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Step Up Medicine > Pulmonary > Flashcards

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
Q

Role of B blockers in COPD

A

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

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26
Q

Why excess O2 should not be given in COPD

A

Because decreased O2 was the stimulus for respiratory drive, giving excess O2 ll lead to apnoea.

O2 saturation should be bw 88-92%

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27
Q

Plethoric ___

Cachectic____

A

Chronic bronchitis

Emphysema

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28
Q

Secondry polycythemia seen in

A

Chronic polycythemia

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29
Q

Smoking inc/dec the effect of theophylline

A

Dec

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30
Q

Hyperinflated lungs classically seen in

A

Only emphysema

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31
Q

DLco in emphysema and chronic bronchitis

A

Emphysema:dec

Chronic bronchitis: inc

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32
Q

Hematocrit is increased in

A

Chronic bronchitis

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33
Q

Why is there dec DLco in emphysema

A

restricted vascular bed because of the loss of pulmonary capillaries from the destroyed alveolar walls

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34
Q

Corpulmonale seen in which types of COPD

A

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

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35
Q

Differences of sign emphysema and chronic bronchitis

A

Thin build(accessory resp muscle use)
hyperinflated
quiet chest

Stocky build(edema)
wheezy
right heart failure

36
Q

Pink puffers and blue bloaters refer to

A

Emphysema

Chronic bronchitis

37
Q

Normal alveolar pressure of O2 and CO2

A

O2: 100 mmhg

CO2: 40 mmhg

38
Q

Why are emphysema patients called pink puffers

A

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
Q

Why chronic bronchitis patients are called blue bloaters

A

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
Q

Scalloping of the expiratory curve seen in

A

Obstructive ds like asthma

41
Q

Rx in COPD exacerbation

A

B agonist+ anticholinergics

Systemic corticosteroids

Antibiotics

Supplemental O2

CXR to r/o other conditions

NPPV/CPPV

Intubation if above measure fails

42
Q

First line therapy chronic and exacerbation of COPDA

A

Chronic:anticholinergics and/or B agonist

Exacerbation:bronchodilator alone or in combination with anticholinergics

43
Q

Role of corticosteroids in COPD

A

Given only in case of acute exacerbation.

Not chronically even in case of severe COPD unlike asthma

44
Q

Only interventions shown to lower mortality in COPD

A

Smoking cesstion

Oxygen therapy

Vaccination

45
Q

Criteria for continuous or intermittent long term O2 therapy in COPD

A

PaO2 : 55mmhg OR

O2 saturation: _< 88% either at rest or during exercise OR

PaO2 : 55-59 mm hg +polycythemia/corpulmonale

46
Q

Mcc of COPD exacerbation

A

Pulmonary infection

47
Q

Mcc of bronchiectasis

A

Cystic fibrosis

48
Q

Diagnostic study of choice in bronchiectasis

A

High resolution CT

49
Q

Sputum.in bronchiectasis is large in amount,mucopurulent and foul smelling than in chroni bronchitis

A

Yes

50
Q

CF of interstitial lung ds

A

Dyspnea(at first with exertion, later at rest)

Cough (nonproductive)

Fatigue

Other symptoms may be present secondry to another condition

51
Q

Drugs that can cause interstitial lung ds

A 
Amiodarone
Bleomycin
Chemotherapeutic drugs
Gold
Pencillamine
Nitrofurantoin
Illicit drugs
52
Q

Typical changes in ILD

A 
DIFFUSE
Reticular
Reticulonodular
Ground glass
Honeycombing
53
Q

Honeycomb lung

A

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
Q

Most accurate diagnosis of ILD is done by

A

Tissue biopsy

55
Q

Causes of clubbing

A 
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
Q

Type of granulomas in sarcoidosis

A

Noncaseating

57
Q

CF of sarcoidosis

A 
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
Q

CXR hallmark of ds

A

Bilateral hilar adenopathy

59
Q

Egg shell calcification typical of

A

Silicosis

Peripheral rim of calcificafion on lymph nodes

60
Q

RX of choice for sarcoidosis

A

Corticosteroids

Methotrexate when refractory

61
Q

Definitive ds of sarcoidosis

A

Transbronchial biopsy:

Must see non vaseating granuloma(not dxistic by itself)+ clinical presentation

62
Q

Characteristic features of churg strauss

A

GRANULOMATOUS VASCULITIS

Asthma
Pulmonary infilterates
Skin:atopy/rash
Eosinophilia
p-ANCA
63
Q

Feautures of wegener granulomatosis

A

GRANULOMATOUS VASCULITIS

URT
LRT
kidneys

c-ANCA

64
Q

Which ds with ANCA are ass with associated ILDs?

A

c-ANCA
wegener granulomatosis

p-ANCA
churg strauss
May also be in goodpasture

65
Q

Asbestosis

A

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
Q

Features of silicosis

A

Localised and nodular peribronchial fibrosis

Upper lobes

Can be acute/chronic

Inc risk of TB

Sources:mining,stine cutting,glass manufacturing

67
Q

Which pneumoconisis is ass with inc risk of TB

A

Silicosis

68
Q

What is pneumoconiosis

A

Environmental lung ds

69
Q

Pleural plaques seen in

A

Asbestosis

70
Q

Air conditioner lung

A

Hypersensitivity pneumonitis/extrinsic allergic alveolitis caused by inhalation of antigenic agent.

Caused by spores of thermophilic actinomycetes.

71
Q

Goodpasture ds

A

Caused by IgG Abs against glomerular amd alveolar BM .

Type II hypersensitivity rxn

72
Q

Bat shaped ground glass opacity seen in

A

Pulmonary alveolar proteinosis

73
Q

Pulmonary alveolar proteinosis

A

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
Q

Drugs for central sleep apnoea

A

Acetazolomide

Progesterone

(Helps to breath faster)

75
Q

Cause of acquired thrombophilia in nephrotic syndrome

A

Lossof antithrombin-III

76
Q

Most accurate/gold std test for pul embolism

A

Angiogram

77
Q

Spiral CT cam miss ____ pul embolism

A

Peripheral

78
Q

Fay embolism triad

A

Acute dyspnoea

Petechiae: neck and axilla

Confusion

79
Q

General criteria for Dx of acute respiratory failure

A

Hypoxia: PaO2<60 mmHg

Hypercapnia : PCO2>50 mm Hg

80
Q

A-a gradient is normal in

A

Hypoventilation
&
Low inspired partial pressure of O2

81
Q

What happens to the A-a gradient in hypoventilation?

A

Remains same

PAO2- PaO2
[(150-1.25×PACO2)-PaO2}
PA CO2 inc and PaO2 dec so difference remain unchanged.

82
Q

Hypoxia due to __ is not responsive to hypoxia

A

Shunt i.e. when the blood directly goes to left heart instead of being oxygenated in lungs.

83
Q

Higher O2 delivery can be attained by which O2 delivery system

A

Nonrebreathing mask

84
Q

Significance of venturi mask as O2 delivery system

A

Controlled oxygenation

85
Q

Why excessive administeration of O2 in hypercapniac respiratory failure case as in COPD should not be given?

A

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

Step Up Medicine (3 decks)

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