NHCON, Calicut

Pharmacology give reason questions and answers

1.ANS

1. Adrenaline along with local anesthetics

Adrenaline has vasoconstrictive properties that can reduce bleeding at the site of injection. This
is particularly beneficial in procedures where minimal bleeding is desirable, such as dental
extractions or surgeries involving delicate tissues.

2. Dobutamine in cardiogenic shock

Dobutamine is a synthetic catecholamine that primarily acts as a beta-1 adrenergic agonist. By
stimulating beta-1 receptors in the heart, it increases myocardial contractility (the force of heart
muscle contraction) and heart rate, leading to improved cardiac output (the amount of blood the
heart pumps per minute).

3. Adrenaline in anaphylactic shock

Vasoconstriction: Adrenaline acts on alpha-1 adrenergic receptors to induce vasoconstriction,
which helps to reverse the vasodilation and increased vascular permeability seen in
anaphylactic shock. This vasoconstrictive effect helps maintain blood pressure and improves
perfusion to vital organs, preventing cardiovascular collapse

4. Tamsulosin in BPH
Alpha-1 Blockade: Tamsulosin belongs to a class of medications known as alpha-1 adrenergic
blockers. It works by selectively blocking alpha-1 receptors in the prostate gland, the prostate
capsule, and the bladder neck. By blocking these receptors, tamsulosin relaxes the smooth
muscle in these areas, leading to improved urinary flow and relief of urinary symptoms
associated with BPH.

5. Beta blockers (Propanalol) contraindicated in asthma

Bronchoconstriction: Beta blockers can block beta-2 adrenergic receptors in the lungs, which
are responsible for bronchodilation (opening up the airways). In individuals with asthma, whose
airways are already hyperresponsive and prone to bronchoconstriction, blocking these receptors
can lead to worsening of asthma symptoms, including wheezing, shortness of breath, and chest
tightness.

6. Atropine i.v. in Organophosphate poisoning

Mechanism of Action: Organophosphates inhibit the enzyme acetylcholinesterase, which results
in the accumulation of acetylcholine at nerve endings and excessive stimulation of cholinergic
receptors throughout the body. Atropine acts as a competitive antagonist of acetylcholine at
muscarinic receptors, blocking its effects and counteracting the cholinergic overstimulation
caused by organophosphates.
2. NSAIDs

1. Aspirin contraindicated in asthmatics

Bronchoconstriction: Aspirin and other NSAIDs can inhibit the cyclooxygenase (COX) enzyme,
leading to decreased production of prostaglandins. In individuals with AERD, this inhibition of
COX pathways results in the accumulation of leukotrienes, potent mediators of
bronchoconstriction and inflammation. As a result, aspirin ingestion can precipitate severe
bronchoconstriction and respiratory distress in asthmatic individuals with AERD.

2. Indomethacin contraindicated with warfarin

Anticoagulant Effect of Warfarin: Warfarin is an anticoagulant medication commonly used to
prevent blood clot formation. It works by inhibiting the synthesis of vitamin K-dependent clotting
factors in the liver, thereby prolonging the time it takes for blood to clot.
NSAID Interaction: Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID) that inhibits
the enzyme cyclooxygenase (COX), thereby reducing the production of prostaglandins, which
are involved in inflammation and pain. Like other NSAIDs, indomethacin can also inhibit platelet
function and prolong bleeding time.
So, When indomethacin is taken concurrently with warfarin, the combination can potentiate the
anticoagulant effect of warfarin, leading to an increased risk of bleeding. This can manifest as
easy bruising, prolonged bleeding from minor cuts or injuries, gastrointestinal bleeding, or even
serious bleeding events such as intracranial hemorrhage.

3. Local and general anesthetics

1. Antihistaminics as preanesthetic medication

Sedation: Some antihistamines, such as diphenhydramine (Benadryl) and hydroxyzine (Vistaril),
have sedative properties. Administering these medications before anesthesia can help induce
drowsiness and calmness in patients, reducing anxiety and promoting relaxation before surgery.

Antiemetic Effects: Certain antihistamines, such as promethazine (Phenergan) and

dimenhydrinate (Dramamine), have antiemetic properties, meaning they can help prevent or
reduce nausea and vomiting associated with anesthesia and surgery. This can be particularly
beneficial for patients who are prone to postoperative nausea and vomiting (PONV).
Anticholinergic Effects: Some antihistamines, like diphenhydramine and hydroxyzine, also
possess anticholinergic properties. This can help reduce secretions in the respiratory and
gastrointestinal tracts, which may be beneficial during anesthesia and surgery to prevent airway
obstruction and decrease the risk of aspiration.
Allergic Reactions: Preanesthetic antihistamines may be administered to patients with a history
of allergic reactions to anesthesia or other medications used during surgery. By blocking
histamine receptors, these medications can help prevent or mitigate allergic reactions.

2. Ketamine is safe in asthmatics, why?

Bronchodilator Properties: Ketamine has bronchodilator effects, meaning it can help relax the
smooth muscles of the airways and improve airflow. This property can be beneficial for
asthmatic patients, as it can alleviate bronchoconstriction and respiratory distress.
Preservation of Airway Reflexes: Unlike many other anesthetic agents, ketamine preserves
airway reflexes and respiratory drive. This means that it does not depress respiratory function to
the same extent as other anesthetics and is less likely to cause respiratory depression in
asthmatic patients.

4. CNS

1. Zolpidem preferred over diazepam as anxiolytics

2. Diazepam used in status epilepticus
Diazepam acts as an anticonvulsant by enhancing the activity of gamma-aminobutyric acid
(GABA), an inhibitory neurotransmitter in the brain that helps regulate neuronal excitability. By
increasing GABAergic inhibition, diazepam suppresses seizure activity and helps terminate
ongoing seizures.
3.Levodopa and carbidopa combination in Parkinsonism
Enhanced Levodopa Bioavailability: The combination of levodopa and carbidopa enhances the
bioavailability and central nervous system penetration of levodopa, allowing for more efficient
conversion to dopamine in the brain. This results in greater efficacy in alleviating motor
symptoms of Parkinson's disease compared to levodopa alone.

4. Fluoxetine as an antidepressant
Mechanism of Action: Fluoxetine works by selectively inhibiting the reuptake of serotonin, a
neurotransmitter involved in regulating mood, emotions, and behavior, into presynaptic neurons.
By increasing serotonin levels in the synaptic cleft, fluoxetine helps enhance neurotransmission
and improve mood regulation.

5. Morphine contraindicated in asthmatics

Respiratory Depression: Morphine is a potent opioid analgesic that acts primarily by binding to
opioid receptors in the central nervous system, including the brainstem respiratory centers. One
of the most significant risks associated with morphine use is respiratory depression, which can
result in decreased respiratory rate and depth, leading to hypoxia and respiratory failure. In
individuals with asthma, who may already have compromised respiratory function due to
bronchoconstriction and airway inflammation, the risk of respiratory depression is particularly
concerning.

6. Morphine contraindicated in patients with head injury

morphine can lead to vasodilation and potentially increase cerebral blood flow, which may
exacerbate elevations in intracranial pressure. Elevated ICP is a significant concern in patients
with head injury, as it can lead to further brain injury, herniation, and neurological deterioration.
Administration of morphine may worsen cerebral edema and increase ICP, potentially
worsening outcomes in these patients.
7. Naloxone in morphine poisoning
Mechanism of Action: Naloxone is a competitive opioid receptor antagonist, meaning it binds to
opioid receptors in the brain and displaces opioids such as morphine, blocking their effects. By
antagonizing opioid receptors, naloxone rapidly reverses the respiratory depression, sedation,
and other central nervous system effects caused by opioids like morphine.

8. Chlorpromazine used in psychosis

Antipsychotic Properties: Chlorpromazine belongs to a class of medications known as typical or
first-generation antipsychotics. It exerts its therapeutic effects by antagonizing dopamine
receptors in the brain, particularly D2 receptors. By blocking dopamine transmission in certain
brain regions, chlorpromazine helps alleviate positive symptoms of psychosis, such as
hallucinations, delusions, and thought disturbances.

9. Rationale for diazepam over phenobarbitone as sedative Less Risk of Respiratory

Depression: While both medications can cause respiratory depression, diazepam generally has
a lower risk compared to phenobarbital, particularly at therapeutic doses. This may make
diazepam a preferred option in patients with compromised respiratory function or those at risk of
respiratory depression, such as individuals with chronic obstructive pulmonary disease (COPD)
or obstructive sleep apnea.
Lower Risk of Hypotension: Diazepam is less likely to cause significant hypotension compared
to phenobarbital, which may be important in patients with hemodynamic instability or
hypovolemia.
Anticonvulsant Properties: Diazepam has anticonvulsant properties and is commonly used in
the management of status epilepticus and acute seizures. In situations where sedation and
seizure control are both desired, diazepam may be preferred over phenobarbital.

5. Drugs acting on kidney

1. Spironolactone combined with hydrochlorothiazide, rationale?Synergistic Mechanisms of

Action: Spironolactone is a potassium-sparing diuretic that acts by antagonizing the aldosterone
receptor in the distal convoluted tubule and collecting ducts of the kidney. By blocking
aldosterone's effects, spironolactone promotes sodium and water excretion while conserving
potassium. Hydrochlorothiazide, on the other hand, is a thiazide diuretic that works by inhibiting
sodium reabsorption in the distal convoluted tubule, leading to increased excretion of sodium,
chloride, and water. By targeting different sites of the renal tubules and employing
complementary mechanisms, the combination of spironolactone and hydrochlorothiazide
provides enhanced diuretic and antihypertensive effects compared to either medication alone.

2. Furosemide contraindicated in patients with aminoglycosides

Nephrotoxicity: Aminoglycoside antibiotics are known to cause nephrotoxicity, particularly acute
tubular necrosis, which can lead to renal impairment and kidney damage. Furosemide, a loop
diuretic, exerts its diuretic effects by inhibiting sodium reabsorption in the renal tubules, leading
to increased urinary excretion of sodium, chloride, and water. When used concurrently with
aminoglycosides, furosemide may exacerbate renal dysfunction and increase the risk of
nephrotoxicity, especially in patients with pre-existing renal impairment or those receiving high
doses of aminoglycosides.

3. Mannitol contraindicated in renal failures

Exacerbation of Electrolyte Imbalances: Mannitol administration can lead to electrolyte
imbalances, including hyponatremia (low sodium levels), hypokalemia (low potassium levels),
and dehydration. In patients with renal failure, who may already have electrolyte disturbances
due to impaired renal excretion, the additional electrolyte losses induced by mannitol can
exacerbate these imbalances and lead to further complications.

6. Drugs affecting blood and CVS

1. Vitamin K in oral anticoagulant toxicity

Vitamin K is an essential cofactor in the synthesis of clotting factors II, VII, IX, and X in the liver.
These clotting factors are inhibited by vitamin K antagonists such as warfarin, which block the
recycling of vitamin K epoxide back to its active form, leading to depletion of functional vitamin K
and decreased synthesis of clotting factors. By administering exogenous vitamin K, the
synthesis of clotting factors can be restored, reversing the anticoagulant effects of warfarin.

2. Beta blockers in CCF

Beta blockers work by blocking the effects of catecholamines (such as adrenaline and
noradrenaline) on beta-adrenergic receptors in the heart and other tissues. By antagonizing
these receptors, beta blockers reduce the heart rate, myocardial contractility, and sympathetic
nervous system activity, leading to decreased myocardial oxygen demand and improved cardiac
function.

3. Enalapril contraindicated in pregnancy, why?

Fetal Renal Damage: Enalapril is an angiotensin-converting enzyme (ACE) inhibitor, which
works by blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor.
Inhibition of the renin-angiotensin-aldosterone system (RAAS) by ACE inhibitors can lead to
decreased fetal renal perfusion and impaired kidney development, resulting in oligohydramnios
(reduced amniotic fluid volume), fetal renal dysplasia, renal failure, and even death.
Fetal Cardiovascular Effects: ACE inhibitors like enalapril can also cause fetal cardiovascular
abnormalities, including hypotension, hypoperfusion, and cardiovascular malformations. These
effects can lead to intrauterine growth restriction (IUGR), fetal distress, and developmental
abnormalities of the heart and blood vessels.

4. ACE inhibitors contraindicated with K+ sparing diuretics

Potassium Retention: ACE inhibitors can reduce aldosterone secretion by inhibiting the
angiotensin-converting enzyme (ACE), which leads to decreased sodium reabsorption and
potassium excretion in the renal tubules. This effect can increase serum potassium levels,
particularly in patients with impaired renal function or other risk factors for hyperkalemia.
Additive Effect: Potassium-sparing diuretics, such as spironolactone and amiloride, work by
blocking the epithelial sodium channels (ENaC) in the distal renal tubules, leading to decreased
sodium reabsorption and potassium retention. When used concomitantly with ACE inhibitors,
the potassium-sparing effect of diuretics can be additive, further increasing the risk of
hyperkalemia.

5. Diltiazem avoided in AV block

Diltiazem has negative chronotropic effects, meaning it slows the heart rate by decreasing the
rate of sinoatrial (SA) node depolarization and impulse conduction. In patients with AV block,
where the conduction of electrical impulses from the atria to the ventricles is already impaired,
further slowing of the heart rate by diltiazem can worsen AV block and lead to bradycardia or
complete heart block.

6. Digoxin contraindicated in hypokalemics

Hypokalemia (low potassium levels) can potentiate the effects of digoxin by increasing its
binding to the sodium-potassium ATPase pump in cardiac myocytes. This can lead to enhanced
cardiac glycoside toxicity, including an increased risk of arrhythmias such as ventricular
tachycardia or fibrillation.

7. Nitrate free interval in patients receiving long term nitrates

patients receiving long-term nitrates for the management of angina or heart failure, a nitrate-free
interval is often recommended to prevent the development of nitrate tolerance. Nitrate tolerance
occurs when the body becomes less responsive to the vasodilatory effects of nitrates over time,
leading to reduced efficacy of nitrate therapy. A nitrate-free interval helps to minimize the
development of tolerance and maintain the effectiveness of nitrate therapy.

8. Sublingual nitroglycerine in acute anginal attack

Rapid Vasodilation: Sublingual nitroglycerin is absorbed quickly through the mucous
membranes under the tongue and enters the bloodstream, where it acts as a vasodilator.
Nitroglycerin primarily dilates veins, leading to venous pooling and reduced preload on the
heart. This decreases cardiac workload and myocardial oxygen demand, helping to relieve
anginal symptoms such as chest pain or discomfort.

9. Statins contraindicated in pregnancy

Fetal Toxicity: Statins can cross the placenta and reach the developing fetus, where they may
interfere with fetal cholesterol synthesis and disrupt normal developmental processes. This can
lead to fetal toxicity and adverse outcomes, including growth restriction, fetal demise, and
neonatal complications.

10. List two drugs used in CPR with their rationale

Epinephrine:

Rationale: Epinephrine is a potent vasoconstrictor and adrenergic agonist that increases

systemic vascular resistance and enhances myocardial contractility. In CPR, epinephrine is
administered to improve coronary and cerebral perfusion pressure, increase cardiac output, and
enhance the chances of successful resuscitation. It acts on alpha-1 adrenergic receptors to
constrict peripheral blood vessels, thereby redirecting blood flow to vital organs such as the
heart and brain. Epinephrine also stimulates beta-1 adrenergic receptors in the heart, leading to
increased myocardial contractility and heart rate. These effects help restore circulation and
improve the likelihood of return of spontaneous circulation (ROSC) during cardiac arrest.
Amiodarone:

Rationale: Amiodarone is an antiarrhythmic medication with multiple mechanisms of action,

including blockade of sodium, potassium, and calcium channels, as well as inhibition of
adrenergic receptors. In CPR, amiodarone is used to treat shock-refractory ventricular fibrillation
(VF) or pulseless ventricular tachycardia (VT) that persists despite defibrillation attempts. By
stabilizing the myocardial cell membrane and prolonging the action potential duration,
amiodarone helps terminate malignant ventricular arrhythmias and restore normal cardiac
rhythm. Additionally, amiodarone has a relatively long half-life, allowing for sustained
antiarrhythmic effects and reducing the likelihood of recurrent ventricular arrhythmias following
successful resuscitation.

11. Beta blockers avaoided in patients receiving insulin, why?

Masking of Hypoglycemia Symptoms: Beta blockers can mask the adrenergic symptoms of
hypoglycemia, such as tremors, tachycardia, and palpitations, which are important warning
signs that help individuals recognize and respond to low blood sugar levels. By blocking the
sympathetic response to hypoglycemia, beta blockers can delay or prevent the recognition of
hypoglycemic episodes, leading to a higher risk of severe hypoglycemia and its associated
complications, including loss of consciousness and seizures.

12.Enalapril used in hypertension, give reason?

Angiotensin-Converting Enzyme (ACE) Inhibitor: Enalapril belongs to the class of medications
known as ACE inhibitors, which work by inhibiting the conversion of angiotensin I to angiotensin
II. Angiotensin II is a potent vasoconstrictor and plays a key role in regulating blood pressure by
constricting blood vessels. By blocking the production of angiotensin II, enalapril causes
vasodilation and reduces systemic vascular resistance, leading to a decrease in blood pressure.