NUR 119 Mod 2

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NUR 119 Mod 2
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Maddie's Lecture Reference
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  1. Stages of Alzheimer's
    1: Normal - No change

    2: Very mild - Forgets object location

    3: Mild (early confusion) -Decreased ability to function in work situation

    4: Moderate - Unable to perform complex tasks

    5: Moderately severe - Usually needs assistance for survival

    6: Severe (dementia) - Forgets names of spouse/family/caregivers and details of their personal lives

    7: Very severe - Unable to speak (5 words or less)
  2. Discuss Alzheimer's treatment with Tacrine(Cognex).
    Improves memory loss by elevating Ach concentration

    Life-threateing: hepatotoxicity
  3. antocholinergics contraindicated with
    glaucoma
  4. Parkinson's

    Tx expectations

    OD signs

    OD actions
    Tx: relieve tremors & rigidity

    OD signs: Agranulocytosis, hemolytic anemia, thrombocytopenia, cardia dysrhythmisa, neroleptic malignant syndrome

    OD action:
  5. Cholinergic drugs tend to AAAA secretions.
    increase
  6. Review Alzheimer's disease & possible causes.
    Incurable dimentia

    Degeneration of cholinergic neuron and deficiency oif acetylcholine
  7. What are adverse effects of Antiparkinson drugs?
    Nausea & vomiting

    Premature ventricular contraction (PVCs)

    Orthostatic hypotension

    • Dyskinesia - involuntary movement
    • of tongue and body

    tachycardia

    CNS stimulation
  8. What are 3 important points about Symmetryl?
    It is an antiparkinson dopaminergic drug.

    It stimulates dopamine receptors.

    It can be used alone or in combination with carbidopa-levodopa (Sinemet)
  9. Which 2 drugs are used in combination to treat Parkinson's disease?
    Tx involves both levadopa and cardopa to increase the dopamine beyond the blood/brain barrier.

    cardopa inhibits the dopa decarboxylase enzyme, whioch would convert 99% of the levadopa to dopamin BEFORE it got to the brain. Use 1p cardopa to 10p levadopa.
  10. How do antiparkinson drugs work?
    Either to reduce the symptoms or replace the domamine deficit
  11. Review Parkinson's disease.
    Degenerative CNS disorder

    Abnormalities in movement (bradykinesia), posture, tremor, joint and muscle

    Rigidity

    Destruction/degenerative changes in dopamine producing nerve cells

    Decreased dopamine/increased acetylcholine

    Can develop with long-term use of antipsychotics (pseudoparkinson's)
  12. Doctor orders Valium 50 mg IV STAT for your patient with severe muscle spasms. Your thoughts?
    OD!!!

    • IV: 5-10mg
    • rpt @ 10-15min
    • MAX 30mg
  13. PHENOBARBITAL
    Anticonvulsant

    2-3 wk steadyt state

    3-4 wk therapeutic levels

    Monitor for anemia

    Drug of choice for less than 2 years
  14. DEPAKENE
    aka Depakote - for grand, petit & psychoM
  15. NEURONTIN
    Tx neuropathy
  16. ATIVAN
    Alcohol WD and anxiety.

    Can be used for status epilepticus, but valium is choice there
  17. VALIUM
    drug of choice for status epilepticus
  18. MYSOLINE
    Barbituate-like drug for grand mal & psychomotor seizures
  19. MAGNESIUM SULFATE
    Anticonvulsant to control seizures in toxemia of pregnancy caused by eclampsia and preeclampsia
  20. CEREBYX
    Anticonvulsant for grand mal seizures
  21. Do not confuse

    CELEBREX, an NSAID

    with

    CEREBYX, a seizure med
  22. Klonopin
    Abrupt WD -> seizures
  23. Tegretal
    anticonvulsant to Tx facial pain assoc w/ triginmenial neural
  24. 8 Important points about anticonvulsants
    Long term oral: Dilantin

    CNS depression

    Contraindicated for renal or liver damage

    May cause bone marroe suppression

    Dilantin will precipitate in D5W - use only 0.9 NS
  25. What prototype drug is used to treat seizures?
    hydantoin (Dilantin)

    Oldest & most widely used

    Also Tx cardiac arythmias

    T1/2 18-24 hr (Maddie)

    Steady Sate 7-21 days

    TSR 10-20 mcg/mL

    • May cause drowsiness
    • Shake oral suspensons well
  26. How are seizures treated?
    Correct the underlying cause

    • Dilantin
    • - T1/2 18-24 hr
    • - Steady state 7-21 days
    • - TDM 10-20 mcg/mL

    If Pt stops dilantin for 2 weeks, seizures may resume

    Need loading dose

    Stop (but not cure) seizure w/ Valium & Ativan
  27. Why do seizures occur?
    Low blood sugar

    Fever

    Check PO2

    WD of drugs: cocain, lidocain, lithium, theophyline

    3-5 days after alcohol WD
  28. Psychomotor seizure
    Complex symptoms: automatisms (repetitive behavior such as chewing or swallowing motions), behavioral changes, and motor seizures
  29. Absense seizure
    Also called petit mal seizure; brief loss of consciousness lasting less than 10 seconds; fewer than three spike waves on the electroencephalogram (EEG) printout; usually occurs in children
  30. Tonic-clonic seizure
    Also called grand mal seizure; most common form of seizure. In the tonic phase, skeletal muscles contract or tighten in a spasm lasting 3 to 5 seconds. In the clonic phase, there is a dysrhythmic muscular contraction, or jerkiness, of legs and arms lasting 2 to 4 minutes.
  31. Clonic seizure
    Dysrhythmic muscle contraction
  32. Tonic seizure
    Sustained muscle contraction
  33. Generalized Seizures
    Convulsive and nonconvulsive; involve both cerebral hemispheres of the brain
  34. SUGGESTED TREATMENT FOR OVERDOSE OF BENZODIAZEPINES
    1. Administer an emetic, and follow with activated charcoal if the client is conscious; use gastric lavage if the client is unconscious.

    2. Administer the benzodiazepine antagonist flumazenil(Romazicon) IV if required.

    3. Maintain an airway, give oxygen as needed for decreased respirations, and monitor vital signs.

    4. Give IV vasopressors for severe hypotension.

    5. Request a mental health consultation for the client.
  35. Treatment schedule for mood disorders with antidepressant meds?
    9 months after symptoms 1st appear

    5 years after 2nd

    long-term after 3rd
  36. Define: Convulsion
    Involuntary paroxysmal mucle contractions.

    The word paroxysm means "sudden attack, outburst".
  37. Define: seizure
    Abnormal electrical discharges of the cerebral neurons and is characterized by a loss or disturbance of conciousness
  38. naloxone HCl (Narcan) Dosage
    • IV: 0.4 to 2 mg
    • may repeat q2-3min
    • max 10mg
  39. flumazenil (Romazicon) Dosage
    • IV: 0.2 mg over 30 sec
    • may repeat with 0.3 mg in 30 sec
    • max: 3 mg total dose

    • Benzodiazepine Antagonists
    • (OD antidote)
  40. Morphine Dosage
    PO: 10 to 30 mg q4h PRN

    SR: 15 to 30 mg, q8-12h PRN

    IV/IM/subQ: 2.5 to 15 mg q2 to 6h PRN

    Epidural: 2 to 10 mg over 24h


    SR=sustained release
  41. Tylenol Dosage
    PO: 325 to 650 mg q4-6h PRN; max: 4000 mg/d

    Rectal supp: 650 mg q.i.d.
  42. ASA Dosage
    • Analgesic:
    • PO: 325 to 650 mg q4h prn; max: 4 g/d

    • TIA and thromboemboliccondition:
    • PO: 81 to 325 mg/d

    • Arthritis:
    • PO: 3.6 to 5.4 g/d in divided doses

    TDM: 15 to 30 mg/dL; 150 to 300 mcg/mL
  43. OD of Tricyclic antidepressents?
    • Symptoms:
    • - CNS depression
    • - Cardiovascular collapse

    • Tx:
    • - Airway
    • - Charcoal
    • - Fluids
    • - EKG monitoring
    • - Antiseizure meds
  44. OD of MAO antidepressents?
    • Symptoms:
    • - Adrenergic

    • Tx:
    • - Diuretics
    • - Acidify urine
    • - Hemodialysis
  45. OD of the antidepressents Welbutrin?
    • Symptoms:
    • - Agitation
    • - Seizures

    • Tx:
    • - Supportive
    • - Charcoal
    • - anti-seizure meds
  46. OD of the antidepressents lithium?
    • Symptoms:
    • - Altered levels of consciousness
    • - Hallucinations
    • - Convulsions (seizure)
    • - Diminished urine output
    • - Low Na+ (Na/K pump shot)
    • - Oliguria
    • - Coma
    • - Death

    • Tx:
    • - Supportive
    • - Fluid and electrolyte correction
    • - Hemodialysis
  47. OD of SSRI antidepressents...
    • Symptoms:
    • - CNS stimulation

    • Tx:
    • - Airway & charcoal
  48. Can polydrug therapy be an effective means of treating depression?
    No becauseof the possible sewrios side effects.
  49. Example(s) of Tricyclic Antidepressants?
    Tofranil
  50. Example(s) of antidepressent Mood Stabilizers?
    Lithium

    anticonvulsants
  51. Example(s) of "misc" antidepressents?
    Wellbuitrin

    Effexor
  52. Example(s) of Serotonin Reuptake Inhibitors?
    Prozac
  53. Example(s) of MAO antidepressents?
    Marplan

    Nardil

    Parnate
  54. What are the 5 types of antidepressents?
    Tricyclic Antidepressants

    Serotonin Reuptake Inhibitors

    MAO's

    Miscellanous

    Mood Stabilizing
  55. Review types of mood disorders.
    Depression

    • 1) Reactive
    • - loss of loved one
    • - possible benzodiazepine

    • 2) Major
    • - loss of interest in work/home
    • - inability to complete tasks
    • - may be primary or secondary to physical or psychiatric problem
    • - antidepressants

    • 3) Bipolar affective disorder
    • - manic (euphoric) or depressive (dysphoria)
    • - Originally lithium, now depakote
  56. Your patient was admitted 2 weeks ago and started on Prolixin for acute psychosis. Your assessment reveals that the patient is restless, unable to sit still, and is uncoordinated with fine hand tremors. What is your interpretation of this data?
    Pt is beginnign ti suffer from the EPS of akathesia and pseudoparkinsonism.
  57. What are the symptoms of Tardive dyskinesia?
    Protrusion and rolling of the tongue

    Sucking and smacking movements of the lips

    Chewing motion

    Facial dyskinesia

    Involuntary movements of the body and extremities
  58. What are the symptoms of Acute dystonia?
    Facial grimacing

    Involuntary upward eye movement

    Muscle spasms of the tongue, face, neck,and back (back muscle spasms cause 'trunk to arch forward)

    Laryngeal spasms
  59. What are the symptoms of Akathisia?
    Restless

    Trouble standing still

    Paces the floor

    Feet in constant motion, rocking back and forth
  60. What are the Pseudoparkinsonism symptoms?
    Stooped posture

    Shuffling gait

    Rigidity

    Bradykinesia

    Tremors at rest

    Pill-rolling motion of the hand
  61. What are the EPS?
    • Pseudoparkinsonism
    • Akathisia
    • Acute dystonia
    • Tardive dyskinesia
  62. How are EPS managed?

    (extrapyramidal symptoms)
    Anticholinergic drugs help decrease:

    pseudoparkinsonism symptoms

    acute dystonia - benztropine (Cogentin)

    akathisia - lorezepam

    BUT has little effect on tardive dyskinesia, which means that the antipsychotic should be stopped for this adverse affect. Other drugs (benzodiazepines, clozapine) have been helpful for some Pt.
  63. What are extrapyramidal symptoms?
    Pseudoparkinsonism:

    Stooped posture

    Shuffling gait

    Rigidity

    Bradykinesia

    Tremors at rest

    Pill-rolling motion of the hand

    (Parkingson's disease affects the extrapyramydal motor tract of nerves)
  64. How long are antipsycotics given?
    Perhaps a lifetime.
  65. One class of "typical" antipsychotics are Nonphenothiazines. Name a few.
    • Haldol
    • Zyprexa
    • Risperdal
  66. One class of "typical" antipsychotics are Phenothiazines. Name a few.
    • thorazine
    • prolixin
    • stelazine (not in our book)
  67. What are advantages of nonphenothiazines?

    What is it?
    I only saw 1 - a dose of 0.5-5mg instead of 10-25mg.

    antipsychotic drug
  68. How do these drugs work?
    They block the action of the neurotransmitter dopamine and thus may be classified as dopaminergic antagonists.

    All antipsychotics block the D2 recepter, which in turn promotes the presense of EPS (extrapyramidal symptoms) resulting in pseudoparkinsonism.

    Atypicals have a weak affinity for D2, but a strong affinity for D4 and they block the serotonine. These cause fewer EPS than typical (phenothiazines)
  69. Name the 1st drug used to treat psychotic disorders.
    Thorazine (1952)
  70. What 2 broad categories of drugs are used to manage psychosis?
    typical (or traditional)

    atypical
  71. What is schizophrenia?
    a mental disorder characterized by a breakdown of thought processes and by poor emotional responsiveness
  72. Discuss signs and symptoms of psychosis.
    It is losing contact with reality.

    • Positive symptoms:
    • incoherent speech
    • hallucinations
    • delusions
    • paranoia

    • Negative symptoms:
    • poverty of speech
    • social withdrawal
    • poor self-cate
  73. Name 2 hyponotic drugs.
    Restoril

    flumazenil (Romazicon)
  74. Def & Tx of myasthenic crisis?
    Generalize muscle weakness that may affect diaphram and intercostal muscles.

    Caused by inadequate dosing of AChE inhibitors

    Tx: neostigmine, a fast-acting AChE inhibitor, but an OD of this can lead to cholinergic crisiis, an exaccerbation of the same symptoms!!!!
  75. Myasthenia Gravis?
    Chronic autoimmune neuro-muscular disease

    • Mostly:
    • women < 30
    • men > 50

    • Cause:
    • lack of ACh receptor sites.
  76. other non-opioid analgesics
    Dolobid

    Motrin

    naproxen (Naprosyn)

    Toradol - IM/IV: 30mg q6h; max 120 mg/d

    Celebrex

    tramadol
  77. Tylenol poisoning?
    Toxic levels > 50 mcg/mLProbably hepatotoxic: > 200 mcg/mL

    Early symptoms: nausea, vomiting , diarrhea and abdominal pain.

    Death could occur in 1-4 days from hepatic necrosis.

    Antidote: Mucomyst
  78. Tylenol Caution:
    Theraputic level: 5-20 mcg/mL

    Toxic levels > 50 mcg/mL

    Probably hepatotoxic: > 200 mcg/mL
  79. Tylenol LIMIT:
    4 g/d, unless taken regularly then it is suggested that the limit be 2 g/d.
  80. Discuss advantages of Tylenol.
    No GI bleeding, nasea or vomiting

    Does not interfere w/ blood clotting, nor does it pose a rsk of excessive bleeding for dysmenorrhea as does ASA/NSAID

    Met-liver, ex-urine

    Peak: 30-120 minutes

    PO, Supp, IV
  81. What is Gold Therapy?
    Is a third type of antiinflammatory drug after NSAIDs & corticosteroids.

    Is a DMARD disease-modifying antirheumatoc drug that can be used although it is more toxic.

    A chrysotheraoy or heavy metal therapy o which Auranofin is the most often used.

    It is for sever arthristis.
  82. Which drug is considered as an ASA substitute?
    Tylenol (acetaminophen)
  83. ASA "intoxication" signs
    Mild intoxication frequently have nausea and vomiting, abdominal pain, lethargy, tinnitus, and dizziness.

    Severe poisonings and include hyperthermia, tachypnea, respiratory alkalosis, metabolic acidosis, hypokalemia, hypoglycemia, hallucinations, confusion, seizure, cerebral edema, and coma.

    The most common cause of death following an aspirin overdose is cardiopulmonary arrest usually due to pulmonary edema.
  84. What is the fluid recommendation for patients taking NSAID's and why?
    2-3 L per day
  85. Drugs that increase the effects of ASA
    Anticoagulants

    Steroids

    Codein hydrocodone (oxycontin)

    Alcohol

    Ascorbic Acid
  86. ASA overdose
    Suction NG tube & add charcoal.

    If no NG tube -> quinton catheter (dialysis)
  87. ASA considersations
    Large doses reequired for arthritis risk GI bleeds, i.e. theraputic blood levels 150-300 ug/mL (or 15-30 mg/dL)
  88. Which drug is different from the other NSAIDs and why?
    6 of the 7 groups of NSAIDs all inhibit the COX-1 enzyme which provides protection for the stomach lining and so for sever arthritis: peptic ulcer and gastric bleeding

    Selective COX-2 inhibitors (2 more than 1, but not 0) such as celecoxib (Celebrex) are good, but have other adverse reactions: peripheral edema.
  89. ASA contraindications:
    Hypersensitivity to salicylates or NSAIDs

    for no reason including fever in children 12 or younger

    third trimester

    Caution: renal or hepatic disorders & may cause bleeding, esp of GI
  90. ASA indications:
    Analgesia

    TIA (transient ischemic attack "small stroke") & Thromboembolic

    Arthritis
  91. NSAID drug & Maddie's note
    She had this in with other analgesics, non of which were anti-inflammatory???

    Indocin (an NSAID) with:

    Potent antiinflammatory effects &

    Graeter incidence of adverse effects.
  92. What is another name used for analgesics antipyretic anti-inflammatory drugs?
    NSAIDs

    They work by inactivation of the cyclooxygenase (PTGS) enzyme required for prostaglandin and thromboxane synthesis.

    But aspirin is different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors.
  93. Name the prototype analgesic antipyretic anti-inflammatory drug.
    ASA or aspirin

    Inhibit "prostaglandins"

    Note #1 - suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (PTGS) enzyme required for prostaglandin and thromboxane synthesis

    Note #2 - Prostaglandins are not endocrine hormones, but autocrine or paracrine, which are locally acting messenger molecules. They differ from hormones in that they are not produced at a discrete site but in many places throughout the human body. Also, their target cells are present in the immediate vicinity of the site of their secretion (of which there are many).

    Note #3 - some actions:

    cause constriction or dilation in vascular smooth muscle cells

    cause aggregation or disaggregation of platelets

    sensitize spinal neurons to pain

    induce labor

    decrease intraocular pressure

    regulate inflammatory mediation

    regulate calcium movement

    control hormone regulation

    control cell growth

    acts on thermoregulatory center of hypothalamus to produce fever

    acts on mesangial cells in the glomerulus of the kidney to increase glomerular filtration rate

    acts on parietal cells in the stomach wall to inhibit acid secretion
  94. Name 3 categories of drugs that could have additive effects when administered with opiods. In other words, when should you be cautious administering an opiod?
    CNS depressants

    Anti-hypertensive drugs

    MAOI - calming drugs
  95. Discuss some important principles the nurse should be aware of with narcotic therapy.
    Pain is subjective

    Morphine is a non-ceiling drug

    Demerol is a ceiling drug - no more than 600mg/24hr and for no longer than 48-72 hrs

    Use least potent analgesic when more than one is ordered.

    Alternate narcotic with non-narcotic (xanax: anti-anxiety) for best pain relief

    PO prefered for long-rterm use

    Dosage should provide good pain relief (down to 3) w/o unacceptable adverse reactions.

    Prompt admin and on regular sched

    Other drugs for Pr comfort (laxatives, antidepressants, anyiemetics)
  96. What is the methadone treatment program?
    No high bu it occupies the receptors which alleviates the eithdrawal symptions of:

    • diarrhea
    • abdominal cramps
    • restlessness
    • watery eyes
    • runny nose
    • nasea
  97. Anabuse?
    Disulfiram is a drug discovered in the 1920s and used to support the treatment of chronic alcoholism by producing an acute sensitivity to alcohol.
  98. Briefly discuss 3 narcotic antagonists.
    NARCAN

    REVEX

    TREXAN

    REVIA - 3-5x more potent than Narcan, not an antidote, Tx after off opioids 7 days

    Observe all for signs of analgesic reversal: tachycardia, nausea, vomiting & sweating.

    Additional observation of rnarcan: bleeding resulting from an elevated partial thromboplastin time.
  99. Give 2 indications for a nurse to administer a narcotic antagonist.
    1) Opioid overdose or post-op respiratory depression.

    2) Respiratory depression in neonates resulting from maternal opioid use.
  100. Define a opioid antagonist
    Antidotes for overdoses of natural or synthetic opioids.

    Higher affinity for the opioid receptors, so it blocks and displaces resulting inthe inhibition of an opioid action.
  101. List 4 examples of opioid agonists-antagonists.
    Buprenex

    Stadol

    Nubain

    Talwin
  102. What is the prototype analgesic agonists-antagonists?
    Nalbuphine
  103. What are analgesic agonists-antagonists?
    They are combinations of opioid antagonists (Narcan) added to opioid agonists in hopes of decreasing opioid abuse, i.e. a lower potential for dependence.
  104. Name other agonists of the prototype MS.
    Codeine

    Vicodin

    Dilaudid

    Demerol

    OxyContin

    Percocet

    Percodan

    Methadone
  105. Codeine v Morphine
    1/15 to 1/20th as potent
  106. Most opioids have antitussive (cough supression) except:
    meperidine (Demerol)
  107. Review contraindications for MS.
    Asthma with respiratory depression

    Increased intracranial prewssure

    Shock

    Caution: respiratory, renal, hepatic diseases, MI, old & young
  108. Review indications for MS.
    Indications: Pain from

    Acute Myocardial Infarction (AMI)

    Cancer

    Dysnea from pulmonary edema

    Preoperative medication
  109. Time to work: fentanyl (opioid) patch
    12 hours
  110. Morphine Sulfate Route Data
    • Peak:
    • IV = 10-20 min
    • IM = 30 min
    • SQ = 60-90 min

    PO as Roxanol & MSContin

    • Other routes:
    • Epidural - space within the canal (formed by the surrounding vertebrae) lying outside the dura mater
    • Intrathecal - space under the arachnoid membrane of the brain or spinal cord

    Met-liver ex-kidney
  111. Compare morphine to dilaudid
    Hydromorphone (Dilaudid)

    semisynthetic opioid

    6X analgesia over morphine

    fewer hypnotic effects

    less GI distress

    faster onset

    shorter duration
  112. What should the nurse be aware of in terms of what effects this prototype has on the CNS?
    life-threatening Respiratory depression

    Nasea & Vomiting

    Pupil Contraction: 3-7 normal, 1=narcotic

    seizures (CNS)

    Slowed GI motility

    Muscle Spasms in bowel & billiary (bile) tract

    life-threatening increased intracranial pressure

    Hypotension

    Urinary retention

    urticaria (hives)
  113. What drug is the prototype opioid analgesic?
    Morphine
  114. What are the effects of narcotic analgesics?
    Reduce the perception of pain

    Produce sedation

    Suppress cough

    Lower BP

    Decrease emotional upset

    Most are Schedule II.
  115. Briefly discuss the body's own system for suppressing the transmission of pain signals.
    The body's enforphins, though not well understood, activate the same receptors as opioids.
  116. What are differences between superficial and deep pain?
    Superficial (skin & mucous membranes) or somatic (skeletal muscles ligaments & joints) are via the sympathetic NS and can increase BP and P.

    Deep (visceral) pain from smooth muscles and organs is parasympathetic (the innervation type) and can lower BP to the point of syncopy.
  117. Gate control for pain seeks to
    Close large diameter (neuro) fibers.
  118. Pain Goal?
    <= 3
  119. What are differences between acute and chronic pain?
    Acute pain is trasnmitted via A delta fibers, which are myelinated and result in a rapid transmission of pain.

    Chronic or dull pain is more often associated with unmyelinated C fibers. Chronic pain lasts longer than 3 months - Maddie.
  120. What can pain receptors be triggered by?
    By origin: Nociceptors (sensory pain receptors, i.e. in tissues, bones, muscles or visceral - organ) are activated by noxious stimuli (mechanical, thermal or chemical) in peripheral tissues.

    Neuropathic pain results from damage or diseasy to the PNS or CNS - burning, tingling or electrical shocks, often caused by a light touch.

    Histamines, Bradykinins and Prostraglandins are chemically involved in the transmission of pain signals.
  121. The brain needs a continuous supply of:
    Oxygen - lack of results in CNS depression

    Normal PO2 is 95-100, but may be as low as 92 for a COPD Pt.

    Glucose - Too much insulin leads to coma

    Thiamine - Deficiency causes degradation of myelin sheath reducing glucose by 1/2
  122. What does excessive CNS stimulation involve?
    Excess Norepinephrine

    Increased Excitatory receptors

    Decreased Inhibitory receptors

    Increased Sensitivity of excitatory receptors

    Decreased Sensitivity of inhibitory receptors

    Decreased GABA
  123. Amino Acids
    BOTH EXCITATORY & INHIBITORY
  124. SEROTONERGIC
    INHIBITORY

    Think turkey - tryptophan from which it is derived - it inhibits CNS
  125. NORADRENERGIC
    EXCITATORY or INHIBITORY

    Mostly sympathetic via norepinephrine
  126. GABA-ERGIC
    USES GABA-INHIBITORY

    Major inhibatory neurotransmitter

    Not enough GABA (gamma-Aminobutyric acid) causes anxiety, hyper-arrousal, seizures.
  127. DOPAMINERGIC
    EXCITATORY or INHIBITORY

    dopamine agonists stimulate the dopamine receptors

    Parkinsons (shuffling gate, intention tremor) is the destruction of the dopamine neurons
  128. CHOLINERGIC neurotransmitter system?
    Excitatory or INHIBITORY

    Memory, arrousal, speech

    Low for Alzheimer's Pt, i.e. Acetylcholine

    Treatment drug: donepezil (Aricept), which is an AChE (acetylecholinesterase inhibitor). AChE is the enzyme that breaks down ACh. If you inhibit that enzyme, you get more ACh by virtue of it not being broken down.
  129. What do neurglial or glial cells do?
    Many fucntions, but chiefly protection. Myelin sheath are Schwann cells - a type if glial cell.
  130. How does hypoxia affect the CNS?
    depression
  131. How does acidosis affect synaptic transmission?
    Makes it nonresponsive
  132. How does alkalosis affect synaptic transmission?
    increases excitability
  133. What 2 factors affect availability and function of neurotransmitters?
    Amino acids from food to create them?

    Oxygen & insulin?
  134. Type of neurotransmitter and action for:

    ACTH (corticotropin)
    ADH (antidiuretic hormone)
    Large Molecule

    ACTH - Corticosteroids release in resp to biological stress

    ADH - Low BP
  135. Type of neurotransmitter and action for
    GABA (gamma-aminobutyric acid):
    • Amino Acids
    • Inhibitor
  136. Type of neurotransmitter and action for:

    Dopamine
    norepinephrine
    serotonin
    • Amines
    • Excite
  137. Type of neurotransmitter and action, and route for acetocholine?
    • Small molecule
    • Inhibitor
    • Parasympathetic
  138. What are neurotransmitters?
    Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse.

    Neurotransmitters are packaged into synaptic vesicles clustered beneath the membrane in the axon terminal, on the presynaptic side of a synapse.

    They are released into and diffuse across the synaptic cleft, where they bind to specific receptors in the membrane on the postsynaptic side of the synapse.
  139. Preganglionic fibers of the parasympathetic nervous system are AAAA to the ganglion and postganglioic fibers are BBBB to the body cells.
    • A. Long
    • B. Short
  140. Preganglionic fibers of the sympathetic nervous system are AAAA to the ganglion and postganglioic fibers are BBBB to the body cells.
    • A. Short
    • B. Long
  141. The Parasympathetic nervous system is also called the AAAA of the ANS because its BBBB originate from the CCCC and the upper DDDD segments of the spinal cord.
    • A. Craniosacral division
    • B. Preganglioic fibers
    • C. Cranial (III, VII, IX and X)
    • D. Sacral (S2, S3 and S4)
  142. The Sympathetic nervous system (not SNS) is also called the AAAA of the ANS because its BBBB originate from the CCCC and the upper DDDD segments of the spinal cord.
    • A. thoraco-lumbar
    • B. preganglioic fibers
    • C. thoracic (T1 - T12)
    • D. Lumbar (L1 & L2)
  143. The sympathetic nervous response is AAAA anf the parasympathetic response is BBBB.
    • A. Excitability
    • B. Inhibition
  144. Becaue organs are innervated by both AAAA and BBBB, CCCC effects can be produced.
    • A. Sympathetic
    • B. Parasympathetic
    • C. Opposite
  145. The Parasympathetic nervous system is called AAAA because its neurotransmitter is BBBB.
    • A. Cholinergic system
    • B. Acetylcholine
  146. The Sympathetic nervous system (not SNS) is called AAAA because its neurotransmitter is BBBB.
    • A. adrenergic system
    • B. norepinephrine
  147. The ANS is further divided into AAAA and BBBB
    • A. Sympathetic
    • B. Parasympathetic
  148. The ANS is AAAA and also called the BBBB. It acts to control & regulate CCCC, DDDD, EEEE, and FFFF
    • A. involunrtary
    • B. Visceral system
    • C. Heart
    • D. respiratory system
    • E. gastrointestonal system
    • F. Glands
  149. The SNS is AAAA and acts on BBBB and CCCC
    • A. Volutary
    • B. Skeletal muscles
    • C. Respiratory muscles
  150. The PNS is composed of?
    Somatic (SNS) & Autonomic (ANS) nervous systems
  151. The Nervous system is composed of
    CNS & PNS
  152. Stimulation of the CNA may...
    Increase or block nerve (neuron) call activity.
  153. What composes the CNS?
    Brain & Spinal cord
  154. Review the components of the central nervous system (CNS).
  155. Contraindications for migrain drugs?
    • Preg Cat X for ergot alkaloids
    • C for all triptans

    • Imitrex
    • Amerge
    • Maxalt
    • Zomig - Avoid for uncontrolled hypertension, IHD (ischemic heart dis) or prior MI

    • Axert
    • Frova
    • Relpax
  156. Treatment of fever in children 12 and younger - what & why?
    No aspirin because of the risk of Reye syndrome -> neurologic prolems assoc w/ viral infects treated with salicylates.

    Usze acetaminophen (Tylenol) instead.
  157. How do the triptan class of drugs work?
    Patho: inflammation and dilation of cranial vessels.

    Etiological theory: neurotransmitter serotonin imbalance, which normally cause vasoconstriction to suppress migrains.

    Triptans are selective serotonin receptor agonists, i.e. they facilitate whatever serotonin present to do what it normally does - cause vasoconstriction.
  158. Migrain drug categories?
    1) Preventative, e.g. beta andrenergic blockers like propanolol (Inderal)

    2) Mild migrain attacks: aspirin thru demerol

    3) Triptans are better than ergot alkaloids for acute migrains.
  159. Regarding drugs used in gout and hyperuricemia, what is recommended to prevent kidney stone development?
    Increased fluid intake and especially alkaline urine, since low pH which precipitates the uric acid into crystals which collect in joints and in kidneys as stones.
  160. When is Benemid also used?
    Effective in alleviating chronic gout, but they should not be used during acute attacks.

    Probenecid can be taken with colchicine.

    Initially w/ small doses of colchicine should be given before adding probenecid.

    If gastric irritation occurs, probenecid should be taken with meals.

    T1/2 8 to 10 hours

    85% to 95% protein-bound. Use caution when administering this drug with other highly protein-bound drugs.
  161. How does Benemid work?
    Probenecid blocks the renal reabsorption of uric acid.

    It can be used to treat chronic gout with colchicine, etc., but should not be used for acute attacks.
  162. Which drug is used for acute attacks of gout because it is able to relieve joint pain and swelling?
    Acute treatment include nonsteroidal antiinflammatory drugs (NSAIDs), colchicine and steroids.

    While indomethacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness.
  163. Name 2 drugs which the nurse may administer for the prevention and treatment of hyperuricemia.
    Uric acid > 6 mg/dL for women and 6.8 mg/dL for men.

    Uric acid is not very soluable, so it crystallizes in the blood and then collects on joints - gouty arthritis.

    Allopurinol (Zyloprim) is a uric acid biosynthesys inhibitor that works by inhibiting the enzyme xanthine oxidase which is needed for the synthesis of uric acid. It is a preventative (prophylactic) measure.

    Uricosurics like probenecid (Benemid) increase the rate of uric acid excresion by inhibiting its reabsorption by the kidneys, but shouylf not be used for acute gout.

    colchicine (Colcrys) is effective at decreasing acute gout symptoms (inflammation), but not at treating gout as the above 2 do.
  164. Your patient is admitted for elective knee surgery. During your admission assessment you discover she has been taking Xanax 1mg tid for the last three years. She has 2 drinks each evening. She is very nervous during interview and asks frequently whether the doctor will order Xanax for her. What is your assessment of this situation?
    Pt may well have a physical or phychological dependence and may very well have developed a tolerance as evidenced by her taking twice the normal dose. Pt should have been instructed not to consume alchhol with this drug because the combination could result in excessive sedation.
  165. HYPNOTIC BENZODIAZEPINES
    • Dalmane
    • Restoril
    • Halcion
  166. ANTIANXIETY BENZODIAZEPINES
    • Xanax
    • Librium
    • Klonopin
    • Valium
    • Ativan
    • Versed
  167. How to discontinue benzodiazepienes?
    taper off
  168. What is another use for Hydroxyzine?
    antiemetic
  169. What effect will caffeine have on antianxiety drugs?
    counteract...
  170. What are the advantages of Chloral Hydrate as an anxiety drug
    Decreased:

    occurrence of hangover

    respiratory depression

    Can be given to clients with mild liver dysfunction
  171. Most anxiolytics are benzodiazepienes. What are the other categories and drug examples for anxiolytics?
    Class of drug: Azapirones

    Drug: buspirone HCl (BuSpar)

    Class of drug: non-benzodiazepines

    • Drug:
    • Chloral Hydrate
    • Ambien
  172. What is the antidote for benzodiazepienes?
    flumazenil

    It is a benzodiazepiene antagonist.
  173. What are 4 contraindications of benzodiazepienes?

    (CNS depressants)
    Hypersensitivity

    CNS depression

    shock

    coma

    narrow-ancle glaucoma

    pregnancy

    lactation

    Caution: Hepatic or renal dysfunction, suicidal
  174. Benzodiazepines enhance the inhibitory effects of?

    (CNS depressants)
    gamma-aminonutyric acid (GABA), an inhibitory neurotransmitter within the CNS
  175. Characteristics of Benzodiazepines:

    (CNS depressants)
    Not meant for long-term use, e.g. > 4 months (Maddie: lose effectiveness after 4 weeks daily use.

    Wide margin of safety between therapeutic and toxic dose

    Lipid-soluble

    May cause CNS depression (respiratory depression and excessive sedation)

    Taper gradually to prevent withdrawal. May cause dependence

    Metabloized - liver

    Excreted - urine

    Steady state- 5 to 7 days

    Therapeutic in 2 to 3 days

    Maddie: Should not be taken every night, but should be taken at bedtime.
  176. Of the drugs used to treat anxiety, which drugs may be prescribed more often?
    alprazolam (Xanax)

    chlordiazepoxide HCl (Librium)

    clorazepate dipotassium (Tranxene)

    diazepam (Valium)

    lorazepam (Ativan)

    oxazepam (Serax)
  177. Which prototype drug can be used to treat anxiety?
    Class: Benzodiazapine

    Generic: Lorazepam

    Trade: Atavan
  178. What is insomnia?
    Insomnia is often defined as a positive response to:

    Do you experience difficulty sleeping? or

    Do you have difficulty falling or staying asleep?

    Transient insomnia lasts for less than a week.

    Acute < 1 month, or chronic
  179. Describe 2 types of anxiety.
    Primary and secondary

    Primary anxiety is not caused by a medical condition or by drug use

    Secondary anxiety is related to selected drug use or medical or psychiatric disorders.

    Anxiolytics are not usually given for secondary anxiety unless the medical problem is untreatable, severe, and causes disability. In this case an, anxiolytic could be given for a short period to alleviate any acute anxiety attacks.

    These agents treat the symptoms but do not cure them.

    Long-term use of anxiolytics is discouraged, because tolerance develops within weeks or months depending on the agent. Drug tolerance can occur in less than 2 to 3 months in clients who take meprobamate or phenobarbital.
  180. What are anxiolytics?
    Antianxiety drugs, used primarily to treat anxiety and insomia.

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