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Sem 3 Neuro > Case 6 > Flashcards

Case 6 Flashcards

1
Q

Describe MS (name, disease type, brief mechanism, end result).

A

MS = Multiple Sclerosis
Slow progressive CNS disease characterised by destruction of the myelin sheath around the axons in the brain and spinal cord.
Complex immune/genetic disease.
Mediated by autoimmune response - Auto-immune attack of oligodendrocytes (CNS) and/or schwann cells (PNS).
Inflammation of the CNS white matter (axons).
Glial scarring.

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2
Q

In the action potential, what causes hyper polarisation, and what is its purpose?

A

Hyper-polarisation results from K+ channels remaining open after re-polarisation (downstroke). This allows resistance to further action potentials. So need more EPSP’s (from dendrites) to reach threshold for another action potential.

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3
Q

In the action potential, what is the purpose of the Na+/K+ ATP pump after re-polarisation?

A

At the end of action potentials, ions are switched around. (extracellular Na+ rushed inside during upstroke, and intracellular K+ rushed outside during downstroke). So pump swaps ions around to re-establish previous gradient.

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4
Q

How big is Node of Ranvier compared to Myelin Sheath?

A

Node of Ranvier much smaller. 1-2um vs 1mm.

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5
Q

What is the composition of the myelin sheath?

A 
Lipids: galactocerebroside
Glycoproteins: 
myelin basic protein (MBP)
myelin oligodendrocyte glycoprotein (MOG)
myelin associated glycoprotein (MAG)
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6
Q

What is saltatory conduction? Where are the Na+ voltage gated ion channels found?

A

Action potentials jump from node to node. Voltage gated Na+ channels found only at nodes of Ranvier.

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7
Q

What are the pathological END results of MS (on neuronal cells and brain/body)?

A

1) Loss of nerve fibres.
2) Pockets of inflammation (Lacunar white dots - breakdown of BBB - sign of local oedema associated with inflammation)
3) Glial scarring or sclerosis (Astrocytes)
4) Several neurological symptoms including loss of sensation (touch, taste), motor co-ordination impairment (cerebellum affected), vision impairment (visual tracts - involuntary eye movements)

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8
Q

What neurological effects can be caused by MS and what is the reason for them (axons)?

A 
Weakness and clumsiness, 
Stiffness and gait disturbances, 
Visual disturbances, 
Mental disturbances
All caused by degradation of the myelin sheath around axons leading to axonal degradation.
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9
Q

Is MS more common in men or women? What race?

A

Women. Unknown why.

Caucasians

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10
Q

What is the aetiology of MS?

A

Unknown but some factors associated with increased incidence.

Combination of genetic and environmental factors

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11
Q

What environmental factors are thought to be associated with/triggers for MS?

A

1) Viruses & bacteria: part of pathogenesis theory of MS (measles, rubella, mumps and herpes).
2) Nutritional and dietary factors: animals, minerals, chemical agents, metals, solvents

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12
Q

How is chromosome 6 involved in MS?

A 
Chromosome 6 found to carry genes for myelin proteins like MOG & MAG.
Also found to contain MHC class genes
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13
Q

What is MHC? Which cells are involved?

A

MHC = Major Histocompatibility Complex
Execution of immune system (1st line defence)
Cass 1, 2 and 3 (depending on nature of infectious agents)
Found on surface of APC cells (antigen-presenting-cells)
APC blood: Macrophages & monocytes
APC skin: dendritic cells
APC liver: Kupfer cells

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14
Q

How do APC’s used MHC’s to initiate immune response?

A

APC’s phagocytose pathogens, and use MHC’s to present antigen of pathogen to immune system (epitopes). T cell receptor detects MHC-epitope complex and release inflammatory mediators to initiate immune response.

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15
Q

What does a MHC-T cell receptor immune repose involve?

A

Inflammatory mediators released by T cell.
Leads to clonal expansion - proliferation (T cytotoxic cells)
Leads to activation of B cells (antibodies)

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16
Q

What is molecular mimicry and how is it related to MS?

A

Molecular mimicry is the homology between foreign proteins (e.g. viral or bacterial) and self proteins (in this case myelin - MBP, MOG, MAG)

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17
Q

With regards to molecular mimicry: what are the two types of homology? Describe them.

A

1) Sequence homology: Same sequence of amino acids in gene (in a row).
2) Structural homology: Amino acids are in same “position” within a sequence of gene (not in a row).

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18
Q

Generally, what is the blood brain barrier?

A

A membrane that controls the passage of substances for the blood into the CNS.
It is a physical barrier between the local blood vessels and most parts of the CNS.
Thus, CNS normally inaccessible to T lymphocytes.

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19
Q

How is the blood brain barrier involved in MS?

A

Blood brain barrier thought to be disrupted in MS, for reasons not fully understood.

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20
Q

Explain briefly the accepted pathogenic pathway of MS.

A

1) Infection by virus/ bacteria
2) Antigen gets into bloodstream, digested by APC
3) Macrophage (APC) displays antigen with MHC molecule
4) MHC-antigen complex recognised by T cell receptors
5) Activated Th cells crosses BBB to CNS
6) In CNS, Th cells encounter local APC’s (microglia)
7) APC’s present MHC-protiein complex with myelin antigens
8) Th cells are RE-ACTIVATED by local APC’s (due to recognition of epitope-self-proteins of MBP, MOG, MAG.
9) Th cell releases cytokines (microglia, astrocytes, macrophages and B-cells from periphery, antibodies) and complement system (mediates myelin sheath attack)
10) results in demyelination and oligodendrocyte degradation.

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21
Q

What are microglial cells?

A

Neuronal glial cells.
Found in brain and spinal cord (CNS)
Local macrophage and APC

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22
Q

What are the types of MS?

A

1) Benign
2) Relapsing-remitting and relapsing-persistent
3) Relapsing-remitting followed by secondary progression (2ndry prog)
4) Primary chronic progression.
5) Progressive relapsing

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23
Q

Explain benign MS.

A

10-20%.
short episodes or mild neurological symptoms.
Symptoms do not worsen.
Returns to normal between attacks.

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24
Q

Explain relapsing-remitting and relapsing-perssistant MS.

A

85-90%
Unpredictable relapses, lasting 24h or more.
Followed by months-years of remission with no new signs of disease activity.
Period between relapse may decrease.
Symptoms become more severe.
relapsing-remitting: no progression between attacks
relapsing-persistant: progression between attacks (partial recovery).

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25
Q

Explain relapsing-remitting followed by secondary progression MS.

A

80% of those with initial relapsing-remitting.
No relapse or remission, linear progression.
More severe neurological symptoms, worsening cognitive function or other deficits.

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26
Q

Explain primary (chronic) progression MS.

A

10% who never have a remission.

Linear-ish progression with no remission or relapse.

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27
Q

Progressive relapsing MS?

A 
Progression from onset, with attacks. 
Rarest form (<5%)
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28
Q

What are the primary and secondary diagnosis methods of MS?

A

Primary:
MRI scan of brain - white lesions - brain atrophy with widened lateral ventricles and cortical sulci.
Secondary:
Blood - raised levels of B and T cells.
CSF electrophoresis - Oligoclonal IgG bands, inflammation indicator.
Visual evoked potential (VEP) - delayed and reduced due to affected visual pathways.

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29
Q

What is the main treatment used for patients with MS?

A 
Prednisolone (main - anti-inflammatory) 
Anti-depressants 
Anti-convulsants 
Tizanidine 
Baclofen 
Dantrolene
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30
Q

Most common form of MS?

A

Relapsing remitting (85-90%)

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31
Q

Rarest form of MS?

A

Progressive relapsing (85-90%)

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32
Q

What is dysarthria?

A

difficult/unclear articulation of speech that is otherwise linguistically normal.

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33
Q

What MS symptoms can arrises from lesions in the cerebrum?

A

cognitive impairment - deficit in attention/reasoning (early)
depression
dementia (late)

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34
Q

What MS symptoms can arrises from lesions in the Optic nerve?

A

Delayed VEP*

Loss of vision - Scotoma, rescued visual acuity, reduced colour vision.

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35
Q

What is Scotoma?

A

Scotoma is a partial loss of vision/ blind spot in an otherwise normal visual field.

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36
Q

What MS symptoms can arrises from lesions in the cerebellum & cerebellar pathways?

A

Tremors, clumsiness/poor balance.

Signs: dysarthria, postural/action tremor, gait ataxia, limb into-ordination.

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37
Q

What MS symptoms can arrises from lesions in the brainstem?

A

Vertigo

Impaired speech and swallowing - Dysarthria.

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38
Q

What MS symptoms can arrises from lesions in the spinal cord?

A

Weakness - Upper MN signs

Stiffness and spasms - Spasticity

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39
Q

Give an example of a main drug treatment MS and explain its function.

A

Prednisolone - anti-inflammatory.
Synthetic glucocorticoid.
Suppresses humoral immune response (B-cells and antibodies).

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40
Q

What is “depression”?

A

State of low mood + aversion to activity.

Can have negative effects on a persons thoughts, behaviours, feelings, world view and physical wellbeing.

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41
Q

Is depression a disease?

A

It is a symptom and can be normal e.g. bereavement.
But can also be a symptom of a clinical disorder or psychiatric disorder. e.g. MS, hypothyroidism, influenza, clinical depression (MDD or DD), isotretinoin, bipolar disorder, schizophrenia.

42
Q

What is “clinical depression”?

A

USA Diagnostics and Statistical Manual (DSM): Classified as Major Depressive Disorder (MDD)
ICD10 (WHO): Depressive Disorder (DD)

‘Clinical depression’ (MDD/DD) is a more severe form of depression. Unipolar!

43
Q

How is clinical depression (MDD) diagnosed?

A

Diagnosed by using “patient health questionnaire”.
MDD: Need to have 5/9 or more of the symptoms present during the same 2 week period - and represents a change from normal.

44
Q

What is anhedonia?

A

Little pleasure in doing things.

45
Q

What specific DSM criteria is needed to diagnose MDD

A

Either anhedonia or depressed mood MUST be present.
Causes significant distress/impairment of function.
Not part of bipolar disorder.
Not due to direct physiological effects of drugs.
Not time-limited depression (e.g. from bereavement)

46
Q

Examples of prominent negative cognitions? How can this be combated?

A 
Negative thoughts about self, world &amp; future. 
"Im a failure, Im shit, Im nothing." 
"The world is shit, the world is bad." 
"Nothing will ever be better." 
CBT combats this.
47
Q

Examples of psychotic guilt?

A

Unfounded guilt.
“Its my fault those people died in Pompeii.”
“Because of me, the bees are dying.”

48
Q

Examples of somatic delusions?

A

Fixed, false belief that one’s bodily functioning, sensation, or appearance is grossly abnormal.
“My heart is literally filled with dust.”
“Im literally dead inside.”

49
Q

What can severe MDD involve?

A 
Psychosis - guilt 
Auditory hallucinations. 
Somatic delusions 
Catatonic retardation 
Suicide
50
Q

What are monoamines?

A

Neurotransmitters.

One amine group, connected to an aromatic/benzene ring.

51
Q

What are catecholamines? Give examples.

A

They are a type of monoamines (NT).
Catechol (benzine with 2 hydroxyl groups) attached to amine. Derived from Tyrosine.
Dopamine and NA/NE*

52
Q

What are Indoleamines? Give examples.

A

They are a type of monoamines (NT)
Derived from Tryptophan.
Seretonin (5-HT)*

53
Q

How is Tyrosine converted to Dopamine?

A

TWO STEP:
Tyrosine hydroxylation to L-DOPA.
L-DOPA decarboxylation to Dopamine.

54
Q

How is dopamine converted to NA?

A

Hydroxylation

55
Q

How is NA converted to Adrenaline?

A

methyl-transferase reaction

56
Q

How is Tyrosine converted to NA?

A

Tyrosine hydroxylation to L-DOPA.
L-DOPA decarboxylation to Dopamine.
Dopamine hydroxylation to NA

57
Q

How is Tryptophan converted to serotonin 5-HT

A

TWO STEP:
Tryptophan hydroxylation to 5-hydroxytryptophan
5-hydroxytryptophan decarboxylation to 5-hydroxytryptamine (5-HT).

58
Q

With regards to NA system: Where is NA made? Why only there? Where does it go?

A

Locus Ceruleus (pons).
Can only be made in cells containing tyrosine hydroxylase.
Actively transported across BBB.
NA system extends extensively throughout brain.

59
Q

With regards to serotonin 5-HT system: Where is 5-HT made? Why only there? Where does it go?

A

Raphé nuclei: chain of brainstem nuclei (midbrain to medulla).
Can only be made in cells containing tryptophan hydroxylase.
5-HT system extends extensively throughout brain.

60
Q

Is tyrosine an essential or non-essential amino acid?

A

essential - must be eaten.

61
Q

Is tryptophan an essential or non-essential amino acid?

A

essential - must be eaten.

62
Q

In what two ways are NA and 5-HT signals terminated during synaptic transmission?

A

Re-uptake and Enzymatic degradation.

some synaptic degradation too

63
Q

What is the MAIN method in which NA and 5-HT signals are terminated?

A

Re-uptake

64
Q

What is the name of the re-uptake transporter for serotonin 5-HT?

A

5-HTT or SERT

65
Q

What is the name of the re-uptake transporter for NA?

A

NAT or NET

66
Q

How is most of the enzymatic depredations of NA and 5-HT done?

A

Uptake through transporters (NET/SERT) into PRE-synaptic terminal.

degraded by MAO-A (monoamine oxidase-A) and COMT (Catechol-O-methyl transferase) only for NA.

67
Q

What is Serotonin 5-HT degraded to by MAO?

A

5-HIAA

68
Q

What is NA degraded to by MAO or COMT?

A

VMA and MHPG

69
Q

What type of receptors do NA and Dopamine (catecholamines) target? How do they work i.e. what class of receptor?

A

Noradrenergic/adrenergic receptors.

GPCR: G-protein coupled receptor. Initiate a intracellular cascade of reactions (involving cAMP).

70
Q

Name the types of adrenergic receptors.

A 
a = alpha 1,2
b = beta 1-3
71
Q

Are a1 adrenergic receptors stimulatory or inhibitory? Where are they normally found?

A

Stimulatory, increase cell firing (lead to smooth muscle contraction).
Normally found on post-synaptic membranes, but can also act on a1 receptors on 5-HT cell bodies.

72
Q

Are a2 adrenergic receptors stimulatory or inhibitory? Where are they normally found?

A

inhibitory, decrease cell firing (lead to decreased cAMP release, smooth muscle contraction).
Normally found on pre-synaptic membranes (auto/hetero)

73
Q

What type of receptors does serotonin 5-HT (Indoleamines) target? How do they work i.e. what class of receptor?

A

Target 5-HT receptors (5-HT1-7).
GPCR’s except 5-HT3.
5-HT3 is ligand gated ion channel.

74
Q

Are 5-HT receptors stimulatory or inhibitory?

A 
5-HT1 &amp; 5-HT5 are inhibitory. 
All others (2,3,4,6,7) are stimulatory.
75
Q

How do NA and 5-HT systems interact?

A

NA act on (post synaptic) a1 receptors - stimulatory (increase cell firing).
NA acts on a1 receptors on 5-HT cell bodies - stimulatory (increase 5-HT cell firing).
NA acts on a2 auto/hetero receptors - inhibitory (regulation/homeostatic).
End result: balancing of stimulation and inhibition of serotonin.

76
Q

Generally, what does the monoamine hypothesis of MDD tell us?

A

4 main things.

1) decrease monoamines = depression.
2) increase monoamines = anti-depressants
3) Transient depletion of monoamines = transient re-ocurance of depression
4) decrease 5-HT = increase 5-HT2A receptors.

77
Q

What is VMAT in the monoamine system?

A

Vesicular monoamine transporter (VMAT) transports free cytoplasmic NA/Dopamine/5-HT in the pre-synaptic terminal into storage vesicles for release. (recycling process).

78
Q

Are 5-HT2A receptors increased or decreased in MDD? (MDD=chronic depletion of 5-HT)

A

Increased.

79
Q

Would blocking up-regulated 5-HT2A receptors lead to increased or decreased anti-depressant potency?

A

increase.

80
Q

Can depression re-occur?

A

Yes, recurrence is the norm. 73% rec. over 15 years.

Progressive disease.

81
Q

Briefly describe the kindling hypothesis in MDD.

A

Depressive episodes become more easily triggered over time.

82
Q

Where is the Ventral Neural System, and what does it do?

A

Inside/underside of brain.
Identification of emotional significance.
Mood states.

83
Q

Where is the Dorsal Neural System, and what does it do?

A

Top side of brain.

Integration of emotions and performance of cognitive executive functions.

84
Q

Which system (Ventral or Dorsal) does the amygdala and hippocampus belong to.

A

Amygdala - Ventral

Hippocampus - Dorsal

85
Q

In MDD, how are are amygdala and hippocampus affected?

A

Amygdala - Overactive with negative cues (causes focusing on negative emotions) and underactive with positive cues (causes anhedonia).

Hippocampus - Underactive and can get smaller. Affects memory, concentration. AD’s can reverse this.

86
Q

How are cortisol levels affected in MDD?

A

Patients show higher levels of cortisol throughout the day.

87
Q

What does axonal transection mean?

A

Axon sectioned. Literally cut.

88
Q

What is Uhthoff’s phenomenon?

A

When there is a worsening of neurological symptoms of MS due to a environmental stimulus.
Flare up of previous lesions.
Sometimes called pseudo-relapse.

89
Q

Is MS a grey or white matter disease?

A

White (axons) but not solely.

Grey matter involvement may be the primary driver of disability is MS.

90
Q

What is Lhermitte’s phenomenon?

A

Bending neck forward gives a shock like sensation going down spine, and maybe arms or legs.

91
Q

What do we mean by “progressive” disease?

A

Gets progressively worse over time.

92
Q

Why is it important to treat MS early?

A

Prevents neuronal cell loss and cerebral atrophy.

93
Q

Are all “relapses” symptomatic?

A

NO

94
Q

Roughly how many neurological lesions does it take to cause a relapsing episode?

A

10-15

95
Q

What is a ‘clinical relapse’?

A

Patient reported symptoms OR objectively observed signs of “acute inflammatory demyelinating event” in the CNS.

Current or in the past. Duration at least 24h. Absence of fever or infection.

96
Q

What are the three types of lesions in MS?

A

Acute Active Plaques (most frequent)
Chronic Active Plaques
Chronic Inactive Plaques

Chronic ones seen in progressive MS.

97
Q

With regards to Oligoclonal IgG band patterning in the CSF: what pattern is observed in the serum and the CSF? What type is it called?

A

Type 2

Bands present in CSF and not in Serum.

98
Q

What is the most abundant neurone TYPE in the nervous system?

A

Interneurone.

99
Q

What do ependymal cells do?

A

They line CSF filled ventricles.

100
Q

What is the most abundant neurone STRUCTURE in the NS?

A

Multipolar.

101
Q

Antidepressants block re-uptake transporters on pre-synaptic membranes, thus blocking re-uptake of 5-HT and NA. This happens almost immediately after taking drug.

So why aren’t antidepressants acutely antidepressant? (i.e why do their effects take long) How long do they take to kick in?

A

Once drug taken (e.g. sertraline blocking SERT aka SSRI’s)

  1. 5-HT is raised also at neurone cell bodies (raphie nuclei)
  2. This acutely increases activity of 5-HT1A auto-receptors. This switches off neurone firing, and thus fails to increase forebrain 5-HT.
  3. CHRONIC SSRI use desensitises somatodendritic 5-HT1A auto-receptors, and also 5-HT re-uptake transporters.
  4. Leads to restored firing and re-uptake remains blocked.

Sem 3 Neuro (8 decks)

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