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patho II > Neuro I(a) > Flashcards

Neuro I(a) Flashcards

1
Q

———–: Accumulation of excess fluid within the brain parenchyma

A

Cerebral odema

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2
Q

what are the 2 types of cerebral odema

A

1) Vasogenic oedema
2) Cytotoxic oedema

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3
Q

Patho of Cytotoxic Oedema

A

Intracelluar fluid accumulation due to Neuronal and glial cell membrane injury caused by hypoxic-ischaemia

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4
Q

Patho of Vasogenic Oedema

A

Extracellular fluid accumulation due to disruption of BBB (caused by isheamia, heamorrahge)

*() extra info

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5
Q

Macroscopic Features:

  • Flattening of the gyri and narrowing of the intervening sulci
  • Compression of the ventricular cavities

features of?

A

Cerebral Oedema

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6
Q

———- : Accumulation of excessive CSF within the ventricular system

A

Hydrocephalus

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7
Q

Causes/patho of Hydrocephalus

A

Choroid plexus tumours –> Overproduction of CSF –> Hydrocephalus (rarely)

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8
Q

Causes of Non-communicating Hydrocephalus

* Obstruction

A

Masses localised to the foramen of Monro or cerebral aqueduct –> Non-communicating Hydrocephalus
(patrial enlargement of the ventricular system)

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9
Q

Causes of Communicating Hydrocephalus

* No obstruction

A

Reduced CSF resorption (by arachnoid granulations) –> Communicating Hydrocephalus
(enlargement of the entire ventricular system)

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10
Q

CM of Hydrocephalus

A

1) Head enlargement, before suture closure
2) Ventricular dilatation and ↑ ICP, after suture fusion

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11
Q

What are the 3 types of Herniation syndromes

A

1) Subfalcine (Cingulate) herniation under Falx cerebri
2) Uncal Transtentorial herniation <>Tentorium cerebelli
3) Cerbellar tonsillar herniation into the Foramen magnum

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12
Q

Compliactions of Herniation in the brain

A

Vascular compromise of the compressed tissue –> Infarction -> Additional swelling –> Further Herniation

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13
Q

————-: Increase of the volume of tissue and fluid inside the skull beyond the limit –> Rise of intracranial pressure

A

Herniation

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14
Q

What are the 3 sites of brain herniation?

A

1) Falx cerebri –> (Subfalcine (Cingulate) herniation)
2) tentorium cerebelli -> (transtentorial [Uncinate] hernia)
3) Foramen magnum –> Tonsillar hernia)

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15
Q

Compression of which artery is caused by Subfalcine (Cingulate) Herniation ?

A

anterior cerebral artery

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16
Q

microscopic features:
- Cortical spongious alteration
- Peri-neuronal/ Peri-vascualar swelling of astrocytic processes

features of?

A

Cytotoxic Cerebal Oedema

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17
Q

Compression ————- nerve in a Transitional (Ucinate) Hernitation –> Pupilary dilatation

A

Third cranial nerve

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18
Q

In a Transtenotorial (Uncinate) Herniation , the compression of ———– –> Kernohan’s notch

A

Contralateral cerebral peduncle against the tentorium

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19
Q

In a Transtentorial (Uncinate) Herniation, the compression of ———– -> Ischaemic injury of the primary visual cortex

A

Posterior cerebral artery

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20
Q

What part of the brain is affected during a transtentorial herniation

A

medial temporal lobe , against the free margin of the tentorium

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21
Q

In a Transtentorial (Uncinate) Herniation , Tearing of penetrating veins and arteries will result in the Development of ————– (in the midbrain and pons)

A

Duret haemorrhages

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22
Q

Patho/ Complications of A Tonsillar Herniation

A

Displacement of the cerebellar tonsils through the foramen magnum –> Brain stem compression –> Life threatening condition, (due to serious damage of vital respiratory and cardiac centers in the medulla oblongata)

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23
Q

The 2 mechanisms that deprive O2 from the brain

A

1) Functional Hypoxia
2) Ischaemia due to tissue Hypoperfusion

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24
Q

Causes of Functional Hypoxia

A
  • Partial pressure of oxygen (e.g. high altitude)
  • Impaired oxygen-carrying capacity (e.g. Sever anaemia)
  • Inhibition of oxygen use by tissue (e.g. Cyanide poisonig
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25
Q

causes of Ischaemia due to tissue hypoperfusion

A

i. Hypotension, ii. Vascular obstruction iii. Both

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26
Q

the 2 froms of Ischaemia due to tissue hypoperfusion

A

1) Transient
2) Permanent

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27
Q

cause of Global Cerebral Ischaemia

A

Severe systemic hypotension (as in cardiac arrest or shock)

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28
Q

Macroscopic Features of Global Cerebral Ischaemia:
* ————-, with ————— and narrowed sulci
* Poor demarcation between gray and white matter

A

Swollen brain, with widened gyri and narrowed sulci

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29
Q

What neuronal cells are affected by Global cerebral Ischaemia

A
  • Pyramidal cells of hippocampus and neocortex
  • Purkinje cells of the cerebellum
30
Q

Which type of Global Cerberal Ischaemia is this?

Macroscopic features:
i. swollen brain and widened Gyri w/ narrowed sulci

Microscopic features:
i. Cytoplasmic eosinophilia,
ii. Nuclear pyknosis and karyorrhexis,
iii. Neutrophil infiltrates

* Pyknosis –> Karyorrehxis are death steps of the cell nucleus

A

Cerebral infarction (Early changes 12-24 hrs)

31
Q

Which type of Global Cerberal Ischaemia is this?

Macroscopic features:
i. swollen brain and widened Gyri w/ narrowed sulci

Microscopic features:
i. Tissue necrosis,
ii. Macrophages,
ii. vascular proliferation,
iv. Reactive gliosis
v.Reactive astrocytes

A

Cerebral infarction (Subacute changes 24 hrs-2 wks)

32
Q

Which type of Global Cerberal Ischaemia is this?

Macroscopic features:
i. swollen brain and widened Gyri w/ narrowed sulci

Microscopic features:
i. Removal of necrotic tissue,
ii. Gliosis

A

Cereral changes (Repair >2wks)

33
Q

Immunohistochemistry used to stain Astrocytes

A

GFAP

34
Q

Marker used for microglia staining

* microglia –> macrophages of the brain

A

CD68

* stains macropahges

35
Q

cause of “Watershed infarcts”

A

Hypotensive episodes
(Anaphylactic shock, sudden blood loss, sever infections)

36
Q

location of “Watershed infarcts”

A

The border-zone between the anterior and middle cerebral artery distributions

37
Q

CF of “watershed” infarcts

A

1) Transient post-ischaemic confusional state –> Complete recovery (mild insult)
2) Sever global cerebral ischaemia–> Widespread neuronal death; Severely neurologically impaired and in a persistent vegetetative state

38
Q

Which is more common an Embolic infarction or thrombotic infarction?

A

Embolic Infarction

39
Q

Most common site of embolic infarction

A

Middle Cerebral Artery (MCA)

40
Q

Sources of emboli in an Embolic Infarction

A
  • Cardiac mural thrombi (Predisposing factor: Atrial fibrillation)
  • Thrombo-emboli from atheromatous plaques
  • Emboli of venous origin + Cardiac defect -> Paradoxical embolism
41
Q

Thrombotic occlusion result to –>

A

Cerberal infactions

42
Q

Patho of Thrombotic occlusions

A

Development of thrombosis on pre-existing atheromatous plaques

43
Q

locations of thrombotic occlusions

A

Carotid bifurcation (,origin of middle cerebral artery)

*carotid bifurcation is the point where the common carotid artery divides into internal and external carotid arteries

44
Q

The 2 types of infarcts

A

1) Non-haemorrhagic (Result of acute vascular occlusions)
2) Haemorrhagic (Result of reperfusion of ischaemic tissue, either through collaterals or dissolution of emboli)

*reperfusion->restortion of blood flow to a tissue that has been blocked

45
Q

Micro features of ?

A

Haemorrhaging infarct

46
Q

Causes of an Intracranial Haemorrhage

A

1) Hypertension
2) Structural lesions (e.g. arteriovenous and cavernous malformations)
3) Traumas
4) Tumours

47
Q

Epi of primary brain parenchymal haemorrhage

A

Peak incidence: ~60 years of age

48
Q

cause of Primary brain parenchymal Haemorrhage

A

Rupture of a small intra-parenchymal vessel, due to chronic hypertension

49
Q

locations of Primary brain parenchymal Haemorrhage

A
  • Basal ganglia
  • Thalamus
  • Pons
  • Cerebellum
50
Q

Clinical manifestions of
Primary brain parenchymal Haemorrhage

A

Depending on the location and size of the haemorrhage

51
Q

Macroscopic Features:
Blood extravasation -> Compression of the neighbouring brain parenchyma –> Cavity formation with brown discoloured rim

Microscopic Findings -Early findings:
* Extra-vasated, clotted blood
* Anoxic neural changes of the adjacent neuropil
* Oedema of the brain parenchyma, around the haemorrhagic focus

features of?

* Anoxic: complete loss of O2 supply

A

Primary brain Parenchymal Haemorrhage (Early findings)

52
Q

Late Microscopic findings of Primary brain parenchymal haemorrhage:
* Pigment and ——————–
* ——————— at the periphery of the lesion

A
  • Pigment and lipid-laden macrophages
  • Reactive astrogliosis at the periphery of the lesion
53
Q

cause/ patho of Cerebral Amyloid Angiopathy

A

Deposition of amyloidogenic peptides in the walls of small- and medium-sized meningeal and cortical vessels

54
Q

location of Cerebral Amyloid Angiopathy

A

Lobes of the cerebral cortex

55
Q

Histochemical stain for Beta Amyloid (in Cerebral Amyloid Angiopathy)

A

Apple-green birefringence on Congo-red

56
Q

stain used for Haemosiderin (in Cerebral Amyloid Angiopathy)

A

Pearl’s/Prassin blue iron staining

57
Q

Pathologocial identifcation of cerebral Amyloid Angiopathy

A

1) Aβ immuno stain/ Congo red stain for Beta Amyloid
2) Pearl’s blue iron stain for Haemosiderin

58
Q

causes of Subarrachnoid haemorrahge & Saccular aneurysms

A
  • Rupture of a berry aneurysm (most common)
  • Vascular malformation
  • Trauma
  • Rupture of an intra-cerebral haemorrhage into the ventricular system
  • Tumours
59
Q

patho of subarachnoid haemorrhage & Saccular Aneurysms

A

Acute increase in intracranial pressure (1/3 of cases) –> Rupture of a saccular aneurysm –> Accumulation of blood in the sub-arachnoidal space

60
Q

loactions of Subarachnoid haemorrhage & Saccular Aneurysms

A

~90% of Berry aneurysms in the anterior circulation

61
Q

Microscopic Findings:
* Absent muscle wall and intimal elastic lamina (thinning of vessels)
* Presence of a thickened hyalinised intima, and the adventitia

features of?

A

Subarachnoid haemorrhage & saccular aneurysms

62
Q

CF of Subarachnoid haemorrhage & saccular aneurysms

A
  • Sudden, severe headache
  • Rapid loss of consciousness
  • Death (from the first bleed in 25-50% of cases)
  • blood in CSF
  • Postive Kernig & Burdzinski sign
63
Q

Complications of Subarachnoid haemorrhage & Saccular aneurysms

A

Ischaemic injury d/t vasospasm (early period after rupture of an aneurysm)

64
Q

the 4 types of Vascular Malformations

A

1) Arterio-Venous Malformations (AVMs)
2) Cavernous Malformations
3) Capillary Telangiectasias
4) Venous Angiomas

65
Q

Epi of AVMs (Anter-venous mal.)

A

Most common vascular malformation
* M:F = 2:1; Age: 10-30 years

66
Q

CM of AVMs

A
  • Seizures
  • Intracerebral or subarachnoid haemorrhage
67
Q

Macroscopic Features:
* Tangled network of worm-like vascular channels
Microscopic Findings:
* Enlarged blood vessels, separated by gliotic tissue (shown w/ GFAP)
* Presence of haemo-siderophages

features of?

A

AVMs (Arterio-venous malformations)

68
Q

loc of Cavernous Malformations

A

Cerebellum, Pons

69
Q

Microscopic Findings:
* Distended, loosely organised vascular channels (Back to back dilated vesseles- Trichome stain)
* Collagenised walls
* No intervening nervous tissue
* Foci of old haemorrhage, infarction and calcification

features of?

A

Cavernous (Vascular) Malformation

70
Q

Micro:
* Dilated thin-walled vascular channels
* Intervening normal brain parenchyma
* several large, thin-walled vascualr spaces
* “Pencil fibers” = white matter tracts of the basal ganglia

features of?

A

Capillary Telangicetasias

71
Q

Micro:
* Aggregates of ectatic venous channels
* Capillary Hindus resembles the head of medusa

features of?

A

Venous Angiomas (Varcies)

patho II (29 decks)

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