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)
Discuss Alzheimer's treatment with Tacrine(Cognex).
Improves memory loss by elevating Ach concentration
antocholinergics contraindicated with
Tx: relieve tremors & rigidity
OD signs: Agranulocytosis, hemolytic anemia, thrombocytopenia, cardia dysrhythmisa, neroleptic malignant syndrome
Cholinergic drugs tend to AAAA secretions.
Review Alzheimer's disease & possible causes.
Degeneration of cholinergic neuron and deficiency oif acetylcholine
What are adverse effects of Antiparkinson drugs?
Nausea & vomiting
Premature ventricular contraction (PVCs)
- Dyskinesia - involuntary movement
- of tongue and body
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)
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.
How do antiparkinson drugs work?
Either to reduce the symptoms or replace the domamine deficit
Review Parkinson's disease.
Degenerative CNS disorder
Abnormalities in movement (bradykinesia), posture, tremor, joint and muscle
Destruction/degenerative changes in dopamine producing nerve cells
Decreased dopamine/increased acetylcholine
Can develop with long-term use of antipsychotics (pseudoparkinson's)
Doctor orders Valium 50 mg IV STAT for your patient with severe muscle spasms. Your thoughts?
- IV: 5-10mg
- rpt @ 10-15min
- MAX 30mg
2-3 wk steadyt state
3-4 wk therapeutic levels
Monitor for anemia
Drug of choice for less than 2 years
aka Depakote - for grand, petit & psychoM
Alcohol WD and anxiety.
Can be used for status epilepticus, but valium is choice there
drug of choice for status epilepticus
Barbituate-like drug for grand mal & psychomotor seizures
Anticonvulsant to control seizures in toxemia of pregnancy caused by eclampsia and preeclampsia
Anticonvulsant for grand mal seizures
Do not confuse
CELEBREX, an NSAID
CEREBYX, a seizure med
Abrupt WD -> seizures
anticonvulsant to Tx facial pain assoc w/ triginmenial neural
8 Important points about anticonvulsants
Long term oral: Dilantin
Contraindicated for renal or liver damage
May cause bone marroe suppression
Dilantin will precipitate in D5W - use only 0.9 NS
What prototype drug is used to treat seizures?
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
How are seizures treated?
Correct the underlying cause
- - 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
Why do seizures occur?
Low blood sugar
WD of drugs: cocain, lidocain, lithium, theophyline
3-5 days after alcohol WD
Complex symptoms: automatisms (repetitive behavior such as chewing or swallowing motions), behavioral changes, and motor seizures
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
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.
Dysrhythmic muscle contraction
Sustained muscle contraction
Convulsive and nonconvulsive; involve both cerebral hemispheres of the brain
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.
Treatment schedule for mood disorders with antidepressant meds?
9 months after symptoms 1st appear
5 years after 2nd
long-term after 3rd
Involuntary paroxysmal mucle contractions.
The word paroxysm means "sudden attack, outburst".
Abnormal electrical discharges of the cerebral neurons and is characterized by a loss or disturbance of conciousness
naloxone HCl (Narcan) Dosage
- IV: 0.4 to 2 mg
- may repeat q2-3min
- max 10mg
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)
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
PO: 325 to 650 mg q4-6h PRN; max: 4000 mg/d
Rectal supp: 650 mg q.i.d.
- PO: 325 to 650 mg q4h prn; max: 4 g/d
- TIA and thromboemboliccondition:
- PO: 81 to 325 mg/d
- PO: 3.6 to 5.4 g/d in divided doses
TDM: 15 to 30 mg/dL; 150 to 300 mcg/mL
OD of Tricyclic antidepressents?
- - CNS depression
- - Cardiovascular collapse
- - Airway
- - Charcoal
- - Fluids
- - EKG monitoring
- - Antiseizure meds
OD of MAO antidepressents?
- - Diuretics
- - Acidify urine
- - Hemodialysis
OD of the antidepressents Welbutrin?
- - Agitation
- - Seizures
- - Supportive
- - Charcoal
- - anti-seizure meds
OD of the antidepressents lithium?
- - Altered levels of consciousness
- - Hallucinations
- - Convulsions (seizure)
- - Diminished urine output- Low Na+ (Na/K pump shot)
- - Oliguria
- - Coma
- - Death
- - Supportive
- - Fluid and electrolyte correction
- - Hemodialysis
OD of SSRI antidepressents...
- - CNS stimulation
Can polydrug therapy be an effective means of treating depression?
No becauseof the possible sewrios side effects.
Example(s) of Tricyclic Antidepressants?
Example(s) of antidepressent Mood Stabilizers?
Example(s) of "misc" antidepressents?
Example(s) of Serotonin Reuptake Inhibitors?
Example(s) of MAO antidepressents?
What are the 5 types of antidepressents?
Serotonin Reuptake Inhibitors
Review types of mood disorders.
- 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
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.
What are the symptoms of Tardive dyskinesia?
Protrusion and rolling of the tongue
Sucking and smacking movements of the lips
Involuntary movements of the body and extremities
What are the symptoms of Acute dystonia?
Involuntary upward eye movement
Muscle spasms of the tongue, face, neck,and back (back muscle spasms cause 'trunk to arch forward)
What are the symptoms of Akathisia?
Trouble standing still
Paces the floor
Feet in constant motion, rocking back and forth
What are the Pseudoparkinsonism symptoms?
Tremors at rest
Pill-rolling motion of the hand
What are the EPS?
- Acute dystonia
- Tardive dyskinesia
How are EPS managed?
Anticholinergic drugs help decrease:
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.
What are extrapyramidal symptoms?
Tremors at rest
Pill-rolling motion of the hand
(Parkingson's disease affects the extrapyramydal motor tract of nerves)
How long are antipsycotics given?
Perhaps a lifetime.
One class of "typical" antipsychotics are Nonphenothiazines. Name a few.
One class of "typical" antipsychotics are Phenothiazines. Name a few.
- stelazine (not in our book)
What are advantages of nonphenothiazines?
What is it?
I only saw 1 - a dose of 0.5-5mg instead of 10-25mg.
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)
Name the 1st drug used to treat psychotic disorders.
What 2 broad categories of drugs are used to manage psychosis?
typical (or traditional)
What is schizophrenia?
a mental disorder characterized by a breakdown of thought processes and by poor emotional responsiveness
Discuss signs and symptoms of psychosis.
It is losing contact with reality.
- Positive symptoms:
- incoherent speech
- Negative symptoms:
- poverty of speech
- social withdrawal
- poor self-cate
Name 2 hyponotic drugs.
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!!!!
Chronic autoimmune neuro-muscular disease
- women < 30
- men > 50
- lack of ACh receptor sites.
other non-opioid analgesics
Toradol - IM/IV: 30mg q6h; max 120 mg/d
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.
Theraputic level: 5-20 mcg/mL
Toxic levels > 50 mcg/mL
Probably hepatotoxic: > 200 mcg/mL
4 g/d, unless taken regularly then it is suggested that the limit be 2 g/d.
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
Peak: 30-120 minutes
PO, Supp, IV
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.
Which drug is considered as an ASA substitute?
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.
What is the fluid recommendation for patients taking NSAID's and why?
2-3 L per day
Drugs that increase the effects of ASA
Codein hydrocodone (oxycontin)
Suction NG tube & add charcoal.
If no NG tube -> quinton catheter (dialysis)
Large doses reequired for arthritis risk GI bleeds, i.e. theraputic blood levels 150-300 ug/mL (or 15-30 mg/dL)
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.
Hypersensitivity to salicylates or NSAIDs
for no reason including fever in children 12 or younger
Caution: renal or hepatic disorders & may cause bleeding, esp of GI
TIA (transient ischemic attack "small stroke") & Thromboembolic
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.
What is another name used for analgesics antipyretic anti-inflammatory drugs?
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.
Name the prototype analgesic antipyretic anti-inflammatory drug.
ASA or aspirin
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
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
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?
MAOI - calming drugs
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)
What is the methadone treatment program?
No high bu it occupies the receptors which alleviates the eithdrawal symptions of:
- abdominal cramps
- watery eyes
- runny nose
Disulfiram is a drug discovered in the 1920s and used to support the treatment of chronic alcoholism by producing an acute sensitivity to alcohol.
Briefly discuss 3 narcotic antagonists.
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.
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.
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.
List 4 examples of opioid agonists-antagonists.
What is the prototype analgesic agonists-antagonists?
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.
Name other agonists of the prototype MS.
Codeine v Morphine
1/15 to 1/20th as potent
Most opioids have antitussive (cough supression) except:
Review contraindications for MS.
Asthma with respiratory depression
Increased intracranial prewssure
Caution: respiratory, renal, hepatic diseases, MI, old & young
Review indications for MS.
Indications: Pain from
Acute Myocardial Infarction (AMI)
Dysnea from pulmonary edema
Time to work: fentanyl (opioid) patch
Morphine Sulfate Route Data
- 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
Compare morphine to dilaudid
6X analgesia over morphine
fewer hypnotic effects
less GI distress
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
Slowed GI motility
Muscle Spasms in bowel & billiary (bile) tract
life-threatening increased intracranial pressure
What drug is the prototype opioid analgesic?
What are the effects of narcotic analgesics?
Reduce the perception of pain
Decrease emotional upset
Most are Schedule II.
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.
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.
Gate control for pain seeks to
Close large diameter (neuro) fibers.
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.
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.
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
What does excessive CNS stimulation involve?
Increased Excitatory receptors
Decreased Inhibitory receptors
Increased Sensitivity of excitatory receptors
Decreased Sensitivity of inhibitory receptors
BOTH EXCITATORY & INHIBITORY
Think turkey - tryptophan from which it is derived - it inhibits CNS
EXCITATORY or INHIBITORY
Mostly sympathetic via norepinephrine
Major inhibatory neurotransmitter
Not enough GABA (gamma-Aminobutyric acid) causes anxiety, hyper-arrousal, seizures.
EXCITATORY or INHIBITORY
dopamine agonists stimulate the dopamine receptors
Parkinsons (shuffling gate, intention tremor) is the destruction of the dopamine neurons
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.
What do neurglial or glial cells do?
Many fucntions, but chiefly protection. Myelin sheath are Schwann cells - a type if glial cell.
How does hypoxia affect the CNS?
How does acidosis affect synaptic transmission?
Makes it nonresponsive
How does alkalosis affect synaptic transmission?
What 2 factors affect availability and function of neurotransmitters?
Amino acids from food to create them?
Oxygen & insulin?
Type of neurotransmitter and action for:
ADH (antidiuretic hormone)
ACTH - Corticosteroids release in resp to biological stress
ADH - Low BP
Type of neurotransmitter and action for
GABA (gamma-aminobutyric acid):
Type of neurotransmitter and action for:
Type of neurotransmitter and action, and route for acetocholine?
- Small molecule
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.
Preganglionic fibers of the parasympathetic nervous system are AAAA to the ganglion and postganglioic fibers are BBBB to the body cells.
Preganglionic fibers of the sympathetic nervous system are AAAA to the ganglion and postganglioic fibers are BBBB to the body cells.
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)
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)
The sympathetic nervous response is AAAA anf the parasympathetic response is BBBB.
- A. Excitability
- B. Inhibition
Becaue organs are innervated by both AAAA and BBBB, CCCC effects can be produced.
- A. Sympathetic
- B. Parasympathetic
- C. Opposite
The Parasympathetic nervous system is called AAAA because its neurotransmitter is BBBB.
- A. Cholinergic system
- B. Acetylcholine
The Sympathetic nervous system (not SNS) is called AAAA because its neurotransmitter is BBBB.
- A. adrenergic system
- B. norepinephrine
The ANS is further divided into AAAA and BBBB
- A. Sympathetic
- B. Parasympathetic
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
The SNS is AAAA and acts on BBBB and CCCC
- A. Volutary
- B. Skeletal muscles
- C. Respiratory muscles
The PNS is composed of?
Somatic (SNS) & Autonomic (ANS) nervous systems
The Nervous system is composed of
CNS & PNS
Stimulation of the CNA may...
Increase or block nerve (neuron) call activity.
What composes the CNS?
Brain & Spinal cord
Review the components of the central nervous system (CNS).
Contraindications for migrain drugs?
- Preg Cat X for ergot alkaloids
- C for all triptans
- Zomig - Avoid for uncontrolled hypertension, IHD (ischemic heart dis) or prior MI
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.
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.
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.
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.
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.
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.
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.
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.
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.
How to discontinue benzodiazepienes?
What is another use for Hydroxyzine?
What effect will caffeine have on antianxiety drugs?
What are the advantages of Chloral Hydrate as an anxiety drug
occurrence of hangover
Can be given to clients with mild liver dysfunction
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
- Chloral Hydrate
What is the antidote for benzodiazepienes?
It is a benzodiazepiene antagonist.
What are 4 contraindications of benzodiazepienes?
Caution: Hepatic or renal dysfunction, suicidal
Benzodiazepines enhance the inhibitory effects of?
gamma-aminonutyric acid (GABA), an inhibitory neurotransmitter within the CNS
Characteristics of Benzodiazepines:
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
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.
Of the drugs used to treat anxiety, which drugs may be prescribed more often?
chlordiazepoxide HCl (Librium)
clorazepate dipotassium (Tranxene)
Which prototype drug can be used to treat anxiety?
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
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.
What are anxiolytics?
Antianxiety drugs, used primarily to treat anxiety and insomia.