Pharm Exam 2

Front 1

Neurotransmitter for All Preganglionic Fibers and what receptor does it act on?

Back 1

Acetylcholine acting on Nicotinic receptors

Front 2

Neurotransmitter for Post-ganglionic Parasympathetic and what receptor does it act on?

Back 2

Acetylcholine, Muscarinic

Front 3

Neurotransmitter for Sympathetic innervation of sweat glands and what receptor does it act on?

Back 3

Acetylcholine, Muscarinic

Front 4

Neurotransmitter for Innervation of adrenal medulla and receptor it acts on?

Back 4

Acetylcholine, Nicotinic

Front 5

Neurotransmitter for Somatic nerves to skeletal muscle, and receptor it acts on?

Back 5

Acetylcholine, Nicotinic

Front 6

Neurotransmitter from post-ganglionic sympathetic fibers (2 exceptions)

Back 6

Norepinephrine
Except sweat glands - ACh, Renal Vasculature - Dopamine

Front 7

Adrenal medulla releases -

Back 7

Epinephrine and Norepinephrine

Front 8

Neurotransmitter for Renal Vasculature

Back 8

Dopamine

Front 9

Ach in Enteric Nerves

Back 9

Parasympathetic - increases peristalsis and acid secretion

Front 10

Parasympathetic fibers leave CNS through:

Back 10

Cranial Nerves (Vagus) and the 3rd/4th sacral spinal roots

Front 11

What does the myenteric plexus do?

Back 11

controls contraction and relaxation within the enteric system

Front 12

What does the submucosal plexus do?

Back 12

controls secretions, absorptions, blood flow

Front 13

Sympathetic Innervation in Enteric system

Back 13

NorEpi/Epi inhibit GI activity and decrease ACh release

Front 14

Serotonin in the enteric system

Back 14

Serotonin (5-hydroxytryptamine) - major intrinsic transmitter, excitatory increasing GI activity

Front 15

Nitric Oxide in Enteric System and Vasoactive Intestinal Peptide

Back 15

NO - major inhibitory transmitter, VIP also inhibits GI activity

Front 16

How do you make ACh

Back 16

Choline + acetyl CoA catalyzed by choline acetyltransferase (ChAT)

Front 17

Mechanism of botulinum toxin

Back 17

Inside the nerve terminal vesicles containing neurotransmitters usually line up and attach to the terminal membrane via Vesicle Associated Membrane Proteins (VAMPs - vSNAREs) and Synaptosomal nerve-associated proteins (SNAPs - tSNAREs) - botulinum toxin degrades the SNAREs inhibiting the release of NTs from the nerve terminal

Front 18

Vesamicol

Back 18

a compound that blocks transport of neurotransmitter ACh into vesicles

Front 19

What causes the termination of ACh activity, what is the duration of ACh activity?

Back 19

Acetylcholinesterase (AChE) hydrolyzes ACh in the synaptic cleft back into choline and Acetate. AChE is very abundant in the synaptic cleft, making the duration of ACh action very short

Front 20

Hemicholinium

Back 20

Post-hydrolysis by AChE acetate and choline are taking back up into the nerve terminal by a high affinity transport mechanism, however this transporter can be blocked by hemicholinium

Front 21

Rate limiting step in catecholamine synthesis

Back 21

Formation of l-dopa from tyrosine via enzyme tyrosine hydroxylase

Front 22

Metyrosine

Back 22

blocks formation of l-dopa from tyrosine via tyrosine hydroxylase

Front 23

VMAT

Back 23

Vesicular Monoamine Transporter is responsible for uptake of Dopamine, NE, and Epi into the synaptic vesicles

Front 24

Reserpine

Back 24

Inhibits VMAT

Front 25

NE in the nerve terminal

Back 25

NE in the nerve terminal is stored in synaptic vesicles and released into the synaptic cleft similarly to ACh, however there is also a free pool of NE in the nerve terminal called the "mobile pool"

Front 26

Termination of NE action in the synaptic cleft, how is this blocked?

Back 26

Norepinephrine transporter (aka reuptake 1) transports NE back into presynaptic terminal - main mechanism. Blocked by antidepressants and cocaine, prolonging the effect of NE

Front 27

Action of Amphetamine, ephedrine, and tyramine

Back 27

taken into nerve terminal by NET and into vesicles by VMAT. NE or DA are displaced from the vesicles and are released by a Ca independent reversal of NET

Front 28

MAO - where is it located and what does it do?

Back 28

MAO is located on the surface of mitochondria in the nerve terminal and breaks down free NE in the mobile pool. MAO is also in the liver and GI tract where it breaks down NE/Epi in circulation. MAO also breaks down tyramine in the GI tract preventing absorption

Front 29

COMT - Where is it located and what does it do?

Back 29

Catechol-O-methyl transferase - found throughout the body, especially in the liver and it breaks down NE and Epi

Front 30

M1 receptors

Back 30

Primarily in CNS and exocrine glands. Gq protein coupled, sitimulates phospholipase C --> IP3/DAG increasing intracellular Ca and depolarization

Front 31

M3 Receptors

Back 31

found in some exocrine glands, smooth muscle, and endothelium. Gq protein coupled - stimulates phospholipase C --> IP3/DAG increased intracellular Ca and depolarization

Front 32

M2 Receptors

Back 32

Heart, some smooth muscle, and on presynaptic neurons. Gi coupled, inhibit adenylyl cyclase reducing cAMP open K channels --> hyperpolarization

Front 33

Nn receptors vs. Nm receptors

Back 33

Nn - autonomic ganglia and adrenal medulla
Nm - skeletal muscle
All nicotinic receptors open Na channels --> depolarization of target cell (neuron/muscle)

Front 34

Alpha 1 receptors

Back 34

Found in smooth muscle - Gq coupled - activate phospholipase C --> IP3/DAG increased intracellular Ca --> depolarization

Front 35

Alpha 2 Receptors

Back 35

Found on presynaptic terminals, in platelets, lipocytes, and smooth muscle. Coupled to Gi protein - inhibits adenylyl cyclase, decreasing cAMP - generally inhibitory

Front 36

Beta 1 receptors

Back 36

Found on many pre and post synaptic sites and in the HEART, Coupled to Gs - stimulates adenylyl cyclase increasing cAMP - excitatory

Front 37

Beta 2 receptors

Back 37

found on postsynaptic sooth muscle, bronchioles, heart, coupled to Gs protein - stimulates adenylyl cyclase, increasing cAMP, effect may be stimulation or relaxation depending on tissue

Front 38

Beta 3 receptors

Back 38

Found on lipocytes, coupled to Gs - stimulate adenylyl cyclase

Front 39

D1/D5 receptors

Back 39

Found in Brain and renal vascular bed, stimulate adenylyl cyclase increasing cAMP

Front 40

D2,D3,D4

Back 40

Found in brain and various other tissues, inhibit adenylyl cyclase decreasing cAMP

Front 41

Trophotrophic

Back 41

Leading to growth - describes the parasympathetic nervous system, "rest and digest"

Front 42

Ergotropic

Back 42

Leading to energy expenditure - describes the sympathetic nervous system, "fight or flight"

Front 43

Muscarinic receptors on endothelium

Back 43

Blood vessels do not constrict or dilate in response to direct parasympathetic innervation, instead the endothelial cells are parasympathetically innervated and they release NO when activated causing vasodilation

Front 44

M2/M3 Heart/Lungs

Back 44

Bronchoconstriction in the lungs - especially asthmatics
Receptors in the heart (primarily atrium) decreases rate at the SA node, slightly decreases atrial contractility and AV conduction

Front 45

Constriction of the cilliary muscle - 2 effects

Back 45

1. Widens space in trabecular meshwork, allowing aqueous humor drainage
2. Makes the lense more convex and shifts it forward - accommodating for near vision (parasympathetic)

Front 46

Cholinergic stimulus in the eye

Back 46

Activates Muscarinic receptors - Causes contraction of the ciliary muscle - increasing aqueous humor outflow and accomodating for near vision. Also causes miosis (pupillary constriction)

Front 47

Sympathetic receptors in the eye, what does their activation cause?

Back 47

Alpha - causes contraction of radial muscle - mydriasis which may promote some drainiage of intraocular fluid. Doesn't affect the ciliary muscle or accommodation because it doesn't affect the parasympathetic tone which is contracting the ciliary muscle
Beta - Increase aqueous humor production, beta blockers can treat glaucoma