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Georgette > Modules 1 and 2 > Flashcards

Modules 1 and 2 Flashcards

1
Q

What is the normal lithium level?

A

0.6-1.2 mEq/L

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2
Q

Baseline labs before initiation of lithium to ensure safety and efficacy

A
  • Thyroid panel (TSH)
  • Serum Creatinine (0.6-1.2 mg/dl) (kidneys)
  • Blood urea nitrogen (BUN) (10-20mg/dl) (kidneys)
  • Pregnancy Test (HCG)
  • ECG for clients older than 50
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3
Q

Side effects of lithium

A

Endocrine: weight gain, impaired thyroid

CNS: fine hand tremors, fatigue, mental cloudiness, headaches, coarse hand tremors with toxicity, nystagmus

Dermatological: Maculopaular rash, pruritus, acne

GI: n/v/d, cramps GI upset, anorexia

Renal: polyuria with polydipsia, diabetes insipidus, edema, microscopic tubular changes

Cardiac: T wave inversions, dysrythmias

Hematological: leukocytosis

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4
Q

Name some drugs reduce renal clearance that may increase serum concentrations of lithium

A

NSAIDs (Ibuprofen, Indocin)
Thiazides (hydrochlorothiazide)
ACE inhibitors (lisinopril)

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5
Q

What are signs of lithium toxicity

A

severe nausea, vomiting, and diarrhea, confusion, convulsions, drowsiness, blurred vision, slurred speech, muscle weakness, heart palpitations, coarse hand tremors, and unsteadiness while standing or walking (ataxia)

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6
Q

If you have a patient that you suspect may have lithium toxicity, what would you do?

A

D/C LITHIUM AND CHECK SERUM LITHIUM LEVELS

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7
Q

What is a dangerous side effect that can occur with MAOIs?

A

hypertensive crisis if taken with foods containing tyramine, a dietary precursor to norepinephrine

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8
Q

What medications should you NOT take while on an MAOI?

A

 Meperidine
 Stimulants and other sympathomimetics
 Decongestants
 TCAs
 Atypical Antipsychotics
 St. John’s wort
 L-tryptophan
 Asthma medication

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9
Q

What are symptoms to watch for in a hypertensive crisis?

A
  • Sudden, explosive-like headache, usually in the
    occipital region
  • Elevated blood pressure
  • Facial flushing
  • Palpitations
  • Pupillary dilation
  • Diaphoresis
  • Fever
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10
Q

How should you treat a hypertensive crisis?

A
  • Discontinue the MAOI.
  • Give phentolamine
  • Stabilize fever
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11
Q

Teratogenic risks of Benzodiazepines:

A

Floppy baby syndrome, cleft palate

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12
Q

Teratogenic risks of Carbamazepine (Tegretol):

A

Neural tube defects

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13
Q

Teratogenic risks of Lithium (Eskalith):

A

Epstein anomaly

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14
Q

Teratogenic risks of Divalproex sodium (Depakote):

A

Neural tube defects, specifically spina bifida,
atrial septal defect, cleft palate, and possible long-term developmental deficits

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15
Q

What anxiolytic is safe in pregnancy?

A

Buspar

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16
Q

What SSRI is safe in pregnancay?

A

zoloft

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17
Q

Black Box warning for Lamotrigine (lamictal) - (anticonvulsant used as mood stabilizer)

A

Steven Johnson Syndrome

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18
Q

What mood stabilizer is safe in pregnancy?

A

lamictal

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19
Q

Black box warning for Carbamazepine (Tegretol)

A

agranulocytosis and aplastic anemia

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20
Q

Black box warning for Valproic acid/divalproex sodium (anticonvulsant used as mood stabilizer)

A

hepatotoxicity and pancreatitis

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21
Q

What are baseline labs you should order before initiating carbamazepine or valproic acid?

A

CBC
LFTs

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22
Q

How long does it take to see a response with lithium or an anticonvulsant?

A

1-2 weeks

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23
Q

Signs and symptoms of Steven Johnson Syndrome

A

* Fever (not included in book)
* Sore throat
* Facial swelling
* Tongue swelling
* Rash
* Skin sloughing
* Prodromal headache, malaise, arthralgia (joint stiffness), and painful mucous membranes may occur before rash occurs

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24
Q

What are some s/s of aplastic anemia?

A

pallor, fatigue, headache, fever, nosebleeds, bleeding gums, skin rash, shortness of breath

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25
Q

Which anticonvulsant is associated with steven johnson syndrome?

A

carbamazepine (tegretol)

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26
Q

If you are going to start an Asian on carbamazepine, what should you screen them for?

A

HLAB-1502 allelle

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27
Q

What should you check before placing any female patient (12-51) on psychotropic medication?

A

pregnancy test

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28
Q

Why would you prescribe folic acid to someone who is pregnant and what is the recommended dosage?

A

Folic acid support neural tube developement
0.4-0.8 mg/day

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29
Q

Does hypokalemia or hyperkalemia cause lithium toxicity?

A

hyperkalemia

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30
Q

A patient on lithium is started on a diuretic, what effect does this have on lithium?

A

Diuretics can reduce renal clearance of lithium.

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31
Q

What is the normal ANC level?

A

2500-6000

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32
Q

What is the normal range for WBC?

A

4500-11000

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33
Q

How often do you monitor clozaril when initiating?

A

During first 6 months: weekly; during second 6 months: every 2 weeks; then monthly if ANC is normal.

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34
Q

What SGA and anticonvulsant can have a serious side effect of agranulocytosis and neutropenia?

A

Clozapine
Carbamazepine

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35
Q

What ANC level suggest neutropenia and what should you do??

A

ANC less than 1000 mm3

DC clozaril/carbamazepine

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36
Q

**What WBC level suggest agranulocytosis?

A

WBC of 2000-3000 (bc of risk of agranulocytosis)

DC clozaril/carbamazepine

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37
Q

A patient on clozaril or carbamazepine develops signs of infection (sudden fever, chills, sore throat, weakness), what should you do?

A

Check ANC and WBC count for neutropenia or agranulocytosis

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38
Q

What are s/s of aplastic anemia and which mood stabilizer can cause this?

A

nosebleeds, bleeding gums, and skin rash

Carbamazepine

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39
Q

What is the normal BMI range?

A

18.5-24.9

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40
Q

What are some presentations that may be seen in someone with bulemia?

A
  • Weight usually within normal range
  • Erosion of dental enamel
  • Russell’s sign – scarring or calluses on the dorsum of the hand secondary to self-induced vomiting.
  • Hypertrophy of salivary glands
  • Rectal prolapse
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41
Q

How d you pharmacologically manage someone with bulimia nervosa?

A
  • Fluoxetine is FDA-approved for bulimia nervosa.
  • SSRIs and tricyclic antidepressants (TCAs) are effective in reducing the frequency of
    bingeing and purging
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42
Q

A person is considered anorexia nervosa when their BMI less than _______

A

15

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43
Q

When would you refer a patient with anorexia nervosa to inpatient hospitalization?

A

Losing 25% of their body weight in 3 months

Severe dehydration

Electrolyte imbalances

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44
Q

How would you manage a patient with anorexia nervosa nonpharmalogically?

A
  • Medical and nutritional stabilization
  • Weight restoration
  • Correction of electrolyte imbalance
  • Vitamin supplementation
  • Nutrition Counseling
  • Dental Care
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45
Q

What psychotherapeutic interventions can you use with someone with anorexia nervosa?

A
  • Behavioral therapy
  • CBT (replacing neg thoughts with positive thoughts)
  • Family therapy
  • Group therapy
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46
Q

**A patient with depression who also presents with fatigue and low energy, what would you give?

A

Wellbutrin

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47
Q

What medication is contraindicated in patients with seizure disorder/history of seizures, or conditions that increase the risk of seizures such as anorexia nervosa or bulimia.

A

Wellbutrin

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48
Q

A patient on an SSRI complains of sexual dysfunction, what medication could you give them that does not have sexual side effects?

A

wellbutrin (buproprion) or remeron (mirtazapine)

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49
Q

What class drug is wellbutrin?

A

NDRI

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50
Q

A patient with depression and neuropathic pain comes to your clinic, what can you give them to help with depression and their neuropathic pain?

A

TCAs or SNRIs

Choose an SNRI first because it is safer than TCAs

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51
Q

What do enzyme inducers do?

A

decrease serum level of other drugs that are substrates of that enzyme, thus possibly causing subtherapeutic drug levels.

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52
Q

Carbamazepine and tobacco are inducers or inhibitors?

A

Inducers

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53
Q

Your patient is on sertraline and decides to start smoking. Because tobacco is an inducer, how should you dose sertraline?

A

Increase dose

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54
Q

What do enzyme inhibitors do and what are two examples?

A

increase the serum level of other drugs that are substrates of that enzyme, thus possibly causing toxic levels

Ex: Clarithromycin and Ketoconazole

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55
Q

What are inducers of CYP450

Mneumonic:
BullShit CRAP GPS

A

Barbiturates
St. John’s Wort
Carbamazepine
Rifampin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenobarbital
Sulfonylureas

**plus cigarette smoking

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56
Q

What are CYP450 inhibitors?

Mneumonic:
SICK FACES.COM

A

Sodium valproate
Isoniazid
Cimetidine
Ketoconazole
Fluconazole
Alcohol (Acute)
Chloramphenicol
Erythromycin
Sulfonamide
Ciprofloxacin
Omeprazole
Metronidazole

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57
Q

Study of what drugs do and how they do it?

A

pharmacology

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58
Q

Study of what the body does to a drugs.

A

pharmacokinetics

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59
Q

Study of what drugs do to the body.

A

pharmacodynamics

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60
Q

What part of the GI are oral medications normally abosrbed?

A

small intestines and liver

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61
Q

Which CYP enzyme is implicated as a tobacco inducer when an individual is treated with clozapine?

A

1A2

Clozapine is an atypical antipsychotic drug that is metabolized to a major extent by the cytochrome P450 enzyme CYP1A2. Smoking is a potent inducer of CYP1A2 enzyme activity, resulting in significant lower clozapine serum concentrations in smokers compared with non smokers, upon a given dose

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62
Q

When treating older adults, you should keep in mind that they are more sensitive to issues of drug toxicity because of which of the following reasons?

A

Decreased protein binding

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63
Q

Where is norepinephrine produce and what does it effect?

A

Produced in locus coeruleus and medullary reticular formation.

Affects attention and focus, mood regulation, sleep-wake cycles,memory formation and involved in the fight or flight response.

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64
Q

An imbalance in norepinephrine can lead to _____

A

depression and anxiety

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65
Q

Where is serotonin produce and what is it responsible for?

A

Produced in raphe nuclei of the brainstem

Regulates mood, appetite, sleep, memory, and learning,

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66
Q

An imbalance in serotonin can lead to ______

A

mood disorders such as depression, anxiety, OCD

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67
Q

Where is dopamine produced and what is it responsible for ?

A

Produced in the substantia nigra (regulate motor movements), nucleus accumbens, and the ventral tegmental area (VTA)

Influences reward and pleasure centers, motivation, and movement

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68
Q

An imbalance in dopamine can lead to ________

A

schizophrenia, bipolar disorder, addiction, depression

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69
Q

Where is acetylcholine produced and what is it involved in?

A

Synthesized by the basal nucleus of Meynert

Involved in memory, learning, and muscle movement

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70
Q

A deficiency in acetylcholine can lead to what disorder?

A

dementia

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71
Q

What does GABA do?

A

GABA reduces neuronal excitability, which helps with relaxation and stress reduction

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72
Q

What does glutamate do?

A

Involved in cognitive functions such as learning and memory

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73
Q

An imbalance in GABA can cause which disorders?

A

anxiety disorders, epilepsy, and other neurological disorders

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74
Q

Increased levels of glutamate can lead to ___

A

anxiety

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75
Q

Glutamate is imbalanced in which disorders?

A

schizophrenia, bipolar disorder, MDD, seizure d/o

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76
Q

Frontal lobe is responsible for:

A
  • Executive functions: working memory, reasoning, planning, prioritizing, sequencing behavior, insight, flexibility, judgment, impulse control, behavioral cueing, intelligence, and abstraction.
  • Language (Broca’s area): expressive speech
  • Personality development
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77
Q

Problems in the frontal lobe can lead to:

A

personality changes, emotional, and intellectual changes.

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78
Q

Temporal lobe is responsible for

A

o Primary auditory area
o Language (Wernicke’s area): Receptive speech or language comprehension
o Memory
o Emotion

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79
Q

Problems in the temporal lobe can lead to ______

A

auditory hallucinations, aphasia, and amnesia

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80
Q

Occipital lobe is responsible for _____

A

o Primary visual cortex
o Integration area: integrates vision with other sensory information.

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81
Q

Problems in the occipital lobe can lead to ________

A

visual field defects, blindness, and visual hallucinations.

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82
Q

The parietal lobe is responsible for _____

A

o Primary sensory area
o Taste
o Reading and writing

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83
Q

Problems in the parietal lobe can lead to ______

A

sensory-perceptual disturbances and agnosia

84
Q

What is agnosia?

A

a rare neurological disorder that prevents people from processing sensory information. People with agnosia can’t recognize objects, people, sounds, shapes, or smells, even though their senses are otherwise functioning normally.

85
Q

What tool is used to screen people for signs of neurological problems, such as Alzheimer’s and other dementia.

A

Clock drawing test

  • It is a very quick way to screen a person for possible dementia
  • It often requires only a minute or two for completion
86
Q

Impairments in the clock drawing test are associated with damage to what parts of the brain?

A

RIGHT PARIETAL LOBE (RIGHT HEMISPHERE)

87
Q

What makes up the limbic system?

A

Hypothalamus
Thalamus
Hippocampus
Amygdala

88
Q

What is the role of the hypothalamus?

A

Plays key roles in various regulatory functions such as appetite, sensations of hunger and thirst, water balance, circadian rhythms (aka sleep), body temperature, libido, and hormonal regulation.

High Yield!!

89
Q

What is the role of the thalamus?

A

Sensory relay station except for smell; modulates low of sensory information to prevent overwhelming the cortex; regulates
emotions, memory, and related affective behaviors

90
Q

What is the role of the hippocampus?

A

Regulates memory and converts short-term memory into long-term memory.

It also regulates motivation, stress, emotion, and learning.

91
Q

What is the role of the amygdala?

A

Responsible for mediating mood, emotional memories, fear, anxiety, anger, emotion, and aggression.

High Yield!

92
Q

The cerebellum is responsible for what?

A

Maintaining equilibrium; acts as a gross movement
control center (e.g., control movement, balance, posture)

93
Q

What test can be done to assess the cerebellum?

A

Romberg Test

94
Q

What differentiates a typical antipsychotic from an atypical?

A

Atypical antipsychotics work on dopamine AND 5HT2A (serotonin) receptor antagonism.

95
Q

Hyperactivity in this dopamine pathway is responsible for psychotic symptoms in schizophrenia.

A

Mesolimbic pathway

96
Q

Decreased levels of dopamine in this pathway are responsible for the negative and depressive symptoms of schizophrenia.

A

Mesocortical pathway

97
Q

Which dopamine pathway is responsible for movement and a decrease in dopamine levels here can lead to EPS, parkinsonism symptoms, akathisia, and TD.

A

Nigrostriatal pathway

98
Q

When dopamine is decreased in the nigrostriatal pathway, what increases which lead to increased salivation, lacrimation, and blurry vision?

A

Acetylcholine

99
Q

What causes EPS?

A

Decrease in dopamine and Increase in Acetylcholine

100
Q

When dopamine is decreased in this pathway, it can lead to increased prolactin levels leading to hyperprolactinemia which manifests as amenorrhea, galactorrhea, sexual dysfunction, and gynecomastia.

A

Tuberoinfundibular Pathway

101
Q

Why is it important to monitor a patient on an antipsychotic medication for hyperprolactinemia?

A

Long-term hyperprolactinemia is associated with osteoporosis.

102
Q

Muscle spasms of face, neck, tongue, especially back or neck muscles; stiff neck, subjectively painful, facial grimacing are s/s of _____

A

Acute dystonia

103
Q

What do you give for acute dystonia and why?

A

Cogentin (benztropine) – give for dystonia; helps because acetylcholine is high in dystonia and cogentin is an anticholinergic that will decrease acetylcholine.

104
Q

What are s/s of akathisa?

A

o Restless (inability to remain still)
o Pacing
o Difficulty standing still
o Feet constantly in motion

Note: Often mistaken for increasing anxiety.

105
Q

What do you give for akathisia?

A

 Betablocker: like propranolol (beta-blockers can cause bronchospasm, beta blockers are contraindicated in patients taking bronchodilators like Albuterol)
 Benztropine (Cogentin)
 Benzodiazepine

106
Q

What tool is used for Akathisa and EPS symptoms?

A

Barnes Akathisia Rating Scale and Extrapyramidal Symptom Rating Scale.

107
Q

Absence of movement, difficulty initiating motion, subjective feeling of lack of motivation to move.

A

Akinesia

Note: often mistaken for laziness or lack of interest.

108
Q

What is the treatment for akinesia?

A

Cogentin (Benztropine)

109
Q

What is pseudo-Parkinsonian symptoms?

A

Presence of symptoms of Parkinson’s disease produced by D2 blockade.
o Muscle rigidity
o Shuffling gait
o Motor slowing
o Mask-like facial expression
o Pill rolling tremors in fingers

Note: mask-like facial expression is often confused as affective blunting or flattening.

110
Q

How do you treat Pseudo-Parkinsonian symptoms?

A

Cogentin (Benztropine)

111
Q

Involuntary abnormal muscle movement of the mouth tongue, face, and jaw that may progress to limbs.

Examples:
o Protrusions and rolling of the tongue
o Lip-smacking and sucking
o Chewing motion
o Facial dyskinesia

A

TD

can be IRREVERSIBLE!!

112
Q

When can TD occur?

A

o Can take up to 1-2 years to occur
o Can occur as an acute process at initiation of medications or as a chronic condition at any point in treatment.

113
Q

What medications are FDA approved to treat TD?

A

Deutetrabenzene (Austedo) and Valbenazine (Ingrezza) which are both vesicular monoamine transporter 2 inhibitor

114
Q

What antiemetic can cause EPS symptoms in TD?

A

Reglan (metoclopramide)

114
Q

True or False, If you give cogentin for TD, it can worsen symptoms.

A

TRUE

115
Q

What is an agonist effect?

A

drug binds to receptors and activates a biological response (opens the ion channel).

116
Q

Which 2 atypical antipsychotics are less likely to cause hyperprolactinemia?

A

Quetiapine (seroquel)
Aripiprazole (abilify)

117
Q

What is an inverse agonist effect?

A

drug causes the opposite effect of agonist; binds to the same receptor (activates a biological response by closing the ion channel).

118
Q

What is a partial agonist effect?

A

drug does not fully activate the receptors

119
Q

What is an antagonist effect?

A

drug binds to the receptor but does not activate a biologic response.

120
Q

What medications can cause mania?

A
  • Steroids
  • Disulfiram (Antabuse)
  • Isoniazid (INH)
  • Antidepressants in person with bipolar disorder
121
Q

What medications can cause depression?

A
  • Steroids
  • Isotretinoin (Accutane) (can also cause birth defects)
  • Beta blockers
  • Interferon
  • Some retroviral drugs
  • Antineoplastic drugs
  • Benzos
  • Progesterone
  • Prednisone/Flonase
122
Q

What kind of labs would you see with NMS?

A
  • Elevated CPK (creatine phosphokinase)- muscle contraction/muscle destruction
  • Myoglobin (rhabdomyolysis)
  • Elevated WBSs (leukocytosis)
  • Elevated LFTs (liver function test)
122
Q

What are s/s of NMS?

A
  • EXTREME MUSCLE RIGIDITY
  • MUTISM
  • Hyperthermia
  • Tachycardia
  • Diaphoresis
  • Altered level of consciousness
123
Q

How do you treat NMS?

A

DC the offending agent (antipsychotic)

  • Bromcriptine (Parlodel) Dopamine (D2) agonist
  • Dantrolene- muscle relaxant (muscle rigidity)
124
Q

What are s/s of serotonin syndrome?

A
  • Caused by antidepressant.
  • Hyperreflexia
  • Myoclonic jerks
  • Agitation, restlessness
  • Rapid heart rate and elevation in blood pressure
  • Headache
  • Sweating, shivering, and goosebumps
  • Confusion, fever, seizures, unconsciousness
125
Q

How do you treat serotonin syndrome

A

 DC offending agent
 Cyproheptadine (Periactin)- first-generation antihistamine with additional anticholinergic, antiserotonergic, and local anesthetic properties.

126
Q

What drug combinations can cause serotonin syndrome?

A

SSRI/TCA/MAO/SNRI
* SSRIs and MAOIs
* Placing a patient on more than one SSRI
* Drug and herbal interactions
* SSRIs and St. Johns wort

127
Q
  1. How long should you wait to switch someone from an SSRI to a MAOI and vice versa (MAOI to SSRI)?
  2. If the SSRI is prozac, how long would you wait?
A
  1. 2 weeks
  2. 5-6 weeks becaues prozac has a long half life
128
Q

What are s/s of serotonin discontinuation syndrome?

A
  • Flu-like symptoms (due to cholinergic rebound, particularly problematic with TCAs)
  • Fatigue and lethargy
  • Myalgia (muscle soreness and achiness)
  • Decreased concentration
  • Nausea and vomiting
  • Ataxia (unsteady)
  • Impaired memory
  • Agitation
129
Q

What can cause serotonin discontinuation sydrome?

A

abruptly stopping SSRIs/TCAs/MAOIs

129
Q

MNEUMONIC for s/s for serotonin discontinuation syndrome:

F.I.N.I.S.H.

A
  • Flu-like symptoms: fatigue, muscle aches, headaches, diarrhea
  • Insomnia
  • Nausea
  • Imbalance: gait instability, dizziness, lightheadedness, vertigo
  • Sensory disturbance: paresthesia, “electric shock” sensation and visual disturbance
  • Hyperarousal: anxiety, agitation
130
Q

How soon can serotonin syndrome start after abruptly stopping a SSRIs/TCAs/MAOIs and how long does it take to resolve?

A
  • Onset: 24-72 hours + Resolution: 1-14 days
131
Q

What are the components of the MSE.

A

Appearance
Behavior
Speech
Mood
Affect
Thought process
Thought content
Insight
Judgement

132
Q

What are the 5 main parts of the mini mental status exam (MMSE) and what does it assess for?

A

Concentration/attention/calculation

Orientation

Registration/ability to learn new material

Recall

Fund of knowledge

-MMSE helps to asses level of cognitive impairment

133
Q

What screening tools can be used to assess level of cognitive impairment

A

-Mini-Mental State Examination (MMSE)
-Montreal Cognitive Assessment (MoCA)
-Mini-Cog
-St Louis University Mental -Status Examination (SLUMS)

134
Q

Suicide risk factors

!!High Yield!!

A
  • Previous suicide attempt
  • Ages 45 and older for male
  • Ages 55 and older for female
  • Divorced, single, or separated
  • White (Caucasian)
  • Living alone
  • Psychiatric disorder
  • Physical illness
  • Substance abuse
  • Family history of Suicide
  • Recent loss
  • Male gender
135
Q

What is the focus of a therapeutic relationship

A

the client’s needs and goals

136
Q

Characteristics of a therapeutic relationship

A
  • Genuineness
  • Acceptance
  • Nonjudgmental
  • Authenticity
  • Empathy
  • Respect
  • Professional boundaries
137
Q

What is transference?

A

displacement of feelings for significant people in the client’s past onto the PMHNP in the present relationship

client onto provider

138
Q

What is countertransference?

A

The nurse’s emotional reaction to the client based on her or his past experience.

provider onto client

139
Q

At what CIWA-AR score do you start medications?

A

score greater than or equal to 8; this is when PRN medications would be given if ordered

140
Q

What are the 3 FDA approved medications used to treat AUD?

A

acamprosate (Campral)
disulfiram (Antabuse)
naltrexone (Vivitrol)

141
Q

What two meds reduce alcohol consumption and increase abstinence?

A

Acamprosate and naltrexone

142
Q

When prescribing a benzo such as ativan or valium, which one do you give to a patient with liver issues?

A

ativan because it has a shorter half life

143
Q

The Alcohol Use Disorders Identification Test (AUDIT)

A
  • The AUDIT is a 10-item screening tool developed by the World Health Organization (WHO) to assess alcohol consumption, drinking behaviors, and alcohol related problems.
  • A score of 8 or more is considered to indicate hazardous or harmful alcohol use.
144
Q

What screening tool is used to assess drug use?

A

Drug Abuse Screening Test (DAST-10)

The DAST-10 is a 10-item brief screening tool that can be administered by a clinician or self administered.

145
Q

How does Disulfiram (anatbuse) help with AUD

A

Aversion effect

When alcohol is consumed while taking disulfiram, this results in a rapid increase of acetaldehyde in the blood, which can be toxic and cause a negative reaction called the disulfiram-alcohol reaction

146
Q

When do delirium tremors usually occur?

A

Within the first 24-72 hours after cessation if alcohol.

147
Q

CIWA scoring

A

0–9 = absent or very mild withdrawal
10–15 = mild withdrawal
16–20 = moderate withdrawal
21–67 = severe withdrawal and possible DTs.

148
Q

s/s of alcohol withdrawal HIGH YIELD

A
  • Nausea and vomiting
  • Tremors
  • Paroxysmal sweats
  • Tactile distrubances
  • Auditory disturbances
  • Visual disturbances
    Headaches
    Anxiety
    Agitation
    Altered sensorium
149
Q

What is a normal score on an MMSE

A

25-30

**the lower the score the more severe/Alz disease

149
Q

Signs and symptoms of opioid withdrawal. !!! HIGH YIELD!!!

A
  • Yawning
  • Irritability/anxiety
  • Pupillary dilation (pinpoint pupils can indicate opioid intoxication)
  • Piloerection
  • Muscle aches
  • Lacrimation
  • Rhinorrhea
    Sweating
    Insomnia
    Nausea, Vomiting, Diarrhea
150
Q

What is a normal score on the MoCA?

A

26-30

**the lower the score the more impaired they are

151
Q

At what score do COWS score do you start treatment?

A

greater than 7

152
Q

For moderate to severe opiate withdrawal, what can you give?

A

Buprenorphine
Suboxone (buprenorphine and naloxone)

153
Q

At what CIWA score do you give both scheduled meds and PRN meds? and what benzos can you give?

A

15 and above

Diazepam (valium)
Lorazepam (ativan)
Librium

154
Q

If prescribing methadone, what is important to remember?

A

Methadone can cause CARDIAC ARRHYTHMIAS AND REQUIRES A LOT OF MONITORING. SHOULD BE IN A RESIDENTIAL TREATMENT CENTER BC IT REQUIRES CLOSE MONITORING

155
Q

If asked, which screening tool you would use (CAGE, AUDIT, or SBIRT), which one do you pick?

A

SBIRT b/c it is more comprehensive

156
Q

Would you administer the CAGE or the AUDIT tool?

A

AUDIT because it is more comprehensive

157
Q

What are the 4 questions asked on the CAGE - AID screening tool for alcohol abuse and drug abuse.

A
  1. Have you ever felt you ought to cut down on your drinking or drug use?
  2. Have people annoyed you by criticizing your drinking or drug use?
  3. Have you felt bad or guilty about your drinking or drug use?
  4. Have you ever had a drink or used drugs first thing in the morning to steady
    your nerves or to get rid of a hangover (eye-opener)?

0 for “no”
1 for “yes”

Score of 1 or mores accurately detects 91% of alcohol users and 92% for drug users

158
Q

What screening tool is used for children/adolescents under the age of 21 to screen for alcohol and other drug use disorders simultaneously.

A

CRAFFT screening tool

  1. Have you ever ridden in a CAR drive by someone who had been using alcohol or drugs?
  2. Do you ever use alcohol or drugs to RELAX, feel better about yourself, or fit in?
  3. Do you ever use alcohol or drugs while you are by yourself ALONE?
  4. Do you ever FORGET things you did while using alcohol or drugs?
  5. Do your FAMILY or FRIENDS ever tell you that you should cut down on drinking or drug use?
  6. have you ever gotten into TROUBLE while you were using alcohol or drugs?

1 point is given for every “yes”

159
Q

What score on the CRAFFT indicates the need for further assessment?

A

2

160
Q

Someone who score mild on anxiety/depression, what is the treatment plan?

A

Therapy, nothing

161
Q

Someone who scores moderate/severe on anxiety/depression, what is the treatment plan?

A

medications and/or therapy

162
Q

If someone scores in the severe range for depression, what should you also assess for?

A

suicidal ideation

163
Q

MMSE scoring ranges

A

25-30 Normal

21-24 Mild cognitive impairment or possibly early stage/mild-Alzheimer’s disease

10-20 Moderate/middle stage/moderate alzheimer’s disease

0-9 severe/late stage/severe Alz disease

164
Q

PHQ-9 Depression scoring

A

0-4 Normal
5-9 Mild
10-14 Moderate
15-19 Moderate to severe
20-27 Severe

165
Q

GAD scoring ranges

A

0-4 Normal
5-9 Mild
10-14 Moderate
15-23 Severe

166
Q

CIWA scoring ranges

A

0-9 None
1-15 Mild
16-20 Moderate
21 > severe

8 and above = PRNs only
15 and above: scheduled meds + PRNs
- Diazepam (valium)
-Lorazepam (Ativan)
-Librium

167
Q

COWS scoring range

A

0-4 None
5-12 Mild - Clonidine
13-24 Moderate
25-35 Moderate to severe
36 > severe

Moderate-Severe: Buprenorphine

Suboxone (Buprenorphine and Naloxone)

168
Q

What is Screening Brief Intervention Referral to Treatment (SBIRT)

A

is an evidence based approach at screening individuals for alcohol/substance abuse and provides recommendations.

169
Q

What can you use to help guide you in delivering brief interventions to someone at risk for alcohol abuse?

A

FRAMES

Feedback - tell them about the risk of their current level of alcohol abuse.

Responsibility -reinforce it is their decision to change.

Advice - based on facts about their drinking, offer simple and direct advice to the service user re impact on them ona offer your advice to change.

Menu - provide them with a menu of options for behavior change.

Empathetic interviewing - consider their perspective,; be non judgemental.

Self-efficacy - encourage the person to believe they can change.

170
Q

In a psychiatric outpatient clinic, a 38-year-old patient with a history of major depressive disorder (MDD) presents for a follow-up appointment. At the initial visit, the patient completed the Beck Depression Inventory (BDI) and scored 30. Based on the assessment, the patient was prescribed 10mg of Escitalopram. At the current visit, eight weeks later, the patient completes the BDI again, and the total score is now 20. What is the most appropriate action for the PMHNP regarding medication?

A. Consider this score improvement as a positive response to the current medication regimen and maintain the treatment plan.
B. Increase the dose of the antidepressant to 20mg
C. Decrease the dose of the antidepressant
. D. Immediately discontinue all medications due to the decrease in BDI score.

A

B. Increase the dose of the antidepressant to 20mg

8 weeks is a long for an SSRI but if they are still scoring moderate, then increase dose*

171
Q

What are s/s of delirium?

A

o Acute onset
o Altered level of consciousness
o Inattention
o Change in cognition (concentration)
o Poor prognosis: 1 year mortality rate of clients with delirium is up to 40 %

172
Q

What are pharmacological and nonpharmacological ways to manage delirium.

A

Pharmacological Management:

Antipsychotic agents
*Haloperidol (Haldol): Haldol is the preferred treatment for agitated delirium patients (as described by the guidelines of the American Psychiatric Association)

Atypical antipsychotic agents

Anxiolytic agents for insomnia

Nonpharmacological Management:

Monitor for safety needs

Pay attention to basic needs

It is helpful to have the client’s room familiar people, familiar pictures or decorations; a clock or calendar; and regular orientation to person, place, or time

173
Q

Dementia is a group of disorders characterized by the gradual development of multiple cognitive deficits such as:

A
  • Impaired executive functioning
  • Impaired global intellect
  • Impaired problem solving
  • Impaired organization skills
  • Altered memory
  • Mutism
  • Seizures
174
Q

What are the 2 types of dementia?

A

Subcorital Dementia

Cortical Dementia

175
Q

Key features in cortical dementia:

A
  1. Cerebral Cortex Affected: Cortical dementia primarily affects the cerebral cortex, the outer layer of the brain responsible for higher cognitive functions.
  2. Memory and Language: Memory loss and language difficulties are hallmark features of cortical dementia.
    * Aphasia: Aphasia, or language impairment, is common in cortical dementia, leading to problems with communication.
  3. Visuospatial Issues: Individuals may experience visuospatial impairments, affecting their ability to navigate and recognize objects.
  4. Apraxia: Cortical dementia can cause apraxia, leading to difficulties in performing purposeful movements.
  5. Personality Changes: Behavioral changes, such as personality shifts and increased impulsivity, can occur.
  6. Hallucinations and Delusions: These symptoms can contribute to agitation and distress.
176
Q

What are common types of cortical dementia?

A

Alzheimer’s disease

Frontotemporal dementia

Primary progressive aphasia are common forms of cortical

177
Q

Key features of subcortical Dementia:

A
  1. Subcortical Structures: Subcortical dementia primarily affects the brain’s subcortical structures, which are located beneath the cerebral cortex.
  2. Cognitive and Motor Symptoms: It is characterized by a combination of cognitive and motor symptoms, including memory problems and movement difficulties.
    * Movement disorders, such as tremors, stiffness, and bradykinesia (slowness of movement), are often prominent in subcortical dementia.
    * Gait and Balance Issues: Problems with walking and balance are common due to the involvement of motor pathways.
  3. Emotional Changes: Mood changes, depression, and apathy can be part of the symptom profile.
  4. Slower Processing Speed: Individuals with subcortical dementia may experience slower thinking and processing speed compared to cortical dementia.
178
Q

What are common types of subcortical dementia?

A

Parkinson’s disease dementia

Huntington’s disease

Vascular dementia.

179
Q

What are some early symptoms of subcortical dementia?

A

Depression
Clumsiness
Irritability
Apathy

180
Q

What is apraxia?

A

neurological disorder that affects a person’s ability to perform tasks or movements, even when they understand the request, are willing to perform the task, and have the necessary muscles

181
Q

What is agnosia?

A

A rare neurological disorder that makes it difficult to process sensory information. People with agnosia may have trouble recognizing objects, people, sounds, shapes, or smells, even though their senses are otherwise functioning normally.

182
Q

loss of ability to understand or express speech, caused by brain damage

A

aphasia

183
Q

Key features of dementia due to HIV disease:

A
  • Classified as a subcortical dementia
  • Early signs of HIV dementia: cognitive decline, motor abnormalities (lack of coordination, tremors, dystonia, and ataxia) and behavioral abnormalities.
184
Q

S/S of late stage HIV related dementia:

A
  • Global cognitive impairment
  • Mutism
  • Seizures
  • Hallucinations
  • Delusions
  • Apathy
  • Mania
185
Q

Key features of Lewy body disease:

A
  • Presents with RECURRENT VISUAL HALLUCINATIONS
  • Parkinson features (bradykinesia, tremor)
  • Adversely react to antipsychotics, especially typical antipsychotic
  • FLUCTUATING COGNITIVE IMPAIRMENT
  • Patients with LBD often exhibit deficits in executive function, including difficulties with LEARNING, PLANNING, ORGANIZING, PROBLEM-SOLVING, AND DECISION-MAKING.
186
Q

Key features of vascular dementia:

A
  • Second most common type
  • Primarily caused by cardiovascular disease and characterized by step-type declines.
  • Most common in men with pre-existing high blood pressure and cardiovascular risk factors

* Hallmarks: carotid bruit, fundoscopic abnormalities, and enlarged cardiac chambers.*

187
Q

Key features of Pick’s disease:

A
  • Also known as frontotemporal dementia/frontal lobe dementia
  • More common in men
  • Personality, behavioral, and language changes (slurred) in early stage
  • Cognitive changes can occur in later stages
188
Q

Key features of Huntington’s Disease

A

(Subcortical type of dementia—think motor abnormalities)

  • Characterized mostly by motor abnormalities (e.g. choreoathetoid movements)
  • Psychomotor slowing and difficulty with complex tasks
  • High incidence of depression and psychosis

Etiology (p.278)
o Diffuse cerebral atrophy and enlarged ventricle in dementia of Alzheimer’s type (DAT)
o Decreased acetylcholine and norepinephrine in DAT
o Genetic loading
 Family history of dementia in first-order relative

189
Q

How do you treat psychosis and agitation in dementia?

A
  • Try nonpharmacological therapies first
  • Atypical antipsychotics should be used as first-line agents in patients with psychosis symptoms of dementia.
  • Use lowest effect dose and attempt to wean periodically.

 Benzodiazepines should be avoided in possible, in most patients with dementia as they are particularly vulnerable to their adverse effects such as sedation, falls, and delirium.

190
Q

Why do try to avoid giving antipsychotics for dementia related psychosis?

A

Because risk of mortality.

Antipsychotics can also increase the risk of death and stroke in older adults with dementia. Elderly patients with dementia-related psychosis treated with antipsychotics are at an increased risk of death compared to placebo.

191
Q

What is the goal of primary prevention?

A
  • Aimed at decreasing incidence (# of new cases) of mental disorders

Helping people avoid stressors or cope with them more adaptively

192
Q

What is the goal of secondary prevention?

A
  • Aimed at decreasing the prevalence (# of existing cases) of mental disorders.
  • Screening
193
Q

What is the goal of Tertiary prevention?

A
  • Aimed at decreasing the disability and severity of a mental disorder
194
Q

What are examples of primary prevention?

A

stress management classes for graduate students,

smoking prevention classes

195
Q

What are examples of secondary prevention?

A

Screenings

Example: telephone hotlines, crisis intervention, disaster responses

196
Q

What are examples of secondary prevention?

A

Rehabilitative services

Examples: day treatment programs; case management for physical, housing, or vocational needs, social skills training

197
Q

Key features of motivational interviewing;

A
  • Focused, goal-directed therapy
  • Builds on the transtheoretical model of change
  • Motivation is elicited from the client
  • Nonconfrontational
  • Listen with a patient-centered empathetic approach
  • Empower the patient. The patient must understand that he is in control of his actions and any change he desires will require him to take steps toward that change
198
Q

OARS can be used to help guide one in motivational interviewing. What does OARS stand for?

A

Ask OPEN ENDED questions

Make AFFIRMATIONS

Use REFLECTIONS

Use SUMMARIZING

199
Q

What are the guiding principles of Motivational Interviewing

A
  1. Express empathy - listen rather than talk
  2. develop discrepancy - promote the client’s awareness; clarify how present behavior is in conflict with important goals.
  3. Roll with resistance - direct the client towards positive change
  4. Support self efficacy - elicit and support hope
  5. Avoid arguing and direct confrontation - avoid confronting denial and make progress towards change
200
Q

What are the 5 phases of the theoretical model of change?

A
  1. Precontemplation - not ready
  2. Contemplation - thinking about changing
  3. Preparation - made decision to change
  4. Action - engaging in actions to change
  5. Maintenance - engaging behaviors to prevent relapse
  6. Relapse - normal part of change process
201
Q
A
202
Q

What ctyochrome P450 metabolizes Clozapine (clozaril)?

A

CYP1A2

Georgette (11 decks)

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