106 final Flashcards
chemical name of a drug
actual chemical structure of a drug (xyz2y)
generic name of a drug
a name assigned by the USAN
official name of a drug
-(generic + USP)
- becomes fully approved by the FDA, then listed in the USP
Trade/Brand Name of a drug
-brand name given by the manufacturer
-this name is “owned” by the manufacturer
Calculate the therapeutic index (TI)
TI= LD50/ED50
-LD = lethal dose
-ED= effective dose
low TI
-unsafe, drugs are safer as TI increases
-No completely safe drug out there
Concomitance
2 drugs given at the same time to produce an effect that is the sum of the effect that each produces on its own. This is pure addition
Synergism
occurs when drugs with similar actions are given concomitantly and produce an effect that is greater than the sum of the effect that each produces on its own.
Potentiation
drugs with unlike actions are given concomitantly and produce an effect that is greater than the sum that each produces on its own
Antagonism
occurs when drugs act concomitantly in a way that one drug causes the actions of the other drug to be reduced
Median lethal dose (LD)
The dose which kills half of test subjects
Median Effective Dose (ED50)
The dose at which half of
tested subjects show the desired therapeutic response
three main uses for aerosols
-humidification of dry inspired gases using bland aerosols
-mobilization and clearance of respiratory secretions, including sputum induction
-delivery of aerosolized drugs to the respiratory tract
2.5 micrometers
useful to treat lower respiratory tract (large airways to periphery) (bronchodilators)
disadvantages of aerosol drug delivery
-many variables affect dose delivered to airways
-cannot measure effectiveness of dosage delivery
-can be difficult for patients to self-administer
-MDs, NPs, and RNs unfamiliar with device use and administration
-many device types lead to confusion among patients and practitioners
advantages of aerosol drug delivery
-doses are smaller than doses fir systemic treatment
-drug delivery is targeted to respiratory system for local effect
-systemic side effects are fewer and less severe than oral/parenteral therapy
-painless and convient
-lungs provide a portal to the body for systemic effects( pain control)
disadvantages of MDIs
-complex hand-breathing coordination required for efficacy
-fixed drug concentrations and dosages
-not easy to know when canister is empty
-reactions to propellants
-high volume loss without use of spacer
advantages of MDIs
-portable, light and compact
-efficient drug delivery
-short treatment time
-easy to use
-more than 100 doses are available
-fine particle sizes are available in HFA form
-not easily contaminated
-no prep drug needed
MDI
small, pressurized canisters for oral or nasal inhalation of aerosol drugs and contain multiple doses of accurately metered drug
DPI
-breath-actuated inhaler where drug is in powder form
-can be unit dose (individually wrapped capsules or multiple doses
disadvantages of DPIs
-limited range of drug availability
-patients not always aware of dose inhaled
-moderate to high inspiratory flow rates necessary
-high oropharyngeal impaction and deposition
-single-dose devices need to be loaded every time
advantages of DPIs
-small and portable
-short preparation and administration times
-breath-actuated, no need for hand-breathing coordination
-no inspiratory hold needed
-no CFC propellants (environmentally friendly)
-built- in dose counter
valve holding chamber
-an extension device
-high-velocity large particles > slower- velocity small particle
-reduces oropharyngeal deposition, amount of drug swallowed, local oropharygneal side effects
disadvantages of valve holding chamber
-large and inconvenient
-additional expense
-possible source of bacterial contamination
-patient error prone
SVN
type of aerosol generator that converts liquid drug solutions or suspensions into aerosol
disadvantages of SVN
-not easily portable (mobile)
-requires assembly
advantages of SVN
-longer treatment time = better deposition
lbs to kgs
1kg= 2.2 lbs
convert % solution to mg/mL
-multiple by 10 or move the decimal point one place to the right
-2% = 20 mg/mL
-0.3% = 3 mg/mL
express ratios as % solutions
-divide the first part by the second part and multiply by 100
-1:500= (1/500) x 100 = 0.2%
convert mL to mg
mg= (mg/mL) x mL
convert mg to mL
mL= mg/ (mg/mL)
ANS branches
-parasympathetic
-sympathetic
ANs keypoints
-drugs either mimic the neurotransmitter (NT) to produce the usual action or block the NT to inhibit it
-ANS is generally efferent-> impulses travel from brain/spinal cord out to body
Parasympathetic branch
-NT is acetylcholine (Ach)
Ach
-located at neuromuscular junction (NJ) and ganglia
-terminated by the enzyme cholinesterase
Parasympathetic
- drugs that mimic/allow/increase Ach transmission
-parasympathomimetic= cholinergic= muscarinic
Parasympatholytic
-drugs that block the transmission of Ach to achieve opposite effects (for us, bronchodilation)
-anticholinergic= antimuscarinic= muscarinic antagonists
Parasympathetic regulation
-craniosacral (from cranial nerves to sacral nerves)
-essential of life
-discrete, finely regulated system (i.e. digestion, bladder discharge, bronchial secretions)
-overstimulation= SLUD syndrome
SLUD Syndrome
-Salivation
-Lacrimation (tears)
-Urination
-Defecation
cholinergic responses to Ach (effects) on cardiopulmonary system
-decreased heart rate
-lower blood pressure
-bronchoconstriction (bronchial smooth muscle)
-increased mucus secretion in airways
Meds of the parasympathetic branch
-parasympatholytic
-antimuscarinic
-antinicotinic
-anticholinergic
-muscarinic
-antagonists
MOA of parasympathetic
M3 receptor = affects airway smooth muscle
sympathetic location
-thoracic nerves - lumber nerves
sympathetic branch
-also called adrenergic
Sympathetic (adrenergic) effects
NT release from sympathetic nerves release catecholamines (norepinephrine and epinephrine) from adrenal medulla and stimulate adrenergic receptors throughout the body
Sympathetic effects on the cardiopulmonary system include:
-Increased heart rate
-Increased contractile force
-Increased blood pressure
-Bronchodilation
-Probable increased secretions from mucous glands in airway
Sympathetic receptor types:
-Alpha
-Beta
Alpha receptors
-excitatory effects
-vasoconstriction (upper airway)
-Alpha -1 = peripheral blood vessels
-meds= racemic epi
Beta receptors
-relaxing effects (inhibit)
-Beta -1 = not important
-Beta -2 = smooth muscle (bronchial and cardiac) dilation
bronchospasm
narrowing of bronchial airways caused by smooth muscle contraction
adrenergic bronchodilators clinical indications:
-used for the treatment of reversible airway obstruction in asthma and COPD
-agents that stimulate sympathetic nerve fibers = bronchodilate
Adrenergic bronchodilators 2 groups:
- SABA (short-acting beta-2 agonists)
-LABA (long-acting beta-2 agonists)
SABA
-albuterol 2.5 mg/ 0.5mL
-levalbuterol= Xopenex= 0.63mg/2mL
-relief of acute reversible airflow obstruction
-‘rescue’ agents or ‘relievers’
LABA
-‘erol’
-salmeterol= serevent
-formoterol= performist (SVN)/ foradil (DPI)
-aformoterol= brovana
-olodaterol= striverdi
maintenance of bronchodilation and control of bronchospasm
-‘controllers’
-not for rescue therapy
special consideration : racemic epinephrine
-svn
-Q 2 hrs
- 11.25% in 0.5 mL
-strong alpha -1 vasoconstrictor
-alpha agonist
Indications for racemic epi
-post-extubation stridor
-croup
-epiglottitis
-upper airway bleeding (endoscopy)
all sympathetic (adrenergic) bronchodilators:
are either catecholamines or derivatives of catecholamines
catecholamines found in the body:
-dopamine
-epinephrine
-norepinephrine
catecholamine structure
-benzine ring
-two hydroxyl groups
-amine side chain
keyhole theory of beta-2 agonists:
the longer the side chain, the greater the beta-2 effect
catecholamines =
sympathomimetic amines that mimic epinephrine
side effects of catecholamines:
-tachycardia
-increased blood pressure
-palpitations
-bronchial smooth muscle relaxation
-CNS stimulation
catecholamines derivatives:
- man-made
-modified nucleus
-not found in the body
-resorcinols
-saligenins (albuterol)
prodrug
-Bitolterol
-drug that is inactive until the body converts it (hydrolysis) to the active drug
SABA/LABA side effects
-muscle tremor
-cardiac effects (tachycardia, palpitations, increased blood pressure)
-headache
-insomnia
-bronchospasm
-hypokalemia
anticholinergic bronchodilator
-agent that blocks Ach transmission at parasympathetic nerve fibers, which allows for relaxation of airway smooth muscle
- blocks Ach at parasympathetic post-ganglionic effector cell receptors
-helps to reduce respiratory secretions
anticholinergic=
parasympatholytic= antimuscarinic= muscarinic antagonists
indications for anticholinergic bronchodilators
-maintenance therapy for COPD
-may be indicated for some with asthma
-often used in combination with other bronchodilators (beta-2 agonists) and inhaled corticosteriods (ICS)
anticholinergic agents 2 groups:
-‘ium’
-SAMA
-LAMA
inhaled corticosteriods (ICS)
- oral inhalation and intranasal delivery agents that produce in anti-inflammatory response
-reduce airway thickening cause by inflammatory process
-recommended for maintenance therapy for COPD
corticosteriods=
glucocorticosteriods= glucocorticiods= steriods
causes of airway inflammation:
-infection (airway, systemic, ARDS)
-allergic and non-allergic stimulation of asthma
-direct or indirect trauma
- inhalation of noxious or toxic substances
antigens
-natural defense mechanism (immune system) is to neutralize, destroy, and eliminate foreign materials
-stimulate both the immune and inflammatory processes
common antigens:
-animal dander
-dust mites
-mold
-pollen
-smoke
-bacteria
mediated by
inflammatory cells (mast cells, eosinophils, T lymphocytes , macrophages)
Airway inflammation
-microvascular leakage
-airway wall swelling
-mucus secretion
-which cause
- wheezing
- shortness of breath
-chest tightness
- cough
-treatments with ICS reduce the basal level of airway inflammation, airway hyperresponsiveness, and exacerbations
systemic corticosteroids
-given orally or by IV
-‘relievers’ for patients in severe acute asthma exacerbations (for COPD)
-reduce inflammation associated with asthma more quickly than ICS
-meds include: prednisone, methlyprednisone (Medrol and Solumedrol), and dexamethasone (Decadron)
-more side effects than ICS
inhaled corticosteroids
- given via SVN, DPI, MDI
-used for maintenance of COPD
-most often work best when combined with LABA
-fewer side effects than systemic steroids - must rinse mouth out after use to prevent oral thrush
nonsteroidal antiasthma agents:
-medications that have an anti-inflammatory effect through mechanisms different from corticosteroids
-used for prophylactic management (control) of mild persistent asthma requiring anti-inflammatory drug therapy
Mast cell mediator:
-i.e. histamine, heparin, leukotrienes
-causes degranulation of mast cells
the effects of degranulation:
-bronchospasm
-mucus production
- airway edema
the goal of all asthma/allergy medication is:
to stop/limit mast cell degranulation
relievers of asthma:
-SABAs (albuterol, levalbuterol)
-systemic corticosteroids (prednisone, dexamethasone)
-SAMAs (atrovent)
controllers of asthma
-ICS
- oral corticosteroids
-cromolyn sodium (mast cell stabilizer)
-LABAs
-Leukotriene modifiers
-monoclonal antibodies
Leukotriene modifiers (antileukotrienes)
-attach to and block the receptor for leukotrienes
-Zileuton (Zyflo) -controller
-Zafirlukast (Accolate) - controller
-Monetlukast (Singulair) - controller (especially good for exercise-induced asthma)
monoclonal antibodies
-Omalizumab (Xolair)
-used to treat uncontrolled moderate - to - severe asthma in ages 12 and up
mucus
-secretion from surface goblet cells and submucosal glands
-composed of water, proteins, and mucins
phlegm
purulent material in the airways
sputum
expectorated phlegm; respiratory tract; oropharyngeal; and nasopharyngeal secretions, bacteria, and products of inflammation
mucoactive agents
- any medication or drug that has an effect on mucus secretion
-also called mucolytics/ mucus controllers
mucolytic agents:
-medication that degrades polymers in secretions (break down mucin, DNA, and actin in sputum)
mucociliary transport:
-how well cilia moves mucus along the respiratory tract and how easy it is for patients to cough mucus out
-is slowed by certain disease processes and substances that cause airway damage
-give med aerosols and CPT (chest physiotherapy) to aid
mucociliary transport:
-COPD
-CF (Cystic Fibrosis)
-Endotracheal suctioning
-airway trauma
-tobacco smoke
-atmospheric pollutants ( Sulfur dioxide, Nitrogen dioxide, Ozone, Allergens)
mucociliary system:
-protects the lungs from inhaled debris
-contains enzymes that give it antimicrobial properties that help prevent infection
-warms and humidifies inspired gases
-prevents excessive loss of heat and moisture from airways
N-Acteylcysteine (Mucomyst)
-comes in 10% and 20% solution
-smells like rotten egg
-ordered as last resort for copious sputum production
-not proven beneficial
-can cause bronchospasm
Pulmozyme (Dornase Alfa)
-indicated ONLY for clearance of purulent secretions in cystic fibrosis (CF)
-reduces viscosity of sputum
-breaks down DNA polymers in sputum
-2.5 mg in 2.5 mL refrigerated vial
Hypertonic saline
-also called hyperosmolar saline or hypersal
-7% saline used for CF
-3% saline used for infant and ped bronchiolitis
-irritates and hydrates the airway to promote cough and loosening of secretions
Antiinfective Agents
nebulized aerosols for pulmonary infections associated with CF, pneumonia, RSV, etc.
Pentamidine (Nebupent)
-Antiinfective agent
-indicated for prevention of PJP/PCP in high-risk HIV-infected patients
-antifungal
-delivered Respirgard II nebulizer
Tobramycin (Tobi)
-Antiinfective
-indicated for management/control of chronic Pseudomonas aeurginosa infection in CF
-must pretreat with bronchodilator (Albuterol) and use separate nebulizer only for Tobi
Aztreonam (Cayston)
-Antiinfective
-indicated to improve pulmonary symptoms in pts with CF and active Pseudomonas aeruginosa infection
-must pretreat with bronchodilator (albuterol)
Diuretics:
-drugs that promote urine production by reducing extracellular fluid volume to decrease blood pressure and/or to rid the body of excess fluid
-affects the metabolic acid-base balance
water loss from diuretics can cause:
acid-base imbalances liek metabolic alkalosis (pH is directly proportional to bicarbonate (HCO3)(fluid)
diuretic indications:
-CHF
-pulmonary edema
-acute respiratory distress syndrome (ARDS)
-fluid build up from trauma
-acute/chronic renal failure
Furosemide (Lasix)
-loop diuretics
-“high ceiling” diuretic
-fast acting (15-20 minutes)
Neuromuscular blocking agents (NMBA) =
Skeletal Muscle Relaxants= paralytics
neuromuscular blockers:
-NMBAs prevent body movement by weakening or paralyzing muscles
-this effect is produced by interfering with the neurotransmitter Ach at the neuromuscular junction
clinical uses of NMBAs:
-to facilitate endotracheal intubation
-to obtain muscle relaxation during surgery
-to enhance patient-ventilator synchrony
-to paralyze pts who must remain immobile (trauma)
NMBA cause:
muscle paralysis without affecting consciousness or the perception of pain
NMBA either:
depolarize the presynaptic and postsynaptic membrane receptors or compete with Ach for binding of the Ach receptors at the NJ site
2 types of NMBAs;
-depolarizing
-nondepolarizing
Succinylocholine
-depolarizing agent (only one)
-ultra short action and duration
-cannot be reversed
-primarily used just prior to intubation
-many severe side effects (not used as much as it used to be)
-subsequent doses have limited effectiveness
nondepolarizing agents:
-‘ium’
-Pancuronium (Pavulon)
-Rocuronium (Zemuron)
-Vecuronium (Norcuron)
-can be reversed by cholinesterase inhibitor Neostigmine
Sedatives
-Propofol (Diprivan)
-Lorazepam (Ativan)
-Midazolam (Versed)
Analgesics (pain control)
-Fentanyl
-Hydromorphone (Dilaudid)
-Morphine
Order given:
Sedatives > NMBAs > Analgesics
Inhaled Nitric Oxide (iNO)
-pulmonary vasodilator
- approved for pulmonary vascular relaxation and is used to treat persistent pulmonary hypertension in newborns (PPHN)
-used in conjunction with ventilatory support
-PPHN diagnosed by cardiac echocardiogram and pre- and post- ductal oxygen saturation differences
- very short half-life (5 seconds)
Epoprostenol
- pulmonary vasodilator
- brand name Flolan (injection) and Veletri (inhalation)
- not indicated for newborns
surfactants:
-used in premature infants who have decreased levels of pulmonary surfactant
-acts as a lubricant to decrease pulmonary surface tension in the alveoli, which aids in ease of breathing
exogenous surfactant:
- manmade
-decrease surface alveolar surface tension, which aids in alveolar inflation and helps prevent atelectasis, thereby improving overall breathing
-made of 85-90% lipids and around 10% protein
Poractant alfa
-Curosurf
-porcine (made from pig lung extract)
Beractant
-Survanta
-Bovine ( made from minced cow lung extract)
Calfactant
-Infrasurf
-Bovine (made from chloroform-methanol extract of fluid lavaged from calf lung)
surfactant risk factors and side effects:
-airway occlusion (clogs the ETT)
-oxygen desaturation (from clogged ETT or oversaturation of alveoli)
-bradycardia
-overoxygenation (High PaO2)
-overventilation
-apnea
-pulmonary hemmorrhage
Surfactants administered through:
via endotracheal tubes directly into the lungs
