2804NRS

• 这门课是用两套完全不同的考核引擎在考你，而且考的模块不一样。[1]Source: asksia-bible-2804nrs-bilingual.pdf3· 考试 It's the End-of-Trimester exam. The MCQ half rewards the fact bullets and trap callouts; the short-answer half rewards re- telling a cascade in prose. Drill the steps() ladders - they ARE model SAQ answers. The blueprint overleaf shows exactly which modules carry the marks. 这是学期末考试。MCQ 部分奖 励事实要点和陷阱提示;简答部 分奖励用文字复述一条级联。反 复演练这些步骤阶梯- -它们本 身就是标准 SAQ 答案。下一页 的蓝图明确显示哪些模块承载着 分数。 2804NRS . Human Pathophysiology & Pharmacology 1 ! The single most important thing to understand about 2804NRS 关于 2804NRS 最需要理解的一件事 The unit is assessed in two completely different engines, and they examine different modules. Modules 1-2 (cells, injury, inflammation, microbiology) are tested by the A1 in-class quiz early in the trimester - and then they vanish from the End-of-Trimester exam study guide. The EoT exam examines Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). So learn M1-2 as scaffolding - they explain everything that follows (inflammation underpins hypersensitivity; cell injury underpins cancer) - but weight your final-exam revision on Modules 3-7. 本单元由两套截然不同的引擎评估,而它们考查的模块各不相同。模块1-2(细胞、损伤、炎症、微生物学)由学期早 期的 A1 课堂测验考核 -- 之后便从学期末考试复习指南中消失。学期末考试考查模块 3-7(免疫、肿瘤、肌肉骨骼/疼 痛、遗传/衰老、神经+自主神经药理学)。所以把 M1-2 当作支架来学 -- 它们解释了后续的一切(炎症支撑超敏反 应;细胞损伤支撑肿瘤) -- 但要把期末考的复习重心放在模块 3-7上。 i How this book was built - and the two-layer rule 本书是如何构建的 -- 以及双层规则 Standard biomedical science (the inflammation cascade, antibody geometry, ADME, dose-response) is stated plainly - it is universal canon, not anyone's copyright. The unit's own framing, sequencing and any example numbers are paraphrased and re-worked, never copied from Learning@Griffith pages, slides or past papers. Texts behind the canon: Gould's Pathophysiology (VanMeter & Hubert, 7e) and Fundamentals of Pharmacology (Bullock & Manias, 9e). Verify dates, weights and exam rules against your own Course Profile, as cohorts shift. 标准的生物医学科学内容(炎症级联、抗体几何结构、ADME、量效关系)以平实方式陈述 -- 它属于通用知识体系, 不归任何人版权所有。本单元自身的框架、编排顺序及任何示例数字都经改写与重新加工,绝不抄自 Learning@Griffith 页面、幻灯片或往年试题。支撑这一知识体系的教材:Gould's Pathophysiology (VanMeter & Hubert,第 7版)与 Fundamentals of Pharmacology (Bullock & Manias,第9版)。由于各届安排会变动,请对照你自己的课程大纲核 实日期、权重与考试规则。 2804NRS . Human Pathophysiology & Pharmacology 1 THE BLUEPRINT - THE EXAM BLUEPRINT EOT EXAM 40% . M3-7 Two engines, Modules 3-7 win the exam 两大引擎,模块 3-7 决定考试成败 A1 in-class quiz ~20% (M1-2) . AZ concept map 40% . A3 EOT exam 40% A1 课堂测验约 20% (M1-2)· A2 概念图 40% · A3 学期末考试 40% Your grade is built from three pieces. The two 40% pieces dominate - and they examine the unit in opposite ways. A2 asks you to draw a cascade; A3 asks you to explain cascades in prose and recognise facts. Same biology, two output formats - which is exactly why this book writes each disease as one reusable cascade. 你的成绩由三部分构成。两个各占40% 的部分占主导 -- 而它们以相反的方式考查本单元。A2 要你画出级联;A3 要你用文 字解释级联并辨识事实。相同的生物学,两种输出格式 -- 这正是本书把每种疾病写成一条可复用级联的原因。 ~20% A1 IN-CLASS QUIZ A1 课堂测验 40% A2 CONCEPT MAP A2 概念图 40% A3 EOT EXAM A3 学期末考试 50+12 MCQ + SHORT -ANSWER MCQ + 简答 The three assessment pieces 三项考核 Component Weight
• 期末（End-of-Trimester, EoT / EOTE）考试只主要考 Modules 3–7：免疫、癌症、肌骨/疼痛、遗传/衰老、神经+自主神经药理；而 Modules 1–2更像“地基”，早期 A1 quiz 考完后在期末复习范围里基本就不再出现。[1]Source: asksia-bible-2804nrs-bilingual.pdf3· 考试 It's the End-of-Trimester exam. The MCQ half rewards the fact bullets and trap callouts; the short-answer half rewards re- telling a cascade in prose. Drill the steps() ladders - they ARE model SAQ answers. The blueprint overleaf shows exactly which modules carry the marks. 这是学期末考试。MCQ 部分奖 励事实要点和陷阱提示;简答部 分奖励用文字复述一条级联。反 复演练这些步骤阶梯- -它们本 身就是标准 SAQ 答案。下一页 的蓝图明确显示哪些模块承载着 分数。 2804NRS . Human Pathophysiology & Pharmacology 1 ! The single most important thing to understand about 2804NRS 关于 2804NRS 最需要理解的一件事 The unit is assessed in two completely different engines, and they examine different modules. Modules 1-2 (cells, injury, inflammation, microbiology) are tested by the A1 in-class quiz early in the trimester - and then they vanish from the End-of-Trimester exam study guide. The EoT exam examines Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). So learn M1-2 as scaffolding - they explain everything that follows (inflammation underpins hypersensitivity; cell injury underpins cancer) - but weight your final-exam revision on Modules 3-7. 本单元由两套截然不同的引擎评估,而它们考查的模块各不相同。模块1-2(细胞、损伤、炎症、微生物学)由学期早 期的 A1 课堂测验考核 -- 之后便从学期末考试复习指南中消失。学期末考试考查模块 3-7(免疫、肿瘤、肌肉骨骼/疼 痛、遗传/衰老、神经+自主神经药理学)。所以把 M1-2 当作支架来学 -- 它们解释了后续的一切(炎症支撑超敏反 应;细胞损伤支撑肿瘤) -- 但要把期末考的复习重心放在模块 3-7上。 i How this book was built - and the two-layer rule 本书是如何构建的 -- 以及双层规则 Standard biomedical science (the inflammation cascade, antibody geometry, ADME, dose-response) is stated plainly - it is universal canon, not anyone's copyright. The unit's own framing, sequencing and any example numbers are paraphrased and re-worked, never copied from Learning@Griffith pages, slides or past papers. Texts behind the canon: Gould's Pathophysiology (VanMeter & Hubert, 7e) and Fundamentals of Pharmacology (Bullock & Manias, 9e). Verify dates, weights and exam rules against your own Course Profile, as cohorts shift. 标准的生物医学科学内容(炎症级联、抗体几何结构、ADME、量效关系)以平实方式陈述 -- 它属于通用知识体系, 不归任何人版权所有。本单元自身的框架、编排顺序及任何示例数字都经改写与重新加工,绝不抄自 Learning@Griffith 页面、幻灯片或往年试题。支撑这一知识体系的教材:Gould's Pathophysiology (VanMeter & Hubert,第 7版)与 Fundamentals of Pharmacology (Bullock & Manias,第9版)。由于各届安排会变动,请对照你自己的课程大纲核 实日期、权重与考试规则。 2804NRS . Human Pathophysiology & Pharmacology 1 THE BLUEPRINT - THE EXAM BLUEPRINT EOT EXAM 40% . M3-7 Two engines, Modules 3-7 win the exam 两大引擎,模块 3-7 决定考试成败 A1 in-class quiz ~20% (M1-2) . AZ concept map 40% . A3 EOT exam 40% A1 课堂测验约 20% (M1-2)· A2 概念图 40% · A3 学期末考试 40% Your grade is built from three pieces. The two 40% pieces dominate - and they examine the unit in opposite ways. A2 asks you to draw a cascade; A3 asks you to explain cascades in prose and recognise facts. Same biology, two output formats - which is exactly why this book writes each disease as one reusable cascade. 你的成绩由三部分构成。两个各占40% 的部分占主导 -- 而它们以相反的方式考查本单元。A2 要你画出级联;A3 要你用文 字解释级联并辨识事实。相同的生物学,两种输出格式 -- 这正是本书把每种疾病写成一条可复用级联的原因。 ~20% A1 IN-CLASS QUIZ A1 课堂测验 40% A2 CONCEPT MAP A2 概念图 40% A3 EOT EXAM A3 学期末考试 50+12 MCQ + SHORT -ANSWER MCQ + 简答 The three assessment pieces 三项考核 Component Weight[2]Source: asksia-bible-2804nrs-bilingual.pdfThe Course Profile does not officially state book status for the End-of-Trimester exam in the materials we worked from - do not assume you can bring notes in. Check your own Course Profile, and revise as if it is closed-book. If it turns out to be open-book, you have lost nothing; if you assume open-book and it is closed, you have lost the unit. 在我们参考的材料中,课程大纲并未正式说明学期末考试是否可带书 -- 不要假设你可以带笔记进场。核对你自己的课 程大纲,并当作闭卷来复习。如果结果是开卷,你毫无损失;如果你假设开卷而它实为闭卷,你就丢掉了整个单元。 2804NRS . Human Pathophysiology & Pharmacology 1 CONTENTS - CONTENTS Foundations first, then the examined five 先打地基,再攻五大考查模块 Part 1 is the A1 scaffold; Parts 2-3 are where the End-of-Trimester marks live 第1部分是A1 的支架;第2-3部分才是学期末分数所在 Ch Topic Core mechanisms Part 1 . Foundations (Al-assessed - and the scaffold for everything) 1 Foundations: cells, injury, inflammation, infection homeostasis . adaptation . cell death . acute inflammation . chain of → infection Part 2 . The examined modules (the End-of-Trimester exam lives here) 2 Immunity & hypersensitivity (M3) innate vs adaptive . antibodies . types I-IV . anaphylaxis → 3 Neoplasia & cancer (M4) cell cycle · oncogenes/suppressors · carcinogenesis · metastasis → 4 Musculoskeletal & pain (M5) fractures . osteoporosis . arthritis . pain . the analgesic ladder → 5 Genetics, congenital disease & ageing (M6) inheritance . chromosomal disorders . ageing pharmacokinetics → 6 Nervous system & autonomic pharmacology (M7) raised ICP · stroke . ANS . adrenergic/cholinergic drugs → Part 3 . Pharmacology toolkit (woven through M3-7) 7 Pharmacokinetics & pharmacodynamics ADME . conc-time . dose-response . therapeutic index → Part 4 . Walk in ready 8 Glossary, cascade bank & exam morning every cascade in one place . SAQ templates . the checklist →[8]Source: asksia-bible-2804nrs-bilingual.pdfi Why this order 为何采用此顺序 We teach the foundations (Modules 1-2) first because they underpin everything - inflammation explains hypersensitivity, cell injury explains carcinogenesis, infection explains immunodeficiency. They are A1-assessed and then drop off the End-of-Trimester guide, so learn them once, well, as scaffolding. Then we spend the bulk of the book on the five examined modules (3-7) that carry the final-exam marks, with the pharmacology toolkit pulled out so the drug mechanisms are in one place. 我们先讲基础(模块1-2),因为它们支撑一切 -- 炎症解释超敏反应,细胞损伤解释致癌作用,感染解释免疫缺陷。它 们由 A1 考核,随后从学期末考试指南中退出,所以一次性把它们当作支架学好。然后我们把本书的主体篇幅用在承载期 末分数的五个被考查模块(3-7) 上,并把药理学工具箱单独抽出,让药物机制集中于一处。 - CHAPTER 1 . FOUNDATIONS OF PATHOPHYSIOLOGY A1-ASSESSED . SCAFFOLD Why a cell fails - the scaffold under every disease 细胞为何衰竭 -- 每一种疾病背后的支架 Homeostasis . adaptation . cell injury . inflammation . infection - Modules 1-2, your A1 quiz 稳态 · 适应 · 细胞损伤 · 炎症 · 感染 -- 模块 1-2,你的A1 测验 2804NRS . Human Pathophysiology & Pharmacology 1 One big idea: pathophysiology = a failure of homeostasis at the cell. Every disease in this whole unit starts the same way - a stressor pushes a cell past what it can cope with, and the body's responses (adaptation, injury, inflammation) produce the signs you see at the bedside. Master these five foundations and the rest of the course is just the same story told about different organs: inflammation explains hypersensitivity, cell injury explains cancer, infection explains immunodeficiency. 一个核心观念:病理生理学=细胞层面稳态的失败。整个单元中的每一种疾病都以同样的方式开始 -- 应激源把细胞推过其 所能应对的极限,而机体的反应(适应、损伤、炎症)便产生了你在床旁所见的体征。掌握这五大基础,课程其余部分不过是 同一个故事在不同器官上的复述:炎症解释超敏反应,细胞损伤解释癌症,感染解释免疫缺陷。 ★ Where these foundations sit in your assessment 这些基础在你的考核中处于何处 Modules 1-2 are assessed by the A1 in-class quiz (20 MCQ, 20 min, no backtracking, Week 4) - and then they do not appear on the End-of-Trimester exam study guide. So this chapter is two jobs: (1) drill the A1 facts now, and (2) bank the mechanisms as scaffolding for the examined Modules 3-7. The cascade format we use here (RF->aetiology->patho->clinical) is also the exact A2 concept-map structure - so you are practising that skill from page 1. 模块 1-2 由 A1 课堂测验考核(20道 MCQ,20分钟,不可回退,第4周) -- 之后它们不会出现在学期末考试复习 指南上。所以本章有两项任务:(1)现在就反复演练 A1的事实点;(2)把这些机制作为被考查模块 3-7的支架储备起 来。我们这里使用的级联格式(RF→病因→病理生理→临床)也正是A2 概念图的结构 -- 所以你从第1页起就在练习 这项技能。 1. 1 Homeostasis & negative feedback 1. 1 稳态与负反馈 Homeostasis is the maintenance of a stable internal environment - temperature, pH, glucose, fluid & electrolytes, blood pressure - within narrow physiological limits despite external change. Disease is, at its core, a failure to maintain homeostasis. The body holds variables steady almost entirely by negative feedback: a deviation from the set point is detected, integrated, and corrected in the opposite direction. I 稳态是指尽管外界变化,仍把内环境 -- 体温、pH、血糖、体液与电解质、血压 -- 维持在狭窄的生理范围内的稳定状态。 疾病本质上就是维持稳态的失败。机体几乎完全依靠负反馈来保持各变量稳定:偏离设定点被探测、整合,并向相反方向加 以纠正。 2804NRS . Human Pathophysiology & Pharmacology 1 P13 Stimulus (variable rises above set point) POSITIVE feedback (rare) AMPLIFIES the change Response (lowers variable) Receptor / sensor Stretch / oxytocin

0）先把分数结构搞清楚（决定你怎么复习、怎么拿分）

• A1 in-class quiz（约 20%）：只考 Modules 1–2（20 MCQ/20 min，不能回退）。[1]Source: asksia-bible-2804nrs-bilingual.pdf3· 考试 It's the End-of-Trimester exam. The MCQ half rewards the fact bullets and trap callouts; the short-answer half rewards re- telling a cascade in prose. Drill the steps() ladders - they ARE model SAQ answers. The blueprint overleaf shows exactly which modules carry the marks. 这是学期末考试。MCQ 部分奖 励事实要点和陷阱提示;简答部 分奖励用文字复述一条级联。反 复演练这些步骤阶梯- -它们本 身就是标准 SAQ 答案。下一页 的蓝图明确显示哪些模块承载着 分数。 2804NRS . Human Pathophysiology & Pharmacology 1 ! The single most important thing to understand about 2804NRS 关于 2804NRS 最需要理解的一件事 The unit is assessed in two completely different engines, and they examine different modules. Modules 1-2 (cells, injury, inflammation, microbiology) are tested by the A1 in-class quiz early in the trimester - and then they vanish from the End-of-Trimester exam study guide. The EoT exam examines Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). So learn M1-2 as scaffolding - they explain everything that follows (inflammation underpins hypersensitivity; cell injury underpins cancer) - but weight your final-exam revision on Modules 3-7. 本单元由两套截然不同的引擎评估,而它们考查的模块各不相同。模块1-2(细胞、损伤、炎症、微生物学)由学期早 期的 A1 课堂测验考核 -- 之后便从学期末考试复习指南中消失。学期末考试考查模块 3-7(免疫、肿瘤、肌肉骨骼/疼 痛、遗传/衰老、神经+自主神经药理学)。所以把 M1-2 当作支架来学 -- 它们解释了后续的一切(炎症支撑超敏反 应;细胞损伤支撑肿瘤) -- 但要把期末考的复习重心放在模块 3-7上。 i How this book was built - and the two-layer rule 本书是如何构建的 -- 以及双层规则 Standard biomedical science (the inflammation cascade, antibody geometry, ADME, dose-response) is stated plainly - it is universal canon, not anyone's copyright. The unit's own framing, sequencing and any example numbers are paraphrased and re-worked, never copied from Learning@Griffith pages, slides or past papers. Texts behind the canon: Gould's Pathophysiology (VanMeter & Hubert, 7e) and Fundamentals of Pharmacology (Bullock & Manias, 9e). Verify dates, weights and exam rules against your own Course Profile, as cohorts shift. 标准的生物医学科学内容(炎症级联、抗体几何结构、ADME、量效关系)以平实方式陈述 -- 它属于通用知识体系, 不归任何人版权所有。本单元自身的框架、编排顺序及任何示例数字都经改写与重新加工,绝不抄自 Learning@Griffith 页面、幻灯片或往年试题。支撑这一知识体系的教材:Gould's Pathophysiology (VanMeter & Hubert,第 7版)与 Fundamentals of Pharmacology (Bullock & Manias,第9版)。由于各届安排会变动,请对照你自己的课程大纲核 实日期、权重与考试规则。 2804NRS . Human Pathophysiology & Pharmacology 1 THE BLUEPRINT - THE EXAM BLUEPRINT EOT EXAM 40% . M3-7 Two engines, Modules 3-7 win the exam 两大引擎,模块 3-7 决定考试成败 A1 in-class quiz ~20% (M1-2) . AZ concept map 40% . A3 EOT exam 40% A1 课堂测验约 20% (M1-2)· A2 概念图 40% · A3 学期末考试 40% Your grade is built from three pieces. The two 40% pieces dominate - and they examine the unit in opposite ways. A2 asks you to draw a cascade; A3 asks you to explain cascades in prose and recognise facts. Same biology, two output formats - which is exactly why this book writes each disease as one reusable cascade. 你的成绩由三部分构成。两个各占40% 的部分占主导 -- 而它们以相反的方式考查本单元。A2 要你画出级联;A3 要你用文 字解释级联并辨识事实。相同的生物学,两种输出格式 -- 这正是本书把每种疾病写成一条可复用级联的原因。 ~20% A1 IN-CLASS QUIZ A1 课堂测验 40% A2 CONCEPT MAP A2 概念图 40% A3 EOT EXAM A3 学期末考试 50+12 MCQ + SHORT -ANSWER MCQ + 简答 The three assessment pieces 三项考核 Component Weight[8]Source: asksia-bible-2804nrs-bilingual.pdfi Why this order 为何采用此顺序 We teach the foundations (Modules 1-2) first because they underpin everything - inflammation explains hypersensitivity, cell injury explains carcinogenesis, infection explains immunodeficiency. They are A1-assessed and then drop off the End-of-Trimester guide, so learn them once, well, as scaffolding. Then we spend the bulk of the book on the five examined modules (3-7) that carry the final-exam marks, with the pharmacology toolkit pulled out so the drug mechanisms are in one place. 我们先讲基础(模块1-2),因为它们支撑一切 -- 炎症解释超敏反应,细胞损伤解释致癌作用,感染解释免疫缺陷。它 们由 A1 考核,随后从学期末考试指南中退出,所以一次性把它们当作支架学好。然后我们把本书的主体篇幅用在承载期 末分数的五个被考查模块(3-7) 上,并把药理学工具箱单独抽出,让药物机制集中于一处。 - CHAPTER 1 . FOUNDATIONS OF PATHOPHYSIOLOGY A1-ASSESSED . SCAFFOLD Why a cell fails - the scaffold under every disease 细胞为何衰竭 -- 每一种疾病背后的支架 Homeostasis . adaptation . cell injury . inflammation . infection - Modules 1-2, your A1 quiz 稳态 · 适应 · 细胞损伤 · 炎症 · 感染 -- 模块 1-2,你的A1 测验 2804NRS . Human Pathophysiology & Pharmacology 1 One big idea: pathophysiology = a failure of homeostasis at the cell. Every disease in this whole unit starts the same way - a stressor pushes a cell past what it can cope with, and the body's responses (adaptation, injury, inflammation) produce the signs you see at the bedside. Master these five foundations and the rest of the course is just the same story told about different organs: inflammation explains hypersensitivity, cell injury explains cancer, infection explains immunodeficiency. 一个核心观念:病理生理学=细胞层面稳态的失败。整个单元中的每一种疾病都以同样的方式开始 -- 应激源把细胞推过其 所能应对的极限,而机体的反应(适应、损伤、炎症)便产生了你在床旁所见的体征。掌握这五大基础,课程其余部分不过是 同一个故事在不同器官上的复述:炎症解释超敏反应,细胞损伤解释癌症,感染解释免疫缺陷。 ★ Where these foundations sit in your assessment 这些基础在你的考核中处于何处 Modules 1-2 are assessed by the A1 in-class quiz (20 MCQ, 20 min, no backtracking, Week 4) - and then they do not appear on the End-of-Trimester exam study guide. So this chapter is two jobs: (1) drill the A1 facts now, and (2) bank the mechanisms as scaffolding for the examined Modules 3-7. The cascade format we use here (RF->aetiology->patho->clinical) is also the exact A2 concept-map structure - so you are practising that skill from page 1. 模块 1-2 由 A1 课堂测验考核(20道 MCQ,20分钟,不可回退,第4周) -- 之后它们不会出现在学期末考试复习 指南上。所以本章有两项任务:(1)现在就反复演练 A1的事实点;(2)把这些机制作为被考查模块 3-7的支架储备起 来。我们这里使用的级联格式(RF→病因→病理生理→临床)也正是A2 概念图的结构 -- 所以你从第1页起就在练习 这项技能。 1. 1 Homeostasis & negative feedback 1. 1 稳态与负反馈 Homeostasis is the maintenance of a stable internal environment - temperature, pH, glucose, fluid & electrolytes, blood pressure - within narrow physiological limits despite external change. Disease is, at its core, a failure to maintain homeostasis. The body holds variables steady almost entirely by negative feedback: a deviation from the set point is detected, integrated, and corrected in the opposite direction. I 稳态是指尽管外界变化,仍把内环境 -- 体温、pH、血糖、体液与电解质、血压 -- 维持在狭窄的生理范围内的稳定状态。 疾病本质上就是维持稳态的失败。机体几乎完全依靠负反馈来保持各变量稳定:偏离设定点被探测、整合,并向相反方向加 以纠正。 2804NRS . Human Pathophysiology & Pharmacology 1 P13 Stimulus (variable rises above set point) POSITIVE feedback (rare) AMPLIFIES the change Response (lowers variable) Receptor / sensor Stretch / oxytocin[20]Source: asksia-cheatsheet-2804nrs.pdf20 MCQ/20 min in class · Mod 1-2 A2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 %
• A2 concept map（40%）：要你“画级联 + 写 500 字解释”。[1]Source: asksia-bible-2804nrs-bilingual.pdf3· 考试 It's the End-of-Trimester exam. The MCQ half rewards the fact bullets and trap callouts; the short-answer half rewards re- telling a cascade in prose. Drill the steps() ladders - they ARE model SAQ answers. The blueprint overleaf shows exactly which modules carry the marks. 这是学期末考试。MCQ 部分奖 励事实要点和陷阱提示;简答部 分奖励用文字复述一条级联。反 复演练这些步骤阶梯- -它们本 身就是标准 SAQ 答案。下一页 的蓝图明确显示哪些模块承载着 分数。 2804NRS . Human Pathophysiology & Pharmacology 1 ! The single most important thing to understand about 2804NRS 关于 2804NRS 最需要理解的一件事 The unit is assessed in two completely different engines, and they examine different modules. Modules 1-2 (cells, injury, inflammation, microbiology) are tested by the A1 in-class quiz early in the trimester - and then they vanish from the End-of-Trimester exam study guide. The EoT exam examines Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). So learn M1-2 as scaffolding - they explain everything that follows (inflammation underpins hypersensitivity; cell injury underpins cancer) - but weight your final-exam revision on Modules 3-7. 本单元由两套截然不同的引擎评估,而它们考查的模块各不相同。模块1-2(细胞、损伤、炎症、微生物学)由学期早 期的 A1 课堂测验考核 -- 之后便从学期末考试复习指南中消失。学期末考试考查模块 3-7(免疫、肿瘤、肌肉骨骼/疼 痛、遗传/衰老、神经+自主神经药理学)。所以把 M1-2 当作支架来学 -- 它们解释了后续的一切(炎症支撑超敏反 应;细胞损伤支撑肿瘤) -- 但要把期末考的复习重心放在模块 3-7上。 i How this book was built - and the two-layer rule 本书是如何构建的 -- 以及双层规则 Standard biomedical science (the inflammation cascade, antibody geometry, ADME, dose-response) is stated plainly - it is universal canon, not anyone's copyright. The unit's own framing, sequencing and any example numbers are paraphrased and re-worked, never copied from Learning@Griffith pages, slides or past papers. Texts behind the canon: Gould's Pathophysiology (VanMeter & Hubert, 7e) and Fundamentals of Pharmacology (Bullock & Manias, 9e). Verify dates, weights and exam rules against your own Course Profile, as cohorts shift. 标准的生物医学科学内容(炎症级联、抗体几何结构、ADME、量效关系)以平实方式陈述 -- 它属于通用知识体系, 不归任何人版权所有。本单元自身的框架、编排顺序及任何示例数字都经改写与重新加工,绝不抄自 Learning@Griffith 页面、幻灯片或往年试题。支撑这一知识体系的教材:Gould's Pathophysiology (VanMeter & Hubert,第 7版)与 Fundamentals of Pharmacology (Bullock & Manias,第9版)。由于各届安排会变动,请对照你自己的课程大纲核 实日期、权重与考试规则。 2804NRS . Human Pathophysiology & Pharmacology 1 THE BLUEPRINT - THE EXAM BLUEPRINT EOT EXAM 40% . M3-7 Two engines, Modules 3-7 win the exam 两大引擎,模块 3-7 决定考试成败 A1 in-class quiz ~20% (M1-2) . AZ concept map 40% . A3 EOT exam 40% A1 课堂测验约 20% (M1-2)· A2 概念图 40% · A3 学期末考试 40% Your grade is built from three pieces. The two 40% pieces dominate - and they examine the unit in opposite ways. A2 asks you to draw a cascade; A3 asks you to explain cascades in prose and recognise facts. Same biology, two output formats - which is exactly why this book writes each disease as one reusable cascade. 你的成绩由三部分构成。两个各占40% 的部分占主导 -- 而它们以相反的方式考查本单元。A2 要你画出级联;A3 要你用文 字解释级联并辨识事实。相同的生物学,两种输出格式 -- 这正是本书把每种疾病写成一条可复用级联的原因。 ~20% A1 IN-CLASS QUIZ A1 课堂测验 40% A2 CONCEPT MAP A2 概念图 40% A3 EOT EXAM A3 学期末考试 50+12 MCQ + SHORT -ANSWER MCQ + 简答 The three assessment pieces 三项考核 Component Weight[5]Source: asksia-bible-2804nrs-bilingual.pdfWhen / detail Map band (colour-code it) What the rubric wants A1 in-class online quiz (Modules 1-2 only) ~20% Week 4 . 20 MCQ in 20 min, no backtracking A2 concept-map written assignment 40% Due ~Wk 9 · A4 colour- coded map + 500 words Pathophysiology (ink/blue) step-by-step sequence - /3 A3 End-of-Trimester exam (Modules 3-7) 40% Exam period . 50 MCQ + 12 short-answer A2 concept map = the cascade, marked A2 概念图 = 被评分的级联 Risk factors (amber) 3 RFs linked to aetiology - /6 Aetiology (red) the trigger that starts it Clinical manifestations (green) 5 signs linked to the mechanism - /10 2804NRS . Human Pathophysiology & Pharmacology 1 ★ What the End-of-Trimester exam actually is 学期末考试到底是什么 50 MCQ = 50% of the exam + 12 short-answer questions = 50% of the exam. The exam study guide highlights only Modules 3-7 as examinable - immunity, cancer, MSK & pain, genetics/ageing, and neuro + autonomic pharmacology. The MCQ half rewards broad recall (every trap callout in this book); the short-answer half rewards explaining a mechanism in prose - literally re-telling a pathophysiology cascade or a drug's mechanism of action. 50 道 MCQ = 占考试 50%+ 12 道简答题= 占考试 50%。考试复习指南仅把模块 3-7 标注为可考范围 -- 免疫、肿瘤、肌肉骨骼与疼痛、遗传/衰老,以及 神经+自主神经药理学。MCQ 部分奖励广泛记忆 (本书中每一个陷阱提示);简答部分奖励用文字解释 一个机制 -- 即字面意义上复述一条病理生理级联或 一种药物的作用机制。 ✓ The strategy this dictates 由此决定的策略 Build everything as the cascade. For A2: pick the case disease, lay out the four colour bands, draw arrows RF - aetiology - pathophysiology -+ manifestations, then in the 500 words give 2 diagnostic investigations + 2 management approaches (≥1 drug). For A3: the SAQ half is the same cascade written out, and the MCQ half is the trap boxes. Learn one cascade per disease and you have answered both 40% pieces. 把一切都构建成级联。A2 方面:选定病例疾病,铺开 四个色带,画出箭头 RF→ 病因→ 病理生理 → 临床 表现,然后在 500 字内给出 2 项诊断性检查+2种 管理方法(≥1种药物)。A3 方面:SAQ 部分就是同 一条级联写出来,而 MCQ部分就是那些陷阱框。每 种疾病学会一条级联,你就同时答好了两个40% 的部 分。 i Open or closed book? 开卷还是闭卷?[16]Source: asksia-cheatsheet-2804nrs.pdf7. 2- 2804NRS Human Pathophysiology & Pharmacology 1 GRIFFITH UNIVERSITY . BACHELOR OF NURSING EXAM REVISION T1 2026 . SIDE 1 OF 2 Pathophysiology . EOTE Modules 3-7 SIDE 1/2 pain PATHOPHYSIOLOGY . Exam blueprint . Immunity . Antibodies . Hypersensitivity I-IV . HIV . Autoimmunity . Cancer . MSK & 0 . Exam Blueprint READ FIRST * Two assessments drive the marks: the A2 concept map (40%) and the End-of-Trimester Exam (40%) (the in-class quiz, ~20%, covers Modules 1-2 only). The EOTE = 50 MCQ (half the marks) + 12 short-answer (half) and examines Modules 3-7: immunity -> cancer > MSK/pain > genetics & ageing > neuro/autonomic + the pharmacology woven through. Train both reflexes: MCQ recall = the tables & trap- facts here; SAQ = explain a mechanism in prose - walk a pathophysiological cascade or a drug's mechanism of action in 3-5 linked steps. SIA > For every SAQ "explain . . . ", answer as a chain: trigger - mechanism step ++ mechanism step - clinical sign. Markers reward the links, not a list of facts. Ob . The A2 Cascade Template CONCEPT-MAP SPINE The A2 concept map (and every "explain the pathophysiology" SAQ) follows ONE colour-coded chain. Learn the shape and slot any disease in: RF > AETIOLOGY -> PATHOPHYSIOLOGY >> MANIFESTATIONS Risk factor - aetiology/trigger - pathophysiology (step-by-step) - clinical manifestations + +1 diagnostic test +1 management Worked (cervical cancer, the A2 case): RF = smoking, immunosuppression, multiple partners -> aetiology = persistent high-risk HPV infection > pathophys = viral oncoproteins inactivate p53/Rb tumour suppressors > dysplasia (CIN) > carcinoma in situ -> invasive squamous-cell carcinoma -> local + lymphatic spread > manifestations = abnormal/post-coital bleeding, discharge, pelvic pain. Dx = Pap/HPV test + biopsy; Mx = surgery/radiotherapy ± chemo. (HIV co-infection accelerates it via CD4 loss. ) Reuse this exact skeleton for stroke, MS, arthritis or any disease the exam throws at you. Oc . Assessment Shape WHERE THE MARKS ARE ITEM WT FORM & SCOPE A1 quiz ~20%
• A3 EoT exam / EOTE（40%）：50 道 MCQ + 12 道简答（SAQ），只考 Modules 3–7。[1]Source: asksia-bible-2804nrs-bilingual.pdf3· 考试 It's the End-of-Trimester exam. The MCQ half rewards the fact bullets and trap callouts; the short-answer half rewards re- telling a cascade in prose. Drill the steps() ladders - they ARE model SAQ answers. The blueprint overleaf shows exactly which modules carry the marks. 这是学期末考试。MCQ 部分奖 励事实要点和陷阱提示;简答部 分奖励用文字复述一条级联。反 复演练这些步骤阶梯- -它们本 身就是标准 SAQ 答案。下一页 的蓝图明确显示哪些模块承载着 分数。 2804NRS . Human Pathophysiology & Pharmacology 1 ! The single most important thing to understand about 2804NRS 关于 2804NRS 最需要理解的一件事 The unit is assessed in two completely different engines, and they examine different modules. Modules 1-2 (cells, injury, inflammation, microbiology) are tested by the A1 in-class quiz early in the trimester - and then they vanish from the End-of-Trimester exam study guide. The EoT exam examines Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). So learn M1-2 as scaffolding - they explain everything that follows (inflammation underpins hypersensitivity; cell injury underpins cancer) - but weight your final-exam revision on Modules 3-7. 本单元由两套截然不同的引擎评估,而它们考查的模块各不相同。模块1-2(细胞、损伤、炎症、微生物学)由学期早 期的 A1 课堂测验考核 -- 之后便从学期末考试复习指南中消失。学期末考试考查模块 3-7(免疫、肿瘤、肌肉骨骼/疼 痛、遗传/衰老、神经+自主神经药理学)。所以把 M1-2 当作支架来学 -- 它们解释了后续的一切(炎症支撑超敏反 应;细胞损伤支撑肿瘤) -- 但要把期末考的复习重心放在模块 3-7上。 i How this book was built - and the two-layer rule 本书是如何构建的 -- 以及双层规则 Standard biomedical science (the inflammation cascade, antibody geometry, ADME, dose-response) is stated plainly - it is universal canon, not anyone's copyright. The unit's own framing, sequencing and any example numbers are paraphrased and re-worked, never copied from Learning@Griffith pages, slides or past papers. Texts behind the canon: Gould's Pathophysiology (VanMeter & Hubert, 7e) and Fundamentals of Pharmacology (Bullock & Manias, 9e). Verify dates, weights and exam rules against your own Course Profile, as cohorts shift. 标准的生物医学科学内容(炎症级联、抗体几何结构、ADME、量效关系)以平实方式陈述 -- 它属于通用知识体系, 不归任何人版权所有。本单元自身的框架、编排顺序及任何示例数字都经改写与重新加工,绝不抄自 Learning@Griffith 页面、幻灯片或往年试题。支撑这一知识体系的教材:Gould's Pathophysiology (VanMeter & Hubert,第 7版)与 Fundamentals of Pharmacology (Bullock & Manias,第9版)。由于各届安排会变动,请对照你自己的课程大纲核 实日期、权重与考试规则。 2804NRS . Human Pathophysiology & Pharmacology 1 THE BLUEPRINT - THE EXAM BLUEPRINT EOT EXAM 40% . M3-7 Two engines, Modules 3-7 win the exam 两大引擎,模块 3-7 决定考试成败 A1 in-class quiz ~20% (M1-2) . AZ concept map 40% . A3 EOT exam 40% A1 课堂测验约 20% (M1-2)· A2 概念图 40% · A3 学期末考试 40% Your grade is built from three pieces. The two 40% pieces dominate - and they examine the unit in opposite ways. A2 asks you to draw a cascade; A3 asks you to explain cascades in prose and recognise facts. Same biology, two output formats - which is exactly why this book writes each disease as one reusable cascade. 你的成绩由三部分构成。两个各占40% 的部分占主导 -- 而它们以相反的方式考查本单元。A2 要你画出级联;A3 要你用文 字解释级联并辨识事实。相同的生物学,两种输出格式 -- 这正是本书把每种疾病写成一条可复用级联的原因。 ~20% A1 IN-CLASS QUIZ A1 课堂测验 40% A2 CONCEPT MAP A2 概念图 40% A3 EOT EXAM A3 学期末考试 50+12 MCQ + SHORT -ANSWER MCQ + 简答 The three assessment pieces 三项考核 Component Weight[5]Source: asksia-bible-2804nrs-bilingual.pdfWhen / detail Map band (colour-code it) What the rubric wants A1 in-class online quiz (Modules 1-2 only) ~20% Week 4 . 20 MCQ in 20 min, no backtracking A2 concept-map written assignment 40% Due ~Wk 9 · A4 colour- coded map + 500 words Pathophysiology (ink/blue) step-by-step sequence - /3 A3 End-of-Trimester exam (Modules 3-7) 40% Exam period . 50 MCQ + 12 short-answer A2 concept map = the cascade, marked A2 概念图 = 被评分的级联 Risk factors (amber) 3 RFs linked to aetiology - /6 Aetiology (red) the trigger that starts it Clinical manifestations (green) 5 signs linked to the mechanism - /10 2804NRS . Human Pathophysiology & Pharmacology 1 ★ What the End-of-Trimester exam actually is 学期末考试到底是什么 50 MCQ = 50% of the exam + 12 short-answer questions = 50% of the exam. The exam study guide highlights only Modules 3-7 as examinable - immunity, cancer, MSK & pain, genetics/ageing, and neuro + autonomic pharmacology. The MCQ half rewards broad recall (every trap callout in this book); the short-answer half rewards explaining a mechanism in prose - literally re-telling a pathophysiology cascade or a drug's mechanism of action. 50 道 MCQ = 占考试 50%+ 12 道简答题= 占考试 50%。考试复习指南仅把模块 3-7 标注为可考范围 -- 免疫、肿瘤、肌肉骨骼与疼痛、遗传/衰老,以及 神经+自主神经药理学。MCQ 部分奖励广泛记忆 (本书中每一个陷阱提示);简答部分奖励用文字解释 一个机制 -- 即字面意义上复述一条病理生理级联或 一种药物的作用机制。 ✓ The strategy this dictates 由此决定的策略 Build everything as the cascade. For A2: pick the case disease, lay out the four colour bands, draw arrows RF - aetiology - pathophysiology -+ manifestations, then in the 500 words give 2 diagnostic investigations + 2 management approaches (≥1 drug). For A3: the SAQ half is the same cascade written out, and the MCQ half is the trap boxes. Learn one cascade per disease and you have answered both 40% pieces. 把一切都构建成级联。A2 方面:选定病例疾病,铺开 四个色带,画出箭头 RF→ 病因→ 病理生理 → 临床 表现,然后在 500 字内给出 2 项诊断性检查+2种 管理方法(≥1种药物)。A3 方面:SAQ 部分就是同 一条级联写出来,而 MCQ部分就是那些陷阱框。每 种疾病学会一条级联,你就同时答好了两个40% 的部 分。 i Open or closed book? 开卷还是闭卷?[16]Source: asksia-cheatsheet-2804nrs.pdf7. 2- 2804NRS Human Pathophysiology & Pharmacology 1 GRIFFITH UNIVERSITY . BACHELOR OF NURSING EXAM REVISION T1 2026 . SIDE 1 OF 2 Pathophysiology . EOTE Modules 3-7 SIDE 1/2 pain PATHOPHYSIOLOGY . Exam blueprint . Immunity . Antibodies . Hypersensitivity I-IV . HIV . Autoimmunity . Cancer . MSK & 0 . Exam Blueprint READ FIRST * Two assessments drive the marks: the A2 concept map (40%) and the End-of-Trimester Exam (40%) (the in-class quiz, ~20%, covers Modules 1-2 only). The EOTE = 50 MCQ (half the marks) + 12 short-answer (half) and examines Modules 3-7: immunity -> cancer > MSK/pain > genetics & ageing > neuro/autonomic + the pharmacology woven through. Train both reflexes: MCQ recall = the tables & trap- facts here; SAQ = explain a mechanism in prose - walk a pathophysiological cascade or a drug's mechanism of action in 3-5 linked steps. SIA > For every SAQ "explain . . . ", answer as a chain: trigger - mechanism step ++ mechanism step - clinical sign. Markers reward the links, not a list of facts. Ob . The A2 Cascade Template CONCEPT-MAP SPINE The A2 concept map (and every "explain the pathophysiology" SAQ) follows ONE colour-coded chain. Learn the shape and slot any disease in: RF > AETIOLOGY -> PATHOPHYSIOLOGY >> MANIFESTATIONS Risk factor - aetiology/trigger - pathophysiology (step-by-step) - clinical manifestations + +1 diagnostic test +1 management Worked (cervical cancer, the A2 case): RF = smoking, immunosuppression, multiple partners -> aetiology = persistent high-risk HPV infection > pathophys = viral oncoproteins inactivate p53/Rb tumour suppressors > dysplasia (CIN) > carcinoma in situ -> invasive squamous-cell carcinoma -> local + lymphatic spread > manifestations = abnormal/post-coital bleeding, discharge, pelvic pain. Dx = Pap/HPV test + biopsy; Mx = surgery/radiotherapy ± chemo. (HIV co-infection accelerates it via CD4 loss. ) Reuse this exact skeleton for stroke, MS, arthritis or any disease the exam throws at you. Oc . Assessment Shape WHERE THE MARKS ARE ITEM WT FORM & SCOPE A1 quiz ~20%

• MCQ：奖励“事实点 + 陷阱点”记得广。[1]Source: asksia-bible-2804nrs-bilingual.pdf3· 考试 It's the End-of-Trimester exam. The MCQ half rewards the fact bullets and trap callouts; the short-answer half rewards re- telling a cascade in prose. Drill the steps() ladders - they ARE model SAQ answers. The blueprint overleaf shows exactly which modules carry the marks. 这是学期末考试。MCQ 部分奖 励事实要点和陷阱提示;简答部 分奖励用文字复述一条级联。反 复演练这些步骤阶梯- -它们本 身就是标准 SAQ 答案。下一页 的蓝图明确显示哪些模块承载着 分数。 2804NRS . Human Pathophysiology & Pharmacology 1 ! The single most important thing to understand about 2804NRS 关于 2804NRS 最需要理解的一件事 The unit is assessed in two completely different engines, and they examine different modules. Modules 1-2 (cells, injury, inflammation, microbiology) are tested by the A1 in-class quiz early in the trimester - and then they vanish from the End-of-Trimester exam study guide. The EoT exam examines Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). So learn M1-2 as scaffolding - they explain everything that follows (inflammation underpins hypersensitivity; cell injury underpins cancer) - but weight your final-exam revision on Modules 3-7. 本单元由两套截然不同的引擎评估,而它们考查的模块各不相同。模块1-2(细胞、损伤、炎症、微生物学)由学期早 期的 A1 课堂测验考核 -- 之后便从学期末考试复习指南中消失。学期末考试考查模块 3-7(免疫、肿瘤、肌肉骨骼/疼 痛、遗传/衰老、神经+自主神经药理学)。所以把 M1-2 当作支架来学 -- 它们解释了后续的一切(炎症支撑超敏反 应;细胞损伤支撑肿瘤) -- 但要把期末考的复习重心放在模块 3-7上。 i How this book was built - and the two-layer rule 本书是如何构建的 -- 以及双层规则 Standard biomedical science (the inflammation cascade, antibody geometry, ADME, dose-response) is stated plainly - it is universal canon, not anyone's copyright. The unit's own framing, sequencing and any example numbers are paraphrased and re-worked, never copied from Learning@Griffith pages, slides or past papers. Texts behind the canon: Gould's Pathophysiology (VanMeter & Hubert, 7e) and Fundamentals of Pharmacology (Bullock & Manias, 9e). Verify dates, weights and exam rules against your own Course Profile, as cohorts shift. 标准的生物医学科学内容(炎症级联、抗体几何结构、ADME、量效关系)以平实方式陈述 -- 它属于通用知识体系, 不归任何人版权所有。本单元自身的框架、编排顺序及任何示例数字都经改写与重新加工,绝不抄自 Learning@Griffith 页面、幻灯片或往年试题。支撑这一知识体系的教材:Gould's Pathophysiology (VanMeter & Hubert,第 7版)与 Fundamentals of Pharmacology (Bullock & Manias,第9版)。由于各届安排会变动,请对照你自己的课程大纲核 实日期、权重与考试规则。 2804NRS . Human Pathophysiology & Pharmacology 1 THE BLUEPRINT - THE EXAM BLUEPRINT EOT EXAM 40% . M3-7 Two engines, Modules 3-7 win the exam 两大引擎,模块 3-7 决定考试成败 A1 in-class quiz ~20% (M1-2) . AZ concept map 40% . A3 EOT exam 40% A1 课堂测验约 20% (M1-2)· A2 概念图 40% · A3 学期末考试 40% Your grade is built from three pieces. The two 40% pieces dominate - and they examine the unit in opposite ways. A2 asks you to draw a cascade; A3 asks you to explain cascades in prose and recognise facts. Same biology, two output formats - which is exactly why this book writes each disease as one reusable cascade. 你的成绩由三部分构成。两个各占40% 的部分占主导 -- 而它们以相反的方式考查本单元。A2 要你画出级联;A3 要你用文 字解释级联并辨识事实。相同的生物学,两种输出格式 -- 这正是本书把每种疾病写成一条可复用级联的原因。 ~20% A1 IN-CLASS QUIZ A1 课堂测验 40% A2 CONCEPT MAP A2 概念图 40% A3 EOT EXAM A3 学期末考试 50+12 MCQ + SHORT -ANSWER MCQ + 简答 The three assessment pieces 三项考核 Component Weight[5]Source: asksia-bible-2804nrs-bilingual.pdfWhen / detail Map band (colour-code it) What the rubric wants A1 in-class online quiz (Modules 1-2 only) ~20% Week 4 . 20 MCQ in 20 min, no backtracking A2 concept-map written assignment 40% Due ~Wk 9 · A4 colour- coded map + 500 words Pathophysiology (ink/blue) step-by-step sequence - /3 A3 End-of-Trimester exam (Modules 3-7) 40% Exam period . 50 MCQ + 12 short-answer A2 concept map = the cascade, marked A2 概念图 = 被评分的级联 Risk factors (amber) 3 RFs linked to aetiology - /6 Aetiology (red) the trigger that starts it Clinical manifestations (green) 5 signs linked to the mechanism - /10 2804NRS . Human Pathophysiology & Pharmacology 1 ★ What the End-of-Trimester exam actually is 学期末考试到底是什么 50 MCQ = 50% of the exam + 12 short-answer questions = 50% of the exam. The exam study guide highlights only Modules 3-7 as examinable - immunity, cancer, MSK & pain, genetics/ageing, and neuro + autonomic pharmacology. The MCQ half rewards broad recall (every trap callout in this book); the short-answer half rewards explaining a mechanism in prose - literally re-telling a pathophysiology cascade or a drug's mechanism of action. 50 道 MCQ = 占考试 50%+ 12 道简答题= 占考试 50%。考试复习指南仅把模块 3-7 标注为可考范围 -- 免疫、肿瘤、肌肉骨骼与疼痛、遗传/衰老,以及 神经+自主神经药理学。MCQ 部分奖励广泛记忆 (本书中每一个陷阱提示);简答部分奖励用文字解释 一个机制 -- 即字面意义上复述一条病理生理级联或 一种药物的作用机制。 ✓ The strategy this dictates 由此决定的策略 Build everything as the cascade. For A2: pick the case disease, lay out the four colour bands, draw arrows RF - aetiology - pathophysiology -+ manifestations, then in the 500 words give 2 diagnostic investigations + 2 management approaches (≥1 drug). For A3: the SAQ half is the same cascade written out, and the MCQ half is the trap boxes. Learn one cascade per disease and you have answered both 40% pieces. 把一切都构建成级联。A2 方面:选定病例疾病,铺开 四个色带,画出箭头 RF→ 病因→ 病理生理 → 临床 表现,然后在 500 字内给出 2 项诊断性检查+2种 管理方法(≥1种药物)。A3 方面:SAQ 部分就是同 一条级联写出来,而 MCQ部分就是那些陷阱框。每 种疾病学会一条级联,你就同时答好了两个40% 的部 分。 i Open or closed book? 开卷还是闭卷?
• SAQ：奖励你能用文字把一条**机制级联（cascade）**讲清楚（3–5 步连起来），不是散点堆知识。[1]Source: asksia-bible-2804nrs-bilingual.pdf3· 考试 It's the End-of-Trimester exam. The MCQ half rewards the fact bullets and trap callouts; the short-answer half rewards re- telling a cascade in prose. Drill the steps() ladders - they ARE model SAQ answers. The blueprint overleaf shows exactly which modules carry the marks. 这是学期末考试。MCQ 部分奖 励事实要点和陷阱提示;简答部 分奖励用文字复述一条级联。反 复演练这些步骤阶梯- -它们本 身就是标准 SAQ 答案。下一页 的蓝图明确显示哪些模块承载着 分数。 2804NRS . Human Pathophysiology & Pharmacology 1 ! The single most important thing to understand about 2804NRS 关于 2804NRS 最需要理解的一件事 The unit is assessed in two completely different engines, and they examine different modules. Modules 1-2 (cells, injury, inflammation, microbiology) are tested by the A1 in-class quiz early in the trimester - and then they vanish from the End-of-Trimester exam study guide. The EoT exam examines Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). So learn M1-2 as scaffolding - they explain everything that follows (inflammation underpins hypersensitivity; cell injury underpins cancer) - but weight your final-exam revision on Modules 3-7. 本单元由两套截然不同的引擎评估,而它们考查的模块各不相同。模块1-2(细胞、损伤、炎症、微生物学)由学期早 期的 A1 课堂测验考核 -- 之后便从学期末考试复习指南中消失。学期末考试考查模块 3-7(免疫、肿瘤、肌肉骨骼/疼 痛、遗传/衰老、神经+自主神经药理学)。所以把 M1-2 当作支架来学 -- 它们解释了后续的一切(炎症支撑超敏反 应;细胞损伤支撑肿瘤) -- 但要把期末考的复习重心放在模块 3-7上。 i How this book was built - and the two-layer rule 本书是如何构建的 -- 以及双层规则 Standard biomedical science (the inflammation cascade, antibody geometry, ADME, dose-response) is stated plainly - it is universal canon, not anyone's copyright. The unit's own framing, sequencing and any example numbers are paraphrased and re-worked, never copied from Learning@Griffith pages, slides or past papers. Texts behind the canon: Gould's Pathophysiology (VanMeter & Hubert, 7e) and Fundamentals of Pharmacology (Bullock & Manias, 9e). Verify dates, weights and exam rules against your own Course Profile, as cohorts shift. 标准的生物医学科学内容(炎症级联、抗体几何结构、ADME、量效关系)以平实方式陈述 -- 它属于通用知识体系, 不归任何人版权所有。本单元自身的框架、编排顺序及任何示例数字都经改写与重新加工,绝不抄自 Learning@Griffith 页面、幻灯片或往年试题。支撑这一知识体系的教材:Gould's Pathophysiology (VanMeter & Hubert,第 7版)与 Fundamentals of Pharmacology (Bullock & Manias,第9版)。由于各届安排会变动,请对照你自己的课程大纲核 实日期、权重与考试规则。 2804NRS . Human Pathophysiology & Pharmacology 1 THE BLUEPRINT - THE EXAM BLUEPRINT EOT EXAM 40% . M3-7 Two engines, Modules 3-7 win the exam 两大引擎,模块 3-7 决定考试成败 A1 in-class quiz ~20% (M1-2) . AZ concept map 40% . A3 EOT exam 40% A1 课堂测验约 20% (M1-2)· A2 概念图 40% · A3 学期末考试 40% Your grade is built from three pieces. The two 40% pieces dominate - and they examine the unit in opposite ways. A2 asks you to draw a cascade; A3 asks you to explain cascades in prose and recognise facts. Same biology, two output formats - which is exactly why this book writes each disease as one reusable cascade. 你的成绩由三部分构成。两个各占40% 的部分占主导 -- 而它们以相反的方式考查本单元。A2 要你画出级联;A3 要你用文 字解释级联并辨识事实。相同的生物学,两种输出格式 -- 这正是本书把每种疾病写成一条可复用级联的原因。 ~20% A1 IN-CLASS QUIZ A1 课堂测验 40% A2 CONCEPT MAP A2 概念图 40% A3 EOT EXAM A3 学期末考试 50+12 MCQ + SHORT -ANSWER MCQ + 简答 The three assessment pieces 三项考核 Component Weight[5]Source: asksia-bible-2804nrs-bilingual.pdfWhen / detail Map band (colour-code it) What the rubric wants A1 in-class online quiz (Modules 1-2 only) ~20% Week 4 . 20 MCQ in 20 min, no backtracking A2 concept-map written assignment 40% Due ~Wk 9 · A4 colour- coded map + 500 words Pathophysiology (ink/blue) step-by-step sequence - /3 A3 End-of-Trimester exam (Modules 3-7) 40% Exam period . 50 MCQ + 12 short-answer A2 concept map = the cascade, marked A2 概念图 = 被评分的级联 Risk factors (amber) 3 RFs linked to aetiology - /6 Aetiology (red) the trigger that starts it Clinical manifestations (green) 5 signs linked to the mechanism - /10 2804NRS . Human Pathophysiology & Pharmacology 1 ★ What the End-of-Trimester exam actually is 学期末考试到底是什么 50 MCQ = 50% of the exam + 12 short-answer questions = 50% of the exam. The exam study guide highlights only Modules 3-7 as examinable - immunity, cancer, MSK & pain, genetics/ageing, and neuro + autonomic pharmacology. The MCQ half rewards broad recall (every trap callout in this book); the short-answer half rewards explaining a mechanism in prose - literally re-telling a pathophysiology cascade or a drug's mechanism of action. 50 道 MCQ = 占考试 50%+ 12 道简答题= 占考试 50%。考试复习指南仅把模块 3-7 标注为可考范围 -- 免疫、肿瘤、肌肉骨骼与疼痛、遗传/衰老,以及 神经+自主神经药理学。MCQ 部分奖励广泛记忆 (本书中每一个陷阱提示);简答部分奖励用文字解释 一个机制 -- 即字面意义上复述一条病理生理级联或 一种药物的作用机制。 ✓ The strategy this dictates 由此决定的策略 Build everything as the cascade. For A2: pick the case disease, lay out the four colour bands, draw arrows RF - aetiology - pathophysiology -+ manifestations, then in the 500 words give 2 diagnostic investigations + 2 management approaches (≥1 drug). For A3: the SAQ half is the same cascade written out, and the MCQ half is the trap boxes. Learn one cascade per disease and you have answered both 40% pieces. 把一切都构建成级联。A2 方面:选定病例疾病,铺开 四个色带,画出箭头 RF→ 病因→ 病理生理 → 临床 表现,然后在 500 字内给出 2 项诊断性检查+2种 管理方法(≥1种药物)。A3 方面:SAQ 部分就是同 一条级联写出来,而 MCQ部分就是那些陷阱框。每 种疾病学会一条级联,你就同时答好了两个40% 的部 分。 i Open or closed book? 开卷还是闭卷?[16]Source: asksia-cheatsheet-2804nrs.pdf7. 2- 2804NRS Human Pathophysiology & Pharmacology 1 GRIFFITH UNIVERSITY . BACHELOR OF NURSING EXAM REVISION T1 2026 . SIDE 1 OF 2 Pathophysiology . EOTE Modules 3-7 SIDE 1/2 pain PATHOPHYSIOLOGY . Exam blueprint . Immunity . Antibodies . Hypersensitivity I-IV . HIV . Autoimmunity . Cancer . MSK & 0 . Exam Blueprint READ FIRST * Two assessments drive the marks: the A2 concept map (40%) and the End-of-Trimester Exam (40%) (the in-class quiz, ~20%, covers Modules 1-2 only). The EOTE = 50 MCQ (half the marks) + 12 short-answer (half) and examines Modules 3-7: immunity -> cancer > MSK/pain > genetics & ageing > neuro/autonomic + the pharmacology woven through. Train both reflexes: MCQ recall = the tables & trap- facts here; SAQ = explain a mechanism in prose - walk a pathophysiological cascade or a drug's mechanism of action in 3-5 linked steps. SIA > For every SAQ "explain . . . ", answer as a chain: trigger - mechanism step ++ mechanism step - clinical sign. Markers reward the links, not a list of facts. Ob . The A2 Cascade Template CONCEPT-MAP SPINE The A2 concept map (and every "explain the pathophysiology" SAQ) follows ONE colour-coded chain. Learn the shape and slot any disease in: RF > AETIOLOGY -> PATHOPHYSIOLOGY >> MANIFESTATIONS Risk factor - aetiology/trigger - pathophysiology (step-by-step) - clinical manifestations + +1 diagnostic test +1 management Worked (cervical cancer, the A2 case): RF = smoking, immunosuppression, multiple partners -> aetiology = persistent high-risk HPV infection > pathophys = viral oncoproteins inactivate p53/Rb tumour suppressors > dysplasia (CIN) > carcinoma in situ -> invasive squamous-cell carcinoma -> local + lymphatic spread > manifestations = abnormal/post-coital bleeding, discharge, pelvic pain. Dx = Pap/HPV test + biopsy; Mx = surgery/radiotherapy ± chemo. (HIV co-infection accelerates it via CD4 loss. ) Reuse this exact skeleton for stroke, MS, arthritis or any disease the exam throws at you. Oc . Assessment Shape WHERE THE MARKS ARE ITEM WT FORM & SCOPE A1 quiz ~20%

1）全课“唯一通用的高分骨架”：级联（Cascade）模板（必背）

• RF（Risk factors）→ Aetiology（触发因素/病因）→ Pathophysiology（分步机制）→ Clinical manifestations（临床表现）
• 然后再补：+ 1 项诊断（Dx）+ 1 种管理/治疗（Rx，最好含药）。[5]Source: asksia-bible-2804nrs-bilingual.pdfWhen / detail Map band (colour-code it) What the rubric wants A1 in-class online quiz (Modules 1-2 only) ~20% Week 4 . 20 MCQ in 20 min, no backtracking A2 concept-map written assignment 40% Due ~Wk 9 · A4 colour- coded map + 500 words Pathophysiology (ink/blue) step-by-step sequence - /3 A3 End-of-Trimester exam (Modules 3-7) 40% Exam period . 50 MCQ + 12 short-answer A2 concept map = the cascade, marked A2 概念图 = 被评分的级联 Risk factors (amber) 3 RFs linked to aetiology - /6 Aetiology (red) the trigger that starts it Clinical manifestations (green) 5 signs linked to the mechanism - /10 2804NRS . Human Pathophysiology & Pharmacology 1 ★ What the End-of-Trimester exam actually is 学期末考试到底是什么 50 MCQ = 50% of the exam + 12 short-answer questions = 50% of the exam. The exam study guide highlights only Modules 3-7 as examinable - immunity, cancer, MSK & pain, genetics/ageing, and neuro + autonomic pharmacology. The MCQ half rewards broad recall (every trap callout in this book); the short-answer half rewards explaining a mechanism in prose - literally re-telling a pathophysiology cascade or a drug's mechanism of action. 50 道 MCQ = 占考试 50%+ 12 道简答题= 占考试 50%。考试复习指南仅把模块 3-7 标注为可考范围 -- 免疫、肿瘤、肌肉骨骼与疼痛、遗传/衰老,以及 神经+自主神经药理学。MCQ 部分奖励广泛记忆 (本书中每一个陷阱提示);简答部分奖励用文字解释 一个机制 -- 即字面意义上复述一条病理生理级联或 一种药物的作用机制。 ✓ The strategy this dictates 由此决定的策略 Build everything as the cascade. For A2: pick the case disease, lay out the four colour bands, draw arrows RF - aetiology - pathophysiology -+ manifestations, then in the 500 words give 2 diagnostic investigations + 2 management approaches (≥1 drug). For A3: the SAQ half is the same cascade written out, and the MCQ half is the trap boxes. Learn one cascade per disease and you have answered both 40% pieces. 把一切都构建成级联。A2 方面:选定病例疾病,铺开 四个色带,画出箭头 RF→ 病因→ 病理生理 → 临床 表现,然后在 500 字内给出 2 项诊断性检查+2种 管理方法(≥1种药物)。A3 方面:SAQ 部分就是同 一条级联写出来,而 MCQ部分就是那些陷阱框。每 种疾病学会一条级联,你就同时答好了两个40% 的部 分。 i Open or closed book? 开卷还是闭卷?[16]Source: asksia-cheatsheet-2804nrs.pdf7. 2- 2804NRS Human Pathophysiology & Pharmacology 1 GRIFFITH UNIVERSITY . BACHELOR OF NURSING EXAM REVISION T1 2026 . SIDE 1 OF 2 Pathophysiology . EOTE Modules 3-7 SIDE 1/2 pain PATHOPHYSIOLOGY . Exam blueprint . Immunity . Antibodies . Hypersensitivity I-IV . HIV . Autoimmunity . Cancer . MSK & 0 . Exam Blueprint READ FIRST * Two assessments drive the marks: the A2 concept map (40%) and the End-of-Trimester Exam (40%) (the in-class quiz, ~20%, covers Modules 1-2 only). The EOTE = 50 MCQ (half the marks) + 12 short-answer (half) and examines Modules 3-7: immunity -> cancer > MSK/pain > genetics & ageing > neuro/autonomic + the pharmacology woven through. Train both reflexes: MCQ recall = the tables & trap- facts here; SAQ = explain a mechanism in prose - walk a pathophysiological cascade or a drug's mechanism of action in 3-5 linked steps. SIA > For every SAQ "explain . . . ", answer as a chain: trigger - mechanism step ++ mechanism step - clinical sign. Markers reward the links, not a list of facts. Ob . The A2 Cascade Template CONCEPT-MAP SPINE The A2 concept map (and every "explain the pathophysiology" SAQ) follows ONE colour-coded chain. Learn the shape and slot any disease in: RF > AETIOLOGY -> PATHOPHYSIOLOGY >> MANIFESTATIONS Risk factor - aetiology/trigger - pathophysiology (step-by-step) - clinical manifestations + +1 diagnostic test +1 management Worked (cervical cancer, the A2 case): RF = smoking, immunosuppression, multiple partners -> aetiology = persistent high-risk HPV infection > pathophys = viral oncoproteins inactivate p53/Rb tumour suppressors > dysplasia (CIN) > carcinoma in situ -> invasive squamous-cell carcinoma -> local + lymphatic spread > manifestations = abnormal/post-coital bleeding, discharge, pelvic pain. Dx = Pap/HPV test + biopsy; Mx = surgery/radiotherapy ± chemo. (HIV co-infection accelerates it via CD4 loss. ) Reuse this exact skeleton for stroke, MS, arthritis or any disease the exam throws at you. Oc . Assessment Shape WHERE THE MARKS ARE ITEM WT FORM & SCOPE A1 quiz ~20%

• SAQ 里凡是 “explain …” 题，你就写成链条：
  • trigger → 机制第1步 → 机制第2步 → 对应临床表现（3–5 步）
  • 老师给分给“链接”，不是给你一堆孤立事实。[16]Source: asksia-cheatsheet-2804nrs.pdf7. 2- 2804NRS Human Pathophysiology & Pharmacology 1 GRIFFITH UNIVERSITY . BACHELOR OF NURSING EXAM REVISION T1 2026 . SIDE 1 OF 2 Pathophysiology . EOTE Modules 3-7 SIDE 1/2 pain PATHOPHYSIOLOGY . Exam blueprint . Immunity . Antibodies . Hypersensitivity I-IV . HIV . Autoimmunity . Cancer . MSK & 0 . Exam Blueprint READ FIRST * Two assessments drive the marks: the A2 concept map (40%) and the End-of-Trimester Exam (40%) (the in-class quiz, ~20%, covers Modules 1-2 only). The EOTE = 50 MCQ (half the marks) + 12 short-answer (half) and examines Modules 3-7: immunity -> cancer > MSK/pain > genetics & ageing > neuro/autonomic + the pharmacology woven through. Train both reflexes: MCQ recall = the tables & trap- facts here; SAQ = explain a mechanism in prose - walk a pathophysiological cascade or a drug's mechanism of action in 3-5 linked steps. SIA > For every SAQ "explain . . . ", answer as a chain: trigger - mechanism step ++ mechanism step - clinical sign. Markers reward the links, not a list of facts. Ob . The A2 Cascade Template CONCEPT-MAP SPINE The A2 concept map (and every "explain the pathophysiology" SAQ) follows ONE colour-coded chain. Learn the shape and slot any disease in: RF > AETIOLOGY -> PATHOPHYSIOLOGY >> MANIFESTATIONS Risk factor - aetiology/trigger - pathophysiology (step-by-step) - clinical manifestations + +1 diagnostic test +1 management Worked (cervical cancer, the A2 case): RF = smoking, immunosuppression, multiple partners -> aetiology = persistent high-risk HPV infection > pathophys = viral oncoproteins inactivate p53/Rb tumour suppressors > dysplasia (CIN) > carcinoma in situ -> invasive squamous-cell carcinoma -> local + lymphatic spread > manifestations = abnormal/post-coital bleeding, discharge, pelvic pain. Dx = Pap/HPV test + biopsy; Mx = surgery/radiotherapy ± chemo. (HIV co-infection accelerates it via CD4 loss. ) Reuse this exact skeleton for stroke, MS, arthritis or any disease the exam throws at you. Oc . Assessment Shape WHERE THE MARKS ARE ITEM WT FORM & SCOPE A1 quiz ~20%

2）你的“复习优先级”（期末 Modules 3–7 的顺序）

• Immunology（免疫） > Cancer（肿瘤） > MSK/Pain（肌骨+疼痛） > Genetics/Ageing（遗传+衰老） > Neuro/Autonomic（神经+自主神经）
• 并且药理学工具（PK/PD）贯穿其中。[20]Source: asksia-cheatsheet-2804nrs.pdf20 MCQ/20 min in class · Mod 1-2 A2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 %[21]Source: asksia-cheatsheet-2804nrs.pdfA2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 % TYPE

3）MCQ 半场：你要死记硬背的“高产陷阱/表格点”（按模块整理）

3.1 Module 3：免疫（MCQ 金矿 + SAQ 常考链）

• Innate：非特异、快、无记忆；包括屏障、炎症、发热、吞噬细胞、NK、补体、干扰素。[20]Source: asksia-cheatsheet-2804nrs.pdf20 MCQ/20 min in class · Mod 1-2 A2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 %[21]Source: asksia-cheatsheet-2804nrs.pdfA2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 % TYPE
• Adaptive：特异、慢、有记忆；分体液（B/抗体）与细胞介导（T）。[20]Source: asksia-cheatsheet-2804nrs.pdf20 MCQ/20 min in class · Mod 1-2 A2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 %[21]Source: asksia-cheatsheet-2804nrs.pdfA2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 % TYPE
• 常见陷阱：炎症与发热属于 innate 的第二道防线，别写成 adaptive。[20]Source: asksia-cheatsheet-2804nrs.pdf20 MCQ/20 min in class · Mod 1-2 A2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 %[21]Source: asksia-cheatsheet-2804nrs.pdfA2 map 40% concept map + 500 words A3 EOTE 40% 50 MCQ + 12 SAQ - Mod 3-7 The MCQ half rewards breadth (recognise the trap); the SAQ half rewards depth (explain a cascade or a mechanism of action in prose). Weight prep on immunology > cancer -> MSK/pain > genetics/ageing > neuro/autonomic. (Modules 1-2 are Al scaffolding, not on the EOTE. ) Od . Foundations (scaffold) MOD 1-2 UNDERPIN Cell adaptation: hypertrophy = bigger cells; hyperplasia = more cells ; metaplasia = reversible cell- type switch; dysplasia = disordered, pre-malignant. Necrosis = swelling + lysis + inflammation, not ATP- needing; apoptosis = shrinkage + apoptotic bodies, no inflammation, ATP-dependent. Healing: resolution / regeneration (same tissue, needs mitosis) / repair-fibrosis (scar, loses function). 1st intention (edges approximated) vs 2nd (open gap, bigger scar). Healing needs age, nutrition (protein, vit C, zinc), oxygenation; corticosteroids impair it. 1 . Immunity . Innate vs Adaptive Innate - non-specific, immediate, no memory . 1st line = barriers (skin, mucosa, cilia, stomach acid, lysozyme, flora); 2nd line = inflammation, fever, phagocytes, NK cells, complement, interferons. Adaptive - specific, slower, has memory; recognises antigens. Two arms: . Humoral = B cells -> plasma cells -> antibodies; hits extracellular pathogens/toxins. · Cell-mediated = T cells; hits intracellular (viruses), cancer, transplants. Inflammation & fever are INNATE (2nd line) - a classic MCQ trap. 1b . Immune Cells WHO DOES WHAT allergy. CELL ROLE 3 . Types of Immunity 3. 3 % TYPE

• 抗原进入 → APC（巨噬/树突）递呈 → 激活 CD4 辅助T → 细胞因子刺激匹配 B 细胞 → 克隆扩增 → 浆细胞分泌抗体 + 记忆B形成。[18]Source: asksia-cheatsheet-2804nrs.pdf1e . How Humoral SAQ Immunity Works CASCADE Antigen enters -> APC (macrophage/dendritic) presents it > activates helper T (CD4) -> cytokines stimulate the matching B cell > clonal expansion > plasma cells secrete antibody + memory B cells form. Antibodies then neutralise, opsonise and activate complement. This is the chain a "describe the immune response" SAQ wants. Antibody functions: neutralisation, opsonisation (tag for phagocytes), complement activation (-> MAC), agglutination, and ADCC (flag cells for NK killing). 1f . Cell-Mediated Immunity THE T-CELL ARM Intracellular antigen (virus, tumour) on the cell surface > cytotoxic T (CD8) -> perforin/granzymes -> apoptosis of the infected/abnormal cell . Helper T amplify; regulatory T enforce tolerance. This arm drives Type IV hypersensitivity and transplant rejection. 2 . The 5 Antibody 3. 1 * MCQ GOLD Classes Y-shaped: 2 heavy + 2 light chains; variable region (Fab) binds antigen , constant region (Fc) = class/effector. IG KEY FACT IgM First & largest (pentamer); primary response; complement IgG Most abundant; only Ig to cross placenta ; secondary response II IgA Secretions - saliva, tears, mucus, breast milk IgE Mast cells/basophils; allergy/anaphylaxis, parasites IgD B-cell surface receptor; role least understood T cells (no Mnemonic: M first, G placenta, A area-secretions, E EXAM REVISION . MODULES 3- 7 Compiled by AskSia . mapped to the 2804NRS syllabus . asksia. ai/cheatsheet/griffith- 2804nrs 3. 1
• 抗体功能：中和、调理作用（opsonisation）、补体激活（MAC）、凝集、ADCC。[18]Source: asksia-cheatsheet-2804nrs.pdf1e . How Humoral SAQ Immunity Works CASCADE Antigen enters -> APC (macrophage/dendritic) presents it > activates helper T (CD4) -> cytokines stimulate the matching B cell > clonal expansion > plasma cells secrete antibody + memory B cells form. Antibodies then neutralise, opsonise and activate complement. This is the chain a "describe the immune response" SAQ wants. Antibody functions: neutralisation, opsonisation (tag for phagocytes), complement activation (-> MAC), agglutination, and ADCC (flag cells for NK killing). 1f . Cell-Mediated Immunity THE T-CELL ARM Intracellular antigen (virus, tumour) on the cell surface > cytotoxic T (CD8) -> perforin/granzymes -> apoptosis of the infected/abnormal cell . Helper T amplify; regulatory T enforce tolerance. This arm drives Type IV hypersensitivity and transplant rejection. 2 . The 5 Antibody 3. 1 * MCQ GOLD Classes Y-shaped: 2 heavy + 2 light chains; variable region (Fab) binds antigen , constant region (Fc) = class/effector. IG KEY FACT IgM First & largest (pentamer); primary response; complement IgG Most abundant; only Ig to cross placenta ; secondary response II IgA Secretions - saliva, tears, mucus, breast milk IgE Mast cells/basophils; allergy/anaphylaxis, parasites IgD B-cell surface receptor; role least understood T cells (no Mnemonic: M first, G placenta, A area-secretions, E EXAM REVISION . MODULES 3- 7 Compiled by AskSia . mapped to the 2804NRS syllabus . asksia. ai/cheatsheet/griffith- 2804nrs 3. 1

• 细胞内抗原（病毒/肿瘤）呈递 → CD8 细胞毒 T → perforin/granzymes → 诱导靶细胞凋亡；CD4 辅助T放大反应；Treg维持耐受。[18]Source: asksia-cheatsheet-2804nrs.pdf1e . How Humoral SAQ Immunity Works CASCADE Antigen enters -> APC (macrophage/dendritic) presents it > activates helper T (CD4) -> cytokines stimulate the matching B cell > clonal expansion > plasma cells secrete antibody + memory B cells form. Antibodies then neutralise, opsonise and activate complement. This is the chain a "describe the immune response" SAQ wants. Antibody functions: neutralisation, opsonisation (tag for phagocytes), complement activation (-> MAC), agglutination, and ADCC (flag cells for NK killing). 1f . Cell-Mediated Immunity THE T-CELL ARM Intracellular antigen (virus, tumour) on the cell surface > cytotoxic T (CD8) -> perforin/granzymes -> apoptosis of the infected/abnormal cell . Helper T amplify; regulatory T enforce tolerance. This arm drives Type IV hypersensitivity and transplant rejection. 2 . The 5 Antibody 3. 1 * MCQ GOLD Classes Y-shaped: 2 heavy + 2 light chains; variable region (Fab) binds antigen , constant region (Fc) = class/effector. IG KEY FACT IgM First & largest (pentamer); primary response; complement IgG Most abundant; only Ig to cross placenta ; secondary response II IgA Secretions - saliva, tears, mucus, breast milk IgE Mast cells/basophils; allergy/anaphylaxis, parasites IgD B-cell surface receptor; role least understood T cells (no Mnemonic: M first, G placenta, A area-secretions, E EXAM REVISION . MODULES 3- 7 Compiled by AskSia . mapped to the 2804NRS syllabus . asksia. ai/cheatsheet/griffith- 2804nrs 3. 1

• IgM：最先出现、五聚体、初次反应、补体。
• IgG：最多、唯一能过胎盘、二次反应更强。
• IgA：分泌液（泪液/唾液/黏膜/乳汁）。
• IgE：肥大细胞/嗜碱，过敏/过敏性休克，寄生虫。
• IgD：B 细胞表面受体，最不常考但要认得。[18]Source: asksia-cheatsheet-2804nrs.pdf1e . How Humoral SAQ Immunity Works CASCADE Antigen enters -> APC (macrophage/dendritic) presents it > activates helper T (CD4) -> cytokines stimulate the matching B cell > clonal expansion > plasma cells secrete antibody + memory B cells form. Antibodies then neutralise, opsonise and activate complement. This is the chain a "describe the immune response" SAQ wants. Antibody functions: neutralisation, opsonisation (tag for phagocytes), complement activation (-> MAC), agglutination, and ADCC (flag cells for NK killing). 1f . Cell-Mediated Immunity THE T-CELL ARM Intracellular antigen (virus, tumour) on the cell surface > cytotoxic T (CD8) -> perforin/granzymes -> apoptosis of the infected/abnormal cell . Helper T amplify; regulatory T enforce tolerance. This arm drives Type IV hypersensitivity and transplant rejection. 2 . The 5 Antibody 3. 1 * MCQ GOLD Classes Y-shaped: 2 heavy + 2 light chains; variable region (Fab) binds antigen , constant region (Fc) = class/effector. IG KEY FACT IgM First & largest (pentamer); primary response; complement IgG Most abundant; only Ig to cross placenta ; secondary response II IgA Secretions - saliva, tears, mucus, breast milk IgE Mast cells/basophils; allergy/anaphylaxis, parasites IgD B-cell surface receptor; role least understood T cells (no Mnemonic: M first, G placenta, A area-secretions, E EXAM REVISION . MODULES 3- 7 Compiled by AskSia . mapped to the 2804NRS syllabus . asksia. ai/cheatsheet/griffith- 2804nrs 3. 1

• I 型：IgE / anaphylaxis（过敏性休克）。
• II 型：细胞毒（IgG/IgM + 补体；固定抗原）。
• III 型：免疫复合物（IgG + 可溶抗原）。
• IV 型：迟发型 / T 细胞介导。[15]Source: asksia-bible-2804nrs-bilingual.pdfSLE (lupus) DNA / RNA (multi-system) Rheumatoid arthritis Synovial joints Module 3 lock-in - the must-knows ★ 模块 3 锁定 -- 必知要点 (1) Innate = non-specific/no memory; adaptive = specific/memory; humoral = B, cell-mediated = T. (2) IgM first, IgG most abundant + placenta, IgE allergy. (3) Hypersensitivity ACID: I IgE/anaphylaxis, II cytotoxic (IgG/IgM + complement, fixed antigen), III immune-complex (IgG + soluble), IV delayed/T-cell. (4) Active makes + remembers; passive is given + no memory. (5) HIV - CD4+ helper T; AIDS = CD4 < 200. Anaphylaxis first-line = adrenaline. (1) 固有=非特异/无记忆;适应性=特异/有记忆;体液= B,细胞介导=T。(2) IgM 最先,lgG 最丰富+胎盘,IgE 过敏。(3)超敏反应 ACID:| 型 IgE/过敏反应,Ⅱ 型 细胞毒(IgG/lgM+补体,固定抗原),ⅢI 型 免疫复合物(IgG+ 可溶性),IV型 迟发/T细胞。(4)主动免疫自己制造+记得住;被动免疫是给予的+无记忆。(5)HIV → CD4+辅助性 T; AIDS = CD4<200。过敏反应一线=肾上腺素。 2804NRS . Human Pathophysiology & Pharmacology 1 EOT CORE . MCQ + SAQ - MODULE 4 . NEOPLASIA & CANCER Cells that forgot how to stop - and learned how to spread 忘记如何停止、却学会扩散的细胞 Benign vs malignant . the cell cycle & checkpoints . carcinogenesis & metastasis . grading vs staging (TNM) 良性 vs 恶性 · 细胞周期与检查点 · 致癌作用与转移 · 分级 vs 分期(TNM) One big idea: cancer is a cell-cycle control failure. A normal cell divides only when told to and stops at checkpoints if its DNA is damaged. Neoplasia is new, uncontrolled, autonomous growth - cells no longer obey those controls. Two things go wrong together: the accelerator gets stuck on (a proto-oncogene mutates into an oncogene, a gain of function) and the brakes fail (a tumour-suppressor such as p53 is lost, a loss of function). The one feature that turns a tumour from dangerous-but-local into deadly is metastasis - the ability to spread to distant sites. 一个核心观念:癌症是一种细胞周期调控的失败。正常细胞只在被指示时分裂,并在DNA 受损时于检查点停止。肿瘤形成是 新生的、不受控制的、自主的生长 -- 细胞不再服从这些调控。两件事同时出错:油门卡在踩下状态(原癌基因突变为癌基 因,一种功能获得)以及刹车失灵(如p53这样的抑癌基因丢失,一种功能丧失)。把肿瘤从“危险但局限”变为“致命”的那个 特征是转移 -- 扩散到远处部位的能力。 ★ What the exam asks here 考试在这里考什么 Module 4 is both MCQ and SAQ. Expect: (1) benign vs malignant features (the headline distinguisher is metastasis); (2) oncogene vs tumour-suppressor - gain vs loss of function, with p53 / BRCA as suppressors; (3) name the steps of carcinogenesis and the routes of metastasis; (4) the perennial trap - grading vs staging (cell appearance vs spread / TNM); and (5) a short-answer risk-factor -+ aetiology - pathophysiology - clinical-manifestation chain for a named cancer. 模块 4 既考 MCQ 又考 SAQ。预期会有:(1)良性 vs 恶性特征(标志性区分点是转移);(2)癌基因 vs 抑癌基因 -- 功 能获得 vs 丧失,以p53/BRCA 为抑癌基因;(3)说出致癌作用的步骤和转移的途径;(4)经久不衰的陷阱 -- 分级 vs 分期(细胞外观 vs 扩散/TNM);以及(5)针对某种指定癌症的简答风险因素 →病因→病理生理→ 临床表现链条。 4. 1 Neoplasia: benign vs malignant 4. 1 肿瘤形成:良性 vs 恶性 Neoplasia = new, uncontrolled, autonomous cell growth not responsive to normal controls; the resulting mass is a neoplasm / tumour. The whole module hinges on one division: benign tumours stay put, malignant tumours (cancer) invade and metastasise. 肿瘤形成=新生的、不受控制的、自主的、不响应正常调控的细胞生长;由此形成的肿块为肿瘤。整个模块的关键在于一个 划分:良性肿瘤原地不动,恶性肿瘤(癌)侵袭并转移。 Feature Benign Malignant (cancer) Growth Slow, expansile Rapid, infiltrative Capsule

• Active：自己产生抗体，有记忆。
• Passive：给你现成抗体，无记忆、会衰减。[7]Source: asksia-bible-2804nrs-bilingual.pdfRe-draw each cascade from a blank page the night before: if you can rebuild Risk - Aetiology - Patho - Clinical - Dx + Rx without the prompt, you can answer almost any SAQ the disease throws at you. 考试前一晚从一张白纸重新画出每条级联:如果你能在没有提示的情况下重建 风险→病因→ 病理生理→临床→ 诊 断+治疗,你就能回答该疾病抛出的几乎任何 SAQ。 MARKER'S NOTE . 2804NRS REVISION 2804NRS . Human Pathophysiology & Pharmacology 1 Type Mechanism Memory? Example Natural active Pathogen enters - illness - you make antibodies Yes Catching chickenpox Artificial active Vaccine given (no illness) - you make antibodies Yes Polio / COVID vaccine Natural passive Antibodies passed mother-baby (placenta / breast milk) No Newborn maternal immunity Artificial passive Pre-formed antibodies injected No Immunoglobulin, antivenom, post- rabies Ig i Analogy - learning to fish vs being handed a fish 类比 -- 学会捕鱼 vs 被递上一条鱼 Active immunity is learning to fish: it takes time to learn, but you can feed yourself forever (memory). Passive immunity is being handed a fish: you eat right now (immediate protection), but when it's gone you've learned nothing (no memory, decays). 主动免疫是学会钓鱼:学起来要花时间,但你可以永远养活自己(记忆)。被动免疫是别人递来一条鱼:你现在就能吃 (即时保护),但吃完后你什么也没学会(无记忆,会衰减)。 - ! The two-axis trap - a frequent MCQ 双轴陷阱 -- 常见 MCQ

• HIV 主要伤 CD4+ helper T；AIDS 典型定义点：CD4 < 200。[15]Source: asksia-bible-2804nrs-bilingual.pdfSLE (lupus) DNA / RNA (multi-system) Rheumatoid arthritis Synovial joints Module 3 lock-in - the must-knows ★ 模块 3 锁定 -- 必知要点 (1) Innate = non-specific/no memory; adaptive = specific/memory; humoral = B, cell-mediated = T. (2) IgM first, IgG most abundant + placenta, IgE allergy. (3) Hypersensitivity ACID: I IgE/anaphylaxis, II cytotoxic (IgG/IgM + complement, fixed antigen), III immune-complex (IgG + soluble), IV delayed/T-cell. (4) Active makes + remembers; passive is given + no memory. (5) HIV - CD4+ helper T; AIDS = CD4 < 200. Anaphylaxis first-line = adrenaline. (1) 固有=非特异/无记忆;适应性=特异/有记忆;体液= B,细胞介导=T。(2) IgM 最先,lgG 最丰富+胎盘,IgE 过敏。(3)超敏反应 ACID:| 型 IgE/过敏反应,Ⅱ 型 细胞毒(IgG/lgM+补体,固定抗原),ⅢI 型 免疫复合物(IgG+ 可溶性),IV型 迟发/T细胞。(4)主动免疫自己制造+记得住;被动免疫是给予的+无记忆。(5)HIV → CD4+辅助性 T; AIDS = CD4<200。过敏反应一线=肾上腺素。 2804NRS . Human Pathophysiology & Pharmacology 1 EOT CORE . MCQ + SAQ - MODULE 4 . NEOPLASIA & CANCER Cells that forgot how to stop - and learned how to spread 忘记如何停止、却学会扩散的细胞 Benign vs malignant . the cell cycle & checkpoints . carcinogenesis & metastasis . grading vs staging (TNM) 良性 vs 恶性 · 细胞周期与检查点 · 致癌作用与转移 · 分级 vs 分期(TNM) One big idea: cancer is a cell-cycle control failure. A normal cell divides only when told to and stops at checkpoints if its DNA is damaged. Neoplasia is new, uncontrolled, autonomous growth - cells no longer obey those controls. Two things go wrong together: the accelerator gets stuck on (a proto-oncogene mutates into an oncogene, a gain of function) and the brakes fail (a tumour-suppressor such as p53 is lost, a loss of function). The one feature that turns a tumour from dangerous-but-local into deadly is metastasis - the ability to spread to distant sites. 一个核心观念:癌症是一种细胞周期调控的失败。正常细胞只在被指示时分裂,并在DNA 受损时于检查点停止。肿瘤形成是 新生的、不受控制的、自主的生长 -- 细胞不再服从这些调控。两件事同时出错:油门卡在踩下状态(原癌基因突变为癌基 因,一种功能获得)以及刹车失灵(如p53这样的抑癌基因丢失,一种功能丧失)。把肿瘤从“危险但局限”变为“致命”的那个 特征是转移 -- 扩散到远处部位的能力。 ★ What the exam asks here 考试在这里考什么 Module 4 is both MCQ and SAQ. Expect: (1) benign vs malignant features (the headline distinguisher is metastasis); (2) oncogene vs tumour-suppressor - gain vs loss of function, with p53 / BRCA as suppressors; (3) name the steps of carcinogenesis and the routes of metastasis; (4) the perennial trap - grading vs staging (cell appearance vs spread / TNM); and (5) a short-answer risk-factor -+ aetiology - pathophysiology - clinical-manifestation chain for a named cancer. 模块 4 既考 MCQ 又考 SAQ。预期会有:(1)良性 vs 恶性特征(标志性区分点是转移);(2)癌基因 vs 抑癌基因 -- 功 能获得 vs 丧失,以p53/BRCA 为抑癌基因;(3)说出致癌作用的步骤和转移的途径;(4)经久不衰的陷阱 -- 分级 vs 分期(细胞外观 vs 扩散/TNM);以及(5)针对某种指定癌症的简答风险因素 →病因→病理生理→ 临床表现链条。 4. 1 Neoplasia: benign vs malignant 4. 1 肿瘤形成:良性 vs 恶性 Neoplasia = new, uncontrolled, autonomous cell growth not responsive to normal controls; the resulting mass is a neoplasm / tumour. The whole module hinges on one division: benign tumours stay put, malignant tumours (cancer) invade and metastasise. 肿瘤形成=新生的、不受控制的、自主的、不响应正常调控的细胞生长;由此形成的肿块为肿瘤。整个模块的关键在于一个 划分:良性肿瘤原地不动,恶性肿瘤(癌)侵袭并转移。 Feature Benign Malignant (cancer) Growth Slow, expansile Rapid, infiltrative Capsule
• Anaphylaxis 一线用药：adrenaline。[15]Source: asksia-bible-2804nrs-bilingual.pdfSLE (lupus) DNA / RNA (multi-system) Rheumatoid arthritis Synovial joints Module 3 lock-in - the must-knows ★ 模块 3 锁定 -- 必知要点 (1) Innate = non-specific/no memory; adaptive = specific/memory; humoral = B, cell-mediated = T. (2) IgM first, IgG most abundant + placenta, IgE allergy. (3) Hypersensitivity ACID: I IgE/anaphylaxis, II cytotoxic (IgG/IgM + complement, fixed antigen), III immune-complex (IgG + soluble), IV delayed/T-cell. (4) Active makes + remembers; passive is given + no memory. (5) HIV - CD4+ helper T; AIDS = CD4 < 200. Anaphylaxis first-line = adrenaline. (1) 固有=非特异/无记忆;适应性=特异/有记忆;体液= B,细胞介导=T。(2) IgM 最先,lgG 最丰富+胎盘,IgE 过敏。(3)超敏反应 ACID:| 型 IgE/过敏反应,Ⅱ 型 细胞毒(IgG/lgM+补体,固定抗原),ⅢI 型 免疫复合物(IgG+ 可溶性),IV型 迟发/T细胞。(4)主动免疫自己制造+记得住;被动免疫是给予的+无记忆。(5)HIV → CD4+辅助性 T; AIDS = CD4<200。过敏反应一线=肾上腺素。 2804NRS . Human Pathophysiology & Pharmacology 1 EOT CORE . MCQ + SAQ - MODULE 4 . NEOPLASIA & CANCER Cells that forgot how to stop - and learned how to spread 忘记如何停止、却学会扩散的细胞 Benign vs malignant . the cell cycle & checkpoints . carcinogenesis & metastasis . grading vs staging (TNM) 良性 vs 恶性 · 细胞周期与检查点 · 致癌作用与转移 · 分级 vs 分期(TNM) One big idea: cancer is a cell-cycle control failure. A normal cell divides only when told to and stops at checkpoints if its DNA is damaged. Neoplasia is new, uncontrolled, autonomous growth - cells no longer obey those controls. Two things go wrong together: the accelerator gets stuck on (a proto-oncogene mutates into an oncogene, a gain of function) and the brakes fail (a tumour-suppressor such as p53 is lost, a loss of function). The one feature that turns a tumour from dangerous-but-local into deadly is metastasis - the ability to spread to distant sites. 一个核心观念:癌症是一种细胞周期调控的失败。正常细胞只在被指示时分裂,并在DNA 受损时于检查点停止。肿瘤形成是 新生的、不受控制的、自主的生长 -- 细胞不再服从这些调控。两件事同时出错:油门卡在踩下状态(原癌基因突变为癌基 因,一种功能获得)以及刹车失灵(如p53这样的抑癌基因丢失,一种功能丧失)。把肿瘤从“危险但局限”变为“致命”的那个 特征是转移 -- 扩散到远处部位的能力。 ★ What the exam asks here 考试在这里考什么 Module 4 is both MCQ and SAQ. Expect: (1) benign vs malignant features (the headline distinguisher is metastasis); (2) oncogene vs tumour-suppressor - gain vs loss of function, with p53 / BRCA as suppressors; (3) name the steps of carcinogenesis and the routes of metastasis; (4) the perennial trap - grading vs staging (cell appearance vs spread / TNM); and (5) a short-answer risk-factor -+ aetiology - pathophysiology - clinical-manifestation chain for a named cancer. 模块 4 既考 MCQ 又考 SAQ。预期会有:(1)良性 vs 恶性特征(标志性区分点是转移);(2)癌基因 vs 抑癌基因 -- 功 能获得 vs 丧失,以p53/BRCA 为抑癌基因;(3)说出致癌作用的步骤和转移的途径;(4)经久不衰的陷阱 -- 分级 vs 分期(细胞外观 vs 扩散/TNM);以及(5)针对某种指定癌症的简答风险因素 →病因→病理生理→ 临床表现链条。 4. 1 Neoplasia: benign vs malignant 4. 1 肿瘤形成:良性 vs 恶性 Neoplasia = new, uncontrolled, autonomous cell growth not responsive to normal controls; the resulting mass is a neoplasm / tumour. The whole module hinges on one division: benign tumours stay put, malignant tumours (cancer) invade and metastasise. 肿瘤形成=新生的、不受控制的、自主的、不响应正常调控的细胞生长;由此形成的肿块为肿瘤。整个模块的关键在于一个 划分:良性肿瘤原地不动,恶性肿瘤(癌)侵袭并转移。 Feature Benign Malignant (cancer) Growth Slow, expansile Rapid, infiltrative Capsule
• “为什么肾上腺素救命”（SAQ 模板）：
  • $\alpha_1$ 血管收缩→升压；$\beta_1$ 增加心输出；$\beta_2$ 支气管扩张 + 抑制肥大细胞介质释放。[22]Source: asksia-cheatsheet-2804nrs.pdfretain void MULTI- 14c . Worked SAQ . Adrenaline RECEPTOR Adrenaline in anaphylaxis hits several receptors at once: al -> vasoconstriction -> ^BP (reverses hypotension); B1 > +cardiac output; 32 > bronchodilation + +mast-cell mediator release. One drug, three life-saving actions - the classic "explain why adrenaline" SAQ. Contrast: a ß-blocker would worsen anaphylaxis and bronchospasm - never give one here. Likewise non- selective ß-blockers can trigger bronchospasm in asthmatics > use cardioselective ß1 agents. ß-blockers are also contraindicated in heart block and cardiogenic shock. 14d . Autonomic Recall MCQ DRILL · SNS post = NA (a/B); PNS post = ACh (muscarinic); all pre = ACh/nicotinic. · Atropine blocks muscarinic ("can't see/pee/spit/poo"). · AChE inhibitors + ACh (myasthenia, Alzheimer's). 15 . Pharmacokinetics * "BODY - · ADME DRUG" Absorption · Distribution · Metabolism · Excretion. ABSORPTION & BIOAVAILABILITY Enteral (oral, SL, rectal) vs parenteral (IV, IM, SC). IV = 100% bioavailability, fastest, no first-pass. Bioavailability (F) = fraction reaching circulation unchanged. Absorption depends on lipid solubility, ionisation/pH, GI motility, surface area, blood flow and food. DISTRIBUTION Drugs bind albumin; only free (unbound) drug is active . valbumin / displacement -> +free drug -> interaction. Vd high = lipophilic/tissue; low = stays in plasma. METABOLISM & EXCRETION Liver (Phase | CYP450; Phase II conjugation) -> water- soluble. First-pass: oral drug via portal vein -> liver before circulation -> voral F. Kidney excretes; renal impairment -> accumulation. 15b . Kinetic Parameters DOSING Half-life (t1/2) = time for conc. to fall 50%; ~ 4-5 t1/2 to clear OR reach steady state (rate in = rate out). Loading dose = reach level fast; maintenance dose = replace what's eliminated. CYP inducers + levels, inhibitors + levels/toxicity. 15c · Worked . Half- Life SHOW THE STEPS

3.2 Module 4：肿瘤/癌症（SAQ 超常考）

• Neoplasia：新生的、不受控、自主生长，不响应正常调控。[15]Source: asksia-bible-2804nrs-bilingual.pdfSLE (lupus) DNA / RNA (multi-system) Rheumatoid arthritis Synovial joints Module 3 lock-in - the must-knows ★ 模块 3 锁定 -- 必知要点 (1) Innate = non-specific/no memory; adaptive = specific/memory; humoral = B, cell-mediated = T. (2) IgM first, IgG most abundant + placenta, IgE allergy. (3) Hypersensitivity ACID: I IgE/anaphylaxis, II cytotoxic (IgG/IgM + complement, fixed antigen), III immune-complex (IgG + soluble), IV delayed/T-cell. (4) Active makes + remembers; passive is given + no memory. (5) HIV - CD4+ helper T; AIDS = CD4 < 200. Anaphylaxis first-line = adrenaline. (1) 固有=非特异/无记忆;适应性=特异/有记忆;体液= B,细胞介导=T。(2) IgM 最先,lgG 最丰富+胎盘,IgE 过敏。(3)超敏反应 ACID:| 型 IgE/过敏反应,Ⅱ 型 细胞毒(IgG/lgM+补体,固定抗原),ⅢI 型 免疫复合物(IgG+ 可溶性),IV型 迟发/T细胞。(4)主动免疫自己制造+记得住;被动免疫是给予的+无记忆。(5)HIV → CD4+辅助性 T; AIDS = CD4<200。过敏反应一线=肾上腺素。 2804NRS . Human Pathophysiology & Pharmacology 1 EOT CORE . MCQ + SAQ - MODULE 4 . NEOPLASIA & CANCER Cells that forgot how to stop - and learned how to spread 忘记如何停止、却学会扩散的细胞 Benign vs malignant . the cell cycle & checkpoints . carcinogenesis & metastasis . grading vs staging (TNM) 良性 vs 恶性 · 细胞周期与检查点 · 致癌作用与转移 · 分级 vs 分期(TNM) One big idea: cancer is a cell-cycle control failure. A normal cell divides only when told to and stops at checkpoints if its DNA is damaged. Neoplasia is new, uncontrolled, autonomous growth - cells no longer obey those controls. Two things go wrong together: the accelerator gets stuck on (a proto-oncogene mutates into an oncogene, a gain of function) and the brakes fail (a tumour-suppressor such as p53 is lost, a loss of function). The one feature that turns a tumour from dangerous-but-local into deadly is metastasis - the ability to spread to distant sites. 一个核心观念:癌症是一种细胞周期调控的失败。正常细胞只在被指示时分裂,并在DNA 受损时于检查点停止。肿瘤形成是 新生的、不受控制的、自主的生长 -- 细胞不再服从这些调控。两件事同时出错:油门卡在踩下状态(原癌基因突变为癌基 因,一种功能获得)以及刹车失灵(如p53这样的抑癌基因丢失,一种功能丧失)。把肿瘤从“危险但局限”变为“致命”的那个 特征是转移 -- 扩散到远处部位的能力。 ★ What the exam asks here 考试在这里考什么 Module 4 is both MCQ and SAQ. Expect: (1) benign vs malignant features (the headline distinguisher is metastasis); (2) oncogene vs tumour-suppressor - gain vs loss of function, with p53 / BRCA as suppressors; (3) name the steps of carcinogenesis and the routes of metastasis; (4) the perennial trap - grading vs staging (cell appearance vs spread / TNM); and (5) a short-answer risk-factor -+ aetiology - pathophysiology - clinical-manifestation chain for a named cancer. 模块 4 既考 MCQ 又考 SAQ。预期会有:(1)良性 vs 恶性特征(标志性区分点是转移);(2)癌基因 vs 抑癌基因 -- 功 能获得 vs 丧失,以p53/BRCA 为抑癌基因;(3)说出致癌作用的步骤和转移的途径;(4)经久不衰的陷阱 -- 分级 vs 分期(细胞外观 vs 扩散/TNM);以及(5)针对某种指定癌症的简答风险因素 →病因→病理生理→ 临床表现链条。 4. 1 Neoplasia: benign vs malignant 4. 1 肿瘤形成:良性 vs 恶性 Neoplasia = new, uncontrolled, autonomous cell growth not responsive to normal controls; the resulting mass is a neoplasm / tumour. The whole module hinges on one division: benign tumours stay put, malignant tumours (cancer) invade and metastasise. 肿瘤形成=新生的、不受控制的、自主的、不响应正常调控的细胞生长;由此形成的肿块为肿瘤。整个模块的关键在于一个 划分:良性肿瘤原地不动,恶性肿瘤(癌)侵袭并转移。 Feature Benign Malignant (cancer) Growth Slow, expansile Rapid, infiltrative Capsule
• Benign vs Malignant：最核心区分点是 恶性会 metastasise（转移）；良性不转移。[6]Source: asksia-bible-2804nrs-bilingual.pdfCheckpoint failure - cervical dysplasia (CIN) - carcinoma in situ - invasive carcinoma; eventual lymphatic / local spread 4 . Clinical manifestations Often asymptomatic early (why screening matters); then abnormal / post-coital bleeding, discharge, pelvic pain; late: spread-related symptoms 1 Risk - aetiology. A risk factor (persistent HPV) supplies the trigger - viral oncoproteins that disable p53 and Rb. 风险→ 病因。一个风险因素(持续性 HPV)提供触发 -- 使 p53和 Rb 失活的病毒癌蛋白。 2 Aetiology - pathophysiology. Lost tumour-suppressors = brakes off at the checkpoint - the morphological arc dysplasia - CIS - invasive (exactly the carcinogenesis ladder from page 3). 病因→ 病理生理。抑癌基因丧失=检查点处刹车失灵→形态学弧线 不典型增生→ 原位癌(CIS)→侵袭(正是第3页的 致癌作用阶梯)。 3 Pathophysiology - clinical. Local invasion and spread produce the bleeding, discharge and pain - but the key teaching point is the silent early phase, which is why screening (Pap / HPV test) and the HPV vaccine are the high-impact interventions. 病理生理→临床。局部侵袭和扩散产生出血、分泌物和疼痛 -- 但关键教学点是那个无声的早期阶段,这正是为什么筛查 (Pap/HPV 检测)和HPV 疫苗是高效干预。 - 2804NRS . Human Pathophysiology & Pharmacology 1 i Why this links back to Module 3 为何这要回链到模块 3 Cervical cancer is the clean bridge between the two modules: an infectious trigger (HPV) disabling tumour- suppressors, prevented by an artificial-active vaccine - immunity (Module 3) and neoplasia (Module 4) in one disease. The same RF-clinical cascade structure works for any cancer the exam names (lung/tobacco, melanoma/UV, breast/BRCA). 宫颈癌是连接这两个模块的清晰桥梁:一个感染性触发因素(HPV)使抑癌基因失活,由一种人工主动疫苗预防 -- 免 疫(模块 3)与肿瘤(模块4)合于一种疾病之中。同样的 RF→临床级联结构适用于考试提到的任何癌症(肺/烟草, 黑色素瘤/紫外线,乳腺/BRCA)。 ★ Module 4 lock-in - the must-knows 模块 4 锁定 -- 必知要点 (1) Benign = no metastasis; malignant metastasises (the distinguisher). (2) Cell cycle G1++S++G2-M; G1/S = key checkpoint; cancer = checkpoint failure. (3) Oncogene = gain of function, tumour-suppressor = loss (p53, BRCA). (4) Carcinogenesis = initiation-promotion-progression; spread by blood / lymph / transcoelomic / local. (5) Grading = cell appearance, Staging = spread (TNM). (6) Be able to run the RF-aetiology++patho-clinical chain. (1) 良性=不转移;恶性会转移(区分点)。(2)细胞周期 G1→S→G2→M;G1/S=关键检查点;癌症=检查点失灵。 (3) 癌基因=功能获得,抑癌基因=功能丧失(p53、BRCA)。(4)致癌作用=启动→促进→进展;通过血液/淋巴/经 体腔/局部扩散。(5)分级=细胞外观,分期=扩散(TNM)。(6)要能跑通RF→病因→病理生理→临床 链条。 Accelerator on, brakes off, boundaries crossed - that is the whole of cancer in six words. 油门开、刹车失、越边界 -- 用六个字概括,这就是癌症的全部。 I THE MODULE 4 MENTAL MODEL 2804NRS . Human Pathophysiology & Pharmacology 1 M5 . MSK & PAIN - MODULE 5 . MUSCULOSKELETAL & PAIN EOTE CORE Joints, bones & the pharmacology of pain 关节、骨骼与疼痛药理学 Inflammatory vs degenerative joint disease . bone & fracture . nociception . NSAIDs, the COX pathway & the WHO ladder 炎症性 vs 退行性关节病 · 骨骼与骨折 · 伤害性感受 · NSAID、COX 通路与 WHO 阶梯 One spine for the whole module: the musculoskeletal system fails in two flavours - degenerative (wear of cartilage/bone, e. g. osteoarthritis, osteoporosis) and inflammatory/autoimmune (the immune system attacking the joint, e. g. rheumatoid arthritis). That same split - is the problem mechanical wear or active inflammation? - decides the drug: you treat inflammation by switching off prostaglandins (NSAIDs, steroids), and you treat the pain itself by climbing the WHO analgesic ladder. Master the COX pathway and the ladder and you own half of Module 5. 贯穿整个模块的一条脊柱:肌肉骨骼系统以两种类型衰败 -- 退行性(软骨/骨的磨损,如骨关节炎、骨质疏松)和炎症性/ 自身免疫性(免疫系统攻击关节,如类风湿关节炎)。同样的划分 -- 问题是机械性磨损还是活动性炎症 ?-- 决定用药:通 过关闭前列腺素(NSAID、类固醇)来治疗炎症,并通过攀登WHO 镇痛阶梯来治疗疼痛本身。掌握 COX 通路与阶梯,你就 掌握了模块 5的一半。 ★ What the EoT exam asks here 学期末考试在这里考什么[15]Source: asksia-bible-2804nrs-bilingual.pdfSLE (lupus) DNA / RNA (multi-system) Rheumatoid arthritis Synovial joints Module 3 lock-in - the must-knows ★ 模块 3 锁定 -- 必知要点 (1) Innate = non-specific/no memory; adaptive = specific/memory; humoral = B, cell-mediated = T. (2) IgM first, IgG most abundant + placenta, IgE allergy. (3) Hypersensitivity ACID: I IgE/anaphylaxis, II cytotoxic (IgG/IgM + complement, fixed antigen), III immune-complex (IgG + soluble), IV delayed/T-cell. (4) Active makes + remembers; passive is given + no memory. (5) HIV - CD4+ helper T; AIDS = CD4 < 200. Anaphylaxis first-line = adrenaline. (1) 固有=非特异/无记忆;适应性=特异/有记忆;体液= B,细胞介导=T。(2) IgM 最先,lgG 最丰富+胎盘,IgE 过敏。(3)超敏反应 ACID:| 型 IgE/过敏反应,Ⅱ 型 细胞毒(IgG/lgM+补体,固定抗原),ⅢI 型 免疫复合物(IgG+ 可溶性),IV型 迟发/T细胞。(4)主动免疫自己制造+记得住;被动免疫是给予的+无记忆。(5)HIV → CD4+辅助性 T; AIDS = CD4<200。过敏反应一线=肾上腺素。 2804NRS . Human Pathophysiology & Pharmacology 1 EOT CORE . MCQ + SAQ - MODULE 4 . NEOPLASIA & CANCER Cells that forgot how to stop - and learned how to spread 忘记如何停止、却学会扩散的细胞 Benign vs malignant . the cell cycle & checkpoints . carcinogenesis & metastasis . grading vs staging (TNM) 良性 vs 恶性 · 细胞周期与检查点 · 致癌作用与转移 · 分级 vs 分期(TNM) One big idea: cancer is a cell-cycle control failure. A normal cell divides only when told to and stops at checkpoints if its DNA is damaged. Neoplasia is new, uncontrolled, autonomous growth - cells no longer obey those controls. Two things go wrong together: the accelerator gets stuck on (a proto-oncogene mutates into an oncogene, a gain of function) and the brakes fail (a tumour-suppressor such as p53 is lost, a loss of function). The one feature that turns a tumour from dangerous-but-local into deadly is metastasis - the ability to spread to distant sites. 一个核心观念:癌症是一种细胞周期调控的失败。正常细胞只在被指示时分裂,并在DNA 受损时于检查点停止。肿瘤形成是 新生的、不受控制的、自主的生长 -- 细胞不再服从这些调控。两件事同时出错:油门卡在踩下状态(原癌基因突变为癌基 因,一种功能获得)以及刹车失灵(如p53这样的抑癌基因丢失,一种功能丧失)。把肿瘤从“危险但局限”变为“致命”的那个 特征是转移 -- 扩散到远处部位的能力。 ★ What the exam asks here 考试在这里考什么 Module 4 is both MCQ and SAQ. Expect: (1) benign vs malignant features (the headline distinguisher is metastasis); (2) oncogene vs tumour-suppressor - gain vs loss of function, with p53 / BRCA as suppressors; (3) name the steps of carcinogenesis and the routes of metastasis; (4) the perennial trap - grading vs staging (cell appearance vs spread / TNM); and (5) a short-answer risk-factor -+ aetiology - pathophysiology - clinical-manifestation chain for a named cancer. 模块 4 既考 MCQ 又考 SAQ。预期会有:(1)良性 vs 恶性特征(标志性区分点是转移);(2)癌基因 vs 抑癌基因 -- 功 能获得 vs 丧失,以p53/BRCA 为抑癌基因;(3)说出致癌作用的步骤和转移的途径;(4)经久不衰的陷阱 -- 分级 vs 分期(细胞外观 vs 扩散/TNM);以及(5)针对某种指定癌症的简答风险因素 →病因→病理生理→ 临床表现链条。 4. 1 Neoplasia: benign vs malignant 4. 1 肿瘤形成:良性 vs 恶性 Neoplasia = new, uncontrolled, autonomous cell growth not responsive to normal controls; the resulting mass is a neoplasm / tumour. The whole module hinges on one division: benign tumours stay put, malignant tumours (cancer) invade and metastasise. 肿瘤形成=新生的、不受控制的、自主的、不响应正常调控的细胞生长;由此形成的肿块为肿瘤。整个模块的关键在于一个 划分:良性肿瘤原地不动,恶性肿瘤(癌)侵袭并转移。 Feature Benign Malignant (cancer) Growth Slow, expansile Rapid, infiltrative Capsule

• G1 → S → G2 → M；G1/S 是关键检查点；癌症常见 = checkpoint failure。[6]Source: asksia-bible-2804nrs-bilingual.pdfCheckpoint failure - cervical dysplasia (CIN) - carcinoma in situ - invasive carcinoma; eventual lymphatic / local spread 4 . Clinical manifestations Often asymptomatic early (why screening matters); then abnormal / post-coital bleeding, discharge, pelvic pain; late: spread-related symptoms 1 Risk - aetiology. A risk factor (persistent HPV) supplies the trigger - viral oncoproteins that disable p53 and Rb. 风险→ 病因。一个风险因素(持续性 HPV)提供触发 -- 使 p53和 Rb 失活的病毒癌蛋白。 2 Aetiology - pathophysiology. Lost tumour-suppressors = brakes off at the checkpoint - the morphological arc dysplasia - CIS - invasive (exactly the carcinogenesis ladder from page 3). 病因→ 病理生理。抑癌基因丧失=检查点处刹车失灵→形态学弧线 不典型增生→ 原位癌(CIS)→侵袭(正是第3页的 致癌作用阶梯)。 3 Pathophysiology - clinical. Local invasion and spread produce the bleeding, discharge and pain - but the key teaching point is the silent early phase, which is why screening (Pap / HPV test) and the HPV vaccine are the high-impact interventions. 病理生理→临床。局部侵袭和扩散产生出血、分泌物和疼痛 -- 但关键教学点是那个无声的早期阶段,这正是为什么筛查 (Pap/HPV 检测)和HPV 疫苗是高效干预。 - 2804NRS . Human Pathophysiology & Pharmacology 1 i Why this links back to Module 3 为何这要回链到模块 3 Cervical cancer is the clean bridge between the two modules: an infectious trigger (HPV) disabling tumour- suppressors, prevented by an artificial-active vaccine - immunity (Module 3) and neoplasia (Module 4) in one disease. The same RF-clinical cascade structure works for any cancer the exam names (lung/tobacco, melanoma/UV, breast/BRCA). 宫颈癌是连接这两个模块的清晰桥梁:一个感染性触发因素(HPV)使抑癌基因失活,由一种人工主动疫苗预防 -- 免 疫(模块 3)与肿瘤(模块4)合于一种疾病之中。同样的 RF→临床级联结构适用于考试提到的任何癌症(肺/烟草, 黑色素瘤/紫外线,乳腺/BRCA)。 ★ Module 4 lock-in - the must-knows 模块 4 锁定 -- 必知要点 (1) Benign = no metastasis; malignant metastasises (the distinguisher). (2) Cell cycle G1++S++G2-M; G1/S = key checkpoint; cancer = checkpoint failure. (3) Oncogene = gain of function, tumour-suppressor = loss (p53, BRCA). (4) Carcinogenesis = initiation-promotion-progression; spread by blood / lymph / transcoelomic / local. (5) Grading = cell appearance, Staging = spread (TNM). (6) Be able to run the RF-aetiology++patho-clinical chain. (1) 良性=不转移;恶性会转移(区分点)。(2)细胞周期 G1→S→G2→M;G1/S=关键检查点;癌症=检查点失灵。 (3) 癌基因=功能获得,抑癌基因=功能丧失(p53、BRCA)。(4)致癌作用=启动→促进→进展;通过血液/淋巴/经 体腔/局部扩散。(5)分级=细胞外观,分期=扩散(TNM)。(6)要能跑通RF→病因→病理生理→临床 链条。 Accelerator on, brakes off, boundaries crossed - that is the whole of cancer in six words. 油门开、刹车失、越边界 -- 用六个字概括,这就是癌症的全部。 I THE MODULE 4 MENTAL MODEL 2804NRS . Human Pathophysiology & Pharmacology 1 M5 . MSK & PAIN - MODULE 5 . MUSCULOSKELETAL & PAIN EOTE CORE Joints, bones & the pharmacology of pain 关节、骨骼与疼痛药理学 Inflammatory vs degenerative joint disease . bone & fracture . nociception . NSAIDs, the COX pathway & the WHO ladder 炎症性 vs 退行性关节病 · 骨骼与骨折 · 伤害性感受 · NSAID、COX 通路与 WHO 阶梯 One spine for the whole module: the musculoskeletal system fails in two flavours - degenerative (wear of cartilage/bone, e. g. osteoarthritis, osteoporosis) and inflammatory/autoimmune (the immune system attacking the joint, e. g. rheumatoid arthritis). That same split - is the problem mechanical wear or active inflammation? - decides the drug: you treat inflammation by switching off prostaglandins (NSAIDs, steroids), and you treat the pain itself by climbing the WHO analgesic ladder. Master the COX pathway and the ladder and you own half of Module 5. 贯穿整个模块的一条脊柱:肌肉骨骼系统以两种类型衰败 -- 退行性(软骨/骨的磨损,如骨关节炎、骨质疏松)和炎症性/ 自身免疫性(免疫系统攻击关节,如类风湿关节炎)。同样的划分 -- 问题是机械性磨损还是活动性炎症 ?-- 决定用药:通 过关闭前列腺素(NSAID、类固醇)来治疗炎症,并通过攀登WHO 镇痛阶梯来治疗疼痛本身。掌握 COX 通路与阶梯,你就 掌握了模块 5的一半。 ★ What the EoT exam asks here 学期末考试在这里考什么[25]Source: asksia-cheatsheet-2804nrs.pdfwell poor (anaplastic) Metastasis No Yes Carcinogenesis = multistep initiation > promotion -> progression ; needs multiple mutations passed to daughter cells. 7b . Oncogenes & Spread GAIN VS LOSS · Tumour suppressor (p53 "guardian", BRCA1/2) -> loss of function = brakes failed. Cell cycle G1->S-> G2->M; cancer = checkpoint failure (esp. G1/S). Metastasis routes: local invasion, lymphatic, haematogenous (blood), transcoelomic seeding. Grading vs Staging: grading = how abnormal cells look; staging = how far it spread (TNM = Tumour, Node, Metastasis). AU risks: tobacco, UV, alcohol, HPV, BRCA, age. 8 . MSK & Pain MODULE 5 % Osteoporosis - bone density (resorption > formation; post-menopausal voestrogen) -> fragility fractures. Fracture healing: haematoma -> soft callus > hard (bony) callus -> remodelling. Compartment syndrome = ^pressure in a closed fascial space -> ischaemia (the 6 Ps) - emergency. Pain cascade (SAQ): tissue injury > mediators (prostaglandins, bradykinin) sensitise nociceptors > signal via A8/C fibres -> dorsal horn -> spinothalamic tract -> thalamus > cortex (perception). Nociceptive vs neuropathic vs referred. 8b . Arthritis & BPH 5. 2 / 4. 4 OA = "wear-and-tear" cartilage loss, mechanical, asymmetrical, large weight-bearing joints. RA = autoimmune (Type III, synovium), symmetrical small joints, systemic, morning stiffness, RF/anti-CCP. BPH = benign hyperplasia of the peri-urethral prostate (age/DHT) -> obstruction (hesitancy, frequency, nocturia, weak stream). Mx: a1-blockers ("-osin", relax smooth muscle) + 5a-reductase inhibitors. Prostate cancer = peripheral zone, PSA marker, androgen-dependent. 8c . Cell-Cycle Recap G1 > S (DNA synthesis) > G2 > M (mitosis) > cytokinesis. Checkpoints (esp. G1/S restriction point) police DNA integrity; p53 halts or apoptoses damaged cells. Cancer = oncogene accelerator stuck ON plus suppressor brakes OFF -> checkpoints bypassed -> autonomous proliferation. Cancer treatment (4. 2. 3): surgery (remove), radiotherapy (DNA damage, local), chemotherapy (cytotoxic, hits rapidly dividing cells -> AEs: myelosuppression, hair loss, GI/mucositis, nausea), and targeted/hormonal therapy. Diagnosis: biopsy + histology, imaging, tumour markers (PSA, CA-125). The cytotoxic AEs come from hitting normal fast-dividing cells (marrow, gut, hair). asksia. ai/cheatsheet/ griffith-2804nrs . side 1/2 AskSia CHEATSHEET SERIES

• Oncogene：功能获得（accelerator stuck on）。
• Tumour suppressor：功能丧失（brakes fail），例：p53、BRCA。[6]Source: asksia-bible-2804nrs-bilingual.pdfCheckpoint failure - cervical dysplasia (CIN) - carcinoma in situ - invasive carcinoma; eventual lymphatic / local spread 4 . Clinical manifestations Often asymptomatic early (why screening matters); then abnormal / post-coital bleeding, discharge, pelvic pain; late: spread-related symptoms 1 Risk - aetiology. A risk factor (persistent HPV) supplies the trigger - viral oncoproteins that disable p53 and Rb. 风险→ 病因。一个风险因素(持续性 HPV)提供触发 -- 使 p53和 Rb 失活的病毒癌蛋白。 2 Aetiology - pathophysiology. Lost tumour-suppressors = brakes off at the checkpoint - the morphological arc dysplasia - CIS - invasive (exactly the carcinogenesis ladder from page 3). 病因→ 病理生理。抑癌基因丧失=检查点处刹车失灵→形态学弧线 不典型增生→ 原位癌(CIS)→侵袭(正是第3页的 致癌作用阶梯)。 3 Pathophysiology - clinical. Local invasion and spread produce the bleeding, discharge and pain - but the key teaching point is the silent early phase, which is why screening (Pap / HPV test) and the HPV vaccine are the high-impact interventions. 病理生理→临床。局部侵袭和扩散产生出血、分泌物和疼痛 -- 但关键教学点是那个无声的早期阶段,这正是为什么筛查 (Pap/HPV 检测)和HPV 疫苗是高效干预。 - 2804NRS . Human Pathophysiology & Pharmacology 1 i Why this links back to Module 3 为何这要回链到模块 3 Cervical cancer is the clean bridge between the two modules: an infectious trigger (HPV) disabling tumour- suppressors, prevented by an artificial-active vaccine - immunity (Module 3) and neoplasia (Module 4) in one disease. The same RF-clinical cascade structure works for any cancer the exam names (lung/tobacco, melanoma/UV, breast/BRCA). 宫颈癌是连接这两个模块的清晰桥梁:一个感染性触发因素(HPV)使抑癌基因失活,由一种人工主动疫苗预防 -- 免 疫(模块 3)与肿瘤(模块4)合于一种疾病之中。同样的 RF→临床级联结构适用于考试提到的任何癌症(肺/烟草, 黑色素瘤/紫外线,乳腺/BRCA)。 ★ Module 4 lock-in - the must-knows 模块 4 锁定 -- 必知要点 (1) Benign = no metastasis; malignant metastasises (the distinguisher). (2) Cell cycle G1++S++G2-M; G1/S = key checkpoint; cancer = checkpoint failure. (3) Oncogene = gain of function, tumour-suppressor = loss (p53, BRCA). (4) Carcinogenesis = initiation-promotion-progression; spread by blood / lymph / transcoelomic / local. (5) Grading = cell appearance, Staging = spread (TNM). (6) Be able to run the RF-aetiology++patho-clinical chain. (1) 良性=不转移;恶性会转移(区分点)。(2)细胞周期 G1→S→G2→M;G1/S=关键检查点;癌症=检查点失灵。 (3) 癌基因=功能获得,抑癌基因=功能丧失(p53、BRCA)。(4)致癌作用=启动→促进→进展;通过血液/淋巴/经 体腔/局部扩散。(5)分级=细胞外观,分期=扩散(TNM)。(6)要能跑通RF→病因→病理生理→临床 链条。 Accelerator on, brakes off, boundaries crossed - that is the whole of cancer in six words. 油门开、刹车失、越边界 -- 用六个字概括,这就是癌症的全部。 I THE MODULE 4 MENTAL MODEL 2804NRS . Human Pathophysiology & Pharmacology 1 M5 . MSK & PAIN - MODULE 5 . MUSCULOSKELETAL & PAIN EOTE CORE Joints, bones & the pharmacology of pain 关节、骨骼与疼痛药理学 Inflammatory vs degenerative joint disease . bone & fracture . nociception . NSAIDs, the COX pathway & the WHO ladder 炎症性 vs 退行性关节病 · 骨骼与骨折 · 伤害性感受 · NSAID、COX 通路与 WHO 阶梯 One spine for the whole module: the musculoskeletal system fails in two flavours - degenerative (wear of cartilage/bone, e. g. osteoarthritis, osteoporosis) and inflammatory/autoimmune (the immune system attacking the joint, e. g. rheumatoid arthritis). That same split - is the problem mechanical wear or active inflammation? - decides the drug: you treat inflammation by switching off prostaglandins (NSAIDs, steroids), and you treat the pain itself by climbing the WHO analgesic ladder. Master the COX pathway and the ladder and you own half of Module 5. 贯穿整个模块的一条脊柱:肌肉骨骼系统以两种类型衰败 -- 退行性(软骨/骨的磨损,如骨关节炎、骨质疏松)和炎症性/ 自身免疫性(免疫系统攻击关节,如类风湿关节炎)。同样的划分 -- 问题是机械性磨损还是活动性炎症 ?-- 决定用药:通 过关闭前列腺素(NSAID、类固醇)来治疗炎症,并通过攀登WHO 镇痛阶梯来治疗疼痛本身。掌握 COX 通路与阶梯,你就 掌握了模块 5的一半。 ★ What the EoT exam asks here 学期末考试在这里考什么[25]Source: asksia-cheatsheet-2804nrs.pdfwell poor (anaplastic) Metastasis No Yes Carcinogenesis = multistep initiation > promotion -> progression ; needs multiple mutations passed to daughter cells. 7b . Oncogenes & Spread GAIN VS LOSS · Tumour suppressor (p53 "guardian", BRCA1/2) -> loss of function = brakes failed. Cell cycle G1->S-> G2->M; cancer = checkpoint failure (esp. G1/S). Metastasis routes: local invasion, lymphatic, haematogenous (blood), transcoelomic seeding. Grading vs Staging: grading = how abnormal cells look; staging = how far it spread (TNM = Tumour, Node, Metastasis). AU risks: tobacco, UV, alcohol, HPV, BRCA, age. 8 . MSK & Pain MODULE 5 % Osteoporosis - bone density (resorption > formation; post-menopausal voestrogen) -> fragility fractures. Fracture healing: haematoma -> soft callus > hard (bony) callus -> remodelling. Compartment syndrome = ^pressure in a closed fascial space -> ischaemia (the 6 Ps) - emergency. Pain cascade (SAQ): tissue injury > mediators (prostaglandins, bradykinin) sensitise nociceptors > signal via A8/C fibres -> dorsal horn -> spinothalamic tract -> thalamus > cortex (perception). Nociceptive vs neuropathic vs referred. 8b . Arthritis & BPH 5. 2 / 4. 4 OA = "wear-and-tear" cartilage loss, mechanical, asymmetrical, large weight-bearing joints. RA = autoimmune (Type III, synovium), symmetrical small joints, systemic, morning stiffness, RF/anti-CCP. BPH = benign hyperplasia of the peri-urethral prostate (age/DHT) -> obstruction (hesitancy, frequency, nocturia, weak stream). Mx: a1-blockers ("-osin", relax smooth muscle) + 5a-reductase inhibitors. Prostate cancer = peripheral zone, PSA marker, androgen-dependent. 8c . Cell-Cycle Recap G1 > S (DNA synthesis) > G2 > M (mitosis) > cytokinesis. Checkpoints (esp. G1/S restriction point) police DNA integrity; p53 halts or apoptoses damaged cells. Cancer = oncogene accelerator stuck ON plus suppressor brakes OFF -> checkpoints bypassed -> autonomous proliferation. Cancer treatment (4. 2. 3): surgery (remove), radiotherapy (DNA damage, local), chemotherapy (cytotoxic, hits rapidly dividing cells -> AEs: myelosuppression, hair loss, GI/mucositis, nausea), and targeted/hormonal therapy. Diagnosis: biopsy + histology, imaging, tumour markers (PSA, CA-125). The cytotoxic AEs come from hitting normal fast-dividing cells (marrow, gut, hair). asksia. ai/cheatsheet/ griffith-2804nrs . side 1/2 AskSia CHEATSHEET SERIES

• grading = 细胞长得多“不像正常”（分化差/间变等外观）。
• staging = 扩散到哪（TNM：Tumour/Node/Metastasis）。[6]Source: asksia-bible-2804nrs-bilingual.pdfCheckpoint failure - cervical dysplasia (CIN) - carcinoma in situ - invasive carcinoma; eventual lymphatic / local spread 4 . Clinical manifestations Often asymptomatic early (why screening matters); then abnormal / post-coital bleeding, discharge, pelvic pain; late: spread-related symptoms 1 Risk - aetiology. A risk factor (persistent HPV) supplies the trigger - viral oncoproteins that disable p53 and Rb. 风险→ 病因。一个风险因素(持续性 HPV)提供触发 -- 使 p53和 Rb 失活的病毒癌蛋白。 2 Aetiology - pathophysiology. Lost tumour-suppressors = brakes off at the checkpoint - the morphological arc dysplasia - CIS - invasive (exactly the carcinogenesis ladder from page 3). 病因→ 病理生理。抑癌基因丧失=检查点处刹车失灵→形态学弧线 不典型增生→ 原位癌(CIS)→侵袭(正是第3页的 致癌作用阶梯)。 3 Pathophysiology - clinical. Local invasion and spread produce the bleeding, discharge and pain - but the key teaching point is the silent early phase, which is why screening (Pap / HPV test) and the HPV vaccine are the high-impact interventions. 病理生理→临床。局部侵袭和扩散产生出血、分泌物和疼痛 -- 但关键教学点是那个无声的早期阶段,这正是为什么筛查 (Pap/HPV 检测)和HPV 疫苗是高效干预。 - 2804NRS . Human Pathophysiology & Pharmacology 1 i Why this links back to Module 3 为何这要回链到模块 3 Cervical cancer is the clean bridge between the two modules: an infectious trigger (HPV) disabling tumour- suppressors, prevented by an artificial-active vaccine - immunity (Module 3) and neoplasia (Module 4) in one disease. The same RF-clinical cascade structure works for any cancer the exam names (lung/tobacco, melanoma/UV, breast/BRCA). 宫颈癌是连接这两个模块的清晰桥梁:一个感染性触发因素(HPV)使抑癌基因失活,由一种人工主动疫苗预防 -- 免 疫(模块 3)与肿瘤(模块4)合于一种疾病之中。同样的 RF→临床级联结构适用于考试提到的任何癌症(肺/烟草, 黑色素瘤/紫外线,乳腺/BRCA)。 ★ Module 4 lock-in - the must-knows 模块 4 锁定 -- 必知要点 (1) Benign = no metastasis; malignant metastasises (the distinguisher). (2) Cell cycle G1++S++G2-M; G1/S = key checkpoint; cancer = checkpoint failure. (3) Oncogene = gain of function, tumour-suppressor = loss (p53, BRCA). (4) Carcinogenesis = initiation-promotion-progression; spread by blood / lymph / transcoelomic / local. (5) Grading = cell appearance, Staging = spread (TNM). (6) Be able to run the RF-aetiology++patho-clinical chain. (1) 良性=不转移;恶性会转移(区分点)。(2)细胞周期 G1→S→G2→M;G1/S=关键检查点;癌症=检查点失灵。 (3) 癌基因=功能获得,抑癌基因=功能丧失(p53、BRCA)。(4)致癌作用=启动→促进→进展;通过血液/淋巴/经 体腔/局部扩散。(5)分级=细胞外观,分期=扩散(TNM)。(6)要能跑通RF→病因→病理生理→临床 链条。 Accelerator on, brakes off, boundaries crossed - that is the whole of cancer in six words. 油门开、刹车失、越边界 -- 用六个字概括,这就是癌症的全部。 I THE MODULE 4 MENTAL MODEL 2804NRS . Human Pathophysiology & Pharmacology 1 M5 . MSK & PAIN - MODULE 5 . MUSCULOSKELETAL & PAIN EOTE CORE Joints, bones & the pharmacology of pain 关节、骨骼与疼痛药理学 Inflammatory vs degenerative joint disease . bone & fracture . nociception . NSAIDs, the COX pathway & the WHO ladder 炎症性 vs 退行性关节病 · 骨骼与骨折 · 伤害性感受 · NSAID、COX 通路与 WHO 阶梯 One spine for the whole module: the musculoskeletal system fails in two flavours - degenerative (wear of cartilage/bone, e. g. osteoarthritis, osteoporosis) and inflammatory/autoimmune (the immune system attacking the joint, e. g. rheumatoid arthritis). That same split - is the problem mechanical wear or active inflammation? - decides the drug: you treat inflammation by switching off prostaglandins (NSAIDs, steroids), and you treat the pain itself by climbing the WHO analgesic ladder. Master the COX pathway and the ladder and you own half of Module 5. 贯穿整个模块的一条脊柱:肌肉骨骼系统以两种类型衰败 -- 退行性(软骨/骨的磨损,如骨关节炎、骨质疏松)和炎症性/ 自身免疫性(免疫系统攻击关节,如类风湿关节炎)。同样的划分 -- 问题是机械性磨损还是活动性炎症 ?-- 决定用药:通 过关闭前列腺素(NSAID、类固醇)来治疗炎症,并通过攀登WHO 镇痛阶梯来治疗疼痛本身。掌握 COX 通路与阶梯,你就 掌握了模块 5的一半。 ★ What the EoT exam asks here 学期末考试在这里考什么[25]Source: asksia-cheatsheet-2804nrs.pdfwell poor (anaplastic) Metastasis No Yes Carcinogenesis = multistep initiation > promotion -> progression ; needs multiple mutations passed to daughter cells. 7b . Oncogenes & Spread GAIN VS LOSS · Tumour suppressor (p53 "guardian", BRCA1/2) -> loss of function = brakes failed. Cell cycle G1->S-> G2->M; cancer = checkpoint failure (esp. G1/S). Metastasis routes: local invasion, lymphatic, haematogenous (blood), transcoelomic seeding. Grading vs Staging: grading = how abnormal cells look; staging = how far it spread (TNM = Tumour, Node, Metastasis). AU risks: tobacco, UV, alcohol, HPV, BRCA, age. 8 . MSK & Pain MODULE 5 % Osteoporosis - bone density (resorption > formation; post-menopausal voestrogen) -> fragility fractures. Fracture healing: haematoma -> soft callus > hard (bony) callus -> remodelling. Compartment syndrome = ^pressure in a closed fascial space -> ischaemia (the 6 Ps) - emergency. Pain cascade (SAQ): tissue injury > mediators (prostaglandins, bradykinin) sensitise nociceptors > signal via A8/C fibres -> dorsal horn -> spinothalamic tract -> thalamus > cortex (perception). Nociceptive vs neuropathic vs referred. 8b . Arthritis & BPH 5. 2 / 4. 4 OA = "wear-and-tear" cartilage loss, mechanical, asymmetrical, large weight-bearing joints. RA = autoimmune (Type III, synovium), symmetrical small joints, systemic, morning stiffness, RF/anti-CCP. BPH = benign hyperplasia of the peri-urethral prostate (age/DHT) -> obstruction (hesitancy, frequency, nocturia, weak stream). Mx: a1-blockers ("-osin", relax smooth muscle) + 5a-reductase inhibitors. Prostate cancer = peripheral zone, PSA marker, androgen-dependent. 8c . Cell-Cycle Recap G1 > S (DNA synthesis) > G2 > M (mitosis) > cytokinesis. Checkpoints (esp. G1/S restriction point) police DNA integrity; p53 halts or apoptoses damaged cells. Cancer = oncogene accelerator stuck ON plus suppressor brakes OFF -> checkpoints bypassed -> autonomous proliferation. Cancer treatment (4. 2. 3): surgery (remove), radiotherapy (DNA damage, local), chemotherapy (cytotoxic, hits rapidly dividing cells -> AEs: myelosuppression, hair loss, GI/mucositis, nausea), and targeted/hormonal therapy. Diagnosis: biopsy + histology, imaging, tumour markers (PSA, CA-125). The cytotoxic AEs come from hitting normal fast-dividing cells (marrow, gut, hair). asksia. ai/cheatsheet/ griffith-2804nrs . side 1/2 AskSia CHEATSHEET SERIES

• 示例（宫颈癌）给你的思路是：
  • RF：持续 HPV（风险因素提供触发）→ 病因：病毒致癌蛋白让 p53/Rb 失活 → 病理：检查点刹车失灵→不典型增生→CIS→侵袭 → 临床：早期沉默、后期出血/分泌物/盆腔痛 → Dx：Pap/HPV 检测 → 高影响干预：筛查 + HPV 疫苗。[6]Source: asksia-bible-2804nrs-bilingual.pdfCheckpoint failure - cervical dysplasia (CIN) - carcinoma in situ - invasive carcinoma; eventual lymphatic / local spread 4 . Clinical manifestations Often asymptomatic early (why screening matters); then abnormal / post-coital bleeding, discharge, pelvic pain; late: spread-related symptoms 1 Risk - aetiology. A risk factor (persistent HPV) supplies the trigger - viral oncoproteins that disable p53 and Rb. 风险→ 病因。一个风险因素(持续性 HPV)提供触发 -- 使 p53和 Rb 失活的病毒癌蛋白。 2 Aetiology - pathophysiology. Lost tumour-suppressors = brakes off at the checkpoint - the morphological arc dysplasia - CIS - invasive (exactly the carcinogenesis ladder from page 3). 病因→ 病理生理。抑癌基因丧失=检查点处刹车失灵→形态学弧线 不典型增生→ 原位癌(CIS)→侵袭(正是第3页的 致癌作用阶梯)。 3 Pathophysiology - clinical. Local invasion and spread produce the bleeding, discharge and pain - but the key teaching point is the silent early phase, which is why screening (Pap / HPV test) and the HPV vaccine are the high-impact interventions. 病理生理→临床。局部侵袭和扩散产生出血、分泌物和疼痛 -- 但关键教学点是那个无声的早期阶段,这正是为什么筛查 (Pap/HPV 检测)和HPV 疫苗是高效干预。 - 2804NRS . Human Pathophysiology & Pharmacology 1 i Why this links back to Module 3 为何这要回链到模块 3 Cervical cancer is the clean bridge between the two modules: an infectious trigger (HPV) disabling tumour- suppressors, prevented by an artificial-active vaccine - immunity (Module 3) and neoplasia (Module 4) in one disease. The same RF-clinical cascade structure works for any cancer the exam names (lung/tobacco, melanoma/UV, breast/BRCA). 宫颈癌是连接这两个模块的清晰桥梁:一个感染性触发因素(HPV)使抑癌基因失活,由一种人工主动疫苗预防 -- 免 疫(模块 3)与肿瘤(模块4)合于一种疾病之中。同样的 RF→临床级联结构适用于考试提到的任何癌症(肺/烟草, 黑色素瘤/紫外线,乳腺/BRCA)。 ★ Module 4 lock-in - the must-knows 模块 4 锁定 -- 必知要点 (1) Benign = no metastasis; malignant metastasises (the distinguisher). (2) Cell cycle G1++S++G2-M; G1/S = key checkpoint; cancer = checkpoint failure. (3) Oncogene = gain of function, tumour-suppressor = loss (p53, BRCA). (4) Carcinogenesis = initiation-promotion-progression; spread by blood / lymph / transcoelomic / local. (5) Grading = cell appearance, Staging = spread (TNM). (6) Be able to run the RF-aetiology++patho-clinical chain. (1) 良性=不转移;恶性会转移(区分点)。(2)细胞周期 G1→S→G2→M;G1/S=关键检查点;癌症=检查点失灵。 (3) 癌基因=功能获得,抑癌基因=功能丧失(p53、BRCA)。(4)致癌作用=启动→促进→进展;通过血液/淋巴/经 体腔/局部扩散。(5)分级=细胞外观,分期=扩散(TNM)。(6)要能跑通RF→病因→病理生理→临床 链条。 Accelerator on, brakes off, boundaries crossed - that is the whole of cancer in six words. 油门开、刹车失、越边界 -- 用六个字概括,这就是癌症的全部。 I THE MODULE 4 MENTAL MODEL 2804NRS . Human Pathophysiology & Pharmacology 1 M5 . MSK & PAIN - MODULE 5 . MUSCULOSKELETAL & PAIN EOTE CORE Joints, bones & the pharmacology of pain 关节、骨骼与疼痛药理学 Inflammatory vs degenerative joint disease . bone & fracture . nociception . NSAIDs, the COX pathway & the WHO ladder 炎症性 vs 退行性关节病 · 骨骼与骨折 · 伤害性感受 · NSAID、COX 通路与 WHO 阶梯 One spine for the whole module: the musculoskeletal system fails in two flavours - degenerative (wear of cartilage/bone, e. g. osteoarthritis, osteoporosis) and inflammatory/autoimmune (the immune system attacking the joint, e. g. rheumatoid arthritis). That same split - is the problem mechanical wear or active inflammation? - decides the drug: you treat inflammation by switching off prostaglandins (NSAIDs, steroids), and you treat the pain itself by climbing the WHO analgesic ladder. Master the COX pathway and the ladder and you own half of Module 5. 贯穿整个模块的一条脊柱:肌肉骨骼系统以两种类型衰败 -- 退行性(软骨/骨的磨损,如骨关节炎、骨质疏松)和炎症性/ 自身免疫性(免疫系统攻击关节,如类风湿关节炎)。同样的划分 -- 问题是机械性磨损还是活动性炎症 ?-- 决定用药:通 过关闭前列腺素(NSAID、类固醇)来治疗炎症,并通过攀登WHO 镇痛阶梯来治疗疼痛本身。掌握 COX 通路与阶梯,你就 掌握了模块 5的一半。 ★ What the EoT exam asks here 学期末考试在这里考什么

3.3 Module 5：肌骨 + 疼痛（“掌握一半模块”的两根主轴）

• MSK 问题两大类：
  • 退行性/磨损（如 OA、骨质疏松）
  • 炎症性/自身免疫（如 RA）
• 这一区分直接决定用药方向：
  • 抗炎：关掉前列腺素（NSAIDs、类固醇）
  • 镇痛：爬 WHO analgesic ladder。[6]Source: asksia-bible-2804nrs-bilingual.pdfCheckpoint failure - cervical dysplasia (CIN) - carcinoma in situ - invasive carcinoma; eventual lymphatic / local spread 4 . Clinical manifestations Often asymptomatic early (why screening matters); then abnormal / post-coital bleeding, discharge, pelvic pain; late: spread-related symptoms 1 Risk - aetiology. A risk factor (persistent HPV) supplies the trigger - viral oncoproteins that disable p53 and Rb. 风险→ 病因。一个风险因素(持续性 HPV)提供触发 -- 使 p53和 Rb 失活的病毒癌蛋白。 2 Aetiology - pathophysiology. Lost tumour-suppressors = brakes off at the checkpoint - the morphological arc dysplasia - CIS - invasive (exactly the carcinogenesis ladder from page 3). 病因→ 病理生理。抑癌基因丧失=检查点处刹车失灵→形态学弧线 不典型增生→ 原位癌(CIS)→侵袭(正是第3页的 致癌作用阶梯)。 3 Pathophysiology - clinical. Local invasion and spread produce the bleeding, discharge and pain - but the key teaching point is the silent early phase, which is why screening (Pap / HPV test) and the HPV vaccine are the high-impact interventions. 病理生理→临床。局部侵袭和扩散产生出血、分泌物和疼痛 -- 但关键教学点是那个无声的早期阶段,这正是为什么筛查 (Pap/HPV 检测)和HPV 疫苗是高效干预。 - 2804NRS . Human Pathophysiology & Pharmacology 1 i Why this links back to Module 3 为何这要回链到模块 3 Cervical cancer is the clean bridge between the two modules: an infectious trigger (HPV) disabling tumour- suppressors, prevented by an artificial-active vaccine - immunity (Module 3) and neoplasia (Module 4) in one disease. The same RF-clinical cascade structure works for any cancer the exam names (lung/tobacco, melanoma/UV, breast/BRCA). 宫颈癌是连接这两个模块的清晰桥梁:一个感染性触发因素(HPV)使抑癌基因失活,由一种人工主动疫苗预防 -- 免 疫(模块 3)与肿瘤(模块4)合于一种疾病之中。同样的 RF→临床级联结构适用于考试提到的任何癌症(肺/烟草, 黑色素瘤/紫外线,乳腺/BRCA)。 ★ Module 4 lock-in - the must-knows 模块 4 锁定 -- 必知要点 (1) Benign = no metastasis; malignant metastasises (the distinguisher). (2) Cell cycle G1++S++G2-M; G1/S = key checkpoint; cancer = checkpoint failure. (3) Oncogene = gain of function, tumour-suppressor = loss (p53, BRCA). (4) Carcinogenesis = initiation-promotion-progression; spread by blood / lymph / transcoelomic / local. (5) Grading = cell appearance, Staging = spread (TNM). (6) Be able to run the RF-aetiology++patho-clinical chain. (1) 良性=不转移;恶性会转移(区分点)。(2)细胞周期 G1→S→G2→M;G1/S=关键检查点;癌症=检查点失灵。 (3) 癌基因=功能获得,抑癌基因=功能丧失(p53、BRCA)。(4)致癌作用=启动→促进→进展;通过血液/淋巴/经 体腔/局部扩散。(5)分级=细胞外观,分期=扩散(TNM)。(6)要能跑通RF→病因→病理生理→临床 链条。 Accelerator on, brakes off, boundaries crossed - that is the whole of cancer in six words. 油门开、刹车失、越边界 -- 用六个字概括,这就是癌症的全部。 I THE MODULE 4 MENTAL MODEL 2804NRS . Human Pathophysiology & Pharmacology 1 M5 . MSK & PAIN - MODULE 5 . MUSCULOSKELETAL & PAIN EOTE CORE Joints, bones & the pharmacology of pain 关节、骨骼与疼痛药理学 Inflammatory vs degenerative joint disease . bone & fracture . nociception . NSAIDs, the COX pathway & the WHO ladder 炎症性 vs 退行性关节病 · 骨骼与骨折 · 伤害性感受 · NSAID、COX 通路与 WHO 阶梯 One spine for the whole module: the musculoskeletal system fails in two flavours - degenerative (wear of cartilage/bone, e. g. osteoarthritis, osteoporosis) and inflammatory/autoimmune (the immune system attacking the joint, e. g. rheumatoid arthritis). That same split - is the problem mechanical wear or active inflammation? - decides the drug: you treat inflammation by switching off prostaglandins (NSAIDs, steroids), and you treat the pain itself by climbing the WHO analgesic ladder. Master the COX pathway and the ladder and you own half of Module 5. 贯穿整个模块的一条脊柱:肌肉骨骼系统以两种类型衰败 -- 退行性(软骨/骨的磨损,如骨关节炎、骨质疏松)和炎症性/ 自身免疫性(免疫系统攻击关节,如类风湿关节炎)。同样的划分 -- 问题是机械性磨损还是活动性炎症 ?-- 决定用药:通 过关闭前列腺素(NSAID、类固醇)来治疗炎症,并通过攀登WHO 镇痛阶梯来治疗疼痛本身。掌握 COX 通路与阶梯,你就 掌握了模块 5的一半。 ★ What the EoT exam asks here 学期末考试在这里考什么

• 组织损伤 → 介质（前列腺素、缓激肽等）致敏 nociceptor → A$\delta$/C 纤维传入 → 脊髓背角 → 脊髓丘脑束 → 丘脑 → 大脑皮层感知。[25]Source: asksia-cheatsheet-2804nrs.pdfwell poor (anaplastic) Metastasis No Yes Carcinogenesis = multistep initiation > promotion -> progression ; needs multiple mutations passed to daughter cells. 7b . Oncogenes & Spread GAIN VS LOSS · Tumour suppressor (p53 "guardian", BRCA1/2) -> loss of function = brakes failed. Cell cycle G1->S-> G2->M; cancer = checkpoint failure (esp. G1/S). Metastasis routes: local invasion, lymphatic, haematogenous (blood), transcoelomic seeding. Grading vs Staging: grading = how abnormal cells look; staging = how far it spread (TNM = Tumour, Node, Metastasis). AU risks: tobacco, UV, alcohol, HPV, BRCA, age. 8 . MSK & Pain MODULE 5 % Osteoporosis - bone density (resorption > formation; post-menopausal voestrogen) -> fragility fractures. Fracture healing: haematoma -> soft callus > hard (bony) callus -> remodelling. Compartment syndrome = ^pressure in a closed fascial space -> ischaemia (the 6 Ps) - emergency. Pain cascade (SAQ): tissue injury > mediators (prostaglandins, bradykinin) sensitise nociceptors > signal via A8/C fibres -> dorsal horn -> spinothalamic tract -> thalamus > cortex (perception). Nociceptive vs neuropathic vs referred. 8b . Arthritis & BPH 5. 2 / 4. 4 OA = "wear-and-tear" cartilage loss, mechanical, asymmetrical, large weight-bearing joints. RA = autoimmune (Type III, synovium), symmetrical small joints, systemic, morning stiffness, RF/anti-CCP. BPH = benign hyperplasia of the peri-urethral prostate (age/DHT) -> obstruction (hesitancy, frequency, nocturia, weak stream). Mx: a1-blockers ("-osin", relax smooth muscle) + 5a-reductase inhibitors. Prostate cancer = peripheral zone, PSA marker, androgen-dependent. 8c . Cell-Cycle Recap G1 > S (DNA synthesis) > G2 > M (mitosis) > cytokinesis. Checkpoints (esp. G1/S restriction point) police DNA integrity; p53 halts or apoptoses damaged cells. Cancer = oncogene accelerator stuck ON plus suppressor brakes OFF -> checkpoints bypassed -> autonomous proliferation. Cancer treatment (4. 2. 3): surgery (remove), radiotherapy (DNA damage, local), chemotherapy (cytotoxic, hits rapidly dividing cells -> AEs: myelosuppression, hair loss, GI/mucositis, nausea), and targeted/hormonal therapy. Diagnosis: biopsy + histology, imaging, tumour markers (PSA, CA-125). The cytotoxic AEs come from hitting normal fast-dividing cells (marrow, gut, hair). asksia. ai/cheatsheet/ griffith-2804nrs . side 1/2 AskSia CHEATSHEET SERIES

• OA：磨损、机械性、常不对称、大关节/负重关节。
• RA：自身免疫（材料提示 Type III）、滑膜，常对称小关节、全身性、晨僵，RF/anti-CCP。[25]Source: asksia-cheatsheet-2804nrs.pdfwell poor (anaplastic) Metastasis No Yes Carcinogenesis = multistep initiation > promotion -> progression ; needs multiple mutations passed to daughter cells. 7b . Oncogenes & Spread GAIN VS LOSS · Tumour suppressor (p53 "guardian", BRCA1/2) -> loss of function = brakes failed. Cell cycle G1->S-> G2->M; cancer = checkpoint failure (esp. G1/S). Metastasis routes: local invasion, lymphatic, haematogenous (blood), transcoelomic seeding. Grading vs Staging: grading = how abnormal cells look; staging = how far it spread (TNM = Tumour, Node, Metastasis). AU risks: tobacco, UV, alcohol, HPV, BRCA, age. 8 . MSK & Pain MODULE 5 % Osteoporosis - bone density (resorption > formation; post-menopausal voestrogen) -> fragility fractures. Fracture healing: haematoma -> soft callus > hard (bony) callus -> remodelling. Compartment syndrome = ^pressure in a closed fascial space -> ischaemia (the 6 Ps) - emergency. Pain cascade (SAQ): tissue injury > mediators (prostaglandins, bradykinin) sensitise nociceptors > signal via A8/C fibres -> dorsal horn -> spinothalamic tract -> thalamus > cortex (perception). Nociceptive vs neuropathic vs referred. 8b . Arthritis & BPH 5. 2 / 4. 4 OA = "wear-and-tear" cartilage loss, mechanical, asymmetrical, large weight-bearing joints. RA = autoimmune (Type III, synovium), symmetrical small joints, systemic, morning stiffness, RF/anti-CCP. BPH = benign hyperplasia of the peri-urethral prostate (age/DHT) -> obstruction (hesitancy, frequency, nocturia, weak stream). Mx: a1-blockers ("-osin", relax smooth muscle) + 5a-reductase inhibitors. Prostate cancer = peripheral zone, PSA marker, androgen-dependent. 8c . Cell-Cycle Recap G1 > S (DNA synthesis) > G2 > M (mitosis) > cytokinesis. Checkpoints (esp. G1/S restriction point) police DNA integrity; p53 halts or apoptoses damaged cells. Cancer = oncogene accelerator stuck ON plus suppressor brakes OFF -> checkpoints bypassed -> autonomous proliferation. Cancer treatment (4. 2. 3): surgery (remove), radiotherapy (DNA damage, local), chemotherapy (cytotoxic, hits rapidly dividing cells -> AEs: myelosuppression, hair loss, GI/mucositis, nausea), and targeted/hormonal therapy. Diagnosis: biopsy + histology, imaging, tumour markers (PSA, CA-125). The cytotoxic AEs come from hitting normal fast-dividing cells (marrow, gut, hair). asksia. ai/cheatsheet/ griffith-2804nrs . side 1/2 AskSia CHEATSHEET SERIES

3.4 Module 6：遗传 + 衰老（MCQ 比较多，套路题要会）

• Down syndrome = trisomy 21（多一整条染色体），不是单基因缺陷。[9]Source: asksia-bible-2804nrs-bilingual.pdfLevel What changes Example Chromosomal - structure Deletion, duplication, translocation Various structural syndromes Multifactorial Genes + environment Neural tube defects, diabetes, many cancers i Gain vs loss of function (ties to cancer) 功能获得 vs 功能丧失(与癌症相关) A point mutation (single base swap) can change one amino acid, make a premature stop codon, or a new start. Gain of function = proto-oncogene - oncogene (accelerator stuck on). Loss of function = tumour suppressor lost (brakes fail, e. g. p53, BRCA). Cancer needs both. 一个点突变(单碱基替换)可改变一个氨基酸、产生 提前终止密码子或新的起始。功能获得 = 原癌基因 → 癌基因(油门卡住)。功能丧失=抑癌基因丧失(刹车 失灵,如 p53、BRCA)。癌症需要二者兼具。 ! Chromosomal vs single-gene 染色体病 vs 单基因病 Down syndrome = trisomy 21 - a whole extra chromosome, NOT a single-gene defect. Cystic fibrosis, Huntington's and haemophilia are single- gene. Confusing the two is a classic MCQ trap. 唐氏综合征=21三体––整条多余的染色体,不是单 基因缺陷。囊性纤维化、亨廷顿病和血友病是单基因 病。把两者搞混是经典的 MCQ 陷阱。 2804NRS . Human Pathophysiology & Pharmacology 1 M6 . GENETICS & AGEING 6. 2 Mendelian inheritance - reading the Punnett square 6. 2 孟德尔遗传 -- 读懂庞纳特方格 Three patterns cover almost every single-gene disorder you must know. The exam will hand you a cross and ask for offspring ratios and carrier risk - so learn to read a Punnett square. Convention: a capital letter = dominant allele, lower-case = recessive. 三种模式涵盖了你必须知道的几乎所有单基因病。考试会给你一个杂交并要求子代比例与携带者风险 -- 故须学会读庞纳特方 格。约定:大写字母=显性等位基因,小写= 隐性等位基因。 P12 Father Aa A a RATIOS AA Aa A homozygous dominant carrier (heterozygous)

• 例如隐性：Aa × Aa → 基因型 $1:2:1$（AA:Aa:aa），表现型 $3:1$，受影响（aa）25%，携带者（Aa）50%。[24]Source: asksia-cheatsheet-2804nrs.pdfDrugs · Antidepressants - SSRIS + synaptic serotonin (reuptake block); SNRIs add noradrenaline. · Anxiolytics - benzodiazepines enhance GABA (sedation, dependence risk). SAQ reflex: answer the verb - "differentiate" = give the contrast, "explain" = give the cascade; for any drug, state the mechanism of action + one key AE. Define a term before applying it (define metastasis, then say why it makes a tumour malignant). asksia. ai/cheatsheet/ griffith-2804nrs . side 2/2 AskSia CHEATSHEET SERIES Revision aid . check the Course Profile for exam conditions . @ 2026 good luck. revise smart. A A A AA Aa a Aa aa Genotype 1 AA : 2 Aa : 1 aa; phenotype 3 unaffected : 1 affected. So 25% affected (aa) , 50% unaffected carriers (Aa). Carriers are healthy but pass the allele on - the key autosomal-recessive MCQ. 10c . Routes & First- WHY ROUTE MATTERS Pass Sublingual, rectal, IV, transdermal, inhaled all bypass first-pass hepatic metabolism (no portal vein) > useful for high first-pass drugs (e. g. GTN sublingual). Oral is convenient but loses bioavailability to first pass + incomplete absorption. IV = fastest onset, 100% F, but no recall once given. 10d · Genetics MCQ Traps Down syndrome = trisomy 21 (extra .[26]Source: asksia-cheatsheet-2804nrs.pdf· Antidepressants - SSRIs + synaptic serotonin (reuptake block); SNRIs add noradrenaline. · Anxiolytics - benzodiazepines enhance GABA (sedation, dependence risk). SAQ reflex: answer the verb - "differentiate" = give the contrast, "explain" = give the cascade; for any drug, state the mechanism of action + one key AE. Define a term before applying it (define metastasis, then say why it makes a tumour malignant). asksia. ai/cheatsheet/ griffith-2804nrs . side 2/2 AskSia CHEATSHEET SERIES Revision aid . check the Course Profile for exam conditions . @ 2026 good luck. revise smart. A A A AA Aa a Aa aa Genotype 1 AA : 2 Aa : 1 aa; phenotype 3 unaffected : 1 affected. So 25% affected (aa) , 50% unaffected carriers (Aa). Carriers are healthy but pass the allele on - the key autosomal-recessive MCQ. 10c . Routes & First- WHY ROUTE MATTERS Pass Sublingual, rectal, IV, transdermal, inhaled all bypass first-pass hepatic metabolism (no portal vein) > useful for high first-pass drugs (e. g. GTN sublingual). Oral is convenient but loses bioavailability to first pass + incomplete absorption. IV = fastest onset, 100% F, but no recall once given. 10d · Genetics MCQ Traps Down syndrome = trisomy 21 (extra . chromosome).

• 总结一句话：老年人更易“药物水平↑、半衰期↑、毒性↑、多重用药相互作用↑”，所以 start low, go slow。[27]Source: asksia-cheatsheet-2804nrs.pdf· Muscarinic agonist (bethanechol, pilocarpine) = more PNS: bradycardia, secretions, miosis ("SLUDGE"). Absorb Distribute +fat, vwater, +albumin + +free drug Metabolise liver mass/flow -> slower Excrete renal GFR > accumulation (biggest) Net: ^levels, +half-life, +toxicity + polypharmacy > "start low, go slow. " 10b . Worked . Punnett RECESSIVE CROSS Two carriers of cystic fibrosis (Aa x Aa): Vessels/BP vasoconstrict +BP — QUICK RECALL PHARMACOLOGY . Genetics & ageing . Raised ICP . Autonomic (adrenergic/cholinergic) . ADME . Dose-response . NSAIDS . EXAM REVISION . MODULES 3- Compiled by AskSia . mapped to the 2804NRS syllabus . asksia. ai/cheatsheet/griffith- 2804nrs MODULE 6[29]Source: asksia-cheatsheet-2804nrs.pdfACh -> receptor -> broken by acetylcholinesterase (AChE). Muscarinic (M1 gastric, M2 heart +rate, M3 smooth muscle/glands); nicotinic (ganglia + skeletal NMJ). · Muscarinic agonist (bethanechol, pilocarpine) = more PNS: bradycardia, secretions, miosis ("SLUDGE"). Absorb Distribute +fat, vwater, +albumin + +free drug Metabolise liver mass/flow -> slower Excrete renal GFR > accumulation (biggest) Net: ^levels, +half-life, +toxicity + polypharmacy > "start low, go slow. " 10b . Worked . Punnett RECESSIVE CROSS Two carriers of cystic fibrosis (Aa x Aa): Vessels/BP vasoconstrict +BP — QUICK RECALL PHARMACOLOGY . Genetics & ageing . Raised ICP . Autonomic (adrenergic/cholinergic) . ADME . Dose-response . NSAIDS . EXAM REVISION . MODULES 3- Compiled by AskSia . mapped to the 2804NRS syllabus . asksia. ai/cheatsheet/griffith- 2804nrs

3.5 Module 7：神经 + 自主神经药理（SAQ 会让你“病+药”一起讲）

• RF：年龄、男性、家族史等。
• 病因：黑质多巴胺能神经元进行性退化。
• 病理：基底节多巴胺缺乏 → 胆碱能相对占优 → 运动控制受损。
• 临床：静止性震颤、强直、运动迟缓、姿势不稳等。
• 治疗：Levodopa（可过 BBB 的多巴胺前体）补充中枢多巴胺，常合并 carbidopa 降低外周分解。[14]Source: asksia-bible-2804nrs-bilingual.pdfCASCADE Parkinson's disease . Module 7 concept-map fuel RISK FACTORS Increasing age, male sex, family history, some environmental toxin exposures. AETIOLOGY Progressive degeneration of dopaminergic neurons in the substantia nigra (cause largely idiopathic). PATHOPHYSIOLOGY Loss of these neurons - dopamine deficiency in the basal ganglia - unopposed cholinergic activity - impaired control of movement. CLINICAL MANIFESTATIONS Resting tremor, rigidity, bradykinesia (slow movement), postural instability; mask-like face, shuffling gait. ONE DIAGNOSTIC Clinical diagnosis on the motor triad + response to dopaminergic therapy (no single definitive test). ONE DRUG MANAGEMENT Levodopa (dopamine precursor that crosses the blood-brain barrier) to replace dopamine - usually with carbidopa to limit peripheral breakdown. i Two more neuro links worth a one-line cascade 另外两条值得一句话级联的神经联系 Alzheimer's: amyloid plaques + tau tangles - acetylcholine - memory loss - treat with AChE inhibitors (donepezil) to raise ACh. Raised intracranial pressure (Monro-Kellie): fixed skull, added volume - NCP - cerebral perfusion - late Cushing's triad (^BP, bradycardia, irregular respiration). Both reuse the same Risk - Aetiology - Patho - Clinical - Dx + Rx skeleton. 阿尔茨海默病:淀粉样斑块 + tau 缠结 →乙酰胆碱减少→记忆丧失→用 AChE 抑制剂(多奈哌齐)治疗以升高 ACh。颅内压升高(Monro-Kellie):颅骨固定,体积增加 → ICP 升高→ 脑灌注下降→ 晚期 Cushing 三联征(血压 升高、心动过缓、呼吸不规则)。两者都复用同一套 风险→病因→病理生理→临床→诊断+治疗 的骨架。 Final Two SAQ-style cascade prompts to self-test 最后 两道 SAQ 式级联自测题 S5 SAO 5 marks . Module 7 + pharmacology Outline the pathophysiology of Parkinson's disease and explain how levodopa addresses it. [5] 5 marks . Module 4 S6 SAQ Explain how a normal cell becomes malignant, referring to oncogenes, tumour suppressor genes and metastasis. [5] 2804NRS . Human Pathophysiology & Pharmacology 1 S5-S6 Model answers 1 S5. Degeneration of dopaminergic neurons in the substantia nigra [1] - dopamine deficiency in the basal ganglia [1] - resting tremor, rigidity, bradykinesia [1]. Levodopa is a dopamine precursor that crosses the blood-brain barrier (dopamine itself cannot) [1] and is converted to dopamine centrally, replacing the deficit and improving movement [1]. S5。黑质中多巴胺能神经元的退化 [1]→基底节多巴胺缺乏[1]→ 静止性震颤、强直、运动迟缓[1]。左旋多巴 (levodopa) 是一种能穿过血脑屏障(多巴胺本身不能)的多巴胺前体[1],在中枢被转化为多巴胺,弥补缺失并改善运 动[1]。 2 S6. Carcinogenesis = stepwise accumulation of mutations (initiation - promotion - progression) [1]. Proto-oncogenes mutate to oncogenes - gain of function - uncontrolled proliferation (accelerator on) [1]; tumour suppressor genes (p53, BRCA) suffer loss of function - checkpoints fail (brakes off) [1]. Cells become poorly differentiated/anaplastic [1] and acquire the ability to metastasise via blood/lymph/seeding - the feature defining malignancy [1]. S6。致癌作用 = 突变的逐步累积(启动→促进→进展)[1]。原癌基因突变为癌基因 -- 功能获得→ 无控制增殖(油 门开启)[1];抑癌基因(p53、BRCA)遭受功能丧失→检查点失灵(刹车失灵)[1]。细胞变得分化差/间变[1],并获 得通过血液/淋巴/种植转移的能力 -- 这是定义恶性的特征 [1]。

• Muscarinic receptor：副交感靶器官/腺体的胆碱能 GPCR；atropine 的靶点。
• Nicotinic receptor：自主神经节 + 骨骼肌 NMJ 的胆碱能离子通道受体。
• Adrenergic receptor：$\alpha_1$ 血管收缩；$\beta_1$ 心脏；$\beta_2$ 支气管舒张。[4]Source: asksia-bible-2804nrs-bilingual.pdfTolerance — Diminished response after repeated use - higher dose needed for the same effect (e. g. opioids). Adverse drug reaction (ADR) — Harmful/unintended response; Type A = dose-related/predictable, Type B = idiosyncratic/unpredictable. H- Autonomic pharmacology 自主神经药理 Muscarinic receptor — Cholinergic GPCR on PNS-innervated organs/glands (M1-M3); atropine's target. Nicotinic receptor — Cholinergic ion-channel receptor at autonomic ganglia + skeletal neuromuscular junction. Adrenergic receptor — Receptor for noradrenaline/adrenaline: a1 (vasoconstriction), ß1 (heart), ß2 (bronchodilation). Acetylcholinesterase (AChE) — Enzyme breaking down ACh; inhibitors RAISE ACh (used in myasthenia gravis & Alzheimer's). i Using the glossary for the bilingual pass 用术语表完成双语通读 The X column is intentionally left as a placeholder (-). In the bilingual pass, fill it with the standard Chinese term (e. g. 生物利用度 for bioavailability, 首过效应 for first-pass,半衰期 for half-life, 治疗指数 for therapeutic index,激动剂 / 拮抗剂 for agonist / antagonist). The English definitions stay as the anchor. 中文列有意留作占位符(一)。在双语处理时,用标准中文术语填充(例如 bioavailability 填 生物利用度,first-pass 填 首过效应,half-life 填 半衰期,therapeutic index 填 治疗指数,agonist/antagonist 填 激动剂/拮抗剂)。英文定 义保留作为锚点。 2804NRS . Human Pathophysiology & Pharmacology 1 PRACTICE . MODULE 3 - CHAPTER . PRACTICE BANK & WORKED SOLUTIONS MIRRORS THE EOTE FORMAT Drill the paper the way the exam asks it 按考试出题方式反复演练试卷 MCQ-style + short answers across Modules 3-7, plus three worked disease cascades - all fresh, all worked 贯穿模块 3-7的 MCQ 式题目与简答,外加三个已解析的疾病级联 -- 全新、全程解析 The one-line frame. The 2804NRS End-of-Trimester Exam is 50 MCQ (50%) + 12 short-answer questions (50%), drawn from the highlighted Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). This bank gives you fresh MCQ-style items and SAQs in that exact style, each worked, plus three disease cascades in the A2 concept-map format you can reuse as study maps. Cover the answer, attempt it, then check. 一句话框架。2804NRS 学期末考试为 50 道 MCQ(50%)+12 道简答题(50%),取自重点标注的模块 3-7(免疫、癌 症、肌骨/疼痛、遗传/衰老、神经+自主神经药理学)。本题库为你提供该风格的全新 MCQ 式题目与 SAQ,每道均有解 析,外加三条 A2 概念图格式的疾病级联,可作复习图复用。遮住答案,先作答,再核对。 3-7 EXAMINABLE MODULES 可考模块

• 抑制 ACh 分解 → 各胆碱能突触 ACh ↑；用于重症肌无力、阿尔茨海默、逆转非去极化型 NM 阻滞。[11]Source: asksia-bible-2804nrs-bilingual.pdf'Less PNS'- HR, dry, mydriasis; bradycardia, pre-op AChE inhibitor Raises ACh - myasthenia gravis (neostigmine), Alzheimer's (donepezil) NM blockers Suxamethonium (depolarising) vs atracurium (non-depolarising, reversed by neostigmine) ! Atropine = 'can't see/pee/spit/poo' 阿托品=“看不见/尿不出/没口水/排不出” Antimuscarinic (anticholinergic) AEs are the opposite of PNS: tachycardia, dry mouth, blurred vision, constipation, urinary retention, flushing - 'can't see, can't pee, can't spit, can't poo. ' A muscarinic agonist does the reverse (SLUDGE-type: salivation, bradycardia, bronchoconstriction). 抗毒蕈碱(抗胆碱能)的不良反应正是 PNS 的反面: 心动过速、口干、视物模糊、便秘、尿潴留、潮红 -- “看不清、尿不出、吐不了口水、排不出便。”毒蕈 碱激动剂的作用则相反(SLUDGE 型:流涎、心动过 缓、支气管收缩)。 ★ AChE inhibitors RAISE ACh AChE 抑制剂升高 ACh Blocking the enzyme that destroys ACh means more ACh at every cholinergic synapse - used to boost weak transmission in myasthenia gravis and to slow cognitive decline in Alzheimer's (where brain ACh is low), plus to reverse non-depolarising NM blockade. Analogy: AChE is the cleanup crew - sack the crew and ACh piles up. Suxamethonium = depolarising (fasciculations, NOT reversed by ACE inhibitors); atracurium = non-depolarising (no fasciculations, reversed by neostigmine). 阻断那个降解 ACh 的酶,意味着每个胆碱能突触处都有更多 ACh -- 用于在重症肌无力中增强微弱的神经传递,在阿 尔茨海默病(脑内 ACh 偏低)中减缓认知衰退,并用于逆转非去极化型神经肌肉阻滞。类比:AChE 是清洁队 -- 解雇 清洁队,ACh 就堆积起来。琥珀胆碱(suxamethonium)=去极化型(肌束颤动,不被 AChE 抑制剂逆转);阿曲库铵 (atracurium)=非去极化型(无肌束颤动,被新斯的明逆转)。 2804NRS . Human Pathophysiology & Pharmacology 1 PHARMACOLOGY . PK/PD - CHAPTER . PHARMACOLOGY CORE (PK / PD) MODULES 6-7 . X EXAMINED What the body does to the drug, and what the drug does to the body 机体对药物做了什么,药物又对机体做了什么 Pharmacokinetics & pharmacodynamics - the spine every other drug in this course hangs from 药代动力学与药效动力学 -- 本课程其余每一种药物所依附的脊柱 The one-line frame. All of pharmacology splits into two questions. Pharmacokinetics (PK) = "what the body does to the drug" - how it moves in, around, gets broken down and out (ADME). Pharmacodynamics (PD) = "what the drug does to the body" - how it binds receptors and produces an effect. Get this split straight and every drug fact in Modules 5-7 slots into one side or the other. 一句话框架。全部药理学分为两个问题。药代动力学(PK)=“机体对药物做了什么” -- 药物如何进入、分布、被分解并排 出(ADME)。药效动力学(PD)=“药物对机体做了什么” -- 它如何结合受体并产生效应。把这一划分理清,模块 5-7 中 的每一条药物事实都会归入其中一侧。 ADME THE 4 PK STEPS: ABSORB- DISTRIBUTE-METABOLISE - EXCRETE PK 四步:吸收-分布-代谢-排泄 Receptor THE PD TARGET : LOCK-AND- KEY DRUG ACTION PD 靶点:锁与钥匙式药物作用 t1/2 HALF-LIFE SETS DOSING & STEADY STATE 半衰期决定给药与稳态浓度 TI THERAPEUTIC INDEX = HOW SAFE THE DRUG IS 治疗指数 = 药物有多安全 Pharmacokinetics (PK)

• 口干、视物模糊、便秘、尿潴留、潮红、心动过速（“看不清、尿不出、没口水、排不出”）。[11]Source: asksia-bible-2804nrs-bilingual.pdf'Less PNS'- HR, dry, mydriasis; bradycardia, pre-op AChE inhibitor Raises ACh - myasthenia gravis (neostigmine), Alzheimer's (donepezil) NM blockers Suxamethonium (depolarising) vs atracurium (non-depolarising, reversed by neostigmine) ! Atropine = 'can't see/pee/spit/poo' 阿托品=“看不见/尿不出/没口水/排不出” Antimuscarinic (anticholinergic) AEs are the opposite of PNS: tachycardia, dry mouth, blurred vision, constipation, urinary retention, flushing - 'can't see, can't pee, can't spit, can't poo. ' A muscarinic agonist does the reverse (SLUDGE-type: salivation, bradycardia, bronchoconstriction). 抗毒蕈碱(抗胆碱能)的不良反应正是 PNS 的反面: 心动过速、口干、视物模糊、便秘、尿潴留、潮红 -- “看不清、尿不出、吐不了口水、排不出便。”毒蕈 碱激动剂的作用则相反(SLUDGE 型:流涎、心动过 缓、支气管收缩)。 ★ AChE inhibitors RAISE ACh AChE 抑制剂升高 ACh Blocking the enzyme that destroys ACh means more ACh at every cholinergic synapse - used to boost weak transmission in myasthenia gravis and to slow cognitive decline in Alzheimer's (where brain ACh is low), plus to reverse non-depolarising NM blockade. Analogy: AChE is the cleanup crew - sack the crew and ACh piles up. Suxamethonium = depolarising (fasciculations, NOT reversed by ACE inhibitors); atracurium = non-depolarising (no fasciculations, reversed by neostigmine). 阻断那个降解 ACh 的酶,意味着每个胆碱能突触处都有更多 ACh -- 用于在重症肌无力中增强微弱的神经传递,在阿 尔茨海默病(脑内 ACh 偏低)中减缓认知衰退,并用于逆转非去极化型神经肌肉阻滞。类比:AChE 是清洁队 -- 解雇 清洁队,ACh 就堆积起来。琥珀胆碱(suxamethonium)=去极化型(肌束颤动,不被 AChE 抑制剂逆转);阿曲库铵 (atracurium)=非去极化型(无肌束颤动,被新斯的明逆转)。 2804NRS . Human Pathophysiology & Pharmacology 1 PHARMACOLOGY . PK/PD - CHAPTER . PHARMACOLOGY CORE (PK / PD) MODULES 6-7 . X EXAMINED What the body does to the drug, and what the drug does to the body 机体对药物做了什么,药物又对机体做了什么 Pharmacokinetics & pharmacodynamics - the spine every other drug in this course hangs from 药代动力学与药效动力学 -- 本课程其余每一种药物所依附的脊柱 The one-line frame. All of pharmacology splits into two questions. Pharmacokinetics (PK) = "what the body does to the drug" - how it moves in, around, gets broken down and out (ADME). Pharmacodynamics (PD) = "what the drug does to the body" - how it binds receptors and produces an effect. Get this split straight and every drug fact in Modules 5-7 slots into one side or the other. 一句话框架。全部药理学分为两个问题。药代动力学(PK)=“机体对药物做了什么” -- 药物如何进入、分布、被分解并排 出(ADME)。药效动力学(PD)=“药物对机体做了什么” -- 它如何结合受体并产生效应。把这一划分理清,模块 5-7 中 的每一条药物事实都会归入其中一侧。 ADME THE 4 PK STEPS: ABSORB- DISTRIBUTE-METABOLISE - EXCRETE PK 四步:吸收-分布-代谢-排泄 Receptor THE PD TARGET : LOCK-AND- KEY DRUG ACTION PD 靶点:锁与钥匙式药物作用 t1/2 HALF-LIFE SETS DOSING & STEADY STATE 半衰期决定给药与稳态浓度 TI THERAPEUTIC INDEX = HOW SAFE THE DRUG IS 治疗指数 = 药物有多安全 Pharmacokinetics (PK)

4）药理学通用“公式/定义”区（几乎所有药题都从这里长出来）

4.1 PK vs PD（先把这句背牢）

4.2 ADME 必背定义点（尤其 PK 相互作用）

4.3 Therapeutic index（TI）治疗指数（常考“安全性”）

• CYP 抑制剂 → 另一药物水平↑ → 毒性↑
• CYP 诱导剂 → 另一药物水平↓ → 治疗失败风险↑ [10]Source: asksia-bible-2804nrs-bilingual.pdfTI 是你脚下那段壁架的宽度:一侧是“不起作用”(低于 ED50),另一侧是悬崖(高于 TD50)。宽壁架(高 TI)让你能 随意行走;窄壁架(低 TI,如华法林)意味着每一步都要精确测量––故而需要血液检测。 - Three modifiers in the real patient 真实患者中的三个修正因素 Concept What it means Exam handle Tolerance Diminished response after repeated use - need a higher dose for the same effect (e. g. opioids; receptor downregulation). Tolerance # dependence # allergy. Adverse drug reaction (ADR) Any harmful/unintended response. Type A = dose-related & predictable (e. g. opioid respiratory depression). Type B = idiosyncratic/hypersensitivity, unpredictable (e. g. penicillin anaphylaxis). Type A = augmented/predictable; Type B = bizarre/unpredictable. Drug interaction Pharmacokinetic - absorption competition, protein-binding displacement, CYP450 induction/inhibition, altered excretion. Pharmacodynamic - additive, synergistic or antagonistic at the receptor. Elderly + polypharmacy = highest ADR/interaction risk. ! Narrow TI - monitor; CYP & albumin drive interactions TI 狭窄 → 监测;CYP 与白蛋白驱动相互作用 Low/narrow therapeutic index = needs monitoring (warfarin, digoxin, lithium, gentamicin). A CYP450 inhibitor raises another drug's level (toxicity); an inducer lowers it (treatment failure). Only free (unbound) drug is active, so a displacing drug that knocks another off albumin raises its free, active fraction - a key PK interaction. 低/窄治疗指数 = 需要监测(华法林、地高辛、锂、庆大霉素)。CYP450 抑制剂升高另一种药的水平(毒性);诱导剂 降低它(治疗失败)。只有游离(未结合)药物才有活性,所以一种把另一种药从白蛋白上置换下来的药会升高其游离、 活性部分 -- 这是关键的 PK 相互作用。 2804NRS . Human Pathophysiology & Pharmacology 1 GLOSSARY 1/ 3 - CHAPTER . GLOSSARY in EN NOW . ++X LATER Bilingual-ready glossary - every examinable term 双语就绪术语表 -- 每一个可考术语 English term . #X (placeholder) . crisp English definition - grouped patho - pharm 英文术语 · 中文(占位)· 简明英文释义 -- 按病理生理→ 药理分组 A fast reference for the vocabulary 2804NRS actually examines - about 55 terms across pathophysiology and pharmacology, each with a one-line English definition. The middle +X column is a placeholder ("-") to be filled in the later bilingual pass. Cover the definition and recite from the term, then flip. 一份针对 2804NRS 实际考查词汇的快速参考 -- 涵盖病理生理学与药理学约 55个术语,每个配一句英文释义。中间的中文 列是占位(“一”),将在后续双语通读中填入。遮住释义,从术语背诵,然后翻看。 Term (EN) 中文 Definition (EN) A -Homeostasis, cell injury & adaptation 稳态与细胞损伤[22]Source: asksia-cheatsheet-2804nrs.pdfretain void MULTI- 14c . Worked SAQ . Adrenaline RECEPTOR Adrenaline in anaphylaxis hits several receptors at once: al -> vasoconstriction -> ^BP (reverses hypotension); B1 > +cardiac output; 32 > bronchodilation + +mast-cell mediator release. One drug, three life-saving actions - the classic "explain why adrenaline" SAQ. Contrast: a ß-blocker would worsen anaphylaxis and bronchospasm - never give one here. Likewise non- selective ß-blockers can trigger bronchospasm in asthmatics > use cardioselective ß1 agents. ß-blockers are also contraindicated in heart block and cardiogenic shock. 14d . Autonomic Recall MCQ DRILL · SNS post = NA (a/B); PNS post = ACh (muscarinic); all pre = ACh/nicotinic. · Atropine blocks muscarinic ("can't see/pee/spit/poo"). · AChE inhibitors + ACh (myasthenia, Alzheimer's). 15 . Pharmacokinetics * "BODY - · ADME DRUG" Absorption · Distribution · Metabolism · Excretion. ABSORPTION & BIOAVAILABILITY Enteral (oral, SL, rectal) vs parenteral (IV, IM, SC). IV = 100% bioavailability, fastest, no first-pass. Bioavailability (F) = fraction reaching circulation unchanged. Absorption depends on lipid solubility, ionisation/pH, GI motility, surface area, blood flow and food. DISTRIBUTION Drugs bind albumin; only free (unbound) drug is active . valbumin / displacement -> +free drug -> interaction. Vd high = lipophilic/tissue; low = stays in plasma. METABOLISM & EXCRETION Liver (Phase | CYP450; Phase II conjugation) -> water- soluble. First-pass: oral drug via portal vein -> liver before circulation -> voral F. Kidney excretes; renal impairment -> accumulation. 15b . Kinetic Parameters DOSING Half-life (t1/2) = time for conc. to fall 50%; ~ 4-5 t1/2 to clear OR reach steady state (rate in = rate out). Loading dose = reach level fast; maintenance dose = replace what's eliminated. CYP inducers + levels, inhibitors + levels/toxicity. 15c · Worked . Half- Life SHOW THE STEPS

5）你考前最省命的“冲刺训练法”（照做就能提分）

• 考前一晚从空白页重建：RF → 病因 → 病理（分步）→ 临床 → Dx + Rx；能做到就能答大多数 SAQ。[7]Source: asksia-bible-2804nrs-bilingual.pdfRe-draw each cascade from a blank page the night before: if you can rebuild Risk - Aetiology - Patho - Clinical - Dx + Rx without the prompt, you can answer almost any SAQ the disease throws at you. 考试前一晚从一张白纸重新画出每条级联:如果你能在没有提示的情况下重建 风险→病因→ 病理生理→临床→ 诊 断+治疗,你就能回答该疾病抛出的几乎任何 SAQ。 MARKER'S NOTE . 2804NRS REVISION 2804NRS . Human Pathophysiology & Pharmacology 1 Type Mechanism Memory? Example Natural active Pathogen enters - illness - you make antibodies Yes Catching chickenpox Artificial active Vaccine given (no illness) - you make antibodies Yes Polio / COVID vaccine Natural passive Antibodies passed mother-baby (placenta / breast milk) No Newborn maternal immunity Artificial passive Pre-formed antibodies injected No Immunoglobulin, antivenom, post- rabies Ig i Analogy - learning to fish vs being handed a fish 类比 -- 学会捕鱼 vs 被递上一条鱼 Active immunity is learning to fish: it takes time to learn, but you can feed yourself forever (memory). Passive immunity is being handed a fish: you eat right now (immediate protection), but when it's gone you've learned nothing (no memory, decays). 主动免疫是学会钓鱼:学起来要花时间,但你可以永远养活自己(记忆)。被动免疫是别人递来一条鱼:你现在就能吃 (即时保护),但吃完后你什么也没学会(无记忆,会衰减)。 - ! The two-axis trap - a frequent MCQ 双轴陷阱 -- 常见 MCQ

• 每句写“箭头关系”，不要写散点。[1]Source: asksia-bible-2804nrs-bilingual.pdf3· 考试 It's the End-of-Trimester exam. The MCQ half rewards the fact bullets and trap callouts; the short-answer half rewards re- telling a cascade in prose. Drill the steps() ladders - they ARE model SAQ answers. The blueprint overleaf shows exactly which modules carry the marks. 这是学期末考试。MCQ 部分奖 励事实要点和陷阱提示;简答部 分奖励用文字复述一条级联。反 复演练这些步骤阶梯- -它们本 身就是标准 SAQ 答案。下一页 的蓝图明确显示哪些模块承载着 分数。 2804NRS . Human Pathophysiology & Pharmacology 1 ! The single most important thing to understand about 2804NRS 关于 2804NRS 最需要理解的一件事 The unit is assessed in two completely different engines, and they examine different modules. Modules 1-2 (cells, injury, inflammation, microbiology) are tested by the A1 in-class quiz early in the trimester - and then they vanish from the End-of-Trimester exam study guide. The EoT exam examines Modules 3-7 (immunity, cancer, MSK/pain, genetics/ageing, neuro + autonomic pharmacology). So learn M1-2 as scaffolding - they explain everything that follows (inflammation underpins hypersensitivity; cell injury underpins cancer) - but weight your final-exam revision on Modules 3-7. 本单元由两套截然不同的引擎评估,而它们考查的模块各不相同。模块1-2(细胞、损伤、炎症、微生物学)由学期早 期的 A1 课堂测验考核 -- 之后便从学期末考试复习指南中消失。学期末考试考查模块 3-7(免疫、肿瘤、肌肉骨骼/疼 痛、遗传/衰老、神经+自主神经药理学)。所以把 M1-2 当作支架来学 -- 它们解释了后续的一切(炎症支撑超敏反 应;细胞损伤支撑肿瘤) -- 但要把期末考的复习重心放在模块 3-7上。 i How this book was built - and the two-layer rule 本书是如何构建的 -- 以及双层规则 Standard biomedical science (the inflammation cascade, antibody geometry, ADME, dose-response) is stated plainly - it is universal canon, not anyone's copyright. The unit's own framing, sequencing and any example numbers are paraphrased and re-worked, never copied from Learning@Griffith pages, slides or past papers. Texts behind the canon: Gould's Pathophysiology (VanMeter & Hubert, 7e) and Fundamentals of Pharmacology (Bullock & Manias, 9e). Verify dates, weights and exam rules against your own Course Profile, as cohorts shift. 标准的生物医学科学内容(炎症级联、抗体几何结构、ADME、量效关系)以平实方式陈述 -- 它属于通用知识体系, 不归任何人版权所有。本单元自身的框架、编排顺序及任何示例数字都经改写与重新加工,绝不抄自 Learning@Griffith 页面、幻灯片或往年试题。支撑这一知识体系的教材:Gould's Pathophysiology (VanMeter & Hubert,第 7版)与 Fundamentals of Pharmacology (Bullock & Manias,第9版)。由于各届安排会变动,请对照你自己的课程大纲核 实日期、权重与考试规则。 2804NRS . Human Pathophysiology & Pharmacology 1 THE BLUEPRINT - THE EXAM BLUEPRINT EOT EXAM 40% . M3-7 Two engines, Modules 3-7 win the exam 两大引擎,模块 3-7 决定考试成败 A1 in-class quiz ~20% (M1-2) . AZ concept map 40% . A3 EOT exam 40% A1 课堂测验约 20% (M1-2)· A2 概念图 40% · A3 学期末考试 40% Your grade is built from three pieces. The two 40% pieces dominate - and they examine the unit in opposite ways. A2 asks you to draw a cascade; A3 asks you to explain cascades in prose and recognise facts. Same biology, two output formats - which is exactly why this book writes each disease as one reusable cascade. 你的成绩由三部分构成。两个各占40% 的部分占主导 -- 而它们以相反的方式考查本单元。A2 要你画出级联;A3 要你用文 字解释级联并辨识事实。相同的生物学,两种输出格式 -- 这正是本书把每种疾病写成一条可复用级联的原因。 ~20% A1 IN-CLASS QUIZ A1 课堂测验 40% A2 CONCEPT MAP A2 概念图 40% A3 EOT EXAM A3 学期末考试 50+12 MCQ + SHORT -ANSWER MCQ + 简答 The three assessment pieces 三项考核 Component Weight[16]Source: asksia-cheatsheet-2804nrs.pdf7. 2- 2804NRS Human Pathophysiology & Pharmacology 1 GRIFFITH UNIVERSITY . BACHELOR OF NURSING EXAM REVISION T1 2026 . SIDE 1 OF 2 Pathophysiology . EOTE Modules 3-7 SIDE 1/2 pain PATHOPHYSIOLOGY . Exam blueprint . Immunity . Antibodies . Hypersensitivity I-IV . HIV . Autoimmunity . Cancer . MSK & 0 . Exam Blueprint READ FIRST * Two assessments drive the marks: the A2 concept map (40%) and the End-of-Trimester Exam (40%) (the in-class quiz, ~20%, covers Modules 1-2 only). The EOTE = 50 MCQ (half the marks) + 12 short-answer (half) and examines Modules 3-7: immunity -> cancer > MSK/pain > genetics & ageing > neuro/autonomic + the pharmacology woven through. Train both reflexes: MCQ recall = the tables & trap- facts here; SAQ = explain a mechanism in prose - walk a pathophysiological cascade or a drug's mechanism of action in 3-5 linked steps. SIA > For every SAQ "explain . . . ", answer as a chain: trigger - mechanism step ++ mechanism step - clinical sign. Markers reward the links, not a list of facts. Ob . The A2 Cascade Template CONCEPT-MAP SPINE The A2 concept map (and every "explain the pathophysiology" SAQ) follows ONE colour-coded chain. Learn the shape and slot any disease in: RF > AETIOLOGY -> PATHOPHYSIOLOGY >> MANIFESTATIONS Risk factor - aetiology/trigger - pathophysiology (step-by-step) - clinical manifestations + +1 diagnostic test +1 management Worked (cervical cancer, the A2 case): RF = smoking, immunosuppression, multiple partners -> aetiology = persistent high-risk HPV infection > pathophys = viral oncoproteins inactivate p53/Rb tumour suppressors > dysplasia (CIN) > carcinoma in situ -> invasive squamous-cell carcinoma -> local + lymphatic spread > manifestations = abnormal/post-coital bleeding, discharge, pelvic pain. Dx = Pap/HPV test + biopsy; Mx = surgery/radiotherapy ± chemo. (HIV co-infection accelerates it via CD4 loss. ) Reuse this exact skeleton for stroke, MS, arthritis or any disease the exam throws at you. Oc . Assessment Shape WHERE THE MARKS ARE ITEM WT FORM & SCOPE A1 quiz ~20%

• 例如：innate vs adaptive、grading vs staging、chromosomal vs single-gene、active vs passive、first-pass 绕行、CYP 抑制/诱导。[5]Source: asksia-bible-2804nrs-bilingual.pdfWhen / detail Map band (colour-code it) What the rubric wants A1 in-class online quiz (Modules 1-2 only) ~20% Week 4 . 20 MCQ in 20 min, no backtracking A2 concept-map written assignment 40% Due ~Wk 9 · A4 colour- coded map + 500 words Pathophysiology (ink/blue) step-by-step sequence - /3 A3 End-of-Trimester exam (Modules 3-7) 40% Exam period . 50 MCQ + 12 short-answer A2 concept map = the cascade, marked A2 概念图 = 被评分的级联 Risk factors (amber) 3 RFs linked to aetiology - /6 Aetiology (red) the trigger that starts it Clinical manifestations (green) 5 signs linked to the mechanism - /10 2804NRS . Human Pathophysiology & Pharmacology 1 ★ What the End-of-Trimester exam actually is 学期末考试到底是什么 50 MCQ = 50% of the exam + 12 short-answer questions = 50% of the exam. The exam study guide highlights only Modules 3-7 as examinable - immunity, cancer, MSK & pain, genetics/ageing, and neuro + autonomic pharmacology. The MCQ half rewards broad recall (every trap callout in this book); the short-answer half rewards explaining a mechanism in prose - literally re-telling a pathophysiology cascade or a drug's mechanism of action. 50 道 MCQ = 占考试 50%+ 12 道简答题= 占考试 50%。考试复习指南仅把模块 3-7 标注为可考范围 -- 免疫、肿瘤、肌肉骨骼与疼痛、遗传/衰老,以及 神经+自主神经药理学。MCQ 部分奖励广泛记忆 (本书中每一个陷阱提示);简答部分奖励用文字解释 一个机制 -- 即字面意义上复述一条病理生理级联或 一种药物的作用机制。 ✓ The strategy this dictates 由此决定的策略 Build everything as the cascade. For A2: pick the case disease, lay out the four colour bands, draw arrows RF - aetiology - pathophysiology -+ manifestations, then in the 500 words give 2 diagnostic investigations + 2 management approaches (≥1 drug). For A3: the SAQ half is the same cascade written out, and the MCQ half is the trap boxes. Learn one cascade per disease and you have answered both 40% pieces. 把一切都构建成级联。A2 方面:选定病例疾病,铺开 四个色带,画出箭头 RF→ 病因→ 病理生理 → 临床 表现,然后在 500 字内给出 2 项诊断性检查+2种 管理方法(≥1种药物)。A3 方面:SAQ 部分就是同 一条级联写出来,而 MCQ部分就是那些陷阱框。每 种疾病学会一条级联,你就同时答好了两个40% 的部 分。 i Open or closed book? 开卷还是闭卷?[9]Source: asksia-bible-2804nrs-bilingual.pdfLevel What changes Example Chromosomal - structure Deletion, duplication, translocation Various structural syndromes Multifactorial Genes + environment Neural tube defects, diabetes, many cancers i Gain vs loss of function (ties to cancer) 功能获得 vs 功能丧失(与癌症相关) A point mutation (single base swap) can change one amino acid, make a premature stop codon, or a new start. Gain of function = proto-oncogene - oncogene (accelerator stuck on). Loss of function = tumour suppressor lost (brakes fail, e. g. p53, BRCA). Cancer needs both. 一个点突变(单碱基替换)可改变一个氨基酸、产生 提前终止密码子或新的起始。功能获得 = 原癌基因 → 癌基因(油门卡住)。功能丧失=抑癌基因丧失(刹车 失灵,如 p53、BRCA)。癌症需要二者兼具。 ! Chromosomal vs single-gene 染色体病 vs 单基因病 Down syndrome = trisomy 21 - a whole extra chromosome, NOT a single-gene defect. Cystic fibrosis, Huntington's and haemophilia are single- gene. Confusing the two is a classic MCQ trap. 唐氏综合征=21三体––整条多余的染色体,不是单 基因缺陷。囊性纤维化、亨廷顿病和血友病是单基因 病。把两者搞混是经典的 MCQ 陷阱。 2804NRS . Human Pathophysiology & Pharmacology 1 M6 . GENETICS & AGEING 6. 2 Mendelian inheritance - reading the Punnett square 6. 2 孟德尔遗传 -- 读懂庞纳特方格 Three patterns cover almost every single-gene disorder you must know. The exam will hand you a cross and ask for offspring ratios and carrier risk - so learn to read a Punnett square. Convention: a capital letter = dominant allele, lower-case = recessive. 三种模式涵盖了你必须知道的几乎所有单基因病。考试会给你一个杂交并要求子代比例与携带者风险 -- 故须学会读庞纳特方 格。约定:大写字母=显性等位基因,小写= 隐性等位基因。 P12 Father Aa A a RATIOS AA Aa A homozygous dominant carrier (heterozygous)[25]Source: asksia-cheatsheet-2804nrs.pdfwell poor (anaplastic) Metastasis No Yes Carcinogenesis = multistep initiation > promotion -> progression ; needs multiple mutations passed to daughter cells. 7b . Oncogenes & Spread GAIN VS LOSS · Tumour suppressor (p53 "guardian", BRCA1/2) -> loss of function = brakes failed. Cell cycle G1->S-> G2->M; cancer = checkpoint failure (esp. G1/S). Metastasis routes: local invasion, lymphatic, haematogenous (blood), transcoelomic seeding. Grading vs Staging: grading = how abnormal cells look; staging = how far it spread (TNM = Tumour, Node, Metastasis). AU risks: tobacco, UV, alcohol, HPV, BRCA, age. 8 . MSK & Pain MODULE 5 % Osteoporosis - bone density (resorption > formation; post-menopausal voestrogen) -> fragility fractures. Fracture healing: haematoma -> soft callus > hard (bony) callus -> remodelling. Compartment syndrome = ^pressure in a closed fascial space -> ischaemia (the 6 Ps) - emergency. Pain cascade (SAQ): tissue injury > mediators (prostaglandins, bradykinin) sensitise nociceptors > signal via A8/C fibres -> dorsal horn -> spinothalamic tract -> thalamus > cortex (perception). Nociceptive vs neuropathic vs referred. 8b . Arthritis & BPH 5. 2 / 4. 4 OA = "wear-and-tear" cartilage loss, mechanical, asymmetrical, large weight-bearing joints. RA = autoimmune (Type III, synovium), symmetrical small joints, systemic, morning stiffness, RF/anti-CCP. BPH = benign hyperplasia of the peri-urethral prostate (age/DHT) -> obstruction (hesitancy, frequency, nocturia, weak stream). Mx: a1-blockers ("-osin", relax smooth muscle) + 5a-reductase inhibitors. Prostate cancer = peripheral zone, PSA marker, androgen-dependent. 8c . Cell-Cycle Recap G1 > S (DNA synthesis) > G2 > M (mitosis) > cytokinesis. Checkpoints (esp. G1/S restriction point) police DNA integrity; p53 halts or apoptoses damaged cells. Cancer = oncogene accelerator stuck ON plus suppressor brakes OFF -> checkpoints bypassed -> autonomous proliferation. Cancer treatment (4. 2. 3): surgery (remove), radiotherapy (DNA damage, local), chemotherapy (cytotoxic, hits rapidly dividing cells -> AEs: myelosuppression, hair loss, GI/mucositis, nausea), and targeted/hormonal therapy. Diagnosis: biopsy + histology, imaging, tumour markers (PSA, CA-125). The cytotoxic AEs come from hitting normal fast-dividing cells (marrow, gut, hair). asksia. ai/cheatsheet/ griffith-2804nrs . side 1/2 AskSia CHEATSHEET SERIES

6）你现在只要回我 3 个问题，我就能把“详细复习重点”变成你个人的冲刺清单

• 你 Final 是哪一天？（我好给你排到每天）
• 你最怕哪两块：
  • A 免疫（抗体/超敏/HIV）
  • B 癌症（细胞周期/转移/分级分期）
  • C MSK+疼痛（OA/RA/疼痛级联/NSAIDs）
  • D 遗传（Punnett/Down 的陷阱）
  • E 神经+自主神经（Parkinson、受体、AChE/atropine）
  • F PK/PD（ADME、首过、半衰期、TI、CYP）
• 你更需要：背“标准答案模板”（SAQ），还是刷 MCQ 陷阱题？