Part 2 moves from organ systems to the CNS, respiratory system, cancer therapy, drug safety, and research ethics. The same four causal threads from Part 1 keep running through every lecture.
Part 2 is dominated by drugs that either slow the CNS down or speed it up. The same electrical logic applies: calm = enhance inhibition (GABA/Cl⁻) or block excitation (Na⁺/Ca²⁺/AMPA); stimulate = reverse that balance.
下篇的藥物主要是讓中樞神經系統變慢或變快。電生理邏輯一樣：冷靜 = 增強抑制（GABA/Cl⁻）或阻斷興奮（Na⁺/Ca²⁺/AMPA）；興奮 = 反過來打破平衡。
| Lecture | English | 中文邏輯 |
|---|---|---|
| L5 CNS | Depressants (benzodiazepines, barbiturates, general anaesthetics) step on the GABA brake. Stimulants (amphetamines, caffeine) press the gas by boosting catecholamines. | 抑制劑（苯二氮䓬、巴比妥、全身麻醉藥）踩下 GABA 剎車。興奮劑（安非他命、咖啡因）提升兒茶酚胺以踩油門。 |
| L6 Respiratory | β2 agonists sit on the muscle itself and open the airway = press the gas. Muscarinic antagonists occupy M3 so acetylcholine can no longer constrict the muscle = take the parasympathetic brake off. | β2 促效劑作用在肌肉本身、把氣道打開 = 踩油門。毒蕈鹼拮抗劑佔住 M3，令 ACh 無法收縮平滑肌 = 放掉副交感這道剎車。 |
| L8 Chemotherapy & Biologics | Cytotoxic chemo cuts the gas for rapidly dividing cancer cells. Biologics can be either brakes (checkpoint inhibitors, TNF blockers) or targeted gas-cutters (monoclonal antibodies). | 細胞毒性化療切斷快速分裂癌細胞的油門。生物製劑可以是剎車（免疫檢查點抑制劑、TNF 阻斷劑）或標靶切油門（單株抗體）。 |
| L7 Drug Safety | Adverse effects are often the same mechanism pushed too far: too much brake = sedation/respiratory depression; too much gas = arrhythmia/seizure. | 不良反應常是同一機制被推到過頭：剎車太多 = 鎮靜／呼吸抑制；油門太多 = 心律不整／癲癇。 |
Diseases in Part 2 are often imbalances between two opposing forces. Therapy restores the midpoint, either by raising the low side or lowering the high side.
下篇許多疾病都是兩股相反力量之間的失衡。治療就是把中點拉回來，可以把低的那端抬高，或把高的那端壓低。
| Lecture | English | 中文邏輯 |
|---|---|---|
| L5 CNS | Parkinson's = dopamine low vs ACh relatively high. Treat with dopaminergics or anticholinergics. Alzheimer's = ACh shortage → cholinesterase inhibitors. | 帕金森氏症 = 多巴胺低、ACh 相對高，用多巴胺藥或抗膽鹼藥。阿茲海默症 = ACh 不足 → 膽鹼酯酶抑制劑。 |
| L8 Chemotherapy & Biologics | Cancer = unchecked cell growth vs immune surveillance. Chemo kills fast growers; biologics restore or redirect immune balance. | 癌症 = 失控的細胞生長對上免疫監視。化療殺死快速分裂細胞；生物製劑恢復或重導免疫平衡。 |
| L7 Drug Safety | Efficacy vs toxicity is itself a seesaw. Dose, route, and special populations determine which side tips. | 療效對毒性本身就是蹺蹺板。劑量、途徑、特殊族群決定了哪一端下沉。 |
Size and lipid solubility decide whether a molecule reaches its target. The BBB excludes most; the gut wall and first-pass liver add further filters. This explains why CNS drugs, biologics, and inhaled agents are designed the way they are.
分子大小與脂溶性決定它能否到達標靶。BBB 排除大多數分子；腸壁與肝臟首渡代謝再加濾網。這解釋了為什麼中樞藥物、生物製劑和吸入劑要這樣設計。
| Lecture | English | 中文邏輯 |
|---|---|---|
| L5 CNS | Small lipid-soluble molecules cross the BBB; proteins and biologics do not. This is why levodopa (prodrug) is used instead of dopamine. | 小分子脂溶性藥物穿過 BBB；蛋白質與生物製劑不行。這就是為什麼用 levodopa（前驅藥）而不是多巴胺。 |
| L6 Respiratory | Inhalation bypasses systemic barriers and deposits drug at the site of disease. The device, not just the molecule, determines efficacy. | 吸入繞過全身屏障，把藥物送到病灶。決定療效的不只是分子，還有裝置。 |
| L8 Chemotherapy & Biologics | Most biologics are too large for oral absorption and must be given parenterally. They also cannot cross the BBB, limiting CNS applications. | 大多數生物製劑太大，無法口服吸收，必須腸胃外給藥。它們也過不了 BBB，限制了中樞應用。 |
| L9 Animals & Alternative Medicine | Animal models predict human ADME and toxicity before human trials. The 3Rs framework tries to reduce the barrier between useful science and ethical limits. | 動物模型在人體試驗前預測人類 ADME 與毒性。3R 框架試圖在有用科學與倫理界限之間取得平衡。 |
The same symptom can be produced through different receptor pathways. A good prescription matches the drug to the lock that is actually being turned.
同一個症狀可以經由不同受體路徑產生。好的處方是把藥對上真正被轉動的那把鎖。
| Lecture | English | 中文邏輯 |
|---|---|---|
| L5 CNS | Pain: μ-opioid (CNS) vs COX (periphery). Vomiting: 5-HT₃, NK1, M, D₂/H₁. Each receptor is a different lock for a different trigger. | 疼痛：μ 鴉片受體（中樞）對 COX（周邊）。嘔吐：5-HT₃、NK1、M、D₂/H₁。每個受體都是不同觸發點的不同鎖。 |
| L6 Respiratory | Asthma/COPD symptoms come from bronchospasm, inflammation, histamine, or leukotrienes. Each pathway has its own drug class. | 哮喘／COPD 症狀來自支氣管痙攣、發炎、組織胺或白三烯。每條路徑都有對應藥物類別。 |
| L8 Chemotherapy & Biologics | Cancer cells are targeted by cell-cycle phase (S, M), receptor tyrosine kinases, immune checkpoints, or hormone receptors. The lock determines the key. | 癌細胞可按細胞週期期別（S、M）、受體酪胺酸激酶、免疫檢查點或荷爾蒙受體來標靶。鎖決定鑰匙。 |
| L7 Drug Safety | Drug-drug interactions happen when two drugs compete for the same metabolic lock (CYP450) or receptor. | 藥物相互作用發生在兩種藥競爭同一把代謝鎖（CYP450）或受體時。 |
Pick any Part 2 drug and ask four questions. (1) Is it a brake or gas? (2) Which side of a seesaw does it push? (3) How does it cross or bypass barriers? (4) Which receptor lock does it fit? If you can answer those, the generic name becomes a consequence rather than a fact to memorise.
隨便挑一個下篇藥物，問四個問題：(1) 它是剎車還是油門？(2) 它推的是蹺蹺板的哪一端？(3) 它如何越過或繞過屏障？(4) 它對上哪一把受體鎖？能答這四題，學名就變成推論結果，而不是要硬背的事實。
The threads are more durable than the drug names. Learn the pattern once, then hang each drug on it.