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Systems Pathology > Exam 2: [CNS Infectious Diseases] > Flashcards

Exam 2: [CNS Infectious Diseases] Flashcards

1
Q

Routes by which Infection can get into the CNS

A

1) Haematogenous (Bacteremia, Virema)
2) Directly from Local Infection
3) Penetrating injuries (Cribiform Plate or Ear Fractures provide pathway to the cranium)

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2
Q

Primary Infections of the MENINGES [CNS] List

A

1) Acute Bacterial (suppurative meningitis)
2) Acute Viral Meningitis
3) Chronic Meningitis: tuberculosis, cryptococcidiosis

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3
Q

Acute Bacterial (Suppurative) Meningitis : Site of Infection, Components Increased/Decreased:

A
  • Infection is in Leptomeningitis
  • CSF shows increased pressure
  • Contains: organisms, increased protein decreased glucose, neutrophils (pus) so CSF looks cloudy
  • Type of organism varies depending on pt. Age
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4
Q

Acute Bacterial (Suppurative) Meningitis: Organisms in Different Age Groups

A

Neonates/Infants: group B strep, E. Coli, Listeria
6 mo-5yrs (FORMER): H. Influenzae strain B
6 mo-5yrs (CURRENT): Streptococcus pneumonia
5yrs-Young Adult: Neisseria Meningitidis
Older Adults: S. Pneumoniae & Gram Negatives

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5
Q

Acute Bacterial (Suppurative) Meningitis: Pathology

A
  • Meninges Congested & Inflamed
  • Neutrophils & Fibrin Present
  • Bacteria are Obvious on CSF Smear
  • Culture Gives Sensitivities
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6
Q

Acute Bacterial (Suppurative) Meningitis: Clinical Features

A
  • Fever, Headaches, Stiff Neck, Altered Mental Status, Kernig’s Sign, Brudzinski’s Sign
  • May have symptoms of the previous infection
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7
Q

Acute Bacterial (Suppurative) Meningitis: Treatment & Progression

A
  • Progresses Very Rapidly
  • Medical Emergency
  • Prognosis related to rapidity of treatment
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8
Q

What should be suspected from an adult who was previously well and may resent as part of an epidemic?

A

N. Meningitidis

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9
Q

Acute Bacterial (Suppurative) Meningitis: Complications

A

1) Epilepsy, Hydrocephalus, Neuro Deficits (mental retardation, CN palsies of CNII & CNVIII, spinal nerve neuropathies)
2) Significant Mortality Rate

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10
Q

Meningococcus Complications

A

1) DIC (Disseminated Intravascular Coagulation) abnormal blood clotting
2) Septic Shock
3) Waterhouse-Friedrichsen Syndrome

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11
Q

Neurosyphilis: Caused by what Organism, Symptoms occur when? Infiltrate & what + Test?

A
  • Cause by organism Treponema Pallidum
  • Symptoms may occur years after infection
  • 2/3 yrs after infection Meninges have Lymphocytic Infiltrate and a (+) VDRL Test (cure=penicillin)
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12
Q

When does Meningovascular Syphillis Occur?

A
  • 3 Years following infection
  • Chronic inflammation of meninges -> cranial nerve palsies
  • Some cases have “Gummas” that act as space-occupying lesions
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13
Q

Neurosyphillis: After 10 years

A
  • “Parenchymous Syphillis” at this Stage
  • General Paresis (dementia & paralysis)
  • Tabes Dorsalis
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14
Q

What Symptoms does Tabis Dorsalis Have?

A
  • In spinal cord (lightning pains, sensory loss, hypotonia, areflexia)
  • Argyll-Robinson Pupils
  • Charcots Joints
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15
Q

What Does General Paresis show?

A

Progressive dementia & psychosis with cerebral atrophy

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16
Q

Causative Agents of Viral Meningitis

A

1) Coxsackievirus B
2) Mumps
3) EBV
4) Echovirus

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17
Q

Viral Meningitis Features

A
  • Produces Aseptic Meningitis (No Bacteria)
  • Benign, Self-Limiting
  • May spread to Encephalitis
  • CSF is clear
  • Cells = Lymphocytes
  • Protein moderately raised, Glucose is Normal
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18
Q

Chronic Meningitis Causative Agents

A

1) Mycobacterium Tuberculosis
2) Cryptococcus
3) Brucella Species
4) Treponema Pallidum

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19
Q

Meningeal Appearance in Chronic Meningitis

A
  • Thick Meninges (all 3)
  • Fibrinous Exudate in the Subarachnoid Space
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20
Q

Chronic Meningitis Leads To:

A

Fibrous Adhesions Causing Obstructive Hydrocephalus

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21
Q

Chronic Meningitis Cellular Components

A

[In CSF]
- Increased # of Mononuclear Cells
- Increased Protein
- Decreased Glucose

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22
Q

Chronic Meningitis: Signs/Symptoms & Prognosis

A
  • Insidious Onset & Less Marked than in the Acute Forms
  • Poor Prognosis
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23
Q

Different Ways Viruses can Affect the Brain

A
  • From Systemic Infection
  • Direct Target of the Brain
  • Specific areas of Brain OR All-Over
  • Specifically target Neurons
  • Specifically Target Neuroglia
  • Healthy OR Immunocompromised Individuals
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24
Q

Viral Encephaltis: Pathological Features

A
  • Perivascular Cuffing of Mononuclear Cells
    (Lymphocytes, plasma cells, monocytes)
  • Microglial Nodules often Present
  • Neuronophagia if Neuron has Dies
  • Inclusion Bodies in Neurons
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25
Q

Viral Encephalitis: Prognosis

A

Very Serious Condition that can lead to Death or Permanent Neurological Defects

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26
Q

Arbovirus Infections

A

1) St. Louis Encephalitis
2) Eastern Equine Encephalitis
3) Venezuelan Encephalitis
4) California Encephalitis
5) West Nile Encephalitis

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27
Q

Sporadic Viral Infections

A

1) Herpes Simplex Encephalitis
2) Cytomegalovirus
3) Progressive Multifocal Leukoencephalopathy
4) Subacute Sclerosing Panencephalitis (SSPE)

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28
Q

Epidemic Viral Infections

A

1) Arbovirus Infections
2) HIV Encephalitis

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29
Q

St Louis Encephalitis: Vector/Reservoir, Time of Year, Population at Risk

A

Vector: Mosquito
Reservoir: Birds (including Poultry)
Late Summer & Early Fall
Very Young & Elderly @ Highest Risk

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30
Q

St. Louis Encephalitis: Histology

A
  • Perivascular Infiltrates
  • Glial Nodules [Brain Stem]
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31
Q

St. Louis Encephalitis: Clinical Signs/Symptoms

A
  • Fever, Photophobia, Meningism
  • Consiousness Disurbances, Convulsions
  • Focal Neurological Signs & Symptoms
    **In fatal cases: Body temp keeps rising, patient goes into a coma, then dies
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32
Q

HIV Encephalitis (AIDS- dementia or HIV Encephalitis): % that Show changes, Change in HIV-1, What does it produce?

A
  • 90% show changes at autopsy
  • 60% show neurological changes
  • In HIV-1, Brain shows Atrophy
  • Produces Progressive Neurological Disease
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33
Q

HIV Encephalitis (AIDS- dementia or HIV Encephalitis): Histology

A
  • Perivascular Infiltrates
  • Glial Nodules
  • Multinucleated Giant Cells
  • Changes most obvious in (White Matter & Basal Ganglia)
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34
Q

Herpes Simplex Encephalitis: MC type in Adults & Neonates

A

Adults: HSV-1 Infection
Neonates: HSV-2

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35
Q

Herpes Simplex Encephalitis: Produced Pathologies, MC Location & Treatment

A
  • Produces: Hemorrhagic Necrotizing Encephalitis
  • MC Location: Temporal Lobes & Frontal Orbital Areas
  • Treatment: Acyclovir (reduces mortality)
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36
Q

Herpes Simplex Encephalitis: Histology

A
  • Perivascular Infiltrates
  • Glial Nodules
  • Inclusion bodies in the nuclei of affected Neurons
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37
Q

Cytomegalovirus Encephalitis: Population Affected & Area of the Brain Affected)

A
  • Neonates & Immunocompromised Individuals
  • Affects Ependyma (may affect any brain area)
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38
Q

Cytomegalovirus Encephalitis: Histology

A
  • Perivascular Infiltrates
  • Glial Nodules
  • Enlarged Neurons with obvious Intranuclear Inclusions
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39
Q

Progressive Multifocal Leukoencephalopathy: Population Affected & Produced Pathologies

A
  • AIDS or Immunocompromised Individuals
  • Acute, rapidly progressive illness with Multifocal Cerebral Dysfunction
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40
Q

Progressive Multifocal Leukoencephalopathy: Cause & Tissue Affected

A
  • Cause: JC Virus (in the papovavirus group)
  • Affects Oligodendrocytes Production in areas of Demyelination
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41
Q

What are the Acute Disseminated Encephalomyelitis Diseases? (Definition)

A

Monophasic Demyelinating Disease that follows a Viral Illness or in Immunization for a Virus

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42
Q

Acute Disseminated Encephalomyelitis: Preceding Viruses

A

1) Measles
2) Chicken Pox
3) Rubella

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43
Q

Acute Disseminated Encephalomyelitis: Preceding Immunizations

A

1) Smallpox
2) Rabies
3) Pertussis

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44
Q

Acute Disseminated Encephalomyelitis: Symptoms

A
  • Occur 1 week following illness
  • Longer if following an Immunization
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45
Q

Subacute Sclerosing Panencephalitis: Definition

A

Slowly progressing Dementia that Occurs a few years after a child has had Measles
(Chronic Measles Infection)

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46
Q

Subacute Sclerosing Panencephalitis: Histology

A
  • Degeneration (Brain) Gray Matter & Basal Ganglia
  • Intranuclear Inclusions seen in Infected Cells
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47
Q

Subacute Sclerosing Panencephalitis: Symptoms

A
  • Personality Changes
  • Myoclonic Type Movements
  • Death in 1-2 Years
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48
Q

Poliomyelitis: Etiological Agent Transmission

A

(Poliovirus) that is transmitted by the fecal-oral route

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49
Q

Poliomyelitis: Internal Pathological Pathway

A
  • Multiplies in Lymphoid Tissues of Oropharynx & Intestine for 2 Weeks
  • Then goes into Blood Stream & Causes Flu-Like Illness
  • Virus then gets into the Meninges producing Acute Lymphocytic Meningitis
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50
Q

Poliomyelitis: Cells Affected

A

[In small % of Individuals]
- Involves the Lower Motor Neurons in the Anterior Horn
- Motor Nuclei of the Medulla

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51
Q

Poliomyelitis: How is the Spinal Cord Affected?

A

Spinal Cord: Asymmetric and Flaccid Paralysis with Muscle Atrophy & Loss of Deep Tendon Reflexes

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52
Q

Poliomyelitis: How is the Medulla Affected?

A

Can be involvement of the muscles for Respiration producing Problems with Ventilation

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53
Q

Poliomyelitis: Long-Term Effects

A
  • Surviving patients have varying degrees of Paralysis
  • Some required assisted Ventilation
  • Post-Polio Syndrome in Long-Term Survivors
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54
Q

Polio Immunizations

A

Injected vaccine > Oral Vaccine
[due to issues of Polio Infections caused by the Oral Vaccine

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55
Q

Rabies: Definition, Prognosis, Incubation Period

A

Definition: Viral disease (rare in humans) but common in animals, both Wild & Domestic
Prognosis: Death is inevitable (no treatment)
Incubation: 1-6 months depending on site of bite

56
Q

How does Rabies enter the body?

A

Enters the Cutaneous Nerve Radicals at the site of Innoculation & travels to the CNS

57
Q

Rabies: Causes what?

A

Severe, Necrotizing Encephalitis

58
Q

Rabies affects what areas of the Brain?

A

1) Brain Stem
2) Basal Ganglia
3) Hippocampus

59
Q

Rabies: Dx & Clinical Features

A

Dx: Negri Body
Clinical: Fever, generalized Convulsios precipitated by Sensory Stimulation

60
Q

Rabies: Prevention

A

1) Controlling Disease in Animal population
2) Vaccination of Dogs & Cats
3) Antirabies Vaccine (humans) immediately after exposure

61
Q

Prion Encephalopathies (Spongiform Encephalopathies): General facts

A

**”Proteinaceous Infectious Particles”
- “slow virus disease”
- Produced ONLY by Protein Agents
- Similar Diseases:
1) Scrapie in Sheep
2) Mad Cow in Cows

62
Q

Prion Encephalopathies (Spongiform Encephalopathies): Histology

A

1) Progressive Neuronal Loss
2) Demyelination
3) Spongiform change in cerebral White Matter

63
Q

Prion Encephalopathies (Spongiform Encephalopathies): 2 Major Diseases

A

1) Creutzfeld-Jakob Disease
2) Kuru

64
Q

Prion Encephalopathies (Spongiform Encephalopathies): Clinical Features

A

Dementia followed by Ataxia followed slowly by Death (No Treatment Known)

65
Q

Prion Encephalopathies (Spongiform Encephalopathies): Transmission Risks

A

1) Through Handling Tissues
(Disease is resistant to Formalin)
2) By Corneal Transplant
3) Pituitary Growth Hormone Extract

66
Q

Demyelinating Congenital Diseases of the CNS

A

1) Metachromatic Leukodystrophy
2) Adrenoleukodystrophy

67
Q

Demyelinating Acquired Diseases of the CNS

A

1) Multiple Sclerosis
2) Acute Disseminated Encephalomyelitis

68
Q

Demyelinating Congenital Diseases of the CNS: Features

A

1) Intrinsic disorder interferes with maintenance of Myelin
2) Genetic Defects
3) Manifests in Early Childhood
4) Progresses Relentlessly
5) Widespread/Symmetric loss of Myelin
6) Brain usually Atrophic

69
Q

Metachromatic Leukodystrophy: Inheritance & What is it?

A
  • Autosomal Recessive
  • Abnormal gene on Chromosome 22
  • Accumulation of Sulfate containing Lipids
70
Q

Metachromatic Leukodystrophy: Symptoms of Late Infantile & Late Juvenile Form

A
  • Motor Symptoms
  • Progressive Disability that leads to Death 5-10 years from Onset of Condition
71
Q

Metachromatic Leukodystrophy: Microscopy Features

A
  • Demyelination with Gliosis
  • Metachromatic with Toluidine Blue
72
Q

Adrenoleukodystrophy: Different Forms

A

[many with different inheritance]
- Some Autosomal recessive
- Some X-Linked Recessive (MC)

73
Q

Adrenoleukodystrophy: Presentation & Progression

A

Presentation:
Early school years with Neurological symptoms & Adrenal Deficiency

Progression:
Rapid & Fatal

74
Q

What is a Defining Characteristic of Adrenoleukodystrophy?

A

Very-Long-Chain-Fatty-Acids
(Why it affects myelin is unknown)

75
Q

Multiple Sclerosis: MC What? Characteristic Lesion/ How many lesions & what they produce?

A

1) MC Aquired Demyelinating CNS Disease
2) Characteristic Lesion=Plaque of Demyelination
3) Multiple CNS Lesions producing focal neurological signs/symptoms

76
Q

Multiple Sclerosis: Geographical Distribution

A
  • MC in climates close to Equator
  • Scandinavia being the Highest
  • Northern Europe 2nd
  • Lowest in the Tropics
77
Q

Multiple Sclerosis: Etiology

A

Unknown

78
Q

Multiple Sclerosis: Associations

A
  • Familial Distribution
  • HLA-DR2 Antigens
  • (Postulated) is associated w/ Measles
79
Q

Multiple Sclerosis: Risk

A

If a person moves from high-risk to low-risk area under the age of 15 (low-risk)

If a person moves after the age of 15 ( high-risk)

80
Q

Multiple Sclerosis: Immune Factors

A

1) Perivascular cuffing of Lymphocytes & Macrophages found in Plaques
2) CDa4+ and CD8+ (cytotoxic) Lymphocytes found in plaques that are destructive to Myelin In-Vitro
3) CSF has increased Gamma Globulins which show increased antibody production int he CNS

81
Q

Multiple Sclerosis: Incidence

A

1) 1:1000 of the population
2) Onset is 20-40 years (any age possible)
3) Earlier the onset = Worse the Disease is
4) 2:1 Female

82
Q

Multiple Sclerosis: Pathology

A

1) Plaques of Demyelination
2) Proliferation of Astrocytes
3) Oligodendrocytes are lost

83
Q

Multiple Sclerosis: Clinical Features

A
  • Chronic w/ Exacerbations & Remissions
  • Lesions occur anywhere, but Optic Neuritis is most common (Unilateral Vision Loss)
84
Q

Multiple Sclerosis: Where does it Affect?

A

Cerebellum, Spinal Cord, Brainstem
(random distribution)

85
Q

Multiple Sclerosis: Produces what?

A

Multitude of neurological deficits over the course of many years

86
Q

Acute Disseminated Encephalomyelitis: Pathology

A
  • Small Foci of Demyelination of White Matter (Brain & Spinal Cord)
  • Lymphocytic Infiltration
  • Lymphocytes that react against Myelin-Basic-Protein are present
87
Q

Acute Disseminated Encephalomyelitis: Clinical Features

A
  • Headache, lethargy & Coma
    (After initial infection or immunization)
88
Q

Acute Disseminated Encephalomyelitis: Prognosis

A
  • 20% Mortality rate
  • Survivors recover slowly over next few months
  • Many have permanent neurological Deficits
89
Q

When does Meningovascular Syphilis Occur? Infection Location and What does it eventually produce?

A

3 Years following infection
Chronic Inflammation involving Meninges -> Producing Cranial nerve Palsies

90
Q

Other term for Poliomyelitis

A

Picornaviridae-RNA

91
Q

Parasitic Infections

A

1) Toxoplasmosis
- Toxoplasma gondii
2) Primary Amoebic Memingocephalopathy
- Naegleria Fowleri (brain-eating amoeba)

92
Q

Brain Abscess: Cause & Location

A

Cause: Blood borne pathogens, Local sinus infections, or direct trauma

Location: Frontal (sinus), Temporal (ear), Parietal (blood)

93
Q

Brain Abcess: Internal Reprocusions

A
  • Liquefactive Necrosis within days
  • Increased ICP
  • Ventricular Seeding, Tonsilar Herniation
94
Q

Brain Abscess: Prognosis

A

100% Fatal without Excision and Chemo

95
Q

Pernicious Anemia: What is it?

A
  • Autoimmune (chronic atrophic gastritis)
  • Leads to lack of intrinsic factor
  • Leads to decreased B12 absorption
96
Q

Pernicious Anemia: Megaloblastic Macrocytic Anemia

A

Subacute combined Degeneration of spinal cord due to demyelination of both tracts
(Sensory & motor)

97
Q

Alzheimer Disease: Features

A
  • Beta-Amyloid Plaques
  • Neuritic (senile) Plaques
  • Granulovascuolar Degeneration
  • Neurofibrillary Tangle
  • Neuronal Loss
  • Lipofusion
  • Astrogliosis
98
Q

Huntington’s Disease: What is it?

A

Enlargement of the Frontal Horns of the Lateral Ventricles of the Brain

99
Q

Tay-Sachs Disease

A

** Cherry red spot in Macula of Eye
- Caused by Deficiency in Beta hexosaminidase A (HEX A)
- Baloon swelling of Nerve Cells

100
Q

Niemann-Pick Disease: Features

A

Kayser-Fleischer Rings (in the eye iris)

101
Q

Wernicke-Korsakoff Syndrome: Features

A
  • Thiamin (B1) deficiency
  • Alcohol Abuse
  • Change in Mental Status
  • Ophthalmoplegia
102
Q

Phenylketonuria

A
  • Musty Body Odor

Phenylalanine -> (PAH) -> Tyrosine
NADH -> (DHPR) -> NAD
Tetrahydrobiopterin -> (PAH) -> Dihydrobiopterin
Dihydrobiopterin -> (DHPR) -> Tetrahydrobiopterin

103
Q

Tuberculous Meningitis: Transmission & Bacteria

A
  • Droplet Inhalation -> Lungs -> Lymph Nodes
  • Mycobacterium Tuberculosis Bacilli
104
Q

CNS TB: Froms

A

1) Tuberculous Meningitis
2) Intracranial Tuberculoma
3) Spinal Tuberculous Arachnoiditis

105
Q

Mycobacterium Tuberculosis Bacilli form:

A
  • Small Subpial/Supependymal Foci of Metastatic Caseous Lesions
  • Progression: Foci enlarge & rupture into subarachnoid space resulting in Meningitis
106
Q

Fungal Encephalitis: Migration Route

A

Into Parenchyma of brain through BBB

107
Q

Fungal Encephalitis: Fungal Species most Pathogenic to Humans

A

Cryptococcus Neoformas

108
Q

Spinocerebellar Degeneration: General Information

A
  • Absense of voluntary muscle control (cerebellum)
  • Autosomal Dominant
  • Gene Affected: AXTN1
109
Q

Spinocerebral Degeneration: Friedreich Ataxia: Areas Affected, Symptoms, What Protein is Affected?

A
  • Spinal Cord, Peripheral nerves, Cerebellum & Heart
  • Muscle weakness & Ataxia, balance/coordination
  • Protein: Frataxin (diminished energy for cells)
    (Iron builds up in the mitochondria)
110
Q

Amyotrophic Lateral Sclerosis (ALS): Pathological Features

A
  • Loss of PYRAMIDAL BETZ CELLS in Ventral Horns of Spinal Cord (motor nuclei & motor cortex)
  • Axonal swelling containing disarrayed neurofillaments
111
Q

Wilson Disease: What is it, Mode of Inheritance & Gene mutated:

A
  • Copper accumulation in the hepatocytes (basal ganglia, cornea & kidneys) -> increased iron
  • Autosomal Recessive
  • ATP7B Mutation (copper transporting ATPase)
112
Q

Hepatic Encephalopathy: Definition

A

Neurocognitive Abnormalities that occur in patients with Acute or Chronic Liver Disease or Portosystemic Shunting

113
Q

Gene AXTN1 does:

A

Provides instructions for making Ataxin-1 protein

114
Q

Amyotrophic Lateral Sclerosis (ALS): Intracellular Aggregates

A
  • Ubiquinated Inclusions
  • Bubina bodies
  • Hyaline Conglomerate
115
Q

Amyotrophic Lateral Sclerosis (ALS): CNS cells activated

A

Microglia & Astrocytes

116
Q

Amyotrophic Lateral Sclerosis (ALS): Genes Associated & Gene Function

A

1) TDP-43
2) FUS
(Function in DNA/RNA processing mechanisms)

117
Q

Hepatic Encephalopathy: Histologic Hallmark

A

Alzheimer Type II astrocyte: enlarged, pale nuclei with rim of chromatin

118
Q

Hepatic Encephalopathy: Lab findings

A

Elevated Blood Ammonia

119
Q

Hepatic Encephalopathy: Epidemiology

A
  • Chronic Alcoholism
  • Acute drop poisoning
  • Hepatic failure
  • Post Portosystemic Bypass
120
Q

Hepatic Encephalopathy: Pathological Cells Found

A

1) Ammonia
2) Inflammatory Cytokines
3) Manganese Deposition in Basal ganglia
4) GABA
5) Microbiota
6) Aromatic Amino Acids

121
Q

Acute Hepatic Encephalopathy: Cause

A

Brain edema caused by swelling of Perivascular Astrocytes

122
Q

Hepatic Encephalopathy: CNS Tissues Affected

A

1) Globes Pallidus
2) Putamen
3) Pons
4) Thalamus
5)Dentate Nucleus
6) Cortical GRAY MATTER (Deep Layers)

123
Q

Concussion: Pathological Features

A
  • Bruising/ Swelling of the Brain
  • Tearing of Blood Vessels
  • Injury to Nerves
124
Q

Concussion: Physical Signs

A

1) Loss of Conciousness
2) Balance Impairment
3) Behavior Changes
4) Slow Reaction Times
5) Sleep Disturbances

125
Q

Concussion: Symptoms

A

Somatic: Headache, Dizziness
Cognitive: “In a Fog”
Emotional: Labillity (unstable)

126
Q

At what point does Post-Concussion Syndrome Occur?

A

When Symptoms persist for longer than 7-10 Days

127
Q

Tertiary Neurosyphilis: Clinical Features

A
  • Gummatous Lesions (Soft Granuloma usually in the liver)
  • Exclusively Neuro Symptoms
  • Develops 10-25 years after infection
128
Q

Tertiary Neurosyphilis: Organs Affected

A
  • Brain Nerves
  • Eyes
  • Heart & Blood Vessels
  • Liver
  • Bones & Joints
129
Q

List of Cerebrovascular Diseases

A

1) Cerebral Vascular Accidents
2) Global/Regional Ischemic Infarction
3) Subarachnoid/Intracerebral Hemorrhage
4) Aneurysm
5) AV Malformations

130
Q

List of MC [Meningitis] Infections of the Nervous System

A

1) Bacterial / Suppurative
2) Neurosyphilis
3) Granulomatous (Tuberculosis)
4) Viral

131
Q

List of MC [Encephalitis] Infections of the Nervous System

A

1) Fungal
2) Viral
3) St. Louis
4) HIV
5) Herpes Simplex
6) Progressive Multifocal Leukoencephalopathy
7) Subacute Sclerosing Panencephalitis (SSPE)
8) Prion Encephalopathies

132
Q

List of Nervous System Demyelinating Disorders

A

1) MLD
2) MS
3) ALD
4) PML
5) Post Infectious Encephalomyelitis
6) Pernicious Anemia

133
Q

List of Inherited Metabolic Nervous System Disorders

A

1) Phenylketonuria
2) Tay-Sachs
3) Niemann-Pick
4) Wilson

134
Q

List of Acquired Metabolic Nervous System Diseases

A

1) Wernicke-Korsakoff
2) Hepatic Encephalopathy
3) Subacute Combined Degen. of the Spinal Cord

135
Q

Tuberculosis may produce

A

Granuloma on the Meningeal Surfaces

Systems Pathology (6 decks)

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