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ACEM Primary VIVA > VIVA: Pathology - CNS and eye > Flashcards

VIVA: Pathology - CNS and eye Flashcards

1
Q

What are the causes of ischaemic cerebral infarction?

A
  • Arterial thrombus*
  • Cerebral emboli
  • Lacunar infarcts from small vessels
  • Cerebral arteritis
  • Arterial dissection
  • Venous infarction

*needed to pass + 1 other

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2
Q

Where are some sources of cerebral thromboemboli?

A

2 to pass:
- Left atrium / ventricle thrombus
- Valvular vegetations
- PFO causing paradoxical emboli
- Carotid plaque

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3
Q

What are the distinguishing pathological features of haemorrhagic and non-haemorrhagic ischaemic cerebral infarcts?

A

Haemorrhagic (red *):
- Multiple, sometimes confluent, petechial haemorrhages typically associated with embolic * events
- Thought to be secondary to reperfusion * either via collaterals or dissolution of materials
- Greater risk if anticoagulated

Non-haemorrhagic (pale/bland anaemic *):
- Usually associated with thrombosis *

*needed to pass

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4
Q

How are the pathological processes involved in haemorrhagic vs non-haemorrhagic ischaemic infarcts important in relation to stroke thrombolysis?

A
  • Complications are higher with embolic/haemorrhagic CVAs
  • Aim is to reverse injury in ischaemic penumbra *
  • In non-haemorrhagic CVA, little macroscopic change can be seen within the first 6hrs: earlier treatment leads to better outcome and less haemorrhagic risk

*needed to pass + concept

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5
Q

What are the types of cerebral ischaemic injury?

A
  1. Global cerebral ischaemia * (ischaemic/hypoxic encephlopathy):
    - Generalised reduction of cerebral perfusion
  2. Focal cerebral ischaemia *:
    - Follows reduction of blood flow to a localised * area of the brain

*needed to pass

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6
Q

What are the pathological effects of HTN on the brain?

A

Needed to pass:
- Lacunar infarcts (in lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, pons)
- Slit haemorrhages
- Hypertensive encephalopathy
- Massive intracerebral haemorrhage

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7
Q

Describe the pathological mechanisms which cause cerebral oedema

A
  1. Vasogenic *:
    - BBB disruption with increased vascular permeability
    - Fluid shift intravascular to intercellular spaces of brain
    - May be generalised or localised (inflammation or neoplasm)
  2. Cytotoxic *:
    - Increased intracellular fluid due to neuronal, glial, or endothelial injury (e.g. generalised hypoxic/ischaemic insult or metabolic damage)
    - Interstitial or ependymal oedema around lateral ventricles due to high pressure of hydrocephalus

*needed to pass or basic understanding of 2 mechanisms

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8
Q

What are the morphological findings of generalised cerebral oedema?

A

3/4 to pass:
- Flattened gyri
- Narrowing of sulci
- Compression of ventricles and/or basal cisterns
- Herniation

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9
Q

Describe the major herniation locations associated with raised ICP

A

2/3 to pass with correct description:
1. Subfalcine:
- Asymmetric expansion of cerebrum displaces the cingulate gyrus under the falx cerebri
2. Transtentorial/uncal:
- Medial aspect of the temporal lobe is compressed against the free margin of the tentorium
3. Tonsillar:
- Displacement of the cerebellar tonsils through the foramen magnum

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10
Q

What are the main pathophysiological causes of spontaneous intracerebral haemorrhage?

A
  • HTN and cerebral amyloid are the main causes *
  • Other causes include systemic coagulation disorders, neoplasms, vasculitis, aneurysms, and vascular malformations

*1/2 needed to pass + 2 others

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11
Q

Which areas of the brain do hypertensive intracerebral haemorrhages most commonly occur?

A

Hypertensive intracerebral haemorrhage may originate in the putamen (50-60% of cases), thalamus, pons, and rarely the cerebellar hemispheres *

*2 needed to pass, basal ganglia and brainstem also accepted

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12
Q

Describe the pathophysiology of cerebral amyloid angiopathy

A

There is deposition of amyloidogenic peptides in the walls of medium- and small-calibre meningeal and cortical vessels
This deposition can result in weakening of the vessel wall and risk of haemorrhage

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13
Q

What are the different types of meningitis?

A
  • Bacterial *
  • Viral
  • Others: Rickettsial, chemical/chemo, autoimmune, TB, syphilis, carcinomatous/lymphomatous, fungi

*needed to pass + 1 other

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14
Q

What are the common organisms that cause bacterial meningitis in different age groups?

A

3/4 groups with 2 examples of each to pass:
1. Neonates:
- E. coli
- Pseudomonas
- Listeria
- Group B streptococcus
- Staphylococcus aureus
2. Children:
- Strep pneumoniae
- Haemophilus influenzae B
- Neisseria meningitidis
3. Adolescents and young adults:
- Neisseria meningitidis
- Strep pneumoniae
4. Older adults:
- Listeria
- Strep pneumoniae
- Neisseria meningitidis

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15
Q

What are the complications of meningitis?

A

3 to pass:
Acute:
- DIC
- Septic shock
- Loss of limbs
- Seizures
- Raised ICP
- CVA
- Hyponatraemia
- Death

Chronic:
- Hearing loss
- Learning difficulties/concentration problems

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16
Q

What is the likely diagnosis based off these CSF results, and why?
- Turbid
- Low sugar
- High protein
- Pleiocytosis with neutrophil predominance
- No bacteria

A

Acute bacterial meningitis

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17
Q

What changes occur in the spinal cord after a traumatic injury?

A
  1. Acute phase *:
    - Haemorrhage
    - Necrosis
    - Axonal swelling in surrounding white matter at level of injury
  2. Late phase *:
    - Area of neuronal destruction becomes cystic and gliotic
    - Secondary Wallerian degeneration involving long white matter tracts
    - Liquefactive necrosis often seen in CNS

*1 example from each to pass

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18
Q

What are the features of irreversible injury at the cellular level?

A
  1. Mitochondrial damage *:
    - Failure of oxidative phosphorylation -> ATP depletion * -> failure of energy-dependent cellular functions
  2. Membrane damage *:
    - Plasma membrane -> loss of osmotic balance
    - Lysosomal membrane -> enzyme leakage * -> cell necrosis

*3/4 to pass

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19
Q

What are the acute clinical consequences of a cervical spinal cord injury?

A

Complete:
- Spinal shock: quadriplegia * / flaccid paralysis, total anaesthesia, areflexia
- If above C4, respiratory compromise * due to diaphragmatic paralysis
- Neurogenic shock: hypotension, bradycardia, warm dry skin

Incomplete:
- E.g. anterior cord, central cord etc

*needed to pass

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20
Q

Which type of vessels have been damaged to produce a subdural haematoma?

A
  • Subdural blood comes from damage to bridging veins between the brain and the venous sinuses * (displacement of the brain with trauma can tear the veins at the point where they penetrate the dura to enter the sinuses)
  • Results in blood between the dura and the arachnoid *

*needed to pass

21
Q

Which groups of patients are most at risk for SDH and why?

A
  1. Elderly *:
    - Veins stretched and more movement due to brain atrophy
  2. Infants:
    - Thin-walled bridging veins

*needed to pass

22
Q

How does an extradural haematoma occur?

A

Extradural haematoma occurs with rupture of a meningeal artery *, usually associated with a skull fracture, leading to accumulation of arterial blood between the dura and the skull *

*needed to pass

23
Q

Define and describe diffuse axonal injury

A
24
Q

Where in the cerebral circulation are saccular (berry) aneurysms commonly located?

A

90% near major arterial branch points *:
- ACA with ACommA (40%) *
- MCA with AChoroidalA (34%)
- ICA with PCommA (20%)
- Basilar artery with PCA
- Multiple in 20-30% of cases at autopsy

*needed to pass

25
Q

What factors increase the likelihood of rupture of these aneurysms?

A
  • Increased likelihood with size * (>10mm carries 50% risk of rupture per year)
  • May occur anytime but in about 1/3 are associated with acute increases in ICP * (e.g. straining at stool, orgasm)

*needed to pass

26
Q

What are the pathological sequelae of subarachnoid haemorrhage?

A

Acute events (hours to days):
- Ischaemic injury (stroke) from vasospasm * (especially basal SAH)
- Raised ICP

Late events (healing process):
- Meningeal fibrosis and scarring *
- Obstruction of CSF flow * and/or to CSF absorption
- Death

*2/3 to pass

27
Q

What is the morphology of a berry aneurysm?

A

Medial muscular layer thins as it approaches the neck of the aneurysm, thickened hyalinised intima, covered with normal adventitia

28
Q

What is the natural history of a ruptured berry aneurysm?

A

3/4 to pass:
- Acute onset of severe headache, often with loss of consciousness (25-50% die at the time)
- Rebleeding is common
- Vasospasm in vessels other than the bleeding site can cause secondary ischaemic injury
- In the healing phase, meningeal fibrosis and scarring can cause secondary hydrocephalus

29
Q

What are the main pathological processes causing ischaemic stroke?

A
  1. Thrombotic occlusion *:
    - Atherosclerosis * most common
  2. Embolism *:
    - E.g. AMI, mural thrombus, valvular heart disease, AF, vascular surgery and shower embolism, fat embolism, endocarditis
  3. Inflammatory process leading to luminal narrowing:
    - E.g. infectious vasculitis, autoimmune vasculitis, primary angiitis of the CNS

*needed to pass + at least 2 causes of embolism + 1 other (embolic or inflammatory)

30
Q

What are the causes of focal cerebral infarction?

A
  1. Emboli:
    - From cardiac mural thrombi, arterial thromboemboli (especially carotid), paradoxical association with cardiac anomalies, tumour/fat/air embolus
  2. Thrombotic arterial occlusion/in situ thrombosis:
    - Large vessel disease
  3. Vasculitis:
    - Small vessel disease
  4. Infectious:
    - Immunosuppression and aspergillus, CMV encephalitis, syphilis, TB
  5. Non-infectious:
    - Polyarteritis nodosa, primary angiitis
  6. Other:
    - Amphetamines, cocaine, heroin
    - Dissecting aneurysm of extracranial arteries
    - Hypercoaguable states
31
Q

What are some of the causes of dementia?

A
  • Alzheimer’s disease (commonest) *
  • Frontotemporal dementia
  • Multi-infarct (vascular) dementia
  • Parkinson’s disease (Lewy bodies)
  • Creutzfeld-Jakob disease
  • Neurosyphilis, toxins etc

*needed to pass + 2 others

32
Q

Describe the pathogenesis of Alzheimer’s disease

A
  • Lysis of transmembrane protein Amyloid Precursor Protein by beta and gamma secretases produces Amyloid-beta and C-terminal portion of APP *
  • Amyloid-beta peptides aggregate into amyloid fibrils and can be directly neurotoxic
  • C-terminal portion of APP involved in cell signalling and transcription regulation
  • Severity of Alzheimer’s disease is related to loss of synapses *

*needed to pass

33
Q

What types of intracranial bleeding can be seen in a patient with a head injury?

A

3/4 to pass:
- Extradural
- Subdural
- Subarachnoid (including intraventricular)
- Intraparenchymal

34
Q

What sequence of events occur in an extradural haemorrhage?

A
  • Dural artery (e.g. middle meningeal) tear, usually associated with a skull fracture *
  • Strips off dura from skull
  • May be a lucid period before loss of consciousness

*needed to pass

35
Q

Define concussion and what are its clinical features

A

Definition:
- Altered consciousness secondary to a head injury *
- Transient neurological dysfunction *
- Transient respiratory arrest
- Transient loss of reflexes
- Pathogenesis unclear, may be dysregulation of reticular activating system

Clinical features:
- Headache
- Amnesia
- Nausea and vomiting
- Concentration and memory issues
- Perseveration
- Irritability
- Behaviour/personality changes
- Dexterity loss
- Neuropsychiatric syndromes

*needed to pass + 3 clinical features

36
Q

What are the typical CSF findings in acute bacterial meningitis?

A
  • Raised pressure
  • Turbid
  • Raised protein
  • Low glucose
  • Raised neutrophils *
  • Bacteria on Gram stain or culture *

*needed to pass + 1 other

37
Q

How do the CSF findings typically differ between acute bacterial and viral meningitis?

A

Bacterial:
- Turbid
- Higher pressure
- More neutrophils *
- Raised protein *
- Low glucose *

Viral:
- Lymphocytes *
- Moderately raised protein *
- Normal glucose *

*needed to pass

38
Q

What are the typical CSF findings in viral meningitis?

A

3/4 to pass:
- Lymphocytes
- Normal glucose
- Mildly elevated protein
- No bacteria on Gram stain or culture

39
Q

What are the common viral causes of viruses?

A

2/4 to pass:
- Echovirus
- Coxsackie (enteroviruses)
- Non-paralytic poliovirus
- Others (HSV, VZV, HIV)

40
Q

What are the clinical features of multiple sclerosis?

A
  • Distinct episodes of neurological deficits separated by time *
  • Myriad of presentations as lesions separated by space
  • Unilateral visual impairment (optic neuritis) is common
  • Brainstem and cord lesions

*needed to pass

41
Q

What is the pathogenesis of multiple sclerosis?

A
  • Exact aetiology not established
  • Autoimmune demyelinating disorder * resulting in white matter lesions separated in space
  • Cellular immune response inappropriate directed against components of myelin sheath *
  • CD4+ TH1 cells react against myelin antigens, release cytokines and activate macrophages
  • Inflammatory cells create plaques
  • Genetic and environmental influences (greater incidence in first degree relatives, ? microbial / viral triggers)

*needed to pass

42
Q

What might be found in CSF of a patient with MS?

A

2 needed to pass:
- Mildly elevated protein
- Moderate pleiocytosis (33%)
- Increased proportion of gamma globulin
- Oligoclonal bands (reflects B cell proliferation)

43
Q

Describe the clinical features of Parkinsonism

A

3/6 to pass:
- Diminished facial expression
- Stooped posture
- Slowness of voluntary movement
- Festinating gait (progressively shortened, accelerated steps)
- Rigidity
- “Pill-rolling” tremor

44
Q

What are the causes of Parkinsonism?

A

Conditions that cause damage to the nigrostriatal dopaminergic system *:
- Parkinson’s disease
- Post-encephalitic
- Familial forms (rare; autosomal dominant and recessive)
- Trauma/injuries
- Drugs (e.g. dopamine antagonists, toxins, pesticides)
- Multiple system atrophy
- Progressive supranuclear palsy

*needed to pass + 2 examples

45
Q

Outline the possible pathogenesis of Parkinson’s disease

A

No unifying pathogenic mechanism identified but possible pathogenesis involves:
- Misfolded protein/stress response triggered by alpha-synuclein aggregation
- Defective proteosomal function due to the loss of the E3 ubiquitin ligase parkin
- Altered mitochondrial function caused by loss of DJ-1 and PINK1
- Genetic variants with gene defects
- Possible damage to dopaminergic cells from toxins, drugs, autoimmune conditions

46
Q

Describe the process of peripheral nerve repair following traumatic injury

A
  • Death of distal part (+/- some of proximal)
  • Axonal cone of growth 1-2mm per day
  • Growth through Schwann cell structure
  • Regenerating clusters
47
Q

What is the most frequent cause of subarachnoid haemorrhage?

A
  • Rupture of an aneurysm *
  • Less common causes include extension of traumatic haemorrhage, hypertensive intracerebral bleed into ventricular system, AVM, bleeding disorders, tumour

*needed to pass

48
Q

What are the genetic risk factors for saccular aneurysms?

A

Generally unknown, not “congenital”

Some genetic risk conferred by (2/6 to pass):
- Polycystic kidney
- Ehlers Danlos type 4
- Neurofibromatosis type 1
- Marfan’s
- Fibromuscular dysplasia
- Aortic coarctation

Predisposing factors:
- Smoking
- HTN

49
Q

Define and describe diffuse axonal injury

A

Axonal microscopic injury *:
- Microscopic findings include axonal swelling and focal haemorrhagic lesions *
- Believed to damage the integrity of the axon at the node of Ranvier * -> alterations in axoplasmic flow *
- Commonly found with “coma” but no cerebral contusions *

*needed to pass

ACEM Primary VIVA (45 decks)

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