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Pharmacology > GI > Flashcards

GI Flashcards

1
Q

Patient-directed drug therapy for GERD

A

INTERMITTENT, MILD HEARTBURN:
lifestyle mod + patient directed therapy w/ antacids and/or OTC H2RA or PPI no more than 2 weeks
ANTACID
1. Mg hydroxide/aluminum hydroxide w/
simethicone (Maalox)
2. antacid/alginic acid (Gaviscon)
3. calcium carb (tums)

OTC H2RA (no more than 2 weeks, up to BID)
1. Cimetidine 200mg
2. famotidine/Pepcid 10mg-20mg
3. nizatidine/Axid AR 75mg

OTC PPI
1. esomeprazole/Nexium 20mg
2. lansoprazole/Prevacid 15mg
3. omeprazole/Prilosec 20mg
4. omeprazole/sodium bicarb (Zegerid)
20mg/1100mg

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2
Q

What are the underlying causes of GERD (physiologically) & what are some things that can worsen GERD symptoms?

A

DECREASE LES PRESSURE:
1. hiatal hernia (increase pressure, lower LES tone)
2. food: fatty, garlic, onion, coffee/tea, soda, chocolate, ETOH, chili peppers
3. Meds: nicotine, nitrates, progesterone, tetracycline, dopamine, estrogen, barbiturates, anticholinergics

IRRITATE ESOPHAGEAL MUCOSA
1. spicy food
2. tomato or orange juice
3. coffee
4. tobacco
5. ASA or NSAIDs
6. irone
7. KCL
etc.

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3
Q

Patho of GERD

A
  1. retrograde gastric content into esophagus, oral cavity, lungs d/t poor tone lower esophageal sphincter (LES).
  2. Slow esophageal clearance, decreased salivary buffering, impaired mucosal resistance, delayed gastric emptying, & increased intra-abdominal pressure can cause
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4
Q

Most common process causing GERD sx

A

slowed esophageal clearance of gastric contents increasing contact time of refluxate w/ esophageal mucosa NOT increased acid

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5
Q

GERD risk factors

A
  1. obesity
  2. high fat diet
  3. smoking
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6
Q

Main typical, atypical, alarm sx GERD

A

Typical: aggravated by activities/food, heartburn waxing/waning, hypersalvation, regurgitation, bleching

atypical (causality only if typical sx also present): chronic cough, hoarseness, wheezing, asthma, non-cardiac chest pain

alarm (GERD complications Barrett esophagus, esophageal strictures, adenocarcinoma): Odynophagia, dysphagia, weight loss, bleeding

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7
Q

How often sx occur for dx GERD & how dx

A

2+ times/week
endoscopy, biopsy to test for Barrett esophagus
ambulatory esophageal reflux monitoring
esophageal manometry

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8
Q

what’s dyspepsia

A

occurs often w/ PUD
epigastric pain and sometimes other upper GI sx like heartburn
consider dx if pain > 1 month

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9
Q

Options of the most appropriate RX drug therapy for gastroesophageal reflux disease

A

***Moderate-severe PPI should be initial therapy, maintenance if recur

H2RA
1. cimetidine/Tagamet 400mg QID or 800mg
BID
2. famotidine/Pepid 20mg BID
3. Nizatidine/Axid 150mg BID

PPI
1. dexlansoprazole/Dexilant 20mg QD x4 weeks
2. esomeprazole/Nexium 20-40ng QD
3. lansoprazole/Prevacid 15mg QD
4. omeprazole/Prilosec 20mg QD
5. pantoprazole/Protonix 40mg QD
6. rabeprazole/Aciphex 20mg QD

**Doses slightly higher or BID or tx erosive esophagitis **

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10
Q

H2RA side effects

A

mild: HA and nausea
drug interactions
cimetidine specifically: gynecomastia & vit B12 deficiency
renally eliminated so dose adjustment in renal dysfunction

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11
Q

how do H2RAs work

A

decrease acid secretion by blocking histamine 2 receptors in gastric parietal cells

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12
Q

how do PPIs work

A

block gastric acid secretion SIGNIFICANTLY by inhibiting gastric H/K ATP in parietal cells= long-lasting antisecretory effect pH > 4 even during postprandial surges

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13
Q

what PPI can be taken w/o regard to food

A

dexlansoprazole or omeprazole-sodium bicarb

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14
Q

PPI side effects

A

Most common= HA, diarrhea, nausea

long-term: AKI/CKD, bone fx, dementia, electrolyte deficiency (ca, mg, B12), bacterial infections (c.diff, PNA)

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15
Q

First line rx tx for GERD

A

PPI x8 weeks
Can do maintenance or on-demand therapy
Can d/c once sx resolve then reinitiate x2-4 weeks if sx 2+ times in week since d/c

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16
Q

rebound hypersecretion

A

can occur w/ continual PPI use of at least 2 months
should be tapered (individualized) slowly using H2RAs for breakthrough sx.
Rebound hypersecretion can last > 3 months

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17
Q

3 most common causes of PUD

A
  1. H pylori
  2. NSAIDs
  3. stress-related mucosal damage (SRMD)
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18
Q

Plan of care for NSAID induced ulcer

A

Prevention:
PPI or misoprostol (prostaglandin E1 analog- GI SE); H2RAs less effective
PPI more tolerated

Treatment:
*PPI x4 weeks, Sucralfate if NSAID stopped, H2RA effective w/ DU only

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19
Q

First line tx H. pylori

A

? amox allergy, ? h/o macrolide abx, ? alcohol (contraindicated metronidazole)

  1. bismuth quadruple
    bismuth 300mg QID
    metronidazole 250-500 QID
    tetracycline 500mg QID
    PPI BID
  2. concomitant
    clarithromycin 500mg BID
    amoxicillin 1g BID
    nitroimidazole 500mg BID
    PPI BID
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20
Q

Meds that end in “-pitant”

Ex: aprepitant, rolapitant, netupitant

A

neurokinin-1 (NK 1) receptor antagonist
act centrally at NK-1 receptors in vomiting centers within the central nervous system to block their activation by substance P released as an unwanted consequence of chemotherapy.

tx acute/delayed CINV when given WITH 5-HT3 antagonist & corticosteroid

prevent PONV

Numerous drug interactions. NOT renally eliminated

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21
Q

Meds that end in “-setron”

Ex: ondansetron, granisetron, dolasetron, palonoestron

A

5-HT3 antagonists (against serotonin) since 5-HT3 stimulates visceral vagal nerve fibers

tx CINV (chemo releases 5-HT3) & PONV

SE: HA, somnolence, diarrhea, constipation, QT interval changes so ECG if at risk

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22
Q

prevention & tx options CINV

A

dexamethasone OR 5-HT3 antagonist (“setron”) OR combo

Moderate= steroid with “setron”

high risk= NK1 receptor antagonist AND 5HT3 antagonist AND dexamethasone AND olanzapine

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23
Q

olanzapine for CINV

A

antipsychotic effects D2, 5HT3, 5HT2C receptors

give in combo therapy for high emetogenic risk chemo

biggest SE= sedation day 2 of chemo

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24
Q

risk factors CINV

A

poor emetic control prior, female, LOW chronic alcohol use, younger age, motion sickness, NVP

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25
Q

what antiemetics for motion sickness & why

A

antihistamines & anticholinergic bc vestibular system replete w/ muscarinic cholinergic & histamine receptors

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26
Q

chemoreceptor trigger zone (CTZ)

A

outside blood-brain barrier so stim by uremia, acidosis, toxins
Has 5HT3/serotonin, NK1, dopamine2 receptors
vagal nerve 5HT3 receptors

NAUSEA/VOMIT

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27
Q

how do anticholinergics & antihistamines work for n/v

A

cholinergic & histamine receptors in vestibular system

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28
Q

meds that end in “-azine”
ex: promethazine, prochlorperazine, chlorpromazine

A

phenothiazines (dopamine2 antagonists) for n/v

SE: sedation, hypoTN, EPS (dystonia, TD, akathesia)

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29
Q

meds that end in “-ridol”
ex: droperidol, haloperidol

A

butyrophenone (dopamine2 antagonist) for n/v

SE: sedation, agitation, restlessness, prolonged QT interval

*Droperidol black box warning Qt interval & cardiac arrhythmias

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30
Q

how do corticosteroids help n/v

ex: dexamethasone & methylprednisolone

A

release of 5HT, reduced permeability blood-brain barrier, decreased inflammation

SE: GI upset, anxiety, insomnia, hyperglycemia
(long term= DM, decreased bone mineral density, cataracts)

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31
Q

meds that end in “ine”

A

usually antihistamINE for n/v
ex: meclizine, hydroxyzine, doxylamine, cyclizine, diphenhydramine

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32
Q

transient causes of retrograde gastric contents & why

A

temp. increase intra-abdominal pressure from straining, exercise, bending, valsalva maneuver

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33
Q

why GERD sx common in older people and during sleep

A

salivation has bicarbonate that buffers acidic gastric content; salivary production decreases in sleep & with age

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34
Q

do people with GERD produce too much acid?

A

NO- most people have slowed esophageal clearance of gastric contents= increase contact time w/ mucosa

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35
Q

non-pharm interventions for GERD

A

lifestyle mod: losing weight, elevate HOB, small meals, no meals 3 hr before HS, avoid foods that exacerbate, smoking cessation, no ETOH

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36
Q

best H2 receptor antagonist for GERD/why?

A

famotidine/Pepcid bc less SE. Cimetidine weak inhibitor w/ many drug interactions. Gynecomastia & b12 deficiency

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37
Q

duodenol ulcer tx

A

H2 receptor antagonist

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38
Q

time to admin PPI

A

am 30-60 min before bkfst NOT with other meds as decrease their efficiency (slow onset/extended release)

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39
Q

what Ca replacement w/ low Ca and GERD on PPI and why

A

Ca citrate NOT carbonate bc better absorption in less acidic environment

40
Q

metoclopramide drug class, mechanism of action, indication, SE, contraindication

A

central dopamine antagonist
accelerates gastric emptying, increases LES pressure

can help n/v from chemo, anesthesia, GERD (w/ PPI), diabetic gastroparesis

SE: EPS/TD. Can affect mental acuity in young and old! Crosses blood/brain barrier

41
Q

on-demand PPI dosing

A

stop PPI when sx resolve
reinstate therapy x2-4 weeks if sx occur >2 times in a week while off therapy

42
Q

when is rebound hypersecretion a concern

A

coming off PPI use of at least 2 months, that’s why titrate slowly
hypersecretion can last > 3 months

43
Q

when is GERD a concern w/ babies

A

vomiting, apnea, poor weight gain, sleep disturbances, refusing to eat

44
Q

why are reflux episodes common during transient LE relaxations not r/t swallowing in babies

A

development immaturity of LES or infant diet
milk protein allergy can mimic GERD

45
Q

when GERD sx resolve in children usually

A

12-18 months old

46
Q

receptors in peripheral nervous system (autonomic [sympathetic/parasympathetic]/somatic) that cause n/v

A

serotonin (5-HT3) and neurokinin

47
Q

corticol (cortex of brain) pathways that cause n/v

A

dopamine & histamine (from sensory glands/vestibular system)

48
Q

Meds that worsen/cause GERD

A

nicotine, nitrates, progesterone or estrogen (OCP), tetracycline, dopamine, barbiturates, anticholinergics

49
Q

zollinger-ellison syndrome (ZES)

A

gastrin-producing tumor (gastrinoma) causing gastric hypersecretion= diarrhea, malabsorption, ulcers

Tx with PPI

50
Q

what kind of ulcers do h.pylori cause

A

more commonly duodenal ulcers

51
Q

what kind of ulcers do NSAIDs cause

A

gastric

52
Q

what stimulates acid secretion in parietal cells

A

histamine, acetylcholine, gastrin

53
Q

NSAID & H.pylori effect on acid secretion

A

NSAIDs dont impact, h.pylori slightly increases acid output

54
Q

how does food effect gastric secretion

A

increases through vagal nerve stim (sight, smell, taste) & stomach distention

55
Q

how do NSAIDs damage gastric mucosa

A

direct irritation & blocks COX-2 which=anti-inflammatory & analgesia but ALSO blocks COX-1 which= gastroprotection

56
Q

duodenal ulcer sx

A

epigastric pain 1-3 hours after meals or night, relieved by food

57
Q

gastric ulcer sx

A

aggravated by food

58
Q

why is acid suppressive therapy alone contraindicated in h.pylori tx

A

associated w/ higher incidence of ulcer recurrence and ulcer-related complications

59
Q

when is bismuth quadruple therapy contraindidcated

A

renal impairment (salicylate toxicity)
issue w/ compliance (QID tx)
SE: stool & tongue discolor, constipation, n/v

60
Q

clarithromycin triple therapy

A

clarithromycin 500mg BID
amoxicillin 1g BID OR metronidazole 500mg TID
PPI BID

61
Q

levofloxacin triple therapy

A

levofloxacin 500mg daily
amoxicillin 1g BID
PPI BID

62
Q

Rifabutin triple therapy

A

*** salvage regimen only
rifabutin 300mg daily
amoxicillin 1g BID or TID
PPI BID

63
Q

common causes constipation

A

Primary
normal-transit
slow-transit (ex low caloric intake)
defecatory evacuation disorder (ex IBD)

Meds (opioids, antihistamine, anticholinergic, andepressant/psychotic, ondansetron, iron, etc)
endocrine (DM, hypercalcemia, hypokalemia, hypomag, hypothyroidism, uremia)
myopathies
neuro (TBI, MS, parkinson)
mechanical obstruction (cancer, stricture)
laxative abuse
immobility

64
Q

lifestyle mod for constipation

A

scheduled bathroom am/pm
elevate feet w/ stool= pelvic relaxation
fiber 20-30g/day
fluids (men 3.7L/day, women 2.7L/day)
exercise
pelvic floor exercise

65
Q

what does soluble fiber do & ex of meds and food

A

dissolved by water, forms gel= slow digestion
lentil, apples, nuts, flax, psyllium

meds: methylcellulose (Citrucel w/ SmartFiber- less likely to cause gas), calcium polycarbophil (FiberCon), wheat dextrin (BeneFiber), psyllium (Metamucil)

66
Q

insoluble fiber & ex

A

doesn’t dissolve in water, decreases time food/feces traverse intestines
whole wheat, corn bran, dark green leafy veggies, skin root veggies

67
Q

What drugs for management of refractory opioid induced constipation?
ex?
SE and what to avoid

A

Peripherally acting μ-opioid receptor antagonists (PAMORAs):
naldemedine, naloxegol, methylnaltrexone

all maintenance laxatives d/c before use, resume after 3 days if PAMORA response suboptimal
stop if opioid stop
don’t use with other opioid antagonists
SE: n/v/d, gas, abd pain, opioid withdrawal sx
avoid with ABX, verapamil, amiodorone

68
Q

bulk producer/fiber supplements
How do they work? examples? when are they NOT effective

A

absorb liquid in the intestines and swell to form a soft, bulky stool… swelling in intestinal fluid, forming gel that aids in fecal elimination & promote peristalsis

ex: psyllium, polycarbophil, methylcellulose (less gas)

NOT effective in delayed transit or obstruct
with 240ml/water

69
Q

emollients

A

soften stool by increasing surface wetting action on stool, reduce friction. Takes up to 72 hrs to work

ex: docusate sodium or calcium
lactulose (osmotic)
mineral oil

70
Q

osmotics and ex

A

water enter lumen in colon > stim. peristalsis

ex: lactulose, sorbitol (may affect blood glucose in DM), glycerin, polythylene glycol/Miralax (BM 1-3 days)

71
Q

lubricants for constipation & SE

A

mineral oil
SE: aspirated into lungs = lipoid PNA in young/old
inhibit fat-soluble vitamins

72
Q

stimulant laxatives & ex
what meds to avoid if take

A

selective action on nerve in intestine smooth muscles > peristalsis

ex: diphenylmethane (bisacodyl) & anthraquinones (senna)

don’t given within 1-2 hrs antacids/H2RA/PPI/milk

73
Q

saline agents for constipation

A

salts of NA, Mg, Ph pull water into lumen increasing enteral pressure

concern of electrolyte imbalances esp. w/ renal impairment & HF

74
Q

intestinal secretagogues & ex

A

Use only after everything else tried

lubiprostone (Amitiza)= derived from prostaglandin E1 > intestinal chloride channels increase intestinal fluid secretion > increase motility. SE: nausea, diarrhea, syncope, distention/pain, gas, hypoTN, dyspnea

linaclotide (Linzess)= activate GC-C increase GNO which stim chloride & bicarb into intestinal lumen= increased fluid & transit. ***ONLY for IBS-C & CIC in adults. Empty stomach 30 min before foot

plecanatide (Trulance)= GC-C agonist ***ONLY for IBS-C & CIC in adults. NOT kids 6-18, concern of dehydration

75
Q

constipation tx pregnant women

A

balanced meal, water intake
bulk producers & stool softeners PROB. safe
lactulose & mg products category B (no risk in animals so prob safe but avoid long term)
laxatives postpartum if not breastfeeding

76
Q

conditions where laxatives should only be used under physician supervision

A

colostomy, DM, heart, renal, swallowing difficulty

77
Q

drugs that may cause acute diarrhea

A

abx, metformin, digitalis, thyroid products, ginseng, st johns warts
poison- arsenic, mercury

78
Q

tx chronic diarrhea

A

calcium polycarbophil (absorbant)
loperamide
diphenoxylate/atropine

bulk-forming products psyllium & methylcellulose may reduce fluid in stool

79
Q

calcium polycarbophil

A

absorbant to tx diarrhea; binds to water leads to formation of gel that enhances stool
***separate from other meds 2-3 hours

80
Q

meds for acute diarrhea

A

loperamide
diphenoxylate/atropine
*bismuth subsalicylate for travel’s & nonspecific acute

81
Q

antiperistaltic (antimotility) agents

A

prolong intestinal transit time in NONINFECTIOUS diarrhea only
loperamide (immodium) & diphenoxylatae/atropine (rx only; Lomotil)
atropine to deter abuse & has anticholinergic effects

loperimide misuse/abuse reported; cardiac arrythmias if OD. Avoid use w/ CYP450 3A4 inhibitors (azole antifungals, clarithromycin, conivaptan, “-mycin”) and 2C8 inhibitors (gemfibrozil, clopidogrel) = increase loperimide concentrations > cardiac

82
Q

antisecretory agents for diarrhea

A

bismuth subsalicylate
cannot give if allergic to salicylates/aspirin. Salicylate absorbed in stomach & small intestine
***stool will turn black

octreotide for severe diarrhea

83
Q

ssx salicylism

A

n/v, tinnitus, hypoTN, hyperventilation, agitation, hallucination, fever, bleeding seizures, confusion, renal fail, resp. fail

84
Q

octreotide

A

antisectory agent for sever diarrhea from chemo, HIV, GM, gastric resection, GI tumor
SQ or IV
nausea, bloating, gallstones

85
Q

botanicals for abd pain & bloating

A

peppermint oil relaxes GI smooth muscle
german chamomile also antispasmodic (avoid w/ warfarin, BZO, ETOH)
primose oil

86
Q

agents for IBS-C

A

bulk producers (psyllium, methylcellulose)
osmotic laxatives (miralax)
linaclotide (Linzess)
lubiprostone (Amitiza) in women only; men can use but only for CIC or OIC
plecanatide (Trulance)- risk diarrhea/dehydration
tegaserod maleate (Zelnorm) women < 65 w/o heart/renal/hepatic disease; monitor for depression & SI

87
Q

what’s the concern with clopidogrel & PPI? What’s the worst PPIs to use w/ this med? Alternative tx?

A

For Plavix (clopidogrel) to work properly in the body, it requires a special protein, or enzyme, called CYP2C19 to help the body digest and use it. PPIs, on the other hand, can stop this enzyme from working. If this happens, the CYP2C19 protein won’t be available to digest the Plavix, meaning it won’t work as well.

Worst PPIs= Omeprazole (Prilosec) and esomeprazole (Nexium) block more CYP2C19 than others

Better PPIs= pantoprazole (Protonix), lansoprazole (Prevacid), or Dexilant (dexlansoprazole)

Alternative= if for heartburn only then H2RA or switch to diff antiplatelet

88
Q

primary method NSAIDs & H pylori cause ulcers

A

inhibit mucosal defense system (prostglandins- buffer acid)

89
Q

important contraindications/considerations for H pylori tx with different drugs

A

QID dosing= issue w/ compliance
PCN allergy= no amox. tx
tx w/ macrolide= no “-ycin” tx (clarithromycin)
alcohol user= no metronidazole
renal impairment= risk of salicylate toxicity w/ bismuth
SE= usually GI, SUPER/OPPORTUNISTIC infections (yeast); bismuth= tongue/stool discolor
pylera & prevac (combo packs) improve adherence but EXPENSIVE
resistance to clarithromycin in areas

90
Q

quinolone abx

A

“floxacin”

91
Q

how to tx h pylori if PCN allergy

A

bismuth regimen (bismuth, metronidazole, tetracycline, PPI) QID

OR

clarithromycin (clarithromycin, metronidazole, PPI) BID/TID

92
Q

best 2 meds to prevent NSAID ulcers or alternative NSAID

A

misoprostol (prostaglandin) or PPI

PPI is better tolerated, misoprostol = GI SE

OR switch NSAID to COX 2 inhibitor (celecoxib)

93
Q

meds for acute AND delayed chemo induced n/v

A

palonosetron (the only 5-HT3 antagonists)

NK1 agonists (-pitant; *Rolapitant doesn’t have as many drug interactions)

94
Q

laxative to avoid in diabetes

A

sorbitol (osmotic) bc affects blood sugar

95
Q

laxative agents heart/renal disease pts must avoid

A

saline agents containing Na, Mg, phosphate bc electrolyte imbalances

96
Q

tx chronic idiopathic constipation (CIC), opioid constipation, IBS-C

A

lubiprostone
linaclotide/Linzess (NOT for opioid)
plecanatide/Trulance not for children= dehydration

97
Q

meds cause constipation

A

diuretics, anticholinergics, Ca/aluminum, analgesics, antidepress/psychotic, antihistamines, calcium channel blockers, iron

Pharmacology (12 decks)

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