Therapeutics Exam 3 (GI - Wendt/Israel/Residents) Flashcards
What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
Antacids
gastric secretion
What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
H2 receptor antagonists
gastric secretion
What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
protectants
gastric secretion
What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
Proton Pump Inhibitors
gastric secretion
What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
Laxatives
increase GI motility
What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
prokinetic drugs
increase GI motility….
What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
Antidiarrheals
reduce motility
What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
anti-emetics
reduce GI motility
Use drugs that affect gastric secretion for the treatment of what things?
indigestion
gastric/duodenal ulcers
GERD (Barretts esophagus)
Zollinger-Ellison Syndrome
What acid related disease is known as a Hypersecretory state
Zollinger Ellison Syndrome
what is the fancy name for indigestion
nonulcer dyspepsia
Pathophys of GI Secretions and Control: (1)
Dietary peptides in the lumen go to ____ cells and they cause release ______
go to G cells
release Gastrin
Pathophys of GI Secretions and Control: (2)
Gastrin from G cells goes to the _____ blood vessel and end up in the _____ area of the stomach
goes to atrium blood vessel –> fundus area
Pathophys of GI Secretions and Control: (3)
When gastrin gets to the fundus it causes ______ cells to make _______
ECL cells; make histamine
Pathophys of GI Secretions and Control: (4)
once ECL cells make histamine – the histamine works on the ______ receptor on ____ cells which leads to the production of ______
Histamine 2 receptor
on parietal cells
leads to production of acid (via proton pump)
Pathophys of GI Secretions and Control: (5)
Production of acid from parietal cells is made via the _______ by using what materials?
Also the acid acts as a negative feedback to ___ cells
made via proton pump – exchanges H+ and K+ 9K+ goes into cell) – NEED ATP to do this
Negative feedback to D CELLS
How does prostaglandin maintain the mucous layer?
it maintains and enhance all mucosal defensive mechanisms working synergistically to nitric oxide
Ulcers = failure of _______protection
mucosal
______ are tight areas to protect something form highly acidic environemnts
gastric crypts
Antacids:
what are the different types/ingredients
NaHCO3
CaCO3
Al(OH)3
Mg(OH)2
Antacids ADEs:
NaHCO3
systemic alkalosis
fluid retention
Antacids ADEs:
CaCO3
hypercalcemia
nephrolithiasis
milk-akali syndrome
Antacids ADEs:
Al(OH)2
constipation hypophosphatemia (constipation = aluminum bat)
Antacids ADEs:
Mg(OH)2
Diarrhea
hypermagnesemia
symptoms of milk-alkali syndrome?
dry mouth and poor appetite
H2 Blockers? examples
and are they competitive or allosteric inhibitors
cimetidine (1st gen)
famotidine (2nd gen)
ranitidine (2nd gen)
Nizatidine (2nd gen)
competitive
Cimetidine:
Drug interactions with what CYP enzymes and then what drugs…
CYP 2D6 or 2D9
warfarin, phenytoin, theophylline, benzos, sulfonylureas
ADEs of Cimetidine
- CNS effects (delirium/confusion/HA) — esp with Elderly pts and IV meds
- Antiandrogen (gynecomastia/impotence)
- Thrombocytopenia
- Can help clear up warts??
Histamine Blockers reduce gastric secretion in response to what things?
histamine
gastrin
acetylcholine
benefits of 2nd gen H2 blockers
longer half life
fewer CYP effects
Greater potency
what is the ratio switch/conversion of H+ and K+ at the proton pump
1:1
what drug is NOT approved for GERD but is a competitive K+ acid blocker (aka works at proton pump)
Vonoprazan
what receptors are on the parietal cells cause a upregulation of proton pump
and what receptors cause downreguation of proton pump
up: Muscarine, gastrin, histamine
down: prostaglandins
Proton pump inhibitors have a _____ as a motif
Benzimidazoles
what is the chiral center in esomeprazole and omeprazole
sulfur
T or F: PPIs are prodrugs and irreversible inhibitors
True!!!!
PPIs need a _____ environment to get activated
and in the end will make a ______ complex with a _____ bond
acidic environment
make a enzyme-inhibitor complex; disulfide bond (leads to irreversible)
T or F: PPIs have a long plasma half life and a long duration of action
FALSE!
SHORT plasma life and LONG duration of action
(long bc covalent inhibition)
PPIs:
should take these when?
first thing in the morning before eating
PPIs:
______ occurs and may result in rebound hypersecretion of gastric acid upon ______
hypergatrenemia
upon withdrawal
PPIs:
Omeprazole CYP interaction and then effects what drugs?
CYP2C19
DECREASE CLOPIDOGREL ACIVITY
diazepam, warfarin, and phenytoin will increase
PPIs or H2 blockers can have tolerance develop?
H2 blockers
process of PPI therapy that affects bone strength
decreased Ca2+ absorption decreased plasma Ca2+ secondary hyperparathyroidism increased PTH!! increased bone resorption = decreased bone strength
Mucosal Protective Agents: Sucralfate
it is a ______ complex of _____
aluminum hydroxide complex of sucrose
Mucosal Protective Agents: Sucralfate
___ pH will activate the complex
works by ________ to form a protective barrier at the ulcer site
acidic
polymerizing
Mucosal Protective Agents: Sucralfate
Absorbed well or poorly?
poorly! (good because there is aluminum in it!!)
Mucosal Protective Agents: Misoprostol
_______ derivative
has ______ effects = enhance _____ and ______ secretion
prostaglandin deriv
cytoprotecant effects = mucus and bicarb
Misoprostol ADEs/
Diarrhea and Abortificeant
Many peptic ulcers are assoc w/ infection of the _______ by ______ bacilli, _________
infection of gastric mucosa, gram negative, H.Pylori
why is bismuth subsalicylate used in h.pylori infection?
can act as a barrier!!
has some antibacterial and antiviral and antisecretory activity
GI muscles are sympathetic are parasympathetic
parasympathtetic
Enteric Nervous System/Muscles of the GI tract are affected by what?
stretching and serotonin??
what are the 2 muscle layers around the lumen that lead to peristalsis
myenteric nerve plexus
submucosal nerve plexus
how do bulk laxatives work?
they are non-absorable sugars and draw in water – -leads to a large hydrophilic mass that acts on stretch receptors = you GOTTA GO!
who does Golytely work (aka isosomtic electrolyte solutions with PEG)
also draw in water = leads to stretch receptors = you gotta go pooooo
how do stool softeners work?
that get incorporated into the stool and decrease water absorption into the body = stool softer and lubricate the lower bowl to reduce fecal impaction
examples of stool softeners?
docusate
mineral oil
glycerin
examples of bulk/saline laxatives
psyllium, methylcellulose, bran, milk of magnesia
what dug is a dephenylmethane derivatives
bisacodyl
what are some common GI hypomotility diseases
gastroparesis
Ileus
what is gastroparesis
neuropathy that can come from diabetes or parkinsons disease (everything gets slowed down)
what is Ileus
small bowels dont recover after surgery (from anethesia)
Clinical uses of metoclopramide
promote gastric emptying
post op and diabetic gastroparesis
GERD
MOA of metoclopramide
Dopamine receptor antagonist in the myenteric plexus that leads to acetylcholine release!
ADEs of Metoclopramide
Sedation, Parkinsons like syndrome, hyperprolactinemia (gynecomastia, galactorrhea, breast tenderness)
what drugs are prokinetic drugs
Erythromycin
Neostigmine
Bethanechol
Prucalopride
what are the toxicities related to using neostigmine and bethanechol
cholinergic effects
why is erythromycin not super useful
rapid tolerance
how do chloride channel activators work
increase chloride rich fluid secretion into intestine = more water comes in!
what drugs are chloride channel activators
Lubiprostone
Linactolide
Plecanatide
Opioid Induced Constipation: Activation of opioid receptors in myenteric plexus: Decrease \_\_\_\_\_\_\_\_ Increase\_\_\_\_\_\_\_ Decrease\_\_\_\_\_\_\_
decrease smooth muscle contraction
Increase rectal sphincter tone
decrease colonic mucosa secretion
what are some peripherally acting opioid antagonists
naloxegol (Movantik)
alvimopan (Entereg)
Naldemedine
Anti-Diarrheals work by slowing _____ and increasing _____ and _____
slow peristalsis
increase water and electrolyte absoroption
what drugs are known as anti-diarrheals
opiates (loperamide and diphenyoxylate)
bismuth
bile salt binding resisn (cholestrymaine, colestipol, and colesavam)
what drugs are anticholinergics and are used to inhibit GI motility
dicyclomine
hyoscymaine
MOA of Aloestron (Lotronex)
serotonin (5HT3) antagonist = blocks visceral afferent pain and decrease colon motility
Aloestron is indicated for who?
for women with IBS + Diarrhea
*IBS = irritable bowel syndrome (not inflamm. bowel disease)
GI side effects of Aloestron
Constipation; Ischemic Colitis
Anticholinergics inhibit _______ receptors which leads to anti______ effects
muscarinic acetylcholine
antispasmodic
Enteric Nervous Systems:
ENS Neuron leads to increased _______
peristalsis
Enteric Nervous Systems:
EC (enterochromoffin cells) release ______ and will act on what two different things
release serotonin
work on IPAN or Extrinsic primary afferent
(IPAN - intrinsic primary afferent neuron)
Enteric Nervous Systems:
IPAN goes and affects ______
EPAN will go to ______
IPAN: goes to ENS neurons
Extrinsic: CNS
Definitions:
Neonate?
0 - 28 days
term + 28 days
Definitions:
Infant
1 - 12 months
Definitions:
Child
1 - 12 years
Definitions:
Adolescent
13 - 18 years
Estimating Renal Function for Kids:
what eqn to use
Beside Schwartz Equation
(0.413 x (ht in cm / SCr) = eGFR
if don’t want to poke kids for blood and get SCr - what is another way to estimate renal function
check urine output: greater than 1 mL/kg/hour
GER vs GERD
GER: passage of gastric contents into the esophagus (normal thing to happen)
GERD: gastric reflux cases trouble some sxs or complications
what is regurgitation?
effortless passage of stomach contents
aka spitting up
GER is caused by _____ of _______
relaxation of LES (lower esophageal sphincter)
In healthy children LES relaxation is TRANSIENT:
frequency of transient LES can be increased by what two things?
infants eat relatively large volumes (100 mL/kg/day)
and
delayed gastric emptying
Most kids older than _____ will have more classic heartburn symptoms
4 years old
GERD Sxs in infants?
Regurgitation
Failure to Thrive
Respiratory Problems (apnea/ALTE - acute life threatening event)
GERD Sxs in Children?
Asthma/lung issues
recurrent pneumonia- like aspiration
dental erosions
what are main non-pharm therapy options for GERD in kids
feeding changes
positioning therapy
lifestyle changes
what are some feeding changes to help with GERD in peds
thickening of feeds (rice cereal)
increase caloric density of feeds while decreasing volume!
Hypoallergenic dieat
Transpyloric feeding (feeding tube in nose)
Indications for pharm therapy in GERD for peds
GERD present w/ complications
no improvement after lifestyle modifications (2 - 4 weeks)
failure to thrive!!!
Pharm therapy for GERD in Peds:
do drug therapy for ______ then reassess - try to take them off this
8 - 12 weeks
H2 Antagonists in Peds:
_____ and _____ agents used most
Requires renal dosing adjustment? yes or no?
______ observed with chronic use
famotidine and ranitidine
yes!! renal adjust!!!
tachyphylaxis observed!
Oral Dosing: (for Peds!!)
Ranitidine?
Famotidine?
Ranitidine: 4 - 8 mg/kg/day divided BID (max: 300 mg)
Famotidine: 1 mg/kg/day divided BID (max 40 mg)
PPI Oral dosing?
Lansoprazole?
and
Omeprazole?
dosing for both is like 1 mg/kg per day (adult caps tho!)
Peds GERD:
agents that are prokinetic?
improve _____ and ______
metoclopramide
erthyromycin
improve esophageal motility and improved LES tone
ADEs of Prokinetic Drugs: metoclopramide --- \_\_\_\_\_\_ ADEs Black box warning of \_\_\_\_\_\_ (may be permanent) \_\_\_\_\_ and \_\_\_\_\_ in neonates
Neurologic ADEs
warning of Tardive dyskinesia
Lactation and Gynecomastia in neonates
ADEs of Prokinetic Drugs: Erythromcin --- \_\_\_\_\_\_ at antimicrobial doses \_\_\_\_\_\_\_\_ --> \_\_\_\_\_\_ Drug interactions
pyloric stenosis (projectile vomiting) QTc prolongation--> arrhythmias
What is the list of QTc prolongation
methadone azole antifungals ondansetron antipsychotics (IV haloperidol) fluoroquinolones antiarrhythmics macrolide abx SSRIs?
want to avoid ____ containing antacid products due to neurotoxicity
aluminum
ADEs of sucralfate with chronic use?
aluminum toxicity
Bezoar formation = “rock in belly”
zinc deficiency
Sucrafalate - used in infants and kids?
NOT in infants
kids ok — typically 7 - 10 days max
4 main pathways of vomiting (from Peds lecture)
Blood borne toxins (chemoreceptor trigger zone)
Motion (vestibular)
Mechanical (vagal)
Emotion
Vomiting Clinical Pearls:
Agents assoc. w/ respiratory depression may have enhanced toxicity with children:
avoid _____ in kids < 2 y.o (CONTRAINDICATED!)
promethazine
Vomiting Clinical Pearls:
Correct ______ and _______
dehydration and electrolyte abnormalities
Vomiting Alarm Symptoms?
Hematemesis/recurrent bilious emesis Clinical dehydration evidence of shock focal neurologic changes abdominal distension/abnormal bowel sounds vomiting that awakes a child from sleep
Definition:
Fecal impaction
large mass unlikely to be passed on command
Definition:
Encopresis
aka fecal incontinence
repeated passage of feces into inappropriate places (?)
often secondary to soft stool leaking around large mass of stool in rectum…
Definition:
Delayed bowel training — bowel continence is expected by age ____
4
Normal Stooling Patterns:
Infants ______ per day
Toddler ______ per day
4 y.o and above - usually similar to adults
infants: 3 - 4 stools / day
toddler: 2 -3 stool/day
How Pooping Happens:
what 4 things “work” together to make productive bowel movements
internal anal sphincter
external anal sphincter
puborectalis muscle
rectum
Circular smooth muscle = ______ control
Skeletal muscle = _______ control
circular: no direct control
skeletal: self control
is it circular or skeletal muscle?
Internal anal sphincter
circular
is it circular or skeletal muscle?
external anal sphincter
skeletal
is it circular or skeletal muscle?
Puborectalis muscle
skeletal
is it circular or skeletal muscle?
rectum
circular
How Pooping Happens: Sitting on the toilet --- relax \_\_\_\_\_\_\_ muscle and relax \_\_\_\_\_ and \_\_\_\_ straighten \_\_\_\_\_\_ increase \_\_\_\_\_\_
relax puborectalis muscle, external anal sphincter and internal anal sphincter
straighten anorectal angle…
increase intraabodominal pressure
definition of withholding (in relation to poop)
occurs when a child fails to recognize or respond to urge to defecate?
issue with repeated withholding?
larger stool load = stretching and possible thinning of rectal wall = increased risk of perforation
Complications of Constipation
Encopresis Bed-wetting recurrent UTIs prolapse (bc thinning) rectal ulcerations social/emotional issues
what meds can cause constipation?
opioids iron supplements CCBs!! TCAs Antihistamines antipsychotics Phenytoin/Carbamazepine
Red Flag Symptoms of constipation?
Delayed passage of meconium (aka first poop) failure to thrive bloody stools severe abdominal distension perianal fistula sacral dimple
what is 1st line tx for infants with constipation
glycerin suppository
what are some definite things to avoid for treating infant constipation
mineral oil/stimulant laxatives/phosphate enemas
NO HONEY! botulisim toxin
steps in managing constipation in kids
educate
disimpaction/cleanout
maintain reg. bowel movements
behavior modification
what is the preferred way to cause disimpaction
oral polyethylene glycol!!
or magnesium citrate
can do rectal if kid cant do oral (enemas - saline, sodium phosphate, or mineral oil – all for 3 consecutive days)
avoid what kind of enemas?
home remedies like soap, herbal, or tap water
other than enemas and oral options for disimpaction - what else can you do
nasogastric - requires hosptiliazation
PEG w/ electrolytes
what is first line for maintenance of constipation
PEG 3550
other maintenance options for constipation? (NOT PEG 3550)
other osmotic agents: lactulose, magnesium hydroxide
stool softeners : docusate
stimulant laxatives
Chronic Diarrhea:
lasting more than _____ consecutive days
14
why is diarrhea such a problem?
dehydration!!!!
electrolyte abnormalities
malnutrition/malabsorption
negatively impacts quality of life
four major categores if diarrhea
secretory
osmotic
excretory
altered motility
Common etiologies for Diarrhea?
viral bacterial parasitic malabsorption syndromes (cystic fibrosis/celiac disease) short gut irritable bowel (crohns and ulcerative colitis) allergic nutrition medications ..........
what are some common meds to cause diarrhea
antibiotics chemo divelant cations (Mg and Ca) PPIs/H2RAs Laxatives.... colchicine digoxin lithium metformin!! food additives - sorbitol
if diarrhea symptoms persist after antibiotics are stopped — consider a _____ infection
c.diff
Amox/Clav – why is the diarrhea so bad?
the clav part wrecks people
way to help prevent amox/clav diarrhea from being so bad…
use the 600 mg Amox/5mL formulation (ratio of amox to clav is much greater which = less clav = less diarrhea!)
How to calculate fluid requirements for peds - use what method
Holliday Segar Method
Holliday Segar Method: – Calculating Fluid Requirements:
Up to 10 kg: ______
100 mL/kg
Holliday Segar Method: – Calculating Fluid Requirements:
10 - 20 kg: _______
1000 mL + 50 mL/kg for every kg over 10!
Holliday Segar Method: – Calculating Fluid Requirements:
> 20 kg: ___________
1500 mL + 20 mL/kg for every kg over 20
Pathogenesis of GERD:
decreased ______ and ______
increased ______ and _______
decreased: esophageal clearance, gastric emptying
increased: gastric pressure, acid production
Sxs of GERD? (adults!)
heartburn - dur regurgitation dysphagia belching bloating nausea globus sensation hypersalivation early satiety
Risk factors/stressors for GERD
overweight/obesity diet diabetes asthma smoking pregnancy delayed stomach emptying
Alarm symptoms assoc w/ GERD
involuntary wt loss anemia continual pain blood in vomit or stool difficulty breathing vomiting chest pain choking painful swallowing hoarseness chronic cough
Foods that trigger REFLUX
coffee
chocolate
fatty foods
alcohol
foods that trigger HEARTBURN
spicy foods
acidic foods
carbonation
Medications can worsen GERD if they _______ or ______
if they are direct irritants to esophageal mucosa; lower esophageal sphincter relaxants
GERD or Heartburn:
which one is mild usually and which one is moderate to severe
mild: heratburn
moderate to severe: GERD
GERD or Heartburn:
which one happens like < 2x/wk (intermittent)
or which one happens >2x/wk (frequent)
intermittent: heartburn
GERD: frequent
what is the bernstein test
put acid soln in esophagus- if painful then the patient has erosiveness going on
definition of strictures?
narrowing of esophagus
why is a strictures a problem
can cause an obstruction
Lifestyle modifications for GERD
exercise/wt loss smoking cessation raise head of bed avoid bending or laying down avoid eating before bedtime increase water intake
what is the max number of tums someone can have in a day
16 tabs
Can avoid most interactions with antacids by doing what?
separate them!!
take med 1 hour before or 4 hours after antacids!!
what drugs can have antacids drug interactions
thyroid medications tetracyclines fluoroquinolones azoles (anti fungals) steroids iron digoxin anti-retrovirals
Aluminum or Magnesium will cause confusion
aluminum
Pros of Antacids?
Quick onset! (~5 minutes)
Relatively safe
use as needed
Cons of Antacids?
short duration (~30 - 60 minutes) Risk of tolerance Frequent dosing
Treatment Overview for GERD (what are the 4 steps)
lifestyle modifications –> prn meds –> scheduled meds –> surgery
H2RA antagonists:
Onset:______
Duration of Action: _____
onset: < 1 hour
DOA: 4 - 10 hours
what are some examples of PRN antacids
Tums Milk of Magnesia Mylanta Gaviscon Alka Seltzer Pepto Bismol
All H2RA meds are dose _______ daily
twice!!!!
which H2RA does NOT come as an IV formulation
Cimetidine
Accumulation of H2RAs can lead to what things?
Mental disturbances
and
insomnia/drowsiness
Need to renally adjust H2RAs when CrCl is < ______
50 mL/min
Beer’s Criteria for H2RAs?
avoid using in pts with delirium
using PPIs and H2RAs as needed? - yay or nay
NAY!
bc MOA - this isn’t the best option — these drugs do not work immediately
For GERD
For H2RAs: Treat for how long?
For PPIs: Treat for how long?
H2RAs: 6 - 12 weeks
PPIs: 4 - 8 weeks
PPIs:
Onset: _______
Duration of Action:_______
onset: 2 -3 hours
duration of action ~ 24 hours
what PPIs do come as an IV solution?
pantoprazole
esomeprazole
when should you typically take PPIs?
which PPI does it not matter when you take it
take 30 - 60 minutes before a meal
dexlansoprazole – take wheneva
which PPI comes ODT
lansoprazole
which PPIs can you not crush
raberprazole
pantoprazole
Drug Interactions of PPIs:
All PPI’s inhibit _______ but this inhibition is seen the most by what two PPIs?
2C19
omeprazole and esomeprazole
Drug Interactions of PPIs:
PPIs will increase the effect of what 3 drugs
MTX
warfarin
phenytoin
Drug Interactions of PPIs:
PPIs will decrease the effect of what 3 drugs
HIV/Hep C meds
Iron
bisphosphonates
also clopidogrel!! - but not clinically significant…
PPIs take ________ to reach max effect
3 - 5 days
PPIs have a chance of causing community acquired pneumonia risk:
seen within ______ of treatment initiation
(how long of tx)
first 30 days
PPIs can cause fractures -
seen more when pts have been on ____________ or they are ______
been on high doses or long term use (>1)
are 50+ y.o.
Metoclopramide is good for GERD if the pt has comorbid ______
gastroparesis
If a pt is pregnant:
what is 1st line after Lifestyle modifications?
antacids!!
what is the surgical procedure done for GERD
fundoplication (laproscopic or Nissen)
reinforces the LES (wrap top of stomach around the lower esophagus)
who qualifies for surgery with GERD?
if the are contraindication to PPIs
or
PPIs and lifestyle modifications do not control symptoms
two most common location so ulcers
stomach
duodenum
what are the defensive factors against Peptic ulcers
prostaglandins
bicarb
mucus
growth factors
main 3 risk factors for PUD
H.pylori infections
NSAID use/antiplatelet meds
smoking/alcohol/diet or stress- hospital
stomach ulcer or duodenum ulcer?
acid production in response to food irritates ulcer quickly
stomach! (stomach comes first…)
stomach ulcer or duodenum ulcer?
pain occurs 2 - 3 hours after food
duodenum!
complications of PUD
upper GI bleeding
perforation
gastric outlet obstruction
Non-Pharm Options of PUD therapy
STOP SMOKING!!! reduce psychological stress avoid food/beverages that can exacerbate symptoms avoid NSAIDs surgery..
how does h pylori cause ulcers:
mucosal damage by _____ factors and _____ enzymes
virulence factors; bacterial enzymes
how does h pylori cause ulcers:
Increased _______ due to cytokine release
gastric acid secretion
4 indications for testing for H pylori
active PUD
Past hx of PUD
Low grade gastric mucosa assoc. lymphoid tissu (MALT lymphoma)
hx of endoscopic resection of early gastric cancer
Treating H. Pylori:
Must include ________ and ______
anti-secretory agent
and 2 - 3 antibiotics
Treating H.Pylori:
treat for ____ days depending on regimen
and continue ____ for at least an additional ____ after eradication
10 - 14 days;
continue PPI; for 2 weeks
2 Questions to ask self when picking H.pylori treatment
PCN allergy?
Previous macrolide exposure (past 6 MOS!!)
what drugs are macrolides
clarithromycin
azithromycin
Treatment Regimens for H.Pylori
Regimen 1 is what drugs and how frequent of dosing?
Amoxicillin Metronidazole Clarithromycin PPI ALL BID!!!!!!! (even PPI!)
Treatment Regimens for H.Pylori
Regimen 2 is what drugs and how frequent of dosing?
Bismuth subsalicylate: QID
Metronidazole: QID
tetracycline: QID
PPI: BID
*good if PCN allergy or macrolide exposure!!
Treatment Regimens for H.Pylori
Regimen 3 is what drugs and how frequent of dosing?
Bismuth subsalicylate: QID Metronidazole: QID tetracycline: QID (at lower doses of regimen 2....) also above 3 drugs are in a single capsule called Pylera PPI: BID
PPIs and H.Pylori:
Continue PPI after infection to prevent further issues?
NO! do not continue a PPI!
PPIs and H.Pylori:
______ a day PPIs are back bone of therapy
twice
What drug class is a good back up for H.pylori treatment…?
Fluroquinolones (levofloxacin)
if H.Pylori treatment fails….
do what 3 things?
use abx not used before/aka no resistance
use drugs with topical effects (bismuth)
extend duration to 14 days
Bismuth salts:
________ effect
topical antimicrobial effect
Bismuth salts:
Improve ______ and relieve _____ in patients
improve ulcer healing
relieve pain
Bismuth Salts:
side effect?
darkening of stool and tongue
Bismuth salts:
concern with ______ allergy and what demographic group?
Aspirin allergy
kids < 12 (bc it is a salicylate)
Abx ADEs:
metronidazole?
avoid with alcohol!!! throwing up while drug is in system (disulfiram like reaction)
Abx ADEs:
Tetracycline?
photosensitvity
Abx ADEs:
Clarithromycin?
Taste disturbances (metallic) QT prolongation
Abx ADEs:
Levofloxacin
tendon rupture
sedation/mental status change
QT prolongation
Risk Factors for NSAID induced ulcer:
High risk if …?
Hx of previously complicated ulcer
2+ risk factors
Risk Factors for NSAID induced ulcer:
Moderate risk if …?
1 - 2 risk factors; Hx of previously uncomplicated ulcer Age 65+ y.o HD NSAID Therapy concurrent ASA, steroids, or anticoags
Primary Prevention Strategies of NSAID induced ulcer:
Combo of _______ with NSAID
PPI (or misprostol)
Primary Prevention Strategies of NSAID induced ulcer:
what agents can be used when the pt is needing an NSAID pain reliever?
COX-2 specific NSAIDs
Naproxen preferred (decreased CV risk compared to others…)
Treating NSAID induced ulcer:
if the patient can discontinue the NSAID what do we do?
discontinue the NSAID…
start PPI/H2RA/or sucralfate
then check for H.pylori – if + - then treat it
Treating NSAID induced ulcer:
if the patient can NOT discontinue the NSAID what do we do?
use NSAID at lowest most effective dose for shortest duration and ADD PPI! (or misoprostol)
and check for H.pylori — if + then treat it
for preventing NSAID induced ulcer: use a PPI how many times a day!
just ONCE a day
Misoprostol:
ADEs/Cons
QID dosing!!
Abortifacient (category X; must do pregnancy test prior to initiation)
ADEs: Diarrhea, abdominal cramping, N/V, flatulence, HA
H2RAs:
use for prevention, maintenance, or treatment for NSAID induced ulcers
ONLY treatment (and do if pt cannot have PPI) do NOT use H2RAs as prevention!!
Sucralfate:
acts like a band aid: _______ complex and can form a physical barrier over an open ulcer
sucrose-sulfate-aluminum
Sucralfate:
_____ times per day
administering instructions?
4x per day(before meals and at bedtime)
administer on an empty stomach 2 hrs before OR 4 hours after other meds
Sucralfate ADEs
constipation, metallic taste
Al toxicity in chronic renal failure!!
for NSAID induced ulcer:
if you can stop the NSAID: treat with PPI for _______
6 - 8 weeks
for NSAID induced ulcer:
if you can NOT stop the NSAID: treat with PPI for _______
8 - 12 weeks
what is SRMD or SRMB and the differences between them?
SRMD: stress related mucosal disease
SRMB: stress related mucosal bleeding
one is visible (bleeding)
disease HAS to come first!
Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one is acute
SRMD
Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one is most superficial
SRMD
Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one has the most severe bleeding?
SRMD
Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one is more chronic?
H.pylori or NSAID
Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one typical has symptoms (of epigastric pain)
H.pylori
why do we care about stress ulcers?
mortality is higher in ICU pts w/ clinically important GI bleeding
Pathophys of Stress Ulcer formation:
(decreased or increased) cardiac output?
decreased!
decreased output = hypoperfusion = decreased motility/decreased mucosal blood flow
Prevention of Stress ulcers:
Prophylactic therapy to prevent bleeding is best when initiated EARLY in a pts course:
- Restore mucosal blood flow thru _________
- use pharmacotherapy to maintain _________ or to provide mucosal gastric protection
thru resuscitative measures
maintain intra-gastric pH >4!!!
ASHP Criteria for Prophylaxis:
Major Criteria?
will just need one or more of the major criteria!
Mechanical ventilation > 48 hours (start at first starting tho)
Coagulopathy (ptc cant clot!!)
others:
severe burn
traumatic brain injury/cervical spinal cord
ASHP Criteria for Prophylaxis:
Minor Criteria?
will need 2 or more of the minor criteria!
HYPOPERFUSION HD corticosteroids AKI Acute organ dysfunction Hx of GI ulcer or bleeding w/in past year Major surgery post op transplant
do NOT do Stress ulcer prophylaxis
for patients with out ______
or _____ patients
w/out risk factors…
NON-ICU pts - should NOT get this
Prophylaxis options for stress ulcers
enteral nutrition and antacids
**Sucralfate, H2RAs, PPIs
Main thing to consider when choosing an agent/route for a patient and stress ulcer prophylaxis
PO or NG or IV?!?..DUH
Which H2RA antagonist can be only oral
cimetidine!!
when do you discontinue stress ulcer prophylaxis
resolution of risk factors
discharge from ICU
extubation
oral intake!!!
out of prophylaxis for stress ulcers - what agent is used most
PPIs (SHOCKING)
what PPIs can be given IV
esomeprazole and pantroprazole
Metoclopramide is a prokinetic agent — how does it work
D2 receptor antagonist
eryhtromycin is a prokinetic agent — how does it work
motilin agonist
Neostigmine is a prokinetic agent — how does it work
acetylcholinesterase inhibitor (aka the drug is a cholinergic drug)
bethanechol is a prokinetic agent — how does it work
agonist of muscarinic receptor (aka a cholinergic drug)
prucalopride is a prokinetic agent — how does it work
selective 5HT4 agonist
