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SA DX & TX I > Exam 2 - Intracranial Disease 2 > Flashcards

Exam 2 - Intracranial Disease 2 Flashcards

1
Q

how would you describe metabolic encephalopathy in terms of disease onset, progression, and pain?

A

onset - can be episodic, slowly progressive, or rapidly progressive

progression - typically worsens over time

pain - not usually painful

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2
Q

T/F: in metabolic encephalopathy, it’s usually forebrain predominant & systemic effects are usually evident

A

true

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3
Q

what is the ‘minimum database’ in regards to metabolic encephalopathy?

A

hypoglycemia - check glucose
hyper/hyponatremia
hypocalcemia - check ionized calcium
ammonia, bile acids - hepatic encephalopathy

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4
Q

what is the general description given for metabolic encephalopathy?

A

waxing/waning forebrain disease with normal neurological exam and vague or symmetrical neurological signs

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5
Q

how low is too low with hypoglycemia?

A

<50mg/dL

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6
Q

what are some common underlying causes of hypoglycemia?

A

excess insulin or insulin-like substances (insulinoma)

decreased glucose production - neonates or severe hepatic insufficiency

excess glucose utilization - sepsis

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7
Q

how high is too high with hypernatremia?

A

> 180mEq/L

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8
Q

what are some causes of free water deficit causing hypernatremia?

A

no intake - denied water or hypodipsic hypernatremia

loss from disease - vomiting/diarrhea or diabetes insipidus

iatrogenic loss - mannitol or activated charcoal

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9
Q

what are some causes of sodium excess causing hypernatremia?

A

sodium rich diet - seawater, jerky, play dough

sodium rich drugs

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10
Q

how does hypernatremia develop?

A

excess sodium causes cells to shrink & you have an increased concentration gradient

when fluids are rapidly given, idiogenic osmoles are created, and the cell rapidly expands causing cerebral edema

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11
Q

how low is too low with hyponatremia?

A

<125 mEq/L

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12
Q

what are some causes of free water excess causing hyponatremia?

A

hypovolemic - cavitary effusions, excessive gi loss, or urinary loss

addison’s

hypervolemic - left heart failure or very severe renal failure

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13
Q

what should you do if you give fluids to a hypernatremic patient & they develop neurological clinical signs?

A

d/c fluids, check their sodium, & give lasix

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14
Q

what happens if there a rapid decrease in free H2O when trying to correct hyponatremia?

A

irreversible demyelination of nerves

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15
Q

T/F: clinical signs of demyelination from rapidly decreasing free H2O in a hyponatremic patient will appear > 24 hours after treatment

A

true

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16
Q

what should you do if an animal with hyponatremia develops clinical signs 24 hours after you started treating it?

A

stop giving high sodium fluids & give free H2O

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17
Q

what clinical signs are associated with severe hepatic insufficiency in dogs and cats with hepatic encephalopathy?

A

increased protein intake, gi disease (hemorrhage or obstruction), acute-or-chronic hepatic injury, dehydration, & sepsis

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18
Q

what medical management/emergency treatment can be used for hepatic encephalopathy patients?

A

lactulose - traps ammonia in the colon & decrease bacterial ammonia production

metronidazole (antibiotics) - decreases ammonia producing bacteria

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19
Q

what is the treatment used for metabolic encephalopathy?

A

correction of the metabolic abnormality should improve neurological signs - diagnostic confirmation

successful resolution of underlying cause can resolve neuro signs but residual seizures are possible if they became epileptic during the incident

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20
Q

what animal is most commonly affected by nutritional encephalopathy caused by thiamine deficiency?

A

cats

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21
Q

how would the onset, progression, and pain status of thiamine deficiency be described?

A

onset - slowly develops

progression - gets worse over time

pain - not usually painful

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22
Q

what are the common neurological localizations given to thiamine deficiency?

A

forebrain, brainstem, & cerebellar - multifocal

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23
Q

T/F: systemic disease may be a risk factor for thiamine deficiency

A

true

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24
Q

what is the most common cause of thiamine deficiency?

A

inadequate dietary intake - cats have a higher requirement

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25
Q

what are the mechanisms that lead to thiamine deficiency?

A
  1. inadequate dietary intake
  2. increased elimination because of increased GFR - hyperthyroid cats
  3. decreased absorption in chronic enteropathy - IBD
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26
Q

what would you expect to see on imaging in a patient with thiamine deficiency?

A

patches in the gray matter

27
Q

what test is used for diagnosing thiamine deficiency & why?

A

high pressure liquid chromatography send out test

more sensitive, specific, & stable

28
Q

what is the prognosis of thiamine deficiency?

A

good

29
Q

what is the treatment for thiamine deficiency?

A

parenteral supplementation given SQ every 3-5 days - not IV!!!

oral supplementation for at least 2-4 weeks & diet change

30
Q

how would the onset, progression, and pain status of toxic encephalopathy be described?

A

onset - variable

progression - single exposure may be static to improving over time while chronic exposure can worsen over time

pain - not usually painful

31
Q

what clinical signs are associated with metronidazole toxicity?

A

central vestibular signs

32
Q

what is metronidazole toxicity associated with?

A

higher doses & longer duration treatments

33
Q

T/F: damage from metronidazole toxicity is reversible

A

true - may resolve faster with oral diazepam treatment

34
Q

a high dose of bromethalin will cause what clinical signs?

A

seizures & death within hours of ingestion

35
Q

a low dose of bromethalin will cause what clinical signs?

A

paresis/paralysis & potentially coma within 1-2 days of ingestion

36
Q

what is the treatment for bromethalin toxicity?

A

gastric lavage with activated charcoal if recent ingestion

37
Q

what is the prognosis of bromethalin toxicity?

A

guarded to poor

38
Q

what anatomic changes are seen with cerebral atrophy?

A

widening of cortical sulci

enlargement of ventricles

thinning of cortex

shrinking of hippocampus

39
Q

how would the onset, progression, and pain status of canine cognitive dysfunction be described?

A

onset - insidious onset with varied/vague signs in older adults

progression - relentlessly progressive

painful - not really

40
Q

what clinical signs are seen if they are confined to the forebrain in canine cognitive dysfunction?

A

disrupted sleep-wake cycle, anxiety, decreased interaction with the owner, and rare seizures

41
Q

how can you confirm canine cognitive dysfunction?

A

rule out systemic & structural brain disease

& distinguishing normal aging from a pathological small interthalmic adhesion

42
Q

T/F: there is a cure for canine cognitive dysfunction

A

false - no cure

43
Q

what treatments/therapies can be used for an animal with suspected canine cognitive dysfunction?

A

l-deprenyl, monoamine oxidase inhibitors (careful of interactions)

diet - combo of high fatty acids, anti-oxidants, & l-carnitine suggested

environmental enrichment in dogs

44
Q

what is a congenital brain malformation?

A

malformation present at birth that may or may not show signs at birth

45
Q

what is the progression of congenital brain malformations causing intracranial disease?

A

underlying problem doesn’t progress but clinical signs may progress

46
Q

what neurological signs are seen with congenital brain malformations?

A

depends on the location of the malformation

47
Q

what animals are typically affected by hydrocephalus?

A

young animals under 6 months of age

inherited - toy breeds & brachycephalic
in utero insult - trauma, toxin, infection, or nutritional deficiency

48
Q

how is hydrocephalus diagnosed?

A

MRI, CT, or even ultrasound - use CSF to rule out meningoencephalitis

49
Q

what treatment can be used for congenital hydrocephalus?

A

omeprazole, glucocorticoids, diuretics - decrease CSF production

control seizures

surgery - ventriculoperitoneal shunt

50
Q

what are the complications associated with the ventriculoperitoneal shunt surgery?

A

blockage, breakage, or infection

51
Q

what is the typical presentation of a traumatic brain injury?

A

emergency - peracute onset & progressive

52
Q

how is a traumatic brain injury diagnosed?

A

based on clinical signs & the recognition of progressive neurological dysfunction after known or suspected trauma because of the increased intracranial pressure

53
Q

why is increased intracranial pressure so bad?

A

causes caudal herniation of the brainstem as it pushes the cerebellum/medulla through the foramen magnum & midbrain under the osseous tentorium

54
Q

what are the clinical signs associated with increased intracranial pressure?

A

progressive signs of forebrain disease, new signs of brainstem disease, central vestibular signs, pupillary/ocular reflex abnormalities, & hypertension with reflex bradycardia (cushing’s reflex)

55
Q

how is increased intracranial pressure diagnosed?

A

neurological exam & indirect diagnostic data

56
Q

what is tier 1 of managing increased intracranial pressure?

A

basic systemic stabilization

57
Q

what is tier 2 of managing increased intracranial pressure?

A

medical reduction of intracranial pressure - mannitol & head elevation

58
Q

what is tier 3 of managing increased intracranial pressure?

A

possible surgical intervention

59
Q

what is the treatment for increased intracranial pressure?

A

maintain normal PO2, PCO2, temperature, perfusion, control seizure activity, & elevate the head without compressing jugular veins

60
Q

what are you looking for on imaging if you suspect increased intracranial pressure?

A

depressed fractures, hematomas, ongoing bleeding (CT) - surgical targets

61
Q

what is a common cause of slowly progressive intracranial disease in older dogs?

A

canine cognitive dysfunction

62
Q

what is a common cause of peracute intracranial disease in older dogs?

A

vascular insult

63
Q

what are the 2 most important parts of managing a traumatic brain injury?

A

systemic stabilization

management of intracranial pressure

SA DX & TX I (59 decks)

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