Pulmonology Flashcards
1
Q
What are conditions that may cause a dry cough?
A
Pluerisy
Laryngeal Cancer
Upper respiratory tract infection
ILD
2
Q
What are conditions that may cause a productive cough? (With sputum)
A
Acute exacerbation of COPD
Pulmonary oedema
Lung abcess
3
Q
What are the causes of an acute cough?
A
PE, Acute bronchitis, pnuemonia
4
Q
What are the causes of a subacute cough?
A
Acute exacerbation of asthma
Post infection cough
5
Q
What are the causes of a chronic cough?
A
ILD
COPD
6
Q
Describe the cough of the following diseases:
Pharyngeal, layryngeal, tracheal and bronchial
A
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
7
Q
Describe the cough of the following lung parenchymal diseases: Pnuemonia TB Pulmonary embolism Interstitial lung diseases
A
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
8
Q
Desecibw the cough associated with plueral diseases
A
Usually dry, associated wirh sharp localized chest pain
9
Q
Give examples pf extra thoracic areas where cough receptors are present (4)
A
Stomach, ear, brain, mouth
10
Q
State 3 non respiratory causes for cough. Describe them
A
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
11
Q
Define expectoration
A
Producing sputum from the throat or lungs
12
Q
Define bronchorrhea
A
Bronchorrhea is the production of more than 100 mL per day of watery sputum
13
Q
Give 3 examples of conditins that cause bronchorrea
A
- suppurative lung diseases:
- lung abcess
- bronchiectasis - Alveolar cell carcinoma
14
Q
What type of bacteria are usually associated with foul smelling sputum?
A
Anaerobic bacteria
15
Q
What are mucolytics
A
Mucolytics are medicines that make the mucus less thick and sticky and easier to cough up
16
Q
State conditions which may cause acute dyspnea
A
Pneumothorax
Pulmonary embolism
Myocardial infarction
17
Q
State conditions which may cause dyspnea progressing over hours or days
A
Acute exacerbation of COPD or asthma
Pneumonia
18
Q
State conditions which may cause dyspnea progressing over weeks or months
A
ILD
Congestive heart failure
19
Q
State the 4 stafes of the mMRC scale for dyspnea
A
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
20
Q
Most common cause of orthopnea?
A
Left ventricular failure
21
Q
State the 2 types of nocturnal dyspnea
A
- Waking after 2 hours of sleep = PND
2. Waking up very early morning with an asthma attack = asthmatic patient (lowest level of cortisol!)
22
Q
What is the diagnosis of breathlessness that gets worse after waking in the morning, and improves after coughing up sputum
A
COPD
23
Q
What is the diagnosis of breathlessness that continues to worsen for 15 – 30 min after stopping physical activity
A
Exercise induced asthma
24
Q
What is the diagnosis of Breathlessness which improves at the weekend or on holiday
A
Occupational asthma
25
What is the diagnosis of dsypnea Associated with feeling of light-headedness, dizziness, tingling in the fingers and around the mouth
Psychogenic dsypnea
26
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.
27
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
28
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
29
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
30
What are the most common causes of haemoptysis
```
Pulmonary embolism
TB
COPD
Bronchiectasis
Malignancy
```
31
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
32
What is considered fatal haemoptysis?
An attack of haemoptysis that exceeds 150mls
33
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
34
Are wheezes an expiratory or inspiratory sound?
Expiratory
35
What are ronchi?
low-pitches wheeze “coarse”, resemble snoring
- Expiration + inspiration
- Due to obstruction or secretion of airways
- Character may change with coughing
36
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.
37
What type of epithelium is presejt in the respiratory tract?
Pseudostratified ciliates columnar epithelium with goblet cells.
38
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
39
What are the 4 types of emphysema?
Centriacinar emphysema
Panacinar emphysema
Paraspetal emphysema
Irregular emphysema
40
Define centriacinar emphysema
Emphysema affecting the respiratory bronchioles, most commonly in the upper lobes, seen in cigarette smokers
41
What type of emphysema seen in alpha 1 antitrypsin deficiency?
Panacinar emphysema
42
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.
43
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
44
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.
45
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
46
What is a characteristic histologies finding of emphysema?
Fragmented, Free floating interalveolar septa
47
Define chronic bronchitis
A persistent productive cough for at least 3 consecutive months for two consecutive years.
48
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)
49
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
50
Causes of death from emphysema?
- pulmonary failure
| - right-sided heart failure
51
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
52
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
-
53
Which is the lung structure responsible for excessive mucous hypersecretion in chronic bronchitis?
Main bronchi
54
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
55
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
```
56
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
57
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
58
What type of cell is associated specifically to bronchial asthma?
Eosinophils
59
What are the 4 histologies findings in bronchial asthma
Narrowed bronchial epithelium
Mucous hyper secretion
Peri bronchial Inflammation
Smooth muscle hypertrophy
60
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
61
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)
62
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)
63
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
```
64
What do we call an asthmatic attack resistant to treatment that continued for days/weeks ?
Status asthmaticus
65
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.
66
What are the clinical manifestations of bronchiectasis
Clinically manifested by cough and expectoration of copious amounts of purulent sputum
67
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
```
68
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
```
69
Which areas of the lung are affected by bronchiectasis?
Bilateral lower lobes
70
What are the 3 stages of a bronchiectatic lesion? Define them.
1. 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
2. HEALING STAGE: Complete regeneration of lining epithelium with persistent abnormal dilation and scarring; Fibrosis of the walls of bronchi and bronchioles;
3. CHRONIC LESION: peribronchiolar fibrosis develops
71
Are chronic interstitial lung diseases obstructive or restrictive?
Restrictive
72
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
73
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
74
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
75
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
76
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
77
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.
78
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
79
State the stages of coal worker’s pneumoconiosis
1. Pulmonary Anthracosis: accumulation of pigment without cellular reaction
2. Simple coal worker’s pneumoconiosis: Accumulation of macrophages with minimal pulmonary dysfunction creating COAL NODULES (macrophages + small amounts of collagen + pigment)
3. Complicated coal worker’s pneumoconiosis: massive fibrosis and pulmonary dysfunction
80
Pathogenesis of silicosis?
Inhaled silica, activation of alveolar macrophages, leading to a continuous inflammatory process and resulting in fibrosis
81
In which lobe of the lung re changes due to silicosis usually found?
Upper lobe
82
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
83
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.
84
What are asbestos bodies?
Macrophages with a engulfed asbestos fibers
85
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.
86
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
87
Most common manifestation of asbestos exposure?
Pleural plaques.
88
Give an example of organic pneumoconiosis
Hypersensitivity pneumonitis.
89
Effects of HP on lung?
Interstitial inflammation by lymphocytes and often granulomas, later fibrosis
90
What is sarcoidosis and which race is it most prevalent in?
Blacks. Systemic disease of unknown aetiology
91
How does sarcoidosis affect the lung
Non - necrotizing granulomatous inflammation
92
What are the findings of idiopathic pulmonary fibrosis?
Extensive interstitial fibrosis with alveolar distortion and interstitial expansion
93
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
94
Out of inspiration and expiration, Which is active and which is passive?
Inspiration: active process
Expiration: passive ( muscle recoil)
95
What is the main cause of the symptoms of COPD patients?
Air trapping
96
What symptoms do COPS patients experience
Wheezes
| Dyspnea due to a hyperinflated lung
97
How does the ABG of COPD patients change as a result of their air trapping!
High CO2, low O2
98
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)
99
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
100
```
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
101
What is the normal value of FEV1/FVC
80%
102
Which lung capacity will be altered in the case of ANY lung pathology?
Vital capacity (IRV+ ERV + RV)
103
What pulmonary disease will lead to increased lung volumes in expiration and inspiration?
Restrictive lung disease such as pulmonary fibrosis.
104
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.
105
What are spirometry requirements
```
No heavy meals 2hrs prior
No smoking 1hr prior
No bronchodilators prior
No tight clothing
No exercise within 30 minutes
```
106
How many times should be spirometry test be run?
A minimum of 3 & no more than 8 should be attempted.
107
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
108
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
109
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
110
What time of curve should we perform to detect upper airway obstruction?
Flow volume loop.
111
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
112
What lung volumes or capacities increase or decrease in restrictive diseases?
```
DECREASES:
TLC
TV
FRC
RV
VC
```
113
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
114
State the columns we look at during spirometry and the normal values
TLC, FVC, FEV1, % predicted: 80 to 120&
FEV1/FVC: actual and predicted within 5% of one another
FRC, RV % predicted: 75 to 120
DLCO % predicted: 60 to 120
115
What do we give patients with hypersensitivity pneumonitis
Steroids
116
What is TLCO/DLCO? Why do we do it?
Transfer Factor’ or ‘Diffusing Capacity of carbon monoxide in the lungs. This is done to assess lungs’ ability to transfer/diffuse gases from air in alveoli to red blood cells in capillary bed. It gives us vital information about the amount of functional capillary bed that is in contact with ventilated alveoli.
117
Why is helium included in the gas mixture given when performing the DLCO test?
We do this to determine the volume of lung available for the transfer of Carbon Monoxide. Due to its inert properties Helium does not transfer across the alveoli, but is instead diluted by the volume of lung present.
118
When we do the DLCO test, we give the patient a gas containing CO. What other gases are present with CO and what are their concentrations?
Gas mixture used to estimate TLCO consists of:
| 0.3% Carbon Monoxide, 14% Helium, 18% Oxygen with the balance being Nitrogen.
119
What reduces DLCO?
A decrease in ventilation or perfusion:
Interstitial lung disease: Pulmonary Fibrosis (be it drug induced, resulting from pneumoconiosis, collagen disease, or whatever the case may be)
• Where the lung surface area is reduced: Emphysema, Pneumonectomy (removal of part of the lung)
• Anemia
• Glaucomatous disease (Sarcoidosis),
120
What increases DLCO?
Increased perfusion:
Polycythemia Vera
Alveolar hemorrhage eg goodpasture’s syndrome
121
How can we measure residual volume?
Not by spirometry but by He method or plethysmography
122
Difference between he dilution and plethysmography?
Helium dilution measures the volume of gas in those parts of the lungs that are ventilated, as oppose to Plethysmography, which measures the amount of gas in the thorax, including areas that are not ventilated – this is referred to as Thoracic Gas Volume (TGV).
123
At which % FEV1/FVC can we say is an obstructive lung?
Less than 70%
124
What is the result of a DLCO test in a COPD patient?
Decreased.
125
State all the different methods of diagnosis of a COPD patient
Clinical (symptoms and signs)
Pulmonary function tests: Spirometery, plethysmography, DLCO, 6 minute exercise test
Radiology (X-ray, CT)
Laboratory tests (ABG, CBC, eosinophils level, alpha 1 anti trypsin, sputum culture and sensitivity)
126
What are the findings in the chest x ray and CT of a COPD patient
X-ray:
Hyperinflated Chest (very large)
Ribbon shaped heart (small heart in comparison to chest size)
Hyper translucency (chest darker than usual due to increased air )
Flattened diaphragm
CT:
Enlarged alveoli and thickened airways.
127
What CBC abnormality ,Amy be present in a patient of COPD
Secondary polycythemia: increased Hb as a compensatory mechanism to the hypoxia (hypoxia is due to the retained expired air, leading to high CO2 and V/Q mismatch in emphysema)
128
Why do we perform sputum culture and sensitivity
to identify causative bacteria and select proper antibiotics
129
Why do we test for alpha one antitrypsin
If low, it confirms hereditary emphysema
130
Why do we test for blood eosinophils in a COPD patient
Blood eosinophil count (if <100 cells/uL = less likely to respond to inhaled corticosteroid (ICS))
131
Complications of COPD?
Respiratory Failure: low PO2 + high PaCO2 (type II)
2- Heart Failure: core pulmonale, pulmonary hypertension
3- Pnuemothorax
4- Bronchiectasis
5- Depression
6- Recurrent Exacerbations
132
What is usually the cause of acute exacerbations in a COPD patient?
Infection
133
State the drugs given to COPD patients
```
Mucolytics
Anti inflammatory
Bronchodilators
Alpha 1 antitrypsin if deficient
Can be given oxygen
```
134
What are the three classes of bronchodilators
B2 agonist
Anti cholinergics/ muscarinics
Methylxanthinws
135
What are the long and short acting B2 agonists and their side effects
SABA: Salbutamol
LABA: Formetorol
Side effects: Arrythmias, anxiety, tremors, hypokalemsi
136
What are the long and short acting anticholimergics and their side effects
Short acting: Ipratropium bromide
LAMA: Tiotropium
Side effects: dry mouth, metallic taste
137
Which has been proven to work better for reducing COPD exacerbation, LAMA or LABA?
LAMA
138
What are the long and short acting methylxanthines and their side effects
Short acting: aminophylline
Long acting: theophylline
SERIOUS SIDE EFFECTS
Cardiac: tachycardia, arrhythmia
CNS stimulation: Headaches, insomnia, dizziness, convulsions
GIT: nausea, vomiting, diarrhea, gastritis
139
When mexylxanthines are given with LABA, what effect does it have on pulmonary function?
Improves FEV1
140
How do anti inflammatory drugs aid a COPD patient?
Decrease FEV1 decline, exacerbation and dsypnea.
141
What are the anti inflammatory drugs we give COPD patients
SPIM:
Systemic / inhaled corticosteroids
Phosphodiesterase inhibitors
Macrolides
142
When are ICs most effective in a COPD patient?
When given with LABA/ LAMA
| If blood eosinophils are over 300
143
What is a common side effect with incorrect ICS use?
Oral candidiasis
144
In what cases do we give a systemic corticosteroid?
Acute exacerbation
145
Side effects of systemic corticosteroids
Immunosuppression: risk of infection/ pneumonia
Muscle weakness
Gastritis/peptic ulcer
Mineralocorticoid action: Hypertension, hyperglycemia (loss of diabetes control), edema
Osteoporosis
loss of endogenous cortisol
146
In what cases do we need to use macrolides and phosphodiesterase inhibitors?
Patient continuing to get exacerbations with combined ICS/LABA/LAMA use.
Phosphodiesterase inhibitor roflumilast only used in patients with FEV1<50%
147
What can we NOT use with phosphodiesterase inhibitors?
Methylxanthines
148
Name the macrolide and phosphodiesterase inhibitor we give COPD patients
Roflumilast (phosphodiesterase inhibitor)
| Azithromycim, 250mg/ day, 1 year.
149
Hallmark of COPD?
Persistent, progressive productive cough with dyspnea
150
Name a common ICS
Budnesonide
151
What are the 4 things we use to asses a COPD patient?
1. mMrc scale = degree of dyspnea
2. GOLD 1-4 scale= looks at FEV1 post bronchodilator to judge airway obstruction
3. Number of exacerbations in the last year
4. Comorbidities and smoking status
152
State what each score in the GOLD 1 to 4 system means.
This system looks at FEV1 post bronchodilator to show the level of airway obstruction
1 (MILD) = FEV1 is equal to or greater than 80% of predicted
2 (MODERATE)= FEV1 is between 50% of predicted and 80% of predicted (can be equal to 50 but not equal to 80)
3. (SEVERE): FEV1 is between 30% of predicted and 50% of predicted (can be equal to 30 but not equal to 50)
4. (VERY SEVERE): FEV1 is less than 30% predicted.
153
In a COPD patient, what is considered mild, moderate or severe exacerbation history?
0-1 NOT LEADING TO HOSPITAL ADMISSION: mild
| 1 leading to hospital admission or 2 or more exacerbations: moderate to severe exacerbation history
154
When creating a treatment plan for a COPD patient, how do we decide the treatment needed?
Do,boned score of GOLD 1 to 4 and GOLD ABCD
155
What is the gold ABCD score
GO TO NOTES AND MEMORIZE IT FROM THERE.
156
State the medication given for each group of the ABCD GOLD system
A: bronchodilator
B: LAMA or LABA
C: LAMA
D: LAMA / LAMA + LABA / ICS + LABA ( if eosinophils are over 300)
157
Management of acute exacerbation?
1. Exclude other differentiatial diagnoses such as PE, acute coronary syndrome, pneumothorax
2. OCS for 5-7 days
3. Rapidly acting B2 agonist and antimuscarinic
4. Oxygen therapy if saturation is less than 88 or if the patient has right heart failure or polycythemia
5. Possible mechanical ventilation
158
When giving a COPD patient O2 therapy, what is our target saturation?
92-94% (Don’t exceed 92% (target: 88-92%) if PCO2 is high = “Type II respiratory failure”). This is because if the hypoxia is corrected the patient may lose his respiratory drive
159
what area in Egypt has a lot of people who get mesothelioma
Mesothelioma = ASBESTOS = HELWAN
160
What do we use in spirometry to confirm bronchial asthma
post BD: 12%+ change
AND
200ml+ change in FEV1
161
What is the main line of treatment of COPD and asthma?
COPD: bronchodilators
Asthma: anti inflammatory drugs
162
Should methylxanthines be used in bronchial asthma?
No due to SERIOUS SIDE EFFECTS:
| Gastritis, convulsions.
163
When should COPD patient be given OCS?
Acute exacerbation, 5-7 days, prednisone from 20-40mg
164
Define lung interstitium
Pulmonary interstitium is a collection of support tissues within the lung that includes the alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues.
165
Gold standard for diagnosis of ILD?
High resolution CT.
166
Which ILD occurs LESS in smokers?
Sarcoidosis
| Hypersensitivity pneumonitis
167
What are the drugs that cause ILD?
Nitrofurantoin (UTI)
Methotrexate (immunosuppressive)
Amiodarone (K channel blocker, class III anti arrhythmic)
168
Major complaint of ILD?
Dry cough and dyspnea
169
Which ILD cause hemoptysis?
ILD associated with collagen vascular disease
| ⁃ Lymphangioleiomyomatosis (hormone related in females below 50)
170
Which ILD present with fever?
Collagen vascular disease–associated ILD
Sarcoidosis (up to one-third of patients)
Acute hypersensitivity pneumonitis Acute interstitial pneumonia
Certain pulmonary eosinophilic diseases
171
ILD associated with smoking?
Idiopathic pulmonary fibrosis
⁃ Pulmonary Langerhans cell histiocytosis
⁃ Respiratory bronchiolitis-associated interstitial lung disease
⁃ Desquamating interstitial pneumonitis
172
What does nitrofurantoin cause in the alveoli ?
Alveolar hemorrhage.
173
What is traction bronchiectasis
Bronchial enlargement due to pulling by fibrosis
174
Which ILD is associated with clubbing
IPF
175
How are Spirometery values affected by ILD?
They are RESTRICTIVE, therefore all lung volumes decrease.
Reduced total lung capacity, ‾ Reduced residual volume ‾ Decreased static compliance ‾ Reduced VC, often with an increased FEV1/FVC ratio ‾ Reduced diffusing capacity for carbon monoxide (DLCO)
176
What are the ILD that present with a substantial component of airway obstruction?
Sarcoidosis
2. Hypersensitivity pneumonia
3. Lymphangioleiomyomatosis
4. Langerhans’ cell histiocytosis
5. Constrictive bronchiolitis (Expiratory wheeze refractory to inhaled bronchodilators)
6. Respiratory bronchiolitis–interstitial lung disease
• In some patients, the coincidence of both restrictive and obstructive components, as occurs in interstitial lung disease associated with asthma or chronic obstructive pulmonary disease, can lead to normalization of lung volumes
177
Why do patients of ILD experience hypoxemia?
Ventilation perfusion inequality.
178
How do we prove the dyspnea on exertion of ILD patients?
6 minute walk test
179
Why do we do bronchoalveolar lavage?
To rule out infections: e.g. 50% eosinophils show’s eosinophilic pneumonia
or malignancy
180
How do we diagnose alveolar hemorrhage?
Increasing red cell count on sequential BALs >20% →Hemosiderin-laden macrophages
181
Describe the BAL of alveolar proteinosis
milky BAL fluid with debris and foamy macrophages)
182
BAL results of langerhaan cell histocytosis?
→Langerhans’ cells >3% total BAL cell count →CD1a & S100 positive
183
Flow-cytometric analysis of lymphocyte subsets in cases of suspected: →Hypersensitivity pneumonitis?
CD4/CD8 <1
184
Flow-cytometric analysis of lymphocyte subsets in cases of suspected: → Sarcoidosis?
CD4/CD8 ≥ 2.5
185
Increased percentage of BAL neutrophils appear to portend a worse prognosis in?
Sarcoidosis
2. Hypersensitivity pneumonitis
3. Idiopathic pulmonary fibrosis
186
What diagnoses sarcoidosis with up to 90% sensitivity?
Trans bronchial biopsy
187
Hallmarks of ILD?
Cough, dyspnea, inspiratory crackles, hypoxia, maybe clubbing
188
Treatment of ILD
Smoking cessation Treatment
• Providing oxygen to hypoxemic patients
• Pulmonary rehabilitation
• Pneumococcal and influenza vaccination
• Removal of offending environmental agents, such as:
→Tobacco smoke in desquamative interstitial pneumonia and respiratory bronchiolitis–ILD →Specific antigens in hypersensitivity pneumonitis →Medications in drug-induced pulmonary reactions
• Corticosteroids and immunosuppressants (cyclophosphamide, azathioprine, methotrexate)
• Plasmapheresis (Diffuse alveolar hemorrhage)
• Avoid pregnancy & give sirolimus in LAM
• Cladribine may be effective in PLCH
• For whole lung lavage & GM-CSF therapy in PAP
• Lung transplantation (definitive management for any end stage lung regardless the
189
State the main features of sarcoidosis
Histologically identified by non caseating granulomas
Occur in people aged 20-40, more common in blacks
Systemic disease of unknown cause, can affect any organ but mostly affect the lungs
Hilar and paratracheal adenopathy, positive d’espine sign
190
What is erythema nodusm and where is it found?
Löfgren's syndrome, acute form of sarcoidosis. They are reddish, painful, tender lumps most commonly located in the front of the legs below the knees
191
What is the initial modality for sarcoidosis staging?
Chest x ray
192
Which modality shows parenchymal involvement in sarcoidosis?
High resolution CT
193
End result of any ILD?
Honeycombing and traction bronchiectasis
194
What are the 4 stages of disease found on chest film for a sarcoidosis patient?
(the stages are not progressive):
1. Bilateral hilar lymphadenopathy
2. Bilateral hilar lymphadenopathy+ pulmonary disease
3. Only pulmonary disease (reticulonodular shadows)
4. Irreversible fibrosis and honey combing
195
State the findings of the following tests in a sarcoidosis patient :
1. Labs
2. Pulmonary function tests
3. Bronchoalveolar lavage
4. Transbronchial biopsy
1. Labs:
Full blood count: may show mild normochromic normocytic anemia with raised ESR
* Biochemistry: (due to increased circulation of vitamin D produced by Macrophages) →Hypercalcemia occurs in 10-20% →Hypercalciuria in 30-50%
* Serum angiotensin-converting enzyme level (ACE):
→Elevated in over 75% of untreated sarcoidosis patients (non-specific) → to monitor disease activity & response to treatment
2. Pulmonary function: restrictive lung defect with reduced gas transfer in patients with parenchymal infiltration or fibrosis
3. BAL: lymphocytosis with raised CD4:CD8 ratio >2.5 is diagnostic
4. Transbronchial biopsy: positive in up to 90% of cases of pulmonary sarcoidosis.
196
What is the definitive diagnosis of sarcoidosis?
Non caseating granulomas on biospy
197
Treatment of sarcoidosis?
First line treatment is with prednisolone(or equivalent) 0.5 mg/kg for 4-6 weeks with gradual tapering to a maintenance dose for at least 12 months.
• Immunosuppressants: ‾ Methotrexate ‾ Azathioprine ‾ Hydoxychloroquine
198
What is the d’espine sign?
d'Espine sign is bronchial breathing heard over the vertebral spines (on the back) below the level of tracheal bifurcation; below the fourth thoracic spine in adults if there is subcarinal (mediastinal) lymphadenopathy.
199
Old man, smoker, chest symptoms. What do you suspect?
Bronchogenic carcinoma.
200
Define pneumonia
Patchy or diffuse inflammation of lung alveoli with consolidation
201
Innate lung defense mechanisms?
Entrapment in mucus blanket
Phagocytosis by alveolar macrophages
Phagocytosis by neutrophils
Complement by alt. pathway =C3b =enhances phagocytosis
Organisms reaching Lymph nodes via Antigen presenting cells à initiate immune response
202
Describe lobar pneumonia
Acute, diffuse inflammation of the Alveoli in one or more lung lobes by droplet infection of pneumococci. Usually in diabetics or cancer patients (immunocompromised)
203
4 stages of lobar pneumonia?
Congestion (early, 1-2 days)
2. Red hepatization (3-4 days): Congested capillaries& Interalveolar :
PNLs, RBCs, Organisms, Fibrin
3. Grey hepatizatiion (1 week): Increased fibrin Disintegrated RBCs&PNLs Clear zone
4. Resolution (1-2 weeks)
204
Complications of lobar pneumonia?
1. Organization of the exudate leaves a firm lung behind.
2. Lung Abscess
3. Septicemia:
- Endocarditis and pericarditis.
- Meningitis.
- Arthritis.
4. Toxemia with toxic myocarditis and heart failure
205
Describe bronchopneumonia
Patchy consolidation of the lung (NOT DIFFUSE)
• Initial affection of bronchi and bronchioles with extension into the surrounding alveoli.
• Affection is bilateral and basal.
• Usually seen in extremes of age (VERY YOUNG OR VERY OLD)
206
Gross picture of bronchopneumonia?
Nodules around bronchi and bronchioles are
bilateral, basal, firm and exude pus on pressure.
Enlarged hilar lymph nodes
207
Microscopic picture of bronchopneumonia?
Lumen: filled by pus and shed epithelial cells.
Mucosa: focal ulceration Submucosa: dilated, congested B.V. & heavy PNL infiltrate
2. Neighboring alveoli filled by PNLs, R.B.Cs, epithelial cells, macrophages & fibrin
208
What are the zones of an early abscess (2)
1, central necrosis
| 2, pyogenic membrane: Zone of inflammation, PNLS, dilated BV, fibrin network
209
What are the zones of an late abscess (3)
1. Central necrosis
2. Pyogenic membrane
3. Granulation tissue
210
Aetiologiy and predisposing factors of lingo abscess?
Aspiration of oropharyngeal contents What are the common predisposing factors in this case?
* Periodontal disease
* Seizure disorder
* Alcohol abuse
* Dysphagia
• Diminished gag or cough reflex, caused by a state of impaired consciousness (examples include: alcohol or other CNS depressants, general anaesthesia, or encephalopathy)
2. Infection of a preexisting bulla or lung cyst
3. Secondary to carcinoma of the bronchusà bronchial
obstruction causes post-obstructive pneumonia à +/- abscess formation
211
What is unique about atypical pneumonia?
No signs of consolidation
212
Organisms causing atypical pneumonia?
```
Mycoplasma pneumoniae
Legionella pneumophilia serogroups 1 & 6
Chlamydia group
Coxiella burnetii
Pneumocystis jiroveci (carinii)
Respiratory viruses
```
213
Complications of atypical pneumonia
Viral etiology = nViremia
* Bacterial infection=Septic bronchopneumonia
* Healing by fibrosis=pulmonary fibrosis& right sided heart failure
214
Who does opportunistic pneumonia happen to?
Immunosuppressed (HIV)
215
What is the most common organism causing an opportunistic infection in HIV patients?
Pneumocystis jiroveci pneumonia (PJP)
216
Define simple pulmonary aspergillosis
Aspergillosis in an already damaged part of the lung. development of a fungal ball in preexisting cavities (old tuberculosis or cystic diseases of the lung). No hyphal invasion occurs when the patient is immunocompetent
NO INVASION OF THE WALL OF THE CAVITY
217
What type of species is Aspergillosis and where is it found
Fungus. Found in air, ground, plants. Found intra pulmonary and in the nasal cavity.
218
Aspergillosis is a hyphae. What are hyphae?
Hyphae are the tubular projections of multicellular fungi that form a filamentous network (mycelium)
219
What is chronic aspergillosis
• A state of transformation from the noninvasive form into the invasive pulmonary disease
• Almost always affects patients with some form of underlying respiratory pathology that results in the formation of an airfilled cavity or bulla
• Takes place when defense mechanisms of the host are hlowered
Pathology:
The cavity wall is eroded and invaded by elongated hyphae Acute and chronic inflammatory infiltrate, fibrosis and necrosis in various degrees
220
Describe invasive aspergillosis
IMMUNOCOMPROMISED HOST
• The clinical presentation is relatively rapid, ranging from days to a few weeks
• Invasion of lung tissue by hyphae
• Invasion of blood vessels, leading to widespread infection
221
What are the two histological patterns of invasive aspergillosis?
1. A discrete nodule of well-demarcated coagulation necrosis in which numerous hyphae are aligned in a radial pattern
• Acute hemorrhage surrounds the area of coagulation necrosis
• Reduced number of inflammatory cells (patients with bone marrow suppression)
2. Lobular consolidation and bronchopneumonia (alveoli filled with neutrophils)
222
What do we call a hypersensitivity reaction to aspergillosis?
Allergic bronchopulmonary aspergillosis
223
What do we use to stain m.TB
Ziehl neelsen.
224
TB routes of infection?
Droplet infection (most common) = Infection of lungs and tonsils
2. Ingestion of raw milk containing bovine bacilli = Infection of tonsils and intestines
3. Contact infection = Skin
* THESE ARE ALL PRIMARY SITES
225
Mechanism of granulomas formation in Aztec?
1. M.TB is ingested by macrophage in the bronchi
2. M.TB prevents macrophages from being engulfed by lysosomes so it stays in the macrophage and replicates
3. Macrophage ruptures and attracts more macrophages
4. Macrophages present bacilli to Th1 cells
5. Th1 cells produce INF gamma to attract more macrophages
6. Activated macrophages secrete IL12 and INF gamma
226
What is a tubercle
Granuloma of m.TB
227
Contents of tubercle
CENTRALLY: macrophages, epithelioid cells ,& giant cells +/- coagulation necrosis
PERIPHERALLY: Peripheral T lymphocytes and fibrosis
228
What do we call a primary TB complex and what is it composed of
GHON’S COMPLEX, COMPOSED OF:
Ghon’s focus [underneath the pleura, middle third of the lung, area of consolidation, circumscribed, yellowish with central necrosis, about 1-1.5cm]
Lymphangitis inflammation of draining lymphatic vessels
Lymphadenitis caseous TB of hilar lymph nodes
229
Fate of primary TB?
1. Healing: with mild infection and good patient’s resistance Lesion gets fibrosed and encapsulated
2. Spread of infection:
a. Direct spread to the lung &/or pleura
b. Blood spread: Depends on the number of bacilli (the more the number of bacilli the more the spread)
3. Encapsulation and reactivation at a time of lowered body resistance
230
What long term effect can secondary TB leave on the lung?
Cavitation
231
Where does secondary TB usually occur?
Apices of the lung
232
Who gets progressive pulmonary TB and what are its types?
```
Elderly or immunosuppressed
• Cavitating TB (Apical lesion enlarges, Expansion of area of caseation creating a ragged cavity)
• Tuberculous bronchopneumonia
• Single organ TB
• Miliary TB
```
233
What does miliary pulmonary TB look like
Scattered small (< 2 mm) consolidation foci of consolidation
• Foci of consolidation may expand and fuse
234
How does pulmonary miliary TB turn systemic?
Infective foci in lungs enter the systemic circulation
• Liver, spleen, bone marrow, adrenals, meninges, kidneys, fallopian tubes and epididymis common
• Prognosis poor despite treatment
235
What is TB of the spine called? What is its prognosis and what imaging modality is used to check for it?
Pott’s disease, prognosis good with treatment. MRI
236
Complications Of secondary TB?
1. Infection of the pleura
2. Infected sputum causes intestinal tuberculosis
3. Erosion of blood vessels traversing the tuberculous cavity leads to severe coughing of blood (hemoptysis)
4. Extensive lung fibrosis = heart failure
237
What is the mycobacterium avum/ intra cellulare complex?
MA and MI are different species
• Atypical mycobacterium
• Opportunistic infection
• Uncommon except in AIDS with low CD4 lymphocytes
• Organisms proliferate in lungs and GI tract
• Clinically: Fever, drenching sweats and weight loss
Abundant acid-fast bacilli within macrophages
• Granulomas and necrosis rare in immunodeficient patients
238
What are the methods we can use for TB diagnosis?
Direct smear microscopy (Ziehl neelsen, fluorescent)
Culture & sensitivity
Detection of metabolic end product of bacilli (radiometeric technology)
Detection of immune response (lymphocyte markers and TST)
239
What are the media that we can use for culture and sensitivity of TB?
```
Egg based
Agar based
• Middlebrook 7H10 or 7H11
Liquid based
• Middlebrook 7H9
```
240
When using radiometric technology to secrete end product of bacilli, what is the agar used and what indicates a positive result for m.tb?
Liquid agar midlebrook 7H12
| Positive culture means that a GI ≥10
241
How do we identify drug resistance to certain TB drugs
PCR to detect mutations of the TB which may cause resistance to certain drugs
242
What are the lymphocyte markers we use confirm TB
Adenosine delaminate
| IFN gamma since it is released by Th1 cells in response to TB
243
What type oh hypersensitivity reaction does the TST count on and what is a positive test?
Tests for memory cells, type IV hypersensitivity reaction
| Induration 5-15mm: positive
244
What is a disadvantage of using TST?
It shares the same antigens as the bcg vaccine. Therefore, after a positive TST, we should do IFN gamma since it does not share antigens with the tuberculin skin test.
245
What is a latent tb infection?
State of persistent immune response to stimulation by Mycobacterium tuberculosis antigens without evidence of clinically manifested active TB ▪ Diagnosis of LTBI →TST
246
First line anti TB drugs?
```
Isoniazid
Rifampicin
Ethambutol
Pyrazinamide
Streptomycin
```
247
Side effects of the anti TB drugs
Rifampicin = red orange discoloration of urine
Ethambutol = should not be used with kidney disease / causes Optic neuritis/ should not be given to children
Isoniazid: peripheral neuropathy
Streptomycin: cannot be used in pregnant females
Pyrazinamide: arthritis, gout like symptoms
248
What is the regimen for TB infection
2 months on Rifampicin, isoniziade, ethambutol, pyrazinamide, then:
4 months on rifampicin and isoniazide only
249
What do we give a patient With TB meningitis
Same drugs but replace ethambutol with streptomycin
250
What do we give patients with TB of any serous sac?(TB meningitis, pericarditis, peritonitis & pleuritis)
Must take adjuvant steroids with anti TB drugs to prevent fibrosis.
251
How can a fetus be born with TB?
Hematogenous dissemination through placenta (50% of cases) = Primary complex formation in liver or lungs
Aspiration or ingestion of infected amniotic fluid = Primary disease in the lungs or gastrointestinal tract
252
Which anti TB drugs are hepatotoxic?
Isoniazid
* Pyrazinamide
* Rifampicin
253
Which TB drugs are safe in pregnancy
All but streptomycin
254
Ways of spread of TB to other parts of the body?
Direct spread from an adjacent organ
Hematogenous dissemination
Lymphatic
255
What do we call the generalized haematogenous spread of TB?
Miliary TB. Uncontrolled massive dissemination can occur during:
⁓ Primary infection
⁓ After reactivation of a latent focus
256
What are the side effects of TB in the bone marrow?
Anaemia
- Thrombocytopenia
- Leukemoid reaction (increased white blood cell count)
257
How can the most dangerous form of TB (TB meningitis) be prevented?
Bcg vaccine in childhood
258
Who commonly gets TB peritonitis?
Alcoholics with cirrhosis
259
TB pericarditis symptoms?
```
FPPP:
Fever
Pleuritic Chest pain
Pericardial tamponade: causing dyspnoea, neck vein distention, paradoxical pulse, muffled heart sounds, and possibly hypotension
Pericardial frictional rub
```
260
What causes decreased immunity in the lung?
Suppressed cough (e.g.,cerebrovascular stroke)
- Inhibited Cilia (e.g., smoking, Immotile Cilia)
- Defective alveolar macrophages, neutrophils defective phagocytosis of microorganisms
(e. g., old age, chronic diseases, HIV, corticosteroid, chemotherapy)
- Impaired Immunoglobulin production in lungs (IgA)
261
Most common organism causing CAP?
Streptococcus pneumoniae
262
Risk Factors for Specific/Resistant Bacteria?
Recent Hospitalization + Receipt of IV antibiotics in last 90 days
2- Previous isolation of Pseudomonas aeruginosa or Methicillin-resistant Staphylococcus aureus (MRSA)
3- Comorbidities (chronic heart, lung “e.g., bronchiectasis, cystic fibrosis”, liver, or renal disease (dialysis); diabetes mellitus; alcoholism; malignancy; or asplenia.
263
In what cases do we hear bronchial breathing?
Pulmonary mass
Collapse
Cavity
Consolidation
264
Clinical examination of pneumonia?
Vital Signs
- Fever
- Tachycardia
- Hypotension (Shock)
- Tachypnea
- SpO2 % (respiratory failure)
Examination
- Cyanosis
- Inspection: Working accessory Muscles
- Percussion: Dullness
- Auscultation:
- Breath sounds
- Bronchial breathing
- Crackles (crepitations
265
How do we differentiate between bacterial and atypical pneumonia on ct?
Atypical: GGOs
Bacterial: consolidation
266
According to the IDSA score, what is severe pneumonia?
1 major criteria or 3 minor criteria (check notes)
267
What tests do we need to do when we suspect pneumonia?
Radiological
- Chest X-ray
- CT Chest
Laboratory
- Complete Blood Picture
- Arterial Blood Gases
- Blood Urea Nitrogen
- ALT AND AST (check liver function to exclude end organ failure due to shock)
- ESR AND CRP
- Coagulation profile
268
In hospitalized patients / severe pneumonia/ resistant strain, what further tests should be done?
Sputum gram stain ( For intubated patients, an endotracheal aspirate sample should be the target sample to test since they cannot cough up the sputum)
Sputumculture and sensitivity
Blood culture and sensitivity
Urinary Antigen Testing for Legionella and Pneumococcal bacteria
PCR in viral outbreaks
269
What is procalcitonin and when do we test for it?
Used to differentiate between bacterial and viral pneumonia . high procalcitonin level (>0.25 mg/L ) correlates with high probability of a bacterial infection
270
How do we decide if the patient should be treated at home, in ward or in ICU?
CURB-65. Check notes
Score 0 – 1 Home (outpatient)
*Score 2 Ward
*Score 3 – 5 (or Severe CAP by IDSA/ATS) ICU
271
According to your curb-65 score, what should your treatment be?
AT HOME:
No comorbidities: B lactam: (amoxicillin) / doxycycline or macrolide
With comorbidities: monotherapy of fluoroquinolones OR amoxicillin with one of the two medications above
INPATIENT NON SEVERE IDSA:
B lactam + macrolide or monotherapy fluoroquinolone and anti mrsa/pseudomonas(Vancomycin) until culture proves there’s no mrsa
INPATIENT SEVERE IDSA:
Beta lactam AND fluoroquinolones AND Anti-MRSA or AntiP. aeruginosa. Based on Culture result: keep/stop the third antibiotic
272
When should we use corticosteroids in CAP.
Corticosteroid should not be used in treatment of CAP EXCEPT in patients with Septic Shock refractory to adequate fluid resuscitation and vasopressor support
273
When do use add anti aneorbic antibiotics to the antibiotics we give to CAP patients?
Add Specific anti-anaerobic Antibiotic to empirical antibiotic ONLY if LUNG ABCESS or EMPYEMA is Suspected
(We get anaerobic bacteria through aspiration pneumonia)
274
How can we prevent CAP
INFLUENZA VACCINE
275
What could seizures, alcohol, stroke mean when it comes to pneumonia?
High risk of aspiration pneumonia
276
What is an example of an anti anaerobic antibody?
Clyndamicin
277
Two most common complications of lung abscesses?
Epmyema and lung abscess
278
Examples of anaerobic bacteria?
Anaerobic bacteria Streptococcus pneumonia; Haemophilus influenzae; Staph aureus;
279
Pretest probability of PE?
Geneva score
280
Mainstay treatment of asthma?
Inhaled corticosteroid (budenoside)
281
When do we give OCS to asthmatics?
Usually in Exacerbations; not for regular treatment Ø Example: Prednisolone 40 mg/day for 5-7 days Ø Not recommended for longer duration Ø Increases risk of pneumonia and systemic side effects!
282
Side effects of B2 agonists?
Tachycardia, Arrhythmia § Hypokalemia § Tremors § Anxiety
283
Triad of aspirin induced asthma?
Triad: rhinitis + sinusitis + asthma
*Avoid Aspirin/NSAID *
Give LTRAs
284
Preferred reliever of asthma?
ICS formeterol
