2 - Altered Mental Flashcards

1
Q

Disorders of consciousness may be divided into?

A

Processes that affect either:

  • arousal
  • content of consciousness

or a combination of both

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2
Q

Where do the neuronal structures responsible for the content of consciousness reside?

A

Cerebral cortex

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3
Q

Content of consciousness includes___

A
  • Self-awareness
  • Reasoning
  • Spatial relationship integration
  • Emotions
  • Complex integral processes that make us human
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4
Q

What is dementia?

A

Failure of the content of portions of consciousness with relatively preserved alerting functions

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5
Q

What is delirium

A

Arousal system dysfunction with the content of consciousness affected as well

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6
Q

What is a coma?

A

Failure of both arousal and content functions

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7
Q

Pts with delirium?

A

Notice symptoms over days with fluctuating effects
They have disordered attention and cognition with either reduced or hyperalert consciousness
Their orientation is impaired and they may have hallucinations, delusions
Their movements are asterixis and often have tremors

Chart on slide 7 if that works better

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8
Q

Pts with dementia?

A

Have an insidious onset with stable symptoms
They are alert with normal attention
Cognition and orientation are impaired
There are generally no hallucinations, delusions or movement abnormalities

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9
Q

Pts with psychiatric disorders?

A

Symptoms have a sudden onset and are stable
Pts are alert with disordered attention and impaired cognition/orientation
Hallucinations are usually auditory and delusions are sustained
Typically no movement disorders

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10
Q

Delirium definition?

A

Transient disorder with impairment of attention and cognition

Aka: 
Acute confusional state
Acute cognitive impairment
Acute encephalopathy
Altered Mental status
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11
Q

Pathophysiology of delirium? (4 general causes)

A
  1. Primary intercranial disease
  2. Systemic diseases secondarily affecting the CNS
  3. Exogenous toxins
  4. Drug withdrawl
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12
Q

With delirium it is not unusual for?

A

Symptoms to be intermittent, not unusual for different caregivers to witness completely different behaviors w/in a brief timespan

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13
Q

Sleep wake cycle for delirium pts?

A

Often disrupted

  • increased somnolence during day
  • agitation at night/sundown
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14
Q

Clinical signs of delirium

A
Tremor
Asterixis
Tachycardic
Sweating 
HTN
Emotional outburst
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15
Q

What type of hallucinations do delirious pts have?

A

Usually visual but auditory is also possible

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16
Q

Symptoms thatre “virtually diagnostic” of delirium?

A

Actue onset of attention deficits and cognitive abnormalities fluctuating in severity throughout the day with worsening symptoms at night

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17
Q

What must be done for a diagnosis of delirium?

Tests

A

R/O drugs, pneumonia, UTI etc

Test electrolytes, hepatic and renal, UA, CBC and chest radiograph

Head CT

Lumbar puncture (post CT)

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18
Q

What are some diagnostic tools that can be used to diagnose delirium?

A

Mini-mental (doesnt do mild impairment)

Quick confusion scale (no reading, writing, or drawing required)

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19
Q

___ often resembles hypoactive delirium but can be differentiated by?

A

Depression

But r/o by:

  • Rapid fluctuation of symptoms
  • Clouding of consciousness (absent)
  • Depressed pts can follow commands
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20
Q

Status epilepticus or complex partial status epilepticus?

A

Unusual cause of confusional state but may be under-recognized

Get an EEG if suspected

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21
Q

Tx for delirium?

A

Detect and treat the underlying cause

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22
Q

Common delirium drugs?

A

Haloperidol (5-10mg PO, IM, IV)

Benzodiazepines: lorazepam (0.5-2.0 PO, IM, IV)

Often combined

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23
Q

Common causes of delirium?

A

Infections

Metabolic/toxic

Neurologic

Cardio

Drugs

Slide 20 has examples of these

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24
Q

Almost all delirium pts get?

A

Admitted

Unless they have a readily reversible cause

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25
Q

What are the largest categories of dementia?

A

Idiopathic dementia
- alzheimers (#1 in US)

Vascular dementia
- diagnosis of exclusion

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26
Q

pathognomonic for alzheimre’s disease?

A

Amyloid deposition

Neurofibrillary tangles and plaques

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27
Q

What is the pathology of vascular dementia?

A

CVD with multiple infarctions

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28
Q

List of possible causes of dementia?

A
Degenerative 
Vascular 
Infectious
Inflammatory
Neoplastic
Traumatic
Toxic (etoh)
Metabolic 
Psychiatric
Hydrocephalic 

(Slide 25 has examples)

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29
Q

Characteristic of the onset of dementia associated with Alzheimer’s?

A

Impaired memory and orientation

with

preserved motor and speech

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30
Q

Early stage of degenerative dementia?

A

Memory loss
Naming problems
Forgetting of items

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31
Q

Middle stage of degenerative dementia?

A
Progression of early stage
\+
Loss of reading
Decreased social function
Loss of direction
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32
Q

Late stage degenerative dementia?

A
Early and middle 
\+ 
Extreme disorientation
Inability to self care
Personality changes
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33
Q

Pts with vascular or multi-infarct dementia show similar symptoms to degenerative but they also often have?

A

Exaggerated/asymmetric DTR
Gait abnormalities
Weakness of an extremity

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34
Q

Presence of focal neurologic signs may suggest?

A

Vascular dementia

Mass lesion

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35
Q

Increased motor tone and extrapyramidal signs (rigidity or movement disorder) indicate?

A

Parkinson’s

36
Q

Labs and images for Dementia?

A
CBC
CMP
UA
Thyroid function
Serum B12
Syphilis test
ESR
Folate level
HIV

CXR
CT/MRI
Lumbar puncture (maybe)

37
Q

You cannot have a diagnosis of probably vascular dementia w/o?

A

Signs of CVD

38
Q

Differentiating between stroke and vascular dementia?

A

Stroke: symptoms w/in 3 mo (temporally related)

VD: fluctuating, stepped course

39
Q

Pseudo dementia?

A

Depression-imitating dementia

40
Q

What may cause a rapid decline in a mild demented pt?

A

UTI
CHF
Hypothyroid

And many more similar things

41
Q

All types of dementia are treatable at least to some degree by?

A

environmental
or
psychosocial interventions

42
Q

Who should antipsychotic drugs be reserved for?

A

Pts with persistent psychotic features
or
those with extreme disruptive or dangerous behaviors

43
Q

How is vascular dementia treated?

A

Tx is limited to tx of risk factors including HTN

44
Q

When should you consider normal-pressure hydrocephalus?

A

If Urinary incontinence and gait disturbance develop early in the disease process

45
Q

Your pt has excessively large ventricles on head CT, what does this suggest? What can you do about it?

A

Normal-pressure hydrocephalus

Consider a trial of lumbar puncture with CSF drainage or ventricular shunting

46
Q

What does the ED do with dementia pts?

A

They r/o thing that are immediately treatable or will kill the pt then attempt to admit or arrange for an outpatient diagnosis.

ED isn’t set up to do all the in depth testing and therapy required for this diagnosis

47
Q

Definition of coma?

A

State of reduced alertness and responsiveness from which the patient cannot be aroused

48
Q

What limitations does the Glasgow coma scale have?

A

Doesn’t acknowledge:

  • hemiparesis
  • focal motor signs

Doesn’t test for
- higher cognitive function

49
Q

GCS

A

Slide 36

50
Q

If a pt is intubated how is their GCS assessed?

A

The verbal testing is not done and a T is written next to the score i.e. 10T

The new lowest score possible is 2T

51
Q

GCS number ranges?

A

13-15: mild head injury
9-12: moderate head injury
= 8: sever head injury (intubate)

52
Q

Common pathophysiology of coma?

A

Deficiency of substrates (hypoxia)

Systemic cause (global)

Primary CNS cause (hemorrhage)

Specific areas (look for CN signs)

53
Q

Do strokes cause comas?

A

Not alone

The function of the brainstem and/or both hemispheres must be impaired for unresponsiveness to occur

54
Q

Cerebral autoregulation maintains cerebral blood flow at a MAP of?

A

50-100mmHg

55
Q

What happens when cerebral MAP is off?

A

Cerebral blood flow is reduced leading to diffuse ischemia

56
Q

What is cerebral perfusion pressure?

A

Cerebral perfusion pressure = MAP - ICP

57
Q

If an unresponsive pt has a hx of seizures you must consider?

A

Ongoing non convulsive seizures
- subtle status epileptics or ictal coma

These may continue in the absence of clinical seizures

58
Q

Coma clinical features?

A

Widely varied:
- increased ICP -> complete loss of motor tone

  • variety of abnormal breath patterns
  • pupillary findings
59
Q

Findings on a toxic-metabolic coma?

A
  • lack of specific brain region findings
  • movements/reflexive posturing is symmetric
  • muscle stretch reflexes symmetric
  • pupils are small but reactive
  • extraocular moments are absent
60
Q

Exception to the rules of toxic coma?

A

Sedative poisoning (barbiturates)

  • pupils = large
  • extraoccular movement absent
  • muscles flaccid
  • apneic (looks like brain death)
61
Q

How do supratentorial lesions present?

A
Progressive hemipareiss
Asymmetric muscle tone/ reflexes
Lateralizing signs
Reflex changes in BP and HR
HTN 
Bradiacardia
62
Q

Coma without lateralizing signs may result from?

A

Decreased cerebral perfusion secondary to increased ICP

63
Q

In reality however supratentorial lesions frequently present how?

A

Large acute supratentorial lesios are seen w/o the features consistent with temporal lobe herniation

64
Q

Signs that a coma may actually be a pseudocoma?

A

Normal and intact

  • Pupilary responses
  • EOM
  • Muscle tone
  • Reflexes

Avoidance of gaze
Nystagmus (strong evidence)

65
Q

The posterior fossa cannot take much expansion so infratentorial lesions often cause?

A

Abrupt coma
Abnormal extensor posturing
Loss of pupillary reflexes
Lose of EOM

66
Q

Pinpoint-sized pupils indicate?

A

Pontine hemorrhage

67
Q

History and PE can vary greatly with coma so:

A

Liberal use of CT scanning is encouraged

68
Q

Abrupt coma suggests?

A

Abrupt CNS failure

  • catastrophic stroke
  • seizure
69
Q

Slow progressive onset coma suggests?

A

progressive CNS lesions

  • tumor
  • subdural hematoma

Also could be metabolic
- hyperglycemia

70
Q

Findings that suggest CNS lesions?

A

Asymmetric findings of CN exam

  • pupillary exam
  • corneal reflexes
  • oculovestibular reflex
71
Q

The goal of the physician when diagnosing coma pts?

A

Rapidly determine if the CNS dysfunction is from

  • diffuse
  • focal

Focal may be treatable with surgery

72
Q

Midline shift and mass lesions?

A

Acute hemorrhage

73
Q

If CT is unremarkable and subarachnoid hemorrhage or CNS infection is suspected?

A

Do a lumbar puncture

74
Q

“Normal” CT with hyperdense basilar artery?

A

Suspect basilar artery thrombosis

Get an MRI or cerebral angiography

75
Q

Continuing state of electrical seizures w/o corresponding motor movements is aka?

A

Nonconvulsive status epileptics

Subtle status epileptics

Electromechanical dissociation of brain and body

76
Q

If a seizing pt stops convulsing and doesnt wake up in 30 min?

A

Consider nonconvulsive status epileptics

77
Q

Tx of coma?

A

Find and fix the problem

Maintain:

  • Airway
  • ventilation
  • circulation
78
Q

Antidotes for some coma’s?

A

Thiamine (before dextrose)
Dextrose
Naloxone

79
Q

What drug is not recommended for routine use as a coma antidote?

A

Flumazenil

80
Q

Elevated ICP tx?

A
  • Paralytic/sedatives
  • Elevate bed 30*
  • mannitol (0.5 - 1.0 gram/kg IV)
  • dexamethasone (10mg IV)
  • hyperventilation (reduce PPCO2)
81
Q

Recommendations for using hyperventilation in ICP pts?

A

Avoid excessive hyperventilation (PPCO2 /= 35 mmHg) in the 1st 24 hrs

Brief hyperventilation for refractory intracranial HTN

82
Q

Haloperidol dose?

A

5-10mg PO, IM or IV

Reduced dosing of 1-2 for elderly

83
Q

Lorazepam dose?

A

0.5 - 2.0mg PO, IM, IV

When combined w haloperidol does = 1-2mg

84
Q

Holy Jesus! What is that? What the fuck is that? WHAT IS THAT, PRIVATE PYLE?

A

Sir, a jelly doughnut, sir!

85
Q

Central herniation syndrome S/S?

A
  • Progressive LOC
  • loss of brainstem reflexes (vitals/pain reaction etc)
  • decorticate posturing
  • irregular respiration
86
Q

S/S Uncal herniation syndrome

A

Medial temporal lobe shifts to compress the upper brainstem, resulting in

  • progressive drowsiness
  • followed by unresponsiveness
  • Ipsilateral pupil is sluggish
  • Dilated/nonreactive pupil (3rd CN compression)

Brain stem is an anchor that gets pushed the opposite direction of the swelling