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M2 Pathology > Neuroscience Pathology 1 (ICP, Stroke, Haemorrhage) > Flashcards

Neuroscience Pathology 1 (ICP, Stroke, Haemorrhage) Flashcards

1
Q

State the 4 common clinical presentations of neuroscience pathology

A
  1. raised ICP (super important!!!)
  2. localising signs
  3. progressive neurodegenerative states
  4. demyelinating diseases
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2
Q

Raised ICP is the increase in mean ____ pressure above __-__ mmHg in supine adult

Raised ICP is due to increased ____ volume from
1. Increase in ____
2. Increase in _____ _____

A

Raised ICP is the increase in mean CSF pressure above 7-15 mmHg in supine adult

Raised ICP is due to increased INTRACRANIAL volume from
1. Increase in CSF
2. Increase in CEREBRAL TISSUES

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3
Q

State the common clinical presentations of raised ICP.

State some presentations associated with advanced raised ICP.

A

Common:
- nausea, vomiting
- headache
- papilloedema (swelling of optic disc)

Advanced:
- loss of consciousness
- altered mental state
- bradycardia
- hypertension
- neurogenic pulmonary oedema (potentially fatal)

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4
Q

State the commonest complication of raised ICP which can be fatal. State the 3 ways this complication can manifest.

A

CEREBRAL HERNIATION = displacement of part of the brain past rigid dural folds or through an opening into another compartment due to increased ICP

  1. subfalcine herniation - herniation of cingulate gyrus through falx cerebri due to cerebral hemisphere lesion
  2. uncal (transtentorial) herniation - herniation of medial temporal lobe through tentorium cerebelli
  3. tonsillar herniation/coning - herniation of cerebellar tonsils through foramen magnum due to posterior fossa space occupying lesions
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5
Q

State the 3 types of cerebral herniation that can occur as a result of raised ICP

A
  1. SUBFALCINE HERNIATION
  2. UNCAL (TRANSTENTORIAL) HERNIATION
  3. TONSILLAR HERNIATION/CONING
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6
Q

State everything you know about SUBFALCINE HERNIATION, which is a type of cerebral herniation that causes raised ICP

A

SUBFALCINE HERNIATION
- herniation of cingulate gyrus through falx cerebri due to cerebral hemisphere lesion
- presentation = clinically silent - asymptomatic
- secondary effects = haemorrhage and necrosis of affected area + compression of ACA leading to infarction and localising signs

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7
Q

State everything you know about UNCAL (TRANSTENTORIAL) HERNIATION, which is a type of cerebral herniation that causes raised ICP

A

UNCAL (TRANSTENTORIAL) HERNIATION
- herniation of medial temporal lobe through tentorium cerebelli
- presentation = loss of consciousness + CN III compression resulting in ipsilateral pupil fixed and dilated + compression of PCA leading to cortical blindness (loss of vision with normal pupillary light reflexes due to bilateral lesions of striate cortex in occipital lobes)

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8
Q

State everything you know about TONSILLAR HERNIATION, which is a type of cerebral herniation that causes raised ICP

A

TONSILLAR HERNIATION
- herniation of cerebellar tonsils through foramen magnum due to posterior fossa space occupying lesions
- presentation = neck stiffness + coning (compression of pons and medullar - compromise of vital centres for respiratory and cardiac function –> cardiorespiratory arrest –> death)

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9
Q

State the causes of raised ICP

A
  1. DIFFUSE CONDITIONS
    - cerebral oedema due to infection, infarction, head trauma
    - hydrocephalus (increase in CSF volume in CNS due to disturbances of formation, flow or absorption of CSF)
    –> NON-COMMUNICATING = due to obstruction between ventricular and subarachnoid space (space-occupying lesions)
    –> COMMUNICATING = due to defective absorption, overproduction and/or venous drainage insufficiency of CSF -> full communication between ventricles and subarachnoid space hence there is no physical block or obstruction
  2. LOCALISED CONDITIONS - space occupying lesions (due to tumours, haemorrhage/infarcts, abscess)
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10
Q

State the common conditions related to non-communicating hydrocephalus and communicating hydrocephalus

A

NON-COMMUNICATING HYDROCEPHALUS
1. Congenital malformations (Arnold Chiari malformation)
2. Mass lesions (cyst, tumour, hematoma)
3. Meningitis (scarring, ventricular outflow obstruction - tuberculous meningitis)

COMMUNICATING HYDROCEPHALUS
1. Subarachnoid haemorrhage (blocked arachnoid villi –> decreased absorption of CSF)
2. Meningitis
3. Normal pressure hydrocephalus (deficiency of arachnoid granulations, head injury, infection)

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11
Q

Cerebrovascular disease, also known as ____, is the ____ signs and symptoms that can be explained by ____ mechanisms, have an ____ onset, and persist > ____ hours.

A

Cerebrovascular disease, also known as STROKE, is the NEUROLOGIC signs and symptoms that can be explained by VASCULAR mechanisms, have an ACUTE onset, and persist > 24 hours.

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12
Q

State the common clinical presentations of cerebrovascular disease/stroke

A
  1. localising signs (site related) - hemiparesis (one-sided weakness)
  2. raised ICP - headache, vomiting, nausea, papilloedema
  3. sudden severe headache
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13
Q

State the risk factors that can predisopose patients to cerebrovascular diseases

A
  1. HTN, DM, atherosclerosis
  2. Transient ischaemic attack (TIA) = transient episode of neurologic dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction –> risk of ischaemic stroke with TIA = 3-4% –> infarction leads to irreversible death of tissues –> neurons unable to replicate –> effects are irreversible
  3. AF, vascular malformations/abnormaltiies, coagulopathy
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14
Q

State the 3 common causes of cerebrovascular disease (stroke)

A
  1. ischaemia and infarction
  2. haemorrhage
  3. hypertensive cerebrovascular disease (CVD)
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15
Q

State the microscopic and macroscopic features of ischaemia and infarction.

A

MICROSCOPIC:
12-48hrs = ischaemic neuronal change (red neurons [coagulation of proteins] + oedema + neutrophils)
2-10days = foamy macrophages (high lipid content in brain in myelin sheath)
1-3weeks = more macrophages, reactive gliosis (reactive astrocytes which appear more cellular than usual and is present at edges of infarcts)

MACROSCOPIC:
12-48hrs = soft, pale, swollen, indistinct grey-white matter junction depending on location of infarct
2-10days = gelatinous, friable
10days-3weeks = liquid filled cavity (liquefactive necrosis)

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16
Q

State the 2 causes of ischaemia and explain everything you know about them.

A

Cause 1: GLOBAL HYPOPERFUSION
- Drop in cerebral perfusion from cardiac arrest, shock, severe hypotension
- Leads to watershed infarcts between MCA and ACA
- Cortical pseudolaminar infarcts (layer of necrosis on brain)

Cause 2: FOCAL CEREBRAL ISCHAEMIA
- Arterial occlusion leading to reduced flow in a localised area of brain due to thrombosis, embolism or vasculitis –> resulting in infarction
- Severity of infarction depends on vessel size and location + presence/lack of collateral blood supply
- 2 types of infarcts = pale/nonhaemorrhagic AND red/haemorrhagic
- PALE INFARCTS = thrombosis due to atherosclerosis/arteriosclerosis/venous thrombosis –> utilise thrombolytic treatment
- RED INFARCTS = thrombosis due to embolism from carotid artery atheroma/ cardiac thrombi (post AMI, AF, vascular disease)/fat emboli –> avoid thrombolytic treatment
- CT scan used to differentiate the 2 infarcts

17
Q

State the 4 causes of haemorrhage leading to cerebrovascular diseases. State everything you know about these causes

A
  1. HYPERTENSION
    - HTN –> hyaline arteriosclerosis + fibrinoid necrosis + charcot bouchard microaneurysms –> rupture of vessels (especially in basal ganglia and thalamus)
    - Histo = blood vessel walls undergo dark-pink appearing change
  2. CEREBRAL AMYLOID ANGIOPATHY
    - Amyloid deposits in leptomeningeal and cortical arteries –> weakens walls –> more prone to bleeding
  3. STRUCTURAL VASCULAR ABNORMALITIES
    - Common in younger population
    - Patients typically present with no known medical history
    - Includes arteriovascular malformations and berry/saccular aneurysms in the circle of Willis
  4. COAGULOPATHY
    - Due to low platelet count (thrombocytopenia) or deficiency in clotting factors
18
Q

State 3 results of hypertensive cerebrovascular disease (CVD)

A

(1) LACUNAR INFARCTS

(2) HYPERTENSIVE ENCEPHALOPATHY

(3) HYPERTENSIVE INTRACEREBRAL HAEMORRHAGE

19
Q

State everything you know about LACUNAR INFARCTS, which is a result of cerebrovascular disease (stroke)

A

LACUNAR INFARCTS
- Found deep in penetrating arteries and arterioles in basal ganglia, cerebral white matter and brainstem
- Caused by arteriolar sclerosis –> leading to occlusion –> multiple small infarcts
- Lacunae = <15mm wide in lenticular nucleus, thalamus, internal capsule, caudate nucleus and pons
- Presentation = silent neurologic impairment

20
Q

State everything you know about HYPERTENSIVE ENCEPHALOPATHY, which is a result of cerebrovascular disease (stroke)

A

HYPERTENSIVE ENCEPHALOPATHY
- Type 1 = Acute Hypertensive Encephalopathy (Malignant HTN)
- Presentation = diffuse cerebral dsyfunction + raised ICP
- Complications = cerebral oedema+herniation –> coma, petechial haemorrhages, fibrinoid necrosis of arterioles
- Type 2 = Multi-Infarct Dementia
- Common in elderly
- Presentation = progressive dementia, gait abnormalities, focal neurologic deficits
- Complications = underlying multifocal vascular diseases throughout brain such as cerebral atherosclerosis + thromboemboli (in carotid vessels and heart)

21
Q

State everything you know about HYPERTENSIVE INTRACEREBAL HAEMORRHAGE, which is a result of cerebrovascular disease (stroke)

A

HYPERTENSIVE INTRACEREBRAL HAEMORRHAGE
- Commonest cause of primary brain parenchymal haemorrhage in older patients
- Causes 15% of death in chronic hypertensives
- Underlying vascular malformations is primary cause of spontaneous brain haemorrhage in young patients
- Causes = arterioles (hyaline arteriosclerosis + fibrinoid necrosis) + Charcot-Bouchard aneurysms in basal ganglia
- Located in putamen, thalamus, pons, minorly in cerebellar hemispheres

22
Q

State the 2 types of intracranial haemorrhage. State any subtypes that may be included.

A
  1. intra-axial (within brain tissue) - intracerebral, intraventricular
  2. extra-axial (within coverings of brain) - extradural, subdural, subarachnoid
23
Q

State the common causes of intra-axial haemorrhagic cerebrovascular disease

A
  1. HTN –> charcot bouchard aneurysm (especially if haemorrhage is located in basal ganglia)
  2. Ruptured Arteriovenous Malformations (espeically if young patient)
  3. Amyloid angiopathy
  4. Trauma
  5. Venous Sinus Thrombosis
  6. Coagulopathy
24
Q

State the common causes of subarachnoid, subdural and epidural haemorrhages.

A

SUBARACHNOID:
- typically non-traumatic
- causes = ruptured saccular/berry aneurysms + ruptured AVM (arteriovascular malformations)

SUBDURAL
- commonly due to trauma
- causes = acute subdural haematoma + chronic subdural haematoma –> cerebral (bridging) veins rupture

EPIDURAL
- commonly due to trauma to pterion –> MMA damaged

25
Q

Berry aneurysms are ____-walled balloon-like ____ outpouching that tends to occur at the junction of ____. It is commonly located at ____ of ____.

A

Berry aneurysms are THIN-walled balloon-like SACCULAR outpouching that tends to occur at the junction of ARTERIES. It is commonly located at CIRCLE of WILLIS.

26
Q

Summarise the features (causes, presentations, predisposing factors) of SUBARACHNOID HAEMORRHAGE.

A

SUBARACHNOID HAEMORRHAGE
- Causes: Rupture of saccular aneurysm + Rupture of AVM
- (1) Rupture of Saccular aneurysm –> affeted arteries bleed easily as vessel walls are weak –> intracerebral haemorrhage –> raised ICP
- Cause (1) commonly associated with - ADPCKD and AORTIC COARCTATION
- (2) AVM = cavernous angioma (clusters of dilated thin-walled blood vessels in CNS) or capillary telangiectasia (lumina of arteries abnormally dilated) or venous angioma (cluster of small veins that drain into larger vein)
- Presentation: Thunderclap headache + warning headaches

27
Q

Summarise the differences between epidural and subdural haemorrhage in terms of…
1. causes
2. site of ruptured vessel
3. bleeding location
4. rate of bleeding
5. prognosis
6. clinical presentation

A
28
Q

State everything you know about the two types of subdural hematomas.

A

ACUTE SUBDURAL HEMATOMA
- due to trauma
- high mortality rate
- raised ICP –> requires rapid surgical decompression

CHRONIC SUBDURAL HEMATOMA
- due to minor head trauma
- can occur for days-wekes and can re-bleed
- good prognosis
- common in young and old

29
Q

State everything you know about epidural hematoma

A
  • due to laceration of MMA leading to arterial bleed
  • commonly accompanied by skull fracture near pterion
  • clinical presentation = lucid interval (patient is conscious and oriented)–> sudden deterioration (vomiting, restlessness, loss of consciousness)
  • immediate surgery required
  • CT scan shows convex appearance
30
Q

Summarise everything you know about INTRACEREBRAL PETECHIAL HAEMORRHAGE

A

PETECHIAL HAEMORRHAGE is a complication of hypertensive intracerebral haemorrhage
- causes = malaria, vasculitis, acute hypertensive encephalopathy, trauma, fat embolism
- presentation = altered mental state due to raised ICP

M2 Pathology (20 decks)

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