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Physio and Psychopharm > Physio and Psychopharm > Flashcards

Physio and Psychopharm Flashcards

1
Q

Dopamine (MMSLR)

A

Mood, Movement, Sleep, Learning, Reinforcement effects of drugs

Abnormal levels related to:

  • Parkinson’s
  • Huntington’s
  • Tourette’s
  • ADHD
  • Depression
  • Schizophrenia
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2
Q

Acetylcholine (MAAM)

A

Muscles (skeletal, smooth, cardiac), Attention, Arousal, Memory

  • Low levels in the hippocampus associated with memory loss in Alzheimer’s
  • Cholinesterase Inhibitors - Reduce the breakdown of Acetylcholine and temporarily reverse or slow down memory loss with mild to moderate Alzheimer’s disease
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3
Q

Glutamate (MMEL)

A

Movement, Memory, Emotions, Learning

  • Involved in LTP - essential for the formation of long-term memories
  • Excessive glutamate = excitotoxicity:
  • Stroke
  • Seizures
  • TBI
  • Huntington’s
  • ALzheimer’s
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4
Q

Norepinephrine (SLAAMM)

A

Sleep, learning, Attention, Arousal, Memory, Mood

Abnormal levels associated with:

  • ADHD
  • Mania
  • Depression

Loss of norepinephrine neurons in the Locus Coeruleus is linked to the non-motor sxs of Parkinson’s:

  • Depression
  • Cognitive deficits
  • Sleep disturbances

**Catecholamine Hypothesis: some forms of depression are due to deficiency of norepinephrine while mania is due to excessive levels

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5
Q

Serotonin (HAAMPSS)

A

Hunger, Arousal, Aggression, Mood, Pain, Sleep, Sex

Low levels:

  • Depression
  • Increased risk for suicide
  • OCD
  • Bulimia
  • Migraines

Excessive levels:

  • Schizophrenia
  • Autism
  • Anorexia
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6
Q

GABA (MMMS)

A

Memory, Mood, Motor Control, Sleep

Abnormally low levels of GABA:

  • Anxiety
  • Mania
  • Insomnia
  • Seizure disorders
  • Parkinson’s disease
  • Huntington’s disease

*Benzos enhance GABA and reduce anxiety and induce sleep

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7
Q

Locus Coeruleus

A
  • Nucleus in the pons

- Involved with physiological responses to stress and panic

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8
Q

Endorphins

A
  • Inhibitory neurotransmitters
  • Effects are similar to opioid drugs
  • Contribute to feelings of pleasure, well-being, and reduce perception of pain
  • Produced by the pituitary gland in the hypothalamus during running and exercise
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9
Q

Hindbrain Structures

A

Cerebellum
Pons
Medulla Oblongata

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10
Q

Medulla

A
  1. Involuntary throat and mouth movements - swallowing, coughing, sneezing
  2. Regulates vital autonomic NS: respiration, HR, BP, digestion

Brain injuries, certain diseases, and other drugs can disrupt the functioning of the medulla and result in death

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11
Q

Pons

A
  1. Connects the 2 parts of the cerebellum (helps coordinate movements on 2 sides of body)
  2. Connected medulla to cerebellum
  3. Connects cerebellum to forebrain

Involved in:

  • Arousal
  • Sleep
  • Regulation of respiration
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12
Q

Cerebellum

A
  1. Coordinates and sequences complex voluntary movements initiated in the motor cortex
  2. Maintains posture and balance
  3. Processes and stores procedural memories

Damage can cause ataxia:

  • Lack of muscle control
  • Impaired balance and coordination
  • Slurred speech
  • Blurred or double vision
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13
Q

Midbrain Structures

A

Reticular Activating System, Substantia Nigra, and Superior and inferior colliculi

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14
Q

Reticular Activating System

A
  1. Alerts cortex to incoming sensory info
  2. Role in: Sleep & wakefulness, Attention, Behavioral arousal, consciousness

Lesions in the RAS can cause: comatose state

Extends from the medulla to the midbrain

Direct electrical stimulation of the RAS or stimulation by sensory input can awaken a sleeping person and cause an awake person to become more alert

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15
Q

Substantia Nigra

A

Plays a role in:

  • Reward seeking behaviors
  • Drug addiction
  • Motor control (thru connection to basal ganglia)

Degeneration of dopamine-producing cells in the Substantia Nigra contributes to the motor sxs associated with Parkinson’s Disease:

  • Slowed movement
  • Tremors
  • Muscle rigidity
  • & other motor sxs
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16
Q

Frontal Lobe

A
  • Execeutive cognitive functions
  • Expressing emotions
  • Speech production (Broca’s area)
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17
Q

Damage to Dorsolateral area

A
  • Damage to dorsolateral:
    - Perseverative responses (inappropriate repetition)
    - Depression, decreased range of emotions
    - Impaired attention, working memory, judgment, abstract thinking
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18
Q

Damage to orbitofrontal area

A

Disinhibited syndrome:
- Behavioral disinhibition, distractibility, emotion lability, inappropriate euphoria, and acquired sociopathy (risk taking behaviors, lack of empathy and insight, and a persistent need for immediate gratification)

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19
Q

Damage to mediofrontal area

A

Apathetic-Akinetic syndrome:

  • Decreased motor behavior and verbal output
  • Lack of motivation and goal-directed activities
  • Apathy and indifference
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20
Q

Broca’s Area

A

Damage results in Broca’s aphasia (expressive aphasia)

  • Slow, labored speech (primarily nouns & verbs)
  • Impaired repetition
  • Anomia (inability to recall the names of familiar objects)
  • Relatively intact comprehension of written and spoken language
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21
Q

Parietal Lobe & Damage

A
  • Somatosensory cortex

Processes sensory info related to: touch, pressure, temp, pain, body position

Result of damage depends on the location:

  1. Somatosensory Agnosias:
    - Tactile agnosia - inability to recognize objects by touch
    - Asomatognosia - Lack of recognition of one or more parts of the body
    - Anosognosia - denial of one’s own illness or disability
  2. Contralateral Neglect - neglect of one side of the body
  3. Gerstmann’s Syndrome:
    - Usually caused by damage to the dominant (usually left) hemisphere:
    • Finger agnosia
    • Right/Left disorientation
    • Agraphia - loss of writing skills
    • Acalculia - loss of math skills
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22
Q

Temporal Lobe

A
  • Auditory cortex & Wernicke’s area

Damage to auditory cortex:

  • Auditory agnosia - impairments in sound perception and identification
  • Auditory hallucinations
  • Cortical deafness (unresponsive to all sounds)

Wernicke’s area:

  • Lives in dominant hemisphere
  • Damage is Wernicke’s Aphasia or Receptive Aphasia
    • Impaired comprehension of written and spoken language
    • Impaired repetition
    • Anomia
    • Speech is fluent! but incoherent and meaningless
23
Q

Arcuate Fasciculus

A

Bundle of axons that connects Broca’s and Wernicke’s area

Damage - Conduction Aphasia!

  • Comprehension is relatively intact
  • Fluent speech w/ many errors
  • Anomia
  • Impaired repetition
24
Q

Occipital Lobe

A
  • Visual cortex
  • Damage to visual cortex:
    • Visual agnosia - patients cannot recognize objects (w/ anomia, they recognize but cannot name them)
    • Visual hallucinations
    • Achromatopsia (loss of color vision)
    • Cortical blindness (loss of vision)
  • Damage (bilateral lesions) to the occipitotemporal junction
  • Prosopagnosia - Inability to recognize the faces of familiar people
25
Q

Structural Neuroimaging Techiques

A
  1. CAT scan - uses x-rays to obtain images of horizontal slices of the brain
    - costs less than an MRI
    - provides images more rapidly
    - doesn’t require motionlessness
    - can be used with pacemakers, metal
  2. MRI - using strong magnetic fields and radio waves
    - cross-sectional images of the brain
    - produces 3 dimensional and more detailed images
    - doesn’t require the use of radiation
    - can be used for brain and other parts of the body
26
Q

Functional Neuroimaging Techniques

A

PET, SPECT, fMRI

  1. PET - patient is injected with radioactive tracer that is taken up by active brain cells
  2. SPECT - similar to PET but easier and less expensive - but less detailed images
  3. fMRI - similar to MRI but provides information on changes in blood oxygenation and flow
27
Q

TBI

A

Open vs. Closed
- Consequences of open injury depend on its location and severity

Closed injuries can share several characteristics:

  • Cause more widespread damage
  • Loss or alternation of consciousness
  • Combo of emotional, cognitive, behavioral, and physical sxs
  • Anterograde and retrograde amnesia are common
  • Duration of anterograde (post-traumatic) amnesia is an indication of severity of TBI and a good predictor of recovery
  • Most ppl and esp with mild TBI, experience significant recovery from sxs in the first 3 months and more recovery in the 1st year
  • However, many ppl continue to have some sxs indefinitely, esp those with moderate to severe injuries
  • Severe MDD is the most common diagnosis regardless of severity of injury
28
Q

Cerebrovascular Accident (CVA) & risk factors

A

Stroke!
*Caused by sudden interruption of blood flow to the brain

Risk factors:

  • Hypertension
  • Cigarette smoking
  • Alcohol use
  • Atrial fibrillation (irregular heartbeat can lead to blood clots)
  • Atherosclerosis (plaque build-up in the arteries)
  • Diabetes
  • High cholesterol
29
Q

Cerebrovascular Accident Sxs & Artery

A

Middle Cerebral Artery:
*Most often involved!
- Supplies blood to the frontal lobe & lateral temporal and parietal lobe
Sxs:
- Contralateral sensory loss
- Weakness or paralysis (esp. in arm or face)
- Impaired vision
- DOMINANT hemisphere - Aphasia (inability to understand or express speech)
- NON-DOMINANT - Contralateral neglect & apraxia (inability to perform correct movement)

Aterior Cerebral Artery
- Supplies blood to frontal lobe and parietal lobes
Sxs:
- Contralateral sensory loss
- Weakness or paralysis, esp. in the leg
- Impaired insight and attention
- Impaired speech
- Confusion
- Apathy

Posterior Cerebral Artery
- Supplies blood to temporal and occipital lobes
Sxs:
- Memory deficits
- Unilateral cortical blindness
- Color agnosia (inability to name colors)
- Other visual impairments

30
Q

Huntington’s Disease

A
  • Caused by autosomal dominant gene
  • Linked to abnormal levels in the basal ganglia of:
    • GABA
    • Glutamate
    • Dopamine
  • Onset of sxs is between 30-50

SEQUENCE of sxs:

  1. Affective
  2. Cognitive
  3. Motor

Initial sxs:

  • Depression
  • Apathy
  • Or other affective sxs

Followed by:

  • Forgetfulness (short term memory loss)
  • Impaired concentration
  • Impaired judgment
  • Other cog sxs

& then:

  • Clumsiness
  • Fidgeting
  • Facial twitches
  • Other motor sxs

As the disease progresses…

  • Athetosis - (slow, writhing movements)
  • Chorea (abnormal involuntary rapid jerky movements in arms, legs, and trunk)
  • Person may eventually develop mild or major neurocognitive disorder
  • *Motor sxs become severe, person has trouble speaking and swallowing
31
Q

Athetosis and Chorea

A

Sxs as Huntington’s Disease progresses

  • Athetosis - (slow, writhing movements)
  • Chorea (abnormal involuntary rapid jerky movements in arms, legs, and trunk)
32
Q

Parkinson’s Disease

A
  • Caused by a loss of dopamine-producing cells in the substantia nigra (which in turn affects the basal ganglia)
  • Cause of the degeneration is not known - but some cases may be related to exposure to some toxins or chemicals

Primary sxs:

  • Impaired balance & equilibrium
  • Muscle rigidity
  • Slowed voluntary movement
  • Tremors (begins in hands, pill rolling)

Many ppl also experience:

  • Depression (up to 50%)
  • Anxiety (up to 40%)
  • Delusions and/or hallucinations (usually in later stages of disorder)
  • Some ppl may eventually develop mild or major neurocogitive disorder
  • No cure for Parkinson’s but tremors and other motor sxs are temporarily alleviated in the early stages with Aldopa!
  • Aldopa acts as a dopamine agonist and increases dopamine
  • Offspring have a 50% chance of inheriting it
33
Q

Seizure Disorders

A

Caused by abnormal electrical activity in the brain

FOCAL ONSET VS. GENERALIZED ONSET

Focal Onset:
- Begin in a localized area in one side of the brain and affect one side of the body
- They may spread and become generalized seizures
Sxs:
- Depend on the origins of the seizure, may include:
- Abnormal sensations
- Hallucinations
- Sense of deja vu
- And/or automatisms (repetitive movements - grunts, founds, walking in circles)

Focal Onset AWARE VS. IMPAIRED AWARENESS SEIZURES

Focal Onset AWARE Seizures (AKA Simple Partial Seizures)

  • Don’t affect consciousness
  • Usually last less than 2 minutes

Focal Onset Impaired Awareness Seizures (AKA Complex Partial Seizures)

  • Cause a change in consciousness
  • May begin with an Aura
  • Usually last 1-2 minutes

GENERALIZED ONSET SEIZURES:

  • Affect both sides of the brain
  • MOTOR VS NON-MOTOR SEIZURES

Generalized onset MOTOR Seizures:

  • AKA Tonic-Clonic Seizures or Grand Mal
  • Change in consciousness
  • Tonic Phase (stiffening of muscles in face and limbs)
  • Followed by Clonic phase (Jerky, rhythmic movements)
  • After - they may be depressed, confused, fatigued, and non memory of event

Generalized onset NON-MOTOR seizures

  • AKA absent seizures and Petit Mal Seizures
  • Loss of consciousness that lasts 10-20 seconds
    • Blank or absent stare
    • For some ppl, eye fluttering, head nodding, hand movements
  • When seizure ends, person often continues doing what he or she was doing
34
Q

First generation/Traditional/Conventional Antipsychotics Names

A
  1. Chlorpromazine (Thorazone)
  2. Haloperidol (Haldol)
  3. Thioridazine (Mellaril)
  4. Fluphenazine (Prolixin)

FLU-CHLOR-HALO-THIOR

35
Q

First generation/Traditional/Conventional Antipsychotics Attributes

A
  1. Chlorpromazine (Thorazone)
  2. Haloperidol (Haldol)
  3. Thioridazine (Mellaril)
  4. Fluphenazine (Prolixin)
  • Used to tx Schizophrenia and other disorders with psychotic sxs and are more effective for positive sxs than negative!
  • Exert their effect by BLOCKING DOPAMINE (supported the dopamine hypothesis of Schizophrenia)
  • Dopamine antagonists

Major Side Effects:

  1. ANTICHOLINERGIC effects (Block acetylcholine)
    - Dry mouth, blurred vision
    - Constipation & Urinary retention
    - Tachycardia (high ass HR)
    - Confusion
    - Impaired attention & concentration
  2. EXTRAPYRAMIDAL Effects
    1) Parkinsonism (resting tremor, muscle rigidity, slowed movement)
    2) Dystonia - uncontrollable muscle spasms in head and neck
    3) Akathisia - restlessness and pacing
    4) Tardive Dyskinesia
    * Potentially life threatening, usually begins after months or years
    - Usually repetitive movements of tongue, face, jaw
    - Over time, may affect limbs and trunk
    * Irreversible for some pts
    * TREATED by gradually waning off and switching to 2nd gen (OR dopamine depleting or GABA enhancing drug)
    * For some, getting off the drug may not lessen sxs and it might get worse before they decrease
  3. NEUROLEPTIC MALIGNANT SYNDROME
    * *Rare, life-threatening side effect
    1) Muscle rigidity
    2) Hyperthermia
    3) Autonomic dysfunction - unstable BP, Tachycardia, rapid breathing
    4) Altered mental state - confusion, disorientation, agitation
  • Have person stop taking the drug at the first sign of sxs
  • Providing medical tx and supportive care for specific sxs
36
Q

First generation/Traditional/Conventional Antipsychotics Attributes

A
  1. Chlorpromazine (Thorazone)
  2. Haloperidol (Haldol)
  3. Thioridazine (Mellaril)
  4. Fluphenazine (Prolixin)
  • Used to tx Schizophrenia and other disorders with psychotic sxs and are more effective for positive sxs than negative!
  • Exert their effect by BLOCKING DOPAMINE (supported the dopamine hypothesis of Schizophrenia)
  • Dopamine antagonists

Major Side Effects:

  1. ANTICHOLINERGIC effects (Block acetylcholine)
    - Dry mouth, blurred vision
    - Constipation & Urinary retention
    - Tachycardia (high ass HR)
    - Confusion
    - Impaired attention & concentration
  2. EXTRAPYRAMIDAL Effects
    1) Parkinsonism (resting tremor, muscle rigidity, slowed movement)
    2) Dystonia - uncontrollable muscle spasms in head and neck
    3) Akathisia - restlessness and pacing
    4) Tardive Dyskinesia
    * Potentially life threatening, usually begins after months or years
    - Usually repetitive movements of tongue, face, jaw
    - Over time, may affect limbs and trunk
    * Irreversible for some pts
    * TREATED by gradually waning off and switching to 2nd gen (OR dopamine depleting or GABA enhancing drug)
    * For some, getting off the drug may not lessen sxs and it might get worse before they decrease
  3. NEUROLEPTIC MALIGNANT SYNDROME
    * *Rare, life-threatening side effect
    1) Muscle rigidity
    2) Hyperthermia
    3) Autonomic dysfunction - unstable BP, Tachycardia, rapid breathing
    4) Altered mental state - confusion, disorientation, agitation
  • Have person stop taking the drug at the first sign of sxs
  • Providing medical tx and supportive care for specific sxs
36
Q

First generation/Traditional/Conventional Antipsychotics Attributes

A
  1. Chlorpromazine (Thorazone)
  2. Haloperidol (Haldol)
  3. Thioridazine (Mellaril)
  4. Fluphenazine (Prolixin)
  • Used to tx Schizophrenia and other disorders with psychotic sxs and are more effective for positive sxs than negative!
  • Exert their effect by BLOCKING DOPAMINE (supported the dopamine hypothesis of Schizophrenia)
  • Dopamine antagonists

Major Side Effects:

  1. ANTICHOLINERGIC effects (Block acetylcholine)
    - Dry mouth, blurred vision
    - Constipation & Urinary retention
    - Tachycardia (high ass HR)
    - Confusion
    - Impaired attention & concentration
  2. EXTRAPYRAMIDAL Effects
    1) Parkinsonism (resting tremor, muscle rigidity, slowed movement)
    2) Dystonia - uncontrollable muscle spasms in head and neck
    3) Akathisia - restlessness and pacing
    4) Tardive Dyskinesia
    * Potentially life threatening, usually begins after months or years
    - Usually repetitive movements of tongue, face, jaw
    - Over time, may affect limbs and trunk
    * Irreversible for some pts
    * TREATED by gradually waning off and switching to 2nd gen (OR dopamine depleting or GABA enhancing drug)
    * For some, getting off the drug may not lessen sxs and it might get worse before they decrease
  3. NEUROLEPTIC MALIGNANT SYNDROME
    * *Rare, life-threatening side effect
    1) Muscle rigidity
    2) Hyperthermia
    3) Autonomic dysfunction - unstable BP, Tachycardia, rapid breathing
    4) Altered mental state - confusion, disorientation, agitation
  • Have person stop taking the drug at the first sign of sxs
  • Providing medical tx and supportive care for specific sxs
37
Q

First generation/Traditional/Conventional Antipsychotics Attributes

A
  1. Chlorpromazine (Thorazone)
  2. Haloperidol (Haldol)
  3. Thioridazine (Mellaril)
  4. Fluphenazine (Prolixin)
  • Used to tx Schizophrenia and other disorders with psychotic sxs and are more effective for positive sxs than negative!
  • Exert their effect by BLOCKING DOPAMINE (supported the dopamine hypothesis of Schizophrenia)
  • Dopamine antagonists

Major Side Effects:

  1. ANTICHOLINERGIC effects (Block acetylcholine)
    - Dry mouth, blurred vision
    - Constipation & Urinary retention
    - Tachycardia (high ass HR)
    - Confusion
    - Impaired attention & concentration
  2. EXTRAPYRAMIDAL Effects
    1) Parkinsonism (resting tremor, muscle rigidity, slowed movement)
    2) Dystonia - uncontrollable muscle spasms in head and neck
    3) Akathisia - restlessness and pacing
    4) Tardive Dyskinesia
    * Potentially life threatening, usually begins after months or years
    - Usually repetitive movements of tongue, face, jaw
    - Over time, may affect limbs and trunk
    * Irreversible for some pts
    * TREATED by gradually waning off and switching to 2nd gen (OR dopamine depleting or GABA enhancing drug)
    * For some, getting off the drug may not lessen sxs and it might get worse before they decrease
  3. NEUROLEPTIC MALIGNANT SYNDROME
    * *Rare, life-threatening side effect
    1) Muscle rigidity
    2) Hyperthermia
    3) Autonomic dysfunction - unstable BP, Tachycardia, rapid breathing
    4) Altered mental state - confusion, disorientation, agitation
  • Have person stop taking the drug at the first sign of sxs
  • Providing medical tx and supportive care for specific sxs
37
Q

First generation/Traditional/Conventional Antipsychotics Attributes

A
  1. Chlorpromazine (Thorazone)
  2. Haloperidol (Haldol)
  3. Thioridazine (Mellaril)
  4. Fluphenazine (Prolixin)
  • Used to tx Schizophrenia and other disorders with psychotic sxs and are more effective for positive sxs than negative!
  • Exert their effect by BLOCKING DOPAMINE (supported the dopamine hypothesis of Schizophrenia)
  • Dopamine antagonists

Major Side Effects:

  1. ANTICHOLINERGIC effects (Block acetylcholine)
    - Dry mouth, blurred vision
    - Constipation & Urinary retention
    - Tachycardia (high ass HR)
    - Confusion
    - Impaired attention & concentration
  2. EXTRAPYRAMIDAL Effects
    1) Parkinsonism (resting tremor, muscle rigidity, slowed movement)
    2) Dystonia - uncontrollable muscle spasms in head and neck
    3) Akathisia - restlessness and pacing
    4) Tardive Dyskinesia
    * Potentially life threatening, usually begins after months or years
    - Usually repetitive movements of tongue, face, jaw
    - Over time, may affect limbs and trunk
    * Irreversible for some pts
    * TREATED by gradually waning off and switching to 2nd gen (OR dopamine depleting or GABA enhancing drug)
    * For some, getting off the drug may not lessen sxs and it might get worse before they decrease
  3. NEUROLEPTIC MALIGNANT SYNDROME
    * *Rare, life-threatening side effect
    1) Muscle rigidity
    2) Hyperthermia
    3) Autonomic dysfunction - unstable BP, Tachycardia, rapid breathing
    4) Altered mental state - confusion, disorientation, agitation
  • Have person stop taking the drug at the first sign of sxs
  • Providing medical tx and supportive care for specific sxs
38
Q

Second Generation Antipsychotics (AKA Atypical) Names

A
  1. Clozapine (Clozaril)
  2. Risperidone (Risperdal)
  3. Olanzapine (Zyprexa)

And…

  1. Quetiapine (Seroquel)
  2. Ziprasidone (Geodon)
  3. Aripiprazole (Abilify)
  4. Paliperidone (Invega)
39
Q

Second Generation Antipsychotics (AKA Atypical) Attributes

A

Used to treat schizophrenia and other disorders with psychotic sxs
- Some are also used for monotherapy or as an adjunctive treatment for bipolar disorder or MDD

  • As effective or more effective than FGA for tx of positive sxs and more affective for tx of negative sxs!
  • SGA may be effective when FGA aren’t (esp Clozapine)
  • SGAs exert their effects by REDUCING DOPAMINE AND SEROTONIN
    • Dopamine and Serotonin antagonists OR inverse agonists
    • And affect several neurotransmitters (dopamine, serotonin, norepinephrine, and glutamate!)

SIDE EFFECTS:

  1. Anticholinergic effects
  2. Neuroleptic Malignant Syndrome
    • Risk for and severity is less than FGA!
  3. Metabolic Syndrome
    • Weight gain, high BP, insulin resistance, increased risk for diabetes and heart disease
  4. Agranulocytosis
    • Potentially life threatening
    • Dangerously low white blood cell count - requires regular blood monitoring
    • Clozapine and to a lesser extent the other atypicals

3 advantages of SGA:

1) Alleviate positive AND negative sxs
2) Typically effective when FGA fail
3) Less likely to cause Tardive dyskinesia
40
Q

SSRIs names

A
  1. Fluoxetine (Prozac, Sarafem)
  2. Sertraline (Zoloft)
  3. Citalopram (Celexa)
  4. Fluvoxamine (Luvox)
  5. Paroxetine (Paxil)
41
Q

SSRI attributes

A

Considered to be the first line psychopharmacological tx to treat depression!

  • Have a faster onset than tricyclics (and are now prescribed more than tricyclics)
  • Less severe cholinergic effects
  • BUT are more likely to cause serotonin syndrome than tricyclics when combined with other serotinergic agents

ALSO CAN TREAT:

  • Premenstrual Dysphoric Disorder
  • OCD
  • Panic disorder
  • GAD
  • PTSD
  • Bulimia
  • Premature ejaculation

Exert their effects by block the reuptake of Serotonin - Increases serotonin! Serotonin agonist

SIDE EFFECTS:

  • Mild cholinergic effects
  • Gastrointestinal issues
  • Insomnia
  • Nausea and vomiting
  • Anxiety
  • Headaches
  • Sexual dysfunction

ADVANTAGES OVER TRICYCLICS:

1) Produce fewer anticholinergic side effects
2) Less cardiotoxic
3) Safer in overdose
4) Faster onset of therapeutic effects

Disadvantages of some SSRIS - Can cause a withdrawal or discontinuation syndrome when decreased or abruptly stopped:

  • Dizziness
  • Headache
  • Numbness or tingling
  • Anxiety, agitation, irritability
  • Mood lability
  • Impaired concentration
  • Sleep disturbances
  • Flu like sxs
  • *SEROTONIN SYNDROME
  • Combining SSRI with MAOI or other serotonergic drug can cause it
  • Potentially fatal!
  • Extreme agitation
  • Confusion
  • Autonomic instability
  • Hyperthermia
  • Tremor
  • Seizures
  • Delirium

TREATMENT FOR SEROTONIN SYNDROME:

  • Immediate withdrawal of the serotonergic drugs
  • Medical treatment for its symptoms
42
Q

SNRI Names

A
  • VennDiagram w/ SSRIs
    1. Venlafaxine (Effexor)
    2. Duloxetine (Cymbalta)
    3. Desvenlafaxine (Pristiq)
43
Q

SNRI attributes

A

Used to treat:

  • Depression
  • Anxiety
  • Chronic Pain & several other dxs
  • Evidence that they are similar to SSRIs in effectiveness to treat depression
  • *And May be more effective than SSRIs for severe depression!

Exert their effects by blocking reuptake of Serotonin and Norepinephrine

SIDE EFFECTS (similar to SSRIs!)

  • Mild anticholinergic effects
  • Insomnia
  • Headaches
  • Sexual dysfunction

Because of their effects on norepinephrine, can ELEVATE BP!! Might be contraindicated for pts with hypertension or heart problems

Also can cause a discontinuation syndrome

And combining an SNRI with an MAOI or other serotonergic drug can cause serotonin syndrome!

44
Q

Tricyclic Antidepressant Names

A
  1. Amitriptyline
  2. Imipramine
  3. Clomipramine
  4. Nortriptyline
  5. Doxepin
45
Q

Tricyclic Attributes

A

**Cardiotoxic!!

Used to treat: depression, anxiety, panic disorder, OCD, and neuropathic pain

EXERT THEIR EFFECTS BY inhibiting uptake of norepinephrine, serotonin, and dopamine

*Most useful for typical depression: Anhedonia and vegetative sxs (appetite and sleep)

SIDE EFFECTS:

  • Anticholinergic effects
  • Gastrointestinal issues
  • Confusion and memory problems
  • Tremor
  • Impaired sexual functioning
  • Hypertension
  • Tachycardia

Because they’re CARDIOTOXIC and can be lethal in overdose, prescribe with caution ppl with heart disease or SI!!

Caridotoxic because you can’t ride a tricycle with heart problems!

46
Q

MAOIs names

A 
o	Phenelzine (Nardil)
o	Isocarboxazid (Marplan)
o	Tranylcypromine (Parnate)
47
Q

MAOI

A
  • Used to treat atypical depression!
  • Include phobic features
  • Hypersomnia
  • Mood reactivity
  • Rejection sensitivity

EXERT THEIR EFFECTS - block the action of enzymes that break down norepinephrine, serotonin, and dopamine and increase these neurotransmitters

SIDE EFFECTS:

  • Anticholinergic effects
  • Orthostatic hypertension
  • Daytime sleepiness
  • Insomnia
  • Headache
  • Confusion
  • Tremor
  • Sexual dysfunction
CAN CAUSE A FATAL HYPERTENSIVE CRISIS:
- When taken in conjunction with other drugs (amphetamines, antihistamines) or foods containing tyramine (cheese, meat, beer, ripe bananas)
- Sxs:
  - Severe throbbing headache
  - Sharp increase in BP
  - Stiff Neck
  - Rapid HR
  - Nausea and vomiting
  - Sweating
  - Photo sensitivity
 - Confusion & dizziness
Extreme cases - Heart Attack or Stroke!
48
Q

Mood Stabilizers names

A
  1. Lithium
  2. Several anticonvulsant drugs:
    • Carbamazepine
    • Valproic acid
49
Q

Mood Stabilizer attributes

A

Lithium is tx of choice to treat bipolar disorder (first line for acute mania and classic bipolar dx - w/out rapid cycling)
- Reduces manic sxs and levels out mood swings

BUT anticonvulsant drugs may be more effective when lithium is not & useful for:

  • Atypical forms of mania
  • Mania with dysphoric mood or rapid cycling
  • Acute mania
  • How lithium and anticonvulsant drugs exert their therapeutic effects is not well understood
    o But both have been linked to alterations in several neurotransmitters:
     Dopamine
     Glutamate
     Norepinephrine
     Serotonin
-	Side effects of Lithium:
o	Nausea
o	Increased thirst & frequency of urination
o	Blurred vision
o	Fine Hand tremor
o	Vomiting
o	Metallic taste
o	Weight gain
o	Fatigue
o	Impaired memory and concentration
-	**Blood lithium levels must be monitored to avoid lithium toxicity:
o	Confusion
o	Slurred Speech
o	Ataxia
o	Course tremor
o	Vomiting
o	Diarrhea
o	**And can lead to:
	Seizures
	Coma 
	Death  
-	**Several factors can precipitate toxicity, including:
o	An overdose of the drug
o	Sodium depletion
o	And simultaneous use of some other drugs:
	Diuretic
	Non-steroidal anti-inflammatory agent 
-	Side effects of anticonvulsant drugs (Carbamazepine):
o	Nausea & vomiting
o	Dizziness
o	Slurred speech
o	Ataxia
o	Tremor
o	Sleepiness 
o	Lethargy
o	Visual disturbances
o	Impaired concentration 
-	To maintain therapeutic levels of Carbamazepine and to avoid toxicity:
o	Blood levels must be monitored!
-	**Blood levels must be monitored to avoid liver failure when taking the anticonvulsants: carbamazepine or valproic acid
o	And to avoid Agranulocytosis and aplastic anemia when taking carbamazepine
50
Q

Benzos

A
  • Central nervous system depressants
  • Stimulate the inhibitory action of GABA
  • Barbiturates and benzos increase GABA

Most common side effects:

  • Drowsiness, lethargy
  • Slurred speech
  • Ataxia
  • Impaired cognitive and psychomotor functioning

Abrupt cessation of a Benzo may produce:
- Rebound excitability
o Produces levels of anxiety, insomnia & other sxs that were more intense than prior to taking the benzo

51
Q

Psychostimulants

A
  • Mimic or increase the activity of dopamine and norepinephrine
  • used to treat ADHD:

Methylphenidate

  • Alleviates the core sxs of ADHD - inattention, hyperactivity, and impulsivity
  • Less evidence for its long-term benefits for academic achievement and social interactions

Pemoline

-	Methylphenidate side effects:
o	Decreased appetite
o	Abdominal pain
o	Insomnia
o	Anxiety and irritability 
o	*Some children experience growth suppression
  • But this sx can be alleviated by providing drug holidays over summer and winter vacations

Physio and Psychopharm (1 decks)

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