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Internal Medicine > Pulmonology > Flashcards

Pulmonology Flashcards

1
Q

Explain tidal volume

A

It’s the normal volume of air within the alveoli during normal respiration
500 ml

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2
Q

Explain inspiratory reserve volume

A

It’s forced inspiration during normal respiration and it’s about 3 litres without tidal volume

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3
Q

Expiratory reserve volume explain

A

It’s forced expiration during normal respiration and it’s 1.5 litres without tidal volume

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4
Q

Explain residual volume

A

Its volume of air remaining in alveoli after forced expiration and it does not include other values and it’s 1 litre

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5
Q

Total lung capacity is

A

6 litres
TV+IRV+ERV+RV=TLC
0.5+3+1.5+1=6

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6
Q

Vital lung capacity or forced vital capacity is

A

Volume of air forcefully expired after forced inspiration and is 5 litres
VLC=TV+IRV+ERV

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7
Q

Inspiratory lung capacity is

A

Forced inspiration after forced expiration is ILC and is 3.5 litres
ILC= IRV+TV

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8
Q

Functional residual capacity is

A

Amount of air remaining in alveoli after normal expiration and is 2.5 litres
FRC=TV+IRV

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9
Q

Forced Expiratory Volume 1 or FEV1 is

A

Volume of air expired in one second after forced inspiration and is 4 litres

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10
Q

FEV1/FVC

A

4/5 is 0.8 or 80%

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11
Q

In Obstructive lung diseases
FEV1/FVC is

A

<70% (less)
Less than 70%

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12
Q

What volume is increased in obstructive lung disease

A

ERV and RV

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13
Q

What happens to FVC in obstructive lung disease

A

Remains same or decreased

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14
Q

What happens to FRC in obstructive lung disease

A

Increased

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15
Q

What happens to TLC in obstructive lung disease

A

Increased

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16
Q

What happens to lung volumes and capacities in restrictive lung diseases

A

All are reduced

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17
Q

Is there any change to Tidal Volume in obstructive and restrictive lung diseases

A

No

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18
Q

In restrictive lung diseases
FEV1/FVC is

A

Usually >70 (greater)
75%
Eg: 3/4=0.75 or 75%

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19
Q

In obstructive lung disease what happens to IRV

A

Decreased

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20
Q

COPD includes

A

Chronic Bronchitis
Emphysema

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21
Q

Productive cough is seen in which type of COPD

A

Chronic bronchitis

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22
Q

Emphysema leads to release of

A

Neutrophilic proteases and elastases

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23
Q

Major contributing factors to COPD

A

Tobacco (90%)
Pollutants

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24
Q

Lack of_______leads specifically to Emphysema

A

Alpha 1 anti trypsin deficiency

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25
Q

Tobacco particles after entering the lungs are ingested by

A

Macrophages

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26
Q

Macrophages releases what

A

Cytokines

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27
Q

Cytokines leads to the activation of

A

Neutrophils

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28
Q

Neutrophils releases

A

Reactive oxygen species
Proteases
Elastases
Free radicals

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29
Q

Bronchiole histological layers

A

Epithelium
Basement membrane
Smooth muscle

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30
Q

Basement membrane is made up of

A

Protiens and
Elastic tissue

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31
Q

Cytokines act on the smooth muscles of bronchioles and leads to

A

Bronchoconstriction

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32
Q

Neutrophils leads to the damage of which layer of bronchioles

A

Basement membrane

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33
Q

Substances released by the neutrophils act on the

A

Mucous producing cells (epithelium) of the bronchioles and increases the production of mucous

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34
Q

TGF beta leads to

A

Fibrosis of bronchioles

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35
Q

DLCO is low when there is

A

Low perfusion and
Low surface area for diffusion

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36
Q

DLCO is high when

A

Perfusion is high

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37
Q

What happens to DLCO in people with asthma end stage

A

Increased because of more (new) vascularisation

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38
Q

Goodpasteur’s syndrome

A

Antibodies against basement membrane of lungs and glomerulus

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39
Q

Smoking leads to what type of acinar formation in emphysema

A

Centrilobular/apex

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40
Q

Alpha 1 anti trypsin deficiency leads to what type of emphysema

A

Panacenar/ at base of lung

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41
Q

Alpha 1 anti trypsin deficiency also leads to what diseases along with emphysema

A

Liver disease

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42
Q

Antigens/ allergens are taken up by

A

APC or dentritic cells or macrophages

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43
Q

Dentritic cells present the antigen on it’s surface by

A

MHC complex 2

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44
Q

Antigen presenting cells present the antigen to

A

T helper cells

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45
Q

CD 4 receptors are present on which cells

A

T helper cells

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46
Q

What is the role of CD 4 receptor

A

To recognize the MHC complex

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47
Q

What is the role of T cell receptor

A

To recognize the antigen presented by APC

48
Q

T helper cells releases

A

IL-4, IL-5

49
Q

IL-4 and IL-5 stimulates

A

Plasma cells

50
Q

Plasma cells release

A

Immunoglobulins specifically IgE

51
Q

IgE activates what cells

A

Mast cells

52
Q

Mast cells upon stimulation releases

A

Leukotrienes
Prostaglandins
Histamines

53
Q

Mast cells after activation binds to

A

Membrane of bronchioles

54
Q

IL-5 specifically stimulates bone marrow to produce more

A

Eosinophils

55
Q

Eosinophils release

A

Major Basic Proteins (MBP)
Cationic Peptide

56
Q

MBP and cationic peptide leads to

A

Damage of smooth muscles and causes inflammation and more production of mucus

57
Q

Bronchiectasis main problem

A

Difficulty clearing mucus

58
Q

Cor pulmonale and RHF leads to

A

Increased JVP
ascitis
Pedal edema
Hepatomagaly

59
Q

Chronic bronchitis signs

A

Cyanosis
Productive cough
Ronchi
Wheezing

60
Q

Emphysema signs

A

Pressed lip breathing
Wheezing
Decreased breath sounds
Barrel chest (increased AP diameter)
But thin or chachexic

61
Q

Chronic bronchitis causes secondary polycythemia by

A

Increasing erythropoietin production by kidneys

62
Q

Primary complication in emphysema is

A

Pneumothorax because of alveolar rupture

63
Q

Bronchiectasis has high risk for pneumonia and fibrosis because of a pathogen called

A

Pseudomonas

64
Q

Other signs that maybe associated with cystic fibrosis are

A

Meconium ileus
Pancreatic insufficiency
Bronchiectasis
Male infertility

65
Q

In bronchiectasis the mucus is thick because of

A

Chloride ion exchange channel damage

66
Q

Role of magnesium in bronchodialation

A

Magnesium blocks calcium channels and causes bronchodilation

67
Q

25 OH CCF is converted to vitamin D by

A

1 alpha hydroxylase

68
Q

Signs of restrictive lung diseases

A

Dyspnea
Dry cough
Bibasilar crackles

69
Q

Restrictive lung diseases include

A

Interstetial Pulmonary Fibrosis
Pneumoconiosis
Sarcoidosis
Systemic sclerosis or scleroderma
Pleural effusion
Kyphoscoliosis
Ankylosing spondylitis
Ascitis
Myasthenia gravis
Polio
LEMS (Lambert Eton Myasthenic Syndrome)
Amyotopic Lateral Sclerosis (ALS)
Gullain Barre

70
Q

TLC in restrictive lung disease is

71
Q

Lambert Eton Myasthenic Syndrome (LEMS)

A

Calcium channel on presynaptic membrane is damaged which disabled neurotransmitter secretion into synaptic cleft

72
Q

Cystic Fibrosis and bronchiectasis are prone to what bacterial infection

A

Pseudomonas

73
Q

Smokers and elderly patients are more prone to

A

Legionella infection

74
Q

COPD patients are more prone to

A

Hemophilus Influenza and M.catharalis

75
Q

Atypical pneumonia pathogens

A

Mycoplasma
Chlamydophilia
Legionella

Influenza
CMV
Sars Cov-2

76
Q

Empyema

A

Is pleural effusion with bacteria

77
Q

Parapneumonic effusion is

A

Pleural effusion without bacteria but adjacent to pneumonia lobe

78
Q

Types of pneumonia

A

Lobar
Broncho
Atypical
Cryptogenic

79
Q

Tuberculosis ghon focus is located in which part of lung

A

Middle or lower lobe of lung
Near the pleura (sub pleural)

80
Q

Ghon focus is made up of

A

Pathogen in centre surrounded by macrophages and lymphocytes

81
Q

Ghon focus is also called a

82
Q

Middle of the ghon focus is what type of necrosis

A

Caseous necrosis

83
Q

Ghon focus then migrates to nearby lymphatic vessels and form

A

Hilar lymphadenopathy

84
Q

Ghon complex includes

A

Ghon focus and hilar lymphadenopathy

85
Q

Lymphocytes in ghon focus release

A

Interferon gamma

86
Q

In primary latent tuberculosis what happens to ghon complex

A

Fibrocalcification

87
Q

Fibrocalcification of ghon complex is called

A

RANKE complex

88
Q

Dormant stage of ghon complex is called

A

RANKE complex

89
Q

Ghon complex in secondary tuberculosis reaches

A

Lung apex and causes fibrocaseous necrosis

90
Q

Secondary TB is because of

A

Reactivation of ghon complex from primary TB

91
Q

Types of TB

A

Primary TB
Secondary TB
Primary progressive TB
Extra pulmonary TB or Miliary TB

92
Q

Miliary TB can lead to

A

TB meningitis
Scrufula or cervical lymphadenitis
Constrictive pericarditis
Hepatitis
Pyuria
Addison’s disease
Pott’s disease
Osteomyelitis

93
Q

TB diagnosis

A

Mantoux skin test
IFGRA (Interferon Gamma Release Assay)
CXR / CT
Sputum culture
Bronchoscopy biopsy

94
Q

TB treatment

A

Izoniacid plus Vitamin B6 (pyridoxin)
Rifamin
Pyrazinamide
Ethambutol
Streptomycin

95
Q

Rifampin

A

Causes red orange urine
Contraindicated in HIV

96
Q

Izoniacid

A

Causes B6 deficiency and peripheral neuritis

97
Q

Pyrazinamide

A

Causes hyperurecaemia (uric acid accumulation)
Contraindicated in GOUT

98
Q

Ethambutol

A

Optic neuritis

99
Q

Streptomycin

A

Ototoxicity
Nephrotoxicity

100
Q

Type 1 respiratory failure is

101
Q

Type 2 respiratory failure is

A

Hypercapnea

102
Q

Types of respiratory failure

A

Type 1
Type 2
Mixed

103
Q

Anatomical dead space

A

No perfusion without ventilation that is expected

104
Q

Physiological dead space

A

No perfusion with good ventilation

105
Q

Chronic bronchitis vs bronchiectasis

A

Bronchitis is temporary
Bronchiectasis is permanent

106
Q

Lung cancer types

A

Large neuroendocrine and
Non small cell

107
Q

Large neuroendocrine carcinoma includes

A

Small cell carcinoma
Bronchial carcinoid tumor

108
Q

Non small cell carcinoma includes

A

Squamous cell carcinoma
Adenocarcinoma
Large cell carcinoma

109
Q

Carcinoid tumor release what hormone

A

Seretonin 5HT

110
Q

Tumor on the lung apex is called

A

Pancoast tumor

111
Q

Voice hoarseness in pancoast tumor is caused by

A

Recurrent laryngeal nerve compression

112
Q

Horner’s syndrome by pancoast tumor is because of

A

Compression of T1 thoracic sympathetic nerve

113
Q

Horner’s syndrome include

A

Ptosis
Myosis
Anhydrosis

114
Q

Pancoast tumor causes flushing by

A

Superior venacava compression

115
Q

Pancoast tumor can cause presthesis by

A

Brachial plexus compression

116
Q

Oxygen induced hypercapnia in COPD is by

A

Pulmonary vasodilation by O2 and increase in physiological dead space

Internal Medicine (5 decks)

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