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# System prepended metadata

title: 103年內專(200題)1-48

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# 103年內專(200題)1-48

## Question 1:

依據2014年新版的JNC 8治療高血壓，強調實證醫學，下列何項的說法不是專家小答組的建議？

---

- A. 大於60歲的高血壓病人以低於160/90 mmHg 為治療目標。 
- B. 介於30-59歲的高血壓病人以心舒血壓低於90 mmHg 為治療目標。 
- C. 60歲以下糖尿病及慢性腎病變病人的血壓治療以140/90 mmHg為治療目標。 
- D. 糖尿病人降壓起始治療以Angiotensin-converting enzyme inhibitor, Angiotensin receptor blocker, Calcium channel blocker及Thiazides-type diuretics為限。 
- E. 降壓劑加用Angiotensin-converting enzyme inhibitor, Angiotensin receptor blocker可改善慢性腎病人之腎功能。

### Correct Answer: A

根據 2014 年成人高血壓治療指引 (JNC 8) 

(1) 建議一: 在年齡大於或等於 60 歲的一般族群,當 其收縮壓大於或等於150mmHg或者舒張壓大於或等於90mmHg時才開始接受藥物控制,其治療目標為收縮壓低於150mmHg和舒張壓低於90mmHg。(強烈建議,等級 A) 

(2) 建議二: 在年齡小於60歲的一般族群,當其舒張壓大於或等於90mmHg時才開始接受藥物控制,其治療目標為舒張壓低於90mmHg。(年齡介於30到59歲,強烈建議,等級A;年齡介於18到29歲 (專家意見,等級E) 

(3) 建議三: 在年齡小於60歲的一般族群,當其收縮壓大於或等於140mmHg時才開始接受藥物控制,其治療目標為收縮壓低於140mmHg。(專家意見,等級 E)
 
(4) 建議四: 在年齡大於或等於18歲合併慢性腎臟疾病(CKD)的族群,當其收縮壓大於或等於140mmHg或者舒張壓大於或等於90mmHg時才開始接受藥物控制,其治療目標為收縮壓低於140mmHg和舒張壓低於90mmHg。(專家意見,等級 E) 

(5) 建議五: 在年齡大於或等於18歲合併糖尿病的族群,當其收縮壓大於或等於140mmHg或者舒張壓大於或等於90mmHg時才開始接受藥物控制,其治療目標為收縮壓低於140mmHg和舒張壓低於 90mmHg。(專家意見,等級 E) 

(6) 建議六: 在非黑人的一般族群,包含糖尿病患者,高血壓的建議起始用藥為thiazide類利尿劑、鈣離子阻斷劑(calcium channel blocker, CCB)、血管收縮素轉化抑制劑 (Angioten- sin converting enzyme inhibitor, ACEI)、或血管收縮素接受體拮抗劑(Angiotensin receptor blocker, ARB)。(中度建議,等級B) 

(7) 建議七: 在黑人的一般族群,包含糖尿病患者, 高血壓的建議起始用藥為 thiazide 類利尿劑或 CCB。( 一般黑人患者,中度建議,等級 B; 黑人合併糖尿病患者 (薄弱建議,等級 C) 

(8) 建議八: 在18歲以上合併CKD與高血壓的患者,起始(或增加)的高血壓藥物應包含ACEI或ARB,以增進腎臟結果。這個建議包含所有CKD患者,不論種族或者有無糖尿病。(中度建議,等級 B) 

(9) 建議九: 在治療高血壓時,應達到並維持目標血壓值。如果在治療的一個月內血壓並未達到目標,應考慮增加起始藥物的劑量,或加上第二類藥物,可參考建議六選取其中一類藥物 (thiazide 類利尿劑、CCB、ACEI 或 ARB)。
Ref: 2014 年成人高血壓治療指引 (JNC 8)

## Question 2:

根據"2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults"，請問下列何項不是建議的指引？

---

- A. 已知粥狀硬化病變相關的心血管病人應給予高強度之Statin治療。 
- B. LDL-C >190 mg/dl的人應給予高強度之Statin治療。 
- C. 年齡40-75的糖尿病人，其LDL-C大於70 mg/dl就應給予中等度之Statin治療。 
- D. 年齡40-75病人，其整體10年風險高於7.5%及LDL-C 70-189 mg/dl就應給予中等度之Statin治療。 
- E. LDL-C之治療目標：心血管病人及糖尿病人應低於70mg/dl；有心血管病危險因子者應低於100mg/dl；其他者應低於160 mg/dl。 

### Correct Answer: E

* **Summary of Statin Initiation Recommendations for the Treatment of Blood Cholesterol to Reduce ASCVD Risk in Adults** 

![](https://hackmd.io/_uploads/rkaX7Ap43.png)
 
* **LDL-C and Non–HDL-C Treatment Goals** 
given the absence of data on titration of drug therapy to specific goals, no recommendations are made for or against specific LDL-C or non–HDL-C goals for the primary or secondary prevention of ASCVD.

 ＊ 揚棄 LDL 及 non-HDL targets 撰寫新指引的專家指出,目前缺乏大型雙盲隨機研究的證據支持要將血脂肪下降至特定的數值,過去我們習慣在不同危險族群使用特定的血脂肪標準參考值和目標值,但這樣做會同時出現 over-treatment 與 under-treatment 的問題,前者有可能會造成 non-statin 藥物的過度使用,而這些藥物並沒有臨床證據支持會改善與降低心血管的風險,因此新的指引將不再建議特定的血脂肪目標。

 ＊ **應積極使用statin therapy之4大重點族群**
  
![](https://hackmd.io/_uploads/rk8_NCaEn.png)
 
Ref：2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults 

## Question 3:

82歲老婦人到院主訴五天來有日趨嚴重的呼吸困難。病史顯示30年前就有醫師告知心臟雜音，因無症狀，未曾有任何治療。近五年來運動耐受逐漸不佳，且偶有突發性悸動及心絞痛，特別在步行樓梯間更加惡化。住院當日清晨3點突然重度呼吸困難，因而急診住院。理學檢查：血壓110/62 mmHg；心跳90/分；頸靜脈怒張。心臟大小正常，但在右上胸骨緣及心尖部有Gr III/VI systolic murmur, S2減輕：其他所見尚無異常。其胸部X光、心臟超音波及心電圖如圖。WBC,5.2 k/micro L；AST,21U/L；CK,111U/L；CK-MB,14.6U/L；Troponin I,0.06 ng/ml。請問下列何項處置最恰當?

![](https://hackmd.io/_uploads/SkZ_HRaV2.png)

---

- A. Percutaneous coronary intervention 
- B. Aortic valve replacement
- C. Nitroglycerin IV infusion at the rate of 15mcg/min 
- D. Titrate PO carvedilol starting from 3.125 mg and reassess in 3 months 
- E. Treating with IV digoxin 0.125mg in conjunction with IV bolus Furosemide 20mg and then 20 mg BID 

### Correct Answer: B

根據 history & PE: 近五年來運動耐受逐漸不佳，且偶有突發性悸動及心絞痛，特別在步行樓梯間更加惡化。在右上胸骨緣及心尖部有Gr III/VI systolic murmur, S2減輕。EKG顯示LVH。CXR發現 cardiomegaly, poststenotic dilation of ascending aorta, pulmonary congestion。Cardiac Echo 測得 increased pressure gradient 和 aortic valve area。

![](https://hackmd.io/_uploads/rJ7ILApVn.png)

由上述history, PE, examination, 可診斷病人患有 severe, decompensated aortic stenosis 

Treatment:

![](https://hackmd.io/_uploads/BykwU064h.png)

*** 病人為有symptoms severe aortic stenosis, 因此最好的治療為 Aortic valve replacement 
Ref: 麻州第四版 1-20 Valvular heart disease, Aortic Stenosis 

## Question 4:

病人67歲男性，自7月起有輕度咳嗽及間斷性發燒高達38度，坊間診所診斷為上呼吸道感染。爾後，發燒仍舊起伏變動，偶有寒顫(chillness)，並有全身倦怠及二公斤體重減輕，直到11月才到院求診。病人僅有高血壓病史，服藥中。理學檢查：血壓 132/70 mmHg；心跳 78/分，正常律動；心臟有Gr II/IV Systolic murmur over left lower sternum border；其他尚無異常所見。Blood cultures 送檢中。 請問本病人的診斷以何項檢查最恰當? 

---

- A. Cardiac MRI 
- B. Chest CT 
- C. Gallium Scan 
- D. Transesophageal echocardiography 
- E. Exploratory chest operation

### Correct Answer: D

根據病人的history, 有fever with chillness的症狀, 病人應有infection 的問題, 加上理學檢查發現心臟有Gr II/IV Systolic murmur over left lower sternum border, 須強烈懷疑是 Infective Endocarditis。因此最恰當的檢查是安排 Transesophageal echocardiography。 

**Infective Endocarditis**: 
 (1) Risk factor:
 * The major risk factor for the development of IE is a structural abnormality of a heart valve, ofter causing a stenotic or regurgitant lesion (e.g., bicuspid aortic valve, myxomatous mitral disease) 
 * Prediposing risk factors for native valve endocarditis (NVE) include degenerative valve disease, age, IV drug use, poor dental hygiene, long-term hemodialysis, and diabetes Mellitus. 

 (2) Clinical presentation: 
 * the most common clinical feature of IE are fever and a new heart disease 

 (3) Diagnostic Criteria 

![](https://hackmd.io/_uploads/SkaX_CaEh.png)

Ref: 
 * The Washington Manual
 * Cardiology subspecialty consult, third edition
 * ＵpToDate 

## Question 5:

心臟衰竭病人常有肝、腎功能等多重器官異常及常要併用多種藥物，可影響藥物的吸收及排泄，導致用藥交互作用禁忌的發生，請問下列何種藥物得使用? 

---

- A. Thiazolidinediones
- B. Dronedarone
- C. Amlodipine
- D. Cyclooxygenase 2 inhibitors
- E. Metformin

### Correct Answer: C

A. Thiazolidinediones(e.g. Rosiglitazone<Avandia>, Pioglitazone<Actos>) 
 (1) Side effect: edema, MI 
 (2) Contraindication: 心肝, ALT> 2.5倍 
 (3) Avandia因為增加心臟病的risk, 目前已被歐盟的EMA禁用, 美國FDA也將它列為沒有其他藥物可選之下才能用的藥。故目前台灣TZD只剩下Actos 

B. Dronedarone:  
 (1) contraindication 
 * atrial fibrillation, permanent (when normal sinus rhythm will not or cannot be restored): risk of death, stroke, and hospitalization for heart failure doubled 
 * atrioventricular block, second- or third-degree (if no pacemaker is present) 
 * bradycardia of less than 50 beats per minute 
 * concomitant use of QT-prolonging drugs or herbal products (eg, phenothiazine antipsychotics, tricyclic antidepressants, certain oral macrolide antibiotics, and Class I and III antiarrhythmics)  
 * concomitant use of strong CYP3A inhibitors (eg, ketoconazole, itraconazole, voriconazole, cyclosporine, telithromycin, clarithromycin, nefazodone, and ritonavir)  
 * heart failure, symptomatic, with NYHA Class IV symptoms or recent decompensation 
requiring hospitalization 
 * hepatic impairment, severe  
 * liver or lung toxicity due to previous use of amiodarone 
 * pregnancy or nursing 
 * QTc Bazett interval of 500 msec or greater or PR interval greater than 280 msec 
 * sick sinus syndrome (if no pacemaker is present) 
 
D. Cyclooxygenase 2 inhibitors 
 (1) USES: Cyclooxygenase-2 (COX-2) inhibitors are nonsteroidal anti-inflammatory drugs (NSAIDs), antipyretics, analgesics, and inhibitors of thrombocyte aggregation. Celecoxib (Celebrex) is used to treat rheumatoid arthritis and osteoarthritis and is the only remaining COX-2 inhibitor on the market in the US. Rofecoxib (Vioxx) was removed from the market in 2004 due to concerns for increased risk of myocardial infarction and stroke, and valdecoxib (Bextra) was removed in 2005 for similar reasons. Etoricoxib (Arcoxia), lumiracoxib (Prexige), and parecoxib (Dynastat) [a prodrug of valdecoxib] are not approved for use in the US, but are available in other countries.  
  (2) PHARMACOLOGY: The cyclooxygenase (COX) enzyme (prostaglandin synthase H) consists of 2 isoforms, COX-1 and COX-2. COX-2 inhibitors decrease the synthesis of prostaglandin H2 by selectively inhibiting COX-2 (from 30- to 433-fold more potent towards COX-2 in vitro) with little or no inhibition of COX-1 at therapeutic doses. Although similar to traditional NSAIDs, selective inhibition of COX-2 may result in fewer gastrointestinal adverse effects usually associated with NSAIDs.  
 (3) TOXICOLOGY: At supratherapeutic doses, selective inhibition of COX-2 is lost, and the usual COX-1 effects may manifest in the GI tract as gastritis, and in the renal system as hypertension, decreased renal perfusion, decreased glomerular filtration rate, edema, and interstitial nephritis.  
 (4) WITH THERAPEUTIC USE 
 (5) ADVERSE EFFECTS: COMMON: GI effects occur most commonly and include dyspepsia, nausea, diarrhea, abdominal pain, pancreatitis, and flatulence. Other fairly common findings 
include headache and fever.  
 (6) SEVERE: Celecoxib is rarely associated with cardiac or renal events. GI bleeding may occur with chronic use. Methemoglobinemia is a rare event. Rofecoxib was voluntarily withdrawn from the market in 2004, due to an increased risk of severe dysrhythmias (ventricular fibrillation, cardiac arrest and sudden death), renal events, and associated with aseptic meningitis. 

E. Metformin: 
 (1) contraindications:  
 * acute or chronic metabolic acidosis including diabetic ketoacidosis 
 * iodinated contrast media, intravascular use in radiologic studies; possible acute alteration of renal function resulting in increased risk of lactic acidosis 
 * renal impairment (ie, serum creatinine 1.4 mg/dL or higher in females or 1.5 mg/dL or higher in males or abnormal creatinine clearance), including that caused by cardiovascular collapse, acute myocardial infarction, or septicemia; increased risk of lactic acidosis 
  (2) Precautions: 
 * lactic acidosis, with some fatal cases, has been reported rarely; monitoring recommended and discontinue with signs or symptoms 
 * Cardiovascular: hypoxic states, including cardiovascular shock, acute congestive heart failure, acute myocardial infarction, and other conditions characterized by hypoxemia increase risk of lactic acidosis 
 * Hepatic: avoid use in patients with clinical or laboratory evidence of hepatic disease due to increased risk of lactic acidosis 
 * Immunologic: sepsis increases risk of lactic acidosis 
Ref: Micromedex 

## Question 6:

72歲老先生，夜間睡覺中突因胸疼伴有寒顫、冷汗而驚醒，疼痛逐漸加劇，並延伸 答後背部，乃急赴急診部求診。當時血壓左手176/98 mmHg；右手164/97 mmHg；脈跳78/分，規則跳動。病人追憶近個月來，時有間歇性的胸痛，有時甚至痛過個把小時。 病人喜好抽煙，但尚無其他疾病。理學只見身高 176 cm及體重64.6 kg，血壓及心跳如前所述，上下肢動脈跳動正常，其他部位並無異常可見。其胸部X光、心電圖及電腦斷層如圖。實驗室檢查如下。經使用IV morphine及鎮靜劑後，病況大有改善。請問此刻病人最合宜的治療策略是? 

![](https://hackmd.io/_uploads/SJ7u20pN3.png)

![](https://hackmd.io/_uploads/SJtK2Ra4h.png)

![](https://hackmd.io/_uploads/SkI53RaN3.png)

---

- A. Endovascular stenting
- B. Urgent aortic repair
- C. Labetalol IV titration
- D. Catheter-based fenestration
- E. Dopamine IV infusion

### Correct Answer: C

Aortic Dissection 

(1) Definition: classic aortic dissection (AD) is a tear in the intima, which allows blood to enter the aortic wall and propagate in an anterograde or retrograde fasion, creating a false lumen or channel. 

(2)Classification: 

![](https://hackmd.io/_uploads/H19e60aEn.png)

(3) History: In contrast to the crescendodiscomfort of angina pectoris, the pain of acute dissection is maximal at its onset, usually sudden and severe, oftendescribed as a sharp, tearing pain in the chest, neck, or interscapular areas. 

(4) Image:  
 * CXR: demonstrate a widened mediastinum or abnormal aortic contour. Therefore, a normal CXR dose not rule out an AD. 
 * If the patient presents with hemodynamic instability or hypotension, rapid evaluation by TEE or CT scan should be performed to assess for complications of dissection, including pericardial effusion, AR, or aortic rupture 

(5) Treatment: 
 * Medications:  
  . When AD is suspected, immediate initiation of beta-blocker therapy to reduce shear forces is paramount while pursuing confirmation of the diagnosis 
  . BP should be reduced to as low a level as possible without compromising organ perfusion. 
  . Beta-blocker therapy is recomened to achieve a target heart rate < 70 beats per minute. 
 * Surgical management: 
                                    ![](https://hackmd.io/_uploads/H1PM6C6Nn.png)
                                 
Ref: Cardiology Subspecialty Consult, third edition, page 358-366

## Question 7:

有關心室快跳(Ventricular tachycardia, VT)的說法，下列何者的說法是錯誤的？ 

---

- A. Monomorphic VT 多見於非器官變異性心臟病。 
- B. Polymorphic VT在EP 實驗室不易電激導誘發(Electric stimulation)。 
- C. 血行力學異常及去顫電激有效的VT多是持續性VT(Sustained VT)。 
- D. 在心前區電極(Precordial leads) 出現同致性(Concordant)QRS型態。 
- E. Monomorphic VT 使用靜注的Procainamide,Lidocaine 或Amiodarone 就有效，不必電擊。

### Correct Answer: E

(1) The QRS complex during VT: 
 * Uniform (monomorphic) 
 * Vary from beat to beat (polymorphic) : torsades de pointes 

(2) Monomorphic VT suggests a stable tachycardia focus in the absence of structural heart disease or a fixed anatomic substrate that can create the substrate for a stable reentrant VT circuit when structural disease is present. 

(3) Monomorphic VT tends to be a reproducible and recurrent phenomenon and may be initiated with pacing and programmed ventricular stimulation. In contrast, polymorphic VT suggests a more dynamic and/or unstable process and, by its very nature, is less reproducible. Polymorphic VT may be produced by acute ischemia, myocarditis, or dynamic changes in the QT interval and enhanced dispersion of ventricular refractoriness. Polymorphic VTs are not reliably initiated with pacing or programmed stimulation. 

(4) A time duration of 30s is frequently used to distinguish sustained from nonsustained VT. Hemodynamically unstable VT that requires termination before 30s or VT that is terminated by therapy from an implantable defibrillator is also typically classified as sustained. 

(5) Sustained polymorphic VT, ventricular flutter, and VF all lead to immediate hemodynamic collapse. Emergency asynchronous defibrillation is therefore required, with at least 200-J monophasic or 100-J biphasic shock. The shock should be delivered asynchronously to avoid delays related to sensing of the QRS complex. If the arrhythmia persists, repeated shocks with the maximum energy output of the defibrillator are essential to optimize the chance of successful resuscitation. Intravenous lidocaine and/or amiodarone should be administered but should not delay repeated attempts at defibrillation. 

(6) ECG clues supporting the diagnosis of ventricular tachycardia: 

![](https://hackmd.io/_uploads/S1pomJR4h.png)

Ref: Ｈarrison 17th Edition, Part 9, page 1436~1437 

## Question 8:

依據美國醫師學院(American College of Physicians)基於醫療成本、臨床實效及病人安全，有下列諸項照護處置：
(1)中年女性，有正常月經週期，也沒有任何心臟症狀，未有三高病史，為早期診斷，達到完全治療效果，應建議電腦斷層冠狀動脈造影檢查，以瞭解冠脈狹窄及冠狀動脈鈣化分數
(2)二尖瓣脫垂病人進行拔牙手術時，除有心內膜炎病史外，可不必服用抗生素預防心內膜炎之發生 
(3)慢性冠心病人，在藥物服用中，未有任何心臟症狀時，不必以冠狀動脈造影追蹤粥狀硬化之進展 
(4)急性下壁心肌梗塞伴發完全房室傳導阻滯，應候等數天，才可決定置放永久性心律調整器 
(5)心臟衰竭病人併有呼吸困難時，仍舊應有BNP檢測，以為治療之參考。
請問下列何組的處置才有高價值的照護？ 

---

- A. (1)+(3)+(5)
- B. (1)+(4)+(5)
- C. (2)+(3)+(4)
- D. (2)+(4)+(5)
- E. (3)+(4)+(5)

### Correct Answer: C

(1) In 2008, the recommendations for endocarditis prophylaxis: 

![](https://hackmd.io/_uploads/HJL4LyR42.png)

![](https://hackmd.io/_uploads/r1xtUyRVh.png)                                                                   
(2) Indications for Permanent Pacemakers:  

![](https://hackmd.io/_uploads/r1_hI1CVh.png)

(3) BNP: B type natriuretic peptide: 是分子量小的心臟荷爾蒙, BNP 在心室中製造, 而且在心肌伸長或是臂張力異常的情況下會釋放到血液中,故是heart failure早期診斷的工具 

Ref: Cardiology subspecialty consult, third edition, chapter 22, chapter24 

## Question 9:

林先生年27歲，於2013年10月初從中國工作回台後，開始有咳嗽、間歇性寒顫、瀉肚及輕度呼吸困難，經過二週，病狀日劇，全身倦怠，並有端坐呼吸困難，腹脹、噁心及體重劇增，乃住院診療。理檢顯示：身高 179公分；體重 84.6公斤；體溫 36.9度：心跳 110/分；呼吸 24/分及血壓 159/119 mmHg；頸靜脈怒張；雙側肺有混濁呼吸聲；心臟，S3及left lift，但無心臟雜音可聞；腹部有shifting dullness，但無肝腫；雙腳浮腫。其心電圖、心臟超音波及胸部X光如圖。 請問這病人最可能的診斷是：

![](https://hackmd.io/_uploads/ry47d1CE3.png)

![](https://hackmd.io/_uploads/rkME_yCE3.png)
                                                                         
---

- A. Acute myocardial infarction
- B. Hypertensive cardiovascular disease
- C. Hypertrophic cardiomyopathy
- D. Acute aortic disease
- E. Acute heart failure

### Correct Answer: Ｅ

(1) 題目中提到的history & PE , 包括dyspnea, orthopnea, abdominal fullness( bowel wall edema), increased body weight, JVE, bilateral crackle breathing sound, S3, left lift, bilateral lower limbs edema 都是heart failure 的臨床表現。CXR showed cardiomegaly with mild bilateral pulmonary edema. EKG: normal sinus rhythm with non specific STT change, Q wave at V1~V2.  2D echo: EF:16.9%, LA dilated, LV dilated, normal Geometry. 根據上述history & PE 和 examination可推論診斷為 acute heart failure. 

(2) Doppler echo 標準值： 
 * IVSd – intraventricular septal width(measured during diastole): normal range: 0.6~1.1cm 
 * LVIDd – Left ventricular internal Dimension(diastole): normal range 3.5~6 cm 
 * LVIDs – left ventricular internal Dimension(systole): normal range 2.1-4 cm 
 * LVPWd – left ventricular posterior wall(diastole): normal range 0.6-1.1 cm 
 * LA – left atrium: 19- 39mm 
 * Aortic root Diameter- normal < 3.7cm 

(3) Acute myocardial infarction: 病人無chest tightness/pain症狀, EKG showed normal sinus rhythm with non specific STT change, Q wave at V1~V2 => old/recent MI, 缺乏 cardiac marker佐證 

(4) Hypertrophic cardiomyopathy  
 * Definition: left ventricular wall thickening in the absence of a cardiac or systemic cause 
 * History: the majority of patients with HCM are asymptomatic. Commonly symptoms include dyspnea, angina, syncope, arrhythmia 
 * PE: crescendo-decrescendo ejection systolic murmur 
 * The usual clinical diagnostic criterion for HCM is maximal LV wall thickness > 15mm 
 * Dynamic obstruction of blood exiting the heart can occur, as the aortic outflow tract is geometrically narrowed due to the thick septum and an elongated mitral valve apparatus causing systolic anterior motion (SAM) and mitral regurgitation. This dynamic process of LV outflow tract(LVOT) obstruction is present in approximately one-third of patients at rest and another third with provocation. 

(5) Heart failure:  

![](https://hackmd.io/_uploads/S1f_5kC4h.png)
    
Ref: 
 * Cardiology subspecialty consult, third edition.  
 * Echocardiographic evaluation of the thoracic and proximal abdominal aorta. UoToDate. 

## Question 10:

先生73 歲，因 H1N1 流行性感冒併發肺炎及呼吸衰竭而於1 月24 日住院。有抽煙病史，但無高血壓、糖尿病或血脂異常病史。住院中呼吸仍舊不適，1 月26 日清晨血氧降低，時T/P/R 36.8/123/26；CVP=8mmHg，BP 140/73mmHg，bilateral crackles，啟用 PEEP輔助呼吸。緊急心電圖及胸部X-光檢查如圖。請問本病人之診斷是：
2011/1/19(發病前心電圖)  

![](https://hackmd.io/_uploads/By6c91CN2.jpg)

2011/1/26/6AM   

![](https://hackmd.io/_uploads/r12s51RE2.jpg)

![](https://hackmd.io/_uploads/S1EzsyAN2.jpg)
    
---

- A. Acute respiratory failure
- B. Acute lungs edema
- C. STEMI, proximal left anterior descending artery occlusion
- D. STEMI, proximal right coronary artery occlusion
- E. NSTEMI, left circumflex artery occlusion

### Correct Answer: C

EKG顯示ST elevation in V2-V6，依以下表格，可得知影響到left anterior descending artery所有流域區域，因此答案選C。

![](https://hackmd.io/_uploads/rkvCjyCVn.png)

A. 題目僅提到血氧降低，但未提及其他data(例如PaO2、PaCO2、A-a gradient等)，且胸部X光沒有明顯infiltration，因此無法確定acute respiratory failure的診斷。 

B. 胸部X光沒有acute lung edema的典型表現。 

C. 正確。 

D. Proximal right coronary artery occlusion的心電圖表現應為ST elevation in V1-V2、V4R、II、III、aVF，或在V1-V3出現ST depression。 

E.  Left circumflex artery occlusion影響主要為V5-V6、I、aVL，而題目選項給NSTEMI，所以應該看到是ST depression。 

Ref: Pocket medicine 5th edition：1-6, 2-18 

## Question 11:

72 歲男性老人，住院主訴突發性呼吸困難。病人在 2007 年有高血壓服用 Bisoprolol(5mg)1/2 #,qd及 Amlodipine(5mg) 1#,qd。2009 年7 月6 日近乎昏厥求醫，心電圖如(A)。2003年4月1日有左眼失明及左手軟弱無力，時血壓164/79 mmHg 及心跳 93/min，不規則律跳，心電圖如(B)。在 2014 年 8 月 6 日清晨突然呼吸困難，乃急往急診部求診，據稱病人已有心悸、胸悶及間歇性呼吸困難一週。理學檢查：T/P/R= 36.9/79/18；BP 119/73 mmHg；急病狀，肺部混濁呼吸音，心臟大小尚可，未有心雜音及 S3 或S4，餘之理檢尚無異常。其心電圖(C) 及胸部X光和血液檢查如圖。請問此病人之心律不整診斷是： 

(A) 2009/07/06 11:17:27   

![](https://hackmd.io/_uploads/SyA6hy0Vh.jpg)

(B) 2013/04/01 08:54:28

![](https://hackmd.io/_uploads/S1B1T1RVn.jpg)

(C) 2014/08/06  

![](https://hackmd.io/_uploads/Hknga1REh.jpg)

![](https://hackmd.io/_uploads/rkYwpkA42.jpg)

![](https://hackmd.io/_uploads/BJUOayA4h.png)


---

- A. Short-run ventricular tachycardia
- B. Torsades de pointes
- C. Atrial fibrillation
- D. Wolff-Parkinson-White (WPW) syndrome with atrial fibrillation
- E. Ventricular fibrillation

### Correct Answer: D

第一張EKG可見到regular sinus rhythm但PR interval約為0.12 sec；
第二張EKG可見atrial fibrillation rhythm(irregularly irregular，且幾乎都沒有P wave)；
而兩張皆可見到delta wave，為preexcitation (WPW) pattern的表現。

![](https://hackmd.io/_uploads/SJaqRJREn.png)

第三張EKG可見wide complex irregular supraventricular tachycardia，當atrial fibrillation合併rapid conduction down accessory pathway時的EKG型態，因此解答為Wolff-Parkinson-White (WPW) syndrome with atrial fibrillation。 

![](https://hackmd.io/_uploads/rkV30kCE3.png)

A. 依Brugada criteria，precordial leads有RS complex、R to S interval沒有>100MS、仍有看到AV association、V1不符合VT morphology，因此不是ventricular tachycardia。 

B. 未見QT prolong，也無使用造成QT prolong的藥物或相關電解質問題(Ca↓)，EKG波形不像Torsades de pointes。 

C. 未見明顯P波、irregular rhythm，可符合atrial fibrillation。 

D. 正確解答。 

E.  仍有R波且有pulse和blood pressures，不是ventricular fibrillation。 

Ref:
 * Pocket medicine 5th edition：1-33, 1-34 
 * Approach to the diagnosis and treatment of wide QRS complex tachycardias. UptoDate.

## Question 12:

現年52 歲男性病人，因急發胸疼並有雙腳麻木急往急診部求診。時有合併冷汗，但無噁心或嘔吐，也未有放散性胸疼。血壓65/52mmHg; 心跳52/分；體溫36.7度；呼吸18/分；其他理學所見尚無重大異常。病人既往病史有十多年高血壓，不規則用藥，家族有冠心病。其緊急生化檢查：CK 78；CK-MB 26.3；Troponin I 0.012。請問本病人的 STEMI最可能的冠狀動脈阻塞位置在：

![](https://hackmd.io/_uploads/HkwJexRVh.jpg)

---

- A. Proximal left anterior descending artery(LAD)
- B. Proximal LAD beyond septal branch
- C. Posterolateral right coronary artery(RCA)
- D. Proximal RCA with Bezold-Jarish reaction
- E. Proximal left circumflex artery

### Correct Answer: D

EKG中顯示II、III、aVF的ST elevation；aVR、aVL的ST depression，可知是inferior wall infarction，有85%是RCA obstruction、15%是LCx obstruction。
**Bezold-Jarisch reaction (reflex)源自於心臟nonmyelinated vagal afferent pathways 的sensory receptors，這些inhibitory receptor主要在左心室的inferoposterior wall，當受到stretch、藥物等等刺激增加parasympathetic activity，就會造成bradycardia、vasodilation、hypotension。**
本題中病患有bradycardia、hypotension，可能因為AV node infarction造成AV block或Bezold-Jarisch reaction，皆是因RCA obstruction所導致。

![](https://hackmd.io/_uploads/B1DDggCV3.png)

A. Proximal LAD應見ST elevation於V1-V6。

B. Proximal LAD beyond septal branch也應於V3-V6有ST elevation。

C. Posterolateral right coronary artery(RCA)包括供應SA node的sinoatrial node artery，病患有bradycardia，但仍是sinus rhythm，因此SA node沒有involvement。
 
D.  正確解答。

E.  Proximal left circumflex artery應見ST elevation於I、aVL。

Ref: 
 * Pocket medicine 5th edition：1-6
 * The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. J Am Coll Cardiol. 1983 Jan;1(1):90-102. 
 * Patterns of coronary compromise leading to bradyarrhythmias and hypotension in inferior myocardial infarction. Coronary Artery Disease 2005, Vol 16 No 5.

## Question 13:

一位42 歲的男性上班族來看體檢報告，他每周慢跑三次，每次跑35 分鐘，跑步時不曾覺得胸悶或氣喘。在工作壓力大的時候偶爾會覺得"心臟少了一跳"的感覺，而這種感覺不會持續，也不會有頭暈。以前沒有住院或開刀，自己感覺健康，沒有抽菸或喝酒。身體檢查血壓 126/72 mmHg，心跳每分鐘68 次，呼吸每分鐘 14 次，身體質量指數(BMI)是23 kg/m2。心音聽診在左下胸骨邊緣有不會放射的第2/6度收縮心雜音，肺部呼吸音正常，四肢脈搏對稱正常，心電圖檢查正常。下一步要安排的檢查是？ 

---

- A. 24 小時心電圖
- B. 食道心臟超音波
- C. 胸前心臟超音波
- D. 運動心電圖
- E. 不用進一步檢查

### Correct Answer: E

左下胸骨邊緣收縮心音可推斷為tricuspid regurgitation。在24-96%的正常人中，即使三尖瓣是正常的，在收縮期並未完全緊閉密合，而在心臟超音波中可見TR jets。另外，tricuspid regurgitation的原因主要為functional(hemodynamic load on the right ventricle)而非valve的structural問題。在心電圖下沒有看到RV strain或RV hypertrophy，且其他檢查都是正常，因此可以當作是正常TR jets造成的murmur。
“心臟少了一跳”可能是bradycardia的心律不整，有明顯誘發因子(工作壓力)，較可能是sinus bradycardia，因為不持續且沒有症狀，不必進一步處置。
 
Ref:
 * Pocket medicine 5th edition：1-32
 * Harrison‘s principles of internal medicine, 18e; Chapter 237. Valvular Heart Disease
 * Goldman: Cecil Medicine, 23rd ed; Chapter 75 – VALVULAR HEART DISEASE
 * Hurst’s The Heart, 10th ed; chapter 59, p.1741

## Question 14:

63 歲男性有第二型糖尿病和高血壓，同時有陣發性心房纖維顫動的病史而接受包含有metoprolol，metformin 和warfarin 的藥物治療。因為糞便潛血篩檢陽性安排大腸鏡檢查，因為可能會有採檢 (biopsy)的需要，要先停用warfarin。他不曾抽菸，沒有中風或四肢動靜脈血管阻塞的過去史，體檢時血壓心跳在正常值，心律則呈現不規則(irregularly irregular)，抽血檢查INR是2.3。在此時需要停止warfarin 的情況下，會採取的較恰當步驟是？ 

---

- A. 改用aspirin
- B. 改用clopidogrel
- C. 改用低分子量肝素(low molecular weight heparin)
- D. 改用肝素(unfractionated heparin)
- E. 不須使用暫時的替代藥品

### Correct Answer: E

在atrial fibrillation病患，當CHADS score ≥2 (此病患=2)時需要使用anticoagulant治療，包括warfarin (keep INR 2-3)或Xa or direct thrombin inhibitor。 Warfarin 作用為抑制vitamin K 的regeneration，因此抑制factor II, VII, IX, X，其Elimination Half Life為7 天，93%病患在停藥約5 天後的INR會降至1.5以下。本題 INR為2.3在治療範圍內，若於 5 日內做完大腸鏡檢查，不需改用其他短效的抗凝血藥物，在追蹤 INR值即可。 
另外，內視鏡 biopsy 屬於low risk bleeding (<1.5%)手術，不須特別矯正INR；但當需執行high risk bleeding手術，則INR需降至1.5以下(intracranial手術要求1.2以下)。 

![](https://hackmd.io/_uploads/HkcVzlR43.png)

(N Engl J Med 2013;368:2113-24. Supplementary Appendix.) 

Ref:
 * Pocket medicine 5th edition：1-36 
 * MicroMedex: warfarin 
 * Management of Antithrombotic Therapy in Patients Undergoing Invasive Procedures; n engl j med 368;22 

## Question 15:

70 歲男性病人，因為嚴重的失代償鬱血性心衰竭(decompensated congestive heartfailure)住院接受治療，因為突發性的心室纖維顫動(Vf)正在進行急救，目前剛進行完 200 焦耳的非同步體外去顫電擊，緊接著去顫電擊之後立刻進行較恰當的動作是？ 

---

- A. 繼續體外按摩 CPR
- B. 給予epinephrine
- C. 給予amiodarone
- D. 確認脈搏
- E. 給予vasopressin

### Correct Answer: A

根據ACLS guideline，心臟電擊後立刻檢查心律與脈搏已不被建議，而是立刻做5個循環的胸外心臟按摩再檢查心律。 

![](https://hackmd.io/_uploads/BJ6k7eRNh.png)

Ref:
 * 高級心臟救命術訓練手冊, 2008年版; III-2頁 
 * 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care 

## Question 16:

52 歲有高血壓的男性患者，排尿正常，因為大於一周的雙下肢水腫和呼吸會喘，爬2層樓梯更喘而住院治療。住院時他接受靜脈注射利尿劑furosemide之後症狀進步，五天後藥物調整到口服的 enalapril 和furosemide，心臟超音波檢查左心室射出率35%，沒有瓣膜疾病，整個左心室運動不良(global hypokinesia); 核子醫學灌流檢查沒有明顯的局部缺血。目前他的血壓是136/88mmHg，心跳每分鐘80 次，呼吸每分15次，身體檢查沒有頸靜脈怒張，沒有第三心音，沒有肺部囉音(moist rales)，雙下肢已經沒有水腫。甲狀腺數值正常，心電圖正常竇性節律，沒有病理性Q波。此時加上下列哪一種藥物較合適？ 

---

- A. Amlodipine
- B. Carvedilol
- C. Hydralazine + isosorbide dinitrate
- D. Doxazosin
- E. Spironolactone

### Correct Answer: B

β blockers在心衰竭治療中是重要的一部分，其阻斷chronic adrenergic stimulation的tocix effect。許多大型研究證實β blockers對於NYHA class II-IV症狀病患的functional status、disease progression、survival等皆有好處，使用後可改善EF、exercise tolerance、functional class。目前正是有好處的β blockers包括carvedilol、metoprolol、bisoprolol。 

A. Amlodipine為dihydropyridine calcium channel blocker，藉由降低peripheral vascular resistance達到vasodilatation而降低血壓。藥物indication包括 hypertension、stable angina、variant angina等，在此病患不需使用。 

B. 正確解答。 

C. 使用於當無法tolerate ACEI/ARB時，此病患可使用enalapril，因此不需要。 

D. Doxazosin為α-adrenergic receptor antagonists，對heart failure病患沒有survival好處，甚至使用doxazocin針對高血壓會增加產生heart failure的風險。 

E. Spironolactone為aldosterone receptor antagonists，對於NYHA class II-IV和EF≦35%患者可以↓25-30%死亡率和降低住院率。但要注意患者的腎功能和血鉀，避免產生hyperkalemia。 

Ref: 
 * Pocket medicine 5th edition：1-16 
 * The Washingron Manual of Medical Therapeutics, 33th ed; chapter 4, p.159-163 
 * Micromedex: amlodipine 

## Question 17:

76 歲女性高血壓病人經歷胸口疼痛三天之後由家人陪同就醫，當她到醫院急診時胸痛已經緩解，初步發現她有 ST節段上升型前壁心肌梗塞。到院兩小時之後她突然發生呼吸不順，劇烈喘息和血壓下降而緊急進行氣管插管，X光檢查發現更擴大的心臟與肺水腫，並需要用 Dopamine開始幫忙維持血壓。身體檢查血壓是90/60mmHg，心跳每分鐘122 次，呼吸每分鐘16 次，在她的左右胸骨邊緣聽到第4/6級全收縮期心雜音，可以觸診到震顫(thrill)，雙側肺部出現囉音(rales)。下列哪一個診斷比較可能要先考慮？ 

---

- A. 主動脈剝離
- B. 左心室瘤
- C. 心室中膈缺損
- D. 右心室梗塞
- E. 心包填塞(cardiac tamponade)

### Correct Answer: C

此病患於myocardial infarction後突然出現decompensated heart failure、cardiogenic shock、pulmonary edema，並有Holo-systolic murmur及thrill。
Holo-systolic murmur的鑑別診斷包括pulmonary stenosis、mitral regurgitation、tricuspid regurgitation、ventricular septal defect。
Free wall rupture是myocardial infarction後嚴重的併發症，導致10%的早期死亡。通常在MI後第一周內，以突然hemodynamic collapse表現，導致PEA、hypotension、
pericardial symptoms、tamponade等等。在有高血壓病史、老年女性、第一次大面積transmural MI中最常見。 
  
A. Aortic dissection不會有heart murmur，且病患沒有劇烈胸痛。

B. Ventricular aneurysm or pseudoaneurysm不會有heart murmur、不會有sudden cardiogenic shock表現。

C. 正確解答。

D. Right ventricular infarction應以general edema表現較pulmonary edema更為明顯，且除非影響到valve function否則沒有murmur。 

E. Cardiac tamponade應是distal heart sound，而非murmur。
 
Ref: 
 * Pocket medicine 5th edition：1-10 
 * The Washingron Manual of Medical Therapeutics, 33th ed; chapter 3, p.153 
 * Bates’ Pocket guide to Physical Examination and History Taking 

## Question 18:

68 歲女性患者因為突然出現的心悸合併頭暈，呼吸會喘等狀況來到急診室。她有高血壓的病史，前一個月剛進行的檢查，心臟超音波顯示左心室收縮功能正常，心跳是竇性心律。目前正使用ACE inhibitor，利尿劑和阿斯匹靈治療。平日血壓控制在正常數值。當她到達急診時，測得的生命徵象：血壓80/60mmHg，心跳150 次/分鐘，呼吸30 次/分鐘，使用 40%氧氣面罩的SpO2 是80%。心臟的身體檢查發現不規則的快速心跳，S1 心音聽診時聲音出現大小變化，雙側下三分之一的肺部有濕囉音，心電圖呈現心房纖維顫動。此時的緊急處理下列比較合適的一項是？ 

---

- A. Adenosine
- B. Amiodarone
- C. Cardioversion
- D. Diltiazem
- E. Metoprolol

### Correct Answer: C

Atrial fibrillation，在ACLS guideline中，當heart rate≥150且出現unstable signs (hypertension、意識狀況改變、shock症狀/徵象、胸痛、心衰竭)，則需要使用 chronized cardioversion。此病患HR=150，且出現hypotension、shock、heart failure(pulmonary edema)等unstable signs，因此需考慮給予同步電擊。 

![](https://hackmd.io/_uploads/SyeFHxCNn.png)
                                    
Ref:
 * 高級心臟救命術訓練手冊, 2008年版;XI-6頁 
 * Pocket medicine 5th edition：ACLS-1

## Question 19:

60 歲的男性因為左側肋膜疼痛感覺而就醫，他的疼痛出現大約一週了，每次發生時會痛數個小時，如果躺下會更疼痛。他曾試著服用普拿疼，只能稍微減輕疼痛感，但他發現如果坐著將上半身傾向前方能暫時讓疼痛感消失。他回憶自己在七個月之前曾被診斷有急性心包膜炎，那時吃了醫師開的止痛藥 7 天之後就好了。患者在最近三天有輕微發燒，但沒有咳嗽或流鼻水，也沒有旅行。身體檢查時生命徵象：血壓 128/68mmHg，呼吸 16 次/分鐘，心跳 98 次/分鐘，沒有頸靜脈鼓脹，但有左側胸骨緣聽到有二個組成成份的心包摩擦音，肺部聽診沒有哮鳴音，手腳沒有水腫，心電圖是竇性心律沒有ST 節段變化。此時會考慮的治療方式，何者比較恰當？

---

- A. 檢查胸部電腦斷層
- B. 心包切除術
- C. Azathioprine
- D. Prednisolone
- E. Colchicine 和 aspirin

### Correct Answer: E

Acute pericarditis:  
  Recurrence in 10% to 15% of patients within the initial 12 mo. The recurrence rate increases up to 50% after the first recurrence. 

Acute treatment: 
(1) **Aspirin 650-1000 mg tid**. NSAIDs can be used in place of aspirin (e.g.,ibuprofen 600-800 mg tid, indomethacin 50mg tid). NSAIDs are contraindicated in patients with recent MI and CHF.

(2) **Colchicine 0.5-0.6 mg bid** should be used in combination with aspirin/NSAIDs.
Several randomized trials (ICAP, COPE, COPPS) have demonstrated that colchicine is effective in both reducing symptoms and the rates of recurrent pericarditis. Its use is recommended for first episodes **++but is not currently approved for recurrent disease++**.

(3) **Use of corticosteroids is controversial**. There is evidence of **their use being associated with increased recurrence**, side effects, and hospitalizations.
Current guidelines recommend that systemic steroid therapy be restricted to patients with underlying connective tissue disease, autoimmune disease or uremia pericarditis. One study found that using a lower dose (0.25 to 0.5 mg/kg per day) maintained for 4 weeks and followed by a slow taper had same efficacy and fewer adverse effects than with higher conventional doses (1 mg/kg/day for 2-4 weeks).
 
(4) Close observation of patients when there is suspicion for cardiac tamponade.
 
(5) Avoidance of anticoagulants (increased risk of hemopericardium). 

病患PE無cardiac temponade sign，選項A及B均無角色 
Azathiopine於acute pericarditis 當中完全沒有角色 
若按照現今guideline, colchicine 也不建議用於recurrent diseae, 因此應該更正為無解,最接近的選項為E
 
Ref: Ferri's Clinical Advisor 2015, pericarditis. 

## Question 20:

73 歲女性有第二型糖尿病，高血壓，高血脂好多年了，她前來回診看最近的檢查報告。目前她正接受 olmesartan, metformin 和pravastatin 的治療。她有接受醫師的建議維持固定運動，高纖低脂飲食，同時常攝取水果與蔬菜。沒有藥物過敏史。回診時生命徵象是：血壓 122/72mmHg，心跳72 次/分鐘，呼吸 15 次/分鐘，心、胸、腹部與四肢的身體檢查則沒有特殊發現。實驗室檢查數值如下：HbA1c : 6.5%，總膽固醇116mg/dL，低密度膽固醇(LDL-C)51mg/dL，高密度膽固醇(HDL-C)57mg/dL，三酸甘油脂(TG)40mg/dL。病人希望接受完善的照顧，請問會給予的用藥建議，下列何者為佳？

---

- A. 使用clopidogrel
- B. 增加降血脂的藥物
- C. 使用aspirin 和dipyridamole
- D. 使用aspirin
- E. 使用aspirin 和clopidogrel

### Correct Answer: D

For now, ADA recommend the following for primary prevention of cardiovascular event with aspirin for patient had diabetes: 
 * **Low-dose (75 to 162 mg/day) aspirin** use for prevention is reasonable for adults with diabetes and no previous history of vascular disease **who are at increased CVD risk (10 year risk of CVD events over 10%) and who are not at increased risk for bleeding** (based on a history of previous gastrointestinal bleeding or peptic ulcer disease or concurrent use of other medications that increase bleeding risk, such as NSAIDS or warfarin). Those adults with diabetes at increased CVD risk include most **men over age 50 years and women over age 60 years** who have **one or more of the following additional major risk factors: smoking, hypertension, dyslipidemia, family history of premature CVD, and albuminuria**. (ACCF/AHA Class IIa, Level of Evidence: B) (ADA Level of Evidence: C) 

 * Aspirin should not be recommended for CVD prevention for adults with diabetes at low CVD risk (men under age 50 years and women under 60 years with no major additional CVD risk factors; 10-year CVD risk under 5%) as the potential adverse effects from bleeding offset the potential benefits. (ACCF/AHA Class III, Level of Evidence: C) (ADA Level of Evidence: C) 

 * Low-dose (75 to 162 mg/day) aspirin use for prevention might be considered for those with diabetes at intermediate CVD risk (younger patients with one or more risk factors, or older patients with no risk factors, or patients with 10-year CVD risk of 5% to 10%) until further research is available. (ACCF/AHA Class IIb, Level of Evidence: C) (ADA Level of Evidence: E) 
 
Hypertension target blood pressure:  
(1) < 140/90 mmHg recommended for most patients 
(2) < 150 mmHg recommended in older patients (age ≥ 60 years or age ≥ 80 years, varies by guideline) 
(3) in patients with diabetes: 
Guidelines vary but targets range from < 130/80 mm Hg to < 140/90 mm Hg. 
BP targets < 140/90 mm Hg (based primarily on diastolic BP) not associated with Reduced mortality or morbidity (level 2 [mid-level] evidence), except in patients with diabetes  
(4) in patients with chronic kidney disease: 
Current guidelines recommend < 140/90 mm Hg, with multiple guidelines suggesting < 130/80 mm Hg if proteinuria or diabetes present. 
Lower blood pressure targets associated with reduced risk of end-stage renal disease in patients with proteinuria (level 2 [mid-level] evidence) 
(5) in patients with coronary artery disease, reaching systolic blood pressure ≤ 130 mm Hg appears associated with reduced risk of heart failure and stroke but no improvement in risk of death or myocardial infarction (level 2 [mid-level] evidence) 
 
Perform HbA1c at least two times a year in patients who are meeting treatment goals and who have stable glycemic control 
(1) HbA1c quarterly in patients whose therapy has changed or who are not meeting glycemic goals 
(2) The HbA1c goal for nonpregnant adults in general is <7% 
(3) In the elderly, those with comorbidities, or those at risk for complications from hypoglycemia, a more moderate glycemic target (HbA1c 7-8) may be appropriate 

![](https://hackmd.io/_uploads/SJXwKgRE2.png)

病患血壓,糖化血色素,血脂均控制在理想目標,因此唯一需要再做的是對DM 的 primary prevention for cardiovascular event. 

Ref: 
 * J Am Coll Cardiol. 2010;55(25):2878-2886. Aspirin for Primary Prevention of Cardiovascular Events in People With Diabetes 
 * Hypertension: Treatment. Dynamed. 
 * Ferri's Clinical Advisor 2015, Diabetes mellitus. 
 * Hypercholesterolemia: treatment. Dynamed. 

## Question 21:

50 歲的女性曾在 13 年前因乳癌接受手術切除右側乳房以及術後的放射線治療。在外科術後的規則追蹤裡，她的狀況穩定，沒有變化。直到她最近三個月裡，她感到運動時會略為胸悶，最近二個月內則慢慢出現爬三層樓梯時有一點喘。身體檢查時她的體溫正常，血壓：150/43mmHg，心跳 80 次/分鐘，呼吸 14 次/分鐘。頸靜脈沒有鼓脹，但會觀察到加強而快速的頸動脈波上升與下降，心音發現減小的S2 心音，但沒有S3，左側第三肋間胸骨緣則出現高頻率，第2/6級的舒張期漸減性心雜音，最大心尖搏動點則向外向下偏移，沒有出現肝－頸靜脈反射波(Hepatojugular reflux)。下列哪一個情況較能解釋前述發現？ 

---

- A. 主動脈瓣迴流(Aortic valve regurgitation)
- B. 心包填塞(Cardiac tamponade)
- C. 限制性心肌病變(Constrictive pericarditis)
- D. 侷限性心包膜炎(Restrictive cardiomyopathy)
- E. 嚴重三尖瓣迴流(Severe tricuspid valve regurgitation)

### Correct Answer: A

Aortic Regurgitation physical examination: 
Aortic regurgitation produces a myriad of signs because a hyperdynamic, enlarged left ventricle ejects a large stroke volume at high pressure into the systemic circulation. Palpation of the precordium finds a **hyperactive apical impulse displaced downward and to the left**. S1 and S2 are usually normal. **S2 is followed by a diastolic blowing murmur heard best along the left sternal border with the patient sitting upright**. In mild disease, the murmur may be short and heard only in the beginning of diastole when the gradient between the aorta and the left ventricle is highest. As the disease worsens, the murmur may persist throughout diastole. A second murmur, a mitral valve rumble, is heard at the LV apex in patients with severe aortic insufficiency. Although the cause is still debated, this Austin Flint murmur is probably produced as the regurgitant jet impinges on the mitral valve and causes it to vibrate. 
 
In chronic aortic regurgitation, the high stroke volume and reduced systemic arterial resistance result in a **wide pulse pressure**, which may generate a number of signs, including **Corrigan's pulse (sharp upstroke and rapid decline of the carotid pulse), de Musset's sign (head bobbing), Duroziez's sign (combined systolic and diastolic bruits created by compression of the femoral artery with the stethoscope), and Quincke's pulse (systolic plethora and diastolic blanching in the nail bed when gentle traction is placed on the nail)**. Perhaps the most reliable of physical signs indicating severe aortic regurgitation is Hill's sign, an increase in femoral systolic pressure of 40 mm Hg or more compared with systolic pressure in the brachial artery. 
 
In contrast to chronic aortic insufficiency with its myriad clinical signs, acute aortic insufficiency may have a subtle manifestation. The eccentric hypertrophy, which compensates for chronic aortic insufficiency, has not yet had time to develop, and the large total stroke volume responsible for most of the signs of chronic aortic insufficiency is absent. The only clues to the presence of acute aortic insufficiency may be a short diastolic blowing murmur and reduced intensity of S1 . This latter sign occurs because high diastolic LV pressure closes the mitral valve early in diastole (mitral valve preclosure) so that when ventricular systole occurs, only the tricuspid component of S1 is heard. 
 
Valvular disease is frequently seen in patients with radiation-induced heart disease. In one postmortem series, the incidence was high with 81% of patients showing evidence of valvular damage. The **++aortic and mitral valves are more commonly involved++** than the tricuspid and pulmonary valves. The reason for preponderance of left-sided lesion and the rarity of pulmonary valve involvement despite its anterior position is not known. This may be related to higher pressure across left-side valves. Only a minority of patients with radiation-associated valvular disease (RAVD) have clinically moderate or severe dysfunction. 

Ref: 
 * Goldman's Cecil Medicine, Aortic valve insufficiency. 
 * Cardiology Research and Practice Volume 2011 (2011), Article ID 317659, 9 pages. Radiation-Induced Heart Disease: A Clinical Update. 

## Question 22:

22 歲的男性，出生時是個早產兒，他記得父母說他從小就被醫師診斷有心雜音但沒有開過刀，但求學中與同班學生在體能運動上的表現相近，沒有特別的地方，不曾因胸部的症狀或不舒服看過病。身體檢查時血壓：116/82mmHg，最大心尖搏動點沒有明顯位移，在左側胸骨緣第二肋間處有一個第3/6級的連續的，像機械的(continuous-machinery )的聲音出現，這個聲音跨越了收縮和舒張期，這個聲音在左側鎖骨下方也可以聽見。他的手腳脈搏強弱是正常對稱，也沒有出現脈搏延遲，沒有杵狀指或發紺。胸部 X光和心電圖檢查則正常。下列哪一個狀況較符合這個發現？

---

- A. Ventricular septal defect
- B. Aortic coarctation
- C. Atrial septal defect
- D. Aortic valve stenosis
- E. Patent ductus arteriosus

### Correct Answer: E

Clinical presentation of PDA:  
  clinical signs are nonspecific and may become more evident and diagnostic after day 4 of life infants with a hemodynamically significant PDA may be asymptomatic and without heart murmur ('silent' duct), especially on days 1-3 of life infants with a symptomatic PDA present with heart murmur most often **a systolic or systolic-diastolic murmur at upper left sternal border moderate-to-large ducts characterized by continuous heart murmur, loudest in the left upper chest or infraclavicular area ('machinery murmur')** 
  Hemodynamically significant PDA may be characterized by additional clinical features including:  
 * bounding peripheral pulses 
 * wide pulse pressure 
 * active precordium 
 * premature infants may also present with 
 * deteriorating respiratory status (tachypnea, grunting, retractions, nasal flaring) 
 * pulmonary edema 
 * loss of lung compliance 

Ref: Patent ductus arteriosus (PDA). Dynamed.

## Question 23:

下列關於急性呼吸窘迫症候群(Acute respiratory distress syndrome,ARDS)的敘述何者錯誤? 

---

- A. severe ARDS其PaO2/FiO2<100mmHg
- B. 因外傷而造成的ARDS預後最好
- C. 俯臥(prone position)可減少90 天死亡率
- D. 肺動脈導管在診斷上很重要
- E. 使用PEEP可改善shunt-associated hypoxemia

### Correct Answer: D

ARDS Definition: A form of noncardiogenic pulmonary edema that results from acute damage to the 
alveoli. 
 
A. Berlin definition in 2011
 (1) Timing: **Within 1 week** of a known clinical insult or new or worsening respiratory 
symptoms
 (2) Chest imaging (chest x-ray or CT scan): **Bilateral opacities**, not fully explained by effusions, lobar/lung collapse, or nodules
 (3) Origin of edema: Respiratory failure **not fully explained by cardiac failure or fluid overload**. Need objective assessment (e.g., echocardiography) to **exclude hydrostatic edema** if no risk factor present 
 (4) Oxygenation (if altitude is higher than 1000 m, the correction factor should be calculated as follows: [Pa o 2 /Fi o 2 × {barometric pressure/760}] 
 * **++Mild: 200 mm Hg <PaO2 /FiO2 ≤300 mmHg++** with **PEEP or CPAP ≥5 cm H2O** (this may be delivered noninvasively in the mild ARDS group) 
 * **++Moderate: 100 mm Hg <PaO2 /FiO2 ≤200 mmHg++** with PEEP or CPAP ≥5 cm H2O 
 * **++Severe; PaO2 /FiO2 ≤100 mmHg++** with PEEP or CPAP ≥5 cm H2O 
 
B. The best chances for a positive outcome occur in **young trauma-related ARDS patients and patients with fewer chronic health problems**. In addition, patients with milder forms of ARDS tend to have a better chance of recovering than those with a more severe form of the illness. 
 
C. Positioning the patient: changes in position can improve oxygenation by improving the distribution of perfusion to ventilated lung regions; repositioning (lateral decubitus positioning) should be attempted in patients with hypoxemia that is not responsive to other medical interventions. Placing patients with moderate and severe hypoxemia in a prone position may improve their oxygenation. Recent trials (Guerin et al) have shown that in patients with severe ARDS, early application of prolonged **prone-positioning sessions significantly decreases 28-day and 90-day mortality**. 
 
D. Maintaining a low-normal intravascular volume may be facilitated by hemodynamic monitoring with a central venous or pulmonary artery (Swan-Ganz) catheter, aimed at achieving a central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) at the lower end of normal. The ARDS clinical trials network of **pulmonary artery catheter versus CVP to guide fluid management in ARDS showed no difference in mortality or ventilator-free days**, regardless of whether fluid status was monitored by pulmonary artery catheter or CVP. 
 
E. PEEP: positive end expirartory pressure: 
 * PEEP maintains expansion of alveoli, increases functional residual capacity (FRC), improves lung compliance, and **decreases ventilation-perfusion (V/Q) mismatch**.  
 * high level of PEEP might reduce mortality in mechanically ventilated adults with acute lung injury or acute respiratory distress syndrome (ARDS) potentially limited to subgroups with ARDS  
 * high PEEP may reduce duration of mechanical ventilation compared to low PEEP 
 * optimize PEEP to reduce FiO2 to < 60% if feasible (oxygen toxicity proportional to duration of time patient exposed to fraction of inspired oxygen [FiO2] > 60%) 
 
Ref: 
 * American lung association: Adult respiratory distress syndrome 
 * Adult respiratory distress syndrome. Medscape. 
 * Adult respiratory distress syndrome: Definition and Acute general treatmenet. Clinical Key.  
 * Acute respiratory distress syndrome: Treatment: mechanical ventilation. Dynamed. 

## Question 24:

下列何者比較不適合使用非侵襲性呼吸器(noninvasive positive pressure ventilation)?

---

- A. 中或重度 COPD急性惡化
- B. 心因性肺水腫(cardiogenic pulmonary edema)
- C. 敗血性休克
- D. 免疫不全病人併發呼吸衰竭
- E. 腹部手術後併發缺氧性呼吸衰竭

### Correct Answer: C

Table 102-1 
Recommendations for the Use of Noninvasive Ventilation During Acute Respiratory Failure According to Disease and Clinical Status

![](https://hackmd.io/_uploads/BJgPrZCN2.png)

![](https://hackmd.io/_uploads/ByMoH-0V3.png)

Ref: Murray and Nadel's Textbook of Respiratory Medicine, 102, 1778-1793.e6. Noninvasive Ventilation.

## Question 25:

下列關於結核性肋膜炎造成的肋膜積水生化及鏡檢之敘述何者錯誤?

---

- A. lymphocyte predominant exudate 
- B. adenosine deaminase>40 IU/L
- C. Interferon gamma (INF-r) >140 pg/ml
- D. mesothelial cell 的比率高
- E. smear 的acid fast stain 陽性率 <5%

### Correct Answer: D

Tuberculous Effusions 
Tuberculosis can cause pleural effusion in up to 30% of patients who reside in endemic locations for tuberculosis. The pleural effusion typically is not due to direct mycobacterial infection itself, but rather to increased vascular permeability of the pleural membrane because of a hypersensitivity reaction to mycobacterial proteins. 
The pleural fluid is generally **++lymphocyte predominant++** and culture negative for acid-fast bacilli. **++Adenosine deaminase levels higher than 50 U/L++** may be helpful in identifying tuberculous pleural effusions. A tuberculous empyema, which is distinct from a tuberculous effusion, is characterized by direct extension of the infection from thoracic lymph nodes or hematogenous spread of tuberculosis into the pleural space. 
 
Eighty-five samples of pleural fluid obtained from 76 patients with biopsy-proven tuberculous pleurisy were examined cytologically. Numerous reactive mesothelial cells were present in only 1,2% of specimens examined. In contrast, 65,3% of pleural fluid aspirates obtained from a control group of patients in congestive cardiac failure contained marked mesothelial exfoliation. The suggestion that **the presence of numerous**, often highly reactive **++mesothelial cells in a pleural aspirate makes the diagnosis of tuberculosis unlikely++** is confirmed. 
 
 Pleural fluid interferon-gamma (IFN-gamma) levels are increased in patients with tuberculosis (TB) pleural effusion. Recent studies from the west have found that estimation of pleural fluid IFN-gamma levels is an excellent diagnostic strategy for these patients. The diagnostic utility of pleural effusion IFN-gamma level estimation has not been evaluated in patients from developing countries, however. This work was carried out to study the diagnostic utility of IFN-gamma level estimation in patients with TB pleural effusion and to define the best cutoff of IFN-gamma for diagnosis TB pleural effusion. We studied 101 patients with pleural effusion. Of these, 64 were found to have a TB etiology, established by means of various conventional modalities. Measurement of pleural fluid IFN-gamma levels was done by ELISA technique. **The median value of pleural fluid IFN-gamma levels in patients with TB (1480 pg/ml, range 3-14,000 pg/ml) was significantly higher (p < 0.001) compared with the non-TB group (3 pg/ml, range 0-900 pg/ml)**. The receiver operator characteristic (ROC) curve for IFN-gamma showed an area under the curve (AUC) value of 0.954, and the best cutoff was computed to be 138 pg/ml. Using this cutoff for IFN-gamma levels in pleural fluid for the diagnosis of TB, sensitivity, specificity, negative predictive value, and positive predictive value were found to be 90.2%, 97.3%, 85.7%, and 98.3%, respectively. Estimation of IFN-gamma levels in pleural fluid is a useful diagnostic modality for TB pleural effusion. **++A cutoff of 138 pg/ml provides the best sensitivity and specificity for diagnosis of TB++**. 

Ref: 
 * Goldman's Cecil Medicine, 332, 1939-1948. Tuberculosis 
 * S Afr Med J. 1980 Jun 7;57(23):937-9. Mesothelial cells in pleural fluid: TB or not TB? 
 * J Interferon Cytokine Res. 2004 Apr;24(4):213-7. Diagnostic utility of pleural fluid IFN-gamma in tuberculosis pleural effusion.

## Question 26:

有關parapneumonic effusion之生化及鏡檢需要進一步考慮胸管引流的狀況下列何者錯誤?

---

- A. glucose <60mg/dl.
- B. pH<7.3
- C. positive Gram stain
- D. positive culture
- E. presence of gross pus

### Correct Answer: B

TABLE 70-2
Categorizing Risk of Poor Outcome in Patients with Parapneumonic Effusion 

![](https://hackmd.io/_uploads/SyJlKZRVh.png)

Drainage is recommended for management of patients in category 3 or 4. On the basis of a literature review, therapeutic thoracentesis and tube thoracostomy appear to be insufficient for managing most patients in category 3 or 4. Fibrinolytic drugs, VATS, and surgery are better choices for these patients. The British Thoracic Society recommends similar parameters with the addition of LDH. **LDH concentrations of less than 1000 IU/L, with glucose levels of greater than 40 mg/dL and negative Gram stains and cultures, are considered simple parapneumonic effusions, which usually resolve with antibiotics alone**. However, LDH levels greater than 1000 IU/L and glucose less than 40 mg/dL suggest a complicated parapneumonic effusion, which will require at minimum chest tube drainage. 

Ref: 
Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 70, 847-854.e2. Pleural Effusion and Empyema. 

## Question 27:

在一位健康的年輕人,感染流感病毒後併發急性肺膿瘍最可能的病原菌為?

---

- A. Legionella pneumophila
- B. Pseudomonas aeruginosa
- C. M. tuberculosis
- D. Aspergillus spp.
- E. Staphylococcus aureus

### Correct Answer: E

Etiology 
• The most important factor predisposing to lung abscess is aspiration. 
• Following aspiration as a major predisposing factor is periodontal disease. 
• Lung abscess is rare in an edentulous person. 
• Approximately 90% of lung abscesses are caused by anaerobic microorganisms 
(peptostreptococci, microaerophilic streptococci such as Streptococcus milleri, Bacteroides species, Fusobacterium nucleatum, Prevotella ). Pulmonary actinomycosis will also generate lung abscess. 
• In most cases anaerobic infection is mixed with aerobic or facultative anaerobic organisms (S. aureus, E. coli, K. pneumoniae, P. aeruginosa). 
• Parasitic organisms including Paragonimus westermani and Entamoeba histolytica. 
• Fungi including Aspergillus, Cryptococcus, Histoplasma, Blastomyces, and Coccidioides spp. 
• Immunocompromised hosts may become infected with Aspergillus, mycobacteria, Nocardia, Legionella micdadei, and Rhodococcus equi. 
• **++Lung necrosis caused by community strains of MRSA (USA 300 strain) in young adults or adolescents after acute influenza was initially reported in 2002 and can be quite fulminant++**. 

Ref: Ferri's Clinical Advisor 2015 , Disease overview: pulmonary abscess. 

## Question 28:

下列關於COPD病生理的敘述何者錯誤? (應選出所有答案) 
(1)增加residual volume 和增加residual volume/total lung capacity 代表air trapping. 
(2)增加total lung capacity代表hyperinflation of thorax. 
(3)一秒量(FEV1)小於50%預測值時PaCO2才會上升
(4)PaO2 下降的主因是shunting 
(5)nonuniform ventilation 也是COPD氣體交換障礙的原因之一 

---

- A. (1)+(2)+(3)
- B. (2)+(3)+(4)
- C. (1)+(5)
- D. (3)+(4)
- E. (3)+(4)+(5)

### Correct Answer: D

COPD典型finding為FEV1持續減少，residual volume(RV)及 RV/total lung capacity增加。特徵為nonuniform distribution of ventilation及ventilation-perfusion mismatching，後者是造成PaO 下降的主因。 

COPD pathophysiology在Harrison分為三個部分討論： 
(1) Airflow obstruction: 由spirometry來看， FEV1/FVC 會慢慢下降，Asthma不同的點在於asthma的 FEV1對bronchodilator有反應，通常可改善達15%。 

(2) Hyperinflation: COPD通常可見有”air-trapping”，即residual volume(RV)及 RV/total lung capacity 增加，且隨COPD病程進展，hyperinflation愈嚴重。 

(3) Gas exchange:  
 * 在FEV1下降到將近50%前，PaO2通常接近正常。FEV1即使下降到更低，休息時的PaO2也有可能是正常的。 
 * FEV1下降到<25%時，PaCO2才會上升。 
 * Pulmonary hypertension嚴重到造成cor pulmonale及right ventricular failure通常見於FEV1 <25%且Chronic hypoxemia(PaO <55mmHg) 

以下為錯誤選項
(3) 一秒量(FEV )小於50%預測值時PaCO 才會上升 → 錯。小於25% 
(4) PaO2下降的主因是shunting → 錯。主因是ventilation-perfusion mismatching 

Ref: Harrison's Principles of Internal Medicine, 19ed, Chapter 314 Chronic obstructive Pulmonary disease

## Question 29:

下列關於COPD的敘述何者錯誤?

---

- A. 氣道的過度反應性(airway hyperresponsiveness)不應該是COPD所具有的特徵
- B. 吸菸是 COPD的危險因子
- C. 燃燒生質燃料(biomass combustion)是不抽菸女性罹患COPD的危險因子
- D. α antitrypsin 缺乏症是COPD的危險因子
- E. 是一種慢性氣道發炎

### Correct Answer: A

COPD包括三個部分： 
(1) Emphysema: 解剖學上的定義，特徵為肺泡的擴張及破壞。 
(2) Chronic bronchitis: 臨床上的定義，慢性咳嗽有黏痰。 
(3) Small airway disease: 小支氣管狹窄。 

Risk factors 
(1) **Cigarette smoking**: FEV1下降的速率與smoking dose(pack per year)成正比。 
     
![](https://hackmd.io/_uploads/rJfWbz0Vn.png)

(2) **Airway responsiveness** 
(3) **Respiratory infections**: 目前尚有爭議，缺乏longitudinal study data。 
(4) **Occupational exposures**: 特定的工作例如：煤礦開採、金礦開採、棉花紡織等，都是COPD的risk factor。 
(5) **Ambient air pollution**: Prolonged exposure to smoke produced by biomass combustion—a common mode of cooking in some countries—also appears to be a significant risk factor for COPD among women in those countries. 
(6) **Passive, or second-hand, smoking exposure** 
(7) **Genetic considerations**: α  Antitrypsin(α AT) deficiency 
 
Ref: Harrison's Principles of Internal Medicine, 19ed, Chapter 314 Chronic obstructive Pulmonary disease 

## Question 30:

下列關於內因性氣喘(intrinsic asthma)的敘述何者錯誤? (應選出所有答案)
(1)內因性氣喘約佔10%的氣喘病人 
(2)內因性氣喘常合併鼻息肉且對阿斯匹林敏感 
(3)與atopy相關的基因在6q 
(4)內因性氣喘與IgE相關的免疫機轉較無關 
(5)氣喘是多基因控制的 

---

- A. (1)+(2)+(3)
- B. (2)+(3)+(4)
- C. (1)+(3)
- D. (3)+(4)
- E. (3)+(4)+(5)

### Correct Answer: D

  大約10%氣喘病患對於常見的吸入性過敏原皮膚試驗呈陰性，且serum IgE濃度正常。這些 nonatopic or intrinsic asthma病患通常疾病的發作較晚，常合併有nasal polyp，且對aspirin敏感，通常有較嚴重、持續的氣喘。病理機轉不明，但氣管切片及痰卻和atopic asthma相似，近來發現呼吸道局部產生的IgE增加，表示可能存在有常見的IgE-mediated mechanism。 
  氣喘是由多基因控制的，近來愈來愈多證據支持。在染色體5q上的基因多樣性包括T helper(T 2)cells IL-4, IL-5, IL-9, IL-13都與Atopy相關， 

以下為錯誤選項
(3) 與atopy相關的基因在6q → 錯誤，在5q 
(4) 內因性氣喘與IgE相關的免疫機轉較無關 → 可能有關。 

Ref: Harrison's Principles of Internal Medicine, 19ed, Chapter 309 Asthma 

## Question 31:

下列何者不是導致氣喘(asthma)死亡的主要危險因子?

---

- A. 成人時期才發生的氣喘
- B. 控制不佳氣喘而需經常使用吸入型支氣管擴張劑的病人
- C. 未使用吸入型類固醇(inhaled corticosteroids)的病人
- D. 之前因瀕死型氣喘(near-fatal asthma)而住院的病人
- E. 以上皆非

### Correct Answer: A

  因氣喘導致死亡近年來已減少，主要是由於inhaled corticosteroids(ICS)的廣泛使用。Asthma death主要risk factor包括：○1 poorly controlled disease with frequent use of bronchodilator inhalers, ○2 lack of or poor compliance with ICS therapy, ○3 previous admissions to hospital with near fatal asthma 

Ref: Harrison's Principles of Internal Medicine, 19ed, Chapter 309 Asthma 

## Question 32:

下列關於肺膿瘍(lung abscess)的敘述何者錯誤?

---

- A. nonspecific lung abscess 與aspiration 有關
- B. 電腦斷層若合併出現淋巴腺腫大(lymphadenopathy),應考慮其他診斷.
- C. 痰液培養的結果,常可代表感染的病原菌
- D. 為了確立細菌學診斷,電腦斷層指引經胸穿刺吸引術,已漸受重視
- E. 有臭味的痰液代表可能有厭氧菌感染

### Correct Answer: C

A&E. When no pathogen is isolated from a primary lung abscess (which is the case as often as 40% of the time), the abscess is termed a nonspecific lung abscess, and the presence of anaerobes is often presumed. **++A putrid lung abscess refers to foul-smelling breath, sputum, or empyema and is essentially diagnostic of an anaerobic lung abscess. The most important factor predisposing to lung abscess is aspiration.++** 
 
B. Similar cavitory disease such as lung abscess includes:  
 * Bacterial (anaerobic, aerobic, infected bulla, empyema, actinomycosis, tuberculosis) 
 * Fungal (histoplasmosis, coccidioidomycosis, blastomycosis, aspergillosis, cryptococcosis, zygomycetes) 
 * Parasitic (amebiasis, echinococcosis) 
 * Malignancy (primary lung carcinoma, metastatic lung disease, lymphoma, Hodgkin’s disease) 
 * Granulomatosis with polyangiitis, sarcoidosis, endocarditis, and septic pulmonary emboli 
  因此出現lymphadenopathy時必須考慮其他疾病 

C&D. Bacteriologic studies 
 (1) Sputum Gram stain and culture **++(commonly contaminated by oral flora)++** 
 (2) Percutaneous transtracheal aspiration 
 (3) Percutaneous transthoracic aspiration 
 (4) Fiberoptic bronchoscopy using bronchial brushings or bronchoalveolar lavage is the most widely used intervention when trying to obtain diagnostic bacteriologic cultures 
 (5) Blood cultures on some occasions (<30%) may be positive 
 (6) If an empyema is present, obtaining empyema fluid via thoracentesis may isolate the organism 
 
Ref: 
 * Ferri's Clinical Advisor 2015 > Pulmonary abscess 
 * Harrison's Principles of Internal Medicine, 19e 154: Lung Abscess 

## Question 33:

以下關於咳嗽的描述何者錯誤？

---

- A. 負責咳嗽的感覺神經是 C-fiber
- B. 急性和慢性咳嗽定義的時間界限一般定為八週
- C. 胃食道逆流是慢性咳嗽常見的原因之一
- D. 鈣離子阻斷劑降血壓藥物是慢性咳嗽常見的原因之一
- E. methacholine誘發試驗可用來排除支氣管氣喘所造成慢性咳嗽的原因

### Correct Answer: D

A. Spontaneous cough is triggered by stimulation of sensory nerve endings that are thought to be primarily rapidly adapting receptors and **C fibers**. Both chemical (e.g., capsaicin) and mechanical (e.g., particulates in air pollution) stimuli may initiate the cough reflex. A cationic ion channel—the type 1 vanilloid receptor—found on rapidly adapting receptors and C fibers is the receptor for capsaicin, and its expression is increased in patients with chronic cough 

B&C&D. **Chronic cough (>8 weeks)** may be caused by a wide variety of cardiopulmonary diseases, including those of inflammatory, infectious, neoplastic, and cardiovascular etiologies. When initial assessment with chest examination and radiography is normal, cough-variant asthma, **gastroesophageal reflux**, nasopharyngeal drainage, and medications (**angiotensin-converting enzyme [ACE] inhibitors**) are the most common causes of chronic cough. 

E. A history suggestive of cough-variant asthma ties the onset of cough to exposure to typical triggers for asthma and the resolution of cough to discontinuation of exposure. Objective testing can establish the diagnosis of asthma (airflow obstruction on spirometry that varies over time or reverses in response to a bronchodilator) or **exclude it with certainty (a negative response to a  bronchoprovocation challenge—e.g., with methacholine)**. In a patient capable of taking reliable measurements, home expiratory peak flow monitoring can be a cost-effective method to support or discount a diagnosis of asthma. 

Ref: Harrison's Principles of Internal Medicine, 19ed, 48: Cough and Hemoptysis 

## Question 34:

以下關於肺解剖生理的描述何者有誤？

---

- A. 人類呼吸道大約有 40 種正常細胞
- B. 從氣管開始約前 14 個分支的呼吸道不具氣體交換功能
- C. 肺尖的通氣量(ventilation)比肺底大
- D. 貧血會降低肺彌散量(diffusion capacity)
- E. 肺氣腫(emphysema)病患的功能肺餘量(functional residual capacity)會偏高

### Correct Answer: C

B. The **first 16 generations of passages form the conducting zone of the airways that transports gas from and to the upper airway described above**. These branches are made up of bronchi, bronchioles, and terminal bronchioles. The conducting airway is made up of a variety of specialized cells that provide more than simply a conduit for air to reach the lung. 
 
C. In the upright position, **++ventilation per unit lung volume is greater at the base of the lung than at the apex++**. The reason for this is that at the start of inspiration, intrapleural pressure is less negative at the base than at the apex, and since the intrapulmonary intrapleural pressure difference is less than at the apex, the lung is less expanded. Conversely, at the apex, the lung is more expanded; that is, the percentage of maximum lung volume is greater. 選項錯誤
    
![](https://hackmd.io/_uploads/S1dsvzA4n.png)

D.  Diffusing Capacity 
This test uses a small (and safe) amount of carbon monoxide to measure gas exchange across the alveolar membrane during a 10-second breath hold. Carbon monoxide in exhaled breath is analyzed to determine the quantity of CO absorbed by crossing the alveolar membrane and combining with hemoglobin in red blood cells. This “single-breath diffusing capacity” [diffusion capacity of the lung for carbon monoxide (DLCO)] value increases with the surface area available for diffusion and the amount of hemoglobin within the capillaries, and varies inversely with alveolar membrane thickness. Thus, DLCO decreases in diseases that thicken or destroy alveolar membranes (e.g., pulmonary fibrosis, emphysema), curtail the pulmonary vasculature (e.g., pulmonary hypertension), or **++reduce alveolar capillary hemoglobin (e.g., anemia)++**. Single-breath diffusing capacity may be elevated in acute congestive heart failure, asthma, polycythemia, and pulmonary hemorrhage. 

E. Emphysema 病患容易airtrapping,造成RV 上升,導致FRC上升 

Ref: 
 * Ganong's Review of Medical Physiology, 24e, Chapter 34. Introduction to Pulmonary Structure and Mechanics 
 * Harrison's Principles of Internal Medicine, 19ed, Chapter 252. Disturbances of Respiratory Function

## Question 35:

下列何者不是阻塞性呼吸睡眠中止症病患常見的臨床表徵?

---

- A.  體重過重
- B.  下巴較小或後縮
- C.  扁桃腺或懸雍垂過大
- D.  打鼾
- E.  無性別差異

### Correct Answer: E

Risk Factors of obstructive sleep apnea 
Elderly persons 65 years and older have a higher prevalence of obstructive sleep apnea secondary to decreased muscle tone. 
**Obesity (body mass index [BMI] greater than 30 kg/m 2 ) is a risk factor for OSA**. A 10% increase in weight is associated with a sixfold increase in risk for development of OSA, and a 10% weight loss is associated with 26% decrease in AHI. There is evidence of a potential link between OSA and insulin resistance. 
Approximately 30% of hypertensive persons have OSA. Patients with moderate to severe OSA have a 2.9 odds ratio of developing hypertension. Up to 50% of patients with cardiovascular disease have OSA, even after adjusting for hypertension and other comorbid conditions. 
**++Male patients are nearly twice as likely to have OSA as female patients++**. Estrogen and progesterone might have a protective role because population-based studies have demonstrated that postmenopausal women have a two- to threefold increased risk of OSA compared to premenopausal women. 
African Americans and Asians are at greater risk for OSA than whites. Being African American is an independent risk factor for severe sleep-disordered breathing, with an odds ratio of 2.55 compared with whites. **Asians have a narrower cranial base, a higher Mallampati score, smaller thyromental distance, and steeper thyromental plane** than whites, which might account for their increased risk. 

Ref: Conn's Current Therapy 2015 > Obstructive sleep apnea. Uptodate.

## Question 36:

78 歲男性，有高血壓及心臟病病史，長期使用鈣離子阻斷劑及利尿劑。此次因這一週呼吸越來越困難而至胸腔科門診求醫。胸部X光檢查發現雙側肋膜積水，但右側較明顯。以細針抽吸後檢驗發現右側肋膜積液的total protein為2.8 g/dL，LDH為112 U/L，同時病患血液中的 total protein 為6.2 g/dL(正常範圍為6.4 - 8.4 g/dL)，LDH為150 U/L(正常範圍為 131 - 250 U/L)。請問下列敘述關於使用 Light's criteria 的判斷，何者正確? 

---

- A. 因為符合三個 criteria 中的一個，所以是exudate
- B. 因為符合四個 criteria 中的兩個，所以是exudate
- C. 因為符合三個 criteria 中的一個，所以是transudate
- D. 因為符合四個 criteria 中的兩個，所以是transudate
- E. 因為血液與肋膜積液的 total protein 差值大於3.1 g/dL，所以是transudate

### Correct Answer: A

TABLE 99-5 
Pleural Fluid Characteristics of Exudates 

![](https://hackmd.io/_uploads/HydCYMCVn.png)

TP: 2.8 / 6.2= 0.45 
LDH= 112/150 = 0.74 
2/3 LDH serum upper limit = 375 > LDH (pleural) 
因符合1項criteria,故選A 
 
Ref: Goldman's Cecil Medicine, Pleural effusion.

## Question 37:

下列何者不是肺栓塞常見的危險因子?

---

- A. 酗酒
- B. 抽菸
- C. 女性賀爾蒙補充治療
- D. 癌症
- E. 長途飛行

### Correct Answer: A

**Etiology of Pulmonary embolism**
  Three primary influences predispose a patient to thrombus formation; these form the so-called Virchow triad, which consists of the following:  
•  Endothelial injury  
•  Stasis or turbulence of blood flow  
•  Blood hypercoagulability  

  The causes for pulmonary embolism are multifactorial and are not readily apparent in many cases. The causes described in the literature include the following:  
•  Venous stasis
•  Hypercoagulable states
•  Immobilization
•  Surgery and trauma
•  Pregnancy
•  Oral contraceptives and estrogen replacement
•  Malignancy
•  Hereditary factors
•  Acute medical illness

A study by Malek et al confirmed the hypothesis that individuals with HIV infection are more likely to have clinically detected thromboembolic disease. The risk of developing a pulmonary embolism or DVT is increased 40% in these individuals. 

**Venous stasis** 
Venous stasis leads to accumulation of platelets and thrombin in veins. Increased viscosity may occur due to polycythemia and dehydration, immobility, raised venous pressure in cardiac failure, or compression of a vein by a tumor. 

**Hypercoagulable states** 
The complex and delicate balance between coagulation and anticoagulation is altered by many diseases, by obesity, or by trauma. It can also occur after surgery. 
Concomitant hypercoagulability may be present in disease states where prolonged venous stasis or injury to veins occurs. 
Hypercoagulable states may be acquired or congenital. Factor V Leiden mutation causing resistance to activated protein C is the most common risk factor. Factor V Leiden mutation is present in up to 5% of the normal population and is the most common cause of familial thromboembolism.  
Primary or acquired deficiencies in protein C, protein S, and antithrombin III are other risk factors. The deficiency of these natural anticoagulants is responsible for 10% of venous thrombosis in younger people. 
 
**Immobilization** 
Immobilization leads to local venous stasis by accumulation of clotting factors and fibrin, resulting in thrombus formation. The risk of pulmonary embolism increases with prolonged bed rest or immobilization of a limb in a cast.  
In the Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) study, immobilization (usually because of surgery) was the risk factor most commonly found in patients with pulmonary embolism.
  
**Surgery and trauma** 
A prospective study by Geerts and colleagues indicated that major trauma was associated with a 58% incidence of DVT in the lower extremities and an 18% incidence in proximal veins. 
Surgical and accidental traumas predispose patients to venous thromboembolism by activating clotting factors and causing immobility. Pulmonary embolism may account for 15% of all postoperative deaths. Leg amputations and hip, pelvic, and spinal surgery are associated with the highest risk.  
Fractures of the femur and tibia are associated with the highest risk of fracture-related pulmonary embolism, followed by pelvic, spinal, and other fractures. Severe burns also carry a high risk of DVT or pulmonary embolism. 

**Pregnancy **
The incidence of thromboembolic disease in pregnancy has been reported to range from 1 case in 200 deliveries to 1 case in 1400 deliveries (see Epidemiology). Fatal events are rare, with 1-2 cases occurring per 100,000 pregnancies.  
Oral contraceptives and estrogen replacement Estrogen-containing birth control pills have increased the occurrence of venous thromboembolism in healthy women. The risk is proportional to the estrogen content and is increased in postmenopausal women on hormonal replacement therapy. The relative risk is 3-fold, but the absolute risk is 20-30 cases per 100,000 persons per year. 
 
**Malignancy** 
Malignancy has been identified in 17% of patients with venous thromboembolism. 
Pulmonary emboli have been reported to occur in association with solid tumors, leukemias, and lymphomas. This is probably independent of the indwelling catheters often used in such patients. The neoplasms most commonly associated 
with pulmonary embolism, in descending order of frequency, are pancreatic carcinoma; bronchogenic carcinoma; and carcinomas of the genitourinary tract, colon, stomach, and breast. 
 
**Hereditary factors** 
Hereditary factors associated with the development of pulmonary embolism include the following: 
•  Antithrombin III deficiency  
•  Protein C deficiency  
•  Protein S deficiency  
•  Factor V Leiden (most common genetic risk factor for thrombophilia)  
•  Plasminogen abnormality  
•  Plasminogen activator abnormality  
•  Fibrinogen abnormality  
•  Resistance to activated protein C  

**Acute medical illness**
Acute medical illnesses associated with the development of pulmonary embolism include the following: 
•  AIDS (lupus anticoagulant)
•  Behçet disease
•  Congestive heart failure (CHF)
•  Myocardial infarction
•  Polycythemia
•  Systemic lupus erythematosus
•  Ulcerative colitis

**Additional risk factors** 
Risk factors for pulmonary embolism also include the following: 
•  Drug abuse (intravenous [IV] drugs)
•  Drug-induced lupus anticoagulant
•  Hemolytic anemias
•  Heparin-associated thrombocytopenia
•  Homocystinemia
•  Homocystinuria
•  Hyperlipidemias
•  Phenothiazines
•  Thrombocytosis
•  Varicose veins
•  Venography
•  Venous pacemakers
•  Venous stasis
•  Warfarin (first few days of therapy)
•  Inflammatory bowel disease
•  Sleep-disordered breathing

In the PIOPED II study, 94% of patients with pulmonary embolism had 1 or more of the following risk factors:  
•  Immobilization
•  Travel of 4 hours or more in the past month
•  Surgery within the last 3 months
•  Malignancy, especially lung cancer
•  Current or past history of thrombophlebitis
•  Trauma to the lower extremities and pelvis during the past 3 months
•  Smoking
•  Central venous instrumentation within the past 3 months
•  Stroke, paresis, or paralysis
•  Prior pulmonary embolism
•  Heart failure
•  Chronic obstructive pulmonary disease
 
結論：綜上所述，酗酒不是肺栓塞常見的危險因子。 

## Question 38:

請問下列關於吸入性類固醇在慢性阻塞性肺病治療的角色，何者爭議最小?

---

- A. 降低死亡率
- B. 減緩肺功能下降的速率
- C. 減少每年急性惡化的次數
- D. 增加肺炎的機率
- E. 減少肺癌發生率

### Correct Answer: C

**Treatment of Chronic Obstructive Pulmonary Disease** 
 * Smoking Cessation 
 * Management of Inflammation 
 * Management of Infection 
 * Management of Sputum Viscosity and Secretion Clearance 
 * PPIs for Exacerbations 
 * Oxygen Therapy 
 * Vaccination to Reduce Infections 
 * Alpha1-Antitrypsin Deficiency Treatment 
 * Bullectomy 
 * Lung Volume Reduction Surgery 
 * Lung Transplantation
    
**Management of Inflammation in Chronic Obstructive Pulmonary Disease** 
 
Inflammation plays a significant role in the pathogenesis of COPD. **++Systemic and inhaled corticosteroids attempt to temper this inflammation and positively alter the course of disease++**. 
The use of systemic steroids in the treatment of acute exacerbations is widely accepted and recommended, given their high efficacy. **++A meta-analysis concluded that oral and parenteral corticosteroids significantly reduced treatment failure and the need for additional medical treatment and that they increased the rate of improvement in lung function and dyspnea over the first 72 hours++**. Note that systemic steroids are not as effective in treating COPD 
exacerbations as they are in treating bronchial asthma exacerbations.  
On the other hand, the use of oral steroids in persons with chronic stable COPD is widely **discouraged**, given their adverse effects, which include **++hypertension, glucose intolerance, osteoporosis, fractures, and cataracts++**. A Cochrane review showed **++no benefit at low-dose therapy and short-lived benefit with higher doses (>30 mg of prednisolone)++**. 
Inhaled corticosteroids provide a more direct route of administration to the airways and, similar to other inhaled agents, are only minimally absorbed. Consequently, aside from the development of thrush, the systemic adverse effects of these medications at standard doses are negligible. **++Despite the theoretical benefit, the current consensus is that inhaled corticosteroids do not decrease the decline in FEV1, although they have been shown to decrease the frequency of exacerbations and improve quality of life for symptomatic patients with an FEV1 of less than 50%. The 2011 ICSI guidelines conclude that inhaled steroids are appropriate in patients with recurrent exacerbations of COPD++**. 
**++Inhaled corticosteroids are not recommended as monotherapy and should be added to a regimen that already includes a long-acting bronchodilator++**. The Towards a Revolution in COPD Health (TORCH) trial showed that a **++combination of an inhaled corticosteroid and a long-acting beta agonist was more beneficial than inhaled corticosteroids alone++**. These data suggest that in patients with COPD, **++inhaled corticosteroids should be used only in conjunction with a long-acting beta agonist++**. 
However, patients treated with inhaled corticosteroids were noted to have an **++increased rate of pneumonia++**. The debate continues on the use of inhaled corticosteroids and the risk for pneumonia in patients with COPD. For example, **++no significant difference in pneumonia risk was found between patients who used inhaled budesonide and those who did not in a study by Sin et al++**. The authors analyzed data from 7 large clinical trials (n = 7042) of patients with stable COPD who used inhaled budesonide (n = 3801), with or without formoterol (Symbicort or Pulmicort, respectively) or a control regimen (placebo or formoterol alone [Oxis]). 
**++Increasing age and decreasing percent of predicted FEV1 were the only variables that were significantly associated with occurrence of pneumonia++**. 
**++Despite the possible increased risk of pneumonia associated with inhaled corticosteroids++**, a retrospective cohort study showed that in patients with COPD hospitalized with pneumonia, **++prior use of inhaled corticosteroids was actually associated with decreased mortality and less mechanical ventilation++**. Therefore the benefit of inhaled corticosteroids in selected patients will likely continue to outweigh the risks. 
Intravenous steroids are often used in high doses for acute exacerbations in the inpatient setting; recent research suggests that there is likely **++no benefit of IV over oral steroid formulations in acute exacerbations, and thus IV steroids should be reserved only for those patients unable to tolerate oral intake++**. 
Nonsteroidal anti-inflammatory medications have not been shown conclusively to have any benefit in COPD. No response has been shown to medications targeting interleukin-8 and tumor necrosis factor-alpha. Leukotriene inhibitors commonly used in asthma have also not proven to be beneficial in COPD. 
However, **++macrolide antibiotics have been shown to have anti-inflammatory effects in the airways of COPD patients. More specifically, azithromycin has been shown to improve the phagocytic function of pulmonary macrophages and to be a potent anti-inflammatory++**. 
**++Azithromycin is used clinically for its anti-inflammatory effects in patients with cystic fibrosis and in lung transplantation patients with chronic rejection. Furthermore, one study showed that erythromycin reduced the frequency of exacerbations in 109 patients with COPD treated over 12 months++**. A subsequent larger randomized controlled trial of 1,142 patients showed a slight decrease in COPD exacerbations for patients given azithromycin over 1 year compared with placebo. However, this study also noted **++an increase in hearing decrements in the patients receiving azithromycin (25% in the treatment group compared with 20% in the placebo group; P =0.04). The noted side effect combined with the concern for breeding antimicrobial resistance continues to prevent widespread use of azithromycin for prevention of COPD exacerbations++**. 
 
結論：**減少每年急性惡化的次數爭議最小；對於增加肺炎的機率、減緩肺功能下降的速率、降低死亡率尚有爭議**！至於減少肺癌發生率，應該不會有人選吧。

## Question 39:

下列何者不是開洞性肺部感染的常見致病菌?  

---

- A. 金黃色葡萄球菌(Staphylococcus aureus)
- B. A型鏈球菌(Group A Streptococcus)
- C. 克雷白氏肺炎菌(Klebsiella pneumoniae)
- D. 嗜肺性退伍軍人桿菌(Legionella pneumophila)
- E. 肺炎黴漿菌(Mycoplasma pneumoniae)


### Correct Answer: E

**Pathophysiology of Cavities** 
A cavity is the result of any of a number of pathological processes including **++suppurative necrosis (e.g., pyogenic lung abscess), caseous necrosis (e.g., tuberculosis), ischemic necrosis (e.g., pulmonary infarction), cystic dilatation of lung structures (e.g., ball valve obstruction and Pneumocystis pneumonia)++**, or **++displacement of lung tissue by cystic structures (e.g., Echinococcus)++**. In addition, malignant processes may cavitate **++because of treatment-related necrosis, internal cyst formation, or internal desquamation of tumor cells with subsequent liquefaction++**. 
The likelihood that the given process wills cavities depends upon both host factors and the nature of the underlying pathogenic process. The prevalence of cavities among persons with a given process varies widely. In general, certain processes tend to form cavities more commonly than others. For example, **++Mycobacterium tuberculosis++** generally has the highest prevalence of cavities among persons with pulmonary disease of any infection, probably because this pathogen causes extensive caseous necrosis. In the case of M. tuberculosis, the tendency to form cavities is clearly advantageous to the propagation of the organism because cavities contain large numbers of organisms, which can then be efficiently aerosolized and transmitted to other susceptible hosts. Other pathogens, such as **++Klebsiella pneumoniae++**, are associated with extensive pyogenic lung necrosis and frequent cavitations. This organism is also disproportionately represented among cases of pulmonary gangrene, in which there is extensive pulmonary necrosis and infarction, suggesting that the organism possesses pathogenic determinants that are more likely to lead to pulmonary necrosis and cavitations than other common causes of pulmonary infection, such as **++Streptococcus pneumoniae++**. The predilection to form necrotic cavities may be due to the priming of the inflammatory response by the concurrent aspiration of stomach acid or factors specific to the organism, such as endotoxin. Unfortunately, there is no single common factor that differentiates organisms that are frequently associated with pulmonary cavitations from organisms that are rarely associated with pulmonary cavitations. However, as a general rule, organisms that cause sub-acute or chronic pulmonary infections (e.g., **++mycobacterium and fungi++**) seem to be more frequently associated with cavities than organisms that cause acute pulmonary infections (e.g., **++viruses and S. pneumoniae++**). This rule has many exceptions (e.g., necrotizing pneumonias associated with **++Staphylococcus aureus and K. pneumoniae++**). 
 
  肺部開洞性病變，在感染性方面需考慮結核菌以及厭氧菌之肺膿瘍，非厭氧菌包含Klebsiella pneumoniae, Staphylococcus 等，其他少見的包含Nocardia spp., Rhodococcus spp., Actinomycosis, 黴菌有Cryptococcus, Aspergillosis, Coccidioides immitis, Histoplasmosis 等等之感染。 
  一般來說肺部開洞性病變若病人有膿痰，且痰味有臭味，先考慮厭氧菌之感染，在痰抹片下會呈現混合性的細菌。若病程很迅速變差，且呈現敗血性表現，需考慮Gram negative bacilli 比如在台灣是K.pneumoniae或Staphylococcus 之肺膿瘍。 
若針對以上常見病原菌治療反應不好時，要針對肺部病變做侵襲性治療，包含胸腔超音波或電腦斷層導引穿刺，甚至開刀取檢體，並排除「非感染性病變」，比如肺癌，自體免疫疾病血管炎等等。送檢需包含gram stain ，acid fast stain, cytology, bacteria, fungus, mycobacterium culture。支氣管檢查可幫忙發現支氣管內病變(endobrochial lesion)，支氣管沖洗培養可以做為參考，但並非代表真正病原菌。 
若病人免疫力差有用免疫抑制劑的病人尤其需要注意Nocardia spp., Rhodococcus spp.以及黴菌之伺機性感染。在國外如美國有一些地區性黴菌造成之肺部病變在台灣較少見，在台灣要注意的是 TB 及Penicillium marneffei和Cryptococcus。若病人查出為以上伺機性感染常見的菌種，必須檢查免疫力是否有問題，常需化驗 HIV 以及詢問有無使用類固醇，或是否有糖尿病等。東南亞含台灣地區愛滋病人最多黴菌感染除了鵝口瘡外的就是隱球菌及青黴菌(Penicillium marneffei)感染。 青黴菌的感染除了常見的典型潰瘍性結節皮膚及軟組織病變外，就是要注意肺部會以空洞或節結性或肺浸潤病兆發生，常常需要侵襲性的組織切片及染色幫忙診斷。一般認為傳染途徑來自土壤中的黴菌，經由呼吸道吸入產生。治療以 Amphotericin B 及Itraconazole為主。 
 
結論：**肺炎黴漿菌(Mycoplasma pneumoniae)  的肺部Ｘ光片呈現瀰漫性的肺炎，不會開洞。** 

## Question 40:

67歲男性，過去無抽菸史，此次因發燒數日至門診就醫，胸部 X光顯示右上肺實質化陰影，投予抗生素治療後無明顯變化，故安排胸部電腦斷層檢查(如圖)，經支氣管鏡切片病理發現為肺腺癌。後來安排全身正子掃描以及腦部核磁共振，發現右上肺腫瘤的SUVmax為4.5，右下氣管旁淋巴結的SUVmax為2.7，此外無其他病灶。請問下一步最適當的處置為何？

![](https://hackmd.io/_uploads/Skhr4mCN3.png)

---

- A. 檢驗EGFR基因是否有突變
- B. 縱膈腔淋巴結切片病理檢查
- C. 手術切除
- D. 化學治療
- E. 同步性化學及放射線治療

### Correct Answer: B

早期肺癌的治療首選手術。近年來，隨著外科技術的進步，亞肺葉（肺段切除或大楔形切除）切除逐漸替代傳統的肺葉切除。然而，由於肺癌的病理組織學的差別很大，對于直徑≦3cm的肺癌患者的術後預後也有很大差別。因此隨著當前亞肺葉切除在無轉移的肺癌中被推崇，使用術前影像學檢查來確定腫瘤惡性程度顯得尤為重要。 
PET/CT和TSCT（薄層CT）對預測肺癌的侵襲性及預后有價值。最大標準吸收值（SUVmax）和腫瘤的大小及分化程度有密切關係。像低分化腺癌，鱗癌，腺癌和大細胞癌往往有一個高的SUVmax值；而分化良好的腺癌，非侵襲性和良好的預後之SUVmax值較低。 
高分化腺癌常顯示為亞實性，在TSCT上表現為磨玻璃樣影；而高惡性度腫瘤顯示為實性，且在TSCT上顯示為單一的實性成分。因此c/t比（TSCT上腫瘤實性成分的最大直徑與腫瘤的最大直徑之比）能被用來預測肺癌侵襲性及預後。 
為了比較SUVmax和c/t比這兩個生物標誌對小體積肺癌患者術后復發的預測價值，日本名古屋大學的Shinji Naganawa教授等對169例直徑≦3cm原發性孤立性肺癌肺癌進行了回顧性研究，發現SUVmax是肺癌預後的良好生物標誌。 
該研究共納入169例孤立性肺癌患者（男性144例，女性55例；年齡：34-87歲）。術後隨訪中位期為42個月。28例suvmax顯著增高的患者術後復發。研究發現，SUVmax≧2.5比suvmax<2.5和c/t=>50%比c/t≦50%的無病生存期顯著降低。19例c/t≦50%的患者未見術後復發。cox風險率模型顯示只有SUVmax為獨立的復發預測因子。 
該研究表明，PDG-PET/CT的SUVmax值是肺癌患者預後密切相關的成像生物標誌，且在預測術後復發方面優於TSCT的c/t比，特別對實性肺癌尤為如此。 
雖然，TSCT的c/t比<50%對應一個較好的預後。在選擇手術方式前通過影像標誌預測腫瘤的侵襲性和預後很重要；因此，對小體積肺癌的SUVmax值在肺葉切除與亞肺葉切除之間的前瞻性比較試驗很有必要。
 
結論：**++先針對右下氣管旁淋巴結進行病理檢查，才能決定下一步的治療計畫++**。 

## Question 41:

78 歲男性，有 25 年的抽菸史，但自從55 歲就戒菸了，此次因近三個月來出現乾咳及呼吸困難且日漸嚴重，故至門診就醫。病患過去有心房顫動病史，最後一次發生rapid ventricular response是四個月前，病患長期使用的藥物包括 metoprolol 和 warfarin，以及自四個月前開始加上的 amiodarone。病患的胸部X光檢查無發現明顯異常，理學檢查除肺底部聽到一些 crackles 以外亦無明顯異常。肺功能檢查結果如下: FEV1= 72%，FEV1/FVC= 78%，VC= 72%，TLC= 65%，DLCO=50%。請問下一步最適當的檢查為何？ 

---

- A. 高解析度胸部電腦斷層檢查
- B. 支氣管鏡檢查
- C. 痰液細胞學檢查
- D. 心臟超音波檢查
- E. 核醫肺臟灌注(perfusion)與通氣(ventilation)掃描

### Correct Answer: A

1. **COPD Staging** 
  The severity of airflow obstruction was the primary means of staging COPD until the American Thoracic Society (ATS) provided criteria for staging COPD based on the presence of obstruction (ratio of FEV  to forced vital capacity **++[FEV /FVC] < 70%++**) and its severity as measured by percent of predicted FEV . The Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification took staging one step further by incorporating the presence of respiratory failure into its most severe stage. Furthermore, GOLD provided guidelines for therapy based on stage.  
ATS and GOLD criteria for assessing the severity of airflow obstruction (based on the percent predicted post-bronchodilator FEV  when the FEV /FVC is < 70%) are as follows:  
 * Stage I (mild) - FEV 1 80% or greater of predicted  
 * Stage II (moderate) - FEV 1 50-79% of predicted  
 * Stage III (severe) - FEV 1 30-49% of predicted   
 * Stage IV (very severe) - FEV 1 less than 30% of predicted or FEV 1 less than 50% and chronic respiratory failure  

2. Metoprolol 「臨床藥理」:   
  **++Metoprolol為一種交感神經β1-感受器之阻斷劑，對心臟而言，具有選擇性，對所有β感受器不具刺激作用。++**
  Metoprolol臨床上常用於治療高血壓，狹心症。凡罹患高血壓之病患，不論為站立或仰臥位置性高血壓，Metoprolol皆能顯著的降低血壓，而從未發生姿態性低血壓或電解質平衡失調。 
  對罹患狹心症者，本劑可降低其發生率，並增加身體的工作能量。  
  Metoprolol抑制心臟的交感神經性活動的作用，其主要是降低節律點細胞的自動性，並且降低上心室的傳導速率。因此Metoprolol能控制上心室搏動過速的心跳速率。本劑亦可能降低罹患心房纖維性顫動或心房顫動病患的心室速率。本劑亦已被證實可減低心室異位搏動的頻率。 
  Metoprolol可以減低心肌梗塞病患的死亡率。而對此作用的機制尚未完全明瞭，但是可能與降低心室纖維性顫動和限制梗塞大小有關。已證實可以降低非致命性心肌梗塞之發病率，此外亦對臨床上甲狀腺機能亢進有降低效果。 
  罹患功能性心臟障礙之病患，心悸為其主要症狀，可能因為增加交感神經性活動之故，對降低心悸和改善患者一般狀況有效。 
  治療劑量較non-selective β-blockers對周邊血管和支氣管之副作用少。因此，**++可投與罹患梗塞性肺疾病患者++**，服用Metoprolol後，呼吸道阻力的程度有時可能會增加，惟極少發生。如果有呼吸道阻力增加時，可併服β2-stimulant來治療。此外，Metoprolol對胰島素釋出和碳水化合物代謝之干擾，較非選擇性藥劑少。並不會明顯地改變心臟血管對低血糖之反應，或延長低血糖後之恢復時間，因此可投與糖尿病患者。 
 
3. Amiodarone仿單節錄：【不良反應】與  【注意事項】 
 (1)呼吸、胸腔及縱膈腔的異常： 
  肺毒性(肺泡性肺炎/間質性肺炎或纖維化、胸膜炎、阻塞性細支氣管炎及肺炎/BOOP，偶爾會致命。 
  嚴重呼吸衰竭病人支氣管痙攣，特別是氣喘患者、成人急性呼吸窘迫症，偶爾會致命，通常在手術後立即發生，可能和高氧濃度產生交互作用所致。 
 (2)肺部症狀： 
 * 如發生呼吸困難或乾咳，不論其是否伴隨整體健康狀況之惡化，都應考慮這有可能是肺部毒性的徵兆，應進一步作胸部X光檢查。 
 * 由於間質性肺炎若可早期停用amiodarone，一般來說是可回復的，應評估是否繼續使用amiodarone治療。 
 
4. 結論 
  **由於本題患者的FEV1/FVC= 78% (>70%)不是COPD；而Metoprolol只有β1的作用，近三個月來出現乾咳及呼吸困難且日漸嚴重，應考慮自四個月前開始加上的Amiodarone造成肺毒性的可能，應先做高解析度胸部電腦斷層檢查才是**。

## Question 42:

請問下列何者是肺癌的高危險群?
(1)抽菸 
(2)二手菸 
(3)糖尿病 
(4)高血壓 
(5)結核病史 
(6)慢性阻塞性肺病
(7)停經 
(8)肺癌家族史 
(9)石綿製造工人 

---

- A. (1)+(2)+(5)+(6)+(7)+(8)
- B. (1)+(2)+(5)+(6)+(8)+(9)
- C. (1)+(2)+(3)+(6)+(8)+(9)
- D. (1)+(2)+(6)+(7)+(8)+(9)
- E. (1)+(2)+(4)+(5)+(6)+(8)

### Correct Answer: B

**Risk factors of lung cancer**
(Ger LP, et al. Journal of the Formosan Medical Association = Taiwan yi zhi. 1992, 91 Suppl 3:S222-31)

Abstract 
The relationship between various risk factors and lung cancer was evaluated in a case-control study. One hundred and forty-one cancer patients newly cytologically or pathologically diagnosed from May 1990 to July 1991 at Tri-Service General Hospital (TSGH) were recruited as cases. 
Two control groups were also studied: 282 hospital controls two-to-one matched with cases on sex, age, hospital of admission and insurance status were selected from  the  TSGH  Ophthalmologic  Department,  and  282  neighborhood  controls two-to-one  matched  on  sex,  age,  and  residence  were  randomly  selected  from eligible neighbors. 
++A comparison of interview data between cases and hospital controls based on multiple conditional logistic regression revealed that cigarette smoking, keeping doves as pet, occupational exposure to cotton dust and working as a cook were risk factors for lung cancer++. 
An inverse association between incense burning and lung cancer was noted. The comparison between cases and neighborhood controls showed lung cancer was significantly associated  with **++cigarette smoking, keeping doves,  prior chronic bronchitis, occupational  exposure to cotton  dust, asbestos  and  radiation, low frequency of burning incense, and low intake of vitamin A derived from vegetables and fruits++**. 
++There was no association between lung cancer and working as a cook++ when cases were compared with neighborhood controls.
    
結論：**肺癌與糖尿病、高血壓、停經等無關。**

## Question 43:

請問下列哪些情況可能導致肋膜積液中的嗜伊紅性白血球比例增加?
(1)氣胸 
(2)乳糜胸 
(3)肝性肋膜積水 
(4)藥物 
(5)結核性肋膜炎 
(6)心臟手術後 
(7)淋巴癌 
(8)肺癌 
(9)石綿肋膜炎  

---

- A. (1)+(2)+(4)+(6)+(8)
- B. (3)+(5)+(6)+(7)+(9)
- C. (2)+(3)+(4)+(5)+(9)
- D. (2)+(4)+(5)+(7)+(9)
- E. (1)+(4)+(6)+(7)+(9)

### Correct Answer: E

**Etiology of eosinophilic pleural effusion** 
Pleural fluid eosinophilia (PFE, also called eosinophilic pleural effusion, EPE) is defined as pleural fluid with a nucleated cell count containing more than 10 percent eosinophils.  It  is  estimated  that  approximately  10  percent  of  exudative  pleural effusions are eosinophilic. The presence of PFE narrows the differential diagnosis of a pleural effusion. The most common cause is air or blood in the pleural space.

![](https://hackmd.io/_uploads/r1UMj7ANn.png)

![](https://hackmd.io/_uploads/B1gL5mCVh.png)

![](https://hackmd.io/_uploads/SJeBw97RN2.png)

**Incidence and etiology of eosinophilic pleural effusion** 
(R. Krenke, et al.) 
ABSTRACT 
  Although eosinophilic pleural effusion (EPE) has been a subject of numerous studies, its clinical significance still remains unclear. The aim of our study was to evaluate:  
(1)  the  relative  incidence  and  aetiology  of  EPE;  
(2)  the  predictors  of malignancy  in  patients  with  EPE;  and  
(3)  the  relationship  between  repeated thoracentesis and pleural fluid eosinophilia. A retrospective analysis of 2,205 pleural fluid samples from 1,868 patients treated between 1995 and 2007 was performed. 
  We identified 135 patients with EPE (7.2% of all patients with pleural effusion) and 153 EPE samples.  The  most  common  condition  associated  with EPE was **++malignancy(34.8%)++**  followed by **++infectious(19.2%), unknown (14.1%), post-traumatic(8.9%) and miscellaneous(23.0%) pleural effusions++**. The incidence of malignancy was significantly higher in patients with a lower (≦40%) pleural fluid eosinophil percentage. 
  40 patients with EPE underwent a second thoracentesis. In 16, eosinophilia was present in both pleural fluid samples, 14 revealed pleural fluid eosinophilia only after the second thoracentesis and 10 had eosinophilia only in the first pleural fluid sample. 
Pleural fluid eosinophilia should not be regarded as a predictor of nonmalignant etiology. Probability of malignancy is lower in  effusions  with  a  high  eosinophil percentage. The incidence of EPE in patients undergoing second thoracentesis is not different to that found during the first thoracentesis. 

結論：**++由上可知，只要有trauma就會造成eosinophilic pleural effusion，所以(1)氣胸、(6)心臟手術後正確，而惡性腫瘤部分為：轉移性肺癌、間皮癌、(7)淋巴癌、多發性骨髓癌、何杰氏淋巴癌所致，而非原發性肺癌，而(4)藥物、(9)石綿肋膜炎也是主因。++** 比較有疑義的應該是(3)肝性肋膜積水、(5)結核性肋膜炎，個人推測是發生的比例不高，又被刪去法而不是不會發生才是！

## Question 44:

請問下列哪些情況導致呼吸困難的機轉包括呼吸功(work of breath)增加? 
(1)慢性阻塞性肺病 
(2)氣喘 
(3)間質性肺病 
(4)肺動脈高壓 
(5)心因性肺水腫 
(6)非心因性肺水腫 
(7)貧血 
(8)失用(deconditioning) 

---

- A. (3)+(4)+(5)+(6)+(8)
- B. (1)+(2)+(4)+(6)+(8)
- C. (3)+(4)+(6)+(7)+(8)
- D. (1)+(2)+(3)+(5)+(6)
- E. (1)+(2)+(4)+(6)+(7)

### Correct Answer: D

On inspection, the rate and pattern of breathing as well as the depth and symmetry of lung expansion are observed. Breathing that is unusually rapid, labored, or associated with the use of accessory muscles of respiration generally indicates either augmented respiratory demands or an increased work of breathing. Asymmetric expansion of the chest is usually due to an asymmetric process affecting the lungs, such as **++endobronchial obstruction of a large airway, unilateral parenchymal or pleural disease, or unilateral phrenic nerve paralysis++**. Visible abnormalities of the thoracic cage include kyphoscoliosis and ankylosing spondylitis, either of which can alter compliance of the thorax, increase the work of breathing, and cause dyspnea.
    
Table 245-1 Typical Chest Examination Findings in Selected Clinical Conditions

![](https://hackmd.io/_uploads/HJXZkVC43.png)

Ref: Harrison’s Principles of Internal Medicine , 17th edition , Chapter 245

## Question 45:

吞嚥困難(dysphagia)可依食物在不同部位受阻情形分成口咽型(oropharyngeal)和食道型(esophageal)兩大類，下列何者不是造成口咽型吞嚥困難的原因？

---

- A. 巴金森病(Parkinson's disease)
- B. 扁桃腺周圍膿瘍(peritonsillar abscess)
- C. Schatzki's ring
- D. Plummer-Vinson syndrome
- E. Zenker's diverticulum

### Correct Answer: C

A. 巴金森病(Parkinson's disease) 
B. 扁桃腺周圍膿瘍(peritonsillar abscess) 
  ++Dysphagia is classified by the deficit area such as oral, pharyngeal, oropharyngeal and esophageal dysphagia. In some patients, no organic cause for dysphagia can be found, and these patients are defined as having functional dysphagia++. 
  Oropharyngeal dysphagia disorders can occur in all age groups, resulting from congenital abnormalities, structural damage, and/or medical conditions. 
  Swallowing problems are a common complaint among older individuals, and the incidence of dysphagia is higher in the elderly, in patients who have had **++strokes++**, and in patients who are admitted to acute care hospitals or chronic care facilities. Other causes  of dysphagia include **++head and neck cancer and progressive neurologic diseases like Parkinson's disease, Dementia, Multiple sclerosis, Multiple system atrophy, or Amyotrophic lateral sclerosis++**. 
  Dysphagia is a symptom of many different causes, which can usually be elicited by a careful history by the treating physician. 
  A formal oropharyngeal dysphagia evaluation is performed by a speech-language pathologistor occupational therapist. 

C. Schatzki's ring 
  A Schatzki ring, also known as a Schatzki-Gary ring, is **a narrowing of the lower part of the esophagus** — ++a muscular tube through which food passes to the stomach++. 
  Schatzki ring is named after Robert Schatzki, the radiologist who first characterized it. The cause of Schatzki rings has not been firmly determined. 
 Some doctors, however, believe that ++it is caused by long-term damage from stomach acid reflux or gastroesophageal reflux disease (GERD)++ — a condition in which stomach liquids shoot up into the esophagus, inflaming and damaging its lining. 
 Treatment for a Schatzki ring includes fracturing with an endoscope, enlargement with a dilator, or expansion with a special balloon. 
 Usually, a Schatzki ring does not ignite any symptoms. ++Awareness, however, is usually triggered by poorly chewed food that gets stuck in the esophagus++, as the patient would consequently have chest pain or have difficulty swallowing — known as dysphagia. This could compel the patient to stick a finger in the back of his or her throat to regurgitate the food — that is, to force it out through the mouth. 

D. Plummer-Vinson syndrome 
 (1) Background 
  The association of **++post-cricoid dysphagia**, **upper esophageal webs**, and **iron deficiency anemia** is known as **Plummer-Vinson syndrome (PVS)**++ in the United States and Paterson-Brown Kelly syndrome in the United Kingdom. The term ++sideropenic dysphagia++ has also been used, since the syndrome can occur with ++iron deficiency (sideropenia)++, but it is not associated with anemia. 

 (2) Pathophysiology 
  The pathogenesis of PVS remains speculative, and the existence of the syndrome has been challenged. Postulated etiopathogenic mechanisms ++include iron and nutritional deficiencies, genetic predisposition, and autoimmune factors++. 
  ++The prevalent iron deficiency theory remains controversial++. Older reports have implicated iron deficiency in the pathogenesis of esophageal webs and dysphagia in predisposed individuals. The depletion of iron-dependent oxidative enzymes may produce myasthenic changes in muscles involved in **++the swallowing mechanism, atrophy of the esophageal mucosa, and formation of webs++** as epithelial complications.

![](https://hackmd.io/_uploads/rkO88SRE3.png)

  ++The improvement in dysphagia after iron therapy provides evidence for an association between iron deficiency and **post-cricoid dysphagia**++. Anecdotal reports have also been made of patients with PVS exhibiting impaired esophageal motility (with dysphagia) that recovers following iron therapy. 
  Moreover, the decline in PVS seems to parallel an improvement in nutritional status, ++including iron supplementation++.  
  However, population-based studies have shown **++no relationship between post-cricoid dysphagia and anemia or sideropenia++**. Other studies have demonstrated that patients with webs are as likely to be iron deficient as controls, and webs are often found in patients without iron deficiency or dysphagia. Lastly, the iron deficiency theory does not explain **++the predilection of webs for the upper esophagus++** and the rarity of the syndrome in populations in which chronic iron deficiency is endemic (eg, eastern and central Africa). 
  PVS has also been viewed as ++an autoimmune phenomenon++. The syndrome has been associated with autoimmune conditions, such as rheumatoid arthritis, pernicious anemia, celiac disease, and thyroiditis. In one study, a significantly higher proportion of patients with PVS had **++thyroid cytoplasmic autoimmune antibodies compared to controls with iron deficiency++**. The autoimmune theory, however, has gained little acceptance to date.  
  A complicated inlet patch (heterotopic gastric mucosa) has also been implicated in the pathogenesis of PVS. **++An ulcerated inlet patch in the upper esophagus can cause stricturing (web-like formation) and bleeding (with subsequent iron deficiency)++**. 
  However, most studies with biopsy or autopsy specimens have not demonstrated the presence of gastric metaplasia in the samples. 

E. Zenker's diverticulum  
 (1) Background
  In anatomy, Zenker's diverticulum, also **++pharyngoesophageal diverticulum, also pharyngeal pouch, also hypopharyngeal diverticulum, is a diverticulum of the mucosa  of  the  pharynx, just above the cricopharyngeal muscle++** (i.e. above the upper sphincter of the esophagus). ++It is a false diverticulum (not involving  all layers of the esophageal wall). It was named in 1877 by German pathologist Friedrich Albert von Zenker++. 
    
![](https://hackmd.io/_uploads/ryJddrAVn.png)

 (2) Epidemiology 
  Zenker's diverticulum mainly affects older adults. It has an incidence of ++2 per 100,000 per year in the UK++, but there is significant geographical variation around the world. 
  (3) Mechanisms and manifestations 
  In simple words, **++when there is excessive pressure within the lower pharynx++**, the weakest portion of the pharyngeal wall balloons out, ++forming a diverticulum which may reach several centimetres in diameter++. 
  More precisely, while traction and pulsion mechanisms have long been deemed the main factors promoting development of a Zenker's diverticulum,  current consensus considers occlusive mechanisms to be most important: ++uncoordinated swallowing, impaired relaxation and spasm of the cricopharyngeus muscle lead to an increase in pressure within the distal pharynx++, so that its wall herniates through the point of least resistance (known as Killian's triangle, located superior to the cricopharyngeus muscle and inferior to the inferior constrictor muscles). The result is an out-pouching of the posterior pharyngeal wall, just above the esophagus. 
  While it may be asymptomatic, Zenker diverticulum can present with the following symptoms: 
 * **Dysphagia** (difficulty swallowing), and **sense of a lump in the neck** 
 * **Food might get trapped in the outpouching**, leading to: 
 * **Regurgitation**, reappearance of ingested food in the mouth
 * **Cough**, due to food regurgitated into the airways
 * **Halitosis**, smelly breath, as stagnant food is digested by microorganisms 
 * **Infection** 
  It rarely, if ever, causes any pain. 
  **++Cervical webs are seen associated in 50% of patients with this condition++**. 
 (4) Diagnosis 
  The simple barium swallow will normally reveal the diverticulum. **++An upper GI endoscopy also shows the diverticulum++**. Sipping contrast and taking a CT also gives definite diagnosis. 
 (5) Treatment 
  ++If small and asymptomatic, no treatment is necessary++. **++Larger, symptomatic cases of Zenker's diverticulum have been traditionally treated by neck surgery to resect the diverticulum and incise the cricopharyngeus muscle++**. 
 However, in recent times non-surgical endoscopic techniques have gained more importance (as they allow for much faster recovery), and the currently preferred treatment is endoscopic stapling (i.e. diverticulotomy with staples). 
 This may be performed through a ++diverticuloscope++. Other methods include ++fibreoptic diverticular repair++. Other non-surgical treatment modalities also exist, such as ++endoscopic laser++, which recent evidence suggests is less effective than stapling. 

## Question 46:

有關巴瑞特氏食道(Barrett's esophagus)的敘述，何者錯誤？

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- A. 是食道腺癌(esophageal adenocarcinoma)的危險因子
- B. 每年有 5%進展成癌症
- C. 依長度分成long-segment 和short-segment，臨床上後者較常見
- D. 可導致食道潰瘍及狹窄
- E. 病理切片有高度化生不良者(high grade dysplasia)有20%進展成癌症機會

### Correct Answer: B

A. 正確，Barrett’s metaplasia can progress to adenocarcinoma 

B. 錯誤，Barrett’s esophagus 進展成癌症的機率應為每年0.5%

C. 正確，Barrett’s esophagus 可分為  
  (1) 3 cm of Barrett's esophagus ("long-segment Barrett's esophagus")  
  (2) less than 3 cm of Barrett's esophagus ("short-segment Barrett's esophagus")  
  Short-segment 較常見

![](https://hackmd.io/_uploads/r16KFrRN2.jpg)

D. 正確，Chronic esophagitis and stricture 為GERD 的 complication  

E. 正確，high grade dysplasia有6-20%進展成癌症機會    
 
Ref:  
 * Harrison's Principles of Internal Medicine, 18ed, Chapter 232 Disease of the esophagus  
 * World J Gastroenterol 2011 October 7; 17(37): 4174-4183

## Question 47:

一位上腹悶痛患者接受胃鏡檢查，並於胃竇部(antrum)切片，其病理如圖，下列敘述何者為真？ (應選出所有正確答案)

![](https://hackmd.io/_uploads/rJ1C9BCE2.png)

(1)因為發炎在胃竇部，所以又稱A 型(type A)胃炎 
(2)容易因此而造成逆流性食道炎
(3)得到十二指腸潰瘍機會增加
(4)與胃淋巴瘤發生有關
(5)會隨時間增長而造成胃黏膜萎縮，且造成該胃炎之細菌量會因黏膜萎縮而增加 

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- A. (1)+(2)
- B. (2)+(3)
- C. (3)+(4)
- D. (4)+(5)
- E. (1)+(5)

### Correct Answer: C

(1) chronic gastritis 分為 
    
![](https://hackmd.io/_uploads/SkcksrC4h.png)

(2) 不會因此容易造成GERD

(3) H. pylori 和十二指腸潰瘍有關

(4) H. pylori 感染和胃淋巴瘤發生有關

(5) H. pylori 反而會因黏膜萎縮而減少

Ref: Harrison's Principles of Internal Medicine, 18ed, Chapter 232 Disease of the esophagus

## Question 48:

承上題，上述患者接受一個療程的抗生素治療，治療後停藥4 週，最合適用於確認治療成效的檢查為何？

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- A. serologic test
- B. urea breath test
- C. endoscopy
- D. histologic examination
- E. endoscopy plus histology

### Correct Answer: B

urea breath test often used to document successful eradication after therapy of H. 
pylori infection 

Ref: Washington manual chapter 18 Gastrointestinal disease 


