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Block 9 Week 3 > Vascular Lung Disease- Baker 3 > Flashcards

Vascular Lung Disease- Baker 3 Flashcards

1
Q

Blood clots in the pulmonary arterial system are almost always (blank). 90% are from a (blank)

A

embolic

DVT

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2
Q

Does a DVT= PE?

A

no, DVT 2x more frequent than PE

BUT you cant get a PE without having a DVT

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3
Q

What is the morbidity associated with PE?

A

1/2 have long term complications (post-thrombotic syndrome):
-pain, swelling, discoloration
1/3 have recurrence over 10 years

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4
Q

What is the mortality associated with PE?

A

50-100k deaths per year

  • 10-30% die within one month of diagnosis
  • 25% first “symptom” is sudden death
  • cause of or contributes to 10% of hospital deaths
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5
Q

DVT with a PFO will give you a (blank) pattern rather than a PE

A

stroke

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6
Q

What are the risk factors for PE?

A

Virchow’s triad

1) endothelial injury
2) blood stasis/turbulent flow
3) hypercoagulability

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7
Q

What are the ways that you can get endothelial injury in virchows triad?

A

trauma
vasculitis
hypertension

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8
Q

What are the ways that you can get blood stasis/turbulent flow in virchows triad??

A
  • immobility (post operative, orthopedic conditions, illness)
  • venous compression
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9
Q

What are the ways that you can get hypercoagulability in virchows triad?

A
  • genetic predisp (factor v leien, prothrombin gene mutation, protein C/S deficiency, AT III deficiency)
  • cancer
  • immobilization
  • pregnancy, HRT, OCP
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10
Q

What are the two main issues in PE pathology?

A
  • respiratory compromise

- hemodynamic compromise

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11
Q

What causes respiratory compromise?

A
  • V (ventilation) not equal Q (perfusion) mismatch

- allows for VQ study that diagnoses PE

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12
Q

What causes hemodynamic compromise?

A

lack of blood flow to the lungs

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13
Q

Severity of symptoms and PE syndrome is all a matter of (blank) of PE

A

size (clot burden)

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14
Q

If you have a large embolic causing a PE what will result?

A

complete loss of blood flow

-acute hypoxemia, right heart failure, death

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15
Q

What is one of the few causes of instantanous death?

A

large PE

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16
Q

What can smaller PEs do?

A

travels deeper into the periphery, less likely to cause death

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17
Q

PEs can cause a hemmorrhagic lesion in (blank) percent of cases, When will this occur? Where does it typically occur?

A

10%
Usually only when underlying cardiopulmonary conditions are present (inability of the bronchial arteries to compensate)

-typically occurs in lower lobes

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18
Q

What are the clinical features of PE?

A 
Tachycardia
Chest pain
Tachypnea
Dyspnea
Hypoxemia 
± cough
± Fever
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19
Q

What is the most common EKG finding with a patient with a PE?
What are some other associated findings?

A

tachycardia!
non-specific ST segment changes and T wave changes
S1Q3T3= right ventricular dilation (present in 12% of massive PE)

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20
Q

What willl a chest x ray look like with a person who has PE?

What will the CT scan look like?

A
  • variable. possibly will show a wedge-shaped infiltrate (infarction)
  • gray spots in white arteries demonstrating perfusion defects
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21
Q

What is normal pulmonary arterial pressure?

A

15-30/4-12 (mean 8-18 mmHg)

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22
Q

How do you calculate MAP?

A

(2x diastolic + systolic) / 3

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23
Q

Pulmonary htn is when you have a sustained elevation of mean pulmonary arterial pressure to more than (blank) at rest or to more than (blank) with exercise

A

25 mm Hg

30 mm Hg

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24
Q

What are the 2 types of pulmonary htn?

A

Primary
-idiopathic pulmonary arterial htn
Secondary
-many causes

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25
What is the histopathology of PAH (pulmonary arterial htn)?
- medial hypertrophy of muscular and elastic arteries - plexiform lesion - pulmonary artery atheromas
26
(blank) are present in idiopathic and familial pulmonary htn (not clear if it is caused of or a result of PH)
plexiform lesions
27
What are the five PAH clinical classifications based on similiarites in pathophysiology, clinical presentation and therapy?
1. Pulmonary Arterial Hypertension 2. PH with left heart disease 3. PH associated with lung disease / hypoxemia 4. PH due to chronic thrombotic/embolic disease 5. Miscellaneous PH
28
How can you cause secondary PAH? Give me 5 examples
anything that increases pressure can lead to PAH - CHRONIC LUNG DISEASE - HEART DISEASE - thromboemboli - CT disease - OBSTRUCTIVE SLEEP APNEA
29
In chronic lung disease, you can get (blank) destruction, fewer (blank), and increased (blanK)
parenchymal destruction capillaries increased resistance
30
What types of heart disease can cause secondary PAH?
left heart failure and mitral stenosis
31
How will thromboemboli cause secondary PAH?
-reduced cross-sectional area, increased resistance
32
What CT disease will cause secondary PAH?
Systemic sclerosis-> leads to vascular inflammation, intimal fibrosis, medial hypertrophy
33
How does OSA cause secondary PAH?
increased pulmonary pressure
34
When you have an obstructive pulmonary artery thrombus what happens?
you get a narrowed lumen which increased flow resistance and increases pulmonary artery BP
35
What causes primary PAH (idiopathic PAH)?
mutation of BMPR2 (bone morphogenetic protein receptor 2) leads to proliferation of vascular smooth muscle cells (may be some association with environmental factors)
36
In whom does primary PAH usually occur in?
females between 20-40 years of age
37
What are the early clinical signs of primary PAH? | What is like as the disease progresses?
- dyspnea, fatigue, anginal chest pain | - respiratory distress, cyanosis, RVH and death from cor pulmonale
38
What is the mortality of primary PAH?
usually die within 2-5 years of diagnosis (80%)
39
What are the conventional therapies of PAH?
``` conventional therapies: O2 CCBs digoxin diuretics ```
40
What are the newer specific therapies of PAH?
- prostacyclin analogues - endothelial receptor antagonist - inhaled NO - phosphodiesterase-5 inhibitors
41
What is the most radical therapy of PAH?
lung transplant
42
What are the diffuse pulmonary hemorrhage syndromes?
- goodpasture syndrome - idiopathic pulmonary hemosiderosis - Vasculitits associated hemorrhage
43
What are the three diseases associated with vasculitis associated hemorrhage?
- Wegener Granulomatosis - Hypersensitivity angiitis - Lupus erythematosus
44
What is this: autoimmune disorder-autoantibodies against the basement membrane in alveoli and glomeruli. What can goodpasture syndrome cause?
Goodpasture syndrome - hemorrhagic interstitial pneumonitis - rapidly progressive glomerulonephritis (RPGN)
45
Who typically gets goodpasture syndome? | What is it caused by?
Males> female; teens to 20s typically | -etiology of antibodies is uknown (viral infections, toxic exposures, smoking)
46
What will the histology look like in good pasture syndrome?
- alevolar wall necrosis w/ intra alveolar hemorrhages - hemosiderin laden macrophages - linear Ig and complement deposits in BM
47
What does good pasture syndrome intially present with? What will an x ray show? What happens after the initial signs?
- hemptysis - focal pulmonary consolidations - renal manifestations folllow-> rapidly progressive glomerulonephritis (RPGN)-> uremia-> death
48
How do you treat goodpasture syndrome?
- Renal Replacement therapy (dialysis) for severe AKI - Plasmapheresis= removes circulating anti-BM antibodies - Immunosuppression
49
What is this: intermittent, diffuse alveolar hemorrhage Who does it typically affect?
Idiopathic pulmonary hemosiderosis | -usually young children
50
What is the clinical course of idiopathic pulmonary hemosiderosis?
productive cough hemoptysis anemia weight loss
51
Idiopathic pumonary hemosiderosis is very similiar to good pasture syndrome but it has no (blank)
anti-BM antibodies
52
How do you treat idiopathic pulmonary hemosiderosis?
immunosuppression
53
What is the new term for Wegener's granulomatosis?
granulomatosis with polyangitis
54
How does granulomatosis with polyangitis (wegener's granulomatosis) cause vasculitis?
C-ANCA activates neutrophils which cause free radicals and protolytic enzymes-> leads to inflammatory cells and vasculitis
55
How does wegener granulomatosis present? | How do you diagnose it?
- necrotizing vasculitis - present w hemoptysis -transbronchial biopsy
56
Granulomatosis with polyangitis also frequently affects the (blank) giving rise to (blank) clinically. Also the (blank) is frequently affected and here mucosal ulcers are seen.
sinuses chronic sinusitis nasopharynx
57
What causes increased lymphatic drainage in noncardiogenic pulmonary edema?
DISRUPTED ENDOTHELIAL BARRIER w/ normal hydrostatic pressure increased permeability-> dirupted epithelial barrier-> neutrophils squeeze in and causes alveolar flooding -> you get increased alveolar edema due to lack of salt transports-> increased lymphatic drainage
58
What is this: engorged alveolar capillaries intra-alveolar pink precipitate heart failure cells
Cardiogenic pulmonary edema
59
What are heart failure cells and what will you see them in?
Hemosiderin-laden macrophages from alveolar microhemorrhages | -cardiogenic pulmonary edema
60
What are the clinical signs of PE?
SOB, DOE, orthopnea, PND, crackkles on ausculatation
61
Where will fluid initially accumulate in PE? | If you have chronic PE what can happen?
lower lobes first | lead to fibrosis and thickening of alveolar wall
62
What are these: are short horizontal lines situated perpendicularly to the pleural surface at the lung base; they represent edema of the interlobular septa.
Kerley's B lines
63
What are these: are linear opacities extending from the periphery to the hila; they are caused by distention of anastomotic channels between peripheral and central lymphatics.
Kerly A lines
64
What are the 3 causes of noncardiogenic pulmonary edema?
- acute lung injury (ALI) - Acute Respiratory Distress Ayndrome - Acute interstitial pneumonia
65
What is severe acute lung injury? What is normal acute lung injury? What is acute lung injury without an identified cause? What do they look like histologically?
- ARDS (acute respiratory distress syndrome) - Noncardiogenic pulm edema - Acute interestitial pneumonia - Diffuse alveolar damage (DAD)
66
What are the causes of ALI/ARDS?
- sepsis - diffuse pulmonary damage - mechanical trauma, including head injuries
67
What does diffuse alveolar damage look like?
- interstitial edema - intra-alveolar edema - inflammation - fibrin deposition - hyaline membranes
68
What do hyaline membranes look like?
fibrin rich edema fluid mixed w/ remnants of necrotic epithelia cells
69
Whats happens to you alveoli in acute lung injury?
you get injured, swollen endothelial cells-> neutrophil migration into alveolus-> cytokines + proteases + leukotrienes + Platelet activating factor-> inactivated surfactant-> sloughed bronchial epithelium
70
SARS demonstrates DAD, what else does?
influenza A
71
What does ALI/ARDs cause, systemic or local insults? Endothelial or epithelial damage? Results in an imbalance between (blank and blank) mediators
both both pro and anti-inflammatory
72
How does ALI/ARDS damage the endothelium or epithelium?
- increase vascular permeability - alveolar flooding - reduced diffusion capacity - microthrombi
73
What are the clinical features of ALI/ARDS? | What is the mortality percentage?
-rapid onset -profound dyspnea -tachypnea -severe cyanosis -respiratory failure -diffuse bilateral pulmonary infiltrates VERY VERY SICK! 40% mortality
74
In infants what causes ARDS? | What causes ARDS in adults?
lack of surfactant | secondary disorder

Block 9 Week 3 (6 decks)

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