Respiratory disease Flashcards
Dx. for dyspnea
diff. breathing due to stimulation of J receptors, decrease full inspiration
Dx: low compliance (interstitial fibrosis)
increased airway resistance (chronic bronchitis, asthma)
chest bellows disease (obesity, kyphoscoliosis)
interstitial inflammation (LHF)
Dx. respiratory acidosis
-decreased PO2 Dx: -pulmonary problems (COPD) -depressed resp. center -epiglotitis blocking trachea -bronchitis -paralyzed muscles of respiration - GB, ALS
Dx. cough
acute vs. chronic?
Dx. postnasal discharge
Nocturnal cough - GERD due to acid reflux to tracheobronchial tree at night, bronchial asthma
Productive cough - chronic bronchitis (smoking), bacterial pneumonia, bronchiestasis
Drugs causing cough - ACE inhibitors, inhibit degradation of bradykinin, causes mucosal swelling and irritation, Aspirin - causes increase in LT-C-D-E4 (broncho-constrictors)
Dx. hemotypsis
coughing up blood tinged sputum
-parenchymal necrosis
-bronchial and pulmonary vessel damage
Dx: chronic bronchitis, pneumonia, bronchogenic carcinoma, TB, bronchiectasis, aspergilloma
Tachypnea
rapid, shallow breathing (> 20 bpm)
Dx: restrictive lung disease, pleuritic chest pain, PE with infarction
Tracheal shift on palpation
pressure in contra. lung, large tension pneumothorax, large pleural effusion
decreased volume in ipsilateral lung - large, spontaneous pneumothorax, resorption atelectasis
Vocal tactile fremitus on palpation
palpable thrill (vibration) transmitted thru CW when patient says “E” or ‘1, 2, 3”
decreased in emphysema, asthma
absent vocal tactile fremitus with atelectasis, fluid, air (pneumothorax) in pleural space
increased as sound travels through consolidations - lobar pneumonia
Percussion: dull? hyperresonant?
Dull - pleural effusion, consolidation, atelectasis
Hyperresonant: percussion with pneumothorax, asthma, emphysema
Inflammation of small airways?
caused by asthma, chronic bronchitis
air trapping –> wheezing –> increased airway resistance
Crackles?
Crackles: usually inspiratory
Early and mid inspiratory crackles: secretions in proximal large to medium-sized airways (CB) clear with coughing
Late inspiratory crackles: reopening of distal airways partially occluded by increased interstitial pressure (e.g., interstitial fluid—pus, transudate in CHF); do not clear with coughing; vary from fine to coarse
Causes: pulmonary edema; lobar pneumonia; interstitial fibrosis (e.g., sarcoidosis)
Wheezing?
high-pitched musical sound usually heard in expiration
Causes: inflammation of segmental bronchi, small airways (e.g., asthma, chronic bronchitis); pulmonary edema constricting airway (called cardiac asthma); pulmonary infarction (release of TXA2 from platelets in embolus causes bronchoconstriction)
Rhonchi?
low-pitched snoring sound heard during inspiration or expiration; due to secretions in large airways (bronchus, trachea); usually clear with coughing; common in chronic bronchitis
Inspiratory stridor
Inspiratory stridor: high-pitched inspiratory sound; sign of upper airway obstruction
Causes: epiglottitis (H. influenzae); croup (parainfluenza virus)
Fixed sound on inspi. and exp. - cancer
Pleural friction rub?
Pleural friction rub: two inflamed surfaces (pleural and parietal) rubbing against each other
Timing: end of inspiration and early part of expiration
Disappears: large effusion is present, holding breath
Causes: pleuritis due to cancer, infarction, pneumonia, serositis (SLE)
Grunting in newborns
Grunting in newborns: always abnormal after 24 hours; common finding in RDS - massive pulmonary shunting (perfusion, no ventilation, lungs collapsed due to lack of enough surfactant)
Transmitted voice sounds
Bronchophony (sound of bronchi)
Alveolar consolidation: syllables/numbers heard louder and more distinctly
Whispered pectoriloquy: clear and intelligible words (e.g., patient whispering “1, 2, 3”)
Egophony: patient saying “E” sounds like “A”
Chronic bronchitis?
CB: daily cough with sputum for at least 3 months per year for 2 consecutive years
- mucous gland hyperplasia, mucus over secretion
- found in smokers mostly
- inflammation and mucous can clog airways - increase resistance - obstructive disease
Emphysema: two types? effects on lungs? risk factors?
Emphysema - destructive lung disease - degradation of pulmonary alveolar with over-distention of terminal bronchioles and alveolar spaces
- confirmed by lung biopsy or CT
- Centriacinar - involves the central and proximal parts of the bronchi, spares distal alveoli, seen in smokers
- panaacinar - involves all the respiratory bronchioles, uniformly enlarged - alpha-1-antitrypsin deficiency
What is COPD?
COPD -used to describe both chronic bronchitis and emphysema
Features: chronic airflow limitations, progressive with an enhanced inflammatory response. Exacerbations are common, contribute to severity
FEV1/FVC in COPD?
Clinical definition: presence of airflow obstruction where FEV1/FVC
What happens when you stop smoking?
- mucous membranes involute within weeks
- cough and sputum production resolves
- airway narrowing, peribronciolar fibrosis, and loss of elastic recoil , destruction of lung parenchyma - irreversible
What causes hypercapnia? (increased PaCO2)
Almost always alveolar hypoventilation
PaCO2 = VCO2/VA, decrease VA increase PaCO2
What is cor pulmonale?
Cor Pulmonale - right heart failure due to pulmonary HTN
Why do we have PA HTN in COPD?
-widespread hypoxic vasoconstriction can increase pulmonary resistance
Persistent PA HTN over supplemental O2?
-destruction of PA vascular bed in emphysema, remaining vessels work very hard
-vessels remodel due to chronic hypoxia - proliferation and hypertrophy which narrow lumen and causes PA resistance
-Polycythemia in chronic hypoxia can occur and cause PA HTN by increasing blood viscosity and increasing resistance
Describe histology of four lung cancers
NSCLC:
Adenocarcinoma: resemble normal glandular tissue with cells arrayed around a central lumen, and with abundant cytoplasm full of mucin ready for secretion
Squamous cell carcinoma: resemble the squamous epithelium of skin, with a keratinizing layer in well-differentiated tumors
Large cell carcinoma: lack these differentiation features on routine light microscopy and appear as a collection of pleomorphic, crowded tumors cells without apparent structure
SCLC
Small cell carcinoma: recognized as a dense collection of hyperchromatic tumor cells which are indeed smaller than all three of the non-small cell subtypes
