BRAIN - Metabolic Flashcards
(39 cards)
DDx hypoglycemia
-
Decreased production
PSS
Acute liver failure
Chronic end-stage hepatopathy
Hypoadrenocorticism
glycogen storage disease -
Increased removal
Insulin: overdose, insulinoma, insulin-like substance-producing tumors (melanoma, carcinoma, hepatoma)
Polycythaemia
Toxic (xylitol)
Renal glycosuria
Unknown: sepsis, renal failure, cardiopulmonary arrest, hunting dog, Babesia
DDx hypocobalaminaemia + breed with increased freq
Exocrine pancreatic insufficiency
Small intestine dysbiosis
Chronic severe ileal disease
Inherited (CUBN gene in giant Schnauzer, Aust Sheperd, Border C, Beagle)
breeds increased freq: the Chinese Shar-Pei, Staffordshire BullTerrier, German Shepherd Dog
What is the Imerslund-Gräsbeck syndrome mechanism? How to make the diagnose?
Decreased intracellular cobalamin
-> Decreased methylmalonic-CoA mutase activity
-> Accumulation of intracellular methylmalonic acid
-> Methylmalonic acidaemia & aciduria
-> Inhibits carbamoyl phosphate synthase I
-> Hyperammonaemia
Diagnosis:
Decreased B12
Increased methylmalonic acid (urine, serum)
Increased homocysteine (serum)
ingestion and absorption of cobalmamin
mainly ingested with food of animal origin (fish, meat, milk product)
intestinal microbiota can produce vit B12 but distally to absorption site
bound to dietary protein -> released in stomach by pepsinogen and gastric acid -> bound to haptocorrin (transcobalamin I) -> separated in duodenum by protease and bound to intrinsic factor -> cubam receptor-mediated endocytosis in ileum -> bound to transcobalamin within bloodstream
1% absorbed via passive diffusion in intestinal mucosa
cobalamin is a cofactor for …
intracellular enzymes methionine synthase and methylmalonyl-CoA mutase
markers that most closely reflect the intracellular availability of cobalamin
serum concentration of methylmalonic acid and homocystein
2 breeds with predisposition to hypocobalaminemia
Giant Schnauzer
Australian Sheperd
Border Collie
Beagle
Chinese Shar-Pei
Komondor
DDx hyperammonaemia
1/ PSS
2/ Fulminating hepatopathy
3/ Urea-cycle deficiency
- Transient (Irish Wolfhound puppies)
- Persistent enzyme deficiency
- Selective cobalamin deficiency
- Arginine deficiency (cats)
4/ Urinary tract obstruction with urea-producing bacteria
5/ L-asparaginase therapy
What are the most common blood works findings with hepatic encephalopathy in dogs and cats?
Serum biochemistry:
Hypoalbuminemia
Hypocholesterolemia
Low BUN
Hypoglycemia
Increased liver enzyme concentration
Specific liver function tests:
Hyperamonaemia
Increased pre and/or post prandial bile acids
Clotting time prolongations
Haematologic: microcytosis
What are the MRI findings associated with hepatic encephalopathy in dogs and cats?
Brain atrophy, maj in dog
symmetric T1 hyperintensity to the lentiform nuclei attributed to increased concentration of manganese, which decreases with treatment of the underlying cause
Bilateral extensive T2 hyperintense lesions in centrum semiovale, corona radiata, cerebellar nuclei
in cat same + medial longitudinal fasciculus and reticular formation
What are the treatment to reduce neurotoxic metabolites with hepatic encephalopathy?
Oral lactulose
Lactulose enemas
Antibiotics (ampicillin or metronidazole or neomycin)
If GI hemorrhage: proton pump inhibitors
Diet alteration: high quality low protein diet (care should be taken not to limit protein intake excessively)
What are the two risk factors for post attenuation neurological signs and seizures after attenuation of single congenital portosystemic shunts in dogs?
Presence of HE preoperatively
Increasing age
other etude PAS: age, WBC
clincial recovery: alb WBC
complete recov alb
Give 3 category of causes of hypernatremia with an example of each.
Free water deficit
Primary hypodipsia
Diabetes insipidus
High Temp
Inadequate access to water
Sodium gain
Salt poisoning
Hypertonic fluid administration
Hyperaldosteronism
Hyperadrenocorticism
Hypotonic fluid loss
Extra-renal: vomiting, diarrhoea, burns, etc.
Renal: osmotic diuresis, chronic renal failure, diuretics, etc.
Give 2 normal physiologic response to correct hypernatremia and plasma hyperosmolality
Increased thirst
Increased production of ADH
What lesion’s type can be induced by too rapid correction of hyper- and hyponatremia?
Hyper: cerebral edema
Hypo: myelinolisis/osmotic demyelination syndrome
Which signs are associated with thiamine deficiency in cats?
Bilateral vestibular: 94%
Altered mentation: 76%
Seizures: 59%
80% with SE or CS
Most remained seizure-free with treatment
Blindness: 59%
What MRI abnormality has been described in cats/ dogs with B12 vitamin deficiency?
Bilateral symmetrical gray matter T2 hyperintense lesions with mild contrast enhancement
Both: vestibular nuclei, caudal colliculi, oculomotor
Dogs: red nucleus, (rostral colliculi), caudate nuclei, cerebellar nodulus
Cats: lat geniculate, periaq grey, facial nucleus, (rostral colliculi), periaqueductal grey, cerebellar nuclei, thalamic nuclei, subthalamus
and pariet/occip, cingulate gyrus, hippocampus if seizures
most common MRI abnomalities with hepatic encephalopathy shunt in dog and cat?
1/ reduced volume of the brain with sometimes cerebellar atrophy (18/20)
T2 hyperintensity in centrum semiovale corona radiata, internal capsue, cerebellar nuclei (and medial longitudinal fasciculus and reticular formation in cat)
no abnomality (2/20)
What MRI abnormality has been described in myelinolysis/osmotic demyelination syndrome ?
T2 hyperintensity: bilateral and symmetric hyperintensities affecting the thalamus and extending into the subthalamus + superior longitudinal fasciculus (lateral to the internal capsule)
Thiamine deficiency in cats: choose the FALSE
1/ The most common clinical sign is bilateral vestibular signs of varying severity, accompanied with altered mentation +/- seizures +/- blindness.
2/ A normal MRI excludes diagnosis of thiamine deficiency
3/ MRI findings may not reflect the neurological status or severity
4/ Most cats, if treated promptly, recover rapidly, within 2 weeks, although more slow recoveries over several months have been documented
2
Which neurological diseases have been associated with syndrome of inappropriate antidiuretic hormone secretion (SIADH) in dogs?
Congenital hydrocephalus
Granulomatous amebic meningoencephalitis
Hypothalamic tumors
Traumatic brain injury (main neurological cause in humans, with spontaneous resolution)
Give the gene, breed, clinical signs, ancillary tests abnormalities, and treatment of medium-chain acyl-coA dehydrogenase deficiency in dogs.
Cavalier King Charles Spaniels
ACADM
Focal seizures and lethargy
β-oxidation, now mediated by medium-chain acyl-CoA dehydrogenase (MCAD), MCFAs serve as energy source for the body
Ancillary tests:
Serum BC, CBC, MRI, CSF, … unremarkable.
Urine: increased medium-chain fatty acids.
Blood: acylcarnitine C8/C12 elevated 43-fold compared to homozygous WT dogs.
Low-fat diet & avoiding prolonged periods of fastings (midnight snack with carbohydrates)
What are the 3 most common presenting clinical signs in dogs with insulinoma?
The most common presenting clinical signs were weakness (59.5%), epileptic seizures (33.6%) and changes in consciousness or behaviour (27.6%).
About postattenuation neurological signs in dogs, what are the 2 prognostic factors positively associated with short-term survival?
History of preoperative seizures
Development of focal seizures only
Mortality associated with PANS was typically related to occurrence of generalized seizure activity.
If affected dogs survived to discharge, survival for several years was possible, and the majority of neurologic signs manifested as part of the phenomenon of PANS appeared to resolve.
