Term
| Nicotinic receptor antagonists are mainly used to produce _______ during general anesthesia so less anesthetic is required. |
|
Definition
| skeletal muscle relaxation |
|
|
Term
Two basic types of neuromuscular blocking
agents: ________. |
|
Definition
| Competitive blockers-non-depolarizing/depolarizing |
|
|
Term
| Competitive blockers-non-depolarizing neuromuscular blockers compete with ________ and act strictly as _______. |
|
Definition
|
|
Term
| Competitive blockers-non-depolarizing neuromuscular blockers prototype __________. |
|
Definition
|
|
Term
| Depolarizing neuromuscular blockers are antagonists/agonists? |
|
Definition
|
|
Term
| Depolarizing neuromuscular blockers act by causing _______ followed by _________. |
|
Definition
| persistent depolarization followed by receptor desens |
|
|
Term
| Depolarizing neuromuscular blockers produce _______ prior to muscle relaxation. |
|
Definition
|
|
Term
| Depolarizing neuromuscular blockers elevate _____ plasma levels. |
|
Definition
|
|
Term
| Depolarizing neuromuscular blockers prototype _________. |
|
Definition
|
|
Term
| _________ neuromuscular blocker has cardiovascular effects. |
|
Definition
|
|
Term
| d-tubocurarine ______ b.p. by releasing __________ and blocking __________. |
|
Definition
lowers
histamine and blocking SNS |
|
|
Term
| __________- not too much cardiovascular action relative to d-tubocurarine but can cause _______ in b.p. if given rapidly also, can cause _________. |
|
Definition
Pancuronium
increase
tachycardia |
|
|
Term
| _________- a non-depolarizing blocker similar to pancuronium. |
|
Definition
|
|
Term
| _______- almost no histamine release- can cause tachycardia (in rare cases). |
|
Definition
|
|
Term
| _________ - a non-depolarizing blocker similar to vecuronium. |
|
Definition
|
|
Term
| Succinylcholine releases _______ & tends to slow ________. |
|
Definition
vasodilator histamine
heart rate |
|
|
Term
Succinylcholine reduces effectiveness
of _______. |
|
Definition
|
|
Term
| Succinylcholine may be unwise to use in patients taking digitalis-like drugs that ________ or _________. |
|
Definition
| compete with K+ to increase ventricular contraction or diuretics that lower plasma K+ levels |
|
|
Term
| Succinylcholine length of duration? |
|
Definition
|
|
Term
| Mivacurium is a slow/fast acting _________ neuromuscular blocker similar to pancuronium, but its onset of action is significantly slower/faster than succinylcholine. |
|
Definition
fast
non-deploarizing blocker
slower |
|
|
Term
| Neuromuscular blockers that _______ such as: ___________ are dangerous to use in asthmatics, because they cause cause __________. |
|
Definition
release histamine
d-tubocurarine, succinylcholine and mivacurium
broncho- constriction |
|
|
Term
| Depolarizing Neuromuscular blocker _______ elevates plasma K+ levels |
|
Definition
|
|
Term
Succinylcholine can trigger an attack
of ________ when its levels greatly elevated. |
|
Definition
| malignant hyperthermia- Ca2+ |
|
|
Term
| _______ neuromuscular blocker can elevate _________ pressure & should not be used in patients with ___________. |
|
Definition
succinylcholine
intraocular
narrow-angle glaucoma |
|
|
Term
| Too much d-tubocurarine causes ________. |
|
Definition
| skeletal muscle paralysis |
|
|
Term
| d-tubocurarine blockade can be overridden with __________. |
|
Definition
|
|
Term
| d-tubocurarine is rarely used bc _______. |
|
Definition
| cardiovascular difficulties |
|
|
Term
| d-tubocurarine administered _________. |
|
Definition
|
|
Term
| d-tubocurarine is only used as a _______ during general anesthesia |
|
Definition
|
|
Term
| d-tubocurarine Duration of action: ________. |
|
Definition
|
|
Term
| Pancuronium+ is short/long acting ________ neuromuscular blocker. |
|
Definition
|
|
Term
| Pancuronium+ doesn't _______ or _______ unlike d-tubocurarine+. |
|
Definition
| release histamine or block ganglionic SNS |
|
|
Term
| Pancuronium+ is a better drug than d-tubocurarine+, to use in _________ and ________. |
|
Definition
| patients with cardiovascular issues or asthama |
|
|
Term
| __________ long-acting competitive blocker similar to pancuronium that also doesn't affect cardio much. |
|
Definition
|
|
Term
| Vecuronium+ ______ acting and has what affect on ganglionic SNS and histamine? |
|
Definition
|
|
Term
| Vecuronium+ is dangerous in ______ patients sensitized to _______. |
|
Definition
hyperthyroid patients sensitized
to catecholamines |
|
|
Term
| Only Depolarizing Neuromuscular Blocking Drug used? |
|
Definition
|
|
Term
| succinylcholine+ has a very short duration of action- 5 min due to breakdown by _______ in the plasma |
|
Definition
|
|
Term
| succinylcholine mainly used for short-term procedures such as _______ & to protect skeletal muscle during _______ therapy |
|
Definition
endotracheal intubation
electroshock |
|
|
Term
| succinylcholine+ cause histamine release? |
|
Definition
| Yes, therefore will lower BP |
|
|
Term
| succinylcholine, a Depolarizing Neuromuscular Blocking Drug, causes ________cardia by ________. |
|
Definition
bradycardia
stimulating Vagus |
|
|
Term
| succinylcholine elevates? |
|
Definition
|
|
Term
| succinylcholine can cause prolonged apnea (or respiratory arrest) in patients with _____________. |
|
Definition
| atypical pseudocholinesterase (can not hydrolyze succinylcholine as effectively) |
|
|
Term
| succinylcholine antidote? |
|
Definition
|
|
Term
| succinylcholine more prone to cause ______ than other skeletal muscle relaxants. |
|
Definition
|
|
Term
| d-tubocurarine and competitive drug antidote? Which does what? |
|
Definition
| Neostigmine inhibits AChE, |
|
|
Term
| Asthma patients should not be given __________ Neuromuscular Blockers. |
|
Definition
Asthma-d-tubocurarine, mivacurium,
and succinylcholine |
|
|
Term
| Narrow-angle glaucoma patients should not be given __________ Neuromuscular Blockers. |
|
Definition
|
|
Term
| Hyperthyroid patients should not be given __________ Neuromuscular Blockers. |
|
Definition
|
|
Term
| Drugs Acting on Skeletal Muscle to Produce Relaxation: ________. |
|
Definition
|
|
Term
| Dantrolene acts to ________ ______junctionally in skeletal muscle by _________. |
|
Definition
Reduce intracellular Ca2+ postjunctionally
reducing Ca2+ realease from the SER. |
|
|
Term
| Dantrolene reduces Intra Ca2+ by acting on the SER and blocking _____. |
|
Definition
| ryanodine receptor channel |
|
|
Term
| Dantrolene causes ________. |
|
Definition
|
|
Term
| Dantrolene is used to provide muscle relaxation for pts. with: ________. |
|
Definition
| Stroke, MS, or Malignant Hyperthemia |
|
|
Term
| Dantrolene causes local or generalized muscle weakness? |
|
Definition
|
|
Term
| Malignant hyperthermia can often occur in surgical patients who are given certain __________ in conjunction with ___________. |
|
Definition
| general anesthetics (e.g., halothane) in conjunction with succinylcholine |
|
|
Term
| Why is Dantrolene used for treating Malignant Hyperthemia? |
|
Definition
| Dantrolene helpful because it reduces Ca2+ release & prevents explosive muscle contraction |
|
|
Term
| Dantrolene influence on prejunctional release of ACh? |
|
Definition
|
|
Term
| Drugs that Act Prejunctionally for muscle relaxation do what ? |
|
Definition
|
|
Term
| Drug that acts Prejunctionally to reduce ACh release? |
|
Definition
|
|
Term
| Botulism toxin is used to treat: ____________. |
|
Definition
eye to treat blepharospasm (twitch of eyelid)
cerebral palsy spasms
into the eye to reduce spasmodic ocular movements |
|
|
Term
| Drugs Acting Centrally to Produce Skeletal Muscle Relaxation: __________ |
|
Definition
|
|
Term
| Cyclobenzaprine is useful for treating ________. |
|
Definition
|
|
Term
| Cyclobenzaprine is useful for treating muscle spasms over Valium because ________. |
|
Definition
|
|
Term
| Cyclobenzaprine overall effect? |
|
Definition
| Blocks the reuptake of NE |
|
|
Term
| Cyclobenzaprine should not be taken simultaneously with a ______. |
|
Definition
|
|
Term
| Cyclobenzaprine side effects? |
|
Definition
dry mouth, drowsiness, tachycardia,
& blurred vision |
|
|
Term
| ACh acts at ______ and ______ receptors once before its hydrolysis by the enzyme AChE. |
|
Definition
|
|
Term
| All of the therapeutically useful cholinesterase inhibitors inhibit _______ |
|
Definition
|
|
Term
| Pseudocholinesterase- more/less sensitive to inhibition by organophosphate compounds than AChE |
|
Definition
|
|
Term
| Organophosphate compounds are __________. |
|
Definition
| irreversible AChE inhibitors |
|
|
Term
|
Definition
| the plasma and glial cells |
|
|
Term
In cases of suspected organophosphate
intoxication, plasma pseudocholinesterase typically inhibited ______% when RBC AChE inhibited _____% |
|
Definition
|
|
Term
| ACh binds to _____ different sites on AChE before its breakdown. |
|
Definition
|
|
Term
| ______ site on AChE binds _______ moiety of ACh. |
|
Definition
Anionic
positively charged choline+ |
|
|
Term
| _______ site- is the active site of AChE & binds _________ of ACh. |
|
Definition
Esteratic
carbonyl carbon |
|
|
Term
| Even _______ can act as an AChE inhibitor, but a very weak one, because it ________ |
|
Definition
choline
binds one of the sites and competes with ACh then |
|
|
Term
| Some AChE inhibitors positively charged & act directly on the ________ to produce a _______ action. |
|
Definition
nicotinic receptor site
positive agonist |
|
|
Term
| Nicotinic receptors at ______ appear more sensitive to agonist action of positively charged AChE inhibitors than nicotinic receptors on ________. |
|
Definition
motor endplate region
ganglia or adrenal medulla |
|
|
Term
| Types of AChE Inhibitors reversible: ____________. |
|
Definition
a. Neostigmine+
b. Edrophonium+
c. Pyridostigmine+
d. Physostigmine
e. Tacrine
f. Donepezil |
|
|
Term
| Types of AChE Inhibitors irreversible: ____________. |
|
Definition
a. Echothiophate+
b. DFP (Diisopropyl flourophosphate)
C. Parathion
d. Sarin |
|
|
Term
| Reversible AChE inhibitors do what? |
|
Definition
compete with ACh for binding to anionic and esteratic sites by
carbamylating esteratic site |
|
|
Term
| Reversible AChE inhibitors form a stronger bond with ________ site than ACh and thus time for breakdown is __________. |
|
Definition
esteric
longer (60-120 min) |
|
|
Term
| Neostigmine-hydrolyzed to _______ by AChE. |
|
Definition
|
|
Term
| Edrophonium is not ______, but irreversibly/reversibly inhibits AChE by ________. |
|
Definition
not hydrolyzed by AChE
competes with ACh for binding to both
esteratic and anionic sites |
|
|
Term
| Edrophonium binds which AChE sites and is ______ acting? |
|
Definition
both esteratic and anionic sites
very short, rapidly excreted |
|
|
Term
| Irreversible AChE Inhibitors act by? |
|
Definition
| Phosphorylate esteratic site |
|
|
Term
| Irreversible AChE Inhibitors act by Phosphorylating esteratic sites which knocks them out for _______ duration and therefore must be ___________. |
|
Definition
2 weeks
new AChE must be synthesized |
|
|
Term
| Irreversible AChE Inhibitors should not be taken ________. |
|
Definition
Extremely dangerous compounds-should not
be taken parenterally |
|
|
Term
| Irreversible AChE Inhibitors can kill by causing __________. |
|
Definition
|
|
Term
| Irreversible AChE Inhibitors can kill by causing Respiratory arrest by __________. |
|
Definition
| Paralyze diaphragm and intercostal muscles by building up ACh at nicotinic receptors to high enough levels that nicotinic receptors are desensitized |
|
|
Term
| Some irreversible AChE inhibitors, __________, can cause delayed ______toxicity. |
|
Definition
organophosphates
neurotoxicity |
|
|
Term
| Delayed neurotoxicity caused by some irreversible AChE inhibitors, organophosphates, can cause: ________ & appears _____ days after drug admin. |
|
Definition
ataxia, muscle paralysis and demyelination and appears 8-14 days
after drug exposure |
|
|
Term
| Therapeutic Uses of AChE Inhibitors for disorders: ___________. |
|
Definition
G.I. tract or bladder atony
Glaucoma - wide and narrow angle
Myasthenia gravis - treatment and diagnosis |
|
|
Term
| AChE Inhibitors can be used to terminate an overdose of a ________ like uncompetitive /competitive blocker. |
|
Definition
| Curare like competitive blocker |
|
|
Term
| AChE Inhibitors can be used to terminate an attack of ________. |
|
Definition
| supraventricular tachycardia |
|
|
Term
| Neostigmine+ is a _______ type of drug. |
|
Definition
| Reversible AChE Inhibitor |
|
|
Term
|
Definition
|
|
Term
| Neostigmine+ drug metabolism? |
|
Definition
| Is hydrolyzed to edrophonium by AChE |
|
|
Term
| Neostigmine+ duration of action? |
|
Definition
|
|
Term
| Neostigmine+ is used to treat? |
|
Definition
paralytic ileus or bladder atony
wide-and narrow-angle glaucoma |
|
|
Term
| Myasthenia gravis Ab against? |
|
Definition
nicotinic receptor at motor endplate of
neuromuscular junction |
|
|
Term
Muscle biopsy will show a decrease in
binding of ______ which correlates with severity of disease. |
|
Definition
|
|
Term
| Myasthenia gravis Ab do not recognize nicotinic receptors on? |
|
Definition
| ganglia or adrenal medulla |
|
|
Term
| ______ are sometimes used if AChE inhibitors are not working for Myasthenia gravis. |
|
Definition
|
|
Term
| Myasthenic Syndrome (_______) |
|
Definition
|
|
Term
| Myasthenic Syndrome (Lambert Eaton) is more common or rarer than MG? |
|
Definition
|
|
Term
| Myasthenic Syndrome (Lambert Eaton) also involves ________. |
|
Definition
|
|
Term
| Myasthenic Syndrome (Lambert Eaton) Ab against? |
|
Definition
| Ca2+ channel mediating ACh release from motor nerve terminal |
|
|
Term
| _______ is used to treat Lambert Eaton. |
|
Definition
|
|
Term
| ______ is drug of treat Myasthenia gravis. |
|
Definition
|
|
Term
| Pyridostigmine is ____ charged and has ______ duration than |
|
Definition
| neostigmine (another reversible AChE inhibitor) |
|
|
Term
| Why is Pyridostigmine better than neostigmine for MG treatment? |
|
Definition
Longer duration
Better absorbed
Fewer side effects |
|
|
Term
|
Definition
Competitively binds to both the esteratic
& anionic sites |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Edrophonium+ excreted by? |
|
Definition
|
|
Term
| Edrophonium+ is the drug of choice for? |
|
Definition
| diagnosis of myasthenia gravis |
|
|
Term
| _______ is the drug of choice for the treatment of MG. |
|
Definition
|
|
Term
| Edrophonium+ can be used to treat disorder? |
|
Definition
| supraventricular tachycardia |
|
|
Term
| Edrophonium+ can be used to treat overdose of? |
|
Definition
|
|
Term
| Physostigmine type of drug? |
|
Definition
| reversible AChE inhibitor |
|
|
Term
|
Definition
|
|
Term
| Physostigmine is mainly used in the ______ in conjunction with _______ for the treatment of _______ until _______. |
|
Definition
eye
pilocarpine
narrow angle glaucoma
iridectomy can be done |
|
|
Term
| Physostigmine can be used as the antidote for? |
|
Definition
|
|
Term
| Tacrine is a _____ type of drug? |
|
Definition
| Reversible AChE inhibitor |
|
|
Term
|
Definition
|
|
Term
| Tacrine crosses the BBB and ________. |
|
Definition
| raises ACh levels centrally |
|
|
Term
| Tacrine is used to treat? |
|
Definition
|
|
Term
| Tacrine & ________ are used to treat Alzheimer's. |
|
Definition
|
|
Term
| Donepezil has a high degree for selectivity of ________. |
|
Definition
|
|
Term
| Donepezil exhibits less ________ than Tacrine (other drug for Alzheimer's) |
|
Definition
|
|
Term
| Irreversible AChE Inhibitors: ________. |
|
Definition
a. Echothiophate+
b. DFP (Diisopropyl flourophosphate)
C. Parathion
d. Sarin |
|
|
Term
|
Definition
|
|
Term
| Echothiophate+ only used ______ to treat ______. |
|
Definition
Only used topically in the eye, mainly for
wide angle glaucoma, |
|
|
Term
| _______ an organophosphate irreversible AChE inhibitor used as an insecticide. |
|
Definition
|
|
Term
| Mipafoxan organophosphate irreversible AChE inhibitor used as an insecticide causes delayed _______ ______days after exposure. |
|
Definition
| delayed neurotoxicity 8-14 days |
|
|
Term
| Parathion is a _______ type of drug. |
|
Definition
| Irreversible AChE Inhibitor |
|
|
Term
| Parathion is a ________ type of compound. |
|
Definition
|
|
Term
| Parathion is a potent _____ & ______. |
|
Definition
|
|
Term
| Parathion does not cause ______, like the insecticide _____ does. |
|
Definition
delayed neurotoxicity
Mipafox |
|
|
Term
| Sarin is a ______ compound. |
|
Definition
|
|
Term
| Antidotes for Organophosphate Intoxication: ___________. |
|
Definition
Pralidoxime+ (2-PAM)
Obidoxime (similar to Pralidoxime+)
Atropine |
|
|
Term
| Pralidoxime+ (2-PAM) MOA? |
|
Definition
"Pulls" organophosphate off esteratic
site of AChE |
|
|
Term
| Atropine (an effective ______ antagonist) |
|
Definition
|
|
Term
| Atropine controls signs of muscarinic excess: ________, caused by ______. |
|
Definition
| Controls signs of muscarinic excess; it blocks muscarinic effects of excess salivation, miosis, bronchoconstriction, bronchiole secretions, &sweating caused by inhibition of AChE at muscarinic receptor sites. |
|
|
Term
|
Definition
| Only needed for approximately two weeks during treatment for myasthenia gravis because muscarinic side effects of AChE inhibitors dissipate. |
|
|
Term
| Myasthenia Gravis An autoimmune disorder of function at the synapse between ______ motor neurons and skeletal muscle |
|
Definition
|
|
Term
| Myasthenia Gravis, antibodies against the ________. |
|
Definition
| nicotinic Acetylcholine (ACh) receptor |
|
|
Term
| Myasthenia Gravis typically affects the _____ muscles. |
|
Definition
|
|
Term
_____ is the transmitter at neuromuscular
junction (NMJ). |
|
Definition
|
|
Term
| Is atrophy present in MG? |
|
Definition
|
|
Term
| Is weakness present in MG? |
|
Definition
|
|
Term
| The weakness of MG is reversed by intravenous injection of inhibitors of acetylcholinesterase (______, _______, ________). |
|
Definition
| edrophonium, pyridostigmine, physostigmine |
|
|
Term
| Neostigmine increases the _____ of ACh. |
|
Definition
|
|
Term
| In MG The amplitude of evoked ______ decreases rapidly. |
|
Definition
| compound action potentials |
|
|
Term
| In MG 15% of patients have a ________. |
|
Definition
|
|
Term
| In MG the density of ______ in muscle fibers is reduced. |
|
Definition
|
|
Term
| ACh receptors are marked and detected using? |
|
Definition
| alpha-bungarotoxin (in MG reduced density on muscle fibers) |
|
|
Term
| Draining ______ from ______ improve symptoms of MG. |
|
Definition
| lymph from the thoracic lymph ducts |
|
|
Term
| In addition to draining the lymph, _______ procedure also improves symptoms of MG. |
|
Definition
|
|
Term
| In the normal neuromuscular junction the amplitude of the end-plate potential is _________ (_________ principle) |
|
Definition
very large,well above the threshold for a muscle action potential
large safety factor |
|
|
Term
| Because of the large amplitude of the end-plate potential (large safety factor) a muscle has _______ under repetitive stimulation. |
|
Definition
| compound muscle action potential is constant and invariable |
|
|
Term
| In MG postsynaptic changes _______ the motor end plate potential, which means that with repetitive stimulation the end plate potential ______. |
|
Definition
reduce the amplitude of
will not meet threshold |
|
|
Term
| Is ACh release impaired in MG? |
|
Definition
|
|
Term
| What happens to geometry of end plate in MG? |
|
Definition
| disturbed and normal infolding is reduced and synaptic cleft is enlarged |
|
|
Term
| The autoimmune reaction of MG depends on: _________ components. |
|
Definition
| antigen (the immunogenic peptide of the ACh receptor), an antigen- specific T cell receptor, and class II molecule of MHC expressed on the APC. |
|
|
Term
| In MG the ___ cells become reactive against the ACh receptor and recognize the receptor in the _______. |
|
Definition
|
|
Term
| Two categories of MG: __________. |
|
Definition
Acquired autoimmune older children/adults
A nonimmune heritable congenital form
without ACh receptor antibodies. |
|
|
Term
| Which type of MG is heterogeneous? |
|
Definition
A nonimmune heritable congenital form
without ACh receptor antibodies. |
|
|
Term
| Slow Channel Syndrome is a form of ________ and results from __________. |
|
Definition
A nonimmune heritable congenital form of MG without ACh receptor antibodies.
alteration in ACh receptor capacity to react with ACh |
|
|
Term
| Slow Channel Syndrome is characterized by ________. |
|
Definition
| little weakness of cranial muscle and major weakness of limbs (opposite pattern usually seen in myasthenia |
|
|
Term
| Slow Channel Syndrome is characterized by end-plate potentials that are _______, despite normal _______, because the ACh Receptor __________. |
|
Definition
Prolonged
normal AChE
stays opened for prolonged periods |
|
|
Term
| Some patients with lung cancer have a neuro-muscular disorder called ________. |
|
Definition
| presynaptic (facilitating) neuromuscular block (Lambert-Eaton Syndrome?) |
|
|
Term
| Lambert-Eaton Syndrome (presynaptic (facilitating) neuromuscular block) physiological response is opposite of myasthenia, showing gradual __________. |
|
Definition
| increase to repetitive stimulation so that the final summated action potential is 2-4 times the amplitude of the first potential. |
|
|
Term
| Lambert-Eaton Syndrome is due to Ab against? |
|
Definition
| voltage-gated calcium channels in the presynaptic terminals |
|
|
Term
| Symptoms in patients with Lambert-Eaton Syndrome often improve after ________ or _______ therapy. |
|
Definition
| plasmapheresis or immunosuppressive |
|
|
Term
| In Lambert-Eaton Syndrome ACh release is? |
|
Definition
|
|
Term
| Impaired ______ in congenital form of MG. |
|
Definition
|
|
Term
| Botulism and Tetanus toxins affect _________ involved in what process? |
|
Definition
| SNARE proteins involved in vesicle fusion (NT release) |
|
|
Term
| Botulism as well as Lambert-Eaton syndrome are treated with ________ & ________ (agents that ________). |
|
Definition
calcium gluconate and guanidine
enhance the release of ACh |
|
|
Term
| Sympathomimetic- ________. |
|
Definition
mimicking action of SNS
(adrenomimetic – action similar to Epi, NE) |
|
|
Term
| Sympatholytic – ________. |
|
Definition
inhibition of adrenergic action
(adrenolytic – blocking action of Epi, NE) |
|
|
Term
| Chronotropic – ____________. |
|
Definition
| altering the rate of rhythmic movement (i.e., heartbeats). |
|
|
Term
| Inotropic – ____________. |
|
Definition
| altering the force of muscular contraction |
|
|
Term
| Direct agents act ________. |
|
Definition
|
|
Term
| Indirect agents act ________. |
|
Definition
|
|
Term
| Indirect agents act prejunctionally by influencing the ______ or ______ of NT. |
|
Definition
- release of transmitter
- reuptake of transmitter |
|
|
Term
| Direct response- ________. |
|
Definition
| response of target organ to agent |
|
|
Term
| Reflex response- ________. |
|
Definition
| an autonomic reaction to peripheral-acting agent |
|
|
Term
| Integrated response- ________. |
|
Definition
|
|
Term
| Isoproterenol is a _______ agonist/antagonist. |
|
Definition
|
|
Term
| Alpha receptors sensitivity with respect to NE, E, and Isoproterenol (Iso)? |
|
Definition
|
|
Term
| Beta receptors sensitivity with respect to NE, E, and Isoproterenol (Iso)? |
|
Definition
|
|
Term
| General Pharmacology of Direct-acting Sympathomimetics categories: ________. |
|
Definition
Catecholamines
Non-catecholamines |
|
|
Term
| Catecholamines (Direct-acting Sympathomimetics) Metabolized? Bioavail? half-life? |
|
Definition
Metabolized quickly
Reduced Bioavail
Reduced Half Life |
|
|
Term
| Catecholamines (Direct-acting Sympathomimetics) more or less polar than non-catecholamines ? and therefore oral bioavail? CNS entry? |
|
Definition
More
low oral bioavail
low CNS entry |
|
|
Term
| Catecholamines (Direct-acting Sympathomimetics) more or less selective than non-catecholamines ? |
|
Definition
|
|
Term
| Non-catecholamines (Direct-acting Sympathomimetics) Metabolized? Bioavail? half-life? |
|
Definition
Resistant to met.
* increased bioavail.
*Longer half life |
|
|
Term
| non-Catecholamines (Direct-acting Sympathomimetics) more or less polar than catecholamines ? and therefore oral bioavail? CNS entry? |
|
Definition
Less polar
*increased oral bioavail.
*Increased in CNS |
|
|
Term
| non-Catecholamines (Direct-acting Sympathomimetics) more or less selective than catecholamines ? |
|
Definition
|
|
Term
| The Chemistry of specificity of Direct-acting Sympathomimetics depends on: __________. |
|
Definition
1.Substitution on the amino group
2.Substitution of the benzene ring
3.Substitution on the alpha carbon
4.Substitution on the beta carbon |
|
|
Term
| Smooth Muscle in vascular, action of alpha1- ________ receptor. |
|
Definition
|
|
Term
| Smooth Muscle in vascular, action of _______ & ________ receptors- relaxation. |
|
Definition
|
|
Term
| Smooth Muscle in bronchioles, action of _______ receptor- relaxation. |
|
Definition
|
|
Term
| Smooth Muscle in Gut/bladder, action of _______ receptor- sphincters to contract |
|
Definition
|
|
Term
| Smooth Muscle in Uterine, action of _______ receptor- relaxation (only in late gestation) |
|
Definition
|
|
Term
| Smooth Muscle in Prostate, action of _______ receptor- contraction. |
|
Definition
|
|
Term
| Smooth Muscle in Eye, action of Alpha1 receptor- contraction of _____ muscle. |
|
Definition
|
|
Term
| Adrenergic receptors in cardiac muscle: ________ |
|
Definition
|
|
Term
| Beta 1 receptors in cardiac muscle are ______tropic. |
|
Definition
* Inotropic
* Chronotropic
much lesser extent |
|
|
Term
| Alpha 1 and Beta 2 receptors in cardiac muscle are ______tropic. |
|
Definition
|
|
Term
| Adrenergic receptors in skeletal muscle: ________ |
|
Definition
|
|
Term
| Beta2 receptors in skeletal muscle cause ____ ion uptake. |
|
Definition
|
|
Term
| Beta2 receptors in skeletal muscle cause ______ with respect to energy stores. |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| a1 Agonists Major Responses in: _______ organs. |
|
Definition
|
|
Term
| a1 Agonists Major Responses in Cardiovascular? |
|
Definition
Direct - vascular contraction
Indirect - slow heart rate |
|
|
Term
| a1 Agonists Major Responses in Eye? |
|
Definition
|
|
Term
| a1 Agonists bc of their _________ Cardiovascular effect, are useful for treating: __________. |
|
Definition
Hypotension
Paroxysmal supraventricular (atrial) tachycardia
Nasal congestion |
|
|
Term
a1 Agonists are used to treat
Paroxysmal supraventricular (atrial) tachycardia because of the _____ response to __________. |
|
Definition
| Reflex response to slow heart (indirect response) |
|
|
Term
| a1 Agonists are used in optical exams to induce _______. |
|
Definition
|
|
Term
| a1 Agonists adverse effects: __________. |
|
Definition
Hypertension
Ischemia to organs
Rebound nasal/sinus hyperemia (desensitization) |
|
|
Term
| Hyperaemia or hyperemia is the increase of blood flow to different tissues in the body. |
|
Definition
|
|
Term
| a1 Agonists are contradicted in patients suffering from: ____________. |
|
Definition
•Hypertension
•Ischemic organ diseases
•Prostate enlargement |
|
|
Term
| a1 Agonists are contradicted with co-administration of: ________. |
|
Definition
–MAO inhibitors
–Indirect-acting sympathomimetics |
|
|
Term
| a2 Agonists major responses: __________. |
|
Definition
vasodilation (a1 constriction)
decrease aqueous humor production (a1 dilation) |
|
|
Term
| a2 Agonists treatments: __________. |
|
Definition
antihypertensive (a1 antihypotensive)
lower intraocular pressure in open angle glaucoma (decrease aqueous humor production)a2 Agonists
minimize withdrawal symptoms |
|
|
Term
| a2 Agonists adverse effects: ________. |
|
Definition
Bradycardia
CNS (>50% population)- Sedation & Dry mouth
Sexual dysfunction |
|
|
Term
| a2 Agonists contradicted in: _______. |
|
Definition
|
|
Term
| B1 Agonists major responses: __________. |
|
Definition
-Cardiovascular:
increases calcium influx
increases rate and force |
|
|
Term
| B1 Agonists treatments: __________. |
|
Definition
|
|
Term
| B1 Agonists adverse effects: ________. |
|
Definition
|
|
Term
| B1 Agonists contradicted in: _______. |
|
Definition
|
|
Term
| B2 major responses: __________. |
|
Definition
Bronchodilation
Uterine dilation |
|
|
Term
| B2 Agonists treatments: __________. |
|
Definition
Bronchodilators
–Asthma
–COPD
Tocolytic agents (reverse effects of?)
-Late term gestation |
|
|
Term
| B2 Agonists adverse effects: ________. |
|
Definition
Symptoms of b1 stimulation
–Tachycardia
–Widening pulse pressure (systolic pressure rise)
Symptoms of b2 stimulation
–Widening pulse pressure (diastolic pressure drop)
–Drop in serum K+ (skeletal muscle uptake)
–Skeletal muscle tremor |
|
|
Term
| B2 Agonists contradicted in: _______. |
|
Definition
Cardiac disease
–Coronary artery disease
–Arrhythmias
Diabetes
Hyperthyroidism
•Co-administration (same as a1)
–MAO inhibitors
–Indirect-acting sympathomimetics |
|
|
Term
| B2 Agonists adverse effects relatively uncommon when given as _______, more likely when given _________– i.e. ____ dependent) |
|
Definition
inhalant
systemically
dose |
|
|
Term
Indirect-acting Drug List:
-Interfere with neurotransmitter metabolism- ___________. |
|
Definition
|
|
Term
Indirect-acting Drug List:
-Block transport at nerve terminal- __________. |
|
Definition
|
|
Term
Indirect-acting Drug List:
Block of vesicular transport- _______. |
|
Definition
|
|
Term
Indirect-acting Drug List:
Promotion of exocytosis and displacement of transmitter- __________. |
|
Definition
|
|
Term
Indirect-acting Drug List:
Prevention of release of transmitter- __________. |
|
Definition
|
|
Term
Indirect-acting Drug List:
Inhibition to transmitter degradation- __________. |
|
Definition
| tranylcypromine: MAO inhibitor |
|
|
Term
| Tyramine is a byproduct of fermentation process that is an intermediate in _____ metabolism |
|
Definition
|
|
Term
| Tyramine can have indirect/direct _______ effect via stimulation of _______. |
|
Definition
indirect
sympathomimetic
NE release |
|
|
Term
| Patients taking ______ should avoid foods high in tyramine |
|
Definition
|
|
Term
| Catecholamine & Sympathomimetic Actions: _______ = prototypical agent |
|
Definition
|
|
Term
Catecholamine & Sympathomimetic Actions:
cardiac ________-> HR _____ & Contraction force _________ |
|
Definition
excitation
Heart rate and contraction force up |
|
|
Term
Catecholamine & Sympathomimetic Actions:
Metabolic effects: __________. |
|
Definition
| Increase glycogenolysis, adipose -> FFA |
|
|
Term
Sympathomimetics /Agonists:
Endogenous to Sympathetic NS: ______. |
|
Definition
* Epinephrine
* Norepinephrine
* Dopamine |
|
|
Term
Sympathomimetics /Agonists:
Exogenous to Sympathetic NS: ______. |
|
Definition
Phenylephrine
Clonidine
Isoproterenol
Dobutamine
Albuterol
Fenoldopam
Bromocriptine |
|
|
Term
| Epinephrine bind what receptors? |
|
Definition
|
|
Term
| Epinephrine has _____ & _____ effects on cardiac. |
|
Definition
|
|
Term
| Epinephrine Non-cardiovascular Effects: ________. |
|
Definition
–Smooth Muscle
–Respiratory
–Metabolic |
|
|
Term
| Epinephrine has a respiratory effect by indirect/direct action on __ receptor causing _______. |
|
Definition
| direct B2: bronchodilation |
|
|
Term
| Epinephrine clinical uses: ________. |
|
Definition
Hypersensitivity
Bronchodilator
•Asthma
•Anaphylaxis
Vasoconstriction
•Angioedema
•Adjunct to local anesthetics
Cardiac stimulant
Lower intraocular pressure in wide angle glaucoma (a2) |
|
|
Term
| Epinephrine Adverse Effects: ________. |
|
Definition
–Arrhythmias
–Cerebral hemorrhage
–Anxiety symptoms (somatic) |
|
|
Term
| Epinephrine Adverse Effects: ________. |
|
Definition
|
|
Term
| Epinephrine in low doses has vascular effects by causing ________. |
|
Definition
| redistribution of blood flow (regional responses) |
|
|
Term
| Epinephrine in low doses has vascular effects by causing redistribution of blood flow: regions rich in ____ see vasoconstriction & regions rich in ____ see vasodilation |
|
Definition
|
|
Term
| Epinephrine in low doses has no vascular effects on __________. |
|
Definition
|
|
Term
| Epinephrine in low doses has results in a ______ cardiac response. |
|
Definition
|
|
Term
| Epinephrine Low Doses- Blood pressure: Increase _______, decrease ________. |
|
Definition
|
|
Term
| Epinephrine in high doses has vascular, cardiac, and blood pressure effects like __________. |
|
Definition
|
|
Term
| Epinephrine in high doses effects vasculature predominately ______ globally and _____ locally resulting in an net effect __________. |
|
Definition
a1 global
b2 local
net effect increase TPR |
|
|
Term
| In high doses Epinephrine has ___ like cardiac effects, giving _____ responses. |
|
Definition
NE Like
direct effects + reflex responses |
|
|
Term
| In high doses Epinephrine has ___ like BP effects, resulting in ______. |
|
Definition
NE like
pulse pressure narrowing |
|
|
Term
| Norepinephrine acts on what receptors? |
|
Definition
adrenergic
a1 a2 B1 (NOT B2 like E) |
|
|
Term
| Norepinephrine effects Vascular directly through ____ receptor causing ___________. |
|
Definition
|
|
Term
| Norepinephrine effects Cardiac ________. |
|
Definition
|
|
Term
| Norepinephrine effects Cardiac directly through ____ receptors and causes ____. |
|
Definition
| B1 [increase in force & HR] |
|
|
Term
| Norepinephrine effects BP by _____ the TPR and ______ the CO. |
|
Definition
|
|
Term
| Norepinephrine non cardiovascular effects? |
|
Definition
|
|
Term
| Norepinephrine clinical use? |
|
Definition
| Limited: Vasoconstriction |
|
|
Term
| Norepinephrine Adverse Effects: __________. |
|
Definition
–Arrhythmias
–Cerebral hemorrhage
(Both same as E, except E also has skeletal somatic tremors) |
|
|
Term
| Dopamine mainly has effects on? |
|
Definition
| Cardiovascular (like NE minimal non cardiovascular) |
|
|
Term
| Dopamine can be used to treat _______ and ________. |
|
Definition
|
|
Term
| Dopamine can be used to treat shock by __________. |
|
Definition
| Increase renal blood flow |
|
|
Term
| Dopamine can be used to treat Cardiac failure by __________. |
|
Definition
acting as cardiac stimulant
&
Increase renal blood flow |
|
|
Term
|
Definition
|
|
Term
| Because of having to give via IV, Dopamine is useful for _____, but not ______. |
|
Definition
| Acute cardiac failure, not chronic |
|
|
Term
|
Definition
| Arrhythmias (just like NE and E) |
|
|
Term
| Oxymethazoline: is a ______ agonist/antagonist? |
|
Definition
| a-adrenergic agonist (a1 and a2) |
|
|
Term
| Oxymethazoline MOA: ______. |
|
Definition
| a1 & a2 adrenergic agonist |
|
|
Term
| Oxymethazoline clinical use? |
|
Definition
| decongestant (a1 main use) |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Oxymethazoline adverse effect? |
|
Definition
| continued use causes rebound congestion |
|
|
Term
| Oxymethazoline adverse effect of continued use causing rebound congestion is a result of? |
|
Definition
| down regulation of a2 receptors |
|
|
Term
| Oxymethazoline is contradicted in those who? |
|
Definition
|
|
Term
| Phenylephrine: is a ______ agonist/antagonist? |
|
Definition
|
|
Term
| Phenylephrine clinical use? |
|
Definition
| Ophthalmological – to produce: - mydriasis (a1 effect) |
|
|
Term
| Phenylephrine MOA: ________. |
|
Definition
|
|
Term
| Phenylephrine adverse effect? |
|
Definition
| Rebound nasal/sinus hyperemia (a1 side effect) |
|
|
Term
| Phenylephrine is contradicted in those who? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| mild-to-moderate hypertension (a2 vasodilation) |
|
|
Term
| Clonidine Adverse effects: _______. |
|
Definition
- drowsiness
- dry mouth
- GI disturbance
- muscle weakness
- withdrawal symp. |
|
|
Term
| Clonidine contraindications: _______. |
|
Definition
|
|
Term
| Isoproterenol MOA: _______. |
|
Definition
|
|
Term
| Isoproterenol Vascular Effects: _______. |
|
Definition
|
|
Term
| Isoproterenol Cardiac Effects: _______. |
|
Definition
| direct b1: force, rate + reflex |
|
|
Term
| Isoproterenol Blood Pressure Effects: _______. |
|
Definition
| widening pulse pressure (B2) |
|
|
Term
| Isoproterenol Non-cardiovascular Effects: _______. |
|
Definition
Smooth muscle
-Bronchial
-GI/Bladder
-Uterine
Metabolic |
|
|
Term
| Isoproterenol Bronchial effect: _______ |
|
Definition
| direct b2: bronchodilation |
|
|
Term
| Isoproterenol Uterine effect- __________. |
|
Definition
| (direct b2: dilation in late gestation) |
|
|
Term
| Dobutamine MOA: __________. |
|
Definition
|
|
Term
| Dobutamine used as a ______? |
|
Definition
|
|
Term
|
Definition
Cardiogenic shock & Cardiac failure
(used as a Cardiac stimulant same as Dopamine and E) |
|
|
Term
|
Definition
IV (just like Dopamine)
–Limits its usefulness in chronic cardiac failure.
–Can be advantage in acute cardiac failure. (just like dopamine) |
|
|
Term
| Dobutamine Adverse Effects: ________. |
|
Definition
Arrhythmias (just like dopamine)
Tolerance develops with use |
|
|
Term
|
Definition
|
|
Term
|
Definition
| - asthma & COPD (Bronchodilator B2) |
|
|
Term
|
Definition
|
|
Term
| Albuterol Adverse Effects: _______. |
|
Definition
|
|
Term
| Albuterol contradictions:________. |
|
Definition
- drug sensitivity
- tachyarrhythmias
- pregnancy |
|
|
Term
|
Definition
| any disturbance of the heart rhythm in which the heart rate is abnormally increased. |
|
|
Term
| Fenoldopam MOA: ________. |
|
Definition
|
|
Term
| Fenoldopam is the ________. |
|
Definition
|
|
Term
| Fenoldopam causes and is used to treat? |
|
Definition
Vasodilation
Severe hypertension |
|
|
Term
| ______ is used to treat Mild-Moderate Hypertension as an a2 agonist. |
|
Definition
|
|
Term
| Fenoldopam Adverse effects? |
|
Definition
|
|
Term
|
Definition
| Short t1/2 & not absorbed by gut (i.v. only) |
|
|
Term
| Bromocriptine MOA: __________. |
|
Definition
|
|
Term
| Bromocriptine Clinical use? |
|
Definition
– hyperprolactinemia
- Parkinson’s |
|
|
Term
| Bromocriptine acts to suppress _______, causing ________ in order to improve ________. |
|
Definition
| suppress prolactin release from adenomas and shrink tumor, improve motor function |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Nonselective a Antagonists: ________. |
|
Definition
| Phenoxybenzamine & phentolamine & Ergot alkaloids |
|
|
Term
| Phenoxybenzamine is used to treat? |
|
Definition
(Nonselective a Antagonist)
Pheochromocytoma
Benign prostatic obstruction |
|
|
Term
| Ergot alkaloids used to treat? |
|
Definition
(Nonselective a Antagonist)
Migranes |
|
|
Term
| Nonselective a Antagonists (Phenoxybenzamine & phentolamine) adverse effects? |
|
Definition
–Cardiovascular
•Tachycardia (reflex)
•Orthostatic hypotension
•Nasal congestion (a1)
–Non cardiovascular
•GI (Phentolamine)
•Impotence (Phenoxybenzamine)
•Potential mutagen
(Phenoxybenzamine) |
|
|
Term
| •Orthostatic hypotension WIKI |
|
Definition
| form of hypotension in which a person's blood pressure suddenly falls when standing up or stretching. |
|
|
Term
| Pheochromocytoma is a ______ tumor of the ___________. |
|
Definition
| neuroendocrine tumor of the medulla of the adrenal glands |
|
|
Term
| Pheochromocytoma is a neuroendocrine tumor of the medulla of the adrenal glands that secretes: __________. |
|
Definition
|
|
Term
| Pheochromocytoma is treated with? |
|
Definition
| prazocin (a1 inhibitor over Phenoxybenzamine a non-selective a inhibitor because of side effects) |
|
|
Term
| Pheochromocytoma ______% with genetic contribution. |
|
Definition
|
|
Term
| Non-selective a blockers have an _____junctional effect on ________ receptors. |
|
Definition
|
|
Term
| The a2 component of Non-selective a blockers causes a ______ blockade leading to a __________. |
|
Definition
| prejunctional blockade -> reflex tachycardia |
|
|
Term
| Because of the tachycardia side effect of the a2 component, Non-selective a blockers are avoided in treating? |
|
Definition
|
|
Term
| The a2 antagonistic component of Non-selective a blockers, blocks _____ release. |
|
Definition
|
|
Term
| Nonselective Adrenergic Antagonists of B and a1: ___________. |
|
Definition
|
|
Term
| Carvedilol is a _____ antagonist and is used as a anti-______ agent and improves the survival |
|
Definition
B and a1
–Anti-ischemic agent
–Improves survival in chronic heart failure |
|
|
Term
| Selective a1 Antagonists have an advantage over non-selective a antagonists, because ________. |
|
Definition
lack a2 component
•less prejunctional blockade -> less reflex tachycardia |
|
|
Term
| Selective a1 Antagonists are used to clinically treat: ________. |
|
Definition
Benign prostatic hyperplasia
Hypertension
Congestive heart failure
Pheochromocytoma (same as nonselective) |
|
|
Term
| Pheochromocytoma is treated by which Selective a1 Antagonist? |
|
Definition
|
|
Term
| Benign prostatic hyperplasia is treated by which Selective a1 Antagonists? |
|
Definition
•Prazosin (BID dosage)
•Doxazosin & Terazosin (QD dosage) |
|
|
Term
| Selective a1 Antagonists Adverse Effects: _______. |
|
Definition
Orthostatic hypotension (just like nonselective) (from a1 obviously)
Nasal congestion (just like nonselective) (from a1) |
|
|
Term
| Selective a1 Antagonists side effect of Orthostatic hypotension usually becomes _______ and requires first does to be __________. |
|
Definition
•Usually becomes tolerated
•Give first dose at night |
|
|
Term
| “Uroselective” a1A Antagonist: ________. |
|
Definition
Tamsulosin (aka flomax)
alfuzosin |
|
|
Term
| Tamsulosin & alfuzosin is used to treat? |
|
Definition
| Benign Prostatic Hyperplasia (BPH) (“Uroselective” a1A Antagonist) |
|
|
Term
| “Uroselective” a1A Antagonist adverse effect? and which one is to a lesser extent? |
|
Definition
| Retrograde ejaculation (less with alfuzosin) |
|
|
Term
| “Uroselective” a1A Antagonist avoids _____ adverse effect in most. |
|
Definition
| orthostatic hypotension (a Selective a1 Antagonist side effect) |
|
|
Term
| B antagonists are used cardiovascularly to treat? |
|
Definition
–Hypertension
–Angina
–Arrhythmias
–Myocardial infarction
–Heart failure
–CV Symptoms of
•Hyperthyroidism
•Pheochromocytoma
•Aortic aneurysm
–Migraine headache |
|
|
Term
| B antagonists are used to treat non-cardiovascularlly? |
|
Definition
–Glaucoma
–Somatic symptoms of anxiety (e.g. stage fright)
–Fine muscle tremors |
|
|
Term
|
Definition
|
|
Term
| Propranolol is a _____ B Antagonist, meaning it has no __________ activity and therefore not a ______ agonist. |
|
Definition
| Pure antagonist, no Intrinsic Sympathomimetic Activity (ISA) (i.e. not a partial agonist) |
|
|
Term
| Propranolol selective or non-selective for _____ receptors. |
|
Definition
| non-selective for B receptors |
|
|
Term
| Propranolol has high ____ and therefore enters __________. |
|
Definition
| High lipid solubility - Enters gut & CNS |
|
|
Term
| Propranolol has _____ first pass metabolism, causing ________ |
|
Definition
|
|
Term
| Propranolol exhibits ______ activity, giving it ______ effects. |
|
Definition
Has membrane-stabilizing activity
Quinidine-like effects, |
|
|
Term
| Propranolol exhibits membrane-stabilizing activity giving it Quinidine-like effects, meaning it causes _______ and acts as a ________ and therefore should be avoided in the treatment of _______. |
|
Definition
Na+ channel blockade, (local anesthetic)
•Avoid for topical administration to eye (glaucoma Tx) |
|
|
Term
| Nonselective B antagonists and their significance: __________. |
|
Definition
–Propranolol
–Nadolol: long half-life
–Timolol: low local anesthetic action - use in glaucoma (can't with Propranolol)
–Pindolol: ISA (Propranolol has none, pure) |
|
|
Term
| Selective B1 antagonists and their significance: __________. |
|
Definition
–Atenolol: low lipid sol.
–Betaxolol: opthal.
–Esmolol: short half-life
–Metoprolol |
|
|
Term
| B Antagonists have adverse effects on the cardivascular system of: _______. |
|
Definition
•Induce CHF or bradycardial arrhythmia
•Sudden withdrawal - in anginal patients may cause sudden death |
|
|
Term
| The sudden withdrawal of B Antagonists from angina pts. is due to ________. |
|
Definition
| receptor supersensitivity |
|
|
Term
| B Antagonists have adverse effect of increasing _______ levels. |
|
Definition
|
|
Term
| B Antagonists non-cardio adverse effects: ________. |
|
Definition
–Bronchiospasm
–CNS - sleep disturbance, depression
–(Mask symptoms & recognition of hypoglycemia) |
|
|
Term
| B Antagonists are the first choice in treating __________ if the patient is _______ stable. |
|
Definition
| hypertensive (1st choice if stable angina present) |
|
|
Term
| B Antagonists being used to treat hypertension in older patients is often used with ______ as the 1st choice. |
|
Definition
|
|
Term
| B Antagonists cardiovascular treatments: ________. |
|
Definition
Hypertension
angina
heart failure – both acute (MI) & chronic |
|
|
Term
| B Antagonists treat heart failure (both acute (MI) & chronic) by ___________. |
|
Definition
| Decrease heart work & protect against arrythmias |
|
|
Term
| B Antagonists are contradicted in pts with: ________. |
|
Definition
Asthma
Diabetes until recently many felt caution needed - still caution in persons with frequent hypoglycemia |
|
|
Term
| B Antagonists are contradicted in Asthma pts. because ____________. |
|
Definition
| bronchoconstriction (adverse effect of bronchospasm) |
|
|
Term
| B Antagonists are contradicted in pts. with Diabetes because ________. |
|
Definition
•(mask symptoms of insulin-induced hypoglycemia & glycogenolysis inhibited)
•(augment insulin-induced hypoglycemia) |
|
|
Term
| B Antagonists effect on cholesterol levels? |
|
Definition
|
|
Term
| B Antagonists are less effective in treating ______ in _____ race. |
|
Definition
|
|
Term
| Phenoxybenzamine MOA: ________. |
|
Definition
|
|
Term
| Phenoxybenzamine used to treat: __________. |
|
Definition
- symptomatic management of pheochromacytoma
- treatment of hypertensive
crisis caused by sympathomimetic amines
- micturition problems |
|
|
Term
| Phenoxybenzamine is a irreversible/reversible a antagonist. |
|
Definition
|
|
Term
| Phenoxybenzamine overall results in a decrease/increase in ________ by ________. |
|
Definition
| decrease vasocon. by Epi & NE |
|
|
Term
| Phenoxybenzamine Adverse effects: ________. |
|
Definition
- decrease blood pressure
- postural hypotens.
- reflex CV stim.
- pupil constriction
- partial agon/antag. (not pure) at 5HT2A |
|
|
Term
| Phenoxybenzamine contradicted in _______. |
|
Definition
|
|
Term
| Prazocin MOA: __________. |
|
Definition
|
|
Term
| Prazocin clinical use: ___________. |
|
Definition
- hypertension
- PTSD
- benign prostatic hyperplasia
- scorpion stings |
|
|
Term
| Prazocin causes _____ muscle to relax/contract resulting in a ________. |
|
Definition
smooth muscle to relax
drop in BP |
|
|
Term
| In addition to being a a1 antagonist, Prazocin, inhibits ________. |
|
Definition
| PDE (phosphodiesterase) breaks down cAMP |
|
|
Term
| Prazocin Adverse effects: __________. |
|
Definition
- postural hypotens. (same as Phenoxybenzamine, non selective a antag)
- syncope |
|
|
Term
|
Definition
|
|
Term
| Yohimbine Clinical Uses: ________. |
|
Definition
- sexual dysfunction*
- diabetic neuropathy
- postural hypotension (side effect of a1 antagonist and non-selective a) |
|
|
Term
| Yohimbine decreases/increases _______ outflow. |
|
Definition
|
|
Term
| Yohimbine overall effect? |
|
Definition
(α2 antagonist)
increases HR and BP (Prazocin: α1 antagonist lowers BP) |
|
|
Term
| Yohimbine Adverse Effets: _______. |
|
Definition
-Increase motor activity
- tremors
- also antagonist of
most 5HT receptors (same w/ Phenoxybenzamine a nonselective a antagonist)
- anxiety
- insomnia |
|
|
Term
| Propranolol MOA: ________. |
|
Definition
| B antagonist (prototypical one) |
|
|
Term
| Propranolol clinical uses: ________. |
|
Definition
- hypertension
- angina
- arrhythmias / tachycardia
- pheochromocytoma
- prophylaxis of migrane
- tremor, Parkinson, alcohol WD* |
|
|
Term
| Propranolol selective or non-selective B antagonist? |
|
Definition
|
|
Term
| Propranolol relaxes/constricts _____ muscle. |
|
Definition
| constricts bronchial smooth muscle |
|
|
Term
| Propranolol Adverse effects: ________. |
|
Definition
| - CV: angina (don't treat HT unless angina stable) |
|
|
Term
| Propranolol Contradictions: _______. |
|
Definition
- congestive heart failure
- COPD (broncho constrictor) |
|
|
Term
| Timolol MOA: ___________. |
|
Definition
|
|
Term
| Timolol Clinical uses: ___________. |
|
Definition
open-angle glaucoma
Ischemic Heart disease |
|
|
Term
| Timolol can be used to treat open-angle glaucoma, unlike ______, bc of its quidine like effect. |
|
Definition
|
|
Term
| Timolol is better tolerated than _______ for treating open-angle glaucoma. |
|
Definition
| Pilocarpine (a parasympathetic akaloid) |
|
|
Term
| Timolol adverse effects: ________. |
|
Definition
- cardiac arrhythmias
- bradycardia (used to treat tacha)
- blurred vision
- bronchospasms |
|
|
Term
| Timolol Contraindications: __________. |
|
Definition
bronchial asthma,COPD (bronchoconstrictor)
heart failure |
|
|
Term
| Carvedilol MOA: ________. |
|
Definition
|
|
Term
| Carvedilol clinical use: ________. |
|
Definition
- Heart failure progression:
reduce sudden death
rate
- Post MI: reduce death rate
-Hypertension |
|
|
Term
| Carvedilol treats hypertension by reducing: ___________. |
|
Definition
| reduce bp & heart rate, plasma renin activity & renal vascular resistence |
|
|
Term
| Carvedilol MOA: α1,b antagonist (a ______ mixture) |
|
Definition
|
|
Term
| Carvedilol adverse effects: __________. |
|
Definition
bradycardia & hypotension (reduces BP and HR)
-CNS: dizziness, abnormal vision
-GI disturbance: diarrhea, nausea, vomiting |
|
|
Term
| Carvedilol Contraindications: ________. |
|
Definition
-bronchial asthma (B2 antagonist),
AV block (B1), severe bradycardia (B1), severe renal impairment (decreases renin and renal vascular resistance) |
|
|
Term
| Atenolol MOA: __________. |
|
Definition
|
|
Term
| Atenolol clinical uses: ___________. |
|
Definition
hypertension
- elderly patients with
isolated systolic HT
- angina
- post MI treatment (Carvedilol B antagonist also) |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Atenolol can be used to treat ______ in the elderly when combined with ________. |
|
Definition
isolated systolic HT
diuretic |
|
|
Term
| Atenolol Adverse effects: ________. |
|
Definition
- CV: bradycardia (B1)
-impotence (Phenoxybenzamine gets a1 in penis) don't know why these B1 does though? |
|
|
Term
| Atenolol Contraindications: ________. |
|
Definition
- bradycardia (adverse effect)
- pregnancy |
|
|
Term
|
Definition
|
|
Term
| Esmolol clinical use: ________. |
|
Definition
supraventricular tachycardia (e.g., atrial fibrillation & atrial flutter)
reduce systolic pressure (Atenolol B1 antagonist also) |
|
|
Term
| Esmolol length of action? |
|
Definition
|
|
Term
| Esmolol Adverse effects: __________. |
|
Definition
-CV: cardiac arrest,hypotension peripheral ischemia
CNS: dizziness,headache, convulsion, anxiety, depression, confusional state, agitation |
|
|
Term
| Esmolol Contraindications: ________. |
|
Definition
- bradycardia
- cardiogenic shock
- pulmonary hypotension |
|
|
Term
| Metoprolol MOA: __________. |
|
Definition
|
|
Term
| Metoprolol clinical use: ________. |
|
Definition
-Hypertension
- Angina
- Heart failure |
|
|
Term
| Metoprolol is more effective at treating HT when? |
|
Definition
| comb. w/ diuretic (same with Atenolol) |
|
|
Term
| Metoprolol Adverse effects: __________. |
|
Definition
- CV: slow heart rate, symptoms of heart
failure
- CNS: dizziness, drowsiness, tiredness, shortness of breath, mood swings, depression (same with Esmolol) |
|
|
Term
| Metoprolol Contraindications: ________. |
|
Definition
- severe bradycardia,
cardiogenic shock, |
|
|
Term
| Betaxolol MOA: __________. |
|
Definition
|
|
Term
| Betaxolol clinical use: ________. |
|
Definition
chronic open angle glaucoma1
hypertension2 |
|
|
Term
| Betaxolol Adverse effects: __________. |
|
Definition
- ocular discomfort1
- bradycardia2
- depression2
- bronchospasm2 |
|
|
Term
| Betaxolol Contraindications: ________. |
|
Definition
|
|
Term
| Butoxamine MOA: ________. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Clozapine Clinical Uses: __________. |
|
Definition
|
|
Term
| Clozapine has weak action on __________. |
|
Definition
| all other DA receptors (α adrenergic, cholinergic, H1 and 5HT as well). |
|
|
Term
| Clozapine Adverse effects: __________. |
|
Definition
- CV: tachy., angin.
- CNS; drowsy, dizzy |
|
|
Term
| Clozapine Contraindications: ________. |
|
Definition
- epilepsy
- CNS depression
- myeloprolif. disor. |
|
|
Term
| BHP treated with ________ or __________ (____________). |
|
Definition
•5-a-reductase inhibitors (Finasteride)
•a1 adrenergic antagonists:
Prazocin and Tamsulosin |
|
|
Term
| Acetylcholine (ACh) acts where? |
|
Definition
postganglionic parasympathetic fibers
Autonomic ganglia
Adrenal medulla
Motor endplate
Sweat glands (Sympathetic postganglionic nerve terminals ACh) |
|
|
Term
| Two basic types of ACh release: _______. |
|
Definition
|
|
Term
| Spontaneous ACh release is ____+ independent/dependent & Evoked ACh release is ____+ independent/dependent. |
|
Definition
Spontaneous- Ca2+- independent
Evoked- Ca2+- dependent |
|
|
Term
| Evoked ACh release occurs where? |
|
Definition
| from synaptic vesicles by exocytosis |
|
|
Term
| Receptor types responding to ACh: __________. |
|
Definition
|
|
Term
| ACh breakdown mediated by ___________. |
|
Definition
| acetylcholinesterase (AChE) |
|
|
Term
| Muscarinic Receptor Mediated Responses ______ acting & ______ lasting. |
|
Definition
|
|
Term
| _______ - classical competitive antagonist for Muscarinic Receptor. |
|
Definition
|
|
Term
| Muscarinic Receptors located: ________. |
|
Definition
| smooth muscle, glands, & the heart |
|
|
Term
| Atropine- a competitive blocker at ______ muscarinic receptors |
|
Definition
|
|
Term
| ________ - a competitive antagonist at M1 receptors |
|
Definition
|
|
Term
| Pirenzepine acts at M_ receptors in _______ & ________. |
|
Definition
1
myenteric plexus (gut muscles) and in cerebral cortex |
|
|
Term
| Known Muscarinic receptor agonists don't/do discriminate between the muscarinic receptor subtypes. |
|
Definition
|
|
Term
| Nicotinic Receptor Mediated Responses ______ acting & ______ lasting. |
|
Definition
|
|
Term
| Nicotinic Receptor Mediated Responses inhibitory/excitatory? |
|
Definition
|
|
Term
| Muscarinic Receptor Mediated Responses inhibitory/excitatory? |
|
Definition
|
|
Term
| Nicotinic Receptor located: _______. |
|
Definition
| autonomic ganglia, adrenal medulla, motor endplate region |
|
|
Term
| Nicotinic receptors on ______ & ______ are similar but differ from those at ___________. |
|
Definition
drenal medulla & ganglia
motor-endplate region |
|
|
Term
| Nicotinic receptors on ganglia- stimulated by _____________. |
|
Definition
| dimethyl 4-phenyl piperazinium (DMPP) |
|
|
Term
| Classical nicotinic receptor antagonist at ganglia: ________, which acts non-competitively/competitively |
|
Definition
hexamethonium (C-6)
competitively |
|
|
Term
| Classical nicotinic receptor antagonist at motor endplate region: _______, which acts non-competitively/competitively |
|
Definition
d-tubocurarine
competitively |
|
|
Term
| Is ACh used therapeutically? Not useful because of its ________. |
|
Definition
|
|
Term
| Muscarinic Receptor Agonists: _____________. |
|
Definition
ACh
Methacholine+
Carbachol+
Bethanechol+
Pilocarpine
Cevimeline |
|
|
Term
| Which Muscarinic Receptor Agonist is broken down by AChE? |
|
Definition
|
|
Term
| Methacholine+ is antagonist/agonist at? |
|
Definition
| mainly agonist muscarinic |
|
|
Term
|
Definition
diagnose bronchial hyperactivity & asthmatic
diagnosis of achalasia |
|
|
Term
| Methacholine+ used to diagnosis achalasia when it causes? |
|
Definition
|
|
Term
| Carbachol+ shorter/longer duration than Methacholine+ and why? |
|
Definition
| Longer, not hydrolyzed by AChE |
|
|
Term
| Methacholine+ is antagonist/agonist at? |
|
Definition
| agonist at both muscarinic and nicotinic |
|
|
Term
| Carbachol+ is clinical use? |
|
Definition
| topically in the eye for wide angle (open-angle) glaucoma |
|
|
Term
| ______ is the best among the three synthetic Muscarinic Receptor Agonists. |
|
Definition
Bethanechol+
(Bethanechol+, Methacholine+ Carbachol+) |
|
|
Term
| Bethanechol+ is antagonist/agonist at? |
|
Definition
|
|
Term
| Bethanechol+ Stimulates __________. |
|
Definition
| smooth muscle of bladder and G.I. tract preferentially over heart |
|
|
Term
| Bethanechol+ clinical use? |
|
Definition
| treat postoperative distension, gastric atony, urinary retention, reflux esophagitis |
|
|
Term
| Bethanechol+ adverse effects? |
|
Definition
| gastric distress & bronchiole constriction |
|
|
Term
| _______ is a naturally occurring muscarinic agonist which is not charged. |
|
Definition
|
|
Term
| Pilocarpine is the ______ drug of choice for treating _____________. |
|
Definition
| ***Cholinergic drug of choice for treatment of wide angle glaucoma (Carbachol+ can also be used) |
|
|
Term
| Pilocarpine in combination with ________ is used to treat ________ preoperatively. |
|
Definition
physostigmine (reversible cholinesterase inhibitor)
narrow angle glaucoma until
surgery |
|
|
Term
| Pilocarpine is also used to treat _______ that follows _________ treatments. |
|
Definition
xerostomia
head & neck radiation treatments |
|
|
Term
| Xerostomia is an autoimmune disease that ________. |
|
Definition
| decreases salivary secretions |
|
|
Term
| Pilocarpine side effects? |
|
Definition
| irritability & restlessness |
|
|
Term
_______ is a relatively new drug used
to treat dry mouth associated with Sjogren's syndrome. |
|
Definition
|
|
Term
| Cevimeline is antagonist/agonist at? |
|
Definition
|
|
Term
| Side Effects of Muscarinic Stimulants (agonists)? |
|
Definition
| Urinary frequency, diarrhea, bronchiole constriction, salivation, nausea, vomiting, bradycardia, increased HCl secretion |
|
|
Term
| Use of cholinergic stimulants contraindicated in: __________. |
|
Definition
| asthma, hyperthyroidism, & peptic ulcer |
|
|
Term
| Anti-Muscarinic Drugs Two major ones: _______. |
|
Definition
|
|
Term
Atropine & Scopolamine: ________.
Antagonist/Agonist of ______
Acting?
Side effect?
Competitive/uncompetitive? |
|
Definition
Anti-Muscarinic
Atropine- long acting & tends to cause anxiety- competitive antagonist
Scopolamine- shorter acting and tends to cause sedation-competitive antagonist |
|
|
Term
|
Definition
|
|
Term
| Atropine is used for Retinal examination, because it causes? |
|
Definition
| mydriasis & loss of accommodation |
|
|
Term
| Atropine is an antidote for? |
|
Definition
| organophosphate intoxication |
|
|
Term
| Atropine is used as an adjunct with ________ in the treatment of _________. |
|
Definition
AChE inhbitors
myasthenia gravis |
|
|
Term
Atropine is used as an adjunct for myasthenia gravis to reduce _______ receptor side effects due to AChE
inhibition at ______ & _______ organs. |
|
Definition
muscarinic
GI tract & bladder |
|
|
Term
| Scopolamine is used to treat? |
|
Definition
motion sickness
bedwetting (enuresis) |
|
|
Term
| Scopolamine gives fewer side effects when administered ______ as ________. |
|
Definition
| topically (rather than orally) Transderm Scop® |
|
|
Term
|
Definition
|
|
Term
| Scopolamine is used to treat bedwetting (enuresis), because it blocks ________ receptors & increases ________. |
|
Definition
muscarinic
bladder capacity |
|
|
Term
| ______ is used in retinal examination in adults, because it is shorter acting than atropine. |
|
Definition
| Homatropine (Anti-Muscarinic ) |
|
|
Term
| ______ is used in retinal examination in adults, because it is shorter acting than atropine & Homatropine. |
|
Definition
| Tropicamide (Anti-Muscarinic ) |
|
|
Term
| Glycopyrrolate+ drug type? |
|
Definition
|
|
Term
| Glycopyrrolate+ reduces _______ and is therefore useful in treating ___________. |
|
Definition
| stomach acid production-used for treating peptic ulcer |
|
|
Term
| Glycopyrrolate+ can be used as a ______ medication surgery to ___________. |
|
Definition
| preanesthetic medication during surgery to dry up mouth, throat & stomach |
|
|
Term
| Glycopyrrolate+ can be injected during surgery to reverse ______-induced _______. |
|
Definition
| vagal-stimulated bradycardia |
|
|
Term
| Glycopyrrolate+ can be used to treat ________ in addition to peptic ulcer disease. |
|
Definition
|
|
Term
| Glycopyrrolate+ drug type? |
|
Definition
|
|
Term
| Unlike the other Anti-Muscarinics, Glycopyrrolate+ has less __________. |
|
Definition
| CNS side effects (unlike atropine, scopolamine) |
|
|
Term
| ________ & ____________ can be used to treat irritable bowel syndrome. |
|
Definition
| Methantheline+ & Propantheline+ |
|
|
Term
| Methantheline+ & Propantheline+ drug type? |
|
Definition
|
|
Term
| Methantheline+ & Propantheline+ do what? |
|
Definition
| Block ganglionic transmission and*** antagonize ACh at muscarinic receptors |
|
|
Term
| Anti Muscarinic Drugs very dangerous in patients with ________. |
|
Definition
|
|
Term
| ______, _______, & ________ have enough antimuscarinic receptor activity to cause atropine- like toxicity |
|
Definition
| antihistamines, phenothiazines, & tricyclic antidepressants |
|
|
Term
| Anti Muscarinic Drugs Contraindicated in: _____________. |
|
Definition
narrow angle glaucoma
prostatic hypertrophy, achalasia, intestinal atony |
|
|
Term
| ______ Indicative of atropine toxicity & especially dangerous in young children |
|
Definition
|
|
Term
| With Atropine flush, ________ must be done to save life. |
|
Definition
| Body temp must be reduced (e.g., ice bath |
|
|
Term
| Classical ganglionic blocker:_________ - competitive antagonist |
|
Definition
|
|
Term
All clinically useful ganglionic blockers
act at ______ receptors |
|
Definition
|
|
Term
| Primary Pathway of Ganglionic Transmission mediated by __________. |
|
Definition
|
|
Term
| Primary Pathway of Ganglionic Transmission fast or slow? |
|
Definition
| fast excitatory potential |
|
|
Term
| Secondary Pathway of Ganglionic Transmission fast or slow? |
|
Definition
| Slow excitatory/inhibitory potential |
|
|
Term
| Slow excitatory potential of Secondary Pathway of Ganglionic Transmission is produced by action of _______ onto _______ receptors. |
|
Definition
|
|
Term
| Slow inhibitory potential of Secondary Pathway of Ganglionic Transmission is produced by action of _______ onto _______ receptors. |
|
Definition
|
|
Term
| Slow inhibitory potential produced by release of ACh from preganglionic nerve terminal, activation of M2 receptor on – SIF cell, and release of _______ or ________ which hyperpolarize ganglia |
|
Definition
| norepinephrine or dopamine |
|
|
Term
|
Definition
| nterneurons of the sympathetic ganglia (postganglionic neurons |
|
|
Term
| _______ blocks dopamine action at ganglia. |
|
Definition
|
|
Term
| Metoclopramide blocks dopamine action at ganglia, which would typically __________. |
|
Definition
|
|
Term
| Metoclopramide blocks dopamine action at ganglia, which leads to increase ________, without _________. |
|
Definition
| G.I. tract motility without stimulating HCl secretion |
|
|
Term
| Ganglionic Stimulants are not used? |
|
Definition
|
|
Term
| Ganglionic Stimulants example? |
|
Definition
|
|
Term
| Nicotine is considered a nonselective/selective _________ receptor antagonist/agonist. |
|
Definition
| nonselective nicotinic Receptor agonist (ganglionic stimulant) |
|
|
Term
| Nicotine activates nicotinic Rc’s on _________. |
|
Definition
|
|
Term
Nicotine activates nicotinic Rc’s on
autonomic ganglia, stimulating
transmission through __________. |
|
Definition
| both parasympath & sympath ganglia |
|
|
Term
| Overall Cardiovascular effect of nicotine? |
|
Definition
|
|
Term
| Cardiovascular: Nicotine increases ________ and ________ by stimulating the ganglia of ______ and ______. |
|
Definition
TPR & Ventricular Contractions
Venous Return and Heart |
|
|
Term
| Overall Respiratory effect of nicotine? |
|
Definition
|
|
Term
| nicotine increases respiration by? |
|
Definition
| activate chemoreceptors in aortic arch & carotid body |
|
|
Term
| In GI tracct ________ has dominant tone in GI tract. |
|
Definition
|
|
Term
| Overall GI effect of nicotine? |
|
Definition
| increase G.I. tract motility & HCl release (Para is dom tone of GI) |
|
|
Term
| Overall CNS effect of nicotine? |
|
Definition
emesis by acting at chemoreceptor trigger zone
Increases ADH release |
|
|
Term
| The Increases ADH release from Nicotine causes? |
|
Definition
|
|
Term
| At high toxic doses, Nicotine becomes? |
|
Definition
| ganglionic blocker at high doses |
|
|
Term
| Nicotine can enter the _____ easily? |
|
Definition
|
|
Term
| Toxic Nicotine kills by __________. |
|
Definition
|
|
Term
| Nicotine in high doses _____ nicotinic receptors at medulla oblongata causing ___________. |
|
Definition
desensitizes
to stop breathing |
|
|
Term
| Nicotine in high doses _____ nicotinic receptors at motor endplate causing ___________. |
|
Definition
desensitizes
paralysis of diaphragm & intercostal muscles |
|
|
Term
| __________ stimulates ganglionic transmission without causing receptor desensitization- only used as laboratory tool |
|
Definition
| DMPP (dimethyl 4-phenyl piperazinium ion) |
|
|
Term
| DMPP (dimethyl 4-phenyl piperazinium ion is specific for _____ receptors on _______ and _______ (doesn't affect _______). |
|
Definition
nicotinic
ganglia & adrenal medulla, not NMJ |
|
|
Term
| DMPP (dimethyl 4-phenyl piperazinium ion) Cardiovascular effects? |
|
Definition
|
|
Term
| Ganglionic Blockers are Only used chronically to control ________ in patients with __________. |
|
Definition
blood pressure
acute dissecting aortic aneurysm |
|
|
Term
| Ganglionic Blockers can be used to produce ______ during surgery to minimize ____________. |
|
Definition
hypotension
minimize hemorrhage at operative site |
|
|
Term
| Ganglionic stimulants: ________. |
|
Definition
|
|
Term
| Ganglionic Blockers: ____________. |
|
Definition
Tetraethylammonium+ (TEA)
Hexamethonium+ (C-6)
Trimethaphan+
Mecamylamine |
|
|
Term
Ganglionic Blockers:
Tetraethylammonium (TEA): ______ charged and & ______ acting. |
|
Definition
1. Positively charged, so does not cross BBB
2. Short duration of action |
|
|
Term
Ganglionic Blockers:
Hexamethonium (C-6): ______ charged and & ______ acting & ______ absorbed. |
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Definition
1. Positively charged, so does not cross BBB
2. Long duration of action
3. Not well absorbed |
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Term
| ______ is only uncharged Ganglionic Blocker that can cause CNS effects. |
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Definition
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Term
| Side Effects of Ganglionic Blockers. |
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Definition
interfere with body's ability to maintain
homeostasis:
1. Abolish autonomic reflexes such as
miosis & accommodation of eyes
2. Reduces transmission through division
of ANS which is dominant to produce
physiological responses (e.g., will
generally increase heart rate by blocking
dominant parasympathetic tone at SA
node)
Also, gastrointestinal tract motility is inhibited,
causing constipation.
- orthostatic hypotension (due to block in
sympathetic tone to veins),
- urinary retention (due to block in
parasympathetic tone) &
- impotence due to block in both
parasympathetic & sympathetic control of
erection & ejaculation |
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