Brainscape's Knowledge GenomeTM

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


See full index

GI Physiology > 46 Gastrointestinal Disorder I > Flashcards

46 Gastrointestinal Disorder I Flashcards

1
Q

GI disorders are the dysfunction of _______ or _______.

A

Secretion; Motility

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

In patients with Achalasia, what can be observed and what are the causes of the disease?

A

Observation:

  • Dysregulation of neural pathway (functional obstruction)
  • Insufficient peristaltic waves
  • Increase in LES pressure
  • Uncoordinated peristalsis and impaired swallowing

Cause of achalasia?
- loss of relaxing factor in ENS neurons (neuropathy of myenteric neurons)

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

How can achalasia be diagnosed?

A 
Barium radiology
Manometric studies (pressure related)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List the 4 types of treatments for achalasia patients.

A
  1. Balloon dilation: Disrupt LES fibers (first line treatment method)
  2. Anti-spasmotic drugs: reduce LES pressure
    (e. g. CCB Ca2+ channel blockers/ amyl nitrate)
  3. Surgical option = myotomy : cut LES fibers (permanent)
  4. Botulinum toxin injection: decrease cholinergic input and thus reduce LES pressure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Manometric studies
Resting pressure of LES is ______ mmHg, while swallowing, the pressure of LES is _______mmHg.

In achalasia patients, the LES pressure is normally _____ mmHg; while in total relaxation the pressure is ________mmHg.

A

30;0

60;45

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

In GERD patients, LES pressure is ______ than normal.

A

Lower

> therefore reflux of gastric contents

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

What are the 3 factors influencing LES motility?

State all the examples and how they affect LES motility.

A

achalasia: neuropathy of myenteric neurons results in loss of VIP/NO relaxing/inhibitory factors

  1. Endocrines (hormones)
    Stimulatory: Gastrin
    Inhibitory: CCK, Secretin
  2. Neurocrines (Vagal and ENS)
    Stimulatory: Acetylcholine, Substance P
    Inhibitory: NO, VIP
  3. Food and others
    Stimulatory: proteins and antacids
    Inhibitory: Chocolate, Ethanol, smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List the 2 causes of Peptic Ulcer Disease (PUD).

A
  1. Excess secretion of HCl and pepsin: Duodenal ulcer (DU)
  2. Diminished ability of the gastric mucosal protection system: Gastric ulcer (GU)
    * acid level is normal/subnormal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List 4 factors affecting the gastric mucosal protection system.

A
  1. Acid (Harmful but can kill bacteria)
  2. Mucus and HCO3- (provides pH gradient)
  3. Replacement of damaged cells (restitution) by gastric neck cells (stem cells)
  4. Prostaglandins
    - Cytoprotective factor
    - Secreted by mucus cells, chief cells and parietal cells in GI
    - Derived from arachidonic acids of cell membrane catalysed by cyclooxygenase COX
    (should be COX2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

State the 3 functions of the gastric mucosal protection system.

A

any 3 of 5
1. Act as anti-secretory effect (directly inhibit acid secretion by parietal cells)

  1. Stimulate mucus and HCO3- secretion (increase gastric mucosal barrier)
  2. Enhance mucosal blood flow (increase mucosal cell metabolism)
  3. Reduce mucosal H+ ion back-diffusion (increase mucosal impermeability to acid)
  4. Accelerate cell turnover of gastric mucosa (increase cell renewal rate/ restitution)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which of the followings are causes of Peptic Ulcer Disease (PUD)?

  1. High pepsin level
  2. Irritation (drug induced, like aspirin)
  3. Rich blood supply
  4. Impaired HCO3- and mucus secretion
  5. Infection (e.g. H.pylori)
A

All except 3

Should be poor blood supply.

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

What are the common sites for PUD?

A
  1. Lower end of esophagus, close to LES
  2. First few cm of duodenum, close to pylorus
  3. Lesser curvature of antral end (not common)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gastrin is produced by antral and duodenal G cells.

Name the 5 physiological roles of gastrin.

A
  1. Stimulate gastric acid secretion by parietal cells (another major stimulants are histamine and Ach)
  2. Stimulate the growth of gastric gland mucosa, especially the trophic action on parietal cells
  3. Increase gastric motility
  4. Increase intestinal secretion of electrolyte and water, esp in excessive elevation of serum gastrin (Gastrinoma patients complain with diarrhea)
  5. Negative feedback mechanisms of gastrin and acid mediated of paracrine action of somatostatin on G cells and parietal cells (to inhibit gastrin release)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In pernicious anemia, (atrophy of gastric mucosa),

Basal acid output is _____; Serum gastrin is _____.

A

0;
very high

In pernicious anemia, the body produces auto antibody to attack parietal cells which produces IF and acid: no acid secretion; high gastrin level

*When acid increases, gastrin release decreases

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

In gastric ulcer:

Basal acid output is _____; Serum gastrin is _____.

A

1.5;
higher than normal

Gastric ulcer (due to diminish gastric mucosal layer function): subnormal acid production, thus high gastrin level

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

In duodenal ulcer:

Basal acid output is _____; Serum gastrin is _____.

A

6;
Lower than normal

Duodenum ulcer (due to excess production of acid): excess acid, lower gastrin levels

17
Q

G cell hyperplasia:

Basal acid output is _____; Serum gastrin is _____.

A

15;
Abnormally high

G cell hyperplasia (over expression of G cells): high acid, high gastrin

18
Q

Gastrinoma (Zollinger-Ellison Syndrome = tumour in pancreas):
Basal acid output is _____; Serum gastrin is _____.

A

20;
Extremely high >1000

Gastrinoma (tumor in pancreas) : high acid output, extremely high gastrin level by the tumour ** in pancreas!

19
Q

Name the pancreatic endocrine tumour (PET) arising from islet cells for each case:

A originated from pancreas that abnormally produces gastrin, hypergastrinemia

B excessive levels of insulin by the pancreas, causing hypoglycemia

C excessive levels of VIP, causing watery diarrhea

D excessive levels of glucagon

A

A: Gastrinoma
B: Insulinoma
C. VIPoma
D: Glucagonoma

20
Q

In gastrinoma,
A. gastrin release is subjected to acid feedback inhibition
B. it results in a constant release of gastric acid
C. Hypergastrinemia leads to hypersecretion of acid

A

B and C only

A: gastrin release is NOT subjected to acid feedback inhibition

(because gastrin stimulates secretion of acid, but over acid secretion does not trigger negative feedback)

21
Q

State the 2 synergistic effects of hypergastrinemia (secretion of excessive gastrin).

A
  1. Overstimulation of gastric parietal cells to secrete acid (stimulatory function)
  2. Increased mass of parietal cells that are susceptible to over stimulation (trophic function)
22
Q

Name the 2 clinical symptomes led by Hypersecretion of acid and hypergastrinemia.

A
  1. Acid peptic ulcer: Duodenal ulcer, NOT GU!!
  2. Persistent diarrhea
    as gastrin increases gastric motility and increases intestinal secretion of water and electrolyte
23
Q

What is a meal test?

A

Standard food bolus (protein) arrive stomach, gastric phase of acid secretion is triggered depending on quality and quantity of food bolus; To test gastrin release

24
Q

Normal person:
Secretin test result: ___
Meal test result: ____

A

Secretin test result: - (inhibitory action on gastrin release)

Meal test result: +

25
Q

In Gastrinoma:
Secretin test result: ___
Meal test result: ____

A

Secretin test result: ++++ (>1000), due to direct activation of secretin receptor which abnormally expressed in gastrinoma cells

Meal test result: no change (high gastrin release but not due to the meal test)

26
Q

In Antral G cell Hyperplasia:
Secretin test result: ___
Meal test result: ____

A

Secretin test result: no change
Meal test result: ++ great increase, due to the increased number of parietal cells reacting to the food, gastrin release will increase

27
Q

Which 2 risk factors are most commonly associated with PUD? (GU and DU)

A
  1. NSAIDS (20%)
    - aspirin, indomethacin
    - inhibition of gastric prostaglandin synthesis (prostaglandin is very protective)

Arachidonic acid —- COX —> Prostaglandins
COX 1 blockade cause gastric irritation
COX 2 blockade improves inflammation

  1. H.pylori (80%)
    - mucosal damage by ammonium ions (NH4+)

Other risk factors include:
3. Ethanol - Vascular damage and stasis, direct cytotoxic (= toxic to living cells) effects

  1. Smoking - Decreases prostaglandin synthesis and increase acid secretion
  2. Corticosteroids - Inhibition of repair of pre-existing damage, interfere with acute inflammatory responses
  3. Methylxanthines - Stimulation of acid secretion
  4. Shock, Trauma, Burns - Decreased blood blow, circulate ulcerogenic mediators

GI Physiology (11 decks)

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