EPPP Part 1 (Examination for Professional Practice in Psychology) — All Questions

After a left-hemisphere stroke, a 62-year-old speaks in slow, effortful, telegraphic phrases, follows everyday conversation reasonably well, and is visibly frustrated by his own errors. Damage to which region best accounts for this picture?

• a.The arcuate fasciculus linking the language areas
• b.The right-hemisphere homologue of Broca's area
• c.Wernicke's area in the left superior temporal gyrus
• d.Broca's area in the left inferior frontal gyrus✓

Nonfluent, effortful speech with relatively preserved comprehension and awareness of errors is the pattern Broca described in 1861 and that NIDCD lists as Broca's (nonfluent) aphasia. Wernicke's area damage produces fluent but meaningless speech with poor comprehension, and arcuate fasciculus damage produces conduction aphasia, marked by poor repetition with fluent speech. Right-hemisphere damage in a right-handed adult does not usually produce aphasia of this kind.

Patient H.M. underwent bilateral removal of medial temporal lobe structures, including most of the hippocampus, to control seizures. Which ability remained largely intact afterward?

• a.Forming lasting memories of new daily events
• b.Getting better at mirror tracing over several days✓
• c.Recalling a word list after a distracting delay
• d.Recognizing people he first met after surgery

Scoville and Milner (1957) described a profound anterograde amnesia after H.M.'s resection: he could not form lasting memories of new events, recognize people met after surgery, or recall material once his attention was diverted. Milner (1962) showed that he nevertheless improved steadily at mirror drawing across days, evidence that procedural (nondeclarative) learning does not depend on the medial temporal lobe.

A night-shift nurse has trouble sleeping during the day because her light exposure is out of step with her body's master circadian clock. Which structure serves as that master clock?

• a.Mammillary bodies of the hypothalamus
• b.Locus coeruleus in the pons
• c.Suprachiasmatic nucleus✓
• d.Pineal gland in the epithalamus

NIH's National Institute of General Medical Sciences identifies the suprachiasmatic nucleus (SCN) as the brain's master clock; it receives light information from the eyes and controls melatonin production. The pineal gland secretes melatonin but takes its timing from the SCN rather than acting as the clock. The locus coeruleus is the main noradrenergic nucleus, and the mammillary bodies are involved in memory circuits.

A client asks how sertraline works. Which description of its primary mechanism is accurate?

• a.It inhibits monoamine oxidase, slowing serotonin breakdown
• b.It blocks dopamine D2 receptors in the mesolimbic pathway
• c.It directly stimulates postsynaptic serotonin receptors
• d.It blocks reuptake of serotonin into the presynaptic neuron✓

The FDA label for sertraline (Zoloft) states that its mechanism is presumed to be linked to inhibition of CNS neuronal uptake of serotonin, which is what makes it a selective serotonin reuptake inhibitor. Inhibiting monoamine oxidase describes MAOIs such as phenelzine, direct receptor stimulation describes agonists, and D2 blockade describes antipsychotics.

A client taking phenelzine eats aged cheese and cured sausage at a party and within an hour develops a severe occipital headache and a sharp rise in blood pressure. What is the most likely explanation?

• a.An allergic reaction to histamine in fermented food
• b.Neuroleptic malignant syndrome triggered by dehydration
• c.A hypertensive crisis caused by dietary tyramine✓
• d.Serotonin syndrome from serotonin precursors in the food

Phenelzine is a monoamine oxidase inhibitor, and its FDA label warns that foods high in tyramine, such as aged cheese and cured meats, can precipitate a hypertensive crisis marked by occipital headache and markedly raised blood pressure. Serotonin syndrome arises mainly from combining serotonergic drugs, neuroleptic malignant syndrome is linked to dopamine-blocking agents, and an allergic reaction does not typically present as an acute hypertensive headache.

Why do prescribers routinely measure serum drug concentrations in clients who take lithium?

• a.Toxicity can occur at levels close to therapeutic levels✓
• b.Lithium forms an active metabolite that must be tracked
• c.Serum levels are needed to confirm a bipolar diagnosis
• d.Lithium levels change only when doses are missed

The boxed warning on lithium labeling states that lithium toxicity is closely related to serum lithium concentrations and can occur at doses close to therapeutic concentrations, so facilities for serum lithium determination should be available before treatment starts. Lithium is an ion that is not metabolized, a blood level cannot diagnose bipolar disorder, and levels shift with many factors such as dehydration, sodium intake and interacting drugs, not only missed doses.

Which description matches how disulfiram supports abstinence from alcohol?

• a.It blocks opioid receptors, reducing the rewarding effect of alcohol
• b.It substitutes for alcohol at GABA-A receptors to prevent withdrawal
• c.It reduces craving by lowering dopamine release in the striatum
• d.It makes drinking aversive by blocking acetaldehyde breakdown✓

The FDA label for disulfiram states that it blocks the oxidation of alcohol at the acetaldehyde stage, so drinking produces an unpleasant disulfiram-alcohol reaction (flushing, nausea, palpitations) that deters use. Opioid-receptor blockade is how naltrexone works, GABA-A modulation describes benzodiazepines used for withdrawal, and disulfiram's action is not described as reducing dopamine release.

For opioid use disorder, buprenorphine differs pharmacologically from methadone chiefly because buprenorphine is:

• a.a partial agonist at the mu-opioid receptor✓
• b.a full agonist at the mu-opioid receptor
• c.an alpha-2 adrenergic receptor agonist
• d.a pure antagonist at the mu-opioid receptor

FDA labeling for buprenorphine products describes buprenorphine as a partial agonist at the mu-opioid receptor, which gives it a ceiling on some opioid effects. Methadone is a full mu agonist, naltrexone is an opioid antagonist, and alpha-2 agonists such as lofexidine ease withdrawal symptoms without acting on opioid receptors.

A twin study estimates the heritability of a trait at 0.60 in the sampled population. Which interpretation is correct?

• a.The trait will be 60% resistant to any environmental intervention
• b.60% of trait variance in that population reflects genetic variance✓
• c.A child has a 60% chance of inheriting the trait from an affected parent
• d.About 60% of each person's level of the trait is caused by their genes

Heritability is a population statistic: the proportion of phenotypic variance in a particular population and environment that is attributable to genetic variance (Visscher, Hill & Wray, 2008; NIH MedlinePlus Genetics). It says nothing about how much of one individual's trait comes from genes, does not mean the trait resists environmental change, and is not a transmission probability for a given child.

A researcher wants to track, millisecond by millisecond, how the brain responds to briefly flashed words. Which method best suits this aim?

• a.Event-related potentials from scalp EEG✓
• b.PET imaging of glucose metabolism
• c.Structural MRI with diffusion tensor imaging
• d.Functional MRI using the BOLD signal

Scalp EEG and the event-related potentials derived from it record electrical activity with millisecond temporal resolution, though with limited spatial precision. The fMRI BOLD signal follows a hemodynamic response that unfolds over seconds (Logothetis, 2008), PET is slower still, and diffusion tensor imaging maps white-matter structure rather than moment-to-moment activity.

A man with a long history of heavy drinking cannot retain new information and fills memory gaps with sincere but fabricated accounts. This syndrome is primarily caused by deficiency of which vitamin?

• a.Folate (vitamin B9)
• b.Niacin (vitamin B3)
• c.Cobalamin (vitamin B12)
• d.Thiamine (vitamin B1)✓

NINDS describes Wernicke-Korsakoff syndrome as a brain disorder caused by thiamine (vitamin B1) deficiency, most often in people with alcohol use disorder, with Korsakoff's psychosis marked by memory loss and confabulation. B12 deficiency causes anemia and neuropathy, folate deficiency is tied to anemia and neural tube defects, and niacin deficiency causes pellagra.