Pulmonary 1 Flashcards
What systems could potentially be source of lung pathology?
respiratory cardiovascular (e.g. CHF) gastrointestinal (GERD) CNS (eg. anxiety) renal (eg. CRF) endocrine (eg. DM) musculoskeletal (herpes zoster, costochrondritis)
What are some environmental exposures that should be assessed in taking history?
Occupation, household chemicals, recent travel, areas of pollution, smoking, pets, hobbies (eg. ceramics, carpentry), Sleep environment, type of pillows, bedding, use of humidifier, Heating system- gas exacerbates allergies, wood exacerbates mold, electric cleanest
What are some common causes of a cough?
Upper respiratory tract infections Asthma Lung infx (pneumonia, acute bronchitis) COPD (emphysema, chronic bronchitis) Rhinosinusitis leading to postnasal drip Lung dz: bronchiectasis, interstitial, tumor Gastroesophageal reflux disease (GERD) Cigarette smoking Second-hand smoke exposure Air pollution exposure ACE inhibitors Aspiration Cystic fibrosis- young individual CHF—unproductive cough at night Anxiety—nervous cough Chronic idiopathic cough
What questions should be asked when taking history to investigate cough?
Duration, sudden or gradual, any recent change in cough?
- Acute cough: < 3 week duration—most likely from infection, exacerbation of underlying lung disease
- Subacute cough: 3-8 wks—often post-infectious
- Chronic cough: >8 wks—often from upper airway cough syndrome (i.e post-nasal drip from allergies, rhinitis, rhinosinusitis), asthma or GERD
What factors affect it? (cold air, talking, eating, posture, drinking, exercise)
Sputum production: amount, quality, color
Any concomitant symptoms? Ie. chest pain, dyspnea, hoarseness, dizziness
Patterns of the cough -
- with posture change suggests chronic lung abscess, TB, bronchiectasis, tumor
- during eating suggests problem with swallowing mechanism
- with cold air or exercise suggests asthma
- in am, that persists until sputum is produced is characteristic of chronic bronchitis
- in am may suggest allergy to something in sleeping quarters
What are some common colors of sputum and corresponding conditions?
- clear: allergy, COPD
- yellow: infection (acute bronchitis, acute pneumonia) (live neutrophils)
- green: chronic infection (chronic bronchitis, pneumonia, bronchiectasis, CF- neutrophil breakdown)
- brown/black/rust: “old blood” eg. chronic bronchitis, chronic pneumonia, TB, lung cancer
- Quantity (scant, profuse) and quality (thin, stringy, thick, etc)
What are some causes of hemoptysis
Airway inflammation
Bronchogenic carcinoma (may be frothy)
Foreign body
Airway trauma
Autoimmune disease
Coagulopathy
Lung parenchymal infection (TB {streaks of blood}, pneumonia, abscess)
Cocaine-induced pulmonary hemorrhage
Pulmonary embolism (bright red)
Esophageal varicesWhat are some causes of physiologic dyspnea?
most common
exertion
high altitude
What are 4 types of pulmonary dyspnea with examples of conditions?
i) restrictive: low compliance of the lungs, usually OK at rest, worse with exertion
- pulmonary fibrosis
- chest deformities: eg pectus excavatum, scoliosis
- broken ribs
- obesity
ii) obstructive: increased resistance to airflow, esp. with expiration
- asthma
- upper airway edema due to allergies, infection
- cystic fibrosis
- COPD (emphesema, chronic bronchitis)
iii) infectious
- pneumonia
- severe acute respiratory syndrome (SARS)
iv) non-infectious
- lung cancer
- sarcoidosis
- pleural effusion
- pneumothorax
- pneumoconiosis
- atelectasis
What are some conditions associated with dyspnea with cardiac origin?
congestive heart failure cardiogenic pulmonary edema valvular heart disease dissecting aortic aneurysm ischemic heart disease cardiomyopathy pericardial effusion malignant hypertension cardiac asthma: acute resp. insufficiency caused by L ventricular failure with bronchospasm, wheezing and hyperventilation
What signs would indicate dyspnea of cardiac origin?
a. Cheyne-Stokes respiration: alternating periods of apnea and hyperpnea (gradually increasing depth and frequency of respiration)
b. Orthopnea: respiratory problems while supine (Left ventricular failure)
c. Paroxysmal Nocturnal Dyspnea (PND): pt awakens gasping for breath and must sit or stand up (eg mitral stenosis, aortic insufficiency, HTN)
Besides physiologic, pulmonary, and cardiac, what are 3 other potential sources of dyspnea?
chemical (acidosis may result in slow, very deep gasping respirations (ie “Kussmaul breathing” - trying to blow off CO2 to compensate for acidosis) - May be seen in diabetes (DKA), chronic anemia, pregnancy, renal failure) neuromuscular (multiple sclerosis, ALS, myasthenia gravis, Guillain Barré Syndrome) Psychological conditions (anxiety, panic attacks)
What are the potential sources of chest pain?
cardiac pulmonary GI musculoskeletal/skin CNS (anxiety)
What are the qualities of cardiac chest pain?
usually crushing, pressing or squeezing, generally aggravated by exertion, cold weather, stress, and after meals. May radiate to neck, jaw or arm
What are the qualities of pulmonary chest pain?
localized, sharp and knifelike; worse breathing or coughing (pleural pain); e.g. - pleurisy, pneumonia, TB, cancer, atelectasis, thromboembolism, pleural effusion, histoplasmosis, pneumothorax
What are the qualities of GI chest pain?
may be sharp, burning, squeezing, or heavy; affected by swallowing (spasm), large meals, certain foods, body position, GERD
What are examples and qualities of musculoskeletal/skin chest pain?
costochrondritis fractured rib (history of fall - pain will be elicited by palpation exam) herpes zoster (prodromal sx, then vesicles erupt along dermatome)
What are the 4 important things to do in lung PE?
Inspection (resp rate, signs of respiratory distress, chest configuration, coloration, etc)
Palpation (assess area of pain, chest expansion, tactile fremitis)
Percussion
Auscultation
What are the notes associated with lung percussion?
Flat: soft, high pitch, short duration – eg. sounds like percussion over thigh muscle
Dull: medium intensity, pitch and duration – eg, sounds like percussion over liver suggests pleural thickening, atelectasis, consolidation, pleural effusion
Hyperresonant: very loud, low pitch, long duration– suggests trapped air as in pneumothorax, severe emphysema
Tympanic: musical quality, e.g., over stomach or puffed cheek
What is diaphragmatic excursion?
Percussion on back between ribs 10-12
During inhalation, lungs should fill to rib 12
During exhalation, lungs should rise to rib 10
What are the normal sounds of lung auscultation?
Vesicular - soft, low pitch, normal over most lungs fields; inspiration lasts longer than expiration I>E
Bronchial – loud, moderately high pitched. Heard over central bronchus. I=E
Bronchovesicular - medium intensity and pitch, normal over main-stem bronchi
Tracheal - loud, high in pitch, normally heard over trachea, E>I (not performed)
When would you hear absence of breath sounds?
Collapsed lung
When would you hear decreased breath sounds?
when normal lung is displaced by air (emphysema or pneumothorax) or fluid (pleural effusion) Increased distance between lung and chest wall
When would you hear bronchial breathing?
consolidation in lower lobes changes sounds from vesicular to bronchial (blockage of passage of air through area of consolidation, prevents vesicular sounds and makes bronchial sounds dominant).
What are crackles?
(prev term “rales”)
popping sounds, usually heard during inspiration, do not clear with cough produced by the passage of air through bronchi that:
1) contain secretions (early inspiratory crackles)
OR
2) are constricted by spasm or thickened walls (pan- or late insp)
What are Rhonchi?
(low pitch wheezes)
originating in upper airways - often have a “snoring “gurgling”, rumbling quality
caused by secretions and resulting obstruction in large bronchi
prominent on expiration, tend to clear with coughing
What are wheezes?
high pitched, musical, or whistling sounds caused by narrowing or obstruction of small bronchi or bronchioles, the walls oscillate creating the sound
may be of one pitch (monophonic) or several pitches (polyphonic) depending on size of airway(s) involved
usually heard during expiration, particularly forced expiration
diffuse over lung fields with asthma, bronchitis, COPD
localized if obstruction in bronchus- eg tumor, secretions or foreign body
What is stridor?
inspiratory wheeze associated with upper airway obstruction (eg Croup)
What are pleural sounds?
pleural friction rub
pleural fluid decreased or absent; usually due to inflammation of pleura; loud creak or grating sound, like the cracking of leather on both inspiration and expiration
Often with concurrent Pleurisy- sharp knife-like localized pain; patient may hold side (“splinting”) to minimize chest wall movement
What is broncophony?
(vocal fremitus)
1 - patient repeats “ninety-nine” in a normal voice
2 - auscultate over area of concern as they repeat it, comparing to opposite side.
3 - “99” will normally be muffled and indistinct. Louder, clearer sounds (called bronchophony) over area of consolidation
What is whispered pectoriloquy?
1 - patient repeats a whispered “1,2,3”
2 - auscultate over area of concern as they repeat it, comparing with opposite side.
3 - Normally faint sounds or nothing at all is heard. Clear “1,2,3” heard over area of consolidation
What is egophany?
1 - patient repeats “ee” in a normal voice
2 - auscultate over area of concern as they repeat it, comparing with opposite side.
3 - Normal: muffled “ee” sound. Abnormal if “ee” turns to “Ay” (E to A change) over area of consolidation (Lower pitched frequencies transmitted)
What are some labs that could be run for pulmary diagnostic measures?
CBC – for infection, allergies etc.
Comprehensive Metabolic Panel (CMP) – electrolytes, glucose, lipids; liver enzymes (serum LDH and protein to compare with pleural fluid expressed from thoracentesis)
Sputum cultures
Arterial Blood Gases (pH, PaO2, PaCO2, HCO 3-)
TB testing—Quantiferon Gold, Mantoux test (older technology)
COPD etiology/risk factors?
Tobacco smoking –primary risk factor. Up to 90% of COPD deaths linked to smoking
air pollution – particulates & gases from the combustion of fossil fuels; hydrocarbons
second-hand smoke- higher in concentration of toxic substances than exhaled smoke
history of childhood respiratory infections - Viral infections (adenovirus, RSV) enhance inflammation & predispose to bronchial hyper-reactivity.
occupational exposure to industrial pollutants (cadmium and silica - coal miners, cement handlers, metal workers, grain handlers, cotton workers, paper mill workers)
alpha-1-antitrypsin (AAT) deficiency (familial emphysema)
asthma increases the risk for developing COPD (12x more likely) later in life
COPD SSx?
Dyspnea (worsens with exertion) chronic productive cough wheezing Barrel chest use of accessory muscles hyperresonance cyanosis
COPD diagnostic workup?
Pulmonary Function Tests (inc TLC) Pulse oximetry CBC Arterial blood gases (ABGs) (hypoxemia, then hypercapnia late) Alpha-1-Antitrypsin level (FHx) CXR Chest CT Forced Expiratory Time (FET) – quick in office test using bell of stethoscope, time the duration of audible expiration after takes a deep breath and blows out as fast as they can (FET > 6 seconds indicates considerable expiratory flow obstruction) Spirometry (FEV1) Normal - >85% Moderate - 50-79% Severe - 30-49% Very severe <30%
Emphysema AAT deficiency?
Familial emphysema: (1-3% of cases)
AAT, produced by the liver, is a “lung protector.” In the absence of AAT, emphysema is almost inevitable. Symptoms of AAT deficiency: emphysema usually begins between 32 - 41 yrs and includes shortness of breath (SOB) and decreased exercise capacity. Blood screening is used to diagnose if a patient is a carrier or AAT-deficient.
Emphysema SSxs?
“pink puffers”
dyspnea
exercise intolerance
cough is rare - scant clear mucus
Emphysema PE findings?
barrel chest (increased A-P diameter) from hyperinflated lungs
thin, can look cachectic (muscle and fat wasting)
Appear uncomfortable.
Purse-lipped breathing
Prominent use of accessory resp muscles
hyperresonance on percussion, decreased diaphragmatic excursion
decreased breath sounds
expiratory crackles, wheezing
PMI may be deviated towards sternum
No peripheral edema
Hoover’s sign: lower ribs pull together with deep inhalation
May see yellowing of fingertips from nicotine stains
Emphysema lab findings?
Hgb normal
ABGs: PaO2 normal to reduced; PaCO2 normal to reduced
reduced FEV1
Chronic bronchitis characteristcs/dx criteria?
mucus hyper-secretion secondary to hypertrophy of the glandular elements of the bronchial mucosa producing a cough most days of the month, 3 months of a year for 2 successive years without another explanation.
Once the bronchial tubes have been irritated over a long period of time, excessive mucus is produced constantly, the lining of the bronchial tubes becomes thickened and scarred, an irritating cough develops and air flow is reduced
Chronic Bronchitis SSxs?
“blue bloaters”
Chronic productive cough with frequent exacerbations (infections)
Mucopurulent sputum; cough usually worse in am
Dyspnea is mild, but can affect activity
Wheezing may occur, particularly during exertion and exacerbations
PE: Patient often overweight and cyanotic (bluish tinge may be seen in oral mucosa, lips, and nail beds)
Respiratory rate and heart rate increases proportionally to disease severity.
Hyperinflation (barrel chest),
Hyperresonance on percussion
Rhonchi, wheezes, diffusely decreased breath sounds, and prolonged expiration
Early inspiratory crackles can be heard (as air passes mucus in upper airways)
Advanced disease: cyanosis, elevated jugular venous pulse (JVP), and peripheral edema
Chronic bronchitis PE findings?
Patient often overweight and cyanotic (bluish tinge may be seen in oral mucosa, lips, and nail beds)
Respiratory rate and heart rate increases proportionally to disease severity.
Hyperinflation (barrel chest),
Hyperresonance on percussion
Rhonchi, wheezes, diffusely decreased breath sounds, and prolonged expiration
Early inspiratory crackles can be heard (as air passes mucus in upper airways)
Advanced disease: cyanosis, elevated jugular venous pulse (JVP), and peripheral edema
Chronic bronchitis lab findings?
Hgb elevated
ABGs: PaO2 reduced; PaCO2 elevated
reduced FEV1
Late stage chronic bronchitis complications?
hypoxemia pneumonia pulmonary hypertension cor pulmonale respiratory failure
Asthma characteristics?
Reversible obstructive lung disorder with an increased reactivity of airways to various stimuli causing episodes (“attacks”) of wide spread broncho-constriction and dyspnea
*Features overlap with COPD (airflow obstruction, underlying inflammation) but what differentiates it is the degree of reversibility
3 major featurs of asthma?
- Airway obstruction– Air moving through the tightened airways causes vibration and a whistling sound known as wheezing. Episodic and Reversible
- Inflammation - red and swollen bronchial tubes.
- Airway irritability– Airways extremely sensitive and tend to overreact to triggers such as pollen, animal dander, dust or fumes.
Common asthma triggers?
Upper respiratory infections - cold and flu, bronchitis or sinus infections
Inhalant allergens- 80% of people have allergies to airborne substances such as pollens, mold, animal dander, dust mites
Medications (aspirin, NSAIDs)
Food and food additives (eg. Sulfite sensitivity - shrimp, dried fruit, beer, wine)
Strenuous exercise may cause a narrowing of the airways in ~80%
Irritants- tobacco smoke, smoke strong odors (perfumes, and cleaning agents); air pollution (SO2, NO2, ozone), occupational dust/vapors
Weather - cold air, changes in temperature and humidity
Strong emotions - anxiety, crying, yelling, stress, anger
Gastroesophageal reflux disease (GERD)
Extrinsic vs Intrinsic asthma?
extrinsic (or allergic) - allergy to external factors such as pollen, mold, animals, lint, insecticides, foods, drugs
intrinsic (or non-allergic) - from infection of upper (nose, sinus) or lower (bronchi, lungs) resp tract, irritants, emotional factors, exercise, cold weather
Asthma SSxs?
(no signs between asthmatic episodes) Cough, especially at night or with exercise (exercise-induced asthma) sputum production Episodic wheezing, SOB Chest tightness, pain, or pressure Decreased exercise tolerance
Asthma PE findings?
With asthma attack: Signs of respiratory distress: increased respiratory rate, increased heart rate, diaphoresis, use of accessory muscles of respiration, anxiousness, can’t speak in full sentences
pulsus paradoxus - slowing of pulse rate during inspiration
Chest hyperinflation can develop chronically
Lung auscultation
Expiratory wheezing or a prolonged expiratory phase
Polyphonic and high pitched wheezes with overall diminished breath sounds
Presence of inspiratory wheezing or stridor may prompt an evaluation for an upper airway obstruction such as vocal cord dysfunction, vocal cord paralysis, thyroid enlargement, or a soft tissue mass (e.g., malignant tumor).
Upper airway
Erythematous or boggy turbinates or the presence of polyps
Allergic rhinitis (pale and swollen nasal mucosa)
Any type of nasal obstruction may result in worsening of asthma
Skin: look for atopic dermatitis, eczema, or other manifestations of allergic skin conditions. (Fingernail clubbing is NOT a feature of asthma)
Asthma lab findings?
Not routinely indicated for asthma but may be used to exclude other diagnoses.
CBC: eosinophilia > 4% (or normal)
Total serum IgE levels > 100 IU (not specific to asthma)
Bronchiectasis characteristics?
Induced by infections, mucus secretions accumulate in the airways causing inflammation, leading to weakening and dilation of the muscle layers of the airway walls– which become irreversibly scarred and deformed, allowing more mucus and bacteria to accumulate, resulting in recurrent infections and progressive injury (thickening, herniation, dilatation)
Similar in ways with COPD (inflamed and collapsible airways, airflow obstruction). It can be complicated by emphysema and chronic bronchitis and commonly is misdiagnosed as asthma or pneumonia.
Common presentation: >50 yo women, but can present in all ages
Bronchiectasis etiology?
Congenital bronchial obstruction: bronchomalacia, bronchial cyst
Immunodeficiency: IgG deficiency, IgA deficiency, HIV, malignancy, chemotherapy
Abnormal secretion clearance: cystic fibrosis, primary ciliary dyskinesia
*Infections: pertussis, measles, bacterial (H flu, staph, klebsiella, TB), virus (adeno, influenza), fungal (pseudomonas aerugnosa, aspergillus)
Other associated conditions: alpha-1 antitrypsin def; rheumatic dz (RA, Sjogren’s), inflammatory bowel dz, inhalation of toxic fumes (ammonia, smoke, talc, silicates), smoking
Bronchiectasis SSxs?
Chronic daily (usually productive) cough.
Sputum: mucopurulent, viscid, and tenacious, without a rancid odor unless concurrent infection
Hemoptysis: blood flecks in purulent sputum occurs in some, may be massive and life threatening secondary to bronchial artery bleeding.
Dyspnea
Rhinosinusitis concurrent in many patients
Wheezing: common, may be due to airflow obstruction following destruction of the bronchial tree. May also be secondary to concomitant conditions, such as asthma.
Pleuritic chest pain can be an intermittent finding, usually secondary to coughing
Chronic fatigue from airflow limitation and chronic infection
Other possible concomitants: reduced sense of smell and urinary incontinence (in women)
Bronchiectasis PE findings?
Findings are nonspecific and may be attributed to other conditions
Fever with acute infectious exacerbations
Weight loss in those with severe disease
Crackles heard bilaterally at lung bases in 70% of patients
Wheezes and Rhonchi can be heard
Digital clubbing (rare), cyanosis, plethora (secondary to polycythemia from chronic hypoxia), wasting, and weight loss
Nasal polyps and signs of chronic sinusitis may also be present
Advanced disease: cor pulmonale; right CHF, including peripheral edema; hepatomegaly; and hypoxia.
Lab/imaging bronchiectasis findings?
CBC, may reveal anemia, polycythemia
Sputum culture
Spirometry (PFT) (low FEV1)
Chest X-ray (CXR)
*Chest HRCT (reveals bronchial wall thickening and luminal dilatation)
Sweat test or other cystic fibrosis testing (CFTR gene)
Serum precipitins (testing for antibodies to aspergillus)
PPD (purified protein derivative) skin test for prior TB infection
CF characteristics?
chronic, progressive disorder from a gene defect that causes the body to produce abnormally thick mucous, primarily affecting respiratory and digestive systems.
Mutations in the cystic fibrosis trans-membrane conductance regulator (CFTR) protein leading to deranged transport of chloride, sodium, bicarbonate and thus thick secretions in lungs (also pancreas, liver, intestine, reproductive tract)
CF etiology?
autosomal recessive inherited disorder
~ 30,000 children and young adults in the U.S. have CF
> 10 million in US carry the CF gene
M=F
CF SSxs?
may exhibit symptoms at birth, others may not develop symptoms for wks, mos, yrs
severity varies, from mild digestive and respiratory problems to severe food-absorption problems and life-threatening respiratory complications.
Lungs: Persistent, productive cough with sputum (thick, viscous secretion), Hyperinflated lungs: barrel chest, Obstructive findings on PFTs
Acute exacerbations of increased cough, tachypnea, dyspnea, inc sputum,wheezing, malaise, anorexia as secretions become colonized with pathogenic bacteria (H flu, S aureus, P aeruginosa, Aspergillis fumigatus, candida albicans)
Chronic infection and inflammation lead to progressive airway damage (air-trapping, spontaneous pneumothorax, hemoptysis)
Sinuses: panopacification of paranasal sinuses, nasal polyposis, chronic rhinosinusitis
Pancreas: insufficient production of digestive enzymes leads to steatorrhea, CF-related diabetes, malabsorption and failure to thrive in infants and children
Bowel: distal intestinal obstructive syndrome (DIOS)
Liver: cirrhosis, portal hypertension, cholelithiasis
Reproductive tract: spermatogenesis defects in males leads to infertility; secondary amenorrhea and tenacious cervical mucus in females leads to infertility
Musculoskeletal: reduced bone density, clubbing of fingers and toes
Kidney: nephrolithiasis
Skin: salty-taste on skin
CF PE findings?
Nose: Rhinitis, may see nasal polyps
Pulmonary system: tachypnea, respiratory distress, wheeze or crackles, cyanosis, cough (usually productive–mucoid or purulent sputum), increased A-P diameter of chest, hyperresonant chest percussion
Gastrointestinal tract: abdominal distention, hepatosplenomegaly, rectal prolapse
Other systems: dry skin (vitamin A deficiency), cheilosis, scoliosis/kyphosis, swelling of submandibular gland or parotid gland
CF lab findings?
Newborns: immunoreactive trypsinogen blood test (IRT), later confirmed with sweat test.
Clinical suspicion in a child who shows poor growth, has repeated respiratory infections, has salty taste on skin, or sibling with CF
Standard diagnostic test: quantitative sweat chloride test (“sweat test,”) - Sweat chloride > 60 mEq/L confirms diagnosis in individual with symptoms
Intermediate results confirmed with DNA genetic screen for CFTR mutations
Chest X-rays, PFTs, (may indicate abnormal airway function)
Stool analysis for steatorrhea
Detection of CF in a fetus is possible through genetic testing.
CF treatment goals?
Focus on both the respiratory and digestive components of the disease
Chest percussion and postural drainage, helps to loosen lung secretions and stimulate coughing. Regular exercise also helps to loosen and move secretions
High-calorie, high-protein diet, fat-soluble vitamins (vitamins A, D, E and K), supplemental pancreatic enzymes, N-acetylcysteine (NAC), Mucolytics, anti-inflammatories
