High Yield Pulm Flashcards
List some etiologies of chronic cough with a NORMAL CXR:
Post nasal drip due to upper airway disease, asthma, or GERD
Compare the appearance of blood from the lungs vs. GI tract:
Lungs: red, frothy, alkaline, with hemosiderin-laden macrophages
GI: dark, often coffee ground appearance, acid pH.
What causes hyperresonance on percussion of the thorax?
Emphysema (barrel chest), pneumothorax
What are the possible etiologies of dullness on thoracic percussion?
Consolidation, atelectasis, pleural effusion
Describe FEV1, VC, and their ratio in a normal patient:
FEV1=4.0 l - volume out in 1st 1 sec
VC= 5.0 l -total volume out
FEV/VC=0.8
Describe the spirometry results (FEV, VC, etc) in a patient with obstructive lung disease:
FEV1 is WAY down (~1.3)
VC is down but not as dramatically (3.1)
*FEV/VC = 0.42–LOWER than in a healthy patient
Describe the spirometry results (FEV, VC, etc) in a patient with restrictive lung disease:
FEV1 is basically normal (2.8)
VC is down more relatively to FEV1 (3.1)
*FEV/VC = 0.90–HIGHER than in a healthy patient because VC is so low.
Obstructive or restrictive: COPD
Obstructive
Obstructive or restrictive: Interstitial lung disease
Restrictive
Obstructive or restrictive: Diffuse parenchymal lung disease (DPLD)
Restrictive
Obstructive or restrictive: Asthma
Obstructive
Obstructive or restrictive: IPF
Restrictive
Describe the V/Q ratio in Chronic Bronchitis:
The physiologic response leads to a drop in ventilation and compensation with the rise in CO. Increased perfusion in the areas of poor ventilation takes place eventually causing hypoxia and secondary polycythemia (elevated Hg).
So V/Q ratio is basically low.
Describe the V/Q ratio in Emphysema:
Since both the terminal bronchioles and alveoli along with the capillary bed have been destroyed, a matched defect exists between the ventilation and perfusion; areas of low ventilation also have poor perfusion. So V/Q ratio is normal.
Describe the V/Q ratio in restrictive disease:
Restricted units are less well ventilated but adequately perfused giving a low V/Q ratio.
Obstructive or restrictive: sarcoidosis
Restrictive
Obstructive or restrictive: CF
Obstructive
Obstructive or restrictive: Nonspecific Interstitial Pneumonia
Restrictive
“simplified” alveolar gas eqn for sea level
PaO2= 150 - (PaCO2/0.8)
Used to determine if diffusion has been affected at alveolar membrane OR by reduced lung volume OR anemia. Difference between expected and actual Pa)2 should be <20, but increases with age.
Describe the 3 major mechanisms of airway obstruction:
- Mucous overproduction (CF, chronic bronchitis)
- Inflammation of airway wall (eg asthma)
- Shrinkage due to destruction of surrounding parenchyma- thin, flabby airways (emphysema).
List risk factors for increased mortality in CAP:
Age>65, ineffective or delay in antibiotic tx, hospitalization in past 1 yr, serious comorbidity (COPD, bronchiectasis, CHF, renal failure, liver disease, immunosuppression, asplenic, DM); Abnormal vital signs (RR>30, hypotension, HR>125, Fever=40); decreased level of consciousness/confusion; evidence of extrapulmonary sites of infection; Lab abnormalities (esp alkalosis).
Common CAP pathogens for alcoholics:
S pneumo, anaerobes (aspiration), gram negs (aspiration), TB
Common CAP pathogens in nursing home
S pneumo, Gram negs (enteric), H flu, S aureus
Common CAP pathogens in pts with poor dental hygeine
Anaerobes
Common CAP pathogens in smokers
S pneumo, H flu, Moraxella, Legionella
Common CAP pathogens in pts with structural lung disease:
Pseudomonas, S aureus
Age>65, alcoholism, exposure to children in daycare, immune suppressive illness, and multiple medical comorbidities all predispose to pneumonia with…
penicillin-resistant pneumococci
Recent antibiotic tx, living in a nursing home, comorbidities (mult) and underlying cardiopulmonary disease all predispose to pneumonia with…
Enteric gram-negatives OR anaerobes
Structural lung disease, recent corticosteroids, use of broad spectrum antibiotics (>7d in last month), and malnutrition all predispose to pneumonia with…
P. aeruginosa
List the common causes of pneumonia in immunocompromised hosts: Bacteria, protozoa, fungi, and viruses
Bacteria: Listeria, Salmonella, Legionella, Nocardia, TB, other mycobacteria
Protozoa: Cryptosporidium
Fungi: Pneumocystis, Histoplasma, Coccidioides, Cryptococcus
Viruses: Varicella-zoster, Herpes, CMV, Epstein-Barr
Compare tx of allergic rhinitis and perennial rhinitis:
Allergic rhinitis: Allergy test, avoid allergens (air filters etc), antihistamines, nasal steroids, immunotherapy if mod-severe
Perennial rhinitis: antihistamines, nasal decongestants, ipratrompium bromide.
List 2 possible mechanisms for hypercapnia:
- Reduction in minute ventilation due to depression of resp. center drive (eg opioids) or loss of neuromuscular coupling (eg COPD)
- Increased dead space ventilation (high V/Q ratio)
As lung volume increases, resistance __________
decreases. Airways are open (larger radius) meaning decreased resistance by Poiseuille’s law.
Describe the typical symptoms (S) of COPD:
Pt. 50-60s, smoking history
Cough, SOB, sputum (mucoid or purulent), increasing DOE
Describe the typical signs of COPD (O):
Gen: Blue bloater (chron. bronchitis) or pink puffer (emphysema)
Pulm: Wheezes, Rhonchi (in chronic bronchitis), prolonged exp time, reduced diaphragmatic excursion, low diaphragmatic position, increased AP:Lat diameter, retractions, late: crackles
Cardio: Accentuated splitting of S2
How do you diagnose COPD?
Spirometry: Obstructive pattern with low FEV1/FVC ratio that is not fully reversible
Stable COPD Tx:
First line: Ipratropium bromide.
Bronchodilators (long or short acting beta-2 agonists), theophylline. No steroids.
Management of COPD exacerbation:
Inhaled bronchodilator
Systemic corticosteroid
Non-invasive intermittent positive pressure ventilation (biPAP, cPAP).
Describe how bronchodilators or a bronchial provocation test can be used to dx asthma:
Significant reversibility of obstruction: increase of >=12% and 200mL in FEV1 or >=15% and 200mL increase in FVC after short-acting bronchodilator
If inconclusive:
Bronchial provocation:
Measure baseline FEV1, FVC. Administer methacholine. >20% decline in FEV1 is positive for airway hyperreactivity.
CXR/HRCT showing dilated, thickened bronchi (train tracks/ring-like markings)
bronchiectasis
Describe the typical symptoms of CF (S)
Pt is typically young, white. Sx are cough, sputum, decreased exercise tolerance, hemoptysis AND evidence of multi-system dysfunction: steatorrhea/diarrhea, ab pain, clubbing,
What are possible etiologies of bronchiectasis?
Post-infectious, CF, allergic bronchopulmonary aspergillosis, bronchial obstruction
What are clinical signs of CF (O)?
Crackles, purulent nasal secretions
How is CF diagnosed?
CFTR gene mutation or sweat Cl concentration >60mEq/L on more than 2 occasions (due to decreased chloride reabsorption).
How many days per week should a patient have symptoms for their asthma to be categorized as Intermittent, Mild, Moderate, or Severe (ANY AGE):
Intermittent: 2 or fewer days/week
Mild: >2 days/week
Moderate: Daily
Severe: Throughout the day
Note: this also applies to use of short-acting B agonists.
How frequently can a pt with asthma have symptoms for their asthma to be considered “well” controlled? What about rescue inhaler use?
2 or fewer times/week (not on same day). Same for rescue inhaler use.
How many exacerbations requiring systemic corticosteroids can an asthma patient have and still be considered intermittent? Mild? Moderate? Severe?
0-1 per year for intermittent. More than 1 per year means they’re persistent.
Exception: kids 1 day and risk factors.
What should FEV1 or Peak flow be for asthma to be considered “well-controlled”?
> 80% of predicted personal best.
What should FEV1 or peak flow be for asthma to be classified as intermittent? Mild? Moderate? or Severe?
What should these look like in a well controlled patient?
Note: only done for kids 5+
Intermittent: FEV/peak flow >80% personal best. FEV/FVC>85% (or normal range if >age 20)
Mild: FEV/peak >80% personal best
FEV/FVC>80% (or normal range if >age 20)
Moderate: FEV/peak 60-80%
FEV/FVC 75-80% (or 5% reduction if older)
Severe: FEV/peak flow 5% if older)
If a patient is well controlled, they should fall in the intermittent category, regardless of baseline severity.
Generally, how do kids under 5 differ from older patients in regards to how night time awakenings affect evaluation of asthma severity?
They are permitted fewer before they get bumped up into higher severity/worse control.
They are considered well controlled only if they have 12, the cut points are 2 or fewer/month; 1-3/week; 4+/week
What is the initial treatment for mild persistent asthma?
All ages: Low-dose ICS
Reevaluate in 2-6 weeks
What is the initial treatment for moderate persistent asthma?
All ages: Med-dose ICS
5-11: can have Low dose ICS + LABA/LRTA/Theophylline
12+: can have Low dose ICS + LABA
Reevaluate in 2-6 weeks
What is the initial treatment for severe persistent asthma?
0-4: Med-dose ICS
5-11: Med-dose ICS or Med-dose ICS+LABA
12+: Med-dose ICS + LABA
Reevaluate in 2-6 weeks
When should you consider stepping down asthma tx?
If it has been well controlled for 3+ months.
Define mild, moderate, and severe asthma exacerbations. How does treatment differ for these?
Mild (PEFR is 70%+ expected): SABA, every 3-4 hours for 24-48 hours. Consider oral corticosteroid.
Moderate (PEFR is 40-69% expected): Continuous admin of SABA, administer oral corticosteroid.
Severe (PEFR is <25% of expected or pt does not respond to Tx.
Which medical interventions for COPD reduce mortality?
Only oxygen therapy.
Emphysema: definition
abnormal enlargement of air spaces distal to terminal bronchiole, with destruction of bronchial walls WITHOUT fibrosis.
Chronic bronchitis: definition
excessive mucous secretions with productive cough for 3 months or more in 2 consecutive years.
How does COPD look on CXR?
Depends on type and severity:
Emphysema: Hyperinflation, flattened diaphragms, diminished vascular markings at apices. CT»plain film for diagnosis.
CB: increased interstitial markings, esp at bases. Diaphragms normal.
Do you order ABGs in a COPD workup? What do you order?
Only order ABGs if you suspect hypoxia. Always get ECG, spirometry, and imaging.
Lung cancer epi:
med. age is 71. w/ smoking or neoplastic Hx.
Lung cancer sx:
Cough (dry or hemoptysis), fever, weight loss, hoarsness
Small cell lung cancer
10-15%. Endocrine cell of bronchial origin, begins centrally, and infiltrates sub-mucosally. Prone to early hematogenous/lymphatic spread. Aggressive course, rarely can be resected.
**May present with elevated ACTH, ADH
What to all non small cell lung cancers have in common?
They can be resected if found early enough.
Squamous cell carcinoma
20%. arises from bronchial epithelium, usually central and intraluminal. More likely to cause hemoptysis, wheeze.
Adenocarcinoma
35-40%. Arises from mucous glands as a peripheral parenchymal mass. Produces mucin.
Large cell carcinoma
3-5%. heterogenous group which can present as a central or peripheral mass.
Bronchioalveolar cell carcinoma
2% arises from epithelial cells distal to terminal bronchiole (clara cells or pneumocyte IIs). Does not damage septa. Slow growing and rarely metastasizes.
Describe the work-up of suspected lung cancer:
Imaging (CT, MRI, PET to confirm/r/o metastasis), sputum cytology (specific but not sensitive), CBC, electrolites. PFTs are required in surgery candidates. Cancer must be confirmed, staged by cytology from bronchoscopy or transthoracic needle biopsy, depending on location.
Describe lung cancer staging:
only NSCLC is staged by the TNM system. Stages I and II can be cured by surgery (Up to T2N1M0 or T3N0M0). N1 means metastasis to ipsilateral peribronchial or perihilar and intrapulmonary nodes only. Those IIIB and worse do not benefit from surgery (usually means N3- affecting contralateral nodes).
Who should be screened for lung cancer?
Low dose CT for persons 55-79 w/30+ pack-year history of smoking & smoked within the past 15 years.
Describe diagnostic possibilities for finding a solitary pulmonary nodule:
> 3cm- usually malignant
40-50% of SPN are malignant.
Get exploratory thoracotomy unless benignity can be established: Benign pattern of calcification (dense, central, or popcorn..NOT eccentric), smooth margin, stability over time, low probability (young age, no tobacco).
Obstructive apnea: definition
complete cessation of airflow for >=10s, O2 desaturation >4% and EEG signs of arousal.
Obstructive hypopnea
Discernible reduction in airflow (>50%) for >=10 sec.
What is diffuse parenchymal lung disease (DPLD)?
A diverse group of pulmonary disorders that cause disruption of distal lung parenchyma (on CXR increased markings and nodules) and worsening SOB. Known causes are inhaled particulates (silica, asbestos), drugs (chemotherapy), collagen vascular disease (lupus, rheumatoid arthritis), granulomatous (like sarcoidosis).
Pathogenesis is inflammatory response, fibrosis, and structural remodeling.
Result is restrictive pattern lung disease.
IFP
Chronic fibrosing interstitial pneumonia. 50-70 yo with Hx of smoking. Will cause progressive DOE, paroxysmal cough, digital clubbing, crackles. Honeycombing on CT. Tx is lung transplant.
NSIP
nonspecific interstitial pneumonitis:
Age 40-50, basilar crackles. GROUND GLASS opacities and fin reticulation on CT.
RB-ILD
Respiratory bronchilitis-associated lung disease. Resp. brionchiolitis is a small airway lesion found in current smokers (intraluminal macrophages). Sx are mild- dyspnea, cough, restrictive pattern. Most patients improve with smoking cessation.
DIP
Desquamative Interstitial Pneumonitis. Age 40s. A more advanced form of RB-ILD that presents with cough, dyspnea. HRCT shows lots of ground glass opacity. Tx: corticosteroids.
Sarcoidosis
Young-middle aged AAs. Presents with bilateral hilar lymphadenopathy, pulm. infiltrates, ocular and skin lesions (and other organ involvement), fatigue, malaise, weight loss.
CT shows non-caseating granuloma (high in CD4s on histology).
Tx: Systemic Steroids
Hypersensitivity pneumonitis
Acute immune-mediated reaction to inhaled small MW organic antigens. Fever, malaise, flu-like sxs, cough, dyspnea 4-8 hrs after inhaling antigen. Includes bird-fancier’s lung and farmer’s lung. Chronic exposure can lead to progressive interstitial lung disease.
Silicosis
Basically chronic exposure to silica and it’s uptake by macrophages eventually causes an immune response with fibroblast proliferation and collagen deposition. On CXR shows tiny dots. If complicated can progress to Cor pulmonale and resp. failure. No increased cancer risk.
**Increased incidence of TB.
Asbestosis
Causes pulmonary fibrosis similar to that seen in silicoses, except it increases cancer risk.
Primarily a pleural disease. Calcifications seen in pleura, with thickening and plaques. Lung biopsy will reveal ferruginous bodies (transparent asbestos fibers coated in iron and protein).
Define pulmonary HTN
Mean pulmonary arterial pressure > 25mmHg
What are the 3 most common symptoms of PE?
SOB, chest pain (pleuritic), anxiety
What are the 3 most common signs of PE?
tachypnea, rales, fever
Describe the PERC rule for Pre-test probability of PE
Age>50, HR>100, O2 sat<2%
What is a d-dimer? When should you order? When will you get a false positive?
d-dimer is the product a degrading clot. Order if you have moderate, but not high suspician of PE (95% sensitive, 50% specific). Will be positive if age>70, pregnant, recent surgery, infection, malignancy, dialysis, shock, hemoptosis
Describe the work up of suspected PE prior to getting imaging (moderate risk)?
D-dimer, ABG (A-a gradient is normal in 50% of PE), Creatinine (to determine kidney function prior to contrast), PT/PTT (as baseline in case anti-coag needed), BNP/Tropoinin (r/o MI), EKG.
Which imaging modalities are preferred for diagnosing PE? What is the gold standard?
Gold standard is angiogram. Chest CT w/ contrast + V/Q scan are great together. You may also want to do an LE dopplar to find embolic sourse.
What should you always order if you suspect a large PE or saddle embolus?
Cardiac echo for RV dysfunction.
Describe management for PE
Admit! (ICU if large or R heart dysfunction)
Manage airway, treat shock with IV fluids (as long as no pulm edema).
Anti-coagulation (Heparin or LMWH)
Thrombolysis (if shock, resp. distress, cardiac arrest)- Does not improve mortality but increases rate of clot resolution. Increased risk of intracranial hemhorrage.
What are the EKG findings of PE?
Sinus tachycardia is most common finding. Look for evidence of R heart strain.
T wave inversions in anteroseptal and inferior leads.
Deep S in I, Q in III, Inverted T in III (S1Q3T3)- only large emboli
PE findings on CXR:
Westermark sign (pulm artery distension), Hampton hump (wedge-shaped opacity). Others: effusion, atelectasis, pleural opacity
What does cardiomegaly look like on CXR?
heart spans >50% of CXR width.
What is the most common cause of COPD exacerbation?
Medication non-compliance.
How does acute pneumothorax usually present?
Usually thin, tall men w/ chest pain lateralizing to affected side and MAYBE SOB. Absent breath sounds, hyperresonance, hypotension.
What is tension pneumothorax?
Pneumothorax with mediastinal shift toward UNAFFECTED side.
What is work up for a suspected pneumothorax?
CXR or CT (more sensitive to visualize small or determine size).
If 15%- chest tube placement.
Spontaneous pneumothorax in setting of pneumonia suggests…
Pneumocystis (PCP), TB, or staph aureus.
What are 2 exam findings that suggest severe airway obstruction in an acute asthma exacerbation?
- Silent chest (no breath sounds)
2. Pulsus paradoxus >20mmHG (decrease in SBP and pulse waves on inspiration).
What are the Wells criteria for evaluation of PE?
Clinical signs and symptoms of DVT (3)
Alternative dx less likely than PE (3)
HR>100 (1.5)
Immobilazation for >3 days or surgery in past 4 weeks (1.5)
Previous DVT or PE (1.5)
Hemoptysis (1.0)
Cancer (w/ treatment in last 6 mo or palliative care) (1)
High probability is >6.0
Moderate is 2-6
Low is < 2.0
