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BCN > E4 > Flashcards

E4 Flashcards

1
Q

What is MAC?

A

Minimum alveolar concentration = measure of potency of anesthetics

Equilibrium concentration required to prevent the response to a painful stimulus in 50% of patients

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2
Q

What is MAC similar to?

A

EC50

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3
Q

What factors decrease MAC/increase potency?

A 
Hypothermia
Pregnancy
Shock
Increasing age
Acute alcohol ingestion
CNS-depressant drugs
Decreased CNS NT release
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4
Q

How do opiates inhibit neurotransmission post-synaptically?

A

Signal via G-proteins –> K+ efflux or Cl- influx –> HYPERpolarizing

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5
Q

What is endogenous analgesia?

A

Endorphins release to cause absence of pain sensation. Stimulation of A-delta and C fibers stimulates release of endogenous opioids B-endorphin and dynorphin

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6
Q

Where are B-endorphin and dynorphin released?

A

B-endorphin: hypothalamus

dynorphin: PAG

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7
Q

How can dynorphins cause pain?

A

Bind to glycine site—which is involved in cross talk—can turn around and affect NMDA receptor and cause pain

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8
Q

How do opioid receptors work?

A

By decreasing synaptic transmission. Binding activates G proteins that, in turn, activate potassium channels or inhibit calcium channels, thereby inhibiting neurotransmitter release.

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9
Q

Naloxone blocks which receptors?

A

Mu receptors

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10
Q

Are opioid receptors presynaptic or postsynaptic?

A

Can be both

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11
Q

Endogenous opioids can be carried by ______, meaning they don’t have to be inside a _______.

A

Leukocytes / nerve

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12
Q

How do endogenous opioids work?

A

They are produced from pro-hormones, released from the synapse, and directly stimulate opioid receptors on the pre- and postysynaptic membranes.

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13
Q

B-endorphin and endomorphin receptor

A

Mu

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14
Q

Enkephalin receptor

A

Delta

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15
Q

Dynorphin receptor

A

Kappa

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16
Q

Which receptor does naloxone NOT act on?

A

ORL-1

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17
Q

Nociceptin receptor

A

ORL-1

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18
Q

Which receptor does morphine/codeine/heroin act on?

A

Mu

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19
Q

Which is more fat soluble: heroin or morphine?

A

Heroin

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20
Q

Opioid receptor location in pain fibers

A

Presynaptic terminal of afferent pain fibers : substantia gelatinosa, dorsal horn

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21
Q

Opioid receptor location in descending pathways

A

Limbic system / thalamus

PAG

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22
Q

How does nociceptin work?

A

Affects how we react to pain, not the pain itself

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23
Q

All opioid receptors are _____ and inhibit _____ _____.

A

GPCRs / adenylate cyclase

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24
Q

What is the net effect of opioid receptors?

A

Hyperpolarization / decreased release of neurotransmitter (e.g. substance P) / decreased pain fiber activity

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25
Q

Opioid receptors are inhibitory/excitatory.

A

Inhibitory. They inhibit the release of some NTs and enable the release of dopamine.

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26
Q

Where are opioid receptors located?

A

CNS, PNS, GI tract

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27
Q

How does heroin’s MOA increase abuse?

A

Rapidly enters the brain and breaks down to morphine

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28
Q

What are the cardiovascular effects of morphine?

A

Vasodilation –> decrease in blood pressure

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29
Q

How does morphine affect respiration?

A

There is a primary and continuous depression of respiration related to dose: decrease rate, volume, and tidal exchange

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30
Q

Which opioid receptor enhances mu agonists?

A

Delta

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31
Q

T/F: Morphine causes histamine release.

A

True

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32
Q

Which drug is similar to morphine, but 10x more potent (IV) and has less of a depressant effect on the respiratory center?

A

Oxymorphone

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33
Q

Fentanyl’s cardiovascular effects are less ____ than morphine, but respiratory effects are more _____.

A

Severe

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34
Q

What is fentanyl’s duration of action?

A

40-60 minutes

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35
Q

How are opiates converted to more polar metabolites?

A

Via hepatic conjugation to glucuronides or N-demethylated

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36
Q

Which opiate does Cytochrome P-450 metabolize?

A

Fentanyl

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37
Q

Where does opioid excretion occur?

A

Kidneys

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38
Q

What is the active metabolite of morphine and what is its potency?

A

Morphine-6-glucuronide –> 2x more potent

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39
Q

What is the triad of acute morphine poisoning?

A

Coma, miosis, cyanosis

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40
Q

What are two examples of synthetic mu-opioid agonists?

A

Fentanyl, meperidine

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41
Q

How long after morphine poisoning does respiratory failure occur?

A

2-4 hours

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42
Q

Oxycodone breaks down to ______.

A

Oxymorphone

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43
Q

Tramadol MOA

A

Blocks NE and 5HT reuptake

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44
Q

Pentazocine MOA

A

K agonist, and delta partial agonist

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45
Q

Which drug has a shorter duration and faster onset of action than morphine when taken orally?

A

Pentazocine

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46
Q

Buprenorphine MOA

A

Mu partial agonist, delta antagonist

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47
Q

Low doses of which drugs, in combination with opiates, have been found to enhance analgesic effect?

A

Opioid antagonists (e.g. naloxone)

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48
Q

Methadone MOA

A

Full opioid agonist on mu receptors
Inhibits serotonin reuptake
Non-competitive antagonist NMDA receptor

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49
Q

Which opiate is an absolute contraindication for taking MAO inhibitors?

A

Meperidine

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50
Q

Which opiate is more potent in women than in men?

A

Buprenorphine

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51
Q

Where does the spinal cord end?

A

L1

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52
Q

Clinical findings of UMN lesion

A 
Spastic muscles
Hyperactive reflexes
Babinski
Clonus (4 beats or more)
Hoffmann's reflex
No sensory changes
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53
Q

When a patient has a bowel/bladder dysfunction, where should you look for the lesion?

A

Conus medullaris

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54
Q

Clinical findings of LMN lesion

A

Flaccid muscles
Hypoactive reflexes
Numbness/tingling

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55
Q

What is the origin of a UMN lesion?

A

Brain or spinal cord

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56
Q

What is the origin of a LMN lesion?

A

Peripheral nerve or lumbar canal or limbs

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57
Q

What is myelopathy and how does it present?

A

Spinal cord compression:
Painless
Non-dermatomal
Clumsiness

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58
Q

What is radiculopathy and how does it present?

A

Nerve root compression:
Painful
Dermatomal muscle weakness
Muscle atrophy and bone loss

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59
Q

What is the calling card of ALS?

A

Tongue fasciculations

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60
Q

How is ALS diagnosed?

A

EMG –> confirms in upper and lower limbs

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61
Q

How is ALS treated?

A

Riluzole

IV Ig therapy

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62
Q

Where is the most common location of syringomyelia?

A

Lower cervical

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63
Q

Life expectancy after ALS diagnosis

A

4-5 years

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64
Q

Cervical syringomyelia symptoms

A 
Loss of sensation in UEs --> shawl distribution
UE weakness
UE reflexes absent
LE spasticity
Hyperhidrosis
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65
Q

Lumbar syringomyelia symptoms

A

LE muscle atrophy
Sensory loss: lumbar and sacral dermatomes
DTRs absent in LEs
Impairment of sphinchter function

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66
Q

Calling card of tabes dorsalis

A

Loss of DTRs at knees and ankles

Argyll Robertson pupils

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67
Q

What aspect of the spinal cord is affected by B12 deficiency?

A

White matter more than grey matter

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68
Q

Exam finding in B12 deficiency

A

Romberg sign

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69
Q

What is the most common inherited neurological disease?

A

Charcot-Marie-Tooth

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70
Q

Lab finding in myasthenia gravis

A

Acetylcholine receptor antibody –> positive in 90% of cases

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71
Q

Myasthenia gravis treatment

A

Pyridostigmine bromide

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72
Q

What is the deficiency in PKU?

A

Phenylalanine hydroxylase –> results in buildup of phenylalanine, which is then converted to phenylpyruvic acid, which is then excreted in the urine

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73
Q

What would be present/elevated in the urine of a PKU patient?

A

Phenylpyruvic acid

Phenylketones

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74
Q

What is the role of tyrosine in PKU?

A

Tyrosine deficiency –> dopamine decrease –> melanin decrease (PKU patients tend to have blonde hair and blue eyes)

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75
Q

What are the three types of neurological alterations in PKU?

***question

A

Interference with normal brain growth
Defective myelination
Diminished pigmentation of substantia nigra and locus ceruleus

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76
Q

What causes Lesch Nyhan?

***question

A

Deficiency in HGPRT (involved in salvage pathway of purine synthesis) –> INCREASED purines (de novo synthesis)

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77
Q

Gaucher cells accumulate ______ in lysosomes.

A

Glucosylceramides

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78
Q

What is the deficit in MLD?

A

Sulfatase A

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79
Q

What is the accumulation in Hurlers?

A

Sulfated polysaccharides in ECM

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80
Q

How do the basal ganglia appear in Wilson disease?

A

Brick red, spongy, small cavities

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81
Q

What is the deficit in Wilson disease?

A

Deficit in Cu transport –> copper accumulates in pericapillary area of astrocytes –> protoplasmic astrocytes

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82
Q

What are the clinical findings of Wilson disease?

A 
Tremor
Dysarthria
Unsteady gait
Speech loss
Drooling
Rigid arms/legs
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83
Q

What is dementia?

A

Disorder characterized by problems with cognition and functional impairment (must have both)

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84
Q

What is the prevalence of Lewy Body dementia?

A

15%

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85
Q

When do cognitive impairment and hallucinations appear in someone with LBD?

A

Before or at the same time as Parkinson-like symptoms

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86
Q

What does a mini mental status exam measure?

A

Global cognitive function by examining memory, language, orientation, and executive function.

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87
Q

What is the MMSE score for normal or mild impairment?

A

25-30

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88
Q

What is the MMSE score for severe dementia?

A

< 10

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89
Q

What are the steps of MMSE?

A
  1. Ask patient to repeat three words
  2. Ask patient to draw face of a clock, then draw hands to read “ten past eleven”
  3. Ask patient to recall three words
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90
Q

What is the most important predisposing factor for delirium?

A

Baseline cognitive impairment

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91
Q

What is the main difference between depression and dementia?

A

Depression: loss of pleasure
Dementia: loss of interest

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92
Q

How is delirium treated?

A

Treat underlying cause:
R/o infection
Check medications
R/o constipation, dehydration, UTI

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93
Q

First line of treatment for partial and tonic-clonic seizures

A

Phenytoin
Valproate
Carbamazepine

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94
Q

Phenytoin MOA

A

Alters Na, Ca, and K conductances

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95
Q

What are the broad spectrum anticonvulsants?

A

Valproic acid

Benzos

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96
Q

How does phenytoin act on Na channels?

A

Increases Na+ channel inactivation / keeps the channel in refractory state

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97
Q

Carbamazepine MOA

A

Increases Na+ channel inactivation (similar to phenytoin)

Potentiates postsynaptic effects of GABA

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98
Q

What is Lamotrigine used for?

A

Add-on therapy with valproic acid

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99
Q

What is a critical side effect of Lamotrigine?

A

Stevens-Johnson syndrome

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100
Q

Which anticonvulsant increases GABA-A action and prolongs opening of Cl- channels and what is it used for?

A

Phenobarbital / partial seizures

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101
Q

Why is valproate contraindicated in pregnancy?

A

Can cause spina bifida

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102
Q

Which anticonvulsant causes a decrease in neuronal calcium currents by binding of alpha-2-delta subunit of the calcium channel?

A

Gabapentin (designed as GABA analog)

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103
Q

Ethosuximide MOA

A

Blocks thalamic T-type Ca2+ channels

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104
Q

Tiagabine MOA

A

Increases GABA by inhibiting reuptake

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105
Q

Increases neuronal GABA
Increases glutamic acid decarboxylase
Binds alpha-2-subunit of VGCC –> decreases calcium

Used for partial seizures, shingles, diabetic neuropathy, fibromyalgia

A

Pregabalin

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106
Q

Major side effect of valproate

A

Hepatotoxicity

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107
Q

What are the safest of all antiepileptic drugs and most free from severe side effects?

A

Benzos

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108
Q

Which anticonvulsant suppresses seizure spread, and is effective in myoclonic and absence seizures?

A

Clonazepam

109
Q

What is the drug of choice for status epilepticus?

A

Benzos (diazepam, lorazepam)

110
Q

Carbamazepine has interactions with….

A

Contraceptives

111
Q

Safest anticonvulsants for pregnancy

A

Lamotrigine
Levetiracetam
Carbamazepine
Phenytoin

112
Q

Which anticonvulsant is used to treat trigeminal neuralgia?

A

Carbamazepine

113
Q

First line anticonvulsant in neonates

A

Phenobarb

114
Q

Vesitbulocerebellar ataxia presentation

A

Vision and gait instability
Wide base stance
Titubation (truncal ataxia and oscillations)
Nystagmus

115
Q

Spinocerebellar ataxia presentation

A

Wide-based “drunken sailor” gait

Less nystagmus

116
Q

Cerebrocerebellar ataxia presentation

A

Incoordination of voluntary, planned movements by the extremities
Scanning speech (explosive variations in voice)
Dysdiadochokinesia
Dysmetria

117
Q

What are the main causes of acute cerebellar ataxia in adults?

A 
Vascular lesions
Cranial traumatisms
Infections
Intoxications
Immune ataxias
Vestibular disorders
118
Q

Which cancers are often associated with paraneoplastic cerebellar degeneration?

A

Small cell lung cancer
Breast/ovarian
Lymphoma

119
Q

What is the most common cerebellotoxic agent?

A

Alcohol

120
Q

What are the main conditions associated with Wernicke encephalopathy?

A 
Alcoholism
Hyperemesis gravidarum
Gastroplasty/intestinal surgery
Prolonged parenteral nutrition
Chemotherapy
121
Q

Wernicke encephalopathy presentation

A

Confused mental state
Oculomotor deficits (nystagmus)
Gait ataxia

122
Q

Lesions associated with what condition commonly affect the cerebellum and its afferent and efferent connections?

A

MS

123
Q

What abnormality can be found in the serum of cerebellar ataxia patients?

A

GAD antibodies

124
Q

Clinically, how is afferent ataxia distinguished from cerebellar ataxia?

A

Heavy dependence on visual guidance
Minor degree of oculomotor deficits
Absence of dysarthria

125
Q

Afferent ataxia is most often associated with ….

A

Impaired DTRs

Sensory deficits

126
Q

PE finding in sensory ataxia

A

Positive Romberg

127
Q

Vestibular ataxia presentation

A

Severe vertigo
Nausea and vomiting
Usually unilateral

128
Q

Disorders affecting the cerebellum

A

VITAMIN C

Vascular
Infectious
Traumatic
Autoimmune
Metabolic
Idiopathic
Neoplastic
Congenital
129
Q

What is the classic clinical presentation of a cerebellar-based movement disorder?

A

Dysmetria
Ataxic gait
Scanning speech
Often with nystagmus

130
Q

Cerebellar nystagmus presentation

A

Slow deviation of the eye with a fast escape beat in the opposite direction

131
Q

Cerebellar nystagmus etiology

A

Pressure/edema/lesions of the deep cerebellar or vestibular nuclei

132
Q

Which anticonvulsant may aggravate myoclonic or absence seizures?

A

Oxcarbazepine

133
Q

Differentials of dementia

A 
Hypothyroidism
Vitamin B12 deficiency
Neurosyphilis
AIDS
Brain tumors
Subdural hematoma
134
Q

Leukodystrophies are caused by an accumulation of…

***question

A

Sulfatides

135
Q

Increased microbiota reduces behavioral symptoms of…

***question

A

Autism

136
Q

What are nociceptors and how are they stimulated?

A

Specialized sensory receptors in free nerve endings of primary afferent A-delta and C fibers. Stimulated by mechanical, thermal, or chemical stimuli. Inflammatory mediators are released from damaged tissue and can stimulate nociceptors directly.

137
Q

What structure is important in the perception of “affective” pain?

A

Anterior cingulate gyrus

138
Q

What is the most important pain-related nucleus in the pons?

A

Locus ceruleus –> contains noradrenaline-containing neurons

139
Q

Which endogenous opiate increase sharply during childbirth?

A

Enkephalin

140
Q

What is the gate control theory of pain?

A

Stimulation by non-noxious input is able to suppress pain

141
Q

What is a guideline for dosing pain meds?

A

The maximum dose within an opioid PRN range should not be greater than four times the minimum dose.

142
Q

How many Americans are addicted to opioid pain relievers?

A

2.1 million

143
Q

What are the most common sites for development of herpes zoster?

A
  1. Thoracic dermatomes

2. CN V-1

144
Q

Testing for herpes zoster

A

Tzanck smear from fresh vesicle will reveal multinucleated giant cells and eosinophilic inclusions

145
Q

First line treatment in palliation of neuritic pain of herpes zoster

A

Gabapentin (if no response, use carbamazepine)

146
Q

What condition usually results from blunt trauma to the greater and lesser occipital nerves?

A

Occipital neuralgia

147
Q

Which disease is almost never seen in patients < 30 years of age unless associated with MS?

A

Trigeminal neuralgia

148
Q

All patients with new diagnosis of trigeminal neuralgia should undergo what imaging and why?

A

MRI of brain/brainstem with and without gadolinium to r/o posterior fossa or brainstem lesions and demyelinating disease

149
Q

What testing should be done for CV-1 neuralgia?

A

Ophthalmologic evaluation to measure intraocular pressure

150
Q

What should be considered in all patients who present with TN before the fifth decade?

A

MS

151
Q

What is the first line of treatment of TN?

A

Carbamazepine

152
Q

Failure to monitor carbamazepine levels can lead to…

A

Aplastic anemia

153
Q

Temporal arteritis will result in _____ within hours to days?

A

Loss of vision

154
Q

How to diagnose temporal arteritis?

A

Inflammatory markers and histology

Palpation of temporal artery can be tender/pulseless

155
Q

Hyponatremia is a side effect of which anticonvulsants?

A

Carbamazepine and oxcarbazepine

156
Q

Which anticonvulsant can make idiopathic generalized epilepsy worse?

A

Carbamazepine

157
Q

What is the risk of seizure recurrence for someone with an epileptiform EEG?

A

60%

158
Q

What does dx of epilepsy primarily rely on?

A

History

159
Q

Autosomal-dominantly inherited epilepsy of the newborn
Onset: 2-4 days
Tonic posture
Ocular symptoms
Other autonomic features
Progression to clonic movements and motor automatisms

A

Benign Familial Neonatal Convulsions

160
Q

How to diagnose BFNC

A

Neonates are normal between seizures
Evaluation for structural, infectious, metabolic disease is negative
Clinical and EEG features SUGGEST seizures are generalized in type

161
Q

Two loci identified in BFNC

A

EBN1 to chromosome 20q13.3

EBN2 to chromsome 8q24

162
Q

Muttion in generalized epilepsy with febrile seizures

A

Mutation in Beta-1 subunit of voltage-gated Na+ channel –> increased excitability

163
Q

____ of children with SMEI have family history of seizures yet de novo SCN1 mutations occur in ___ of cases

A

50% / 80%

164
Q

Which seizure patients should have an MRI?

A

Complex febrile seizures
Unrprovoked seizures with focal features and/or abnormal exam
EEG not “benign”

165
Q

What are the AAN guidelines for emergent imaging for seizure patients?

A

Postictal focal deficit without rapid resolution (<1 hour)

Failure to return to baseline within 3-4 hours

166
Q

Why is treatment after first unprovoked seizure not recommended?

A

Does not reduce long-term recurrence risk

Does not prevent development of epilepsy

167
Q

When would you consider treatment after first unprovoked seizure?

A

In circumstances where risk of a second seizure outweighs the risks of pharmacologic and psychosocial side effects

168
Q

How long after a seizure should an EEG be ordered?

A

5-6 days

169
Q

What is a major contraindication for Tramadol?

A

Patients under 18 who have undergone tonsillectomy or adenoidectomy

170
Q

Which seizure patients are prone to SUDEP?

A

Tonic seizure patients

171
Q

Why syndrome has the best prognosis following AED discontinuation?

A

Benign rolandic epilepsy (0%)

compared to juvenile myoclonic epilepsy at 80% and temporal lobe epilepsy at 53%

172
Q

What is the key aspect of administrating a SPECT scan?

A

Must give within 5 seconds of the seizure starting

173
Q

What kind of epilepsy is amenable to surgical resection?

A

Focal seizures

174
Q

What are some causes of cervical radiculopathy?

A

Herniated disc
Foraminal stenosis
Tumor
Osteophyte formation

175
Q

What are some common causes of cervical myelopathy?

A

Midline herniated disc
Spinal stenosis
Tumor

176
Q

What are LE symptoms of cervical myelopathy?

A

LE weakness

Bowel/bladder symptomatology

177
Q

Which pain syndromes mimic cervical radiculopathy?

A 
Cervicalgia
Cervical bursitis
Cervical fibromyositis
Inflammatory arthritis
Disorders of C spinal cord, roots, plexus, nerves
178
Q

What is double crush syndrome?

A

Compression of an axon at one location makes it more sensitive to effects of compression in another location because of impaired axoplasmic flow

179
Q

In the majority of lissencephaly cases, where is the mutation?

A

LIS1 or DCX gene

180
Q

• Normal intelligence
• Epilepsy – intractable partial seizures (unreactive to drug
therapy)
• Sex ratio = females > males
• FLNA gene mutated (X-linked gene), mutation in males is lethal

A

Periventricular heterotropia

181
Q
  • Intractable seizures (neonate or infancy)
  • Hemiparesis
  • Developmental delay
A

Hemimegalencephaly

182
Q
  • Intellectual impairment
  • Epilepsy
  • Ophthalmological disorders
  • Facial dysmorphism
  • Cleft palate
  • Anomalies (heart, kidneys, urinary tract, skeletal, & GI tract)
  • Causes = mutations in genes encoding proteins associated with CENTROSOME or centrosome-related activities, perinatal brain injury
A

Microcephaly

183
Q

Cerebrum and cerebellum are reduced or absent
Hindbrain is present
Part of NTD spectrum

A

Anencephaly

184
Q

What can protect against anencephaly?

A

Folic acid during pregnancy

185
Q

What is the diagnostic biochemical test for anencephaly?

A

Amniotic alpha-fetoprotein during 1st/2nd trimester

186
Q

NTD characterized by sac-like protrusions of the brain and membranes through openings in the skull
Results from failure of the ectoderm to separate from the neuroectoderm

A

Encephalocele

187
Q

Where is the most common site of encephalocele?

A

Occiput

188
Q

Benign cysts that occur in the cerebrospinal axis in relation to the arachnoid membrane
Do not communicate with the ventricular system

A

Arachnoid cyst

189
Q

Consists of a downward displacement of the cerebellar tonsils through the foramen magnum
Causes non-communicating hydrocephalus as a result of CSF outflow obstruction

A

Chiari malformation

190
Q

Abnormal accumulation of CSF in the ventricles of the brain
May cause increased intracranial pressure and progressive enlargement of the head
Convulsions
Tunnel vision
Mental disability

A

Hydrocephalus

191
Q

What conditions can cause hydrocephalus?

A 
Aqueductal stenosis
Chiari malformations
Dandy-Walker
Trisomy chromosomal defects
Tumors and hemorrhages
192
Q

Overactivation of the kynurenine pathway has been detected in what conditions?

A

Various autoimmune diseases

MS

193
Q

NMDA receptor-mediated excitotoxicity is involved in what disorders?

A

Neurodegenerative disorders (e.g. Huntington’s, Parkinson’s, Alzheimer’s)

194
Q

Most metabolites of the kynurenine pathway are _____.

A

neuroactive

195
Q

What is the anaerobic fate of pyruvate?

A

No TCA cycle to burn up reduced NADH, therefore NADH must be recycled to NAD+ (otherwise glycolysis will stop). Electrons are a waste product, and microbes dispose of them by making ethanol and lactate.

196
Q

Which bacterial species produce GABA?

A

Lactobacillus and Bifidobacterium

197
Q

Which bacterial species produce NE?

A

Escherichia, Bacillus, Saccharomyces

198
Q

Which bacterial species produce 5HT?

A

Candida, Streptococcus, Escherichia, Enterococcus

199
Q

Which bacterial species produces dopamine?

A

Bacillus

200
Q

Which bacterial species produces acetylcholine?

A

Lactobacillus

201
Q

All movement disorders except _____ and ______ abate during sleep.

A

Palatal myoclonus / some tic disorders

202
Q

What is hypokinesia?

A

Decreased amount of movement

203
Q

Involuntary muscle movements, including movements similar to tics or chorea and diminished voluntary movements

A

Dyskinesias

204
Q

Voluntary rigidity seen in dementia

A

Paratonia

205
Q

Abnormal distorted position of limb, trunk, face, or eyes

A

Dystonia

206
Q

Sudden brief action that is preceded by an urge to perform it and followed by relief
Usually involves face or neck

A

Tic disorder

207
Q

Fastest movement disorder
Sudden rapid muscular jerk
Can be unilateral, focal, or bilateral
Can be caused by LBD, Alzheimer’s, CBD, CJD, and more

A

Myoclonus

208
Q 
Rigidity
Tremor at rest (asymmetric, avoids head and neck)
Bradykinesia
Gait shuffling
Masked fascies
Anosmia
Stooped posture
Reduced arm swing
A

Parkinson’s

209
Q

Parkinsonism with patchy skin/iris depigmentation
Susceptibility to infection
Giant white cell inclusions
LBD with early hallucinations/delusions

A

Chediak-Higashi

210
Q 
Autosomal recessive disorder of biliary copper excretion causing hepatolenticular degeneration
Dysarthria
Dystonia
Rigidity
Psychiatric disturbances
A

Wilson disease

211
Q

Unilateral, large amplitude tremor due to a lesion of the red nucleus

A

Holmes / midbrain / rubral tremor

212
Q

Which proteins regulate migration and cytoskeleton?

A

LIS1, Ndel1, DCX

213
Q

Promotes microtubule stability

Disruption abolishes centrosome-nucleus coupling

A

LIS1

214
Q

Required for targeting LIS1 and dynein to the centrosome
Facilitates LIS1-dynein interaction
Regulates dynein-mediated retrograde transport

A

Ndel1

215
Q

Promotes polymerization and stabilization of microtubules

Regulates nucleokinesis

A

DCX

216
Q

Majority of cases (80%) involve mutation in LIS1 or DCX gene

A

Lissencephaly type I

217
Q

Intellectual disability
Hypotonia
Epilepsy
Feeding problems

A

Lissencephaly type I

218
Q

Microdeletin 17p13

Mental retardation, dysmorphic faces, lissencephaly

A

Miller Dieker

219
Q

DCX gene is ___-linked

A

X

220
Q

Poorly organized cerebral grey matter
Mild-moderate intellectual disability
Mixed seizure disorder with onset at any age
No dysmorphic features

A

Subcortical band heterotropia

221
Q

Which condition is caused by mutation in LIS1 or DCX gene?

A

Subcortical band heterotropia

222
Q

Shh+Fgf8=

A

dopamine neurons (substantia nigra)

223
Q

Fgf4, Shh+Fgf8=

A

serotonin neurons (raphe)

224
Q

Fgf8+Bmp4=

A

noradrenaline neurons locus ceruleus)

225
Q

Most rapid onset of action and recovery of halogenated GAs

Used for maintenance of anesthesia

A

Desflurane

226
Q

Safest inhalation GA
Useful induction agent (especially in children)
Not irritating to airway
Low blood:gas partition coefficient with pretty rapid onset of action and recovery

A

Sevoflurane

227
Q 
General anesthetic
Most frequently used barbiturate
Most commonly used induction agent
Binds to GABA-A receptor
Poor analgesia
Decreased blood pressure
Depressed respiration
A

Thiopental

228
Q

A 7yo patient presents for emergent surgery on a damaged liver and the preceptor anesthesiologist asks you which inhaled general anesthetic you should use

A

Sevoflurane

229
Q

All inhaled anesthetics are used primarily for ____ and all IV anesthetics are used for _____.

A

Maintenance / induction

230
Q

What GA would you use for a patient who has significantly low blood pressure and hypovolemia?

A

Opiates

231
Q

What are the inhalation GAs?

A

HEISMN- Halothane, Enflurane, Isoflurane, Sevoflurane, Methoxyflurane, and NO

232
Q

What are the IV GAs?

A 
Barbiturates
Benzodiazepines
Etomidate
Ketamine
Propofol
233
Q

Which GAs can cause liver toxicity?

A

Halothane and methoxyflurane

234
Q

The speed of induction of anesthesia depends on what factors?

A

Inspired gas partial pressure
Ventilation rate
GA solubility

235
Q

GAs that enhance GABA effect on GABA-A receptors

A 
Inhaled anesthetics
Barbiturates
Benzos
Etomidate
Propofol
236
Q

GAs that inhibit NMDA (glutamate) receptors

A

NO
Ketamine
Xenon
High dose barbiturates

237
Q

Which inhalant is most soluble in blood?

A

Halothane

238
Q

MAC > 100%
Good analgesia
Rapid onset and recovery

A

NO

239
Q

Not pungent (used for children)
Sensitizes the heart to epi-induced arrhythmias
Rarely induces hepatitis

A

Halothane

240
Q

Most rapid onset of action and recovery of the halogenated GAs
Irritating to the airway
Poor induction agent
Used for maintenance of anesthesia

A

Sevoflurane

241
Q

Loss of ability to recognize objects, faces, voices, or places

A

Agnosia

People with agnosia can still think, speak, and interact with the world normally

242
Q

State in which a person is unable to speak or move

A

Akinetic mutism

243
Q

Disorder of brain and nervous system in which person is unable to perform tasks or movements when asked, even though the request is understood, muscles work properly, and the task may have already been learned

A

Apraxia

244
Q

Characteristics of a coma

A

No eye-opening
Unable to follow instructions
No speech or other forms of communication
No purposeful movement

245
Q

GCS: E

A
  1. Opens eyes spontaneously
  2. Opens eyes to voice
  3. Opens eyes to pain
  4. No eye opening
246
Q

GCS: M

A
  1. Obeys commands
  2. Localized to pain
  3. Withdraws to pain
  4. Abnormal flexor response
  5. Abnormal extensor response
  6. No movement
247
Q

GCS: V

A
  1. Appropriate and oriented
  2. Confused conversation
  3. Inappropriate words
  4. Incomprehensible sounds
  5. No sounds
248
Q

Large pupils that dilate and contract automatically, but do not react to light suggest….

A

Tectal lesion

249
Q

Halogenated GA + succ can cause

A

Malignant hyperthermia

250
Q

What is the treatment for malignant hyperthermia?

A

Dantrolene

251
Q

Which anesthetic is least likely to cause nausea and vomiting?

A

Isoflurane

252
Q

What is the mechanism of action of Ondansetron?

A

5HT antagonist

253
Q

What are the safest AEDs?

A

Lamotrigine
Levetiracetam
Carbamazpine
Phenytoin

254
Q

In the lateral perforant pathway, dendrites of CA3 communicate with CA1 via….

A

Schaffer Collaterals

255
Q

Which pathway is important for long term potentiation?

A

Lateral perforant pathway

256
Q

What comprises the alvear pathway?

A

Axons from entorhinal cortex –> dendrites of CA1 and CA3 –> subiculum

257
Q

Corticomedial group of amygdala –> septal area and hypothalamus

A

Stria terminalis

258
Q

Stratum oriens contains

A

Basal dendrites of pyramidal cells

259
Q

Stratum radiatum contains

A

Apical dendrites of pyramidal cells

260
Q

Which hippocampal field is closest to the subiculum?

A

CA1

261
Q

Where do basal dendrites extend in the hippocampus?

A

Laterally toward ventricular surface

262
Q

Where do apical dendrites extend in the hippocampus?

A

Toward dentate gyrus

263
Q

What is the principal cell type in the dentate gyrus?

A

Granule cell

Axons (mossy fibers) contact pyramidal cells in CA3 and polymorphic layer

264
Q

Where is the transition between the entorhinal cortex and the hippocampus?

A

Subiculum –> pyramidal cell layer thicker here

265
Q

Anterior nucleus –> cingulate gyrus –> entorhinal cortex (via subiculum) –> hippocampus

A

Papez circuit

266
Q

Urbach Wiethe disease

A

Inability to process fear

267
Q

What is spared in Urbach Wiethe disease?

A

Hippocampal formation

268
Q

Thalamic nuclei associated with emotion

A

MD

BCN (6 decks)

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