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Flashcards in Pathology Deck (71):
1

What are the cellular components of the CNS?

Neurones
Glial cells: astrocytes, oligodendrocytes, ependymal cells
Microglia
Supporting structures: connective tissue, meninges, blood vessels

2

What are the 2 ways that neurones will respond to injury?

Rapid necrosis with sudden acute functional failure
Slow atrophy with gradually increasing dysfunction - seen in age related cerebral atrophy

3

When will you see a red neurone?

Context of hypoxia/ ischaemia
Visible 12-24 hours after an irreversible insult to the cell
Results in neuronal cell death

4

What is the pattern to acute neuronal injury?

Shrinking and angulation of nuclei
Loss of nucleolus
Intensely red cytoplasm

5

How will axons respond to injury?

Increased protein synthesis; cell body swelling and enlarged nucleolus
Chromatolysis; margination and loss of nissl granules
Degeneration of axon and myelin sheath distal to the injury - wallerian degeneration

6

What is simple neuronal atrophy?

Shrunken, angulated and lost neurones
Small dark nuclei
Lipofuscin pigment
Reactive gliosis

7

What is gliosis?

Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system
Hypertrophy and hyperplasia of astrocytes

8

What are sub-cellular alterations (inclusions)?

Common in neurodegenerative conditions such as neurofibrillary tangles in alzheimer's
Inclusions appear to accumulate with ageing
Will get inclusions in viral infections

9

What is the function of an oligodendrocyte?

Wraps around axons to form a myelin sheath to facilitate salutatory conduction

10

What will occur with damage to an oligodendrocyte?

Variable pattern of demyelination
Apoptosis

11

Are oligodendrocytes sensitive to oxidative damage?

Yes

12

What is an astrocyte?

Star shaped cell with multipolar cytoplasmic processes

13

Where can strocytes be found?

Present throughout the CNS
Astrocytic process; envelops synaptic plates
Wraps around vessesl and capillaries within the brain

14

What are the roles of astrocytes?

Ionic, metabolic and nutritional homeostasis
Work in conjunction with endothelial cells to maintain the BBB
Main cell involved in repair and scar formation - gliosis

15

Where can you find ependymal cells?

Ventricular system

16

What occurs with disruption to these cells?

Local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulations

17

What is the microglia response to injury?

Proliferation
Recruited through inflammatory mediators; forms aggregates around areas of necrotic and damaged tissues

18

What is the difference between M1 and M2 microglia?

M2; anti-inflammatory, phagocytic, more acute
M1; pro-inflammatory, more chronic

19

What are causes of nervous system injury?

Hypoxia
Trauma
Toxic insult - exogenous and metabolic disruption within brain releasing noxious substances
Metabolic abnormalities
Nutritional deficiencies
Infections
Genetic abnormalities
Ageing

20

What can result in hypoxia?

Cerebral ischaemia
Infarct
Haemorrhage
Trauma
Cardiac arrest
Cerebral palsy

21

What occurs in the brain cells after the onset of ischaemia?

Mitochondrial inhibition of ATP synthesis leading to ATP reserves being consumed within a few minutes - underlies rapid loss of consciousness in hypoxia

22

What occurs in terms of glutamate in excitotoxicity?

Glutamate released by depolarising neurone
Uptake of glutamate inhibited at astrocytes
Glutamate storm and excitation
Increased calcium resulting in protease activation, mitochondrial dysfunction and oxidative stress

23

What results in cytotoxic oedema?

Intoxication
Reye's
Severe hypothermia

24

What results in ionic oedema?

Hyponatraemia
Excess water intake; SIADH

25

What results in vasogenic oedema?

Trauma
Tumours
Inflammation
Infection
Hypertensive encephalopathy

26

Which areas of the brain does the anterior cerebral artery supply?

Midline portions of the frontal lobes and superior medial parietal lobes.

27

Which areas of the brain does the middle cerebral artery supply?

Portion of the frontal lobe and the lateral surface of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hand and arm, and in the dominant hemisphere, the areas for speech

28

Which areas of the brain does the posterior cerebral artery supply?

Occipital cortex

29

What is global hypoxic ischaemia?

Generalised reduction in blood flow/ oxygenation

30

What can cause global hypoxic ischaemic damage?

Cardiac arrest
Severe hypotension; trauma with hypovolaemic shock

31

What can cause focal cerebral ischemia?

Vascular obstruction

32

What is a watershed area?

Zone between 2 arterial territories e.g. parieto-occipital

33

Which neurones are particularly sensitive to hypoxic ischaemic damage?

Neocortex - cerebellum
Hippocampus

34

What is a stroke?

Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours

35

What can cause a cerebral infarction?

Interruption of cerebral blood flow due to thrombosis or emboli

36

What artery most commonly become thrombotic?

Middle cerebral artery

37

Where will emboli arise from commonly that affect the brain?

Atheroma in internal carotid and aortic arch

38

What are risk factors for a stroke?

Atheroma
Hypertx
Serum lipids, obesity, diet
DM
Heart disease
Diseases of neck arteries
Drugs
Smoking

39

What is the location, distribution and extent of parenchymal damage determined by in cerebral infarction?

Arterial territory of affected artery
Timescale of occlusion
Extent of collateral circulatory relief
Systemic perfusion pressure

40

What will be seen macroscopically 12-24hrs after a cerebral infarction?

Pale, soft, swollen with ill defined margins between injured and normal brain

41

What will be seen macroscopically 2-14 days after a cerebral infarction?

Brain becomes gelatinous and friable
Reduction in surrounding tissue oedema demarcating the lesion

42

What will be seen macroscopically several months after a cerebral infarction?

Increasing liquefaction apparent
Eventual formation of cavity lined by dark grey tissue

43

What will be seen microscopically 12-24 hours after a cerebral infarction?

Red neurone, oedema (cytotoxic and vasogenic) with generalised cell swelling

44

What will be seen microscopically 24-48hrs after a cerebral infarction?

Increasing neutrophils
Extravasation of red blood cells (haemorrhagic conversion)
Activation of astrocytes and microglial cells

45

What will be seen microscopically 2-14 days after a cerebral infarction?

Microglia become predominant cell type
Myelin breakdown
Reactive gliosis begins from as early as 1 week

46

What will be seen microscopically several months after a cerebral infarction?

Ongoing phagocytosis brings increasing cavitation and surrounding gliotic scar formation

47

What is a haemorrhagic infarct?

BBB disruption
Hemorrhagic conversion
Thrombolysis resulting in occlusion of vessel, usually by an embolus, with reperfusion and leakage through a damaged capillary bed following lysis of the embolus

48

What results from a middle cerebral artery lesion?

Weakness predominantly in contralateral face and arm

49

What results from anterior cerebral artery lesion?

Weakness and sensory loss in contralateral leg

50

What results from vertebrobasilar artery disease?

Vertigo
Ataxia
Dysarthria
Dysphasia

51

What results from a carotid artery lesion?

Contralateral weakness or sensory loss
If dominant hemisphere; aphasia or apraxia

52

What does hypertension in the brain result in?

Extra and intracranial vascular disease
Vascular remodelling: accelerated atherosclerosis, arteriosclerosis, fibrinoid necrosis of vessel walls
Lacunes
Micro-aneurysms; charcot-bouchard

53

What is charcot-bouchard?

Result of chronic hypertension occuring in small middle cerebral artery branches within the basal ganglia resulting in rupturing leading to an intracerebral haemorrhage

54

What is a lacunar infarct?

Occlusion of small penetrating arteries that provide blood to the brain's deep structures such as the basal ganglia

55

What is hypertensive encephalopathy?

Global cerebral oedema, tentorial and tonsillar herniation, petechiae and arteriolar fibrinoid necrosis

56

What are the types of spontaneous intracranial haemorrhages?

Intracerebral haemorrhage
Subarachnoid haemorrhage
Haemorrhagic infarct

57

What are the types of traumatic intracranial haemorrhages?

Extra-dural haematoma
Subdural haematoma
Contusion
Intracerebral haemorrhage
Subarachnoid

58

What can cause an intracerebral haemorrhage?

Hypertx
Aneurysms
Systemic coag disorders
Anticoaga
Vascular malformations
Cerebral myloid angiopathy
Open heart surgery
Neoplasms
Vasculitis
Diabetes
Drugs: cocaine, alcoholism

59

What are common locations for an intracerebral haemorrhage?

Basal ganglia
Thalamus
Cerebral white matter
Cerebellum

60

What will be seen morphologically with an intracerebral haemorrhage?

Asymmetric distortion
Various shifts and herniations
Well demarcated intraparenchymal haematoma
Softening of adjacent tissue
Surrounding oedema

61

Why will amyloid angiopathy result in intracerebral haemorrhage?

Accumulation of amyloid can cause a plaque, making the blood vessel very stiff and resistant to changes to BP - can easily rupture

62

What are the different types of vascular malformations?

Arteriovenous malformation
Cavernous angioma
Venous angioma
Capillary telangiectasia

63

What is an AVM?

Abnormal tangle of blood vessels connecting arteries and veins, which disrupts normal blood flow and oxygen circulation

64

Why can an AVM result in a bleed?

Veins have a much higher pressure than they are anatomically structured for resulting in bursting and bleeding

65

What is a cavernous angioma?

Blood vessel abnormality characterized by large, adjacent capillaries with little or no intervening brain. The blood flow through these vessels is slow

66

Will AVMs form aneurysms?

Yes

67

What is the most common cause for a subarachnoid haemorrhage?

Saccular/ berry aneurysm

68

What genetic assoc do subarachnoid haemorrhages have?

PKD
Collagen gene abnormalities

69

Why does hydrocephalus occur in subarachnoid haemorrhage?

Lack of CSF flow; can be acute or progress to chronic

70

What are risk factors for a SAH?

Smoking
Hypertx
Kidney disesae

71

What are the symptoms of SAH?

Severe headache
Vomiting
Loss of consciousness