Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Life maintenance > Gastric acid secretion disorders > Flashcards

Gastric acid secretion disorders Flashcards

1
Q

What are the mechanisms of peptic ulcer formation?

A
  • Breakage of mucosal barrier – imbalance between protective and
    damaging factors
  • Exposure of tissues to the erosive effects of HCl and pepsin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the sites affected by peptic ulcers?

A

Oesophagus
stomach
duodenum

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

What are factors pre-disposing to peptic ulceration?

A

-H.pylori
-Smoking
-Stress
-NSAIDs

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

What are protective factors that prevent autodigestion of the stomach?

A
  • Secretion of alkaline mucus and HCO3-
  • Protein content of food
  • Presence of tight junction between the epithelial cells lining the stomach
    and fibrin coat
  • Replacement of damaged cells within the gastric pits
  • Prostaglandins (E and I): inhibit acid secretion and enhance blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does mucus layer protect in the stomach?

A

Mucus layer protects the gastric mucosa
from the low pH of the gastric juice

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

How do NSAIDs play a role in gastric acid secretion disorders?

A

Aspirin blocks the synthesis of PGE2 and TXA2

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

What synthesis do NSAIDs suppress?

A

-Suppresses gastric prostaglandin synthesis

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

What do NSAIDs decrease flow of?

A

↓ gastric mucosal blood flow

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

What do NSAIDs inhibit in stomach?

A

Inhibit platelet aggregation

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

What do NSAIDs interfere with?

A

Interferes with the haemostasis process

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

What gram is H.pylori?

A

Gram negative

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

What shape is H.pylori?

A

Spiral shaped; can be coccoid too

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

What does H.pylori penetrate?

A

Penetrates gastric mucosa (able to survive
under the harsh condition of the stomach

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

What does the flagella of h.pylori enable?

A

The flagella enable its
‘corkscrew’ motility towards
the gut epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a peptic ulcer?

A

ulcer in the digestive tract (in the
stomach or duodenum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What virulence activity does h.pylori have?

A

Mucinase activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does H.pylori produce and what does this do to gastric acid and what does this produce?

A

Produces urease (converts urea to ammonia, which buffers gastric acid
and produces CO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does cytotoxin-associated antigen(CagA) in H.pylori insert?

A

inserts pathogenicity islands and
confers ulcer-forming potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does vacuolating toxin A in h.pylori alter?

A

alters the trafficking of intracellular protein
in gastric cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the commonest cause of peptic ulcers?

A

H.pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does H.pylori infection dysregulate?

A

H.pylori infection dysregulates gastrin secretion → ↑gastrin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the mechanism of H.pylori in mucosal damage?

A

1, H.pylori moves with corkscrew motility and attaches to gastric epithelial cells
2. This h.pylori relesases urease which forms NH3 to neutralise gastric acid.
3. This allows more h.pylori to colonise the gastric epithelial cells
4. Bacterial mucinase then causes mucosal damage
5. Mucosal cell death occurs due to cytotoxins and ammonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the common cause of mucosal damage and ulceration caused by both H.pylori and NSAIDs?

A

-Hydrogen ions
-Pepsin

24
Q

Where are peptic ulcers common in the duodenal cap?

A

first part of the duodenal cap

25
Q

Where are peptic ulcers common in in the stomach?

A

junction of antrum and body

26
Q

What are diagnostic tests for peptic ulcers?

A
  1. Low dose PPI(Omeprazole)
  2. Endoscopy
  3. Histological examination and staining of an EGD biopsy
27
Q

What is a test for the presence of H.pylori?

A
  1. Stool antigen test
  2. Evaluate urease activity through urea breath test
28
Q

What are the steps involved in urea breath test?

A
  1. Take 14C or 13C labelled urea tablet
  2. There is H14CO3- bicarbonate in bloodstream which comes out as 14CO2 in breath
  3. You then collect 2L breath in mylar balloon
  4. Then transfer CO2 to counting vial
  5. Add 10ml scintillation fluid
  6. Scintillation counter will give total count
29
Q

What aer clinical symptoms of peptic ulcers?

A
  1. Nausea
  2. Anorexia
  3. Vomiting
  4. Epigastric pain
  5. Chest discomfort/weight loss
  6. Black, tarry stools
30
Q

Where does chronic peptic ulcer occur?

A

Occurs in upper GIT (pepsin and HCl)

31
Q

Where does acute peptic ulcer develop?

A

Develops from areas of corrosive gastritis (oesophagus, stomach,
proximal duodenum), severe stress or shock (burns, trauma)

32
Q

What happens to surface epithelium by acute peptic ulcer?

A

Acute hypoxia of surface epithelium

33
Q

What are the outcomes of peptic ulcers?

A
  1. Severe bleeding
  2. Heal with no scarring
  3. Chronic peptic ulcer
34
Q

What are complications of peptic ulcer?

A
  1. Haemorrhage (GI bleeding)
  2. Perforation (peritonitis) and penetration (liver and pancreas may be affected); leakage of luminal contents
  3. Narrowing of pyloric canal(stricture causing acquired pyloric stenosis in
    the stomach) or oesophageal stricture
35
Q

What are examples of H2 receptor antagonists?

A

Cimetidine
Famotidine
Nizartidine

36
Q

What are clinical uses of H2 receptor antagonists?

A
  1. Peptic ulcer
  2. Reflex oesophagitis
37
Q

What is the mechanism of action of H2 receptor antagonists?

A

-Inhibit histamine action at H2 receptors on parietal cells
* Reduce gastric acid secretion and as a consequence reduce pepsin
secretion – do you know how it does that?
* Inhibit histamine-, ACh- and gastrin-stimulated acid secretion

38
Q

What are unwanted effects of H2 receptor antagonists?

A

diarrhoea, muscle cramps, transient rashes,
hypergastrinaemia

39
Q

What effect can cimetidine bring in men?

A

Cimetidine → gynaecomastia in men

40
Q

What enzymes may cimetidine inhibit and what may that cause?

A

Cimetidine also inhibits P450 enzymes → ↓ metabolism of a number of
drugs metabolised by P450 enzymes, e.g. anticoagulants, tricyclic
antidepressants (e.g. imipramine, dosulepin, amytriptyline, etc.)

41
Q

What are examples of proton pump inhibitors?

A

omeprazole, lanzoprazole, pantoprazole, rabeprazole

42
Q

What are the clinical uses of proton pump inhibitors?

A

-Peptic ulcer
-Reflux oesophagitis
-Zollinger-Ellison syndrome

43
Q

What is the mechanism of action of proton pump inhibitors?

A
  • Weak bases; inactive at neutral pH and irreversibly inhibit the H+/K+-
    ATPase pump
  • Decreases basal and food-stimulated gastric acid secretion
44
Q

What are unwanted effects of proton pump inhibitors?

A

Headache, diarrhoea, mental confusion, rashes, somnolence, impotence,
gynaecomastia; dizziness

45
Q

What are the combination therapies for H.pylori infection?

A
  • Omeprazole, amoxicillin and metronidazole
  • Omeprazole, clarythromycin and amoxicillin or tetracycline, metronidazole and
    bismuth chelates
  • Lansoprazole, clarithromycin, tinidazole and bismuth chelates
46
Q

What is an example of a drug that protects the gastric mucosa?

A

Bismuth chelate

47
Q

What does bismuth chelate provide?

A

Provide a physical barrier (coat) over the surface/base of the ulcer

48
Q

What does bismuth chelate enhance local synthesis of?

A

Enhances local synthesis of PGs

49
Q

What does bismuth chelate promote secretion of?

A

Promote bicarbonate secretion

50
Q

What are the side effects of bismuth chelate?

A

-Nausea
-Vomiting
-Blackening of tongue and faeces

51
Q

What can bismuth chelate do to patients with renal impairments?

A

May rise causing encephalopathy

52
Q

What type of reaction do we get if metronidazole is taken with alcohol and how will patient feel?

A

Disulfiram-like reaction
-Patient will feel severely ill

53
Q

What does disulfiram inhibit and what deos this cause?

A

Disulfiram inhibits acetaldehyde dehydrogenase, build up of
acetaldehyde → unpleasant flushing and nausea & headache

54
Q

When do you not give metronidazole to pregnant women?

A

First trimester

55
Q

What are examples of drugs that protect the gastric mucosa?

A

Prostanoids
-PGE2
-PGI2
-TXA2

56
Q

What is misoprostol?

A

Misoprostol (a synthetic analogue of PGE1)

Life maintenance (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions