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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)

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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

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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

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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
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24
Q

what is the management

A
  1. diuretics to treat decrease ICP
  2. optic nerve sheath fenestration (in severe cases)
  3. monitor vision
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25
bell's palsy vs horner's syndrome
bell's: LMN lesion of CN7 =
26
pathophysiology of bell's palsy
LMN lesion of CN7 = ipsilateral paralysis of facial muscles = loss of wrinkles ON AFFECTED SIDE
27
what is the pathophysiology of horner's syndrome
disruption of sympathetic pathway to eye and face preganglionic: pancoast tumour = compression of sympathetic chain in apex of lung
28
Pathophysiology of alzheimer's (dementia) disease
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
what are the radiological findings
enlarged sulci and ventricles, NO raised ICP progressive neuronal death = brain atrophy = ventricles compensate by expanding
30
which parts of the brain are affected in alzhimers?
FTPH frontal temporal parietal hippocampus
31
what are the histo features of alzhimers
1. neurofibrillary tangles 2. thickened blood vessel walls with amyloid deposits 3. bundles of paired helical filaments as basophilic fibrillar structures in neuronal cytoplasm
32
what are the lifestyle risk factors for alzhimers? (think what reduces the blood flow to the brain)
1. hypercholesterol 2. lack of physical exercise 3. lack of mental exercise
33
what is the tau protein hypothesis? I DONT UNDERSTAND
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 =
34
which medication is used to treat seizures?
diazepam
35
what are the likely causes of seizures?
1. acute stroke - haemorragic: rupture of blood vessel - non haemorragic: clot formation 2. alzheimer's disease 3. hypoglycemia 4. CNS infections 5. tumour
36
what is the best distinguishing fact of a seizure vs stroke
seizure: deja vu
37
Stroke vs seizure vs faint definition
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
38
Stroke vs seizure vs faint symptoms before event
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
39
Investigations for faint, seizure vs stroke
Faint: bood pressure, ECG Seizure: EEG to identify brain activity Stroke: CT/MRI to identify haemorrage
40
what is dermatomyositis? and what are the signs of it
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)
41
UMN vs LMN lesions
UMN: loss of inhibition of reflex arc = hyper reflexia LMN: nerve pulls away from the muscle = hypo reflexia
42
What is wenicke korsakoff syndrome associated with? (low yield)
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
43
(high yield) how fast do we need to give rTPA when stroke?
4.5 hours
44
what is the cardinal rule of stroke?
time is brain (1 min = 2 million neurons)
45
what are the risk factors for stroke/ how to manage stroke?
"think of coffeeshop uncles" 1. smoking 2. diabeties 3. hypercholesterol 4. hypertension
46
What tests to run for stroke?
1. CT scan 2. test for the risk factors (smoking, diabeties, hypercholesterol, hypertension)
47
What medications to give for stroke? Classify into the 2 different types of stroke
Haemorragic 1. focus on blood pressure control Non-haemorragic (ischemic) 1. antiplatelets [started within first 24 hours] - asprin - clopridrogel - ticagrelor 2. anticoagulants (inhibit the coagulation cascade) [started 5 days later] - wafarin - rivaroban - apixaboan
48
LEFT SUPERIOR quadrantopia means lesion in...
RIGHT temporal lobe affecting MYER's LOOP
49
LEFT INFERIOR quadrantopia means lesion in...
50
what are the different types of bone neoplasms to know
Malignant (SARCOMA) 1. osteosarcoma 2. chondroSARCOMA 3. ewing sarcoma 4. multiple myeloma Benign 1. osteoCHONDROMA 2. giant cell tumour 3. fibrous dysplasia
51
what is the most common BENIGN bone chondroid tumour? - state tumour - mutation in which gene - what is the gene responsible for + what happens when it is unregulated - what would you see on x ray
osteoCHONDROMA mutation in EXT1 or 2 genes function of EXT1/2 genes: transcription of EXT1/2 protein = synthesis of heparin sulfate = allow for regulated growth plate activity = without synthesis of heparin sulfate, there would be uncontrolled growth plate activity (called EXOSTOSIS) what is EXOSTOSIS? bone extension containing cortex and periosteum = covered by thin cartilaginous cap
52
what is the SECOND most common BENIGN bone tumour? - what are the risk factors - location of tumour - pathophysiology - recurrence rate
Giant cell tumour Risk factors: 1. trauma 2. radiation exposure 3. female Location: epiphyseal - metaphysal region pathophysiology: ostoblasts develop into ABUNDANT GIANT CELLS WITH NUMEROUS NUCLEI (50-100 nuclei per cell) 30% recurrence rate, and potential to become malignant
53
which is the MOST common primary bone cancer in young children - definition - where does it affect - who does it usually affect - pathophysiology
osteoSARCOMA "high grade malignant bone tumour that produces osteoid directly from tumour cells" Location: metaphysis of long bones (since there is a lot of cell division going on here) Who: - 75% adolescents (10-25 yo) males - if affecting elderly, usually associated with pagets disease!! pathophysiology: p53 or pRB mutations in mesenchymal stem cells = uncontrolled cell division and proliferation of new immature bone = local invasion of surrounding tissues histology (x ray): 1. large destructive lytic mass 2. permeative margins 3. sunburst pattern because of new bone formation in soft tissue 4. (slide) cytological atypia 5. (slide) lace like pattern of osteoid produced by eosinophillic matrix entrapping anaplastic tumour cells
54
what is the most common MALIGNANT CHONDROID tumour? - definition - who does it usually affect - pathophysiology (what mutation) - gross vs microscopic histology - grading system
chondrosarcoma "malignant bone tumour that produces cartildge, BUT NOT OSTEOID" usually affects male adults (30-70 yo) pathophysiology: arise from IDH1/2 mutations in chondrocytes (mesenchymal cells) histology: 1. cartilaginous matrix 2. permeation of bone trabeculae 3.soft tissue and marrow invasion gross histology: 1. large lobulated tumour 2. focal calcification 3. areas of hemorrhagic necrosis 4. myxoid change (malignant changes) grading - grade 1-3 (higher means worse)
55
what is the 1. site it is commonly found 2. pathophysiology 3. histology of osteosarcomas
commonly found: metaphysis of LONG bones pathophysiology (x ray) 1. large destructive lytic mass 2. permeative margins 3. may break through cortex and elevate periosteum 4. new bone formation in soft tissue = SUNBURST pattern histology:
56
what are the 3 parts to a bone?
1. epiphysis (containing epiphyseal plate) 2. ARTICULAR CARTILDGE 3. diaphysis 4. metaphysis
57
what are the common x ray findings in OA?
LOSS loss of joint space osteophyte formation subchondral cyst subARTICULAR sclerosis ------------------ constant friction = loss of ARTICULAR cartildge = 1. loss of joint space = body tries to fill up the joint space = osteophyte formation 2. eburnation (smooth bone surface) = thickening of bone = subarticular sclerosis exposed subchondral bone with gaps in between = SYNOVIAL FLUID leaks in = intraosseous accumulation of synovial fluid
58
what is the common drug used to treat OA? - list what class of drugs it belongs to - describe the MoA
inter articular hydraulonic acid (IAHA) - symptomatic slow acting drug for OA MoA: IAHA is a large aminosaglycan found naturally in synovial fluid = induces the endogenous production of HA
59
what are the drugs that are involved in
60
what are the common X ray findings in RA?
SUB 1. swan neck deformity 2. ulnar deviation 3. boutonniere deformity
61
what is the pathophysiology of RA? (and how does this lead to the histology of RA)
APCs recognise self antigens = being self antigens to the lymph node = lymph node activated = T and B cells proliferate = form anti Ab against self antigens = Abs reach joints = secrete proinflammatory cytokines = macrophages attracted = synovial cell proliferation PPC 1. pannus formation = damage cartildge and bone 2. synovial cells secrete protease = break down of articular cartildge 3. chondrocytes release matrix melloproteinases = break down cartildge
62
what is pannus in RA?
abnormal layer of fibrovascular/ granulation tissue
63
what are chondrocytes in RA?
cells at articular cartildge
64
what are the genetic associations for RA?
HLA DR1, HLA DR4
65
what is the type of pain that last for more than 1hr?
Inflammatory pain
66

M2 (36 decks)

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