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Advanced Pharmacology- NU 607 > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

Antihistamines do not have an effect on…

A

Common colds or nasal congestion

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2
Q

MOA- produces accumulation of cAMP at beta 2 receptors, bronchodilator, used long-term on a fixed schedule

A

Beta 2 adrenergic agonists, salmeterol

long acting beta agonists- LABA

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3
Q

Employs the use of oxygen therapy in conjunction with treatment provided during stages I-III

A

GOLD Step IV

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4
Q

Maintenance phase lithium levels

A

0.4-0.6

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5
Q

More cAMP =…

A

More bronchodilation

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6
Q

AEs: neuroleptic malignant syndrome, anticholinergic effects, orthostatic hypotension, neuroendocrine effects, seizures, sexual dysfunction, agranulocytosis, severe dysrhythmias, doubled rate of mortality in elderly

A

1st gen antipsychotics

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7
Q

Requires short acting beta agonist to manage acute episodes of difficulty breathing

A

GOLD Step I

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8
Q

MOA- suppresses leukotrienes to decrease bronchoconstriction and inflammatory responses like edema and mucus secretion

A

Leukotriene modifiers/leukotriene receptor antagonists- zafirlukast

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9
Q

EPS- protrusion and rolling of the tongue, sucking and smacking movements of the lips, chewing motion, facial dyskinesia, involuntary movements of the body and extremities

A

Tardive dyskinesia

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10
Q

 6-8 hours after initiation/increased dose
 Autonomic changes
 Mental status changes- confusion, hallucinations,
 Neurologic excitability- lack of coordination
 Mostly with SSRIs, MAOIs, serotonin releasers (amphetamines)• Begins 2-72 hours after onset of treatment
• Altered mental status, incoordination, myoclonus, hyperreflexia, excessive sweating, tremor, fever, death sometimes
• Syndrome resolves after stopping the drug
• Increased risk with concurrent use of MAOIs and other drugs

A

Serotonin syndrome

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11
Q

Lithium toxicity starts at…

A

2.0

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12
Q

What competes with lithium in the proximal tubule of the nephron?

A

Sodium

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13
Q

MOA- blocks muscarinic receptors in the bronchi, reducing bronchoconstriction

A

Anticholinergics- ipratropium

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14
Q

What drug can cause an increase in lithium levels?

A

NSAIDS

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15
Q

MOA- inhibits MAO in nerve terminals, increasing the amount of NE and 5-HT available for release, intensifying transmission at noradrenergic and serotonergic junctions

A

Monoamine oxidase inhibitors

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16
Q

MOA- binds selectively to H1 receptors, can also bind to muscarinic receptors, causing vasoconstriction, decreased capillary permeability, bronchodilator, CNS depression, helps with itching

A

1st generation antihistamine- diphenhydramine

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17
Q

For asthma and COPD-antagonizes the action of acetylcholine by blocking receptors, leading to decreased contractility of the smooth muscle and reducing bronchospasm

A

Anticholinergic bronchodilators (ipratropium- Atrovent)

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18
Q

MOA- blocks receptors for dopamine and serotonin- more serotonin than dopamine, so less EPS

A

Second generation antipsychotics- clozapine

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19
Q

High potency 1st gen antipsychotic

A

Haloperidol (Haldol)

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20
Q

More likely with high or low potency?:
 Extrapyramidal side effects, dysrhythmias
 less sedation, HoTN, and anticholinergic effects

A

High potency

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21
Q

At high levels (toxicity), can cause dysrhythmias (VF) and convulsions that can be resistant to treatment, resulting in death

A

Theophylline

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22
Q

First choice antidepressants

A

SSRIs, SNRIs, bupropion and mirtazapine

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23
Q

AEs- seizures, anxiety, HA, insomnia, arrhythmia, tachycardia, angina, palpitations, n/v

A

Theophylline

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24
Q

AEs: sedation, weight gain, orthostatic hypotension, anticholinergic effects, agranulocytosis, metabolic effects (weight gain, increased risk of CV events), seizures, myocarditis, doubles mortality rate in elderly

A

2nd generation antipsychotics

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25
Q

MOA- decreases the synthesis and release of inflammatory mediators, decreases infiltration/activity of inflammatory cells, decreases edema of airway mucosa (secondary to decrease in vascular permeability)

A

Glucocorticoids- flunisolide

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26
Q

Use in combination with glucocorticoids- not indicated for mono therapy

A

LABAs

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27
Q

EPS- restlessness, trouble standing or sitting still, pacing the floor, feet in constant motion (rocking back and forth)

A

Akathisia

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28
Q

AEs- sexual dysfunction, weight loss, nervousness/anxiety, insomnia/drowsiness, sweating, seizures, serotonin syndrome, withdrawal syndrome,

A

SSRIs

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29
Q

Low potency 1st gen antipsychotic

A

Chlorpromazine (Thorazine)

30
Q

Theophylline toxicity occurs once levels reach…

A

20mcg/ml

at 30mcg/m- hyperglycemia, hypotension, seizures, brain damage and death can occur

there is no antidote for theophylline toxicity

31
Q

Increases the amount of cAMP in the lungs…

A

Adrenergics and methylxanthines

32
Q

MOA- Blocks serotonin and norepinephrine

A

SNRIs (serotonin/norepinephrine reuptake inhibitors)- venlafaxine (Effexor) and duloxetine (Cymbalta)

33
Q

AEs- can cause neuropsychiatric effects (depression, anxiety, agitation, abnormal dreams, hallucinations, insomnia, irritability, restlessness, suicidal thinking/behavior), HA, GI upset, arthralgia/myalgia, Churg-Strauss syndrome (weight loss, flu-like symptoms, pulmonary vasculitis, can be fatal)

A

Leukotriene modifiers/receptor antagonists- zafirlukast

34
Q

Theophylline toxicity starts at

A

20mcg/ml

35
Q

AEs- orthostatic hypotension, anticholinergic effects, sweating, sedation, cardiac toxicity, seizures, hypomania, suicide risk, many drug interactions

A

TCAs

36
Q

AEs- CNS stimulation (anxiety, insomnia, agitation, hypomania, mania), orthostatic hypotension, hypertensive crisis if patient eats food risk in tyramine

A

MAOIs

37
Q

What needs to be done when prescribing theophylline in patients who smoke?

A

Smoking decreases theophylline levels, so dosage needs to be increased (sometimes up to 50%)

38
Q

Drugs that interact with MAOIs

A

Meperidine (demerol) and pseudoephedrine, both can cause hypertensive crisis because they release norepi

39
Q

Decrease the release of histamine in COPD/asthma- inhibits rupture and degranulation of mast cells after contact with an antigen

A

Mast cell stabilizers- cromolyn

40
Q

Black box warning for LABA

A
  • If taken as abortive therapy for bronchospasm, could result in unrelieved bronchospasm, resulting in death, intubation, or hospitalization
  • No longer recommended as monotherapy for asthma
  • To be used in combination with corticosteroids and in treatment of COPD
41
Q

Promote smooth muscle constriction, blood vessel permeability, and inflammatory responses through direct action and recruitment of eosinophils and other inflammatory cells

A

Leukotrienes

42
Q

MOA- suppresses inflammation by stabilizing cytoplasmic membrane of mast cells, preventing release of histamine and other mediators

  • *Also inhibits eosinophils, macrophages, and other inflammatory cells
  • *Mostly used for asthma
A

Mast cell stabilizers- cromolyn

43
Q

Lithium levels are affected by….

A

sodium

44
Q

An enzyme found in the liver, intestinal wall, and terminals of monoamine-containing neurons, converts monoamine neurotransmitters into inactive products but also acts on dietary tyramine

A

Monoamine oxidase

45
Q

MOA- altered distribution of certain ions (calcium, sodium mag) that are critical to neuronal function, altered synthesis and release of NE, serotonin, and dopamine

A

Lithium

46
Q

Anticholinergic effects:

A

Dry mouth, urinary retention, blurred vision, wheezing

47
Q

MOA- binds to H1 receptors but does not cross BBB (less sedating), also less anticholinergic effects

A

2nd generation antihistamine- fexofenadine (allegra)

48
Q

Blocks the binding of LTD4 to its receptor (predominant leukotriene in the airways and lung)- inhibits leukotriene synthesis by preventing conversion of arachidonic acid into leukotrienes
• Hepatotoxic, monitor LFTs
• Interacts with theophylline, warfarin, ASA, drugs metabolized through P450

A

Leukotriene receptor antagonists- zafirukast, montelukast

49
Q

MOA- binds to beta 2-adrenergic receptors in the airway smooth m muscle, leading to increased levels of cAMP, relaxing smooth muscle in the airways

A

Beta 2 adrenergic agonists- albuterol

short acting beta agonists- SABA

50
Q

 Lead pipe rigidity, sudden high fever, sweating, autonomic instability (dysrhythmias, fluctuations in BP), alterations in LOC
 Death can result from respiratory failure, CV collapse, dysrhythmias, and other causes
 More likely with high-potency FGAs

A

Neuroleptic malignant syndrome

51
Q

AEs- nausea, HA, anorexia, nervousness, sweating, somnolence, insomnia, sexual dysfunction, diastolic hypotension

A

SNRIs

52
Q

What affects the metabolism of theophylline, decreasing the half-life of the drug?

A

Tobacco smoking

53
Q

Includes the addition of inhaled steroids along with the scheduled LABA and SABA PRN

A

GOLD Step III

54
Q

AEs- nervousness, restlessness, tremor, HA, insomnia, chest pain, palpitations, n/v, paradoxical bronchospasm

A

beta 2 adrenergic agonists

55
Q

EPS- stooped posture, shuffling gait, rigidity, bradykinesia, tremors at rest, pill-rolling motion of the hand

A

Pseudoparkinson

56
Q

AEs- candidiasis, dysphonia (hoarseness, speaking difficulty) with inhaled route
(Adrenal suppression, growth suppression, bone loss in long-term oral use)

A

Glucocorticoids

57
Q

Low sodium =

A

lithium toxicity

58
Q

o CNS- nervousness, tremors, insomnia
o CVS- tachycardia, palpitations, increased BP
o GI- n/v

A

Adrenergic agonists (albuterol, salmeterol)

59
Q

Major interactions with caffeine and tobacco smoke

A

Theophylline

60
Q

Includes a short acting beta agonist bronchodilator as needed in addition to long acting anticholinergic bronchodilator for symptom management
o Consideration is given to combination therapy with theophylline for those with breakthrough symptoms

A

GOLD Step II

61
Q

MOA- relaxes smooth muscle of the bronchi, most likely from blockade of receptors for adenosine.
Impacts many areas of the body:
o Powerful CNS stimulants
o CVS effects- dilates coronary vessels
o Diuretic effects
o Increases force of contraction of diaphragmatic muscles to draw more air into the lungs

A

Theophylline (methylxanthines)

62
Q

MOA- blocks neuronal uptake of serotonin (5-HT), CNS excitation rather than suppression

A

SSRIs- fluoxetine

63
Q

MOA- blocks receptors for dopamine, acetylcholine, histamine, and norepinephrine, causes more extrapyramidal SEs due to dopamine blockade

A

1st generation antipsychotics

64
Q

Acute phase lithium levels

A

0.8-1.2

65
Q

More likely with high or low potency?:
 Anticholinergic effects, sexual side effects/dysfunction, agranulocytosis
 Sedation, orthostatic HoTN, antichol. Effects
 Lowers seizure threshold
 Prolongs QT interval

A

Low potency

66
Q

EPS-facial grimacing, involuntary upward eye movement, muscle spasms of the tongue, face, neck, and back (causing trunk to arch forward), laryngeal spasms, rigidity/stiffness

A

Acute dystonia

67
Q

MOA- Blocks reuptake of norepinephrine and serotonin, has anticholinergic effects

A

Tricyclic antidepressants- amitriptyline and nortriptyline

68
Q

AEs- very few SEs, some cough or bronchospasm

A

Mast cell stabilizers- cromolyn

69
Q

Theophylline toxicity becomes potentially fatal at

A

30mcg/ml

70
Q

For what condition is lithium contraindicated?

A

Leukemia

Advanced Pharmacology- NU 607 (5 decks)

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