Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro Critical Care > 328 Coma > Flashcards

328 Coma Flashcards

1
Q

Deep sleeplike state from which the patient cannot be aroused

A

Coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Higher degree of arousability in which the patient can be transiently awakened by vigorous stimuli, accompanied by motor behavior that leads to avoidance of uncomfortable or aggravating stimuli

A

Stupor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Simulates light sleep characterized by easy arousal and the persistence of alertness for brief periods

A

Drowsiness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Signifies an awake-appearing but nonresponsive state in a patient who has emerged from coma

A

Vegetative state / “awake coma”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T or F: Respiratory and autonomic functions are retained in vegetative state

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Term used once vegetative had supervened after a year, wherein the prognosis for regaining mental faculties are almost nil

A

Persistent vegetative state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A partially or fully awake state in which the patient is able to form impressions and think, but remains virtually immobile and mute

A

Akinetic mutism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

A milder form of akinetic mutism characterized by mental and physical slowness and diminished ability to initiate activity; usually a damage to the frontal lobes

A

Abulia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Curious hypomobile and mute syndrome that occurs as part of a major psychosis, usually schizophrenia or major depression

A

Catatonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type of pseudocoma in which an awake patient has no means of producing speech or volitional movement but retains voluntary vertical eye movements and lid elevation, thus allowing the patient to signal with a clear mind

A

Locked-in state

Common cause: infarction or hemorrhage of ventral pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Eyelid elevation is actively resisted, blinking occurs in response to visual threat, eyes move concomitantly with head rotation, limbs to retain postures in which they have been placed by the examiner (catalepsy or “waxy flexibility”)

A

Catatonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Principal causes of coma

A
  1. Lesions that damage the reticular activating system (RAS) in the upper midbrain or its projections
  2. Destruction of large portions of both cerebral hemispheres
  3. Suppression of reticulocerebral function by drugs, toxins, or metabolic derangements (hypoglycemia, anoxia, uremia, hepatic failure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Displacement of brain tissue by an overlying or adjacent mass into a contiguous compartment that it normally does not occupy

A

Herniation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T or F: “False localizing” signs can be seen in herniation since they are derived from compression of brain structures at a distance from the mass

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Brain tissue is displaced from the supratentorial to the infratentorial compartment through the tentorial opening

A

Transtentorial herniation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Impaction of the anterior medial temporal gyrus (uncus) into the tentorial opening just anterior to and adjacent to the midbrain

A

Uncal transtentorial herniation

Figure 328-1, p. 1772

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The nerve that traverses the subarachnoid space and when compressed by the uncus, causes enlargment of the ipsilateral pupil

A

Third nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hemiparesis contralateral to the hemiparesis that resulted from the mass (in short, ipsilateral to the mass)

A

Kernohan-Woltman sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Symmetric downward movement of the thalamic structures through the tentorial opening with compression of the upper midbrain

A

Central transtentorial herniation

Figure 328-1, p.1772

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Displacement of cingulate gyrus under falx and across the midline

A

Transfalcial herniation

Figure 328-1, p. 1772

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Downward forcing of the cerebellar tonsils into the foramen magnum

A

Foraminal herniation

Figure 328-1 p. 1772

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Level of arousal based on horizontal displacement of pineal calcification in cases of acutely enlarging masses

A

3-5mm : drowsiness
6-8mm : stupor
>9mm : coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cerebral blood flow (CBF) in gray matter and white matter

A

Gray matter: ~75ml per 100 g/min

White matter: ~55ml per 100g/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Oxygen consumption of cerebral neurons

A

3.5ml per 100g/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Glucose utilization of cerebral neurons

A

5mg per 100g/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How long will brain stores of glucose last after blood flow is interrupted?

A

~2 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How long will oxygen stores in the brain last after cessation of blood flow?

A

8-10 seconds

28
Q

Unlike hypoxia-ischemia which cause neuronal destruction, what metabolic disorders cause minor neuropathologic changes and are thus reversible

A
  1. Hypoglycemia
  2. Hyponatremia
  3. Hyperosmolarity
  4. Hypercapnia
  5. Hypercalcemia
  6. Hepatic failure
  7. Renal failure
29
Q

Sodium levels that induce confusion

A

<125 mmol/L

30
Q

Sodium levels associated with coma and convulsions

A

<115 mmol/L

31
Q

Serum osmolarity in hyperosmolar coma

A

> 350 mosmol/L

32
Q

T or F: In the approach to a coma patient, most instances, complete medical evaluation, except VITAL SIGNS, FUNDOSCOPY, EXAM FOR NUCHAL RIGIDITY, may be deferred until the neurologic evaluation has established severity and nature of coma

A

True

33
Q

Useful points in the history of a patient in coma

A
  1. Circumstances and rapidity with which neurologic symptoms developed
  2. Antecedent symptoms (confusion, weakness, headache, fever, seizures, dizziniess, double vision, vomiting)
  3. use of medications, drugs, alcohol
  4. chronic liver, kidney, lung, heart of medical disease
34
Q

At what temperature does hypothermia cause coma?

A

<31 C (87.8 F)

35
Q

What can fundoscopy reveal in a coma patient?

A
  1. Subarachnoid hemorrhage (subhyaloid hemorrhages)
  2. Hypertensive encephalopathy (exudates, hemorrhages, vessel-crossing changes, papilledema)
  3. Increased intracranial pressure (papilledema)
36
Q

In a drowsy or confused patient, what is a certain sign of metabolic encephalopathy or drug intoxication

A

Bilateral asterixis

37
Q

Flexion of elbows and wrists and supination of arm suggesting bilateral damage rostral to midbrain

A

Decorticate posturing

38
Q

Extension of elbows and wrists with pronation indicating damage to motor tracts in midbrain or caudal diencephalon

A

Decerebrate posturing

39
Q

Pupillary signs and probable causes

A

> 6mm, unilateral, poorly reactive pupils : compression of Third nerve from cerebral mass

1-2.5mm, bilaterally small, reactive pupils but not pinpoint: metabolic enceph, hydrocephalus, thalamic hemorrhage

<1mm, smaller reactive pupils : narcotic or barbiturate overdose, extensive pontine hemorrhage

40
Q

This phenomenon is summarized as: The eyes look toward a hemispheral lesion and away from a brainstem lesion

A

Conjugate horizontal roving

41
Q

Brisk downward and slow upward movements of eyes associated with loss of horizontal eye movements and is diagnostic of bilateral pontine damage

A

“Ocular bobbing”

42
Q

Slower arrhythmic downward movement followed by a faster upward movement in patients with normal reflex horizontal gaze; indicates diffuse cortical anoxic damage

A

“Ocular dipping”

43
Q

Reflex elevation of eyelids with flexion of neck, normally suppressed in the awake patient

A

“doll’s eyes”

44
Q

Eliciting this response reflects both reduced cortical influence on brainstem and intact brainstem pathways; coma is caused by lesion or dysfunction in cerebral hemispheres

A

Positive “doll’s eyes”

45
Q

Useful test of pontine function

A

Corneal reflex

46
Q

Breathing pattern described as typical cyclic form, ending with a brief apneic period, signifying bihemispheral damage or metabolic suppression

A

Cheyne-Stokes respiration

47
Q

Breathing pattern that is rapid and deep, usually implies metabolic acidosis

A

Kussmaul breathing

48
Q

Result of lower brainstem (medullary) damage recognized as terminal respiratory pattern of severe brain damage

A

Agonal gasps

49
Q

Studies most useful in diagnosis of coma

A
  1. Chemical-toxicologic analysis of blood and urine
  2. Cranial CT or MRI
  3. EEG
  4. CSF examination
50
Q

Ethanol levels in nonhabituated patients that causes impaired mental activity and stupor

A

Impaired mental activity: 43 mmol/L (0.2g/dL)

Stupor : >65 mmol/L (0.3g/dL)

51
Q

Chronic alcoholics develop tolerance which makes them awake at what ethanol levels?

A

> 87 mmol/L (0.4g/dL)

52
Q

T or F:

CT or MRI in coma patients is prudent

A

False.

Imprudent because most cases of coma are metabolic or toxic in origin.

If source of coma remains unknown, a scan should be obtained

53
Q

EEG findings in metabolic coma (e.g. hepatic failure)

A

Predominant high-voltage slowing delta or triphasic waves in frontal regions

54
Q

EEG findings implicating sedative drugs (e.g. BDZ)

A

Widespread fast beta activity

55
Q

T or F:

For patients with altered level of consciousness, imaging study should be performed prior to lumbar puncture

A

True.

To exclude a large intracranial mass lesion.

56
Q

3 broad categories on causes of coma

A
  1. Cases without focal neurologic signs (metabolic and toxic enceph)
  2. Meningitis syndromes (fever, stiff neck, excess of cells in spinal fluid)
  3. Diseases associated with prominent focal signs (stroke, cerebral hemorrhage)
57
Q

Conditions that cause sudden coma

A
  1. Drug ingestion
  2. Cerebral hemorrhage
  3. Trauma
  4. Cardiac Arrest
  5. Epilepsy
  6. Basilar artery occlusion (due to embolism)
58
Q

Coma in cerebrovascular disease is associated with

A
  1. basal ganglia and thalamic hemorrhage
  2. pontine hemorrhage
  3. cerebellar hemorrhage
  4. basilar artery thrombosis
  5. subarachnoid hemorrhage
59
Q

T or F:

Infarction in territory of MCA can cause coma

A

False.

Edema surrounding the large infarctions can cause coma from mass effect.

60
Q

Characterized by headache and sometimes vomiting that may progress quickly to coma with extensor posturing of the limbs, bilateral Babinski signs, small unreactive pupils, impared oculocephalic movements in vertical direction

A

Syndrome of acute hydrocephalus (particulary subarachnoid hemorrhage)

61
Q

State of irreversible cessation of all cerebral function with preservation of cardiac activity and maintenance of respiratory and somatic function by artificial means

A

Brain death

62
Q

Three essential elements of brain death

A
  1. widespread cortical destruction reflected by deep coma and unresponsiveness to all forms of stimulation
  2. global brainstem damage (absent pupillary light reaction and loss of oculovestibular and corneal reflexes)
  3. destruction of medulla (complete and irreversible apnea)
63
Q

Apnea testing procedure

A
  1. Preoxygenation with 100% oxygen thru tracheal cannula
  2. CO2 tension increases ~0.3-0.4 kPa/min (2-3 mmHg/min ) during apnea
  3. arterial PCO2 should be atleast >6.6 - 8.0 kPa (50-60mmHg)

Apnea confirmed if no respiratory effort has been observed in presence of sufficiently elevated PC02

64
Q

Immediate goal in comatose patient

A

Prevention of further nervous system damage

65
Q

Indications for tracheal intubation in comatose patients

A
  1. Apnea
  2. Upper airway obstruction
  3. Hypoventilation

Neuro Critical Care (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions