Pulmonary Flashcards
Samter’s triad
asthma
sinus inflammation with recurring nasal polyps
aspirinsensitivity
Avoid aspirin and other NSAIDS in them
Is MDI with a spacer as effective as a nebuliser in rx of acute asthma
Yes
First line Rx in Mx of acute severe asthma
Short acting B - blockers
When is monteleukast-leukotriene imhibitor used in asthma.
It is used to prevent the uptake of oral steroids or dec the dose in case if they cant be avoided in asthma
When is cromolyn used in asthma
Usually used in children to prevent intake of oral steroids
Rarely used in adults as their ds is more severe.
S/e of inhaled corticosteroids
Due to oropharyngeal deposition:
Sore throat
Oral candidiasis
Hoarseness
Using a spacer with MDIs and rinsing the mouth after use helps minimize these side effects.
Chronic Rx for various types of asthma
MILD INTERMITTENT (Symptoms 2 or fewer /week):none
MILD PERSISTANT
(2 or more times/week but not everyday)
LDIC
MODERATE PERSISTANT
(daily, frequent exacerbation)
LDIC+ LABA, alternative include adding leukotriene modifier
SEVERE PERSISTANT
(Continual symptoms, frequent exacerbation, limited physical activity)
M/HDIC+LABA
If poor control oral steroid may be added
Asthma can begin at any age
Yes
C/f of asthma
SOB
wheezing
Chest tightness
Cough
Worse at night
Reversibility of asthma is checked by
Spirometry before and after bronchodilator.
Inc in FEV1>12%
Chest x ray finding in asthma
Normal in mild
Severe: hyperinflation
Mainly done to exclude other conditions:pneumonia, pnemothorax, foreign body)
ABG of a person with asthma
Due to hyperventilation: hypocarbia/alkalosis
If hypercarbia/acidosis develop :it indicates muscle fatigue-need for intubation
Wheeze DD
Asthma
CHF—due to edema of airways and congestion of bronchial mucosa
- COPD—inflamed airways maybe narrowed,or bronchospasm may be present
- Cardiomyopathies,pericardial diseases can lead to edema around thebronchi
- Lungcancer—due to obstruction of airways (central tumor or mediastinal invasion)
Emphysema pathogenesis
Relative excess in protease(elastase which is produced by PMNs and macrophages) or deficiency in alpha 1 antitrysin
Chronic bronchitis pathogenesis
Excess mucus production-enlargement in mucus gland-smooth muscle hyperplasia- scarring of airwys lead to obstruction
COPD consists of
Chronic bronchitis: clinical dx
Emphysema:pathological dx
How ll u dx chronic bronchitis
Chronic cough productive of sputum for atleast 3 months per yr for atleast 2 consecutive years
Pathological change in emphysema
Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls
Centrilobular emphysema
Smokers
Proximal acini/respiratory bronchioles involved
Upper zones
Panlobular emphysema
Alpha 1 antityrpsin deficiency
Whole acini(proximal/distal)
Lung base mostly
Lung acini
Consists of:
Respiratory bronchioles
Alveolar duct
Alveoli
Even if CXR show no evidence of pneumonia in COPD, should antibiotics be given?
Yes
Inflammation in COPD
Chronic form: no
Acute exacerbation: inflammation present so steroids have to be given like in asthma
When is theophylline used in COPD
When std Rx fails i.e in refractory COPD
Role of B blockers in COPD
DOC : anticholinergics
But B blockers can be given in acute state with anticholinergics.
They should be given cautiously as the person with COPD may have corpulmonale and Bb may worsen the ds
Why excess O2 should not be given in COPD
Because decreased O2 was the stimulus for respiratory drive, giving excess O2 ll lead to apnoea.
O2 saturation should be bw 88-92%
Plethoric ___
Cachectic____
Chronic bronchitis
Emphysema
Secondry polycythemia seen in
Chronic polycythemia
Smoking inc/dec the effect of theophylline
Dec
Hyperinflated lungs classically seen in
Only emphysema
DLco in emphysema and chronic bronchitis
Emphysema:dec
Chronic bronchitis: inc
Hematocrit is increased in
Chronic bronchitis
Why is there dec DLco in emphysema
restricted vascular bed because of the loss of pulmonary capillaries from the destroyed alveolar walls
Corpulmonale seen in which types of COPD
Chronic bronchitis
both alveolar hypoxia and acidosis (secondary to chronic hypercapnia) stimulate pulmonary arterial vasoconstriction, and hypoxemia stimulates erythrocytosis.
So due to vasoconstriction and high blood viscosity, pul arterial hypertension develops
Differences of sign emphysema and chronic bronchitis
Thin build(accessory resp muscle use)
hyperinflated
quiet chest
Stocky build(edema)
wheezy
right heart failure
Pink puffers and blue bloaters refer to
Emphysema
Chronic bronchitis
Normal alveolar pressure of O2 and CO2
O2: 100 mmhg
CO2: 40 mmhg
Why are emphysema patients called pink puffers
Emphysema sufferers are called “pink puffers”. That is they hyperventilate. Alternatively, because they hyperventilate, emphysema sufferers are able to maintain adequate blood PaO2/CO2 levels: they are not cyanotic, which would suggest a low blood oxygen level.
Called puffers because they breathe with pursed lips leaning forward which generate postive pressure , helps to maintain open airways and prevent their collapsing
Why chronic bronchitis patients are called blue bloaters
In bronchitis, there is a disproportionate loss of perfusion versus ventilation (ie. blood passing through the capillaries surround an alveolus which has no air supply due to a blocked bronchiole, will shunt into the pulmonary veins without picking up oxygen.) so even if people with bronchitis hyperventilate (up their tidal volume by breathing more) they will be unable to maintain adequate blood oxygen levels; so people with bronchitis, and not emphysema, will appear cyanotic.
Bloaters:because of the edema from rt heart failure
Scalloping of the expiratory curve seen in
Obstructive ds like asthma
Rx in COPD exacerbation
B agonist+ anticholinergics
Systemic corticosteroids
Antibiotics
Supplemental O2
CXR to r/o other conditions
NPPV/CPPV
Intubation if above measure fails
First line therapy chronic and exacerbation of COPDA
Chronic:anticholinergics and/or B agonist
Exacerbation:bronchodilator alone or in combination with anticholinergics
Role of corticosteroids in COPD
Given only in case of acute exacerbation.
Not chronically even in case of severe COPD unlike asthma
Only interventions shown to lower mortality in COPD
Smoking cesstion
Oxygen therapy
Vaccination
Criteria for continuous or intermittent long term O2 therapy in COPD
PaO2 : 55mmhg OR
O2 saturation: _< 88% either at rest or during exercise OR
PaO2 : 55-59 mm hg +polycythemia/corpulmonale
Mcc of COPD exacerbation
Pulmonary infection
Mcc of bronchiectasis
Cystic fibrosis
Diagnostic study of choice in bronchiectasis
High resolution CT
Sputum.in bronchiectasis is large in amount,mucopurulent and foul smelling than in chroni bronchitis
Yes
CF of interstitial lung ds
Dyspnea(at first with exertion, later at rest)
Cough (nonproductive)
Fatigue
Other symptoms may be present secondry to another condition
Drugs that can cause interstitial lung ds
Amiodarone Bleomycin Chemotherapeutic drugs Gold Pencillamine Nitrofurantoin Illicit drugs
Typical changes in ILD
DIFFUSE Reticular Reticulonodular Ground glass Honeycombing
Honeycomb lung
Refers to scarred shrunken lung and is an end stage finding with poor prognosis.
Air spaces are dilated and there are fibrous scars in interstium.
It can arise feom many different types of ILD
Most accurate diagnosis of ILD is done by
Tissue biopsy
Causes of clubbing
PULMONARY DS Lung cancer CF ILD Empyema Sarcoidosis Mesothelioma
HEART
Comgenital heart ds
Bacterial endocarditis
GIT
Biliary cirrhosis
Inflammatory bowel ds
Primary biliary cirrhosis
Familial clubbing
Hypertrophic osteoarthropathy
Type of granulomas in sarcoidosis
Noncaseating
CF of sarcoidosis
CONSTITUTIONAL Malaise Fever Anorexia Weight loss
LUNGS
Dry cough
Dyspnoea
SKIN
Erythema nodosum
Plaques
S.c. nodules
EYES
Ant uveitis
HEART
Arrythmia
Conduction disturbances
Sudden death
MUSCULOSKETAL
Arthralgia
Arthritis
Bone lesions
NERVOUS Bells palsy Otic n dysfunction Papilledema Peripheral neuropathy
CXR hallmark of ds
Bilateral hilar adenopathy
Egg shell calcification typical of
Silicosis
Peripheral rim of calcificafion on lymph nodes
RX of choice for sarcoidosis
Corticosteroids
Methotrexate when refractory
Definitive ds of sarcoidosis
Transbronchial biopsy:
Must see non vaseating granuloma(not dxistic by itself)+ clinical presentation
Characteristic features of churg strauss
GRANULOMATOUS VASCULITIS
Asthma Pulmonary infilterates Skin:atopy/rash Eosinophilia p-ANCA
Feautures of wegener granulomatosis
GRANULOMATOUS VASCULITIS
URT
LRT
kidneys
c-ANCA
Which ds with ANCA are ass with associated ILDs?
c-ANCA
wegener granulomatosis
p-ANCA
churg strauss
May also be in goodpasture
Asbestosis
Diffuse interstial fibrosis
Lower lobes
Develops insidiously
Inc risk of bronchogenic ca(synergistic with smoking,Smoking + asbestos exposure has a synergistic effect on increasing risk for lung cancer rather than a mesothelioma. ) and mesothelioma but the risk of bronchogenic ca is more.
Asbestos bodies:rusty colored, dumbbell shaped bodies in the lung tissue. These represent asbestos fibers coated by iron.
Features of silicosis
Localised and nodular peribronchial fibrosis
Upper lobes
Can be acute/chronic
Inc risk of TB
Sources:mining,stine cutting,glass manufacturing
Which pneumoconisis is ass with inc risk of TB
Silicosis
What is pneumoconiosis
Environmental lung ds
Pleural plaques seen in
Asbestosis
Air conditioner lung
Hypersensitivity pneumonitis/extrinsic allergic alveolitis caused by inhalation of antigenic agent.
Caused by spores of thermophilic actinomycetes.
Goodpasture ds
Caused by IgG Abs against glomerular amd alveolar BM .
Type II hypersensitivity rxn
Bat shaped ground glass opacity seen in
Pulmonary alveolar proteinosis
Pulmonary alveolar proteinosis
Accumulation of surfactant like protein amd phospholipids in alveoli.
CxR: ground glass appearance with bilateral alveolar infilterates that resemble a bat shape lung.
It is an alveolar filling ds.
Drugs for central sleep apnoea
Acetazolomide
Progesterone
(Helps to breath faster)
Cause of acquired thrombophilia in nephrotic syndrome
Lossof antithrombin-III
Most accurate/gold std test for pul embolism
Angiogram
Spiral CT cam miss ____ pul embolism
Peripheral
Fay embolism triad
Acute dyspnoea
Petechiae: neck and axilla
Confusion
General criteria for Dx of acute respiratory failure
Hypoxia: PaO2<60 mmHg
Hypercapnia : PCO2>50 mm Hg
A-a gradient is normal in
Hypoventilation
&
Low inspired partial pressure of O2
What happens to the A-a gradient in hypoventilation?
Remains same
PAO2- PaO2
[(150-1.25×PACO2)-PaO2}
PA CO2 inc and PaO2 dec so difference remain unchanged.
Hypoxia due to __ is not responsive to hypoxia
Shunt i.e. when the blood directly goes to left heart instead of being oxygenated in lungs.
Higher O2 delivery can be attained by which O2 delivery system
Nonrebreathing mask
Significance of venturi mask as O2 delivery system
Controlled oxygenation
Why excessive administeration of O2 in hypercapniac respiratory failure case as in COPD should not be given?
Since central receptors are for CO2 and they adapt in 12- 24 hrs ,it is only the peripheral receptore that are left which are responding to Low PO2. If PaO2 is corrected ,no respiratory drive , leading to apnoea
