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Pharmacology > Exam 2 Mechanism of Action, Drug Classes & Drugs, Side Effects > Flashcards

Exam 2 Mechanism of Action, Drug Classes & Drugs, Side Effects Flashcards

1
Q

What does histamine cause?

A
  • vasodilation
  • ↑ capillary permeability
  • smooth muscle constriction
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2
Q

Antihistamine Mechanism of Action

A

act as antagonist (block) at H1 receptors

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3
Q

Antihistamine Side Effects

A
  • dizziness
  • tinnitus
  • incoordination
  • blurred vision
  • nervousness
  • constipation
  • weight gain
  • insomnia
  • tremors
    *** paradoxical reaction
  • drowsiness
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4
Q

First Generation Antihistamine Drugs

A
  • hydroxyzine
  • meclizine
  • promethazine
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5
Q

What are first generation antihistamines used for?

A

nausea & vomiting

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6
Q

Second Generation Antihistamine Drugs

A
  • Cetirizine (zyrtec)
  • Levocetirizine
  • Loratadine (Claritin)
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7
Q

Which antihistamines are sedating & which are non-sedating?

A

1st Generation = sedating

2nd Generation = non-sedating

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8
Q

Second Generation Antihistamine Mechanism of Action / what is unique about them?

A

C- cannot cross BBB
- not as effective for N/V

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9
Q

Characteristics of Parkinson’s

A
  • limb rigidity
  • tremor
  • bradykinesia (slow moving)
  • depression, psychosis, anxiety, dementia, etc.
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10
Q

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

A

vast majority of drugs help the brain make more dopamine or are drugs that act like dopamine. You can also use drugs that block ACh.

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11
Q

What is the main underlying pathophysiological deficit in Parkinson’s Disease?

A

loss of dopamine releasing neurons in the nitro-striatal pathway

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12
Q

How do drugs that stimulate Dopamine effect the CNS & PNS / what do Dopamine stimulating drugs cause in the CNS & PNS?

A

CNS: voluntary movement, cognition, motivation, reward/punishment, sleep, inhibition of prolactin

PNS: BP regulation, regulation of peristalsis (inhibition), N/V

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13
Q

Drug Classes used for Parkinson’s Disease

A
  • Dopamine Precursor
  • Dopamine Agonists
  • Anticholinergic Agents
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14
Q

Drugs for Parkinson’s Disease

A
  • Levodopa (DA precursor)
  • Pramipexole (DA agonist)
  • Ropinirole (DA agonist)
  • Benztropine (Anticholinergic)
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15
Q

Dopamine Precursor Drugs for Parkinson’s Disease

A

Levodopa

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16
Q

Levodopa Mechanism of Action

A

neurons can turn Levodopa into dopamine

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17
Q

What is Levodopa given with and why?

A

Carbidopa to prevent Levodopa from becoming dopamine outside of the brain

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18
Q

Side Effects of Levodopa (Dopamine Precursor)

A
  • Dyskinesia (80%)
  • “Wearing Off”
  • “On-Off”
  • N/V
  • Orthostatic Hypotension
  • Psychosis
  • Sedation
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19
Q

What is “Wearing Off”?

A

↓ Drug Concentrations = ↑ symptoms

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20
Q

What is “On-Off”?

A

can happen at any time; not related to concentration

  • pt is doing well, then suddenly symptoms come back
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21
Q

Dopamine Agonist Drugs

A
  • Pramipexole
  • Ropinerole
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22
Q

Side Effects of Dopamine Agonists

A
  • ↑ hallucinations
  • sleepiness
  • orthostatic hypotension
  • **Impulse Control Disorder **
  • N/V
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23
Q

Dopamine Precursor Drugs for Parkinson’s, Mechanism of Action, Contraindications, & Side Effects

A

Levodopa

MOA: neurons can convert it to dopamine

SE: dyskinesia, “wearing off”, “On-Off”, N/V, orthostatic hypotension, psychosis

Contraindication: do NOT give with food, it’ll slow absorption

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24
Q

Dopamine Agonist Drugs & Side Effects

A

Pramipexole & Ropinirole

SE: hallucinations, sleepiness, orthostatic hypotension, N/V, syncope, & IMPULSE CONTROL DISORDERS

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25
Q

What are Anticholinergic / Anti-muscarinic effects?

A

Block the parasympathetic NS (rest & digest)

CAUSES SLUD
- dry mouth
- dry eyes
- urinary hesitancy
- constipation
- tachycardia

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26
Q

Anticholinergic Drugs for Parkinson’s Disease

A

Benztropine

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27
Q

Anticholinergic Mechanism of Action

A

block Acetylcholine at muscarinic receptors

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28
Q

Side Effects of Antichoinergic Drugs for Parkinson’s Disease

A
  • drowsiness
  • inattention
  • confusion
  • delusions
  • memory problems
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29
Q

Anticholinergic Drugs for Parkinson’s Disease, MOA, & Side Effects

A

Benztropine

MOA: blocks ACh at muscarinic receptors

SE: drowsiness, confusion, memory problems, delusions, inattention

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30
Q

Donepezil Mechanism of Action

A

↑ acetylcholine in the brain
- first line of action for Alzheimer’s

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31
Q

Donepezil (cholinesterase inhibitor) side effects

A
  • N/V
  • diarrhea
  • headache
  • bradycardia
  • salivation
  • sweating
  • muscle weakness

AVOID STOPPING SUDDENLY

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32
Q

Alzheimer’s Drugs

A
  • Donepezil
  • Memantine
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33
Q

Memantine Mechanism of Action

A

blocks glutamate receptor activation

  • moderate to severe alzheimer’s
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34
Q

Donepezil (cholinesterase inhibitor) side effects

A
  • N/V
  • diarrhea
  • headache
  • bradycardia
  • salivation
  • sweating
  • muscle weakness

AVOID STOPPING SUDDENLY

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35
Q

Memantine Side Effects

A
  • constipation
  • confusion
  • dizziness
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36
Q

(Organic) Nitrate Drugs

A
  • Nitroglycerin
  • Isosorbide mononitrate
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37
Q

What is the shelf-life of Nitrates?

A

3-5 months after you first open the bottle

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38
Q

What is asynchronous dosing?

A

an uneven interval of time between doses

  • BID could mean one dose at breakfast, one with lunch, & nothing until breakfast the next day
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39
Q

What are Nitrates used to treat?

A
  • angina
  • hypertension
  • heart failure
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40
Q

Nitrate mechanism of action

A

vasodilator (mainly the veins)

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41
Q

Side Effects of Nitrates

A
  • headache
  • orthostatic hypotension
  • reflex tachycardia
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42
Q

Contraindications of Nitrates

A

Risk of Rapid Development of Resistance
- use lowest dose possible
- need 8 hrs without drugs in system per day

Cannot be used with hypotensives

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43
Q

(Organic) Nitrate Drugs, Mechanism of Action, Side Effects, & Contraindications

A
  • Nitroglycerin
  • Isosorbide mononitrate

MOA: vasodilator (donates a nitric oxide to blood vessels)

SE: headache, orthostatic hypotension, reflex tachycardia

Contraindications:
- need 8 hr / 24 hrs drug free
- do not take with hypotensive (can ↓ BP too much)

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44
Q

Hypothyroidism Drugs

A

Levothyroxine - synthetic T4

Thyroid - synthetic T3 & T4

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45
Q

Contraindications of Hypothyroidism Drugs

A

Give on EMPTY STOMACH

  • Chelation (↓ absorption)
  • Enzyme Inducers (↑ metab)
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46
Q

Symptoms of Hypothyroidism

A
  • lethragy
  • fatigue
  • cold, dry skin
  • cold intolerance
  • hair loss
  • ↑ cholesterol
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47
Q

Hypothyroidism Drugs & Contraindications

A

Levothyroxine (T4)
Thyroid (T3 & T4)

CONTRAINDICATIONS
- give on empty stomach
- chelation (↓ absorption)
- enzyme inducers (↓ metab)

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48
Q

Symptoms of Hyperthyroidism

A
  • heat intolerance
  • palpitations
  • weight loss
  • exophthalmos
  • anxiety
  • diaphoresis
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49
Q

Drugs for Hyperthyroidism

A

Methimazole

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50
Q

Anti-Thyroid Drugs Mechanism of Action

A
  • inhibits synthesis of T3 & T4
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51
Q

Side Effects of Anti-Thyroid Drugs

A
  • agranulocytosis
  • hepatitis or hepatic failure
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52
Q

Anti-Thyroid (Hyperthyroidism) Drugs, MOA, & SE

A

Methimazole

MOA: blocks synthesis of T3 & T4

SE: agranulocytosis & liver disease

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53
Q

Types of Opioids

A

Opioid Agonists
Mixed Agonist-Antagonist
Opioid Antagonist

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54
Q

Opioid Agonist Drugs

A
  • Morphine
  • Oxycodone
  • Hydrocodone
  • Hydromorphone
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55
Q

Mixed Opioid Agonist-Antagonist Drugs

A

Buprenorphine

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56
Q

Opioid Antagonist Drugs

A

Naloxone (narcan)

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57
Q

Side Effects of Opioid Agonists

A

**Respiratory Depression **

  • Constipation
  • Sedation
  • orthostatic hypotension
  • urinary retention
  • ↑ intracranial pressure
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58
Q

Opioid Agonist Drugs, Mechanism of Action, & Side Effects

A

Morphine
Oxycodone
Hydrocodone
Hydromorphone

MOA: agonist at mu & kappa receptors

SE: Respiratory Depression, constipation, sedation, euphoria, orthostatic hypotension, emesis, cough reflex, ↑ intracranial pressure

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59
Q

What is cross-tolerance?

A

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

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60
Q

How do you prevent cross-tolerance with opioids?

A

Reduce “equianalgesic” dose by 25-50%

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61
Q

When does physical dependence of opioids become a concern?

A
  • with chronic use (2+ weeks)
  • do NOT stop suddenly

1.) yawning, rhinorrhea, sweating

2.) anorexia, irritability, tremor

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

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62
Q

What is Pharmacogenetics?

A

how genetics influence people’s responses to drugs

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63
Q

What role dose CYP2D6 play in terms of Codeine?

A

CYP2D6 turns Codeine into Morphine in the liver

64
Q

Dual Action Opioid Agonist Drugs

A

Tramadol

  • weak receptor agonist
  • less potent opioid-like effects
  • can treat neuropathic pain
65
Q

Mixed Agonist-Antagonist Drugs

A

Buprenorphine (suboxone)

66
Q

What is Buprenorphine used to treat in some cases?

A

opioid dependence

67
Q

Side Effects of Mixed Agonist-Antagonist Drugs

A

hallucinations
dysphoria (negative feeling)
potential

68
Q

Mixed Agonist-Antagonist Drugs & Side Effects

A

Buprenorphine (suboxone)

Se: hallucinations, dysphoria (negative feelings), analgesic ceiling

69
Q

What is Analgesic “Ceiling”?

A

there’s a maximum pain relief effect you can expect

70
Q

Opioid Antagonist Mechanism of Action

A

block or prevent the activation of opioid receptors

71
Q

Opioid Antagonist Drugs

A

Naloxone (narcan)

72
Q

How do Opioid Antagonists work centrally and peripherally?

A

CENTRAL: overdose, abuse deterrent (also weight loss & EtOH dependence)

PERIPHERAL: treatment of opioid-related constipation & post-operative ileus

73
Q

Opioid Antagonist Drugs, Mechanism of Action, & How they work centrally & peripherally

A

Naloxone (narcan)

MOA: block / prevent activation of opioid receptors

CENTRALLY: overdose, abuse deterrent (also for weight loss & EtOH dependence)

PERIPHERALLY: treatment of opioid-related constipation

74
Q

Nonsteroidal Antiinflammatory Drugs (NSAIDs) Mechanism of Action

A

Prevent the production of prostaglandins by blocking COX-1 & COX-2

75
Q

How do NSAIDs effect temperature set point, pain, & inflammation?

A

↓ temperature set point
↓ pain
↓ inflammation

76
Q

NSAID Drugs

A
  • Ibuprofen
  • Meloxicam
  • Naproxen
    -Diclofenac
    -Celecoxib
77
Q

Which NSAIDs are Non-specific & which are specific?

A

Non-specific: inhibit COX-1/2
- iburprofen
- meloxicam
- naproxen
- diclofenac

Specific: inhibit COX2
- Celecoxib

78
Q

Side Effects NSAID Toxicicites

A
  • hypertension
  • ↓ renal function
  • ↓ platelet function
  • fluid retension
  • GI bleeds / ulcers
  • hepatotoxicity
  • bronchospasm
79
Q

NSAID Drugs, Mechanism of Action, & Side Effects from Toxicities

A
  • Ibuprofen
  • Meloxicam
  • Naproxen
  • Diclofenac
  • Celecoxib (inhibit COX-2)

MOA: prevent the production of prostaglandins by inhibiting / blocking COX-1 & COX-2

SE: ↓ renal function, ↓ platelet function, hypertension, GI bleeds / ulcers, fluid retention, bronchospasm, hepatotoxicity

80
Q

NSAID Related GI Bleed Management

Who is at high risk?
What are treatment options?

A

HIGH RISK
- on aspirin, warfarin, steroids
- prior hx of GI bleeds/ulcers
- 65+ years old

TREATMENT OPTIONS
- misoprostol (synthetic prostaglandin)
- PPI (↓ stomach acid)
- change to COX-2 agent

81
Q

What does it mean that COX-1 is constitutively expressed?

A

COX-1 is always around, all day every day

82
Q

What does it mean that COX-2 is inducible?

A

COX-2 is only present during injury or inflammation

83
Q

What is the difference in terms of when COX-1 & COX-2 are present?

A

COX-1 is ALWAYS around (constitutively expressed) & COX-2 is only present during injury or inflammation (inducible)

84
Q

Guidelines & Contraindications of Ketorolac (Toradol)

A
  • Super NSAID
  • maximum of 5 days use
  • dose adjustment for 65+ or less than 50 kg

CONTRAINDICATIONS
- prior / active ulcer
- advanced renal dx or ↑ risk
- ↑ risk of bleeding
- on aspirin, NSAID, or probenecid (for gout)

85
Q

Acetaminophen Mechanism of Action

A

blocks prostaglandin production, but only works in the brain (centrally)

  • reduces pain & lowers temperature (does not help with swelling)
86
Q

Toxicity associated with Acetaminophen

A

liver damage / toxicity is a concern but is much LESS common than GI bleeds with NSAIDs

87
Q

Acetaminophen Risk Factors & FDA Actions

A

leading cause of acute liver failure

Hi

Risk Factors: ↑ doses, EtOH use, chronic liver disease

FDA ACTIONS: restrict dose in combo products to 325 mg & consider limiting maximum doses

88
Q

Acetaminophen MOA, toxicity, risk factors, & FDA Actions

A

MOA: inhibits production of prostaglandins in the brain (centrally)

Toxicity: concerned with liver toxicity, but is less common than GI Bleeds with NSAIDs (leading cause of acute liver failure)

Risk Factors: ↑ doses, EtOH use, chronic liver disease

FDA Actions: restrict dose in combo products to 325 mg & consider limiting maximum doses

89
Q

Steroids Mechanism of Action

A

Change gene transcription

  • increase / decrease translation of certain genes
90
Q

What do steroids play an important role in?

A

maintaining blood glucose levels & blood pressure

91
Q

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

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.)

92
Q

Side Effects of Steroids

A
  • ↑ risk of infection
  • leukocytosis (↑ WBC count not from infection)
  • growth retardation
  • cataracts
  • oral candidiasis
93
Q

Steroid Related Immunosupression

A

Doses greater than 20 mg / day for 2+ weeks

94
Q

What is Mineralcorticoid Potency in terms of Steroid Comparison?

A

ability of the kidneys to hold onto sodium & water

95
Q

Compare the mineralocorticoid potency of prednisone, methylprednisolone, & hydrocortisone from highest to lowest potency.

A

Hydrocortisone (2)
- ↑ability to retain H2O & NA+

Prednisone (1)

Methylprenisolone (0)
- no ability to retain Na+ & H2O; can lead to ↓ BP

96
Q

Corticosteroid Drugs

A
  • fluticasone
  • budesonide
  • triamcinolone
  • beclomethasone
97
Q

Corticosteroid Drugs, MOA, & SE

A

Fluticasone
Budesonide
Triamcinolone
Beclomethasone

MOA: change gene translation

SE: HPA-Axis Suppression; leukocytosis (↑ WBC count); ↑ risk of infection; growth retardation; cataracts

98
Q

What are the 2 ways to treat Gout?

A

1.) ↓ uric acid concentrations in the blood & body

2.) ↓ immune response to uric acid crystals

99
Q

Drugs for treating Gout

A

Allopurinol (chronic)

Colchicine (acute)

100
Q

Xanthine Oxidase Inhibitor Drug, purpose, SE, & contraindications

A

Allopurinol
- for chronic gout

SE: liver damage (abnormal LFTs); SCAR (severe skin rxn); genetic predisposition

Contraindications: anti-cancer drugs

101
Q

Colchicine Purpose, MOA, & SE

A

for acute gout episodes

MOA: impairs WBCs (leukocytes) so they cannot get to the tissue & cause inflammation (prevents inflammation)

SE: N/V, Diarrhea, abdominal pain, rhabdomyolysis, seizures, bone marrow suppression, renal failure, hepatotoxicity

102
Q

Colchicine MOA

A

impairs WBCs so they cannot migrate to tissue & cause inflammation

103
Q

Colchicine Side Effects

A
  • N/V
  • Diarrhea
  • Abdominal Pain
  • Bone marrow suppression
  • Renal failure
  • Hepatotoxicity
  • Seizures
  • Rhabdomyolysis
104
Q

Drug classes used for migraine treatment

A
  • aspirine, NSAID, opioids
  • antiemetics
  • ergot alkaloids
  • serotonin receptor agonists
  • prophylactic agents
105
Q

Ergot Alkaloid (DHE) Mechanism of Action

A

Serotonin agonist at the 5-HT1 receptors - stimulates serotonin production

  • also stimulates alpha, beta, & dopamine receptors
106
Q

Side Effects of Ergot Alkaloids

A

chest tightness
cold, numb, painful extremities
paresthesias
↓ peripheral puulses

107
Q

Contraindications of Ergot Alkaloids

A

avoid with uncontrolled HTN, CAD/CVD, PVD, & pregnancy

108
Q

Ergot Alkaloids should not be taken within 24 hours of taking what other drug class?

A

Serotonin Receptor Agonists (Triptans)

109
Q

Ergot Alkaloids (DHE) MOA, SE, & Contraindications

A

MOA: serotonin agonist at 5-HT1 receptor (stimulates serotonin; also works to stimulate alpha, beta, & dopamine receptors)

SE: chest tightness; cold, numb, painful extremities; paresthesias; ↓ perisperhal pulses

CONTRAINDICATIONS: avoid with uncontrolled HTN, CAD/CVD, PVD, pregnancy

110
Q

Serotonin Receptor Agonists Mechanism of Action

A

stimulate specific serotonin receptors (5-HT 1B/1D)

  • normalize dilated intracranial arteries
111
Q

Serotonin Receptor Agonists Side Effects

A
  • paresthesias
  • fatigue
  • dizziness
  • flushing
  • “chest symptoms” (15-50%
112
Q

Serotonin Receptor Agonists Contraindications

A
  • don’t take within 24 hours of an ergot alkaloid
  • be careful with SSRIs
113
Q

Serotonin Receptor Agonist Drugs

A

Rizatriptan (maxalt)
Sumatriptan (imitrex)

114
Q

Serotonin Receptor Agonist Drugs, MOA, SE, & Contraindications

A

Rizatriptan (maxalt)
Sumatriptan (imitrex)

MOA: stimulates specific serotonin receptors (5-HT 1B/1D)

SE: paresthesias, fatigue, dizziness, flushing, “chest symptoms” (15-50%

Contraindications: avoid within 24 hrs of ergot alkaloid & be careful with SSRIs

115
Q

Antiemetic Drugs

A

** Ondansetron (Zofran)

ANTIHISTAMINES: hydroxyzine & meclizine

ANTIPSYCHOTIC: promethazine (phenergan)

116
Q

Antiemetic Mechanism of Action

A

5-HT3 Antagonist - blocks serotonin receptor

117
Q

Side Effects of Antiemetics

A
  • prolonged QT-interval
  • constipation
  • headache
118
Q

Beta-2 Adrenergic Agonists Mechanism of Action

A

Binds to & activates the Beta-2 receptor

  • smooth muscle relaxation (in bronchioles)
  • mast cell stabilization (makes it harder for mast cells to release histamine)
119
Q

What are Beta-2 Adrenergic Agonists used to treat?

A

Asthma & COPD

120
Q

Side Effects of Beta-2 Adrenergic Agonists

A
  • tremor
  • tachycardia
  • nervousness
  • hypokalemia
121
Q

FDA Warnings of Long-Acting Beta-Agonists (LABAs)

A

1.) must be used with another controller agent

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

3.) used for as short a duration as possible

4.) when possible use combo products

122
Q

What can overuse of a long-acting beta agonist cause?

A

↓ beta receptor sensitivity

123
Q

Beta-2 Adrenergic Agonist Drugs

A

SHORT ACTING: albuterol

LONG ACTING
- Salmeterol
- Formoterol
- Vilanterol

124
Q

Short Acting Beta-Adrenergic Agonist Drugs

A

Albuterol

125
Q

Long Acting Beta-Adrenergic Agonist Drugs

A

Salmeterol
Formoterol
Vilanterol

126
Q

What are the advantages & disadvantages of using inhalers?

A

ADVANTAGES
1.) more direct access & a faster onset
2.) less systemic side effects (works directly on the lungs)

DISADVANTAGES
1.) technique (adequate spacing from mouth & timing of breath)
2.) Very severe asthma - patient must be able to move air in order for these to work

127
Q

Beta-2 Adrenergic Agonist Drugs, Mechanism of Action & Side Effects

A

Albuterol (short acting)
Salmeterol (long acting)
Formoterol (long acting)
Vilanterol (long acting)

MOA: smooth muscle relaxation (of bronchioles) & mast cell stabilization (harder for mast cells to release histamine)

SE: tremor, tachycardia, nervousness, hypokalemia

128
Q

Leukotriene Modifying Agents Mechanism of Action

A

reduce inflammation & bronchoconstriction

129
Q

Leukotriene Modifiers (LTD4 Antagonists) Drugs

A

Montelukast

130
Q

Leukotriene Modifiers - LTD4 Antagonist Side Effects

A
  • headache
  • GI upset
  • ↑↑ LFTs
  • suicide risk
  • vivid nightmares
  • agression & depression
131
Q

Leukotriene Modifiers Drugs, MOA, & SE

A

Montelukast

MOA: reduces inflammation & bronchoconstriction

SE: headache, GI upset, ↑ LFTs, suicide risk, anxiety & depression, vivid nightmares, aggression

132
Q

Inhaled Anticholinergic Agent Drugs

A

Ipratropium
Tiotropium
Umeclidinium

133
Q

Inhaled Anticholinergic Agents Mechanism of Action

A

dilate airways by blocking acetylcholine

134
Q

Side Effects of Inhaled Anticholinergic Agents

A

ANTICHOLINERGICS CAUSE SLUD

- dry mouth
- dry eyes
- urinary hesitancy
- constipation - Tachycardia
135
Q

Which of these is LEAST likely to cause sedation?

a.) meclisine
b.) cetirizine
c.) loratadine
d.) hydroxyzine

A

loratadine (c)

136
Q

Which of these drugs is used to treat nausea & vomiting via its antihistamine, anticholinergic, & anti-dopamine effects?

a.) promethazine
b.) carbidopa
c.) loradatine
d.) benztropine

A

promethazine (a)

137
Q

Impulse control disorders have been most often associated with what drugs?

a.) Gen. 1 antihisatmines
b.) levodopa /carbidopa
c.) central anticholinergics
d.) dopamine receptor agonists

A

dopamine receptor agonists (c)

138
Q

Which of these describes the phenomenon where a patient’s Parkinson’s symptoms abruptly return, despite adequately high serum levodopa concentrations?

a.) wearing off
b.) dyskinesia
c.) food-drug interaction
d.) on / off

A

on / off (d)

139
Q

Disorientation, confusion, dementia, & memory problems are all side effects most likely to be seen with what drug?

a.) levodopa / carbidopa
b.) pramipexole
c.) ropinerole
d.) benztropine

A

benztropine (d.)

140
Q

How is food likely to impact levodopa therapy?

a.) it may substantially enhance its actions by enhancing its appearance in the brain

b.) it may delay its absorption & onset of actions

c.) it is unlikely to have any significant impact

d.) patients need to eat a low protein diet to ensure levodopa still works

A

it may delay its absorption & onset of actions (b.)

141
Q

which of these drugs is a dopamine receptor agonist?

a.) benztropine
b.) pramipexole
c.) promethazine
d.) levodopa

A

pramipexole (b.)

142
Q

“Antimuscarinic effects” would be expected to include which of the following?

a.) bradycardia
b.) diarrhea
c.) excessive salivation
d.) dry eyes

A

dry eyes (d.)

143
Q

Math the given drugs to their actions or class:

isosorbide mononitrate (Ismo)
memantine (namenda)
donepezil (aricept)
hydromorphone (dilaudid)
methimazole (tapazole)

1.) opioid receptor agonist
2.) NMDA glutamate receptor
3.) anti-thyroid agent
4.) organic nitrate
5.) cholinesterase inhibitor

A

1.) opioid receptor agonist: HYDROMORPHONE (Dilaudid)

2.) NMDA glutamate receptor: MEMANTINE (Namenda)

3.) anti-thyroid agent: METHIMAZOLE (Tapazole)

4.) organic nitrate: ISOSORBID MONONITRATE (Ismo)

5.) cholinesterase inhibitor: DONEPEZIL (Aricept)

144
Q

Which of these drugs must be taken on an empty stomach, either 30-60 minutes before a meal or 3-4 hours after eating?

a.) hydrocodone (Vicodin)
b.) levothyroxine (Synthroid)
c.) donepezil (Aricept)
d.) nitroglycerin (Nitrostat)

A

levothyroxine (b.)

145
Q

You look on your hospital’s opioid conversion chart & see 30 mg of oral morphine is equivalent to 20 mg of oral oxycodone. You want to switch your patient from 30 mg of oral morphine per day to oral oxycodone before sending them home. What is the most appropriate daily dose of oral oxycodone to start with?

a.) 20 mg, since that is the equivalent dose

b.) 15 mg, to allow for incomplete cross-tolerance

c.) 30 mg, due to accumulated tolerance on morphine

d.) 5 mg, since oxycodone is more potent

A

15 mg, to allow for incomplete cross tolerance (b.)

146
Q

Your patient is using sublingual nitroglycerin, & they open a new bottle of 25 tablets today. When do they need to replace their bottle of tablets with a refill?

a.) one year from today

b.) whenever they’re down to 2-3 remaining tablets in the bottle

c.) on the expiration date listed on the bottle

d.) approximately 3-5 months from today

A

approximately 3-5 months from today (d.)

147
Q

You must ensure patients taking which class of drugs has a minimum period of 8 hours each day where their body is free of drug in order to prevent rapid development of resistance?

a.) organic nitrates
b.) anti-thyroid agents
c.) cholinesterase inhibitors
d.) opioid receptor agonists

A

organic nitrates (a.)

148
Q

Which of these represents an approach for treating Alzheimer’s Disease?

a.) ↑ CNS acetylcholine
b.) ↑ CNS dopamine activity
c.) ↑ CNS histamine
d.) ↑ CNS glutamate

A

↑ CNS acetylcholine (a.)

149
Q

Which of these steroids is MOST likely to cause salt-retention and, as a result, fluid retention, edema, & hypertension?

a.) hydrocortisone
b.) prednisone
c.) they are all equally likely
d.) methylprednisolone

A

hydrocortisone (A.)

150
Q

Nightmares, aggressive behavior, depression, & anxiety are all side effects associated with what drug?

a.) salmeterol (Serevent)
b.) iprattropium (Atrovent)
c.) montelukast (Singular)
d.) albuterol (Proventil)

A

montelukast (C.)

151
Q

Which of these is true regarding Long-Acting Beta 2 Agonists (LABAs)?

a.) must be used with a steroid or leukotriene antagonist to prevent negative morbidity & mortality effects

b.) associated with substantially positive effects on morbidity & mortality but only useful when used without other medications

c.) not any more effective than placebo

d.) should only be used on an ‘as needed’ basis to treat acute exacerbations to prevent negative effects

A

must be used with a steroid or leukotriene antagonist to prevent negative morbidity & mortality effects (A.)

152
Q

Which of these is a disadvantage of inhaled anti-asthma medicines vs. oral administration?

a.) there is no difference in safety or effectiveness when given by inhalation

b.) optimal effectiveness relies on proper technique

c.) inhaled administration results in substantially more side effects overall

d.) inhaled administration is not effective because the drug can only work on the airway surface & not deeper into the lung tissue

A

optimal effectiveness relies on proper technique (B.)

153
Q

Which of these drugs is associated with severe cutaneous adverse reactions, for which there is a genetic predisposition such that patients may benefit from having a genetic test prior to its use?

a.) colchicine (Colcrys)
b.) ondansetron (Zofran)
c.) rizatriptan (Maxalt)
d.) allopurinol (Zyloprim)

A

allopurinol (D.)

154
Q

Which of these drug classes is most likely to cause paresthesias, chest tightness, cold & numb extremities, & abdominal pain?

a.) Xanthine oxidase inhibitors
b.) Leukotriene D4 antagonist
c.) 5-HT3 antagonists
d.) Ergot alkaloids

A

ergot alkaloids (D.)

155
Q

For a patient who is altering use of a “triptan” & use of an ergot alkaloid, how long must they wait after to use an ergot alkaloid after using sumatriptan (Imitrex)?

a.) at least 24 hours
b.) at least 12 hours
c.) at least 2 weeks
d.) at least 1 week

A

at least 24 hours (A.)

156
Q

Which of these is an inhaled anticholinergic?

a.) colchicine
b.) triamcinolone
c.) tiotropium
d.) formoterol

A

tiotropium (C.)

Pharmacology (5 decks)

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