Term
| beta 1 location and function |
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Definition
| cardiac SM, increase rate and force of contraction |
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Term
| beta 2 location and function |
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Definition
| smooth muscle and secretory glands, ciliary body. Bronchioles (dilating). Constrict Blood Vessels. Decreases GI Tract motility. Relaxes Uterus. Increase insulin secretion. |
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Term
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Definition
| Vasoconstrict skin, mucosa, conjunctiva, GI Tract (like M3). Contracts sphincters of GI Tract, bladder and stomach. Contracts uterus. IP3 DAG PLC. |
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Term
|
Definition
| Relax GI Tract. Decrease cAMP, decrease calcium channels. Increase potassium channels. Decrease insulin secretion. |
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Term
|
Definition
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Term
|
Definition
| decrease aqueous humor production |
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Term
|
Definition
| increase aqueous humor production, also relaxes the ciliary muscle |
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|
Term
| All beta receptors second messenger/effector: |
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Definition
|
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Term
|
Definition
| alpha 1 (vaso constrict), causes reflex badycardia |
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Term
|
Definition
| Bronchodilates (beta 2 agonist) |
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Term
|
Definition
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Term
|
Definition
| indirect stimulation of NE release and blocks reuptake - CNS stimulation. D isomer is best. |
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Term
|
Definition
| Direct beta 2 stimulation and indirect NE release. Both alpha and beta effects. Increases blood pressure, relaxes bronchioles, dilates the eyes, constricts blood vessels in conjunctiva. |
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Term
|
Definition
| oral decongestant (used to make speed) |
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Term
|
Definition
| ophthalmic decongestant (visine, alpha agonist) |
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Term
|
Definition
|
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Term
|
Definition
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Term
|
Definition
| alpha 2 agonist, antihypertensive |
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Term
|
Definition
| alpha 2 agonist, anti-glaucoma. (decreases aqueous humor production) |
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Term
|
Definition
| beta 2 agonist given to relax uterine smooth muscle during premature labor |
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Term
|
Definition
| alpha 1 blocker. 100x more alpha 1 than alpha 2. decreases TPR, leads to increased Heart Rate and cardiac output. Irreversible. |
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Term
|
Definition
| Alpha blocker, not very selective. Reversible. Stimulates cardiac, increased NE release. |
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Term
|
Definition
| Very selective alpha 1 blockers. Little tachycardia, effective as antihypertensive. First dose effect will cause syncope, so don't stand 30-90 minutes after first dose. |
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Term
|
Definition
| hypertension, pheocromocytoma, shock, peripheral vascular disease (will vaso-dilate), reverse eye dilation (Dapiprazole), BPH (will relax muscle of prostate and bladder neck - drug is tamsulosin a.k.a. flomax. |
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Term
|
Definition
|
|
Term
|
Definition
| block rate and force of contraction of heart, decrease CO, decreases angina, decreases blood pressure. |
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Term
|
Definition
| long duration beta blocker |
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|
Term
|
Definition
| partial beta agonist, but acts like beta blocker. Doesn't lower HR as much. |
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|
Term
|
Definition
| ophthalmic glaucoma drug, decreases aqueous production. If used orally is called Blocadren. |
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|
Term
| Non selective beta blockers have a risk to: |
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Definition
|
|
Term
|
Definition
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|
Term
|
Definition
|
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Term
|
Definition
| beta 1 selective blocker, not as effective in lowering IOP as the non-selective beta blocker |
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Term
|
Definition
| beta blocker (non selective) and alpha 1 blocker. Double action against hypertension. |
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|
Term
| Cautions for beta blockers: |
|
Definition
| asthmatics, severe heart failure, rapid withdrawal (rebound hypersensitivity), labile diabetic. |
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|
Term
|
Definition
| hypertension, arrhythmias, angina, migrane, panic attack, glaucoma, myocardial infarct |
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|
Term
|
Definition
| adrenergic neuron blocker. Inhibits sympathetic nerve stimulation. Depletes NE. Does not penetrate CNS. Last resort for HTN. Toxicities include: postural hypotension, diarrhea, nasal stuffiness, increased fluid retention, bradycardia, supersensitivity to direct agonists (chemical denervation). Very toxic. |
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|
Term
|
Definition
adrenergic neuron blocker. Depletes NE including in CNS (also DA and 5-HT), prevents storage in granules. Anti-HTN. Produces sedation, depression, bradycardia, postural hypotension, increased GI Tract activity.
Used for centuries as the Rauwolfia alkyloid to calm people. |
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Term
|
Definition
| Ganglionic stimulant - no therapeutic uses. |
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Term
|
Definition
| Ganglionic blocker - no therapeutic uses. Can cause tachycardia, dilation of eye, orthostatic hypotension due to block of SNS reflex control. Used to be used as anti-HTN. |
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|
Term
| Neuromuscular Blockers (two types) |
|
Definition
| Competitive (Do not depolarize, antagonist) and Depolarizing |
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Term
|
Definition
| Prototype competitive neuromuscular blocker. (D-tubocurarine) Paralyzes the skeletal muscle. Effect can be reversed by AchE inhibitors i.e. physostigmine. |
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Term
|
Definition
| like curare but not absorbed into CNS or across placenta |
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|
Term
|
Definition
| decreased blood pressure, ganglionic blockade and histamine release. |
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|
Term
|
Definition
| depolarizing neuromuscular blocker. fasciculation then paralysis. Short duration (5 mins). Not overcome by Anti-cholinesterases. Mainly used as adjunct to anesthesia to relax skeletal muscle. Toxicity is malignant hyperthermia. |
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|
Term
| Anti neuromuscular toxicities |
|
Definition
| Apnea, CV collapse, histamine release, |
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|
Term
| First Line anti-HTN agents: |
|
Definition
| ACE inhibitor, ANG II antagonist at the AT1 receptor, beta blocker, calcium channel blocker, diuretic |
|
|
Term
| hydrochlorothiazide, furosemide, triamterene are all |
|
Definition
|
|
Term
|
Definition
| decrease BV, TPR, and decrease CO. |
|
|
Term
| Thiazides and Loop diuretics ____ K+ |
|
Definition
|
|
Term
|
Definition
| directly related to diuresis, in addition to decreasing BV it may involve decreasing Na+ load in the body and in the vessel walls. |
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|
Term
| Non selective versus selective beta blockers |
|
Definition
| are not different when treating HTN. All will decrease HR, decrease CO and thus decrease BP. They also decrease renin release as well as decreasing CNS sympathetic outflow. Some might decrease TPR. |
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|
Term
|
Definition
| bradycardia, asthma aggravation, congestive heart failure |
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|
Term
| beta blockers (ending in olol) |
|
Definition
| propranolol, nadolol, metoprolol, atenolol, carvedilol |
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|
Term
|
Definition
| non-selective beta blocker |
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|
Term
|
Definition
| non selective beta blocker |
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|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| beta blocker that also blocks alpha 1 (prevents vaso-constriction) |
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|
Term
| centrally acting anti-hypertensive agents that decrease SNS activity: |
|
Definition
| clonidine (catapres), guanfacine, alpha methyl-dopa |
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Term
|
Definition
| selective alpha 2 agonist. |
|
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Term
|
Definition
| selective alpha 2 agonist |
|
|
Term
|
Definition
| directly stimulates central alpha 2 receptors, indirectly as alpha-methyl-norepinephrine which has selective alpha 2 agonist actions. |
|
|
Term
| clonidine and guanfacine MOA |
|
Definition
| directly stimulate central alpha 2 receptors, possibly inhibitory neurons to vasomotor control center. |
|
|
Term
| central acting agents which decrease SNS activity will _____ TPR and _____ HR |
|
Definition
|
|
Term
| toxicities of agents that decrease SNS activity |
|
Definition
| sedation, dizziness, dry mouth. Rapid withdrawal will cause BP spike, anxiety, palpitations and sweating. |
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|
Term
| peripheral SNS activity blockers |
|
Definition
| terazosin, guanethidine (not first line agents) |
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