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62 Cards in this Set
- Front
- Back
how often is CSF exchanged? what is CSF glucose compared with blood?
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every 3-4 hrs
CSF glucose is 2/3 of blood's. |
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where is the infection located in a patient with meningitis?
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the subarachnoid space
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what is encephalities? myelitis?
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e: inflammation of brain
m: inflammatin of spinal cord |
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where is a subdural empyema located?
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it's an infection between dura mater and arachnoid
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where is an epidural abscess located?
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it's a localized infection between the dura mater and overlying skull or vertebral column.
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how can antibiotic therapy aggravate an infection of the brain? what is the significance of the pH?
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it may lyse cells and release immunogenic cell wall components and allow for a more vigorous immune response.
an altered pH in infected tissues may INACTIVATE antibiotics. |
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what is a normal serum/CSF antibody ratio? what immune components are present in CSF?
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800:1
small # of lymphocytes NO plasma or PMNs. NO complement. |
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what is the primary site of breach in the BBB during inflammation? what can cause a breach?
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microvascular endothelium.
a breach may be caused by bacterial components activating macrophages to secrete cytokines in the SUBARACHNOID space. |
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what components are able to enter the CSF during inflammation of the BBB?
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serum proteins
polymorphonuclear leukocytes plasma cells T-lymphocytes antibiotics *antibody production may occur* |
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what are some possible routes of infection of the CNS?
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hematogenous via extracranial foci or retrograde propagation of infected thrombi within emmissary veins.
neurotropic (viruses) bone injury surgery congenital problems otitis sinusitis |
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what are some symptoms of acute bacterial meningitis? where does the infection occur and how does it get there?
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fever, stiff neck, coma
organisms enter subarachnoid space, infection is blood borne and crosses the vascular endothelium or choroid plexus. |
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where does bacterial meningitis often colonize before entering brain? what types of cells is it found within?
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the organisms often enter the subarachnoid space AFTER nasopharyngeal colonization.
they are found within circulating monocytes. |
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how can bacterial meningitis be acquired thru extension?
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otitis media
paranasal sinusitis |
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describe the pathogenenesis of bacterial meningitis.
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1.organisms multiply within the subarachnoid space.
2.cell wall components accumulate in CSF and are inflammatory. 3.migration of neutrophils. 4.loosen BBB 5.cerebral edema 6.obstruct flow of CSF to blood 7.increased ICP |
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what is haemophilus influenzae?
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1.gram - rod, requires X & V
2.transmitted via respiration 3.antiphag capsule 4.1/3 survivors - deaf 5.usual spread hematogenously 6.fimbriae mediate attachment |
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what are predisposing factors to haemophilus influenzae? what vaccine is available?
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predisposed via pharyngitis or otitis media.
Hib conjugate vaccine at 2 months. |
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what is streptococcus pneumoniae?
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a gram + diplococcus
optichin positive antiphag capsule transported via receptors cause pneumonia, otitis media MOST FREQUENT CAUSE OF MENINGITIS IN ADULTS AND KIDS UNDER 5!! |
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what often causes the meningitis associated with s.pneumonia? what is another common factor?
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bacteremia causes the meningitis. often follows a head wound.
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what bacteria are associated with bacterial meningitis?
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h.influenza
s.pneumonia n.meningitidis l.monocytogenes s.agalactiae |
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what aerobic gram - bacteria are associated with bacterial meningitis?
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e.coli
klebsiella serratia marcescens |
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what is n.meningitidis?
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a g-diplococcus
oxidase + antiphag capsule (c, b & y) dz in young, overcrowd, fatigue. epidemic late winter, early spring. |
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what is characterisitic about the meningitis caused by n.meningiditis?
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1.adherence to endothelium of choroid plexus and meninges.
2. DIC is COD 3.11-20% survivors suffer neurologic disability and hearing loss. |
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describe l.monocytogenes
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g+ motile rod
usually food borne pregnant/immunocompromised are predisposed. |
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what is streptococcus agalactiae?
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GBS
found in vagina, rectum cause meningitis, pneumonia, sepsis in newborn. |
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what type of aerobic gram- bacilli is especially likely to cause meningitis?
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e.coli, K1 capsular type gram- rod from perineal flora of mother.
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what defines chronic meningitis?
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neuro signs progress
CSF remains abnormal for at least 4 weeks. MORE RARE than acute causes: m.tuberculosis brucellosis syphilis lyme dz |
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what bacteria cause chronic meningitis?
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m.tuberculosis
brucellosis syphilis lyme dz |
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what is a brain abscess? where is it often from?
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it's a focal infection in the brain, often mixed.
spread from contiguous source (otitis media, mastoiditis, sinusitis, dental trauma, penetrating trauma). |
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what are some common etiological factors for a brain abscess?
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streptococci
bacteroides staph aureus RARELY gram- rods toxoplama gondii (HIV) |
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what is an epidural abscess? a subdural empyma?
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epi ab: lesion has created space between dura mater and skull
sub emp: leasion has created space btwn dura mater and arachnoid |
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what are the most common causes of intracranial epidural abscesses and subdural empyemas?
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aerobic and anaerobic strep
s.aureus anaerobes g- rods |
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what is characteristic of a spinal epidural abscess or subdural empyema?
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1.fills actual space within spine.
2.extension of osteomylitis or paravertebral infection. 3.hematogenous spread. |
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what is the etiology of spinal abscess/subdural empyema?
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s.aureus
aerobic/anaerobic strep g- bacilli organisms from distant sepsis. |
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how do viruses invade the CNS?
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1.directly across cerebral capillary endothelial cells
2.directly infect cerebral microvasculature endothelial cells before infection of adjacent glia and neurons. 3.traverse choroid plexus epithelium, disperse virus in CSF with resultant contact of meningeal cells. 4.carried btwn cerebral endothelial cells in infected immune cells after BBB disruption. |
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most viruses infect the CNS via ________ except for _____ and _______.
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hematogenous spread
herpes rabies |
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how does herpes infect the CNS?
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rxn with trigeminal ganglion
de novo infection olfactory nerve |
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how does rabies enter the CNS?
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via retrograde movement within neurons.
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what is aseptic meningitis? how severe is it?
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it's an inflammation of the meninges, choroid plexus. no etiological agent identified from gram stain/CSF.
this is a MILD form |
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describe fatal viral encephalitis.
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an inflammatory rxn: meninges and perivascular distribution.
neural cells show degenerative changes, phag of neurons via macrophages. giant cells + viral antigens present. |
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what class does enterovirus belong to?
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it's a picornovirus, +ss, unenveloped.
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what is considered the leading cause of aseptic meningitis? what are some characteristics?
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enterovirus:
1.summer/fall 2.fecal-oral 3.resist stomach acid, disinfectant. 4.kids 5.echovirus, coxsackievirus |
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what cell types does poliomyelitis effect? HSV?
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pm: motor neurons on anterior horn cells of spinal cord and brain stem.
hsv: cells of temporal lobes |
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describe poliomyelitis.
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the virus multiplies in neurons on ant. horn of cord and stem and kills them. can be excreted by the vaccinated. IPV recommended to prevent VAPP.
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what is post-polio syndrome?
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25-35 yrs post-recovery gradual progression of muscle weakness.
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what type of virus is mumps? describe it.
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large ss-RNA virus
respiratory spread late winter/spring 16-18 day incubation orchiditis symptomatic meningitis 4-6% encephalitis rare |
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what types of viruses require an extrinsic incubation period?
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arboviruses.
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name 6 arboviruses.
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1.togavirus (small, enveloped +ssRNA)
2.east/west/venez equine encephalitis. mosquito-birds-human. 3.flavivirus (small, enveloped +ssRNA) 4.st.louis encephalitis 5.west nile 6.bunyavirus (enveloped -ssRNA w.segments) |
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describe colorado tick fever virus.
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1.reovirus
2.ds RNA, segmented, capsid. 3.w and nw US 4.infects erythroid precursor cells (phag protection) 5.neonatal infxn can lead to meningitis or enceph. 6.usually benign, some nuchal rigidity and pleocytosis. |
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what type of virus is herpes?
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large ds DNA, enveloped. characterized by latency. type I infects 95% of population.
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what is common in HSV I?
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1.most common nonepidemic fatal encephalitis.
2.spread via infected secretions (oral). 3.primary: virus goes up local sensory nerve and is latent in ganglia. 4.enceph can be primary or not. |
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what type of virus is rabies?
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rhabdovirus (bullet shaped)
-ssRNA with lipoprotein sensitive to heat and drying |
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what is the pathogenesis of rabies?
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1.bite implants infected saliva in mm near n.
2.multiplies (10-240 days) 3.to CNS 4.replicates in nuerons of gray matter, makes cytoplasmic inclusion bodies(negri) 5.centrifugal migration to organs/tissue. |
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what are some manifestations of rabies?
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1.prodromal-nonspecific.
2.anxiety, eye problems 3. paralytic, coma death. |
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is the rabies vaccine enough if someone is suspected of having a bite?
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NO, also give human rabies immunoglobin.
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what are some unusual neuro outcomes of viral illness?
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postinfection encephalomyelitis
experimental autoimmune encephalomyelitis subacute sclerosing panencephalitis progressive rubella panencephalitis guillain-barre syndrome |
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what characterizes postinfectious encephalomyelitis?
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1.short time lag
2.perivenular inflammation, demyelination (rxn to myelin of brain, spinal cord and optic nerve). |
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what are some causes of postinfectious encephalomyelitis?
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varicella
mumps vaccinia measles *now commonly seen after nonspecific URI* |
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what is experimental autoimmune encephalomyelitis?
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animal immunized with MBP, PLP, adjuvant. get enceph characterized by perivascular infiltrates, demyelination of brain and spinal cord. neuro lesions can be mild or chronic.
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what is SSPE?
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caused by MEASLES.
occurs YEARS later, most common in those infected with measles pre-2yrs. more common in males. onset is insidious, early dementia. disturbed motor & seizures later. death 1-3 yrs. |
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what is the pathogenesis of SSPE?
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it's a variant measles virus with less/no matrix protein, fusion protein and hemaglutin. mature virus particles are not produced.
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what are some characteristics of progressive rubella panencephalitis?
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RARE.
pr- raised in CSF (IgG) more common after CONGENITAL rubella. |
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what is gullain-barre syndrome?
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acute inflammatory demyelinating polyradiculonueropathy.
associated with virusy resp or GI illness. occurs 1-4 wks after infection due to sensitization to periperal nerve myelin ascending motor weakness 85% recover (up to 6 months) MOST FREQUENT: acute severe generalized human paralytic dz in US |