ANS Flashcards
1
Q
list cellular bonds from weak to strong
A
van der walls , hydrophobic, hydrogen, ionic, covalent
2
Q
1st messenger leads to?
A
1st messenger > receptor > effector > 2nd messenger > cell response
3
Q
4 types of recetors
A
- transmembrane GPCR
- Transmembrane ligand gated
- transmembrane enzyme linked receptor
- soluble intracelular (nucelar) receptors
4
Q
what is faster metabotropic or ionotropic receptors?
A
ionotropc
5
Q
list the ionotropic receptors
A
nicotinic
GABAaR
5HT-3R
Glycine - R
NMDA
AMPA
6
Q
glutamate binds what two receptors
A
NMDA and AMPA
7
Q
list the metabotropic receptors
A
muscarinic
adrenergic
GABAbR
opioid
5HT1-R
D1-D5
8
Q
2 other receptors besides the main 4 and the drugs that bind them
A
- extracelllar targets (dabigatran)
- Adhesion molecules (eptifibatide)
9
Q
what to kinases do?
A
they add a phosphate
10
Q
what is the first step in depolarization of all the neurons in this unit?
A
Action potential then Ca++ influx through the N-type Ca channel
11
Q
when are GPCR is the off mode?
A
when GDP is bound to alpha subunit
12
Q
when are GPCR in the on mode?
A
when GTP is bound to alpha subunit
13
Q
what happens after GPCR is activated?
A
alpha subunit with GTP seperates from Y and B subunits
14
Q
how are GPCRs turned off?
A
alpha subunit has built in GTPase that turns GTP back to GDP turning it off
15
Q
what does Gs do?
A
stimulates adenylyl cyclase
16
Q
what does Gi do?
A
inhibits adenylyl cyclase
17
Q
what does Gq do?
A
stiulates PLC
18
Q
action of adenylyl cylcase?
A
converts ATP to cAMP
19
Q
PLC action
A
converts PIP2 to IP3 and DAG, also increases Ca++
20
Q
what does PLA2 do?
A
PLA2 plus Ca liberate arachadonic acid from cell membranes
21
Q
neurotransmitters can be divided into what two main groups?
A
conventional and non conventional
22
Q
what are the subgroups of conventional neurotransmitters?
A
choline esters
amino acids
biogenic amines
neuropeptides
23
Q
what are the subgroups of non-conventional neurotransmitters
A
Gases and lipids
24
Q
list the choline esters
A
acetylcholine
25
list the amino acids
Glutamate
GABA
Glycine
26
what is the main excitatory and inhibitor neurtransmitters in the brain?
excitatory: glutamate
inhbitory: GABA
27
what is the main inhibitory neurotransmitter in the spinal cord?
glycine
28
what are the 3 subgroups of biogenic amines and neurtransmitters in each group?
catecholamines
dopamine
NorEpi
Epi
indoleamine
serotonin
imidazole amine
histamine
29
what are all catecholamiens made out of?
tyrosine
30
what is serotonin made out of?
trypophan
31
what is histamine made out of?
histidine
32
list the neuropeptides
hypothalamic peptides
opioids
substance p
neuropeptide Y
VIP- glucagon family
33
what are the two subtypes of non-conventional neurtransmitters and the neurotrnasmitters in each group
Gases
NO and CO
lipids
endocannabinoids
34
where does Ach synthesis take place?
pre-synaptic nerve terminal
35
list the steps for Ach synthesis, relese, and elimination. what is the rate limiting step?
1. glucose enters cell
2. glucose converted to pyruvate
3. pyruvate goes into mitochondria, acetyl from pyruvate added to co-enzyme A. Acetyl CoA moves back inot cytoplasm
4. choline is transported into presynaptic nerve terminal (rate lmiiting step)
5. acetyl CoA + Choline = Ach
6. Ach is transported into synaptic vesicle until release
7. Ca triggers fusion of vesicle, Ach release via exocytosis
8. AchE hydrolyzes Ach to acetate and choline. choline re-enters nerve terminal and is re-used.
36
explain how Mag can caues muscle weakness and potentiate NMBs
mag is antagonist for Ca++ ar presynaptic nerve terminal, so it can inhibit Ca++ triggers Ach release.
37
how does gultamate interact with BBB?
doesn't cross, so it must be synthesized in the brain.
38
what can the brain do with glutamate and GABA? how?
it can convert Glutamate to GABA and vice versa via the krebs cycle
39
what are the three safety mechanisms of NMDA R? why is this important?
1. voltage dependence
2. 2 gluatmate bindings
3. 2 glycine bindings
important because hyper activation of NMDA receptor could lead to Ca flooding neuron > cell death
40
how does mag interact with NMDA receptor?
mag blocks NMDA receptor in the resting state
41
what are the 2 common enzymatic reactions of biogenic amine neurotransmitters biosynthesis?
1. Hydroxylation (adding a OH)
2. decarboxylation - Removes (CO2)
42
what is the main precurrosr for dopamine, NE, and Epi synthesis?
tyrosine
43
what is another name for tyrosine
hydroxyphenylalanine
44
what will the body use to synthesize dopamine, NorEpi, or Epi if there is no tyrosine
converts phenylalanine to tyrosine if tyrosine levels are low
45
what is the rate lmiting step in biogenic amine biosynthesis?
tyrosine hydroxylation to L-DOPA
46
steps of Dopamine/NE/Epi synthesis
1. tyrosine > L-DOPA (hydroxylation)
2. L-DOPA > Dopamine (decarboxylated)
3. dopamine into vesicle (stops here for dopaminergic neurons)
4. Dopamine > NorEpi in vessicle (hysroxylation) (stops here if noradrenergic neuron)
5. NorEpi > Epi (methylation)
47
describe NE and Epi metabolism
NE and Epi broken down by both COMT and MAO in any order and produce VMA (vanillymandelic acid
48
describe doapmine metabolism
dopamine > homovanillicacid (HVA) by COMT and MAO
49
question bank info about COMT and MAO
NE broken down by MOA at terminal nerve endings and both MOA and COMT at extraneural locations
50
where is the largest concentration of dopamine receptors? what does thsi area do? what diseae is this important for?
substania nigra
critical for coordinating movement, degeneration of these neurons > parkinsons disease.
51
how many Dopamine receptors are there?
D1-D5
52
effects of D1 & D5
activate adneylyl cylcase > ^cAMP > PKA activation
D5 also actives PLC > activates PKC
53
effects of D2, D3 & D4
inhibit adenylyl cyclase> decreased PKA activity
54
averactivae D2 receptors have a role in what disease?
schizophrenia
55
how are alpha and beta receptor classes distinguised?
by their responsiveness to isoproterenol
56
NE preferentially binds what receptors
alpha 1 alpha 2 and beta 1
57
Epi is mostly what at low doses? what about high doses?
mostly beta activity at low doses and you add in alpha activity at higher doses
58
what are the purinergic neurotransmitters?
ATP ADP and Adenosine
59
cardiac effects of B1 stimulation
increased inotropy, luistropy, chronotropy, dromotropy
60
what is dromotropy
conduction velocity
61
opioid exert inhibtory effects where on neurons?
both pre-synaptic and post-synpatic inhibitory effects
62
what PDE inhibitors do you need to konw for boards?
PDE3 PDE4 PDE5
63
effects of PDE3
bind cAMP and cGMP, but 10x the affinity for cGMP
64
where is PDE3 found?
heart, vascular and placlental smooth muscle
65
how is milrinone excreted?
renal excretion and 80% unchanged
66
where is PDE5 found?
every tissue in the body but more in the penis and clitoris, vascular smooth muscle, and platelets
67
what does PDE4 do?
modulates B2 adrenergic responsivness in pulm smooth muscle. cAMP specific
68
M2 and M4 are what GPCR
Gi
69
M1 M3 M5 are what GPCR
Gs
70
what is the substarte for NO synthesis
l-arginine
71
where is NorEpi converted to Epi?
adrenergic cells and neurons
72
what converts tyrosine to L-Dopa?
tyrosine hydroxylase
(dont forget this is the rate limiting step)
73
how many pairs of spinal nerves
31
74
CN 2 is part of which nervous system?
CNS becasue it is covered by the three meningeal layers
75
what kind of receptors are insulin receptors?
enzyme liked tyrosine receptors
76
where are steroid receptors?
in the cytoplasm
77
where are thyroid receptors?
in teh cell nucleus
78
which 5 second messengers should I know?
cAMP
cGMP
IP3
DAG
Ca++
79
what allows for amplification
2nd messenger
80
what receptors are Gs
B1 B2 B3
D1
V2
Histamine 2
81
what receptors are Gq
A1
V1
Histamine 1
M1 M3 M5
82
what receptors at Gi
A2
M2 M4
D2
83
which receptors does not use effector or 2nd messengers?
nicotinic receptors are just ion channels and dont have effectors of 2nd messengers
84
what receptors on the heart?
B1 and M2
85
what receptors in the lungs
B2 and M3
86
what does M3 stimulation in the lungs cause?
bronchoconstriction and ^ gland secretions
87
what receptors in the GI tract? What do they do when stimulated?
A1: vasoconstriction and sphincter contraction
M3: ^ motility, sphincter relaxation, gland secretion
88
what receptors in glands? What do they do when stimulated?
A1: ^ sweating and decreased pancreatic activity
M1:
M3: ^ salivation ^ lacrimation ^pancreatic activity
89
what receptors in the urinary tract and what do they do when stimulated?
A1 & B2: bladder sphincter contraction and ^ renin secretion
M3: bladder sphincter relaxation
90
receptors in skin and what they do when stimulated?
A1: vasoconstriction
91
S muscle receptors and what they do when stimulated
B2: vasodilation
92
Receptors in the Eyes and what they do when stimulated
A1: dilation
M3: constriction
93
expain eye receptors and actions at deeper level
PNS > M3 stim > spincter muscle contraction > miosis
SNS > Alpha1 > radial muscle contraction > mydriasis
94
Arteries and Veins have what kind of innervation? what are the exceptions?
No PNS input, only SNS
exception: coronary arteries (vasodilation)
cerebral vessels (receptor specific vasodilation or vasoconstriction)
95
A1 receptor stimulation affects arerties or veins?
vasoconstriction
96
A2 receptor stimulation affects arteries or veins?
venouconstriction
97
where are alpha 2 receptors located and what are their effects?
presynaptic NE releasing neurons in PNS and SNS
post synaptic in smooth muscle and several organs
non-synaptic: platelets causes platelet aggregation.
98
where are alpha 2 receptors that provide analgesia located?
dorsal horn of the spinal cord
99
Alpha 2 effects in the renal tubules
inhibit ADH release > diuresis
100
in the presence of O2, 1 mole of glucose creates how much ATP?
38 moles of ATP
101
What does PEE3 do?
turns off cAMP by converting cAMP to AMP
102
^cAMP in the hear has what effect?
^ contractility
103
^cAMP in smooth muscle has what effect?
cAMP in vascular smooth muscle inhibits myosin light chain > vasodilation
104
PDE3 inhibitors work independently of what?
independently of the SNS
105
what is the prototype drug for PDE inhibitors
theophylline is non-selective PDE inhibitor prototype
106
^cAMP in the heart inceases what? and what two effects does this have?
^cAMP in the heart ^ Ca++ > force of contraction
^cAMP > ^ rate of Ca++ to sacroplasmic reticulum > ^ lusitropy
107
NE inhibitis its own release via what receptor?
presynaptic A2 receptor
108
NE augments its own release via what receptor?
presynaptic B2 receptor
109
catecholamines are removed from syanptic cleft via what three mechanisms? and specific to know about each way?
1. re-uptake into pre-synaptic cleft about 80% (requires energy) (most is repackaged into vesicle but some metabolised by MAO)
2. diffusion away > COMT &MAO metabolism
3. reuptake by extraneural tissue > MAO and COMT metabolism
110
reuptake of catecholamines is blocked by what two drugs
cocaine and TCAs
111
what is the main site of extra neural catecholamine metabolism
liver and kidneys
112
main things to know about Ach metabolism
no re-uptake
metabolized to choline and acetate
choline transported back into nerve terminal
Ach must be rapidly metabolized for precise control of effector organs
113
what nerves in PNS and SNS have myelin?
the pre-ganglionic PNS and SNS neurons
114
SNS nerves originate from?
T1-L3 "thoracolumbar"
115
PNS originates from where?
CN 3,7,9,10 and S2-S4 "craniosacral"
116
post to preganglionic ration for PNS and SNS
SNS 30:1
PNS 1:1 to 3:1
117
preganglionic fibers are what?
both PNS and SNS preganglionic fibers are myelinated B Fibers
118
post ganglionic fibers are what?
both PNS and SNS postganglionic fibers are unmyelinated C fibers
119
post ganglionic SNS neurons synapse on what receptors on sweat glands?
muscarinic receptors
120
how many paired sympathetic ganglia make of the sympathetic chain?
22
121
ganglion impar are in what region?
coccygeal
122
preganglionic sympathetic fibers originate from where?
T1-L2
123
post ganglionic sympathetic fibers supply
body from head to toe. as opposed to just T1-L2 where the preganglionic fibers originate.
124
what makes up the stellate ganglion?
inf. cervical ganglion and T1 ganglion
AKA cericothoracoganglion
125
what does the stellate ganglion innervate?
SNS innervation to ipsilateral head, neck, and UE
126
s/s of horners syndrome
ptosis, miosis, anhidrosis, flushed skin, nasal congestion, enopthalamos
127
waht does the renal medulla and renal cortex secrete?
cortex: glucocorticoids, mineralcorticoids, and androgens
medulla: catecholamines
128
adrenal glands recive what innervation
preganglionic sympathetic B fibers release Ach on medulla > NorEpi and Epi release
129
how much epi and norepi does adrenal medulla release?
Epi 0.2mcg/kg/min 80%
NorEpi 0.05mcg/kg.min 20%
130
how long to catecholamiens stay in blood compared to synaptic cleft?
5-10x longer
131
name two non selective alpha blockers
phenoxybenzamine and phentolamine
132
name two A1 specific blockers
doxazosin and prazosin
133
what should you anticipate after a pheochromocytoma is removed?
HoTN and hypoglycemia
134
drugs to avoid with pheo if possible
histamine releasing: Sux, atracurium, mivacurium, morphine
indirect acting: ephedrine
SNS activators: ketamine, pancuronium, naloxone
135
classic s/s of pheochromocytoma
HTN headache and diaphoresis
136
what are the effects of SNS activity on the Liver?
^ BG
^K initially
also ^ insulin from actiivty on pancrease so body can use the BG.
adrenal medulla also recives SNS innervation > ^ catechoamines > bind B2 receptors > K shift into cell (this is how SNS activity ultimately leads to hypokalemia.
137
4 things that shift K into cells
alkolosis
beta 2 agonists
theopylline
insulin
138
4 thins that shift K out of cells
acidosis
cell lysis
hyperosmolarity
Sux
139
mnemonic to remember the ANS reflexes
3 Bees in the CV Ouch!
baroreceptor
bainbridge
bezold jarish
chemo receptor
vasovagal
occulocardiac
140
whre are baro receptors
aortic arch and carotid sinus
141
how do baro receptors affect the set point?
set point can adapt over 1-3 days
142
drugs that impair the baro receptor reflex
VA dose dependent
propofol (usually)
BB (may impair)
CCB
PDE i
ACEi with any other dilator
all catecholamines besides NE
143
drugs that preserve the baro receptor reflex
thiopental
hyralazine
Nitro
Nipride
NE (only B1 at lower dose, but with higher dose A1 outweights effects on B1 R so you can still get reflex bradycardia
144
