Pulmonology Flashcards
What are conditions that may cause a dry cough?
Pluerisy
Laryngeal Cancer
Upper respiratory tract infection
ILD
What are conditions that may cause a productive cough? (With sputum)
Acute exacerbation of COPD
Pulmonary oedema
Lung abcess
What are the causes of an acute cough?
PE, Acute bronchitis, pnuemonia
What are the causes of a subacute cough?
Acute exacerbation of asthma
Post infection cough
What are the causes of a chronic cough?
ILD
COPD
Describe the cough of the following diseases:
Pharyngeal, layryngeal, tracheal and bronchial
Pharyngeal disease: painful, associated with nausea and vomiting, post nasal drip
Laryngeal disease: stridor, hoarsness of voice
Tracheal disese: metallic sound, retrosternal soreness
Bronchial disease such as asthma or COPD: associated with wheezes
Describe the cough of the following lung parenchymal diseases: Pnuemonia TB Pulmonary embolism Interstitial lung diseases
Pnuemonia: starts off dry, eventually becomes productive
TB: lasts from weeks to months, blood timged sputum
Pulmonary embolism: associated with haemoptysis
Interstitial lung disease: dry, persistent cough with dsypnea
Desecibw the cough associated with plueral diseases
Usually dry, associated wirh sharp localized chest pain
Give examples pf extra thoracic areas where cough receptors are present (4)
Stomach, ear, brain, mouth
State 3 non respiratory causes for cough. Describe them
Gastro-oesophageal: GERD. Chronic persistent dry or productive cough, following meals and in supine position
Cardiac: like left sided heart failure causing pulmonary congestion, associated with orthopnea
Neurological: brain tumors, encephalitis
Drug induced: ACE inhibitors as they cause the accumulation of bradykinin which irritates nerve wndings at the lung
Define expectoration
Producing sputum from the throat or lungs
Define bronchorrhea
Bronchorrhea is the production of more than 100 mL per day of watery sputum
Give 3 examples of conditins that cause bronchorrea
- suppurative lung diseases:
- lung abcess
- bronchiectasis - Alveolar cell carcinoma
What type of bacteria are usually associated with foul smelling sputum?
Anaerobic bacteria
What are mucolytics
Mucolytics are medicines that make the mucus less thick and sticky and easier to cough up
State conditions which may cause acute dyspnea
Pneumothorax
Pulmonary embolism
Myocardial infarction
State conditions which may cause dyspnea progressing over hours or days
Acute exacerbation of COPD or asthma
Pneumonia
State conditions which may cause dyspnea progressing over weeks or months
ILD
Congestive heart failure
State the 4 stafes of the mMRC scale for dyspnea
GRADE 0= Dyspnea only with strenuous exercise
GRADE 1= Dyspnea when hurrying or walking up a hil
GRADE 2= Dyspnea after walking for 15 mins that forces him to stop or go slower
GRADE 3= dsypnea after walking for less than 15mins
GRADE 4= dyspnes while talking or so severe that the patient cannot leave his home
Most common cause of orthopnea?
Left ventricular failure
State the 2 types of nocturnal dyspnea
- Waking after 2 hours of sleep = PND
2. Waking up very early morning with an asthma attack = asthmatic patient (lowest level of cortisol!)
What is the diagnosis of breathlessness that gets worse after waking in the morning, and improves after coughing up sputum
COPD
What is the diagnosis of breathlessness that continues to worsen for 15 – 30 min after stopping physical activity
Exercise induced asthma
What is the diagnosis of Breathlessness which improves at the weekend or on holiday
Occupational asthma
What is the diagnosis of dsypnea Associated with feeling of light-headedness, dizziness, tingling in the fingers and around the mouth
Psychogenic dsypnea
What are the two layers of the pleura and which of the two is sensitive to pain?
Visceral and parietal pleura
Only the parietal pleura is sensitive to pain.
Describe pleural chest pain
Stitching pain.
Sharp, stabbing and intensified by inspiration or coughing. Localized pain. May be referred to the neck, shoulder tip, or the upper abdomen
Describe anginal/ MI pain
Crushing pain.
Burning, aching, squeezing or just sense of tightness or pressure. Reterosternal region, radiating to neck or left arm, left shoulder. Increase by exertion, tense emotion , heavy meal. reduced by: rest, sublingual nitroglycerin
Describe oesophageal pain
Sharp or constricting simulating angina
usually burning pain, may radiate as angina. Associated with dysphagia abdominal
discomfort, and/or vomiting. Related to meals. Increase in supine; relieved by H2 blockers,
antacid, and prokinetic drugs
What are the most common causes of haemoptysis
Pulmonary embolism TB COPD Bronchiectasis Malignancy
How can the frequency of haemoptysis identify the reason behind it?
Intermittent: respiratory tract infection over years (bronchiectasis, COPD)
Daily for a week: lung cancer, tuberculosis, lung abscess
Single episode, associated with chest pain and dyspnea: pulmonary embolism and infarction
What is considered fatal haemoptysis?
An attack of haemoptysis that exceeds 150mls
What intervention should be done in patientd with an attack of fatal haemoptysis?
Resuscitation (IV fluid/blood)
- Cough suppressants
- Bronchoscopy interventions: e.g., blood aspiration, balloon temponade, bronchial artery embolization
Are wheezes an expiratory or inspiratory sound?
Expiratory
What are ronchi?
low-pitches wheeze “coarse”, resemble snoring
- Expiration + inspiration
- Due to obstruction or secretion of airways
- Character may change with coughing
What is the difference between the wheeze of an asthamtic vs a COPD patient?
COPD: wheezes shortly after waking up
Asthma: patient awaknes with wheezes.
What type of epithelium is presejt in the respiratory tract?
Pseudostratified ciliates columnar epithelium with goblet cells.
Define emphysema
Abnormal permanent enlargement of air spaces distal to the terminal bronchioles. There is an associated destruction of alveolar walls without significant fibrosis and loss of alveolar capillaries
What are the 4 types of emphysema?
Centriacinar emphysema
Panacinar emphysema
Paraspetal emphysema
Irregular emphysema
Define centriacinar emphysema
Emphysema affecting the respiratory bronchioles, most commonly in the upper lobes, seen in cigarette smokers
What type of emphysema seen in alpha 1 antitrypsin deficiency?
Panacinar emphysema
What does alpha 1 anti trypsin do?
It stops the inflammatory process that occurs in the alveoli which causes the breakdown of the alveolar wall as a result of the release of proteases and elastases during the inflammatory process.
Define paraseptal emphysema
Emphysema (expanded alveoli) affecting the everything distal to the respiratory bronchiole, so that includes the alveolar duct and the alveoli. It affects the areas adjacent to the pleura, therefore some patients of this type of emphysema develop pneumothorax randomly. Occurs mostly in the upper lung lobes
Pathophysiology of emphysema?
Bronchioles are exposed to an irritant such as tobacco. We then get an inflammatory cell reaction from neutrophils, lymphocytes and macrophages that leads to the release of elastases, cytokines, proteases and oxidants. These will lead to the damage of the alveolar wall , endothelium, epithelium and mesenchymal damage. Elastin products will be produced which drive the inflammatory process forward, however this can be stopped by alpha anti trypsin. Eventually, there will not be enough mesenchyme to undergo the repair process, leading to permanent enlargement of these alveoli.
Emphysema is known as damaged alveoli but without much fibrosis. What proves that no fibrosis has occurred in the alveoli?
If fibrosis has occurred, the alveoli would have shrunken and would not be enlarged
What is a characteristic histologies finding of emphysema?
Fragmented, Free floating interalveolar septa
Define chronic bronchitis
A persistent productive cough for at least 3 consecutive months for two consecutive years.
What is the difference between early and late forms of chronic bronchitis ?
Early: productive cough with NO AIRWAY OBSTRUCTION
late: productive cough WITH airflow obstruction, associated with emphysema (especially in smokers)
What is the difference between an emphysema patient WITH chronic bronchitis and without?
PINK PUFFER: emphysema without chronic bronchitis
- barrel chest, hyper-inflated lungs with flattened diaphragm
- Older, thinner
- NOT cyanotic, adequate blood oxygenation
- Progressive dyspnea
- Prolonged expiration with a hunched over sitting position in an attempt to squeeze air out.
BLUE BLOATER: EMPHYSEMA ON TOP OF CHRONIC BRONCHITIS
- Obese, cyanotic due to hypoxia, retains CO2
- History of recurrent infections and purplent sputum
- dyspnea is less prominent
- Ronchi AND wheezing
- productive cough for at least 3 consecutive months for at least 2 consecutive years
- diminished respiratory drive
Causes of death from emphysema?
- pulmonary failure
- right-sided heart failure
Why do all COPD and the emphysema patients develop gradual, secondary pulmonary hypertension?
- Due to loss of capillaries as a result of the alveolar damage
- hypoxia induced pulmonary vascular spasm
Describe the Pathogenesis of chronic bronchitis
EXPOSURE TO IRRITANTS:
- submucosal inflammation (Cd8, neutrophils, and macrophages)
- hyperplasia of mucous glands and goblet cells in bronchi and bronchioles (where they shouldn’t be), leading to mucous hyper secretion
- squamous cell metaplasia from the normal pseudo stratified ciliated columnar epithelium
-
Which is the lung structure responsible for excessive mucous hypersecretion in chronic bronchitis?
Main bronchi
Which is the lung structure responsible for airway obstruction?
Since it is a peripheral small airway disease, mucous plugging, inflammation and bronchiolar wall fibrosis occur
What are the symptoms of an asthmatic patient
A chronic inflammatory disorder causing: Cough at night or early morning Episodes of wheezes Chest tightness Breathlessness
What is the end result of the difficulty in expiration in an asthmatic patient?z
Progressive hyperinflation of the lungs with air trapped distal to the bronchi, which are constricted and filled with mucus and debris
What are the hallmarks of asthma?
Intermittent and reversible airway obstruction
Chronic bronchial inflammation with eosinophils
Bronchial smooth muscle cell hypertrophy and hyperreactivity
Increased mucus secretion
This causes a DECREASED LUMEN DIAMETER
What type of cell is associated specifically to bronchial asthma?
Eosinophils
What are the 4 histologies findings in bronchial asthma
Narrowed bronchial epithelium
Mucous hyper secretion
Peri bronchial Inflammation
Smooth muscle hypertrophy
What makes atopic asthma different to non atopic asthma?
BOTH HAVE THE SAME TREATMENT LINE, HOWEVER:
ATOPIC ASTHMA:
- positive family history
- type I, IgE hypersensitivity
- triggered by environmental antigens, such as dusts, pollen and food also by Infections
- positive skin test
- preceded by allergic rhinitis, urticaria, eczema, infections
NON ATOPIC:
- negative skin test
- no family history
- triggers are respiratory infections and air pollutants
- no allergen sensitization
What are the contents of the mucous plug that block bronchi and bronchioles in asthmatic patients?
- eosinophils
- whorls (spirals) of shed epithelium (Curschmann spirals)
- crystalloids from eosinophil proteins. (Charcot- Leyden crystals)
What are the contents of the mucous plug that block bronchi and bronchioles in asthmatic patients?
- eosinophils
- whorls (spirals) of shed epithelium (Curschmann spirals)
- crystalloids from eosinophil proteins. (Charcot- Leyden crystals)
What are the morphologic changes in the airway of an asthmatic patient?
THICKENED WALL Sub basement membrane fibrosis Smooth muscle hyperplasia Increased vascularity in submucosa Increased size of submucosal glands and goblet cell metaplasia of airway epithelium
What do we call an asthmatic attack resistant to treatment that continued for days/weeks ?
Status asthmaticus
Define bronchiectasis
Permanent dilation of bronchi(especially distal) and bronchioles caused by destruction of the muscle and the supporting elastic tissue. It is secondary to persisting infection or obstruction of any cause.
What are the clinical manifestations of bronchiectasis
Clinically manifested by cough and expectoration of copious amounts of purulent sputum
What are the causes of obstructive and non obstructive bronchiectasis?
OBSTRCUTIVE 1. Tumor 2. Foreign body 3. Mucous plug NON OBSTRUCTIVE 1.congenital 2. Infection: suppurative pneumonia
How do obstruction and infection relate to one another to cause bronchiectasis?
Obstruction = hampered clearing, leading to infection Infection = damage to bronchial wall leading to dilation and obstructive secretions
Which areas of the lung are affected by bronchiectasis?
Bilateral lower lobes
What are the 3 stages of a bronchiectatic lesion? Define them.
- ACTIVE LESION: Intense acute and chronic inflammatory exudate within the walls of the bronchi and bronchioles. Desquamation of lining epithelium extensive areas of ULCERATION ( since there is Squamous metaplasia of bronchiectatic wall lining epithelium). Culture from involved bronchi shows mixed flora
- HEALING STAGE: Complete regeneration of lining epithelium with persistent abnormal dilation and scarring; Fibrosis of the walls of bronchi and bronchioles;
- CHRONIC LESION: peribronchiolar fibrosis develops
Are chronic interstitial lung diseases obstructive or restrictive?
Restrictive
What is the meant by lung interstitium?
Lung interstitium comprises of alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues.
The interstitium refers to the tissue area in and around the wall of the airsacs (alveoli) of the lung area where oxygen moves from the alveoli into the the capillary network (small blood vessels) that covers the lung like a thin sheet of blood. Once the oxygen crosses the intersitial space it enters the bloodstream and is delivered to the vital organs of your body. ILDs cause this interstitial space to become inflammed or scarred making it more difficult for oxygen to get into the bloodstream. This inflammation and scarring also makes the lung a bit stiffer which can increase the ‘work’ of breathing and make you feel more breathless than normal, especially with exertion such as walking up stairs. The changes in the lung tissue can also cause a dry, hacky cough for some patients
What happens to lung interstitium in interstitial lung diseases?
Inflammation and fibrosis to the interstitium ( the space between the alveoli and pulmonary capillaries) leading to difficulty in oxygen transport, reducing lung compliance and gas exchange
What can be seen on the chest X-ray of a patient with interstitial lung disease?
Ground glass opacities. infiltrative pattern of small nodules, irregular lines or ground glass shadows
Define pneumoconiosis
Pneumoconiosis is one of a group of interstitial lung disease caused by breathing in certain kinds of dust particles that damage your lungs. Because you are likely to encounter these dusts only in the workplace, pneumoconiosis is called an occupational lung disease. Pneumoconiosis usually take years to develop
Pneumoconiosis can be caused by inorganic material, organic material and chemical fumes. State the inorganic material and the effect they have on the lung interstitium
Asbestos= asbestosis
Silica= silicosis
Coal dust= Anthracosis
THEY ALL CAUSE DIRECT FIBROSIS OF INTERSITIUM AFTER MANY YEARS OF EXPOSURE
Which cell responsible for initiation and perpetuation of lung injury and fibrosis in ILD due to mineral inhalation?
Macrophages. The more reactive particles trigger the macrophages to release a number of products that mediate an inflammatory response and initiate fibroblast proliferation and collagen deposition.
Out of coal, silica, asbestos, which are the most reactive?
Coal is relatively inert, requiring massive exposure to create a reaction
Asbestos and silica are more reactive, resulting in lung fibrosis at lower concentrations
State the stages of coal worker’s pneumoconiosis
- Pulmonary Anthracosis: accumulation of pigment without cellular reaction
- Simple coal worker’s pneumoconiosis: Accumulation of macrophages with minimal pulmonary dysfunction creating COAL NODULES (macrophages + small amounts of collagen + pigment)
- Complicated coal worker’s pneumoconiosis: massive fibrosis and pulmonary dysfunction
Pathogenesis of silicosis?
Inhaled silica, activation of alveolar macrophages, leading to a continuous inflammatory process and resulting in fibrosis
In which lobe of the lung re changes due to silicosis usually found?
Upper lobe
WHY is silicosis associated with an increased susceptibility to tuberculosis
Silicosis results in depression of cell- mediated immunity. Crystalline silica may inhibit the ability of pulmonary macrophages to kill phagocytosed mycobacteria
What are the effects of asbestosis on the body
1.cellular and fibrotic lung reactions
2. tumor initiator and promoter
asbestos fibers generate reactive free radicals which localize in the distal lung close to the mesothelial layer causing their oncogenic effect on mesothelium.
What are asbestos bodies?
Macrophages with a engulfed asbestos fibers
Describe the appearances of the lung of an asbestos patient
Diffuse pulmonary interstitial fibrosis with asbestos bodies. It begins in the lower lobes and sub-pleural area WHICH CAUSES THICKENING OF VISCERAL PLEURA. With time, the fibrosis progresses to the middle& upper lobes.
What are the grades of asbestosis?
Grade 1 asbestosis: fibrosis involving the bronchiolar wall and extending to the first layer of alveoli, asbestos bodies embedded within the fibrous tissue.
Grade 2 asbestosis: fibrosis involving more distant alveolar walls but spares at least some alveoli
Grade 3 asbestosis: fibrosis involving all alveoli between 2 adjacent bronchioles
Most common manifestation of asbestos exposure?
Pleural plaques.
Give an example of organic pneumoconiosis
Hypersensitivity pneumonitis.
Effects of HP on lung?
Interstitial inflammation by lymphocytes and often granulomas, later fibrosis
What is sarcoidosis and which race is it most prevalent in?
Blacks. Systemic disease of unknown aetiology
How does sarcoidosis affect the lung
Non - necrotizing granulomatous inflammation
What are the findings of idiopathic pulmonary fibrosis?
Extensive interstitial fibrosis with alveolar distortion and interstitial expansion
Treatment and prognosis of pneumoconiosis and other ILD ?
Pneumoconiosis
• Stop exposure to stop progression
• Any damage is irreversible
Other interstitial lung diseases
• Steroid or further immunosuppression
• Response is variable
• Often progress to significant fibrosis
Out of inspiration and expiration, Which is active and which is passive?
Inspiration: active process
Expiration: passive ( muscle recoil)
What is the main cause of the symptoms of COPD patients?
Air trapping
What symptoms do COPS patients experience
Wheezes
Dyspnea due to a hyperinflated lung
How does the ABG of COPD patients change as a result of their air trapping!
High CO2, low O2
What are the consequences of the chronic hypoxia in COPD
Pulmonary vasoconstriction—> pulmonary hypertension —> cor pulmonale (tight sided heart failure leading to ascites, lower limb oedema, hepatomegaly, etc)
State the differences between the pink puffer and blue bloater.
THIN/ OBESE
WHEEZES / WHEEZES AND CRACKLES (secretions)
MORE DYSPNEA / MORE COUGH AND SPUTUM
TACHYPNEA, PURSED LIPS / PROLONGED EXPIRATION
PINK / BLUE (cyanotic)
LESS HYPOXEMIC, (CORRECTED BY TACHYPNEA) / HYPOXEMIC
WORKING ACCESSORY MUSCLES DURING INSPIRATION/ WORKING ACCESSORY MUSCLES DURING EXPIRATION
BARREL CHEST/ LOWER LIMB OEDEMA
Define: Total Lung Capacity Vital Capacity Residual Volume Tidal Volume Functional Residual Capacity Expiratory Reserve Volume Inspiratory Capacity Inspiratory Reserve Volume
-Total Lung Capacity (TLC)
The volume of gas present in the lungs and airways at the position of full inspiration
-Vital Capacity (VC)
The maximum volume of gas that can be expired from the lungs during a relaxed expiration from the position of full inspiration
-Residual Volume (RV)
The volume of gas in the lungs and airways at the position of full expiration
-Tidal Volume (VT )
The volume of gas expired or inspired during one breathing cycle
-Functional Residual Capacity (FRC)
The volume of gas in the lungs and airways at the end of a tidal expiration
-Expiratory Reserve Volume (ERV)
The maximum volume of gas which can be expired from the position of FRC
-Inspiratory Capacity (IC)
The maximum volume of gas which can be inspired from the position of FRC
-Inspiratory Reserve Volume (IRV)
The maximum volume of gas which can be inspired from the position of end-inspiratory tidal volume
What is the normal value of FEV1/FVC
80%
Which lung capacity will be altered in the case of ANY lung pathology?
Vital capacity (IRV+ ERV + RV)
What pulmonary disease will lead to increased lung volumes in expiration and inspiration?
Restrictive lung disease such as pulmonary fibrosis.
How is the FEV1/FVC changed in a restrictive lung disease,
The ratio itself may be normal or only slightly reduced , however the volume expired when compared to a normal lung is reduced.
Restrictive lung disease, such as pulmonary fibrosis or interstitial lung disease : ALL lung volumes are reduced.
What are spirometry requirements
No heavy meals 2hrs prior No smoking 1hr prior No bronchodilators prior No tight clothing No exercise within 30 minutes
How many times should be spirometry test be run?
A minimum of 3 & no more than 8 should be attempted.
Requirements of a valid spirometry?
Good test initiation ⁃ Maximal inspiration ⁃ Quick & forceful onset of exhalation ⁃ No coughing, leak, or obstruction ⁃ Smooth curves ⁃ Absence of early termination of expiration (MINIMUM EXHALATION TIME OF 6 SEC with no change in volume for last 1 sec) ⁃ Reproducible efforts agree within 5% or 100 mL with other
efforts
In what cases is a flow volume loop rejected?
Leak at the mouth
- Obstructed mouthpiece due to tongue, false teeth
- Poorly coordinated start to maneuver (delay before forced expiration)
- cough
- Early termination of blow
- Initial inspiration not maximal
- Slow expiration / poor peak obtained
What instructions do we give the patient performing spirometry?
Sit (or stand) straight ⁃ Loosen tight clothing ⁃ Put feet flat on the floor ⁃ Elevate chin and neck ⁃ Patient is asked to place teeth & lips around tube
creating an airtight seal ⁃ Make sure teeth & tongue are not blocking
mouthpiece ⁃ Nose clip is attached occluding air flow from nose ⁃ Patient is asked to breath quietly, then once tidal breathing is established, ask patient to breath to lung capacity then expire to residual volume. Breath as fast and as hard as possible throughout the test. Repeat 3-8 times
What time of curve should we perform to detect upper airway obstruction?
Flow volume loop.
How can we differentiate asthma/ reversible airway obstruction from other types of obstruction?
Give bronchodilator. If the change in FEV1 increases by 12% or more, and FVC increases by 200ml, this is a reversible disease
If no improvement = COPD
What lung volumes or capacities increase or decrease in restrictive diseases?
DECREASES: TLC TV FRC RV VC
What lung volumes or capacities increase or decrease in obstructive diseases?
Decreases:
ERV, IRV, VT
Increases (air trapping) ANYTHING THAT INCLUDES RESIDUAL VOLUME:
RV, TLC, FRC, ratio of RV to TLC
