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Neurological System > 3-Pathology > Flashcards

3-Pathology Flashcards

1
Q

Describe Guillain-Barré syndrome

A

active inflammatory demyelinating polyradiculoneuropathy.
Features:
1. Ascending paralysis (starts in feet; normally).
2. Segmental demyelination of spinal and peripheral nerves (primary lesion).
3. Weakness (distal limbs first).
4. Life threatening (respiratory arrest; cardiac electrical system).
5. Decreased conduction velocity; increased CSF protein.

Onset: acute. Preceded by “flu-like” symptoms.
Causes: Campylobacter jejuni, CMV, Mycoplasma pneumoniae, vaccination.

Treat: plasmapheresis.
Lymphocyte and macrophage mediated

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2
Q

Define wallerian degeneration and its etiology

A

Degeneration of dorsal columns after a spinal cord injury.

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3
Q

Describe the various reactions of astrocytes to injury

A

Astrocytosis: local proliferation of glial cells in response to injury

Congenital hydrocephalus: gestational viral infection of ependymal cells

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4
Q

Red Neurons

A

Ischemic/Dead neurons at the site of injury

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5
Q

Astrocytes

A

Astrocytes: support neurons and promote repair. Star shaped. Outnumber neurons throughout CNS.
Fibrillary astrocytes (white matter).
Protoplasmic astrocytes (grey matter).
Glial Fibrillary Acidic Protein (GFA): stain specific for astrocytes.
Function: BBB (metabolic buffers); repair and scar formation.

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6
Q

Gliosis

A

Astrocytosis (reactive gliosis): proliferation locally in response to injury (trauma, abscess, tumors, infarcts, hemorrhage).

Most important histopathalogic indicator of CNS injury!

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7
Q

Rosenthal Fibers

A

bright, thick, elongated eosinophilic structures associated with long standing gliosis.

Also associated with pilocytic astrocytoma and reactive structures adjacent to craniopharyngioma

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8
Q

Corpora Amylacea

A

Astrocytes make and store these proteins

When slow turnover of these processes

Proteins tagged with stuff and stored

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9
Q

Differentiate between vasogenic and cytotoxic edema

A

Vasogenic edema: due to disruption of BBB (increased permeability). May be focal or generalized.

Cytotoxic edema: increase intracellular volume (hypoxia/ischemia inhibiting active pumps).
White matter more edematous. Increased salt due to pump inhibition. Affects ponds and midbrain more.

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10
Q

Define hydrocephalus

A

Hydrocephalus: increased CSF in the ventricular system.

Non-communicating: there is an obstruction in the normal path of CSF flow.

Communicating: no obstruction. Removal via subarachnoid granulations (into venous system) is insufficient to keep up with production.

Aqueduct of Sylvius: most common location of obstruction (congenital malformation; viral ependymitis during emgryogenesis results in stenosis).

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11
Q

Describe Chiari Type I and Type II (Arnold-Chiari) malformations.

A

CM: brainstem (medulla) and cerebellum compacted into bowl-shaped posterior fossa (flattening of base of skull; enlarged foramen magnum).

Associated with: syringomyelia; lumbar meningomyelocele.

Type I: NO meningomyelocele. Present infant to adolescence.

Type II, III: adults. Meningomyelocele.

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12
Q

Define concussion and its immediate and long term effects

A

Transient loss of consciousness due to trauma (mainly brainstem reticular formation). Mildest type of spinal cord injury (transient/reversible).

“Knock-out”: quick deflection of head up and posteriorly places torque on brainstem and causes functional paralysis of neurons of reticular formation.

Temporal-parietal blow: skull fracture (generally not a concusision; lateral movement prevented by Falx).

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13
Q

Epidural vs Subdural Hematoma

A

Epidural: convex tear-drop shape, MMA hemorrhage usually from fracture

Subdural: rupture of bridging veins slow bleed, concave with contour of head.

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14
Q

Charcot-Bouchard microaneurysms

A

Charcot-Bouchard aneurysm: occur in small blood vessels.

Cause: chronic hypertension.

Pathogenesis: thickened vascular walls; lipid deposits.

Location: brainstem.

Prognosis: thrombus in ICA sends emboli into MCA.

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15
Q

Describe congenital saccular “berry” aneurysms

A

arterial defect that arises during embryogenesis. 90% of secular aneurysms occur at branch points in carotid system.
Younger women. Saccular.

Rupture: life-threatening subarachnoid hemorrhage. ~35% mortality.

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16
Q

AV malformations, discuss them

A 
ArterioVenous Malformation (AVM): most common congenital vascular malformation. Onset 2nd-3rd decade.
Features: seizures; intracranial hemorrhage (subarachnoid).
Location: cerebral cortex (typically).

Pathology: abnormal vessesl replace cortical grey matter and extend deeply into white matter.

17
Q

4 main routes of entry for infection in the CNS

A

Hematogenous spread: most common. Usually via arterial route, or retrogradely (veins).
Direct implantation: trauma; iatrogenic (rare; lumbar puncture); congenital (meningomyelocele).
Local extension: secondary to established infections. Most from mastoid and frontal sinuses.
PNS to CNS: viruses (rabies, herpes zoster).

18
Q

Acute pyogenic meningitis and the causative organisms

A

Neonates: streptococcus agalactiae; E. Coli; Listeria monocytogenes.

Adolescents and young adults: Neisseria meningitidis (most common); Haempohilus influenza (reduced due to immunization; most common in infants is no S. pneumoniae).

Children and adults: Strep. Pneumonia.

IV Drug Users with HIV: Staph aurues.

19
Q

Brain abscesses and their possible sources/causing agents

A

Brain abscess: produces ring enhancement lesion on imaging.

Routes: movement from primary infected site (heart; lungs; tooth decay; bones).

Causes: staph, strep.

Pathogenesis: destructive lesions (central liquifactive necrosis surrounded by fibrous (collagenous) cap; edema surrounding).

Location: frontal lobe; parietal lobe; cerebellum.
Presentation: progressive focal deficits (increased ICP).

CSF: increased pressure; increased WBC; increased protein; glucose normal.

Thrombophlebitis: result of abscess. Develops in bridging veins, leading to occlusion (infarct).

S&S: febrile; headache; neck stiffness; lethargy/coma (if untreated).
CSF: similar to abscess.

Extradural abscess: associated with osteomyelitis (arise from adjacent site of infection).

Sources: sinusitis; surgical procedure.

20
Q

Tabes Dorsalis

A

demyelination of sensory neurons (ataxia; weakness; loss of coordination).

Result of neurosyphilis 3rd degree.

21
Q

List the most common sites of primary thrombosis.

A

MCA

22
Q
  1. List and describe the two groups of infarcts.
A

Ischemic

Hemorrhagic

23
Q
  1. Discuss lacunar infarcts and their etiology.
A

noncortical infracts caused by occlusion of penetrating arteries.

24
Q
  1. Describe hypertensive encephalopathy and Binswanger disease
A

Fibronoid necrosis: hypertensive encephalopathy. Malignant hypertension.
Petechiae: minute hemorrhages.

Binswanger disease: subcortical arteriosclerotic encephalopathy (multiple infarcts in white matter).

25
Q
  1. List the major cause of nontraumatic intraparenchymal hemorrhages
A

Most commonly seen in systemic hypertension.

i.e. charcot-bouchard aneurysm

26
Q
  1. Describe the types of neurologic dysfunction associated with HIV infections
A

~60% of patients develop neurologic dysfunction. Aseptic meningitis within 1-2 weeks of seroconversion in ~10% of patients.

HIV meningoencephalitis (subacute encephalitis): dementia (mental slowing; memory loss; mood disturbances); ataxia; bladder/bowl incontinence; seizure.
Chronic inflammatory reaction: microglial infiltrates (nodules); multinucleated giant cell.
Vacuolar Myelopathy: spinal cord. 20-30% of paitients in US.
Similar to subacute combined degeneration (Vit B12 deficiency; Vit B12 levels are normal).
Myopathy and Peripheral Neuropathy: inflammatory myopathy. Most described disorder in patients with HIV.
S&S: proximal weakness; pain; increased serum creatine kinase.

Most commonly reported syndromes: acute/chronic inflammatory ~60% of patients develop neurologic dysfunction. Aseptic meningitis within 1-2 weeks of seroconversion in ~10% of patients.

HIV meningoencephalitis (subacute encephalitis): dementia (mental slowing; memory loss; mood disturbances); ataxia; bladder/bowl incontinence; seizure.
Chronic inflammatory reaction: microglial infiltrates (nodules); multinucleated giant cell.
Vacuolar Myelopathy: spinal cord. 20-30% of paitients in US.
Similar to subacute combined degeneration (Vit B12 deficiency; Vit B12 levels are normal).

Myopathy and Peripheral Neuropathy: inflammatory myopathy. Most described disorder in patients with HIV.
S&S: proximal weakness; pain; increased serum creatine kinase.
Most commonly reported syndromes: acute/chronic inflammatory

27
Q
  1. Describe progressive multifocal leukoencephalopathy (PML)
A

Demyelination of CNS due to destruction of oligodendrocytes. Associated with JC virus. Usually fatal. Rapidly progressive

28
Q
  1. Define kuru plaques.
A

Kuru: prion disease. Ritualistic cannibalism.

S&S: symptomatic coordinative malfunctions; inappropriate episodes of laughter (“laughing death”).

29
Q
  1. Describe CJD.
A

Prion disease
rapidly progressive
dementia with myoclonus
Spongiform cortex

30
Q
  1. Describe Pick’s disease
A

Dementia, aphasia, parkinsonian aspects, personality changes, Spares parietal lobe.

Find pick bodies on histo, spherical tau protein aggregates.

31
Q
  1. List the four major classes of brain tumors
A

Gliomas
Neuronal Tumors
Poorly Differentiated
Meningiomas

32
Q
  1. List the three major types of gliomas.
A

Astrocytoma
Oligodendroglioma
Ependymoma

33
Q
  1. Describe astrocytomas and glioblastomas.
A

Fibrillary astrocytoma: most common (80% of adult primary tumors). Onset 20-40s (rare after).
Location: cerebral hemispheres.
Presenting signs: seizures; headache; no focal neurological dificits.
Prognosis: WHO classification; grades 1-4.

Glioblastoma multiformes: death sentence (8-10 months after diagnosis). 2 distinct clinical histories:
1. Short, rapidly progressive, arising without preexisting low grade tumor. Typically in older patients (primary glioblastoma).
2. Previously diagnosed low grade astrocytoma (secondary astrocytoma). Young. P53 mutation.
Pathology: necrosis (well-circumscribed).

34
Q
  1. Describe pilocytic astrocytomas
A

young adults, children. Relatively benign. Rare p53 mutation.

Location: cerebellum; anterior optic pathway; floor of 3rd ventricle; cerebral hemispheres.

Features: cystic appearance (solid, brightly contrast-enhancing mural component and associated cyst); grows slowly; WHO grade 1.

Diagnosis: labeled by antisera to B-crystallin; immunoreactive for α-1-antitrypsin.

35
Q
  1. Describe oligodendrogliomas.
A

young, middle-aged adults. 5-15% of gliomas.

Location: frontal and temporal lobes (mainly within white matter).

Features: calcification.

Pathology: loss of chromosome 1p and 19q (80% of patients).

Prognosis: 5-10 year survival.

36
Q
  1. Briefly describe general ependymomas
A

young (ventricular system); adults (spinal cord).

Location: next to ependymal-lined ventricular system. Central canal of spinal cord.

4th ventricle: young (1st 2 decades).

Spinal cord: adults. Associated with Neurofibromatosis-2. Pain.

Clinical features: posterior fossa ependymoma with hydrocephalus secondary to obstruction.

Histology: form rosettes or perivascular pseudorosettes.

37
Q
  1. Describe primary brain lymphoma
A

Primary CNS lymphomas: most common CNS neoplasm in immunosuppressed (HIV; SLE) patients. Elderly (> 60; nonimmunosuppresed).

Location: brain; spinal cord; meninges.

Pathology: B-cell origin (EBV).

Pathogenesis: invades deep structure of brain (cerebral hemispheres; corpus callosum; basal ganglia); cerebellum; brainstem; spinal cord (rarely). Crosses corpus callosum.

Features: perivascular localization (rosettes).

38
Q
  1. Briefly describe schwannomas
A

Schwannomas: benign. Arise from neural crest cells. SOL (brainstem, spinal cord).
NF2 gene: inactivating mutations of chromosome 22.

Merlin: product of 22. Loss of expression consistent finding in schwannomas. Normally controls/restricts actions of cell surface growth factor (EGFR). Absence results in hyperproliferation.

Acoustic neuroma: occur in cerebellopontine angle (attached to CN VIII).
Features: tinnitus; hearing loss.

Neurological System (10 decks)

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