resp Flashcards
(37 cards)
how to diagnosed pleural effusion ?
- Is it exudate or transudate?
This is the first question to ask when analyzing pleural effusion. It guides further workup.
Transudate:
Mechanism: Pressure imbalance
(↑ hydrostatic or ↓ oncotic pressure)
Cause: Systemic conditions (e.g. CHF, cirrhosis, nephrotic syndrome)
Pathophysiology:
No inflammation
No cytokine release
Intact capillaries
Minimal protein or LDH leakage
Result:
Low protein
Low LDH
Clear, watery fluid
Exudate:
Mechanism: Inflammation or local disease
Cause: Pneumonia, TB, malignancy, PE, autoimmune
Pathophysiology:
Cytokine release → increased capillary permeability
Protein leaks into pleural space
Cell destruction → LDH release
Result:
High protein
High LDH
Often cloudy or turbid fluid
what is light criteria ?
Light’s criteria, a pleural effusion is exudative if any of the following are true:
1/Pleural fluid protein / serum protein > 0.5
2/Pleural fluid LDH / serum LDH > 0.6
3/Pleural fluid LDH > 2/3 the upper limit of normal for serum LDH
type of pneumothorax ?
1/Spontaneous
A/Primary:
Occurs in healthy people (no lung disease)
Risk factors: Tall, thin, young males
Path: rupture of subpleural blebs
B/Secondary:
Due to underlying lung disease (obstrictive - air can not get ou) (e.g. COPD,ASTHMA)
or necrotic mechanism ( TB,)
Path: weakened alveoli rupture due to hyperinflation or infection
2/Traumatic PTX
Cause: Chest trauma (e.g., stab, rib fracture, thoracentesis, central line placement) ot mechanical ventilation with highe pressure .
diagnostic approach to plural effusion ?
CXR → Locate effusion → CXR or Chest CT → Best: Chest CT
↓
Perform Thoracentesis
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Clear fluid Cloudy fluid
↓ Pleural Protein ↑ Pleural Protein
↓ Pleural LDH ↑ Pleural LDH
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Transudative Effusion Exudative Effusion
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↑ PCWP → CHF → Obtain Pleural Glucose
↓ Albumin → Nephrotic ↓ Pleural Glucose
↔ Albumin → Cirrhosis → Causes:
→ Malignancy (abnormal cytology)
→ Empyema (culture +, ↓↓ pH)
→ Autoimmune (ANA/RF+)
→ Tuberculosis (AFB stain+)
→ Normal Pleural Glucose
→ ↑ Pleural TG → Chylothorax
→ ↑ Pleural RBCs → Hemothorax
→ ↑ Pleural Amylase
→ Pancreatitis
→ Esophageal rupture
diagnostic approach to pneumothorax ?
Suspected Pneumothorax?
→ Confirm with CXR or bedside US
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Type of Pneumothorax?
→ Tension PTX
→ Spontaneous PTX (Primary or Secondary)
→ Traumatic PTX
→ Iatrogenic PTX
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If Tension Pneumothorax
→ Immediate needle decompression (2nd ICS midclavicular or 5th ICS anterior axillary)
→ Then chest tube (tube thoracostomy)
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If Spontaneous PTX
Stable?
→ Small PTX (<2 cm rim / <20% lung volume)
→ Observe + O2
→ Large PTX / symptomatic
→ Needle aspiration (if primary)
→ If fails or secondary: Chest tube
Unstable?
→ Chest tube immediately
ninja
What is the complication of COPD?
- Pneumonia
• Airway obstruction due to excess mucus and inflammation leads to:
• ↓ Clearance of bacteria
• Cilia degeneration → impaired mucociliary escalator
• This makes them more prone to bacterial pneumonia.
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- Respiratory Failure (AECOPD)
• Can be triggered by:
• Viral URI, medication non-compliance, or bacterial infections
• All lead to:
• ↑ CO₂ retention, ↓ O₂ exchange due to airway obstruction and alveolar collapse
• Result = Type II Respiratory Failure (↑ CO₂, ↓ O₂)
• You’ll see ↑ RR and ↑ work of breathing
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- Cor Pulmonale (Right Heart Failure due to Lung Disease)
• Chronic hypoxia causes pulmonary vasoconstriction:
• decreased O2 strong stimulus to↑ Pulmonary Vascular Resistance (PVR)
• This can lead to Type III Pulmonary Hypertension
• Over time, this increases afterload on the right heart → Right-sided heart failure
• Clinical signs:
• JVD, Hepatomegaly, Peripheral edema, Ascites
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- Polycythemia
• Chronic hypoxia stimulates erythropoietin (EPO) release from the kidneys
• This increases RBC production to compensate for hypoxia
• Result = ↑ Hematocrit (HCT) → blood becomes more viscous, increasing thrombosis risk
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- Pneumothorax
• Patients with Emphysema have bullae (thin-walled air sacs)
• These can rupture → allowing air to escape into the pleural space
• This leads to a secondary spontaneous pneumothorax
• Air traps in pleural space, collapsing lung
• Emergency!
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This visual ties together the domino effects of chronic lung disease:
• Airway obstruction → infection
• Infection + poor clearance → respiratory failure
• Hypoxia → heart strain + blood changes
• Bullae formation → lung collapse risk
Diagnostic approach to COPD ?
Management of COPD?
Management of acute exarpation COPD
Bronchodilation
• Give SAMA + SABA (e.g., Ipratropium + Albuterol)
2. Reduce Airway Inflammation
• Use systemic corticosteroids, either IV or oral (e.g., Prednisone or Methylprednisolone)
3. Reduce Work of Breathing
• Start BiPAP to support ventilation and reduce respiratory effort
4. Treat Possible Bacterial Infection
• Give Azithromycin or Doxycycline
what indicate bad prognosis for pneumonia ?
CURP 65
Confusion
urea > 7
RR>30
BP SYS<90 DIS<60
AGE 65
A score of ≥2 suggests hospitalization; higher scores indicate worse prognosis.
what type of inflammation is most common in asthma ?
- Type 2 (T2) Asthma – Most common (especially in children and allergic adults)
Driven by Th2 cells, IL-4, IL-5, IL-13
Involves eosinophils, IgE, FeNO
Responds well to steroids and biologics (e.g., anti-IL-5, anti-IgE)
- Non-Type 2 Asthma – Often in adults, more severe, steroid-resistant
Neutrophilic asthma:
Involves neutrophils instead of eosinophils
Possibly linked to Th1 or Th17 immune responses
Often triggered by infections, pollutants, or smoking
Poor response to corticosteroids
May benefit from macrolides (like azithromycin) or non-biologic options
what is the pathophysiology of asthma ?
- Trigger Exposure (e.g., allergens, cold air, smoke)
→ activates dendritic cells in the airways. - Dendritic Cells stimulate
→ TH2 cells (a type of helper T cell). - TH2 Cells release IL-4 and IL-5, which:
• Activate eosinophils (inflammation)
• Stimulate plasma cells to produce IgE antibodies - IgE binds to mast cells, making them sensitive to allergens.
- On re-exposure to the allergen, mast cells release:
• Histamine → bronchoconstriction, mucus
• Leukotrienes → inflammation and airway narrowing
What is biomarker of asthma ?
biomarkers used in asthma to help diagnose inflammation type, assess treatment response, and guide therapy choices—especially with corticosteroids and biologics.
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- Blood Eosinophils• What it is: A type of white blood cell involved in allergic inflammation.
• Elevated levels:
• ≥300 cells/μL indicates Type 2 (T2) inflammation
• Clinical value:
• Predicts good response to corticosteroids
• Helps select patients for biologics targeting IL-5 (e.g., mepolizumab, benralizumab)
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- Exhaled Nitric Oxide (FeNO)
• What it is: A marker of eosinophilic airway inflammation measured in exhaled breath.
• Elevated levels:
• 35–40 ppb suggests eosinophilic asthma
• Clinical value:
• Monitors adherence to inhaled corticosteroids
• Predicts response to ICS and biologics
• Non-invasive and useful for ongoing monitoring
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- Total and Specific IgE
• Total IgE:
• Elevated in patients with atopy (genetic tendency to develop allergies)
• Specific IgE:
• Identifies particular allergen sensitivities
• Assists in determining eligibility for anti-IgE therapy (e.g., omalizumab)
Gold stander in asthma diagnoses?
No gold stander
Challenge test = physiological evidence
Biomarkers = inflammatory insight
Both are complementary. A positive challenge test may suggest asthma, but biomarkers help confirm the type of asthma and guide appropriate therapy.
Main co-morbidities associated with asthma and affect treatment?
Rhinosinusities
GERD
Obesity
Physiological factor (exm.GAD/depression)
OSA
Step-wise asthma Mangment?
General Principles:
• Use a stepwise approach: start at the step appropriate for the patient’s symptoms and severity, then step up or down as needed.
• Ensure correct inhaler technique and good adherence.
• Identify and reduce exposure to asthma triggers.
• Reassess symptoms within 2–6 weeks after changes (step up)
note Before stepping up treatment , Assess adherence and review proper inhaler technique.
Identify any persistent exposures to asthma triggers.
• Consider step-down if well-controlled for ≥ 2 months (step down).
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Step 1: Intermittent symptoms (<4–5 days/week)
• As-needed (PRN) low-dose ICS/formoterol (e.g., budesonide/formoterol)
Step 2: Mild persistent symptoms
• Continue PRN low-dose ICS/formoterol
Step 3: Symptoms on most days OR nighttime symptoms ≥1/week
• Maintenance and reliever therapy with low-dose ICS/formoterol (both scheduled and PRN)
note : Advise patients to seek medical care if they require > 12 inhalations from their ICS/LABA inhaler in a single day
Step 4: Daily symptoms OR low lung function
• Medium-dose ICS/formoterol (scheduled)
• PLUS PRN low-dose ICS/formoterol
Step 5: Inadequate control despite step 4
• Ensure adherence to step 4
• Consider:
• Trial of high-dose ICS/LABA for 3–6 months
• Add-on LAMA (e.g., tiotropium)
• Biologics (e.g., anti-IgE, anti-IL-5/5R, anti-IL-4R)
• Low-dose oral glucocorticoids (last resort)
Dignostic approach to asthma ?
Summary:
This flowchart guides through:
• Initial workup (CXR, ECG, ABG)
•1 Function-based confirmation (PFTs: FEV₁/FVC, PEFR) •2 Reversibility testing (bronchodilator/methacholine) • biomarker (atopic vs non-atopic)
⸻detail:
- Initial Evaluation
Obtain:
• CXR (Chest X-ray): Usually normal; may show hyperinflation.
• ECG: Usually normal.
• ABG (Arterial Blood Gas):
• In severe asthma exacerbation:
• ↓ pH (acidosis)
• ↑ pCO₂ (hypercapnia)
→ Indicates respiratory acidosis
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- Pulmonary Function Tests (PFTs)
From here, two main paths:
A. Stable Asthma: Check FEV₁/FVC ratio
• FEV₁/FVC < 70% → Suggests obstructive pattern → asthma likely
Then:
Check FEV₁ (Forced Expiratory Volume in 1 sec)
• Administer bronchodilator, re-check FEV₁: > 12% increase in FEV₁ → Suggests asthma
If uncertain:
Administer methacholine, re-check FEV₁:
• > 20% drop → Suggests asthma
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B. Exacerbation: Check PEFR (Peak Expiratory Flow Rate)
• PEFR < 40% predicted → Severe asthmatic exacerbation
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Note : DLCO (Diffusing Capacity of the Lungs for Carbon Monoxide)
• Use this if diagnostic doubt remains.
• Normal or ↑ DLCO → Suggests asthma
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Ddx diagnosis’s of asthma?
-COPD
-Vocal cord dysfunction
-Bronchiectasis
-Heart failure
-Eosinophilic pneumonias
-Allergic bronchopulmonary aspergillosis.
Detail :
COPD: Older age, smoking history, fixed airflow limitation
Vocal cord dysfunction: Inspiratory stridor, normal PFTs, laryngoscopy findings
Bronchiectasis: Chronic productive cough, CT findings, recurrent infections
Heart failure: Cardiac history, BNP levels, echocardiogram findings
Eosinophilic pneumonias: Pulmonary infiltrates, systemic symptoms, BAL eosinophilia
Allergic bronchopulmonary aspergillosis: Central bronchiectasis, high IgE, Aspergillus sensitivity
Asthma in pregnancy
Pediatric mangment + asthma exarbation
Area to improve
classification of asthma severity ?
- Intermittent Asthma
Symptoms: ≤2 days/week
Nighttime awakenings: ≤2 times/month
SABA use: ≤2 days/week
Interference with normal activity: None
Exacerbations: 0–1/year requiring oral steroids
- Mild Persistent Asthma
Symptoms: >2 days/week but not daily
Nighttime awakenings: 3–4 times/month
SABA use: >2 days/week but not daily
Interference with normal activity: Minor limitation
Exacerbations: ≥2/year requiring oral steroids
- Moderate Persistent Asthma
Symptoms: Daily
Nighttime awakenings: >1 time/week but not nightly
SABA use: Daily
Interference with normal activity: Some limitation
Exacerbations: ≥2/year requiring oral steroids
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4. Severe Persistent Asthma
Symptoms: Throughout the day
Nighttime awakenings: Often 7x/week
SABA use: Several times/day
Interference with normal activity: Extremely limited
Exacerbations: Frequent
Mangment of acute asthma exacerbation with dose ?
- Inhaled Short-Acting Beta-Agonist (SABA – Albuterol)
• Adults (nebulized): 2.5 mg every 20 minutes for 3 doses, then 2.5–10 mg every 1–4 hours as needed, or continuous at 10–15 mg/hour.
• Adults (MDI with spacer): 4–8 puffs every 20 minutes for up to 4 hours, then as needed.
• Children (nebulized): 0.15 mg/kg (minimum dose 2.5 mg) every 20 minutes for 3 doses, then 0.15–0.3 mg/kg every 1–4 hours as needed. - Inhaled Short-Acting Muscarinic Antagonist (SAMA – Ipratropium)
• Adults and children (nebulized): 0.5 mg every 20 minutes for 3 doses, then as needed.
• MDI (with spacer): 4–8 puffs every 20 minutes for up to 3 hours. - Systemic Glucocorticoids
• Prednisone/prednisolone (oral):
• Adults: 40–60 mg once daily for 5–7 days.
• Children: 1–2 mg/kg/day (max 60 mg/day) in 1–2 divided doses for 3–5 days.
• Methylprednisolone (IV):
• Adults: 60–80 mg/day in divided doses.
• Children: 1–2 mg/kg/dose every 6 hours. - Inhaled Corticosteroid + LABA (e.g., Budesonide/Formoterol)
• Maintenance and reliever therapy: 1–2 inhalations (each with 80/4.5 mcg or 160/4.5 mcg) as needed, max 12 inhalations/day for adults. - IV Magnesium Sulfate (for severe exacerbations)
• Adults: 2 grams IV over 20 minutes.
• Children: 25–75 mg/kg IV over 20 minutes (max 2 grams).
