Appendix J ATI FORM A & B PHARMOCOLOGY
Cholinesterase Inhibitors
* Neostigmine (Prostigmin)
ACTION: Prevent the enzyme cholinesterase (CHE) from inactivating acetycholine (ACh), thereby increasing the amount of ACh available at receptor sites. Transmission of nerve impulses is increased at all sites responding to ACh as a transmitter
Therapeutic Use (TU)
increases muscle strength by increasing ACh effects at motor neurons in Myasthenia Gravis
Causes reversal of nondepolarizing neuromuscular blocking agents (tubocurarine) following surgery
Side Effects/Adverse Effects
Increased GI motility and secretion, bradycardia & urinary Urgency due to excessive muscarinic stimulation
* 1) If effects become intolerable notify primary care provider, Side effects can be treated with ATROPINE
Cholinergic Crisis- excessive muscarinic stimulation and respiratory depression from neuromuscular blockade
* Treat with Muscarinic effects with ATROPINE
* Provide resp. support through mechanical ventilation
Contraindications (CI) :
In clients with obstruction of GI and GU system
Pregnancy Risk Category C
Med food/ Interaction
Atropine : counteracts the effects of Neostigmine (Nursing interventions: ATROPINE is used to treat NEOSTIGMINE TOXICITY……….if no recovery is noted apply mechanical ventilation until full muscle function is regained)
Tubocurarine : Neostigmine reverses neuromuscular blockade after surgical procedures and overdose
Succinylcholine (increase neuromuscular blockade) : Avoid concurrent use
Client Education : Start at low dosages and titrate until desired muscle function is achieved, Encourage the client to keep track of self doasage administration, recognize signs of INADEQUATE DOSING, such as difficulty swallowing and signs of overmedication, such as urinary urgency, Advise the client to wear a medical alert bracelet
Effectiveness : Decreased fatigued, improved muscle strength as demonstrated by chewing, swallowing and performing hygiene
Neuromuscular blocking agent
Drug : Tubocuraine (non-depolarizing) & Succinycholine (Depolarizing)
Action: Neuromuscular blocking agents block Ach at the neuromuscular junction resulting in muscle relaxation and hypotension. They d/n cross the blood-brain barrier so complete paralysis can be achieved w/o loss of consciousness or decreased pain sensation
USE:
Used as adjuncts to general anesthesia to promote muscle relaxation
Used to control spontaneous respiratory movements in clients receiving mechanical ventilation
These Meds are used to diagnosis MYASTHENIA GRAVIS
Succinycholine is preferred for : Seizure contol during electroconvulsive therapy, endotracheal tubation, endoscopy
S/E
Respiratory Arrest from paralyzed respiratory muscles (NI: monitor respirations and vitals continuously, equipment ready for resuscitation)
Hypotension resulting from HISTAMINE RELEASE and GUANGLIONIC BLOCKADE, Bradycardia and dysrhythmias
S/E of SUCCINYLCHOLINE (ANECTINE)
Malignant hyperthermia: 109.4 F (NI: Monitor vitals, stop med, ice or ice saline to cool the client, Administer Dantrolene: decreases metabolic activity of the skeletal muscle)
Prolonged Apnea due to low Pseudocholinesterase (NI : Test clients blood and hold med if pseudo levels are low)
HyperKalemia
Med/food Int
General anesthetics are often used concurrently in surgery
Aminoglycosides, tetracyclines : increase effects of neuromuscular blockade
Neostigimine & Prostigmin) and other Cholinesterase inhibitors : decrease the effects of non-depolarizing neuromuscular blockers, such as Tubucurarine; increase the effects of depolarizing neuromuscular blockers, such as Succinylcholine
Education: Continous Cardiac and respiratory monitoring (have life support equipment handy)
Effectiveness: Muscle relaxation during surgery, absence of seizures in EC Therapy, Successful Endotracheal intubation, No spontaneous respiratory movements
Classification : Adrenergic Agonist
Drug : Epinephrine (Adrenaline) other drugs Dopamine and Dobutamine
Action : Catecholamine adrenergic agonists c/n be taken by the oral route, d/n cross the blood brain barrier and the duration is short
Receptors
Alpha1 : Activation of receptors in arterioles of skin, viscera ad mucous membranes, and veins lead to vasoconstriction
Beta1 : Heart stimulation leads to increased HR. increased Myocardial contractility, increased rate of conduction through the AV node, Activation of receptors in the kidney lead to release of rennin
Beta2 : Activation of receptors in the arterioles of the heart, lungs, and skeletal muscles leading to vasodilation, Bronchial stimulation leads to bronchodilation, activation of receptors in the uterine smooth muscles causes relaxation, activation of receptors in the liver causes glycogenesis, activation of skeletal muscles leads to muscle contraction
Dopamine : activation of receptors in the kidney cause the renal blood vessels to dilate
Estrogen acting on Alpha1
VASOCONSTRICTION
TU: Increases B/P, decreases congestation of nasal mucosa, Manages superficial bleeding, slows absorption of local anesthetics
Estrogen acting on Beta 1
Increases HR, Myocardial contractility, rate of conduction through the AV
Tx: AV Block and Cardiac Arrest
Estrogen acting on Beta2
Bronchodilation
Tx : Asthma
S/E :
Hypertensive crisis : Due to Vasoconstriction of Alpha 1 receptors (NI: Continuous Cardiac monitor).Dysrhythmias : Do to activating Beta1 receptors which increases the workload of the heart and the oxygen demand of the heart
Contraindications- Pregnancy Risk C, In clients with Tachydysrhythmias and v.Fib
Med/Food Int- Avoid use of MAOI’s in clients receiving Epinephrine.Tricylic Antidepressants increase the effects of epinephrine, may need to lower epinephrine dosage.General Anesthetics and epi can cause Dsyrhythmias so monitor ECG and notify primary care provider for signs of chest pain, increased HR
Phentolamine Treats Epinephrine Toxicity
Propranolol treats Chest Pain and dysrhythmias
Education- Must be administered IV by continuous infusion, continuous ECG monitoring
Effectiveness- urine output greater than 30ml/hr, improved mental status, systolic blood pressure maintained at greater than equal to 90mm hg
Classification : Alpha Adrenergic Blockers (Sympatholytics)
Drug : PRAZOSIN (MINIPRESS)
Action: Venous and arterial dilation. Smooth muscle relaxation of the prostatic capsule and bladder neck
TU: Tx: HTN
Doxazosin mesylate (Cardura) may be used to decrease symptoms of benign prostatic hypertrophy (BPH) (e.g urgency, frequency, dysuria)
S/E
First-Dose Orthostatic Hypotension (NI: first dose may be given at night, monitor blood pressure for 2hr after the initiation of tx, instruct clients to avoid activity for the first 12-24hr, encourage pt. to change positions slowly)
Contraindications (CI) : Pregnancy risk C. CI in clients with hypersensitivity to medication
Med/Food Int
Anti-hypertensive Medications
NSAID’s and Clonidine decrease Anit-HTN effects
Effectiviness
*decrease in b/p, reduction in benign prostatic hypertrophy symptoms
Classification : Centrally Acting Alpha2 Agonists
Drug : Clonidine (Catapres)
Action :
Act in the CNS to decrease sympathethic outflow. This results in a decrease of norepinephrine (NE) released from sympathetic nerves, thereby decreasing the amount of NE that is available to stimulate the adrenergic receptors (both alpha and beta receptors) of the heart and peripheral vascular system
decreases sympathetic outflow to myocardium, results in bradycardia and decrease cardiac output (CO)
decreases in synmpathetic outflow to peripheral vasculature results in, vasodilation, which leads to decrease blood pressure
S/E
Drowsiness and Sedation
Dry Mouth (encourage the client to chew gum or hard candy, symptoms resolves in 2 to 4 weeks)
Rebound HTN: Discontinue CLONIDINE gradually over the course of 2 to 4 days
Med & Food Int
Antihypertensive Meds (may have hypotensive additive effects)
Prazosin, MAOI’s and Tricyclic Antidepressants (May counteract anti-hypertensive effects)
Alcohol : CNS Depressants
Education- Pregnancy must be ruled out before treatment is begun
Administer Twice a day in divided doses
Transdermal patches applied every seven days
Effectiveness- decreased blood pressure, absence of pain
Classification : Adrenergic Neuron-Blocking Agents
Drug: Reserpine
Action- Depletion of NE from postganglionic symphathetic neurons which decreases the activation of alpha and beta adrenergic receptors…………..This slows HR and Reduces Cardiac Output
TU: Tx HTN and Can be, but is less commonly used to treat Psychotic States
S/E-
Severe Depression (NI: educate about signs of depression such as early morning insomnia, decreased appetite, change in mood
Cardiovascular Effects : Bradycardia, orthostatic hypotension, nasal congestion ((due to depletion of Noreepinephrine (NE))………Bradycardia caused by decreased activation at the beta1 receptors, hypotension and nasal congestion caused by dec. activation at alpha receptors
GI Effects : Increase secretion of gastric acid causing Ulcer Formation
CI: Patients who have a hx of Depression
Classification : Beta Adrenergic Blockers (Sympatholytics)
Drugs : Propranolol and Metoprolol
Action : decrease HR, Myocardial contractility (inotropic), rate of conduction through the AV.Metoprolol blocks at Beta1 receptor, Propranolol (Inderal) blocks at Beta 2 receptor
TU: Angina Pectoris, HTN, Cardiac Dysrhythmias, MI, Heart Failure,
Other uses : hyperthyroidism, migraine headache, stage fright, glaucoma
S/E of Metoprolol (lopressor): Bradycardia (Administer Atropine and Isoproterenol) Decrease In Cardiac output (Metoprolol may take like 1 to 3 months for effects to work) AV Block (D/n administer beta-blocker) Orthostatic hypotensive, rebound myocardium excitation (use of beta blockers shouldn’t be abruptly stopped, discontinue over 1 to 2 weeks)
S/E of Propranolol (Inderal) : Bronchoconstriction (Avoid in asthmatic clients), Glycogenolysis is inhibited (Contraindicated in Diabetic pt.s treat diabetic pt.s with Beta1 agent)
Contraindications
Beta adrenergic blockers are contraindicated in clients with AV block and Sinus BradyCardia
Non-Selective beta-adrenergic blockers are contraindicated in clients with asthma, bronchospasms and heart Failure
Use cardioselective Beta-adrenergic blockers cautiously in clients with heart failure, asthma, bronchospasm, diabetes, hx of allergies and depression
MED and Food Int
CCB’s (Verapamil &Diltiazem (Cardizem) : intensifies the effects of beta-blockers………monitor closely
Antihypertensive Meds : Increases Hypotensive effects……monitor b/p
Insulin- prevents glycogenolysis: may need to adjust dosage of insulin when using Propranolol (Inderal)
Education- Self monitor HR and B/p, D/N crush or chew extended release tablets, avoid sudden changes in position
Effectiveness- Absence of chest pain, cardiac dysrhythmias, normal b/p, control of signs of HF
Classification : Muscarinic Agonists
Drug : Bethanechol (Urecholine)
Action : Binds reversibly to muscarinic cholinergic receptors and causes activation, the principal structures affected by muscarinic activation are the heart, exocrine glands, smooth muscles, and eye
At the heart : Causes Bradycardia
At Exocrine Glands : Causes increase sweat, salivation, bronchial secretions, and secretion of gastric acid
In the Smooth muscles of the lung and GI Tract : Promote contraction
In the bladder : contracts the detrusor muscle and relaxs the trigone and sphincter causeing BlADDER EMPTYING
TU : Tx for Urinary Retention in post opt and post pardum pt. NOT urinary retention caused by physiological obstruction…..b/c it cam cause injury due to increased pressure
S/E : Hypotension and bradycardia. Excessive salivation ,increased sec. of gastric acid, abdominal cramps and diarrhea
CI : Patients with low blood pressure, gastric ulcers, intestinal obstruction (can rupture the bladder) patients with asthma (it causes bronchoconstriciton), hyperthyroid patients (Can cause dysrhythmias)
Classification : Muscarinic Antagonists (Anticholinergic Drugs)
Drug: Atropine
Action : completely block the action of acetylcholine at muscarinic receptors. Exerts it’s influence primarily on the heart, exocrine glands, smooth muscles, and eye, just like the muscarinc agonist
At the heart : increase HR
Exocrine Glands : decrease secretion of salivation, bronchial glands, sweat glands and decreases gastric secretions
Smooth muscles: Atropine causes relaxation of the bronchi, decreased tone of the urinary bladder detrusor and decreased tone and motility of the GI
Eye : Dilates the pupil (mydriasis) focuses the lens for far vision (cycloplegia)
CNS: can cause mild excitation at therapeutic doses, Toxic doses can causes delirium & hallucinations
TU:Helps during eye examinations for disorders of the eye. Tx Bradycardia. Tx : diverticulitis by decreasing tone and motility in the smooth muscles of the intestine. Used to Reverse Muscarinic Poisioning, Can treat Peptic Ulcers disease, Asthma (by bronchodilating)
S/E : Xerostomia (Dry Mouth), Blurred Vision (paralyze ciliary muscle focus on far objects causes blurred vision) photophobia (paralysis of iris sphincter prevents constriction of the pupil) (NI: where glasses 4photophobia-when unable to adapt to bright light)
Urinary Retention and Constipation (blockade of muscarinic receptors increase the pressure w/in bladder and increases the tone of the urinary sphincter and trigone)
Anhidrosis (absence of sweat), Tachycardia, Asthma(cause thickening and drying of bronchial secretions
Drug Interactions : Anti-histamines, phenothiazines, antipsychotics, tricyclic antidepressants…have anticholinergic effects and can enhance the effects of Atropine
Note : Anti-cholinergic means blockade at Muscarinic Receptors-not blockade at all cholinergic receptors
Classification : Ganglinic Blocking Agents
Drugs : Mecamylamine
Action : Blocks transmission through the ganglia of the ANS by completing with Ach for binding to nicotinic receptors
TU : Are used ONLY to decrease blood pressure, treats primary HTN in selected patients, only used when b/p c/n be reduced by all other medications
S/E :
Antimuscarinic effects (dry mouth, blurred vision, photophobia, urinary retention, constipation, tachycardia, anhidrosis)
Orthostatic hypotension (by dilating veins causes pooling of blood decreasing blood return to the heart, reducing CO and subsequent fall in b/p)
CNS Effects ( tremor convulsions, and mental aberrationds)
Central Nervous System Drugs
Drugs for Parkinson’s disease
Dopaminergic Drugs:
Anti-Parkinson’s Medications
Dopaminergics: Levodopa (increases dopamine [DA] synthesis)
-levodopa plus carbidopa (Sinemet)
-Carbidopa (blocks levodopa destruction)
Dopamine agonists: pramipexole (Mirapex)
Centrally acting anticholinergics: Benztropine (Cogentin)
Dopamine releaser (Antiviral): Amantadine (Symmetrel)
Classification:
Dopaminergics:
Medications: Levodopa (Dopar, Larodopa), levodopa plus carbidopa (Sinemet)
Actions:
-Levodopa crosses the blood brain barrier and is taken up by dopaminergic nerve terminals and converted to dopamine (DA). This newly synthesized DA is released into the synaptic space and causes stimulation of DA receptors
- Carbidopa does not possess any therapeutic effects, but is used to augment levodopa. Carbidopa inhibits conversion of levodopa to DA in the intestine and periphery, and thereby allows for increase amounts of levodopa to reach the CNS
Dopamine agonists:
Medications: Pramipexole (Mirapex), Ropinirole (Requip), bromocrptine (Parlodel)
Actions:
-Act directly on DA receptors
Centrally Acting Anticholinergics:
Medications: Benztropine (Cogentin), Trihexyphenidyl (Artane)
Actions: These medications block acetylcholine at muscarnic receptors, which assists in maintaining the balance between dopamine and acetylcholine in the brain.
Dopamine releaser (Antiviral):
Medications: Amantadine (Symmetrel)
Actions: Antiviral stimulate DA release, prevent dopamine reuptake, and may block cholinergic and glutamate receptors
Therapeutic Uses:
- These medications do not halt the progression of Parkinson’s disease (PD): however, they do offer symptomatic relief from dyskinesias (e.g., bradykinesis, resting tremors, and muscle rigidity).
- Levodopa may be used as a first-line medication for PD treatment
- Pramipexole (Mirapex) is used as monotherapy in early-stage PD, and used in conjunction with levodopa in late- stage PD. It is used often in younger clients who are more able to tolerate daytime drowsiness and postural hypotension
Side/Adverse Effects: Nursing Interventions and Client Education
Dopaminergics: levodopa- usually dose dependant
- N&V, drowsiness
o Administer in small doses at the start of treatment and with food
- Dyskinesias (e.g.), head bobbing, tics, grimacing, tremors)
o Decrease dosage of medication, but the decrease may result in resumption of PD symptoms
- Orthostatic hypotension
o Monitor the clients b/p
o Instruct the client about signs of postural hypotension
- Cardiovascular effects from beta1 stimulation (e.g., tachycardia, palpitations, irregular heartbeat)
o Monitor the clients vital signs
o Use cautiously in clients with cardiovascular disorders
o Monitor ECG
- Psychosis (e.g., visual hallucinations, nightmares)
o Administer antipsychotic medications such as clozapine (Clozaril) if symptoms occur.
- Discoloration of sweat and urine
o Advise the client that this is a harmless side effect
- Activation of malignant melanoma
o Avoid use of medication in clients with skin lesions that have not been diagnosed
Dopamine Agonists: Pramipexole (Mirapex)
- Sleep attacks
- Daytime sleepiness
o Advise the client to avoid the use of other CNS depressants such as alcohol
- Orthostatic hypotension
- Psychosis