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SRNA3AdvancedPatho2 > Final NEURO Degenerative > Flashcards

Final NEURO Degenerative Flashcards

1
Q

Explain the mechanism of Huntington Disease

A

Results in altered Huntington protein that damages neurons

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2
Q

What is Huntington disease? Genetic

A

Inherited disease
Autosomal dominant gene
Carried on Huntington gene (chromosome 4)

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3
Q

When does Huntington manifests?

A

Does not usually manifest until 3rd to 5th

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4
Q

In Huntington’s Disease there is

A

Progressive atrophy of brain

Particularly in caudate nucleus

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5
Q

Huntington’s Disease and neurotransmitters

A

Depletion of GABA in the basal nuclei

Reduced levels of ACh in the brain

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6
Q

How is huntington’s disease diagnosed?

A

DNA analysis for the protein mutation

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7
Q

Huntington’s disease Cure?

A

No cure

Supportive treatments

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8
Q

Huntington’s disease Treatment: Medication use?

A

Tetrabenazine – suppresses hyperkinetic movements (central monoamine depleting agent)

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9
Q

Huntington Disease Anesthesia Considerations: Airway

A

Dysphagia & ↑ risk of aspiration

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10
Q

Huntington Disease Anesthesia Considerations: Depolarizing agents

A

Caution with Succinylcholine- ↑ sensitivity

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11
Q

Huntington Disease Anesthesia Considerations: NONDepolarizing agents

A

↑ ↑ ↑ sensitivity to nondepolarizing muscle relaxants

– titrate carefully

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12
Q

Huntington Disease Anesthesia Considerations: Prepare for

A

Prepare pt. and family for poss. Post-op. Ventilation

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13
Q

Explain the mechanism of Myasthenia Gravis

A

Auto-antibodies attack ACh receptors @ NMJ
Skeletal muscle weakness (without atrophy)
Ocular & facial muscles usually affected first

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14
Q

Explain the mechanism of Myasthenia Gravis

A

Auto-antibodies attack ACh receptors @ NMJ
Skeletal muscle weakness (without atrophy)
Ocular & facial muscles usually affected first

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15
Q

What are the signs and symptoms of Myasthenia Gravis?

PSW CD

A 
Ptosis, diplopia
Slurred speech, dysphagia, aspiration
Weakness in arms & legs
Chronic muscle fatigue
Difficulty breathing
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16
Q

DIAGNOSIS Myasthenia Gravis Diagnostic tests:

A

Electromyography
Serum antibody test
Edrophonium (acetylcholinesterase inhibitor) temp. reversal

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17
Q

Treatment of Myasthenia Gravis : Medications primary

A

Anticholinesterase agents

Pyridostigmine

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18
Q

Treatment of Myasthenia Gravis : Steroids

A

Glucocorticoids

Suppress immune system

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19
Q

Myasthenia Gravis: Surgery

A

Thymectomy (70% of cases have thymus hyperplasia)

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20
Q

Treatment of Myasthenia Gravis: Antibodies

A

Plasmaphoresis (Removal of antibodies from the blood)

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21
Q

Myasthenia Gravis – Anesthesia : What can aggravate Myasthenia?

A

Aminoglycosides (aggravate MG)

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22
Q

For Myasthenia, When is Post-op. ventilation required?

DPDV

A

Disease with duration > 6 yrs.
Presence of COPD
Daily dose of pyridostigmine > 750mg
Vital capacity < 2.9 L

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23
Q

Do all patients with Myasthenia gravis require Post op ventilation?

A

NO

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24
Q

Myasthenia Gravis – Anesthesia

Pts may be resistant to

A

succinylcholine

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25
Q

Myasthenia Gravis avoid preop

A

Avoid opioids pre-op. (respiratory effects)

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26
Q

Myasthenia Gravis and IV anesthetic?

A

Use short-acting IV anestheic for induction

Consider intubation without muscle relaxants

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27
Q

Myasthenia Gravis and NDNMB

A

↑ sensitivity to nondepolarizing muscle relaxants – if used, initial dose should be titrated to response according to
peripheral nerve stimulator.

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28
Q

Myasthenia Gravis: Atracurium and vecuronium

A

potency is increased twofold compared to response in normal pt.

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29
Q

For Myasthenia Gravis, If maintenance requires nondepolarizing drugs,

A

decrease intial dose by half to two thirds

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30
Q

Your patient has recent changes that include loss of arm swings when walking and absence of head rotation when turning the body. A loss of facial expression, and decreased emotional response is also noted. what would these signs indicate?

A

Parkinson’s Disease

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31
Q

Loss of facial expression, and decreased emotional response

A

Parkinson’s Disease

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32
Q

Mechanism of the Disease PARKINSON’S: what is it?

A

Progressive degeneration of the substantia nigra in the

midbrain

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33
Q

Parkinson’s and location of dopamine production

A

Substantia nigra normally produces Dopamine which

controls unwanted movements

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34
Q

Parkinson’s and Dopamine

A

↓ Dopamine leads to unopposed firing of LMNs & tremor

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35
Q

Parkinson’s and CLASSIC Triad of major signs:

A

Rigidity (first in neck muscles)
Akinesia
Tremor

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36
Q

Treatment of Parkinson’s (DAA SPOT)

A

Dopamine replacement therapy with Levodopa w/
decarboxylase inhibitor (prevents peripheral conversion)
Anticholinergic drugs
Amantadine
Speech and language pathologist
PT
OT ( Improve balance, coordination)

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37
Q

What is the role of Decarboxylate inhibitor in Parkinsons?

A

decarboxylase inhibitor (prevents peripheral conversion)

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38
Q

Medication management for the patient with Parkinson’s undergoing surgery? When should it be administered?

A

Parkinson Disease – Anesthesia Mgmt.
Maintain Levodopa peri-op.
- Oral levodopa can be administered ~20 min. before inducing anesthesia

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39
Q

Anesthesia considerations with Parkinson’s Interruption of levodopa?

A

Interruption of therapy can lead to muscle rigidity interfering with lung ventilation

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40
Q

Important anesthesia considerations for Parkinson’s

What medication to avoid?

A

Avoid Butyrophenones - antagonize effects of dopamine

ex. droperidol, haloperidol

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41
Q

Hemodynamics instability for the patient with parkinson’s disease ?

A

Hypotension & cardiac arrhythmias possible during

anesthesia

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42
Q

Your patient is a 27 year old who states that she has been experiencing, numbness, tingling, and burning that started in legs and later included her arms. She has also begun to notice some loss of coordination and vision disturbances. Her MRI Appears below? What does it indicate?

A

Multiple Sclerosis

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43
Q

Tests that can be ordered to diagnosis MS? (MECE)

A

MRI for diagnosis and monitoring
Evoked potential tests (VER)
CSF (antibodies, abnormal cells)
EEG if seizures present

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44
Q

Seizures and Multiple Sclerosis

A

Increase incidence of Seizures in MS patiens

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45
Q

Explain the mechanism of Multiple Sclerosis : Progressive

A

Progressive autoimmune demyelination of CNS neurons &

Cranial Nerves

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46
Q

Explain the mechanism of Multiple Sclerosis loss of

A

Loss of myelin interferes with conduction of impulses
Affects motor, sensory, & autonomic fibers
Occurs in diffuse patches in the nervous system

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47
Q

Course of MS

A

Course variable: subacute w/ relapse and remission or

chronic and aggressive

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48
Q

MS Cure? and what is the role of treatment options

A

No cure. Treatments control symptoms and slow progression.

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49
Q

MS medications for treatments?

A

Corticosteroids
Interferon β
Low-dose Methrotrexate
PT, OT

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50
Q

MS Anesthesia Considerations:and the Use of SPINAL ANESTHESIA? which one do not cause that effect?

A

Spinal anesthesia known to cause Post-op. exacerbations

Epidural and peripheral blocks usually do not

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51
Q

MS and GA

A

General anesthesia usually tolerated well

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52
Q

MS and SUCC

A

Avoid succinylcholine - ↑ risk of hyperkalemia

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53
Q

MS and Steroids

A

Continue steroids peri-op.

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54
Q

Amyotrophic Lateral Sclerosis (ALS) - AKA

A

Lou Gehrig disease

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55
Q

ALS cause and genetic

A

No identified cause
Genes on various chromosomes have been linked to the
disease

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56
Q

ALS Mechanism of disease

A

Progressive degenerative disease affecting upper motor
neurons in the cerebral cortex and lower motor neurons in
brainstem and spinal cord (at anterior horns)

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57
Q

Inflammation and cognition in ALS

A

No indication of inflammation around the nerves

Cognition unimpaired

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58
Q

Amyotrophic Lateral Sclerosis (ALS) Anesthesia Considerations: GETA

A

General anesthesia associated with exaggerated ventilatory depression

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59
Q

ALS and SUCC

A

Avoid Succinylcholine (↑ risk of hyperkalemia)

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60
Q

ALS and NDNMB –> There is

A

prolonged response to nondepolarizing muscle relaxants

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61
Q

ALS and Regional: and why?

A

Avoid regional anesthesia – exacerbates disease symptoms

62
Q

ALS and EPIDURAL

A

Epidural anesthesia ok

63
Q

Causes of Alzheimer’s : Progressive

A

Progressive cortical atrophy

64
Q

Pathophysiology of Alzheimer’s BCD

A

Beta-amyloid plaques & neurofibrillary tangles form destroy neuron microtubules
Disrupt neurotransmitter function
↓ choline acetyltransferase = ↓ ACh levels

65
Q

Most common neurodegenerative disease

A

Alzheimer’s Disease

66
Q

Alzheimer’s is responsible for

A

Responsible for 40-80% of all cases of dementia

67
Q

Affected with Alzheimer’s

A

Affects ~20% of pts. over 80

68
Q

Alzheimer’s Specific cause

A

unknown

69
Q

Alzheimers cause unknown but repetitive

A

Repetitive DNA sequences on different chromosomes have been associated with AD

70
Q

ALzheimer’s and diagnosis (PCP)

A

PET scan exhibits areas of ↓ cerebral blood flow
CT demonstrates ventricular dilation & cortical atrophy
Postmortem examination of brain tissue

71
Q

Alzheimer’s detection other tests

A

Peanutbutter detection Test

72
Q

Explain why cholinesterase inhibitors are used to treat Alzheimer’s Disease?

A

Because there is decrease ACH in Alzheimer’s. Cholinesterease break down ACH. Cholinesterase inhibitors prevent further breakdown of ACh

73
Q

Why is glycopyrrolate a preferred anticholinergic for AD patients?

A

It does not cross BBB

74
Q

AD – Anesthesia Considerations

Preoperative sedation

A

usually avoided - may aggravate dementia & precipitate postop. confusion.

75
Q

AD Pts. Taking cholinesterase inhibitors and SUCC

A

may have prolonged duration of action with succinylcholine.

76
Q

AD and NDNMB

A

Resistance to nondepolarizing muscle relaxants with

acetylcholinesterase inhibitors.

77
Q

AD is preferred anticholinergic - doesn’t cross

BBB.

A

Glycopyrrolate

78
Q

Atropine and scopolamine

A

Atropine & scopolamine may cause increased confusion

79
Q

Your patient has a distorted sense of reality. See CT , what are the abnormalities seen? What do they indicate? Common changes include Schizophrenia are REEAD

A

–Reduced gray matter in temporal lobes
–Enlarged third and lateral ventricles
– Excessive dopamine secretion
Indicate Schizophrenia

80
Q

Schizophrenia has both

A

positive and negative symptoms.

81
Q

Schizophrenia Positive symptoms

A

exaggeration of normal behavior with hallucinations & delusions

82
Q

Schizophrenia Negative symptoms

A

Reflect decline in normal function with apathy, flattened affect
changes in hygiene & appearance, and occupational or social withdrawal.

83
Q

Schizophrenia Tx of positive symptoms

A

Dopamine receptor blockers (D2 & D4)

Improve the ‘positive’ symptoms

84
Q

Schizophrenia Tx of negative symptoms

A

“Atypical” serotonin receptor blockers (5-HT2A)

Improve the ‘negative’ symptoms

85
Q

Schizophrenia – Anesthesia Mgmt.

A

–Be mindful of the effects of antipsychotic medications
->Prolonged QT interval can lead to torsades de pointes
–sedation that may lessen anesthetic requirements
– seizures

86
Q

Schizophrenia – anesthesia Mgmt. Hepatic enzymes and hypotension?

A

↑ hepatic enzymes
postural hypotension caused by alpha adrenergic
blockade

87
Q

What is ECT used for ?

A

ECT - Electroconvulsive therapy may be used in severe

depression unresponsive to medications.

88
Q

Used of ECT include

A

For treatment of medically resistant depression, schizophrenia or bipolar disorder w/ suicidal tendencies

89
Q

ECT is Performed

A

under anesthesia

90
Q

During ECT , small

A

Small electric currents used to induce brief small seizures

91
Q

ECT does what?

A

Effectively reverses certain mental illnesses

92
Q

ECT CV effects

A

10-15 second stimulation of the parasympathetic nervous
system produces bradycardia & hypotension followed by hypertension and tachycardia that lasts for
several minutes as a result of sympathetic nervous system
activation.

93
Q

Other side effects of ECT

A 
Other side effects:
 ↑ intragastric pressure
 ↑ ICP
 ↑ IOP
 ↑ cerebral blood flow
 Memory impairment (most common long-term effect)
94
Q

Other side effects of ECT

A 
↑ intragastric pressure
↑ ICP
↑ IOP
↑ cerebral blood flow
Memory impairment (most common long-term effect)
95
Q

2 most common causes of death related to ECT:

A

Cardiac dysrhythmias & MI

96
Q

ECT – Anesthesia Mgmt.

Glycopyrrolate

A

IV 1-2 min. before induction decreases excess salivation & bradycardia

97
Q

ECT – Anesthesia Mgmt. Beta Blocker

A

Esmolol 1 mg/kg IV just prior to induction can attenuate

tachycardia & HTN

98
Q

ECT – Anesthesia Mgmt. HTN

A

HTN can be ameliorated w/ nitroglycerine

99
Q

ECT and Methohexital

A

Methohexital (0.5-1.0 mg/kg IV) is standard for induction
Has rapid onset & recovery
Short duration of action and minimal anticonvulsant effects

100
Q

ECT beside methohexital

A

Propofol is alternative but has anticonvulsant effect

101
Q

ECT – Anesthesia Mgmt. Succinylcholine and dose

A

Succinylcholine IV promptly after induction reduces risk of potentially dangerous muscle contractions/bone fxs
Dose of 0.3 to 0.5 mg/kg IV sufficient to attenuate contractions but still permit visual confirmation of seizure activity

102
Q

ECT and anesthesia mgmt. EEG

A

most reliable way to confirm seizure

103
Q

ECT and anesthesia mgmt: Use of Tourniquet

A

Alternatively, a tourniquet can be applied to a limb
before administration of Succ. – subsequent tonic/clonic
movement of limb provides evidence that seizure has
occurred.

104
Q

ECT and Anesthesia Management: Pacemakers and defibrillators

A

Pacemakers/defibrillators are shielded and not affected
by ECT, however – external magnet should be available
Ensure capability of converting pacemakers to asynchronous modes if malfunction does occur

105
Q

ECT and Cardioverter/defibrillators

A

should be turned off prior to ECT and reactivated afterward

106
Q

ECT Methods to monitor Pacemaker function PPPE

A

External MAGNET SHOULD BE AVAILABLE

107
Q

What is Neuroleptic Malignant Syndrome?

.

A

A rare complication of antipsychotic drug treatment that is
potentially fatal and is hypothesized to be caused by
central nervous system depletion of dopamine.

108
Q

Neuroleptic Malignant Syndrome usually occurs ?

A

Usually occurs within the first few weeks of treatment, or

when there is an increase in the dose of the drug

109
Q

Causes of death in NMS: CCRH

A

–CHF
–RF
–cardiac dysrhythmias
–hypoventilation

110
Q

Neuroleptic Malignant Syndrome Signs/Symptoms: (SHRD)

A

Severe muscle rigidity (may require mechanical ventilation)
Hyperpyrexia (pts. have ↑ susceptibility to developing MH)
Rhabdomyolysis
Dehydration & myoglobinuria (can lead to renal failure)

111
Q

Shy-Drager Syndrome aka

A

Multiple System Atrophy (MSA) a.k.a. “Shy-Drager Syndrome”

112
Q

Shy-Drager Syndrome Develops in

A

50s

113
Q

Shy-Drager Syndrome there is

A

Chronic degeneration of the ANS w/ ↓ Norepi levels
Characterized by severe orthostatic hypotension & urinary
involvement (urgency/incontinence)

114
Q

Multiple System Atrophy (MSA) or SHY DRAGER – Anesthesia Considerations- ANS and CV

A

↓ ANS / Cardiovascular responses with change in body

position, positive airway pressure & acute blood loss

115
Q

Avoid what drugs with Multiple System Atrophy (MSA) aka. Shy DRAGER ; monitor what?

A

Avoid drugs with negative inotropic effects

Closely monitor systemic BP

116
Q

BP correction for Multiple System Atrophy (MSA) Aka shy drager

A

Prompt correction of hypotension w/ crystalloid or colloid
Phenylephrine is preferred direct-acting vasopressor
Administer small doses initially

117
Q

Alpha receptors and MSA:

A

α-receptors are up-regulated in MSA 2o to ANS chronic
denervation and produce exaggerated response to small
doses of the drug

118
Q

MSA aka SHY drager

A

Continuous infusion of phenylephrine may be used to maintain BP during GA

119
Q

MSA aka SHY DRAGER – Anesthesia Considerations

Volatile anesthetics

A

can diminish C.O. & contractility leading to exaggerated hypotension

120
Q

Absent with MSA

A

Compensatory vasoconstrictive/tachycardic responses absent

121
Q

MSA aka shy drager, treat with bradycardia

A

Atropine or glycopyrrolate to treat bradycardia

122
Q

MSa aka shy drager “ NDNMB

A

Vecuronium preferred muscle relaxant

Has less effect on systemic circ.

123
Q

MSA aka Shy drager: Adjust

A

propofol or thiopental dose & rate according to pt’s

↓ compensatory responses

124
Q

Risk factors for Parkinson’s (AGE)

A

Risk Factors:
Age
Genetic associations
Exposure to manganese in welders has been identified

125
Q

ALS loss of UMN leads to (US ) “ think US”

A

Loss of upper motor neurons
Spastic paralysis & hyperreflexia

 Decreased muscle tone and reflexes
 Progressive muscle weakness and loss of fine
motor coordination
 Stumbling and falls are common.
 Death occurs due to respiratory failure
126
Q

ALS loss of LMN leads to (FL) “ think FL”

A 
Flaccid paralysis (decrease muscle tone and reflexes)
 Damage to Lower motor neurons
127
Q

ALS there is

A

Progressive muscle weakness and loss of fine
motor coordination
Stumbling and falls are common.

128
Q

ALS death occurs due to

A

Death occurs due to respiratory failure.

129
Q

ALS and Autonomic NS

A

Autonomic dysfunction : Orthostatic hypotension and Resting tachycardia

130
Q

ALS sx where first

A

Skeletal muscle weakness w/ fasciulations

Intrinsic muscles of the Hands first

131
Q

Myasthenia Gravis affected first

A

Ocular & facial muscles usually affected first

132
Q

Myasthenia Gravis population affected

A

Women 20 – 30 yrs. most often

Men > 60 yrs.

133
Q

What are the 4 subtypes of schizophrenia (DCUP)

A

Disorganized
Catatonic
Undifferentiated
Paranoid

134
Q

Depression

A

Most common psychiatric disorder

characteristics associated with major depression:

135
Q

Depression : Suicide rate

A

15% suicide rate among pts. with major depression

136
Q

Depression Unipolar

A

Diagnosis based on biologic factors or personal characteristics

137
Q

Depression Bipolar

A

Alternating periods of depression and manic episodes

138
Q

Depression distinction ?

A

length and degree of the disturbances in mood

distinguish depression from ordinary grief and sadness

139
Q

Treatments: Psychotherapy Antidepressant drugs that:

A

increase norepinephrine activity

140
Q

Antidepressant medications:

A

SSRIs (ex. zoloft, prozac)
SNRIs (ex. cymbalta, effexor)
Tricyclics (ex. amitriptyline, nortriptyline)
MAOIs

141
Q

Spondylosis aka

A

Spinal Stenosis
Transverse osteophytes compress cord in canal and/or
nerve roots at intervertebral foramina.

142
Q

Ankylosing Spondylitis and HLA

A

90% of pts. are HLA-B27 positive

143
Q

Ankylosing Spondylitis Causes:

A

Decreased mobility of vertebral column

144
Q

Ankylosing Spondylitis And systemic manifestation : EYE

A

Conjunctivitis/Uveitis

Unilateral w/ visual impairment, photophobia & eye pain

145
Q

Ankylosing Spondylitis And systemic manifestation: LUNGS

A

Apical cavitary lesions with fibrosis & pleural thickening in the lung (mimics TB)

146
Q

Ankylosing Spondylitis And systemic manifestation: SPINE and RESP

A

T-spine involvement = ↓ chest wall compliance and

↓ vital capacity

147
Q

Ankylosing Spondylitis And systemic manifestation: CV

A

Aortic regurgitation from fibrosis may also be present

148
Q

Ankylosing Spondylitis Anesthesia Considerations Stiffened/deformed C-spine may cause_____

A

difficult intubation- Awake fiberoptic intubation may be neede

149
Q

Ankylosing Spondylitis Restrictive lung disease results in

A

↓ vital capacity

150
Q

Ankylosing Spondylitis Anesthesia Considerations : SVR

A

Sudden increases in systemic vascular resistance poorly

tolerated if aortic regurgitation present

151
Q

Ankylosing Spondylitis Anesthesia Considerations : Neuraxial

A

Regional anesthesia may be difficult 2o to limited jt. mobility
Epidural or spinal anesthesia is acceptable alternative to
general

SRNA3AdvancedPatho2 (15 decks)

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