principles of pharmacology and autonomic nervous system

additive interactions

when two drugs are combined and produce a response that is a sum of their individual effects, each drug acting independently without altering the effects of the other.

synergistic interactions

occurs when two drugs together produce an effect substantially greater than either drug alone

agonist effects

drugs that activate receptors and produce a desired response

antagonist effects

block or reduce the effects of other drugs by preventing receptor activation

peak drugs levels measure

the highest plasma concentration and indicate the rate of absorption

collection of peak levels for oral medications

2-3 hours after administration

collection of peak levels for IV medications

30-60 minutes after the infusion is complete

collection of peak drug levels for IM medications

2-4 hours after injection

trough levels measure

the lowest plasma concentration and indicate the rate at which the drug is eliminated

trough levels are collected

just before the next dose of the drug, regardless the route of administration

if peak levels are too low

effective concentration has not been reached

peak levels help determine

if dose needs adjustment to achieve therapeutic effects

measuring trough levels ensures

the drug is being eliminated properly

measuring trough levels prevents

drug accumulation that could lead to toxicity

pharmacokinetics

the process of how drugs move through the body, including absorption, distribution, metabolism, and excretion.

absorption

the movement of drugs into bloodstream after administration

main organs involved in administration

GI tract especially small intestine, skin, lungs, muscle (dependent on route of administration)

patient factors that strongly affect absorption

foood, diarrhea, constipation, poor circulation, route, pain, stress, hunger, and pH

distribution

the movement of the drug from circulation to body tissues

main organs involved in distribution

heart, liver, kidneys, blood vessels, and body tissues

patient factors that strongly affect distribution

perfusion, albumin levels, body fat/water, edema, dehydration, pregnancy, and age

metabolism

the process by which the body chemically changes into a form that can be excreted

main organs involved in metabolism

liver

patient factors that strongly affect metabolism

liver function, age, genetics, other medications, alcohol use, and enzyme induction/inhibition

excretion

elimination of drugs from the body

main organs involved in excretion

mainly kidneys, also bile/GI tract, lungs, sweat

patient factors that strongly affect excretion

kidney function, GFR, urine output, hydration status, age, medications, renal disease

liver dysfunction effects

• elevated drug levels: excess drug accumulation occurs when metabolism is impaired

• prolonged half-life: reduced hepatic metabolism extends how long the drug is in the body

• increased toxicity risk: drug accumulation from lowered clearance can result in toxicity

renal failure effects

• drug accumulation: impaired excretion prevents drugs from being eliminated improperly

• adverse drug reactions: accumulation increases risk of toxicity

• prolonged half life: decreased renal function extends presence in the body

main pharmacokinetic concern with vomiting after oral meds

absorption

nursing considerations when vomiting after oral meds

• timing

• drug characteristics

• underlying cause

• need for antiemetics

• alternative routes

alpha 1 receptors location

smooth muscle

alpha 1 receptors when stimulated

causes vasoconstriction and increases blood pressure.

alpha 1 receptors when blocked

results in vasodilation and decreased blood pressure

alpha 2 receptors location

presynaptic nerve terminals.

alpha 2 receptors when stimulated

inhibits norepinephrine release and decreases sympathetic outflow.

alpha 2 receptors when blocked

results in increased norepinephrine release and increases sympathetic outflow.

beta 1 receptors location

heart

beta 1 receptors when stimulated

increase heart rate and contractility, leading to increased blood pressure

beta 1 receptors when blocked

decrease heart rate and contractility, leading to decreased blood pressure.

beta 2 receptors location

smooth muscles of lungs, GI tract, liver, and uterine muscles

beta 2 receptors when stimulated

• lungs: relaxation os smooth muscle causing bronchodilation

• GI tract: decreased tone and motility

• liver: activation of glycogenesis with increased blood sugar

• uterus: relaxation of uterine muscle, decreased contraction

beta 2 receptors when blocked

causes brohncial constriction

muscarinic receptor location

organs, tissues, and glands innervated by cholinergic nerve endings

muscarinic receptor action

stimulates smooth muscle and slows heart rate

muscarinic when stimulated

• increased gi motility and peristalsis

• bladder contraction promoting urination

• bradycardia

• miosis (pupil contraction)

• bronchial constriction

muscarinic when blocked

• increased HR by blocking vagus stimulation

• mydriasis (pupil dilation)

• decreased salivation and respiratory secretions

• decreased GI motility

nicotinic receptor location

skeletal muscles (neuromuscular) and ganglions

nicotinic receptor actions

affect skeletal muscles

nicotinic receptor when stimulated

• skeletal muscle contraction and increased muscle tone

• increased force of muscular contraction

• enhanced neuromuscular transmission

nicotinic receptors when blocked

skeletal muscle weakness or paralysis

how do alpha 1 agonist relieve nasal congestion

They cause vasoconstriction of nasal blood vessels, reducing blood flow and edema in nasal passages.

pseudoephedrine

an alpha-adrenergic agonist (a decongestant) that works by constricting blood vessels in the nasal passages, leading to reduced swelling and congestion.

cardiovascular effects to monitor with alpha 1 agonist used to treat nasal congestion

• hypertension: alpha 1 stimulation causes vasoconstriction THROUGHOUT body

• tachycardia: pseudoephedrine increases hr because it also stimulates beta 1 receptors in heart

• palpations

• cardiac dysrhythmias

Why can an alpha1 blocker improve symptoms of benign prostatic hyperplasia

Alpha-1 blockers relax the smooth muscle in the prostate and bladder neck, leading to improved urine flow and reduced urinary symptoms associated with benign prostatic hyperplasia (BPH).

Why can an alpha1 blocker improve symptoms of benign prostatic hyperplasia but also cause orthostatic hypotensional?

the same alpha-1 blockers that relax prostatic smooth muscle can also cause vasodilation in blood vessels, leading to decreased vascular resistance. This may result in a drop in blood pressure upon standing, causing orthostatic hypotension.

alpha 1 blocker for bph safety teaching

• orthostatic hypotension prevention

• includes getting up slowly and avoiding sudden position changes.

• avoid with alcohol

fluid management with apla 1 blockers

alpha blockers can cause sodium and water retention with edema, so diuretics are frequently given cocomitantly to manage to decrease fluid accumulation

identify alpha 1 antagonist by name

typically end with the suffix “-zosin”.

Why can a nonselective beta blocker be dangerous for a client with asthma?

can exacerbate asthma by blocking beta-1(heart) and beta-2 (bronchial) adrenergic receptors in the lungs, leading to bronchoconstriction and difficulty breathing.

finding that requires prompt reporting for nonselective beta blockers used for asthma

bronchospam or any signs of respiratory distress:

• wheezing

• dyspnea

• diffuclty breathing

• chest tightness

• use of accessory muscles for breather

• dropped o2 sats

safe alternatives instead of nonselective beta blockers for asthma

cardioselective beta blockers are preferred because they act mainly on beta1 receptors rather than beta2 receptors, making bronchoconstriction less likely to occur.

how to identify a beta blocker drug by its name

typically end with the suffix "-olol," such as metoprolol or atenolol.

what do cholinergic agonist do to the pupils

miosis (constriction of the pupils)

what do cholinergic agonist do to the heart rate

bradycardia

what do cholinergic agonist do to secretions

increase salivation and respiratory secretions

what do cholinergic agonist do to gi motility

increase gastrointestinal motility and peristalsis.

what do cholinergic agonist do to urination

increase urinary frequency and urgency.

what do cholinergic agonist do to muscle tone

increase muscle tone and contractions

what do anticholinergics do to the pupils

mydriasis (dilate)

what do anticholinergics do to heart rate

tachycardia

what do anticholinergics do to secretions

decrease salivations and respiratory secretions

what do anticholinergics do to gi motility

decrease gastrointestinal motility

what do anticholinergics do to urination

decrease urinary frequency and urgency

what do anticholinergics do to muscle tone

decrease rigidity and tremors

what do acetylcholinesterase inhibitors do to pupils

miosis (constriction of pupils)

what do acetylcholinesterase inhibitors do to heart rate

bradycardia

what do acetylcholinesterase inhibitors do to secretions

increase secretions

what do acetylcholinesterase inhibitors do to gi motility

increase gi motility

what do acetylcholinesterase inhibitors do to urination

increase urination

what do acetylcholinesterase inhibitors do to muscle tone

increase muscle tone and force

how to identify a cholinergic drug by its name

typically end with the suffix “-chol”

how to identify an acetylcholinesterase inhibitor drug by its name

typically end with the suffix “-stigmine”

bethanechol promotes urination by

stimulating muscarinic cholinergic receptors in the bladder. this stimulation causesthe bladder to contract and facilitates voiding.

receptors bethanechol targets

muscarinic cholinergic receptors

how metoclopramide affects gastrointestinal motility and gastric emptying.

increases gastrointestinal motility and accelerates gastric emptying by blocking dopamine receptors and enhancing the action of acetylcholine on muscarinic receptors.

A client touches a scopolamine patch and then rubs one eye. Explain why unilateral blurred vision and pupillary dilation may occur and what teaching could prevent it.

its an anticholinergic medication that can cause unilateral blurred vision and pupillary dilation due to its effects on muscarinic receptors in the eye. To prevent this, clients should be advised to avoid touching their eyes after handling the patch.

What causes anticholinergic toxicity?

Overdose or excessive effects of anticholinergic/cholinergic-blocking drugs.

What causes a cholinergic crisis?

Excessive acetylcholine, often from an overdose of acetylcholinesterase inhibitors or other cholinergic drugs.

What happens to the pupils in anticholinergic toxicity?

mydriasis (dilate)

What happens to the pupils in a cholinergic crisis?

miosis (constrict)

What happens to heart rate in anticholinergic toxicity?

tachycardia

What happens to heart rate in a cholinergic crisis?

bradycardia

What happens to oral secretions in anticholinergic toxicity?

they decrease, causing dry mouth

What happens to secretions during a cholinergic crisis?

They increase, including saliva, tears, and bronchial secretions.

What happens to GI motility in anticholinergic toxicity?

It decreases, leading to constipation and reduced gastrointestinal activity.

What happens to GI motility during a cholinergic crisis?

It increases, potentially causing diarrhea and increased bowel sounds.

What happens to urination in anticholinergic toxicity?

It decreases, leading to urinary retention and difficulty in urination.

What happens to urination during a cholinergic crisis?

It increases, causing frequent urination and urgency.

What CNS symptoms can occur with anticholinergic toxicity?

Confusion, agitation, delirium, hallucinations, and possibly coma.