1. sympathatic
1.1. sympaathomimetics
1.1.1. Direct
1.1.1.1. recepotres agonists
1.1.1.1.1. B recepotres agonist
1.1.1.1.2. A receptor agonists
1.1.1.1.3. Dopamin agonist
1.1.1.2. epinephrine
1.1.1.2.1. 1-natural catecholamine neurotransmeitter , 2- synthitic epineohrine is poorly absorbed and does not pass BBB, 3- Admeinistered parenterallu im and sc , hpwever sc is slow duo to local vc, 4-metabp;ozed by MAO(cell cytoplasm) and COMT(synapatic space)
1.1.1.3. N/A
1.1.1.3.1. It activates α (mainly) and β1receptors leading to increase both systolic and diastolic BP with reflex bradycardia. It has little activity on β2-receptors. It is used as VC (by slow i.v. infusion) in acute hypotensive states.
1.1.1.4. Dopamine
1.1.1.4.1. It is a natural catecholamine given by i.v. infusion because it has very short duration of action (2 min). In low doses: stimulates dopamine D1 receptors in renal and mesenteric vascular beds leading to VD and increase renal and hepatic blood flow.
1.1.2. Inderict
1.1.2.1. Amphetamine
1.1.2.1.1. mechanism
1.1.2.1.2. USE
1.1.2.1.3. Its derivatives
1.1.2.2. Cocaine
1.1.2.2.1. Cocaine is an alkaloid derived from the coca plant. It is widely abused as a recreational stimulant. It inhibits neuronal uptake of norepinephrine, dopamine, and serotonin leading to their accumulation in the synaptic spaces with profound CNS stimulation. Adverse effects: similar to amphetamine Manifestations of cocaine toxicity is managed by benzodiazepines.
1.1.3. Mixed
1.1.3.1. Ephedrine
1.1.3.1.1. 2- planed alkaoid
1.1.3.1.2. USE
1.1.3.1.3. Mechanism
1.2. sumpathoplegic
1.2.1. Centraly acting
1.2.1.1. Alpha-merhyldopa
1.2.1.1.1. comoete with dopa for dopa decarbxylase enzyme--> formation of alophamethylenorepinephrine which is an a2 stimulater(central)
1.2.1.1.2. USE
1.2.1.1.3. Advers effects
1.2.1.2. clonidin
1.2.2. Receotores blockers
1.2.2.1. a-adrenergic blockers
1.2.2.1.1. non-selective alpha receptor blocker
1.2.2.1.2. slelctive alpha a(a1)
1.2.2.1.3. selective alpha tow(a2)
1.2.2.2. B blockers
1.2.2.2.1. types
1.2.2.2.2. mechanism and pharmagologicaleffects
1.2.2.2.3. USE
1.2.2.2.4. Advers effects
1.2.2.2.5. Contra indication
1.2.3. Neuron blockers
1.2.3.1. Reserpine
1.2.3.1.1. block vseicular uptake--> accumulation in cytoplasm-->depletion by MAO enzyme(Thats why we dont use them with MAO inhibiters), used to treat mildhypertension ( third line drug)
1.2.3.1.2. Adverse effects
2. parasympatharic
2.1. parasympathomimetics(cholinergic)
2.1.1. Direct
2.1.1.1. muscarinic agonists
2.1.1.1.1. Phrmacolofical effects
2.1.1.1.2. Types
2.1.1.1.3. Advers effects
2.1.1.1.4. contraidications
2.1.1.2. Nicotinic agonists
2.1.1.2.1. Nicotin
2.1.1.2.2. Varenicline
2.1.2. Indirect
2.1.2.1. Mechanism
2.1.2.1.1. inhibit AChE enzyme--> accumulation of ACh
2.1.2.2. Types
2.1.2.2.1. reversible
2.1.2.2.2. Irreversible
2.2. parasympatholetics (anticholinergic)
2.2.1. Muscarinic antagonist
2.2.1.1. mechanism and pharmacological effects
2.2.1.1.1. cvs
2.2.1.1.2. Respiratory
2.2.1.1.3. GIT
2.2.1.1.4. urinary bladder
2.2.1.1.5. sweat galnds
2.2.1.1.6. eye
2.2.1.1.7. CNS
2.2.1.2. USE
2.2.1.2.1. GIT
2.2.1.2.2. CVS
2.2.1.2.3. respiratory
2.2.1.2.4. urinary
2.2.1.2.5. eye
2.2.1.2.6. CNS
2.2.1.2.7. other
2.2.1.3. Adverse effects
2.2.1.3.1. Blurred vision (due to mydriasis and cycloplegia). Rise of IOP (glaucoma). Dryness of all body secretions: dry mouth, dry skin, dry eyes, etc.. Urine retention especially in patients with senile enlarged prostate. Tachycardia. In children: atropine fever (due to blockade of thermoregulatory sweating resulting in hyperthermia) and flush . Children are more sensitive to this effect.
2.2.1.4. contrindication
2.2.1.4.1. Narrow angle glaucoma Obstructive diseases of the GIT (e.g. pyloric stenosis), paralytic ileus, intestinal atony of the elderly, etc. Urine retention due to senile enlarged prostate It should be used with caution in children.
2.2.2. ganglion blocking drugs
2.2.2.1. Trimethaphan and mecamylamine are competitive blockers of ACh at nicotinic receptors at both sympathetic and parasympathetic ganglia. ■ Because of lack of selectivity and numerous adverse effects, they are used rarely in the clinical setting hypertensive emergencie
2.2.3. Neuromuscular blockers
2.2.3.1. Non-depolarizing
2.2.3.1.1. بالكتاب
2.2.3.2. Depolrizing
2.2.3.2.1. بالكتاب