GI Flashcards

1
Q

Drugs categories that affect gastric secretion?

A

Antacids
H2RAs
PPIs
Protectants

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2
Q

When are drugs affecting gastric treatment used?

A
Dyspepsia (indigestion)
Gastric/duodenal ulcers
GERD
Barrett's Esophagus
Hypersecretory states (Zollinger-Ellison)
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3
Q

What are the steps that lead to gastric acid release?

A

Dietary peptides in lumen bind to G cells
G cells produce gastrin
Gastrin stimulates ECL cells to make histamine
Histamine binds to parietal cells
Parietal cells produce H+ ions that go into the stomach

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4
Q

What inhibits gastric acid production? (molecule and cell that makes it)

A

Somatastatin released by D cells in response to stomach acid

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5
Q

Ulcers: A failure of _____ _____

A

mucosal protection

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6
Q

_____ maintains the mucosal layer

A

prostaglandins

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7
Q

Parietal cells have what pump for acid production?

A

H/K/ATPase (proton pump)

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8
Q

What do NSAIDs inhibit?

A

PGE production –> decreased mucous production

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9
Q

What controls histamine release by ECL cells (besides gastrin)

A

ENS - by releasing acetylcholine

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10
Q

Does chloride move out of parietal cells with or against its gradient?

A

Against

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11
Q

How do antacids work?

A

They neutralize acids

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12
Q

What are the antacids?

A

Sodium bicarb
Calcium bicarb
Aluminum hydroxide
Magnesium hydroxide

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13
Q

Side effects: Sodium bicarb

A

systemic alkalosis, fluid retention

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14
Q

Side effects: calcium bicarb

A

hypercalcemia, nephrolithiasis, milk-alkali syndrome

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15
Q

Side effects: aluminum hydroxide

A

Constipation, hypophosphatemia

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16
Q

Side effects: Magnesium hydroxide

A

Diarrhea, hypermagnesemia

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17
Q

AlternaGEL

A

Aluminum hydroxide

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18
Q

Tums

A

Calcium carbonate

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19
Q

Maalox/Mylanta

A

Aluminum hydroxide & mag hydroxide

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20
Q

Rolaids

A

Calcium bicarb & mag hydroxide

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21
Q

Alka-Seltzer

A

ASA & NaHCO3 (for hangovers)

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22
Q

Gaviscon

A

Sodium alginate + antacids (weak base)

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23
Q

What does Gaviscon do?

A

Prevent reflux and effective in GERD

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24
Q

What are the dosage forms of commercial antacids?

A

chewable tablets

Liquid suspension

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25
Q

What’s the first-gen H2RA?

A

Cimetidine

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26
Q

H2RAs reduce gastric acid secretion in response to what?

A

Histamine, gastrin, acetylcholine (things upstream of histamine)

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27
Q

Cons of cimetidine?

A

DRUG INTERACTIONS
CNS effects (esp elderly)
Antiandrogen
Thrombocytopenia

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28
Q

What’s the benefit of cimetidine?

A

Clears up warts

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29
Q

What CYPs does cimetidine inhibit?

A

2C6 and 2D9

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30
Q

2nd gen H2RAs?

A

Ranitidine
Nizatidine
Famotidine

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31
Q

2nd gen h2RAs have longer or shorter half-life?

A

Loner –> daily dosing

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32
Q

2nd gen H2RA more or less potent?

A

More

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33
Q

Where do PPIs work?

A

Directly on proton pump in parietal cell

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34
Q

What’s vanoprazan?

A

Potassium-competitive acid blocker (NOT PPI - acts on transmembrane region)

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35
Q

What are the PPIs?

A
-Oprazole's
Esomeprazole
Omeprazole
Lansoprazole
Pantoprazole
Rabeprazole
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36
Q

T/F: PPIs are prodrugs

A

True - activated by acid in parietal cells

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37
Q

PPIs should be taken when?

A

In the morning

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38
Q

PPIs are reversible/irreversible?

A

Irreversible

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39
Q

PPIs have a short/long half life?

A

Short - but long effect b/c they irreversibly inhibit PPIs until protein is turned over

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40
Q

Side effect of PPIs?

A

Hypergastrinemia –> hypsecretion upon drug withdrawal

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41
Q

Why does hypergastrinemia occur?

A

B/c PPIs are inhibiting negative feedback of acid onto G cells, which causes lots of gastrin to be produced

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42
Q

How do PPIs react w/ PP?

A

Disulfide bond - via sulfur

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43
Q

How long do PPIs take for full effect?

A

1-4 days

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44
Q

ADEs of PPIs?

A
Nausea
CYP2C19 interactions (w/ omeprazole)
Increased infection
Vit B12 deficiency
Decreased Ca absorption/increased bone fractures
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45
Q

Do PPIs decrease acid more or less than H2RAs?

A

More

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46
Q

Do H2RAs or PPIs work faster?

A

H2RAs

47
Q

What is acid rebound?

A

Gastric acid secretion increased upon wtihdrawal of meds

48
Q

PPI –> decreased Ca absorption –> what?

A

Increased parathyroid hormone
Increased bone resorption
decrease bone strength
Fractures

49
Q

Do PPIs cause dementia?

A

No - just correlation

50
Q

PPI recommendations: which patients?

A

GERD

Barret esophagus

51
Q

Should patients on PPIS for GERD stay on PPIs forever?

A

No try to stop/reduce if uncomplicated GERD

52
Q

What should NOT be taken with PPIs?

A

Probiotics!

53
Q

T/F: Take Ca, Vit B12, mag with PPI

A

No - don’t raise intake above daily recommended allowance

54
Q

What are mucosal protectants?

A

Sucralfate
Misoprostol
Bismuth subsalicylate

55
Q

Sucralfate is a ____ complex of ___

A

Aluminum hydroxide complex of sucrose

56
Q

Sucralfate works how?

A

Polymerizes at ulcer site to prevent protective barrier

57
Q

Sucralfate activated by __ pH

A

Acidic

58
Q

Misoprostol MOA?

A

PGE1 derivative –> enhanced mucus and bicarb secretion

59
Q

ADEs of misoprostol?

A

Diarrhea, abortifacient

60
Q

What causes peptic ulcers?

A

H Pylori

61
Q

How does H Pylori cause peptic ulcers?

A

Reduces D-cell production of somatastatin

Increase gastrin secretion

62
Q

Therapy to eradicate H Pylori?

A

Bismuth salt (PeptoBismol)
Antibiotic
H2 blocker/PPI
Ranitidine bismuth citrate (Tritec)

63
Q

What antibiotics for H Pylori?

A

Metronidazole
Tetracycline
Amoxicillin
Clarithromycin

64
Q

Use of peptobismol?

A

Mild diarrhea

H Pylori eradication

65
Q

What is bismuth subsalicyate converted to in GI

A

bismuth salt and salicylic acid

66
Q

What controls GI motility?

A

ENS innervation (enteric nervous system)

67
Q

Myenteric plexus receives input and signals what?

A

Parasympathetic and sympathetic response

68
Q

Submocal plexus signas what?

A

Parasympathetic only

69
Q

Threet ypes of laxatives?

A

Bulk/saline
Stool softeners
Secretory/stimulant

70
Q

How do bulk/saline laxatives work?

A

Non-absorbale, hydrophilic mass in the presence of water - draws water into the intestines, which leads to distention/stretch response

71
Q

What are bulk/saline laxatives?

A

Psyllium, methylcellulose, bran, milk of mag, non absorbable sugars (also PEG is similar)

72
Q

How do stool softeners work?

A

Surfactant/lubricant to increase H20 absorption and pass stool more easily

73
Q

What are stool softener examples?

A

Docusate, mineral oil, glycerin

74
Q

Stool softeners can decrease absorption of ___

A

fat solubler vitamins

75
Q

Secretory/stimulant laxative examples

A
Castor oil
Dephenylmethane derivatives (Bisacodyl)
Anthraquinones (Cascara, senna, aloes)
76
Q

How do secretory/stimulant work?

A

Irritate mucous, affects fluid balance and induces peristalsis

77
Q

What is gastroparesis?

A

Neuropathy that slows GI - usually from diabetes or PD

78
Q

What is ileus?

A

Small bowel doesn’t recover after surgery

79
Q

What receptors affect the cholinergic motor neuron that stimulates smooth muscle?

A

5-HT4
Motilin
D2
M3 on smooth muscle cells

80
Q

Metoclopramide mechanism?

A

D2 receptor antagonist –> increased Ach release

81
Q

What are metocolopramide side effects?

A

Sedation, PD, hyperprolactinemia

82
Q

Metoclopramide uses?

A

Gastric emptying, gastroparesis, GERD

83
Q

What’s erythromycin?

A

Motillin agonist - rapid tolerance

84
Q

What’s neostigmine?

A

Ach esterase inhibitor (Toxicity)

85
Q

What’s bethanechol

A

Agonist of muscarinic acid receptors (toxicity)

86
Q

Prucalopride?

A

5HT4 agonist (not approved yet)

87
Q

What drugs activate GCC to activate the chloride channel?

A

Plecanatide

Linaclotide

88
Q

What drug directly activates chloride channel?

A

Lubiprostone

89
Q

What are chloride channel activators used in?

A

IBS + Constipation

90
Q

What do Cl channel activators do?

A

Increase Cl-fluid secretion into intestine

91
Q

What opioid pathway causes constipation?

A

B-arrestin

92
Q

Opioid receptors ___ smooth muscle contraction

A

Decrease

93
Q

What strategy to overcome opioid constipation?

A

Drug that only works on G protein pathway, not Beta arrestin (Oliceridine)

94
Q

WHat are centrally acting opioid antagonist?

A

Naloxone
Naltrexone
Nalmefene

95
Q

What are peripherally acting opioid antagonists?

A

Naloxegol
Alvimopan
Naldemedine

96
Q

Where do anti-diarrhealas work?

A

On smooth muscle innervation to slow process - allows increased water absorption

97
Q

Opiate anti-diarrheals?

A

Loperamide and diphenoxylate (w/atropine) - have poor CNS penetration

98
Q

What are anti-diarrheal options?

A

Bismuth

Cholestyramine/colestipol/colesevam

99
Q

What do bile-salt binding resins do for diarrhea?

A

Ion exchange resins - correct osmotic imbalance

100
Q

ADE of bile-salt binding resins?

A

Decrease abs or drugs and fat-soluble vitamins

101
Q

IBS?

A

Abdominal pain + distension + diarrhea/constipation

102
Q

What is alosetron?

A

5HT3 antagonist for women w/IBS + diarrhea

103
Q

What are the drugs to inhibit GI motility?

A

Anti-diarrheals
opiates
ANticholinergics

104
Q

What are anticholinergic drugs for GI?

A

Dicyclomine

Hysoscyamine

105
Q

Side effect of 5HT3 receptor antagonists?

A

Constipation!

106
Q

What’s the effect of serotonin in the GI?

A

Stimulates peristalsis and signals to CNS emetic centers

107
Q

What’s Akynzeo?

A

Combo of neutpitant and palonosetron

108
Q

When are 5ht3 antogonists used?

A

For chemo-induced NV

109
Q

Cannabinoid use?

A

N/V with chemo - refractory

110
Q

Cannabinoid drugs?

A

Dranobinol

Nabilone

111
Q

Motion sickness anti-emetics?

A

Antihistamines/anticholinergics
Diphenhydramine
Meclizine
Scopolamine

112
Q

Does scopolamine or meclizine have more anticholinergic effects?

A

scopolamine

113
Q

Dopamine antagonists?

A
Prochlorperazine
Promethazine
Thiethylperazine
Droperidol
Metocolopramide
Trimethobenzamine