NEUROLOGY Flashcards

1
Q

subarachnoid haemorrhage
type of hydrocephalus

A

communicating
(CSF cant be absorbed via arachnoid granulations)

subarachnoid space widening
usually inflammatory or trauma cause

blood is inflammatory if leaked i.e. leaking aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

causes of communicating hydrocephalus

A

subarachnoid haemorrhage
post-meningitis
scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

causes of non-communicating hydrocephalus

A

Dnay Walker
Arnold Chiari II
Medulloblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

chorioretinitis,
hydrocephalus
intracranial calcifications
+/− “blueberry muffin” rash

A

toxoplasma gondii

mother asymptomatic or lymphaenopathy

cat faeces or undercooked meat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

in regionalisation of the neural tube, where does basal ganglia develop from (___cephalon)

A

prosencephalon –> telencephalon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

in regionalisation of the neural tube, where does the retina develop from

A

prosencephalon –> diencephalon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are derived from neural crest cells

A

Melanocytes
Odontoblasts
Tracheal cartilage
Enterochromaffin cells
Laryngeal cartilage
Parafollicular (C) cells of the thyroid
Adrenal medulla & autonomic ganglia
Schwann cells
Spiral (aorticopulmonary) septum

MOTEL PASS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what mutation is holoprosencephaly associated with

A

SHH
(sonic hedgehog)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SHH is crucial for

A

embryonic patterning
(brain and limbs)

Holoprosencephaly (failure of forebrain division)
Midline defects (cleft lip/palate, cyclopia)
Polydactyly (abnormal limb patterning)
CNS malformations (affecting dorsal-ventral axis formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are Chiari I and II each associated with

A

I = syringomyelia
II = myleomeningocele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what actions do these tongue muscle do
styloglossus
genioglossus

And what innervates them

A

stylo = draws sides upward
genio = protudes

XII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is present in cell bodies and dendrites but not axons that stains on Nissl staining

A

RER
(not present in axon)
stained by Nissl stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are (2) neuron cell markers

A

neurofilament protein
synaptophysin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

neuro cell derived from mesoderm
not dissernible on nissl stain

A

microglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

neuro cell positive for GFAP+

A

astrocyte

glial fibrillary acidic protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

neuro cell with marker S100
injured in Guillian Barre

A

Schwann cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

round cellular swelling
displacement nucleus to periphery
dispersion nissl substance in cytoplasm

A

chromatolysis

reaction of neuronal cell body (soma) to axonal injury

increased protein sysnthesis aimed to repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

disintegration of axon/myelin sheath distal to site of axonal injury.

A

wallerian degeneration

macrophages remove debris

proximal to injury - axon retracts and sprouts new protrusions

20
Q

injury to middle meningial artery often bleeds into what space

A

epidural space

21
Q

lucid interval, rapid deterioration

A

epidural haematoma

haematoma expansion

22
Q

injury to bridging veins

A

subdural

shaking baby
midline shift
crosses suture lines

23
Q

conductive aphasia caused by damage to

A

arcuate fasciculus

repetition

24
Q

saccular aneurysms assocaited with

A

ADPKD
elher danlos

common site ACA, AComm

25
Q

gait instability
cognitive disturbance
urinary incontinence

A

normal pressure hydrocephalus “wet, wacky, and wobbly”

develops faster than vascvular dementia
reversible

mood changes, amnesia, aphasia

26
Q

seen in

A

Alzheimers disease
neurofibrillary tangle

hyperphosphorylates tau protein

27
Q

area of brain critial for memory formation

A

hippocampus

medial temporal lobe
affected in Alzhiemers diease

28
Q

AD
early-onset alzhiemers overproduction of b-amyloid
amyloid plaques

mutation causing

A

presenilin 1

29
Q

Alzhiemers characterised by loss of -? neurons

A

cholinergic

decreased Ach

30
Q

prosopagnosia can occur due to

artery

A

PCA stroke

‘face blindness’

31
Q

familial (early-onset) alzhiemers associated with

genes

A

Presenilin 1 (PSEN1) Ch 14
Presenilin 2 (PSEN2) Ch 1
Amyloid precursor protein (APP) Ch 21

increased Aβ (beta-amyloid) deposition, amyloid plaque formation

32
Q

late onset alzhiemers is associated with

gene

A

APOE (apolipoprotein E) Ch19

33
Q

Damage to the DRG disrupts -? that rely on -? input

A

reflex arcs
sensory

would see hyporeflexia
DTR diminished

34
Q

dorsal root gangion carries

A

afferent sensory info
periphery to SC

affects reflex arc

34
Q

MDD
SSRI
Na 122mEq/L

what might be seen in this patient

A

SAIDH
(adverse effect of SSRI)

hyponatremia - dilutional effect of ADH (H20 retained)

35
Q

older patient
acute confusional state
memory or language deficit
fluctuating consciousness, lethargy
disorientation, hallucinations
perceptual awareness, cognition changes

A

delirium

deficient Ach signalling suggested

causes: infection, medications, withdrawal, or electrolyte imbalances* i.e. SIADH from SSRI*

36
Q

dementia + hallucinations

A

lewy body dementia

37
Q

dementia + personality changes

A

pick disease
(frontotemporal dementia)

50yo

38
Q

huntingtons disease demonstrates what characteristic

A

anticipation

each future generation is affected at a younger age & more severely

AD
One copy of the mutated gene is sufficient to cause the disease
CAG repeats

39
Q

localised motor or sensory symptoms
oral/manual automatisms - lip smacking, picking
auras
altered consciousness
postictal confusion

rhythmic slowing on EEG

A

complex partial seizure
(focal onset impaired awareness)

40
Q

Blank stare
3Hz spike EEG
no postictal confusion

rapid blinking, mouth twitching

A

absense seizure

often children

41
Q

motor or sensory symptoms
no impaired consciousness
no postictal confusion

A

simple partial sensory seizure

numbness, paraesthesias, pain (sensory)

42
Q

label A, C, E

A

right inferior cerebellar peduncle (vestibular)
right medial lemnisci (sensation)
right medullary pyrimidal tract (motor)

43
Q

identify the vessel

A

PCA

will see: contralateral visual field defecf

contralateral homonymous hemianopsia with macular sparing

originates rostral end, near basilar artery

44
Q

what would an anesthesiologist change to increase intracranial pressure?

A

decreasing RR

decrease RR or TV = increased CO2 = increase PaCO2 = increase CBF + ICP

autoregulation between 10-160mmHg
CBF increases with:
increased metabolic demand
hypercarbia (biggest effect)
hypoxemia
hyperthermia
increased central venous pressure (CVP)

CO2 combines with H2O to form carbonic acid –> disolves to H+ and HCO3 –> pH decreased (H+) –> causes vasodilation in arteries/arterioles brain –> increases blood flow to flush out co2, deliver O2

45
Q

loss of pain & temperature on Left LL. Where in SC is injured

A

(D)

right spinothalamic tract

will see symptoms 2-3 levels below SC decussation (Lasseurs tract).

see s/s CONTRALATERLAL
CST and DC will see ipsilateral