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Anwser,s Dr :ANAS SAHLE 1. Chest xr cases. 2. Chest clinical case. 3. Chest ct cases. 4. Collicum exam. :http://www.facebook.com/dranas224 7/3/22
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Page 1: Anwser,s7

Wednesday, April 12, 2023

Anwser,sDr :ANAS SAHLE

1. Chest xr cases.2. Chest clinical case.

3. Chest ct cases.4. Collicum exam.

:http://www.facebook.com/dranas224

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chest xr casesDr :anas sahle

http://www.facebook.com/dranas224

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CXR-26-a

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CXR26-b

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CXR26-c

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CXR26-dDiagnosis for CXR26 is: Ankylosing Spondylitis

Bamboo spine

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CXR27

Diagnosis is: Aneurysm Arch of Aorta

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CXR28-a

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CXR28-b

Old film

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Wednesday, April 12, 2023

CXR28:Aneurysm Arch of Aorta

Leaking Blood into Pleural Space • Mediastinal mass • Calcification of periphery evident along upper margin • Loss of silhouettes of

– aortic knob– left heart margin– left diaphragm

• Left pleural effusion • Tracheal indentation

• Lateral view• Middle mediastinal mass • Calcification of periphery in lateral view • left diaphragm not visible due to fluid in pleural space

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CXR29

Diagnosis is: Pectus Excavatum

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Pectus Excavatum

• Indistinct right heart margin. • Vague density in right lower lung field• Lateral view • reveals protruding sternum and flattening

heart

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CXR30-a

Diagnosis is: Pulmonary Sequestration

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CXR30-b

Aortogram

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CXR30-c

Aortogram

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Pulmonary Sequestration

• Anomalous Arterialization of Lung:• Increased vascular markings at right base• Smaller right pulmonary artery

Big anomalous artery arising from aorta supplying right lung

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chest clinical casesDry Cough and Clubbing in a 45-Year-Old Woman

Submitted byJamie L. Garfield, MDFellowPulmonary and Critical Care MedicineTemple University School of MedicinePhiladelphia, PennsylvaniaVictor Kim, MDAssistant Professor of MedicineTemple University School of MedicinePhiladelphia, Pennsylvania

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History• A 45-year-old white female presents to pulmonary clinic for evaluation of increasing chest

tightness, cough and dyspnea. • She has a history of chronic respiratory symptoms since childhood and frequent exacerbations of

bronchitis, but no history of respiratory failure. • She reports that until 1 year ago she was limited by mild pleuritic chest tightness and shortness

of breath with heavy exertion. • She now reports daily symptoms of fatigue, dyspnea, and exercise intolerance with minimal

exertion. • She has persistent dry cough and occasionally expectorates granular mucus. • She has been using 3 liters per minute of supplemental oxygen via nasal cannula for the past

year.• Her past medical history is significant for polycythemia, gastroesophageal reflux disease,

fibronodular breast disease, chronic tinnitus with hearing loss and genital herpes. • Her current medications include famotidine, diltiazem, valacyclovir, inhaled fluticasone,

salmeterol and albuterol. • She has a 30 pack-year smoking history, having quit smoking 5 years ago. • She drinks 1-2 beers per week and she denies illicit drug use. • She is a homemaker and reports no occupational exposures. • Her parents, siblings and 2 children (ages 16 and 24) are alive and well with no respiratory

disease or malignancy.

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Physical Exam• her heart rate is elevated at 112 beats per minute. • Oxygen saturation on 2 liters of oxygen via nasal cannula is

89%. • Her vital signs are otherwise normal. • Her head and neck exam is benign. • Her pulmonary exam is significant for diffuse inspiratory and

expiratory dry crackles, more prominent at the bases bilaterally.

• Cardiac exam reveals regular rhythm with no murmurs, rubs or gallops.

• There is clubbing but no cyanosis or edema of her extremities.

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Lab • White blood cell count 12,900/mm3, • Hemoglobin 15.5 mg/dl, • Platelet count 473,000/mm3.• BUN 9 mg/dl, creatinine 1.0 mg/dl, • calcium 8.8 mg/dl and phosphate 4.9 mg/dl.• PT, PTT, electrolytes, glucose and liver function tests

were within normal limits.• Arterial blood gas on 3L/min supplemental oxygen

revealed a – pH of 7.39, PCO2 40 mm Hg and PaO2 62 mm Hg.

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Studies

• Echocardiogram: – left ventricular ejection fraction was 55-65% and – grade 1 diastolic dysfunction was noted; – right ventricle was mildly dilated and had mildly depressed systolic function; – pulmonary artery systolic pressure was estimated to be 48-52 mm Hg; right atrium was mildly

dilated and there was mild tricuspid regurgitation.

• Cardiac Catheterization: PAP: 30/6/13; PCWP: 2; CO: 3.38; CI: 2.16.

• Pulmonary Function Tests: – FEV1/ FVC: 74%;

– FEV1: 0.96 L, 39%; – FVC: 1.29L, 42%; – TLC: 2.27L, 53%; RV: 1.14L, 79%; DLCO: 3.11L, 57%.

• 6-Minute Walk Test: – Resting SpO2: 86% RA; 92% on 2L/min; 8L/min was required to maintain oxygen saturation

above 90% – at the end of 6 minutes; the patient was able to walk 211 meters.

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CXR

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Coronal view of high-resolution chest CT

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Bronchoalveolar lavage

Slightly mucoid, tan fluid; cultures revealed no growth; cytology showed no evidence of malignancy; a few white blood cells were noted, predominantly macrophages; laminated calcified concretions and debris were also present. Von Kossa stain positive.

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Question 1• What is the most likely diagnosis?• A. Idiopathic pulmonary fibrosis • B. Pulmonary alveolar proteinosis • C. Diffuse alveolar hemorrhage syndrome • D. Pulmonary alveolar microlithiasis • E. Broncheoloalveolar carcinomatosis

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Pulmonary Alveolar Microlithiasis (PAM) • is a rare disorder of unknown etiology in which microliths occupy the alveolar space (1). • The mean age of diagnosis is in the fourth decade of life, although the onset of disease may occur

in childhood (2, 3).• Idiopathic pulmonary fibrosis (IPF) tends to present later in life than PAM. • Dyspnea and hypoxemia are common to both disease entities, but the honeycombing classically

seen on HRCT in IPF would not be expected in PAM.• Pulmonary alveolar proteinosis (PAS), another alveolar filling disorder, is also a rare but deadly

entity. • Patients with PAS may have dry crackles and clubbing as in PAM. • The patchy ground glass opacities with a “crazy-paving” pattern described in PAS can usually be

distinguished from the microcalcifications seen on HRCT in PAM. Rarely, “crazy-paving” can be seen in PAM (4).

• Bronchoalveolar carcinomatosis can radiographically mimic many diseases with alveolar infiltrates. • Classically this condition is less diffuse than PAM, and as such, hypoxemia and diffusion impairment

are less common.• Diffuse alveolar hemorrhage (DAH) can present with hypoxia and diffuse alveolar infiltrates similar

to PAM. • The onset of DAH is usually more abrupt than PAM. • While frank hemoptysis can be absent in up to one third of DAH cases, hemosiderin-laden

macrophages are commonly found in BAL.

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Question 2• Which of the following statements is true regarding

pulmonary alveolar microlithiasis?• A. Dyspnea is described in proportion to the severity of the

radiographic abnormalities. • B. The diagnosis can only be made by lung biopsy

demonstrating microliths within the alveoli. • C. Pathologically, the lungs are soft and boggy. • D. Familial disease is inherited in an autosomal dominant

fashion. • E. PAM is found in all geographic regions, across all races,

and equally between men and women.

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PAM• is present on all continents with no particular geographic or racial distribution, is reported

equally in males and females, and has been described in all age groups, but most frequently from birth to age 40.

• A family history was noted in 37% of patients in one large review .• Simultaneous cases of PAM have been described in siblings, supporting an autosomal

recessive inheritance pattern.• A hallmark feature of PAM is the striking dissociation between clinical and radiographic

findings. • Often there is extensive radiographic evidence of disease and only mild symptomatology• Children that present with PAM are often asymptomatic.• The diagnosis can often be made in the absence of a biopsy, with radiographic imaging

demonstrating the classic “sand-storm” appearance. • Bronchoalveolar lavage may demonstrate laminated calcified concretions. • Diagnosis can be confirmed with open, transbronchial or transthoracic needle biopsy. • Histologically, the characteristic finding is that of bluish-violet bodies of varying shape and

sizes, many of which are fissured with radial cracks .• On gross pathology, lungs are hard and gritty and do not collapse upon removal from

thorax .

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Question 3• PAM may be associated with all of the

following conditions/exposures EXCEPT which of the following?

• A. Milk-alkali syndrome • B. Calcium containing powdered tobacco • C. Inflammatory bowel disease • D. Printing ink • E. Renal transplant

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discussion• PAM has been described in many patients with no discernable risk

factors for the disease. • An increased risk of PAM has been reported in individuals with

exposure to printing ink and among those with a history of smoking powdered tobacco containing calcium salts .

• Systemic diseases associated with calcium and phosphate deregulation, such as milk-alkali syndrome renal transplant and nephrolithiasis have been linked to PAM.

• It is not known if these associations are causational or coincidental.

• Inflammatory bowel disease, while can be associated with electrolyte abnormalities related to malabsorption, has not been described in patients with PAM.

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Question 4• Which of the following signs/symptoms

is not commonly associated with PAM?• A. Pleural plaques • B. Pneumothorax • C. Hemoptysis • D. Lithoptysis • E. Emphysema

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discussion

• On gross pathology, the pleural surfaces are generally free, though appear granular owing to the sand-like particles that can be seen and felt beneath.

• Pleural plaques are not commonly seen in PAM .• Emphysematous blebs are commonly seen in patients

with PAM and may represent early lung fibrosis. • Pneumothorax resulting from bleb rupture is not rare .• Some patients report coughing up blood, while others

describe lithoptysis, or expectorating granular-like mucus or microliths with coughing.

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Question 5• Which of the following statements is FALSE regarding the

underlying pulmonary process in this patient?• A. Microliths are derived from the alveolar capillary blood and not a

result of pathological changes in the tissue cells of the alveoli. • B. Inborn errors in metabolism at the alveolar interface leads to

local accumulation of calcium salts. • C. Alveolar hemorrhage is commonly associated with this disease. • D. PAM usually occurs in patients without evidence of systemic

derangement in calcium metabolism. • E. Dysfunction of SLC34A2 may reduce the clearance of phosphate

leading to the formation of microliths.

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discussion• The metabolic abnormality in PAM results in precipitation of calciferous salts in an otherwise

normal alveolus. • The components of the microliths are therefore thought to be derived from the alveolar

capillary blood and not a result of pathological changes in the tissue cells of the alveoli .• It has been suggested that inborn errors in metabolism at the alveolar interface lead to

increased alkalinity or mucopolysaccharide deposition, promoting the local accumulation of calcium salts.

• Studies of calcium metabolism in affected patients have been consistently normal, suggesting it is unlikely that PAM is due to a systemic derangement of calcium metabolism .

• Hemoptysis is not uncommon in PAM when inspissated microliths irritate and erode bronchial epithelium. Diffuse alveolar hemorrhage, however, is not known to be associated with PAM.

• Homozygous inactivating mutations in the SLC34A2 gene, are present in patients with PAM. • SLC34A2 encodes a sodium phosphate transporter that is highly expressed in alveolar type II

cells. • Normally, type II alveolar cells recycle and degrade surfactant and subsequently release

phosphate into the alveolar space. • Dysfunction of this sodium phosphate transporter may reduce the clearance of phosphate

from the alveolar space, thereby leading to the formation of microliths .

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Question 6• Treatment for PAM currently includes all

of the following except?• A. Bilateral lung transplant • B. Gene replacement therapy • C. Whole lung lavage • D. Systemic steroids • E. Dibisphosphonates

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discussion• Various treatment regimens have been explored for PAM, most of which have

not altered the natural course of the disease. • Borrowing from the therapeutic strategy for PAS, whole lung lavage has been

tried without success in patients with PAM. • Systemic corticosteroids and bisphosphonates have also been used but fail to

preserve lung function or improve symptoms. • Bilateral lung transplant remains the only option for patients with severe

symptoms related to PAM . • There remains very little information on long term survival and whether the

disease will return in the donor lungs .• As more is learned about the SLC34A2 gene and its role in PAM, there is growing

interest in the possibility of gene replacement therapy to treat PAM .• While this therapy is not available today, early data suggest that targeting

phosphate rather than calcium metabolism may be beneficial for the treatment of PAM.

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chest ct cases-6Dr :anas sahle

http://www.facebook.com/dranas224

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HRCT-1

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HRCT-1

• What is the distribution of the abnormal densities?

• a) Bronchovascular• b) Interlobular septal• c) Pleural• d) Centrilobular

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HRCT-1

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HRCT-1

• Find an example in the right lung of combined bronchovascular and interlobular septal thickening with distortion of the architecture.

• Find an example in the left lung of thickened bronchovascular interstitium.

• Find a centrilobular nodule, representing thickening of the terminal bronchiolovascular interstitium, in the left lung.

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HRCT-1

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Gross Appearance

This slice of lung shows vessels, bronchi, and enlarged lymph nodes.

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• Find lymph nodes. • Find the main pulmonary artery. • The adjacent thinner-walled vessel is the vein.• Find and outline a longitudinally-cut, segmental

bronchus with thickened bronchovascular interstitium that narrows the lumen.

• This bronchovascular interstitial involvement corresponds to that seen in the HRCT image above.

• Architectural distortion may result.• Find other airways cut in cross-section that are also

narrowed.

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Gross Appearance

This slice of lung shows vessels, bronchi, and enlarged lymph nodes.

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Histologic Appearance

This picture shows thickening of the interstitium.

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• Find an airway and name its type.• Find the accompanying pulmonary artery

branch.• Find and identify 5 rounded, interstitial,

cellular structures.• Find and identify the composition of the pink

matrix.

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Histologic Appearance

This picture shows thickening of the interstitium.

Bronchiole (airway has no cartilage)

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Differential diagnosis

• Differential diagnosis of nodular bronchovascular and interlobular septal thickening on HRC:............

• Histologic differential diagnosis:………

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Differential diagnosis

• Differential diagnosis of nodular bronchovascular and interlobular septal thickening on HRC:

–Sarcoidosis.–lymphangitic tumor. –Lymphoma. –Kaposi's sarcoma

• Histologic differential diagnosis:………

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Differential diagnosis

• Differential diagnosis of nodular bronchovascular and interlobular septal thickening on HRC:

–Sarcoidosis.– lymphangitic tumor. –Lymphoma. –Kaposi's sarcoma

• Histologic differential diagnosis: – Infectious granulomatous disease (tuberculous

or fungal).–hypersensitivity pneumonia.– reaction to tumor or drug should be considered.

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Diagnosis:

Chronic sarcoidosis

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Summary of diagnostic features of sarcoidosis on HRCT

• Bronchovascular, interlobular septal and pleural thickening

• Upper lung predominance common • Architectural distortion frequent

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04/12/202357

Collicum EXAMRespiratory

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A1 الذى لم تقترحه ما هو الصاد الحيوي•

عند تطبيق IDSA 2002توصيات. معالجة ذات رئة في مرضى لديهم

Neutropeniaسرطان مع نقص عدالت•Cefepime .A•Ceftazidime .B•Imipenem .C•Meropenem .D•Tazobactam and Piperacillin sodium .E

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A2 ق • من المقترحة الخطة هي IDSA. 2002لبما

لديهم مرضى في رئة ذات معالجة عند: عدالت نقص مع عند Neutropeniaسرطانالتخبرية الفموية المعالجة empiricalتطبيق

•Amoxicillin-clavulanate + Moxifloxacin .A•Amoxicillin-clavulanate + Ciprofloxacin .B•Amoxicillin-clavulanate + Levofloxacin .C•Amoxicillin-clavulanate + Azithromycin .D•Cefixime .E

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A3 أي من األمراض التالية يجب عزل •

المريض ؟.Aالسل الرئوي.Bخراجة الرئة.Cذات الرئة بالعقديات.Dذات الرئة بالمكورات الرئوية.E .ذات الرئة بالحمضات

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A4 استخدامها • يمكن التالية األدوية من أي

لمعالجة الحمل من األول الثلث خالل : ناجمة مختلطة فطريةغير رئة ذات

coccidioidalعن• .Amphotericin-B .A•Caspofungin .B•.Fluconazol .C•.Voriconazole .D

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A5 عمرها • سوابق 40مريضة وبدون مدخنة غير سنة،

أسبوعين من شكت مهمة، منتج مرضية سعال منظهر رفيعة دموية خيوط مع مترافق قيحي مخاطي

شديد زكام بعد . d حاليdا تشكو الصدر صورة كذلك طبيعي السريري الفحص

التوصيات هي ما بالصدر، حارق ألم ؟ من المقترحة.A للصد محوري رطبقي.B الرئوي السل لنفي للقشع جرثومي فحص.C قصبي تنظير.D فقط المراقبة.E.إعطائهاPrednisone

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A6 متوسطة، 63مريض • حرارة منتج، بسعال راجع كحولي، سنةالصدر • صورة في :أظهرت متجانس غير رئوي تكثف وجود

قليل جنب انصباب مع األيسر السفلي المقدار الفصنتحي • كان للسائل الكيماوي exudate،الفحص•: أن ذلك أفسر

.A .مرافق جنب انصباب مع رئة ذات لديه المريضparapneumonicلإلنتان

.B بفحص إال إنتان بوجود أجزم أن أستطيع الجنب PHال سائل

.C . السائل كولسترول بفحص إال إنتان بوجود أجزم أن أستطيع ال

.D الثالثية الشحوم بفحص إال االنصباب سبب أجزم أن أستطيع البالسائل.

.E السائل سكر بفحص إال إنتان بوجود أجزم أن أستطيع ال

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A7 بانصباب. • يتعلق فيما احتماال األقل الخيار هو ما

الجنب:.A كبدية خراجة تمزق عند يشاهد الغامق األصفر اللون

الجنب amebic liver abscessزحارية إلى.B الرشاشيات عن الناجم أسود vا غالب لونه .Aspergillusيكون.C الداء في الغالب على يشاهد المخضر األصفر اللون

الرثياني ..D الكيلوسي حليبي أبيض لون ذو .Chylothoraxيكون.E في يشاهد االحتشاء pulmonary infarctionالمدمى

الرئوي

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A8 •: يلي فيما الخاطئ الخيار هو ما

.A الذأب في متدنية حدود إلى الجنب سكر ينخفض أن يمكن lupus pleuritisالجنبي

.B انخفاض يشكل الصدر LDHال تبلون في Urinothoraxالجنب.. سريريه أهمية

.C النقوي الورم في الجنب بروتين يرتفع أن الشائع من ليسعالية المتعدد لألرقام

.D يرتفع ما ~ا إلى LDHغالب يصل قد كبير بشكل 1000الجنبIU/LD الجنب تقيح .في

.E في حاد بشكل المدرات إعطاء عند الجنب بروتين يرتفع قداالحتقاني القلب congestive heart failureقصور

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A9 عمرها • قصور 65مريضة لديها أول، نمط سكرية سنه،

لها أجري خفيف، مزمن إكليلي كلية جراحي عملبعد • مدمى جنب انصباب مع تامور انصاب لديها تطور

الجراحةاحتما • األكثر التفسير أن أعتقد ،dال: حدوث هو

.ACardiac tamponade قلبي سطام.B.Dressler's syndrome درسلر تناذر.CPulmonary Embolus رئوية صمة.D . معvا والقلب الكلية قصور بسبب وعائي حمل فرط.E . اإلكليلي التداخل اختالطات

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A10 احتما • األقل الخيار أن بأسباب لأعتقد يتعلق بما dا

النتحي الجنب الظروف انصباب بعض في الذي: d نتعيا يكون قد

.A اإلنسدادي . اإلنخماص قصبي ورم عن الناجمobstructive atelectasis

.B . قلب قصور مع المترافقة الرئوية الخباثات

.C . Nephrotic syndrome. النفروزي التناذر.DPulmonary Embolus. الرئوية الصمة.E قصور سياق في القلبية العضلة اعتالل

Hypothyroidالدرق

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