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Pharmacology II - Emily Britton > Respiratory Medications > Flashcards

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

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2
Q

M2 Receptor location and function

A

Location: Atria, conducting tissues of heart | Function: cardiac inhibition

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3
Q

M3 Receptor location and function

A

Location: Exocrine glands, smooth muscle, lungs, eye, GI tract | Function: Lacrimal, salivary, mostly stimulatory

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4
Q

M4 Receptor location and function

A

Location: CNS | Function: Direct regulatory action on K and CA channels

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5
Q

M5 Receptor locatioin and function

A

Location: Substantia nigra, CNS | Function: May regulate dopamine release

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6
Q

Muscarinic Recetors (Stimulatory)

A

M1, M3, M5

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7
Q

Muscarinic Receptors (Inhibitory)

A

M2 and M4

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8
Q

Review MOA

A

slide 5

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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

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10
Q

T/ F Inhaled medications have the same side effects as their oral counterparts

A

TRUE

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11
Q

Most effective in treating bronchospasm due to beta ANTAGONISTS

A

Ipratropium

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12
Q

Atrovent (Ipratropium) has slower onset than __________. More selective in lungs, less readily absorbed in the heart.

A

Atropine

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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

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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

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15
Q

Would you used Tiotropium (Spiriva) for acute bronchospasm

A

NO, because this is a long acting but NOT fast acting

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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

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17
Q

Tiotropium (Spiriva) blocks muscarinic receptor subtypes ___ and ____, which fascilitates _______ and reduces ______ secretion

A

M1 and M3 / bronchodilation / mucous

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18
Q

Difference between Spiriva and Aclidinium (Tudorza)

A

Aclidinium is given twice daily and has a faster onset to peak

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19
Q

Umeclidiuium is another ________________

A

long -acting Anticholinergic

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20
Q

What are some Beta Agonsist respiratory drugs? (Adrenergic Agents)

A

Epinephrine, Isoproterenol, Albuterol, Terbutaline

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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

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22
Q

Primatene mist is inhaled ________

A

epinephrine

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23
Q

Isoproterenol can be used for the treatment of _____________. However, this drug is highly ______.

A

bronchospasms / proarrhythmic

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24
Q

Review slide 17.

A

MOA for beta 2 agonists

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25
Q

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.

A

therapeutic / COMT / sustained

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26
Q

________ 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.

A

Beta 2 agonists / asthma / COPD / Tocolytic

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27
Q

Intermediate acting Beta 2 agonists DOA

A

3-6 hrs

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28
Q

Long acting Beta 2 Agonists DOA

A

12 hrs

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29
Q

If you are giving beta 2 agonists and steroids, which would you give first?

A

Beta 2 agonists first followed by steroids

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30
Q

Beta 2 agonists preferred route of administration is _______, but oral and parenteral (SQ or IV) are also possible

A

inhaled

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31
Q

Beta 2 agnoist inhalation technique

A

Deep breath, blow it all out. Dishcarge MDI with slow deep breath over 5-6 sec and hold breath for 10 seconds. Repeat

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32
Q

Issues with inhalation technique

A

12% delivered to the lungs, rest to mouth, pharynx and larynx.

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33
Q

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.

A

50-70%

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34
Q

Dose delivered by a nebulizer requires ___ to ___ times that of a MDI dose to produce the same degree of bronchodilation

A

6-10 times

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35
Q

Tremors from beta 2 agonists is due to stimulation of beta 2 receptors in ________ __________. Tachycardia is from direct stimulation of receptors on the ______.

A

skeletal muscle / heart

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36
Q

Beta 2 Agonsists metabolic response includes what?

A

Hyperglycemia, Hypokalemia, Hypomagnesemia

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37
Q

The preferred beta2 agonist for bronchospasm is ___________. Is this long or short acting?

A

albuterol / Short acting

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38
Q

Levoalbuterol is the _________ of racemic albuterol. Little or no clincially significant difference in adverse effects compared to albuterol.

A

R-enantiomer

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39
Q

Does xopenex still cause tachycardia

A

yes

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40
Q

Metaproterenol is a ___________ beta 2 agonist

A

selective

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41
Q

Terbutaline is used for the treatment of ___________. It can also be used as a ___________ to reduce contractions and postpone labor for hours to days

A

asthma / tocolytic

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42
Q

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.

A

long / prophylaxis

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43
Q

Vilanterol is a _______ acting beta 2 agonist

A

long

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44
Q

LABAs have a black box warning that says it should not be used _________ and there is an increased risk of asthma related ___________

A

alone / death

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45
Q

Cromolyn sodium is considered a _________ ____________. Also known to taste like a handful of _________.

A

membrane stabilizer / pennies

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46
Q

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.

A

antigen-induced / secretory / NOT / NO

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47
Q

Cromolyn is used for the _________ treatment of bronchial asthma with no use for an ______ attack. Side effects are RARE.

A

prophylactic / acute

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48
Q

Methylxanthines include what drugs?

A

theophylline/aminophylline (that’s the IV form), caffeine, theobromine

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49
Q

Uses for methylxanthines

A

stimulate the CNS, increase BP, incrase myocardial contractility, relax smooth muscle (airways)

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50
Q

Daliresp is a PDE4 ________

A

inhibitor

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51
Q

MOA for methylxanthines are they are non-selective _______ inhibitors

A

phosphodiesterase

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52
Q

Methylxanthines are competitive antagonists of __________ receptors

A

adenosine

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53
Q

Theophylline is more active than _____________ or __________

A

Caffeine / theobromine

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54
Q

Theophylline inhibits PDE 3,4 and 7 to cause _________. It inhibits PDE5 to ________ inflammatory cells

A

bronchodilation / decrease

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55
Q

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.

A

asthma

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56
Q

Caffeine and other methylxanthines all block the ______ enzyme

A

a2a (adenosine)

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57
Q

Theophylline level 15-25 mcg/ml

A

GI upset, N/V, tremor

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58
Q

Theophylline level 25-35

A

tachycardia and PVCs

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59
Q

Theophylline level >35

A

Vtach and seizures

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60
Q

Theophylline has a very narrow _____ window

A

therapeutic

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61
Q

Effects of caffeine

A

CNS stimulant, cerebral VASOCONSTRICTOR, secretion of gastric acid

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62
Q

Uses for caffeine

A

apnea of prematurity, PDPH, cold remedies (offset sedation from antihistamines)

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63
Q

Ritodrine is considered a ______ and ________. Most frequently used as a tocolytic though.

A

tocolytic and beta2 agonists

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64
Q

Ritodrine stimulates beta 2 receptors and activates _______ ______. Has some beta 1 effects which may cause _________.

A

adenyl cyclase / tachycardia

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65
Q

Does ritodrine cross the placenta?

A

Yes

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66
Q

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).

A

mother and fetus / increased / Na and water / K+ and HCO3 /

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67
Q

T/F Pulmonary edema can result from ritodrine admin?

A

TRUE

68
Q

With ritodrine there can be an exaggerated systemic BP _________. Also, hyperglycemia in mother may cause a reactive ________ in fetus.

A

decrease / hypoglycemia

69
Q

T/F Histamine is a LOW molecular weight, naturally occuring HYDROPHYLLIC endogenous amine that produces a cariety of physiologic and pathologic responses

A

TRUE

70
Q

Histamine acts through _________ membrane receptors

A

G-protein coupled

71
Q

Chemical meidator of inflammation in allergic disease

A

histamine

72
Q

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.

A

TRUE

73
Q

T/F Histamine easily crosses the blood-brain barrier

A

FALSE, does not easily cross the BBB

74
Q

H1 receptors

A

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
Q

Through H1 and H2 receptors histamine causes

A

increased capillary permeability, hypotension, tachycardia, flushing, headache

76
Q

H2 receptors will activate AC and INCREASE _______ __________

A

intracellular cAMP

77
Q

H2 receptors activates proton pump of gastric _____ _____ to secrete hydrogen ion

A

parietal cells

78
Q

H2 receptor activation increases myocardial _____ and _______. Vasodilating effects on coronary vasculature opposes the vasoconstricting effects of ___ receptors.

A

contractility and heart rate / H1

79
Q

H1 receptor activation you should think what?

A

increase capillary permeability and vasodilation

80
Q

What do you need to completely block the vasodilatory effects of histamine?

A

H1 and H2 blockers

81
Q

Cardiovascular effects of histamine

A

dilation of aterioles and capillaries resulting in flushing, decreased SVR (H1 and H2 effect), decreased BP, increased capillary permeability leading to edema

82
Q

Additional cardiovascular effects of histamine

A

inotropic effects, chronotropic effects, antidromic efffects, coronary vasodilation (H2), and vasoconstriction (H1)

83
Q

Triple response to histamine is AKA

A

Wheal and Flare

84
Q

What is the triple response

A

(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
Q

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 _____ _______

A

H1 / airway resistance

86
Q

H2 receptor activation in the airway results in ____________

A

bronchial smooth muscle relaxation

87
Q

Histamine evokes secretion of ________ fluid containing high concnetrations of hydrogen ions. Can occur without enough histamine to alter ______. It is due to ____ receptor stimulation.

A

gastric / BP / H2

88
Q

T/F Vagal activity also increases H+ ion secretion

A

TRUE

89
Q

Histamine receptor antagonists are considered to be ______ and ________ antagonists of histamine receptors

A

competetive and reversible

90
Q

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)

A

TRUE

91
Q

H1 receptor antagonists are highly selective for ____ receptors. First gen are very _______ while second gen are not _______

A

H1 / sedating / sedating

92
Q

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.

A

inverse agonists

93
Q

H1 antagonists first generation CNS side effects

A

somnolence, decreased alertness, slowed reaction time, and impaired cognitive function

94
Q

H1 antagonists first generation anticholinergic side effects

A

dry mouth, blurred vision, urinary retention, and constipation

95
Q

H1 antagonists first generation Cardiovascular side effects

A

tachycardia, QT prolongation, heart block, and cardiac dysrhythmias

96
Q

H1 antagonists second generation facts

A

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
Q

H1 antagonists clinical uses

A

allergic rhinits, less effective for nasal congestion, pretreatment may provide potection against bronchospasm, antipruritic, sedative, antiemetic

98
Q

Benadryl is used for Type __ allergic reactions. Administer with epi, and addition of ___ antagonist speeds the resolution of the symptoms

A

I / H2

99
Q

Anaphylactic reactions from IV contrast or blood products, antihistamines are more effective in ________ and __________.

A

preventing and controlling

100
Q

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.

A

motion sickness and PONV / vestibular nuclei

101
Q

Second Gen H1 antagonists

A

cetirizine, loratadine, fexofenadine

102
Q

H1 anatagonist summary

A

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
Q

HPA axis

A

Hypothalmus, Anterior Pituitary, Adrenal Cortex

104
Q

CRH is released from the _______. ACTH is release from the ________. Cortisol is released from the ________.

A

Hypothalmus, Anterior Pituitary, Adrenal Cortex

105
Q

The outer layer of the adrenal cortex is the Zona ______ and releases _________

A

glomerulosa / mineralcorticoid

106
Q

The middle layer of the adrenal cortex is the Zona ______ and releases __________

A

Fascicula / glucocorticoids

107
Q

The inner layer of the adrenal cortex is the Zona ________ and releases ________

A

reticularis / weak androgens

108
Q

_________ 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 ____ _____.

A

cortisol / stress / stress response

109
Q

T/F Cortisol alters carbohydrate, protein and fat metabolism as well as fluid and electrolyte. They also can inhibit the inflammatory and allergic response.

A

TRUE

110
Q

Steroid do not provide acute relief because the way it alters and _______

A

protein

111
Q

Aldosterone is released in response to _____

A

AT II

112
Q

Aldosterone is secreted secondary to increased ____, decreased ____ and decreased ____/______

A

K / Na / blood and fluid volume

113
Q

What are the effects of aldosterone

A

increased K excretion, Increased Na retention, increased water retention and increased blood volume

114
Q

Circadian rhythm is releated to ________ secretion

A

cortisol

115
Q

Secretory reates of CRH, ACTH, and cortisol are _______ in the early morning and ______ in the late evening

A

high / low

116
Q

T/F Changing daily sleeping habits causes a corresponding change in the cycle of cortisol secretion

A

TRUE, so damn true

117
Q

Primary adrenocortical insufficiency is AKA ________ disease. With this the adrenals do not secrete ____ or _____ so replacement therapy must include _____ and ________.

A

Addison’s / cortisol or aldosterone / glucocorticoid and mineralcorticoid

118
Q

Secondary adrenocortical insufficiency is usually due to _________ and suppression of the _____ axis.

A

chronic steroid use / HPA

119
Q

With secondary adrenocortical insufficiency _______ secretion is maintained and replacement usually requires only _________

A

aldosterone / glucocorticoid

120
Q

Long term supplementation due to a negative ffeedback loop creating a lack of natural corticoids

A

secondary adrenocortical insufficency

121
Q

Physiologic effects of cortisol secretion

A

increased CO, increased RR, increased gluconeogenesis, decreased inflammation, decreased immune response, inhibition of digestion, enhanced analgesia, redistribution of CNS blood flow

122
Q

Glucocorticoid effect relates to what?

A

anti-inflammatory response

123
Q

Mineralocorticoid effect evokes distal renal tubular re-absorption of ___ in exchange for ___

A

Na / K

124
Q

Naturally occuring steroids

A

cortisol, cortisone, corticosterone, desoxycorticosterone, aldosterone

125
Q

Synthetic corticosteroids

A

prednisolone, prednisone, methylprednisolone, betamethasone, dexamethasone, triamcinolone

126
Q

Synthetic mineralocorticoids

A

fludrocortisone

127
Q

Review Slide 67

A

Cortisol equivalents

128
Q

Steroids are ______ lipophilic and that is how it gets into the cells

A

highly

129
Q

The only FDA approved use for corticosteroids is

A

replacement therapy for deficiency states

130
Q

Water soluble forms of corticosteroids

A

cortisol succinate

131
Q

Prolonged effects of come from what form of corticosteroids

A

cortsione ACETATE

132
Q

Will cortisol cross the placenta

A

YES, will cross any barrier and will ALWAYS absorb

133
Q

Review Corticosteroid side effects

A

Slide 71

134
Q

Most common side effect from steroids?

A

hyperglycemia

135
Q

HTN from steroids is from what?

A

fluid retention

136
Q

Most common electrolyte abnormality from corticosteroids?

A

Hypokalemic Metabolic Alkalosis which can also lead to weight gain

137
Q

Hypokalemic metabolic alkalosis is due to the _________ effect of cortisol on DISTAL renal tubules leading to enhanced absorption of ____ and loss of ____

A

mineralocorticoid / Na / K

138
Q

Corticosteroids inhibit glucose USE in peripheral tissues and promote hepatic __________

A

gluconeogenesis

139
Q

dose of oral hypoglycemic or insulin may need to be increased when steroids are administered to _______

A

Type II diabetics

140
Q

Chronic steroid used leads to redistribution of fat. You get a _______ obesityt from moving amino acids and fast from the ________

A

central / periphery

141
Q

Catabolic effeects of steroids

A

decreased skeletal muscle mass, osteoporosis, thinning of skin, negative nitrogen balance

142
Q

Cataracts can develop from long term steroid use of greater than ___ years

A

4 years

143
Q

Long term corticosteroids tend to increase ______ and number of _________

A

hematocrit / leukocytes

144
Q

Single dose of cortisol decreases circulating lymphocytes by ____ % and monocytes by ______% (steroid induced leukemia). Cells are actually _________ rather than destroyed.

A

70% / 90% / sequestered

145
Q

T/F admin of small doses of GLUCOCORTICOIDS in children can stunt growth by inhibiting DNA synthesis and cell division

A

TRUE

146
Q

If someone has thyroid storm would you want to use a steorid?

A

NO

147
Q

Relative contraindications for corticosteroids

A

active systemic infection, immunosuppression, acute psychosis, primary glaucoma, hypokalemia, CHF, Cushing’s syndrome, diabetes, HTN, osteoporosis, HYPERthyroidism

148
Q

Surgeons concerns about intraop use of corticosteroids

A

aseptic necrosis of femoral head, failure of bone fusion, altering glucose in DM, masking infection or further complicating surgery inteded to treat infection

149
Q

T/F Any corticosteroid at any dose may result in suppression of HPA axis?

A

TRUE, so damn true

150
Q

The longer the duration and dose of steroid, the higher the possibility of ___________

A

suppressing the HPA axis

151
Q

Aldosterone secretion remains intact in ____________

A

secondary adrenocortical insufficency

152
Q

Therapies unlikely to suppress the HPA axis

A

prednisone 5mg/ day or 10mg QOD and long term QOD dosing associated with less suppression.

153
Q

Glucocorticoids, any dose < _____ ______ does not clinically suppress the HPA axis

A

3 weeks

154
Q

Prednisosne or dexamethasone (evene physiologic doses) given as single daily dose at ________ is associated more commonly with HPA axis suppression

A

BEDTIME

155
Q

Baseline cortisol secretion is about ____ mg per day and during stressful times can release ___ times that.

A

10 mg/ ten

156
Q

Therpaies assumed to suppress the HPA axis

A

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
Q

After cessation of steroid therapy, recovery of the HPA function can take ____ or longer

A

12 months

158
Q

Review slide 85

A

therapies that may or may not suppress the HPA axis

159
Q

Patients who have diagnosed secondary adrenal insufficiency as demonstrated by the short acting ACTH test will require perioperative ____ _____ steroids

A

stress dosed

160
Q

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

A

supplementation

161
Q

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

A

required

162
Q

Patients at intermediate risk, may consider ___________ testing

A

HPA

163
Q

Review slide 88

A

surgical stress dose by procedure recommendations

164
Q

Burns or sepsis could exaggerate the need for _______ corticosteroid supplementation

A

exogenous

165
Q

Signs and symptoms of ACUTE adrenal crisis

A

hypotension unresponsive to vasopressors, hyperdynamic circulatioin, hypoglycemia, hyperkalemia, hyponatremia, hypovolemia, metabolic acidosis, decreased LOC

Pharmacology II - Emily Britton (5 decks)

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