Introduction to Pulmonary Pathology and Diseases of Pulmonary Vascular Origin Flashcards
At end of gestation
These are 5 lobes
Bronchi progress through 23 divisions to increase airway volume and decrease the resistance to flow
Acinus of the lung
Area that gas exchange is taking place
Trachea and bronchi histology
Mucosa is psdeuostratified columnar epithelium with goblet cells
Submucosa contains sero-mucinous glands
Wall is mix of smooth muscle and cartilage
Bronchiole histology
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
Alvoeli histology
95% of surface covered by flat Type 1 penumocytes…there for gas exchange
5% by cuboidal penumocytes
Atelectasis types
Obstructive - resorption…part distal to obstruction will collapse
Non-obstructie - compression or contraction…something on outside is squeezing it down
Obstructive atelectasis
Causes
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
Non-obstructive atelectasis
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
Pulmonary edema
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
Etiologies of hemodynamic edema
Increeased HS pressurei n capillaries…CHF, fluid overload
Decreased oncotic pressure…hypoalbuminemia, liver dz, nephrotic syndrome
Etiologies of MV pulmonanry edema
Anything that damages capillaries
Pneumonia, spesis, shock, trauam
Sx and signs of Pulm edema
Orthopnea (can’t lay down), PND (wake up at night), SOB, and weight gain
Crackles in lung bases
CXR “butterfly” findings
Gross pathology and micropathology of pulm edema
Heavy wet lungs with grothy pink fluid
Septa are engorged, pink fluid in alveolar space…if chronic then hemosiderin laden macrophages
ARDS
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
Acute phase of ARDS
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
Prolif phase of ARDS
Fibroblasts proliferate within the interstitium and alveolar space and can produce sscarring of the lung
After 7 days
Tx of ARDS
ID underlying cause
high positive end esxp pressure (PEEP)
Mortality is 40-60
Many suriving will have residual scarring
Pulm HTN
Pulm artery is normally low (15 mm)…definition of HTN when it reaches 25 mm Hg
Groups 1 -4 of Pulm HTN
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
Group 1
Idiopathic
Very rare
Most common is 20-40 y/o women
Poor prognosis
Group 2,3, and 4
2 - Left sided CHF
3 - COPD, interstitial lung dz…COPD results in hypoxia with arterial constriction of pulm vasculature
4 - chronic thromboemobli
Pulmonary embolus
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
PE microscopic and clinical findings
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
Dx of pulm embolus
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
