Term
| The advantages of morphine sulfate |
|
Definition
| Analgesic, amensic +, reversible w/ Narcan, longer duration |
|
|
Term
| Disadvantages of morphine sulfate |
|
Definition
| Respiratory depression, longer duration |
|
|
Term
| Morphine sulfate is used for... |
|
Definition
| Pain relief, pacing, and Post ETT |
|
|
Term
| The advantages of Fentanyl |
|
Definition
| Analgesic, amnesic +, reversible w/ Narcan, short duration |
|
|
Term
| Disadvantages of Fentanyl |
|
Definition
| Respiratory depression, short duration |
|
|
Term
|
Definition
| Pain relief, pacing, and post ETT |
|
|
Term
| Advantages of Versed (midazolam) |
|
Definition
| Quick acting, IN/IM/IV, somnolence, amnesic ++++, short duration |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Combative pts, post ETT, pacing, and severe anxiety |
|
|
Term
| Advantages of Valium (diazepam) |
|
Definition
| Short acting, IV/IM, somnolence, and amnesic ++ |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Combative pts, post ETT, pacing, and sever anxiety |
|
|
Term
|
Definition
| Rapid onset, IV/IM, somnolence |
|
|
Term
| Disadvantages of Haldol (hypnotic) |
|
Definition
|
|
Term
|
Definition
| Acute psychosis and aggressive pts |
|
|
Term
| Advantages of Etomidate (hypnotic) |
|
Definition
|
|
Term
| Disadvantages of Etomidate |
|
Definition
|
|
Term
|
Definition
|
|
Term
| These are small-diameter afferent fibers that cause sensation of pain when activated. |
|
Definition
|
|
Term
| This is the primary pain inducing neurotransmitter. |
|
Definition
|
|
Term
| What do nociceptors release when stimulated? |
|
Definition
|
|
Term
| These drugs act at the tissue site to reduce pain and inflammation by interfering with prostaglandin synthesis/release. |
|
Definition
| Peripherally acting drugs |
|
|
Term
| How do peripherally acting drugs reduce pain/inflammation? |
|
Definition
| Interfere with prostaglandin synthesis/release |
|
|
Term
| Centrally acting drugs are... |
|
Definition
|
|
Term
| These neuro pathways, located in the dorsal horn of the spinal cord, release substance P upon nociceptor stimulation, which results in pain and analgesia system activation. |
|
Definition
|
|
Term
| These neuro pathways, located in the spinal cord, release NE when stimulated, inhibiting Substance P. |
|
Definition
|
|
Term
| Drugs or meds produced exclusively from opium. |
|
Definition
|
|
Term
| Synthetic drugs that mimic opium products. |
|
Definition
|
|
Term
| Any substance that induces a dream-like sleep. |
|
Definition
|
|
Term
| What are the three types of opioid receptors? |
|
Definition
|
|
Term
| These opioid receptors cause analgesia, respiratory depression, meiosis (pin-pt pupils, euphoria and physical dependence. |
|
Definition
|
|
Term
| These opioid receptors are located primarily in the dorsal horn of the spinal cord, and produce analgesia by depressing pain transmission. To a lesser degree, also produce miosis and sedation. |
|
Definition
|
|
Term
| What are the benefits of targeting Kappa opioid receptors? |
|
Definition
| They do not cause respiratory depression or euphoria. |
|
|
Term
| These opioid receptors are poorly understood; may cause analgesia and respiratory depression. |
|
Definition
|
|
Term
| This group of opioids exhibits a high affinity for Mu receptors, and a moderate affinity for Kappa receptors. |
|
Definition
|
|
Term
| This is a commonly carried agonist opioid. |
|
Definition
|
|
Term
| This opioid is 6-10x more potent than morphine sulfate. |
|
Definition
|
|
Term
| This is a naturally occuring opioid, is 1/10th as potent as morphine, but is absorbed better orally. |
|
Definition
|
|
Term
| Codeine is often combined with... |
|
Definition
| ASA (aspirin) or APAP (tylenol) |
|
|
Term
| This is an oral opioid that is less potent than codeine, and is a commonly abused street med. |
|
Definition
|
|
Term
| This is a synthetic opioid that is 1/10th as potent as morphine, works well for extremity fractures, but was pulled due to manufacturing issues. |
|
Definition
|
|
Term
| This is a short acting opioid, 100x more powerful than morphine, but short acting. Commonly administered via IV. |
|
Definition
|
|
Term
| This is an oral opioid analgesic, removed by the manufacture in 2003, often used illegally as a heroin substitute. |
|
Definition
|
|
Term
| Why was LAAM discontinued? |
|
Definition
| Side-effect of severe ventricular dysrhythmia |
|
|
Term
| This is used in Europe as a med, 3x more potent than morphine, high lipid solubility, and is metabolized to morphine. |
|
Definition
|
|
Term
| These opioids bind to opioid receptors with varying affinity, but they do not exert agonist activity at any receptor (ex. Narcan). |
|
Definition
|
|
Term
|
Definition
| Blocks prostaglandin synthesis (analgesic), lowers temp by causing direct vasodilation (antipyretic), and 100 mg will inhibit platelet aggregation for the life span of the platelet |
|
|
Term
|
Definition
| Classic signs of Aspirin toxicity include febrile, tachycardia, and tachypnea; 400 mg/kg to reach LD50, and non-enteric coated forms clump in the stomach (slowing absorption) |
|
|
Term
|
Definition
| Blocks prostaglandin synthesis (analgesic) and resets the hypothalamus (the body's thermostat/antipyretic) |
|
|
Term
| Acetaminophen toxicity info |
|
Definition
| Liver dies over the course of 7-8 days, treatment is with NAC w/in 24 hr, and levels are 15 g for an adult, 10 g for a child |
|
|
Term
|
Definition
| Block prostaglandin synthesis (analgesic); antipyretic effects are unclear. |
|
|
Term
|
Definition
| Rare, takes 1255 mg/kg in mice, but may cause GI disturbances/bleeding and renal failure in extreme cases |
|
|
Term
| These meds stabilize cell membranes to prevent the release of harmful bronchoconstricting substances and inflammation mediators. |
|
Definition
|
|
Term
| Corticosteroids are indicated for... |
|
Definition
| Severe chronic asthma and COPD |
|
|
Term
| These meds prevent inflammation in the lungs, maintain bronchiole relaxation, decrease mucus production, and prevent vascular permeability. |
|
Definition
| Antileukotrienes/Leukotriene Receptor Agonists (LTRAs) |
|
|
Term
| These meds are indicated for prophylaxis and chronic treatment of asthma in adults and children older than 12. |
|
Definition
|
|
Term
| Although drugs from this class are not recommended in the use of children under 12, this specific drug is acceptably used in children over 2 to treat chronic asthma and prophylaxis. |
|
Definition
|
|
Term
| T or F, antileukotrienes are indicated for acute asthma attack. |
|
Definition
|
|
Term
| These drugs, used to prevent chronic bronchospasm, stabilize mast cells walls to limit degranulation, but possess ZERO direct bronchodilation properties. |
|
Definition
|
|
Term
| Mast cell stabilizers are indicated for... |
|
Definition
| Rx of severe, chronic asthma (but not acute asthma attacks) |
|
|
Term
| These drugs, used to prevent and treat bronchospasm, work by stimulating cAMP action resulting in bronchodilation. |
|
Definition
|
|
Term
| What are the respiratory effects of xanthine derivatives? |
|
Definition
-Stimulates medulla to stimulate respiratory activity
-Relaxes bronchial smooth muscle
-Decreases mast cell degranulation |
|
|
Term
| What are the cardiovascular effects of xanthine derivatives? |
|
Definition
-Positive inotrope/chronotrope
-Vasodilation |
|
|
Term
| What are the CNS effects of xanthine derivatives? |
|
Definition
-Decreases drowsiness and fatigue
-Improves concentration and clarity of thought
-Interferes w/ delicate muscle coordination and timing |
|
|
Term
| In addition to asthma Rx, xanthine derivatives can be used as _______. |
|
Definition
|
|
Term
| Indications for xanthine derivatives: |
|
Definition
-Asthma
-Chronic bronchitis
-Chronic emphysema |
|
|
Term
| These drugs, used in the Rx of bronchospasm, blocks the parasympathetic-controlled J receptors in the lungs that cause bronchoconstriction, and inhibits secretions. |
|
Definition
|
|
Term
| What are the indications for anticholinergics? |
|
Definition
-Prevention of bronchoconstriction (asthma/COPD)
-Early use in PNS-induced bronchospasm |
|
|
Term
| Why do you not want to use anticholinergics in late stage asthma attacks? |
|
Definition
| Inhibits secretions, which results in thicker mucus. |
|
|
Term
| These drugs are used in the Rx of acute bronchospasm, they are nonspecific A and B agonists which increase the HR and have a potent vasoconstrictive effect (reduces swelling). |
|
Definition
| Non-selective Adrenergics |
|
|
Term
| What are the indications for use of non-selective adrenergics? |
|
Definition
|
|
Term
| These non-selective adrenergics are mainly used for group in peds as its primary benefit is the reduction of swelling. |
|
Definition
|
|
Term
| These drugs, used in the Rx of acute bronchospasm, cause rapid relaxation of smooth muscle in the bronchioles adn the GI tract via stim of B2 receptors. |
|
Definition
| Non-selective Beta-agonists |
|
|
Term
| What are the indications for use of non-selective beta-agonists? |
|
Definition
|
|
Term
| Used for the Rx of acute bronchospasm, this is a rapid onset, short duration drug with rapid tolerance development. |
|
Definition
| Non-selective Beta-Agonists |
|
|
Term
| These drugs, used in the Rx of acute bronchospasm, stimulate B2 receptors resulting in relaxation of the smooth muscles of the airway and bronchial dilation. |
|
Definition
|
|
Term
| What are the indications for B2 selective agonists use? |
|
Definition
-Asthma attack
-Exacerbated COPD Pts
-Allergic rxn
-Toxic inhalation
-Pneumonia (off-label use)
-Cardiac asthma (off-label and controversial) |
|
|
Term
| T or F, you should not give Beta2's to CHF Pts w/ reflex bronchospasm. |
|
Definition
|
|
Term
| These drugs, used to Rx acute bronchospasm, block Ca++ through smooth muscle Ca++ channels, resulting in smooth muscle relaxation. |
|
Definition
|
|
Term
| What are the indications for smooth muscle dilators? |
|
Definition
| -Bronchospasm refractory to B2 agonists and oxygenation |
|
|
Term
| HA, nausea, diahhrea and liver dysfunction are side-effects of... |
|
Definition
|
|
Term
| Nervousness/restlessness/insomnia, tremors, myocardial irritability, and seizures refractory to anticonvulsants are side-effects of... |
|
Definition
|
|
Term
| What kind of side effects do non-selective adrenergics have? |
|
Definition
| Significant cardiovascular side-effects |
|
|
Term
| What are the side-effects of non-selective beta-agonists? |
|
Definition
| Positive inotrope, chronotrope, and dromotrope (and increases BP) |
|
|
Term
| What drugs are used in the prevention of bronchospasm? |
|
Definition
-Corticosteroids
-Antileukotrienes/LRTAs
-Mast Cell Stabilizers
-Xanthine Derivatives
-Anticholinergics |
|
|
Term
| What drugs are used in the Rx of acute bronchospasm? |
|
Definition
-Non-selective Adrenergics
-Non-selective Beta-agonists
-Beta2 Selective Agonists
-Smooth Muscle Dilators |
|
|
Term
| These meds block the Pt's physiologic repsonses to intubation, minimizing bradycardia, hypoxia, cough/gag relex, increases in intracranial, intraocular, and intragastric pressure. |
|
Definition
|
|
Term
| T or F, you would not use pre-sedation meds in peds or Pts with head injury. |
|
Definition
| False (these are the circumstances you WOULD use them) |
|
|
Term
| This medication is thought to blunt the rise of ICP associated with intubation, and is given to Pt's with suspected head injury. |
|
Definition
|
|
Term
| What is the pre-sedation dosage of lidocaine? |
|
Definition
| 1.5-3 mg/kg (avg 100 mg) given 3 min prior to intubation |
|
|
Term
| This pre-sedation drug minimizes vagal effects (which minimizes bradycardia and secretions). |
|
Definition
|
|
Term
| What is the pre-sedation dosage of atropine? |
|
Definition
| 0.02 mg/kg, minimum 0.1 mg IV, max 1 mg, three minutes prior to intubation |
|
|
Term
| T or F, children develop profound bradycardia during intubation. |
|
Definition
|
|
Term
| What drug would be used to minimize bradycardia in a child? |
|
Definition
|
|
Term
| Used to decrease muscle fasciculations caused by depolarizing agents and attenuates rise in ICP. |
|
Definition
|
|
Term
| What does a defasciculating dose consist of? |
|
Definition
| Non-depolarizing blocking agents usually 1/10 standard dose |
|
|
Term
| These are agents administered at doses capable of producing unconsciousness, and should nearly always be used when paralyzing a Pt. |
|
Definition
|
|
Term
| Which sedative agent has minimal hemodynamic effects, and can be used on hypotensive Pts? |
|
Definition
|
|
Term
| This sedative is a non-barbituate hypnotic that decreases ICP/IOP, and has a rapid onset/short duration. |
|
Definition
|
|
Term
| What is the intubation dose of etomidate? |
|
Definition
|
|
Term
| This sedative is a dissociative anesthetic, has rapid onset/short duration, is a potent bronchodilator and increases secretions. |
|
Definition
|
|
Term
| This sedative increases ICP/IOP/IGP and emergence phenomenon can occur, though rarely in children less than 10 y/o. |
|
Definition
|
|
Term
| Would you use Ketamine in a Pt with a head injury? |
|
Definition
| No (increases ICP/IOP/IGP) |
|
|
Term
| What is the sedative dose of Ketamine? |
|
Definition
|
|
Term
| This sedative has a slower onset, does not increase ICP, but does cause respiratory/cardio depression. |
|
Definition
|
|
Term
| What is the sedative dose of midazolam? |
|
Definition
| 2-5 mg (adults), 0.1 mg/kg (peds) |
|
|
Term
| This sedative is moderate/long lasting, but has a longer onset than Midazolam. May be more beneficial for post-ETT sedation. |
|
Definition
|
|
Term
| What is the sedative dose of diazepam? |
|
Definition
| 5-10 mg (adult), 0.2-0.3 mg/kg (ped) |
|
|
Term
| These opiates are used as sedatives. |
|
Definition
| Fentanyl and Morphine Sulfate |
|
|
Term
| This is a rapid acting sedative, with a short duration (30 min). It can be reversed with naloxone, and may decrease tachycardia/hypertension associated with ETT. |
|
Definition
|
|
Term
| What is the sedative dosage of fentanyl? |
|
Definition
| 25-50 mcg (adult), 2-5 mcg/kg (ped) IV |
|
|
Term
| This opiate sedative has a longer onset and duration (4-6 hr), but may not blunt tachycardia, HTN, and ICP as well as Fentanyl. |
|
Definition
|
|
Term
| What is the sedative dose of morphine sulfate? |
|
Definition
| 2-5 mg (adult), 0.2-0.3 mgkg (ped) IV |
|
|
Term
| What are the two types of paralyzing agents? |
|
Definition
| Depolarizing and Non-depolarizing Agents |
|
|
Term
| These paralyzing agents bind with ACh receptors at the NMJ, causing sustained depolarization. |
|
Definition
|
|
Term
| These paralyzing agents bind to ACh receptors in a competitive, non-stimulatory manner preventing depolarization. |
|
Definition
|
|
Term
| What type of paralyzing agent is succinylcholine? |
|
Definition
|
|
Term
| With this paralyzing agent, you must be cautious of malignant hyperthermia and trismus. |
|
Definition
|
|
Term
| This paralyzing agent stimulates nicotinic/muscarinic receptors, has a 45 sec onset, an 8 min duration and is the standard for paralytics. |
|
Definition
|
|
Term
| How is masseter spasm treated? |
|
Definition
| BVM and non-depolarizing NMJB |
|
|
Term
| Pancuronium, vecuronium, and rocuronium are what type of paralytics? |
|
Definition
|
|
Term
| What is the dosage of succinylcholine? |
|
Definition
| 1.5 mg/kg (adult) and 2.0 mg/kg (ped) |
|
|
Term
| What is the dosage for pancuronium? |
|
Definition
|
|
Term
| What is the dosage for vecuronium? |
|
Definition
| 0.1 mg/kg, priming dose 0.01 mg/kg |
|
|
Term
| What is the dosage for rocuronium? |
|
Definition
|
|
Term
| If you needed a longer lasting non-depolarizing paralytic, which drug would you use? |
|
Definition
|
|
Term
| What drugs can be used to reverse non-depolarizing agents? |
|
Definition
| Edrophonium or neostigmine |
|
|
Term
| List the pre-sedation drugs. |
|
Definition
|
|
Term
| List the drugs used for sedation. |
|
Definition
Etomidate
Ketamine
Midazolam
Diazepam
Fentanyl
Morphine |
|
|
Term
| List the drugs used for post-ETT sedation. |
|
Definition
Midazolam
Diazepam
Fentanyl
Morphine |
|
|
Term
| List the drugs used as paralyzing agents. |
|
Definition
Succinylcholine
Vecuronium
Pancuronium
Rocuronium |
|
|
Term
| Discuss asthma in pregnant Pts. |
|
Definition
| Those with a Hx of asthma tend to have an increase in bronchospasm, but Rx remains the same. |
|
|
Term
| This condition is characterized by HTN, proteinuria, and edema (at least 2 of 3) in Pt of 20 wk or more gestation. |
|
Definition
|
|
Term
| In pregnancy, HTN is defined as... |
|
Definition
| BP of 140/90, or a rise of at least 20 mmHg in systolic or 10 mmHg diastolic above pre-pregnancy levels. |
|
|
Term
| Rx for HTN in pregnant Pts. |
|
Definition
| Labetolol or hydralazine are preferred, nitroglycerin may be used in some systems. |
|
|
Term
| This is pre-eclampsia with generalized seizure or coma. |
|
Definition
|
|
Term
| Drug use/dosage to prevent eclampsia seizures |
|
Definition
| MgSO4, admin 4-6 g (in 50 mL) over 20-30 min |
|
|
Term
| Primary drug use/dosage for Rx of eclampsia seizures |
|
Definition
| MgSO4, admin 2-4 g (in 50 mL) over 2 min |
|
|
Term
| What is option #2 for Rx of eclampsia seizures? |
|
Definition
|
|
Term
| What is the Rx of pediatric bradycardia? |
|
Definition
| Usually caused by hypoxia, Rx involves oxygenation and ventilation, epi or atropine admin (>12 y/o epi is the drug of choice). |
|
|
Term
| What is the Rx of pediatric tachycardia? |
|
Definition
| Rx is fluid, rather than drugs (10-20 cc/kg). For PSVT use adenosine and cardioversion, and treat ventricular dysrhythmias with electiricity. |
|
|
Term
| What tends to cause pediatric tachycardia? |
|
Definition
|
|
Term
| These are the physiological changes in geriatric pts that influence pharmacological interventions... |
|
Definition
-Decreased muscle mass/body wt
-Slower metabolizm
-Reduced liver/kidney fxn
-Alterations in receptor site fxn
-Reduced proteins (for drugs to bind to)
-Reduced cognition/memory |
|
|
Term
| This occurs when a Pt is taking multiple meds for the Rx of several medical disorders. |
|
Definition
|
|
Term
| What are the med considerations for geriatric Pts? |
|
Definition
| Doses not altered for geriatric Pts, but desired action may be delayed or hindered due to physiological changes/polypharmacy issues. |
|
|
Term
| These are used primarily for Rx of HTN, but some are also used to maintain kidney fxn. |
|
Definition
|
|
Term
| These diuretics inhibit carbonic anhydrase (an enzyme in RBCs) and NaCl reabsorption in the DCT. |
|
Definition
|
|
Term
| These diuretics increase Ca++ reabsorption, which can decrease cardiac fxn. |
|
Definition
|
|
Term
| Basically, thiazides stop _____ reabsorption. |
|
Definition
|
|
Term
| Thiazides may also cause _______ in the proximal tubule. |
|
Definition
| Natriuresis (excessive excretion of sodium in the urine) |
|
|
Term
| This type of diuretics inhibits the Na+/K+2Cl- transport system in the luminal membrane of the ascending Loop of Henle. |
|
Definition
|
|
Term
| These diuretics inhibit NaCl reabsorption, which leads to increased Mg++ and Ca++ excretion. |
|
Definition
|
|
Term
| These diuretics antagonize the effects of aldosterone in the collecting tubules and ducts. |
|
Definition
| Postassium-sparing Diuretics |
|
|
Term
| This type of diuretic is most useful in Pts taking Digitalis. |
|
Definition
|
|
Term
| This is the major side-effect of potassium-sparing diuretics. |
|
Definition
|
|
Term
| These are the three types of meds used in the Rx of UT infections. |
|
Definition
| Antimicrobials, antispasmodics, and antiseptics |
|
|
Term
| This type of drug, used to Rx UT infections, blocks DNA transcription or weakens bacterium cell walls. |
|
Definition
|
|
Term
| These drugs, used to Rx UTIs, have parasympatholytic properties which cause an increase in bladder capacity, thus decreasing UTI related incontinence. |
|
Definition
|
|
Term
| This class of drug, used to Rx UTIs, produces high levels of formaldehyde to kill bacteria. |
|
Definition
|
|
Term
| Hyponatremia is defined as Na+ levels less than _____. |
|
Definition
|
|
Term
| Hyperkalemia is defined as K+ levels greater than ______. |
|
Definition
|
|
Term
| Dilution, cardiac/renal/liver failure, sepsis and SIADH can all cause... |
|
Definition
|
|
Term
| What is the Rx of hyponatremia? |
|
Definition
| IV of sodium solutions, possible diuretics. |
|
|
Term
| What are the four meds used to Rx hyperkalemia? |
|
Definition
| Calcium chloride, Bicarb, D50W, and Beta-adrenergic Agents (albuterol) |
|
|
Term
| What is the MOA, dose and route of calcium chloride admin? |
|
Definition
MOA-antagonizes K+ (doesn't alter levels, just overcomes negative effects)
Dose-250-500 mg slow IVP
Route-IV |
|
|
Term
| What is the MOA, dose and route of bicarb admin? |
|
Definition
MOA-tends to reduce serum K+ by driving it into cells
Dose-50-100 mEq
Route-IV |
|
|
Term
| What is the MOA, dose and route of D50W? |
|
Definition
MOA-increases blood sugar, triggering pancreas to release insulin which drives K+ into cells
Dose-25-50 g
Route-IV |
|
|
Term
| What is the MOA, dose and route of abluterol (used to Rx hyperkalemia)? |
|
Definition
MOA-drives K+ into the cell equivalent to insulin
Dose-@ least 10 mg, and must keep it coming
Route-Nebulizer |
|
|
Term
| These classes of meds are used to Rx hyperacidity. |
|
Definition
-Protein pump inhibitors
-H2-Receptor blockers
-Cytoprotective agentgs
-Antacids |
|
|
Term
| This class of drug is used for Rx of esophageal reflux and both chronic/acute erosive esophagitis. |
|
Definition
|
|
Term
| This class of drug is used to Rx esophageal reflux/ulcers. Works by inhibiting actions of hydrochloric acid producing cells in the stomach. |
|
Definition
|
|
Term
| This class of drugs, used to Rx hyperacidicty, does not decrease acidity, rather it binds w/ stomach proteins to form a barrier over exposed tissue ulcerations. |
|
Definition
|
|
Term
| Through various buffers, this class of meds neutralizes excessive acid in the stomach (temp relief only). |
|
Definition
|
|
Term
| These drugs work locally, irritating gastric mucosa and centrally stimulating the emetic center in the medulla to induce vomiting. |
|
Definition
|
|
Term
| These meds are used to treat NV, and variously work by blocking neurotransmitters in the emetic center of the brain, or at the end of the vagus nerve; and some block histamine, serotonin, or dopamine. |
|
Definition
|
|
Term
| When do anti-emetics tend to work best? |
|
Definition
| Before the Pt experiences NV |
|
|
Term
| Drugs that Rx IBS block serotonin centrally and peripherally. How does this Rx the hyperkinetic state of IBS? |
|
Definition
| -Decreases NV (centrally) and decreases peristaltic activity (peripherally) |
|
|
Term
| What are the two different actions of anti-diarrheal meds? |
|
Definition
-Block ACh to limit peristaltic activity
-Bind with toxins to eliminate peristaltic activity |
|
|
Term
| This class of drugs tends to have generic names that end in "-one" or "-ide. |
|
Definition
|
|
Term
| This class of drugs tends to end in "-phylline". |
|
Definition
|
|
Term
| T or F, anticholinergics are effective in the Rx of late stage asthma attacks. |
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Definition
| False, won't stop chem mediators that are causing bronchospasm, and will inhibit secretions, causing mucus to become a thick glob. |
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Term
| This drug is used to Rx croup. |
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Definition
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Term
| Bronchosol, albuterol and levalbuterol belong to what class of drug? |
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Definition
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Term
| Albuterol has two parts, S. albuterol and R. albuterol. Which part is responsible for side-effects, and often results in reflex bronchospasm 2-6 hr after taking large amts of albuterol? |
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Definition
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Term
| Racemic means that two drugs are... |
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Definition
| Mirror images of each other. |
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Term
| Which is responsible for bronchodilation, S. albuterol or R. albuterol? |
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Definition
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