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Summary WGU D345 Comprehensive Study Guide: Dr Cole Remediation for OA | latest Update wit, Summaries of Advanced Education

Western Governors University (WGU)Advanced Education

Summary WGU D345 Comprehensive Study Guide: Dr Cole Remediation for OA | latest Update with complete solutions.

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2025/2026

Available from 05/21/2026

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Comprehensive Study Guide
D345
1
Summary WGU D345 Comprehensive Study Guide:
Dr Cole Remediation for OA | latest Update with
complete solutions.
Section
1
Highlight
Guide
•
1. Neurotransmitters: know all the
neurotransmitters, the role of various
neurotransmitters in various diagnosis and
symptoms. Recommendation: Make a chart
with various diagnosis and the role various
neurotransmitters play in that
diagnosis/symptom.
•
The study of the magnitude and variation of
drug response is the definition of
pharmacodynamics. Psychodynamics is
the study of
what the body does to a drug and helps
explain the relationship between the dose and
response.
o
Dopamine produced in substantia nigra
and ventral tegmental area
▪
D: Drive/Drugs
▪
O: psychOsis
▪
P: Prolactin Inhibition
▪
A: Attention
▪
M: Motivation
▪
I: Involuntary Movements
▪
N: Nausea
▪
E: Energy
o
Serotonin is produced mostly in Raphe nucleus
▪
DOMAINS: Depression, Obsession,
Migraines, Anxiety, Intestines,
Nausea, and Sexual.
▪
Serotonin Syndrome: Shits
and SHIVERS. Shits(diarrhea),
Shivering, Hyperreflexia,
Increased temperature, Vital
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D

Summary WGU D345 Comprehensive Study Guide:

Dr Cole Remediation for OA | latest Update with

complete solutions.

Section 1 Highlight Guide

    1. Neurotransmitters: know all the neurotransmitters, the role of various neurotransmitters in various diagnosis and symptoms. Recommendation: Make a chart with various diagnosis and the role various neurotransmitters play in that diagnosis/symptom.
  • The study of the magnitude and variation of drug response is the definition of pharmacodynamics. Psychodynamics is the study of what the body does to a drug and helps explain the relationship between the dose and response. o Dopamine produced in substantia nigra and ventral tegmental area ▪ D: Drive/Drugs ▪ O: psychOsis ▪ P: Prolactin Inhibition ▪ A: Attention ▪ M: Motivation ▪ I: Involuntary Movements ▪ N: Nausea ▪ E: Energy o Serotonin is produced mostly in Raphe nucleus ▪ DOMAINS: Depression, Obsession, Migraines, Anxiety, Intestines, Nausea, and Sexual. ▪ Serotonin Syndrome: Shits and SHIVERS. Shits(diarrhea), Shivering, Hyperreflexia, Increased temperature, Vital

D

sign instability, Encephalopathy, Restlessness, and Sweating. o Norepinephrine is produced in locus ceruleus of the pons ▪ Receptors A1, A2, B1, B2, and B3. More blood vessels. ▪ Fight or flight. Sympathetic nervous system. ▪ Concentrating, focusing, burst of energy, increased BP/HR, mobilizing glucose o Epinephrine produced by the adrenal glands ▪ More heart ▪ Fight or flight. Sympathetic nervous system. o Acetylcholine synthesized by the Basal Nucleus of Meynart ▪ Parasympathetic Nervous system. Rest and Digest. Feed and breed. o Muscarinic Receptors

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    1. Pharmacokinetics and Pharmacodynamics are factors that affect both. o Pharmacokinetics- What the BODY does to the drug or how it is processed by the body. o Pharmacodynamics- What the Drug does to the body and how it produces the therapeutic effect. The MOA. o Pharmacokinetics processes vary between patients because they are affected by body factors such as gender, age, weight, genetics, and also drug-drug interactions. The process is affected by a pregnancy and a patient's pathophysiology. o Pharmacodynamics is another process involving the relationship between drug concentration at the site of action and its effects. Medication binding determines drug impact at the site of movement with a receptor. Understanding each medication's full range of receptor interactions is critical
    1. Agonist, antagonist, partial agonist, inverse agonist, depolarization, repolarization o Agonist- Substance which initiates a physiological response when combined with a receptor. o Antagonist- Substance that interferes/inhibits the physiological action of another. o Partial Agonist- Binds to a receptor and activates it, but to a lesser extent than a full agonist.

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sedation, anticonvulsant actions, and possibly to amnesia.

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ii. A2 and A3 subtype receptors are linked to anti- anxiety, muscle relaxant, and alcohol- potentiating actions. iii. A5 is mostly in the hippocampus and may be linked to cognition. c. Dual Orexin Receptor Antagonists(DORAS): Block wake stabilizing orexin 1&2 receptors. Reversible so when the orexin levels rise in the morning, it goes back to normal. Lemborexant has a faster reversal due to dissociation kinetics at receptor 2(orexin). i. Suvorexant and Lemborexant. Promote sleep without side effects of Benzo or Z-drug(hypnotic). d. Serotonergic Hypnotics: 5HT2A/A1/H1 antagonist. TRAZADONE. Reduces the arousal in insomnia. REDUCES AROUSAL vs enhancing sleep drive. Blockade of arousal neurotransmitters(serotonin, norepinephrine, and histamine). Used for depression but insomnia is a non-intended treatment effect. e. Histamine 1 Antagonists: Diphenhydramine/Benadryl(allergy meds) or doxylamine. Doxepin(depression med/other tricyclic antidepressants too), and psychosis meds(chlorpromazine and quetiapine). Low doses for them function as hypnotics. f. Anticonvulsants: Gabapentin and pregabalin. i. Gabapentin

  1. Short half life 5-7 hours. Can experience withdrawal.
  2. For partial seizures, post herpetic neuralgia, RLS. a. Off Label anxiety, withdrawal of alcohol or benzo, alcohol dependence. b. Dizzy, somnolence, ataxia, weight gain. c. Blocks voltage dependent CA channels. d. Not metabolized, excreted unchanged by kidneys. g. Oxcarbazepine(Trileptal): i. Seizure disorder in children and adults.
  3. Off label Bipolar. ii. Dizzy, somnolence, headache, ataxia, N, S. iii. Serious Stevens Johnson. Angioedema. Monitor serum sodium(especially first 3 months). iv. NA channel blocker. POTENT INDUCE CYP3A4.

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Section 2 Highlight Guide

  1. GABA(y-aminobutyric acid). a. Inhibitory. Like a gabber who goes on and on and puts everyone to sleep. b. Specifically, GABA is produced, or synthesized, from the amino acid glutamate (glutamic acid) via the actions of the enzyme glutamic acid decarboxylase (GAD). c. GABA’s synaptic actions are terminated by the presynaptic GABA transporter (GAT), also known as the GABA reuptake pump or by the enzyme GABA transaminase (GABA-T), which converts GABA into an inactive substance. d. GABA Receptor Subtypes (GABA-a, GABA-b, and GABA- c). A/C are ligand-gated and B are G Proteins. e. f. GABA-a is subtypes a1-a6. B is b1 to b3. And y1-y3. Ther are also δ, ε, π, θ, and ρ (with three isoforms ρ1 to ρ3).

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g. Y subunit tend to be synaptic to mediate phasic neurotransmission and be sensitive to Benzodiazepines. h. GABA-a with δ subunit are extrasynaptic and mediate tonic(low level release of neurotransmitters) neurotransmission. Insensitive to benzos. i.

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ii. Varenicline(Chantix): A selective A4B2 nicotinic acetylcholine receptor partial agonists. Stabilizes the channel in the closed state but does not desensitize the receptors. iii. Less used is reducing cravings by boosting dopamine with the norepinephrine-dopamine reuptake inhibitor(NDRI) bupropion(Wellbutrin).

  1. Releases a bit of dopamine in the nucleus accumbens making the craving less. b. Opioid: i. Both clonidine and lofexidine are α2-adrenergic agonists that reduce signs of autonomic hyperactivity during withdrawal and aid in the detoxification process. ii. Naltrexone: Shortens the withdrawal time of an A agonist administered with methadone or buprenorphine.
  2. Monthly injections and assist in adherence. Chooses once to take every 30 vs choosing to take a pill daily. iii. Non-pharmacologic: running out of money, drug supply, and incarceration. iv. Pharmacological: Methadone and buprenorphine(combo of naloxone/buprenorphine is Suboxone). v. Buprenorphine: Buprenorphine is a μ-opioid partial agonist that has less powerful agonist effects, yet can suppress withdrawal symptoms especially when mild withdrawal has already begun after stopping abused opioids.
  3. Sublingual. Several day supply.
  4. Can be 6-month implantable or 1 month injection. vi. Naloxone: injection. Narcan(nasal) and zimhi(injection). c. Alcohol: i. The actions of alcohol on opioid synapses create the rationale for blocking μ-opioid receptors with antagonists such as naltrexone(Vivitrol) or nalmefene(Outside the US: Opvee, Zurnai, Revex, and Selincro).
  5. μ-opioid antagonists and block the euphoria and “high” of heavy drinking. ii. Acamprosate(Campral): Interacts with glutamate to inhibit and enhances GABA system. It is like

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“artificial alcohol”. Can substitute for alcohol in patients during withdrawal. Blocks certain receptors GluR receptors.

  1. Used for alcohol. Best when started after a period of abstinence.

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  1. Monthly injections and assist in adherence. Chooses once to take every 30 vs choosing to take a pill daily. c. Vivitrol: indications, formulations, contraindications, side effects
  2. Pharmacological agents useful in treating cravings and maintaining abstinence. Use Stahl’s book.

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a. See Above

  1. ADHD Medication Times.