Respiratory Medications Flashcards
M1 Receptor Location and function
endocrine glands, autonomic ganglia, CNS, Salivary galnds, stomach. Function is arousal, attention, REM, emotional response
M2 Receptor location and function
Location: Atria, conducting tissues of heart | Function: cardiac inhibition
M3 Receptor location and function
Location: Exocrine glands, smooth muscle, lungs, eye, GI tract | Function: Lacrimal, salivary, mostly stimulatory
M4 Receptor location and function
Location: CNS | Function: Direct regulatory action on K and CA channels
M5 Receptor locatioin and function
Location: Substantia nigra, CNS | Function: May regulate dopamine release
Muscarinic Recetors (Stimulatory)
M1, M3, M5
Muscarinic Receptors (Inhibitory)
M2 and M4
Review MOA
slide 5
Atropine antagoinizes ACh effects on airway smooth muscle in large and medium sized airways. Atropine affects airways that respond to ______ stimulation. This _________ airways resistance and _______ dead space
vagal / decreases / increases
T/ F Inhaled medications have the same side effects as their oral counterparts
TRUE
Most effective in treating bronchospasm due to beta ANTAGONISTS
Ipratropium
Atrovent (Ipratropium) has slower onset than __________. More selective in lungs, less readily absorbed in the heart.
Atropine
Ipratropium has a slower onset and less effectvie than ______ _______ in treating broncnhial asthma. It is not useful in _____ attacks. More effective than beta agonists in _______ or _______.
beta agonists / acute / chronic bronchitis / emphysema
With Ipratropium it has minimal systemic absorption (<1%) but paradoxical bronchospasm may occur due to ____ blockade. Limited absorption results in prolonged local site effect. Tolerance has not been observed to the _______ effect.
M2 / bronchodilator
Would you used Tiotropium (Spiriva) for acute bronchospasm
NO, because this is a long acting but NOT fast acting
Long-acting anticholinergic bronchodilator with once daily dosing. Used for maintenance treatment of bronchospasm associated with COPD including chronic bronchitis and emphysema
Spiriva
Tiotropium (Spiriva) blocks muscarinic receptor subtypes ___ and ____, which fascilitates _______ and reduces ______ secretion
M1 and M3 / bronchodilation / mucous
Difference between Spiriva and Aclidinium (Tudorza)
Aclidinium is given twice daily and has a faster onset to peak
Umeclidiuium is another ________________
long -acting Anticholinergic
What are some Beta Agonsist respiratory drugs? (Adrenergic Agents)
Epinephrine, Isoproterenol, Albuterol, Terbutaline
Ephedrine and epinephrine provide bronchodilating effects from activation of ____________ receptors; however, there is a significant amount of ______ side effects
beta 2 / non-respiratory
Primatene mist is inhaled ________
epinephrine
Isoproterenol can be used for the treatment of _____________. However, this drug is highly ______.
bronchospasms / proarrhythmic
Review slide 17.
MOA for beta 2 agonists
Beta 2 agonists relax bronchial smooth muscle. They lack stimulating effects on the heart at ________ doses. Their structure makes them resistant to _________, which contributes to their ______ duration of action.
therapeutic / COMT / sustained
________ are preferred treatment for acute episodes of asthma. They can also be used for prevention of exercise-induced ________, as well as improve airflow and exercise tolerance in patients with __________. Can also be used as a _______ to stop premature uterine contractions.
Beta 2 agonists / asthma / COPD / Tocolytic
Intermediate acting Beta 2 agonists DOA
3-6 hrs
Long acting Beta 2 Agonists DOA
12 hrs
If you are giving beta 2 agonists and steroids, which would you give first?
Beta 2 agonists first followed by steroids
Beta 2 agonists preferred route of administration is _______, but oral and parenteral (SQ or IV) are also possible
inhaled
Beta 2 agnoist inhalation technique
Deep breath, blow it all out. Dishcarge MDI with slow deep breath over 5-6 sec and hold breath for 10 seconds. Repeat
Issues with inhalation technique
12% delivered to the lungs, rest to mouth, pharynx and larynx.
Presence of ETT decreases by ___ to ____% the amount of drug delivered by a MDI that reaches the trachea. However, administering during mechanial ventilation increases the amount of drug that passes beyond the distal end of the ETT.
50-70%
Dose delivered by a nebulizer requires ___ to ___ times that of a MDI dose to produce the same degree of bronchodilation
6-10 times
Tremors from beta 2 agonists is due to stimulation of beta 2 receptors in ________ __________. Tachycardia is from direct stimulation of receptors on the ______.
skeletal muscle / heart
Beta 2 Agonsists metabolic response includes what?
Hyperglycemia, Hypokalemia, Hypomagnesemia
The preferred beta2 agonist for bronchospasm is ___________. Is this long or short acting?
albuterol / Short acting
Levoalbuterol is the _________ of racemic albuterol. Little or no clincially significant difference in adverse effects compared to albuterol.
R-enantiomer
Does xopenex still cause tachycardia
yes
Metaproterenol is a ___________ beta 2 agonist
selective
Terbutaline is used for the treatment of ___________. It can also be used as a ___________ to reduce contractions and postpone labor for hours to days
asthma / tocolytic
Salmeterol (serevent) is considered a _______ acting beta 2 agonist. It is frequently administered with a steroid. Salmaterol/Fluticasone (Advair) is used for the ________ of asthma.
long / prophylaxis
Vilanterol is a _______ acting beta 2 agonist
long
LABAs have a black box warning that says it should not be used _________ and there is an increased risk of asthma related ___________
alone / death
Cromolyn sodium is considered a _________ ____________. Also known to taste like a handful of _________.
membrane stabilizer / pennies
Cromolyn works by inhibiting _______-________ release of histamine and other mediators from pulmonary mast cells during ANTIBODY mediated allergic response. Cromolyn suppresses the _______ response NOT the Ag-AB interaction. It does ______ relax bronchial or vascular smooth muscle. There is ____ use for this in an acute asthma attack.
antigen-induced / secretory / NOT / NO
Cromolyn is used for the _________ treatment of bronchial asthma with no use for an ______ attack. Side effects are RARE.
prophylactic / acute
Methylxanthines include what drugs?
theophylline/aminophylline (that’s the IV form), caffeine, theobromine
Uses for methylxanthines
stimulate the CNS, increase BP, incrase myocardial contractility, relax smooth muscle (airways)
Daliresp is a PDE4 ________
inhibitor
MOA for methylxanthines are they are non-selective _______ inhibitors
phosphodiesterase
Methylxanthines are competitive antagonists of __________ receptors
adenosine
Theophylline is more active than _____________ or __________
Caffeine / theobromine
Theophylline inhibits PDE 3,4 and 7 to cause _________. It inhibits PDE5 to ________ inflammatory cells
bronchodilation / decrease
Theophylline can be used to treat bronchospasm due to acute exacerbation of _____________. It is adminstered PO or IV, but has really been replaced by beta 2 agonists.
asthma
Caffeine and other methylxanthines all block the ______ enzyme
a2a (adenosine)
Theophylline level 15-25 mcg/ml
GI upset, N/V, tremor
Theophylline level 25-35
tachycardia and PVCs
Theophylline level >35
Vtach and seizures
Theophylline has a very narrow _____ window
therapeutic
Effects of caffeine
CNS stimulant, cerebral VASOCONSTRICTOR, secretion of gastric acid
Uses for caffeine
apnea of prematurity, PDPH, cold remedies (offset sedation from antihistamines)
Ritodrine is considered a ______ and ________. Most frequently used as a tocolytic though.
tocolytic and beta2 agonists
Ritodrine stimulates beta 2 receptors and activates _______ ______. Has some beta 1 effects which may cause _________.
adenyl cyclase / tachycardia
Does ritodrine cross the placenta?
Yes
Ritodrine will cause cardiac and metabolic effects in both the _____ and _________. This includes dose related tachycardia, ________ renin secretion, decreased ____ and _____ secretion. Increased ____ and ___ loss (hypokalemia).
mother and fetus / increased / Na and water / K+ and HCO3 /
T/F Pulmonary edema can result from ritodrine admin?
TRUE
With ritodrine there can be an exaggerated systemic BP _________. Also, hyperglycemia in mother may cause a reactive ________ in fetus.
decrease / hypoglycemia
T/F Histamine is a LOW molecular weight, naturally occuring HYDROPHYLLIC endogenous amine that produces a cariety of physiologic and pathologic responses
TRUE
Histamine acts through _________ membrane receptors
G-protein coupled
Chemical meidator of inflammation in allergic disease
histamine
T/F Mast cells in the skin, lungs, GI tract and circulating basophils contain large amounts of histamine. Histamine release can be in response to certain drugs and Ag-AB reactions.
TRUE
T/F Histamine easily crosses the blood-brain barrier
FALSE, does not easily cross the BBB
H1 receptors
Evoke smooth muscle contraction in the respiratory and GI tracts, cause pruritis and sneezing by sensory nerve stimulation, causes NO mediated vasodilation, slow the heart rate by decreasing the A-V nodal conduction, mediate epicardial coronary vasoconstriction
Through H1 and H2 receptors histamine causes
increased capillary permeability, hypotension, tachycardia, flushing, headache
H2 receptors will activate AC and INCREASE _______ __________
intracellular cAMP
H2 receptors activates proton pump of gastric _____ _____ to secrete hydrogen ion
parietal cells
H2 receptor activation increases myocardial _____ and _______. Vasodilating effects on coronary vasculature opposes the vasoconstricting effects of ___ receptors.
contractility and heart rate / H1
H1 receptor activation you should think what?
increase capillary permeability and vasodilation
What do you need to completely block the vasodilatory effects of histamine?
H1 and H2 blockers
Cardiovascular effects of histamine
dilation of aterioles and capillaries resulting in flushing, decreased SVR (H1 and H2 effect), decreased BP, increased capillary permeability leading to edema
Additional cardiovascular effects of histamine
inotropic effects, chronotropic effects, antidromic efffects, coronary vasodilation (H2), and vasoconstriction (H1)
Triple response to histamine is AKA
Wheal and Flare
What is the triple response
(edema, flare, pruitis) edema due to increased permeability, dilated arteries around the Edema resulting in the Flare, Pruritis due to histamine in the superficial layers of the skin
The effect of histamine on the airway is due to _____ receptor activation that constricts bronchial smooth muscle. In the normal patient this action is neglible but in patients with asthma or bronchitis, more likely to develop increases in _____ _______
H1 / airway resistance
H2 receptor activation in the airway results in ____________
bronchial smooth muscle relaxation
Histamine evokes secretion of ________ fluid containing high concnetrations of hydrogen ions. Can occur without enough histamine to alter ______. It is due to ____ receptor stimulation.
gastric / BP / H2
T/F Vagal activity also increases H+ ion secretion
TRUE
Histamine receptor antagonists are considered to be ______ and ________ antagonists of histamine receptors
competetive and reversible
T/F Histamine receptor antagonists DO NOT inhibit the release of histamine, but rather attach to receptors and prevent the response mediated by histamine. They basically stabilize the receptor in the inactive form (INVERSE AGONIST)
TRUE
H1 receptor antagonists are highly selective for ____ receptors. First gen are very _______ while second gen are not _______
H1 / sedating / sedating
H1 receptor antagonists have been re-classified as _____ ________. Basically the drugs combine and stabilize the inactive form of the H1 receptor shifting the equilibrium toward the inactive state.
inverse agonists
H1 antagonists first generation CNS side effects
somnolence, decreased alertness, slowed reaction time, and impaired cognitive function
H1 antagonists first generation anticholinergic side effects
dry mouth, blurred vision, urinary retention, and constipation
H1 antagonists first generation Cardiovascular side effects
tachycardia, QT prolongation, heart block, and cardiac dysrhythmias
H1 antagonists second generation facts
unlikely to produce CNS side effects unless recommneded doses are exceeded, enhancement of sedatives or alcohol is unlikely, older second generation antihistamines associated with prolongation of the QT interval have been removed from the market
H1 antagonists clinical uses
allergic rhinits, less effective for nasal congestion, pretreatment may provide potection against bronchospasm, antipruritic, sedative, antiemetic
Benadryl is used for Type __ allergic reactions. Administer with epi, and addition of ___ antagonist speeds the resolution of the symptoms
I / H2
Anaphylactic reactions from IV contrast or blood products, antihistamines are more effective in ________ and __________.
preventing and controlling
Dimenhydrinate (dramamine), is used to treat ______ and _______. It works by inhibiting the integrative functioning of ______ ______ by decreasing vestibular and visual input. Not associated with prolonged sedation.
motion sickness and PONV / vestibular nuclei
Second Gen H1 antagonists
cetirizine, loratadine, fexofenadine
H1 anatagonist summary
If taking benadryl think about more sedation, possible agitation, thicker secretions that may complicate intubation or extubation. 2nd generation side effect profile is not as sedating as first
HPA axis
Hypothalmus, Anterior Pituitary, Adrenal Cortex
CRH is released from the _______. ACTH is release from the ________. Cortisol is released from the ________.
Hypothalmus, Anterior Pituitary, Adrenal Cortex
The outer layer of the adrenal cortex is the Zona ______ and releases _________
glomerulosa / mineralcorticoid
The middle layer of the adrenal cortex is the Zona ______ and releases __________
Fascicula / glucocorticoids
The inner layer of the adrenal cortex is the Zona ________ and releases ________
reticularis / weak androgens
_________ is a hormone produced in the adrenal cortex. It is released by stimulation of the HPA axis due to ______. It initiates a series of metabolic effects directed at relieving the damaging nature of the ____ _____.
cortisol / stress / stress response
T/F Cortisol alters carbohydrate, protein and fat metabolism as well as fluid and electrolyte. They also can inhibit the inflammatory and allergic response.
TRUE
Steroid do not provide acute relief because the way it alters and _______
protein
Aldosterone is released in response to _____
AT II
Aldosterone is secreted secondary to increased ____, decreased ____ and decreased ____/______
K / Na / blood and fluid volume
What are the effects of aldosterone
increased K excretion, Increased Na retention, increased water retention and increased blood volume
Circadian rhythm is releated to ________ secretion
cortisol
Secretory reates of CRH, ACTH, and cortisol are _______ in the early morning and ______ in the late evening
high / low
T/F Changing daily sleeping habits causes a corresponding change in the cycle of cortisol secretion
TRUE, so damn true
Primary adrenocortical insufficiency is AKA ________ disease. With this the adrenals do not secrete ____ or _____ so replacement therapy must include _____ and ________.
Addison’s / cortisol or aldosterone / glucocorticoid and mineralcorticoid
Secondary adrenocortical insufficiency is usually due to _________ and suppression of the _____ axis.
chronic steroid use / HPA
With secondary adrenocortical insufficiency _______ secretion is maintained and replacement usually requires only _________
aldosterone / glucocorticoid
Long term supplementation due to a negative ffeedback loop creating a lack of natural corticoids
secondary adrenocortical insufficency
Physiologic effects of cortisol secretion
increased CO, increased RR, increased gluconeogenesis, decreased inflammation, decreased immune response, inhibition of digestion, enhanced analgesia, redistribution of CNS blood flow
Glucocorticoid effect relates to what?
anti-inflammatory response
Mineralocorticoid effect evokes distal renal tubular re-absorption of ___ in exchange for ___
Na / K
Naturally occuring steroids
cortisol, cortisone, corticosterone, desoxycorticosterone, aldosterone
Synthetic corticosteroids
prednisolone, prednisone, methylprednisolone, betamethasone, dexamethasone, triamcinolone
Synthetic mineralocorticoids
fludrocortisone
Review Slide 67
Cortisol equivalents
Steroids are ______ lipophilic and that is how it gets into the cells
highly
The only FDA approved use for corticosteroids is
replacement therapy for deficiency states
Water soluble forms of corticosteroids
cortisol succinate
Prolonged effects of come from what form of corticosteroids
cortsione ACETATE
Will cortisol cross the placenta
YES, will cross any barrier and will ALWAYS absorb
Review Corticosteroid side effects
Slide 71
Most common side effect from steroids?
hyperglycemia
HTN from steroids is from what?
fluid retention
Most common electrolyte abnormality from corticosteroids?
Hypokalemic Metabolic Alkalosis which can also lead to weight gain
Hypokalemic metabolic alkalosis is due to the _________ effect of cortisol on DISTAL renal tubules leading to enhanced absorption of ____ and loss of ____
mineralocorticoid / Na / K
Corticosteroids inhibit glucose USE in peripheral tissues and promote hepatic __________
gluconeogenesis
dose of oral hypoglycemic or insulin may need to be increased when steroids are administered to _______
Type II diabetics
Chronic steroid used leads to redistribution of fat. You get a _______ obesityt from moving amino acids and fast from the ________
central / periphery
Catabolic effeects of steroids
decreased skeletal muscle mass, osteoporosis, thinning of skin, negative nitrogen balance
Cataracts can develop from long term steroid use of greater than ___ years
4 years
Long term corticosteroids tend to increase ______ and number of _________
hematocrit / leukocytes
Single dose of cortisol decreases circulating lymphocytes by ____ % and monocytes by ______% (steroid induced leukemia). Cells are actually _________ rather than destroyed.
70% / 90% / sequestered
T/F admin of small doses of GLUCOCORTICOIDS in children can stunt growth by inhibiting DNA synthesis and cell division
TRUE
If someone has thyroid storm would you want to use a steorid?
NO
Relative contraindications for corticosteroids
active systemic infection, immunosuppression, acute psychosis, primary glaucoma, hypokalemia, CHF, Cushing’s syndrome, diabetes, HTN, osteoporosis, HYPERthyroidism
Surgeons concerns about intraop use of corticosteroids
aseptic necrosis of femoral head, failure of bone fusion, altering glucose in DM, masking infection or further complicating surgery inteded to treat infection
T/F Any corticosteroid at any dose may result in suppression of HPA axis?
TRUE, so damn true
The longer the duration and dose of steroid, the higher the possibility of ___________
suppressing the HPA axis
Aldosterone secretion remains intact in ____________
secondary adrenocortical insufficency
Therapies unlikely to suppress the HPA axis
prednisone 5mg/ day or 10mg QOD and long term QOD dosing associated with less suppression.
Glucocorticoids, any dose < _____ ______ does not clinically suppress the HPA axis
3 weeks
Prednisosne or dexamethasone (evene physiologic doses) given as single daily dose at ________ is associated more commonly with HPA axis suppression
BEDTIME
Baseline cortisol secretion is about ____ mg per day and during stressful times can release ___ times that.
10 mg/ ten
Therpaies assumed to suppress the HPA axis
Prednisone 20mg/day (or equivalent) for > 3 weeks within the previous year | Patient with signs of Cushing’s syndrome from ANY steroid dose | NO NEED TO TEST THE HPA AXIS IN THESE PATIENTS, JUST SUPPLEMENT WITH STRESS DOSE STEROIDS
After cessation of steroid therapy, recovery of the HPA function can take ____ or longer
12 months
Review slide 85
therapies that may or may not suppress the HPA axis
Patients who have diagnosed secondary adrenal insufficiency as demonstrated by the short acting ACTH test will require perioperative ____ _____ steroids
stress dosed
Patients at high risk of HPA suppression, including those treated with at least 20mg/day of prednisone for > 3weeks or who have s/sx of Cushings, __________ is recommended
supplementation
Patients at low risk for HPA suppression - any steroid for < 3 weeks, less than 5mg/day of prednisone (or 10 mg QOD) - steroids are not ________ unless s/sx of HPA suppression are observed
required
Patients at intermediate risk, may consider ___________ testing
HPA
Review slide 88
surgical stress dose by procedure recommendations
Burns or sepsis could exaggerate the need for _______ corticosteroid supplementation
exogenous
Signs and symptoms of ACUTE adrenal crisis
hypotension unresponsive to vasopressors, hyperdynamic circulatioin, hypoglycemia, hyperkalemia, hyponatremia, hypovolemia, metabolic acidosis, decreased LOC
