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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
Q

What are complex behaviors associated with sedative-hypnotics?

A

Engaging in activities while not fully awake or aware, such as eating, sleepwalking or sleepdriving

These behaviors can occur without the individual being aware of them.

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26
Q

What is a common gastrointestinal effect of sedative-hypnotics?

A

GI discomfort; also dry mouth and sore throat

This may manifest as nausea, constipation, or abdominal pain.

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27
Q

What are the clinical categories of anxiety disorders?

A
  • Generalized anxiety disorder
  • Social anxiety disorder
  • Panic disorder
  • Obsessive-compulsive disorder
  • Posttraumatic stress syndrome

These categories help in the diagnosis and treatment of anxiety disorders.

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28
Q

What are the primary types of antianxiety drugs?

A

Benzodiazepines, Buspirone, Antidepressants, Other (e.g., Beta adrenergic antagonist)

This categorization includes various classes of medications used to treat anxiety.

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29
Q

What is the mechanism of action for Buspirone?

A

Increased 5-HT effects

5-HT refers to serotonin, a neurotransmitter that Buspirone interacts with to exert its effects.

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30
Q

What is the efficacy level of Buspirone?

A

Moderate efficacy

This indicates that Buspirone is effective but not as potent as some other antianxiety medications.

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31
Q

True or False: Benzodiazepines are a type of antidepressant.

A

False

Benzodiazepines are specifically categorized as antianxiety drugs, not antidepressants.

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32
Q

What is a common adverse effect of anxiolytics?

A

Sedation

Sedation can lead to drowsiness and decreased alertness.

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33
Q

What type of impairment can result from the use of anxiolytics?

A

Psychomotor impairment

Psychomotor impairment affects coordination and reaction times.

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34
Q

True or False: Anxiolytics can lead to addiction and abuse.

A

True

Anxiolytics are associated with a risk of developing dependency.

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35
Q

What are the primary symptoms of depression?

A

Depressed mood, lack of energy, sleep disturbance, abnormal eating, feelings of despair

These symptoms can significantly impact daily functioning.

36
Q

What type of depression is triggered by unpleasant life experiences and negative thinking?

A

Situational depression

This form of depression often arises in response to specific life stressors.

37
Q

What is post-stroke depression?

A

A type of depression that occurs following a stroke

It is considered a pathological form of depression.

38
Q

What is seasonal affective disorder?

A

A type of depression that occurs at certain times of the year, typically in winter

It is linked to changes in light exposure.

39
Q

What role does genetics play in depression?

A

Genetic factors can influence the risk of developing depression

Family history may increase susceptibility.

40
Q

What is one theory regarding the pathophysiology of depression?

A

Increased receptor sensitivity leading to down regulation

This refers to either presynaptic or postsynaptic receptors.

41
Q

What role does neurogenesis play in the pathophysiology of depression?

A

Lack of neurogenesis in the hippocampus

Neurogenesis is crucial for maintaining mood regulation and cognitive function.

42
Q

How long does it typically take for medications to begin to work for depression?

A

2 to 4 weeks

This delay is due to the time needed for compensatory changes in the CNS.

43
Q

What are the primary classes of antidepressants?

A
  • Selective Serotonin Reuptake Inhibitors (SSRI)
  • Selective Serotonin-Norepinephrine Reuptake Inhibitors (SNRI)
  • Monoamine Oxidase Inhibitors (MAOi)
  • Tricyclic Antidepressants (TCA)

These classes of antidepressants differ in their mechanisms of action and side effects.

44
Q

What does Serotonin-Nonepinephrine
Re-uptake Inhibitors (SNRI) do?

A

Decrease Serotonin and norepinephrin uptake

45
Q

What do Tricyclics do?

A

Blocks re-uptakes of amine neurotranmitters (Such as: Serotonin and norepinephrine reuptake)

46
Q

What neurotransmitters do antidepressants enhance the action of?

A
  • Norepinephrine
  • Serotonin

These neurotransmitters are crucial for mood regulation and are targeted by various classes of antidepressants.

47
Q

Fill in the blank: The class of antidepressants known as _______ primarily works by inhibiting the reuptake of serotonin.

A

[Selective Serotonin Reuptake Inhibitors (SSRI)]

SSRIs are commonly prescribed for depression and anxiety disorders.

48
Q

What is the mechanism of action for Monoamine Oxidase Inhibitors (MAOi)?

A

Inhibit the enzyme monoamine oxidase, increasing levels of neurotransmitters

MAOis are typically used when other antidepressants have failed due to their dietary restrictions and potential side effects.

49
Q

How are antidepressants usually delivered?

A

Orally

50
Q

What factors influence the dosages of antidepressants?

A

Each drug and each individual

51
Q

What is the typical approach to initial dosages of antidepressants?

A

Start low and increase slowly within the therapeutic range

52
Q

Where do antidepressants eventually reach to exert their effects?

A

The brain

53
Q

Where does metabolism of antidepressants primarily take place?

A

In the liver

54
Q

What happens to the metabolites of several antidepressants?

A

They continue to show significant antidepressant activity

55
Q

What processes are involved in the elimination of antidepressants?

A

Biotransformation and renal excretion

56
Q

Fill in the blank: Antidepressants are usually delivered _______.

A

Orally

57
Q

True or False: Initial dosages of antidepressants are usually started at a high level.

A

False

58
Q

Fill in the blank: Metabolism of antidepressants primarily takes place in the _______.

A

Liver

59
Q

What are common gastrointestinal symptoms associated with SSRIs and SNRIs?

A

Nausea, vomiting, diarrhea, constipation

These symptoms can vary in severity among individuals taking these medications.

60
Q

What central nervous system effects can MAO inhibitors produce?

A

CNS excitation, restlessness, irritability, agitation, sleep loss

These effects can significantly impact a patient’s daily functioning.

61
Q

What neurotransmitters do antidepressants modulate?

A

Serotonin, norepinephrine, and dopamine

Antidepressants can influence mood and pain perception by affecting these neurotransmitters.

62
Q

What do animal models suggest about serotonergic pathways and chronic pain?

A

Decreased activity in descending (efferent) serotonergic pathways may lead to chronic pain syndromes

This indicates a potential link between serotonin regulation and the experience of pain.

63
Q

What are the main components that modulate signals transmitted to the brain?

A

Brain stem and descending controls via neurotransmitters

The brain stem plays a crucial role in the modulation of sensory signals.

64
Q

Which neurotransmitter is considered a key inhibitory transmitter?

A

Noradrenaline

Noradrenaline is important for regulating various functions, including mood and attention.

65
Q

What role does serotonin (5-HT) play in neurotransmission?

A

Serotonin acts as both an inhibitory and stimulatory transmitter

Serotonin is involved in many functions, including mood regulation and the sleep-wake cycle.

66
Q

What is Bipolar Disorder?

A

A mental health condition associated with mood swings from mania to depression

Mood swings can range from extreme euphoria to deep sadness.

67
Q

What characterizes manic episodes in Bipolar Disorder?

A

Euphoria, hyperactivity, and talkativeness

These episodes are marked by heightened energy and mood.

68
Q

What are the characteristics of depressive episodes in Bipolar Disorder?

A

Similar to those described in major depressive disorder

Symptoms may include sadness, fatigue, and loss of interest.

69
Q

What is a theory regarding the causes of Bipolar Disorder?

A

Genetic and environmental factors alter neurotransmitter balance in the brain

This theory suggests a complex interaction between heredity and environment.

70
Q

Which neurotransmitters are involved in the imbalance related to Bipolar Disorder?

A

Inhibitory: serotonin, GABA;
Excitatory: norepinephrine, dopamine, glutamate, aspartate

The balance between these neurotransmitters is crucial for mood regulation.

71
Q

What is the focus of treatment for Bipolar Disorder?

A

Preventing the start of mood swings by preventing manic episodes

Treatment often involves the use of mood stabilizers.

72
Q

With Bipolar disorder, what are mood stabilizers also known as?

A

Antimanic drugs

These medications help to control manic and depressive episodes.

73
Q

Name a commonly used mood stabilizer for Bipolar Disorder.

A

Lithium salts

Examples include lithium carbonate and lithium citrate.

74
Q

What is the primary drug used to treat bipolar disorder?

A

Lithium

Lithium is the most commonly prescribed medication for managing bipolar disorder.

75
Q

What type of ion is lithium?

A

Monovalent cation

Lithium is categorized as an alkali metal.

76
Q

How does the size and charge of lithium influence neural excitability?

A

It competes with other cations

Lithium competes with sodium, potassium, and calcium.

77
Q

List some aspects of neuronal function that lithium can affect.

A
  • Enzymes
  • Second messenger systems
  • Release of neurotransmitters
  • Normalization of receptor sensitivity

Lithium’s effects on these functions contribute to its therapeutic action.

78
Q

What protective effects does lithium have on neurons?

A

Neuroprotective effects

These effects help prevent neuronal damage associated with mood swings in bipolar disorder.

79
Q

How is Lithium administered?

A

Orally

80
Q

Where is Lithium absorbed?

A

From the GI tract

81
Q

How is Lithium distributed in the body?

A

Throughout all the tissues in the body

82
Q

Is Lithium metabolized in the body?

A

No, Lithium is not metabolized

83
Q

How is Lithium eliminated from the body?

A

Almost exclusively through excretion in the urine

84
Q

What is a major problem associated with lithium use?

A

Danger of accumulation within the body

Accumulation can lead to toxic levels.

85
Q

What can frequently occur during the administration of lithium?

A

Toxic levels can be reached

This is a significant concern for patient safety.

86
Q

What serious neurological complications can result from the progressive accumulation of lithium?

A
  • Seizures
  • Coma
  • Death

These complications highlight the need for careful monitoring.

87
Q

What should clinicians be aware of in patients taking lithium?

A

Any changes in behavior

Behavioral changes may indicate lithium toxicity.

Term 3 (44 decks)

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