This document summarizes various drugs that affect the nervous system. It discusses analgesics like opioids and non-opioids that decrease pain sensation. It covers anesthetics that cause loss of sensation and consciousness. Anti-anxiety and sedative drugs like benzodiazepines and barbiturates are described as promoting the inhibitory neurotransmitter GABA. Anti-seizure medications decrease neuronal hyperexcitability through various ion channel mechanisms. The document provides an overview of the categories and examples of drugs that impact the nervous system.
7. Opioids
Opioids
•• Generic reference to
Generic reference to
morphine-like
morphine-like
drugs/actions
drugs/actions
–– Opiate: derivative of opium
Opiate: derivative of opium
•• Prototype: morphine
Prototype: morphine
–– Morpheus: god of dreams
Morpheus: god of dreams
•• Act on endorphin
Act on endorphin
receptors:
receptors:
––
––
Mu (most important)
Mu (most important)
Kappa
Kappa
8. Actions of Opioid Receptors
Actions of Opioid Receptors
Response
Mu
Kappa
Analgesia
Respiratory
Depression
Sedation
Euphoria
Physical Dependence
⇓ GI motility
9. Actions at Opioid Receptors
Actions at Opioid Receptors
Drugs
Mu
Kappa
Pure Agonists
Agonist
Agonist
-morphine, codeine, meperidine (Demerol®),
fentanyl (Sublimaze®), remifentanil (Ultiva®),
propoxyphene (Darvon®), hydrocodone (Vicodin®),
oxycodone (Percocet®)
Agonist-Antagonist
-nalbuphine (Nubaine®), butorphanol (Stadol®)
Antagonist Agonist
Pure Antagonist
Antagonist Antagonist
-naloxone (Narcan®)
10. General Actions of Opioids
General Actions of Opioids
••
••
••
••
••
••
••
Analgesia
Analgesia
Respiratory depression
Respiratory depression
Constipation
Constipation
Urinary retention
Urinary retention
Cough suppression
Cough suppression
Emesis
Emesis
Increased ICP
Increased ICP
– Indirect through CO2 2
– Indirect through CO
retention
retention
••
••
••
Euphoria/Dysphoria
Euphoria/Dysphoria
Sedation
Sedation
Miosis
Miosis
– Pupil constriction
– Pupil constriction
∀ ⇓ Preload & afterload
∀ ⇓ Preload & afterload
– Watch for
– Watch for
hypotension!
hypotension!
11. Non-opioid Analgesics
Non-opioid Analgesics
•• Salicylates
Salicylates
– Aspirin (Bayer®® )) * (prototype for class)
– Aspirin (Bayer * (prototype for class)
•• Non-Steroidal Anti-Inflammatory Drugs
Non-Steroidal Anti-Inflammatory Drugs
•• Ibuprofen (Motrin®, Advil®®)
Ibuprofen (Motrin®, Advil)
–– Propionic Acid derivative
Propionic Acid derivative
•• Naproxen (Naprosyn®®)
Naproxen (Naprosyn)
•• Naproxen sodium (Aleve®®)
Naproxen sodium (Aleve)
•• All compete with aspirin for protein binding sites
All compete with aspirin for protein binding sites
– Ketorolac (Toradol®®)
– Ketorolac (Toradol )
13. Aspirin Mechanism of Action
Aspirin Mechanism of Action
•• Inhibit synthesis of cyclooxygenase (COX)
Inhibit synthesis of cyclooxygenase (COX)
– Enzyme responsible for synthesis of:
– Enzyme responsible for synthesis of:
Prostaglandins
Prostaglandins
––Painresponse
Pain response
––Suppressionof gastric acid secretion
Suppression of gastric acid secretion
––Promotesecretion of gastric mucus and bicarbonate
Promote secretion of gastric mucus and bicarbonate
––Mediationof inflammatory response
Mediation of inflammatory response
––Productionof fever
Production of fever
––Promoterenal vasodilation (⇑ blood flow)
Promote renal vasodilation (⇑ blood flow)
––Promoteuterine contraction
Promote uterine contraction
Thromboxane A22
Thromboxane A
––Involvedin platelet
Involved in platelet
––aggregation
aggregation
14. Aspirin Effects
Aspirin Effects
Good
Good
•• Pain relief
Pain relief
∀ ⇓ Fever
∀ ⇓ Fever
∀ ⇓ Inflammation
∀ ⇓ Inflammation
Bad
Bad
•• GI ulceration:
GI ulceration:
⇑ Gastric acidity
⇑ Gastric acidity
⇓ GI protection
⇓ GI protection
∀ ⇑ Bleeding
∀ ⇑ Bleeding
∀ ⇓ Renal elimination
∀ ⇓ Renal elimination
∀ ⇓ Uterine contractions
∀ ⇓ Uterine contractions
during labor
during labor
15. ®
Acetaminophen (Tylenol®))
Acetaminophen (Tylenol
••
••
NSAID similar to aspirin
NSAID similar to aspirin
Only inhibits synthesis of CNS
Only inhibits synthesis of CNS
prostaglandins
prostaglandins
– Does not have peripheral side effects of ASA:
– Does not have peripheral side effects of ASA:
•• Gastric ulceration
Gastric ulceration
∀ ⇓ Platelet aggregation
∀ ⇓ Platelet aggregation
∀ ⇓ Renal flow
∀ ⇓ Renal flow
∀ ⇓ Uterine contractions
∀ ⇓ Uterine contractions
16. Acetaminophen Metabolism
Acetaminophen Metabolism
Major Pathway
Non-toxic
Non-toxic
metabolites
metabolites
Acetaminophen
Acetaminophen
Induced by
Induced by
ETOH
ETOH
P-450
Toxic
Toxic
metabolites
metabolites
Minor Pathway
Depleted by ETOH &
Depleted by ETOH &
APAP overdose
APAP overdose
Glutathione
Non-toxic
Non-toxic
metabolites
metabolites
17. Anesthetics
Anesthetics
•• Loss of all sensation
Loss of all sensation
– Usually with loss of consciousness
– Usually with loss of consciousness
⇓ propagation of neural impulses
⇓ propagation of neural impulses
•• General anesthetics
General anesthetics
– Gases
– Gases
•• Nitrous oxide (Nitronox®®),halothane, ether
Nitrous oxide (Nitronox), halothane, ether
– IV
– IV
•• Thiopental (Pentothal®®),methohexital (Brevitol®®),
Thiopental (Pentothal), methohexital (Brevitol),
diazepam (valium®), remifentanil (Ultiva®®)
diazepam (valium®), remifentanil (Ultiva)
18. Anesthetics
Anesthetics
•• Local
Local
– Affect on area around injection
– Affect on area around injection
– Usually accompanied by epinephrine
– Usually accompanied by epinephrine
•• Lidocaine (Xylocaine ®®),topical cocaine
Lidocaine (Xylocaine ), topical cocaine
20. Mechanism of action
Mechanism of action
•• Both promote the effectiveness of GABA
Both promote the effectiveness of GABA
receptors in the CNS
receptors in the CNS
– Benzodiazepines promote only
– Benzodiazepines promote only
– Barbiturates promote and (at high doses)
– Barbiturates promote and (at high doses)
stimulate GABA receptors
stimulate GABA receptors
•• GABA = chief CNS inhibitory
GABA = chief CNS inhibitory
neurotransmitter
neurotransmitter
– Promotes hyperpolarization via ⇑ Cl- - influx
– Promotes hyperpolarization via ⇑ Cl influx
25. Anti-seizure Medications
Anti-seizure Medications
••
••
Seizures caused by hyperactive brain areas
Seizures caused by hyperactive brain areas
Multiple chemical classes of drugs
Multiple chemical classes of drugs
– All have same approach
– All have same approach
– Decrease propagation of action potentials
– Decrease propagation of action potentials
∀ ⇓ Na+,+,Ca++++influx (delay depolarization/prolong
∀ ⇓ Na Ca influx (delay depolarization/prolong
repolarization)
repolarization)
∀ ⇑ Cl- -influx (hyperpolarize membrane)
∀ ⇑ Cl influx (hyperpolarize membrane)
27. Ion Diffusion
Ion Diffusion
••
••
Key to neurophysiology
Key to neurophysiology
Dependent upon:
Dependent upon:
– Concentration gradient
– Concentration gradient
– Electrical gradient
– Electrical gradient
•• Modified by:
Modified by:
– ‘Gated ion channels’
– ‘Gated ion channels’
28. Where Does Diffusion Take the
Where Does Diffusion Take the
Ion?
Ion?
Na++
Na
150 mM
150 mM
K++
K
5 mM
5 mM
Cl- Cl
High
High
Exterior
II
N
N
Na++
Na
15 mM
15 mM
O
O
U
U
T
T
II
N
N
K++
K
150 mM
150 mM
Cl- Cl
Low
Low
Interior
31. 0
Na + Influx
+30
K+ Efflux
Membrane Potential (mV)
What Happens to the Membrane If Cl-What Happens to the Membrane If Cl
Rushes Into the Cell During Repolarization?
Rushes Into the Cell During Repolarization?
It gets
It gets
hyperpolarized!
hyperpolarized!
Threshold
Threshold
Potential
Potential
-50
-70
Resting Membrane
Resting Membrane
Potential
Potential
Time (msec)
32. Membrane Potential (mV)
What Happens to the Frequency of Action
What Happens to the Frequency of Action
Potentials If the Membrane Gets
Potentials If the Membrane Gets
Hyperpolarized?
Hyperpolarized?
+30
0
It
It
decreases!
decreases!
-50
-70
Time (msec)
33. Clinical Correlation
Clinical Correlation
•• Remember that it is the rate of action potential propagation
Remember that it is the rate of action potential propagation
that determines neurologic function.
that determines neurologic function.
–– Determined by frequency of action potentials.
Determined by frequency of action potentials.
What is a seizure?
What would be the
What is a seizure?
What would be the
effect on the membrane
effect on the membrane
of ⇑ Cl-- influx
of ⇑ Cl influx
Hyperpolarization & …
during a seizure?
during a seizure?
⇓ seizure
activity!
36. Are You Ready for a Big
Are You Ready for a Big
Surprise?
Surprise?
Many CNS drugs act on GABA
receptors to effect the frequency
and duration of action potentials!
37. SNS Stimulants
SNS Stimulants
•• Two general mechanisms:
Two general mechanisms:
– Increase excitatory neurotransmitter release
– Increase excitatory neurotransmitter release
– Decrease inhibitory neurotransmitter release
– Decrease inhibitory neurotransmitter release
•• Three classes:
Three classes:
•• Amphetamines
Amphetamines
•• Methylphendidate
Methylphendidate
•• Methylxanthines
Methylxanthines
39. ®
Methylphenidate (Ritalin®))
Methylphenidate (Ritalin
•• Different structure than other stimulants
Different structure than other stimulants
– Similar mechanism
– Similar mechanism
– Similar side effects
– Similar side effects
•• Indication: ADHD
Indication: ADHD
– Increase ability to focus & concentrate
– Increase ability to focus & concentrate
41. A patient is taking theophylline and
A patient is taking theophylline and
becomes tachycardic (SVT). You want to
becomes tachycardic (SVT). You want to
give her adenosine. Is there an interaction
give her adenosine. Is there an interaction
you should be aware of? How should you
you should be aware of? How should you
alter your therapy?
alter your therapy?
Methylxanthines blocks
Methylxanthines blocks
adenosine receptors. A
adenosine receptors. A
typical dose of adenosine
typical dose of adenosine
may not be sufficient to
may not be sufficient to
achieve the desired
achieve the desired
result.
result.
Double the
Double the
dose!
dose!
42. News You Can Use…
News You Can Use…
Source
Amount of Caffeine
Coffee
•Brewed
•Instant
40 – 180 mg/cup
30 – 120 mg/cup
Decaffeinated Coffee
2 - 5 mg/cup
Tea
20 – 110 mg/cup
Coke
40 – 60 mg/12 oz
43. Psychotherapeutic
Psychotherapeutic
Medications
Medications
•• Dysfunction related to neurotransmitter
Dysfunction related to neurotransmitter
imbalance.
imbalance.
– Norepinephrine.
– Norepinephrine.
– Dopamine.
– Dopamine.
– Seratonin.
– Seratonin.
Monoamines
•• Goal is to regulate excitory/inhibitory
Goal is to regulate excitory/inhibitory
neurotransmitters.
neurotransmitters.
44. Anti-Psychotic Drugs
Anti-Psychotic Drugs
(Neuroleptics)
(Neuroleptics)
•• Schizophrenia
Schizophrenia
– Loss of contact with reality & disorganized
– Loss of contact with reality & disorganized
thoughts
thoughts
– Probable cause: increased dopamine release
– Probable cause: increased dopamine release
– Tx. Aimed at decreasing dopamine activity
– Tx. Aimed at decreasing dopamine activity
Two Chemical
Two Chemical
Classes:
Classes:
•• Phenothiazines
Phenothiazines
••
chlorpromazine (Thorazine ®®)
chlorpromazine (Thorazine )
••
haloperidol (Haldol ®)
haloperidol (Haldol )
•• Butyrophenones
Butyrophenones
®
45. Other Uses for Antipsychotics
Other Uses for Antipsychotics
••
••
••
••
••
Bipolar depression
Bipolar depression
Tourette’s Syndrome
Tourette’s Syndrome
Prevention of emesis
Prevention of emesis
Dementia (OBS)
Dementia (OBS)
Temporary psychoses from other illness
Temporary psychoses from other illness
46. Antipsychotic MOA
Antipsychotic MOA
••
••
Mechanism is similar
Mechanism is similar
Strength ([]) vs. Potency (‘oomph’)
Strength ([]) vs. Potency (‘oomph’)
– Phenothiazines – low potency
– Phenothiazines – low potency
– Butyrophenones – high potency
– Butyrophenones – high potency
•• Receptor Antagonism
Receptor Antagonism
– Dopamine2 2in brain
– Dopamine in brain
– Muscarinic cholinergic
– Muscarinic cholinergic
– Histamine
– Histamine
– Norepi at alpha1 1
– Norepi at alpha
Therapeutic effects
Uninteded effects
47. Antipsychotic Side Effects
Antipsychotic Side Effects
••
••
••
Generally short term
Generally short term
Extrapyramidal symptoms (EPS)
Extrapyramidal symptoms (EPS)
Anticholinergic effects (atropine-like)
Anticholinergic effects (atropine-like)
••
••
••
••
Orthostatic hypotension
Orthostatic hypotension
Sedation
Sedation
Decreased seizure threshold
Decreased seizure threshold
Sexual dysfunction
Sexual dysfunction
– Dry mouth, blurred vision, photophobia, tachycardia,
– Dry mouth, blurred vision, photophobia, tachycardia,
constipation)
constipation)
48. Extrapyramidal Symptoms
Extrapyramidal Symptoms
Reaction
Onset
Features
Acute dystonia
Hours to 5 days
Spasm of tongue, neck, face &
back
Parkinsonism
5 – 30 days
Tremor, shuffling gait, drooling,
stooped posture, instability
Akathesia
5 – 60 days
Compulsive, repetitive motions;
agitation
Tarditive
dyskinesia
Months to years
Lip-smacking, worm-like tongue
movement, ‘fly-catching’
49. Treatment of EPS
Treatment of EPS
•• Likely caused by blocking central
Likely caused by blocking central
dopamine22 receptors responsible for
dopamine receptors responsible for
movement
movement
•• Anticholinergic therapy rapidly effective
Anticholinergic therapy rapidly effective
– diphenhydramine (Benadryl®®)
– diphenhydramine (Benadryl )
51. Antidepressants
Antidepressants
••
••
Likely cause: inadequate monoamine levels
Likely cause: inadequate monoamine levels
Treatment options:
Treatment options:
– Increasing NT synthesis in presynaptic end
– Increasing NT synthesis in presynaptic end
bulb
bulb
– Increasing NT release from end bulb
– Increasing NT release from end bulb
– Blocking NT ‘reuptake’ by presynaptic end
– Blocking NT ‘reuptake’ by presynaptic end
bulb
bulb
54. Selective Serotonin Reuptake
Selective Serotonin Reuptake
Inhibitors (SSRIs)
Inhibitors (SSRIs)
•• Block only serotonin (not NE) reuptake
Block only serotonin (not NE) reuptake
– Elevate serotonin levels
– Elevate serotonin levels
•• Fewer side effects than TCS
Fewer side effects than TCS
– No hypotension
– No hypotension
– No anticholinergic effects
– No anticholinergic effects
– No cardiotoxicity
– No cardiotoxicity
•• Most common side effect
Most common side effect
– Nausea, insomnia, sexual dysfunction
– Nausea, insomnia, sexual dysfunction
55. Monoamine Oxidase Inhibitors
Monoamine Oxidase Inhibitors
(MAOIs)
(MAOIs)
•• Monoamine oxidase
Monoamine oxidase
– Present in liver, intestines & MA releasing
– Present in liver, intestines & MA releasing
neurons
neurons
– Inactivates monoamines
– Inactivates monoamines
– Inactivates dietary tyramine in liver
– Inactivates dietary tyramine in liver
•• Foods rich in tyramine: cheese & red wine
Foods rich in tyramine: cheese & red wine
56. MAOI Side Effects
MAOI Side Effects
•• CNS Stimulation
CNS Stimulation
– Anxiety, agitation
– Anxiety, agitation
••
••
Orthostatic hypotension
Orthostatic hypotension
Hypertensive Crisis
Hypertensive Crisis
– From increased tyramine consumption
– From increased tyramine consumption
•• Excessive arteriole constriction, stimulation of heart
Excessive arteriole constriction, stimulation of heart
60. Parkinson’s Disease
Parkinson’s Disease
•• Fine motor control dependent upon balance
Fine motor control dependent upon balance
between excitatory and inhibitory NT
between excitatory and inhibitory NT
– Acetylcholine = excitatory
– Acetylcholine = excitatory
– Dopamine =inhibitory
– Dopamine =inhibitory
GABA= inhibitory
GABA= inhibitory
Control GABA
release
62. Parkinson’s Symptoms:
Parkinson’s Symptoms:
••
••
Similar to EPS
Similar to EPS
Dyskinesias
Dyskinesias
– Tremors, unsteady gait, instability
– Tremors, unsteady gait, instability
••
••
Bradykinesia
Bradykinesia
Akinesia in severe cases
Akinesia in severe cases
63. Parkinson’s Treatment
Parkinson’s Treatment
•• Dopaminergic approach
Dopaminergic approach
⇑ Release of dopamine
⇑ Release of dopamine
⇑ [Dopamine]
⇑ [Dopamine]
⇓ Dopamine breakdown
⇓ Dopamine breakdown
•• Cholinergic approach
Cholinergic approach
⇓ Amount of ACh released
⇓ Amount of ACh released
– Directly block ACh receptors
– Directly block ACh receptors
•• All treatment is symptomatic and temporary
All treatment is symptomatic and temporary
64. Levodopa
Levodopa
••
••
••
Sinemet ® = levodopa + carbidopa
Sinemet ® = levodopa + carbidopa
Increase central dopamine levels
Increase central dopamine levels
Side effects:
Side effects:
– Nausea and vomiting
– Nausea and vomiting
– Dyskinesia (~80% of population)
– Dyskinesia (~80% of population)
– Cardiovascular (dysrythmias)
– Cardiovascular (dysrythmias)
66. Other Agents
Other Agents
•• amantadine (Symmetrel®®))
amantadine (Symmetrel
⇑ release of dopamine from unaffected neurons
⇑ release of dopamine from unaffected neurons
•• bromocriptine (Parlodel®®))
bromocriptine (Parlodel
– Directly stimulated dopamine receptors
– Directly stimulated dopamine receptors
•• selegiline (Carbex®®,, Eldepryl®®))
selegiline (Carbex Eldepryl
– MAOI selective for dopamine (MAO-B)
– MAOI selective for dopamine (MAO-B)
•• benztropine (Cogentin®®))
benztropine (Cogentin
– Centrally acting anticholinergic
– Centrally acting anticholinergic
67. Drugs That Affect the
Drugs That Affect the
Autonomic Nervous System
Autonomic Nervous System
Word of Warning
Word of Warning
Carefully review the A&P material &
Carefully review the A&P material &
tables on pages 309 – 314 and 317 – 321!
tables on pages 309 – 314 and 317 – 321!
68. PNS Drugs
PNS Drugs
•• Cholinergic
Cholinergic
– Agonists & Antagonistis (Anticholinergics)
– Agonists & Antagonistis (Anticholinergics)
– Based on response at nicotinic(N&M) & muscarinic
– Based on response at nicotinic(N&M) & muscarinic
receptors
receptors
70. Cholinergic Agonists
Cholinergic Agonists
Cholinergic agents
cause SLUDGE!
HINT!
These effects are
predictable by knowing
PNS physiology (table 9-4)
Salivation
Salivation
Lacrimation
Lacrimation
Urination
Urination
Defecation
Defecation
Gastric motility
Gastric motility
Emesis
Emesis
71. Direct Acting Cholinergics
Direct Acting Cholinergics
•• bethanechol (Urecholine) prototype
bethanechol (Urecholine) prototype
– Direct stimulation of ACh receptors
– Direct stimulation of ACh receptors
– Used for urinary hesitancy and constipation
– Used for urinary hesitancy and constipation
72. Indirect Acting Cholinergics
Indirect Acting Cholinergics
•• Inhibit ChE (cholinesterase) to prolong the
Inhibit ChE (cholinesterase) to prolong the
duration of ACh stimulation in synapse
duration of ACh stimulation in synapse
•• Reversible
Reversible
•• Irreversible
Irreversible
73. Reversible ChE Inhibitors
Reversible ChE Inhibitors
•• neostigmine (Prostigmine®®))
neostigmine (Prostigmine
– Myasthenia Gravis at nicotinicMMreceptors
– Myasthenia Gravis at nicotinic receptors
– Can reverse nondepolarizing neuromuscular
– Can reverse nondepolarizing neuromuscular
blockade
blockade
•• physostigmine (Antilirium®)
physostigmine (Antilirium®)
– Shorter onset of action
– Shorter onset of action
– Used for iatrogenic atropine overdoses @
– Used for iatrogenic atropine overdoses @
muscarinic receptors
muscarinic receptors
74. Irreversible ChE Inhibitors
Irreversible ChE Inhibitors
••
••
Very rarely used clinically
Very rarely used clinically
Very common in insecticides & chemical
Very common in insecticides & chemical
weapons
weapons
– VX and Sarin gas
– VX and Sarin gas
– Cause SLUDGE dammit and paralysis
– Cause SLUDGE dammit and paralysis
•• Tx: atropine and pralidoxime (2-PAM®®))
Tx: atropine and pralidoxime (2-PAM
– Anticholinergics
– Anticholinergics
75. Anticholinergics
Anticholinergics
•• Muscarinic
Muscarinic
antagonists
antagonists
– Atropine
– Atropine
•• Ganglionic antagonists
Ganglionic antagonists
– block nicotinicNN
– block nicotinic
receptors
receptors
– Turns off the ANS!
– Turns off the ANS!
– trimethaphan
– trimethaphan
(Arfonad®®)
(Arfonad)
•• Hypertensive crisis
Hypertensive crisis
•• Atropine Overdose
Atropine Overdose
– Dry mouth, blurred
– Dry mouth, blurred
vision, anhidrosis
vision, anhidrosis
Hot as Hell
Hot as Hell
Blind as aaBat
Blind as Bat
Dry as aaBone
Dry as Bone
Red as aaBeet
Red as Beet
Mad as aaHatter
Mad as Hatter
76. Neuromuscular Blockers
Neuromuscular Blockers
•• Nicotinic Cholinergic Antagonists
Nicotinic Cholinergic Antagonists
– Given to induce paralysis
– Given to induce paralysis
•• Depolarizing
Depolarizing
– succinylcholine (Anectin®®)
– succinylcholine (Anectin )
•• Nondepolarizing
Nondepolarizing
– tubocurarine from curare
– tubocurarine from curare
– rocuronium (Zemuron®®)
– rocuronium (Zemuron )
– vecuronium (Norcuron®®)
– vecuronium (Norcuron )
77. Warning!
Warning!
•• Paralysis without loss of consciousness!
Paralysis without loss of consciousness!
– MUST also give sedative-hypnotic
– MUST also give sedative-hypnotic
– Common agents:
– Common agents:
•• fentanyl (Sublimaze®®)
fentanyl (Sublimaze)
•• midazolam (Versed®®)
midazolam (Versed)
78. SNS Drugs
SNS Drugs
•• Predictable response based on knowledge of
Predictable response based on knowledge of
affects of adrenergic receptor stimulation
affects of adrenergic receptor stimulation
•• HINT: Know table 9-5, page 321
HINT: Know table 9-5, page 321
•• Each receptor may be:
Each receptor may be:
– Stimulated (sympathomimetic)
– Stimulated (sympathomimetic)
– Inhibitied (sympatholytic)
– Inhibitied (sympatholytic)
79. Alpha11 Agonists
Alpha Agonists
•• Profound vasoconstriction
Profound vasoconstriction
– Increases afterload & blood pressure when
– Increases afterload & blood pressure when
given systemically
given systemically
– Decreases drug absorption & bleeding when
– Decreases drug absorption & bleeding when
given topically
given topically
84. Web Resources
Web Resources
•• Web based synaptic transmission project
Web based synaptic transmission project
– http://www.williams.edu/imput/index.html
– http://www.williams.edu/imput/index.html