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Clinical Neuroscience 2 > Clinical- 3 > Flashcards

Clinical- 3 Flashcards

1
Q

What is a coma?

A

A state of unconsciousness where the pt doesnt respond to environmental stimuli and cannot be awaken

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2
Q

Where in the brainstem are the disturbances to cause the coma?

A

reticular activating system ABOVE the midpons or of both cerebral hemispheres

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3
Q

What are the 5 defining characteristics of comas?

A
  1. eyes closed
  2. no speaking
  3. cant move
  4. cant respond to verbal stimuli
  5. cannot respond to pain
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4
Q

What is the first thing u should do when treating a coma?

A

establish ABCs

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5
Q

What is the next procedure to do for Dx in a coma?

A

blood labs for CBC, hepatic/renal panels, serum glucose/electroltes, PT/PTT

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6
Q

What 2 easy things should you rule out (which are easily correctible) in the cause of the coma?

A

hypoglycemia and opiate OD

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7
Q

How can u evaluate the metabolic cause of the coma?

A

blood gas and pH studies

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8
Q

What happens if the coma pt has szrs?

A

treat it

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9
Q

Why do u give 25g of dextrose?

A

tosee if its a hypoglycemic cause

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10
Q

Why do u give 100mg of thiamine for the comapt?

A

prevents dextrose precipitation and prevents exasterbation of Wenicke’s encephalopathy

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11
Q

Why do u gie 0.4-1.2mg naloxone for the come pt?

A

to see if its an opiate OD

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12
Q

Why do u NOT give flumenazil for the coma pt?

A

cuz it can precipitate status epilepticus

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13
Q

What causes a SUDDEN onset of coma?

A

vascular origin, esp brainstem stroke or subarachnoid hemorrhage

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14
Q

What is the cause of rapid progression from hemispheric signs to a coma?

A

intracerrebral hemorrhage

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15
Q

What are some cuases for a slower/longer progresison for the coma?

A

tumors, abscesses, or chronic subdural hematomas

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16
Q

What is the cause for a coma that follows a confusional state or agitated delirium w/o lateralizing signs or Sx?

A

metabolic

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17
Q

What are raccoon eyes?

A

periorbital ecchymoses

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18
Q

What is battle sign?

A

swelling or bruising over the mastoid bone behind the ear

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19
Q

What is hemotympanum?

A

blood behind the tympanic membrane

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20
Q

What is CSF rhinorrhea/otorrhea?

A

CSF coming out of nose or ear

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21
Q

Coon eyes, battle sign, hemotympanium, or CSF rhinorrhea/otorrhea are all signs of what?

A

basilar skull Fx from head trauma

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22
Q

What are the early diencephalic findings of the coma pt?

A

small pupils (<2mm), reactive, reflex intact, motor response is purposeful and asymmetric

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23
Q

What ar ethe late diencepalic findings of coma?

A

similiar to early but pain causes decorticate posturing (lol neuroanatomy)

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24
Q

What are the sign for midbrain coma?

A

pupils fixed and midsized (5mm), reflex in adducion is impaired, decerebrate (eeee)

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25
Q

What are the signs of pons/medulla involvement in comas?

A

fixed, midsized pupils, loss of abduction and adduction, flaccid

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26
Q

When do u get decorticate positioning?

A

. Decorticate posturing is indicative of lesions involving the thalamus either directly or from large hemispheric masses above it.

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27
Q

When do u get decerebreate posturing?

A

This posture occurs when midbrain function is compromised and implies a more severe brain dysfunction than decorticate posturing.

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28
Q

What are the Sx of an uncal herniatioN?

A

The medial portion of the temporal lobe (uncus) is forced across the cerebellar tentorium and on to the rostral brainstem causing ipsilateral pupillary dilation and impaired adduction of the eye (uncal syndrome) before losing consciousness.

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29
Q

What happen sin cheyne-stokes respirations?

A

there is alteration between apnea and hypernea

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30
Q

True or False: cheyne-stokes and central hyperventilation are not useful in localizing the cause of coma.

A

True. They’re also seen with metabolic disturbacnes and structural lesions

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31
Q

Where is the lesion to cause ataxic and gasping ventialtions?

A

pontomedulla

32
Q

What is the classic finding for metabolic encephalopathy?

A

the presence of reactive pupil even with impaired brainstem function.

33
Q

What are the 2 classes of drugs to treat cerebral edema?

A

glucocorticoids and osmotic diuretic agents.

34
Q

The drugs dexamethasone, prednisone, methylprednisone, and hydrocortisone belong to which class?

A

Glucocorticoids

35
Q

The drugs mannitol and hypertonic saline belong to which class?

A

Osmotic diuretic agents.

36
Q

Subdural hematoma (SH)- cause

A

trauma

37
Q

SH- pathogenesis

A

shearing of bridging veins

38
Q

SH- clinical findings

A

headache and altered consciousness with comes and goes. CL hemiparesiss, IL miosis

39
Q

SH- Tx

A

surgical evaculation

40
Q

Epidural Hematoma (EH)- cause

A

trauma to lateral skull

41
Q

EH- pathogensis

A

tearing of MMA

42
Q

EH- clinical findings

A

heaedache, vomiting, obtundation, srs, and focal signs

43
Q

EH- tx

A

prompt surgical evacuation

44
Q

Intercerebral hemorrhage (IH)- cause

A

chronic HTN

45
Q

IH- pathogenesis

A

transentorial heriation –> nuchal rigidity, eyes deviate toward side of hemorrhage and away from hemiparetic side.

46
Q

IH clinical findings

A

headache, N/V, hemiparesis

47
Q

IH- Tx

A

limited, as these are usually brief

48
Q

Brain abscess (BA)- cause

A

metastasis of infection > direct infection > unknown source of infection > infection with recent or remote head trauma > infection assocaited with cyanotic congential heart disease

49
Q

BA- clinical findings

A

headache, focal signs, hyperthermia, ↑ WBC count

50
Q

BA- Tx

A

antibiotics and/or surgery (if there is a big ass mass)

51
Q

Which pts typically have pontine hemorrhages?

A

HTN pts

52
Q

What is the hallmark of pontine hemorrhages?

A

apoplectic onset

53
Q

Which artery is screwed up in pontine hemorrhages?

A

basilar a.

54
Q

Sx of pontine hemorrhages?

A

ocular bobbing (quick downward movement, slow return to normal position), pinpoint pupils, and loss of lateral eye movements

55
Q

Global cerebral ischemia (GCI)- cause

A

Cardiac arrest

56
Q

GCI- pathogenesis

A

encephalopathy that leads to coma

57
Q

GCI- clinical Sx

A

rapid pupil dilation, opisthotonic posture (hyperextension and spasticity)

58
Q

GCI- Tx

A

prompt re-establishment of cerebral perfusion

59
Q

GCI- prognosis

A

good if u return blood quickly. bad if u cant get pupillary reactivity within 1 day or consciousness within 4 days

60
Q

The intoxication of which drug is the most common cause of coma?

A

Sedative-hypnotic drugs

btw middle-aged women LOVE trying to commit suicide by ODing on this. Classic 2 bottles of wine + bottle of sedatives = 5150 UP IN HERE.

61
Q

What the 2 classes of drugs that are sedative-hypnotic drugs?

A

barbituates and benzos

62
Q

What is the progression for sedative-hypnotic drug comas?

A

drug intoxication –> nystagmus in all directions + dysarthria + ataxia –> coma –> presents with UMN lesion-like Sx

63
Q

What are the Sx of sedative-hypnotic drug comas?

A

absence of extraocular movements with preserved pupillary reflex

64
Q

What is the Tx to sedative-hyponotic drug comas?

A

Be supportive and maintain adequate ventilation and circulation. Dialysis may be used to reduce the drug intoxication.

65
Q

What are the Sx to alcohol-induced comas?

A

produces a similar syndrome without nystagmus during wakefulness, impairment of lateral eye movements, or progression to coma.

66
Q

What are the Sx to opiate-induced comas?

A

Characterized by pupillary constriction similar to miotic eye drops, pontine hemorrhage, Argyll Robertson pupils, and organophosphate poisoning

67
Q

How can you Dx opiate OD’s?

A

Naloxone

68
Q

What are the complications to hepatic encephalopathy?

A

Somnolence, delirium, and ultimately coma due to severe liver disease

69
Q

What are the Sx to hepatic encephalopathy?

A

Patients will present with increased muscle tone, hyperreflexia, alternating hemiparesis, and decorticate or decereberate posturing

70
Q

What causes hepatic encephalopathy?

A

inability to detoxify ammonia

71
Q

What happens in persistent vegetitative state?

A

Happens when you eat too much salad. Patients who go into a coma because of cerebral hypoxia or ischemia, will sometimes “wake up.” These patients will show an ability to spontaneously open their eyes but they cannot comprehend or produce language and cannot produce purposeful movements. That are in what is called a minimally conscious state where they are “awake but not aware.”

72
Q

Where is the damage to cause locked-in syndrome?

A

damage to the brainstem below the midpons (the reticular formation above this area is responsible for consciousness)

73
Q

So if I say: not awake and not aware. What am I?

A

hepatic encephalopathy

74
Q

So if I say: awake and aware. What am I?

A

locked-in syndrome

75
Q

So if I say: awake and not awake. What am I?

A

persistent vegitative state

76
Q

What are the 4 factors to determine brain death?

A

1) Patient must be unresponsive to sensory input such as pain and speech.
2) Brainstem reflexes are absent, attempts to elicit eye movements passively via oculocephalic (doll’s head) and vestibuloocular (cold caloric) maneuvers are unsuccessful. Respiratory responses are also absent, when PCO2 is raised to 60mmHg, the patient does not respond.
3) The brain dysfunction is irreversible. In order to determine this, the cause of coma must be known.
4) Time is also a factor: 6 hours with a confirmatory isoelectric (flat) EEG, 12 hours without a confirmatory isoelectric EEG, and 24 hours for anoxic brain injury without a confirmatory isoelectric EEG.

Clinical Neuroscience 2 (16 decks)

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