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TPX: Opthal/Derma/Nutrition/GI > Exam 2 > Flashcards

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

  1. Disorders of balance
    * motion sickness: vestibular system
    * vertigo
    * Dizziness
  2. NVP (N/V of pregnancy)
    * hyperemesis gravidarum (severe N/V) during pregnancy and weightloss>5% of pre-pregnancy body weight
  3. 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
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2
Q

N/V

Signs and Symptoms

A

Nausea-> Retching (dry heaving)->vomiting

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3
Q

N/V

Acute complications

A

1.dehydration
2.electrolyte imbalances
(1&2 especially in kids)
3.esophageal tears
4. aspiration
5. malnutrition

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4
Q

N/V

approach to management

A
  1. provide symptomatic relief
  2. identify and correct the underlying cause
  3. identify, prevent, and correct consequences/ complications that have occurred as a result
  4. prevent future occurrences
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5
Q

N/V

General N/V therapies

A
  1. metaclopramide
  2. phenothiazines
  3. 5-HT3 (seretonin receptor) antagonists
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6
Q

N/V

gastroenteritis

  1. 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
  1. 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

  1. phosphorated Carbohydrate solution (Emetrol)
    15-30 mL once. may repeat q15 min until episode subsides .do not take for more than 1 hour.
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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

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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
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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…

  1. 5HT3 antagonists
  2. choose a drug of a different class (i.e metaclopramide, phenothiazine etc.)
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10
Q

N/V Therapies specific

antihistamines indication examples

H1 antagonists
H2 antagonists;

A

H1 antagonists:
indication: disorder of balance, NVP

ex:
1. dimenhydronate

  1. diphenhydramine
  2. meclizine
  3. doxylamine
    a. OTC generally but also available as rx for NVP called declegis (delayed release) or bonjesta (extended) coformulated with b6.
  4. scopolamine
    a. (transdermal patch)
    b. applied on ear q72hr

6.Hydroxyzine

H2: N/V associated w. over eating
ex: ranitidine, famotidine

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11
Q

N/V Therapies specific

H1 antihistamine adverse effects

A

sedation

dry mouth

constipation

paradoxical effect

insomnia

irritability

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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.
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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)

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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

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15
Q

N/V Therapies specific

5ht3 side effets

A

constipation

headache

qt prolongation

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16
Q

N/V Therapies specific

prokinetics

indication
moa
ex:

A

indication: gastroparesis

  1. 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
  2. erythromycin
    * gastroparesis (2nd line)
    * work on motion receptors
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17
Q

N/V Therapies specific

pro kinetic side effects

A
  1. metaclopramide
    AE: extrapyramidal symptoms, dystonia (esp. if IV), QT prolongation, diarrhea
  2. erythromycin: N/V, diarrhea, QT prolongation
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18
Q

N/V therapies specific

corticosteroids

indication
MOA:
side effects

A
  1. dexamethasone
    indication: PONV
    moa: largely unknown

AE:
short term use

agitation
insomnia
increased appetite
hyperglycemia

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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:

  1. N/V
  2. abdominal cramping
  3. stool characteristics
  4. fever
  5. dehydration
  6. qnorexia
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20
Q

Therapy for diarrhea

  1. OTC (self care)
  2. 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

  1. Loperamide OTC
    * opioid derivatives
    * act on mu and gamma receptors in the gut, delays transit
  2. Bismuth salicylate (peptobismol):
    * antimicrobial effects
    * salicylate has antisecretory effects
    * black staining of stool and tongue
  3. probiotics
    * can help with infectious diarrhea
  4. digestive enzymes (Lactaid)
    * lactose intolerance

RX

  1. 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
  2. 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
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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

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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

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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:

  1. 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

  1. 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

  1. stimulant laxatives
    * sennosides, senna (senokot) PO, Bisacodyl (Dulcolax) direct stimulant
    moa: direct stimulant on colonic mucosa (stimulates myenteric plexus)
  2. saline laxatives (magnesium citratePO, milk of magnesia PO)
    pulls fluid into intestines increasing intraluminal pressure

6.lubricant laxatives (mineral oil)

RX

  1. Osmotic
    * PEG3350 (miralax)
    * Lactulose- nonabsorbale sugar metabolized by colonic bacteria. used in hepatic encephalopathhy for cirrhosis
    * tastes really sweet
  2. chronic idiopathic constipation
    a. Lubiprostone (amities): 24 mcg PO
    b. lanaditide <45 mcg daily po
    c. placanatide : 3mg po daily
  3. opiod receptor antagonists
    * used for opioid induced constipation
    a. methylnaltrexone (resistor) SQ
    b. naloxigol (movantile) po
    c. Naldenedine (symproic) po
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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
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25
Q

Irritable bowel syndrome (IBS)

treatment approach

A

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

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26
Q

Irritable bowel syndrome (IBS)

IBS -C characteristics

A

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

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27
Q

Irritable bowel syndrome (IBS)

IBS-D charcateristics

A

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

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28
Q

Irritable bowel syndrome (IBS)

IBS M

A

have a mix of both types 1 and 2, as well as 6 and 7 > 25% of the time

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29
Q

Irritable bowel syndrome (IBS)

goals of IBS treatment

A
  1. improve the stool frequency and consistency

2. improve global symptoms (abdominal pain, bloating, reductions in QOL)

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30
Q

Irritable bowel syndrome (IBS)

IBS-C treatment

A

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

  1. 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

  1. 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
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31
Q

Irritable bowel syndrome (IBS)

IBS-D treatment

A

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

  1. 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

  1. 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

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32
Q

Irritable bowel syndrome (IBS)

IBS treatment
any subtype treatment

A

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

  1. 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

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33
Q

Irritable bowel syndrome (IBS)

IBS NON pharm treatment (can be used n any subtype)

A

psychotherapy

counseling

relaxation (stress management techniques),

hypnosis,

cognitive behavioral treatment

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34
Q

Gastro esophageal reflux disease (GERD)

A

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)

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35
Q

Self treatment for heartburn

A

lifestyle modifications

antacids

H2RA’s

PPIS

36
Q

GERD treatment goals

how is it achieved (what is the treatment)

A

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
Q

why must you limit PPI therapy in use of gerd

A

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
Q

lifestyle modifications of GERD

A

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
Q

Peptic Ulcer Disease (PUD)

types:

depth

complications

SS

effect of food

causes

A

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
Q

PUD

H. pylori gram

dx

A

1 cause of PUD

gram negative rod

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
Q

h. pylori treatment goals

A

ACID SUPRESSION
relieve pain
heal ulcer

ABX
prevent recurrence
elimante h pylori.

42
Q

h. pylori tripple therapy

A

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
Q

NSAID INDUCED PUD

A

said said toxicity #1 drug related toxicity in the US

44
Q

epithelial affects due to prostaglandin depletion by nsaids

A 
INCREASE HCL SECRETION
decrease mucin secretion
decrease HCO3 secretion
decreased surface active phospholipid secretion 
decreased epithelial cell proliferation
45
Q

risks for nsaid PUD

A

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
Q

diagnosis of said induces PUD

A

dyspepsia
NSAID taking history
endoscopy

47
Q

NSAID induced PUD treatment

A

atleast 4 weeks PPI daily

up to 8 weeks or even ironically long tern if pt continues NSAIDS

48
Q

nsaid induced PUD prevention

A

switch to APAP

add PPI w. NSAID

add misoprostol to nsid (prostaglandin analog)

use cox2 selective NSDAID

49
Q

stress related mucosal bleeding related to critical illness (SRMB) OR (SRMD)

A

altered defense mechanisms

reductions in blood flow to GI tract (mucosa)

release of damaging mediators (cytokines, free radicals, etc. )

50
Q

stress related mucosal bleeding related to critical illness (SRMB) OR (SRMD)

risk factors

A

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
Q

stress related mucosal bleeding related to critical illness (SRMB) OR (SRMD)

prophylaxis

A

H2RAs (PPi’s less favorable b/c they have increased infection risk)

52
Q

Zollinger Ellison Syndrome

A

gastrin producing tumor

causes recurrent ulcers

treatment : PPI q8-12 hours

53
Q

upper GI bleeding (UGIB)

A 
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
Q

upper GI bleeding (UGIB) treatment

A

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
  1. 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
  2. oral daily PPI after iv PPI therapy
55
Q

upper gi bleed while on ASA, and other p2y12 inhibitor like ticagrelor/ clopidogrel etc.

A

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
Q

Inflammatory Bowel Disease (IBD)

what is it

results in what

general treatment requirements

A

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
Q

types of IBD

A

ulcerative colitis and chrons disease

58
Q

patho of IBD

A

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
Q

SS of ibd

A

Diarrhea

blood in stool

abdominal pain

weight loss

fatigue

change in daily activities

60
Q

dx of IBD

A

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
Q

IBD disease location

A

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
Q

complications of IBD

A

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
Q

IBD drug treatment options

A

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
Q

IBD treatment

5 amino salicylic acid 5-ASA

A

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
Q

ex of 5-ASA

sulfasalazine

A
  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
Q

ex of 5-ASA

olsalazine

A

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
Q

ex of 5-ASA

balsa;azide (colazal)

A

sulfalazine without the sulfa

lots of drug to take . 3 725 mg product)

68
Q

ex of 5-ASA

mesalamine

A

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
Q

Immunomodulators

A

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
Q

immunomodulator monitorinf

A

cbc q3 mo: bone marrow suppression possible

lots and pancreatic enzymes *hepatotoxicity
*pancreatitis (6 MP/aza)

Lymphomas`

71
Q

corticosteroids for IBD

A

work to quickly decrease inflammation

72
Q

budesonide for IBD

A

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
Q

biologics for IBD

A

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
Q

infusion related reactions of biologics (all IV products)

A

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
Q

BBW for TNF-A inhibitors and JAK

A

infections

  • active tuberculosis
  • assessment of HBV
  • note; pts on biologic should not get a live vaccination
  • malignancy (TNF inhibitors)
76
Q

natalizumab AE

A

PROGRESIVE MULTIFOCAL LEUKOCEPHALAPOTHY (pml)

fatal

must be admin as mono therapy

last line therapy

77
Q

ABX in IBD

A

metronidazole
ciprofloxacin
best for perianal (fistulas, fissures) so basically chrons disease

78
Q

goals of therapy for IBD

A

reduce or eliminate. SS
reduce inflammation
keep pts out of hospital

Induce remission (treat flare)
maintain remission
79
Q

chrons disease severity

A

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
Q

cd treatment

active therapy

A

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
Q

maintenance therapy for chrons diseas

A

maintenance

1stline: 6-MP/AZA/MTX take for 4 months until full effect

other options-budesoinde can be used 3 months

biologics:

82
Q

ulcerative colitis

active vs maintenance SS

A

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
Q

UC active disease

A

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
Q

UC maintenance disease therapy

A 
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
Q

which tnf-a inhibitors used for what disease

A 
Anti-TNF
Inflixamab → Crohn’s, UC, 
Adalimumab → Crohn’s, UC
Certolizumab → Crohn’s, 
Golimumab → UC
86
Q

biologic indications

A 
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
Q

how to remember biologic indications

A

Certolizumab: chrons
Golimumab: UC
Natalizumab: chrons
Tofacitinib: UC

everything else, indicated for both

TPX: Opthal/Derma/Nutrition/GI (3 decks)

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