THIRD BHMS
PHARMACOLOGY QUESTION BANK
question bank according to CBDC syllabus
M - MCQ | S - SAQ | L - LAQ | V - VIVA/PRACTICAL | Ø - NON
Major Drug Classifications
A = ANS AND AUTACOID
1. Cholinergic and Anticholinergic Drugs
A] Introduction
-Definition of cholinergic (parasympathomimetic) and anticholinergic (parasympatholytic) drugs.
-Overview of acetylcholine receptors – muscarinic (M₁–M₅) and nicotinic (Nₙ, Nₘ)
B] Mechanism of Action
-Cholinergic drugs:
–Mimic acetylcholine → increase parasympathetic activity.
-Anticholinergic drugs:
–Block muscarinic receptors → inhibit parasympathetic actions
C] Classification
-Direct-acting cholinergic agonists (e.g., acetylcholine, pilocarpine).
-Indirect-acting cholinergic agonists (anticholinesterases) (e.g., neostigmine, physostigmine).
-Muscarinic antagonists (e.g., atropine, scopolamine).
D] Clinical Applications
-Glaucoma (pilocarpine)
-Myasthenia gravis (neostigmine)
-COPD and asthma (ipratropium)
-Motion sickness (scopolamine)
E] Adverse Effects
-Cholinergic: Bradycardia, diarrhea, sweating.
-Anticholinergic: Dry mouth, tachycardia, blurred vision, urinary retention.
F] Key Comparison
a) Cholinergic drugs:
–Action – Mimic the action of acetylcholine (ACh).
–System Effect -Stimulate the parasympathetic nervous system.
–Example -Neostigmine
b) Anticholinergic drugs:
–Action – Block the action of acetylcholine (ACh).
–System Effect -Inhibit the parasympathetic nervous system.
–Example -Atropine
2. Adrenergic & Antiadrenergic Drugs, T/t of Glaucoma
A] Introduction
-Adrenergic drugs (sympathomimetics): Stimulate the sympathetic nervous system (SNS).
-Antiadrenergic drugs (sympatholytics): Inhibit SNS activity.
-Act on adrenergic receptors – α (alpha) and β (beta) types- (α₁, α₂, β₁, β₂, β₃).
B] Mechanism of Action
a) Adrenergic agonists:
–Stimulate α or β receptors → increase heart rate, BP, bronchodilation.
b) Antiadrenergic drugs:
–Block adrenergic receptors → decrease HR, BP, and cardiac output.
C] Classification
a) Adrenergic agonists
–Direct-acting: act on receptors directly (e.g., adrenaline, noradrenaline).
–Indirect-acting: increase release of noradrenaline (e.g., amphetamine).
–Mixed-acting: both direct and indirect (e.g., ephedrine).
b) Antiadrenergic drugs/Adrenergic blockers
–Alpha blockers: Prazosin (α₁-selective), Phenoxybenzamine.
–Beta blockers: Atenolol (β₁-selective), propranolol (non-selective).
D] Miller’s Principles for Antiadrenergic Drugs
-Selective blockade: Target α₁ or β₁ to minimize side effects.
-Sympathetic inhibition: Reduce HR and BP.
-Receptor affinity and potency: Guide drug selection (e.g., atenolol for cardiac patients).
E] Clinical Applications
a) Adrenergic drugs:
–Asthma (β₂ agonists – salbutamol)
–Hypotension and shock (α agonists – norepinephrine)
–Cardiac arrest (epinephrine)
–Glaucoma: Reduce intraocular pressure using α₂ agonists (e.g., brimonidine)
b) Antiadrenergic drugs:
–Hypertension (β₁ blockers – atenolol)
–Angina, arrhythmias, heart failure (β blockers)
–Glaucoma: Reduce aqueous humor production using β-blockers (e.g., timolol)
F] Adverse Effects
a) Adrenergic drugs:
– Tachycardia, hypertension, tremors, insomnia.
b) Antiadrenergic drugs:
– Bradycardia, hypotension, fatigue, dizziness, possible bronchospasm in asthma patients.
G] Key Comparison
a) Adrenergic drugs –
–Stimulate SNS → ↑ heart rate, ↑ BP, bronchodilation.
b)Antiadrenergic drugs –
–Block SNS → ↓ heart rate, ↓ BP, vasodilation.
H] Treatment of Glaucoma
The aim of glaucoma treatment is to reduce intraocular pressure (IOP) and prevent optic nerve damage. Treatment can be medical, laser, or surgical.
1. Medical (Drug) Therapy
a) Cholinergic (Miotics) –
–Increase aqueous humor outflow
–Example: Pilocarpine
–Action: Constricts the pupil (miosis), opens trabecular meshwork to reduce IOP.
b) Adrenergic Agonists –
–Reduce aqueous humor production
–Example: Brimonidine
–Action: Decreases fluid production and increases outflow.
c) Beta-Blockers –
–Reduce aqueous humor production
–Example: Timolol
–Action: Lowers IOP by decreasing fluid secretion.
d) Carbonic Anhydrase Inhibitors –
–Reduce aqueous humor formation
–Example: Acetazolamide (oral), Dorzolamide (topical)
e) Prostaglandin Analogues –
–Increase uveoscleral outflow
–Example: Latanoprost, Bimatoprost
–Action: Improve drainage of aqueous humor, lowering IOP.
2. Laser Therapy
-Trabeculoplasty: Improves drainage through trabecular meshwork.
-Iridotomy: Creates a hole in the iris for fluid flow in angle-closure glaucoma.
3. Surgical Therapy
-Trabeculectomy: Creates a new drainage pathway for aqueous humor.
-Glaucoma drainage implants: Used in refractory cases.
3. Autacoids: Serotonin and drugs acting or Serotonergic System
A] Introduction
-Autacoids: Locally acting biological mediators (e.g., serotonin, histamine).
B] Serotonin
-Serotonin (5-HT): Neurotransmitter in CNS and periphery; regulates mood, sleep, appetite, vascular tone, and GI motility.
C] Serotonergic Drugs
a) SSRIs (Selective Serotonin Reuptake Inhibitors):
–Increase serotonin levels in synapses → treat depression and anxiety.
b) SNRIs (Serotonin-Norepinephrine Reuptake Inhibitors):
–Increase serotonin and norepinephrine → treat depression and neuropathic pain.
c) 5-HT1B/1D Agonists (Triptans):
–Constrict cranial blood vessels → relieve migraine attacks.
d) 5-HT3 Antagonists:
–Block serotonin receptors in GI → prevent nausea and vomiting.
e) 5-HT4 Agonists:
–Increase GI motility → treat constipation-related disorders.
f) Serotonin Modulators:
–Adjust serotonin signaling for various CNS and peripheral effects.
D] Mechanism of Action
-SSRIs/SNRIs: Block reuptake → ↑ serotonin (and norepinephrine for SNRIs).
-Triptans: Activate 5-HT1B/1D receptors → vasoconstriction and reduced neurogenic inflammation.
-5-HT3 antagonists: Prevent serotonin-induced nausea.
-5-HT4 agonists: Enhance peristalsis in GI tract.
E] Clinical Applications
-SSRIs: Depression, anxiety.
-SNRIs: Depression, neuropathic pain.
-Triptans (5-HT1B/1D agonists): Acute migraine attacks.
-5-HT3 antagonists: Chemotherapy-induced nausea.
-5-HT4 agonists: GI motility disorders.
4. Autacoids: Histamine and Antihistaminic & T/t of Migraine
A] Histamine:
-Biogenic amine formed from histidine; acts as a local mediator in allergic reactions, inflammation, gastric acid secretion, and CNS neurotransmission.
-Released from mast cells, basophils, and neurons in response to allergens or injury.
-Causes vasodilation, increased capillary permeability, bronchoconstriction, and itching.
b] Antihistaminics:
-Drugs that block histamine receptors (H₁, H₂, H₃, H₄) to counter histamine’s effects.
-H₁ blockers: Relieve allergic symptoms, motion sickness, and vertigo.
-H₂ blockers: Reduce gastric acid secretion → used in peptic ulcer and GERD.
-H₃ and H₄ antagonists: Under study for neurological and inflammatory disorders.
-Classified as first-generation (sedating) or second-generation (non-sedating) depending on CNS penetration
C] Migraine Treatments
a) Acute Treatments (Stop migraine attacks):
–NSAIDs: Reduce pain and inflammation.
–Ergot Alkaloids: Constrict cranial blood vessels.
–Anti-nausea medications: Prevent or treat vomiting associated with migraine.
b) Preventive Treatments (Reduce frequency/severity):
–Beta-blockers: Reduce sympathetic activity; useful in migraine prophylaxis.
–Anticonvulsants: Stabilize neuronal activity to prevent attacks.
–Calcium Channel Blockers: Prevent vascular changes triggering migraines.
–CGRP (Calcitonin Gene-Related Peptide) Antagonists: Block CGRP → reduce migraine attacks.
–Tricyclic Antidepressants (TCAs): Modulate neurotransmitters for migraine prevention.
D] Pathophysiology
-Migraines involve neurovascular changes, serotonin signaling, and CGRP pathways.
E] Migraine Types
a) With aura: Visual or sensory disturbances before headache.
b) Without aura: Headache without warning signs.
F] Therapy Classification
-Acute therapy: Stop attacks once they start.
-Preventive therapy: Reduce frequency, intensity, or duration of attacks.
G] Key Points
-Histamine and serotonin are important mediators in migraine pathophysiology.
-Treatments are chosen based on migraine type and whether the goal is acute relief or prevention.
B = NSAID
1. Drugs used in Rheumatoid Arthritis
A] Understand Pathophysiology
-Explain the autoimmune nature of rheumatoid arthritis.
-Describe the role of cytokines such as TNF-α and IL-6 in joint inflammation and destruction.
B] Classify Drugs Used in RA
Differentiate between major drug groups:
–NSAIDs – for symptomatic relief
–Corticosteroids – for short-term inflammation control
–DMARDs (Disease-Modifying Antirheumatic Drugs) – for long-term disease control
–Biologic Agents – targeting specific cytokines (e.g., TNF inhibitors, IL-6 blockers)
C] Select Appropriate Therapies
-Choose treatment based on disease severity, progression, and response to prior therapy.
-Combine conventional DMARDs and biologics when indicated.
D] Monitor for Adverse Effects
Recognize and prevent toxicities:
–Methotrexate: hepatotoxicity, bone marrow suppression
–Biologics: increased infection risk, especially tuberculosis reactivation
2. Drugs used in Gout
A] Identify Pathophysiology
-Explain the role of hyperuricemia and urate crystal deposition in joint inflammation.
B] Classify Drugs Used in Gout
a) Acute Gout: NSAIDs, colchicine, corticosteroids
b) Chronic Gout: Xanthine oxidase inhibitors (e.g., allopurinol, febuxostat), Uricosuric agents (e.g., probenecid)
C] Manage Comorbidities
-Consider renal function and cardiovascular health when selecting therapy.
-Avoid drugs that exacerbate gout (e.g., thiazide diuretics).
C = CNS
1. Anxiolytics
A] Introduction
-Drugs that reduce anxiety and promote calm without sedation.
B] Key Principles of Use
-Treatment should be individualized for each patient.
-Minimize long-term use to avoid dependence or tolerance.
-Balance efficacy and safety.
-May be used in combination with psychotherapy or other medications.
-Educate patients on safe use and potential side effects.
C] Mechanism of Action
a) Benzodiazepines:
–Enhance GABA activity → CNS inhibition → anxiolytic effect.
b) SSRIs:
–Increase serotonin in CNS → reduce anxiety over long-term use.
c) Buspirone:
–Partial serotonin receptor agonist → anxiolytic effect without sedation.
D] Clinical Applications
-Generalized anxiety disorder, panic disorder, social anxiety, short-term relief of severe anxiety.
E] Adverse Effects
-Sedation, dizziness, cognitive impairment (benzodiazepines).
-Gastrointestinal upset, sleep disturbances (SSRIs).
-Minimal sedation with buspirone.
2. Antiepileptics
A] Introduction
-Drugs used to prevent or control seizures in epilepsy.
B] Key Principles of Use
-Personalized treatment: Choose drug based on seizure type, age, comorbidities.
-Monotherapy preferred when possible.
-Dose titration and monitoring to balance efficacy and toxicity.
-Minimize drug interactions.
-Long-term management: Regular follow-up and monitoring.
-Consider non-pharmacological treatments as adjuncts.
-Patient education and adherence are critical.
-Aim for seizure-free outcome.
-Discontinuation considered only after sustained seizure control
C] Mechanism of Action
-Na⁺ channel blockers: Stabilize neuronal membranes.
-GABA enhancers: Increase inhibitory neurotransmission.
-Ca²⁺ channel blockers: Reduce neuronal excitability.
-Glutamate inhibitors: Decrease excitatory signaling.
D] Clinical Applications
-Tailor AEDs to type of epilepsy: generalized, focal, or absence seizures.
-Adjust dose based on patient-specific factors and previous response.
E] Monitoring & Safety
-Therapeutic drug monitoring to maintain effective serum levels.
-Watch for side effects: cognitive impairment, liver/kidney toxicity, hematologic effects.
-Monitor for drug interactions that may alter efficacy or increase toxicity.
F] Key Points
-Understanding pharmacology, mechanism, and individualized patient care is essential.
-Safe use and adherence improve long-term outcomes in epilepsy and anxiety disorders.
3. Antipsychotics and Antidepressants
A] Introduction
-Drugs used to manage psychiatric disorders such as schizophrenia, bipolar disorder, and depression.
B] Key Principles of Use
-Early and accurate diagnosis is essential.
-Choice of medication should be individualized.
-Personalized treatment based on patient needs and comorbidities.
-Minimize side effects through careful drug selection and dose adjustment.
-Use non-pharmacological support like psychotherapy or lifestyle interventions.
-Ongoing monitoring and dose adjustments improve outcomes.
-Patient education and adherence are critical for effectiveness.
-Consider tapering when discontinuing therapy to prevent withdrawal.
C] Mechanism of Action
a) SSRIs & SNRIs:
–Increase serotonin (and norepinephrine) in CNS → treat depression and anxiety.
b) Typical antipsychotics:
–Dopamine D₂ receptor antagonists → reduce psychotic symptoms.
c) Atypical antipsychotics:
–Dopamine and serotonin receptor modulators → fewer motor side effects.
D] Clinical Applications
-Depression, anxiety, schizophrenia, bipolar disorder, and other psychiatric conditions.
E] Key Points
-Tailor treatment: Start low, go slow.
-Understand pharmacology, pharmacokinetics, and clinical indications for each drug class.
4. Opioid Analgesics
A] Introduction
-Drugs used for moderate to severe pain management, both acute and chronic.
B] Key Principles of Use
a) Accurate pain assessment:
–Evaluate intensity, location, and cause using tools like Numeric Pain Rating Scale or Visual Analog Scale.
b) Appropriate indications:
–Acute pain (postoperative, trauma)
–Chronic pain (cancer, palliative care)
–Severe pain unresponsive to non-opioid therapy
c) Individualized treatment plans for each patient.
d )Risk mitigation:
–Monitor for tolerance, dependence, or addiction.
e) Side effect management:
–Constipation: Prophylactic laxatives
–Nausea/vomiting: Antiemetics
–Sedation: Dose adjustment or alternative medications
g) Avoid long-term use when possible.
C] Mechanism of Action
a)Full agonists:
–Activate opioid receptors fully → strong analgesia (e.g., morphine).
b)Partial agonists:
–Activate receptors partially → moderate analgesia, lower risk (e.g., buprenorphine).
c)Antagonists:
–Block receptors → reverse opioid effects (e.g., naloxone).
D] Clinical Applications
-Pain management in surgical, traumatic, or palliative settings.
-Adjust doses based on pain severity and patient-specific factors.
E] Key Points
a) Dosing and titration: Ensure adequate pain relief while minimizing side effects.
b) Patient-centered care: Educate patients on benefits, risks, and naloxone use.
c) Monitoring: Regular follow-up to assess efficacy and detect adverse effects.
D = Respiratory system
1. Drugs for cough
A] Accurate Diagnosis of the Underlying Cause
a) Conduct thorough assessment to identify the origin of cough:
–Respiratory infections: viral or bacterial
–Asthma or COPD
–Post-nasal drip
–Cardiac causes (e.g., heart failure)
b) Focus treatment on underlying cause rather than symptom suppression alone:
–Antibiotics for bacterial infections
–Bronchodilators for asthma
B] Classification of Cough
a) Dry (Non-productive) Cough: Treated with antitussives like dextromethorphan or codeine.
b) Productive Cough: Treated with expectorants such as guaifenesin to aid mucus clearance.
c) Acute vs. Chronic Cough:
–Acute: <3 weeks, often self-limited
–Chronic: >8 weeks, requires evaluation for underlying disease
C] Symptomatic Treatment
-Use antitussives for persistent dry cough interfering with daily life.
-Use expectorants or mucolytics to facilitate clearance in productive coughs.
D] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes:
–Pharmacology: Understand mechanisms, pharmacokinetics, and pharmacodynamics of antitussives and expectorants.
–Etiology Awareness: Identify causes of acute vs. chronic cough and match drug therapy to cough type.
–Drug Safety: Recognize side effects of opioid and non-opioid cough medications, ensuring safe use across populations.
2. Bronchial asthma and COPD
A] Accurate Diagnosis and Differentiation
a) Asthma: Reversible airway obstruction and inflammation, often triggered by allergens, irritants, or exercise.
b) COPD: Progressive, irreversible airflow limitation, usually due to smoking or environmental exposures.
c) Diagnosis guided by clinical symptoms, spirometry, and patient history.
B] Individualized Pharmacological Treatment
a) Asthma: Control inflammation, relieve bronchoconstriction, prevent exacerbations.
b) COPD: Focus on symptom relief, reduce exacerbations, slow disease progression.
c) Medication choice should consider age, disease severity, comorbidities, and exacerbation frequency.
C] Stepwise Approach to Asthma Management
a) Step 1 (Mild): Short-acting beta-agonists (SABA, e.g., albuterol) for symptom relief.
b) Step 2 (Persistent): Add inhaled corticosteroids (ICS, e.g., beclometasone, budesonide).
c) Step 3 (Moderate): Combine long-acting beta-agonists (LABA, e.g., salmeterol) with ICS.
d) Step 4 (Severe): Consider leukotriene receptor antagonists (LTRAs, e.g., montelukast) or biologics (omalizumab, dupilumab).
D] COPD Pharmacological Management
a) Short-Acting Bronchodilators:
–SABA (salbutamol), SAMA (ipratropium) for quick symptom relief.
b) Long-Acting Bronchodilators:
–LABA (formoterol), LAMA (tiotropium) for long-term management.
c) Inhaled Corticosteroids:
–Used with bronchodilators for patients with frequent exacerbations (e.g., fluticasone).
E] Monitoring and Adjusting Treatment
-Track lung function, symptoms, and exacerbation frequency.
-Asthma: step up or down therapy based on symptom control.
-COPD: adjust treatment considering symptoms, exacerbation history, and comorbidities.
F] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes:
–Pathophysiology: Understand inflammation, bronchoconstriction, and airway remodeling in asthma and COPD.
–Pharmacological Principles: Know drug classes (bronchodilators, corticosteroids, adjuncts) and their mechanisms.
–Diagnosis and Differentiation: Distinguish asthma vs. COPD using clinical and diagnostic criteria.
–Exacerbation Management: Recognize appropriate use of systemic corticosteroids, bronchodilators, and antibiotics during flare-ups.
–Inhaler Technique & Patient Education: Teach correct inhaler use, lifestyle modification, and non-pharmacological interventions to optimize outcomes.
E = Hormones
1. Insulin and oral Hypoglycemic drugs
A] Diabetes Mellitus: Diagnosis and Classification
a) Type 1 Diabetes (T1D):
–Autoimmune destruction of pancreatic beta cells; requires lifelong insulin therapy.
b) Type 2 Diabetes (T2D):
–Insulin resistance and progressive beta-cell dysfunction; managed with lifestyle and pharmacological therapy.
B] Insulin Therapy
a) For Type 1 Diabetes
–Basal insulin (e.g., glargine, detemir)
–Bolus insulin (e.g., aspart, lispro)
–Continuous insulin infusion (insulin pump)
b) For Type 2 Diabetes
–Initially managed with oral hypoglycemics
–Combination therapy with insulin + oral agents (e.g., metformin, sulfonylureas)
C] Oral Hypoglycemic Agents (OHAs)
a) Biguanides:
–Metformin – reduces hepatic glucose production, increases insulin sensitivity
b) Sulfonylureas:
–Glibenclamide, Glimepiride – stimulate insulin secretion
c) Thiazolidinediones (TZDs):
–Pioglitazone – increase insulin sensitivity via PPAR-γ
d) DPP-4 Inhibitors:
–Sitagliptin, Saxagliptin – enhance incretin action
e) SGLT2 Inhibitors:
–Empagliflozin, Dapagliflozin – increase urinary glucose excretion
f) GLP-1 Receptor Agonists:
–Exenatide, Liraglutide – increase insulin, reduce glucagon, delay gastric emptying
D] Monitoring and Treatment Adjustment
-Self-Monitoring of Blood Glucose (SMBG)
-Hemoglobin A1c (HbA1c) targets
-Renal function monitoring
E] Prevention and Management of Hypoglycemia
-Patient education on recognition and management
-Drug selection to minimize risk (SGLT2 inhibitors, DPP-4 inhibitors)
F] Management of Comorbidities
-Cardiovascular: SGLT2 inhibitors, GLP-1 agonists
-Renal: Regular monitoring in patients on metformin, insulin, SGLT2 inhibitors
G] Long-Term Management
-Lifestyle support: diet, exercise, weight management
-Patient engagement and follow-up
H] Standard Learning Outcomes(SLO)
a)Knowledge-Based Outcomes
–Pharmacodynamics, pharmacokinetics, and therapeutic use of insulin and OHAs
–Understanding of diabetes types and pathophysiology
–Awareness of drug safety, adverse effects, and contraindication
2. Adrenocortical and Androgenic Steroids
A] Adrenocortical Steroids
a) Glucocorticoids (Prednisone, Dexamethasone)
–Role: Anti-inflammatory, immunosuppressive
–Uses: asthma, autoimmune diseases, allergies
–Adverse effects: osteoporosis, diabetes, adrenal suppression
b) Mineralocorticoids (Fludrocortisone)
–Role: Regulate electrolytes and water balance
–Uses: Addison’s disease
–Adverse effects: sodium retention, hypokalemia, hypertension
c) Rational Use
–Short-acting: Hydrocortisone
–Intermediate-acting: Prednisone, Methylprednisolone
–Long-acting: Dexamethasone, Betamethasone
d) Management of Adverse Effects
–Monitor for Cushing’s syndrome, osteoporosis, hypertension, hyperglycemia, infections
e) Therapeutic Uses
–Anti-inflammatory, immunosuppressive therapy, transplantation
B] Androgenic Steroids
a) Natural Androgens (Testosterone)
–Role: Development and maintenance of male secondary sexual characteristics; anabolic effects on muscle and bone.
–Uses: Male hypogonadism, delayed puberty in males.
–Adverse effects: Acne, baldness, gynecomastia, infertility, hepatic dysfunction.
b) Synthetic Anabolic Steroids (Nandrolone, Stanozolol, Oxandrolone)
–Role: Promote protein synthesis, muscle growth, and bone strength.
–Uses: Anemia, muscle wasting, osteoporosis, catabolic states.
–Adverse effects: Liver toxicity, virilization in females, growth retardation in children, psychological dependence.
c) Rational Use
–Use only for documented androgen deficiency or specific medical indications.
–Avoid use for performance enhancement or cosmetic purposes.
d) Management of Adverse Effects
–Regular liver function tests, lipid profile, and hormonal monitoring.
–Watch for signs of aggression, acne, edema, and testicular atrophy.
e) Therapeutic Uses
–Replacement therapy in hypogonadism.
–Anabolic therapy in chronic wasting diseases.
–Adjunct therapy in certain anemias and osteoporosis.
3. Estrogens, Progesterone and OCPs
A] Estrogens
a) Physiological roles:
–secondary sexual characteristics, menstrual cycle, bone density
b) Therapeutic uses:
–HRT, hypogonadism, osteoporosis, certain cancers
c) Rational use:
–combine with progestins in women with intact uterus, lowest effective dose
d) Monitoring/adverse effects:
–thromboembolism, breast/endometrial cancer, liver/lipid profile
B] Progesterone
a) Physiological roles:
–menstrual cycle regulation, pregnancy maintenance
b)Therapeutic uses:
–HRT, abnormal uterine bleeding, endometriosis
c) Rational use:
–combine with estrogens, lowest effective dose
d) Monitoring/adverse effects:
–mood changes, weight gain, cardiovascular risks
C] Oral Contraceptive Pills (OCPs)
a) Types:
–Combined oral contraceptives (COCs) – estrogen + progestin
–Progestin-only pills (POPs) – preferred for breastfeeding or estrogen contraindications
b) Therapeutic applications:
–contraception, menstrual disorders, endometriosis, cancer risk reduction
c) Selection:
–based on patient history and side effects
d) Safety and monitoring:
–contraindications (thromboembolism, cancers, hypertension, migraines)
e) Managing side effects:
–dose adjustment, patient educationb)
D] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Pharmacodynamics, pharmacokinetics
–Indications and contraindications
4. Vitamin D, Calcium and Drugs affecting Calcium Balance
A] Physiological Roles
a) Vitamin D: regulates calcium/phosphate absorption, bone mineralization (Calcitriol, Cholecalciferol)
b) Calcium: bone structure, muscle contraction, nerve transmission, blood clotting
B] Therapeutic Applications
a)Vitamin D: rickets, osteomalacia, hypocalcemia, osteoporosis
b)Calcium: supplementation, hypocalcemia, osteoporosis, cardiac arrest
C] Rational Use
-Ensure adequate calcium intake with vitamin D therapy
-Use active forms in renal impairment
-Tailor dosage to patient needs
D] Monitoring and Adverse Effects
-Monitor serum calcium and vitamin D
-Avoid hypercalcemia, renal calculi, toxicity
E] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanisms of action on bone remodeling and calcium homeostasis
–Appropriate indications, dosages, formulations
–Recognition of side effects
F = CVS
1. T/t of Hypertension/Hypertension Management
A] Etiology and Pathophysiology
Identify the cause of hypertension:
a) Primary (essential) hypertension:
–Idiopathic but influenced by genetic and lifestyle factors.
b) Secondary hypertension:
–Caused by conditions such as renal artery stenosis, endocrine disorders, or medication use.
c) Understand the pathophysiological mechanisms:
–Increased systemic vascular resistance, volume overload, and sympathetic nervous system activation.
B] Therapeutic Goals
a) The primary goal is to reduce blood pressure to recommended targets:
– <140/90 mmHg for most adults.
– <130/80 mmHg for patients with diabetes, chronic kidney disease, or a history of cardiovascular disease.
b) Prevent complications such as stroke, myocardial infarction, and organ damage.
C] Pharmacological Treatment Options
Hypertension treatment requires patient-specific drug selection based on comorbidities, age, and ethnicity:
1. First-Line Agents:
a) Thiazide Diuretics (e.g,Hydrochlorothiazide, Chlorthalidone):
–Reduce blood volume by increasing urinary excretion of sodium and water.
b) ACE Inhibitors (e.g., Enalapril, Ramipril):
–Inhibit the renin-angiotensin aldosterone system (RAAS), reducing vasoconstriction and aldosterone secretion.
c) Angiotensin II Receptor Blockers (ARBs) (e.g., Losartan, Valsartan):
–Block angiotensin II receptors, reducing vasoconstriction.
d) Calcium Channel Blockers (CCBs) (e.g., Amlodipine, Nifedipine):
–Cause vasodilation by inhibiting calcium influx in vascular smooth muscle.
2. Second-Line and Add-On Agents:
a) Beta-Blockers (e.g., Metoprolol, Atenolol):
–Reduce heart rate and cardiac output.
b) Aldosterone Antagonists (e.g., Spironolactone, Eplerenone):
–Effective in resistant hypertension.
c) Alpha-Blockers (e.g., Doxazosin):
–Relax vascular smooth muscle to lower BP.
3. Other Agents:
a) Centrally Acting Drugs (e.g., Clonidine, Methyldopa):
–Reduce sympathetic outflow.
b) Direct Vasodilators (e.g., Hydralazine, Minoxidil):
–Reserved for severe or refractory hypertension.
D] Non-Pharmacological Measures
Emphasize lifestyle modifications for all patients:
a) Dietary Approaches to Stop Hypertension (DASH) diet: Rich in fruits, vegetables, and low-fat dairy.
b) Salt reduction: <2.3 grams of sodium/day.
c) Regular exercise: At least 150 minutes of moderateintensity aerobic activity per week.
d) Weight loss: Aim for BMI <25 kg/m².
e) Smoking cessation and limiting alcohol intake.
E] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Understanding Pathophysiology: Describe the mechanisms contributing to hypertension and the pharmacological targets of antihypertensive drugs.
–Therapeutic Principles: Understand the indications, mechanisms, and contraindications of different antihypertensive drugs.
–Risk Stratification: Learn to assess cardiovascular risk and tailor treatment to reduce complications.
b) Skill-Based Outcomes
–Blood Pressure Measurement: Accurately measure and interpret blood pressure values using standard techniques
2. Angina, MI
A] Types of Angina
a) Stable Angina: Caused by a fixed coronary artery obstruction.
b) Unstable Angina: Part of acute coronary syndrome (ACS), often due to plaque rupture.
c) Prinzmetal (Variant) Angina: Caused by coronary vasospasm.
B] Goals of Therapy - Angina
-Alleviate symptoms by improving oxygen supplydemand balance.
-Prevent progression to MI or sudden cardiac death.
-Improve quality of life and physical activity tolerance.
C] Drug Classes for Angina
1. Nitrates:
-E.g., Nitroglycerin, Isosorbide Dinitrate
-Mechanism: Reduce preload and afterload by venodilation; improve coronary blood flow.
-Indication: Acute relief (sublingual nitroglycerin) and long-term prophylaxis (oral or transdermal nitrates).
-Adverse Effects: Headache, hypotension, reflex tachycardia.
2. Beta-Blockers:
-E.g., Metoprolol, Atenolol
-Mechanism: Reduce heart rate and contractility, lowering myocardial oxygen demand.
-Indication: First-line for stable angina; reduce mortality in post-MI patients.
-Adverse Effects: Bradycardia, fatigue, bronchospasm.
3. Calcium Channel Blockers:
-E.g., Amlodipine, Verapamil
-Mechanism: Reduce afterload by vasodilation and decrease myocardial oxygen demand.
-Indication: Prinzmetal angina, stable angina in patients intolerant to beta-blockers.
-Adverse Effects: Hypotension, peripheral edema, constipation.
4. Antiplatelet Agents:
-E.g., Aspirin, Clopidogrel
-Mechanism: Prevent platelet aggregation and thrombus formation.
-Indication: Prevent acute coronary syndromes.
-Adverse Effects: Bleeding, gastrointestinal irritation.
5. Ranolazine:
-Mechanism: Inhibits late sodium currents, reducing ischemia.
-Indication: Chronic stable angina refractory to standard therapy.
-Adverse Effects: QT prolongation.
D] Pathophysiology - MI
-MI is caused by complete or partial coronary artery occlusion, leading to ischemia and myocardial necrosis.
E] Goals of Therapy - MI
-Restore coronary perfusion and limit infarct size.
-Prevent complications such as arrhythmias, heart failure, and reinfarction.
-Reduce mortality and improve long-term outcomes.
F] Drug Classes for MI
1. Thrombolytics (Fibrinolytics):
-E.g., Alteplase, Streptokinase
-Mechanism: Dissolve thrombi by activating plasminogen to plasmin.
-Indication: STEMI when percutaneous coronary intervention (PCI) is unavailable.
-Adverse Effects: Bleeding, intracranial hemorrhage.
2. Antiplatelet Agents:
-Aspirin: Irreversible COX-1 inhibition reduces thromboxane A2, preventing platelet aggregation.
-P2Y12 Inhibitors (e.g., Clopidogrel, Ticagrelor): Block ADP-mediated platelet activation.
-Used in dual antiplatelet therapy (DAPT) for ACS and post-PCI.
3. Anticoagulants:
-E.g., Enoxaparin, Heparin
-Mechanism: Prevent clot propagation by inhibiting clotting factors.
-Indication: Acute phase of MI to reduce thrombotic risk.
-Adverse Effects: Bleeding, heparininduced thrombocytopenia (HIT).
4. Beta-Blockers:
-Reduce myocardial oxygen demand, preventing arrhythmias and infarct expansion.
5. ACE Inhibitors/ARBs:
-Prevent ventricular remodeling and reduce afterload.
-Indication: Post-MI with heart failure or reduced ejection fraction.
-Adverse Effects: Cough (ACE inhibitors), hyperkalemia.
6. Statins:
-E.g., Atorvastatin, Rosuvastatin
-Mechanism: Lower LDL cholesterol and stabilize plaques.
-Indication: All MI patients irrespective of baseline cholesterol levels.
7. Nitrates:
-Relieve ischemic pain by improving coronary perfusion.
8. Aldosterone Antagonists:
-E.g., Spironolactone
-Indication: Post-MI with heart failure or reduced ejection fraction.
G] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Pathophysiology Understanding: Describe the mechanisms underlying angina and MI, including the role of oxygen supply-demand mismatch and thrombosis.
–Drug Mechanisms and Indications: Understand the mechanism of action, indications, and contraindications of drugs used in angina and MI.
–Guideline Awareness: Familiarity with current guidelines for managing stable angina, unstable angina, and MI.
b) Skill-Based Outcomes
–Drug Selection: Select the most appropriate therapy for angina or MI based on patient-specific factors, such as comorbidities and contraindications.
–Acute Management Skills: Administer appropriate acute therapies for MI (e.g., thrombolysis, dual antiplatelet therapy).
–Monitoring and Adjustment: Monitor therapy effectiveness (e.g., relief of chest pain, BP control) and adjust based on patient response and side effects.
c) Attitude-Based Outcomes
–Patient-Centered Care: Prioritize patient preferences and risk factors in designing treatment plans.
–Preventive Focus: Educate patients on lifestyle changes (e.g., smoking cessation, diet, exercise) to prevent angina and recurrent MI.
–Ethical Prescribing: Avoid polypharmacy and adhere to evidence-based practices for reducing cardiovascular morbidity and mortality.
3. Cardiac Glycosides and Drugs for Heart failure
A] Cardiac Glycosides
1. Mechanism of Action
Digoxin, the primary cardiac glycoside, works by:
–Inhibiting the Na⁺/K⁺-ATPase pump, leading to increased intracellular sodium.
–Increased sodium decreases calcium extrusion via the sodium-calcium exchanger, leading to higher intracellular calcium and stronger myocardial contractions (positive inotropy).
–Slowing conduction through the atrioventricular (AV) node and increasing vagal tone (negative chronotropy).
2. Indications
-Symptomatic relief in chronic heart failure (especially in patients with reduced ejection fraction).
-Management of atrial fibrillation with rapid ventricular rates, especially in heart failure patients.
3. Adverse Effects
a) Cardiac: Arrhythmias (e.g., ventricular tachycardia, AV block).
b) Gastrointestinal: Nausea, vomiting, diarrhea.
c) Neurological: Visual disturbances (e.g., yellow vision), confusion.
d) Toxicity: Narrow therapeutic index necessitates careful monitoring of drug levels(normal range: 0.5–2 ng/mL).
4. Monitoring
-Regular assessment of digoxin levels, renal function, and electrolytes (hypokalemia and hypomagnesemia increase toxicity risk).
B] Drugs Used in Heart Failure
Heart failure management varies based on the type:
–Heart Failure with Reduced Ejection Fraction (HFrEF): EF ≤40%.
–Heart Failure with Preserved Ejection Fraction (HFpEF): EF >50%.
1. Goals of Therapy
-List the scope and limitations of HMM(MSLV)
-Discuss the scope and limitations of HMM(MSLV)
-Discuss the solutions to overcome the limitations of HMM(MSLV)
2. Drug Classes
1) First-Line Drugs:
a) Angiotensin-Converting Enzyme (ACE) Inhibitors (e.g., Enalapril, Ramipril):
–Mechanism: Reduce afterload and preload by blocking the renin-angiotensin-aldosterone system (RAAS).
–Benefits: Decrease mortality and slow disease progression.
–Adverse Effects: Cough, hyperkalemia, angioedema.
b) Angiotensin II Receptor Blockers (ARBs) (e.g., Losartan, Valsartan):
–Alternative to ACE inhibitors in patients with intolerance.
–Beta-Blockers (e.g., Bisoprolol, Carvedilol, Metoprolol):
–Mechanism: Block sympathetic overactivation.
–Benefits: Reduce mortality and improve left ventricular function.
–Adverse Effects: Bradycardia, fatigue, hypotension.
c) Mineralocorticoid Receptor Antagonists (MRAs) (e.g., Spironolactone, Eplerenone):
–Mechanism: Block aldosterone, reducing fluid retention and fibrosis.
–Benefits: Mortality reduction in HFrEF.
–Adverse Effects: Hyperkalemia, gynecomastia (spironolactone).
2) Symptomatic Relief:
a) Loop Diuretics (e.g., Furosemide, Torsemide):
–Mechanism: Increase urinary excretion of sodium and water.
–Indication: Relieve fluid overload symptoms (e.g., pulmonary congestion, peripheral edema).
–Adverse Effects: Hypokalemia, hypovolemia.
b) Thiazide Diuretics (e.g., Hydrochlorothiazide):
–Used in mild fluid retention or combination therapy.
3) Novel Therapies:
–Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors (e.g., Dapagliflozin, Empagliflozin)
–Benefits: Mortality reduction, symptom improvement, regardless of diabetes status.
4) Other Agents:
a) Ivabradine:
–Mechanism: Reduces heart rate by inhibiting the If current in the sinoatrial node.
–Indication: HFrEF with resting heart rate >70 bpm despite beta-blocker use.
b) Hydralazine and Isosorbide Dinitrate:
–Indication: HFrEF in African-American patients or those intolerant to ACE inhibitors/ARBs.
5) Anticoagulation and Antiplatelets:
–Indicated in HF patients with atrial fibrillation or thromboembolic risk.
C] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Understanding Mechanisms: Describe the pharmacological actions of cardiac glycosides and other HF drugs.
–Pathophysiology: Understand the role of neurohormonal dysregulation in HF and the impact of pharmacotherapy.
–Evidence-Based Practices: Learn to apply current guidelines in the pharmacological management of HF.
b) Skill-Based Outcomes
–Drug Selection: Select appropriate drugs for HFrEF, HFpEF, and symptom management.
–Toxicity Monitoring: Identify and manage digoxin toxicity and other drug-related adverse effects.
c) Patient Counseling:
–Educate patients on medication adherence, recognizing symptoms of fluid overload, and dietary restrictions.
4. Hypolipidemic drugs
A] Classes of Hypolipidemic Drugs
1. HMG-CoA Reductase Inhibitors (Statins)
-Examples: Atorvastatin, Rosuvastatin, Simvastatin.
-Mechanism: Inhibit HMGCoA reductase, the ratelimiting enzyme in cholesterol synthesis, reducing LDL cholesterol.
-Benefits:
–Decrease LDL by 20–60%.
–Modest increase in HDL and decrease in triglycerides.
–Anti-inflammatory and plaquestabilizing effects.
-Indications:
–Primary and secondary prevention of atherosclerotic cardiovascular disease (ASCVD).
–Hypercholesterolemia.
2. Fibrates
-Examples: Fenofibrate, Gemfibrozil.
-Mechanism: Activate peroxisome proliferatoractivated receptor-alpha (PPAR-α), increasing fatty acid oxidation and lipoprotein lipase activity, leading to reduced triglycerides.
-Benefits:
–Decrease triglycerides by 3050%.
–Modest increase in HDL.
Indications: Hypertriglyceridemia, prevention of pancreatitis.
3. Bile Acid Sequestrants
-Examples: Cholestyramine, Colestipol.
-Mechanism: Bind bile acids in the intestine, preventing reabsorption and promoting cholesterol excretion.
-Benefits:
–Lower LDL by 1020%.
–May slightly increase HDL.
-Indications: Hypercholesterolemia, particularly in statin-intolerant patients.
4. Cholesterol Absorption Inhibitors
-Example: Ezetimibe.
-Mechanism: Inhibits Niemann-Pick C1-Like 1 (NPC1L1) protein in the intestine, reducing dietary and biliary cholesterol absorption.
-Benefits:
–Reduces LDL by 1825%.
–Additive effect with statins.
-Indications: Hypercholesterolemia, adjunct to statins.
5. PCSK9 Inhibitors
-Examples: Evolocumab, Alirocumab.
-Mechanism: Monoclonal antibodies that inhibit PCSK9, increasing LDL receptor recycling and reducing LDL levels.
-Benefits:
–Lower LDL by 50-70%.
–Reduce cardiovascular events.
Indications: Severe hypercholesterolemia, familial hypercholesterolemia, and patients with ASCVD.
6. Nicotinic Acid (Niacin)
-Mechanism: Reduces hepatic synthesis of triglycerides and VLDL, increasing HDL.
-Benefits:
–Reduces triglycerides and LDL.
–Significantly increases HDL.
-Adverse Effects: Flushing, hyperglycemia, hepatotoxicity.
-Indications: Mixed dyslipidemias.
7. Omega-3 Fatty Acids
-Examples: Eicosapentaenoic acid (EPA), Docosahexaenoic acid (DHA).
-Mechanism: Reduce hepatic triglyceride synthesis.
-Benefits:
–Decrease triglycerides.
–Anti-inflammatory and anti-arrhythmic properties.
-Indications: Hypertriglyceridemia.
B] Principles of Therapy
-Lifestyle Modifications: Emphasize diet, exercise, and smoking cessation alongside pharmacotherapy.
C] Monitoring and Safety
-Lipid Levels: Monitor baseline and follow-up lipid profiles to assess efficacy.
-Liver Function: Regularly check liver enzymes, especially with statins and niacin.
-Muscle Toxicity: Monitor for myalgia or rhabdomyolysis in statin-treated patients.
-Glycemic Control: Be cautious of hyperglycemia in susceptible individuals on statins or niacin
D] Adverse Effects of Hypolipidemic Drugs
-Statins: Myopathy, rhabdomyolysis, hepatotoxicity, increased diabetes risk.
-Fibrates: Myopathy(especially with statins), gallstones.
Bile Acid Sequestrants: Gastrointestinal discomfort, vitamin deficiencies (A, D, E, K).
-Niacin: Flushing, pruritus, hepatotoxicity.
-PCSK9 Inhibitors: Injection site reactions, rare hypersensitivity.
G = Renal system
1. Diuretics & Antidiuretics
A] Diuretics: Classes and Mechanism of Action
Diuretics are classified based on their site of action in the nephron and their mechanism of action.
1. Thiazide Diuretics
-Examples: Hydrochlorothiazide, Chlorthalidone.
-Mechanism: Inhibit sodiumchloride symporters in the distal convoluted tubule, promoting sodium and water excretion.
-Effects: Decrease blood volume and lower blood pressure.
-Indications: Hypertension, mild heart failure, edema due to kidney disease, and nephrolithiasis (calciumcontaining stones).
-Adverse Effects: Hypokalemia, hyponatremia, hyperglycemia, hyperuricemia.
2. Loop Diuretics
-Examples: Furosemide, Bumetanide, Torsemide.
-Mechanism: Inhibit the sodium-potassium-chloride co-transporter in the thick ascending limb of the loop of Henle, preventing sodium reabsorption.
-Effects: Cause significant diuresis, lowering fluid overload rapidly.
Indications: Acute heart failure, pulmonary edema, chronic kidney disease, severe edema.
-Adverse Effects: Hypokalemia, dehydration, hypotension, ototoxicity.
3. Potassium-Sparing Diuretics
-Examples: Spironolactone, Eplerenone, Amiloride, Triamterene.
-Mechanism: Aldosterone antagonists (e.g., Spironolactone, Eplerenone) block the effects of aldosterone in the collecting ducts, preventing sodium retention and potassium excretion & Epithelial sodium channel blockers (e.g., Amiloride, Triamterene) inhibit sodium reabsorption in the collecting tubules.
-Effects: Reduce sodium retention without causing significant potassium loss.
-Indications: Hyperaldosteronism, heart failure (as adjunct), hypertension, and cirrhosis with ascites.
-Adverse Effects: Hyperkalemia, gynecomastia (with spironolactone), metabolic acidosis.
4. Carbonic Anhydrase Inhibitors
-Examples: Acetazolamide.
-Mechanism: Inhibit carbonic anhydrase in the proximal convoluted tubule, preventing bicarbonate reabsorption and increasing urine output.
-Effects: Mild diuresis, alkalinization of urine.
-Indications: Glaucoma, metabolic alkalosis, altitude sickness.
-Adverse Effects: Metabolic acidosis, kidney stones, hypokalemia.
5. Osmotic Diuretics
-Examples: Mannitol.
-Mechanism: Increase osmolarity of the filtrate, preventing water reabsorption in the proximal tubule and descending loop of Henle.
-Effects: Draw water into the renal tubules, promoting diuresis.
-Indications: Cerebral edema, increased intraocular pressure, acute renal failure.
-Adverse Effects: Dehydration, hyperkalemia, electrolyte imbalances.
B] Antidiuretics: Mechanism and Use
Antidiuretics, or diuretic inhibitors, are used to reduce urine output, typically by increasing water reabsorption in the kidneys.
1. Antidiuretic Hormone (ADH) Analogs
-Examples: Desmopressin, Vasopressin.
-Mechanism: Mimic the action of endogenous ADH, promoting water reabsorption in the collecting ducts by activating V2 receptors.
-Indications: Diabetes insipidus, nocturnal enuresis.
-Adverse Effects: Hyponatremia, water retention, hypertension.
2. Vasopressin Receptor Antagonists
-Examples: Tolvaptan, Conivaptan.
-Mechanism: Block the V2 receptors, inhibiting water reabsorption and promoting diuresis.
-Indications: Syndrome of inappropriate antidiuretic hormone (SIADH), hypervolemic hyponatremia.
-Adverse Effects: Hypernatremia, thirst, dehydration.
H = Blood
1. Hematinics
a] Definition:
-Hematinics are agents that promote the formation of hemoglobin and red blood cells (RBCs). They are used to prevent and treat various types of anemia by supplying essential components required for blood formation.
b] Main Components:
-Iron: Essential for hemoglobin synthesis.
-Folic Acid: Required for DNA synthesis and maturation of RBCs.
-Vitamin B₁₂ (Cyanocobalamin): Necessary for normal RBC development and prevention of megaloblastic anemia.
c] Uses:
-Treatment and prevention of iron-deficiency anemia, megaloblastic anemia, and nutritional anemia.
-Commonly given during pregnancy, lactation, and recovery from chronic illness to improve hemoglobin levels.
2. T/t of Iron deficiency anemia and Megaloblastic anemia
a) Iron Preparations (Ferrous sulfate, Ferrous fumarate, Ferric carboxymaltose)
-Role: Essential for hemoglobin synthesis and oxygen transport.
-Uses: Treatment and prevention of iron deficiency anemia.
-Adverse effects: Nausea, constipation, black stools, abdominal discomfort (oral); pain, staining at injection site (parenteral).
b) Vitamin B₁₂ (Cyanocobalamin, Hydroxocobalamin)
-Role: Required for DNA synthesis and red blood cell maturation.
-Uses: Megaloblastic anemia due to Vitamin B₁₂ deficiency (e.g., pernicious anemia).
-Adverse effects: Rare; possible hypersensitivity reactions with injections.
c) Folic Acid
-Role: Essential for nucleic acid synthesis and normal RBC production.
-Uses: Megaloblastic anemia due to folate deficiency, prevention of neural tube defects in pregnancy.
-Adverse effects: Rare; may mask Vitamin B₁₂ deficiency if given alone.
d) Rational Use
-Identify the specific cause of anemia before treatment.
-Combine iron + folic acid in nutritional anemia.
-Parenteral therapy only when oral therapy is not tolerated or ineffective.
e) Management of Adverse Effects
-Take iron after meals to reduce gastric irritation.
-Monitor Hb and reticulocyte count during therapy.
-Treat underlying causes (e.g., blood loss, malabsorption).
f) Therapeutic Uses
-Iron deficiency anemia
-Megaloblastic anemia (Vitamin B₁₂ / folate deficiency)
-Anemia of pregnancy and chronic illness (supportive therapy)
I = GIT
1. Drugs for Peptic Ulcer and GERD
A) Peptic Ulcer Disease (PUD)
-Peptic ulcers are lesions in the mucosal lining of the stomach, duodenum, or esophagus caused by an imbalance between aggressive factors (e.g., gastric acid, pepsin) and protective factors (e.g., mucus, bicarbonate). Common causes include Helicobacter pylori infection, long-term NSAID use, and excess gastric acid production.
b) Drug Classes Used for PUD
1. Proton Pump Inhibitors (PPIs)
-Examples: Omeprazole, Lansoprazole, Esomeprazole, Pantoprazole, Rabeprazole.
-Mechanism: PPIs irreversibly inhibit the H+/K+ ATPase (proton pump) in parietal cells, which reduces gastric acid secretion.
-Indications: Firstline therapy for peptic ulcers, H. pylori eradication (as part of combination therapy), GERD, Zollinger-Ellison syndrome.
-Adverse Effects: Long-term use may lead to vitamin B12 deficiency, n test, MCQ Medicine Physiology hypomagnesemia, osteoporosis, and increased susceptibility to Clostridium difficile infections.
2. H2-Receptor Antagonists (H2RAs)
-Examples: Ranitidine, Famotidine, Cimetidine, Nizatidine.
-Mechanism: H2RAs block histamine receptors (H2 receptors) on parietal cells, reducing gastric acid secretion.
-Indications: Used in the treatment of mild to moderate PUD, GERD, and Zollinger-Ellison syndrome. They are also used in the prevention of stress ulcers in critically ill patients.
-Adverse Effects: Headache, dizziness, fatigue, and gastrointestinal symptoms. Cimetidine has significant drug interactions due to its inhibition of cytochrome P450 enzymes.
3. Antacids
-Examples: Magnesium hydroxide, Aluminum hydroxide, Calcium carbonate, Sodium bicarbonate.
-Mechanism: Antacids neutralize gastric acid, increasing gastric pH and providing symptomatic relief.
-Indications: Shortterm relief of symptoms in PUD and GERD, as adjunctive therapy in combination with other agents.
-Adverse Effects: Constipation (aluminum-based), diarrhea (magnesiumbased), and metabolic alkalosis with overuse of sodium bicarbonate.
4. Mucosal Protective Agents
-Examples: Sucralfate, Misoprostol.
-Mechanism: Sucralfate forms a protective barrier over the ulcer, while Misoprostol, a prostaglandin analog, increases mucus and bicarbonate secretion to protect the gastric mucosa.
-Indications: Used in the healing of ulcers, particularly NSAIDinduced ulcers (Misoprostol), and in combination with other drugs for H. pylori eradication.
-Adverse Effects: Sucralfate can cause constipation and nausea, while Misoprostol may cause diarrhea, abdominal cramping, and is contraindicated in pregnancy due to its abortifacient effects.
5. Antibiotics (for H. pylori infection)
-Examples: Amoxicillin, Clarithromycin, Metronidazole, Tetracycline.
-Mechanism: Antibiotics target and eradicate Helicobacter pylori, which is a primary cause of peptic ulcers.
-Indications: Used in combination therapy with PPIs for the eradication of H. pylori in PUD.
-Adverse Effects: Nausea, vomiting, diarrhea, and the risk of developing antibiotic resistance.
c] Gastroesophageal Reflux Disease (GERD)
-GERD is a chronic condition where gastric contents, including acid, reflux into the esophagus, causing symptoms such as heartburn, regurgitation, and potential esophageal damage (e.g., esophagitis, Barrett’s esophagus).
d] Drug Classes Used for GERD
1. Proton Pump Inhibitors (PPIs)
-Indications: Firstline therapy for GERD to heal esophagitis, provide symptomatic relief, and prevent complications like strictures or Barrett’s esophagus.
-Adverse Effects: Similar to those seen in PUD therapy, including risk of long-term complications like vitamin B12 deficiency and osteoporosis.
2. H2-Receptor Antagonists (H2RAs)
-Indications: Used for mild GERD symptoms or in patients who do not require more potent acid suppression (PPIs).
-Adverse Effects: As noted above, particularly with cimetidine due to its interaction with cytochrome P450 enzymes.
3. Antacids
-Indications: Provide short-term relief from heartburn symptoms in GERD.
-Adverse Effects: As noted in PUD treatment, particularly with overuse leading to metabolic alkalosis, constipation, or diarrhea.
4. Prokinetic Agents
-Examples: Metoclopramide, Domperidone.
-Mechanism: These drugs increase lower esophageal sphincter tone and enhance gastric emptying, reducing acid reflux.
-Indications: Used in GERD with delayed gastric emptying or in patients with esophageal motility issues.
-Adverse Effects: Metoclopramide can cause extrapyramidal symptoms, tardive dyskinesia, and sedation.
5. Alginate-based Products
-Examples: Gaviscon.
-Mechanism: Alginate forms a gellike barrier that floats on the stomach contents, preventing acid from refluxing into the esophagus.
-Indications: Used for mild to moderate GERD and in combination with other agents.
-Adverse Effects: Typically welltolerated but may cause bloating or discomfort.
e] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanisms of Action: Understand how PPIs, H2RAs, and other drugs reduce gastric acid secretion, promote ulcer healing, and protect the gastrointestinal mucosa.
–Indications and Contraindications: Identify when to use PPIs, H2RAs, antacids, and mucosal protectants based on the underlying etiology of PUD or GERD.
–Adverse Effects and Drug Interactions: Recognize the potential side effects of each class of drug (e.g., bleeding risks with mucosal protectants, infection risks with PPIs, or drug interactions with cimetidine). Skill-Based Outcomes
–Therapeutic Decision Making: Select appropriate drug therapy based on the clinical scenario, balancing the severity of the condition with the potential for adverse effects and long-term complications.
–Monitoring and Adjustment: Monitor patient progress, adjust therapy as needed based on symptom control, adverse effects, and response to treatment (e.g., for H. pylori eradication or healing of ulcers).
–Patient Education: Educate patients on the importance of adherence to therapy, lifestyle modifications (e.g., diet, weight management), and potential side effects.
b) Attitude-Based Outcomes
–Patient-Centered Care: Address patient concerns regarding long-term treatment (e.g., PPI use) and emphasize the importance of managing GERD and PUD to prevent complications.
–Rational Prescribing: Prescribe drugs for PUD and GERD based on current guidelines, considering the risk of complications, especially with long-term therapy.
–Preventive Approach: Advocate for preventive measures such as H. pylori screening and eradication, lifestyle modifications, and careful monitoring of patients at risk for complications.
2. Drugs for constipation and diarrhea
A] Drugs for Constipation
-Constipation is characterized by infrequent, difficult, or painful bowel movements, often associated with hard stools. Treatment typically involves dietary and lifestyle changes, but pharmacotherapy is used in more severe or chronic cases.
b] Drug Classes Used for Constipation
1. Bulk-Forming Laxatives
-Examples: Psyllium, Methylcellulose, Polycarbophil.
-Mechanism: These drugs increase stool volume by absorbing water, which softens the stool and promotes peristalsis.
-Indications: Firstline therapy for chronic constipation, especially in patients with low fiber intake.
-Adverse Effects: Bloating, flatulence, and abdominal discomfort. Rarely, they can cause obstruction if not taken with adequate water.
2. Stool Softeners
-Examples: Docusate sodium, Docusate calcium.
-Mechanism: These agents increase the water content of the stool, making it softer and easier to pass.
-Indications: Used for mild constipation, particularly in patients with hemorrhoids or postoperative patients who should avoid straining.
-Adverse Effects: Generally well tolerated but may cause mild abdominal cramping.
3. Osmotic Laxatives
-Examples: Lactulose, Polyethylene glycol (PEG), Magnesium hydroxide.
-Mechanism: These agents draw water into the colon through osmosis, softening the stool and promoting bowel movement.
-Indications: Used in chronic constipation, fecal impaction, and in patients with hepatic encephalopathy (lactulose).
-Adverse Effects: Bloating, flatulence, diarrhea, and electrolyte imbalances (especially with magnesium-based agents).
4. Stimulant Laxatives
-Examples: Bisacodyl, Senna, Castor oil.
-Mechanism: These drugs stimulate the smooth muscle of the colon, enhancing peristalsis and accelerating bowel movements.
-Indications: Used in cases of acute constipation or as a second-line treatment for chronic constipation.
-Adverse Effects: Cramping, dehydration, and long-term use may lead to dependence or bowel atony.
5. Chloride Channel Activators
-Examples: Lubiprostone, Linaclotide.
-Mechanism: These agents increase chloride secretion into the intestinal lumen, enhancing water secretion and improving stool consistency.
-Indications: Used for chronic idiopathic constipation (CIC) and constipationpredominant irritable bowel syndrome (IBS-C).
-Adverse Effects: Nausea, diarrhea, bloating, and abdominal discomfort.
6. Guanylate Cyclase-C Agonists
-Examples: Plecanatide, Linaclotide.
-Mechanism: These drugs increase cyclic GMP levels in the intestines, stimulating fluid secretion and promoting bowel motility.
-Indications: Used for chronic constipation and IBS-C.
-Adverse Effects: Diarrhea, flatulence, and abdominal pain.
c] Drugs for Diarrhea
-Diarrhea is defined as the passage of loose or watery stools more than three times a day and can be caused by infections, medications, or gastrointestinal disorders. The goal of treatment is to restore fluid balance, relieve symptoms, and treat the underlying cause.
d] Drug Classes Used for Diarrhea
1. Antidiarrheal Agents
-Examples: Loperamide, Diphenoxylate with atropine (Lomotil).
-Mechanism: These drugs work by slowing intestinal motility, allowing more time for fluid absorption in the colon.
-Indications: Used for acute diarrhea (including traveler’s diarrhea), chronic diarrhea (e.g., in IBS), and to reduce the frequency of stool in conditions like inflammatory bowel disease (IBD).
-Adverse Effects: Constipation, bloating, and abdominal cramps. Loperamide should be avoided in cases of dysentery or bacterial infections involving the gut.
2. Adsorbents
-Examples: Activated charcoal, Kaolin, Pectin.
-Mechanism: Adsorbents bind to toxins or pathogens in the gut, preventing them from causing diarrhea.
-Indications: Used for mild diarrhea and toxin-related diarrhea (e.g., from bacterial infections).
-Adverse Effects: Constipation, bloating, and reduced effectiveness of other medications if used concurrently.
3. Bismuth Subsalicylate
-Examples: Pepto-Bismol.
-Mechanism: It has antimicrobial, antiinflammatory, and antacid properties, which help reduce diarrhea, nausea, and abdominal discomfort.
-Indications: Used for acute diarrhea (including traveler’s diarrhea), indigestion, and nausea.
-Adverse Effects: Blackened stools, tongue discoloration, and in large doses, salicylate toxicity.
4. Probiotics
-Examples: Lactobacillus, Saccharomyces boulardii.
-Mechanism: Probiotics restore the natural balance of gut flora, which can be disrupted in diarrhea.
-Indications: Used for antibiotic-associated diarrhea, gastroenteritis, and inflammatory bowel disease (IBD).
-Adverse Effects: Generally well tolerated but may cause bloating and gas in some individuals.
5. Octreotide
-Mechanism: Octreotide is a somatostatin analog that inhibits the secretion of various gastrointestinal hormones, slowing motility and reducing secretions.
-Indications: Used for diarrhea caused by neuroendocrine tumors, chemotherapy, and certain gastrointestinal disorders.
-Adverse Effects: Nausea, abdominal cramps, and flatulence.
6. Antibiotics (for Infectious Diarrhea)
-Examples: Ciprofloxacin, Metronidazole, Rifaximin.
-Mechanism: These drugs treat bacterial infections causing diarrhea by targeting the pathogen directly.
-Indications: Used for diarrhea caused by specific bacterial infections, such as Salmonella, Shigella, or Clostridium difficile.
-Adverse Effects: Diarrhea, nausea, and potential development of antibiotic resistance.
e] Monitoring and Safety
1. Constipation
-Regular monitoring for adverse effects with long-term laxative use, especially stimulant laxatives, to avoid dependency and bowel atony.
2. Diarrhea
-Close monitoring of hydration status, especially in children and elderly patients, to prevent complications like electrolyte imbalances and dehydration.
f] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanisms of Action: Understand how each class of drug for constipation and diarrhea works to alleviate symptoms and restore normal bowel function.
–Indications and Contraindications: Recognize the appropriate use of bulk-forming agents, laxatives, antidiarrheals, and probiotics based on the underlying cause and clinical scenario.
–Adverse Effects and Drug Interactions: Identify potential side effects and interactions of these drugs (e.g., electrolyte imbalances with osmotic laxatives, constipation with antidiarrheals).
b) Skill-Based Outcomes
–Therapeutic Decision Making: Be able to select the appropriate pharmacotherapy based on the type of constipation or diarrhea and its underlying cause (e.g., osmotic laxatives for chronic constipation, loperamide for acute diarrhea).
–Monitoring and Adjustment: Monitor patients for adverse effects, treatment response, and the resolution of underlying causes (e.g., adjusting therapy based on stool frequency and consistency).
–Patient Education: Provide guidance on proper use of medications, potential side effects, and lifestyle modifications (e.g., increasing fluid and fiber intake for constipation).
c) Attitude-Based Outcomes
–Patient-Centered Care: Ensure that treatment decisions are tailored to the individual patient, taking into account their preferences, lifestyle, and specific medical conditions.
–Rational Prescribing: Prescribe drugs for constipation and diarrhea based on the clinical severity, while minimizing risks of adverse effects, especially in vulnerable populations (e.g., the elderly).
–Preventive Approach: Advocate for preventive measures like diet modification (increasing fiber intake), hydration, and regular exercise for constipation, and proper sanitation to prevent infections that cause diarrhea
3. Antiemetics
A] Mechanisms of Nausea and Vomiting
Nausea and vomiting are complex physiological processes that involve multiple pathways and brain regions, including:
1. Central mechanisms:
-Activation of the vomiting center in the medulla oblongata via signals from the chemoreceptor trigger zone (CTZ), vestibular system, and higher brain centers.
2. Peripheral mechanisms:
-Inflammation or irritation of the gastrointestinal tract, involving neurotransmitters like serotonin (5-HT), dopamine, and substance P.
3. Key Neurotransmitters Involved:
-Serotonin (5-HT): Plays a central role in chemotherapy induced nausea and vomiting (CINV) and post-operative nausea.
-Dopamine (D2 receptors): Involved in motion sickness, CINV, and gastroparesis.
-Histamine (H1 receptors): Responsible for motion sickness and vestibular nausea.
-Substance P (NK1 receptors): Involved in chemotherapy-induced and post-operative nausea.
B] Drug Classes Used for Nausea and Vomiting (Antiemetics)
1. Serotonin (5-HT3) Antagonists
-Examples: Ondansetron, Granisetron, Dolasetron, Palonosetron.
-Mechanism: These drugs block serotonin receptors in the central and peripheral nervous system, specifically 5-HT3 receptors, which are involved in triggering nausea and vomiting.
-Indications: Primarily used for chemotherapyinduced nausea and vomiting (CINV), postoperative nausea, and radiation therapyinduced nausea.
-Adverse Effects: Headache, constipation, dizziness, and potential QT prolongation.
2. Dopamine (D2) Antagonists
-Examples: Metoclopramide, Prochlorperazine, Domperidone.
-Mechanism: These drugs block dopamine receptors in the CTZ and gastrointestinal tract, which helps control nausea and vomiting.
-Indications: Used for gastrointestinal disorders (e.g., gastroparesis), postoperative nausea, motion sickness, and CINV.
-Adverse Effects: Extrapyramidal symptoms (EPS) like dystonia, parkinsonism, and tardive dyskinesia, sedation, and increased prolactin levels (domperidone is less likely to cause EPS).
3. Histamine (H1) Antagonists
-Examples: Diphenhydramine, Meclizine, Promethazine.
-Mechanism: These drugs block histamine receptors in the vestibular system, helping prevent nausea related to motion sickness and vertigo.
-Indications: Used for motion sickness, vertigo, postoperative nausea, and as adjunct therapy in CINV.
-Adverse Effects: Sedation, dry mouth, blurred vision, and urinary retention.
4. Neurokinin (NK1) Receptor Antagonists
-Examples: Aprepitant, Fosaprepitant, Rolapitant.
-Mechanism: These drugs block substance P at the NK1 receptors in the brain, reducing the signal that triggers vomiting.
-Indications: Mainly used in combination with 5-HT3 antagonists and corticosteroids for CINV, especially for highly emetogenic chemotherapy regimens.
-Adverse Effects: Fatigue, dizziness, diarrhea, and liver enzyme elevation.
5. Corticosteroids
-Examples: Dexamethasone.
-Mechanism: The exact mechanism of action is unclear, but corticosteroids may reduce inflammation and affect the central nervous system’s response to nausea.
-Indications: Used in combination with 5HT3 antagonists and NK1 receptor antagonists for CINV and postoperative nausea.
-Adverse Effects: Increased appetite, weight gain, insomnia, and elevated blood glucose levels.
6. Cannabinoids
-Examples: Dronabinol, Nabilone.
-Mechanism: These agents act on the cannabinoid receptors in the brain, which play a role in the regulation of nausea and vomiting.
-Indications: Used for CINV in patients who do not respond to standard antiemetics or in cases of appetite stimulation in patients with cancer or HIV/AIDS.
-Adverse Effects: Euphoria, sedation, dizziness, dry mouth, and psychosis in susceptible individuals.
7. Anticholinergic Agents
-Examples: Scopolamine.
-Mechanism: These drugs block acetylcholine receptors in the vestibular system and gastrointestinal tract,
helping prevent nausea and vomiting caused by motion sickness.
-Indications: Used for motion sickness and postoperative
-Adverse Effects: Dry mouth, blurred vision, urinary retention, and confusion.
C] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanism of Action: Understand how different classes of antiemetic drugs act on the various pathways involved in nausea and vomiting, such as serotonin, dopamine, histamine, and substance P.
–Clinical Indications: Recognize the appropriate indications for the use of specific antiemetic drugs, including CINV, PONV, motion sickness, and gastrointestinal disorders.
–Adverse Effects: Identify the potential adverse effects and safety concerns associated with antiemetic drugs, such as sedation, extrapyramidal symptoms, and electrolyte imbalances.
b) Kill-Based Outcomes
–Therapeutic Decision Making: Be able to select the most appropriate antiemetic treatment based on the type of nausea/vomiting (e.g., CINV, motion sickness) and the patient’s clinical condition.
–Combination Therapy: Develop the ability to combine antiemetics (e.g., 5-HT3 antagonists with NK1 antagonists and corticosteroids) to provide effective control of nausea and vomiting in complex conditions like CINV.
–Monitoring and Adjustment: Monitor patients for adverse effects, especially in chemotherapy and postoperative settings, and adjust treatment based on the patient’s response and side effects.
c) Attitude-Based Outcomes
–Patient-Centered Care: Ensure that antiemetic therapy is tailored to the individual patient’s needs, considering factors such as chemotherapy regimens, comorbidities, and personal preferences.
–Rational Prescribing: Prescribe antiemetics based on the severity and cause of nausea and vomiting, while minimizing side effects and drug interactions, especially in vulnerable populations.
–Patient Education: Provide thorough education to patients about the appropriate use of antiemetics, potential side effects, and when to seek medical attention for any adverse reactions.
J = Chemotherapy
1. Sulfonamides and Cotrimoxazole
A] Sulfonamides
Sulfonamides are bacteriostatic agents that inhibit the synthesis of dihydropteroic acid, an essential precursor in the folate pathway of bacteria.
1. Mechanism of Action
-Sulfonamides act as competitive inhibitors of the enzyme dihydropteroate synthase.
-They block the incorporation of para-aminobenzoic acid (PABA) into folic acid, preventing bacterial replication.
2. Examples
-Short-acting sulfonamides: Sulfisoxazole.
-Intermediate-acting sulfonamides: Sulfamethoxazole.
-Long-acting sulfonamides: Sulfadoxine.
-Topical sulfonamides: Sulfacetamide (eye infections), Silver sulfadiazine (burn infections).
3. Clinical Uses
-Urinary tract infections (UTIs).
-Nocardiosis.
-Trachoma.
-Toxoplasmosis (in combination with pyrimethamine).
-Burn wound infections (topical silver sulfadiazine).
4. Adverse Effects
-Hypersensitivity reactions: Rash, Stevens-Johnson syndrome.
-Hematologic effects: Hemolytic anemia (especially in G6PD-deficient patients).
-Kernicterus in neonates due to bilirubin displacement.
-Crystalluria: Formation of crystals in urine leading to renal damage.
B] Cotrimoxazole
Cotrimoxazole is a combination of sulfamethoxazole (SMX) and trimethoprim (TMP) in a 5:1 ratio. The combination provides synergistic bactericidal activity.
1. Mechanism of Action
-Sulfamethoxazole: Inhibits dihydropteroate synthase, blocking folic acid synthesis.
-Trimethoprim: Inhibits dihydrofolate reductase, further blocking folate metabolism.
-Together, they inhibit two consecutive steps in folate synthesis, leading to bacterial cell death.
2. Clinical Uses
-Respiratory infections: Pneumocystis jirovecii pneumonia (PCP).
-Urinary tract infections (UTIs): First-line treatment.
-Gastrointestinal infections: Shigellosis, Traveler’s diarrhea (caused by E. coli).
-Nocardiosis and toxoplasmosis (alternative to sulfonamides and pyrimethamine).
3. Adverse Effects
-Same as sulfonamides (hypersensitivity, hematologic effects, crystalluria).
-Trimethoprim-specific effects: Hyperkalemia (due to potassium-sparing effects), megaloblastic anemia, leukopenia (due to folate deficiency).
C] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanisms of Action: Understand how sulfonamides and trimethoprim target bacterial folate synthesis.
–Spectrum of Activity: Recognize the broad spectrum of sulfonamides and the synergistic effects of Cotrimoxazole.
–Therapeutic Applications: Know the specific indications for sulfonamides and Cotrimoxazole, including bacterial, parasitic, and opportunistic infections.
–Adverse Effects: Identify common side effects and contraindications, including their use in neonates, pregnant women, and G6PD deficient individuals.
b) Skill-Based Outcomes
–Rational Drug Selection: Select appropriate sulfonamide or Cotrimoxazole therapy based on infection type, organism susceptibility, and patient factors.
–Therapeutic Monitoring: Monitor for clinical efficacy and adverse effects, including renal function, electrolyte levels, and signs of hypersensitivity.
–Drug Interactions: Manage potential interactions, such as the displacement of warfarin or methotrexate by sulfonamides, increasing their toxicity.
c) Attitude-Based Outcomes
–Patient Education: Counsel patients on the importance of hydration to prevent crystalluria and adherence to therapy to avoid resistance.
–Antimicrobial Stewardship: Avoid unnecessary use to reduce the development of resistance, particularly with Cotrimoxazole in Pneumocystis infections.
–Holistic Care: Consider patient comorbidities (e.g., renal impairment, G6PD deficiency) and adjust therapy accordingly.
2. Quinolones
A] Definition
-Quinolones are synthetic antibiotics that inhibit bacterial DNA replication by targeting DNA gyrase (topoisomerase II) and topoisomerase IV.
B] Mechanism of Action
1. DNA Gyrase Inhibition:
-Primarily in gram negative bacteria, it prevents the unwinding of supercoiled DNA, which is essential for replication.
2. Topoisomerase IV Inhibition:
-Predominantly in gram-positive bacteria, it interferes with the separation of replicated DNA strands during cell division.
3. Classification and Examples
a) First-Generation Quinolones
–Examples: Nalidixic acid.
–Spectrum: Limited to gram negative bacteria.
–Use: Uncomplicated urinary tract infections (UTIs).
b) Second-Generation Fluoroquinolones
–Examples: Ciprofloxacin, Norfloxacin, Ofloxacin.
–Spectrum: Broad spectrum, effective against gramnegative bacteria and some gram-positive organisms.
–Use: UTIs, gastroenteritis, prostatitis, bone/joint infections.
c) Third-Generation Fluoroquinolones
–Examples: Levofloxacin.
–Spectrum: Improved activity against gram-positive bacteria (e.g., Streptococcus pneumoniae).
–Use: Respiratory tract infections (e.g., community acquired pneumonia, bronchitis).
d) Fourth-Generation Fluoroquinolones
–Examples: Moxifloxacin, Gemifloxacin.
–Spectrum: Broad spectrum, effective against anaerobes and atypical pathogens.
–Use: Respiratory tract infections, intra-abdominal infections.
C] Adverse Effects
1. Gastrointestinal: Nausea, vomiting, diarrhea.
2. Central Nervous System (CNS): Headache, dizziness, insomnia, seizures (rare).
3. Tendinopathy: Risk of tendonitis and Achilles tendon rupture, especially in older adults or those on corticosteroids.
4. QT Prolongation: Particularly with moxifloxacin, leading to arrhythmias.
5. Photosensitivity: Increased sensitivity to sunlight.
6. Resistance Development: Widespread use has led to significant bacterial resistance.
D] Contraindications and Precautions
1. Pregnancy and Breastfeeding: Contraindicated due to potential cartilage damage in the fetus or neonate.
2. Children (<18 years): Avoid unless benefits outweigh risks (e.g., severe infections like anthrax).
3. Drug Interactions: Antacids, iron, and calcium reduce absorption and Increased risk of seizures with NSAIDs or theophylline
E] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanisms of Action: Explain how quinolones inhibit bacterial DNA synthesis by targeting DNA gyrase and topoisomerase IV.
–Spectrum of Activity: Differentiate between generations and their bacterial targets (e.g., gram-negative, gram positive, atypicals).
–Therapeutic Uses: Identify clinical conditions where quinolones are firstline or alternative treatments.
–Adverse Effects: Recognize side effects and the patient populations at higher risk.
b) Skill-Based Outcomes
–Rational Drug Selection: Prescribe appropriate quinolones based on infection type, bacterial susceptibility, and patient factors.
–Therapeutic Monitoring: Monitor for adverse effects such as tendinopathy, QT prolongation, or photosensitivity.
–Resistance Management: Avoid overuse or inappropriate prescribing to minimize antimicrobial resistance.
c) Attitude-Based Outcomes
–Patient Counseling: Educate patients on proper usage, adherence, and the need to avoid direct sunlight.
–Ethical Prescribing: Limit use to infections where quinolones are clearly indicated, reducing unnecessary exposure.
–Safety Awareness: Prioritize patient safety by considering contraindications and drug interactions.
d) Clinical Pearls
–Ciprofloxacin is highly effective for UTIs and gastrointestinal infections but has limited activity against gram-positive cocci.
–Levofloxacin and moxifloxacin are preferred for respiratory infections due to better activity against S. pneumoniae.
–Resistance is a growing concern; restrict use to confirmed or strongly suspected bacterial infections.
3. Beta Lactam Antibiotics
A] Penicillin
a) Natural Penicillins:
–E.g. Penicillin G, Penicillin V.
–Spectrum: Grampositive bacteria (Streptococcus spp., Treponema pallidum).
b) Penicillinase-Resistant Penicillins:
–E.g. Methicillin, Nafcillin, Oxacillin.
–Spectrum: Penicillinase producing Staphylococcus aureus.
c) Aminopenicillins:
–E.g. Amoxicillin, Ampicillin.
–Spectrum: Broader gram-negative activity (e.g., E. coli, H. influenzae).
d) Extended-Spectrum Penicillins:
–E.g. Piperacillin, Ticarcillin.
–Spectrum: Includes Pseudomonas aeruginosa.
B] Cephalosporins
Classified into five generations:
–1st Generation: Cefazolin, Cephalexin (Grampositive activity).
–2nd Generation: Cefuroxime (Broader gram-negative coverage).
–3rd Generation: Ceftriaxone, Ceftazidime (Expanded gramnegative activity, some penetrate CNS).
–4th Generation: Cefepime (Pseudomonas coverage).
–5th Generation: Ceftaroline (MRSA coverage).
C] Carbapenems
-Examples: Imipenem, Meropenem, Ertapenem.
-Spectrum: Broadest among beta-lactams, covering grampositive, gram-negative, and anaerobes.
D] Monobactams
-Example: Aztreonam.
-Spectrum: Gram-negative aerobes, including Pseudomonas.
E] Beta-Lactamase Inhibitors
-Examples: Clavulanic acid, Sulbactam, Tazobactam.
-Used in combination with beta-lactams to inhibit bacterial beta-lactamase enzymes.
F] Clinical Applications
1. Gram-Positive Infections
-Penicillin: Streptococcus, Enterococcus, Listeria.
-Cephalosporins (1st generation): Skin infections caused by Staphylococcus aureus.
2. Gram-Negative Infections
-Aminopenicillins: H. influenzae, E. coli.
-Cephalosporins (3rd and 4th generations): Severe gram negative infections.
-Carbapenems: ESBL producing organisms.
3. Anaerobic Infections
-Carbapenems and penicillins with beta-lactamase inhibitors.
4. Special Cases
-Meningitis: Ceftriaxone or Cefotaxime (good CNS penetration).
-Pseudomonas infections: Piperacillin-tazobactam, Ceftazidime, Cefepime.
-MRSA(Methicillin-Resistant Staphylococcus aureus): Ceftaroline.
G] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanism of Action: Understand how beta-lactams inhibit bacterial cell wall synthesis.
–Spectrum of Activity: Differentiate between various classes and their antibacterial coverage.
–Resistance Mechanisms: Recognize common mechanisms of resistance and strategies to overcome them.
–Adverse Effects: Identify common and serious side effects associated with betalactams.
b) Skill-Based Outcomes
–Rational Drug Selection: Prescribe appropriate beta-lactams based on infection type, organism susceptibility, and patient-specific factors.
–Therapeutic Monitoring: Monitor for signs of efficacy and toxicity, including hypersensitivity and GI disturbances.
–Combination Therapy: Use beta-lactamase inhibitors appropriately to enhance the efficacy of beta-lactam antibiotics.
c) Attitude-Based Outcomes
–Antimicrobial Stewardship: Avoid unnecessary or prolonged use to reduce resistance development.
–Patient Education: Counsel patients on completing the course of antibiotics and recognizing signs of adverse effects.
–Ethical Prescribing: Balance effective treatment with the need to minimize resistance and preserve antibiotics for future use.
d) Clinical Pearls
–Cephalosporins have a generation-specific spectrum, with newer generations covering more gram-negative organisms.
–Carbapenems are last-resort antibiotics, reserved for multidrug-resistant infections.
–Avoid beta-lactams in patients with a history of severe hypersensitivity reactions.
–Combining beta-lactams with beta-lactamase inhibitors significantly broadens their spectrum against resistant bacteria.
4. Tetracyclines, Chloramphenicol
A] Tetracyclines
1. Mechanism of Action
-Tetracyclines inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit, preventing the attachment of aminoacyl-tRNA to the mRNA-ribosome complex. This action halts bacterial growth, making them bacteriostatic.
2. Classification and Examples
a) Short-acting: Tetracycline.
b) Intermediate-acting: Demeclocycline.
c) Long acting: Doxycycline, Minocycline.
3. Clinical Uses
a) Respiratory Infections: Atypical pathogens (Mycoplasmapneumoniae, Chlamydia pneumoniae).
b) Zoonotic Infections: Rickettsial diseases (e.g., Rocky Mountain spotted fever), Lyme disease (Borrelia burgdorferi).
c) Sexually Transmitted Infections: Chlamydia, syphilis (alternative to penicillin).
d) Acne: Long-term therapy for severe acne.
e) Malaria Prophylaxis: Doxycycline.
4. Adverse Effects
a) Gastrointestinal: Nausea, vomiting, diarrhea.
b) Photosensitivity: Increased sensitivity to sunlight.
c) Teeth Discoloration: Avoid in children <8 years and pregnant women.
d) Hepatotoxicity: Rare but severe in high doses.
e) Fanconi Syndrome: Result of using expired tetracycline.
5. Resistance Mechanisms
a) Efflux Pumps: Actively expel tetracyclines from bacterial cells.
b) Ribosomal Protection Proteins: Prevent tetracycline binding.
B] Chloramphenicol
1. Mechanism of Action
-Chloramphenicol inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit, preventing peptide bond formation during translation. This action is primarily bacteriostatic but may be bactericidal at high concentrations against certain pathogens.
2. Clinical Uses
a) Serious Infections:
–Meningitis (Haemophilus influenzae, Neisseria meningitidis).
–Typhoid fever (Salmonella typhi).
b) Rickettsial Infections:
–Alternative for tetracyclines in pregnant women or children.
c) Topical Use:
–Eye infections (conjunctivitis).
3. Adverse Effects
a) Bone Marrow Suppression:
–Reversible suppression (dose dependent).
–Aplastic anemia (idiosyncratic and potentially fatal).
b) Gray Baby Syndrome:
–In neonates due to immature liver enzymes, leading to toxicity.
c) Gastrointestinal:
–Nausea, vomiting, diarrhea.
4. Resistance Mechanisms
a) Chloramphenicol Acetyltransferase: Inactivates the drug via acetylation.
b) Efflux Pumps: Reduce intracellular drug concentration.
c] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanisms of Action: Explain how tetracyclines target the 30S ribosome and chloramphenicol targets the 50S ribosome to inhibit protein synthesis.
–Spectrum of Activity: Recognize their broad-spectrum activity, covering gram-positive, gram negative, atypical, and intracellular pathogens.
–Clinical Applications: Identify appropriate conditions for their use, such as rickettsial infections, typhoid fever, and acne.
–Adverse Effects: Understand the risks of bone marrow suppression, gray baby syndrome, and photosensitivity.
b) Skill-Based Outcomes
–Rational Drug Selection: Select tetracyclines or chloramphenicol based on the infection type, pathogen susceptibility, and patient factors.
–Therapeutic Monitoring: Monitor for toxicity, such as hepatotoxicity (tetracyclines) or bone marrow suppression (chloramphenicol).
–Resistance Management: Prescribe only when indicated to avoid resistance development.
c) Attitude-Based Outcomes
–Antimicrobial Stewardship: Promote responsible use to prevent resistance.
–Patient Counseling: Educate patients on completing therapy, avoiding sunlight exposure (tetracyclines), and recognizing signs of adverse effects.
–Safety Considerations: Avoid use in vulnerable populations (e.g., pregnant women, neonates, and children) unless absolutely necessary.
5. Aminoglycosides
A] Mechanism of Action
Aminoglycosides irreversibly bind to the 30S ribosomal subunit, leading to:
a) Misreading of mRNA.
b) Production of defective proteins.
c) Disruption of bacterial cell membrane integrity, resulting in bactericidal activity.
B] Unique Feature
-Aminoglycosides exhibit a concentration-dependent killing effect and postantibiotic effect (PAE), meaning bacterial suppression continues even after drug levels drop below the minimum inhibitory concentration (MIC).
-Common Aminoglycosides: The most common aminoglycoside in clinical use are gentamicin, tobramycin, and amikacin
C] Clinical Applications
a) Gram-Negative Infections
–Effective against Enterobacteriaceae (e.g., E. coli, Klebsiella), Pseudomonas aeruginosa, and other gramnegative aerobes.
b) Combination Therapy
–Used synergistically with betalactams or glycopeptides for:
––Endocarditis(Enterococcus spp., Staphylococcus spp.).
––Serious grampositive infections (e.g., MRSA).
c) Tuberculosis
–Streptomycin as a second-line agent.
d) Topical/Local Use
–Neomycin for skin infections.
–Gentamicin in ophthalmic or otic preparations.
D] Adverse Effects
a) Ototoxicity (Cochlear and Vestibular):
–Irreversible damage to auditory and vestibular function.
–Risk increases with prolonged therapy, high doses, and renal impairment.
b) Nephrotoxicity:
–Reversible renal tubular damage.
–Risk factors include high trough levels, prolonged therapy, and co-administration with other nephrotoxic drugs.
c) Neuromuscular Blockade:
–Rare but can cause respiratory paralysis, especially in patients with myasthenia gravis.
E] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanism of Action: Explain how aminoglycosides disrupt bacterial protein synthesis by binding to the 30S ribosomal subunit.
–Spectrum of Activity: Recognize their primary activity against aerobic gram negative bacteria and synergistic potential with other antibiotics.
–Pharmacokinetics: Understand their poor oral bioavailability, renal elimination, and concentration dependent killing.
–Adverse Effects: Identify key toxicities (ototoxicity, nephrotoxicity) and their risk factors.
b) Skill-Based Outcomes
–Rational Prescribing: Select appropriate aminoglycosides based on infection type, pathogen susceptibility, and patient-specific factors.
–Therapeutic Monitoring: Use therapeutic drug monitoring (TDM) to maintain effective peak levels while minimizing toxic trough levels.
–Resistance Management: Apply appropriate combination therapy to minimize resistance.
c) Attitude-Based Outcomes
–Patient-Centered Care: Educate patients on potential toxicities and monitor closely for early signs of adverse effects.
–Antimicrobial Stewardship: Avoid overuse or misuse of aminoglycosides aminoglycosides to prevent resistance and toxicity.
–Ethical Use: Reserve aminoglycosides for serious infections to preserve their efficacy.
d) Clinical Pearls
–Monitor renal function (serum creatinine, urine output) and auditory/vestibular function during therapy.
–Avoid aminoglycosides in patients with pre-existing renal or auditory impairment unless absolutely necessary.
–Use combination therapy for gram-positive infections to enhance efficacy and reduce resistance.
6. Anti-tubercular drugs and Antileprosy drugs
A] Antitubercular Drugs
1. Classification
-Antitubercular drugs are classified into first-line and second-line agents based on their efficacy, safety, andtolerability.
a) First-Line Drugs (Used for drug-susceptible TB):
–Isoniazid (INH)
–Rifampicin (Rifampin)
–Pyrazinamide
–Ethambutol
–Streptomycin
b)Second-Line Drugs Used for multidrug-resistant TB (MDR-TB):
–Fluoroquinolones (e.g., Levofloxacin, Moxifloxacin).
–Aminoglycosides (e.g., Amikacin, Kanamycin).
–Linezolid, Bedaquiline, Delamanid.
2. Mechanism of Action
a) First-Line Drugs:
1) Isoniazid (INH)
–Inhibits mycolic acid synthesis (cell wall).
2) Rifampicin
–Inhibits DNA-dependent RNA polymerase → blocks RNA synthesis.
3) Pyrazinamide
–Disrupts mycobacterial membrane transport; active in acidic pH.
4) Ethambutol
–Inhibits arabinosyl transferase → blocks arabinan (cell wall).
5) Streptomycin
–Binds 30S ribosome → inhibits protein synthesis.
b) Second-Line Drugs (MDR-TB)
1) Fluoroquinolones (Levofloxacin, Moxifloxacin)
–Inhibit DNA gyrase / Topoisomerase IV → block DNA replication.
2) Aminoglycosides (Amikacin, Kanamycin)
–Bind 30S ribosome → misreading of mRNA → ↓ protein synthesis.
3) Linezolid
–Binds 50S ribosome → inhibits initiation of protein synthesis.
4) Bedaquiline
–Inhibits ATP synthase → blocks mycobacterial energy production.
5) Delamanid
–Inhibits mycolic acid synthesis (similar to INH).
3. Clinical Uses
a) Active TB:
–Initial phase: Combination of 4 drugs (INH, RIF, PZA, EMB) for 2 months.
–Continuation phase: Combination of 2 drugs (INH and RIF) for 4-7 months.
b) Latent TB:
–Monotherapy (e.g., INH for 6-9 months) or combination (RIF + INH for 3 months).
c) Drug-Resistant TB:
–Individualized regimens with second-line drugs.
4. Adverse Effects
a) Isoniazid: Peripheral neuropathy (prevented with pyridoxine), hepatotoxicity.
b) Rifampin: Hepatotoxicity, red-orange body fluids, drug interactions (CYP inducer).
c) Pyrazinamide: Hyperuricemia, hepatotoxicity.
d) Ethambutol: Optic neuritis, reversible with discontinuation.
e) Streptomycin: Ototoxicity, nephrotoxicity.
5. Resistance Mechanisms
a) Mutations in drug targets (e.g., katG for INH, rpoB for RIF).
b) Efflux pumps.
c) Enzymatic inactivation of drugs.
b] Antileprosy Drugs
1. Classification
-Antileprosy drugs are used in combination therapy to prevent resistance and ensure effective eradication of Mycobacterium leprae.
a) First-Line Drugs (WHO MDT Drugs)
-These are the main drugs used routinely.
–Dapsone
–Rifampicin
–Clofazimine
b) Second-Line / Alternative Drugs (Used when intolerance or resistance)
–Ofloxacin
–Minocycline
–Clarithromycin
–Rifabutin
–Ethionamide / Prothionamide
c) Newer / Experimental Agents
–Bedaquiline (studied)
–Moxifloxacin (off-label)
2. Mechanism of Action
a) Dapsone
–Inhibits dihydropteroate synthase → blocks folic acid synthesis.
b) Rifampicin
–Inhibits DNA-dependent RNA polymerase → stops RNA synthesis (bactericidal).
c) Clofazimine
–Binds to mycobacterial DNA → inhibits replication; also anti-inflammatory.
d) Ofloxacin
–Inhibits DNA gyrase (Topoisomerase II) → blocks DNA replication.
e) Minocycline
–Blocks 30S ribosome → inhibits protein synthesis.
f) Clarithromycin
–Blocks 50S ribosome → inhibits protein synthesis.
3. Clinical Uses
a) Multibacillary Leprosy (MB):
–Dapsone + Rifampin + Clofazimine for 12 months.
b) Paucibacillary Leprosy (PB):
–Dapsone + Rifampin for 6 months.
c) Reactions in Leprosy:
–Type I Reaction: Use corticosteroids.
–Type II Reaction (Erythema Nodosum Leprosum): Use thalidomide or corticosteroids.
4. Adverse Effects
a) Dapsone: Hemolysis (especially in G6PD deficiency), methemoglobinemia.
b) Rifampin: Hepatotoxicity, red-orange body fluids. Clofazimine: Skin pigmentation (reddish-brown), gastrointestinal symptoms.
c] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanisms of Action: Describe how antitubercular and antileprosy drugs target bacterial cell walls, protein synthesis, and metabolic pathways.
–Drug Regimens: Understand standard treatment regimens for TB (e.g., DOTS strategy) and leprosy.
–Adverse Effects: Recognize potential toxicities and their prevention (e.g., pyridoxine for INH induced neuropathy).
–Drug Resistance: Explain the mechanisms and management of drug resistant TB.
b) Skill-Based Outcomes
–Rational Prescribing: Prescribe appropriate combinations of drugs to avoid resistance and ensure efficacy.
–Monitoring: Monitor liver function (for hepatotoxicity), vision (ethambutol), and other toxicities during therapy.
–Public Health Implementation: Apply national TB control program guidelines and strategies for leprosy eradication.
c) Attitude-Based Outcomes
–Patient Education: Educate patients on the importance of adherence to long term therapy to prevent resistance.
–Antimicrobial Stewardship: Promote the rational use of drugs in TB and leprosy management.
–Community Engagement: Advocate for early diagnosis and treatment in endemic regions to reduce transmission.
7. Antimalarial drugs
A] Classification of Antimalarial Drugs
1. Based on Mechanism of Action
a) Blood Schizonticides(Act on asexual blood-stage parasites)
–Chloroquine
–Artemisinin derivatives
–Quinine/Quinidine
–Mefloquine
–Atovaquone
–Proguanil (with atovaquone)
b) Tissue Schizonticides (Act on liver-stage parasites)
–Primaquine
–Proguanil
–Atovaquone
c) Gametocides (Act on sexual forms of parasite – prevent transmission)
–Primaquine
–Artemisinin derivatives (against P. falciparum)
d) Sporontocides (Act inside mosquito – inhibit development of oocysts)
–Primaquine
–Proguanil
2. Key Antimalarial Agents
-Chloroquine, Artemisinin Derivatives, Quinine/Quinidine, Mefloquine, Primaquine, Proguanil and Pyrimethamine, Atovaquone
B] Clinical Applications
1. Treatment of Malaria
a) Uncomplicated Malaria:
–P. vivax and P. ovale: Chloroquine + Primaquine.
–P. falciparum (chloroquineresistant): Artemisinin-based Combination Therapy (ACT).
b) Severe Malaria:
–IV Artesunate is the drug of choice.
–Alternatives: IV Quinine or Quinidine.
c) Radical Cure:
–Primaquine or Tafenoquine to eradicate hypnozoites in relapsing malaria (P. vivax and P. ovale).
2. Prophylaxis of Malaria
a) Casual Prophylaxis (prevents hepatic infection): Atovaquone-Proguanil.
b) Suppressive Prophylaxis (prevents blood-stage infection): Mefloquine, Doxycycline.
3. Drug-Resistant Malaria
-ACTs (e.g., Artemether Lumefantrine, Artesunate Mefloquine).
4. Mechanisms of Resistance
a) Chloroquine: Mutations in the PfCRT (Plasmodium falciparum chloroquine resistance transporter) gene.
b) Artemisinin: Delayed parasite clearance due to mutations in the K13 gene.
c) Pyrimethamine/Proguanil: Mutations in the dihydrofolate reductase (DHFR) enzyme
5. Adverse Effects
a) Chloroquine – causes itching, visual disturbances (retinopathy with long use).
b) Quinine – can cause “cinchonism” (ringing in ears, headache, nausea).
c) Artemisinin derivatives – may cause mild gastrointestinal upset.
d) Mefloquine – may cause vivid dreams, anxiety, or depression.
e) Primaquine – can cause hemolysis (breakdown of red blood cells) in people with G6PD deficiency
C] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Mechanisms of Action: Explain how antimalarial drugs target specific stages of the parasite lifecycle.
–Drug Selection: Describe first-line and alternative therapies for uncomplicated, severe, and relapsing malaria.
–Resistance Patterns: Understand mechanisms of resistance and how they influence therapy.
–Adverse Effects: Recognize common toxicities and preventive measures (e.g., testing for G6PD deficiency).
b) Skill-Based Outcomes
–Rational Prescribing: Prescribe appropriate antimalarials based on species, resistance patterns, and patient factors.
–Monitoring and Safety: Monitor for adverse effects, such as QT prolongation and hemolysis.
–Preventive Strategies: Develop prophylactic regimens tailored to travel destinations and patient risks.
c) Attitude-Based Outcomes
–Patient Education: Counsel patients on the importance of adherence to treatment to prevent resistance.
–Global Health Awareness: Advocate for malaria prevention and treatment programs in endemic regions.
–Antimicrobial Stewardship: Use antimalarials judiciously to avoid resistance development
K = Miscellaneous
1. Disinfectants
A] Classification of Disinfectants Based on Chemical Composition
-Ethanol/Isopropanol
-Sodium Hypochlorite
-Glutaraldehyde
-Hydrogen Peroxide
-Quaternary Ammonium Compounds
B] Mechanism of Action
-Targeting Microbial Structures: Disinfectants act on cell walls, membranes, or intracellular components to inhibit or kill microbes.
-Broad-Spectrum Activity: Effective against bacteria, viruses, fungi, and spores (depending on the type and concentration).
C] Principles of Disinfectant Use
1. Selection Based on Purpose
a) High-Level Disinfection: Required for medical instruments that contact mucous membranes (e.g., glutaraldehyde, peracetic acid).
b) Intermediate-Level Disinfection: For surfaces that come in contact with intact skin (e.g., alcohols, chlorine compounds).
c) Low-Level Disinfection: Suitable for general cleaning of floors, walls, and furniture (e.g., QACs).
2. Concentration and Contact Time
a) Alcohols: Effective at 6090%, with optimal contact time of 10–15 minutes.
b) Sodium Hypochlorite: Typically used in 0.1–0.5% solutions for surface disinfection.
c) Hydrogen Peroxide: Usually applied in 3% solutions for general use.
D) Commonly Used Disinfectants and Applications
a) Ethanol and Isopropanol (Alcohols) – These act by denaturing proteins and disrupting microbial cell membranes. They are most effective in 60–90% concentrations. Commonly used for hand sanitization, skin antisepsis before injections, and disinfecting small surfaces such as thermometers and stethoscopes.
b) Sodium Hypochlorite (Bleach) – A strong oxidizing agent that destroys microbial proteins and nucleic acids. Usually used in concentrations of 0.1–0.5% for disinfecting surfaces, cleaning contaminated spills, hospital floors, and medical equipment (non-metallic surfaces).
c) Glutaraldehyde – A high-level disinfectant that alkylates proteins and nucleic acids, leading to microbial death. It is mainly used to disinfect medical instruments such as endoscopes, respiratory equipment, and surgical tools that contact mucous membranes.
d) Hydrogen Peroxide – Acts by releasing free radicals that damage microbial proteins and DNA. A 3–6% solution is used for wound cleansing, surface disinfection, and sterilization of instruments.
e) Quaternary Ammonium Compounds (QACs) – These disrupt microbial cell membranes and cause leakage of cell contents. They are suitable for low-level disinfection of environmental surfaces like floors, walls, and furniture in hospitals and laboratories.
f) Peracetic Acid – A strong oxidizing agent that denatures proteins and disrupts cell walls. It is used for high-level disinfection and sterilization of medical instruments and endoscopes.
g) Phenolic Compounds – These work by disrupting cell walls and precipitating proteins. They are used for environmental disinfection in healthcare and laboratory settings but are less preferred today due to toxicity concerns.
E] Adverse Effects and Precautions
a) Alcohols may cause skin dryness and irritation and are highly flammable. They should be used in well-ventilated areas and kept away from flames.
b) Sodium Hypochlorite can irritate the skin and eyes and is corrosive to metals. It should never be mixed with acids or ammonia, as this releases toxic chlorine gas. Gloves and eye protection should be worn when handling it.
c) Glutaraldehyde can irritate the skin, eyes, and respiratory tract, and prolonged exposure may cause dermatitis or asthma-like symptoms. Use it only in a well-ventilated area with protective gear.
d) Hydrogen Peroxide can irritate the skin and eyes and may bleach fabrics. It should be handled carefully and stored in dark bottles since it is light-sensitive.
e) Quaternary Ammonium Compounds may cause mild skin irritation and are ineffective against spores and certain viruses. Avoid ingestion and eye contact.
f) Peracetic Acid is corrosive and can irritate the skin, eyes, and respiratory tract. It has a strong odor and should be used with gloves, goggles, and good ventilation.
g) Phenolic Compounds are toxic to tissues and particularly harmful to infants; they can cause skin irritation. They should not be used on food-contact surfaces or directly on skin.
f] Standard Learning Outcomes (SLO)
a) Knowledge-Based Outcomes
–Classification: Categorize disinfectants based on chemical composition and use.
–Mechanism of Action: Explain how disinfectants kill or inhibit microbes.
–Application: Recognize the appropriate disinfectant for specific situations (e.g., surgical instruments vs. general surfaces).
b) Skill-Based Outcomes
–Preparation: Demonstrate correct preparation and dilution of disinfectants.
–Application Techniques: Apply disinfectants effectively to achieve optimal microbial control.
–Monitoring: Evaluate the effectiveness of disinfection and identify potential failures.
c) Attitude-Based Outcomes
–Judicious Use: Encourage responsible use of disinfectants to prevent resistance and environmental harm.
–Safety Practices: Adhere to safety guidelines to protect users and patients.
2. Vitamins
A] Classification and Sources
Vitamins are organic compounds essential for normal metabolism, growth, and health. They are classified based on their solubility into:
1. Fat-Soluble Vitamins
-Vitamins A, D, E, and K
-Sources: Dairy products, fish oils, liver, egg yolk, green leafy vegetables, nuts, and vegetable oils.
2. Water-Soluble Vitamins
-Vitamin C and the B-Complex group (B₁, B₂, B₃, B₅, B₆, B₇, B₉, B₁₂).
-Sources: Fresh fruits, vegetables, cereals, legumes, meat, milk, and eggs.
B] Fat-Soluble Vitamins and Deficiency Disorders
1. Vitamin A (Retinol)
-Function: Essential for vision, growth, epithelial tissue maintenance, and immune function.
-Deficiency Disorders: Night blindness, xerophthalmia (dry eyes), keratomalacia, and increased susceptibility to infections.
-Sources: Liver, milk, butter, egg yolk, green leafy vegetables, and carrots.
2. Vitamin D (Calciferol)
-Function: Regulates calcium and phosphate metabolism; maintains bone health.
-Deficiency Disorders: Rickets in children, osteomalacia in adults, and osteoporosis.
-Sources: Sunlight exposure, fish liver oils, fortified milk, and egg yolk.
3. Vitamin E (Tocopherol)
-Function: Acts as an antioxidant, protects cell membranes from oxidative damage.
-Deficiency Disorders: Neuromuscular disorders, hemolytic anemia in newborns, and peripheral neuropathy.
-Sources: Vegetable oils, nuts, seeds, and green leafy vegetables.
4. Vitamin K
-Function: Required for synthesis of clotting factors (II, VII, IX, X) in the liver.
-Deficiency Disorders: Prolonged bleeding time, easy bruising, and hemorrhagic disease of the newborn.
-Sources: Green leafy vegetables, liver, and gut bacterial synthesis.
C] Water-Soluble Vitamins and Deficiency Disorders
1. Vitamin C (Ascorbic Acid)
-Function: Collagen synthesis, wound healing, antioxidant activity, and iron absorption.
-Deficiency Disorders: Scurvy (bleeding gums, delayed wound healing, fatigue).
-Sources: Citrus fruits, tomatoes, guava, and green vegetables.
2. B-Complex Vitamins
-Functions: Serve as coenzymes in metabolism of carbohydrates, proteins, and fats.
-Deficiency Disorders:
–B₁ (Thiamine): Beriberi, Wernicke-Korsakoff syndrome.
–B₂ (Riboflavin): Cheilosis, glossitis, dermatitis.
–B₃ (Niacin): Pellagra (dermatitis, diarrhea, dementia).
–B₆ (Pyridoxine): Anemia, dermatitis, peripheral neuropathy.
–B₉ (Folic Acid): Megaloblastic anemia, neural tube defects in fetus.
–B₁₂ (Cobalamin): Pernicious anemia, neurological symptoms.
D] Supplementation Principles
1. Deficiency-Based Supplementation:
-Vitamin supplements are prescribed to correct specific deficiencies, e.g., Vitamin D in rickets, Vitamin B₁₂ in pernicious anemia.
2. Therapeutic Use:
-High-dose vitamin therapy is used for certain medical conditions, e.g., Vitamin D for osteoporosis, Folic acid in pregnancy, and Vitamin C for wound healing.
E] Safety Considerations
1. Fat-soluble vitamins
-Are stored in body tissues and may cause hypervitaminosis (toxicity) if taken in excess.
2. Water-soluble vitamins
-Are generally safe as excess amounts are excreted in urine, but very high doses should still be avoided.
F] Standard Learning Outcomes(SLO)
a) Knowledge-Based Outcomes
–Understand the physiological role of vitamins in metabolism and disease prevention.
–Identify clinical signs and symptoms of vitamin deficiencies and their appropriate management.
b) Skill-Based Outcomes
–Prescribe appropriate vitamin supplements based on individual or clinical needs.
–Educate patients about natural dietary sources of vitamins and the importance of balanced nutrition.
c) Attitude-Based Outcomes
–Promote healthy and balanced dietary habits to prevent vitamin deficiencies.
–Encourage responsible use of vitamin supplements and discourage unnecessary or excessive intake.