9/10/26 quiz

wheres the location of alpha 1 receptors - 7

blood vessels, bladder sphincter, penis, uterus, Pupillary muscles of the iris, GI smooth muscle (with beta2), Liver (with beta2)

response when Alpha1 Blood vessels activates

Vasoconstriction

Bladder sphincter Alpha1 response

Constriction

Alpha1 Penis response

Ejaculation`

Uterus alpha 1 response

Contraction

Pupillary muscles of the iris alpha 1 repsonse

Mydriasis (pupil dilation)

GI smooth muscle (with beta2) alpha 1 response

Decreased motility (relaxation)

Liver (with beta2) alpha 1 response

Glycogenolysis

Alpha2 location

Presynaptic nerve terminals

Alpha2 Presynaptic nerve terminals response

Inhibits further norepinephrine release (feedback "brake" on SNS) — reverses/limits sympathetic activity

Beta1 locations

Cardiac muscle, SA node / AV node, Kidney

Beta1 Cardiac muscle response

Increased contractility (positive inotropic

SA node / AV node Beta1 response

Increased heart rate (positive chronotropic); increased AV conduction (positive dromotropic)

Kidney beta1 repsonse

Increased renin secretion

Beta2 locations

Bronchial smooth muscle, Blood vessels, Uterus, Liver (with alpha1)

Bronchial smooth muscle Beta2 response

Dilation (bronchodilation/relaxation)

Beta2 Blood vessels response

Vasodilation

Uterus Beta2 repsonse

Relaxation

Liver (with alpha1) Beta2 response

Glycogenolysis

there's also a dopaminergic receptor — stimulated only by dopamine that does what

that dilates renal, mesenteric, coronary, and cerebral vessels

beta3 receptors on the bladder detrusor muscle, which do what

decrease contraction frequency and increase bladder capacity

Catecholamines definitions

these are a specific chemical family your body makes naturally

Adrenergic drugs mimic

norepinephrine (NE), epinephrine, and dopamine

explain the Mechanisms of Adrenergic Receptor Activation

Adrenergic drugs mimic norepinephrine (NE), epinephrine, and dopamine — the endogenous catecholamines. When released from nerve vesicles into the synaptic cleft, these neurotransmitters (or drugs that act like them) bind to adrenergic receptors on the effector organ and trigger a physiologic response. There are three activation mechanisms:

• Direct-acting — the drug binds directly to the receptor and causes the response (e.g., epinephrine).

• Indirect-acting — the drug causes release of stored catecholamines from nerve vesicles, which then bind to receptors (e.g., amphetamines).

• Mixed-acting — the drug does both: direct receptor binding and stimulates neurotransmitter release (e.g., ephedrine).

• The response is terminated by reuptake of NE back into the nerve (active transport) and by enzymatic breakdown via MAO (inside the nerve ending) and COMT (at the synaptic cleft). Drugs can also be selective (act on one receptor subtype, e.g., phenylephrine on alpha1) or nonselective (act on multiple receptor types, e.g., epinephrine on alpha and beta), and effects can even shift with dose — dopamine, for example, is dopaminergic at low doses, beta1 at moderate doses, and alpha1 at high doses.

• Direct-acting —

• the drug binds directly to the receptor and causes the response (e.g., epinephrine).

• Indirect-acting —

• the drug causes release of stored catecholamines from nerve vesicles, which then bind to receptors (e.g., amphetamines).

Alpha1 receptors Located

• 
  

Located on the effector organ itself (postsynaptic) — on blood vessels, the bladder, the uterus, the eye

Alpha1 receptors stimulated

vasoconstriction, pupil dilation, bladder/uterine contraction. TIGHTENING / CONSTRICTING

Alpha2 receptors Located

the nerve ending itself (presynaptic) — not on the target organ, but on the nerve that's releasing the NE

Alpha2 receptors stimulating

• Their job is basically a feedback brake: when NE builds up, alpha2 receptors sense that and tell the nerve to stop releasing more NE

• So stimulating alpha2 actually reduces sympathetic activity — the opposite flavor from alpha1

Beta1 receptors located

on heart

Beta1 receptors stimulated

• 
  

• When stimulated → increased heart rate, increased force of contraction, faster conduction

• 
  

Beta2 receptors mainly

• Located mainly on smooth muscle — bronchioles (lungs), blood vessels, uterus

• 
  

Beta2 receptors whenstimulated

relaxation of that smooth muscle → bronchodilation, vasodilation

3. Nursing Implications for Prototype Drugs

Epinephrine

• High-alert drug; verify concentration carefully (now labeled mg/mL, not ratios, since 2016 — a past source of fatal dosing errors)

• Monitor vital signs, ECG, IV site for infiltration (can cause tissue necrosis — phentolamine is the antidote)

  • Use only clear solutions, infusion pump, continuous cardiac monitoring

Metoprolol nursing implications

• Available as tartrate (immediate-release, dosed BID) and succinate (extended-release, dosed once daily) — these are not interchangeable, and mix-ups on medication reconciliation orders are a documented, high-risk error. Nurses must clarify with the prescriber which salt form is intended.

• IV metoprolol is a high-alert medication requiring close monitoring

• Assess apical pulse for a full minute and blood pressure (supine and standing) before administration; hold and notify the prescriber if HR < 60 bpm or systolic BP < 100 mmHg

• Never discontinue abruptly — taper per prescriber's schedule to avoid rebound hypertension/angina/MI

• Monitor for bradycardia, fatigue, depression, hypotension, edema (early sign of heart failure), and — since it's cardioselective — bronchospasm risk is lower but not zero at higher doses

• Teach the patient to weigh daily, report weight gain (≥2 lb/24 hr or ≥5 lb/week), and avoid abrupt position changes

Phentolamine nursing implications

• Used to treat extravasation of vasopressors (norepinephrine, epinephrine, dopamine) — injected subcutaneously around the site to prevent tissue necrosis

• Monitor IV sites hourly during vasopressor infusions to catch infiltration early

  • Contraindicated in MI/coronary artery disease

Alpha1 agonist therpautic use

Raise BP in shock/hypotension (phenylephrine, midodrine); nasal/ocular decongestion; pupil dilation for eye exams

Alpha1 agonist advese effects

Hypertension, reflex bradycardia, vasoconstriction-related chest pain, headache, restlessness, insomnia

Alpha2 agonist theraputic use

Less clinically prominent as agonist therapy here (discussed more with antihypertensives like clonidine, Ch. 22)

Alpha2 agonist adverse effect

none

Beta1 agonist theraptuic use

Cardiac support in shock/heart failure (dobutamine, dopamine); cardiac arrest (epinephrine)

Beta1 agonist adverse effects

Tachycardia, palpitations, dysrhythmias, chest pain

Beta2 agonist theraputic use

Bronchodilation for asthma/COPD (albuterol); tocolysis

Beta2 agonist adverse effects

Tremors, nervousness, tachycardia (from some beta1 crossover)

Beta3 agonist theraputic use

Overactive bladder (mirabegron)

Beta3 agonist adverse effects

Hypertension, UTI, headache, dizziness

Alpha1 blockade theraputic use

Hypertension, BPH (relaxes bladder neck/prostate smooth muscle), pheochromocytoma-related hypertension, reversing vasopressor extravasation (phentolamine)

Alpha1 blockade adverse reaction

First-dose phenomenon (sudden severe hypotension), orthostatic hypotension, dizziness, headache, reflex tachycardia, nasal congestion, constipation

Beta1 blockade thearputic use

Hypertension, angina, post-MI cardioprotection, heart failure (select agents), dysrhythmias

Beta1 blockade adverse reaction

Bradycardia, decreased contractility, AV block, fatigue, depression, hypotension

Beta2 blockade theraputic use

(Usually an unwanted effect of nonselective agents, not a treatment goal)

Beta2 blockade adverse reaction

Bronchoconstriction, masked hypoglycemia symptoms (except sweating), delayed hypoglycemia recovery, hyperlipidemia

Nonselective alpha+beta blockade (carvedilol, labetalol) thearputic use

Heart failure, severe hypertension/hypertensive emergency

Nonselective alpha+beta blockade (carvedilol, labetalol) adverse reaction

Combination of the above + orthostatic hypotension

All beta blockers carry a —- due to

black box warning against abrupt withdrawal (taper over 1–2 weeks) due to risk of rebound hypertension, angina, or MI. Nonselective beta blockers are contraindicated/cautioned in asthma/COPD (bronchoconstriction) and diabetes (masked hypoglycemia).

Agonist explain

a drug that flips the switch ON. It binds to the receptor and activates it, causing the same effect the body's natural chemical would cause.

• 
  

antagonist explain

a drug that blocks the switch from being flipped. It sits on the receptor but does NOT activate it — instead, it just occupies the spot so the natural chemical (or another drug) can't get in and turn it on.