Neurovascular Disease Flashcards

(57 cards)

1
Q

arteriovenous malformation

A

complex tangle of abnormal arteries and veins connected together with fistulas creating a shunt that connects them directly - bypassing the normal capillary network

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2
Q

are AVM congenital?

A

some are, can occur later in life

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3
Q

do AVM cause any problems as they are?

A

they tend to be silent until there is a big problem, can cause a progressive neurological deficit as they steal the blood flow to tissue

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4
Q

what acute problems can AVM cause

A

haemorrhage (1), seizure (2), headache

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5
Q

AVM occuring in which areas of the brain are more likely to caue focla and general seizures

A

frontal lobe - generalised

temporal lobe - focal

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6
Q

investigation of AVM

A

catheter angiography - navigated under x ray guidance

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7
Q

investigation of AVM in acute setting

A

CT angiography is faster than catheter so may be used

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8
Q

what procedure may be performed pre surgery on AVM

A

embolization - decrease blood flow through AVM allowing surgery to take place in a more blood less and controlled way

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9
Q

surgical options for AVM

A
  • open craniotomy
  • stereotactic radiosurgery
  • endovascular coiling
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10
Q

which blood vessels cause SAH

A

circle of Willis (90%), also vertebro basilar circulation

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11
Q

which areas of the blood vessels are high risk sites for damage (SAH)

A

bifurcation

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12
Q

2y damage caused by SAH

A

damage surrounding parenchyma due to haemorrhage, infarcts due to disruption of blood supply

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13
Q

most common place for berry aneurysm

A

bifurcation of anterior cerebral and communicating artery

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14
Q

what are fusiform aneurysms associated with

A

diffuse atheromatous degeneration of arterial wall assoicated with hypertension

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15
Q

are females or males more at risk of aneurysm rupture

A

females

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16
Q

are aneurysms in the posterior or the anterior circulation more likely to rupture

A

posterior

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17
Q

risk factors for aneurysms (and rupture)

A

bigger aneurysm, comorbidities (hypertension, smoking, alcohol), bleeding disorder

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18
Q

name 2 drugs that increase blood pressure

A

cocaine, methamphetamine - inc risk of aneurysm rupture

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19
Q

which connective tissue disease is assoicated with aneurysms

A

ehlers danlos - assoicated with very fragile blood vessels

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20
Q

fibromuscular dysplasia

A

abnormal development of arteries leads to narrowing in some places - this creates a string of beads appearance

found in renal, cerebral and carotid arteries. are prone to haemorrhage, aneurysm etc

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21
Q

what problems can aneurysms cause as they are - think compression

A

can compress specific CN

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22
Q

which CN is at risk of compression from a posterior communicating aneurysm

A

CN III

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23
Q

what is at risk of compresion from an ACOM aneurysms

24
Q

presentation of SAH

A
  • thunderclap headache - sudden onset, vvv severe, occipital typically
  • n and v, collapse, seizures, coma, drowsiness (may persist for days)
25
what symptoms arise in SAH due to irritation of the meninges from blood
meningitis - neck stiffness, photophobia, fever, Kernigs sign
26
what is teh diagnostic test for SAH
CT
27
SAH: what investigation do you perform if CT is normal, when would you do it and what findings would you expect
lumbar puncture - wait at least 12 hours from start of headache to allow time for blood cells to lyse and xanthochromia to develop CSF has blood in it (circulates in subarachnoid space), blood turns yellow due to breakdown and bilirubin release - xanthochromia
28
management of SAH
* endovascular coiling - block blodo flow into aneurysms by inducing clotting of the aneurysm * craniotomy and microsurgical clipping - wide necked aneurysm
29
most common cause of death after SAH treatment
re bleeding - 20% occur in the first few days
30
who is at the biggest risk of rebleeding after SAH
elderly and hypertensives
31
managmenet of SAH re bleeding
surgical clipping or coiling again
32
what problems can vasospasm cause after SAH
* blood products can irritate arterial walls and cause spasm * this can cause ischaemia --\> focal neurological deficit/altered state of consciousness
33
how long after SAH does vaosospasm occur
3-10 days
34
how to confirm diagnosis of vasospasm?
angiogram
35
management of vasospasm
nimodipine - a Ca channel blocker than relaxes narrowed blood vessels
36
SAH leading to hydrocephalus?
communicating - arachnoid granulations are blocked by blood
37
seizures after SAH?
yes
38
what is the most common electrolyte disorder after SAH
hyponatraemia - either through SIADH or CSWS
39
SAIDH
the hypothalamus is stimulated by trauma/ischaemia adn there is excessive release of ADH - increased water reabsorption by the kidneys - this results in fluid retention and dilutional hyponatraemia
40
CSWS
for some reason in reponse to brain injury or trauma the kidneys excrete too much Na - fluid follows
41
do SIADH and CSWS create a hypo/eu volaemia hyponatraemia
SIADH - euvolaemia hyponatraemia CSWS - hypovol hyponat
42
does hyponatraemia indicate poor outcome?
it may, hyponatraemia can cause a shift in water from the EC to the IC space - worsen cerebral oedema and intracranial hypertension - inc risk of seizures and neurological injury
43
management of hyponatraemia after SAH
**avoid fluid restriction** (normally part of SIADH management) supplement Na intake fludrocortisone - aldosterone replacement (increase Na absoprtion)
44
where does the blood accumulate in extradural haematoma
between blood and dura
45
what is the most common cause of an epidural haematoma
pterion fracture - injures middle meningeal artery which runs over the inner aspect of it
46
what is the classical history of an epidural haematoma
young adult sustains closed head trauma - lucid interval (brief loss of consciousness, regain consciousness), then deteriorating state 3-4 hours later as blood accumulates
47
how quickly is the decline in epidural haematoma, and why
froma high pressure arterial source, so rapid
48
how does an epidural haematoma appear on ct
biconvex shape - midline shift due to pressure it does not cross teh suture lines as the dura adheres tightly here to the skull
49
where does the blood collect in a subdural haematoma and from which vessels
between the dura and arachnoid layer. the cerebral veins drain blood from the brain out to the dural venous sinuses (located between the 2 layers of dura)
50
why are teh elderly more prone to subdural haematima
as you get older, the brain atrophies - the bridging veins are stretched and so are more likely to rupture even with minor trauma can present acute or be chrnoic
51
what other things cause brain atrophy
epilepsy, dementia, chronic alcoholism
52
how does a subdural haematoma present in an acute situation
decreased state of consciousness, confusion
53
how does a chronic subdural haematoma present
insidiously, progressive headache and confusion
54
if there is a subdural haematoma and it is non fatal, so not treated, what does the blood form on the surface of the brain?
a yellow neo-membrane
55
subdural haematoma ct
some of the blood may be hypodense (black) if it is chronic may see acute on chronic
56
what is coup and countercoup, and which often causes the most severe injuries?
coup = damage at point of impact countercoup = damage occuring when brain rebounds and hits back of skull countercoup
57