Peptic Ulcer Disorder Flashcards Preview

Pathophysiology > Peptic Ulcer Disorder > Flashcards

Flashcards in Peptic Ulcer Disorder Deck (50):
1

______ comes up from the blood flow to neutralize the mucus layer on top of the stomach lining

bicarbonate

2

anything that _____ blood flow, you can start getting stress induced ulcers

reduces

3

What do superficial epithelial cells do?

Produce mucus and bicarbonate to neutralize acid and prevent damage to the lining of the stomach

4

What do chief cells do?

produce digestive enzymes (pepsinogen, chymotrypsin, gastric lipase)

5

What do parietal cells do?

produce HCl

6

What do G cells do?

produce gastrin

7

What do enterochromaffin-like cells (ELC) do?

release histamine

8

How does a drug like Zantac work?

Zantac surpresses the parietal cells that produce acid (HCl)

9

_____ binds to receptor on parietal cell and increases acid production

histamine

*see slide 6

10

What are examples of gastric acid producers?

acetylcholine
gastrin
histamine

11

What are examples of gastric acid (HCl) reducers ?

prostaglandins
somatostatin

* these are good for stomach, it increases bicarbonate and mucous layer

12

Are NSAIDS (ex. aleve) good for people with stomach problems?

NO. They block production of prostaglandins.

13

Describe the layers of the stomach

-mucus layer
-bicarbonate layer
-superficial epithelial ells
-mucosal capillaries and sub mucosal arteries (blood)

14

What is the purpose of having mucus?

-physical barrier that pepsin and other proteases cannot penetrate
-slows pH gradient from 2-6

15

What is the purpose of the bicarbonate layer?

neutralizes H+

16

mucosal blood flow is critical for supplying ____

bicarbonate

17

What happens if there is an imbalance between gastric acid and mucosal defences?

-it can result in inflammation and damage to stomach lining leading to ulcerations

18

What 5 things reduce blood flow and therefore can lead to stomach ulcerations?

*IMPORTANT

-drugs
-alcohol
-stress
-smoking
-immobility

19

Define: erosion

superficial injury caused by either:
-decrease in mucosal defences
-increase in gastric acid

20

Define: ulcer

complete erosion through the GI mucosa

21

What are the 3 main causes of PUD (peptic ulcer disease) ?

-helicobacter pylori (most common)
-NSAID induced
-stress induced (uncommon)

22

Can you die from a stomach ulcer?

Yes

23

Define: gastritis

inflammation in the stomach

24

Define: duodenitis

inflammation in the duodenum

25

What kind of ulcers are more common: duodenal or gastric?

duodenal

26

Describe H. pylori

-gram neg bacteria
-spiral shaped
-spread from person to person by fecal-oral route
-it attaches to cells of the stomach and can stimulate the production of excess stomach acid
-contracted through food and water

27

What are the 3 virulence factors of H. pylori ?

*ON EXAM

H. pylori has genes that make it more capable of:
-colonizing the stomach
-penetrating through the mucous layer to evade the low gastric pH (kills superficial epithelial cells which produce mucus)
-causing inflammation and cell death

28

Pathological properties of H. pylori:
Describe urease

ammonia produced can neutralize gastric acid allowing it to move from the stomach to the gastric mucosa

29

Pathological properties of H. pylori:
Flagella

allow penetration to mucus layer of the epithelial cells

30

Pathological properties of H. pylori:
Vac A = vacuolating toxin

-induces inflammation/apoptosis
-promotes formation of acidic vacuoles inc ells
-forms pores in epithelial cell membranes

31

Pathological properties of H. pylori:
LPS

recruits and activates immune cells - resulting in inflammation which kills epithelial cells

32

What is the most common symptom of PUD?

a gnawing or burning abdominal pain, usually in the area just beneath the ribs

other symptoms:
weight loss
loss of appetite
bloating
burping
nausea
etc.

33

If symptoms improve from eating = ____ ulcer

duodenal

34

If symptoms don't improve from eating = ____ ulcer

gastric

35

H. pylori attacks the normal gastric mucosa and causes _____ ______

acute gastritis

36

Acute gastritis then worsens into ____ ____ _____

chronic active gastritis

37

What can chronic active gastritis develop into?

Either:
antral gastritis which produces a duodenal ulcer
Or
pan gastritis which produces a gastric ulcer

38

Describe the general pathogenesis of ulcers (either gastric or duodenal)

1. H. pylori infection
2. Inflammation stimulates increased release of gastrin
3. gastrin induces acid secretion from body of stomach
4. increased acid and inflammation damages mucosa causes ulceration

39

Describe 2 PUD symptoms of a gastric ulcer

-burning pain over a wide area below the breast bone
-precipitated by food!!

40

Describe 3 PUD symptoms of a duodenal ulcer

-focal pain between breast bone and belly button
-pain releived by eating but will reoccur 1-3 hours after meals
-pain worse at night

41

What is the most common noninvasive diagnostic method for PUD?

urea breath test
*downside - it's expensive

42

What is the most common invasive diagnostic method for PUD?

histology
*requires expert pathologist and biopsy

43

What are the 3 main lifestyle effects relating to PUD?

-alcohol consumption
-smoking
-cocaine/amphetamine (reduce blood flow which means less bicarbonate)

44

Are prostaglandins good in PUD? Why or why not?

Yes
-stimulate bicarbonate secretion
-mucous secretion
-stimulate mucosal cell growth
-decrease acid production

45

Why are NSAIDs bad? Why can they cause PUD?

Because they inhibit prostaglandin synthesis!! And prostaglandins are good!

46

Are muscarinic antagonists used?

Not really

47

What is the main treatment method to kill H. pylori ?

antibiotics

48

Are histamine H2 receptor antagonists used?

They are but are less common.

49

What is another part to the treatment of H. pylori ?

block H+ K+ ATPase

50

How many CCK2 receptor antagonists exist?

none