GIT - stomach Flashcards

1
Q

diseases of the stomach

congenital (2) and acquired (6)

A

congenital

  • diaphragmatic hernia
  • pyloric stenosis

acquired

  • gastropathy
  • acute gastritis
  • chronic gastritis
  • peptic ulcer (PUD)
  • neoplasm
  • uncommon forms of gastritis (eosinophilic, lymphocytic, granulomatous)
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2
Q

gastropathy definition

A

inflammation of gastric mucosa

absence of inflammatory cells

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3
Q

acute gastritis

+ symptoms

A

inflammation of gastric mucosa
presence of neutrophils
causes superficial erosions and gastric ulcers
cause congestion also -> petechial hemorrhage / erosions

symptoms: epigastric pain, indigestion, n/v, bleeding
may be asymptomatic also

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4
Q

causes of acute gastritis/gastropathy (6)

A
  • reflux - alcohol, bile
  • drugs: NSAIDs
  • cigarettes
  • chemo/radiation therapy
  • stress-induced mucosal injury: sepsis/ trauma/ burns/ cushing’s (cause intracranial disease?)
  • uremia
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5
Q

pathogenesis of acute gastritis/gastropathy

A
  • NSAIDs: inhibit COX dependent synthesis of prostaglandins - prostaglandins are the one that stimulate defence mechanisms in stomach
  • chemo/radiation therapy + chemicals/alcohol/cigarettes: direct injury to mucosal epithelium and stroma cells
  • stress-induced mucosal injury: results in local ischemia
    cushing’s cause IC disease stimulates vagal nuclei -> hypersecretion of acid
  • uremia: inhibits gastric bicarbonate transporters
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6
Q

chronic gastritis pathogenesis

A

Chronic mucosal inflammation -> mucosal atrophy and intestinal metaplasia
metaplasia -> carcinoma

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7
Q

chronic gastritis forms (2)

A
  • associated chronic gastritis: H.pylori**

- autoimmune gastritis

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8
Q

H.pylori

- diseases associated (4)

A

most common cause of chronic gastritis
asymptomatic

diseases associated:

  • Chronic gastritis
  • Peptic ulcer
  • Gastric carcinoma
  • Gastric lymphoma
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9
Q

H.pylori associated chronic gastritis characteristics

A
  • active inflammation: inflammatory cells (neutrophils, lymphocytes, lymphoid aggregates)
  • regenerative changes: epithelium undergoes mitosis
  • eptithelium metaplasia (now looks like intestines)
  • atrophy: loss in glands
  • may undergo dysplasia -> invasive adenocarcinoma
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10
Q

H.pylori diagnosis

A
  • urea breath test: H/pylori produces urease which breaks down the urea -> radioactive CO2 detected in breath
    CO2 detected = pos of H.pylori infection
  • serology
  • histology
  • culture: curved microaerophilic organism
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11
Q

autoimmune gastritis (chronic gastritis)

A

rarer (<10%)

  • Diffuse gastritis of oxyntic mucosa (in body and fundus of stomach)
  • > antibodies to gastric parietal cells and intrinsic factor can be detected in serum/gastric secretions
  • extensive intestinal metaplasia and pseudopyloric metaplasia
  • severe gastric body-fundal atrophy
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12
Q

effects of autoimmune gastritis (4)

A
  • Defective gastric acid secretion – hypo- or achlorhyridia
  • Endocrine cell hyperplasia - hypergastrinemia
    associated w/ endocrine disorders: hashimoto’s/graves/DM
  • Disabled ileal Vit B12 absorption - Megaloblastic anemia
  • Chief cell destruction - reduced serum pepsinogen I concentration

could lead to Pernicious anemia (vit B12 def), adenocarcinoma, carcinoid tumor

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13
Q

peptic ulcer disease (PUD)

A

chronic mucosal ulceration affecting the duodenum or stomach
- more common in 1st part of duodenum
- affects lesser curve of stomach
penetrates muscularis mucosae

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14
Q

other rarer PUD caused diseases

A

Heterotopic gastric mucosa - at merkel diverticulum (umbilical cord remains that cause an outpouching)

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15
Q

risk factors/ causes of PUD

A
  • H,pylori
  • cigarettes
  • COPD
  • drugs that reduce mucosal blood flow (cocaine)
  • NSAIDs
  • alcohol -> alcoholic cirrhosis
  • psychological stress - increase gastric acid secretion
  • Endocrine hyperplasia - stimulate parietal cell growth
  • Zollinger-Ellison syndrome in distal duodenum
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16
Q

H.pylori -> PUD pathogenesis**

A

produce urease, protease & phospholipases:

  • Urease: generates NH3 and CO2 from endogenous urea. NH3 inhibits bicarbonate channels -> decrease bicarbonate secretion
  • Protease: breaks down glycoprotein in gastric mucosa
  • Phospholipases: damage epithelial cells -> thrombotic occlusion of capillaries

inflammatory effects:
attracts neutrophils - release myeloperoxidase -> damages mucosa -> leakage of tissue nutrients

17
Q

gross PUD appearance

A
  • ‘punched out’ defect
  • Base is smooth and clean
  • Scarring and puckering of the wall
18
Q

PUD clinical symptoms

A
  • Epigastric burning or aching pain
    Pain tends to occur 1-3 hours after meals during the day and worse at night. Relieved by alkali or food
  • Nausea, vomiting bloating belching, weight loss
  • anemia, hemorrhage and perforation
19
Q

PUD complications

A
  • bleeding (most common)
  • perforation
  • obstruction
  • gastric adenocarcinoma
20
Q

causes of upper GIT bleeding

A
  • duodenal/gastric ulcers
  • gastric erosion
  • esophageal varices
  • Mallory-Weiss tear: tear of tissue in lower esophagus - caused by violent coughing/vomiting
  • esophagitis
  • erosive duodenitis
  • neoplasm
21
Q

microscopic PUD appearance (4 features)

A
  • fibrinopurulent exudate
  • necrotic debris
  • granulation tissue
  • fibrinosis
22
Q

definition of intestinal metaplasia

A

Change of gastric columnar mucosa to that of intestinal type (with goblet cells)

23
Q

definition of dysplasia

A

Pre-malignant / neoplastic changes of the gastric mucosa - w/ potential for further steps in malignant transformation

24
Q

stomach defense mechanism

A
  • thick mucosal layer
  • epithelial mucous producing cells
    secrete bicarbonate and mucus -> neutralise stomach acidity + pepsin
25
Q

intestinal metaplasia clinical symptoms

A
  • black tarry stools cause of hemorrhage
  • altered bowel movement: constipation, nausea/vomitting
  • pain in epigastrium