29.CNS pathophys Flashcards Preview

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Flashcards in 29.CNS pathophys Deck (36):

4 ventricles or fluid filled cavities in CNS

1. lateral ventricles (one within ea hemisphere)--foramina2. third ventricle (diencephalon)--mesencephalic aqueduct3. fourth ventricle (ventral to cerebellum)--lateral apertures into subarachnoid space**choroid plexus makes CSF**


3 layers of connective tissue surrounding brain and spinal cord

1. pia mater--intimate contact with parenchyma--subarachnoid space (CSF)2. arachnoid--lies in contact with outermost layer--subdural (blood vessels)3. dura mater--outer layer


epidural space

space surrounding dura in the area of the spinal cord; fat is stored hereno such space exists in the calvarium (dura is next to skull)


most common area of brain herniation

caudally--tentorium --foramen magnum


resting membrane potential of neuronal cell body

-80 mV depol w rapid Na channel influxdepol w closing Na channel and opening K channel to allow for efflux of K out


myelin characteristics

fatty, insulationproduced by oligodendrocytesallows fast rapid efficient conduction over long distancesinterrupted by nodes of ranvier which are UNmyelinated


pressure auto regulation of CNS

perfusion should remain constant despite fluctuations btwn MAP 50-160 mm Hgbrain vasodilates during hypotensionbrain vasoconstricts during hypertensionmyogenic mx of smooth muscle cells


metabolic auto regulation of CNS

astrocytes detect chemical changes--extremely sensitive to PaCO21 mm Hg change PaCO2 changes cerebral perfusion 5%sense incr PaCO2 -->vasodilation-->incr intracranial vol/P (risk herniation)sense decr PaCO2-->vasoconstriction->decr intracranial vol/P (may cause ischemic damage)


define Cushings reflex

bradycardia w hypertensionduring marked peripheral hypotension, bodies response is to vasoconstrictor but damages organs (ie. kidneys). Systemic hypertension causes reflex bradycardia


T/Fblood flow is more affected by changes in PaO2 within the physiologic range

FALSE blood flow is LESS affected by changes in PaO2 within a physiologic rangebut if PaO2 is severely low (50 mm Hg), vasodilation to increase perfusion in CNSMajority of regulation is under control of PaCO2 unless oxygenation status is severely decreased


how is cerebral blood flow determined

cerebral blood flow depends on cerebral perfusion pressure (CPP)CPP = MAP-ICP


marked peripheral hypotension may do what to cerebral perfusion pressure

reduce cerebral perfusion pressure


marked elevation in intracranial pressure may do what to cerebral perfusion pressure

reduce cerebral perfusion pressure


brain --heart syndrome

during peripheral hypotension and vasoconstriction (Cushings reflex hypertension w reflex bradycardia)sustained release of catecholamines may result in myocardial ischemia and arrhythmias (brain-heart syndrome)


normal intracranial pressures

8-15 mm Hgminimal intracranial compliance to adjust (one compensatory mx is CSF and blood flow) fig 29-3 page 376


how much does a durotomy decreases intracranial pressure

durotomy 65%craniotomy 15%


what compromises the BBB

--endothelial cell and astrocyte processes tight junctions--basal lamina--pericytes--perivascular microglia**selectively permeable: depends on size, lipophilicity, ionization


antibiotics with good penetration into CNS

--3rd generation cephalosporins--fluoroquinolones--metronidazole--sulfonamides//trimethoprim--chloramphenicolCCFMS


antibiotics that penetration BBB with inflammation present

--tetracyclines (doxy/minocycline)--erythromycin--penicillins--rifampinPERT


POOR antibiotic penetration into CNS

--1st and 2nd generation cephalosporins--aminoglycosides--clindamycin--vancomycinVCCA


T/Fthe meninges and choroid plexus do NOT have a BBB

TRUEthe meninges and choroid plexus do NOT have a BBBtherefor they can undergo inflammatory responses similar to those in peripheral tissue


immune system of CNS

immunologically privileged --complex molecules for lymphocyte activation (B7)--cell adhesion molecules--perivascular macrophages (antigen presenting cells)--microglial cells (phagocytic, resident cells)


neuronal stem cells are a type of adult stem cellwhere does neurogenesis occur within the brain

1. OLFACTORY system/subventricular zone2. dentate gyrus of the HIPPOCAMPUS


contusion leading to primary and secondary damage

(contusions more common in spinal cord due to dynamic nature)1. primary mechanical damage--in the brain contusion leads to focal and diffuse changes2. secondary injury--series of biochemical and metabolic changes causing neuronal and glial cell death which may lasts for weeks (acute hemorrhage-->multi located cavitations with apoptosis (gray matter)-->central cavitation with apoptosis (white matter), wallerian degeneration and cell death


hypothesis why GCC are avoided and potentially deleterious for patients with acute spinal cord injury

CNS response to injury is one that internally depresses lymphocyte and monocyte numbers for several days after injurythat is accompanied by endogenous release of ACTH and catecholamines which can damage distant organs "CNS injury induced immunodepression"GCC may enhance this affect and be potentially deleterious


clinical signs of compressive injury depends on...



pathological changes associated with compression injury

demyelinationvasogenic edema (favors white matter)axonal degenerationneuronal necrosiswith chronic compressions--necrosis/apoptosis of glial cells


role of oligodendrocytes

produce and maintain myelin sheath


hypothesis of worsening or clinic deterioration seen after decompressive surgery

1. mechanical insult from surgery2. reperfusion injury


Is gray matter or white matter affected more with thomboembolic disease

gray matter dz includes: FCE (nucleus pulposus), feline ischemic encephalopathy (Cuterebra vasotoxin), thrombotic "stroke", septic or neoplastic emboli


most common tumors to metastasize to the CNS



difference btwn cytotoxic and vasogenic edema

cytotoxic--intracellular fluid from failure of ion pumps from ischemic/hypoxic injury; most pronounced in astrocytesvasogenic--extracellular fluid from increased vascular permeability along white matter; like interstitial edemacytotoxic edema is best treated by alleviating inciting causevasogenic edema responds well to GCC


types of IVDD

most common cause of myelopathy in dogs1. nucleus has progressive decr in proteoglycan (dehydrates) and replaced with mineral; seen in chondrodystrophic; acute compression with tear in annulus2. nucleus dehydrates and replaced with fibrinoid tissue; chronic wear and tear of annulus with compression3. peracute type 1; low volume, high velocity' acute non compressive nucleus pulpous extrusions


T/FContusive effect, rather than compression, is probably responsible for most of the observe clinical signs after acute IVDD



T/Fneurons/axon damage is likely irreversibleoligodendrocytes/astrocyte damage can be regenerated



define hydrocephalus, hydromyelia, syringomelia

hydrocephalus--fluid accumulation in ventricleshydromyelia--fluid accumulation in spinal cordsyringomyelia--fluid within spinal cord parenchyma

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