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Adams 10th Ed > Chap 41-43: Nutriotional Deficiency, Alcohol & Neurotoxicology > Flashcards

Chap 41-43: Nutriotional Deficiency, Alcohol & Neurotoxicology Flashcards

1
Q

Important factor in the causation of nutritional diseases of the nervous system

A

Alcoholism

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2
Q

Triad of Wernicke’s disease

A

Ophthalmoplegia / nystagmus
Ataxia
Mental confusion

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3
Q

Korsakoff amnesic state defined as:

A

Retentive memory impairment out of proportion to other cognitive function in otherwise alert & responsive px

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4
Q

T/F. Wernicke’s disease; ¾ of cases are not recognized during life

A

TRUE

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5
Q

Most important medical circumstances that may precipitate Wernicke’s encephalopathy

A

Administration of IV glucose to a malnourished or alcoholic patient

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6
Q

Highly characteristic symptom of Wernicke’s disease, wherein improvement of this symptom w/ thiamine confirms diagnosis

A

Oculomotor abnormalities

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7
Q

Most common oculomotor feature of Wernicke’s disease

A

Gaze-evoked nystagmus (vertical/ horizontal)

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8
Q

Oculomotor abnormalities seen in Wernicke’s disease

A

1) Gaze-evoked nystagmus
2) Lateral rectus weakness
3) Conjugate gaze weakness

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9
Q

T/F. Having two of three signs is common in Wernicke’s Dz.

A

FALSE. One is most common (37% of cases)

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10
Q

Most common clinical feature in Wernicke’s dz

A

Mental confusion

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11
Q

Most common disturbance of mentation in Wernicke’s dz

A

Global confusional state; - drowsiness common feature under this

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12
Q

The core of amnesic disorder is:

A

Anterograde & retrograde amnesia; but able to register

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13
Q

Distinguishing feature of Wernicke’s from Korsakoff:

A

If confusional state is sustained despite treatment; then prominent is Korsakoff-amensic state

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14
Q

As a rule Korsakoff patients are:

A
  • No insight to illness
  • Apathetic & inert
  • Lacking spontaneity & initiative
  • Indifferent
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15
Q

Generally been considered to be a specific feature of Korsakoff psychosis

A

Confabulation

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16
Q

Other clinical abnormalities seen in Wernicke’s dz

A
  • Alcohol withdrawal
  • Peripheral neuropathy
  • Postural hypotension
  • Hypothermia
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17
Q

Lesion attributable to impaired olfactory discrimination among Korsakoff amnesic state

A

Mediodorsal thalamic lesion

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18
Q

Acute lesions in MRI (T2/FLAIR/DWI) & may enhance in Wernicke-Korsakoff syndrome

A
  • Mammillary bodies
  • Medial thalami
  • Periaqueductal areas
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19
Q

T/F. Normal MRI rules out Wernicke’s-Korsakoff syndrome

A

FALSE. Normal MRI does not precludes the dx, typical MRI occurs 58%

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20
Q

Has been explored but not sufficient to be sensitive to dx Wernicke’s dz

A

Serum thiamine & RBC transketolase measure

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21
Q

Mortality of acute Wernicke’s is around 17% with fatalities attributable to:

A

Hepatic failure & infection (septicemia as most common)

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22
Q

Most dramatic improvement upon giving thiamine in Wernicke’s dz

A

Oculomotor manifestation

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23
Q

T/F. improvement of Ataxia upon tx w/ thiamine is delayed

A

TRUE. 60% have residual or never improved

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24
Q

T/F. Wernicke’s & Korsakoff are not separate diseases instead the signs & symptoms are successive stages in a single disease process

A

TRUE

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25
Q

IEM that resembles the neuropathologic finding of Wernicke’s dz

A

Leigh encephalomyelopathy

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26
Q

Hypothermia w/c is an early feature in Wernicke’s is localized lesion in

A

Posterolateral nuclei of hypothalamus

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27
Q

Lesion responsible for memory disorder in Korsakoff

A

Mediodorsal nuclei of thalamus NOT mammillary bodies

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28
Q

Initial doses thiamine to tx Wernicke’s to fully reverse manifestation

A

500mg

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29
Q

Chronic alcoholic exhaust thiamine in how many weeks?

A

7-8 weeks

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30
Q

Acute fatal disease of infants, common among rice-eating countries.

Acute cardiac symptoms dominate w/ neurologic symptoms

A

Infantile Wernicke-Beriberi Disease

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31
Q

Cardiac manifestation (tachycardia, exertional dyspnea, heart failure) w/ neuropathic manifestation of weakness, paresthesia, usually having burning feet syndrome

A

Beri-beri

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32
Q

Common manifestation of alcohol-induced nutriotional neuropathy

A

Excessive sweating of feet & hands

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33
Q

Cardiac manifestation w/ symmetrical impairment, loss of tendon reflex, motor & sensory affecting legs more than arms, distal more than proximal

A

Nutritional polyneuropathy

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34
Q

Essential pathologic feature of Nutritional neuropathy

A

Axonal degeneration, pronounced in longest & largest myelinated fibers

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35
Q

T/F. ASA & paracetamol is sufficient to control hyperpathia & allodynia in Beriberi polyneuropathy

A

TRUE.. Phenytoin, CBZ, & gabapentin has been inconsistent

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36
Q

T/F. Recovery of nutritional polyneuropathy is a slow process.

A

TRUE

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37
Q

In developed countries, Pellagra is confined among

A

Alcoholics

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38
Q

Clinical triad of Pellagra

A

3D’s: diarrhea, dermatitis, dementia (neuroasthenia)

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39
Q

In Pellagra, neurons are swollen and rounded, w/ eccentric nuclei & loss of Nissl bodies most pronounced in the:

A

Brainstem nuclei

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40
Q

Spinal cord lesions in Pellagra take in the form of:

A

Symmetrical degeneration of dorsal column likely secondary to degeneration of dorsal root ganglion

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41
Q

Pellagra is a deficiency of what vitamin

A

Nicotinic acid / Niacin / Vit B3

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42
Q

The amino acid precursor of nicotinic acid

A

Tryptophan

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43
Q

IEM that resembles pellagra in most respects including dermatitis

A

Hartnup disease

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44
Q

Prominent features were confusional state, paratonic rigidity, ataxia, polymyoclonia. Skin lesion absent

A

Nicotinic acid-deficiency Encephalopathy

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45
Q

T/F. Pyridoxine deficiency & excess causes sensory polyneuropathy

A

TRUE

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46
Q

Drugs that may cause Pyridoxine neuropathy

A

INH, Hydralazine

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47
Q

Pyridoxine (B6) deficiency results to:

A

Neuropathy
Vascular thrombosis (excessive homocysteine)
Seizures

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48
Q

Excessive consumption of pyridoxine will manifest as:

A

Sensory polyneuropathy : no weakness, ONLY ataxia, areflexia

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49
Q

Drugs that may cause Folate deficiency (B9)

A

MTX & Phenytoin

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50
Q

Constituent of coenzyme A (CoA)

A

Pantothenic acid

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51
Q

Vitamin deficiency related to Subacute combined degeneration

A

Vit B12 (Cobalamin)

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52
Q

Classic neurologic syndrome of Cobalamin deficiency

A

Spinal cord
Optic nerve
Peripheral nerve involvement

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53
Q

Hematologic effect of Vit B12 deificiency

A

Pernicious anemia

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54
Q

Spinal cord (ataxic paraplegia w/ spasticity), optic nerve, peripheral nerve involvement w/ pernicious anemia

A

Vit B12 deficiency

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55
Q

Interference of methionine synthase, a methylcobalamin dependent enzyme results to subacute combined degeneration

A

Nitrous oxide (anesthesia paresthetica)

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56
Q

Most consistent sign in SCD / Vit B12 deficiency

A

Loss of vibration sense

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57
Q

Earliest histologic event in Vit B12 deficiency is

A

Swelling of myelin sheath representing myelinopathy

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58
Q

Essential cofactor in conversion of homocysteine to methionine

A

Methylcobalamin

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59
Q

Chief obstacle to early diagnosis of SCD

A

Lack of parallelism between hematologic & neurologic sign particularly who have taken dietary or medicinal folate

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60
Q

Main Ddx of SCD

A
  • Cervical spondylosis
  • MS
  • Adrenoleukodystrophy
  • Low serum copper level
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61
Q

Serum B12 level that is associated w/ neurologic symptoms signs of deficiency

A

100 pg/dL

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62
Q

Other additional reliable indicators of intracellular cobalamin deficiency

A

Methylmalonic acid levels

Homocysteine levels

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63
Q

In patient who receive Vit B12 parenterally, this test is more reliable than indicator for cobalamin deficiency

A

2-stage Schilling test

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64
Q

Diagnosis of pernicious anemia demands

A

Giving Vit B12

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65
Q

Improvement of gait upon treatment of Vit B12 is usually seen in

A

Less than 3 months

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66
Q

Ataxia, dec sensation, loss of DTRs, ophthalmoparesis, proximal muscle weakness, w/ elevated serum CKs is seen in

A

Vit E deificiency

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67
Q

In familial Vit E deficiency, the hepatic incorporation of tocopherol (active form Vit E) in to VLDL is defective due to mutation of

A

TTP, gene encoding a-tocopherol transfer protein

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68
Q

Excess of Vit A may result to what neurologic condition

A

Pseudotumor Cerebri

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69
Q

Uniform type of degeneration of what areas in the cerebellum among alcoholics

A

Vermian & anterior lobes, particularly degeneration of Purkinje cells

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70
Q

T/F. Alcoholic cerebellar degeneration is a result of direct toxic effects of alcohol

A

FALSE. It is a result of nutritional deficiency

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71
Q

Unique alteration of of the corpus callosum confined to the middle lamina due to loss of myelin among chronic alcoholic px

A

Marchiafava-Bignami Disease

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72
Q

Impressive feature of Marchiafavi-Bignami dz:

A

Varied neurologic features remits upon restoration of nutrition

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73
Q

Chronic alcoholism, w/ frontal lobe syndrome should suggest the diagnosis of:

A

Marchiafava-Bignami Disease

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74
Q

Most common cause of nutritional deficiency secondary to malabsorption

A

Celiac sprue

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75
Q

Alcohol is oxidized to acetaldehyde by

A

Alcohol dehydrogenase

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76
Q

The flushing reaction from alcohol is traced to deficiency in

A

Alcohol dehydrogenase

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77
Q 
Level of alcohol in blood relating to various degree of symptoms in nonhabituated person:
•	Euphoria
•	Mild incoordination
•	Ataxia
•	Confusion 
•	Stuporous
•	Deep anesthesia
A 
Euphoria: 30 mg/dL
Mild incoordination: 50 mg/dL
Ataxia: 100mg/dL
Confusion: 200mg/dL
Stuporous: 300 mg/dL
Deep anesthesia: 400 mg/dL

Provided blood rises steadily for 2 hours

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78
Q

T/F. Ethanol is oxidized at a constant rate independent of its concentration in blood

A

TRUE

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79
Q

T/F. The tolerance of alcohol is related to rate of alcohol metabolism.

A

FALSE. It depends in the increase of neuronal adaptation to alcohol

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80
Q

Early effects of aggressiveness, excessive activity, inc excitability of cortex is caused by:

A

Inhibition of subcortical structure

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81
Q

Effect of alcohol causing outburst of fury w/ assaultive & destructive behavior, attack terminates w/ sleep, no memory of the episode

A

Idiosyncratic alcohol intoxication / Pathologic intoxication

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82
Q

Main disorders to be distinguish from pathologic intoxication

A

Temporal lobe epilepsy & Sociopathy

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83
Q

Degree of intoxication interferes w/ registration of events & formation of memories

A

Alcoholic Blackouts

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84
Q

Main objective for treatment in Severe alcohol intoxication

A

Prevent respiratory depression & its complications

Use of HD is need if alcohol is extremely high w/ acidosis

85
Q

Most common source of methyl alcohol intoxication

A

Adulterated alcoholic beverage drink

86
Q

Characteristic feature of methyl alcohol intoxication

A

Damage to retinal ganglion & bilateral degeneration of putamen

Survivors may have blindness & parkinsonism

87
Q

By-product of methyl alcohol w/ ADH

A

Formaldehyde & formic acid

88
Q

Formation of oxalate crystal & CSF, among px w/ severe metabolic acidosis, altered sensorium & convulsions aids the diagnosis of

A

Ethylene glycol intoxication

89
Q

More effective drug inhibiting alcohol dehydrogenase for nonethanol alcohol intoxication

A

Fomepizole

90
Q

Mutiple craniopathies most common in CNs __ & ___ is a complication of ingestion of ethylene glycol as a result of _____ which develops after 6-18 days

A

CN 7 & 8

Deposition of oxalate crystals along the subarachnoid portions of the affected nerves

91
Q

Major alcohol withdrawal symptoms are seen mainly among

A

Binge drinker or Periodic drinkers

Steady drinker abruptly stopped due to hospitalization

92
Q

Most common single manifestation of alcohol abstinence syndrome

A

Tremulousness

93
Q

Feeling of uneasiness may not leave the patient completely for

A

10-14 days

94
Q

Most common hallucination in alcohol withdrawal

A

Auditory hallucination (human voices), prominent at night & duration varies

95
Q

90% of withdrawal seizures from alcohol occurs during ____ period following cessation of drinking

A

7-48 hrs

96
Q

Distinctive feature of seizure in alcohol withdrawal

A

Number of seizures is SINGLE. 2% have status epilepticus

97
Q

Seizure semiology commonly seen in alcohol withdrawal

A

GTC

98
Q

Most dramatic & grave of all acute alcoholic illness presenting as profound confusion, delusions, vivid hallucinations, tremor agitation, sleeplessness & inc sympathetic activity

A

Delirium tremens

99
Q

Most important obligate factor in genesis of delirium tremens is:

A

Withdrawal of alcohol following a period of sustained chronic intoxication & rapid decline of blood alcohol

100
Q

Treatment of delirium tremens begins w/ search of:

A

Injuries
Infections
Pancreatitis
Liver disease

101
Q

Drug used in alcohol dependence resulting nausea, vomiting & hypotension

A

Disulfiram (Antabuse)

102
Q

Neurotoxin affecting melanin-bearing dopaminergic nigral neurons explaining the production of parkinsonism

A

MPTP

103
Q

Opioids activate _______ receptors influencing neuronal activity through intermediate cAMP .

A

G-coupled transmembrane receptors

mu, delta, kappa

104
Q

Opioid receptors are concentrated in these areas of the brain

A 
Thalamus
Dorsal root ganglion  (mu receptor pain)
Amygdala (affect)
Brainstem raphe (alertness)
Edinger-Westphal nuclei (pupillary miosis)
Respiratory drive
105
Q

Well recognized clinical manifestation of acute opioid toxicity

A 
Unresponsiveness
Shallow & slow respiration
Pinpoint pupils
Hypothermia
Bradycardia
106
Q

Immediate cause of death in opioid toxicity

A

Respiratory depression

107
Q

Drugs administered to treat opioid toxicity or overdose

A

Naloxone (0.5mg in rpt increments every 2 mins until 15 mg IV

Nalmefene (long-acting)

108
Q

Dramatic change when naloxone is administered in opioid toxicity

A

Improved circulation and respiration
Reversal of miosis
Sensorium no immediate improvement
Observed for 24 hours or more.

109
Q

Once patients regains consciousness from opioid toxicity they complain of

A 
Pruritis
Sneezing / Tearing
Piloerection
Diffuse body pains
Yawning
Diarrhea
110
Q

Antidote for opioid toxicity should be used w/ great caution among:

A

Addicts may precipitate withdrawal phenomenon

111
Q

Opioid addiction consists of three recognizable phases:

A

Intoxication / Euphoria
Addiction
Relapse after period of abstinence

112
Q

Most important factor of genesis of addiction

A

Repeated self-administration of opioid

113
Q

Mechanism of tolerance in opioid addiction

A

Desensitization of opioid receptors through uncoupling of receptors from G-protein complex

114
Q

Intensity of opioid withdrawal depends on

A

Dose

Duration of addiction

115
Q

Symptoms of opioid withdrawal peaks at

A

48-72 hours

116
Q

Clinical signs of opioid withdrawal are no longer evident by

A

7-10 days

117
Q

Refers to the substitution of drug-seeking activities for all other aims and objectives in life (Emotional/ psychological dependence)

A

Habituation

118
Q

Reason methadone is used for treatment of morphine and heroin dependency

A

It is long-acting hence abstinence syndrome is evident around 3-4 days after withdrawal

119
Q

Areas of activation or depression in opioid addiction

A

Mesolimbic structures: Nucleus accumbens, ventral tegmentum of midbrain, locus ceruleus

120
Q

T/F. Diagnosis of addiction is usually made when patient admits using and needing drugs

A

TRUE

121
Q

Confirmatory evidence of opioid addiction

A

Urine test confirms use within 24 hours of test

122
Q

Alternative drug for opioid withdrawal that counteracts noradrenergic withdrawal symptoms but may induce hypotension

A

Clonidine (0.2-0.6 mg bid x 1 week)

123
Q

Treatment for heroin & cocaine abuse, both w/ opioid agonist and antagonist, mutes effect of withdrawal, serves as aversive agent which demonstrated superiority over methadone

A

SL buprenorphine

124
Q

Neurologic complication of opioid use

A
  • Vasculitis (stroke)
  • Amblyopia
  • Transverse myelopathy
  • Peripheral neuropathy
  • Subacute progressive leukoencephalopathy
125
Q

Sequelae of venous thrombosis resulting from administration of heroin and adulterants via IM or SC

A 
Brawny edema
Volkmann contracture (fibrosing myopathy)
126
Q

Advantages of benzodiazepine drugs

A

Relatively low toxicity & addictive potential

Minimal interactions with other drugs

127
Q

MOA of barbiturates

A

Enhancing GABA inhibition at pre-post synaptic receptor sites and reduce excitatory postsynaptic potentials

128
Q

Duration of hypnotic-sedative effect of phenobarbital

A

6 hours (usually coma is slow & prolonged)

129
Q

Dose of phenobarbital & lowest plasma concentration that is fatal

A

Dose: 6-10g

Plasma conc: 60mg/mL

130
Q

Oldest, safest, most effective, inexpensive sedative-hypnotic drug excreted in urine as glucuronide

Resembles acute barbiturate intoxication except for miosis

A

Chloral hydrate

131
Q

MOA of benzodiazepine

A

Activate GABA receptors opening chloride channel & hyperpolarize postsynaptic neurons & reducing firing rate

132
Q

Primary sites of action that accounts for its anticonvulsant and anxiolytic effects

A

Cerebral cortex

Limbic system

133
Q

Disadvantage of benzodiazepine

A

Causes unsteadiness, drowsiness, confusion, impairment of memory especially in the elderly

134
Q

Specific pharmacologic antagonist for benzodiazepine, w/c is diagnostically useful in cases of coma of unknown cause, & hepatic encephalopathy

A

Flumazenil

135
Q

Benzodiazepine withdrawal occurs when

A

3rd day of withdrawal but peaks at 5th day

136
Q

In chronic benzodiazepine users, gradual tapering of dosage over ______ minimizes withdrawal effect

A

1-2 weeks

137
Q

MOA of antipsychotic drugs

A

Blocking postsynaptic mesolimbic dopamine receptors (D1 to D4 receptors)

138
Q

D2 receptors are located mainly in what areas

A

Frontal cortex, hippocampus, limbic cortex (hence accounts for the psychosis)

139
Q

D1 receptors are located mainly in what area

A

Striatum (hence parkinsonism)

140
Q

Atypical antipsychotic drugs has less extrapyramidal symptoms because

A

Acts more on D2 & D4 receptors of temporal & limbic lobes more than the D1 receptors in the striatum

141
Q

Widest application in treatment of major psychosis & bipolar psychosis, as well as for hyperactive, delirious, combative px

A

Phenothiazines (chlorpromazine)

142
Q

Frequent SE of phenothiazines

A
  • Extrapyramidal symptoms (most important)
  • Cholestatic jaundice
  • Agranulocytosis
  • Seizures
  • Orthostatic hypotension
  • Skin sensitivity reactions
  • Mental depression
143
Q

Most extreme complication of phenothiazines & haloperidol

A

Neuroleptic malignant syndrome (NMS)

144
Q

Extrapyramidal symptoms seen in phenothiazines (chlorpromazine)

A
  • Parkinsonian syndrome
  • Acute dyskinetic / dystonia
  • Akathisia
  • Tardive dyskinesia
  • NMS
145
Q

Most common extrapyramidal symptom in phenothiazines that appear several days after tx

A

Parkinsonian syndrome

146
Q

Drug to treat acute dyskinesia and dystonia from drug-induced

A

Diphenhyrdamine IV

147
Q

Inner restlessness, reflected by persistent shifting of body and feet, responsive w/ propranolol

A

Akathisia

148
Q

Late and persistent complication of neuroleptic drugs appearing as dyskinesia, choreoathetosis and dystonic movements. 40 % of px taking antipsychotic meds have this

A

Tardive dyskinesia

149
Q

Postulated cause for tardive dyskinesia

A

Hypersensitivity of dopamine receptor in the BG, secondary to prolonged blockade

150
Q

Only Butyrophenone member approved for antipsychotic and management of acute psychosis

A

Haloperidol

151
Q

Drugs that can be used for neuroleptic side effects

A
  • Diphenhydramine (acute dystonia)
  • Anticholinergic drugs
  • Amantadine (postphenothiazine)
152
Q

Approach to neuroleptic SE

A
  • Gradual decrease of dose of antipsychosis to a minimum enough to control symptoms
  • Substitute atypical ones
153
Q

Neuroleptic malignant syndrome consist of:

A
  • Hyperthermia
  • Rigidity
  • Stupor
  • Unstable BP
  • Diaphoresis
  • Sympathetic overactivity
  • High CK values
  • Renal failure (myoglobinuria)
154
Q

Treatment of NMS

A
  • Bromocriptine (for altered consciousness & temp rising)
  • Dantrolene (for severe cases)
155
Q

One pitfall in managing NMS

A

Mistaken as worsening psychosis therefore administer more antipsychosis medications

156
Q

Most common adverse effect of all MAO inhibitors

A

Postural hypotension

157
Q

Enzyme located on outer surface of mitochondria in neurons for catabolism of catecholamines

A

Monoamine oxidase

158
Q

MAO-A inhibitors must be warned against

A
  • Phenothiazines
  • CNS stimulants
  • Tricylic antidepressants
  • SSRI
  • Sympathomimetic amines
  • Tyramine containing foods (cheese, red wine, beer, preserved meat and fish)
159
Q

TCAs MOA & indications & SE
Examples of:

Tertiary amines

Secondary amines

A
  • Blocks reuptake of amine NTs, hence increase NTs in the synaptic cleft; used for depression
  • Has anticholinergic effect
  • Amitryptiline (reuptake inhibitor for serotonin & NE)
  • Nortriptyline (more selective for NE)
160
Q

SSRI examples

A
  • Paroxetine
  • Fluoxetine
  • Sertraline
  • Escitalopram
161
Q

Concurrent use of MAO inhibitors results to confusion, restlessness, tremor, tachycardia, hypertension, clonus, hyperreflexia, shivering, diaphoresis

A

Serotonin syndrome

162
Q

Drug used for treatment of manic phase of bipolar disorder and prevention of recurrences of cyclic mood shifts

A

Lithium

163
Q

SE of Lithium

A
  • Altered consciousness
  • Delirium
  • Dizziness
  • Nystagmus
  • Ataxia
  • Diffuse myoclonic twitching
  • Nephrogenic DI
164
Q

Lithium concentration proved to be fatal

A

3.5meqs/L

165
Q

T/F. Discontinuation of lithium results to immediate disappearance of toxicity

A

FALSE. May be delayed until two weeks and DI may persist even longer

166
Q

Proven treatment for rapid reduction of lithium blood concentration and used for lithium comatose

A

Hemodialysis

167
Q

Zinc dependent protease blocking NT release by cleaving synaptic protein vesicles hence unable to exocytose, mainly GABA in _____

A
  • Tetanospasmin

* Renshaw cells

168
Q

Most sensitive part of the body for tetanospasmin

A

Masseter innervation (hence trismus first frequent manifestation)

169
Q

For Tetanus clinical features:

Most common
Most benign
Proven fatal

A

Generalized (common)
Localized (benign)
Cephalic (fatal)

170
Q

Most characteristic for tetanus is the loss of ____ that occurs after reflex contraction normally produced by recurrent inhibition by _____

A

Physiologic silent period

Renshaw cells

171
Q

Antibiotics used for tetanus

A

Metronidazole
Penicillin
Tetracyline

172
Q

Most common clinical type of Diptheria

A

Faucial-pharyngeal type: exudate of throat and pharynx w/c is source of exotoxins affecting heart and nervous system

173
Q

Distinguishing feature of diphtheria from other polyneuropathy

A
  • Early oropharyngeal symptoms
  • Ciliary paralysis w/ relatively retained pupillary response to light
  • Subacute delayed symmetrical sensorimotor neuropathy
174
Q

Toxin of diphtheria causes what pathology of the nerves

A

Demyelination in spinal nerves, spinal roots & dorsal root ganglion

175
Q

Clinical diagnosis of botulism can be confirmed by electrophysiologic studies showing

A

Decrease amplitude of evoked muscle potential but increasing amplitude by RNS

176
Q

Block neural Na channel resulting from eating fish fed on toxin-containing dinoflagellates (red tide)

A

Ciguatera poisoning

177
Q

Most prominent manifestation of ciguatera that distinguishes it from GBS

A

Perioral parasthesia

178
Q

Develops among children over 3-6 weeks who vomits, apathetic, altered sensorium, seizures then coma.

A

Plumbism

179
Q

Non-CNS manifestation that may give clue for plumbism

A
  • Lead lines in metaphyses of long bones

* Basophilic stippling of RBC esp in bone marrow erythroblast

180
Q

To test for lead using UCP, urine is added w/ acetic acid, then shaken with eq vol of ether. This will result to _____ which under Wood lamp is color ____

A
  • Coproporphyrin

* Reddish fluorescence

181
Q

Positive UCP means the lead level exceeds in blood by

A

80 mg/dL

182
Q

Diagnosis for plumbism can be confirmed by

A

Measuring 24 hr urine lead over 500 mg using calcium EDTA

183
Q

Treatment of acute plumbism & goal lead level

A
  • Chelation therapy of BAL & Ca EDTA, then followed by oral penicillamine
  • 40mg/dL
184
Q

Most of lead stores in

A 
Soft tissue (which is readily chelated)
Bone (not chelated)
185
Q

Oral lead chelator used for outpatient asymptomatic children w/ lead >45mg/dL given for 3 weeks

A

Succimer

186
Q

Adult lead intoxication usually manifest as

A
  • Colic (poorly localize severe abdominal pain w/o fever & leukocytosis)
  • Anemia
  • Peripheral neuropathy
187
Q

Diagnostic test for plumbism for adults are same for children EXCEPT

A

Bone films (no value for adults)

188
Q

Heavy metal poisoning presenting as:
Encephalopathy or distal axonopathy (subacute distal sensorimotor areflexic syndrome)
Diffuse scaly desquamation
Transverse white lines, 1-2mm above lanula (Mess lines)

A

Arsenic

189
Q

Diagnosis of arsenic poisoning depends in the demonstration of increased level in the:

A

Urine & hair

190
Q

Heavy metal poisoning that has delayed manifestation including concentric visual field constriction, tremors, mental confusion & progressive cerebellar syndrome

A

Organic mercury (methylmercury) poisoning / Minamata disease

191
Q

Pathologic changes characterized by organic mercury poisoning / Minamata disease:

A
  • degeneration of granular layer of cerebellar cortex w/ relative sparing of Purkinje cells
  • Gliosis of calcarine cortex compared to other cortices
192
Q

Heavy metal poisoning presenting as parasthesia, lassitude, incoordination, intentional tremors, & erethism

A

Inorganic mercury poisoning

193
Q

Drug of choice for chronic mercury poisoning

A

Penicillamine

194
Q

Delayed effects of acute organophosphate ingestion after 2-5 weeks

A

Distal symmetrical sensorimotor (more motor) polyneuropathy

195
Q

Appears 24 to 96 hours after acute cholinergic phase of organophosphate poisoning consisting of weakness of proximal limbs, neck flexors, motor cranial nerves, respiratory muscle proven to be fatal

A

Intermediate syndrome

196
Q

T/F. Intermediate and delayed symptoms of organophosphate poisoning does not respond to atropine

A

TRUE

197
Q

Most important SE of Vincristine occurring w/in few weeks of the beginning of treatment

A
  • Peripheral neuropathy (sensory w/ reflex loss)

* Other: Reversible posterior leukoencephalopathy

198
Q

Heavy metal that inhibits DNA synthesis, dose limiting factors of nephrotoxicity, vomiting, peripheral neuropathy (primary axonal degeneration), ototoxicity, retrobulbar neuritis

A

Cisplatin

199
Q

Derived from bark of western yew, w/ predominantly sensory polyneuropathy, due to inhibition of depolymerization of tubulin in axons in the axon, hence axonal neuropathy

A

Paclitaxel / Docetaxel

200
Q

MAO inhibitor that is antineoplastic effective for oligodendroglioma.

May cause somnolence, confusion, agitation, depression

A

Procarbazine

201
Q

Enzyme inhibitor of protein synthesis causing drowsiness, confusion, stupor, coma, diffuse EEG slowing, may occur days upon tx. Also w/ cerebrovascular complications

A

L-asparaginase

202
Q

Pyrimidine analogue causing cerebellar syndrome usually mild and subside within 6 weeks

A

5-FU

203
Q

Most common complication of IT MTX

A

Aseptic meningitis

204
Q

Most common & serious complication of systemic & even IT MTX

A

Leukoencephalopathy

205
Q

Nitrosoureas used to treat malignant cerebal gliomas causing diffuse vasculopathy

A

Carmustine & Lomustine

206
Q

Long term treatment for leukemia which is usually not neurotoxic at usual doses but if high doses will cause cerebellar degeneration

A

Cytarabine

207
Q

Most frequent SE of calcinuerin inhibitors (Cyclosporine, Tacrolimus)

A
  • Tremor & myoclonus (most frequent)
  • Seizure (sign of toxicity)
  • PRES
208
Q

Antibiotic causing seizures at higher doses

A

Penicillin
Imipenem
Cephalosporins

209
Q

Antibiotic that may cause reversible cerebellar syndrome assoc w/ dentate nuclei signal changes in MRI.

Dysarthria, confusion & gait ataxia are core clinical syndrome

A

Metronidazole

Adams 10th Ed (8 decks)

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