Lecture 18 Word Scramble
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Question | Answer |
Definition of demyelinating diseases | A disruption of normal myelin causing neurologic disease |
Definition of dysmyelinating diseases | A disruption of abnormal myelin causing neurologic disease |
A neurologic disease characterized by a history of remissions and exacerbations of at least 2 separate neurologic abnormalities with multiple plaques found on MRI. | Multiple sclerosis |
What are the clinical forms of MS? | (1) Relapsing-remitting MS (2) Primary progressive MS (3) Secondary-progressive MS |
Pathologic characteristics of multiple sclerosis plaques | (1) Demyelination with relative preservation of axons (2) Infiltration of lymphocytes and macrophages (3) Gliosis (4) Variable remyelination |
A clinical type of MS characterized by acute attacks with full recovery or minor residual deficit upon recovery. | Relapsing-remitting MS |
A clinical type of MS characterized by progression of disability from the onset of the disease without remissions. This form more commonly affects males and has a later onset. | Primary progressive MS |
A clinical form of MS characterized by an initial course of relapsing-remitting MS, followed by progression of disability. | Secondary-progressive MS |
Common clinical symptoms of relapsing-remitting form of MS | (1)Optic neuritis (2)sensory(less motor) symptoms (3)brain stem involvement (4)cerebellar involvement |
What are the type of MS plaques? | (1)Active plaque (2)Inactive plaque (3)Shadow plaque |
Histologic characteristics of active MS plaques | (1)Active myelin destruction with relative axonal preservation (2)Inflammatory reaction (T cells>>B cells) (3) Mild astrocytosis (4) Periphery of the plaque is hypercelluar with lymphocytes and macrophages |
Histologic characteristics of chronic MS plaques | (1)Demyelination with "naked" axons (2)Minimal inflammatory reaction (3)Dense gliosis (4)Periphery of the plaque is hypocellular |
Histologic characteristics of shadow MS plaques | (1)Myelin content is reduced but not totally absent (2)Remyelinated axons present with relatively thin myelin sheaths |
Distribution of MS plaques | (1)Periventricular areas (2)Cortical gray/white matter transition zone (3)Optic nerves, chiasm, tracts (4)Periaqueductal area (5)Cerebellum white matter (6)Cerebellar peduncles (7)Dorsal spinal cord (8)Subpial region of spinal cord (10)Pericentral canal |
A very aggressive form of MS where the disease progresses rapidly to disability or death. | Marburg type |
A rare variant of MS characterized by lesions consisting of rings of demyelination alternating with rings of intact myelin. | Balo type (Concentric sclerosis) |
Treatment for an acute attack of MS | High dose steroids |
Treatment for relapsing forms of MS | Interferon Beta (1a and 1b) or Natalizumab. |
An acute demyelinating disorder characterized by widely scattered small foci of periventricular inflammation and demyelination most frequently associated with antecedent immunization or infection. | Acute Disseminated Encephalomyelitis (ADEM) |
Most common preceding infections of postinfectious encephalomyelitis | Measles, mumps, chickenpox (varicella), rubella, influenza, mononucleosis (EBV) |
Most common preceding vaccinations of postvaccinal encephalomyelitis | Smallpox, rabies, influenza vaccination |
Biochemical abnormality associated wtih X-linked Adrenoleukodystrophy (ALD) | Leukodystrophy caused by abnormality in peroxisomal beta-oxidation resulting in an excess of very long chain fatty acid (VLCFA) esters in the plasma, cultured fibroblasts and affected tissues. |
A rare inherited progressive neurologic disease with adrenal insufficiency. | Childhood form of X-linked adrenoleukodystrophy |
The distribution of lesions of X-linked adrenaleukodystrophy | Lesions are bilateral and symmetrical and mainly limited to the white matter. The typical locations include occipital, parietal, and temporal lobes. Brain stem and the spinal cord are less involved. |
A neurologic condition with a hallmark finding of needle-like trilaminar bodies in CNS macrophages, adrenal cells, Schwann cells, testes, and cultured fibroblasts. | X-linked adrenaleukodystrophy |
Pathogenesis of X-linked adrenoleukodystrophy | Dysmyelination results from the myelin membrane insability induced by very long chain fatty chain acid (VLCFA) esters while the demyelination is initiated by cyotkines from an inflammatory response. |
Criteria for prenatal diagnosis of X-linked adrenoleukodystrophy | (1) very long chain fatty acid esters levels in chorionic villus samples (CVS) (2) needle-like trilaminar bodies in cultured fibroblasts of culture of amniotic fluid cells. |
Treatment option for neurologically intact or verly mildly affected children in X-linked adrenoleukodystrophy | Bone marrow transplant |
Treatment options for X-linked adrenoleukodystrophy | (1) X-linked adrenoleukodystrophy (2) Lorenzo's oil (3) glucocorticoid replacement for adrenocortical insufficiency |
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