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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
What are the metabolism, half life and major side effects of phenothiazines?
- Hepatic Metabolism - T 1/2= 4-8 hours * Highly sedating** watch when giving other sedating meds - EPS
26
What are H1 antagonists?
Diphenhydrinate (Dramamine)—combo of diphenhydramine and chlorotheophylline - anti- histamine—> may increase BP - highly sedating - Benadryl falls into this category
27
What do H1 (Dramamine) antagonists do?
``` Block dizziness (CN VIII) Treat nausea ```
28
What is scopalamine and what are some side effects to warn pts of?
``` - anticholinergic Side effects: - blurred vision - dry mouth - urinary retention - constipation - dilated pupil on ipsilateral side as patch ```
29
What is Arepetiant (Emend)?
- 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
How is Aprepitant metabolized?
``` 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
What is Metoclopramide (Regan) and what does it do?
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
How is metoclopramide metabolized?
- 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
What are side effects of metoclopraminde?
- 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
What can be give instead of metoclopramide?
Erythromycin stimulates peristalsis without the EPS (can give to pts with Parkinson’s)
35
What are interactions and cautions with metoclopramide?
- 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
With metoclopramide, which should you avoid administration in conjunction with?
- pts with seizures - pts with existing EPS - pts with mechanical gastric outlet obstruction: will just push against obstruction
37
What dose of reglan is administered to pre-operatively decrease gastric fluid volume?
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
What do H2 receptor antagonists do?
- inhibit histamine binding to the receptors on gastric parietal cells - selective and reversal inhibition - used in PUD and GERD
39
What are drug names of some H2 antagonists?
cimetidine (tagament) Ranitidine (Zantac) Famotidine (pepcid) Nizatidine (axid)—> EXPENSIVE
40
What is the mechanism of action of H2 antagonists?
—> 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
Which H2 antagonist is the most potent? Least potent?
Most potent—> famotidine | Least potent—> cimetidine (and shortest acting)
42
What are clinical uses for H2 histamine receptor antagonists?
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
How would you give an H2 histamine receptor antagonist to prevent an allergic reaction during a procedure?
- 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
What will happen if you only give and H2 antagonist to treat drug-induced histamine release?
Effects of drug induced histamine release may be exaggerated (Always give H1 and H2 antagonists for this)
45
What are side effects of H2 histamine receptor antagonists?
``` Most common: - diarrhea - HA - fatigue - skeletal muscle pain Rare: - thrombosis - mental confusion (in non-ambulatory pts) - Brady arrythmias (mostly with rapid IV administration) ```
46
What are drug interactions with H2 histamine receptor antagonists?
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
Having a low gastric pH is important for the absorption of which elements?
Fe Mg Ca Increasing pH can lead to anemia, atypical fractures and low Mg side effects
48
What medications fall under the classification of proton pump inhibitors?
``` Omeprazole (Prilosec) Esomeprazole (nexium) Pantoprazole (protonix) Lansoprazole (Prevacid) Rabeprazole (aciphex) ```
49
What disorders are PPIs used to treat?
Moderate to severe GERD Hypersecretory disorders PUD
50
How is a PPI given preop?
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
What are adverse reactions of PPIs?
- 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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