Gastroenterology Flashcards
(162 cards)
1
Q
________ in saliva helps neutralize the acid in gastric reflux
A
bicarbonate
2
Q
LES maintains tonic (sustained) contraction and relaxes through ___________ to allow the passage of food into the stomach
A
parasympathetic, vagal stimuli
3
Q
The LES is a smooth muscle. What drugs could inhibit (or antagonize) the tonic contraction of this muscle?
A
Dihydropyridine CCBs
can cause relaxation of LES –> reflux of food
4
Q
What do parietal cells do?
A
secreted HCl, which:
1) helps prevent microbial foodborne illnesses
2) activates certain enzymes
3) secretes IF –> allows body to absorb Vit B12
5
Q
Antacids MOA
A
acid buffer, luminal side
6
Q
Antacids pharmcokinetics
A
1) onset: immediate (< 5 min)
2) DOA: short (20-30 min) - limited to activity only while w/in stomach
**food can prolong DOA, potentially up to 3-hr
7
Q
Which antacid is preferred?
A
they are generally interchangeable when doses appropriately
*just because a majority of OTC contain Calcium carbonates, does not make it a superior agent
8
Q
What age group are OTC antacids indicated for?
A
> /= 12 y/o
calcium is approved for infants
9
Q
What is/are the calcium carbonate antacid(s)?
A
Tums
Maalox (tabs)
Alka-Mints
10
Q
What is/are the magnesium hydroxide antacid(s)?
A
Milk of Magnesia
11
Q
What is/are the sodium bicarbonate antacid(s)?
A
Alka-Seltzer
original formula also contained 325mg aspirin
12
Q
What is/are the bismuth subsalicylate antacid(s)?
A
Pepto-Bismol
13
Q
What is/are the mixed antacid(s)?
A
Rolaids
Maalox (liquid)
Gaviscon
Mylanta
14
Q
caution should be used when using antacids with medications that ______
A
can chelate
15
Q
Calcium carbonate ADRs
A
- Ca++ may cause constipation/flatulence
- about 10% of Ca++ is absorbed into blood
16
Q
Magnesium hydroxide ADRs
A
- Mg++ may cause diarrhea
- about 20% is absorbed into blood
17
Q
Sodium bicarbonate ADRs
A
- forms NaCl
- may not be great for pt. on sodium-restrictive diets
18
Q
Bismuth subsalicylate ADRs
A
- dark stools (an unnecessary pt. panic)
- tongue discoloration
- hearing loss
19
Q
Aluminum hydroxide ADRs
A
some Al is absorbed and can accumulate –> altered mental statues (esp. in CKD)
**generally avoided
20
Q
Natural product interactions of antacids
A
Lilly of the Valley and Strophanthus
*Both have major interactions w/ Ca++ and moderate interactions with aluminum hydroxide and bismuth subsalicylate
21
Q
Which antacid can cause constipation?
A
calcium carbonate (Tums, Maalox tabs, Alka-Mints)
22
Q
Which antacid can cause diarrhea?
A
magnesium hydroxide (milk of magnesia)
23
Q
Histamine_2 Receptor Antagonists (H2RA) MOA
A
selective, competitive blockage of type 2 histamine receptors on basolateral side of parietal cells –> prevents stimulation of proton pump w/out blocking it directly
24
Q
Histamine_2 Receptor Antagonists (H2RA) pharmacokinetics
A
1) onset: 30-45 min
2) DOA: 4-10 hr
25
Which Histamine_2 Receptor Antagonists (H2RA) is preferred?
products are considered interchangeable
26
What are the main Histamine_2 Receptor Antagonists (H2RA) drugs?
Famotidine (Pepcid)
Ranitidine (Zantac)
Cimetidine (Tagamet HB)
Nizatidine (Axid AR)
27
How long should pt. take antacids for?
= 2 wks OTC
therapy can be indefinite
28
How long should pt. take Histamine_2 Receptor Antagonists (H2RA) for?
< 2x/day for = 2 wks OTC
therapy can be indefinite under supervision
29
Histamine_2 Receptor Antagonists (H2RA) ADRs
- anti-androgenic (reversible gynecomastia, rarely impotence w/ cimetidine)
- arrhythmias (IV)
- HA
- dizziness
- GI disturbance
- tachyphylaxis (taking for more than a couple days can lead to tolerance and reduced effectiveness...should only taken prn)
30
Which Histamine_2 Receptor Antagonists (H2RA) is rarely used b/c it has lots of s/e and many drug interactions?
Cimetidine
**it is a CYP450 inhibitor
31
Histamine_2 Receptor Antagonists (H2RA) natural product interactions
- Caffeine (cimetidine)
- Hypericum (ranitidine and cimetidine
- many other moderate interactions
32
Dose of Histamine_2 Receptor Antagonists (H2RA) needs to be reduced in people with _________
renal disease
33
Proton Pump Inhibitors (PPI) MOA
selective, irreversible H/K/ATPase inhibition on luminal side of parietal cells
34
Proton Pump Inhibitors (PPI) pharmacokinetics
1) onset: 2-3 hr
2) DOA: 24 hr**
3) T1/2: 1 hr (except tenatoprazole is 8-9hr)
4) acid-labile medication so 50% decrease in bioavailability if taken with food (recommended to take qd 30 min before breakfast)
5) Takes up to 1-4 days for full effect of drug when initiating tx
6) Drugs become MORE bioavailable and absorption INCR. with repeat dosing
7) Metabolism: CYP2C19 and CYP3A4 (hepatic impairment and old age decr. clearance)
35
Proton Pump Inhibitors (PPI) drugs
```
Omeprazole (Prilosec)
Esomeprazole (Nexium)
Lansoprazole (Prevacid)
Pantoprazole (Protonix)
Rabeprazole (Aciphex)
```
36
How long should a patient take PPIs for?
< 1x/day for = 2 wks OTC
therapy can be indefinite and up to bid under supervision
37
Which PPI can be taken with food?
Dexlansoprazole
38
How long does it take for secretory activity to return after stopping PPIs?
3-5 days
39
Proton Pump Inhibitors (PPI) ADRs
- Mg++ depletion (monitor levels)
- osteoporosis (dietary Ca++ absorption requires acidic environment)
- Clostridium difficile infx
- community acquired pneumonia
- HA
- dizziness
- GI disturbance
40
Proton Pump Inhibitors (PPI) natural product interactions
- Grapefruit
- Hypericum
many other moderate interactions
41
Are PPIs or H2RAs better at immediate sx relief?
H2RAs
42
Which site of action do PPIs and H2RAs have in common?
Parietal cells
43
Lactose intolerance is very common in
Black (90%) and Asian (75%) populations
44
Lactose is a disaccharide composed of
glucose + galactose
45
Do probiotics help with lactose intolerance?
questionable
May improve bloating w/ lactase deficiency
46
Simethicone (Gas-X, Mylicon Infant's drops) MOA
inert silicone polymer, "de-foaming" agent --> reduces surface tension of gas bubbles --> relieves gas
47
Simethicone pharmacokinetics
1) Not absorbed
48
Simethicone drug interactions
can bind to thyroid products (e.g. levothyroxine) and decr. absorption of thyroid med
49
Activated charcoal MOA
highly absorptive charcoal; possible adsorbent effects --> gas relief
**this product is charcoal plus w/ simethicone)
50
Activated charcoal pharmacokinetics
1) not absorbed
51
Activated charcoal drug interactions
may significantly impact absorption of medications
52
Alpha-Galactoside (Beano, Gaz away) MOA
mold-derived enzyme, cleaves oligosaccharides before reaching colonic bacteria
recommended for gas prevention with high-fiber diets
53
Alpha-Galactoside (Beano, Gaz away) cautions
avoid with DM and galactosemia
No known drug interactions
54
Pt. with flatulence would like OTC to relieve gas sx. Pt. has DM and would like to avoid a product that could interfere w/ absorption of medications. He has not food restrictions/intolerances. What drug should he try?
Simethicone
55
What is the recommended supplementation for lactose intolerance?
Lactaid (lactase enzyme)
**take at FIRST bite of lactose containing food
56
___________ laxatives are preferred if there is any concern for intestinal obstruction or if rapid onset is required
rectally administered
57
Senna (Senokot, Ex-Lax) classification
stimulant laxative
58
Senna (Senokot, Ex-Lax) MOA
anthraquinone --> direct action on intestinal mucosa or nerve plexus --> stimulates peristaltic activity
59
Senna (Senokot, Ex-Lax) pharmacokinetics
1) Onset: 6-24 hr
60
How long should pt. use Senna (Senokot, Ex-Lax) for?
less than 1 wk OTC
61
Senna (Senokot, Ex-Lax) ADRs
cramps, N/V, diarrhea, *melanosis coli*
**AVOID with actual/possible bowel obstruction
62
Senna (Senokot, Ex-Lax) natural products interactions
- Jalap (electrolyte/fluid depletion)
| - Oleander (incr. risk of cardiac glycoside toxicity d/t K+ depletion
63
Bisacodyl (Dulcolax) class
Stimulant laxative
64
Bisacodyl (Dulcolax) MOA
directly irritates sm. mm. in intestine --> stimulates peristalsis
65
Bisacodyl (Dulcolax) pharmacokinetics
1) onset: 6-12 hr (oral); < 60 min suppository; < 20 min enema
2) minimal absorption (< 5%)
66
Bisacodyl (Dulcolax) ADRs
cramps, diarrhea, N/V, electrolyte disturbances, local irritation
**AVOID with actual/possible bowel obstruction
67
Bisacodyl (Dulcolax) natural product interactions
- Jalap (electrolyte/fluid depletion)
| - Oleander (incr. risk of cardiac glycoside toxicity d/t K+ depletion
68
Polyethylene Glycol 3350 Electrolyte Sol'n (Miralax) class
osmotic (electrolyte) laxative
69
Polyethylene Glycol 3350 Electrolyte Sol'n (Miralax) MOA
osmotic water retention in stool and incr. stool frequency
**AVOID w/ actual/possible bowel obstruction
70
Polyethylene Glycol 3350 Electrolyte Sol'n (Miralax) pharmacokinetics
1) onset = 24-96 hr
| 2) minimal absorption
71
How long should a pt. use Bisacodyl (Dulcolax)?
< 1 week OTC
72
How long should a pt. use Polyethylene Glycol 3350 Electrolyte Sol'n (Miralax)?
< 1 week OTC
73
Polyethylene Glycol 3350 Electrolyte Sol'n (Miralax) ADRs
cramps, diarrhea, urticaria
74
Magnesium Citrate class
osmotic (electrolyte) laxatives
75
Magnesium Citrate MOA
osmotic retention of fluid in bowel
**AVOID with actual/potential bowel obstruction
76
Magnesium Citrate pharmacokinetics
1) onset = 30-60min
| 2) up to 30% absorbed
77
How long should pt. take Magnesium Citrate?
< 1 wk OTC
78
Magnesium Citrate ADRs
cramps, diarrhea, flatulence
magnesium toxicity early signs = hypotn, N/V, facial flushing, retention or urin, ileus, depression, lethargy
magnesium toxicity later signs = mm. weaknes, difficulty breathing, extreme hypotn, irregular heartbeat, cardiac arrest
**risk of magnesium toxicity incr. w/ renal failure
79
Magnesium Citrate natural product interactions
magnesium chelation and various moderate interactions
overall, osmotic lax are less likely to cz electrolyte abnormalities than stimulant lax
80
Docusate (Colace) class
bowel softener
81
Docusate (Colace) MOA
dioctyl dosium sulfosuccinate reduces surface tension of oil-water interface of the stool --> enhances incorporation of water and fat into stool
may also stimulate the secretion of water and electrolytes on contact w/ the mucosa
82
Docusate (Colace) pharmacokinetics
1) onset: 12-72 hr (oral); 2-15 min (rectal)
| 2) absorbed and excreted into bile
83
Docusate (Colace) ADRs
throat irritation (liquid formulation)
84
Docusate (Colace) natural product interactions
many moderate, may incr. absorption of various oral agents, including mineral oil (avoid combination)
theoretical concern that docusate salts can emulsify mineral oil, leading to systemic absorption and toxicity
85
A patient already taking senna could add which other agent(s) (with a different mechanism) for help with persistent constipation?
Docusate (Colace) - stool softener
| mush and push
86
Psyllium (Metamucil) class
Bulk laxative
87
Psyllium (Metamucil) MOA
soluble fiber, absorbes water in the intestine --> viscous liquid --> promotes peristalsis AND reduces transit time
**AVOID if bowel is obstructed
88
Psyllium (Metamucil) pharmacokinetics
1) onset: 12-72 hrs
89
Psyllium (Metamucil) ADRs
cramps, respiratory distress (if inhaled in susceptible individuals), constipation (MUST incr. fluid intake as well)
may cause bowl obstruction
90
Psyllium (Metamucil) interactions
many moderate
can affect absorption (e.g. digoxin) d/t slowed GI transit
91
_________ are being used to reverse opioid induced constipation in the gut
opiate receptor antagonists
naloxone is esp. useful b/c it isn't absorbed well so it stays in the gut and blocks opiate receptors there (relieving constipation) but it does not really get into the bloodstream so opiates can still act systemically
92
anti-diarrheal meds that are OTC rely on an ______________ mechanism, so there is abuse potential; especially with __________
opiate-based
loperamide
93
Loperimide (Immodium) class
opiate-like antidiarrheal
94
Loperimide (Immodium) MOA
decr. GI motility by effects on the circular and longitudinal mm.
reduced GI secretions produced by opiod receptor binding effects in the intestinal mucosa
95
Loperimide (Immodium) pharmacokinetics
1) onset: < 1 hr
| 2) poorly absorbed (when absorbed, metabolism via hepatic oxidative N-demethylation)
96
Loperimide (Immodium) ADRs
dizziness, cramps, nausea, toxic megacolon and rashes (rare), **pro-arrhythmic cz QTC prolongation (high doses and in combination)
**At high doses leads dependence and abuse
97
Loperimide (Immodium) natural product interactions
1) Henbane (additive anticholinergic effects)
2) Scopolia (additive anticholinergic effects)
3) Hypericum (induction of PgP)
98
Diphenoxylate and Atropine (Lomotil) class
opioid-like antidiarrheal
**This is a controlled substance
99
Diphenoxylate and Atropine (Lomotil) MOA
opiate receptor agonist (stimulates mu receptors) --> inhibits excessive GI motility and GI propulsion
100
Diphenoxylate and Atropine (Lomotil) pharmacokinetics
1) onset: 45-60min
| 2) extensively absorbed (hydrolyzed to active diphenoxylic acid)
101
OTC preparations of __________ contain a subtherapeutic amt of atropine to discourage abuse
Diphenoxylate and Atropine (Lomotil)
102
Diphenoxylate and Atropine (Lomotil) ADRs
many anti-cholinergic s/e d/t atropine (inhibited SLUD and dry skin) and CNS depressant effects
103
Diphenoxylate and Atropine (Lomotil) natural product interactions
1) Henbane (additive anticholinergic effects)
| 2) Scopolia (additive anticholinergic effects)
104
Lamotil and Imodium exert their anti-diarrheal effects based on what similar mechanism?
reducing GI motility (and also acting on opioid receptors)
105
What are the primary drug categories used to tx IBD?
1) Corticosteroids/Glucocorticoids
2) Aminosalicylates (5-ASA)
3) Immunosuppressants/Biologics
4) Antibiotics
106
Prednisone/prednisolone class
corticosteroid (includes both glucocorticoid and mineralcorticoid)
107
Prednisone/prednisolone MOA
1) modulates protein synthesis --> reduced migration of polymorphonuclear leukocytes and fibroblasts
2) reverses capillary permeability and lysosomal stabilization --> controls inflammation
3) immunosuppression
**use for IBD is limited to acute flares or salvage therapy
108
Prednisone/prednisolone pharmacokinetics
1) onset: days-weeks
| 2) DOA: 12-18 hr
109
Budesonide (Entocort EC) class
glucocorticoid
110
Budesonide (Entocort EC) MOA
synthesis --> reduced migration of polymorphonuclear leukocytes and fibroblasts
2) reverses capillary permeability andlysosomal stabilization --> controls inflammation
3) immunosuppression
4) **Release mechanism of enteric-coated tablets (Uceris) and capsules (Entocort) delay release until pH > 5.5
111
Budesonide (Entocort EC) pharmacokinetics
1) onset: days - weeks
2) absorption varies, overall minimal absorption (11%)
3) rapid and extensive first-pass (major CYP3A4)
4) Glucocorticoid >> mineralcorticoid receptor affinity (15-fold compared to prednisolone)
5) good topical activity w/ low systemic bioavailability
112
Budesonide (Entocort EC) natural product interactions
1) Grapefruit (CYP3A4 inhibitor)
| 2) Hypericum (CYP3A4 inducer)
113
Which corticosteroid(s) cover the duodenum/ jejunum?
1) Beclomethasone
| 2) Prednisone (PO/IV)
114
Which corticosteroid(s) cover the ileum?
1) Entocort EC
| 2) Budesonide
115
Which corticosteroid(s) cover the colon?
1) Budesonide
116
Which corticosteroid(s) cover the anus/rectum?
1) topical hydrocortisone
| 2) budesonide
117
Mesalamine class
aminosalicylates (5-ASA)
118
Mesalamine MOA
1) modulates local chemical mediators of inflammation (anti-inflammatory), esp. leukotrienes
2) free radical scavenger
3) inhibitor of TNF
119
Mesalamine pharmacokinetics
1) onset: 3-4 wks
2) absorption varies (baled on dosage form), overall minimal absorption (10%)
3) activity is mostly topical
120
Sulfasalazine class
aminosalicylates
121
Sulfasalazine MOA
1) **Prodrug of mesalamine (the Azo, N=N, bond is cleaved by colonic bacteria)
122
Sulfasalazine ADRs
1) dose dependent: nausea, anorexia, folate deficiency, HA, alopecia
2) dose independent: male infertility, rash, hemolytic anemia, hepatitis, pancreatitis, agranulocytosis
123
Sulfasalazine pharmacokinetics
1) onset: 3-4 wks
2) metabolism: intestinal bacteria --> sulfapyridine and 5-ASA --> 5-ASA is poorly absorbed and continues thru GI
3) absorption: sulfasalazine (< 15%); sulfapyridine (60%), 5-ASA (10%)
124
Sulfasalazine metabolism is dependent on
NAT (N-acetyltransferase) phenotype
* 5-ASA is metabolized in colonic mucosa by NAT1
* sulfapyridine is metabolized in liber by NAT 2
125
Which 5-ASA drug(s) cover the duodenum/jejunum?
1) Pentasa (ER caplet)
126
Which 5-ASA drug(s) cover the ileum?
1) Asacol (enteric coated tablet)
2) Claversal
3) Salofack
127
Which 5-ASA drug(s) cover the colon?
1) Sulfasalazine
| 2) Osalazine
128
Which 5-ASA drug(s) cover the anus/rectum?
1) topical 5-ASA
129
Which folic acid derivative immunosuppressant is MC used in Crohn's and UC?
methotrexate
130
Which purine analog immunosuppressant is MC used in Crohn's and UC?
6-mercaptopurine
131
Azathioprine class
purine analog antimetabolite (immunosuppressant)
132
Azathioprine MOA
inhibits purine synthesis and DNA replication --> anti-proliferative effect and apoptosis of T-cells
133
Azathioprine pharmacokinetics
1) onset: 1-3 mo.
2) absorption 60%
3) pro-drug (imidazolyl derivative) which is converted to active form 6-mercaptopurine
134
Azathioprine has a major interaction with
Ethanol (incr. risk for hepatotoxicities)
135
Tumor Necrosis Factor-alpha class
monoclonal Abs
| immunosuppressant
136
Tumor Necrosis Factor-alpha MOA
inhibit TNFa
137
Tumor Necrosis Factor-alpha pharmacokinetics
1) onset: 1-2 wks
2) T1/2: 7-12 days
3) DOA: 8-48 wks
4) metabolisms: mononuclear phagocyte system
138
Tumor Necrosis Factor-alpha C/I
- active HepB
- MS, optic neuritis
- active serious infx
- chronic/recurrent infx
- current neoplasia
- Hx TB or positive PPD (untx)
- CHF (class III or IV)
139
Tumor Necrosis Factor-alpha ADRs
- infusion rxn/anaphylaxis
- infection (TB and HepB re-activation)
- HA
- transaminitis
- N/V
140
Premedication with __________ may be considered to prevent and manage infusion-related rxn to Tumor Necrosis Factor-alpha
antihistamines (H1-antag. +/- H2-antag.), acetaminophen, and/or corticosteroids
141
Infliximab (Remicade) class
anti-TNFa monoclonal Ab
(immunosuppressant)
```
xi = chimera (human-mouse)
mab = monoclonal Ab
```
142
Infliximab (Remicade) MOA
chimeric IgGk that binds to both free and membrane bound TNFa
143
Infliximab (Remicade) major interaction
DMSO
144
Adalimumab (Humira) class
anti-TNFa
(immunosuppressant)
```
lim = immune/immunomodulator
u = mouse
mab = monoclonal antibody
```
145
Adalimumab (Humira) MOA
human mAb (IgGk) against TNFa
146
Drugs used for nausea/emesis
1) Serotonin (5-HT3) antagonists
2) Dopamine (D2) antagonists/prokinetics
3) Antipsychotics
4) Steroids
5) Cannabinoids
6) Antihistamines
147
Ondanstron class
Serotonin (5-HT3) antagonist
148
Ondanstron MOA
selectively antagonizes serotonin at 5-HT3-receptors (both peripherally on vagal n. terminals and centrally in chemoreceptor trigger zone)
149
Ondanstron pharmacokinetics
1) onset: 30 min
2) DOA: 3-6 hr (prolonged T1/2 w. hepatic impairment)
3) metabolism: 1' hepatic - hydroxylation, glucuronide, sulfate conjugation, demethylation (involves CYP450 enzymes)
150
Ondanstron ADRs
- CV (QTc prolongation)
- HA
- fatigue/malaise
- diarrhea
- transient transaminitis
151
Ondanstron natural product interactions
1) Grapefruit (CYP3A4 inhibitor)
| 2) Hypericum (CYP3A4 inducer)
152
If serotonin antagonists prevent/treat nausea...what would you expect SSRIs to do?
s/e of nausea
153
Promethazine class
dopamine (D2) antagonist
154
Promethazine MOA
- blocks postsynaptic mesolimbic dopaminergic receptors in the brain
- exhibits a strong alpha-adrenergic blocking effect
- depresses release of hypothalamic and hypophyseal hormones
155
Promethazine pharmacokinetics
1) onset: 20 min (PO, IM) or 5 min (IV)
2) DOA: 4-6 hr
3) metabolism: significant first-pass, hydroxylation via CYP2D6 and N-demethylation via CYP2B6
156
Promethazine ADRs
- CV (arrhythmia, hypotension)
- dopamine suppression "extrapyramidal" effects (e.g. akathisia, acute dystonia, pseudoparkinsonism, tardive dyskinesia)
- endocrine (amenorrhea, gynecomastia, hyperglycemia)
157
Promethazine natural product interactions
1) Henbane (additive anticholinergic effects)
2) Scopolia (potentiate s/e and ADRs of anticholinergic drugs)
(anticholinergic = anti-SLUD)
158
Metoclopramide class
Dopamine (D2) antagonist
159
Metoclopramide MOA
- antagonizes dopamine receptors
| - at high doses blocks serotonin receptors in chemoreceptor trigger zone of CNS (antiemetic)
160
Metoclopramide pharmacokinetics
1) onset: 30-60 min (PO), 10-15 min (IM), 1-3 min (IV)
2) DOA: 1-2 hr
3) metabolism: extensive absorption, N-demethylation and N-hydroxylation via CYP2D6 and CYP1A2
161
Metoclopramide ADRs
relatively few at low doses
at higher doses may see dopamine-suppression "extrapyramidal" effects (e.g. akathisia, acute dystonia, pseudoparkinsonism, tardive dyskinesia)
162
Metoclopramide has effects on which receptors?
both D2 receptors and 5-HT4 receptors
