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Path II > Neurodegen > Flashcards

Neurodegen Flashcards

1
Q

What is demyelination?

A

Acquired loss of myelin WITH AXONAL SPARING
CNS: MS, viral (PML from JC), metabolic
PNS: Toxic, Inflammatory, Guillain-Barre

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2
Q

What is dysmyelination?

A

Inherited, myelin not formed or is abnormally formed

  • Axons tend to undergo degeneration
  • LEUKODYSTROPHIES
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3
Q

What is MS?

A

Autoimmune DEMYELINATING disease

Well defined episodes of neuro deficits, separated by time, white matter lesions that are separated by space

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4
Q

Who most often gets MS?

A

Young Women

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5
Q

What is the spectrum of MS disease?

A

Relentless to little progression

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6
Q

What are the Genetic factors of MS?

A

CLASS II MHC-DR2, DR4, DR15, DQ6

15-20x if 1st degree relative

MZ twins have a greater magnitude

May be environmental: Pacific theatre WII outbreak

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7
Q

What is the pathogenesis of MS?

A

CD4 T cells that attack oligos

Target: MOG (myelin oligo glycoprotein), MBP (myelin basic protein, and alpha beta crystallin

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8
Q

What is the mechanism of injury for MS?

A

Antibodies and complement
- T cell induced B cell clonal expansion in CSF

Produces IgG1, IgG3

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9
Q

What is the diagnostic hallmark of MS?

A

Oligoclonal banding of CSF

Ag-Ab complex recognized by Macrophages

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10
Q

What is the mechanism of injury for MS?

A

Antibodies and complement
- T cell induced B cell clonal expansion in CSF

Produces IgG1, IgG3

Ag-Ab complex recognized by Macrophages and is recognized by Fc receptor

Fc receptor binding with complement causes damage to myelin leading to phagocytosis

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11
Q

What is the diagnostic hallmark of MS?

A

Oligoclonal banding of CSF

Ag-Ab complex recognized by Macrophages and is recognized by Fc receptor

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12
Q

What is the mechanism of injury for MS?

A

Antibodies and complement
- T cell induced B cell clonal expansion in CSF

Produces IgG1, IgG3

Ag-Ab complex recognized by Macrophages and is recognized by Fc receptor

Fc receptor binding with complement causes damage to myelin leading to phagocytosis

Lympocyte mediated injury

  • T lymph prominent in early plaque formation
  • Oligos are targets of cytolytic T cells

Macrophages
-Activated macros produce ROS and NOS, proteolytic enzymes, cytokines (TNF) that damage myelin

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13
Q

What is the diagnostic hallmark of MS?

A

Oligoclonal banding of CSF

Ag-Ab complex recognized by Macrophages and is recognized by Fc receptor

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14
Q

What are plaques in MS?

A

Actively demyelinating plaques (loss of myelin, retention of axons, myelin-laden macros
-Center of plaque is Perivascular T-cells

Inactive: Axons undergo demyleination
-Leave astros to repair (GLIOSIS)

Shadow: Remyleination occurring slowly
-LFB stain

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15
Q

What are different types of MS?

A

Classic (Charcot)
Acute (Marburg)
Neuromyelitis Optica (spinal cord and optic nerves)
-Aquaporin 4 abnormalities
Schilder’s disease: Children, fulminant to remiting with steroid therapy
Concentric sclerosis (balo’s type): Very rare and diagnosed at autopsy

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16
Q

What is the cause of MS neuromyelitis optica?

A

Aquaporin 4 mutation (associated with BBB abnormalities

17
Q

Who is affected by Schilder’s disease most often?

A

Children, young adults

Acute/subacute with symmetrical bilateral plaques

2x3cm involving central semiovale

No other lesions seen

18
Q

Who is affected by Schilder’s disease most often?

A

Children

19
Q

What is central pontine myelinolysis?

A

Toxic demyelination disorder

Too rapid overcorrection of hyponatremia

Due to swelling and damage to myelin sheath during the too rapid change

20
Q

What is the clinical picture of CPM?

A

Confusion, limb weakness, conjugate gaze palsies, dysarthria, dysphagia, hypotension

21
Q

What is the prognosis of CPM?

A

Poor most patients succumb within weeks

22
Q

What is Guillain Barre syndrome?

A

Acute inflammatory demyelinating polyradiculopathy

Due to infectious causes (viral, campy)

Ascending paralysis

Few patients progress to MS

23
Q

WHat is ADEM?

A

Acute disseminated encephalomyelitis

Few weeks after viral infections

HA, Vomiting, Rapid weakness, sensory loss, ataxia, visual impairment, stupor, LOC, seizures

20% succumb to disease

5-10% have relapses

24
Q

What is the range of complications with alcohol and fetal development?

A

Binge drinking results in the severe abnormalities

Behavioral and minor learning disabilities to severe facial (ocular) and cardiac defects

25
Q

What is the most common cause of Alch related death in adolescents young adults?

A

Alc poisoning and trauma

26
Q

What are the nutritional deficiencies in the alcoholic?

A

Thiamine (B1)

B12

27
Q

What is a consequnce of thiamine def?

A

Wernickes encephalopathy

  • Necro encephalopathy with mamillary bodies, periaqueductal grey, pons and medulla
  • Ataxia, gaze palsies, alterned mental state

Korsakoffs syndrome: Thalamic disease
- Severe antegrade amnesia with confabulation

28
Q

What is a consequnce of thiamine def?

A

Wernickes encephalopathy

  • Necro encephalopathy with mamillary bodies, periaqueductal grey, pons and medulla
  • Ataxia, gaze palsies, alterned mental state

Korsakoffs syndrome: Thalamic disease
- Severe antegrade amnesia with confabulation

29
Q

What is a consequence of B12 deficiency?

A

Subacute combined degeneration of spinal cord

Ascending and descending tract

Slow onset of ataxia, tingling of legs

paraplegia can develop

30
Q

What happens to the cerebellum due to alcohol?

A

Atrophy

Toxic to internal granular layer of cortex (vermix) atrophy in particular

31
Q

What are alcoholics also at risk for?

A

Central pontine myelinolysis

Hepatic encephalopathy

Stroke

Peripheral neuropathy

Optic neuropathy

Marchiafava-bignamic Disease

32
Q

What is marchiafava-bignami disease?

A

Itatlina men who drank red wine

Toxic demyelination of corpus callosum

33
Q

What happens in lead toxicity?

A

ALtered heme prodution

Delayed cognitive and intellectual development

Retarded growth

Learning diff and behavioral changes

34
Q

What happens in lead toxicity in adults?

A

Neurocog disease, peripheral neuropathy IRREVERSIBLE

35
Q

What happens in mercury poisoning?

A

Mild congnitive to psychiatric abnormalities to coma and death

Minamata disease: Hypoesthesia of hands, feet, ataxia, visual field disturbance, dysarthria, severe encephalopathy

Not reversible

36
Q

Radiology effects on CNS?

A

Methotrexate in particular and radiation causes encephalopathy with development of learning disabilities

37
Q

What does CO poisoning do?

A

It causes globus pallidus necrosis, survivors suffer movement and memory disorders

38
Q

WHat is ADEM?

A

Acute disseminated encephalomyelitis
T-CELL MEDIATED HS REACTION

Few weeks after viral infections

HA, Vomiting, Rapid weakness, sensory loss, ataxia, visual impairment, stupor, LOC, seizures

20% succumb to disease

5-10% have relapses

39
Q

What are characteristic lesions of MS?

A

Flame lesions

Path II (11 decks)

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