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Pharmacology > Pharmacology Exam 3 > Flashcards

Pharmacology Exam 3 Flashcards

1
Q

Immunosupressant Drugs

A

Calcineurin Inhibitor
- cyclosporin (Neoral)

Anti-TNF-Alpha
- Adalimumab (Humira)

Other Drugs for RA
- Hydroxychloroquine (Plaquenil)

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2
Q

What must individuals on immunosuppresants avoid?

A

live, attenuated vaccines
- may need additional boosters

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3
Q

Individuals on immunosuppresants have increased risks of what?

A
  • rate of malignancy
  • infection
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4
Q

What type of skin cancer are individuals on immunosupressants most likely to develop?

A

squamous cell

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5
Q

Mechanism of Action & Side Effects of Calcineurin Inhibitors

A

MOA
- blocks T-cell activation

Side Effects
- nephrotoxicity
- hyperkalemia
- HTN
- dyslipidemia

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6
Q

Calcineurin Inhibitor Drug

A

cyclosporine

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7
Q

Side effects of Calcineurin inhibitors

A
  • nephrotoxicity
  • hyperkalemia
  • HTN
  • dyslipidemia
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8
Q

Calcineurin Inhibitors Mechanism of Action

A

blocks T-cell activation

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9
Q

What are Cytotoxic Agents & the two classes?

A

kill certain types of cells

1.) Non-specific
2.) Specific

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10
Q

Non-Specific Cytotoxic Agent Mechanism of Action

A

Target rapidly-dividing cells (like T & B cells)

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11
Q

Specific Cytotoxic Agents Mechanism of Action

A

inhibit enzymes required for lymphocyte production of purines or pyrimidines

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12
Q

What is the difference in specific and non-specific Cytotoxic Agents?

A

Specific Cytotoxic Agents target the immune system more accurately and are less likely to have side effects

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13
Q

Non-Specific Cytotoxic Agent Drug

A

Methotrexate

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14
Q

Side Effects of Cytotoxic Agents

A
  • Myelosuppression (bone marrow suppression)
  • N/V
  • Diarrhea
  • Fatigue
  • Hepatotoxicity
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15
Q

What is the drug of choice for Rheumatoid Arthritis & what are the most common side effects?

A

Methotrexate

  • Nausea
  • Vomiting
  • Fatigue
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16
Q

What are biologic agents?

A

large molecules produced by living cells

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17
Q

Antibodies (biologic agents) end in what suffix?

A

“-mab”

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18
Q

SHORT ANSWER

What are Biosimilars? What is unique about them & what must the drug manufacturer prove?????

A

Biosimilars: similar to generic for biologics

Unique:
- amino acid sequence must be the same as the biologic
- biosimilars cannot be substituted for one another, you have to order / prescribe the specific version you want

Drug companies must prove: the same amount of active ingredient / molecule reaches the bloodstream

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19
Q

Monoclonal Antibody Drug Name

A
  • Adalimumab (Humira)
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20
Q

What are 3 unique things about monoclonal antibodies?

A

1.) IV or SQ (require injection)

2.) ↑ risk of infection, myelosuppression (bone marrow suppression)

3.) Infusion-related reactions (pre-medicate with antihistamines, NSAIDs, steroids, etc.)

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21
Q

Side Effects of Hydroxychloroquine (Plaquenil)

A
  • neuromuscular toxicity
  • N/V/D
  • ataxia
  • nervousness
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22
Q

What is disinhibition?

A

take away barriers you may have formed about whether or not to do certain things based on social norms, fear of how others may react, etc.

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23
Q

What is the difference in the dose response curves of Barbiturates & Benzodiazepines???

A

Barbiturates:
- linear dose response curve
- can be more dangerous
- rate of change is same at ANY dose

Benzodiazepines
- flat dose response curve
- you don’t get as “deep” of an effect as you would with barbiturates (like a medically-induced coma)

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24
Q

Benzodiazepine Mechanism of Action

A

Facilitate GABA Actions
- GABA = inhibitory neurotransmitter

benzodiazepines stabilize neurons making it much LESS likely that they become activated

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25
Q

What is unique about Zolpidem (Ambien)?

A

it is NOT a benzodiazepine, but it works on benzodiazepine receptors

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26
Q

Benzodiazepines used for Anxiety

A
  • Alprazolam (Xanax)
  • Clonazepam (Klonopin)
  • Diazepam (Valium)
  • Lorazepam (Ativan)
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27
Q

Drugs used for Anxiety Disorder

A

*Benzodiazepines
- Alprazolam (Xanax)
- Clonazepam (Klonopin)
- Diazepam (Valium)
- Lorazepam (Ativan)
- Zolpidem (Ambien)

Non-Benzodiazepines
- Buspirone (Buspar)

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28
Q

Adverse Effects of Benzodiazepines

A
  • CNS Depression: drowsiness, sedation, dizziness, confusion
  • rebound insomnia (after discontinuing)
  • paradoxical reaction: irritation, aggression, excitement
  • amnesia
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29
Q

Benzodiazepine Dependence

A

If someone has been on a benzodiazepine at a HIGH dose for a LONGER period of time, then they need a taper

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30
Q

Drugs for Insomnia

A
  • Zolpidem (Ambien)
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31
Q

What is unique about Buspirone (Buspar)?

A
  • treats anxiety & panic without causing sedation (unique sedative-hypnotic mechanism)
  • takes a few weeks to work
  • metabolized by CYP3A4
  • Short half-life (2.5 hours); may need multiple doses per day
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32
Q

Explain the Monoamine-Deficiency Hypothesis for Major Depressive Disorder

A

Depression is likely caused by relative lack of monoamine neurotransmitters (serotonin, norepinephrine, dopamine, etc.) in the brain

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33
Q

3 Drug Classes used to treat Antidepressants

A
  • Tricyclic Antidepressants
  • SSRIs (Selective Serotonin Reuptake Inhibitor)
  • SNRIs (Selective Norepinephrine Reuptake Inhibitor)
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34
Q

Tricyclic Antidepressant drugs, mechanism of action, & side effects

A
  • Amitriptyline (Elavil)
  • Nortriptyline (Pamelor)

MOA
- block neuronal reuptake of monoamine neurotransmitters (NE, 5-HT)
- also antagonize (block) H1, Acetylcholine (ACh), & norepinephrine (NE) receptors
- NOT SPECIFIC

*Side Effects
- Orthostatic hypotention
- Sedation
- Anticholinergic Effect (anti-SLUD + Tach)
- Cardiac toxicity

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35
Q

Tricyclic Antidepressant MOA

A
  • blocks neuronal uptake of monoamine neurotransmitters (NE, 5-HT)
  • antagonizes (blocks) H1, ACh, & NE receptors
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36
Q

Tricyclic Antidepressant Side Effects

A
  • Orthostatic Hypotension
  • Sedation
  • Anticholinergic Effects
    - dry mouth
    - dry eyes
    - urinary hesitancy
    - constipation
    - tachycardia
  • Cardiac Toxicity
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37
Q

SSRI Drugs

A
  • Fluoxetine (Prozac)
  • Paroxetine (Paxil)
  • Sertraline (Zoloft)
  • Citalopram (Celexa)
  • Escitalopram (Lexapro)
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38
Q

SSRI Drugs, Mechanism of Action, & Side Effects

A
  • Fluoxetine (Prozac)
  • Paroxetine (Paxil)
  • Sertraline (Zoloft)
  • Citalopram (Celexa)
  • Escitalopram (Lexapro

MOA
- block neuronal reuptake of serotonin
- no anti-SLUD, tachy, or sedation

Side Effects
- Sexual dysfunction
- Weight gain
- Serotonin syndrome
- Withdrawal syndrome
- Anti-platelet activity
- Osteoporosis

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39
Q

Symptoms of Serotonin Syndrome

A
  • Altered mental staus
  • Incoordination
  • Hyperreflexia
  • Excessive sweating
  • Tremor
  • Fever
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40
Q

What 3 side effects do SSRIs NOT cause?

A
  • Sedation
  • Tachycardia
  • Anti-SLUD (dry mouth / eyes, urinary hesitancy, & constipation)
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41
Q

What side effects are associated with SSRIs & SNRIs?

A
  • sexual dysfunction
  • weight gain
  • serotonin syndrome
  • withdrawal syndrome
  • antiplatelet activity
  • osteoporosis
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42
Q

SNRI drugs, MOA, & side effects

A
  • Duloxetine (Cymbalta)
  • Venlafaxine (Effexor)
  • Desvenlafaxine (Pristiq)

MOA
- selective inhibition of both serotonin & norepinephrine

Side Effects
- sexual dysfunction
- weight gain
- serotonin syndrome
- withdrawal syndrome
- anti-platelet activity
- osteoporosis

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43
Q

SNRI Drugs

A
  • Venlafaxine (Effexor)
  • Desvenlafaxine (Pristiq)
  • Duloxetine (Cymbalta
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44
Q

SNRI Mechanism of Action

A

selective inhibition of both serotonin & norepinephrine

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45
Q

Side Effects of SNRIs

A
  • sexual dysfunction
  • weight gain
  • serotonin syndrome
  • withdrawal syndrome
  • anti-platelet activity
  • osteoporosis
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46
Q

Atypical Antidepressant Drugs (Miscellaneous)

A
  • Bupropion (Wellbutrin)
  • Mirtazapine (Remeron)
  • Trazodone (Oleptro)
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47
Q

What neurotransmiter does Bupropion (Wellbutrin) work on?

A

dopamine

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48
Q

What side effects are associated with Mirtazapine (Remeron)?

A
  • sedation
  • orthostatic hypotention
  • tachycardia
  • Anti-SLUD (dry eye/mouth, urinary hesitancy, constipation)
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49
Q

Which neurotransmitter does Trazodone (Oleptro) work on?

A

serotonin

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50
Q

Side Effects of Bupropion (Wellbutrin)

A
  • neutral / no weight gain
  • lowest risk of sexual side effects
  • can lead to seizures at high doses
    - could be an issue for epileptics
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51
Q

Side Effects of Trazodone (Oleptro) & Mirtazapine (Remeron)

A
  • sedation
  • orthostatic hypotension
  • tachycardia
  • anti-SLUD (dry eyes, dry mouth, urinary hesitancy, constipation)
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52
Q

In prostatic hypertrophy, what are glandular / epithelial muscle regulated by?

A

testosterone / DHT-regulated

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53
Q

In prostatic hypertrophy, what are muscular / smooth muscle regulated by?

A

alpha-1 receptor mediated

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54
Q

Which drug classes are used to treat prostatic hypertrophy?

A
  • alpha-1 antagonists
    - non-selective
    - selective
  • 5-alpha-reductase inhibitors
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55
Q

Alpha-1 Antagonist Drugs for prostatic hypertrophy

A

NON-SELECTIVE
- Terazosin (Hytrin)
- Doxazosin (Cardura)
- Prazosin (Minipress)

SELECTIVE
- Tamsulosin (Flomax)

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56
Q

Non-Selective Alpha-1 Antagonist Drugs

A
  • Terazosin (Hytrin)
  • Doxazosin (Cardura)
  • Prazosin (Minipress)
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57
Q

Selective Alpha-1 Antagonist Drugs

A

Tamsulosin (Flomax)

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58
Q

Alpha-1 Antagonist Mechanism of Action & Side Effects

A

MOA
- inhibition of alpha-1 receptors leads to relaxation / vasodilation

Side Effects
- Hypotension
- fainting
- dizziness
- fatigue
- nasal congestion
- ↓ ejaculation volume

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59
Q

Tamsulosin (Flomax) can be used to treat what condition in both males and females?

A

kidney stones

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60
Q

What are the main differences in selective & non-selective alpha-1 antagonists????? KNOW THIS

A
  • Non-Selectives block alpha-1 receptors throughout the ENTIRE body while Selectives block alpha-1 receptors in the prostate
  • Non-Selectives have a greater risk of hypotension because they cause vasodilation throughout the entire body
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61
Q

Are Non-Selective or Selective Alpha-1 Antagonists more likely to cause hypotension and why? KNOW THIS

A

Non-selective alpha-1 antagonists because they cause relaxation / vasodilation throughout the entire body

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62
Q

5-alpha-reductase inhibitor drug for treatment of prostatic hypertrophy

A

Finasteride (Flomax)

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63
Q

What do 5-alpha reductase inhibitors do?

A

prevent the body from turning testosterone into DHT (dihydrotestosterone)

 - **allows body to "starve" prostate of its growth factor**
 - **drug does NOT actively shrink the prostate itself** (prostate shrinks over time due to lack of growth factor, cell turnover / death, etc.)
64
Q

What drug class can PDE5 Inhibitors not be taken with?

A

NITRATES

65
Q

What drug class is used to treat erectile dysfunction?

A

PDE-5 Inhibitors

66
Q

PDE-5 Inhibitor Drug

A

Sildenafil (Viagra)

67
Q

Erectile Dysfunction drug & class, MOA, & side effects

A

Sildenafil (Viagra) PDE-5 Inhibitor

MOA
- prevents the breakdown of cGMP
- cGMP causes vascular relaxation

Side Effects
- hypotension
- headache
- flushing
- visual changes
- myalgia / back pain
- hearing problems

68
Q

PDE-5 Inhibitor Mechanism of Action

A

** prevents the breakdown of cGMP**

  - cGMP causes vascular relaxation
69
Q

PDE-5 Inhibitor Side Effects

A
  • Hypotension
  • Headache
  • Flushing
  • Visual changes
  • Myalgia / back pain
  • Hearing problems
70
Q

Which two drugs are vitamins or minerals containing salts?

A

Potassium salts & calcium salts

71
Q

Side Effects of Potassium Salts

A
  • fatigue
  • muscle weakness / weak pulses
  • N/V & abdominal pain
  • vesicant at high concentrations
72
Q

What is a vesicant????? KNOW THIS

A

blister causing because the substance is toxic to the tissue

73
Q

Be cautious when taking potassium salts with __________.

A

anticholinergics (can cause dry secretions)

74
Q

What is unique about Calcium Salts? What is the primary risk & what are the drug interaction risks?

A
  • gut can only absorb 500 mg at once
  • hypercalcemia (GI & CNS toxicities)
  • chelation can occur with levothyroxine, antibiotics, etc.
75
Q

Vitamin D Drugs & Which form of Vitamin D are these drugs?

A
  • Ergocalciferol = D2 (Calciferol, Drisdol)
  • Cholecalciferol = D3 (Delta-D)
76
Q

Drug name for Vitamin D2

A

Ergocalciferol (Calciferol, Drisdol)

77
Q

Drug name for Vitamin D3

A

Cholecalciferol (Delta-D)

78
Q

What is the biggest risk when taking Vitamin D?

A

hypercalcemia (↑ calcium in blood)

79
Q

Which Vitamin D supplement is more effective?

A

Cholecalciferol (D3) (Delta-D)

80
Q

Iron Supplement Drugs

A

Ferrous sulfate (20% elemental iron)

81
Q

What can improve the absorption of non-heme iron?

A
  • ↑ gastric acidity
  • ascorbic acid (vitamin C to ↑ acidity)
82
Q

Side Effects of taking Iron Supplements

A
  • N/V
  • constipation
  • dark stool
  • can be highly toxic in OD situations; especially with kids
83
Q

What should be kept in mind when giving oral iron supplements?

A
  • administer on empty stomach
  • divide total into 2-3 doses to ↑ tolerability
84
Q

Vitamin B Drugs

A
  • Folic Acid
  • Cyanocobalamin = B12
85
Q

What is another name for Vitamin B12?

A

Cyanocobalamin

86
Q

SHORT ANSWER

How does Folic Acid mask Vitamin B12 Deficiency???? KNOW THIS!!!!!!

A

1.) Folic acid will treat the anemia of B12 deficiency meaning you will no longer have symptoms of anemia.

2.) This is BAD because B12 deficiency can lead to CNS effects (like ↓ muscle tone, impaired concentration, muscle weakness, dizziness, syncope, etc.) & which can be IRREVERSIBLE if the deficiency is prolonged

87
Q

What can prolonged Vitamin B12 deficiency lead to?

A

irreversible damage (specifically CNS damage)

88
Q

What are some CNS effects associated with B12 deficiency?

A

↑ muscle tone, syncope, dizziness, impaired concentration, etc.

89
Q

Anti-Platelet Drugs

A
  • Aspirin
  • Clopidogrel (Plavix) = ADP Receptor Inhibitor
90
Q

Aspirin MOA

A

binds to COX-1 to prevent the production of TXA2 (Thromboxine-A2)

  • irreversibly binds COX-1
91
Q

How long do the effects of Aspirin last for?

A

life-span of the platelet (8-10 days)

92
Q

What is the job / goal of Aspirin?

A

makes it harder to form a platelet plug, but your blood still clots

get rid of new platelets that were made that day

93
Q

Side Effects of Aspirin

A
  • GI bleeding & other bleeding
  • hemorrhagic stroke
  • dyspepsia
94
Q

Which drug is an ADP Inhibitor (ADP Receptor Inhibitor) & what is it used for?

A

Clopidogrel (Plavix)

Antiplatelet drug

95
Q

Clopidogrel (Plavix) MOA

A

blocks ADP-dependent platelet activation

96
Q

What is unique about Clopidogrel (Plavix)?

A

patient responses are highly variable

97
Q

Side Effects of Antiplatelet Drugs / Clopidogrel (Plavix)

A

bleeding

98
Q

Most antiplatelet drugs are given in conjunction with what other medication?

A

Aspirin

99
Q

Anticoagulant Drug Classes

A
  • Vitamin K Antagonists
  • Specific Xa (10-A) Inhibitors
  • Direct Thrombin Inhibitor
  • Heparins (UFH & LMWH)
100
Q

Anticoagulant Drugs: Vitamin K Antagonists

A

Warfarin

101
Q

Vitamin K Antagonists (Warfarin) MOA

A
  • warfarin prevents the liver from making new functional clotting factors by inhibiting Vitamin K Epoxide Reductase (prevents body from recycling vitamin K)
  • ↓ activity of factors II, VII, IX, X, Protein C, & Protein S
102
Q

What drug is Warfarin always started in conjunction with and why?

A

Heparain because it works right away while Warfarin takes days to work

103
Q

Side Effects of Warfarin

A
  • bleeding
  • skin necrosis
  • purple toe syndrome
  • osteoporosis
104
Q

What is used to measure the effectiveness of Warfarin?

A

INR

  • normally want INR = 2-3
105
Q

What do you do if a patient comes into a clinic who’s on Warfarin & has an INR of 8 but they aren’t actively bleeding?

A

↑ vitamin K intake

106
Q

What do you do if a patient comes into a clinic on Warfarin with an INR of 8 and is actively bleeding? Will giving them Vitamin K help?

A

NO, because vitamin K takes 5-7 days to start working. Instead, give the patient fresh frozen plasma

107
Q

Specific Xa Inhibitor Drugs

A
  • Rivaroxaban (Xarelto)
  • Apixaban (Eliquis)
108
Q

Specific Xa Inhibitor Drugs MOA

A

bind & inhibit Xa (10-A) factor in the blood

109
Q

Side Effects of Specific Xa Inhibitor Drugs

A
  • bleeding
  • Caution with renal dysfunction
110
Q

If an individual presents to a clinic actively bleeding & is on a specific Xa Inhibitor, should plasma or whole blood be given?

A

no, because the patient’s body will continue to inhibit the clotting factors that are being introduced

111
Q

What is the Antidote for Specific Xa Inhibitors?

A

Recombinant Factor Xa (10-A) (inactivated-zhzo [Andexxa])

112
Q

Direct Thrombin Inhibitor Drugs

A

Dabigatran (Pradaxa)

113
Q

Direct Thrombin Inhibitor Drugs MOA

A

targets Factor II

114
Q

What is unique about Dabigatran (Pradaxa) / Direct Thrombin Inhibitors?

A

must be discarded 120 days after opening because they are incredibly sensitive to humidity

115
Q

What is the Antidote for Dabigatran (Pradaxa)?

A

Idarucizumab (Praxbind) = monoclonal antibody

  • binds Dabigatran in blood & inactivates it
116
Q

Heparin Anticoagulant Drugs

A

Unfractionated Heparin (UFH)

Low Molecular Weight Heparin (LMWH)

117
Q

What is the difference in Unfractionated Heparin (UFH) & Low Molecular Weight Heparin (LMWH)?

A

LMWH are short molecules & only enhance the removal of Factor Xa (10-A)

UFH are long & short molecules

118
Q

What do the short molecules of Low Molecular Weight Heparin do?

A

enhance removal of Factor Xa (10-A)

119
Q

What do the long molecules of Unfractionated Heparin do?

A

allow for significant antithrombin effect

120
Q

What is the job of Heparin?

A

helps antithrombin work more effectively

121
Q

Which form of Heparin (UFH or LMWH) has more variable pharmacokinetics and why?

A

UFH because the long molecules remain in the body longer than short molecules

122
Q

What labs are required for monitoring of Unfractionated Heparin?

A

aPPT (partial thromboplastin time)

123
Q

What labs can be used to monitor Low Molecular Weight Heparin but are not required?

A

anti-Xa activity

124
Q

What is the antidote of Heparin?

A

protamine sulfate

125
Q

Side Effects of Heparin (UFH & LMWH)

A
  • Heparin Induced Thrombocytopenia
  • Osteoporosis (w/ long-term use)
126
Q

What is Heparin Induced Thrombocytopenia?

A

autoimmune reaction to a patient’s platelets

127
Q

Opthalmic Drugs & what are they used to treat?

A
  • Latanoprost (Xalatan)
  • Timolol (Timoptic)
  • Brimonidine (Alphagan P)

Treat Glaucoma

128
Q

Opthalmic Products (for glaucoma) mechanism of action

A

1.) ↑ outflow of fluid
- prostaglandin analogs & alpha-2 agonists

2.) ↓ production of fluid
- alpha-2 agonists & beta-blockers

129
Q

Lantanoprost (Xalatan) MOA

A

↑ outflow of fluid (prostaglandin analog)

130
Q

Timolol (Timoptic) MOA

A

↓ production of fluid (beta-blocker)

131
Q

Brimonidine (Alphagan P) MOA

A
  • ↑ outflow of fluid (alpha-2 agonist)
  • ↓ production of fluid (alpha-2 agonist)
132
Q

Mechanism of Action for:

1.) Lantanoprost (Xalatan)
2.) Timolol (Timoptic)
3.) Brimonidine (Alphagan P)

A

1.) Lantanoprost (Xalatan): ↑ outflow of fluid

2.) Timolol (Timoptic): ↓ production of fluid

3.) Brimonidine (Alphagan P): ↑ outflow of fluid & ↓ production of fluid

133
Q

Side Effects of Lantanoprost (Xalatan)

A
  • darkens the color of the iris
  • makes eyelashes longer & thicker
134
Q

Side Effects of Timolol (Timoptic)

A
  • bradycardia
  • ↓ in strength of contraction
  • exercise intolerance
  • hypotension
135
Q

Side Effects of Brimonidine (Alphagan P)

A
  • significant bradycardia & HTN
  • severe sedation
  • can cause depression & mood/behavior side effects
136
Q

What preservative is commonly contained in ophthalmic products that can cause irritation & inflammation?

A

Benzalkonium Chloride

137
Q

What are “Positive” symptoms of Schizophrenia?

A

seen in patients with schizophrenia (abnormal in patients WITHOUT schizophrenia)

  • Hallucinations
  • Dellusions
  • Paranoia
  • Agitation & Combative
138
Q

What are “Negative” symptoms of Schizophrenia?

A

symptoms seen in patients with schizophrenia
- patients without schizophrenia would not exhibit these (they’d be “normal”)

  • Social & Emotional Withdrawal
  • Blunt Affect
  • Poor Self-Care
139
Q

Positive vs. Negative Symptoms of Schizophrenia

A

Positive Sx
- Hallucinations
- Delusions
- Paranoia / Agitation / Combativeness

Negative Sx
- Social & Emotional Withdrawal
- Blunted Affect
- Poor Self-Care / Judgement / Insight

140
Q

Etiology / MOA of Schizophrenia

A
  • Glutamatergic Dysfunction
    - ↑ DA = glutamate deficiency
  • Serotonergic Influence
    - ↑ 5-HT in the blood
141
Q

What are the two drug classes of antipsychotics for schizophrenia?

A
  • Typical (1st generation)
  • Atypical (2nd generation)
142
Q

What are the differences in Typical & Atypical Antipsychotics?

A

Typical (1st gen)
- Dopamine Receptor Antagonist
- ↑ risk of extrapyramidal symptoms
- few adverse metabolic effects
- mainly effective for “positive” symptoms

Atypical (2nd gen)
- works on 5-HT receptors (little / no DA activity)
- low risk of extrapyramidal symptoms
- ↑ risk of metabolic effects (weight gain)
- effective for positive & negative symptoms

143
Q

What is unique about Atypical Antipsychotics (1st gen)?

A
  • Dopamine Receptor Antagonist
  • ↑ risk of extrapyramidal symptoms (acute dystonia, Parkinsonism, akathisia, tardive dyskinesia)
  • few adverse metabolic effects
  • effective for “positive” symptoms (hallucinations, combativeness, paranoia)
144
Q

What is unique about Atypical Antipsychotics (2nd gen)?

A
  • 5-HT antagonist (strong) & weak on dopamine
  • low risk of extrapyramidal symptoms (acute dystonia, Parkinsonism, akathisia, tardive dyskinesia)
  • ↑ risk of adverse metabolic effects (weight gain, DM, HTN, ↑ LDL)
  • effective for positive & negative symptoms
145
Q

What is similar about Typical & Atypical Antipsychotics?

A

Both have strong antihistamine actions (sedation), anticholinergic effects (dry mouth, dry eyes, urinary hesitancy, constipation, & tachycardia), * block peripheral alpha-1 receptors (risk of orthostatic hypotension)

146
Q

What are the similarities & differences between Typical & Atypical Antipsychotics? KNOW THIS

A

Similarities
- strong antihistamine actions (sedation)
- anticholinergic effects (SLUD + tachycardia)
- block peripheral alpha-1 receptors (risk of orthostatic hypotension)
- both work on positive symptoms

Differences

  • Typical = Dopamine Receptor Antagonist, ↑ risk of EPS, ↓ metabolic effects, work on “Positive (+)” symptoms
  • Atypical = strong 5-HT effect, weak on dopamine, ↓ risk of EPS, ↑ metabolic effects (weight gain, DM, HTN, bad cholesterol), work on “Positive (+)” & “Negative (-)” symptoms
147
Q

What are Extrapyramidal Symptoms (EPS)?

A
  • Acute Dystonia: sustained muscle contractions causing twisting, abnormal, and/or repetitive movement
  • Parkinsonism: limb muscle rigidity, tremor, bradykinesia
  • Akathisia: (profound restlessness)
  • Tardive Dyskinesia: involuntary movements of the face & tongue (can be come permanent!!!)
148
Q

Side Effects of Antipsychotics

A
  • Neuroleptic Malignant Syndrome
  • Anticholinergic Effects (SLUD + Tach)
  • Orthostatic hypotension (alpha-1 inhibition)
  • Sedation (antihistamine effects)
149
Q

What is Neuroleptic Malignant Syndrome (NMS)? KNOW THIS

A

sustained contraction of opposing muscle groups at the same time causing limb rigidity (limbs are frozen / stiff)

  • biceps & triceps fire at the same time
150
Q

What are the similarities & differences in Neuroleptic Malignant Syndrome (NMS) & Serotonin Syndrome????? KNOW THIS

A

NMS is only caused from taking antipsychotics. Serotonin Syndrome is due to taking antidepressants & causes involuntary muscle contraction & ↑ temperature

Similarities
- caused by taking certain medications
- fever & sweating
- altered consciousness / mental status

Differences
- NMS: caused by antipsychotics (dopamine antagonists); “lead-pipe” rigidity, hyporeflexia

  • *Serotonin Syndrome: caused by antidepressants (serotonergic agents); hyperreflexia, myoclonus (sudden, brief involuntary twitching / jerking of muscles)
151
Q

Features of Neuroleptic Malignant Syndrome & what is the cause?

A

Cause: antipsychotics (dopamine antagonists) - contraction of opposing muscle groups at the same time

Features
- “lead pipe” rigidity
- hyporeflexia
- fever & sweating
- autonomic instability (altered BP & dysrhythmias)
- altered consciousness

152
Q

What is the cause of Serotonin Syndrome & what are some unique features?

A

Cause: antidepressants (serotonergic agents)

Features
- hyperreflexia
- altered mental status
- fever & sweating
- tremor & incoordination
- myoclonus (sudden, brief involuntary twitching / jerking of muscles)

153
Q

Adverse / Side Effects of Antipsychotics

A
  • ↑ prolactin
    - can lead to gynecomastia, menstrual cycle irregularities, & sexual dysfunction
  • Seizures
    - reduced threshold / ↑ risk of seizures
  • Sexual Dysfunction
  • QT Prolongation
    • ↑ risk of potentially fatal form of V-Fib (Torsades de Pointes)
154
Q

What is the most common typical (1st gen) antipsychotic?

A

Haloperidol (Haldol)

155
Q

Atypical Antipsychotic Drugs

A
  • Olanzapine (Zyprexa)
  • Risperidone (Risperdal)
  • Clozapine (Clozaril) = LAST RESORT
  • Aripiprazole (Abilify)
  • Quetiapine (Seroquel)
156
Q

What is unique about Clozapine (Clozaril) & what side effects are associated with it?

A
  • first atypical (2nd gen) antipsychotic on the market (one of, if not the, most effective antipsychotic)

Side Effects
- Agranulocytosis (MUST monitor WBS & ANC)
- Weight Gain (DM, obesity, heart disease, etc.)
- > 40% of patients gain >7% TBW

157
Q

SHORT ANSWER

Which ophthalmic medications (drops for glaucoma) cause darkening of the iris, bradycardia, & depression??? KNOW THIS

A

Latanoprost (Xalatan) = darkening of iris

Timolol (Timoptic) = bradycardia

Brimonidine (Alphagan P) = depression

Pharmacology (5 decks)

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