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CPR II Exam 2 > Clinical Approach to Asthma/COPD and pHTN/PE/OSA/ILD > Flashcards

Clinical Approach to Asthma/COPD and pHTN/PE/OSA/ILD Flashcards

1
Q

What is the largest epidemiological risk factor In Utero for the development of Asthma?

A

PREMATURITY

  • has a 4x increased risk
  • also ethnicity, low socioeconomic status, stress, and C-section
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2
Q

What are common Postnatal risk factors for the development of Asthma? (A/I/AP/Abx/A/O)

A
  • 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
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3
Q

Asthma diagnosis with Spirometry

A
  • 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
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4
Q

Intermittent Asthma

What is the Rule of 2’s?

A
  • symptoms < 2x/week
  • nighttime awakenings < 2x/month
  • SABA use < 2x/week

lung function > 80%, use Step 1 therapy

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5
Q

Mild Persistent Asthma

When do pts have symptoms, nighttime awakenings, and asthma exacerbations?

A

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

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6
Q

Moderate Persistent Asthma

When do pts have symptoms, nighttime awakenings, and when is SABA used for symptom control?

A

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)

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7
Q

Severe Persistent Asthma

When do pts have symptoms, nighttime awakenings, and when is SABA used for symptom control?

A

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)

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8
Q

Asthma Treatment and Management

A
  • 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

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9
Q

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
A
  1. SABA as needed
  2. low-dose ICS (inhaled corticosteroid)
  3. low-dose ICS + LABA (or medium-dose ICS)
  4. medium-dose ICS + LABA
  5. high-dose ICS + LABA (and omalizumab for allergies)
  6. high-dose ICS + LABA + oral corticosteroid (and omalizumab for allergies)
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10
Q

What is the most common complication of Asthma and how is it treated?

A

ASTHMA EXACERBATION = acute worsening of symptoms

  • often triggered by benign viral infections, allergies
  • want to prevent this from happening

Tx: bronchodilators, systemic glucocorticoids, oxygen

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11
Q

What is one of the most studied preventative measures for Asthma?

What are other ways to prevent asthma?

A

BREASTFEEDING –> microbiome transfer still occurs

  • also avoid tobacco smoke, reduce obesity (eat balanced diet), get vaccinations

early exposure to microorganisms dec. risk of asthma

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12
Q

What is COPD and who does it commonly affect?

What are its biggest risk factors for development?

A
  • 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

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13
Q

How is COPD diagnosed and what are the 4 Gold classifications of COPD?

How should each Gold stage be managed?

A

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)

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14
Q

What are the two goals of COPD treatment?

What are two nonpharmalogic treatment options for COPD patients?

A

Goal: reduce symptoms and reduce risk

  1. Pulmonary Rehabilitation (individually tailored)
    • improve physical activity and daily living
  2. Lung Volume reduction surgery/transplant
    • evidence-based intervention to improve quality life
    • usually for patients with severe disease
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15
Q

What are the 3 main pharmalogical treatments for COPD? (B/C/O)

A
  1. Bronchodilators = MAINSTAY (address breathlessness)
    • prefer LONG-ACTING (inc. lung function, exercise)
    • LAMA + LABA = 2x lung function ONLY
  2. Inhaled Corticosteroids (high risk of exacerbations)
    • improve lung function, dec. breathlessness
  3. OXYGEN (15 hrs/day if SaO2 < 88%)
    • REDUCED MORTALITY
    • B/ICS are only for SYMPTOM reduction
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16
Q

What are the ABCD groups for COPD?

What treatment should each group be given?

A

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

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17
Q

COPD Treatment (OC/Abx/O) and Prevention for Acute Exacerbations (V/LABA/ICS)

A

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%)

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18
Q

What is Pulmonary Hypertension and what is it importance?

What are its symptoms? (DOE/F/PCP/HF)

A
  • 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

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19
Q

How can Pulmonary Hypertension be diagnosed?

What is the Swan-Ganz Catheter?

A

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

20
Q

How is Pulmonary Hypertension treated?

What are 4 medications that can be used to treat Pulmonary Hypertension? (PA/PDI/EA/CCBs)

A

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
21
Q

What is Virchow’s Triad and what condition does it relate to?

A

Hypercoagulability, Venous Stasis, Endothelial Injury

  • related to venous thromboembolisms
22
Q

What do Proteins C/S and Antithrombin III block in the coagulation pathway?

A

Proteins C/S - blocks factor VIII and V to inhibit cascade

ATIII - blocks factor II and X

23
Q

What state do Protein C/S deficiency, Antithrombin III deficiency, and Factor V Leiden mutation cause?

A
  • 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

24
Q

How is Pulmonary Embolism diagnosed? (WC/L)

What imaging is used to visualize PE?

A

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
25
Q

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?

A
  • 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

26
Q

What are the symptoms of Unstable PE (H/RVS/ECE) and what are its 2 treatment options?

A

Sx: HYPOTENSION, RV strain, elevated cardiac enzymes

  1. Resuscitation: ventilation (oxygen) and IVF/vasopressors
  2. Thrombolytics: ensure NO contraindications

if systemic thrombolysis fails –> repeat thrombolysis, attempt catheter thrombolysis, and proceed to surgery for thrombectomy

27
Q

What are treatment options for Stable PE? (H/LMWH/W/DOACs)

A

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
28
Q

What are the reversal agents for LMWH, Warfarin, and DOACs used to treat Pulmonary Embolism?

A

LMWH: protamine sulfate
Warfarin: Vitamin K, fresh frozen plasma
DOACs: andexanent alpha (Xa Inhibs) and idarucizumab (Thrombin Inhib)

29
Q

What is the common duration of treatment for pts. with Pulmonary Embolism?

A

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)
30
Q

What is Obstructive Sleep Apnea (OSA), what is apnea, and how is OSA measured?

A
  • 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
31
Q

What are risk factors for OSA? (O/LT/CA/ET/ELN/M)

A
  • OBESITY - #1 cause/predictor of OSA
  • large tongue
  • craniofacial abnormalities (retrognathia/micrognathia)
  • enlarged Tonsils or LNs
  • Male sex
32
Q

What is the STOPBANG risk criteria for OSA?

A

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

33
Q

How is OSA diagnosed and what are two treatment options for patients with it? (CPAP/OA)

A

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
34
Q

What are the 4 common characteristics of Interstitial Lung Disease? (RPFTs/DLCO/DOE/A)

A
  1. restrictive pattern on PFTs
  2. dec. DLCO
  3. dyspnea on exertion
  4. absence of primary infection or malignancy
35
Q

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)

A
  • 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)

36
Q

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?

A
  • 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)

37
Q

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)

A

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

38
Q

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)?

A
  • small-vessel vasculitis affecting sinuses/lungs/kidneys in middle-aged caucasians

PE: saddle nose deformity (relapsing polychondritis)
Lab: c-ANCA (+)
Tx: steroids and cyclophosphamide

39
Q

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)

A
  • 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

40
Q

What 3 Connective Tissue disorders are most commonly associated with ILD? (SS/RA/DP)

A
  1. Systemic Sclerosis = MC CT disease with ILD
  2. Rheumatoid Arthritis = more common in males
  3. Dermatomyositis/Polymyositis
    • (+) for anti-synthetase Abs
41
Q

Hypersensitivity Pneumonitis

How does it present clinically, what is seen on radiographs, what is seen on histology, and how is it treated?

A

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

42
Q

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?

A
  • 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
43
Q

Asbestosis

Who does it affect, what is seen on radiography, and what are pts. at inc. risk of developing?

A
  • 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)
44
Q

Coal Worker Pneumoconiosis

Who does it affect and what is the difference between Simple and Complicated?

A
  • 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

45
Q

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)?

A
  • 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

CPR II Exam 2 (10 decks)

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