Pulmonary Medicine Flashcards
Define dyspnea
- subjective experience of shortness of breath
- common from pulmonary and cardiac disease
Define tachypnea
- increased rate of breathing
>20 breaths/min
Define hyperpnea
- deep and rapid breathing
Define hyperventilation
- increased alveolar ventilation, leading to an alveolar CO2 level below normal
Where is respiratory control centre?
Medulla
What inputs into respiratory control centre?
- cortical (voluntary) control
- mechanical/stretch receptors in chest wall and diaphragm
- PCO2/pH chemoreceptors in medulla
- PCO2, PO2, pH receptors in carotid body and aortic arch
What mechanism leads to sensation of dyspnea?
- mechanical receptors in chest wall that feed back to respiratory motor neurons
- lung stretch receptors
- irritant receptors in bronchial mucosa activated by stimulation of bronchial mucosa and increased muscle tone and flow
- central and peripheral chemoreceptors (even in absence of activation of respiratory muscles)
What is Homan sign?
- pain with foot dorsiflexion -> DVT
What does brain natriuretic peptide differentiate?
heart failure vs. lung disease
- BNP released by myocytes being stretched
- cleaved into pro-BNP then to biologically active form and inactive amino terminal fragment NT-pro-BNP
-> used to guide CHF therapy
BNP <100 pg/mL or NT-pro-BNP <400 pg/mL: CHF unlikely
BNP >400 pg/mL or NT-pro-BNP >2000 pg/mL: CHF likely
What do you exclude by checking Hct in patient with dyspnea?
Anemia
Normal ABG values (sea-level)?
- pH 7.4 (7.36 - 7.44)
- PCO2: 40 (37 - 42)
- HCO3: 24 (22 - 26)
- PO2: 80-100 mmHg
Direction of change with respiratory pH change re: pH and PCO2?
Opposite directions
Appropriate compensation for acute resp acidosis
HCO3 increase by 10
PCO2 increase by 1
Appropriate compensation for chronic resp acidosis
HCO3 increase by 10
PCO2 increase by 3
Appropriate compensation for acute resp alkalosis
HCO3 decrease by 10
PCO2 decrease by 2
Appropriate compensation for chronic resp alkalosis
HCO3 decrease by 10
PCO2 decrease by 4
What is next step with metabolic acidosis?
Anion gap
Calculate anion gap? Normal range?
Na - Cl + HCO3
= 14 +/- 2
What is delta gap?
- change in anion gap minus change in HOC3
>+6 = another metabolic process (e.g. metabolic alkalosis)
What does + C-ANCA in patient with dyspnea suggest?
- granulomatosis with polyangitis (Wegener’s)
What investigation is suggestive of FB?
- insp and exp X-ray views to look for gas trapping
Resp acidosis or alkalosis causes?
- CNS depression
- Neuromuscular disorders
- Upper and lower airway abnormalities
- Lung parenchyma abnormalities
- Thoracic cage abnormalities
Resp acidosis
Resp acidosis or alkalosis causes?
- hypoxia: pneumonia, pulmonary deem, restrictive lung disease
- primary hyperventilation: CNS disorder, drugs (salicylate), sepsis, hepatic failure
Resp alkalosis
Treatment AECOPD?
- oral/ IV steroids x5d
- abx (increased sputum, purulence, volume): amoxicillin, doxycycline, septra, or 2/3rd gen cephalosporin
- > likely pathogens H. flu, M. catarrhalis, S. pneumonia
- second line abx: b-lactam, resp fluoroquinolone
Organisms for CAP?
- S. pneumonia, H. flu, atypicals (C. pneumonia, M. pneumonia, L. pneumophilia)
Treatment CAP?
uncomplicated outpt- extended spectrum macrolide or doxycycline
complicated outpt: resp fluoroquinolone (levofloxacin), second line amoxil-clav or 2nd get cephalosporin and macrolide
hospitalized based on pneumonia severity index score
hospital-acquired pneumonia >48h often resistant organisms or gram-negative bacteria - need broad-spectrum abx
ARDS (acute lung injuries) 4 criteria
- acute onset (within 1 wk clinical insult)
- bilateral patchy airspace disease
- PCWP <18 mmHg or no clinical evidence of increased LVEDP
- PO2/FiO2 <300 mmHg (<300 mild, 100-200 moderate, <100 severe)
ARDS dx
- bilateral pulmonary infiltrates
- resp distress
- hypoxemia
ARDS etiologies
- aspiration/ toxin inhalants
- sepsis
- shock
- trauma
- DIC
- pancreatitis
- embolism
- drugs
- head trauma
ASA toxicity
- metabolic acidosis and resp alkalosis
- mild: n/v, abdominal pain, tinntus
- more serious: hyperthermia, tachypnea, resp alkalosis, metabolic acidosis, hypoglycaemia, hypokalmeia, seizure, coma, death
- > decontamination of gut with charcoal
- > alkalinize urine and dialysis if severe
What has pauci-immune necrotizing and crescentic glomerulonephritis and pulmonary capillaritis?
Granulomatosis and polyangiitis (Wegners) and microscopic polyangiitis
-> high dose steroids and pulsed cyclophosphamide to induce remission then slow taper
What is chronic dyspnea?
dyspnea >1mo
2/3 cardiopulmonary
Ddx chronic dyspnea
- COPD
- asthma
- CHF/ coronary artery/ CIRCU
- obesity
- psychogenic
- interstitial lung disease
COPD in nonsmoker or pt presenting early condition to r/o?
alpha-1-antitrypsin deficiency
Spirometry dx of COPD?
FEV1/FVC <0.7
What does cardiopulmonary exercise testing differentiate?
- cardiac and pulmonary pathology
FVC severity COPD?
FEV1/FVC >70% = at risk FEV1 >80% predicted =mild FEV1 50-80% predicted = moderate FEV1 30-49% predicted = severe FEV1 <30% predicted = very severe
Steps to manage COPD
- education, modulate RF, etc \+ SABD \+ LABD \+/- pulmonary rehav \+ inhaled steroid to LABD \+ long-term supplemental O2, surgery, end-of-life care
Nodular pattern of ILD on CXR ddx
- fungal disease
- metastatic/ lymphangitis carcinomatosis
- silicosis
- sarcoidosis
- histiocytosis X
Dx IPF
- progressive dyspnea
- bibasilar inspiratory crackles
- restrictive pattern on PFT and impaired gas exchange
- bilateral peripheral reticular opacities and sub pleural honeycombing with basal predominance on high resolution CT
- r/o other causes
What is bronchiectasis
- permanent dilation of airways due to repeat cycles of infection and inflammation
etiology
- postinfectious
- idiopathic
- genetic dz
- aspiration//GERD
- immune deficiency
- rheumatoid arthritis
- ulcerative colitis
- ABPA (allergic bronchopulmonary aspergillosis)
What is stridor?
- high-pitched sound caused by oscillation of narrowed airway, signifying significant obstruction of large airways -> always prompts urgent airway evaluation
What does wheezing indicate?
- obstructing airway = pathology
- requires sufficient airflow
PFT pattern with obstructive
- FVC normal or reduced
- FEV1/FVC reduced <70%
- TLC increased or normal (increased = hyperinflation)
- RV increased or normal (increased = gas trapping)
- DLCO normal or reduced in mod-severe emphysema
PFT pattern with restrictive lung
- FVC reduced
- FEV1/FVC normal
- TLC reduced <80%
- RV reduced
- DLCO reduced
PFT pattern with restrictive chest wall
- FVC reduced
- FEV1/ FVC normal
- TLC reduced <80%
- RV reduced
- DLCO normal
PFT pattern with pulmonary vascular dz
- FVC normal
- FEV1/FVC normal
- TLC reduced <80%
- RV reduced
- DLCO normal
Do flow volume curves indicate obstruction?
- yes they give clues to the presence and location of obstruction (upper vs. lower airways) or presence of restriction
3 anatomic areas for obstruction
- extra thoracic upper airways (nose to extrathroacic trachea)
- intrathoracic upper airways (intrathroacic trachea)
- lower airways (intrathoracic airways below carina)
Monophasic vs. polyphonic wheeze signifies what?
- monophonic: large airway obstruction
- polyphonic: small airway obstruction
What type of stridor is extrathroacic obstruction?
Inspiratory stridor
What type of stridor is intrathroacic obstruction?
Expiratory stridor
Initial wheeze investigations
- CBC (re: WBC)
- ABG (re: hyperpnea, hypoxemia)
- CXR (re: consolidation, pleural effusion, pneumothorax, heart failure)
- EKG (re: ACS)
Management acute wheeze/ asthma
- O2
- short acting b-agonist
- prednisone
- ipratropium
- magnesium (very severe re: bronchodilates)
- epinephrine/ anesthetic gases in ICU
Define cyanosis
- physical sign of bluish coloration of skin due to >50 g/L deO2 hemoglobin in blood vessels near skin surface
- O2 saturation of arterial blood falls <85%
What is abnormal deficiency in the concentration of O2 in arterial blood which can be reversed with supplemental O2?
Hypoxemia
What is the term when the total body is deprived of O2?
Hypoxia
Central vs peripheral cyanosis
Central
- circulatory or ventilatory problem -> poorer blood oxygenation in lungs or greater O2 extraction due to slowing down of blood circulation in skin bv
- hypoventilation: normal A-a gradient, elevated PCO2
- high A-a gradient: shunt, V/Q mismatch
Peripheral
- blood reaching extremities not O2 rich = skin appears blue
- can be due to central causes or other etiologies
If A-a gradient increased but supplemental O2 doesn’t correct hypoxemia what does that indicate?
R-L shunt
What is the A-a gradient?
Alveolar-Arterial gradient = PAO2 - PaO2
- normal <10mmHg (5-20 normal range)
- increased = diffusion defect, V/Q defect or right to left shunt
Common causes of cough?
- PND
- asthma
- GERD
- drugs (ACEi)
Where are cough receptors (mechanical and chemical)?
- resp epithelium
- pericardium
- esophagus
- diaphragm
- stomach
-> stimulate via afferent nerves the medullary cough centre that activates exp muscles through efferent nerves
Do patients die of asphyxiation or exsanguination with massive hemoptysis?
Asphyxiation
Define massive hemoptysis
- expectoration >100-600 mL blood over 24h period
+ features hemodynamic instability, altered gas exchange, or resp difficulties
What is most common site of hemoptysis?
- bronchial arteries due to higher pressures (vs. pulmonary arteries)
What do bronchial arteries supply?
- airways
- hilarious LN
- visceral pleura
- some of mediastinum
Can blood from respiratory source present as coffee ground emesis?
Yes if swallowed
Anatomic classification of lower resp tract (LRT) disorders
- large airways (obstructive lung dz)
- small airways
- interstitium
- vascular
- extra pulmonary
Diagnosis of: - nocturnal wheeze, cough or dyspnea - chest tightness - waxing and waning sx - nocturnal sx - seasonal variation - sx exacerbated by cold, exercise, dust \+/- nasal polyps CXR often normal
Asthma
Diagnosis of: - dyspnea (hallmark), esp on exertion - chronic cough, sputum production - hx smoking - frequent resp infection o/e - prolonged expiration on forced exhalation (>6sec), reduced breath sounds, increased AP diameter, paradoxical breathing if severe - pulmonary HTN if severe CXR - increased AP diameter, hyperinflation, bullae
COPD
Diagnosis of: - chronic resp infection - chronic cough - purulent sputum production - fever - weakness - wt loss - hemoptysis - dyspnea (less frequently) \+/- nasal polyps or sinusitis crackles on auscultation CXR - normal; dilated bronchi, tram tracks
Bronchiectasis
Diagnosis of: - orthopnea - nocturnal wheeze, cough, dyspnea - leg swelling - dyspnea on exertion - fatigue o/e - bibasilar crackles, elevated JVP, valvular disease, leg swelling CXR - vascular redistribution to apical area, fluid in fissures, fluffy opacities, pleural effusions, Kerly B lines, peribronchial cuffing
CHF
Diagnosis of:
- progressive dyspnea on exertion then at rest
- hypoxia (later stages)
- dry cough
- occupation/ drug exposure
- autoimmune history
o/e - clubbing, fine crackles, rheumatologist dz, pulmonary HTN
CXR variable - may have nodules or reticulations
Interstitial lung
Diagnosis of: - history stroke/ seizure - neuromuscular dz - EtOH or drug abuse affecting LOC - use of sedating medications - elderly - GERD o/e - crackles, wheeze, fever CXR - range to pneumonia or ARDS
Aspiration
Diagnosis of:
- sudden dyspnea on exertion or rest
- leg swelling
- risk factors DVT
o/e - fever, tachypnea, tachycardia
- hypotension, elevated JVP, pulses if large
CXR - often normal- may have Hampton hump (infarction); Westermark sign (oligemia)
PE
Asthma paroxysmal or persistent symptoms?
- dyspnea
- wheeze
- chest tightness
- cough
- sputum production
What is associated with allergies, atopic dermatitis, seasonal allergic rhinitis, conjunctivitis
Asthma
How do you diagnose asthma?
Reversible airway obstruction (FEV1 gold standard)
- clinical history + spirometry
- peak expiratory flow variability
- metacholine challenge
- exercise challenge
Positive response to bronchodilators in diagnosis of asthma?
> 12% and 200mL increase in FEV1 or FVC = positive response
Define properly controlled asthma
- daytime sx <4/wk
- night sx <1/wk
- capable of normal physical activity, no work/school absence
- mild/few exacerbations
- rescue puffer <4 dose/wk
- FEV1 >90% patient’s best
- PEF >90% patient’s best
- PEF diurnal variation <10-15%
- sputum eosinophils <2-3%
Treatment of asthma
education re: trigger avoidance
mild intermittent - short acting b-agonist
mild persistent - low dose inhaled corticosteroids plus short acting b-agonist for sx relief
moderate persistent - medium-dose inh corticosteroids or low-medium dose inh corticosteroid with long acting b-agonist plus short acting b-agonist (sx)
severe persistent - high-dose inh corticosteroid and long acting bronchodilator +/- anti-IgE tx (omalizumab) +/- leukotriene receptor antagonist +/- oral corticosteroid
Main cellular mechanisms involved in asthma?
Mast cells - early phase allergen; release histamine, tryptase, leukotriene, cytokines -> smooth muscle contraction
Eosinophils - late phase allergen; release major basic protein, eosinophilic cationic protein, leukotrienes -> airway narrowing and hyperactivity, mucous secretion -> airway remodelling
T cells - initiation and sustaining airway inflammation -> Th2 immune deviation (IL4, 13) -> increased IgE production by B lymphocytes
Treatment for mast cell mechanism in asthma?
- b2-agonist/ anticholinergic for smooth muscle relaxation
- anti-IgE Ab to prevent activation
Treatment for eosinophil mechanism in asthma?
- leukotriene receptor antagonists (mast cells and eosinophil action)
Treatment for T cell mechanism in asthma?
Corticosteroids to inhibit pro inflammatory cytokines
Types of lung cancer?
Small cell lung cancer (SCLC)
Non-small cell lung cancer (NSCLC)
- adenocarcinoma
- SCC
- large cell carcinoma
What does pancoast tumor involve?
- often in apical tumor
- involves brachial plexus -> shoulder pain
What is SVC syndrome?
- common in central tumors
- SVC compression -> dyspnea, venous distention in neck, swelling of face
Common lung mets sites?
- brian
- bone
- liver
- adrenal
- skin
Paraneoplastic syndromes with lung cancer?
- cushing (SCLC)
- hypercalcemia (SCC)
- SIADH (SCLC)
What is a pleural effusion?
- imbalance between formation and removal of pleural fluid
- pulmonary, pleural or extrapulmonary dz
Symptoms of pleural effusion?
- dyspnea most common
+/- cough, chest pain, orthopnea
Does pleural fluid have low or high protein? pH? Glucose?
- low protein (<2g/dL)
- pH and glucose similar to blood
How is pleural fluid formed?
- mainly from parietal pleura
- turnover re: vascular and interstitial exchange
Does parietal or visceral pleura have higher hydrostatic pressure? Flow of fluid in which direction?
- parietal = 30 mmHg
- visceral = 10 mmHg
fluid: parietal -> visceral pleura
What is exudative pleural effusion? Causes?
- inflammation in lung/ pleural or impaired lymphatic drainage, including movement of fluid from extrathoracic spaces
- local factors
Causes = DELII MICE - drugs (amiodarone, nitrofurantoin, cytotoxic)
- extrapulmonary
- lymphatic abnormalities
- infectious (empyema, parapneumonic, abscess, TB)
- inflammatory (pancreatitis, PE, sarcoidosis, radiation, radiation, ARDS, asbestos, ureic pleurisy)
- malignancy (carcinoma, lymphoma, mesothelioma, chylothroax)
- iatrogenic
- connective tissue dz
- endocrine
What is transudative pleural effusion? Causes?
- imbalance of hydrostatic and oncotic pressures in chest, including movement of fluid from extra thoracic spaces (peritoneal/ retroperitoneal)
- systemic factors
Causes
- CHF
- cirrhosis
- nephrotic syndrome
- peritoneal dialysis
- hypoalbuminemia
- constrictive pericarditis
- atelectasis
- SVC obstruction
- urinothorax
- Meig syndrome
Lights criteria for exudates
- pleural fluid protein divided by serum protein >0.5
- pleural fluid LDH divided by serum LDH >0.6
- pleural fluid LDH > 2/3 upper limes of normal serum LDH
any of these 3 criteria = pleural effusion exudative
Physical exam signs of pleural effusion
- reduced breath sounds
- dullness to percussion
- reduced tactile fremitus
- egophony
- pleural friction rub
Complications of thoracentesis
- pneumothorax
- reexpansion pulmonary edema
- hemothorax/ bleeding
- infectoin
- abdominal puncture
Common tests to order for pleural fluid analysis?
Pleural fluid
- LDH
- total protein
- glucose
- pH
- cell count
- differential
- cytology (gram stain)
Serum
- LDH
- total protein
- glucose
Define pneumothroax
- air in pleural space
Sx tension pneumothorax?
- rapid, laboured breathing
- cyanosis
- tachycardia
- hypotension
- tracheal shift away from side of pneumo
- absent breath sounds on ipsilateral side
- JVP distended
- pulses paradoxus
- abdominal distention
Sx spontaneous pneumothorax? Classification?
variable sx re: size
- dyspnea
- chest pain
primary - unknown cause
secondary - underlying etiology
Causes of secondary pneumothorax?
- airway dz - emphysema, COPD, CF, asthma
- infectious - pneumocystis jiroveci pneumonia, necrotizing pneumonia
- interstitial dz - IPF, pulmonary Langerhans cells histiocytosis, sarcoidosis, LAM
- CT disorder - Marfan, RA, ankylosing spondylosis, Ehlers-Danlos syndrome
- malignancy - lung CA, metastatic
- trauma/ iatrogenic
What is postthrombotic syndrome?
- chronic pain, swelling, ulceration of skin
- 1/3 pt with DVT
- latency up to 10yr
Are thrombi resulting in PE often from proximal or distal leg veins?
proximal leg veins
- can begin as calf vein thrombi and extend proximally
What do you want to rule out in patients with no obvious cause for DVT, recurrent idiopathic thrombosis or patients >60yr?
Malignancy
Ddx unilaterla/ local edema
- DVT
- lymphatic obstruction
- ruptured popliteal cyst
- cellulitis
- postphlebitic syndrome
- trauma
- thyroid dz
Classic triad for DVT?
- calf pain
- edema
- pain on dorsiflexion of food - Woman sign
Sx PE
- dyspnea
- pleuritic CP
- RR> 20
- cough
- hemoptysis
DVT risk factors?
- pregnancy
- malignancy
- hip surgery
- major knee surgery
- immobilization
- OCP
- nephrotic syndrome
- sepsis
- anticardiolipin Ab
- protein C and S and antithrombin deficiency
- previous VTE
Wells criteria (DVT)
Sx
- active cancer = 1
- paresis, paralysis, recent plaster cast = 1
- recently bedridden >3d or major surgery <4wk = 1
- localized tenderness over deep veins = 1
- entire leg swollen = 1
- calf swelling >3cm compared to other leg measured 10cm below tibial tuberosity = 1
- pitting edema = 1
- collateral superficial veins = 1
- alternative dx as likely or greater than DVT = -2
Wells pretest probability (DVT)
0 = low risk = 3% probability 1-2 = moderate risk = 17% probability >3 = high risk = 75% probability
Wells criteria (PE)
- clinical sx DVT = 3
- PE as likely as alternative dx = 3
- HR >100 bpm = 1.5
- immobilization or surgery <4wk = 1.5
- prior DVT or PE = 1.5
- hemoptysis = 1
- malignancy = 1
Wells pretest probability (PE)
0-2 pt = low risk = 3% probability
2-6 pt = intermediate risk = 20% probability
>6 pt = high risk = 60% probability
What anticoagulant works right away to manage DVT/PE?
Heparin - inhibits activated coagulation factors
unfractionated
- inhibits thrombin and factor Xa
- PTT monitoring
- difficult to maintain therapeutic range
LMWH
- inhibits factor Xa
- no monitoring
- more reliable dose relation
- not safe with renal failure
Slower anticoagulant for managing DVT/PE?
Coumadin
- inhibits synthesis of vitamin K-dependent coagulation factors
- follow INR with 2-3 target
-> overlap start with heparin x5d
Anticoagulant complications?
- bleeding
- thrombocytopenia (HIT) with heparin
- osteoporosis with long term use of LMWH
- drug interactions with warfarin
- teratogenicity with warfarin
Length of anticoagulant tx?
- time-limited factor: 3mo
- idiopathic - 6 mo
- ongoing RF or second event - life
Thromboprophylaxis guidelines
Low risk - early ambulation
Moderate risk - low dose unfractionated heparin q12
- LMWH (dalteparin or enoxaparin)
- pneumatic compression stockings
High risk - low dose unfractionated heparin q8
- LMWH (dalteparin or enoxaparin)
- pneumatic stockings + elastic stockings
Very high risk - LMWH (dalteparin or enoxaprin)
- PO coumadin
- pneumatic stockings/ elastic stockings + low dose heparin/ LMWH
Treatment unilateral cellulitis
Mild
- no systemic infection
tx - PO abx
- Penicillin or Ceftriaxone or Cefazolin or Clindamycin
Moderate
- systemic infection
tx - IV abx
- Penicillin or Ceftriaxone or Cefazolin or Clindamycin
Severe
- decompensated or immunocompromised
- r/o necrotizing process, send cultures, empiric broad spectrum IV abx
- Vancomycin + Piperacilin/ Tazobactam
What is a genetic condition resulting from hypersensitivity reactions to allergens?
Atopy
With Ig do mast cells have high affinity for surface receptor?
IgE
- coated with IgE antibody
How is mast cell activated in allergies? What happens?
- allergin binds IgE on surface of mast cell and cross-linking activates mast cell
- > release of granules = histamine, proteoglycans (heparin), serine proteases
- > make and release prostaglandin D2, leukotriene C4 and cytokines
What causes:
- dilation of post capillary venules
- bronchial and smooth muscle contraction
- increase in nasal mucus production
- increase in blood vessel permeability leading to edema
Histamine
Do you need previous sensitization for IgE allergies?
Yes - need to have made IgE Ab
Sx allergic rhinitis?
- sneezing
- itchy eyes
- rhinorrhea
What is angioedema?
- rapid swelling of skin, mucosa and submucosal tissue
- often associated with allergy, can be hereditary
Ddx wheeze
- asthma
- FB
- aspiration
- GERD
- CF
- bronchitis
- tumor
- COPD
