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CNS diseases Flashcards

1
Q

what are meninges?

A

membranes between the inner side of the skull and the neurons of the brain

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2
Q

where is the CSF formed?

A

in the ventricle’s choroid plexus

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3
Q

where does CSF flow? how does it get absorbed?

A

through the ventricles into the subarachnoid space via the median and lateral apertures. Some CSF flows through the central canal of the spinal cord.
Gets absorbed in the dural venous sinuses via the arachnoid villi.

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4
Q

what are the 3 types of glial cells? describe

A
  • oligodendrocytes: analogs of the Schwann cells in periphery (production of myelin sheath on axons)
  • astrocytes: control neuron’s microenvironment. caretaker cells of the neurons.
  • microglia: variant macrophages (immune cells in the brain)
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5
Q

what’s an abscess?

A

local area of tissue destruction due to infection.
liquefaction inside the brain.

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6
Q

what brain bacterial infections are neonatal and young children most prone to?

A

E. coli and haemophilus influenzae

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7
Q

does tha brain have good immune response?

A

it is very resistant, but has weak defense if a bacteria establishes itself.

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8
Q

where in the brain does inflammation happen?

A

meninges

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9
Q

where do microorganisms often grow?

A

subarachnoid space

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10
Q

layers of meninges from inner to outer

A

pia mater, arachnoid, dura mater

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11
Q

what is meningitis and name the symptoms

A

inflammation of the meninges, usually confined to subarachnoid space.
fever, headache, stiff neck, mental alterations, photophobia

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12
Q

what fills the subarachnoid space in meningitis?

A

purulent exudate (neutrophils and bacteria)

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13
Q

what 3 bacterias can cause meningitis in adults?

A

E. coli, streptococcus pneumoniae, Neisseria meningitis

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14
Q

where is Neisseria meningitis most present?

A

Africa

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15
Q

how does Neisseria meningitis infect people?

A

it colonizes the nasopharynx and secretes proteases that inactivate IgA so they can cross the epithelium and enter the bloodstream which gives them access to the brain where they invade non-ciliated cells

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16
Q

pathogenesis of meningitis caused by Neisseria meningitis (like the steps)

A
  1. Adhesion to non-ciliated epithelium
  2. Production of an IgA protease.
  3. Has a polysaccharide capsule that inhibits phagocytosis. The capsule can mimic
    neural cell adhesion molecules.
  4. They can vary the surface expression antigen.
  5. Immune system is triggered by endotoxin.
  6. Neutrophil proteolytic enzymes damage the endothelium.
  7. Shock, intravascular thrombosis, and system failure
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17
Q

what does the inflammatory reaction following meningitis cause?

A
  • vasculitis and cerebral ischemia
  • BBB disruption, hydrocephalus, cellular swelling causing cerebral edema
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18
Q

what bacteria can pass through the endothelium of the cerebral vasculature
without any disruption of the endothelium?

A

E. coli with a K1 capsule

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19
Q

what are the 2 forms of neural injury in meningitis?

A

necrotic cortical injury and apoptotic hippocampal injury

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20
Q

how can we cure meningitis?

A

no therapy found, only antimicrobial treatment

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21
Q

meningitis can arise from complication of what disease?

A

tuberculosis

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22
Q

what can viral meningitis be caused by?

A

mostly herpes viruses and HIV, also echovirus, coxsackie, mumps, measles, adenovirus

23
Q

is viral or bacterial meningitis most dangerous?

A

bacterial has more morbidity and mortality

24
Q

what are consequences of HIV affecting the CNS?

A

causes demyelination, peripheral neuropathy, dementia

25
Q

how does HIV get in the brain?

A

it can cross the BBB directly if theres a gap, or be transported with monocytes or t cells

26
Q

what brain cells does HIV target the most?

A

microglial cells and astrocytes

27
Q

can you get rid of HIV?

A

Once infected, the Herpes virus remains latent for the rest of our lives

28
Q

what is the most common parasitic infection of CNS? what bacteria? how can you catch it?

A

cerebral malaria: P. Falciparum.
from mosquitos

29
Q

what are symptoms of cerebral malaria (parasitic)

A

causes inflammation, damage to the vasculature and to the blood brain barrier

30
Q

describe prion diseases

A

abnormal protein formation and build up causing spongiform change (can destroy neurons).
a mutated protein can mutate other proteins! (loop chain reaction)

31
Q

give one example of prion disease

A

Mad cow: transmitted to humans through food

32
Q

explain the different types of prion diseases

A
  • spongiform encephalopathy: holes in the
    brain form, giving a sponge-like appearance to the brain
  • Creutzfeldt-Jakob disease CJD: damages cerebrocortex. formation of damaging plaques
  • Gerstmann-Straussler-Scheinker: damages the cerebellum
  • Kuru: damages the cerebellum
  • mad cow (bovine spongiform encephalopathy BSE): damages brain stem
  • Fatal familial insomnia: damage to thalamus
33
Q

what are the two phases of head trauma?

A
  • immediate: primary change, physical damage
  • delayed: secondary damage, ischemia, hypoxia, swelling, hypercarbia, hypo/hypertension, infections
34
Q

what can secondary brain injuries lead to?

A

initial damage, decrease in autoregulation of blood flow by the brain, compensatory mechanism

35
Q

Consequences of Traumatic Brain Injury (TBI)?

A
  • BBB breakdown = toxic compounds, neutrophils get in, cause inflammation, neuronal cell death from cytotoxicity
  • secondary immune reactions with T cells injury
  • sepsis
  • usually multi-trauma
36
Q

what is herniation?

A

increase intracranial pressure due to subdural hematoma (ex brain pushes on brainstem, which pushes on cerebellum, causing herniation and cerebellar tonsil)

37
Q

what are the common sites of trauma?

A

frontal lobe, occipital lobe and cerebellum

38
Q

how do we evaluate someone’s unconsciousness?

A

with the Glasgow coma scale - classify the damage as being either mild (13), moderate (9-12) or severe (8 or less)

39
Q

what are cortical Lewy bodies and beta-amyloid plaques each related to?

A

cortical Lewy bodies = parkinson’s
beta-amyloid plaques = alzheimer’s

40
Q

symptoms of Parkinson’s disease

A

lack of balance, blank face, tremor, joint rigidity, dementia

41
Q

what brain region is affected by Parkinson’s?

A

substantia nigra (dopaminergic neurons) in the basal ganglia.
Lewy bodies accumulate in neuron’s cell bodies

42
Q

describe Lewy Body

A

accumulation of α- synuclein proteins, which compact into fibrils

43
Q

what minimum % of neurons must be destroyed in substantia nigra to see an effect?

A

80%

44
Q

describe the hypothesis for Prakinson’s pathogenesis

A
  • microbiome hypothesis: The Lewy body gets in through the Vagus nerve (CNX) from the GI tracts where there’s an abnormal microbiome
  • viral hypothesis: long-term risk of Parkinson disease following influenza and other infections
45
Q

can we treat parkinson’s and alzheimer’s?

A

no. we only have treatment that can improve the quality of life of Parkinson’s patients

46
Q

is Alzheimer’s genetic?

A

no. 98% of causes are environmental

47
Q

why do we see more cases of Alzheimer’s?

A

because we live longer now!

48
Q

what are alzheimer’s symptoms?

A

dementia, cognitive impairment, as well as motor, language and sensory impairments.

49
Q

what brain areas are affected by Alzheimer?

A

cholinergic neurons in hippocampus and cortex. whole .brain atrophies (gets smaller and looses neurons)

50
Q

what are physical features of Alzheimer’s?

A
  • Intraneuronal tangles of tau proteins and b-amyloid plaque-like structures on the brain
  • changes in mitochondrial function, neuro inflammation, cholinergic
    insufficiency, autophagy dysfunction
  • angiopathy
51
Q

how are amyloid plaques formed?

A

amyloid precursor
-> cleaved with gamma and beta secretase = tau tangles
-> cleaved with gamma and alpha = no danger

52
Q

is dementia a natural consequence of aging?

A

no

53
Q

name dementia preventable risk factors

A

no education, mid-life hearing loss, smoking, untreated depression, lack of exercise, social isolation, high BP, obesity, type 2 diabetes

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