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
Does not cure seizures it manages the symptoms
Antiseizure Drugs
26
Taken for lifetime
Antiseizure Drugs
27
If not seizure activity for 3-5 years
Antiseizure Drugs
28
First group of anti seizure meds developed in 1938. prototype for antiseizure drugs
Hydantoins
29
Phenytoin (Dilantin)
Hydantoins
30
Phenytoin (Dilantin) Action
Inhibits sodium influx into the nerves cells, decreasing neuron from firing
31
Phenytoin (Dilantin) Dosing
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.
32
Phenytoin (Dilantin) Therapeutic serum level
10 to 20 mcg/mL
33
Phenytoin (Dilantin) Contraindications
Pregnancy- Teratogenic drug
34
Phenytoin (Dilantin) Benefit
Slightly sedating and not addictive- benefit
35
Phenytoin (Dilantin) Highly protein bound=
more free drug= more risk of toxicity
36
Psychiatric effects- Depression or suicidal ideation
Phenytoin (Dilantin) Side effect
37
Nystagmus- involuntary eye movement, diplopia- double eye vision
Phenytoin (Dilantin) Side effect
38
Headache, dizziness, drowsiness(can occur at a therapeutic drug level)
Phenytoin (Dilantin) Side effect
39
N/V, constipation
Phenytoin (Dilantin) Side effect
40
Gingival hyperplasia- overgrowth of the gums that causes easily bleeding, normal side effect at a therapeutic level
Phenytoin (Dilantin) Side effect
41
Alopecia- hair loss hirsutism- excessive body hair
Phenytoin (Dilantin) Side effect
42
Discolored urine- pink or red, brownish. educate clients, normal side effect
Phenytoin (Dilantin) Side effect
43
Hyperglycemia- happens in long-term use, inhibits release of insulin. Blood sugar checks
Phenytoin (Dilantin) Side effect
44
Blood dyscrasias0 thrombocytopenia(low platelet) leukopenia(low WBC counts)
Phenytoin (Dilantin) Side effect
45
Purple glove syndrome- swelling discoloration and decrease blood flow to the hands can require amputation
Phenytoin (Dilantin) Side effect
46
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
Phenytoin (Dilantin) Side effect
47
Phenytoin Drug Interactions: Anticoagulants & ASA-
displace the anticoagulant (beats it), adds longer acting time of the anticoagulant
48
Phenytoin Drug Interactions: Barbiturates, rifampin, & alcohol-
increase metabolism, may need a higher dose
49
Phenytoin Drug Interactions: Sulfonamides and cimetidine-
can increase action of a hydantoin by inhibiting liver metabolism.
50
Phenytoin Drug Interactions: Antacids, calcium preparations, sucralfate, and antineoplastic-
Decrease the absorption
51
Phenytoin Drug Interactions: Antipsychotics and certain herbs-
decrease the seizure threshold, lowers drug therapeutic range, low enough so a seizure can be induces.
52
Highly protein bound drug it competes with other highly protein bound drugs for the receptor sites
Phenytoin
53
Phenytoin Assessment
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.
54
Phenytoin NSG Interventions
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.
55
Phenytoin Education
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.
56
Phenobarbital
Barbiturate
57
Phenobarbital Action
Enhances GABA activity, reduce the excitability of the CNS
58
Phenobarbital Used to tx
Tonic–clonic, partial, status epilepticus
59
Longer than 5 minutes seizures or so close together that the pt cannot recover in-between
status epilepticus
60
Phenobarbital Therapeutic serum range
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)
61
Phenobarbital Side effects
Sedation tolerance-gradually withdrawal decreased teratogenic risk- safest drugs for pregnancy and seizures
62
Phenobarbital Discontinuation
Should be gradual
63
What type of acting barbiturate is Phenobarbital
Long acting barbiturate
64
What type of acting are Sedative hypnotics
Short acting
65
Ethosuximide (Zarontin)
Succinimides
66
Ethosuximide (Zarontin) Action
Decreases calcium influx which prevents the electrical current generated by the calcium ions
67
Ethosuximide (Zarontin) Use to tx
Absence seizures (petit mal)- found in children
68
Ethosuximide (Zarontin) Therapeutic serum range-
40 to 100 mcg/mL wide therapeutic range
69
GI upset- educate to take with food
Ethosuximide (Zarontin) Side effects/Adverse effects
70
Dizziness, drowsiness, headache, nightmares
Ethosuximide (Zarontin) Side effects/Adverse effects
71
Suicidal ideation
Ethosuximide (Zarontin) Side effects/Adverse effects
72
Gingival hyperplasia- measurable side effect and manageable, does not mean toxic level
Ethosuximide (Zarontin) Side effects/Adverse effects
73
Ataxia- lack of coordination
Ethosuximide (Zarontin) Side effects/Adverse effects
74
Blood dyscrasias
Ethosuximide (Zarontin) Side effects/Adverse effects
75
Renal and liver impairment
Ethosuximide (Zarontin) Side effects/Adverse effects
76
Systemic lupus erythematous -Once med is stopped= SLE will stop
Ethosuximide (Zarontin) Side effects/Adverse effects
77
Can have anti seizure effects
Benzodiazepines
78
Benzodiazepines that have anti seizure effects
Clonazepam (Klonopin) Clorazepate dipotassium (Tranxene) Diazepam (Valium)
79
Treats absence seizures Tolerance may occur in 6 months of starting therapy, increase dosage after that time frame
Clonazepam (Klonopin)-
80
Treats partial seizures and anxiety, alcohol withdrawal
Clorazepate dipotassium (Tranxene)
81
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
Diazepam (Valium)
82
Carbamazepine (Tegretol)- most commonly used drug in this drug class
Iminostilbenes
83
Carbamazepine (Tegretol) Tx
Tonic–clonic, partial seizures Also used for psychiatric disorders (BPD), nerve pain (trigeminal neuralgia, diabetic neuropathy), and alcohol withdrawal
84
Carbamazepine (Tegretol) Therapeutic serum range
4 to 12 mcg/mL (narrow TR) Monitor drug serum level closely
85
Carbamazepine (Tegretol) Side Effects
Dizziness, drowsiness, headache, blurred vision GI distress Ataxia Weakness Anemia Agranulocytosis- low WBC count Stevens-Johnson syndrome- rare
86
Grapefruit juice increases bioavailability of this drug, increasing risk for drug toxicity
Carbamazepine (Tegretol)
87
Valproic Acid (Depakote) Uses
tonic–clonic & absence
88
Valproic Acid (Depakote) Therapeutic serum range
50 to 100 mcg/mL Wide therapeutic range
89
Valproic Acid (Depakote) Side effects/Adverse reactions
Dizziness Drowsiness Insomnia Diplopia Weakness GI distress Suicidal ideation Thrombocytopenia Hepatotoxicity- major adverse reaction, monitor liver labs closely
90
Not safe for children under the age of 2
Valproic Acid (Depakote)
91
Antiseizure Drugs and Pregnancy: Seizure episodes can increase and
Teratogenesis
92
Antiseizure Drugs and Pregnancy: ____ are linked to cardiac defects, cleft lip, palate defects
Phenytoin & Carbamazepine
93
Antiseizure Drugs and Pregnancy: Occur in small percentage of infants, 4-8% chance of congenital defects if they take it during pregnancy
Valproic acid
94
Antiseizure Drugs and Pregnancy: least amount of effects on fetus
Phenobarbital
95
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
Vitamin K
96
Antiseizure Drugs and Pregnancy: Risk for neural tube defects.
Increase Folic acid
97
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)
25%
98
More than one drug to have a decrease seizure activity in pregnancy bc of metabolic rate
increases
99
Antiseizure Drugs and Febrile Seizures: Febrile Seizures-
increase in body temp, most commonly seen of 3 month-5yrs. About 2.5% of children who have febrile seizures develop epilepsy.
100
Antiseizure Drugs and Febrile Seizures: Seizures associated with
fever
101
Antiseizure Drugs and Febrile Seizures: Development of epilepsy is
uncommon
102
Antiseizure Drugs and Febrile Seizures: Prophylactic treatment for high-risk patients- if using preventative meds
Phenobarbital Diazepam
103
Preventative seizures meds are not indicative Only at a high risk for developing seizures
Antiseizure Drugs and Febrile Seizures
104
Antiseizure Drugs and Status Epilepticus: Medical
emergency
105
Antiseizure Drugs and Status Epilepticus: Needs
Tx
106
Antiseizure Drugs and Status Epilepticus: Diazepam IV (drug of choice, benzo) or Lorazepam IV followed by
Followed by IV Phenytoin or Phenobarbital
107
Antiseizure Drugs and Status Epilepticus: Continued Seizures worry about (sedation, depression, respiratory) Used for surgical procedures, depression of CNS
Midazolam-versed Propofol
108
If not treated it can result in death
Status epilepticus
109
What is the highest priority nursing diagnosis for a patient taking phenytoin (sedative effect, dizziness, ataxia)?
Risk for falls
110
Before administering a daily dose of phenytoin, it is most important for the nurse to
check phenytoin levels. 10-20 therapeutic range, narrow
111
When assessing a patient taking hydantoin therapy for seizure disorder, which indicates an adverse reaction to this therapy?
Thrombocytopenia (blood dyscrasias)
112
A patient is experiencing status epilepticus. The nurse anticipates immediate administration of which drug?
Diazepam
113
Chronic progressive neurologic disorder
Parkinson’s Disease Pathophysiology
114
Degeneration of dopaminergic neurons leading to a lack of dopamine
Parkinson’s Disease Pathophysiology
115
Imbalance of neurotransmitters not enough dopamine compared to acetylcholine
Parkinson’s Disease Pathophysiology
116
No cure, effects the extrapyramidal system, controls out posture balance and locomotion
Parkinson’s Disease
117
Results from loss of neurons that are producing dopamine, part of the brain called the substantia nigra
Parkinson’s Disease
118
Dopamine controls excitatory response from the acetylcholine
Parkinson’s Disease
119
Too much acetylcholine stimulates too much GABA which causes the symptoms
Parkinson’s Disease
120
Effects more men than women
Parkinson’s Disease
121
Can occur with Carbon monoxide and manganese poisoning
Parkinson’s Disease
122
Pseudoparkinsonism
Result of getting Parkinson like symptoms that are caused by other drugs Frequently occurs as an adverse reaction to various drugs
123
Pseudoparkinsonism causing meds
Chlorpromazine Haloperidol Lithium Metoclopramide Methyldopa Reserpine
124
Parkinson’s Disease Characteristics
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
125
Nonpharmacologic measures for Parkinson’s Disease:
Exercise, Nutrition, and Group support
126
Exercise-
Improve mobility and flexibility, used to help slow the decline in the quality of life
127
Nutrition-
fiber and fluids diet to prevent weight loss and constipation. Constantly tremoring, caloric intake and output equal imbalanced
128
Group support-
family members/caregivers because of chronic progressive disease, coping
129
Parkinson’s Disease Treatment
Anticholinergics, Dopamine replacements, Dopamine agonists, MAO-B inhibitors, COMT inhibitors,
130
Anticholinergics-
blocking receptors of acetylcholine bc too much. Allows dopamine balance to be restored
131
Dopamine replacements-
replacing endogenous dopamine and binding with dopamine receptors
132
Dopamine agonists-
dopamine replacement, stimulating dopamine receptor
133
MAO-B inhibitors-
inhibits monoamine oxidase b enzyme, involved in the metabolism of dopamine, decrease dopamine metabolism to increase dopamine receptors. Inhibiting the break down
134
COMT inhibitors- catechol o methyltransferase
Enzyme that deactivates dopamine, inhibiting that from occurring. Allows more dopamine to be available. Antagonist agonist
135
Replace dopamine and reduce symptoms
Parkinson’s Disease Treatment
136
Antiparkinson Drugs
Anticholinergics
137
Anticholinergics Example
Benztropine & Trihexyphenidyl
138
Benztropine & Trihexyphenidyl Action
Reduces rigidity and some of the tremors Minimal effect on bradykinesia
139
Benztropine & Trihexyphenidyl Side effects
Blurred vision Mydriasis Ocular hypertension (Glaucoma contra) Weakness Dry mouth (regulate drooling), Constipation Anhidrosis(decreased sweating) Urinary retention
140
Activating the nicotinic receptors and muscuenic receptors through out the body
Anticholinergics
141
Helps reduce the muscle tone and tremors, does not have good effect on the bradykinesia
Anticholinergics
142
Also used to treat pseudo Parkinson, drug induced Parkinson's
Anticholinergics
143
Antiparkinson: Anticholinergic Agent Assessment
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
144
Antiparkinson: Anticholinergic Agent NSG Interventions
vital signs urinary retention bowel movements watch for increase pulse rate hypervolemia constipation, monitor effects on drugs and how effective they are on symptoms.
145
Antiparkinson: Anticholinergic Agent Education
Safety measures- safety bar in shower, elevated toilet seat, shower chair, removing throw rugs. Adding extra lighting, eliminating danger.
146
Dopaminergics
Antiparkinson Drugs
147
Dopaminergics Example
Carbidopa-levodopa
148
Carbidopa
Prolongs the effect of levodopa
149
Carbidopa-levodopa action
Converts to dopamine and increases mobility
150
Carbidopa-levodopa Side effects
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
151
Dopamine itself cannot cross BBB but
levodopa can by converting into dopamine
152
___ inhibits the enzyme decarboxylase that’s breaking down levodopa in the body
Carbidopa
153
levodopa turns into dopamine = increasing levels of
dopamine
154
When levodopa is used alone, only __ reaches the brain because __ converts to dopamine while in the peripheral nervous system
1% 99%
155
By combining carbidopa with levodopa, carbidopa can inhibit the enzyme __ in the periphery, thereby allowing more levodopa to reach the brain.
decarboxylase
156
Levodopa taken alone-
10mg of 500mg reaches the brain, 5%
157
When carbidopa given with levodopa a smaller dose-
10mg of 100mg gets to the brain = 10% effectiveness, decreases side effects
158
Dopaminergics (carbidopa-Levodopa) Asessment
vital sign baseline, drug history, medical history, s/sx
159
Dopaminergics (carbidopa-Levodopa) Nursing Interventions-
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
160
Dopaminergics (carbidopa-Levodopa) Education
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.
161
Bromocriptine(dopaminergic)
Dopamine Agonists
162
Bromocriptine(dopaminergic) Action
Acts directly on dopamine receptors in CNS, cardiovascular system, & GI tract Used when pts do not tolerate carbidopa-levodopa
163
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
Bromocriptine(dopaminergic)
164
Selegiline
Monoamine Oxidase B Inhibitors
165
Selegiline Action
Inhibit MAO-B enzyme that interferes with dopamine
166
Selegiline Interaction
Food high in tyramine can cause hypertensive crisis CNS toxicity with tricyclic antidepressants or SSRIs
167
Breaks down dopamine enzyme, Inhibiting from occurring
Selegiline
168
The action of dopamine in levodopa is prolonged
Selegiline
169
Used as early tx before carbadop-levodopa
Selegiline
170
Large doses of MAO B inhibitor can inhibit MAO A enzyme
Selegiline
171
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
Selegiline
172
Tolcapone & Entacapone
Catechol-O-Methyltransferase COMT Inhibitors
173
Tolcapone & Entacapone Action
Inhibit COMT enzyme that inactivates dopamine. Increase the amount of dopamine Often combined with carbidopa-levodopa. Can decrease both dosages
174
Hepatoxic (liver enzymes)
Tolcapone
175
less risk for liver toxicity but cause brown/orange urine. No effect on liver fxn
Entacapone
176
Form of Incurable dementia illness
Alzheimer’s Disease
177
Chronic, progressive neurodegenerative disorder
Alzheimer’s Disease
178
Onset usually between ages 45 and 65
Alzheimer’s Disease
179
Alzheimer’s Disease Pathophysiology
Cholinergic neuron degeneration and acetylcholine deficiency Neuritic plaques/neurofibrillary tangles
180
Alzheimer’s Disease Etiology- unknown
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
Neurodegenerative disorder
Alzheimer’s Disease
182
Increased marked cognitive dysfunction
Alzheimer’s Disease
183
Can give meds to try and slow progression of symptoms
Alzheimer’s Disease
184
Can cause sedentary lifestyle.
Alzheimer’s Disease
185
Occur more in women than in men, risk more occurrence bc women live longer
Alzheimer’s Disease
186
Alzheimer’s Disease Pathophysiology Histologic changes
Neuron affected by Alzheimer’s disease showing characteristic neuritic plaques and cellular neurofibrillary tangles.
187
Alzheimer’s Disease Mild (early stage)
still living independently, trouble planning and organizing, memory loss
188
Alzheimer’s Disease Moderate (middle stage)
increased memory loss, personality changes, not able to perform routine tasks, loss of bowel and bladder control
189
Alzheimer’s Disease Severe (late stage)-
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
Rivastigmine & Donepezil
Acetylcholinesterase/ Cholinesterase Inhibitors
191
Rivastigmine & Donepezil Action
Inhibit the action of acetylcholinesterase Cause increased levels of acetylcholine in the CNS Increase cognitive function and delay loss of brain function
192
Rivastigmine & Donepezil Side effects
Related to an increase in acetylcholine in the peripheral nervous system as well Parasympathetic response- bronchoconstriction, bradycardia, hypotension
193
Rivastigmine & Donepezi Treats
Mild to moderate Alzheimer's disease
194
Rivastigmine (Exelon) Side effects/Adverse effects (results from parasympathetic nervous system activation)
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
Rivastigmine (Exelon) Drug Interactions
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
Transdermal patch or tablet form, 2x a day, mild to moderate Alzheimer's
Rivastigmine (Exelon)
197
Rivastigmine Assessment
Stage of disease, physically and mentally able to do, support system look like. Maintain consistency and care- same staff members.
198
Rivastigmine NSG interventions
Assisting with ambulation and activity. Goal to help independence as possible. Monitor side effects. Noting improvement or decline in function
199
Rivastigmine Education
home safety, side effects, reason for drug regimen, info about support groups
200
Memantine (Namenda)
NMDA receptor antagonist
201
Memantine (Namenda) Action
Blocks effects of neurotransmitter glutamate at NMDA receptors
202
Memantine (Namenda) Side effects/adverse effects
Fewer than acetylcholinesterase inhibitors Most common: Dizziness, HA, drowsiness, confusion, constipation or diarrhea Stevens-Johnson syndrome Depression, Hallucinations Hyper or hypotension, urinary incontinence
203
Learning capability and memory- NMDA
Memantine (Namenda)
204
Tx moderate to severe Alzheimer's
Memantine (Namenda)
205
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
unknown.”
206
Which comment to the nurse indicates more teaching is needed for a patient taking carbidopa/levodopa?
“I know I need to take this drug once a day.”
207
Which side effect/adverse effect of carbidopa/levodopa does the nurse realize is most important to monitor?
Agranulocytosis- decrease in WBCs
208
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
glaucoma
209
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,
“The carbidopa helps the levodopa reach the brain.”
210
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
slow the progression of symptoms of Alzheimer disease.
211
Autoimmune disorder
Myasthenia Gravis Pathophysiology
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Antibodies attach to acetylcholine receptor sites, obstruct binding of acetylcholine, and destroy receptor sites
Myasthenia Gravis Pathophysiology
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Lack of acetylcholine impairs transmission of messages at neuromuscular junctions
Myasthenia Gravis Pathophysiology
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Non-curable
Myasthenia Gravis
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Myasthenia Gravis Result
Respiratory, facial, and extremity weakness Muscles that are not getting their receptor sites fulfilled
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___ is the neurotransmitter for the parasympathetic nervous system
Acetylcholine
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Myasthenia Gravis occurs more in women of child bearing age years =
20-40yrs
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Myasthenia Gravis peak male age
50-70
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Tend to run in families
Myasthenia Gravis
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Lymph organ
Myasthenia Gravis: Thymus Gland
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Produces T cells
Myasthenia Gravis: Thymus Gland
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Enlarged in 60% of MG patients- produce antibodies that add acetylcholine to receptor sites. Over production of antibodies occur.
Myasthenia Gravis: Thymus Gland
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Remove the thymus gland, reduce number of antibodies
Myasthenia Gravis: Thymectomy
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Skeletal muscle weakness
Myasthenia Gravis Characteristics
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Fatigue, ptosis, diplopia, dysphagia, dysarthria
Myasthenia Gravis Characteristics
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Respiratory muscle weakness, paralysis, and arrest
Myasthenia Gravis Characteristics
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Fluctuating muscle weakness especially when someone is using that muscle a lot
Myasthenia Gravis Characteristics
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Respiratory arrest due to
paralysis of muscles in the lungs, Myasthenia Gravis
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Facial muscles-
Ptosis, difficulty chewing, drooping eyelids, and dysphagia, Myasthenia Gravis
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Extremities are the most effected
Myasthenia Gravis
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Causes Severe generalized muscle weakness- involve respiratory muscles = death
Myasthenic crisis
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Involves diaphragm and intercostal muscles
Myasthenic crisis
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Myasthenic crisis triggers
Inadequate dosing of AChE inhibitors Emotional stress, menstrual cycle, pregnancy Infection, surgery, trauma Hypokalemia, alcohol intake Temperature extremes Medication interactions
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Treat with neostigmine- a fast acting ACHe inhibitor, prevents breakdown of acetylcholine
Myasthenic crisis
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Myasthenic crisis can occur 3-4 hours after taking certain meds=
Aminoglycoside antibiotics, Phenytoin, CCBs, Psychotropics
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Usually occurs within 30 to 60 minutes after taking excess anticholinergic medications
Cholinergic crisis
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Triggered by overdosing
Cholinergic crisis
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Cholinergic crisis symptoms
Severe muscle weakness Possible respiratory paralysis and arrest Miosis (pupil constriction) Pallor, sweating, vertigo Excess salivation, GI distress, vomiting Bradycardia, fasciculations (muscle twitching)
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Occurs when too much of an Acetylcholinesterase inhibitor at the receptor sites Nerves are over stimulated when having too much Acetylcholine
Cholinergic crisis
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Can cause respiratory arrest
Cholinergic crisis
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Antidote: Atropine
Cholinergic crisis
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Acetylcholinesterase inhibitors
Edrophonium (Tensilon), Neostigmine, Pyridostigmine
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Acetylcholinesterase inhibitor action
Increases muscle strength in patients with myasthenia gravis
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Medication differentiating between myasthenic (if it works) and cholinergic crises (if it worsens)
Edrophonium (Tensilon)
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Ultra-short-acting- (worsened symptoms resolve quickly), need emergency precautions
Edrophonium (Tensilon)
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Short-acting
Neostigmine
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Intermediate-acting
Pyridostigmine
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Decreasing break down the the acetylcholine at the sites
Acetylcholinesterase Inhibitors
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Acetylcholinesterase Inhibitors Side effects
Miosis Blurred vision Bradycardia Hypotension GI distress- Nausea, vomiting, diarrhea, abdominal cramps
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PNS stimulation Increase acetylcholine Activates both muscarinic and nicotinic receptor sites
Acetylcholinesterase Inhibitors
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Patients Unresponsive to Acetylcholinesterase Inhibitors
Prednisone, Plasma exchange, Intravenous immune globulin, Immunosuppressive drugs
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Prednisone-
If the AChe are not effective Drug of choice
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Intravenous immune globulin-
IGG
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Immunosuppressive drugs
Azathioprine- Intense drug, need to be monitored for hepatotoxicity and leukopenia
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Pyridostigmine Assessment-
Drug history Labs S/Sx if being effective or over effective Ability to swallow,
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Pyridostigmine Nursing Interventions-
Monitoring and watching for drug effectiveness, S/Sx or myasthenic crisis or cholinergic crisis Make sure family is involved (addressing psychosocial needs)
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Pyridostigmine Education-
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)
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Autoimmune disorder Attacks myelin sheath of nerve fibers in brain and spinal cord Causes lesions (plaques)
Multiple Sclerosis Pathophysiology
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Multiple Sclerosis Motor Characteristics
Motor symptoms- Weakness or paralysis of extremities, fatigue, muscle spasticity, paresthesia
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Remissions and exacerbations
Multiple Sclerosis
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Multiple Sclerosis Sensory symptoms
Numbness and tingling, double vision (first symptom that they experience), vertigo, tinnitus
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Multiple Sclerosis Cerebellar symptoms-
nystagmus, ataxia, dysarthria, and dysphagia
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May have neuropathic pain in lower back or abdominal area
Multiple Sclerosis
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Slows down nerve impulse transmission
Multiple Sclerosis
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No cure Can give meds to slow disease process and improve symptoms
Multiple Sclerosis
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Multiple Sclerosis diagnosis is
difficult
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Multiple Sclerosis diagnosis
Medical history Neurologic exam MRI Cerebrospinal fluid analysis Evoked potential test
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MRI-
lesions in the brain or spinal column
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Cerebrospinal fluid analysis-
may have elevated IgG antibodies
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Evoked potential test-
measuring electric activity in the brain as the response of stimulation of a nerve pathway
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Oligoclonal bands-
proteins that are the product of the myelin sheath breakdown
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Multiple Sclerosis Tx:
Immunomodulators and immunosuppressants
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Immunomodulators
disease modifying drugs
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immunosuppressants
slowing disease process and prevention of relapse of an exacerbation
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First-line treatment Slows disease progression and prevents relapses
Immunomodulators and immunosuppressants
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Immunomodulators and immunosuppressants example
Beta interferon
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Beneficial in reducing edema or acute inflammation that is occurring at the direct area of myelin sheath breakdown.
Multiple Sclerosis tx: Corticosteroids
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Used for acute exacerbations not for long term (sick symptoms can worsen), increases BGL on long term meds
Multiple Sclerosis tx: Corticosteroids
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Reduces edema and acute inflammation
Multiple Sclerosis tx: Corticosteroids
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Corticosteroid example
Methylprednisolone(solumedrol)
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Skeletal muscle relaxants
Centrally acting muscle relaxants Direct acting muscle relaxant
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Centrally acting muscle relaxants
Relieves muscle spasm and spasticity Have sedative effect
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Direct acting muscle relaxants
Decreases muscle spasm pain and increases range of motion Suppresses hyperactive reflex
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Skeletal Muscle Relaxants side effects
Drowsiness, dizziness, headache, nausea, vomiting
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Used to alleviate muscle spasms and injury that causes it
Skeletal Muscle Relaxants
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Sedative effect, do not give any other cns depressants
Skeletal Muscle Relaxants
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All muscle relaxants Can cause drug dependence except cyclobenzaprine
Skeletal Muscle Relaxants
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Do not put someone on long-term
Skeletal Muscle Relaxants
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Can have anticholinergic side effect
Skeletal Muscle Relaxants
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Cyclobenzaprine
Skeletal Muscle Relaxants
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Cyclobenzaprine action
Relax skeletal muscles
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Cyclobenzaprine uses
Relieves muscle spasm
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Cyclobenzaprine side effects
Anticholinergic effects- Blurred vision, dry mouth, urine retention, constipation, tachycardia Drowsiness, dizziness Headache, nervousness, confusion GI distress, unpleasant taste Dysrhythmias
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Prototype drug of skeletal relaxants
Cyclobenzaprine
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Only skeletal relaxant that does not cause dependence
Cyclobenzaprine
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Benefits SUD
Cyclobenzaprine
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Weaning off drug because can cause muscle spasm rebound
Cyclobenzaprine
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Baclofen Carisoprodol (Soma) Chlorzoxazone (Parafon Forte) Methocarbamol
Skeletal Muscle Relaxants
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PO, Intrathecally (spinal column)-pump is surgically implanted, catheter into the spinal column. Can be continues or scheduled, gives low continual dose (steady state)
Baclofen
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Cyclobenzaprine- Assessment
Drug history and medical history
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Cyclobenzaprine- Nsg interventions
Hepatic functions (can become toxic) Observing S/E for CNS depression (still need to function)
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Cyclobenzaprine- Education
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
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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?
Neostigmine
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The patient is admitted to the emergency department with cholinergic crisis. The nurse anticipates administration of
atropine.
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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?
Edrophonium
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A patient with myasthenia gravis is prescribed neostigmine. The nurse identifies that the medication is effective when the patient experiences
increased muscle strength.
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A patient with multiple sclerosis is being treated with large doses of corticosteroids. Which nursing diagnosis would be the priority at this time?
Risk for infection
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A child with cerebral palsy is ordered to receive baclofen. The nurse is aware that this medication is prescribed to
reduce muscle spasticity.
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Depression Etiology
Genetic predisposition Social and environmental factors
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Depression Pathophysiology theories
Decreased levels of monoamine neurotransmitters- predisposed to depression when decreased neurotransmitters
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Monoamine neurotransmitters
Norepinephrine, serotonin, dopamine
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Depression S/Sx
Depressed mood, despair, weight loss or gain Loss of interest in most activities Fatigue, insomnia, hypersomnia Decreased ability to think or concentrate Suicidal thoughts
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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?
Suicidal thoughts
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Most common mental illness, 1/3 of people experience depression ½ of people seek treatment, 2/3 of the tx have remission
Depression
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Depression contributing factors:
Hx of abuse Genetic component Experience of illness Traumatic life event Personal problems and Substance abuse (self medicating prescription or elicit)
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Types of depression
Reactive depression, Major depression, Bipolar disorder
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Reactive depression-
Occur after a precipitating event- death of a loved one, divorce. Can last months.
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Major depression Primary-
unrelated to any health problems.
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Major depression Secondary-
Related to physical (postpartum depression) or psychiatric disorder or drug misuse
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Bipolar disorder-
Mood is fluctuating between manic state (euphoria) and really low depression state
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Complementary and Alternative Therapy for Depression
Ginkgo biloba and St. John’s wort, Psychotherapy Somatic therapies, Exercise, Light therapy
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Ginkgo biloba and St. John’s wort- decreased reuptake of monoamine neurotransmitter
Discontinue use of herbal products 1 to 2 weeks before surgery. Check with the health care provider before taking herbal treatments.
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Somatic therapies
ECT Transcranial magnetic stimulation
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ECT
short acting neuromuscular blocker, short acting IV is given
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Transcranial magnetic stimulation
magnetic pulses that are directed to the areas of the brain that control mood
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Exercise-
releases endorphins
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Light therapy-
experiencing seasonal effective disorder
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Not be combines with prescription antidepressants- ginkgo. Causes:
Extreme dizziness, headache, sweating= Serotonin syndrome
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Antidepressant Groups
Tricyclic antidepressants (TCAs) Selective serotonin reuptake inhibitors (SSRIs) Serotonin norepinephrine reuptake inhibitors (SNRIs) Atypical antidepressants Monoamine oxidase inhibitors (MAOIs)
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TCAs and MAOIs=
more side effects, not used as often, developed in 1950s. older med.
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SSRIs and SNRIs=
1980s, less side effects, more used
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Tricyclic Antidepressants Examples:
Amitriptyline Imipramine Trimipramine Doxepin Nortriptyline Protriptyline
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Blocks uptake of neurotransmitters norepinephrine and serotonin in brain
Tricyclic Antidepressants Action
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Elevates mood, increases interest in ADLs, decreases insomnia
Tricyclic Antidepressants Action
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Blocks histamine receptors which leads to sedation
Tricyclic Antidepressants Action
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Blocks cholinergic receptors which leads to anticholinergic effects
Tricyclic Antidepressants Action
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As effective as SSRIs but have a lot of side effects
Tricyclic Antidepressants
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Tricyclic Antidepressants Use
Major depression
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It takes 2-4 weeks to become effective, if ineffective in that time frame they need to be tapered off of the med
Tricyclic Antidepressants
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Tricyclic Antidepressants Side effects/adverse reactions
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
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Sedation is the major side effect
Tricyclic Antidepressants
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Also have anticholingeric effects- tachycardia, urine retention, blurred vision
Tricyclic Antidepressants
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Can cause leukopenia, thrombocytopenia, agranulocytosis
Tricyclic Antidepressants
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Amatriptaline- Extrapyramidal symptoms
Tricyclic Antidepressants
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Clomipramine- cause neuroleptic malignant system, fever, rigidify to muscles, autonomic hyperactivity(SNS stimulation)
Tricyclic Antidepressants
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__ can lower seizure threshold- if have epilepsy they need to increase seizure medications
Tricyclic Antidepressants
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High doses of __ cause cardiotoxicity and dysrhythmias, can be lethal
Tricyclic Antidepressants
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Tricyclic Antidepressants Interactions
Alcohol and other CNS depressants potentiate CNS depression MAOIs may lead to toxic psychosis, cardiotoxicity Antithyroid drugs may increase dysrhythmias
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Must wait 2 weeks after stopping MAOI to give ___
Tricyclic Antidepressants
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Increased risk for dysrhythmia when taking
methimazole, Tricyclic Antidepressants
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Selective Serotonin Reuptake Inhibitors Example
Fluoxetine(Prozac), sertraline, paroxetine, citalopram
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Fluoxetine(Prozac)-
Positive results in 50-60% who don’t respond well to a TCA (prototype)
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Selective Serotonin Reuptake Inhibitors Action
Block uptake of neurotransmitter serotonin which allows more serotonin to effect the receptor sites=more availability of serotonin
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Selective Serotonin Reuptake Inhibitors Uses
Major depression (primary use) Anxiety disorders Prevention of migraine headaches Decrease premenstrual tension syndrome Eating disorders Substance use disorder
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Can have Weekly delayed dose, must see daily dosing first
Selective Serotonin Reuptake Inhibitors
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Selective Serotonin Reuptake Inhibitors Interactions
Increased sedation with alcohol and other CNS depressants Grapefruit juice with SSRIs can lead to toxicity
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Selective Serotonin Reuptake Inhibitors Side effects/adverse reactions
Headache, insomnia Blurred vision Dry mouth, GI distress Erectile dysfunction Suicidal ideation Side effects often decrease over 1 to 4 weeks
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More popular than TCA bc they cause less side effects
Selective Serotonin Reuptake Inhibitors (SSRI)
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Not much a risk of cardiotoxicity
Selective Serotonin Reuptake Inhibitors (SSRI)
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Dosage should be decreased in older clients bc of CNS depression and lower metabolism
Selective Serotonin Reuptake Inhibitors (SSRI)
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Can cause increase appetite so weight gain is common
Selective Serotonin Reuptake Inhibitors (SSRI)
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S/E decrease libido, nervousness, insomnia, can decreased overtime
Selective Serotonin Reuptake Inhibitors (SSRI)
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Monitor for suicidal ideation especially when first beginning tx
Selective Serotonin Reuptake Inhibitors (SSRI)
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Should be tapered off, not stopped abruptly
Selective Serotonin Reuptake Inhibitors (SSRI)
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Serotonin Norepinephrine Reuptake Inhibitors examples
Venlafaxine, duloxetine, desvenlafaxine
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Serotonin Norepinephrine Reuptake Inhibitors Action
Inhibit the reuptake of serotonin and norepinephrine
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Serotonin Norepinephrine Reuptake Inhibitors Use
Major depression Generalized anxiety disorder Social anxiety disorder
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Serotonin Norepinephrine Reuptake Inhibitors Interactions
St. John’s wort- high risk for serotonin syndrome and neuroleptic malignant syndrome
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Serotonin Norepinephrine Reuptake Inhibitors Side effects
Drowsiness, dizziness Insomnia, euphoria Headache, amnesia Blurred vision Erectile/ejaculation dysfunction Elevated liver enzymes
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Serotonin Norepinephrine Reuptake Inhibitors Adverse effects
Tachycardia, hypertension Orthostatic hypotension Seizures, suicidal ideation, insomnia
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Don’t give to someone with liver disease or alcohol abuse issues
Serotonin Norepinephrine Reuptake Inhibitors
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More of a stimulant effect bc of norepinephrine
Serotonin Norepinephrine Reuptake Inhibitors
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Atypical Antidepressants examples
Amoxapine, maprotiline, trazadone(common, hypnotic)
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Atypical Antidepressants action
Affects neurotransmitters: serotonin, norepinephrine, and dopamine. (effects one or two)
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Atypical Antidepressants uses
Major depression, reactive depression, anxiety
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Atypical Antidepressants interactions
MAOIs
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Atypical Antidepressants Side effects/adverse effects
Dry mouth, blurred vision, orthostatic hypotension Constipation, erectile/ejaculatory dysfunction
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Called second generation antidepressants
Atypical Antidepressants
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Must be stopped 2 weeks before starting an MAOI
Atypical Antidepressants
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Monoamine Oxidase Inhibitors Examples
Tranylcypromine sulfate, isocarboxazide, selegiline, & phenylzine sulfate
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Monoamine Oxidase Inhibitors action
Monoamine oxidase enzyme inactivates norepinephrine, dopamine, epinephrine, and serotonin
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Monoamine Oxidase Inhibitors use
Depression not controlled by TCAs and second-generation antidepressants (Atypical Antidepressants)
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Enzyme that inactivates neurotransmitters-
Monoamine Oxidase
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High risk of severe adverse effects
Monoamine Oxidase Inhibitors
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Should not be taken at the same time of another antidepressant Use is limited
Monoamine Oxidase Inhibitors
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Monoamine Oxidase Inhibitors drug interactions
CNS stimulants such as vasoconstrictors and some cold medications containing phenylephrine and pseudoephedrine can cause a hypertensive crisis when taken with an MAOI
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Monoamine Oxidase Inhibitors food interactions
Foods containing tyramine
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MAOI can be fatal due to
interactions
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Phenylephrine- Tylenol (OTC sudafed), Pseudoephedrine with an MAOI can cause
hypertensive crisis
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Foods high in tyramine-
Cheese, Yogurt, coffee, chocolate, bananas, raisins, Italian green beans, liver, pickled foods, cured meats (salami, pepperoni), soy sauce, yeast, beer, red wine
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Monoamine Oxidase Inhibitors Side effects/adverse effects
Agitation, restlessness, insomnia Anticholinergic effects Orthostatic hypotension Hypertensive crisis from tyramine interaction Suicidal ideation
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Cause CNS stimulation
Agitation, restlessness, insomnia
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Antidepressant Agents Assessment
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
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Antidepressant Agents Nursing Interventions
Giving someone entire list of foods when taking MAOIs. If not compliant need to find different drug
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Antidepressant Agents Education-
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.
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Mood Stabilizer: Lithium
Mood Stabilizer
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Lithium therapeutic serum range
0.8 to 1.2 mEq/L (narrow)
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Serum lithium levels greater than __ may lead to toxicity
1.5 mEq/L
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Lithium Action
Alteration of ion transport in muscle and nerve cells (in sodium) Increased receptor sensitivity to serotonin
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Lithium use
Bipolar disorder, manic episodes
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Help decrease wide ranges of mood swings that they experience
Lithium
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First drug to tx bipolar disorder and still commonly used
Lithium
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Need lithium drug serum levels frequently
Lithium
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Lithium Side effects/adverse reaction
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
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Lithium Early s/sx of toxicity=
diarrhea, drossiness, N/V, slurred speech, and trembling
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Lithium Late s/sx of toxicity
burred vision, confusion, large output of dilute urine, and convulsions
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Lithium Interactions Increased lithium level with
Thiazides diuretics', methyldopa, haloperidol, NSAIDs, antidepressants, phenothiazines
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Lithium Interactions Decreased lithium level with
Caffeine, loop diuretics, theophylline
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Lithium Assessment
Evaluating neurological status, gait, LOC, reflexes, and tremors. History- drug/health. Watching renal and hepatic lab functions
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Lithium Nursing Interventions-
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).
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Lithium Education-
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
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A patient with reactive depression is ordered to receive fluoxetine (SSRI). Which information will the nurse include when teaching this patient?
The medication may cause headaches and insomnia. (take in evening)
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Before administering a monoamine oxidase inhibitor, it is most important for the nurse to assess the patient’s
dietary intake.
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Which laboratory test is most important for the nurse to monitor when a patient is receiving lithium?
Serum electrolytes (sodium)
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When providing dietary teaching for a patient taking monoamine oxidase inhibitors, the nurse should teach the patient to avoid which food?
Yogurt
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Which advice will the nurse include when teaching the patient about lithium therapy?
It may take 1 to 2 weeks before you have any benefits from taking the medication. (common for all antidepressants)
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Which statement about amitriptyline (TCAs) does the nurse identify as being true?
The drug should be discontinued slowly.
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