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Module 4: Laxatives, Antidiarrhea Digavalli Flashcards

Dr. Digavalli EXAM V (40 cards)

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1
Q

Definition of Constipation

A

< 3 Bowel movements per week !!!

-too little mass
-too dry (reabsorption)
-incomplete evacuation
-too little dietary fiber, too little physical activity

-women 2x as prone
-older adults (25-50%)

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2
Q

What are neuro or endocrine disorders causing constipation?

A

-Neuro: Parkinson’s disease
-Endocrine: diabetes (degeneration of neurons in the gut system), hypothyroidism
-drug-induced

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3
Q

Drugs causing constipation

A

-Anticholinergics (e.g. atropine, dicyclomine )
-Antihistaminics (first gen only)
-Tricyclic antidepressants (e.g. )
-Ca++ channel blockers
-NSAIDS
-Al+3 containing antacids
-Alosetron (Lotronex) - used in diarrhea-predominant IBS
-Opiates (e.g. loperamide)

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4
Q

Why do anticholinergics cause constipation?

A

Blockage of ACh receptors
-ACh stimulates gut motility

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5
Q

Why do TCAs and Antihistamines (1st) cause constipation?

A

due to their anticholinergic effect
-dry mouth, slow gut, …

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6
Q

Why do NSAIDs cause constipation?

A

-prostaglandins cause smooth muscle contraction

-NSAIDs block prostaglandin production

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7
Q

How do Bulk-forming agents work as a Laxative?

A

-absorbing water
-swells and distends -> distends the wall -> stimulation of peristalsis

-Methylcellulose
-Polycarbophil
-Psyllium (natural fiber -> prebiotic)

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8
Q

Which bulk-forming agent may cause bloating and gas?

A

Psyllium (Metamucil, a fiber)

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9
Q

How do Lubricating agents work as Laxatives?

A

reduces water absorption, prevents fecal impaction, keeps the feces wet
-often used for kids (suppository)

-Glycerin
-Mineral oil (oral)
-Magnesium hydroxide and mineral oil

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10
Q

Where are Stool softeners used?

A

-hospital-setting
-preventing strain of the rectum
-hydrates the stool as a surfactant by reducing the barrier between water and the stool

-Docusate sodium

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11
Q

Saline (Lactulose, sorbitol, PEG)

A

hydration of the stool by osmotic pressure
-colonoscopy

-magnesium hydroxide
-PEG (Golytely, Nulytely) -> salts added to compensate for salt loss when water is absorbed and excreted with feces
-Miralax

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12
Q

Stimulants

A

-triggering peristalsis
-stimulates nitric oxide synthase (NOS) and release of platelet active factor -> secretion and motility

-Bisacodyl
-Sodium bicarbonate and potassium bitartrate
-Sennosides
-Castor oil
-Senna

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13
Q

Signs of abuse from laxatives

A

-loss of fluids/electrolytes
-steatorrhea (fat in stool)
-hypoalbuminemia
-osteomalacia (bone softening)

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14
Q

How does Lubiprostone work?

A

-PGE2 agonist (prostaglandin) -> EP4 receptor
-Chloride channel activator

-works locally, not absorbed
-stimulates Cl(-) channel efflux (G2 coupled)
-Na+ will follow through the paracellular pathway
-water will follow

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15
Q

Indication of Lubiprostone

A

-for chronic idiopathic constipation
-IBS-C and opioid-induced constipation

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16
Q

MOA of Linaclotide (Linzess) and Plecanatide

A

-MOA similar to cholera toxin for IBS-C
1. Guanylate cyclase C activation -> increase in GMP 2. secretion of Cl(-) and HCO3(-)
3. Na+ follows passively the negative ion gradient
4. H20 follows the osmotic gradient

cGMP reduces visceral pain
-> increases of 1–2 bowel movements per week

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17
Q

How is Linaclotide different from other laxatives?

Study These Flashcards
A

no dependence

18
Q

How does Tegaserod work

Study These Flashcards
A

5-HT4 agonist (serotonin)

-stimulates peristaltic reflex on 5HT4
receptors on the enteric nervous system

-proximal contraction and distal relaxation

-for IBS-C

19
Q

Which drugs antagonize peripheral opioid
agonist effects?

Postop ileus

Study These Flashcards
A

-Methylnaltrexone Br
-Alvimopan

-work systemically but do not cross the BBB! (the other laxatives work locally)
-reverse postop opioid-induced constipation (paralyzation of the gut)

20
Q

How do opioids cause constipation?

Study These Flashcards
A

-enhance moisture reabsorption
-reduce motility
-increase sphincter tone (it doesn’t relax)
-prolong postop ileus (paralyzed colon - no contraction) -> opioids bind to mu receptors

(Loperamide (Imodium), an opioid is used to treat diarrhea by its constipating effect, but doesn’t cross BBB)

21
Q

What is the non-pharmacological approach to increasing bowel movement?

Study These Flashcards
A

-dietary fiber
-30g/day

-soluble: gel-forming (pectin, psyllium inulin) - may cause bloating

-insoluble: bulk-forming (methylcellulose, cellulose, lignin, synthetic fiber) -> doesn’t feed bacteria

22
Q

Benefits of fibers

Study These Flashcards
A

-Improves regularity (bulk and hydration)
- Increases transit time (and nutrient absorption; why?)
- Improves blood glucose profile -> slows down glucose absorption into the bloodstream
- Reduces blood cholesterol -> absorbs cholesterol -> feces
- Nurtures “good bacteria” (why?)
- Improves barrier function (butyric acid feeds gut epithelia)
- Healthy weight and longevity

23
Q

Definition of diarrhea

Study These Flashcards
A

more than 3 Bowel movements/week

-hypersecretion (ions/paracellular fluid draw)
-osmotic imbalance (ions, protein, AAs exudation)
-Accelerated motility

24
Q

How do PPIs cause diarrhea?

Study These Flashcards
A

-increased risk for C. diff with long-term use
-> diarrhea

25
Treatment for diarrhea
-Loperamide (peripheral acting opioid agonists (mu receptor) increases transit time - Eluxadoline (Viberzi) (peripheral mu/kappa opiate agonist, delta opiate antagonist): approved for IBS-D
26
What is the consequence of an overdose of Loperamide and which patients to avoid using it?
may cause constipation and paralytic ileus (gut paralyzation) Caution in IBD patients (bc of long-term use): toxic megacolon
27
Which anti-diarrheal drug is an opioid?
Diphenoxylate and Difenoxin -> crosses the BBB -formulated with atropine to prevent abuse -atropine is an anticholinergic: photophobia, dry mouth, loss of accommodation of the eye reflex -> unpleasant effects to prevent abuse -long-term use in IBD may cause megacolon
28
How is the emesis reflex regulated?
-sensory stimuli (smell, eyes, sound, sensation) -> stimulates prefrontal cortex -> central pattern generator in the brain stem -central pattern generator in the brain: triggering a sequence of events from the bottom (stomach) to the top pharynx -stomach contraction, opening of lower esophagus sphincter then upper esophagus sphincter, closure of the airway
29
Different factors stimulating the vomiting center?
-sensory stimuli (smell, eyes, sound, sensation) -vagal afferent nerves from the stomach and heart: via mechanoreceptors, chemoreceptors, 5-HT receptors -> radiation, cytotoxic drugs (chemo), emetine, bacteria, virus -vestibular system in the ear: may be stimulated by aminoglycosides (histamine and M-receptors) -chemoreceptor trigger zone: doesn't have BBB so it can sense toxic molecules in the blood an activate the vomiting center -> chemoreceptors, D-receptors, 5-HT receptors -vomiting center itself: has H1 receptors, M-receptors, 5-HT 3 receptors
30
How do 5-HT3 antagonists work?
-"setrons" Ondansetron, Granisetron, Dolasetron -reduces the activity of vagal afferents that go to the brain (by blocking 5-HT3 receptors in the brain???) -it may also reduce motility by binding to 5-HT3 receptors -> Constipation (Alosteron used for IBS-D) -CAUTION: prolong QT interval
31
What may be co-administered to counter severe nausea-inducing chemotherapy?
-dexamethasone -Corticosteroids -NK-1 antagonists
32
What is the role of steroids in nausea therapy?
adjuvant, in combination with "setrons" and NK1 antagonists fe: Dexamethasone, methylprednisolone
33
MOA of NK1 antagonists
-block NK1 receptors in the chemoreceptor trigger zone (CTZ) and vomiting center
34
Why is NK1 so effective and what type of cancer regimen is it used?
-because it directly acts on the vomiting center remember that nausea-causing signals are sent from different sources to the center -> NK1 antagonists are more effective by blocking the center, and don't rely on blocking every single nausea-causing pathway -it has a long halflife it is used for the second wave of cancer treatment which is slowly and longer-lasting -combined with 5-HT setrons and dex (steroids) covering the first wave of nausea -> short-halflife
35
Examples of NK1 antagonists
-Aprepitant -Netupitant -Ranolapitant
36
D2 antagonists
-Antagonize D2, also anticholinergic and anti-histaminergic activity -for motion sickness and chemotherapy-induced nausea -low to moderate nausea -antiemetic + sedative -Prochlorperazine, promethazine and droperidol
37
CB1 antagonists
-present in the CTZ and vomiting center -for AIDS-induced loss of appetite/weight loss and chemotherapy-induced nausea -has a euphoric and dysphoric effect -> counteracted when given with antipsychotic -eg Dronabinol (synthetic delta9-THC, tetrahydro-cannabinol) Nabilone (THC analog)
38
Where are D2 and CB1 receptors in the brain?
-D2: vomiting center -chemoreceptor trigger zone (CTZ) + vomiting center
39
H1 antagonists
-used for motion sickness -> blocking H1 and M1 in the vestibulocerebellar pathway (balance) -used for pregnancy-related nausea -sedative + anticholinergic side effects (dizziness, dry mouth, constipation), hypotension (block alpha1-receptor) -Diphenhydramine -Dimenhydrinate -Cyclizine -Meclizine
40
Scopolamine
-transdermal (most effective, others are oral) -for prevention of motion sickness, apply before traveling -side effects: dry eyes, dry mouth, photosensitivity

GI (19 decks)

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