PATIENT PROFILE & PATIENT COUNSELING

ADRENALINE
 SYMPATHETIC NERVOUS SYSTEM

Fight or flight response results in:

1. Increased BP
2. Increased blood flow to brain, heart and skeletal muscles
3. Increased muscle glycogen for energy
4. Increased rate of coagulation
5. Pupil dilation
ADRENERGIC RECEPTORS
• Alpha—A1 and A2
• Beta—B1, B2, B3
• Dopamine—subsets D1-5
REVIEW OF FUNCTIONS OF SYMPATHETIC NERVOUS SYSTEM RECEPTORS

• Alpha 1—smooth muscle contraction

• Alpha 2-negative feedback causes less
norepinephrine to be released so BP is reduced
• Beta 1—increased heart rate
• Beta 2—bronchodilation
• Beta 3—actual site for lipolysis
 MECHANISMS OF ACTION AND EFFECTS OF ADRENERGIC DRUGS …1

• Direct adrenergic drug action

• Affects postsynaptic alpha 1 and beta
receptors on target effector organs
• Examples: epinephrine, Isuprel,
norepinephrine, phenylephrine
 MECHANISMS OF ACTION

2. Indirect adrenergic drug action occurs by stimulation of

postsynaptic alpha 1, beta 1 and beta 2 receptors.Cause
release of norepinephrine into the synapse of nerve endings or
prevent reuptake of norepinephrine.
• Examples include cocaine and TCAs
• 3. mixed action. Combination of direct and indirect receptor
stimulation
• Examples are ephedrine and pseudoephedrine
 ADRENALINE
 Secreted from Adrenal Adrenal Medulla (Adrenal Gland).
 Sympathomimetic drug
 What is Adrenaline (C9H13NO3) ?

• Catecholamine
– belongs to the family of biogenic amines
• A hormone and a neurotransmitter
• Enzymes responsible for fast degradation of
Adrenaline
1. Catecholamine-O-methyltransferase
(COMT)

2. Monoaminoxidase (MAO)
 Adrenaline as an Internal Drug

• Hyperarousal
• Increased blood flow
• Heightened pulse rate
• Increased physical
performance
 Brain During Stress Subcortical
Fight or Flight Areas
• Subcortical Fight or Flight areas includes thalamus, hippocampus,
brainstem, and hypothalamus
• Mobilize body for action
• Bypass frontal executive functioning and trigger stress response
 ADRENALINE
ADMINISTRATION
 S/C and I/M
 Orally doesn’t absorbed
 NOTE: If given I/V it causes hypertensive crises and causes cerebral
hemorrhages.
METABOLISES
 Metabolized in liver by the process of conjugation and sulfation.
 Metabolized by MAO and COMT.
 Monoamine catecholeamine transferase
 Catechol-O-methyl transferase
 ADRENALINE
EXCRETION
 Excreted as Vinyl Mandelic Acid (VMA).
MECHANISM
 Acts on adrenergic receptor (α and β), coupled by G-Protein
Coupled receptor.
INDICATIONS
 Anaphylactic shock
 Cardiac arrest
 Status asthmaticus (severe asthma)
 Epitaxis (bleeding from nose)
 Along with local anesthetic, it incresesea the duration of
action of local anesthetic.
 ADRENALINE
CONTRAINDICATIONS
 Hypertensive patients
 Ischemic heart diseases (because adrenaline will increase
myocontractility and heart rate and oxygen demand which
may lead to worsen the condition)
 Anxiety (because it result in heart diseases)
 Hyperthyrodism (because it stimulate the sympathetic
nervous system, adrenaline will further increase it which will
cause harm to organ).