Unit 3 Flashcards by Katherine Milley

Antihistamines do not have an effect on…

Common colds or nasal congestion

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

Beta 2 adrenergic agonists, salmeterol

long acting beta agonists- LABA

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

GOLD Step IV

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Maintenance phase lithium levels

0.4-0.6

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More cAMP =…

More bronchodilation

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

1st gen antipsychotics

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

GOLD Step I

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

Leukotriene modifiers/leukotriene receptor antagonists- zafirlukast

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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

Tardive dyskinesia

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 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

Serotonin syndrome

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Lithium toxicity starts at…

2.0

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

Sodium

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MOA- blocks muscarinic receptors in the bronchi, reducing bronchoconstriction

Anticholinergics- ipratropium

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What drug can cause an increase in lithium levels?

NSAIDS

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

Monoamine oxidase inhibitors

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

1st generation antihistamine- diphenhydramine

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

Anticholinergic bronchodilators (ipratropium- Atrovent)

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

Second generation antipsychotics- clozapine

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High potency 1st gen antipsychotic

Haloperidol (Haldol)

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

High potency

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

Theophylline

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First choice antidepressants

SSRIs, SNRIs, bupropion and mirtazapine

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

Theophylline

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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

2nd generation antipsychotics

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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)

Glucocorticoids- flunisolide

Use in combination with glucocorticoids- not indicated for mono therapy

LABAs

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

Akathisia

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

SSRIs

Low potency 1st gen antipsychotic

Chlorpromazine (Thorazine)

Theophylline toxicity occurs once levels reach...

20mcg/ml at 30mcg/m- hyperglycemia, hypotension, seizures, brain damage and death can occur ***there is no antidote for theophylline toxicity***

Increases the amount of cAMP in the lungs...

Adrenergics and methylxanthines

MOA- Blocks serotonin and norepinephrine

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

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)

Leukotriene modifiers/receptor antagonists- zafirlukast

Theophylline toxicity starts at

20mcg/ml

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

TCAs

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

MAOIs

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

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

Drugs that interact with MAOIs

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

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

Mast cell stabilizers- cromolyn

Black box warning for LABA

* 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

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

Leukotrienes

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

Mast cell stabilizers- cromolyn

Lithium levels are affected by....

sodium

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

Monoamine oxidase

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

Lithium

Anticholinergic effects:

Dry mouth, urinary retention, blurred vision, wheezing

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

2nd generation antihistamine- fexofenadine (allegra)

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

Leukotriene receptor antagonists- zafirukast, montelukast

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

Beta 2 adrenergic agonists- albuterol | short acting beta agonists- SABA

 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

Neuroleptic malignant syndrome

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

SNRIs

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

Tobacco smoking

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

GOLD Step III

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

beta 2 adrenergic agonists

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

Pseudoparkinson

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

Glucocorticoids

Low sodium =

lithium toxicity

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

Adrenergic agonists (albuterol, salmeterol)

Major interactions with caffeine and tobacco smoke

Theophylline

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

GOLD Step II

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

Theophylline (methylxanthines)

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

SSRIs- fluoxetine

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

1st generation antipsychotics

Acute phase lithium levels

0.8-1.2

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

Low potency

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

Acute dystonia

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

Tricyclic antidepressants- amitriptyline and nortriptyline

AEs- very few SEs, some cough or bronchospasm

Mast cell stabilizers- cromolyn

Theophylline toxicity becomes potentially fatal at

30mcg/ml

For what condition is lithium contraindicated?

Leukemia

Unit 3 Flashcards

(70 cards)