Module B Flashcards
(106 cards)
1
Q
Provocholine (Methacoline)
A
- Direct-acting cholinergic with greater M3 muscarinic specificity
- Broad systemic effects, but mainly respiratory (SLUDGE), decreased heart rate, increased PR, decreased gastric secretions and GI motility
- Used in the methacholine challenge test (MCT) for asthma. Small doses of methacholine may induce bronchospasm and excessive mucus production in those with reactive airways
2
Q
Branches of the sympathetic nervous system arise from:
A
T1 through L3
3
Q
Sympathetic nerves have ________ pre-ganglionic neurons and ________ post-ganglionic neurons
A
short, long
4
Q
Black Widow spider venom exerts its toxic effects by _________ (stimulating / inhibiting) release of _________
A
stimulating, acetylcholine
5
Q
M3 muscarinic receptors, belong to the class ________ and are found in ________
A
they are Gαq GPCRs (therefor stimulute phospholipase C activity and increase IP3 and DAG contentrations) and are found in smooth muscle, glands, and vascular smooth muscle
6
Q
The GI and GU effects of muscarinic activation are:
A
- Increased salivary, gastric, and other secretions
- Increased smooth muscle contraction (except sphincters) leading to increased GI motility
- Micturition due to detrussor stimulation and internal urethral sphincter relaxation
Overdose may lead to “all faucets turned on” syndrome of excessive salivation, diarrhea, incontinence.
7
Q
Name, compare and contrast the two common kinds of indirect-acting cholinergic drugs:
A
The two types are reversible and quasireversible cholinesterase inhibitors. Both inhibit the function of acetylcholinesterase and thereby functionally increase the concentration of ACh in the synapse.
Reversible cholinesterase inhibitors (Edrophonium, neostigmine) are slowly hydrolyzed by AChase, and are rapidly excreted, leading to a short duration of action
Quasireversible cholinesterase inhibitors act in a similar way but form a covalent bond with AChase and take much longer to be hydrolyzed (ex: isofluorophate). These are common causes of organophosphate poisoning.
8
Q
Three reasons the sympathetic nervous system tends to have broad, systemic effects when activated are:
A
- The sympathetic nervous system tends to discharge as a unit
- Each sympathetic preganglionic neuron innervates many post-ganglionic neurons
- Sympathetic activation triggers release of epinephrine and norepinephrine into the systemic circulation
9
Q
Branches of the parasympathetic nervous system arise from:
A
CN III, VII, IX, and X, and S2-S4
10
Q
the ENS _____ (can / can not) function independently of the CNS after autonomic denervation
A
can!
11
Q
All somatic motor neurons use ________ as a neurotransmitter at the neuromuscular junction
A
All somatic motor neurons use acetylcholine as a neurotransmitter at the neuromuscular junction
12
Q
Nicotinic receptors belong to the receptor class _________
A
ligand-gated sodium channels
13
Q
parasympathetic pre-ganglionic neurons synapse with ________ (many / few) post-ganglionic neurons and therefore produce ________ (broad / specific) effects.
A
parasympathetic pre-ganglionic neurons synapse with few post-ganglionic neurons and therefore produce specific effects.
14
Q
Tensilon (Edrophonium)
A
- Short-acting reversible cholinesterase inhibitor (indirect-acting cholinnergic)
- rapidly increases ACh concentrations
- may be used to reverse neuromuscular blockade
- used to diagnose between myasthenic crisis (not enough ACh) and a cholinergic crisis (too much ACh) in myasthenia gravis
15
Q
Botulinum toxin A ________ (stimulates / inhibits) the release of ________ which results in ________
A
Botulinum toxin A inhibits the release of acetylcholine which results in decreased neuromuscular transmission
This is used to treat disorders of innapropriate muscle tone/activation as in parkinsons, CP, bladder spasm, strabismus, etc.
16
Q
Paraympathetic nerves have ________ pre-ganglionic neurons and ________ post-ganglionic neurons
A
long, short
17
Q
Prostigmin (Neostigmine)
A
- Reversible cholinesterase inhibitor (indirect-acting cholinergics)
- Relatively long-acting (compared to edrophonium)
- Used in long-term treatment of myasthenia gravis and in reversal of NMBA blockade
18
Q
The bronchial effects of muscarinic activation are:
A
bronchoconstriction, hypersecretion of mucus
19
Q
Describe the general process of acetylcholine synthesis, storage, and release
A
- Synthesized from choline and acetate by choline acetyltransferase
- Stored in presynaptic vesicles
- Action potential triggers vesicle fusion with presynaptic membrane
- ACh released across synapse to bind with post-synaptic receptors
- ACh hydrolyzed acetylcholinesterase back to acetate and choline
- Choline is recycled through presynaptic reuptake
20
Q
The ocular effects of M3 muscarinic receptor activation are:
A
miosis (pupillary constriction), accomodation (ciliary muscle contraction for near vision), and lacrimation
21
Q
______________ is similar to acetylcholinesterase but is found in blood plasma and is important in breakdown of cholinergic drugs
A
pseudocholinesterase
22
Q
Expain why direct cholinergic agonists have limited clinical use.
A
it is difficult to produce specificity in thse drugs for particular nicotinic or muscarinic receptors, so the rate of adverse reaction is very high (low TI and CSF)
23
Q
The effect of stimulating M3 muscarinic receptors in non-vascular smooth muscle is
A
increased calcium release and muscle contraction
24
Q
The effect of stimulating M2 muscarinic receptors is
A
decreases cAMP production in cardiomyocytes, slowing heart rate and conduction
25
Describe the difference between **direct-acting** and **indirect-acting cholinergics**
**direct-acting cholinergics** directly stimulate an ACh recptor (ex: **Provocholine** (Methacholine))
**indirect-acting cholinergics** increase the concentration of ACh or augment ACh signal transduction in some way (ex: **Tensilon** (Edrophonium)) *prominent examples are acetylcholinesterase inhibitors*
26
the **enteric nervous system (ENS)** is innervated by the ________ (sympathetic / parasympathetic / both) branch of the ANS
both sympathetic and parasympathetic
27
The cardiac effects of muscarinic activation are:
Decrease SA diastolic depolariztion (slows heart rate), Slow AV nodal conduction (prolonged P-R interval)
28
sympathetic pre-ganglionic neurons synapse with ________ (many / few) post-ganglionic neurons and therefore produce ________ (broad / specific) effects.
sympathetic pre-ganglionic neurons synapse with **_many_** post-ganglionic neurons and therefore produce **_broad_** effects.
29
The vascular effects of muscarinic activation are
vasodilation due to nitrous oxide release, stimulated by increased IP3 and DAG levels.
30
muscarinic receptors belong to the receptor class \_\_\_\_\_\_\_\_\_
G-protein coupled receptors (GPCRs)
31
List three uses of reversible cholinesterase inhibitors (indirect-acting cholinergics)
* reversal of neuromuscular blockade by curariform drugs
* Diagnose/treat disorders of ACh (ex: **edrophonium** for myasthenia gravis)
* Treat glaucoma (ex: **pilocarpine**)
32
The two types of nicotinic receptors are:
neuronal type (nN) and muscle type (mN)
33
The two types of acetylcholine receptors are:
**nicotinic** and **muscarinic**
34
Nicotinic receptors are found at: (list 3)
all **autonomic ganglia**, **neuromusuclar junctions**, and in the **CNS**
35
The effect of stimulating M3 muscarinic receptors in vascular smooth muscle is:
nitric oxide synthesis and smooth muscle relaxation
36
The neurotransmitter released at sympathetic preganglionic synapses and at all parasympathetic synapses is \_\_\_\_\_\_\_\_\_
acetylcholine
37
Muscarinic receptors are found at: (list 3)
**smooth muscle**, **cardiac tissue**, and **glands** innervated by the parasympathetic nervous system. They are also found at some **sympathetic** neuroeffector junctions, specifically sweat glands and chromaffin cells.
## Footnote
*Muscarinic receptors may also be found on sympathetic terminals where the PNS exerts an inhibitory effect on norepinephrine release*
38
The effect of stimulating M3 muscarinic receptors in glands is
increased glandular secretion
39
The purpose of ACh autoreceptors is:
to provide **negative feedback** at cholinergic synapses
40
M2 muscarinic receptors, belong to the class ________ and are found in \_\_\_\_\_\_\_\_
they are Gαi GPCRs (therefor inihibit adenylyl cyclase activity) and are found in cardiac muscle tissue.
41
**Viagra** (sildenafil)
* Type 5 phosphodiesterase inhibitor (PDE5 inhibitor)
* PNS innervation of vascular smooth muscle causes vasodilation and cGMP release (causing further smooth muscle relaxation). PDE5 inhibitors slow the breakdown of cGMP leading to increased/prolonged vasodilation.
* As **Viagra**, sildenafil is used to treat erectile dysfunction
42
What are the three primary clinical uses of muscarinic receptor antagonists?
1. relax smooth muscle (vasodilation)
2. reduce glandular secretions
3. increase heart rate
43
What is the primary clinical use of nicotinic receptor antagonists?
relax skeletal muscle during medical procedures
44
Three examples of belladonna alkaloids are \_\_\_\_\_, \_\_\_\_\_\_\_, and \_\_\_\_\_\_\_\_\_. These drugs belong to the class \_\_\_\_\_\_\_\_\_.
atropine, scopolamine, and hyoscyamine. They belong to the class muscarinic receptor antagonists (parasympatholytics).
45
A mnemonic to remember the effects of atropine toxicity is:
**dry as a bone**: *dry mouth and decreased sweating*
**blind as a bat**: *mydriasis and loss of accomadation*
**mad as a hatter**: *hallucinations and delirium at extremely high doses*
**red as a beet**: *inhibits sweating, leading to hot, dry, flushed skin*
46
The most significant difference between tertiary and quaternary amine muscarinic receptor antagonists is:
only tertiary compounds (atropine, scopolamine) are well-absorbed into the CNS
47
**Atropine** (atropine)
* muscarinic receptor antagonist (belladonna alkaloid, tertiary amine)
* toxixicity is dose dependent, remember; dry as a bone, red as beet, mad as a hatter, blind as a bat
* causes dilatation, positive chronotropy, decreased secretions, decreased GI motility, bronchodilation, etc.
* used to reverse cholinesterase overdose and as a positive chronotrope
48
**Buscopan** (Scopolamine)
* muscarinic receptor antagonist (belladonna alkaloid, tertiary amine)
* toxixicity is dose dependent, remember; dry as a bone, red as beet, mad as a hatter, blind as a bat
* causes dilatation, positive chronotropy, decreased secretions, decreased GI motility, bronchodilation, etc.
* **greater CNS effect than atropine** therefore used to treat motion sickness
49
**Robinul** (Glycopyrrolate)
* Quaternary amine muscarinic receptor antagonist
* not absorbed by CNS
* used in the setting of surgery to dry secretions and inhibit muscarinic effects of cholinesterase inhibitors during NMBA reversal
50
**Atrovent** (Ipratropium bromide)
* Muscarinic-selective receptor antagonist (synthetic atropine analog)
* used for bronchodilation and reduced mucus secretion in asthma/COPD
51
**Spiriva** (Tiotropium bromide)
* Muscarinic-selective receptor antagonist (synthetic atropine analog)
* used for bronchodilation and reduced mucus secretion in asthma/COPD
52
The primary clinical use of nicotinic receptor antagonists is as:
neuromuscular blocking agents (NMBAs) to induce paralysis during medical procedures
53
The two major classes of NMBA are:
Non-depolarizing (ND) and depolarizing (D)
## Footnote
*the only depolarizing NMBA is succinylcholine*
54
Non-depolarizing neuromuscular blocking agents (NMBAs) are also known as \_\_\_\_\_\_\_\_, after their biological source
curariform drugs
55
The ND NMBAs (curariform drugs) generally function by:
acting as competitive muscle-type nicotinic acetylcholine receptor antagonists
56
ND NMBAs may potentiate hypotension, bronchocostriction, and tachycardia by stimulating release of __________ from mast cells
histamine
57
The advantage of modern curariform drugs (rocuronium, vecuronium) over older ones (pancuronium) is:
they cause less histamine release and have higher mN nicotinic receptor specificity (lower ganglionic blockade)
58
Describe the general strategies for countering NMBA overdose
* use cholinesterase inhibitors (neostigmine) to increase ACh concentration at neuromuscular junction. Quaternary amine muscarinic antagonists may be given to limit muscarinic side effects of this strategy.
* Sugammadex directly binds NMBAs for excretion
59
The only depolarizing neuromuscular blocking agent (D NMBA) is:
succinylchline
60
transient muscle contractions during the onset of succinylcholine are called
fasciculations
61
**Zemuron** (Rocuronium)
* non-depolarizing neuromuscular blocking agent (ND NMBA)
* competitive inhibitor of muscle-type nicotinic ACh receptors
* induction of paralysis during medical procedures (ex: intubation)
* **intermediate acting** consider pancuronium for longer duration of action
62
**Anectine** (Succinylcholine)
* depolarizing neuromuscular blocking agent (D NMBA)
* non-competitive agonist of muscle-type nicotinic ACh receptors causes protracted depolariztion
* induction of paralysis during medical procedures (ex: intubation)
* **short onset and short-acting**
63
**Tracium** (Atracurium)
* non-depolarizing neuromuscular blocking agent (ND NMBA)
* competitive inhibitor of muscle-type nicotinic ACh receptors
* induction of paralysis during medical procedures (ex: intubation)
* intermediate acting, may have increased histamine release but lower hepatotoxicity vs. rocuronium
64
Differentiate between myasthenic and cholinergic crisis and name a drug used in differential diagnosis of the two
myasthenic crisis: insufficient effect of acetylcholine at the neuromuscular junction as in undertreated myasthenia gravis
Cholinergic crisis: too much ACh at the NMJ as in overtreatment of MG with cholinesterase inhibitors
Edrophonium is used to distinguish between the two
65
use the provided chart to organize the acetylcholine receptor drugs
66
The only type of adrenergic receptor that does not involve the adenylyl cyclase pathway is
alpha-1
## Footnote
*alpha 1 receptors are Gαq GPCRs which result in activation of the phospholipase C - IP3/DAG pathway, and an increase in intracellular calcium*
67
list and compare the activation effects of the adrenergic receptors:
**α1:** Smooth muscle contraction (vasoconstriction), glandular secretion
**α2: **Autoreceptor for negative feedback inhibition of catecholamine release
**β1: **Increase in heart rate, contractility, conduction. Increased renin secretion
**β2:** Smooth muscle relaxation (vasodilation (esp. skeletal muscle), bronchodilation), glycogenolysis, skeletal muscle potassium intake
**β3:** Lipolysis, thermogenesis, uterine relaxation
68
Describe the synthesis and release of Norepinephrine at sympathetic neuroeffector junctions
1. Tyrosine is converted to dopa by tyrosine hydroxylase
2. Dopa is converted to dopamine by dopa decarboxylase
3. Dopamine is converted to norepinephrine by dopamine β-hydroxylase
4. Norep is stored in presynaptic vesicles and released by calcium-mediated exocytosis
69
Describe the roles of **MAO**, **COMT**, and the **catecholamine transporter** in the reuptake and metabolism of both endogenous and exogenous catecholamines
Norepinephrine (endogenous) is taken back into the sympathetic neuron through the catecholamine transporter through **uptake 1** and is metabolized intracellularly by **MAO**
Exogenous catecholamines (dobutamine, epinephrine) are either directly metabolized in the synapse by **COMT** or are taken into the non-neuronal cell through **uptake 2** and metabolized by **MAO** and **COMT**. **MAO** is the major enzyme of exogenous catecholamine metabolism
70
Describe the effect of **cocaine** on sympathetic neurotransmission
**cocaine** inhibits reuptake of norep into the neuronal cell for MAO metabolism
71
Describe the processes of **reflex bradycardia** and **reflex tachycardia** as part of the **baroreceptor reflex**
The **baroreceptor reflex** arises from stimulation of mechanoreceptors in the aortic arch and carotid arteries which send impulses to the **vasomotor center** and influence **vagal outflow.**
Drugs or diseases that cause increased BP will cause an increased stretch of the baroreceptors, leading to **reflex bradycardia**, aka a **vagal reflex**.
72
Describe the effects of β1 activation on cardiac muscle cells
β1 receptors are GPCRs of the Gs type which means activation leads to adenylyl cyclase stimulation and increased cAMP. This leads to an increase of intracellular Ca2+, resulting in a positive **inotropic**, **chronotropic**, and **dromotropic** effect.
73
Describe the effects of β2 activation on vascular smooth muscle and decribe the locations in the body where β2 concentrations are highest
β2 receptors are GPCRs of the Gs type which means activation leads to adenylyl cyclase stimulation and increased cAMP. This leads to a decrease of intracellular Ca2+, resulting in **smooth muscle relaxation**. This effect is most pronounced in **bronchial smooth muscle** and **vascular smooth muscle of the skeletal muscles**.
74
The three classes of adrenergic agonists are:
Direct-acting (dobutamine), indirect acting (cocaine), and mixed acting (ephedrine).
75
Why must catecholamines be delivered parenterally?
because otherwise they will be rapidly degraded by GI COMT and MAO
76
**Levophed** (Norepinephrine)
* Direct-acting adrenergic agonist, endogenous catecholamine
* Has high α1 specificity, so minimal cardiac effects with signigicant peripheral vasoconstriction
* incr. BP due to incr. SVR. **high potential for reflex bradycardia** (no beta effect)
* used in treatment of shock and hypotension
77
**Adrenalin** (Epinephrine)
* Direct-acting adrenergic agonist, endogenous catecholamine
* Has equal α and β affinity, so both cardiac and vascular effects
* effects are highly **dose dependent!** at lower doses there is greater β activation, so there is MSK vasodilation and positive cardiac effects leading to increased systolic, decreased diastolic. At higher doses there is increased α1 effect and diastolic may increase as well.
* used in treatment of shock and hypotension
78
**Isuprel** (Isoproterenol)
* Direct-acting adrenergic agonist, exogenous catecholamine
* Has **only β affinity**, so produces positive cardiac effects and vasodilation (as well as bronchodilation)
* Strong positive chronotrope! Causes increased HR and SBP, with decreased SVR and diastolic BP
* Risk of tachyarrhythmias, useful in treatment of heart blocks and bradycardia
79
**Dobutrex** (Dobutamine)
* Direct-acting adrenergic agonist, exogenous catecholamine
* Has only β affinity, so produces positive cardiac effects and vasodilation
* Positive **inotrope** and **dromotrope** without significant **chronotropic** effects! Increases SBP and stroke volume without increasing HR while dropping SVR
* preferred drug for treating cradiogenic shock or heart failure
80
**Inotropin** (Dopamine)
* Direct-acting adrenergic agonist, endogenous catecholamine
* Effect is **highly dose-dependent**. At **low** doses it is D1 selective and promotes renal perfusion (uncommon). At **medium** doses it stimulates β1 receptors (incr. inotropy and decr. SVR). At **high** doses it stimulates α1 receptors, causing vasoconstriction
* used in treatment of shock and hypotension
81
List 5 common catecholamine vasopressors and describe their receptor specificities
1. Epinephrine: activates both α and β receptors. Increasing α-affinity with higher doses
2. Dopamine: at low doses only D1-affinity, with increasing doses it activates β and then α
3. Norepinephrine: High α1 specificity, little to no β effect
4. *Dobutamine*: has only β affinity with a strong inotropic and almost no chronotropic effect
5. *Isoproterenol*: has only β affinity with a strong chronotropic effect
82
Which tissues in the body primarily experience vasoconstriction in response to SNS activation
skin, kidneys, GI (high α1 concentration relative to β2)
## Footnote
*These tissues at rest have blood supplies that vastly exceed their metabolic needs. Their high perfusion is related to their function (thermoregulation, excretion, absorption)*
83
explain why dobutamine, dopamine, isoproterenol, and epinephrine should be used with caution in diabetic patients.
These drugs are all β2-agonists and therefore promote glycogenolysis and may cause iatrogenic hyperglycemia
84
Hypovolemia should always be treated with IV fluid administration ________ (before / after) vasopressor treatment.
before!
85
Name the vasopressor of choice for treating each of the following forms of shock:
1. Septic
2. Cardiogenic (tachy/post-arrest)
3. Cardiogenic (brady)
4. Anaphylactic
1. Septic: Dopamine followed by Norep
2. Cardiogenic (tachy/post-arrest): Dobutamine
3. Cardiogenic (brady): Isoproterenol
4. Anaphylactic: Epinephrine
86
Non-catecholamine direct-acting adrenergics (phenylephrine) ________ (may / may not) be given enterally and ________ (are / are not) metabolized by COMT
they **_may_** be given enterally *because* they **_are not_** metabolized by COMT
87
**Neosynephrine** (Phenylephrine)
* Non-catecholamine direct-acting adrenergic
* relatively pure **α1-agonist**
* Used to promote **mydriasis**
* Used as a nasal **decongestant**
* Used in the emergency or surgical setting as a **vasopressor** (prominent push-dose vasopressor)
88
Non-catecholamine direct adrenergics have a _______ (shorter / longer) duration of action than the catecholamines
longer because they are not metabolized by COMT or perhaps even MOA
89
Non-catecholamine direct adrenergics are _______ (more / less) receptor-selective than the catecholamines
more!
90
**Ventolin** (Salbutamol)
* Non-catecholamine direct-acting adrenergic
* selective, short-acting β2 agonis (**SABA**). May activate β1 reeptors at higher doses.
* used to promote bronchodilation in COPD and asthma as a **rescue medication**
* adverse effects include tachycardia, tremor, and nervousness
91
**Bricanyl** (Terbutaline)
* Non-catecholamine direct-acting adrenergic
* selective, short-acting β2 agonis (**SABA**). May activate β1 reeptors at higher doses.
* used to promote bronchodilation in COPD and asthma as a rescue medication
* adverse effects include tachycardia, tremor, and nervousness
92
Compare the effects of Cocaine and Amphetamine on the PNS
both are **indirect acting adrenergics**. Cocaine prevents uptake 1 of Norep at neuroeffector junction. Amphetamine is a potent CNS stimulant and inhibits vesicular storage of norep in the neuron, causing it to "leak out" through the catecholamine transporter into the synapse.
93
The primary clinical use for selective α1-blocking drugs like **tamsulosin** is:
treatment of urinary sysmptoms of benign prostatic hyperplasia (BPH). Possible due to high selectively of these drugs for α1 receptors of the urinary subtype, they have essentially no vascular smooth muscle side effects (i.e. hypotension)
94
use the provided chart to organize the Adrenoceptor drugs
95
The first β receptor antagonist drugs were ________ (specific / non-specific). Give an example of one such drug
non-specific. Propranolol is the prototype. Need to be especially careful with diabetics and asthmatics.
96
Indications for selective β-blockers include:
* Migraine prevention
* Glaucoma treatment
* Antihypertensive
* Antiarrhythmic
* Antianginal
97
Adverse effects of β-antagonist treatment are generally due to _________ and include: (list 2)
β2 antagonism and include bronchoconstriction and hypoglycemia due to inhibition of glycogenolysis.
98
**Inderal** (Propranolol)
* Non-selective β-antagonist (beta-blocker)
* Primarily given orally but may be given parenterally
* One of the first developed and thus has the ridest range of approved clinical uses
* hypertenion, angina, cardiac dysrhythmias, migraine, AMI, pheochromocytoma
* Has more CNS side effects than other non-selective beta-blockers
99
**Tenormin** (Atenolol)
* Selective β1-antagonist (beta-blocker)
* oral or parenteral
* good antihypertensive, antianginal, antiarrhythmic
* Low rate of CNS side effects due to poor lipid solubility
100
**Brevibloc** (Esmolol)
* Selective β1-antagonist (beta-blocker)
* IV-only!
* good antihypertensive, antianginal, antiarrhythmic
* very short half-life compared to other beta-blockers, used in emergent settings (check out that trade name!)
101
**Lopressor** (Metoprolol)
* Selective β1-antagonist (beta-blocker)
* oral or parenteral
* good antihypertensive, antianginal, antiarrhythmic
* relatively short half-life (3-4hr)
102
The combination α and β blockers have the added benefit of \_\_\_\_\_\_\_\_\_
anti-oxidant activity
103
**Coreg** (Carvedilol)
* α and β blocker
* used in the treatment of hypertension and for its potent anti-oxidant effects
* non-selctive beta effect, so should **not** be used in persons with asthma
104
**Normodyne** (Labetalol)
* α and β blocker
* used in the treatment of hypertension and for its potent anti-oxidant effects
* non-selctive beta effect, so should not be used in persons with asthma
105
Explain how muscarinic antagonists like atropine cause a decrease in sweating
Sweat glands are stimulated by muscarinic receptors, and are an unusual case where the sympathetic postganglionic neuroeffector junction is mediated by acetylcholine!
106
Compare and contrast the effects of the different beta-adrenergic antagonists (beta-blockers) and suggest clinical indications for each.
* lopressor (metoprolol) and tenormin (atenolol) are both beta-1 selective, intermediate acting, and used in management of hypertension, angina, and tachyarrhythmia. Atenolol has fewer CNS side-effects and a longer half-life.
* Brevibloc (esmolol) has a very short half-life and is given parenterally in acute hypertensive emergencies and SVT
* Inderal (propranolol) is a non-selective beta-blocker that has many indications since it was the first developed. There are better options for cardiac indications, due to beta-2 side effects of propranolol
