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193 Cards in this Set
- Front
- Back
what is nausea?
|
the inclination to vomit
|
|
what is vomiting?
|
expulsion of refluxed gastric contents from the mouth
|
|
define retching?
|
labored movement of abdominal and thoractic muscles before vomiting.
|
|
what are the GI mechanisms leading to NV?
|
-peptic ulcer disease
-gastric cancer -pancreatic disease |
|
what are the neurologic processess that cause NV?
|
-midline cerebellar hemorrhage
-increase ICP -migraine headaches -vestibular disorders -head trauma |
|
list the motility disorders to cause NV?
|
-gastroparesis
-IBS -postgastric surgery -anorexia |
|
what are the 3 metabolic disorders to cause NV?
|
-Diabetes, DKA
-addison's disease -renal disease |
|
list the intra-abdominal emergencies that have caused NV
|
1. intestinal obstruction
2. acute pancreatitis 3. actue cholecystitis 4. acute viral hepatitis 5. acute pyelonephritis |
|
Self induced and anticipatory NV are considered ___ causes of NV?
|
psychogenic
|
|
what are the pathogens for acute gastroenteritis?
|
-viral
-salmonellosis -shigellosis -enterotoxins |
|
What are the therapies know to cause NV?
|
-chemo
-radiation -theophylline tox -anticonvulsants -opiates -dig tox -antibiotics -amphotericin |
|
what are the cardiovascular disorders known to cause NV?
|
-AMI
-CHF -shock and circulatory collapse |
|
whta are the miscellaneous causes of NV?
|
-pregnancy
-noxious odor -operative procedures -any swallowed irritant |
|
the vomiting center or ___ center is located int he nucleus __ __ of the __
|
emetic; tractus solitaries; medulla
|
|
what does the vomiting center contain?
|
-histamine
-acetylcholine -serotonin receptors |
|
how does the VC coordinate the act of vomiting?
|
Stimulates the
-salivary center -vasomotor center -respiratory center -cranial nerves |
|
the VC can be activated by what signals from the body?
|
1. Visceral afferents (GI tract)
2. Chemoreceptors trigger zone 3. vestibular system 4. limbic system 5. midbrain ICP reveptors |
|
the chemoreceptor trigger zone is located in the area ___ of the ___
|
postrema; medulla
|
|
the CTZ contains dopamine, ___, acetylcholine and ___ receptors
|
histamine; serotonin
|
|
The CTZ is a major area of stimulation by ___
|
chemotherapy
|
|
What are the 4 types of chemo induced NV?
|
-actue
-delayed -anticipatory -breakthrough: despite prophylaxis |
|
what is delayed CINV?
|
after 24 hours of chemotherapy
|
|
What are the risk factors of CINV?
|
-age (younger)
-sex (females) -concomitant radiation therapy -history of ethanol use or motion sickness -emetogenicity |
|
ToF: a person with a hx of ethanol use on chemo is at higher risk for CINV?
|
false: they are less likely to have chemo induced NV
|
|
What are level 1 emetogenic chemo agents?
|
the lowest level that has frequency of NV <10% of the patients
|
|
Level 2 emetogenics have what frequency of CINV?
|
10-30%
|
|
If an chemo agents causes NV in 30-60% of patients, what level emetogenic is it?
|
level 3
|
|
how many patients on level 5 emetogenics will have NV?
|
>90%
|
|
ToF: the route of administration of a chemo agent does not change its emetogenic potentia?
|
false! intrathecal admin of methotrexate(level 1) and cytarabine (level 2) increase them to level 3
|
|
What are the antihistaminc agents?
|
Anticholingeric agents (diphenhydramine (benadryl), Hydroxazine (atarax), scopolamine (transderm scop)
|
|
what is the MOA of the anticholinergic agents?
|
interrupt various visceral afferent pathways that stimulate nausea and vomiting
|
|
What place in chemotherapy do anticholingeric agents have?
|
simple nausea and vomiting; useful to prevent EPS
|
|
List the SE of anticholinergic agents.
|
-drowsiness
-constipation -dry mouth -confusion -blurred vision -urinary retention |
|
what are the 2 therapeutic considerations for anticholinergic use in chemo?
|
-low potency
-pediatric considerations |
|
List the dopamine antagonists.
|
Class: phenothiazines
-chlorpromazine (Thorazine) -prochlorperazine (Compazine) -promethazine (phenergan) black box warning Class: butyrophenones -Haloperidol (Haldol) -droperidol (inapsine) CLass: benzamides -metoclopramide (reglan) |
|
the MOA of the phenothiazines is...
|
to block dopamine receptors (CTZ)
|
|
what are the most widely prescribed antiemetics?
|
the phenothiazines (dopamine antagonists)
|
|
what type of NV is indicated for phenothiazines?
|
simple NV; mild emetogenic chemo
|
|
what are the SE of phenothiazines?
|
-sedation
-lethargy -cardiovascular -EPS -hypersensitivity reactions -liver dysfunction |
|
what are the 3 therapeutic considerations with phenothiazines?
|
-adverse effects
-pediatric considerations -inexpensive agents; useful for long term treatment |
|
what is the MOA of the butyrophenones?
|
block dopamine stimulation (CTZ)
|
|
what types of emetogenics can be treated with butyrophenones?
|
Haldol and inapsine
the mild emetogenic chemotherapy agents |
|
what are the SE of the butyrophenones?
|
Droperidol causes QT prolongation and/or torsades de points
general SE of the class: -sedation -hypotention -tachycardia -dystonic reaction |
|
What are the indications for butyrophenones?
|
reserved for the patients that fail other treatment modalities for NV
|
|
what is the MOA of metoclopramide?
|
Reglan
-Blocks dopamine receptors -blocks serotonin receptors at high doses -increase LES tone, aides gastric emptying and transit time |
|
what is the place in therapy for metoclopramide?
|
used for moderate emetogenic chemo agents
|
|
what are the Side effects fo metoclopramide?
|
Reglan
-EPS! -sedations -restlessness and agitation -Diarrhea -fatigue |
|
what are the therapeutic considerations for reglan?
|
consider for breakthrough or patients allergic to serotonin antagonists
|
|
What are the serotonin antagonists?
|
-ondansetron (zofran)
-granisetron (Kytril) -dolasetron (Anzemet) |
|
what is the MOA for the serotonin antagonists?
|
-block serotonin receptors in the GI tract and CNS
|
|
the serotonin antags are used with ____ emetogenic chemo agents?
|
moderate to high
|
|
what are the SE of the serotonin antags?
|
-headache
-diarrhea -Increased LFTs (zofran) -somnolence (kytril) -constipation (kytril) -fatigue (anzemet) -ekg changes (anzemet) |
|
what are the therapeutic considerations with the serotonin antags?
|
-used in combo with corticosteroids (dexamethosone)
-these agents DO NOT CAUSE EPS or DYSTONIA -dolestron (anzamet) associated with drug interactions (cimetidine and rifampin) |
|
what class of drugs aid with delayed NV and typically used in combo with dopamine and or serotonin antags?
|
corticosteroids
|
|
what are the 2 corticosteroids often used for NV?
|
dexamethosone and methylprednisolone
|
|
what are the SE of the corticosteroids?
|
-GI upset
-anxiety/excitation -increased appetite -hyperglycemia -euphoria -headache -insomnia |
|
what are the therapeutic considerations for corticosteroids>
|
not indicated for patients with simple NV; may be associated with unacceptable risks
|
|
what drug falls under the calass of the cannabinioids?
|
dronabinol (marinol)
|
|
what are the SE of dronabinol?
|
-drowsiness
-euphoria -somnolence -vasodilation -vision difficulties -dysphoria -hallucinations -memory loss -hunger |
|
what are the therapeutic considerations for dronabinol?
|
cannabis:
use this agent should only be considered when other regimens do not provide desired efficacy (not first line) |
|
what drug has been found useful for anticipatory NV?
|
benzodiazapines: lorazepam (ativan)
|
|
what are the SE for lorazepam?
|
-sedation
-amnesia -lethargy |
|
ToF: lorazepam is usually a monotherapy for CINV
|
false: mainly used in combo with others
|
|
what is the general approach to treatment of CINV?
|
-determine emetrogenic potential of chemo
-know potential ADRs -understand pharmacologic and kinetic properties -cost awareness |
|
what is the best treatment for the prevention of acute CINV (levels 2-5)?
|
dexamethosone + serotonin receptor antag (30 mins prior to therapy
|
|
what are the guidelines for treatment of anticipatory CINV?
|
benzodiazapine +or- phenothiazine
|
|
what is the best treatment for delayed NV?
|
dopamine antag + dexamethosone
|
|
What are the drugs used for treatment of post-operative NV?
|
-dolasetron
-ondansetron -lorazepam -diphenhydramine -promethazine -proclorperazine -metoclopramide |
|
what is the best treatment for radiation induced emesis?
|
serotonin receptor antag prior to radiation
|
|
what are retrograde movement of gastric contents from the stomach to esophagus?
|
GER
|
|
what is GERD?
|
symptoms or damage that results from reflux
|
|
define reflux esophagitis.
|
inflammation of the esophagus due to repeated refluxed material
|
|
what is erosive esophagitis?
|
visible damage on endoscopy (redness, bleeding, superficial ulcerations, and exudates)
|
|
what is the passage of refluxed gastric contents into the oral pharynx?
|
regurgitation
|
|
what are the aggressive factors in the patho of GERD?
|
-gastric acid
-pepsin -bile salts -pancreatic enzymes |
|
what is the body's defense mechs against GERD?
|
-lower esophageal sphincter
-esophageal mucus -esophageal clearance -acid neutralization by saliva -gastric emptying |
|
list the risk factors for having GERD?
|
-decreased/increased LES pressure
-delayed gastric emptying (motility) -increased gastric acid secretion or is a direct irritant -impaired gastroesophageal pressure gradient |
|
what are the possible complications of GERD?
|
-esophageal stricture formation
-esophageal ulceration/hemorrhage -erosive esophagitis -barretts's esophagitis -extra-esophageal complications |
|
what is barrett's esophagitis?
|
esophagus ends up looking like the intestines. Increase risk of cancer
|
|
LIst the clinical presentation (symptoms) of GERD.
|
-Recurrent vomiting
-heartburn (pyrosis) -early satiety -acid regurg -epigastric pain -dysphagia or feeding refusal -odynophagia -irritability in infants -sandifer syndrome |
|
what are the atypical manifestations of reflux?
|
-respiratory complaints
-apnea or ALTE (acute life threatening event) -noncardiac chest pain -nausea -hoarseness -cough |
|
what are the diagnosis methods for GERD?
|
-patient history
-endoscopy -barium swallow -ambulatory pH testing -esophageal manometry (monitor pressure and pH) |
|
List the goals of therapy of gERD?
|
-promote normal weight gain and growth
-heal inflammation -prevent resp and other comps |
|
what are the dietary modifications for infants and children to prevent gerd?
|
infant: alter formula to alimentum or hypoallergenic formula
children -avoid foods that decrease LES pressure -avoid foods that have a direct irritant effect (citric, spice) -eat small meals -avoid eating immediately prior to sleep |
|
what are some medications that can cause GERD?
|
KCl, Fe, NSAIDs
|
|
infants with gerd should be placed in the __ position
|
supine
|
|
how should children and adolescentes with gerd be positioned?
|
-elevate head of bed
-avoid reclining after meals |
|
what are some lifestyle modifications for adolescents to prevent gerd?
|
-stop smoking
-avoid alcohol -avoid tight-fitting clothes -reduce weight -do not exercise immediate after eating |
|
what are the antacids and the alginic acid?
|
-tums
-maalox -mylanta algininc (gaviscon) |
|
list the MOAs of antacids.
|
-neutralize stomach acid
-deactivate pepsin -decrease acidity of reflux -form viscous solution, coast esophagus (alginic acid) |
|
describe the place that antacids have in therapy.
|
-mild GERD; in conjunction with lifestyle modifications
-used in combo with other suppression therapies |
|
when are antacids dosed?
|
-after meals and at bedtime
-as needed |
|
what are the SE of antacids?
|
-diarrhea (Mg ones: mylanta)
-constipation (Al ones: maylox) -alteration in mineral metab -acid rebound |
|
what are the therapeutic considerations of antacids?
|
-effective for mild or breakthrough symps
-avoid in patients with renal insufficiency -drug interactions (tetracycline etc) |
|
List the H2 receptor antagonists.
|
-Cimetidine (Tagamet)
-nizatidine (Axid) -ranitidine (zantac) -famotidine (pepcid) |
|
what are the MOAs of H2s?
|
-block histamine-mediated gastric acid secretion
-decrease acidity of reflux |
|
what place in therapy do H2's have?
|
-mild to mod GERD
-severe GERD (non-erosive disease) |
|
LIst the SE of H2's
|
-Tachyphylaxis (stops working after a few weeks)
-headache!! -mental confusion -somnolence -fatigue -dizziness -gastrointestinal complaints -gynecomatia (cimetidine) -impotence -thrombocytopenia |
|
which GERD medication can be used under age 1?
|
H2's: Zantac
|
|
what are the therapeutic considerations for H2s?
|
-ped consideration
-drug interactions (cimetidine) -dose adjust for renal insuff -approx 50% of patients have resolution of esophagitis |
|
List the PPIs
|
-omperazole (prilosec)
-lansoprazole (prevacid) -pantoprazole (protonix) -rabeprazole (aciphex) -esomperazole (nexium) |
|
what is the MOA of the PPIs?
|
-block acid secretion by inhibiting (irreversibly the H+, K+-ATPase enzyme system in the parietal cells)
-cause profound, prolonged decrease in gastric acid secretion -decrease acidity of reflu |
|
which class of drugs are the of the ones of choice for GERD?
|
PPIs
|
|
what has been found to help with nocturnal rebound symptoms of GERD?
|
H2s in combo with PPIs
|
|
WHat are the SEs of the PPIs?
|
-diarrhea
-flatulence -abd pain -dizziness -headache |
|
what are the therapeutic consids for PPIs?
|
-superior to H2s in Tx of mod-to-severe esophagitis
-not many drug interactions -cost considerations -pediatric considerations |
|
what are the prokinetic agents?
|
-cisapride (propulsid)
-metoclopramide (reglan) |
|
what is the MOA of the prokinetic agents?
|
-increase gastric emptying
-increase LES pressure |
|
What is the place in therapy for prokinetic agents?
|
-mild-to-moderate Gerd
-severe GERD; in combo with others -useful in pts with belching, early satiety, nocturnal symps |
|
what are the SE of prokinetic drugs?
|
-diarrhea, cramping
-somnolences -fatigue -dizziness -weakness -rash -EPS -anxiety, nervousness -insomnia |
|
what are the therapeutic considerations for prokinetic agents?
|
-side effect profile (EPS)
-tachyphylaxis |
|
what are the maintenance therapy suggestions for FERD ?
|
-more likely necessary in patients with esophagitis or comlications
-PPI are highly effective -H2s are less effective -surgery is last line |
|
What is IBD?
|
term used to describe a family of closely related intestinal disorders including UC and crohns
|
|
what is UC?
|
a mucosal inflammatory condition confined to the recum and colon
|
|
what is Crohns?
|
a transmural inflammation of the GI tract that can affect any part, from the mouth to the anus
|
|
what groups have the highest rates of IBD?
|
ashkenazi Jews>>whites>blacks and asians
|
|
ToF: males have higher incidence of IBD than females
|
false: they are =
|
|
what are the proposed etiologies of IBD?
|
-infectious agent
-genetics -environmental -immune defects -psychologic factors (stress increases flare up) |
|
which disorder, (UC or CD), is common to have fistulas/abcesses/strictures?
|
Crohns
|
|
what is the location of the sores of UC? of crohns?
|
UC: mucosal (superficial)
Crohns: transmural |
|
which disorder has crypt abscess, cryptitis?
|
UC
|
|
which disorder has tissue granuloma and cobble stone appearance?
|
Crohns
|
|
what are the minor complications of UC?
|
-hemorrhoids
-anal fissures -perirectal abscesses |
|
what are the major complications of UC?
|
-toxic megacolon (rapid dilation: severe)
-colonic carcinoma |
|
what are the systemic issues of UC?
|
-hepatobiliary complications
-joint complications -ocular complications -dermatologic complications -mucosal complications |
|
what are the local complicatios of Crohns?
|
-small bowel stricture/obstruction
-fistula formation -hypochromic anemia (due to bleeding) -colonic carcinoma |
|
what are the systemic issues of crohns?
|
-similar to UC
-renal stones more common in CD than UC -NUTRITIONAL DEFICIENCIES |
|
what are the SxS of UC?
|
-abd cramping
-increase BMs with rectal bleeding -weight loss -systemic involvement (fever, tachy, joint, ocular and dermatologic complications) |
|
what are the PE findings for UC?
|
-local complications (hemorrhoids, anal fissures, perirectal abscesses)
-ocular complications (iritis, uveitis, and conjucntivitis) -dermatologic findings |
|
what are the lab findings for UC?
|
-decreased Hgb/Hct
-increased ESR -leukocytosis and hypoalbuminemia |
|
what is mild UC?
|
fewer than four BMs per day containing minimal or no blood; no systemic symptoms such as fever; and an ESR wtihin nml limits
|
|
what is moderate UC?
|
> 4 BMs/day but with minimal systemic compliations
|
|
what is the definition of severe UC?
|
> 6 BMs a day with blood; evidence of systemic complications (fever, tachy, anemia, and or ESR > 30
|
|
what are the SxS of crohns?
|
-abd pain
-increased BM -hemotachezia -systemic involvement -weight loss -fistula |
|
what are some of the PE findings for crohns?
|
-adb mass and tenderness
-local complications |
|
what are the lab findings of Crohns?
|
Increased WBC and ESR
|
|
what IBD commonly has an abdominal mass?
|
Crohns
|
|
what is the distribution of UC and CD?
|
UC: continuous
CD: dicontiuous (skip lesions) |
|
what are the diagnostic procedures for IBD?
|
-patient hx
-PE -lab tests -biopsy -stools studies -sigmoidoscopy/colonoscopy -histologic exam -barium studies |
|
what ist he goal of IBD therapy?
|
-develop a regimen of medical, surgical and nutritional interventions that reverese the mucosal inflammatory response, maintain disease remission, prevent malignancy, optimize nutrition, and max QOL.
|
|
what are the 4 general approaches to treatment of IBD?
|
-pharmacologic
-surgical -nutritional -disease complications considered |
|
what are the aminosalicylates?
|
-sulfasalazine
-Mesalamine -Olsalazine -Balsalzide |
|
what is the MOA of the aminosalicylates?
|
UNKNOWN: data suggests that they work topically to inhibit the generation of potent pro-inflammatory cytokines; other daya say they inhibit inflammatory trasncription factor NF-kB, block of prostaglandin and leukotriene production
|
|
what are the place in therapy of aminosalicylates?
|
-mild to moderate disease (both)
-maintenance of remission (both) |
|
what are the SE of the aminosalicylates?
|
-headache
-N -photosensitivity -diarrhea, -colitis -pancreatitis -hepatitis -anemia -interstitial nephritis -proteinuria |
|
WHat are the therapeutic considerations for aminosalicylates?
|
-patients treated with sulfasalazine should receive daily folate to prevent deficiency complications (anemia, neural tube defects)
-patients treated with sulfasalazine or mesalamine should undergo annual urinalysis, bi-annual CBC, and periodic LFT and pancreatic tests -site of activity |
|
___ patients on steroids go into remission
|
3/4
|
|
what are the commonly used corticosteroids of IBD?
|
prednisone
prenisolone hydrocortisone methyprednisone |
|
what is the place in therapy of IBD for corticosteroids?
|
-Moderate to severe disease (UC and CD)
--remission (induction) rates are 60-80% in moderates UC and CD and 55% in severe cases) -ineffective for maintenance therapy, dose taper after remission is induced |
|
what are the SE of the corticosteroids?
|
-excessive bone loss
-weight gain -cataracts -glucose intolerance -HTN -neuropsyhiatric complaints -facial swelling, acne, striae -decreased linear growth |
|
what are the therapeutic considerations of corticosteroids for IBD?
|
-minimize incidence and severity of steroid induced adverse effects
-consider calcium and vit D supplement -budesonide associated with less adverse effects (adrenal suppression, acne); remission rates slightly lower than prednisolone group |
|
what are the Abx that are often used in IBD?
|
metronidazole and cipro
|
|
what is the place in therapy of Abx for IBD?
|
-treat both mucosal inflammation as well as complications (abscesses)
-metronidazole used in treatment of active CD of the colon and rectum; ineffective for inducing remission in patients with active UC but may play a role in UC maintenance -cipro used in treatment of CD and UC |
|
What are the side effects of metronidazole?
|
-Reversible peripheral neuropathy
-abdominal pain -nausea and vomiting -pancreatitis -neutropenia -disulfiram-like reaction (teenagers and adults) |
|
What are the SE of cipro?
|
-tendonitis
-NVD -skin and urogenital complaints |
|
list the therapeutic considerations for abx in IBD treatment.
|
-used in combo with a mesalamine product or steroid therapy when those agents alone are not effective
|
|
What are the immunomodulatory drugs used for IBD?
|
-azathioprine
-mercaptopurine -methotrexate |
|
what is the MOA of azathrioprine?
|
inhibits inflammatory response such as interfering with protein synthesis, nucleic acid metabolism,and the clonal expansion of lymphocytes
|
|
what is the MOA of methotrexate in IBD?
|
inhibition of proinflammatory cytokines as well as down-regulation of activated T cells and neutrophils
|
|
describe the instances when immunomodulatory agents help prevent clinical relapse of IBD?
|
-where aminosalicylate therapy failed
-who failed weaning of corticosteroids -who required mercaptopurine/azathioprine as part of induction regimen -that are weaned from cyclosporine and tacrolimus therapy |
|
ToF: azathiprine/mercaptopurine demonstrated induction of mucosal and clinical remission of IBD
|
true
|
|
when is methotrexate used for IBD?
|
reserved for patients that failed azath/mercapto therapy due to administration concerns and hepatotoxicity
|
|
what are the SE of immunomodulatory therapy for IBD?
|
-BONE MARROW SUPPRESSION
-HEPATOTOXICITY -INFECTION -pancreatitis -malaise, ND -rahs -hypersensitivity -risk of malignancy |
|
what are the SE for methotrexate?
|
-BONE MARROW TOX
-Pulmonary disease -hepatitis -ND -anorexia -fatigue |
|
What should patients receiving methotrexate also be taking?
|
folate supplementation to decrease incidence and severity of adverse effects
|
|
ToF: methotrexate has shown to effectively treat CD
|
false; not as effective
|
|
What are the immunosuppresants used for IBD?
|
cyclosporine and tacrolimus
|
|
what are the MOA of the immunosuppresants for iBD?
|
inhibit production of IL2 and other cytokines that encourage proliferation of Tcells
|
|
What place in therapy do immunosuppresants have for IBD?
|
-severe disease refractory to intravenous corticosteroids
-if discontinued, most patients require colectomy -concomitant azathio/mercapto therapy results in decrease need for surgery |
|
what are the SE of cyclosporine?
|
-ACNE, HIRSUTISM, Gingival hyperplasia
-Hyperlipidemia, HTN -nephrotoxic -seizures, confusions, tremor -ND -diabetes |
|
what are the SE of tacro>?
|
-TREMOR, seizures, confusion
-ALOPECIA -ND -nephrotoxic -HTN -diabetes |
|
what are the therapeutic considerations for the immunosuppresants?
|
-therapuetic drug monitoring needed
-don't switch between formulations -adverse reaction decrease compliance -patients with low serum cholesterol levels may be better for tacro |
|
what are the biologic agents used in IBD?
|
MoAbs
-infliximab -adalimumab |
|
what is the mechanism of the biologic agents?
|
-neutralize proinflammatory cytokine TNK; activbates complement-mediated cytolysis of TNF-producing monocytes
|
|
what are biologic agents used for with IBD?
|
treatment of moderate to severe crohns
|
|
What are the SE of the biologic agents ?
|
-infusion-related reactions
-hypersensitivity |
|
whta are the therapeutic considerations for the biologic agents>
|
-may develop antibodies to infliximab: use steroids to reduce this
-smoking reduces the response of infliximab -discontinue with hypersensitivity -limited data for use in pediatric UC |
|
what are the additional agents for IBD?
|
-thalidomide
-mycophenolate |
|
what is the MOA of thalidomide?
|
inhibition of TNF production and angiogenesis
|
|
what is the MOA of mycophenolate?
|
suppresses lymphocyte prolif through an inhibition of DNA synthesis
|
|
what place does thalidomide have in therapy of IBD?
|
-restricted to corticosteroid dependent patients with CD
-results in improvements in clinical symptoms, biochemical papremeters, endoscopic/histo appearance, reduction in corticosteroid dose, and QOL |
|
what is the place in therapy for mychophenalate?
|
-Alternative to mercapto/azathio therapy
-conflicting data in regards to efficicay |
|
what are the SE of thalidomide>
|
-sedation
-peripheral neurop -constipation, rash, fatigue, and dizziness |
|
what are the SE for mycophenolate?
|
-DV, abd pain
-HTN -Headache -fever -infection |
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What does thalidomide cause that limits its use?
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congenital defects
-controlled studies have found use in CD is warranted |
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What alternative treatment has been found to help with UC, but not crohns>?
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nicotine therapy
-results based on onset of symptoms after smoking cessations in some individuals |
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what has enetral nutrition been found to do in IBD>?
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-induced disease remission in children with small bowel CD
-role in maintenance therapy in peds patients with CD -compliance concerns |
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what has been found with parenteral nutrition with IBD?
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-assists in treatment of severe disease
-allows bowel rest and remission -required in long-term therapy patients (short gut) |
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what have probiotics been found to do?
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-reestablish normal bacterial flora within the gut
-mixed success with IBD remission -potentially effective in preventing pouchitis |
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what is a curative approach for UC?
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surgery
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what is pouchitis?
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inflammation of the ileal pouch made during surgical intervention for UC.
need abx, probiotic therapy and removal and revert to ileostomy |
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what is a proctolectomy?
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permanent ileostomy
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describe surgery for crohns?
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needed for patients with strictures, fistulizing disease, abscesses formation, and extraintestinal complications
-resection of major intestinal area -colostomy placement -multiple surgical intervential usually required within 15years |