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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
Classification of vasculitis & those occurring lungs
- classified by size of vessels effected | - occurring in lungs: microscopic polyangitis, granulomatosis w/ polyangitis
26
Suggestive features of vasculitis
- mononeuritis multiplex (asymmetric polyneuropathy) - palpable purpura - pulmonary-renal - fevers, myalgias, athralgias
27
Diagnosis of ANCA vasculitis
- clinical picture - radiographs - histology (BIOPSY) - lab - ANCA
28
What is essential to diagnosis of vasculitis
- Tissue Biopsy
29
Features seen on biopsy w/ vasculitis
- granulomas | - inflammatory cells around vessels
30
Epidemiology of ANCA vasculitis: incidence & prevalence
- incidence: 15-20 per million/year | - prevalence: 90-300/million
31
Survival with ANCA vasculitis
1 year: 88% 3 year: 85% 5 year: 78%
32
Clinical features of granulomatosis with polyangitis
- airway: nose involvement, otitis, sinusitis (85%) - lung parenchyma: focal consolidation/infiltrates/nodules (80%) - alveolar hemorrhage: 5-10% - extrapulmonary: glomerulonephritis, skin
33
ANCA lab testing
c-ANCA: cytoplasmic, proteinase-3 (PR3) antigen | p-ANCA: perinuclear, myeloperoxidase (MPO) antigen
34
ANCA associated vasculitis (AAV) treatment
- RITUXIMAB, corticosteroids, cyclophosphamide (immunosuppression) - rarely plasma exchange
35
AAV remission and relapse
- remission rate: 90-94% | - time to remission
36
AAV survival
- 5 months if untreated GPA | - 21.7 years in treated GPA
37
Pulmonary hypertension: definition
- pathophysiological & hemodynamic condition | - increase in resting MAP > 25 mmHg by right heart catheterization
38
Right heart failure w/ PH
- 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
Essential to diagnosis of PH
- right heart catheterization
40
Right heart catheterization: where is the problem
- pre capillary: low wedge | - post capillary: high wedge
41
Groups of pulmonary hypertension
1. pulmonary arterial hypertension (PAH) 2. left heart disease 3. chronic lung disease 4. chronic thromboembolic PH 5. unclear mechanisms
42
Cause of PAH
- idiopathic - hereditary: BMPR2 mutation (70%) - connective tissue disease: scleroderma - drugs: appetite suppressants, meth, cocaine, st. johns wart - HIV (1/200 patients)
43
Definition of PAH
- right heart cath - resting mean PAP > 25mmHg - exercise mean PAP > 30mmHg - wedge
44
Left heart disease PH
- most COMMON cause (65%) - systolic or diastolic dysfunction - valvular disease, cardiomyopathy, pericardial disease
45
Lung disease PH (group 3)
- COPD, ILD, CPFE, sleep disorder, alveolar hypoventilation, chronic exposure to high altitude - obliteration of vascular bed - hypoxic vasoconstriction
46
Chronic thromboembolic disease PH
- 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
Idiopathic PH survival
- median survival 2.8 years by early NIH registry | - has now improved drastically
48
Why does PH occur
- genetic predisposition, then some sort of injury (hypoxia, meth) leading to inflammation and scarring
49
PAH histologic features
- intimal and medial thickening | - intimal fibrosis and in situ thrombosis (complex plexiform lesions)
50
How to treat PH in groups 2-4
- FIND and treat underlying disease
51
How to treat idiopathic PAH
- therapies that relax pulmonary arteries | - if accompanied by HF then treat that as well
52
Treatment pathways of PAH
- endothelial: endothelin receptor antagonists - nitric oxide: phosphodiesterase 5 inhibitor (prevent breakdown), exogenous nitric oxide (riociguat) - prostacyclin pathway: prostacyclin derivatives (systemic vasodilation)
53
Diseases of pulmonary vasculature
- obstruct: PE - malform/connect: AVM - inflame: vasculitis - scar: pulmonary arterial hypertension - leak: ARDS, CHF
54
Why do people get low oxygen in PE
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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