Peptic Disease and Gastritis

Question 1

Gastric glands and what they secrete

Answer 1

• Parietal Cells: found throughout the gastric complex and secrete HCL
• Chief Cells: Secrete pepsinogen
• Mucous cells: Found in neck. Bicarbonate rich mucous
• G cells: only found in antrum and they secrete gastrin

Question 2

What are the three receptors on the serosal side of the parietal cell?

Answer 2

Acetylcholine receptor- receive Ach which comes from the vagus nerve (parasympathetic) which is stimulated by eating. Increases intracellular calcium

Gastrin receptor- Increases intracellular calcium

Histamine Receptor- Receives histamine. activates adenylate cyclase which increases cAMP levels which aids in acid secretion

Basically, high intracellular calcium concentrations trigger the H/K ATPase to pump hydrogen out and potassium in

Question 3

What is the significance of the protaglandin receptor on the serosal surface of the parietal cell

Answer 3

Allows negative feedback as prostaglandin binding leads to low cAMP.

Question 4

What stimulates Ach release via the Vagus nerve?

Answer 4

Taste, smell, chewing

Question 5

Three phases of acid secretion

Answer 5

1) Cephalic- taste, smell, chewing
2) Gastric- chemical effects of food and distension of teh stomach stimulate gastrin release by G cells
3) Intestinal- Food and acid in small bowel causes release of CCk and secretin which inhibit acid production

Question 6

Duodenal ulcer and acid secretion

Answer 6

Pts with duodenal ulcer=

• Basal acid output twice as high in pts with duodenal ulcer
• Peak acid output higher in pts with duodenal ulcer
• Serum gastrin is higher in pts with duodenal ulcer

Question 7

Mucous secretion in the stomach creates a bicarbonate layer which makes a pH gradient that prevents autodigestion

Answer 7

ok….pts with peptic ulcer disease may have decreased bicarb

Question 8

Most common symptoms of peptic ulcer

Answer 8

abdominal pain in 80%
- may be nocturnal or relieved by food
Nausea

Question 9

Risk factors for PUD

Answer 9

• Heliobacter Pylori gastritis
• Medicines like NSAIDS
• Smoking
• genetics

Question 10

PUD in chrinic diseases such as

Answer 10

• ICU pts on ventillators
• those with cirrhosis
• organ transplant pts
• COPD

These pts usualy get prophylactic PPI’s while in ICU

Question 11

Morphology of Heliobacter Pyloris

Answer 11

spiral shaped gram neg organism with 4-6 flagella

Question 12

H. Pylori makes what substance which makes it resistant to gastric acid

Answer 12

Urease

Question 13

H. Pylori resides where?

Answer 13

In the mucous layer overlying the gastric epithelium.

Question 14

H. Pylori and inflammation?

Answer 14

H. Pylori releases a Peptide and Lipopolysaccharide which are chemotactic for neutrophils and monocytes. These inflammatory cells release oxygen radicals, prostaglandins, IL-1 and TNF which then promote addittional inflammation

Question 15

Slide 19 is a good summary

Answer 15

ok

Question 16

H Pylori is most likely trasnsmitted how?

Answer 16

Person to person

Question 17

High risk for NSAID GI Toxicity?

Answer 17

two criteria:

• History of complicated ulcer in the past OR…
• more than one of the moderate risk factors which are (over the age of 65, high dose NSAID therapy, previous uncomplicated ulcer, concurrent use of aspirin, gluccocorticoids, or corticosteroid)

Question 18

Dx of H. Pylori

Answer 18

Barium x ray of stomach

Endoscopy (this also allows for biopsy for H. Pylori testing)

Question 19

Complications of PUD

Answer 19

• Bleeding: hematemesis, melena, anemia
• Perforation; need surgery
• Penetration- may penetrate into adjacent organ
• Gastric outlet obstruction

Question 20

Treatment of PUD

Answer 20

• Anti-secretory agents (H2 blockers) or PPIs for 6-8 wks
• Treat H. Pylori
• Avoid smoking, NSAIDS.

Question 21

Gastritis

Answer 21

Pathological diagnosis of gastric inflammation of mucosa

- may be acute or chronic

Question 22

Causes of Gastritis

Answer 22

NSAIDS, H. Pylori, Alcohol, ischemia, extreme stress

Question 23

Endoscopic erosive gastritis

Answer 23

multiple erosive and hemorrhagic lesions on endoscopy

Question 24

Alcoholic hemorrhagic gastritis

Answer 24

multiple subepithelial hemorrhages without without any visible breaks in the mucosa (blood under plastic wrap)

Question 25

Helicobacter Pylori Gastritis (Type B) most commonly affects which part of the stomach most

Answer 25

Antrum (whereas type A (genenrally autoimmune) affects the body and fundus most frequently)).

Question 26

What type of immune cells are most common in helicobacter pylori gastritis

Answer 26

Lymphocytes, they commonly form germinal centers with neutrophils present (this is why it is referred to as a “chronic active gastritis”). MUST KNOW THIS

Question 27

Which type of Gastritis increases your risk of cancer?

Answer 27

Helicobacter Pylori Gastritis— Increased risk of adenocarcinoma or low grade lymphoma
KNOW

Question 28

Most important Helicobacter Pylori Toxin

Answer 28

Cag A protein - disables p53 and allows cell proliferation pathways to activate. Injected into cels by the syringe like Type 4 Secretion System (T4SS)

Question 29

What is autoimmune atrophic gastritis

Answer 29

ab to parietal cells and intrinsic factor, Causes achlorhydria and loss of Intrinsic factor

Question 30

Layers in peptic ulcer disease micro histology

Answer 30

N= necrosis
I- Inflammtion
G- Granulation Tissue
S- scarring

Question 31

Benign ulcer vs malignant ulcer characteristics

Answer 31

Benign- Round-oval, flat or overhanging margins, deep and punched out, smaller (less than 2cm), radiating rugal folds

Malignant- Irregular shape, heaped up margins. shallower, ulcerated mass, bigger (over 3 cm)

Question 32

Cushing ulcer

Answer 32

Occurs with brain injury- leads to persistent vagal stimulation and high Ach levels. thus high acid.

Question 33

Curling ulcer

Answer 33

burns