Exam 2 Flashcards
1
Q
N/V
Potential Etiologies:
A
Etiologies:
a. General N/V:
* Gastroenteritis(stomach flu): body bring to rid itself of harmful organisms
* Pancreatitis
- Disorders of balance
* motion sickness: vestibular system
* vertigo
* Dizziness - NVP (N/V of pregnancy)
* hyperemesis gravidarum (severe N/V) during pregnancy and weightloss>5% of pre-pregnancy body weight - Post operative N/V (PONV)
a: opioids/ anesthetics
b. Apfels risk score
* female- non smoker
- hx of motion sickness or previous PONV
- expected use of postoperative opioids.
* 1 pt for each criteria, higher the score, higher the risk
2
Q
N/V
Signs and Symptoms
A
Nausea-> Retching (dry heaving)->vomiting
3
Q
N/V
Acute complications
A
1.dehydration
2.electrolyte imbalances
(1&2 especially in kids)
3.esophageal tears
4. aspiration
5. malnutrition
4
Q
N/V
approach to management
A
- provide symptomatic relief
- identify and correct the underlying cause
- identify, prevent, and correct consequences/ complications that have occurred as a result
- prevent future occurrences
5
Q
N/V
General N/V therapies
A
- metaclopramide
- phenothiazines
- 5-HT3 (seretonin receptor) antagonists
6
Q
N/V
gastroenteritis
- quick self care overview
a. what is it (self care)
b.causes: (self care)
c. non pharm (self care and tpx)
* how to give
d. pharm (self care)
* how does it work
* how to give
A
- quick self care overview
a. what is it (self care): intestinal infection
b.causes: (self care)
most common viral (norovirus, rotavirus etc.), can also be bacterial
c. transmission: food borne, fecal-oral
c. non pharm (self care and tpx): oral rehydration salts ESPECIALLY IN PEDS!
* pedialyte
* <10 kg: 60-120 mL after each episode
* >10 kg: 120-140 mL after each episode
* mild to moderate: 50-100 mL/kg over 3-4 hrs
d. pharm (self care)
1. bismuth subsalicylate (PEPTOBISMOL)
* antisecretory and antimicrobial against bacterial and viral GI pathogen
* give 524 mg pm q30-60 min prn for uptimes to 2 days
* not indicated for <12. y.o
- phosphorated Carbohydrate solution (Emetrol)
15-30 mL once. may repeat q15 min until episode subsides .do not take for more than 1 hour.
7
Q
N/V associated with motion sickness
non pharm: (self care)
pharm: (self care and tpx)
A
non-pharm (self care:
- avoid reading during take
- focus on the line of vision fairly straight ahead
- stay where motion is least experienced
- avoid excess food or alcohol before and during extended travel
pharm:
ANTIHISTAMINES: H1 receptor antagonists
OTC:
*Meclizine (bonine) 25-50 mg 1 hr prior to travel. MDD 50 mg (less sedating)
*dimenhydrinate (dramamine) 50-100 mg 14-6h. MDD: 400 mg
8
Q
NVP
(nausea and vomiting of pregnancy)
non pharm (self care)
pharm (self care and tpx)
1.OTC
2.RX
A
non pharm:
*ensure fresh air
*eat several dry crackers and relax for 10-15 min prior to leaving bed
*eat 4-5 small meals per day
avoid greasy or fatty foods
* ginger
*acupuncture bands (sea band, bio band, relief band)
Pharm: self care and tpx: OTC *Doxylamine 12.5 mg TID-QID (antihistamine) *Pyridoxine 10-25 mg (vitamin b6 * usually use din combo (pyridoxine/ + doxylamine) *5HT3 antagonists *metaclopramide *prochlorperazine
9
Q
PONV
(Post operative nausea and vomiting)
therapies based on apfels score
what happens if the therapy doesn’t work
A
using Apfels criteria
score
4- high risk:
*scopolamine patch. apply 2 hr prior to anesthesia
* IV dexamethesone after anesthesia induction
* 5HT3 antagonist @ end of surgery
2-3 moderate risk:
*5T3 antagonist @ end of surgery
=1 Low risk:
*no therapy needed
doesn’t mean that this is definitive. if needed, rescue therapies can be use such as…
- 5HT3 antagonists
- choose a drug of a different class (i.e metaclopramide, phenothiazine etc.)
10
Q
N/V Therapies specific
antihistamines indication examples
H1 antagonists
H2 antagonists;
A
H1 antagonists:
indication: disorder of balance, NVP
ex:
1. dimenhydronate
- diphenhydramine
- meclizine
- doxylamine
a. OTC generally but also available as rx for NVP called declegis (delayed release) or bonjesta (extended) coformulated with b6. - scopolamine
a. (transdermal patch)
b. applied on ear q72hr
6.Hydroxyzine
H2: N/V associated w. over eating
ex: ranitidine, famotidine
11
Q
N/V Therapies specific
H1 antihistamine adverse effects
A
sedation
dry mouth
constipation
paradoxical effect
insomnia
irritability
12
Q
N/V Therapies specific
phenothiazines
moa:
indications
ex and dosage forms
A
moa: inhibit dopaminergic, histamine, and muscuranic receptors
indication: general N/V, rescue PONV, lower line therapy for NVP
ex: promethazine Prochlorperazine Chlorpromazine *dosage forms: PO, IM(deep IM preferred route),IV (can cause tissue damage), prochlorperazine also available as rectal supp.
13
Q
N/V Therapies specific
phenothiazines
adverse effects
A
tissue damage
hypotension: esp if IV. make sure it is given slow IV push, pt must lie down for at least 30min after administration
QT prolongation:
dystonia (
extrapyramidal symptoms (i.e tardive dyskenesis)
14
Q
N/V Therapies specific
5HT3 antagonists
moa
indications
ex
A
moa: inhebt 5ht3 receptors in the gut
indications: general N/V, PONV, lower line in NVP
ex:
ondansetron (zofran): used the most. available po, IV, and oral dissolving tab (ODT)
dulasetron
granisetron
palonosetron
15
Q
N/V Therapies specific
5ht3 side effets
A
constipation
headache
qt prolongation
16
Q
N/V Therapies specific
prokinetics
indication
moa
ex:
A
indication: gastroparesis
- metaclopramide
* moa: d2 antagonists. also helps increase speed of gastric emptying
* indication: General N/V, rescue PONV, gastroparesis,lower line in NVP.
* first line therapy for diabetic gastroparesis - erythromycin
* gastroparesis (2nd line)
* work on motion receptors
17
Q
N/V Therapies specific
pro kinetic side effects
A
- metaclopramide
AE: extrapyramidal symptoms, dystonia (esp. if IV), QT prolongation, diarrhea - erythromycin: N/V, diarrhea, QT prolongation
18
Q
N/V therapies specific
corticosteroids
indication
MOA:
side effects
A
- dexamethasone
indication: PONV
moa: largely unknown
AE:
short term use
agitation
insomnia
increased appetite
hyperglycemia
19
Q
Diarrhea
what is it
criteria
risk factors
potential etiologies
diarrhea associated symptoms
A
what is it: abnormal increase in frequency, liquidity or weight
> 3bm/ day abnormal
risk factors: day care exposure food handling close quarters immunosupression diverticular disease
potential etiologies: infectious diarrhea (viral or bacterial transmitted via fecal oral route or food borne) 2.food borne gastroenteritis/ diarrhea 3. travelers diarrhea 4. medication: ABX, chemo, 5. food intolerance (like lactose) 5. inflammatory bowel syndrome (IBD) 6. irritable bowel syndrome - (IBS) 7.
Diarrhea associated symptoms:
- N/V
- abdominal cramping
- stool characteristics
- fever
- dehydration
- qnorexia
20
Q
Therapy for diarrhea
- OTC (self care)
- RX (tpx)
A
OTC:
1. Oral rehydration solution (pedialyte): ESP. IN PEDS
6mo-5 yo. 100-150 ml/kg over 3-4 hrs
>5 y.o 2-4L over 3-4 hrs
generally ors not needed for adults w. diarrrhea
- Loperamide OTC
* opioid derivatives
* act on mu and gamma receptors in the gut, delays transit - Bismuth salicylate (peptobismol):
* antimicrobial effects
* salicylate has antisecretory effects
* black staining of stool and tongue - probiotics
* can help with infectious diarrhea - digestive enzymes (Lactaid)
* lactose intolerance
RX
- Diphenoxylate (with atropine)
* limited abuse potential
* donot use in pplwith bacterial gastroenteritis b/cus u don’t want to trap bacterial pathogen in GI tract
* used in IBD - Octreotide
* moa: somatostatin analog->reduces intestinal secretion, which reduces idea
* used in intestinal carnicoid tumors, chemo induced diarrhea
* given SQ initially, then pt converted to IM depot injection
21
Q
who is not a candidate for self care of diarrhea
A
< 6 months old
pregnancy
severe dehydration
high fever (39 C or 102.2 F
protracted vomiting
blood, mucus, or pus in stool
severe abdominal pain
DM, CHF
immunosuppression
diarrhea lasting > 14 days
recent ABX use
22
Q
Constipation
what is it
risk factos
SS
A
what is it
decreased frequency of bowel movements (< 3 BM/ week
risk factors: older age, female, pregnancy, highly processed diet (no fiber sedentary lifestyle drugs (opiates, anticholinergic, TCAs, Parkinson's meds, iron, Calcium channel blocker) comorbidities, IBS, DM, hypothyroid
SS: hard dry stool
staring to pass a stool
passage of a small stool
feelings of incomplete bowel evacuation
23
Q
Constipation treatment
lifestyle changes (self care)
OTC options (self care)
Rx (tpx)
A
lifestyle (self care): water fiber exercise establish a bowel regimen
OTC options:
- bulk-forming laxatives:
ex: *psyllium seed husks(metamucil)
* calcium polycarbophil (fiber con)
* methylcellulose (citrucel)
moa: increases absorption of water in the small and large intestine to create a viscous like gel. fluid ingestion is crucial. avoid us win chf
- emollient laxatives: doccusate (colace) po.
stool softener, increases water content of stool. best for hard stool complaints, not infrequent stool completes. CAN BE USED IN PREGNANCY
3.hyperosmotic laxatives
*polyethylene glycol 3350 (miralax): large poorly absorbed molecules that draw water into the colon
PO and rectal. INCREASES FREQUENCY
- stimulant laxatives
* sennosides, senna (senokot) PO, Bisacodyl (Dulcolax) direct stimulant
moa: direct stimulant on colonic mucosa (stimulates myenteric plexus) - saline laxatives (magnesium citratePO, milk of magnesia PO)
pulls fluid into intestines increasing intraluminal pressure
6.lubricant laxatives (mineral oil)
RX
- Osmotic
* PEG3350 (miralax)
* Lactulose- nonabsorbale sugar metabolized by colonic bacteria. used in hepatic encephalopathhy for cirrhosis
* tastes really sweet - chronic idiopathic constipation
a. Lubiprostone (amities): 24 mcg PO
b. lanaditide <45 mcg daily po
c. placanatide : 3mg po daily - opiod receptor antagonists
* used for opioid induced constipation
a. methylnaltrexone (resistor) SQ
b. naloxigol (movantile) po
c. Naldenedine (symproic) po
24
Q
Irritable bowel syndrome (IBS)
what is it
criteria
SS
causes
A
what is it: GI syndrome characterized by chronic abdominal pain with altered bowel habits
criteria for dx: Rome IV criteria
*@least 1 day recurrent abdominal pain in last 3 months associated with defecation, change in frequency, or change in form/appearance. ATLEAST 2 OF THESE
most commonly dx gi condition
symptoms:
abdominal pain
bloating
decrease in bowel habits\
causes: gut hypersensitivity contributing factors *genetic *motility factors *colonic infection (gastroenteritis, bowel flora) *psychological factors
25
Irritable bowel syndrome (IBS)
treatment approach
based on IBS subtype
1. IBS-C (constipation dominant)
2. IBS-D (diarrhea dominant)
3. IBS-M mixed
only type c and d have approved therapies
26
Irritable bowel syndrome (IBS)
IBS -C characteristics
predominantly having type 1 (separate hard lumps, like nuts) and type 2 (sausage shaped but lumpy) bowel movement types >25% of the time. and types 6 &7 stool < 25% of the time
27
Irritable bowel syndrome (IBS)
IBS-D charcateristics
predominantly having type 6 (fluffy pieces of ragged edges mushy stool) and type 7 (watery, no solid pieces, entire liquidity) >25% of the time and types 1 and 2 <25% time
28
Irritable bowel syndrome (IBS)
IBS M
have a mix of both types 1 and 2, as well as 6 and 7 > 25% of the time
29
Irritable bowel syndrome (IBS)
goals of IBS treatment
1. improve the stool frequency and consistency
| 2. improve global symptoms (abdominal pain, bloating, reductions in QOL)
30
Irritable bowel syndrome (IBS)
IBS-C treatment
FIRST LINE
1. Lubiprostone (Amitiza)
moa: activates chloride channel on epithelium, increasing CL-secretion. increasing motility
approved in women only
8mg BID w. food to decrease diarrhea and nausea
2. secretagogues:
linaclotide(Linzess) + Plecanatide (tuulance)
moa: increase secretion of chloride and bicarb. increase motility
linzess: 290 mcd qd PO
tulane: 3 mg po qd
AE: diarrhea
if pt hasnt responded to first line therapy
3. tegaserod: 5ht4 agonist.
moa: increased gi secretion,
decreased visceral pain.
caused an increased in cardiac events in pl with preexisting risk factors. so now its use recommended in...
*women <65 y.o w. out cardiac history and = 1 cv risk factor such as
HTN, smoking, BMI>30, DM,HLD, age > 55
31
Irritable bowel syndrome (IBS)
IBS-D treatment
firstline
1. rifaxim (Xifaxn): abx
SIBO small intestinal bacterial overgrowth
*14 day course of therapy. 550 mg TID po
can be repeated up to twice within a year
2. Eluxadoline (Vibrezi)
moa; mu agonist/ delta antagonist: inhibits bowel contraction
can cause sphincter of ddi dysfunction
CI: in pts with hx of pancreatitis, w.o a gallbladder, hx of alcoholism, pts who ingest 3 or more alcoholic beverages a day
second line
3. Alosetron: 5HT3 antagonist
mao: slow transit time, slow movement of fecal water, increase water absorption
can cause severe constiation + ischemic colitis. REMS program-
indication: women who have failed conventional therapy w. IBS-D
d/c if no improvement after 4 weeks of therapy
32
Irritable bowel syndrome (IBS)
IBS treatment
any subtype treatment
antidepressants:
1.Tricyclic antidepressants (TCA's)
*amitriptyline-50-100 mg qd
*Nortriptyline-25-75 mg qd
help treat pain and global symptoms of IBS
start @10 mg daily due to antihistaminic side effects
side effects: sedation, drowsiness, dry mouth, anticholinergic se profile, constipation
2. soluble fiber-IBS-C would probably be more beneficial, but trials found it could be used for both
* soluble fiber(dissolves and pulls water into gut, creating gel, resists colonic fermentation causing gas): psyllium, oat bran, barley, brans.
SOLUBLE FIBER IS RECOMMENDED FOR IBS
*insoluble(doesn't dissolve,bulks stool, fermented by bacteria causing gas and bloating) causing : wheat bran, whole grain, vegetables
33
Irritable bowel syndrome (IBS)
IBS NON pharm treatment (can be used n any subtype)
psychotherapy
counseling
relaxation (stress management techniques),
hypnosis,
cognitive behavioral treatment
34
Gastro esophageal reflux disease (GERD)
key symptom:
* heart burn >3 months and /or refractory to OTCs therapies
* dyspepsia: paint bra line, burning, fullness, bloating, gnawing, early satiety.
dx: symptoms, trial therapy, endoscopy (esophagitis, barretts's)
35
Self treatment for heartburn
lifestyle modifications
antacids
H2RA's
PPIS
36
GERD treatment goals
how is it achieved (what is the treatment)
relieve symptoms
heal damaged mucosa
prevent complications
achieved by using PPI x8 weaks
chronic PPI in setting of GERD
*complications present such as damaged mucosa or barretts
*symptoms return in PPI d/c- must titrate to lowest effective dose or prn
( can also use H2RA or antacids for episodic relief )
37
why must you limit PPI therapy in use of gerd
limit adverse effects such as increased risk of infections (C.Diff, pneumonia,) renal injury (Aki, cod), THROMBOCYTOPENIA, cns EFFECTS, osteoporosis and fracture risk (b/c decrease calcium absorption)
38
lifestyle modifications of GERD
small frequent meals
remain upright after/ during eating
dont eat before bed or atleast 3 hours before
avoid trigger foods (spice , fried/high fat, caffeine, alcohol)
weightloss
smoking cessation
prop the head of the bed using a foam wedge
avoid tight fitting clothing
39
Peptic Ulcer Disease (PUD)
types:
depth
complications
SS
effect of food
causes
imbalance between mucosal defense and corrosive mechanisms
types:
1. gastric
2. duodenal
depth:
1. superficial (protrudes into the GI wall no deeper than the lamina propria) (gastritis duodenitis)
complications of PUD: gi bleed
Sign and symptoms
dyspepsia associated with food
Duodenal ulcer(du)-food helps
*Most common 2/3 DU pts report pain btw 12-3 am
gastric ulcer: FOOD WORSENS
causes:(causes ulcers) H. Pylori, NSAIDS
critical illness, alcohol use(gastritis)
40
PUD
H. pylori gram
dx
gram negative rod
#1 cause of PUD
usually causes gastritis but 10-15% of pts develop ulcers due to oh pylori due to differences in bacteria and host
causes more DU than GU.
H. Pylori can escape acid killing due to spiral shape, flagellum, adherance pedestal, and conversion of urea to ammonia and bicarb to protect itself from acid (buffering), produce lipase and proteases, to
dx:
1. invasive measures
*endoscopyDX
*tissue sample h. pylori culture
2. non invasive
*bloodtestsDX
*urea breath testsERADICATION
*fecal antigen testERADICATION
for eradication: wait 4 weeks after therapy is completed
41
h. pylori treatment goals
ACID SUPRESSION
relieve pain
heal ulcer
ABX
prevent recurrence
elimante h pylori.
42
h. pylori tripple therapy
traditionally was
* PPI BID
* clarithromycin 50 mg bid
* amoxicillin 1 gram bid
```
NOW PREFERRED
bismuth quadruple therapy
*PPI BID
*Bismuth subsalicylate or subsitrate QID
*tetracycline 500 mg QID
*metronidazole QID
*more first line due to increasing macrolide resistance)
```
Levofloxacin based tripple therapy
*PPI BID
levofloxacinQD
amox 1g BID
PCN allergy?
bismuth quad therapy work
treatment length: 10-14 but closer to 14. confirm eradication with urea breath test or fecal antigen test
*note: tetracycline and bismuth have interaction but b/cus in PUD the indications are for the stomach and not systemic, interaction doesn't effect the stomach where they will be doing their job
43
NSAID INDUCED PUD
said said toxicity #1 drug related toxicity in the US
44
epithelial affects due to prostaglandin depletion by nsaids
```
INCREASE HCL SECRETION
decrease mucin secretion
decrease HCO3 secretion
decreased surface active phospholipid secretion
decreased epithelial cell proliferation
```
45
risks for nsaid PUD
age >65
previous hx ulcer
contaminant use of steroid
selectivity (non selective COX)
* *note: selective(COX2) are celecoxib
* *some cox 2 selective: meloxicam, etodulac, nabumetone
anticoagulation
antiplatelets
if p has 1 of these risk factors, might want to consider use of ppt chronically
also if pt requires baby ASA, plavix, require daily NSAID regimen
46
diagnosis of said induces PUD
dyspepsia
NSAID taking history
endoscopy
47
NSAID induced PUD treatment
atleast 4 weeks PPI daily
up to 8 weeks or even ironically long tern if pt continues NSAIDS
48
nsaid induced PUD prevention
switch to APAP
add PPI w. NSAID
add misoprostol to nsid (prostaglandin analog)
use cox2 selective NSDAID
49
stress related mucosal bleeding related to critical illness (SRMB) OR (SRMD)
altered defense mechanisms
reductions in blood flow to GI tract (mucosa)
release of damaging mediators (cytokines, free radicals, etc. )
50
stress related mucosal bleeding related to critical illness (SRMB) OR (SRMD)
risk factors
MAJOR
1. resp. failure (ventilator for >/= 48hrs)
2. coagulopathy
* inR > 1.5
* platelets < 50
only need to have 1 major risk factor
minor (need 2 or more)
* sepsis
* hypotensive require pressors
* hx GI bleeding
* use of high dose steroids >250mg/day of hydroquartisone equivalents
if they meet criteria, they need stress ulcer prophylaxis until risk factors are gone (when pt leaves the ICU)
51
stress related mucosal bleeding related to critical illness (SRMB) OR (SRMD)
prophylaxis
H2RAs (PPi's less favorable b/c they have increased infection risk)
52
Zollinger Ellison Syndrome
gastrin producing tumor
causes recurrent ulcers
treatment : PPI q8-12 hours
53
upper GI bleeding (UGIB)
```
suspected in:
hematemesis
melena
NSAID users
hx of PUD
```
```
pts present w.
epigastric pain
dyspepsia
some pts. can be asymptomatic
tachycardic
hypotensive
low hgb/hct
```
54
upper GI bleeding (UGIB) treatment
achieve hemodynamic stability
*IV Bolus NS/ lactated ringers
*restore bloodloss (packed rbc for plasma expansion)
1 unit ~ 1 point increase in hgb
target to get hgb>7
*supplemental oxygen 92%
*reverse anticoagulant
*fresh frozen plasma (ffp) has clotting factors
```
2.endoscopy:
local targeted therapies
*epinephrine
*targeted contact thermal therapy
* if don't do endoscopic treatment, have a 50% rebleed rate
```
3. Acid suppression
* usually b4 endoscopy
* high dose short term IV therapy
* IV 80 mg bolus of pantoprazole or esomeprazole, then 9 mg 1 hr infusion for x72 hr
4. oral daily PPI after iv PPI therapy
55
upper gi bleed while on ASA, and other p2y12 inhibitor like ticagrelor/ clopidogrel etc.
evaluate risk vs benefit
A.*for post stent pt, cardiac risk outweighs GI bleeding risk
*resume agents after making sure hgb is stable
*antiplatelet needs to be resumed within 7days, esp. 1-3 days
B.*for pt on ASA daily with no cv risk (primary prevention). D/C ASA bc risk of gi bleed outweighs risk of cardiac event
56
Inflammatory Bowel Disease (IBD)
what is it
results in what
general treatment requirements
chronic inflmmatory disease of the gi tract
results in edema, ulceration, tissue destruction
relapsing and remitting in nature
treatment requires flare therapy 9active disease therapy) and maintenance therapy which helps prevent flare recurrence
57
types of IBD
ulcerative colitis and chrons disease
58
patho of IBD
pts have defectivese mucosa genes, leaky junction which allow things to flow into lamina propria. tigers antigen presenting cell to mount an immune response.
causes tissue destruction and inflammation.
low t regular cells and too many t helper cells.
59
SS of ibd
Diarrhea
blood in stool
abdominal pain
weight loss
fatigue
change in daily activities
60
dx of IBD
symptoms
lab tests : increase ESR, CP
stool studies: leukocytes, lactoferrin, calprotectin ( oninvasie marker of ibd),
endoscopy (colonoscopy), ct scan, MRI
MAIN THING IS ENDOSCOPY
61
IBD disease location
ulcerative colitis: confined to rectum and colon.
can move up overtime if not treated. extent of disease matters
if just has recutum, its called proctitis.
left sided distal colitis: goes up the descending colon up to the sphelnic flexure.
extended disease: past the sphlenic disease.
does not include anus
have continues superficial inflammation
Chrons disease: from mouth to anus
* 2/3 of pts have it in terminal ileum
* more perineal involvement
* deep penetration, but patchy, cobblestone like
62
complications of IBD
uc: toxic megacolon, colon cancer, colectomy (removal bowel). only curative modality for UC is surgery
chrons disease: malnutrition, vitamin deficiency, strictures, fistulas that connect bowel to bladder, other pets of gi tracts, etc.-> might need surgery/drainage to deal with this.
disease cannot be cured with surgery
63
IBD drug treatment options
5-Aminosalicylates
* sulfasalazine
* Meesalamine
* Alsalazine
* Balsalazide
Immunomodulator
* azathioprine
* 6-mercaptopurine
* methotrexate
* cyclosporine*tacrolimus
ABX
* metronidazole
* ciprofloxacin
Corticosteroids
* prednisone
* methylprednision
* hydrocortisone
* budesonide
Biologics
* inflixamab
* adalimumab
* certolizumab
* Golimumab
* natalizumab
* vedolizumab
* ustekinumab
* tofacitinib
64
IBD treatment
5 amino salicylic acid 5-ASA
moa: act to reduce inflammation in gi tract. (aka aspirin for the gut lol) decrease prostaglandins, leukotrienes and the rproinflammatory cytokines through COX
require multiple daily dosages
must need to get to intestine but py bassing absorption. need a carrier to large intestine because it is readily absorbed in small intestine
65
ex of 5-ASA
sulfasalazine
1. Sulfasalazine
cleaved by colonic bacteria to sulfa and 5 asa moieties
sulfa is the carrier, 5-asa active component
sulfa is responsible for ADR. GI, rash, photosensitivity, blood dycrasias
frequent dosing
66
ex of 5-ASA
olsalazine
two 5 asa linked together and cleaved by gut so no sulfa moiety
better tolerated than sulfasalazine but still has diarrhea but not generic available
less frequent dosing
67
ex of 5-ASA
balsa;azide (colazal)
sulfalazine without the sulfa
lots of drug to take . 3 725 mg product)
68
ex of 5-ASA
mesalamine
available in oral(delayed/controlled)
and rectal:
* enema: can reach rectum and go up distal colon
* supp. can only stay at rectum
olsalazine can release in terminal ileum
asacol can release in ileum
pentasa can release in jejunum. DO NOT USE IN CHRONS DISEASE
69
Immunomodulators
maintain therapy remission
1. 6-mercaptopurine 6-MP)
2. azathioprine: mainly used. can be used for UC or chrons disease. can take 4 months to full effect
3. methotrexate
70
immunomodulator monitorinf
cbc q3 mo: bone marrow suppression possible
lots and pancreatic enzymes *hepatotoxicity
*pancreatitis (6 MP/aza)
Lymphomas`
71
corticosteroids for IBD
work to quickly decrease inflammation
72
budesonide for IBD
used because allows for more local with less systemic side effects
has a enteric coat capsule:
*stimulated for releas ein Terminal Ileum: Entocort (for use in chrons disease)
released throughout colon (Uceris) formulated for ulcerative colitis
should be eventually tapered off
73
biologics for IBD
anti tnfs
infixamab IV
adalminumab sc
certolizumab sc
golimumab SC
selective adhesion molecule (intern) inhibitor
natalizumab IV
vedolizumab IV
IL-12, IL23 inhibitor
*ustekinumab IV
JAK inhibitor
*tofacitinib oral
74
infusion related reactions of biologics (all IV products)
acute(1-2 hrs): headache, dizziness, nausea, flushing, fever, chest pain, cough, dyslexia, pruritis
delayed: 3-14 days: myalgia, fever, rash, pruritis,
sq: injection site reactions
75
BBW for TNF-A inhibitors and JAK
infections
* active tuberculosis
* assessment of HBV
* note; pts on biologic should not get a live vaccination
* malignancy (TNF inhibitors)
76
natalizumab AE
PROGRESIVE MULTIFOCAL LEUKOCEPHALAPOTHY (pml)
fatal
must be admin as mono therapy
last line therapy
77
ABX in IBD
metronidazole
ciprofloxacin
best for perianal (fistulas, fissures) so basically chrons disease
78
goals of therapy for IBD
reduce or eliminate. SS
reduce inflammation
keep pts out of hospital
```
Induce remission (treat flare)
maintain remission
```
79
chrons disease severity
remisson: asymptomotmatic
mild to moderaye: ambulatory, no abdominal pain, fever or extreme weightloss (<10)
moderate to severe: failed mild-mod diseae, fever >38, ?10% weightloss, and pain, N/V w o obstruction, anemia
severe tp fulminant
persistent symptoms despite steroid or biologic therapy, requires int stay. severe abdominal pain, not eating
80
cd treatment
active therapy
active therapy
1. mild-mod:
* po budesoinde x 8 weeks
* 5-ASA not used unless sulfasalazinecolonic involvement
2. mod-severe
* if budesonide doesn't work after 4 weeks,
* po prednisone
* biologic therapy (infliximab first line)
* can try other biologics if not getting symptom relief within 2-4 weeks
* steroid or biologic cane used with azathioprine. all take several months to work, but canreduce steroid dose and can increase response in biologic therapy
3. severe fulminate
* surgery
* IV steroids
* IV infliximab if personhavet used infliximab.
perianal disease: fistulas or fissures, can use ABX, not any other time
81
maintenance therapy for chrons diseas
maintenance
1stline: 6-MP/AZA/MTX take for 4 months until full effect
other options-budesoinde can be used 3 months
biologics:
82
ulcerative colitis
active vs maintenance SS
remission:
formed stools
no bleed
hgb normal
mild:
less than 4 stool per day
intermittent stools with blood
gi normaL
```
mod-severe
> 6 STOOLDS /DAY
hgb <75% normal
cap
ear, cap
frequent blood in stool
```
Fulminant
>10stools per day
continuous blood in stool
83
UC active disease
mild
a. distal
* topical 5-ASA supp or enema
* 2nd line: oral 5-ASA or combo oral and rectal
* if those don't work, cause budesonide
b.extensive:
oral 5-ASA +/- budesonide
MODERATE:
a. distal and extensive
* budesonide
* prednisone
* biologic +/- 6-MP/AZA
fulminant disease
a. distal and extensive
* IV STEROID
* IV INFLIXIMAB
* IV CYCLOSPORINE
* SURGERY COLECTOMY
84
UC maintenance disease therapy
```
mild
a: distal
*topical 5-ASA (mesalamine)
or po 5-ASA
b. extensive
*oral ASA
```
mod-severe or fulminant:
* depends on what induced your remission
* if budesonide induced rem. use 6-MP/AZA
* if biologic continue biologic + AZA
* if cyclosporine, use 6-MP/AZA
85
which tnf-a inhibitors used for what disease
```
Anti-TNF
Inflixamab → Crohn’s, UC,
Adalimumab → Crohn’s, UC
Certolizumab → Crohn’s,
Golimumab → UC
```
86
biologic indications
```
Anti-TNF
Inflixamab → Crohn’s, UC,
Adalimumab → Crohn’s, UC
Certolizumab → Crohn’s,
Golimumab → UC
Selective adhesion molecule (integrin)inhibitor
Natalizumab → Crohn’s
Vedolizumab → Crohn’s, UC
IL-12, IL-23 inhibitor
Ustekinumab → Crohn’s, UC
JKA Inhibitor
Tofacitinib → UC
```
87
how to remember biologic indications
Certolizumab: chrons
Golimumab: UC
Natalizumab: chrons
Tofacitinib: UC
everything else, indicated for both
