Andrenergic Agonists, Andrenergic Antagonists, Indirect-Acting Antiandrenergic Agents
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Adrenergic agonists mimic the effects of ______
sympathetic nervous system
Most adrenergic agonists work by _______ receptor binding
3 indirect methods of binding by adrenergic agonists
- promote release of NEblock NE reuptake
- inhibit inactivation of NE
Amphetamines and ephedrine work by which method of binding?
promoting release of NE
Cocaine and tricyclic antidepressants work by which method of binding?
blocking reuptake of NE
MAO inhibitors work by which method of binding?
inhibiting NE inactivation
2 classes of Adrenergic Agonists
Three properties of catecholamines
- Can't be taken orally
- Brief duration of action
- Can't cross BBB
Why can't catecholamines be taken orally?
Inactivated too quickly by liver and MAO/COMT (intestinal enzymes)
Why is the duration of action for catecholamines brief?
inactivated quickly by liver/MAO/COMT
Why can't catecholamines cross the BBB? What does this mean for their therapeutic use?
- polar molecules
- Don't affect CNS
What color should catecholamines be? what color can they turn, and what should you do if that happens?
- should be colorless
- turn pink/brown from oxidation
- throw it away if it is discolored
How do non-catecholamines differ from catecholamines?
- Can take them orally
- Metabolized slowly -> longer duration of action
- less polar -> can cross BBB
If the dose is high, will the drug be more or less selective?
- Low dose = more selective
2 therapeutic responses of activation of alpha1 receptors
- -skin, viscera, mucous membranes
- -most common use
- mydriasis (pupil dilation)
3 drugs that activate alpha1 receptors
epinenphrine, NE, dopamine
Therapeutic effects of alpha1 activation
- stop bleeding in skin/mucous membranes
- elevate BP
- nasal decongestion
- combined with local anesthetics to delay their absorption
pupil constriction for eye exams/ocular surgery
why use a1 agonists to delay absorption of anesthesia? which drug is most commonly used?
- prolong anesthesia
- ->reduce dosage
- ->reduce systemic effects
clinical term for dilation of pupils
Adverse Effects of a1 activation
- necrosis (lack of blood flow due to extreme vacoconstriction)
- bradycardia (elevates BP -> triggers baroreceptor reflex -> heart rate declines)
What does activation of alpha2 receptors do?
inhibit NE release
What drugs can activate a2 receptors?
Clinical effects of activation of a2 receptors?
- no therapeutic application
- Some effects in CNS, discussed in later chapters
change heart rate
changes force of heart contractions
changes conduction velocity in heart
therapeutic responses of beta1 activation in kidneys
none that are clinically relevant
Drugs that can activate beta1 receptors
Therapeutic effects of beta1 activation in heart
- -Positive chronotropy (increase heart rate)
- -Positive inotropy (increase force of myocardial contraction)
- -> increased cardiac output
- -positive dromotropy (increase speed of AV conduction)
- -initiate contraction in cardiac arrest
Adverse effects of beta 1 activation in heart
- angina pectoris (chest pain)
Drugs that activate beta2 receptors
therapeutic effects of beta2 activation occur in which organs?
therapeutic effects of beta2 activation in lungs
how is it administered?
- -treat asthma, coronary artery disease, tachycardia
therapeutic effects of beta2 activation in uterus
- relax uterine smooth muscle
- -> delay preterm labor
adverse effects of beta 2 activation
- hyperglycemia (elevation of blood glucose)
- -only in patients with diabetes
- -b2 enhances skeletal muscle contraction
what drug activates dopamine receptors?
effect of dopamine receptor activation
-used to treat what?
dilation of renal blood vessels
- used to treat shock (reduces risk of renal failure)
- -also enhances cardiac performance
Symptoms of anaphylactic shock
- hypotension (widespread vasodilation)
- edema of glottis
Drug used to treat anaphylactic shock
activates which receptors?
- activates a1, b1, b2
Epinephrine activates which receptors?
a1, a2, b1, b2
Chemical classification of epinephrine
effects of epinephrine
pupil dilation (mydriasis)
activate b1 receptors -> overcome AV heart block, restore cardiac function
Routes of administration for epinephrine
- Oral inhalation (1%)
- Subcutaneous, IM, Intraspinal ((0.1%)
- IV, Intracardiac (0.01%)
- In combination with local anesthetics (0.001%)
adverse effects of epinephrine
- hypertensive crisis
- angina pectoris
- necrosis following extravasation
- hypergylcemia (in patients with diabetes)
Adrenergic Antagonists affect which receptors?
alpha and beta
Two main categories of adrenergic antagonists
- alpha-adrenergic blockers
- beta-adrenergic blockers
effects of Alpha1 antagonists
- vasodilation -> reduce BP
- bladder: promotes voiding
Prostate: reduces contraction of smooth muscle in prostatic capsule and bladder neck
Alpha1 antagonists can be used to treat which conditions?
- reverse toxicity from alpha1 agonists
- Benign prostatic hyperplasia
- Raynaud's disease
Therapeutic effects of alpha2 antagonists
no therapeutic application
Adverse effects of alpha1 antagonists
nasal congestion (vasodilation in nasal mucosa)
inhibition of ejaculation
sodium retention/increased blood volume
how can a1 antagonists cause reflex tachycardia?
vasodilation -> reduced BP -> baroreceptor reflex overcompensates -> tachycardia
how can a1 antagonists cause increased blood volume?
-> decreased renal blood flow, reduced perfusion
-> less sodium and water excreted
-> retention of na+/h20 = elevated BP
What can/should a1 antagonists be combined with when treating hypertension?
- so kidney doesn't "neutralize" hypotensive actions by retaining salt/water and raising BP again
Most therapeutic effects of beta-adrenergic antagonists result from blocking ________ in the ______.
beta1 receptors in the heart
beta blockers can be used to treat which conditions?
- angina pectoris
- cardiac dysrythmias
- myocardial infarction
- decrease risk of mortality in noncardiac surgery in high-risk patients
- heart failure
what causes angina pectoris?
how do beta blockers treat it?
blood flow (oxygen supply) to heart is insufficient to meet cardiac oxygen demand
decrease cardiac work, i.e. oxygen demand of heart, to match oxygen supply
how do beta blockers treat cardiac dysrhythmias?
suppress rate of SA node and AV conduction
how can beta blockers treat heart failure?
improve LV ejection fraction, increase exercise tolerance
adverse effects of beta1 antagonists
decreased cardiac output
AV heart block (stops atrial impulses from reaching ventricles)
- rebound cardiac excitation
- -chest pain
- -cardiac dysrhythmias
what should you teach patients about regarding the adverse effects of beta1 blockers?
early signs of heart failure (shortness of breath, night coughs, swelling of extremities)
- warn against abruptly stopping treatment
- -sudden withdrawal can cause hypersensitivity to catecholamines -> sudden increase of cardiac activity
- -carry adequate supply of beta blocker when traveling
therapeutic effects of beta2 blockade
no therapeutic application
adverse effects of beta 2 blockade
bronchoconstriction (opposite of activation of receptors which is sympathetic response -> dilation)
hypoglycemia (activation causes glycogenolysis)
Since beta2 blockers can cause bronchoconstriction and hypoglycemia, they are contraindicated in patients with which conditions?
what the hell does an indirect-acting antiadrenergic do?
prevents activation of peripheral adrenergic receptors by indirect methods
2 categories of indirect-acting antiadrenergics
- central alpha2 agonists
- adrenergic neuron blocking agents
how and where do central alpha2 agonists work?
- in CNS
- reduce firing of sympathetic neurons
- (less release of NE?)
The effect of a central alpha2 agonist is similar to that of a _________
direct-acting adrenergic receptor blocker
In addition to treating hypertension, what is the other therapeutic use for central alpha2 agonists?
primary use of indirect acting central alpha2 agonists and targets
- heart and blood vessels
how do central alpha2 agonists treat hypertension?
- inhibit firing of sympathetic neuron
- -> decrease release of NE
- -> decrease in activation of adrenergic receptors in cardiovascular system
- -> lowers heart rate and cardiac output
Adverse effects of central alpha2 agonists
Rebound hypertension (following abrupt withdrawal)
drowsiness (from CNS repression)
dry mouth (xerostomia)
self-medication (euphoria, hallucination, etc)
clinical term for dry mouth
how do adrenergic neuron-blocking agents work?
decrease release of NE
therapeutic uses for adrenergic neuron-blocking agents?
CNS drugs act on the ______ and ________
brain and spinal cord
what are the neurotransmitters for the peripheral nervous system? how many are in the central nervous system?
- PNS: aceytlcholine, E, NE
- CNS: 21 neurotransmitters
What is the function of the blood brain barrier?
- impedes entry of drugs into brain
- (protects brain from injury and potentially toxic substances)
what drugs can cross the BBB?
lipid-soluble and drugs with a transport system
what drugs CAN'T cross BBB?
protein bound drugs
highly ionized drugs
Describe the state/efficacy of BBB in infants
- BBB is not fully developed yet
- infants sensitive to CNS drugs
5 categories of CNS neurotrasmitters
-for reference, with examples (not likely to memorize)
Monoamines (MOA)-- E/NE, dopamine, seratonin
Amino Acids, GABA
Opioid peptides- endorphins
Nonopioid peptides- substance P, oxytocin
How much do we know about the mechanisms of action of CNS drugs?
not much-- don't have enough definite understanding of brain or pathophysiology of CNS disorders
most MOA's are proposed hypotheses
CNS drugs may have altered effects as a result of _____ use
- chronic (prolonged drug exposure)
- --> adaptation
three adaptations that may occur as a result of prolonged exposure to CNS drugs
how do they occur?
increased therapeutic effects
- effects are produced as a result of CNS adaptation, take a few weeks to take place
decreased side effects-
brain adapts to side effects, they go away while therapeutic effects remain
- tolerance/physical dependence- CNS adapts to drug, response to drug decreases
- -abrupt discontinuation -> withdrawl
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