Pulmonary Flashcards
Asthma
- Chronic cough
- Characterized by: variable/recurring symptoms + airflow obstruction + bronchospasm + bronchial inflammation + airway hyper-reactivity
- Treatment:
- inhaled corticosteroid —> reduce bronchial inflammation
- beta-adrenergic agonist—> dilate bronchial smooth muscle
COPD
Exacerbation of asthma
- Iv corticosteroid
- SABA
- Mg sulfate
- O2 supplementation
Bronchiectasis ( permanent damage like fibrosis)
- bronchioles are filled with mucus (توسع قصبات)—> due to childhood infection ( like TB…)
- cough with pelghm + SOB
- treatment: antibiotics
CYCLE:
1. Inflammation
2. Permanent airway dilation, loss of cilia —> airway remodeling
3. Mucus accumulation —> bacterial accumulation
4. Infection
- pulmonary edema + heart issue
- biPAP —> patient is ventilated —>
1. she is in oxygen
Nasal cannula
تعب قلب ….احتقان…. و تجمع سواال….
CPAP vs. BiPAP
- BiPAP delivers higher air pressure when you breathe in. The CPAP, on the other hand, delivers the same amount of pressure at all times. So the BiPAP makes it easier to breathe out than the CPAP.
—> used in patient with many comorbidities
—————-
- While CPAP generally delivers a single pressure, BiPAP delivers two: an inhale pressure and an exhale pressure. —-> used in patient with obstructive sleep apnea —> less morbidities
Chronic silicosis
( factory manufacturing granite & quartz)
- dyspnea slowly worsening in the past couple of years
- upper lobe fibrosis + calcified hilar adenopathy
- due to fibrotic occupational lung disease
Asbestosis
( home insulation & pulmonary company)
- symptoms develops 20 years after initial exposure
- progressive dyspnea+ nonproductive cough + end inspiratory bibasilar fine crackles + clubbing + pleural plaque
- increase risk for lung cancer & mesothelioma
- PFT shows restrictive lung disease = decreased lung volume & normal/increased FEV1/FVC ratio
Obstructive vs restrictive lung disorders
Obstructive lung disorder
1. Increase lung volume capacity
2. Decrease FEV1/FVC ratio
Restrictive lung disorder
1. Decrease lung volume capacity
2. Normal or increase FEV1/FVC ratio
3. Decreased DLCO
—-> 5-10 dont treat
Pulmonary function test (PFT)
- Low FEV1/FVC ratio
- obstructive disease (asthma, COPD/ chronic bronchitis + empyema, bronchiectasis)
- Low DLCO: COPD
- Normal/High DLCO: Asthma
- Norma/ high FEV1/FVC ratio
- restrictive disease (
- Low DLCO:
- Interstitial lung disease (progressive fibrosis)
- occupational dust exposure= inhalation of asbestos, beryllium, silicon dioxide
- drug toxicity = amiodarone, bleomycin, nitrofurantoin
- radiation
- systemic connective tissue disorders = RA, scleroderma ),
- granulomatous disease (sarcoidosis)
- Interstitial lung disease (progressive fibrosis)
- Normal DLCO: chest wall weakness
- Low DLCO:
Scleroderma ( CREST Syndrome)
- extensive production of collagen that target skins, GI, Lung , kidneys
- Calcinosis ( deposit of calcium in the skin)
- Raynaud’s phenomenon ( spasm of blood vessels in response to cold or stress)
- Esophageal dysfunction ( acid reflex & decrease in motility of esophagus)
- Sclerodactyly ( thickening & tightening of the skin on the finger & hand)
- Talengectasia ( dilation of the capillary causing red marks on surface of skin)
Sarcoidosis
( restrictive lung disease)
- systemic granulomatous disorder ( normal/low FEV1, normal/low FVC, high FEV1/FVC ratio, low DCLO)
- CLUES: hypercalcemia + hilar lymphadenopathy (mediastinal fullness & scattered reticular opacity in the upper lobe)
Interstitial lung disease
( excessive collage deposit in the extracellular matrix around alveoli = low DLCO = high alveolar-arterial oxygen gradient = lead to hypoxemia)
- Interstitial lung disease (progressive fibrosis)
1. occupational dust exposure= inhalation of asbestos, beryllium, silicon dioxide
2. drug toxicity = amiodarone, bleomycin, nitrofurantoin
3. radiation
4. systemic connective tissue disorders = RA, scleroderma ) - granulomatous disease (sarcoidosis)
Signs:
1. Low fev1, low fvc, normal to high fev1/fvc, low DLCO
2. Fine crackles + clubbing
3. X-ray: honeycombing + fibrosis + traction of bronchiectasis
Causes of hypoxemia
Normal A-a gradient: (between 5–10 mmHg)
1. Low PiO2 due to high altitude —> corrected with O2 supplement
- hypoventilation due to morbid obesity, CNS depression —> corrected with O2 supplement
Increase A-a gradient:
1. Diffusion limitation due to ILD, emphysema —> corrected with O2 supplement
- V/Q mismatch due to small PE, lobar pneumonia, ARDS ( right-to-left intrapulmonary shunt)—> can be corrected with O2 supplement or not ( depend on how much of lung is affected)
- Large intrapulmonary shunt due to diffuse pulmonary edema —> not corrected with O2 supplement
- Large dead space ventilation due to massive PE, right to left intracardiac shunt —> not corrected with O2 supplement
hypersensitivity pneumonitis (HP)
( can be mistaken for bacterial pneumonia)
- recurrent, short-lived episodes of sudden fever, dyspnea, non productive cough
- exaggerated autoimmune response to antigen (mold, bacteria, animal protein)
Acute-HP:
1. Recurrent episodes of sudden fever, dyspnea, nonproductive cough + hypoxemia + fine crackles + leukocytosis + x-ray shows scattered micro-nodular interstitial opacities (that resolves between episodes) + self resolves within few hours or days, after removal of antigen exposure + treated with antibiotics
Chronic cough (causes)
- Upper-airway cough syndrome ( postnasal drip)
- Asthma
- GERD
- Upper-airway cough syndrome ( postnasal drip)
Diagnosis:
1. Elimination of nasal discharge & cough with H1-histamine receptor antagonist ( chloropheniramine)
Recurrent pneumonia causes
- Same lung lobe
- bronchial obstruction ( neoplasm, adenopathy, bronchiectasis, foreign body)
- recurrent aspiration ( GERD, Dysphagia, altered consciousness, seizure, alcohol) (advanced Parkinson disease = impaired cough reflex) ( use of sedating antipsychotic medication) ( dental issues)
- Different lung lobe
- HIV, leukemia
- cystic fibrosis
- vasculitis
Symptoms:
- dyspnea, cough, leukocytosis, pulmonary infiltrates —> CAP
Patient with recurrent aspiration
( due to advanced Parkinson disease = impaired cough reflex)
- major cause of death in patient with advanced Parkinson disease is aspiration pneumonia
- require:
- Swallow study (to evaluate & alter food consistency or eating position)
- Video-fluoroscopic modified barium swallow
Hospital acquired pneumonia
- caused by bacterial aspiration pneumonia associated with:
1. Sedative & anti-psychotic medication
2. Gastric suppression medication
3. Incubation
4. Nasogastric feeding
5. Anesthesia
Symptoms:
1. Fever, dyspnea, leukocytosis, nonproductive cough , pulmonary infiltrates
Bronchiectasis
( bronchial thickening & dilation due to recurrent cycles of bacterial infection, inflammation, & tissue damage)
Symptoms:
- recurrent episodes of fever, dyspnea, productive sputum, hemoptysis, clubbing, crackles
- impaired bacterial clearance ( patients do not clear infection after antibiotic course)
- bronchiectasis is associated with cystic fibrosis in young patients—> due to defective chloride & sodium transport ( defective chloride channel) —> associated with upper lung lobe & pseudomonas infection found in sputum
Chronic bacterial infection
- Lead to neutrophil recruitment + extensive elastase activity —> bronchial airway damage
Seen with:
- Bronchiectasis due to cystic fibrosis—> recurrent episodes of fever, dyspnea, sputum, hemoptysis, fine crackles, clubbing, upper lobe involvement, pseudomonas in sputum
- Alpha-1-antitrypsin deficiency —> associated with emphysema & lower lung lobe
Sickle cell anemia lead to bronchiectasis
—>
Sickle cell disease —> splenic dysfunction —> encapsulated bacteria —> predispose to bronchiectasis
Bronchiectasis
Associated with:
1. hemoptysis (chronic blood-streaked sputum) + fever + dyspnea + sputum + clubbing + fine crackles
- Diagnosed with:
—> diffuse bronchiectasis ( immunodeficiency) : high-resolution CT scan of the chest—> focal bronchiectasis: bronchoscopy ( to exclude upstream obstructing lesion)
—> regular PFT is ordered to monitor lung function
Endocarditis
- lead to valvular dysfunction
- caused left-sided heart failure + with increased left atrial pressure (pulmonary capillary wedge pressure) + bibasilar crackles
Pulmonary HTN
- gradual SOB + Hypoxemia —> no fever
- massive left-to-right shunt —> right-sided volume over load
Miliary TB complication is Primary adrenal insufficiency
(TB adrenalitis = infectious adrenalitis)
Primary adrenal insufficiency (addison disease):
- destruction of all 3 layers of adrenal cortex
- low aldosterone —> lightheadedness + orthostasis —> renal sodium wasting (weight loss, hypovolemia) + hyponatremia + hyperkalemia
- low cortisol —> hypotension + hypoglycemia + peripheral eosinophilia
- low androgen —> decrease libido
- Miliary TB:
1. Patchy airspace disease ( daily cough) + upper lobe + hiliar Lymphadenopathy
Typical vs atypical pneumonia
Typical pneumonia: (lobar)
- strep pneumonia, H. Influenza, Moraxella
- treatment:
1. Inpatient: mostly fluoroquinolone
2. Outpatient: amoxicillin
Atypical pneumonia: (interstitial)
- chlamydia, legionella, myoplasma
- treatment:
1. Inpatient: mostly fluoroquinolone
2. Outpatient: azithromycin
Hospital acquired:
- pseudomonas, e.coli, staph aureus
- Treatment:
1. Pipercillin-tazobactem
2. Cefepim
Aspiration pneumonia:
- treatment: clindamycin
Community acquired pneumonia (inpatient)
- beta lactam + macrolide
—> ceftriaxone + azythromycin
Or
- fluoroquinolone (moxifloxacin)
—> should be avoided in elderly people due to risk of C. Difficile, tendon rupture, or aortic dissection
Invasive aspergillosis
- affect immunocompromised patient (neutropenia, HIV, recent transplant)
- triads: fever + pleuritic chest pain + hemoptysis
- x-ray: pulmonary nodule/mass surrounded by ground-glass opacity (indicates alveolar hemorrhage)
- treatment: azole (variconazole) + echinocandin (caspofungin)
CHF- exacerbation with pneumonia
Vs.
CHF-exacerbation with pulmonary edema
- treatment:
1. Ceftriaxone + azithromycin + furosemide
If,
1. Pulmonary infiltration rapidly resolves—> CHF-exacerbation with pulmonary edema
- Pulmonary infiltration resolves in weeks to months—> CHF- exacerbation with pneumonia
Note:
1. Left-sided heart failure lead to bilateral pulmonary infiltrates —> administration of diuretics improves pulmonary edema (pulmonary infiltrates, dyspnea, hypoxemia)
2. Heart failure is precipitated by URI & exacerbated by NSAIDS (increase sodium retention in the kidney)
Transudative vs. exudative pleural effusion
Massive pulmonary embolism
- patient with massive pulmonary embolism usually present with:
- Low arterial perfusion ( hypotension, syncope) + acute dyspnea + pleuritic chest pain + tachycardia
- The thrombus increases pulmonary vascular resistance & right ventricular pressure
- Causing right ventricular hypokinesis & dilation & hypotension
Multifocal atrial tachycardia
Signs:
1. More than 3 different P-WAVE morphologies
2. Rate > 100
3. Irregular rhythm
- precipitated by Acute respiratory illness in patient with underlying lung disease ( acute COPD exacerbation in COPD patient)
- treatment: monitor rate while correcting COPD exacerbation
Pulmonary embolism
- sudden dyspnea + chest pain + tachycardia + no consolidation on x-ray
- PE lead to pleural effusion ( exudative, small, bloody)
Pulmonary embolism
- present initially as syncope & shock
- right heart catheterization shows:
1. High right atrial pressure
2. High pulmonary artery pressure
3. Normal PCWP
Sickle cell disease
- associated with:
1. Asthma (obstructive lung disease)
2. Pulmonary HTN:- chronic intravascular hemolysis + pulmonary
vascular remodeling - excertional dyspnea + signs of right sided heart
failure ( hepatomegaly + edema)- Pulmonary fibrosis ( restrictive lung disease)
- chronic intravascular hemolysis + pulmonary
Left-sided heart failure
- Cardiomegaly:
- displace point of maximum impulse (PMI)
- S3 sound - Pulmonary edema
- dyspnea
- orthopnea
- PND
- Crackles
Pulmonary (edema, embolism, HTN)
- Pulmonary edema
- Dyspnea
-orthopnea
-Paroxysmal nocturnal dyspnea
- crackles - Pulmonary Embolism
- sudden dyspnea
- pleuritic chest pain
- tachycardia (tachypnea, hypoxemia, fever JVD)
- hypotension, syncope, shock - Pulmonary HTN
- excertional dyspnea
- signs of right-sided heart failure ( hepatomegaly, edema)
Normal pleural fluid pH is 7.60
Trasudative pleural effusion:
- due to decrease oncotic pressure or increase hydrostatic pressure
- hypoalbuminemia ( cirrhosis, nephrotic syndrome)
- congestive heart failure
- pleural fluid pH is 7.4-7.55
Exudative pleural effusion:
- due to increase capillary permeability
- due to PE, malignancy, TB, fungus, pneumonia, empyema
- pH of 7.30-7.45
Obstructive shock (pre-pulmonary)
- pulmonary embolism, pneumothorax
- high CVP (vena cava)
- low PCWP. ( pulmonary artery/vein)
- low CO (aorta)
- high SVR (arterioles)
Obstructive shock (post-pulmonary)
- aortic dissection, severe aortic stenosis
- high CVP
- high PCWP
- low CO
- high SVR
Hypovolemic shock
- decrease blood volume ( dehydration, vomiting, diarrhea, diuretics)
- low CVP
- low PCWP
- low CO
- high SVR
Septic shock (distributive)
- peripheral vasodilation
- low CVP
- low PCWP
- high CO
- low SVR
NOTE:
- opposite to obstructive shock (post-pulmonary)
Cardiogenic shock
- left ventricular failure
- high CVP
- high PCWP
- looow CO
- high SVR
NOTE:
- similar to obstructive shock (post-pulmonary)
Granulomatosis with polyangiitis (GPA)
( Wegener granulomatosis)
- small/ medium vessel vasculitis —> upper and lower respiratory tract and glomerulonephritis most commonly affected
- recurrent sinusitis & otitis + bloody nasal discharge + auditory canal ulceration + fatigue + anemia + microscopic hematuria
- diagnosis: positive p-ANCA & c-ANCA & tissue biopsy
NOTE:
- HIV can increase the chances of false-positive ANCA —> thus, HIV should be ruled out
Treatment:
- high-dose corticosteroid
Symptoms of respiratory tract involvement
Upper respiratory tract:
- sinusitis + otitis + auditory canal ulceration + bloody nasal discharge
Lower respiratory tract:
- dyspnea + cough + hemoptysis
Acute chest syndrome ( vasoocclusion of pulmonary vasculature)
(seen with sickle cell disease)
Symptoms:
- Acute vasoocclusion pain
A) fat emboli ( from bone marrow necrosis, lead to thrombocytopenia) —> pulmonary infarction/inflammation
B) atelectasis ( from splinting/pain/opioid therapy) —> regional alveolar hypoxia
- A&B —> increase RBC sickling & vasoocclusion in pulmonary vasculature —> acute chest syndrome
- Pulmonary infection (chlamydia, mycoplasma, strep pneumonia; lead to leukocytosis) & asthma exacerbation
- regional alveolar hypoxia —> increase RBC sickling & vasoocclusion in pulmonary vasculature —> acute chest syndrome
Signs:
- life-threatening
- present with a new pulmonary density ( new multifocal, bilateral opacities)
- fever
- respiratory symptoms ( hypoxia & chest pain)
Acute respiratory (lung) failure due to transfusion
- Transfusion- related acute lung injury ( TRALI)
(occurs within min-hrs after transfusion)
- Acute dyspnea
- diffused, bilateral infiltrate on x-ray
- crackles/rales on auscultation
- absent of JVD
- normal EF & BNP
- Transfusion-associated circulatory overload (TACO)
- acute dyspnea
- diffused, bilateral infiltrate on x-ray
- crackles/rales ± S3
- JVD present
- decrease EF
- increase BNP
Anti-GBM disease ( anti-glomerular basement membrane disease) ( GoodPasture syndrome)
Symptoms:
1. Pulmonary: dyspnea + cough + hemoptysis
2. Renal : hematuria
Caused by:
- autoantibodies against alpha- 3 chain of collagen 4 ( expressed on alveolar & glomerulus basement membrane)
Diagnosis:
- Biopsy shows: Linear IgG deposit along the glomerular basement membrane
Scenario (diabetes with pyelonephritis develop septic shock)
- diabetic patient with pyelonephritis ( fever, dysuria, flank pain) —> develops septic (distributive) shock —> lead to peripheral vasodilation & further hypotension
- management: IV- norepinephrine (vasopressor) to increase systemic vascular resistance (increase SVR = vasoconstriction) —> increase MAP to provide circulation to brain & thus reduce perfusion to peripheral tissue ( digits) —> lead to bilateral digit (finger) ischemia & tissue necrosis (dry gangrene)
Acute respiratory distress syndrome (ARDS)
( involves acute pulmonary edema + diagnosed with hypoxemia & bilateral alveolar infiltrates + not explained by cardiac dysfunction —> pulmonary edema lead to decrease lung compliance, decrease gas exchange, & pulmonary HTN )
- ARDS develops in the setting of acute lung injury:
1. Direct: aspiration, pneumonia,
2. Indirect: pancreatitis, trauma, sepsis - the lung releases inflammatory cytokines & neutrophils in the alveolar space —> leading to leakage of fibrinous proteinaceous fluid in the airspace & alveolar collapse due to loss of surfactant
- pulmonary edema changes result in:
- Impaired gas exchange —> hypoxemia due to V/Q mismatch due to intrapulmonary shunt
- Decrease lung compliance —> due to loss of surfactant & increase weight of edematous lung
- Increase pulmonary arterial pressure (pulmonary HTN) —> due to hypoxic vasoconstriction & destruction of lung parenchyma. Treatment with mechanical ventilation or NIPP lead to further increase in pulmonary arterial pressure
Symptoms:
1. severe hypoxemia + Respiratory distress + diffuse crackles + bilateral alveolar infiltrate within 1 week of clinical insult
2. PaO2 decrease & require higher FiO2 to maintain oxygenation —> as a result PaO2/FiO2 ratio is decreased < 300
3. Lower ratio of (PaO2/FiO2) indicates more severe ARDS
Mechanical ventilation in respiratory alkalosis patient ( hyperventilation)
- ventilation is the product of tidal volume & respiratory rate
- if patient is administered appropriate tidal volume of (6 mL/kg) & ABG shows that pH is high & PCO2 is low —> this is respiratory alkalosis secondary to hyperventilation—> than, next step is to adjust respiratory rate
Amyotrophic lateral sclerosis (ALS) & hypoventilation
- causes diaphragmatic weakness with resultant hypoventilation ( respiratory insufficiency)
—> Arterial blood gas (ABG) analysis should be performed to assess for hypercapnia —> suggested by elevated serum bicarbonate level
Patients with ARDS & mechanical ventilation
( lower FiO2 & compensatory increase PEEP, if PO2 on ABG is > 90)
- mechanical ventilation improves oxygenation by:
- Increasing FiO2
- Increasing positive end-expiratory pressure (PEEP)
- to prevent alveolar collapse
Goal:
1. Maintain PO2 at 60-90 mmHg (corresponds to oxygen saturation of 92%-96%)
- immediately after intubation —> high FiO2 ( > 60%) is administered —> can later be adjusted after ABG results
- PaO2 is mainly affected by FiO2 & PEEP
EXAMPLES:
1. ABG analysis shows ( PaO2 > 90 = excessive oxygenation) & respiratory acidosis ( low pH & high PCO2)
2. If, the high FIO2 is continuously administered —> this will lead to oxygen toxicity & lung injury & worsen the atelectasis
3. Therefore,
- decrease FiO2 (< 60%) is required to prevent toxicity
&
- compensatory increase PEEP is required to maintain adequate oxygenation by recruiting collapsed alveolar & keeping them open
Pneumothorax development in COPD
Pneumothorax symptoms:
- sudden onset pleuritic chest pain + dyspnea + tachycardia + tachypnea + Hypoxemia + decrease or absent breath sounds
- the collapsed lung ( air within the pleural cavity)—> receives stable volume of air from ventilator —> this results in:
- increase peak pressure ( measure of the increased resistance to air flow from the ventilator)
- Increase plateau pressure ( measure of the lung’s decrease ability to expand/compliance)
- management of pneumothorax involves chest tube to allow reexpantion of the lung
Orthostatic hypotension (due to hypovolemia in elderly patient)
Diagnosis:
1. SBP decreases > 20 mmHg
2. DBP decreases > 10 mmHg
Example:
- supine position is 120/80
- standing within 2-5 min lead to: 100/70
Can be caused by:
- hypovolemia —> which leads decrease renal perfusion & activation of renin-angiotensin- aldosterone system —> stimulates Na & water reabsorption —> thus, decrease Na in urine
ARDS & low tidal Volume ventilation (LTVV)
- Low-tidal volume ( almost 4-6 ml/kg) is delivered to the remaining non-collapsed alveolar (only open alveolar)
- prevents overdistension of these alveolar
- LTVV improves mortality in ARDS patient
Effect of alcohol, BDZ, opioid on respiration
( lead to respiratory acidosis —> adjust mechanical ventilation with increase RR or Tv)
- alcohol, BDZ, opioid lead to respiratory depression & hypoventilation & acute hypercapnia respiratory failure
- Arterial Blood Gas will shows respiratory acidosis ( low pH & high PaCO2)
- correction of the hypercapnia requires increase respiratory rate or tidal volume
Criteria for extubation readiness
( wean off the patient from mechanical ventilation)
Criteria:
- PH > 7.25
- Adequate oxygenation (PaO2 > 60 mmHg) on minimal ventilator support ( FiO2 < 40% & PEEP < 5 cm H2O)
- Intact inspiratory effort & sufficient mental alertness to protect airway
Next step:
1. Patient should go undergo spontaneous breathing trial to help confirm candidacy for successful extubation
Complication of positive pressure ventilation
- Alveolar damage
- Penumothorax
- Hypotension
Anaphylaxis ( laryngeal edema + urticarial rash)
Symptoms:
- acute onset of respiratory distress + hypo-dynamic instability + urticarial rash
Risk factors:
- asthma
- NSAID can worsen anaphylaxis —> non-immunologic mast cell activation
Treatment:
1. IM Epinephrine
2. Anti-histamine or glucocorticoids
Criteria for lung cancer screening
- Method: low-dose CT scan of chest
- annually
- Age: 50-80 years old
- Eligibility: > 20 packs per year or currently smoking or quit smoking within 15 years ago
- No need for test if ( patient quit smoking > 15 years or patient have other conditions that limits life expectancy)
Smoking cessation before surgery
Smoking cessation within 4-8 weeks before surgery to prevent post-operation complication (pneumonia, respiratory distress requiring mechanical ventilation)
Hyponatremia
Lung cancer ( long-standing cough, hemoptysis, dyspnea, large/irregular pulmonary nodule)
Adenocarcinoma
- peripheral located
- clubbing + hypertrophic osteoarthropathy
- non-smoker, women
Squamous cell carcinoma
- centrally located
- hypercalcemia + necrosis & cavitation
- smoker + hemoptysis + hypercalcemia + hilar mass
Small-cell carcinoma
- centrally located
- Cushing syndrome, SIADH, Lambert-Eaton syndrome
Large-cell carcinoma
- peripherally located
- gynecomastia, galactorrhea
Obstructive sleep apnea
- obesity + chocking during night + snoring + excessive daytime sleepiness + morning headache + impotence + poor judgement + depression
- caused by transient upper airway obstruction + nocturnal hypoventilation
Untreated OSA lead to:
1. HTN
2. Pulmonary HTN ( can lead to tricuspid regurgitation = holosystolic murmur on the left lower sternal border)
3. Right-sided heart failure
Alpha-1 antitrypsin (AAT) deficiency
( presents like other obstructive lung disease = COPD…)
Result in:
1. Emphysema
2. Destruction of lower lung lobe
3. Presents in the 30th (smoker) & in the 40th (non-smoker)
4. Chronic dyspnea, productive cough, destruction of lower lung lobe
5. Associated with liver disease —> result in neonatal hepatitis, cirrhosis, hepatocellular carcinoma
Think of alpha 1 antitrypsin deficiency when:
- COPD in young age (< 45 years)
- COPD with no history of smoking
- Basilar-predominant COPD
- History of unexplained liver disease
Diagnosis:
- measure serum AAT level
- PFT testing
Treatment:
- IV supplementation with pooled human AAT
Patient with cured Hodgkin lymphoma
-Have 30% increased risk for secondary malignancy
- secondary malignancy ( lung, breast GI, acute leukemia, non-HL) can arise after 10 years after initial treatment for HL with chemotherapy & radiation
Hilar mass region refers to centrally located mass
Seen with:
- Squamous cell carcinoma ( hilar mass + hemoptysis + hypercalcemia + smoking)
- Small lung cancer ( associated with cushing, SIADH, Lambert-Eaton disorder)
Asbestos exposure ( pleural plaques on x-ray) and smoking have (synergistic effect)
Increase risk for :
- Bronchogenic carcinoma ( most common)
- Mesothelioma ( rare)
Investigation of solitary lung nodule/mass
Start with:
- Compare current chest x-ray with previous X-ray —> if stable lesion for 2-3 years —> no further testing
- If no previous x-ray available or growth has been seen —> order chest CT scan —>
- Benign feature —> serial CT scan
- Indeterminate or suspicious for malignancy —> further investigation with biopsy or PET
- Highly suspicious for malignancy. —> surgical excision
Pneumothorax ( thoracocentesis or diuretics )
Undiagnostic pleural effusion is best evaluated with thoracocentesis, EXCEPT in patient with clear-cut evidence of congestive heart failure
Obstructive sleep apnea is associated with motor vehicle collision
- diagnosis with: nocturnal polysomnography
Superior pulmonary sulcus tumor (SPST) (pancoast tumor)
Symptoms:
1. Shoulder pain
2. Ipsilateral Horner syndrome ( ptosis, miosis, anhidrosis)
3. Neurologic symptoms of the arm (weakness)
4. Supraclavicular LAD
5. Weight loss
Tumor location:
- in the right or left superior sulcus ( pulmonary apex)
Caused by:
- adenocarcinoma or squamous cell carcinoma of the lung
- smoking
Diagnosis:
-MRI
