Exam 2 - Intracranial Disease 2

Question 1

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

Answer 1

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

progression - typically worsens over time

pain - not usually painful

Question 2

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

Answer 2

true

Question 3

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

Answer 3

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

Question 4

what is the general description given for metabolic encephalopathy?

Answer 4

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

Question 5

how low is too low with hypoglycemia?

Answer 5

<50mg/dL

Question 6

what are some common underlying causes of hypoglycemia?

Answer 6

excess insulin or insulin-like substances (insulinoma)

decreased glucose production - neonates or severe hepatic insufficiency

excess glucose utilization - sepsis

Question 7

how high is too high with hypernatremia?

Answer 7

> 180mEq/L

Question 8

what are some causes of free water deficit causing hypernatremia?

Answer 8

no intake - denied water or hypodipsic hypernatremia

loss from disease - vomiting/diarrhea or diabetes insipidus

iatrogenic loss - mannitol or activated charcoal

Question 9

what are some causes of sodium excess causing hypernatremia?

Answer 9

sodium rich diet - seawater, jerky, play dough

sodium rich drugs

Question 10

how does hypernatremia develop?

Answer 10

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

Question 11

how low is too low with hyponatremia?

Answer 11

<125 mEq/L

Question 12

what are some causes of free water excess causing hyponatremia?

Answer 12

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

addison’s

hypervolemic - left heart failure or very severe renal failure

Question 13

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

Answer 13

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

Question 14

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

Answer 14

irreversible demyelination of nerves

Question 15

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

Answer 15

true

Question 16

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

Answer 16

stop giving high sodium fluids & give free H2O

Question 17

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

Answer 17

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

Question 18

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

Answer 18

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

metronidazole (antibiotics) - decreases ammonia producing bacteria

Question 19

what is the treatment used for metabolic encephalopathy?

Answer 19

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

Question 20

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

Answer 20

cats

Question 21

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

Answer 21

onset - slowly develops

progression - gets worse over time

pain - not usually painful

Question 22

what are the common neurological localizations given to thiamine deficiency?

Answer 22

forebrain, brainstem, & cerebellar - multifocal

Question 23

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

Answer 23

true

Question 24

what is the most common cause of thiamine deficiency?

Answer 24

inadequate dietary intake - cats have a higher requirement

Question 25

what are the mechanisms that lead to thiamine deficiency?

Answer 25

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

Question 26

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

Answer 26

patches in the gray matter

Question 27

what test is used for diagnosing thiamine deficiency & why?

Answer 27

high pressure liquid chromatography send out test more sensitive, specific, & stable

Question 28

what is the prognosis of thiamine deficiency?

Answer 28

good

Question 29

what is the treatment for thiamine deficiency?

Answer 29

parenteral supplementation given SQ every 3-5 days - not IV!!! oral supplementation for at least 2-4 weeks & diet change

Question 30

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

Answer 30

onset - variable progression - single exposure may be static to improving over time while chronic exposure can worsen over time pain - not usually painful

Question 31

what clinical signs are associated with metronidazole toxicity?

Answer 31

central vestibular signs

Question 32

what is metronidazole toxicity associated with?

Answer 32

higher doses & longer duration treatments

Question 33

T/F: damage from metronidazole toxicity is reversible

Answer 33

true - may resolve faster with oral diazepam treatment

Question 34

a high dose of bromethalin will cause what clinical signs?

Answer 34

seizures & death within hours of ingestion

Question 35

a low dose of bromethalin will cause what clinical signs?

Answer 35

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

Question 36

what is the treatment for bromethalin toxicity?

Answer 36

gastric lavage with activated charcoal if recent ingestion

Question 37

what is the prognosis of bromethalin toxicity?

Answer 37

guarded to poor

Question 38

what anatomic changes are seen with cerebral atrophy?

Answer 38

widening of cortical sulci enlargement of ventricles thinning of cortex shrinking of hippocampus

Question 39

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

Answer 39

onset - insidious onset with varied/vague signs in older adults progression - relentlessly progressive painful - not really

Question 40

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

Answer 40

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

Question 41

how can you confirm canine cognitive dysfunction?

Answer 41

rule out systemic & structural brain disease & distinguishing normal aging from a pathological small interthalmic adhesion

Question 42

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

Answer 42

false - no cure

Question 43

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

Answer 43

l-deprenyl, monoamine oxidase inhibitors (careful of interactions) diet - combo of high fatty acids, anti-oxidants, & l-carnitine suggested environmental enrichment in dogs

Question 44

what is a congenital brain malformation?

Answer 44

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

Question 45

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

Answer 45

underlying problem doesn't progress but clinical signs may progress

Question 46

what neurological signs are seen with congenital brain malformations?

Answer 46

depends on the location of the malformation

Question 47

what animals are typically affected by hydrocephalus?

Answer 47

young animals under 6 months of age inherited - toy breeds & brachycephalic in utero insult - trauma, toxin, infection, or nutritional deficiency

Question 48

how is hydrocephalus diagnosed?

Answer 48

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

Question 49

what treatment can be used for congenital hydrocephalus?

Answer 49

omeprazole, glucocorticoids, diuretics - decrease CSF production control seizures surgery - ventriculoperitoneal shunt

Question 50

what are the complications associated with the ventriculoperitoneal shunt surgery?

Answer 50

blockage, breakage, or infection

Question 51

what is the typical presentation of a traumatic brain injury?

Answer 51

emergency - peracute onset & progressive

Question 52

how is a traumatic brain injury diagnosed?

Answer 52

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

Question 53

why is increased intracranial pressure so bad?

Answer 53

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

Question 54

what are the clinical signs associated with increased intracranial pressure?

Answer 54

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

Question 55

how is increased intracranial pressure diagnosed?

Answer 55

neurological exam & indirect diagnostic data

Question 56

what is tier 1 of managing increased intracranial pressure?

Answer 56

basic systemic stabilization

Question 57

what is tier 2 of managing increased intracranial pressure?

Answer 57

medical reduction of intracranial pressure - mannitol & head elevation

Question 58

what is tier 3 of managing increased intracranial pressure?

Answer 58

possible surgical intervention

Question 59

what is the treatment for increased intracranial pressure?

Answer 59

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

Question 60

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

Answer 60

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

Question 61

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

Answer 61

canine cognitive dysfunction

Question 62

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

Answer 62

vascular insult

Question 63

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

Answer 63

systemic stabilization management of intracranial pressure