NEET MDS Lessons
Pharmacology
Aquaretics
An aquaretic is a class of drug that is used to promote aquaresis, the excretion of water without electrolyte loss.
Lithium, demeclocycline
Mechanism of Action
1. Block ADH action on distal tubule and collecting duct. Blocking ADH decreases H2O permeability. H2O is not recovered (distal tubule) using osmotic draw of counter-current multiplier so aquaretics reduce water reabsorption (tubule to blood stream).
2. Net effect is an increase in free water clearance
Operator position
For the right-handed operator, the 8 and 10 o’clock position and for left-handed operators, the corresponding 2 and 4 o’clock position almost always allows for optimal visualization of the injection field.
Antiplatelet Drugs:
Whereas the anticoagulant drugs such as Warfarin and Heparin suppress the synthesis or activity of the clotting factors and are used to control venous thromboembolic disorders, the antithrombotic drugs suppress platelet function and are used primarily for arterial thrombotic disease. Platelet plugs form the bulk of arterial thrombi.
Acetylsalicylic acid (Aspirin)
• Inhibits release of ADP by platelets and their aggregation by acetylating the enzymes (cyclooxygenases or COX) of the platelet that synthesize the precursors of Thromboxane A2 that is a labile inducer of platelet aggregation and a potent vasoconstrictor.
• Low dose (160-320 mg) may be more effective in inhibiting Thromboxane A2 than PGI2 which has the opposite effect and is synthesized by the endothelium.
• The effect of aspirin is irreversible.
Properties of inhalation anesthetics
The lower the solubility, the faster the onset and the faster the recoverability.
All general anesthetics:
1. inhibit the brain from responding to sensory stimulation.
2. block the sensory impulses from being recorded in memory.
3. prevent the sensory impulses from evoking “affect”.
Most general anesthetic agents act in part by interacting with the neuronal membranes to affect ion channels and membrane excitability.
· If the concentration given is too low:
1. Movement may occur
2. Reflex activity present (laryngeal spasm)
3. Hypertension
4. Awareness
Premedication of analgesic drugs and muscle relaxants are designed to minimise these effects
· If the concentration given is too high:
1. Myocardial depression
2. Respiratory depression
3. Delayed recovery
Second Generation Cephalosporins
Prototype drug is CEFUROXIME (IV) and CEFUROXIME AXETIL (oral). CEFOXITIN has good activity vs. anaerobes.
1. Expanded activity against gram negative bacilli. Still have excellent activity against gram positive (Staph. and Strep.) bacteria.
Activity for Gram negative bacteria
Neisseria sp. (some gonococci resistant)
H. influenzae (including some ampicillin-resistant strains)
Moraxella catarrhalis (some resistance esp. to cefaclor)
E. coli
Proteus mirabilis
Indole + Proteus (some strains resistant)
Morganella morganii (some strains resistant)
Klebsiella pneumoniae
Serratia sp. (many strains resistant)
2. Anaerobic infections - CEFOXITIN & CEFOTETAN only
Moderate activity against Bacteroides fragilis group.
Good activity for other Bacteroides sp., Peptostreptococcus, Fusobacterium, Clostridium sp
Uses
1. Community-acquired pneumonia - Cefuroxime is widely used for empiric therapy. Has activity vs. many ampicillin-resistant H. influenzae strains.
2. Skin and soft tissue infection
3. Urinary tract infections
4. Upper respiratory tract infections (otitis media, sinusitis). Some resistance to H.influenzae to cefaclor (20-30%).
5. Mixed aerobic & anaerobic infections - Cefoxitin & Cefotetan. Resistance to B.fragilis is increasing.
6. Surgical prophylaxis - Cefoxitin or cefotetan are widely used in cases where mixed aerobic & anaerobic infections may occur, esp. intra-abdominal, colorectal, and gynecologic operations. For cardiovascular and orthopedic procedures, cefuroxime and others may be used, but cefazolin is cheaper and appears to work well.
Adverse effects
Nitrates
– Headache, hypotension, dizziness, lightheadedness, tachycardia, palpitations
Beta-adrenergic blocking agents
– hypotension, bradycardia, bronchospasm, congestive heart failure
Calcium channel blockers
– hypotension, dizziness, lightheadedness, weakness, peripheral edema, headache, congestive heart failure, pulmonary edema, nausea, and constipation
Drugs that increase effects of Antianginal drugs
• Antihypertensive
• Diuretics
• Phenothiazine antipsychotic agents
• Cimetidine
• Digoxin
Drugs that decrease effects of Antianginal
• Adrenergic drugs - epinephrine
• Anticholinergic
• Calcium salts
• Phenobarbital, Phenytoin
Adjunctive Antianginal Drugs
In addition to antianginal drugs, several other drugs may be used to control risk factors and prevent progression of myocardial ischemia to myocardial infarction and sudden cardiac death.
These may include:
• Aspirin. This drug has become the standard of care because of its antiplatelet (ie, antithrombotic) effects. Recommended doses vary from 81 mg daily to 325 mg daily or every other day; apparently all doses are beneficial in reducing the possibility of myocardial reinfarction, stroke, and death. Clopidogrel 75 mg/day,
Is an acceptable alternative for individuals with aspirin allergy.
• Antilipemics. These drugs may be needed by clients who are unable to lower serum cholesterol levels sufficiently with a low-fat diet. Lovastatin or a related “statin” is often used. The goal is usually to reduce the serum cholesterol level below 200 mg/dL and lowdensitylipoprotein cholesterol to below
130 mg/dL.
• Antihypertensives. These drugs may be needed for clients with hypertension. Because beta blockers and calcium channel blockers are used to manage hypertension as well as angina, one of these drugs may be effective for both disorders.
Diclofenac
Short half life (1‐2 hrs), high 1stpass metab., accumulates in synovial fluid after oral admn., reduce inflammation, such as in arthritis or acute injury
Mechanism of action
inhibition of prostaglandin synthesis by inhibition of cyclooxygenase (COX). There is some evidence that diclofenac inhibits the lipooxygenase pathways, thus reducing formation of the
leukotrienes (also pro-inflammatory autacoids). There is also speculation that diclofenac may inhibit phospholipase A2 as part of its mechanism of action. These additional actions may explain the high potency of diclofenac - it is the most potent NSAID on a molar basis.
Inhibition of COX also decreases prostaglandins in the epithelium of the stomach, making it more sensitive to corrosion by gastric acid. This is also the main side effect of diclofenac and other drugs that are not selective for the COX2-isoenzyme.