Pulmonary Pathology 1/2 Flashcards
alveolar pores (of Kahn)
allow aeration but also bacteria/cells/exudate to travel between alveoli
type 2 pneumocytes
produce surfactant and replace type 1 pneumocytes
resorption atelectasis
airway obstruction with gradual resorption of air reduces lung expansion
compression atelectasis
accumulated material in pleural cavity compresses the lung parenchyma
*pleural effusion
contraction atelectasis
fibrotic or other innate restrictive process in the pleura or peripheral lung restricts lung expansion
hemodynamic “pushing out” causes of pulmonary edema
- left sided heart failure
- volume overload
- pulmonary vein obstruction
hemodynamic “leaking out” pulmonary edema
- hypoalbuminemia
- nephrotic syndrome
- liver disease
injury to alveolar wall causes of pulmonary edema
- bacterial pneumonia
- sepsis
- smoke inhalation
- aspiration
What will show pink proteinaceous material in the alveolar spaces histologically?
pulmonary edema
acute lung injury
acute onset, hypoxemia, bilateral infiltrates, NO evidence of cardiac failure
Acute respiratory distress syndrome
- worsening hypoxemia
- PaO2/FiO2 < 200
- bilateral infiltrates
- abrupt onset of Sx
Diffuse alveolar damage
histologic manifestation of ARDS
DAD formula
Edema + fibrin + cell debris = HYALINE MEMBRANES
What is the difference between ARDS and Acute interstitial pneumonia?
acute interstitial pneumonia cannot be attributed to a specific etiology
(same clinical presentation and histology as ARDS)
stages of ARDS
1) exudative
2) proliferative
3) fibrotic
What happens after the fibroproliferative phase of ARDS?
Either
Resolution- restoration of normal cellular structure and function
-OR-
Fibrosis- destruction and distortion of normal cellular structure (irreversible)
Pathogenesis of neonatal respiratory distress syndrome
immature lungs with limited pulmonary surfactant lead to development of RDS at birth
Restrictive lung disease characteristics
- volume restriction
- FEV1/FVC normal
- FVC reduced
Obstructive lung disease characteristics
- decreased flow
- low FEV1/FVC ratio
Dx criteria for chronic bronchitis
persistent cough with sputum production for 3 months out of 2 consecutive years
lung sounds chronic bronchitis
rhonchi and wheezing
lung sounds emphysema
quiet chest
airway remodeling
- occurs with asthma
- progressive structural changes to airways (fibrosis, smooth muscle hyperplasia, increased goblet cells)
- may be irreversible
- decreased response to therapeutic agents
status asthmaticus
- potentially fatal asthma attack
- bronchial occlusion by thick mucus
- eosinophils and breakdown product (charot leyden crystals)
Curschmann spirals
coiled mucus plugs found in status asthmaticus
Kartagener’s syndrome
or primary ciliary dyskinesia; dysfunction of dynein arm of microtubules
What is cause of death with a saddle pulmonary embolism?
Acute cor pulmonale (no pulmonary infarct)
who have Talc embolisms?
IV drug users
pulmonary HTN Dx criteria
pulmonary artery pressure (PAP) greater than 25 mmHg
pulmonary HTN subgroups
1) pulmonary arterial HTN (primary vascular Dz)
2) secondary to left heart failure
3) secondary to chronic pulmonary parenchymal Dz or hypoxia
4) secondary to thromboembolic pulmonary Dz
5) multifactorial
pathology pulmonary HTN
1) plexiform lesion
2) medial hypertrophy
Three pulmonary hemorrhage syndromes
1) goodpasture syndrome
2) granulomatosis with polyangiitis
3) idiopathic pulmonary hemosiderosis
immunofluorescence showing linear pattern of deposition is related to..
Good pasture syndrome (due to anti-basement membrane antibodies)
goodpasture syndrome is what type of hypersensitivity reaction?
type II
Who does good pasture syndrome affect?
male patients in their 2nd or 3rd decade
Goodpasture syndrome pathophys
Abs against a noncollagenous subunit of collagen IV
Cause of clinical Sx of goodpasture syndrome
Ab-mediated damage to basement membranes in lung and kidneys
Stages of lobar PNA
1) congestion
2) red hepatization
3) grey hepatization
4) resolution
complications of lobar PNA
- abscess
- empyema
- bacteremia
typical pneumonia features
- abrupt onset
- respiratory Sx
- consolidation on chest x-ray
- in older adults or children
atypical/walking pneumonia features
- slower onset
- systemic symptoms
- patchy infiltrates on chest x-ray
- in young adults/teens/older children
antigenic drift
- causes epidemics
- minor changes to antigens on virus, allowing for increased spread
- similar enough to original virus to allow for some immunity in many individual
antigenic shift
- causes pandemics
- genomic alterations with major resulting changes to protein structure
- Naive immunity for almost all people
where does bacterial PNA show infiltrates on histology?
in the alveolar spaces
where does viral PNA show infiltrates on histology?
in the interstitium
general presentation bacterial PNA
- abrupt onset
- high grade fever
- crackles on lung exam
- lobar or consolidated appearance
- may involve pleura
general presentation viral PNA
- gradual onset
- epidemics are common
- no or low grade fever
- wheezes on lung exam
- diffuse infiltrates on CXR
lung abscess causes
1) complication on PNA
2) aspiration
what histological finding is highly associated with TB?
caseating granuloma
ghon complex
- radiological/histo finding with TB
- lesion has a ghon focus (primary lesion) and pulmonary lymphadenopathy
chronic pneumonia
pneumonic process lasting for months in an immunocompetent patient
what does histo of lung transplant rejection look like?
mononuclear infiltrates around vessel
