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NSG > Pharm #4 > Flashcards

Pharm #4 Flashcards

1
Q

Seizure disorder

A

Epilepsy

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2
Q

Abnormal electric discharges from cerebral neurons

A

Seizure disorder

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3
Q

Seizure disorder Characteristics

A

Loss of consciousness
Involuntary, uncontrolled movements

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4
Q

Seizure disorder Causes

A

Idiopathic
Secondary
Isolated seizures

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5
Q

Neurological disorder

A

Epilepsy

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6
Q

____ of the seizures are unknown reason

A

75% Epilepsy

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7
Q

____ related to brain injury, trauma, anoxia, infection, cerebral vascular disorders (Stroke)

A

25% Epilepsy

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8
Q

Chronic condition lasting a lifetime-

A

epilepsy, long term tx

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9
Q

If seizure nonrelated to epilepsy

A

electrolyte imbalance and hypoglycemia

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10
Q

International Classification of Seizures

A

Generalized and Partial

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11
Q

Generalized seizure definition

A

Both hemispheres of the brain

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12
Q

Types of Generalized Seizures

A

Tonic-Clonic (Grand-Mal)
Absence (petit mal)

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13
Q

Tonic-Clonic (Grand-Mal)

A

Most common generalized alternating muscle spasms, extremities jerking, tonic phase of the muscles contracting, colonic phase spasming and jerking.

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14
Q

Absence (petit mal)-

A

seen in children, causes sudden and brief loss of consciousness

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15
Q

Partial Seizure Definition

A

One hemisphere of the brain, can progress into generalized seizures

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16
Q

Types of Partial Seizure

A

Simple Partial and Partial complex

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17
Q

Simple Partial-

A

No loss of consciousness

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18
Q

Partial complex-

A

Loss of consciousness

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19
Q

Antiseizure Drugs

A

Anticonvulsants or antiepileptic drugs

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20
Q

Antiseizure Drugs Basic Action:

A

Stabilize nerve cell membranes
Suppress abnormal electric impulses in cerebral cortex

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21
Q

Antiseizure Drugs Specific Types of Action:

A
  • Suppress sodium influx into the cells which inactivates the sodium channel, prevents neurons from firing the electrical impulses
  • Suppress calcium influx- preventing the electrical current generated by those calcium ions
  • Enhance action of GABA- amino acid that is inhibiting the neurotransmitters in the brain
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22
Q

Antiseizure Drugs Dosing

A
  • Start low of antiseizure medication to get a therapeutic drug serum level
  • Consistency- need to take these medications at the same time everyday
  • Hard to control so they have to try multiple meds
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23
Q

CNS depressants because it depresses CNS function

A

Antiseizure Drugs

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24
Q

Effective in 75% of patients with seizures

A

Antiseizure Drugs

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25
Q

Does not cure seizures it manages the symptoms

A

Antiseizure Drugs

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26
Q

Taken for lifetime

A

Antiseizure Drugs

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27
Q

If not seizure activity for 3-5 years

A

Antiseizure Drugs

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28
Q

First group of anti seizure meds developed in 1938. prototype for antiseizure drugs

A

Hydantoins

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29
Q

Phenytoin (Dilantin)

A

Hydantoins

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30
Q

Phenytoin (Dilantin) Action

A

Inhibits sodium influx into the nerves cells, decreasing neuron from firing

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31
Q

Phenytoin (Dilantin) Dosing

A

Decrease dose with lower metabolism and liver disease. Increased dose for someone (children with high function liver) with a high metabolic rate.
Age-related
Based on serum drug levels.

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32
Q

Phenytoin (Dilantin) Therapeutic serum level

A

10 to 20 mcg/mL

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33
Q

Phenytoin (Dilantin) Contraindications

A

Pregnancy- Teratogenic drug

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34
Q

Phenytoin (Dilantin) Benefit

A

Slightly sedating and not addictive- benefit

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35
Q

Phenytoin (Dilantin) Highly protein bound=

A

more free drug= more risk of toxicity

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36
Q

Psychiatric effects- Depression or suicidal ideation

A

Phenytoin (Dilantin) Side effect

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37
Q

Nystagmus- involuntary eye movement, diplopia- double eye vision

A

Phenytoin (Dilantin) Side effect

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38
Q

Headache, dizziness, drowsiness(can occur at a therapeutic drug level)

A

Phenytoin (Dilantin) Side effect

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39
Q

N/V, constipation

A

Phenytoin (Dilantin) Side effect

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40
Q

Gingival hyperplasia- overgrowth of the gums that causes easily bleeding, normal side effect at a therapeutic level

A

Phenytoin (Dilantin) Side effect

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41
Q

Alopecia- hair loss
hirsutism- excessive body hair

A

Phenytoin (Dilantin) Side effect

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42
Q

Discolored urine- pink or red, brownish. educate clients, normal side effect

A

Phenytoin (Dilantin) Side effect

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43
Q

Hyperglycemia- happens in long-term use, inhibits release of insulin. Blood sugar checks

A

Phenytoin (Dilantin) Side effect

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44
Q

Blood dyscrasias0 thrombocytopenia(low platelet) leukopenia(low WBC counts)

A

Phenytoin (Dilantin) Side effect

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45
Q

Purple glove syndrome- swelling discoloration and decrease blood flow to the hands can require amputation

A

Phenytoin (Dilantin) Side effect

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46
Q

Stevens-Johnson syndrome- Rare, effects skin, mucus membranes, genitals and eyes. Flu-like symptoms and painful rash that causes blisters. Educate flulike or rash report immediately. Life threatening

A

Phenytoin (Dilantin) Side effect

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47
Q

Phenytoin Drug Interactions: Anticoagulants & ASA-

A

displace the anticoagulant (beats it), adds longer acting time of the anticoagulant

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48
Q

Phenytoin Drug Interactions: Barbiturates, rifampin, & alcohol-

A

increase metabolism, may need a higher dose

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49
Q

Phenytoin Drug Interactions: Sulfonamides and cimetidine-

A

can increase action of a hydantoin by inhibiting liver metabolism.

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50
Q

Phenytoin Drug Interactions: Antacids, calcium preparations, sucralfate, and antineoplastic-

A

Decrease the absorption

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51
Q

Phenytoin Drug Interactions: Antipsychotics and certain herbs-

A

decrease the seizure threshold, lowers drug therapeutic range, low enough so a seizure can be induces.

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52
Q

Highly protein bound drug it competes with other highly protein bound drugs for the receptor sites

A

Phenytoin

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53
Q

Phenytoin Assessment

A

Med history
Renal and hepatic lab function values
Urinary output
Kidney function is appropriate to excrete the drugs
Level of knowledge(compliance)
Ask about seizure history, is it chronic, is it related to a fever etc.

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54
Q

Phenytoin NSG Interventions

A

Monitor drug levels of antiseizure drugs to determine therapeutic range.
If increased number of seizures ask them about drug regimen and assess serum drug level.
Use seizure precautions.
Always address nutritional intake (electrolytes balanced, well balanced diet) because the amount of caloric intake.

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55
Q

Phenytoin Education

A

Compliant and consistent with medication regimen.
If female client is taking an oral contraceptive and taking an antiseizure drugs they need to change contraceptive.
Do not stop abruptly.
Once in steady state in the system they must be weaned off of it.
If the client is already diabetic, blood sugar levels will increase so they have to monitor BGL.
Avoid alcohol, decrease serum drug levels, effectiveness.
Any seizure meds, keep a log of their seizure medications for neurologist to show times and triggers.

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56
Q

Phenobarbital

A

Barbiturate

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57
Q

Phenobarbital Action

A

Enhances GABA activity, reduce the excitability of the CNS

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58
Q

Phenobarbital Used to tx

A

Tonic–clonic, partial, status epilepticus

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59
Q

Longer than 5 minutes seizures or so close together that the pt cannot recover in-between

A

status epilepticus

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60
Q

Phenobarbital Therapeutic serum range

A

15 to 40 mcg/mL
Wider therapeutic range, longer half life, allows for once daily dosing regimen.
More effective for someone because its a longer acting drug (once a day)

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61
Q

Phenobarbital Side effects

A

Sedation
tolerance-gradually withdrawal
decreased teratogenic risk- safest drugs for pregnancy and seizures

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62
Q

Phenobarbital Discontinuation

A

Should be gradual

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63
Q

What type of acting barbiturate is Phenobarbital

A

Long acting barbiturate

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64
Q

What type of acting are Sedative hypnotics

A

Short acting

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65
Q

Ethosuximide (Zarontin)

A

Succinimides

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66
Q

Ethosuximide (Zarontin) Action

A

Decreases calcium influx which prevents the electrical current generated by the calcium ions

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67
Q

Ethosuximide (Zarontin) Use to tx

A

Absence seizures (petit mal)- found in children

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68
Q

Ethosuximide (Zarontin) Therapeutic serum range-

A

40 to 100 mcg/mL
wide therapeutic range

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69
Q

GI upset- educate to take with food

A

Ethosuximide (Zarontin) Side effects/Adverse effects

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70
Q

Dizziness, drowsiness, headache, nightmares

A

Ethosuximide (Zarontin) Side effects/Adverse effects

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71
Q

Suicidal ideation

A

Ethosuximide (Zarontin) Side effects/Adverse effects

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72
Q

Gingival hyperplasia- measurable side effect and manageable, does not mean toxic level

A

Ethosuximide (Zarontin) Side effects/Adverse effects

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73
Q

Ataxia- lack of coordination

A

Ethosuximide (Zarontin) Side effects/Adverse effects

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74
Q

Blood dyscrasias

A

Ethosuximide (Zarontin) Side effects/Adverse effects

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75
Q

Renal and liver impairment

A

Ethosuximide (Zarontin) Side effects/Adverse effects

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76
Q

Systemic lupus erythematous -Once med is stopped= SLE will stop

A

Ethosuximide (Zarontin) Side effects/Adverse effects

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77
Q

Can have anti seizure effects

A

Benzodiazepines

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78
Q

Benzodiazepines that have anti seizure effects

A

Clonazepam (Klonopin)
Clorazepate dipotassium (Tranxene)
Diazepam (Valium)

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79
Q

Treats absence seizures
Tolerance may occur in 6 months of starting therapy, increase dosage after that time frame

A

Clonazepam (Klonopin)-

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80
Q

Treats partial seizures and anxiety, alcohol withdrawal

A

Clorazepate dipotassium (Tranxene)

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81
Q

Treats status epilepticus (drug of choice)
Must be administered IV for status epilepticus
Short-term effect- used with longer acting seizure medications
Used for anxiety and induce sedation

A

Diazepam (Valium)

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82
Q

Carbamazepine (Tegretol)- most commonly used drug in this drug class

A

Iminostilbenes

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83
Q

Carbamazepine (Tegretol) Tx

A

Tonic–clonic, partial seizures
Also used for psychiatric disorders (BPD), nerve pain (trigeminal neuralgia, diabetic neuropathy), and alcohol withdrawal

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84
Q

Carbamazepine (Tegretol) Therapeutic serum range

A

4 to 12 mcg/mL (narrow TR)
Monitor drug serum level closely

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85
Q

Carbamazepine (Tegretol) Side Effects

A

Dizziness, drowsiness, headache, blurred vision
GI distress
Ataxia
Weakness
Anemia
Agranulocytosis- low WBC count
Stevens-Johnson syndrome- rare

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86
Q

Grapefruit juice increases bioavailability of this drug, increasing risk for drug toxicity

A

Carbamazepine (Tegretol)

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87
Q

Valproic Acid (Depakote) Uses

A

tonic–clonic & absence

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88
Q

Valproic Acid (Depakote) Therapeutic serum range

A

50 to 100 mcg/mL
Wide therapeutic range

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89
Q

Valproic Acid (Depakote) Side effects/Adverse reactions

A

Dizziness
Drowsiness
Insomnia
Diplopia
Weakness
GI distress
Suicidal ideation
Thrombocytopenia
Hepatotoxicity- major adverse reaction, monitor liver labs closely

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90
Q

Not safe for children under the age of 2

A

Valproic Acid (Depakote)

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91
Q

Antiseizure Drugs and Pregnancy: Seizure episodes can increase and

A

Teratogenesis

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92
Q

Antiseizure Drugs and Pregnancy: ____ are linked to cardiac defects, cleft lip, palate defects

A

Phenytoin & Carbamazepine

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93
Q

Antiseizure Drugs and Pregnancy: Occur in small percentage of infants, 4-8% chance of congenital defects if they take it during pregnancy

A

Valproic acid

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94
Q

Antiseizure Drugs and Pregnancy: least amount of effects on fetus

A

Phenobarbital

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95
Q

Antiseizure Drugs and Pregnancy: Inhibits vitamin k- seizure medications, baby has an increased risk of clotting.
Should take a vitamin K supplement a week-10 days before delivery and baby receive vitamin k injection

A

Vitamin K

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96
Q

Antiseizure Drugs and Pregnancy: Risk for neural tube defects.

A

Increase Folic acid

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97
Q

Seizures in pregnant women can increase by __ because of increased metabolism rate during pregnancy
Hypoxia can occur- mother and fetus at risk (placental blood flow)

A

25%

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98
Q

More than one drug to have a decrease seizure activity in pregnancy bc of metabolic rate

A

increases

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99
Q

Antiseizure Drugs and Febrile Seizures: Febrile Seizures-

A

increase in body temp, most commonly seen of 3 month-5yrs.
About 2.5% of children who have febrile seizures develop epilepsy.

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100
Q

Antiseizure Drugs and Febrile Seizures: Seizures associated with

A

fever

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101
Q

Antiseizure Drugs and Febrile Seizures: Development of epilepsy is

A

uncommon

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102
Q

Antiseizure Drugs and Febrile Seizures: Prophylactic treatment for high-risk patients- if using preventative meds

A

Phenobarbital
Diazepam

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103
Q

Preventative seizures meds are not indicative
Only at a high risk for developing seizures

A

Antiseizure Drugs and Febrile Seizures

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104
Q

Antiseizure Drugs and Status Epilepticus: Medical

A

emergency

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105
Q

Antiseizure Drugs and Status Epilepticus: Needs

A

Tx

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106
Q

Antiseizure Drugs and Status Epilepticus: Diazepam IV (drug of choice, benzo) or Lorazepam IV followed by

A

Followed by IV Phenytoin or Phenobarbital

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107
Q

Antiseizure Drugs and Status Epilepticus: Continued Seizures worry about (sedation, depression, respiratory)
Used for surgical procedures, depression of CNS

A

Midazolam-versed
Propofol

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108
Q

If not treated it can result in death

A

Status epilepticus

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109
Q

What is the highest priority nursing diagnosis for a patient taking phenytoin (sedative effect, dizziness, ataxia)?

A

Risk for falls

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110
Q

Before administering a daily dose of phenytoin, it is most important for the nurse to

A

check phenytoin levels.
10-20 therapeutic range, narrow

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111
Q

When assessing a patient taking hydantoin therapy for seizure disorder, which indicates an adverse reaction to this therapy?

A

Thrombocytopenia (blood dyscrasias)

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112
Q

A patient is experiencing status epilepticus. The nurse anticipates immediate administration of which drug?

A

Diazepam

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113
Q

Chronic progressive neurologic disorder

A

Parkinson’s Disease Pathophysiology

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114
Q

Degeneration of dopaminergic neurons leading to a lack of dopamine

A

Parkinson’s Disease Pathophysiology

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115
Q

Imbalance of neurotransmitters not enough dopamine compared to acetylcholine

A

Parkinson’s Disease Pathophysiology

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116
Q

No cure, effects the extrapyramidal system, controls out posture balance and locomotion

A

Parkinson’s Disease

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117
Q

Results from loss of neurons that are producing dopamine, part of the brain called the substantia nigra

A

Parkinson’s Disease

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118
Q

Dopamine controls excitatory response from the acetylcholine

A

Parkinson’s Disease

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119
Q

Too much acetylcholine stimulates too much GABA which causes the symptoms

A

Parkinson’s Disease

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120
Q

Effects more men than women

A

Parkinson’s Disease

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121
Q

Can occur with Carbon monoxide and manganese poisoning

A

Parkinson’s Disease

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122
Q

Pseudoparkinsonism

A

Result of getting Parkinson like symptoms that are caused by other drugs
Frequently occurs as an adverse reaction to various drugs

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123
Q

Pseudoparkinsonism causing meds

A

Chlorpromazine
Haloperidol
Lithium
Metoclopramide
Methyldopa
Reserpine

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124
Q

Parkinson’s Disease Characteristics

A

Involuntary tremors of limbs (extremities)
Rigidity of muscles
Bradykinesia – slow movements
Postural changes- head and chest pushed forward and shuffling gait
Lack of facial expression
Pill-rolling motion of hands
Extrapyramidal system- posture effected, rebalance themselves by compensating

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125
Q

Nonpharmacologic measures for Parkinson’s Disease:

A

Exercise, Nutrition, and Group support

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126
Q

Exercise-

A

Improve mobility and flexibility, used to help slow the decline in the quality of life

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127
Q

Nutrition-

A

fiber and fluids diet to prevent weight loss and constipation.
Constantly tremoring, caloric intake and output equal imbalanced

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128
Q

Group support-

A

family members/caregivers because of chronic progressive disease, coping

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129
Q

Parkinson’s Disease Treatment

A

Anticholinergics, Dopamine replacements, Dopamine agonists, MAO-B inhibitors, COMT inhibitors,

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130
Q

Anticholinergics-

A

blocking receptors of acetylcholine bc too much. Allows dopamine balance to be restored

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131
Q

Dopamine replacements-

A

replacing endogenous dopamine and binding with dopamine receptors

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132
Q

Dopamine agonists-

A

dopamine replacement, stimulating dopamine receptor

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133
Q

MAO-B inhibitors-

A

inhibits monoamine oxidase b enzyme, involved in the metabolism of dopamine, decrease dopamine metabolism to increase dopamine receptors. Inhibiting the break down

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134
Q

COMT inhibitors- catechol o methyltransferase

A

Enzyme that deactivates dopamine, inhibiting that from occurring. Allows more dopamine to be available. Antagonist agonist

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135
Q

Replace dopamine and reduce symptoms

A

Parkinson’s Disease Treatment

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136
Q

Antiparkinson Drugs

A

Anticholinergics

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137
Q

Anticholinergics Example

A

Benztropine & Trihexyphenidyl

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138
Q

Benztropine & Trihexyphenidyl Action

A

Reduces rigidity and some of the tremors
Minimal effect on bradykinesia

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139
Q

Benztropine & Trihexyphenidyl Side effects

A

Blurred vision
Mydriasis
Ocular hypertension (Glaucoma contra)
Weakness
Dry mouth (regulate drooling),
Constipation
Anhidrosis(decreased sweating)
Urinary retention

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140
Q

Activating the nicotinic receptors and muscuenic receptors through out the body

A

Anticholinergics

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141
Q

Helps reduce the muscle tone and tremors, does not have good effect on the bradykinesia

A

Anticholinergics

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142
Q

Also used to treat pseudo Parkinson, drug induced Parkinson’s

A

Anticholinergics

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143
Q

Antiparkinson: Anticholinergic Agent Assessment

A

Full medical history looking for glaucoma and parkinsonism
Worried if they already have GI constipation, dysfunction, urinary retention, myasthenia gravis
Drug history, Antihistamine can increase the effect of an anticholinergic (trihexyphenidyl)
Baseline vital signs
See the stage of Parkinson disease progression, current s/sx.
Know ability for drug regimen.
Baseline urinary output for urinary retention

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144
Q

Antiparkinson: Anticholinergic Agent NSG Interventions

A

vital signs
urinary retention
bowel movements
watch for increase pulse rate
hypervolemia
constipation,
monitor effects on drugs and how effective they are on symptoms.

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145
Q

Antiparkinson: Anticholinergic Agent Education

A

Safety measures- safety bar in shower, elevated toilet seat, shower chair, removing throw rugs. Adding extra lighting, eliminating danger.

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146
Q

Dopaminergics

A

Antiparkinson Drugs

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147
Q

Dopaminergics Example

A

Carbidopa-levodopa

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148
Q

Carbidopa

A

Prolongs the effect of levodopa

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149
Q

Carbidopa-levodopa action

A

Converts to dopamine and increases mobility

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150
Q

Carbidopa-levodopa Side effects

A

Fatigue, insomnia, dry mouth, blurred vision
Orthostatic hypotension- seen beginning the TX, decreases overtime, palpitations, dysrhythmias, Agranulocytosis
Constipation, N/V, urinary retention, urine discoloration
Dyskinesia- involuntary movements, psychosis, severe depression- report immediately

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151
Q

Dopamine itself cannot cross BBB but

A

levodopa can by converting into dopamine

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152
Q

___ inhibits the enzyme decarboxylase that’s breaking down levodopa in the body

A

Carbidopa

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153
Q

levodopa turns into dopamine = increasing levels of

A

dopamine

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154
Q

When levodopa is used alone, only __ reaches the brain because __ converts to dopamine while in the peripheral nervous system

A

1%
99%

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155
Q

By combining carbidopa with levodopa, carbidopa can inhibit the enzyme __ in the periphery, thereby allowing more levodopa to reach the brain.

A

decarboxylase

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156
Q

Levodopa taken alone-

A

10mg of 500mg reaches the brain, 5%

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157
Q

When carbidopa given with levodopa a smaller dose-

A

10mg of 100mg gets to the brain = 10% effectiveness, decreases side effects

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158
Q

Dopaminergics (carbidopa-Levodopa) Asessment

A

vital sign baseline, drug history, medical history, s/sx

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159
Q

Dopaminergics (carbidopa-Levodopa) Nursing Interventions-

A

orthostatic hypotension
increase water and salt intake
take carbidopa and levodopa with low protein foods.
High protein food effects/blocks how the drug goes to the CNS

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160
Q

Dopaminergics (carbidopa-Levodopa) Education

A

Family support and educating support system
drug regimen is taken properly
Short half life- 1-2 hrs.
Need to take frequently through out the day, cannot abruptly stop med can cause rebound symptoms.
Can cause urine discoloration-will darken with exposure to the air- harmless.
Perspiration(Sweat) not clear, educate.
Can be taken with food (low protein), can cause GI upset.
If given with food, absorption can be delated.
Therapeutic response takes several months, educate to not stop taking med.

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161
Q

Bromocriptine(dopaminergic)

A

Dopamine Agonists

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162
Q

Bromocriptine(dopaminergic) Action

A

Acts directly on dopamine receptors in CNS, cardiovascular system, & GI tract
Used when pts do not tolerate carbidopa-levodopa

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163
Q

Dopamine agonist direct acting
Can be taken alone or with carbidopa-levodopa, when given together the dosages of each can be decreased. Can reduce side effects and drug tolerance

A

Bromocriptine(dopaminergic)

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164
Q

Selegiline

A

Monoamine Oxidase B Inhibitors

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165
Q

Selegiline Action

A

Inhibit MAO-B enzyme that interferes with dopamine

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166
Q

Selegiline Interaction

A

Food high in tyramine can cause hypertensive crisis
CNS toxicity with tricyclic antidepressants or SSRIs

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167
Q

Breaks down dopamine enzyme, Inhibiting from occurring

A

Selegiline

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168
Q

The action of dopamine in levodopa is prolonged

A

Selegiline

169
Q

Used as early tx before carbadop-levodopa

A

Selegiline

170
Q

Large doses of MAO B inhibitor can inhibit MAO A enzyme

A

Selegiline

171
Q

When drug is not metabolized well it can cause hypertensive crisis- too much tyramine in the body= aged cheese, beer, red wine, bananas. Educate to prevent tyramine

A

Selegiline

172
Q

Tolcapone & Entacapone

A

Catechol-O-Methyltransferase COMT Inhibitors

173
Q

Tolcapone & Entacapone Action

A

Inhibit COMT enzyme that inactivates dopamine. Increase the amount of dopamine
Often combined with carbidopa-levodopa. Can decrease both dosages

174
Q

Hepatoxic (liver enzymes)

A

Tolcapone

175
Q

less risk for liver toxicity but cause brown/orange urine.
No effect on liver fxn

A

Entacapone

176
Q

Form of Incurable dementia illness

A

Alzheimer’s Disease

177
Q

Chronic, progressive neurodegenerative disorder

A

Alzheimer’s Disease

178
Q

Onset usually between ages 45 and 65

A

Alzheimer’s Disease

179
Q

Alzheimer’s Disease Pathophysiology

A

Cholinergic neuron degeneration and acetylcholine deficiency
Neuritic plaques/neurofibrillary tangles

180
Q

Alzheimer’s Disease Etiology- unknown

A

Genetics, can be caused by damage of the brain cells, virus, infection, nutritional deficiencies folic acid decrease

Others. Cholinergic neurons that produce acetylcholine degernate which leads to decreased acetychoe. It is crucial in forming memoires

181
Q

Neurodegenerative disorder

A

Alzheimer’s Disease

182
Q

Increased marked cognitive dysfunction

A

Alzheimer’s Disease

183
Q

Can give meds to try and slow progression of symptoms

A

Alzheimer’s Disease

184
Q

Can cause sedentary lifestyle.

A

Alzheimer’s Disease

185
Q

Occur more in women than in men, risk more occurrence bc women live longer

A

Alzheimer’s Disease

186
Q

Alzheimer’s Disease Pathophysiology
Histologic changes

A

Neuron affected by Alzheimer’s disease showing characteristic neuritic plaques and cellular neurofibrillary tangles.

187
Q

Alzheimer’s Disease Mild (early stage)

A

still living independently, trouble planning and organizing, memory loss

188
Q

Alzheimer’s Disease Moderate (middle stage)

A

increased memory loss, personality changes, not able to perform routine tasks, loss of bowel and bladder control

189
Q

Alzheimer’s Disease Severe (late stage)-

A

severe cognitive impairment, not recognize people, a lot of adl assistance, not walking or talking often, ability to lose swallow effect worried about aspiration

190
Q

Rivastigmine & Donepezil

A

Acetylcholinesterase/Cholinesterase Inhibitors

191
Q

Rivastigmine & Donepezil Action

A

Inhibit the action of acetylcholinesterase
Cause increased levels of acetylcholine in the CNS
Increase cognitive function and delay loss of brain function

192
Q

Rivastigmine & Donepezil Side effects

A

Related to an increase in acetylcholine in the peripheral nervous system as well
Parasympathetic response- bronchoconstriction, bradycardia, hypotension

193
Q

Rivastigmine & Donepezi Treats

A

Mild to moderate Alzheimer’s disease

194
Q

Rivastigmine (Exelon) Side effects/Adverse effects (results from parasympathetic nervous system activation)

A

Anorexia
Abdominal pain
N/V
Diarrhea or constipation
Weight loss
Dizziness
HA
Depression
Confusion
Peripheral edema
Dry mouth
Dehydration
Nystagmus
Seizures
Bradycardia
Orthostatic hypotension
Cataracts
MI, HF, dysrhythmias
Hepatoxicity
Suicidal ideation
Steven-Johnson’s syndrome

195
Q

Rivastigmine (Exelon) Drug Interactions

A

Theophylline, general anesthetics- increase effect, if going into surgery they may discontinue before
TCAs- decrease effect
Cimetidine- increase effect
NSAIDs- for other pain/inflammation, increases GI effects
Tobacco

196
Q

Transdermal patch or tablet form, 2x a day, mild to moderate Alzheimer’s

A

Rivastigmine (Exelon)

197
Q

Rivastigmine Assessment

A

Stage of disease, physically and mentally able to do, support system look like. Maintain consistency and care- same staff members.

198
Q

Rivastigmine NSG interventions

A

Assisting with ambulation and activity.
Goal to help independence as possible.
Monitor side effects.
Noting improvement or decline in function

199
Q

Rivastigmine Education

A

home safety, side effects, reason for drug regimen, info about support groups

200
Q

Memantine (Namenda)

A

NMDA receptor antagonist

201
Q

Memantine (Namenda) Action

A

Blocks effects of neurotransmitter glutamate at NMDA receptors

202
Q

Memantine (Namenda) Side effects/adverse effects

A

Fewer than acetylcholinesterase inhibitors
Most common: Dizziness, HA, drowsiness, confusion, constipation or diarrhea
Stevens-Johnson syndrome
Depression, Hallucinations
Hyper or hypotension, urinary incontinence

203
Q

Learning capability and memory- NMDA

A

Memantine (Namenda)

204
Q

Tx moderate to severe Alzheimer’s

A

Memantine (Namenda)

205
Q

A patient has been diagnosed with Alzheimer disease. The patient’s daughter asks the nurse what the cause of Alzheimer disease is. The best response by the nurse is “The cause of Alzheimer disease is

A

unknown.”

206
Q

Which comment to the nurse indicates more teaching is needed for a patient taking carbidopa/levodopa?

A

“I know I need to take this drug once a day.”

207
Q

Which side effect/adverse effect of carbidopa/levodopa does the nurse realize is most important to monitor?

A

Agranulocytosis- decrease in WBCs

208
Q

Before administering carbidopa–levodopa for the treatment of Parkinson’s disease, it is most important for the nurse to assess the patient for a history of

A

glaucoma

209
Q

A patient with Parkinson’s disease is being treated with carbidopa–levodopa. The daughter asks the nurse why he needs both agents. The nurse responds,

A

“The carbidopa helps the levodopa reach the brain.”

210
Q

A nurse at an adult day care center notes that many patients are on rivastigmine. The nurse knows that the function of this medication is to

A

slow the progression of symptoms of Alzheimer disease.

211
Q

Autoimmune disorder

A

Myasthenia Gravis Pathophysiology

212
Q

Antibodies attach to acetylcholine receptor sites, obstruct binding of acetylcholine, and destroy receptor sites

A

Myasthenia Gravis Pathophysiology

213
Q

Lack of acetylcholine impairs transmission of messages at neuromuscular junctions

A

Myasthenia Gravis Pathophysiology

214
Q

Non-curable

A

Myasthenia Gravis

215
Q

Myasthenia Gravis Result

A

Respiratory, facial, and extremity weakness
Muscles that are not getting their receptor sites fulfilled

216
Q

___ is the neurotransmitter for the parasympathetic nervous system

A

Acetylcholine

217
Q

Myasthenia Gravis occurs more in women of child bearing age years =

A

20-40yrs

218
Q

Myasthenia Gravis peak male age

A

50-70

219
Q

Tend to run in families

A

Myasthenia Gravis

220
Q

Lymph organ

A

Myasthenia Gravis: Thymus Gland

221
Q

Produces T cells

A

Myasthenia Gravis: Thymus Gland

222
Q

Enlarged in 60% of MG patients- produce antibodies that add acetylcholine to receptor sites. Over production of antibodies occur.

A

Myasthenia Gravis: Thymus Gland

223
Q

Remove the thymus gland, reduce number of antibodies

A

Myasthenia Gravis: Thymectomy

224
Q

Skeletal muscle weakness

A

Myasthenia Gravis Characteristics

225
Q

Fatigue, ptosis, diplopia, dysphagia, dysarthria

A

Myasthenia Gravis Characteristics

226
Q

Respiratory muscle weakness, paralysis, and arrest

A

Myasthenia Gravis Characteristics

227
Q

Fluctuating muscle weakness especially when someone is using that muscle a lot

A

Myasthenia Gravis Characteristics

228
Q

Respiratory arrest due to

A

paralysis of muscles in the lungs, Myasthenia Gravis

229
Q

Facial muscles-

A

Ptosis, difficulty chewing, drooping eyelids, and dysphagia, Myasthenia Gravis

230
Q

Extremities are the most effected

A

Myasthenia Gravis

231
Q

Causes Severe generalized muscle weakness- involve respiratory muscles = death

A

Myasthenic crisis

232
Q

Involves diaphragm and intercostal muscles

A

Myasthenic crisis

233
Q

Myasthenic crisis triggers

A

Inadequate dosing of AChE inhibitors
Emotional stress, menstrual cycle, pregnancy
Infection, surgery, trauma
Hypokalemia, alcohol intake
Temperature extremes
Medication interactions

234
Q

Treat with neostigmine- a fast acting ACHe inhibitor, prevents breakdown of acetylcholine

A

Myasthenic crisis

235
Q

Myasthenic crisis can occur 3-4 hours after taking certain meds=

A

Aminoglycoside antibiotics, Phenytoin, CCBs, Psychotropics

236
Q

Usually occurs within 30 to 60 minutes after taking excess anticholinergic medications

A

Cholinergic crisis

237
Q

Triggered by overdosing

A

Cholinergic crisis

238
Q

Cholinergic crisis symptoms

A

Severe muscle weakness
Possible respiratory paralysis and arrest
Miosis (pupil constriction)
Pallor, sweating, vertigo
Excess salivation, GI distress, vomiting
Bradycardia, fasciculations (muscle twitching)

239
Q

Occurs when too much of an Acetylcholinesterase inhibitor
at the receptor sites
Nerves are over stimulated when having too much Acetylcholine

A

Cholinergic crisis

240
Q

Can cause respiratory arrest

A

Cholinergic crisis

241
Q

Antidote: Atropine

A

Cholinergic crisis

242
Q

Acetylcholinesterase inhibitors

A

Edrophonium (Tensilon), Neostigmine, Pyridostigmine

243
Q

Acetylcholinesterase inhibitor action

A

Increases muscle strength in patients with myasthenia gravis

244
Q

Medication differentiating between myasthenic (if it works) and cholinergic crises (if it worsens)

A

Edrophonium (Tensilon)

245
Q

Ultra-short-acting- (worsened symptoms resolve quickly), need emergency precautions

A

Edrophonium (Tensilon)

246
Q

Short-acting

A

Neostigmine

247
Q

Intermediate-acting

A

Pyridostigmine

248
Q

Decreasing break down the the acetylcholine at the sites

A

Acetylcholinesterase Inhibitors

249
Q

Acetylcholinesterase Inhibitors Side effects

A

Miosis
Blurred vision
Bradycardia
Hypotension
GI distress- Nausea, vomiting, diarrhea, abdominal cramps

250
Q

PNS stimulation
Increase acetylcholine
Activates both muscarinic and nicotinic receptor sites

A

Acetylcholinesterase Inhibitors

251
Q

Patients Unresponsive to Acetylcholinesterase Inhibitors

A

Prednisone, Plasma exchange, Intravenous immune globulin, Immunosuppressive drugs

252
Q

Prednisone-

A

If the AChe are not effective
Drug of choice

253
Q

Intravenous immune globulin-

A

IGG

254
Q

Immunosuppressive drugs

A

Azathioprine- Intense drug, need to be monitored for hepatotoxicity and leukopenia

255
Q

Pyridostigmine Assessment-

A

Drug history
Labs
S/Sx if being effective or over effective
Ability to swallow,

256
Q

Pyridostigmine Nursing Interventions-

A

Monitoring and watching for drug effectiveness,
S/Sx or myasthenic crisis or cholinergic crisis
Make sure family is involved (addressing psychosocial needs)

257
Q

Pyridostigmine Education-

A

Follow drug regimen
Notifying about other meds to physician
Side effects
Take meds before meals for best absorption.
If taking med at least 30 mins before meals it can increase muscle capability for chewing.
Encourage to wear Medical identification bracelet for emergencies (myasthenia and cholinergic crisis)

258
Q

Autoimmune disorder
Attacks myelin sheath of nerve fibers in brain and spinal cord
Causes lesions (plaques)

A

Multiple Sclerosis Pathophysiology

259
Q

Multiple Sclerosis Motor Characteristics

A

Motor symptoms- Weakness or paralysis of extremities, fatigue, muscle spasticity, paresthesia

260
Q

Remissions and exacerbations

A

Multiple Sclerosis

261
Q

Multiple Sclerosis Sensory symptoms

A

Numbness and tingling, double vision (first symptom that they experience), vertigo, tinnitus

262
Q

Multiple Sclerosis Cerebellar symptoms-

A

nystagmus, ataxia, dysarthria, and dysphagia

263
Q

May have neuropathic pain in lower back or abdominal area

A

Multiple Sclerosis

264
Q

Slows down nerve impulse transmission

A

Multiple Sclerosis

265
Q

No cure
Can give meds to slow disease process and improve symptoms

A

Multiple Sclerosis

266
Q

Multiple Sclerosis diagnosis is

A

difficult

267
Q

Multiple Sclerosis diagnosis

A

Medical history
Neurologic exam
MRI
Cerebrospinal fluid analysis
Evoked potential test

268
Q

MRI-

A

lesions in the brain or spinal column

269
Q

Cerebrospinal fluid analysis-

A

may have elevated IgG antibodies

270
Q

Evoked potential test-

A

measuring electric activity in the brain as the response of stimulation of a nerve pathway

271
Q

Oligoclonal bands-

A

proteins that are the product of the myelin sheath breakdown

272
Q

Multiple Sclerosis Tx:

A

Immunomodulators and immunosuppressants

273
Q

Immunomodulators

A

disease modifying drugs

274
Q

immunosuppressants

A

slowing disease process and prevention of relapse of an exacerbation

275
Q

First-line treatment
Slows disease progression and prevents relapses

A

Immunomodulators and immunosuppressants

276
Q

Immunomodulators and immunosuppressants example

A

Beta interferon

277
Q

Beneficial in reducing edema or acute inflammation that is occurring at the direct area of myelin sheath breakdown.

A

Multiple Sclerosis tx: Corticosteroids

278
Q

Used for acute exacerbations not for long term (sick symptoms can worsen), increases BGL on long term meds

A

Multiple Sclerosis tx: Corticosteroids

279
Q

Reduces edema and acute inflammation

A

Multiple Sclerosis tx: Corticosteroids

280
Q

Corticosteroid example

A

Methylprednisolone(solumedrol)

281
Q

Skeletal muscle relaxants

A

Centrally acting muscle relaxants
Direct acting muscle relaxant

282
Q

Centrally acting muscle relaxants

A

Relieves muscle spasm and spasticity
Have sedative effect

283
Q

Direct acting muscle relaxants

A

Decreases muscle spasm pain and increases range of motion
Suppresses hyperactive reflex

284
Q

Skeletal Muscle Relaxants side effects

A

Drowsiness, dizziness, headache, nausea, vomiting

285
Q

Used to alleviate muscle spasms and injury that causes it

A

Skeletal Muscle Relaxants

286
Q

Sedative effect, do not give any other cns depressants

A

Skeletal Muscle Relaxants

287
Q

All muscle relaxants Can cause drug dependence except cyclobenzaprine

A

Skeletal Muscle Relaxants

288
Q

Do not put someone on long-term

A

Skeletal Muscle Relaxants

289
Q

Can have anticholinergic side effect

A

Skeletal Muscle Relaxants

290
Q

Cyclobenzaprine

A

Skeletal Muscle Relaxants

291
Q

Cyclobenzaprine action

A

Relax skeletal muscles

292
Q

Cyclobenzaprine uses

A

Relieves muscle spasm

293
Q

Cyclobenzaprine side effects

A

Anticholinergic effects- Blurred vision, dry mouth, urine retention, constipation, tachycardia
Drowsiness, dizziness
Headache, nervousness, confusion
GI distress, unpleasant taste
Dysrhythmias

294
Q

Prototype drug of skeletal relaxants

A

Cyclobenzaprine

295
Q

Only skeletal relaxant that does not cause dependence

A

Cyclobenzaprine

296
Q

Benefits SUD

A

Cyclobenzaprine

297
Q

Weaning off drug because can cause muscle spasm rebound

A

Cyclobenzaprine

298
Q

Baclofen
Carisoprodol (Soma)
Chlorzoxazone (Parafon Forte)
Methocarbamol

A

Skeletal Muscle Relaxants

299
Q

PO, Intrathecally (spinal column)-pump is surgically implanted, catheter into the spinal column.
Can be continues or scheduled, gives low continual dose (steady state)

A

Baclofen

300
Q

Cyclobenzaprine- Assessment

A

Drug history and medical history

301
Q

Cyclobenzaprine- Nsg interventions

A

Hepatic functions (can become toxic)
Observing S/E for CNS depression (still need to function)

302
Q

Cyclobenzaprine- Education

A

Cannot be abruptly stopped, should not drive,
Not taken more than 3 weeks or less
Avoid alcohol.
Take with food to decrease GI upset and report other side effects, avoid other CNS depression meds

303
Q

A patient with myasthenia gravis comes to the emergency department in respiratory distress. He has been diagnosed with myasthenic crisis. The nurse anticipates administration of which drug?

A

Neostigmine

303
Q

The patient is admitted to the emergency department with cholinergic crisis. The nurse anticipates administration of

A

atropine.

304
Q

A patient with myasthenia gravis comes to the emergency department in respiratory distress. To determine if the patient is in myasthenic crisis or cholinergic crisis, the nurse anticipates administration of which drug?

A

Edrophonium

305
Q

A patient with myasthenia gravis is prescribed neostigmine. The nurse identifies that the medication is effective when the patient experiences

A

increased muscle strength.

306
Q

A patient with multiple sclerosis is being treated with large doses of corticosteroids. Which nursing diagnosis would be the priority at this time?

A

Risk for infection

307
Q

A child with cerebral palsy is ordered to receive baclofen. The nurse is aware that this medication is prescribed to

A

reduce muscle spasticity.

308
Q

Depression Etiology

A

Genetic predisposition
Social and environmental factors

309
Q

Depression Pathophysiology theories

A

Decreased levels of monoamine neurotransmitters- predisposed to depression when decreased neurotransmitters

310
Q

Monoamine neurotransmitters

A

Norepinephrine, serotonin, dopamine

311
Q

Depression S/Sx

A

Depressed mood, despair, weight loss or gain
Loss of interest in most activities
Fatigue, insomnia, hypersomnia
Decreased ability to think or concentrate
Suicidal thoughts

312
Q

Whoever is discussing this w them needs to openly address this issue. Ask if they have thought about hurting themselves or others? Do they have plan?

A

Suicidal thoughts

313
Q

Most common mental illness, 1/3 of people experience depression
½ of people seek treatment, 2/3 of the tx have remission

A

Depression

314
Q

Depression contributing factors:

A

Hx of abuse
Genetic component
Experience of illness
Traumatic life event
Personal problems and
Substance abuse (self medicating prescription or elicit)

315
Q

Types of depression

A

Reactive depression, Major depression, Bipolar disorder

316
Q

Reactive depression-

A

Occur after a precipitating event- death of a loved one, divorce. Can last months.

317
Q

Major depression Primary-

A

unrelated to any health problems.

318
Q

Major depression Secondary-

A

Related to physical (postpartum depression) or psychiatric disorder or drug misuse

319
Q

Bipolar disorder-

A

Mood is fluctuating between manic state (euphoria) and really low depression state

320
Q

Complementary and Alternative Therapy for Depression

A

Ginkgo biloba and St. John’s wort, Psychotherapy
Somatic therapies, Exercise, Light therapy

321
Q

Ginkgo biloba and St. John’s wort- decreased reuptake of monoamine neurotransmitter

A

Discontinue use of herbal products 1 to 2 weeks before surgery.
Check with the health care provider before taking herbal treatments.

322
Q

Somatic therapies

A

ECT
Transcranial magnetic stimulation

323
Q

ECT

A

short acting neuromuscular blocker, short acting IV is given

324
Q

Transcranial magnetic stimulation

A

magnetic pulses that are directed to the areas of the brain that control mood

325
Q

Exercise-

A

releases endorphins

326
Q

Light therapy-

A

experiencing seasonal effective disorder

327
Q

Not be combines with prescription antidepressants- ginkgo. Causes:

A

Extreme dizziness, headache, sweating= Serotonin syndrome

328
Q

Antidepressant Groups

A

Tricyclic antidepressants (TCAs)
Selective serotonin reuptake inhibitors (SSRIs)
Serotonin norepinephrine reuptake inhibitors (SNRIs)
Atypical antidepressants
Monoamine oxidase inhibitors (MAOIs)

329
Q

TCAs and MAOIs=

A

more side effects, not used as often, developed in 1950s. older med.

330
Q

SSRIs and SNRIs=

A

1980s, less side effects, more used

331
Q

Tricyclic Antidepressants Examples:

A

Amitriptyline
Imipramine
Trimipramine
Doxepin
Nortriptyline
Protriptyline

332
Q

Blocks uptake of neurotransmitters norepinephrine and serotonin in brain

A

Tricyclic Antidepressants Action

333
Q

Elevates mood, increases interest in ADLs, decreases insomnia

A

Tricyclic Antidepressants Action

334
Q

Blocks histamine receptors which leads to sedation

A

Tricyclic Antidepressants Action

335
Q

Blocks cholinergic receptors which leads to anticholinergic effects

A

Tricyclic Antidepressants Action

336
Q

As effective as SSRIs but have a lot of side effects

A

Tricyclic Antidepressants

336
Q

Tricyclic Antidepressants Use

A

Major depression

337
Q

It takes 2-4 weeks to become effective, if ineffective in that time frame they need to be tapered off of the med

A

Tricyclic Antidepressants

338
Q

Tricyclic Antidepressants Side effects/adverse reactions

A

Drowsiness, dizziness, blurred vision
Dry mouth and eyes, GI distress
Urinary retention, sexual dysfunction
Weight gain, seizures
Suicidal ideation
Orthostatic hypotension (Common, CNS depression), dysrhythmias
Blood dyscrasias, cardiotoxicity
EPS, NMS

339
Q

Sedation is the major side effect

A

Tricyclic Antidepressants

340
Q

Also have anticholingeric effects- tachycardia, urine retention, blurred vision

A

Tricyclic Antidepressants

341
Q

Can cause leukopenia, thrombocytopenia, agranulocytosis

A

Tricyclic Antidepressants

341
Q

Amatriptaline- Extrapyramidal symptoms

A

Tricyclic Antidepressants

342
Q

Clomipramine- cause neuroleptic malignant system, fever, rigidify to muscles, autonomic hyperactivity(SNS stimulation)

A

Tricyclic Antidepressants

343
Q

__ can lower seizure threshold- if have epilepsy they need to increase seizure medications

A

Tricyclic Antidepressants

344
Q

High doses of __ cause cardiotoxicity and dysrhythmias, can be lethal

A

Tricyclic Antidepressants

345
Q

Tricyclic Antidepressants Interactions

A

Alcohol and other CNS depressants potentiate CNS depression
MAOIs may lead to toxic psychosis, cardiotoxicity
Antithyroid drugs may increase dysrhythmias

346
Q

Must wait 2 weeks after stopping MAOI to give ___

A

Tricyclic Antidepressants

347
Q

Increased risk for dysrhythmia when taking

A

methimazole, Tricyclic Antidepressants

348
Q

Selective Serotonin Reuptake Inhibitors Example

A

Fluoxetine(Prozac), sertraline, paroxetine, citalopram

349
Q

Fluoxetine(Prozac)-

A

Positive results in 50-60% who don’t respond well to a TCA (prototype)

350
Q

Selective Serotonin Reuptake Inhibitors Action

A

Block uptake of neurotransmitter serotonin which allows more serotonin to effect the receptor sites=more availability of serotonin

351
Q

Selective Serotonin Reuptake Inhibitors Uses

A

Major depression (primary use)
Anxiety disorders
Prevention of migraine headaches
Decrease premenstrual tension syndrome
Eating disorders
Substance use disorder

352
Q

Can have Weekly delayed dose, must see daily dosing first

A

Selective Serotonin Reuptake Inhibitors

353
Q

Selective Serotonin Reuptake Inhibitors Interactions

A

Increased sedation with alcohol and other CNS depressants
Grapefruit juice with SSRIs can lead to toxicity

354
Q

Selective Serotonin Reuptake Inhibitors Side effects/adverse reactions

A

Headache, insomnia
Blurred vision
Dry mouth, GI distress
Erectile dysfunction
Suicidal ideation
Side effects often decrease over 1 to 4 weeks

355
Q

More popular than TCA bc they cause less side effects

A

Selective Serotonin Reuptake Inhibitors (SSRI)

356
Q

Not much a risk of cardiotoxicity

A

Selective Serotonin Reuptake Inhibitors (SSRI)

357
Q

Dosage should be decreased in older clients bc of CNS depression and lower metabolism

A

Selective Serotonin Reuptake Inhibitors (SSRI)

358
Q

Can cause increase appetite so weight gain is common

A

Selective Serotonin Reuptake Inhibitors (SSRI)

359
Q

S/E decrease libido, nervousness, insomnia, can decreased overtime

A

Selective Serotonin Reuptake Inhibitors (SSRI)

360
Q

Monitor for suicidal ideation especially when first beginning tx

A

Selective Serotonin Reuptake Inhibitors (SSRI)

361
Q

Should be tapered off, not stopped abruptly

A

Selective Serotonin Reuptake Inhibitors (SSRI)

362
Q

Serotonin Norepinephrine Reuptake Inhibitors examples

A

Venlafaxine, duloxetine, desvenlafaxine

363
Q

Serotonin Norepinephrine Reuptake Inhibitors Action

A

Inhibit the reuptake of serotonin and norepinephrine

364
Q

Serotonin Norepinephrine Reuptake Inhibitors Use

A

Major depression
Generalized anxiety disorder
Social anxiety disorder

365
Q

Serotonin Norepinephrine Reuptake Inhibitors Interactions

A

St. John’s wort- high risk for serotonin syndrome and neuroleptic malignant syndrome

366
Q

Serotonin Norepinephrine Reuptake Inhibitors Side effects

A

Drowsiness, dizziness
Insomnia, euphoria
Headache, amnesia
Blurred vision
Erectile/ejaculation dysfunction
Elevated liver enzymes

367
Q

Serotonin Norepinephrine Reuptake Inhibitors Adverse effects

A

Tachycardia, hypertension
Orthostatic hypotension
Seizures, suicidal ideation, insomnia

368
Q

Don’t give to someone with liver disease or alcohol abuse issues

A

Serotonin Norepinephrine Reuptake Inhibitors

369
Q

More of a stimulant effect bc of norepinephrine

A

Serotonin Norepinephrine Reuptake Inhibitors

370
Q

Atypical Antidepressants examples

A

Amoxapine, maprotiline, trazadone(common, hypnotic)

371
Q

Atypical Antidepressants action

A

Affects neurotransmitters: serotonin, norepinephrine, and dopamine. (effects one or two)

372
Q

Atypical Antidepressants uses

A

Major depression, reactive depression, anxiety

373
Q

Atypical Antidepressants interactions

A

MAOIs

374
Q

Atypical Antidepressants Side effects/adverse effects

A

Dry mouth, blurred vision, orthostatic hypotension
Constipation, erectile/ejaculatory dysfunction

375
Q

Called second generation antidepressants

A

Atypical Antidepressants

376
Q

Must be stopped 2 weeks before starting an MAOI

A

Atypical Antidepressants

377
Q

Monoamine Oxidase Inhibitors Examples

A

Tranylcypromine sulfate, isocarboxazide, selegiline, & phenylzine sulfate

378
Q

Monoamine Oxidase Inhibitors action

A

Monoamine oxidase enzyme inactivates norepinephrine, dopamine, epinephrine, and serotonin

379
Q

Monoamine Oxidase Inhibitors use

A

Depression not controlled by TCAs and second-generation antidepressants (Atypical Antidepressants)

380
Q

Enzyme that inactivates neurotransmitters-

A

Monoamine Oxidase

381
Q

High risk of severe adverse effects

A

Monoamine Oxidase Inhibitors

382
Q

Should not be taken at the same time of another antidepressant
Use is limited

A

Monoamine Oxidase Inhibitors

383
Q

Monoamine Oxidase Inhibitors drug interactions

A

CNS stimulants such as vasoconstrictors and some cold medications containing phenylephrine and pseudoephedrine can cause a hypertensive crisis when taken with an MAOI

384
Q

Monoamine Oxidase Inhibitors food interactions

A

Foods containing tyramine

385
Q

MAOI can be fatal due to

A

interactions

386
Q

Phenylephrine- Tylenol (OTC sudafed), Pseudoephedrine with an MAOI can cause

A

hypertensive crisis

387
Q

Foods high in tyramine-

A

Cheese, Yogurt, coffee, chocolate, bananas, raisins, Italian green beans, liver, pickled foods, cured meats (salami, pepperoni), soy sauce, yeast, beer, red wine

388
Q

Monoamine Oxidase Inhibitors Side effects/adverse effects

A

Agitation, restlessness, insomnia
Anticholinergic effects
Orthostatic hypotension
Hypertensive crisis from tyramine interaction
Suicidal ideation

389
Q

Cause CNS stimulation

A

Agitation, restlessness, insomnia

390
Q

Antidepressant Agents Assessment

A

Drug history,
Hepatic and renal function study
Health history
S/Sx having of depression to treat correctly,
Serotonin syndrome and Neuroleptic malignant syndrome.
Already on the meds and effectiveness

391
Q

Antidepressant Agents Nursing Interventions

A

Giving someone entire list of foods when taking MAOIs.
If not compliant need to find different drug

392
Q

Antidepressant Agents Education-

A

Drug effectiveness is not going to be immediate.
Can take 1-3 weeks to become effective.
Cannot stop abruptly.
Side effects will decrease overtime.
Take meds in the morning, that it will be causing stimulation.
Take drugs that cause sedation take in evenings.
Don’t consume alcohol or there CNS depressants.
If drug has Anticholinergic side effects, not giving this to someone with glaucoma.
No driving until they know how they are effected by the meds.

393
Q

Mood Stabilizer: Lithium

A

Mood Stabilizer

394
Q

Lithium therapeutic serum range

A

0.8 to 1.2 mEq/L (narrow)

395
Q

Serum lithium levels greater than __ may lead to toxicity

A

1.5 mEq/L

396
Q

Lithium Action

A

Alteration of ion transport in muscle and nerve cells (in sodium)
Increased receptor sensitivity to serotonin

397
Q

Lithium use

A

Bipolar disorder, manic episodes

398
Q

Help decrease wide ranges of mood swings that they experience

A

Lithium

399
Q

First drug to tx bipolar disorder and still commonly used

A

Lithium

400
Q

Need lithium drug serum levels frequently

A

Lithium

401
Q

Lithium Side effects/adverse reaction

A

Drowsiness, dizziness
Blurred vision, headache
Restlessness, tremors
Memory impairment
Dry mouth, thirst, metallic taste,
GI distress, weight gain/loss
Hypotension, dysrhythmias
Edema of hands and ankles
Increased urination, dehydration

402
Q

Lithium Early s/sx of toxicity=

A

diarrhea, drossiness, N/V, slurred speech, and trembling

403
Q

Lithium Late s/sx of toxicity

A

burred vision, confusion, large output of dilute urine, and convulsions

404
Q

Lithium Interactions Increased lithium level with

A

Thiazides diuretics’, methyldopa, haloperidol, NSAIDs, antidepressants, phenothiazines

405
Q

Lithium Interactions Decreased lithium level with

A

Caffeine, loop diuretics, theophylline

406
Q

Lithium Assessment

A

Evaluating neurological status, gait, LOC, reflexes, and tremors.
History- drug/health.
Watching renal and hepatic lab functions

407
Q

Lithium Nursing Interventions-

A

Early s/sx of toxicity.
Monitoring intake and output.
Intervening clients who are in manic phase of their bipolar disorder to conserve energy.
Checking cardiac function.
Electrolytes (sodium important).

408
Q

Lithium Education-

A

cautious about driving bc of lithium level.
Increase fluid intake in hot weather.
Always have adequate intake of 2/3 liters.
Avoid caffeine.
Can take w meals to decrease GI upset.
Teratogenic.
Need to be aware of appropriate birth control options to prevent pregnancy

409
Q

A patient with reactive depression is ordered to receive fluoxetine (SSRI). Which information will the nurse include when teaching this patient?

A

The medication may cause headaches and insomnia. (take in evening)

410
Q

Before administering a monoamine oxidase inhibitor, it is most important for the nurse to assess the patient’s

A

dietary intake.

411
Q

Which laboratory test is most important for the nurse to monitor when a patient is receiving lithium?

A

Serum electrolytes (sodium)

412
Q

When providing dietary teaching for a patient taking monoamine oxidase inhibitors, the nurse should teach the patient to avoid which food?

A

Yogurt

413
Q

Which advice will the nurse include when teaching the patient about lithium therapy?

A

It may take 1 to 2 weeks before you have any benefits from taking the medication. (common for all antidepressants)

414
Q

Which statement about amitriptyline (TCAs) does the nurse identify as being true?

A

The drug should be discontinued slowly.

415
Q
A

NSG (13 decks)

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