Toxic/Metabolic and Degenerative Diseases Flashcards
(63 cards)
1
Q
intoxication
A
exposure to organic and inorganic compounds: pesticides, heavy metals, plants, microbial products
2
Q
deficiency
A
inadequate levels of minerals, vitamins, metabolites, etc
3
Q
peracute to acute neurologic signs
A
headpressing, ataxia, disorientation, motor deficits, recumbency, tonic-clonic seizures, partial seizures
4
Q
T/F: age is a generalized feature of neurologic issues
A
FALSE: age is NOT a generalized feature. certain toxins/deficiencies do express predilections
5
Q
outbreaks of neuro deficits
A
- commonly a herd health or household issue
- individual exposure is also relatively common
6
Q
how do neuro issues often present grossly?
A
BILATERAL AND SYMMETRIC !!
7
Q
are gross lesions of neuro issues often generalized or specific?
A
SPECIFIC anatomic areas, cell types of the CNS.
- vascular geography
- concentration of receptors
patterns and features can often clue into a diagnosis: can be difficult to definitively diagnose
8
Q
what are the 3 major patterns of toxic/metabolic neuro diseases?
A
- malacia: common pathway: +/- hemorrhage
- selective necrosis: neurons, axons, myelin
- spongiform state (status spongiosis): irregular cavities within the neuropil secondary to neuronal loss
9
Q
what is the major common pathway of toxic/metabolic issues?
A
malacia: +/- hemorrhage
10
Q
what is the spongiform state?
A
status spongiosis: irregular cavities within the neuropil secondary to neuronal loss
11
Q
what are the 3 big malacic diseases?
A
- polioencephalomalacia
- leukoencephalomalacia
- encephalomalacia
12
Q
what are the polioencephalomalacia diseases?
A
- polioencephalomalacia of ruminants
- salt toxicity (water deprivation encephalopathy) of pigs
- thiamine (B1) deficiency of carnivores
- equine nigropallidal encephalomalacia (yellow star thistle poisoning)
13
Q
what is the leukoencephalomalacia disease?
A
equine leukoencephalomalacia: moldy corn disease
14
Q
what is the encephalomalacia disease?
A
focal symmetric encephalomalacia: overeating disease
15
Q
polioencephalomalacia in large animals
A
- cerebrocortical necrosis (CCN)
- cerebral cortex: basal/thalamic nuclei, colliculi and cerebellar cortex (less common)
- diagnosis of PEM is almost exclusively postmortem
16
Q
what are the etiologies of polioencephalomalacia in large animals?
A
- sulfur toxicity
- thiamine deficiency
- water deprivation encephalopathy
- lead toxicity
17
Q
diagnosis of polioencephalomalacia is almost exclusively
A
postmortem
18
Q
sulfur toxicity
A
- sulfur ingested in excess: feed or water or contamination
- rumen microbes produce excess Hydrogen Sulfide (H2S) : accumulates in ruminal gas cap, accumulate in ruminal fluid and diffuse across rumen wall
- H2S decreases mitochondrial respiration!! inhibition of cytochrome oxidases (which decrease GLU production)
- brain has high demand for O2, GLU, energy metabolites = neuronal dysfunction, degeneration and necrosis
19
Q
how does hydrogen sulfide affect the brain?
A
- sulfur ingestion in excess: rumen microbes produce excess H2S (hydrogen sulfide) = accumulates in ruminal fluid and diffuse across the rumen wall
- H2S decreases mitochondrial respiration!!!
20
Q
H2S decreases/increases mitochondrial respiration
A
decreases!! inhibition of cytochrome oxidases: within mitochondria = decreases GLU production
21
Q
what part of the body produces excess hydrogen sulfide?
A
rumen microbes
22
Q
how does hydrogen sulfide affect mitochondrial respiration?
A
inhibits cytochrome oxidases
23
Q
what causes thiamin deficiency?
A
- high carbohydrate diets lead to overgrowth of thiaminase producing bacteria: Clostridium sporogenes, Bacillus thiaminolyticus
- grazing of thiaminase-containing plants (Bracken fern, Nardoo)
- Amprolium: coccidiostat
24
Q
what are thiaminase containing plants?
A
Bracken Fern, Nardoo
25
why is thamin deficiency bad?
- Vitamin B1: crucial cofactor for GLU metabolism and glial-neuronal membrane interactions
- ruminal microbes produce thiamin, and balance out microbes
- imbalances can lead to increased lactate and subsequent ruminal acidosis!!
- insufficient thiamin = neuronal dysfunction, degeneration and necrosis
26
insufficient thiamin =
neuronal dysfunction, degeneration and necrosis
27
what are gross findings of PEM in ruminants?
less distinct sulci, multifocal to coalescing yellow foci (necrosis), cerebellar hemorrhage = herniation, flattened gyri
28
what is the *classic* finding with PEM
deep laminar necrosis resulting in perisulci cystic cavities
degeneration/loss of neurons in the deep lamina of the grey matter: "band like" pattern
29
what diagnostic can be used to detect PEM?
wood's lamp/UV: neurons release pigments when they are damaged, and macrophages come to "eat" them and the pigments fluoresce in the macrophages
30
histologic findings of PEM
- spongy change = emedatmous
- neuronal necrosis: BAND-LIKE PSEUDO LAMINAR!!
- gliosis
- vascular proliferation
- infiltration of macrophages with phagocytic ability: "gitter cells"
31
how is thiamin deficiency similar/different in carnivores?
- similar in pathogenesis/presentation to thiamine deficiency of PEM in ruminants
- carnivores are dependent on DIETARY intake of thiamin
- topography and nature of the lesions are DIFFERENT
- ***caudal colliculi, medial vestibular nuclei and lateral geniculate bodies***
- often hemorrhagic
32
where are lesions of thiamin deficiency in carnivores found?
caudal colliculi, medial vestibular nuclei and lateral geniculate bodies
often hemorrhagic
33
how do carnivores become thiamin deficient?
starvation (cats)
raw fish
thiamin inactivation: commercial dog foods incorrect measurements?
34
what is Chastek's Paralysis?
thiamin deficiency in farmed mink and foxes
35
water deprivation encephalopathies
- salt poisoning, water intoxication
- PEM/CCN lesions
- pigs fed a high salt ration!!
- occurs in other animals as a result of water deprivation: environment, broken water pipes, frozen water, neglect
- revolves around osmotic gradients between blood stream and CNS
36
what species is salt toxicity most common in?
pigs
37
what is the pathogenesis of salt toxicity?
- water intake restriction in pigs being fed a high salt diet
- blood becomes HYPERNATREMIC
- following an osmotic gradient, fluid from the brain moves into vessels
- brain becomes dehydrated
- equilibrium of NaCl between plasma and extracellular space of CNS is SLOW
38
what happens when pigs being fed a high salt diet get given water?
blood becomes hypotonic in comparison to the brain
- excess fluid from blood now moves into the dehydrated brain
- development of PEM unclear but hypothesized to be secondary to compression, anoxia
39
what histologic findings are pathognomonic for salt toxicity?
perivascular infiltrate of eosinophils
40
water toxicity
- PEM/CCN
- excess water consumption following deprivation
- hemodilution and then hyponatremic blood: following osmotic gradient, intravascular fluid moves into the brain
- similar necropsy findings to salt toxicity
- eosinophilic perivascular infiltrates are NOT a feature on histology!
41
T/F: eosinophilic perivascular infiltrates are common histologic findings in salt toxicity and water toxicity
false- just salt toxicity. the are not a feature in water toxicity
42
lead toxicity
- PEM/CCN
- occurs in any animal: young, birds/carnivores
- oxidative stress leads to erythrocytic and vascular damage: anemia
- can occur with other heavy metals, zinc, mercury, manganese
43
lead toxicity causes
young: milk substitutes, paint, plumbing, batteries, crankcase oil
birds/carnivores: lead shot, fishing sinkers, coins, secondary poisoning
44
ingestion of yellow star thistle or Russian knapweed causes what problem in what species?
equine nigropallidalencephalomalacia
- dry summer pastures, chronic exposure, acute onset of disease
- REPIN is the suspected toxic compond
45
what is the suspected toxic compound of yellow star thistle and russian knapweed?
repin
46
what plants cause equine nigropallidalencephalomalacia?
yellow star thistle or russian knapweed
47
what signs are seen with equine nigropallidalencephalomalacia?
abnormal tongue movement, difficulty with prehension, swallowing, drinking
48
what gross/histologic lesions are seen with equine nigropallidalencephalomalacia?
- bilaterally symmetrical malacia of substantia nigra and globus pallidius
- conscious proprioception and movement ^
- pseudolaminar necrosis is NOT a feature!!
49
T/F: pseudolaminar necrosis is also a common feature of equine nigropallidalencephalomalacia
FALSE. it is NOT a feature
50
equine leukoencephalomalacia
- mycotoxic leukoencephalomalacia: "moldy corn disease"
- fatal neurological disorder with sudden clinical onset: chronic exposure
- ingestion of mold corn contaminated with Fusarium moniliforme: FUMONINSIN B1 is the bad part
51
moldy corn disease
equine leukoencephalomalacia
Fusarium moniliforme contaminated corn
Fumoninsin B1!
52
what is the toxic component of moldy corn disease?
Fumoninsin B1
53
pathogenesis of moldy corn disease/equine leukoencephalomalacia
- ingestion of moldy corn contaminated with Fusarium moniliforme
- Fumoninsin B1: vascular damage selectively in the white matter with secondary encephalomalacia
- bilateral, ASYMMETRICAL, centrum semiovale, corona radiata
- may also cause concurrent hepatic necrosis
54
general characteristics of degenerative diseases
- selective degeneration and loss of cells or cell components
- bilaterally symmetric
- individual animals
55
is degenerative disease bilateral or unilateral?
bilaterally symmetric
56
clinical presentation of degenerative diseases
- younger animals/early age of onset
- slow clinical progression, depends on parts affected
- many genetic origin or breed predilections
- poor understanding of pathogenesis
- no standardized terminology: classified by main cellular target
57
lesions of degenerative diseases are almost always
bilateral, symmetric of restricted to a cell type/structure
58
if you suspect a degenerative condition, what is absolutely necessary to get?
an adequate history!
59
major patterns of degenerative disease
- loss of neurons, axons and/or myelin
- pallor of white matter
- spongy state
- intracellular storage: most easily recognizable, accumulation of abnormal material
- malacia
60
neuroaxonal dystrophy
- axonopathies with prominent axonal swelling
- axonal changes start at preterminal portion of axons and in synaptic terminals
- dystrophic axons mostly seen in nuclei of grey matter, secondary neuronal injury
- equine degenerative myeloencephalopathy
61
pathogenesis of equine degenerative myeloencephalopathy
- occurs sporadically in many breeds: appaloosa, standardbred, Paso Fino, Lusitano, Zebras
- hereditary defect that predisposes to pathology related to environmental or nutritional factors
- VITAMIN E DEFICIENCY
- onset around 6 months
- chronic, progressive and irreversible
- ataxia and tetraparesis
62
what nutritional deficiency has been demonstrated in equine degenerative myeloencephalopathy?
vitamin E
63
differentials for equine degenerative myeloencephalopathy
- equine motor neuron disease: similar older horses, brainstem degeneration
- wobbler syndrome: cervical stenotic myelopathy: restricted to site of compression
