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Pharm 1 > GI Meds > Flashcards

GI Meds Flashcards

1
Q

What are timeframes for early, late, delayed and post- discharge PONV?

A
  • early: 2-6 hours
  • late: 6-24 hours
  • delayed: >24 hours
  • post- discharge: > 24 hours post-discharge
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2
Q

What are the top 3 risks factors that have the strongest correlation with PONV?

A
  1. ) female
  2. ) history of PONV
  3. ) non-smoker
  4. ) age <50
  5. ) general vs regional (GA 9xs the risk as regional)
  6. ) volatile anesthetics and nitrous oxide
  7. ) post-op opiods
  8. ) duration of procedure (>30 min increases risk by 60%)
  9. ) type of procedure
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3
Q

What types of procedures are associated with PONV?

A
  • cholecystectomy
  • gynecological
  • laparoscopic
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4
Q

Having one risk factor increases the risk of PONV by ______, two risk factors increases risk of PONV by _______, and so on.

A

20%

40%

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5
Q

What are risk factors for Post Discharge NV?

A
  • female
  • <50 years of age
  • hx of PONV
  • opiates in PACU
  • nausea in PACU
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6
Q

What are PONV risk factors for children?

A
  • procedure >30 min
  • age >3 years
  • strabismus surgery
  • hx of PONV or PONV in relatives
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7
Q

Who would you pretreat for PONV?

A

Moderate to high risk patients —> 3 or more risk factors

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8
Q

What are anesthesia considerations?

A
  • propofol: good for early PONV
  • GA vs regional: GA 9xs more likely to have PONV than regional
  • NSAIDS over opiates: consider alternatives to opiates
  • it is no longer recommended to reduce neostigmine dose to prevent PONV as risk of inadequate reversal is greater problem
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9
Q

What are pretreatment options?

A
    • THE BEST THING WE CAN DO IS PRE-TREAT **
  • dexamethasone
  • 5HT3 antagonists serotonin antagonists)
  • H1 blockers
  • Scopolamine patch
  • NK1 antagonists: dopaminergic
  • droperidol
  • hydration
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10
Q

What are rescue meds for PONV?

A
  • 5HT3 antagonists (serotonin)
  • D2 blockers
  • Reglan
  • H1 blocker
    • try something with a different mechanism of action than med used for pre-treatment **
  • continue to assess
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11
Q

What do you give pts who are high risk for post discharge NV?

A
  • dexamethasone
  • scopalamine patch
  • education

Rescue meds

  • zofran ODT
  • phernergan suppos/tab
  • scopalamine patch
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12
Q

Almost all of the PONV meds are recommended to be given at the end of surgery. When are the meds to be given that are the exceptions?

A
  • dexamethasone: before induction
  • scopalamine patch: 4 hours prior to pt awakening or the evening prior—> 4 hours to onset
  • Emend: 1-3 hours prior
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13
Q

What were the findings of a study done comparing 4mg zofran vs 1.25mg droperidol vs 4 mg dexamethasone?

A

They were all equally effective—> 25% reduction in PONV vs placebo

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14
Q

What are 5HT3 antagonists?

A 
Serotonin receptor 3 antagonists located in the gut (what you eat can also affect your mood)
- ondansetron
- granisetron
- dolasetron
- palonosetron 
—> ends in SETRON
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15
Q

What is the metabolism and half life like for 5HT3 meds?

A

Metabolized by CYP450

T 1/2 of ondansetron= 4 hours

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16
Q

What are side effects of 5HT3 meds?

A 
Constipation
Diarrhea 
Nausea
Dizziness
 * when 32mg given —> QTC prolongation noted (watch daily total)
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17
Q

What does dexamethasone do?

A

It’s a corticosteriod responsible for endorphin release

  • prostaglandin antagonist—> decreases inflammatory response. Blocks signals that boost NV
    • augments other antiemetics
  • decreases pain as well
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18
Q

What are side effects of dexamethasone?

A

Impaired wound healing/infection
Increased glucose
Hypertension/edema
Altered mental status
** if you only give 1 or 2 doses you won’t see much of these unless the pt is high risk—> DM, dementia, impaired wound healing already
—> side effects are usually mild unless it exacerbates something else they have

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19
Q

What is the half life for dexamethasone?

A

T1/2= 35-45 hours

—> steroids have to go into cell and adjust how that cell is making proteins- this is a process that takes some time

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20
Q

What is Droperidol?

A
  • anti-dopaminergic (D2) drug
  • mild antihistamine and antiserotonergic
    Works on the chemoreceptor trigger zone
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21
Q

What are side effects of droperidol?

A

QT prolongation if >5mg (usually give 2.5mg)
- dysphoria
- hypotension
- EPS(extra pyramidal symptoms
Very closely related to haloperidol, which is an antipsychotic— can have anxiety, detachment

22
Q

What are Extra Pyrimidal Symptoms (EPS)?

A

Not enough dopamine (Parkinson’s like symptoms)
- torticallis (neck jerking)
- lip smacking
- nystagmus
- tremors
- gait abnormalities
- feeling that if you don’t get up and move you will just die
—-> if not recognized early, may become permanent

23
Q

What is the metabolism and half life of droperidol?

A
  • hepatic metabolism

- t 1/2= 2.3 hours

24
Q

What are Phenothiazines?

A

Promethazine (phenergan) and prochlorpromazine (Compazine)
- close to Thorazine: at low psychoactive doses, really good at controlling N/V

D2 receptor antagonists

25
Q

What are the metabolism, half life and major side effects of phenothiazines?

A
  • Hepatic Metabolism
  • T 1/2= 4-8 hours
  • Highly sedating** watch when giving other sedating meds
  • EPS
26
Q

What are H1 antagonists?

A

Diphenhydrinate (Dramamine)—combo of diphenhydramine and chlorotheophylline

  • anti- histamine—> may increase BP
  • highly sedating
    • Benadryl falls into this category
27
Q

What do H1 (Dramamine) antagonists do?

A 
Block dizziness (CN VIII)
Treat nausea
28
Q

What is scopalamine and what are some side effects to warn pts of?

A 
- anticholinergic 
Side effects:
-  blurred vision
- dry mouth 
- urinary retention
- constipation
- dilated pupil on ipsilateral side as patch
29
Q

What is Arepetiant (Emend)?

A
  • Neurokinin 1 receptor Antagonist
    • works on the brain stem and dorsal vagal complex
    • blocks substance P
    • very expensive, reserved for very advanced nausea states (end of life, pancreatic CA)
30
Q

How is Aprepitant metabolized?

A 
CYP 3A4 substrate and weak inhibitor
T 1/2= 9-3 hours 
Highly protein bound
—> give 1-3 hours prior to induction 
Dose: daily 
(Almost no side effects/great safety profile)
31
Q

What is Metoclopramide (Regan) and what does it do?

A

Dopamine antagonist - antagonizes dopamine’s effect on the CTZ and theoretically contributes to an antiemetic effect

  • increases lower esophageal sphincter tone
  • enhances peristalsis-> accelerates rate of gastric emptying
  • does NOT change pH
32
Q

How is metoclopramide metabolized?

A
  • undergoes hepatic metabolism with an extensive first-pass effect
  • undergoes renal elimination—> adjust dose for renal impairment
  • readily crosses BBB and placenta
  • excreted in breast milk
33
Q

What are side effects of metoclopraminde?

A
  • abdominal cramping with rapid IV admin (<3 minutes)
  • akathesia: feeling of unease, restlessness in legs
  • dystonic extrapyrimidal reactions with chronic use and doses 40-80mg/day
34
Q

What can be give instead of metoclopramide?

A

Erythromycin stimulates peristalsis without the EPS (can give to pts with Parkinson’s)

35
Q

What are interactions and cautions with metoclopramide?

A
  • Inhibitory effects on cholinesterase
    • prolongs succ and mivacurium
    • slows metabolism of ester LAs
  • may increase sedative effect of CNS depressants
  • may increase EPS of other drugs
    • avoid admin in combo with phenothiazines or butyrophenones
36
Q

With metoclopramide, which should you avoid administration in conjunction with?

A
  • pts with seizures
  • pts with existing EPS
  • pts with mechanical gastric outlet obstruction: will just push against obstruction
37
Q

What dose of reglan is administered to pre-operatively decrease gastric fluid volume?

A

10-20 mg IV over 3-5 minutes

 - give 15-30 minutes before induction  - may not reverse opioid-induced inhibition of gastric mobility  - faster administration can produce gastric cramping
38
Q

What do H2 receptor antagonists do?

A
  • inhibit histamine binding to the receptors on gastric parietal cells
    • selective and reversal inhibition
    • used in PUD and GERD
39
Q

What are drug names of some H2 antagonists?

A

cimetidine (tagament)
Ranitidine (Zantac)
Famotidine (pepcid)
Nizatidine (axid)—> EXPENSIVE

40
Q

What is the mechanism of action of H2 antagonists?

A

—> H2 antagonists competitively and selectively inhibit binding of histamine to H2 receptors and prevent the release of H+ ions from parietal cells
(No effect on gastric emptying)

41
Q

Which H2 antagonist is the most potent? Least potent?

A

Most potent—> famotidine

Least potent—> cimetidine (and shortest acting)

42
Q

What are clinical uses for H2 histamine receptor antagonists?

A

The thought is to administer before induction to increase pH of gastric fluid to prevent damage in the case of aspiration- actually did more harm since gastric pH is acidic to kill organisms, this change in pH allowed them to live and caused more problems.
—> they have no effect on pH of gastric fluid that is already in the stomach anyway
*** remember, they increase pH, but don’t necessarily change volume

The real clinical use:

  • pre-op prophylaxis of pts with allergic hx that are undergoing procedure with likelihood of allergic reaction (IV contrast)
  • to treat drug induced histamine release—> must give H1 and H2 antagonist—> won’t prevent s/s but hypotension will be less
43
Q

How would you give an H2 histamine receptor antagonist to prevent an allergic reaction during a procedure?

A
  • Give oral H1 antagonist (diphenhydramine) 0.5-1mg/kg
  • and give H2 antagonist (cimetidine) 4mg/kg q 6 hours 12-24 hours prior
  • can also give corticosteroid 24 hours prior as well
44
Q

What will happen if you only give and H2 antagonist to treat drug-induced histamine release?

A

Effects of drug induced histamine release may be exaggerated
(Always give H1 and H2 antagonists for this)

45
Q

What are side effects of H2 histamine receptor antagonists?

A 
Most common:
- diarrhea
- HA
- fatigue
- skeletal muscle pain
Rare:
- thrombosis 
- mental confusion (in non-ambulatory pts)
- Brady arrythmias (mostly with rapid IV administration)
46
Q

What are drug interactions with H2 histamine receptor antagonists?

A

Usually seen with cimetidine and ranitidine

  • inhibit CYP 450 oxidase system
  • slows metabolism of drug that metabolize via this pathway:
    • diazepam, propranolol, meperidine, lidocaine
  • alters absorption of some drugs by increasing gastric pH
    • decreased absorption of ketoconazole, iron products and calcium carbonate (ca citrate less effected)
47
Q

Having a low gastric pH is important for the absorption of which elements?

A

Fe
Mg
Ca
Increasing pH can lead to anemia, atypical fractures and low Mg side effects

48
Q

What medications fall under the classification of proton pump inhibitors?

A 
Omeprazole (Prilosec)
Esomeprazole (nexium)
Pantoprazole (protonix)
Lansoprazole (Prevacid)
Rabeprazole (aciphex)
49
Q

What disorders are PPIs used to treat?

A

Moderate to severe GERD
Hypersecretory disorders
PUD

50
Q

How is a PPI given preop?

A

One given PO the onset is 2-6 hours
Duration >24 hours
Give the night before or 3 hours prior
Can give IV form 1 hour prior to decrease gastric fluid and pH

51
Q

What are adverse reactions of PPIs?

A
  • C. diff diarrhea—> long term PPI use can cause C. Diff, especially if you are a carrier—> gastric pH changes so now C.diff can survive, even if no antibiotics were given
  • kidney injury
  • dementia
  • reduced absorption of Ca (fractures), Fe (anemia), Mg (arrhythmias, muscle weakness, confusion), B12
  • ** we are finding, the longer people are on theses the worse the effects ***

Pharm 1 (9 decks)

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