Pulmonology Flashcards by ACE MASTER

Explain tidal volume

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

How well did you know this?

Not at all

Perfectly

Explain inspiratory reserve volume

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

How well did you know this?

Not at all

Perfectly

Expiratory reserve volume explain

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

How well did you know this?

Not at all

Perfectly

Explain residual volume

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

How well did you know this?

Not at all

Perfectly

Total lung capacity is

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

How well did you know this?

Not at all

Perfectly

Vital lung capacity or forced vital capacity is

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

How well did you know this?

Not at all

Perfectly

Inspiratory lung capacity is

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

How well did you know this?

Not at all

Perfectly

Functional residual capacity is

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

How well did you know this?

Not at all

Perfectly

Forced Expiratory Volume 1 or FEV1 is

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

How well did you know this?

Not at all

Perfectly

FEV1/FVC

4/5 is 0.8 or 80%

How well did you know this?

Not at all

Perfectly

In Obstructive lung diseases
FEV1/FVC is

<70% (less)
Less than 70%

How well did you know this?

Not at all

Perfectly

What volume is increased in obstructive lung disease

ERV and RV

How well did you know this?

Not at all

Perfectly

What happens to FVC in obstructive lung disease

Remains same or decreased

How well did you know this?

Not at all

Perfectly

What happens to FRC in obstructive lung disease

Increased

How well did you know this?

Not at all

Perfectly

What happens to TLC in obstructive lung disease

Increased

How well did you know this?

Not at all

Perfectly

What happens to lung volumes and capacities in restrictive lung diseases

All are reduced

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

In restrictive lung diseases
FEV1/FVC is

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

How well did you know this?

Not at all

Perfectly

In obstructive lung disease what happens to IRV

Decreased

How well did you know this?

Not at all

Perfectly

COPD includes

Chronic Bronchitis
Emphysema

How well did you know this?

Not at all

Perfectly

Productive cough is seen in which type of COPD

Chronic bronchitis

How well did you know this?

Not at all

Perfectly

Emphysema leads to release of

Neutrophilic proteases and elastases

How well did you know this?

Not at all

Perfectly

Major contributing factors to COPD

Tobacco (90%)
Pollutants

How well did you know this?

Not at all

Perfectly

Lack of_______leads specifically to Emphysema

Alpha 1 anti trypsin deficiency

How well did you know this?

Not at all

Perfectly

Tobacco particles after entering the lungs are ingested by

Macrophages

Macrophages releases what

Cytokines

Cytokines leads to the activation of

Neutrophils

Neutrophils releases

Reactive oxygen species Proteases Elastases Free radicals

Bronchiole histological layers

Epithelium Basement membrane Smooth muscle

Basement membrane is made up of

Protiens and Elastic tissue

Cytokines act on the smooth muscles of bronchioles and leads to

Bronchoconstriction

Neutrophils leads to the damage of which layer of bronchioles

Basement membrane

Substances released by the neutrophils act on the

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

TGF beta leads to

Fibrosis of bronchioles

DLCO is low when there is

Low perfusion and Low surface area for diffusion

DLCO is high when

Perfusion is high

What happens to DLCO in people with asthma end stage

Increased because of more (new) vascularisation

Goodpasteur’s syndrome

Antibodies against basement membrane of lungs and glomerulus

Smoking leads to what type of acinar formation in emphysema

Centrilobular/apex

Alpha 1 anti trypsin deficiency leads to what type of emphysema

Panacenar/ at base of lung

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

Liver disease

Antigens/ allergens are taken up by

APC or dentritic cells or macrophages

Dentritic cells present the antigen on it’s surface by

MHC complex 2

Antigen presenting cells present the antigen to

T helper cells

CD 4 receptors are present on which cells

T helper cells

What is the role of CD 4 receptor

To recognize the MHC complex

What is the role of T cell receptor

To recognize the antigen presented by APC

T helper cells releases

IL-4, IL-5

IL-4 and IL-5 stimulates

Plasma cells

Plasma cells release

Immunoglobulins specifically IgE

IgE activates what cells

Mast cells

Mast cells upon stimulation releases

Leukotrienes Prostaglandins Histamines

Mast cells after activation binds to

Membrane of bronchioles

IL-5 specifically stimulates bone marrow to produce more

Eosinophils

Eosinophils release

Major Basic Proteins (MBP) Cationic Peptide

MBP and cationic peptide leads to

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

Bronchiectasis main problem

Difficulty clearing mucus

Cor pulmonale and RHF leads to

Increased JVP ascitis Pedal edema Hepatomagaly

Chronic bronchitis signs

Cyanosis Productive cough Ronchi Wheezing

Emphysema signs

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

Chronic bronchitis causes secondary polycythemia by

Increasing erythropoietin production by kidneys

Primary complication in emphysema is

Pneumothorax because of alveolar rupture

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

Pseudomonas

Other signs that maybe associated with cystic fibrosis are

Meconium ileus Pancreatic insufficiency Bronchiectasis Male infertility

In bronchiectasis the mucus is thick because of

Chloride ion exchange channel damage

Role of magnesium in bronchodialation

Magnesium blocks calcium channels and causes bronchodilation

25 OH CCF is converted to vitamin D by

1 alpha hydroxylase

Signs of restrictive lung diseases

Dyspnea Dry cough Bibasilar crackles

Restrictive lung diseases include

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

TLC in restrictive lung disease is

Decreased

Lambert Eton Myasthenic Syndrome (LEMS)

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

Cystic Fibrosis and bronchiectasis are prone to what bacterial infection

Pseudomonas

Smokers and elderly patients are more prone to

Legionella infection

COPD patients are more prone to

Hemophilus Influenza and M.catharalis

Atypical pneumonia pathogens

Mycoplasma Chlamydophilia Legionella Influenza CMV Sars Cov-2

Empyema

Is pleural effusion with bacteria

Parapneumonic effusion is

Pleural effusion without bacteria but adjacent to pneumonia lobe

Types of pneumonia

Lobar Broncho Atypical Cryptogenic

Tuberculosis ghon focus is located in which part of lung

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

Ghon focus is made up of

Pathogen in centre surrounded by macrophages and lymphocytes

Ghon focus is also called a

Granuloma

Middle of the ghon focus is what type of necrosis

Caseous necrosis

Ghon focus then migrates to nearby lymphatic vessels and form

Hilar lymphadenopathy

Ghon complex includes

Ghon focus and hilar lymphadenopathy

Lymphocytes in ghon focus release

Interferon gamma

In primary latent tuberculosis what happens to ghon complex

Fibrocalcification

Fibrocalcification of ghon complex is called

RANKE complex

Dormant stage of ghon complex is called

RANKE complex

Ghon complex in secondary tuberculosis reaches

Lung apex and causes fibrocaseous necrosis

Secondary TB is because of

Reactivation of ghon complex from primary TB

Types of TB

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

Miliary TB can lead to

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

TB diagnosis

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

TB treatment

Izoniacid plus Vitamin B6 (pyridoxin) Rifamin Pyrazinamide Ethambutol Streptomycin

Rifampin

Causes red orange urine Contraindicated in HIV

Izoniacid

Causes B6 deficiency and peripheral neuritis

Pyrazinamide

Causes hyperurecaemia (uric acid accumulation) Contraindicated in GOUT

Ethambutol

Optic neuritis

Streptomycin

Ototoxicity Nephrotoxicity

Type 1 respiratory failure is

Hypoxemia

Type 2 respiratory failure is

Hypercapnea

Types of respiratory failure

Type 1 Type 2 Mixed

Anatomical dead space

No perfusion without ventilation that is expected

Physiological dead space

No perfusion with good ventilation

Chronic bronchitis vs bronchiectasis

Bronchitis is temporary Bronchiectasis is permanent

Lung cancer types

Large neuroendocrine and Non small cell

Large neuroendocrine carcinoma includes

Small cell carcinoma Bronchial carcinoid tumor

Non small cell carcinoma includes

Squamous cell carcinoma Adenocarcinoma Large cell carcinoma

Carcinoid tumor release what hormone

Seretonin 5HT

Tumor on the lung apex is called

Pancoast tumor

Voice hoarseness in pancoast tumor is caused by

Recurrent laryngeal nerve compression

Horner’s syndrome by pancoast tumor is because of

Compression of T1 thoracic sympathetic nerve

Horner’s syndrome include

Ptosis Myosis Anhydrosis

Pancoast tumor causes flushing by

Superior venacava compression

Pancoast tumor can cause presthesis by

Brachial plexus compression

Oxygen induced hypercapnia in COPD is by

Pulmonary vasodilation by O2 and increase in physiological dead space

Pulmonology Flashcards

(116 cards)