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47 Cards in this Set

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  • Back
What are the catecholamine direct acting adrenergic agonists?
Never enter into debt during medschool
What do the catecholamine direct acting adrenergic agonists have in common?
They all act directly at the adrenergic receptors, and have a catechol group
Receptor selectivity of NE
a1, a2, b1
3 Main effects of NE
-increase TPR
-Increase contractility
-Reflex bradycardia
Result of increased TPR/contractility
TPR - increased diastolic bp
Contractility - increased systollic bp
Result = increased MAP
How does NE cause reflex bradycardia?
The increased BP is detected by carotid baroreceptors and stimulates vagal output to slow heartrate
Receptor selectivity of Epi:
All - a1/a2/b1/b2
3 types of effects of Epi:
How does Epi affect the heart?
-Increases Heartrate
-Increases contractility
-Increases Cardiac output
How does Epi effect TPR at low concentrations? Via what receptors?
Decreases TPR by vasodilating skeletal muscle vessels - B2
How does Epi effect TPR at high concentrations? Via what receptors?
Increases TPR by global vasoconstriction - a1
How does Epi affect MAP?
-Decreases Diastolic (vasodilation of skeletal m)
-Increases Systolic (heart effects)
-No change in MAP
What is the result of there being no change in MAP by Epi?
There is no reflex bradycardia so the heartrate is elevated
What are the respiratory effects of NE and via what receptor?
Bronchodilation - via B2
What are the 2 metabolic effects of Epi?
-Increased gluconeogenesis and glycogenolysis
-Increased lipolysis (FFA)
What is norepinephrine used to treat?
Neurogenic shock
3 uses of Epinephrine:
-Tx Cardiovascular collapse
-Tx Anaphylactic shock
-Prolong effects of local anesthetics
What is the difference between Norepi/Epi and Isoproterenol?
Isoproterenol is synthetic
What receptors is Isoproterenol selective for?
B1 and B2
Where are the 2 main effects of Isoproterenol seen?
How does Isoproterenol affect blood pressure?
-Increases systolic (heart contractility)
-Decreases diastolic (no alpha constriction, only b2 dilation)
-Decreases MAP
How does Isoproterenol affect TPR?
TPR - decreased
Heartrate - Significantly increased
Respiration - bronchdilation
What are 2 things Isoproterenol is used to treat?
-AV block
Why isn't Isoproterenol given as an inhalant for asthmatics?
Because of the cardiac side effects - there are now more B2 selective agonists.
What is the receptor selectivity of Dopamine?
-Dopa1 receptors
What determines the receptor selectivity of dopamine?
The concentration
What is the receptor selectivity of dopamine at low dose and what is the effect?
low = D1 in renal vasculature; response is dilation, increased renal perfusion, decreased TPR and better urine output
What is the receptor selectivity of dopamine at med dose and what is the effect?
-Still renal effects
-Also B1 effects - increased HR, Contractility, and CO
What is the receptor selectivity of dopamine at high dose and what is the effect?
-All 3 - Dopa1, B1, and a1
How does Dopamine affect BP at high conc then?
-Increased Systolic BP
-Increased diastolic (a1)
-Increased MAP
How does Dopamine affect BP at low conc then?
-Decreased diastolic BP (renal)
-Decreased MAP
How does Dopamine affect BP at med conc then?
-Increased systolic BP (heart)
-Decreased diastolic BP (renal)
-No change in MAP
What is Dopamine used to treat?
Acute cardiogenic shock - it temporarily gets the patient through
What is the receptor selectivity of Dobutamine?
So what effect will Dobutamine have?
Only cardiovascular
-increased HR, contractility, CO
How does dobutamine change BP?
Minimally increases it
What is the main use of Dobutamine then?
Cardiogenic shock - to increase cardiac output
What is something else Dobutamine is often used in?
Cardiac stress testing for patients that can't exercise, to see if they have CAD
What is the method of administration for all of the direct acting adrenergic agonists except methyldopa?
IV - given in an inpatient setting and via constant infusion
Why do the direct acting catechol agonists have to be given via IV?
Because they are all quickly metabolized by MAO and COMT
Which direct acting catechol adrenergic agonist can be given orally?
What is Methyldopa?
A prodrug
How is the prodrug Methyldopa activated?
By replacing NE in the presynaptic nerve terminals and being metabolized by the same enzymes that synthesize NE
What are the steps in Methyldopa activation and what is the final active metabolite?
1. Methyldopa is acted on by Aromatic AA decarboxylase
2. alpha-Methyldopamine accumulates in synaptic vesicles and is acted on by Dopamine B-hydroxylase
3. A-methylnorepinephrine is released
So the final active metabolite of Methyldopa is?
Where is the predominant site of a-methylnorepinephrine action?
-What receptors
-What is its effect
In the CNS on a2 receptors
-Effect is reduced sympathetic outflow, decreased symp tone, bradycardia
What is Methyldopa primarily used to treat?