Brainscape's Knowledge GenomeTM

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


See full index

GI > Module 2: Acid Suppression Pharmacology > Flashcards

Module 2: Acid Suppression Pharmacology Flashcards

Dr. Digavalli

1
Q

Difference between Erosion and ulcers

A

Erosion: superficial lesions

Ulcer: deep lesions across layers

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

Complication of untreated ulcers

A

Bleeding and perforation (hole)

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

What may cause Barretts esophagus

A

-precancer stage
-chronic inflammation (esophagitis/gastritis) leading to epithelial changes (squamous to columnar)

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

What are the ways to protect the GI tract?

A

-epithelial cells secreting mucus and bicarbonate: buffer and protection

-prostaglandins, hydrogen sulfide, nitric oxide, trefoil factors: microcirculation and protection

-continuous regeneration of mucosal tissue

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

Function of prostaglandins and hydrogen sulfide

A

microcirculation and protection

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

Factors contributing to peptic ulcers

A

Imbalance between damaging and protecting factors
-H. pylori
-poorly functioning of the sphincter
-excessive use of NSAIDs, aspirin (inhibit COX enzyme and PG)
-dietary and lifestyle (alcohol, smoking, caffeine)
-stress

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

What are the damaging and protective factors?

A

-damaging: acid/pepsin/H.pylori/stress

-protecting: Prostaglandins, bicarbonate, hydrogen sulfide, mucosal repair

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

Which cells in the stomach produce acid?

A

Parietal cells
1.5l per day

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

How is the acid produced by parietal cells?

A

the enzyme carbon anhydrase (CA) converts CO2 to H2CO3 (carbonic acid)

H2CO3 dissociates to H+ and HCO3 (bicarbonate) -> goes into the blood as BUFFER after a meal (alkaline tide, exchange HCO3 with Cl-)

H+ is secreted into the gastric duct via the H+/K+ antiporter

Cl- diffuses from the blood (then through the parietal cell) into the gastric duct too
-> forms HCl- (acid)

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

What is secreted by Parietal cells and Chief cells?

A

-Parietal cells:

Chief cells: Pepsinogen

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

What is secreted by G cells and ECL cells?

A

G cells: Gastrin -> CCK B receptors

Enterochromaffin-like cells: Histamine -> H2 receptors

Postganglionic cholinergic neurons: ACh -> muscarinic M3 receptors

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

What is secreted by Goblet cells and D cells?

A

Goblet cells: Mucous (protection)

D cells: Somatostatin (inhibits acid secretion)

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

What is the role of histamine, ACh and gastrin in the stomach?

A

-histamine (via ECL) and ACh (via vagal/anticholinergic neurons) stimulate parietal cells

-gastrin stimulates acid secretion -> parietal cells and ECL

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

What are the functions of Somatostatin and gastrin?

A

Somatostatin (via D cells): inhibits ECL, G cells, and parietal cells

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

Drug formulation of Omeprazole

A

-enteric coated -> prevents early activation -> absorption

-Weak base pKa 4.5

-take on empty stomach (food reduces the bioavailability by 50%)

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

MOA of omeprazole

A

-Protonation and conversion into Sulphenamide intermediate

-irreversibly binds to proton pumps

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

Clinical use of PPIs

A

-GERD
-Peptic ulcer disease
-NSAID-induced ulcers
-Esophagitis
-Zollinger-Ellison syndrome

18
Q

Side effects of PPIs

A

-Diarrhea, risk of C diff induced diarrhea
-Nausea
-Abdominal pain
-headache
-inhibit CYP450
-induce CYP450 (omeprazole, lansoprazole, pantoprozole)

19
Q

Which of the PPIs induce CYP450?

A

-Pantoprazole
-Lansoprazole
-Omeprazole

20
Q

Which molecule do PPIs interfere with?

A

absorption of Vitamin B12
-may worsen osteoporosis with long-term use (1-2y)

21
Q

How are PPIs metabolized?

A

liver (CYP450) -> excreted through the urine and feces

22
Q

Onset duration of PPIs

A

4 hours

23
Q

Which PPIs can be administered IV?

A

Esomeparzole and Pantoprazole

24
Q

MOA of H2 receptor antagonists

A

-competitive inhibition of H2 receptor on parietal cells -> decrease in gastric acid secretion

-protection for 10-12h

25
Q

Clinical use of H2RA

A

-effective against nocturnal acid release
-prophylaxis for ulcers, GERD, heartburn
-GERD
-Zollinger-Ellison syndrome
-Peptic ulcer disease

26
Q

Side effects of H2RA (Cimetidine)

A

-Headache
-Gynecomastia (blocks production of testosterone)
-inhibits P450 enzyme (except Famotidine)
-Vitamin B12 deficiency with long-term use

27
Q

Side effects Famotidine

A

-Diarrhea
-Headache
-dizziness
-confusion in the elderly

28
Q

How are H2RA eliminated?

A

-Metabolized in the liver (CYP450)
-excreted in the urine

29
Q

What might be a consequence of prolonged acid suppression?

A

C. diff infection
Vitamin B12 deficiency

30
Q

Antacids

A

-short onset, short duration
-sodium an calcium bicarbonate may cause bloating and belching

31
Q

MOA of Antiacids

A

-directly buffers the acid -> forming a salt and water
-increases the gastric pH -> pH > 4 deactivates pepsin (protein degrading enzyme)

32
Q

Clinical use of Antacids

A

-Symptoms of GERD, PUD, esophagitis, gastric hyperacidity
-safe for pregnant women
-works better for duodenal ulcers than in gastric ulcers

-calcium carbonate is helpful in hypocalcemia
-magnesium hydroxide is used as a laxative

33
Q

Side effects of Antacids

A

-Aluminum hydroxide: constipation (elderly), not in patients with CKD, hypophosphatemia

-Calcium carbonate: Hypercalcemia, metabolic alkalosis

-Magnesium hydroxide: strong laxative effect -> diarrhea

-sodium bicarbonate: metabolic alkalosis

34
Q

Which of the Antacids have poor oral bioavailability?

A

Aluminium hydroxide
Magnesium hydroxide

35
Q

Which of the Antiacids cause bloating and belching?

A

Carbonate containing

-Sodium carbonate
-Calcium carbonate

36
Q

Which of the Antacids cause metabolic alkalosis?

A

-Sodium bicarbonate
-Calcium bicarbonate

37
Q

Which antacids should be avoided in CKD?

A

-Aluminium hydroxide
-Magnesium hydroxide

-also caution with sodium carbonate and calcium carbonate bc of metabolic alkalosis

aluminum and magnesium accumulation due to decreased kidney function

38
Q

How does absorption of Antacids cause DDIs?

A

due to being administered in large amounts (grams) they easily bind (adsorb) to drugs given in mg (warfarin, digoxin)

39
Q

Antacids DDI

A

-chelation with FQ, tetracyclines space with 3-4h
-reduces dissolution of weakly basic drugs, acid environment is needed (antivirals, conazole, tk inhibitors) and poorly soluble drugs

40
Q

Use of Cytotec (Misoprostol)

A

-NSAID-induced and mucosal restoration
-increases local blood flow and bicarbonate buffering

-PGE1 (porstaglandin E1) analog
-can cause smooth muscle contraction -> contraindicated in pregnancy, SSRIs, anticoagulants, steroids

41
Q

Use of Sucralfate

A

-forms a sticky wax-like coating on ulcers
-ulcer healing, PG secretion

-can interfere with phosphate absorption by binding to phosphate

42
Q

Use of Bismuth Salicylate

A

-coats the ulcers
-stimulates mucous and PG synthesis
-antibacterial effect
-causes black tongue and black stool -> reacts with sulfide (Bisulfide) causing the black color

GI (19 decks)

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