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GASTRITIS Flashcards

1
Q

what is the stomach?

A

J shaped muscle organ located in the left upper abdominal cavity inferior to the diaphragm

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2
Q

what is the pathophys of what the stomach does?

A

contributes to mechanical and chemical digestion of food from the esophagus before releasing it, as CHYME, to the small intestine

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3
Q

what is the greater curvature of the stomach?

A

convex lateral surface of stomach

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4
Q

what is the lesser curvature of the stomach?

A

concave medial surface of the stomach

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5
Q

what is the stomach held in place by?

A

greater omentum
lesser omentum

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6
Q

where is the greater omentum?

A

runs from the greater curvature to the posterior abdominal wall

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7
Q

where is the lesser omentum?

A

extends from liver to lesser curvature

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8
Q

what are the 4 regions of the stomach?

A
  1. cardia
  2. fundus
  3. body
  4. pylorus
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9
Q

what is the cardia of the stomach?

A

region where food passes from the esophagus and into the stomach

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10
Q

what is the fundus of the stomach?

A

dome-shaped region located above and to the left of the cardia
stores undigested food and gases

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11
Q

what is the body of the stomach?

A

largest region of the stomach

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12
Q

what is the pylorus of the stomach?

A

funnel shaped region that connects to the duodenum

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13
Q

what is the pyloric antrum ?

A

wider end of pylorus

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14
Q

what is the pyloric canal?

A

narrow end of pylorus

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15
Q

what is the pyloric sphincter?

A

smooth muscle that controls gastric emptying

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16
Q

what are the 3 physiology aspects about the mucosa of the stomach

A
  1. forms large folds when stomach is empty known as rugae
  2. contains a protective alkaline mucus
  3. gastric pits are depressions that mark entry to gastric glands
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17
Q

what is the in the submucosa of the stomach?

A

contains blood vessels, lymphatic vessels and nerves

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18
Q

what is the muscularis externa responsible for?

A

responsible for mechanically breaking down food into smaller particles

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19
Q

what are the layers of the muscularis externa?

A

inner oblique layer
middle circular layer
outer longitudinal layer

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20
Q

what do chief cells do?

A

secrete pepsinogen, the inactive proenzyme of pepsin

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21
Q

what 2 things to the parietal cells produce?

A
  1. HCl
  2. intrinsic factor
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22
Q

what is entailed in the HCl production of parietal cells?

A

-high acidity (pH 1.5-3.5) of stomach
> kill ingested bacteria
> denatures proteins
- activates digestive enzyme, pepsin

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23
Q

what is intrinsic factor? (produced by parietal cells)

A

glycoprotein necessary for the absorption of vitamin B12 in the small intestine

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24
Q

-WHY IS B12 VITAL TO SURVIVE?

A

its a cofactor in heme production -> Hgb

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25
Q

what do mucous neck cells secrete?

A

alkaline mucus

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26
Q

what are the 2 types of enteroendocrine cells?

A

D cells and G cells

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27
Q

what do D cells secrete?

A

somatostatin - inhibitory

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28
Q

what do G cells secrete?

A

they secrete gastrin that then stimulates parietal cells

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29
Q

what do gastric enzymes have the potential to do?

A

digest themselves

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30
Q

what are the 3 things that protect the stomach from self-digestion?

A
  1. mucosal barrier
  2. tight junctions
  3. stem cells
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31
Q

what is the mucosal barrier?

A

thick coating of bicarbonate-rich mucus that acts as a physical barrier. the bicarb ions neutralize the acid.

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32
Q

what are tight junctions?

A

they block gastric juice from penetrating underlying tissues

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33
Q

where are stem cells located?

A

they are located at the junction of gactric pits and gastric glands

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34
Q

what do stem cells do?

A

they replace damaged epithelial mucosal cells

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35
Q

when it eh surface epithelium of the stomach replaced?

A

it is completely replaced every 3-6 days

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36
Q

what is gastritis?

A

a general term for a group of conditions in which there is histologic evidence of inflammation, irritation, or erosion of the lining of the stomach

37
Q

what is acute gastritis called?

A

neutrophilic infiltration

38
Q

what is chronic gastritis called?

A

lymphocyte and plasma cell infiltration

39
Q

what are the 2 types of gastritis?

A

1.erosive
2. nonerosive

40
Q

what is erosive gastritis?

A
  • gastric mucosal erosion caused by damage to the mucosal defenses
  • superficial erosions and punctate mucosal lesions
41
Q

where does erosive gastritis occur?

A

typically occurs in the body of the stomach

42
Q

what are the common causes of erosive gastritis?

A
  1. NSAIDS, ASA, BISPHOSPHONATES
  2. ALCOHOL
  3. PHYSIOLOGICAL STRESS
    • severe medical or surgical illness
      >5% of critically ill patients
      >incidence increases with duration of intensive
      care unit stay and length of time the patient is
      not receiving enteral feeding
43
Q

what are the s/sx of MILD erosive gastritis?

44
Q

what are the s/sx of MOD/SEVERE erosive gastritis?

A

-develop within 2-5 days of inciting event
1. dyspepsia (indigestion)
2. N and/or V
3. epigastric pain
4. GI bleeding
- mild-mod
- hematemesis, “coffee grounds” emesis, and/or
melena

45
Q

what is the dx study of choice for erosive gastritis?

A

ENDOSCOPY

-most sensitive method for dx

46
Q

when is endoscopy performed?

A

within 24 hrs of UPPER GI bleedwh

47
Q

what is the tx of erosive gastritis?

A
  1. REMOVAL OF OFFENDING AGENT IF POSSIBLE
  2. endoscopic hemostasis (cautery, sclerotherapy) if bleeding
  3. acid suppression w/ H2 blocker or PPI for 4-8 week trial

(H2 mild, PPI severe)

48
Q

what are the 3 types of non-erosive gastritis?

A
  1. H. Pylori
  2. pernicious anemia gastritis
  3. gastric metaplasia

A= AUTOIMMUNE- PERNICIOUS
B= BACTERIA- H. PYLORI
C= CANCER- METAPLASIA

49
Q

What is the most common type of non-erosive gastritis?

50
Q

what is H. pylori?

A

spiral gram-neg bacterium that resides beneath gastric mucosa layer causing mucosal inflammation with PMNs (neutrophils) and lymphocytes

51
Q

what are the mechanisms of H. Pylori that allows it to survive the acidic environment of the stomach?

A
  1. it gives off ammonia that erodes the mucus barrier
  2. cytotoxins and mucolytic enzymes cause mucosal damage and lead to ulcerogenesis
52
Q

what does h. pylori commonly cause?

A

gastritis
PUD
gastric adenocarcinoma
low-grade B-Cell gastric lymphoma

53
Q

what is the epidemiology of h. pylori infection?

A

increases with age
50% over age 60 infected

54
Q

what is the transmission of h. pylori?

A

oral-oral or fecal-oral route

55
Q

what ethnicity is h. pylori more common in?

A

blacks, hispanics, and asians

56
Q

what is h. pylori also known as?

A

type b gastritis

57
Q

what are the s/sx of acute H. pylori gastritis infxn?

A

-transient illness for several days
-nausea
-abdominal pain -epigastric

58
Q

what are the s/sx of chronic H. pylori gastritis infxn?

A

most patients are asx (80%)
-dyspepsia
> early satiety
> postprandial fullness
> gnawing or burning upper abdominal discomfort

59
Q

what are the types of chronic H. pylori gastritis?

A
  1. mild diffuse gastritis
  2. antral- predominant gastritis
  3. body- predominant gastritis
60
Q

what is the pathophys of antral- predominant gastritis?

A
  1. increased gastrin production
    > gastrin: stimulated secretion of gastric acid (HCl) by
    the parietal cells
  2. resultant hypersecretion fo acid predisposes the patient to developing PEPTIC ULCERS and GASTRIC ADENOCARCINOMA
61
Q

what is the pathophys of body- predominant gastritis?

A

destruction of acid-secreting glands resulting in gastric atrophy and decreased acid production
- predisposes patients to NEUROENDOCRINE TUMORS

62
Q

what is the dx screening of choice for asx patients of h. pylori gastritis?

A

not indicated

63
Q

what is the initial dx studies for h. pylori gastritis?

A
  1. stool (fecal) antigen immunoassay
    (similar sensitivity and specificity to that of urea breath test)
  2. urea breath test
64
Q

what is entailed in the urea breath test for h. pylori gastritis?

A
  • oral dose o 13c or 14c- labeled urea (capsule)
  • infected patient –H. Pylori will metabolize the urea and liberate labeled CO2 which is exhaled and quantified in breath samples taken 20-30 min after ingestion of the urea
65
Q

what should patients do prior to urea breath test?

A

PPI’s should be d/c for 14 days and abx should be d/c for 28 days

66
Q

what dx study is performed in patients with sx that suggest upper GI disease related to h. pylori gastritis?

67
Q

what should be done during endoscopy for h. pylori gastritis?

A

gastric mucosal biopsy for histology and rapid urease test (RUT)

68
Q

is endoscopy recommended solely for dx of H. pylori?

69
Q

why should all H. pylori positive patients be treated?

A

d/t the chance it turns into gastric cancer

BAD

70
Q

what are the 2 tx options for h. pylori gastritis?

A
  1. triple therapy
  2. quadruple therapy
71
Q

what is the most frequent prescribed regimen for h. pylori gastritis?

A

triple therapy

72
Q

what is the best initial h. pylori gastritis therapy in areas where the clarithromycin resistance rate is >15% ?

A

quadruple therapy

73
Q

how long is the triple therapy tx duration? (for h. pylori infxn)

A

10-14 days

74
Q

how long is the quadruple therapy tx duration? (for h. pylori infxn)

75
Q

what is entailed in triple therapy for tx of h. pylori?

A
  1. PPI X2 DAILY PO -> OMEPRAZOLE
  2. AMOXICILLIN 1 G PO X2 DAILY ORRR METRONIDAZOLE 500 MG PO X3 DAILY
  3. CLARITHROMYCIN 500 MG PO X2 DAILY
76
Q

what is entailed in quadruple therapy for tx of h. pylori?

A
  1. PPI X2 DAILY PO -> OMEPRAZOLE
  2. BISMUTH SUBSALICYLATE 300 MG PO X4 TIMES DAILY
  3. METRONIDAZOLE 250-500 MG PO X4 TIMES DAILY
  4. TETRACYCLINE 500 MG PO X4 TIMES DAILY
77
Q

in addition to triple or quadruple therapy for h. pylori infxn, what should a patient who has duodenal or gastric ulcers do?

A

they must continue their acid suppression therapy for at least 4 weeks

78
Q

how can eradication of h. pylori be confirmed?

A

with a urea breath test, stool antigen test, or endoscopy > or equal to 4 weeks after completion of therapy

79
Q

what is pernicious anemia gastritis also known as? (what type)

A

type A gastritis

80
Q

what 2 antibodies are involved in pernicious anemia gastritis?

A

parietal cells antibodies (PCA) and intrinsic factor antibodies (IFA)

81
Q

what is arguably the biggest thing that occurs in pernicious anemia gastritis?

A

achlorhydria
- impaired iron absorption
- hyperplasia of G-cells -> increase in GASTRIN
secretion

82
Q

what is the pathophys of pernicious anemia gastritis?

A
  1. achlorhydria
  2. vita b12 malabsorption
  3. destruction of chief cells leading to decrease in pepsinogen
83
Q

where is pernicious anemia gastritis located?

A

typically restricted to the fundus and body of the stomach

84
Q

what is involved in the dx of pernicious anemia gastritis?

A
  1. measuring anti-parietal cell and anti-intrinsic factor antibodies
  2. serum gastrin
  3. serum pepsinogen
  4. endoscopic biopsy
85
Q

what is gastric metaplasia?

A
  • pre-cancerous changes characterized by histologic change from a normal gastric cardia, fundic, and antral mucosa to epithelium that resembles the small intestine
86
Q

why does gastric metaplasia occur?

A

d/t chronic irritation and inflammation of stomach lining caused by various factors such as gastric acid, bile salts, H. Pylori infxn, smoking, alcohol, and environmental contaminants

87
Q

what can gastric metaplasia lead to?

A

an increased risk of dysplasia leads to stomach cancer

88
Q

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GI (22 decks)

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