32 respa Flashcards
congenital anomalies
acute lung injury
manifest as
congestion edema surfactant disruption atelactasis and progress to ards
pulm. edema
define
causes
accumulation of fluid in lungs
hemodynamic edema
edema due to microvascukar injury
edema of undetermined origin
hemodynamic edema
define due to
example cause
histology
lung appearance
due to hydrostatic pressure
left sided chf
hemosiderin laden macrophages prsent
chronic firm and brown induration
ARDS is caused by
diffuse alveolar capillary damage
Clinical features
Hypoxemia and cyanosis with respiratory distress—due to thickened diffusion
barrier and collapse of air sacs (increased surface tension)
‘White-out’ on chest x-ray (Fig. 9.I7B)
alveloar wall become…………. in ARDS
hyalinized
injury is to………..in ARDS
pathogenesis
endothelial and alveolar epi injury
il1
il8 and TNF increase
neutrophil activated
phases of ARDS
EXUDATIVE
proliferative
fibrotic
NEONATAL RESPIRATORY DISTRESS SYNDROME
due to
what cell
associtaed with
Respiratory distress due to inadequate surfactant levels
1. Surfactant is made by type II pneumocytes; phosphatidylcholine (lecithin) is the
major component.
2. Surfactant decreases surface tension in the lung, preventing collapse of alveolar
air sacs after expiration.
3. Lack of surfactant leads to collapse of air sacs and formation of hyaline
membranes.
prematurty
cesarian section
maternal diabetes
why prematurity affect
—Surfactant production begins at 28 weeks; adequate levels are not
reached until 34 weeks.
i. Amniotic fluid lecithin to sphingomyelin ratio is used to screen for lung
maturity.
ii. Phosphatidylcholine (lecithin) levels increase as surfactant is produced;
sphingomyelin remains constant.
iii. A ratio > 2 indicates adequate surfactant production.
why cesearian section cause NARDS
—due to lack of stress-induced steroids; steroids
increase synthesis of surfactant,
why maternal DM causes NARDS
—Insulin decreases surfactant production,
Clinical features OF NARDS
3
- Increasing respiratory effort after birth, tachypnea with use of accessory muscles,
and grunting - Hypoxemia with cyanosis
- Diffuse granularity of the lung (‘ground-glass’ appearance) on x-ray
acute interstitial pneumonia
like ARDS but unknown etiology
Obstructive versus restrictive pulmonary diseases
Obstructive characterized by an increase in resistance to airflow, owing to partial or complete obstruction at any level from the trachea and large bronchi to the terminal and respiratory bronchi restrictive disease characterized by reduced expansion of lung Panka, which is decreases total lung capacity
COPD diseases list
Chronic bronchitis, bronchiectasis , asthma, emphysema
Emphysema
Is characterized by abnormal, permanent enlargement of airspace distal to the terminal bronchioles, accompanied by destruction of their walls , without obvious fibrosis
Types of emphysema
Central Panacinar paraseptal, irregular
From the types of emphysema, which are clinically significant
Central and panacinar
Central or centri acinar emphysema affects
lesions are
What is seen in the walls occurs predominantly in?
Proximal parts of the acinar are affected and distal parts are spared. Lesions are more common in the upper lobe
wall often contain large amounts of black pigments.
Predominantly in heavy smokers
Panacinar emphysema
Involves both proximal and distal bronchioles
it’s more common in the lower lobe and
is associated with alpha 1 anti-trypsine deficiency
Distal or paraseptal emphysema
Spares the proximal acinus
Emphysema is adjacent to the plural along the lobular connective tissue septa, and the margins of the lobules
Occurs adjacent to areas of fibrosis and scarring
More severe in the upper half of the lung
Under lies many cases of spontaneous pneumothorax in adults
Forms blebs and bullous
Most plausible hypothesis to account for the destruction of Alveolar walls
Protease anti-protease mechanism
Can you call manifestations of emphysema do not appear until
1/3 of functioning, pulmonary paranchyma is damaged
Clinical features of emphysema include
- Dyspnea and cough with minimal sputum
- Prolonged expiration with pursed lips (‘pink-puffers’)
- Weight loss
- Increased anterior-posterior diameter of chest {‘barrel-chest,’ )
- Hypoxemia (due to destruction of capillaries in the alveolar sac) and cor
pulmonale are late complications.
Other types of emphysema list
Compensatory hyper inflation, emphysema obstructive over inflation, bullous emphysema interstitial emphysema
Compensatory hyperinflation emphysema
Hyper inflation of the residual lung parenchyma that follow surgical removal of a diseased lung or lobe
Obstructive over inflation, define and give example
Refers to the condition in which the lung expands because air is trapped within it. Common cause is obstruction by tumor or foreign object. Example is congenital labor over inflation in infants.
Interstitial emphysema
Presence of air or gas within the interstitial space of the lung
CHRONIC BRONCHITIS
Chronic productive cough lasting at least 3 months over a minimum of 2 years;
highly associated with smoking
c. bronchitis Characterized by
hypertrophy of bronchial mucinous glands
1. Leads to increased thickness of mucus glands relative to overall bronchial wall thickness (Reid index increases to > 50%; normal is < 40%)
reurrent infection because of of mucus plus and smoking
metaplasia of brochiol epithelium follows
Chronic bronchitis patients known as
blue bloaters
asthma define and types
Reversible airway broncho constrict ion, most often due to allergic stimuli (type I
hypersensitivity)
Atopic
non atopic
drug induced
occupational
atopic asthma
define
pathogenesis
Presents in childhood; often associated with allergic rhinitis, eczema, and a family
history of atopy
Pathogenesis
1. Allergens induce TH2
2. TH2 cells secrete IL-4 (mediates class switch to IgE), IL-5 (attracts eosinophils),
and IL-10 (stimulates T|}2 cells and inhibits T^l).
3. Reexposure to allergen leads to lgE-mediated activation of mast cells.
IL4 IL5 IL10 functions
TH2 cells secrete IL-4 (mediates class switch to IgE), IL-5 (attracts eosinophils),
and IL-10 (stimulates TH2 cells and inhibits TH1).
early phase rxn and late phase rxn in asthma
i. Release of preformed histamine granules and generation of leukotrienes C4,
D4, and E4 lead to broncho constrict ion, inflammation, and edema (earlyphase reaction),
ii. Inflammation, especially major basic protein derived from eosinophils,
damages cells and perpetuates bronchoconstrict ion (late-phase reaction).
clinical triads in asthma
cough
wheezing
dyspnea
macroscopic and microscopic finding of asthma
tnecious mucus
crushman spirals
and
charcot leydon crystals
made of eosinophil membrane proteins
if asthma persists
status athmaticus
BRONCHIECTASIS
define
due to
Permanent dilatation of bronchioles and bronchi ; loss of airway tone results in air trapping.
1. Cystic fibrosis
2. Kartagener syndrome
3. Tumor or foreign body
4. Necrotizing infection
5. Allergic bronchopulmonary aspergillosis
kartagener syndrome
inherited defect of the dynein arm, which is necessary
for ciliary movement. Associated with sinusitis, infertility (poor motility of
sperm), and situs inversus (position of major organs is reversed, e.g., heart is on
right side of thorax)
etiology and pathogenesis of BRONCHECTASIS
obstruction and infection
bronchial obstruction
normal clearing mechanism impaired
pooling of secretion distal to obstruction
inflammation
