Obstructive Lung Diseases CIS Flashcards
40 yo male presents with gradual onset of dyspnea, cough, and wheezing over the last 2-3 years.
Family History is remarkable for a father deceased at age 53 with cirrhosis.
Social History: 20 pack year history of tobacco use
Physical Examination: decreased breath sounds to auscultation, lungs are hyperinflated by percussion, peripheral cyanosis and clubbing of the digits
Pulmonary Function Testing
FEV1 1.06 L 36% of predicted
FEV1/FVC 38%
No significant improvement with bronchodilator treatment
Pick the letter that best describes this patient’s disorder
A) Sweat testing confirms diagnosis
B) Purified protein derivative skin testing will confirm diagnosis
C) This disorder is caused by an imbalance in neutrophil elastase
D) Sputum cytology will confirm diagnosis
E) Acid fast sputum stain will confirm diagnosis
C) This disorder is caused by an imbalance in neutrophil elastase
Alpha-1 Antitrypsin Deficiency
Genetic risk factor for COPD
Etiology of 1-2% of COPD cases
Serine protease inhibitor secreted by the liver that protects the lung tissue against the action of neutrophil elastase and serine proteases.
Patients are very susceptible to damage from cigarette smoking.
Should be considered in young patients with COPD
Can lead to LFT abnormalities and cirrhosis
19 year old male presents to the emergency room in acute respiratory distress. He has had a productive cough for several days
Past Medical History: Frequent bouts of sinusitis, hospital admission 2 years ago with pneumonia, and meconium ileus at birth
Physical Examination: Oxygen Saturation 93% on 2L NC, nostril flaring, subcostal retractions, wheezes, rhonchi, and clubbing of the fingers
Pulmonary Function Testing with moderate airway obstruction.
Which statement is true regarding this disorder?
A) B Vitamin Malabsorption is common in this disorder.
B) 95% of males with this disorder are sterile.
C) This disease is characterized by non-caseating granulomas
D) This is an autosomal dominant disorder
E) All siblings will be gene carriers
95% of males with this disorder are sterile.
Cystic Fibrosis
Autosomal recessive disorder caused by mutation of the cystic fibrosis transmembrane conductance regulator protein.
Organs affected include lungs, pancreas, intestines, liver, sweat gland, sinuses, and the vas deferens.
Lung disease leads to death in 90% of patients.
Median survival 37 years
Lung Manifestations in CF
Cough, dyspnea, decreased exercise tolerance, fatigue, and increased sputum production
Steep decline in lung function at adolescence
Daily productive cough
Airway infection with Pseudomonas aeruginosa is the primary pathogen. Staphylococcus aureus, and methicillin resistant Staphylococcus aureus are also common.
Other infections include bronchopulmonary mycoses, and nontuberculous mycobacterial infections
Pancreatic Manifestations of CF
Exocrine pancreatic insufficiency can lead to impaired growth
Signs of malabsorption include bulky, foul smelling stools and flatulence.
Malabsorption of fat soluble vitamins occur.
Liver Manifestations of CF
Hepatomegaly
Splenomegaly
Hematemesis secondary to esophageal or gastric varices from portal hypertension
Sweat Gland in CF
Failure of chloride absorption from the lumen into the ductal lining cell.
Marked elevation of chloride and sodium in sweat
Vas deferens in CF
almost all male are sterile
Other clinical manifestations in CF
Endocrine Pancreas: 1/3 of patients have diabetes by age
30
Electrolyte abnormalities can lead to nausea/vomiting, decreased appetite, circulatory collapse, and seizures
Musculoskeletal: decreased bone density secondary to decreased absorption of vitamin D, glucocorticoid treatment, and decreased exercise.
Kidney: nephrolithiasis
Cystic Fibrosis Diagnosis
Screening with immunoreactive trypsinogen which is a marker of pancreatic injury
Genetic mutation analysis
Diagnosis confirmed with sweat testing
The sweat test measures chloride concentration in sweat that is stimulated by pilocarpine iontophoresis.
5% of diagnosis are made after the age of 18
Pulmonary function testing in CF
obstruction
Chest x-ray in CF
Hyperinflation
Bronchiectasis
Oral Antibiotics in CF
Azithromycin [25-40 kg] 250 mg PO every Mon, Wed, Fri; [> 40 kg] 500 mg PO every Mon, Wed, Fri
Patients ≥ 6 years of age with Pseudomonas aeruginosa meet criteria for use
Trimethoprim/sulfamethoxazole 20 mg/kg/day PO divided every 6-8 hours
Ciprofloxacin 40 mg/kg/day PO divided every 12 hours
IV antibiotics in CF
Aztreonam 200 mg/kg/day IV divided every 6-8 hours
Cefepime 150 mg/kg/day IV divided every 8 hours
Ceftazidime 200 mg/kg/day IV divided every 8 hours
Ciprofloxacin 30 mg/kg/day IV divided every 8-12 hours
Meropenem 120 mg/kg/day IV divided every 8 hours
Piperacillin/tazobactam 400 mg/kg/day divided every 4-6 hours
Tobramycin 7.5-15 mg/kg/day IV divided every 8-24 hours
[Higher dose, extended interval dosing may be more effective and less nephrotoxic]
Vancomycin 60 mg/kg/day divided IV every 6-8 hours
Inhaled antibiotics in CF
Tobramycin 300 mg inhaled twice daily in 28 day cycle
Aztreonam 75 mg inhaled three times daily in 28 day cycle
Other CF Treatments
Pancreatic enzymes, vitamin supplementation, bronchodilators, hypertonic saline inhalation, dornase alfa(rhDNase), ibuprofen, oxygen, bronchodilators, lung transplant
Chest percussion and postural drainage
55 year old male with a history of chronic obstructive pulmonary disease complains of increased shortness of breath, dyspnea with minimal exertion, and decreased exercise tolerance.
Past Medical History : Multiple hospital admissions for COPD exacerbations, intubated last admit
Social History: 40 pack year history of tobacco use
Medications: maximal doses of inhaled steroid, salmeterol, and tiotropium. He frequently has been treated with oral antibiotics and oral steroids.
Which of the following Pulmonary Function Test results are most likely in this patient?
A) Decreased FEV1/FVC
B) Decreased functional residual capacity
C) Decreased total lung capacity
D) Increased FEV1
E) Increased FEV1/FVC
A) Decreased FEV1/FVC
Chronic Obstructive Pulmonary Disease
Progressive, mostly irreversible airflow obstruction
Onset: Middle age or elderly 20-30 years after exposure
4th leading cause of mortality in the United States
Cigarette smoking is the leading cause of COPD
Smokers have a 40ml/year reduction in FEV1 after age 30
Lung growth can be impaired by maternal smoking in pregnancy and second hand smoke in childhood
Other exposures: workplace dusts from mining, cotton mills, and grain handling facilities
Lung Mechanics in COPD
Elastic recoil is the lungs innate ability to deflate following inflation.
Elastic fibers in the lung parenchyma, along with surface tension at the alveolar air-liquid interface are responsible for elastic recoil
Elastic recoil maintains the patency of small airways
Elastic recoil is markedly decreased in COPD
Airway resistance is increased in COPD
The sites of airflow obstruction are distal airways less than 2mm diameter
COPD History
Current or past cigarette use
Dyspnea with slow progression
History of acute bronchitis
History of a chronic cough
Sputum production
Wheezing
Physical Findings COPD
Barrel Chest
Prolonged expiratory phase
Accessory muscle use
Low Diaphragm
Distant Heart Sounds
Diminished Breath Sounds
Rhonchi
Wheezing
Cyanosis
Pedal Edema
Distended Jugular Veins
Hepatic congestion
Cachexia
“Blue Bloaters”
“Pink Puffers”
Pulmonary Function Testing in COPD
I Mild
FEV1/FVC = 80% of predicted
Pulmonary Function Testing in COPD
II Moderate
FEV1/FVC
Pulmonary Function Testing in COPD
III Severe
FEV1/FVC
Pulmonary Function Testing in COPD
IV Very Severe
FEV1/FVC
Chest x-ray in COPD
Hyperinflation Flattened Diaphragms Increased restrosternal space Bullae Can be normal in mild to moderate COPD
Differential Diagnosis COPD
Asthma
Bronchiectasis
Bronchiolitis obliterans
Emphysema
Enlargement of the air spaces distal to the terminal bronchiole with destruction of the alveolar walls
Centriacinar: affects respiratory bronchioles distal to the terminal bronchiole, remainder of the acinus spared. Occurs with smoking
Panacinar: alveolar ducts, adjacent alveoli, coalescence and bullae formation. Common in alpha 1 antitrypsin deficiency. Occurs in smoking
Most severe COPD patients have a combination of centriacinar and panacinar emphysema
Chronic Bronchitis
Enlargement of bronchial mucous glands and increased epithelial goblet cell production leads to cough and increased mucous production.
45 year old female with a history of asthma complains of a daily cough and increased dyspnea. She now wakes up 2 or 3 nights a week with symptoms. Her current medicine is a medium dose inhaled steroid and albuterol inhaler as needed.
Physical Examination: Pulse 80, Respiratory Rate 16 Lung examination is remarkable for bilateral expiratory wheezing
How would you categorize this patient’s asthma?
A) Intermittent asthma
B) Mild persistent asthma
C) Moderate persistent asthma
D) Severe persistent asthma
What is the most appropriate addition to this patient’s treatment?
A) Add a long acting B2-agonist inhaler
B) Add an ipratropium metered-dose inhaler
C) Double the dose of inhaled corticosteroid
D) Start a 10-day course of a macrolide antibiotic
mild persistant asthma
Asthma
Clinical syndrome of unknown etiology with 3 distinct components
1) Recurrent airway obstruction that resolves spontaneously or with treatment.
2) Airway hyperresponsiveness: exaggerated bronchoconstrictor response to stimuli that have little or no effect on nonasthmatic patients.
3) Airway Inflammation
Population Affected by Asthma
8% of Adults
Boys more common than girls before puberty
Women more common than men
Most cases start before age 25, but can occur at any age
15 million outpatient visit per year
2 million hospitalizations per year
Asthma Pathology
Mild Asthma: edema and hyperemia of the mucosa and infiltration of the mucosa with mast cells, eosinophils, and lymphocytes.
Moderate Asthma: chemokines eotaxin, RANTES, macrophage inflammatory protein 1 alpha, and interleukin 8 lead to inflammation and smooth muscle constriction
Severe: hypertrophy and hyperplasia of airway glands and smooth muscle lead to severe airway thickening
Airway Obstruction
Caused by a combination of
1) constriction of airway smooth muscle 2) thickening of airway epithelium 3) liquids in the airway
Asthma Triggers
Atopy
Occupational
Allergy
Food
Cold Air
Smoking or Smoke in the
environment
Pollution
Climate Changes
Emotion
Medication
Asthma Mediators
Acetylcholine: released from intrapulmonary motor nerves stimulate M3 muscarinic receptors causing airway smooth muscle constriction
Histamine: released from mast cells – minor role
Leukotrienes and Lipoxins: derived by the lipoxygenation of arachidonic acid released from the target cell membrane phospholipids during cellular activation
Nitric Oxide: produced by airway epithelial cells and by inflammatory cells found the asthmatic lung. High levels found during asthma attacks
Asthma History
Dyspnea, cough, wheezing, and anxiety
Exercise induced, aspirin ingestion, extrinsic(allergen induced), or intrinsic(unknown)
Cough, hoarseness, or inability to sleep through the night
Rapid changes in temperature or humidity may lead to an attack
Consider occupation exposures
Differential Diagnosis with asthma
COPD
Congestive Heart Failure
Pneumothorax
Pulmonary Embolism
Large Airway Obstruction
Vocal Cord Dysfunction
Asthma Categories
Mild intermittent: symptoms present for 2 days/week or less, or 2 nights/month or less
Mild persistent: symptoms present for > 2 days/week but less than once daily, or > 2 nights/ month
Moderate persistent: symptoms present daily or greater than once/night
Severe persistent asthma: symptoms are continual during the day and frequent at night
Asthma Physical Examination
Often normal between attacks
Vital Signs tachypnea with respiratory rate often between 25-40 breaths per minute, tachycardia, and pulsus paradoxus.
Accessory muscle use, hyperinflation, prolonged expiratory phase
Wheezing loudest during expiration, but can also be heard during inspiration. Wheezing is polyphonic.
Decreased breath sounds in asthma patients is an indication of severe obstruction.
Ominous signs are inability to speak or drink, fatigue, drowsiness, confusion, and cyanosis.
Asthma Testing
ABG Often mild hypocapnea. If PaCO2 normalizes during a severe attack, this may indicate impending respiratory failure.
PFT: obstruction
CBC: Eosinophilia(Hypersensitivity Only), Elevated IgE
Chest X-ray is often normal, hyperinflation, in severe asthma may have pneumothorax or pneumomediastinum
EKG: sinus tachycardia is usual, May see right axis, RBBB, P pulmonale, and even ST-T changes in a severe attack that will resolve after treatment.
Sputum often contains eosinophils
Outpatient Treatment of Asthma
Step 1 Intermittent Asthma
No daily medication
Short-acting beta-2 agonist as needed
Outpatient Treatment of Asthma
Step 2 Mild Persistent Asthma
Short acting beta-2 agonist as needed
Inhaled corticosteroid
Alternate treatments mast-cell stabilizer, leukotriene-receptor antagonist, or theophylline
Outpatient Treatment of Asthma
Step 3 Moderate Persistent Asthma
Short-acting beta-2 agonist as needed
Low to medium dose inhaled corticosteroid
Long-acting beta-2 agonist
Alternate treatments: increase in inhaled corticosteroids within medium dose range; or low to medium dosed inhaled corticosteroids and either a leukotriene-receptor antagonist or theophylline
Outpatient Treatment of Asthma
Step 4 Severe Persistent Asthma
Short-acting beta-2 agonist as needed
High-dose inhaled corticosteroid and long-acting beta-2 agonist
If symptoms persist, 2mg/kg/day of prednisone may be required, generally not to exceed 60mg/day
Outpatient Treatment of Asthma
Other Treatments
Omalizumab: monoclonal antibody in patients with moderate to severe persistent asthma who have shown reactivity to an allergen and whose symptoms are inadequately controlled by an inhaled corticosteroid.
60 year old male presents with a complaint of increased cough productive of purulent sputum, dyspnea, hemoptysis, pleuritic chest pain, and weight loss.
Physical Examination: wheezing and rales on auscultation of the lungs.
X-ray: see next slide
Which of the following disorders is the most likely cause of this patient’s airway dilation? A) Asthma B) Atelectasis C) Adult Respiratory Distress Syndrome D) Bronchiectasis E) Churg-Strauss Syndrome
D) Bronchiectasis
Bronchiectasis
Abnormal permanent dilatation of the bronchi and bronchioles caused by repeated cycles of airway infection and inflammation.
Abnormalities of cilia, mucous clearance, mucus rheology, airway drainage, and host defenses can lead to bronchiectasis.
Patients develop chronic infections that lead
to lung destruction.
Abnormal permanent dilatation of the bronchi and bronchioles caused by repeated cycles of airway infection and inflammation.
Abnormalities of cilia, mucous clearance, mucus rheology, airway drainage, and host defenses can lead to bronchiectasis.
Patients develop chronic infections that lead
to lung destruction
Bronchiectasis Etiologies
One half of patients have cystic fibrosis
One third have an infectious etiology often years before the onset of disease.
Infectious etiologies include pertussis, TB, Mycobacterium avium-intracellulare. MAI typically involve the right middle lobe and lingula
Genetic etiologies include cystic fibrosis, primary ciliary dyskinesia, and alpha 1 antitrypsin deficiency.
Anatomic etiologies include esophageal dysfunction with aspiration, COPD, allergic bronchopulmonary aspergillosis, endobronchial tumors, extrinsic compression by lymph nodes and foreign bodies.
Immune and autoimmune etiologies include primary hypogammaglobulinemia, immunoglobulin G deficiencies, HIV, Sjogren’s syndrome, and rheumatoid arthritis
Bronchiectasis Symptoms
Chronic cough with purulent sputum production
Dyspnea
Intermittent hemoptysis
Pleuritic chest pain
Weight loss
Fatigue
Bronchiectasis Physical Exam
Wheezing, rales
Slow decline in pulmonary function
Decline more rapid if patient has Pseudomonas aeruginosa
Bronchiectasis Imaging
High Resolution CT used to make diagnosis
Findings:
Lack of bronchial tapering
Bronchi visible in the peripheral 1 cm of the lungs
Internal bronchial diameter greater than the diameter of the accompanying bronchial artery
Bronchiectasis Location
Cystic Fibrosis: upper lobe predominance
Aspiration: lower lobe predominance
MAI: right middle lobe and lingular predominance
Bronchopulmonary aspergillosis: central bronchiectasis
Bronchiectasis Testing
PFT: demonstrates obstruction
Bronchoscopy: Used to detect airway abnormalities including tumors, structural deformities, and foreign bodies. Most helpful if the bronchiectasis is localized
Sputum cultures and bronchial alveolar lavage used to assess infectious etiologies
Bronchiectasis Testing
Other Testing
Serum Immunoglobulin levels
Genetic disease screening
Sweat chloride to diagnose cystic fibrosis
Electron microscopy of airway mucosal cilia to diagnose primary ciliary dyskinesia
Alpha 1 antitrypsin levels
Rheumatoid Factor for rheumatoid arthritis
SSA, SSB for Sjogren’s Syndrome
Bronchiectasis Treatment
Treat underlying condition
Specific antimicrobials
Anti-inflammatory – inhaled steroids, macrolide antibiotics
Surgery for localized or refractory disease
Transplantation for end-stage disease
A 63 year-old has worsening dyspnea, there is no fever or chills. He has a long history of COPD and has had exacerbations in the past. He is in moderate respiratory distress and has trouble speaking in full sentences.
Vital Signs: T98.6, BP 148/90, P 112, RR 28/min, Pulse Ox 84% on room air
Chest examination reveals diffusely diminished breath sounds, scattered end-expiratory wheezes, and rare rhonchi. The rest of the examination is normal
ABG pH 7.3, PCO2 65 mm Hg, and PO2 55 mm Hg
CXR hyperinflation and flattened diaphragms
The intern caring for this patient orders continuous nebulized breathing treatments with albuterol and ipratropium, starts IV methylprednisolone, and places the patient on 6L NC O2.
The patient continues to have respiratory distress and becomes increasingly somnolent, becoming arousable only to pain. A repeat ABG reveals a pH of 7.24, PCO2 of 82 mm Hg, and a PO2 of 72 mm Hg.
The patient is prepared for intubation and transferred to the ICU
Which of the following may have prevented this patient’s acute increase in PCO2?
A. Chest physiotherapy and mucolytics B. Delay supplemental oxygen C. Early administration of IV antibiotics D. Theophylline E. Use of a Venturi mask
use a venture mask
41 year old nonsmoking carpenter is referred to you for treatment of asthma. He initially described cough, wheezing, and dyspnea in the evening which was controlled with his albuterol inhaler.
He now experiences symptoms during work hours and is using his inhaler more frequently. During vacation last month, at the beach, he had no symptoms, but upon returning to his work his symptoms have returned. His exam is unremarkable. A bronchoprovocation test with western red cedar produces a 30% decrease in his FEV1
The best way to manage this patient’s occupational asthma is ?
A. Continue symptomatic treatment with his albuterol
B. Avoid any further exposure to wood dust
C. Wear a specialized respirator at work
D. Add inhaled corticosteroids
E. Daily oral corticosteroids
inhaled corticosteroids
35 year old white male come to your office complaining of difficulty breathing that has been worsening over the last 8 months.
He states he is now short of breath even when not moving. He has a 5 pack year history of smoking and quit 3 years ago when he first noticed difficulty breathing. This has persisted until now.
His family history is unknown because the patient was adopted. The patient denies sputum production, fever, or chills.
His blood pressure is 105/70 mm Hg in his right arm, pulse is 120/min and regular, RR 29/min at rest.
Examination shows intercostal retraction during breathing. On auscultation of his chest there are diminished breath sounds throughout both lungs and wheezes bilaterally. The rest of his examination is unremarkable
PFT TLC 115% of predicted RV 110% of predicted FEV1/FVC 30% or predicted DLco 55% of predicted
Which of the following is the most likely diagnosis?
A. Alpha-1 antitrypsin deficiency B. Bronchial asthma C. Bronchiectasis D. Chronic bronchitis E. Chronic obstructive pulmonary disease of the emphysematous type
alpha 1 antitrypsin deficiency
65 year old white female is seen with a chronic productive cough. She produces over 2 tablespoons of sputum each day and her current cough has been present for 3 months. History reveals that she had a similar episode of chronic, productive cough that lasted more than 3 months each year for the last 2 years, but at different seasons of the year.
The most appropriate diagnosis of this patient is:
A. Seasonal allergies B. Emphysema C. Chronic bronchitis D. Asthma E. Sino-bronchial syndrome
chronic bronchitis
20 year old female with symptoms of wheezing and shortness of breath for the past 3 months.
It is worse with exercise. Her past medical history is consistent with seasonal conjunctivitis and rhinitis.
She moved into her college dormitory 4 months ago and noticed she became worse after the move. Her roommate has a pet cat that sleeps on her bed.
Which of the following would best assess the possible etiology of her condition?
A. Serum IGE level B. Circulating eosinophil count C. Nasal smear for eosinophils D. Antibody titers for Mycoplasma pneumonia E. Reid index
antibody titers for mycoplasma pneumonia
35 year old dairy farmer who has never smoked. He has a chronic cough for the past two years. On physical examination he is afebrile, he has a mild wheeze heard on expiration. Spirometry reveals a mild decreased FEV1, and a decreased FVC.
Chest x-ray is normal. Lab reveals an eosinophilia and clusters of eosinophils are noted in his sputum.
He has serum precipitins to Thermoactinomyces vulgaris in his blood work
The most likely diagnosis is
A. Farmer’s lung B. Chronic bronchitis C. Bronchial asthma D. Sarcoidosis E. Wegner’s granulomatosis
farmers lung
Acute Farmer’s Lung
Develops after large exposure to moldy hay or contaminated compost
Symptoms often spontaneously resolve within 12 hours to days if antigen exposure is eliminated or avoided
Acute farmer’s lung manifest as new onset of fever, chills, nonproductive cough, chest tightness, dyspnea, headache , and malaise.
If the inhalational exposure is large, patients may develop acute respiratory failure
Subacute Farmer’s Lung
Manifest as chronic cough, dyspnea, anorexia, and weight loss
Subacute disease is insidious in onset and may occur over weeks to months.
Chronic Farmer’s Lung
Results from prolonged and continuous exposure to antigen
Patients may have irreversible lung damage
Patients may experience severe dyspnea at rest or with exertion
42 year old male with asthma since childhood. He has never smoked cigarettes but does smoke marijuana. He now has low grade fevers, a productive cough, and mild exercise induced dyspnea. He denies chest pain or hemoptysis. Six weeks ago a persistent cough had developed with sputum production. His temperature is 100.6 F, and he has expectorated thick brown cords in the phlegm. The patient was given a diagnosis of pneumonia and received a dose of azithromycin without benefit. His WBC count is 11, 200 with 35% eosinophils. His chest x-ray shows diffuse pulmonary infiltrates.
The most likely diagnosis is?
A. Acute asthma B. Pneumococcal pneumonia C. Acute bronchopulmonary aspergillosis D. Tuberculosis E. Wegner’s granulomatosis
acute bronchopulmonary aspergillosis
35 year old woman come to the ER with urticaria, SOB, and wheezing. She is stabilized with epinephrine and antihistamines. One hour prior to symptoms she had a headache and took an OTC cold medication. She ate a meal of a tuna fish sandwich on white bread with lettuce, tomato, and a diet cola. She has no known food allergies and has not had this problem prior. Her PMH is positive for perennial nasal congestion treated with a nasal steroid. She was diagnosed with asthma 5 years earlier and takes an inhaled steroid and rescue inhaler. She saw an allergist one year ago and all “prick tests” to common allergies were negative.
Physical exam reveals small bilateral nasal polyps, the chest is clear to auscultation now.
The most likely cause of her reaction is:
A. Tuna fish allergy B. Scombroid poisoning C. Allergy to food coloring in the diet cola D. Sensitivity to ASA or NSAIDS E. Aspergillosis
sensitivity so asa or nsaids
Samter’s Triad
Asthma
Nasal Polyps
ASA, NSAID sensitivity
32 year old white female who is a ranch hand from Craig, CO. She presents with signs and symptoms of COPD. She has hypoxia, a prolonged expiratory phase of respiration, and a poor FEV1. She has never smoked , but does have a family history of early emphysema.
This person should be evaluated for which of the following disorders?
A. Farmer’s lung B. Silo fillers lung C. Alpha 1 antitrypsisn deficiency D. Agammaglobulinemia E. Pulmonary fibrosis
alpha 1 antitrypsin deficiency
23 year old female has a history of asthma. She is using an albuterol rescue inhaler about 4 times a week and wakes up once a week with symptoms.
How would you classify her asthma?
A. Mild intermittent B. Mild persistent C. Moderate persistent D. Severe persistent E. Sleep induced
mild persistent
42 year old nurse is evaluated because of coughing, wheezing, and shortness of breath for the past 2 months. She relates the onset of her illness to a heavy exposure during an accidental spill of glacial acetic acid at work. At the time of exposure, she experienced dyspnea, eye irritation, and nasal congestion. She now complains of frequent paroxysms of cough, chest tightness, and awakening at night with SOB. Her physical exam is normal and her spirometry only reveals a decreased FEF25-75 at 45% of predicted. This improves to 65% of predicted with inhalation of albuterol.
Which of the following is the most likely diagnosis?
A. Reactive airways dysfunction syndrome (RADS) B. Atopic asthma C. Allergic occupational asthma D. Chronic bronchitis E. Alpha-1-antitrypsin disease
rads
44 year old female has progressive difficulty with breathing for several years since her hysterectomy/bilateral oophorectomy. She takes thyroid supplements for borderline thyroid function, hormone therapy, eye drops for signs of early glaucoma, and water pills for weight gain. She does not smoke. Her mother has hay fever. Physical exam reveals a slender nervous woman with wheezing noted only on forced expiration. The rest of the exam is normal, Chest x-ray is normal and her FEF25-75 is 45% of predicted.
The most likely cause of her respiratory disorder is:
A. Psychological dyspnea B. Beta-blocker induced asthma C. NSAID induced asthma D. Sarcoidosis E. Pulmonary artery hypertension
b
she is on a beta blocker for the glaucoma
topical beta blocker exacerbates copd or asthma
22 year old male with a 2 year history of asthma has worsening respiratory function. He has seen a couple of doctors and tried a couple of inhalers, but has not had much success in controlling his asthma exacerbations. He has had two episodes of pneumonia in the last 2 years and often suffers from episodes of coughing and wheezing. These episodes are associated with blood-tinged, greenish sputum, fever, malaise, and expectoration of brownish mucous plugs. Past medical history and review of symptoms are otherwise unremarkable. Vital signs: T 98.6, BP 120/72 mm Hg, pulse 68/min, RR 28/min.
Examination reveals an ill appearing male in moderate distress. Respiratory examination reveals rare inspiratory crackles in the left lung base and coarse breath sounds in both upper lung lobes. The rest of the examination is normal. A chest x-ray reveals a small amount of parenchymal infiltrates in the upper lobes, some plate-like atelectasis at the left lung base, and some branched tubular radiodensities that the radiologist describes as “gloved finger” shadows. Serum IgE levels are sent and come back as 1,500ng/mL (normal is less than 1,000 ng/mL
Which of the following is the most appropriate therapy?
A. Amphotericin B B. Caspofungin C. Fluconazole D. Prednisone E. Surgery
diagnosis is allergic bronchoplumonary aspergillosus
treated with prednisone
modifys immune resonse to decrease ir and obstuction
Allergic bronchopulmonary aspergillosis
Occurs in asthmatics and CF patients from a hypersensitivity reaction to Aspergillus colonization of the tracheobronchial tree
This syndrome may cause fever and pulmonary infiltrates that are unresponsive to antibacterial therapy.
Patients often have a cough and produce mucous plugs, which may form bronchial casts. Possible hemoptysis.
People with asthma who have ABPA are usually poorly controlled asthmatics with difficulty tapering off oral corticosteroids
ABPA may occur in conjunction with allergic fungal sinusitis, with symptoms including chronic sinusitis with purulent sinus drainage.
65 year old woman with a long-standing history of smoking quit smoking 10 years ago when she was told that she had severe emphysema. She has been treated since then with prednisone 15 mg daily, albuterol, and ipratropium inhalers, inhaled steroids, theophylline, and leukotriene inhibitors. She is also on 24 hour supplemental oxygen. She now comes to the office with increasing shortness of breath and an inability to complete the minimal activities of daily living. She is essentially bedridden now. She denies a cough, fever, chills, shakes, shortness of breath, or chest pain.
Her oxygen saturation is 69% on 4 liters of oxygen. Lungs have poor air movement with no wheezing. Heart is regular, rate, and rhythm. She has no pedal edema. Laboratory studies are unremarkable. Electrocardiogram is normal sinus rhythm with evidence of right sided strain. Chest x-ray shows hyperinflated lungs. PFTs indicate an FEV1 that is 18% of predicted value
Which of the following is the next appropriate step in management?
A. Increase the dose of prednisone B. Increase the frequency of inhalers C. Obtain a CT of the chest D. Refer for lung transplant E. Schedule an echocardiogram
lung transplant
purified protein derivative skin testing will confirm diagnsos
tb
sweat testing confrims
cf
imbalance of neutrophil elastase
emphysema antialpha1
sputum cytology diagnosis
cancer
acid fast sputum stain
tb
meconium ilesu
cf
sticky stool small bowel obstruction
inhaled abs in cf
are for prophylaxis
ibuprofen in cf
preserves lung function
blue boaters
overweight retain co2
pin puffers
thin elderly males
breathing rapidly
ards cxr
whiteout in whole xray
churg strauss syndrom
cough wheezing gi complants with pain diarrhea and blood in stool
venture mask
it titrates up the po2 so you slowly increase the oxygen
chest physiotherapy and mucolytics
cf
sarcoidosis
granulomas on cxr mediastinal lymphadenoptahy
do a serum ace level
pneumococcal pneumonia sputum
rusty colord
tb chest xray
cavitary lesions in upper love
scombroid poisoning
tuna not put on ice so bacteria grows andit produces histidine, like histamine
sensitivity to asa or nsaids
nasal polyps and asthma
she is on a beta blocker
glaucoma
topical beta blocker exacerbates copd or asthma
