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Therapeutics > Exam 3 lecture 2 > Flashcards

Exam 3 lecture 2 Flashcards

1
Q

How does transport into pre-synaptic neuron or neighboring glial cell affect neurotransmission

A

slows it down

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2
Q

Effect of destruction of neurotransmitter in neurotransmission

A

slows it down

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3
Q

can post synaptic receptors be agonists or antagonists

A

both

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4
Q

how do drugs act on neurotransmitters

A

Some drugs act as agonists
some act as antagonists
some act as partial agonists
some drugs target the removal of transmitters from synaptic cleft

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5
Q

What are the different ways drugs can target drugs removal of neurotransmitters from cleft

A

Enzymatic metabolism
transport into presynaptic neuron or neighboring glial cell

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6
Q

Glycine MOA

A

similar to GABA but acts in spinal cord

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7
Q

Common aa neurotransmitters

A

GABA
Glycine
Glutamate

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8
Q

What is GABA

A

a major inhibitory neurotransmitter in the brain.

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9
Q

How does GABA work

A

Depresses neuronal excitability by increasing flux of Cl- ions into neurons

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10
Q

What are the GABA receptors

A

GABA-a
GABA-B

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11
Q

Drugs that interact with GABA pathways are generally

A

CNS depressants

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12
Q

What are some drug types that interact with GABA pathways

A

Sedatives
Anticonvulsants
anxiolytics

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13
Q

What is the difference between GABA a and GABA b

A

GABA a- GABA receptors that are ion channels and allow influx of Cl- ions

GABA b- GPCR

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14
Q

What kind of neurotransmission does glutamate have?

A

It is a major excitatory neurotransmitter

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15
Q

What is the effect of excessive glutamate

A

can cause neuronal damage by allowing excessive Ca2+ influx into neuron

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16
Q

What are glutamate receptors

A

Metabotropic (GPCR) or ionotropic (NMDA and AMPA)

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17
Q

what are metabotropic? what are ionotropic?

A

Metabotropic are GPCRs
Ionotropic re receptors that bind glutamate and allow influx of ions

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18
Q

Common non aa neurotransmitters

A

Ach
Dopamine (DA)
Norepinephrine
Serotonin , 5 hydroxytryptamine (5-HT)

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19
Q

What are particular regions of the brain that have more prominent Ach signalling

A

Basal forebrain (alzheimers)
Pons
Cortex
Basal ganglia

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20
Q

types of Ach receptors

A

Nicotinic (ionotropic Na channels)
Muscarinic (GPCR)

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21
Q

Ach is important in

A

Nicotinic dependence
Cognitive function/disorder
Movement disorder

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22
Q

examples of drugs that target this Ach receptor

A

Cholinesterase inhibitors like aricept (to treat alzheimers)

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23
Q

Dopamine transmission has a role in

A

Parkinsons disease
schizophrenia
addiction
depression
ADHD

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24
Q

What are some places where dopamine signalling is important

A

Midbrain (substantia nigra and pons compacta)
(used in voluntary motor function)

Ventral tegmental area
(used in reward and addiction)

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25
Q

Dopamine receptor types

A

Only GPCR

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26
Q

what are the different groups of dopamine receptors

A

D1 group (D1 and D5)
D2 group (D2, D3 and D4)

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27
Q

D1 group effect on CAMP? What is it coupled to?

A

Coupled to Gs protein, leads to increase in CAMP

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28
Q

D2 group effect on CAMP? what is it coupled to?

A

GI coupled, lead to decrease in CAMP concentration

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29
Q

What is parkinsons caused by

A

Insufficient dopamine signalling due to loss of dopamine producing neurons in substantia nigra

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30
Q

What is schizophreia caused by>

A

Excess dopamine signalling

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31
Q

what is DAT

A

dopamine transporter

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32
Q

what happens when drugs that block DAT are taken

A

drugs that block extracellular dopamine (amphetamine and cocaine) can produce euphoria and lead to addiction

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33
Q

drugs that interact with dopamine pathways include

A

Antipsychotics (D2 receptor antagonists)
D2/D3 and D1 receptor agonists for PD

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34
Q

region in brain important for norepinephrine signaling

A

Pons (locus coeruleus)

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35
Q

what type of receptors are used for norepinephrine transmission

A

GPCR receptors

36
Q

Norepinephrine is important in

A

Memory
Depression
addiction
Pain

37
Q

What are the receptors for norepinephrine transmission

A

alpha and beta adrenergic receptors (GPCRs)
Norepinephrine transporter (NET)

38
Q

What are NET inhibitors used to treat

A

Depression

39
Q

serotonin transmission is important in what part of brain

A

Mid brain/pons (raphe nuclei) important

40
Q

serotonin is important in

A

Depression
Mood disorders/anxiety
Schizophrenia

41
Q

What type of receptors are serotonin receptors

A

14 are GPCRs
1 is ion channel

42
Q

5-HT meaning

A

serotonin

43
Q

drug targets for serotonin

A

serotonin receptors (14 GPCRs, 1 gated ion channel)
and serotonin transporter (SERT)

44
Q

5-HT axons arise from a group of cell bodies called

A

Raphe nuclei

45
Q

Drugs that interact with 5-HT receptors

A

5-HT 2A- antagonist as a typical antipsychotics
5-HT 1D- Agonist for migraine
SERT- uptake inhibitor for depression
5-HT 2A- agonists are hallucinogenic (LSD)

46
Q

Multiple sclerosis meaning

A

immune mediated inflammatory disorder involving destruction of the myelin sheath that surrounds neuronal axons

47
Q

symptoms of MS

A

Visual problems (monooccular blindness, double vision)
Numbness, tingling
Fatigue, motor weakness

48
Q

potential role for viral infection in MS

A

Epstein barr virus (EBV) may be involved in MS

49
Q

why is EBV bad?

A

There is a sequence similarity between EBV and self peptides that results in activation of autoreactive T or B cells (molecular mimicry)

An immune response to EBV will lead to recognition of self myelin protein and leads to autoreactive immune cells

50
Q

EBNA meaning

A

EBV nuclear antigen antibody

51
Q

What does EBNA do in our bodies

A

EBNA proteins will mimic myelin base protein (which is endogenous to each of us) and an immune response will lead to targeting of our own myelin basic protein

52
Q

When do individuals with a particular HLA phenotype have an increased risk of developing MS

A

when they have anti EBNA antibody

53
Q

know figure showing different clinical forms of MS (RRMS, SPMS, etc)

A
54
Q

in what order do the clinical forms of MS occur on the graph

A

Pre- symptomatic MS
RRMS
SPMS

55
Q

do inflammatory episodes occur continously of intermittently for MS

A

intermittently

56
Q

what is cytodegeneration

A

Neural degeneration that occurs gradually (loss of myelin sheath and loss of axons)

57
Q

according to the graph, what must happen to see symptoms

A

An orange bar or blue line must cross threshold to see any symptoms

58
Q

according to graph, do initial inflammatory episodes cross threshold? what does this lead to?

A

do not cross threshold, lead to pre- symptomatic MS (no symptom)

59
Q

When will there be an inflammatory episode according to the graph for MS? What is this called?

A

there will be an inflammatory episode the 1st orange bar that crosses the threshold. It is called CIS (clinically isolated syndrome)

60
Q

What is RRMS

A

relapsing of symptoms and disappearing, multifocal areas of damage are revelaed by magnetic resonance imagine in white matter

initial symptoms disappear but less remission with each relapse
Most RRMS enter SPMS

61
Q

Where do we see more inflammation RRS or SPMS

A

RRMS

62
Q

What is SPMS

A

SLowly progressive neurological decline and CNS damage with little remission

63
Q

what is PPMS?

A

resembles SPMS at initial stages, mean age of onset is later than RRMS (40 vs 30)

64
Q

do inflammatory episodes of RRMS pass symptomatic threshold?

A

yes

65
Q

compare SPMS and PPMS

A

Orange bar does not cross threshold or touch the line. SPMS does.
PPMS not visible to patient and no relapsing remitting phase.

66
Q

what is a CIS

A

an initial episode of neurologic symptoms lasting >24 hr

67
Q

What happens to antigens released from CNS or cross reactive foreogn antigens

A

They are presented to B and T cells in the lymph nodes

68
Q

What happens to the B and T cells that have a high affinity receptors for the antigens presented to it by CNS or cross reactive foreign antigens (autoimmune phase)

A

B and T cells with high affinity receptors for these antigens are expanded and migrate to CNS sites where they re encounter and are activated by their target ligands

Activated B and T cells then carry out immune functions (release of antibodies and cytokines respectivelly) at CNS sites

69
Q

explain degenerative phases of MS

A

CNS damage is triggered by activated B and T cells. Or by other insults like infection or stroke.
Antigens released from damaged sites in CNS further prime immune cells in periphery, thus completing a vicious cycle

70
Q

Explain autoimmune responses in MS

A

Leakage of antigen out into periphery will either directly stimulate a B cell by interacting with it or it will be picked up by a dendritic cell

dendritic cells activate T cell responses in peripheral lymphoid tissue

activated B and T cells proliferate and infiltrate the CNS and BBB

71
Q

How do B and T cells make it into the brain?

A

They use a protein expressed on surface of both B and T cells called α-4 integrin.

72
Q

What do α-4 integrins do?

A

allow B and T cells to anchor to BB and start process leading to penetration

73
Q

WHat happens when B cells and T cells make it into the brain

A

B cells mature into plasma cells and release IgG antibodies that cause demyelination

T cells interact with target ligands presented by oligodendrocytes, neurons or microglia on MHC molecules, which leads to T cell activation. T cell activation results in cytokine release and macrophage stimulation leading to damage of myelin sheath.

74
Q

T cells engage oligodendrocytes via

A

MHC class I interactions

75
Q

cytokines released by T cells include

A

IFN-gamma
TNF-α
perforin

76
Q

macrophages also harm myelin sheath via

A

Phagocytosis

77
Q

What happens to action potentials in zones of demyelination

A

In MS, demyelination leads to slowing down of action potential of axon signaling (inefficient action potentials are the result of demyelination)

78
Q

SPaces between myelins are called

A

Nodes of ranvier

79
Q

explain remyelination

A

Remyelination (myelin repair) involves the recruitement OPCs to the lesion and the differentiation of these cells into myelin- producing oligodendrocytes.

Remyelination typically fails in MS because of a lack of OPC or failure of OPC to differentiate

80
Q

What is astrogliosis

A

Involves the invasion and propagation of astrocytes resulting in irreversible formation of gliotic plaques or scaring

81
Q

explain steps of remyelination

A

Demyelination (loss of myelin and oligodendrocytes) results in the activation of microglia and astrocytes.

Activated microglia and astrocytes release pro-migratory factors and mitogens that recruit OPCs to the lesion and stimulate their proliferation. Macrophages eliminate the myelin debris.

Recruited OPCs differentiate into oligodendrocytes via a process involving axon engagement and myelin sheath formation. OPC differentiation is the key step where remyelination fails in MS.

82
Q

what is less pronounced in SPMS compared to RRMS

A

T cell priming in peripheral lymphoid tissue
Infiltration of B cells in CNS

these are both autoimmune events (orange bar), axon degeneration (blue line) is more pronounced in SPMS)

83
Q

Describe pathogenic mechanisms that are current or potential targets for MS therapies.

A

immunomodulatory therapies
- interference with T cell or B cell activation
- inhibition of T cell or B cell proliferation movement into CNS
- inhibition of α-4 integrin mediated binding and penetration of BBB

rescue strategy
remyelination (agents that facilitate OPC recruitment or promote OPC differentiation)

84
Q

Understand how gadolinium-enhanced MRI can be used to
visualize lesions in MS patients.

A

Gadolinium is a contrast agent used to visualize breakdown of BBB and formation of lesions in brain of MS patients
(penetrates regions where BBB is compromised)

85
Q

Know the symptoms, pathophysiology, and treatments of Guillain-Barré syndrome.

A

Many similarities to MS but is peripheral instead of CNS

infection leading to autoimmune response
can be fatal
leads to demyelination

treatment
Ventilation
plasmapharesis (eliminating auto antibody)
IV mmunoglobin admission

symptoms
weakness in distal muscles and lower extremities
can progress to total paralysis with death from respiratory failures in days

Therapeutics (38 decks)

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