Respiratory Medications Flashcards
1
Q
M1 Receptor Location and function
A
endocrine glands, autonomic ganglia, CNS, Salivary galnds, stomach. Function is arousal, attention, REM, emotional response
2
Q
M2 Receptor location and function
A
Location: Atria, conducting tissues of heart | Function: cardiac inhibition
3
Q
M3 Receptor location and function
A
Location: Exocrine glands, smooth muscle, lungs, eye, GI tract | Function: Lacrimal, salivary, mostly stimulatory
4
Q
M4 Receptor location and function
A
Location: CNS | Function: Direct regulatory action on K and CA channels
5
Q
M5 Receptor locatioin and function
A
Location: Substantia nigra, CNS | Function: May regulate dopamine release
6
Q
Muscarinic Recetors (Stimulatory)
A
M1, M3, M5
7
Q
Muscarinic Receptors (Inhibitory)
A
M2 and M4
8
Q
Review MOA
A
slide 5
9
Q
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
A
vagal / decreases / increases
10
Q
T/ F Inhaled medications have the same side effects as their oral counterparts
A
TRUE
11
Q
Most effective in treating bronchospasm due to beta ANTAGONISTS
A
Ipratropium
12
Q
Atrovent (Ipratropium) has slower onset than __________. More selective in lungs, less readily absorbed in the heart.
A
Atropine
13
Q
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 _______.
A
beta agonists / acute / chronic bronchitis / emphysema
14
Q
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.
A
M2 / bronchodilator
15
Q
Would you used Tiotropium (Spiriva) for acute bronchospasm
A
NO, because this is a long acting but NOT fast acting
16
Q
Long-acting anticholinergic bronchodilator with once daily dosing. Used for maintenance treatment of bronchospasm associated with COPD including chronic bronchitis and emphysema
A
Spiriva
17
Q
Tiotropium (Spiriva) blocks muscarinic receptor subtypes ___ and ____, which fascilitates _______ and reduces ______ secretion
A
M1 and M3 / bronchodilation / mucous
18
Q
Difference between Spiriva and Aclidinium (Tudorza)
A
Aclidinium is given twice daily and has a faster onset to peak
19
Q
Umeclidiuium is another ________________
A
long -acting Anticholinergic
20
Q
What are some Beta Agonsist respiratory drugs? (Adrenergic Agents)
A
Epinephrine, Isoproterenol, Albuterol, Terbutaline
21
Q
Ephedrine and epinephrine provide bronchodilating effects from activation of ____________ receptors; however, there is a significant amount of ______ side effects
A
beta 2 / non-respiratory
22
Q
Primatene mist is inhaled ________
A
epinephrine
23
Q
Isoproterenol can be used for the treatment of _____________. However, this drug is highly ______.
A
bronchospasms / proarrhythmic
24
Q
Review slide 17.
A
MOA for beta 2 agonists
25
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
26
________ 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
27
Intermediate acting Beta 2 agonists DOA
3-6 hrs
28
Long acting Beta 2 Agonists DOA
12 hrs
29
If you are giving beta 2 agonists and steroids, which would you give first?
Beta 2 agonists first followed by steroids
30
Beta 2 agonists preferred route of administration is _______, but oral and parenteral (SQ or IV) are also possible
inhaled
31
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
32
Issues with inhalation technique
12% delivered to the lungs, rest to mouth, pharynx and larynx.
33
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%
34
Dose delivered by a nebulizer requires ___ to ___ times that of a MDI dose to produce the same degree of bronchodilation
6-10 times
35
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
36
Beta 2 Agonsists metabolic response includes what?
Hyperglycemia, Hypokalemia, Hypomagnesemia
37
The preferred beta2 agonist for bronchospasm is ___________. Is this long or short acting?
albuterol / Short acting
38
Levoalbuterol is the _________ of racemic albuterol. Little or no clincially significant difference in adverse effects compared to albuterol.
R-enantiomer
39
Does xopenex still cause tachycardia
yes
40
Metaproterenol is a ___________ beta 2 agonist
selective
41
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
42
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
43
Vilanterol is a _______ acting beta 2 agonist
long
44
LABAs have a black box warning that says it should not be used _________ and there is an increased risk of asthma related ___________
alone / death
45
Cromolyn sodium is considered a _________ ____________. Also known to taste like a handful of _________.
membrane stabilizer / pennies
46
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
47
Cromolyn is used for the _________ treatment of bronchial asthma with no use for an ______ attack. Side effects are RARE.
prophylactic / acute
48
Methylxanthines include what drugs?
theophylline/aminophylline (that's the IV form), caffeine, theobromine
49
Uses for methylxanthines
stimulate the CNS, increase BP, incrase myocardial contractility, relax smooth muscle (airways)
50
Daliresp is a PDE4 ________
inhibitor
51
MOA for methylxanthines are they are non-selective _______ inhibitors
phosphodiesterase
52
Methylxanthines are competitive antagonists of __________ receptors
adenosine
53
Theophylline is more active than _____________ or __________
Caffeine / theobromine
54
Theophylline inhibits PDE 3,4 and 7 to cause _________. It inhibits PDE5 to ________ inflammatory cells
bronchodilation / decrease
55
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
56
Caffeine and other methylxanthines all block the ______ enzyme
a2a (adenosine)
57
Theophylline level 15-25 mcg/ml
GI upset, N/V, tremor
58
Theophylline level 25-35
tachycardia and PVCs
59
Theophylline level >35
Vtach and seizures
60
Theophylline has a very narrow _____ window
therapeutic
61
Effects of caffeine
CNS stimulant, cerebral VASOCONSTRICTOR, secretion of gastric acid
62
Uses for caffeine
apnea of prematurity, PDPH, cold remedies (offset sedation from antihistamines)
63
Ritodrine is considered a ______ and ________. Most frequently used as a tocolytic though.
tocolytic and beta2 agonists
64
Ritodrine stimulates beta 2 receptors and activates _______ ______. Has some beta 1 effects which may cause _________.
adenyl cyclase / tachycardia
65
Does ritodrine cross the placenta?
Yes
66
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 /
67
T/F Pulmonary edema can result from ritodrine admin?
TRUE
68
With ritodrine there can be an exaggerated systemic BP _________. Also, hyperglycemia in mother may cause a reactive ________ in fetus.
decrease / hypoglycemia
69
T/F Histamine is a LOW molecular weight, naturally occuring HYDROPHYLLIC endogenous amine that produces a cariety of physiologic and pathologic responses
TRUE
70
Histamine acts through _________ membrane receptors
G-protein coupled
71
Chemical meidator of inflammation in allergic disease
histamine
72
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
73
T/F Histamine easily crosses the blood-brain barrier
FALSE, does not easily cross the BBB
74
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
75
Through H1 and H2 receptors histamine causes
increased capillary permeability, hypotension, tachycardia, flushing, headache
76
H2 receptors will activate AC and INCREASE _______ __________
intracellular cAMP
77
H2 receptors activates proton pump of gastric _____ _____ to secrete hydrogen ion
parietal cells
78
H2 receptor activation increases myocardial _____ and _______. Vasodilating effects on coronary vasculature opposes the vasoconstricting effects of ___ receptors.
contractility and heart rate / H1
79
H1 receptor activation you should think what?
increase capillary permeability and vasodilation
80
What do you need to completely block the vasodilatory effects of histamine?
H1 and H2 blockers
81
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
82
Additional cardiovascular effects of histamine
inotropic effects, chronotropic effects, antidromic efffects, coronary vasodilation (H2), and vasoconstriction (H1)
83
Triple response to histamine is AKA
Wheal and Flare
84
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
85
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
86
H2 receptor activation in the airway results in ____________
bronchial smooth muscle relaxation
87
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
88
T/F Vagal activity also increases H+ ion secretion
TRUE
89
Histamine receptor antagonists are considered to be ______ and ________ antagonists of histamine receptors
competetive and reversible
90
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
91
H1 receptor antagonists are highly selective for ____ receptors. First gen are very _______ while second gen are not _______
H1 / sedating / sedating
92
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
93
H1 antagonists first generation CNS side effects
somnolence, decreased alertness, slowed reaction time, and impaired cognitive function
94
H1 antagonists first generation anticholinergic side effects
dry mouth, blurred vision, urinary retention, and constipation
95
H1 antagonists first generation Cardiovascular side effects
tachycardia, QT prolongation, heart block, and cardiac dysrhythmias
96
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
97
H1 antagonists clinical uses
allergic rhinits, less effective for nasal congestion, pretreatment may provide potection against bronchospasm, antipruritic, sedative, antiemetic
98
Benadryl is used for Type __ allergic reactions. Administer with epi, and addition of ___ antagonist speeds the resolution of the symptoms
I / H2
99
Anaphylactic reactions from IV contrast or blood products, antihistamines are more effective in ________ and __________.
preventing and controlling
100
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
101
Second Gen H1 antagonists
cetirizine, loratadine, fexofenadine
102
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
103
HPA axis
Hypothalmus, Anterior Pituitary, Adrenal Cortex
104
CRH is released from the _______. ACTH is release from the ________. Cortisol is released from the ________.
Hypothalmus, Anterior Pituitary, Adrenal Cortex
105
The outer layer of the adrenal cortex is the Zona ______ and releases _________
glomerulosa / mineralcorticoid
106
The middle layer of the adrenal cortex is the Zona ______ and releases __________
Fascicula / glucocorticoids
107
The inner layer of the adrenal cortex is the Zona ________ and releases ________
reticularis / weak androgens
108
_________ 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
109
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
110
Steroid do not provide acute relief because the way it alters and _______
protein
111
Aldosterone is released in response to _____
AT II
112
Aldosterone is secreted secondary to increased ____, decreased ____ and decreased ____/______
K / Na / blood and fluid volume
113
What are the effects of aldosterone
increased K excretion, Increased Na retention, increased water retention and increased blood volume
114
Circadian rhythm is releated to ________ secretion
cortisol
115
Secretory reates of CRH, ACTH, and cortisol are _______ in the early morning and ______ in the late evening
high / low
116
T/F Changing daily sleeping habits causes a corresponding change in the cycle of cortisol secretion
TRUE, so damn true
117
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
118
Secondary adrenocortical insufficiency is usually due to _________ and suppression of the _____ axis.
chronic steroid use / HPA
119
With secondary adrenocortical insufficiency _______ secretion is maintained and replacement usually requires only _________
aldosterone / glucocorticoid
120
Long term supplementation due to a negative ffeedback loop creating a lack of natural corticoids
secondary adrenocortical insufficency
121
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
122
Glucocorticoid effect relates to what?
anti-inflammatory response
123
Mineralocorticoid effect evokes distal renal tubular re-absorption of ___ in exchange for ___
Na / K
124
Naturally occuring steroids
cortisol, cortisone, corticosterone, desoxycorticosterone, aldosterone
125
Synthetic corticosteroids
prednisolone, prednisone, methylprednisolone, betamethasone, dexamethasone, triamcinolone
126
Synthetic mineralocorticoids
fludrocortisone
127
Review Slide 67
Cortisol equivalents
128
Steroids are ______ lipophilic and that is how it gets into the cells
highly
129
The only FDA approved use for corticosteroids is
replacement therapy for deficiency states
130
Water soluble forms of corticosteroids
cortisol succinate
131
Prolonged effects of come from what form of corticosteroids
cortsione ACETATE
132
Will cortisol cross the placenta
YES, will cross any barrier and will ALWAYS absorb
133
Review Corticosteroid side effects
Slide 71
134
Most common side effect from steroids?
hyperglycemia
135
HTN from steroids is from what?
fluid retention
136
Most common electrolyte abnormality from corticosteroids?
Hypokalemic Metabolic Alkalosis which can also lead to weight gain
137
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
138
Corticosteroids inhibit glucose USE in peripheral tissues and promote hepatic __________
gluconeogenesis
139
dose of oral hypoglycemic or insulin may need to be increased when steroids are administered to _______
Type II diabetics
140
Chronic steroid used leads to redistribution of fat. You get a _______ obesityt from moving amino acids and fast from the ________
central / periphery
141
Catabolic effeects of steroids
decreased skeletal muscle mass, osteoporosis, thinning of skin, negative nitrogen balance
142
Cataracts can develop from long term steroid use of greater than ___ years
4 years
143
Long term corticosteroids tend to increase ______ and number of _________
hematocrit / leukocytes
144
Single dose of cortisol decreases circulating lymphocytes by ____ % and monocytes by ______% (steroid induced leukemia). Cells are actually _________ rather than destroyed.
70% / 90% / sequestered
145
T/F admin of small doses of GLUCOCORTICOIDS in children can stunt growth by inhibiting DNA synthesis and cell division
TRUE
146
If someone has thyroid storm would you want to use a steorid?
NO
147
Relative contraindications for corticosteroids
active systemic infection, immunosuppression, acute psychosis, primary glaucoma, hypokalemia, CHF, Cushing's syndrome, diabetes, HTN, osteoporosis, HYPERthyroidism
148
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
149
T/F Any corticosteroid at any dose may result in suppression of HPA axis?
TRUE, so damn true
150
The longer the duration and dose of steroid, the higher the possibility of ___________
suppressing the HPA axis
151
Aldosterone secretion remains intact in ____________
secondary adrenocortical insufficency
152
Therapies unlikely to suppress the HPA axis
prednisone 5mg/ day or 10mg QOD and long term QOD dosing associated with less suppression.
153
Glucocorticoids, any dose < _____ ______ does not clinically suppress the HPA axis
3 weeks
154
Prednisosne or dexamethasone (evene physiologic doses) given as single daily dose at ________ is associated more commonly with HPA axis suppression
BEDTIME
155
Baseline cortisol secretion is about ____ mg per day and during stressful times can release ___ times that.
10 mg/ ten
156
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
157
After cessation of steroid therapy, recovery of the HPA function can take ____ or longer
12 months
158
Review slide 85
therapies that may or may not suppress the HPA axis
159
Patients who have diagnosed secondary adrenal insufficiency as demonstrated by the short acting ACTH test will require perioperative ____ _____ steroids
stress dosed
160
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
161
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
162
Patients at intermediate risk, may consider ___________ testing
HPA
163
Review slide 88
surgical stress dose by procedure recommendations
164
Burns or sepsis could exaggerate the need for _______ corticosteroid supplementation
exogenous
165
Signs and symptoms of ACUTE adrenal crisis
hypotension unresponsive to vasopressors, hyperdynamic circulatioin, hypoglycemia, hyperkalemia, hyponatremia, hypovolemia, metabolic acidosis, decreased LOC
