Introduction to Pulmonary Pathology and Diseases of Pulmonary Vascular Origin

Question 1

At end of gestation

Answer 1

These are 5 lobes

Bronchi progress through 23 divisions to increase airway volume and decrease the resistance to flow

Question 2

Acinus of the lung

Answer 2

Area that gas exchange is taking place

Question 3

Trachea and bronchi histology

Answer 3

Mucosa is psdeuostratified columnar epithelium with goblet cells

Submucosa contains sero-mucinous glands

Wall is mix of smooth muscle and cartilage

Question 4

Bronchiole histology

Answer 4

Epithelium is ciliated in large and non ciliated in smaller

No goblet cells but are Clara cells

Submucosa has mooth muscle but no cartialge

As you move down you lose cilia and cartilage but maintain smooth muscle

Question 5

Alvoeli histology

Answer 5

95% of surface covered by flat Type 1 penumocytes…there for gas exchange

5% by cuboidal penumocytes

Question 6

Atelectasis types

Answer 6

Obstructive - resorption…part distal to obstruction will collapse

Non-obstructie - compression or contraction…something on outside is squeezing it down

Question 7

Obstructive atelectasis

Causes

Answer 7

Mucous plugs, excess secretions, tumor or foreign bodies

Early after obstruction area is perfused but not ventilated…this can lower O2

Witth time, other areas will increase ventilation and normalize O2

Mediatinum shifts towards affected side

If remoxed soon enough, the lung can return to normal…if not, area canscar

Question 8

Non-obstructive atelectasis

Answer 8

Compression by fluid, blood, air, or tumor in pleural space

Can be reversible

Tend to push away from the lung

If etiology is fibrosis of the pleural space, then not reversible

Question 9

Pulmonary edema

Answer 9

Fluid build up in the lungs

Hemodynamic PE due to increase intravascular pressure or decreased oncotic pressure

Microvascular pulmonary edema due to damage ot alveolar capillaries

Question 10

Etiologies of hemodynamic edema

Answer 10

Increeased HS pressurei n capillaries…CHF, fluid overload

Decreased oncotic pressure…hypoalbuminemia, liver dz, nephrotic syndrome

Question 11

Etiologies of MV pulmonanry edema

Answer 11

Anything that damages capillaries

Pneumonia, spesis, shock, trauam

Question 12

Sx and signs of Pulm edema

Answer 12

Orthopnea (can’t lay down), PND (wake up at night), SOB, and weight gain
Crackles in lung bases

CXR “butterfly” findings

Question 13

Gross pathology and micropathology of pulm edema

Answer 13

Heavy wet lungs with grothy pink fluid

Septa are engorged, pink fluid in alveolar space…if chronic then hemosiderin laden macrophages

Question 14

ARDS

Answer 14

Resp failure and decreased O2 associated with acute pulmonary injury and resulting diffuse alvoelar cpaillaries

NOTHING to do with HF

Most occur from diffuse lung infection, spesis, or gastric aspiration

Alveolar injury with damage to capillaries and leakiness probably due to imbalance of pro and anti inflammatories

Question 15

Acute phase of ARDS

Answer 15

Day 1-4 shows early exudate with intersitital and alveolar edema

day 4-7 Hyaline membranes form…these are the hallmark and classic findings of ARDS…very pink pretty hyaline membranes

Question 16

Prolif phase of ARDS

Answer 16

Fibroblasts proliferate within the interstitium and alveolar space and can produce sscarring of the lung

After 7 days

Question 17

Tx of ARDS

Answer 17

ID underlying cause

high positive end esxp pressure (PEEP)

Mortality is 40-60

Many suriving will have residual scarring

Question 18

Pulm HTN

Answer 18

Pulm artery is normally low (15 mm)…definition of HTN when it reaches 25 mm Hg

Question 19

Groups 1 -4 of Pulm HTN

Answer 19

1 - primary d of pulm arterioles

2 - secondary to disorder of left heart with increase is PCWP

3 - secondary to lung dz

4 - secondary to chronic thromboemboli

Question 20

Group 1

Answer 20

Idiopathic

Very rare

Most common is 20-40 y/o women

Poor prognosis

Question 21

Group 2,3, and 4

Answer 21

2 - Left sided CHF

3 - COPD, interstitial lung dz…COPD results in hypoxia with arterial constriction of pulm vasculature

4 - chronic thromboemobli

Question 22

Pulmonary embolus

Answer 22

Substance travels through venous system to lung

THromboemoblus most common

95% from deep leg veins

Gross pathology -
Depend on embolus and time since vscular occlusion

HEart trying to pump BUT can’t get out of the right heart

Question 23

PE microscopic and clinical findings

Answer 23

Puggled vessel and infarction IF heart or lung dz. present

Dyspena and tachypnea frequent

Syncopoe, hypotension, cyanosis, pleuritic pain and hemopysis

Sudden death or EMD

Question 24

Dx of pulm embolus

Answer 24

Ultrasensitive D-dimer test with poor specificity so

If negative, then probably not PE

If positive, t hen ay be PE but could be many other things

CT/angiography with contrast is best imaging

If filling defect seen and tracking of contrast around the clot

Can detect down to 2 mm

Question 25

Venous ultrasound of deep leg veins

Answer 25

Does not show DVT 1/3 of the time because clot has already broken off and emoblized

Question 26

V/Q scan

Answer 26

Radiolabeld albumin injected IV and look for cold spots where lung not perfused

Radiolabeled gas is inhaled and get dark spots if not ventilated

Matched up to look for ventilation perfusion kismatch

Question 27

Pulmonary ateriography

Answer 27

Reserved for pts that have decreased renal function

Invasive but specific for PE

Risk due to catheteriation o the groin and into the lung vessels

Question 28

PE txx

Answer 28

Best is to prevent

Mobilization

Anticoagulation both in prevention and after PE

Thrombolytic meds

Greenfield filter in IVC