exam 2 Flashcards
1) B2 adrenergic agonists (sympathomimetics)
2) Antimuscarinics/Anticholinergics
Relax airway smooth muscle (bronchodilators)
asthma RELIEVERS
o 1) Glucocorticoids
o 2) Leukotriene Modifiers
o 3) Cromones
o 4) Biologic Therapies
Decrease underlying inflammation
controllers
Methylxanthines (Theophylline)
Both Relievers and Controllers
MOA
B2 receptor couples to a “Gs” protein activation of adenylyl cyclase increased cAMP increased PKA increased bronchodilation
B2 Adrenergic Agonists (Sympathomimetics)
Major effector tissues: smooth muscle including bronchiolar, liver, skeletal muscle
Major functions: relaxes/dilates smooth muscle + gluconeogenesis + glycogenolysis
B2 Adrenergic Agonists (Sympathomimetics)
- Terbutaline: SC and oral
- Albuterol: oral and nebulizer
Short Acting Beta2 Agonists (SABAs)
- Formoterol* (this has rapid onset for inhaler, can be used as rescue inhaler)
- Salmeterol
- Indacaterol (only used for COPD)
all of these MUST be combined with glucocorticoid
Long Acting Beta2 Agonists (LABAs)
MOA:
Normally: Ach stimulates M3 couple with Gq increases IP3 intracellular calcium calmodulin binding myosin and actin contract bronchoconstriction + increased pulmonary secretions
^^ _________________/__________________ block this!
Anticholinergics/antimuscarinics
Ipratropium (Atrovent)
Also used for rhinorrhea
Short Acting Muscarinic Antagonists (SAMAs)
- Tiotropium (Spiriva): once daily
- Glycopyrrolate: once daily
Long-Acting Muscarinic Antagonists (LAMAs)
B2 agonists > Antimuscarinics: _________
B2 agonists = Antimuscarinics: ______
B2 agonists > Antimuscarinics: ASTHMA
B2 agonists = Antimuscarinics: COPD
MOA
Inflammatory stimuli increase in inflammatory proteins
________________ binds to intracellular receptors goes to cell nucleus decreases expression of genes encoding for inflammatory proteins
Glucocorticoids
Inhalers
Beclomethasone (QVAR)
Budesonide (Pulmicort)
Fluticasone (Flovent)
Oral/IV
Hydrocortisone: short acting (½ life: <12 hours)
Prednisone: intermediate acting (½ life: 12-36 hours)
Methylprednisone: intermediate acting (½ life: >48 hours)
Dexamethasone: long acting (½ life: >48 hours)
all have “SON” in them
glucocorticoids
________________ _____________: existing in the cell membrane
Types
1) CysLT1 Antagonists
* Not as effective as glucocorticoids
2) 5-Lipoxygenase Inhibitor
Leukotriene Modifiers
Mild persistent asthma
Exercise induced bronchospasm/asthma
Allergic rhinitis
May reduce the need for glucocorticoids in select patients
CysLT1 Antagonists
Montelukast (Singulair)
What drug class decreases both COX (prostaglandins) + lipoxygenase (leukotrienes) pathways*
Glucocorticoids
NSAIDS will block COX, which will shunt over to the lipoxygenase/leukotriene pathway (this will cause “aspirin exacerbated respiratory disease”; more bronchoconstriction
MOA
Elevated IgE antibodies and sensitivity to perennial allergens (pollen)
Anti-IgE Therapy: anti-IgE antibody binds to circulating IgE and INHIBITS its interaction with receptors on mast cells and other effector cells
biologic therapies
(OmalizuMAB)
MOA
Increase in cAMP = increase in bronchodilation
Increases cAMP by:
1) Inhibiting phosphodiesterase
AND
2) Blocks adenosine receptor, thereby, INCREASING adenylyl cyclase
AND
Enhances histone deacetylation, decreasing inflammation
Methylxanthines (Theophylline)
Both a Reliever and a Controller
Narrow therapeutic index!
Large variation in ½ life (due to it being metabolized in the liver)
o Very similar to caffeine
o CNS excitation (can cause seizures)
o Weak diuretic
o CV stimulation (chronotropy, inotropy, arrhythmias)
o N/V
theophylline
Inducers = ______________ blood levels of theophylline
DECREASED
Inhibitors = ______________ blood levels of theophylline (toxicity risk)
INCREASED
major triggers of asthma attack (4)
beta adrenergic receptor antagonists
aspirin/NSAIDS
histamine (morphine, demerol, Sch, atracurium)
preservatives
______________ is a reliever + controller of asthma but is 2nd line therapy due to risk of AEs
Theophylline
_______________________ is used in select patients to decrease need or dose of glucocorticoid inhaler
Montelukast (Singular)
COPD best treatment option
Long-Acting Muscarinic Antagonists (LAMAs)
MOA
o Mild mucolytic activity via inhalation or intratracheal instillation
o Thins secretions, reduces risk of exacerbations
N-acetylcysteine
Nasocort
Flonase
Intranasal glucocorticoids
used for allergic rhinitis
Chlorpheniramine
Hydroxyzine (Vistaril)
1st gen “sedating” antihistamines
Impaired cognition (caution with elderly) *
Antimuscarinic effects (opposite of DUMBBELSS)
1st gen “sedating” antihistamines
MOA
Primarily stimulates alpha adrenergic (A1) receptors, causing vasoconstriction
Some also release NE
decongestants (sympathomimetics)
- Direct + indirect (NE release): mixed acting
- Can create meth, that is why you show your license
Pseudoephedrine
- Direct acting only
- Not as effective
Phenylephrine
____________ route is preferred for decongestants (does not go systemic) however, overuse can cause rebound vasodilation
topical (limit to < 5 days!)
- Ipratropium (Atrovent)
short acting muscarinic agent (SAMA)
- Tiotropium (Spiriva): once daily
- Glycopyrrolate: once daily
long acting muscarinic agent (LAMA)
best treatment for COPD!
the only methylxanthine
theophylline
select drug triggers of asthma attack
morphine
meperidine
atracurium
Sch
you notice the presence of oral candidiasis in a patient with asthma. Which of the following is most likely the cause?
fluticaSONe (flovent)
more common with AEROSOL use!
(flovent, pulmicort, QVAR)
man with history of BPH, asthma, and allergic rhinitis has developed urinary retention following surgery. Which drug contributed to the urinary retention?
Diphenhydramine (Benadryl)
antimuscarinic! (trop)
this is because it is oral! it is NOT TIOTROPIUM because that is an inhaler
Ach and monoamines come from
biogenic amines
serotonin and catecholamines (NE, Epi, Dopamine) come from
monoamines
3 ways of termination of NT activity
reuptake
enzymatic degradation
diffusion
Drugs can block everything except diffusion
BLOCKING muscarinics/cholinergic (aka antimuscarinics) receptors causes:
opposite of DUMBBELSS
* Hypomania
* Constipation
* Urinary retention (especially BPH)
* Blurred vision, glaucoma
* Bronchodilation
* Tachycardia
* Dry mouth/eyes
* Overheating/hypohidrosis
Altered cognition
BLOCKING dopaminergic receptors causes*
there is LESS dopamine
Extrapyramidal symptoms (parkinsonian-like)
Prolactin release (lactation, impotence)
BLOCKING histaminergic receptors causes*
sedation
impaired cognition
BLOCKING alpha1 adrenergic receptors causes*
orthostatic hypotension
reflex tachycardia
major antidepressant drug targets (4)
NET
SERT
MAO
DAT
antidepressant drug classes (6)*
Most Commonly Used/Frontline Therapy:
1) SSRIs: increases serotonin
2) SNRIs: increases serotonin + NE
3) Atypical antidepressants: increases NE and dopamine
4) Serotonin modulator
Least Commonly Used/Secondary Therapy:
1) TCAs: tricyclic antidepressants: increases serotonin + NE + additional actions
2) MAOIs: monoamine oxidase inhibitors
MOA
Blockage/inhibition of serotonin-5HT reuptake transporter (SERT) only
NO blockage of H1, Ach, or NE!
SSRIs
o Sertraline (Zoloft)
o Fluvoxamine (Luvox)
o Fluoxetine (taken once a week)
o Paroxetine
o Citalopram
o Escitalopram
SSRIs
o Serotonin Syndrome
o Hyponatremia
o Withdrawal Syndrome
o Bleeding
SSRIs
Inhibition of CYP2D6 (codeine, hydrocodone effectiveness would be decreased)
Fluvoxamine
Fluoxetine
Bupropion
MOA
Increases serotonin + NE activity; blocks SERT + NET activity
NET blockade: treats multiple pain syndromes
NO blockage of H1, Ach, or muscarinic receptors!
SNRIs
o Effexor
o Cymbalta
Often used for fibromyalgia and pain associated with neuropathy*
SNRIs
o Increase in BP* (this is unique to _______)
with Effexor only !
o Serotonin Syndrome
o Hyponatremia
o Bleeding
SNRIs
MOA
o Increase NE + dopamine (DA) activity; blocks NET and DAT
o Noncompetitive antagonist/blocker of nicotinic receptors
atypical antidepressants
Buproprion
bupropion
atypical antidepressant
Use:
Individuals who do not want any sexual dysfunction*
o Depression
o Smoking cessation
bupropion; atypical antidepressant
MOA
o Low doses: hypnotic/sedation/sleep aid
o High doses: increases serotonin activity; blocks serotonin (5HT2)
Blocks H1, and adrenergic receptors
serotonin modulator (trazadone)
Hypnotic/sedation/sleep aid
serotonin modulator (trazadone)
MOA:
MAOIs will block MAO enzyme, leading to _______________ of monoamines:
MAOI-A
MAOI-B
MAOIs
ACTIVATION of monoamines
MAOI-A: an increase in: ____________________
MAOI-B: an increase in: _____________
MAOI-A: tyramine + NE +serotonin
MAOI-B: dopamine only
Only Refractory/Severe/Atypical Depression due to adverse effects*
Exception: Selegiline: patch/SQ is less likely to cause adverse effects
MAOIs (nonselective, irreversible)
what drugs can cause
Life-threatening HYPERtensive crisis due to interactions with foods + drugs
Orthostatic hypotension (normal doses)
MAOIs
MOA
Blocks NE + serotonin (5HT) reuptake into presynaptic nerve terminal, increased NT activity at postsynaptic neuron and increased subsequent neurological events
and blocks H1, A1, muscarinic receptors
TCAs
o AmiTRIptyline
o NorTRIptyline
TCAs
Life threatening arrythmias is main reason not to use them! (QT prolongation)
Cardiotoxicity, caution with other cardiac depressive drugs
TCAs
Hyperreflexia, clonus (of the muscles), agitation, AMS, diaphoresis, autonomic instability, fever, death
serotonin syndrome
4 opioids that can cause serotonin syndrome
tramadol
meperidine (demerol)
methadone
fentanyl
drug classes that can cause serotonin syndrome (4)
Direct 5HT Stimulators: triptans (sumatriptan)
SSRIs, SNRIs, TCAs
Opioids: Tramadol, Meperidine, Methadone, Fentanyl
Zofran
what is the direct serotonin stimulator
sumatriptan
only SSRI that can be used for OCD
fluvoxamine
lithium
bipolar disorder
chlorpromazine
promethazine
haldol
droperidol
phenergan* (actually an antiemetic)
conventional (1st gen) antipsychotics
risperidone
ziprasidone (geodon)
seroquel
zyprexa
abilify (partial dopamine agonist)
atypical (2nd gen) antipsychotics
dantrolen
bromocriptine (parlodel)
benzos
TREATMENT for neuroleptic malignant syndrome
benztropine (cogentin)
benadryl
TREATMENT for antipsychotic acute dystonia
o Narrow therapeutic index
o Renal excretion
contraindications to ___________ use:
o Hyponatremia (dehydration, diarrhea, diuretics): can cause lithium levels to increase
o Renal impairment
o Pregnancy and lactation (teratogenic)
lithium
Monitor thyroid levels, __________ level, fluid, and electrolytes (hyponatremia)!
may prolong NMBs
lithium
positive symptoms, high dopamine =
1st generation OR 2nd generation
Negative symptoms + cognitive symptoms = low dopamine =
2nd generation
o Schizophrenia
o Delusional disorders
o Bipolar disorder
o Psychoses (depressive, drug-induced reaction)
o Drug-resistant depression
Other Uses
ANTIEMETICS
Tourette’s syndrome
Huntington’s chorea
Antipsychotics
HIGHER risk of:
sedation
hypotension
antimuscarinic effects
Chlorpromazine
LOW potency antipsychotics
phenergen
medium potency antipsychotic/antiemetic
LOWER risk of sedation
HIGHER risk of extrapyramidal symptoms
haldol
droperidol
With LOW levels of synaptic DA: increases activity
With HIGH levels of synaptic DA: decreases activity
Abilify
DA system stabilizer/2nd gen
Least amount of side effects of all antipsychotics
abilify (DA system stabilizer)
severe muscle spasm including torticollis, oculogyric crisis, trismus
Acute dystonic reaction
treatment for acute dystonic reaction
antimuscarinic
Benadryl, Benztropine
Lower risk of extrapyramidal symptoms
2nd Generation/Atypicals
Block A1 adrenergic, muscarinic, H1 receptors (leads to adverse effects discussed earlier)
Decreased seizure threshold (increased risk of seizures)
Prolonged QT interval/arrythmias
Neuroleptic malignant syndrome
antipsychotics
“lead-pipe” muscle rigidity, dysautonomia, AMS, fever
cause: blocking dopamine receptors
neuroleptic malignant syndrome
what drugs BLOCK dopamine, leading to a DECREASE in dopamine
1st generation antipsychotics (most common)
2nd generation antipsychotics
DA2 antagonist/blockers: antiemetics (Droperidol)
prokinetics (REGLAN)
what drugs INCREASE dopamine
drugs used for parkinsons
Benzodiazepines
Dantrolene
Bromocriptine (dry up lactation)
treatment for neuroleptic malignant syndrome
causes of prolonged QT interval (6)
TCAs (high doses)
Antipsychotics/antiemetics
High risk: Haldol (especially IV), Droperidol, Geodon
Methadone
Zofran
Perioperative Drugs
* Sevoflurane, Desflurane, Isoflurane
* Amiodarone