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neurology FA + STEP 2 > tumor, headache, dementia, Parkinson > Flashcards

tumor, headache, dementia, Parkinson Flashcards

1
Q

Adult primary brain tumors - types

A
  1. Glioblastoma multiforme (grade IV astrocytoma)
  2. Meningioma
  3. Hemangioblastoma
  4. Schwannoma
  5. Oligodendroglioma
  6. Pituitary adenoma
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2
Q

Meningioma - treatment / histology

A

resection and/or radiosurgery

  • spindle cells concentrically arranged in a whorled pattern
  • psammoma bodies (laminated calcification)
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3
Q

Hemangioblastoma - most often area / can produce

A

cerebellum / erytrhopoietin (2ry polycethemia)

- associated with VHL

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4
Q

Schwannoma stain / treatment

A

S-100 positive

- resectable or treated with stereotactic radiosurgery

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5
Q

Childhood primary brain tumors - types

A
  1. Pilocytic (low grade) astrocytoma
  2. Medulloblastoma
  3. Ependymoma
  4. Craniopharyngioma
  5. pinealoma
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6
Q

ependymoma can cause / histology

A

Hydrocephalus
- characteristic perivascular rosettes.
Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus

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7
Q

craniopharyngioma can cause

A
  1. bitemporal hemianopia
  2. hypopituitarism
  3. hyperphagia (destruction of ventromedial area - satiety area of hypothalamus)
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8
Q

Medulloblastoma - histology / gross appearance / complications

A
  1. Homer-Wright rosettes
  2. small blue cells
    gross: solid
    complications: 1. compress 4th ventricle causing hydrocephalus
  3. send “drop metastases” to spinal cord
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9
Q

Pinelioma can cause … (and mechanism)

A
  1. Parinaud syndrome: compression of tectum –> vertical gaze palsy
  2. obstructive hydrocephalus (compression of cerebral aqueduct)
  3. precosious puberty in males (increased β-HCG production)
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10
Q

headache - definition / MC in (sex)

A
  • pain due to irritation of of structure such as dura, cranial nerves or extracranial structures
  • MC in women, except clusters
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11
Q

main types of headache - duration

A
  1. cluster –> 15min-3h repetitive
  2. tension –> more than 30 min (typically 4-6h)
    constant
  3. migraine –> 4-72h
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12
Q

Migraine mnemonic

A

POUND

Pulsatile, One-day duration, Unilateral, Nausea, Disabling

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13
Q

cluster headache - characteristic of pain and other symptoms

A
  • Repetitive brief headaches
  • Excruciating periorbital pain with lacrimation
  • Rhinorrhea
  • may present with HORNER syndrome
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14
Q

cluster headache - treatment

A

acute: 1. 100% 02 2. sumatriptan
prophylaxis: verapamil

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15
Q

tension headache - treatment

A
  1. Analgesics
  2. NSAID
  3. acetaminophen
  4. Amitryptyline for chronic pain
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16
Q

Migraine - treatment

A

Acute: triptans, NSAIN, dihydroergotamine
ProphylaxiS: lifestyle changes (sleep, exercisem diet eg,) propranolol, topiramate, Ca2+ channel blockers, amitriptyline, valproate

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17
Q

triptans - clinical use

A
  1. acute migraine

2. cluster headache attacks

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18
Q

triptans - mechanism of action

A

5-HT (1B/1D) agonists (seretonin) –>

a. inhibit trigeminal nerve activtion
b. prevent vasoactive peptide release
c. induce vasoconstriction

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19
Q

triptans - toxicity

A
  1. coronary vasospasm

2. mild paresthesia

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20
Q

triptans are contraindicated in

A

patients with CAD or Prinzmetal angina

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21
Q

Menierre disease - symptoms

A
  1. recurrent attacks of vertgio (>20 mins)
  2. tinnitus
  3. hearing loss
  4. fullness sensation
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22
Q

familiar form of Alzheimer disease - proportion and proteins

A

10%

APP, presenilin-1, presenilin-2

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23
Q

Altered proteins - Alzheimer disease

A

altered proteins:
ApoE2: decreased risk of sporadic
ApoE4: increased risk of sporadic
APP: increased risk for early onset (familiar)
presenilin-1: increased risk for early onset (familiar)
presenilin-2: increased risk for early onset (familiar)

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24
Q

Alzheimer disease - histology

A
  1. loss of ach neurons
  2. senile plaques in gray matter (extracellular β-amyloid (Aβ) core)
  3. Neurofibrillary tangles (intracellular, hyperphosphorylated tau protein)
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25
Q

Alzheimer disease - senile plaques CAN CAUSE (how)

A

amyloid angiopathy –> intracranial haemorrhage

deposition around vessels

26
Q

Lewy body dementia - clinical course

A

initially dementia and visual hallucinations followed by parkinsonian features

27
Q

Lewy body dementia - histology

A
  1. loss of pigmented neurons in substantial nigra

2. lewy bodies (PRIMARILY CORTICAL)

28
Q

Lewy bodies

A

round eosinophilic inclusion of α-synuclein (PRIMARILY CORTICAL)

29
Q

Frontotemporal dementia (Pick disease) - histology

A
  1. silver-staining spherical tau protein aggregates (Pick bodies)
  2. inclusions of ubiquitinated TDP-43
30
Q

Frontotemporal dementia (Pick disease) - symptoms

A
  1. Dementia
  2. aphasia (early) (primary progressive aphasia)
  3. movement disorders (eg. parkinsonism, ALS-like UMN/LMN degeneration)
  4. early change in personality and behaviour
31
Q

vitamins deficiency associated dementia - vitamins

A

Vitamins B1, B3 or B12

32
Q

Parkinson disease - histology

A
  1. Lewy bodies (composed of a-synuclein - intracellilar eosnophilic inclusions)
  2. loss of dopaminergic neurons of substantia nigra pars compacta (de-pigmentation)
33
Q

Parkinson disease - neurotransmitter alternations

A
  1. decreased dopamine
  2. increased Ach
  3. Increased serotonin
34
Q

Parkinson disease - symproms

A

MNEMONIC: TRAP

  1. Tremor (pill-rolling tremor at rest)
  2. Rigidity (cogwheel)
  3. Akinesia (or bradykinesia)
  4. Postural instability
  5. Shuffling gait
35
Q

Huntington disease - chromosome of trinucleotide / trinucleotide repeat / age / mode of inference

A

ch 4
CAG
20-50
AD

36
Q

Huntington disease - symptoms

A
  1. choreiform movements (athetosis, chorea)
  2. aggression
  3. depression
  4. dementia
37
Q

Huntington disease - neurotransmitter alternations

A
  1. increased dopamine
  2. decreased GABA
  3. decreased Ach
38
Q

Huntington disease - MRI

A

Atrophy of caudate and putamen nuclei with hydrocephalus ex vacuo

39
Q

Huntungton is sometimes mistaken for

A

substance abuse

40
Q

Huntington disease - pathogenesis

A

neuronal death via NMDA-R binding and glutamate toxicity

41
Q

neurons cell bodies and dendrites can be seen on

A

Nissle staining (stains RER)

42
Q

Injury of axon of neuron –> .. ..

A

Wallerian degeneration: degeneration distal to injury and axonal retraction proximally –> allows for potential regeneration of axon (if in peripheral)

43
Q

Myelin is made of

A
  • CNS - oligodendrocytes

- PNS - Schwann cells

44
Q

astrocytes, microglia, Schwann cells, oligodendroglia - derived from

A

astrocytes –> neuroectoderm
microglia –> mesodermal, mononuclear origin
Schwann cells –> neural crest
oligodendroglia –> neuroectoderm

45
Q

correcting of serum Na+ too fast can cause

A

from low to high –> Osmotic demyelination syndrome

from high to low –> cerebral edema/herniation

46
Q

Huntington Drugs and mechanims of action

A
  1. Haloperidol –> D2 receptor antagonist –
  2. Tetrabenazine –> VMAT inhibitor
  3. reserpine –> VMAT inhibitor –> limits dopamine vesicle packagings and release
    VMAT: vesicular monoamine transporter
47
Q

Alzheimer disease - drugs and mechanism of action

A
  1. Memantine –> NMDA receptor antagonists –> helps prevent exctitoxicity (mediated by Ca2+)
  2. Donepezil –> Ache inhibitors
  3. galantamine –> Ache inhibitors
  4. rivastigmine –> Ache inhibitors
  5. tacrine –> Ache inhibitors
48
Q

Memantine - side effects

A
  1. Dizziness
  2. confusion
  3. hallucinations
49
Q

Alzheimer disease - Ache inhibitors - side effects

A
  1. nausea
  2. dizziness
  3. insomnia
50
Q

Parkinson disease drug - dopamine agonists (drugs)

A
  1. bromocriptine (ergot)
  2. pramipexole (non-ergot)
  3. ropinirole (non-ergot)
51
Q

Parkinson disease drug - increase dopamine availability - drugs and mechanism?

A

amantadine –> increases dopamine release and decreases dopamine reuptake

52
Q

amantadine - toxicity

A
  1. ataxia

2. livedo reticularis

53
Q

Parkinson desease drugs - increase L-DOPA availability - mechanism

A

agents prevent peripheral (pre-BBB) L-DOPA degradation –> increase L-DOPA entering CNS –> increase central L-DOPA available for conversion to dopamine

54
Q

agents that prevent peripheral (pre-BBB) L-DOPA degradation

A
  1. carbidopa
  2. entacapone (peripheral COMT)
  3. tolcapone (central and peripheral COMT)
55
Q

selegiline - clinical use

A

adjunctive agen to L-dopa in treatment of Parkinson

56
Q

selegiline - mechanism of action

A

blocks conversion of dopamine into DOPAC by selectively inhibiting MAO-B

57
Q

L-dopa to dopamine - enzyme?

A

DOPA decarboxylase

58
Q

L-dopa - toxicity

A
  1. arrhythmias from increased peripheral formation of catecholamines
  2. Long term use can lead to dyskenesia following administration (on-off phenomeno), akinesia between doses
59
Q

Parkinson disease drug - curb excess cholinergic activity - drugs and action

A

Benzotropine (antimuscarinic) –> improves tremor and rigidity but has little effect on bradykinesia

60
Q

all Parkinson drugs and mechanism of action (shortly)

A
  1. Bromocriptine (dopamine agonist)
  2. Pramipexole (dopamine agonist)
  3. ropinirole (dopamine agonist)
  4. amantadine (incr dopamine release and inh reuptake)
  5. Levodopa (increases dopamine levels in CNS)
  6. carbidopa (DOPA decarboxylase inhibitor)
  7. entacapone(peripheral COMT inhibitor)
  8. tolcapone (central and peripheral COMT inhibitor)
  9. selegiline (MAO-B inhibitor) (and rasagilini)
  10. benzotropine (antimuscarinic)

neurology FA + STEP 2 (8 decks)

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