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Pulmonary Flashcards

1
Q

Samter’s triad

A

asthma
sinus inflammation with recurring nasal polyps
aspirinsensitivity

Avoid aspirin and other NSAIDS in them

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2
Q

Is MDI with a spacer as effective as a nebuliser in rx of acute asthma

A

Yes

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3
Q

First line Rx in Mx of acute severe asthma

A

Short acting B - blockers

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4
Q

When is monteleukast-leukotriene imhibitor used in asthma.

A

It is used to prevent the uptake of oral steroids or dec the dose in case if they cant be avoided in asthma

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5
Q

When is cromolyn used in asthma

A

Usually used in children to prevent intake of oral steroids

Rarely used in adults as their ds is more severe.

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6
Q

S/e of inhaled corticosteroids

A

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.

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7
Q

Chronic Rx for various types of asthma

A 
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

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8
Q

Asthma can begin at any age

A

Yes

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9
Q

C/f of asthma

A

SOB

wheezing

Chest tightness

Cough

Worse at night

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10
Q

Reversibility of asthma is checked by

A

Spirometry before and after bronchodilator.

Inc in FEV1>12%

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11
Q

Chest x ray finding in asthma

A

Normal in mild

Severe: hyperinflation

Mainly done to exclude other conditions:pneumonia, pnemothorax, foreign body)

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12
Q

ABG of a person with asthma

A

Due to hyperventilation: hypocarbia/alkalosis

If hypercarbia/acidosis develop :it indicates muscle fatigue-need for intubation

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13
Q

Wheeze DD

A

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)
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14
Q

Emphysema pathogenesis

A

Relative excess in protease(elastase which is produced by PMNs and macrophages) or deficiency in alpha 1 antitrysin

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15
Q

Chronic bronchitis pathogenesis

A

Excess mucus production-enlargement in mucus gland-smooth muscle hyperplasia- scarring of airwys lead to obstruction

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16
Q

COPD consists of

A

Chronic bronchitis: clinical dx

Emphysema:pathological dx

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17
Q

How ll u dx chronic bronchitis

A

Chronic cough productive of sputum for atleast 3 months per yr for atleast 2 consecutive years

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18
Q

Pathological change in emphysema

A

Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls

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19
Q

Centrilobular emphysema

A

Smokers

Proximal acini/respiratory bronchioles involved

Upper zones

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20
Q

Panlobular emphysema

A

Alpha 1 antityrpsin deficiency

Whole acini(proximal/distal)

Lung base mostly

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21
Q

Lung acini

A

Consists of:

Respiratory bronchioles

Alveolar duct

Alveoli

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22
Q

Even if CXR show no evidence of pneumonia in COPD, should antibiotics be given?

A

Yes

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23
Q

Inflammation in COPD

A

Chronic form: no

Acute exacerbation: inflammation present so steroids have to be given like in asthma

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24
Q

When is theophylline used in COPD

A

When std Rx fails i.e in refractory COPD

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25
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
26
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%
27
Plethoric ___ | Cachectic____
Chronic bronchitis Emphysema
28
Secondry polycythemia seen in
Chronic polycythemia
29
Smoking inc/dec the effect of theophylline
Dec
30
Hyperinflated lungs classically seen in
Only emphysema
31
DLco in emphysema and chronic bronchitis
Emphysema:dec Chronic bronchitis: inc
32
Hematocrit is increased in
Chronic bronchitis
33
Why is there dec DLco in emphysema
restricted vascular bed because of the loss of pulmonary capillaries from the destroyed alveolar walls
34
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
35
Differences of sign emphysema and chronic bronchitis
Thin build(accessory resp muscle use) hyperinflated quiet chest Stocky build(edema) wheezy right heart failure
36
Pink puffers and blue bloaters refer to
Emphysema Chronic bronchitis
37
Normal alveolar pressure of O2 and CO2
O2: 100 mmhg CO2: 40 mmhg
38
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
39
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
40
Scalloping of the expiratory curve seen in
Obstructive ds like asthma
41
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
42
First line therapy chronic and exacerbation of COPDA
Chronic:anticholinergics and/or B agonist Exacerbation:bronchodilator alone or in combination with anticholinergics
43
Role of corticosteroids in COPD
Given only in case of acute exacerbation. Not chronically even in case of severe COPD unlike asthma
44
Only interventions shown to lower mortality in COPD
Smoking cesstion Oxygen therapy Vaccination
45
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
46
Mcc of COPD exacerbation
Pulmonary infection
47
Mcc of bronchiectasis
Cystic fibrosis
48
Diagnostic study of choice in bronchiectasis
High resolution CT
49
Sputum.in bronchiectasis is large in amount,mucopurulent and foul smelling than in chroni bronchitis
Yes
50
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
51
Drugs that can cause interstitial lung ds
``` Amiodarone Bleomycin Chemotherapeutic drugs Gold Pencillamine Nitrofurantoin Illicit drugs ```
52
Typical changes in ILD
``` DIFFUSE Reticular Reticulonodular Ground glass Honeycombing ```
53
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
54
Most accurate diagnosis of ILD is done by
Tissue biopsy
55
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
56
Type of granulomas in sarcoidosis
Noncaseating
57
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 ```
58
CXR hallmark of ds
Bilateral hilar adenopathy
59
Egg shell calcification typical of
Silicosis Peripheral rim of calcificafion on lymph nodes
60
RX of choice for sarcoidosis
Corticosteroids Methotrexate when refractory
61
Definitive ds of sarcoidosis
Transbronchial biopsy: Must see non vaseating granuloma(not dxistic by itself)+ clinical presentation
62
Characteristic features of churg strauss
GRANULOMATOUS VASCULITIS ``` Asthma Pulmonary infilterates Skin:atopy/rash Eosinophilia p-ANCA ```
63
Feautures of wegener granulomatosis
GRANULOMATOUS VASCULITIS URT LRT kidneys c-ANCA
64
Which ds with ANCA are ass with associated ILDs?
c-ANCA wegener granulomatosis p-ANCA churg strauss May also be in goodpasture
65
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. 
66
Features of silicosis
Localised and nodular peribronchial fibrosis Upper lobes Can be acute/chronic Inc risk of TB Sources:mining,stine cutting,glass manufacturing
67
Which pneumoconisis is ass with inc risk of TB
Silicosis
68
What is pneumoconiosis
Environmental lung ds
69
Pleural plaques seen in
Asbestosis
70
Air conditioner lung
Hypersensitivity pneumonitis/extrinsic allergic alveolitis caused by inhalation of antigenic agent. Caused by spores of thermophilic actinomycetes.
71
Goodpasture ds
Caused by IgG Abs against glomerular amd alveolar BM . | Type II hypersensitivity rxn
72
Bat shaped ground glass opacity seen in
Pulmonary alveolar proteinosis
73
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.
74
Drugs for central sleep apnoea
Acetazolomide Progesterone (Helps to breath faster)
75
Cause of acquired thrombophilia in nephrotic syndrome
Lossof antithrombin-III
76
Most accurate/gold std test for pul embolism
Angiogram
77
Spiral CT cam miss ____ pul embolism
Peripheral
78
Fay embolism triad
Acute dyspnoea Petechiae: neck and axilla Confusion
79
General criteria for Dx of acute respiratory failure
Hypoxia: PaO2<60 mmHg Hypercapnia : PCO2>50 mm Hg
80
A-a gradient is normal in
Hypoventilation & Low inspired partial pressure of O2
81
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.
82
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.
83
Higher O2 delivery can be attained by which O2 delivery system
Nonrebreathing mask
84
Significance of venturi mask as O2 delivery system
Controlled oxygenation
85
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

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