resp Flashcards
Indication for pleural space drainage
– Large free flowing pleural effusion more than 50% hemithorax OR
– Positive culture OR
– Positive gram stain OR
– pH of <7.2 suggesting the presence of Pus.
- pus
RAPID score
-pleural infection.
- Age
- Urea
- Albumin
- Source of infection
- Purulence.
Patients were stratified into:
low-risk (0-2)
medium-risk (3-4)
high-risk (5-7) groups.
A RAPID score of 3 to 4 and >4 was associated with an OR of 24.4 (95% CI, 3.1-186.7; P=.002) and 192.4 (95% CI, 25.0-1480.4; P
Malignant pleural effusion
LENT score (prognostic scoring system)
- lactate dehydrogenase (pleural fluid),
- ECOG
- neutrophil-to-lymphocyte ratio
- tumour type
Perfirnidone
no significant between-group difference in dyspnea scores.
riociguat
CTPEH
AHI
Mild: 5-15 events per hour of sleep
Moderate: 15-30 events per hour of sleep
Severe: greater than 30 events per hour of sleep
Kartegener syndrome
- subunit of primary ciliary dyskinesia (PCD),
- autosomal recessive disorder with genetic heterogeneity.
KS is caused by ciliary immotility or dysmotility due to ultrastructural abnormalities of respiratory cilia and flagella of spermatozoa and Fallopian tube.
Clinical characteristic features are ;
- situs inversus,
- respiratory distress of various severity leading to chronic sinusitis and bronchiectasis.
Flagella defects of spermatozoa and Fallopian tube results in infertility or subfertility.
Situs inversus is probably due to the absence of ciliary motility in Hensen’s node in the embryo.
In terms of investigations:
- Mutations in DNAI1 and DNAH5 have been detected in 38% of patients with primary ciliary dyskinesia.
- Ciliary beat pattern analysis via digital high speed video imaging is a more sensitive and specific test for PCD with positive predictive value.
- Bronchoscopy reveals mucosal inflammation and mucopurulent secretions. It can also be used to confirm the reversal of bronchial anatomy in those patients with situs inversus.
- Nasal biopsy (brush or curettage) samples are obtained from inferior surface of turbinates. Electron microscopy reveals the abnormalities in the cilia.
- Pulmonary function testing has shown reduced values for FEV1. However, longitudinal studies have shown a high degree of variation in the course of lung function after diagnosis that was not related to either age or lung function level at the time of diagnosis- so does not actually help in establishing a diagnosis of PCD.
ICS withdrawal
mod fev1 reduction
CODEX index
CODEX
- comorbidity
- obstruction
- dyspnea
- previous severe eXacerbations
can accurately predict mortality, hospital readmission, and their combination for the period from 3 months to 1 year after discharge in patients hospitalized for COPD.
Löfgren syndrome
Löfgren syndrome is a type of acute sarcoidosis
Triad of Löfgren syndrome:
1) erythema nodosum
2) bilateral hilar adenopathy on CXR
3) arthritis.
Löfgren syndrome is associated with a good prognosis,with >90% of patients experiencing disease resolution within 2 years.
EGFR Tyrosine Kinase inhibitor
- Erlotinib and Gefitinib
improved survival in
- colorectal,
- head, neck
- lung cancer
Erlotinib
interstitial pneumonitis
R
-characterized by cough and increased dyspnea occurs in patients taking Erlotinib.
This may be severe and must be considered among those patients whose breathing acutely worsens.
Higher response rate with Erlotinib if
1) EGFR mutation
2) Wild type K-ras
3) EGFR polysomy >4 copies
higher likelihood of responding to oral TKI
Asian, female, never-smoker, adenocarcinoma
lung abscess
IV clindamycin is drug of choice for lung abscess.
-predominantly anaerobic flora of the gingival crevice.
The most common organisms are Peptostreptococcus, Prevotella, Bacteroides spp (usually not B. fragilis), and Fusobacterium app
- Charateristic sign on X-ray is air fluid level.
- On CT is seen as the “split pleura” sign
Mycoplasma pneumoniae
atypical pneumonia younger pt characteristic complications: - erythema multiforme and - cold autoimmune haemolytic anaemia.
-may not respond to penicillins or cephalosporins
Features
- flu-like symptoms classically precede a dry cough
- bilateral consolidation on x-ray
- complications may occur as below:
Complications
- cold agglutins (IgM) may cause an haemolytic anaemia, thrombocytopenia
- erythema multiforme, erythema nodosum
- meningoencephalitis, Guillain-Barre syndrome
- bullous myringitis: painful vesicles on the tympanic membrane
- pericarditis/myocarditis
- gastrointestinal: hepatitis, pancreatitis
- renal: acute glomerulonephritis
Diagnosis
* Mycoplasma serology
Management
- erythromycin/clarithromycin
- tetracyclines such as doxycycline are an alternative
Paraneoplastic features of lung cancer
- squamous cell: PTHrp, clubbing, HPOA
- small cell: ADH, ACTH, Lambert-Eaton syndrome
Lambert-Eaton syndrome occurs almost exclusively in small cell lung cancer
Paraneoplastic features:
Small cell
* ADH
* ACTH – not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc
* Lambert-Eaton syndrome (bilateral proximal muscle weakness,absent deep tendon reflexes,autonomic dysfunction and improvement of the ptosis after sustained upward gaze )
Squamous cell
- PTH-rp
- clubbing
- hypertrophic pulmonary osteoarthropathy (HPOA)
- hyperthyroidism due to ectopic TSH
Adenocarcinoma
* gynaecomastia
PCP & steroid
Prednisone protects against a vigorous immune response in the lung from dead pneumocysts.
Administration of corticosteroids within the first 72 hours of anti-Pneumocystis treatment helps to prevent respiratory failure and death in AIDS patients.
All patients with an A-a gradient greater than 35 mm Hg or a PaO2 of less than 70 mm Hg should receive cortico-steroids when antimicrobial therapy is initiated.
The standard approach is to use prednisone for 21 days
80mg/day for 5 days
40mg/day for 5 days
20mg/day until completed.
flow- vol curves
Normal Inspiration = A variable Intrathoracic problem.
Normal Expiration = A variable Extrathoracic problem.
Variable intrathoracic obstruction (eg, tracheomalacia). During a forced inspiration,negative pleural pressure holds the ‘floppy’ trachea open. With forced expiration, loss of structural support results in tracheal narrowing of the trachea and a plateau of diminished flow. Flow is maintained briefly before airway compression occurs.
lung fn test
Low FEV1 (<80%) suggest obstruction
Low FVC and high FEV/FVC ratio (>80%) suggest restriction.
TLC (<80%)confirms a restrictive pattern
Low DLCO and High KCO suggest restrictive disease: – previous lobectomy – severe pleural disease – kyphoscoliosis – diaphragmatic paralysis
increase DLCO
mnemonic “SAMPPLE”
–Severe obesity –Asthma –Mild LVF –Polycythaemia –Pulmonary hemorrhage –Left to right intracardiac shunting –Exercise just prior to test session(due to increased cardiac output)
low DLCO
Low DLCO with obstruction:
- emphysema
- cystic fibrosis
- alpha-1 antitrypsin deficiency
Low DLCO with restriction:
– interstitial lung disease or pneumonitis.
Low DLCO with mixed picture: – sarcoidosis – asbestosis – miliary TB – heart failure
Low DLCO with normal spirometry: – pulmonary vascular disease: PE, pulmonary HT, Scleroderma. – early interstitial lung disease – anemia – increased carboxyhemoglobin level
Normal DLCO with restriction
Consistent with extrapulmonary restriction such as – Obesity – Kyphoscoliosis – Neuromuscular weakness – Pleural effusion or thickening
Gas calc
PA02 = FiO2 x [Patm – p H2o] – (PaCO2/Resp quotient)
changes in PAO2 with changes in Patm (changes in altitude) if all other factors remain constant = FiO2 x diff of Patm
Hypoxemia
5 mechanism
1) Hypoventilation
2) V/Q mismatch
3) Right to left shunt
4) Diffusion limitation
5) Reduced inspired oxygen tension
Hypoventilation causes hypoxemia in the following conditions:
1) CNS dpression- drug overdose, structural CNS lesion
2) Obesity hypoventilation syndrome
3) Impaired neuronal conduction-GBS, MND
4) Muscular weakness- myasthenia gravis
5) Poor chest wall elasticity- kyphoscoliosis.
Hypoventilation is characterized by:
– correction with increase in FiO2.
– normal A-a gradient
Ventilation/perfusion (V/Q) mismatch
In the normal lung, there is V/Q mismatch because perfusion and ventilation are heterogenous.
Both ventilation and perfusion are greater in bases more than apices.
But difference between apical and basilar ventilation is smaller than apical basilar perfusion.
V/Q ratio is usually higher in apices than the bases.
V/Q mismatch is responsible for the normal A-a gradient.
Conditions from V/Q mismatch:
– Obstructive lung disease
– Pulmonary vascular disease
– Interstitial lung disease
Narcolepsy
– 100% will have HLA DQB1*0602 (HLA DR2)
Mx: – scheduled naps – reduce heavy carbo meals – good night’s sleep – psychosocial support
– Avoid Prazosin- may induce cataplexy
antigen clusters associated with SCLC
- Serum neurone specific enolase can be found in 75% of small cell lung cancer
– dopa decarboxylase
– calcitonin
– chromogranin A
– CD 56 or neural cell adhesion molecule (NCAM)
– gastrin releasing peptide
– insulin like growth factor 1
NSCL ca rx
Stage I and II- surgical resection
**surgical resection plus adjuvant chemo(For completely resected stage II and III)
Stage IIIa- Induction chemotherapy followed by surgery OR chemoradiotherapy
Stage IIIb- chemoradiotherapy
Stage IV- Chemotherapy AND palliative radiotherapy.
– if solitary brain mets consider surgical excision.
If patient is not suitable for optimal regimen, treat depending on symptom and performance status.
-observation if not symptomatic
or palliative management
(ie: Palliative radiotherapy for Stage IIIa to IV)
small cell lung ca
- Limited disease:
Optimal management:
- Platinum based chemotherapy combined with thoracic radiotherapy.
AND
- Prophylactic cranial irradiation for complete responders.
If not for optimal management:
Palliative chemotherapy +/- radiotherapy.
2. Extensive disease: Optimal management: Combination chemotherapy AND Prophylactic cranial irradiation for complete responders
If not for optimal management:
Symptom control.
DEFINITIONS:
Limited disease:
(a) disease confined to one hemithorax, although local extensions may be present;
(b) no extrathoracic metastases except for possible ipsilateral, supraclavicular nodes if they can be included in the same (radiotherapy) portal as the primary tumour;
(c) primary tumour and regional nodes which can be adequately treated and totally encompassed in every (radiotherapy) portal.
Extensive disease:
Inoperable patients who cannot be classified as having limited disease
Constrictive Bronchiolitis Obliterans
Constrictive bronchiolitis or bronchiolitis obliterans is concentric submucosal fibrosis of the bronchiolar airway leading to narrowing and obliteration.
Shortness of breath is the most common presenting symptom and early inspiratory crackles are heard by lung auscultation.
Pulmonary function demonstrates irreversible airflow obstruction with decreased FEV1:FVC ratio, although a restrictive pattern may be seen.
The chest radiograph shows normal lungs or hyperinflation, while the chest CT shows air trapping by the expiratory view, a mosaic pattern, bronchiolectasis and small airway wall thickening.
Corticosteroid therapy is effective for the inflammatory component of the illness and for exacerbations. Immunosuppressive agents may be effective in some individuals. Antifibrotic agents may be effective in the future. Lung transplantation is an option for life-threatening, disabling disease.
Principles of Asthma management
- Use preventer if asthma symptoms >3x per week or use
SABA >3x per week - Start with a low dose of inhaled ICS.
Once control is achieved, titrate the dose of ICS to the lowest dose at which effective control of asthma is maintained.
Those with moderate persistent asthma will need the addition of a LABA.
Little additional improvement in symptoms or lung function is gained by increasing doses above:
800 mcg/day budesonide(Pulmicort),
500 mcg/day fluticasone(Flixotide)
In adults, initial therapy with ICS is superior to treatment with a leukotriene receptor antagonist (LTRA), cromone or theophylline for improving lung function and reducing symptoms.
Samter’s triad
Samter’s triad characterized by presence of aspirin intolerance, asthma and nasal polyposis.
The disorder is caused by overproduction of leukotrienes.When prostaglandin production is blocked by NSAIDS like aspirin, the cascade shunts entirely to leukotrienes, causing overproduction of LT-4 and producing the severe allergy-like effects.
Treatment is with leukotrienes antagonist(Montelukast) for symptom relief but the preferred treatment is now aspirin desensitization.
H1N1
Severe H1N1 infection is associated with IgG(2) deficiency, which appears to persist in a majority of patients. Pregnancy-related reductions in IgG(2) level may explain the increased severity of H1N1 infection in some but not all pregnant patients. The role of IgG(2) deficiency in the pathogenesis of H1N1 infection requires further investigation, because it may have therapeutic implications.
Association between severe pandemic 2009 influenza A (H1N1) virus infection and immunoglobulin G(2) subclass deficiency.
Galactomannan
– major constituents of aspergilus cell wall
– released during growth of hyphae
– used to diagnose invasive aspergillosis in immunocompromised patients.
BODE index
predicting the risk of death from any cause and from respiratory causes among patients with COPD
- BMI
- Obstruction(FEV1)
- Dyspnea(MMRC)
- Exercise(6MWD)
Contraindications to surgery in non-small cell lung cancer
– stage IIIb or IV – FEV1 <1.5 – malignant pleural effusion – tumour near hilum – vocal cord paralysis – SVC obstruction
Small cell lung ca
Small cell lung cancer(SCLC) comprises about 20% of lung cancers. This type of lung cancer is the most aggressive and rapidly growing of all the types.
SCLC is strongly related to cigarette smoking with only 1% of these tumors occurring in non-smokers.
SCLC metastasize rapidly to many sites within the body and are most often discovered after they have spread extensively.
infrequently present with:
- SVC obstruction
- Pancoast syndrome
- Paraneoplastic syndrome
poor prognosis in patients with cystic fibrosis
1) Low FEV1
2) High CO2
3) High WCC
4) Females
Ivacaftor - which CF?
augment the chloride-transport activity of G551D-CFTR protein in vitro.
Ivacaftor was associated with improvements in lung function at 2 weeks that were sustained through 48 weeks. Substantial improvements were also observed in the risk of pulmonary exacerbations, patient-reported respiratory symptoms, weight, and concentration of sweat chloride.
Spontanenous pneumothorax
In primary pneumothorax, risk factors include: – smoking – positive family history in 10% – Marfan’s syndrome – Homocytinuria – Thoracic endometriosis
In secondary pneumothorax, risk factors include:
– COPD for 70% of cases (Increased risk with worsening obstruction)
– PCP
– AIDS
– CF
– TB
Management of Primary pneumothorax:
– supplemental oxygen (100% humidified oxygen)
– simple pleural aspiration or intercostal tube drainage (similar 12 months outcome)
– But Simple aspiration is associated with a reduction in hospitalization.
PAH (NOT same as pul htn)
def:
- pre-capillary PH (mean PAP of >25mmHg),
- pulmonary artery wedge pressure (PAWP) ≤15 mmHg
- PVR >3 Wood units (WU)
in the absence of other causes of pre-capillary PH such as PH due to lung diseases, CTEPH or other rare diseases.
May be classified into 5 WHO groups:
Group 1: due to idiopathic,familial or associated dx (ie: connective tissue disease, HIV, portal hypertension, congenital heart disease, schistosomiasis).
Group 2: due to left heart disease (LV systolic dysfunction, LV diastolic dysfunction, valvular disease, congenital heart disease)
Group 3: due to respiratory disease (COPD, ILD, sleep disordered breathing, alveolar hypoventilation disorders,etc)
Group 4: due to chronic thromboembolic HT (CTEPH)
Group 5: due to unclear or multifactorial mechanisms (hematological disorders, systemic disorders like sarcoidosis, etc).
Three important hormones in pathogenesis of PAH and their function:
1) Prostacyclin causes vasodilation and anti-proliferation.
2) Nitric oxide causes vasodilation and anti-proliferation
3) Endothelin 1 causes vasocontriction of smooth muscle.
What happens in PAH?
1) Low prostacyclin production.
2) Low nitric oxide synthesis.
3) High Endothelin 1 and thromboxane production.
4) Impaired voltage gated potassium - calcium
5) Mutation of Bone morphogenetic protein(BMPR) gene resulting in increased smooth muscle proliferation.
Other gene mutations: Activin 1 like kinase receptor, serotonin transporter gene.
How to treat?
Treat the cause.Treatment depends on Group of PAH.
Group 1
– treat underlying condition like HIV, scleroderma.
– warfarin for IPAH, familial PAH.
– lung transplant for IPAH if refactory to medical Rx.
Group 2- optimize heart failure therapy.
Group 3- oxygen
Group 4- warfarin. consider heart lung transplant
Group 5- treat underlying condition if possible.
Pharmacotherapy:
1) Low prostacyclin- Treat with prostacyclin (Epoprostenol, Treprostinil)
2) Low nitric oxide- Treat with phosphodiesterase Type 5 inhibitor (Sildenafil)
3) High endothelin 1- Treat with endothelin receptor antagonist (Bosentan, Ambrisentan)
4) Calcium blocker-Trial in patients with positive vasoreactivity test but most patient are non-responders (No role for PAH with scleroderma)
Absolute contraindications to thrombolysis
– intracranial disease
– uncontrolled hypertension
– recent major surgery or trauma (within the past 3 weeks).
Percutaneous mechanical thrombectomy (thrombus fragmentation and aspiration) and surgical embolectomy should be restricted to high-risk patients with an absolute contraindication to thrombolytic treatment and those in whom thrombolytic treatment has not improved hemodynamic status; percutaneous mechanical thrombectomy is an alternative to surgical embolectomy in cases in which immediate access to cardiopulmonary bypass is unavailable.
A-a gradient
< (age/4) + 4
PA02 - Pa02
PA02 =
[FiO2 x (Patm - PH20) ] - (PCo2 / 0.8)
PH20 = 47
Patm at sea level = 760
at room air and sea level
PA02 =
150 - 5/4 (PCo2)
