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KLowe Pharm 2 > Lecture 6-Respiratory Medications > Flashcards

Lecture 6-Respiratory Medications Flashcards

1
Q

Inhalation administration recommendations–discharge MDI with a ___ (slow/fast) deep breath in (over ___-___ seconds); hold breath for ___ seconds; repeat

A

discharge MDI with a slow deep breath in (over 5-6 seconds); hold breath for 10 seconds; repeat

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2
Q

Issues with inhalation technique–___% delivered to the lungs, the rest to the mouth, pharynx, and larynx

A

12% delivered to the lungs

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3
Q

Issues with inhalation technique–presence of an ETT decreases the amount of drug delivered by a MDI to the trachea by ___-___%

A

presence of an ETT decreases the amount of drug delivered by a MDI to the trachea by 50-70%

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4
Q

Administering inhalers during mechanical ventilation ___ (increases/decreases) the amount of drug that passes beyond the distal end of the ETT

A

increases the amount of drug that passes beyond the distal end of the ETT

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5
Q

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

A

Dose delivered by a nebulizer requires 6-10x that of a MDI dose to produce the same degree of bronchodilation

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6
Q

What should be administered first, bronchodilators or corticosteroids?

A

Bronchodilators should be administered before corticosteroids

^ because the bronchodilator will open up the lungs and increase the surface area that the corticosteroid can work on

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7
Q

What are the (6) classes of respiratory medications?–anti___; ___ agonists; membrane ___; ___thines; ___lytics; cortico___

A
  • Anticholinergics
  • Adrenergic agonists
  • Membrane stabilizers
  • Xanthines
  • Tocolytics (related drug)
  • Corticosteroids
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8
Q

What are the 5 types of muscarinic receptors?

A

M1-M5 receptors

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9
Q

M___ receptors are located in the heart and are responsible for cardiac inhibition

A

M2 receptors

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10
Q

M___ receptors are located in the CNS and have direct regulatory action on K and Ca channels

A

M4 receptors

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11
Q

What (3) muscarinic receptors are stimulatory?

A

M1, M3, M5

Odd = stimulatory

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12
Q

What (2) muscarinic receptors are inhibitory?

A

M2, M4

Even = inhibitory

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13
Q

Antimuscarinic = anti___

A

anticholinergic

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14
Q

Antimuscarinic/anticholinergic both mean that we are blocking ___ from binding to ___ receptors

A

we are blocking ACH from binding to muscarinic receptors

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15
Q

Atropine antagonizes ___ effects on airway smooth muscle in large and medium sized airways; it affects airways that respond to vagal stimulation; it ___ (increases/decreases) airway resistance; ___ (increases/decreases) dead space

A

Atropine antagonizes ACH effects on airway smooth muscle in large and medium sized airways; it affects airways that respond to vagal stimulation; it decreases airway resistance; increases dead space

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16
Q

What is the main issue with nebulized atropine?

A

A lot of CV complications, tachyarrhythmias

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17
Q

Atropine is ___ (more/less) lipophilic than glycopyrrolate

A

atropine is more lipophilic than glyocpyrrolate

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18
Q

Atropine is a ___ amine

A

tertiary amine

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19
Q

Atropine ___ (can/cannot) cross the BBB

A

can cross the BBB (because it’s a tertiary amine and more lipophilic)

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20
Q

Glycopyrrolate is a ___ ammonium; it ___ (does/does not) absorb systemically as much as atropine

A

glycopyrrolate is a quaternary ammonium; it does not absorb systemically as much as atropine

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21
Q

Glycopyrrolate is an inhaled anticholinergic medication used for treatment of ___

A

COPD

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22
Q

Is glycopyrrolate indicated for acute symptom management?

A

No–used for management of chronic disease like COPD

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23
Q

Glycopyrrolate has ___ (more/less) risk of tachyarrythmias than atropine

A

less risk of tachycarrhythmias than atropine (because there’s less systemic absorption of glycopyrrolate)

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24
Q

Ipratropium has minimal ___ absorption

A

minimal systemic absorption (<1%)–less systemic absorption than atropine

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25
Q

Ipratropium is a ___ (short/long) acting muscarinic antagonist

A

short-acting muscarinic antagonist

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26
Q

What may occur due to the M2 blockade that ipratropium causes?

A

Paradoxical bronchospasm–this is true for all muscarinic antagonists d/t M2 blockade

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27
Q

Limited systemic absorption of ipratropium results in prolonged local site effect–T/F?

A

True

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28
Q

Ipratropium is most effective in treating bronchospasm due to ___

A

treating bronchospasm due to beta antagonists (i.e.: propranolol which has non-selective beta blockade)

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29
Q

Compared to beta agonists, ipratropium has a ___ (slower/faster) onset and is ___ (more/less) effective in treating bronchial asthma

A

ipratropium has a slower onset (30-90 minutes) and is less effective in treating bronchial asthma than beta agonists

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30
Q

Ipratropium is useful in acute attacks–T/F?

A

False–is NOT useful in acute attacks because it has a slower onset of 30-90 mins

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31
Q

Albuterol is better than ipratropium for acute asthma attacks because it has a faster onset of action–T/F?

A

True

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32
Q

Ipratropium is more effective than beta agonists in treating what two diseases?

A

Chronic bronchitis or emphysema

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33
Q

Ipratropium is usually not given alone–T/F?

A

True–it is usually given in combo with a beta agonist (i.e.: albuterol)

Ipratropium is only given alone if a person can’t tolerate a beta agonist like albuterol

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34
Q

Ipratropium alone = ___

A

atrovent

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35
Q

Ipratropium given in combo with albuterol = ___ or ___

A

duoneb or combivent (MDI with ipratropium/albuterol)

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36
Q

Tiotropium (Spiriva) is a ___ (short/long) acting anticholinergic bronchodilator

A

long-acting anticholinergic bronchodilator

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37
Q

Tiotropium (Spiriva) is used as maintenance treatment of bronchospasm associated with COPD, including chronic ___ and ___

A

chronic bronchitis and emphysema

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38
Q

Tiotropium (Spiriva) blocks muscarinic receptor subtypes M___ and M___ to facilitate broncho___ and reduce ___ secretion

A

blocks muscarinic receptor subtypes M1 and M3 to facilitate bronchodilation and reduce mucous secretion

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39
Q

Tiotropium is a little more specific to the M___ receptors than other medications

A

M3 receptors

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40
Q

Tiotropium (Spiriva) is administered as ___ by inhalation

A

dry powder

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41
Q

Long-acting bronchodilators ___ (should/should not) be used to treat acute anything

A

should NOT be used to treat acute anything

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42
Q

Is glycopyrrolate used for acute symptom management or chronic disease management?

A

Chronic disease management

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43
Q

Is atropine used for acute symptom management or chronic disease management?

A

Acute symptom management (i.e.: acute bronchospasm)

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44
Q

Aclidinium (Tudorza) is similar to Spiriva…what’s the major difference between these two medications?

A

Aclidinium (Tudorza) is given twice daily vs. once daily like Spiriva

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45
Q

Warnings for inhaled anticholinergics–can cause ___ and severe ___

A

narrow angle glaucoma and severe urinary retention

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46
Q

At normal inhaled doses, the risk of systemic absorption of inhaled anticholinergics is very low–T/F?

A

True

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47
Q

Reports of constipation/CNS side effects that typically come along with anticholinergics–i.e.: agitation, cognitive decline, confusion–are far less with inhaled anticholinergics than IV anticholinergics–T/F?

A

True–less with inhaled than IV

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48
Q

Beta 2 agonists ___ (relax/contract) bronchial smooth muscle

A

relax bronchial smooth muscle

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49
Q

Newer beta 2 agonists lack stimulating effects on the heart at therapeutic doses–T/F?

A

True

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50
Q

Beta 2 agonists ___ (do/do not) have a catecholamine structure

A

do NOT have a catecholamine structure

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51
Q

The non-catecholamine structure of beta 2 agonists makes them resistant to what enzyme? What effect does this have on their duration of action?

A

Beta 2 agonists are resistant to COMT (because they are non-catecholamines); this contributes to their LONGER duration of action

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52
Q

Uses of beta 2 agonists–preferred treatment for ___ (acute/chronic) episodes of asthma; prevention of ___-induced asthma; improve airflow and exercise tolerance in patients with ___; tocolytic to stop premature ___ contractions; treatment of ___kalemia

A

preferred treatment for acute episodes of asthma; prevention of exercise-induced asthma; improve airflow and exercise tolerance in patients with COPD; tocolytic to stop premature uterine contractions; treatment of hyperkalemia

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53
Q

Classes of beta 2 agonists–short acting = ___-___ hours; long acting = > ___ hours

A

short acting = 3-6 hours; long acting = > 12 hours

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54
Q

What is the preferred route of administration for beta 2 agonists?

A

Inhaled

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55
Q

What is a useless route of administration for beta 2 agonists like albuterol?

A

Oral–4 mg albuterol tablets are worthless

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56
Q

Beta 2 agonists can be given subQ or IV–T/F?

A

True

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57
Q

What are (2) beta 2 agonists that have a significant amount of non-respiratory side effects?

A

Ephedrine and epinephrine

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58
Q

In spite of their non-respiratory side effects, ephedrine and epinephrine do have ___ effects from activation of beta 2 receptors

A

bronchodilating effects from activation of beta 2 receptors

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59
Q

What are some of the non-respiratory side effects of ephedrine and epinephrine?–___arrhythmias; ___tension; increased blood ___

A

tachyarrhythmias; hypertension; increased blood glucose

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60
Q

Isoproterenol is a ___ (selective/non-selective) sympathomimetic that acts at ___ and ___ receptors

A

non-selective sympathomimetic that acts at beta 1 and beta 2 receptors

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61
Q

Isoproterenol is highly pro-___

A

pro-arrhythmic

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62
Q

Isoproterenol is often used as a last resort medication for a respiratory issue–T/F?

A

True (because it is so pro-arrhythmic)

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63
Q

What medication is the preferred beta 2 agonist for acute bronchospasm?

A

Albuterol

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64
Q

Albuterol is a ___ (short/long) acting beta agonist

A

short acting beta agonist

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65
Q

Albuterol given alone is known as ___ or ___

A

Proventil or ventolin

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66
Q

Albuterol given in combo with ipratropium is known as ___ or ___

A

combivent or duoneb

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67
Q

Levoalbuterol (Xopenex) is the (___)-enantiomer of racemic albuterol

A

(R)-enantiomer of racemic albuterol

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68
Q

(___)-enantiomer has cardio-stimulatory effects

A

(S)-enantiomer has cardio-stimulatory effects

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69
Q

What was the main point of levoalbuterol (xopenex) for being marketed?

A

Because it is an (R)-enantiomer, it was expected to have little to no cardiac effects

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70
Q

Studies have shown that there is little or no clinically significant difference in adverse effects of levoalbuterol (xopenex) compared to albuterol–T/F?

A

True

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71
Q

Terbutaline can be used in the treatment of asthma and is also a ___

A

tocolytic–reduces contractions of the uterus to postpone labor for hours to days

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72
Q

Terbutaline has fallen out of use by pulmonologists and obstetricians–T/F?

A

True

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73
Q

Ritodrine is a beta 2 agonist used as a ___ to stop ___

A

used as a tocolytic to stop uterine contractions of premature labor

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74
Q

Ritodrine has been removed from the market–T/F?

A

True

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75
Q

Ritodrine was removed from the market d/t ___ complications and 24 maternal ___

A

d/t CV complications and 24 maternal deaths

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76
Q

Side effects of ritodrine–crosses the ___; causes ___ and ___ effects in both the mother and fetus; dose-related ___cardia (because it’s slightly non-selective, beta1 and beta 2 agonism), ___ (increased/decreased) cardiac output; increased ___ secretion d/t beta1 stimulation; exaggerated systemic BP ___ (increase/decrease); ___glycemia in the mother (from beta2 effects) may cause reactive ___glycemia in the fetus

A

crosses the placenta; causes CV and metabolic effects in both the mother and fetus; dose-related tachycardia (because it’s slightly non-selective, beta1 and beta2 agonism), increased cardiac output; increased renin secretion d/t beta1 stimulation; exaggerated systemic BP decrease; hyperglycemia in the mother (from beta2 effects) may cause reactive hypoglycemia in the fetus

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77
Q

Side effects of ritodrine–increased renin secretion from beta1 stimulation causes ___ (increased/decreased) sodium; water ___ (reabsorption/secretion); ___ (increased/decreased) K+ and H+; pulmonary ___ may occur

A

increased renin secretion from beta1 stimulation causes increased sodium; water reabsorption; decreased K+ and H+; pulmonary edema may occur

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78
Q

Terbutaline and ritodrine are both ___ (short/long) acting beta agonists, just like albuterol and levoalbuterol

A

short acting beta agonists

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79
Q

Long acting beta agonists ___ (are/are not) used for acute effect

A

are NOT used for acute effect–used for long-term management

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80
Q

Long acting beta agonists are often given in combo with something else–T/F?

A

True–can be administered with a short acting beta agonist or steroid

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81
Q

Salmeterol (serevent) and vilanterol are both ___ (short/long) acting beta agonists

A

long acting beta agonists

82
Q

Salmeterol (serevent) is frequently administered with a ___

A

steroid–i.e.: salmeterol/fluticasone = Advair used for the prophylaxis of asthma

83
Q

Formoterol and aformoterol are two other ___ (short/long) acting beta agonists

A

long acting beta agonists

84
Q

Corticosteroids end in -___

A

-sone–i.e.: fluticasone, mometasone

Be able to recognize corticosteroids in inhalers…need to know what is in the product

85
Q

Side effects of beta 2 agonists–___ usually occurs with overdose/systemic absorption due to stimulation of beta 2 receptors on ___ muscle; ___cardia from direct stimulation of receptors on the heart; metabolic response–___glycemia, ___kalemia, ___magnesemia

A

tremor usually occurs with overdose/systemic absorption due to stimulation of beta 2 receptors on skeletal muscle; tachycardia from direct stimulation of receptors on the heart; metabolic response–hyperglycemia, hypokalemia, hypomagnesemia

86
Q

Why do you see hypokalemia/hypomagnesemia with beta 2 agonists?

A

When you give a beta 2 agonist, potassium is pulled into the cell in exchange for sodium; magnesium follows potassium into the cell

87
Q

Black box warning for LABAs–increased risk of ___; ___ (should/should not) be used alone

A

increased risk of asthma related death; should not be used alone

88
Q

How can LABAs (when used alone) lead to asthma related death?–LABAs have no ___ action

A

LABAs have no anti-inflammatory action–so if someone is having an asthma attack and you only give them an LABA, their lungs won’t react to the inflammatory response that is going on, leading to death

89
Q

Cromolyn sodium is a ___; it inhibits antigen-induced release of ___ and other mediators from pulmonary mast cells during antibody mediated allergic responses

A

membrane stabilizer; it inhibits antigen-induced release of histamine and other mediators from pulmonary mast cells during antibody mediated allergic responses

90
Q

Cromolyn sodium suppresses the ___ response, NOT the Ag-Ab interaction

A

secretory response

91
Q

Cromolyn sodium ___ (does/does not) relax bronchial or vascular smooth muscle

A

does NOT relax bronchial or vascular smooth muscle

92
Q

Cromolyn sodium is used for ___ (acute/chronic) management; has no use in ___

A

used for chronic management; has no use in an acute asthma attack

93
Q

What do most patients complain about when taking cromolyn sodium?

A

Metal taste

94
Q

Cromolyn sodium is no longer available as an ___ but is available as a ___

A

no longer available as an inhaler but is available as a nebulizer

95
Q

What are (3) types of methylxanthines?

A
  • Theophylline/aminophylline
  • Caffeine
  • Theobromine
96
Q

Methylxanthines ___ (stimulate/inhibit) the CNS; ___ (increase/decrease) BP; ___ (increase/decrease) myocardial contractility and heart rate; ___ (contract/relax) smooth muscle in the airways

A

stimulate the CNS; increase BP; increase myocardial contractility and heart rate; relax smooth muscle in the airways

97
Q

Methylxanthines are non-selective ___ inhibitors

A

non-selective phosphodiesterase inhibitors–inhibit all fractions of PDE isoenzymes

98
Q

PDE4 = ___ effects

A

respiratory effects

99
Q

PDE3 = ___ effects

A

CV effects

100
Q

PDE5 = ___ effects

A

vasodilatory effects–PDE5 inhibitors are used to treat pulmonary HTN and erectile dysfunction

101
Q

Phosphodiesterase breaks down ___

A

cAMP/cGMP

102
Q

Methylxanthines are also competitive antagonists of ___ receptors

A

competitive antagonists of adenosine receptors

103
Q

Theophylline has more competitive antagonism for adenosine receptors than caffeine and theobromine–T/F?

A

True

104
Q

Theophylline is used for acute or chronic asthma management?

A

Acute asthma management

105
Q

Theophylline is also used to treat ___ in infants

A

apnea of prematurity in infants (because it is a CNS stimulant)

106
Q

Theophylline toxicities–___-___ mcg/ml = GI upset, nausea/vomiting, tremor

A

15-25 mcg/ml = GI upset, nausea/vomiting, tremor

107
Q

Theophylline toxicities–___-___ mcg/ml = tachycardia, PVCs

A

25-35 mcg/ml = tachycardia, PVCs

108
Q

Theophylline toxicities– >___ mcg/ml = fatal VTach, seizures

A

> 35 mcg/ml = fatal VTach, seizures

109
Q

Caffeine effects–CNS ___ (stimulant/inhibitor); cerebral vaso___ (dilator/constrictor); secretion of ___

A

CNS stimulant; cerebral vasoconstrictor; secretion of gastric acid

110
Q

Caffeine uses–apnea of ___; ___ headache; ___ remedies (to offset sedation from antihistamines)

A

apnea of prematurity; post-dural puncture headache; cold remedies (to offset sedation from antihistamines)

111
Q

The methylxanthine class has a high risk of ___ and ___

A

high risk of toxicity and withdrawal

112
Q

This substance is a naturally occurring hydrophilic endogenous amine that produces a variety of physiologic and pathologic responses; it acts through G-protein coupled membrane receptors; it is a chemical mediator of inflammation in allergic disease

A

Histamine

113
Q

What cells contain large amounts of histamine?

A

Mast cells in the skin, lungs, GI tract, and circulating basophils

114
Q

Histamine ___ (does/does not) easily cross the blood-brain barrier

A

does not easily cross the blood-brain barrier

115
Q

Histamine receptors = ___-___ receptors

A

H1-H4 receptors

116
Q

H1 receptors are mostly ___ effects and are triggered during ___ reactions

A

H1 receptors are mostly respiratory effects and are triggered during allergic reactions

117
Q

H2 receptors are mostly ___ effects

A

H2 receptors are mostly GI effects

118
Q

___ effects come from both H1 and H2 receptors

A

CV effects come from both H1 and H2 receptors

119
Q

Through H1 and H2 receptors, histamine causes ___ (increased/decreased) capillary permeability; ___tension; ___cardia; ___ing; ___ache

A

increased capillary permeability; hypotension; tachycardia; flushing; headache

120
Q

What receptor(s) need to be blocked in order to completely block the vasodilatory effects of histamine release?

A

Both H1 and H2 receptors need to be blocked in order to completely block the vasodilatory effects of histamine release

So–if someone is having a severe allergic reaction, give Benadryl and pepcid to block H1 and H2 receptors

121
Q

Histamine triple response (wheal and flare)–___ due to increased permeability; ___ (dilated/constricted) arteries around the edema (flare); ___ due to histamine in the superficial layers of the skin

A

edema due to increased permeability; dilated arteries around the edema (flare); pruritus due to histamine in the superficial layers of the skin

122
Q

Histamine effects on organ systems–airway–H1 receptor activation ___ (constricts/dilates) bronchial smooth muscle; in normal patients, this action is ___; in patients with asthma or bronchitis, they are more likely to develop increases in airway ___

A

H1 receptor activation constricts bronchial smooth muscle; in normal patients, this action is negligible; in patients with asthma or bronchitis, they are more likely to develop increases in airway resistance

123
Q

Histamine effects on organ systems–airway–H2 receptor activation ___ (constricts/relaxes) bronchial smooth muscle

A

H2 receptor activation relaxes bronchial smooth muscle

124
Q

Histamine evokes secretion of gastric fluid containing ___ (low/high) concentrations of hydrogen ions; due to H__ receptor stimulation; ___ activity also increases H+ secretion

A

Histamine evokes secretion of gastric fluid containing high concentrations of hydrogen ions; due to H2 receptor stimulation; vagal activity also increases H+ secretion

125
Q

Histamine receptor antagonists are ___ (competitive/noncompetitive) and ___ (reversible/irreversible) antagonists of histamine receptors

A

competitive and reversible antagonists of histamine receptors

126
Q

Histamine receptor antagonists ___ (do/do not) inhibit the release of histamine

A

do NOT inhibit the release of histamine–histamine is still released from the mast cells, but it is unable to bind to its receptor

127
Q

Histamine receptor antagonists attach to receptors and prevent the responses mediated by histamine–T/F?

A

True–competitive antagonism

128
Q

Histamine receptor antagonists stabilize the receptor in the ___ (active/inactive) form, making them ___ agonists

A

stabilize the receptor in the inactive form, making them inverse agonists

129
Q

H1 receptor antagonists are highly selective for H__ receptors

A

H1 receptors

130
Q

Two generations of H1 receptor antagonists–first generation = ___; second generation = ___

A

first generation = sedating; second generation = non-sedating

131
Q

First generation H1 receptor antagonists are ___; they may also activate ___ or ___-adrenergic receptors; they block ___ receptors

A

First generation H1 receptor antagonists are sedating; they may also activate serotonin or alpha-adrenergic receptors; they block muscarinic receptors

132
Q

H1 receptor antagonists have been reclassified as ___ agonists–they combine and stabilize the ___ (active/inactive) form of the H1 receptor, shifting equilibrium toward the ___ (active/inactive) state

A

Inverse agonists–they combine and stabilize the inactive form of the H1 receptor, shifting equilibrium toward the inactive state

133
Q

First generation H1 receptor antagonist CNS side effects–___ence; ___ (increased/decreased) alertness; ___ (slower/faster) reaction time; impaired ___ function

A

somnolence; decreased alertness; slower reaction time; impaired cognitive function

134
Q

First generation H1 receptor antagonist anticholinergic side effects–___ mouth; ___ vision; urinary ___; ___ation

A

dry mouth; blurred vision; urinary retention; constipation

135
Q

First generation H1 receptor antagonist CV side effects–stimulate the ___ (alpha/beta) adrenergic receptor, leading to ___cardia, QT ___ heart ___, and cardiac ___

A

stimulate the alpha adrenergic receptor, leading to tachycardia, QT prolongation, heart block, and cardiac dysrhythmias

136
Q

Benadryl is a ___ (first/second) generation H1 antagonist

A

first generation H1 antagonist

137
Q

Second generation H1 antagonists are unlikely to produce CNS side effects unless recommended doses are exceeded–T/F?

A

True

138
Q

H1 antagonists uses–prevent and relieve the symptoms of allergic ___itis; less effective for nasal ___; pretreatment may provide some protection against ___ induced by various stimuli; anti___; ___; anti___

A

prevent and relieve the symptoms of allergic rhinoconjunctivitis; less effective for nasal congestion; pretreatment may provide some protection against bronchospasm induced by various stimuli; antipruritic; sedative; antiemetic

139
Q

Diphenhydramine (Benadryl) is used as a ___, anti___, anti___; is used for treatment of type ___ allergic reactions; is used for ___ reactions

A

Benadryl is used as a sedative, antipruritic, antiemetic; is used for treatment of type 1 allergic reactions; is used for anaphylactic reactions

140
Q

Dimenhydrinate (dramamine) is used to treat ___ sickness and post-op ___/___; it inhibits the integrative functioning of vestibular nuclei by ___ (increasing/decreasing) vestibular and visual input

A

dimenhydrinate (dramamine) is used to treat motion sickness and post-op nausea/vomiting; it inhibits the integrative functioning of vestibular nuclei by decreasing vestibular and visual input

141
Q

Dimenhydrinate (dramamine) ___ (is/is not) associated with prolonged sedation

A

dimenhydrinate (dramamine) is NOT associated with prolonged sedation

142
Q

(3) second generation H1 antagonists

A
  • Zyrtec (cetirizine)
  • Claritin (loratidine)
  • Allegra (fexofenadine)
143
Q

Second generation H1 antagonists are ___ (more/less) sedating than first generation H1 antagonists

A

less sedating

144
Q

HPA axis–hypothalamus releases ___, anterior pituitary releases ___, adrenal cortex releases ___

A

hypothalamus releases corticotropin releasing hormone (CRH), anterior pituitary releases adrenocorticotropic hormone (ACTH), adrenal cortex releases cortisol

145
Q

Adrenal cortex–zona glomerulosa = ___ layer; releases ___

A

outer layer; releases mineralocorticoids

146
Q

Adrenal cortex–zona fasciculata = ___ layer; releases ___

A

middle layer; releases glucocorticoids

147
Q

Adrenal cortex–zona reticularis = ___ layer; releases ___

A

inner layer; releases weak androgens

148
Q

What hormone is produced in the adrenal cortex in response to stress?

A

Cortisol (hydrocortisone)

149
Q

What is the major mineralocorticoid?

A

Aldosterone

150
Q

Aldosterone is secreted secondary to ___ (increased/decreased) K+; ___ (increased/decreased) sodium; ___ (increased/decreased) BP/fluid volume

A

aldosterone is secreted secondary to increased K+; decreased sodium; decreased BP/fluid volume

151
Q

Review of RAAS

A

renin is released by the kidneys in response to low BP –> angiotensinogen (released by the liver) converts renin to angiotensin I –> angiotensin I is converted to angiotensin II by ACE (released from the lungs) –> angiotensin II is potent vasoconstrictor, stimulates release of aldosterone from the adrenal cortex

152
Q

Aldosterone ___ (increases/decreases) K+ excretion; ___ (increases/decreases) Na+ retention; ___ (increases/decreases) water retention; ___ (increases/decreases) blood volume

A

Aldosterone increases K+ excretion; increases Na+ retention; increases water retention; increases blood volume

153
Q

Circadian rhythm–secretory rates of CRH, ACTH, and cortisol are ___ (low/high) in the early morning; ___ (low/high) in the late evening

A

high in the early morning; low in the late evening

154
Q

Changing daily sleeping habits causes a corresponding change in circadian rhythm–T/F?

A

True

155
Q

Primary adrenocortical insufficiency is AKA ___ disease

A

Addison’s disease

156
Q

Addison’s disease–the adrenals do not secrete ___ or ___; replacement therapy must include ___corticoid and ___corticoid

A

the adrenals do not secrete cortisol or aldosterone; replacement therapy must include glucocorticoid and mineralocorticoid

157
Q

Secondary adrenocortical insufficiency is due to chronic ___ use and suppression of the ___ axis

A

due to chronic steroid use and suppression of the HPA axis

158
Q

In secondary adrenocortical insufficiency, ___ secretion is maintained

A

aldosterone secretion is maintained

159
Q

Replacement therapy for secondary adrenocortical insufficiency usually requires only ___corticoid

A

glucocorticoid

160
Q

Physiological effects of corticosteroids–___ (increased/decreased) cardiac output; ___ (increased/decreased) respiratory rate; ___ (increased/decreased) gluconeogenesis; ___ (increased/decreased) inflammation; ___ (increased/decreased) immune response; ___ (stimulation/inhibition) of digestion; ___ (enhanced/reduced) analgesia; redistribution of ___ blood flow

A

increased cardiac output; increased respiratory rate; increased gluconeogenesis; decreased inflammation; decreased immune response; inhibition of digestion; enhanced analgesia; redistribution of CNS blood flow

161
Q

How are corticosteroids classified?

A

They are classified according to their potencies

162
Q

Glucocorticoid effect = anti-___ response

A

glucocorticoid effect = anti-inflammatory response

163
Q

Mineralocorticoid effect = evoke distal renal tubular reabsorption of ___ in exchange for ___

A

mineralocorticoid effect = evoke distal renal tubular reabsorption of Na+ in exchange for K+

164
Q

What are (5) naturally occurring corticosteroids?

A
  • cortisol (hydrocortisone)
  • cortisone
  • corticosterone
  • desoxycorticosterone
  • aldosterone
165
Q

Prednisolone, prednisone, methylprednisolone, betamethasone, dexamethasone, triamcinolone, and fludrocortisone are all ___ (natural/synthetic) corticosteroids

A

synthetic corticosteroids

166
Q

Which (2) corticosteroid medications have the greatest anti-inflammatory potency?

A
  • Betamethasone
  • Dexamethasone

^ Both are synthetic glucocorticoids

167
Q

What corticosteroid medication has the greatest sodium-retaining potency?

A

Fludrocortisone–synthetic mineralocorticoid

168
Q

Fluticasone, budesonide, beclometasone, mometasone, cicleonide are all inhaled ___

A

inhaled corticosteroids

169
Q

What should you do after you give an inhaled corticosteroid?

A

Have patient rinse mouth so they don’t get thrush

170
Q

What is the main clinical use of corticosteroids?

A

Replacement therapy for deficiency states

171
Q

Pharmacokinetics of corticosteroids–___ (lipid/water) soluble forms can be administered IV; prolonged effects with ___ administration; able to cross the ___

A

water soluble forms can be administered IV (cortisol succinate); prolonged effects with IM administration (cortisone acetate); able to cross the placenta

172
Q

Corticosteroid use can lead to ___kalemic metabolic ___osis due to ___corticoid effect of cortisol on distal renal tubules, leading to enhanced absorption of ___ and loss of ___; also leads to ___ and weight ___

A

corticosteroid use can lead to hypokalemic metabolic alkalosis due to mineralocorticoid effect of cortisol on distal renal tubules, leading to enhanced absorption of Na+ and loss of K+; also leads to edema and weight gain

173
Q

Corticosteroids ___ (stimulate/inhibit) glucose use in peripheral tissues and ___ (promote/inhibit) hepatic gluconeogenesis; resultant ___glycemia may require diet changes, insulin, or both to manage

A

inhibit glucose use in peripheral tissues and promote hepatic gluconeogenesis; resultant hyperglycemia may require diet changes, insulin, or both to manage

174
Q

Peripherally, corticosteroids mobilize amino acids from tissues, leading to ___ (increased/decreased) skeletal muscle mass; ___porosis; ___ of the skin; negative nitrogen balance

A

decreased skeletal muscle mass; osteoporosis; thinning of the skin; negative nitrogen balance

175
Q

Steroid use is associated with an increased incidence of neurosis and psychosis–T/F?

A

True

176
Q

Behavioral changes associated with steroid use include manic depression and suicidal tendencies–T/F?

A

True

177
Q

Cataracts can develop with long term ( > ___ years) steroid usage

A

> 4 years

178
Q

Long term corticosteroids tend to ___ (increase/decrease) hematocrit and number of leukocytes

A

increase hematocrit and number of leukocytes

179
Q

Single dose of cortisol decreases circulating lymphocytes by ___%; decreases circulating monocytes by ___%; cells are sequestered rather than destroyed

A

decreases circulating lymphocytes by 70%; decreases circulating monocytes by 90%

180
Q

Arrest of growth can result from the administration of relatively small doses of glucocorticoids to children–T/F?

A

True

181
Q

Acute systemic infection; immunosuppression; acute psychosis; primary glaucoma; hypokalemia; CHF; Cushing’s syndrome; diabetes; hypertension; osteoporosis; and hyperthyroidism are all ___ (relative/absolute) contraindications to steroid administration

A

relative contraindications

182
Q

Surgeons concerns about Intraoperative use of corticosteroids–masking ___ or further complicating surgery intended to treat ___; altering ___ control in diabetics; aseptic ___ of the femoral head; failure of bone ___

A

masking infection or further complicating surgery intended to treat infection; altering glucose control in diabetics; aseptic necrosis of the femoral head; failure of bone fusion

183
Q

Any corticosteroid administration may result in suppression of the HPA axis–T/F?

A

True

184
Q

Likelihood of HPA axis suppression is increased with longer duration/larger dose of steroid administration–T/F?

A

True

185
Q

Aldosterone secretion remains intact in ___ (primary/secondary) adrenal insufficiency

A

secondary adrenal insufficiency

186
Q

Prednisone 5 mg/day or less or 10 mg every other day is ___ (likely/unlikely) to suppress the HPA axis

A

unlikely to suppress the HPA axis

187
Q

Long term every other day dosing is associated with ___ (more/less) suppression

A

less suppression

188
Q

Glucocorticoids any dose < ___ weeks does not clinically suppress the HPA axis

A

any dose < 3 weeks

189
Q

Prednisone or dexamethasone (even physiologic doses) given as a single daily dose at bedtime is associated more commonly with HPA axis suppression–T/F?

A

True

190
Q

Therapies assumed to suppress HPA axis–prednisone 20 mg/day (or equivalent) for > ___ weeks within the previous year; patient with clinical signs of ___ syndrome from any steroid dose

A

> 3 weeks; patient with clinical signs of Cushing syndrome

191
Q

In patients on therapies assumed to suppress the HPA axis, you don’t need to test the HPA axis, just supplement with stress dose steroids–T/F?

A

True

192
Q

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

A

12 months or longer

193
Q

H-P function returns to normal before adrenal function–T/F?

A

True

194
Q

What test can assess the responsiveness of the adrenals?

A

Cosyntropin (ACTH) stimulation test

195
Q

If you’re unsure if the patient’s HPA axis is suppressed, you can give stress doses of glucocorticoids prophylactically–T/F?

A

True

196
Q

Patients who have diagnosed secondary adrenal insufficiency as demonstrated by the short acting ACTH test ___ (will/will not) require perioperative stress dose steroids

A

will require stress dose steroids

197
Q

Patients at high risk of HPA suppression, including those treated with at least 20mg/day of prednisone for > 3 weeks or who have signs and symptoms of Cushings–unless data states otherwise, supplementation ___ (is/is not) recommended

A

supplementation is recommended

198
Q

Patients at low risk of HPA suppression–any dose of steroid for < 3 weeks, less than 5 mg/day of prednisone (or 10 mg every other day)–steroids ___ (are/are not) required unless signs and symptoms of HPA suppression are observed

A

are not required unless signs and symptoms of HPA suppression are observed

199
Q

Patients at intermediate risk, consider HPA testing, exercise clinical judgement based on hemodynamic stability and surgical risk–T/F?

A

True

200
Q

What two conditions could exaggerate the need for exogenous corticosteroid supplementation?

A

Burns or sepsis

201
Q

Signs and symptoms of acute adrenal crisis–___tension unresponsive to ___; ___dynamic circulation; ___glycemia; ___kalemia; ___natremia; ___volemia; metabolic ___osis; ___ (increased/decreased) level of consciousness

A

hypotension unresponsive to vasopressors; hyper dynamic circulation; hypoglycemia; hyperkalemia; hyponatremia; hypovolemia; metabolic acidosis; decreased level of consciousness

KLowe Pharm 2 (10 decks)

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