Partial preview of the text
Download MARYVILLE NURS660 PSYCHOPHARMACOLOGY EXAM 4 100% DETAILED VERIFIED CORRECT ANSWERS STUD and more Exams Health sciences in PDF only on Docsity!
MARYVILLE NURS
PSYCHOPHARMACOLOGY EXAM 4
100% DETAILED VERIFIED CORRECT
ANSWERS STUDY SET 2025/
CORTICO-STRIATAL-THALAMIC LOOP IN ADHD
- IMPULSIVITY AND HYPERACTIVITY ARE MODULATED HERE.
- MOTOR ACTIVITY, SUCH AS HYPERACTIVITY AND PSYCHOMOTOR AGITATION OR
RETARDATION, CAN BE MODULATED BY CSTC LOOP FROM THE PREFRONTAL MOTOR CORTEX
TO THE PUTAMEN (LATERAL STRIATUM) TO THE THALAMUS AND BACK TO THE PREFRONTAL
MOTOR CORTEX.
- COMMON SYMPTOMS OF HYPERACTIVITY IN CHILDREN WITH ADHD INCLUDE FIDGETING,
LEAVING ONE'S SEAT, RUNNING/CLIMBING, BEING CONSTANTLY ON THE GO AND HAVING
TROUBLE PLAYING QUIETLY.
MESOLIMBIC DOPAMINE PATHWAY IN ADHD
- TOO LITTLE OF NOREPI OR DOPAMINE-HAVE ISSUES WITH BEING DISTRACTED, ORGANIZED,
FORGETFUL, OR FATIGUED. (NOREPI AND DOPAMINE ARE THE TWO KEY
NEUROTRANSMITTERS IN ADHD)
PATHOPHYSIOLOGY OF ADHD
INEFFICIENT TUNING OF PREFRONTAL CORTEX BY DYSREGULATION OF DOPAMINE AND
NOREPINEPHRINE.
SYMPTOMS: INATTENTION, HYPERACTIVITY, AND IMPULSIVITY.
ATOMEXETINE (STRATTERA)
- ADHD NON-STIMULANT
- INHIBITS NET IN THE PREFRONTAL CORTEX INCREASES BOTH DA AND NE. AS ONLY A FEW
NET EXIST IN THE NUCLEUS ACCUMBENS, ATOMOXETINE DOES NOT INDUCE AN INCREASE
IN DA AND NE IN THE NUCLEUS ACCUMBENS, THE REWARD CENTER OF THE BRAIN, THUS
ATOMOXETINE DOES NOT HAVE ABUSE POTENTIAL.
- REQUIRES BUILD-UP OVER TIME, NOT SHORT ACTING, NO CONCERN FOR ABUSE/MISUSE.
- CAN'T BE TAKEN WITH PAXIL OR WELLBUTRIN
- ADVERSE EFFECTS: PRIAPISM, LIVER INJURY
METHLYPHENIDATE
RITALIN, CONCERTA, ADHD STIMULANT.
- METHYLPHENIDATE BINDS TO THE DOPAMINE TRANSPORTER AND TO THE
NOREPINEPHRINE TRANSPORTER, IN BOTH CASES ACTING AS AN ALLOSTERIC MODULATOR.
STOPS THE ACTION OF THE TRANSPORTERS, PREVENTING REUPTAKE AND THUS ALLOWING
DOPAMINE AND NOREPINEPHRINE TO ACCUMULATE IN THE SYNAPSE.
AMPHETAMINE
ADDERALL, ADHD
- COMPETITIVELY INHIBITS DOPAMINE TRANSPORTER AND VMAT TRANSPORTER.
- BLOCKS THE TRANSPORTER FOR DOPAMINE AND NOREPINEPHRINE.
- INCREASES DOPAMINE AT SYNAPTIC CLEFT.
- HIGH RISK FOR ABUSE
GUANFACINE
INTUNIV, NONSTIMULANT FOR ADHD.
SELECTIVE AGONIST FOR ALPHA 2A.
BETTER TOLERATED THAN CLONIDINE.
CLONIDINE
DONEPEZIL (ARICEPT)
- REVERSIBLE, LONG-ACTING SELECTIVE INHIBITOR OF ACETYLCHOLINESTERASE (ACHE),
- TRANSIENT GASTROINTESTINAL SIDE EFFECTS
- TAKEN ONCE DAILY
GALANTAMINE
ACHE INHIBITION AND POSITIVE ALLOSTERIC MODULATION (PAM) OF NICOTINIC
CHOLINERGIC RECEPTORS.
- CHOLINESTERASE INHIBITOR, ENHANCES ACTIONS OF ACETYLCHOLINE
- CONTRAINDICATED IN PATIENTS WITH RENAL OR HEPATIC IMPAIRMENT
RIVASTIGMINE
CHOLINESTERASE INHIBITOR
AVAILABLE AS ORAL AND TRANSDERMAL
THE ORAL FORMULATION MAY RESULT IN MORE GASTROINTESTINAL SIDE EFFECTS THAN
DONEPEZIL,
- INHIBITION OF BOTH ACHE AND BUTYRYLCHOLINESTERASE (BUCHE) IN THE PERIPHERY.
MEMANTINE
- NMDA RECEPTOR ANTAGONIST
- STOPS THE EXCESSIVE GLUTAMATE FROM INTERFERING WITH THE RESTING GLUTAMATE
NEURON'S PHYSIOLOGICAL ACTIVITY AND THUS IMPROVING MEMORY.
BIOMARKERS OF ALZHEIMER'S
- PRESYMPTOMATIC STAGE OF ALZHEIMER'S DISEASE, A-BETA PEPTIDES ARE SLOWLY AND
RELENTLESSLY DEPOSITED INTO THE BRAIN RATHER THAN ELIMINATED VIA THE CSF,
PLASMA, AND LIVER. CSF LEVELS OF AMYLOID BETA DECREASE.
- WITH PROGRESSION, TAU AND PHOSPHORYLATED TAU PROTEIN LEVELS IN THE CSF
INCREASE.
- BRAIN AMYLOID SEEN ON AMYLOID-PET SCANS
PATHOPHYSIOLOGY OF ALZHEIMERS
- EXTRACELLULAR AMYLOID PLAQUE BUILD UP- INTRACELLULAR FORMATION OF
NEUROFIBRILLARY TANGLES (MADE UP OF TAU PROTEIN)
IMPULSIVITY IS HYPOTHESIZED TO BE RELATED TO THE _____, WHILE COMPULSIVITY IS
HYPOTHESIZED TO BE RELATED TO THE _____.
VENTRAL STRIATUM, DORSAL STRIATUM
DC
IV
NALTREXONE
OPIOID ANTAGONIST
BLOCKING MU-OPIOID RECEPTORS INTERRUPTS REWARD PATHWAYS IN BRAIN.
CONTRAINDICATED IN PTS WITH SEVERE LIVER IMPAIRMENT
CAN'T USE UNTIL PATIENT HAS BEEN OFF OPIOIDS FOR 7-10 DAYS, LONG HALFLIFE
IM 30 DAY OPTION (TRIAL ORAL FIRST)
DISULFIRAM
USED IN TX OF ALCOHOL CESSATION. ANTABUSE
INHIBITS ACETALDEHYDE DEHYDROGENASE-->INCREASED ACETALDEHYDE WHEN DRINKING
(TOXIC)-->N/V, FLUSHING, HYPOTENSION-->INCENTIVE NOT TO DRINK
CAN'T INITIATE UNTIL PT HASN'T DRANK ALCOHOL FOR 12 HOURS+. LONG HALF-LIFE, CAN
TAKE UP TO TWO WEEKS TO CLEAR.
MAY REACT TO ANY ALCOHOL/ETHANOL, INCLUDING HAND SANITIZER, KOMBUCHA, ETC.
ACAMPROSATE
DECREASES UNPLEASANT EFFECTS RESULTING FROM ABSTINENCE LIKE DYSPHORIA, ANXIETY,
RESTLESSNESS.
MODULATES OVERACTIVE GLUTAMATE BRAIN ACTIVITY THAT OCCURS AFTER STOPPING
QUICK ADMINISTRATION (SNORTING) CAUSES PHASIC FIRING OF DOPAMINE, THE TYPE
ASSOCIATED WITH REWARD AND SALIENCY.
HOW IS THE BRAIN AFFECTED BY HALLUCINOGENICS?
HALLUCINOGENS WORK BY AGONIZING 5H2A RECEPTORS- CAUSES HALLUCINATIONS
ALCOHOL WITHDRAWAL
- ABSTINENCE LEADS TO WITHDRAWAL BECAUSE YOU NO LONGER HAVE INHIBITION OF
GABA RECEPTORS AND NMDA RECEPTORS ARE UPREGULATED WHICH LEADS TO
UNCONTROLLED EXCITATION THROUGH GLUTAMATE ACTIVITY.
- TREAT ALCOHOL WITHDRAWAL WITH BENZOS AND ANTICONVULSANTS TO TRY TO GET PTS
BACK TO BASELINE INHIBITION OF GABA RECEPTOR AND BASELINE EXCITATION, WE WANT
TO GET IT BALANCED AND NOT OVER EXCITATION BECAUSE OF UPREGULATION NMDA
RECEPTORS AND OVERLY DOWN REGULATED GABA RECEPTORS
- OCCURS WITHIN 24-72 HOURS
PHASES OF ALCOHOL WITHDRAWAL
MILD WITHDRAWAL: 6-24 HOURS. MILD ANXIETY, TREMORS, GI UPSET, HEADACHE,
PALPITATIONS, STILL COHERENT
ALCOHOL HALLUCINOSIS: 12-24 HOURS. HALLUCINATIONS
MODERATE & SEVERE WITHDRAWAL: 24-72 HOURS. MARKED AGITATION & DIAPHORESIS,
HYPERTENSION, TACHYPNEA, TACHYCARDIA, HYPERTHERMIA, CONFUSION MAY BE PRESENT
WITHDRAWAL SEIZURES: 8-48 HOURS (PEAK 24 HOURS).
ALCOHOL WITHDRAWAL DELIRIUM: 72-96 HOURS. HALLUCINATIONS (MAINLY VISUAL),
DISORIENTATION, AUTONOMIC INSTABILITY, SEVERE TACHYCARDIA, AGITATION,
DIAPHORESIS
LABS WITH ALCOHOL USE
AST/ALT-IF RATIO IS 2:1 IT IS SUGGESTIVE OF ALCOHOLIC INDUCED LIVER DISEASE
- TAKES ABOUT 3 TO 7 DAYS TO ELEVATE AND HOURS (HALF-LIFE)? TO NORMALIZE AFTER
ABSTINENCE
AST: 10- 34
ALT: 8- 34
CDT (CARBOHYDRATE DEFICIENT TRANSFERRIN) IS VERY SPECIFIC AND RELIABLE FOR
DETECTING EXCESSIVE ALCOHOL USE AND MORE RELIABLE THAN GGT BUT IS NOT AS
AVAILABLE.
CDT TAKES ABOUT 2 TO 3 WEEKS TO ELEVATE AND 2 TO 4 WEEKS TO NORMALIZE AFTER
ABSTINENCE
GGT (GAMMA-GLUTAMYLTRANSFERASE)-IT CAN TELL YOU IF THERE IS EXCESSIVE ALCOHOL
USE WHICH CHANGES FROM MALE TO FEMALE (45) AND TELLS YOU IF SOMEONE HAS
REMAINED SOBER FROM ALCOHOL
- GGT IS USUALLY USED IN COMBINATION WITH MCV (>100 MACROCYTOSIS AND
PANCYTOPENIA) WHICH IS PRETTY RELIABLE FOR ALCOHOL USE
- GGT TAKES ABOUT 24 HOURS TO 2 WEEKS TO ELEVATE AND 2 TO 6 WEEKS TO NORMALIZE
AFTER ABSTINENCE
- MCV TAKES 6 WEEKS TO ELEVATE AND 3 MONTHS TO NORMALIZE
WERNICKE'S ENCEPHALOPATHY
A BRAIN DISORDER CAUSED BY THIAMINE DEFICIENCY AND CHARACTERIZED BY VISUAL
DISTURBANCES, ATAXIA, SOMNOLENCE, STUPOR, AND , WITHOUT THIAMINE REPLACEMENT,
DEATH.
TREAT WITH THIAMINE, IM OR IV
KORSAKOFF'S SYNDROME
- MCV TAKES 6 WEEKS TO ELEVATE AND 3 MONTHS TO NORMALIZE
