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M2 > Neuroscience patho > Flashcards

Neuroscience patho Flashcards

1
Q

describe the pathophysiology of parkinsons disease

A

*neurodegenerative disease
death of dopaminergic neurons in substantia niagra
= decrease dopamine levels
= unable to modulate direct (excitatory D1 receptor) and indirect (inhibitory D2 receptor) pathway
= no inhibition of D2 pathway
= increase inhibition of GP externa
= increase inhibition of cortex
= uncontrolled D2 pathway
= involuntary movement

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2
Q

describe neuronal circuity through the basal ganglia

A

movement initiated by motor cortex

BASAL GANGLIA
1. putamen + caudate nucleus = striatum (recieves multple affrent projections)
2. global pallidus (EXTERNA)
3. SUBthalamic nucleus
4. global pallidus (INTERNA)
5. thalamus
6. cortex

no dopamine
= D2 pathway is free
= inhibition of GP externa
= inhibition of cortex
= supress movement

direct: initiate voluntary movement
indirect: PREVENT involuntary movement

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3
Q

what are the symptoms of parkinson? (“trapped in their own body”)

A

Tremor –> resting tremor which subsides with voluntary moevment
Cogwheel rigitity –> increasing resistance on passive joint movement
Akinesia + bradykinesia –> everything is slowed down significantlly
Postural instabilty + shuffling gait

late stages:
1. autonomic dysfunction
2. issues sleeping
3. cognitive abnormalities
4. falls

  1. bradykinesia (slow movement)
  2. akinesia (cannot initiate movement) + rigidity
  3. resting tremor (cannot prevent involuntary movement) +
  4. postural instability (cannot initiate voluntary movement)
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4
Q

Histology of parkinsons disease

A
  1. depigmentation of dopamine producing neurons in substantia nigra
  2. cytoplasmic inclusions and lewy bodies
  3. neuronal death in substantia niagra
    = dopamine producing neurons are usually highly pigmented, but death means DEPIGMENTATION
  4. cytoplasmic inclusions and lewy bodies
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5
Q

What are the hypothesis for parkinsons

A
  1. mitochondrial compplex 1 ETC inhibition

complex inhibition
= disrupt electron flow
= electrons leak
= react with oxygen
= ROS formed
= superoxide radicals –> toxic hydroxyl radical
= decomposition of lipid peroxides
= formation of neurotoxic 4-HNE
= neuronal death

2 . PARK 2 mutation = disrupt proteasome function

PARK2 mutation
=parkin cannot tag disfunctional MITOCHONDRIA with ubiquitin
= accumulation of faulty mitochondria
= ROS accumulation
= neuronal death

  1. alpha synuclein gene hypothesis

alpha synuclein gene misfolds
= oligomers formed
= aggregate into insoluble fibrils
= accumulates lewy bodies
= acts as Ca2+ channels
= influx of Ca2+
= degredative enzymes and proteins released into the cell
= cell death

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6
Q

what are the markers used for parkinsons disease (think of the hypothesis + use ur brain)

A
  1. increase ROS = increase inflammatory levels
  2. alpha synuclein aggregates
  3. decrease dopamine levels
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7
Q

Drugs used for parkinsons

A

L DOPA + carbidopa

  1. L-DOPA
    dopamine precursor that can cross the BBB
    = DOPA decaryboxylase converts L-DOPA to dopamine
  2. carbidopa
    DOPA decarboxylase inhibitor that does not cross the BBB
    = prevents early coversion of L DOPA to dopamine before the BBB
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8
Q

What are the headache red flags

A

“elderly TCM”

  1. increase ICP
  2. neurological deficits
  3. elderly
    - jaw claudiation (pain when chewing) –> giant cell artheritis
    - new onset headache –> tumours
  4. Tempo
    - not getting bettrer
    - sudden onset
  5. constituitional features –> cancer
    - weight loss
    - night sweats
    - confusion + seizures
  6. meningitis
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9
Q

what is a thunderclap headache

A

subarachnoid haemorrage

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10
Q

what are 3 causes of rapidly evolving sinister headaches?

A
  1. subarachnoid haemorrage (lens shaped)
    - thunderclap
    - meningism (blood irritates the meninges)
  2. sinus thrombus
    = blood cannot drain into the IJV
    = venous congestion
    = increase ICP
    = ischemia
    = seizures and neuro deficit
  3. dissection
    = tearing of intima layer of blood vessel
    = false lumen created
    = stretching of outer layers of vessel, which contain pain sensitive nerve endings
    = ‘tearing’ ‘ripping’ headache
  • dissection usually in ACA, ICA, or MCA
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11
Q

what is the flow of blood from the heart to the HnN?

A

left ventricle
arch of aorta
brachiocephallic trunk
subclavian artery & common carotid artery (bificuation at sternoclavicular joint)
commmon carotid artery bificuaration at C4 behind thyroid cartildge, into internal carotid and external carotid
internal carotid –> circle of willis (brain)
external carotid –> superficial structures on face

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12
Q

draw out the circle of willis + where is most likely to get haemorraged

A

ACA (40%) –> middle of frontal and parietal lobe
ICA (20%)
MCA –> lateral cerebral cortex, temporal lobe

PCA –> everything else

berry annureysm
= most common cause of non traumatic SAH [circle of willis is in the subarachnoid space]

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13
Q

First line treatment for headaches

A
  1. CT scan –> diagnose
  2. lumbar puncture –> look for xanthochromia

SAH: surgical clipping of ruptured aneurysm
GCA: corticosteroids + temporal artery biopsy
Meningitis: empirical Abx
Dissection: anticoagulants or antiplatelets

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14
Q

what genetic abnormality is associated with berry annyuerysm?

A

ADPKD (autosomal dominant polycystic kidney disease)

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15
Q

what are the CT findings of berry annyuerysm

A

no contrast CT: HYPOdense fissures in CT
= blood fills sulci

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16
Q

what modality does MRI imaging use?

A

MRI = magnetic resonance imaging
= no radiation

T1 weighted: fat bright
T2: fluid bright

good for visualising soft tissue swelling and venous system

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17
Q

how to differentate betwen CT vs MRI scan

A

CT: bone is hyperdense
MRI: brain is more obvious

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18
Q

what are the primary causes of intraparenchymal haemorrage

A

primary causes:
1. hypertension
2. amyloid angiopathy
3. trauma

  1. vascular malformation
  2. anticoagulant use
  3. tumour
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19
Q

list the difference between epidural vs subdural haemorrage

A

epidural:
1. clear history of trauma
= pterion fracture
2. MMA rupture
3. BICONVEX

subdural:
1. brain atrophy
2. bridging veins
3. CRESENT

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20
Q

what are the branches of the 1st part of the maxillary artery?

A

DAMIA:
1. Deep auricular artery (External acoustic meatus)
2. Anterior tympanic artery
3. Middle meningeal artery (FS)
4. Inferior alveolar artery (MF)
5. ACCESSORY meningeal artery (FO)

21
Q

what is the pathophysiology + symptoms of GCA?

A

temporal artheritis
= inflammation of medium - large arteries of the HnN
= macrophages activated
= macrophage fusion
= giant cell formation
= granulomatous inflammation in TUNICA MEDIA
= disruption of elastic lamina
= increase hyperplasia and fibrosis (due to inflammation)
= narrowing of lumen
= decrease blood flow
= ischemia
= jaw claudication, new onset headache in >50yo

22
Q

How does papilloedema come about?

A

Increase ICP
= transmitted to optic nerve sheath
= swelling of optic disc

Clinical features
1. blurred vision
2. CN6 palsy = failure of aBduction of the eye + double vision
3. enlarged blindspot

23
Q

what are the fundoscopic examination findings?

A
  1. blurred disc margins = due to swelling
  2. venous engorgement
  3. increase venous pressure/ inflammation
    = increase blood flow in capillaries of the optic disc
    = disc appears red and congested
24
Q

what is the management

A
  1. diuretics to treat decrease ICP
  2. optic nerve sheath fenestration (in severe cases)
  3. monitor vision
25
Q

bell’s palsy vs horner’s syndrome

A

bell’s: LMN lesion of CN7

26
Q

pathophysiology of bell’s palsy

A

LMN lesion of CN7
= ipsilateral paralysis of facial muscles
= loss of wrinkles ON AFFECTED SIDE

27
Q

what is the pathophysiology of horner’s syndrome

A

disruption of sympathetic pathway to eye and face

preganglionic: pancoast tumour
= compression of sympathetic chain in apex of lung

28
Q

Pathophysiology of alzheimer’s (dementia) disease

A

NORMAL
amyloid protein precursor cleaved by ALPHA senatase

ABNORMAL
amyloid protein precursor cleaved by BETA senatase
= insoluble fragments formed
1. works as a radical and causes damage
2. aggregates to form oligomers
= acts as Ca2+ channel
= influx of Ca2+ into the cell
= proteases released into the cell
= cell death
3. activate macrophages
= pro inflmmatory mediators
= ROS
= neurons undergo bystander damage

29
Q

what are the radiological findings

A

enlarged sulci and ventricles, NO raised ICP

progressive neuronal death
= brain atrophy
= ventricles compensate by expanding

30
Q

which parts of the brain are affected in alzhimers?

A

FTPH

frontal
temporal
parietal
hippocampus

31
Q

what are the histo features of alzhimers

A
  1. neurofibrillary tangles
  2. thickened blood vessel walls with amyloid deposits
  3. bundles of paired helical filaments as basophilic fibrillar structures in neuronal cytoplasm
31
Q

what are the lifestyle risk factors for alzhimers? (think what reduces the blood flow to the brain)

A
  1. hypercholesterol
  2. lack of physical exercise
  3. lack of mental exercise
32
Q

what is the tau protein hypothesis? I DONT UNDERSTAND

A

dysregulation of kinases + decrease activity of phosphotases
= tau is excessively phosphorylated
= cannot assemble microtubules
= hyperphosphorylated tau becomes insoluble
= aggregates of tau proteins form
= formation of neurofibrillary tangles
= loss of axonal transport and communication between neurons
=

33
Q

which medication is used to treat seizures?

A

diazepam

34
Q

what are the likely causes of seizures?

A
  1. acute stroke
    - haemorragic: rupture of blood vessel
    - non haemorragic: clot formation
  2. alzheimer’s disease
  3. hypoglycemia
  4. CNS infections
  5. tumour
35
Q

what is the best distinguishing fact of a seizure vs stroke

A

seizure: deja vu

36
Q

Stroke vs seizure vs faint definition

A

Faint: Temporary loss of consciousness due to transient global hypoperfusion

Seizure: Abnormal electrical activity in the brain

Stroke: Ischemia or haemorrage to the brain = sudden loss of neurological function

37
Q

Stroke vs seizure vs faint symptoms before event

A

Faint:
1. light headed
2. sweat
3. nausea
4. pallor

Seizure:
1. aura
2. deja vu
3. focal symptoms before full blown seizure

Stroke: Sudden headache

38
Q

Investigations for faint, seizure vs stroke

A

Faint: bood pressure, ECG
Seizure: EEG to identify brain activity
Stroke: CT/MRI to identify haemorrage

39
Q

what is dermatomyositis? and what are the signs of it

A

inflammatory myopathy
- proximal muscle weakness (shoulder and hip)

signs:
1. heliotrope rash (violaceous rash) on face and hanfs
2. scaly ermathous patches over knuckles
3. mechanics hands
4. elevated CK levels (to indicate inflammation)

40
Q

UMN vs LMN lesions

A

UMN: loss of inhibition of reflex arc = hyper reflexia

LMN: nerve pulls away from the muscle = hypo reflexia

41
Q

What is wenicke korsakoff syndrome associated with? (low yield)

A

B1 thiamine deficiency

triad of symptoms:
1. confusion
2. occulomotor dysfunction
3. gait ataxia

wernicke’s encephalopthy: acute and reversible
korsakoff syndrome: chronic and irreversible

MRI findings:
1. symmetrical lesions in mamillary bodies, thalamus, periaqueductal grey matter

42
Q

(high yield) how fast do we need to give rTPA when stroke?

A

4.5 hours

43
Q

what is the cardinal rule of stroke?

A

time is brain (1 min = 2 million neurons)

44
Q

what are the risk factors for stroke/ how to manage stroke?

A

“think of coffeeshop uncles”

  1. smoking
  2. diabeties
  3. hypercholesterol
  4. hypertension
45
Q

What tests to run for stroke?

A
  1. CT scan
  2. test for the risk factors (smoking, diabeties, hypercholesterol, hypertension)
46
Q

What medications to give for stroke? Classify into the 2 different types of stroke

A

Haemorragic
1. focus on blood pressure control

Non-haemorragic (ischemic)
1. antiplatelets [started within first 24 hours]
- asprin
- clopridrogel
- ticagrelor

  1. anticoagulants (inhibit the coagulation cascade) [started 5 days later]
    - wafarin
    - rivaroban
    - apixaboan
47
Q

what are the different types of bone neoplasms to know

A

Malignant (SARCOMA)
1. osteosarcoma
2. chondroSARCOMA
3. ewing sarcoma
4. multiple myeloma

Benign
1. giant cell tumour
2. fibrous dysplasia
3. osteoCHONDROMA

48
Q
A

M2 (21 decks)

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