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idk emergencies Flashcards

1
Q

Mentation change in which the animal has abnormal response to stimulus but still able to respond to their environment to some degree?

A

Obtunded

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2
Q

Mentation chance in which the animal appears comatose but will respond to noxious stimuli

A

Stuporous

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3
Q

Mentation change which the animal has HR, may or may not be breathing but is otherwise unresponsive

A

Comatose

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4
Q

Obtunded mentation change can be located to forebrain, brainstem or both?

A

Both, and forebrain injuries can extend to the brainstem as well

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5
Q

Stuporous and Comatose mentation can be located to forebrain or brainstem?

A

Brainstem

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6
Q

What are the 4 most common causes of mentation change?

A

Neoplasia, Toxin, Trauma and Infectious (MUE)
-vascular is less common than N, T, T or I

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7
Q

Important factors to consider when you see a mentation change

A

-HISTORY (rule out trauma, toxin or metabolic cause)
-Exam (forebrain, brainstem, multifocal or systemic)
+check temp, BP, BW and look for signs of increased ICP
-Do minimum database

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8
Q

What is the primary neurological cause of mentation change?

A

If the cerebral perfusion pressure is not maintained (CPP is directly related to cerebral blood flow)

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9
Q

What is the equation for Cerebral Perfusion Pressure (CPP)?

A

MAP- ICP = CPP
-normal MAP is 50-150mmHg
-normal ICP is 0-15mmHg
-normal CPP is 70-100mmHg

DANGER if CPP < 50mmHg

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10
Q

Causes of increased intracranial pressure (ICP)?

A

edema, inflammation, CSF, tumor or trauma

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11
Q

What needs to happen if ICP increases significantly and what are we protecting?

A

Need to increase MAP or decrease ICP to maintain perfusion to the brain. But you don’t want to increase MAP…

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12
Q

What will you see with the cushings reflex?

A

-severe hypertension! (MAP > 200mmHG)
-reflex bradycardia HR = 30(due to carotid baroreceptors causing vagal stimulation)
-increased PaCO2 in brain
-the brain’s protective mechanism has failed

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13
Q

Other than cushing’s reflex, what are other signs of increased ICP?

A

-pupil changes or asymmetry
+miotic (constricted pupil)–bad
+mydriasis (dilated pupil) –TERRIBLE
-tetraparesis and ataxia
-proprioceptive deficits
-cranial nerve deficits
-decerebrate postures (increased tone in all limbs)

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14
Q

How to decrease ICP (in general terms)?

A

-decrease edema with meds/fluids
-craniectomy
-remove space occupying lesion (tumor, granuloma, depressed skull fracture)

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15
Q

What treatment do you use to decrease edema (in order to decreased ICP)?

A

Acute:
-mannitol (1G/kg over 20 minutes)
+DON’T USE if the animal is dehydrated
-7.2% hypertonic saline (4mL/kg over 15 minutes)

Long-term:
-Corticosteroids (anti-inflammatory dose)
-diuretics (carbonic anhydrase inhibitor)

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16
Q

How do you diagnose a stroke?

A

-MRI! MRI! MRI!
-may be able to see on CT but not likely
-CSF analysis?

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17
Q

What are signs of a stroke?

A

Peracute/acute onset focal non-progressive or convulsive brain signs

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18
Q

What are the 2 types of stroke?

A

-ischemic stroke (ex. blood clot thats decreasing blood flow to certain area of brain)
-hemorrhagic stroke (bleed that increases ICP)

want to test for underlying cause

19
Q

What is difference between decerebrate postures and decerebellate posture?

A

Decerebrate: ALL limbs extended
Decerebellate: front limbs extended, pelvic limbs flexed

20
Q

What qualifies as Status Epilepticus?

A

-failure of a seizure to terminate
-any seizure lasting longer than 5 minutes
- > 2 seizures w/o return to normal consciousness

21
Q

How does Status Epilepticus cause brain damage?

A

-glutamate released–> NMDA receptors–> cause either sodium or calcium influx:
+sodium influx leads to cytotoxic edema
+calcium influx leads to mitochondrial damage
-both cytotoxic edema and mitochondrial damage leads to cell death (irreversible damage)

22
Q

What are the systemic effects of status epilepticus?

A

-hypertension
-tachycardia
-arrhythmias
-hyperglycemia (exacerbate neuronal damage)
-respiratory compromise (poor ventilation, noncardiogenic pulmonary edema, asp. pneumonia)
-hyperthermia
-acidosis
-myoglobinuria

23
Q

How can status epileptics cause death?

A

-ventricular arrhthmias
-respiratory compromise
-renal failure

24
Q

How do you treat status epilepticus?

A

STOP THE SEIZURE!
-check temperature—active cooling
-oxygen supplementation
-anti-epiletic therapy (benzos then propofol if didn’t work)

25
Q

What is the anti-epileptic therapy used for status epilepticus?

A

BENZOs:
-diazepam (IV 0.5mg/kg)
-midazolam (IN or IV 0.25mg/kg)

After 3 failed benzos –> Propofol (IV 4-6mg/kg to effect)

May need to do CRI (benzo or propofol) if seizure continues

Add in long-term treatment:
-phenobarbital (15mg/kg IV loading dose)
-levetiracetam “keppra” (60mg/kg IV loading dose)

26
Q

What are causes of a reactive seizure?

A

-toxin (meds, plants, food, insecticides)
-metabolic:
+hypoglycemia
+hepatic encephalopathy
+renal encephalopathy

27
Q

What are causes of epilepsy?

A

-idiopathic epilepsy
-structural epilepsy
-epilepsy of unknown cause (less common)

28
Q

If ICP is increased, what does it do to MAP and CPP?

A

-MAP must increase (but also increases ICP)
-CPP decreases

29
Q

During a seizure, edema and inflammation occur which causes what?

A

An increased ICP–> Decreased Cerebral Perfusion Pressure (CPP)

30
Q

What is the modified glasgow coma scale (MGCS)
used for?

A

-It assesses head trauma and helps determine prognosis (when assessed over 48hrs)
-can monitor trends for pts w/ intracranial signs
+evaluate every 4-24 hrs depending on severity

31
Q

What are the 3 categories that modified glasgow coma scale (MGCS) evaluates?

A

-motor activity
-brain-stem reflexes
-level of consciousness

32
Q

What is the prognosis for different MGCS scores? Hint: it’s out of 18

A

-3-8 grave
-9-14 guarded
-15-18 good

33
Q

Steps to caring for a traumatic brain injury

A
  1. Does it have seizures–if so treat that (benzo, phenobarbital or keppra)
  2. No seizures–> do systemic evaluation and ABC emergency therapy (O2, ventilator, TPR, BW, etc)
  3. Do modified Glasgow coma scale once patient is stable. Depending on score or trends may need to do more interventions
  4. Imaging
34
Q

What are signs of tetanus and when would you expect to see them?

A

-signs: RIGIDITY in all limbs and posture
+localized tetanus more common in cats where dogs tend to be more generalized

-Expect to see at 5-10 days of infection

35
Q

Is there a specific treatment for Clostridium tetani, if so what is it?

A

YES, antimicrobial therapy (metronidazole) +/- anti-toxin

36
Q

What are the signs of botulism and when would you expect to see them?

A

-Signs: FLACCID paralysis (LMN) often autonomic signs too

-Expect to see w/in 12 hours of exposure

37
Q

Is there a specific treatment for Clostridium botulinum, if so what is it?

A

No, treatment is supportive care.

38
Q

How does Clostridium botulinum toxin act on the body?

A

It binds to synaptobrevin or SNAP-25 –> this prevents the release of Ach and therefore can’t get excitation in muscle
——flaccid paralysis

39
Q

How does Clostridium tetani toxin act on the body?

A

It binds to synaptobrevin in the inhibitory cells in the spinal cord and brainstem (Renshaw cells)—-no inhibition of excitation —–muscle rigidity

40
Q

What are clinical signs of metabolic encephalopathies?

A

-seizures
-behavior changes (aggression, anxiety, dementia, mania)
-mentation change
-cortical blindness

41
Q

How does hypoglycemia cause seizures?

A

-lack of glucose causes lack of phosphorus –> ATPase pumps don’t have energy to pump Na out of cell in K in cell
-Na accumulates in cell and K accumulates outside of cell—> membrane cannot relax (can’t go back to resting potential)—-> causes seizure

42
Q

How does hyponatremia cause seizures?

A

-when there is low systemic Na (less Na outside cell than in cell), the water will flow into cells
-this causes swelling of the neuron/axon itself which can lead to cell death
-want to fix this slowly!

43
Q

How does hypocalcemia lead to seizures?

A

-Ca bind to the sodium channels, when in low quantities, it will not be bound to the channels allowing for Na to enter the cell more easily
-More Na in the cell leads to depolarization —> seizures

44
Q

How does hepatic encephalopathy cause seizures?

A

There is excess NH3 (ammonia), converts glutamate (excitatory NT) back into glutamine
—this leads to neuronal dysfunction

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