Pulmonary - Week 7 - Notes

Question 1

Define and describe the classification of pulmonary hypertension.

Answer 1

Pulmonary hypertension (PH) is defined by an elevation in mean pulmonary arterial pressure (mPAP)[cite: 4]. It is classified into 5 WHO Groups based on etiology/mechanism[cite: 4].

Question 2

Identify the etiology and explain the epidemiology of pulmonary hypertension.

Answer 2

Etiology varies by WHO Group (e.g.# Group 1: PAH# Group 2: Left heart disease# Group 3: Lung disease/hypoxia# Group 4: CTEPH)[cite: 5]. Epidemiology is variable across the groups[cite: 5].

Question 3

Describe the pathophysiology and microscopic features of vascular remodeling.

Answer 3

Vascular remodeling involves medial hypertrophy# intimal proliferation# and plexiform lesions in the pulmonary arteries# leading to increased pulmonary vascular resistance (PVR) and right ventricular strain[cite: 6].

Question 4

Explain clinical features of pulmonary hypertension.

Answer 4

Clinical features include progressive dyspnea (especially on exertion)# fatigue# chest pain# syncope# and signs of right heart failure (e.g.# peripheral edema# elevated JVP)[cite: 7].

Question 5

Discuss the evaluation of pulmonary hypertension.

Answer 5

Evaluation includes echo# V/Q scan# CT# and right heart catheterization (RHC) which is required for definitive diagnosis and measurement of mPAP[cite: 8].

Question 6

Explain the management of pulmonary hypertension.

Answer 6

Management includes treating the underlying cause# and specific therapies like pulmonary vasodilators (for Group 1 PAH) or pulmonary endarterectomy (for Group 4 CTEPH)[cite: 9].

Question 7

Describe the complications and prognosis of pulmonary hypertension.

Answer 7

The major complication is Right Ventricular Failure (Cor Pulmonale)[cite: 10]. Prognosis is generally poor without treatment# but has improved with modern therapies[cite: 10].

Question 8

Define and identify the etiology and epidemiology of cardiac and noncardiac pulmonary edema.

Answer 8

Pulmonary edema is the accumulation of fluid in the extravascular spaces of the lung[cite: 16]. Etiology is either Cardiogenic (elevated hydrostatic pressure due to left heart failure) or Noncardiogenic (increased capillary permeability due to alveolar-capillary barrier injury# e.g.# ARDS)[cite: 16].

Question 9

Compare non-cardiogenic pulmonary edema from cardiogenic in terms of pathophysiology# microscopic findings and clinical features.

Answer 9

Cardiogenic pathophysiology: elevated hydrostatic pressure# Microscopic: hemosiderin-laden macrophages (“heart failure cells”)# Clinical: Cardiomegaly# S3 gallop# perihilar edema on CXR[cite: 17]. Noncardiogenic pathophysiology: increased capillary permeability# Microscopic: hyaline membranes# Clinical: Normal heart size# patchy peripheral infiltrates on CXR[cite: 17].

Question 10

Define pulmonary embolism.

Answer 10

Pulmonary embolism (PE) is the obstruction of the pulmonary artery or one of its branches# most commonly by a thrombus originating from a deep vein thrombosis (DVT)[cite: 21].

Question 11

Identify the etiology and explain the epidemiology of thromboembolism.

Answer 11

Etiology is typically DVT# often associated with Virchow’s Triad (endothelial injury# stasis# hypercoagulability)[cite: 22]. Epidemiology is common# with incidence increasing with age[cite: 22].

Question 12

Describe the pathophysiology# pathology and clinical features of thromboembolism and infarction.

Answer 12

Pathophysiology: obstruction leads to increased PVR# RV overload# and V/Q mismatch[cite: 23]. Pathology: Infarcts (rare) are typically hemorrhagic and wedge-shaped[cite: 23]. Clinical: Sudden onset dyspnea# pleuritic chest pain# tachypnea# or circulatory collapse (massive PE)[cite: 23].

Question 13

Explain the evaluation and management of embolism.

Answer 13

Evaluation: CT Pulmonary Angiography (CTPA) is the gold standard[cite: 24]. Management: Anticoagulation (e.g.# LMWH# DOACs) is the mainstay# thrombolysis or embolectomy for unstable PE[cite: 24].

Question 14

List the complications and differential diagnosis of pulmonary embolism and infarction.

Answer 14

Complications include acute RV failure# shock# and Chronic Thromboembolic Pulmonary Hypertension (CTEPH)[cite: 25].

Question 15

Describe the prognosis of pulmonary embolism.

Answer 15

Prognosis is highly dependent on the severity and hemodynamic stability at presentation (massive PE has the worst prognosis)[cite: 26].

Question 16

Explain and distinguish the etiology# pathophysiology# clinical features# evaluation# and management of Nonthrombotic pulmonary embolism: Fat embolism.

Answer 16

Etiology: Typically follows long bone fractures[cite: 34]. Pathophysiology: Mechanical obstruction by fat globules and toxic/inflammatory injury[cite: 34]. Clinical: FES triad (respiratory insufficiency# neurologic dysfunction# petechial rash) 12-72 hrs post-injury[cite: 34# 39]. Management: Supportive care (oxygen# ventilation)[cite: 34].

Question 17

Explain and distinguish the etiology# pathophysiology# clinical features# evaluation# and management of Nonthrombotic pulmonary embolism

Answer 17

Gas embolism.#Etiology: Iatrogenic (central lines# surgery) or decompression sickness[cite: 35]. Pathophysiology: Gas bubbles cause mechanical obstruction[cite: 35]. Clinical: Acute cardiopulmonary collapse[cite: 35]. Management: 100% oxygen# left lateral decubitus/Trendelenburg position# Hyperbaric Oxygen Therapy (HBOT)[cite: 35].

Question 18

Describe the classification of pulmonary vasculitis in terms of ANCA and non-ANCA associated small vessel vasculitis.

Answer 18

Small vessel vasculitis is classified into ANCA-associated (e.g.# GPA# MPA) and non-ANCA-associated (e.g.# Goodpasture Syndrome)[cite: 42].

Question 19

Compare and contrast pathogenesis# pathologic findings# and clinical features of the ANCA related small vessel vasculitis.

Answer 19

Pathogenesis involves ANCA activating neutrophils and causing endothelial injury[cite: 43]. Pathologic findings are necrotizing capillaritis that is “pauci-immune”[cite: 43]. Clinical features often present as a Pulmonary-Renal Syndrome[cite: 43].

Question 20

Compare granulomatosis with polyangiitis with Goodpasture syndrome in terms of pathogenesis and clinical features.

Answer 20

GPA (Wegener’s) pathogenesis involves ANCA (anti-PR3/c-ANCA)[cite: 44]# Clinical: Upper airway# lung# and kidney involvement[cite: 44]. Goodpasture pathogenesis involves Anti-GBM antibodies[cite: 44]# Clinical: Pulmonary-renal syndrome[cite: 44].

Question 21

Describe the diagnostic approach to vasculitis.#Diagnosis involves clinical presentation# serology (ANCA# Anti-GBM)# and biopsy (lung or kidney)[cite: 45].

Question 22

Explain the treatment of vasculitis.#Treatment is immunosuppression# typically with high-dose glucocorticoids plus cyclophosphamide or rituximab[cite: 46].

Question 23

Define and illustrate the different types of atelectasis with examples.#Atelectasis is the incomplete expansion or collapse of a part of the lung[cite: 56]. Types include Resorption/Obstructive (e.g.# mucous plug)# Compression (e.g.# pleural effusion)# Contraction/Cicatrization (e.g.# pulmonary fibrosis)# and Patchy (e.g.# ARDS)[cite: 56].

Question 24

Describe the etiology and pathophysiology of flail chest.

Answer 24

Etiology is severe blunt chest trauma[cite: 61]. Pathophysiology is three or more consecutive ribs fractured in two or more places# causing a free-floating segment that moves paradoxically (inward on inspiration)[cite: 61].

Question 25

Describe the clinical features and evaluation of flail chest.

Answer 25

Clinical features include the hallmark paradoxical movement of the chest wall# severe localized pain# and dyspnea[cite: 62]. Evaluation uses clinical exam# CXR# and CT to assess fractures and associated pulmonary contusion[cite: 62].

Question 26

Explain the management# complications and prognosis of flail chest.

Answer 26

Management is primarily supportive: aggressive pain control# pulmonary hygiene# and often mechanical ventilation[cite: 63]. Complications include hypoxia# pneumonia# and severe pulmonary contusion[cite: 63]. Prognosis depends mainly on the severity of the underlying lung injury[cite: 63].

Question 27

Define and describe the classification of pulmonary hypertension

Answer 27

Pulmonary hypertension is classified into five groups: pulmonary arterial hypertension (PAH)# PH due to left heart disease# PH due to lung diseases/hypoxia# chronic thromboembolic PH# and PH with unclear multifactorial mechanisms.

Question 28

Identify the etiology and explain the epidemiology of pulmonary hypertension

Answer 28

Etiologies include idiopathic PAH# connective tissue diseases# congenital heart disease# portal hypertension# HIV# and drugs; prevalence varies by subtype# with PAH being rare but more common in females.

Question 29

Describe the pathophysiology and microscopic features of vascular remodeling in PH

Answer 29

Vascular remodeling involves intimal proliferation# medial hypertrophy# adventitial fibrosis# and plexiform lesions leading to increased pulmonary vascular resistance.

Question 30

Explain clinical features of pulmonary hypertension

Answer 30

Symptoms include dyspnea on exertion# fatigue# chest pain# syncope; signs include loud P2# right ventricular heave# and jugular venous distension.

Question 31

Discuss the evaluation of pulmonary hypertension

Answer 31

Evaluation includes echocardiography# right heart catheterization# pulmonary function tests# V/Q scan# CT angiography# and serologic tests for underlying causes.

Question 32

Explain the management of pulmonary hypertension

Answer 32

Treatment includes vasodilators (e.g.# endothelin receptor antagonists# PDE-5 inhibitors)# oxygen therapy# anticoagulation# and lung transplantation in advanced cases.

Question 33

Describe the complications and prognosis of pulmonary hypertension

Answer 33

Complications include right heart failure# arrhythmias# hemoptysis; prognosis depends on etiology and response to therapy# with idiopathic PAH having poor outcomes.

Question 34

Define and identify the etiology and epidemiology of cardiac and noncardiac pulmonary edema

Answer 34

Pulmonary edema is fluid accumulation in alveoli; cardiogenic causes include left heart failure# while noncardiac causes include ARDS# high altitude# neurogenic injury; epidemiology varies by cause.

Question 35

Compare non-cardiogenic pulmonary edema from cardiogenic in terms of pathophysiology# microscopic findings and clinical features

Answer 35

Cardiogenic edema shows transudate with alveolar fluid and engorged capillaries; non-cardiogenic shows exudate# hyaline membranes# and inflammatory infiltrates; clinical features differ in onset and associated conditions.

Question 36

Define pulmonary embolism

Answer 36

Pulmonary embolism is obstruction of pulmonary arteries by thrombus# usually from deep veins of the legs.

Question 37

Identify the etiology and explain the epidemiology of thromboembolism

Answer 37

Etiology includes DVT# hypercoagulable states# surgery# trauma; PE is common in hospitalized patients and major cause of sudden death.

Question 38

Describe the pathophysiology# pathology and clinical features of thromboembolism and infarction

Answer 38

PE causes ventilation-perfusion mismatch# increased pulmonary artery pressure# and right heart strain; infarction shows hemorrhagic wedge-shaped lesions; symptoms include dyspnea# chest pain# hemoptysis.

Question 39

Explain the evaluation and management of embolism

Answer 39

Diagnosis via D-dimer# CT pulmonary angiography# V/Q scan; management includes anticoagulation# thrombolysis# and supportive care.

Question 40

List the complications and differential diagnosis of pulmonary embolism and infarction

Answer 40

Complications include pulmonary infarction# chronic thromboembolic PH; differentials include pneumonia# MI# pericarditis# pneumothorax.

Question 41

Describe the prognosis of pulmonary embolism

Answer 41

Prognosis depends on clot burden# right heart function# and prompt treatment; massive PE has high mortality.

Question 42

Explain and distinguish the etiology# pathophysiology# clinical features# evaluation# and management of fat embolism

Answer 42

Fat embolism occurs after long bone fractures; fat globules enter circulation causing mechanical obstruction and inflammation; symptoms include hypoxia# petechiae# neurologic signs; diagnosis is clinical; management is supportive.

Question 43

Explain and distinguish the etiology# pathophysiology# clinical features# evaluation# and management of gas embolism

Answer 43

Gas embolism arises from trauma# surgery# or diving; air enters venous system causing obstruction; symptoms include dyspnea# chest pain# neurologic deficits; diagnosis via imaging; treatment includes hyperbaric oxygen.

Question 44

Describe the classification of pulmonary vasculitis in terms of ANCA and non-ANCA associated small vessel vasculitis

Answer 44

ANCA-associated includes granulomatosis with polyangiitis (GPA)# microscopic polyangiitis (MPA); non-ANCA includes Goodpasture syndrome# IgA vasculitis.

Question 45

Compare and contrast pathogenesis# pathologic findings# and clinical features of the ANCA related small vessel vasculitis

Answer 45

GPA shows necrotizing granulomas and upper/lower respiratory involvement; MPA lacks granulomas; both show glomerulonephritis and systemic symptoms.

Question 46

Compare granulomatosis with polyangiitis with Goodpasture syndrome in terms of pathogenesis and clinical features

Answer 46

GPA: ANCA-mediated# granulomatous inflammation# sinusitis# hematuria; Goodpasture: anti-GBM antibodies# alveolar hemorrhage# glomerulonephritis.

Question 47

Describe the diagnostic approach to vasculitis

Answer 47

Includes ANCA testing# renal biopsy# imaging (CT# CXR)# bronchoscopy with lavage# and serologies.

Question 48

Explain the treatment of vasculitis

Answer 48

Treatment includes corticosteroids# immunosuppressants (cyclophosphamide# rituximab)# and plasmapheresis in severe cases.

Question 49

Define and illustrate the different types of atelectasis with examples

Answer 49

Atelectasis is lung collapse; types include resorption (e.g.# mucus plug)# compression (e.g.# pleural effusion)# contraction (e.g.# fibrosis)# and microatelectasis (e.g.# surfactant deficiency).

Question 50

Describe the etiology and pathophysiology of flail chest

Answer 50

Flail chest results from multiple rib fractures causing paradoxical chest wall movement; leads to impaired ventilation and hypoxia.

Question 51

Describe the clinical features and evaluation of flail chest

Answer 51

Features include chest pain# respiratory distress# paradoxical movement; evaluation via physical exam and imaging (CXR# CT).

Question 52

Explain the management# complications and prognosis of flail chest

Answer 52

Management includes pain control# oxygen# mechanical ventilation; complications include pneumonia# ARDS; prognosis depends on severity and comorbidities.