Module 7 Pulmonary

Question 1

How do you get single vs. multiple abscesses in the lung?

Answer 1

Single is via Aspiration: alcoholics, bedridden, intubated, seizures, and stroke patients (due to decreased gag reflex)(usually in right lung because the bronchus is straight) (if sitting up then bottom of lung) (if laying back then top of lung). Alzehemiers.
Multiple: Hematogenous spread via septicemia and septic emboli but it would be infective endocarditis on tricuspid valve so IV drug users. Wegener’s Granulomatosis. Bronchopneumonia

Question 2

Bronchopneumonia can do multiple lung abscesses esp. angio invasive organisms, like

Answer 2

Klebsiella

Pseudomonas

Question 3

How does a lung abscess present?

Answer 3

Finger clubbing (hypoxia) 
SOB 
Weight loss 
Spike in fever (separates it from bronchiectasis) 
Halitosis 
Productive sputum

Question 4

What is the best investigation for a lung abscess?

Answer 4

CT looking for cavities with air fluid level

–remember liquefactive necrosis due to pyogenic bacteria

Question 5

what would the sputum of patients with lung abscess be?

Answer 5

mixed flora anaerobes (foul smelling) and aerobe

Question 6

What are complications of a lung abscess?

Answer 6

Empyema 
Compression atelectasis
Bronchopleural fistula 
AA amyloidosis 
Septicemia --- DIC

Question 7

What are other causes of a lung abscess?

Answer 7

Lymphomatoid Granulomatosis
Wegener’s Granulomatosis (multiple)
Churg Strauss

Question 8

If the cavity of an abscess gets colonized by aspergillus, what forms?

Answer 8

Aspergilloma (fungal ball)

Question 9

What is pulmonary edema?

Answer 9

Fluid accumulation in air spaces and parenchyma of lungs; leads to impaired gas exchange

Question 10

The first type of pulmonary edema is cardiogenic pulmonary edema, what is the etiology?

Answer 10

Left heart failure (dyspnea, orthopnea, paroxysmal dyspnea, pink frothy sputum)

Question 11

What is the pathogenesis for cardiogenic pulmonary edema?

Answer 11

less than 2 weeks = transudate due to increased hydrostatic pressure
Greater than 2 weeks= alveolar wall fibrosis and therefore hemosiderin laden macrophages

Question 12

What is the presentation of cardiogenic pulmonary edema?

Answer 12

Increased pulmonary capillary wedge pressure ( because its due to heart failure)
No hyaline membrane so therefore not refractory to oxygen
At 2 weeks hemosiderin laden macrophages/heart failure cells

Question 13

Now on the exam they are going to make you compare the cardiogenic pulmonary edema to ARDS, what are feature of ARDS that are different?

Answer 13

ARDS:

1. Pulmonary edema is fibrinous exudate because its acute inflammation (Either due to direct or indirect damage to type II pneumocyts)
2. Diffusion barrier to oxygen due to hyaline membrane
3. Pul wedge pressure is normal (again no heart involvement)

Question 14

In slide 11, what is the time frame on this for cardiogenic pulmonary edema?

Answer 14

less then 2 weeks due to engourgement of capillaries

and lack of alveolar wall thickening

Question 15

What are complications of cardiogenic pulmonary edema?

Answer 15

Can lead to pulmonary HTN — right heart failure

Will not lead to cor pulmonale (due to cardiac problem not a lung problem)

Question 16

The second type of pulmonary edema is non cardiogenic, what disorders fall into this category?

Answer 16

ARDS
high altitude
neurogenic
PE

Question 17

What is the etiology of a pulmonary embolism (PE)?

Answer 17

DVT due to stasis caused by long flights, birth control pills, adenocarcinoma and Factor V leiden mutations

Question 18

What veins is a DVT associated with?

Answer 18

Popliteal
Iliac 
Femoral 
--at or above knee
---unilateral

Question 19

What is the pathogenesis of a DVT?

Answer 19

Virchows Triad:

• -hypercoagulability
• -endothelial injury
• –turbulence of blood flow

Question 20

What are the three presentations of PE?

Answer 20

Massive Saddle Emboli: at bifurcation of pulmonary trunk: sudden death therefore no effect on the lungs
Major with CHF: dyspnea, pleuritic CP, hemoptysis, coagulative necrosis in the lung
–CHF compromised the bronchial artery —red infarct and coagulative necrosis
—no compromise of bronchial artery — pulmonary hemorrhage and at 2 weeks hemosiderin laden macrophages
Minor: no effect unless recurrent — Pul HTN – right heart failure (Cor pulmonale) and nutmeg liver after 2 weeks

Question 21

What is the best investigation for a PE?

Answer 21

CT angiogram 
Spiral CT (3D CT)

Question 22

What is pulmonary HTN?

Answer 22

Pulmonary pressure is over 1/4th of the systemic arterial pressure

Question 23

What is the etiology of pulmonary HTN?

Answer 23

Secondary to decreased cross sectional area of blood flow

• -chronic obstructive or interstitial lung disease
• –recurrent PE

Question 24

There is secondary and primary HTN. Lets start with primary HTN, what is the etiology?

Answer 24

Idiopathic
–usually associated with a mutation in BMPR2 (bone morphogenic protein receptor) — binds to TGFbeta and causes hyperplasia and increased vascular resistance

Question 25

Primary HTN is common in what individuals?

Answer 25

Young females 20-40

Question 26

Primary HTN is initially asymptomatic, what happens when the HTN becomes long standing/chronic and severe?

Answer 26

Plexiform lesions: vasculature channels within the intima

• -small capillaries cant take extreme pressure and undergo fibrinoid necrosis, dilations and hemorrhage
• -think of it as a form of recannalization of intima of small pulmonary arteries

Question 27

Now what is the etiology of secondary pulm HTN?

Answer 27

Pulmonary Etiology: ALL obstructive lung diseases (Except asthma), recurrent minor emboli and all restrictive lung diseases
Cardiac Etiology: Left to right shunts, VSD, ASD, PDA and also mitral and aortic valve problems

Question 28

How do patient present with secondary pulm HTN?

Answer 28

SAD
syncope
angina
dyspnea

Question 29

What findings on physical exam will you find in a patient with secondary pulmonary HTN?

Answer 29

Loud P2 (pulmonary valve closing under pressure) due to higher right sided pressure 
--differentiates from aortic stenosis

Question 30

What is the best investigation for secondary pulmonary HTN?

Answer 30

Cardiac Cath and pressures on the right side will be pretty high

Question 31

If you take a biopsy of the pulmonary arteries what will you see?

Answer 31

Pulmonary Trunk: atherosclerosis – atheroma due to increased pressure
Medium Vessels: intimal and smooth muscle cell proliferation — wall thickening (this is slide 13)
Small vessels – thickening, medial hypertrophy and reduplication of the IEL and EEL

Question 32

What are complications of secondary pulmonary HTN?

Answer 32

Right heart failure (Because the right ventricle is hypertrophy) — nutmeg liver
–pitting peripheral edema, ascites, distended jular edema and hepatosplenomegaly

Question 33

what is a Diffuse pulmonary hemorrhagic syndrome?

Answer 33

Active bleeding into lungs and fibrotic thickening of alveolar spaces

Question 34

Primary immune mediated diseases which manifest as a triad of what symptoms?

Answer 34

1. Iron deficiency anemia
2. Cough with hemoptysis
3. Pulmonary infiltrates on xray

Question 35

What type of heterogeneity is seen in diffuse pulmonary hemorrhagic syndrome?

Answer 35

Temporal:
coexistence of old (hemosiderin laden macrophages) and new hemorrhage with alveolar wall fibrosis
–so in the pic slide 14: the blue indicates old blood, if no blue then fresh blood

Question 36

There are three conditions that have diffuse pulmonary hemorrhagic syndrome involvement, each card will go through the different conditions. The first is Goodpastures, what are some characteristics?

Answer 36

1. Young men, type II HSR
   - -antibodies attacking glomerular and pulmonary BM (type IV collagen)
   - –see triad but also affects kidney so glomerular nephritis – hematuria
   - -never see URT so no nasal ulceration or sinusitis
   - -anti-glomerular BM (GBM) antibodies to the alpha 3 chain of type IV collagen and linear deposits of IgG and C3

Question 37

What would you see on renal biopsy immunofluorescent for Goodpasture’s?

Answer 37

Linear deposits of IgG and complement

Question 38

The next conditions involving diffuse pulmonary hemorrhagic syndrome is Wegener’s, what are some characteristics?

Answer 38

URT: nasal ulceration and sinusitis
LRT: cough with hemoptysis
Causes glomerular nephritis – hematuria
cANCA and PR3 antibodies
Renal biopsy with immunoflurescence — see nothing pauci immune

Question 39

The final condition involving pulmonary hemorrhagic syndrome is Idiopathic pulmonary hemosiderosis, what are some characteristics?

Answer 39

No renal involvement and no hematuria

• –children more affected than adults
• -self limiting therefore resolves on its own