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Cellular Science > Neuropathology > Flashcards

Neuropathology Flashcards

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Biology 101 flashcards
1
Q

What is a Lysosome

A

“Digestive system” of cell. Small membrane-bound organelles containing hydrolases that degrade macromolecules arriving by endocytosis, phagocytosis or autophagy

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2
Q

What’s the difference between phagocytosis and pinocytosis?

A

Phagocytosis is the cytosis of a solid particle whereas pinocytosis deals with (extracellular) fluids

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3
Q

What’s the difference between a phago/pinocytosed vesicle and receptor-mediated endocytosed vesicle

A

Receptor-mediated endocytosed vesicles have coat proteins on the outside becoming a coated vesicle

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4
Q

What is the name of a phagocytosed particle engulfed in a vesicle

A

Phagosome (cytosome)

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5
Q

What is an autophagosome

A

?

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6
Q

What gets packaged in vesicles

A

Damaged organelles, lipids, denatured proteins (happens around pH 6)

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7
Q

What happens to lysosomes in the rER before they’re finally packaged

A

They’re fly soulmates and tagged with mannose-6-phosphate ligand which allows the package to be easily picked up by cells with mannose-6-phosphate receptors

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8
Q

How many enzymes does a lysosome contain

A

Over 50

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9
Q

Brief description of what happens if lysosomes lose function

A

Accumulation of substrate that’s meant to be broken down. This can affect the brain, bones, muscles etc.

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10
Q

How many lysosomal storage disorders are there

A

Over 50

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11
Q

What does MPS disease stand for

A

MucoPolySaccharide Disease

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12
Q

What is the cause of Mucopolysaccharide disease

A

Caused by enzymatic defect in the breakdown glycosaminoglycans (long chain sugars) —> different GAG sugars being stored

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13
Q

What happens in MPS that causes the storage of Heparin Sulphide?

A

exhibit lysosomal swelling l, neuroinflammation, sever brain dysfunction and behavioural problems.

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14
Q

What’s the name for MPS type 1

A

Hurler’s syndrome

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15
Q

What is hurlers syndrome

A

An autosomal recessive disease resulting in progress neurodegeneration. Some treatments are available through HSCT and ERT

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16
Q

What are some symptoms of Hurlers syndrome (MPS Type 1)

A

Cloudy corneas, deafness, intellectual disability, halted growth, bone and joint problems

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17
Q

What’s the name MPS type 3

A

Sanfilippo disease

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18
Q

Characteristics for MPS Type 3

A

Sanfilippo disease affects the first decade of life, leads to death in adolescence and progressive cognitive function & latter mother decline.
Stores heparin sulphide and also secondary storage if GM gangliosides

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19
Q

What can the storage of GAG sugars lead to

A

Lysosomal swelling and dysfunction. Can be leaked into bloodstream to cause problems for immune system

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20
Q

There is a natural multi step process of heparin degradation. What happens if one of these steps/enzymes is disrupted

A

Accumulation of HS over time leading to storage of GAGs

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21
Q

How can the sulphation heparin sulphide be monitored

A

Disaccharide analysis

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22
Q

What do we see in the neuropathology if lysosomal disorder

A

Enlarged lysosomal compartment due to lysosomal swelling

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23
Q

What can MPS disease lead to the secondary storage of

A

GM2 ganglioside

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24
Q

What other organelle may we see under the microscope when looking at neuronflamation

A

Microglia - proliferate to deal with presence (Depredation) of GAGs - sort of like macrophages

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25
Q

What is cross-correction is enzyme production and uptake

A

10% of enzyme produced is released from cell, taken up via mannose-6-phosphate receptors by RM endocytosis and secretion is determined by presence of one single peptide on the enzyme

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26
Q

Why can’t you just deliver the enzyme into the bloodstream as a treatment

A

Because the bbb limits it making the process ineffectual and the immune system could recognise it as foreign and degrade it (a way to avoid this is HSCT so the immune system changes with it)

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27
Q

Why doesn’t ERT work with sever MPS disorders

A

Enzymes can’t pass bbb from blood stream to brain where they’re needed for hurlers and sanfilippo.

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28
Q

How do you overcome the bbb to deliver an enzyme treatment

A

Physical injection or overproduction of enzyme

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29
Q

What ERTs are available atm

A

Direct enzyme delivery to brain through spinal cord, monthly injections and intra CSF delivery in MPS nice corrects disease if delivered early enough (in clinical trials)
Intracranial enzyme - direct injection to brain
Modifying enzyme allowing it to pass through bbb

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30
Q

How does the skull cope with increased pressure and how does this affect a person in the long run.

A

Brain is able to push some CSF or blood out of the skull. Eventually the process fails at about 30mgH2O intracranial pressure where the pressure starts to rise rapidly again.
Pats of the brain may herniate or get squeezed out of profaned or over rigid folds of the dura.

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31
Q

What are the effects of an increase in cerebral pressure

A

As pressure increases, perfusion pressure decreases leading to decreased cerebral blood flow —> hypoxia or cell death

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32
Q

Define hypoxia

A

?

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33
Q

Define perfusion

A

?

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34
Q

What are the 3 layers called that cover the brain

A

Dura mater, arachnoid, pia mater (from top to bottom) - collectively the meninges

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35
Q

What is obstructive hydrocephalus

A

When the flow of CSF is blocked anywhere along it’s pathway, obstructive hydrocephalus develops rapidly

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36
Q

Where are CSF samples taken from

A

Lumbar puncture (lower spinal chord)

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37
Q

How are blood vessels in the brain unique

A

Have thinner tunica media and no external elastic lamina - have to be sensitive and able to change the construction and dilation quickly & easily

38
Q

What is the Blood Brain Barrier

A

Separation of circulatory blood and extra cellular fluids - blocks diffusion if microscopic objects e.g. bacteria and large hydrophilic molecules into CSF
Will allow small molecules like o2, co2, hormones etc.

39
Q

Why does dinner is have a limited pthophysiology

A

Because it’s only really studied at onset

40
Q

Does havin amyloid plaques or tau deposites in brain mean you will develop dimentia

A

No not necessarily

41
Q

What are two standard procedures when physically examining the brain

A 
Covering of brain I.e. the meninges
Gurus patterning (mapping)
42
Q

What is the name of the peak of a deep fold in the brain

A

A gyrus

43
Q

What is the name of the trough of a deep fold in the brain

A

The sulcus

44
Q

Why is cranial nerve examinations good for tricky diagnostics

A

Symptoms may not always be enough pointing in the direction of a route cause whereas if we know that sight has been affected (as an affect of nerve damage), we also know the nerve that’s linked to it and can help find the route cause

45
Q

What features is the occipital lobe linked with

A

Vision

46
Q

What features is the parietal lobe linked with

A 
SENSORY
Intelligence
Language
Reading
Sensation
47
Q

What features is the temporal lobe linked with

A 
Behaviour
Hearing
Memory 
Speech
Vision
48
Q

What features is the frontal lobe linked with

A 
MOTOR
Behaviour (emotion)
Intelligence
Memory
Movement
Problem solving
49
Q

What features is the cerebellum linked with

A

Balance

Coordination

50
Q

What features is the brain stem linked with

A 
REGULATES BASIC BODY FUNCTIONS
Blood pressure
Breathing
Consciousness
Heartbeat
Swallowing
51
Q

What are the 3 different body and brain planes

A

Sagittal, coronal, transverse

52
Q

Name some temporal lobe disease symptoms

A

Hearing disturbances
Alteration to personality and behaviour
Language comprehension problem

53
Q

Name some techniques to study brain function

A 
Case study patients
Remove part to examine
Stimulate and monitor
Record activity
-fMRI
-MRI
54
Q

What does the fusiform face area do and where is it

A

Located in temporal lobe, when stimulated it leads to movement in facial muscles

55
Q

Symptoms of ICP Intercranial pressure

A 
Bradychardia
Papilloedema
Headaches in morning
Drowsiness
Seizures
56
Q

True or false: The brain has no nerve sensors with which to feel pain or pressure

A

True

57
Q

Describe what a grade is in the WHO grading system

A

A grade is the degree to which a tumour cell is different from a normal cell under the microscope

58
Q

Describe a Grade 1 Tumour

A

Benign cytological features

59
Q

Describe a Grade 2 Tumour

A

Moderate cellularity - no anaplasia or mitotic activity

60
Q

Describe a grade 3 tumour

A

Cellularity, anaplasia, mitosis

61
Q

Describe a Grade 4 Tumour

A

Grade 3 + vascular proliferation and necrosis. Permeate adjacent to normal brain tissues. Blastomas.
Most malignant, highly proliferating

62
Q

Define necrosis

A

?

63
Q

What variables can affect the survival rate with a tumour

A

Age, severity of metastasis, location and size, grade and type

64
Q

True or false: surgery alone can be a sufficient treatment for Grade 1 Tumours

A

True

65
Q

True or false: surgery alone can be a sufficient treatment for Grade 4 Tumours

A

False

66
Q

What is a glioma?

A

50% of all primary Tumours

67
Q

Give an example of a non-glial brain tumour

A

Meningioma: very common meninges tumour

68
Q

What organisms can infect the brain other than the usual 3

A

Parasites and Prions

69
Q

What is meningitis

A

Inflammation of meninges caused by bacteria

70
Q

What is encephalitis

A

Inflammation of brain (general term) - meningitis is a type of encephalitis

71
Q

What is the process of diagnosing meningitis

A

Same ole of CSF through lumbar puncture, ID bacteria, give treatment. Prognosis: untreated —> generally fatal

72
Q

Common cause of meningitis in neonates?

A

E. Coli

73
Q

Common causes for meningitis?

A

N. Meningitidis, S. Pneumoniae

74
Q

What are the 3 types of meningitis

A

Pneumococcal, chronic, cryptococcal (fungal)

75
Q

Describe the characteristics of a Toxiplasmosis gondii infection

A

Limited to immunosuppressed/compromised people I.e. most common cause of mass lesions in HIV infected patients. In most cases causes necrotising cerebritis

76
Q

What is fatal familial insomnia

A

A prion disease affecting familia, thalamus disorder

77
Q

Name some diseases associated with CNS deredatation

A

Disorders of Myelin or neuronal degenerations

78
Q

Myelin disorders - Describe the difference between demyelinating (MS) and dysmyelenating (Leukodystrophies)

A

?

79
Q

What are the characteristics of neuronal degeneration

A

Primary degeneration happens either globally (e.g. Lew my body, Alzheimer’s) or selective/system (e.g. Parkinson’s or Huntington’s)
Secondary is based on metabolic storage, toxic, infections, nutrition or even alcohol and b12 deficiency

80
Q

Describe briefly what MS is

A

An autoimmune response primarily against CNS myelin (white matter). Regions of white demyelination are called plaques

81
Q

What are plaques in the brain

A

Regions of demyelination white matter

82
Q

True or false: plaques in the cortex may lead to dementia’s

A

True

83
Q

True or false: plaques in the basal ganglia and brain stem can lead to dementia’s

A

False, they lead to Parkinsonian diseases

84
Q

What are the primary causes of denial CNS degradation

A

Alzheimer’s, left body, Huntington’s, picks disease

85
Q

What are some secondary causes to senile CNS degradation

A

Stroke, infections, drugs, toxins, vitamin deficiency

86
Q

What are some pathological hallmarks of CNS degradation

A

Deposition of amyloid plaques around blood vessels and neurons
Abnormal form of microtubule protein (tau) in neurons neurofibrillary intracellular tangles.
Degeneration starts in hippocampus
Use Silver stain

87
Q

What is silvers stain used for

A

?

88
Q

Characteristics of frontotemporal dementia (& picks disease)

A

Personality changes followed by memory loss, affected personality, behaviour and speech
Pathology: neurons with round intracytoplasmic Picks bodies

89
Q

Characteristics of Vascular dementia

A

Associated with multiple undercard, he served the name multiple infarct dementia.
2nd most common form of dementia after Alzheimer’s

90
Q

What are Lewy bodies and Tau

A

Irregular densely packed proteins that develop inside nerve cells and disrupt neurosignalling causing cells to die
Found in cortex or brain stem

91
Q

What are neurofibrillary tangles

A

Primary marker of Alzheimer’s disease, tau protein stabilises the structure of microtubules so when aggregates of hyperphosphorylated tau protein form away from the tubules, they destabilise and start to fall apart.

Cellular Science (19 decks)

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