Acid Dz@ Flashcards

1
Q

Which meds dec risk of gastric ulcers when on NSAIDs?

A

Misoprostol, PPI, BID H2B (not once daily H2B)

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2
Q

Which BAO:PAO ratio would make ZES likely after pentagastrin?

A

> 0.6

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3
Q

Which type of HP preferentially affects D cells and leads to dec SS release?

A

Antral predominant with body sparing

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4
Q

Which type of HP preferentially affects parietal cells and leads to dec acid production?

A

Body predominant

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5
Q

Which type of HP leads to inc risk of ulcers and gastric AC?

A

Pangastritis

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6
Q

What should make you suspect ZES?

A

Recurrent PUD, multiple ulcers, post bulbar ulcer, non HP/NSAID ulcer, diarrhea, erosive esophagitis, FH/PH MEN1

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7
Q

MEN1 vignette

A

Hypercalcemia (HPTH), diarrhea, ulcers (ZES)

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8
Q

What test to obtain to screen for ZES?

A

Fasting serum gastrin level and if elevated, gastric pH assessment +/- secretin stim test

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9
Q

MC carcinoid type?

A

Type 1 (70-80%) AW chronic atrophic gastritis

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10
Q

Which type of carcinoid AW gastrinomas/MEN1?

A

Type 2

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11
Q

Which carcinoid has highest MAL potentia’?

A

Type 3

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12
Q

Tx of Type 3 carcinoid?

A

Surgical resection if possible or EMR

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13
Q

Which ICU pts at highest risk of stress ulcers? Name 2 biggest risks

A

MV > 48hrs, coagulopathy

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14
Q

Once perform endoscopic tx of ulcer (like vis vessel), what tx should be done?

A

72 hours IV BID dosing

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15
Q

Once find ulcer without HR features, what tx should be done?

A

PPI BID oral

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16
Q

T/F: Chronic renal fx is a cause of appropriate hypergastrinemia?

A

True

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17
Q

List the causes of appropriate hypergastrinemia?

A

CRF, PPI tx, atrophic gastritis, vagotomy, chronic HP with pangastritis

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18
Q

Tx regimens for HP with pen allergy and recent clarithro use?

A

Bismuth + metro + tetra + ranitdiine OR

Levo + Omep + nitazoxanide + doxy

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19
Q

Which NSAIDs have highest ulcer risk?

A

piroxicam, indomethacin, ketorolac (KIP)

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20
Q

T/F: COX2 inhibitor is safer than standard NSAID in pts with CVD?

A

False

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21
Q

Which NSAID is preferred in pts with CV risk and low GI risk?

A

Naproxen

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22
Q

T/F: Pts with CVD on ASA and NSAID should be on ppi or misoprostol?

A

True

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23
Q

IF secreted by which part of stomach?

A

Parietal cells which is in body and fundus

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24
Q

Role of gastric acid in B12 abs?

A

Breaks bonds of R protein to B12 to allow IF to bind; If take PO supps of B12, no R protein present so acid not important

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25
Q

CagA strain does what/

A

Inc risk of gastric AC or MALToma, inc risk of gastric/duod ulcers; protects against esoph dz

26
Q

Which ulcer locations have higher risk of rebleeding?

A

Posterior duodenal ulcers or higher lesser curvature in the stomach

27
Q

HP pt with duodenal ulcer typically have dz of what?

A

Antrum –> dec SS from D cells –> inc gastrin –> duod ulcer

28
Q

What is most common location(s) of gastrinoma?

A

Prox duodenum or panc head

29
Q

How does gastrin fcn?

A

Stims histamine release from ECLs leading to inc acid

30
Q

Which two NTs induce acid secretion?

A

ACh and Histamine

31
Q

Which cells secrete acid?

A

Parietal cells

32
Q

Which NT inhibits acid secretion?

A

Somatostatin

33
Q

Which cells release gastrin?

A

G cells

34
Q

T/F: Peptide YY induces secretion of gastric acid.

A

False, it inhibits it

35
Q
Name fcn of each cell type
G cell
ECL cells
Chief cells
D cells
Vagal nerve
A

G cells - secrete gastrin which inc acid production and stims ECLs
ECL cells - secrete histamine which leads to acid
Chief cells - secrete pepsinogen to break down protein
D cells - secrete SS which inhibits G and ECL cells
Vagal - secrete ACh which inc acid production

36
Q

What is the dose of epi for injection?

A

1:10,000

37
Q

How does GOO lead to inc acid?

A

Distention of stomach leads to gastric phase of acid release triggered by gastrin which leads to high acid output

38
Q

What are the 2 biggest RFs for stress ulcers?

A

MV > 48 hrs, coagulopathy

39
Q

How long after tx to use urease breath test for cure if sxs remain?

A

4 weeks after tx of H pylori

2 weeks off of PPI

40
Q

If a gastric ulcer is present which requires tx due to visible vessel, what is the best PPI regimen?

A

IV BID PPI therapy for 72 hours followed by oral dosing

41
Q

If gastric ulcer is present which has pigmented spot, which is best PPI tx?

A

BID dosing immediately

42
Q

T/F: Duodenal bulb ulcer in H pylori infxn likely to be due to HP of the antrum. This leads to dec in SS.

A

True - antral D cells are inflamed and secrete less SS, therefore, inc in gastrin production

43
Q

T/F: Both Cag PAI and VacA have inc risk of HP ulcers.

A

True

44
Q

What is the MC location of a gastrinoma?

A

“Gastrinoma triangle” - jxn of cystic and common hepatic ducts, jxn of 2nd and 3rd portions of duodenum, jxn of H&N of panc

45
Q

How do each of these fxn?
Gastrin
Histamine
ACh

A

Gastrin stims histamine secretion from ECL

Histamine and ACh directly lead to acid release from parietal cells

46
Q

Where are G cells located?

A

Gastric epithelium

47
Q

What role do prostaglandins play in mucosal barrier protection of stomach?

A

Play role in mucous layer thickness, mucosal blood flow, and HCO3 secretion

48
Q

Name conditions that lead to appropriate hypergastrinemia (where acid is deficient).

A

CRF, chronic HP pangastritis, atrophic gastritis, PPIs, vagotomy

49
Q

Name conditions that lead to inappropriate hypergastrinemia (where acid is not deficient).

A

ZES, GOO, antral predominant HP, retained antrum syndrome, massive SI resection

50
Q

Which NSAIDs have the highest ulcer risk?

A

Piroxicam, indomethacin, tometin, ketorolac, azapropazone, meclofenamate

51
Q

N/V, satiety, bloating, discomfort - name which symptoms are MOST to LEAST likely to respond to PPIs.

A

Discomfort, satiety, bloating, N/V

52
Q

Pt on ASA 81, which NSAID is best to use in combo?

A

Naproxen and should add PPI or misoprostol also

53
Q

If high gastrin level and suspect ZES, what should be done next?

A

Assess gastric pH.

54
Q

How do PPIs work?

A

Irreversibly inhibit H-K ATPase

55
Q

What level of gastric pH tells us that PPI is working?

A

pH > 4

56
Q

T/F: PPIs delay gastric emptying

A

True

57
Q

How does CRF lead to high gastrin and acid?

A

Poor clearance of gastrin allows it to circulate longer

58
Q

Where does IF come from?

A

Parietal cells, mainly located in fundus and body

59
Q

What basal to peak acid output is suggestive of ZES?

A

Basal:Peak of 0.6 or greater

60
Q

What are the effects of HP of the antrum only?

A

D cells affected and so more acid and gastrin

61
Q

What are the effects of HP of the body only?

A

Parietal cells affected in large part leading to decreased acid

62
Q

What other condition besides ZES can lead to gastrin ~1000? How do you differentiate the two?

A

Pernicious anemia; Secretin stim test - will lead to decreased acid in pernicious anemia but not in ZES