Path 2 - Neuro

drraythe's version from 2016-03-07 18:24

Do 'em backwards!

*Cross-referenced w/ Muzzy's review!*

Quick & Dirty Neuro Review

Question Answer
**What lesion is both CONGENITAL & ACQUIRED hydroencephalus have? Major difference?BOTH = LAT VENTRICULAR DISTENTION!! Congenital will have an ENLARGED CRANIUM & acquired will NOT
**HYDRANENCEPHALY vs PORENCEPHALY → which is MORE SEVERE? What is the major defect in hydra, what is the major defect in poren?HYDRA IS WAY MORE SEVERE - ABSENCE OF CEREBRAL HEMISPHERES
POREN is CYSTS (white matter defect)
**Which viruses cz cerebellar hypoplasia?Feline panleukopenia
BVD in cattle
Herpesvirus in dogs
**What samples to you send off to Dx prion dzs w/ Histopathy???Lesions in the brain stem >> obex. Variant forms may be seen in: olfactory bulb, cerebral cortex, hippocampus (associated w/ amyloid plaques)
**Explain Dx of prion dzs via Immunohistochemistry. Where do you take samples from? (Not post mortem)Dx via detection of prion protein. Lymphoid tissue of the 3rd eyelid in live sheep w/ scrapie
**ABIOTROPHY is WHAT KIND of defect? (& happens bc of?)1° metabolic defect/degen due to premature programmed cell loss (APOPTOSIS). Which czs a Loss of Purkinje cells
*Moldy corn has what toxin, which czs what in who?Fumonisin B1, mycotoxicosis (focal necrosis of cerebreal hemispheres), Leukoencephalomalacia in the Horse
**Know the vascular, hypoxic, toxin, infectious & nutritional czs of necrosis (& possible type of necrosis they cz)Toxins are:
Yellow star thistle (Nigropallidal malacia)
Pb, Na, Cl, Se (Poliomyelomalacia) (Lead Posioning in Cattle = CCN)
Moldy corn (Leukoencephalomalacia)
***Clostridium perfringens D czs what in who?Focal Symmetrical Encephalomalacia (FSE) in SHEEP
**LAMINAR CORTICAL NECROSIS → aka (2 aka) & this occurs why?Aka “cerebrocortical necrosis” (CCN), “polioencephalomalacia” – specific layer. Softening of the cerebrocortical grey matter in a laminar (layered) pattern based on susceptibility of cells to hypoxia
**Lead poisoning-chronic (cattle) → CCN, POLIO OR BOTH?“Cerebrocortical necrosis” (CCN), (You're gonna get a lead bullet, C?)
**Salt poisoning (pigs) → CCN, POLIO OR BOTH?POLIO (Black Himalayan salt) Softening in a specific layer cerebrocortical GREY matter
**Se poisoning-acute (pig) → CCN, POLIO OR BOTH?BILATERAL POLIO (Se casts on BOTH legs bc pig polio)
**Thiamine depletion/def (Rumi/Cat) → CCN, POLIO OR BOTH?BOTH
**Cell Susceptibility to Laminar Cortical Necrosis (most to least)"NOAM" Neurons > Oligodendrocytes > Astrocytes > Microglia
*EDEMA LEADS TO WHAT MAJOR PROBLEM?↑ INTRACRANIAL PRESSURE (from inflam, hypoxia, ischemia, toxins)
***If the exudate from an inflam. brain is nonsuppurative, what is the causative agent? What will you see?VIRAL INFXNS!
Neuronal degen
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***
*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. septicemia!!)
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. The MAIN LESION IS SEPTICEMIC THROMBI & the polyarthritis (Histophilus somnieeeee)
**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 cellsinfxn 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 TRI TO 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 in sheep
**Cuterebra spp → what dz does this cz in who?(Larval migration to the brain via vasculature of dogs & CATS) → Feline Ischemic Encephalopathy - Hemorrhage, Thrombosis, Vasculitis
***TME - THROMBOTIC MENINGOENCEPHALITIS → CZD BY WHAt? MAJOR LESION? What do you see grossly?Histophilus somni, Major lesion = Septic Infarct (Thrombosis) (histo made me want to damage blood vessels)
Grossly: The most characteristic lesion are single or multiple hemorrhagic foci (septic thrombosis) located in any part of the brain &/orin organs & tissues
***Listeriosis has an affinity for WHERE & what is the major lesion?Affinity for BRAINSTEM (medulla+pons), will see a circumscribed collections of MONONUCLEAR CELLS (1(MONO) swish of Listerine will get the MONO out of your brain stem)
***Viral histological changes → vascular rxn to viral infxn is? Neuronal change? White matter change? Meningeal change? Inclusion body types?Vascular = Perivascular cuffing (of MONONUCLEAR cells (Lymphocytes, plasma cells, macrophages) )
Neuronal = Neuronal degen
White matter = DEMYELINATION
Meninges = Lympho (+/-plasma) cytic meningitis
Inclusion bodies: Intranuc = canine distemper & Rabies
Cytoplasm: Rabies
***FELINE ISCHEMIC ENCEPHALOPATHY is czd by what? What are the 3 major VASCULAR signs?Cuterebra!
***In RUMIs: "Polioencephalomalacia" or Central Cortical Necrosis (CCN)" affects WHICH part of the brain & what is the etiology?CEREBRAL CORTEX, BRACKEN FERN & HORSETAIL
*Which part of the horse's brain is damaged from eating corn? (Fumosin B1)WHITE MATTER!! FOCAL NECROSIS of the CEREBRAL HEMISPHERES
**#1 most common CNS tumor of DOG+CATMENINGIOMA
**What does a meningioma grossly look like?WELL CIRCUMSCRIBED & encapsulated, w/ STREAMS & WHORLS
**Most common glial tumor?Astrocytoma
***CONTREcoup means dmg where?Opposite side of the point of injury
**MENINGIOMA#1 MOST COMMON 1° tumor of dog + cat
*Hansen Type I vs Type II disk deformities(I) Acute rupture, multiple discs involved, early degen, younger age, Chondroystrophoid breeds
(II) Gradual rupture, less disc involved, older age, all breeds
**What is Syringomyelia? How common is it? Who does it usually occur in?Tubular cavitation (cavities) (syrinx) of the spinal cord extending over several segments. Rare, except in the Weimaraners
**Acquired hydrocephalus → which type of hydro. Is this usually (internal, external or communicating)? What is causing this? How does it appear?Seen most commonly as an internal hydrocephalus. It is a progressive condition. There is obstruction of flow due to an accumulation of & organization of exudate, but no malformation of the cranium!
*Lysosomal storage Dzs (LSDs) → in essence, what is happening to cz this storage dz?(Normally, lysosomes perform catabolic activities by degrading stuff not needed anymore) Hydrolytic enzyme is absent or inoperational → catabolic degradation of the substrate interrupted → accumulates w/in the lysosomes= "storage dz"
*Prion Dzs → Transmissible spongiform encephalopathies (TSE's): are these Dzs inflammatory? Are they transmissible?NO, but ARE transmissible!
*What are 3 major lesions of prion DZs (TSEs)(1) Spongiform change of the neuropil (broad term defined as any area in the nervous system composed of mostly unmyelinated axons, dendrites & glial cell processes that forms a synaptically dense region containing a relatively low number of cell bodies.)
(2) Neuronal degen, apoptosis & loss >> prominent cytoplasmic vacuoles
(3) Astrocytosis (mild to severe)
*What is Abiotrophy? What is it NOT?This is PRIMARY premature neuronal degen. IT ISNT 2° (which would mean it happened bc of a toxin or infectious agent)
*Abiotrophy → 1° neuronal degen may have 2 different patterns of involvement. What are they?(1) Restricted to the cerebellar cortex
(2) Involve connected neural systems
*FOCAL lesions → explain this pattern of lesions. What are the 4 situations where you see a focal pattern of necrosis?Necrosis in selective areas in the CNS. Usually due to a specific toxin/nutritional def.
(1) FSE (Focal Symmetrical Encephalomalacia) in sheep (Clostridium perfringens D)
(2) Eequine Leukoencephalomalacia (moldy corn dz)
(3) Equine Nigropallidal Encephalomalacia (Yellow star thistle toxicity)
(4) Avian Encephalomalacia (Hypovitaminosis E)
(D CORN is STAR E...lets FOCUS on it)
**NaCl toxicity czs what kinda necrosis in who?Laminar necrosis + eosinophilic ME (meningoencephalitis); pig (poliomyelomalacia) (Pigs are allergic to salt & allergic to watching CNN)
*Leukomalacia?White matter necrosis
*Poliomalacia?Gray matter necrosis
*Encephalomalacia?Brain as a whole necrosis
*Myelomalacia?Spinal cord necrosis
*Yellow Star Thistle czs what in who?Nigropallidal malacia; horse (BLACK & YELLOW HORSES)
*Pb poisoning czs what in who?Laminar necrosis; cattle/horse/dog
*Se poisoning czs what in who?Poliomyelomalacia; pig (a pig w/ a selenium cast bc it had polio)
*NaCl poisoning czs what in who?Laminar necrosis + eosinophilic ME; Pig
*The lesions from Enterotoxemia due to C. 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
*How does Listeriosis manifest in young rumis & mono animals?Septicemia w/ focal hepatic necrosis (Listerine soaks from your blood (septic) to your brain stem)
**Inflam of the dura mater is?Pachymeningitis
*Inflam of the pia-arachnoid is?Leptomeningitis
*Inflam of the choroid (plexus in the ventricles of the brain where cerebrospinal fluid (CSF) is produced) is?Choroiditis
*Can you have an embolism INSIDE a spinal disc?NO!
**Salt (NaCl) poisoning in swine → what are the microscopic lesions from this & what is the PATHOGNOMIC LESION?Microscopically: Eosinophilic Meningoencephalitis (eosinophils in the meninges & around blood vessels), encephalomalacia & laminar necrosis. The "pathognomonic" lesion is: eosinophils+laminar necrosis = salt poisoning
**Eosinophils+laminar necrosis =?SALT POISONING
*Describe the salt poisoning of swine, the symptom of convulsions are characteristic in pattern & regularity?Tremors of the snout
Rapidly extend as colonic spasms of the neck muscles w/ jerky opisthotonus → pig walks backward & sits down
**Salt toxicosis-aka? Who is most affected by this?Aka Water Deprivation Syndrome, swine & sheep.
*GROSS lesions of Yellow Star Thistle tox? Microscopic?GROSS: Sharply demarcated foci of yellow discoloration & malacia
Microscopically: Necrosis w/ loss of neurons, axons, glia & blood vessels, influx of macrophages
**If the signs of Cu def have a delayed onset up to 6mo, what is it called? Who does it usually happen in? What do these lesions look like & where are they?Enzootic ataxia in lambs & kids. They grey & white matter will both be affected & you will see chromatolysis, neuronal necrosis, degen of myelinated axons
**What CS would you see in a Thiamine (B1) def?Anorexia
Convulsions (responsive to thiamine Tx)
Coma (irreversible)
**What do the brain lesions look like in a Thiamine (B1) def? (general)Edema
Perivascular dilation
BILATERALLY SYMMETRICAL Necrosis (Periventricular Gray Matter)**!
*Acute lead poisoning in CATTLE czs dead in how much time? What are the CS in calves? Adults?Death in 12-24 hours. In CALVES you will see: staggering, muscular tremors, recumbency, convulsions, death ADULTS you will see: Head pressing, blindness, convulsions, death
*Cholesteatosis (cholesteatoma) → what is this? What is this not? WHO gets this?Degen of the choroid plexus (plexus in the ventricles of the brain where cerebrospinal fluid (CSF) is produced). IT IS not a true neoplasm!!!! It occurs in OLD HORSES. GRANULOMATOUS INFLAMMATION w/ CHOLESTEROL CRYSTALS
*Osseous metaplasia of the dura (Pachymeningitis ossificans) → whats happening?Formation of bony plaques in the cranial or spinal dura (the plaques often contain marrow & may appear WHITE & RED)
**Hansen Type I vs Hansen Type II disk deformities(I) Acute rupture, multiple disc involved, early degen, younger age, Chondroystrophoid breeds
(II) Gradual rupture, less disc involved, older age, all breeds
*What is happening w/ the brain, what hits the head & the energy that happens from this in a CONTRECOUP lesionMoving head hits a stationary object (usually the ground). There will be a coup injury at the point of impact & then energy dissipation at the beginning or end of the head motion → contrecoup injury opposite the point of impact due to movement of the brain w/in the head
**Glial tumors: Major diffs btwn astrocytomas & Oligodendroglioma?ASRO: COMMON, POORLY DEMARCATED