Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
350 Cards in this Set
- Front
- Back
|
Sensory impulses go by what to CNS
|
afferent nerve,
|
|
|
What are NT characteristics
|
chemical, unidirectional, sodium-dependent, and caclium dependent
|
|
|
What is unidirectional
|
nerve releases and affect tissue, (NOT other way around)
|
|
|
What is involved in docking, fusion and release of NTs
|
proteins on outside of vesicles,a nd proteins inside nerve terminal
|
|
|
What is a protein on outstide of vesicle
|
synaptobrevin
|
|
|
What is a protein inside of nerve terminal that helps with fusion
|
syntaxin
|
|
|
What is general mechanism of NT synthesis and release
|
1. NT stored in Nerve ending, and is release by stimulation, diffuses across synpatic cleft,
|
|
|
What happens after NT diffuses across synatpic cleft
|
activates recpetors on postsynpatic cell to elicit response
|
|
|
The effect on the cell is dictated by
|
receptors be activated and intracellular 2nd messenger cascade acitavted
|
|
|
If different nerve innervate a tissue, the net effect will be dtermined by
|
balance of excitorary and inhibitory inputs
|
|
|
What are efferent 2 divisions of PNS
|
somatic and autonomic
|
|
|
What tissues are innervated by somatic nerves and automic nerves
|
Somatic-Skeletal muscle
autonomic-viscera |
|
|
What does somatic and autonomic nerves control
|
Somatic-volunatry
Autonomic-INvoluntary |
|
|
What is anatomy of somatic nerves and autonomic nerves
|
somatic-cell bodies inCNS
autonomic nerves-preganglionic cell bodies in CNS |
|
|
What si nueroeffector junction of somamtic nerves, and autonomic nerves
|
somatic--specialized (terminal arborizations)
autonomic-NOT specialized "en passant innervation" |
|
|
What is physiology of somatic nerves adn autonomic nerves
|
somatic--breathing, motion
autonomic-visceral homeostatis |
|
|
What are effect of somtic nerves
|
EXCITATORY
|
|
|
What are effects of autonomic nerves
|
excitory or inhibitory
|
|
|
Where does ANS originate
|
in nuclei within CNS
|
|
|
What types of nerve comprise the ANS
|
preganglionic and postganglionic nerves
|
|
|
If gnaglionic transmission is blocked, what nerves are affected
|
only autonomic
|
|
|
Autonomic nerves are divided on the basis of
|
anatomic or NT criteria
|
|
|
What is anatmoic classification based solely on
|
location in the CNS from which the preganglionic nerve emerges from the CNS
|
|
|
Where can the preganglinic nerve emerge
|
next to spinal cord or next to tissue
|
|
|
PNS divides into somatic, and autonomic, which further divides
|
ANS divides into parasympathic and sympathetic
|
|
|
Where do sympathetic pregranflionic fivers exit
|
exit CNS via thoracic and lumbar spinal nerve
|
|
|
Which is longer in sympathetic pregranglinoic or postganglionic
|
postganlionic nerve
|
|
|
In sympathetic may one preganglionic axon synapse with many postganglinoic nerves
|
YES
|
|
|
Characteristic of sympathetic Neuroeffector junction
|
not specialized and varies in size
|
|
|
What happens in smapathetic if preganglionic can connect with 20 postganglioic neurons
|
diffuse response
|
|
|
Where do preganglionic PARAsympathetic fibers exit
|
via cranial and sacral spinal nerves
|
|
|
Where are ganglia genrally located
|
in tissue
|
|
|
What is characterisitc of postganlgionic nerve in parasympathetic
|
SHORT
|
|
|
Are there ONLY single conections of preganglionic to postganglionic in what
|
YES---parasympathetic
|
|
|
Where are somatic ganglion
|
NO--GANGLION--only para symathic and sympathic
|
|
|
Somatic axons dives into many branches, each inneravate
|
ONE muscle fiber
|
|
|
What are the NTs of the PNS
|
cholingeric an adregneric
|
|
|
What is cholingeric NT
|
Ach
|
|
|
What is the NT of all preganglionic nerves
|
AcH
|
|
|
AcH is NT of
|
ALL preganglinoic nerves, and all PARAsympathetic postganglionic nerves, adn FEW sympathic postganglionic nerves and ALL SOMATIC NERVES
|
|
|
What are NTs of adrenergic
|
CCAs
|
|
|
What are the CCA
|
norepniherine, epinherine, and (dopamine)
|
|
|
What is the NTs of most SYMpathetic postganlionic nerves
|
CCAs
|
|
|
Orgin of CCA
|
adrenal medulla
|
|
|
All efferent nerves leaving the CNS are
|
cholinergic or Ach
|
|
|
All postganlionic nerves are
|
cholinergic or aderegic
|
|
|
Which sympathetic nerves are cholinergic
|
ALL
|
|
|
What happens to pupils during sympathetic
|
DILATION
|
|
|
What happens to heart during sympathetic
|
increased HR, increase cardiac conduction, increased contractility
|
|
|
What increase salivation, nasal secrtions and tear formation
|
PARAsymathetic
|
|
|
What does PARAsympathetic do to heart
|
decrease HR, conduction---NO EFFECT ON CONTRACILITY
|
|
|
What does sympatehtic do to blood vessels and blood vessels in SKM
|
constriction of blood vessels,and dialation of SKM
|
|
|
What symstion causes porstate capsule contraction
|
sympathetic
|
|
|
What system causes bronchoconstriction
|
parasympathetic
|
|
|
What system causes erection
|
parasympathetic
|
|
|
What system causes ejaculation
|
sympathetic
|
|
|
What system causes uterine smooth muscle relaxation
|
sympatehtic
|
|
|
What system increases sweating
|
sympathetic
|
|
|
What system causes glycolysis and gluconeogensis
|
sympathetic
|
|
|
Can symathetic/parasympathetic work together or against each other
|
YES
|
|
|
What are the nonadrenergic noncholinergic nervous systems
|
tachykinergic nerves
NO enteric nervous system |
|
|
What are acute/reversible dysautonomias
|
acute pandysautonomia, Guillain-Barre syndrome, vasovagal syndrome
|
|
|
What are chronic/progessive dysautonomias
|
Shy-drager syndrome, postural orthostatic tachycardia
|
|
|
What are indirect dysautonomia
|
spinal cord damage, diabetes, alcoholism
|
|
|
What is drug indiced dysautonomia
|
caffeine, OTC medications
|
|
|
What happens when you have a full bladder with a spinal cord injury
|
Increase in sympathetic outflow, b/c blocked from going to brain, causing widespread vasoconstrtion, leading to hypertension, which baroreceptor tell brain and decrease HR
|
|
|
What is cause of acute pandysautonomia
|
autoimmune reaction whre antibodies bind ganglionic nicontinic receptors
|
|
|
The more antibodies what happens
|
more autonomic blocked
|
|
|
What are symptoms of aute pandysautonomia
|
FAG DAD IO
Fixed heart rate (both blocked), anhydrosis, GI dysfunction, dry eyes, altered bowel/blader, dry mouth, imparied pupillary reflex to light, and orthostatic hypotension |
|
|
Orthostatic hypotension is greatest sign of autepandysautonomia, by what blockage
|
sympathetic blockage,
|
|
|
If BP decreases, what should be activated
|
sympathetic
|
|
|
What are 2 cases in which sympathetic is not activated
|
autonomic failure and vasovagal syncope
|
|
|
What causes Guillain-Barre Syndrome
|
autoimmume reaction against myelin sheath-leading to nerve demyelination
|
|
|
Guillain-Barre Syndrome primarily affect
|
somatic nerves (most likely to have mylein)
|
|
|
What are symptoms of Guillan Barre Syndrome
|
DART PPD HU
diffuse muscle weakness, anhydrosis, repiraotry failure, tachycardia, parethesia, pain, dysreflexia, hypertension and urinary hesitancy |
|
|
What causes the diffuse muscle weakness and respiratory failure of Guillain 0Barre syndrome
What is causing paresthesia, pain and dysreflexia issues |
blockage of sympathetic
sensory blockage |
|
|
What is Familial dysautonomia AKA
|
Riley-Day syndrome
|
|
|
What is cause of Familia dysautonomia (Riley-Day)
|
incomplete development of sensory and ANS, hereditary
|
|
|
What are symptoms of Familial dysautonomia
|
BCP PIGS DEL
Breath-holding episodes corenal anestesia poor suck and swallow as infants Poor growth incapable of producing tears GI dysmotility sweating/spinal curvature Labile blood pressure |
|
|
Labile blood pressure is assoicated with
|
Familial dysautonomia and sympathetic
|
|
|
What is cause of Horner's syndrome
|
interruption of the oculo-sympathetic nerve pathway
|
|
|
What are symptoms of Horner's syndrome (block sympathetic)
|
facial anhydrosis
miosis and ptosis dilation of arterioles |
|
|
What is cause of progressive Shy-drager Syndrome
|
failure of CNS and ANS
|
|
|
Symptoms of Shy-drager syndrome
|
PUP parkinsonian symptoms, loss of balance/ and unstable pressure leads to severe HA, and postural hypotension
|
|
|
What is cuase of Postural Orthostatic Tachycardia Sydrome
|
restricted from of autoimmune neuropathy
|
|
|
What happens in postural orthostatic tachcardia syndrome
|
inapproprate tachycardia response to orthostatis
|
|
|
What are symtoms of Postural orthostatic tachycardia
|
excess tachycardia, dry eyes mouth and N/V
|
|
|
What is cause of Vasovagal syndrome
|
sudden increase in vagal activation coupled with large drop in PVR
|
|
|
What are symptoms of vasovagal syndrome
|
bradycardia, and fainting
|
|
|
Is fainting a good homeostaic response
|
YES
|
|
|
What is cause of Diabetic neuropathy
|
hyperglycemia causing alter autonomic, sensory and somatic nerve function
|
|
|
What are symtoms of diabetic neuopathy
|
PPP excruiating pain, paresthesisa, burning, loss of pain sensation/temperature
|
|
|
What are the general mechanism of adrenergic
|
syntheis, storage, release, termination of acition, receptor interaction and 2nd messenger cascade activation
|
|
|
The pharmacological actions of CCAs on the effector tissue are dictated in large part by the specfic types of
|
adrenegic recetpors present on the cell
|
|
|
Often are there mroe than one type of adrenergic receptor on a cell--do they often have opposing actions
|
YES
|
|
|
Blood vessel have
|
alpha 1-contstion
beta2--dilate |
|
|
CCAs are synthesised in multistep process from
|
tyrosine
|
|
|
What happens 1st
|
tyrone is taken up into nerve terminal
|
|
|
What happens after tyrosine is taken up into nerve terminal
|
Tyrosine is converted to DOPA by tyrosine hydroxylase
|
|
|
Tyrosine hydroxylase is activated by
|
nerve stimulation or adrenal stimulation
|
|
|
What type of enzyme is Tyrosine hydroxylase
|
cAMP-dependent protien kinase
protein kinase C Ca++/calmodulin dependent |
|
|
What is the rate limiting step in CCA synthetisis
|
tyrosine hydroxylase
|
|
|
DOPA is converted into
|
Dopamine by DOPA decarboxylase
|
|
|
What also does DOPA decaroxylase do, besides converting DOPA to DOPAMINE
|
converts alpha methyldopa to alpha methly dopamine
|
|
|
What is alpha mehtly dopamine converted into and do
|
alpha methly NE, by dopamine B-hydroxlase, A2 agonist, which decrease sympathetic function
|
|
|
DOPA decarboxylase is inhibted by
|
alpha mehtlydopa and carbidopa
|
|
|
What does carbidopa do
|
prevents PERIPHERAL L-DOPA being converted to Dopamine
|
|
|
Dopamine is then converted into
|
NE by dopamine Beta hydroylase
|
|
|
Where is dopamine B-hydroxlase located
|
inside vesicle
|
|
|
NE is converted to
|
epineprhine by phenylethanolamine N-methly transferase (PE-N-methylransferase)
|
|
|
Where is phenylethanolamine N-methaly transferase (PE-N-methyltransferase
|
located in adrenal chromaffin cells
|
|
|
Tyrosine taken up in nerve, converted into Dopamine Storage---50% of dopamine is taken up into vesicles in nerve terminal by
|
Vesicular monoamine transport VMAT-2
|
|
|
What is Vesicular monoamine transports (VMAT-2)
|
ATP dependent prton translocase
|
|
|
What is exchanged in VMAT-2,
|
2H+ leave cell, and DA enters vesicle
|
|
|
What happens to remained of DA in nerve teminal not in vesicles
|
metabolized by MAO
|
|
|
DA in vesicle is converted to NE and Epi--which are stored in
|
adrenal chronaffin granules
|
|
|
Some NE is in extravesicular pool of terminal and not subject to
|
metabolism
|
|
|
Reserpine is taken up into
|
nerve ending and binds tightly to vesicle
|
|
|
What does Reserpine do
|
inhibit VMAT-2, which decrease CCA uptake into vesicles
|
|
|
IF there is decreased uptake of CCA into vesicles what happens
|
increase CCA metabolism and decreases CCA in vesicles
|
|
|
Recovery from reserpine requires
|
synthesis of new vesicles-
|
|
|
Recovery from respine requires synthesis of new vesciles, is there a delay in recovery when cease therapy
|
YES
|
|
|
What causes release of vesicles
|
action potential reaches the nerve terminal (Na+ dependent), causes Ca+ influx, and fuse with temrinal membrane
|
|
|
Ca+ influx into nerve terminal via
|
N-type Ca+2 channel
|
|
|
All vesicular contents are rlease into the
|
neuroeffector juction (quantal release)
|
|
|
What are modulators of release
|
adrenegic neurone blocking drugs, presynatic receptors, and indirectly acting sympathomimetic drugs
|
|
|
What are examples of adrenegic neurone blocking drugs
|
guanethidine, and bretylium
|
|
|
Guanethidine and bretylium do
|
CCA depeltion
|
|
|
How does Aderengic neurone blocking drugs ANBD do
|
enter the nerve terminal via NET (norepinephrine transporter) and concentrate in vesicles
|
|
|
If ANBD are taken up and concentrated in vesicles, what happens
|
displace CCAs leading to CCA depletion
|
|
|
How does body respond to CCA depeltion
|
postjunctional supersensitivity--leads to more adrenoceptors
|
|
|
What should one beware about
|
increased respone to EXGouenous sympatomemtic, such as products that contain alpha agonists--such as psedophed
|
|
|
What happens when you take an alpha agonist such as pseuophed with guanethidine or bretylium
|
leads to massive vasoconstriction
|
|
|
Where are presynaptic receptors
|
located on nerve terminals
|
|
|
What do presynaptic receptors do
|
control NT release by modulating the number release or nerve impulses
|
|
|
What do the a2, adn D2 and M2 presynaptic receptors do
|
inhbit rlease of CCA
|
|
|
What do B2 presynatic receptors do
|
faciltate relase of CCA
|
|
|
WHat does M2 do
|
ihbitits release of NT
|
|
|
What does angiotensin II do
|
increase release
|
|
|
Do Ach and NE have there own feedback inhibition
|
they regulate their own release
|
|
|
What do indirectly-acting sympathomimetic drug do
|
increase CCA release from sympathetic nerve to simulate adrenergic receptors
|
|
|
Tyramine and amphetamine is an example of indirectly acting sympathomimetic drug, which does what
|
enters nerve terminal, and inject NE from vesicle into synapse
|
|
|
Indirectly acting sympathetimetic agents do NOT directa cton adrenoceptors, what does
|
NE---released from vesicles caused by tyramine and amphetamine
|
|
|
What are indirectly acting sympathomietic drugs
|
A PET
amphetamine, tyramine, ephedrine, and pseuodephedrine |
|
|
What are characeristic of amphetmaine
|
indirectly acting, and CNS action, non-polar not substrate for MAO
|
|
|
Wht are chacteristic of ephedrine
|
indirectly acting, directlty through a, B, and CNS action
|
|
|
What are characteristics of pseudoephrein
|
indirectly acting, directly a, and CNS action
|
|
|
What are characteristic of tyramine
|
indirectly acting ONLY and metabolism by MAO/COMT
|
|
|
What drugs are only indirectly acting
|
amphetamine and tyramine
|
|
|
Tyramine is present in foodstuff, continued tyramine exposure can lead to
|
tachyphylaxis and decrease sympathomimetic response
|
|
|
Tyramine is NOT a pharmacologial agent, however it has important interactions with
|
MAO inhbitors
|
|
|
What are 2 mechanism that are involved in terminating the actiosn of CCA's
|
uptake (most important)
metabolism |
|
|
What is the most important mechansism regulating the activity of RELEASED CCAs
|
uptake
|
|
|
Nerve mediated responses are enchanced by
|
neuronal uptake inhibitors NOT enzyme inhbitors
|
|
|
Extraneuronal uptake, metabolism and diffusion more importatant when
|
synaptic cleft wide
|
|
|
What are 2 types of uptake
|
1. neuronal uptake NET
2. extraneuronal uptake ENT |
|
|
Where does neuronal uptake occur
|
nerve terminal membrane
|
|
|
The transport mechanism concentrates CCA in nerve terminal by what co-transport mechaism
|
uses Na+ and and Cl-
|
|
|
Does neuronal uptake have different affinites for CCAs,
|
NET-- greater affinity for NE, then EPI
|
|
|
Why is NE more efficently taken up by neuronal uptake
|
b/c N-substrituted derivates are less efficently taken up--epi has a CH3--instead of NH2
|
|
|
What are 2 things that can happen when CCAs are taken up into terminal cytoplasm
|
1. reincorporated in vesicle
2 metabolized by MAO |
|
|
What are inhibitors of neuronal uptake
|
Cocacine, tricycylic antidepressants (desipramine, and imipramine), and chlorpromazine
|
|
|
If you inhibit neruonal uptake,what happens
|
increases the effects of CCAs
|
|
|
Is the CCA ispropernol taken up by neuronal uptake
|
NO
|
|
|
What would a neuronal uptake inhibtor do to SYMPATHETIC nervous effects on heart
|
increase HR, contractility and conduction
|
|
|
With respect to abuse, euphroic effects of cocaine are indistinguishable from amphetamine why
|
cocacine increases dopamine directly
amphenatmine increase dopaine indirectly |
|
|
Where is extraneruonal uptake
|
effector tissues such as lliver, kidney smooth muscle
|
|
|
Extraneuronal uptake has greatest affinity for what CCAs
|
ISO>EPI>NE
|
|
|
What are 2 enzymes responsible for CCA metabolism
|
MAO
COMT (catechol-o-mehtly transferase) |
|
|
What are 2 isozymes of MAO
|
MAO-A
MAO-B |
|
|
What does MAO-A have preferance for
|
NE, EPI and 5-HT
|
|
|
What does MAO-B have a preferance for
|
DA and phenlyethalmines
|
|
|
Where does MAO work
|
nerve terminal cytoplasm
|
|
|
MAO inhibitios influences concentrations of
|
CCA available for vesicular uptake
|
|
|
Oral phenylethalamines (tyramine) normally metabolized by MAO-B in
|
liver and GI tract
|
|
|
What happens if inhibit MAO in periphery
|
tyramine is not broken down so absobed into systemic ciruclation, release NE, adn sympathetmitic effect
|
|
|
Whay is tyramine less of a problem with reversible inhbitiors of MAO (RIMAS)
|
allows tyramine to be metabolized, leads to decreased sympathoemtic SEs
|
|
|
What are MAO inhibitors
|
MR SPIT C
mocolbemide rasgiline selegiline phenelzine isocarboxazid tranylcypromine clorglyine |
|
|
What does Moclobemide inhibit
|
MAO-A, AND REVERSIBLE
|
|
|
What does Rasagiline inhibit
|
MAO-B, irrervesible
|
|
|
What does selegiline inhibit
|
MAO-B, irrevesible
|
|
|
What does Phenelzine inhibit
|
MAO A, B and irreversible
|
|
|
What does isocarboxazid inhibit
|
MAO-A and B, and irreversbile
|
|
|
What does tranylcypromine inhibit
|
MAO-A and B, adn irreversbile
|
|
|
What does clorglyine inhibit
|
MAO-A and irreversible
|
|
|
Inhibition of MAO for short-term use does what
|
increases SYMPATHETIC function
|
|
|
Inhibiotion leads to accumulation of CCAs in nerve terminal which means
|
more availabe to be release
|
|
|
inhibition of MAO is used for
|
antidepressants
|
|
|
What would happen is a depressed preson treated with an irreversible MAO-A inhibitor ate a food containing tyramine
|
can lead to hypotensive crisis
|
|
|
Where is location of COMT
|
cytoplasm of extraneuronal tissues
|
|
|
COMT may play a important role for
|
metbolism of circulating CCAs
|
|
|
What is entacapone
|
COMT inhbitior
|
|
|
What does entacapone do
|
inhibit peripheral COMT only, and prevents peripheral utilization of levadopa
|
|
|
The physiological actions induce by NE and Epi are release from
|
sympathetic nerve or adernal medulla
|
|
|
THe physiological action induced by NE and Epi are dependent on
|
effector tissue
adenergic receptor |
|
|
What are 2 major categories of adrenergic agoinsts
|
a-adrenoceptors
b-adrenoceptors |
|
|
Whhich CCAs has greatest potency on a-adrenoceptors
|
EPI, NE, ISO
|
|
|
What are a-adrenceptors response on smooth muscle
|
EXCITORY---contraction
|
|
|
Which CCA have great agonist petncy on b-adrenoceptors
|
ISO, EPI, NE
|
|
|
What do b-adrenoceptors do to smooth msucle
|
inhibitory (relaxtion) adn Excitiory in heart
|
|
|
What activates BOTH a-adrenoceptors and b-adrenoceptors
|
NE and Epi
|
|
|
What are Alpha adrenceptors substypes
|
A1 adn A2
|
|
|
What are specific locations of A1
|
SMOOTH MUSCLE
BEST PR Blood vessels ejaculation Spinchters, sweat, salviary The radial muscle Piolomotor muscles Renin secretion |
|
|
What are specific location of A2
|
Presynatic nerve endings
Platelets Pancreatic Beta cells |
|
|
What effects do Alpha receptors have A1
|
Blood vessel (constrict)
Ejaulation Sphinters contract, inrease sweating The raidal mussle dilates Pilomotor (googebumps) Renin secretion |
|
|
What are A1 agonists
|
phenylephrine, methoxamine
|
|
|
What is A1 antagonist
|
prazosin
|
|
|
What is A2 agonist
|
clonidine
|
|
|
What is an A2 antagonist
|
yohimbine
|
|
|
The effects on cells are mediated by
|
G-protein linked transduction systmes
|
|
|
What are the B-adrenoceptor subtypes
|
B1,B2, B3
|
|
|
What are effects of B receptors
|
inhibitory on smooth muscle (vasodilation) and EXCITYOATY on HEART
|
|
|
What are specific tissue locations of B1
|
Heart-increase HR, C,C
Kidney-stimulates JG-release Renin |
|
|
What are specific tissue locations of B2
|
Smooth muscle (Blood vessels, airways, and GI
Liver-increase glucose synthetsis SKM contractility |
|
|
What are locations of B3
|
Fat cells-lipolyisis
Bladder relaxtion Heart-decrease contractility |
|
|
What is relative potency of agonists B1
|
ISO, EPI=NE
|
|
|
What is relative potency of B2
|
ISO, EPI, NE
|
|
|
What is relative potency of B3
|
ISO=NE>EPI
|
|
|
Continual stimulation of B1 and B2 adrenoceptors leads to
|
receptor desensitaization
|
|
|
What is a non-selective Alpha angonist
|
NE
|
|
|
What is a non-selective Beta agonist
|
isproterenol
|
|
|
What are B1 agonsts
|
dobutamine
|
|
|
What are B2 agonists
|
BRAT-PM
Bitolerol ritordrine albuterol terbutaline pirbuterol metaproterenol |
|
|
What are non-selective Beta antagoints
|
propranolol
|
|
|
What is a B1 antagonist
|
metoprolol
|
|
|
What is non-selective Alpha antagaonist
|
phentolamine
|
|
|
What is a A1 antagonist
|
prazosin
|
|
|
What is a A2 antagoinst
|
yohimbine
|
|
|
What is physiolgocial and therapetic effect of A1 agonist
|
vasoconstriction--decongestion
|
|
|
What is physiolgocial and therapetic effect of A2
agonist |
A2-decrease NE release from presynaptic end-antihypertensive
|
|
|
What is physiolgocial and therapetic effect of B1 agonist
|
stimulates heart for HF
|
|
|
What is physiolgocial and therapetic effect of B2 agoinst
|
relaxes smooth muscle broncodilator
|
|
|
What is physiolgocial and therapetic effect of A1 ANTAGOINST
|
vasodilation antihypertensive
|
|
|
What is physiolgocial and therapetic effect of A2 ANTAGONIST
|
yohibbine-penis engourment
|
|
|
What is physiolgocial and therapetic effect of B1 ANTAGONIST
|
Decrease HR, C C, and renin, antihypertensive
|
|
|
What is physiolgocial and therapetic effect of B2 ANTAGOINST
|
NONE
|
|
|
What happens if you inhibit phosphodiesterase
|
increase physological response
|
|
|
Where is NE released
|
sympahteic postganlgionic nerves
|
|
|
Where is EPI released from
|
chroaffin cells of adrenal medulla
|
|
|
EPI exerts its effects on what receptors
|
A1, A2, B1, and B2
|
|
|
NE exerts its effects on what receptors
|
A1, A2, B1, B3
|
|
|
DA exerts its effects on what receptors
|
D1, D2, and A1,A2, and B1 (with increase conc)
|
|
|
What are A1 agoinst
|
methoxamine, and phenylephrine
|
|
|
What are A2 agoinsts
|
Clonidine, guanfacine, guanabenz, and alpha methly norepinephrine
|
|
|
What are the 4 parital agoinst ISA (tickle)
|
acebutolol, carteolol, penbutolol, and pindolol
|
|
|
Acebutolol
|
B2>B1
|
|
|
Carteolol
|
B1=B2
|
|
|
Penbutolol
|
B1=B2
|
|
|
Pindolol
|
B1=B2
|
|
|
What are B2 agoinsts
|
BRAT PM
Bitolerol ritodrine albuterol terbutaline pirbuterol metaproternol |
|
|
What 3 B2 agoinsts are broncholdiatlors
|
albuterol, metaproteronol,and terbutaline
|
|
|
What is special about ritodrine
|
uterine relaxant
|
|
|
What B2 agoinst is a pro-drug
|
bitolerol
|
|
|
What are the other indirectly acting sympathometics besides A PET
|
methylphenidate, and metaraminol
|
|
|
Methylpheidates
|
indirectly acting, CNS stimulate
|
|
|
Metraaminol
|
inidrectly acting, directly acting alpha, and NOT CNS stimulate
|
|
|
What are 3 drugs that are ONLY indirectly acting
|
Amphetamine, tyramine, and methylphenidate
|
|
|
What are actions of Al agonitsts
|
contsrtict blood vessels, which increase PVR
|
|
|
What are methoxamine and phenylephrine used for
|
hypotension
|
|
|
How does methoxamine and pheylephrine work
|
constrict blood vessels, increasing PVR, increaing BP, which decrease sympathetic outflow
|
|
|
What happens to HR taking methoxamine and phenylephrine (A1 agonists)
|
decrease HR
|
|
|
Increased vasoconstrction does what to heart
|
slows HR, and increases BP
|
|
|
What increases duration of local anesthetics through al
|
epinephrine--increase local anestetic action, by constricting Blood vessels
|
|
|
Phenylephirne and pseudepherdine are useful in nasal vasoconstrtion for alpha 1, how
|
decrease nasal mucosa volume and nasal congestion
|
|
|
Can one get rebound hyperemia and worsening of symptoms chonically using phenyleprine and pseud
|
YES
|
|
|
Why are Alpha 1 epineprhien and cocaine used in hemostatis in surgery
|
vasoconstrtion, decreases blood flow and increases blood clotting
|
|
|
Does cocaine promote vasoconstrtion
|
blocks neuronal uptake and increases sympathetic vasoconstrtion
|
|
|
What do a1 do to eye
|
contracts radial muscle of iris leading to dilation and myrasis, and increases aquesous humor outflow
|
|
|
What are topicals used on eye
|
epinehprine and phenylephrine
|
|
|
What drugs are used to treat hypotension
|
methoxamine, and phenylephrine
|
|
|
What does topical epinehprine and phenyleprine do to eye
|
dilation-with NO cyclopeglia
|
|
|
Epinehprine and phenylephrine are contraindicated in
|
NAG (narrow angle glucoma)
|
|
|
Can epinehprine treat open angle glaucoma
|
YES
|
|
|
How does epinephrine treat open agnle glaucoma
|
decreases intraocular pressure by increase aqueous humor outflow and decrease aquous humor production
|
|
|
What do a2 agonists do to brainstem (CNS) in cardiovascular system
|
decrease symathetic outflow decreases BP
and increases vagal outflow decrease HR |
|
|
Decrease in sympathetic outflow does what
|
decrease BP
|
|
|
Increase in vagal outflow
|
decreases HR (bradycardia)
|
|
|
What do A2 presynatic receptors on sympathetic nerves do on heart
|
Decrease NE release, results in dialtion, decrease PVR, and decrease CO
|
|
|
What are Alpa 2 agoints used for
|
antihypertensive
|
|
|
Alpha 1 agoinsts are used for
|
hypotension
|
|
|
What are antihypertensive agents for A2
|
clonidine, guanfacine, guanabenz, and methlydopa
|
|
|
What are clonidine side effects
|
xerostomia (dry mouth)
sedation |
|
|
What happens with sudden discontinuation of clonidine
|
HA, sweating, tachycardia, and rebound hypertension
|
|
|
What does sudden discontinuation of clonidine cause HA, sweating, tachycardia,and rebound hypertension
|
A2 turns off sympathetic, have sudden increase in sympathetic
|
|
|
What do alpha 2 agoinsts do to eye
|
decrease aqueous humor production
|
|
|
What condition can alpha 2 agoinsts treat
|
open angle glucoma
|
|
|
What alpha 2 agoinst treats open angle glucoma
|
apraCLONIDINE
|
|
|
What do B1 agoinsts do
|
Increase HR, Conduction and contractility
|
|
|
How do B1 agoinsts increase HR
|
increase SA node rate, depolaries more quickly
|
|
|
How does B1 agoinst increase contractility (1st step
|
activates cAMP, which phospharlates VOC which increase Ca influx into cells
|
|
|
2nd step on B1 agoinst increasing contractility
|
ATPase increase Ca+ upatke in SR, increase rate of relaxation
|
|
|
3rd step on B1 agoinst increasing contractility
|
phosphorlatino of troponin, increase rate of Ca+ reelase from tropoin, more powerful and shorter DOA
|
|
|
B1 agoinsts ALSO increase rate of conduction how
|
decrease the effective refractory period, increase impulses get through and cause ventricular contraction
|
|
|
What happens when B1 agoinsts decrease effective refractory period of AV node
|
increases amount of impulses to ventricles, and increases ventricular rates
|
|
|
What do B1 treat
|
short term cardaic decompensation
|
|
|
What is short term cadiac decompensation
|
heart not contracting forecfully enough
|
|
|
Does Dobutamine have a short termn half life, and where are its effects greater inotropic or chronotropic
|
YES--easier to control level of stimulation---greater INOTROPIC--contraction
|
|
|
3 Characteristic of Dobutamine
|
short half-life, inotropic effects, and No effects on PVR
|
|
|
What are adverse effects of B1 (dobutamine)
|
increased risk of ventricular tachyrhythms in atrial fib
increase BP increase infartion size |
|
|
Why do infarcation increase in size
|
oxygen deprivation, cells using more oxygen
|
|
|
B1 agoinsts use is only in
|
HEART
|
|
|
A2 aoinsts use is only in
|
HEART and eye
|
|
|
A1 agoinsts use is only in
|
HEART, local anesthetics, congestion, and hemostatis in surgery and eye
|
|
|
B2 agoinst use is only in
|
Airways and Uterus
|
|
|
What are B2 agoinst used for airways
|
relaxes airway smooth muscle and used for broncodilation and reversible airway obstruction
|
|
|
Albuterol, metaproternol, and terbuatline may also
|
inhibit mediator release
|
|
|
What do B2 do to uterus
|
relaxes uterine smooth muscle
|
|
|
What are B2 used for in uterus
|
delay or prevent premature parturtion
|
|
|
What B2 agoinsts are used to delay or prevent premature parturition
|
ritodrine or terbutaline
|
|
|
What are side effects of B2 agoints
|
skeltal msucle termor, tachycardia, ventilation perfusion mismatching, and tolerane
|
|
|
What causes SKM tremor with B2
|
increase muscle spindle discharge
|
|
|
What causes tachycardia
|
B2 have direct effect on heart
|
|
|
What causes ventiltion perfusion mismatching with B2
|
pulmonary vasodilation, decrease BP, increases sympathetic dischange increasing HR
|
|
|
What do B3 affect
|
Adipose cells, and bladder
|
|
|
What do B3 do to adipose cells
|
increase expression of mitochondrial uncoupling proteins, increase glucose metabolism
|
|
|
WHat does increaed expression of mitrochonrdial uncoupling do
|
increase substrate oxidation and increases thermogensis,
|
|
|
What does inducing expression of mitochondrial uncouling proteins treat
|
obesity
|
|
|
Adipose cells also increase glucose metabolism, which do what
|
increase insulin sensitivty
|
|
|
WHat does incrase insulin sensityity treat
|
non-insulin dependent diabetics
|
|
|
Can B3 also suppress appetite, and may B3 polymorphism be involved in obestity and insulin resistance
|
possibly
|
|
|
What effect do B3 have on bladder, and treats
|
relaxes bladder smooth muscle, and treat overactive bladder
|
|
|
What are types of Dopamine receptors
|
D1 and D2
|
|
|
Where are D1 located, and effects
|
blood vessels, renal tubules and JGA (dialtion BV), and increases Na exretion (diuresis, and increase renin release increase BP
|
|
|
What are effects of LOW doses of Dopamine on D1 BLOOD vessels
|
dilation of blood vessels, renal tubules, which decreases BP and PVR
|
|
|
What recpetors have to do with preload
|
D1
|
|
|
Where are D2 located
|
presynaptic nerve--inhibitory
|
|
|
What are effects of D2
|
inhibit sympathetic nerves
|
|
|
What do high doses of DA affect
|
A1, causing constrtion
|
|
|
High DA doses has affects on A1 receptors causing constrition which does
|
increases Afterload, increase preload, and increases BP
|
|
|
Intermediate doses of DA affect
|
B1 receptors
|
|
|
Intermediate doses of DA affect B1 agoisnts how
|
increase contractility, CO, and BP
|
|
|
What are Dopamine recetor agonist used for
|
acute heart filaure and LOW output failure condutions, severe hypertension, and renal failure
|
|
|
What treats acute HEART FAILURE and LOW OUTPUT
|
Doamine, and dopexamine
|
|
|
What is receptor selectivty for Dopamine
|
D1=D2 >B1> a1=a2
|
|
|
What is dopexamine receptor selectivity
|
D1,D2, and B2
|
|
|
How does dopamine and dopexamine treat heart failure
|
Dopamine affects B1, increases HR, C, C, and D receptors cause increased diuresis, and decrease BY
|
|
|
How does dopamine and dopeamine improve renal perfusion
|
increase diuresis, and decresase BV
|
|
|
What treats severe maligant hypertension
|
Fenoldopam
|
|
|
What receptor does Fenoldopam work
|
D1
|
|
|
What does Fenoldopam do
|
decrease PVR, and afterload, and increase diuresis decreases BP
|
|
|
What is used to treat renal failure, and how
|
dopamine, increase renal blood flow and GFR
|
|
|
What are side effects of D1 agoinst
|
flushing and HA
|
|
|
What are side effects of D2 agoinsts
|
N/V
|
|
|
What are Dopamine Agoinsts
|
DID CPR FBP
Dopamine ibopamine dopexamine cabergoline pramipexole ropinirole fenoldopam bromocryptine pergolide |
|
|
Cabergoline
|
D2
|
|
|
Prampipexole
|
D2, D3
|
|
|
Ropinirole
|
D2,D3
|
|
|
Fenoldopam
|
D1
|
|
|
Bromocyptine
|
D2 (D1 partial agoinst)
|
|
|
Pergolide
|
D2 (D1 ANTAGOINST)
|
