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ACVIM Specialty 2023 > Neurology > Flashcards

Neurology Flashcards

1
Q

How many dogs with portosystemic shunts display neurologic signs?

A

95%

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2
Q

Name 4 neurologic signs of hepatic encephalopathy

A

Decreased ability to learn, behavioral changes, head pressing, seizures, blindness

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3
Q

Are neurologic signs more common when shunts insert cranial to or caudal to the liver

A

Caudal

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4
Q

Name 3 endotoxins thought to be involved in the development of hepatic encephalopathy

A

Ammonia, amino acids (tryptophan), GABA, mercaptans

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5
Q

Hyperammonemia has been documented in young Irish Wolfhounds due to what deficiency?

A

Deficiency in urea cycle enzymes

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6
Q

What neurologic signs can be seen in hypothyroid dogs?

A

Acute or chronic, progressive central vestibular signs

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7
Q

Name 4 clinical signs of myxedema coma in dogs

A

Mentation changes due to brain edema, hypothermia without shivering, non-pitting skin edema, bradycardia

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8
Q

Name 3 mild CNS signs noted in cats with hyperthyroidism

A

Hyperactivity, changes in sleep/wake cycles, aggression, obtundation

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9
Q

How large are pituitary tumors before they result in neurologic signs?

A

Typically >1 to 1.5cm diameter

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10
Q

Pituitary tumors result in neurologic signs in what percent of dogs before or after diagnosis of hyperadrenocorticism?

A

15-30%

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11
Q

Name 4 neurologic signs of a pituitary macroadenoma

A

Obtundation, pacing, circling, disorientation, ataxia, seizures

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12
Q

How does persistent hypoglycemia results in neurologic damage?

A

Leads to vasoconstriction and hypoxia

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13
Q

Name two tumors capable of resulting in hypoglycemia

A

Insulinoma, leiomyosarcoma

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14
Q

What drug can be used to treat insulin producing tumors because it inhibits insulin secretion, stimulates production of glucose by the liver, and inhibits uptake of glucose by cells?

A

Diazoxide

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15
Q

What role does thiamine play in the body?

A

Essential cofactor for carbohydrate metabolism - essential for utilization of pyruvic acid in the TCA cycle and pentose phosphate pathway. Absence of thiamine leads to excessive lactic acid buildup as anaerobic metabolism occurs

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16
Q

How can thiamine deficiency result in dogs and cats?

A

Fed meats preserved with sulfur dioxide, thiaminase-containing raw fish

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17
Q

What are the histopathologic findings associated with thiamine deficiency?

A

Polioencephalomalacia

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18
Q

Name 3 clinical signs of thiamine deficiency

A

Vestibular signs, spastic cervical ventroflexion in cats, vision loss, mydriasis without pupil light reflexes, incoordination, ataxia, and seizures

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19
Q

How does hypocalcemia alter membrane excitability?

A

Increases it

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20
Q

Name 3 neurologic signs of hypocalcemia

A

Facial rubbing, stiffness, muscle twitching, nervousness, tetany, and seizures

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21
Q

Severe hyponatremia results in what changes to the brain?

A

Cerebral edema, diffuse encephalopathy

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22
Q

Rapid correction of hyponatremia can result in what histopathologic changes in the brain? How long after correction do these signs manifest?

A

Central pontine myelinolysis; occurs 48 hours to days after correction

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23
Q

When correcting hyponatremia, the serum sodium concentration should not rise by more than ____ in 24 hours?

A

10 mEq/L

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24
Q

Acute hypernatremia can cause what changes to the brain?

A

Decrease in brain volume from osmotic shifts, leading to vascular rupture and focal hemorrhage

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25
Q

In chronic hypernatremia, the brain adjusts to hypertonicity by producing what substance?

A

Idiogenic osmoles

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26
Q

Rapid correction of hypernatremia results in what changes to the brain?

A

Cerebral edema

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27
Q

T4 stimulates mitochondrial respiratory activity, thereby leading to ATP production. In hypothyroidism, how does ATP deficiency affect peripheral nerves?

A

Impairs the function of the Na/K pump, leading to decreased axonal transport ==> leads to axonal degeneration and demyelination

28
Q

List 3 neurologic signs of hypothyroidism

A

Weakness, muscle atrophy, laryngeal paralysis, megaesophagus facial paralysis, peripheral vestibular signs

29
Q

What hormonal disease causes fibrotic myopathy and polyneuropathy?

A

Hyperadrenocorticism

30
Q

Name 3 clinical signs of fibrotic myopathy

A

Stiff, stilted gain, difficulty flexing the limbs, generalized muscle atrophy

31
Q

Name 3 signs of diabetic polyneuropathy in cats

A

Plantigrade stance, difficulty jumping, CP deficits, decreased tendon reflexes, muscle atrophy

32
Q

Name two feline diseases that may result in hypokalemia

A

CKD, hyperaldosteronism

33
Q

What is the reticular activating system and what is it responsible for?

A

Network of nuclei in the brainstem. Activate the cerebral cortex to maintain consciousness

34
Q

What is the function of the cerebrum?

A

Integrates sensory info, plans motor activity, responsible for emotion and memory

35
Q

Diffuse, bilateral forebrain lesions will result in stupor/coma. How will they affect movement and reflexes?

A

Tetraparesis, postural deficits are present. Reflexes are normal but vision is absent

36
Q

Lesions of the rostral brainstem will result in stupor/coma. How will they affect movement and reflexes?

A

Bilateral lesions will cause tetraparesis, unilateral lesions will cause hemiparesis. Postural deficits present. Reflexes are exaggerated with increased extensor tone

37
Q

Name 3 brainstem reflexes

A

Pupil size/symmetry and response to light. Physiologic nystagmus. Dazzle reflex. Palpebral reflex

38
Q

If a patient has unilateral mydriasis with no pupillary response to light, where is the lesion located?

A

Cranial nerve III

39
Q

If a patient has unilateral mydriasis AND ventrolateral strabismus with no response to light, where is the lesion located?

A

Midbrain

40
Q

Describe Cheyne-Stokes breathing

A

Alternating hypernea and apnea

41
Q

Describe apneusis. Where is the lesion located

A

Breathing raises for a full inspiratory period with otherwise normal breathing. Pontine lesions

42
Q

What equation describes cranial perfusion pressure (CPP)

A

CPP = MAP - ICP

43
Q

Describe the Cushing’s reflex

A

If ICP rises, the MAP increases to maintain CPP. Systemic hypertension triggers the baroflex, leading to bradycardia

44
Q

Name 3 causes of hepatic encephalopathy

A

A = acute, fulminant liver disease
B = bypass (portosystemic shunts)
C = cirrhosis (cirrhotic liver, portal hypertension, acquired shunting)

45
Q

Acute, fulminant liver disease can result in hepatic encephalopathy by what pathologic change?

A

Cytotoxic brain edema. Can lead to intracranial hypertension and brain herniation

46
Q

What causes cytotoxic brain edema?

A

Failure of ion pumps, so no sodium efflux occurs. Water shifts to the intracellular space to maintain iso-osmotic state => edema. BBB is intact

47
Q

What causes vasogenic edema?

A

Disruption of the BBB, which triggers a cascade of inflammatory and vasoactive mediators. Often causes by tumors

48
Q

Chronic hepatic disease can result in hepatic encephalopathy by what pathologic change?

A

Alzheimer type II astrocytosis - astrocytes change structure and function. Very minimal brain edema

49
Q

Name 2 non-hepatic causes of hyperammonemia

A

Vitamin B12 deficiency. Arginine deficiency in cats

50
Q

Name 3 sources of ammonia in the body

A

Bacteria breakdown of proteins, urease bacterial breakdown of urea, intestinal breakdown of glutamine

51
Q

Which form of ammonia is absorbed from the gut (NH3 or NH4+)?

A

NH3

52
Q

In the periportal hepatocytes, ammonia is converted into _____ via the _____ pathway

A

Urea, urea cycle

53
Q

How does arginine deficiency in cats lead to hyperammonemia?

A

Arginine is an important component of the urea cycle. Without it, ammonia cannot be converted into urea. Essential amino acid in cats

54
Q

How does ammonia affect glutamate in the brain?

A

Ammonia is added to glutamate (a major neurotransmitter) to form glutamine. Glutamine is taken up by astrocytes and is osmotically active, leading to edema formation

55
Q

What hepatic synthetic parameter is NOT affected by PSS?

A

Bilirubin (hyperbilirubinemia is not a feature of congenital PSS)

56
Q

What is the major excitatory neurotransmitter?

A

Glutamate

57
Q

What is the major inhibitory neurotransmitter?

A

GABA

58
Q

Name two catecholamine based neurotransmitters

A

Dopamine, norepinephrine

59
Q

What type of amino acids are precursors to catecholamines?

A

Aromatic amino acids: phenylalanine, tyrosine, tryptophan

60
Q

Aromatic amino acids are usually removed by the liver. How do they contribute to hepatic encephalopathy

A

Can build up and become false neurotransmitters

61
Q

What amino acids may be decreased with liver failure?

A

Branched chain amino acids: leucine, valine, isoleucine

62
Q

How does lactulose reduce hyperammonemia?

A

Broken down into acid byproducts in the gut. The acidity traps NH3 in the NH4 form, which is not absorbed

63
Q

How do antibiotics reduce hyperammonemia?

A

Reduce the number of urease producing bacteria

64
Q

What is dialysis disequilibrium syndrome?

A

A rapid decline in peripheral osmolality results from dialysis => cerebral edema => increased ICP

65
Q

What is kernicterus?

A

Deposition of bilirubin in the grey matter and spinal cord => neuronal degeneration

ACVIM Specialty 2023 (38 decks)

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