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Pharmacology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

How does histamine impact mast cells?

A
  • vascular / mucosal permeability
  • pruritus (itching)
  • stimulation of irritant receptors
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2
Q

How do kinins impact mast cells?

A

vascular permeability

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3
Q

List mediators that impact mast cells

A
  • HISTAMINE
  • neutrophil & eosinophil chemotactic factor
  • kinins
  • leukotrienes
  • thormboxanes
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4
Q

What does histamine cause?

A
  • vasodilation (of small blood vessels)
  • ↑ capillary permeability
  • Constriction of extravascular smooth muscle
  • gastric acid secretion (H2-mediated)
  • Neurotransmission
    * pain, itching, awake, suppress appetite
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5
Q

Histamines Mechanism of Action

A

act as antagonists (blocks) at the H1 receptor

 * causes vasodilation
 * ↑ capillary permeability 
 * itching
 * redness
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6
Q

Are Antihistamines effective or ineffective for hypersensitivity reactions / severe allergic reactions?

A

limited effectiveness (not very effective)

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7
Q

Antihistamines can be both __________.

A

sedative and CNS stimulating

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8
Q

What is a paradoxical reaction?

A

a patient experiences the opposite of what you would expect the drug to do

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9
Q

Paradoxical Reaction with Antihistamines

A
  • Dizziness
  • Tinnitus
  • Incoordination
  • Insomnia
  • Tremors
  • Nervousness
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10
Q

Side Effects of Antihistamines

A
  • CONSTIPATION
  • WEIGHT GAIN
  • DROWSINESS
  • loss of appetite
  • nausea & vomiting
  • diarrhea
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11
Q

What is a major difference between first generation and second generation antihistamines?

A

First generation agents are sedating & second generation agents are non-sedating (less sedating)

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12
Q

What are first generation Antihistamine agents are often used for?

A

anti-nausea and anti-vomiting

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13
Q

First Generation Antihistamine Drugs

A

Hydroxizine (good for severe itching)

Meclizine

Promethazine

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14
Q

Stimulation of ______ can trigger nausea & vomiting.

A

chemoreceptor trigger zone (CTZ)

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15
Q

Which antihistamine is good for severe itching?

A

hydroxyzine

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16
Q

Effects of Hydroxyzine & Meclizine on the body

A

↑↑ CNS-depressant effects

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17
Q

Effects of Promethazine on the body

A
  • Anti-Acetylcholine (anti-ACh), Anti-Dopamine, & Antihistamine effects
  • ↑↑ sedation
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18
Q

Promethazine is mainly used as _______

A

antiemetic

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19
Q

Second Generation Antihistamine Mechanism of Action

What do second generation antihistamines cause?

A

H1 antagonist

  • Less Sedation … ↓ CNS penetration
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20
Q

Second Generation Antihistamine Drugs

A
  • Cetirizine (Zyrtec) - can be sedating
  • Levocetirizine (Xyzal)
  • Loratadine (Claritin)
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21
Q

What is unique about second generation antihistamines?

A
  • work peripherally (not in the CNS)
  • don’t work well for anti-nausea / anti-vomiting
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22
Q

Characteristics of Parkinson’s Disease

A
  • Limb muscle rigidity
  • Resting tremor
  • Bradykinesia (slow movement)
  • Postural instability
  • depression, psychosis, dementia
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23
Q

What is the cause of Parkinson’s Disease?

A

loss of dopamine releasing neurons in the nigrostriatal pathway

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24
Q

Explain what is meant by inhibiting the inhibitor in Parkinson’s Disease

A

When dopamine releasing neurons are lost, the ability to turn off GABA neurons is lost.

Therefore, GABA neurons are turned on more often releasing more & more GABA which affects movement (ACTIVE GABA SLOWS MOVEMENT)

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25
Q

What compound in the brain enhances the effects of GABA (slowing of movement)

A

Acetylcholine

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26
Q

If Parkinson’s Disease is caused by too much activity of the GABA neuron due to the loss of dopamine releasing neurons, what are the main options for treating Parkinson’s Disease?

A
  • drugs that help the brain make more dopamine
  • drugs that act like dopamine
  • blocking acetylcholine in the brain
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27
Q

What is Levodopa?

A

dopamine precursor meaning neurons turn it INTO dopamine

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28
Q

Why is Levodopa often given with Carbidopa?

A

Carbidopa PREVENTS Levodopa from being turned into Dopamine OUTSIDE of the brain. This allows Levodopa to get into the brain before it is synthesized into Dopamine

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29
Q

What is one important fact to remember when giving / for patients who take Levodopa?

A

It should not be taken with food to minimize competition with transport pumps which can lead to delayed uptake of the drug

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30
Q

What is the most common side effect associated with Levodopa?

A

Dyskinesia (occurs in up to 80% of patients)

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31
Q

What is “Wearing Off” in regard to Parkinson’s Disease?

A

as Parkinson’s progresses (declining dopamine concentrations) each dose of Levodopa lasts for a shorter amount of time

↓ drug concentration = ↑ symptoms

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32
Q

What is “On-Off” in regard to Parkinson’s Disease?

A

patient is doing well on medication (Levodopa) and suddenly symptoms come back

  • NOT related to concentration
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33
Q

What is the difference in “Wearing Off” and “On-Off” in regard to Levodopa and Parkinson’s Disease?

A

WEARING OFF: as Parkinson’s progresses, the dose of Levodopa lasts for a shorter amount of time
* ↓ drug concentrations = ↑ symptoms

ON-OFF: patient is doing well on Levodopa and suddenly their symptoms come back
* NOT related to drug concentration

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34
Q

Side Effects of Levodopa

A
  • DYSKINESIA (most common)
  • Nausea / Vomiting
  • Orthostatic Hypotension
  • Psychosis
  • Sedation
  • ↑ risk of Melanoma
  • discoloration of sweat & urine
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35
Q

What does Dopamine do in the Central Nervous System (CNS)?

A
  • voluntary movement
  • cognition
  • motivation
  • reward / punishment
  • sleep
  • inhibition of prolactin (hormone from pituitary)
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36
Q

What does Dopamine do in the Peripheral Nervous System (PNS)?

A
  • Blood Pressure regulation
  • Regulation of peristalsis (inhibition)
  • Nausea / Vomiting
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37
Q

Dopamine Agonist Drugs

A
  • Pramipexole (Mirapex)
  • Ropinirole (ReQuip)
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38
Q

Dopamine Agonists Mechanism of Action

A

bind to and activate dopamine receptors

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39
Q

Side Effects of Dopamine Agonists

A
  • Hallucinations
  • Sleepiness
  • Orthostatic Hypotension
  • Impulse Control Disorders (ICD)
  • Nausea & Vomiting
  • Syncope
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40
Q

What Parkinson’s Disease Drug Class causes Impulse Control Disorder (ICD)?

A

Dopamine Agonists

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41
Q

How do Dopamine Agonists differ from Levodopa?

A
  • Less effective
  • Don’t treat movement disorders
  • Better tolerated (than Levodopa), less side effects
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42
Q

What occurs when Anticholinergic (antimuscarinic) receptors in the body are blocked?

A
  • dry mouth (Salivation)
  • dry eyes (Lacrimation)
  • urinary hesitancy (Urination)
  • constipation (Defecation)
  • Tachycardia
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43
Q

What do Procholinergic drugs do to the body?

A
  • Salivation = ↑ saliva production
  • Lacrimation = ↑ tears
  • Urination = ↑ frequency
  • Defecation = diarrhea
  • Bradycardia
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44
Q

What do Anticholinergic (antimuscarinic) drugs do to the body?

A
  • Salivation = dry mouth
  • Lacrimation = dry eyes
  • Urination = urinary hesitancy
  • Defecation = constipation
  • TACHYCARDIA
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45
Q

What do anticholinergics (antimuscarinics) to the parasympathetic nervous system?

A

BLOCK the PNS causing dry mouth, dry eyes, constipation, urinary hesitancy, & tachycardia

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46
Q

What compound activates cholinergic receptors?

A

acetylcholine

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47
Q

What do anticholinergics (antimuscarinics) block?

A

histamine AND muscarinic receptors (blocks effects of acetylcholine at muscarinic receptors)

  • leads to dry eyes, dry mouth, urinary hesitancy, constipation, & tachycardia *
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48
Q

Anticholinergic Agent Drugs

A

Benztropine (Cogentin)

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49
Q

Anticholinergic Agent Drugs Mechanism of Action

A

Block muscarinic receptors in the brain (and entire body)

  • block ACh at muscarinic receptors *
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50
Q

Which drug class does NOT work well for Parkinson’s Disease?

A

Anticholinergic Agents

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51
Q

When are Anticholinergic Drugs used?

A

to enhance the actions of Levodopa or to enhance the actions of a dopamine receptor agonist

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52
Q

Anticholinergic Drugs are often used in conjunction with what other drug classes?

A

Levodopa (Dopamine Precursor)

Dopamine Receptor Agonist

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53
Q

Adverse Side Effects of Anticholinergic Drugs

A
  • Dry mouth
  • Dry eyes
  • Urinary hesitancy
  • Constipation
  • Tachycardia
  • Drowsiness
  • Confusion
  • Memory Problems
  • Delusions
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54
Q

Symptoms of Alzheimer’s Disease

A

COGNITIVE DYSFUNCTION
* memory loss
* aphasia (speech)
* apraxia (movement)
* disorientation
* loss of executive function

NEUROPSYCHIATRIC SYMPTOMS
* psychotic symptoms
* inappropriate behavior
* depression

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55
Q

Cognitive Dysfunction Symptoms Associated with Alzheimer’s Disease

A

memory loss
aphasia
apraxia
disorientation
loss of executive funciton

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56
Q

Neuropsychiatric Symptoms Associated with Alzheimer’s Disease

A

psychotic symptoms
inappropriate behavior
depression

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57
Q

What drug class is the first line of action for patients with mild to moderate Alzheimer’s Disease?

A

Cholinesterase Inhibitors

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58
Q

Cholinesterase Inhibitors Mechanism of Action

A

Inhibit Cholinesterase by breaking down Acetylcholine (ACh)

ACh –> Choline + Acetic Acid

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59
Q

What cholinesterase inhibitor is used in the treatment of MILD–MODERATE Alzheimer’s Disease?

A

Donepezil (ODT - orally disintegrating tablet)

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60
Q

What cholinesterase inhibitor is used in the treatment of MODERATE–SEVERE Alzheimer’s Disease?

A

Memantine (Namenda)

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61
Q

Memantine Mechanism of Action

A

Blocks activation of glutamate receptors

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62
Q

Adverse Side Effects of Memantine

A
  • Confusion
  • Constipation
  • Coughing
  • Dizziness
  • Hallucinations
  • Headache
  • Hypertension
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63
Q

What is unique about Memantine?

A
  • long half-life (60-80 hours)
  • NMDA Antagonist
    - NMDA = specific glutamate receptor
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64
Q

What is important to avoid when using cholinesterase inhibitors?

A

avoid abrupt discontinuation

  • can result in acute impairment in cognition and / or behavioral problems
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65
Q

Blocking cholinesterase does what to acetylcholine levels?

A

↑ ACh in the brain

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66
Q

What type of drug are cholinesterase inhibitors?

A

procholinergic (Muscarinic drugs)

cause:
   * diarrhea
   * bradycardia
   * urinary frequency
   * ↑ salivation
   * ↑ tears
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67
Q

Side Effects of Cholinesterase Inhibitors

A
  • Bradycardia
  • ↑ Salivation
  • ↑ Lacrimation (tears)
  • Urinary frequency
  • Diarrhea
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68
Q

What Drug Classes & Medications in each Class are used to treat Parkinson’s Disease

A
  • Dopamine Precursor (Levodopa)
  • Dopamine Agonists (Pramipexole, Ropinirole)
  • Anticholinergic Agents (Benztropine)
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69
Q

Which Drug Classes are used in the treatment of Parkinson’s Disease?

A
  • Dopamine Precursor
  • Dopamine Agonists (activate dopamine)
  • Anticholinergic Agents
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70
Q

Which drugs are used in the treatment of Parkinson’s Disease?

A
  • Levodopa
  • Pramipexole
  • Ropinirole
  • Benztropine
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71
Q

What is asynchronous dosing?

A

uneven interval of time between dosing; doses are crammed together and then there is a window with no drug in your body

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72
Q

Give an example of asynchronous dosing BID.

A

Take one dose with breakfast, the next dose at lunch, & then nothing until breakfast the next day

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73
Q

Organic Nitrates Mechanism of Action

A

donate nitric oxide (NO) to blood vessels making it a STRONG VASODILATOR

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74
Q

Organic Nitrate Therapeutic Use

A

ANGINA

  • also used for HTN & heart failure
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75
Q

What is Tachyphylaxis?

A

rapid development of drug resistance

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76
Q

Risks & Drug Interactions associated with Organic Nitrates

A

RISKS: tachyphylaxis (rapid development of drug resistance) – must have 8 hours per day drug-free

DRUG INTERACTIONS
* hypotensives, PDE5 inhibitors (Treat ED)

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77
Q

Adverse Side Effects of Organic Nitrates

A
  • Headache
  • Orthostatic hypotension
  • Reflex tachycardia (HR ↑ due to ↓ in BP)
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78
Q

What is reflex tachycardia?

A

Increase in heart rate due to a drop in blood pressure

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79
Q

Organic Nitrate Drugs

A
  • Nitroglycerin
  • Isosorbid mononitrate
80
Q

What is the shelf-life of nitroglycerin?

A

3-5 months from when you FIRST OPEN THE BOTTLE.

  • nitroglycerin is very unstable
81
Q

Nitroglycerin contraindications…who should not use Nitroglycerin?

A

individuals taking anticholinergics due to potentially having a dry mouth

82
Q

What are signs and symptoms associated with Hypothyroidism?

A
  • Lethragy
  • Fatigue
  • Cold & dry skin
  • Cold / Heat intolerance
  • Hair loss
  • ↑ cholesterol
83
Q

How to diagnose hypothyroidism based on labs.

A

↑ TSH
↓ T4

84
Q

Medication for hypothyroidism & facts about it.

A

Levothyroxine
* synthetic T4
* give on an empty stomach

85
Q

Drug interactions with Levothyroxine

A

Enzyme inducers

Chelation

86
Q

Why can’t Levothyroxine be taken with Enzyme Inducers?

A

Enzyme inducers ↑ metabolism and therefore metabolize Levothyroxine more quickly

87
Q

Why is Levothyroxine given on an empty stomach?

A

During chelation minerals & drugs in the gut at the same time bind together meaning you cannot absorb another drug at the same time because that drug will bind to the minerals & other drugs

88
Q

What is levothyroxine?

A

synthetic T4

89
Q

What is bioequivalence?

A

two drugs have an equal rates and extents of absorption

90
Q

When proving bioequivalence of two drugs, what do drug companies have to prove?

A

there is between 80 - 125% of the drug in the blood stream with the generic drug as there is with the brand name of the drug

91
Q

What are two thyroid products used most often?

A

Levothyroxine - T4

Thyroid (Armour Thyroid) - T3 & T4

92
Q

Symptoms of Hyperthyroidism

A
  • Palpitations
  • Heat Intolerance
  • Diaphoresis
  • Tremor
  • Weight Loss
  • Anxiety
  • Psychosis
  • Exophthalmos (eye bulging)
93
Q

What is another name for Hyperthyroidism?

A

Graves Disease

94
Q

Treatment for Graves Disease

A
  • Beta Blockers
  • Anti-Thyroid Drugs
95
Q

What anti-thyroid drug is used for graves disease and mechanism of action

A

Methimalzole

*blocks thyroid gland from producing T3 & T4

96
Q

Severe Side Effects of Methimalzole

A
  • Agranulocytosis
  • Hepatitis or Hepatic Failure
97
Q

What are the 3 types of opioids?

A

1.) Pure Agonists

2.) Mixed Agonist-Antagonists

3.) Antagonists

98
Q

What is a Pure Agonist Opioid?

A

acts as agonist at the receptor

  * μ & k receptors
99
Q

What is a Mixed Agonist-Antagonist Opioid?

A

Acts one way at the mu (μ) receptor & another way at the kappa (k) receptor

  • gives you what you DO want (pain relief) and DON’T want (addiction, euphoria, etc.)
100
Q

What is an Antagonist Opioid?

A

completely blocks the receptors preventing activation

*μ & k receptors

101
Q

Adverse Effects of Pure Opioid Agonists

A
  • RESPIRATORY DEPRESSION
    • tolerance develops
    • less sensitive to CO2
    • ↑ by CNS depressants
  • CONSTIPATION
    • ↓ speed of GI tract motion
    • usually need stool softener & stimulant

OTHER
- sedation
- euphoria / dysphoria
- miosis (pupil constriction)
- ↓ cough reflex
- orthostatic hypotension
- ↑ intracranial pressure

102
Q

Primary Adverse Effects of Opioid Agonists

A
  • Respiratory Depression
  • Constipation
  • Sedation
  • Euphoria / dysphoria
  • ↓ cough reflex
  • orthostatic hypotension
  • ↑ intracranial pressure (due to build up of CO2)
103
Q

Opioid Agonist Tolerance

A

As your body gets used to the drug, you need a higher dose in order to get the same effects

104
Q

What is Cross-Tolerance (in terms of opioids)?

A

occurs when developing a tolerance for 1 substance leads to a tolerance for another substance

105
Q

What should “equianalgesic” doses be reduced by (opioids)?

A

25 - 50% decrease

 - helps prevent overdose
106
Q

3 Phases of the Signs of Opioid Agonist Physical Dependence

A

1.) yawning, rinorrhea, sweating

2.) anorexia, irritability, tremor

3.) violent sneezing, weakness, N/V, abdominal cramps, muscle spasms

107
Q

When does opioid dependence become a concern?

A

when someone is on opioids for greater than 2 weeks

108
Q

Opioid Agonist Drugs

A
  • Morphine
  • Oxycodone
  • Hydrocodone
  • Hydromorphine
109
Q

Patients with what condition should not be given Morphine?

A

impaire renal function

110
Q

What liver enzyme turns Codeine into Morphine?

A

CYP2D

  • individuals without this enzyme do NOT get pain relief from morphine
111
Q

Pharmacogenetics

A

how genes influence an individual’s response to certain drugs

112
Q

Dual Action Opioid Agonist

A

Tramadol

113
Q

What is unique about dual action opioid agonists like tramadol?

A

it’s a weak receptor agonist (mu receptor) & has less potent opioid-like effects

114
Q

Mixed Agonist-Antagonists

A
  • Lower potential for abuse & respiratory depression
  • Analgesic ‘ceiling’
  • Psychotomimetic effects (hallucinations, dysphoria, etc.)
  • some use treating opioid dependence
115
Q

What is an analgesic ‘ceiling’?

A

maximum pain relief effect you can experience

116
Q

Mixed Agonist-Antagonist Drug

A

Buprenorphine (Buprenex, Suboxone)

117
Q

What can mixed agonist-antagonists be used to treat?

A

opioid dependence

118
Q

Opioid Antagonist Drug

A

Naloxone (Narcan)

119
Q

How do Opioid Antagonists work?

A

block or prevent the activation of opioid receptors

1.) find opioid receptor

2.) push off any agonists on the receptor

3.) occupies the receptor without activating it
120
Q

How do opioid antagonists act centrally?

A

Centrally
- overdose
- abuse deterrent
- weight loss
- EtOH dependence

121
Q

How do opioid antagonists act peripherally?

A

Peripherally
- treatment of opioid-related constipation

  • treatment of post-operative ileus
  • do not cross BBB or enter the brain
122
Q

What 2 ways do opioid antagonists work?

A

CENTRALLY - cross BBB & work on the brain

PERIPHERALLY - do NOT cross BBB & work on receptors outside the brain

123
Q

Nonsteroidal Antiinflammatory Drugs (NSAIDs) mechanism of action

A

block the production of prostaglandins by inhibiting COX-1 & COX-2

124
Q

NSAID Drugs

A
  • Ibuprofen
  • Meloxicam
  • Naproxen
  • Diclofenac
  • Celecoxib
125
Q

Which NSAID Drugs are non-specific?

A
  • Ibuprofen
  • Meloxicam
  • Naproxen
  • Diclofenac
126
Q

What do non-specific NSAIDs inhibit?

A

COX-1 & COX-2

127
Q

What does Celecoxib inhibit?

A

COX-2

128
Q

Side Effects of NSAIDs

A
  • Hypertension
  • ↓ renal function
  • ↓ platelet function
  • Fluid retention
  • Bronchospasms
  • Hepatotoxicity
  • GI Bleeds & Ulcers
129
Q

Why do NSAID Toxicities occur and what do they do?

A
  • make the stomach / GI system more vulnerable to damage by stomach acid
  • cause constriction / tightening of the afferent arteriole (kidneys)
130
Q

Who is at high risk of NSAID-related GI Bleeding?

A
  • patients on aspirin, warfarin, or steroids
  • patients with a prior history of ulcers or GI bleeds
  • patients over 65 years old
131
Q

What is the difference in COX-1 & COX-2?

A

COX-1 is constitutively expressed meaning it is always around all day long, everyday, regardless

COX-2 is inducible meaning it is not always expressed & is only around when you have an injury inflammation

132
Q

Treatment options to prevent NSAID-Related GI Bleeds

A
  • concurrent misoprostol (synthetic prostaglandin - uncommon)
  • concurrent PPI (common)
  • change to COX-2 selective agent
133
Q

What is unique about Ketorolac (Toradol)?

A
  • super NSAID (considered to be equivalent to an opioid in terms of pain relief)
  • used for a maximum of 5 days
  • dose adjustment for anyone 65+ or under 50 kg
134
Q

Ketorolac (Toradol) Contraindications

A
  • prior or active ulcer disease
  • high risk of bleeding
  • concurrent Aspirin, NSAIDs, or probenecid (gout)
  • advanced / high risk of renal disease
135
Q

Acetaminophen Mechanism of Action

A

inhibits CENTRAL prostaglandin synthesis

  • only works IN the brain
136
Q

Contraindications / Side Effects of Acetaminophen Toxicity

A
  • Caution concerning hepatotoxicity
    • liver toxicity / damage is a a concern with acetaminophen but is much LESS common than GI bleeds with NSAIDs
137
Q

What do NSAIDs and Acetaminophen do to temperature & pain?

A

reduce pain & temperature set point

138
Q

Explain Acetaminophen Hepatotoxicity

A

1.) CYP2E1 turns acetaminophen into NAPQU which is a highly reactive byproduct.

2.) Once NAPQI is formed, it looks for other things to bind to.

3.) The liver produces Glutathione which neutralizes reactive byproducts.

** IN THE CASE OF HEPATOTOXICITY, THERE IS NOT ENOUGH GLUTATHIONE TO NEUTRALIZE THE NAPQI

139
Q

How is most Acetaminophen broken down?

A

by Phase II Metabolism

- liver attaches acetaminophen to a large water molecule so that it is inactive & can easily leave the body
140
Q

2 Ways Acetaminophen is Broken Down

A

1.) Phase II Metabolism (95% of Acetaminophen)

2.) CYP2E1 (5% of Acetaminophen) into NAPQI

141
Q

Acetaminophen Contraindications & Side Effects / Risk Factors

A
  • leading cause of acute liver failure
  • RISK FACTORS: higher doses, EtOH use, chronic liver disease
142
Q

What actions has the FDA taken to help prevent hepatotoxicity from Acetaminophen?

A
  • restrict dose in combo products to 325 mg
  • consider limiting maximum dose
143
Q

Steroid Mechanism of Action

A

steroids change gene transcription

144
Q

Glucocorticoids / Corticosteroids Mechanism of Action

A

Inhibit COX-1 & COX-2

145
Q

What do Steroids help regulate?

A

blood glucose levels & BP / vascular tone

146
Q

What is the HPA Axis?

A

how the body auto-regulates its on steroid production (Hypothalamus signals Pituitary which signals Adrenal glands to ↑ cortisol production)

147
Q

Key Glucocorticoid Toxicities

A

** HPA-Axis Suppression*

  • ↑ infection risk, leukocytosis
  • Growth retardation
  • Cataracts (can worse with glaucoma)
  • Inhaled: oral candidiasis, dysphonia
148
Q

What is HPA-Axis Suppression & when does it occur?

KNOW THIS - SHORT ANSWER QUESTION!!!!!

A

OCCURS: pt is on steroids high dose for long period of time

  • The body senses the steroid as similar to cortisol. This causes the body to think there is enough cortisol & the body / HPA axis tells the adrenal glands to stop producing cortisol

(H –> P –> A = no cortisol production if on ↑ dose steroids for long enough time)

149
Q

Explain HPA Axis Suppression in 1-2 Sentences (SHORT ANSWER)

A

If a patient takes steroids at a high dose for a long enough period of time, the body recognizes steroids as cortisol. This causes the HPA axis to tell the adrenal glands to stop producing cortisol, therefore causing the HPA Axis to shut off & less cortisol is produced.

150
Q

What is HPA Axis Suppression & what are the 2 clinical consequences of HPA Axis Suppression?

A

HPA AXIS SUPRESSION: if a patient takes steroids at a high dose for a long time, the body recognizes the steroids as cortisol which tells the HPA Axis to stop producing cortisol & shut off.

CONSEQUENCES:

1.) ADRENAL ATROPHY (shrink/shrivel) - TAPER OFF
- NOT stop steroid suddenly (taper dose allows HPA axis / adrenal glands to ‘wake up’)

2.) STRESS DOSING - short term ↑ in steroid dose to account for physical stress (prior to surgery, after a trauma / MVA, etc.)

151
Q

When does Steroid-Related “Immunosuppression” occur?

A

doses greater than 20 mg/day (pt over 10 kg) for 2+ weeks

152
Q

Steroid Drugs

A
  • Hydrocortisone
  • Prednisone
  • Methylprednisolone
  • Prednisolone
153
Q

What is Mineralcorticoid Potency?

A

ability of the kidneys to hold onto sodium & water

  • hydrocortison (2) has better ability to retain salt & water
  • dexamethasone (0) does not have the ability to retain salt or water (pt can become hypotensive over time or have intravascular volume depletion / ↓ BP)
154
Q

Use Steroid Comparison regarding Mineralcorticoid Potency for Prednisone, Hydrocortisone, & Methylprednisolone from HIGHEST to LOWEST Potentcy

A

1.) Hydrocortisone (2 - high ability to retain H2O & Na+)

2.) Prednisone (1)

3.) Methylprednisolone (0)

155
Q

Corticosteroid Drugs

A
  • Fluticasone
  • Budesonide
  • Triamcinolone
  • Beclomethasone
156
Q

What are the 2 ways / methods for treating Gout?

A

1.) ↓ amount of uric acid in the blood & body

2.) ↓ immune response to uric acid crystals

157
Q

Allopurinol Mechanism of Action

A

Allopurinol blocks xanthine oxidase so that the body does NOT make as much uric acid & over time there is ↓ uric acid in the blood

158
Q

Drugs for Gout

A

Allopurinol (allopurinol oxidase inhibitor)

Colchicine

159
Q

Which Gout medication is used for chronic episodes & which is used for acute episodes?

A

ACUTE: Colchicine

CHRONIC: Allopurinol

160
Q

Side Effects of Allopurinol

A
  • Liver damage (abnormal LFTs)
  • SCAR (severe skin rxn)
    • Severe Cutaneous Adverse Reactions
  • Genetic predisposition (HLA-B*58:01)
161
Q

Contraindications of Allopurinol, what drugs can allopurinol not be taken with?

A

anti-cancer drugs

162
Q

Colchicine Mechanism of Action

A

makes WBCs less flexible so they cannot get into tissue & cause inflammatory response

163
Q

Side Effects of Colchicine

A
  • GI toxicity (N/V, diarrhea, abdominal pain)
  • bone marrow suppression
  • renal failure
  • hepatotoxicity
  • seizures
  • rhabdomyolysis
164
Q

Drug categories used for migraines

A
  • Aspirin / NSAIDs/ Opioids
  • Antiemetics
  • Ergot Alkaloids
  • Serotonin Receptor Agonists
  • Prophylactic Agents
165
Q

Ergot Alkaloids Mechanism of Action (Ergotamine & Dihydroergotamine (DHE))

A

Serotonin Agonists at the 5-HT receptors - stimulate serotonin production

  • also stimulate alpha, beta, & dopamine receptors
166
Q

What do Ergot Alkaloids cause?

A

vasoconstriction in the brain (centrally) & prevent neurogenic inflammation

167
Q

Side Effects of Ergot Alkaloids

A
  • chest pain
  • paresthesias
  • ↓ peripheral pulses
  • cold, numb, painful extremities
168
Q

Who should avoid Ergot Alkaloids?

A
  • pt’s with uncontrolled HTN
  • Pregnant patients
  • pt’s with CAD/CVD
    pt’s with PVD
169
Q

Serotonin Receptor Agonists (Triptans) Mechanism of Action

A

selective serotonin agonist at 5-HT (1b / 1d) receptor

  • stimulate specific serotonin receptors
    • work in intracranial arteries, but do not work as much on the rest of the body
170
Q

Side effects of Serotonin Receptor Agonists (Triptans)

A
  • paresthesias
  • fatigue
  • dizziness
  • flushing
  • somnolence
  • “chest symptoms” (15-50%)
171
Q

What drugs should be avoided when taking Serotonin Receptor Agonists (Triptans)?

A
  • do NOT use within 24 hours of ergot alkaloids
  • be careful when using with an SSRI
  • avoid within 2 weeks of MAO inhibitor
172
Q

Serotonin Receptor Agonist (Triptan) Drugs

A
  • Rizatriptan (Maxalt)
  • Sumatriptan (Imitrex)
173
Q

Preventative Drug Therapies for Migraines

A
  • CGRP monoclonal antibodies
    - erenumab (Aimovig)
    - fremanezumab (Ajovy)
    - galcanezumab (Emgality)
  • Beta-blockers
  • Calcium channel blockers
  • Antidepressants
    • TCAs
    • SSRIs
  • Antiepileptics
    • Valproic acid
    • Topiramate
174
Q

Antiemetics Mechanism of Action

A

Chemoreceptor Trigger Zone (CTZ - not protected by BBB) & vomiting center are primarily responsible

  • can be caused by chemicals (serotonin, dopamine, histamine, neurokinin, ACh), GI & vestibular signals, smell, sight, pain, chemotherapy, anesthesia, pregnancy, migraines, radiation, infections, etc.
175
Q

Antiemetic Drugs

A

Odansetron (Zofran)

176
Q

Ondansetron (Zofran) Mechanism of Action

A

Serotonin receptor antagonist / blocker

177
Q

Side Effects of Serotonin Receptor Antagonists like Ondansetron (Zofran)

A
  • prolonged QT interval
    *can increase risk of ventricular arrhythmia as it continues to increase in length
  • constipation
  • headache
178
Q

List of all drugs on top 200 that can be used as antiemetics

A

Serotonin Receptor Antagonist
- Ondansetron (Zofran)

Antihistamines
- hydroxyzine
- meclizine (Antivert)

Antipsychotics
- promethazine (Phenergan)

179
Q

Beta-2 Adrenergic Agonists Mechanism of Action

A

** SMOOTH MUSCLE RELAXATION (in bronchioles)
- less obstructed to airflow

** MAST CELL STABILIZATION
- harder to release histamine

180
Q

Side Effects of Beta-2 Adrenergic Agonists

A
  • tremor
  • nervousness
    -hypokalemia
  • tachycardia (due to crossover to B1 receptors)
181
Q

What are Beta-2 Adrenergic Agonists useful in treating?

A

Asthma & COPD

182
Q

Long-Acting Beta-Agonists FDA Warning / Recommendations

A

1.) must be used with another controller agent (glucocorticoids, etc.)

2.) only used if asthma isn’t controlled by the glucocorticoid (or other controller agent)

3.) used for as SHORT a duration as possible

4.) when possible use combo products

183
Q

Why does a steroid need to be used in combination with a Long-Acting Beta-Agonist?

A

steroids work on beta receptors to ensure they maintain sensitivity

  • if sensitivity was lost, the LABAs would no longer work to control asthma or COPD
184
Q

Long Acting Beta-Agonists
(LABA) Drugs

A
  • Salmeterol
  • Formoterol
  • Vilanterol
185
Q

Short Acting Beta-Agonist Drugs

A
  • Albuterol
186
Q

What are the advantages and disadvantages of using inhalers?

SHORT ANSWER QUESTION - KNOW THIS!!!

A

ADVANTAGES
1.) more direct access & faster onset
2.) Less systemic side effects

DISADVANTAGES
1.) Technique - you need adequate spacing from the mouth & timing of the breath

2.) Very severe asthma attacks - pt must be able to move air in order for inhalers to work
187
Q

Leukotriene Mechanism of Action

A
  • reduce inflammation & bronchoconstriction
188
Q

Leukotriene Drugs

A
  • Zileuton
    ** Montelukast (KNOW THIS ONE ONLY)
    -Zafirlukast
189
Q

Mechanism of Action for Zileuton

A

stops production of ALL leukotrienes

190
Q

Montelukast Mechanism of Action

A

LTD4 Antagonist - blocks receptor of Leukotriene D4

191
Q

What is Montelukast used to treat?

A

asthma & allergies

192
Q

Side Effects of Leukotriene Modifiers

A
  • headaches
  • GI upset
  • ↑ LFTs
  • ↑ suicide risk
  • aggression
  • anxiety
  • depression
  • nightmares (realistic, vivid, memorable)
193
Q

(inhaled) Anticholinergic Drugs

A
  • Ipratropium
  • Tiotropium
  • Umeclidinium
194
Q

(inhaled) Anticholinergics Mechanism of Action

A

dilate airways by blocking acetylcholine

  • can cause dry secretion
195
Q

Side Effects of (inhaled) Anticholinergics

A
  • SLUD
    • dry mouth
    • dry eyes
    • urinary hesitancy
    • constipation
  • Tachycardia
  • blocks parasympathetic (rest & digest) nervous system

Pharmacology (5 decks)

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