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
2
Q
Issues with inhalation technique–___% delivered to the lungs, the rest to the mouth, pharynx, and larynx
A
12% delivered to the lungs
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%
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
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
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
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
8
Q
What are the 5 types of muscarinic receptors?
A
M1-M5 receptors
9
Q
M___ receptors are located in the heart and are responsible for cardiac inhibition
A
M2 receptors
10
Q
M___ receptors are located in the CNS and have direct regulatory action on K and Ca channels
A
M4 receptors
11
Q
What (3) muscarinic receptors are stimulatory?
A
M1, M3, M5
Odd = stimulatory
12
Q
What (2) muscarinic receptors are inhibitory?
A
M2, M4
Even = inhibitory
13
Q
Antimuscarinic = anti___
A
anticholinergic
14
Q
Antimuscarinic/anticholinergic both mean that we are blocking ___ from binding to ___ receptors
A
we are blocking ACH from binding to muscarinic receptors
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
16
Q
What is the main issue with nebulized atropine?
A
A lot of CV complications, tachyarrhythmias
17
Q
Atropine is ___ (more/less) lipophilic than glycopyrrolate
A
atropine is more lipophilic than glyocpyrrolate
18
Q
Atropine is a ___ amine
A
tertiary amine
19
Q
Atropine ___ (can/cannot) cross the BBB
A
can cross the BBB (because it’s a tertiary amine and more lipophilic)
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
21
Q
Glycopyrrolate is an inhaled anticholinergic medication used for treatment of ___
A
COPD
22
Q
Is glycopyrrolate indicated for acute symptom management?
A
No–used for management of chronic disease like COPD
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)
24
Q
Ipratropium has minimal ___ absorption
A
minimal systemic absorption (<1%)–less systemic absorption than atropine
25
Ipratropium is a ___ (short/long) acting muscarinic antagonist
short-acting muscarinic antagonist
26
What may occur due to the M2 blockade that ipratropium causes?
Paradoxical bronchospasm--this is true for all muscarinic antagonists d/t M2 blockade
27
Limited systemic absorption of ipratropium results in prolonged local site effect--T/F?
True
28
Ipratropium is most effective in treating bronchospasm due to ___
treating bronchospasm due to beta antagonists (i.e.: propranolol which has non-selective beta blockade)
29
Compared to beta agonists, ipratropium has a ___ (slower/faster) onset and is ___ (more/less) effective in treating bronchial asthma
ipratropium has a slower onset (30-90 minutes) and is less effective in treating bronchial asthma than beta agonists
30
Ipratropium is useful in acute attacks--T/F?
False--is NOT useful in acute attacks because it has a slower onset of 30-90 mins
31
Albuterol is better than ipratropium for acute asthma attacks because it has a faster onset of action--T/F?
True
32
Ipratropium is more effective than beta agonists in treating what two diseases?
Chronic bronchitis or emphysema
33
Ipratropium is usually not given alone--T/F?
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
34
Ipratropium alone = ___
atrovent
35
Ipratropium given in combo with albuterol = ___ or ___
duoneb or combivent (MDI with ipratropium/albuterol)
36
Tiotropium (Spiriva) is a ___ (short/long) acting anticholinergic bronchodilator
long-acting anticholinergic bronchodilator
37
Tiotropium (Spiriva) is used as maintenance treatment of bronchospasm associated with COPD, including chronic ___ and ___
chronic bronchitis and emphysema
38
Tiotropium (Spiriva) blocks muscarinic receptor subtypes M___ and M___ to facilitate broncho___ and reduce ___ secretion
blocks muscarinic receptor subtypes M1 and M3 to facilitate bronchodilation and reduce mucous secretion
39
Tiotropium is a little more specific to the M___ receptors than other medications
M3 receptors
40
Tiotropium (Spiriva) is administered as ___ by inhalation
dry powder
41
Long-acting bronchodilators ___ (should/should not) be used to treat acute anything
should NOT be used to treat acute anything
42
Is glycopyrrolate used for acute symptom management or chronic disease management?
Chronic disease management
43
Is atropine used for acute symptom management or chronic disease management?
Acute symptom management (i.e.: acute bronchospasm)
44
Aclidinium (Tudorza) is similar to Spiriva...what's the major difference between these two medications?
Aclidinium (Tudorza) is given twice daily vs. once daily like Spiriva
45
Warnings for inhaled anticholinergics--can cause ___ and severe ___
narrow angle glaucoma and severe urinary retention
46
At normal inhaled doses, the risk of systemic absorption of inhaled anticholinergics is very low--T/F?
True
47
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?
True--less with inhaled than IV
48
Beta 2 agonists ___ (relax/contract) bronchial smooth muscle
relax bronchial smooth muscle
49
Newer beta 2 agonists lack stimulating effects on the heart at therapeutic doses--T/F?
True
50
Beta 2 agonists ___ (do/do not) have a catecholamine structure
do NOT have a catecholamine structure
51
The non-catecholamine structure of beta 2 agonists makes them resistant to what enzyme? What effect does this have on their duration of action?
Beta 2 agonists are resistant to COMT (because they are non-catecholamines); this contributes to their LONGER duration of action
52
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
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
53
Classes of beta 2 agonists--short acting = ___-___ hours; long acting = > ___ hours
short acting = 3-6 hours; long acting = > 12 hours
54
What is the preferred route of administration for beta 2 agonists?
Inhaled
55
What is a useless route of administration for beta 2 agonists like albuterol?
Oral--4 mg albuterol tablets are worthless
56
Beta 2 agonists can be given subQ or IV--T/F?
True
57
What are (2) beta 2 agonists that have a significant amount of non-respiratory side effects?
Ephedrine and epinephrine
58
In spite of their non-respiratory side effects, ephedrine and epinephrine do have ___ effects from activation of beta 2 receptors
bronchodilating effects from activation of beta 2 receptors
59
What are some of the non-respiratory side effects of ephedrine and epinephrine?--___arrhythmias; ___tension; increased blood ___
tachyarrhythmias; hypertension; increased blood glucose
60
Isoproterenol is a ___ (selective/non-selective) sympathomimetic that acts at ___ and ___ receptors
non-selective sympathomimetic that acts at beta 1 and beta 2 receptors
61
Isoproterenol is highly pro-___
pro-arrhythmic
62
Isoproterenol is often used as a last resort medication for a respiratory issue--T/F?
True (because it is so pro-arrhythmic)
63
What medication is the preferred beta 2 agonist for acute bronchospasm?
Albuterol
64
Albuterol is a ___ (short/long) acting beta agonist
short acting beta agonist
65
Albuterol given alone is known as ___ or ___
Proventil or ventolin
66
Albuterol given in combo with ipratropium is known as ___ or ___
combivent or duoneb
67
Levoalbuterol (Xopenex) is the (___)-enantiomer of racemic albuterol
(R)-enantiomer of racemic albuterol
68
(___)-enantiomer has cardio-stimulatory effects
(S)-enantiomer has cardio-stimulatory effects
69
What was the main point of levoalbuterol (xopenex) for being marketed?
Because it is an (R)-enantiomer, it was expected to have little to no cardiac effects
70
Studies have shown that there is little or no clinically significant difference in adverse effects of levoalbuterol (xopenex) compared to albuterol--T/F?
True
71
Terbutaline can be used in the treatment of asthma and is also a ___
tocolytic--reduces contractions of the uterus to postpone labor for hours to days
72
Terbutaline has fallen out of use by pulmonologists and obstetricians--T/F?
True
73
Ritodrine is a beta 2 agonist used as a ___ to stop ___
used as a tocolytic to stop uterine contractions of premature labor
74
Ritodrine has been removed from the market--T/F?
True
75
Ritodrine was removed from the market d/t ___ complications and 24 maternal ___
d/t CV complications and 24 maternal deaths
76
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
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
77
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
increased renin secretion from beta1 stimulation causes increased sodium; water reabsorption; decreased K+ and H+; pulmonary edema may occur
78
Terbutaline and ritodrine are both ___ (short/long) acting beta agonists, just like albuterol and levoalbuterol
short acting beta agonists
79
Long acting beta agonists ___ (are/are not) used for acute effect
are NOT used for acute effect--used for long-term management
80
Long acting beta agonists are often given in combo with something else--T/F?
True--can be administered with a short acting beta agonist or steroid
81
Salmeterol (serevent) and vilanterol are both ___ (short/long) acting beta agonists
long acting beta agonists
82
Salmeterol (serevent) is frequently administered with a ___
steroid--i.e.: salmeterol/fluticasone = Advair used for the prophylaxis of asthma
83
Formoterol and aformoterol are two other ___ (short/long) acting beta agonists
long acting beta agonists
84
Corticosteroids end in -___
-sone--i.e.: fluticasone, mometasone
Be able to recognize corticosteroids in inhalers...need to know what is in the product
85
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
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
Why do you see hypokalemia/hypomagnesemia with beta 2 agonists?
When you give a beta 2 agonist, potassium is pulled into the cell in exchange for sodium; magnesium follows potassium into the cell
87
Black box warning for LABAs--increased risk of ___; ___ (should/should not) be used alone
increased risk of asthma related death; should not be used alone
88
How can LABAs (when used alone) lead to asthma related death?--LABAs have no ___ action
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
Cromolyn sodium is a ___; it inhibits antigen-induced release of ___ and other mediators from pulmonary mast cells during antibody mediated allergic responses
membrane stabilizer; it inhibits antigen-induced release of histamine and other mediators from pulmonary mast cells during antibody mediated allergic responses
90
Cromolyn sodium suppresses the ___ response, NOT the Ag-Ab interaction
secretory response
91
Cromolyn sodium ___ (does/does not) relax bronchial or vascular smooth muscle
does NOT relax bronchial or vascular smooth muscle
92
Cromolyn sodium is used for ___ (acute/chronic) management; has no use in ___
used for chronic management; has no use in an acute asthma attack
93
What do most patients complain about when taking cromolyn sodium?
Metal taste
94
Cromolyn sodium is no longer available as an ___ but is available as a ___
no longer available as an inhaler but is available as a nebulizer
95
What are (3) types of methylxanthines?
- Theophylline/aminophylline
- Caffeine
- Theobromine
96
Methylxanthines ___ (stimulate/inhibit) the CNS; ___ (increase/decrease) BP; ___ (increase/decrease) myocardial contractility and heart rate; ___ (contract/relax) smooth muscle in the airways
stimulate the CNS; increase BP; increase myocardial contractility and heart rate; relax smooth muscle in the airways
97
Methylxanthines are non-selective ___ inhibitors
non-selective phosphodiesterase inhibitors--inhibit all fractions of PDE isoenzymes
98
PDE4 = ___ effects
respiratory effects
99
PDE3 = ___ effects
CV effects
100
PDE5 = ___ effects
vasodilatory effects--PDE5 inhibitors are used to treat pulmonary HTN and erectile dysfunction
101
Phosphodiesterase breaks down ___
cAMP/cGMP
102
Methylxanthines are also competitive antagonists of ___ receptors
competitive antagonists of adenosine receptors
103
Theophylline has more competitive antagonism for adenosine receptors than caffeine and theobromine--T/F?
True
104
Theophylline is used for acute or chronic asthma management?
Acute asthma management
105
Theophylline is also used to treat ___ in infants
apnea of prematurity in infants (because it is a CNS stimulant)
106
Theophylline toxicities--___-___ mcg/ml = GI upset, nausea/vomiting, tremor
15-25 mcg/ml = GI upset, nausea/vomiting, tremor
107
Theophylline toxicities--___-___ mcg/ml = tachycardia, PVCs
25-35 mcg/ml = tachycardia, PVCs
108
Theophylline toxicities-- >___ mcg/ml = fatal VTach, seizures
> 35 mcg/ml = fatal VTach, seizures
109
Caffeine effects--CNS ___ (stimulant/inhibitor); cerebral vaso___ (dilator/constrictor); secretion of ___
CNS stimulant; cerebral vasoconstrictor; secretion of gastric acid
110
Caffeine uses--apnea of ___; ___ headache; ___ remedies (to offset sedation from antihistamines)
apnea of prematurity; post-dural puncture headache; cold remedies (to offset sedation from antihistamines)
111
The methylxanthine class has a high risk of ___ and ___
high risk of toxicity and withdrawal
112
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
Histamine
113
What cells contain large amounts of histamine?
Mast cells in the skin, lungs, GI tract, and circulating basophils
114
Histamine ___ (does/does not) easily cross the blood-brain barrier
does not easily cross the blood-brain barrier
115
Histamine receptors = ___-___ receptors
H1-H4 receptors
116
H1 receptors are mostly ___ effects and are triggered during ___ reactions
H1 receptors are mostly respiratory effects and are triggered during allergic reactions
117
H2 receptors are mostly ___ effects
H2 receptors are mostly GI effects
118
___ effects come from both H1 and H2 receptors
CV effects come from both H1 and H2 receptors
119
Through H1 and H2 receptors, histamine causes ___ (increased/decreased) capillary permeability; ___tension; ___cardia; ___ing; ___ache
increased capillary permeability; hypotension; tachycardia; flushing; headache
120
What receptor(s) need to be blocked in order to completely block the vasodilatory effects of histamine release?
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
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
edema due to increased permeability; dilated arteries around the edema (flare); pruritus due to histamine in the superficial layers of the skin
122
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 ___
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
Histamine effects on organ systems--airway--H2 receptor activation ___ (constricts/relaxes) bronchial smooth muscle
H2 receptor activation relaxes bronchial smooth muscle
124
Histamine evokes secretion of gastric fluid containing ___ (low/high) concentrations of hydrogen ions; due to H__ receptor stimulation; ___ activity also increases H+ secretion
Histamine evokes secretion of gastric fluid containing high concentrations of hydrogen ions; due to H2 receptor stimulation; vagal activity also increases H+ secretion
125
Histamine receptor antagonists are ___ (competitive/noncompetitive) and ___ (reversible/irreversible) antagonists of histamine receptors
competitive and reversible antagonists of histamine receptors
126
Histamine receptor antagonists ___ (do/do not) inhibit the release of histamine
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
Histamine receptor antagonists attach to receptors and prevent the responses mediated by histamine--T/F?
True--competitive antagonism
128
Histamine receptor antagonists stabilize the receptor in the ___ (active/inactive) form, making them ___ agonists
stabilize the receptor in the inactive form, making them inverse agonists
129
H1 receptor antagonists are highly selective for H__ receptors
H1 receptors
130
Two generations of H1 receptor antagonists--first generation = ___; second generation = ___
first generation = sedating; second generation = non-sedating
131
First generation H1 receptor antagonists are ___; they may also activate ___ or ___-adrenergic receptors; they block ___ receptors
First generation H1 receptor antagonists are sedating; they may also activate serotonin or alpha-adrenergic receptors; they block muscarinic receptors
132
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
Inverse agonists--they combine and stabilize the inactive form of the H1 receptor, shifting equilibrium toward the inactive state
133
First generation H1 receptor antagonist CNS side effects--___ence; ___ (increased/decreased) alertness; ___ (slower/faster) reaction time; impaired ___ function
somnolence; decreased alertness; slower reaction time; impaired cognitive function
134
First generation H1 receptor antagonist anticholinergic side effects--___ mouth; ___ vision; urinary ___; ___ation
dry mouth; blurred vision; urinary retention; constipation
135
First generation H1 receptor antagonist CV side effects--stimulate the ___ (alpha/beta) adrenergic receptor, leading to ___cardia, QT ___ heart ___, and cardiac ___
stimulate the alpha adrenergic receptor, leading to tachycardia, QT prolongation, heart block, and cardiac dysrhythmias
136
Benadryl is a ___ (first/second) generation H1 antagonist
first generation H1 antagonist
137
Second generation H1 antagonists are unlikely to produce CNS side effects unless recommended doses are exceeded--T/F?
True
138
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___
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
Diphenhydramine (Benadryl) is used as a ___, anti___, anti___; is used for treatment of type ___ allergic reactions; is used for ___ reactions
Benadryl is used as a sedative, antipruritic, antiemetic; is used for treatment of type 1 allergic reactions; is used for anaphylactic reactions
140
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
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
Dimenhydrinate (dramamine) ___ (is/is not) associated with prolonged sedation
dimenhydrinate (dramamine) is NOT associated with prolonged sedation
142
(3) second generation H1 antagonists
- Zyrtec (cetirizine)
- Claritin (loratidine)
- Allegra (fexofenadine)
143
Second generation H1 antagonists are ___ (more/less) sedating than first generation H1 antagonists
less sedating
144
HPA axis--hypothalamus releases ___, anterior pituitary releases ___, adrenal cortex releases ___
hypothalamus releases corticotropin releasing hormone (CRH), anterior pituitary releases adrenocorticotropic hormone (ACTH), adrenal cortex releases cortisol
145
Adrenal cortex--zona glomerulosa = ___ layer; releases ___
outer layer; releases mineralocorticoids
146
Adrenal cortex--zona fasciculata = ___ layer; releases ___
middle layer; releases glucocorticoids
147
Adrenal cortex--zona reticularis = ___ layer; releases ___
inner layer; releases weak androgens
148
What hormone is produced in the adrenal cortex in response to stress?
Cortisol (hydrocortisone)
149
What is the major mineralocorticoid?
Aldosterone
150
Aldosterone is secreted secondary to ___ (increased/decreased) K+; ___ (increased/decreased) sodium; ___ (increased/decreased) BP/fluid volume
aldosterone is secreted secondary to increased K+; decreased sodium; decreased BP/fluid volume
151
Review of RAAS
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
Aldosterone ___ (increases/decreases) K+ excretion; ___ (increases/decreases) Na+ retention; ___ (increases/decreases) water retention; ___ (increases/decreases) blood volume
Aldosterone increases K+ excretion; increases Na+ retention; increases water retention; increases blood volume
153
Circadian rhythm--secretory rates of CRH, ACTH, and cortisol are ___ (low/high) in the early morning; ___ (low/high) in the late evening
high in the early morning; low in the late evening
154
Changing daily sleeping habits causes a corresponding change in circadian rhythm--T/F?
True
155
Primary adrenocortical insufficiency is AKA ___ disease
Addison's disease
156
Addison's disease--the adrenals do not secrete ___ or ___; replacement therapy must include ___corticoid and ___corticoid
the adrenals do not secrete cortisol or aldosterone; replacement therapy must include glucocorticoid and mineralocorticoid
157
Secondary adrenocortical insufficiency is due to chronic ___ use and suppression of the ___ axis
due to chronic steroid use and suppression of the HPA axis
158
In secondary adrenocortical insufficiency, ___ secretion is maintained
aldosterone secretion is maintained
159
Replacement therapy for secondary adrenocortical insufficiency usually requires only ___corticoid
glucocorticoid
160
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
increased cardiac output; increased respiratory rate; increased gluconeogenesis; decreased inflammation; decreased immune response; inhibition of digestion; enhanced analgesia; redistribution of CNS blood flow
161
How are corticosteroids classified?
They are classified according to their potencies
162
Glucocorticoid effect = anti-___ response
glucocorticoid effect = anti-inflammatory response
163
Mineralocorticoid effect = evoke distal renal tubular reabsorption of ___ in exchange for ___
mineralocorticoid effect = evoke distal renal tubular reabsorption of Na+ in exchange for K+
164
What are (5) naturally occurring corticosteroids?
- cortisol (hydrocortisone)
- cortisone
- corticosterone
- desoxycorticosterone
- aldosterone
165
Prednisolone, prednisone, methylprednisolone, betamethasone, dexamethasone, triamcinolone, and fludrocortisone are all ___ (natural/synthetic) corticosteroids
synthetic corticosteroids
166
Which (2) corticosteroid medications have the greatest anti-inflammatory potency?
- Betamethasone
- Dexamethasone
^ Both are synthetic glucocorticoids
167
What corticosteroid medication has the greatest sodium-retaining potency?
Fludrocortisone--synthetic mineralocorticoid
168
Fluticasone, budesonide, beclometasone, mometasone, cicleonide are all inhaled ___
inhaled corticosteroids
169
What should you do after you give an inhaled corticosteroid?
Have patient rinse mouth so they don't get thrush
170
What is the main clinical use of corticosteroids?
Replacement therapy for deficiency states
171
Pharmacokinetics of corticosteroids--___ (lipid/water) soluble forms can be administered IV; prolonged effects with ___ administration; able to cross the ___
water soluble forms can be administered IV (cortisol succinate); prolonged effects with IM administration (cortisone acetate); able to cross the placenta
172
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 ___
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
Corticosteroids ___ (stimulate/inhibit) glucose use in peripheral tissues and ___ (promote/inhibit) hepatic gluconeogenesis; resultant ___glycemia may require diet changes, insulin, or both to manage
inhibit glucose use in peripheral tissues and promote hepatic gluconeogenesis; resultant hyperglycemia may require diet changes, insulin, or both to manage
174
Peripherally, corticosteroids mobilize amino acids from tissues, leading to ___ (increased/decreased) skeletal muscle mass; ___porosis; ___ of the skin; negative nitrogen balance
decreased skeletal muscle mass; osteoporosis; thinning of the skin; negative nitrogen balance
175
Steroid use is associated with an increased incidence of neurosis and psychosis--T/F?
True
176
Behavioral changes associated with steroid use include manic depression and suicidal tendencies--T/F?
True
177
Cataracts can develop with long term ( > ___ years) steroid usage
> 4 years
178
Long term corticosteroids tend to ___ (increase/decrease) hematocrit and number of leukocytes
increase hematocrit and number of leukocytes
179
Single dose of cortisol decreases circulating lymphocytes by ___%; decreases circulating monocytes by ___%; cells are sequestered rather than destroyed
decreases circulating lymphocytes by 70%; decreases circulating monocytes by 90%
180
Arrest of growth can result from the administration of relatively small doses of glucocorticoids to children--T/F?
True
181
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
relative contraindications
182
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 ___
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
Any corticosteroid administration may result in suppression of the HPA axis--T/F?
True
184
Likelihood of HPA axis suppression is increased with longer duration/larger dose of steroid administration--T/F?
True
185
Aldosterone secretion remains intact in ___ (primary/secondary) adrenal insufficiency
secondary adrenal insufficiency
186
Prednisone 5 mg/day or less or 10 mg every other day is ___ (likely/unlikely) to suppress the HPA axis
unlikely to suppress the HPA axis
187
Long term every other day dosing is associated with ___ (more/less) suppression
less suppression
188
Glucocorticoids any dose < ___ weeks does not clinically suppress the HPA axis
any dose < 3 weeks
189
Prednisone or dexamethasone (even physiologic doses) given as a single daily dose at bedtime is associated more commonly with HPA axis suppression--T/F?
True
190
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
> 3 weeks; patient with clinical signs of Cushing syndrome
191
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?
True
192
After cessation of steroid therapy, recovery of the HPA function can take ___ months or longer
12 months or longer
193
H-P function returns to normal before adrenal function--T/F?
True
194
What test can assess the responsiveness of the adrenals?
Cosyntropin (ACTH) stimulation test
195
If you're unsure if the patient's HPA axis is suppressed, you can give stress doses of glucocorticoids prophylactically--T/F?
True
196
Patients who have diagnosed secondary adrenal insufficiency as demonstrated by the short acting ACTH test ___ (will/will not) require perioperative stress dose steroids
will require stress dose steroids
197
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
supplementation is recommended
198
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
are not required unless signs and symptoms of HPA suppression are observed
199
Patients at intermediate risk, consider HPA testing, exercise clinical judgement based on hemodynamic stability and surgical risk--T/F?
True
200
What two conditions could exaggerate the need for exogenous corticosteroid supplementation?
Burns or sepsis
201
Signs and symptoms of acute adrenal crisis--___tension unresponsive to ___; ___dynamic circulation; ___glycemia; ___kalemia; ___natremia; ___volemia; metabolic ___osis; ___ (increased/decreased) level of consciousness
hypotension unresponsive to vasopressors; hyper dynamic circulation; hypoglycemia; hyperkalemia; hyponatremia; hypovolemia; metabolic acidosis; decreased level of consciousness
