HSBTE D Pharm. Pharmacology & Toxicology Sample Paper.

HSBTE February 2022.

SECTION-A

Note: Multiple choice questions. All questions are compulsory (8x1=8)

Q.1 Example of Catecholamine is

a) Adrenaline b) Paracetamol c) Quinine d) Heparin

Ans: a) Adrenaline

Q.2 Example of Cholinesterase inhibitor is

a) Paracetamol b) Neostigmine c) Furosemide d) Lignocaine

Ans: a) Adrenaline

Q.3 Which one is used in Bronchial Asthma

a) Methotrexate b) Primaquine c) Salbutamol d) Phenylbutazone

Ans: c) Salbutamol

Q.4 Phenothiazines are used as

a) Major Tranquillizers/ psycholeptics    b) Anti Cancer

c) Anti Fungal      d) Anti Viral

Ans: a) Major Tranquillizers/ psycholeptics

Q.5 Chloroform is used as

a) Local Anaesthetic b) General Anesthetic c) Tranquillizers d) Analeptic

Ans: b) General Anesthetic

Q.6 Penicillin is

a) Steroidal Drug b) Non Steroidal drug c) Antibiotics d) Analgesic

Ans: c) Antibiotics

Q.7 Which one drug is used as an Antimalarial drug

a) Primaquine b) atropine c) Proguanil d) Nystatin

Ans: c) Proguanil

Q.8 Cisplatin Drug is used as

a) Antimalarial             b) Antileprotic Drug

c) Antithyroid drug     d) Anti Neoplastic drug

Ans: d) Anti Neoplastic drug

SECTION-B

Note: Objective/completion type questions. All questions are compulsory. (8x1=8)

Q.9 Define the term Analgesics

Ans: Analgesics are used to relieve pain, either by reducing the perception of pain or by blocking the transmission of pain signals.

Note: Analgesics can be categorized on their mechanisms of action. They are nonsteroidal anti-inflammatory drugs (NSAIDs), opioids, and adjuvant analgesics. They are commonly used to reduce pain associated with various conditions such as headaches, arthritis, injuries, surgeries, and chronic illnesses.

Q.10 Mention one drug used in Myasthenia Gravis

Ans: Pyridostigmine.

Note: Pyridostigmine works by inhibiting the enzyme acetylcholinesterase. Thus it prolongs the action of acetylcholine at the neuromuscular junction. This helps improve muscle strength and reduce symptoms of weakness in individuals with Myasthenia Gravis.

Q.11 Mention one example of Anti Histaminic drugs

Ans: Loratadine.

Note: Loratadine is commonly used to relieve symptoms of allergies such as hay fever, allergic rhinitis, and hives. It works by blocking the action of histamine, a substance in the body that causes allergic symptoms such as itching, sneezing, runny nose, and watery eyes. It blocks the peripheral H1 receptor.

Q.12 Mention one use of furosemide

ANS: Diuretics (loop diuretics)

Furosemide is used as a diuretic to treat conditions such as edema (fluid retention) associated with congestive heart failure, liver disease, or kidney disorders. It helps the body to expel excess water and salt through urine, thus reducing swelling and fluid buildup in the body.

Q.13 Mention one example of Antithyroid Drugs.

Ans: Methimazole.

Note: It is used to treat hyperthyroidism by inhibiting the production of thyroid hormones in the thyroid gland.

Q.14 Define the term Mydriatics

Ans: Mydriatics are drugs that cause dilation of the pupil (mydriasis or pupil dilator) by relaxing the radial muscles of the iris.

Note: They are commonly used in ophthalmology for various purposes, such as dilating the pupil for eye examinations or surgeries, aiding in the diagnosis and treatment of certain eye conditions, and facilitating intraocular procedures.

Mydriatics block acetylcholine from binding with cholinergic receptors. Mydriatics work by blocking the action of the iris sphincter muscle, (the Iris sphincter constricts the pupil). Mydriatics also paralyze the ciliary muscles. (Ciliary muscle adjusts the lens thickness to focus the vision). This allows the pupil to enlarge and more light to enter the eye. An example of a mydriatic is tropicamide.

Q.15 Define the term Analeptics

Ans: Analeptics are drugs that act as central nervous system stimulants.

Note: They are used primarily to stimulate respiration in cases of respiratory depression or arrest,. Analeptics work by stimulating the respiratory centers in the brain, increasing the rate and depth of breathing. Examples of analeptic drugs include doxapram and nikethamide. However, it's important to note that the use of analeptics has become less common due to safety concerns and the availability of other treatment options.

Q.16 Define the term Anti tussive Agents

Ans: Antitussive agents are used to suppress or relieve coughing.

Note: They work by acting on the cough reflex center in the brain, reducing the urge to cough. One example of an antitussive agent is dextromethorphan, Dextromethorphan works by affecting the signals in the brain that trigger the cough reflex. It is often used to provide temporary relief from cough associated with colds, flu, or other respiratory conditions.

SECTION-C

Note: Short answer type questions. Attempt any eight questions out of ten questions. (8x5=40)

Q.17 Explain at least 8 factors modifying drug action

Ans: Several factors can modify the action of drugs in the body. The following are eight important factors:

• i. Genetics: Genetic factors play a significant role in drug response. Genetic variations can affect drug metabolism, efficacy, and susceptibility to adverse effects. Pharmacogenomics is the study of how genetic variations influence drug response that helps in personalized medicine.

• ii. Age: Age-related changes in physiology can alter drug action. For example, infants (pediatrics) and elderly individuals (geriatrics) reduced drug metabolism or clearance, leading to increased drug concentrations inside body and increased toxicity. Dosage adjustments may be necessary based on age.

• iii. Body weight and composition: Body weight and composition influence drug distribution and clearance. Drugs with a high lipophilicity tend to accumulate in fatty tissues. This leads to prolonged effects in individuals with higher body fat percentages.

• iv. Gender: Biological differences between males and females can affect drug pharmacokinetics and pharmacodynamics. Hormonal fluctuations, body composition, and enzyme activity vary between genders. This leads to differences in drug response.

• v. Disease State: Underlying medical conditions alter drug metabolism, distribution, and elimination. Diseases affecting liver or kidney function impair drug clearance. This leads to toxicity.

• vi. Drug Interaction: Concurrent use of multiple drugs leads to interactions. This alters drug action. Interactions may involve competition for metabolic pathways, changes in drug absorption or distribution, or synergistic or antagonistic effects on pharmacological activity.

• vii. Route of Administration: The route through which a drug is administered affects its onset of action, intensity, and duration of effect. Different routes, such as oral, intravenous, or topical, have varying absorption rates and bioavailability. This influences drug action.

• viii. Tolerance and Sensitization: Prolonged use of certain drugs leads to tolerance. The higher doses are required to achieve the same therapeutic effect. Conversely, sensitization may occur, where repeated exposure leads to an increased response to the drug.

Q.18 Write a detailed note on Drug Procaine.

Ans: Procaine (novocaine) is a local anesthetic.

Pharmacology: Procaine blocks the impulses along nerve fibers. This prevents the transmission of pain signals to the brain.

Clinical Uses:

• 1. Dental Procedure: Procaine is commonly used in dentistry such as dental fillings, root canals, and tooth extractions to provide local anesthesia.

• 2. Minor Surgical Procedure: It is also used in minor surgical procedures, dermatological procedures, and certain diagnostic procedures to provide local anesthesia.

Administration: Procaine is administered via injection, either subcutaneously, intramuscularly, or by infiltration into the tissues surrounding the site requiring anesthesia. It is available in combination with vasoconstrictors like epinephrine. Ephedrine helps to prolong the duration of anesthesia by acting as a vasoconstrictor. Ephedrine reduces local blood flow and delays the systemic absorption of procaine.

Onset and Duration of Action: The onset of action of procaine occurs within a few minutes. Its duration of action ranges from 30 minutes to 2 hours. It depends on factors such as the dose, the site of injection, and the addition of vasoconstrictors.

Adverse Effects: Some adverse effects may occur.

• 1. Allergic Reactions: Procaine causes allergic reactions ranging from mild skin rashes to severe anaphylaxis in susceptible individuals.

• 2. Systemic Toxicity: Excessive doses or rapid absorption of procaine into the bloodstream lead to systemic toxicity uch as dizziness, confusion, convulsions, and cardiovascular collapse.

Contraindications: Procaine should be used with caution or avoided in individuals with:

• 1. Known hypersensitivity or allergy to ester local anesthetics.

• 2. Pre-existing cardiac conduction abnormalities or severe cardiovascular disease.

• 3. Porphyria, a rare genetic disorder affecting heme metabolism.

Drug Interactions: Procaine may interact with certain medications.

• 1. Antiarrhythmic drugs: Increased risk of cardiac toxicity when administered with drugs that affect cardiac conduction.

• 2. Monoamine oxidase inhibitors (MAOIs): Prolonged and intensified effects of procaine due to inhibition of procaine metabolism.

Special Consideration

• 1. Pregnancy and Lactation: it should be used carefully in these populations.

• 2. Pediatric and Geriatric Use: Lower doses of procaine may be required in pediatric and geriatric patients due to differences in drug metabolism and sensitivity to its effects.

• 3. Renal or Hepatic Impairment: Procaine should be used with caution in patients with renal or hepatic impairment. Impaired drug metabolism and clearance may increase the risk of systemic toxicity.

Q.19 Write a detailed note on Drug Morphine.

Morphine is a powerful opioid analgesic derived from the opium poppy plant. It is the oldest known pain-relieving substance and remains one of the most effective medications for the management of severe pain.

Pharmacology: Morphine works by binding to opioid receptors and activating them in the central nervous system, particularly the mu-opioid receptors. This results in a change in pain perception, leading to analgesia. Additionally, morphine can produce other effects such as sedation, euphoria, respiratory depression, and cough suppression.

Medical Uses: Morphine is used for the management of moderate to severe pain, particularly if less potent analgesics are not effective. It is administered via various routes: oral tablets, injectable formulations, and transdermal patches. The following are medical uses of morphine:

• 1. Pain Management: Morphine is highly effective in relieving pain associated with conditions such as cancer, post-surgical recovery, severe injuries, and terminal illnesses.

• 2. Anesthesia: Morphine is used as an adjunct to general anesthesia or regional anesthesia to provide pain relief during surgical procedures.

• 3. Palliative Care: In palliative care for patients with advanced cancer or other terminal conditions to ease painful symptoms and improve quality of life.

Side Effects: The following are side effects associated with morphine:

• 1. Respiratory Depression: It can be life-threatening, especially in high doses or when combined with other respiratory depressants.

• 2. CNS Effects: Drowsiness, confusion, and impairment of cognitive and motor functions.

• 3. Constipation: Morphine causes constipation due to its effects on gastrointestinal motility. Laxatives are often prescribed with morphine to lessen this side effect.

• Tolerance and Dependence: Prolonged use of morphine leads to the development of tolerance. This requires higher doses to achieve the same level of pain relief. It can also lead to physical dependence and withdrawal symptoms upon discontinuation.

Contraindications and Precautions: Morphine use is contraindicated in certain situations:

• 1. Respiratory insufficiency or severe asthma

• 2. Paralytic ileus (intestinal obstruction)

• 3. Acute alcohol intoxication or fever

• 4. Known hypersensitivity to morphine or other opioids

• 5. Special precautions should be taken when prescribing morphine to elderly patients, individuals with impaired hepatic or renal function, and those with a history of substance abuse or addiction.

Q.20 Explain in detail the Pharmacology of Non- Barbiturates.

Non-barbiturates under sedative-hypnotic drugs are used for their sedative, anxiolytic (anxiety-reducing), and hypnotic (sleep-inducing) properties. Nonbarbiturates have similar effects as barbiturates under sedative-hypnotic drugs. Non barbiturates have replaced barbiturates due to the high potential for addiction, dependence, and overdose of barbiturates.

Chemical Classification: Non-barbiturate sedative-hypnotics encompass various chemical classes, such as benzodiazepines, non-benzodiazepine receptor agonists (e.g. Z-drugs), and miscellaneous agents like melatonin receptor agonists. Each class has distinct pharmacological properties and mechanisms of action.

Mechanism of Action:

• Benzodiazepines: They act by enhancing the activity of gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system (CNS). Benzodiazepines bind to specific sites on the GABA-A receptor complex, which contains chloride ion channels. Benzodiazepines increase the frequency of chloride channel opening By binding to these receptors, This leads to hyperpolarization of the neuronal membrane and inhibition of neuronal excitability. This results in sedative, anxiolytic, muscle relaxant, and anticonvulsant effects.

• Non-Benzodiazepine Receptor Agonists (Z-drugs): Drugs in this class are zolpidem, zaleplon, and eszopiclone. They also act on the GABA-A receptor complex but bind to a specific subset of receptors distinct from those targeted by benzodiazepines. They selectively bind to receptors containing the alpha-1 subunit, which is associated with sedative and hypnotic effects. Z-drugs promote sleep initiation and maintenance by enhancing the effects of GABA-Z. They have minimal effects on other neurotransmitter systems.

Pharmacokinetics: The pharmacokinetic properties of non-barbiturate sedative-hypnotics vary depending on the specific drug and its formulation. Many of these drugs are well-absorbed after oral administration. The peak plasma concentrations reached within 1-2 hours for most benzodiazepines and Z-drugs. They typically undergo extensive hepatic metabolism via the cytochrome P450 (CYP) enzyme system. Their metabolites are excreted through renal excretion

Clinical Uses: Non-barbiturate sedative-hypnotics have various clinical applications:

• 1. Treatment of insomnia: These drugs are commonly used to promote sleep initiation and maintenance in patients with insomnia.

• 2. Anxiolysis: Benzodiazepines and some Z-drugs are used to alleviate symptoms of anxiety and agitation.

• 3. Muscle relaxation: Benzodiazepines possess muscle relaxant properties and may be used to relieve muscle spasms and stiffness.

Adverse Effects: Common adverse effects associated with non-barbiturate sedative-hypnotics include drowsiness, dizziness, impaired coordination, and cognitive impairment. Benzodiazepines and Z-drugs can also cause rebound insomnia and dependence with long-term use. Additionally, these drugs carry a risk of respiratory depression if used concomitantly with other CNS depressants such as opioids or alcohol.

Q.21 Explain in detail Pharmacology of Phenothiazines

Phenothiazines have diverse pharmacological effects known for their antipsychotic properties.

Mechanism of Action: The exact mechanism of action of phenothiazines is not fully understood. It is believed to involve complex interactions with multiple neurotransmitter systems in the central nervous system (CNS), including dopamine, serotonin, histamine, and adrenergic receptors. The mechanisms of action include:

• 1. Dopamine Receptor Blockade: Phenothiazines primarily exert their antipsychotic effects by antagonizing D2 subtype dopamine receptors in the brain. Phenothiazines reduce the hyperactivity of dopaminergic neurotransmission by blocking dopamine receptors,

• 2. Serotonin Receptor Antagonism: Some phenothiazines also possess antagonistic activity at serotonin (5-HT) receptors (5-HT2A subtype). This action contributes to their antipsychotic efficacy and may also be involved in the management of anxiety disorders.

• 3. Histamine H1 Receptor Blockade: Phenothiazines have potent antagonistic effects on histamine H1 receptors. This leads to sedation, antiemetic effects, and weight gain commonly observed with their use.

• 4. Alpha-Adrenergic Receptor Blockade: Phenothiazines exhibit varying degrees of antagonism at alpha-adrenergic receptors. This contributes to their hypotensive effects and helps lessen symptoms such as agitation and anxiety.

Pharmacokinetics: Well-absorbed after oral administration. The peak plasma concentrations were achieved within 1-4 hours. They undergo extensive hepatic metabolism via the cytochrome P450 (CYP) enzyme system. This results in active metabolites that contribute to their pharmacological effects. The elimination half-life of phenothiazines varies but generally ranges from several hours to several days.

Clinical Uses: Phenothiazines have several clinical uses:

• 1. Treatment of schizophrenia and other psychotic disorders: Phenothiazines are effective in reducing the symptoms of schizophrenia, such as hallucinations and delusions, by blocking dopamine receptors in the brain.

• 2. Management of bipolar disorder: They may be used as mood stabilizers in the treatment of bipolar disorder. They are used in combination with mood-stabilizing agents such as lithium.

• 3. Control of severe nausea and vomiting: Phenothiazines possess antiemetic properties and are used to manage nausea and vomiting associated with chemotherapy, surgery, and other medical conditions.

• 4. Treatment of anxiety and agitation: Some phenothiazines have sedative and anxiolytic effects, making them useful in managing anxiety, agitation, and behavioral disturbances.

Adverse Effects: Common adverse effects associated with phenothiazines include:

• 1. Sedation and drowsiness

• 2. Extrapyramidal symptoms (e.g., parkinsonism, dystonia, akathisia)

• 3. Anticholinergic effects (e.g., dry mouth, constipation, urinary retention)

• 4. Orthostatic hypotension

• 5. Weight gain and metabolic disturbances

Phenothiazines should be used with caution in elderly patients, individuals with cardiovascular disease, and those with a history of seizures or hepatic impairment.

Q.22 Write a detailed note on the drug Noradrenaline.

Noradrenaline, also known as norepinephrine, is a neurotransmitter and hormone that affects the sympathetic nervous system's response to stress. It belongs to a class of compounds called catecholamines.

Synthesis and Release: The noradrenaline synthesis pathway involves the conversion of tyrosine to L-DOPA (di hydroxyl phenylalanine) by the enzyme tyrosine hydroxylase, followed by the conversion of L-DOPA to dopamine by aromatic L-amino acid decarboxylase. Dopamine is then converted to noradrenaline by the enzyme dopamine beta-hydroxylase. Noradrenaline is primarily synthesized in the nerve terminals of sympathetic neurons located in the central nervous system (CNS) and peripheral sympathetic ganglia.

Stimulation of sympathetic nerves releases noradrenaline from synaptic vesicles into the synaptic cleft.. The released noradrenaline interacts with adrenergic receptors on target cells, producing various physiological responses.

Physiological Effects: Noradrenaline exerts its effects by binding to adrenergic receptors, which are G protein-coupled receptors located on the surface of target cells. There are two main classes of adrenergic receptors: alpha-adrenergic receptors and beta-adrenergic receptors. Each class is further divided into subtypes (e.g., alpha-1, alpha-2, beta-1, beta-2), each with distinct physiological effects.

• 1. Alpha-adrenergic receptors: Activation of alpha-adrenergic receptors by noradrenaline leads to vasoconstriction of blood vessels, pupillary dilation (mydriasis), and contraction of smooth muscle in organs such as the gastrointestinal tract and urinary bladder.

• 2. Beta-adrenergic receptors: Activation of beta-adrenergic receptors by noradrenaline results in various effects such as vasodilation of blood vessels in skeletal muscle, relaxation of smooth muscle in the bronchi and gastrointestinal tract, and stimulation of cardiac muscle contraction (positive inotropic and chronotropic effects).

Noradrenaline is also a hormone when released into the bloodstream by the adrenal medulla. In this capacity, noradrenaline acts as a stress hormone. It mobilizes the body's resources in response to acute stress. It increases heart rate, blood pressure, and glucose levels, among other effects.

Clinical Applications: Noradrenaline is used clinically as a medication to treat hypotension (low blood pressure) and shock, particularly in critically ill patients. It is administered intravenously as a vasopressor agent to increase blood pressure. It is administered intravenously to restore adequate tissue perfusion in situations such as septic shock, cardiogenic shock, or hypovolemic shock.

Adverse Effects: Hypertension, tachycardia, arrhythmias. and tissue necrosis if extravasation occurs during intravenous infusion. Close monitoring of blood pressure and cardiac function is essential during noradrenaline therapy to avoid adverse cardiovascular effects.

Q.23 Write a detailed note on the Drug Neostigmine

Neostigmine is used in the treatment of myasthenia gravis, a neuromuscular disorder characterized by muscle weakness and fatigue. It belongs to a class of drugs known as acetylcholinesterase inhibitors. It works by inhibiting the activity of the enzyme acetylcholinesterase.

Mechanism of Action: Neostigmine exerts its pharmacological effects by inhibiting the activity of acetylcholinesterase (AChE), an enzyme responsible for breaking down the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. Neostigmine increases the concentration of ACh in the synaptic cleft by inhibiting AChE. This prolongs ACh action and enhances neuromuscular transmission.

At the neuromuscular junction, ACh released from motor nerve terminals binds to nicotinic acetylcholine receptors (nAChRs) on the postsynaptic membrane of skeletal muscle fibers. This leads to muscle contraction.

In myasthenia gravis, there is a reduction in the number of functional nAChRs due to autoimmune destruction. This results in muscle weakness and fatigue. Neostigmine helps compensate for this deficit by increasing the availability of ACh at the neuromuscular junction. Thereby improving muscle strength and function.

Pharmacokinetics: Neostigmine is administered orally or via injection (intramuscular or intravenous). It is poorly absorbed from the gastrointestinal tract and undergoes extensive metabolism in the liver. The onset of action after intramuscular injection is rapid. The peak effects occur within 30 minutes to 1 hour. The duration of action is relatively short, necessitating frequent dosing.

Clinical Uses:

• 1. Myasthenia Gravis: Neostigmine is used in myasthenia gravis, a chronic autoimmune disorder characterized by muscle weakness and fatigability. It is used in combination with other medications such as corticosteroids and immunosuppressants to manage symptoms and improve muscle strength.

• 2. Reversal of Neuromuscular Blockade: Neostigmine is commonly used to reverse the effects of nondepolarizing neuromuscular blocking agents (e.g., vecuronium, rocuronium) following surgery or during anesthesia. By inhibiting acetylcholinesterase, neostigmine enhances the transmission of nerve impulses at the neuromuscular junction, leading to the reversal of muscle paralysis.

• 3. Urinary Retention: Neostigmine is used to alleviate urinary retention by enhancing detrusor muscle contraction and promoting bladder emptying. It is particularly useful in patients with neurogenic bladder dysfunction or postoperative urinary retention.

Adverse Effects: The following are common adverse effects associated with neostigmine therapy:

• 1. Cholinergic Excess: Neostigmine can cause symptoms of cholinergic excess, including nausea, vomiting, diarrhea, abdominal cramps, excessive salivation, sweating, bradycardia, bronchoconstriction, and miosis (pupil constriction).

• 2. Bradycardia: Neostigmine causes bradycardia and severe cardiovascular effects, particularly in patients with underlying cardiac disease.

• 3. Respiratory Depression: In high doses or when administered rapidly, neostigmine causes respiratory depression or bronchoconstriction, particularly in patients with compromised respiratory function.

Q.24 Write a brief note on Coagulants.

Coagulants are used to promote blood clotting. They are used to manage bleeding disorders or to control excessive bleeding during surgical procedures. These drugs work by accelerating the process of coagulation, which involves the formation of a blood clot to stop bleeding. There are several types of coagulants:

• 1. Vitamin K: Vitamin K is essential for the synthesis of clotting factors in the liver. It is commonly used to treat bleeding disorders caused by vitamin K deficiency.

• 2. Recombinant clotting factors: Recombinant forms of clotting factors, such as Factor VIII and Factor IX, are used to treat hemophilia, a genetic disorder characterized by a deficiency in these clotting factors.

• 3. Desmopressin: Desmopressin is a synthetic hormone that stimulates the release of factor VIII from endothelial cells. It is used to treat bleeding disorders like hemophilia A.

• 4. Antifibrinolytic agents: Antifibrinolytic drugs work by inhibiting the breakdown of blood clots. They are used to prevent or control bleeding in various clinical settings, including surgery, trauma, and certain medical conditions. Examp;e tranexamic acid and aminocaproic acid,

Coagulants play a critical role in the management of bleeding disorders and in ensuring hemostasis during surgical procedures. However, their use requires careful monitoring to avoid complications such as thrombosis or excessive clot formation, which can lead to serious health risks. These drugs are typically administered under the supervision of healthcare professionals who can monitor their effects and adjust dosages as necessary to achieve optimal outcomes. Top of Form

Q.25 Write a brief note on Sex Hormones

Sex hormones are a group of steroid hormones that play crucial roles in the development and regulation of sexual characteristics and reproductive functions in humans. The primary sex hormones in humans include:

• 1. Estrogens: Estrogens are produced in the ovaries in females and in smaller quantities in the testes and adrenal glands in males. They are responsible for the development and maintenance of female secondary sexual characteristics, regulation of the menstrual cycle, and support of pregnancy.

• 2. Progesterone: Progesterone is mainly produced in the ovaries following ovulation and plays a vital role in preparing the uterus for implantation of a fertilized egg and maintaining pregnancy.

• 3. Androgens: Androgens, such as testosterone, are produced in the testes in males and in smaller amounts in the ovaries and adrenal glands in females. Testosterone is the primary male sex hormone and is responsible for the development of male secondary sexual characteristics such as facial hair, deep voice, and muscle mass. In females, androgens contribute to libido and play a role in ovarian function.

These sex hormones exert their effects by binding to specific receptors located in target tissues throughout the body, including the reproductive organs, brain, bones, and muscles. They regulate various physiological processes, including puberty, fertility, libido, bone density, mood, and metabolism.

Imbalances in sex hormone levels can lead to various health issues and reproductive disorders. For example, deficiencies or excesses of estrogen or testosterone can result in menstrual irregularities, infertility, decreased libido, osteoporosis, and mood disturbances. Hormone replacement therapy (HRT) may be used to restore hormone levels in individuals with deficiencies or to manage symptoms associated with hormonal imbalances. 

Q.26 Write a brief note on Emetics.

Emetics induce vomiting when ingested or administered. They are used to treat poisoning by expelling toxic substances from the stomach before they are absorbed into the bloodstream. Emetics work by stimulating the vomiting reflex either directly on the stomach lining or indirectly through the central nervous system. The following are examples of emetics:

• 1. Ipecac syrup: Ipecac syrup contains emetine and cephaeline. These are alkaloids that irritate the stomach lining and trigger vomiting. It was historically used as a household remedy for inducing vomiting in cases of accidental poisoning. However, its use has declined due to its doubtful effectiveness and side effects.

• 2. Apomorphine: Apomorphine is a dopamine agonist that acts on the chemoreceptor trigger zone in the brain, stimulating the vomiting reflex. It is administered subcutaneously or intramuscularly and is primarily used in clinical settings for emergency treatment of poisoning.

• 3. Hydrogen peroxide: Hydrogen peroxide is a strong oxidizing agent that irritates the gastric mucosa, leading to vomiting. It is sometimes used as a home remedy for inducing vomiting after ingestion of toxic substances. However, its effectiveness and safety are debatable. its use is generally discouraged.

The use of emetics to induce vomiting in poisoning should only be done under the guidance of medical professionals. Indiscriminate use of emetics can cause complications such as aspiration pneumonia, esophageal rupture, and electrolyte imbalances. In many cases, other methods such as activated charcoal administration or gastric lavage may be more appropriate for decontamination in cases of poisoning.

SECTION-D

Note: Long answer type questions. Attempt any three questions out of four questions. (3x8=24)

Q.27 Define and Classify Cholinergic Drugs. Write a detailed note on Acetylcholine & Physostigmine.

Cholinergic drugs (Parasympathomimetic drugs) mimic or enhance the actions of the neurotransmitter acetylcholine (ACh) in the body. Acetylcholine is a neurotransmitter found in the central nervous system, as well as the autonomic nervous system (ANS). ACh acts on both muscarinic and nicotinic receptors to regulate various physiological processes, including muscle contraction, heart rate, glandular secretion, and neurotransmission.

Classification: Cholinergic drugs (Parasympathomimetic drugs) are classified into groups on the basis of their mode of action.

• 1. Direct-acting parasympathomimetic drugs: These drugs interact with cholinergic receptors to produce action similar to the action of Acetylcholine (parasympathetic nervous system stimulation): Examples: Acetylcholine, Bethanechol, Carbachol, Natural alkaloids Pilocarpines, Muscarine

• 2. Indirect-acting parasympathomimetic drugs: These drugs increase the availability of endogenous acetylcholine (increase duration of action of acetylcholine) by blocking the enzyme Acetyl Choline esterase (AChE). AChE inactivates acetylcholine by hydrolysis. Thus these drugs increase the availability of acetylcholine at the synaptic cleft which increases its duration of action.

Indirect-acting parasympathomimetic drugs are also called anticholinesterase or cholinesterase inhibitors. These drugs are further subdivided into two groups depending on nature and stability.

• · Reversible anticholinesterase: Anticholinesterase Drug and cholinesterase enzyme complex are not stable. Thus, they are called reversible anticholinesterase. Physostgmine, Neostigmine, Pyridostigmine, Edrophonium, Carbamates

• · Irreversible anticholinesterase: Anticholinesterase drug and cholinesterase enzyme complex is very stable and irreversible. Examples of organophosphorus compounds. Organophosphorus compounds Such as Isoflurophate, Ecothiophate

Acetylcholine (ACh)

Acetylcholine is a neurotransmitter in the parasympathetic nervous system (PNS) and at neuromuscular junctions.

• 1. In the PNS, acetylcholine activates muscarinic receptors on smooth muscle, cardiac muscle, and glands. This leads to various physiological responses such as increased glandular secretion, smooth muscle contraction, and decreased heart rate.

• 2. Acetylcholine also activates nicotinic receptors at the neuromuscular junction, resulting in skeletal muscle contraction.

• 3. Dysregulation of acetylcholine levels or signaling is associated with various neurological and neuromuscular disorders, including Alzheimer's disease, myasthenia gravis, and certain autonomic dysfunctions.

Physostigmine Physostigmine is an indirect-acting cholinergic agonist and a reversible acetylcholinesterase inhibitor. It is derived from the Calabar bean (Physostigma venenosum) and has been used therapeutically for its cholinergic effects.

• 1. Physostigmine increases the concentration of acetylcholine at cholinergic synapses by inhibiting acetylcholinesterase. This leads to prolonged stimulation of cholinergic receptors.

• 2. It is used clinically to treat conditions associated with reduced cholinergic activity, such as myasthenia gravis, and to reverse the effects of anticholinergic toxicity (e.g., from atropine or certain other drugs).

• 3. Physostigmine can cross the blood-brain barrier. Thus it is useful in the treatment of central anticholinergic toxicity and certain neurological conditions.

However, physostigmine has a narrow therapeutic window and can cause adverse effects such as bradycardia, bronchoconstriction, and gastrointestinal disturbances. Therefore, it should be used cautiously and under medical supervision. 

Q.28 Write a detailed note on Routes of Administration of Drugs

Routes of drug administration are the pathways through which medications are introduced into the body. The choice of route of administration depends on factors such as the drug's properties, the desired onset and duration of action, the patient's condition, and the intended therapeutic outcome. There are several routes of drug administration, each with its advantages, and disadvantages:

• 1. Oral (Enteral or PO) route of administration: Oral administration involves ingesting drugs through the mouth. They are absorbed through the gastrointestinal tract.

• Advantages: Convenient, non-invasive, suitable for self-administration, and allows for prolonged drug release (e.g., sustained-release formulations).

• Disadvantages: Variable absorption, first-pass metabolism in GIT and liver, high dose, and inability to administer to unconscious or vomiting patients.

• 2. Sublingual (SL) and Buccal: Sublingual administration involves placing medications under the tongue, while buccal administration involves placing them between the cheek and gum.

• Advantages: Rapid absorption due to the rich blood supply in the oral mucosa, no first-pass metabolism, and suitable for drugs with poor oral bioavailability or that degrade in the gastrointestinal tract.

• Disadvantages: Limited to small doses and specific drug formulations, risk of irritation to the oral mucosa, and difficulty administering to uncooperative or unconscious patients.

• 3. Rectal (PR): Rectal administration involves inserting medications into the rectum, where they are absorbed into the bloodstream via the rectal mucosa or transported to the systemic circulation via the mesenteric veins.

• Advantages: Useful when oral administration is not feasible (e.g., nausea, vomiting), no first-pass metabolism, and suitable for patients unable to swallow.

• Disadvantages: Variable absorption due to differences in rectal mucosal blood flow, irritation or discomfort, and patient acceptability issues.

• 4. Parenteral: Parenteral routes involve administering drugs via injection directly into the body tissues or bloodstream. Subcutaneous (SC), intramuscular (IM), and intravenous (IV) injections are common parenteral routes.

• Advantages: Rapid onset of action, predictable drug levels, suitable for drugs with poor oral bioavailability, and useful for emergencies.

• Disadvantages: Requires healthcare professional for administration, risk of infection, tissue damage, patient discomfort, and needlestick injuries.

• 5. Topical: Topical administration involves applying medications directly to the skin or mucous membranes. Examples include creams, ointments, patches, eye drops, ear drops, nasal sprays, and inhalers.

• Advantages: Non-invasive, localized effect, reduced systemic side effects, and suitable for treating skin conditions or delivering drugs to specific sites.

• Disadvantages: Limited penetration of drugs through the skin barrier, potential for skin irritation or allergic reactions, and difficulty achieving consistent drug levels.

• 6. Inhalation: Inhalation involves administering drugs via inhalation into the respiratory tract. Drugs are absorbed into the bloodstream or exert local effects. Examples include metered-dose inhalers (MDIs), dry powder inhalers (DPIs), nebulizers, and vaporized medications.

• Advantages: Rapid onset of action, direct delivery to the lungs for respiratory conditions, and reduced systemic side effects.

• Disadvantages: Requires patient cooperation and proper inhalation technique, risk of local irritation or bronchospasm, and difficulty administering to unconscious or pediatric patients.

• 7. Transdermal: Transdermal administration involves applying medications to the skin for systemic absorption over an extended period. Drugs are delivered through specialized patches or formulations designed to penetrate the skin barrier.

• Advantages: Continuous drug delivery, no first-pass metabolism, convenient, and non-invasive administration.

• Disadvantages: Limited to drugs with favorable physicochemical properties, slow onset of action, potential for skin irritation or allergic reactions, and difficulty adjusting doses.

Each route of administration has its unique characteristics, and the selection of the most appropriate route depends on various factors such as the drug's properties, the patient's condition and preferences, and the therapeutic goals. Healthcare professionals consider these factors when prescribing medications to optimize treatment outcomes and patient safety.

Q.29 Define and Classify Tubercular Drugs. Write a detailed note on INH (Isonicotinic Acid Hydrazide ) & Pyrazinamide.

Tubercular drugs are used to treat tuberculosis (TB), a bacterial infection caused by Mycobacterium tuberculosis. Tuberculosis treatment involves a combination of several drugs to prevent the development of drug-resistant strains and improve treatment efficacy.

Tubercular drugs are classified into several categories based on their mechanism of action and therapeutic properties. Common classes of tubercular drugs include:

• 1. First-line anti-tubercular drugs: These drugs are considered the most effective and are the first choice for treating TB. Examples are isoniazid (INH), rifampicin (RIF), pyrazinamide (PZA), ethambutol (EMB), and rifabutin.

• 2. Second-line anti-tubercular drugs: These drugs are used when first-line drugs are ineffective or when drug-resistant TB is suspected. Examples are fluoroquinolones (e.g., moxifloxacin, levofloxacin), aminoglycosides (e.g., streptomycin, amikacin), and other agents such as bedaquiline and linezolid.

Isonicotinic Acid Hydrazide (INH): INH, also known as isoniazid. It is one of the most widely used and effective drugs for treating TB.

• 1. Mechanism of action: INH inhibits the synthesis of mycolic acids, essential components of the bacterial cell wall. It blocks the enzyme enoyl-acyl carrier protein reductase (InhA). This disrupts cell wall formation and ultimately leads to bacterial cell death.

• 2. Pharmacokinetics: INH is well-absorbed orally and penetrates well into tissues where TB infection primarily occurs. It is metabolized in the liver by acetylation. The rate of metabolism varies among individuals. Genetic factors influence acetylation rates, which can affect INH's efficacy and toxicity.

• 3. Clinical use: INH is a cornerstone of TB treatment and is included in all standard TB treatment regimens. It is usually administered orally, either as a single daily dose or as part of combination therapy with other anti-TB drugs. INH is also used for prophylaxis in individuals at high risk of developing active TB, such as close contacts of TB patients or individuals with latent TB infection.

• 4. Adverse effects: Common side effects of INH include hepatotoxicity, peripheral neuropathy, and gastrointestinal disturbances. Hepatotoxicity is the most serious adverse effect and can occur idiosyncratically. Thus regular monitoring of liver function tests during INH therapy is essential. Peripheral neuropathy can be prevented or minimized by co-administering pyridoxine (vitamin B6).

Pyrazinamide (PZA): Pyrazinamide is another first-line drug used in the treatment of TB, particularly in the intensive phase of therapy.

• 1. Mechanism of action: The exact mechanism of action of PZA is not fully understood, but it is believed to disrupt bacterial metabolism by inhibiting fatty acid synthetase-I, an enzyme involved in mycobacterial fatty acid synthesis. This impairs mycobacterial growth and survival.

• 2. Pharmacokinetics: PZA is well-absorbed orally and penetrates well into tissues, including the acidic environment of macrophages where M. tuberculosis resides. It is metabolized in the liver to its active form, pyrazinoic acid.

• 3. Clinical use: PZA is typically used as part of combination therapy for TB, particularly in the initial phase of treatment. It is usually administered orally, either daily or intermittently, depending on the treatment regimen.

• 4. Adverse effects: Common side effects of PZA include hepatotoxicity, gastrointestinal disturbances, arthralgia, and hyperuricemia. PZA can also exacerbate gout due to its effect on uric acid metabolism, requiring caution in patients with pre-existing gout or hyperuricemia.

Q.30 Define and Classify Antihypertensives. Write a detailed note on any two antihypertensive drugs.

Antihypertensive drugs are used to treat high blood pressure (hypertension). Hypertension is a risk factor for cardiovascular diseases such as heart attack, stroke, and heart failure. Antihypertensive drugs work by lowering blood pressure through various mechanisms. It includes reducing cardiac output, decreasing peripheral vascular resistance, and promoting sodium and water excretion.

Classification

• 1. Diuretics: Diuretics increase urine production, leading to decreased blood volume and reduced fluid retention, which ultimately lowers blood pressure. Examples are thiazide diuretics (e.g., hydrochlorothiazide), loop diuretics (e.g., furosemide), and potassium-sparing diuretics (e.g., spironolactone).

• 2. Beta-blockers: Beta-blockers block the effects of adrenaline (epinephrine) and noradrenaline (norepinephrine) on beta-adrenergic receptors in the heart and blood vessels. This results in decreased heart rate, contractility, and cause vasodilation. Examples are atenolol, metoprolol, and propranolol.

• 3. Angiotensin-converting enzyme (ACE) inhibitors: ACE inhibitors block the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This leads to vasodilation and decreased blood pressure. Examples are lisinopril, enalapril, and ramipril.

• 4. Angiotensin II receptor blockers (ARBs): ARBs block the binding of angiotensin II to its receptors. It prevents vasoconstriction and aldosterone release. This leads to vasodilation and decreased blood pressure. Examples are losartan, valsartan, and irbesartan.

• 5. Calcium channel blockers (CCBs): Calcium channel blockers inhibit the influx of calcium ions into vascular smooth muscle cells, leading to vasodilation and decreased peripheral vascular resistance. Examples are amlodipine, diltiazem, and verapamil.

• 6. Alpha-blockers: Alpha-blockers block alpha-adrenergic receptors in blood vessels. This leads to vasodilation and decreased peripheral vascular resistance. Examples are doxazosin, prazosin, and terazosin.

Lisinopril (ACE inhibitor): Lisinopril is an ACE inhibitor commonly used to treat hypertension and heart failure.

• 1. Mechanism of action: Lisinopril inhibits the enzyme ACE, which converts angiotensin I to angiotensin II. By blocking this enzyme, lisinopril reduces the production of angiotensin II. This leads to vasodilation, decreased peripheral vascular resistance, and reduced blood pressure.

• 2. Clinical use: Lisinopril is typically administered orally once daily. It is effective as monotherapy or in combination with other antihypertensive drugs. Lisinopril is also used to improve outcomes in patients with heart failure and to prevent kidney damage in individuals with diabetes.

• 3. Adverse effects: cough, dizziness, headache, hypotension, and hyperkalemia. Rare but serious adverse effects include angioedema, renal dysfunction, and fetal toxicity during pregnancy.

Amlodipine (Calcium channel blocker): Amlodipine is a calcium channel blocker used to treat hypertension and angina (chest pain).

• 1. Mechanism of action: Amlodipine inhibits the influx of calcium ions into vascular smooth muscle cells by blocking L-type calcium channels. This leads to vasodilation, decreased peripheral vascular resistance, and reduced blood pressure.

• 2. Clinical use: Amlodipine is administered orally once daily. It is often used as first-line therapy for hypertension, either alone or in combination with other antihypertensive drugs. Amlodipine is also used to relieve symptoms and improve exercise tolerance in patients with angina.

• 3. Adverse effects: Common side effects of amlodipine include peripheral edema, headache, dizziness, flushing, and fatigue. Serious adverse effects are rare but may include hypotension, bradycardia, and exacerbation of heart failure symptoms.