BRAIN - Metabolic

Question 1

DDx hypoglycemia​

Answer 1

• 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

Question 2

DDx hypocobalaminaemia​

Answer 2

Exocrine pancreatic insufficiency
Small intestine dysbiosis
Chronic severe ileal disease
Inherited

Question 3

What is the Imerslund-Gräsbeck syndrome mechanism? How to make the diagnose?​

Answer 3

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)

Question 4

ingestion and absorption of cobalmamin

Answer 4

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

Question 5

cobalamin is a cofactor for …

Answer 5

intracellular enzymes methionine synthase and methylmalonyl-CoA mutase

Question 6

markers that most closely reflect the intracellular availability of cobalamin

Answer 6

serum concentration of methylmalonic acid and homocystein

Question 7

2 breeds with predisposition to hypocobalaminemia

Answer 7

Giant Schnauzer
Australian Sheperd
Border Collie
Beagle
Chinese Shar-Pei
Komondor

Question 8

DDx hyperammonaemia

Answer 8

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

Question 9

What are the most common blood works findings with hepatic encephalopathy in dogs and cats?

Answer 9

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

Question 10

What are the MRI findings associated with hepatic encephalopathy in dogs and cats?

Answer 10

Brain atrophy (widening of the sulci, grey matter atrophy)

Bilaterally 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 along the cerebral cortex

Question 11

What are the treatment to reduce neurotoxic metabolites with hepatic encephalopathy?

Answer 11

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)

Question 12

What are the two risk factors for post attenuation neurological signs and seizures after attenuation of single congenital portosystemic shunts in dogs?

Answer 12

Presence of HE preoperatively
Increasing age

Question 13

Give 3 category of causes of hypernatremia with an example of each.

Answer 13

Free water deficit
Primary hypodipsia
Diabetes insipidus
High Temp.
Fever
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.

Question 14

Give 2 normal physiologic response to correct hypernatremia and plasma hyperosmolality

Answer 14

Increased thirst
Increased production of ADH

Question 15

What lesion’s type can be induced by too rapid correction of hyper- and hyponatremia?

Answer 15

Hyper: cerebral edema
Hypo: myelinolisis

Question 16

Which signs are associated with thiamine deficiency in cats?

Answer 16

Bilateral vestibular: 94%
Altered mentation: 76%
Seizures: 59%
80% with SE or CS
Most remained seizure-free with treatment
Blindness: 59%

Question 17

What MRI abnormality has been described in cats/ dogs with B12 vitamin deficiency?

Answer 17

Bilateral symmetrical gray matter T2 hyperintense lesions with mild contrast enhancement

Both: vestibular nuclei, caudal colliculi, cerebellar nodulus

Dogs: red nucleus, rostral colliculi, caudate nuclei, oculomotor nuclei

Cats: LGN, PAG, facial nucleus, rostral colliculi, periaqueductal grey

Question 18

most common MRI abnomalities with hepatic encephalopathy shunt in dog and cat?

Answer 18

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)

Question 19

What MRI abnormality has been described in myelinolysis/osmotic demyelination syndrome ?

Answer 19

T2 hyperintensity: bilateral and symmetric hyperintensities affecting the thalamus and extending into the subthalamus + superior longitudinal fasciculus (lateral to the internal capsule)

Question 20

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

Answer 20

2

Question 21

Which neurological diseases have been associated with syndrome of inappropriate antidiuretic hormone secretion (SIADH) in dogs?

Answer 21

Congenital hydrocephalus
Granulomatous amebic meningoencephalitis
Hypothalamic tumors
Traumatic brain injury (main neurological cause in humans, with spontaneous resolution)

Question 22

Give the gene, breed, clinical signs, ancillary tests abnormalities, and treatment of medium-chain acyl-coA dehydrogenase deficiency in dogs.

Answer 22

Cavalier King Charles Spaniels
ACADM
Focal seizures and lethargy

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)

Question 23

What are the 3 most common presenting clinical signs in dogs with insulinoma?

Answer 23

The most common presenting clinical signs were weakness (59.5%), epileptic seizures (33.6%) and changes in consciousness or behaviour (27.6%).

Question 24

About postattenuation neurological signs in dogs, what are the 2 prognostic factors positively associated with short-term survival?

Answer 24

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.

Question 25

The use of prophylactif AED (such as LV) prevent and reduce the incidence of postattenuation seizures in dogs and cats: true or false?

Answer 25

False for both