Drug/Application Clinical Mechanism Drug Interactions/ Comments Uses Side Effects Cholinergic Agonists Direct Acting Cause vasodilation by stimulating muscarinic type receptors on arteries Increase Low viscosity saliva CONTRAINDICTIONS: Bradycardia, hypotension, asthma, and peptic ulcer All acetylcholine receptors are nicotinic except parasympathetic end organ receptors which are muscarinic 1 st adrenergic receptor is nicotinic Acetylcholine Eye surgery - topical Coronary angiography - Coronary vasodilatation Nicotinic and Muscurinic agonist Broken down by AchE - Brief duration of action No CNS NT as sympathetic ganglia, pre and post- parasympathetic ganglia, adrenal medulla, and NMJ Carbachol Nicotinic and Muscarinic agonist NOT broken down by AchE No CNS Bethanechol Used to stimulate intestine and bladder - increase contraction and tone Muscarinic agonist Long duration of action NOT broken down by AchE No CNS Decrease HR , decrease pupil diameter, increased secretions , bronchospasms , and increase GI and urinary function In high does - causes vasodilatation and decreased BP due to activation of M 3 receptors that release NO Pilocarpine Glaucoma management - Muscarinic agonist 2 - 3 hr duration of Cholinergic crisis - salvation, 1
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Drug/Application Clinical Mechanism Drug Interactions/ CommentsUses Side Effects
Cholinergic Agonists Direct Acting Cause vasodilation by stimulating muscarinic type receptors on arteries
Increase Low viscosity saliva
CONTRAINDICTIONS: Bradycardia, hypotension, asthma, and peptic ulcer
All acetylcholine receptors are nicotinic except parasympathetic end organ receptors which are muscarinic
1st adrenergic receptor is nicotinic
Acetylcholine Eye surgery - topical Coronary angiography -
Coronary vasodilatation
Nicotinic and Muscurinic agonist
Broken down by AchE - Brief duration of action
No CNS
NT as sympathetic ganglia, pre and post- parasympathetic ganglia, adrenal medulla, and NMJ
Carbachol Nicotinic and Muscarinic agonist
NOT broken down by AchE No CNS
Bethanechol Used to stimulate intestine and bladder - increase contraction and tone
Muscarinic agonist Long duration of action NOT broken down by AchE No CNS
Decrease HR , decrease pupil diameter, increased secretions, bronchospasms, and increase GI and urinary function
In high does - causes vasodilatation and decreased BP due to activation of M3 receptors that release NO
Pilocarpine Glaucoma management - topical
Dry mouth - oral
Muscarinic agonist 2 - 3 hr duration of action NOT broken down by AchE CNS
Sulfa drug allergy, hypercalciuria, calcium kidney stones
K+ Wasting (does not require supplement)
Spironlactone Refractory edema associated with secondary hyperaldosteronism
HTN and edema Primary
hyperaldosteronism Co-administered with loop
diuretics and thiazides
Aldosterone receptor antagonist Late distal and collecting ducts
Hyperkalemia K sparing
Triamterene Used with loop diuretics and thiazides
Inhibit Na channels Late distal and collecting ducts
Hyperkalemia K sparing
B agonist Dobutamine Stimulate heart in
cardiogenic shock Short term - cardiac
decomensation
1 Agonist
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Abuterol (metaproterenol) Dilate bronchial airways - used to manage asthma, COPD
2 Agonist Given orally - decrease BP and increase HR
Given via inhalation - jitters and tremors
Drug/Application Clinical Mechanism Drug Interactions/ CommentsUses Side Effects
Isoproterenol Mild or transient episodes of heart block
For cardiac arrest until cardioversion can be performed
Bronchodilator (minimum)
1 2 Agonist Tachycardia
-Blockers (Sympatholytic drugs)
HTN Cardiac arrhythmias (AF -
after cardiac inversion) Angina
Chronic use (months) - Increased ejection fraction, contractility, and improvement in systolic performance with decrease in systolic and diastolic volumes and left ventricular mass
DO NOT use with asthma patients, COPD, unstable CHF, Occlusive peripheral vascular disease
Can cause AV Heart block High Doses With Ca+ blockers With Digoxin
Gradual removal due to upregulation of receptors
In persons with mild, moderate, or severe heart failure - reduces morbidity (40%) and mortality (30%)
Use with ACE inhibitor when treating CHF
Propanolol Management of Hypertension Angina Cardiac arrhythmias Migraine headaches Anxiety
1 2 –Antagonist (non-selective) - Decrease cardiac work and CO
Noon-enzymatic protein Activates the fibrinolytic system Forms Plasminogen-
streptokinase activating complex to convert plasminogen to plasmin. Plasmin break fibrin.
Risk of bleeding CONTRAINDICTIONS: hx
of peptic ulcers, IDDM, internal bleeding, CVA, recent surgery or trauma, brain tumor, aneurysm, bleeding diathesis, age over 70, or uncontrolled severe HNT
Prolongation of PT or APTT indicates lytic state
Follow by use of heparin
t-PA Thrombolytic drug $2000
Converts plasminogen to plasmin. Plasmin break fibrin
t-PA selectively binds to bound fibrin-plasminogen
Releases plasmin – systemic fibrinolytic
Not used to treat: DVT or PE
Prolongation of PT or APTT indicates lytic state
Must be followed up with Heparin
Anticoagulants Heparin - Injection Hemodialysis
Cardiopulmonary bypass DVT (IV) and DVT
prevention (subcu) PE and PE prevention
SEE BELOW Hemorrhage Thrombocyopenia Arterial thromboembolism Hypersensitivity Osteoporosis
Monitored by APTT of >50 sec and PTT - heparin plasma [0.2 - 0.4 U/ml)
IV Only Does NOT cross
placenta Unfractionated (UFH) Initial treatment for
DVT PE
Enhances antithrombin III and IIa, which deactivates Thrombin and Factors Xa and Iia
Short half-life (0.5 - 1 hour)
Heparin induced thrombocytopenia (HIT) - Activates antiplatelet Ab (IgG) that activate platelets via their Fc Iia receptors
OK for breast feeding or pregnancy
Widespread binding - unpredictable
Low molecular weight(LMWH)
Subcutaneous b.i.d DVT - prophylaxis Venous
thromboembolism
Enhances antithrombin IIIa only , which deactivates factor Xa more than Iia
Long half-life (4 - 6 hours) Eliminated in kidney
Spinal or epidural hematoma
Less likely: HIT, but if already HIT DON’T use
Predictable ↑ ½ life, ↑
bioavailability
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Drug/Application Clinical Mechanism Drug Interactions/ CommentsUses Side Effects
Warfarin - Oral DVT - begin during heparin treatment
PE - begin during heparin treatment
Atrial fibrillation Acute MI Valvular heart disease Recurrent systemic
embolism
Interferes with vit K therefore reducing factors VII, IX, X, and Thrombin
Long duration (35-45 hrs) Metabolized by cytochrome
P-450
Hemorrage Teratogenic - CROSSES
placenta CONTRAINDICTIONS:
Rifampin - increases metabolism; Nafcillin - loss of activity; alcohol - chronic: decrease activity, acute: increased; Metronidazole, trimethoprim, and sulfamethoxazole - decreases metabolism of S isomer; Amiodarone - decreases metabolism of S and R isomer; Aspirin - risk of bleeding
½ life 35-45 hrs Therapeutic delay (3-4
days) PT or INR 2-3 Treat OD with Vit K
Protamine Sulfate Reversal of Heparin's (LMWH) actions
Basic protein that binds the acidic heparin to for a stable compound
Partially reveses the anti-factor Xa activity
Vitamin K Reverse warfarin's anticoagulant effects
In the process of carboxylation of Factors Vii, IX, X and thrombin, vit. K is oxidized to am epoxide - a required step
Pulmonary All 2 agonists Palpitations 2 dilation
which leads to barrow receptors increasing HR
Tremor – caused by stimulation of 2 in skeletal muscles - Na-K ATPase causing hypokalemia
For abortion - follow with prostaglandin after 48 hours
Hydrocortisone 1 or 2 adrenal insufficiency
Congenital adrenal hyperplasia
Cortisol - increase gluconeogenesis, potentiation of effects of lipolytic agents, improve stress response
Cushing like symptoms Oral or parenterally
Prednisone Treat diseases with strong inflammatory reactions
Glucocorticoids - potent glucorticoid effects
Longish duration of action Very potent
HTN Hypokalemia Edema
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Drug/Application Clinical Mechanism Drug Interactions/ CommentsUses Side Effects
Dexamethasone Decrease cerebral edema Diagnostic agent to
suppress endogenous secretion of mineralcorticoid activity
Potent glucocorticoid Long duration of action
See above
9-fluorohydrocortisone Aldosterone replacement Very potent mineralcorticoid - adrenocorticoid analog
125 times more active than hydrocortisone
Metyrapone Diagnostic test of pituitary, eliciting a compensatory ACTH release, which is reflected in increased 11-deoxycortisol in plasma and urine
Inhibits 11-beta-hydroxylation in adrenocortical cells
Decreases hydrocortisone production
Cholestyramine an Colestipol Decrease plasma LPL High molecular weight Ion- exchange resins that bind bile acids in intestine
Forces the formation of new bile acids from cholesterol
Nausea, vomiting, constipation, and steatorrhea
Reduced absorption of compounds that depend on bile acids - fat soluble vit, thyroid hormone, iron, digitalis, thiazide diuretics, tetracycline, and anticoagulants