Reading...
Play button
Play button
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;
29 Cards in this Set
- Front
- Back
|
Encephalitis vs Meningoencephalitis
|
Encephalitis: inflammation of brain parenchyma
Meningoencephalitis: inflammation of brain parenchyma AND meninges |
|
|
What is myelitis?
|
Inflammation of SC tissue
|
|
|
Examples of suppurative space-occupying lesions?
|
suppurative = pus
Any sort of abscess (brain, epidural, spinal) Subdural empyema |
|
|
Examples of postinfectious inflammatory lesions? Relevance to CNS infections?
|
Examples:
Guillain-Barre Postinfectious encephalomyelitis All may mimic infection! |
|
|
Leptomeninges vs Parameninges
|
Leptomeninges: pia + arachnoid mater
Parameninges: dura mater |
|
|
What does the BBB do?
|
Serves as:
1) Barrier to microorganisms 2) Impedes passage of humoral and cellular immune system components into CSF 3) Reduces penetration of many antimicrobial drugs; thus, reducing the effectiveness of tx |
|
|
Describe the hematogenous route of CNS infection.
|
Nasopharyngeal colonization of bacteria evade nasociliary clearance and secretory IgA (many bact injure nasopharyngeal cell, bind non-ciliated cells; produce IgA proteases)
Invasion of nasopharyngeal epithilium Some may gain entry at sites where BBB is less restrictive (lack of tight jns, ex: choroid plexus-->direct access to CSF-->ependymal cells lining ventricles-->periventricular brain tissue) Evade cmplement via polysaccharide capsule Some viruses directly infect endothelial cells |
|
|
Examples of bacteria/viruses that take hematogenous route.
|
Meningococcus (pili-facilitate endocytosis)
H. flu B (creates separations between epithelial cells) |
|
|
Provide three examples of bacteria/viruses that take the neural route. Describe mechanism of entry.
|
Rabies: enters axons of peripheral nerves and travels via axoplasmic ransport to reach cell bodies in sensory ganglia and SC
HSV: travels from nerves in oropharynx/genital area to infect CN V or sacral ganglia where virus becomes latent in sensory neurons Herpes, arboviruses, N. fowleri (freshwater amoeba) enter olfactory nerve endings |
|
|
What is contiguous spread? Examples?
|
Adjacent focus infects CNS (sinusitis, otitis media, rupture of nearby brain abscess)
|
|
|
What is direct inoculation? Example?
|
Introduction of foreign bacteria which colonize and infect; ex: skull fracture, ventricular shunts, meningomyelocoele, dermal sinuses
|
|
|
Why does the CNS exhibit local immunodeficiency?
|
Complement levels low in CSF
No immunoglobulins, thus, no opsonization CSF fluid less able to clear bacteria (cannot mediate phagocytosis) |
|
|
What immunologic surveillance does the CNS utilize? Mediators of inflammation? Effects of inflammation?
|
Microglial Cells (derived from monocytes)
Lymphlike system: Virchow-Robin spaces (sheaths surrounding BV's as they enter brain and contain macs and lymphocytes) IL-1, TNF, IL-6 Inflammation results in: -Increased permeability of BBB -Vasogenic edema (separation of intercellular tight jns) -Cerebrocortical hypoperfusion (loss of autoreguln) -Increased intracranial P |
|
|
What are the pathological findings of inflammation?
|
Exudates in subarachnoid spaces
Narrowing of large arteries due to P from exudate Vasculitis of small vessels Infection, localized bleeding/throbosis in dural sinuses Neutrophils degenerate, removed by macs |
|
|
How do fibrinopurulent exudates lead to brain herniation?
|
Exudates impede absorption of CSF-->Cerebral edema-->focal neurologic defects-->brain herniation
|
|
|
What is asceptic meningitis? Subtypes? Examples?
|
Asceptic meningitis = meningeal inflammation sans bacterial cultures (infection)
Infectious subtype: Viruses (enterovirus) Mycobacteria (TB) Fungi (cryptococcus) Spirochetes (syphilis, lyme) Noninfectious: Automimmune (lupus) Sarcoid Dug Induced (NSAIDS, bactrim, IVIG) Neoplasm (tumor) |
|
|
Acute vs Subacute Infectious Meningitis
Provide examples of each. |
Acute:
Viral >> Bacteria Onset over hours to days Fever, HA, photophobia, stiff neck Altered mental state Ex: S. Pneumonia > N. meningococcus > Group B Strep; Entero virus, abrovirus, HIV Subacute: Fluctuation of syx over weeks, months, years (CHRONIC) Ex: TB, syphilis, cryptococcus, enteroviral infection |
|
|
CSF Cultures:
Bacterial vs Viral vs TB meningitis |
Bacterial: bacterial culture positive 80% of time
Viral: CSF pleocytosis (increase cell count) with lymphocyte predominance (early on may be nphil) TB: Elevated protein, low glucose with mononuclear pleocytosis |
|
|
Abnormal findings of CSF Analysis?
|
1) >10K WBC; NO NPHILS!!
2) Elevated protein 3) Low glucose (altered cerebral metabolism, not bacterial or leukocyte consumption) |
|
|
Protocol for patient suspected to have bacterial meningitis?
|
Blood cultures, lumbar puncture, THEN ANTIBX
If pt is >60 with known CNS dz/tumor, immunocompromised, seizure, etc; GET CT BEFORE LUMBAR PUNCTURE Children should also get CT prior to LP AntiBX: IV at HIGH DOSES that don't bind prots (or won't penetrate BBB well) Supportive therapy to preserve blood flow to brain (corticosteroids) |
|
|
Mechanism of corticosteroids in CNS?
|
inhibit cytokine production by CSF microglia
attenuate LPS release by lysed bacteria Decrease cerebral edema, decrease intracranial pressure, increase blood flow |
|
|
Complications of meningitis?
|
Seizures
Herniation of cerebral tissue as result of increased intracranial pressure Focal neurologic deficits (vasculitis, infarcts, necrosis) HYDROCEPHALUS (obstruction of CSF flow) |
|
|
Next step if patient suspected of having meningitis has negative cultures?
|
send viral culture and/or PCR
|
|
|
What does the presence of seizures in a patient with meningitis suggest?
|
Parenchymal involvement, CN palsies (IV, V, VII)
|
|
|
How does acute encephalitis differ in presentation from meningitis?
Etiology? |
Encephalitis: absence of normal brain fn!
Includes altered mental status, motor/sensory deficits, altered bhvr/personality changes, hallucinations, deliriuim, ataxia Etiology: viral most common; asceptic meningitis causes can also cause acute encephalitis |
|
|
What diagnostic results would confirm acute encephalitis?
|
CSF pleocytosis (lymphocytic)
CSF cultures negative usually PCR of DNA for HSVI Focal areas of inflammn on imaging (HSV--temporal lobes) Brain bx |
|
|
What is a brain abscess? Methods of infection?
Most common cause? |
Brain abscess: focal suppurative (pus) infection localized in brain parenchyma and surrounded by vascular capsule
Methods of infection: Hematogenous (gray-white jn--poor collateral circuln) Contiguous spread from otic, sinus or dental infection Direct inoculation from h ead trauma 25% cryptogenic (no source) Most common organism: strep, staph |
|
|
Phases of brain abscess formation?
|
Early cerebritis: perivascular infiltration, coagulative necrosis; edema
Late cerebritis: pus formation leads to necrotic center Capsule formation: enhances on MRI on side of cortex Late capsule formation: gliosis and reactive astrocytes |
|
|
Treatment of brain abscess?
|
Antimicrobial tx w/surgical drainage/excision
Antileptic meds Steroids ONLY if mass effect (Small abscesses--<3-4 cm--respond to antibx alone maybe) Bactericidal drugs wh ich penetrate BBB well Mannitol (diuretic) and hyperventilation to decrease intracranial pressure 6-8 weeks of antibx usually req'd |
