Peptic Diseases and Gastritis (Jackson/Nichols)

Question 1

gastric cells that make HCl

Answer 1

parietal

Question 2

gastric cells that make pepsinogen

Answer 2

chief

Question 3

gastric cells that make bicarbinate rich mucos

Answer 3

mucous cells

Question 4

gastric cells that make gastrin

Answer 4

g cells

Question 5

what intracellular processes drigger H/K ATPase activity

Answer 5

↑ Ca (thru IP3) and ↑ cAMP (thru AC)

Question 6

exert a negative feedback on acid secretion in partial cells?

Answer 6

distention, low pH, somatostatin, and prostaglandins inhibit parietal cell H+ secretion

CCK and secretin inhibit action of gastrin

Question 7

what is the cephalic phase of acid secretion

Answer 7

Taste, smell, and chewing food stimulates acetylcholine release via the vagal nerve → partial cells secrete HCl (30% of total secretion)

Question 8

What is the gastric phase of acid secretion?

Answer 8

Chemical effects of food and distension of stomach causes:

• release of gastrin by the G cells (indirect stim of parietal cells)
• release of Ach from vagal N to directly act on parietal cells

Question 9

how does gastric acid secretion in pts with DUODENAL ulcers compare to secretion in normal patients? GASTRIC ulcers?

Answer 9

Duodenal: ↑H+ (2x nml) and ↑gastrin

Gastric: ↓H+ and ↑gastrin (H+ leaks out due to damage to the mucosa and gastin ↑ to compensate)

Question 10

what prevents auto digestion?

Answer 10

mucos-bicarb layer in stomach

Question 11

how does duodenal bicarb secretion in pts with DUODENAL ulcers compare to secretion in normal patients

Answer 11

↓ basal [bicarb] and ↓ acid stimulated secretion of bicarb

Question 12

definition of PUD

Answer 12

defect in GI mucose extending THROUGH THE MUSCULARIS MUCOSA

Question 13

Risk factors for PUD

Answer 13

PUD HANGS around with H pyloir:

H pylori
ASA
NSAIDs
Genetics
Smoking

Question 14

What chronic diseases is PUD assc with? how is it prevented in these conditions (i.e. what is the prophylactic treatment?)

Answer 14

Stress
Transplanted organs
Cirrhosis
COPD

prophylactic PPIs

Question 15

symptoms of PUD

Answer 15

abd pain (nocturnal or with food)
nausea
anorexia
**may be asympomatic and present with complication = bleeding or perforation

Question 16

morphology of H pylori

Answer 16

gram - spiral shaped with 4-6 flagella

Question 17

pts infected with h pylori will have ↑ or ↓ response to gastrin/acid production. why?

Answer 17

↑ due to ↓somatostatin release

Question 18

Since H pylori colonize gastric mucosa, how do they cause a duodenal ulcer?

Answer 18

1. inhibit somatostatin secretion → gastrin → ↑H+ secretion
2. inhibits duodenal HCO3- secretion → duodenal contents become abnormally acidic → mucosa eroded
3. ↑ gastrin has trophic effect on parietal cells →↑H
4. increased inflammatory cells and cytokines

Question 19

top 2 causes of PUD

Answer 19

H pylori and NSAIDs

Question 20

How does H pylori elicit an inflammatory response

Answer 20

secretes LPS and peptides that will cross gastric epithelium and are then chemotactic for neutrophils and monocytes in the lamina propria → monocytes secrete TNF< IL-1, O2-, Prostaglandins

Question 21

how does NSAID use leas to PUD

Answer 21

NSAIDS
▪︎ ↑HCl
▪︎ ↓bicarb
▪︎ ↓glutathione → ↑ROS

Question 22

pareital cell hyperplasia occurs as a result of

Answer 22

↑ vagal stimulation and gastrin

Question 23

how is the diagnosis of PUD made

Answer 23

UGI barium X ray

upper endoscopy **also allows for biopsy

Question 24

What are the complications of PUD?

Answer 24

bleeding → hematemesis, melana, anemi
perforation
penetration into adj organs (pancreas, liver, colon)
obstruction (due to edema or fibrosis)

Question 25

perforated duodenal ulcers are assc with

Answer 25

ZES, NSAIDs, cocaine

Question 26

Acute PUD → obstruction due to ____. | Chronic PUD → obstruction due to _____.

Answer 26

Acute PUD → obstruction due to edema. | Chronic PUD → obstruction due to fibrosis.

Question 27

Obstruction causes pt to _____ several hours after they eat

Answer 27

vomit

Question 28

Treatment of PUP

Answer 28

H2 blockers or PPIs | Abx

Question 29

can you assume a pt with a + serological test for H pyloru has an active H pylori infection

Answer 29

no, they may have cleared it but they still have Abs made to it

Question 30

defn of gastritis. How is this diff than the defn of PUD?

Answer 30

``` gastritis = infalmmation of mucosa PUD = inflammation and damage extends thru the muscularis mucosa ```

Question 31

common causes of gastritis:

Answer 31

H pylori NSAIDs alcohol extreme stress (ICU (less common: chemo, bile reflux, truama, burns, sepsis, shock)

Question 32

“blood under plastic wrap” on endoscopy indicates

Answer 32

multiple subepi hemorrhages without any breaks in mucosa = assc with alcohol use

Question 33

numerous petechiae and erosions of on gastric mucosa

Answer 33

acute hemorrhagic gastritis

Question 34

causes of chronic gastritis

Answer 34

H pylori > autoimmune and bile reflux

Question 35

chronic gastritis can lead to

Answer 35

atrophy, intestinal metaplasia/dysplasia/neoplasia

Question 36

WHere is the stomach is chronic gastritis due to H pylori likely to affect? autoimmune?

Answer 36

ABBA Bacteria = Antrum Autoimmune = Body

Question 37

what type of cells will predominate in chronic active gastritis

Answer 37

neutrophils = ACTIVE!!

Question 38

chronic gastritis due to (autoimmune or H pylori) commonly displays lymphoid follicles/germinal centers

Answer 38

H pylori

Question 39

where will the H pylori organisms be found in chronic gastritis

Answer 39

superficial MUCOUS layer (above the epi)

Question 40

most important virulence factors for H pylori

Answer 40

CagA protien **degrades p53** also, T4SS (found in CagPAI)

Question 41

characteristics of autoimmune chronic gastritis

Answer 41

4 A's Abs to parietal cells Achlorhydria pernicious Anemia (Abs to intrinsic factor) Atrophy*all chronic gastritis cuases atrophy, so maybe only 3 A's?

Question 42

↑ risk for MALT lymphoma

Answer 42

H pylori chronic gastritis

Question 43

assc with G cell and partial cell hyperplasia | assc with parietal cell hyperplasia (No G cell)

Answer 43

BOTH: autoimmune chronic gastritis **loss of parietal cells at the same time since there are Abs made against it Parietal only: PUD (due to ↑Ach/vagal stim and gastrin)

Question 44

seen in histo of chronic PUD

Answer 44

NIGS | necrosis, inflammation, granulation tissue, scar

Question 45

bigger or smaller ulcers are signs of benignity

Answer 45

smaller

Question 46

deeper or shallow ulcers are signs of benignity

Answer 46

deeper

Question 47

stress ulcers occur with

Answer 47

Brain injury = Cushing ulcer (↑vagal stim → inc Ach and H+ secretion) **C(r)ush the brain and you may get stress ulcer** Burns = Curling ulcer (↓plasma volume → sloughing of gastric mucosa) **burned by a curling iron**

Question 48

describe appearance of stress ulcer

Answer 48

deep, single, small (<1 cm) penis to DEEPly penetrate Katniss which makes her BLEED You are welcome.