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Obstructive Lung Diseases
- COPD mostly results from chronic bronchitis or emphysema
- also be seen with asthma and bronchiectasis
- -Cystic Fibrosis is included
- -Decreased FEV1/FVC leads to obstructive defect
- -~14.2 million people in the US have COPD
- Patients may have bronchitis, emphysema, asthma, or a combination of these
- -Most patients with COPD have chronic bronchitis and emphysema (subset 5)
- -Asthmatic patients with emphysema and/or bronchitis (subsets 6, 7, 8) are considered to have “asthmatic bronchitis”
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COPD Risk Factors
- Aging: elastic recoil in lungs and number of alveoli and lung capillaries diminishes with age,
- Smoking: effect is additive over a lifetime. Paralyzes the cilia in the lungs.
- Genetics: Alpha1-antitrypsin deficiency can lead to neutrophil elastase damaging the alveoli. Increased risk with smoking.
- Exposure to environmental toxins
- Deconditioning: reduced peripheral muscle strength, decreases lung’s compliance. Vicious cycle of dyspnea causing anxiety, which induces dyspnea and tachypnea. Can also be associated with poor nutrition due to dyspnea
- Heart Disease
- Obesity
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Emphysema
- -Destruction of alveolar septa leads to distention of air spaces distal to terminal bronchioles and diminished elastic recoil (PINK PUFFER)
- Leads to small airway collapse during expiration
- -Patient usually has severe dyspnea caused by hyperinflation of the lungs (alveoli cannot empty, induces uncomfortable sensation and reduces exercise tolerance)
- -Hypoxemia and CO2 retention occurs LATE in course of disease
- -NOT associated with cyanosis, hence “pink puffer”
- -Chest cavity appearance is lifted upwards=BARREL CHESTED
- -Enlarged lungs with clusters of dilated air spaces is characteristic during autopsy
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Chronic Bronchitis
- -Lumen of airways are decreased (excessive tightening of lumen and over secretion of mucous)
- -“BLUE BLOATER”associated with hypoxemia and cyanosis EARLY in the disease
- -Obstruction occurs because of mucus gland enlargement and secretion, inflammation and fibrosis (elastic recoil is usually normal)
- -Associated with a productive cough that has lasted at least 3 months/year for at least 2 consecutive years
- -Patient is less dyspneic than emphysema
- -More shunting of arterial blood through unventilated alveoli, more severe hypoxemia and cor pulmonale
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Obstructive Diagnosis
- Chest X-Ray: shows overinflated (hyperblack) lungs, more so with emphysema than chronic bronchitis
- -Pulmonary Function Tests:
- 1) TLC: increased in emphysema, usually normal or slightly decreased in chronic bronchitis
- 2) RV: increased in both
- 3) Diffusing Capacity (ability to exchange gases): markedly decreased in obstructive emphysema, less so in chronic bronchitis
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Obstructive Symptoms
- features of both emphysema and chronic bronchitis at the same time:
- 1) Dyspnea
- 2) Cough
- 3) Sputum Productionscant in emphysema, but often copious and purulent in chronic bronchitis
- 4) Clubbing of Fingersexcessive enlargement at the ends of digits, profile of finger tip loses angle between nailbed and skin, due to excess of fluid and edema in extremities
- 5) Increased antero-posterior diameter of chest
- 6) Tachypnea
- 7) Decreased lung sounds and abnormal sounds
- 8) Cyanosis (in severe cases)
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Obstructive Treatment
- 1) Avoid causative agents smoking
- 2) Treat intermittent infections provide necessary vaccinations
- 3) Oxygen Therapy needs to be done very carefully as some patients rely on hypoxemia for their ventilator drive
- 4) Drugs to decrease airway constriction and inflammation (beta-agonists, anti-cholinergics, combination)
- **THIS IS NOT A REVERSIBLE DISEASE!!! The best we can do is treat the symptoms, prevent further damage and provide lifestyle changes
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Obstructive Complications
- -Exacerbations of COPD are associated with transient decreases in lung function
- **Must distinguish from pneumonia, pneumothorax and pulmonary embolism
- -Severe hypoxia may lead to angina, acute coronary syndrome and heart failure
- In elderly smokers, COPD may coexist with heart failure (Cor pulmonale and right sided failure are common)
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Asthma
- -Hyper-reactivity of bronchial musculature that involves airway inflammation and reversible airway obstruction
- -Affects 3-6% of the population
- -Most common in children younger than 5
- -A variety of inflammatory cells, cytokines and other mediators appear to be involved in an attack -Cause remains unknown, but appears to involve an intense allergic sensitivity to environmental factors
- Common Aeroallergens: animal dander, dust mite, mold, cockroaches, pollens
- -May also be precipitated by exercise, medications (ex/ aspirin) and infections (ex/ viral) -Tightness of chest
- -Dyspnea
- -Sometimes cough may be only symptom (in mild cases)
- -Wheezing
- -Retraction of respiratory muscles
- Questions to ask:
- -Do you actually get attacks?
- -When was the last time you had an attack?
- -What precipitates these attacks?
- -Is it sports-induced?
- -Is it allergy induced?
- -Is it stress induced? -Pulmonary Function Test:
- Decreased FEV1
- Decreased maximal mid-expiratory flow rates
- -Drugs: To reverse bronchial muscular constriction
- beta-adrenergic agonisits (short and long-acting)
- Anti-inflammatory drugs to treat and prevent attacks (ex/corticosteroids)
- -Avoid causal agents
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Bronchiectasis
- -Irreversible dilation of the bronchial walls
- destruction of the muscular elastic components
- -People get xerostoma and very thick secretions due to increased salt content
- -Sweat is also effected -Congenital: a rare condition in which the lung periphery fails to develop
- -Acquired: recurrent inflammation or infection of the airways
- 1) Cystic Fibrosis (CF): more than 50% of cases are related to CF
- 2) Infections: ex/ pneumonia, TB, fungal infections
- 3) Inhalation of noxious chemicals
- 4) Immune mediated
- -Associated with chronic bronchitis and/or emphysema and some fibrosis
- -Most patients have chronic cough and sputum productionmost characteristic and common symptoms
- -Complications: Cor pulmonale (damage to RV due to pulmonary HTN) excessive secretions are a furtile ground for bacterial growth, respiratory tract type of infections are extremely common
- - High Resolution CT scan can be used for diagnosis
- - Antibiotics, bronchodilators, physiotherapy, occasionally surgical resection and rarely lung transplant
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Restrictive Lung Diseases
- Reduced lung volumes either because of an alteration in lung parenchyma, a disease of the pleura, a defect in the chest wall or the neuromuscular apparatus
- -Mortality and morbidity depends on the type
- Several risk factors are associated with poorer outcome
- Ex/ Older age, male sex, history of smoking
- -Interstitial disease within the parenchyma itself
- Resistance to movement is coming from something outside of the lung such as the chest wall
- NOT AS COMMON AS OBSTRUCTIVE!
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Scleroderma:
- Multi-organ disease due to presence of collagen everywhere
- 1. Progressive Systemic Sclerosis: progressive interstitial fibrosis with atrophy and sclerosis of many organ systems (skin, internal organs, walls of blood vessels)
- 2. Pulmonary Scleroderma: Excessive amount of bad collagen is replacing normal tissue, causes excessive tightening and fibrosis. CXR will show fibrocystic spaces (honeycomb) mostly at lung bases
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Systemic Lupus Erythematosus (SLE):
- disorder of immune regulation
- 1. Tissues damaged by autoantibodies and immune complexes
- 2. Characteristic butterfly rash on face
- 3. Intraoral Presentation: significant submucosal inflammation that leads to exfoliation of the mucous membraneslarge ulcers inside of the mouth
- 4. Cardiopulmonary Involvement: pleural effusion, pericarditis, endocarditis
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Ankylosing Spondylitis:
- A type of spondyloarthropathy of the axial skeleton (Inflammation at the site where the ligament attaches to the bone, get excessive bone deposition here)
- 1. Involves new bone formation and joint ankylosis “Bamboo Spine” (Vertebrae fused together, patients usually suffocate to death)
- 2. Frequently involves extra-articular featuresEx/ conjunctivitis, uveitis, urethritis, nail changes
- 3. Associated with certain HLA antigens (Ex/ HLA B27)
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Restrictive Lung Certain medications:
- i. Gold: severe immunosuppressant agent
- ii. Dilantin
- iii. Bleomycin
- iv. Mehotrexate
- v. Radiation: may lead to various forms of lung damage ranging from edema to fibrosis, pneumonia may set in the damaged lungs
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Inorganic or Organic Dust Exposure:
- may result in restrictive lung disorder
- usually contains bacteria or fungus that causes severe immune response inside of the lung
- i. Silicosis
- ii. Coal Work’s Pneumoconiosis: Fibrosis and scarring of the lungs due to prolonged inhalation of coal dust
- 1. Mortality and morbidity are strictly related to the type of coal dust and the length of exposure (silica is one of the worst things to inhale)
- iii. Hypersensitivity Pneumonitis: seen with farmer’s or mushroom worker lung
- 1. Presents acutely as flu-like illness with cough; subacutely as recurrent “pneumonia”; chronically as exertional dyspnea, productive cough and weight loss
- 2. Environmental microbial agents (Ex/ compost, peat moss), organic materials (Ex/ dust) and chemicals (ex/ plastics, resins, paints) identified as being causitive
- d. Idiopathic Fibrotic Disorders:
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Idiopathic Pulmonary Fibrosis (IPF):
- Pathology is unidentified, overtime the disease gets worse, life expectancy is ~2-3yrs
- 1. Clinical features include hypoxia and digital clubbing
- 2. Patients may benefit from anti-inflammatories in early stages, but advanced disease is associated with O2 dependency and poor prognosiscandidate for lung transplantation
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Sarcoidosis:
- Granulomatous tissue changes involving the lung and many other organ systems (lymph nodes, skin, eyes, liver, salivary glands, oral mucosa), prevalence higher among women and African Americans
- 2) Extrinsic Disorders
- a. Neuromuscular or skeletal diseases
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Restrictive Clinical Manifestations
- Diagnosis:
- Pulmonary Function Tests: Interstitial tissue changes lead to DECREASED VC, TLC, TV (Overall lung capacity has decreased vs. obstructive diseases where overall lung capacity has increased)
- Signs and Symptoms:
- -Progressive dyspnea especially with exercise
- -Cough, especially after deep breath, sputum not likely
- -Cyanosis seen in LATE stages
- Treatment:
- -Attempt to treat underlying problem
- -Corticosteriods, cytotoxic drugs
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Bronchitis
- -Inflammation of larger airways extending to tertiary bronchi, to be distinguished from:
- Bronchiolitis: acute inflammation of small airways
- Bronchiectasis: permanent dilation of bronchi and chronic cough
- -Most acute cases have viral etiology (all those implicated in common cold)
- -In young adults, atypical bacteria may be responsible
- Mycoplamsa pneumoniae and Chlamydia pneumoniae
- -In adults, Bordetella species are being recognized more frequently
- B. pertussis causes whooping cough
- -Non- productive cougha cough that extends for 1-3 weeks after a cold, usually lungs sound normal
- -Cough with an absence of clinical or radiographic evidence of pneumonia
- -Culture or serology for atypical bacteria (for patients with advanced or progressive disease)
- -Usually no treatment is needed
- at least 70% of pts with acute bronchitis in the US receive antibiotics
- (Mycoplamsa and C. pneumoniae may respond to erythromycin)
- (Bordetella is toxin mediated therefore antibiotics are not useful except very early on)
- Subsets of pts with bronchial hyperresponsiveness may benefit from beta-agonist inhalers
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Lung Abscess
- -Collection of pus within a destroyed portion of the lung
- -Variety of pathogens can cause it but oral anaerobes are most common (periodontal disease)
- -Consciousness impairing conditions (Ex/ seizures, drug overdoses), decreased ciliary function (Ex/smoking and alcoholism) and the use of nasogastric or endotrachial tubes
- -Sputum is usually putrid smelling
- -Usually requires prolonged antibiotic therapy
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Tuberculosis
- -Existed centuries before the dawn of civilization
- -“Phthisis”= Consumption
- -Incidence of TB declined in the US until 1985 when there was resurgence of TB that continued until 1993 (Increase in prison populations, immigration, HIV+)
- -Caused by Mycobacterium tuberculosis
- Non-motile rods with high lipid content in the wall, remarkable capacity to endure unfavorable conditions
- -Can circumvent destruction within macrophages
- -Able to limit access to bacterial targets of hydrophilic antiseptics and antibiotics
- -Very cold resistant, but heat, sunlight, and UV sensitive
- -Mounts an immune response -1/3 of the world’s population is currently infected
- -5-10% of people infected with TB become sick or infectious at sometime during their life
- -Environmental factors: poverty, malnutrition, stress, overcrowding
- -Risk of developing TB increases when TB co-exists with an alteration in the immune system like with HIV -Cough
- -Hemoptysis (coughing up blood)
- -Weight loss
- -Night sweats
- -Initial Infection: usually occurs in lungs and is controlled by immune system
- -Latent TB: after control of primary TB, bacilli remain dormant for the rest of the pts life
- -TB Reactivation: occurs when immunosuppressed
- GRANULOMA
- -Primary infectionusually in the middle to lower lobes
- -Secondary infectionusually in the upper lobes
- -Acid Fast Bacillus in body fluids (Gold Standard)
- -Culture
- -CXR (May take 6 weeks to become +)
- -Serologic Diagnosis (PPD skin test)
- -PCR
- -Enzyme linked immunospot (Like an ELISA)
- -Acid Fast Staining (Ziehl-Neelsen)
- -Post WWII: Isoniazid was very specific for TB
- -Problem with drug resistance: Multi-Drug Resistance (MDR) TB
- can develop when second-line drugs are misused or mismanaged and become ineffective
- -Active disease needs more than 1 drug: INH, rifampin, pyrazinamide, ethambutol
- PREVENTION: BCG Vaccine
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TYPCIAL PNEUMONIA
- -Bacteria commonly enter the lower airways but are contained by the host defenses
- -More than 50% of cases, physician doesn’t know what is causing it, but they just treat for broad range
- -With Strep Pneumonia, don’t need to do a sputum test
- -If only one lobe is infected, it is usually bacterial
- -Viral airway infections
- -Previous hospitalizations
- -Immuno-compromised
- -Aspiration altered state of consciousness, esophageal problems
- -Periodontal disease
- -Alcoholism
- -Tumors
- -COPD Symptoms:
- -Fever, Cough, Sputum Production, Various degrees of respiratory failure
- Signs:
- -Decreased breath sounds, Rales, Bronchovesicular breath sounds, Rhonchi, Dullness to percussion (abdomen and/or chest cavity should be hollow) -Suspect in pts with new respiratory symptoms (cough, sputum, dyspnea esp w/ fever), abnormal chest sounds
- -Presentation: Toxic appearance, fever, pleuritic chest pain, rusty colored sputum
- -TB test, fungal test (KOH), CXR, blood culture -Clarithro-mycin or erythromycin is good for Strep pneumoniae -Vaccine:
- should be given to patients 65+ or people with cardiac, pulmonary, diabetes, chronic liver, or alcoholism diseases
- -HIB vaccine
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Community-Acquired Pneumonia (CAP)
- -Not-institutionalized, not nosocomial
- -Through droplet nuclei, you can inhale pneumonia
- -Bacteria populates oropharynx
- -Aspirate some bacteria into lungs
- -Mostly related to Streptococcus pneumoniae
- Still causing over 20,000 deaths/yr in US
- Recent penicillin resistance cases are bad
- Vaccine available
- -Viral cases are mostly related to Influenza viruses and SRS
- To be suspected when epidemic is ongoing; associated with myalgias, vaccine available
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Severe Acute Respriatory Syndrome (SARS)
- -Type of CAP
- -Atypical Pneumonia
- -First described in China in late 2002
- -Caused by novel Coronavirus
- Cats and ferrets harbor the virus
- -Suspect with history of travel in areas with reported cases
- -Rapid onset of fever (>100F)
- -Chills and malaise
- -cough
- -dyspnea
- -watery diarrhea
- -CXR for evidence of pneumonia
- -Requires respiratory isolation precautions (N95 masks)
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Hospital Acquired (Nosocomial) Pneumonia
- -Usually acquired by health care workers or patients in hospital longer than 2-3 days
- -Mostly related to g-organisms (enteric bacilli) but can also be due to Staph Aureus and Strep pneumoniae
- -MRSA (Methicillin Resistant S. aureus) is the main concern
- -After 48-72 hrs of hospitalization, pt may develop fever, purulent bronchopulmonary secretions, lung infiltrate on CXR
- -CXR
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Immune Compromised Host pneumonia
- -Usually caused by a weird type of bacteria, but regular types are possible too -Variety of organisms including Fungi:
- Bacterial: Chlamydia, pseudomonas, TB, Strep pneumonia, Haemophilus influenzae
- Viral: cytomegalovirus, herpes zoster, respiratory syncytial virus, picornaviruses
- Fungal: aspergillus, cryptosporidium, candidia -Usually in HIV+ patients and other immunosuppressed people
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Pulmonary HTN
- -Increased pressure in the pulumonary circulation
- -Mean Pulmonary arterial pressure is >25mmHg at rest or >35mmHg during exercise
- -Primary Pul HTN (PPH): with unknown etiology
- -Secondary Pul HTN (SPH): occurring after a variety of conditions
- -LEADS TO R ventricular overload and failure
- -Also involves increased risk of coagulation
- -Cardiac: congenital heart disease (LR shunt with Eisenmenger’s complex, patent ductus arteriousus), Left Ventricular diastolic dysfunction
- -Connective Tissue Diseases/Vasculitis: Scleroderma, SLE
- -Pulmonary: COPD, restrictive lung disease, chronic high altitude exposure, obstructive sleep apnea
- -Portal Hypertension/Liver Failure
- -Pulmonary HTN can develop as a result of something happening on the Left side of the Heart (Secondary HTN)
- -Conditions that increase blood flow to the lungs will increase pressure too.
- -Pulmonary Embolism
- -Hepatic circulation is highly sensitive to pressure.
- -Fatiuge, exertional dyspnea, chest discomfort and syncope
- -PPH: pulmonary vessels become constricted and hypertrophied
- -Caused by endothelial dysfunction: enhanced remodeling, increased activity of vasoconstrictors, reduced activity of vasodilators
- -May be sporadic or familial
- -Measuring pulmonary artery pressure (PA catherization)
- -Vasodilators
- -In selected advanced cases, lung transplantation
- -Treatment of SPH involves management of the underlying disorder
- -At a high risk of PE
- -Over time, the degree of SOB increases. May experience some chest pain and will have problems with syncope.
- -Can lead to systemic HTN eventually.
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Pulmonary Embolism
- -Causes 50,000 deaths peryear
- -Occlusion of one or more pulmonary arteries by thrombi that originate elsewhere
- -Typical origins: pelvic vein, lower deep veins
- -Non-Thrombotic emboli: fat, usually following bone trauma, amniotic fluid and more uncommonly from a septic, foreign body and tumor origin.
- -Conditions that impair venous return and that cause endothelial injury or dysfunction
- -Hypercoagulable states
- -Women with breast cancer
- -Deep Vein Thrombosis
- -Blood clots form usually in the deep veins due to blood stasis
- -When they dislodge, they will travel in blood stream until they get stuck, which is usually in the lungs -Dyspnea and Tachypnea
- -Pleuritic chest pain
- -Cough
- -Leg swelling and pain
- -Anxiety
- -Diaphoresis (sweating)
- -Hypotension (affects CO)
- -Hemoptysis (if infarction has occurred)
- -Blood gas
- -CXRusually not helpful, but can rule out other issues
- -Ventilation-Perfusion scan (perfusion is usually more effected than ventilation)
- -Compression ultrasound
- -D-Dimer Test (a fibrin degradation product)
- -Angiography (invasive)
- -Spiral CT scanning and MRI angiography
- -Homan’s Test for DVT
- -Anti-coagulation
- -Fibrinolytic agents (clot-busting drugs)
- -Tying off inferior vena cava for recurrent embolisame can be achieved with an umbrella device in IVC
- -If not treated properly, can result in sudden death due to pulmonary artery complete blockage
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Pleural Diseases:
- A disease process leading to fluid accumulation in pleural space (Effusions)
- Exudative: caused by inflammation of the pleura, anything in the parenchyma of the lung
- increased protein, LDH and cells
- Pneumonia, TB, Meothelioma, PE, Sarcoidosis
- -Transudative: Caused by abnormal lung pressure, comes from the circulatory side
- CHF, Cirrhosis, Nephrotic Syndrome
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Exudative:
- pleural disease caused by inflammation of the pleura, anything in the parenchyma of the lung
- increased protein, LDH and cells
- Pneumonia, TB, Meothelioma, PE, Sarcoidosis
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Transudative:
- pleural disease caused by abnormal lung pressure, comes from the circulatory side
- CHF, Cirrhosis, Nephrotic Syndrome
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Mesothelioma:
- 50% due to asbestos exposure
- -30-35yrs after exposurepredisposes to it
- -Median age, 60; 5X more in men than women
- -Rest due to radiation and Simian Virus 40
- -CXR showing effusion
- -Biopsy through thoracoscopy
- -Surgery: pleurectomy, pneumonectomy, radiation and chemotherapy not improving survival
- -Very Poor prognosis
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Pneumothorax:
- gas in the pleural space (lung pressure is -)
- -Perforation of visceral pleura, penetration of chest wall, diaphragm or esophagus
- -Gas can be generated via microorganisms
- -Smoking (esp in females) and genetic factors increase risk
- -High Male:Femail ratio (6:1 for primary, 3:1 for secondary)
- Spontaneous: acute pain, dyspnea, cough, decreased breath sounds, CXR
- Secondary: result of trauma or pulmonary diseases
- -Severe emphysema, asthma, sarcoidosis, neoplasms, infections
- -May need chest tube placement
- -Surgery for severe cases
- Can see collapsed lung
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Hyperventilation Syndrome
- -Increase in Ventilation
- -Most of the time this syndrome is associated with anxiety
- -When you breathe too fast, you don’t build up CO2 and have too much O2
- -Will cause blood alkalosis
- -Tightness of the chest, Sweating, Flushing, Paresthesias, Tingling of fingertips, Sometimes even tetany (cramps)
- -Breaths/ minute
- -Treat the anxiety
- -Rebreathing of exhaled air
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Hypoventilation Syndrome
- -Decrease in Ventilation
- -Will cause a buildup of CO2 in the lungs and acidosis in the blood
- -Due to an imbalance between air flow and lung perfusion, there is a fall in the alveolar and capillary PO2 while the PCO2 increases (Hypercapnia and hypoxemia)
- -Continued hypoventilation may lead to cardiac arrhythmias, hypercapnic respiratory failure, acidosis and cor pulmonale.
- -Causes:
- COPD, asthma, pneumonia, pneumothorax, restrictive lung diseases, heart failure, pulmonary edema
- CNS inhibition (stroke, drug overdose)
- Neuromuscular (polio, myasthenia gravis)
- Musculoskeletal (severe kyphoscoliosis or ankylosing spondylitis)
- Upper airway problem (obstruction or swelling due to allergic rxn or infection)
- -Hypoxia after a long duration of hypoventilation
- -Very slow breathing
- -Can be an emergency like with a foreign object obstruction, or can be chronic
- -Relatively small increases in alveolar ventilation is associated with significant reduction in PCO2, so hypercapnic state can be easily compensated with restoring adequate ventilation
- -Treat the underlying problem
- Heimlich maneuver for obstructions
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Hypoventilation:
- Sleep Apnea Syndrome
- -Periods of dyspnea during the night
- -Can eventually affect the heart
- -Incompetence of the breathing muscles
- Lose their tone
- Tongue falls behind and causes the obstruction to be very drastic
- -Prolonged episodes of hypoventilation during sleep, loud snoring, daytime hypersomnolence, insomnia, obesity, hypertension
- -Sleep test
- -CPAP machine, dental devices, uvulopalatoplasty, removal of the intranasal adenoids, Correction of a deviated septum.
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Acid/Base Balance
- -Healthy individuals have normal [H+] that is maintained with a narrow range by body’s buffering system
- Most effective buffers are weak acids with pK’s close to the physiological pH (7.4) ex/H2CO3, H3PO4)
- The buffer system most commonly measured clinically to determine a patient’s acid/base status is the H2CO3/HCO3-.
- -Slight reductions or increases in blood pH can drastically effect body systems
- blood must remain in the very narrow range of 7.35-7.45pH
- -Achieved by normal respiratory and renal functions
- -On a daily basis large quantities of CO2 are generated in two forms:
- Volatile acids: produced by carbohydrate and fat metabolism, Lungs are responsible for this CO2, rapidly hydrated to produced carbonic acid and revered in the lungs for CO2 excretion
- **If the lungs cannot excrete the CO2, will get Respiratory Acidosis
- Non-Volatile Acids: produced from protein and phospholipid metabolism, Kidneys are responsible for excretion of these acids
- **If the kidneys are damaged, will get decreased bicarbonate stores and metabolic acidosis
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Respiratory Acidosis-Clinical Aspects
- -Caused by elevated PCO2 (Hypercapnia) and when a steady state cannot be achielved
- Usually as a result of reduced alveolar ventilation
- Can occur as acute or chronic acidosis
- Lab Findings: Increased PCO2 and H2CO3, reduced pH
- Body’s ability to defend acidity with shifts in PCO2 depends on buffer stores
- Compensatory mechanisms are primarily RENAL
- **Increased renal acid excretion (NH4Cl), increased synthesis and reduced reabsorption of bicarbonate
- Acute Effects: drowsinessstuporcoma
- Chronic Effects: headache and drowsinessfatigue, lethargy, confusion
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Metabolic Acidosis-Clinical Aspects
- -Reduction in effective levels of HCO3-
- -This can be due to either bicarbonate loss or build up of too much non-volatile acids
- Caused by renal failure, diabetic ketoacidosis, severe diarrhea
- anion gap refers to a disproportionate increase in non-volatile acids relative to the available bicarbonate
- **The higher the gap, the worse the acidsosis
- Lab Findings: Reduced plasma HCO3-, reduced pH
- Compensatory mechanisms are primarily respiratory, increased respiration to lower PCO2
- Mild Acidosis: may be asymptomatic, but usually have nausea, vomiting, fatigue, deeper and faster breathingextreme weakness, drowsiness, confusion and increasing nausea
- Severe Acidosis: severe hypotension, shock, coma and death.
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Nasopharyngitis (Common Cold)
- -Transmission from person to person of non-normal flora viruses
- -Over 90% are caused by viruses:
- Rinoviruses (50%), coronaviruses, respiratory syncytial (RSV) are the most common ones
- Adenovirus, influenza and parainfluenza are common too
- -Typical common cold
- -Symptomatic treatments with OTC meds
- -When flying, decongestants can reduce barotrauma
- ANTIBIOTICS HAVE NO ROLE!
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Influenza
- -Influenza types A or B cause epidemics of disease almost every winter (Usually originates in SE Asia)
- -Influenza type C infections cause a mild respiratory illness and are not thought to cause epidemics -Transmission: expired air from an infected person and also by direct contact with respiratory droplets
- Incubation period is usually 2 days, but can range from 1-5 days
- -Abrupt onset of fever, aching muscles, sore throat, non-productive cough
- -Runny nose, headache, burning in the chest, eye pain, sensitivity to light
- -Pneumonia is the major complication of the flu
- Can develop 5 days after viral influenza
- Worsened cough, difficulty breathing, persistent or recurring fever, bloody sputum
- -Reye’s Syndrome: occurs almost exclusively in children; severe vomiting and confusion, may lead to coma
- Treatment: Oseltamivir (Tamiflu), Zanamivir (Relenza) protection against both A and B viruses
- -Amantadine Simmetrel) and Rimantadine (Flumadine)protection against A only
- **Medication use limited to vulnerable, unvaccinated persons when an outbreak is underway
- Vaccines: New vaccine every year due to new emerging subgroups. Most common Flu A and B strains are included in each year’s vaccine
- Inactivated Form (IM): recommended for people over 50, children b/w 6mos and 2yrs, pregnant women in their second trimester, long-term care facility residents, anyone with chronic heart, lung, or kidney conditions, diabetes or immunosuppressed
- Live attenuated form (Nasal Spray): healthy, non-pregnant people ages 4-59.
- -Influenza Type A viruses are divided into subtypes based on two proteins on the surface of the virus
- Hemagglutinin (H) and neuraminidase (N)
- Current subtypes of influenza A viruses found in people are H1N1, H1N2, H3N2
- -Influenza Type B are not divided into subgroups
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Pharyngitis
- -“Strep Throat”
- -Intense, burning in the back of the throat
- -Caused by a variety of agents:
- Viral: EBV, adenovirus, influenza, parainfluenza, RSV
- Bacterial: GAS, gonococcus, anaerobes
- -Soreness, scatchiness, or irritation of the throat, fever
- -Erythema, edema, exudates of the throat, cervical adenopathy may be present, inflamed salivary glands -Diagnosis: Can take a throat culture of an pus or exudates in throat
- ”Rapid Strep Test”: False negatives are possible, usually want a culture
- -Complications: Rheumatic Fever (RF), Peritonsillar abscess, Glomerulonephritis can also follow GAS infection, Scarlet fever is strep pharyngitis with an allergy-mediated skin rash (Will see a rash and raspberry appearance on the tongue due to enlarged taste buds)
- Will rarely lead to: Necrotizing fasciitis (deep seated infection of subcutaneous tissue destroying facia and fat) or Toxic Shock Syndrome (bacteremia, shock and multiorgan failure.
- -Treatment: No treatment if cause is viral
- Appropriate antibiotic if bacteria is the cause:
- **Streptococcus Pyogenes (GAS)Penicillin for 10-14 days
- -You can’t distinguish between bacterial and viral by clinical appearance
- Dysphagia more characteristic of GAS pharyngitis
- Some may cause a rash like GAS.
- Ulcerated lesions are usually from EBV, but sometimes from coxsackie
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Laryngo-Tracheo-Bronchitis (Croup)
- -Intense cough -Mostly caused by viruses
- -Fever, Hoarseness, “seal’s” bark cough, inspiratory stridor, rales, ronchi, wheezing Diagnosis: Lab Tests (WBC, X-ray may show narrowing of air shadow of the trachea, hypoxemiaPresent in most)
- Treatment: Oxygen, steroids may be of some benefit to reduce inflammation
- Complications: Occasional respiratory compromise requiring hospitalization.
- Bronchiolitis: severe form with significant hypoxemia, usually caused by RSV, especially in infants, treated with an antiviral agent (Ribavirin in an aerosolized form). Extremely rare!!
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Epiglottitis
- -Rapidly progressive celluitis of the epiglottis
- -Usually caused by HIB (Hemophilus influenzae B)
- -Can be life threatening but has been dramatically reduced with HIB vaccine.
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Otitis Media
- -Ear Infection
- -In children, it is commonly bacterial:
- S. pneumonia, HIB, S. pyogenes
- -Can be viral
- -Pain, often severe
- -inflammation of the middle ear
- -Tympanic membrane wil show signs of inflammation
- -Loss of light reflex Diagnosis: Pneumatic otoscopy, impedance tympanography, must check the hearing and pressure of the middle ear
- Treatment: Antibiotics! improve symptoms (but close to 90% improve w/o antibiotics); Analgesics, Decongestants new protein conjugated pneumococcal vaccines.
- sometimes a tube must be placed to drain the middle ear. Will compromise hearing somewhat
- Complications: chronic serous otitis, hearing loss
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Otitis Externa
- -Infection of the external canal
- -usually associated with moisture
- -Pseudomonas aeruginosa is most common, sometimes S. aureus
- -Malignant form in diabetics (may invade cartilage, bone, CNShigh mortality
- Treatment: Topical (if not complicated, keep ears dry)
- Malignant Form: surgical debridement and systemic antibiotics
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Sinusitis
- -Usually follows the common cold
- -Increased frequency in HIV patients who have more unusual orgnansims
- -Most cases are bacterial: S. pneumonia, H. influenza (acute), anaerobes (chronic)
- -Post-nasal drip, in some cases mucous can get caught in the sinuses and can result in a serious infection. -Facial pain, frontal headaches
- -Purulent nasal discharge
- -Tenderness over sinuses
- Diagnosis: CT and MRI scans are best, but are expensive.
- Routine X-Rays are insensitive (Water’s View: will show cloudiness in the sinus, but CT will also show if there is a deviation)
- Treatment: ANTIBIOTICS!
- Lavage may be helpful
- Role of decongestants is not proven yet.
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Relal Disease
- Patients with renal dysfunction exhibit signs and symptoms of renal disease regardless of etiology or other accompanying systemic conditions
- -RENAL FUNCTIONS:
- 1) Clearance of Nitrogenous waste
- 2) Regulation of electrolytes and pH
- 3) Regulation of Volume
- 4) Synthesis of active forms of vitamin D
- 5) Synthesis of erythropoietin
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Evaluation of Kidney Function
- Blood Tests:
- -Blood-urea nitrogen (BUN), 8-20mg /dLproduct of protein catabolism, may be affected by higher protein intake
- -Creatinine, 0.7-1.5mg/dL: result of liver conversion of creatine produced by myocytes
- -BUN/Creatinine Ratio: used to determine the body’s volume status
- -GFR: can be calculated based on patient’s ethnicity, age and gender
- Urine Analysis:
- -Examine RBC, WBC, protein, casts and crystals
- -Look for proteinuria, microalbuminuria, Na, K, and creatinine
- -Do the DIP TEST
- Imaging:
- -Structural evaluation using ultrasound, radionuclide scanning and MRI
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Acute Kidney Injury:
- functional or structural kidney abnormality manifested within 48hrs by tests
- -Involves a reduction in renal GFR causing N waste retention
- -Can lead to Azotimea (buildup of N, but not that much) or Uremia (too much N waste in the blood)
- Pre-Renal: mostly caused by renal hypoperfusion
- decreased intravascular volume, but increased extracellular volume
- Renal autoregulatory systems usually preserve GFR
- Renal: variety of diseases involving renal parenchyma (tubules, interstitium, vasculature, glomerulous
- Acute Tubular Necrosis (ATN): tubular injury usually due to ischemia or toxins (aminoglycosides, chemotherapy)
- Acute Interstitial Nephritis (AIN): injury to renal interstitium due to medications, infection, inflammatory conditions
- Vascular damage (Thrombotic events)
- Glomerulonephritis: glomerular damage caused by many conditions such as SLE and polyarteritis nodosa
- Post-Renal: bilateral urinary outflow obstruction due to precipitation of uric acid crystals in tubules, bilateral kidney stones, or enlarged prostate
- -Usually occurs in the hospital with mortality rates as high as 86%
- Pre-Renal: dehydration, bleeding, burns
- Pre-Renal: easily reversible unless it progresses to tubular damage
- -Depending on the underlying cause, some are easily reversed with hydration in pre-renal cases.
- -Some will go on to chronic renal failure
- -Careful monitoring of volume and electrolytes especially during recovery period is important
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Chronic Kidney Disease:
- Spectrum of clinical problems beginning with lab abnormalities in kidney function to a late stage labeled “Uremia”
- -End-Stage Renal Disease (ESRD): when kidneys fail to perform most of their functions (BUN>60mg/mL)
- -Kidney damage for more than 3 months as defined by structural or functional abnormalities of the kidneys with or without decreased GFR
- -Two important causes: Diabetes mellitus, HTN
- Uremia: clinical condition that results from renal failure
- -Causes many clinical problems: metabolic acidosis, hyperkalemia, volume overload, osteodystrophy (replacing structures with bone that shouldn’t be), osteomalacia (softening of the bone), hyperuricemia, neuropatheis, myopathies, seizures, pericarditis, HTN, pruritus, anemia, platelet dysfunction
- -GFR values less than 90 mL/min=Stage 1
- -With decreasing GFR, stages 2-5 are identified
- -Renal Failure defined as GFR < 15mL/min requiring hemodialysis
- -Dyspnea on exercise, nail changes, bone pain, edema, myopathy, peripheral neuropathy, bruising -Slow down the process by decreasing protein intake and controlling underlying causes
- -ESRD: Hemodialysis, peritoneal dialysis (associated with infections) or renal transplant
- -Not requiring dialysis: control BP!
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Glomerular Diseases:
- usually immune mediated
- 1) Antibodies directed against glomerular Basement Membrane
- 2) Antibody-Antigen complex deposition mostly leading to vasculitis
- These lead to red cell casts, hematuria, proteinuria, renal insufficiency, HTN, nephritic syndromes
- -Renal biopsy is usually needed to establish diagnosis
- -Treatment depends on cause
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Useful Serologic Tests for Diagnosis
- 1) Antinuclear Antibody (ANA): suggestive of glomerular disease and SLE (and really any autoimmune), not that specific
- 2) Anti Double stranded DNA and Anti-Smith Antibodies: seen in SLE
- 3) Rheumatoid Factor (RF): seen in vasculitis
- 4) Complement (C3 and C4): seen in glomerulo-nephritis
- 5)Urine Bens Jones Proteins: seen in myeloma kidney, amyloidosis and lymphoma (cases with excessive Ig production)
- 6) Antiglomerular basement membrane antibody: seen in Goodpasture’s syndrome
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Tubulointerstitial Diseases:
- damage the tubules and interstitum, can be chronic or acute.
- -Causes: drugs, obstruction, infections, toxins, vascular problems
- -Tubular defects can lead to a variety of metabolic problems: Renal tubular acidosis, aminoaciduria, salt, K, Mg wasting, concentrating defect
- -Urine contains RBCs, WBCs, and WBC casts
- -Proteinuria
- -Treatment depends on underlying causes
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Hematuria
- -Blood in the urine
- ->5 erythrocytes per high powerfield
- -cause may originate anywhere in the GI tract
- -infections, stones, malignancies
- -connective tissue diseases
- -renal diseases
- -bleeding tendencies
- -usually requires urinalysis and evaluation of urinary tract such as an IVP (Intravenous pilogram; uses dye to track the path)
- -Tests: PSA, BUN creatinine, PT, PTT, ANA
- -Depends on underlying cause
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Proteinuria
- -Protein in the urine
- ->150mg of protein excretion in 24hrs
- -Nephrotic Syndrome: protein excretion >3.5 mg/day, hyperlipidemia, hypertension and edema
- -renal diseases, infections, drugs
- -diabetes, Connective Tissue diseases, vasculitis
- -malignancies
- -proceeds along differential possibilities
- -depends on underlying cause
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Hyponatremia
- Disorders of Na Balance:
- -Normal Na Level=135-145 meq/L
- -Too little Na in the system
- -Can lose water along with Na
- -Can be classified along volume status, usually associated with hypo-osmolal state
- -Brain cells can dehydrate and shrink if too little water or Na in the blood. Will lead to unconsciousness, seizures or confusion -Hypovolemia (More Water loss than Na): diarrhea, vomiting, diuretics, mineralocorticoid deficiency
- -Euvolemia (Same Water loss as Na): SIADH (Syndrome of Inappropriate ADH), postoperative, psychogenic polydipsia
- -Hypervolemia (More Na than water lost): CHF, liver disease, renal failure
- -Blood test
- -Depends on underlying cause
- -Fluid restriction with SIADH
- -Replacement in hypovolemic states: needs to be done carefully if patient has difficulty handling volume
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Hypernatremia
- Disorders of Na Balance:
- -Too much Na buildup in the system
- -Usually from free water loss coupled with impairment of thirst mechanism
- -Usually a CNS problem
- -Water loss may be through kidneys (Hyperglycemia, diabetes insipidus) or nonrenal (excess sweating, osmotic diarrhea)
- -Usually has a mental status change
- -Replace fluids
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Hypokalemia
- -Too little K in the blood
- -Normal K level=3.5-5.0 meq/L
- -Usually 98% of the K is INSIDE the cell
- -Cellular shifts: induced by glucose load, insulin, beta-agonists
- -Losses through GI tract or kidneys (diuretics, antibiotics, diarrhea, renal diseases, mineraloglucocortico excess)
- -Fatigue, weakness, hypoflexia, cramps
- -Cardiac manifestations= arrhythmias
- -EKG: T wave flattening and U waves (repolarization is lost)
- -Treat underlying conditions and replace the K
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Hyperkalemia
- -Too much K buildup in the blood
- -Can lead to bradycardia (when the myocytes contract, they require active transport in order to bring K back into the cell)
- -Renal failure
- -Adrenal insufficiency
- -Excess K intake or K sparing diuretics -EKG changes include peaked T waves and loss of P waves
- -Refractory period is sometimes extended because the relative concentration of K in and out of the cell is different due to buildup of K outside of the cell
- -T waves will be spiking due to fast repolarization
- -In acute emergencies, cellular shifting of K by infusion of Ca, glucose, and insulin
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Nephrolithiasis
- -Kidney Stone (5% of people will have one in life)
- -hypercalcuira, hyperuricosuria, hyperoxaluria, hypocitraturia, hypomagnesiuria
- -Visualization of GI tract using ultrasound or CT
- -<5mm will pass on own
- ->10mm will require lithotripsy
- -Treat underlying condition to prevent stone formation
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Dental Implications of Renal Disease
- • In Patients with End Stage Renal Disease
- o Pretreatment screening for bleeding tendencies, anemia, and susceptibility to infections and potential for HTN
- o Avoid drugs excreted by kidneys or nephrotoxic drugs
- o Questions to Ask:
- What kind of kidney disorder do you have?
- Do you have problems with BP management?
- Are you on Anti-Virals? (One of the drugs that can cause renal problems is acyclovir)
- Are you on Dialysis? (Can’t treat them the same day as dialysis because they have too much heparin in their system)
- • In Patients on Renal Dialysis
- o Use all the precautions above
- o The risk for bacterial endarteritis of the AV fistula but prophylaxis not universally used
- o Best to treat on the day after dialysis due to high heparin levels on the day of dialysis
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