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Pulmonary Week 4 > ICL 3.6: Pathology of Pulmonary Vascular Diseases > Flashcards

ICL 3.6: Pathology of Pulmonary Vascular Diseases Flashcards

1
Q

eosinophilia in the context of pulmonary diseases

A
  1. asthma
  2. sarcoidosis
  3. Churg-Strauss
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2
Q

hypertrophy of smooth muscles

A

asthma

bronchi are constricted

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3
Q

blue bloated

A

chronic bronchitis

cyanosis around the mouth and nails

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4
Q

spontaneous pneumothorax

A

paraseptal emphysema

usually in young males who develop sudden sharp chest pain

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5
Q

cirrosis and emphysema in young patient

A

alpha-one antitrypsin deficiency with PZZ phenotype

panacinar emphysema

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6
Q

insulation industry

A

asbestos

can cause pulmonary fibrosis, cancer, pleural plugs, mesothelioma etc.

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7
Q

sand balsting

A

silicosis

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8
Q

egg shell calcification in the mediastinum

A

silicosis

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9
Q

pleural plug

A

asbestos

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10
Q

Caplan syndrome

A

RA and any pneumoconosis

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11
Q

serositis

A

associated with SLE

inflammation of a serous membrane

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12
Q

alveolitis

A

**it’s the pathogenesis of restrictive lung disease

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13
Q

smoking

A
  1. chronic bronchitis

2. emphysema

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14
Q

constipation and hypercalcemia

A

sarcoidosis

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15
Q

paniculitis in the legs/inflammation of subcutaneous fat

A

erythema nodosum

sarcoidosis

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16
Q

infertility

A

Kartageners

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17
Q

65 year old male smoker with a known history of hypertension and hyperlipidemia presents to the ER with severe shortness of breath and productive cough with frothy sputum PE reveals bilateral basal crackles in the lungs.

Tests: His BNP is 500

diagnosis?
pathogenesis?

A

pulmonary edema due to CHF!!

frothy sputum = water + air together = water and air in the alveoli!

crackles = alveoli

risk factors = HTN, hyperlipidemia, smoker

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18
Q

what are some of the things that can cause pulmonary edema?

A
  1. increased hydrostatic pressure
  2. decreased oncotic pressure
  3. lymphatic obstruction
  4. microvascular injury
  5. undetermined origin
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19
Q

what can cause pulmonary edema due to increased hydrostatic pressure?

A
  1. increased pulmonary venous pressure like in CHF*
  2. volume overload
  3. pulmonary vein obstruction
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20
Q

what can cause pulmonary edema due to decreased oncotic pressure?

A
  1. hypoalbuminemia
  2. nephrotic syndome*
  3. liver disease
  4. protein losing enteropathies
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21
Q

what can cause pulmonary edema due to microvascular injury?

A
  1. infections: pneumonia, septicemia*
  2. inhaled gases: oxygen, smoke
  3. liquid aspiration: gastric contents, near-drowning
  4. drugs and chemicals: chemotherapeutic agents (bleomycin), other medications (amphotericin B), heroin, kerosene, paraquat
  5. shock, trauma*
  6. transfusion related (TRALI)*
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22
Q

why are we worried about pulmonary edema due to microvascular injury?

A

this is what causes ARDS!!!

there is leakage of fibrin from the capillaries due to the damage which cements the walls of the alveoli so that they can’t diffuse gas and they become really hypoxic and giving oxygen doesn’t even help

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23
Q

what can cause pulmonary edema due to undetermined origin?

A
  1. high altitude

2. neurogenic (CNS trauma)

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24
Q

what are the gross changes seen in pulmonary edema?

A
  1. heavy, wet lungs and frothy blood tinged fluid
  2. fluid accumulates in the lower lobes where hydrostatic pressure is greater

changes lead to impaired function (interstitial edema) and predisposes one to infections (intra-alveolar edema)

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25
Q

what are the microscopic changes seen in pulmonary edema?

A
  1. intra-alveolar granular pink (eosinophilic) precipitate
  2. alveolar microhemorrhages and hemosiderin-laden macrophages (“heart-failure cells”) present in chronic cases

with long-standing chronic passive congestion (e.g. mitral stenosis), lungs become visibly brown and firm due to numerous hemosiderin-laden macrophages and interstitial fibrosis which is termed “brown induration”***

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26
Q

This thirty-four year old white male collapsed suddenly while waiting for his baggage at the airport after arriving from a business trip to Tokyo on a non-stop, private charter flight. CPR was begun at the airport and continued until his arrival at the ER. At that time, he was found to have electromechanical dissociation and, in spite of all efforts, he could not be resuscitated.

His family history was positive for early death from heart disease, and he had been warned about his elevated cholesterol. He had sustained a recent fracture to his right tibia while skiing, and his right lower leg was in a walking cast.

diagnosis?

A

pulmonary embolism

was on the plane not moving for a super long time

electromechanical dissociation = pulsus paradoxicus associated with cardiac tamponade

recent fracture to tibia = immobilization

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27
Q

what is a pulmonary embolism?

A

blood clots that occlude the large pulmonary artieres

most common cause is DVTs in the legs

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28
Q

what are the predisposing factors for developing a PE?

A

Virchow’s triad:
1. immobilization

  1. hypercoagulable states
    - factor V bleeder
    - contraceptive pills (especially estrogen)
    - SLE
  2. endothelial injury
29
Q

what are the consequences of having a PE?

A

depends on the size of the embolus

large emboli may occlude main pulmonary artery, major branches or lodge at the bifurcation –> if it’s at the bifurcation it’s called a saddle embolus and this is what kills people most often

if it’s small the emboli may travel to more peripheral vessels and may or may not cause infarction

30
Q

what are the outcomes of a PE?

A
  1. most of the time they’re clinically silent because they’re so small so there is none! one (~60-80% are clinically silent)
  2. hemorrhage (~10-15%): tissue viability sustained by collateral blood flow
  3. transient chest pain and cough
  4. only 10% develop infarction if they have inadequate collateral blood flow; often coexisting heart and lung disease is present
  5. acute right heart failure, cardiovascular collapse and sudden death
  6. pulmonary hypertension caused by multiple emboli over time; can cause chronic right heart straight and hypertrophy
  7. secondary embolus (30% chance)
31
Q

what is the morphology of a PE?

A
  1. embolus:

red cells, platelets and fibrin (lines of zahn) fill arterial lumen adhering to endothelial surface

may dissolve or organize and recanalize

  1. hemorrhage

blood in alveoli and interstitium, preserved architecture

32
Q

what are Lines of Zahn?

A

characteristic feature of premoretem clots; not seen postmortem

they are intermingled areas of pale pink platelets and fibrin mixed with red areas of RBCs which form the Lines of Zahn

33
Q

what is an infarct due to a PE?

A

usually wedge-shaped and peripheral, with embolus at apex–> the apex points to hilum

sharp pain due to irritation of the pleura

¾ infarcts are in the lower lobe

in over 50% of cases there are multiple pulmonary infarcts

  1. acute (recent) infarct

coagulative necrosis with hemorrhage (“red infarct”); overlying pleura with fibrinous pleuritis

  1. remote (old) infarct

Inflammatory response followed by regeneration and fibrosis (scar); often with hemosiderin macrophages

34
Q

45 year old male falls while skiing and he factures his femur, he goes to the ER his fracture is realigned and he gets a cast 24 hours after he develops severe dyspnea and reports back to the ER.

What happened?

What would you see if you had lung tissue to examination under the microscope?

A

fat embolus

you’ll see fat droplets in his lungs

35
Q

what are fat embolisms?

A

most common form of clinically significant embolism second to thromboembolism

occurs generally as a result of fracture of a long bone, most typically the femur

histological examination shows fat globules in the capillaries and small vessels of the lung

36
Q

A 14 year old 2 months gestation goes to a friends house to get rid of the pregnancy because she is afraid to tell her Mom. Her friend inject air and insert wire rod through her cervix. The girl develops vaginal bleeding and she goes home but 4 hours later she develops severe dyspnea and is rushed to the ER.

What happened?

A

air embolism

37
Q

what is an air embolism?

A

can be caused by rauma, surgery, intravenous injections, obstetrical procedures, criminal abortion

may cause sudden death

frothy blood is present in the right ventricle and pulmonary artery at autopsy

on histological examination, empty spaces resembling fat emboli are seen

38
Q

what is a septic embolism?

A

infected (bacteria or fungus) fragments of venous thrombi or tricuspid valve vegetations that travel to the lungs

“Septic infarct” made of neutrophils and organisms can convert to abscess

39
Q

Postmortem examination of a 41 year old male who collapsed while hiking reveals bone marrow emboli in the lung vessels.

How did this happen?

A

bone marrow emboli in the lungs are an incidental finding at autopsy in patients who have undergone CPR

40
Q

what is an amniotic fluid embolism?

A

embolus usually at time of delivery

can cause shock and diffuse alveolar damage in severe cases

41
Q

what are starch or talc particle emboli?

A

contained in drug solutions injected by addicts

injections are mixed with talc powder

42
Q

what is the clinical presentation of a large PE?

A
  1. chest pain
  2. dyspnea
  3. shock
  4. fever
  5. elevated (LDH3**)
  6. mimics MI
43
Q

what is the clinical presentation of a small PE?

A
  1. transient chest pain or cough
  2. dyspnea
  3. tachypnea
  4. chest pain
  5. hemoptysis
44
Q

how do you diagnose a PE?

A
  1. spiral computed tomographic angiography

dangerous because it could mobilize the clot but it’s the most accurate

  1. D-dimer
45
Q

what is D-dimer?

A

a product of the degradation of fibrin when a blood clot is degraded by fibrinolysis it has 2 cross-linked D-fragments of the fibrin protein which is what is called D-dimer

usually elevated in patients with a PE

46
Q

how do you prevent PE?

A
  1. early post-surgical and postpartum ambulation
  2. elastic stockings and leg exercises for the bedridden
  3. anticoagulation for high risk patients
  4. filter in inferior vena cava
47
Q

what is pulmonary HTN?

A

mean pulmonary pressures reach 1/4 of the systemic levels

48
Q

how is pulmonary HTN classified?

A
  1. primary

idiopathic;rare

  1. secondary

structural cardiopulmonary conditions which increase pulmonary blood flow or pressure, pulmonary vascular resistance, or left heart resistance to blood flow

49
Q

what are some of the causes of secondary pulmonary HTN?

A
  1. chronic obstructive or interstitial lung diseases
  2. antecedent congenital or acquired heart disease
  3. recurrent thromboemboli due to scarring
  4. autoimmune disorders (progressive systemic sclerosis, scleroderma, NOT SLE)
50
Q

what does elevated LDH3 indicated?

A

pulmonary infarction

LDH1 = heart and RBC

LDH5 = liver

LDH2 and 4 = nonspecific

51
Q

electromechanical dissociation in the context of the lungs?

A

PE

in the heart, it’s cardiac tamponade

52
Q

brown induration

A

severe mitral stenosis causing severe congestion of the lungs

53
Q

fracture femur

A

fat emoblism

54
Q

criminal abortion

A

air embolism

55
Q

lines of Zahn

A

premortum blood clot

56
Q

uremia

A

causes pulmonary edema = uremic pneumonitis

57
Q

25 year old female with progressive dyspnea, leg edema and hemoptysis

discomfort in right upper quadrant. no CHF or autoimmune disease or work in the mines, insulation, etc.

A

primary HTN

58
Q

what is primary pulmonary HTN?

A

aka idiopathic pulmonary HTN

usually in females: 24 – 40 yrs; occasionally young children

presenting features: dyspnea, fatigue common. Some patients angina

leads to right ventricular hypertrophy

80% die in 2-5 years of cor pulmonale, often with superimposed thromboembolism & pneumonia

59
Q

what is the pathogenesis of primary pulmonary HTN?

A

mutation/inactivation of BMPR2 = bone morphogenetic protein

linkage to BMPR2 locus on 2q33 gene rearrangement deletions can also be found

BMPR2 mutation in the vascular smooth muscles causes:

  1. embryogenesis
  2. cell proliferation and differentiation
  3. apoptosis

normally BMPR2 results in inhibition of proliferation so without it there is proliferation of smooth muscles

60
Q

what is the morphology of pulmonary HTN?

A
  1. atheromatous plaques in the main elastic arteries –> secondary PH
  2. medial hypertrophy, intimal proliferation and fibrosis in the small arteries and arterioles –> primary PH
  3. plexogenic pulmonary arteriopathy = capillary tuft formation (“plexiform lesion”**) which indicates severe and irreversible hypertension

this is the classic change in primary PH

61
Q

what are the microscopic changes seen in pulmonary HTN?

A

mainly affects arterioles and small arteries (40 -300 mm in diameter)

medial thickness, intimal fibrosis, and narrowing of the lumen

62
Q

which syndromes are diffuse pulmonary hemorrhage syndromes?

A
  1. Goodpasture syndrome
  2. idiopathic pulmonary hemosiderosis
  3. vasculitis-associated hemorrhage
63
Q

what is Goodpasture syndrome?

A

simultaneous renal and pulmonary disease associated with antibasement membrane antibodies

patients have necrotizing hemorrhagic interstitial pneumonitis

they also have rapidly progressive glomerulonephritis

immunofluorescence shows linear deposits of immunoglobulins and complement on the glomerular basement membrane and in the alveolar septa = type II hypersensitivity reaction

64
Q

what is idiopathic pulmonary hemosiderosis?

A

pulmonary hemorrhage due to capillary dilation and breakage and release of blood that gets metabolized to hemosiderin which is then taken up by alveolar macrophages

presents in children and young adults as cough, hemoptysis, anemia, weight loss

we have no idea why it happens

no kidney involvement; no antibodies

65
Q

what is vasculitis-associated hemorrhage

A

hypersensitivity angiitis

granulomatous polyangiitis = Wegner syndrome

lupus erythematosus

66
Q

plexiform lesions

A

primary pulmonary HTN

67
Q

anti GBM

A

Goodpasture syndrome

68
Q

BMPR2 mutation

A

primary pulmonary HTN

Pulmonary Week 4 (6 decks)

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