Neuro and Ophtho Flashcards

1
Q

What is transcranial magnetic stimulation?

A

Technique to evaluate the fxnal integrity and conduction speed of the fastest conducing descending motor pathways in the brain and spinal cord. Used to assess integrity of spinal cord, intraop monitoring, and prognosis in humans. De Decker, JAVMA, 2011, DAWS

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2
Q

What is x-linked muscular dystrophy?

A

Deletion of dystrophin gene. C/S - stunted growth, muscle atrophy, pelvic limp weakness, coughing, aspiration pneumonia, hyperinflation of lungs, cervical musculature hypertrophy,

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3
Q

Lomustine MOA

A

alkylating agent; acts via induction of intrastrand and interstrand DNA cross-linking by transferring a chloroethyl group from the chloroethyl-nitrosurea to the O6 methyl group of guanine; lipophilic, crosses BBB; WBC nadir 7 d

GME and NE - no *difference in survival time vs pred alone, RBC count lower with lomustine after first dose, then normalized; able to taper pred faster in GME dogs JAVMA, 2011

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4
Q

GME affects what part of brain?

A

white matter, diffuse or multifocal

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5
Q

Necrotizing encephalitis affects what part of brain?

A

multifocal with 1 or more cavitating lesions on MRI

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6
Q

What is glaucoma?

A

Degenerative dz of retinal ganglion cells and optic nerve; incresed IOP major risk for development

Primary almost always results in vision loss

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7
Q

What antifibrotic used to decrease firboris around gonioimplant?

A

mitomycin C

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8
Q

What IHC confirms diagnosis of nephroblastoma?

A

Wilms tumor-1 (WT-1)

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9
Q

Findings, nephroblastomas, JAVMA, 2011, Brewer.

A

WT-1 stained in 9/11 dogs, females more common, age 5-48 mos, signs: progressive paresis, paraplegia, ataxia, MST 30 d, MST w/ sx 70 d

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10
Q

Where do nephroblastomas come from?

A

kidneys, arise from primitive metanephric blastema (which normally forms nephrons and connective tissue of kidneys)

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11
Q

What breeds get nephroblastomas more commonly?

A

GSD (not in JAVMA study tho) and Goldens; T 10-13, intradural

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12
Q

Most common ocular finding in dogs with systemic hypertension?

A

retinal hemorrhage

>1 lesion 62% sens, 61% spec for identification of hypertension

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13
Q

Ocular manifestations of systemic hypertension

A

retinal hemorrhage, retinal detachment, hyphema, tortuous vessels, subretinal edema

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14
Q

What caused most significant changes in IOP from JAVMA, 2011, Klein study on eyelid manipulation and manual jugular compression?

A
  1. Lateral eyelid extesion with compression of both jugulars
  2. Lateral eyelid extension alone

Both increased IOP ~17 mm Hg

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15
Q

What were risk factors identified for development of seizures after myelography (JAVMA, 2011, da Costa)

A
large dogs (35 X more likely than small dogs)
location (cervical 7.4X more likely than lumbar injection)
lesion location (cervical 4.6X more likely than other areas)
total volume iohexol (but NOT dose)

No relationship with ace and seizures

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16
Q

Findings of DECRA (Decompressive Craniectomy) trial for TBI patients, NEJM, 2011.

A

Craniectomy had * less time with ICP above tx threshold, fewer interventions for increased ICP, and fewer days in ICU and on MV; HOWEVER, worse scores on Extended Glasgow Outcome Scale, higher risk of unfavorable outcome (70% vs. 50%), and no difference in rates of death at 6 months

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17
Q

Ways to treat ICH?

A

sedation, decrease CO2, mannitol, HTS, NMB, external ventricular drainage

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18
Q

What is the ICH index?

A

end hourly measurements of ICP >20 divided by total # measurements x 100

19
Q

Betaxolol MOA

A

selective B1 antagonist - decreases prod’n aqueous humor via blockade at ciliary body, topical
Side effects: bradycardia, syncope, reduced myocardial contracility

20
Q

Timolol maleate MOA

A

nonselective B antagonist, topical, causes mild miosis and may increase aqueous humor outflow in addn’n to inhibiting prodn
Side effects: bradycardia, syndope, decreased contractility, bronchoconstriction

21
Q

MOA carbonic anhydrase inhibitors (CAIs) for tx glaucoma

A

Decrease aqueous humor production by inhibiting CA and decreasing synthesis of bicarbonate in ciliary body

22
Q

Oral CAIs

A

acetazolamide, methazolamide
Adverse efects: GI upset, metabolic acidosis, hypokalemia

Not used much b/c adverse effects

23
Q

Topical CAIs

A

brinzolamide, dorzolamide

Few systemic side effects, local irritation

24
Q

Cholinergic MOA for glaucoma

A

parasympathomimetics - not used with intraocular inflammation. MOA: induce contraction of ciliary body musculature and severe miosis which subsequently opens the drainage angle, facilitating aqueous humor outflow
Contraindicated with anterior lens lux and anterior uveitis

25
Q

Pilocarbine

A

cholinergic, stimulates Ach on iris and ciliary body, locally irriating, not used anymore

26
Q

Demecarium

A

Inirect acting parasympathomimetic, increases duration of ACh normally produced by ciliary body, can cause cholinergic signs if overdose (SLUD)

27
Q

Prostaglandin analogues MOA glaucoma

A

lower IOP by increasing uveoscleral outflow of aqueous humor via action on iris and ciliary body musculature

Contraindicated with lens lux or uveitis.

28
Q

Prostaglandin analogues

A

latanoprost, travoprost, bimatoprosts

29
Q

Other methods to decrease IOP

A

mannitol (works in 15 min), oral glycerin (works in 30 min)

use topical prostaglandin analogue first, then recheck IOP in 20 min, if not lower than use mannitol

30
Q

What did the CRASH trial show?

A

No reduction in mortality with methylpred, slight increase in relative risk of death with steroids (21.1% vs. 17.9%)

31
Q

JVIM, 2009, Status epilepticus in dogs.

A

Dogs with intoxications had a higher risk of developing SE as 1st manifestation of a seizure disorder. Dogs with SE from toxin better prognosis than SE from symptomatic epilepsy.

Dogs that were poisoned 2.7X higher risk of status epilepticus compared to symptomatic/idiopathic (2X higher if compared to all with first seizure)

32
Q

Toxins that can cause SE

A
carbofurane
metaldehyde
paraoxone
crimidine
zinc phosphide
strychnine
diazinon
amphetamine
33
Q

Mannitol beneficial effects

A

Immediate RHEOLOGIC effect: expand plasma volume, reduce HCT, increase RBC deformability, reduce blood viscosity, increase CBF, increase cerebral O2 delivery

Osmotic effect: delayed for 15-30 min while gradients established

34
Q

Risks of mannitol

A

Patients with arterial hypotension, sepsis, nephrotoxic drugs, preexisting renal dz place patients at increased risk for renal failure.
Rebound phenomenon
Renal failure in general b/c hyperosmotic

35
Q

Hypertonic saline MOA

A

Osmotic mobilization of water across the intact BBB to decrease cerebral content, dehydrates endothelial cells and erythrocytes which increases diameter of vessels and deformability of erythrocytes and leads to plasma volume expansion and improved blood flow, reduces leukocyte adhesion in traumatized brain, no rebound effect

36
Q

HTS risks

A

If chronic hyponatremia - central pontine myelinosis, must exclude hyponatremia first, pulmonary edema, CHF

37
Q

ICP monitoring gold standard

A

ventricular catheter (gold standard) connected to an external strain gauge (gold standard) most accurate, low-cost, and reliable. Can be recalibrated in situ. ICP transduction via fiberoptic or microstrain gauge placed in ventricular catheters provide similar benefits but at higher costs.

38
Q

Downside to parencymal ICP monitoring?

A

Cannot be recalibrated in situ

39
Q

What monitoring locations less acurate?

A

subarachnoid, subdural, epidural

40
Q

Where can ICP be measured? (order from gold standard to least accurate)

A

ventricular fluid filled external strain gauge, ventricular micro strain gauge fiberoptic, parencymal, subdural, subarachnoid, epidural

41
Q

Benefits of barbiturates with ICH

A

Cerebroprotective and lowers ICP - Alterations in vascular tone and resistance, suppression of metabolism, inhibition of free radical-mediated lipid peroxidation, inhibition of excitotoxicity

42
Q

Risk factors for seizures after TBI (human)

A
GCS <10
cortical contusion
depressed skull fracture
subdural hematoma
epidural hematoma
intracerebral hematoma
penetrating head wound
seizure within the first 24 hours
43
Q

Fuente, JVIM, 2012. Fibrinolytic activity in CSF in dogs with different neurological disorders.

A

D-dimers were significantly higher in dogs with steroid responsive meningitis-arteritis so may be diagnostic marker of SRMA.

CRP significantly higher in SRMA compared to other diseases, except dogs with SIRS w/o CNS involement.