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Sem3 > Case 6 > Flashcards

Case 6 Flashcards

1
Q

What are the two types of astrocytes?

A

Fibrous astrocytes - round in white matter

Protoplasmic astrocytes - round in grey matter

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2
Q

What is the precursor of astrocytes called?

A

Radial glial

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3
Q

What does the cytoskeleton consist of?

A

Microtubules, microfilaments and neurofilaments

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4
Q

What are the different types of neurones?

A

Unipolar - sensory
Pseudounipolar - sensory
Bipolar - interneuron
Multipolar - motor/interneuron/pyramidal cell

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5
Q

Which neurones are myelinated?

A

Some in PNS and those in the Sympathetic nervous system

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6
Q

Where is neurotransmitters produced?

A

In the neurones cell body and then actively transported to axonal end

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7
Q

What is an electrotonic potential?

A

Non-propagated local potential caused by a local change in ionic conductance - it reduces as it spreads across the membrane

Used to trigger AP

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8
Q

What is an Action Potential?

A

Propagated impulse

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9
Q

How is a resting potential set?

A

Set through Na/K pump and also the open potassium ion channels which increases the membrane permeability of potassium.

The is more potassium inside the cell than outside (opposite for sodium)

RP = -70mV

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10
Q

What happens during depolarisation?

A

Depolarising stimulus causes the activation of voltage-gated sodium ions, if threshold is met, influx of sodium causes an AP

At +30mV the sodium channels become inactive before returning to resting state

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11
Q

What happens during repolarisation?

A

Voltage-gated potassium channels open slowly and causes efflux of potassium reducing the membrane potential

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12
Q

What is hyperpolarisation?

A

This is a process where a high stimulus is required to cause AP because of slow return of potassium channels to close state

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13
Q

What are the two gates of the sodium voltage-gated sodium channels?

A

M-gate - activation gate outside the cell

H-gate - inactivation gate inside the cell

RP = m-gate closed and h-gate open
Depolarisation = m-gate open and h-gate open 
Repolarisation = m-gate open and h-gate closed

(Potassium only has h-gate)

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14
Q

What is the all-or-none law?

A

Once threshold is met an AP is produced and further increase in intensity of a stimulus won’t produce changes in AP

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15
Q

What are the two refractory periods?

A

Absolute - no stimulus will excite the nerve (due to inactivation of Na channel)

Relative - stronger than normal stimuli can cause excitation (due to K channel)

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16
Q

What are the two types of receptors?

A

Ionotropic - ion channels
Metatropic - g-protein coupled

In metatropic, the g-protein will activate ion channels or enzymes that generate 2nd messengers - there are then slower and longer lasting than ionotropic

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17
Q

What are the two types of demyelinating disease?

A

Primary demyelination - myelin sheath damage without axonal damage

Secondary demyelination - myelin sheath damage resulting from axonal damage

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18
Q

What are the CNS and PNS demyelinating disease to know?

A

CNS: MS and Vitamin B12 deficiency

PNS: Gullain-Barre Syndrome

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19
Q

What is MS?

A

Disease characterised by inflammation, demyelination and gliosis with lesions seen in CNS white matter

It may be relapsing (85%) or progressive (10-15%)

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20
Q

What are the symptoms of MS?

A

Loss of or changes in sensitivity (tingling, pins and needles, numbness)

Muscle weakness, pronounced reflexes, spasms, difficulty moving

Incoordination: ataxia, speech and swallowing problems (dysarthria and dysphargia) and visual problems (nystagmus, optic neuritis or dyplopia)

Depression and unstable mood

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21
Q

What is the epidemiology of MS?

A

1/800 in UK
Onset 20-40yo
Risk = low levels of vitamin D, exposure to human herpes virus and Epstein-Barr virus , smoking and stress

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22
Q

What are the types of MS?

A
  • Relapsing and remitting (85-90%) - relapses (symptoms worsen) then complete or partial recovery and then remission (symptoms don’t worsen)
  • secondary progressive - progression of disease following RRMS
  • Primary Progressive (10-15%) - gradual progression from onset with no remissions or relapses
  • progression relapsing (<5%) - progresses gradually but interrupted with sudden relapses
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23
Q

What are the three characteristics of MS

A

Inflammation, demyelination and

Lesions (plaques)

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24
Q

What happens during inflammation?

A

An infection causes damage to BBB which allows T-cells into CNS - there is recruitment of lymphocytes and monocytes > the chemokines released cause adhesion molecules on lymphocytes and monocytes which interact with Endothelial cells on BBB activating expression of MMP to degrade barrier leading to swelling and activation and infiltration of macrophages and lymphocytes that directly attack myelin sheath within CNS

Cytokines and antibodies are also recruited

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25
Q

What is the demyelination process?

A

Relapse:
Th-1 and Th-17 activated by IL-12 (over production of IL-12 =inflammation) which then attack myelin sheath (oligodendrocytes)

Remission:
Oligodendrocytes cells can’t fully repair so CNS gets stem cells but the new formed myelin is thin and not as effective so remission causes worsening until scar-like plaques (sclerosis) builds around damage axons

26
Q

What do Th1 and Th17 cells do?

A

Th 1 secrete IFN-gamma for macrophages

Th-17 promoter leukocyte recruitment

27
Q

Where do lesions tend to form?

A

White matter in:

Optic nerve, corpus callosum, cerebellum, brainstem, basal ganglia and spinal cord

28
Q

What is Optic Neuritis?

A

Diminished visual acuity, dimness, or colour desaturation in centre of vision

Afferent pupillary defect

Pallor of optic disc (optic atrophy)

29
Q

How is MS diagnosed?

A

Requires documentation of two or more episodes of symptoms and two or more signs that reflect pathology in anatomically noncontiguous white matter tracts of the CNS

30
Q

What are diagnostic tests for MS?

A

MRI - shows increased vascular permeability due to breakdown of BBB, and lesions

Evokes Potentials Test - shows electrical activity of brain

CSF - elevated levels of IgG antibodies, oligoclonal bands via electrophoresis, and proteins that are breakdown products of myelin

31
Q

How do Glucocorticoids (Methylprednisolone/Prednisone) work?

A

They inhibit the generation of vasodilators and function of APC; they reduce prostaglandin, leukotriene and platelet-activating factor synthesis that result from activation of phospholipase A2; reduce expression of COX-2

reducing inflammation

Side effects: hyperglycaemia, decreased resistance to infection, swelling of face, weight gain, fluid retention, oedema, hypertension

32
Q

How do Beta-Interferon work?

A

Inhibit T cells activation, prevent T cells proliferation and block T cells migration across BBB

Treat relapsing and remitting disease via subcutaneous injection (alternating days) preventing relapse rates and increased lesions

33
Q

What do Immune-modulators do?

A

Glatiramer Acetate/Copaxane

bind to MHC class 2 preventing binding of other antigen

Compete with myelin basic protein (MBP) for T cell receptor

Inhibiting activation of MBP-reactive T cells suppressing inflammatory response

34
Q

What does Fingolimod/Gilenya do?

A

For relapsing-remitting MS

Bind to sphingosine 1-phosphate receptor 1 blocking capacity of autoreactive lymphocytes to egress from lymph nodes - reducing migration to CNS

35
Q

What does Natalizumab/Tysabri do?

A

Monoclonal antibody that inhibits migration of leukocytes into CNS by preventing binding to VCAM-1

Used in severe relapsing remitting MS

Associated with progressive multi focal leukoencephalopathy (PML) due to reactivation of John-Cunningham Virus (JVC)

36
Q

What are the two immunosuppressants?

A

Teriflunomide and Dimethyl Fumarate

37
Q

What is depression?

A

A state of low mood and aversion to activity that can have a negative effect on a person’s thoughts, behaviour, feelings, world view and physical well-being

It is a symptom not a psychiatric disorder lasting 4-12months

38
Q

How is Major Depression Diagnosed?

A

PHQ-9

Questionnaire of symptoms and freq. Over 2weeks

39
Q

What are symptoms of MDD?

A 
Negative cognition (feeling worthless, hopeless) 
Psychosis (psychotic guilt and catatonic retardation)
40
Q

What are risks of MDD?

A

Life stress, family history, earlier age of onset

41
Q

What are the two groups of monoamines?

A

Catecholamines - dopamine, noradrenaline, adrenaline

Indoleamines - serotonin

42
Q

What are the precursors of monoamines?

A

Dopamine - Tyrosine to L DOPA

Noradrenaline - hydrolysis of dopamine

Adrenaline - conversion from noradrenaline

Serotonin - tryptophan

43
Q

How do we intake the monoamines precursors?

A

Tyrosine and Tryptophan is taken from diet

44
Q

What are the enzymes for serotonin and noradrenaline breakdown?

A

MAO-A

MAO-A and COMT

There are two types of MAO:
• MAO-A: deaminate noradrenaline, adrenaline, serotonin, melatonin and dopamine
• MAO-B: deaminate phenylethylamine and dopamine

45
Q

What are the reuptake transporters for serotonin and noradrenaline?

A

5-HTT,SERT

NET, NAT

46
Q

What are the receptors of noradrenaline and serotonin?

A

Alpha receptors - a1 (stimulators) a2 (inhibitory)

Beta receptor - b1,2,3 (stimulators)

5-HT family

47
Q

What is the interaction between serotonin and noradrenaline?

A

Noradrenaline acts on noradrenergic receptors on serotonin systems stimulating or inhibiting the release of serotonin

(The two systems act individually)

48
Q

What is the MOA of Resperine?

A

Used to control Blood Pressure

Irreversible VMAT blocker so prevents transport of serotonin and catecholamines through vesicles from cytoplasm

Causes depression

49
Q

What is the MOA of Imipramine?

A

SNRI antidepressant that inhibits reuptake of serotonin and noradrenaline

50
Q

What is the MOA of Iproniazid?

A

Antidepressant that irreversibly inhibits MAO so increase levels of monoamines (especially serotonin)

Moclobomide reversibly inhibits MAOs

A tyramine diet is required while on MAOI to prevent increase in blood pressure

Side effects:
Dry mouth, nausea, headache, drowsiness, high BP, weight gain

51
Q

What are the three type of antidepressants?

A

Tricyclics Antidepressants (TCAs):
• block reuptake of noradrenaline, serotonin and Dopamine
• amitriptyline and clomipramine

Serotonin-Noradrenaline Reuptake Inhibitors (SNRIs):
• reversibly block SERT and NET
• imipramine and venlafaxine

Selective-Serotonin Reuptake Inhibitors (SSRIs):
• reversibly block SERT
•fluoxetine, sertraline, paroxetine, fluvoxamine, escitalopram, citalopram

52
Q

What is Mirtazapine?

A

Alpha-2 adrenergic receptor antagonist

Blocks the negative feedback loop to inhibit the release of noradrenaline and serotonin therefore there is an increase of both

53
Q

What does the amygdala do?

A

Part of the Ventral Neural System

Modulates visual and attentional processing, particularly of facial expression

In MDD it is overly activated when shown sad stimuli but under-activated when shown positive stimuli

54
Q

What is the function of the hippocampus?

A

Part of the Dorsal Neural system

Deals with memory consolidation

In MDD there is a reduction in the hippocampal volume leading to a decrease in memory consolidation

55
Q

What does diasthesis mean?

A

Prédisposition to illness

56
Q

What is the diasthesis-stress hypothesis of mood disorder?

A

Hyperactivity in HPA system

Hypothalamus releases increase of CRH > stimulates increased ACTH release from anterior Pituitary gland > stimulates increased cortisol release from adrenal cortex

Cortisol dysregulates amygdala function and increases activity of MAO decreasing levels of serotonin, noradrenaline and dopamine
It also causes reduction in BDNF resulting in reduction in neurogenesis and decreased hippocampal volume

57
Q

Which genes are linked with depression?

A

5HTT genes

Short/short = greater risk of developing depression

Short/long = most common in population

Long/long = lesser risk of developing depression

58
Q

How is depression treated?

A
  • Mild - low intensity psychosocial intervention
  • moderate - ADs + high-intensity psychological intervention such as CBT
  • ECT - most effective for depression and involves inducing seizures activity in the temporal lobes
  • psychotherapy - CBT, IPT, PST
59
Q

What is coping?

A

Process of managing stressors that have been appraised as taxing or exceeding a person’s resources

60
Q

What are types of coping?

A

Approach

Avoidance

Problem focused

Emotion focused

Sem3 (10 decks)

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