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patho II > Neuro I (b) > Flashcards

Neuro I (b) Flashcards

1
Q

HTN in the brain leads to?

A

1) Hyaline arterioscelrosis
2) Charcot-Bouchard Micro-Aneurysm
3) Lacunar Infarcts
4) Rupture of the small-caliber penetrating vessels
5) Acute Hypertensive Encephalopathy

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2
Q

loc of Hyaline Arteriosclerosis

A

basal ganglia and brain stem

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3
Q

———-: Small cavitary infarcts in basal ganglia, thalamus, internal capsule, pons, etc which is a result in Occlusion of a penetrating artery

A

Lacunar infarcts

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4
Q

CF of Acute Hypertensive Encephalopathy

A

Sudden, sustained increase in diastolic blood pressure (>130mm Hg) –> Increased intracranial pressure –> Headaches, confusion, vomiting, convulsions

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5
Q

DD of Acute Hypertensive Encephalopathy

A

Stroke

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6
Q

Rupture of the small-caliber penetrating vessels suplying deep structures if the brain will result in?

A

Slit haemorrhage (slit-like cavity)

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7
Q

———: Infectious arteritis of small and large vessels

A

Vasculitis

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8
Q

cause of Vasculitis

A

Opportunistic infections in immunocompromised individuals

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9
Q

Vasculitis

In systemic forms of Vasculitis there is Involvement of ———— (e.g. polyarteritis nodosa) –> ————

A

In systemic forms of Vasculitis there is Involvement of cerebral vessles (e.g. polyarteritis nodosa) –> -Multiple infarcts

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10
Q

————: Form of vasculitis, affecting small- to medium-sized parenchymal and subarachnoid vessels

A

Primary Angiitis of the CNS

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11
Q

Microscopic Findings:
* Chronic inflammatory cell infiltrates
* Multinucleate giant cells (+/- granuloma formation)
* Destruction of vessel walls
* Amyloid-β deposits
* Lumen Oblitertion

features of?

A

Primary Angiitis of the CNS

* Form fo Vasculitis

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12
Q

———: Rapid tissue displacement –>Damage of vessels -> Haemorrhage, tissue injury and oedema

A

Contusion

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13
Q

Contusion Will cause?

A

haemorrhage, tissue damage and oedema in the brain

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14
Q

Loc of a Contusion

A

1) Orbito-frontal regions
2) Temporal lobe tips

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15
Q

the 2 types of Contusion

A

Coup and Contre-Coup injuries

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16
Q

Macroscopic Features:
* Cross-section: Wedge-shaped
* Old lesions: Depressed, yellowish-brown patches (Crests of gyri)

Microscopic Findings:
* Involvement of superficial layer
* Neuronal cell body injury (nuclear pyknosis and cytoplasmic eosinophilia) within 24 hours
* Inflammatory response: Initially neutrophils and later also macrophages
* Old lesions: Gliosis and haemo-siderophages

features of?

A

Contusion

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17
Q

Contusion

Macroscopic Features:
* Cross-section: ———– -shaped
* Old lesions: Depressed, ————– patches (Crests of gyri)

Microscopic Findings:
* Involvement of superficial layer
* Neuronal cell body injury (————- and cytoplasmic eosinophilia) within 24 hours
* —————: Initially neutrophils and later also macrophages
* Old lesions: Gliosis and —————-

A

Macroscopic Features:
* Cross-section: Wedge-shaped
* Old lesions: Depressed, yellowish-brown patches (Crests of gyri)

Microscopic Findings:
* Involvement of superficial layer
* Neuronal cell body injury (nuclear pyknosis and cytoplasmic eosinophilia) within 24 hours
* Inflammatory response: Initially neutrophils and later also macrophages
* Old lesions: Gliosis and haemo-siderophages

* pyknosis: nuclear shrinking

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18
Q

cause/ patho of Diffuse Axonal injury

A

Angular acceleration –> Axonal injury and haemorrhage

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19
Q

location of Diffuse Axonal injury (DAI)

A
  • Near the angles of the lateral ventricles
  • Corpus callosum
  • Brain-Stem
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20
Q

Microscopic Findings:
* Axonal swellings (“bulbs”), within hours of the injury
* Axonal Spheroids
* Immuno-histochemistry : β-APP

features of?

A

Diffuse Axonal injury

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21
Q

Diffuse Axonal injury

Microscopic Findings:
* Axonal swellings (“——-”), within hours of the injury
* Axonal ——-
* Immuno-histochemistry : ——-

A

Microscopic Findings:
* Axonal swellings (“bulbs”), within hours of the injury
* Axonal Spheroids
* Immuno-histochemistry : β-APP

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22
Q

Histochemical stain for diffuse Axonal Injury ?

A

Silver stain
(detects axonal swelling)

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23
Q

Immuno-Histochemistry findings in Diffuse Axonal Injury

A

Amyloid Precussor ProteinAPP

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24
Q

————– :Penetration of the brain by a projectile (e.g. bullet, bone fragment of the skull –> Tissue tearing, vascular disruption and haemorrhage

A

Laceration

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25
Q

——–: Reversible altered consciousness from head injury in the absence of contusion

A

Concussion

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26
Q

CM of Concussions

A
  • Loss of consciousness
  • Temporary respiratory arrest (Due to sever perssure ont the brain stem)
  • Loss of reflexes
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27
Q

CNS trauma –> Disruption of the vessel wall -> ———–

A

Haemorrhage

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28
Q

The 4 types of Haemorrahge

A

1) Epidural
2) Subdural
3) Subarachnoid
4) Intra-parenchymal

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29
Q

Cause of Epidural Haematoma

A

Traumatic injury of the middle meningeal artery, after a skull fracture

30
Q

CM of Epidural Haematoma

A

Neurosurgical emergency; If left untreated –> Death

31
Q

causes of Subdural Haematoma

A

Tear of the bridging veins, after trauma

32
Q

Cause of Subdural Haematoma in Elderly?

A

Elderly individuals with brain atrophy, due to stretching of the bridging veins

33
Q

patho of Subdural Haematoma

A

Vein disruption (tear of bridging veins) –> Bleeding into the subdural space

34
Q

location of Subdural Haematoma

A

lateral aspects of the cerebral hemispheres

35
Q

CM of Subdural Haematoma

A

Within 48 hrs after injury:
* Headache
* Confusion
* Slowly progressive neurologic deterioration

36
Q

Macroscopic Features:
* Collection of freshly clotted blood, over the brain convexity
* Flattening of the underlying brain
* Ruprture of Bridging veins
* star-like invasion of Collagen fibers
* Immuno-histo: Combined leukocyes-macrophage rxn, Siderophages

features of ?

A

Subdural Haematoma

37
Q

?? not sure if we need to know this

stain for Siderophages

A

Prussian-blue reaction

38
Q

?? not sure if we need know this

Stain used for Erythrophagocytosis

A

Azan

39
Q

Progression of Subdural Haematoma

  • ——— of the clot (~1 week)
  • Development of ————– from dura (2 weeks)
  • ——– (1-3 months)
  • ———- of the fibrosing lesion -> Thin layer of connective tissue (————”)
  • Commonly, ————– (chronic subdural haematoma)
A
  • Lysis of the clot (~1 week)
  • Development of Granulation tissue from dura (2 weeks)
  • Fibrosis (1-3 months)
  • Retraction of the fibrosing lesion -> Thin layer of connective tissue (“Subdural membrane”)
  • Commonly, re-bleeding (chronic subdural haematoma)
40
Q

Most frequent type of CNS malformation?

A

Neural tube malformations

41
Q

Risk factors of Neural tube defects

A

Folate deficiency during the initial weeks of gestation

42
Q

Defects in the posterior end of the Neural Tube will result in

A

1) Spina Bifida Occulta
2) Meningocele and
3) Myelo-Meningocele

43
Q

Defects in the anterior end of the Neural Tube

A

1) Anencephaly: Absence of the brain and the top of skull
2) Encephalocele

44
Q

————: Abnormally large brain volume

A

Megaloencephaly

45
Q

———: Abnormally small brain volume, which occurs together with a small head

A

Micro(en)cephaly

46
Q

Risk factors of Microencephaly

A

Fetal alcohol syndrome, HIV infection
(acquired in utero), Zika virus

47
Q

patho of Microencephaly

A

Decreased generation of neurons that will populate the cerebral cortex

48
Q

Which condition is known as “Smooth brain” ?

A

Lissencephaly

49
Q

patho of Lissencephaly

A

Total absence of gyration or pachygyria (patchy involvement) –> “Smooth brain”

50
Q

Macroscopic features:
* Complete absence of Gyration –> “Smooth brain”
* Abnormally thickened cortex
* Four cortical layers

Microscopic features:
* Mylein sheath
* reactive astrocytes around vessles
* reticullar pattern of the deep cortical layer

features of?

A

Lissencephaly

51
Q

Patho of Polymicrogyria

A

Numerous irregularly formed gyri –> Cobblestone-like surface

52
Q

Macroscopic features:
* Numerous irregulary formed gyri –> Cobbelstone - like surface
* Many gyri

Microscopic features:
* A festooned cortex w/ fusion of Gyri

features of?

A

Polymicrogyria

53
Q

pathophysio of Holoprosencephaly

A

Absence of the olfactory bulbs
(Arrhinencephaly)

54
Q

Absence of the olfactory bulb is known as ?

A

Arrhinencephaly

* Mild form of Holoprosencephaly

55
Q

Mild form of Holoprosencephaly?

A

Arrhinencephaly - Absence of The Olfactory bulbs

56
Q

sever forms of Holoprosecncephaly are associated w?

A

facial midline defects (e.g. cyclopia)

57
Q

Macroscopic features:
* Fused cerebral hemispheres and thalamus
* Absent sulci
* Absence of Olfactory nerve

features of?

A

Alobar Holoprosencephaly

58
Q

Posterior Fossa Anomalies

A

1) Chiari Type I malformation
2) Arnold-Chiari (Chiari Type II) Malformation
3) Dandy-Walker Malformation

59
Q

CM of Chiari Type I Malformation

A

partial Obstruction of the CSF flow and compression of the medulla –> Sever headaches or Cranial nerver deficits

* manifested in adulthood

60
Q

Macroscopic features:
* Low-lying cerebellar tonsils, extending through the
foramen magnum
* Protrusion of the tonsils into the foramen magnum

features of?

A

Chiari Type I malformation

61
Q

Arnold-Chiari (Type II) Malformation Coexists w?

A

hydrocephalus and lumbar myelo-meningocele

62
Q

Macroscopic features:
* Small posterior fossa
* Misshaped midline cerebellum
* Protrusion of tonsil and vermis below the foramen magnum
* Hydrocephalus
* Narrowing of the 4th Ventricle
* Elongation of the brain stem and Vermis

features of?

A

Arnold-Chiari Malformation

63
Q

Macroscopic features:
* Enlarged posterior fossa
* Absence of the cerebellar vermis
* Large midline cyst
* Cystic dilatation of the 4th Ventricle

Microscopic features:
* Agenesis of the cerebellar Vermis
* Microgyri in the cerebral cortex

features of?

A

Dandy-Walker Malformation

64
Q

Spinal cord Abnormalities examples

A

1) Hydromyelia
2) Syringomyelia

65
Q

Hydromyelia are associated w?

A

hydrocephalus or Chiary malformation
type II and Dandy-Walker syndrome

66
Q

Pathophysio of Hydromyelia
Abnormal ————— of the central canal of the ——– –> Cavity connected to the 4th ventricle, with possible build up of ———-–> pressure on the spinal cord–> ————- of nerve cells and their connections

A

Abnormal widening of the central canal of the spinal cord –> Cavity connected to the 4th ventricle, with possible build up of CSF–> pressure on the spinal cord–> Damage of nerve cells and their connections

67
Q

Syingomyelia commonly coexists w?

A

Chiari malformation type I or have
experienced spinal cord trauma

68
Q

Cerebral palsy is a non-progressive neurological motor deficit, characterized by?

A

1) Ataxia or Athetosis
2) Spasticity
3) Dystonia
4) Paresis (muscle weakness)

69
Q

Types of Brain Injuries in the Perinatal Period

A

1) Haemorrhages (Eventually causes Hydrocephalus)
2) Infarcts

70
Q
A

patho II (29 decks)

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