Pulmonology Flashcards
Main difference between asthma and COPD
Both are obstructive lung diseases
asthma = reversible
Why is oral temperature not accurate when a patient is having an asthma exacerbation?
Rapid mouth breathing cools the thermometer
The best initial test during an acute asthma exacerbation
Peak expiratory flow (PEF)
or
ABG
CXR is often normal, and although PFTs are the most accurate diagnostic test, they cannot be performed during an acute attack
What constitutes a positive methacholine test
A >20% decrease in FEV1
Metacholine is synthetic ACh
PFTs in Asthma
Decreased FEV1/FVC
Decrease in FEV1 >20% with the use of methacholine or histamine
Increase in FEV1 >12% and 200 mL with the use of albuterol
Increase in DLCO
Treatment of asthma
- SABA (albuterol)
- Low-dose ICS (beclomethasone)
- LABA or increase the dose of ICS
- Increase dose of ICS to maximum in addition to LABA and SABA
- Omalizumab (if IgE level is increased)
- Oral corticosteroids (prednisone)
Adverse effects of inhaled steroids
Dysphonia
Oral candidiasis
Alternative control agents if a patient with asthma refuses inhaled steroids
Cromolyn and nedocromil (inhibit mast cell mediator release)
Theophylline
Leukotriene modifiers: montelukast, zafirlukast*, or zileuton (best wiith atopic patients)
*Zafirlukast is hepatotoxic and has been associated with Churg-Strauss syndrome (inflammation of small and medium sized blood vessels)
True/False
High-dose inhaled steroids rarely lead to the adverse effects associated with prednisone
True
What is a good indication of the severity of an asthma exacerbation?
Respiratory Rate
Accessory muscle use is subjective, pulse ox will not show hypoxia until the patient is nearly at the point of imminent respiratory failure
The severity of an asthma exacerbation is quantified by:
Decreased peak expiratory flow (PEF)
ABG with an increased A-a gradient
The PEF is an approximation of…
Force Vital Capacity
There is no precise “normal” value; look to see how much difference there is from a patient’s baseline
When is magnesium indicated during an asthma attack
During a severe exacerbation that is not responsive to several rounds of albuterol while waiting for steroids to take effect (take 4-6 hours)
Best initial therapy = oxygen with SABA and a bolus of steroids
How does a patient acquire COPD?
Smoking or alpha-1 antitrypsin deficiency
Tobacco destroys elastin fibers; most of the ability to exhale is from elastin fibers in the lungs passively allowing exhalation
PFTs with COPD
Decreased FEV1/FVC (under 70%)
Increased Total Lung Capacity (d/t increase in residual volume)
Decreased DLCO*
Incomplete improvement with albuterol
Little or no worsening with methacholine
*Only with emphysema; a normal DLCO is indicative of chronic bronchitis predominant COPD
What improves mortality and delays the progression of COPD
- Stop smoking
- Oxygen therapy if pO2 <55 or saturation <88%
- Influenza and pneumococcal vaccinations
Next step:
Asthmatics not controlled with albuterol…
vs
COPD not controlled with albuterol…
Asthma = inhaled steroids
COPD = anticholinergic (tiotropium) then inhaled steroiods if ineffective
Treatment of acute exacerbations of chronic bronchitis
Bronchodilators and corticosteroid therapy combined with antibiotics
Coverage should be provided against Strep pneumo, H influenza, and Moraxella
Why do you avoid placing a patient with COPD on very-high flow 100% nonrebreather mask?
Dyspneic, hypoxic patients with COPD must get oxygen; however, too much creates a V/Q mismatch (damaged airways that are normally constricted, open when exposed to O2)
The idea of “eliminating hypoxic drive” is NOT accurate
Define bronchiectasis
Chronic dilation of the large bronchi (permanent anatomic abnormality)
The single mot common cause of bronchiectasis is…
cystic fibrosis
Define ABPA
AKA Allergic Bronchopulmonary Aspergillosis
Hypersensitivity of the lungs to fungal antigens that colonize the bronchial tree (occurs almost exclusively in patients with asthma and a history of atopic disorders)
Treatment for ABPA
- Oral steroids (prednisone) for severe cases
-
Itraconazole for recurrent episodes
* Note: inhaled steroids are NOT effective for ABPA (inhaler cannot deliver a high enough dose of steroids)*
Meconium ileus
Recurrent pancreatitis
Biliary cirrhosis
Think cystic fibrosis
Why are men and women with CF infertile?
Men: 95% have azoospermia, with the vas deferens missing in 20%
Women: chronic lung disease alters the menstrual cycle and thick cervical mucus blocks sperm entry
For CF, which test is more accurate:
increased sweat chloride
or
genotyping
Increased sweat chloride: > 60 (use pilocarpine to induce sweating)
Genotyping is not as accurate because there are many different types of mutations leading to CF
Treatment for CF
- Antibiotics (Nontypable H influenza, Pseudomonas, Staph aureus, Burkholderia)*
- Recombinant human deoxyribonuclease: rhDNase (breaks down the massive amounts of DNA left by neutrophils in respiratory mucus)
- Inhaled bronchodilators (albuterol)
- Pneumococcal and influenza vaccinations
- Lung transplantation
- Ivacaftor (increases activity of CFTR in some patients)
- Daily postural drainage and percussion
* *Until adulthood, children with CF are most likely to suffer from Staph aureus infections (pseudomonas becomes predominant in adulthood); if a pt has a history of pulmonary infections it is safe to assume that they are colonized with MRSA and you should tailor abx appropriately*
The most common infectious cause of death in the US
CAP: defined as pneumonia occurring before hospitilization or within 48 hours of hospital admission
Strep pneumo is the most common cause
Pneumonia vs bronchitis
Pneumonia = dyspnea, high fever, and an abnormal CXR
Organism-specific association of pneumonia on presentation:
- Hemoptysis, “currant jelly” sputum
- Foul-smelling sputum, “rotten eggs”
- Dry cough, rarely severe, bullous myringitis (inflammation of the tympanic membrane)
- GI symptoms or CNS symptoms
- AIDS with CD4 < 200
- Klebsiella
- Anaerobes
- Mycoplasma
- Legionella
- Pneumocystis
What does the term atypical pneumonia refer to?
An organism not visible on Gram stain and not culturable on standard blood agar
Mycoplasma, Chlamydophila, Legionella, Coxiella, and viruses
Outpatient treatment of pneumonia
If healthy and no abx in last 3 months = macrolide (azithro or clarithromycin) or doxycycline
Comorbidities or abx within the last 3 months = respiratory fluoroquinolone (levofloxacin or moxifloxacin)
Inpatient treatment of pneumonia
respiratory fluoroquinolone (levofloxacin or moxifloxacin)
or
ceftriaxone and azithromycin
Reasons to hospitalize patients for pneumonia
Hypoxia and hypotension (<90) as single factors are a reason to hospitalize a patient
CURB-65
Confusion, Uremia, Respiratory distress, BP low, Age >65
0-1 point = go home
2 or more = admit
Pt admitted for CAP with CXR showing a lobar infiltrate and a large effusion. Started on ceftriaxone and azithromycin. What is the next step?
Thoracentesis to determine if a chest tube is warranted
Pleural effusion with pH <7.2, LDH >60% serum, or protein >50% serum suggests an exudate (caused by infection or cancer)
Empyema reponds rapidly to drainage by chest tube or thoracostomy (acts like an abscess)
Who should receive a pneumococcal vaccine?
Everyone above the age of 65 should receive the 13 polyvalent vaccine, followed in 6-12 months with the 23 polyvalent vaccine
Also recommended for those age <65 with very high risk comorbid conditions (CSF leaks, SCD, cochlear implants, congenital or aquired asplenia, immunocompromised).
For adults <65 with other chronic medical conditions that increase the risk of invasive pneumococcal disease (heart or lung disease, DM, smoking, chronic liver disease), PPSV23 alone is recommended, followed by sequential PCV13 and PPSV23 at age 66
Define HAP
Pneumonia developing more than 48 hours after admission or after hospitalization in the last 90 days
Important to define because we worry about MRSA and pseudomonas in these patients: aka macrolides are not acceptable as empiric therapy
Which drugs have activity against Pseudomonas?
Aminoglycosides (gentamicin, tobramycin, amikacin)
Ciprofloxacin (not as effective)
Pip/tazo (and other ureidopenicillins)
Ceftazidime, Cefepime (good for neutropenic fever)
Colistin
Carbapenems (except Ertapanem)
Aztreonam
KNOW THIS
Treatment for VAP
- Antipseudomonal beta-lactam: cephalosporin or penicillin or carbapenem
- Second antipseudomonal: aminoglycoside or fluoroquinolone
- Methicillin-resistant antistaphylococcal agent: vanc or linezolid
Patient is treated for VAP and subsequently develops seizures. What medication were they likely started on?
Imipenem
Risk of seizure increases with renal failure
Can daptomycin be used for pulmonary infections?
No
Daptomycin is inactivated by surfactant
Which abx are good for a lung abscess?
Clindamycin or penicillin
Sputum culture is always the wrong answer for diagnosing a lung abscess
What is the best initial test for Pneumocystis Pneumonia
CXR showing bilateral interstitial infiltrates or an ABG showing hypoxia or an increased A-a gradient
The most accurate test is a bronchoalveolar lavage
A normal LDH level means what about PCP
That it is NOT the diagnosis
In PCP LDH is ALWAYS elevated
Treatment for PCP
TMP/SMX for therapy and for prophylaxis
Add steroids to decrease mortality if: pO2 < 70 or an A-a gradient >35
Toxicity with TMP/SMX for PCP, what do you switch to?
Clindamycin and primaquine
OR
Pentamidine
Clindamycin with primaquine has more efficacy than pentamidine; however, it is contraindicated in G6PD deficiency (look for AA man with bite cells on smear) – in this case pentamidine would be the answer if they experienced side effects with TMP/SMX (i.e., neutropenia and a rash)
How does treatment for PCP prophylaxis differ from treatment when a patient experiences adverse side effects with TMP/SMX
Treatment = clindamycin and primaquine* OR pentamidine
Prophylaxis = atovaquone OR dapsone*
*Both dapsone and primaquine are contraindicated in those with G6PD deficiency
True/False
The use of prophylatic medication for HIV is based on CD4 count and the viral load
False
Prophylatic treatment is NOT based on the viral load
Recent immigrants
Prisoners
HIV positive
Steroid use
Hematologic malignancy
Alcoholics
DM
Risk factors for TB
Also includes: healthcare workers and close contacts
Best initial test for TB
CXR
Sputum stain and culture must be done 3 times to fully exclude TB
Pleural biopsy is the single most accurate diagnostic test
True/False
PPD skin testing is never the best test for TB in a symptomatic patient
True
Treatment for TB
RIPE
Rifampin, Isoniazid, Pyrazinamide, and Ethambutol
Use RIPE for the first 2 months, then stop ethambutol and pyrazinamide and continue rifampin and isoniazide for the next 4 months (standard of care is 6 months)
When can you treat TB with just “RIP”
You do not need ethambutol if it is known at the beginning of therapy that the organism is sensitive to all TB medications
(RIPE is used as a 4-drug empiric therapy prior to knowing the sensitivity of the organism)
In what cases should you consider extending TB treatment past 6 months?
For cases complicated by:
Osteomyelitis
Miliary TB
Meningitis
Pregnancy (or any other time pyrazinamide is not used)
Adverse effects of RIPE
R = red color to body secretions
I = peripheral neuropathy (coadminister with pyridoxine/B6)
P = hyperuricemia (contraindicated in pregnancy)
E = optic neuritis/color vision (decrease dose in RF)
When should steroids be added to TB treatment?
To decrease the risk of pericarditis
OR
To decrease neurologic complication in TB meningitis
No risk factors, what constitutes a positive PPD
> 15 mm of induration (erythema is irrelevant)
When should a patient have a second PPD within 1-2 weeks if there first PPD was negative?
When they have never had a PPD skin test before (the first test may be falsely negative)
Everyone with a reactive PPD test should have a…
CXR to exclude active disease
9 months of isoniazid (decreases lifetime risk of developing TB from 10% to 1%) regardless of BCG vaccine status
The PPD test should not be repeated once it is positive (it will always be positive in the future)
PET is most accurate with…
larger lesions (>1 cm)
This is a way of telling whether the content of a lesion is malignant without a biopsy. Malignancy has increased uptake of glucose (sensitivity is 85-95%)
Drugs that cause pulmonary fibrosis
Bleomycin
Busulfan
Amiodarone
Methylsergide
Nitrofurantoin
Cyclophosphamide
Dyspnea, worse on exertion
Fine rales or “crackles”
Loud P2 heart sound
Finger clubbing
Pulmonary fibrosis
PFTs for pulmonary fibrosis
Decrease of everything proportionately (FEV1, FVC, TLC, and RV)
FEV1/FVC ratio will be normal
DLCO is decreased
What type of pneumoconioses responds best to steroids?
Berylliosis (due to the presence of granulomas, which are a sign of inflammation)
Associated with electronic manufacturing
Diagnostic test for sarcoidosis?
CXR is the best initial test: hilar adenopathy is present in more than 95% of patients
Lymph node biopsy is the most accurate: noncaseating granulomas
Elevated ACE, Hypercalciuria, Hypercalcemia, and restrictive PFTs
Treatment for sarcoidosis
Prednisone
Diagnostic test for PE
CXR, EKG, and ABG are the best initial tests
Angiography is the most accurate test, but can be fatal in 0.5% of cases
After doing an ABG, CXR, and EKG, the “best next step” is most often a CT angiogram
What are the most common findings of PE on the best initial tests?
CXR: usually normal (may show atelectasis)
EKG: usually shows sinus tachycardia (nonspecific ST-T wave changes are the most common abnormality, NOT S1, Q3, T3)
ABG: hypoxia and respiratory alkalosis
When is V/Q scan the answer (over Spiral CT)?
In pregnant patients with suspected PE
The CXR must be normal for the V/Q scan to have any degree of accuracy
What is D-dimer good at?
A negative test excludes a clot, but a positive test doesn’t mean anything
(AKA very sensitive, but poor specificity)
D-dimer is the answer when the pretest probability of PE is low and you need a simple, noninvasive test to exclude thromboembolic disease
True/False
You do not need a spiral CT or V/Q scan to confirm a PE if there is a clot in the legs
True
(therapy does not change)
LE Dopplers are a good test if the V/Q and spiral CT do not give a clear diagnosis
Best initial therapy for PE
Heparin (Warfarin should be started at the same time in order to achieve a therapeutic INR of 2-3 x normal as quick as possible)
Fondaparinux is an alternative to heparin
Rivaroxaban
Dabigatran
Oral agents that do not require INR monitoring and can be used for the treatment of pulmonary emboli (reach therapeutic effect in several hours, instead of several days like warfarin)
When is IVC filter the right answer after a PE?
- Contraindication to anticoagulants (e.g., melena, CNS bleed)
- Recurrent emboli while on heparin or fully therapeutic warfarin (INR of 2-3)
- RV dysfunction with an enlarged RV on echo (filter is placed because the next embous could be fatal)
When are thrombolytics the right answer after a PE?
Hemodynamically unstable patients (systolic BP < 90 and tachycardia)
Acute RV dysfunction
There is no specific time limit in which to use thombolytics as there is in stroke or MI
Define pulmonary hypertension
systolic > 25 or diastolic > 8
Primary pulmonary hypertension is by definition idiopathic
Diagnostic test for pulmonary hypertension
CXR and CT = best initial test (shows dilation of the proximal pulmonary arteries with narrowing of distal vessels)
Right heart or Swan-Ganz catheter = most accurate
EKG showing R axis deviation, RA an RV hypertrophy
Treatment for pulmonary hypertension
Only lung transplantation is curative for idiopathic pulmonary hypertension
- Prostacyclin analogues (PA vasodilators): epoprostenol, treprostinil, iloprost, beraprost
- Endothelin antagonists: bosentan, ambrisentan
- Phosphodiesterase inhibitors: sildenafil
These are all better than CCBs, hydralazine, and nitroglycerin
What is the most accurate test for OSA
Polysomnography (sleep study) which shows multiple episodes of apnea
AHI = Apnea Hypopnea Index
- None/Minimal: AHI < 5 per hour*
- Mild: AHI ≥ 5, but < 15 per hour*
- Moderate: AHI ≥ 15, but < 30 per hour*
- Severe: AHI ≥ 30 per hour*
Define ARDS
Defined as having a pO2/FiO2 ratio below 300
< 200 = moderately severe
< 100 = severe
Respiratory failure from overwhelming lung injury or systemic disease leading to severe hypoxia with a CXR suggestive of CHF but normal cardiac hemodynamic measurements (ARDS decreases surfactant and makes the lung cells “leaky” so that the aveoli fill up with fluid)
Treatment for ARDS
LTVV (low tidal-volume mechanical ventilation)
Use 6 mL per kg of tidal volume
PEEP to decreases FIO2 requirement (levels of FIO2 above 50% are toxic to the lungs)
Maintain the plateau pressure of less than 30 cm of water
