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Pharm > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Donepezil

A

Alzheimer’s Disease medication

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2
Q

Memantine

A

Alzheimer’s Disease medication

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3
Q

Atypical antipsychotics (ex. risperdone and olanzapine (SGAs))

A

Alzheimer’s Disease medication (help but increase mortality)

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4
Q

Donepezil mechanism and effects

A

Increases acetylcholine levels
FDA approved for all stages
Side effects:
GI discomfort (common)
Bradycardia (rare)

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5
Q

Memantine mechanism and effects

A

Helps regulate glutamate (too much glutamate = gas mephrotoxc)
FDA approved for only moderate and severe stages
Well tolerated

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6
Q

Do Alzheimer’s medication work

A

Little window of improvement and then it goes to a normal digression. No other alternate

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7
Q

What is a seizure

A

too much electrical activity in the brain

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8
Q

3 types of seizures

A
  1. Tonic-clonic = shaking
  2. Absense = no shaking and just drifts
  3. Myoclonic = just fall and hit the ground (brief shock-like jerks of a muscle or group of muscles)
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9
Q

Generalized seizures

A

Whole brain

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10
Q

Partial (focal) seizures

A

Restricted to one part of the brain

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11
Q

Phenytoin

A

Antiepileptic

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12
Q

Carbamazepine

A

Antiepileptic (used also for neuropathic pain)

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13
Q

Valproic Acid

A

Antiepileptic

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14
Q

Lamotrigine

A

Antiepileptic

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15
Q

Levetiracetam

A

Antiepileptic (Used the most in clinical)

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16
Q

Antiepileptic mechanism of action

A

slow down CNS either by promoting GABA activity or a different mechanism

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17
Q

Antiepileptic common themes

A

lots of drug-drug interactions
All have CNS side effects
Must avoid pregnancy

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18
Q

Phenytoin side effects

A
  1. Very narrow therapeutic index (keep your pheny between 10 and 20)
  2. Gingival hyperplasia (make sure to brush teeth)
  3. Abnormal hair growth (hirsutism)
  4. Vitamin D and K interference
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19
Q

Valproic Acid side effects

A
  1. May upset stomach (take with food)

2. Risk for hepatotoxicity (Monitor LFTs (AST and ALT 1-36) and watch for jaundice)

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20
Q

Lamotrigine side effects

A
  1. Risk for Stevens-Johnson syndrome

2. Start LOW and go sLOW with LAMOtrigine (start a low dose and gradually go up)

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21
Q

Antiepileptic client teaching

A
  1. These drugs help control seizures, but they are not a cure
  2. Don’t abruptly stop them - that can precipitate a seizure
  3. Carry extra medication when traveling
  4. You may need an alternative form of contraception
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22
Q

What do you give for status epileptions (seizure that won’t stop)

A

benzodiazepine

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23
Q

Parkinson’s Disease major symptoms

A
  1. Rest tumor
  2. Rigidity
  3. Bradykinesia
  4. Postural instability
  5. Dysarthria - trouble producing words
  6. Micrographia- writing very small
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24
Q

Parkinson’s Disease treatment strategies

A
  1. Increase dopamine levels
  2. Decrease acetylcholine levels
  3. Slow the destruction of neurons
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25
Q

Levodopa/Carbidopa

A

Parkinson’s Disease Med

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26
Q

Selegiline

A

Parkinson’s Disease Med

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27
Q

Benztropine

A

Parkinson’s Disease Med

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28
Q

Trihexyphenidyl

A

Parkinson’s Disease Med

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29
Q

Levodopa/Carbidopa mechanism and effects

A
  1. Increases dopamine
  2. Most effective treatment
  3. Carbidopa enables more levodopa to enter the CNS = smaller dose and decreasing many side effects
  4. Avoid high protein meals, vitamin B6, and pyridoxine (if not a carb, probably can’t eat it).
  5. Psychosis
  6. Orthostatic Hypotension
  7. Takes several weeks to start working and only last about 5 years
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30
Q

Selegiline mechanism and effects

A
  1. MAO-B inhibitor ( increases serotonin and dopamine)
  2. Avoid tyramine foods
  3. Avoid drugs that increase monoamines (ex. antidepressants, meperidine, and sympathomimetics)
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31
Q

Benztropine & Trihexyphenidyl mechanism of action and effects

A
  1. Decreases acetylcholine
  2. Centrally acting anticholinergics
  3. Second-line therapy for tremors
  4. Anticholinergic effects
  5. Drowsiness/sedation
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32
Q

Symptoms of Diabetes Insipidus (DI)

A
  1. Polydipsia (extra thirsty)

2. Large volumes of dilute urine (polyuria)

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33
Q

Causes of Diabetes Insipidus (DI)

A
  1. Head trauma
  2. Neurosurgery
  3. Cancer
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34
Q

Vasopressin

A

Diabetes Insipidus (DI) med (only parenteral) (used in cardiac arrest) (identical copy of ADH)

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35
Q

Desmopressin

A

Diabetes Insipidus (DI) med (PO and parenteral) (real close copy of ADH)

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36
Q

Diabetes Insipidus (DI) medication common uses

A
  1. Diabetes Insipidus (DI)

2. Cardiac arrest (vasopression)

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37
Q

Diabetes Insipidus (DI) medication mechanism of action

A

Synthetic version of ADH. Once absorbed, they help kidneys hold onto urine. Vasopression causes vasoconstriction

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38
Q

Evaluating Diabetes Insipidus (DI) medication

A
  1. Too much of the medication, they don’t pee.

2. If peeing 3 L, dose needs to go down

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39
Q

Diabetes Insipidus (DI) medication adverse effects

A
  1. Over hydration (headache)

2. Excessive vasoconstriction (chest pain) (caused by vasopressin)

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40
Q

NSAIDs (Non steroid anti-inflammatory drug) common uses

A
  1. pain
  2. fever
  3. inflammation
  4. Stroke & MI prevention (aspirin only) (every other drug increases risk)
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41
Q

Aspirin

A

NSAIDs

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42
Q

Ibuprofen

A

NSAIDs

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43
Q

Naproxen

A

NSAIDs

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44
Q

Ketorolac

A

NSAIDs

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45
Q

Celecoxib

A

NSAIDs

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46
Q

COX-1 prostaglandin helps with what

A
  1. gastric protection
  2. renal perfusion
  3. platelet aggregation
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47
Q

COX-2 prostaglandin helps with what

A
  1. pain
  2. fever
  3. inflammations
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48
Q

NSAIDs mechanism of action

A

Inhibit the conversion of arachidonic acid into prostaglandins by inhibiting COX-1 and COX-2.

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49
Q

NSAIDs common themes

A
  1. GI issues
  2. Renal impairment
  3. Heart attacks and strokes
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50
Q

GI issues caused by NSAIDs

A
  1. Damage to gastric mucosa
  2. Watch for signs of bleeding (black stool, blood in vomit, and/or small bruising)
  3. Take with food or milk
  4. Consider giving a proton pump inhibitor or histamine-2 blocker
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51
Q

Renal impairment by NSAIDs

A
  1. Contraindication with clients with kidney problems. one kidney
  2. Use cautiously if client has decreased renal funtion
  3. Monitor intake and output, BUN, and creatinine
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52
Q

Heart Attacks and strokes by NSAIDs

A
  1. All NSAIDs except aspirin increase risk

2. High risk with selective COX-2 inhibitors (ex. celecoxib)

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53
Q

Aspirin effects

A
  1. Reduces risk of stroke and MI
  2. Contraindicated for children (due to risk of Reye’s syndrome). Especially with the flu. Only use for Kawasaki’s disease
  3. Antiplatelet effect occurs at low doses and lasts the lifetime of the platelet
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54
Q

Salicylism is what

A 
Aspirin poisoning
Manifestations:
1. Tinnitus
2. Sweating
3. Headache
4. Dizziness
5. Acid-base disturbances (breathe faster/Kussmal respiration's)
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55
Q

Salicylism treatment

A
  1. activated charcoal with 1-2 hours.
  2. a lot of IV fluid
  3. sodium bicarbon increases blood pH (dialysis)
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56
Q

Ketorolac effects

A
  1. Pain relief similar to morphine
  2. Short-term use only (up to 5 days)
  3. Can be given IV or PO
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57
Q

Acetaminophen mechanism of action

A

Only works in the CNS and only decreases pain and fever.

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58
Q

Acetaminophen problems

A

Liver toxicity

  1. Max dose is 3 or 4 g daily
  2. Contraindicated for malnourished (not enough glutathione), heavy drinkers (turns toxic too fast), and people with liver disease
  3. Hidden acetaminophen in other medications
  4. Jaundice
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59
Q

Antidote for acetaminophen overdose

A

Acetylcysteine

  1. it replaes depleted glutathione
  2. very effective when given within 8-10 hours
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60
Q

Opioids common uses

A
  1. Moderate to severe pain
  2. Sedation
  3. Cough suppresion (codeine)
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61
Q

Codeine

A

moderate to strong opioid

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62
Q

Hydrocodone and Acetaminophen

A

moderate to strong opioid

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63
Q

Oxycodone and Acetaminophen

A

moderate to strong opioid

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64
Q

Meperidine

A 
Strong opioid (doesn't effect the pupils) 
short term use only (less than 48 hours) due to seizure risks
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65
Q

Morphine

A

Strong opioid

66
Q

Hydromorphone

A

Strong opioid

67
Q

Fentanyl

A

Strong opioid

68
Q

Opioid mechanism of action

A

Activate mu and kappa receptors in the CNS and elsewhere. This decreases neuronal activity, causing sedation and decreased pain transmission

69
Q

Opioid most serious side effects

A
  1. Respiratory depression (monitor respiratory rate)

2. Constipation (increase fluid/fiber intake, walking, give prophylactic laxative and/or stool softener)

70
Q

Opioid regular side effects

A
  1. Cough suppression (encourage coughing)
  2. Itching (may need diphenhydramine)
  3. Nausea/vomiting (may need ondansetron)
  4. Sedation (avoid other CNS depressants and machinery)
  5. Urinary retention (encourage to void every 4 hours)
71
Q

Administration of Opioids

A
  1. Double-checks
  2. Hold and contact provider if Respiratory Rate (RR) is < 12
  3. Another nurse witness waste
  4. Administer IV slowly (usually 4-5 minutes)
72
Q

Patient Controlled Analgesia administration

A
  1. double check settings during handoff
  2. only patient can push button
  3. teach to stay ahead of their pain
  4. guardrails prevent patient from overdosing
73
Q

Fentanyl patches administration

A
  1. Apply to intact, clean, dry, hair-free skin
  2. Maximum effect in 1 day
  3. Change every 72 hours
  4. Fold and flush to dispose
74
Q

Antidote for Opioids

A

Naloxone

75
Q

Migraine characteristics

A
  1. last 42 hours
  2. unilateral (half the head)
  3. pulsating
  4. debilitating pain
  5. worsening by movement
  6. nausea and/or vomiting
  7. photophobia (light) and phonophobia (sound)
76
Q

What causes migraines

A

has something to do with vasodilation and inflammation of the brain’s vasculature. The trigeminal nerve (CN V) innervates these blood vessels and plays a key role

77
Q

2 types of migraine meds

A
  1. Abortive Agents (Stop)

2. Prophylactic Agents (Prevent)

78
Q

Triptans

A

Migraine medications (Stop) (Serotonin 1B/1D blockers)

79
Q

Triptans mechanism of action

A

activate a subset of serotonin receptors. This causes the intracranial vessels to vasoconstrict and decreases their inflammation. 80% effective

80
Q

Sumatriptan

A

Triptans to know

81
Q

Issues with triptans

A
  1. Chest pressure/heavy arms is common
  2. Drug interactions
    - Ergot alkaloids (wait 24 hours)
    - Antidepressants (serotonin syndrome)
82
Q

Triptans client teaching

A
  1. not use for prevention
  2. take immediately after symptoms start
  3. avoid migraine triggers
  4. report continuous or severe chest pain
83
Q

Muscle relaxers and antispasmodics common uses

A
  1. Muscle spasms due to injury/surgery
  2. Spasticity due to cerebral palsy, spinal cord injury, or multiple sclerosis
  3. Malignant (bad) hyperthermia (antidote = dantrolene)
84
Q

diazepam

A

benzodiazepine (in this case muscle relaxer

85
Q

Cyclobenzaprine

A

Muscle relaxer

86
Q

Baclofen

A

Muscle relaxer

87
Q

Dantrolene

A

antidote for malignant hyperthermia

88
Q

Muscle relaxers and antispasmodics mechanism of action

A
  1. Most act within the CNS by enhancing GABA activity
  2. Dantrolene works directly on skeletal muscle. Suppresses the release of calcium, making the muscle weaker and less able to contract
89
Q

Muscle relaxers and antispasmodics problems

A
  1. all cause CNS depression.
  2. Clients should avoid hazardous activity
  3. avoid other CNS depressants
90
Q

Baclofen extra problems

A

Visual hallucinations, paranoid ideation, and seizures if discontinued abruptly

91
Q

Dantrolene extra problems

A
  1. Hepatoxicity (jaundice)
  2. Women older than 35 highest risk
  3. Check liver function before treatment and monitor afterwards
92
Q

Medications for Neuropathic pain

A
  1. TCAs
  2. SNRIs
  3. Antiepileptics
    - Carbamazepine
    - Gabapentin (only prescribe for neuropathic pain)
    - Pregabalin (only prescribe for neuropathic pain)
93
Q

Carbamazepine, gabapentin, and pregabalin mechanism of action

A

They suppress the spontaneous firing of damaged neurons

94
Q

Carbamazepine problems

A
  1. Bone marrow suppression (leukopenia, anemia, thrombocytopenia)
  2. Stevens-Johnsons Syndrome
  3. Lots of interactions (warfarin, oral contraceptives, grapefruit juice)
95
Q

Gabapentin problems

A
  1. Fewer side effects
  2. No significant interactions
  3. Most common side effects: sedation, fatigue, ataxia
96
Q

What does a new nurse need to know about neuropathic pain medications

A

They are to be used in combination with other drugs (opioids). Not by themselves

97
Q

Local anesthetic common uses

A
  1. Surgical procedures
  2. Minor procedures (IV)
  3. Chronic pain
98
Q

Lidocaine (patch, Injection)

A

Local Anesthetic

99
Q

Lidocaine/Epinephrine (vasoconstriction last longer)

A

Local Anesthetic

100
Q

Lidocaine 2.5%/Prilocaine 2.5 (Cream)

A

Local anesthetic

101
Q

Local anesthetic mechanism of action

A
  1. Block the electrical conduction of axons by blocking sodium channels along the axons.
  2. affected neurons can’t transmit their signals, which leads to loss of sensation or loss of movement
102
Q

Lidocaine problems

A
  1. Lidocaine injections work fast (about 5 minutes)
  2. Lidocaine cream work slower (wait 1 hour)
  3. Does not last long
  4. Cardiac toxicity (bradycardia, heart block, cardiac arrest)
  5. CNS toxicity (seizures, respiratory depression, coma)
103
Q

Never give Lidocaine where

A
  1. Finger
  2. Toes
  3. Nose
  4. “Hose” (penis)
104
Q

Lidocaine cream administration

A
  1. squeeze from the tube onto site
  2. don’t rub it
  3. place a Tegaderm on top
  4. Wait a least one hour
  5. Remove dressing and cleanse sight
105
Q

Glaucoma medication mechanism of action

A
  1. Prostaglandin analogs- increase the outflow of aqueous humor
  2. Beta-adrenergic blockers- decreases the production of aqueous humor
  3. Alpha2-adrenergic agonist- do both
106
Q

Latanoprost

A

Glaucoma med (Prostaglandin analog)

107
Q

Timolol

A

Glaucoma med (Beta-adrenergic blockers)

108
Q

Brimonidine

A

Glaucoma med (Alpha2-adrenergic agonists)

109
Q

Glaucoma medication side effects (all)

A
  1. temporary stinging
  2. conjunctivitis
  3. blurred vision
110
Q

Prostaglandin analog extra side effects

A
  1. very few systemic effects

2. Permanent increased pigmentation of iris and/or eyelids (30% of time)

111
Q

Beta-adrenergic blockers extra side effects

A
  1. Some are nonselective (timolol); others are beta1 selective
  2. Bradycardia
  3. Hypotension
  4. Bronchoconstriction (small airway)
112
Q

Alpha2-adrenergic agonists problems

A
  1. hypotension

2. drowsiness (crosses the BBB)

113
Q

Antihistamine common uses

A
  1. Allergies
  2. Itchiness
  3. Hives (urticaria)
  4. Nausea and vomiting
  5. Anaphylaxis
114
Q

Diphenhydramine

A

Antihistamine- 1st generation H1 blocker (crosses BBB)

115
Q

promethazine

A

Antihistamine- 1st generation H1 blocker (crosses BBB)

116
Q

hydroxyzine

A

Antihistamine- 1st generation H1 blocker (crosses BBB)

117
Q

loratadine

A

Antihistamine- 2nd generation H1 blocker (doesn’t cross BBB)

118
Q

cetirizine

A

Antihistamine- 2nd generation H1 blocker (doesn’t cross BBB)

119
Q

fexofenadine

A

Antihistamine- 2nd generation H1 blocker (doesn’t cross BBB)

120
Q

desloratadine

A

Antihistamine- 2nd generation H1 blocker (doesn’t cross BBB)

121
Q

Antihistamine mechanism of action

A

Block H1 receptors, decreasing the effects of excessive histamine (runny nose, sneezing, itchy eyes, itchy rash, vasodilation)

122
Q

Antihistamine common adverse effects

A 
1st generation
- sedation
- anticholinergic effects
2nd generation
- well tolerated
-longer duration
123
Q

Nasal glucocorticoids common uses

A
  1. seasonal rhinitis

2. perennial (never ending) rhinitis

124
Q

mometasone

A

nasal glucocorticoid

125
Q

fluticasone

A

nasal glucocorticoid

126
Q

nasal glucocorticoid mechanism of action

A

prevent the immune system from creating the chemical triggers of inflammation

127
Q

nasal glucocorticoid effectiveness

A
  1. the most effective drugs for allergic or perennial rhinitis
  2. maximal effect takes about 1 week
  3. use proper technique
128
Q

nasal glucocorticoid side effects

A
  1. drying of nasal mucosa

2. epistaxis (nosebleeds)

129
Q

Epinephrine common uses

A
  1. anaphylactic shock
  2. cardiac arrest
  3. local anesthetics
130
Q

Epinephrine mechanism of action

A

activates alpha1, beta1, and beta2 receptors, causing vasoconstriction. Increasing cardiac contractility, and bronchodilation

131
Q

Hypothyroidism symptoms

A
  1. depression
  2. fatigue
  3. weight gain
  4. cold intolerance
  5. constipation
    and many more..
132
Q

causes of hypothyroidism

A
  1. Iodine deficiency
  2. Hashimoto’s thyroiditis
  3. Lithium therapy
133
Q

Levothyroxine

A

Hypothyroidism med

134
Q

Hypothyroidism med mechanism of action

A

levothyroxine is a synthetic version of T4. It is then converted to T3

135
Q

Levothyroxine adverse effects

A
  1. insomnia
  2. anxiety
  3. weight loss
  4. sweating
  5. increased HR and BP
136
Q

Levothyroxine other issues

A
  1. Many food/drug interactions
  2. Narrow therapeutic index
  3. Generic does same thing but do not change brands
137
Q

Asthma controllers

A

taken daily and are not for acute symptoms

138
Q

Asthma rescue medication

A

taken as needed and have a quick onset

139
Q

Asthma and COPD med options

A
  1. Beta2 agonist (use first and then wait 5 minutes)
  2. Anticholinergics
  3. Inhaled glucocorticoids
  4. Combinations
140
Q

Asthma and COPD med mechanism of action

A
  1. Beta2 agonists- activate beta 2 receptors in lungs causing bronchodilation
  2. Anticholinergics- block muscarinic receptors in the lungs, causing bronchodilation
  3. Inhaled glucocorticoids- suppress the inflammatory/immune response in the lungs
141
Q

Albuterol

A

Short-acting Beta2 agonist (asthma)

142
Q

Levalbuterol

A

Short-acting Beta2 agonist (asthma)

143
Q

Formeterol

A

Long-acting Beta2 agonist (COPD)

144
Q

Salmeterol

A

Long-acting Beta2 agonist (COPD)

145
Q

ipatropium

A

Short-acting anticholinergic

146
Q

tiotropium

A

Long-acting anticholinergic

147
Q

beclomethasone

A

inhaled glucocorticoid

148
Q

fluticasone (for asthma)

A

inhaled glucocorticoid

149
Q

Long-acting beta2 agonist must not be what?

A

used as monotherapy in asthma

150
Q

Beta2 agonist adverse effects

A

Tachcardia and tremors

151
Q

Anticholinergic adverse effects for asthma and COPD

A

Dry mouth and hoarseness (since it doesn’t go into the stomach

152
Q

Inhaled glucocorticoid adverse effects

A

oral candidiasis (wash mouth after use)

153
Q

Glucocorticoids common uses

A
  1. asthma and COPD
  2. Allergic reactions
  3. Autoimmune disorders
    and many more…
154
Q

Prednisone

A

oral glucocorticoid

155
Q

prednisolone

A

oral glucocorticoid

156
Q

methylprednisolone

A

oral glucocorticoid

157
Q

dexamethasone

A

oral glucocorticoid

158
Q

glucocorticoid mechanism of action

A

Decrease the body’s immune response

159
Q

glucocorticoid adverse effects

A 
C- cataracts
U- ulcer (GI)
S- skin thinning
H- hypertension and hypokalemia
I- insomnia
N- Neck and face fat
G- glucose elevation
O- osteoporosis, obesity
I- infections
D- depression/mood changes
160
Q

Adrenal insufficiency caused by glucocorticoids

A
  1. Cortisol will stop being made
  2. Don’t stop abruptly if taken more than 7-14 days
  3. flu-like symptoms and hypotension

Pharm (7 decks)

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