• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/39

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

39 Cards in this Set

  • Front
  • Back
Prions (3 types of illnesses)
Sporadic - No family hx
Genetic - Disease is in the genome and will occur in all generations of family.
Infectious - Individual exposed to infectious material in someone else's CNS.
Prions - General
No cell or DNA associated. Creates a subacute disease (progression over months)

The abnormal protein has notation PrP^(sc) - normal is PrP^c (and this one is normal in the CNS)

Prions can't replicate, but the abnormal prion can induce normal prions to be abnormal and gradual aggregation causes severe damage.
Types of prion diseases
Kuru
Creutzfeldt-Jakob Disease
New Variant CJD (AKA mad cow disease)
Gerstmann-Straussler
Scrapie...
Histo features of prion diseases
SPONGIFORM CHANGE (bubbles)

extensive neuronal loss, gliosis, kuru-like plaques, white matter changes
If you see plaques with spongiform, you must think...
new variant Creutzfeldt-Jakob disease!
Virus - general
Acute, rapidly progressive, serious and life-threatening.
Herpes encephalitis
Virus

Prefers temporal lobe - causes necrosis and edema.

Onset is quick and it can be grave.
Histo characteristics of viruses
Lymphocytes and macrophages diffusely through neuropil (inflammation)

Perivascular lymphocyte cuffs

Microglial nodules AKA neuronophagia (site where a neuron has died and has been eaten by microglial cells)

Inclusion bodies - In the nuclei there are big red things that push chromatin against the side of the nuclear membrane.
Acute poliomyelitis
Virus

Infects grey matter of spinal cord (motor neurons) - anterior horn area.
HIV-1
Mainlty affect immune system, and then CNS.

Non-transforming retrovirus of lentivirus family.

dsRNA
How is CNS affected by HIV-1
Macrophages carrying virus get to CNS within a week or two of primary infection. These secrete cytokines to damage the parenchyma and form nodules histologically (perivascular).

HAART (Highly active antiretroviral therapy) doesn't get to CNS that well so these pts die of a disease similar to Alzheimers.

Can progress to HIV encephalitis and the pt will die.

Will also see perivascular giant cells.
4 CNS opportunistic infections seen in HIV immunodeficiency
Toxoplasma gondii cerebral abscess/encephalitis

Cryptococcal meningitis or disseminated cryptococosis

Progressive multifocal leukoencephalopathy

B-cell lymphoma (cerebral or disseminated)
CNS lymphoma
Common with AIDS pts

Anaplastic B cells in parenchyma of brain.
Progresive multifocal leukocencephalopathy (PML)
Due to JC virus. Common in immunosupp (HIV)

Extensive oligodendo-->myelin loss.

Small demyelinating foci

Develops to an encephalopathic state and the pt drifts into coma and dies.

Oligos look huge, lose fried-egg appearance.

Won't have inflamm bc pt is immunosupp.
Toxoplasmosis
Intracellular parasite - not a virus.
Associated with AIDS and cats.

Cats play a role in spreading infection.

Pregnant women are in danger.

Hemorrhagic lesions. They replicate in cells, make them burst, and then go to other cells.

Can form toxoplasma pseduocyst - these are multiple organisms of the replicating toxoplasma in one cell.
Bacteria CNS - 3 main categories
Empyema

Meningitis

Abscess
Empyema
Collection of pus in a POTENTIAL space. Not in the tissue proper (this would be an abscess)

e.g. subdural
Bacterial meningitis - agents affecting infants (0-2 months)
E. Coli, Group B strep, Listeria
Bacterial meningitis - agents affecting 2 months - 5 years
Hemophlus, pneumococcus, meningococcus, m. tuberculosis

***"My Harry's Potty Trained
Bacterial meningitis - agents affecting > 5 years
Pneumococcus, meningococcus, m. tuberculosis

**Those my pencils!
(starting school)
Bacterial meningitis - agents affecting elderly
Listeria, hemophilus, pneumococcus, m. tuberculosis.

***Lavern and hokie potty train
Pus in neonatal meningitis
Creamy and white. May block CSF outflow.
Adult bacterial meningitis - general features
Pus along vessels over surface of the brain (this is the subarachnoid space)

Infection stays in subarachnoid space and neutrophils come in and secrete things to cause BV dilatation and edema.

Can cause infarcts or hydrocephalus
Latest stage bacterial meningitis
Pts if cured, may come back with big infarct bc the antigens of dead bacteria were in csf of subarachnoid space causing complement to be fixed and vasculitis.
Post meningitis hydrocephalus
Massively dilated ventricles bc scarring closes off CSF exit sites.
M. Tuberculosis
Can cause 1. diffuse BASAL meningitis (not rapidly progressive) or 2. localized tuberculoma (fibrotic mass).

typically, but not always, you will get one or the other.
Diffuse BASAL meningitis from tuberculosis
This is a fibrosing process in the brain stem that goes down to the spinal cord.
Localized tuberculoma
Fibrotic mass - causes granulomatous inflammation where fibroblasts lay down collagen and entrap BVs to cause infarctions.
Brain abscess
Presents like tumor.
Induces swelling (after rupture especially) and fibrosis (one of the few things that deposits collagen in the brain parenchyma).

Often due to staph or strep.

The rim on the outside of these abscesses in collagen.
Typical pattern of brain abscesses
Neutrophils - macrophages - b cells/plasma cells - necrosis - fibroblasts.
Abscess rupture into ventricular system
Will get REALLY bad edema
Candida
Yeast/fungi

Common only in immunosupp.

Necrotizing, non-hemorrhagic. Ischemic.

Can form fungus balls (colonies) in the brain parenchyma.

Minimal inflammation and yeast/pseudohyphal forms exist together.
Cyyptococcus
Yeast/fungi

Smoldering meningitis that progresses very slowly.

Common in non-immunosupp.

Produces large jelly-like masses, small ischemic lesions.

No hyphal form - all yeast.

India ink.
Aspergillosis
Very grave. Ubiquitious in soil.

In immunosupp only.

Comes to CNS from BVs of lungs and causes emboli in CNS. As it is wedged in small BVs, it proliferates then the hyphae kill surrounding tissue and eat it as food.
Histologically seen as hyphae branching at 45 degrees
Think aspergillus.
Mucormycosis
Closely related to aspergillus. Their hyphae look similar.

Common in diabetics. No good tx.

Usually directly spreads from infected sinus to inferior surface of frontal lobe.
Coccidioidomycosis
Fungi/yeast

In dry arid areas (SW USA)

Seen in immunosupp. Can produce a nasty meningitis.

Found in soil. Parasitic cycle in resp tract.

Cold-like sx before progressing to meningitis.

Better seen with silver stain.
Coccidioidomycosis - Meningitis presentation
Entrapped BVs, fibrosis and vasomeningitis in meninges.

Hard to tx bc not dividing rapidly and their presence stimulates macrophages.

Chronic disease.
Cysticercosis
Infestation with larval form of a tape worm.

If humans eat undercooked pork and then get fecal-oral contamination, the cysticerci may move to brain or muscles.

Growing disease bc more population from central/south america.

Causes large cysts.

TYPICALLY DON'T CAUSE PROBLEMS UNTIL THE ORGANISM DIES BECAUSE THIS IS WHEN IMMUNE SYSTEM BEGINS TO ATTACK IT.

Tx - excise and surgery.