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Pathobiology > Block 4 > Flashcards

Block 4 Flashcards

1
Q

What is the brain? What are the three main functions of the central nervous system?

A

the brain is an information processor that interfaces with the environment: condition, stimulus, receptor, signal, integration, signal release, effect (motor function)

Brain + Spinal Chord
input–>process–>output
1. input: receptors convert the environment into electrochemical signals for processing by the brain
2. cognition: interpretation
3. output: motor movement

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2
Q

What are the three sectional planes used to examine the brain?

A
  1. frontal plane (coronal)
  2. sagittal plane (side)
  3. transverse plane
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3
Q

What is the hippocampus?

A

critical region for new memory formation; often affected in neural degeneration; looks like a seahorse

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4
Q

What happened to HM?

A
  • bilateral medial temporal lobe removal from epilepsy
  • developed anterograde amnesia
  • moderate retrograde amnesia
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5
Q

Difference between anterograde and retrograde amnesia?

A

not able to form new memories vs. loss of memory access to events from the past

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6
Q

List the anatomic levels of the CNS

A
  1. Telencephalon: cerebral hemispheres, hippocampus
  2. Diencephalon: thalamus
  3. Cerebellum
  4. Brainstem: midbrain, pons, medulla oblongata
  5. Spinal chord
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7
Q

What is a lesion? How are they organized?

A

any pathology finding that affects function
1. focal brain disorder: localize pathology to a focal area of the brain
2. Diffuse brain disorder: many areas involved and can’t localize; causes encephalopathy –> from primary brain disease or secondary to metabolic disease

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8
Q

Break down the sections of the brain

A

2 cerebral hemispheres: dominant is opposite side of handedness
- language problems localize here
4 lobes per hemisphere
1. Frontal: motor cortex (motor homunculus), speech (Broca’s Area), executive function
2. Parietal: somatosensory cortex
3. Temporal: auditory cortex (Wernicke’s dom side), memory (hippocampus)
4. Occipital: visual cortex

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9
Q

Parts of the brain you have to know

A
  • basal ganglia: initiation and coordination of movement
    LESION: movement difficulties, PK, HT disease
    CLINICAL: tremor, rigidity; hypokinesia, hyperkinesia
  • thalamus: sensory relay station of the brain
    LESION: inability to feel things, hemorrhagic stroke in
    hypertension
  • brainstem: cranial nerves, consciousness, cardiorespiratory function
    LESION: impaired movement, death from intracranial pressure
  • cerebellum: balance and posture
    LESION: ataxia = incoordination or clumsy movement (alcohol)
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10
Q

What happens where there is focal injury to the dominant frontal lobe?

A

aphasia: disorder or speech
Broca’s: problem of speech production (BROKEN)

motor cortex: inability to coordinate movement
PFC: impaired cognition, mood changes

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11
Q

What happens when there is focal injury to the parietal lobe?

A

dominant: apraxia = difficulty in performing a complex learned action
non-dominant: neglect of the opposite side (person is unaware of half their body)

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12
Q

What happens when there is focal injury to the temporal lobe?

A

damage to hippocampus: amnesia
dominant: Wernicke’s area, verbal learning
non-dominant: visual learning, face recognition =prosopagnosia

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13
Q

What happens when there is focal injury to the occipital lobe?

A

visual deficits, blindness

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14
Q

What are the cells of the CNS?

A

Neurons
- acute: red-dead neurons
- chronic: neurodegeneration: progressive loss of synapses, neurons, gliosis, atrophy
1. astrocytes: physical support, repair, reactive gliosis (proliferation/fibers/scarring) in response to injury
2. oligodendrocytes: myelinate CNS neurons-> myelin insulates axons; swelling, loss (MS), inclusion (viral infection) during injury
3. microglia: immune cells of CNS, phagocytic, release immune mediators in response to injury
4. Ependymal cells: help produce, circulate, and absorb CSF; dysfunction leads to hydrocephalus
5. Schwann cells: promote axon regneration

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15
Q

What are the challenges neurons face?

A

large cell size, metabolically active, long-lived, highly polarized, long cell processes, functionally diverse

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16
Q

Difference between acute, subacute, and chronic?

A

acute: seconds to hours
- focal: vascular (stroke), seizure (focal), trauma (contusion)
- diffuse: vascular (SAH), seizure (generalized), trauma (DAI), metabolic (hypoglycemia)

subacute: days to weeks
- focal: infection (abscess), inflammation (MS), auto-immune
- diffuse: infection (meningitis), inflammation (AI encephalitis)

chronic: months to years
- focal: neoplasm (GBM)
- diffuse: degenerative, metabolic

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17
Q

When is the lesion? Where is the lesion? What is the lesion?

A
  1. acute, subacute, chronic
  2. which of the 5 CNS levels or more than 1
  3. focal, multifocal and diffuse
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18
Q

What is hydrocephalus? What is edema and its causes?

A

increased CSF volume leads to expansion of the ventricles and increase intracranial pressure
1. Too much CSF being made (ie: tumor of cells that make CSF)
2. CSF flow is obstructed (ie: tumor/anatomy blocking ventricles)
3. CSF is not being reabsorbed (ie: meningitis with residual scarring)

too much fluid in brain tissue leads to increased intracranial pressure, fatal brain herniation
1.) vasogenic: abnormal increased permeability from breakdown of BBB
2.) cytotoxic: direct cell injury and swelling
3.) hydrocephalic: breakdown in ventricular lining
common after complete cessation of blood to brain

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19
Q

What are the lethal reactions?

A

hemorrhage, herniation, hydrocephalus, hypoxia

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20
Q

Herniation? Hemorrhage?

A

complication of RICP: brain expands into other structures, affecting blood flow; midline shift
1) subfalcine: anterior cerebral artery
2) transtentorial: posterior cerebral artery; causes duret hemorrhage: fatal upper brainstem
3) WORST: tonsillar ‘coning’, compresses brainstem = death

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20
Q

What kills people with intracranial disease?

A
  1. RICP due to mass lesion: hydrocephalus, hemorrhage, or other lesions; herniation with brainstem compression and Duret hemorrhage
  2. Cerebral ischemia: problem of arterial blood supply
    - occlusion or rupture of vessel: stoke, aneurysm
    - malformation of vessel: AVM
    - compression of vessel
  3. cerebral hypoxia: neurons are not getting oxygen
  4. brain ‘poisoning’: toxic substances lethal to neurons
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21
Q

How is the CNS assembled? What happens when there is failure?

A

neurulation is the process of neural tube closure and CNS formation

neural tube defects:
-anencephaly: absence of brain
-myelomeningocele: spine is exposed
- encephalocele: brain protrudes through a midline skull defect

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22
Q

Diagnostic techniques?

A
  1. CT scan: first pass; bleeds, abscess, edema, changes to ventricles
  2. MRI: more detail about brain structure, strokes, tumors, trauma, MS
  3. Angiogram: blood vessels (bleeds, occlusions, aneurysms, malformations); invasive with contrast
  4. EEG: brainwave activity, useful for seizures
  5. Lumbar puncture: analyze CSF to look for RBCs/WBCs that would tell us about bleeding, infections, tumors
  6. biopsy: gold standard to look at brain under microscope; tumor diagnosis/prognosis
  7. neuropsychological testing: cognition
  8. autopsy: cause of death
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23
Q

What is the MCA?

A

middle cerebral artery: major artery of the cerebrum
supplies most of motor cortex and motor homunculus

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24
Q

What is a stroke? Causes? Risk Factors?

A

sudden damage to the brain of vascular origin; lack of blood flow -> cell death

caused by ischemia or bleeding
- cerebral infarct caused by atherosclerosis
- intracranial hemorrhage
- subarachnoid hemorrhage

hypertension, diabetes, high cholesterol, smoking, history, alcohol/drugs

ischemic (80%): usually atherosclerosis (plaque)
hemorrhagic: hypertension (DEEP in brain) or superficial (amyloid, AVM = high pressure vascular anomaly)

paralysis, weakness, numbness

develop over time, present acutely

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25
Q

What is amyloid angiopathy?

A

abnormal beta amyloid protein deposits in the blood vessel walls; superficial acute lobar hemorrhage

sporadic: age-associated, common with AD
familial: mutations in AB

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26
Q

What is an aneurysm? Risk factors?

A

focal pathological swellings of a blood vessel; sudden onset ‘thunderclap headache’
factors: size, location, morphology

ruptured aneurysm cause of SAH

hypertension, cocaine, pregnancy, trauma, history

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27
Q

What is an arteriovenous malformation?

A

high-pressure vascular abnormality; tangled network of arteries and veins lacking a capillary bed

bleeding is the most common presentation; usually in cerebral hemispheres

28
Q

What is an abscess?

A

pus-filled swelling in the brain; necrosis and inflammation caused by infection; subacute lesion

can expand or rupture; can be multifocal = source of infection is in the bloodstream or they are immunosuppressed

headache, fever

‘ring-enhancing lesion’ = abscess, lymphoma or glioblastoma

29
Q

Focal chronic brain lesions?

A

primary brain neoplasms = tumors = excessive abnormal tissue growth; compress blood vessels, increase ICP with edema/inflammation; can be multifocal; rarely metastasize

1.) intra-axial = brain + spinal chord: glial
astrocytoma, glioblastoma, oligodendroglioma, medulloblastoma
2.) extra-axial = CNS accessories (nerves, bone): not glial
meningioma, Schwannoma, pituitary adenoma

30
Q

What are the categories of gliomas?

A

circumscribed: good margins; surgery works
diffuse: infiltrating margins; can’t be removed with surgery

primary: older patients, de novo, EGFR amplified, IDH WT
secondary: younger patients, IDH driver mutations

31
Q

What is the most common CNS tumor?

A

meningioma: benign tumor of meningothelial cells; external surfaces of the brain; slow-growing; most common in women; NF2 gene mutations

CLINICAL: headache, nausea/vomiting, blurred vision

causes: sporadic, irradiation

32
Q

Metastatic brain tumors?

A

~25% of tumors
usually carcinoma, melanoma, lymphoma
Top cause = lung

33
Q

Common malignant brain tumor?

A

glioblastoma: found in cerebral hemispheres
butterfly patterning on imaging

34
Q

What do diffuse brain lesions cause?

A

encephalopathy: any diffuse brain disorder that alters brain structure or function
- ALTERED MENTAL STATE (AMS): confusion, delirium, dementia, concussion, coma, loss of consciousness
- acute, subacute, chronic
- symmetric across brain

35
Q

Secondary encephalopathy?

A

caused by disturbances outside the brain
- organ failure
- nutritional deficiencies
- diabetes: hyperglycemia
- disturbances of water and Na balance
- sepsis

ex) hepatic encephalopathy = liver failure due to cirrhosis
ex) hypoxic-ischemic from cardiac arrest

36
Q

What are multifocal brain lesions?

A

separation in space and time
- vascular: multiple infarcts, vasculitis
- infectious: multiple abscesses = bacterial endocarditis
- tumor: multiple metastases, multifocal primary tumor (glioblastoma), tumor predisposition syndrome (NF2)

37
Q

What is MS?

A

multiple sclerosis: multifocal demyelinating disorder of the brain; autoimmune response targeting the myelin sheath causes selective demyelination; plaques

25-35 years old; optic nerves, brainstem, spinal chord are commonly affected

38
Q

Diffuse acute lesions?

A
  1. Trauma: diffuse axonal injury, traumatic brain injury
  2. Vascular: subarachnoid hemorrhage
  3. Metabolic: hypoglycemia
  4. Seizure (generalized)
39
Q

Diffuse subacute lesions?

A

infection: meningitis, encephalitis
- HSV, PML, bacteria
inflammation

40
Q

Diffuse chronic lesions?

A

metabolic: alcohol, central pontine myelinolysis, fetal alcohol syndrome
neurodegenerative: dementia, motor neuron disorders, movement disorders

41
Q

Describe TBI?

A
  • # 1 cause of death in people <45 years old
  • can be focal or diffuse: immediate AMS tells us diffuse
  • primary: immediately at impact
  • secondary: 4 H’s
42
Q

Describe DAI?

A

axotomy (neurons separate) with formation of spheroids

risks: hypoxia, edema, RICP, herniation, compression of posterior cerebral artery

43
Q

What is HSV encephalitis?

A

herpes simplex virus: targets limbic system (cerebral cortex and brainstem that regulates behaviors needed for survival)

CLINICAL: rapid onset fever, headache, impaired consciousness; CSF is abnormal ; EEG has encephalopathy pattern

necrosis, hemorrhage, inflammation –> edema –> RICP –> herniation

44
Q

What is progressive multifocal leukoencephalitis (PML)?

A
  • caused by JC virus in immunosuppressed patients with focal and diffuse signs over months
  • all 3 primary responses to infection (perivascular cuffs of lymphocytes, viral inclusions, microglial nodules) and secondary changes
  • demyelination of white matter; focal (visual disturbance, ataxia, seizures) and diffuse (AMS) signs that develop over months
45
Q

What is a diffuse acute on subacute lesion?

A

meningitis: inflammation of the meninges and CSF usually caused by infection
- fatal within hours of acute onset
- clinical is diffuse: fever, headaches, neck stiffness, AMS, seizures
- confirmed with blood cultures and lumbar puncture
- meningeal fibrosis can develop after inflammation: focal = optic or cranial nerves –> blindness; diffuse = block CSF reabsorption causing hydrocephalus, AMS, paralysis

46
Q

What is an acute SDH? How does it relate to chronic alcoholism?

A

subdural hemorrhage: space occupying lesion that splits the dura from the arachnoid caused by tearing of the bridging veins from motion/impact
- causes midline shift and life-threatening brain compression and herniation

patients with brain atrophy from alcoholism are at a greater risk for SDH from stretching the bridging veins

47
Q

What are the CNS lesions of chronic alcoholism?

A

hepatic encephalopathy, trauma, cerebellar degeneration (ataxia, atrophy, <1%), central pontine myelinolysis (CPM), nutritional deficiencies, fetal alcohol syndrome

48
Q

Hepatic encephalopathy?

A

major complication of cirrhosis
- confusion, altered consciousness, coma
- asterixis (tremors of hands)
- increased bleeding risk due to liver disease makes brain trauma hard to treat in alcoholics (contusions spread, RICP)

49
Q

What can chronic alcoholism induce?

A

mamillary body degeneration: connect hippocampi to other brain regions

Wernicke encephalopathy: global confusion, apathy, disorientation, ataxia

Korsakoff psychosis: retrograde amnesia, anterograde amnesia

50
Q

What is central pontine myelinolysis (CPM)?

A

focal demyelination of the pons; not multifocal + has clear cause normally

  • alcoholic liver disease is associated with low sodium–> rapid infusion of saline can cause CPM –> rapid onset confusion, quadriplegia
51
Q

What is fetal alcohol syndrome (FAS)?

A

most common cause of preventable neurodevelopmental defects

mom maintains high level of alcohol intake during pregnancy

52
Q

What is acute methanol intoxication?

A

ingested as a cheap substitute for ethanol, oxidized by the liver to produce formaldehyde that is neurotoxic

loss of vision, AMS, convulsions, coma, death
global hypoxic brain damage; acute hemorrhage in the basal ganglia is common

53
Q

What is neurodegeneration?

A

progressive selective neuron loss with LOF in NDDs
- neuronal connections (synapses) are lost during normal ageing
- normal age-related cognitive decline is associated with that than neuronal loss
- synaptic degeneration is associated with abnormal protein aggregation and occurs early in AD

54
Q

What are the risk factors and hallmarks of NDD?

A
  • ageing: neurons do not divide
  • classified by major protein deposit: protein misfolding disorders = ‘proteinopathies’
  • neuronal/glial inclusions from misfolded protein accumulation
55
Q

Which proteins are associated with which NDD?

A

AD: amyloid beta, tau
ALS: TDP-43
PK: synuclein

56
Q

What are the common features of NDDs?

A
  • age-dependent relentlessly progressive disorders
  • affect selectively vulnerable populations of specific neuronal subpopulations
  • characterized by the accumulation of abnormal insoluble protein
    aggregates in the form of inclusion bodies
57
Q

What are the 3 groups of NDDs?

A
  1. Dementia
    - AD, vascular brain injury, Lewy body dementia, frontotemporal dementia
  2. Movement disorders
    - PK, HD
  3. Motor neuron disorders
    - ALS, spinal muscular atrophy
58
Q

What is dementia?

A

persistent cognitive impairment across multiple domains
- loss of previously attained occupational or social function due to acquired and persistent impairment of memory, emotion, personality, or cognition with normal consciousness

59
Q

What is AD?

A

most common cause of dementia; slowly progressive diffuse brain disease with global cerebral atrophy
- synaptic and neuron loss from pathological accumulation of tau and AB
- 3 phases: preclinical, mild cognitive impairment, dementia
- dilation of ventricles, atrophy of hippocampus and amygdala

60
Q

AB and tau protein role in AD?

A

produced from the amyloidogenic pathway and is neurotoxic
- loss of synapses, impairs mitochondrial function
- APP is on chromosome 21; trisomy 21 have early onset AD
- plaques cause astrocyte and microglia responses

tau protein becomes phosphorylated in AD which forms intracellular tangles (NFTs); destabilize microtubules

61
Q

What causes AD?

A

sporadic (>95%): late-onset; age, genetic, environmental

familial: early onset (<60 yo); autosomal dominant

AB plaques and tau neurofibrillary tangles, neuronal and synaptic dysfunction, neurodegeneration –> neuron loss, gliosis, microglial activation, amyloid angiopathy

62
Q

What is amyloid angiopathy?

A

Abnormal Aꞵ protein deposits in the blood vessel walls
* Sporadic (age-associated) amyloid = common and is
associated with AD
* Familial causes are uncommon and caused by mutations in Aβ
**can cause lobar hemorrhage

63
Q

What are the 3 reasons for intracranial hemorrhage in AD?

A
  1. lobar hemorrhage from amyloid angiopathy
  2. subdural hemorrhage from bridging veins stretching from cortical atrophy
  3. hypertensive hemorrhage from cardiovascular disease (risk factor for AD)
64
Q

What is parkinsonism?

A

most common cause is Parkinson disease
- tremor, rigidity, akinesia, postural instability

65
Q

What is Parkinson Disease?

A
  • selective loss of pigmented substantia nigra neurons
    —> motor symptoms of PD are due to decreased dopaminergic stimulation of the striatum
  • Lewy bodies begin in the brainstem and end in cerebrum; aggregates made of alpha-synuclein protein cause neuron death–> astrocyte and microglial reactions
66
Q

Lewy body disorders classifications?

A

brain region affected
LB dementia: cortex/limbic = cognition
PD: midbrain = motor
PD dementia: cortex/limbic + midbrain = cognition and motor

67
Q

What is Huntington’s Disease?

A

progressive basal ganglia degeneration with movement disorder and progression to dementia
- autosomal dominant inheritance due to mutations in HTT
- causes hyperkinetic movement
- atrophy of caudate and putamen –> enlarged ventricles
- severe neuronal loss with activated astrocytes and microglia

**greater polyglutamine repeats, earlier age of onset

68
Q

What is ALS?

A

amyotrophic lateral sclerosis: progressive loss of motor neurons in the motor cortex, brainstem, and spinal cord
- profound muscle weakness, paralysis, loss of ability to walk, move, breathe
- 100% fatal
- 80% sporadic
-TDP43 cytoplasmic inclusions is hallmark –> neuron degeneration –> activation of astrocytes and microglia
- frontotemporal lobar degeneration

Pathobiology (3 decks)

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