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Fall 2018/P3 Year' > Therapeutics Exam 3 (Foster/Scott) > Flashcards

Therapeutics Exam 3 (Foster/Scott) Flashcards

1
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

mucosal inflammation confined to rectum to colon

A

UC

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2
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

transmural inflammation

A

CD (deeper = transmural)

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3
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

inflammation of GI tract (can affect any part from mouth to anus)

A

CD

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4
Q

6 Possible Causes of IBD

A 
immunologic
microbial
genetic 
Psychological
environmental
Drug related causes
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5
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

is more superficial than the other one

A

UC

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6
Q

What are some local complications of UC

A

hemorrhoids
anal fissures
perirectal abscesses

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7
Q

what is a systemic complication of UC

A

toxic megacolon!

systemic toxicity — could be fatal – fever/tachycardia/elevated WBCs/abdominal distension

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8
Q

UC leads to a decrease or increase in colorectal cancer risk?

A

increase AF!

colonoscopies + biopsies should be done q 1 - 2 years…

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9
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

will have a cobblestone appearance

A

CD

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10
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

is often discontinuous (normal bowel parts separating disease bowel)

A

CD

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11
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

which one has bleeding being more common?

A

UC

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12
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

which one has a greater risk of colorectal cancer/carcinoma

A

UC

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13
Q

Complications of CD?

A

small bowel stricture/obstruction
fistula common
nutritional deficiencies

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14
Q

Extraintestinal Manifestations of IBD

A 
Hepatobiliary
Ocular
Bone/joint (ARTHRITIS and Osteoporosis)
Hematologic
Coagulation (INCREASED RISK FOR VTE)
Dermatologic and Mucocutaneous
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15
Q

Extraintestinal Manifestations of IBD
Pts may experience arthritis—
it is asymmetrical or symmetrical

A

asymmetrical

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16
Q

Extraintestinal Manifestations of IBD
Arthritis seen a lot during _______
and is hard to treat why?

A

seen during FLARES (control disease = control arthritis)

hard to treat - because we can’t just give NSAIDs!

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17
Q

Extraintestinal Manifestations of IBD

Patients are at an increased risk of ______ – higher risk during flares - CONSIDER PROHPYLAXIS for this!!

A

risk VTE —- ahhhh

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18
Q

Clinical Presentation of UC and its disease extent/location:

if it is distal – that means the disease is where?

A

distal = left sided

= distal to splenic flexure

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19
Q

Clinical Presentation of UC and its disease extent/location:

if it is extensive – that means the disease is where?

A

extending proximal to the splenic flexure

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20
Q

Clinical Presentation of UC and its disease extent/location:

if it is proctitis – that means the disease is where?

A

involving the rectal area

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21
Q

Clinical Presentation of UC and its disease extent/location:

if it is proctosigmoiditis – that means the disease is where?

A

involves rectum and sigmoid colon

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22
Q

Clinical Presentation of UC and its disease extent/location:

if it is pancolitis– that means the disease is where?

A

majority of colon is involved

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23
Q

Disease Classification of UC:

what are the 4 categories of severity?

A

mild
moderate
severe
fulminant

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24
Q

Disease Classification of UC:
Mild, Moderate, Severe, or Fulminant?
< 4 stools / day

A

mild

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25
Q

Disease Classification of UC:
Mild, Moderate, Severe, or Fulminant?
> 4 stools/day

A

moderate

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26
Q

Disease Classification of UC:
Mild, Moderate, Severe, or Fulminant?
> 6 stools/day

A

severe

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27
Q

Disease Classification of UC:
Mild, Moderate, Severe, or Fulminant?
> 10 stools/day

A

fulminant

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28
Q

Disease Classification of UC:
Mild, Moderate, Severe, or Fulminant?

no systemic disturbance; normal ESR; normal fecal calprotectin and lactoferrin

A

mild (with < 4 stools +/- blood)

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29
Q

Disease Classification of UC:
Mild, Moderate, Severe, or Fulminant?

minimal systemic disturbance

A

moderate (also > 4 stools/day)

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30
Q

Disease Classification of UC:
Mild, Moderate, Severe, or Fulminant?

evidence of systemic disturbance (fever, tachycardia, anemia, or ESR > 30 mm/h)

A

Severe (> 6 stools/day)

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31
Q

Disease Classification of UC:
Mild, Moderate, Severe, or Fulminant?

continuous bleeding with stools, toxicity - severe systemic disturbances; abdominal tenderness; need for transfusion; colonic dilation

A

fulminant (> 10 stools/day)

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32
Q

Lab Tests to look at for CD?

A

Hgb/Hct
CRP, ESR, WBCs
+ anti-saccharamycses cervisiae antibodies!!!! (diff from UC!!!0
fecal calprotectin and lactoferrin

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33
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

will have skip lesions

A

Crohns

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34
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

cigarette smoking is actually protective

A

UC

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35
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

fistulas and strictures are uncommon

A

UC

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36
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

cigarette smoking is a risk factor

A

CD

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37
Q

IBD Treatment:

what is the best diet to be beneficial?

A

none to be known!!!

people have own specific trigger foods

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38
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

Surgery/colectomy seen to be used more

A

UC

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39
Q

T or F: There are only a couple agents to cure IBD

A

false! there are NONE!

No agents are curative!!

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40
Q

Pharm options for IBD:

5 main classes?

A 
ASAs
Corticosteroids
Immunomodulators/immunosuppresives 
Biologics
Antimicrobials
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41
Q

what drugs are ASA agents for tx IBD

A

sulfasalazine

mesalamine

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42
Q

what is 5-ASA

A

mesalamine

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43
Q

what is the active component in sulfasalazine

and what is the inactive part that causes ADE’s

A

active: 5-ASA

inactive + ADEs = sulfapyridine

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44
Q

UC (Ulcerative colitis) or CD (Crohns Disease):

which one has (+) perinuclear antineutrophil cytoplasmic antibodies

A

UC

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45
Q

what drugs are ASAs for IBD therapy

A

sulfasalazine

mesalamine

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46
Q

what drugs are immunomodulators for IBD therapy

A

azathioprine
mercaptopurine
cyclosporine
methotrexate

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47
Q

Sulfasalazine MOA:

_____ by colonic bacteria to release _______ and _____

A

cleaved; release sulfapyridine; 5-ASA

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48
Q

You can administer mesalamine alone - but why do we not?

A

rapidly and completely absorbed in small intestine but NOT colon (booooo)

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49
Q

Mesalamine topical is a good option:
use enemas for _______
use suppository for ______
(use them for when the disease is where)

A

enemas - when LEFT sided disease

suppositories: proctitis

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50
Q

Mesalamine:

which one is typically more effective - topical or oral?

A

topical!

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51
Q

A lot of oral mesalamine drugs are either ____ or ____ related

A

pH or ER/DR

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52
Q

what are the oral mesalamine options

A 
Apriso
Lialda
Pentasa
Asacol HD/Delzicol
Osalazine
Balasalazide

(“BOA PAL”)

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53
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
where does Apriso work in?

A

colon

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54
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
where does Lialda work in?

A

terminal ileum

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55
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
where does Pentasa work in?

A

duodenum, ileum

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56
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
where does Asacol HD/Delzicol work in?

A

terminal ileum

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57
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
where does Osalazine work in?

A

colon

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58
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
where does Balsalazide work in?

A

colon

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59
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
which ones work in the colon?

A

Apriso
Osalazine
Balsalazide

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60
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
which ones work in the terminal ileum?

A

Lialda

Asacol HD/Delzicol

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61
Q

The Oral mesalamine drugs acting in different parts of the GI tract due to pH or ER stuff —
which ones work in the duodenum/ileum

A

Pentasa

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62
Q

Drug Interactions for sulfasalazine vs mesalamine

A

BOTH: since ASA agents - anticoag/antiplatelets/NSAIDs

but mesalamine is affected by acid reducing agents!!

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63
Q

Monitor CBCs and LFTs in sulfasalazine why?

A

bc pneumoitis/lymphma/anemia/thrombocytopenia risk

also hepatoxicity

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64
Q

Sulfasalazine can lead to a ______ reaction if allergy

A

hypersensitivity/rash

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65
Q

Mesalamine derivs:

which one commonly causes diarrhea

A

Olsalazine

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66
Q

Budesonide:
Given PO for up to ______
ok to give because of ______ = less systemic exposure

A

8 - 16 weeks!

first pass metab

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67
Q

Budesonide:

drug interactions?

A

CYP3A4 inhibitors – since heavy first pass!!!

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68
Q

AZA/6-MP:

which one is the prodrug of the other

A

AZA = prodrug of 6-MP

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69
Q

AZA/6-MP:

ADEs?

A 
(remember it is chemo!)
Bone marrow suppression 
N/V/D
Stomatitis
pancreatitis
hepatoxicity
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70
Q

what monitoring to do for AZA/6-MP:

A

TPMT!!!!! (homozygous mutation – hell no to these drugs)
CBC - bc bone marrow
LFTs - bc hepatotoxicity

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71
Q

Cyclosporine:good for (induction or maintenance) of remission

A

induction!!

NOT for long term use!!/just bridge therapy

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72
Q

Cyclosporine ADEs?

A

metabolic - HTN, hyperlipidemia, hyperglycemia
nephro and neurotoxicity
gingival hyperplasia/hirsutism

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73
Q

Cyclosporine : good for _____
MTX: good for ____
(UC or CD)

A

Cyclo: UC
MTX: CD

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74
Q

MOA of the Biologic:

Infliximab

A

anti TNF-a antibody

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75
Q

MOA of the Biologic:

adalimumab

A

anti TNF-a antibody

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76
Q

MOA of the Biologic:

golimumab

A

anti TNF-a antibody

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77
Q

MOA of the Biologic:

certolizumab

A

anti TNF-a antibody

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78
Q

MOA of the Biologic:

Natalizumab

A

anti integrins/prevent leukocyte adhesion

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79
Q

MOA of the Biologic:

Ustekinumab

A

IL12/IL23 antagonist

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80
Q

MOA of the Biologic:

Tofacitinib

A

janus kinase inhibitor

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81
Q

Indicated for UC or CD or both:

Infliximab

A

CD/UC

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82
Q

Indicated for UC or CD or both:

adulimumab

A

CD/UC

mod - severe; steroid dependent or fistulizing disease

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83
Q

Indicated for UC or CD or both:

Golimumab

A

UC

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84
Q

Indicated for UC or CD or both:

Certolizumab

A

CD

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85
Q

Indicated for UC or CD or both:

Natalizumab

A

CD

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86
Q

Indicated for UC or CD or both:

Vedolizumab

A

CD/UC

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87
Q

Indicated for UC or CD or both:

ustekinumab

A

CD

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88
Q

Indicated for UC or CD or both:

tofacitinib

A

UC

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89
Q

Indicated for UC or CD or both:

tofacitinib

A

UC

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90
Q

ADRs of TNF-a inhibitors:

A

increase risk of infections, demyelinating disease, and malignancy (also HSTCL risk)

inj site rxns

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91
Q

For TNF-a inhibitors must check for what things prior to therapy

A

if up to date on vaccines

for tuberculosis and hep B/C

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92
Q

Contraindication with TNF a inhibitors (what other biologic)

A

live vaccines!during tx and 3 mos after

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93
Q

All TNF a inhibitors are given _____ route except infliximab is given ______

A

all given SQ

inflix: is IV!

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94
Q

what is HSTCL

A

hepatosplenic T cell lymphoma

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95
Q

How to prevent ADA’s with Infliximab

A

take immunomodulators too! (Aza)

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96
Q

what are ADAs

A

anti drug antibodies

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97
Q

T or F:

all TNF a inhibitors are for induction and maintenance

A

TRUE!

all anti-TNFs are!!

98
Q

what drug has risk of PML (bc of JC virus that lies dormant)

A

Natalizumab

99
Q

what drug is similar to Natalizumab but does NOT have PML/JC virus issue

A

Vedolizumab

100
Q

all NON TNF a inhibitors are IV except which one

A

Ustekinumab! induction is IV but maintenance is SQ

101
Q

TDM of Biologics and Strategy:

typically check therapeutic levels when?

A

when loss of response to an anti-TNF agent

102
Q

TDM of Biologics and Strategy:

if pt loss of response to an anti-TNF agent AND pt has subtherapeutic level with no/low ADA – do what

A

increase dose or dosing interval! (dose just isnt high enough!)
can add immunomodulator

103
Q

TDM of Biologics and Strategy:

if pt loss of response to an anti-TNF agent AND levels are at therapeutic level – do what

A

switch to vedolizumab with or w/out immunomodulator (drug just wont work in this pt)

104
Q

TDM of Biologics and Strategy:

if pt loss of response to an anti-TNF agent AND pt has subtherapeutic level with high ADA – do what

A

switch within the class (pt has built immunity against this drug)

105
Q

what drugs for UC/CD treatment should NOT be used contaminantly with immunosuppressants

A

Natalizumab (NO Aza/6-MP)

Tofacitinib - NO Aza or biologics with it!!!

106
Q

T or F: Tofacitnib is best as monotherapy

A

true because it should NOT be used with immunosuppressants or biologics!!

107
Q

ADE’s of tofacitnib

A

NEUTROPENIA!!

increased risk of infections/tuberculin test/ avoid if active infection

108
Q

Tofacitinib and Neutropenia - how to deal with it

A

do NOT give drug if ANC < 500

if 500 - 1000 (dose reduce if 10 mg BID or d/c 5 mg BID until ANC > 1000)

109
Q

Antimicrobial options for UC/CD —

A

cipro and metronidazole

110
Q

ADRs of antimicrobials for UC/CD

A

resistance and C.DIFF!!!

111
Q

Antimicrobials are used in (UC or CD) if it is associated with fistulas/abscesses

A

CD!

112
Q

N/V during pregnancy:
Usually worst during what time of the day
and usually limited to what trimester?

A

morning

first

113
Q

N/V during pregnancy:

Non-pharm options

A 
ginger root/gum
Peppermint oil
(Best for mild cases!)

Morning Sickness “magic” = ginger + vitamin B6 +folic acid

114
Q

N/V during pregnancy: Pharm options?

A

Diclegis or Bonjesta

all have Pyridoxine (vit. B6) TID or Doxylamine TID

115
Q

Diclegis or Bonjesta?

is 1 tab BID

A

bonjesta

116
Q

Diclegis or Bonjesta?

is 2 tabs qhs +/- 1 tab in AM and noon

A

diclegis

117
Q

what antiemetic drugs during pregnancy have minimal risk to the fetus and which one is used but has less data to support its safety to fetuses?

A

safe: antihistamines; phenothiazines, metoclopramide

not a lot of data: ondansetron!

118
Q

what are some rx drugs that can be used for N/V during pregnancy?

A 
metoclopramide
ondansetron
meclizine
dimenhydrinate
promethazine
prochlorperazine
119
Q

PONV stands for?

A

post op nausea/vomiting

120
Q

Risk factors for PONV
F ___ M
_____ status
Hx of _____ or _____

A

F > M
non-smoking status (smoking = protective!)
hx of PONV or motion sickness

121
Q

Risk factors for PONV – Anesthetic Risk Factors:
intra-operative use of _____ but less with ______
use of ______
Type of _____

A

use of volatile anesthetics; less with propofol

use of nitrous oxide

122
Q

what surgeries increase peoples risk of PONV

A

laparoscopy
craniotomy
ENT

123
Q

Treating PONV:

N/V is seen ______ surgery so give the agents when?

A

seen AFTER surgery; give agents at the end of the procedure

124
Q

for treating PONV:

use # agent(s) for when propofol is used

A

1

125
Q

for treating PONV:
for treating mod - high risk -
______ are drug of choice

A

5-HT3 antagonisists

126
Q

for treating PONV:
for highest risk
always use # agents
what are possible agents?

A

2 agents!

5-HT3 + metoclopramide or aprepitant

127
Q

for treating PONV:
low risk if # of risk factors
mod - high risk if # of risk factors
high risk if # of risk factors

A

low: 0 -1
mod - high: 2+
high: 3+ or if prior hx of PONV

128
Q

for treating PONV:

aprepitant: give how?

A

40 mg 1 -3 hours prior to induction of anesthesia

129
Q

definition of constipation?

A

decreased frequency PLUS signs/sx > 25% of the time

130
Q

need 2 or more of the symptoms to chronic constipation – what are the symptoms

A 
straining
lumpy/hard stools
sensation of incomplete evacuation
sensation of obstruction/blockage
manual maneuvers to facilitate defecations
<3 defecations per week
131
Q

Peristalsis is mediated predominantly thru _______

A

serotonin transmitter

132
Q

when food/stool distends the gut walls, _____ cells will release _____ (will cause colonic motility)

A

enterochromaffin cells; release 5HT3

133
Q

mouth - anus transit time?

A

20 - 72 hours

134
Q

Acute Constipation:
less than __#__ bowel movements per week
Chronic Constipation:
sxs lasting > ____

A

Acute: 3
chronic: 6 weeks

135
Q

Common Causes of Constipation?

A

Elderly – things are just slower
Dietary (poor fluid intake)
Disease states that slow down GI motility
lack of privacy - long term care facilities
opioids

136
Q

what disease states can slow down GI motility?

A

diabetes
parkinsons
CNS injury/disease
MS

137
Q

Antacid ingredients that wil cause constipation?

A

Aluminim/Calcium

138
Q

______ scale to asses poops

A

Bristol Stool

139
Q

Bristol Stool:
Type 1 - 7
which end means slow transit time and which one means fast transit

A

type 1: slow

7: fast

140
Q

Adding fiber to diet to promote regular bowel habits:
Add fiber ______
____ g of fiber per day

A

SLOWLY

20 - 30 g/day

141
Q

Adding fiber to diet to promote regular bowel habits:

increase fiber over ____ days

A

7 - 10

142
Q

why are prunes awesome for bowel habits:

A

lots of sorbitol (sugar)
12 g of fiber
and has dihydrophenylsatin (natural laxative)

143
Q

pts should defecate when colonic activity is greatest - this is when?

A

first thing in the morning!

within 30 minutes after meals

144
Q

Bulk Laxatives:

advantages and disadvantages

A

advantages: soften stool better than docusate/well tolerated
disadvantages: must have adequate fluid intake!! impact on drug absorption

145
Q

examples of bulk laxatives

A

psyllium
methylcellulose
calcium polycarbophil

146
Q

T or F: stool softeners are great to increase peristalsis

A

hell no—- not effective for creating peristalsis (NOT good for active constipation)

147
Q

examples of a lubricant laxative

A

mineral oil

148
Q

example of surfactant/emollient

A

docusate

149
Q

examples of saline laxatives

A

Milk of magnesia/ Mg Citrate

150
Q

examples of hyperosmotic laxatives/agents

A

sorbitol (karo corn syrup)
lactulose
PEG!!
glycerin

151
Q

advantages of hyperosmotic laxatives/agents

and disadvantages of hyperosmotic laxatives/agents

A

advantages: well tolerated; softens and stimulates BM
great for CHRONIC constipation!!

Disadvantages takes 1-3 days for onset at usual doses &
minor nausea/cramping

152
Q

stimulant laxative choices?

A

senna
bisacodyl
castor oil

153
Q

advantages for stimulant laxatives

A

6 - 12 hours onset
Drug of choice for pts on opioids
works well if pts have motility disorders

154
Q

disadvantages for stimulant laxatives

A

risk of nausea/cramping;

avoid long term continuous use in pts with normal GI motility

155
Q

Lubiprostone MOA

A

Cl- channel activator

156
Q

linaclotide MOA

A

Guanylate cyclase C receptor

157
Q

if treating acute constipation and pt wants relief in 6 - 24 hours - what can they do

A

MOM
std. dose of PEG
bisacodyl or senna tablets

158
Q

if treating acute constipation and pt wants relief in 0.5 - 3 hours - what can they do

A

large doses of PEG

magnesium citrate

159
Q

if treating acute constipation and pt wants relief in 0.5 - 1 hours - what can they do

A

enemas

or suppositories

160
Q

Follow up when? for constipation:
if acute: _____
if chronic constipation: ______

A

acute: 1 -2 DAYS
chronic: 1 -2 WEEKS

161
Q

Chronic Constipation Treatment:

step 1?

A

dietary interventions have been tried

162
Q

Chronic Constipation Treatment:

step 2?

A

bulk forming laxative + adequate fluid intake

163
Q

Chronic Constipation Treatment:

step 3?

A

sorbitol/lactulose/PEG

164
Q

Chronic Constipation Treatment:

step 4?

A

stimulant laxative

165
Q

Chronic Constipation Treatment:

step 5?

A

lubiprostone

linactolide

166
Q

pregnancy pts that are constipated should use what?

A

diet, fiber, and docusate

167
Q

spinal cord injury pts and laxative use?

A

since they have damage to nerves they do not have adequate function for peristalsis — will use routine use of bowel stimulants

168
Q

when a patient is taking an opioid medication – what kind of laxative medication should they avoid?

A

bulk!!! not going to help (will make it worse)

they need stimulant laxatives

169
Q

what is the perk of methylnaltrexone and naloxegol?

A

they are mu opioid receptor antagonist — to be used for opioid induced constipation

170
Q

methylnaltrexone vs naloxegol

which one is SC and which one is PO

A 
SC = methylnaltrexone
naloxegol = PO
171
Q

what disease states are worrisome with bowel prep regimens?

A

heart failure
renal disease
electrolyte abnormalities

172
Q

Classifying Diarrhea:

Acute?

A

< 14 days (usually an infection process caused this)

173
Q

Classifying Diarrhea:

Persistent

A

> 14 days

174
Q

Classifying Diarrhea:

Chronic?

A

> 30 days

175
Q

Classifying Diarrhea:

Chronic Idiopathic

A

> 4 weeks w/out identifiable cause

176
Q

How diarrhea happens:

The _____ intestine water absorptive capacity is exceeded and _____ overloads the colon = diarrhea

A

small intestine

chyme overloads

177
Q

What is chyme?

A

thick semifluid mass of partially digested food and digest secretions formed in stomach/intestine during digestion

178
Q

where does most of the fluid that gets to the small intestine come from?
our diet/intake or GI secretions

A

GI secretions (fluids from stomach, bile, pancreas, salivary glands, and intestines)

179
Q

How diarrhea happens:
________ typically delay passage and mix of intestinal contents which allows for greater absorption

*ppl w/ diarrhea often have fewer of these

A

segmenting contractions

180
Q

How diarrhea happens:

(decrease or increase) in intestinal osmolarity leads to diarrhea

A

increase! (more Cl- in lumen = water and Na+ follow!!)

181
Q

4 pathopys causes of diarrhea

A

secretory
osmotic
exudative
altered intestinal transit

182
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
is a change in active ion transport (either decreased Na+ absorption or increase in Cl- secretion)

A

secretory

183
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
Sxs will NOT be helped if the patients stops eating

A

secretory

184
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
caused when poorly absorbed substances are retained in the intestinal fluids

A

osmotic

185
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
Sxs will be improved if the patient stops eating

A

osmotic

186
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
Seen in lactose intolerance

A

osmotic

187
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
seen with pancreatic tumors/unabsorbed fat/laxatives

A

secretory

188
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
seen with consumption of poorly soluble CHOs (lactulose/sorbitol)

A

osmotic

189
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
is actually a subset of secretory

A

exudative

190
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
characterized by large stool volumes
and
mucus/protein/blood is in the gut — pts will need work up if UC or CD

A

exudative

191
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
decrease time of exposure b/w intestinal epithelium and chyme = irregular absorption/secretion

A

altered intestinal transit

192
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
typically caused by bowel resection or pro-motility meds

A

altered intestinal transit

193
Q

Secretory, osmotic, exudative, or altered intestinal transit diarrhea?
altered motility due to neuropathy in diabetes

A

altered intestinal transit

194
Q

common medications that can cause diarrhea

A 
cholinergic meds
Mg+ containing medications
chemo (irinotecan!!)
Monoclonal ABs
ACEIs
misoprostol
colchicine
sorbitol containing meds
metformin
(Laxatives, motility agents)
195
Q

how to evaluate if a pt is dehydrated

A 
skin turgor test/skin tenting
dry mucous membranes (tongue)
dizziness when standing
orthostatic hypotension
concentrated urine
196
Q

Diarrhea Treatment – Diet management:
More important in ______ diarrhea (need to remove causative agent)
____ diet

A

osmotic

BRAT

197
Q

T or F:

Do not stop feedings in children w/ bacterial diarrhea

A

true!!

198
Q

Pharm Treatment goals of Diarrhea:
(decrease or increase) fluid accum. in the lumen
(decrease or increase) propulsive contractions
(decrease or increase) mixing contractions

A

decrease
decrease
increase

199
Q

Treating Acute Diarrhea:

First check if the have ______

A

fever or systemic symptoms

200
Q

Treating Acute Diarrhea:

If NO fever/systemic symptoms – how to treat?

A

Symptomatic Therapy
fluid/electroylyte replacement
loperamide/diphenoxylate or absorbet
diet

201
Q

Treating Acute Diarrhea:

If they do have fever/systemic symptom- what to check next?

A

check feces for WBC/RBC/and parasites

202
Q

Treating Acute Diarrhea:

If they do have fever/systemic symptom and negative for things when checked feces – do what?

A

symptomatic therapy
fluid/electroylyte replacement
loperamide/diphenoxylate or absorbet
diet

203
Q

Treating Acute Diarrhea:

If they do have fever/systemic symptom and positive for things when checked feces – do what?

A

use appropriate abx and symptomatic therapy

204
Q

Chronic Diarrhea:

T or F: always refer to doctor

A

True!!

205
Q

Possible Causes of Chronic Diarrhea?

A 
intestinal infection
IBD
malabsorption
secretory hormonal tumor
drug induced
motility disturbance
206
Q

How to prevent travelers diarrhea

A

drink bottled water/drinks
wash fresh fruits/veggies
consider pepto 1 - 4 x daily

207
Q

what drugs are antimotility agents used for diarrhea

A 
diphenoxylate (+atropine)
difenoxin (+atropine)
loperamide
paregoric
tincture of opium
208
Q

for diphenoyxlate + atropine - do not exceed ______ /day

A

20 mg

209
Q

for loperamide - do not exceed ______ / day

A

16 mg (8 tabs)

210
Q

for difenoxin + atropine do not exceed ____ /day

A

8 tabs

211
Q 
which anti motility agent is OTC
diphenoxylate (+atropine)
difenoxin (+atropine)
loperamide
paregoric
tincture of opium
A

loperamide

212
Q

which anti motilty agents should not be used in kids < 2 bc of high sensitivity => toxic megacolon

A

diphenyoxylate and difenoxin

213
Q

Antimotility agents:

activate the ____ receptors on smooth muscle of the bowel to reduce ______ and increase _____

A

activate mu opioid receptors; reduce peristalsis; increase segementation

214
Q

what are examples of absorbents for treating diarrhea

A

polycarbophil/fibercon

attapulgite/kaopectate

215
Q

what drugs are antisecreotry agents

A

bismuth subsalicylate (pepto)
enzymes - lactase
probiotics
octrotide

216
Q

Pepto: max dose of?

A

8 doses in 24 hours

217
Q

T or F: IBS has just as much inflammation as IBD does

A

false! (IBS does not have an inflammatory component)
IBS - irritable bowel syndrome
IBD = inflammatory

218
Q

Subtypes of IBS?

A

IBS- C (constipation)
IBS-D (diarrhea)
IBS-M (mixed)
untyped IBS

219
Q

which Subtype of IBS?
Hard/lumpy stools at least 25 % of the time

loose water stools less than 25% of the time

A

IBS-C

220
Q

which Subtype of IBS?
Hard/lumpy stools less than 25 % of the time

loose water stools at least 25% of the time

A

IBS-D

221
Q

which Subtype of IBS?
Hard/lumpy stools at least 25 % of the time

loose water stools at least 25% of the time

A

IBS-M

222
Q

which Subtype of IBS?
Hard/lumpy stools less than 25 % of the time

loose water stools less than 25% of the time

A

untyped

223
Q

4 non pharm options for IBS

A

diet - pts have a food sensitivity/trigger
low FODMAP diet
physical activity
cognitive behavioral therapy

224
Q

what is the low FODMAP diet

A

fermentable, oligosaccharides, disaccharides, monosaccahrides, polyols — aka avoid poorly absorbed carbs

225
Q

pathophys of IBS:

thought to be due to ______ and ______ of intestine

A

somatovisceral and motor dysfunction

226
Q

what drugs are antispasmodics

A

hycosamine

dicyclomine

227
Q

Antispasmodics:
use caution in what pts

and avoid in pts that have what things?

A

use caution in elderly — BEERS

avoid in pts w/ glaucoma, and IBS w/ constipation…

228
Q

TCAs are helpful in what kind of IBS?
and
SSRIs have seen to be helpful in what IBS?

A

TCAs – for IBS-D pts

SSRIs - IBS-C

229
Q

why are antidepressants helpful in IBS

A

reduce visceral sensitivity

230
Q

Tx IBS- C:

what to do for diet?

A

increase fiber/fluid intake
avoid foods that increase sxs
gluten free
Low FODMAP diet

231
Q

what drugs can be used for IBS-C?

A

add a bulk laxative!!
(maybe antispasmodic/anticholinerigcs to relieve painful bowel spasms)
consider Lubiprostone/linactolide: for constipation and abdom pain
TCA/SSRI for pain, anxiety, and depression
serotonin 4 antag - as last resort

232
Q

what drugs are pro-secretory agents

A

lubiprsotone and linactolide

233
Q

Contraindication for Lubiprostone?

A

if suspected intestinal block

234
Q

black box warning for linaclotide

A

against use in kids under 17 (dehydration risk)

235
Q

lubiprsotone and linactolide
which one to take with food/water
which one to take 30 ins before first meal

A

lubiprostone: take w/ food
linactolide: before first meal

236
Q

MOA of teagserod:

A

stimulates peristalsis and GI secretions – 5Ht4 agonist

237
Q

when is tegaserond used?

A

in emegency situations/under FDA investigaiton right now —

238
Q

diet for IBS-D?

A

avoid lactose and caffeine

239
Q

MOA of eluxadoline

A

multiple mu opioid receptor agonist

240
Q

lubiprsotone and linactolide

which one should be avoided in pregancy

A

lubiprostone

Fall 2018/P3 Year' (16 decks)

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