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MODHIII - Unit 3 > Pulmonary Vascular Disease > Flashcards

Pulmonary Vascular Disease Flashcards

1
Q

Pulmonary Arteriovenous Malformations (PAVM): definition

A
  • abnormal communication between artery and vein
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2
Q

Why do patients get hypoxemic with an AVM

A

Shunt: no O2 exchange

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3
Q

Mechanisms of injury to pulmonary vasculature

A
  • pulmonary embolus
  • pulmonary arteriovenous malformation
  • inflammation of vessels
  • scarring of vessels
  • pulmonary edema
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4
Q

Types of pulmonary embolisms

A
  • thrombus
  • tumor
  • fat
  • air
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5
Q

What is a saddle PE

A

lodges in bifurcation of the pulmonary artery

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6
Q

Method of increased mortality of PE

A
  • unstable: hypotesion (SBP15 min

- much higher mortality up to 72 hrs

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7
Q

Individuals at risk for PE

A
  • Women have increased risk

- obesity, smoking, hypertension, prolonged travel, immobilization, oral contraceptives

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8
Q

Populations at risk for PE

A
  • malignancy, pregnancy, stroke, hospitalized patients, nephrotic syndrome, acute spinal cord injury, joint replacements, inherited disorders
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9
Q

Prediction model of PE & probability

A
  • Wells Score

- probability: high>6, moderate: 2-6, low

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10
Q

Diagnosis: labs & imaging

A
  • labs: D-dimer (fibrin degradation product indicating recent coagulation) **do this first, then proceed if positive
  • imaging: CT angiogram (gold standard), VQ scan
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11
Q

Why do PEs occur

A
  • Virchow’s Triad: venous stasis, endothelial injury, hypercoagulable state
  • arise from lower extremity proximal veins usually
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12
Q

What happens when you get PE

A
  • lung infarction
  • low oxygen
  • impairs CO
  • V/Q mismatch
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13
Q

Why do you get impaired CO w/ PE

A
  • increased PVR leads to RV dilation, flattening IV septum, compressing LV space, which ultimately leads to decreased CO
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14
Q

Treatment of PE

A
  • supportive care: oxygen, vasopressors, ventilator
  • thrombolytics
  • anticoagulation (minimum of 3 months): heparin or fondaparinux then go home with oral coumadin, factor Xa inhibitors, or direct thrombin inhibitors
  • IVC filter (rarely used): net that catches things in IVC
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15
Q

What does presentation with cyanosis tell you?

A
  • CHRONIC hypoxia
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16
Q

Pulmonary AVM: how are they grouped

A
  • defined by size and how many feeding/draining vessels
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17
Q

Pulmonary AVM: location

A
  • usually lower lobe (70%)
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18
Q

Pulmonary AVM associated with

A
  • HHT (30%)
  • trauma
  • hepatopulmonary syndrome
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19
Q

Causes of mortality with pulmonary AVM

A
  • stroke
  • cerebral abscess
  • hemoptysis
  • hemothorax
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20
Q

Treatment of pulmonary AVM

A
  • embolization: clot off vessels

- surgery

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21
Q

Differential Dx of cavitating lung nodules

A
  1. infection: septic emboli, fungal infection
  2. malignancy
  3. vasculitis
  4. primary rheumatologic disease
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22
Q

Lab presentation of ANCA vasculitis (granulomatous with polyangitis)

A
  • elevated creatinine w/ sediment in urine

- C-ANCA elevated along w/ anti-PR3

23
Q

Vasculitis most common location

A
  • small vessels of the lung
24
Q

Vasculitis types that present w/ kidney disease

A
  • granulomatosis w/ polyangitis (Wengener’s/C-ANCA vasculitis)
  • goodpasture’s disease (antibodies to collagen in basement membrane-autoimmune disease)
  • lupus
25
Q

Classification of vasculitis & those occurring lungs

A
  • classified by size of vessels effected

- occurring in lungs: microscopic polyangitis, granulomatosis w/ polyangitis

26
Q

Suggestive features of vasculitis

A
  • mononeuritis multiplex (asymmetric polyneuropathy)
  • palpable purpura
  • pulmonary-renal
  • fevers, myalgias, athralgias
27
Q

Diagnosis of ANCA vasculitis

A
  • clinical picture
  • radiographs
  • histology (BIOPSY)
  • lab - ANCA
28
Q

What is essential to diagnosis of vasculitis

A
  • Tissue Biopsy
29
Q

Features seen on biopsy w/ vasculitis

A
  • granulomas

- inflammatory cells around vessels

30
Q

Epidemiology of ANCA vasculitis: incidence & prevalence

A
  • incidence: 15-20 per million/year

- prevalence: 90-300/million

31
Q

Survival with ANCA vasculitis

A

1 year: 88%
3 year: 85%
5 year: 78%

32
Q

Clinical features of granulomatosis with polyangitis

A
  • airway: nose involvement, otitis, sinusitis (85%)
  • lung parenchyma: focal consolidation/infiltrates/nodules (80%)
  • alveolar hemorrhage: 5-10%
  • extrapulmonary: glomerulonephritis, skin
33
Q

ANCA lab testing

A

c-ANCA: cytoplasmic, proteinase-3 (PR3) antigen

p-ANCA: perinuclear, myeloperoxidase (MPO) antigen

34
Q

ANCA associated vasculitis (AAV) treatment

A
  • RITUXIMAB, corticosteroids, cyclophosphamide (immunosuppression)
  • rarely plasma exchange
35
Q

AAV remission and relapse

A
  • remission rate: 90-94%

- time to remission

36
Q

AAV survival

A
  • 5 months if untreated GPA

- 21.7 years in treated GPA

37
Q

Pulmonary hypertension: definition

A
  • pathophysiological & hemodynamic condition

- increase in resting MAP > 25 mmHg by right heart catheterization

38
Q

Right heart failure w/ PH

A
  • used to low pressure system of right side
  • less reserve than left ventricle
  • right coronary blood flow occurs ONLY in diastole in PH (normally throughout entire cycle)
  • RV ischemia in the setting of increased RV metabolic demand
39
Q

Essential to diagnosis of PH

A
  • right heart catheterization
40
Q

Right heart catheterization: where is the problem

A
  • pre capillary: low wedge

- post capillary: high wedge

41
Q

Groups of pulmonary hypertension

A
  1. pulmonary arterial hypertension (PAH)
  2. left heart disease
  3. chronic lung disease
  4. chronic thromboembolic PH
  5. unclear mechanisms
42
Q

Cause of PAH

A
  • idiopathic
  • hereditary: BMPR2 mutation (70%)
  • connective tissue disease: scleroderma
  • drugs: appetite suppressants, meth, cocaine, st. johns wart
  • HIV (1/200 patients)
43
Q

Definition of PAH

A
  • right heart cath
  • resting mean PAP > 25mmHg
  • exercise mean PAP > 30mmHg
  • wedge
44
Q

Left heart disease PH

A
  • most COMMON cause (65%)
  • systolic or diastolic dysfunction
  • valvular disease, cardiomyopathy, pericardial disease
45
Q

Lung disease PH (group 3)

A
  • COPD, ILD, CPFE, sleep disorder, alveolar hypoventilation, chronic exposure to high altitude
  • obliteration of vascular bed
  • hypoxic vasoconstriction
46
Q

Chronic thromboembolic disease PH

A
  • persistent pulmonary hypertension 6 months after PE
  • 2-4% of patients after PE
  • small vessel arteriopathy distal to thrombosis
  • SURGICAL treatment w/ cure
  • *only type of PH you can surgically treat**
47
Q

Idiopathic PH survival

A
  • median survival 2.8 years by early NIH registry

- has now improved drastically

48
Q

Why does PH occur

A
  • genetic predisposition, then some sort of injury (hypoxia, meth) leading to inflammation and scarring
49
Q

PAH histologic features

A
  • intimal and medial thickening

- intimal fibrosis and in situ thrombosis (complex plexiform lesions)

50
Q

How to treat PH in groups 2-4

A
  • FIND and treat underlying disease
51
Q

How to treat idiopathic PAH

A
  • therapies that relax pulmonary arteries

- if accompanied by HF then treat that as well

52
Q

Treatment pathways of PAH

A
  • endothelial: endothelin receptor antagonists
  • nitric oxide: phosphodiesterase 5 inhibitor (prevent breakdown), exogenous nitric oxide (riociguat)
  • prostacyclin pathway: prostacyclin derivatives (systemic vasodilation)
53
Q

Diseases of pulmonary vasculature

A
  • obstruct: PE
  • malform/connect: AVM
  • inflame: vasculitis
  • scar: pulmonary arterial hypertension
  • leak: ARDS, CHF
54
Q

Why do people get low oxygen in PE

A

V/Q mismatch: bases of lungs better V/Q matching and if they get blocked off the upper lobes are only place for O2 exchange and they don’t have as good V/Q matching

MODHIII - Unit 3 (20 decks)

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