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ABPP > Psychopharmacology & Toxins > Flashcards

Psychopharmacology & Toxins Flashcards

1
Q

How do monoamine oxidase inhibitors (MAOIs) work?

A

Inhibit the enzyme MAO (which deactivates DA, NE, & serotonin)

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1
Q

Drug potentiation

A

Synergistic action of 2+ drugs when this is more powerful than their additive effects

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2
Q

Cognitive deficits associated with long-term MDMA use

A

Persist up to 1 year postabstinence Learning & memory, exec fx & planning, attention & vigilance, verbal fluency, visual scanning

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2
Q

Mercury exposure is associated with

A

Encephalopathy of cerebellum, BG, primary visual corteix, spinal cord Motor slowing, clumsiness, tremor, paresthesia, visual & hearing defects, agitation Long-term exposure associated with depression, slowing, impaired STM

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2
Q

Dialysis dementia

A

Caused by high brain aluminum levels Marked by stuttering & dysfluent speech, myoclonus & difficulty swallowing, concentration & memory problems

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3
Q

Neuroimaging findings among cocaine users

A

Cerebral atrophy correlated w/ length of use, demyelination, hyperintensities, vasospasm, stroke-like defects, multiple patchy areas of hypoperfusion, EEG - marked reduced alpha power in frontal & temporal regions

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4
Q

Typical antipsychotics work by

A

Blocking dopamine

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4
Q

How do beta-blockers work?

A

Block beta-adrenergic receptors, which respond to epinephrine & NE

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5
Q

How do tricyclics work?

A

Block reuptake of NE & serotonin (DA?)

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6
Q

Name some common tricyclics

A

ANDI: amitriptyline, nortirptyline, doxepin, imipramine

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7
Q

How do benzodiazepines work?

A

Inhibit GABA

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7
Q

Side effects of benzodiazepines

A

Can cause sedation/drowsiness, confusion, disorientation in elderly, disturbed sleep, potential for withdrawal If stopped, see rebound hyperexcitability leading to seizures, depersonalization, panic, & stroke

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8
Q

Neuroimaging findings in recently detoxified alcoholics

A

Cerebral atrophy & white & gray matter volume loss

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9
Q

Neuropsych deficits associated with glue sniffing

A

Dose-related deficits in attention, memory, visuospatial fx, complex cognition, naming, reading/writing

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10
Q

How do barbiturates work?

A

Interrupt impulses to RAS

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11
Q

MAOIs are used for

A

Used for atypical depression, hostility, anxiety, hypochondriasis

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12
Q

Alcohol-induced persisting dementia

A

Dysfx of general intellectual abilities, memory, visuospatial abilities, abstraction, problem solving Orientation to time & place, language abilities remain well-preserved May be on average 10 yrs younger than those w/ other dementias, 2x the avg length of institutionalization

14
Q

Symptoms of cocaine withdrawal

A

Crash, disrupted sleep, appetite, psychomotor fx, vivid disturbing dreams due to REM rebound

15
Q

How do amphetamines work in the CNS?

A

Provoke discharge of DA & then blocks reuptake Increases activity of NE that produces sympathomimetic effects

16
Q

Tricyclics are used for

A

Used for somatic & vegetative symptoms of depression, panic attacks, agoraphobia, & obsessive states

18
Q

Long term cognitive deficits among amphetamine users

A

Attentional & motor skills, verbal memory & attention

19
Q

How do atypical antipsychotics work?

A

Work on D2 & other DA receptors, serotonin, & glutamate

20
Q

Neuroleptic malignant syndrome

A

High fever, severe muscle rigidity, altered consciousness, ANS dysregulation

22
Q

Hepatic encephalopathy

A

Perform worse on STM, eye tracking, hand-eye coordination Many deficits improve following liver transplantation, memory does not Subclinical can cause sig. memory impairment & motor slowing w/ intact intellectual fx & abstraction

23
Q

Primary CNS target of manganese

A

Dopaminergic neurons in striatum

25
Q

NP findings among sober moderate-heavy cocaine users

A

Memory flexibility & control, attention & concentration, visuomotor ability, verbal & visual learning/memory

26
Q

Multiple exposures to PCP may produce what chronic impairments?

A

Memory & confusion

27
Q

How do SSRIs work, and what are they used for?

A

Block reuptake of serotonin; used for depression, OCD, eating disorders

28
Q

CNS damage from carbon monoxide is centered in

A

GP, cortex, hippocampus, cerebellum, fornix, CC

29
Q

Characteristic triad of opioid overdose

A

Coma, miosis, respiratory depression

31
Q

Long-term cognitive deficits associated with alcohol use

A

Complex memory deficits due to use of inefficient organization strategies during encoding; problem-solving, perceptuomotor abilities, visual learning & memory, contextual memory

32
Q

What are beta-blockers used for?

A

used for physical manifestations of anxiety, high BP, angina, tremors, migraines, glaucoma

33
Q

How does MDMA work in the CNS?

A

Provokes sudden emptying of presynaptic serotonin stores With continued use, destroys serotoninergic neurons & creates cognitive impairments

34
Q

Symptoms of mercury exposure

A

Cerebral encephalopathy, oral hemorrhage, auditory/visual hallucinations, fine motor tremor, insomnia, agitation

35
Q

What are some contraindications for psychostimulants?

A

anxiety & tension, anorexia, HTN, hx of psychosis, recent hx of drug or ETOH abuse, pre-existing motor tics

36
Q

How do psychostimulants work?

A

Works on catecholamines (DA, NE, epinephrine)

37
Q

Neuroimaging findings among heavy MDMA users

A

Global decreases in 5-HT transporter densities in parieto-occipital, occipital, & sensory cortex

38
Q

NP findings in current cocaine users

A

Deficits in verbal & visual recall, WM, attention

39
Q

How does cocaine work in the CNS?

A

Provokes a discharge of DA from presynaptic storage vesicles & then blocks its reuptake (particularly in mesolimbic system) Blocks reuptake of NE => pronounced sympathomimetic effects (arrhythmias, HTN, vasospasm, pupillary dilation) Blocks reuptake of serotonin => euphoria

40
Q

Central serotonin syndrome

A

Severe HA, nystagmus, tremor, dizziness, unsteady gait, irritability, confusion, delirium, cardiac arrhythmia

ABPP (34 decks)

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