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ACEM Viva > Pathology - CNS & Eye > Flashcards

Pathology - CNS & Eye Flashcards

1
Q

Common locations of saccular aneurysms in the cerebral circulation

A

90% near major arterial branch points, more common at anterior circulation around the Circle of Willis

  • ACA & ACoA 40%
  • MCA & AChoroidalA 34%
  • ICA & PCoA 20%
  • Basilar & PCoA

Multiple in 20-30% cases at autopsy

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2
Q

Risk factors for saccular aneurysm rupture

A
  1. Size: > 10 mm with 50% risk of rupture per year
  2. Acute increase in ICP (straining at stool, orgasm)
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3
Q

Pathological sequelae of SAH

A

Acute - ischaemic injury (stroke) from vasospasm

Late - meningeal fibrosis and scarring, obstruction of CSF flow and absorption

Death

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4
Q

Morphology of berry aneurysm

A

Medial muscular layer thins as approaching the aneurysm’s neck and gets thickened hyalinised intima, covered with normal adventitia

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5
Q

Natural history of a ruptured berry aneurysm

A
  1. Acute onset of headache, ALOC
  2. Initial mortality 25-50%
  3. Rebleeding is common
  4. Vasospasm in vessels other than the bleeding site -> secondary ischaemic injury
  5. During healing, meningeal fibrosis and scarring -> secondary hydrocephalus
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6
Q

Causes of ischaemic cerebral infarction

A

Arterial thrombosis
Cerebral emboli
Lacunar infarcts from small vessels
Cerebral arteritis
Arterial dissection
Venous infarction

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7
Q

Sources of cerebral thromboemboli

A 
Left atrium/ventricle thrombus
Valvular vegetations
Carotid plaque
PFO with paradoxical emboli
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8
Q

Main pathological processes causing ischaemic stroke

A

Thrombus - atherosclerosis

Embolism - AMI with mural thrombus, valvular heart disease, AF, vascular surgery/shower embolism, fat embolism, endocarditis

Vasculitis - infective vasculitis, autoimmune vasculitis, primary angiitis of CNS

Arterial dissection

Venous infarction - venous sinus thrombosis

Drugs - amphetamines, cocaine, heroin

Hypercoagulable state

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9
Q

Distinguishing pathological features of haemorrhagic and non-haemorrhagic stroke?

A

Haemorrhagic (red) - multiple, confluent, petechial haemorrhages associated with emboli, secondary to reperfusion via collaterals or dissolution of materials, greater risk if anticoagulated

Non-haemorrhagic (pale/bland anaemic) - usually associated with thrombosis

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10
Q

Importance of stroke pathology in relation to stroke thrombosys

A
  • Complications higher with embolic/haemorrhagic CVAs
  • In non-haemorrhagic CVA, little macroscopic change can be seen within the first 6 hours
  • Reversible ischaemic penumbra
  • Early treatment leads to better outcome and less haemorrhagic risk
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11
Q

Types of cerebral ischaemic injury

A

Global (e.g. hypoxic encephalopathy) - generalised reduction of cerebral perfusion

Focal - reduction of blood flow to a localised area of the brain

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12
Q

Pathological effects of HTN on brain

A

Lacunar infarcts (lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, pons)

Massive ICH

Hypertensive encephalopathy

Slit haemorrhages

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13
Q

Pathological mechanisms of cerebral oedema

A

Vasogenic - BBB disruption, incr vasc perm, fluid shift from intravascular to intercellular space

Cytotoxic - neuronal/glial/endothelial injury, from hypoxic or ischaemic insults or metabolic damage, leads to cellular swelling and intracellular oedema

Interstitial or ependymal oedema from high pressure hydrocephalus

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14
Q

Morphological findings of generalised cerebral oedema

A
  • Flattened gyri
  • Narrowing of sulci
  • Compression of ventricles and basal cisterns
  • Herniation
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15
Q

Major brain herniation locations

A

Subfalcine - cingulate gyrus under the falx cerebri

Transtentorial - medial aspect of the temporal lobe against the free margin of the tentorium

Tonsillar - cerebellar tonsils through the foramen magnum

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16
Q

Causes of dementia

A
  • Alzheimer
  • FTD
  • Vascular
  • Parkinson
  • Creutzfeld-Jakob
  • Neurosyphilis
  • Toxins (heavy metals, alcohol)
17
Q

Pathogenesis of Alzheimer

A
  • Lysis of transmembrane protein Amyloid Precursor Protein (APP) by beta and gamma secretases produce Aβ and C-terminal portion of APP
  • Aβ peptides aggregate into amyloid fibrils and can be directly neurotoxic
  • C-terminal portion of APP is involved in cell signalling and transcription regulation
  • Severity of AD is related to the loss of synapses
18
Q

Main pathophysiological causes of spontaneous intracerebral haemorrhage

A
  • Hypertension
  • Cerebral amyloid
  • Other: coagulopathy, neoplasm, vasculitis, aneurysm, vascular malformation
19
Q

Areas of brain where hypertensive intracerebral haemorrhages most commonly occur

A
  • Putamen 50-60%
  • Thalamus
  • Pons
  • Cerebellum
20
Q

Pathophysiology of cerebral amyloid angiopathy

A
  • Deposition of amyloidogenic peptides in the walls of medium and small calibre meningeal and cortical vessels
  • Results in weakening of the vessel wall and risk of haemorrhage
21
Q

Types of intracranial bleeding in head injury

A

Extradural
Subdural
Subarachnoid and intraventricular
Intra-parenchymal

22
Q

Sequence of events in extradural haemorrhage

A
  • Dural artery tear (middle meningeal), usually associated with skull fracture
  • Strips off the dura from the skull
  • May be a lucid period before ALOC
23
Q

Define concussion and clinical features

A

Altered consciousness secondary to a head injury, with
- transient neurological dysfunction
- transient respiratory arrest
- transient loss of reflexes

Features: headache, amnesia, n & v, concentration and memory impairment, perseveration, irritability, behaviour/personality change, dexterity loss, neuropsychiatric syndromes

24
Q

Types of meningitis. Common organisms of bacterial meningitis in different age groups.

A

bacterial, viral, fungal, chemical/drug induced, chronic (TB, carcinomatous)

Neonate: E coli, GBS
Children: S pneumoniae, H influenzae
Adolescent/young adult: Neisseria meningiditis, S pneumoniae
Older adults: S pneumoniae,, Listeria

By organisms:
E coli & GBS: neonates
Pneumococci and Meningococci: all age groups beyond neonates
Haemophilus: children but decreased incidence with immunisation
Listeria: extremes of age
Unusual organisms: staph post neurosurgery, G neg in immunocompromised

25
Q

CSF findings in acute bacterial meningitis

A
  • raised pressure
  • turbid
  • raised protein
  • decreased glucose
  • raised neutrophils
  • positive gram stain or culture
26
Q

Difference in CSF findings between acute bacterial and viral meningitis

A

Bacterial: cloudy, high pressure, more neutrophils, raised protein, reduced glucose

Viral: lymphocytes, moderately raised protein, normal glucose

27
Q

Common viral causes of meningitis

A

Echovirus, Coxachievuris (non polio enteroviruses)
HSV
VZV
mumps
measles
HIV
Arboviruses (WNV, JEV)
Non paralytic polio

28
Q

Clinical features of MS

A
  • distinct episodes of neurological deficits separated by time
  • myriad of presentations as white matter lesions separated by space
  • relapsing-remitting course
  • unilateral visual impairment from optic neuritis
29
Q

Pathogenesis of MS

A

Autoimmune, demyelinating disorder, to white matter lesions separated in space

Cellular immune response inappropriately directed against components of myelin sheath

Genetic linkage, environmental influences, microbial/viral trigger, CD4+ Th1 cells react against myelin antigens, release cytokines, activate macrophages

Inflammatory cells create plagues

30
Q

CSF findings in MS

A
  • elevated protein
  • pleocytosis
  • increased proportion of gamma globulin
  • oligoclonal bands
31
Q

Clinical features of Parkinsonism

A
  • diminished facial expression
  • stooped posture
  • slowed voluntary movement
  • festinating gait
  • rigidity
  • pill rolling tremors
32
Q

Causes of Parkinsonism

A

Conditions that cause damage to nigrostriatal dopaminergic system
- PD
- post encephalitis
- familial forms
- trauma
- drugs: dopamine antagonists, toxins, pesticides
- multiple system atrophy, progressive supranuclear palsy

33
Q

Pathogenesis of PD

A

No unifying pathogenic mechanism identified
- misfolded protein/stress response triggered by alpha-synuclein aggregation
- defective proteosomal function due to the loss of E3 ubiquitin ligase parkin
- altered mitochondrial function by loss of DJ-1 and PINK1
- damage to dopaminergic cells from toxins, drugs, autoimmune conditions

34
Q

Process of peripheral nerve repair following injury

A
  1. death of distal part
  2. axonal cone of growth 1-2 mm per day
  3. growth through Schwann cell structure
  4. regenerating clusters
35
Q

Changes in spinal cord after traumatic injury

A

Acute phase: haemorrhage, necrosis, axonal swelling in the surround white matter at level of injury

Late phase: area of neuronal destruction becomes cystic and gliotic, secondary wallerian degeneration involving long white matter tracts

Liquefactive necrosis often seen in CNS

36
Q

Features of irreversible injury at the cellular level

A

Mitochondrial damage:
failure of oxidative phosphorylation -> ATP depletion -> failure of energy dependent cellular functions

Membrane damage:
- plasma membrane -> loss of osmotic balance
- lysosomal membrane -> enzyme leakage -> cell necrosis

Nuclear changes
- chromatin condensation and fragmentation
- pyknosis, karyorhexis, karyolysis

37
Q

Acute consequences of cervical spinal cord injury

A
  • complete or incomplete
  • spinal shock: quadriplegia, flaccid paralysis, total anaesthesia, areflexia
  • if above C4, respiratory compromise from diaphragmatic paralysis
  • neurogenic shock: hypotension, bradycardia, warm dry skin
  • incomplete syndromes (anterior cord, central cord etc)
38
Q

Genetic risk factors for saccular aneurysms

A

Generally unknown, not congenital
Linked to:
Polycystic kidney
EDS type 4
NF1
Marfan
FMD
Aortic coarctation

ACEM Viva (39 decks)

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