Chapter 3: Biological Basis for Understanding Psychiatric Disorders and Treatments Flashcards

1
Q

Function and activities of the brain

A

Maintenance of homeostasis. Regulation of ANS and hormones. Control of biological drives and behavior. Cycle of sleep and wakefulness. Circadian rhythms. Conscious mental activity. Memory. Social skills.

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2
Q

Neuronal action

A

Neurons can release more than one chemical at the same time. Neuropeptides: long-term changes in cells. Neurotrophic facts: proteins, gases. Effect of steroid hormones.

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3
Q

Core: regulaties internal organs and vital functions.
Hypothalamus: basic drives and link between thought and emotion and function of internal organs.
Brainstem: processing center for sensory information

A

Function of brainstem

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4
Q

Involved in fine muscle movement. Involved in integration of emotions and thoughts. Involved in decision making. Stimulates hypothalamus to release hormones.
Receptors: D1-5
Decrease: Parkinson’s disease, depression. Increase: Schizophrenia, mania

A

Dopamine

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5
Q

Level in brain affects mood. Attention and arousal. Stimulates sympathetic brand of the ANS for “fight or flight” in response to stress.
Receptors: alpha-1 and 2; beta-1 and 2.
Decrease: depression.
Increase: mania, anxiety states, schizophrenia

A

Norepinephrine

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6
Q

Plays a role in sleep regulation, hunger, mood states, and pain perception. Hormonal activity. Plays a role in aggression and sexual behavior. Receptors: 5-HT 1-4
Decrease: depression
Increase: Anxiety states

A

Serotonin (5-HT)

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7
Q

Involved in alertness. Involved in inflammatory response. Stimulates gastric secretion.
H1 and H2 receptors.
Decrease: sedation, weight gain

A

Histamine

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8
Q

Plays a role in inhibition; reduces aggression, excitation, and anxiety. May play a role in pain perception. Has anticonvulsant and muscle-relaxing properties. May impair cognition and psychomotor functioning.
Decrease: anxiety disorders, schizophrenia, mania, huntington’s reissues

A

GABA

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9
Q

Is excitatory. Plays a role in learning and memory.
Decrease: psychosis.
Increase: prolonged increased state can be neurotoxic, neurodegeneration in Alzheimer’s disease, improvement of cognitive performance in behavioral tasks

A

Glutamate (NMDA, AMPA)

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10
Q

Potentiate, or promote the activity of GABA by binding to a specific receptor on the GABA A receptor complex (binding results in an increased frequency of chloride channel opening causing membrane hyper polarization which inhibits cellular excitation). Nonselective. Can cause sedation at higher therapeutic doses. Treatment of insomnia with a predominantly hypnotic (sleep-inducing) effect: flurazepam (Dalmane), temazepam (Restoril). Lorazepam (Ativan) and alprazolam (Xanax) reduce anxiety without being as soporific (sleep producing) at lower therapeutic doses. Can be used as anticonvulsants.

A

Benzodiazepines

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11
Q

Addictive. Should only be used a few days at a time. Ataxia is a common side effect secondary to the abundance of GABA receptors in the cerebellum.
-“pams”

A

Benzodiazepines.

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12
Q

Zolpidem (Ambien), Zalepon (Sonata), Eszopiclone (Lunesta). Inform about the chance of doing things while asleep. Addictive, should only be used short-term. Sedative effects without the anti-anxiety, anticonvulsant, or muscle relaxant effects of BZDs. Potential for amnestic and ataxic s/es. Onset of action faster than most BZDs.

A

Short-acting sedative-hypnotic sleep agents (Z-hypnotics)

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13
Q

Ramelteon (Rozerem). Approved for tx of insomnia that is not classified as a scheduled substance. S/es: HA, dizziness. Can increase depression.

A

Melatonin receptor agonists

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14
Q

Silenor. Tx of insomnia characterized by difficulty in maintaining sleep. Histamine-1 blockade. Pts with severe urinary retention or on MAOIs should avoid. not with narrow angle glaucoma, severe sleep apnea.

A

Doxepin

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15
Q

Reduces anxiety without having strong sedative-hyponotic properties. Does not leave the pt sleepy or sluggish. Not a CNS depressant and thus does not have as great a danger of interaction.

A

Buspirone (BuSpar)

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16
Q

Widely used prior to the development of SSRIs. No longer first-line medications since they have more s/e’s, take longer to reach an optimal dose, and are far more lethal in OD. Act primarily by blocking the reiptake of norepinephrine for the secondary amines (i.e. nortriptyline) and both norepi and serotonin for the tertiary amines (i.e. amitriptyline, imipramine). Blockage prevents norepi from coming into contact with its degrading enzyme, MAO, and thus increases the level of norepi at the synapse.
Nortriptyline (Pamelor), Amitriptyline (elavil), IMipramine (Tofranil).
Blurred vision, dry mouth, tachycardia, urinary retention, constipation. Have bad effect on heart. Easy to OD on. Highly suicidal drug

A

Tricyclic antidepressants

17
Q

Have to avoid tyramine containing foods. Don’t “play well” with a lot of other drugs. Lots of pt education is required. Going on or off- 2 week dry out period.
Isocarboxazid (Marplan), phenelzine (nardil), selegiline (EMSAM), tranylcypromine (parnate)

A

Monoamine oxidase inhibitors (MAOIs)

18
Q

Fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), citalopram (Celexa), escitalopram (Lexapro). Preferentially block the repute and the degradation of serotonin, but each have different effects on neurotransmitter.

A

Selective Serotonin Reuptake Inhibitors

19
Q

Venlafaxine (effexor)- can increase anxiety, N/V, dizziness. Desvenlafaxin (Pristine), duloxetine (Cymbalta).

A

Serotonin-norepinephrine reuptake inhibitors (SNRIs)

20
Q

mirtazapine (remeron). Increases norepi and serotonin transmission by antagonizing (blocking) presynaptic alpha-2 noradrenergic receptors.
Anti anxiety and antidperessent effects with minimal sexual dysfunction and improved sleep.
S/e’s: weight gain, sedation

A

Serotonin-Norepinephrine disinhibitors