Clinical Approach to Asthma/COPD and pHTN/PE/OSA/ILD Flashcards
What is the largest epidemiological risk factor In Utero for the development of Asthma?
PREMATURITY
- has a 4x increased risk
- also ethnicity, low socioeconomic status, stress, and C-section
What are common Postnatal risk factors for the development of Asthma? (A/I/AP/Abx/A/O)
- levels of endotoxins/allergens in home (DUST MITES)
- viral and bacterial infections (RSV/adenovirus) that generate vigorous inflammation (unbalanced immunity)
- also air pollution, Abx use, Acetaminophen exposure, obesity
Asthma diagnosis with Spirometry
- diagnosis can be difficult! –> Normal spirometry does NOT EXCLUDE the disease
- treat pt. if you think they have asthma
- spirometry in symptomatic asthma often associated with FEV1 < 80% and FEV1/FVC < 75%
- helps to see REVERSIBILITY of airway OBSTRUCTION like 12% improvement in FEV1 over baseline and total improvement of at least 200mL
Intermittent Asthma
What is the Rule of 2’s?
- symptoms < 2x/week
- nighttime awakenings < 2x/month
- SABA use < 2x/week
lung function > 80%, use Step 1 therapy
Mild Persistent Asthma
When do pts have symptoms, nighttime awakenings, and asthma exacerbations?
Symptoms: > 2/week but not daily
NA: 1-2/month (0-4) and 3-4/month (5-12+)
AE: 2 exacerbations in 6 months or wheezing 4x year lasting > 1 day AND risk factors for persistent asthma
Moderate Persistent Asthma
When do pts have symptoms, nighttime awakenings, and when is SABA used for symptom control?
Symptoms: daily
NA: 3-4/month (0-4) and 1/week but not nightly (5-12+)
SABA use daily (asthma causes some interference with daily activity)
Severe Persistent Asthma
When do pts have symptoms, nighttime awakenings, and when is SABA used for symptom control?
Symptoms: throughout the day
NA: 1/week (0-4) and often 7/week (5-12+)
SABA use several times a day (asthma causes extremely limited normal activity)
Asthma Treatment and Management
- want personalized, pt.-centered approach with individualized written asthma action plan
- fosters CO-MANAGEMENT (best quality of life)
- show appropriate medication use!
**want to provide best quality of life through minimizing disease symptoms and abolishing exacerbations
What is the treatment for each step of Asthma treatment:
Intermittent Asthma
Step 1
Persistent Asthma Step 2 Step 3 Step 4 Step 5 Step 6
- SABA as needed
- low-dose ICS (inhaled corticosteroid)
- low-dose ICS + LABA (or medium-dose ICS)
- medium-dose ICS + LABA
- high-dose ICS + LABA (and omalizumab for allergies)
- high-dose ICS + LABA + oral corticosteroid (and omalizumab for allergies)
What is the most common complication of Asthma and how is it treated?
ASTHMA EXACERBATION = acute worsening of symptoms
- often triggered by benign viral infections, allergies
- want to prevent this from happening
Tx: bronchodilators, systemic glucocorticoids, oxygen
What is one of the most studied preventative measures for Asthma?
What are other ways to prevent asthma?
BREASTFEEDING –> microbiome transfer still occurs
- also avoid tobacco smoke, reduce obesity (eat balanced diet), get vaccinations
early exposure to microorganisms dec. risk of asthma
What is COPD and who does it commonly affect?
What are its biggest risk factors for development?
- persistent airflow limitation that is usually progressive with enhanced chronic inflammatory response in airways and lungs (airflow limitation is largely IRREVERSIBLE)
- mortality rates higher in men with strong associations to poverty
RF: smoking/tobacco exposure (MC), history of TB (more of a worldwide problem)
- first-degree relatives have 3x risk of development
How is COPD diagnosed and what are the 4 Gold classifications of COPD?
How should each Gold stage be managed?
Dx: FEV1/FVC < 0.7 (MUST HAVE)
- pts with low FEV1 and < 12% reversibility
Gold 1 = mild (FEV1 > 80% predicted)
- educate and manage risk
Gold 2 = moderate (50% < FEV1 < 80% predicted)
- consider rehabilitation
Gold 3 = severe (30% < FEV1 < 50% predicted)
- rehabilitation (possible lung reduction/transplant)
Gold 4 = very severe (FEV1 < 30% predicted)
- lung reduction/transplant (possible rehabilitation)
What are the two goals of COPD treatment?
What are two nonpharmalogic treatment options for COPD patients?
Goal: reduce symptoms and reduce risk
- Pulmonary Rehabilitation (individually tailored)
- improve physical activity and daily living
- Lung Volume reduction surgery/transplant
- evidence-based intervention to improve quality life
- usually for patients with severe disease
What are the 3 main pharmalogical treatments for COPD? (B/C/O)
- Bronchodilators = MAINSTAY (address breathlessness)
- prefer LONG-ACTING (inc. lung function, exercise)
- LAMA + LABA = 2x lung function ONLY
- Inhaled Corticosteroids (high risk of exacerbations)
- improve lung function, dec. breathlessness
- OXYGEN (15 hrs/day if SaO2 < 88%)
- REDUCED MORTALITY
- B/ICS are only for SYMPTOM reduction
What are the ABCD groups for COPD?
What treatment should each group be given?
A - mMRC 0-1, CAT < 10, 0-1 exacerbations (no hospital)
Tx: SABA
B - mMRC > 2, CAT > 10, 0-1 exacerbations (no hospital)
Tx: long acting bronchodilator (LABA/LAMA)
C - mMRC 0-1, CAT < 10, 2+ exacerbations (1 hospital)
Tx: LAMA
D - mMRC > 2, CAT > 10, 2+ exacerbations (1 hospital)
Tx: LAMA or LAMA + LABA or ICS + LABA
groups B-D should also receive Pulmonary Rehab
COPD Treatment (OC/Abx/O) and Prevention for Acute Exacerbations (V/LABA/ICS)
Treatment: ORAL CORTICOSTEROIDS (mainstay), oral antibiotics (if inc. sputum purulence), oxygen if needed (noninvasive mechanical ventilation if respiratory acidosis)
Prevention: flu vaccine, pneumococcal vaccine, long-acting bronchodilator and ICS (each reduces risk by 25%)
What is Pulmonary Hypertension and what is it importance?
What are its symptoms? (DOE/F/PCP/HF)
- mean pulmonary artery pressure (PAP) > 20 mmHg
- importance: inc. mortality if left untreated and onset can be insidious/overlooked (vague symptoms or co-morbid conditions)
Symptoms: dyspnea (exertion), fatigue, pleuritic chest pain, signs of right-sided heart failure
How can Pulmonary Hypertension be diagnosed?
What is the Swan-Ganz Catheter?
Transthoracic Echocardiogram (TTE) is the MOST COMMON way to diagnose pulmonary hypertension
- can look at RV and LV chamber size
- estimates PASP indirectly
- can also use electrocardiogram (right ventricular hypertropy), labs (inc. BNP), and cardiac catheterization (Swan-Ganz catheter)
SGC: catheter placed into pulmonary arteries with balloon that can be inflated/deflated
How is Pulmonary Hypertension treated?
What are 4 medications that can be used to treat Pulmonary Hypertension? (PA/PDI/EA/CCBs)
Tx: treat underlying causes and use symptom-based treatments
- graded exercise, supplemental oxygen, diruetics
Meds: Prostacyclin agonist (vasodilation), Phosphodiesterase inhibitors (dec. NO breakdown = vasodilation), Endothelium antagonists (block vasoconstriction), CCBs (least prescribed)
- PD inhibitor = Tadalafil
- Endothelium antagonists = ambrisentan
What is Virchow’s Triad and what condition does it relate to?
Hypercoagulability, Venous Stasis, Endothelial Injury
- related to venous thromboembolisms
What do Proteins C/S and Antithrombin III block in the coagulation pathway?
Proteins C/S - blocks factor VIII and V to inhibit cascade
ATIII - blocks factor II and X
What state do Protein C/S deficiency, Antithrombin III deficiency, and Factor V Leiden mutation cause?
- all 3 lead to hypercoagulable states
PC/SD - ineffective regulation of VIIIa/Va
ATIIID - ineffective regulation of Xa and IIa (thrombin)
FVLM - mutation of Factor V preventing protein C bind
How is Pulmonary Embolism diagnosed? (WC/L)
What imaging is used to visualize PE?
Wells Criteria (point-based scoring system to determine PE probability)
Labs: D-dimer serum lvls are good at RULING OUT PE if lvls are normal (SENSITIVE TEST)
- other inflammatory states can have (+) D-dimers
I: CT chest with Contrast (primary test for PE diagnosis)
- GOLD standard (visualize vasculature/vessels)
- also used V/Q scan (second-line study)
- for pts. w/contrast allergy and end stage renal disease
What is seen on ECG of a patient with Pulmonary Embolism? (ST/RV/BB/SQT)
What is seen on Echocardiogram of a patient with Pulmonary Embolism?
- Sinus Tachycardia is most common finding (44%)
- RV strain: inverted T waves in leads V1-4
- incomplete/complete RBBB
- S1, Q3, T3: deep S-wave in lead 1, Q-wave in lead 3, and inverted T-wave in lead 3
ECHO = D-shaped LV chamber due to RV enlargement
- pathomneumonic for PE until proven otherwise
What are the symptoms of Unstable PE (H/RVS/ECE) and what are its 2 treatment options?
Sx: HYPOTENSION, RV strain, elevated cardiac enzymes
- Resuscitation: ventilation (oxygen) and IVF/vasopressors
- Thrombolytics: ensure NO contraindications
if systemic thrombolysis fails –> repeat thrombolysis, attempt catheter thrombolysis, and proceed to surgery for thrombectomy
What are treatment options for Stable PE? (H/LMWH/W/DOACs)
Heparin: inhibits Factor II/X via antithrombin III
- continuous drip, but quick onset/easy to stop
LMW Heparin: enoxaparin
- requires injection, but quick onset (SubQ)
Vitamin K Antagonist: WARFARIN (blocks F 2, 7, 9, 10)
- oral, cheap but requires INR check and LMWH bridge
DOACs: rivaro/api/endoxaban and dabigatran
- do NOT need LMWH bridge (Xa inhibitors)
- oral, no labs or dietary restrictions, less bleeding
- cost and reversible agents are cons
What are the reversal agents for LMWH, Warfarin, and DOACs used to treat Pulmonary Embolism?
LMWH: protamine sulfate
Warfarin: Vitamin K, fresh frozen plasma
DOACs: andexanent alpha (Xa Inhibs) and idarucizumab (Thrombin Inhib)
What is the common duration of treatment for pts. with Pulmonary Embolism?
MINIMUM 3 months for all patients
- extended treatment not typically needed for pts. with provoked DVT/PE (travel, surgery, hormone therapy)
- indefinite anticoagulation intended for those with underlying disease (malignancy and genetic mutations)
What is Obstructive Sleep Apnea (OSA), what is apnea, and how is OSA measured?
- disruption of breathing pattern while sleeping that results in excessive daytime somnolence despite adequate sleep periods and not explained by other causes = snoring, gasping for air, breathing pause
apnea = red. breathing for 10 sec with drop in SpO2 > 3%
- OSA measured by Apnea-Hypopnea Index (AHI) calculated by taking # of apnea episodes/hours
What are risk factors for OSA? (O/LT/CA/ET/ELN/M)
- OBESITY - #1 cause/predictor of OSA
- large tongue
- craniofacial abnormalities (retrognathia/micrognathia)
- enlarged Tonsils or LNs
- Male sex
What is the STOPBANG risk criteria for OSA?
S - snoring
T - tired
O - observed (has someone seen you stop breathing)
P - pressure (high blood pressure)
B - body mass index > 35
A - age (older than 50)
N - neck size
G - gender
Low risk = 0-2, intermediate = 3-4, high risk = 5-8
How is OSA diagnosed and what are two treatment options for patients with it? (CPAP/OA)
Dx: Polysomnogram (PSG) = GOLD STANDARD
- records sleep activity for 6-7 hours overnight
- monitors EEG, ECG, ocular movement, airflow, O2
- generates AHI, diagnose severity of sleep apnea
Tx: CPAP or Oral Appliances
- CPAP - provides positive pressure ventilation
- improved compliance rate with education/support
- OA - thrust mandible forward (opens airway)
- for mild OSA, requires adjustments, jaw pain
What are the 4 common characteristics of Interstitial Lung Disease? (RPFTs/DLCO/DOE/A)
- restrictive pattern on PFTs
- dec. DLCO
- dyspnea on exertion
- absence of primary infection or malignancy
Idiopathic Pulmonary Fibrosis
Who does it affect, what are its symptoms, what does it sound like of physical exam, and what is seen on CT imaging? (BH/TB)
How is it treated? (SC/S/IM/AF)
- affects pts older than 60 yo, M = F
Sx: progressive dyspnea, dry cough, fatigue, inability to perform ADLs
PE: inspiratory CRACKLES (“velcro lung”)
CT: bilaterally honeycombing, traction bronchiectasis
Tx: supportive care (O2/rehab), steroids, immunomodulators, anti-fibrotic therapy (pirfenidone - fibroblast prolif. and nintedanib - TK inhibitor)
Sarcoidosis
Who does it affect, what is it characterized by, what are two cutaneous manifestations (LP/EN), and what are two syndromes pts have (LS/HS)?
What are Lofgren’s (EN/HL/F/A) and Heerfordt’s (AU/P/F/CNP) Syndromes?
- affects African American females the most, either in 2nd-3rd or 6th decade (biomodal)
- characterized by NONCASEATING GRANULOMA
CM: lupus pernio and erythema nodosum
S: Lofgren’s (EN/hilar lymphadenopathy/fever/arthritis) and Heerfordt’s (ant. uveitis/parotitis/CN 7 palsy/fever)
Sarcoidosis
What is the most common radiological finding, what are stages 0-4 of radiographic sarcoidosis, and how is it treated? (S/M/A/C)
I: most common finding is HILAR LYMPHADENOPATHY
Stages:
- 0 = no pulmonary involvement
- 1 = Hilar LAD
- 2 = Hilar LAD + infiltrates
- 3 = infiltrates only
- 4 = fibrosis
Tx: supportive, steroids (1st line therapy), methotrexate, azathioprine, cyclophosphamide
Granulomatosis with Polyangiitis
Who does it affect, what does it affect, what is a clinical manifestation it can cause, what lab is it positive for, and how is it treated (S/C)?
- small-vessel vasculitis affecting sinuses/lungs/kidneys in middle-aged caucasians
PE: saddle nose deformity (relapsing polychondritis)
Lab: c-ANCA (+)
Tx: steroids and cyclophosphamide
Goodpasture’s Syndrome
Who does it affect, what does it affect, what is seen on radiology, what lab is it positive for, and how is it treated (P/S/C)
- autoimmune condition with Abs against basement membrane of alveoli and glomerular parenchyma in caucasians (usually pediatrics, or bimodal adult distrib)
Radio: bilateral ground glass opacities
Lab: anti-GBM (+)
Tx: PLASMAPHERESIS, steroids, cyclophosphamide
What 3 Connective Tissue disorders are most commonly associated with ILD? (SS/RA/DP)
- Systemic Sclerosis = MC CT disease with ILD
- Rheumatoid Arthritis = more common in males
- Dermatomyositis/Polymyositis
- (+) for anti-synthetase Abs
Hypersensitivity Pneumonitis
How does it present clinically, what is seen on radiographs, what is seen on histology, and how is it treated?
PE: symptoms IMPROVE when patient goes on vacation, otherwise cough, dyspnea, +/- fevers
Radio: chronic forms have honeycomb patterns that SPARE the base of the lungs (unlike IPF)
Histo: possible NON-caseating granulomas, PLASMA CELLS
Tx: remove pt. from antigen
Silicosis
Who does it affect, what is the difference in radiographs between long and progressive disease, and what are pts. at inc. risk of developing?
- affects miners, stone cutters, sand blasters, quarry workers
Long exposure - Simple Silicosis
- nodular disease and calcified hilar LN
Progressive - Complicated Silicosis
- large nodules (> 1cm) with extensive fibrosis
- pts at inc. risk of infections, ESPECIALLY TB
Asbestosis
Who does it affect, what is seen on radiography, and what are pts. at inc. risk of developing?
- affects construction, INSULATION, demolition, automobile workers (“needle-like”)
Radio: multiple nodular opacities, pleural effusion/fibrosis, blurred diaphragm/cardiac silhouette
- pts. at inc. risk of mesothelioma and lung cancer (asbestos and cigarette smoke have SYNERGISTIC effect on lung cancer rates)
Coal Worker Pneumoconiosis
Who does it affect and what is the difference between Simple and Complicated?
- affects miners who inhale coal dust (high lvls of silica)
Simple: asymptomatic
- Radio: small nodules (< 1cm) at APEX of lung
Complicated: cough, dyspnea, sputum
- Radio: large nodules (> 1cm) with patchy infiltrates at BASE, with fibrosis
Berylliosis
Who does it affect, what is the difference between acute and chronic versions, what are pts. at inc. risk of developing, and how is it treated (S/R)?
- affects pts. in alloy or electronic device manufacturing (beryllium exposure)
Acute: similar rxn to hypersensitivity pneumonitis
Chronic: insidious onset, from cumulative exposure
- Radio: hilar LAD, diffuse infiltrates
- pts are at inc. risk of LUNG CANCER
Tx: steroids, removal from beryllium environment
