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Neuroinfectious Diseases > Neuroinfectious Diseases Exam 2 > Flashcards

Neuroinfectious Diseases Exam 2 Flashcards

1
Q

what does MNS stand for

A

mental, neurological, and substance abuse disorders

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2
Q

what are the heterogenous range of diseases and disorders of MNS

A

Mental: schizophrenia, depression, autism
Neurological: dementias, ALS, Huntington
Substance-abuse: alcohol, illicit drugs, pain killers, sleep aids

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3
Q

Symptoms and measurable impairments of MNS disorders are in part due to…?

A

some degree of brain dysfunction

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4
Q

What 4 factors affect MNS disorders

A
  1. genetic
  2. biological
  3. psychological
  4. social
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5
Q

Why are MNS disorders hard to study

A

bc of the high number of variables due to the brain being the most complex organ

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6
Q

What are some examples of the genetic factors of MNS disorders?

A
  • mutated SOD1 gene-> ALS
  • Mutated MECP2 gene -> Rett syndrome
  • Trisomy 21 -> Down Syndrome
  • Loss of FMR1 -> Fragile X Syndrome
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7
Q

Biological factors of MNS disorders

A

Age and gender (not necessarily sex)

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8
Q

Psychological factors of MNS disorders

A
  • mood disorders
  • education/religion -> psychological strength
  • depression (not sadness or unhappiness)
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9
Q

what types of diseases are not very well understood?

A

biology of psychological diseases

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10
Q

Social factors of MNS disorders

A
  • socioeconomic status
  • neighborhood factors
  • environmental events
  • large or sudden social changes (gentrification)
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11
Q

what is the cyclical pattern in MNS disorders

A

social adversities increase risk for MNS disorders -> promotes poverty -> increase risk for MNS disorders

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12
Q

What does YLLs stand for

A

Years of life lost

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13
Q

What does YLDs stand for

A

Years lived with disability

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14
Q

what does DALYs stand for and how do you calculate it?

A

Disability adjusted life years
YLL+YLD=DALYs

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15
Q

In terms of medical burden, why are MNS disorders hard to measure?

A

MNS disorders increase the risk of premature death without being the actual cause

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16
Q

By how much have MNS disorders increased from 1990 to 2010?

A

Increased by 41%

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17
Q

Why have mns disorders increased from 1990s?

A
  • Aging
  • social factors (drug dealers targeting young people)
  • population growth
  • lifestyle factors (poor nutrition, excessive work hours)
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18
Q

What are the substantial social and economic consequences of MNS disorders?

A
  • maternal mental -> transmission to children
  • correlation of substance use disorders and criminal behavior -> incarceration, lost of productivity
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19
Q

what are the effects of mns disorders on family members engaged in caregiving

A

immigration and pop displacement due to conflict or climate change -> increased burden on healthcare system -> effects on equality of service

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20
Q

what is the economic output lost to mns disorders globally in 2010?

A

$8.5 trillion

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21
Q

what are the nonphysiological interventions?

A
  1. behavioral therapy
  2. life-skills education (adulting)
  3. psychosocial stimulation (for infants and kids)
  4. population based interventions (i.e. targeting risk factors affecting communities)
  5. promote healthier diet
  6. excise taxes
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22
Q

what are the most effective mns disorder interventions

A
  • use platforms: schools, hospitals
    1. population - legislative and regulatory measures
    2. community - workplace rules, teacher training
    3. healthcare - detection and management of mns disorders
  • erase stigma of MNS disorders
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23
Q

what are 2 problems that prevent effective intervention delivery for mns disorders?

A
  • lack of evidence that it confers wider economic and social benefits (households-> society -> country)
  • very cost effective but lower and middle income countries cannot afford it
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24
Q

what MNS disorders is the lifestyle disorder diabetes mellitus associated with

A

diabetes mellitus ->cognitive disorders

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25
Q

what common lifestyle disorders (4) are associated with all mns disorders?

A
  • atherosclerosis
  • heart disease
  • stroke
  • obesity
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26
Q

what do all lifestyle disorders that are associated with mns disorders cause?

A

they all weaken the immune system ->infections ->medical and economic burden

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27
Q

what two aspects of healthcare are essential for treating mns disorders?

A

quantity (ease of access) and quality (effectiveness of treatment)

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28
Q

what are the three main non-infectious neurodiseases/disorders

A
  1. progressive neurodegenerative diseases
  2. neuropsychiatric disorders
  3. addictive disorders
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29
Q

what are the 4 main examples of progressive neurodegenerative diseases?

A
  1. Alzheimer’s
  2. Parkinson’s
  3. Guillain-Barre Syndrome
  4. Multiple Sclerosis
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30
Q

what lifestyle disorders is alzheimer’s associated with

A

amyloidosis and tauopathy

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31
Q

what lifestyle disorder is Parkinson’s associated with

A

Synucleinopathy

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32
Q

what two diseases discussed in class autoimmune?

A

Guillian-Barre syndrome and Multiple Sclerosis

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33
Q

what are the two examples of neuropsychiatric disorders?

A

depression and schizophrenia

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34
Q

what are mental illnesses examples

A

neuropsychiatric and addictive disorders

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35
Q

What is a disorder

A

it effects your mood, thinking and behavior

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36
Q

what are some examples of disorders (5)?

A
  • depression
  • schizophrenia
  • anxiety disorders
  • addictive behaviors
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37
Q

what are severe caes of disorders called

A

psychosis

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38
Q

what percent of us population has schizophrenia?

A

less than 1%

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39
Q

what percent of us population experience psychosis

A

3.5-5%

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40
Q

What are three factors that cause changes in brain leading to mental illnesses?

A

genetics- higher risks if close relative have mental illnesses
environment - poverty, addiction, violence, military struggles
experiences - death of loved one, diseases, stressful situations

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41
Q

what type of chronic imbalances in neurotransmission occur that lead to mental illnesses

A

nerve circuits involved in rewards and emotions

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42
Q

Example of nerve circuits involved in rewards and emotions that lead to mental illnesses and where it occurs?

A
  1. abnormally high amounts of dopamine and low amounts of glutamate
  2. unbalance can happen in diff parts of brain
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43
Q

Structural changes are visible in mental illnesses but…?

A

inconclusive and nonspecific (see twin MRI images in lecture 24)

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44
Q

what is the commonality bw all the MNS disorders?
a. all exhibit symptoms and measurable impairments attributable to brain dysfunction
b. all are consequence of uncontrolled inflammation
c. all have plaques, or proteinaceous aggregates
d. all are transmissible from person-to-person

A

a. all exhibit symptoms and measurable impairments attributable to brain dysfunction

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45
Q

which of the following are clinical therapeutic interventions for mns disorders?
a. increased presence of behaviora therapists at schools
b. use of antipsychotic drugs for schizophrenia or antidepressants for mood disorders
c. policies and legislations to reduce access to the means of suicide
d. better training of teachers and nurses to recognize and identify MNS disorder symptoms

A

b. use of antipsychotic drugs for schizophrenia or antidepressants for mood disorders

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46
Q

there are various ways to treate mns disorders. These are?
a. targeting vectors, or vehicles of mns disorders
b. by enacting legislation that protects children from sources of mental or physical sickness
c. through use of antipsychotics
d. by a combination of therapeutic, psychological, and social interventions

A

d. by a combination of therapeutic, psychological, and social interventions

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47
Q

to implement and maintain an effect mns disorder intervention, lawmakers and funding agencies need …?
a. to be able to recover the costs incurred
b. evidence of a positive effect on health and their costs and cost-effectiveness
c. to familiarize themselves with the problem by hiring affected individuals to lead the efforts
d. to familiarize themselves with the problem by infecting communities to see the outcome

A

b. evidence of a positive effect on health and their costs and cost-effectiveness

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48
Q

the mortality of mns disorders is difficult to measure or estimate because…?
a. mns disorders result in stillbirths
b. mns disorders increase the risk of premature deaths without being the actual cause of death
c. mns disorders are chronic diseases that do not result in death
d. mns disorders are overrepresented in certain populations but absent in others

A

b. mns disorders increase the risk of premature death without being the actual cause of death

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49
Q

mns disorders are complex because they can be affected and modulated by?
a. age, genetics, religion, and socioeconomic status of the patient
b. month of birth, weight, height, and horoscope
c. all of the above
d. a and b only

A

a. age, genetics, religion, and socioeconomic status of the patient

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50
Q

Which of the following attributes of health systems must be considered when analyzing possible interventions for MNS disorders

A

Inclusiveness of MNS disorders in health care packages or insurance schemes

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51
Q

which of the following is the best definition for mns disorders?

A

a heterogenous group of clinical manifestations that are affected, and caused, by a complex array of genetic, biological, psychological, and social factors

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52
Q

which of the following states is true for mns disorders

A

they are grouped together because they all owe their symptoms to a brain disfunction

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53
Q

what is the monoamine hypothesis referring to mental illnesses?

A

it is a disbalance of proteins in the brain resulting in neurodegeneration

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54
Q

what are the three vehicles or means to deliver interventions against mns disorders

A

population, community, and healthcare

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55
Q

under the healthcare platform, there are various levels at which interventions can take place. These are:

A

self management and care, primary healthcare, and hospital care

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56
Q

hree factors that have contributed to the steady increase in mns disorders in recent times are:

A

population growth, lifestyle changes, and aging

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57
Q

mns disorders manifest broadly and differently because they can be modulated by several factors including:

A

social, biological, and psychological factors

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58
Q

T or F: mns disorders are a catchall term for diseases and disorders that are usually treated equally

A

F; although mns disorders apply to broad spectrum of diseases, they are not always treated equally

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59
Q

T or F: interventions to reduce or prevent mns disorders have benefits for society (i.e. less injuries due to alcohol or drug use)

A

True

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60
Q

T or F: if we want to make a positive change on how we manage and prevent mns disorders, political will and commitment from development agencies to allocate the necessary resources and provide technical leadership is essential

A

True

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61
Q

T or F: Crude mortality numbers are used to estimate the medical burden of mns disorders because they are the direct cause of substantial deaths

A

False; mns disorders are hard to estimate because they can increase the risk of premature death without being the direct cause of death

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62
Q

what are the four main mneurotransmitters in the monoamine hypothesis that can lead to an imbalance in the brain

A
  1. serotonin
  2. dopamine
  3. norepinephrine
  4. epinephrine
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63
Q

what is dementia

A

loss of intellectual and cognitive abilities

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64
Q

what are the main three characteristics of dementia in alzheimers?

A
  1. acquired
  2. progressive/chronic
  3. broad clinical picture, but dominated by personality, mental and motor changes
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65
Q

all patients exhibiting dementia deserve a thorough diagnostic evaluation because…

A

a treatable cause may be discovered

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66
Q

the progressive neurodegenerative diseases cause progressive destruction of what and what does it lead to?

A

progressive destruction of nerve cells lead to death

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67
Q

what age group is most likely to have a progressive neurodegenerative disease?

A

most often present in older people

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68
Q

what is senile dementia

A

decreases in mental abilities experienced by some people in old age

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69
Q

why is studying progressive neurodegenerative diseases important

A

because as population ages, the field becomes more imp as it affects more people

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70
Q

what is the most common form of dementia

A

alzheimer’s

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71
Q

there is evidence that many progressive neurodegenerative diseases are a type of what?

A

prion disease

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72
Q

what evidence is there that progressive neurodegnerative diseases being a type of prion disease

A
  1. accumulation of protein plaques
  2. nerve cell necrosis
  3. gliosis
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73
Q

what is nerve cell necrosis

A

Nerve cell necrosis, also known as neuronal necrosis, is a type of cell death that occurs in response to an unplanned injury to a neuron

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74
Q

what is gliosis

A

Gliosis is a nonneoplastic reaction that occurs when the body produces more or larger glial cells, which support nerve cells. This process can cause scars in the brain that impact how the body functions

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75
Q

what is amyloidosis and what disease is this seen in?

A

Amyloidosis is a rare disease that occurs when amyloid proteins build up in the body, causing abnormal protein build-up in tissues and eventually leading to organ dysfunction and death
- seen in alzheimer’s

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76
Q

what is tauopathy and what disease is this associated with?

A

Tauopathies are a group of neurodegenerative disorders that cause abnormal tau protein to accumulate in the brain. These deposits can be found in neurons, glial cells, and the extracellular space. The misfolded tau proteins stabilize microtubules in cells, but eventually accumulate and form neurofibrillary tangles (NFTs). These NFTs can lead to neuronal toxicity and degeneration.
- seen in alzheimer’s

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77
Q

when was alzheimer’s disease (AD) first described and by who

A

first described in 1906 by Alois Alzheimer

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78
Q

who was the first patient that was used to describe AD and what evidence supported this

A
  • a 51 yo suffering from severe dementia
    1. described the symptoms and the pathological manifestations
    2. extracellular deposits of a “peculiar substance”
    3. intracellular fibrillary bundles
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79
Q

what were the peculiar substance and intracellular fibrillary bundles described by Alois Alzheimer

A

the peculiar substance was amyloids and the bundles were tau tangles

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80
Q

what year was AD accepted to be the cause of most senile dementias

A

1976

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81
Q

what rare mutation confirmed the hypothesis of AD causing senile dementia

A

a rare mutation discovered in chromosome 21, this also helped to explain incidence of dementia in down syndrome

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82
Q

how many APP mutations have been linked to AD since its discovery

A

more than 50

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83
Q

what percent of adults over 65 have AD

A

5%

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84
Q

what percent of adults over 85 have AD

A

30 to 40%

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85
Q

out of the top 10 global causes of deaths in 2016, what place was AD?

A

5th leading cause

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86
Q

out of the top 10 causes of deaths in high income countries in 2016, what place was AD?

A

3rd place

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87
Q

what is imp to note about the top 10 causes of deaths in high vs low income countries in terms of AD?

A

It is very prevalent in high income countries but not in the low income countries (not part of the top 10)

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88
Q

AD is disproportionally prevalent in the developed world, including in these two regions

A

USA and EU

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89
Q

women are ( ) more likely to get AD

A

2 times, according to Framingham study since 1948 (a still ongoing study)

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90
Q

African women are ( ) more likely to get AD

A

5 times, possibly due to diabetes

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91
Q

what is a risk factor for AD

A

diabetes

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92
Q

what type of possible factors are correlated with AD

A

environmental factors, but nothing conclusive

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93
Q

what seems to be protective for AD

A

education, maybe due to brain activity or just socioeconomic status

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94
Q

what percent of AD patients start with memory problems

A

75%

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95
Q

what type of function goes last with AD

A

motor function

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96
Q

what changes are seen in AD (6)

A
  1. language becomes less fluid
  2. comprehension declines
  3. mood changes common (mild depression and social withdrawal)
  4. memory loss more pervasive, involving older memories (capgras)
  5. sever interference with normal activities like driving
  6. motor skill problems
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97
Q

what is capgras syndrome

A

people replaced by identical impostors, symptom of AD

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98
Q

what are examples of motor skill problems associated with AD

A

problems walking, eating, taking care of themselves

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99
Q

how does motor skill loss of AD burden caregivers

A

not being able to take care of themselves places an economic and psychological burden on caregivers

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100
Q

what is the onset of death for AD

A

8 to 10 years

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101
Q

what are the two main types of dementia

A

cortical and subcortical

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102
Q

AD is a classic example of what type of dementia

A

cortical because of loss of the cerebral cortex

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103
Q

the senile plaques found in AD are made up of ?

A

amyloid Beta

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104
Q

what role does cell necrosis play in AD?

A

Necroptosis is a type of programmed cell death that can contribute to the development of Alzheimer’s disease (AD). It can cause cell death and neuroinflammation, and may also contribute to other AD pathological events such as: Aβ aggregation, Axonal degeneration, Mitochondrial dysfunction, and Granulovacuolar degeneration.

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105
Q

AD tangles are?

A

hyperphosphorylated tau protein

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106
Q

the immune system reaction to the plaques in AD are?

A

inflammation that causes damages

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107
Q

the inflammation of AD inhibits what brain function

A

inflammation impairs clearance of waste from brain

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108
Q

in AD, what is the neuronal transport system interrupted by

A

its interrupted by the tau tangles

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109
Q

what is the effect of the tau tangles interrupting the neuronal transport system in AD

A

causes less neurotransmitters, and other components, to be delivered to synapses

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110
Q

what acts as catalysts that lead to dissemination and spread of AD

A

Plaques

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111
Q

what kind of response do plaques elicit in AD

A

elicit inflammatory response

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112
Q

the inflammatory response caused by plaques lead to what in AD

A

lead to neuron killing

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113
Q

how many fda approved drugs are there to treat AD

A

4`

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114
Q

is there a cure for AD

A

no

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115
Q

how do the 3 inhbitor medications for AD function

A

they are inhibitors of cholinesterase which causes increase of neurotransmitter availability

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116
Q

how does the NMDA receptor antagonist used to treat AD work?

A

the NMDA is involved in learning and allows for glutamate import which leads to glutamate toxicity

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117
Q

what is key to help treating AD

A

early diagnosis which is difficult to find volunteers at early stages of disease

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118
Q

do AD drugs combine both inhibitors and NMDA receptor antagonists?

A

yes, some treatments combine both classes

119
Q

current research is targeting the clearance of ?

A

plaques, has been found to be promising and was based on learning about prion research

120
Q

Parkinson’s (PD) is the ( ) most common form of dementia?

A

2nd most common

121
Q

when was PD first described

A

1817

122
Q

PD is also known as

A

Shaking palsy

123
Q

what was the main description of PD

A

described by tremors

124
Q

what are the 3 classical symptoms of PD

A

tremors, abnormal posture and gait, and reduced muscle strength

125
Q

what type of dementia is PD and what are of brain is being affected

A

it is a subcortical dementia that causes the degeneration of the substantia nigra in which neurons produce a black pigment

126
Q

what percent of dopamine neurons are lost by the time of death for PD patients

A

70%

127
Q

what are the main factors associated with PD

A

genetic and environmental factors

128
Q

what percent of PD patients have a relative that was affected by PD as well

A

up to 25%

129
Q

Is pd more common in men or women?

A

more common in men

130
Q

what ethnicity is more likely to have PD?

A

caucasians are 3 times more likely to get PD

131
Q

what age is the typical onset for PD

A

greater than 65 yo

132
Q

are there early onset cases of PD?

A

yes, it is very rare, and due to genetic cases

133
Q

how many genes are believed to be associated with PD?

A

7

134
Q

What are the earliest symptoms of PD

A

tremors which are autorecognized

135
Q

what are the 6 main symptoms seen in PD?

A
  1. tremors
  2. slowness of motion
  3. overall rigidity and stiffness
  4. loss of olfaction
  5. mood changes
  6. dementia
136
Q

slowness of motion in PD affects movement how?

A

impairs initiation of movement

137
Q

overall rigidity and stiffness in PD leads to

A

walking instability which leads to frequent falls

138
Q

what symptom is a telltale sign of PD

A

loss of olfaction

139
Q

what mood changes are seen in PD

A

depression and behavioral problems

140
Q

dementia in PD affects what?

A

mostly daily function but WITHOUT memory loss

141
Q

what disease is very well studied, aka is the oldest movement disorders identified and is also seen in lots of celebrities

A

PD

142
Q

what neurotransmitter is associated with the mood disorders seen in PD

A

dopamine which play a role in the rewards system

143
Q

how does dementia occur in PD

A

lewy bodies cause aggregates of alpha synuclein and in later stages of PD causes dementia due to build up

144
Q

What are Lewy bodies?

A

Lewy bodies (LBs) are abnormal protein clumps that build up in the brain in people with Parkinson’s disease. These deposits are found in areas of the brain responsible for thinking, visual perception, and muscle movement. The formation of LBs has been considered to be a marker for neuronal degeneration, because neuronal loss is found in the predilection sites for LBs

145
Q

Lewy bodies role in PD

A

it is unclear but seem to be involved in the propagation/spread over the brain

146
Q

what is the normal role of lewy bodies

A

not known

147
Q

how do lewy bodies cause aggregates in PD

A

lewy bodies bind to the outside of vesicles (mostly alpha helical) causing the misfolds to form into beta sheets which promote aggregation

148
Q

what is a possible marker for PD diagnosis

A

Lewy bodies

149
Q

Prion like hypothesis

A

The prion-like hypothesis suggests that Lewy bodies and other pathological α-synuclein aggregates spread in a prion-like manner throughout Parkinson’s disease (PD). This spreading can happen through a process of secretion and uptake, and some pathological forms of α-syn can seed healthy cells, which promotes a self-sustained cycle of inclusion formation, amplification, and spreading. This cycle ultimately underlies the progression of the disease.

150
Q

what is the main causative pathology in PD

A

death of dopaminergic neurons

151
Q

what kills neurons in PD and why are those the only neurons targeted?

A

mitochondrial function and ROS generation

152
Q

how does mitochondrial function and ROS generation play a role in PD

A

Mitochondrial dysfunction is a major factor in the development of Parkinson’s disease (PD). Mitochondria are the cell’s powerhouse, performing important reactions such as energy production, calcium metabolism, and cell death regulation. They also produce free radicals that can lead to oxidative stress (OS), which can damage intracellular components and cause cell death
- ROS modification of alpha synuclein promotes aggregation

153
Q

what sign presents early onset of PD

A

carriers of alpha synuclein mutations present early onset of PD leading to an increased level of alpha synuclein

154
Q

What are the three main treatments for PD

A
  1. dopamine and dopamine replacement therapy
  2. deep brain stimulation
  3. neuroprotection - nonmotor symptoms treatment
155
Q

how does dopamine and dopamine replacement therapy for PD work?

A

it targets the motor problems only, and will wear off after some years before it can actually start to cause motor years

156
Q

how does deep brain stimulation to treat PD work?

A

it is a surgical procedure that is given to patients who do not respond to medication, and it works by blocking electrical signals that cause the motor symptoms

157
Q

how does neuroprotection, nonmotor symptoms treatment to treat PD work?

A

this is cholinesterase inhibitors, antidepressants, caffeine and nicotine supplements

158
Q

study the lecture 25 graph on how the BBB is disrupted in AD

A

lecture 25

159
Q

There are various causes for dementia, many treatable. Which of the following is treatable?

A

Certain dementias as a result of stroke

160
Q

the molecular composition of the Alzheimer’s plaques and fibers are?

A

amyloid-Beta and tau protein, respectively

161
Q

what may explain the relatively common occurrence of dementia in young adults with down syndrome?

A

increased levels of amyloid-beta due to extra copy of the APP gene

162
Q

which of the following are correct comparisons between prion disease and dementia syndromes

A

both exhibit pathologically clear proteinaceous aggregates

163
Q

which of the following describes PD

A

a motor disorder, that is an excess or deficiency of movement impulse, movement automaticity, and/or muscle tone

164
Q

Inflammation negatively affects AD and PD pathology because?

A

it removes the protein aggregates but, as collateral damage, kills the neurons

165
Q

why inhibitors of cholinesterase alleviate AD and PD early symptoms

A

they increase the neurotransmitter availability which is affected in these diseases

166
Q

Senile plaques, kuru plaques, lewy bodies, are all examples of ?

A

abnormal cellular debris

167
Q

which of the following are common hallmarks of neurological diseases (infectious and noninfectious)?

A

neuronal death, gliosis, and inflammation

168
Q

which of the following are main symptoms of PD

A

tremors, abnormal posture and gait

169
Q

T or F: Most cases of what was previously called “senile dementia: we know now were cases of AD

A

True

170
Q

T or F: The epidemiology of both AD and PD are similar

A

False; AD affects more people in high income countries and PD is more common in men than women

171
Q

T or F: Lewy bodies disease is just one of many synucleinopathies, like Alzheimers

A

False, like PD not AD

172
Q

T or F: All of the neurodegenerative diseases mentioned in class are pathologically defined by intracellular or extracellular protein aggregates

A

True

173
Q

T or F: In PD, tau tangles disrupts the cellular transport machinery while amyloid plaques are involved in dissemination/spread of disease

A

False, Amyloid plaques and tau tangles lead to AD not PD

174
Q

The mainstay Parkinson’s treatment that can also be used as a diagnostic is…?

A

dopamine replacement therapy

175
Q

All dementias can be classified into two broad types:

A
  1. cortical
  2. subcortical
176
Q

Specific anatomical part of brain affected in PD

A

substantia nigra

177
Q

Oligmers and plaques of ___________ drive the inflammation in AD

A

Oligmers and plaques of ___________ drive the inflammation in AD

178
Q

what are the two classical examples of neuromuscular diseases/disorders

A

GBS and MS

179
Q

what do diseases of motor neurons and neuromuscular junctions (NMJ) affect)?

A

They affect the signaling from the brain to the muscles aka the motor system

180
Q

what areas of the motor system are affected by motor neuron and NMJ diseases?

A
  1. motor neurons themselves
  2. their axons
  3. presynaptic terminal
  4. postsynaptic terminal
181
Q

what part does NMJ affect in progressive neurodegenerative diseases?

A

pre and post synaptic terminals

182
Q

what area of the motor system does the GBS affect?

A

the motor axon, from the spinal cord to the muscles

183
Q

what area of the motor system is affected in MS?

A

the corticospinal tract from the primary motor cortex all the way down to the caudate medulla

184
Q

what is the most common acute paralytic neuropathy

A

Guillain Barre Syndrome aka GBS

185
Q

how many cases of GBS are there a year

A

more than 100000

186
Q

Why is GBS a syndrome and not a disease?

A

because there are various subtypes

187
Q

what are the two subtypes of GBS and what is their difference

A
  1. targeting myelin membrane - acute inflammatory demyelinating polyneuropathy, antibody injures myelin membranes
  2. targeting axonal membrane - acute motor axonal neuropathy or acute motor and sensory axonal neuropathy, antibody injures axonal membranes
188
Q

How long does it take for GBS to develop?

A

Develops days/weeks after infection or vaccination

189
Q

How does molecular mimicry play a role in GBS?

A

Molecular mimicry occurs when the antigenic structures of pathogens and humans are similar enough to cause an autoreactive response of T or B lymphocytes after infection, which contributes to disease pathogenesis. In GBS, microbial carbohydrate epitopes induce IgM, IgA, and IgG subclasses, which challenges the classic concept of thymus-dependent (TD) versus thymus-independent (TI) antibody responses

190
Q

How long does it take people to recover from GBS

A

most pp recover spontaneously in 3 to 4 wks

191
Q

what percent of GBS people recover completely

A

70%

192
Q

what percent of GBS patients retain residual weakness

A

30%

193
Q

20 to 30% of people with GBS develop…?

A

into severe cases that can lead to complete paralysis, including respiratory muscles

194
Q

in severe cases of GBS, how long does rapid progression occur after onset

A

in 3 to 4 days

195
Q

there is strong evidence of GBS related with?

A

C. jejuni infection

196
Q

what viruses is GBS associated with

A

flu, zika, CMV, and epstein barr

197
Q

how is GBS related to C. jejuni infection?

A

Lipooligosaccharides (LOS) are glycolipids that are expressed on the outer membrane of mucosal Gram-negative bacteria. The LOS core of Campylobacter jejuni can mimic human antigens like gangliosides, and some strains of C. jejuni can trigger Guillain-Barré syndrome (GBS) by mimicking LOS.

198
Q

Lipooligosaccharides (LOS) are glycolipids that are expressed on the outer membrane of mucosal Gram-negative bacteria. The LOS core of Campylobacter jejuni can mimic human antigens like gangliosides, and some strains of C. jejuni can trigger Guillain-Barré syndrome (GBS) by mimicking LOS.

A

Antibody production

199
Q

immunopathology of GBS is mostly driven by?

A

mostly a humoral driven pathogenesis (antibody mediated)

200
Q

How is immunopathology of GBS antibody mediated in each GBS subtype?

A
  1. humoral driven pathogenesis against gangliosides in axonal membranes (exposed at nodes of Ranvier)
  2. humoral driven pathogenesis against broad range of myelin sheet proteins (moesin was suggested)
201
Q

what GBS subtype is most severe

A

Axonal subtype

202
Q

what are humoral effects of GBS

A

Antibody deposits, complement activation of the immune system, macrophage recruitment

203
Q

when is diagnosis for GBS best

A

early diagnosis correlates to better recovery

204
Q

how is GBS syndrome treated (3 ways)

A
  1. Intravenous Ig infusion
  2. Plasma exchange
  3. physical therapy for sever cases
205
Q

how does IV Ig infusion treat GBS?

A

The addition of normal antibodies overcomes effect of autoreactive antibodies (lots of mechs, but most end up reducing inflammation)

206
Q

how does plasma exchange treat GBS?

A

removal of autoreactive antibodies and other damaging humoral factors

207
Q

why are treatments for GBS not as effective in lower income countries

A

because treatments are very expensive and often unavailable, so new therapeutics are needed

208
Q

what percent of patients with GBS die and why?

A

10 to 15% of patients die due to lack of treatment and medical support

209
Q

What is the most common autoimmune mediated disease of the CNS?

A

Multiple Sclerosis (MS)

210
Q

MS is also known as

A

Disseminated Encephalomyelitis

211
Q

How many MS cases are there in the US and worldwide?

A

350000 in US and 2.5 to 3 million worldwide

212
Q

what is the most common age period to get MS

A

can occur at any age, but most commonly occurs at 20 to 40 yo

213
Q

what are the clinical telltale signs of MS (5 signs)

A
  1. sudden onset of muscle weakness
  2. loss of sensation
  3. numbness
  4. pain
  5. vision problems
214
Q

what is protective against MS

A

pregnancy

215
Q

are women or men more likely to get MS

A

women are 3x more likely

216
Q

what are the four major types of MS

A
  1. relapsing remitting MS
  2. primary progressive MS
  3. secondary progressive MS
  4. progressive relapsing MS
217
Q

after how long of of relapsing remitting MS does it turn into Secondary progressive MS

A

15 to 25 years

218
Q

relapsing manifestation of MS is associated with?

A

autoimmune inflammation

219
Q

progressive manifestation of MS is associated with?

A

neurodegeneration

220
Q

Why is history of patient important for MS diagnosis?

A

the recurrence of isolated neurological symptoms is important to identify MS

221
Q

what is the best way to see lesions of MS

A

MRI which shows aggregation of immune cells

222
Q

the presence of lesions predicts MS development with what percent of accuracy?

A

more than 80% accuracy

223
Q

T or F: size and number of lesions correlate with severity of MS

A

False

224
Q

what is most critical when it comes to MS lesions

A

location is most critical, but steady increase is correlated with severity as well

225
Q

how does MRI show lesions due to MS

A

the contrast enhancing media shows the BBB breaches due to inflammation

226
Q

MS is due to?

A

chronic inflammation

227
Q

In MS, does inflammation affect white or grey matter first?

A

white matter early on then spreads to grey matter

228
Q

How does inflammation occur in MS?

A
  1. autoreactive microglia and astrocytes signal for immune recruitment
  2. activated T cells enter and bind their targets exposed by microglia and astrocytes
  3. T cells now are programmed to bind and destroy myelin, oligodendrocytes, or axons
  4. B cells are activated to generate autoantibodies
  5. T cells release cytokines that activates astrocytes and microglia causing uncontrolled inflammation
229
Q

Why is MS such a chronic disease with months of no symptoms between attacks?

A

When myelin is destroyed, the axon redistributes the ion channels and switches to continuous signaling rather than saltatory signaling
- there is also remyelination in which Oligodendrocyte progenitor cells (OPCs) are responsible for remyelination in the central nervous system (CNS) in health and disease.
BUT as MS progresses, remission periods are shorter and fewer

230
Q

What occurs as MS progresses and remission periods are shorter?

A
  1. correlates with decline in remyelination
  2. with less remyelination, axon dies
  3. OPCs ability to differentiate declines with age
  4. once axonal death starts, progression into advanced MS is inevitable
231
Q

Is there a cure for MS?

A

no

232
Q

What is one of the leading causes of death in MS?

A

Suicide

233
Q

What are the supportive treatments available for MS

A
  1. amelioration of acute attack symptoms
  2. anti-inflammatory agents
234
Q

what is the problem with MS treatments

A
  1. very expensive with single dose averaging about $60000
  2. can make you immunosuppressed aka susceptible to infections
235
Q

Ms is is an example of what in regards to neurodegenerative diseases?

A

MS is example that not all neurodegenerative diseases involve prion like component

236
Q

current disease modifying drugs for MS target what?

A

target the immune reaction not the actual causative pathology (axonal destruction)

237
Q

what is the 2 hits theory

A

The two-hit hypothesis, also known as the Knudson hypothesis, is a cancer genetics theory that states that most tumor suppressor genes (TSGs) require both alleles to be inactivated to cause a change in phenotype. This can happen through mutations or epigenetic silencing. The first hit can be promoter hypermethylation, and the second hit can be a nonsense or frameshift mutation, or loss of heterozygosity (LOH). The two-hit hypothesis provides a model for understanding cancer that occurs in individuals who carry a susceptibility gene and cancers that develop because of randomly induced mutations in otherwise normal genes.

238
Q

What are the 2 types of GBS

A

axonal and demyelinating

239
Q

Which of the following would be the most accurate definition of molecular mimicry in disease?

A

Similarities between the antigens and microbe and a host

240
Q

What can be affected in diseases of motor neurons?

A

neuromuscular junctions

241
Q

In MS, the pathology is driven by an humoral and cellular response towards

A

oligodendrocytes

242
Q

In MS, there are ______________ as well as _________________ epidemiological oddities

A

geographical; dietary

243
Q

T or F: in developed countries, MS is the most common peripheral nervous system disease that arises in young adults and causes permanent disability

A

False; MS is most common CNS disease

244
Q

T or F: The pathology in GBS is driven by a cellular response towards motor neuron axons

A

False; driven by humoral response

245
Q

T or F: GBS occurs when the autoreactive antibodies bind to the myelin sheath on the CNS nerves

A

False, it affects the peripheral nerves

246
Q

T or F: MS can strike at any age, but most cases are in people over 40

A

False; ms affects pp bw 20 and 40 yo

247
Q

T or F: a temporary remission from GBS symptoms occurs when women are pregnant

A

False, it is in MS where recovery of symptoms occurs

248
Q

Compare and contrast the two effective treatments for GBS

A

One form of treatment for GBS is IV Ig infusion which causes macrophage receptors to be blocked by Igs and makes macrophages unable to bind to motor neurons (basically adds normal antibodies to overcome effect of autoreactive antibodies) while plasma exchange removes the autoreactive antibodies along with other damaging humoral factors. The more severe cases are treated with IV ig infusions and patients averse to immunoglobulin therapy are recommended to use plasma exchange

249
Q

IN class we discussed leading theories explaining the development of autoimmune reactions in GBS and MS. State them and briefly discuss why one is temporary (GBS) while the other is permanent (MS)

A

In GBS, there is a molecular mimicry in which C. jejuni infection results in gangliosides in PNS axons. In MS, the reaction is due to chronic inflammation where autoreactive microglia signal for immune recruitment causing T and B cells to activate and result in uncontrolled inflammation. GBS is temporary in that the symptoms can eventually ease up and patient can recover while MS causes permanent damage to nerve fibers

250
Q

Do microbes directly influence the brain?

A

there are clear examples of alter brain function by infections

251
Q

3 examples of how infections alter brain function

A
  1. rabies ->vampirism or werewolf myth because of altered behavior
  2. Toxoplasma and “cat ladies” (or taking away fear of cats in rodents)
  3. Herpes virus infection linked to increased risk to develop MS
252
Q

What are some other infections linked to nervous disorders (2 examples)?

A
  1. C. jejuni infection as driver of GBS
  2. AD can be result of brain infection -> AB plaques are a defensive mech in overdrive against infection
253
Q

what is the gut brain axis?

A

The bidirectional link between the CNS and the GI track, mediated by endocrine, immune, and neural signaling

254
Q

What are the 5 main gut brain axis players?

A
  1. microbiota
  2. gut-immune link
  3. vagus nerve
  4. bacterial mediators
  5. hypothalamic-pituitary-adrenal (HPA) circuit
255
Q

what is the microbiota

A

Individual microbial species in a biome - bacteria, fungi, archaea and viruses; all microorganisms living in stable association with their host

256
Q

what does disruption to the microbiota lead to

A

allergies and metabolic disorders

257
Q

what is the Gut-immune link

A

acquisition of microbiota during birth essential to train immune intolerance, the microbial signature of a baby

258
Q

what is the vagus nerve

A

it is the 10th cranial nerve, the longest nerve in the ANS connecting the GI tract to the brain stem

259
Q

What are bacterial mediators

A

precursors to, or actual, neurotransmitters (Serotonin)

260
Q

what is the HPA circuit

A

the brain’s stress response system

261
Q

ow does the gut brain axis work?

A
  1. bacterial metabolites act upon the different interfaces in the gut: the epithelial, the immune and neural
  2. SCFAs: short chain fatty acids
  3. Balance of pro and anti inflammatory cytokines
  4. response of the HPA to neuroactive metabolites
  5. reaction of the gut and immune cells to HPA response
  6. Counter reaction of microbiota to gut and immune cells response
262
Q

Balanced vs unbalanced gut brain axis

A

Balanced State: the epithelial and immune cells are trained in tolerance to correct microbiota AND microbiota is adapted to host’s biochemical normal response
Unbalanced state: small change in either microbiota composition or host’s biochemical response can lead to uncontrolled dysregulation (butterfly effect, leading to pathology)

263
Q

What are four ways the gut brain axis is seen in disease?

A

four ways the gut brain axis is seen in disease?
1. autoimmune diseases (hygiene hypothesis)
2. autism
3. depression and anxiety
4. obesity

264
Q

how does the gut brain axis and autoimmune disease correlate?

A

When the immune system training is disrupted and leads to aberrant immune reactions such as asthma, allergies, and MS

265
Q

How are autism and the gut brain axis correlated?

A

The correlation between autism and dysbiosis of the gut. Picky eating habits, genetics, or environmental factors (this is not always clear)

266
Q

what is the correlation between the gut brain axis and depression and anxiety?

A

high correlation between intestinal disorders and mental illness

267
Q

what is the correlation between the gut brain axis and obesity

A

correlation between gut microbiota and misregulation in the CNS control of food intake

268
Q

what are 5 ways the gut brain axis can affect health/disease?

A
  1. gut microbiota dysbiosis
  2. inflammation ->leaky gut
  3. leaky gut -> LPS exposure ->inflammation
  4. chronic stress -> high cortisol levels
  5. high cortisol -> go back to 1 and 2
269
Q

Study of AD, a faulty defense or dysbiosis of the brain? What are the main findings?

A
  • response to infection where AB plaques are a defense strategy
  • correlation bw brain herpes infection and risk to develop AD
  • animal studies suggest plaque are a response to infection and are protective
270
Q

What is the first brain? or fist two brains

A

the actual brain in skull
- brain stem and limbic system (oldest, emotional brain)
- neocortex (youngest, higher processing brain)

271
Q

what is the third brain?

A

your enteric nervous system aka gut brain
- influenced by microbiota

272
Q

what is the fourth brain?

A

brain microbiota
- same way gut microbiota influences our brain, but without the intermediary

273
Q

what is the significance of the UAB med school findings?

A

they studied brain slices from healthy and schizophrenia patients and found rod shaped objects in EM images that were consistent with bacteria but did not know how they got there. it could represent a previously unknown mechanism by which the immune system activity within brain is regulated

274
Q

what is fuel for the brain

A

neurotransmitters

275
Q

what produces the same type of brain fuel

A

microbes

276
Q

what is the chicken egg problem in the gut brain axis

A

what affects gut/brain also affects the gut/brain

277
Q

what highlights the connection between mental and physical health

A

MS

278
Q

Which of the following is not a player in the Gut brain axis

A

the stomach

279
Q

mental illnesses can be classified into the following categories

A

mood disorders, cognition disorders, and behavioral disorders

280
Q

which of the following statements best describe the gut brain axis

A

a bidirectional link between the gut and the brain mediated by several signals

281
Q

which of the following is an example of a microbe influencing behavior

A

rabies infection turning the infected aggressive

282
Q

how is the hygiene hypothesis related to the gut microiota

A
  • the human microbiota is necessary to train immune system, and this period of immune training is disrupted by extremely clean household environments
  • the lack of exposure to microbes early in life increases risk for autoimmune diseases like asthma
  • constant, low grade exposure to antibiotics or hormones (like diary or cattle industry) changes ratio of bad and good gut microbes, which throws off the immune system, promoting aberrant reactions
283
Q

T or F: mental illnesses are considered disorders rather than diseases because the causative agent is unknown

A

True

284
Q

T or F: there are 3 mediators between the gut and the brain: hormones, cytokines, and neuroreactive compounds

A

True

285
Q

T or F: a small changes in the gut microbiota can affect the brain, but small changes in the brain does not affect the microbiota

A

False, the gut brain link is bidirectional meaning changes in brain also affect microbiota

286
Q

T or F: the monoamine hypothesis states that a disbalance in levels of serotonin, norepinephrine (or epinephrine), and dopamine is behind mental illnesses

A

true

287
Q

The 3 types of bacterial metabolites that can affect brain function

A

SCFAs, neurotransmitters, and immune modulatory metabolites

288
Q

the 3 mental disease/disorders where there is a clear correlation with gut dysbiosis

A

autism, depression, and anxiety

289
Q

4 ways by which the gut brain axis can affect health and disease

A
  1. gut microbiota dysbiosis
  2. inflammation leading to leaky gut
  3. leaky gut leading to LPS exposure/inflammation
  4. chronic stress causing high cortisol
290
Q

what is essential to train and promote immune intolerance

A

gut immune link

291
Q

collection of microorganisms living in stable association with their host

A

microbiota

292
Q

part of our brain that coordinates the response to external stresses like hunger

A

HPA circuit

293
Q

one of the cranial nerves that serve as a link between the gut and the CNS

A

vagus nerve

294
Q

compounds produced by bacteria that can have an effect on the gut brain axis

A

bacterial mediators

Neuroinfectious Diseases (8 decks)

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