Pharmacology Test 2 L1 Autonomics

Front 1

What NT do ALL preganglionic nerve fibers release?
What Receptor type does this act on?

Back 1

Ach

acts on nicotinic receptors

Front 2

Where do preganglionic PNS nerves come from?

Back 2

Cranial sacral, CN's and S3/S4

Front 3

How long are postganglionic PNS fibers?

Back 3

very short

Front 4

What NT do postganglionic PNS nerves use?

On what receptor type?

Back 4

Ach

on Muscarinic

Front 5

Where do preganglionic SNS nerves come from?

Back 5

T1-L2

Front 6

Where are pregnaglionic SNS cell bodies located?

Back 6

lateral horn of the gray matter

Front 7

Where do most pre-ganglionic SNS fibers terminate?

Back 7

in the paravertebral chain ganaglions

Front 8

How does the paravertebral chain fire?

Back 8

in a coordinated discharge
(this gives you the chill up your spine effect!)

Front 9

What NT do post ganglionic SNS nerves that innervated sweat glands release?

Back 9

Ach

Front 10

What NT do post ganglionic SNS nerves that innervate renal vasculature release?

Back 10

Dopamine

Front 11

What NT do MOST Post-ganglionic SNS nerves release

Back 11

NE (nore epi)

Front 12

What place do pre-ganglionic SNS fibers go to, that releases Epi?

Back 12

the adrenal medulla

Front 13

What three places, is ACh released, acting on Nicotinic receptors?

Back 13

Pre-ganglionics of both SNS/PNS

Nerves to the adrenal medulla (causes epi release)

and Motor neurons (NMJ)

Front 14

What two places is ACh released, acting on Muscarinic receptors

Back 14

post-ganglionic PNS

sweat glands (from SNS)

Front 15

Where is NE release from? What two receptor types does it act on?

Back 15

this is released from post ganglionic SNS fibers.

acts on Alpha and Beta 1 (NOT 2) receptors

Front 16

Where is Dopamine released from? acting on?

Back 16

SNS nerves, acts on renal vasculature smooth muscle

(note, Dopaminergic nerves MUST lack dopamine-B-hydroylase to prevent it begin converted into NE!)

Front 17

What functions does the myenteric plexus control?

Back 17

this controls the muscle functions, contraction and relaxation

Front 18

what functions does the submucosal plexus control?

Back 18

this controls secretions, absorption, and blood flow

Front 19

What does Vagal input do to the enteric nerves? what NT?

Back 19

this uses ACh, and is excitatory.
causes stimulation of smooth muscle motion, AND secretions

Front 20

What does sympathetic input to the enteric nerves do? What NT?

Back 20

this uses NE, and is inhibitory on GI motion

Front 21

What does PNS and SNS overall do to the GI tract?

Back 21

this is modulatory, GI activity can occur in the absence of these signals

Front 22

What is the major intrinsic transmitter in the GI system? what does it do?

Back 22

Serotonin (5-HT) is the major intrinsic transmitter. this si excitatory- increase GI motility and activity

Front 23

What does NO do to the GI tract?

Back 23

this is inhibitory

Front 24

What are the 3 major inhibitors of GI motility?

Back 24

NO
VIP
ATP (on a P2Y)

Front 25

What 3 things are released with ACh to excite the GI system?

Back 25

Substance P
Neurokinin A
ATP (on P2X)

Front 26

What does the compound Vesamicol do?

Back 26

this blocks TRANSPORT of ACh into Vesicles

(vesicle- may-clot-, clots block things)

Front 27

What does botulinum toxin do

Back 27

this blocks the RELEASE of ACh (which messes with the snaps and snares)

Front 28

What drug blocks Choline reuptake (to be repacked into ACh by choline acetyltransferase)

Back 28

Hemicholinium

Front 29

What is the rate limiting step in NE synthesis?

Back 29

Tyrosine-> L-dopa (done by tyrosine hydroxylase)

Front 30

What drug blocks the tyrosine-> L dopa conversion?

Back 30

metyrosine

(this is just a methylated tryosine, and thus blocks the conversion! just like hemicholinium blocks choline transport- look for a random molecule stuck on the intended molecules name)

Front 31

What regulates (increases) the expression of tyrosine hydroxylase (and this NE production)

Back 31

this is increased during increased SNS activity (SNS activity goes up, needs more NE, induces tyrosine hydroxylase)

Front 32

What slows down tyrosine hydroxylase activity?

Back 32

NE feed back through presynaptic alpha 2 receptors
(as all alpha 2 receptors are inhibitory)

Front 33

Where are the catecholamines stored (DA, NE, Epi)? by what?

Back 33

these are store in vesicles by VMAT (vesciular monoamine transporter)

Front 34

What prevents VMAT's actions?

Back 34

reserpine
(causes all the catecholamines to Re surface, rather than be stored)

Front 35

What terminates the actions of NE in a normal cleft?

Back 35

NET (NE transporter)

Front 36

What drugs block the reuptake of NE?
(both illicit and prescription)

Back 36

antidepressants and cocaine

Front 37

What do amphetamine, ephedrine, and tyramine do in a nerve terminal?

Back 37

these get taken up by NET, into vesicles by VMAT. pushing NE and DA out- where they are released by NON-Ca+ dependent process

(maybe this could be blocked by Reserpine?)

Front 38

What must be intact for Amphetamine to work?

Back 38

the noradrenergic innervation (aka the presynaptic process)

Front 39

What two enzymes break down NE?

Back 39

Monoamine Oxidase

and

Catechol-O-methyl Transferase

Front 40

Where is MAO located?

Back 40

on the outer surface of mitochondria in the nerve terminal

Front 41

Where is COMT located?

Back 41

most places in the body (especially the liver)

Front 42

What metabolite does a urine test for NE and EPI look for?

Back 42

VMW

(NE/EPI are hormones you would have in your body when your all jacked up driving your BMW (or VMW) fast!)

Front 43

What metabolite does a urine test for Dopamine look for?

Back 43

HVA

Front 44

Where are M1 receptors found?

Back 44

in the CNS, and exocrine glands

Front 45

What do M1 receptors do? mechanism?

Back 45

these are Gq, PLC-> IP3/DAG. increases calcium and depolarizes the cell

Front 46

Where are M3 receptors?

Back 46

these are found in exocrine glands, smooth muscle, and endothelium.

Front 47

What is the mechanism of M3 receptors?

Back 47

Gq, PLC-> IP3/DAG, increased Ca2+ and depolarizing.

Front 48

Where are M2 receptors found?

Back 48

Heart, some smooth muscle, and Presynaptically

Front 49

What is the mechanism of M2 receptors?

Back 49

these are Gi,- inhibit adenylyl cyclase, lower cAMP.

Opens K+ channels, and Hyperpolarizes cells

Front 50

How does M2 receptor affect heart rate?

Back 50

this SLOWS heart rate, by hyperpolarizing the cells reducing thier NT release rate

Front 51

Where are N(n) receptors found?

Back 51

autonomic gangila and adrenal medulla

Front 52

Where are N(m) receptors found?

Back 52

in skeletal muscle

Front 53

What do ALL nicotinic receptors do?

Back 53

these ALL open Na+ channels and depolarize neurons or muscle cells.

Front 54

What is the mechanism of alpha 1 receptors?

Back 54

these are Gq (PLC, IP3, DAG)

depolarizes the cell

Excititory

Front 55

What is the mechanism of Alpha 2 receptors?

Back 55

Gi

this inhibits adenylyl cyclase, decreasing cAMP levels

Inhibitory

Front 56

What is the mechanism of Beta 1 receptors?

Back 56

These are Gs, they increase cAMP, and are excitiory

Front 57

Where are B1 receptors found?

Back 57

these are found are pre and post synaptic sites on the heart

Front 58

where are alpha 1 receptors found?

Back 58

these are found in smooth muscle

Front 59

where alpha 2 receptors found?

Back 59

these are found in presynaptics, platelets, lipocytes, and smooth muscle

Front 60

What is the mechanism of Beta 2 receptors?

Back 60

these are Gs, stimulated adenylyl cyclase

Front 61

Where are B2 receptors found?

Back 61

smooth muscle, bronchioles, heart

(may stimulate, OR relax depending on the tissue)

Front 62

Where are B3 receptors found, mechanism?

Back 62

these are found on lipocytes.
Gs (like all B's)

Front 63

Where are D1/D5 receptors located?

Back 63

these are in the brain and renal vascular bed

Front 64

Where are D2,D3,D4 receptors located?

Back 64

brain and other random tissues

Front 65

What is the mechanism of action of D1, D5 receptors?

Back 65

these stimulate adenylyl cyclase, increasing cAMP

Front 66

What is the mechanism of action of D2, D3, D4 receptors?

Back 66

these inhibit adenylyl cyclase

Front 67

What is the end result of increased intracellular cAMP?

Back 67

activates PKA, and thus intracelular enzymes
Ion channels Ca2+ and K+
and contractile proteins

Front 68

What 3 receptor types are linked to Gq?

Back 68

M1, M3, and A1 (PLC)

Front 69

What 2 receptor types are linked to Gi?

Back 69

M2, A2 (inhibits adenylyl cyclase)

Front 70

What receptors are linked to Gs?

Back 70

all beta receptors (stimulate adenylyl cyclase)

Front 71

What two receptor types inhibit NE release from presynaptic terminals?

Back 71

Alpha 2a, and Alpha 2c
(these are auto receptors, as they prevent the release of the NT that binds them)

Front 72

What receptor types increase NE release from presynaptic terminals?

Back 72

presynaptic B receptors
(these are auto receptors, as it promotes the release of the NT that binds it)

Front 73

What do presynaptic M2 receptors on noradrenergic terminals do?

Back 73

these DECREASE NE release
(called a heteroreceptor- as it uses a different NT than the one it regulates)

Front 74

What input do blood vessels primarily receive?

Back 74

SNS input

Front 75

What innervates sweat glands

Back 75

SNS releasing ACh

Front 76

Where are M2's located on the heart? What do they do?

Back 76

Located at the Atrium.

Decrease SA node HR

Slows AV conduction (PNS)

Front 77

What do M2/ M3 receptors do to the lungs?

Back 77

these cause Bronchoconstriction, especially in asthmatics

Front 78

What do B1/B2' receptors do in the heart?

Back 78

These increase Heart Rate,
Automaticity, and Contractility

Front 79

What do B2 receptors do in the lung?

Back 79

these respond to circulating EPI

relax bronchioles (epi pen!)

Front 80

What do B2 receptors do in skeletal muscle?

Back 80

these relax BV's here, increasing blood flow.

Front 81

What do B2's do in coronary arteries?

Back 81

these dilate coronary arteries

Front 82

What do Alpha 1's do to skin BV's?

Back 82

the SNS acts on Alpha 1's (Gq) to Constrict blood vessels in skin, and constrict veins.

Front 83

What do M3's do to salivary and lacrimal glands?

Back 83

these cause profuse secretion (PNS)

Front 84

What do M3 receptors do to the eye?

Back 84

(PNS)
MIosis, contraction of ciliary muscle- for near vision (and reduces intraocular pressure)

Front 85

What type receptors incruease sweating?

Back 85

M1/M3 (SNS)

Front 86

What do Alpha 1's do to the eye?

Back 86

(SNS)- these constrict the radial muscle, DILATION of the pupils

Front 87

What do alpha receptors do in the nose?

Back 87

these cause vasoconstriction in nasal passes- reducing swelling, allowing decongestion

Front 88

What Parasympathetic receptor is in the bowel and bladder? 4 man actions in these regions?

Back 88

Contraction of GI
Secretion in GI
Contract bladder- peeing
promote erection
M3 receptors for all

Front 89

What SNS receptor promotes ejaculation?

Back 89

Alpha 1

Front 90

What SNS receptor promotes Renin release?

Back 90

B1

Front 91

What does the SNS do to the bowel and bladder?

Back 91

Relaxes GI tract, decreases secretions
Relaxes bladder/uterus
Contractions sphincters in the bladder

Front 92

What 3 metabolic effects are related to SNS stimulation?

Back 92

glycogenolysis
Lipolysis
potassium uptake in skeletal muscle

Front 93

What does a Fast infusion of NE do to BP? how?

Back 93

this is a vasopressor via Alpha 1's which constrict BV's.

Rapid NE also causes B1 to increase HR.

This creates a Large BP increase

Front 94

What does a Slow infusion of NE do to BP? how?

Back 94

This still constricts BV's via Alpha 1 receptors,

but there is compensation- with decrease SNS outflow, and increased PNS input. Results in Bradycardia...

So increase BP, but not too much.

Front 95

What causes Miosis? For what range of vision?

Back 95

Cholinergic input (PNS)

used for near vision

Front 96

What agents are used to treat glaucoma? why?

Back 96

cholinergic (PNS) ones, these contract the ciliary muscles, increasing outflow and decreasing intraocular pressure.

Front 97

What is cycloplegia?

Back 97

this is ciliary muscle blocked by cholinergic antagonists (so no pupil constriction or near vision accommodation)

Front 98

What do alpha receptors do to the eye?

Back 98

these cause Mydriasis (pupil dilation)

Front 99

What class of drugs can lower interocular pressure by limiting aqueous humor production?

Back 99

beta blockers

Front 100

What do Beta receptors do the aqueous humor?

Back 100

these increase production of aqueous humor