Transcript Biomedicine Review of the Respiratory System

Biomedicine Review of the
Respiratory System
Felix Hernandez, M.D.
Facts about the Respiratory System
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1. open-ended and in direct contact with the environment
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Allows for a high number of URI
2. exposed to many allergens inhaled in air
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Allows for a high number of immunologic diseases
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3. Inhaled air contains pollutants, airborne particles, and
gases that may cause disease
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4. The heart and the lungs for a functional unit
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Pathology in one leads to pathology in the other
5. inhaled air contains many potential carcinogens
Locating Findings on the Chest
To locate findings around the circumference
of the chest, imagine a series of vertical lines
Lungs, Fissures, and Lobes
Each lung is divided roughly in half by an oblique (major) fissure
The right lung is further divided by the horizontal (minor) fissure
These fissures divide the lungs into lobes
The right lung is divided into upper, middle, and lower lobes
The left lung is divided into upper and lower lobes
The Trachea and Major Bronchi
The trachea bifurcates into its mainstem
bronchi at the levels of the sternal angle
anteriorly and the T4 spinous process posteriorly
The Pleurae
The pleurae are serous membranes that cover
the outer surface of each lung (visceral
pleura), and also the inner rib cage and upper
surface of the diaphragm (parietal pleura)
Figure 17-4: Branching of the airways
Inspiration:
Contraction of diaphragm / intercostal muscles 
Expansion of thorax  expansion of lungs 
Pressure in lungs ↓ 
Air inflow
Expiration:
Relaxation of muscles 
Thorax / lung recoil back 
Pressure in lungs ↑ 
Air outflow
Hypothalamus (emotions / pain)
Cortex (voluntary control)
Chemoreceptors:
Central (in medulla oblongata): responds to CO2 ↑
CO2 passes blood brain barrier
CO2 + H2O
H2CO3
H+ + HCO3-
H+ stimulates receptors  breathing depth ↑ + rate ↑
Peripheral (in aortic / carotid bodies):
responds when O2 < 60 mm Hg  increase ventilation
Responds to pH ↓  increase ventilation
Marieb, Human Anatomy & Physiology, 7th edition
Diaphragm & rib cage are pumps for inspiration
Alveolar surface exchanges O2 & CO2 with blood
The gasses in air act independently & move
down a pressure gradient
Airway resistance can limit ventilation efficiency
Typically ventilation matches blood perfusion via
local regulators of vasodilation & bronchodilation
URI Etiology
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Recognized as common colds
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Acute inflammation of the nose, sinuses, throat
or larynx
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Most are caused by viruses
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Most commonly influenza virus,
parainfluenza virus, and rhinovirus
Predisposing factors include physical
exhaustion, old age, and general poor health
URI Clinical Presentation
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Rhinorrhea
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Throat pain, discomfort in swallowing, sneezing
and a hacking cough
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Lasts from a few days to 1 to 2 weeks
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Heal spontaneously
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Signs of purulent discharge indicates a bacterial
superinfection
Intranasal Steroids
 Drugs:
 Budesonide
(Rhinocort)
 Triamcinolone
 Fluticasone
(Nasacort)
(Flonase)
 Mometasone
(Nasonex)
 MOA:
inhibit inflammatory cells in the nasal
mucosa thus reducing the symptoms of rhinitis
 Side
effects: may increase the risk of thrush and
prevent healing of damaged nasal mucosa
Lobar Pneumonia
Widespread/diffuse alveolar pneumonia
Figure 8-07B
Common Causes of Pneumonia
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Bacteria- 75% of cases
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Viruses
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influenza virus
Fungi
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Streptococcus pneumoniae #1
Pneumocystis carinii
Bacteria-like organisms
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Mycoplasma pneumoniae
Bronchopneumonia
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Bacterial invasion of the bronchial mucosa
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PMN move into the lumen of the airways and
starts an inflammatory response
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The inflammation spreads form the bronchi into
the adjacent alveoli
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Lobular  single lobules
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Lobar  large portions of entire lobes
Intra-alveolar exudate accumulates and replaces
the air causing the lung parenchyma to become
consolidated
Bronchopneumonia
Limited to the segmental bronchi and
surrounding lung parenchyma
Figure 8-07A
Interstitial Pneumonia
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Inflammation primarily affects the alveolar septa
and does not result in exudation of PMNs into
the alveolar lumen
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Caused by viruses or M. pneumoniae that attach
to the surface of respiratory epithelial cells
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Cause cell necrosis and induce an infiltrate in
the alveolar septa
Interstitial Pneumonia
Diffuse and bilateral
Infection caused by Mycoplasma pneumiae or
viruses
Figure 8-07C
Clinical Features of Pneumonia
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Systemic signs of infection—fever, chills,
prostration
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Local signs of irritation—cough
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Airway obstruction—shortness of breath
(dyspnea), rapid breathing (tachypnea)
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Inflammation and tissue destruction—
expectoration of rusty sputum, hemoptysis
Common Antibiotics Used to Treat Pneumonia
Amoxicillin
DOC for: empiric therapy in otitis media, sinusitis and pneumonia
Side Effects: Diarrhea
2nd generation Cephs
moderate gram + and gram - coverage
Vancomycin
MOA: prevents transfer of cell wall precursors from plasma membrane
to cell wall
Clinical Use: DOC for penicillin or methicilliin resistant staph and strep
Side Effects: thrombophlebitis, Red Man Syndrome
Common Antibiotics Used to Treat Pneumonia
Erythromycin
MOA: Inhibits protein synthesis
DOC for Mycoplasma pneumonia
Pulmonary Tuberculosis
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Key feature is the formation of granulomas which are
composed of lymphocytes, macs and giant cells.
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The central portion of the granuloma is necrotic and consists of
caseous necrosis
Primary infection
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Hasn’t been exposed and results in localized lung inflammation
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The lession is called the Ghon complex and it consists of granulomas in
the lung parenchyma and enlarged regional lymph nodes.
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95% of the times the complex heals spontaneously and undergoes
calcification
Pulmonary Tuberculosis
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Secondary infection
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Develops as a result of reactivation of a dormant
primary infection or reinfection
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most are due to reactivation
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Bacteria spread to the apex of the lung and cause a
granulomatous lobular pneumonia
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Confluent granulomas can form cavities which
become a source of hemoptysis
Ghon Complex
Figure 8-10
Drugs Used to TreatTuberculosis
Isoniazid
MOA: inhibits mycolic acid synthesis in the wall
Side Effects: peripheral neuropathies (prevent with treatment with pyridoxine)
Rifampin
MOA: stopping bacterial RNA synthesis
Side Effects: urine and sweat turn red
Pyrazinamide
Side Effects: hepatitis, hyperuricemia with gouty arthritis.
Ethambutol
MOA: inhibits mycolic acid synthesis in bacterial cell wall
Chronic Obstructive Pulmonary Disease
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A group of diseases characterized by chronic
airway obstruction
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Includes the following diseases:
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Chronic bronchitis
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Emphysema
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Bronchiectasis
Bronchiectasis
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A permanent dilatation of the bronchi
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Occurs as a result of persistent inflammation inside the
airways
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Larger bronchi show saccular dilatation, smaller bronchi
show cylindrical dilatation
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Dilated bronchi are filled with mucopurulent material
which cannot be cleared by coughing
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Infection spreads to adjacent alveoli causing recurrent
pneumonias
Bronchiectasis
Figure 8-12
Chronic Bronchitis
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Excessive production of tracheobronchial mucus causing cough
and expectoration for at least three months during 2 consecutive
years
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Smoking is the cause in more than 90% of cases
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Non-specific pathology
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The walls of the bronchi are thickened and the lumen contains
thick mucus
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The mucosa becomes infiltrated with lymphocytes, macs and
plasma cells
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The submucosa shows marked mucous gland hyperplasia,
chronic inflammation and fibrosis
Emphysema
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Enlargement of the airspaces distal to the terminal
bronchioles with destruction of alveolar walls
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Is linked to chronic cigarette smoking but can be found in
non-smokers with Alpha-1-antitrypsin deficiency
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Irritants in smoke cause an influx of inflammatory cells into
the alveoli.
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proteolytic enzymes are released from leukocytes and destroy the
alveolar walls
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Oxygen radicals produced by cigarettes kill alveolar cells and
leukocytes which releases even more enzymes
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Elastase breaks down elastin fibers and its activity is increased
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Oxygen radicals also inactivate antiproteolytic enzymes (Alpha 1 theory)
Emphysema
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Centrilobular
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Widening of the airspaces in the center of a lobule
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MC form and is found in smokers
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Remaining bronchioles are infiltrated with antracotic
macs and chronic inflammatory cells
Panacinar
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Involves all the airspaces distal to the terminal
bronchioles
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Occurs with alpha 1 def.
COPD—Emphysema (Pink Puffer)
Figure 8-14A
COPD—Chronic Bronchitis
(Blue Bloater)
Figure 8-14B
Comparison of Chronic Bronchitis
and Emphysema
Table 8-2
Asthma
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Extrinsic
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Intrinsic—attacks precipitated by:
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Physical factors
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Exercise
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Psychological stress
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Chemical irritants and air pollution
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Bronchial infection
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Aspirin
Pathogenesis of Asthma
Figure 8-15
Histopathology of Asthma
Figure 8-16
Bronchodilators
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Sympathomimetics
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Albuterol (Ventolin)
MOA:
beta-2 agonist which causes bronchodilation
 Rapid
onset of action
Indications:
DOC for the treatment of acute asthma
symptoms and prevent exercise induced asthma.
Side
Effects: vasodilation, tachycardia, CNS
stimulation.
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Levalbuterol (Xopenex)
Less
side effects than albuterol
Bronchodilators
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Salmeterol
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MOA: long acting beta-2 agonist
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Indications: chronic treatment of asthma or bronchospasm in
adults.
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Is not used for acute exacerbations
Epinephrine (Primatene Mist)
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MOA: beta-2 bronchdilation, alpha-1 vasoconstriction and
decreased secretions
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Indications: emergent use for sever
bronchoconstriction/vasodilation seen in anaphylaxis
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Side Effects: tachycardia, CNS stimulation
Bronchodilators
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Ipratropium (Atrovent)
 MOA:
muscarinic antagonist which reverses AcH
induced bronchconstriction
 Indications:
bronchospasm associated with
COPD in adults
 Side
effects: very few systemic anticholinergic
s/sx because it poorly crosses into the systemic
circulation
Corticosteroids
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Drugs: Beclomethasone (Beclovent), Triamcinolone (Azmacort), Dexamethasone
(Decadron)
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Systemic
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MOA: decrease inflammation and edema in respiratory tract.
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Indications: asthma which can not be controlled by sympathomimetics alone
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Side Effects: sodium/water retention, osteoporosis, PUD, avascular necrosis of
the femoral head
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Should be discontinued ASAP
Inhaled
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MOA: same as systemic
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Indications: same as systemic
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Side Effects: don’t induce systemic toxicity. Their action is mostly in the lungs.
They have an increased risk of oral thrush (Candida albicans infection)
Lung Carcinoma
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Most common malignant tumor of internal
organs in the United States
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Most often related to cigarette smoking
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Rare before the age of 40 years, but its
incidence rises with age
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Poor prognosis
Histogenesis of Lung Carcinoma
Figure 8-25
Histopathology of Lung Tumors
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Squamous cell carcinoma
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Adenocarcinoma
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Large-cell undifferentiated carcinoma
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Small-cell carcinoma
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Mesothelioma --> Asbestos
Clinical Features of Lung Cancer
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Bronchial irritation
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Local extension into the mediastinum or pleural
cavity—pleural effusion
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Distant metastases
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Systemic effects of neoplasia
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Paraneoplastic syndromes
Metastases of Lung Carcinoma
Figure 8-27