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Flashcards in Exam 2 Gastro Deck (44):
1

Name the condition: acid regurgitation back into the esophagus and oral cavity

GERD

2

Name the condition: excessive acid production

hypersecretory condition

3

Name the condition: ulceration of the walls of the esophagus

erosive esophagitis

4

Name the condition: lining of esophagus altered to resemble that in intestines

Barrattes esophagus

5

4 symptoms of common GI disorders

1. acidic taste
2. pain/burning sensation
3. difficulties with digestion
4. ulceration and bleeding

6

6 oral symptoms of common GI disorders

1. tooth erosion
2. irritation of the buccal mucosa
3. glossitis
4,. burning mouth/tongue
5. inflammation of oropharynx
6. ulceration of pillars and pharyngeal walls

7

MOA for antacids

weak bases that interact with stomach acid to form water and salt, act local locally to treat excess acidity, raise gastric pH

8

Antacids do NOT inhibit ____ production by ____ cells

HCL
parietal
(need HCL for digestion, pepsin maximally active at pH = 2, when pH >4, pepsin activity decreases, best antactids are those that buffer to a pH of 3-4)

9

2 examples given in class of antacids

milk of magnesia
Maalox

10

MOA for aluminum products

aluminum is an astringent to stop bleeding, coats and protects ulcers from H+, and interferes with absorption of tetracyclines

11

example of an aluminum product discussed in class

Amphojel

12

another name for buffered aspirin

aluminum glycinate

13

What drug form complexes with albumin, fibrinogen, and globulin on ulcer surfaces, thus creating protective barrier to acid and pepsin?

Carafate - interferes with the absorption of many medications

14

4 examples of histamine H2 receptor antagonists discussed in class

Tagament
Pepcid
Axid
Zantac - preferred by GI docs

15

Histamine H2 receptors are most know for what?

Nocturnal acid control - address multiple symptoms

16

Proton pump inhibitors - Bind to ______ enzyme system in parietal cells, ____ gastric secretions, ______ gastric acid after release, and protect _____ _____ from damage. Used as a long term acid suppression with ___ onset and ___ nocturnal acid control.

H+/K+ ATPase
reduces
neutralize
gastric mucosa
slow
poor

17

5 discussed PPIs

1. Nexium
2. Prevacid
3. Prilosec
4. Protonix
5. Aciphex

18

Which PPI drug is second generation and better at healing erosive lesions than Prilosec? Used in the prevention and treatment of NSAID induced GI lesions

Nexium

19

4 antibiotics used in the treatment of H. pylori

1. amoxicillin
2. metronidazole
3. clarithromycin
4. tetracycline

20

Antibiotics plus what other 2 drugs are used in combination to treat H. pylori

1. PPI
2. H2 receptor blocker

21

When treating H. pylori, what is the standard first line therapy?

1 week triple therapy consisting of amocicillin, clarithromycin and a PPI

22

If treating clarithromycin resistant strain of H pylori, what drug is added as part of the therapy?

levofloxacin (Levaquin)

23

Important drug interactions with GI medications: binding of drugs in stomach = _____. Also interferes with the _____ and ____ of many drugs.

Metals
bioavailability
elimination

24

Histamine antagonists decrease _____

antifungals

25

histamine antagonists alter ____

warfarin

26

Tagament increases serum concentration of what 3 things?

1.. benzodiazepines
2. lidocaine
3. Cipro

27

PPIs decrease absorption of ____ ____

systemic antifungals

28

5 side effects of GI medications

1. xerostomia
2. taste alteration
3. aphthous stomatitis
4. candidiasis (esophageal)
5. excessive salivation (mediated by vagus nerve in response to excessive gastric acid)

29

Higher prevalence of stomach ulcers seen is association with these 6 things

1. smokers
2. heavy drinkers
3. hyperparathyroidism
4. renal dialysis patients
5. uses of NSAIDS (chronic)
6. elderly (death from disease more likely)

30

H. pylori lives naturally where?

resides in the oral cavity but infects at the interface between surface of gastric epithelium and overlying mucous gel - usually acquired in childhood

31

4 contributing factors to ulcer formation

1. acid hypersecretion
2. smoking
3. stress - increase acid secretion
4. Use of NSAID > 1 month

32

H. pylori is associated with cancer of ____ ____ = lymphoma. Peptic ulcers rarely undergo transformation to _____. Ulcers in _____ _____ of stomach more likely to become malignant. ____ ____ caused by chronic use of PPis increases risk for stomach cancer

gastric mucosa
carcinoma
greater curvature
atrophic gastritis

33

2 oral manifestations of peptic ulcer disease

1. vascular malformation of lip
2. enamel erosion

34

In patients with peptic ulcer disease, what medications should be avoided? and which one is ok?

Avoid aspirin and NSAIDS
acetaminophen ok

35

Where is the site of ulcerative colitis?

large intestines and rectum

36

Where does Crohn disease manifest?

entire wall of bowel - focal ulcerations along any point of alimentary canal - most common in the terminal ileum

37

4 oral manifestations of Crohns

1. apthous ulcerations
2. mucosal ulcerations
3. diffuse swelling of lips/cheeks
4. cobblestone mucosal lesions

38

In pts with IBS why is the use of corticosteroids questionable

risk for adrenal suppresssion

39

3 categories of antidiarrheal agents and an example of each

1. Absorbents - Pepto-Bismol (caution with salicylate allergy)
2. Opioids-paregoric - Lomotil (codeine and diphenoxylate)
3. Ioperamide - Imodium (muscle relaxant, decreases gut motility)

40

4 classes of laxatives

1. Bulk
2. Osmotic
3. Contact
4. Lubricants

41

Which class of laxative uses magnesium salts? - used as prep for colonoscopy

Osmotic

42

Which class of laxative uses mineral oil/glycerin?

Lubricants, acts as emollients

43

Which class of laxative uses bisacodyl (dulcolax) or caster oil?

Contact - also can be used as colonoscopy prep

44

Which class of laxative uses carboxymethyl cellulose with psyllium? What does it do?

Bulk- absorbs water to form softened stools by increasing bulk of intestinal contents