Exam 1 Review Flashcards

1
Q

Why do drugs modify psychology?

A
  1. Cognitive and emotional brain systems evolved in animals because they increased adaptive fitness in evolutionary history
  2. What evolution actually selects for are genes (nucleotide sequences) that encode blueprints for proteins (amino acid sequences) that build the nervous system (development) and control its operation (through the constant regulation of genes that encode things like neurotransmitter receptors or enzymes that influence neurons)
  3. Most psychiatric drugs directly disrupt synaptic communication, which can have secondary effects on larger brain systems and ultimately on psychological states
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2
Q

Why is it important for mental health workers to understand psychopharmacology?

A
  1. Use is widespread. Example: About 12% of all US adults, and 25% of US women over 60, currently use antidepressants
  2. Use of psychotropic medication is increasing
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3
Q

What are the ways therapists interact with clients or prescribing physicians around drug use?

A
  1. refer patients for evaluation for medication (usually by referring them to a psychiatrist)
  2. discuss drug use with clients and prescribing clinicians
  3. manage clients’ expectations for therapeutic and adverse effects of prescribed drugs
  4. recognize behavioral problems that might arise from drug use
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4
Q

What is pharmakinetics?

A

The process of drug absorption, distribution, metabolism, and elimination, i.e., what the body does to the drug.

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5
Q

What does “LADME” stand for?

A
  1. liberation (of drug molecules from ingested form)–>
  2. absorption (into blood; blood is the only route to the brain)–>
  3. distribution through the body via blood–>
  4. metabolism (first pass metabolism in liver for orally ingested drug)–>
  5. elimination (excretion in urine or feces)
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6
Q

What is the blood brain barrier? What does it do?

A
  1. Tight insulation of brain blood vessels by specialized vessel wall cells and glial cells
  2. Prevents potentially harmful chemicals in blood from entering brain
  3. Drugs must cross the BBB to be psychoactive; a big limitation to psychopharmacology
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7
Q

What makes up the central nervous system (CNS)? What does it do?

A

Brain and spinal cord. General function is sensory-motor integration

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8
Q

What makes up the peripheral nervous system (PNS)? What does it do?

A

Connects brain to body via the spinal and cranial nerves. There are somatic and autonomic branches of PNS

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9
Q

What does the somatic branch of the PNS do?

A

conscious sensation & voluntary motor control

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10
Q

What does the autonomic branch of the PNS do?

A

automatic control of smooth muscle, glands, viscera

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11
Q

What are the branches of the autonomic branch?

A

Sympathetic NS and Parasympathetic NS

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12
Q

What does the sympathetic branch of the Autonomic PNS do? What is it associated with?

A

Fight or Flight. Associated with anxiety, panic disorder seeing activation in this area. Adrenaline & epinephrine, increased heart rate.

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13
Q

What does the parasympathetic branch of the Autonomic PNS do? What is it associated with?

A

Rest & Digest. Acetylcholine, reduces heart rate.

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14
Q

What do neurons and ALL cells have in common?

A

Neurons like all cells have a plasma membrane, nucleus, genes, ribosomes, membrane channels

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15
Q

What are the specialized structures of a neuron? Define them?

A

Dendrites: synaptic input zone.

Axons: action potential conductance zone.

Synapses: gap between neurons.

Neurotransmitter (NT): chemical signal released from pre synaptic neurons.

Vesicles: presynaptic membrane spheres with stored NT ready for release.

NT receptors: post-synaptic proteins that bind NT and alter post synaptic cell function

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16
Q

What is electrochemical signaling?

A

Neurochemical signaling complexity is greatly increased by multiple receptor types for each neurotransmitter and genetic diversity in genes encoding receptors, ion channels, and other synaptic proteins.

17
Q

What does “excitatory” mean in terms of electrochemical signaling?

A

Synaptic input causes positively charge ions (Na+, Ca++) to enter a neuron, which can generate an action potential (a signal sent to postsynaptic cells).

18
Q

What does “inhibitory” mean in terms of electrochemical signaling?

A

Synaptic input causes negatively charged ions (Cl-) to enter, decreasing the likelihood of an action potential.

Neurons at rest have a negative electrical charge. Synaptic input can alter electric charge to excite or inhibit neurons.

19
Q

What is an ionotropic neurotransmitter receptor?

A

Same protein contains NT binding site and a selective ion channel. NT binding opens the ion channel, rapidly and briefly altering postsynaptic cell voltage.

20
Q

What is a metabotropic neurotransmitter receptor?

A

When receptor binds NT it releases an intracellular second messenger (called a G protein) that can (a) open ion channels from inside the neuron and (b) alter gene regulation. Slower and longer lasting effects on post synaptic cells than ionotropic receptor. Also called a GPCR.

21
Q

What is a nuclear neurotransmitter receptor?

A

Use by hormone-type neurotransmitters such as thyroid hormone, estrogens, and androgens. The receptor resides inside neurons. Hormone transmitters cross neuron membranes, bind to intracellular receptors, and the receptor/hormone complex then moves to the nucleus and directly interacts with DNA at specific locations on the genome to suppress or enhance expression of specific genes.

22
Q

What are Endogenous vs exogenous receptor ligands?

A

Receptors exist to bind natural NT’s (endogenous ligands), drugs bind to receptors because drugs mimic natural NT (drugs are exogenous ligands)

23
Q

What are pharmacogenetics?

A

Individual differences in drug responses resulting from differences in genes encoding synaptic proteins

24
Q

What are pharmacodynamics?

A

The process of how drugs affect receptors, cells, and brain systems, i.e., what a drug does to the body

25
Q

What are Pre synaptic vs Post synaptic drug actions?

A

Pre-synaptic example: SSRI’s like sertraline block presynaptic serotonin transporters.

Post-synaptic example: Benzodiazepine anxiolytics like valium activate GABA receptors.

26
Q

What are Agonistic and Antagonistic drug effects on receptors?

A

Agonists - drugs that occupy receptors and activate them.

Antagonists - drugs that occupy receptors but do not activate them. Antagonists block receptor activation by Agonists.

27
Q

Give examples and explain the following: full agonist, partial agonist, agonist, and inverse agonist.

A

Full Agonist: Binds and strongly activates, e.g., Opioids, Benzodiazepines

Partial Agonist: Binds and weakly activates, e.g., Buprenorphine

Agonist: Binds and blocks
e.g., Caffeine, SSRI

Inverse Agonist: Binds and reverses action, e.g., Amphetamine

28
Q

What are opponent processes?

A

Initial drug effects are opposed by homeostatic processes working to keep neurons stable, and these opponent processes produce delayed effects that are opposite to initial drug effects (eg, drug withdrawal symptoms, including SSRI).

Opponent processes in drug effects leading to discontinuation withdrawal symptoms that tend to be opposite from immediate drug effects.

May result from compensatory changes in receptor expression (Downregulation or Upregulation) after long-term use that counteracts direct drug effects to restore homeostasis.

29
Q

What are the 5 clinically important NTs that are affected by psychotropic drugs?

A

Serotonin
Dopamine
Acetylcholine
GABA
Glutamate

30
Q

What is Serotonin? Explain its function.

A

Main functions: emotion regulation, sensation, impulsiveness, aggression

Anatomy: Cell bodies are located in the brainstem (raphe nuclei) and long axons project to limbic system, cortex, and spinal cord. Also used in the body and PNS. Discovery of serotonin in the brain by Betty Tworog in 1950’s

Receptors: There are > 15 known serotonin receptor types, more than any other NT. Fits with serotonin being an ancient NT that has diversified

Drugs that directly influence Serotonin, examples: SSRI antidepressants boost serotonin by blocking transporters; classic psychedelics are serotonin receptor agonists

31
Q

What is Dopamine? Explain its function.

A

Main functions: movement, motivation, emotion, experience of pleasure and pain, learning.

Anatomy: Cell bodies located in midbrain nuclei. Axons project to limbic, motor, and cortical areas (below left)
MDS = midbrain dopamine reward system. Projects from ventral tegmentum to nucleus accumbens
Nigrostriatal motor pathway: other major dopamine pathway, from midbrain to striatum. Damaged in Parkinson’s

Receptors: There are at least 5 dopamine receptors types, all metabotropic

Drugs that directly influence Dopamine - examples: Antipsychotic drugs are dopamine receptor antagonists; ADHD drugs boost dopamine by blocking transporters

32
Q

What is Acetylcholine? Explain its function.

A

Main functions: Neurotransmitter used at the neuromuscular junction, in the sympathetic nervous system, and throughout the brain.

Anatomy: Acetylcholine cell bodies are located deep in the brain and have long axons that project to cortex and elsewhere (like dopamine)

Receptors: 2 types: Nicotinic (ionotropic) and Muscarinic (metabotropic)

Drugs that directly influence Acetylcholine - examples:
Nicotine is an agonist at a type of ACh receptor in the brain
Anti-Alzheimer’s drugs block Acetylcholine breakdown enzymes

33
Q

What is GABA? Explain its function.

A

Most abundant inhibitory (GABA) and excitatory (glutamate) neurotransmitters

Main functions: inhibitory and excitatory synaptic transmission in nearly all neural circuits in brain and spinal cord

Anatomy and receptors: GABA and glutamate releasing neurons, and diverse receptors for glutamate and GABA, occur in all brain regions

Drug examples: benzodiazepines and alcohol are GABA receptor agonists

34
Q

What is Glutamate? Explain its function.

A

Most abundant inhibitory (GABA) and excitatory (glutamate) neurotransmitters

Main functions: inhibitory and excitatory synaptic transmission in nearly all neural circuits in brain and spinal cord

Anatomy and receptors: GABA and glutamate releasing neurons, and diverse receptors for glutamate and GABA, occur in all brain regions

Drug examples: benzodiazepines and alcohol are GABA receptor agonists