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Pharmacology > GI Pharm Class > Flashcards

GI Pharm Class Flashcards

1
Q

What are antacids for?

A

Short term temporary relief from mild pain and symptoms of PUD/GERD

Also used to promote headline of duodenal ulcers

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2
Q

Are there better drugs for PUD/GERD than antacid

A

Year with more effective, more convientnt, longer lasting effects

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3
Q

What are the two types of antacids

A

Low systemic agents

High systemic agents

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4
Q

Name the low systemic agents

A 
Aluminum salts (aluminum hydroxide)
Calcium salts(calcium carbonate)
Magnesium salts(magnesium hydroxide/carbonate/trisilicate)
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5
Q

What are high systemic agents antacids

A

Sodium salts (sodium bicarbonate)

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6
Q

What is a supplemental agent for antacids

A

Simethicone

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7
Q

How do antacids work

A

They are weak bases that form a salt and water upon reaction with gastric HCl. The net result is to increase the pH and thereby reduce the acidity of the gastric contents. Furthermore, since pepsin is inactivated at pH>4, antacids may also act to decrease the peptic activity of protein breakdown. Also it has been postulated that antacids may increase the mucosal barrier of the gastric lining by stimulating prostagladin synthesis

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8
Q

Side effect aluminum hydroxide

A

Constipation

Hypophosphatemia (can treat hyperphosphatemia)

Renal osteodystrophy (ESRD)
Encephalopathy
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9
Q

Side effect magnesium hydroxide

A

Diarrhea(stool soft/laxative)

Hypermagnesemia

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10
Q

Side effects calcium carbonate

A

Hypercalcemia; milk alkali syndrome resulting in nephropathy and metabolic alkalosis

Constipation

Hypophosphatemia (effective treatment for hyperphosphatemia)

Calcium based kidney stones

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11
Q

Side effects sodium bicarbonate

A

Flatulence, metabolic acidosis

Hypernatremia

Metabolic alkalosis

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12
Q

What is sucralfate

A

Compound to promote healing of duodenal ulcers. It enhances mucosal barrier through prostagladin synthsis stimulation or by acting as a physical barrier itself and thereby protecting the delicate mucosal lining from the acidic stomach contents. Since sucrlfate requires an acidic environment for activation, it should not be taken with antacids H2 blockers, or protein pump inhibitors

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13
Q

Do antacids reduce acid secretion or production

A

No

Can get rebound acid production

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14
Q

How do antacids work

A

Combine with H ions in stomach acid , capturing the loose H atoms

Forming common byproducts that depend on the antacid agent . (Water, carbon dioxide, chloride salts)

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15
Q

At _ doses, antacids increase LES tone

A

High

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16
Q

Calcium vs magnesium onset

A

Both rapid

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17
Q

Calcium vs magnesium DOA

A

Both long

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18
Q

Acid neutralizing capcity of calcium and Magnesium

A

Both good (calcium a bit better)

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19
Q

Aluminum and sodium

A

Fair good acid neutralizing and short duration of action

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20
Q

Simethicone

A

A surfactant-decreases surface tension

AIDS in expulsion of gas GAS RELIEF and given as a supplement with antacids

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21
Q

Why use combinations of antacids

A

Enhance efficacy and reduce side effects (use of lower doses of each and opposing side effects)
Bc side effects are dose related

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22
Q

How decide which antacid/combination to use

A

What works best for patient, trial and error, and experience

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23
Q

What are patient factors that we have to take into account what prescribing antacids

A

Dosage form and palatability

Presence of renal or heart disease

Electrolyte status

Diseases associated with diarrhea and constipation

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24
Q

If on other meds, when should you are antacids

A

1-2 hours before other medications OR 2-4 hours after other meds

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25
Q

What are anti-ulcer agents

A

H2 receptor

Proton pump inhibitors

Surface acting agents

PGE1 analogs

Bismuth compounds

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26
Q

Name H2 receptor antagonists

A

Cimetidine (po/iv)
Famotidine (po/iv)
Nizatidine (po/iv)
Ranitidine (po)

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27
Q

Name proton pump inhibitors

A 
Lansoprazole
Dexlansoprazole
Omeprazole
Esmoprazole
Pantoprazole
Rabeprazole
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28
Q

Name a surface acting agent

A

Sucralfate

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29
Q

Name a PGE1 analog

A

Misoprostol

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30
Q

Name a bismuth compounds

A

Bismuth subsalicylate

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31
Q

How do H1 blockers work

A

Reversible block the binding of histamine to the H2 receptor (basolateral membrane of parietal cell) that is present not he parietal cells of the gastric mucosa. By inhibiting stimulation of the H2 receptor, cyclic AMP levels are decreased, which then eventually leads to the decreased activity of the H/K proton pump. The end result is that gastric acid secretion is decreased

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32
Q

Onset Histamine type 2 blockers

A

.5-2 hours (longer than antacids, shorter than PPI)

QB to BID

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33
Q

Clinical use of histamine type 2 blockers

A

Treat GERD< peptic ulcer disease, and other diseases associated with gastric ulcers and get ulcer healing in 4-8 weeks

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34
Q

H2 blockers inhibit __% of acid production

A

20-50

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35
Q

Adverse effects H2 blockers

A

Headache (CNS)

Nausea/diarrhea/constipatoin (GI)

Gynecomastia

Cimetidine is also associated with decreased hepatic metabolism of certain drugs (warfarin, phenytoin, diazepam)

Cimetidine decreases testosterone binding to androgen receptor (weak anti androgen effects) -gynecomastia in men, galactorrhea in women

Blood dyscrasias-neutropenia, thrombocytopenia

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36
Q

Cimetidine interesting

A

Prototypical inhibitor of several CYP450 isoenzymes

Lots of drug drug interactions

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37
Q

Ranitidine interesting

A

Inhibits but 10% of what is with cimetidine

Pregnancy only if necessary!! Contraindicated in preg

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38
Q

Name PPI

A 
Omeprazole po
Esomeprazole po/iv
Lansoprazole po
Dexlansoprazole po
Pantoprazole po/iv
Rabeprazole po
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39
Q

MOA PPI

A

Covalently/irreversibly bind sulfhydryl groups of HKATPas at parietal cell secretory sites, thereby inhibiting gastric acid secretion by irreversibly inhibiting functions ase pumps, suppressing gastric secretion

Inhibits pump induced egress of gastric acid

Takes several days to create new steady state of pump activite

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40
Q

Use of PPI

A

PUD, GERD, zollinger ellison syndrome, and esophagitis, and in regimen for H pylori

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41
Q

why QD dosing PPI

A

Effects last 24 hours

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42
Q

PPI inhibit _% of acid

A

50-90

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43
Q

Onset PPI

A

Days -longer than H2 and ulcerations heal 4-8 weeks

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44
Q

Adverse effects of PPI

A

CNS-headache

GI-diarrhea, dyspepsia/nausea, *additional risk of Clostridium Difficile Associated Diarrhea

Rash

Rare-generalized myalgia, fatigue, myopathies

Other-kidney disease, bone fractures, MI

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45
Q

Special omeprazole

A

P450 inhibition many drug drug interactions

Not for preg

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46
Q

Contraindications PPI

A

Pregnancy, but if 1100% necessary, can try lasoprazole

AVOID omeprazole

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47
Q

Sucralfate

A

A sulfate polysaccharide-an octasulfate of sucrose and ALOH3 added

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48
Q

MOA sucralfate

A

Undergoes cross linking from interaction with stomach acid, creating a viscous, sticky polymer which adheres to epithelial cells around ulcer’s crater, preventing acid access to ulcer sites

May also stimulate local prostagladin and mucous productiona nd epidermal growth factor (cytoprotection) but does not affect pH

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49
Q

What use sucralfate for

A

DU*

But also aphthous ulcers, mucositis/stomatitis
Radiation procitis/ulcers (enema)
Bile reflux gastropathy

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50
Q

Adverse effects sucralfate

A

Constipation

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51
Q

Contraindication sucralfate

A

Severe renal failure

Aluminum containing antacids should be avoided

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52
Q

Drug interaction sucralfate

A

Possible therefore take 2 hours after other meds

QID for active ulcers so plan dosing other meds accordingly if possible

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53
Q

Misoprostol

A

Prostagladin E1 analog that provides protective prostagladin to gastric mucosa and reduces gastric acid release from parietal cells (providing cytoprotection by increasing mucosal defenses-stimulates bicarbonate and mucous production, increases mucosal blood flow)

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54
Q

Misoprostol and acid output

A

Reduce basal and nocturnal acid output but lesss than H2 antagonist and PPI

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55
Q

Indication misoprostol

A

Prevention of NSAID induced gastric ulceration in patients at high risk of ulcerations and complications

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56
Q

Off label uses of misoprostol

A

With/without mifepristone (pregnancy termination)

Alone for cervical ripening

Post partum hemorrhaging (high dose)

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57
Q

Adverse effects misoprostol

A

GI-diarrhea with or without N/V and cramping

CNS-related: headache/dizziness

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58
Q

Contraindications misoprostol

A

Pregnancy

IBD

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59
Q

Bismuth compounds MOA

A

Not precisely delineated; but as a salicylate derivative can function similar to asprin and inhibit prostagladin synthesis

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60
Q

What was bismuth originally developed as

A

Antidiarrheal

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61
Q

What is bismuth most well known for

A

Antimicrobial actions which prevent microbial attachment to mucosa, possible inactivation of enterotoxins, and disruption of bacterial cell wall

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62
Q

OTC bismuth compounds

A

Alone for reflux (heartburn), indigestion and diarrhea

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63
Q

RX bismuth compounds

A

In combination with antibiotics and acid suppressant for H pylori

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64
Q

Adverse effects bismuth compounds

A

Constipation from antidiarrheal

Black/dark stools but regularly formed

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65
Q

Drug interactions bismuth

A

LOTS take 2 hours after other meds

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66
Q

Contraindications bismuth compounds

A

Severe renal failure

Antiplatelets and anticoagulatnts (bismuth subsalicylate)

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67
Q

Absolute contraindications bismuth

A

GI bleeding

Salicylate hypersensitivity

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68
Q

Treat H pylori

A

Combination therapy-at least 2 antibiotics and an acid reducer (PPI or H blocker)

14 days of triple drug regimen
(PPI, clarithromycin, and either amoxicillin or metronidazole) on BID

Or

10-14 days quadruple therapy
PPI BID
Metronidazole QID
Tetracycline QID
Bismuth subsalicylate QID
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69
Q

What drugs may lead to false negative urea breath test with h pylori

A

Bismuth, antimicrobials, PPI suppress H pylori

Avoid the use of agents known to suppress H pylori

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70
Q

Prevpac for PUD

A

Amoxicillin
Clarithromycin
Lansoprazole

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71
Q

Omeclamox for PUD

A

Amoxicillin
Clarithromycin
Omeprazole

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72
Q

Helidac for PUD

A

Bismuth
Metronidazole
Tetracyclines
Plus additional PPI

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73
Q

Pylera for PUD

A

Bismuth subcitrate potassium
Metronidazole
Tetracycline
Plus addition of PPI omeprazole

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74
Q

Why consider PPI for a few/several weeks after 10-14 days h pylori combo therapy

A

For complete healing of ulcers

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75
Q

What do if failure to eradicate h pylori with metronidazole containing triple therapy

A

Follow up with non metronidazole containing quadruple therapy

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76
Q

H pylori with PCN allergy

A

No amoxicillin

Substitute metronidazole (consider bismuth quad)

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77
Q

H pyloric ith metronidazole resistance

A

Substitute tetracycline

Consider quadruple therapy (with clarithromycin and amoxicillin)

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78
Q

H pylori with clarithromycin resistance

A

Substitute either amoxicillin or tetracycline

Consider bismuth quadruple therapy

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79
Q

Pregnant patient with PUD without h pylori

A

Short course of antacids or sucralfate

  • if moderate symptoms consider ranitidin
  • if severe consider iansoprazole
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80
Q

PUD if nsaid at risk

A

If nsaid not required, consider acetaminophen and D/C NSAID

If NSAID required, consider COX-2 NSAID and/or consider PPI or misoprostol

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81
Q

What are common causes of nausea and vomiting

A 
Chemotherapy/radiation
Post op
Vestibular dysfunction
Gastrointestinal obstruction/dysmotility
Metabolic conditions
Pregnancy
Infections
Intracranial lesions
Non chemo medications
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82
Q

Receptors of nausea/vomiting

A

Receptors in Brain and GI stimulate, which we can use antiemetic agents in combinations since have different MOA , espicially for chemo and radiation induced N/V

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83
Q

Categories of emetic potential for chemotherapy

A

High (90%)
Moderate (30-90%)
Low(10-30%)
Minimal (fewer than 10%)

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84
Q

what are the important receptors for N/V

A

5-HT3

Neurokinin (NK1)

Histamine (H1)

Dopamine(D2)

Muscarinic (M1)

Cannabinoid

*antagonize them all except agonist cannabinoid

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85
Q

What are commonly used to treat N/V

A

Glucocorticosteroids

Benzodiazepines

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86
Q

Name serotonin 5HT3 receptor antagonists

A

Dolasetron
Granisetron
Ondansetron
Palonosetron

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87
Q

Name neurokinin receptor antagonists (NK1)

A 
Aprepitant 
Fosaprepitant
Netupitant
Fosnetupitant
Rolapitant
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88
Q

Name histamine receptor antagonists

A 
Diphenhydramine
Dimenhydrinate
Hydroxyzine
Promethazine
Meclizine
Cyclizine
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89
Q

Name dopamine receptor antagonists

A

Phenothiazines
-chlorpromazine
-perphenazine
Prochlorperazine

Other

  • metoclopramide
  • haloperidol, olanzapine and trimethobenzamide
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90
Q

Name muscadine M1 receptor antagonists

A

Scopolamine

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91
Q

Name cannabinoid receptor agonists

A

Dronabinol

Nabilone

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92
Q

Indication for aldosterone

A

IBS-D

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93
Q

Serotonin are strong antiemetic agents, what were they developed for

A

Chemotherapy induced N/V (CINV)

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94
Q

How do serotonin 5-HT3 receptor antagonists work

A

Block serotonin type-3 receptors at vagal nerve terminals and blocks signal transmission to CTZ
-blocks serotonin receptor activation after serotonin release from intestinal enterochromaffin cells

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95
Q

Uses for serotonin 5-HT2 receptor antagonists

A

CINV
RINV
Post op NV (PONV)
NV of pregnancy (NVP)

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96
Q

Adverse effects serotonin receptor antagonists

A

CNS-headache
GI-constipation/diarrhea
—-serotonin syndrome (IF WITH OTHER 5-HT AFFECTING DRUGS)

BUT MOST WORRISOME
-DOSE DEPENDENT QT PROLONGATION AND TORSADES

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97
Q

Dose dependent QT prolongation and torsades with serotonin receptor antagonsits

A

Extreme caution required when using with other QT-prolonging agents (anti-arrhythmatics ) or in patients with electrolyte imbalances (hypokalemia or hypomagnesmia )
-dolasetron high risk; no longer recommended for CINV prophylaxis

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98
Q

All serotonin 5-HT3 receptor antagonists have short half lives, except which one

A

Palonosetron and sustained release formulation of grainisetron

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99
Q

Long half life makes palonosetron and 2 branded granisetron agents effective for :

A

Delayed CINV as a single dose

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100
Q

Drug interactions H2 receptor antagonists

A

QT prolonging agents

Antiarrhythmics

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101
Q

Name neurokinin NK1 receptor antagonists

A 
Aprepitant
Fosaprepitant
Netuputitant
Fosnetupitant
Rolapitant
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102
Q

Fosaprepitant is a prodrug of ___

A

Aprepitant

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103
Q

Fosnetupitant is a prodrug of __

A

Netupitant

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104
Q

Netupitant and fosnetupitant are in combo only.. what what

A

Palonosetron

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105
Q

Neurokinin1 receptor antagonist is a __ antiemetic

A

Moderate

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106
Q

Blockade of neurokinin receptors (subastant P) in CTZ/VC

A

Peripheral blockade of NK1 receptors located on vagal terminals in gut an additional hypothesized actio

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107
Q

Therapeutic uses NK1 antagonist

A

Chemotherapy induced NV

-most effected when used in combo with a glucocoticosteroid and 5HT3 antagonist

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108
Q

Prophylaxis NK1 antagonist

A

PONV

Only aprepitant given up to 3 hours prior to anesthesia induction

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109
Q

Adverse effects NK1 antagonist

A

GI-dyspepsia/constipation/diarrhea

CNS-dizzy/fatigue/somnolence

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110
Q

Neutupitant/rolapitant

A

Moderate major active metabolites

Longer half lives

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111
Q

NK1 cyp450

A

Mild moderate inhibition

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112
Q

Name H2 receptor antagonists

A 
Diphenhydramine
Dimenhydroxyine
Promethazine
Meclizine
Cyclizine
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113
Q

Doxylamine

A

Initial therapy for NVP

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114
Q

Histamine receptor antagonists are __ antiemetic agents

A

Weak

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115
Q

Use of histamine receptor antagonist

A

PONV

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116
Q

MOA histamine receptor antagonist

A

Block histamine type 1 receptors in VC and vestibular system

-*agents exhibitvarying levels of central anticholinergic properties at level CTZ

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117
Q

Therapeutic uses histamine receptor antagonist

A 
Idiopathic mild NV
Post op NV
NVP (doxylamine/B6)
Motion sickness/vertigo(only indication for meclizine and cyclizine)
Chemotherapy-induced NV
RINV
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118
Q

Adverse effects histamine->CLASSIC ANTICHOLINERGIC EFFECTS

A 
Drowsiness
Dry mouth
Constipation
Urinary retention
Blurred vision
Decreased BP
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119
Q

Hydroxyzine pharmacokinetics

A

Active metabolism=cetirizine

IM route

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120
Q

Promethazine pharmacokinetics

A

IV administration requires dilution and lower dose (than oral)

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121
Q

Interactions histamine receptor antagonist

A

Other agents that also induce anticholinergic-related side effects (cumulative)

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122
Q

Name the dopamine receptor antagonists

A

Phenothiazines

  • chlorpromazine
  • perphenazine
  • prochlorperazine

Other
-metoclopramide

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123
Q

Dopamine receptor antagonists are ___ antiemetic agents

A

Weak to moderate

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124
Q

How do dopamine receptor antagonists work

A

Block dopamine type 2 receptors in CTZ
-agents exhibit varying levels of anticholinergic properties; affect other receptors (histamine, muscarinic, adrenergic receptors)

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125
Q

Metoclopramide also stimulates _____ in GI. Doing what

A

Acetylcholine
Enhancing GI motility (dysmotility use) and increases lower esophageal sphincter tone
-no impact on GI secretions
-also has weak 5HT inhibition

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126
Q

Therapeutic dopamine receptor antagonist

A

Idiopathic mild NV
Gastroparesis/dysmotility
-specifically metoclopramide
Post operative NV
NV of pregnancy
Chemotherapy induced NV and radiation induced NV
-as single agents only weak moderate antiemetic activity;olanzapine used in combination with other agents for CINV RINV

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127
Q

Adverse effects dopamine effects-classic anticholinergic effects

A 
Drowsy
Dry mouth
Constipation
Urinary retention
Blurred vision
Hypotension
-arrhythmias and extrapyramidal SE are possible;usually seen with larger psychiatric doses
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128
Q

Dopamine receptor antagonists interactions

A

Other agents that also induce anticholinergic related side effects

Antiarrhythmics, espicially QT prolonging agents

Antihypertensives

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129
Q

Name muscarinic receptor antagonists

A

Scopolamine

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130
Q

Scopolamine transdermal scop

A

Worn for 73 Horus

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131
Q

Scopolamine is a _ antiemetic agent

A

Weak

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132
Q

What is scopolamine used for

A

Motion sickness

And also in end of life care foe excessive secretions

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133
Q

MOA scopolamine

A

Block acetylcholine stimulates muscarinic receptors in neural pathways fromt he vestibular nuclei in inner ear to brain stem and from reticular formation to VC

  • significant anticholinergic properties
  • usually put behind ear
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134
Q

Adverse effects scopolamine -classic anticholinergic effects

A 
Drowsy
Dry mouth
Constipation
Urinary retention
Blurred vision
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135
Q

Interactions scopolamine

A

Other agents that also induce anticholinergic related side effects (cumulative)

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136
Q

Name cannabinoid receptor agonist

A

Dronabinol

Nabilone

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137
Q

What are cannabinoid

A

Synthetic preparations of cannabinol (THC)

  • synthetic cannabinoids are FDA schedules(controlled) medications
  • limits on quantities/refill
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138
Q

Cannabinoids are _ antiemetic agents

A

Strong

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139
Q

Cannabinoids are reserved for treatment of what

A

CINV

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140
Q

Stimulation of cannabinoid receptors stimulates what

A

Central (CB1) and peripheral (CB2) cannabinoid receptors in VC/CTZ

This exerts signal transduction effects through G protein coupled receptors, resulting in decreased excitability of neurons
-minimizing serotonin 5HT3 release from vagal afferent terminals

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141
Q

Therapeutic uses of cannabinoids

A

CINV

Appetites stimulation in select (anorexic) patients due to severe disease (cancer or AIDS)

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142
Q

Why are cannabinoids commonly reserved for treatment resistant clinical scenarios

A

FDA scheduling

Can be used in combination with other agents

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143
Q

Adverse effects of cannabinoids

A 
Euphoria/irritability
Vertigo
Sedation/drowsiness
Impaired cognition/memory
Alterations in perception of reality
Xerostomia
Sympathomimetic
Appetite stimulation
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144
Q

Pharmacokinetics dronabinol

A

Large first pass effect and metabolized to one active metabolite

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145
Q

Nabilone pharmacokinetics

A

Metabolized to several active metabolites

-both have a short time to onset of activity and a long duration of action (34-36 hours) so can use fewer doses a day

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146
Q

Interactions cannabinoids

A

Caution in use with other CNS depressants and cardiovascular agents and sympathomimetics

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147
Q

Acute CINV

A

<24 hours after chemo given

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148
Q

Chronic CINV

A

> 24 hours after chemo given

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149
Q

Anticipatory CINV

A

Occurs before chemo give, customarily in non treatment naive patients

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150
Q

You should add ___ to antiemetic regimens for adults who receive high emetic risk, antineoplastic agents or who experience breakthrough nausea and vomiting

A

Olanzapine

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151
Q

High emetogenic regimen for CINV

A

NK1 receptor antagonist
5HT3 receptor antagonist
Corticosteroid (dexamethasone)

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152
Q

When should the region for CINV be started

A

Day of (prior to therapy) and 3 days after

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153
Q

What can you add to the high emetogenic regim to make it a four drug regimen

A

Olanzapine (D2 antagonist)

Cannabinoid in treatment resistance

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154
Q

Also provide therapy for breakthrough NV for all patients and provide therapy for anticipatory NV as needed

A

Ok

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155
Q

Moderate emetogenic regimen

A

5HT3 receptor antagonist (palonos/granis SQ)

Corticosteroid (dexamethasone)

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156
Q

When give the moderate emetogenic regimen

A

Day of (prior) to chemo and for 2 days after

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157
Q

What can you add to the moderate emetogenic regimen

A

NK1 antagonist or olanzapine

May add cannabinoid in treatment resistsance (make.4 drug after 3)

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158
Q

Provide therapy breakthrough NV for all patients

Provide therapy for anticipatory NV as needed

A

Ok

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159
Q

Low emetogenic regimen for CINV

A 
Corticosteroid (dexamethasone)
Or
5HT3 receptor antagonist
Or
Metoclopramide
Or
Prochlorperazine
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160
Q

Same timing thing here

A

Ok

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161
Q

Minimal emetogenic regimen for CINV

A

No routine prophylaxis therapy recommended

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162
Q

Breakthrough emesis regimen

A

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

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163
Q

Motion sickness

A

Scopolamine or dimenhydrinate or meclizine

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164
Q

Vertigo

A

Meclizine or cyclizine

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165
Q

Diabetic gastroparesis

A

Metoclopramide

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166
Q

Pregnancy induced (stepped therapy)

A
  1. Vitamin B6 or histamine antagonist w/B6 or 5 HT2 antagonist
  2. Dopamine antagonist
  3. Steroid or different dopamine antagonist
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167
Q

Take home points

A

Targeted therapy of NV by first determining cause

Multiclass combination therapy appropriate for moderate to high emetogenic chemotherapy regimens

Prevention is more cost effective and clinically accepted than attempting to treat after it develops

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168
Q

What groups of drugs are for diarrhea

A

Prostagladin inhibitors

Opoid agonists

Serotonin antagonists

Chloride channel inhibitors

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169
Q

Name prostagladin inhibitors

A

Bismuth

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170
Q

Name opoid agonists

A

Loperamide
Diphenoxylate
Eluxadoline

171
Q

Name serotonin antagonists

172
Q

Name chloride channel inhibitors

A

Crofelemer

173
Q

Loperamide

A

Chemically related to opoids but does not exhibit analgesic/opiate-like effects or appear to produce physical dependence

174
Q

Loperamide OTC or Rex

175
Q

Misuse with loperamide

A

Overdose

FDA issues drug safety communication-cardiac toxicities leading to death

176
Q

MOA loperamide

A

Interferes with peristalsis direct action on circular and longitudinal muscles of intestinal wall, slowing motility
-the slowed motility allows for fluid/electrolyte reabsorption and increasing bulk/density of feces

177
Q

Side effects loperamide

A

Dizziness, fatigue, drowsiness and urinary retention (anticholinergic)
-long half life; increases with increasing dose

178
Q

Diphenoxylate

A

Synthetic opiate agonist (chemically similar to meperidine)

  • opoid effects only seen at very high doses
  • small quantity of atropine added to discourage deliberate abuse/over-dosage
179
Q

MOA diphenoxylate

A

Locally and centrally on GI smooth muscle cells; inhibits GI motility and slows excess GI propulasion

180
Q

Side effects diphenoxylate

A

Dizzy, drowsi, urinary retention (anticholinergic; atropine)

181
Q

Kinetics diphenoxylate

A

Active metabolite with long half life

182
Q

MOA eluxadoline

A

Agonist at opoid mu and kappa receptors in GI tract (slows peristalsis/delays digestion)
Antagonist-a delta opoid receptors in GI
-stomach, pancreas, and biliary tract secretions decreased

183
Q

Indication for eluxadoline

A

IBS, diarrhea predominant subtype (IBS-D)

184
Q

Side effects eluxadoline

A

GI-related
Hepatic /pancreatic toxicity
-PANCREATITIS HI-RISK IN PTS W/O GALLBLADDER—>DEATHS HAVE OCCURED

CNA-related (dizzy/fatigue/sedation/euphoria/impaired)

185
Q

Contraindications eluxadoline

A 
Biliary duct obstruction
Sphincter of oddi dysfunction
Alcoholism
History pancreatitis
Severe hepatic impairment

Stop therapy if severe constipation develops and lasts 4+ hours

186
Q

MOA alosetron

A

Selectively blocks GI based 5HT2 receptors

-antagonism in GI modulate regulation of visceral pain, colonic transit and GI secretions

187
Q

Alosetron indication

A

Chronic, severe IBS-D not responsive to other conventional therapies (women)
-severe diarrhea predominant IBS includes diarrhea, and one or more of the following
—frequent/severe abdominal pain
—frequent bowel urgency or fecal incontinence
—restriction of daily activities due to IBS
——anatomical or biochemical GI abnormalities must be excluded before prescribing

188
Q

Alosetron side effects

A

GI-constipation, dyspepsia, GERD and NV

Ischemic colitis (black bow warning)

  • no refills without a follow up exam by prescriber
  • physicians must enroll in prescribing program
  • patients and physicians must sing a risk benefit statement and agree to adhere to therapy plans
  • additional self training and testing by physicians to learn to appropriately diagnose IBS required
189
Q

Alosetron contraindications

A

GI obstruction, perforation, stricture, adhesions, or toxic megacolon

Diverticulitis, crohns, UC

Impaired intestinal circulation, thrombophlebitis or hypercoagulable state

Severe constipation; DC immediately if develops on alosetron therapy

190
Q

Crofelemer

A

Derived from dark red sap of croton lechleri tree

191
Q

MOA crofelemer

A

Inhibitis chloride ion secretion by blocking cAMP-stimulated CFTR and calcium activated chloride channels
-channels regulate fluid secretion ny intestinal epithelial cells

192
Q

Indication crofelemer

A

Non infectious diarrhea in HIV AIDS on antiretroviral therapy

193
Q

Side effects crofelemer

A

GI -abdominal distention, elevated AST/ALT/bilirubin

Infections-respiratory/urinary

194
Q

Name antimuscarinic agents

A

Hyoscyamine
Dicyclomine
Clidinium
Chlordiazepoxide

195
Q

What are antimuscarinic for

A

Abdominal pain IBS

196
Q

MOA antimuscarinic

A

Competitively inhibit autonomic, post ganglionic cholinergic receptors to decrease GI motility and spasms

197
Q

Indication antimuscarinic

A

Abdominal pain/spasm espicially when associated with IBS

198
Q

Side effects antimuscarinic

A 
Dry mouth
Urinary retention
Constipation
Drowsy
Mental confusion
Blurred vision
199
Q

What do we use for constipation

A

Laxative and cathartic agents

Peripheral opoid antagonists

Guanylate cyclase C

Agonists

Selective chloride channel activators

200
Q

Linaclotide MOA

A

Selective guanylate cyclase C agonist

  • binds to GC-C on luminal surface of intestinal epithelium and increases intracellular/extracellular concentrations of cGMP
  • stimulates secretion of chloride/bicarbonate into intestinal lumen cia activation of CFTR ion channel-results in increased intestinal fluid and accelerated transit
201
Q

Linaclotide indication

A

IBS-C IBS constipation

CIC chronic idiopathic constipation

202
Q

Side effects linaclotide

A

GI-diarrhea (dehydration/electrolyte imbalance), GERD/dyspepsia NV

203
Q

Lubiprostone MOA

A

A bicyclist fatty acid, prostagladin E1 derivative
-increases intestinal fluid secretion by activating GI specific chloride channels in luminal cells of intestinal epithelium

204
Q

Lubiprostone indications

A

IBS-C
CIC
OIC opoid induced. Constipation

205
Q

Side effects lubiprostone

A

Nausea, dyspepsia, dizziness

206
Q

Methylnaltrexone and naloxegol and alvimopan MOA

A

Peripheral mu opoid receptor antagonists

-no common significant CNS penetrations/actions or induction of withdrawal/pain symptoms

207
Q

Methylnaltrexone, naloxegol and alvimopan indications

A

OIC

Alvimopan only for accelerating time to GI recovery following bowel resection surgery with primary anastomoses (prevention of postoperative ileus)
-therapeutic doses of opoids for <7 consecutive days immediately before starting alvimopan

208
Q

Side effects methylnaltrexone and naloxegol and alvimopan

A

Abdominal pain, diarrhea, nausea, flatulence, vomiting

209
Q

Warning alvimopan

A

Carries risk of MI with use; REMS program requires use only in approved institutions for max of 15 doses

Only for short term hospital use

210
Q

Laxative and cathartic agents stimulants

A 
Bisacodyl
Castor oil
Glycerin
Senna
Na picosulfate
211
Q

Laxative and cathartic agents osmotic

A

Lactulose
Mag citrate
Polyethylene glycerol (PEG)
Sorbitol (glycerin)

212
Q

Laxative and cathartic agents saline’s

A

Mag. Hydroxide

Na phosphate

213
Q

Laxative and cathartic agents bulk forming

A 
Dietary (fiber/bran fruits/grains/cereal)
Psyllium
Methylcelluose
Carboxymethylcellulose
Calcium polycarbophil
214
Q

Laxative and cathartic agents stool softeners

A

Docusate

Mineral oil

215
Q

Dietary fiber/brain

A

Fruits, bran, whole grains, cereals, wheat

216
Q

Methylcellulose/carboxymethylcellulose

A

Bulk forming/hydrophilic colloidal agents

217
Q

What do bulk forming hydrophilic colloidal agents do

A

Work to increase bulk volume and water content thereby increasing GI motility

Fiber can also support colonic bacteria, fermentation and digestion’s

Efficacy seen in 2-4 days

218
Q

Adverse effects bulk forming/hydrophilic colloidal agents

A

Bloating/obstruction

-drink fluids

219
Q

Drug interactions bulk forming/hydrophilic colloidal agents

A

LOTS (recommendation similar to that f the bile acid sequesterants and antacids)
-mainly with psyllium and cellulose

220
Q

Stool softeners (surfactant or emollient)

A

Docusate salts

Mineral oil

221
Q

Stool softeners-anionic surfactants

A

Soften/lubricate fecesvia reduction in surface tension

Increase fluid secretion into GI tract

222
Q

Mineral oil is a hydrocarbon

A

Ingestible and penetrates still thereby softening it

-may also inhibit water reabsorption from GI tract

223
Q

When is efficacy seen with stool softeners

224
Q

Stool softeners laxative

A

Minimal, softening mainly

225
Q

Adverse effects stool softeners

A

GI-bloating/flatulence, abdominal cramps

Can leak past anus in some-aspiration caution in elderly/delibitated stroke

226
Q

Stimulants

A

Senna
Bisacodyl
Castor oilglycerin
Sodium picosulfate-OSMOTIC, also has magnesium oxide/anhydrous citric acid, metabolically converted to magnesium citrate

227
Q

MOA stimulatnts

A

Irritant to enterocytes, GI smooth muscle leading to inflammation
-Na K ATPas inhibition and/or increase in prostagladin synthesis/secretion (via cAMP/GMP)

Promote water/electrolyte accumulation in GI
-castor oil is hydrolyzed to ricinoleic acid

Glycerin is a tri-hydroxyl alcohol and functions as an irritant and an osmotic and lubricant agent

228
Q

Efficacy of usual stimulants

A

12-36 hours

229
Q

Adverse effects stimulants

A

Abdominal cramping

Urine discoloration (yellow brown/red pink)-senna

Fluidelectrolyte disturbances (long use)

230
Q

Stimulants contraindications

A

GI obstruction/ileus/impaction

231
Q

Caution stimulants

A

Several of these agents pass into break milk

232
Q

Bisacodyl and glycerin PR route

A

Faster onset via this route (.5-3 hours)

233
Q

Prepopik and large doses PEG-3350 for precolonoscopy only

A

Classically given evening prior; with bisacodyl

234
Q

Magnesium/phosphate

A

Ions poorly absorbed

Hyperosmolar solutions;osmotically retain water in GI tract

Greater volume shortens transit time

235
Q

Drug interactions saline agents

A

Diuretics (electrolyte balance)

236
Q

Caution saline agents

A

Renal disease (electrolytes)

CHF/HTN (sodium)

237
Q

Osmotic agents

A

Lactulose
Magnesium citrate
Sorbitol
Polyethylene glycol (PEG-3350)

238
Q

Lactulose

A

Disaccharide of galactose and fructose which aids in retaining fluid in GI

239
Q

Sorbitol

A

Non absorbable sugar hydrolyzed to short chain FA retaining fluid in GI

240
Q

In general osmotic agents provide effects in 1-2 days with laxative doses; larger doses may provide catharsis sooner

241
Q

Lactulose also used for what

A

Severe liver disease patients (hyperammonemia) changes in pH traps ammonia in GI

242
Q

Adverse effects osmotic agents

A

Electrolyte disturbances;watch closely

Abdominal pain/distention/flatulence

243
Q

Polyethylene glycol (PEG-3350)

A

Also used for bowel prep prior to GI scopes radiological procedures or surgery

Smaller doses for constipation

Isotonic solution of long chain PEGs, not absorbed which retain water in GI (osmotically)

244
Q

PEG products can provide a large volume of fluid to consume in a short period
-bloating/distension and NV
Palatability

A

Efficacy may be seen within 1-3 hours of large volume administration
-smaller, daily doses provides effects in .5-3 days

245
Q

What drugs do we use for UC

A

5-ASA
JAK inhibitors
TNF-a inhibitors
1-4 integrins inhibitors

246
Q

Name 5-ASA

A

Sulfasalazine
Mesalamine
Olsalazine
Balsalazide

247
Q

Name JAK inhibitors

A

Tofacitinib

248
Q

Name TNF-a inhibitors

A

Adalimumab
Golimumab
Infliximab

249
Q

Name a-4 integrin inhibitor

A

Vedolizumab

250
Q

__, ______, and ___ are also used as first line therapy for UC and crohnsbut not officially indicated, and covered elsewhere…not one exam

A

Steroids, immune modulators, antibiotics

251
Q

What can we use to treat CD

A

IL-12/23 inhibitors
TNF-a inhibitors
A-4 inhibitors

252
Q

Name IL-12/23 inhibitors

A

Ustekinumab

253
Q

Name TNF-a inhibtors

A

Adalimumab
Certolizumab
Infliximab

254
Q

Name a-4 integrin inhibtors

A

Natalizumab

Vedolizumab

255
Q

5-ASA MOA

A

Inhibit PG and LT production via arachidonic acid pathway
-COX and LIPOX

Inhibiton of PG and LT produciton via arachidonic acid pathway

Reduction in PMN and macrophage chemotaxis
-may also inhibit the activation of NFKB which regulated transcription of genes for pro inflammatory proteins

256
Q

Name the 5-ASA agents

A

Sulfasalazine (sulfapyridine and 5-ASA)

Mesalamine (single 5-ASA)

Olsalazine (2 molecules of 5-ASA)

Balasalazide (inert carrier +5-ASA)

257
Q

The extend of disease impacts how 5-ASA are given.

A

Oral-make distal ileum, colon or throughout GI

Rectal exam-may reach the splenic flexure, so not frequently concentrate in the rectum

Rectal suppositories-reach the upper rectum

258
Q

Side effects 5-ASA agents

A 
Izzy/headache/fatigue
Epigastric distress (anorexia, abdominal pain, NVD)

Fewer systemic SE with pure 5-ASA products and topical formulations

259
Q

Contraindication of 5-ASA

A

ASA allergic paintings

260
Q

Contraindication for sulfasalazine

A

Sulfonamide allergic patients

261
Q

Indications for 5-ASA agents

A

Active and maintence of mild to moderate UC

Olsalazine-only for maintence of remission

Balasalazide-only for active disease approval in males

262
Q

MOA TNF-a inhibitors

A

Binding to TNF receptors and mediating upregulation of surface adhesion molecules-VCAM-1, E-selectin, MAdCAM-1 for leukocyte adhesion

Binds to and neutralized membrane-associated and soluble human TNF-a mediated proinflammatory cell signaling, ultimately blocking leukocyte migration to its of inflammation

263
Q

Name TNF-a inhibitors

A

Adalimumab
Infliximab
Golimumab
Certolizumab

264
Q

What are TNF-a inhibitors used for

265
Q

Side effects TNF-a inhibtors

A

Infections (TB testing pre therapy)

266
Q

Adalimumab black bow

A

Serious warning of infection that may lead to hospitalization or death. Most who developed these infections were also taking immunosuppressants

267
Q

When discontinue adalimumab

A

Serious infection or sepsis
TB

Closely monitor

268
Q

Side effects TNF-a inhibtors

A

Infections-TB treat pre therapy recommended

Liver toxicity (increased enzymes)

Headache/arthralgias/fatigue

Rare-but-severe

  • dermatological related (EM, SJS, TEN)
  • malignancies
269
Q

Indications adalimumab and infliximab

270
Q

Indication golimumab

271
Q

Indication certolizumab

272
Q

Administration adalimumab

A

SQ every 2 weeks

273
Q

Administer infliximab

A

IV every 8 weeks

274
Q

Administer golimumab

A

SQ every 4 weeks

275
Q

Certolizumab

A

SQ every 4 weeks

276
Q

A-4 integrin MOA

A

Limits integrins associated cell adhesion and subsequent treansendothelial migration of leukocytes to cite of inflammation

277
Q

Name a-4 integrin inhibitors

A

Natalizumab (recombinant humanized IgG4 monoclonal antibody)

Vedolizumab (humanized IgG1 monoclonal antibody)

278
Q

Side effects a-4 integrin inhibitors

A

Infections (only natalizumab)
-PML

Infusion related SE

Anti medication antibodies (decrease efficacy)rare-malignancies (vedolizumab)

279
Q

What are the 3 risk factors for PML with a-4 integrin inhibtors

A

Treatment over 2 years

Prior immunosuppressant treatment

Anti-JC virus antibodies

280
Q

Black bow warning a-4 integrin

A

PML
Natalizumab only available through TOUCH prescribing program (only prescribers, infusion centers, and pharmacies associated with infusion centers registered with the program are able to prescribe, distribute, or infuse)

281
Q

How diagnose PML

A

Evaluation that includes a gadolinium enhanced MRI scan of brain and when indicated, CSF analysis for John Cunningham viral DNA are recommended

282
Q

Indication a-4 inhibtors

A

Used after inadequate response to conventional or TNF-a therapy

Vedolizumab-moderate to severe CD and UC

Natalizumab-moderate to severe CD

283
Q

What is natalizumab not requested with

A

Moderate to severe CD

Not recommended in combination with immunosuppressants; including TNF-a agents

284
Q

Dose natalizumab

A

Administration IV infusion every 4 weeks

285
Q

Dose vedolizumab

A

IV every 8 weeks

286
Q

IL-23 and 12 MOA

A

Bind to respective receptors on naive T cells to induce differentiation and production of pro inflammatory cytokines

Bind p40 subunit of IL12 and IL23 blocking activation and differentiation of naive T cells and activation of NK cells
-thereby inhibiting production of pro inflammatory cytokines; INFg (TH1), TNFa, IL17(TH12), IL21,

287
Q

Ustekinumab

A

Fully human igG1k monoclonal antibody

Also indicated for plaque psoriasis and psoriatic arthritis
IBD

288
Q

Side effects IL12/23

A

Infections-TB testing pre therapy recommendation

Infusion/injection related allergic reactions

Headache/arthralgias/fatigue

Rare-malignancies

289
Q

Indications IL12/23

A

Active and maintence CD

For patients intolerant or inadequate response (resistant) to conventional immune modulators, steroids or TNFa therapy

290
Q

Dosing ustekinumab

A

IV as a single infusion
For induction

SQ every 8 weeks for maintence

291
Q

JAK

A

Intracellular enzymes that transmit signals arising from cytokine interactions on cellular membrane to influence pro inflammatory gene transcription and expression

292
Q

MOA JAK inhibtors

A

Bind to and inhibit free floating and bound JAK1 and JAK3 (lesser extent JAK2)
-thereby ultimately inhibiting gene transcription and more cytokine release

293
Q

Tofacitinib

A

Oral jak1/3 inhibitor

Also indicated for psoriatic and RA

294
Q

Side effects JAK inhibitors

A

Lymphopenia/lymphocytosis
Neutropenia

Fatigue

Increases in LDL and HDL

Rare-increased risk of malignancies/serious infections
-from RA indication data

295
Q

Indication JAK inhibitors

A

Moderate to severe UC active and maintence

Concomitant use in biologic therapies or potent immunosuppressants not recommended

296
Q

Siding tofacitinib

297
Q

Indications for steroid agents

A

Acute and/or severe UC and CD uncontrolled by other conventional medications
-not for mainance of remission unless absolutely required

298
Q

Dosing steroid agents

A

Use the lowest dose for shortest duration possible

299
Q

C diff

A

Gram positive spore forming anaerobic rod

Antibiotic associated pseudo membranous diarrhea

300
Q

C diff toxins

A

Toxin a-enterotoxin_>diarrhea

Toxin b-cytotoxic->cytotoxic to the colonic cells

301
Q

Treat C diff

A

Cessation antibiotic

Supportive, fecal transplant

Vancomycin , metronidazole
Fidaxomixin

302
Q

Vancomycin c diff

A glycoprotein

A

Severe or mild

303
Q

Metronidazole for c diff

A 5 nitroimidazole

A

Mild

If oral administation wont work

304
Q

Fidaxomicin c diff

A macrolide

A

Recurrent cdi

Spares anaerobic colic flora

305
Q

Name Protozoa

A

Entamoeba histolytica

Giardia lamblia

Cryptosporidium

306
Q

Treat entamoeba histolytica

A

Metronidazole or tinidazole to eliminate trophozoites

Paromomycin or iodoquinol to eradicate intestinal carriage or organism

307
Q

How treat entamoeba histolytica asymptomatic carriage

A

Cysts or trophozoites without internalized RBC

With amebicide

308
Q

Why must metronidazole and tinidazole be given with a luminal amebicide

A

Ensure eradication of e histolytica

309
Q

Do paromomucin and lodoquinol effect extraintestinal organisms

310
Q

MOA lodoquinol

A

Halogenated hydrocyquinolone unknown mechanism of e histolytica

311
Q

Pharmacokinetics lodoquinol

A

90% retained in the intestines and excreted in feces

312
Q

SE lodoquinol

A

Diarrhea, anorexia, nausea, vomiting, abdominal pain, headache, rash pruritus

313
Q

Paromomycin is a aminoglycosides

314
Q

Treat giardia lamblia

A

Tinidazole first line
Metronidazole maybe
Nitazoxanide

315
Q

Nitrazoxanide MOA

A

Inhibit pyruvate ferredoxin oxidoreductase enzyme essential to anaerobic energy metabolism

Prodrug active metabolite is tizoxanide

316
Q

Pharmacokinetics nitazoxanide

A

Rapidly absorbed, excreted in urine and feces

317
Q

SE nitazoxanide

A

Nausea, anorexia, flatulence, increased appetites, enlarged salivary glands, yellow eyes, dysuria, bright yellow urging

318
Q

Key drugs for g lamblia

A

Nitazoxanide

5-nitroimidazoles-metronidazole, tinidazole

319
Q

Cryptosporidium partum

A

Water day care, immunocompromised severe life threatening diarrhea

4 motile sporophytes

320
Q

Treat cryptosporidium parvum

A

Antidiarrheal-loperamide

Fluid management

Antimicrobial-nitazoxanide, paromomcin

321
Q

Cryptosporidium treatment in HIV

A

Antiretroviral therapy+ nitazoxanide

322
Q

Cryptosporidium therapy not HIV

A

Reduce dose of immunosuppressant and nitazoxanide

323
Q

Main goal of treating cryptosporidium in immunocompromised

A

Restore immune function

324
Q

Key drugs for c parvum

A

Nitazoxanide

Aminoglycosides-paromomycin

325
Q

Nematodes

A

Round worms need to visualize microscopic eggs in feces

Elevate eosinophils

326
Q

Necator americanus and ancylostoma duodenal (hook worms)

A

Penetrate skin between toes
Larva to lungs
To SI where worms populate and release effs into feces

Diarrhea, ab pain, weight loss, anemia, itching at penetration site

327
Q

Ascaris lumbricoides

A 
Consume eggs
Large penetrate intestine and travel to lung
Grow and cough hp
Adult worms in fertilized eggs
Eggs excreted in feces
Eggs hatch in soil and live

Ab cramping. Malnutrition, worm invasion

328
Q

Strongyloides

A

Larva in soil penetrate skin to lung
Mature in SI release eggs that ARE NOT PASSED IN STOOL
Hatched eggs autoinfect excrete larva

329
Q

Clinical signs and diagnosis strongyloides

A

Vomit, ab bloating, diarrhea, anemia, weight loss,

330
Q

Treat stronglyoides

A

Prednisone and asthma

331
Q

Diagnose strongyloides

A

Larva in feces, enterohepatic

332
Q

Trichuris trichuria whip worm

A

Ingest in food with eggs they hatch in SI mature thousands of eggs per day for a year

No large no lung, no transit, no eosinophilia, no auto infection

Diagnose eggs in feces

333
Q

Enterobius vermicularis pin worm

A

Eggs ingested mature, migrate o perianal area to lay eggs

Severe perianal itching scotch tape test

334
Q

Treat nematode

A 
Albendazole
Mebendazole
Ivermectin
Ivermectin
Thiabendazole
Pyrantel pamoate
335
Q

MOA albendazole and mebendazole which are broad spectrum oral anti helmithic agents

A

Inhibit microtubules synthesis, paralyzes worms,

Prodrug , active metabolite produced after first pass effect

336
Q

Thiabendazole MOA

A

Same as albendazole and mebendazole

337
Q

Pharmacokinetics thiabendazole

A

Rapidly absorbed after ingestion, largely excreted in uring, can be absorbed from the skin

338
Q

Adverse effects thiabendazole

A

Toxic, dizzy, anorexia, vomit,

Irreversible liver fail and SJS

339
Q

Ivermectin MOA

A

Intensifies GABA mediated transmission of signals in peripheral nerves of the nematode

340
Q

What should ivermectin not be given with

A

Other drugs that enhance GABA (barbiturates, benzodiazepines, valproic acid)

341
Q

Pyrantel pamoate MOA

A

Neuromuscular blocking agent causes release of acetylcholine and inhibito cholinesterase resulting in paralysis and expulsion fo the nematode

342
Q

N americanus and A duodenal

A

Albendazole

343
Q

A lumbricoides

A

Albendazole

Mebendazole

344
Q

S stercoralis

A

Ivermectin

345
Q

T trichuria

A

Mebendazole

346
Q

E vermicularis

A

Albendazole
Mebendazole
Pyrantel pamoate

347
Q

Schistosoma

A

Eggs in fresh water hatch larva infect and mature in snail
Get into skin
Mature in intrahepatic portion of portal venous migrate to veins surrounding intestine of bladder to lay effs

Dermatitis, katakana fever, chronic fibrosis

348
Q

Drug for schistomiasis

A

Praziquantel

349
Q

Praziquantel MOA

A

Increase permeability of nematode and cestodes cell membranes to calcium resulting in paralysis , dislodgement and death

350
Q

Adverse effects praziquantel

A

Headache, dizzy, drowsylow grade fever, itchy, rash

351
Q

Tania solium (pork) and Tania saginata (beef)

A

Weight loss malnutrition

Pigs and cows ingest from field contaminated with human feces larva disseminate through he intestine into the muscle of the animal
Human ingest undercooked meat, tape worm matures in intestine

Proglottids in stool or eggs

352
Q

Diphyllobothrium datum

A

Acquired by intestine fresh water larva

Proglttids and eggs in feces

353
Q

Echinococcus granulosis

A

Extra intestinal tapeworm infection humans ingest eggs from dog feces

Eggs hatch in intestine and larva form hydration cysts

354
Q

Treat cestodes

A

Praziquantel

Niclosamide

Albendazole

355
Q

Nicolsamide

A

Alternative drug for treatment of most tape worms

Not effective against hydration cysts

356
Q

MOA niclosamide

A

Inhibitoin of oxidative phosphorylation or stimulation of ATPase

357
Q

INTERFERON A

A

Host cytokines that exert antiviral , immunomodulatory and antiprolifeative actions

Interferon a-2B
PEGylated interferon a-2B

PEGylated interferon a-2a

Treat with well compensated liver disease, not wanting long term treatment, pregnant within next 2-3 years

358
Q

Pros of interferons in chronic HBV infection

A 
Shorter course
Efficacious
Decreased HBV DNA
Decreased HBeAg
Resistance rare
359
Q

Cons interferons chronic HBV infection

A

Parenteral administation
Expensive
Side effects

DANGEROUS IN DECOMPENSATED CIRRHOSIS

360
Q

Pharmacokinetics interferon a-2B vs PEGylated interferon a-2a/2B

A
  1. Short

2. Long

361
Q

MOA endogenous interferons

A

Infected cells release interferons to protect nearby healthy cells by allowing them to mount a defense

Signal nearby macrophages and NK cells to clear infected cell

Interferons act in an autocrine fashion to stimulate lysosomes lysis which leads to the lysis of the infected cell

362
Q

Interferon a MOA

A

Bind to type 1 interferon receptor and activates JAK1 and TYK2 which phosphorylation the intracellular domains of the type 1 interferon receptos

Phosphorylation of type 1 interferon leads to recruitment , phosphorylation and dimerization of signal transducer and activator of transcription 1 and 2 STAT1 and 2
Which translocate to the nucleus and activate the transcription of interon stimulated genes

363
Q

Antiviral mechanism of ISG

A

Inhibit multiple steps of viral replication

Viral protein synthesis and translocation
Zap, IFIT family, OAS RNAseL path PKR

364
Q

Immunomodulatory molecular mechanisms of interferon a

A

Inhibits HBV replciation and depends on immune clearance of HBV infected cells increased inflammation and fibrosis

365
Q

PEGylated interferon a treatment induced an increase in ALT during seroconversion

A

Hepatitis flare can be a sign that seroconversion is in progress
ALT up!

366
Q

Contraindication PEGylated interferon a

A

Decompensated cirrhosis

367
Q

Adverse effects interferon a and PEGylated interferon a

A

Flu like
Headache, fever, chills, myalgia, malaise, fatigue and mental depression

Bone marrow suppression, neurotoxicity

368
Q

Nucleosides for HBV treatment

A

HBV DNA reverse transcriptase DNA polymerase inhibitors

Oral agents that are used to suppress HBV

Better tolerated than interferon a

Higher response rate than interferon a

Can be used in decompensated cirrhosis

369
Q

NRTI

A

Nucleotide reverse treansciptase inhibitors stops synthesis

Require conversion into their corresponding nucleotide triphosphates
-cellular kinases convert both synthetic and endogenous nucleosides into nucleotides, the synthetic nucleotide triphosphate is the active antiviral aren’t

370
Q

NRTA

A

Terminated HBV replication via viral DNA polymerase reverse transcriptase

371
Q

HBV resistance to nucleosides/nucleotides

A

Impaired purine/pyramiding kinase activity

  • patient resistant to nucleoside analogs (lamivudine, entecavir, telbivudine)
  • patient responsive to nucleoside analogs (tenofovir)
  • resistance due to slow or low conversion of nucleosides into a nucleotide monophosphate form

Mutation DNA polymerase

372
Q

Why get HBV viral breakthrough

A

Resistance or non compliance

373
Q

Nucleosides for treat HBV

A

Lamivudine
Telbivudine
Entecavir

374
Q

Nucleotides for HBV infection

A

Tenofovir

Adefovir

375
Q

Factors affecting the selection of antiviral nucleosides/nucleotides

A

Resistance
Efficacy
Usefulness with HIV co infection
Pregnancy

376
Q

Tenofovir

A

First line treatment for wild type HBV
Used in patients with lamivudine, telbivudine or entecavir resistance

Resistance rare
Nephrotoxicity-proximal renal tubule

377
Q

Entecavir-guanosine nucleoside analog

A

First line HBC

Potent antiviral and low resistance
-resistance in patients resistant to lamivudine

Better choice than adefovir or tenofovir in patients with renal insuffiency

Well tolerated

378
Q

Long term efficacy of lamivudine limited by frequent emergence of drug resistance

A

YMDD to YVDD mutant in catalytic domain of HBV polymerase

Leads to subsequent virological breakthrough

379
Q

Lamivudine resistance increases over __

380
Q

Important to remember about HBV therapies

A

Therapies fail to eradicate the virus

Relapse of hepatitis induced by HBV is always possible

381
Q

Key drugs for HBV

A

Interferons-interferon a-2b, PEGylated interferon a-2B, PEGylated interferon a-2a

Nucleosides-lamivudine, telbivudine, entecavir

Nucleotides-tenofovir, adefovir

382
Q

Can HCV be cured

A

Yup its an RNA virus not incorporated into DNA

PEGylated interferon a plus ribavirin
24-48 week wegimen
Less than 50% cure rate

383
Q

Ribavirin

A

Interferes with the synthesis of GTP
Inhibits capping of viral messenger RNA
Inhibits the viral RNA dependent polymerase of certain viruses

Potentiation the action of PEGylated interferon a-2a and a-2B
-upregulated interferon stimulated genes (ISGs)

Broad spectrum r

384
Q

Contraindications ribavirin

A

Anemia

Pregnant

385
Q

Protease inhibitors for HCV

A

Simeprevir
Telaprevir
Boceprevic

386
Q

MOA protease inhibitors

A

Block NS3 catalytic site or the NS3/NS4 interaction

387
Q

Simeprevir

A

Second generation

Administered in combination with PEGylated interferon a-2a or a-2B

Or sofosbuvir and ribavirin for chronic genotype 1 infection

388
Q

Telaprevir and boceprevir

A

First generation protease inhibitors
Administered in combination with PEGYlated interferons a-2a or a-2B and ribavirin

Simeprevir better tolerated

389
Q

NS5B

A

RNA dependent RNA polymerase needed for HCV

390
Q

Sofosbuvir

A

Nucleotide analog

First NS5B inhibitor available in US
Disrupts all genotypes of HCV

391
Q

NS5A proteins

A

Important for viral replciation and assembly of HCV

Exact MOA unknown

392
Q

Ledipasvir, elbasvir, velpatasvir

A

Inhibit NS5a
Effective across all genotypes
Low barrier to resistsance, not given as a monotherapy

Ledipasvir traditionally given in combination with ribavirin and PEGylated interferon a-2a or a-2B
-significant reduction HCV RNA

393
Q

Genotype 1 HCV no ribavirin

A

Ledipasvir+sofosbuvir

394
Q

Genotype 1,2,3 HCV no ribavirin

A

Velpatasvir+sofosbuvir

Elbasvir+grazoprevir

395
Q

How manage coinfection HBV HCV

A

Treat predominant circus

PEGylated interferon a-2a or a-2B and ribavirin for 48 weeks

396
Q

Interferons for HCV

A

PEGylated interferon a-2B

PEGylated interferon a-2a

397
Q

Nucleoside HCV

398
Q

Nucleotide HCV

A

Sofosbuvir

399
Q

Protease inhibtiors for HCV

A

Simeprevire
Telaprevir
Boceprevir
Grazoprevir

400
Q

NA5A inhibitors for HCV

A

Ledipasvir
Elbasvir
Velpatasvir

401
Q

Enterotoxin
Enteroadherent
Cytotoxin

A

Watery diarrhea

Cramp fever

High fever abdominal pain

402
Q

Day care

A

Shigella, giardia, cryptosporidium, rotavirus

403
Q

Infectious diarrhea treatment

A

Usually self limited ,

Do work up if blood, high fever, pain, immunocomp

404
Q

What order for work up diarrhea

A

CBC, electrolytes, BUN Cr, stool cultures

405
Q

hemolytic uremic syndrome

A

Anemia, thrombocytopenia, renal fail

406
Q

Salmonella typhimurium

A

Gram neg rod

No antibiotics

Septic arthritis osteomyelitis

407
Q

Vaccination

A

Hep, roar, shigella, salmonella typhi, CHOLERA

408
Q

Vibrio parahemolyticus (cytotoxin) vs vulnificus

A

Bloody diarrhea seafood
Gram neg bacillus
Seafood

Bulbous skin leasion coasatal salt water gram negative bacillus
Cirrhosis hemochromatosis

409
Q

Aeromonas hydrophilia

A

Gram negative, nonspore forming, rod shaped facultatively anaerobic bacteria, motile with flagellum

Fresh water

Necrotizing fasciitis, flesh eating bacteria

Cholera like or blood stool

Scuba divers with enteritis

410
Q

Traveler diarrhea most common

A

Enterotoxigenic from ETEC

Clinical diagnosis

411
Q

EHEC and fever (cytotoxin)

412
Q

Shiva toxin

413
Q

Yersinia enterocolitica

A 
Gram negative coccobacilli
Iron metabolism (hemochromatosis)

Bloody
Appendicitis, crohns

Clinically indistinguishable from salmonella or shigella

Dairy

414
Q

Listeria monocytogenes

A

Gram positive rod
Water diarrhea
Dairy

Need select media to grow

415
Q

What antibiotics cause c diff

A

Clindamycin, cephalosporin, fluoroquinolones

PO or IV metronidazole PO vancomycin

416
Q

Cmv

A

Double stranded linear DNA immunosuppressed

Endoscopy ulcerations

417
Q

Giardia lamblia

A

Watery
Steatorrhea
Flatulence

418
Q

Cryptosporidium

A

Watery diarrhea
Direct microscopy acid fast

Self limited imuunook
Continuous and biliary disease-acalculous cholecystitis if not RUQ pain, fever

419
Q

Cyclospora cayentanesis

A

Produce travel subtropical and tropical
Watery
21 days in immunocompetent
Indefinetely in immunosuppressed

Cl resistant

420
Q

Cystosporia belli

A

Tropical subtropical

Malabsorption weight loss 
Acid fast
Non bloody 
Eosinophilia
Need repeat stool exam
421
Q

Schistomiasis

A

Bloody fresh water snails varices

422
Q

Enteric fever

A

Samonalle yersinia

423
Q

Reactive arthritis

A

Salmonella, camp, shigella, yersinia

Pharmacology (52 decks)

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