the signs and Sx of stomach disease?

A

hematmesis;

melena

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2
Q

most common cause of hematemesis w/ stomach disorder?

A

PUD (most common);

esophageal varices and hemorrhagic gastritis

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3
Q

What mechanism causes melena? what does this signify?

A

Hb is converted into hematin (black pigment) by acid;

signifies bleed proximal to duodenojejunal jxn (90%)

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4
Q

Gastric analysis is included when stomach disease is suspected?

A

measurement of basal acid output (BAO), maximal acid output (MAO) and the BAO: MAO ratio

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5
Q

define basal acid output

A

acid output of gastric juice collected via NG tube over 1hr period on empty stomach => normally less than 5mEq/hr

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6
Q

define maximal acid output

A

acid output of gastric juice that is collected over 1hr after pentagastrin stimulation normally 5-20mEq/hr

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7
Q

what is normal BAO:MAO ratio?

A

0.2 : 1

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8
Q

Epidemiology congenital pyloric stenosis

A

probable genetic basis w/ parent having disease increases risk for child w/ CPS
males > females;

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9
Q

How does acquired pyloric obstruction occur?

A

complication of chronic duodenal ulcer disease w/ pyloric scarring

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10
Q

Pathophys of congenital pyloric stenosis

A

progressive hypertrophy of circular muscles in pyloric sphincter;
Deficiency of NO synthase precipitates CPS

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11
Q

when does congenital pyloric stenosis present?

A

not at birth but occurs over 3-5wks

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12
Q

clinical findings of congenital pyloric stenosis

A

projectile vomit of NON-BILE stained fluid;
hypertrophied pylorus palpated in epigastrium (70%) => “olive mass”;
visible hyperperistalsis

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13
Q

Tx for congenital pyloric stenosis

A

myotomy IF it does not resolve

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14
Q

Define gastroparesis and what may cause it

A 
decreased stomach motility => 
autonomic neuropathy (diabetes mellitus);
previous vagotomy
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15
Q

clinical findings in gastroparesis

A

early satiety and bloating;

vomiting of undigested food a few hrs after eating

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16
Q

Tx for gastroparesis

A

small volume frequent feeding;

metoclopramide

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17
Q

What 2 pathologies are associated w/ acute hemorrhagic (erosive) gastritis?

A

erosions => breach in epithelium of mucosa;

ulcers => breach in mucosa w/ extension into submucosa or deeper

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18
Q

What are the causes of acute hemorrhagic (erosive) gastritis?

A 
NSAIDs; 
alcohol, H. pylori;
CMV (AIDS), smoking;
Burns (Curling ulcers);
CNS injury (Cushing ulcer); 
Uremia;
anisakis
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19
Q

How does anisakis cause acute hemorrhagic gastritis?

A

worm associated w/ eating raw fish

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20
Q

clinical findings of acute hemorrhagic gastritis?

A

hematemesis;
melena;
Fe deficiency

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21
Q

Non pharm Tx for acute hemorrhagic gastritis excluding H. pylori?

A

avoid mucosal irritants (NSAIDs, alcohol);

cessation of smoking

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22
Q

pharm Tx for acute hemorrhagic gastritis excluding H. pylori?

A

misoprostol;

proton pump inhibitors

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23
Q

Differentiate 2 types of chronic atrophic gastritis

A

Type A=> body and fundus

Type B=> antrum and pylorus

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24
Q

What is the most often cause of type A chronic atrophic gastritis?

A

pernicious anemia

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25
Q

complications of type A chronic atrophic gastritis

A

Achlorhydria w/ hypergastrinemia (loss of - cycle);
macrocytic anemia due to vit B12 deficiency;
increased risk for gastric adenocarcinoma

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26
Q

most common cause of type B chronic atrophic gastritis

A

H. pylori (gram neg, curved rod)

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27
Q

Epidemiology of type B chronic atrophic gastritis

A

30-50% population in US;
increases w/ age;
transmitted by fecal-oral/ oral-oral route usually in poor sanitation areas

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28
Q

pathophys of type B chronic atrophic gastritis

A

gram neg, curved rod;
produces urease, proteases, cytotoxins;
colonizes mucus layer lining

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29
Q

What does H. pylori attach to? does it invade?

A

attaches to blood group O receptors on mucosal cells;

NOT invasive

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30
Q

microscopic findings in type B chronic atrophic gastritis

A 
chronic inflammatory infiltrate in lamina propria;
intestinal metaplasia (precursor lesion for adenoCA)
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31
Q

Tests for H. pylori ID

A

Urea breath test > 90%;
stool antigen test (pos when active, neg when not);
detect urease in gastric Bx;
Serologic tests (only 1st infection)

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32
Q

Tx for type B chronic atrophic gastritis

A

sequential therapy =>

1) Rabeprazole and amoxicillin;
2) Rabeprazole + clarithromycin + tinidazole

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33
Q

What is the test of cure for type B chronic atrophic gastritis?

A

stool antigen test => neg 8wks after Tx

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34
Q

Other than type B chronic atrophic gastritis, what other diseases are associated w/ H. pylori?

A

duodenal and gastric ulcers;
gastric adenoCA;
low grade B cell malignant lymphoma

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35
Q

Other than type A and B chronic atrophic gastritis, what other disease is associated w/ chronic atrophic gastritis?

A

Menetrier’s disease (hypertrophic gastropathy)

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36
Q

What is associated w/ Menetrier’s disease?

A
  • Giant rugal folds => hyperplasia of mucus secreting cells causing hypoproteinemia (protein losing enteropathy)
  • Atrophy of parietal cells (achlorhydria) => increase risk for adenoCA
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37
Q

Epidemiology of PUD

A

H. pylori (70% in US) => duodenal ulcers more common than gastric ulcers;
increased recurrence rate for untreated PUD

38
Q

Gross appearance of PUD ulcers

A

clean, sharply demarcated and slightly elevated around edges

39
Q

Which PUD ulcers should always be Bx?

A

gastric ulcers as can rarely become malignant;

duodenal ulcers NEVER malignant

40
Q

What may be found in the histo section of ulcers?

A

necrotic debris;
inflammation w/ predominance of neutrophils;
granulation tissue (repair tissue);
fibrosis

41
Q

Epidemiology and pathogen of ZE syndrome

A

majority are malignant pancreatic islet cell tumors;
secrete excess gastrin causing hyperacidity;
sporadic 2/3;
usually single ulcers but can be multiple;
MEN type I association (20-30% cases)

42
Q

What would give suspicion of ZE syndrome?

A 
multiple ulcers in usual places;
ulcers resistant to Tx;
ulcers distal to 1st part of duodenum;
PUD plus diarrhea; 
fam Hx of PTH or pituitary tumors;
PUD w/o H. pylori or NSAIDs
43
Q

clinical findings of ZE syndrome?

A

epigastric pain w/ weight loss;
heartburn from GERD;
peptic ulceration (usually solitary duodenal ulcers);
acid hypersecretion w/ diarrhea;
maldigestion of food (acid interferes w/ pancreatic enzyme activity

44
Q

Lab findings in ZE syndrome

A

increased BAO, MAO and BAO:MAO ratio;

increased gastrin > 1000pg/mL

45
Q

Tx for ZE syndrome

A

CTX and PPI

46
Q

What are gastric polyps typically complications of?

A

chronic gastritis and achlorhydria

47
Q

What is the most common type of gastric polyp? malignant potential?

A

hyperplastic polyp;

hamartoma w/ no malignant potential

48
Q

What is a neoplastic gastric polyp?

A

adenomatous polyp w/ potential for malignant transformation

49
Q

name the 3 gastric tumors

A

leiomyoma;
primary stomach adenoCA;
primary gastric malignant lymphoma

50
Q

most common site of leiomyoma? what is a common complication?

A

stomach;

may ulcerate or bleed

51
Q

primary stomach adenoCA epidemiology

A

decreasing incidence in US;
increasing incidence in Japan;
increased incidence in blood group A ppl

52
Q

What are the 2 types of primary stomach adenoCA? which is most common

A

intestinal&raquo_space; diffuse

53
Q

Risk factors for intestinal type of gastric adenoCA

A 
intestinal metaplasia due to H. pylori (important);
nitrosamines;
smoked foods (japan);
diets lacking fruit/veggies; 
type A chronic atrophic gastritis;
Menetrier's disease
54
Q

What are the 2 types of intestinal type of gastric adenoCA?

A

polypoid or ulcerated

55
Q

locations of intestinal type of gastric adenoCA

A

lesser curvature of pylorus and antrum (50-60%);
cardia (25%);
body and fundus

56
Q

T/F diffuse type of gastric adenoCA is NOT associated w/ H. pylori

A

true

57
Q

What characterizes diffuse type of gastric adenoCA?

A

diffuse infiltration of malignant cells in stomach wall

58
Q

What malignant cells infiltrate in diffuse type of gastric adenoCA?

A

linitis plastica;
does NOT peristalse;
Signet ring cells ;
produces Krukenberg tumor of ovaries

59
Q

How signifies a krukenberg tumor has spread to ovaries?

A

hematogenous spread of signet ring cells

60
Q

clinical findings of gastric adenoCA

A

cachexia and weight loss;
epigastric pain;
vomiting often w/ melena;
mets to left supraclavicular node => Virchow’s node;
paraneoplastic skin lesions;
mets to umbilicus (Sister Mary joseph sign)

61
Q

What are paraneoplastic skin lesions associated w/ gastric adenoCA?

A

acanthosis nigricans;

multiple outcroppings of seborrheic keratosses => Leser Trelat sign

62
Q

where are common mets of gastric adenoCA?

A

liver, lung, ovaries

63
Q

Tx for gastric adenoCA?

A

surgery; local radiation; CTX

64
Q

Px of overall 5yr survival rate

A

10-15%

65
Q

what is the most common site for extranodal malignant lymphoma

A

stomach (primary gastric malignant lymphoma)

66
Q

What are the types of primary gastric malignant lymphoma

A

low grade B cell lymphoma;

High grade B or T cell lymphoma

67
Q

What is the pathogenesis of low grade B cell lymphoma?

A

H. pylori related;

MALToma (mucosa assoc lymphiod tissue)

68
Q

Tx for primary gastric malignant lymphoma

A

H. pylori produces 50% cure rate

69
Q

What is the most common GI ulcer?

A

Duodenal&raquo_space; Gastric

70
Q

epidemiology of gastric ulcers

A

male = female;

smoking does NOT cause PUD but delays healing

71
Q

epidemiology of duodenal ulcers and what causes increases risk?

A

male > female;
risk increased w/ MEN I;
increased risk in cirrhosis, COPD, renal failure, hyperparathyroidism

72
Q

H. pylori frequency in gastric and duodenal ulcers

A

gastric => 80%;

duodenal=> 90-95%

73
Q

Pathogenesis for gastric ulcers

A

defective mucosal barrier due to H. pylori leading to mucosal ischemia (reduced PGE), bile reflux, delayed gastric emptying

74
Q

How is the gastric analysis for gastric ulcers?

A

BAO and MAO normal to decreased

75
Q

Pathogenesis for duodenal ulcers

A

defective mucosal barrier due to H. pylori but causing increased acid production so increased parietal cell mass

76
Q

gastric analysis for duodenal ulcers?

A

BAO and MAO both increased

77
Q

Location of gastric ulcers. how does this relate to cancer?

A

single ulcer on lesser curvature of antrum;

sam location for cancer

78
Q

location for duodenal ulcers

A

single ulcer on anterior portion of 1st part of duodenum followed by single ulcer on posterior portion

79
Q

what risk does a duodenal ulcer on the posterior portion have?

A

danger of perforation into pancreas and pancreatitis

80
Q

Complications of gastric ulcers

A

bleeding (MC is left gastric artery);

perforation

81
Q

complications of duodenal ulcers

A

bleeding (MC is gastroduodenal artery);
perforation (air under diaphragm, pain radiates to left or right shoulder);
gastric outlet obstruction;
pancreatitis

82
Q

Clinical findings in gastric ulcers

A

epigastric pain made worse by eating

83
Q

Clinical findings in duodenal ulcers

A

epigastric pain relieved by eating

84
Q

How is gastric ulcer Dx?

A

Endoscopy (90-95% accurate) and MUST BIOPSY;

upper GI barium study: ID’s 70-80% PUD

85
Q

Why must gastric ulcers be biopsied?

A

potential for malignancy is 1-4%

86
Q

How are duodenal ulcers Dx?

A

endoscopy (90-95%);

upper GI barium study to ID 70-80% of PUD

87
Q

should duodenal ulcers be biopsied?

A

no bc they are never malignant

88
Q

Nonphram Tx for gastric ulcers

A

stop smoking;
avoid NSAIDs and alcohol;
avoid foods causing Sx

Surgery=> antrectomy or hemigastrectomy w/o vagotomy

89
Q

Pharm Tx for gastric ulcers

A

eradicate H. pylori;
H2 receptor antagonists;
PPI;
antacids

90
Q

Nonpharm Tx of duodenal ulcers

A

stop smoking;
avoid NSAIDs and alcohol;
avoid foods causing Sx

Surgery=> highly selective vagotomy

91
Q

Pharm Tx for duodenal ulcers

A

eradicate H. pylori;
H2 receptor antagonists;
PPI;
antacids

GI block (11 decks)

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