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Objectives for NS 2: You should be able to define, describe pathogenesis, list lesions and know how to diagnose the following conditions: Cytotoxic, osmotic.

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Presentation on theme: "Objectives for NS 2: You should be able to define, describe pathogenesis, list lesions and know how to diagnose the following conditions: Cytotoxic, osmotic."— Presentation transcript:

1 Objectives for NS 2: You should be able to define, describe pathogenesis, list lesions and know how to diagnose the following conditions: Cytotoxic, osmotic and vasogenic brain edema) Thiamine-responsive polioencephalomalacia of ruminants Thiamine deficiency in carnivores Lead poisoning Salt poisoning Toxin-induced vasogenic brain edema

2 Brain swelling (cerebral edema)
Response to injury - Brain edema Brain swelling (cerebral edema) Increased intracranial pressure E. Simko WCVM

3 Blood perfusion pressure Intracranial pressure
Response to injury - Brain edema Brain swelling (edema) Blood perfusion pressure Intracranial pressure Ischemic necrosis E. Simko WCVM

4 Brain edema Cytotoxic (intracellular) Extra cellular edema Osmotic
Response to injury - Brain edema Brain edema Cytotoxic (intracellular) Extra cellular edema Osmotic Vasogenic E. Simko WCVM

5 Diagnosis: Gross: cerebellar coning (herniation) cerebral herniation
Response to injury - Brain edema Diagnosis: Gross: cerebellar coning (herniation) cerebral herniation flattened gyri Microscopically neuronal necrosis edema is not evident in most cases E. Simko WCVM

6 Polioencephalomalacia (PEM)
Thiamine-responsive PEM of ruminants Lead poisoning in ruminants Salt poisoning in pigs & occ. in rumin. Hypoxia

7 Thiamine-responsive polioencephalomalacia
Response to injury - Brain edema Cytotoxic edema (cellular degeneration) Thiamine-responsive polioencephalomalacia in ruminants Etiology Disturbance of thiamine production/absorption concentrate ruminal pH change in flora Bacterial thiaminase [sulfur, sulfates, sulfides] in diet or water E. Simko WCVM

8 Pathogenesis Cytotoxic edema - Thiamine deficiency
Thiamine interferes with glucose metabolism and Krebs cycle in CNS ATP production Na/K transport is impaired Intacellular H2O (hydropic degeneration) Cellular swelling (Cytototoxic edema) Energy exhaustion Intacranial pressure & blood perfusion Ischemic necrosis E. Simko WCVM

9 Lesions Histology Brain swelling Cytotoxic edema - Thiamine deficiency
(flattened gyri, cerebellar coning) Yellow cortical discoloration (autofluorescence under UV light) Cortical liquefaction and cavitation Histology Laminar cortical necrosis E. Simko WCVM

10 Diagnosis History Response to thiamine Gross and histologic lesions
Cytotoxic edema - Thiamine deficiency Diagnosis History Response to thiamine Gross and histologic lesions Rule out the other causes of PEM E. Simko WCVM

11 Dietary thiamine deficiency in carnivores
Cytotoxic edema - Thiamine deficiency Dietary thiamine deficiency in carnivores Dog, cat, mink (Human – Wernicke’s encephalopathy) Depend on exogenous source of vitamin Pathogenesis: diet with thiaminase, sulfur preservatives or exposed to high temperature Lesions: Symmetrical necrosis of thalamic and mid-brain nuclei E. Simko WCVM

12 Lead poisoning Brain edema Lesions: Source: Old batteries and paint
Polioencephalomalacia similar to thiamine resp. Cattle Lead shotgun pellets PNS degeneration (Esophageal/crop dilation and impaction) Waterfowl E. Simko WCVM

13 Pathogenesis in cattle
Brain edema - Lead poisoning Pathogenesis in cattle Direct endothelial injury vasogenic edema Damaged metabolism cellular swelling Energy exhaustion Increased intracranial pressure Failure of blood perfusion Ischemic necrosis E. Simko WCVM

14 Diagnosis Gross and histologic lesions Lead particles in the rumen
Brain edema - Lead poisoning Diagnosis Gross and histologic lesions Lead particles in the rumen Lead level in liver and kidney E. Simko WCVM

15 Osmosis and semi-permeable cellular membrane
Swelling Hypo Os Hypo Os Shrinkage Hyper Os Hyper Os

16 N N Osmotic brain edema Water intoxication ( IV H2O, behavioral, ADH)
Dehydr. Dehydr. BRAIN PLASMA BRAIN PLASMA E. Simko WCVM

17 N N Water deprivation +/- high salt
Osmotic brain edema - Salt toxicity Water deprivation +/- high salt NaCl H2O t = 0 hr Edema Edema N N Cl- Na+ Cl- Na+ Cl- Cl- Na+ Dehydr. Cl- Na+ Dehydr. Cl- Na+ Na+ Na+ Na+ Na+ Na+ Cl- Cl- Cl- Na+ Cl- BRAIN PLASMA NormoNa HyperNa BRAIN PLASMA NormoOs HyperOs Dehydration Dehydration

18 N N Equilibration of CNS hyperNa Osmotic brain edema - Salt toxicity
t = > 36 hr Edema Edema N N AA Cl- Na+ Cl- Cl- Na+ Cl- Na+ Cl- Dehydr. Cl- Cl- Na+ Cl- AA Na+ Cl- Dehydr. Cl- Na+ Na+ Na+ Cl- Na+ Na+ Cl- Na+ Na+ Na+ Cl- BRAIN PLASMA BRAIN PLASMA NormoNa HyperNa HyperNa HyperNa HyperOs HyperOs HyperOs HyperOs Dehydration Dehydration Dehydration Dehydration

19 N N Water access Osmotic brain edema - Salt toxicity H2O Edema Edema
t = > 36 hr H2O Edema Edema N N AA AA Cl- Na+ Na+ Cl- Na+ Cl- Cl- Dehydr. Cl- Dehydr. Na+ AA Na+ AA Cl- Cl- Na+ Na+ Na+ Cl- Na+ Cl- Na+ BRAIN PLASMA BRAIN PLASMA NormoNa HyperNa NormoNa NormoNa HyperOs HyperOs HyperOs NormalOs Dehydration Dehydration Edema Normal hydr.

20 Lesions Histology Brain swelling Osmotic brain edema - Salt toxicity
Cerebrocortical necrosis (occ) Histology Laminar cerebrocortical necrosis Perivascular eosinophilic infiltrate (Po) E. Simko WCVM

21 Diagnosis History Gross and histologic lesions Na level in the brain
Osmotic brain edema - Salt toxicity Diagnosis History Gross and histologic lesions Na level in the brain E. Simko WCVM

22 Vasogenic brain edema Vasogenic brain edema
The most common type of brain edema Pathogenesis: damaged BBB Examples: Toxins Inflammatory processes (H. somnus) E. Simko WCVM

23 White matter Grey matter E. Simko WCVM

24 Toxin-induced Toxins Vasogenic brain edema - Salt toxicity
Shigella toxin type II (Edema disease) Po Fibrinoid vasculitis Epsilon toxin (C. perfringens D enterotoxemia) Ov Symmetrical encephalomalacia Fumonisin B1 (Fusarium momiliforme) Moldy corn Equine leucoencephalomalacia E. Simko WCVM

25 Necrosis Trauma Thiamine deficiency Lead poisoning Salt poisoning
Response to injury - Necrosis Necrosis Trauma Thiamine deficiency Lead poisoning Salt poisoning Edema disease Clostridial eterotoxemia Equine leucoencephalomalacia Infarction

26 Infarction

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