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Pathophysiology > Peptic Ulcer Disorder > Flashcards

Peptic Ulcer Disorder Flashcards

1
Q

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

A

bicarbonate

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2
Q

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

A

reduces

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3
Q

What do superficial epithelial cells do?

A

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

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4
Q

What do chief cells do?

A

produce digestive enzymes (pepsinogen, chymotrypsin, gastric lipase)

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5
Q

What do parietal cells do?

A

produce HCl

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6
Q

What do G cells do?

A

produce gastrin

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7
Q

What do enterochromaffin-like cells (ELC) do?

A

release histamine

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8
Q

How does a drug like Zantac work?

A

Zantac surpresses the parietal cells that produce acid (HCl)

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9
Q

_____ binds to receptor on parietal cell and increases acid production

A

histamine

*see slide 6

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10
Q

What are examples of gastric acid producers?

A

acetylcholine
gastrin
histamine

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11
Q

What are examples of gastric acid (HCl) reducers ?

A

prostaglandins
somatostatin

  • these are good for stomach, it increases bicarbonate and mucous layer
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12
Q

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

A

NO. They block production of prostaglandins.

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13
Q

Describe the layers of the stomach

A
  • mucus layer
  • bicarbonate layer
  • superficial epithelial ells
  • mucosal capillaries and sub mucosal arteries (blood)
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14
Q

What is the purpose of having mucus?

A
  • physical barrier that pepsin and other proteases cannot penetrate
  • slows pH gradient from 2-6
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15
Q

What is the purpose of the bicarbonate layer?

A

neutralizes H+

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16
Q

mucosal blood flow is critical for supplying ____

A

bicarbonate

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17
Q

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

A

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

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18
Q

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

*IMPORTANT

A
  • drugs
  • alcohol
  • stress
  • smoking
  • immobility
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19
Q

Define: erosion

A

superficial injury caused by either:

  • decrease in mucosal defences
  • increase in gastric acid
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20
Q

Define: ulcer

A

complete erosion through the GI mucosa

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21
Q

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

A
  • helicobacter pylori (most common)
  • NSAID induced
  • stress induced (uncommon)
22
Q

Can you die from a stomach ulcer?

A

Yes

23
Q

Define: gastritis

A

inflammation in the stomach

24
Q

Define: duodenitis

A

inflammation in the duodenum

25
Q

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

A

duodenal

26
Q

Describe H. pylori

A
  • 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
Q

What are the 3 virulence factors of H. pylori ?

*ON EXAM

A

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
Q

Pathological properties of H. pylori:

Describe urease

A

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

29
Q

Pathological properties of H. pylori:

Flagella

A

allow penetration to mucus layer of the epithelial cells

30
Q

Pathological properties of H. pylori:

Vac A = vacuolating toxin

A
  • induces inflammation/apoptosis
  • promotes formation of acidic vacuoles inc ells
  • forms pores in epithelial cell membranes
31
Q

Pathological properties of H. pylori:

LPS

A

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

32
Q

What is the most common symptom of PUD?

A

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
Q

If symptoms improve from eating = ____ ulcer

A

duodenal

34
Q

If symptoms don’t improve from eating = ____ ulcer

A

gastric

35
Q

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

A

acute gastritis

36
Q

Acute gastritis then worsens into ____ ____ _____

A

chronic active gastritis

37
Q

What can chronic active gastritis develop into?

A

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

38
Q

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

A
  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
Q

Describe 2 PUD symptoms of a gastric ulcer

A
  • burning pain over a wide area below the breast bone

- precipitated by food!!

40
Q

Describe 3 PUD symptoms of a duodenal ulcer

A
  • 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
Q

What is the most common noninvasive diagnostic method for PUD?

A

urea breath test

*downside - it’s expensive

42
Q

What is the most common invasive diagnostic method for PUD?

A

histology

*requires expert pathologist and biopsy

43
Q

What are the 3 main lifestyle effects relating to PUD?

A
  • alcohol consumption
  • smoking
  • cocaine/amphetamine (reduce blood flow which means less bicarbonate)
44
Q

Are prostaglandins good in PUD? Why or why not?

A

Yes

  • stimulate bicarbonate secretion
  • mucous secretion
  • stimulate mucosal cell growth
  • decrease acid production
45
Q

Why are NSAIDs bad? Why can they cause PUD?

A

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

46
Q

Are muscarinic antagonists used?

A

Not really

47
Q

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

A

antibiotics

48
Q

Are histamine H2 receptor antagonists used?

A

They are but are less common.

49
Q

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

A

block H+ K+ ATPase

50
Q

How many CCK2 receptor antagonists exist?

A

none

Pathophysiology (15 decks)

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