Path 2 - Neuro 4

drraythe's version from 2016-03-07 17:41

Circulatory disturbances continued

Question Answer
What are the sequelae to cerebral edema?↑ intracerebral pressure → life threatening
What are some etiologies of LOCALIZED cerebral edema? (In essence & specifics)In essence, SOLs (Space occupying lesions):
Focal necrosis
What are the lesions you'd see in a LOCALIZED cerebral edema?The brain is swollen, soft, depressed & moist appearance on cut surface, there will be faint yellow discoloration, displacement & distortion of the brain (depending on the localization of the lesion)
How can you detect localized edema in the brain?detected by assessing the symmetry of the brain (whole or when sectioned fixation)
What are some etiologies of GENERALIZED cerebral edema (in essence & specifics)SYSTEMIC CONDITIONS:
Diffuse meningitis
Diffuse viral encephalitis
Heartwater (Ehrlichia ruminatum)
Acute bacterial toxemias
Chemical intoxications (lead acid organomercurials)
CCN (Cerebrocortical necrosis, aka Polioencephalomalacia) of cattle & sheep
What are the 2 types of cerebral edema?Intracellular (cytotoxic) & vasogenic
Which cells help control fluid movements across vascular compartments & nerve parenchyma?Astrocytes
Explain what is going on in intracellular or cytotoxic edema (brain swelling) (what czs this? what is the pathogenesis?)This is due to direct cellular injury & damage to osmoregulation (effect of reduced levels of ATP on the sodium-potassium pump), so swelling is due to accumulation of fluid in the astrocytes, oligodendrocytes, neurons, endothelial cells. This czs nuclear & cytoplasmic swelling & accumulation of glycogen granules
Which parts of the brain are affected by intracellular or cytotoxic edema (brain swelling)? What does the brain/cut surface look like?This affects the Grey & White matter are both affected. The brain looks swollen & turgid. It is NOT moist on cut surface
Explain what is going on in vasogenic edema (what czs this? which part of the brain is especially affected?)Usually czd by acute inflammation >> ↑ in vascular permeability. BC of the ↑ permeability, there is extracellular accumulation of fluid due to vascular damage. This also results in leakage of plasma & protein into the interstitial tissue (esp. white matter)
What is the macroscopic appearance of a cerebral edema which is recent & severe?Brain is swollen, pale, soft & wet. The hemispheres droop over the edges of cut bone of the cranium prior to the removal of the brain from the cranium
What is the macroscopic appearance of a cerebral edema which is severe & of long duration?Gyri are flattened, sulci are shallow & there is displacement due to ↑ in volume
If there is displacement of the brain (which type of cerebral edema do you see this in?) how can you tell the diff/describe btwn a MODERATE displacement & a severe compression?(Displacement happens in severe, long-duration edema) In the MODERATE DISPLACEMENT you will see posterior surface of the cerebellar hemispheres are compressed & depressed. In SEVERE COMPRESSION, you will see medulla oblongata & the posterior portion of cerebellum (the vermis) herniate through the foramen magnum ['lipping' of the cerebellum]
What are the problems that happen bc of a severe compression of the brain? (3)(1) Lipping in → obstruction of the flow of CSF through the foramina in the roof of the 4th ventricle → internal hydrocephalus
(2) Cerebrum → impaction on the tentorium (tent.=an extension of the dura mater that separates the cerebellum from the inferior portion of the occipital lobes.)
(3) Brain stem → compression ±hemorrhages
What is the Macroscopic appearance of a cerebral edema which is less severe but long duration?Brain is relatively firm & dry. Gyri are pale, have a faint yellowish color. Displacement caudally. Brain appears elongated.
Macroscopic appearance of cerebral edema in all cases of cerebral edema-what do the nerves look like? What is blood flow like? What blood-related problem MIGHT form?The nerves may be stretched & flattered, blood flow is inhibited & there may or may not be thrombosis of the superficial sagittal sinus
Thromboembolism → septicemia can cz thromboembolisms. Give 5 examples of things that can cz this (& a species if it's species specific)Erysipelas in pigs
Sleepy foal dz
Pasteurellosis in ruminants & pigs
Haemophilus spp (bact)
Coliforms (bact)
Thromboembolism → what are 2 common thromboses in cats?Atrial & aortic thrombosis in cats
When would bone marrow cz a thromboembolism which can cz a circ. disturbance in the brain?During fractures
Which condition related to the spinal canal in dogs can possibly cz a thromboembolism to create circulatory disturbances in the CNS?Cartilaginous or nucleus pulposus in dogs
*Can you have an embolism INSIDE a spinal disc?NO!


Question Answer
**Inflammation of the dura mater is?Pachymeningitis
*Inflammation of the pia-arachnoid is?Leptomeningitis
*Inflammation of the choroid (plexus in the ventricles of the brain where cerebrospinal fluid (CSF) is produced) is?Choroiditis
Inflammation of the ependyma (the thin epithelium-like lining of the ventricular system of the brain & the central canal of the spinal cord) is?Ependymitis
Inflammation of the brain is?Encephalitis
Inflammation of the spinal cord is?Myelitis
Inflammation of the brain & spinal cordis?Encephalomyelitis
If the exudate from an inflammatory brain is suppurative, what is the causative agent & what is this called? What will you see?Bacterial infxns >> Septic meningoencephalitis. (You’ll see abscessation, neutrophils)
***If the exudate from an inflammatory brain is nonsuppurative, what is the causative agent? What will you see?VIRAL INFXNS!
Neuronal degeneration
Perivascular cuffing by mononuclear cells (Lymphocytes, Plasma Cells, Macrophages)
Gliosis & Demyelination in the white matter
Lympho(+/- plasma)cytic Meningitis
Inclusion bodies (Nuclear (CDV) & Cytoplasmic(Rabies) )
***Demyelination & NUCLEAR Inclusion Bodies in Canine Distemper*(**
Granulomatous exudates would be due to what 2 causative agents?Higher bacteria, mycotic infxns
*Thrombotic meningoencephalitis (TME) → what czs this? What is this dz characterized by? (CS)Czd by a BACTERIAL infxn → Histophilus somni infxn. It is an acute infectious dz, primarily affecting the CNS that is characterized by fever, depression, weakness, ataxia, blindness, polyarthritis, coma & death. Oftentimes peracute & CS may not be observed
***Thrombotic meningoencephalitis (TME) → (once again, what czs this?) What are the gross lesions? What are the microscopic lesions?(Histophilus somni. Produces septicemia as well)
Grossly: the most characteristic lesions are single or multiple hemorrhagic foci (infarcts) located in any part of the brain. However, gross lesions may be found in many organs & tissues (heart, kidneys, etc.).
Microscopically:**characteristic lesion is VASCULITIS w/ THROMBOSIS & septic infarction in the brain as well as in other organs. In less acute cases, the dz is characterized by signs referable to the septicemia & the polyarthritis (Histophilus somnieeeee)
Listeriosis → what is this czd by?Sporadic BACTERIAL infxn, czd by Listeria monocytogenes
INFECTIOUS MENINGOENCEPHALITIS vs IDIOPATHIC INFLAMMATORY BRAIN DISORDERS. Which 1 of these do cats get, which do dogs get?Cats = infectious
Dogs = idiopathic
How does Listeriosis manifest in Adult Rumis?Encephalitis or meningoencephalitis
*How does Listeriosis manifest in young ruminants & monogastric animals?Septicemia w/ focal hepatic necrosis (Listerine soaks from your blood (septic) to your brain stem)
How does Listeriosis manifest in fowl?Septicemia & myocardial degeneration or focal hepatic necrosis
What 2 bad things can happen in all pregnant susceptible mammals from Listeriosis?Abortion & prenatal infxn
**Listerial encephalitis occurs chiefly in who? How does the bacteria get in & what does it do from there?Mainly affects ADULT RUMIS. Ingestion of organisms >> organisms survive & multiply in phagocytic host cells >> infxn of monocytes, macrophages, PMNs
***What are the gross lesions for Listeriosis?Gross lesions are usually not observed in the brain; however, occasionally grayish foci of malacia may be found in cross sections of the medulla. Listeria has an affinity for the BRAIN STEM & lesions are most severe in the **MEDULLA & PONS**. There is evidence that infxn reaches the brain by passing along cranial nerves ascending infxn (especially the trigeminal) ((LISTERINE WILL SOAK UP INTO YOUR BRAIN STEM)
**What are the microscopic lesions for Listeriosis? (Whats the 1° microscopic lesion?)Microscopically, the 1° lesion is circumscribed collections of MONONUCLEAR CELLS, w/ or w/o neutrophils, in close proximity to blood vessels. Well-defined microabscesses may occur, but they are most common I `sheep
Enterotoxemia due to Clostridium perfringens type D → which kind of encephalopathy does this cz? Who does this usually affect & when do the brain lesions occur?Focal Symmetrical Encephalomalacia [FSE]. In sheep (lambs) that survive the acute form of enterotoxemia type D, brain lesions may occur.
*The lesions from Enterotoxemia due to Clostridium perfringens type D are of 2 morphologic patterns. What do both patterns have in common & how are they different?Both patterns are bilaterally symmetrical
(1) The more common pattern is hemorrhage & softening of the basal ganglia (caudate nuclei, putamen, Globus pallidus, subthalamic nuclei), internal capsule, dorsal lateral thalamus & substantia nigra\
(2) The 2nd pattern is characterized by lysis & liquefaction of the white matter of the frontal gyri, which spares only the common "U" fibers (connections btwn adjacent gyri are U-shaped which run in the white matter just beneath the lowest layers of cortex); the overlying gray matter is edematous
What is the pathogenesis of Enterotoxemia due to Clostridium perfringens type D (start w/ what kinda toxin it is, end w/ necrosis) & what is a feature of the dz in lambs (not brain related)Pathogenesis: epsilon toxin → vascular injury → ↑ vascular permeability → edema → hypoxia-ischemia → necrosis. Glucosuria is a feature of the Dz in lambs
Edema Dz (enterotoxemic colibacillosis) of pigs . What kinda pathogen czs this? How does it cz CNS necrosis?E. coli infxn → toxin (Shiga-like) production → angiopathy → vasculitis → edema, hypoxia-ischemia → bilaterally symmetrical foci of malacia/necrosis (brainstem) (Edema Ecoli)
What are the CS of Edema Dz (enterotoxemic colibacillosis) of pigs?Incoordination
Hindlimb paralysis
Tremors, convulsions
What type of response does the CNS usually have to viruses?NON suppurative & NON specific
Histological changes associated w/ viral infxns in the CNS → perivascular cuffing. WHAT KINDA CELLS are doing this w/ a VIRAL infxn? What can result from perivascular cuffing?MONONUCLEAR CELLS (lymphocytes, plasma cells & macrophages) do the cuffing in viral infxns. Thrombosis is rare & damage to the vascular wall & endothelium only occurs in certain Dzs, however large infiltrates may cz compression of vessels & ischemia. (These rxns are non-specific & may also be czd by malacia & immunological rxns)
**Histological changes associated w/ viral infxns (non-suppurative) in the CNS incld: (5 things)Perivascular cuffing (monocytes)
Neuronal degeneration, gliosis
Demyelination (Canine Distemper)
Inclusion bodies (Rabies, Canine Distemper, Herpesvirus)
Demyelination is characteristic for which viral dz?CANINE DISTEMPER (Paramyxo-fyi)
Parasitic dzs → Cerebral nematodiasis: what kinda damage does this parasitic infxn cz?Hemorrhage, malacia, migratory tracts, space-occupying cysts
Cerebral nematodiasis → Baylisascaris procyonis (definitive hosts? how/when does this cz CNS destruction?)Definitive hosts:
Raccoon (raccoon roundworm)
Larvae → blood → nervous tissue → destructive lesions (malacia, inflammation)
What are 6 parasitic dzs of the CNS?Cerebral nematodiasis
Oestrus ovis
Hypoderma bovis
Cuterebra spp (Feline ischemic encephalopathy)
Cestodes (Larval stage: Cysticercus)
Protozoa (Sarcocystosis, Toxoplasmosis, Neosporosis)
Hypoderma bovis does what in who?Larval migrans in spinal cord in cattle
***Cuterebra spp → what dz does this cz in who?(Larval migration into the brain via vasculature of dogs & CATS) → Feline Ischemic Encephalopathy - Hemorrhage, Thrombosis, Vasculitis