Pt 713: Cns Drugs Ii

Front 1

What are sedative-hypnotic drugs used for?

Back 1

to promote sleep (hypnotic), calm patient (sedative), and induce general anesthesia (at high doses)

Front 2

What is a main type of sedative hypnotic drug?

Back 2

benzodiazapines

Front 3

What are other indications for using benzodiazapine drugs other than for sedative-hypnotic uses?

Back 3

epilepsy or producing muscle relaxation

Front 4

how are sedative-hypnotic drugs administered? What effect do they have that could be problematic for PT?

Back 4

- they are administered orally
- reservoir effect that may cause the patient to be tired even after the dose should have worn off
- metabolized in liver and excreted by kidneys

Front 5

What is a specific example of a benzodiazepine used for sedative-hypnotic purposes?

Back 5

flurazepam (Dalmane)

Front 6

What are uses for benzodiazepines for sedative-hypnotic drugs?

Back 6

used to promote sleep, specificially for short-term, acute situations

Front 7

What is the benefit of using benzodiazepines vs. a different type of sedative-hypnotic drug?

Back 7

less chance of fatal overdose than barbituratesq

Front 8

What are problems associated with benzodiazepines as sedative-hypnotic drugs?

Back 8

residual effects, risk of tolerence and physical dependence if used long-term

Front 9

What is the benzodiazepine mechanism?

Back 9

increases GABA's inhibitory effec`t by binding to a site on the GABA-benzodiazepine-chloride ion channel complex

- acts primarily on GABAa receptor subtype

Front 10

Describe the use for barbiturates as hypnotic-sedative agents.

Back 10

occasionally used to promote sleep, but more often used for general anesthesia

Front 11

What is another use for barbiturates (other than sedative-hypnotic)?

Back 11

used as antiseizure drugs

Front 12

What is the primary mechanism of barbiturates for sedative-hypnotics?

Back 12

- increases GABAs inhibitory effects by binding to a distinct site on GABAa receptor

- low doses: affects reticular formation and limbic system

- high doses: affects spinal cord and other areas of brain

Front 13

What are problems associated with barbiturate use for sedative-hypnotics?

Back 13

low TI, risk of dependence, abuse, fatal overdose

Front 14

What is an example of a newer sedative-hypnotic?

Back 14

Zolpidem (Ambien)

Front 15

What are uses/mechanisms for zolpidem (Ambien)?

Back 15

promote sleep

affects GABAa receptor but is selective for sedation subunit

Front 16

What are the benefits of using the newer sedative-hypnotics?

Back 16

as effective as benzodiazepines, but have fewer side effects and less risk of dependenceq

Front 17

What are the residual effects a patient may experience when taking sedative-hypnotic drugs?

Back 17

drowsiness and decreased motor performance the next day (reservoir effects)

- this is milder in the newer drugs (Ambien/zolpidem)

Front 18

What are the risks of tolerance/physical dependence associated with sedative-hypnotics?

Back 18

WITHDRAWAL SYMPTOMS:
- lead to sleep disturbances
- milder with newer drugs

Front 19

What is the indication for using antianxiety drugs?

Back 19

drugs are used to decrease patient's level of anxiety

Front 20

What are the main types of antianxiety drugs?

Back 20

- benzodiazepines
- antidepressants
- drugs that increaes some of seratonin's effects
- beta blockers

Front 21

What is the prototypical antianxiety drug?

Back 21

diazepam (Valium)

** used as first-line antianxiety drugs

Front 22

What are problems associated with benzodiazepine drugs used for antianxiety?

Back 22

sedation
residual effects
risk of tolerence and physical dependence

Front 23

What are PT implications for sedative-hypnotic and antianxiety drugs?

Back 23

- scheduling treatment (during peak effect = calmer, participator vs. sedation)

- increased falls risk

- PT treatments may help decrease need for these drugs (breathing exercises, music, soft tissue massage, flexibility and relaxation)

Front 24

What are affective disorders?

Back 24

mental illnesses that are characterized by marked distrubance in mood

Front 25

What are the 2 typical presentations we may see for affective disorders?

Back 25

major depressive disorder (clinical depression)

bipolar disorder (manic depression is old name)

Front 26

What is major depressive disorder?

Back 26

characterized by intense feelings of sadness, despair, lack of interest in previously enjoyable activities

Front 27

What is the hypothesized pathology behind depression?

Back 27

a possible problem with amine neurotransmitters (NE, serotonin, dopamine)

Front 28

What are the 3 amine neurotransmitters?

Back 28

1. NE
2. serotonin
3. dopamin

** metabolism of NT, uptake of NT seem to be the problematic areas

Front 29

What are 3 examples of antidepressant drugs?

Back 29

1. tricyclics
2. monamine oxidase (MAO) inhibitors)
3. second-generation drugs (SSRIs)

Front 30

What is the goal for using antidepressant drugs in general?

Back 30

increase amine neurotransmission

Front 31

What are the pharmacokinetics associated with antidepressant drugs?

Back 31

oral administration

metabolism in liver

Front 32

What are other uses for antidepressant drugs?

Back 32

adjuct treatment in chronic pain (neuropathic, fibromyalgia, chronic LBP)

Front 33

What is a drug example of tricyclic antidepressants?

Back 33

amitriptyline (Elavil)q

Front 34

When are tricyclics used for antidepressants?

Back 34

to treat the most severe depression

Front 35

What are side effects associated with tricyclic antidepressants?

Back 35

1. sedation
2. central/peripheral anticholinergic effects (confusion, CV)
3. highest potential for suicidal cases (fatal overdose) -- closely monitored

Front 36

What is the mechanism of tricyclic antidepressants?

Back 36

block reuptake of amine NTs into presynaptic terminal

Front 37

What is the mechanism of MAO inhibitor antidepressants?

Back 37

they inhibit monoamine oxidase (MAO), the enzyme that metabolizes amine NTs in the nerve ending

Front 38

What is the use for MAO inhibitor antidepressants?

Back 38

possibly used if patient is not responsive to other antidepressants or has intolerable side effects

not frequently used

Front 39

What are MAO inhibitor interactions that are seen?

Back 39

interactions can lead to a hypertensive crisis

- fermented cheese/wines
- other drugs that cause an increase in sympathetic activity

Front 40

What are side effects/adverse effects of MAO inhibitors?

Back 40

1. CNS excitation (restlessness, irritability)
2. anticholinergic effects (similar to tricyclics, but to lesser extent)
3. risk of hypertensive crisis

Front 41

What is the mechanism of SSRIs?

Back 41

slectively block seratonin reuptake

Front 42

What are drug examples of SSRIs?

Back 42

fluoxetine (Prozac)
sertraline (Zoloft)

Front 43

What is the indication for using SSRIs?

Back 43

the initially prescribed drug for depression

Front 44

What are side effects of SSRIs?

Back 44

- depends on specific drug
- fewer than other antidepressants
- GI problems, insomnia
- seratonin syndrome (NM symptoms such as shivering, restlessness, dystonia d/t having more seratonin in synaptic cleft so there is more potential for it to have an effect on the post synaptic membrane

Front 45

What is bipolar affective disorder?

Back 45

characterized by mood swings from one extreme (mania) to another (depression)

Front 46

What are manic episodes characterized by?

Back 46

euphoria, hyperactivity, talkativeness

Front 47

What is the goal for treating bipolar affective disorder?

Back 47

to stop the mania from beginning which inhibits the huge mood swings from occuring

Front 48

What is the mechanism of Lithum (an antimanic drug treatment)?

Back 48

complete with other positively charged ions influencing neural excitability

Front 49

What are the pharmacodynamics of Lithium?

Back 49

absorbed easily from GI tract

Front 50

What are adverse effects of Lithum?

Back 50

accumulation in body to toxic levels

Front 51

What are other drug that can be used to inhibit mania in bipolar disorder?

Back 51

antiseizure drugs (valproic acid)

antipsychotic drugs (risperidone)

** these are helpful because they act on CNS neurons directly to prevent excitation

Front 52

What are rehab concerns for patients on antidepressant medications?

Back 52

- depression may or may not be related to the reason pt is doing PT

- by taking antidepressants/antimanic meds patient can be more active in PT

- suidical ideations may occur as the meds start to take effect

Front 53

What are psychoses?

Back 53

group of mental disturbances characterized by marked thought disturbances and impaired perception of reality

Front 54

What is included under the term psychoses?

Back 54

- delusions (false beliefs)
- hallucinations
- grossly disorganized thinking

Front 55

What diagnoses are included with psychoses?

Back 55

- schizophrenia
- psychotic depression
- severe paranoid disorder
- sometimes bipolar is classified in this category

Front 56

What is schizophrenia?

Back 56

neurodevelopmental psycotic disorder indicated by periods with marked disturbance in though process which may include delusions and hallucinations

Front 57

What are antipsychotic drugs called?

Back 57

neuroleptics

(traditional and atypical)

Front 58

What do antipsychotic drugs do for schizophrenia?

Back 58

normalize behavior and thinking during an acute psychotic event and prevent recurrence of psychotic events to improve a patient's quality of life

** do NOT cure disease

Front 59

What are 2 other areas that antipsychotic drugs might be used for?

Back 59

- during the manic phase of bipolar disorder (with Lithium)
- to decrease psychotic symptoms in patients with PD or Alzheimer's disease dementia

Front 60

What is the pathophysiology of antipsychotics?

Back 60

THOUGHT that overactivity of dopamine pathways in parts of brain (limbic system) is responsible for disease

Front 61

What do most antipsychotic drugs block?

Back 61

central dopamine receptors

Front 62

What is the drug name for traditional antipsychotic drugs?

Back 62

haloperidol (Haldol)

Front 63

Which has more side effects: traditional or atypical antipsychotic drugs?

Back 63

traditional antipsychotic drugs (more extrapyramidal)

Front 64

Which binds to more dopamind receptors: traditional or atypical antipsychotic drugs?

Back 64

traditional binds to more dopamine receptor subtypes (especially those influencing motor function)

Front 65

Which has the least patient to patient variability: traditional or atypical antipsychotic drugs?

Back 65

atypical antipsychotic drugs have less variability in beneficial effects between patients

Front 66

Which the first choice for treating psychoses (tradtional or atypical drugs)? Why?

Back 66

atypical becaues they are better at preventing relapse than traditional drugs (which also have increased side effects)

Front 67

Explain what one might see in terms of extrapyramdial symptoms primarily with traditional drugs.

Back 67

- abnormal movement patterns
- tardive dyskinesias
- pseudoparkinsonism
- restlessness
- neuroletic malignant syndrome

Front 68

What is tardive dyskinesias?

Back 68

- characterized by involuntary, fragmented movements
- rhythmic tongue and mouth movments
- not alway reversible

Front 69

What is neuroleptic malignant syndrome?

Back 69

life threatening
rigidity
problems with temperature regulation

Front 70

What are non-motor symptoms seen with antipsychotic drugs?

Back 70

sedation
OH (specifically in first several days)

Front 71

What are PT implications for drugs of abuse? (4)

Back 71

1. CNS stimulants and hallucinogens are CV stimulants (withdrawal = decreased cognition and psychomotor function)

2. CNS depressants = decreased respiratory drive

3. falls risk

4. cognitive/behavioral changes

Front 72

What class is EtOH in?

Back 72

sedative-hypnotic class

Front 73

What is the mechanism of EtOH?

Back 73

modulate several signaling proteins (increases GABA's inhibition)

Front 74

What is the pharmacokinetics of EtOH?

Back 74

absorbed quickly after indigestion and metabolized in the gut

Front 75

What are acute effects of EtOH?

Back 75

CNS depression, decreased cardiac contractility, vasodilation

Front 76

What are drug-drug EtOH interactions?

Back 76

1. more accentuated CNS depression if EtOH is used with other sedative-hypnotics
2. EtOH increases effects of vasodilators and oral hypoglycemic agents

Front 77

What are symptoms of alcohol withdrawal syndrome?

Back 77

insomnia, tremors, anxiety, seizures, and DTs (delirium tremens)

Front 78

How can EtOH withdrawal syndrome be treated?

Back 78

thiamine and sedative-hypnotics

also treating electrolyte imbalances

Front 79

What is the major goal for treating EtOH withdrawal?

Back 79

1. seizures
2. DTs
3. arrhythmias

Front 80

What are delirium tremens (DTs)?

Back 80

characterized by total disorientation, hallucinations, and marked abnormalitiy of vital signs