NEET MDS Lessons
Pharmacology
Nystatin
Candida spp. are sensitive to nystatin.
Uses: Cutaneous, vaginal, mucosal and esophageal infections.
Candida infections can be treated with nystatin.
Cryptococcus is also sensitive to nystatin.
Nystatin is often used as prophylaxis in patients who are at risk for fungal infections, such as AIDS patients with a low CD4+ count and patients receiving chemotherapy.
MOA
nystatin binds to ergosterol, the main component of the fungal cell membrane. When present in sufficient concentrations, it forms a pore in the membrane that leads to K+ leakage and death of the fungus.
Examples of calculations of doses of vasoconstrictors
Ratio concentrations represent grams per millilitre
1:100,000 = 0.01 mg/mL or 10 µg/mL
1:200,000 = 0.005 mg/mL or 5 µg/mL
1:50,000 = 0.02 mg/mL or 20 µg/mL
1 cartridge of epinephrine 1:200,000 = 9 µg
1 cartridge of epinephrine 1:100,000 = 18 µg
1 cartridge of epinephrine 1:50,000 = 36 µg
1 cartridge of levonordefrin 1:20,000 = 90 µg
Class III Potassium Channel Blockers
Prolong effective refractory period by prolonging Action Potential
Treatment: ventricular tachycardia and fibrillation, conversion of atrial fibrillation or flutter to sinus rhythm, maintenance of sinus rhythm
– Amiodarone (Cordarone) – maintenance of sinus rhythm
– Bretylium (Bretylol)
– Ibutilide (Corvert)
– Dofetilide (Tykosyn)
– Sotalol (Betapace)
Amiodarone
- Has characteristics of sodium channel blockers, beta blockers, and calcium channel blockers
- Has vasodilating effects and decreases systemic vascular resistance
- Prolongs conduction in all cardiac tissue
- Decreases heart rate
- Decreases contractility of the left ventricles
Class III - Adverse Effects
- GI- Nausea vomiting and GI distress
- CNS- Weakness and dizziness
- CV-Hypotension, CHF, and arrhythmias are common.
- Amiodarone associated with potentially fatal Hepatic toxicity, ocular abnormalities and serious cardiac arrhythmias.
Drug – Drug Interactions
These drugs can cause serious toxic effects if combined with digoxin or quinidine.
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 |
- |
Heparin:
- Inhibits blood coagulation by forming complexes with an α2-globulin (Antithrombin III) and each of the activated proteases of the coagulation cascade (Kallikrein, XIIa, XIa, IXa, Xa, and Thrombin). After formation of the heparin-ATIII-coagulation factor, heparin is released and becomes available again to bind to free ATIII.
- Blocks conversion of Prothrombin to Thrombin and thus inhibits the synthesis of Fibrin from Fibrinogen.
- Inhibits platelet function and increases vascular permeability. May induce moderate to severe thrombocytopenia.
- Is prescribed on a “unit” basis.
- Heparin is not effective after oral administration and is generally administered by intravenous or subcutaneous injection. Intramuscular injections should be avoided.
- Heparin does not cross the placenta and does not pass into the maternal milk.
- is contraindicated in any situation where active bleeding must be avoided.
Ulcerative lesions, intracranial hemorrhage, etc.
Overdosage:
• Simple withdrawal.
• Protamine sulfate: Highly basic peptide that binds heparin and thus neutralizes its effects.
Pramlintide -Amylin mimetics
Mechanism
synthetic analogue of human amylin that acts in conjunction with insulin
↓ release of glucagon
delays gastric emptying
Clinical use
type I and II DM
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.