Unit 3 Flashcards
Antihistamines do not have an effect on…
Common colds or nasal congestion
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
Employs the use of oxygen therapy in conjunction with treatment provided during stages I-III
GOLD Step IV
Maintenance phase lithium levels
0.4-0.6
More cAMP =…
More bronchodilation
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
Requires short acting beta agonist to manage acute episodes of difficulty breathing
GOLD Step I
MOA- suppresses leukotrienes to decrease bronchoconstriction and inflammatory responses like edema and mucus secretion
Leukotriene modifiers/leukotriene receptor antagonists- zafirlukast
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
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
Lithium toxicity starts at…
2.0
What competes with lithium in the proximal tubule of the nephron?
Sodium
MOA- blocks muscarinic receptors in the bronchi, reducing bronchoconstriction
Anticholinergics- ipratropium
What drug can cause an increase in lithium levels?
NSAIDS
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
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
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)
MOA- blocks receptors for dopamine and serotonin- more serotonin than dopamine, so less EPS
Second generation antipsychotics- clozapine
High potency 1st gen antipsychotic
Haloperidol (Haldol)
More likely with high or low potency?:
Extrapyramidal side effects, dysrhythmias
less sedation, HoTN, and anticholinergic effects
High potency
At high levels (toxicity), can cause dysrhythmias (VF) and convulsions that can be resistant to treatment, resulting in death
Theophylline
First choice antidepressants
SSRIs, SNRIs, bupropion and mirtazapine
AEs- seizures, anxiety, HA, insomnia, arrhythmia, tachycardia, angina, palpitations, n/v
Theophylline
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
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
