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Term 3 > Pharmacology Unit 6 > Flashcards

Pharmacology Unit 6 Flashcards

1
Q

What is the function of the Blood Brain Barrier?

A

Acts as a selective filter and protects CNS by limiting substances that enter the brain and spinal cord

The Blood Brain Barrier is crucial for maintaining the homeostasis of the central nervous system.

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2
Q

What causes the barrier effect of the Blood Brain Barrier?

A

The tight junctions that occur between capillary endothelial cells

These tight junctions prevent the free passage of substances and help maintain the integrity of the barrier.

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3
Q

Which non-neuronal cells contribute to the Blood Brain Barrier?

A

Astrocytes and the capillary basement membrane

Astrocytes play a significant role in the maintenance and regulation of the Blood Brain Barrier.

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4
Q

What are exceptions to the Blood Brain Barrier’s selective permeability?

A

The presence of carrier-mediated transport systems

These transport systems allow certain essential substances to cross the barrier.

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5
Q

What are the two general categories of sedative hypnotic drugs?

A

Benzodiazepines and Nonbenzodiazepines

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6
Q

What is the primary function of sedative hypnotic drugs?

A

Promote sleep

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7
Q

What calming effect do sedative hypnotic drugs have on patients?

A

Helps relax the patient

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8
Q

What are non-benzodiazepines in the context of sedative hypnotic drugs?

A

A class of sedative hypnotic drugs that includes various agents like zolpidem, zaleplon, and eszopiclone.

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9
Q

What is the therapeutic index (TI) of barbiturates?

A

Small therapeutic index (TI = TD/ED).

Can be addictive

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10
Q

What is the mechanism of action of barbiturates at low doses?

A

Potentiates GABA but at a unique site.

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11
Q

What happens to the mechanism of action of barbiturates at higher doses?

A

Increases the release of inhibitory neurotransmitters. (Glycine)

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12
Q

Name three examples of non-benzodiazepine sedative hypnotics.

A
  • Zolpidem (Ambien)
  • Zaleplon (Sonata)
  • Eszopiclone (Lunesta)
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13
Q

How do non-benzodiazepines affect GABA?

A

They increase chloride influx.

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14
Q

What is a notable advantage of non-benzodiazepines compared to barbiturates?

A

Less side effects and shorter duration of action.

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15
Q

What is the structure and function of Ramelteon similar to?

A

Similar to melatonin.

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16
Q

What is the primary route of administration for benzodiazepines and nonbenzodiazepines?

A

Oral administration

Highly lipid soluble, absorbed easily

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17
Q

Describe the distribution of benzodiazepines and nonbenzodiazepines.

A

Fairly uniform

Indicates that these drugs distribute evenly throughout the body

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18
Q

How are benzodiazepines and nonbenzodiazepines metabolized?

A

Oxidative enzymes in liver cells

The liver plays a crucial role in the metabolism of these substances

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19
Q

What mechanisms are involved in the termination of effect for benzodiazepines and nonbenzodiazepines?

A

Hepatic enzymes or storage in non-CNS tissues (sequestering)

This can lead to a prolonged effect or hangover

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20
Q

What is a common side effect associated with the use of benzodiazepines and nonbenzodiazepines?

A

Hangover effect

  • This can include drowsiness, confusion, or impaired motor function

Refers to residual effects after the drug’s active effects have worn off

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21
Q

Where are benzodiazepines and nonbenzodiazepines excreted from the body?

A

Kidneys

The kidneys play a vital role in the elimination of these drugs

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22
Q

With the adverse effects of Sedative-Hypnotics, what is anterograde amnesia?

A

Inability to form new memories after the onset of drug effects

This can lead to gaps in memory for events that occur while under the influence.

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23
Q

What does tolerance refer to in sedative-hypnotics?

A

A condition where increasing doses are required to achieve the same effect

This can lead to higher consumption and increased risk of adverse effects.

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24
Q

What is physical dependence in relation to sedative-hypnotics?

A

A state where the body adapts to the drug, leading to withdrawal symptoms upon discontinuation

Symptoms can include anxiety, tremors, and seizures.

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25
What are complex behaviors associated with sedative-hypnotics?
Engaging in activities while not fully awake or aware, such as eating, sleepwalking or sleepdriving ## Footnote These behaviors can occur without the individual being aware of them.
26
What is a common gastrointestinal effect of sedative-hypnotics?
GI discomfort; also dry mouth and sore throat ## Footnote This may manifest as nausea, constipation, or abdominal pain.
27
What are the clinical categories of anxiety disorders?
* Generalized anxiety disorder * Social anxiety disorder * Panic disorder * Obsessive-compulsive disorder * Posttraumatic stress syndrome ## Footnote These categories help in the diagnosis and treatment of anxiety disorders.
28
What are the primary types of antianxiety drugs?
Benzodiazepines, Buspirone, Antidepressants, Other (e.g., Beta adrenergic antagonist) ## Footnote This categorization includes various classes of medications used to treat anxiety.
29
What is the mechanism of action for Buspirone?
Increased 5-HT effects ## Footnote 5-HT refers to serotonin, a neurotransmitter that Buspirone interacts with to exert its effects.
30
What is the efficacy level of Buspirone?
Moderate efficacy ## Footnote This indicates that Buspirone is effective but not as potent as some other antianxiety medications.
31
True or False: Benzodiazepines are a type of antidepressant.
False ## Footnote Benzodiazepines are specifically categorized as antianxiety drugs, not antidepressants.
32
What is a common adverse effect of anxiolytics?
Sedation ## Footnote Sedation can lead to drowsiness and decreased alertness.
33
What type of impairment can result from the use of anxiolytics?
Psychomotor impairment ## Footnote Psychomotor impairment affects coordination and reaction times.
34
True or False: Anxiolytics can lead to addiction and abuse.
True ## Footnote Anxiolytics are associated with a risk of developing dependency.
35
What are the primary symptoms of depression?
Depressed mood, lack of energy, sleep disturbance, abnormal eating, feelings of despair ## Footnote These symptoms can significantly impact daily functioning.
36
What type of depression is triggered by unpleasant life experiences and negative thinking?
Situational depression ## Footnote This form of depression often arises in response to specific life stressors.
37
What is post-stroke depression?
A type of depression that occurs following a stroke ## Footnote It is considered a pathological form of depression.
38
What is seasonal affective disorder?
A type of depression that occurs at certain times of the year, typically in winter ## Footnote It is linked to changes in light exposure.
39
What role does genetics play in depression?
Genetic factors can influence the risk of developing depression ## Footnote Family history may increase susceptibility.
40
What is one theory regarding the pathophysiology of depression?
Increased receptor sensitivity leading to down regulation ## Footnote This refers to either presynaptic or postsynaptic receptors.
41
What role does neurogenesis play in the pathophysiology of depression?
Lack of neurogenesis in the hippocampus ## Footnote Neurogenesis is crucial for maintaining mood regulation and cognitive function.
42
How long does it typically take for medications to begin to work for depression?
2 to 4 weeks ## Footnote This delay is due to the time needed for compensatory changes in the CNS.
43
What are the primary classes of antidepressants?
* Selective Serotonin Reuptake Inhibitors (SSRI) * Selective Serotonin-Norepinephrine Reuptake Inhibitors (SNRI) * Monoamine Oxidase Inhibitors (MAOi) * Tricyclic Antidepressants (TCA) ## Footnote These classes of antidepressants differ in their mechanisms of action and side effects.
44
What does Serotonin-Nonepinephrine Re-uptake Inhibitors (SNRI) do?
Decrease Serotonin and norepinephrin uptake
45
What do Tricyclics do?
Blocks re-uptakes of amine neurotranmitters (Such as: Serotonin and norepinephrine reuptake)
46
What neurotransmitters do antidepressants enhance the action of?
* Norepinephrine * Serotonin ## Footnote These neurotransmitters are crucial for mood regulation and are targeted by various classes of antidepressants.
47
Fill in the blank: The class of antidepressants known as _______ primarily works by inhibiting the reuptake of serotonin.
[Selective Serotonin Reuptake Inhibitors (SSRI)] ## Footnote SSRIs are commonly prescribed for depression and anxiety disorders.
48
What is the mechanism of action for Monoamine Oxidase Inhibitors (MAOi)?
Inhibit the enzyme monoamine oxidase, increasing levels of neurotransmitters ## Footnote MAOis are typically used when other antidepressants have failed due to their dietary restrictions and potential side effects.
49
How are antidepressants usually delivered?
Orally
50
What factors influence the dosages of antidepressants?
Each drug and each individual
51
What is the typical approach to initial dosages of antidepressants?
Start low and increase slowly within the therapeutic range
52
Where do antidepressants eventually reach to exert their effects?
The brain
53
Where does metabolism of antidepressants primarily take place?
In the liver
54
What happens to the metabolites of several antidepressants?
They continue to show significant antidepressant activity
55
What processes are involved in the elimination of antidepressants?
Biotransformation and renal excretion
56
Fill in the blank: Antidepressants are usually delivered _______.
Orally
57
True or False: Initial dosages of antidepressants are usually started at a high level.
False
58
Fill in the blank: Metabolism of antidepressants primarily takes place in the _______.
Liver
59
What are common gastrointestinal symptoms associated with SSRIs and SNRIs?
Nausea, vomiting, diarrhea, constipation ## Footnote These symptoms can vary in severity among individuals taking these medications.
60
What central nervous system effects can MAO inhibitors produce?
CNS excitation, restlessness, irritability, agitation, sleep loss ## Footnote These effects can significantly impact a patient's daily functioning.
61
What neurotransmitters do antidepressants modulate?
Serotonin, norepinephrine, and dopamine ## Footnote Antidepressants can influence mood and pain perception by affecting these neurotransmitters.
62
What do animal models suggest about serotonergic pathways and chronic pain?
Decreased activity in descending (efferent) serotonergic pathways may lead to chronic pain syndromes ## Footnote This indicates a potential link between serotonin regulation and the experience of pain.
63
What are the main components that modulate signals transmitted to the brain?
Brain stem and descending controls via neurotransmitters ## Footnote The brain stem plays a crucial role in the modulation of sensory signals.
64
Which neurotransmitter is considered a key inhibitory transmitter?
Noradrenaline ## Footnote Noradrenaline is important for regulating various functions, including mood and attention.
65
What role does serotonin (5-HT) play in neurotransmission?
Serotonin acts as both an inhibitory and stimulatory transmitter ## Footnote Serotonin is involved in many functions, including mood regulation and the sleep-wake cycle.
66
What is Bipolar Disorder?
A mental health condition associated with mood swings from mania to depression ## Footnote Mood swings can range from extreme euphoria to deep sadness.
67
What characterizes manic episodes in Bipolar Disorder?
Euphoria, hyperactivity, and talkativeness ## Footnote These episodes are marked by heightened energy and mood.
68
What are the characteristics of depressive episodes in Bipolar Disorder?
Similar to those described in major depressive disorder ## Footnote Symptoms may include sadness, fatigue, and loss of interest.
69
What is a theory regarding the causes of Bipolar Disorder?
Genetic and environmental factors alter neurotransmitter balance in the brain ## Footnote This theory suggests a complex interaction between heredity and environment.
70
Which neurotransmitters are involved in the imbalance related to Bipolar Disorder?
Inhibitory: serotonin, GABA; Excitatory: norepinephrine, dopamine, glutamate, aspartate ## Footnote The balance between these neurotransmitters is crucial for mood regulation.
71
What is the focus of treatment for Bipolar Disorder?
Preventing the start of mood swings by preventing manic episodes ## Footnote Treatment often involves the use of mood stabilizers.
72
With Bipolar disorder, what are mood stabilizers also known as?
Antimanic drugs ## Footnote These medications help to control manic and depressive episodes.
73
Name a commonly used mood stabilizer for Bipolar Disorder.
Lithium salts ## Footnote Examples include lithium carbonate and lithium citrate.
74
What is the primary drug used to treat bipolar disorder?
Lithium ## Footnote Lithium is the most commonly prescribed medication for managing bipolar disorder.
75
What type of ion is lithium?
Monovalent cation ## Footnote Lithium is categorized as an alkali metal.
76
How does the size and charge of lithium influence neural excitability?
It competes with other cations ## Footnote Lithium competes with sodium, potassium, and calcium.
77
List some aspects of neuronal function that lithium can affect.
* Enzymes * Second messenger systems * Release of neurotransmitters * Normalization of receptor sensitivity ## Footnote Lithium's effects on these functions contribute to its therapeutic action.
78
What protective effects does lithium have on neurons?
Neuroprotective effects ## Footnote These effects help prevent neuronal damage associated with mood swings in bipolar disorder.
79
How is Lithium administered?
Orally
80
Where is Lithium absorbed?
From the GI tract
81
How is Lithium distributed in the body?
Throughout all the tissues in the body
82
Is Lithium metabolized in the body?
No, Lithium is not metabolized
83
How is Lithium eliminated from the body?
Almost exclusively through excretion in the urine
84
What is a major problem associated with lithium use?
Danger of accumulation within the body ## Footnote Accumulation can lead to toxic levels.
85
What can frequently occur during the administration of lithium?
Toxic levels can be reached ## Footnote This is a significant concern for patient safety.
86
What serious neurological complications can result from the progressive accumulation of lithium?
* Seizures * Coma * Death ## Footnote These complications highlight the need for careful monitoring.
87
What should clinicians be aware of in patients taking lithium?
Any changes in behavior ## Footnote Behavioral changes may indicate lithium toxicity.

Term 3 (50 decks)

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