Exam 2 Flashcards
Sympathetic Nervous System (SNS)- fight or flight
- Responsible fight, flight, and fright functions
- Speeds everything up except the GI tract
- Epinephrine/Norepinephrine gets released by neurons of SNS and activates adrenergic receptors (alpha and beta receptors), Alpha 1&2, and Beta 1&2.
Alpha Receptors
- Alpha 1- constricts smooth muscles, especially vessels.
- Alpha 2- inhibitory
Beta Receptors
1 heart, 2 lungs
- Beta 1- on the heart, increased heart rate, increases contractility (squeeze of the heart), increases blood pressure.
- Beta 2- present throughout the airway–>relax smooth muscle–>bronchodilation.
Non-selective adrenergic agonist: Epinephrine
MOA:
Activates Alpha 1, Beta 1&2
Non-selective adrenergic agonist: Epinephrine
Uses:
o Asthmatic and allergic emergencies
o Cardiogenic shock
o Cardiac arrest
o Has a rapid onset, short duration of action.
Non-selective adrenergic agonist: Epinephrine
SEs/ADRs:
o Nervousness
o Restlessness
o Tremors
o Headache
o Angia (chest pain)
o Arrhythmias
o Hypertension
o Tachycardia
o Hyperglycemia
o GI upset
Non-selective adrenergic agonist: Epinephrine
Nursing Action:
o Monitor vital signs.
o CM (cardiac monitor)
o Monitor blood glucose closely.
Epi-pen autoinjector
“Blue to sky, orange to thigh”
o Remove the blue cap.
o Inject the orange end into the lateral thigh.
o Hold at a 90-degree angle. Insert until you hear a click. HOLD for 10 secs, remove, then gently massage the area.
o Call 911. Effects are brief. The second dose may be given in 10 mins if the patient is not better before help arrives.
Adrenergic Blockers: Beta-blockers
Action:
o Blocking Beta 1–> dec heart rate, dec blood pressure
o Blocking Beta 2–> bronchoconstriction ——-ADR
o Non-selective BBs (beta blockers) (N-Z) ex/propranolol. Block Beta 1&2
o Selective BB (A-M) ex/atenolol. Preferentially target Beta minimizes ADRs of non-selective.
Adrenergic Blockers: Beta-blockers
Uses:
o Antihypertensive
o Cardioprotective benefits post MI (heart attack)
o Heart failure (not acute)
o Arrhythmias
Adrenergic Blockers: Beta-blockers
SEs:
o Drowsy
o Dizzy
o Decreases sex drive.
o Orthostatic hypotension
Adrenergic Blockers: Beta-blockers
ADRs:
o Bronchoconstriction
o Hypoglycemia
o Bradycardia
- Selective beta-blockers may be used with caution in patients with asthma/COPD.
Adrenergic Blockers: Beta-blockers
Contraindications:
o Bradycardia
o Heart block (arrhythmia where heart rate is very slow)
o Cardiogenic shock
o Acute heart failure – pt must be stable before initiating beta blockers (no hypotension). Once stable, begin very low-dose BB (beta-blocker).
o Asthma
o COPD
o Sick sinus syndrome (pts heart rate is tachy then brady, tachy then brady, etc.)
Adrenergic Blockers: Beta-blockers
Nursing Interventions:
o Check baseline vital signs- report heart rate less than 60.
o Check history- diabetic, asthma, or COPD.
o Counsel pt to change positions slowly.
Parasympathetic Nervous System (PNS)- rest and digest
- Responsible for “rest and digest” functions
- Acetylcholine (ACH) is released by neurons of PNS and activates muscarinic/nicotinic receptors (cholinergic receptors).
Muscarinic Receptors: M1
Found in exocrine- salivation and gastric acid secretions.
Muscarinic Receptors: M2
Found in the heart- slow heart rate.
Muscarinic Receptors: M3
Found in smooth muscle- bronchoconstriction, bladder contraction, GI contractility, produce vasodilation, pupil constriction, also found in pancreas–>insulin release.
Effects of cholinergic stimulation (when they are activated)
- Hypotension, decreased heart rate
- Inc secretions (saliva, GI, sweat)
- Inc GI motility- diarrhea, nausea, abdominal pain
- Increased detrusor tone–> Micturition (peeing), incontinence
- Pupillary constriction
- Bronchospasm
Effects of cholinergic blockade (anti)
- Inc heart rate
- Dec secretions (dry mouth, eyes)
- Dec GI motility (constipation)
- Dec detrusor muscle tone (urinary retention)
- Pupillary dilation/ciliary muscle–> Blurred vision.
- Bronchodilation
Cholinergic agonists
“bind to and activate cholinergic receptors.”
Cholinergic agonists: Bethanechol
Action:
o Stimulates receptors on the smooth muscle of the bladder and GI tract.
Cholinergic agonists: Bethanechol
Uses:
o Urinary retention
o MUST rule out urinary/intestinal tract obstruction.
Cholinergic agonists: Bethanechol
SEs/ADRs:
o Blurred vision
o Inc secretions
o Orthostatic hypotension
o Bronchoconstriction
o Hypotension
o Bradycardia
Cholinergic agonists: Bethanechol
Interactions:
o Other drugs that dec heart rate and blood pressure
o Atropine (reversal agent)- block PNS activity
Cholinergic agonists: Bethanechol
Contraindications:
o Bradycardia
o Hypotension
o COPD/asthma
o Peptic ulcer disease
o Parkinson’s disease
o Intestinal/urinary obstruction
Cholinergic agonists: Bethanechol
Nursing Actions:
o Check vital signs.
o Be familiar with the medications/medical history of the patient.
o Give 1 hour before, 2 hours after meals to avoid nausea and vomiting.
o Teach pt to change positions slowly.
o Monitor input and output.
Cholinergic agonists: Pilocarpine
Action:
o Directly stimulates cholinergic receptors in eye–> miosis (constrict pupil). This allows aqueous humor to exit.
Cholinergic agonists: Pilocarpine
Use, Administration:
- Use:
o Eye drops to treat glaucoma. - Administration: pg 86
o Eye drops – punctal occlusion (a mechanical treatment that blocks the tear drainage system in order to aid in the preservation of natural tears on the ocular surface).
Cholinergic agonists: Pilocarpine
Nursing Actions:
o Teach proper administration of eye drops and punctual occusion technique.
o Causes difficulty in dark adaptation- advise pts to use caution while night driving or performing tasks in poor lighting.
Anticholinergic: Atropine
Action:
Opposes actions of PNS (Parasympathetic Nervous System)
Anticholinergic: Atropine
Uses:
o Eyes: mydriatic agent (dilates pupils)
o CV (cardiovascular): inc heart rate (used for symptomatic sinus bradycardia)
o Pulmonary: anti-secretory (used to dry up secretions, pre-op)
o GI: antispasmodic (dec GI motility, relieves cramps and diarrhea)
o Urinary tract: for incontinence (replaced by other drugs)
o Antidote: for cholinergic toxicity
Anticholinergic: Benztropine
Action:
o Inhibits cholinergic activity.
o Inhibits reuptake of dopamine
o Explanation: dopamine depletion–>inc ACH release–>activation of muscarinic receptors–>overstimulation of neurons by ACH–>tremors/rigidity
Overall effect: Benztropine blocks effects of ACH–>dec tremors, dec rigidity, dec drooling.
Anticholinergic: Benztropine
Uses:
o Dec tremors
o Dec rigidity
o Dec drooling
Urinary Anticholinergic: Tolterodine
Action:
Inhibits muscarinic receptors in bladder and urinary tract which helps retain bladder volume
Urinary Anticholinergic: Tolterodine
Use:
o Urge incontinence (dec frequency of urination/OAB (overactive bladder))
General Anticholinergics
Common SEs:
- Constipation
- Dry mouth/eyes
- Tachycardia
- Blurred vision
- Urinary retention
General Anticholinergics
ADRs:
- Confusion/hallucinations
- inc fall risk in the elderly.
General Anticholinergics
Contraindications:
- DO NOT GIVE to pts with a history of glaucoma.
- GI motility issues
- May worsen MG (myasthenia gravis)
- Tachycardia
- BPH (Benign prostatic hyperplasia-enlarged prostate that is not cancerous)
General Anticholinergics
Interactions:
- Other drugs with anticholinergic effects ex. TCAs, antihistamines, cyclobenzaprine (muscle relaxer), grapefruit juice
General Anticholinergics
Nursing Considerations:
- Asses for contraindications: glaucoma, Gi/bladder obstruction, MG (myasthenia gravis)
- Assess neurological status.
- Monitor vital signs.
- Assess abdomen, monitor bowel sounds.
- Monitor urine output.
- Oral care
- Safety – inc risk for falls in elderly.
- Inc FFF (fluid, fiber, fitness)
- Wear sunglasses in bright light due to pupil dilation
Parkinson’s Disease
Neurological disorder that results in progressive loss of coordination and movement.
Parkinson’s Disease
Etiology/Pathophysiology:
- Loss of dopaminergic neurons in the brain.
- Dec dopamine–>inc ACH (acetylcholine) levels–>abnormal signaling between neurons.
- Imbalance–> signs and symptoms such as impaired mobility, resting tremor, bradykinesia, rigidity, and postural instability.
Parkinson’s Disease
Drug treatment goals:
- Replace dopamine.
- Mimic dopamine’s action
- Antagonize excitatory effects of cholinergic neurons.
Anti-Parkinson’s Drug: Carbidopa/Levodopa
Dopamine replacement
Anti-Parkinson’s Drug: Carbidopa/Levodopa
Action:
Levodopa is a dopamine precursor. Dopamine itself cannot get across the blood-brain barrier. Levodopa can, with a little bit of help from carbidopa. Carbidopa prevents peripheral breakdown of levodopa so it can reach the brain.
Anti-Parkinson’s Drug: Carbidopa/Levodopa
Benefits of Carbidopa/Levodopa:
Less rigidity/hypokinesia
Anti-Parkinson’s Drug: Carbidopa/Levodopa
ADRs:
Due to inc dopamine activity in the brain
o Behavioral effects: confusion, sleep disturbances, vivid dreams, anxiety, schizophrenia-type symptoms
o Dyskinesia (involuntary movement)
o Peripheral effects: postural hypotension
o Mydriasis (dilation of the pupil)–>precipitate an attack of glaucoma.
o Alteration of smell and taste
o Altered labs: inc BUN and LFTs
o Brownish discoloration of body fluids
“Wearing-off effect”-as the disease advances, more neurons are lost, and the dose of the drug (carbidopa/levodopa) “wears off” before the next one is due.
Anti-Parkinson’s Drug: Carbidopa/Levodopa
Interactions, Contraindications:
- Interactions: MAOIs
- Contraindications:
o Psychosis
o Glaucoma
o Melanoma
Anti-Parkinson’s Drug: Carbidopa/Levodopa
Administration:
o With or without food
o inc protein, food may dec absorption
Anti-Parkinson’s Drug: Carbidopa/Levodopa
Nursing Actions:
o Monitor vital signs: may cause orthostatic hypotension.
o Drug is taken with food, take with low protein.
o Do not abruptly discontinue (may–>NMS (neuroleptic malignant syndrome)
Anti-Parkinson’s Drug:
Tolcapone
COMT- inhibitor, used in combination with carbidopa/levodopa.
Anti-Parkinson’s Drug:
Tolcapone
Action:
Inhibits COMT so that additional loss of levodopa is prevented and more enters the brain.
Anti-Parkinson’s Drug:
Tolcapone
Benefits:
o Prolongs the time dopamine is available to the brain.
o Lower doses of carbidopa/levodopa
o Dec wearing off effect.
Anti-Parkinson’s Drug:
Tolcapone
ADRs:
serious liver toxicity (entacapone preferred)
Alzheimer’s Dementia
Most common form, diagnosis of exclusion. Pt slowly loses orientation to time, place, then person.
Alzheimer’s Dementia
Etiology/Pathophysiology:
- Cortical atrophy- brain “shrinks.”
- Abnormal proteins in the brain called “plaques and tangles” accumulate in the brain and
destroy neurons–>dec ACH (acetylcholine)–>loss of memory and learning.
Alzheimer’s Dementia
Management:
o Palliative, aimed at reducing symptoms.
o Drugs improve symptoms but have no effect on the cause of disease.
o Approximate time between diagnosis of death is 8 yrs.
Alzheimer’s Dementia
Drug treatment:
Rivastigmine- acetylcholinesterase inhibitor
Alzheimer’s Dementia:
Rivastigmine
Action:
Inhibits enzymes from breaking down ACH (acetylcholine)–>inc levels/duration of action of ACH
Alzheimer’s Dementia:
Rivastigmine
SEs:
o Nausea and vomiting
o Diarrhea
o Insomnia
Alzheimer’s Dementia:
Rivastigmine
ADRs:
o Bradycardia
o Hypotension
o Syncope (a loss of consciousness for a short period of time)
o Lack of appetite
o Weight loss
Alzheimer’s Dementia:
Rivastigmine
Contraindications:
o Cardiac conduction abnormality
o Liver/renal disease
Alzheimer’s Dementia:
Rivastigmine
Administration:
o Transdermal patch or capsule BID
o Take with food.
Alzheimer’s Dementia:
Rivastigmine
Interactions:
o NSAIDs
o Other drugs that cause bradycardia/hypotension
o TCAs
Alzheimer’s Dementia:
Rivastigmine
Patient Teaching:
DON’T SMOKE – smoking inc clearance of drug–>dec amount of drug in the body.
Myasthenia Gravis
A disorder at the neuromuscular junction. It affects the nerve’s ability to communicate with muscles.
Myasthenia Gravis
Etiology/Patho:
Caused by antibodies that block ACH (acetylcholine) at receptors–>absence of muscle contraction–>weakness.
Myasthenia Gravis
Signs & Symptoms:
Systemic muscle weakness
o Primarily facial muscle weakness–>difficulty with eye-opening, talking, chewing.
o Also, proximal limb muscles
o Sever cases: may affect respiratory muscles- EMERGENCY!
Myasthenia Gravis
Drug treatment:
Pyridostigmine: acetylcholinesterase inhibitor
Myasthenia Gravis:
Pyridostigmine
Benefits:
- inc ACH (acetylcholine)levels in the synapse
- inc levels of ACH “outcompete” the antibodies.
- Improves muscle weakness (inc muscle strength).
Myasthenia Gravis:
Pyridostigmine
Caution:
o Hyperthyroidism
o Renal impairment
Myasthenia Gravis:
Pyridostigmine
Contraindications:
Intestinal/urinary obstruction