Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
Effects of substitutions of the beta carbon
|
Hydroxylation at beta carbon increases activity on alpha and beta receptors but also decreases lipid solubility. This explains the transformation from dopamine to NE and Epi and also why dopamine is mainly active in CNS
|
|
Substitutions at amino groups
|
Seen in NE to E transformation and leads to increase in activity at beta Rs.
|
|
Isoproterenol
|
Has 3 and 5 C OH groups plus large group on amino leading to increased beta2 R activity
|
|
Substitutions on ring of sympathomimetics
|
3, 4 C OH groups leads to maximum alpha and beta activity. Removal of one deceases activity, especially beta. 3, 5 OH is specific for beta 2 Rs.
|
|
Are catecholamines affected when administerd orally? Why or why not?
|
No because both MAO's and COMT metabolize them.
|
|
What changes to catecholamines render them resistant to MAO and COMT degradation?
|
1) Large amino groups
2) Methylation on alpha C 3) Removal of 3 or 4 OH group This combo leads to oral effective, long lasting drug. |
|
Epinephrine Effects on alpha receptors
|
Think fight and flight
alpha Rs on mucosal, cutaneous, and renal --> vasoconstriction Plus GI m. tone decreased |
|
Epinephrine receptor specificity
|
Acts on all adrenergic receptors
|
|
Epinephrine effects on beta1 Rs
|
beta1--> HR and force up
|
|
Epinephrine effects on beta2 Rs
|
beta2 Rs on skeletal m., cerebral, and coronary --> vasodilation also bronchodilation and GI tone inhibition
|
|
Epinephrine Side Effects
|
Fear, palpitation, discomfort. Seen more in hypertensive and hyperthyroid pts.
|
|
Epinephrine Administration
|
IM or SC
|
|
Epinephrine Therapeutic Uses
|
Acute hypersensitivity reactions (allergies) and local vasoconstriction to keep local anesthetics restricted to area. Also, pupillary dilation via alpha 1 Rs for opthalmic procedures.
|
|
Receptor specificity of NE
|
More specific than Epi. Potent stimulant of all alpha R and also B1 Rs. Almost no stimulation of B2 Rs.
|
|
Is NE used to treat shock? Why or why not?
|
No because does not activate B2 Rs and therefore BP greatly increases with administration leading to a greater reflex compensation.
|
|
Phenylephrine
|
Alpha 1 R agonist: Epi without one OH. Used to treat hypotension, mydriasis, and as nasal decongestant.
|
|
Clonidine
1) Drug Class 2) Sites of action 3) Therapeutic uses |
1) Alpha 2 agonist
2) Works at both vasomotor control center in brain on postsynaptic Rs to reduce sympathetic outflow, and presynaptically in the periphery to reduce sympathetic input into vasculature 3) Used widely as antihypertensive |
|
Isoprotereno: class?
1) Most resembles Epi or NE? 2) Effects 3) Administration 4) Metabolized by what? |
Nonselective beta agonist
1) Epi with extra CH3 on N 2) Same as Epi, B1 activity -> transient incrase in systolic BP but B2 binding -> vasodilation so BP lowered. B2 also relaxes bronchial and GI muscles. 3) IV 4) COMT b/c amino CH3 group makes it insensitive to MAO |
|
Terbutaline
1) Drug type 2) Therapeutic use? Why? |
1) Beta2 agonist
2) Asthma, b/c does not have beta1 affects like isoproterenol and it is resistant to COMT degradation. |
|
Albuterol
1) Drug type 2) Therapeutic use? Why? |
1) Beta2 agonist
2) Asthma, b/c does not have beta1 affects like isoproterenol and it is resistant to COMT degradation. |
|
Ritodrine
1) Drug class 2) Therapeutic use? 3) Administration route? |
1) Beta 2 agonist
2) To inhibit uterine contractions in premature labor, questionable efficacy 3) IV and oral |
|
Indirect vs. Direct Sympathomimetics
|
Direct: Bind directly to alpha or beta R
Indirect: Causes and increase in NE |
|
Two Indirect Sypathomimetic Strategies
|
1) Reverse NET activity, causing outflow (amphetamine, tyramine)
2) Simply inhibiting NET activity, as in cocaine |
|
Tyramine
1) Drug class 2) Made from what? |
1) Indirect sypathomimetic amine
2) Tyrosine, looks a lot like dopamine |
|
Explain the relationship between MAO inhibitors, tyramine, and hypertensive crisis
|
MAO inhibitor --> NE up
Food consumption including cheese and wine leads to ingestion of tyramine which is not metabolized by missing MAO --> hypertensive crisis |
|
Tyramine mechanism of action
|
Acts as false transmitter. Taken up into synaptic terminal and storage vesicle. Can also be converted to octopamine, via BPH, which stay in granule. Therefore, it is released but can't interact with receptor.
|
|
Amphetamine
1) Drug class 2) Administration and why? |
1) Indirect sympathomimetic
2) Effective orally due to alpha methyl group and lack of OH groups --> long lasting |
|
Amphetamine site of action?
|
CNS stimulants. Can get there because do not have OH group.
|
|
Tachyphylaxix
|
When repeated doses of a drug given at short intervals produce successively smaller responses. This is seen for indirect sympathomimetics.
|
|
Ephedrine
1) Drug class 2) Therapeutic uses |
1) Direct and Indirect Sympathomimetic
2) To treat hypotension |