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

(259 cards)

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
symptoms of milk-alkali syndrome?
dry mouth and poor appetite
26
H2 Blockers? examples and are they competitive or allosteric inhibitors
cimetidine (1st gen) famotidine (2nd gen) ranitidine (2nd gen) Nizatidine (2nd gen) competitive
27
Cimetidine: | Drug interactions with what CYP enzymes and then what drugs...
CYP 2D6 or 2D9 warfarin, phenytoin, theophylline, benzos, sulfonylureas
28
ADEs of Cimetidine
- CNS effects (delirium/confusion/HA) --- esp with Elderly pts and IV meds - Antiandrogen (gynecomastia/impotence) - Thrombocytopenia - Can help clear up warts??
29
Histamine Blockers reduce gastric secretion in response to what things?
histamine gastrin acetylcholine
30
benefits of 2nd gen H2 blockers
longer half life fewer CYP effects Greater potency
31
what is the ratio switch/conversion of H+ and K+ at the proton pump
1:1
32
what drug is NOT approved for GERD but is a competitive K+ acid blocker (aka works at proton pump)
Vonoprazan
33
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
34
Proton pump inhibitors have a _____ as a motif
Benzimidazoles
35
what is the chiral center in esomeprazole and omeprazole
sulfur
36
T or F: PPIs are prodrugs and irreversible inhibitors
True!!!!
37
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)
38
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)
39
PPIs: | should take these when?
first thing in the morning before eating
40
PPIs: | ______ occurs and may result in rebound hypersecretion of gastric acid upon ______
hypergatrenemia | upon withdrawal
41
PPIs: | Omeprazole CYP interaction and then effects what drugs?
CYP2C19 DECREASE CLOPIDOGREL ACIVITY diazepam, warfarin, and phenytoin will increase
42
PPIs or H2 blockers can have tolerance develop?
H2 blockers
43
process of PPI therapy that affects bone strength
``` decreased Ca2+ absorption decreased plasma Ca2+ secondary hyperparathyroidism increased PTH!! increased bone resorption = decreased bone strength ```
44
Mucosal Protective Agents: Sucralfate | it is a ______ complex of _____
aluminum hydroxide complex of sucrose
45
Mucosal Protective Agents: Sucralfate ___ pH will activate the complex works by ________ to form a protective barrier at the ulcer site
acidic polymerizing
46
Mucosal Protective Agents: Sucralfate | Absorbed well or poorly?
poorly! (good because there is aluminum in it!!)
47
Mucosal Protective Agents: Misoprostol _______ derivative has ______ effects = enhance _____ and ______ secretion
prostaglandin deriv | cytoprotecant effects = mucus and bicarb
48
Misoprostol ADEs/
Diarrhea and Abortificeant
49
Many peptic ulcers are assoc w/ infection of the _______ by ______ bacilli, _________
infection of gastric mucosa, gram negative, H.Pylori
50
why is bismuth subsalicylate used in h.pylori infection?
can act as a barrier!! | has some antibacterial and antiviral and antisecretory activity
51
GI muscles are sympathetic are parasympathetic
parasympathtetic
52
Enteric Nervous System/Muscles of the GI tract are affected by what?
stretching and serotonin??
53
what are the 2 muscle layers around the lumen that lead to peristalsis
myenteric nerve plexus | submucosal nerve plexus
54
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!
55
who does Golytely work (aka isosomtic electrolyte solutions with PEG)
also draw in water = leads to stretch receptors = you gotta go pooooo
56
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
57
examples of stool softeners?
docusate mineral oil glycerin
58
examples of bulk/saline laxatives
psyllium, methylcellulose, bran, milk of magnesia
59
what dug is a dephenylmethane derivatives
bisacodyl
60
what are some common GI hypomotility diseases
gastroparesis | Ileus
61
what is gastroparesis
neuropathy that can come from diabetes or parkinsons disease (everything gets slowed down)
62
what is Ileus
small bowels dont recover after surgery (from anethesia)
63
Clinical uses of metoclopramide
promote gastric emptying post op and diabetic gastroparesis GERD
64
MOA of metoclopramide
Dopamine receptor antagonist in the myenteric plexus that leads to acetylcholine release!
65
ADEs of Metoclopramide
Sedation, Parkinsons like syndrome, hyperprolactinemia (gynecomastia, galactorrhea, breast tenderness)
66
what drugs are prokinetic drugs
Erythromycin Neostigmine Bethanechol Prucalopride
67
what are the toxicities related to using neostigmine and bethanechol
cholinergic effects
68
why is erythromycin not super useful
rapid tolerance
69
how do chloride channel activators work
increase chloride rich fluid secretion into intestine = more water comes in!
70
what drugs are chloride channel activators
Lubiprostone Linactolide Plecanatide
71
``` 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
72
what are some peripherally acting opioid antagonists
naloxegol (Movantik) alvimopan (Entereg) Naldemedine
73
Anti-Diarrheals work by slowing _____ and increasing _____ and _____
slow peristalsis | increase water and electrolyte absoroption
74
what drugs are known as anti-diarrheals
opiates (loperamide and diphenyoxylate) bismuth bile salt binding resisn (cholestrymaine, colestipol, and colesavam)
75
what drugs are anticholinergics and are used to inhibit GI motility
dicyclomine | hyoscymaine
76
MOA of Aloestron (Lotronex)
serotonin (5HT3) antagonist = blocks visceral afferent pain and decrease colon motility
77
Aloestron is indicated for who?
for women with IBS + Diarrhea *IBS = irritable bowel syndrome (not inflamm. bowel disease)
78
GI side effects of Aloestron
Constipation; Ischemic Colitis
79
Anticholinergics inhibit _______ receptors which leads to anti______ effects
muscarinic acetylcholine antispasmodic
80
Enteric Nervous Systems: | ENS Neuron leads to increased _______
peristalsis
81
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)
82
Enteric Nervous Systems: IPAN goes and affects ______ EPAN will go to ______
IPAN: goes to ENS neurons Extrinsic: CNS
83
Definitions: | Neonate?
0 - 28 days | term + 28 days
84
Definitions: | Infant
1 - 12 months
85
Definitions: | Child
1 - 12 years
86
Definitions: | Adolescent
13 - 18 years
87
Estimating Renal Function for Kids: | what eqn to use
Beside Schwartz Equation | (0.413 x (ht in cm / SCr) = eGFR
88
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
89
GER vs GERD
GER: passage of gastric contents into the esophagus (normal thing to happen) GERD: gastric reflux cases trouble some sxs or complications
90
what is regurgitation?
effortless passage of stomach contents | aka spitting up
91
GER is caused by _____ of _______
relaxation of LES (lower esophageal sphincter)
92
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
93
Most kids older than _____ will have more classic heartburn symptoms
4 years old
94
GERD Sxs in infants?
Regurgitation Failure to Thrive Respiratory Problems (apnea/ALTE - acute life threatening event)
95
GERD Sxs in Children?
Asthma/lung issues recurrent pneumonia- like aspiration dental erosions
96
what are main non-pharm therapy options for GERD in kids
feeding changes positioning therapy lifestyle changes
97
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)
98
Indications for pharm therapy in GERD for peds
GERD present w/ complications no improvement after lifestyle modifications (2 - 4 weeks) failure to thrive!!!
99
Pharm therapy for GERD in Peds: | do drug therapy for ______ then reassess - try to take them off this
8 - 12 weeks
100
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!
101
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)
102
PPI Oral dosing? Lansoprazole? and Omeprazole?
dosing for both is like 1 mg/kg per day (adult caps tho!)
103
Peds GERD: agents that are prokinetic? improve _____ and ______
metoclopramide erthyromycin improve esophageal motility and improved LES tone
104
``` 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
105
``` ADEs of Prokinetic Drugs: Erythromcin --- ______ at antimicrobial doses ________ --> ______ Drug interactions ```
``` pyloric stenosis (projectile vomiting) QTc prolongation--> arrhythmias ```
106
What is the list of QTc prolongation
``` methadone azole antifungals ondansetron antipsychotics (IV haloperidol) fluoroquinolones antiarrhythmics macrolide abx SSRIs? ```
107
want to avoid ____ containing antacid products due to neurotoxicity
aluminum
108
ADEs of sucralfate with chronic use?
aluminum toxicity Bezoar formation = "rock in belly" zinc deficiency
109
Sucrafalate - used in infants and kids?
NOT in infants | kids ok --- typically 7 - 10 days max
110
4 main pathways of vomiting (from Peds lecture)
Blood borne toxins (chemoreceptor trigger zone) Motion (vestibular) Mechanical (vagal) Emotion
111
Vomiting Clinical Pearls: Agents assoc. w/ respiratory depression may have enhanced toxicity with children: avoid _____ in kids < 2 y.o (CONTRAINDICATED!)
promethazine
112
Vomiting Clinical Pearls: | Correct ______ and _______
dehydration and electrolyte abnormalities
113
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 ```
114
Definition: | Fecal impaction
large mass unlikely to be passed on command
115
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...
116
Definition: | Delayed bowel training --- bowel continence is expected by age ____
4
117
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
118
How Pooping Happens: | what 4 things "work" together to make productive bowel movements
internal anal sphincter external anal sphincter puborectalis muscle rectum
119
Circular smooth muscle = ______ control | Skeletal muscle = _______ control
circular: no direct control skeletal: self control
120
is it circular or skeletal muscle? | Internal anal sphincter
circular
121
is it circular or skeletal muscle? | external anal sphincter
skeletal
122
is it circular or skeletal muscle? | Puborectalis muscle
skeletal
123
is it circular or skeletal muscle? | rectum
circular
124
``` 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
125
definition of withholding (in relation to poop)
occurs when a child fails to recognize or respond to urge to defecate?
126
issue with repeated withholding?
larger stool load = stretching and possible thinning of rectal wall = increased risk of perforation
127
Complications of Constipation
``` Encopresis Bed-wetting recurrent UTIs prolapse (bc thinning) rectal ulcerations social/emotional issues ```
128
what meds can cause constipation?
``` opioids iron supplements CCBs!! TCAs Antihistamines antipsychotics Phenytoin/Carbamazepine ```
129
Red Flag Symptoms of constipation?
``` Delayed passage of meconium (aka first poop) failure to thrive bloody stools severe abdominal distension perianal fistula sacral dimple ```
130
what is 1st line tx for infants with constipation
glycerin suppository
131
what are some definite things to avoid for treating infant constipation
mineral oil/stimulant laxatives/phosphate enemas NO HONEY! botulisim toxin
132
steps in managing constipation in kids
educate disimpaction/cleanout maintain reg. bowel movements behavior modification
133
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)
134
avoid what kind of enemas?
home remedies like soap, herbal, or tap water
135
other than enemas and oral options for disimpaction - what else can you do
nasogastric - requires hosptiliazation | PEG w/ electrolytes
136
what is first line for maintenance of constipation
PEG 3550
137
other maintenance options for constipation? (NOT PEG 3550)
other osmotic agents: lactulose, magnesium hydroxide stool softeners : docusate stimulant laxatives
138
Chronic Diarrhea: | lasting more than _____ consecutive days
14
139
why is diarrhea such a problem?
dehydration!!!! electrolyte abnormalities malnutrition/malabsorption negatively impacts quality of life
140
four major categores if diarrhea
secretory osmotic excretory altered motility
141
Common etiologies for Diarrhea?
``` viral bacterial parasitic malabsorption syndromes (cystic fibrosis/celiac disease) short gut irritable bowel (crohns and ulcerative colitis) allergic nutrition medications .......... ```
142
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 ```
143
if diarrhea symptoms persist after antibiotics are stopped --- consider a _____ infection
c.diff
144
Amox/Clav -- why is the diarrhea so bad?
the clav part wrecks people
145
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!)
146
How to calculate fluid requirements for peds - use what method
Holliday Segar Method
147
Holliday Segar Method: -- Calculating Fluid Requirements: | Up to 10 kg: ______
100 mL/kg
148
Holliday Segar Method: -- Calculating Fluid Requirements: | 10 - 20 kg: _______
1000 mL + 50 mL/kg for every kg over 10!
149
Holliday Segar Method: -- Calculating Fluid Requirements: | > 20 kg: ___________
1500 mL + 20 mL/kg for every kg over 20
150
Pathogenesis of GERD: decreased ______ and ______ increased ______ and _______
decreased: esophageal clearance, gastric emptying increased: gastric pressure, acid production
151
Sxs of GERD? (adults!)
``` heartburn - dur regurgitation dysphagia belching bloating nausea globus sensation hypersalivation early satiety ```
152
Risk factors/stressors for GERD
``` overweight/obesity diet diabetes asthma smoking pregnancy delayed stomach emptying ```
153
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 ```
154
Foods that trigger REFLUX
coffee chocolate fatty foods alcohol
155
foods that trigger HEARTBURN
spicy foods acidic foods carbonation
156
Medications can worsen GERD if they _______ or ______
if they are direct irritants to esophageal mucosa; lower esophageal sphincter relaxants
157
GERD or Heartburn: | which one is mild usually and which one is moderate to severe
mild: heratburn moderate to severe: GERD
158
GERD or Heartburn: which one happens like < 2x/wk (intermittent) or which one happens >2x/wk (frequent)
intermittent: heartburn GERD: frequent
159
what is the bernstein test
put acid soln in esophagus- if painful then the patient has erosiveness going on
160
definition of strictures?
narrowing of esophagus
161
why is a strictures a problem
can cause an obstruction
162
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 ```
163
what is the max number of tums someone can have in a day
16 tabs
164
Can avoid most interactions with antacids by doing what?
separate them!! | take med 1 hour before or 4 hours after antacids!!
165
what drugs can have antacids drug interactions
``` thyroid medications tetracyclines fluoroquinolones azoles (anti fungals) steroids iron digoxin anti-retrovirals ```
166
Aluminum or Magnesium will cause confusion
aluminum
167
Pros of Antacids?
Quick onset! (~5 minutes) Relatively safe use as needed
168
Cons of Antacids?
``` short duration (~30 - 60 minutes) Risk of tolerance Frequent dosing ```
169
Treatment Overview for GERD (what are the 4 steps)
lifestyle modifications --> prn meds --> scheduled meds --> surgery
170
H2RA antagonists: Onset:______ Duration of Action: _____
onset: < 1 hour DOA: 4 - 10 hours
171
what are some examples of PRN antacids
``` Tums Milk of Magnesia Mylanta Gaviscon Alka Seltzer Pepto Bismol ```
172
All H2RA meds are dose _______ daily
twice!!!!
173
which H2RA does NOT come as an IV formulation
Cimetidine
174
Accumulation of H2RAs can lead to what things?
Mental disturbances and insomnia/drowsiness
175
Need to renally adjust H2RAs when CrCl is < ______
50 mL/min
176
Beer's Criteria for H2RAs?
avoid using in pts with delirium
177
using PPIs and H2RAs as needed? - yay or nay
NAY! | bc MOA - this isn't the best option --- these drugs do not work immediately
178
For GERD For H2RAs: Treat for how long? For PPIs: Treat for how long?
H2RAs: 6 - 12 weeks PPIs: 4 - 8 weeks
179
PPIs: Onset: _______ Duration of Action:_______
onset: 2 -3 hours | duration of action ~ 24 hours
180
what PPIs do come as an IV solution?
pantoprazole | esomeprazole
181
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
182
which PPI comes ODT
lansoprazole
183
which PPIs can you not crush
raberprazole | pantoprazole
184
Drug Interactions of PPIs: | All PPI's inhibit _______ but this inhibition is seen the most by what two PPIs?
2C19 omeprazole and esomeprazole
185
Drug Interactions of PPIs: | PPIs will increase the effect of what 3 drugs
MTX warfarin phenytoin
186
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...
187
PPIs take ________ to reach max effect
3 - 5 days
188
PPIs have a chance of causing community acquired pneumonia risk: seen within ______ of treatment initiation (how long of tx)
first 30 days
189
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.
190
Metoclopramide is good for GERD if the pt has comorbid ______
gastroparesis
191
If a pt is pregnant: | what is 1st line after Lifestyle modifications?
antacids!!
192
what is the surgical procedure done for GERD
fundoplication (laproscopic or Nissen) | reinforces the LES (wrap top of stomach around the lower esophagus)
193
who qualifies for surgery with GERD?
if the are contraindication to PPIs or PPIs and lifestyle modifications do not control symptoms
194
two most common location so ulcers
stomach | duodenum
195
what are the defensive factors against Peptic ulcers
prostaglandins bicarb mucus growth factors
196
main 3 risk factors for PUD
H.pylori infections NSAID use/antiplatelet meds smoking/alcohol/diet or stress- hospital
197
stomach ulcer or duodenum ulcer? | acid production in response to food irritates ulcer quickly
stomach! (stomach comes first...)
198
stomach ulcer or duodenum ulcer? | pain occurs 2 - 3 hours after food
duodenum!
199
complications of PUD
upper GI bleeding perforation gastric outlet obstruction
200
Non-Pharm Options of PUD therapy
``` STOP SMOKING!!! reduce psychological stress avoid food/beverages that can exacerbate symptoms avoid NSAIDs surgery.. ```
201
how does h pylori cause ulcers: | mucosal damage by _____ factors and _____ enzymes
virulence factors; bacterial enzymes
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how does h pylori cause ulcers: | Increased _______ due to cytokine release
gastric acid secretion
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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
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Treating H. Pylori: | Must include ________ and ______
anti-secretory agent | and 2 - 3 antibiotics
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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
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2 Questions to ask self when picking H.pylori treatment
PCN allergy? | Previous macrolide exposure (past 6 MOS!!)
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what drugs are macrolides
clarithromycin | azithromycin
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Treatment Regimens for H.Pylori | Regimen 1 is what drugs and how frequent of dosing?
``` Amoxicillin Metronidazole Clarithromycin PPI ALL BID!!!!!!! (even PPI!) ```
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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!!
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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 ```
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PPIs and H.Pylori: | Continue PPI after infection to prevent further issues?
NO! do not continue a PPI!
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PPIs and H.Pylori: | ______ a day PPIs are back bone of therapy
twice
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What drug class is a good back up for H.pylori treatment...?
Fluroquinolones (levofloxacin)
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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
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Bismuth salts: | ________ effect
topical antimicrobial effect
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Bismuth salts: | Improve ______ and relieve _____ in patients
improve ulcer healing | relieve pain
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Bismuth Salts: | side effect?
darkening of stool and tongue
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Bismuth salts: | concern with ______ allergy and what demographic group?
Aspirin allergy kids < 12 (bc it is a salicylate)
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Abx ADEs: | metronidazole?
avoid with alcohol!!! throwing up while drug is in system (disulfiram like reaction)
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Abx ADEs: | Tetracycline?
photosensitvity
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Abx ADEs: | Clarithromycin?
``` Taste disturbances (metallic) QT prolongation ```
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Abx ADEs: | Levofloxacin
tendon rupture sedation/mental status change QT prolongation
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Risk Factors for NSAID induced ulcer: | High risk if ...?
Hx of previously complicated ulcer 2+ risk factors
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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 ```
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Primary Prevention Strategies of NSAID induced ulcer: | Combo of _______ with NSAID
PPI (or misprostol)
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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...)
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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
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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
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for preventing NSAID induced ulcer: use a PPI how many times a day!
just ONCE a day
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Misoprostol: | ADEs/Cons
QID dosing!! Abortifacient (category X; must do pregnancy test prior to initiation) ADEs: Diarrhea, abdominal cramping, N/V, flatulence, HA
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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!! ```
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Sucralfate: | acts like a band aid: _______ complex and can form a physical barrier over an open ulcer
sucrose-sulfate-aluminum
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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
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Sucralfate ADEs
constipation, metallic taste | Al toxicity in chronic renal failure!!
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for NSAID induced ulcer: | if you can stop the NSAID: treat with PPI for _______
6 - 8 weeks
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for NSAID induced ulcer: | if you can NOT stop the NSAID: treat with PPI for _______
8 - 12 weeks
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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!
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Comparing Ulcers: (H.pylori induced, NSAID induced, or SRMD) which one is acute
SRMD
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Comparing Ulcers: (H.pylori induced, NSAID induced, or SRMD) which one is most superficial
SRMD
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Comparing Ulcers: (H.pylori induced, NSAID induced, or SRMD) which one has the most severe bleeding?
SRMD
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Comparing Ulcers: (H.pylori induced, NSAID induced, or SRMD) which one is more chronic?
H.pylori or NSAID
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Comparing Ulcers: (H.pylori induced, NSAID induced, or SRMD) which one typical has symptoms (of epigastric pain)
H.pylori
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why do we care about stress ulcers?
mortality is higher in ICU pts w/ clinically important GI bleeding
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Pathophys of Stress Ulcer formation: | (decreased or increased) cardiac output?
decreased! | decreased output = hypoperfusion = decreased motility/decreased mucosal blood flow
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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!!!
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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
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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 ```
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do NOT do Stress ulcer prophylaxis for patients with out ______ or _____ patients
w/out risk factors... NON-ICU pts - should NOT get this
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Prophylaxis options for stress ulcers
enteral nutrition and antacids | **Sucralfate, H2RAs, PPIs
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Main thing to consider when choosing an agent/route for a patient and stress ulcer prophylaxis
PO or NG or IV?!?..DUH
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Which H2RA antagonist can be only oral
cimetidine!!
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when do you discontinue stress ulcer prophylaxis
resolution of risk factors discharge from ICU extubation oral intake!!!
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out of prophylaxis for stress ulcers - what agent is used most
PPIs (SHOCKING)
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what PPIs can be given IV
esomeprazole and pantroprazole
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Metoclopramide is a prokinetic agent --- how does it work
D2 receptor antagonist
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eryhtromycin is a prokinetic agent --- how does it work
motilin agonist
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Neostigmine is a prokinetic agent --- how does it work
acetylcholinesterase inhibitor (aka the drug is a cholinergic drug)
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bethanechol is a prokinetic agent --- how does it work
agonist of muscarinic receptor (aka a cholinergic drug)
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prucalopride is a prokinetic agent --- how does it work
selective 5HT4 agonist