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GI2- AM > GI2- Ex2 Pharm > Flashcards

GI2- Ex2 Pharm Flashcards

1
Q

5HT receptor antagonist with patch

A

Granisetron

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2
Q

5HT receptor anatagoinst only for IBS-D

A

Alosetron

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3
Q

Causes prolonged QT time
Dont use w/

Which one high risk

A

Serotonin (5-HT3) receptor antagonists

Dont use w/ anti-arrhythmics or in patients w/ electrolyte imbalance

Dolasetron

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4
Q

5HT receptor antagonist with extended-release SQ injection

A

Granisetron

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5
Q

5HT receptor antagonist pharmacokinetics

A

All have short half lives

Except Palonosetron and Sustained release formulation of Granisetron (SQ)
- 24hr +

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6
Q

What two drugs work well for delayed-CINV as a single dose

A

Long half life

Palonosetron & Granisetron (patch & SQ injection)

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7
Q

5HT receptor antagonist

A

-setron

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8
Q

Neurokinin (NK1) receptor antagonists

A
  • pitant
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9
Q

Neurokinin (NK1) receptor antagonists types (5)

A

Aprepitant (PO)

Fosaprepitant (prodrug, IV)

Netupitant (combo only w/ palonosetron, PO)

Fosnetupitant (prodrug, combo only w/ palonosetron, IV)

Rolapitant (PO/IV)

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10
Q

Strength of antiemetic drugs

  • 5-HT receptor antagonist
  • NK1 receptor antagonist
  • H1 receptor antagonist
  • D2 receptor antagonist
  • M1 receptor antagonist
  • Cannabinoid receptor AGONST
A

1) 5-HT= Strong
2) NK1= Moderate
3) H1= Weak
4) D2= Weak to moderate
5) M1= Weak
6) Cannabinoid= strong

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11
Q

Uses of antiemetic drugs

  • 5-HT receptor antagonist
  • NK1 receptor antagonist
  • H1 receptor antagonist
  • D2 receptor antagonist
  • M1 receptor antagonist
  • Cannabinoid receptor AGONST
A

1) 5-HT
- CINV
- Radiation induced RINV
- Post-operative PONV
- N/V of pregnancy (NVP)

2) NK1
- CINV
- PONV

3) H1
- Idiopathic, mild N/V
- PONV
- NVP (doxylamine/ B6)
- Motion sickness/ Vertigo
- CINV (add-on therapy)
- RINV (add-on therapy)

4) D2
- Idiopathic mild N/V
- Gastroparesis/ Dysmotility (metoclopramide)
- PONV
- NVP
- CINV & RINV (only weak; olanzapien used in combo)

5) M1
- Motion sickness
- End of life care for excessive secretions

6) Cannabinoids
- *CINV (treatment resistant scenarios)
- Appetite stimulation

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12
Q

Only NT1 receptor antagonist used for porphylaxis of post-operative N/V (PONV)

A

Aprepitant

Given 3 hrs PRIOR to anesthesia

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13
Q

Pharmacokinetics of NK1 receptor antagonists

A

Netupitant/ Rolapitant have moderate-major active metabolites, longer half lives

Inhibition of few key CYP450 enzymes

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14
Q

Initial therapy for NVP

A

Doxylamine with pyridoxine (B6) PO

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15
Q

HIstamine receptor antagonist (7)

A

1) Diphenhydramine (PO, IV, IM)
2) Dimenhydrinate (PO, IV, IM)
3) Hydroxyzine (PO, IM)
4) Promethazine (PO, IV, IM, PR)
5) Meclizine (PO) vestibular issues
6) Cyclizine (PO) vestibular issues
7) Doxylamine (PO) NVP only

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16
Q

Drugs for vestibular issues

A

Histamine receptor antagonists

Meclizine and Cyclizine (PO)

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17
Q

Doxylamine

A

Only used for nausea in pregnancy

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18
Q

Receptor antagonists that has anti-cholinergic properties at level of CTZ

A

Histamine receptor antagonists

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19
Q

Classic anticholinergic effects

A 
Drowsiness (CNS depression)
Dry mouth
Constipation
Urinary retention
Blurred vision
Decreased BP
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20
Q

Hydroxyzine

A

H1 receptor antagonist
Converted to active metabolite
IM

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21
Q

Promethazine

A

IV

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22
Q

Dopamine Receptor Antagonists (4)

A

Phenothiazines

1) Chlorpromazine (PO, IV, IM)
2) Perphenazine (PO)
3) Prochlorperazine (PO, IV, IM PR)

4) Metoclopramide (PO, IV, IM, ODT)

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23
Q

Metoclopramide

A

Blocks D2 receptor and

Stimulates acetycholine (ACh) in GI
-enhancing GI motilitly (dysmotility use) & increases lower esophageal sphincter tone
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24
Q

Muscarinic receptor blocker (1)

A

Scopolamine
- patch
72 hrs

Motion sickness

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25
Q 
Stimulates acetycholine (ACh) in GI
-enhancing GI motilitly (dysmotility use) & increases lower esophageal sphincter tone
A

Metoclopramide

Blocks D2 receptor

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26
Q

Cannabinoid receptor agonists (2)

A

1) Dronabinol (C-III) PO

2) nabilone (C-22) PO

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27
Q

Patient with diabetes that has peripheral nerve transmission issues such that GI tract isnt fxn is not sychronous, prescribe what

A

Metoclopramide

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28
Q

Reserved for treatment resistant CINV

A

Cannabinoids

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29
Q

Cannabinoids MOA

A

CB1 adn CB2 cannabinoid receptors are stimulated in VC/CTZ exert signal transduction through G protein-coupled receptors

Results in decreased excitability of neurons

Minimizing serotinon 5-HT3 release from vagal afferent terminals

Suppress Emesis and nausea feeling in the brain

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30
Q

Adverse effects Cannadbinoids (8)

A

1) Euphoria/ Irritability
2) Vertigo
3) Sedation/ drowsiness
4) Impaired congition/ memory
5) Alterations in perception of reality
6) Xerostomia (dry mouth)
7) Sympathomimetic (Increasd HR/BP)
8) Appetite stimulation

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31
Q

Pharmacokinetics of Cannabinoids

A

1) Dronabinol: large first pass effect metabolized to ONE active metabolite
2) Nabilone: metabolized to SEVERAL active metabolites

Short time of onset of activity
Long duration of action 24-36 hrs

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32
Q

High Emetogenic Regimen

A

3-drug regimen

  1. NK1 receptor antagonist (-pitant)
  2. 5-HT3 receptor antagonist (-setron)
  3. Corticosteroid (Dexamethasone)

Give treatment regimen day of (prior to) chemotherapy (for acute) and for 3 days following chemotherapy (for delayed N/V)

A. May add olanzapine (D2)
- increase to 4-drug regimen

B. May add cannabinoid (4 drug)

C. Provide therapy for break through

D. Provide therapy for anticipatory

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33
Q

Moderate-Emetogenic Regimen

A

2 drug regimen

  1. 5-HT3 receptor antagonist (-setron)
  2. Corticosteroid (Dexamethasone)

Give treatment regimen day of (prior to) chemotherapy (for acute) and for 2 days following chemotherapy (for delayed N/V

A. May add NK antagonist or olanzapine (3 drug)

B. May add cannabinoid (4 drug after step A)

C. Provide therapy for break through

D. Provide therapy for anticipatory

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34
Q

Low Emetogenic regimen

A

1 drug regimen

  1. Corticosteroid (Dexamethasone) or
  2. 5-HT receptor antagonist or
  3. Metoclopramide or
  4. Prochlorperazine or

Give day of (prior to) chemo (acute)

A. Provide break through
B. Provide anticipatory

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35
Q

Minimal Emetogenic Regimen

A

0 drug regimen

A. Provide break through
B. Provide anticipatory

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36
Q

Break through

A

Add one agent from a different drug class to the current regimen

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37
Q

Anticipatory Emesis Regimen

A

Avoid strong smells

Relaxation exercises

Lorazepam PO beginning on night before treatment and repeated the next day 1-2 hrs before chemo begins

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38
Q

Motion sickness

A

Scopolamine (patch)
Dimenhydrinate
Meclzine

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39
Q

Vertigo

A

Meclizine or Cyclzine

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40
Q

Diabetic Gastroparesis

A

Metoclopramide

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41
Q

Pregnancy induce nausea/vomiting (NVP)

A

(stepped therapy)

  1. Vitamin B6 or H1 antagonist w/ Vit B6 or 5-HT3 antagonist
  2. Dopamine Antagonist
  3. Steroid or Different dopamine antagonist
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42
Q

Antacids 3 groups

A

1) Low-systemic agents
- Aluminum salts
- Calcium salts
- Magnesium salts

2) High-systemic agents
- sodium salts

3) Supplemental agents
- simethicone

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43
Q

Antacids that work the fastest

A

Calcium and magnesium

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44
Q

Prodrug that tacts the surface tension ofthe little bubbles, lessens it breaks it up and makes one gigantic bubble makes it easier to pass

A

Simethicone

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45
Q

Adverse effects Antacids

  • Aluminum
  • magnetsium
  • calcium
  • sodium
A

1) Aluminum
- Constipation
- Hypophosphatemia

2) Magnesium
- Diarrhea
- Hypermagnesemia

3) Calicum
- Constipation
- Hypercalcemia
- Hypophosphatemia
- Kidney stones

4) Sodium
- Gas
- Hypernatreia
- Metabolic alkalosis

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46
Q

Antacids w/ other medications

A

AVOID

Take all antacids 1-2 hrs before other medications or 2-4 hrs after

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47
Q

Antiulcer agents (5)

A

1) H2 receptor antagonists
2) Proton Pump inhibitors
3) Surface acting agents
4) PGE analogs
5) Bismuth Compounds

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48
Q

Histamine type 2 blockers (4)

A
  • TIDINE
    1) Cimetidine (PO/IV)
    2) Ranitidine (PO/IV)
    3) Famotidine (PO/IV)
    4) Nizatidine (PO)
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49
Q

Only HIstamine Type 2 blocker not IV form

A

Nizatidine

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50
Q

Adverse effects H2 blocker

A

Rare

Cimetidine
- decreases testosterone binding to androgen receptor
(Gynecomastia in men, breast development)
(Galactorrhea in women, liquid from breasts)

Blood dyscrasias in elderly

  • Neutropenia
  • Throbocytopenia
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51
Q

Drug interactions H2 blockers

A

Cimetidine: CYP450 inhbitior

Ranitidine
-10% of cyp450 inhibition

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52
Q

Contraindications for H2 blockers

A

Pregnancy

Use Ranitidine if must

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53
Q

Proton Pump Inhibitors (PPI’s) 6

A
  • PRAZOLE
    1. Omeprazole (PO)
    2. Esomeprazole (PO/IV) isomer
    3. Lansoprazole (PO)
    4. Dexlansoprazole (PO) Isomer
    5. Pantoprazole (PO/IV)
    6. Rabeprazole (PO)
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54
Q

Given enough of what has potential to make patients echolithidric

A

PPIs

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55
Q

PPI characteristics

A

Last 24 hrs
QD dosing
50-90% acid secretion
Takes several days to feel effects

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56
Q

PPI adverse effects

A

Diarrhea

- At risk clostirdium difficile associated diarrhea (CDAD)

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57
Q

PPI drug interactions

A

Omeprazole (CYP450 inhibition)

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58
Q

PPI contraindicated

A

Pregnancy

If necessary Lansoprazole

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59
Q

Surface acting agent

A

Sucralfate

Has alumnium in it –> constipation

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60
Q

Covers ulcer like bandaid, cross-linking from interaction w/ stomach acid

A

Sucralfate

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61
Q

Sucralfate contraindictaions

A

Severe renal failure (aluminum)

Avoid aluminum antiacids

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62
Q

Drug interactions sucralfate

A

avoid taking w/ other drugs, get stuck in viscous membrane

take 2 hrs after other medications

4x day

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63
Q

Prostaglandin analog

-fxn

A

Misoprostol

Makes mucus, bicarb, good blood flow, good healing cell regeneration

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64
Q

Misoprostol indicated in

A

Patients on non-steroidals who cant stop

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65
Q

Misoprostol MOA

A

works on both parietal cell and superficial epithelial cell

1) H2 antagonist, effect on cAMP to tell HK ATPase pump to not release H
2) Stimulatory effect in epithelial cells, make mucus, bicarb, quality blood supply and tissue regeneration

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66
Q

off label use of misoprostol (3)

A

Contractions
Post partum hemorrhaging
Pregnancy termination

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67
Q

Misoprostol adverse effect

A

Diarrhea

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68
Q

Contraindications Misoprostol

A

Pregnancy (contractions/termination)

IBD

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69
Q

Bismuth compounds FXN

A

Anti-diarrheal

Anti-microbial

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70
Q

Bismuth can be added in which situations

A

Ulcers w/ H. pylori

Situations w/ high resistance

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71
Q

Bismuth adverse effects

A

Constipation

Black stools

Lots of drug interactions

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72
Q

Dont use Bismuth salicylate in what patients

can lead to

A

those w/ asprin allergies & GI bleeding

–> renal failure

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73
Q

Treatment of H. pylori

A

Need at least 2 antibiotics and PPI or H2 blocker

10-14 days

Triple therapy (All BID)

1) PPI
2) Clarithromycin
3) Amoxicillin (or metronidazole)

(or metronidaole & tetracycline)

Quadruple Therapy (10-14 days)

  • PPI at BID and all other QUID
    1) PPI
    2) MEtrnoidazole
    3) Tetracycline
    4) Bismuth subsalicylate
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74
Q

PUD in pregnancy w/o H.pylori

A

1) short course antiacids or sucralfate

2) Moderate symptoms
- Ranitidine

3) Severe symptoms
- Lansoprazole

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75
Q

PUD if NSAIDS at risk

A

NSAID no required

  • D/C NSAID
  • acetaminophin

NSAID required

  • COX-2 NSAID and/or
  • PPI or misoprostol
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76
Q

Gram positive spore forming anaerobic rod

A

Clostridium difficile (C. diff)

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77
Q

Severe diarrhea
Abdominal cramping
Fever
Red inflamed mucosa with areas of white exudate on surface of large intestine

A

Pseudomembranes

C. DIff

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78
Q

C. diff frequently associated with what drugs (4)

A
  1. Fluoroquinoles
  2. Clindamycin
  3. Cephalosporins
  4. Pencillins
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79
Q

Treatment for Severe CDI

A

Vancomycin

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80
Q

Treatment for mild CDI

A

Metronidazole

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81
Q

Treatment for recurrent CDI

A

Fidaxomicin

Spares many anaerobic colonic flora

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82
Q

Vancomycin adverse effect

A

Red man syndrome

  • hypotension
  • flushing
  • tachycardia
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83
Q

CDI treatment if patient is vomiting

A

Metronidazole

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84
Q

H. pylori tx (4)

A
  1. Bismuth subsalicylate
  2. Metronidazole
  3. Tetracycline
  4. Omeprazole (PPI)
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85
Q

GI Infections

  • Bacteria (2)
  • Protozoa (3)
  • Nematodes (6)
  • Platyhelminthes (5)
A

Bacteria

1) Clostrudium difficile
2) Helicobacter pylori

Protozoa

1) Entamoeba histolytic
2) Giardia lamblia
3) Cryptosporidium parvum

Nematodes

1) Necator americanus
2) Ancyclostoma duodenale
3) Ascaris lumbricoides
4) Stronglyloides stercoralis
5) Trichuris trichiura
6) Enterobius Vermicularis

Platyhelminthes

1) Scistosomas
2) Taenia solium
3) Taenia saginata
4) Diphyllobothrium latum
5) Echinococcus granulosus

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86
Q

Entamoeba histolytic life cycle

A

Trophozoite –> binucleated precyst –> tetranucleated cyst

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87
Q

During which part of entamoeba life cycle does invasion happen

A

Trophozoites

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88
Q

Liver abscess pathogen

A

Entamoeba histolytica

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89
Q

Tx of Entamoeba histolytic (2)

A

1) Eliminate invading trophozoites
- Metronidazole
- Tinidazole

2) Eradicate intestinal carriage of the organism
- Paromomycin
- Iodoquinol

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90
Q

Paromomycin MOA (3)

A

Bind to 30 S subunit
Irreversible inhibitor protein syn

3 mechanisms

1) inhibit initiation by fixing 50S and 30S to AUG start codon

2) Inhibit continuation of translation, promote early termination
- Inhibition of translation: inhibition of formation 70S
- Promote early termination: induce misreading of mRNA by binding 30S

3) Introduction of errors in protein synthesis, incorportation incorrect AA –> non functional proteins

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91
Q

Iodoquinol MOA

A

Used as a luminal amebicide
No effect extrainestinally

Unknown MOA

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92
Q

Iodoquinol contraindicated in

A

Patient w/ iodine sensitivity

Iodine group

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93
Q

Drug of choice for extraluminal amebiasis

A

Metronidazole

Tinidazole is better tolerated tahn metronidazole

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94
Q

Luminal agent of choice for intestinal carriage in US

A

Paromomycin

Remains in GI

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95
Q

Giardia lamblia life cycle

A

Trophozoite –> Cyst

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96
Q

Characteristics of Giardia lamblia

A 
Coats small intestine interferes w/ fat absorption
Steatorrhea
No invasion of intestinal wall
No blood in stool
Gas and cramps
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97
Q

Giardia first line agent (FDA approved)

A

Tinidazole

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98
Q

Giardia agents

A

Tinidazole
Metronidazole (Not FDA approved)
Nitazoxanide

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99
Q

Nitazoxanide

  • MOA
  • type
  • pharmacokinetics
  • AE
A

Inhibition of pyruvate-ferredoxin oxidoreductase enzyme
-Essential for anaerobic energy metabolism

Prodrug

Rapidly absorbed, excreted in urine and feces

AE

  • Nausea, anorexia, flatulence, increased appetitie, enlarged salivary glands
  • YELLOW EYES, DYSURIA, BRIGHT YELLOW URINE
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100
Q

Inhibition of pyruvate-ferredoxin oxidoreductase enzyme

A

Nitazoxanide

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101
Q

Frothy smelly diarrhea
Gas
Cramps

A

Giardia

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102
Q

Bind to 30 S subunit
Irreversible inhibitor protein syn

3 mechanisms

1) inhibit initiation by fixing 50S and 30S to AUG start codon

2) Inhibit continuation of translation, promote early termination
- Inhibition of translation: inhibition of formation 70S
- Promote early termination: induce misreading of mRNA by binding 30S

A

Paromomycin

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103
Q

Yellow eyes
Dysuria
Bright yellow urine

A

AE to nitazoxanide

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104
Q

Metallic mouth

Vomit w/ alcohol

A

Metronidazole

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105
Q

Metronidazole

  • MOA
  • AE
A

Anaerobic pathogen donates electron to metronidazole

When donated, highly reactive nitro radical anion formed

Ion mediates the killing of organism by means of radical mediated DNA damage

AE= Metallic mouth, vomit w/ alcohol

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106
Q

Vancomycin

  • type
  • MOA
  • route
  • AE
A

Glycopeptide

Cell wall synthesis inhibitors

Bind- D-alanyl-D-alanine terminus of cell wall precursor units w/ high affinity

Leads to inhibition of transglycoslyase and prevents extension and cross linking of the peptidoglycans

Poorly absorbed orally, IV

Red man syndrome: hypotension, tachycardia, flushing

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107
Q

Fidaxomicin

  • type
  • MOA
  • AE
A

Macrolide

Not systemically absorbed

Protein synthesis inhibitor, reversibly binds 50S subunit

Prevents translocation of tRNA from A site to P site
Conformation change, indirect inhibition of transpeptidation

Can induce arrhythmias
Hypersensitivity: eosinophilia, fever

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108
Q

Tetracycline

  • MOA
  • route
  • AE
A

Bind 30S subunit and prevent aminoacyl tRNA from entering acceptor A site

Inhibits synthenis by indirectly blocking polypeptide elongation

Incompletely absorbed in GI

Binds calcium

  • Permanent discoloration of teeth
  • Bone deformaties
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109
Q

Discoloration of teeth

Bone deformity

A

Tetracycline

110
Q

Contaminated water
Daycare
travelers

Diarrhea and abdominal pain
-Self limiting in immunocompetent

Life threatening diarrhea

A

Cryptosporidium parvum

111
Q

Cryptosporidium parvum tx

A

Antidiarrhea agents
- Loperamide

Fluid management

Antimicrobial agents
-Nitazoxanide (preferred)
Paromomycin

112
Q

Preferred drug for cryptosporidium parvum

A

Nitazoxanide

113
Q

Nematodes

  • diagnosed
  • look
  • extra note
A

Eggs in feces

Round worms

No immune response to worms

  • response to dead worms and eggs
  • elevation of eosinophils
114
Q

Necator americanus and Ancylostoma duodenale

  • look
  • life cycle
A

hook worms

Penetrate the skin in-between toes

  • larvae to lungs
  • grow coughed up and swallowed
  • adults in small intestine
  • eggs in feces
  • larvae live in soil
115
Q 
Diarrhea
Abdominal pain
Weight loss
Anemia
Itching at wound in between toes
A

Necator americanus

Ancylostoma duodenale

116
Q

Ascaris lumbricoides

-life cycle

A

Consumption of eggs (contaminated food)

Larvae penetrate intestine and travel to lung
Grow cough up
Swallow
Adult worms in small intestine
Eggs in feces
Eggs hatch, larvae in soil
117
Q

Abdominal cramping
Malnutrition
Worm invasion

A

Ascaris lumbricoides

Worm load so heavy can block GI tract

118
Q

Stronglyoides stercoralis

  • life cycle
  • diagnosis
A 
Larvae in soil
Penetrates human skin, travels to lungs
Larve in lungs, coughed up swallowed
Adult worms in small intestine
Release eggs 
EGGS NOT PASSED IN STOOL
Larvae in stool

Hatched larvae can

1) autoinfect
2) Excrete in feces, infect (direct)
3) Excrete in feces, mature, lay eggs, new larvae infect (indirect)

119
Q 
Vomiting
Abdominal bloating
Diarrhea
Anemia 
Weight loss
Enterotest

Risk w/

A

Strongyloides stercoralis

Risk w/ immunosuppressive medication –> severe auto infection

Prednisone and asthma

Enterotest: swallow a piece of string, pull it back out

120
Q

Organism which eggs are not passed in stool

A

Stronglyloides stercoralis

121
Q

Dont use immunosuppressive medication with what pathogen

A

Strongyloides stercoralis –> severe autoinfection

122
Q

Trichuris trichiura

  • type
  • life cycle
  • diagnosis
  • unique descriptor
A

Whip worm

Ingestion of food w/ infective eggs
Eggs hatch in SI migrate to cecum and ascending large intestine

No larvae
No lung involvment
No eosinophilia

Football shaped worms

123
Q

Enterobius vermicularis

  • type
  • life cycle
  • transmission
  • diagnosis
A

Pin worms

Eggs ingested
Pinworms mature in cecum and ascending large intestine

Female to perianal at night to lay eggs

Severe perianal itching

Scotch tape test

124
Q

Organism w/ larvae in stool not eggs

A

Stronglyloides stercoralis

125
Q

Autoinfect

A

Stronglyloides stercoralis

126
Q

Nematode treatment

A 
Albendazole
Mebendazole
Ivermectin
Thiabendazole
Pyrantel pamoate
127
Q

Albendazole and mebendazole MOA

A

Inhibits microtubule synthesis, paralyzes worms, worms passed in stool

Prodrug

128
Q

Thiabendzole

  • MOA
  • AE
A

Inhibits microtubule synthesis, paralyzes worms, worms passed in stool

Dizziness, nausea, vomiting
Irreversible liver failure
Fatal steven johnson syndrome

129
Q

Ivermectin

  • MOA
  • route
  • contraindicated
A

Intensifies GABA mediated transmision of singals in peripheral nerves of the nematode

Oral only

Not combine w/ drugs that enhance GABA activity

130
Q

Pyrantel pamoate

-MOA

A

Neuromuscular blocking agent, causes release of acetylcholine and inhibit of cholinesterase, paralysis worm

131
Q

Irreversible liver failure

A

Thiabendzole

132
Q

Neuromuscular blocking agent, causes release of acetylcholine and inhibit of cholinesterase, paralysis worm

A

Pyrantel pamoate

133
Q

Intensifies GABA mediated transmision of singals in peripheral nerves of the nematode

A

Ivermectin

134
Q

Inhibits microtubule synthesis, paralyzes worms, worms passed in stool

A

Albendazole
Mebendazole
Thiabendazole

135
Q

Bind 30S subunit and prevent aminoacyl tRNA from entering acceptor A site

Inhibits synthenis by indirectly blocking polypeptide elongation

A

Tetracycline

136
Q

Protein synthesis inhibitor, reversibly binds 50S subunit

Prevents translocation of tRNA from A site to P site
Conformation change, indirect inhibition of transpeptidation

A

Fidaxomicin

137
Q

Bind- D-alanyl-D-alanine terminus of cell wall precursor units w/ high affinity

Leads to inhibition of transglycoslyase and prevents extension and cross linking of the peptidoglycan

A

Vancomycin

138
Q

Drug for N. americanus

A

Albendazole

139
Q

Drug for A. duodenale

A

Albendazole

140
Q

Drug for A. lumbricoides

A

Albendazole or mebendazole

141
Q

Drug for S. stercoralis

A

Ivermectin

142
Q

Drug for T. trichiura

A

Mebendazole

143
Q

Drug for E. vermicularis

A

Albendazole
Mebendazole
Pyrantel pamoate

144
Q

Pathogen that does molecular mimicry posts antigens on surface, confuse host

A

Schistosoma spp. (blood flukes)

145
Q

Schistosoma spp

  • location
  • moa
  • special
  • life cycle
  • clinical
A

fresh water
Invades venous system through exposed skin
Survive for years, no immune rxn
-molecular mimicry

Eggs hatch fresh water
Larvae infect snail
Mature leave snail, infect humans (exposed skin)
Portal venous system
-Mating mature worms veins surrounding intestine and bladder to lay eggs
Eggs enter lumen to be excreted

Dermatitis (immediate)
Katayma fever (4-8 wks)
Chronic fibrosis (years)
146
Q

Katayma fever

A

fever hives
enlarged liver and spleen
bronchospasms

Schistosoma

147
Q

Chronic fibrosis pathogen

A

Schistosoma

148
Q

Dermatitis pathogen

A

Scistosoma

149
Q

Schistosoma tx

A

Praziquantel

150
Q

Praziquantel

  • MOA
  • route
  • AE
A

Increases permeability of nematode and cestodes cell membrane to calcium resulting in paralysis, dislodgement and death

Oral
Rapid
Throughout

AE

  • Immediate: HA, dizziness, drowsiness, lassitude
  • several days: fever, pruritis, skin rash
151
Q

Cestodes

  • type
  • part found in feces
A

Flat worms

Gravid proglottids

152
Q

Taenia

  • 2 types
  • attachment
  • life cycle
A

T. solium= pork, hooks

T. saginata= beef, suckers

Pigs/cows ingest eggs from field contaminated w/ human feces

  • larve into cysts
  • humans ingest undercooked meat

weight loss
Malnutrition

153
Q

Raw fresh water fish

A

Diphyllobothrium Latum

154
Q

Diphyllobothrium Latum

  • acquired
  • life cycle
  • clinical
A

Raw fresh water fish

Absorbs vitamin B12 (anemia)

155
Q

Echinococcus granulosus

  • type
  • cycle
A

Extra intestinal tape worm infection

dog eat sheep meat, poop, sheep eat something near poop

Humans injest eggs from dog feces

Form hydatid cysts

156
Q

Hydatid cysts

A

Echinococcus granulosus

157
Q

Echinococcus granulosus cyst removal

A

Inject albendzole and ethanol to kill everythign with in

surgically remove

158
Q

Cestode treatment

A

Praziquantel
Niclosamide
Albendazole

159
Q

Niclosamide

A

Not effective against hydatid cysts

Inhibition of ox phos or stimualtion of ATPase activity

Oral

160
Q

Inhibition of ox phos or stimualtion of ATPase activity

A

Niclosamide

161
Q

Used for patients with compensated liver disease who do not want to be on long-term treatment
-Prenant next 2-3 years

A

Interferon-a

162
Q

Cons of Inteferon-alpha treatment (4)

A
  1. Parenteral administration
  2. expensive
  3. Side effects
    - Flu like syndrome w/ fever, HA, chills, myalgia, malaise
  4. Dangerous in decompensated cirrhosis
163
Q

Interferon-alpha vs Pedylated interferon alpha -2a/2b

A

Interferon alpha-2b
- agents dont last long

Pegylated interferon alpha-2a

  • Inferon has slower clearance
  • longer half life
  • Steady concentration
  • Left frequently dosage
164
Q

Endogenous Interferon alpha (3)

A
  1. Protect nearby cells
  2. signal macrophages and NK cells
  3. Induce lysosome lysis of infected cell
165
Q

Interferon alpha MOA (4)

A
  1. Interferon alpha binds type 1 interferon receptor and activates JAK1 and TYK2
  2. Activated JAK1 and TYK2 phosphorylate and type 1 interferon receptor
  3. Phosphorylation of receptor leads to recruitment, phosphorylation and dimerization of siganl transducer and activator of transcrition 1 STAT1 and STAT2
  4. STAT1 and STAT2 translocate to the nucleaus and activate the transcirption of interferion stimulated gens (ISGs)
166
Q

ISGs inhibit viral replication at multiple steps (4)

A
  1. ZAP
  2. IFIT family
  3. OAS-RNAseL pathway
  4. PKR
167
Q

Why do you not give Interferon alpha treatment to patients w/ decompensated cirrhosis?

A

As treat w/ interferon alpha, levels of ALT drop.
HBV DNA present
HBeAg present

As the cells start to lyse the level of ALT is going to spike

Bad w/ Decompensated cirrhosis

  • If already have bad liver disease dont want to have spike to make disease even worse
  • might send over edge
168
Q

Nucleosides/ Nucleotides reverse transcriptase inhibitor (NRTI) MOA (2)

A

1) Inhibit Plus-strand synthesis by DNA polymerase

2) Inhibit Minus-strand syntheiss by reverse transcriptase

169
Q

Which NRTI require converstion

A

Nucleosides have to be converted into triphospahte to be active

170
Q

NTRIs list (5)

A

Nucleosides

  1. Lamivudine
  2. Telbivudine
  3. Entecavir

Nucleotide

  1. Tenofovir
  2. Adefovir
171
Q

Patient with impair purine/ pyrimidine kinase activity

A

Use Tenofovir ( nucleotide)

172
Q

Factors that affect selection of antiviral nucleosides/nucleotides for HBV

A
  1. Resistance profile
  2. Efficacy (clearance of HBV DNA)
  3. Usefulness w/ HIV co-infection
  4. Pregnancy
173
Q

First line treatment for wild-type HBV

174
Q

Used in patients with lamivudine, telbivudine or entecavir resistance

175
Q

Tenofovir

  • characteristic
  • AE
A

Resistance is rare

Nephrotoxicity
-Proximal renal tubule

176
Q

First line HBV infection agent

-characteristic

A

Entecavir

  • Resistance rare in nucleoside naive patients
  • 50% in patients resistant to lamivudine
  • well tolerated
  • limited SE
177
Q

Use in patients with HBV and renal insufficiency

A

Entecavir

Better than Adefovir or tenofovir

178
Q

HBV vs HCV treatment

A

HBV can not be fully eradicated

HCV can be cured

179
Q

HCV

- characteristic

A

RNA virus

Can be cured

180
Q

Tx for HCV through 2011

A

PEGylated interferon alpha plus ribavirin

181
Q

Ribavirin

  • what is it
  • MOA (3)
  • Use (2)
  • Contraindications
A

Nucleoside
MOA not fully known

Interferes w/ synthesis GTP
Inhibits capping viral messenger RNA
Inhibits viral RNA-dep polymerase

Potentiates actions of PEGylated interferon alpha-2a and alpha-2b

Also upregulates interferon stimulated genes (ISGs)

Contraindicated

  • patients w/ anemia
  • PREGNANCY
182
Q

HCV Tx new approaches (4, 3)

A

Target translation & processing step
- no generation of new viral particles

1) Protease inhibitors
- Simeprevir
- Telaprevir
- Boceprevir
- (and grazoprevir)

2) NS5B inhibitor
- Ledipasvir
- Elbasvir
- Velpatasvir

183
Q

Protease inhibitors

A

Block the NS3 catalytic site or the NS3/NS4A interaction

184
Q

Simeprevir

A

Second generation protease inhibitor

Administered in combination:
-Simeprevir + PEGylated interferon 2a or 2b + ribavirin

  • Simeprevir + sofosbuvir +- ribavirin (chronic genotype 1 infection)
185
Q

Telaprevir and Boceprevir

A

First generation protease inhibitors

Administed in combo w/ PEGylated interferon alpha-2a or alpha-2b + ribavirin (chronic genotype 1 infection)

Diminished clinical use due to simeprevir

186
Q

Sofosuvir

A

novel NS5B inhibitor
Nucleotide analog
First N5Sb inhibitor available in US

Use in combo w/ other antivirals ledipasvir

Disrupts all genotypes

187
Q

NS5B inhibitor

A

RNA dependent RNA polymerase needed for HCV replication

188
Q

HCV drug that disrupts all genotypes

189
Q

Ledipasvir
Elbasvir
Velpatasvir

A

Inhibit NS5A
All genotypes effective
Low barrier to resistance

Ledipasvir traditonally given in combination w/ ribavirin adn PEGylated interferon alpha -2a or 2b

190
Q

HCV Tx FDA approval 2016

A

Genotype 1
- Ledipasvir + Sofosbuvir

Genotype 1, 2, 3

  • Velpatasvir + sofosbuvir
  • Elbasvir + grazopevir (once daily w/ fixed dosage)
191
Q

Coinfection HBV and HCV

A

Severe liver damage
Decompensation cirrhosis
Greater incidence HCC

Treatment directed at predominant virus

PEGylated interferion alpha-2a or alpha 2b + ribavirin for 48 weeks

  • effective against HBV infection
  • just as effective against HBV and HCV co infection
192
Q

HCV drugs

A

Interferons

  • PEGylated interferon alpha-2b
  • PEGYlated interferon alpha-2a

Nucleoside= ribavirin

Nucleotide= Sofosbuvir

Protease inhibitors

  • Simeprevire
  • Telaprevir
  • Boceprevir
  • Grazoprevir

NS5A Inhibitors

  • Ledipasvir
  • Elbasvir
  • Velpatasvir
193
Q

-asvir

A

NS5A inhibitor

194
Q

-previr

A

Protease inhibitor

195
Q

Ulcerative Colitis (UC) agents(4,1,3,1,4)

A

1) 5-ASA
- Sulfasalazine
- Mesalamine
- Olsalazine
- Balsalazide

2) Janus Kinase (JAK) inhibitors
- Tofacitinib

3) TNF-alpha inhibitors
- Adalimumab
- Golimumab*
- Inflixmab

4) Alpha-4 integrin inhibitors
- Vedolizumab

5) Corticosteroids
- Prednisone
- Dexamethasone
- Hydrocortisone
- Methylprednisone

196
Q

Crohns Disease (CD)

A

1) IL-12/23 inhibitors
- Ustekinumab

2) TNF-alpha
- Adalimumab
- Certolizumab*
- Infliximab

3) ALpha-4 integrin inhibitors
- Natalizumab*
- Vedolizumab

4) Corticosteroids
- Prednisone
- Dexamethasone
- Hydrocortisone
- Methylprednisone

197
Q

Sulfasalazine

A

Sulfapyridine + 5-ASA

SE w/ Sulfa part

198
Q

Mesalamine

A

Single 5-ASA

199
Q

Olsalazine

A

2 molecules of 5-ASA

200
Q

Balsalazide

A

Inert carrier + 5-ASA

201
Q

5-ASA MOA

A

Blocks cycloxygenase and all prostaglandin mediators down stream

Blocks Lipoxygenase and downstream leukotriene

Blocks both via arachidonic acid pathway

Also inhibit activation of NFkB

202
Q

5-ASA contraindicated

A

All 5-ASA CI in ASA-allergic patients

Sulfasalazine CI in sulfonamide allergic patients

203
Q

Use 5-ASA agents in

A

Mild to moderate U.C

204
Q

Use only in active UC in women

A

Balsalazide

205
Q

Use only for maintenance of UC

A

Olsalazine

206
Q

IV inj TNF-alpha inhibitor

A

Infliximab

207
Q

Mild to moderate U.C use

A

5-ASA agents (active and maintenance)

  • Sulfasalazine
  • Mesalamine
  • except Olsalazien (maintance only)
  • except balsalazide (only for active disease)
208
Q

TNF-inhibitors (4)

- derived

A

-mab

Adalimumab
Infliximab
Golimumab
Certolizumab

All monoclonal Ab derived from IgG except certolizumab
-recombinant humanized antibody freagment (Fab)

209
Q

Recombinatn humanize antibody fragment (Fab) assoc w/

A

Certolizumab

210
Q

TNF-alpha inhibitors MOA

A

Bind to an neutralizes membrane-associated and soluble human TNF-alpha mediated pro-inflammatory cell signaling

Ultimately blocking, leukocyte migration to site inflammation

211
Q

TNF-alpha inhibitors SE

A

1) Worry about drugs suppressing immune system
- TB testing pre-therapy

2) Liver toxicity
- have baseline LFT, ALT/AST

3) Rare, dermatologic adn malignancies

212
Q

Adalimumab

A

Moderate to severe UC & CD

213
Q

Infliximab

A

Moderate to severe UC and CD

214
Q

Golimumab

A

Moderate to severe UC ONLY

215
Q

Certolizumab

A

Moderate to severe CD ONLY

216
Q

Moderate to severe UC ONLY

A

Golimumab (TNF)

Tofacitinib (JAK inhibitors)

217
Q

Moderate to severe CD ONLY

A

Certolizumab (TNF)
Resistant
-Natalizumab (a-4)
-Ustekinumab (IL-12/23)

218
Q

Moderate to severe UC and CD

A

Adalimumab (TNF)
Infliximab (TNF)
Vedolizumab (a-4)

219
Q

TNF-alpha inhibitors maintenance dosing (4)

A

1) Adalimumab
- SQ every 2 wks

2) Infliximab
- IV infusion every 8 wks

3) Golimumab
- SQ every 4 weeks

4) Certolizumab
- SQ every 4 weeks

220
Q

Alpha-4 Beta-7 inhibitors
-targets

Alpha 4 Beta 1 inhibitors
-targets

A

Can decreased lymphocyte migration and immune response to tissue damage adn inflammation that IBD patients have

MAdCAM-1

Inhibit most leukocytes except neutrophils

VCAM1

221
Q

Alpha-4 Integrin inhibitors (2)

A

1) Natalizumab (IV)
- Recombinatnt IgG4 monoclonal Ab
- ALpha4beta1 (VCAM-1) & Alpha4Beta7 (MAdCAM-1)

2) Vedolizumab (IV)
- humanized IgG1 monoclonal Ab
- Alpha4beta7 (MAdCAM1)

222
Q

Alpha -4 integrin inhibitors MOA

A

Limits integrins associated cella dhesion and subsequent transendothelial migration of leukocytes to cite of inflammation

223
Q

Alpha-4 Integrin inhibitors SE

A

Natalizumab

  • Infections
    • Progressive multifocal leukoencephalopathy (assoc w/ John Cunningham virus), 3 risk factors
      1) Treatment >2 yrs
      2) Prior imunosuppressant tx
      3) Anti-JC virus (JCV) Antibodies

Infusion related SE

Anti-medication antibodies

224
Q

Progressive multifocal leukoencephalopathy PML

A

Alpha-4 Integrin inhibitor

-Natalizumab

225
Q

Natalizumab indications

A

Moderate to severe CD

Not recommend in combination w/ immunosuppressants

226
Q

Vedolizumab indications

A

Moderate to severe CD & UC

227
Q

Alpha-4 Integrin inhibitors are use when

A

After inadequate response to convential or TNF-alpha therapy

Treatment resistance

228
Q

Alpha 4 maintenance dosing

A

1) Natalizumab
- IV every 4 weeks

2) Vedolizumab
- IV every 8 weeks

229
Q

Interleukin IL-12/23 inhibitors

  • name
  • type
  • MOA
A

Ustekinumab
- fully human IgG1 monoclonal Ab

Bind to a P40 subunit of IL-12/23 receptor located on surface of T cells and NK cells

Thereby inhibiting signal transduction related activites and production of pro-inflammatory TH1 and TH17 cells

230
Q

Interleukin IL-12/23 inhibitors

-SE

A

Infections

-TB testing therapy recommended

231
Q

Moderate to severe CD for patients w/ intolerant or inadequate response (resistant) to conventional, steroids or TNF-alpha therapy

A

Interleukin IL-12/23

Ustekinumab

232
Q

Dosing Interleukin IL-12/23 inhibitors

A

Ustekinumab
-IV as single infusion for induction

-SQ every 8 weeks (for maintenance)

233
Q

Janus Kinase (JAK) inhibitors MOA

A

Bind to and inhibit free-floating and bound JAK1 and JAK3

Thereby ultimately inhibiting gene transcription and more cytokine release

234
Q

JAK inhibitors

-SE (4)

A

Tofacitinib
-Oral

SE

  • Lymphopenia/ lymphocytosis
  • Neutropenia/ Anemia
  • Fatigue
  • Increased LDL & HDL
235
Q

JAK inhibitors indications

-dosage

A

Moderate to severe U.C

PO BID

Dont use w/ other drugs

236
Q

Steroid agents Indications

A

Acute and/or Severe UC & CD uncontrolled by other conventional medications

NOT for maintenance of remission unless absolutely required

Use when have very acute very severe hospitalized requiring flair of their disease

Use in conjunction w/ other therapies

Lowest dose for shortest duration possible

237
Q

Agents for Diarrhea (1,3,1,1)

A

1) Prostaglandin inhibitors
- Bismuth

2) Opiod Agonists
- Loperamide
- Diphenoxylate
- Eluxadoline

3) Serotonin (5HT3) antagonist
- Alosetron

4) Chloride channel inhibitors
- Crofelemer

238
Q

Loperamide

  • death
  • MOA
  • SE
A

Structurally related to opiods

No opiate like effects

OTC status

Cardiac toxicites –> death

Interferes w/ peristalsis (slows transit time)
-Direct action on circular and longitudinal muscles of intestinal wall

Dizziness, fatigure, urinary retention

239
Q

Diphenoxylate

  • Fun fact
  • MOA
  • SE
A

Opiate agonist
(similar to meperidine)
C-V

Atropine added to discourage abuse
- Cant spit or pee

Exert effect locally & centrally on GI smooth muscle cells; inhibits GI motility adn slows excess GI propulsion

SE= dizzy, drowsy, urinary retention

240
Q

Eluxadoline

  • Indication
  • MOA
A

C- IV
Specific to GI tract, opiod receptors

Specifically for IBS-D

Agonist at opioid Mu & kappa receptors in GI tract
Antagonist at delta opioid receptors
-stomach, pancreas, biliary tract, secretions decreased

241
Q

Eluxadoline SE

A

Hepatic/ pancreatic toxicity (increased enzymes)

- Pancreatitis high risk w/o gallbladder

242
Q

Eluxadoline contraindicated in (5)

A
  1. Biliary duct obstruction
  2. Sphincter of Oddi dysfunction
  3. Alcoholism
  4. History of pancreatitis
  5. Severe hepatic impairment
243
Q

Serotonin Antagonists

  • MOA
  • indicated
A

Alosetron
-Selectively blocks GI-based 5HT receptors

Chronic severe IBS-D not responsive to other conventional therapies (women)

244
Q

Serotonin Antagonists SE

A

Constipation

Be concerned if over shoot –> Ischemic colitis

245
Q

Alosetron contraindicated (5,3,3,1)

A

1) GI obstruction, perforation, stricture, adhesions or toxic megacolon
2) Diverticulitis, Crohns, UC
3) Impaired intestinal circulation, thormbophlebitis, or hypercoagulable state
4) Severe constipation; D/C immediately if develops

246
Q

Cl- channel inhibitors

  • from
  • MOA
A

Crofelemer
- derived from dark red sap of Croton lechleri tree

MOA

  • inhibits chloride ion secretion by blocking cAMP stimulated CFTR & Calcium activated (CaCC) chloride channels
  • slows GI secretions
247
Q

Crofelemer indicated in

A

Non-infection diarrhea in HIV/AID pts on anti-retroviral therapy

248
Q

Abdominal pain drugs

A

Antimuscarinics

  • Hyoscyamine
  • Dicyclomine
  • Clidinium/ Chlordiazepoxide
249
Q

Antimuscarinics

  • MOA
  • Indications
  • Se
A

Competitively inhibit autonomic, post-ganglionic cholinergic receptors
-decreases GI motility and spasms (pain)

Indications: Abd pain/ spasms, esp when assoc w/ IBS

SE: Classic anticholinergic
-Dry mouth, urinary retention, constipation, drowsiness, blurred vision

250
Q

Meds for Constipation (2,3,1,1)

A

1) Laxative & Cathartic agents

2) Peripheral Opiod Antagonists
- Methylnaltrexone
- Naloxegol
- Alvimopan

3) Guanylate cyclase-C agonists
- Linaclotide

4) Selective chloride (C2) channel activators
- Lubiprostone

251
Q

Non-infection diarrhea in HIV/AID pts on anti-retroviral therapy

A

Crofelemer

252
Q

Linaclotide

  • MOA
  • Indications
  • SE
A

Guanylate cyclase C agonist

Binds to GC-C on luminal surface or intestinal epitehlium and increases intracellular/extracellualr concentrations of cGMP

  • Stimulate secretion of chloride/bicarb into lumin
  • Activate CFTR
  • Results in increased intestinal fluid and accelerated transit

IBS-C
Chronic idiopathic constipation (CIC)

SE:
- Diarrhea, GERD

253
Q

Lubiprostone

  • MOA
  • Indication
  • SE
A

Selective chloride (C2) channel activator

Prostaglandin analog
Increases intestinal fluid secretion by activating GI specific chloride channels (CIC-2) in luminal cells of intestinal epitehlium

IBS-C
CIC
Opiod induced constipation (OIC)

254
Q

Peripheral opiods

  • MOA
  • Indications
A

Methylnaltrexone (IV/PO)
Naloxegol (PO)
Alvimopan (PO, hospital use only)

Block Mu-opioid receptor

Opiod induced constipation (OIC)

Alvimopan only for accelerating time to GI recovery following bowel resection surgery w/ primary anastomosis (prevention of postop ileus)

255
Q

only for accelerating time to GI recovery following bowel resection surgery w/ primary anastomosis (prevention of postop ileus)

256
Q

Risk w/ Alvimopan

A

Risk of MI

REMS program requires use only in approved institutions for max of 15 doses

257
Q

Cathartics

A

Quickly empty the bowel now

Few hours

258
Q

Laxative (5,4,2,4,2)

A

Can stimulate things, can soften things, can make osmotically draw in water

1) Stimulants
- Bisacodyl
- Castor oil
- Glycerin
- Senna
- Na Picosulfate

2) Osmotics
- Lactulose
- Mag citrate
- Polyethylene glycol (PEG)
- Sorbitol (glycerin)

3) Salines
- Mag. hydroxide
- Na phosphate

4) Bulk forming
- Dietary (fiber/ bra, fruits, grains, cereal)
- Psyllium
- Methylcellulose/ Carboxymethylcellulose
- Calcium polycarbophil

5) Stool softener
- Docusate
- Mineral oil

259
Q

Bulk-forming/ Hydrophilic Colloidal agents

  • MOA
  • AE
  • Interactions
A

Work to increase bulk-volume and water content, therby increasing GI motility

Bloating/ Obstruction

Lots of drug interactions

260
Q

Stool softeners

  • Known as
  • 2 examples
  • time
  • MOA (2)
A

Known as surfactant or emollient laxatives

Docusate ‘salts’
Mineral oil

Takes a few days for effect 1-3 days

Soften/lubricate feces via reduction in surface tension
Increased fluid secretion in GI tract

261
Q

Stimulants (Irritants)

-MOA (3)

A 
Senna
Bisacodyl
Castor Oil
Glycerin
Sodium Picosulfate
(*- also has magnesium oxide/ anhydrous citric acid, converted to mag. citrate (osmotic)

Stimulate peristalsis

1) Irritant to enterocytes, GI smooth muscle leading to inflammation
- Na/K inhibition and/or increased in prostaglandin synthesis and secretion (via cAMP)

2) Promote water/ electrolyte accumulate in GI
- Castor oil is hydrolyzed to ricinoleic acid

3) Glycerin is a tri-hydroxyl alcohol and fxns as an irritant & an osmotic & lubricant agent

262
Q

Stimulants

  • Time
  • AE
  • CI
A

12-36 hrs

AE: cramping

  • Urine discoloration (yellow-brown to red-pink) Senna
  • fluid electrolyte disturbances

CI: GI obstruction, Ileus, impaction

263
Q

Urine discoloration (yellow-brown to red-pink)

264
Q

Stimulant and Osmotic, use to completely evacuate GI tract before surgery or scope

A

Bisacodyl & Glycerin (PR)
- Fast onset 0.5 -2 hr

Prepopik

  • large dose PEG 3350 for pre-colonoscopy only
  • given evening before w/ bisacodyl
265
Q

Saline Agents

  • 3 examples
  • MOA
A

Magnesium salts

  • Mag. sulfate
  • Mag. hydroxide

Sodium phospahte

Magnesium/ Phospahte poorly absorbed, hyperosmolar solutions; osmotically retain water in GI tract

266
Q

Saline agents

  • Drug interactions
  • Caution
A

Interactions: Diuretics (electrolyte balance)

Caution:

  • renal disease (electolytes)
  • CHF/ HTN (sodium)
267
Q

Osmotic agents

  • time
  • AE
A

Lactulose
Magnesium citrate
Sorbitol
Polyethylene glycol (PEG-3350)

1-2 days

Electrolyte distrubance

268
Q

Lactulose

A

Osmotic agent

Disaccharide of galactose and fructose aids in retaining fluid in GI

Also used for severe liver disease patients

  • Hyperammonemia
  • Change in pH traps ammonia in GI
269
Q

Sorbitol

A

Osmotic agent

Non-absorbable sugar, hydrolyzed to short chain fatty acids retaining fluid in GI
Increased motility

270
Q

Polyethylene glycol (PEG-3350)

A

Osmotic agent

Also use in bowel prep for scopes

Smaller doses for constipation (MIralax)

Isotonic solution of long chain PEGs not absorbed with retain water in GI

1-3 hrs large vol administration
0.5-3 days small dose

GI2- AM (11 decks)

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