Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Summer pharm 4 > IBD > Flashcards

IBD Flashcards

1
Q

What is comprised in IBD

A

UC: mucosal inflammatory condition confined to rectum and colon
Crohn’s: transmural inflammation of GI tract, mouth to anus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes IBD

A

Combo of infectious, genetic, environmental, and immunologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pharm Tx for IBD involves

A

anti-inflammatories
1. Aminosalicylates (Sulfasalazine, Mesalamine)
2. Corticosteroids (prednisone, budesonide)
(Also Tx with abx, immunosuppressives, biologics, and anti-integrins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are Sx of UC

A 
rectal bleeding 
abd ttp 
Continuous distribution 
rectal involvement 
crypt abscesses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are Sx of Crohn’s

A 
Fever, malaise 
rectal bleeding 
abd pain 
abd mass 
fistulas
aphthous ulcers 
discontinuous distribution 
ileal involvement 
strictures 
transmural 
granulomas 
linear clefts 
cobblestoning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Drugs that are less effective but with fewer ADE

A

Budesonide
Topical steroids
Antibiotics
5-aminosalicylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Agents that are most effective but with a lot of ADE

A

Natalizumab
Cyclosporine
TNF antagonists
IV corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens to aminosalicylates in the body

A

Sulfasalazine: converted to mesalamine in the colon
Asacol: Release is delayed until terminal ileum and cecum, then released as a bolus in right colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What constitutes mild (low risk) Crohn’s

A 
No/Mild Sx 
Nl/mils elevation of CRP
Diagnosed 30+ 
Limited distribution 
No prior resections 
No strictures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do you treat mild, low risk crohn’s

A

Budesonide to induce remission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the Aminosalicylates (5-ASA)

A

Azo compounds: Sulfasalazine, Olsalazine, Balsalazide

Mesalamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the significance of Azo compounds

A

The structure reduces absorption from small intestine

In the terminal ileum and colon, bacteria cleave the azo bond and release active 5-ASA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the formulations of Mesalamine

A

Pentasa: timed release microgranules throughout small intestine
Asacol/Apriso: Coating dissolves at pH 6-7; distal ileum and proximal colon
Lialda: Dissolves in pH of colon. Slow release throughout colon
Rowasa: enema
Canasa: Suppository

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the site of action of the IBD drugs

A

Jejunum: Pentasa
Ileum: Asacol, Lialda
Proximal colon: Sulfasalazine, Balsalazide
Rectum: Rowasa, Canasa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the PK of IBD drugs

A

Absorption of 5-ASA from colon is very low
Absorbed 5-ASA undergoes N-Acetylation in the gut and liver and is converted to a metabolite that is not anti-inflammatory
That metabolite is excreted by kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the MOA of 5-ASA

A

Modulates inflammatory mediators derived from COX and LOX pathways
Interferes with production of inflammatory cytokines (NF-Kb)
Inhibit cell fxn of NK cells, lymphocytes, macrophages
Scavenge reactive oxygen metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does 5-ASA work in UC and Crohn’s

A

UC: Induce and maintain remission

Crohn’s: efficacy unproven, used mainly for mild-mod involving colon or distal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is first lint Tx for mild-mod UC

A

5-ASA!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Efficacy of 5-ASA depends on

A

achieving high drug concentration at site of active disease

  • Rowasa and Canasa good for dz confined to rectum or distal colon
  • azo compounds and mesalamine for dz in proximal colon
  • pentasa, asacol, lialda for dz involving small bowel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are ADE of Sulfasalazine

A 
nausea 
vomiting 
HA 
rash 
hepatotoxicity, nephritis 
-monitor folate, CBC, LFT, SrCr, BUN 
*Has more ADE than others bc it is a fast acetylator
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are ADE of Olsalazine

A

secretory diarrhea

-monitor oligospermia (reverses on drug d/c)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are ADE of Mesalamine

A

N/V
Headache
High dose: Interstitial nephritis

23
Q

How do glucocorticoids work in IBD

A

Inhibit inflammatory cytokines (TNF, IL1) and chemokines (IL8)
Reduce expression of inflammatory cell adhesion
Inhibit gene transcription of NO synthase, phospholipase A2, COX2, and NF-Kb

24
Q

What is the MC steroid used in IBD

A

Prednisone and prednisolone

Oral, QD

25
What are other steroids used in IBD
Hydrocortisone: maximize colon effects, minimize systemic absorption. Topical Tx in rectum and sigmoid Budesonide: prednisolone synthetic analog. rapid first pass hepatic metabolism (low oral bioavailability) (entocort, uceris- PO forms in US)
26
What is Entocort
Controlled release budesonide released thru distal ileum and colon PO
27
What are steroids used for
mod-severe active IBD- a flare! NOT to maintain remission (need 5-ASA or biologics for that) Higher doses are NOT more effective, just more ADE After response (1-2 weeks), slowly taper If very ill, can give IV If involving rectum or sigmoid colon, rectally administered preferred
28
ADE of corticosteroids are
``` hyperglycemia dyslipidemia osteoporosis HTN acne edema infection myopathy psychosis -Monitor BP, fasting lipids, glucose, vit. D, bone density ```
29
What are the pruine analogs
Azathioprine (more bioavailable!)- converted to 6-MP 6-Mercaptopurine -They are anti-metabolites with immunosuppressive properties
30
What ahppens to 6-MP in the body
Biotransformed via competing catabolic enzymes; Xanthine oxidase, Thiopurine methyltransferase
31
What should you not give Xanthine oxidase with
Allopurinol (XO inhibitor)- so you get double XO inhibition | Increases active 6-thioguanine nucleotides= severe leukopenia
32
What is the PK of purine analogs
Half life <2 hours | Takes 17 weeks before therapeutic benefit or oral purine analogs
33
What are clinical uses of purine analogs
Induce and maintain remission of UC and Crohn's after 3-6 months of Tx Allow reduction and elimination of steroids in most pts
34
What are ADE of purine analogs
N/V bone marrow depression (anemia, low plt, wbc) hepatic toxicity (monitor CBC, LFT) hypersensitivity to azathioprine (fever, rash, pancreatitis, diarrhea, hepatitis Increased risk of lymphoma
35
Can purine analogs be used in pregnancy
CAN cross placenta but many women used during pregnancy and teratogenicity is small
36
How can Abx influence the course of IBD
Decrease bacteria and fungi in gut/lumen Alter composition of mictobiota Decrease bacterial tissue invasion and Tc microabscess Decrease bacterial translocation and systemic dissemination
37
How does Methotrexate work
Inhibit dihydrofolate reductase enzyme (needed to make thymidine and purines) Can interfere with inflammatory actions of IL Can stimulate increased release of adenosine, and apoptosis/death of active T lymphocytes
38
What disorders does methotrexate treat
Crohn's RA Cancer -oral (50% bioavailable), subQ, IM (appx 100% bioavailable)
39
Clinically, methotrexate is used to
induce and maintain remission in crohn's (1x wk subQ)- if effective after 8-12 weeks, can reduce dose
40
ADE of high dose methotrexate are
bone marrow depression megaloblastic anemia alopecia mucositis -reduce the dose! and reduce risk of ADE with FOLATE* -permanent peripheral neuropathy if used for prolonged periods
41
Other ADE of methotrexate are
if w/ psoriasis: hepatic damage | hepatic accumulation and toxicity if w/ renal insufficiency
42
How do anti-TNF agents work in IBD
Dysregulate helper T cella type 1 (Th1) response and regulatory T cells
43
Wha are the biologic actions of TNF
release proinflammtory cytokines from macrophages Activate and proliferate T cells Up regulate adhesion molecules (leukocyte migration) Stimulate hepatic acute phase reactants
44
What anti-TNF (TNF MAB's) are approved for use in Crohn's
``` Infliximab Adalimumab Certolizumab Natalizumab Vedolizumab (golimumab, Inflixi, adalim, and Vedo in UC) ```
45
How do anti-TNF work
Bind soluble and membrane bound TNF prevent cytokine from binding to receptors Cause reverse signaling that suppresses cytokine release -Inflix/Adalim/Golim: Fc portion promotes Ab mediated apoptosis. Also complement activation, and cytotoxicity to T lymphocytes and macrophages Certo: No Fc portion= no apoptosis
46
What are the clinical uses of anti-TNF
Acute and chornic mod-severe Crohn's not responsive to Tx | 1/3 of pts eventually lose response (may be 2/2 development of Abs to TNF Ab (Abs to the Abs; ATA)
47
What are ADE of anti-TNF
*Infection! 2/2 supprssion of T helper cells (Th1)- sepsis, TB, invasive fungal, reactivation of Hep B or latent TB -Increased risk if also on steroids Less serious: URI (sinusitis, bronchitis, PNA), cellulitis *Delayed serum sickness-like Rxn: myalgia, arthralgia, jaw tightness, fever, rash, urticaria, edema +ANA and anti-ds DNA Lupus like syndrome (goes away w/ drug d/c) Hepatic reactions, demyelinating d/o, hematologic d/o, new or worse CHF, psoriatic skin rash, lymphoma
48
What does concomitant use of anti-TNF and immunomodulators do
increase risk of lymphoma
49
What makes the likelihood of developing antibodies to antibodies while using anti-TNF
Using immunomodulators like 6-MP or methotrexate
50
What are Integrins
Adhesion molecules on the surface of leukocytes interact with selectins, adhesion molecules on vascular endothelium Allow leukocytes to adhere to vascular endothelium and move thru vessels into tissue
51
What is Natalizumab
Anti-integrin; IgG4 MAB that blocks integrins and prevents migration into surrounding tissues
52
What is Natalizumab used for
Mod-severe crohn's who fail Tx | CArefully restricted program
53
ADE of Natalizumab are
Acute infusion reaction Opportunistic infections -Monitor brain MRI, mental status, PMI
54
What is Vedolizumab
Similar to natalizumab but: Selectively blocks the gut (NOT brain) Prevents JC virus (more selective) Can be used in crohn's ad UC

Summer pharm 4 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions