Module 7 Pulmonary Flashcards Preview

Pathology Pre-Midterm > Module 7 Pulmonary > Flashcards

Flashcards in Module 7 Pulmonary Deck (39):
1

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

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

2

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

Klebsiella
Pseudomonas

3

How does a lung abscess present?

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

4

What is the best investigation for a lung abscess?

CT looking for cavities with air fluid level
--remember liquefactive necrosis due to pyogenic bacteria

5

what would the sputum of patients with lung abscess be?

mixed flora anaerobes (foul smelling) and aerobe

6

What are complications of a lung abscess?

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

7

What are other causes of a lung abscess?

Lymphomatoid Granulomatosis
Wegener's Granulomatosis (multiple)
Churg Strauss

8

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

Aspergilloma (fungal ball)

9

What is pulmonary edema?

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

10

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

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

11

What is the pathogenesis for cardiogenic pulmonary edema?

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

12

What is the presentation of cardiogenic pulmonary edema?

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

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?

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)

14

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

less then 2 weeks due to engourgement of capillaries
and lack of alveolar wall thickening

15

What are complications of cardiogenic pulmonary edema?

Can lead to pulmonary HTN --- right heart failure
Will not lead to cor pulmonale (due to cardiac problem not a lung problem)

16

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

ARDS
high altitude
neurogenic
PE

17

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

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

18

What veins is a DVT associated with?

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

19

What is the pathogenesis of a DVT?

Virchows Triad:
--hypercoagulability
--endothelial injury
---turbulence of blood flow

20

What are the three presentations of PE?

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

21

What is the best investigation for a PE?

CT angiogram
Spiral CT (3D CT)

22

What is pulmonary HTN?

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

23

What is the etiology of pulmonary HTN?

Secondary to decreased cross sectional area of blood flow
--chronic obstructive or interstitial lung disease
---recurrent PE

24

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

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

25

Primary HTN is common in what individuals?

Young females 20-40

26

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

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

27

Now what is the etiology of secondary pulm HTN?

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

28

How do patient present with secondary pulm HTN?

SAD
syncope
angina
dyspnea

29

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

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

30

What is the best investigation for secondary pulmonary HTN?

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

31

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

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

32

What are complications of secondary pulmonary HTN?

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

33

what is a Diffuse pulmonary hemorrhagic syndrome?

Active bleeding into lungs and fibrotic thickening of alveolar spaces

34

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

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

35

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

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

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?

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

37

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

Linear deposits of IgG and complement

38

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

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

39

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

No renal involvement and no hematuria
---children more affected than adults
--self limiting therefore resolves on its own