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acid/pepsin txt Flashcards

1
Q

what are the two major groups of drugs for acid/pepsin disorders?

A
  1. decrease acid from gastric lumen

2. promote mucosal defense (promote HCO3- secretion)

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2
Q

what are the 3 groups of drugs that decrease acid from gastric lumen?

A

anatacids, H2 blockers, PPIs

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3
Q

what are the 3 drugs that promote mucosal defense?

A

prostoglandin analogs (Misoprostol aka Cytotec)
Bismuth (aka Pepto Bismol)
Sucaralfate (aka Carafate)

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4
Q

MOA of antacids

A

they are all weak bases that react w/ gastric acid to produce H2O and salt.
This raises the pH (decreasing acid effects)

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5
Q

DOA or antacids

A

2 hours (cover post-mealtime)

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6
Q

how to use antacids: what do they treat? when do you take them? how many times a week can you use them?

A

treat heartburn/dyspepsia,
take after meals for symptoms
use < 2 days/week

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7
Q

antacids can combine ___ and ___ to decrease ADRs

A

Al (ADR is constipation)
Mg (ADR is diarrhea)
- antacids may combine these to counteract the ADRs of each

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8
Q 
ADRs for antacids: 
Na+
Al 
Mg
Ca
A

Na+: burping (which may provide relief), Na+ retention, metabolic alkalosis (rare)
Al: CONSTIPATION, hypophosphatemia
Mg:DIARRHEA, high Mg+
Ca: high Ca++

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9
Q

Antacids: A ffect _____, ______ or _____ of other drugs by altering gastric and urinary pH or by delaying gastric emptying

A

Affect absorption, bioavailability or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying

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10
Q

contraindications for Antacids:
Sodium bicarb
Al and Mg

A 
CHF (for sodium bicarb)
renal impairment (Al and Mg ones will accumulate b/c youre not excreting them)
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11
Q

Abx like fluroquinolones, tetracyclines and ketoconazoles are given before or after antacids?

A

before, they need acidic enviornment for them to work!

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12
Q

what are the four H2 blockers (antagonists) ?

A 
"tidines"
Cimetidine (Tagamet)
Famotidine (Pepcid)
Ranitidine (Zantac)
Nizatidine (Axid)
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13
Q

Which H2 blocker has the most ADRs?

A

Cimetidine (tagamet)

  • lots of drug/drug- (warfarin for example)
  • imbalance of androgen - prolactin produced =gynecomastia
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14
Q

MOA of H2 blockers

A

Reversible H2 block on parietal cells

Decreases cAMP = decreased H+ secretion into gastric lumen

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15
Q

PKs of H2 blockers (maybe weeds): Abs, metabolism, 1/2 life, onset, excretion

A 
Absorption-rapid
Metabolism-hepatic
½ life – 2 hours; prolonged with renal impairment
Onset – 45 min-2 hours
Excretion – primarily renal
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16
Q

4 ADRs of H2 blockers (weeds)

A
  1. May reduce efficacy of drugs that require an acidic environment for absorption
  2. CIMETIDINE: DRUG/DRUG, GYNECOMASTIA
  3. Elderly- confusion after IV administration (dont really know why)
  4. B-12 deficiency with long term use (although mostly with PPIs)
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17
Q

what do we use H2 blockers for?

A

mild esophageal reflux (best use for them)
Peptic ulcer
gastritis

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18
Q

which drugs do we use for pregnant pts?

A

Antacids, then H2, then PPIs

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19
Q

what are the PPI drugs?

A 
"prazoles"
 Esomeprazole (Nexium)
Omeprazole (Prilosec)
Lansoprazole (Prevacid)
Pantoprazole (Protonix)
Rabeprazole (Aciphex)
Dexlansoprazole (Dexilant)
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20
Q

MOA of the PPIs, why is this so effective?

A

Irreversibly binds to H+/K+ ATPase enzyme of parietal cell preventing H+ secretion into gastric lumen
(stop acid secretion at its source! = very effective)
Also, Effective because it take 18 hours for enzyme to be resynthesized

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21
Q

All PPIs are ____, what does this mean?

A

ALL are Prodrugs: have acid resistant enteric coatings to prevent degradation by gastric acid
Coating removed in alkaline duodenum, prodrug is weak base an is absorbed/taken to parietal cell

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22
Q

PKs of PPIs : abs, onset, 1/2life (weeds)

A

Rapid absorption
Onset 30 min – 2 hours
½ life – 1-2 hours

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23
Q

why is there a long DOA of PPIs?

A

Long DOA due to irreversible binding with enzyme

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24
Q

metabolism and excretion for PPIs

A

Hepatic metabolism

Excretion: urine, feces, bile

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25
Q

3 ADRs of PPIs

A
  1. Increased risk of C difficile infection (acidic env. is there to kill Cdiff and we are taking that away)
  2. hypomagnesemia (increased excretion through GI)
  3. B-12 deficiency, iron and calcium malabsorption (fracture risk)
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26
Q

what do we use PPIs for?

A

Peptic ulcer, gastritis, esophageal reflux, H pylori (in combination), stress ulcer prophylaxis, NSAID associated ulcer

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27
Q

when do we take PPIs? why do we take them at this time? (maybe weeds)

A

Administration: 30-60 minutes before meal

Greatest amount of H+/K+ ATPase enzyme is present after prolonged fast

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28
Q

PPIs for pregnancy? (keep in mind, antacids are class A - aka first choice for pregnant)

A

omeprazole/esomeprazole class C; all others class B

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29
Q

why do we use PPIs for H pylori?

A

if we dont irradicate Hpylori, pt is more at risk for certain cancers : we use PPI b/c H pylori in acidic env is dormant (we want it to start replicate so that the abx can target the replicating cyle of the Hpylori)

(wake the monster and kill it !)

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30
Q

what is the controversy of using PPIs on someone taking clopidegrel?

A

both Omeprazole + Esomeprazole and Clopidegrel are prodrugs- CYP C19 converts both into their active forms -some think if you take them together, the PPI is inhibiting the Clopidegrel but pt may just be poor metabolizers of Clopidegrel!

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31
Q

what is the MOA of sucralfate?

A

Binds to positively charged proteins of both the normal and necrotic mucosa

  • Forms a gel with epithelial cells to create physical barrier
  • Protects ulcer from pepsin and acid-promoting healing
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32
Q

overall PKs of sucralafate?

A

overall: nonsystemic, urine excretion

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33
Q

ADRs of sucralafate?

A 
Aluminum base (which causes constipation) 
kidney- Al may accumulate if chronic kidney disease
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34
Q

Uses for sucralafate?

A

duodenal ulcers

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35
Q

Drug/drug problems with most anti- acid-pepsin drugs ?

A

problem for drugs that need the acidic GI environment to become biologically available.

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36
Q

Sucralafate: Need _____ for activation – shouldn’t be given with ____, ____ or _____

A

acidic pH

PPI, H2 antagonist, antacids

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37
Q

why is compliance difficult with sucralafate?

A

QID dosing (4xday)

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38
Q

misoprostol MOA

A

Prostaglandin E1 analog
binds receptors- slows H/K pump
–>slows acid secretion
–>increase of mucus and HCO3- secretion

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39
Q

misoprostol: Contraindicated in …

A

pregnancy – induces/augments uterine contractions

however, this can be inserted into cervix, used for induced labor

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40
Q

what do we use for prevention of gastric and duodenal ulcers in patients taking NSAIDs long-term

A

misoprostol!

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41
Q

PKs of misoprostol (weeds.. not very significant)

A

Absorption: rapid with onset of action within 30 minutes
Hepatic metabolism
Renal excretion

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42
Q

MOA of bismuth subsalicylate (pepto bismol) (4 parts)

A

Inhibit proliferation of H pylori
Inhibits activity of pepsin
Increases secretion of mucus

-still unsure of exactly how this one works but we know it interacts with proteins in necrotic tissue to coat/protect ulcers (biggest MOA we care about)

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43
Q

Bismuth Subsalicylate:
Absorption: bismuth-__%; subsalicylate__%
Metabolism: …
Excretion: …

A

Abs: bismuth: <1% Subsalicylate >80%

metab: converted to bismuth and salicylic acid in GI tract
excretion: bismuth – urine/bile; salicylate- urine

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44
Q

ADR of bismuth subsalicylate

A

if it works too well… fecal impaction

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45
Q

what do we use Bismuth Sucsalicylate for?

A

in quadruple therapy for peptic ulcers

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46
Q

what is pepsin?

A

the chief digestive enzyme in the stomach, which breaks down proteins into polypeptides.

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47
Q

Eradication of H pylori leads to …

A

rapid healing of ulcer and low recurrence rates

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48
Q

triple and quadruple therapy for H pylori eradication

A

Triple Therapy
Clarithromycin
Amoxicillin or metronidazole
PPI

Quadruple Therapy
Tetracycline
Metronidazole
Bismuth subsalicylate
PPI
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49
Q

what 3 groups of drugs do we use for constipation?

A
  1. laxatives (big group)
  2. Guanylate Cyclase-C (GC-C) Agonist
  3. Peripherally Acting Mu-Opioid Receptor Antagonist (PAMORA) (for opiod induced consipation)
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50
Q

what are the 6 different groups of laxatives?

A
  1. stimulant
  2. bulk forming
  3. saline and osmotic
  4. stool softner
  5. lubricants
  6. Cl channel activator
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51
Q

what are the stimulant laxatives? are they Rx or OTC?

A

Senna (Senokot) (“natural” plant-derived),
bisacodyl (Dulcolax)
castor oil

all OTC

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52
Q

MOA of stimulant laxatives

A

DIRECTLY STIMULATE NERVE PLEXUS IN COLON to alter water and electrolyte secretion in order to CAUSE PERISTALSIS

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53
Q

onset oral vs suppository for stimulant laxatives?

A

Onset: oral 6-12 hours; suppositories 1-2 hours

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54
Q

ADRs of Senna (Senokot)

A

Senna – melanosis coli (browning of colon wall)
when people abuse the product- use longterm. a dependent cycle is created (relief, constipation, laxative, relief … colon “forgets” how to function)

*browning itself isnt bad but indicates you’ve been taking the drug longterm, which may indicate you’ve put yourself into a dependent cycle

55
Q

ADR of Bisacodyl (Dulcolax)

A

abdominal cramping

56
Q

longterm use of any stimulant laxative can lead to …

A

dependence

57
Q

oral or suppository stimulant laxatives are used more for prophylaxis? (to partner with a drug that may cause constipation)

A

oral

58
Q

what are the 4 bulk-forming laxatives?

A

Psyllium (Metamucil)
Methylcellulose (Citrucel)
Polycarbophil (FiberCon)
Wheat Dextrin (Benefiber)

59
Q

MOA of the bulk-forming laxatives

A 
Hydrophilic colloids (from indigestible fruits and vegetables) that absorb water to form gel
Causes intestinal distention and increases peristaltic activity
60
Q

onset of bulk-forming laxatives

A

12-72 hours

61
Q

ADRs of bulk-forming laxatives

A

Abdominal cramps, Gas

these both limit pt compliance- never recommend that they take a full dose to start- start low, go slow

62
Q

special considerations with bulk-forming laxatives? (how do we want to advise these be taken, are they ok for daily use? what about immobile pts? )

A

Take with 8oz H2O
Start with low dose and titrate to desired effect
Use cautiously in immobile patients because of their potential for obstruction

63
Q

are bulk-forming agents ok for daily use?

A

yes, no dependency issue for these

64
Q

when might a DM pt not want to take a bulk-forming agent?

A

if its one that has had sugar added for better taste

65
Q

what are the saline/osmotic laxatives?

A

Sorbitol
Lactulose (Chronulac)
Magnesium citrate
Magnesium hydroxide (MOM)
Sodium phosphate (Fleets Enema, OsmoPrep)
Polyethylene glycol (PEG) (Colyte, GoLYTELY, Miralax)

66
Q

MOA of saline/osmotic laxatives

A

Non absorbable salts that hold H2O in intestine by osmosis

Causes bowel distention, increasing peristalsis and BM

67
Q

ADRs of saline/osmotic laxatives

A

ABD CRAMPS, bloating, nausea

68
Q

onset for saline/osmotic laxatives depend on..

A

dose, at least over an hour

69
Q

_____ also used for hepatic encephalopathy to decrease ammonia levels (converts NH3 to ammonium- liver dysfunction issue)

A

lactulose

70
Q

saline/osmotic laxatives:Can alter fluid and electrolyte balance, so what patients do we want to caution with?

A

Caution in patients with reduced kidney function, elderly, CHF

71
Q

which are the more sugar-based saline/osmotic laxatives?

A

sorbitol and lactulose

72
Q

which is more powerful and used for bowel prep for colonoscopies? Mg citrate or Mg OH?

A

citrate!

73
Q

what is the stool softener laxative?

A

Docusate (Colace)

74
Q

MOA of Colace?

A

Surfactants that become emulsified with the stool
Incorporates water and fat into stool
Produce softer feces and ease passage

75
Q

onset for stool softeners (weeds maybe) ? oral vs rectal.

A

Onset: oral 12-82 hours; rectal 15 minutes

76
Q

are stool softeners safe for daily use? pregnancy?

A

yes and yes

77
Q

what are the the lubricant laxatives? which is NOT recommended for use?

A 
Glycerin
Mineral oil (OTC but bad ADRs so don’t reccomend using)
78
Q

MOA of lubricant laxatives (glycerin)?

A

Slows colonic absorption of water and lubricates the intestine

79
Q

onset time mineral oil vs glycerin ? (weeds)

A

Onset:
Mineral oil - oral 6 hours; rectal 15 minutes
Glycerin – 30 minutes

80
Q

major ADRs of lubricant laxatives (glycerin)

A

Abdominal cramps
Long term use can decrease absorption of fat soluble vitamins (A, D, E, K)
May leak from anus causing soiling + itching

81
Q

ADR of mineral oil: why must you remain upright when you take it? (weeds..maybe)

A

Mineral oil:

must remain upright after oral administration to prevent aspiration and lipid pneumonitis

82
Q

what is the Chloride channel activator laxative?

A

Lubiprostone (Amitiza)

83
Q

MOA of lubiprostone (amitiza) ?

A

ACTIVATES CHLORIDE CHANNEL-2 (CIC-2) of the apical membrane of the intestine to INCR. FLUID SECRETION AND TRANSIT

84
Q

which laxative is Metabolized within stomach and jejunum by carbonyl reductase to M3 (active metabolite) ? (weeds)

A

lubiprostone (amitiza)

85
Q

how is lubiprostone eliminated? (weeds)

A

fecal

86
Q

what 3 things do we use lubiprostone for?

A

Idiopathic chronic constipation, Irritable bowel w/ constipation in women, Opioid induced constipation

87
Q

ADRs of lubiprostone?

A

going too far with its effects… Abdominal pain, flatulence, abdominal distention, vomiting

88
Q

what are the two Guanylate Cyclase-C (GC-C) Agonist drugs?

A

Linaclotide (Linzess)
Plecanatide (Trulance)

(“tides”)

89
Q

MOA of the GC-C agonists?

A

Bind and agonize guanylate cyclase-C of intestinal epithelium.
Increases cGMP increasing Cl- and HCO3- secretion
GI transit time is accelerated

90
Q

metabolism and absorption of GC-C agonists

A

Minimal systemic absorption

Metabolized by GI tract to active metabolite

91
Q

what do we use the GC-C agonists for ?

A

Chronic idiopathic constipation, irritable bowel with constipation
* slightly more specific than Cl channel blockers

92
Q

GC-C agonists:

Contraindication for patients ___ years old. Recommended to avoid in pts ___ years old, due to _____

A

contraindicated: pediatric patients <6 years
avoid: in patients <17
severe dehydration

93
Q

what drugs do we use for opiod-induced consipation?

A

Peripherally Acting Mu-Opioid Receptor Antagonist (PAMORA)

94
Q

what are the PAMORA drugs ?

A

Methylnaltrexone (Relistor)
Naloxegol (Movantik): most common
Naldemedine (Symproic)
Alvimopan (Entereg)

95
Q

MOA of Naloxegol (Movantik) (and all drugs in its class) ?

A

work in GI tract ONLY:
Peripheral acting mu receptor antagonist
Inhibits opioid induced-decreased GI motility/transit time

96
Q

3 groups of anti-diarrheal agents? which is the biggest group?

A

Antimotility agents (biggest group)

Adsorbants

Fluid/electrolyte transport modifier

97
Q

what are the 2 antimotility agents ?

A

Loperamide (Imodium)

Diphenoxylate/atropine (Lomotil)

98
Q

what are the 2 adsorbants?

A

Aluminum hydroxide

Methylcellulose

99
Q

what is the fluid/electrolyte transport modifier agent for anti-diarrheal?

A

Bismuth subsalicylate (pepto bismol)

100
Q

which drug has similar structure to meperidine with opioid-like activity in gut?

A

the antimotility agents for constiplation:

imodium and lomotil

101
Q

MOA of imodium and lomotil?

A

Activate presynaptic opioid receptors in the enteric nervous system
Inhibits Ach release resulting in decreased peristalsis

102
Q

which antimotility agent is OTC and which is Rx?

A

OTC: imodium
Rx: lomotil

103
Q

imodium or lomotil have risk for addiction and tolerance/dependence?

A

imodium: Doesn’t cross blood brain barrier, so no analgesia, potential for addiction & no tolerance.

lomotil:
Low doses it doesn’t cross BBB
Higher doses get risk of dependence & addiction.

104
Q

lomotil may be combined with ____ to incr. antidiarrheal action. But what is the risk if using this for a narcotic effect?

A

Combined with atropine to increase antidiarrheal action and if abusing for narcotic effect, will have unpleasant anticholinergic side effects

105
Q

brief pathophys for N/V?

A

irritants irritate the gut, sensory and/or motion input —> feedback to brain —> afferent effect —> vomitting

106
Q

8 groups of anti-emetic drugs

A 
Phenothiazines
Serotonin 5HT3 antagonists 
Benzamides
Dronabinol
Substance P/neurokinin-1 receptor blocker
Anti-histamines
Scopolamine
Corticosteroids
107
Q

what are the 2 phenothiazines?

A

Prochlorperazine (Compazine)
Chlorpromazine (Thorazine)

“azines”

108
Q

MOA for phenothiazines, what are these drugs also used for?

A

Blocks postsynaptic dopamine (D2) receptors and M1 receptors

-antipyschotics

109
Q

Use for phenothiazines?

A

Nausea/vomiting from motion sickness
Chemotherapy induced N/V (but we still have better agents for this)

*Many ADRs: so we don’t use unless we have to

110
Q

3 ADRs of phenothiazines

A

Sedation
EPS (dystonia) (continuous spasms and muscle contractions)
Hypotension

111
Q

what are the serotonin 5HT3 Antagonist

A

Ondansetron (Zofran)
Granisetron (Kytril)
Dolasetron (Anzemet)
Palonosetron (Aloxi)

“-setron” like “serotonin”

112
Q

MOA of serotonin 5HT3 receptors antagonists

A

Blocks 5-HT3 receptors to prevent serotonin action peripherally on visceral vagal afferent fibers and centrally in chemoreceptor trigger zone

113
Q

use for serotonin 5HT3 receptor antagonists

A

Chemotherapy-induced N/V
Radiation & post-op N,V

highly efficacious, long DOA

114
Q

ADRs of the serotonin 5HT3 anatgonists

A 
Common: HA, dizziness &amp; constipation 
Prolong QT (all but palonosetron)
115
Q

what is the bezamide drug (for nausea/vomiting) ?

A

metoclopramide (reglan)

116
Q

MOA for metoclopramide?

A

Blocks dopamine receptors in chemoreceptor trigger zone, also serotonin receptors at higher doses
Increases effect of ACh on muscarinic receptors to promote gastric emptying

117
Q

what are the 2 uses for metoclopramide?

A 
Diabetic gastroparesis  (mostly) - a gastric-emptying propulsive effect. 
Chemotherapy induced N/V (not great for)
118
Q

ADRs for metoclopramide?

A

CNS effects (drowsiness, & agitation), drug induced Parkinson’s

119
Q

MOA for dronabinol (marinol)

A

THC derivative that ACTIVATES ANNABINOID CB1 receptors in chemoreceptor trigger zone
Results in euphoria, increased sensation, analgesia, increased appetite, DECREASED NAUSEA

120
Q

what do we use dronabinol (marinol) for ?

A

Chemotherapy induced N/V, stimulate appetite

121
Q

what are the 3 Substance P/neurokinin-1 receptor blocker?


A

Aprepitant (Emend)
Rolapitant (Varubi)
Fosaprepitant (emend)

“pitant”

122
Q

what is the MOA of the substance P/neurokinin-1 blockers (“pitants”)?

A

Blocks substance P/neurokinin 1 (NK1) receptor

123
Q

PK for “pitants”?

metabolism, onset, DOA

A

Hepatic metabolism – substrate of CYP3A4
Onset – 4 hours
DOA: Up to 3 days and beyond

124
Q

what do we use the “pitants” for?

A

Delayed onset chemotherapy induced N/V with 5HT3 antagonist and glucocorticoids
- targets the late phase emesis for chemo

125
Q

what are the 5 anti-histamine drugs?

A 
Promethazine (Phenergan)
Diphenhydramine (Benadryl)
Dimenhydrinate (Dramamine)
Meclizine (Antivert)
Doxylamine (Unisom)
126
Q

what is the MOA of the anti-histamines?

A

H1 (histamine) receptor antagonist that suppresses vestibular system

127
Q

what do we use anti-histamines for as far as nausea and vomitting?

A 
Motion sickness (mostly), vertigo
Postoperative vomiting
128
Q

ADR of anti-histamines?

A

sedation (as they the generation 1)

129
Q

what drug is used for hospice pts- last days of life to dry up secretions (last few hours before death)

A

scolpolamine (transderm-scop)

130
Q

MOA and use for scolpolamine ?

A

Blocks muscarinic receptors at PNS sites in smooth muscle, secretory glands and CNS
Use:
N/V associated with motion sickness

131
Q

ADR for scolpolamine?

A

drowsiness, confusion, blurred vision, dry mouth, urinary retention

132
Q

what glucocorticoids are utilized for N/V?

A

Dexamethasone & prednisone in particular are used

133
Q

clinical use for glucocorticoid? (3)

A

Clinical use:
Acute & delayed N/V due to chemotherapy (make 5HT3 work better when used in combination)
Post-op N/V
Don’t use in simple N/V

pharmacology (24 decks)

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