E4 IBD Flashcards
rectum and colon
UC
any part of Gi tract
CD
mucosal inflammation
UC
transmural inflammation
CD
more common in men
UC
or
CD
UC
more common in women
UC
or
CD
CD
T or F: IBD has both autoimmune and non-autoimmune mechanisms
tru
what happens when the gut wall is infiltrated by WBCs
granuloma formation and cytokine dysregulation
T or F: IBD has genetic etiology
true
diet stuff:
refined sugars, diets low in fruit/vege, high in unsat fats = _______
high protein= ____
CD
UC
smoking:
protective in ___
bad with _____
UC - good
CD - bad
T or F:
NSAIDs are a mainstay therapy in both IBD conditions
no fuck NSAIDs
T or F:
UC affects mucosal and submucosal layers
true
mucosal damage from UC can result in what two things
diarrhea and bleeding
3 local complications of UC
hemorrhoids
anal fissures
perirectal absesses
whats the potentially fatal UC complication we talked about?
toxic megacolon
what is the physiological result of toxic megacolon
segmental or total colonic distension with acute colitis and signs of systemic toxicity
cobblestone appearance
CD pathophys
what is the most common site of inflammation in CD
terminal ileum
UC or CD: ulcers tend to be deeper
CD
UC or CD: small bowel stricture and obstruction possible
CD
T or F: CD pts typically have more bleeding than UC
false
UC or CD: More risk of nutritional deficiencies
CD because whole GI tract = more things absorbed and shit
hepatic manifestations of IBD
fatty liver, pericholangitis, autoimmune hepatitis, cirrhosis
biliary manifestations of IBD
primary sclerosing cholangitis (PSC), cholangiocarcinoma, cholelithiasis
what extraintestinal manifestation of IBD should you immediately refer an evaluation for
anything with eyes
Bone and joint manifestations:
symmetrical or asymmetrical
asymmetrical
super common manifestation of IBD (hematologic)
anemia
when is the risk of VTE highest?
during flares
lab tests for UC:
- (increased/decreased) Hb/HCT
- (increased/decreased) ESR/CRP
- fecal calprotein (FC)
increased
increased
what does fecal calprotein (FC) correlate with?
degree of inflammation
T or F:
fecal calprotein (FC) is less sensitive and specific than serum markers
false, more
what are the main ways to diagnose UC
-oscopies
- negative stool exam for infectious causes
distal to splenic flexure
A. Left-sided
B. Extensive
C. Proctitis
D. Proctosigmoiditis
E. Pancolitis
A
extending proximal to splenic flexure
A. Left-sided
B. Extensive
C. Proctitis
D. Proctosigmoiditis
E. Pancolitis
B
involving the rectal area
A. Left-sided
B. Extensive
C. Proctitis
D. Proctosigmoiditis
E. Pancolitis
C
involving rectum and sigmoid colon
A. Left-sided
B. Extensive
C. Proctitis
D. Proctosigmoiditis
E. Pancolitis
D
involving majority of colon
A. Left-sided
B. Extensive
C. Proctitis
D. Proctosigmoiditis
E. Pancolitis
E
typical presentation of CD includes what 2 things
diarrhea and abdominal pain
what is hematochezia
blood in stool
when running an FC test, what does it help distinguish from?
IBD from IBS
clinical presentation of CD:
- (increased/decreased) Hb/HCT
- (increased/decreased) WBCs, ESR, CRP
decreased
increased
what is the most frequently used thing in research to gauge response to therapy and determine remission
CDAI (Chrons disease activity index)
mild/mod
A. CDAI 150-220
B. CDAI 220-450
C. CDAI>450
A
mod/sev
A. CDAI 150-220
B. CDAI 220-450
C. CDAI>450
B
sev/fulminant
A. CDAI 150-220
B. CDAI 220-450
C. CDAI>450
C
severe-fulminant CD:
- persistent sxs or evidence of systemic _______ despite _______ or biologic treatment
or
- presence of _______, rebound tenderness, intestinal obstruction, or _______
toxicity
corticosteroid
cachexia
abscess
which diet has shown to be beneficial for IBD
none shown
what to do with PN in regards to nutrition support in IBD
avoid unless absolutely necessary
UC or CD:
indications for surgery
UC (still for CD but less established)
which agents are considered curative?
none, no drugs at all cure either
what are the 2 ASAs?
sulfasalazine and mesalamine
what are the 4 immunomodulators
azathioprine
mercaptopurine
cyclosporine
MTX
what 2 antimicrobials are indicated in IBD tx
metronidazole
cipro
sulfasalazine is cleaved by _______ _______ to release _________ and 5-ASA
colonic bacteria
sulfapyridine
5-ASA mainly remains in ______ and is excreted in ______
lumen
stool
T or F:
sulfapyridine is active and associated with ADRs
false, inactive but still associated
2 things listed under MOA of 5-ASA
anti-inflam
free radical scavenging
T or F:
mesalamine can be administered alone
true
mesalamine rapidly and completely absorbed in ______ _______ but not ______
small intestine
colon
what form of mesalamine do you give for left-sided disease
topical (enemas)
what form of mesalamin do you give for proctitis
suppository
what form of mesalamine do you give for delayed/controlled release
oral
T or F:
topical mesalamine is more effective than oral
true
better tolerated
A. Sulfasalazine
B. Mesalamine
B
significance of olsalazine
more diarrhea
2 drug interactions for mesalamine
anything that increases bleeding
drugs affecting ph (ppil, H2RA, antacids)
T or F:
corticosteroids are used for induction and maintenance
False, induction of remission but not maintenance
what is budesonide and how is it administered
cortico
PO in CR formulation
T or F:
budesonide associated with extensive first pass metabolism
true
1 drug interaction for budesonide
CYP3A inhibitors (grapefruit, ketoconazole) -> increase systemic exposure
how much oral prednisone/prednisolone a day
40-60mg/day
do we need to taper off of the preds?
yes
oral preds may be used for disease _______ or ________
flares or induction
4 short term ADRs with cortico
hyperglycemia
gastritis
mood changes
inc BP
6 long term ADRs with cortico
necrosis
cataracts
obesity
growth failure
HPA suppression (what?)
osteoporosis*
what 2 things should you give pts on corticos and for what reason
calcium and vitamin d for risk of osteoporosis
AZA and 6-MP can be effective in long term treatment of ?
UC AND CD
T or F:
you can combine AZA with prednisone
true
AZA is a prodrug rapidly converted to?
6-MP
T or F:
AZA and 6-MP primarily play a role in maintenance
false, primarily maintenance with little to no role in induction
ADR “we worry about most” with AZA and 6-MP
hematologic -> bone marrow suppression and he said something about deadly anemia too
niche thing to monitor with AZA and 6-MP
TPMT
cyclosporine can be effective in ______ in pts with refractory IBD (not recommended for __)
inducing remission
not rec for CD
3 AEs for cyclosporine
nephrotoxicity (dose related)
neurotoxicity
metabolic effects
weird monitoring thing for cyclosporine
cya tr. conc.
goal is 200-400
2 drug interactions with cyclosporine
CYP3A and PgP !!
MTX used in?
just CD
T or F:
MTX may have steroid sparing effects
truee
what do we want to add to MTX and why?
folic acid for bone marrow suppression (I think)
few main CI’s for MTX
pregnancy
CrCL <40
liver disease
pleural effusions
niche monitoring for MTX
chest xray
TNF inhibitor class ADRs:
test for which two things before starting?
tuberculin test, hep b/c
TNF inhibitor class ADRs:
contraindicated
live vaccines
TNF inhibitor class ADRs:
weird risk of what?
lymphoma and hepatosplenic T-cell lymphoma
oh my fucking god another one for demyelinating disease
TNF inhibitor class ADRs:
may exacerbate?
CHF, dont give in class III/IV
Infliximab:
indication:
class:
mod/sev CD and UC
TNF inhibitor
what do you need to know about combining infliximab with immunosuppressives
basically makes the risk of everything exceptionally worse
Adalimumab:
indication:
class:
mod/sev CD and UC
TNF inhibitor
Adalimumab may use for pts with poor response to ______
infliximab
T or F:
Infliximab has lower likelihood of developing ADAs than adalimumab
false, backwards
Golimumab:
indication:
class:
UC only
TNF inhibitor
T or F:
All 4 tnf inhibitors are used in induction and maintenance therapy
true
Certolizumab pegol:
indication:
class:
CD only
TNF inhibitor
Natalizumab:
indication:
class:
CD only
anti a-subunit integrin
(prevents leukocyte adhesion/migration)
Natalizumab induction or maintenance
both
can use natalizumab in pts who fail/dont tolerate ?
TNF-a inhibitors
Do we use natalizumab in combo with immunosuppressants?
no
when to d/c natalizumab in pts that start it
pts w/ no benefit by 12 weeks and/or who are still steroid dependent within 6 months (fuck this is so much info)
Natalizumab associated with ? (scary thing from past topics)
PML
T or F:
can see hypersens reactions and ADAs
true
natalizumab increased risk of PML with what 3 things
- Longer duration of therapy
- prior immunosuppressant use
- JC antibody positive
Vedolizumab:
indication:
class:
UC and CD
anti-a4-b7-integrin
Vedolizumab induction or maintenance
both
T or F:
PML also observed in Vedolizumab
false
where is a4-b7 integrin expressed?
subset of T-lymphocytes
Ustekinumab:
indication:
class:
CD and UC
IL-12 and IL-23 antagonist
Ustekinumab induction or maintenance
both
Reports of rapidly developing cutaneous cell carcinoma in pts with risk factors:
A. Natalizumab
B. Vedolizumab
C. Methotrexate
D. Ustekinumab
D