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BRAIN - Metabolic Flashcards

1
Q

DDx hypoglycemia​

A
  • 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

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2
Q

DDx hypocobalaminaemia​

A

Exocrine pancreatic insufficiency
Small intestine dysbiosis
Chronic severe ileal disease
Inherited

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3
Q

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

A

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)

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4
Q

ingestion and absorption of cobalmamin

A

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

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5
Q

cobalamin is a cofactor for …

A

intracellular enzymes methionine synthase and methylmalonyl-CoA mutase

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6
Q

markers that most closely reflect the intracellular availability of cobalamin

A

serum concentration of methylmalonic acid and homocystein

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7
Q

2 breeds with predisposition to hypocobalaminemia

A

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

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8
Q

DDx hyperammonaemia

A

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

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9
Q

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

A

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

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10
Q

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

A

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

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11
Q

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

A

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)

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12
Q

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

A

Presence of HE preoperatively
Increasing age

other etude PAS: age, WBC
clincial recovery: alb WBC
complete recov alb

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13
Q

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

A

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.

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14
Q

Give 2 normal physiologic response to correct hypernatremia and plasma hyperosmolality

A

Increased thirst
Increased production of ADH

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15
Q

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

A

Hyper: cerebral edema
Hypo: myelinolisis

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16
Q

Which signs are associated with thiamine deficiency in cats?

A

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

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17
Q

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

A

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

18
Q

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

A

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)

19
Q

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

A

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

20
Q

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

A

2

21
Q

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

A

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

22
Q

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

A

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)

23
Q

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

A

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

24
Q

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

A

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.

25
Q

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

A

False for both

26
Q

Signs/ cause of hypervitaminosis A in cat

A

Feed with raw liver diet
Extensive bone proliferation, can fuse cervical column

27
Q

risk factor associated with post att seizures

A

dog: immediate post-op encephalopthy
increasing age

cat: low post opr serum osmolarity

28
Q

complication post attenuation PSS + freq in dog and cat

A

ataxia, blindness, seizures (within 96h, often refract for first AED treat)

dog (4-17%)
cat (40-60%):

mortality rate in animals with signs 4-22%

29
Q

mechanism neuroglycopenia

A

dysfunction Na/K ATPase pump

-> neuronal swelling, uptake glutamate from astrocytes, stim NO synthase, rapid celllular influx K/Ca

-> neuronal apoptosis and necrosis, eve, after glc normalised

30
Q

neurologioc signs assoc with hypoadrenocorticism

A

seizures due to hypoglycemia
muscle cramps
generalised neuromusc weakness

hyperK, hypoNa, non regen anemia

31
Q

diff hematologic variable extra/intrahepatic shunt

A

intra: higher freq anemia, micocytosis, hypochromia, more GI signs

IHPSS ulceration 15% before treat, 21% after

32
Q
A
33
Q

breed w

A
34
Q
A
35
Q

MRI abnomalies in a dog with mitochondrial fatty acid oxydation defect

A

hyperlactatemia hypogly
bilat necrotic lesion in caudate nucleus + abnom in cerebellar nuclei + multi organ lipid accumul including lipid storage myopathy

malonic aciduria and ketonuria

36
Q

causes of hyponatremia

A

vomiting, diarhea, third space fluid loss
urological, cardiovascular (cong heart failure), hepatobiliary
hypoadrenocort
diabetus melit/ketoacidosis

severity of hypo/hyperNa lineary assoc with fatality rate

37
Q

causes of hyperNa

A

most fqt dog GI fluid loss, cat chronic kidney disease/IRA

+neurological
central diab insip
hypertyroidism
fever/hyperthermia

38
Q

origin of ammonium

A

urea producing anaerobic/colif bact in colon +/- helicobacter in stomach

from glutamine by intestinal mucosa

endogenous breakdown protein

39
Q

mechanism lesion from ammonia

A

astrocyte swelling (Alzeimer type II)
glutamate release by astrocytes
increase BBB permeability
inflam change
accumul manganèse/neurosteroids
oxidative stress
ammoniac umbalance

40
Q

thiamine metabolic pathway

A

absorbed in ileum and jejunum, passive + active carrier transport, maj carried within RBC
maj in phosphorilated form

Krebs cycle (TCA cycle) in carbonydrate metab ->cofactor for conversion of pyruvate to acetyl coA
pentose phosphate pathway

41
Q

presurgical treatment for shunt

A

hepative support diet + lactulose

42
Q

blood anomaliies in cat with PSSS

A

microcytosis, rarely anem/leucocytosis/thrombocytopenia
increase coag profile but no bleeding risk

surgical treat increase hct, mcv

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