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Plan for study pharmacology

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Here is a focused, practical 2–3 month pharmacology study plan for a preclinical medical student targeting university exams.

📚 Pharmacology Study Plan — 2–3 Months (Preclinical, Exam-Focused)

🔑 Core Principles Before You Start

Understand mechanisms first, memorize second. If you know why a drug works, you can reason through effects and side effects without pure memorization.
Group drugs by class. Study drug families together (e.g., all beta-blockers, all ACE inhibitors) rather than individually.
Use active recall — flashcards, self-quizzing — not passive re-reading.
Spaced repetition (Anki or similar) is non-negotiable for retaining drug names and details.

🗓️ Phase 1 — Foundations (Weeks 1–2)

Goal: Build the conceptual framework everything else hangs on.

Topic	What to Cover
Pharmacokinetics	ADME — absorption, distribution, metabolism, excretion; half-life; bioavailability; first-pass effect
Pharmacodynamics	Receptor types, agonists vs antagonists, dose-response curves, EC50/ED50, therapeutic index
Drug interactions	Pharmacokinetic vs pharmacodynamic interactions
Autonomic pharmacology	Cholinergic & adrenergic receptors, agonists, antagonists — this underpins many later systems

Autonomic pharmacology is the most important foundation. Get it solid before moving on.

🗓️ Phase 2 — System-by-System Coverage (Weeks 3–9)

Tackle one system per week. Each week: learn the class mechanism → drugs → clinical uses → key side effects → contraindications.

Week	System	Key Drug Classes
3	Cardiovascular	Anti-hypertensives (ACEi, ARBs, CCBs, diuretics, beta-blockers), anti-arrhythmics, heart failure drugs
4	Cardiovascular (cont.)	Anticoagulants, antiplatelets, thrombolytics, lipid-lowering agents
5	CNS	Sedatives, anxiolytics (benzodiazepines), antidepressants (SSRIs, TCAs, MAOIs), antipsychotics
6	CNS (cont.)	Antiepileptics, opioid analgesics, NSAIDs, local/general anesthetics
7	Endocrine & Metabolic	Insulin, oral hypoglycemics, thyroid drugs, corticosteroids, sex hormones
8	Antimicrobials	Antibiotics (penicillins, cephalosporins, macrolides, quinolones, aminoglycosides), antivirals, antifungals
9	Respiratory, GI, Renal	Bronchodilators, antihistamines, PPIs, antiemetics, diuretics

🗓️ Phase 3 — Consolidation & Exam Prep (Weeks 10–12)

Week	Activity
10	Full review of high-yield drug tables; identify weak areas from Phase 2
11	Past paper questions / MCQ banks — at least 30–50 questions/day; review explanations
12	Final weak-area revision; timed mock exam; stop learning new material 3 days before exam

🧠 Daily Study Structure (2–3 hrs/day)

Time	Activity
0–15 min	Anki review (previous cards)
15–90 min	New material (textbook/notes/video)
90–120 min	Self-quiz / MCQs on today's material
120–150 min	Write a brief summary / drug table from memory

📖 Recommended Resources

Resource	Purpose
Katzung's Basic & Clinical Pharmacology	Primary textbook — comprehensive
Lippincott's Illustrated Pharmacology	More visual and exam-friendly
Anki (shared decks or custom)	Spaced repetition — use daily
Sketchy Pharm / Ninja Nerd (YouTube)	Visual/mnemonic learning for tough classes
Past university MCQs	Exam pattern familiarization

⚠️ Common Pitfalls to Avoid

Trying to memorize every drug name before understanding the class
Skipping pharmacokinetics (it explains why dosing matters)
Not doing MCQs until the last week — start from Week 3
Cramming the antibiotic chapter in one sitting — spread it over 2 days minimum

This plan covers the full preclinical pharmacology curriculum in a logical, progressive order. Adjust the pace based on your syllabus — if your exam focuses heavily on one system, allocate more time there. Let me know if you'd like a deeper breakdown of any specific week or topic.

Endocrine in detail explanation chapterwise in pharmacology

Reading File

Finding Sources

All content is in block 8 of Katzung. Let me read the major endocrine sections in parallel.

Reading File

Finding Sources

Reading File

Here is the complete chapterwise endocrine pharmacology breakdown, drawn from Katzung's Basic & Clinical Pharmacology (16th ed.).

🧬 Endocrine Pharmacology — Chapterwise Detailed Explanation

CHAPTER 1 — Thyroid Pharmacology

🔬 Thyroid Physiology (Foundation)

The thyroid gland secretes two active hormones:

T3 (triiodothyronine) — more potent, shorter half-life
T4 (thyroxine / tetraiodothyronine) — longer half-life, converted to T3 peripherally

Both contain iodine as an essential component (T3 = 59% iodine, T4 = 65% iodine).

Iodide Metabolism:

Daily requirement: 150 mcg/day (200 mcg in pregnancy)
Iodide is absorbed, enters extracellular fluid pool → thyroid takes ~75 mcg/day
Excess iodide → fractional thyroid uptake decreases

Biosynthesis of Thyroid Hormones (Step-by-Step)

Step	Process	Drug Target
1	Iodide uptake via NIS (Na/I symporter)	Blocked by thiocyanate, perchlorate, large doses of iodide
2	Iodide transported across apical membrane via pendrin	—
3	Thyroid peroxidase (TPO) oxidizes I⁻ → I₂	Blocked by thioamides (PTU, methimazole)
4	Organification — iodination of tyrosine residues → MIT, DIT	Blocked by thioamides
5	Coupling — DIT + DIT → T4; MIT + DIT → T3	Blocked by thioamides
6	Proteolysis of thyroglobulin → releases T3, T4 into blood	—

💡 Pendred syndrome: mutation in SLC26A4 gene (pendrin) → goiter + deafness

💊 Thyroid Preparations (Hypothyroidism Treatment)

Drug	Type	Key Points
Levothyroxine (T4)	Synthetic T4	Drug of choice; long half-life (~7 days); taken on empty stomach
Liothyronine (T3)	Synthetic T3	Faster onset; shorter half-life; used when rapid correction needed
Liotrix	T4:T3 (4:1 mix)	Less commonly used
Desiccated thyroid	Natural (porcine/bovine)	Contains T3+T4; variable potency

Clinical notes:

TSH is the best monitor for levothyroxine therapy
Bioavailability affected by calcium, iron, antacids (take separately)
Interactions: warfarin (↑ effect), digoxin (↓ effect)

⚠️ Antithyroid Drugs (Hyperthyroidism Treatment)

1. Thioamides

Drug	Mechanism	Special Feature
Propylthiouracil (PTU)	Inhibits TPO; also blocks T4→T3 conversion peripherally	Preferred in 1st trimester pregnancy and thyroid storm
Methimazole (MMI)	Inhibits TPO only	Preferred outside pregnancy (once-daily dosing, safer)

Side effects: agranulocytosis (most serious — stop drug, check WBC), rash, hepatotoxicity (PTU >> MMI)

Onset: Both take 3–4 weeks to work (depleting stored hormone)

2. Radioactive Iodine (¹³¹I)

Destroys thyroid follicular cells by beta radiation
Treatment of choice for Graves' disease in adults (not in pregnancy)
Leads to hypothyroidism in most patients long-term

3. Iodide (High-dose)

Wolff-Chaikoff effect — high iodide paradoxically inhibits TPO transiently
Uses: pre-operative preparation (Lugol's iodine), thyroid storm
Escape occurs after ~10 days — cannot be used long-term

4. Beta-blockers (Propranolol)

Controls symptomatic hyperthyroidism (tachycardia, tremor, anxiety)
Propranolol also blocks peripheral T4→T3 conversion at high doses
Does NOT reduce hormone synthesis

5. Teprotumumab

IGF-1 receptor inhibitor — approved for thyroid eye disease (Graves' ophthalmopathy)

Thyroid Storm Management

PTU (blocks synthesis + peripheral conversion)
High-dose iodide (given 1 hour after PTU to prevent organification)
Propranolol (symptomatic control)
Hydrocortisone (blocks T4→T3 conversion)
Supportive: antipyretics, fluids

CHAPTER 2 — Pancreatic Hormones & Antidiabetic Drugs

🔬 Endocrine Pancreas — Basic Structure

Cell	% of Islet	Product
Beta (B)	75%	Insulin, C-peptide, amylin
Alpha (A)	20%	Glucagon
Delta (D)	3–5%	Somatostatin
Epsilon	<1%	Ghrelin

Insulin — Chemistry & Physiology

Molecular weight: 5808 Da; 51 amino acids in A chain + B chain linked by disulfide bridges
Synthesized as preproinsulin → proinsulin → cleaved by proteases into insulin + C-peptide (in equimolar amounts)
C-peptide: marker of endogenous insulin secretion (absent in exogenous insulin injection)
Stored as hexamers (with Zn²⁺) in beta cell granules; dissociates into monomers for absorption

Mechanism of insulin secretion:

Glucose enters beta cell → metabolized → ATP rises
ATP-sensitive K⁺ channel closes → membrane depolarizes
Voltage-gated Ca²⁺ channel opens → insulin granule exocytosis

💡 Sulfonylureas mimic step 2 by blocking K⁺-ATP channels

Insulin Preparations

Category	Examples	Onset	Peak	Duration
Rapid-acting analogs	Lispro, Aspart, Glulisine	5–15 min	30–90 min	3–5 h
Short-acting (Regular)	Regular insulin	30–60 min	2–3 h	5–8 h
Intermediate-acting	NPH (isophane)	1–2 h	4–10 h	14–18 h
Long-acting analogs	Glargine, Detemir	1–2 h	No peak	20–24 h
Ultra-long acting	Degludec	1–2 h	No peak	>42 h

💡 Glargine precipitates at SC site (slightly acidic pH), giving slow release — cannot be mixed with other insulins

Oral Antidiabetic Drugs (Type 2 DM)

1. Biguanides — Metformin (First-line)

Feature	Detail
Mechanism	Activates AMPK → inhibits hepatic gluconeogenesis; improves insulin sensitivity
Does NOT cause	Hypoglycemia (no insulin release); weight gain
Key side effects	GI upset (nausea), lactic acidosis (rare, especially in renal failure)
Contraindications	eGFR <30, IV contrast, liver failure, heavy alcohol use
Benefit	Reduces CV events; weight neutral to modest weight loss

2. Sulfonylureas (2nd generation preferred)

Drug	Example
1st gen	Tolbutamide, chlorpropamide
2nd gen	Glipizide, Glyburide, Glimepiride

Mechanism: Bind SUR1 subunit of K⁺-ATP channel → channel closes → insulin release (glucose-independent)
Side effects: Hypoglycemia (most common), weight gain
Avoid in sulfa allergy; renally cleared (glyburide) — use glipizide in elderly

3. Meglitinides (Glinides)

Repaglinide, Nateglinide
Same mechanism as sulfonylureas but shorter acting → taken with each meal
Less hypoglycemia risk between meals

4. Thiazolidinediones (TZDs / Glitazones)

Pioglitazone, Rosiglitazone
Mechanism: Activate PPARγ nuclear receptor → improve insulin sensitivity in fat and muscle
Side effects: Weight gain, fluid retention, heart failure (CI in HF), bone fractures
Rosiglitazone withdrawn due to CV concerns; pioglitazone still in use

5. Alpha-Glucosidase Inhibitors

Acarbose, Miglitol
Mechanism: Inhibit intestinal α-glucosidase → delay carbohydrate absorption → blunt post-meal glucose spike
Side effects: Flatulence, diarrhea (fermentation of undigested carbs)
Only active at gut level; no systemic hypoglycemia

6. DPP-4 Inhibitors (Gliptins)

Sitagliptin, Saxagliptin, Linagliptin, Alogliptin
Mechanism: Inhibit DPP-4 enzyme → prolongs GLP-1 and GIP → glucose-dependent insulin secretion
Side effects: Nasopharyngitis, rare pancreatitis
Weight neutral; no hypoglycemia alone

7. GLP-1 Receptor Agonists (Incretin Mimetics)

Exenatide, Liraglutide, Semaglutide, Dulaglutide
Mechanism: Mimic GLP-1 → stimulate insulin (glucose-dependent), suppress glucagon, slow gastric emptying, central satiety
Benefits: Weight loss, CV protection (liraglutide, semaglutide)
Side effects: Nausea/vomiting, rare pancreatitis; do not use in MEN2 or medullary thyroid cancer (rodent risk)
Semaglutide available orally (Rybelsus) and as injectable

8. SGLT-2 Inhibitors (Gliflozins)

Canagliflozin, Dapagliflozin, Empagliflozin
Mechanism: Inhibit SGLT-2 in proximal tubule → prevent glucose reabsorption → glucosuria
Benefits: CV protection (empagliflozin, canagliflozin), heart failure reduction, renoprotection
Side effects: UTI, genital mycotic infections, DKA (euglycemic), volume depletion, lower limb amputation (canagliflozin)
Weight loss ~2–3 kg; blood pressure lowering

Glucagon & Hypoglycemia Treatment

Glucagon — stimulates hepatic glycogenolysis; used in severe hypoglycemia when IV access unavailable
Glucagon kit (1 mg IM/SC) or intranasal glucagon

CHAPTER 3 — Adrenocortical Hormones & Antagonists

🔬 Adrenal Cortex — Zones and Products

Zone	Product
Zona glomerulosa	Mineralocorticoids (aldosterone)
Zona fasciculata	Glucocorticoids (cortisol)
Zona reticularis	Androgens (DHEA, androstenedione)

All steroids synthesized from cholesterol.

Glucocorticoids

Endogenous: Cortisol (hydrocortisone) Pharmacological: Prednisone, prednisolone, methylprednisolone, dexamethasone, betamethasone

Mechanism:

Steroid diffuses into cell → binds cytoplasmic glucocorticoid receptor (GR)
GR–ligand complex → translocates to nucleus
Binds GRE (glucocorticoid response elements) → activates or represses gene transcription
Key effect: induces lipocortin → inhibits phospholipase A2 → blocks arachidonic acid release → reduces prostaglandins, leukotrienes, thromboxanes

Physiological effects:

Carbohydrate: ↑ gluconeogenesis, ↑ blood glucose (counter-regulatory)
Protein: catabolic — ↑ muscle breakdown
Fat: Redistribution (central obesity, buffalo hump, moon face)
Immune: Anti-inflammatory; suppress T-cells, macrophages, cytokines
Bone: ↓ osteoblast activity, ↑ osteoclast activity → osteoporosis
Sodium: Mild Na⁺ retention (weak mineralocorticoid effect)

Relative Potencies:

Drug	Anti-inflammatory	Mineralocorticoid	Duration
Hydrocortisone	1	1	Short
Prednisone	4	0.8	Medium
Methylprednisolone	5	0.5	Medium
Dexamethasone	25–30	0	Long
Betamethasone	25–30	0	Long

💡 Dexamethasone — no mineralocorticoid activity; preferred for cerebral edema, dexamethasone suppression test (Cushing's), fetal lung maturity

Clinical uses:

Inflammatory/autoimmune: RA, SLE, IBD, asthma, allergic reactions
Organ transplant rejection prevention
Adrenal insufficiency (replacement therapy)
Cerebral edema (dexamethasone)
Antenatal fetal lung maturation (betamethasone/dexamethasone)
Shock (septic shock — controversial)

Side effects (chronic use):

Cushing's syndrome (iatrogenic): moon face, buffalo hump, central obesity, striae
Adrenal suppression — HPA axis suppression; never stop abruptly (taper)
Hyperglycemia (steroid diabetes)
Osteoporosis
Peptic ulcer
Infections (immunosuppression)
Cataract, glaucoma
Growth retardation in children
Psychosis / mood changes

Mineralocorticoids

Endogenous: Aldosterone Pharmacological: Fludrocortisone (most potent oral mineralocorticoid)

Mechanism: Acts on collecting duct → ↑ Na⁺ reabsorption, ↑ K⁺ excretion, ↑ H⁺ excretion
Use: Adrenal insufficiency (Addison's disease), salt-losing congenital adrenal hyperplasia
Side effects: Hypertension, hypokalemia, edema

Mineralocorticoid Antagonists:

Spironolactone — competitive aldosterone antagonist; used in heart failure, hypertension, hyperaldosteronism, hirsutism; causes gynecomastia
Eplerenone — more selective, less gynecomastia

Adrenal Androgens

DHEA (dehydroepiandrosterone), androstenedione, testosterone
Converted peripherally to more potent androgens or estrogens
Clinical role: contribute to adrenarche (pubic/axillary hair)
Therapeutic use of DHEA: studied in SLE and adrenal insufficiency with modest benefit; no proven role in athletic performance or memory

Inhibitors of Adrenal Steroid Synthesis

Drug	Mechanism	Use
Aminoglutethimide	Blocks cholesterol → pregnenolone	Cushing's, breast cancer (now replaced)
Metyrapone	Blocks 11β-hydroxylase (cortisol synthesis)	Cushing's diagnosis/treatment
Ketoconazole	Inhibits multiple CYP enzymes in steroid synthesis	Cushing's syndrome
Mifepristone (RU-486)	Glucocorticoid + progesterone receptor antagonist	Cushing's; also used as abortifacient
Mitotane	Adrenolytic (destroys adrenal cortical cells)	Adrenocortical carcinoma

CHAPTER 4 — Sex Hormones

Estrogens

Endogenous: Estradiol (E2) — most potent; estrone (E1); estriol (E3 — predominant in pregnancy)

Mechanism: Nuclear receptor (ER-α, ER-β) → gene transcription

Pharmacological estrogens:

Ethinyl estradiol, conjugated equine estrogens, estradiol valerate

Uses:

HRT (hormone replacement therapy) — menopausal symptoms
Combined oral contraceptives
Hypogonadism
Osteoporosis prevention (less common now)
Prostate cancer (high-dose)

Side effects: Nausea, fluid retention, DVT/PE (↑ clotting factors), breast cancer risk, endometrial hyperplasia (unopposed estrogen)

SERMs (Selective Estrogen Receptor Modulators):

Drug	Agonist at	Antagonist at	Use
Tamoxifen	Bone, uterus	Breast	Breast cancer treatment
Raloxifene	Bone	Breast, uterus	Osteoporosis, breast cancer prevention
Clomiphene	Pituitary (↑ GnRH pulse)	Hypothalamus	Ovulation induction (infertility)

Progestins

Endogenous: Progesterone

Pharmacological: Medroxyprogesterone acetate (MPA), norethindrone, levonorgestrel, desogestrel, drospirenone

Uses:

Combined OCP (with estrogen)
Progestin-only pill ("mini-pill")
Endometrial protection in HRT
Emergency contraception (levonorgestrel — Plan B)
Endometriosis
Threatened abortion

Mechanism of OCP contraception:

Inhibit LH surge → prevent ovulation (primary)
Thicken cervical mucus
Thin endometrial lining
Impair tubal motility

Androgens

Endogenous: Testosterone, DHT (dihydrotestosterone)

Pharmacological: Testosterone esters (cypionate, enanthate), methyltestosterone, oxandrolone

Uses:

Hypogonadism (male)
Delayed puberty
Anemia (erythropoiesis)
Anabolic use in catabolic states (wasting diseases)

Side effects:

Virilization (females): hirsutism, voice deepening, clitoromegaly
Males: testicular atrophy, gynecomastia (conversion to estrogen), prostate growth
Hepatotoxicity (17α-alkylated oral androgens)
Polycythemia

Antiandrogens:

Drug	Mechanism	Use
Finasteride	5α-reductase inhibitor (blocks T→DHT)	BPH, male-pattern baldness
Dutasteride	5α-reductase inhibitor (both types I+II)	BPH
Flutamide, Bicalutamide	Competitive androgen receptor antagonist	Prostate cancer
Spironolactone	Weak androgen receptor antagonist	Hirsutism, PCOS
Cyproterone	Androgen receptor antagonist	Hirsutism, prostate cancer

CHAPTER 5 — Hypothalamic & Pituitary Hormones

Hypothalamic Releasing Hormones & Drug Targets

Hormone	Effect	Pharmacological Analogs/Uses
GnRH (LHRH)	↑ LH, FSH	Leuprolide, goserelin, nafarelin — pulsatile = fertility; continuous = suppress LH/FSH (prostate cancer, endometriosis, precocious puberty)
GHRH	↑ GH	Sermorelin — GH deficiency
TRH	↑ TSH, prolactin	Protirelin — diagnostic
CRH	↑ ACTH	Corticorelin — Cushing's diagnosis
Somatostatin	↓ GH, TSH, insulin	Octreotide, lanreotide — acromegaly, carcinoid, varices

Pituitary Hormones

Hormone	Drug	Use
GH	Somatropin	GH deficiency, Turner syndrome, Prader-Willi, chronic renal failure
GH antagonist	Pegvisomant	Acromegaly
Prolactin inhibitor	Bromocriptine, Cabergoline (dopamine agonists)	Hyperprolactinemia, prolactinoma, acromegaly
ADH (Vasopressin)	Desmopressin (DDAVP)	Diabetes insipidus, bedwetting, von Willebrand disease, hemophilia A
ADH antagonist	Conivaptan, tolvaptan (vaptans)	SIADH (hyponatremia)
Oxytocin	Oxytocin	Induce/augment labor, postpartum hemorrhage
Oxytocin antagonist	Atosiban	Tocolysis (preterm labor)

CHAPTER 6 — Drugs Affecting Calcium & Bone Metabolism

Calcium Homeostasis Regulators

Hormone	Source	Action
PTH	Parathyroid	↑ Ca²⁺ (↑ bone resorption, ↑ renal Ca reabsorption, ↑ vitamin D activation)
Calcitriol (Vit D3)	Kidney (1α-hydroxylase)	↑ Ca²⁺ absorption in gut; ↑ bone mineralization
Calcitonin	Thyroid C-cells	↓ Ca²⁺ (↓ bone resorption)

Drugs for Osteoporosis

Drug	Mechanism	Notes
Bisphosphonates (alendronate, risedronate, zoledronate)	Inhibit osteoclast farnesyl pyrophosphate synthase → osteoclast apoptosis	Most widely used; oral taken fasting with water; osteonecrosis of jaw (rare)
Denosumab	Monoclonal antibody against RANK-L → inhibits osteoclastogenesis	SC injection q6 months; do not stop abruptly (rebound fractures)
Teriparatide	PTH analog → stimulates osteoblasts (anabolic)	Black box: osteosarcoma (rodent data); limited to 2 years
Abaloparatide	PTHrP analog, anabolic	Similar to teriparatide
Romosozumab	Anti-sclerostin antibody → ↑ bone formation + ↓ resorption	CV risk warning
Raloxifene	SERM — ↑ bone density	Also reduces breast cancer risk
Calcitonin (nasal)	Inhibits osteoclasts	Mild effect; mainly used for pain in vertebral fractures

Quick Summary — High-Yield Exam Points

Topic	High-Yield Fact
PTU vs Methimazole	PTU preferred in pregnancy 1st trimester + thyroid storm; MMI for everything else
Levothyroxine	Take on empty stomach; TSH is the monitoring parameter
Metformin	1st-line T2DM; causes lactic acidosis; contraindicated in CKD <30
Sulfonylureas	Cause hypoglycemia + weight gain; block K-ATP channel
SGLT-2 inhibitors	Glucosuria, UTI, euglycemic DKA, heart + kidney protection
GLP-1 agonists	Weight loss, nausea, CV benefit; avoid in medullary thyroid Ca
Dexamethasone	No mineralocorticoid activity; used for cerebral edema, Cushing's test
Fludrocortisone	Most potent oral mineralocorticoid; used in Addison's disease
Tamoxifen	ER antagonist in breast, agonist in uterus → endometrial cancer risk
Raloxifene	ER agonist at bone, antagonist at breast AND uterus (safer)
GnRH agonists (continuous)	Paradoxically suppress LH/FSH → used in prostate cancer, endometriosis
Bisphosphonates	Take fasting, stay upright; osteonecrosis of jaw risk
Teriparatide	Anabolic (only PTH analog that builds bone); osteosarcoma concern

Sources: Katzung's Basic & Clinical Pharmacology, 16th Edition — Chapters 38, 39, 40, 41, 42

---This covers all 6 major chapters of endocrine pharmacology. Here's a quick navigation guide:

Chapter	Topic
1	Thyroid — physiology, hypothyroidism drugs, antithyroid drugs, thyroid storm
2	Pancreas — insulin types, oral antidiabetics (metformin, sulfonylureas, SGLT-2, GLP-1, DPP-4, TZDs)
3	Adrenal — glucocorticoids, mineralocorticoids, adrenal androgens, synthesis inhibitors
4	Sex hormones — estrogens, progestins, SERMs, androgens, antiandrogens, OCPs
5	Hypothalamic/Pituitary — GnRH analogs, oxytocin, desmopressin, dopamine agonists
6	Calcium & Bone — PTH, Vitamin D, bisphosphonates, denosumab, teriparatide

Let me know if you want any chapter explained in even more depth, want practice MCQs, or want a drug comparison table for any specific class.

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