Chap 41-43: Nutriotional Deficiency, Alcohol & Neurotoxicology Flashcards
1
Q
Important factor in the causation of nutritional diseases of the nervous system
A
Alcoholism
2
Q
Triad of Wernicke’s disease
A
Ophthalmoplegia / nystagmus
Ataxia
Mental confusion
3
Q
Korsakoff amnesic state defined as:
A
Retentive memory impairment out of proportion to other cognitive function in otherwise alert & responsive px
4
Q
T/F. Wernicke’s disease; ¾ of cases are not recognized during life
A
TRUE
5
Q
Most important medical circumstances that may precipitate Wernicke’s encephalopathy
A
Administration of IV glucose to a malnourished or alcoholic patient
6
Q
Highly characteristic symptom of Wernicke’s disease, wherein improvement of this symptom w/ thiamine confirms diagnosis
A
Oculomotor abnormalities
7
Q
Most common oculomotor feature of Wernicke’s disease
A
Gaze-evoked nystagmus (vertical/ horizontal)
8
Q
Oculomotor abnormalities seen in Wernicke’s disease
A
1) Gaze-evoked nystagmus
2) Lateral rectus weakness
3) Conjugate gaze weakness
9
Q
T/F. Having two of three signs is common in Wernicke’s Dz.
A
FALSE. One is most common (37% of cases)
10
Q
Most common clinical feature in Wernicke’s dz
A
Mental confusion
11
Q
Most common disturbance of mentation in Wernicke’s dz
A
Global confusional state; - drowsiness common feature under this
12
Q
The core of amnesic disorder is:
A
Anterograde & retrograde amnesia; but able to register
13
Q
Distinguishing feature of Wernicke’s from Korsakoff:
A
If confusional state is sustained despite treatment; then prominent is Korsakoff-amensic state
14
Q
As a rule Korsakoff patients are:
A
- No insight to illness
- Apathetic & inert
- Lacking spontaneity & initiative
- Indifferent
15
Q
Generally been considered to be a specific feature of Korsakoff psychosis
A
Confabulation
16
Q
Other clinical abnormalities seen in Wernicke’s dz
A
- Alcohol withdrawal
- Peripheral neuropathy
- Postural hypotension
- Hypothermia
17
Q
Lesion attributable to impaired olfactory discrimination among Korsakoff amnesic state
A
Mediodorsal thalamic lesion
18
Q
Acute lesions in MRI (T2/FLAIR/DWI) & may enhance in Wernicke-Korsakoff syndrome
A
- Mammillary bodies
- Medial thalami
- Periaqueductal areas
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%
20
Q
Has been explored but not sufficient to be sensitive to dx Wernicke’s dz
A
Serum thiamine & RBC transketolase measure
21
Q
Mortality of acute Wernicke’s is around 17% with fatalities attributable to:
A
Hepatic failure & infection (septicemia as most common)
22
Q
Most dramatic improvement upon giving thiamine in Wernicke’s dz
A
Oculomotor manifestation
23
Q
T/F. improvement of Ataxia upon tx w/ thiamine is delayed
A
TRUE. 60% have residual or never improved
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
25
IEM that resembles the neuropathologic finding of Wernicke’s dz
Leigh encephalomyelopathy
26
Hypothermia w/c is an early feature in Wernicke’s is localized lesion in
Posterolateral nuclei of hypothalamus
27
Lesion responsible for memory disorder in Korsakoff
Mediodorsal nuclei of thalamus NOT mammillary bodies
28
Initial doses thiamine to tx Wernicke’s to fully reverse manifestation
500mg
29
Chronic alcoholic exhaust thiamine in how many weeks?
7-8 weeks
30
Acute fatal disease of infants, common among rice-eating countries.
Acute cardiac symptoms dominate w/ neurologic symptoms
Infantile Wernicke-Beriberi Disease
31
Cardiac manifestation (tachycardia, exertional dyspnea, heart failure) w/ neuropathic manifestation of weakness, paresthesia, usually having burning feet syndrome
Beri-beri
32
Common manifestation of alcohol-induced nutriotional neuropathy
Excessive sweating of feet & hands
33
Cardiac manifestation w/ symmetrical impairment, loss of tendon reflex, motor & sensory affecting legs more than arms, distal more than proximal
Nutritional polyneuropathy
34
Essential pathologic feature of Nutritional neuropathy
Axonal degeneration, pronounced in longest & largest myelinated fibers
35
T/F. ASA & paracetamol is sufficient to control hyperpathia & allodynia in Beriberi polyneuropathy
TRUE.. Phenytoin, CBZ, & gabapentin has been inconsistent
36
T/F. Recovery of nutritional polyneuropathy is a slow process.
TRUE
37
In developed countries, Pellagra is confined among
Alcoholics
38
Clinical triad of Pellagra
3D’s: diarrhea, dermatitis, dementia (neuroasthenia)
39
In Pellagra, neurons are swollen and rounded, w/ eccentric nuclei & loss of Nissl bodies most pronounced in the:
Brainstem nuclei
40
Spinal cord lesions in Pellagra take in the form of:
Symmetrical degeneration of dorsal column likely secondary to degeneration of dorsal root ganglion
41
Pellagra is a deficiency of what vitamin
Nicotinic acid / Niacin / Vit B3
42
The amino acid precursor of nicotinic acid
Tryptophan
43
IEM that resembles pellagra in most respects including dermatitis
Hartnup disease
44
Prominent features were confusional state, paratonic rigidity, ataxia, polymyoclonia. Skin lesion absent
Nicotinic acid-deficiency Encephalopathy
45
T/F. Pyridoxine deficiency & excess causes sensory polyneuropathy
TRUE
46
Drugs that may cause Pyridoxine neuropathy
INH, Hydralazine
47
Pyridoxine (B6) deficiency results to:
Neuropathy
Vascular thrombosis (excessive homocysteine)
Seizures
48
Excessive consumption of pyridoxine will manifest as:
Sensory polyneuropathy : no weakness, ONLY ataxia, areflexia
49
Drugs that may cause Folate deficiency (B9)
MTX & Phenytoin
50
Constituent of coenzyme A (CoA)
Pantothenic acid
51
Vitamin deficiency related to Subacute combined degeneration
Vit B12 (Cobalamin)
52
Classic neurologic syndrome of Cobalamin deficiency
Spinal cord
Optic nerve
Peripheral nerve involvement
53
Hematologic effect of Vit B12 deificiency
Pernicious anemia
54
Spinal cord (ataxic paraplegia w/ spasticity), optic nerve, peripheral nerve involvement w/ pernicious anemia
Vit B12 deficiency
55
Interference of methionine synthase, a methylcobalamin dependent enzyme results to subacute combined degeneration
Nitrous oxide (anesthesia paresthetica)
56
Most consistent sign in SCD / Vit B12 deficiency
Loss of vibration sense
57
Earliest histologic event in Vit B12 deficiency is
Swelling of myelin sheath representing myelinopathy
58
Essential cofactor in conversion of homocysteine to methionine
Methylcobalamin
59
Chief obstacle to early diagnosis of SCD
Lack of parallelism between hematologic & neurologic sign particularly who have taken dietary or medicinal folate
60
Main Ddx of SCD
* Cervical spondylosis
* MS
* Adrenoleukodystrophy
* Low serum copper level
61
Serum B12 level that is associated w/ neurologic symptoms signs of deficiency
100 pg/dL
62
Other additional reliable indicators of intracellular cobalamin deficiency
Methylmalonic acid levels
| Homocysteine levels
63
In patient who receive Vit B12 parenterally, this test is more reliable than indicator for cobalamin deficiency
2-stage Schilling test
64
Diagnosis of pernicious anemia demands
Giving Vit B12
65
Improvement of gait upon treatment of Vit B12 is usually seen in
Less than 3 months
66
Ataxia, dec sensation, loss of DTRs, ophthalmoparesis, proximal muscle weakness, w/ elevated serum CKs is seen in
Vit E deificiency
67
In familial Vit E deficiency, the hepatic incorporation of tocopherol (active form Vit E) in to VLDL is defective due to mutation of
TTP, gene encoding a-tocopherol transfer protein
68
Excess of Vit A may result to what neurologic condition
Pseudotumor Cerebri
69
Uniform type of degeneration of what areas in the cerebellum among alcoholics
Vermian & anterior lobes, particularly degeneration of Purkinje cells
70
T/F. Alcoholic cerebellar degeneration is a result of direct toxic effects of alcohol
FALSE. It is a result of nutritional deficiency
71
Unique alteration of of the corpus callosum confined to the middle lamina due to loss of myelin among chronic alcoholic px
Marchiafava-Bignami Disease
72
Impressive feature of Marchiafavi-Bignami dz:
Varied neurologic features remits upon restoration of nutrition
73
Chronic alcoholism, w/ frontal lobe syndrome should suggest the diagnosis of:
Marchiafava-Bignami Disease
74
Most common cause of nutritional deficiency secondary to malabsorption
Celiac sprue
75
Alcohol is oxidized to acetaldehyde by
Alcohol dehydrogenase
76
The flushing reaction from alcohol is traced to deficiency in
Alcohol dehydrogenase
77
```
Level of alcohol in blood relating to various degree of symptoms in nonhabituated person:
• Euphoria
• Mild incoordination
• Ataxia
• Confusion
• Stuporous
• Deep anesthesia
```
```
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
78
T/F. Ethanol is oxidized at a constant rate independent of its concentration in blood
TRUE
79
T/F. The tolerance of alcohol is related to rate of alcohol metabolism.
FALSE. It depends in the increase of neuronal adaptation to alcohol
80
Early effects of aggressiveness, excessive activity, inc excitability of cortex is caused by:
Inhibition of subcortical structure
81
Effect of alcohol causing outburst of fury w/ assaultive & destructive behavior, attack terminates w/ sleep, no memory of the episode
Idiosyncratic alcohol intoxication / Pathologic intoxication
82
Main disorders to be distinguish from pathologic intoxication
Temporal lobe epilepsy & Sociopathy
83
Degree of intoxication interferes w/ registration of events & formation of memories
Alcoholic Blackouts
84
Main objective for treatment in Severe alcohol intoxication
Prevent respiratory depression & its complications
| Use of HD is need if alcohol is extremely high w/ acidosis
85
Most common source of methyl alcohol intoxication
Adulterated alcoholic beverage drink
86
Characteristic feature of methyl alcohol intoxication
Damage to retinal ganglion & bilateral degeneration of putamen
Survivors may have blindness & parkinsonism
87
By-product of methyl alcohol w/ ADH
Formaldehyde & formic acid
88
Formation of oxalate crystal & CSF, among px w/ severe metabolic acidosis, altered sensorium & convulsions aids the diagnosis of
Ethylene glycol intoxication
89
More effective drug inhibiting alcohol dehydrogenase for nonethanol alcohol intoxication
Fomepizole
90
Mutiple craniopathies most common in CNs __ & ___ is a complication of ingestion of ethylene glycol as a result of _____ which develops after 6-18 days
CN 7 & 8
Deposition of oxalate crystals along the subarachnoid portions of the affected nerves
91
Major alcohol withdrawal symptoms are seen mainly among
Binge drinker or Periodic drinkers
| Steady drinker abruptly stopped due to hospitalization
92
Most common single manifestation of alcohol abstinence syndrome
Tremulousness
93
Feeling of uneasiness may not leave the patient completely for
10-14 days
94
Most common hallucination in alcohol withdrawal
Auditory hallucination (human voices), prominent at night & duration varies
95
90% of withdrawal seizures from alcohol occurs during ____ period following cessation of drinking
7-48 hrs
96
Distinctive feature of seizure in alcohol withdrawal
Number of seizures is SINGLE. 2% have status epilepticus
97
Seizure semiology commonly seen in alcohol withdrawal
GTC
98
Most dramatic & grave of all acute alcoholic illness presenting as profound confusion, delusions, vivid hallucinations, tremor agitation, sleeplessness & inc sympathetic activity
Delirium tremens
99
Most important obligate factor in genesis of delirium tremens is:
Withdrawal of alcohol following a period of sustained chronic intoxication & rapid decline of blood alcohol
100
Treatment of delirium tremens begins w/ search of:
Injuries
Infections
Pancreatitis
Liver disease
101
Drug used in alcohol dependence resulting nausea, vomiting & hypotension
Disulfiram (Antabuse)
102
Neurotoxin affecting melanin-bearing dopaminergic nigral neurons explaining the production of parkinsonism
MPTP
103
Opioids activate _______ receptors influencing neuronal activity through intermediate cAMP .
G-coupled transmembrane receptors
| mu, delta, kappa
104
Opioid receptors are concentrated in these areas of the brain
```
Thalamus
Dorsal root ganglion (mu receptor pain)
Amygdala (affect)
Brainstem raphe (alertness)
Edinger-Westphal nuclei (pupillary miosis)
Respiratory drive
```
105
Well recognized clinical manifestation of acute opioid toxicity
```
Unresponsiveness
Shallow & slow respiration
Pinpoint pupils
Hypothermia
Bradycardia
```
106
Immediate cause of death in opioid toxicity
Respiratory depression
107
Drugs administered to treat opioid toxicity or overdose
Naloxone (0.5mg in rpt increments every 2 mins until 15 mg IV
Nalmefene (long-acting)
108
Dramatic change when naloxone is administered in opioid toxicity
Improved circulation and respiration
Reversal of miosis
Sensorium no immediate improvement
Observed for 24 hours or more.
109
Once patients regains consciousness from opioid toxicity they complain of
```
Pruritis
Sneezing / Tearing
Piloerection
Diffuse body pains
Yawning
Diarrhea
```
110
Antidote for opioid toxicity should be used w/ great caution among:
Addicts may precipitate withdrawal phenomenon
111
Opioid addiction consists of three recognizable phases:
Intoxication / Euphoria
Addiction
Relapse after period of abstinence
112
Most important factor of genesis of addiction
Repeated self-administration of opioid
113
Mechanism of tolerance in opioid addiction
Desensitization of opioid receptors through uncoupling of receptors from G-protein complex
114
Intensity of opioid withdrawal depends on
Dose
| Duration of addiction
115
Symptoms of opioid withdrawal peaks at
48-72 hours
116
Clinical signs of opioid withdrawal are no longer evident by
7-10 days
117
Refers to the substitution of drug-seeking activities for all other aims and objectives in life (Emotional/ psychological dependence)
Habituation
118
Reason methadone is used for treatment of morphine and heroin dependency
It is long-acting hence abstinence syndrome is evident around 3-4 days after withdrawal
119
Areas of activation or depression in opioid addiction
Mesolimbic structures: Nucleus accumbens, ventral tegmentum of midbrain, locus ceruleus
120
T/F. Diagnosis of addiction is usually made when patient admits using and needing drugs
TRUE
121
Confirmatory evidence of opioid addiction
Urine test confirms use within 24 hours of test
122
Alternative drug for opioid withdrawal that counteracts noradrenergic withdrawal symptoms but may induce hypotension
Clonidine (0.2-0.6 mg bid x 1 week)
123
Treatment for heroin & cocaine abuse, both w/ opioid agonist and antagonist, mutes effect of withdrawal, serves as aversive agent which demonstrated superiority over methadone
SL buprenorphine
124
Neurologic complication of opioid use
* Vasculitis (stroke)
* Amblyopia
* Transverse myelopathy
* Peripheral neuropathy
* Subacute progressive leukoencephalopathy
125
Sequelae of venous thrombosis resulting from administration of heroin and adulterants via IM or SC
```
Brawny edema
Volkmann contracture (fibrosing myopathy)
```
126
Advantages of benzodiazepine drugs
Relatively low toxicity & addictive potential
| Minimal interactions with other drugs
127
MOA of barbiturates
Enhancing GABA inhibition at pre-post synaptic receptor sites and reduce excitatory postsynaptic potentials
128
Duration of hypnotic-sedative effect of phenobarbital
6 hours (usually coma is slow & prolonged)
129
Dose of phenobarbital & lowest plasma concentration that is fatal
Dose: 6-10g
Plasma conc: 60mg/mL
130
Oldest, safest, most effective, inexpensive sedative-hypnotic drug excreted in urine as glucuronide
Resembles acute barbiturate intoxication except for miosis
Chloral hydrate
131
MOA of benzodiazepine
Activate GABA receptors opening chloride channel & hyperpolarize postsynaptic neurons & reducing firing rate
132
Primary sites of action that accounts for its anticonvulsant and anxiolytic effects
Cerebral cortex
| Limbic system
133
Disadvantage of benzodiazepine
Causes unsteadiness, drowsiness, confusion, impairment of memory especially in the elderly
134
Specific pharmacologic antagonist for benzodiazepine, w/c is diagnostically useful in cases of coma of unknown cause, & hepatic encephalopathy
Flumazenil
135
Benzodiazepine withdrawal occurs when
3rd day of withdrawal but peaks at 5th day
136
In chronic benzodiazepine users, gradual tapering of dosage over ______ minimizes withdrawal effect
1-2 weeks
137
MOA of antipsychotic drugs
Blocking postsynaptic mesolimbic dopamine receptors (D1 to D4 receptors)
138
D2 receptors are located mainly in what areas
Frontal cortex, hippocampus, limbic cortex (hence accounts for the psychosis)
139
D1 receptors are located mainly in what area
Striatum (hence parkinsonism)
140
Atypical antipsychotic drugs has less extrapyramidal symptoms because
Acts more on D2 & D4 receptors of temporal & limbic lobes more than the D1 receptors in the striatum
141
Widest application in treatment of major psychosis & bipolar psychosis, as well as for hyperactive, delirious, combative px
Phenothiazines (chlorpromazine)
142
Frequent SE of phenothiazines
* Extrapyramidal symptoms (most important)
* Cholestatic jaundice
* Agranulocytosis
* Seizures
* Orthostatic hypotension
* Skin sensitivity reactions
* Mental depression
143
Most extreme complication of phenothiazines & haloperidol
Neuroleptic malignant syndrome (NMS)
144
Extrapyramidal symptoms seen in phenothiazines (chlorpromazine)
* Parkinsonian syndrome
* Acute dyskinetic / dystonia
* Akathisia
* Tardive dyskinesia
* NMS
145
Most common extrapyramidal symptom in phenothiazines that appear several days after tx
Parkinsonian syndrome
146
Drug to treat acute dyskinesia and dystonia from drug-induced
Diphenhyrdamine IV
147
Inner restlessness, reflected by persistent shifting of body and feet, responsive w/ propranolol
Akathisia
148
Late and persistent complication of neuroleptic drugs appearing as dyskinesia, choreoathetosis and dystonic movements. 40 % of px taking antipsychotic meds have this
Tardive dyskinesia
149
Postulated cause for tardive dyskinesia
Hypersensitivity of dopamine receptor in the BG, secondary to prolonged blockade
150
Only Butyrophenone member approved for antipsychotic and management of acute psychosis
Haloperidol
151
Drugs that can be used for neuroleptic side effects
* Diphenhydramine (acute dystonia)
* Anticholinergic drugs
* Amantadine (postphenothiazine)
152
Approach to neuroleptic SE
* Gradual decrease of dose of antipsychosis to a minimum enough to control symptoms
* Substitute atypical ones
153
Neuroleptic malignant syndrome consist of:
* Hyperthermia
* Rigidity
* Stupor
* Unstable BP
* Diaphoresis
* Sympathetic overactivity
* High CK values
* Renal failure (myoglobinuria)
154
Treatment of NMS
* Bromocriptine (for altered consciousness & temp rising)
* Dantrolene (for severe cases)
155
One pitfall in managing NMS
Mistaken as worsening psychosis therefore administer more antipsychosis medications
156
Most common adverse effect of all MAO inhibitors
Postural hypotension
157
Enzyme located on outer surface of mitochondria in neurons for catabolism of catecholamines
Monoamine oxidase
158
MAO-A inhibitors must be warned against
* Phenothiazines
* CNS stimulants
* Tricylic antidepressants
* SSRI
* Sympathomimetic amines
* Tyramine containing foods (cheese, red wine, beer, preserved meat and fish)
159
TCAs MOA & indications & SE
Examples of:
Tertiary amines
Secondary amines
* 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
SSRI examples
* Paroxetine
* Fluoxetine
* Sertraline
* Escitalopram
161
Concurrent use of MAO inhibitors results to confusion, restlessness, tremor, tachycardia, hypertension, clonus, hyperreflexia, shivering, diaphoresis
Serotonin syndrome
162
Drug used for treatment of manic phase of bipolar disorder and prevention of recurrences of cyclic mood shifts
Lithium
163
SE of Lithium
* Altered consciousness
* Delirium
* Dizziness
* Nystagmus
* Ataxia
* Diffuse myoclonic twitching
* Nephrogenic DI
164
Lithium concentration proved to be fatal
3.5meqs/L
165
T/F. Discontinuation of lithium results to immediate disappearance of toxicity
FALSE. May be delayed until two weeks and DI may persist even longer
166
Proven treatment for rapid reduction of lithium blood concentration and used for lithium comatose
Hemodialysis
167
Zinc dependent protease blocking NT release by cleaving synaptic protein vesicles hence unable to exocytose, mainly GABA in _____
* Tetanospasmin
| * Renshaw cells
168
Most sensitive part of the body for tetanospasmin
Masseter innervation (hence trismus first frequent manifestation)
169
For Tetanus clinical features:
Most common
Most benign
Proven fatal
Generalized (common)
Localized (benign)
Cephalic (fatal)
170
Most characteristic for tetanus is the loss of ____ that occurs after reflex contraction normally produced by recurrent inhibition by _____
Physiologic silent period
Renshaw cells
171
Antibiotics used for tetanus
Metronidazole
Penicillin
Tetracyline
172
Most common clinical type of Diptheria
Faucial-pharyngeal type: exudate of throat and pharynx w/c is source of exotoxins affecting heart and nervous system
173
Distinguishing feature of diphtheria from other polyneuropathy
* Early oropharyngeal symptoms
* Ciliary paralysis w/ relatively retained pupillary response to light
* Subacute delayed symmetrical sensorimotor neuropathy
174
Toxin of diphtheria causes what pathology of the nerves
Demyelination in spinal nerves, spinal roots & dorsal root ganglion
175
Clinical diagnosis of botulism can be confirmed by electrophysiologic studies showing
Decrease amplitude of evoked muscle potential but increasing amplitude by RNS
176
Block neural Na channel resulting from eating fish fed on toxin-containing dinoflagellates (red tide)
Ciguatera poisoning
177
Most prominent manifestation of ciguatera that distinguishes it from GBS
Perioral parasthesia
178
Develops among children over 3-6 weeks who vomits, apathetic, altered sensorium, seizures then coma.
Plumbism
179
Non-CNS manifestation that may give clue for plumbism
* Lead lines in metaphyses of long bones
| * Basophilic stippling of RBC esp in bone marrow erythroblast
180
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 ____
* Coproporphyrin
| * Reddish fluorescence
181
Positive UCP means the lead level exceeds in blood by
80 mg/dL
182
Diagnosis for plumbism can be confirmed by
Measuring 24 hr urine lead over 500 mg using calcium EDTA
183
Treatment of acute plumbism & goal lead level
* Chelation therapy of BAL & Ca EDTA, then followed by oral penicillamine
* 40mg/dL
184
Most of lead stores in
```
Soft tissue (which is readily chelated)
Bone (not chelated)
```
185
Oral lead chelator used for outpatient asymptomatic children w/ lead >45mg/dL given for 3 weeks
Succimer
186
Adult lead intoxication usually manifest as
* Colic (poorly localize severe abdominal pain w/o fever & leukocytosis)
* Anemia
* Peripheral neuropathy
187
Diagnostic test for plumbism for adults are same for children EXCEPT
Bone films (no value for adults)
188
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)
Arsenic
189
Diagnosis of arsenic poisoning depends in the demonstration of increased level in the:
Urine & hair
190
Heavy metal poisoning that has delayed manifestation including concentric visual field constriction, tremors, mental confusion & progressive cerebellar syndrome
Organic mercury (methylmercury) poisoning / Minamata disease
191
Pathologic changes characterized by organic mercury poisoning / Minamata disease:
* degeneration of granular layer of cerebellar cortex w/ relative sparing of Purkinje cells
* Gliosis of calcarine cortex compared to other cortices
192
Heavy metal poisoning presenting as parasthesia, lassitude, incoordination, intentional tremors, & erethism
Inorganic mercury poisoning
193
Drug of choice for chronic mercury poisoning
Penicillamine
194
Delayed effects of acute organophosphate ingestion after 2-5 weeks
Distal symmetrical sensorimotor (more motor) polyneuropathy
195
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
Intermediate syndrome
196
T/F. Intermediate and delayed symptoms of organophosphate poisoning does not respond to atropine
TRUE
197
Most important SE of Vincristine occurring w/in few weeks of the beginning of treatment
* Peripheral neuropathy (sensory w/ reflex loss)
| * Other: Reversible posterior leukoencephalopathy
198
Heavy metal that inhibits DNA synthesis, dose limiting factors of nephrotoxicity, vomiting, peripheral neuropathy (primary axonal degeneration), ototoxicity, retrobulbar neuritis
Cisplatin
199
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
Paclitaxel / Docetaxel
200
MAO inhibitor that is antineoplastic effective for oligodendroglioma.
May cause somnolence, confusion, agitation, depression
Procarbazine
201
Enzyme inhibitor of protein synthesis causing drowsiness, confusion, stupor, coma, diffuse EEG slowing, may occur days upon tx. Also w/ cerebrovascular complications
L-asparaginase
202
Pyrimidine analogue causing cerebellar syndrome usually mild and subside within 6 weeks
5-FU
203
Most common complication of IT MTX
Aseptic meningitis
204
Most common & serious complication of systemic & even IT MTX
Leukoencephalopathy
205
Nitrosoureas used to treat malignant cerebal gliomas causing diffuse vasculopathy
Carmustine & Lomustine
206
Long term treatment for leukemia which is usually not neurotoxic at usual doses but if high doses will cause cerebellar degeneration
Cytarabine
207
Most frequent SE of calcinuerin inhibitors (Cyclosporine, Tacrolimus)
* Tremor & myoclonus (most frequent)
* Seizure (sign of toxicity)
* PRES
208
Antibiotic causing seizures at higher doses
Penicillin
Imipenem
Cephalosporins
209
Antibiotic that may cause reversible cerebellar syndrome assoc w/ dentate nuclei signal changes in MRI.
Dysarthria, confusion & gait ataxia are core clinical syndrome
Metronidazole
