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Medical Neuropathology > Exam 3 powerpoints > Flashcards

Exam 3 powerpoints Flashcards

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USMLE® Step 1 flashcards
1
Q

What is GFAP

A

a glial stain, used to find glial cell tumors, turns glial cells brown

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2
Q

What are the charactersitics of neoplastic cells

A

They grow autonomously, are insensitive to inhibitory signals, dont die off, are malignant, limitless replication

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3
Q

What are the tumor classifications

A
  1. primary (originate inside brain) or secondary (outside brain)
  2. Intra-axial (inside brain) or extra axial (in nerves, skull, meninges, or pituitary gland)
  3. Benign or malignant
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4
Q

What are the three neuroglial cell tumors

A

Glial cell tumor, neuronal tumor, embryonal tumors

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5
Q

What are two types of Glial cell tumors

A

Astrocytic tumors, and glioblastoma

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6
Q

What is an example of a Neuronal tumor

A

ganglioglioma

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7
Q

what is a type of embyronal tumor

A

medulloblastoma

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8
Q

What is the most common type of tumor in adults

A

Glioblastoma (55%)

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9
Q

what is the most common type of tumor in infants

A

Medulloblastoma

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10
Q

What are the two grades for histology in tumors

A

High grade: malignant/fast growing

Low grade: benign/slow growing

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11
Q

What are the 4 classifications of tumors. Describe them

A

Grade 1: Pilocytic astrocytoma, circumscribed childhood
Grade 2: Diffuse astrocytoma, diffusely infiltrating, nuclear atypia
Grade 3: Anaplastic astrocytoma, mitotic figures
Grade 4: glioblastoma, endothelial proliferation/ necrosis

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12
Q

What do both grade 3 and 4 tumors show

A

mitosis Angiogenesis

Necrosis

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13
Q

How do you determine whether a tumor is malignant in a histology slide

A

There are more than three mitotic cells present

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14
Q

What are the 4 cell markers of malignancy

A

Nuclear pleomorphism (weird shaped) and atypia
Mitoses
Microvascular proliferation
Necrosis

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15
Q

Why are Low grade tumors hard to detect

A

They grow so slowly that they look like their cells of origin ( blend in with the cells)

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16
Q

What are the direct effects of a tumor

A

Space occupying effects with increased intracranial pressure (ICP)

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17
Q

What are the causes of ICP

A

Direct compression of brain, hemorrhage within tumor, Edema, Impaired CSF flow

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18
Q

What are symptoms of a brain tumor

A

Headaches that awaken you, increased ICP, seizures (most common in adults), focal neurological deficits, hormonal changes

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19
Q

What does a pilocytic astrocytoma present as

A

Tumor of cerebellum, often with cyst, rosenthal fibers, and piloid cells, no mitosis

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20
Q

What is the most common tumor in children

A

Pilocytic astrocytoma

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21
Q

Describe a meningioma

A

Extra-axial, attatched to dura, meningothelial whorls, psammoma bodies, affect women twice as much as men

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22
Q

Describe Neuronal and axonal injury

A

Injury of the white matter that causes impaired axoplasmic transport

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23
Q

What is Azarcon

A

Remedy for diarrhea that contains 85-96% lead

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24
Q

What is the primary neurological effect of neurotoxicity of lead in childhood

A

Cerebral edema

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25
Q

What are some adverse outcomes of Neurotoxicity of lead in childhood

A

Aggression
Hyperactivity
Antisocial behavior
Learning disability

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26
Q

What type of neurons do metals kill

A

Brain and peripheral neurons

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27
Q

What is a symptom of Arsenic poisoning

A

Severe abdominal pain

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28
Q

What are some symptoms of Mercury poisoning

A

numbness in fingers and toes, and a rash with no fever

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29
Q

What is a treatment for mercury poisoning

A

Chelation, EDTA

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30
Q

What does inhalation of Mercury cause

A

necrotizing bronchitis, pneumonitis, death

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31
Q

What are the early symptoms of mercury poisoning

A

insomnia, forgetfulness, anorexia, mild tremor

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32
Q

What are the late symptoms of mercury poisoning

A

progressive tremor and erethism

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33
Q

What are the most common symptoms of Wernicke-Korsakoff syndrome (WKS)

A

Eye abnormalities (nystagmus), Ataxia, and mental symptoms

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34
Q

What is the pathology of WKS

A

Lesions in the midline: mammillary bodies, hypothalamus, thalamus, periaqueductal gray, colliculi, and floor of the fourth ventricle

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35
Q

What is WKS caused by

A

Vitamin B1 (thiamine) deficiency

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36
Q

What is Midline alcoholic cerebellar degeneration

A

Ataxia of stance and gait more than arms. Insidious onset and chronic course

Pathologically, there is loss of Purkinje and granular neurons

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37
Q

What does Vitamin E deficiency cause

A

causes sensory peripheral neuropathy, ataxia, retinitis pigmentosa, and skeletal and cardiac myopathy

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38
Q

What is the pathology for Vitamin E deficiency

A

Dorsal root neurons: Early loss of distal region of central projection
Spinal cord: Loss of fibers in posterior & Clarke column
Axon swelling: in cuneate & gracile nuclei

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39
Q

What does Vitamin B12 deficiency cause

A

Subacute combined degeneration

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40
Q

How does Vitamin B12 deficiency affect the spinal cord and peripheral nerve

A

Spinal cord: multifocal axonal loss & demyelination
Cervical & thoracic cord
Posterior column

Peripheral nerve: Axonal loss ± demyelination

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41
Q

The most common cause of vitamin B12 deficiency is

A

pernicious anemia, an autoimmune disorder against parietal cells and so loss of intrinsic factor

42
Q

What are the kinds of Neural tube defects?

A

Anencephaly, Encephalocele, and Spina bifida.

43
Q

What are the pathological findings for Anencephaly?

A

The absence of a major portion of the brain, skull, and scalp that occurs during embryonic development and underdeveloped hypothalamus. Results from a neural tube defect that occurs when the anterior neuropore of the neural tube fails to close, usually between the 23rd and 26th day following conception. Frog-like facies; always fatal. (Folic acid supplementation)

44
Q

What are the pathological findings for Encephalocele?

A

Encephalocele, is a neural tube defect characterized by sac-like protrusions of the brain and the membranes that cover it through openings in the skull. These defects are caused by failure of the hindbrain neuropore in the neural tube to close completely during fetal development. Usually occipital, rarely anterior at the bridge of nose.

45
Q

What are the pathological findings for Spina bifida?

A

Spina bifida is caused by the incomplete closing of posterior neuropore of the embryonic neural tube. Some vertebrae overlying the spinal cord are not fully formed and remain unfused and open. If the opening is large enough, this allows a portion of the spinal cord to protrude through the opening in the bones.

46
Q

When subarachnoid space is small, the membranous ring is narrow and the neural plate hardly protrudes in Spina bifida is refer to as what?

A

Myelocele

47
Q

When subarachnoid space is very large, the membranous ring is wide and neural plate is elevated in Spina bifida is refer to as what?

A

Myelomeningocele

48
Q

What are pathological findings for Craniorachischisis?

A

Craniorachischisis is a severe form of neural tube defect in which both the brain and spinal cord remain open to varying degrees. Failure closing of Closing 1.

49
Q

What are the pathological findings for Myelomeningocele?

A

Herniation of malformed cord and meninges through vertebrae defect. Usually with Chiari malformation and hydrocephalus.

50
Q

Spina bifida Occulta presents what pathological finding?

A

Sacral dimple

51
Q

Describe Holoprosencephaly and its clinical findings?

A

Cerebral hemispheres fail to separate. Clinical findings are cyclopia (cyclop), proboscis (elongated appendages), agnathia (absent of lower jaw), and cleft lip/palate

52
Q

Common causes for holoprosencephaly is?

A

TORCH infections, fetal alcohol syndrome, and trisomy 13.

53
Q

Describe Agenesis of corpus callosum (ACC).

A

Failure of the axons to form the corpus callosum or cross it.

54
Q

Cortical development in Neuronal migration defects (NMDs) entails?

A
  1. generation of stem cells
  2. differentiation into neurons/glia
  3. migration to cortex
  4. organization into functional layers
55
Q

In NMDs, neurons that do not migrate at all from the ventricle is called?

A

Periventricular heterotopia

56
Q

In NMDs, neurons that migrate half way from the ventricles is called?

A

Subcortical band heterotopia

57
Q

In NMDs, some neurons reach cortex and some do not form normal cortical layers is refers to as?

A

Lissencephaly
Pachygyria
Cobblestone cortex

58
Q

In NMDs, neurons that over-shoot in the cortex and end up in the subarachnoid space can be refers to as?

A

Marginal-leptomeningeal heterotopia

Cobblestone cortex

59
Q

In NMDs, late stage of migration and cortical organization of neurons is disrupted is called?

A

Polymicrogyria

60
Q

What clinical findings are associated with Lissencephaly?

A

Cortical sulci are absent except for the Sylvian fissure. The cortex is thick but has only three neuronal layers.

61
Q

What pathological findings are associated with Chiari I Malformation?

A

Chronic protrusion of cerebellar tonsils below the foramen magnum. Some develop hydrocephalus and most patients are asymptomatic.

62
Q

What pathological findings are associated with Chiari II Malformation?

A 
Cerebellar tonsillar herniation
Small posterior fossa
Kinked medulla (z-formation)
Myelomeningocele
Hydrocephalus
63
Q

What is Dandy-Walker Malformation

A

Malformation consist of agenesis of cerebellar vermis. Cystic dilation of 4th ventricle/enlargement of posterior fossa.

64
Q

What are two kinds of neurogenesis disorders (disorders of brain size)

A

Microcephaly and Megalencephaly

65
Q

What is a possible diagnosis when the brain is hard to touch or feel like a potatoes with candle guttering in caudate nucleus. Clinical findings involve butterfly distribution of acne on the face but not refer to as acne.

A

Tuberous sclerosis

66
Q

What are pathological findings in Polymicrogyria

A

More cell growth in the fold of the cortical cortex with lead to bigger gray matter with more neuron than white matter.

67
Q

What happens in metabolic disorders

A

metabolic abnormalities block amino acid, carbohydrate or lipid metabolism, or impair oxidative phosphorylation

68
Q

Most inherited metabolic disorders are categorized as what?

A

autosomal recessive disorders

69
Q

What are the major categories of inherited metabolic disorders

A

Lysosomal (most common)
Peroxisomal
Mitochondrial
Amino acid disorders

70
Q

What is the gray matter inherited metabolic disorder

A

Lysosomal/Peroxisomal (neuronal storage) diseases

71
Q

What is the white matter inherited metabolic disorder

A

Leukodystrophies

72
Q

What is the inherited metabolic disorder associated with neurons

A

Mitochondrial encephalomyopathies

73
Q

Describe the three general principles of Lysosomal storage disorders

A

Deficiencies of lysosomal enzyme function caused by mutant enzyme proteins and cofactors.
Accumulation (storage) of undegraded products in lysosomes
Causes ballooning, cellular dysfunction, and cell death; the stored products are membrane-bound

74
Q

what are the five Putative mechanisms of disease in LSDs

A

Altered trafficking of molecules through lysosomal network.
inflammatory response, through activation of microglia
Oxidative stress
Disruption of autophagy
Initiation of apoptosis

75
Q

What are the initial signs of Tay-Sach disease

A

arrest of development, neurologic regression, blindness, and seizures. Inexorable progression leads to vegetative state

76
Q

Describe the gray matter pathology in Tay-Sach disease

A

Storage causes neuronal ballooning and torpedo-like swellings of proximal axons and dendrites.
This leads to loss of neurons and their axons

77
Q

Describe the white matter pathology in Tay-Sach disease

A

myelin is not primarily affected. Storage in retinal ganglion cells causes blindness.

78
Q

what is the Laboratory diagnosis of LSDs in Tay-Sach

A

The gold standard is enzyme assay. Gene analysis is useful for carrier detection

79
Q

Describe Peroxisomal disorders

A

Peroxisomes use O2 to generate hydrogen peroxide via peroxidase. H2O2oxidizes/detoxifies ethanol and other toxins

80
Q

What do peroxisomal enzymes do

A

catalyze plamologen syntheis and very long chain fatty acid (VLCFA) beta oxidation

81
Q

What are the two types of peroxisomal disorders

A

single peroxisomal enzyme deficiencies andperoxisomal biogenesis disorders

82
Q

what are some manifestations found in peroxisomal disorders

A

Manifestations include dysmorphic features, liver dysfunction and skeletal abnormalities

83
Q

What is a key determining biochemical sign of a peroxisomal disorder

A

elevated VLCFAsanddecreased RBC plasmalogens

84
Q

What are the clinical findings in the zellweger spectrum

A

dysmorphic faces, neurologic deficits (hypotonia, decreased sucking, decreased tendon reflexes, seizures, nystagmus), liver disease. Most patients fail to thrive and die by six months of age

85
Q

What happens in Mitochondrial disorders

A

when generating ATP , oxygen is converted to free oxygen radicals. These are detoxified by protective enzymes and vitamin antioxidants. If not, free radicals damage lipids, proteins, and nucleic acids

86
Q

What is a cause of amino acid metabolism disorders

A

Defective conversion of the amino group to urea, and many of the organic acidemias, which are caused by defects in disposal of the carbon skeletons of branched chain amino acids.

87
Q

What are the clinical findings of Amino acid disorders

A

fatal metabolic encephalopathy due to accumulating amino acids, hyperammonemia, impaired energy and synthetic pathways, and defective synthesis of glutamate,
Respiratory depression, seizures, and HIE

88
Q

What age group are Amino acid disorders typically found in

A

Most present in the neonatal period with severe or fatal metabolic encephalopathy

89
Q

Which metabolic disease category presents with hyperammonemia?

A

Amino acid (urea cycle)

90
Q

Which metabolic disease category presents with failure to thrive (short stature, muscle weakness, deafness)

A

Mitochondrial

91
Q

Which metabolic disease category presents with big livers?

A

Lysosomal or Peroxisomal

92
Q

Name one of Angelina Jolie’s kids (don’t google it)

A

Shiloh, Knox, Vivienne, Maddox, Pax, Zahara

93
Q

Describe type 1 muscle fibers

A

protracted slow action fibers

94
Q

Describe type 2 fibers

A

capable of fast, powerful contraction

95
Q

Muscle disease is divided into myopathy and denervation atrophy. Describe myopathy.

A

Primary disease of muscle. Includes muscular dystrophies and inflammatory myopathies

96
Q

Muscle disease is divided into myopathy and denervation atrophy. Describe denervation atrophy

A

Often causes distal weakness and atrophy.

97
Q

Why do our muscles shrink/die as we age?

A

Because our nerves that provide muscles with growth factor die off

98
Q

Describe histology of myopathy

A

necrosis/phagocytosis and regeneration. Atrophic fibers are scattered among normal or hypertrophic fibers.

99
Q

What is nuclear change

test question

A

displacement of nuclei from periphery of fibers to the central zone

100
Q

What is polymyositis?

think of the name

A

too many inflamed muscles

101
Q

What is the most severe of the muscular dystrophies?

A

Duchenne’s muscular dystrophy

Medical Neuropathology (10 decks)

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