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APEX UNIT 2 ANS Flashcards

(121 cards)

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1
Q

ACh at the NMJ is an example of

A

Ion channel

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2
Q

Norepinephrine at vascular smooth muscle is an example of what kind of receptor?

A

G-Protein Couple Receptor

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3
Q

The process by which a cell converts an extracellular signal into a intracellular response?

A

Signal transduction

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4
Q

Name the 4 different types of signal transduction mechanisms?

A

Ion channels
G Protein Couple receptor
Enzyme linked receptors
Intracellular receptors

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5
Q

3 categories of membrane bound receptors are?

A

1) ion channel
2) G-protein couple receptor
3) Enzyme linked Receptor

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6
Q

What kind of channel prevents ion from flowing along concentration gradient?

A

Closed channel

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7
Q

What kind of channel allow ion to flowing along a concentration gradient?

A

Open channel

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8
Q

What are the 2 ways a GPRC work?

A

It opens or closes a channel
It activate or inhibits an enzyme inside the cells

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9
Q

For enzyme linked receptor, the receptor is also an

A

Enzyme

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10
Q

For enzyme linked receptor, the catalytic domain is _____at rest. When the signal binds, what happens the catalytic domain?

A

Inactive; becomes activated

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11
Q

Steroids binds to what receptors in the _____

A

cytoplasm

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12
Q

Thyroid hormone binds to receptors in the _____

A

Nucleus

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13
Q

Name 5 second messengers

A

IP3
DAG
Calcium
cGMP
cAMP

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14
Q

List the sequence when GPCR gets a first messenger

A

First messenger
GPCR
Effector
Second messenger
Cellular response

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15
Q

The first messenger is described as a what?

A

A ligand that binds to the GPCR

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16
Q

What are examples of ligands?

A

Neurotransmitter and hormone

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17
Q

The G protein itself resides where

A

inside of the cells

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18
Q

What are the 3 subunits of the GPCR (BAG)

A

Beta
alpha
Gamma

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19
Q

What is the first messenger for the NDMA receptor?

A

Glutamate

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20
Q

G protein and effector

A

Either stimulates it to do something or prevents it from doing something

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21
Q

What are the stimulator G proteins

A

Gs or Gq

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22
Q

What is the inhibitory G protein

A

Gi (Turns a signal off)

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23
Q

What happens when a ligand bind to the GPCR? 3 steps

A

1.The interaction of the ligand with the receptor activates G-protein
2. This causes the alpha subunit to dissociate from the beta and gamma subunits
3. The alpha subunit of a Gs or Gq protein will turn on an effector, while the alpha subunit of a Gi protein will turn off an effector.
4. Then when the ligand unbinds from the receptor, it goes back to join the beta and gamma subunits, and its interaction with the effector is done.

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24
Q

What is the function of the effector?

A

It is to activate the 2nd messenger

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25
Name 2 enzymatic effectors?
Phospholipase C and Adenylate cyclase
26
What are examples of ion channel effectors?
GABA-A and M2 Receptors at the SA node
27
What does the 2nd messenger do?
Modulates a series of activities involving phosphatases and protein kinases that elicit a reaction in a particular cell type.
28
The intracellular response to a 2nd messenger is _________
tissue specific (meaning different cell types have different response to ICP)
29
Name the receptors that are involved in Gq signal transduction?
Alpha-1 Muscarinic 1,3,5 Vasopressin 1 Histamine 1
30
Name the receptors that are involved in Gs signal transduction?
Beta 1, 2 D1, Vasopression 2 Histamine 2
31
Is Gq stimulatory or inhibitory?
Stimulatory
32
Is Gs stimulatory or inhibitory?
Stimulatory
33
Name the receptors that are involved in Gi signal transduction? MAD
M2, 4 Alpha 2 D2
34
Gq effector is ________which 2nd messenger are?
(qP) Phospholipase C ; IP3, DAG and Calcium
35
Gs effector is _________ Which 2nd messenger is
Adenylate cyclase ; Stimulate adenylate cyclase leads to an INCREASE in cAMP (converts ATP into cAMP)
36
Gi effector is __________
Adenylate cyclase: INHIBITS adenylate cyclase leading to a DECREASE in cAMP (inhibits ATP to be converted to cAMP)
37
Skeletal muscle vasodilation via what receptor
Beta-2
38
Increase automaticity via what receptor
Beta-1
39
Receptor that can cause bronchoconstriction?
M3
40
Receptor that can lead to diuresis?
Alpha 2
41
Increase contractility through what recepotr?
B1
42
Increase automaticity through what receptor?
B1
43
Increase conduction speed through
B1
44
Decrease contractility, automaticity and conduction speed through
M2
45
ANS action on bronchial tree and via what receptor?
Bronchodilation via B2
46
Parasymp. NS action on bronchial tree and via what receptor?
Bronchoconstriction via M3
47
SNS action on kidney as far as renin and what receptor?
Increase renin via B1
48
SNS action on renal tubules
Diuresis (ADH inhibition)
49
Vasculature Arteries SNS action
Alpha 1 > Alpha 2
50
Vasculature Veins SNS action
Alpha 2 > Alpha 1
51
SNS action of myocardium via what receptor?
Vasodilation B2
52
SNS action of skeletal muscle via what receptor?
Vasodilation B2
53
Mydriasis is through stimulation of
Alpha 1
54
Decrease insulin release through what receptor
Alpha 2
55
Increase insulin release through what receptor?
Beta 2
56
Miosis is
Near vision , constriction though PNS
57
Mydriasis does what to pupils?
Dilation
58
NO PNS action of those areas
Arteries and veins, Specific vascular beds.
59
SNS action on the trigone and sphincter muscle
Contraction through alpha 1
60
SNS action on the detrusor
Relaxation through Beta 2
61
SNS on liver through what 2 receptors?
Increase serum glucose through alpha 1 and beta 2
62
SNS on skin and sweat glands
Alpha 1
63
SNS and motility
Decrease through Alpha 1, 2, Beta 1, 2
64
PNS and motility
Increase
65
Radial muscle (iris) and SNS
Contraction (mydriasis) through alpha 1
66
PNS and Sphincter muscle
Contraction (miosis)
67
SNS action on gallbladder and duct
Relaxation through B2
68
Radial muscle is in the white part of the eye or black?
White
69
Sphincter muscle is in the white part of the eye or black?
Black
70
Detrusor muscle with SNS
Relaxation via Beta 2
71
Detrusor muscle with PNS
Contraction via M
72
Uterus contraction through PNS
M
73
Uterus relaxation through SNS
Beta 2
74
Uterus contraction with SNS
Alpha 1
75
Radial muscle with SNS
Contraction through
76
Stimulation of this receptor reduces shivering
Alpha 2
77
Alpha 2 receptor stimulation and insulin
Inhibits insulin secretion
78
Stimulation of alpha 2 and platelet aggregation
Promotes platelet aggregation
79
Stimulation of alpha 2 and SNS outflow
Reduces SNS outflow
80
Stimulation of alpha 2 produces 3 main effects
sedation , analgesia and hypnosis
81
Alpha 2 in present throughout the body, in 3 locations
Presynaptic, post synaptic and nonsynaptic
82
Alpha 2 is present Presynaptic in
NE releasing neurons in the CNS and PNS Negative feedback mechanism reduces NE release
83
Postsynaptic NE
Smooth Muscle and several organs
84
Nonsynaptic locations of alpha 2 receptors
Platelets
85
Alpha 2 effect on the Medulla
Decrease SNS tone
86
Alpha 2 effect on vagus nerve
Increase PNS tone
87
Where in the Nervous system does the alpha 2 produces its Sedation and hypnosis effect?
Locus Coerulus.
88
Where in the Nervous system does the alpha 2 produces its analgesic effect?
Spinal Cord (dorsal horn)
89
Where in the Nervous system does the alpha 2 produces its antishivering effect?
unknown
90
Effect of alpha 2 on vasculature?
Vasoconstrictions then vasodilation (HTN then HoTN )
91
Alpha 2 effects on renal tubules
Inhibits ADH release (diuresis)
92
Decrease insulin resistance through stimulation of
Alpha 2
93
Dexdemetomidine is what kind of medication? Effect on SNS tone ? sedation?
Alpha 2 agonist, centrally acting, reduces SNS tone, causes sedation, MAC reduction, analgesia, bradycardia and vasodilation.
94
Dexmedetomidine can cause both
Hypotension, then transient HTN
95
What enzyme metabolizes cyclic adenosine monophosphate?
Phosphodiesterase III
96
Action of cAMP
Activates protein kinase A which initiates a variety of phosphorylation reaction inside the cells.
97
Phosphodiesterase and action on cAMP
Turns it off by metabolizing it to AMP
98
In the presence of Oxygen 1 mol glucose leads to
38 moles of ATP
99
Beta 1 are present in the ______while beta 2 are present in ______And _________ such as the _______
Heart Skeletal muscle and other vascular bed such as the myocardium
100
What is the function of cAMP?
Responsible to turn on a variety of protein kinases that instruct the cell to perform a specific function.
101
What does the PHOPHODIESTERASE III do?
Metabolizes cAMP to AMP these turn off these protein kinases and the cell is no longer instructed to perform that specific function.
102
What does the PHOSPHODIESTERASE III inhibitor do?
Inhibit the turn off mechanism, of phosphodiesterase III directly increase intracellular cAMP and maintains the protein kinases in the turned on state.
103
When protein kinases are maintained in the turned on state how is that good?
Its good because in the cardiac muscle it increases inotropy and lusitropy In the vascular muscle: It causes relaxation and vasodilation.
104
What is the role of cAMP in the cardiac muscle cell
It increases intracellular calcium and the force of contraction
105
What is the role of the cAMP with increasing cardiac performance?
It increasing the rate of relaxation by accelerating the return of calcium to the Sarcoplasmic reticulum, this is called lusitropy.
106
Role of cAMP in the vascular smooth muscle cell?
Inhibits myosin light chain kinase causing vasodilation and decreased SVR.
107
What is considered the prototype nonselective phosphodiesterase inhibitor?
Theophylline
108
PDE III inhibitors example
Milrinone also called Inodilators.
109
Why is a PDE III Inhibitor a good choice?
because they augment myocardial performance independently of the SNS.
110
3 conditions in which PDE III inhibitor is a good choice?
Beta blocker induced myocardial depression Acute HF Unresponsive to IV catecholamines.
111
Catecholamines synthesis what is the rate limiting step?
Tyrosine Hydroxylase catalyzes the rate limiting step in the norepinephrine release.
112
Where does NE inhibit its own release?
In the synaptic cleft.
113
Where is Norepinephrine converted to Epinephrine ?
In the adrenal medulla
114
The adrenal medulla releases Epi and NE at what %?
80% epinephrine 20% norepinephrine.
115
What is the main site of NE synthesis?
Post-ganglionic nerve terminal
116
What is the rate limiting step of the catecholamine synthesis?
Tyrosine is transported actively in the axoplasm and converted to DOPA(DihydrOxyPhenylAlanine)
117
What triggers the exocytosis of NE
Intracellular calcium that accompanies an action potential
118
What terminates the effects ofNE at the effector site?
Active re-uptake of NE in the presynaptic terminal 80%
119
What is responsible for the metabolism of the small amount of NE that enters the cytoplasm after neuronal uptake?
Monoamine oxidase.
120
2 main enzymes responsible for NE metabolism for NE that is not reabsorbed
Catechol-O-Methyltransferase
121
What is the primary neurotransmitter in the SNS?
Norepinephrine

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