Characteristics of NTs Flashcards

1
Q

Norepi is released from

A

the locus ceruleus of midbrain

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2
Q

Norepi is released from which system ?

A

SNS

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3
Q

Norepi binds to what receptors

A

alpha or beta

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4
Q

Norepi release is enhanced by

A

amphetamines

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5
Q

Reuptake of norepi is blocked by

A

TCA (tricyclics), Cocaine

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6
Q

Reserpine has what effect on Norepi? leads to?

A

Reserpine decreases Norepi levels –> depression

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7
Q

Norepi is metabolized by

A

MAO and COMT

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8
Q

Metabolites of Norepi are:

A
  • 3,4-Dihydroxymandelic acic (DOMA)
  • Normethanephrine
  • 3-methoxy-4-hydroxyphenyglycol (MOPEG)
  • Vanillylmandelic acid (VMA)
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9
Q

In phenochromocytoma, what is excreted?

A

increased VMA excretion in urine

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10
Q

ACh is mainly what kind of NT?

A

Excitatory

-inhibitory on heart

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11
Q

ACh is secreted by:

A

motor neuron at NMJ
pre-ganglionic fibers of SNS and PNS
post-ganglionic fibers of PNS and some of SNS

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12
Q

this prolongs the effect of acetylcholine

A

organophosphate
nerve gas

*acts as AChE blocker –> prolonging effects of ACh

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13
Q

Treatment for organophosphate toxicity?

A

Atropine

-blocks muscarinic receptors

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14
Q

Release of ACh is inhibited by

A

botulinum toxin

- muscle paralysis

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15
Q

ACh receptors are blocked by

A

Curare

-muscle paralysis

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16
Q

this NT is decreased in Alzheimer’s disease

A

ACh

*give AChE blockers (Rivastigmine) to help

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17
Q

The ACh receptors are destroyed in

A

Myasthenia gravis

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18
Q

Epi is secreted, along with norepi from

A

adrenal medulla

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19
Q

Dopamine releases from

A

substantia nigra

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20
Q

dopamine inhibits

A

prolactin secretion

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21
Q

Dopamine is decreased in what disease process? why?

A

parkinson’s disease

-degeneration of dopamenergic neurons of substantia nigra

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22
Q

Dopamine is increased in what disease?

A

schizoprenia

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23
Q

Serotonin (or 5-HT) is formed from

A

tryptophan

24
Q

Serotonin (5-HT) is produced by the

A

Raphe nuclei, dorsal horn of spinal cord

25
Q

Serotonin is an ____ of pain pathways in the spinal cord

A

inhibitor

feeling good NT

26
Q

Fluoxetine is

A

Prozac

*SSRI

27
Q

SSRI’s inhibit

A

reuptake (recycling) of serotonin –> increasing serotonin levels

–antidepressant action

28
Q

Histamine is present in the

A

hypothalamus

29
Q

Histamine is formed from

A

histidine

30
Q

Histamine is released by

A

mast cells

31
Q

For increased stomach acid secretion, we’d give

A

H2 blockers

32
Q

The most common excitatory NT is

A

Glutamate

“Go Glutamate Go”

33
Q

This NT is known as the “stroke NT”

A

Glutamate

excites the cells to death in stroke

34
Q

after a stroke, Glutamate increases intracellular

A

Na+ and Ca++

35
Q

How many glutamate receptors are there?

A

four

  • three subtypes
  • including NMDA receptor
36
Q

GABA-A receptors increase

A

Cl- conductance

37
Q

The site of action of benzodiazepines (Valium) and barbiturates:

A

GABA A receptors

38
Q

GABA-B receptors incease

A

K+ conductance

39
Q

This is an inhibitory NT in the spinal cord, basal ganglia, cerebellum and cerebral cortex

A

GABA

40
Q

This is an inhibitory NT mainly in the SPINAL cord

A

Glycine

41
Q

Glycine is in the

A

spinal cord

42
Q

Glycine increases

A

Cl- conductance

43
Q

Tetanus toxin (clostridium tetanus) blocks

A

glycine –> tetanus

44
Q

A short acting inhibitory NT

A

NO (nitric oxide)

45
Q

NO acts in the

A

GIT
blood vessels
CNS

46
Q

This NT acts via cGMP

A

Nitric Oxide (NO)

47
Q

These are natural opiates

A

endorphins

48
Q

Name types of endorphins

A

Dynorphin

Enkephalins

49
Q

Endorphins inhibit release of

A

Substance P

no sub p to brain = no pain

50
Q

This NT mediates pain sensation in PNS

A

Substance P

51
Q

Somatostatin is what kind of NT hormone?

A

very inhibitory hormone

52
Q

This NT has an anti-GH effect

A

Somatostatin

53
Q

What NT also affects REM sleep

A

ACh

54
Q

What NT’s affect Huntington’s

A

Ach and GABA

55
Q

Acidosis on neuronal activity

A

depresses neuronal activity

-pH change from 7.4 to 7.0 will induce coma

56
Q

Alkalosis effect on neuronal activity

A

increases neuronal excitability

-ph change from 7.4-8.0 will induce Seizures