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GIT > Stomach > Flashcards

Stomach Flashcards

1
Q

What do parietal cells secrete, what do chief cells secrete, what do G cells secrete

A

P = Acid, Intrinsic Factor
C = Pepsin
G = Gastrin

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2
Q

WHat are 2 congenital diseases of the stomach?

A

Diaphragmatic Hernia
Congenital Pyloric STenosis

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3
Q

What are 6 acquired diseases of the stomach

A
  1. Gastropathy
  2. Acute Gastritis
  3. Chronic Gastritis
  4. Peptic Ulcer
  5. Special forms of Gastritis
  6. Neoplasms
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4
Q

What is the difference between acute gastritis and gastropathy?

A

Acute gastritis is when neutrophils are present, while in gastropathy inflammatory cells are rare/absent

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5
Q

How does acute gastritis present?

A
  1. Asymptomatic
  2. Epigastric Pain
  3. Indigestion
  4. Nausea & Vomitting
  5. Bleeding
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6
Q

What two things can result from acute gastritis?

A

Superficial Erosions
Acute Ulcers

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7
Q

What can be seen on an endoscope in acute gastritis?

A
  1. Petechial Hemorrhages
  2. Erosions
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8
Q

What are 5 causes of gastropathy/gastritis?

A

Reactive Gastritis
- Chemical/reflux (alcohol, bile, corrosives)
- NSAIDs
- CIgarette smoking
Chemotherapy/radian
Vascular gastropathy
- portal hypertension
Stress-induced mucosal injury (local ischemia)
- shock, sepsis, post MI, trauma
- severe burns
- intracranial disease
Uremia

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9
Q

How does uremia causes gastric injury?

A

Inhibition of gastric bicarbonate transporters by ammonium ions

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10
Q

How do NSAIDs cause gastric injury

A

Inhibit COX, no PGs, PGs needed for bicarbonate production, mucus production, regulation of acid secretion

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11
Q

Why are elderly more susceptible to gastric injjury?

A

Reduced mucin and bicarbonate secretion

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12
Q

How do people get acute gastritis at high altitudes?

A

Decreased oxygen delivery

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13
Q

How does chemotherapy/radiation cause gastric injury?

A

Direct Injury

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14
Q

pathogenesis of stress associated gastric injury

A

Local Ischemia

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15
Q

pathogenesis of intracranial injury related gastritis

A

Direct stimulation of vagal nuclei, hypersecretion of acid

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16
Q

What can chronic gastritis lead to?

A

Mucosal atrophy, intestinal metaplasia, dysplastic, development of carcinoma

17
Q

What are 2 main causes of chronic gastritis?

A
  1. H. pylori
  2. Autoimmune gastritis
18
Q

4 disease a/w H. Pylori

A
  1. Chronic Gastritis
  2. Peptic Ulcer
  3. Gastric Carcinoma
  4. Gastric Lymphoma
19
Q

Mechanism of injury of H. Pylori

A
  1. Urease generates free ammonia from endogenous area
  2. Protease breaks don glycoprotein in mucus
  3. Phospholipase damages epithelial cells, release leukotrienes
  4. Neutrophils attracted by H. pylori release MPO
  5. H Pylori colonisation damages epithelial and endothelial cells; thrombotic occlusion of capillaries promoted by bacterial platelet-activating factor
  6. Recruitment of more inflammatory cells to mucosa
  7. Chronically inflamed mucosa more susceptible to acid injury
  8. damaged mucosa permits leakage of tissue nutrients into surface microenvironment, sustaining bacillus
20
Q

4 features relating H. Pylori virulence

A
  1. Flagella
  2. Urease
  3. Adhesin
  4. Toxin (CAG-A)
21
Q

Progression of H. Pylori in Chronic Gastritis

A

Active Inflammation –> Regenerative Changes (mitoses in epithelium, loss of mucus vacuoles) –> Metaplasia (intestinal type) –> Atrophy (loss of glandular structures and specialised cells) –> Dysplasia –> Invasive adenocarcinoma

22
Q

How to diagnose H .Pylori

A
  1. Urea Breath Test
  2. Serology
  3. Histology
  4. CUlture
23
Q

What happens in autoimmune gastritis?

A

Diffuse gastritis of oxynitic mucosa in the body and fundus with extensive intestinal metaplasia and pseudopyloric metaplasia and severe gastric body-fundal atrophy

24
Q

What antibodies can be detected in autoimmune gastritis?

A

Ab to Gastric Parietal Cells & IF

25
Q

What are the consequencs of autoimmune gastritis>

A

Defective gastric acid secretion
Endocrine cell hyperplasia
Disabled VB12 absorption = megaloblastic anemia
chief cell destruction - reduced pepsinogen

26
Q

What are 3 complications of autoimmune gastritis?

A

Pernicious Anemia
Adenocarcinoma
Carcinoid Tumour

27
Q

3 diseases that are associated with autoimmune gastritis?

A

Hashimoto
DM
Graves

28
Q

3 uncommon forms of gastritis?

A
  1. Eosinophilic Gastritis (a/w peripheral eosinophilia and increased IgE)
  2. Lymphocytic Gastritis (a/q celiac and H pylori)
  3. Granulomatous Gastritis (Mycobacteria, Sarcoidosis, Crohn’s)
29
Q

What is peptic ulcer disease?

A

Chronic mucosal ulceration due to hyperacidity

30
Q

What is peptic ulcer disease associated with commonly?

A

H. Pylori Infection

31
Q

How does PUD appear morphologically

A

Breach in mucosa, sharply punched put defect with smooth base; may penetrate the muscularis mucosae and deeper or even perforate
scarring and puckering of the wall

32
Q

Common site of PUD

A

Duodenum, Stomach

33
Q

Risk factors for GERD

A

H. Pylori, NSAIDs, Zollinger-Ellison Syndrome

34
Q

microscopic appearance of chronic peptic ulcer

A

surface zone of necrotic debris
acute inflammatory cells
zone of granulation tissue
zone of dense scar/fibrous tissue

interuption of muscularis propria
proximation of muscularis propria and mucosae
endarteritis obliterans (lumen occluded by fibrosis of blood vessel)

35
Q

Clinical features of peptic ulcer disease

A

Epigastric burning or aching pain 1-3h after meals during day/worse at nigh

Relieved by alkali or food

Nausea, vomitting bloating belching, weight loss

Anemic symptoms, hemorrhage, perforation

36
Q

Complications of PUD

A
  1. Bleeding
  2. Perforation
    Obstruction
    - edema or scarring/strictures (inflammation = scarring; scarring = distortion, distortion = strictures)
    Gastric adenocarcinoma
37
Q

Causes of Upper GI Bleeding

A

Duodenal ulcer
Gastric erosions
Gastric ulcers

Esophageal varices
Mallory-Weiss Tear
Esophagitis
Erosive Duodenitis
Neoplasm

GIT (3 decks)

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