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Respiratory > Pulmonary Vascular Disease > Flashcards

Pulmonary Vascular Disease Flashcards

1
Q

Acute Pulmonary Embolism – Venous Thromboembolism

  • What are the characteristics and recognized risk factors?
A
  • Common
  • Often Fatal
  • Idiopathic
  • Recognized Risk Factors: Thrombophilias
  • Many Preventable !
    • DVT prophylaxis
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2
Q

Where do the majority of PEs originate?

A
  • 60-90% of PE originate in proximal deep veins of the legs
    • Calf vein thrombus – problem if propagates
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3
Q

What is Virchow’s Triad?

A
  1. Stasis
  2. Injury
  3. Hypercoagulability
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4
Q

What are the risk factors for venous thromboembolism?

A
  • Virchow’s Triad
  • Thrombophilias: Prot C, S, ATIII, Factor V Leiden, Prothrombin gene mutation, MTHFR; Factor VIII
  • Medical Risks:
    • Hip, Knee Surgery
    • Immobility
    • CHF, Obesity
    • Malignancy ( may be cause of “Idiopathic VTE”)
    • Acquired Hypercoagulability
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5
Q

Pulmonary Embolism

Natural History

A
  • 30% Mortality if untreated
  • 2.5% In-Hospital Mortality, due to
    • Recurrent, Acute PE
    • Massive Obstruction of Vessels
    • RV Failure, Infarct
  • Vast Majority will resolve with treatment
  • 1-3% with Chronic PE
    • Main Risk Factor: Recurrent Events
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6
Q

What symptoms are associated with PE?

A

Nonspecific

  1. Dyspnea; Acute or Subacute
  2. Dizziness, Syncope:
    • Large PE, Massive, “Saddle”
  3. Chest Pain – Pleuritic, (Infarct, Bloody Effusion)
  4. Palpitations, Tachycardia
  5. Hemoptysis (infarct)
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7
Q

What methods are used to diagnose a venous thromboembolism (DVT & PE)?

A
  • DVT:
    • Doppler Ultrasound (US)
  • PE:
    • Ventilation perfusion scans
    • CT pulmonary angiogram
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8
Q

How is a PE identified on a ventilation perfusion lung scan?

A

Mismatched Perfusion defects

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9
Q

Diseases in Group IV Pulmonary Hypertension:

  • What characterizes this classification?
A

Chronic Thrombotic, Embolic Diseases

  • Thromboembolic obstruction of proximal pulmonary arteries
    • Surgical candidates
  • Obstruction of distal pulmonary arteries too
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10
Q

**Pulmonary Hypertension: Chronic Disorders **

Classification (Groups I-V)

A
  1. Pulmonary Arterial Hypertension
    • “Pre-Capillary “ by Catheterization and not III, IV, V
  2. Pulmonary Venous Hypertension
    • Ex: Common Left Heart Disease
  3. Pulm HTN: Respiratory Disorders (FVC < 70%)
  4. Pulm HTN: Thromboembolic Disorders
  5. Pulm HTN: Miscellaneous (Ex:Sarcoidosis)
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11
Q

Define Group I PAH:

A
  • Criteria:
    • Mean pulmonary arterial pressure (mPAP) >25 mm Hg at rest
    • normal wedge pressure (PCWP)
      • PCWP ⇒ estimates left heart filling pressure
    • “pre-capillary” pattern
  • not Groups III, IV, or V
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12
Q

What are the etiologies of Group I Pulmonary Arterial Hypertension (“Pre-capillary”)?

A
  • Idiopathic = IPAH (“Primary = PPH”)
  • Heritable (BMPR2 Genetic Mutations, Others):
    • The “Keyhole” to the Disease
  • Associated with: APAH
    • CVD (Scleroderma, SLE, RA),
    • Congenital Heart Disease,
    • Portal Hypertension, HIV, Drugs, Other Disorders
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13
Q
  • How would pulmonary HTN present on an echocardiogram?
  • Why is this test used?
  • What correlates with prognosis?
A
  • Best noninvasive test for diagnosis of PH
  • Right atrial and Right Ventricular Changes
    • Right Ventricular Overload
  • Estimate PA Pressure
  • Look for:
    • Congenital Ht Dis; PFO; shunt (bubble study)
  • Pericardial Effusion: Prognosis
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14
Q

How is the prognosis determined in pulmonary HTN?

A
  • Decreased RV function:
    • RA P> 10 mmHg, CI < 2.2 L/min m2
    • POOR PROGNOSIS ⇒ Elevated RAP and low CO parameters
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15
Q

How do BMPR-2 mutations play a role in PAH?

A
  • 10% IPAH (PPH) is familial , heritable
  • Mapped to long arm chromosome 2: 2q31-32
  • Bone Morphogenic Protein Receptor-2 (BMPR2)
    • Deng, et al 2000
    • ~55% familial PHT have mutations in this gene
    • Autosomal dominant with low penetrance
    • TGF-ß superfamily of receptors
    • **Exon mutations **⇒ Stop codons, but more than 40 distinct mutations identified to date
    • 25% Sporadic IPAH (PPH) have BMPR2 mutations
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16
Q

NYHA/WHO Functional Assessment of Pulmonary Arterial Hypertension

  1. Class 1:
  2. **Class 2: **
  3. **Class 3: **
  4. **Class 4: **
A
  1. Class 1:
    • Symptoms do not limit physical activity.
    • Ordinary physical activity does not cause undue discomfort
  2. **Class 2: **
    • Slight limitation of physical activity
    • The patient is comfortable at rest, yet experiences symptoms with ordinary physical activity
  3. Class 3:
    • Marked limitation of physical activity
    • The patient is comfortable at rest, yet experiences symptoms with minimal physical activity
  4. Class 4:
    • Inability to carry out any physical activity.
    • The patient may experience symptoms even at rest.
    • Discomfort is increased by any physical activity.
    • These patients manifest signs of right heart failure
17
Q

What are the symptoms of pulmonary HTN?

A
  • **Breathlessness **
  • Fatigue
  • Near Syncope, Syncope (suggestive if particularly with exertion in young adult)
  • Chest Pain: Angina
  • Palpitations
18
Q

What is the pathophysiology of Group I PAH?

A
  • Large Pulm. Artery Thickening
  • Medial Wall Smooth Muscle Hypertrophy
  • “Plexiform” Lesion in small vessel
    • Specific to GROUP I PAH diseases
19
Q

What defects lead to the pathophysiology seen in pulmonary HTN?

A
  • ENDOTHELIAL CELL DEFECTS
    • Decreased Prostacyclin
    • Increased Endothelins
    • Decreased Nitric Oxide Synthase
  • PLATELET DEFECTS
    • Thromboxane
    • Serotonin
  • SMOOTH MUSCLE CELLS
    • Distal muscularization
  • CONNECTIVE TISSUE MATRIX
  • GENETIC STUDIES (Familial PAH):
    • BMPR2 Gene
20
Q

Key Pathways Implicated in PAH Pathogenesis:

  • What is targeted for therapy in each pathway?
A
  1. Endothelin Pathway
    • Endothelin receptor antagonists
  2. Nitric Oxide Pathway
    • PDE type 5 inhibitor
    • endogenous nitric oxide
  3. Prostacyclin Pathway
    • Prostacyclin derivatives
    • Probably the most potent pathway
21
Q

What are the clinical manifestations of pulmonary vasculitis?

A
  • Pulmonary and Alveolar Hemorrhage
    • ex.: Goodpasture’s Syndrome
  • Lung Infitrates
    • nodular
    • cavitary lesions
    • associated ILD
    • Acute, bilateral, diffuse
  • Pulmonary Hypertension
22
Q

Alveolar (Capillary) Hemorrhage Syndromes: Classification

A
  1. Antibasement Membrane Antibody Disease (ABMAb)
    • Goodpasture’s Syndrome
  2. Anti Neutrophil Cytoplasmic Antibody (ANCA) Associated Vasculitis
    • Wegener’s
  3. Idiopathic Pulmonary Hemosiderosis
  4. Collagen Vascular Diseases
    • Systemic Lupus Erythematosis
23
Q

Alveolar (Capillary) Hemorrhage Syndromes

  • What is the classic triad?
  • What are some life threatening complications?
A
  • Classic Triad
    1. hemoptysis
    2. pulmonary infiltrates
    3. anemia
  • Life threatening complications
    • respiratory failure
    • acute renal failure
    • severe anemia
24
Q

What can be used to diagnose an alveolar (capillary) hemorrhage syndrome?

A
  • sputum, tracheal aspirate
  • Urine; other organ problems
  • Serial Hgb: - 2 gm in 24 hr
  • Serial Chest x-rays
  • Serologies: ABMAb, ANCA, ANA, other
  • Bronchoalveolar lavage, Open Lung Biopsy
  • OTHER ORGANS:
    • Skin Biopsy;
    • Renal Biopsy
25
Q

What are “siderophages” and when are they seen?

A

“Siderophages”

  • Hemosideran laden macrophages seen in alveolar hemorrhage syndrome
26
Q
  • Define Wegener’s Granulomatosis:
  • What areas are affected?
  • What are the signs/symptoms?
A
  • Definition: Systemic vasculitis - granulomatous inflammation
  • Upper (73%) before Lower Respiratory (45%) Tract; and Kidney (18%)
  • SIGNS/SYMPTOMS:
    • Nasal, sinus, otitis
    • Cough, hemoptysis
    • Constitutional (joint, fever)
27
Q

Wegener’s Vasculitis:

  • What is the incidence?
  • What organs are involved?
  • What diagnostic studies can be done?
A
  • 5th decade; male > female
  • Constitutional symptoms prominent
  • Organ Involvement:
    • Upper respiratory tract 80%
    • Dyspnea, Obstructive PFT 55%
    • Infiltrates, Cough, Hemoptysis 45%
    • Arthralgias 45%, Renal
    • Skin 40%, Neuro 40%
    • DVT, increased risk
  • Diagnostic Studies
    • tissue biopsy
    • Serologies (c-ANCA)
28
Q

How does Wegener’s vasculitis affect the lung?

A
  • Perivascular, Necrotizing Granulomatous Inflammation
  • Lung Necrosis and Cavitation, Hemorrhage
29
Q

What lung problems are caused by Weger’s Granulomatosis?

A
  • Capillaritis, Alveolar Hemorrhage
  • Nodules, Cavitary Lesions
  • Large Airways
  • Interstitial lung disease

Respiratory (31 decks)

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