MSN 671 Final Exam Focus Points FINAL EXAM 2026
COMPLETE TEST APPROVED QUESTIONS AND CORRECT
VERIFIED ANSWERS (A NEW UPDATED VERSION)
|GUARANTEED PASS A+ Northern Kentucky University
Sodium-charged ion channel
Essential for action potentials
Made of 4 subunits forming a central alpha pore; each subunit is made
of 6 transmembrane segments:
-Segment 4= voltmeter
-Segment 5-6= ionic filter (only allows Na through)
-Between 3rd and 4th subunits= amino acid plug/pore inactivator
Site of action of many anticonvulsants
,Presynaptic transporter
Collects NTs from the synapse and transports them back into the
neuron for packaging and release
Monoamine: SERT, DAT,
NET GABA: GAT
Glutamate: EAAT
Norepinephrine role
helps control alertness and arousal, stress response, cognitive
functioning, attention/focus
Linked to fight or flight
Acetylcholine role
Motivation, memory, cognitive functioning, sleep
Melatonin role
Sleep
Released from the pineal gland (increased in darkness)
,Serotonin role
Sleep, mood, sexuality, appetite, pain
Dopamine role
Reward/pleasure, executive functioning, wakefulness, learning,
motor control
GABA role
Inhibitory
Sleep, mood regulation
Histamine role
inflammation, alertness/wakefulness
Process of melatonin production
-During darkness, there is no input from the retinohypothalamic tract
to the suprachiasmatic nucleus (SCN) in the hypothalamus-->Signals
the pineal
gland to produce melatonin
-MT1 receptor then inhibits neurons in the suprachiasmatic nucleus
, decreasing the wake-promoting actions there
, Process causing tardive dyskinesia with an antipsychotic
· Chronic blockade of D2 receptors in the nigrostriatal pathway (D2
receptors are normally inhibitory of the "STOP" pathway, making it
"GO"--> acute blockade causes "STOP" to predominate, resulting
in slow and rigid Parkinsonism-like movements)
-->Receptors then upregulate, causing supersensitivity of receptors
and the opposite situation (not enough "STOP") and, therefore,
the rapid, hyperkinetic, involuntary movements of TD)
· Late and delayed in onset (months to years of treatment)
· Can be irreversible
How can antipsychotics cause breast discharge
· By blocking the tuberoinfundibular pathway (projects from
hypothalamus to pituitary gland), which is normally tonically
active and inhibits prolactin release
· This blockade causes a rise in prolactin--> galactorrhea
Metabolic monitoring/labs for antipsychotics
· Weight/BMI
· Fasting triglycerides
· Fasting glucose
· BP
Liver
fnt
COMPLETE TEST APPROVED QUESTIONS AND CORRECT
VERIFIED ANSWERS (A NEW UPDATED VERSION)
|GUARANTEED PASS A+ Northern Kentucky University
Sodium-charged ion channel
Essential for action potentials
Made of 4 subunits forming a central alpha pore; each subunit is made
of 6 transmembrane segments:
-Segment 4= voltmeter
-Segment 5-6= ionic filter (only allows Na through)
-Between 3rd and 4th subunits= amino acid plug/pore inactivator
Site of action of many anticonvulsants
,Presynaptic transporter
Collects NTs from the synapse and transports them back into the
neuron for packaging and release
Monoamine: SERT, DAT,
NET GABA: GAT
Glutamate: EAAT
Norepinephrine role
helps control alertness and arousal, stress response, cognitive
functioning, attention/focus
Linked to fight or flight
Acetylcholine role
Motivation, memory, cognitive functioning, sleep
Melatonin role
Sleep
Released from the pineal gland (increased in darkness)
,Serotonin role
Sleep, mood, sexuality, appetite, pain
Dopamine role
Reward/pleasure, executive functioning, wakefulness, learning,
motor control
GABA role
Inhibitory
Sleep, mood regulation
Histamine role
inflammation, alertness/wakefulness
Process of melatonin production
-During darkness, there is no input from the retinohypothalamic tract
to the suprachiasmatic nucleus (SCN) in the hypothalamus-->Signals
the pineal
gland to produce melatonin
-MT1 receptor then inhibits neurons in the suprachiasmatic nucleus
, decreasing the wake-promoting actions there
, Process causing tardive dyskinesia with an antipsychotic
· Chronic blockade of D2 receptors in the nigrostriatal pathway (D2
receptors are normally inhibitory of the "STOP" pathway, making it
"GO"--> acute blockade causes "STOP" to predominate, resulting
in slow and rigid Parkinsonism-like movements)
-->Receptors then upregulate, causing supersensitivity of receptors
and the opposite situation (not enough "STOP") and, therefore,
the rapid, hyperkinetic, involuntary movements of TD)
· Late and delayed in onset (months to years of treatment)
· Can be irreversible
How can antipsychotics cause breast discharge
· By blocking the tuberoinfundibular pathway (projects from
hypothalamus to pituitary gland), which is normally tonically
active and inhibits prolactin release
· This blockade causes a rise in prolactin--> galactorrhea
Metabolic monitoring/labs for antipsychotics
· Weight/BMI
· Fasting triglycerides
· Fasting glucose
· BP
Liver
fnt
