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Fall 2018/P3 Year' > Therapeutics Exam 3 (GI - Wendt/Israel/Residents) > Flashcards

Therapeutics Exam 3 (GI - Wendt/Israel/Residents) Flashcards

1
Q

What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
Antacids

A

gastric secretion

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2
Q

What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
H2 receptor antagonists

A

gastric secretion

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3
Q

What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
protectants

A

gastric secretion

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4
Q

What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
Proton Pump Inhibitors

A

gastric secretion

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5
Q

What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
Laxatives

A

increase GI motility

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6
Q

What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
prokinetic drugs

A

increase GI motility….

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7
Q

What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
Antidiarrheals

A

reduce motility

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8
Q

What drug class does this belong to:
Affect gastric secretion, increase GI motility, and reduce GI motility?
anti-emetics

A

reduce GI motility

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9
Q

Use drugs that affect gastric secretion for the treatment of what things?

A

indigestion
gastric/duodenal ulcers
GERD (Barretts esophagus)
Zollinger-Ellison Syndrome

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10
Q

What acid related disease is known as a Hypersecretory state

A

Zollinger Ellison Syndrome

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11
Q

what is the fancy name for indigestion

A

nonulcer dyspepsia

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12
Q

Pathophys of GI Secretions and Control: (1)

Dietary peptides in the lumen go to ____ cells and they cause release ______

A

go to G cells

release Gastrin

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13
Q

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

A

goes to atrium blood vessel –> fundus area

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14
Q

Pathophys of GI Secretions and Control: (3)

When gastrin gets to the fundus it causes ______ cells to make _______

A

ECL cells; make histamine

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15
Q

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 ______

A

Histamine 2 receptor
on parietal cells
leads to production of acid (via proton pump)

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16
Q

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

A

made via proton pump – exchanges H+ and K+ 9K+ goes into cell) – NEED ATP to do this

Negative feedback to D CELLS

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17
Q

How does prostaglandin maintain the mucous layer?

A

it maintains and enhance all mucosal defensive mechanisms working synergistically to nitric oxide

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18
Q

Ulcers = failure of _______protection

A

mucosal

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19
Q

______ are tight areas to protect something form highly acidic environemnts

A

gastric crypts

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20
Q

Antacids:

what are the different types/ingredients

A

NaHCO3
CaCO3
Al(OH)3
Mg(OH)2

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21
Q

Antacids ADEs:

NaHCO3

A

systemic alkalosis

fluid retention

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22
Q

Antacids ADEs:

CaCO3

A

hypercalcemia
nephrolithiasis
milk-akali syndrome

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23
Q

Antacids ADEs:

Al(OH)2

A 
constipation
hypophosphatemia
(constipation = aluminum bat)
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24
Q

Antacids ADEs:

Mg(OH)2

A

Diarrhea

hypermagnesemia

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25
Q

symptoms of milk-alkali syndrome?

A

dry mouth and poor appetite

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26
Q

H2 Blockers? examples

and are they competitive or allosteric inhibitors

A

cimetidine (1st gen)
famotidine (2nd gen)
ranitidine (2nd gen)
Nizatidine (2nd gen)

competitive

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27
Q

Cimetidine:

Drug interactions with what CYP enzymes and then what drugs…

A

CYP 2D6 or 2D9

warfarin, phenytoin, theophylline, benzos, sulfonylureas

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28
Q

ADEs of Cimetidine

A
  • CNS effects (delirium/confusion/HA) — esp with Elderly pts and IV meds
  • Antiandrogen (gynecomastia/impotence)
  • Thrombocytopenia
  • Can help clear up warts??
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29
Q

Histamine Blockers reduce gastric secretion in response to what things?

A

histamine
gastrin
acetylcholine

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30
Q

benefits of 2nd gen H2 blockers

A

longer half life
fewer CYP effects
Greater potency

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31
Q

what is the ratio switch/conversion of H+ and K+ at the proton pump

A

1:1

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32
Q

what drug is NOT approved for GERD but is a competitive K+ acid blocker (aka works at proton pump)

A

Vonoprazan

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33
Q

what receptors are on the parietal cells cause a upregulation of proton pump
and what receptors cause downreguation of proton pump

A

up: Muscarine, gastrin, histamine
down: prostaglandins

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34
Q

Proton pump inhibitors have a _____ as a motif

A

Benzimidazoles

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35
Q

what is the chiral center in esomeprazole and omeprazole

A

sulfur

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36
Q

T or F: PPIs are prodrugs and irreversible inhibitors

A

True!!!!

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37
Q

PPIs need a _____ environment to get activated

and in the end will make a ______ complex with a _____ bond

A

acidic environment

make a enzyme-inhibitor complex; disulfide bond (leads to irreversible)

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38
Q

T or F: PPIs have a long plasma half life and a long duration of action

A

FALSE!
SHORT plasma life and LONG duration of action
(long bc covalent inhibition)

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39
Q

PPIs:

should take these when?

A

first thing in the morning before eating

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40
Q

PPIs:

______ occurs and may result in rebound hypersecretion of gastric acid upon ______

A

hypergatrenemia

upon withdrawal

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41
Q

PPIs:

Omeprazole CYP interaction and then effects what drugs?

A

CYP2C19
DECREASE CLOPIDOGREL ACIVITY

diazepam, warfarin, and phenytoin will increase

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42
Q

PPIs or H2 blockers can have tolerance develop?

A

H2 blockers

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43
Q

process of PPI therapy that affects bone strength

A 
decreased Ca2+ absorption
decreased plasma Ca2+
secondary hyperparathyroidism
increased PTH!!
increased bone resorption = decreased bone strength
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44
Q

Mucosal Protective Agents: Sucralfate

it is a ______ complex of _____

A

aluminum hydroxide complex of sucrose

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45
Q

Mucosal Protective Agents: Sucralfate
___ pH will activate the complex
works by ________ to form a protective barrier at the ulcer site

A

acidic

polymerizing

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46
Q

Mucosal Protective Agents: Sucralfate

Absorbed well or poorly?

A

poorly! (good because there is aluminum in it!!)

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47
Q

Mucosal Protective Agents: Misoprostol
_______ derivative
has ______ effects = enhance _____ and ______ secretion

A

prostaglandin deriv

cytoprotecant effects = mucus and bicarb

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48
Q

Misoprostol ADEs/

A

Diarrhea and Abortificeant

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49
Q

Many peptic ulcers are assoc w/ infection of the _______ by ______ bacilli, _________

A

infection of gastric mucosa, gram negative, H.Pylori

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50
Q

why is bismuth subsalicylate used in h.pylori infection?

A

can act as a barrier!!

has some antibacterial and antiviral and antisecretory activity

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51
Q

GI muscles are sympathetic are parasympathetic

A

parasympathtetic

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52
Q

Enteric Nervous System/Muscles of the GI tract are affected by what?

A

stretching and serotonin??

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53
Q

what are the 2 muscle layers around the lumen that lead to peristalsis

A

myenteric nerve plexus

submucosal nerve plexus

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54
Q

how do bulk laxatives work?

A

they are non-absorable sugars and draw in water – -leads to a large hydrophilic mass that acts on stretch receptors = you GOTTA GO!

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55
Q

who does Golytely work (aka isosomtic electrolyte solutions with PEG)

A

also draw in water = leads to stretch receptors = you gotta go pooooo

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56
Q

how do stool softeners work?

A

that get incorporated into the stool and decrease water absorption into the body = stool softer and lubricate the lower bowl to reduce fecal impaction

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57
Q

examples of stool softeners?

A

docusate
mineral oil
glycerin

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58
Q

examples of bulk/saline laxatives

A

psyllium, methylcellulose, bran, milk of magnesia

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59
Q

what dug is a dephenylmethane derivatives

A

bisacodyl

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60
Q

what are some common GI hypomotility diseases

A

gastroparesis

Ileus

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61
Q

what is gastroparesis

A

neuropathy that can come from diabetes or parkinsons disease (everything gets slowed down)

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62
Q

what is Ileus

A

small bowels dont recover after surgery (from anethesia)

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63
Q

Clinical uses of metoclopramide

A

promote gastric emptying
post op and diabetic gastroparesis
GERD

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64
Q

MOA of metoclopramide

A

Dopamine receptor antagonist in the myenteric plexus that leads to acetylcholine release!

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65
Q

ADEs of Metoclopramide

A

Sedation, Parkinsons like syndrome, hyperprolactinemia (gynecomastia, galactorrhea, breast tenderness)

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66
Q

what drugs are prokinetic drugs

A

Erythromycin
Neostigmine
Bethanechol
Prucalopride

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67
Q

what are the toxicities related to using neostigmine and bethanechol

A

cholinergic effects

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68
Q

why is erythromycin not super useful

A

rapid tolerance

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69
Q

how do chloride channel activators work

A

increase chloride rich fluid secretion into intestine = more water comes in!

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70
Q

what drugs are chloride channel activators

A

Lubiprostone
Linactolide
Plecanatide

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71
Q 
Opioid Induced Constipation:
Activation of opioid receptors in myenteric plexus:
Decrease \_\_\_\_\_\_\_\_
Increase\_\_\_\_\_\_\_
Decrease\_\_\_\_\_\_\_
A

decrease smooth muscle contraction
Increase rectal sphincter tone
decrease colonic mucosa secretion

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72
Q

what are some peripherally acting opioid antagonists

A

naloxegol (Movantik)
alvimopan (Entereg)
Naldemedine

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73
Q

Anti-Diarrheals work by slowing _____ and increasing _____ and _____

A

slow peristalsis

increase water and electrolyte absoroption

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74
Q

what drugs are known as anti-diarrheals

A

opiates (loperamide and diphenyoxylate)
bismuth
bile salt binding resisn (cholestrymaine, colestipol, and colesavam)

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75
Q

what drugs are anticholinergics and are used to inhibit GI motility

A

dicyclomine

hyoscymaine

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76
Q

MOA of Aloestron (Lotronex)

A

serotonin (5HT3) antagonist = blocks visceral afferent pain and decrease colon motility

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77
Q

Aloestron is indicated for who?

A

for women with IBS + Diarrhea

*IBS = irritable bowel syndrome (not inflamm. bowel disease)

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78
Q

GI side effects of Aloestron

A

Constipation; Ischemic Colitis

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79
Q

Anticholinergics inhibit _______ receptors which leads to anti______ effects

A

muscarinic acetylcholine

antispasmodic

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80
Q

Enteric Nervous Systems:

ENS Neuron leads to increased _______

A

peristalsis

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81
Q

Enteric Nervous Systems:

EC (enterochromoffin cells) release ______ and will act on what two different things

A

release serotonin
work on IPAN or Extrinsic primary afferent
(IPAN - intrinsic primary afferent neuron)

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82
Q

Enteric Nervous Systems:
IPAN goes and affects ______
EPAN will go to ______

A

IPAN: goes to ENS neurons

Extrinsic: CNS

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83
Q

Definitions:

Neonate?

A

0 - 28 days

term + 28 days

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84
Q

Definitions:

Infant

A

1 - 12 months

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85
Q

Definitions:

Child

A

1 - 12 years

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86
Q

Definitions:

Adolescent

A

13 - 18 years

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87
Q

Estimating Renal Function for Kids:

what eqn to use

A

Beside Schwartz Equation

(0.413 x (ht in cm / SCr) = eGFR

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88
Q

if don’t want to poke kids for blood and get SCr - what is another way to estimate renal function

A

check urine output: greater than 1 mL/kg/hour

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89
Q

GER vs GERD

A

GER: passage of gastric contents into the esophagus (normal thing to happen)

GERD: gastric reflux cases trouble some sxs or complications

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90
Q

what is regurgitation?

A

effortless passage of stomach contents

aka spitting up

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91
Q

GER is caused by _____ of _______

A

relaxation of LES (lower esophageal sphincter)

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92
Q

In healthy children LES relaxation is TRANSIENT:

frequency of transient LES can be increased by what two things?

A

infants eat relatively large volumes (100 mL/kg/day)
and
delayed gastric emptying

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93
Q

Most kids older than _____ will have more classic heartburn symptoms

A

4 years old

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94
Q

GERD Sxs in infants?

A

Regurgitation
Failure to Thrive
Respiratory Problems (apnea/ALTE - acute life threatening event)

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95
Q

GERD Sxs in Children?

A

Asthma/lung issues
recurrent pneumonia- like aspiration
dental erosions

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96
Q

what are main non-pharm therapy options for GERD in kids

A

feeding changes
positioning therapy
lifestyle changes

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97
Q

what are some feeding changes to help with GERD in peds

A

thickening of feeds (rice cereal)
increase caloric density of feeds while decreasing volume!
Hypoallergenic dieat
Transpyloric feeding (feeding tube in nose)

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98
Q

Indications for pharm therapy in GERD for peds

A

GERD present w/ complications
no improvement after lifestyle modifications (2 - 4 weeks)
failure to thrive!!!

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99
Q

Pharm therapy for GERD in Peds:

do drug therapy for ______ then reassess - try to take them off this

A

8 - 12 weeks

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100
Q

H2 Antagonists in Peds:
_____ and _____ agents used most

Requires renal dosing adjustment? yes or no?

______ observed with chronic use

A

famotidine and ranitidine

yes!! renal adjust!!!

tachyphylaxis observed!

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101
Q

Oral Dosing: (for Peds!!)
Ranitidine?

Famotidine?

A

Ranitidine: 4 - 8 mg/kg/day divided BID (max: 300 mg)

Famotidine: 1 mg/kg/day divided BID (max 40 mg)

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102
Q

PPI Oral dosing?
Lansoprazole?
and
Omeprazole?

A

dosing for both is like 1 mg/kg per day (adult caps tho!)

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103
Q

Peds GERD:
agents that are prokinetic?
improve _____ and ______

A

metoclopramide
erthyromycin

improve esophageal motility and improved LES tone

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104
Q 
ADEs of Prokinetic Drugs:
metoclopramide ---
\_\_\_\_\_\_ ADEs
Black box warning of \_\_\_\_\_\_ (may be permanent)
\_\_\_\_\_ and \_\_\_\_\_ in neonates
A

Neurologic ADEs
warning of Tardive dyskinesia
Lactation and Gynecomastia in neonates

105
Q 
ADEs of Prokinetic Drugs:
Erythromcin ---
\_\_\_\_\_\_ at antimicrobial doses
\_\_\_\_\_\_\_\_ --> \_\_\_\_\_\_
Drug interactions
A 
pyloric stenosis (projectile vomiting)
QTc prolongation--> arrhythmias
106
Q

What is the list of QTc prolongation

A 
methadone
azole antifungals
ondansetron
antipsychotics (IV haloperidol)
fluoroquinolones
antiarrhythmics
macrolide abx
SSRIs?
107
Q

want to avoid ____ containing antacid products due to neurotoxicity

A

aluminum

108
Q

ADEs of sucralfate with chronic use?

A

aluminum toxicity
Bezoar formation = “rock in belly”
zinc deficiency

109
Q

Sucrafalate - used in infants and kids?

A

NOT in infants

kids ok — typically 7 - 10 days max

110
Q

4 main pathways of vomiting (from Peds lecture)

A

Blood borne toxins (chemoreceptor trigger zone)
Motion (vestibular)
Mechanical (vagal)
Emotion

111
Q

Vomiting Clinical Pearls:
Agents assoc. w/ respiratory depression may have enhanced toxicity with children:
avoid _____ in kids < 2 y.o (CONTRAINDICATED!)

A

promethazine

112
Q

Vomiting Clinical Pearls:

Correct ______ and _______

A

dehydration and electrolyte abnormalities

113
Q

Vomiting Alarm Symptoms?

A 
Hematemesis/recurrent bilious emesis
Clinical dehydration
evidence of shock
focal neurologic changes
abdominal distension/abnormal bowel sounds
vomiting that awakes a child from sleep
114
Q

Definition:

Fecal impaction

A

large mass unlikely to be passed on command

115
Q

Definition:

Encopresis

A

aka fecal incontinence
repeated passage of feces into inappropriate places (?)

often secondary to soft stool leaking around large mass of stool in rectum…

116
Q

Definition:

Delayed bowel training — bowel continence is expected by age ____

A

4

117
Q

Normal Stooling Patterns:
Infants ______ per day
Toddler ______ per day
4 y.o and above - usually similar to adults

A

infants: 3 - 4 stools / day
toddler: 2 -3 stool/day

118
Q

How Pooping Happens:

what 4 things “work” together to make productive bowel movements

A

internal anal sphincter
external anal sphincter
puborectalis muscle
rectum

119
Q

Circular smooth muscle = ______ control

Skeletal muscle = _______ control

A

circular: no direct control
skeletal: self control

120
Q

is it circular or skeletal muscle?

Internal anal sphincter

A

circular

121
Q

is it circular or skeletal muscle?

external anal sphincter

A

skeletal

122
Q

is it circular or skeletal muscle?

Puborectalis muscle

A

skeletal

123
Q

is it circular or skeletal muscle?

rectum

A

circular

124
Q 
How Pooping Happens:
Sitting on the toilet ---
relax \_\_\_\_\_\_\_ muscle and relax \_\_\_\_\_ and \_\_\_\_
straighten \_\_\_\_\_\_ 
increase \_\_\_\_\_\_
A

relax puborectalis muscle, external anal sphincter and internal anal sphincter

straighten anorectal angle…
increase intraabodominal pressure

125
Q

definition of withholding (in relation to poop)

A

occurs when a child fails to recognize or respond to urge to defecate?

126
Q

issue with repeated withholding?

A

larger stool load = stretching and possible thinning of rectal wall = increased risk of perforation

127
Q

Complications of Constipation

A 
Encopresis
Bed-wetting
recurrent UTIs
prolapse (bc thinning)
rectal ulcerations
social/emotional issues
128
Q

what meds can cause constipation?

A 
opioids
iron supplements
CCBs!!
TCAs
Antihistamines
antipsychotics
Phenytoin/Carbamazepine
129
Q

Red Flag Symptoms of constipation?

A 
Delayed passage of meconium (aka first poop)
failure to thrive 
bloody stools
severe abdominal distension
perianal fistula
sacral dimple
130
Q

what is 1st line tx for infants with constipation

A

glycerin suppository

131
Q

what are some definite things to avoid for treating infant constipation

A

mineral oil/stimulant laxatives/phosphate enemas

NO HONEY! botulisim toxin

132
Q

steps in managing constipation in kids

A

educate
disimpaction/cleanout
maintain reg. bowel movements
behavior modification

133
Q

what is the preferred way to cause disimpaction

A

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)

134
Q

avoid what kind of enemas?

A

home remedies like soap, herbal, or tap water

135
Q

other than enemas and oral options for disimpaction - what else can you do

A

nasogastric - requires hosptiliazation

PEG w/ electrolytes

136
Q

what is first line for maintenance of constipation

A

PEG 3550

137
Q

other maintenance options for constipation? (NOT PEG 3550)

A

other osmotic agents: lactulose, magnesium hydroxide

stool softeners : docusate

stimulant laxatives

138
Q

Chronic Diarrhea:

lasting more than _____ consecutive days

A

14

139
Q

why is diarrhea such a problem?

A

dehydration!!!!
electrolyte abnormalities
malnutrition/malabsorption
negatively impacts quality of life

140
Q

four major categores if diarrhea

A

secretory
osmotic
excretory
altered motility

141
Q

Common etiologies for Diarrhea?

A 
viral
bacterial
parasitic
malabsorption syndromes (cystic fibrosis/celiac disease)
short gut
irritable bowel (crohns and ulcerative colitis)
allergic 
nutrition
medications 
..........
142
Q

what are some common meds to cause diarrhea

A 
antibiotics
chemo
divelant cations (Mg and Ca)
PPIs/H2RAs
Laxatives....
colchicine
digoxin
lithium
metformin!!
food additives - sorbitol
143
Q

if diarrhea symptoms persist after antibiotics are stopped — consider a _____ infection

A

c.diff

144
Q

Amox/Clav – why is the diarrhea so bad?

A

the clav part wrecks people

145
Q

way to help prevent amox/clav diarrhea from being so bad…

A

use the 600 mg Amox/5mL formulation (ratio of amox to clav is much greater which = less clav = less diarrhea!)

146
Q

How to calculate fluid requirements for peds - use what method

A

Holliday Segar Method

147
Q

Holliday Segar Method: – Calculating Fluid Requirements:

Up to 10 kg: ______

A

100 mL/kg

148
Q

Holliday Segar Method: – Calculating Fluid Requirements:

10 - 20 kg: _______

A

1000 mL + 50 mL/kg for every kg over 10!

149
Q

Holliday Segar Method: – Calculating Fluid Requirements:

> 20 kg: ___________

A

1500 mL + 20 mL/kg for every kg over 20

150
Q

Pathogenesis of GERD:
decreased ______ and ______
increased ______ and _______

A

decreased: esophageal clearance, gastric emptying
increased: gastric pressure, acid production

151
Q

Sxs of GERD? (adults!)

A 
heartburn - dur
regurgitation
dysphagia
belching
bloating
nausea
globus sensation
hypersalivation
early satiety
152
Q

Risk factors/stressors for GERD

A 
overweight/obesity
diet
diabetes
asthma
smoking
pregnancy
delayed stomach emptying
153
Q

Alarm symptoms assoc w/ GERD

A 
involuntary wt loss
anemia
continual pain
blood in vomit or stool
difficulty breathing
vomiting
chest pain
choking
painful swallowing
hoarseness
chronic cough
154
Q

Foods that trigger REFLUX

A

coffee
chocolate
fatty foods
alcohol

155
Q

foods that trigger HEARTBURN

A

spicy foods
acidic foods
carbonation

156
Q

Medications can worsen GERD if they _______ or ______

A

if they are direct irritants to esophageal mucosa; lower esophageal sphincter relaxants

157
Q

GERD or Heartburn:

which one is mild usually and which one is moderate to severe

A

mild: heratburn

moderate to severe: GERD

158
Q

GERD or Heartburn:
which one happens like < 2x/wk (intermittent)
or which one happens >2x/wk (frequent)

A

intermittent: heartburn

GERD: frequent

159
Q

what is the bernstein test

A

put acid soln in esophagus- if painful then the patient has erosiveness going on

160
Q

definition of strictures?

A

narrowing of esophagus

161
Q

why is a strictures a problem

A

can cause an obstruction

162
Q

Lifestyle modifications for GERD

A 
exercise/wt loss
smoking cessation
raise head of bed
avoid bending or laying down
avoid eating before bedtime
increase water intake
163
Q

what is the max number of tums someone can have in a day

A

16 tabs

164
Q

Can avoid most interactions with antacids by doing what?

A

separate them!!

take med 1 hour before or 4 hours after antacids!!

165
Q

what drugs can have antacids drug interactions

A 
thyroid medications
tetracyclines
fluoroquinolones
azoles (anti fungals)
steroids
iron
digoxin
anti-retrovirals
166
Q

Aluminum or Magnesium will cause confusion

A

aluminum

167
Q

Pros of Antacids?

A

Quick onset! (~5 minutes)
Relatively safe
use as needed

168
Q

Cons of Antacids?

A 
short duration (~30 - 60 minutes)
Risk of tolerance
Frequent dosing
169
Q

Treatment Overview for GERD (what are the 4 steps)

A

lifestyle modifications –> prn meds –> scheduled meds –> surgery

170
Q

H2RA antagonists:
Onset:______
Duration of Action: _____

A

onset: < 1 hour
DOA: 4 - 10 hours

171
Q

what are some examples of PRN antacids

A 
Tums
Milk of Magnesia 
Mylanta
Gaviscon
Alka Seltzer
Pepto Bismol
172
Q

All H2RA meds are dose _______ daily

A

twice!!!!

173
Q

which H2RA does NOT come as an IV formulation

A

Cimetidine

174
Q

Accumulation of H2RAs can lead to what things?

A

Mental disturbances
and
insomnia/drowsiness

175
Q

Need to renally adjust H2RAs when CrCl is < ______

A

50 mL/min

176
Q

Beer’s Criteria for H2RAs?

A

avoid using in pts with delirium

177
Q

using PPIs and H2RAs as needed? - yay or nay

A

NAY!

bc MOA - this isn’t the best option — these drugs do not work immediately

178
Q

For GERD
For H2RAs: Treat for how long?
For PPIs: Treat for how long?

A

H2RAs: 6 - 12 weeks

PPIs: 4 - 8 weeks

179
Q

PPIs:
Onset: _______
Duration of Action:_______

A

onset: 2 -3 hours

duration of action ~ 24 hours

180
Q

what PPIs do come as an IV solution?

A

pantoprazole

esomeprazole

181
Q

when should you typically take PPIs?

which PPI does it not matter when you take it

A

take 30 - 60 minutes before a meal

dexlansoprazole – take wheneva

182
Q

which PPI comes ODT

A

lansoprazole

183
Q

which PPIs can you not crush

A

raberprazole

pantoprazole

184
Q

Drug Interactions of PPIs:

All PPI’s inhibit _______ but this inhibition is seen the most by what two PPIs?

A

2C19

omeprazole and esomeprazole

185
Q

Drug Interactions of PPIs:

PPIs will increase the effect of what 3 drugs

A

MTX
warfarin
phenytoin

186
Q

Drug Interactions of PPIs:

PPIs will decrease the effect of what 3 drugs

A

HIV/Hep C meds
Iron
bisphosphonates
also clopidogrel!! - but not clinically significant…

187
Q

PPIs take ________ to reach max effect

A

3 - 5 days

188
Q

PPIs have a chance of causing community acquired pneumonia risk:
seen within ______ of treatment initiation
(how long of tx)

A

first 30 days

189
Q

PPIs can cause fractures -

seen more when pts have been on ____________ or they are ______

A

been on high doses or long term use (>1)

are 50+ y.o.

190
Q

Metoclopramide is good for GERD if the pt has comorbid ______

A

gastroparesis

191
Q

If a pt is pregnant:

what is 1st line after Lifestyle modifications?

A

antacids!!

192
Q

what is the surgical procedure done for GERD

A

fundoplication (laproscopic or Nissen)

reinforces the LES (wrap top of stomach around the lower esophagus)

193
Q

who qualifies for surgery with GERD?

A

if the are contraindication to PPIs
or
PPIs and lifestyle modifications do not control symptoms

194
Q

two most common location so ulcers

A

stomach

duodenum

195
Q

what are the defensive factors against Peptic ulcers

A

prostaglandins
bicarb
mucus
growth factors

196
Q

main 3 risk factors for PUD

A

H.pylori infections
NSAID use/antiplatelet meds
smoking/alcohol/diet or stress- hospital

197
Q

stomach ulcer or duodenum ulcer?

acid production in response to food irritates ulcer quickly

A

stomach! (stomach comes first…)

198
Q

stomach ulcer or duodenum ulcer?

pain occurs 2 - 3 hours after food

A

duodenum!

199
Q

complications of PUD

A

upper GI bleeding
perforation
gastric outlet obstruction

200
Q

Non-Pharm Options of PUD therapy

A 
STOP SMOKING!!!
reduce psychological stress
avoid food/beverages that can exacerbate symptoms
avoid NSAIDs
surgery..
201
Q

how does h pylori cause ulcers:

mucosal damage by _____ factors and _____ enzymes

A

virulence factors; bacterial enzymes

202
Q

how does h pylori cause ulcers:

Increased _______ due to cytokine release

A

gastric acid secretion

203
Q

4 indications for testing for H pylori

A

active PUD
Past hx of PUD
Low grade gastric mucosa assoc. lymphoid tissu (MALT lymphoma)
hx of endoscopic resection of early gastric cancer

204
Q

Treating H. Pylori:

Must include ________ and ______

A

anti-secretory agent

and 2 - 3 antibiotics

205
Q

Treating H.Pylori:
treat for ____ days depending on regimen
and continue ____ for at least an additional ____ after eradication

A

10 - 14 days;

continue PPI; for 2 weeks

206
Q

2 Questions to ask self when picking H.pylori treatment

A

PCN allergy?

Previous macrolide exposure (past 6 MOS!!)

207
Q

what drugs are macrolides

A

clarithromycin

azithromycin

208
Q

Treatment Regimens for H.Pylori

Regimen 1 is what drugs and how frequent of dosing?

A 
Amoxicillin
Metronidazole
Clarithromycin
PPI
ALL BID!!!!!!! (even PPI!)
209
Q

Treatment Regimens for H.Pylori

Regimen 2 is what drugs and how frequent of dosing?

A

Bismuth subsalicylate: QID
Metronidazole: QID
tetracycline: QID

PPI: BID

*good if PCN allergy or macrolide exposure!!

210
Q

Treatment Regimens for H.Pylori

Regimen 3 is what drugs and how frequent of dosing?

A 
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
211
Q

PPIs and H.Pylori:

Continue PPI after infection to prevent further issues?

A

NO! do not continue a PPI!

212
Q

PPIs and H.Pylori:

______ a day PPIs are back bone of therapy

A

twice

213
Q

What drug class is a good back up for H.pylori treatment…?

A

Fluroquinolones (levofloxacin)

214
Q

if H.Pylori treatment fails….

do what 3 things?

A

use abx not used before/aka no resistance
use drugs with topical effects (bismuth)
extend duration to 14 days

215
Q

Bismuth salts:

________ effect

A

topical antimicrobial effect

216
Q

Bismuth salts:

Improve ______ and relieve _____ in patients

A

improve ulcer healing

relieve pain

217
Q

Bismuth Salts:

side effect?

A

darkening of stool and tongue

218
Q

Bismuth salts:

concern with ______ allergy and what demographic group?

A

Aspirin allergy

kids < 12 (bc it is a salicylate)

219
Q

Abx ADEs:

metronidazole?

A

avoid with alcohol!!! throwing up while drug is in system (disulfiram like reaction)

220
Q

Abx ADEs:

Tetracycline?

A

photosensitvity

221
Q

Abx ADEs:

Clarithromycin?

A 
Taste disturbances (metallic)
QT prolongation
222
Q

Abx ADEs:

Levofloxacin

A

tendon rupture
sedation/mental status change
QT prolongation

223
Q

Risk Factors for NSAID induced ulcer:

High risk if …?

A

Hx of previously complicated ulcer

2+ risk factors

224
Q

Risk Factors for NSAID induced ulcer:

Moderate risk if …?

A 
1 - 2 risk factors;
Hx of previously uncomplicated ulcer
Age 65+ y.o
HD NSAID Therapy
concurrent ASA, steroids, or anticoags
225
Q

Primary Prevention Strategies of NSAID induced ulcer:

Combo of _______ with NSAID

A

PPI (or misprostol)

226
Q

Primary Prevention Strategies of NSAID induced ulcer:

what agents can be used when the pt is needing an NSAID pain reliever?

A

COX-2 specific NSAIDs

Naproxen preferred (decreased CV risk compared to others…)

227
Q

Treating NSAID induced ulcer:

if the patient can discontinue the NSAID what do we do?

A

discontinue the NSAID…
start PPI/H2RA/or sucralfate

then check for H.pylori – if + - then treat it

228
Q

Treating NSAID induced ulcer:

if the patient can NOT discontinue the NSAID what do we do?

A

use NSAID at lowest most effective dose for shortest duration and ADD PPI! (or misoprostol)

and check for H.pylori — if + then treat it

229
Q

for preventing NSAID induced ulcer: use a PPI how many times a day!

A

just ONCE a day

230
Q

Misoprostol:

ADEs/Cons

A

QID dosing!!

Abortifacient (category X; must do pregnancy test prior to initiation)
ADEs: Diarrhea, abdominal cramping, N/V, flatulence, HA

231
Q

H2RAs:

use for prevention, maintenance, or treatment for NSAID induced ulcers

A 
ONLY treatment (and do if pt cannot have PPI)
do NOT use H2RAs as prevention!!
232
Q

Sucralfate:

acts like a band aid: _______ complex and can form a physical barrier over an open ulcer

A

sucrose-sulfate-aluminum

233
Q

Sucralfate:
_____ times per day
administering instructions?

A

4x per day(before meals and at bedtime)

administer on an empty stomach 2 hrs before OR 4 hours after other meds

234
Q

Sucralfate ADEs

A

constipation, metallic taste

Al toxicity in chronic renal failure!!

235
Q

for NSAID induced ulcer:

if you can stop the NSAID: treat with PPI for _______

A

6 - 8 weeks

236
Q

for NSAID induced ulcer:

if you can NOT stop the NSAID: treat with PPI for _______

A

8 - 12 weeks

237
Q

what is SRMD or SRMB and the differences between them?

A

SRMD: stress related mucosal disease
SRMB: stress related mucosal bleeding

one is visible (bleeding)
disease HAS to come first!

238
Q

Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one is acute

A

SRMD

239
Q

Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one is most superficial

A

SRMD

240
Q

Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one has the most severe bleeding?

A

SRMD

241
Q

Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one is more chronic?

A

H.pylori or NSAID

242
Q

Comparing Ulcers:
(H.pylori induced, NSAID induced, or SRMD)
which one typical has symptoms (of epigastric pain)

A

H.pylori

243
Q

why do we care about stress ulcers?

A

mortality is higher in ICU pts w/ clinically important GI bleeding

244
Q

Pathophys of Stress Ulcer formation:

(decreased or increased) cardiac output?

A

decreased!

decreased output = hypoperfusion = decreased motility/decreased mucosal blood flow

245
Q

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
A

thru resuscitative measures

maintain intra-gastric pH >4!!!

246
Q

ASHP Criteria for Prophylaxis:
Major Criteria?
will just need one or more of the major criteria!

A

Mechanical ventilation > 48 hours (start at first starting tho)
Coagulopathy (ptc cant clot!!)

others:
severe burn
traumatic brain injury/cervical spinal cord

247
Q

ASHP Criteria for Prophylaxis:
Minor Criteria?
will need 2 or more of the minor criteria!

A 
HYPOPERFUSION
HD corticosteroids
AKI
Acute organ dysfunction
Hx of GI ulcer or bleeding w/in past year
Major surgery
post op transplant
248
Q

do NOT do Stress ulcer prophylaxis
for patients with out ______
or _____ patients

A

w/out risk factors…

NON-ICU pts - should NOT get this

249
Q

Prophylaxis options for stress ulcers

A

enteral nutrition and antacids

**Sucralfate, H2RAs, PPIs

250
Q

Main thing to consider when choosing an agent/route for a patient and stress ulcer prophylaxis

A

PO or NG or IV?!?..DUH

251
Q

Which H2RA antagonist can be only oral

A

cimetidine!!

252
Q

when do you discontinue stress ulcer prophylaxis

A

resolution of risk factors
discharge from ICU
extubation
oral intake!!!

253
Q

out of prophylaxis for stress ulcers - what agent is used most

A

PPIs (SHOCKING)

254
Q

what PPIs can be given IV

A

esomeprazole and pantroprazole

255
Q

Metoclopramide is a prokinetic agent — how does it work

A

D2 receptor antagonist

256
Q

eryhtromycin is a prokinetic agent — how does it work

A

motilin agonist

257
Q

Neostigmine is a prokinetic agent — how does it work

A

acetylcholinesterase inhibitor (aka the drug is a cholinergic drug)

258
Q

bethanechol is a prokinetic agent — how does it work

A

agonist of muscarinic receptor (aka a cholinergic drug)

259
Q

prucalopride is a prokinetic agent — how does it work

A

selective 5HT4 agonist

Fall 2018/P3 Year' (16 decks)

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