NEET MDS Lessons
Pharmacology
Antianginal Drugs
Organic Nitrates :
Short acting: Glyceryl trinitrate (Nitroglycerine, GTN), Amyl Nitrate
Long Acting: Isosrbide dinitrate (Short acting by sublingual route), Erythrityl tetranitrate, penta erythrityl tetranitrate
Beta-adrenergic blocking agents : Propanolol, Metoprolol
Calcium channel blockers Verapamil, Nifedipine, Dipyridamole
Mechanism of action
– Decrease myocardial demand
– increase blood supply to the myocardium
Uses of NSAIDs
NSAIDs are usually indicated for the treatment of acute or chronic conditions where pain and inflammation are present. Research continues into their potential for prevention of colorectal cancer, and treatment of other conditions, such as cancer and cardiovascular disease.
NSAIDs are generally indicated for the symptomatic relief of the following conditions.
rheumatoid arthritis, osteoarthritis, inflammatory arthropathies (e.g. ankylosing spondylitis, psoriatic arthritis, Reiter's syndrome), acute gout, dysmenorrhoea, metastatic bone pain ,headache and migraine, postoperative pain, mild-to-moderate pain due to inflammation and tissue injury, pyrexia, renal colic
Aspirin, the only NSAID able to irreversibly inhibit COX-1, is also indicated for inhibition of platelet aggregation; an indication useful in the management of arterial thrombosis and prevention of adverse cardiovascular events.
Balanced Anesthesia
A barbiturate, narcotic analgesic agent, neuromuscular blocking agent, nitrous oxide and one of the more potent inhalation anesthetic.
Thiazide diuretics
Chlorothiazide, Hydrochlorothiazide
Mechanism(s) of Action
1. Block facilitated Na/Cl co-transport in the early distal tubule. This is a relatively minor Na absorption mechanism and the result is modest diuresis
2. Potassium wasting effect
a. Blood volume reduction leads to increased production of aldosterone
b. Increased distal Na load secondary to diuretic effect
c. a + b = increase Na (to blood) for K (to urine) exchange which produces indirect K wasting
3. Increase distal Ca re-absorption (direct effect)
o causes an increase in plasma calcium.This is unimportant NORMALLY but makes thiazides VERY inappropriate choice for hypercalcemic patients.
4. Anti-diuretic effect in nephrogenic diabetes insipidus patients secondary to depletion of Na and Water.
Toxicity
• Electrolyte imbalance (particularly hypokalemia) ,Agranulocytosis , Allergic reactions
• Hyperuricemia , Thrombocytopenia
Dissociation constants
|
Local anesthetic |
pKa |
% of base(RN) at pH 7.4 |
onset of action(min) |
|
Lidocaine |
7.8 |
29 |
2-4 |
|
Bupivacaine |
8.1 |
17 |
5-8 |
|
Mepivacaine |
7.7 |
33 |
2-4 |
|
Prilocaine |
7.9 |
25 |
2-4 |
|
Articaine |
7.8 |
29 |
2-4 |
|
Procaine |
9.1 |
2 |
14-18 |
|
Benzocaine |
3.5 |
100 |
- |
Antihypertensives Drugs
CATEGORIES
I. Diuretics to reduce blood volume
Chlorothiazide (Diuril)
II. Drugs that interfere with the Renin-Angiotensin System
A. Converting enzyme inhibitors Captopril , enalapril, Lisinopril
B. Angiotensin receptor antagonists Saralasin Losartan
III. Decrease peripheral vascular resistance and/or cardiac output
A. Directly acting vasodilators
1. calcium channel blockers Nifedipine , Diltiazem, amlodipine
2. potassium channel activators Minoxidil
3. elevation of cGMP Nitroprusside
4. others Hydralazin e
B. Sympathetic nervous system depressants
1. α-blockers Prazosin, phentolamine, phenoxybenzamine
2. β-blockers Propranolol ,Metoprolol, atenolol
3. norepinephrine synthesis inhibitors Metyrosine
4. norepinephrine storage inhibitors Reserpine
5. transmitter release inhibitors Guanethidine
6. centrally acting: decrease
sympathetic outflow Clonidine , methyldopa
Eicosanoid compounds
Prostaglandines, Leukotriens and Thromboxanes.
They are produced in minute amounts by all cells except RBCs and they act locally at the same site of synthesis.
These agents have many physiological processes as mediators and modulators of inflammatory reactions.