Transcript The lung and the Upper Respiratory Tract
The lung and the Upper Respiratory Tract -1 Atelectasis Obstructive Lung Disease
Thoracic Assessment
Breath Sounds absent or decreased – –
Atelectasis: Pneumothorax: Emphysema: Pleural Effusion.
Tactile fremitus – Increased = consolidation of pneumonia – Decreased =
pleural effusion, pleural thickening (fibrosis) ,Pneumothorax, bronchial obstruction, COPD/emphysema.
Hyperresonant =
COPD, hyperinflation
.
Atelectasis (collapse)
Definition: collapse of the lung.
Major types of atelectasis: 1. Resorption atelectasis.
obstruction of bronchus by mucous plug, peanut → absorption of air → collapse.
2. Compression atelectasis Accumulation of fluid, blood, and air in the plural cavity → Compression → collapse of lung.
Atelectasis
Clinical: sudden respiratory distress, no breath sound at that part, mediastinal shift towards the effected area.
Atelectasis: morphology of lung
Airless, Heavy
Dark purple
wrinkled pleura
Tracheal shifting
Resp. distress
Obstructive Vs Restrictive lung disease
Obstructive (COPD): increased resistance to airflow: due to obstruction in airway.
Restrictive: decreased lung capacity and volume. Due to fibrosis.
Points Total lung capacity FEV1 Forced Vital capacity (FVC)
Remember this
Obstructive lung disease Increased Restrictive lung disease Decreased Decreased ( > FVC).
Normal / Decreased Reduced Reduced FEV1: FVC Decreased.
Ratio may be normal.
Chronic Obstructive Lung Diseases (COPD) Def : group of disorder characterized by airflow obstruction.
Major obstructive disorders: 1. Asthma.
2. Emphysema.
3. Chronic bronchitis.
4. Bronchiectasis.
BRONCHIAL ASTHMA
Bronchial Asthma
Definition : stimulation of hyperactive airways → episodic bronchospasm.
Age: older people.
Types: 1. Extrinsic asthma (immune asthma)
Atopic.
Aspergeliosis 2. Intrinsic asthma (non-immune).
Extrinsic Asthma
Mechanism: A Type I hypersensitivity reaction involve IgE bound to mast cell.
Feature: begins in child hood with a family history of asthma.
Atopic: asthma) (most common type of Extrinsic IgE and eosinophils are elevated in the serum
.
Caused by antigens like: pollen, fumes, animal dander, molds.
Pathogenesis of atopic asthma: 1 st exposure by antigen ( childhood with h/o allergic rhinitis, urticaria, or eczema ) Ag. presentation by APC ↓ CD4 activation ↓ Cytokine release ( IL4) ↓ Th2 cell activation →activating B cell ↓ IgE production ↓ Coating of the mast cell by IgE Recruitment of these cells in resp. Mucosa = Sensitization of patient.
Pathogenesis of atopic asthma: 2 nd exposure by that antigen ( adult or young age) Binding of the antigen to the IgE (to
Fab part
) on Mast cell ↓ 1. Early phage reaction = Release of histamine from mast cell ( duration: few hours) ↓ 2. Late phage reaction by Eosinophils (IL-5 fetch these cell) ↓ Release of major basic protein etc. (duration: 12-24 hr)
Early phase Mediators : mast cells
Mediators: –
Histamine: Increased capillary permeability →
mucous formation.
– Prostaglandins D2, E2 and F2 alpha : smooth muscle contraction → bronchospasm ( asthma!!
) – Stimulation of
subepithelial vagal receptors by antifgen.
Late
phase
mediators
Major basic protein Similar function :: bronchospasm and mucous production
Intrinsic Asthma
Onset: adult life
Triggering mechanisms are non-immune:
Aspirin (
by inhibiting the cyclooxygenase pathway without affecting the lipoxygenase route
),
infection (
like virus- by stimulating sub epithelial vagal receptors
).
Cold, Psychological stress, Exercise
No personal or family history of allergy, & IgE levels are normal in the serum.
Morphology of airways in atopic asthma Inflated lung Eosinophil in mucosa Thick basement membrane Hypertrophy of smooth muscle in the bronchial wall.
Clinical Course of atopic Asthma
Presentation of asthmatic attack : Severe dyspnea, coughing, and episodic wheezing.
Severe case: Status asthmaticus:
Severe paroxysm of broncho-constriction that last for days or weeks and does not respond to
therapy. May be fatal.
http://video.google.com/videoplay?docid= 4964654399832185717&q=status+asthmaticus&total= 2&start=0&num=10&so=0&type=search&plindex=1
Lab findings : sputum Curschmann spiral : Inspissated sputum and epithelial cells.
→ Charcot leyden crystal: developed from eosinophil.
→
Chronic Bronchitis
Definition
Persistent productive cough for at least 3 consecutive months in at least 2 consecutive years ( usually all winter).
Etiology:
–
Smoking, Air pollution (Sulfur dioxide and Nitrogen).
–
Infection
Chronic Bronchitis: morphology of airways
Following ratio ( Reid index) is increased Thickness of the mucous gland layer Thickness of the wall (epithelium to cartilage) Squamous metaplasia
dysplasia
cancer.
Clinical Course of Chronic Bronchitis
Persistent cough productive of sputum.
Others:
–
Hypercapnia.
–
Hypoxemia.
May lead to
infection , CorPulmonale and lung cancer.
Emphysema
Definition:
–
Permanent abnormal dilatation of the distal airways and alveolar space (ACINI).
Etiology: smoking ( strong association) Types: 4
Pathogenesis
↑ Protease (Elastase) and ↓ antiprotesase ( alpha- 1 anti trypsin – AAT) ↓ Loss of elastic tissue around the acini Dilatation of acini= Emphysema
Emphysema
1.
2.
3.
4.
Types ( according to its anatomical distribution).
Centriacinar.
Panacinar.
Distal Acinar.
Irregular
Centriacinar (centrilobular) emphysema
• Seen in cigarette smokers.
• Involvement central or proximal parts of the acini.
• Location : Upper lobes (apical).
Pathogenesis: Centrilobular emphysema Smoking ↓ Attract Neutrophils ↓ Secret elastase ↓ Reduce AAT (acquired deficiency) ↓ Loss of elastic tissue around the acini ↓ Dilatation of acini = emphysema
Panacinar (panlobular) emphysema
Etiology: congenital alpha 1 antitrypsin deficiency Involved respiratory bronchiole to the terminal alveoli.
Location: lower lung zones.
Genetic factor
Hereditary
alpha 1 anti-trypsin deficiency.
–
lack of secretion of anti-trypsin from liver… accumulate in liver (PAS positive) .
Homozygous : piZZ gene Other organ effected: Cirrhosis of liver
Distal Acinar or paraseptal emphysema: AKA: bullous emphysema 1.
Involvement of the distal potion of the acinus (close to pleura).
2. Location: upper part of the lungs.
3. Complication : may rupture and produce Pneumothorax.
Collapse of lung, shifting of trachea to other side and acute resp. distress.
Clinical Course of Emphysema Progressive dyspnea → barrel-chested individual, flat diaphragm. Increase AP length (diameter) of lung.
Dyspnea, cyanosis and respiratory acidosis.
Weight loss
patients are thin.
hyperresonant lung.
Respiratory acidosis.
Respiratory Acidosis
↑ pCO2 .
Compensation by: ↑ HCO3
Initial value / after Compensation
Without Compensation pH (<7.35) PaCO2 (>47 mm Hg) HCO3 20-26 mmol/L After Compensation pH ( ~ 7.35) PaCO2 (>47 mm Hg) HCO3: 32mmol/L ( acute) HCO3: 44mmol/L ( chronic)
Bronchiectasis
Definition: permanent abnormal dilation due to necrosis and chronic inflammation of the airways.
Factor responsible :
–
Obstruction : Tumor, foreign body, mucous Cystic fibrosis: increased sweat chloride and pancreas aciner atrophy.
Kartagener syndrome
Conditions that predispose to bronchiectasis
Kartagener syndrome:
Defect in motility of the cilia of bronchus, ear and sperm cilia ( tail).
Features: Sinusitis, bronchiectasis, male sterility and hearing loss.
Morphology of Bronchiectasis
Location:
Lower lobes
(often bilateral).
Dilated bronchiole take saccular appearance .
Complications
Lung Abscess Septic emboli - Metastatic brain abscesses. Reactive amyloidosis extra cellar deposit of Amyloid Associate type of Amyloid protein ( congored positive pink hyaline material ).
Clinical
1.
2.
3.
4.
High Fever Copious, purulent sputum ( may contain blood) Clubbing of the fingers.
In severe wide-spread cases
hypoxia, hypercapnia, pulmonary hypertension, & cor pulmonale.