NEET MDS Lessons
Pharmacology
Nalidixic acid:
Nalidixic acid is the basis for quinolone antibiotics. It acts bacteriostatically (that is, it inhibits growth and reproduction) or bactericidally (it kills them) on both Gram positive and Gram negative bacteria, depending on the concentration. It is especially used in treating urinary tract infections, caused for example by Escherichia coli, Proteus, Enterobacter and Klebsiella.
Pharmacology is the study of drugs and the way they interact with living systems. Clinical pharmacology is the study of drugs in humans.
A drug is any chemical that can effect living processes.
Therapeutics: the medical use of drugs.
An ideal drug has several important properties. Three of these properties are of utmost importance: effectiveness, safety and selectivity.
Effectiveness: This is the most important quality that a drug can have. Effectiveness refers to the drug's ability to do what it is supposed to do.
Safety: Although no drug can be totally safe, proper usage can lessen the risks of adverse effects.
Selectivity: A truly selective drug would have no side effects, and would effect only the body process' for which it is designed and given. Therefore, there is no such thing as a selective drug.
Pharmacokinetics: The way the body deals with a drug. Pharmacokinetics is concerned with the processes of absorption, distribution, metabolism and excretion.
Pharmacodynamics: What a drug does to the body.
Pharmacokinetics and pharmacodynamics are two of the processes that determine how a person will respond to a drug. Other factors include how a drug is administered (dose, route, and timing of administration), interactions with other drugs, and individual physiological variables (weight, age, function of body systems).
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.
Anticonvulsant Drugs
A. Anticonvulsants: drugs to control seizures or convulsions in susceptible people
B. Seizures: abnormal neuronal discharges in the nervous system produced by focal or generalized brain disturbances
Manifestations: depend on location of seizure activity (motor cortex → motor convulsions, sensory cortex → abnormal sensations, temporal cortex → emotional disturbances)
Causes: many brain disorders such as head injury (glial scars, pH changes), anoxia (changes in pH or CSF pressure), infections (tissue damage, high T), drug withdrawal (barbiturates, ethanol, etc.), epilepsy (chronic state with repeated seizures)
C. Epilepsy: most common chronic seizure disorder, characterized by recurrent seizures of a particular pattern, many types (depending on location of dysfunction)
Characteristics: chronic CNS disorders (years to decades), involve sudden and transitory seizures (abnormal motor, autonomic, sensory, emotional, or cognitive function and abnormal EEG activity)
Etiology: hyperexcitable neurons; often originate at a site of damage (epileptogenic focus), often found at scar tissue from tumors, strokes, or trauma; abnormal discharge spreads to normal brain regions = seizure
Idiopathic (70%; may have genetic abnormalities) and symptomatic epilepsy (30%; obvious CNS trauma, neoplasm, infection, developmental abnormalities or drugs)
Neuropathophysiology: anticonvulsants act at each stage but most drugs not effective for all types of epilepsy (need specific drugs for specific types)
Seizure mechanism: enhanced excitation (glutamate) or ↓ inhibition (GABA) of epileptic focus → fire more quickly → ↑ release of K and glutamate → ↑ depolarization of surrounding neurons (=neuronal synchronization) → propagation (normal neurons activated)
Paracetamol
Paracetamol or acetaminophen is analgesic and antipyretic drug that is used for the relief of fever, headaches, and other minor aches and pains.
paracetamol acts by reducing production of prostaglandins, which are involved in the pain and fever processes, by inhibiting the cyclooxygenase (COX) enzyme.
Metabolism Paracetamol is metabolized primarily in the liver. At usual doses, it is quickly detoxified by combining irreversibly with the sulfhydryl group of glutathione to produce a non-toxic conjugate that is eventually excreted by the kidneys.
Beta-Adrenergic blocking Agents
• Prototype - Propranolol
• Prevent or inhibit sympathetic stimulation
– Reduces heart rate
– Myocardial contractility
– Reduce BP - decreases myocardial workload and O2 demand
• In long-term management used to decrease frequency and severity of anginal attacks
• Added when nitrates do not prevent anginal episodes
• Prevents exercise induced tachycardia
• Onset of action 30 min after oral dose. 1-2 min IV
Therapeutic Actions
• Block Beta adrenergic receptors in the heart and juxtaglomerular apparatus
• Decrease the influence of the sympathetic nervous system decreasing excitability of the heart
• Decrease cardiac output.
• Indicated for long term management of anginal pectoris caused by atherosclerosis
Atenolol, metoprolol, and nadolol have the same actions, uses, and adverse effects as propranolol, but they have long half-lives and can be given once daily. They are excreted by the kidneys, and dosage must be reduced in clients with renal impairment.
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