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NURA 671 Advanced Pharmacology > GI Pharm/Diuretics > Flashcards

GI Pharm/Diuretics Flashcards

1
Q

Patient risk factors of PONV

A
  • female
  • age < 50
  • nonsmokers
  • hx of PONV/motion sickness
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2
Q

Surgical risk factors of PONV.

A
  • length of surgery
  • laparotomies
  • laparoscopic procedures
  • ENT
  • breast
  • OBGYN
  • plastic surgeries
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3
Q

anesthetic risk factors of PONV

A
  • use of inhalational agents
  • N2O
  • neostigmine
  • etomidate
  • opioids
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4
Q

PONV is assicated with what complications?

A
  • increased morbidity
  • dehydration
  • electrolyte imbalances
  • wound dehiscence
  • bleeding
  • esophageal rupture
  • airway compromise
  • low patient satisfaction
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5
Q

What is the vomitting center and where is It located?

A
  • nucleus of neurons in the medulla oblongota
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6
Q

What are some direct stimuli of nausea?

A
  • noxious odors
  • pain
  • motion sickness
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7
Q

What are some indirect stimuli of nausea?

A
  • first activate the chemoreceptor trigger zone (CTZ) in area postrema/floor of 4th ventricle which then activates the vomitting center
    • CTZ is stimulated by signals in the stomach/small intestine or by direct stimulation (ex. opioids, chemotherapy)
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8
Q

What are the 5 receptor types targeted by our antiemetic drugs?

A
  • 5HT3 = serotonin3
  • DA2 = dopamine2
  • M = muscarinic cholinergic
  • H1 = histamine1
  • NK1 = neurokinin1
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9
Q

Explain the antiemetic effect of midazolam.

A
  • may work to decrease synthesis and release of dopamine in the CRTZ and decrease anxiety related to signaling in the vomitting center
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10
Q

What class of drug is dexamethasone?

Explain the antiemetic effect.

When is typically given?

What is the dose?

A
  • corticosteroid
  • antiemetic mechanism unclear
  • typically given post induction for antiemetic effect - needs to be given at the beginning of a case
  • works synergistically with ondansetron
  • 4 - 8 mg
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11
Q

Scopolamine: Class, structure, MOA, dosing, SE

A
  • Class
    • Anticholinergic at muscarinic receptor
  • structure
    • Tertiary amine = crosses the BBB
  • MOA
    • Competitively and reversibly binds to muscarinic receptors to inhibit binding of Ach
  • dose
    • Most often used transdermal
      • 5 mcg/hour for 72 hours
      • Best when placed at least 4 hours prior to noxious stimuli for prophylaxis
  • Side Effects:
    • Pupillary dilation, increased IOP → avoid in glaucoma (especially narrow angle)
    • Bronchodilation
    • Antisialogogue
    • Anticholinergic syndrome (restlessness, hallucinations, somnolence and unconsciousness. Tx: Physostigmine)
    • Sedation
    • Dry mouth
    • Moderate increase in HR/CO - not as much as atropine and glyco
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12
Q

amisulpride (barhemsys): class + use

A
  • class
    • dopamine (D2/D3) antagonist approved by FDA in 2020 for PONV
  • use
    • proposed as a replacement for droperidol in multimodal PONV mgt.
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13
Q

amisulpride (barhemsys): PK

A
  • Rapid onset of action (1-2 minutes) - give slowly over 1 -2 min
  • E1/2 life – 4-5 hours (less than droperidol)
  • Vd in surgical patients: 127 to 144 L
  • Minimal metabolism/no cytochrome P450 metabolism (excreted unchanged in urine 58%/feces 23%)
    • avoid in renal failure (OK in mild to moderate renal disease GFR>30 ml/min
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14
Q

amisulpride (barhemsys): SE (chart with drug vs placebo)

A
  • dose dependent QT prolongation
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15
Q

amisulpride (barhemsys): cautions/contraindications/drug interactions

A
  • Dose dependent QT prolongation warning in package insert
    • Avoid doses >10mg
    • Avoid in known prolonged QT
    • Avoid with other drugs with prolonged QT as SE.
  • Minimal drug interactions
    • neither inhibits nor promotes liver enzyme activity
    • exhibits limited plasma protein binding (25-30%)
  • AVOID with Parkinson’s patients
  • Adverse effects similar to placebo group
  • Well-tolerated in elderly patients
  • Avoid in renal failure (OK in mild to moderate renal disease GFR>30 ml/min)
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16
Q

amisulpride (barhemsys): dose + misc notes

A
  • Prevention of PONV (either alone or in combination):
    • 5 mg as a single intravenous dose infused over 1-2 minutes at anesthesia induction
  • treatment of PONV
    • 10 mg as a single intravenous dose infused over 1-2 minutes post-operatively
  • Photodegradation an issue: administer within 12 hours of removal from the protective carton.
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17
Q

List some additional 5HT3 antagonists besides zofran.

A
  • Dolasetron
  • Grainsetron
  • Palonosetron
  • Ramosetron
  • Tropisetron
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18
Q

aprepitant (emend): class, MOA, use, Vd, PB, Metabolism, 1/2 life, dose

A
  • class
    • Neurokinin- 1 (NK1) antagonist
  • MOA
    • Serves to antagonize substance P
    • Little to no affinity for serotonin, dopamine, and corticosteroid receptors
  • use
    • PONV and nausea/vomiting related to cancer chemotherapy (typically in combination with other antiemetics)
      • Moderate effectiveness- usually as part of multi-modal approach
  • Vd: 70L
  • PB: >95%
  • Primary metabolism by liver: CYP3A4
  • Half-life 9-13 hours
  • Dose PONV: 40 mg IV prior to induction (better if given prior to exposure of “offending agents”)
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19
Q

List potential side effects of NK1 antagonists

A
  • diarrhea
  • neutropenia, anemia, leukopenia (concern in CA population)
  • peripheral neuropathy
  • dyspepsia
  • UTI
  • injection site pain

**remember these SE may be more notable with chronic use and not so much with single time use**

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20
Q

What are the potential drug interactions of NK1 antagonists?

A
  • CYP3A4 metabolism inhibition:
    • metabolized by CYP3A4, but also inhibits CYP3A4
    • many drug interactions including many chemotherapeutic drugs and corticosteroids… adjusted doses important).
  • CYP2D6 inducer
    • warfarin (would be subtherapeutic)
    • oral contraceptives (would be subtherapeutic)
    • codeine (more of drug metabolized to morphine – resp depression and OD)
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21
Q

List two cannabionoid agents that a patient might be taking.

A
  • Dronabinol [Marinol]
  • Nabilone [Cesamet]
  • both chemically related to the active ingredient in marijuana
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22
Q

What is the use and MOA of cannabionoids?

A
  • Unknown MOA: activation of cannabinoid receptors adjacent and within vomiting center
  • Improves chemotherapy induced nausea and improves appetite in HIV patients
  • NOT currently FDA approved for use in PONV
23
Q

What are adverse effects of cannabinoids?

A
  • same as marijuana
    • sedation (additive with other sedatives)
    • temporal disintegration
    • dysphoria
    • personality changes
    • tachycardia and hypotension
    • Abuse potential (*Schedule III DEA controlled substance)*
24
Q

What is the occurence of aspiration in the perioperative period?

A
  • 1/3 with laryngoscopy
  • 1/3 w/ extubation
  • 1/3 during the procedure
25
Q

What are the primary determinants of pulmonary complications regarding aspiration?

A
  • volume and acidity of apsirated gastric contents
26
Q

What are some foods/factors that precipitate effects of GERD? Lifestyle modifications to treat GERD?

A
  • smoking
  • alcohol
  • fatty meals
  • caffeine
  • acidic foods
  • citrus
  • chocolate
  • eat smaller meals throughout day
  • sleep with HOB elevated
27
Q

Briefly describe pharmacologic management of GERD.

A
  • PPIs - ↓ acid secretion
  • H2 blockers - ↓ acid secretion
  • Antacids - ↑ gastric pH
  • Metoclopramide - prokinetic functions, encourgage gastric emptying, increase tone of LES
  • Sucralfate / misoprostol – cytoprotective (not used in aspiration prophylaxis)
28
Q

What is the MOA of antacids?

A
  • Neutralize hydrogen ions in gastric contents or decrease the secretion of hydrogen chloride into the stomach
  • Aluminum, calcium and magnesium salts
    • Hydrogen ions in the stomach acid react with the base, forming a stable compound- consuming the hydrogen ions and increase pH >5.
  • Relieves symptoms of gastritis, improves rate of gastric ulcer healing and duodenal ulcer pain relief, increases gastric motility (neutralized pH increases gastrin release and gastric motility).
29
Q

What are some considerations for long term use and potential drug interactions of antacids?

A
  • If pH too high, impaired food digestion
  • Electrolyte abnormalities
  • Drug interactions: increase rate of absorption for salicylates, indomethacin and naproxen; decreased bioavailability of PO cimetidine
30
Q

Sodium bicarbonate: MOA, cautions

A
  • Prompt rapid neuralization of stomach pH, may result in acid rebound
  • Pts with HTN, heart disease may not tolerate sodium load
31
Q

Magnesium hydroxide (milk of magnesia): MOA, cautions

A
  • Prominent laxative, osmotic diarrhea
  • Caution in renal impairment- results in metabolic alkalosis, neurologic, neuromuscular and cardiovascular impairments
32
Q

Calcium carbonate: MOA, cautions

A
  • Metabolic alkalosis with chronic therapy
  • Symptomatic hypercalcemia in renal disease, hypophosphatemia, acid rebound
33
Q

Aluminum hydroxide: MOA, cautions

A

•Renal disease, excessive aluminum concentration → encephalopathy

•SLOWS gastric emptying → (could increase aspiration risk), constipation

•Phosphorous depletion leading to anorexia, muscle weakness, osteoporosis

34
Q

What is histamine?

Where is It synthesized and stored?

Why is It relased?

What does It cause upon release?

Which receptors mediate effects?

A
  • Naturally occurring endogenous amine
  • Synthesized in tissues –decarboxylation of histadine
  • Stored in vesicles- mast cells (skin, lung, gastric mucosa) & circulating basophils
  • Released in response to antigen-antibody reaction/ certain drugs
  • Induces contraction of smooth muscle in the airways, increases secretion of acid in the stomach, and stimulates release of neurotransmitters in CNS
  • Effects mediated by H1, H2 and H3 receptors
35
Q

Where are H1 receptors expressed?

What effects do they exhibit?

A
  • smooth muscle-contraction lung & GI, vascular endothelium- release of NO, sensory nerve stimulation
  • Lungs - bronchoconstriction – asthma/bronchitis → increased airway resistance
  • Vascular smooth muscle – predominant effect of histamine= dilation – hypotension/erythema
  • Vascular endothelium – increased capillary permeability - edema
  • Peripheral nerves - sensitization - itching, pain, sneezing
  • Heart-found in A-V node-slow HR by slowing conduction
36
Q

Where are H2 receptors expressed?

What effects do they exhibit?

A
  • gastric parietal cells, cardiac muscle, mast cells
  • Heart – Positive inotropic and chronotropic effects → increase in heart rate and contractility
    • Coronary vasculature- vasodilation (offsets H1 constriction)
  • Airways - relaxes bronchial smooth muscle
  • Stomach
    • Activation of cAMP → activates proton pump of parietal cells to secrete hydrogen ions
    • Effects due to direct stimulation of gastric parietal cells- increases gastric acid secretion – increased risk of PUD, GERD
37
Q

Where are H3 receptors expressed?

What effects do they exhibit?

A
  • sort of analagous to alpha 2 receptors with negative feedback mechanisms
  • Location- Heart & Presynaptic postganglionic SNS fibers
  • Stimulation causes Inhibition of synthesis and release of histamine
  • Activity impaired by H2 antagonists → enhanced histamine release. AVOID rapid administration of these agents esp when in combo with a histamine releaser (eg. Atracurium)
    • should coadminister an H1 blocker because of the impaired inhibition of histamine release by H2 antagonists
38
Q

How do H1 and H2 antagonists work?

A
  • H1 or H2 antagonists- Competitive and reversible inhibition.
    • The drugs occupy receptors on effector cell membranes.
    • Histamine receptors are seven-transmembrane G protein-coupled receptors
  • H1 antagonists- Allergic rhinitis treatment
  • H2 antagonists-inhibit acid gastric fluid secretion
  • H1 and H2 antagonists do not inhibit the release of histamine- they block the response to histamine!
39
Q

H1 antagonists are classically known as _________ and are used to treat what conditions?

A
  • anithistamines
  • mild allergy
    • rhinitis, conjunctivitis, uticaria, pruritis
  • motion sickness
  • chemotherapy induced NV
  • PONV
  • insomnia
40
Q

H1 antagonists block which actions of histamine at H1 receptors?

A
  • vasodilation
  • increased capillary permeability
  • bronchoconstriction
  • CNS effects
  • Itching
  • pain
  • do not block H2 receptors
  • some bind to muscarinic receptors
41
Q

List first generation H1 antagonists and their characteristics.

A
  • diphenhydramine
  • hydroxizine
  • chlorpheniramine
  • promethazine (phenergan)
  • doxepin
  • sedation
  • less specific for H1 receptors
    • active at muscarinic, serotonin and alpha receptors
  • lipophilic
  • nonionized
  • cross BBB
42
Q

List second generation H1 antagonists and their characteristics.

A
  • loratidine
  • desloratidine
  • acrivastine
  • fexofenadine
  • non drowsy
  • more selective for H1
  • less crosses BBB → decreases CNS toxicity
  • ionized at physioloic pH
43
Q

Name an anitcholinergic used for PUD/GERD.

What is the MOA and primary use?

Adverse Effects?

A
  • Dicyclomine
    • Muscarinic ACh receptor antagonist
    • Decreases acid secretion
    • Primarily used to treat irritable bowel syndrome
  • Less effective than H2 antagonists and PPIs
  • Adverse effects
    • •Dry mouth, constipation, blurred vision, cardiac arrhythmia, urinary retention
    • doesn’t have sedative issue like scopolamine so good for daily use
44
Q

PUD TX: chart

A
45
Q

Misoprostol: Class + use

A
  • Methyl analog of prostaglandin E1
  • In US, only indicated in the prevention of NSAID-induced ulcers
46
Q

misoprostol: MOA

A
  • Inhibits gastric acid secretion by inhibiting histamine-stimulated cAMP production
  • Mucosa-protective; binds to prostaglandin E receptors, facilitates production of mucus and bicarbonate
47
Q

misoprostol: Pregnancy category, adverse effects

A
  • Pregnancy category X
    • Stimulates uterine contraction
    • Used in combination with mifepristone to induce pregnancy termination
  • ADE
    • Diarrhea (up to 40%)
    • Abdominal cramps (7 – 20%)
48
Q

sucralfate: class, use, MOA

A
  • Aluminum salt of a sulfated disaccharide
  • Used for acute/maintenance tx of duodenal ulcers
  • MOA
    • In acidic environment (pH < 4), forms a gel-like substance that selectively binds to mucosa; forms protective barrier against acid, pepsin etc…
    • No acid-neutralizing activity
    • Does not treat cause of ulcer, just coats/protects it
49
Q

sucralfate: PK, adverse effects, administration considerations

A
  • Minimal systemic absorption; >90% excreted in feces
  • ADE:
    • Constipation (2%)
    • Aluminum toxicity
  • Separate administration of other drugs by 2 hours before or 4 hours after
    • This prevents 1) changes in pH 2) inhibition of absorption of other drugs (common with co-administration)
  • Pills are difficult to swallow for many patients
50
Q

Triamterene: class and MOA, cautions

A
  • potassium sparing diuretic
    • CB says this is a weak diuretic - often used in bombo with a thiazide or loop diuretic
  • Site of action: Collecting duct
  • Action: Na+ channel blockade (luminal membrane; independent of aldosterone)
  • precautions: can cause hyperkalemia
51
Q

spironolactone: class, use

A
  • class
    • synthetic 17-lactone drug
    • competitive aldosterone antagonist
      • ***aldosterone is a hormone that increases the reabsorption of Na and H2O & seceretion of poatssium → increases volume and BP
  • use
    • primarily to treat heart failure, ascites, hypertension, hypokalemia, and Conn’s syndrome
  • spironolactone is a weak diuretic, and is usually combined with other diuretics (HCTZ)
52
Q

Acetazolamide (diamox): class, use, MOA

A
  • class
    • carbonic anhydrase inhibitor
    • Carbonic Anhydrase catalyzes H+ and HCO3- released from CO2 and H2O. H+ is then excreted in exchange for Na+ on the renal luminal membrane & HCO3- is reabsorbed with Na+
  • Use
    • Glaucoma, altitude sickness, ICP
  • MOA
    • blocks the action of carbonic anhydrase therefore increasing amounts of Na+, and H2O in the urine (and decreasing bicarb reabsorption)
53
Q

Dopaminergic agents, low dose dopamine: dose, uses and considerations

A
  • dose: 1 - 3 mcg/kg/min
  • Renal vasodilation
  • Inhibition Na-K-ATPase pump/decreases renal O2 consumption
  • Effect diminished after 48 hours-down-regulation of dopaminergic receptors/contraction intravascular volume
  • No evidence dopamine has a renal protective effect despite increased urine output
54
Q

Dopaminergic agents, fenoldopam: class, MOA, PK

A
  • Selective for D1 receptor with moderate action at alpha 2
    • arterial/arteriolar dilation leading to a decrease in BP via activation of peripheral D1 receptors
    • Increases renal perfusion and urine output
  • Rapid onset, short half-life (10 minutes)
  • Short term treatment of severe HTN

NURA 671 Advanced Pharmacology (9 decks)

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