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Medical Pathophysiology > Neurodegeneration > Flashcards

Neurodegeneration Flashcards

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USMLE® Step 1 flashcards
1
Q

what are the symptoms of Parkinson’s disease?

A

resting tremor, rigidity, bradykinesia, flexed posture, postural instability, loss of dopaminergic neurones, presence of Lewy bodies

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2
Q

why is Parkinson’s misdiagnosed?

A

mistaken for an essential tremor, Alzheimers, drug induced conditions

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3
Q

what are the risk factors of parkinsons?

A

age, twice as common in men, potential genetic cause, environmental factors

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4
Q

what is bradykinesia?

A

difficulty with everyday activities such as writing, shaving, using a knife and fork, opening buttons, decreasing blinking and slowed eating

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5
Q

what is rigidity?

A

muscle tone increase in flexor and extensor muscles providing constant resistance to passive movements

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6
Q

what autonomic functions are affected by parkinsons?

A

impotence, slower bowel motility, orthostatic hypotension

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7
Q

what effect does parkinsons have on cognition and mood?

A

slow executive functions, depression, apathy, frustration

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8
Q

what is caused by dysfunction of autonomic nervous system?

A

impaired GI motility, bladder dysfunction, excessive sweating

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9
Q

what are lewy bodies?

A

eosinophilic intracytoplasmic inclusions

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10
Q

where are Lewy bodies mainly found?

A

substantia nigra

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11
Q

how are Lewy bodies formed?

A

deposition of Alpha synuclein

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12
Q

what type of cells are affected by Lewy bodies?

A

neurons, rarely glial cells

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13
Q

what is the substantial nigra?

A

the major origin of the dopaminergic innervation of the striatum

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14
Q

what is the major function the striatum?

A

regulation of posture and muscle tone

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15
Q

how does depleting levels of dopamine correlate with PD?

A

symptoms begin when around 50-60% of DA containing neurones are lost

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16
Q

how is dopamine started?

A

tyrosine to L-DOPA to dopamine

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17
Q

what receptors does dopamine act on?

A

D 1-5 receptors

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18
Q

what effects take place in a cell after dopamine binds?

A

excitability, metabolism and gene expression of the cell

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19
Q

what is the nigrostriatal pathway?

A

pathway connecting substantially nigra and the striatum in the forebrain

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20
Q

what is the purpose of the nigrostriatal pathway?

A

for dopamine transport

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21
Q

how is movement regulated by signals to the spinal cord regulated in normal people using acetylcholine?

A

acetylcholine has a damoing effect on dopamine release in the basal ganglia, meaning signals to spinal cord are regulated

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22
Q

how is the acetylcholine damping effect on the spinal cord signals effected in someone with PD?

A

a lack of dopamine means that the signal to the spinal cord is larger meaning there is a constant on/off causing tremors

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23
Q

what is stage I of PD?

A

unilateral involvement

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24
Q

what is stage II of PD?

A

bilateral involvement but no postural abnormalities

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25
Q

what is stage III of PD?

A

bilateral involvement with mild postural imbalance on examination, leads independent life

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26
Q

what is stage IV of PD?

A

bilateral involvement with postural instability, requires substantial help

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27
Q

what is stage V of PD?

A

severe, fully developed disease, restricted to bed or wheelchair

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28
Q

how does L-DOPA treat PD?

A

is a precursor to dopamine and so crosses the BBB to restore DA levels in the brain

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29
Q

what are the issues with L-DOPA?

A

some converted before it reaches the brain

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30
Q

how can issues with L-DOPA be resolved?

A

issued with an inhibitor of decarboxylase so it does not get broken down before the BBB

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31
Q

how can half life of L-DOPA be increased?

A

COMT inhibitor prevents the breakdown

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32
Q

what other drugs can be used to treat PD?

A

oral dopamine agonists to mimic the dopamine, MAO-B inhibitor to reduce breakdown, anticholinergics to restore DA/ACh balance

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33
Q

what do MAO-B inhibitors do?

A

reduce metabolism of dopamine in the brain

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34
Q

what are the side effects of anticholinergics?

A

dry mouth, constipation, sedation

35
Q

what is dyskinesia?

A

uncontrollable writhing and choreiform movements

36
Q

what are the non-drug options of treating PD?

A

deep brain stimulation and ablative surgery

37
Q

what is deep brain stimulation?

A

implantation of wire and high frequency stimulation to create a functional lesion

38
Q

what is ablative surgery?

A

create a lesion on one or both sides of the brain which addresses the motor symptoms

39
Q

what is the pathogenic cascade in PD?

A

protein aggregation, oxidative stress and mitochondrial impairment

40
Q

what is the synaptic dysfunction in Alzheimers?

A

decreased neurotransmitters

41
Q

what are the abnormal protein deposits in alzheimers?

A

neurofibrillary tangles and amyloid plaques

42
Q

what is the very mild stage of alzheimers?

A

incidents go unnoticed and taken as a sign of getting old

43
Q

what is the mild stage of alzheimers?

A

more frequent memory loss, unable to concentrate, difficulty remembering people or objects, misplacing things

44
Q

what is the moderate stage of alzheimers?

A

failure to recall events, cannot plan or organise, become withdrawn

45
Q

what is the moderately severe stage of alzheimers?

A

unknown address, date, season, still remembers own name and family members

46
Q

what is the severe stage of alzheimers?

A

may forget spouse, need help dressing or personal hygiene, tendency to wander

47
Q

what is the very severe stage of alzheimers?

A

speech lost, help needed for all aspects of life, unable to walk or sit without help, muscles rigid

48
Q

what are the visual effects of alzheimers on the brain?

A

ventricles enlarged, loss in memory region, smaller gyri and areas missing

49
Q

what are the amyloid plaques made up of?

A

amyloid beta

50
Q

what are the enzymes involved in amyloid beta production?

A

alpha/beta/gamma secretases

51
Q

what is the function of alpha secretases?

A

cleave secretes at a particular point

52
Q

what is the function of beta secretases?

A

cleaves at the end terminus of the beta amyloid

53
Q

what is the function of gamma secretases?

A

cleaves beta amyloid at the C- terminus

54
Q

what are the 5 proteins that make up gamma secretase?

A

presinillin, nicastrin, APH-1, PEN-2, CD147

55
Q

what mutations can cause early onset alzheimers?

A

mutations in chromosome 1 and 14 cause abnormal presenilins, mutation in chromosome 21 leads to abnormal amyloid precursor protein

56
Q

where are precursor mutations found?

A

in certain residues close to alpha and gamma secretase which affect how amyloid beta is processed and can make it more likely to aggregate

57
Q

where Is amylin or islet polypeptides found?

A

in type II diabetic pancreas

58
Q

why are amyloid beta proteins made?

A

they are useful in small doses as they can protect from cell toxicity and prevent brain damage

59
Q

what things can diagnose alzheimers?

A

blood tests for macro globulin and amyloid beta structures or mini-mental state exams

60
Q

how can PET scans be used to investigate alzheimers?

A

use radioactive materials to track aspects of brain function

61
Q

what radioactive materials can be used for PET scans? how does this work?

A

radioactive water or glucose and attach to amyloid plaques

62
Q

why are PET scans important?

A

potential to diagnose at the preclinical stage and used to track changes

63
Q

what things are assessed in a brain ageing index?

A

Brain stress, neurones function, brain amyloid, genetic risk, memory scores and shrinkage level

64
Q

where is infected with amyloid beta aggregation less?

A

cerebellum and the pons

65
Q

what is ApoE?

A

involved in the breakdown and uptake of amyloid beta

66
Q

what are cholinergic defects?

A

reduced cholineacetyltransferase, acetylcholine release and choline uptake in the neocortex

67
Q

what changes occur in terms of receptors in cholinergic defects?

A

reduced muscarinic M2 and nicotinic receptors

68
Q

what are the current drugs used to treat alzheimers?

A

donezepil, galantamine, rivastigmine and memantine

69
Q

what is donezepil?

A

acetylcholinesterase inhibitor

70
Q

what is galantamine?

A

acetylcholinesterase inhibitor and nicotinic agonist

71
Q

what is rivastigmine?

A

acetylcholinesterase and butyrylcholinesterase inhibitor

72
Q

what is memantine?

A

NDMA receptor agonist

73
Q

what is antiamyloid immunotherapy?

A

immunising against A beta peptide

74
Q

what is a prion?

A

type of protein that can trigger normal proteins in the brain to fold abnormally

75
Q

when do prion diseases occur?

A

when normal prion proteins becomes abnormal and clumps in the brain causing damage

76
Q

what is sporadic CJD?

A

most common and occurs when the brain undergoes a spontaneous change to the abnormal form which results in disease

77
Q

what is iatrogenic CJD?

A

accidentally transmitted during the course of medical or surgical treatment

78
Q

what is familial CJD?

A

inherited abnormal gene

79
Q

what is new variant CJD?

A

caused by ingestion of infected meat which causes conversion of normal prion to pathogenic form

80
Q

what is fatal familial insomnia?

A

autosomal dominant disorder that is characterised by degeneration of thalamus and progressive insomnia

81
Q

what are the symptoms of fatal familial insomnia?

A

vegetative state of sleep, inability to produce tears and well as poor reflexes and dementia

82
Q

what is the cause of prions becoming infectious?

A

conformational change so a soluble protease sensitive form to an insoluble resistant form accumulates in the brain

83
Q

what are the acquired forms of human prion diseases?

A

kuru, variant CJD and iatrogenic CJD

Medical Pathophysiology (16 decks)

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