The lung and the Upper Respiratory Tract -1

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The lung and the Upper Respiratory Tract -1

• Atelectasis
• Obstructive Lung Disease

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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.

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Atelectasis (collapse)

• Definition collapse of the lung.
• Major types of atelectasis
• Resorption atelectasis.
• obstruction of bronchus by mucous plug, peanut ?
  absorption of air ? collapse.
• Compression atelectasis
• Accumulation of fluid, blood, and air in the
  plural cavity ? Compression ? collapse of lung.

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Atelectasis
Clinical sudden respiratory distress, no breath
sound at that part, mediastinal shift towards the
effected area.
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Atelectasis morphology of lung

• Airless, Heavy
• Dark purple
• wrinkled pleura
• Tracheal shifting
• Resp. distress

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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.

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Remember this
Points Obstructive lung disease Restrictive lung disease
Total lung capacity Increased Decreased
FEV1 Decreased ( gt FVC). Reduced
Forced Vital capacity (FVC) Normal / Decreased Reduced
FEV1 FVC Decreased. Ratio may be normal.
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Chronic Obstructive Lung Diseases(COPD)

• Def group of disorder characterized by airflow
  obstruction.
• Major obstructive disorders
• Asthma.
• Emphysema.
• Chronic bronchitis.
• Bronchiectasis.

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BRONCHIAL ASTHMA
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Bronchial Asthma

• Definition stimulation of hyperactive airways ?
  episodic bronchospasm.
• Age older people.
• Types
• Extrinsic asthma (immune asthma)
• Atopic.
• Aspergeliosis
• Intrinsic asthma (non-immune).

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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 (most common type of Extrinsic asthma)
• IgE and eosinophils are elevated in the serum.
• Caused by antigens like pollen, fumes, animal
  dander, molds.

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Pathogenesis of atopic asthma 1st 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.

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Pathogenesis of atopic asthma 2nd 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)

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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.

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Late phase mediators

• Major basic protein
• Similar function bronchospasm and mucous
  production

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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.

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Morphology of airways in atopic asthma

• Inflated lung
• Eosinophil in mucosa
• Thick basement membrane
• Hypertrophy of smooth muscle in the bronchial
  wall.

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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.

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Lab findings sputum

• Curschmann spiral Inspissated sputum and
  epithelial cells.?
• Charcot leyden crystal developed from
  eosinophil.?

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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

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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.

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Clinical Course of Chronic Bronchitis

• Persistent cough productive of sputum.
• Others
• Hypercapnia.
• Hypoxemia.
• May lead to infection , CorPulmonale and lung
  cancer.

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Emphysema

• Definition
• Permanent abnormal dilatation of the distal
  airways and alveolar space (ACINI).
• Etiology smoking ( strong association)
• Types 4

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Pathogenesis

• ? Protease (Elastase) and ? antiprotesase (
  alpha- 1 anti trypsin AAT)
• ?
• Loss of elastic tissue around the acini
• Dilatation of acini Emphysema

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Emphysema

• Types ( according to its anatomical
  distribution).
• Centriacinar.
• Panacinar.
• Distal Acinar.
• Irregular

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Centriacinar (centrilobular) emphysema

• Seen in cigarette smokers.
• Involvement central or proximal parts of the
  acini.
• Location Upper lobes (apical).

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Pathogenesis Centrilobular emphysema

• Smoking
• ?
• Attract Neutrophils
• ?
• Secret elastase
• ?
• Reduce AAT (acquired deficiency)
• ?
• Loss of elastic tissue around the acini
• ?
• Dilatation of acini emphysema

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Panacinar (panlobular) emphysema

• Etiology congenital alpha 1-antitrypsin
  deficiency
• Involved respiratory bronchiole to the terminal
  alveoli.
• Location lower lung zones.

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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

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Distal Acinar or paraseptal emphysema AKA
bullous emphysema

• Involvement of the distal potion of the acinus
  (close to pleura).
• Location upper part of the lungs.
• Complication may rupture and produce
  Pneumothorax.
• Collapse of lung, shifting of trachea to other
  side and acute resp. distress.

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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.

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Respiratory Acidosis

• ? pCO2 .
• Compensation by ? HCO3

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Initial value / after Compensation

• Without Compensation
• pH (lt7.35)
• PaCO2 (gt47 mm Hg)
• HCO3 20-26 mmol/L

• After Compensation
• pH ( 7.35)
• PaCO2 (gt47 mm Hg)
• HCO3 32mmol/L ( acute)
• HCO3 44mmol/L ( chronic)

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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

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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.

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Morphology of Bronchiectasis

• Location Lower lobes (often bilateral).
• Dilated bronchiole take saccular appearance.

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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).

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Clinical

1. High Fever
2. Copious, purulent sputum ( may contain blood)
3. Clubbing of the fingers.
4. In severe wide-spread cases ? hypoxia,
   hypercapnia, pulmonary hypertension, cor
   pulmonale.

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