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GI- Week 5 > Fitzaekerly: Laxatives, Anti-diarrheals and Treatments for IBS > Flashcards

Fitzaekerly: Laxatives, Anti-diarrheals and Treatments for IBS Flashcards

1
Q

What regulates GI motility independent of extrinsic SNS and PNS input?

A

Enteric nervous system

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2
Q

What NTs are important regulators of motility and water absorption?

A

ACh
5HT
DA
Enkephalins

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3
Q

What drug enhances or disrupts the afferent limb?

A

5HT

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4
Q

What drugs effect interneuron function?

A

DA

Enkephalins

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5
Q

What drugs affect effector neurons innervating circular muscle?

A

ACh

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6
Q

What drugs affect muscle cells?

A

motilin

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7
Q

How do ECL cells act as sensory receptors?

A

Release 5HT> stimulates afferent neurons

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8
Q

What are afferent neurons NTs?

A

cGRP
glutamate
substance P

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9
Q

What are the three SSRIs?

A

Fluoxetine
Paroxetine
Sertraliine

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10
Q

SSRI TU?

A

antidepressants (depbression comorbid w/ IBS)

*most beneficial in constipation predominant IBS

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11
Q

How do SSRIs increase peristalsis? (MOA)

A

decreased reuptake of 5HT into EC cells>
increased 5HT at synapse>
increased afferent activity>
increased peristalsis

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12
Q

What is a SE of SSRIs?

A

diarrhea

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13
Q

What are 4 bulk laxatives?

A

Dietary fiber
Methylcellulose
Polycarbophil
Psyllium

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14
Q

What is the TU for bulk laxatives?

A

Stool stabilizers

If you have diarrhea> decrease BM, more solid stool and decrease pain

If you have constipation> increase BM, losen stool, decrease pain

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15
Q

What is the MOA for bulk laxatives?

A 
bulk attracts water to lumen and increases stool mass>
increased distension of lumen>
increased release of 5HT from EC cells>
increased afferent activity>
increased peristalsis
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16
Q

What two factors limit the use of bulk laxatives?

A
  1. neurons that generate the peristaltic reflex must be functional (afferent, interneurons, motorneurons)
  2. cause of constipation must be known
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17
Q

What are the SE of bulk laxatives?

A

allergies
flatulence
increased obstruction

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18
Q

What are contact cathartics?

A

anthraquinone derivatives
Bisacodyl
Castor oil

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19
Q

Where do bisacodyl and anthraquinones act?

A

ONLY on the LARGE INTESTINE

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20
Q

Where does castor oil act?

A

ENTIRE GI TRACT (sml and larg intestine) as a prokinetic more than a laxative

It’s a prodrug that must be converted to ricinoleic acid to be in its active form

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21
Q

How does the timing and potency of bisacodyl and anthraquinones differ from castor oil?

A

Bisacodyl and anthraquinones: longer latency, decreased potency

Castor oil: shorter latency, potent effects (more SE)

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22
Q

How long does it take bisacodyl to be active?

A

6 hours to be converted to active

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23
Q

What is the MOA of contact cathartics?

A

increase irritation>
Increased EC activity>
same as bulk laxatives

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24
Q

Wha tis hte SE of contact cathartics?

A

dependency (need drug to have BM)
destroy myenteric plexus w/ chronic use
pigmenation of mucosa

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25
Q

What are SE of castor oil?

A

UTERINE CONTRSCTION

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26
Q

What is a 5HT3 receptor antagonist?

A

Alosetron

considered an anti-emetic but doesn’t work as an anti-emetic

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27
Q

What is alosetron used for?

A

diarrhea (causes constipation)

IBS (when everything else has failed)

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28
Q

What is the MOA of alosetron?

A

blocks 5HT receptor>
decreases afferent stimulation>
decreased peristalsis

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29
Q

What are SE of Alosetron?

A

Constipation
hospitalization
IsCHEMIC COLITIS> can be fatal

*compassionate use program b/c of SE

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30
Q

What exagerates the SE of Alosteron?

A

inhibitors of CYP1A2

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31
Q

What are 5HT4 receptor agonists?

A

Cisapride (also a 5HT3 antagonist)

Tegaserod (more selective)

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32
Q

What is the TU for Tegaserod?

A

IBS**

constipation

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33
Q

What is hte TU for cisapride?

A

diabetic gastroporesis

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34
Q

What is the MOA of cisapride and tegaserod?

A

stimulation of 5HT4 receptors on PRE-SYNAPTIC CELL BODIES>
increase release of NT (subst P/glutamate) from aff neuron>
increased peristalsis

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35
Q

What are SE of cisapride and tegaserod?

A

cardiovascular toxicity (arrythmias–LONG QT)

*esp w/ pre-existing condtions or co-administration of CYP3A4 inhibitors

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36
Q

What are two opiates?

A

loperamide

diphenoxylate

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37
Q

What distinguishes diphenoxylate from loperamide?

A

DI has MORE CNS penetration

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38
Q

Why is loperamide OTC?

A

little potential for addiction, doesn’t cross BBB

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39
Q

Why is DI typically combined w/ ATROPINE?

A

blocks muscarine receptors on sm muscle cells>
decreased contraction>
synergy

ALSO atropine has bad SE so pts are less liekly to use drug

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40
Q

How does the chronic intake of morphine and codeine cause constipation?

A

Same mechanism as DI

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41
Q

What are the most effective antidiarrheals?

A

loperamide nad DI

42
Q

What is hte MOA of loperamide and DI?

A

decrease motility and decrease secretion

43
Q

What are hte SE of loperamide and DI?

A

TOXIC MEGACLOLON (in pt w/ ulcerative colitis)

EUPHORIA> physical dependence (w/ hi doses of DI)

44
Q

What are u receptor antagonists?

A

Alvimopam

Methylnaloxone

45
Q

Who are u receptor antagonists given to? Why?

A

Pts who are on opiates for pain control to prevent constipation caused by opiate therapy.

The goal is for the central action to work but peripheral action of opiates in GI to be blocked

46
Q

When are alvimopam given?

A

Same time as opiates–> selective antagonists that DONT cross the BBB

47
Q

What is the TU of alvimopam?

A

short term, hospitalized pts (d/t SE)

48
Q

What is the TU of methylnaloxone?

A

long term, palliative care

49
Q

What drug increases your risk of MI?

A

alvimopam

50
Q

Where do enkephalins act?

A

interneurons

51
Q

Where does DA act?

A

interneurons

52
Q

What are D2 receptor antagonists?

A

Doperidone (compassionate use)

Metoclopramide

53
Q

What is the MOA of D2 receptor antagonists?

A

inhibit DNA inhibition> increased ACh in gut>

increased motility in entire gut

54
Q

What is the TU of D2 receptor antagonists?

A

impaired GI motility– vagotomy or gastroporesis)

Metoclopramide crosses BBB so tx CONSTANT HICCUPS

55
Q

What are SE of D2 receptor antagonists?

A

dystonia
parkinsonism
tardive dyskinesia (irreversible–occurs in high dose pt/chronic use)

Increased prolactin release> impotance, menstural disorders, galactorrhea

56
Q

Where does ACh act?

A

motor neurons

57
Q

Post ganglionic parasympathetic fibers that are innervating muscarinic receptors on circular sm muscle secrete?

A

ACh

58
Q

When is ACh used to treat diarrhea or constipation?

A

NOT usually used…exceptions:

  1. TCAs–to counter decreased motility
  2. Atropine included w/ diphenoxylate to decrease peristalsis
59
Q

How does erythromycin affect motilin?

A

stimulates motilin receptors on sm muscle>

activation of MCC

60
Q

What drugs primarily affect water balance?

A
  1. chloride secretion
  2. osmotic cathartics
  3. Bile acid binding resins
61
Q

What is Lubiprostone?

A

CIC-2 activator that is poorly absorbed so it has almost no systemic effects

62
Q

What is lubiprostone used for?

A

CONSTIPATION (IBS)

63
Q

What is the MOA of lubiprostone?

A

Activates CIC-2 (Cl channel in lumen of mucosal crypt cells)> increase Cl secretion

64
Q

What drug can increase the risk of fetal loss?

A

Lubiprostone

65
Q

What is Linaclotide?

A

CG-C activator

Verry little systaemic absorption

66
Q

What is the TU of linaclotide?

A

same as lubiprostone

67
Q

What is the MOA of linaclotide?

A 
activates guanylyl cyclase C>
generates cGMP>
activates CFTR>
increased Cl secretion>
increased water in lumen
68
Q

What drug can increase maternal death?

A

linaclotide

69
Q

What drug is a CFTR inhibitor?

A

Crofelemer

70
Q

What is the TU of Crofelemer?

A

anti-HIV drug Tx (PI and NRTIs)

71
Q

What is the MOA of crofelemer?

A

voltage independent inhibition of CFTR>
decreased Cl secretion>
decreased Na/water excretion>
firmer stool

72
Q

What drug is a somatostatin analogue?

A

ocreotide (has longer t 1/2 than somatostatin)

73
Q

What is the off label use for ocreotide?

A

severe diarrhea d/t dumping syndrome, shortbowel sydnrome, vagotomy, AIDS

74
Q

What is the MOA of ocreotide?

A 
decreased fluid secretion
decreased motility (esp at HIGH doses)
75
Q

What drug can cause fat soluble vit def, gallstones, and hypo or hyperglycemia?

A

Ocreotide

76
Q

What drug is used to prevent and treat travelers diarrhea?

A

bismuth subsalicylate

77
Q

What is te MOA of bismuth subsalicylate?

A

Decreases PG and CL secretion in LI
Antimicrobial
binds enterotoxins

78
Q

What are SE of bismuth subsalicylate?

A

blackens stools and tognue

79
Q

What are osmotic cathartics?

A

Lactulose
Mg HYdroxide (WB)
Na PHosphate (WB)
Polyethylene Glycol Electrolyte Solution

80
Q

When are osmotic cathartics used?

A

constipation (esp when enteric nervous system has been disrupted)

81
Q

What is the MOA of osmotic cathartics?

A

not absorbed>

increase water in lumen by osmosis

82
Q

What is a SE of ALL osmostic laxatives?

A

intravascular volume depletion and electrolyte imbalance

83
Q

What drugs can cause hypokalemia that can lead to arrythmias?

A

Osmotic Cathartics

84
Q

What are bile acid binding resins?

A

cholestyramine and colestipol

85
Q

What are cholestyramine and colestipol used for?

A 
decreased reabsorption of bile salts>
secretory diarrhea (MCC Chrons/resection of terminal ileum)
86
Q

What is hte MOA of cholestyramine and colestipol?

A

bind uabsorbed bile acids>

decrease water secretion

87
Q

What drugs can impair absorption of other drugs and fat soluble vitamins?

A

Cholestyramine and Colestipol

88
Q

What can be used as a stool softener?

A

docusate and mineral oil

89
Q

What is the MOA of docusate?

A

surfactant

90
Q

What is hte MOA of MO?

A

lubricates

91
Q

What is a SE of Mineral Oil?

A

lipid pneumonitis if aspirated

decreased absorption of fat soluble vits w/ long term use

92
Q

What are prokinetics and what are they used for?

A

dramatically increase motility throughout enter GI tract (not just colon)

Used for impaired gastric emptying and constipation (vagotomy gastroparesis)

93
Q

What are three types of prokinetics?

A
  1. D2 receptor Antag: Metochlopromaide
  2. Erythromycin
  3. 5HT4 Agonists: Cisapride
94
Q

When are anti-diarrheals NOT recommended?

A

bloody diarrhea
high fever
systemic toxicity

95
Q

What are 5 types of anti-diarrheals?

A
  1. opiates: loperamide/DI
  2. Bile acid binding resins: bile salt malabsorption
  3. octreotide: dumping syndrome
  4. Bismuth: travelers diarrhea
  5. crefelemer: AIDS diarrhea
96
Q

You should only use laxatives/cathartics after….

A

you’ve made dietary modificaitons, increased fluid intake and physical activity

97
Q

What are mild effect, long/day laxatives that soften feces and take 1-3 days to work?

A

Cl channel activators
Stool softeners
bulk forming laxatives

98
Q

What are intermediate effect laxatives that make soft semi-solid stool after 6-8 hrs?

A

contact cathartics

99
Q

What are strong effect cathartics that have a short latency and cause a watery evacuation in 1-3 hours?

A

osmotic cathartics

castor oil

100
Q

What do you use to tx constipation predominant IBS?

A

laxatives and cathartics

Tegaserod (restricted availability)

101
Q

What do you use to tx diarrhea predominant IBS?

A 
opiates
Alossetron (restricted availability)

GI- Week 5 (9 decks)

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