Drug Classes Flashcards
Local Anaesthetics
- MOA
- Indications
- Side Effects
Penetrate into interior of nerve cell to plug Na channel. Use dependent (open and inactive). More effective in unmyelinated cells. Lipid soluble and basic increases rate of action. Sometimes given with vasoconstrictor to localise effects and prolong.
Surgical procedures, topical/nerve block etc.
CNS (dose-dependent): shivering, tongue numbness/metalic taste, convulsions, resp depression
CVS: cardiac depression, vasodilation, hypotension
NSAIDs
- MOA
- Side Effects/Contraindications
Arachidonic Acid is converted by COX enzymes into prostaglandins, producing leukotrienes as part of the pathway. COX-1 involved in platelets and gastric cell protection. COX-2 prostaglandins sensitize and amplify pain by opening more Na channels, cause vasodilation. They are anti-inflammatory, pyretic and analgesic.
COX-1 gastric disturbances
CVS hypertension due to vasoconstriction in kidneys and sodium retention
DMARDs
- Indications
- Side Effects/Contraindications
RA or Gout
Specific to drug, immunosuppressant
Opioids
- MOA
- Indications
- Side Effects
Opioids active the mu receptor to relieve pain. mu receptor hyperpolarise the cell through activating K channels and inhibiting Ca channels. Target dorsal horn of spine and periaqueductal grey in brain. Target slow dull pain. Effects include euphoria, resp depression, suppression of cough, GIT effects.
Long, difficult to endure pain. Avoided if possible
Extension of therapeutic effects: GIT, sedation, resp depression, bronchconstriction, hypotension.
SAIDs
- MOA
- Indications
- Side Effects
Doses above normal levels have anti-inflammatory effects. Inhibition of WBC at site, suppression of transcription of inflam mediators.
Addison’s, inflam conditions regardless of cause, RA, allergic reactions
Diabetes (hyperglycaemia), growth suppresion, osteoporosis, hypertension, Cushing’s syndrome
ANS drugs
- MOA
- Side Effects
Blocks stuff. AD: Alpha-1 promotes vasoconstriction, relaxed GIT mm, dilate pupil. Alpha-2 on presynaptic nerve. Beta-1 increase force and rate of heart, increase renin. Beta-2 dilate lungs, vascular mm.
Organophosphate poisoning, too much ACh. Atropine to treat muscarinic effects.
ACE inhibitors
- MOA
- Indications
- Side Effects
- Contraindications
Renin -> angiotensin I -> angiotensin II-> vasocontriction and aldosterone secretion (salt retention). Blocks this which vasodilates and rids water
Hypertension, heart failure
Hypotension, hyperkalaemia, dry cough from bradykinin
Renal failure and pregnancy, K sparing diuretics
Angiotensin Receptor Blocker
- MOA
- Indications
Blocks angiotensin receptors.
When coughing is too much for ACE inhibitors
Beta Blocker
- MOA
- Indications
- Side Effects
- Contraindications
Blocking beta-1 to decrease SNS of heart, decreasing CO, HR and TPR. Beta-2 acts to dilate bronchi, relax vascular mm.
Hypertension, angina, arrhythmias, stable heart failure
Bronchoconstriction, rebound hypertension/angina, exercise intolerance, sleep problems.
Asthma
Calcium Channel Blocker
- MOA
- Indications
- Side Effects
- Contraindications
Inhibit L-type voltage Ca channels in heart (no reflex tachycardia) and vasculature (drop BP, reflex tachycardia).
Angina, hypertension, tachyarrhythmias
Cardiac depression, oedema, dizziness, constipation/nausea
Heart failure, with beta blockers
Diuretics
- MOA
- Indications
- Side Effects
Prevent sodium reabsorption, less water retention. Less blood volume, oedema and stress on heart.
Congestive heart failure, hypertension
Hyperkalaemia
Positive Inotropes
- MOA
- Indications
- Side Effects
Inhibit Na/K ATPase, increase Ca and contractibility. Slows AV node conduction.
Class I anti-arrhythmic
Can cause arrhythimias, GIT, vagal centers, hypokalaemia
Nitrates
- MOA
- Indications
- Contraindications
Converted to NO, vasodilation, reduction of pre and afterload. Reduce ventricular wall tension and oxygen demand.
??
Viagra
Adenosine
- MOA
- Indications
- Side Effects
Hyperpolarises conduction tissue and slows pacemaker activity through alpha-1 receptors.
??
Bronchospasms in asthmatics
Lipid lowering drugs Statins -MOA -Indications Fibrates -MOA -Indications Bile acid binding resins Nicotinic acid
Angina, hypertension, tachyarrhythimias
Statins inhibit HMG CoA reductase, inhibiting cholesterol synthesis. Promotes LDL receptors and HDL.
Hypercholesterolaemia
Fibrates stimulate lipoprotein lipase and break down TAG, increase LDL receptors and HDL.
Hypertriglyceridemia
Bile acid binding resins prevent reabsorption of cholesterol , requiring more bile acid to be made from cholesterol.
Nicotinic acid lowers LDL and TAG, increase HDL.
