Pulmonary Path 2 Flashcards
Pulmonary infections
pneumonia, acute resp distress syndrome, pulmonary abscess and TB
Pneumonia
one of the leading causes of death, often complicates other chronic debilitating diseases
-any organism can cause pneumonia (bac common, viral, fungal (immunocomp pts.), parasites)
bacterial pneumonia predisposing factors
loss of cough reflex, injury to cilia and decreased phagocytosis (all 3 above from smoking) pulmonary edema, immunocomp condition (ex. pregnancy complication)
clinical presentation
cough, dyspena, fever, chills, sputum production (blue/green from myloperoxase and neutrophils but also bloody from destruction)
bronchopneumonia
patchy, begins around the small bronchi
-common in the very young and very old
lobar pneumonia
involves the entire lobe
- happens in healthy adults
- strep pneumonia is the cause in 90% of cases
2 forms of bacterial pneumonia
bronchopneumonia and lobar pneumonia
2 stages of the infammatory process in LOBAR pneumonia
- congestion - increased red blood cells with (WBC) neutrophils that start to fill the air spaces
- red hepatization - purulent exudate with many RBC (looks like the liver)
- gray hepatization - rbc lyse and get taken out and replaced with exudate with fibrin and macrophages
- resolution - doesn’t completely repair - the air spaces will open and the scaring will be in the interstitium
complicaitons of pneumonia
abcess, pleuritis, pericarditits (lung wrapped around teh heart) and bacteremia (because there is so much vascularization
interstitial/atypical/walking pneumonia
seen with mycoplasma pneumonia and viruses
clinical interstitial pneumonia
highly variable - fever, DRY cough (b/c no PMNs), myalgia (mm. cramps) to life threatening
pathologay of interstitial pneumonia
intersitital inflammation (in the walls), mononuclear cells (macrophages), congestion and hyaline membrane (diffuse alveolar damage) -pneumocytes (type 1 ) can be injured by macros and neutrophils and cause hyaline membrane formation
Acute Respiratory Distress Syndrome (ARDS)
rapidly developing serious condition with same histologic features as interstitial pneumonia
- serious complication of that has many triggers
- *can cause death in a few days
- 30% mortality
what causes ARDS?
many triggers
shock (ex. prego complications), infections, trauma (ex. vehicle accident), drug overdoses, irritants etc..
pathology ARDS
injury to endothelium and alveolar epithelium and increased endothelial permeability
- cytokines activate “ases” and macrophages so shit is ripped up like bronchial epithelium and hyaline membranes form
- alveolar spaces are there, but all the type 1 pneumocytes are damaged and the type 2 are trying to regenerate and fill in the spaces
clinical pulm abscess
cough, fever, purulent sputum (PMN, possibly blood)
** pulm abcess have air-fluid lines on a radiograph dileniating where the pus is vs. air
predisposing factors pulm abcess
bronchiectasis, aspiration, septic emboli, airway ob, dental sepsis (aspiration form procedures)
**harder to cause an abcess in the lung than in the mouth from say an extraction
course of a pulm abcess
scar, cavitate, progressively enlarge
-cavities will only heal through scarring, tissue not coming back
TB frequency
myobacterium tuberculosis
- 1/3 of the world infected - most infectious cause of death in the world (3 million deaths/yr)
- in 80s (with HIV) the US cases rose, but since 1992, have been declining
exceptions to TB decline in frequency in the US
HIV infections (immunocomp), overcrowding, poor living conditions, patches of immigrant populations
myobacterium tuberculosis
acid fast bacillus (rod), aerobe, non-motile, slow groeht
- waxy coat that is resistant to acid destaining (but we have a special stain to find it in the tissues
- caseating (cheesy) granulomatous inflammation - tissue reaction
pathology TB
casseating granuloma (multinuc giant cells)
TB pathogenesis
- almost always airborne (inhalation) b/c bacillus 3-4 micros in size
- Ghon lesion (site of early infec) - inflammation trying to wall off the infection in the lung
- Ghon complex (lung lesion + hilar lymph nodes) - nodes are the secondary area of infection from spread of bacteria
cavitary TB
- apex of the lung
- when destruction out weighs the isolation of the granulmoa
- significant scarring (can only heal through scarring, will not regen)
- this much destruction may seed the large airways, lymph nodes or blood (bacteremia)
- -> sputum from the airways may lead to TB infection in the mouth
- direct extension to the pleura (thickening) - effusion