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  1. 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”
  2. 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
  3. 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
  4. 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
  5. 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
  6. Obstructive Symptoms
    • features of both emphysema and chronic bronchitis at the same time:
    • 1) Dyspnea
    • 2) Cough
    • 3) Sputum Productionscant in emphysema, but often copious and purulent in chronic bronchitis
    • 4) Clubbing of Fingersexcessive 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)
  7. 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
  8. 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)
  9. 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
  10. 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 productionmost 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
  11. 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
  12. 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
  13. 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 membraneslarge ulcers inside of the mouth
    • 4. Cardiopulmonary Involvement: pleural effusion, pericarditis, endocarditis
  14. 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 featuresEx/ conjunctivitis, uveitis, urethritis, nail changes
    • 3. Associated with certain HLA antigens (Ex/ HLA B27)
  15. 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
  16. 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:
  17. 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 prognosiscandidate for lung transplantation
  18. 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
  19. 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
  20. 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 cougha 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
  21. 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
  22. 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
    • -Primary infectionusually in the middle to lower lobes
    • -Secondary infectionusually 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
    • -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
  24. 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
  25. 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)
  26. 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
  27. 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
  28. 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 (LR 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.
  29. 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
    • -CXRusually 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 embolisame can be achieved with an umbrella device in IVC
    • -If not treated properly, can result in sudden death due to pulmonary artery complete blockage
  30. 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
  31. 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
  32. Transudative:
    • pleural disease caused by abnormal lung pressure, comes from the circulatory side
    • CHF, Cirrhosis, Nephrotic Syndrome
  33. Mesothelioma:
    • 50% due to asbestos exposure
    • -30-35yrs after exposurepredisposes 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
  34. 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
  35. 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
  36. 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
  37. 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.
  38. 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
  39. 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: drowsinessstuporcoma
    • Chronic Effects: headache and drowsinessfatigue, lethargy, confusion
  40. 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 breathingextreme weakness, drowsiness, confusion and increasing nausea
    • Severe Acidosis: severe hypotension, shock, coma and death.
  41. 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
  42. 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
  43. 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
  44. 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, hypoxemiaPresent 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!!
  45. 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.
  46. 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
  47. 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, CNShigh mortality
    • Treatment: Topical (if not complicated, keep ears dry)
    • Malignant Form: surgical debridement and systemic antibiotics
  48. 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.
  49. Relal Disease
    • Patients with renal dysfunction exhibit signs and symptoms of renal disease regardless of etiology or other accompanying systemic conditions
    • 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
  50. Evaluation of Kidney Function
    • Blood Tests:
    • -Blood-urea nitrogen (BUN), 8-20mg /dLproduct 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
  51. 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
  52. 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!
  53. 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
  54. 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
  55. 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
  56. 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
  57. 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
  58. 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
  59. 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
  60. 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
  61. 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
  62. 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
  63. 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
Card Set
Younai Systems Lung Renal
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