GI - Peptic Ulcer Disease (PUD) Flashcards

1
Q

What is PUD? Where is it located? Provide %.

A

Ulceration in the upper GIT.

Located in duodenum (80%) and stomach (20%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Incidence %?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Is it curable? If yes, how so?

A

Yes. Antibiotics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What protection does the stomach have that the duodenum does not? and vice versa

A

The stomach has a mucous layer that secrete mucous to protect from HCl

Pancreatic juice is released to the duodenum to neutralize acid with bicarbonate ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why are incidents higher in duodenum?

A

It depends on the action of pancreatic juice. If acid enters duodenum with no pancreatic juice then it is damaged.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which layers of GIT is mostly impacted and where most ulcers are found?

A

The Mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Can acid penetrate to deeper layers?

A

YES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Patient can experience chronic ____ and ____ if ___ and ____ or if _____ occur

A

remission and exacerbation

untreated and uneradicated

reinfection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Etiology: what bacteria is found in PUD?

A

Heliobacter pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Etiology: The site of attachment is ____. H. Pylori is part of the ____ flora.

A

epithelial lining

transient flora (colonizes in GIT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Etiology: H. Pylori secretes ____ ____ to attach on surface of the duodenal/stomach wall

A

adhesion proteins/factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Etiology: What enzyme does H. Pylori secrete? What does the enzyme do? How does it benefit the bacteria?

A

Urease = converts urea to CO2 and NH2

Ammonia (NH2) is basic and can neutralize the gut acid in the vicinity of the bacteria

CO2 combines with H2O in the stomach to produce H2CO3 (carbonic acid) which dissociates rapidly to bicarbonate ion and hydrogen ions. Bicarbonate ions buffers the HCl to protect bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The bacteria creates a _______. How does it benefit the bacteria?

A

Microenvironment/micro-niche:

an area surrounding the bacteria that is neutralized to protect the bacteria from the gut acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the protective factors of the GIT? (4)

A
  1. mucous lining of the stomach
  2. regeneration of the mucosa
  3. regulation of the acid secretion
  4. good perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the risk factors of PUD? (5)

A
  1. HCl and biliary acid (secreted in stomach and found in bile)
  2. Chronic Gastritis (acid impact damaged tissues d/t inflm)
  3. NSAIDs (impairs healing and regeneration of mucosa, irritate mucosa, decrease syn. of PG)
  4. Smoking and alcohol (aggravate lining of the gut)
  5. H. Pylori
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Patho: PUD (2)

A
  1. Due to proposed role of H. Pylori

2. Risk factors overcomes the defense of the gastric acid

17
Q

Patho: How does H. Pylori cause tissue damage? (2)

A
  1. infection–> inflammation–> tissue damage

2. hypergastrinemia–> increase acid secretion–>tissue damage

18
Q

How does HCl and biliary acid affect tissues?

A

HCl and biliary acids acts readily on damaged tissues causing additional damage and impedes cell protection (cells are unable to secrete mucous).

19
Q

What are the defense against gastric acids? (4)

A
  1. mucous lining in stomach
  2. good perfusion
  3. regeneration of the mucosa
  4. regulation of acid secretion
20
Q

Manifestations (2)

A
  1. abdominal pain - burning and cramping: d/t inflm and acid affecting the wall
    - can be confused w/ angina
    - there’s no gastric content so acid act on stomach wall more easily
  2. nausea and vomiting: d/t infection and irritation by acid in stomach and duodenum
21
Q

Manifestation depends on ___, ___, and ____

A
  1. size: single or multiple
  2. site: stomach and duodenum
  3. penetration: how deep
22
Q

Manifestations can _____ and __

A

come and go

eg. w/ full or empty stomach

23
Q

Complications of PUD (3)

A
  1. perforation: penetrating ulcers perforate thru stomach and duodenum wall—> HCl spills into ab. cavity—> chemical peritonitis
  2. hemorrhage: occurs in upper GIT and appears as dark occult blood in feces (blood mix with stool and not easily detected)
  3. obstruction: d/t several reason
    - –> pyloric sphincter is narrow
    - -> edema from inflm
    - –> increase secretion of exudate or muscle spasms
    - –> scar tissue contraction: scar tissue brings two edges together and contracts
24
Q

Diagnosis of PUD (5)

A
  1. UBT: urea breath test
  2. serology
    - measures antibodies that is formed to fend off the bacteria
  3. fecal antigen
    - looking at antigens from H. Pylori
  4. barium x-ray
    - barium is ingested and attaches to GIT and is shown thru specialized x-ray to shows presence of ulcers
  5. gastroscopy
    - scope inserted to the upper GIT thru the mouth into the beginning of duodenum
25
Q

How does UBT work?

A
  • carbon-13 is a radioisotope that can be traced
  • Pt ingest soln containing urea labelled w/ C-13
  • after 30min to 2hrs a patient blows into a bag to collect exhaled air
  • If the person has H Pylori in stomach or duodenum it will secrete urease, and the urea that is ingested will convert to CO2 and NH2
  • CO2 will get picked up in blood and transported to lungs to be exhaled
  • When patient blows in the bag the air is analyzed for radioactivity (came from urea)
26
Q

What is an Ulcer?

A

an open sore in external/internal body surface caused by a break in skin or mucous mem. that fails to heal

27
Q

How does H. Pylori cause ulcer formation?

A

H Pylori–> attach to wall–> inflm–> damage to tissue–> xs prod. of acid furthering damage–> ulcer formation

28
Q

Ulceration is where most _____ occurs and where _____ has most impact

A

inflm

acid

29
Q

Treatment of PUD

A
  • anaticid
  • triple regimen: PPI or H2RA + 2 antibiotics
  • sx if req (d/t complications eg hemorrhage)
30
Q

How does antacids aid PUD?

A

Decrease acidity to cause less aggravation of the ulcers

31
Q

How does antibiotics treat PUD? Does it heal ulcers? Examples (3)?

A

eradicate the bacteria

no

  • flagyl
  • biaxin
  • amoxicil
32
Q

What does PPI do? Examples? What antibiotics are normally used with PPI?

A

Proton Pump Inhibitors

Action: inhibits the pumping of hydrogen ions which is needed to form HCl and to heal ulcers

Examples: Losec –> decrease acid secretion to allow ulcers to heal

Antibiotics:  Flagyl and biaxin

33
Q

What does H2RA do? Example? What antibiotics are normally used with H2RA?

A

Histamine receptor antagonists

Action: blocks hydrogen synthesis and decrease secretion of acid

Examples: Zantac (newer)and Tagamet (older and less common)

Antibiotics: Amoxil + biaxin

34
Q

What is the first line therapy of triple regimen?

A

PPI + amoxicil + biaxin

35
Q

How long are antibiotics used?

A

7-10 days to get rid of infections

36
Q

How long are PPI and H2Ra used?

A

used up to 6-8 weeks to heal ulcers