Week 6 Flashcards
(194 cards)
1
Q
What thoracic cage disorders cause restrictive conditions?
A
- Kyphosis
- Scoliosis
- Ankylosing spondylitis (an inflammatory disease that, over time, can cause some of the bones in the spine (vertebrae) to fuse)
- Flail chest
2
Q
Why does kyphosis, scoliosis, ankylosing spondylitis cause restrictive conditions?
A
- mechanical restriction of the rib cage causing reduced compliance of chest wall and therefore inability to bring in large volumes during inspiration
3
Q
What symptoms are seen with restrictive conditions caused by kyphosis, scoliosis, ankylosing spondylitis?
A
- rapid, shallow breathing
- dyspnea on exertion
- reduction in all lung volumes (for PFTs)
4
Q
What is flail chest?
- Explain the changes during inspiration and expiration
A
When there is a flail segment that moves paradoxically to the rest of the chest wall
- On inspiration the chest wall is supposed to expand while the flail segment moves inwards
- On expiration chest wall comes inwards while flail segment moves outwards - bulge
5
Q
What is poliomyelitis?
A
- Polio virus that leads to paralysis, muscular atrophy, and often disability and deformity
6
Q
What is guillan-barre syndrome?
A
- A rare neurological disorder in which the body’s immune system mistakenly attacks part of its peripheral nervous system
7
Q
What is amyotrophic lateral sclerosis (ALS)?
A
- Progressive nervous system disease that affects nerve cells in the brain and spinal cord, causing loss of muscle control
8
Q
Myasthenia Gravis
A
- A chronic autoimmune disorder in which antibodies destroy the communication between nerves and muscle, resulting in weakness of the skeletal muscles
9
Q
Why do neuromuscular disease cause restrictive disorders?
A
- Difficulty in increasing the volume of the thoracic cavity during inspiration due to weakness of the respiratory muscles
- symptoms don’t present until diaphragm is involved
10
Q
What are major manifestations of respiratory muscle weakness? (2)
A
- insufficient ventilation - decreased tidal volume → compensated by increased respiratory frequency
- ineffective cough - caused by weakness of respiratory muscles so individual is unable to expel mucus which predisposes patients to aspiration, pneumonia, respiratory failure
11
Q
With neuromuscular disease what are the changes in
- FVC
- FEV
- FEV/FVC ratio
- TLC
- DLCO (diffusing capacity)
A
- decreased
- decreased
- normal
- decreased
- normal because lung parenchyma is unaffected
12
Q
What is
- FVC
- FEV1
A
- Forced vital capacity ; This is the amount of air exhaled forcefully and quickly after inhaling as much as you can.
- Forced expiratory volume: measures how much air a person can exhale during a forced breath in the first second
13
Q
How does nicotine act on nervous system of a user? (3)
A
- Nicotine enters brain in 10-20 seconds and acts on mesolimbic reward pathways
- With mesolimbic reward pathway activated → there is release of large amounts of dopamine
- This produces mood-elevating and behaviorally reinforcing effects
14
Q
How does nicotine cause hypercoagulable states?
A
- There are oxidant gasses in tobacco smoke that induce hypercoagulable state leading to platelet aggregation and thrombosis
- This increases risk of MI
15
Q
How does nicotine affect sympathetic nervous system?
A
- It activates the sympathetic NS and leads to increase heart rate, increase BP, myocardial contractility, increase coronary artery vasoconstriction
16
Q
What are the types of nicotine replacement therapies? (5)
A
- patch
- gum
- lozenge
- oral inhaler
- nasal spray
17
Q
How does nicotine replacement therapies (NRTs) affect a smoker?
A
- work on same addiction pathways to help reduce withdrawal syndromes
- Nicotine delivery is slower to the mesolimbic reward pathways - so smokers doesn’t get the same pleasurable experiences but also don’t get extreme withdrawal symptoms
18
Q
What are the non-nicotine medicators?
A
- bupropion
- varenicline
19
Q
- What is the mechanism of action of bupropion (zyban)?
- What individuals should not get this drug?
A
- Blocks neural reuptake of dopamine and/or norepinephrine to relieve cravings
- Patients with history of seizures
20
Q
What is the best effective first line smoking cessation treatment?
A
two nicotine replacement therapies at the same time
- a long acting formulation + a short acting formulation
* this is to prevent onset of severe withdrawal symptoms
21
Q
Out of the Nicotine replacement therapies which ones are long acting formulation and short acting formulation?
A
- Long acting - nicotine patch
- short acting -everything else (gum, lozenge, inhaler, or nasal spray)
22
Q
What is the difference between obstructive vs restrictive lung disease?
A
Obstructive lung diseases include conditions that make it hard to exhale all the air in the lungs.
People with restrictive lung disease have difficulty fully expanding their lungs with air.
23
Q
What diseases are included in obstructive lung disease? (4)
A
- emphysema → lead to COPD
- chronic bronchitis → lead to COPD
- asthma
- bronchiectasis
24
Q
Obstructive Lung Disease
What are the changes in spirometry values
- FVC
- FEV1
- FEV1/FVC ratio
A
- FVC - decreased
- FEV1 - very decreased
- Decreased FEV1/FVC ratio
25
Restrictive Lung Disease
What are the changes in spirometry values
1. FVC
2. FEV1
3. FEV1/FVC ratio
1. Decreased FVC
2. Decreased FEV1
3. Normal or even increased FEV1/FVC ratio
26
What disease categories are included in restrictive lung disease? (3)
1. Chest wall disorders
2. Acute interstitial lung disease such as ARDS (acute respiratory distress syndrome)
3. Chronic interstitial lung diseases
27
1. What are bullae in lungs?
2. What complications can this lead to?
1. Air pockets within lung parenchyma that have thin or poorly defined wall
2. Can rupture and cause pneumothorax because air goes into chest cavity and can lead to collapse of the lung
3. Bullae can get to a point where it acts as a pump → pumping air into thorax and causing tension pneumothorax
28
How does emphysema occur after inhaling irritants such as smoking? (4)
1. Tobacco smoke makes ROS which starts inflammatory response, inactivates antiproteases
2. Neutrophils work against ROS and increase production of proteases which can no longer be regulated by antiproteases and leads to tissue damage - loss of elastic tissue in alveoli
3. Since there is less elastic tissue then compliance is larger - alveoli fill up more but have no elastic recoil so air gets trapped in alveoli. This also leads to collapse at alveolar opening/respiratory bronchiole
4. It is harder for person to breathe out
29
Differentiate between the different types of emphysema?
Centriacinar
1. What part of respiratory system and pathophysiology
2. What part of lungs
3. What is risk factor
1. Pulmonary emphysema mainly localized to the proximal respiratory bronchioles with focal destruction
2. Predominantly found in the upper lung zones
3. Seen with smoking
30
Differentiate between the different types of emphysema?
Panacinar
1. What part of respiratory system and pathophysiology
2. What part of lungs
1. Includes entire alveolar duct and associated with deficiency antiprotease activity (alpha -1- antitrypsin deficiency)
2. Lower lung zones
31
Differentiate between the different types of emphysema?
Paraseptal
1. What part of respiratory system
2. What part of lungs
3. What is risk factor
1. Proximal part of acinus (gas exchanging unit of lung) is normal but distal part is primarily involved
2. common in upper half of lungs, adjacent to pleura, areas of fibrosis, scarring, or atelectasis
3. Young adults with spontaneous pneumothorax
32
Differentiate between the different types of emphysema?
Irregular
1. What part of respiratory system
2. What part of lungs
3. What is risk factor
1. Acinus irregularly involved - almost always associated with scarring
2. variable parts of lung
3. inflammatory conditions can cause this type
33
What are some symptoms of emphysema?
1. Age range
2. Breathing
3. Lung noises
4. Description of patient
5. Shape of thorax/chest
6. Cough?
1. 50-75 years old
2. dyspnea - severe and early in disease (in panacinar dyspnea presents 20-30 yrs earlier than what is seen in centriacinar)
3. Wheezing
4. Pink puffer- difficulty catching their breath and their faces redden while gasping for air.
5. Barrel-chest
6. cough - late in disease with scanty sputum
34
What radiographic findings will you find with emphysema?
1. elongated thorax
2. flattened diaphragm
3. increased radiolucency (darkness) of lungs
35
What risk factor is very common for emphysema?
smoking
36
What is the pathophysiology and clinical description of chronic bronchitis?
1. Clinical diagnosis of persistent cough for at least 3 consecutive months in at least 2 consecutive years
2. Results from continuous inhalation of irritants resulting in mucus hypersecretion due to mucus gland and goblet cell hyperplasia
37
What are risk factors for chronic bronchitis?
Tobacco smoking and air pollution
38
What are some symptoms of chronic bronchitis?
1. Age range
2. Cough?
3. Breathing abnormalities?
4. Description of patient
5. complications from this?
1. 40-45 years old
2. chronic PRODUCTIVE cough
3. dyspnea on exertion - mild and occurs late in disease
4. Blue bloater- cyanosis because often take deeper breaths but can't take in the right amount of oxygen.
5. Chronic infections can occur
39
What changes in pathology can be seen with chronic bronchitis?
1. with mucous gland and goblet cell hyperplasia you see airway remodeling
2. the amount of remodeling can be determined by the Reid Index
40
What is the Reid Index?
1. ratio of thickness of mucous gland layer to bronchial wall
2. \< 0.4 is normal
3. 0.7 is severe
41
differentiate between chronic bronchitis and emphysema in…
1. age
2. dyspnea
3. cough
4. infections
5. airway resistance
6. elastic recoil
7. chest radiograph
8. clinical appearance
image
42
What are the four types of asthma?
1. Atopic (allergic or extrinsic)
2. Nonatopic (intrinsic)
3. Drug induced
4. Occupational
43
What is asthma?
* Episodic and reversible disease that is defined by increased irritability of the bronchial tree in response to stimuli
44
Describe early and late phase of atopic asthma?
1. Early phase - mast cells release histamine, prostaglandins, and leukotrienes to cause bronchoconstriction, increased mucus production, vasodilation
2. Late phase - leukocytes recruited and activated to initiate asthma + damage to epithelium
45
Describe with more details the process/steps to late phase atopic asthma? (3)
1. inhaled allergens elicit a TH2 response
2. IL - 4 is sent to B cells so B cells now favor IgE production
3. IL-5 does eosinophil recruitment - cause damage to epithelium and induce remodeling
46
What does remodeling look like in atopic asthma?
1. thickened mucus layer
2. goblet cell hyperplasia
3. thickening of smooth muscle
4. increased glands
5. angiogenesis
47
what causes lungs to be uncollapse on autopsy for a person with asthma/
* mucus plug, air cannot escape and leads to inflated lungs at autopsy
48
1. What are Curschmann spirals and charcot-leyden crystals and what do they look like?
2. In what condition are they found?
1. **Curschmann** - spiral-shaped mucus plugs from subepithelial mucous gland ducts of bronchi ;;;; **Charcot-leyden** -microscopic crystals composed of eosinophil protein galectin-10 found in people who have allergic diseases such as asthma;;; *image (spirals on left and crystals on right)*
2. asthma
49
1. What risk factors for nonatopic asthma?
2. Onset?
-not well understood
* triggers are respiratory viral infections and inhaled air pollutants
* adult age
50
1. What drugs cause drug induced asthma?
1. aspirin/NSAIDs
51
1. What risk factors for occupational asthma?
2. Onset?
1. fumes, chemical dust, gases, etc
2. adult age
52
What is bronchiectasis?
* Dilation of segments of airway which causes pooling of mucous which is subject to infection
* Sleep allows mucus to pool making the condition worse in the morning
53
What are some symptoms of bronchiectasis?
1. Fever
2. Dyspnea
3. Hemoptysis (spitting of blood that originated in the lungs or bronchial tubes)
4. and more
54
What are some pathology findings of bronchiectasis in gross anatomy?
dilated airways and mucous
55
What disease(s) causes bronchiectasis?
1. cystic fibrosis
2. Ciliary dyskinesia
56
What is the pathophysiology of cystic fibrosis? (3)
* Disorder of epithelial ion transporters affecting/inhibiting fluid secretion
* Dehydrated mucus is formed which is difficult to move and plugs up airway
* This type of mucus is also a good place for infection to occur - persistent lung infections can occur
57
1. Is cystic fibrosis autosomal recessive or dominant?
2. What mutation is associated with CF?
1. autosomal recessive
2. mutation in CFTR gene on chromosome 7
58
What is ciliary dyskinesia?
* Primary structural disorder of cilia causing abnormal ciliary motility
* Cilia look normal under the microscope but don’t function properly
59
1. What complications/disorders can be seen along with ciliary dyskinesia?
2. is ciliary dyskinesia autosomal recessive or dominant?
1. Kartagener syndrome/situs inversus: flipped organs on the wrong side of body
2. autosomal recessive
60
What is type A vs type B COPD?
1. Type A is typically emphysema
2. Type B is typically chronic bronchitis
61
What are the three factors that affect airway resistance?
1. Pattern of airflow
2. Diameter of airway
3. Lung volume
62
How does pattern of airflow affect airway resistance?
**If flow becomes turbulent, and the pressure difference is increased to maintain flow, this response itself increases resistance**. This means that a large increase in pressure difference is required to maintain flow if it becomes turbulent.
63
How does diameter of airway affect airway resistance?
1. airway resistance is inversely proportional to radius4
2. so if radius doubles then airway resistance decreases 16 fold
* extra info:
* airway resistance is proportional to length - so double the length you double the resistance
64
If larger radius in airway decreases resistance then why do small airways have such low resistance?
1. small airways are large in number and together have large surface area. This means that in fact together they have a large radius which decreases resistance in airway
65
How does lung volume affect airway resistance?
* as lung volume increases, airway resistance decreases
* with more lung volume, there is more expansion of alveoli
* As the alveoli expand they also exert tension on airways, pulling them open (known as radial traction) - thus airway diameter increases as lung inflates and reduces airway resistance
66
Why do individuals with obstructive disease ventilate at high lung volumes?
Because airway resistance is minimized at high volumes due to radial traction
67
What are three major causes of increased alveolar CO2?
1. increased CO2 production
2. hypoventilation
3. increased dead space
68
What happens during forced expiration that limits the amount of air expired at the end of exhalation?
1. peripheral ariways collapse and this limits flow
2. When you force expiration you cause positive intrapleural pressure which is greater than airway pressure
3. this causes collapse of airway
69
Describe the differences in airway pressures and pleural pressure to determine if airway closes or opens
* If PAW \> PPL then airway stays open
* If PPL \> PAW then airway closes
70
What is FRC and RV?
1. Functional residual capacity (FRC) is the volume of air present in the lungs at the end of passive expiration
2. Residual volume is the amount of air that remains in a person's lungs after maximal exhalation.
71
Describe how FRC and RV change in obstructive lung disease and why?
1. FRC is increased
2. RV is increased
* Both are increased because there is air trapping in obstructive lung disease
72
Describe how FRC and tidal volume change in restrictive lung disease and why?
1. Decreased tidal volume and FRC
2. Restrictive diseases stop the lungs from fully expanding. This limits the volume of air and amount of oxygen that a person breathes in
73
1. What does a spirometer measure? (two values that are similar)
1. volume of air inspired and expired with time
2. FEV1 (volume of air exhaled in first second of expiration)
3. FVC (total volume of air exhaled before next inspiration)
74
1. Why is FEV1 reduced in obstructive disease?
2. Why is FVC reduced?
* FEV1 is reduced because of increased airway resistance
* FVC is reduced because increased airway resistance causes earlier airway collapse/airway closure/etc
75
What is typically the ratio of FEV1/FVC for obstructive lung disease?
1. less than 80%
normal is 80%
76
1. Why is FEV1 reduced in restrictive disease?
2. Why is FVC reduced?
* FEV1 is reduced because of low total lung volume
* FVC is reduced because there is lower lung volume typical for these patients
77
What is typically the ratio of FEV1/FVC for restrictive lung disease?
1. can be higher than 80%
normal is 80%
78
What does DLCO test indicate or look at?
1. looks at how well diffusion capacity is at capillaries.
2. With conditions that interfere diffusion like decreased alveolar surface area, or thickness of membrane there are lower DLCO values
79
What is hypoxemia vs hypoxia?
1. Hypoxemia is low levels of oxygen in blood
2. Hypoxia is low levels of oxygen being able to be taken to tissue
80
What are the 5 causes of hypoxemia and describe if they have normal or increased A-a gradient?
1. Hypoventilation - normal A-a
2. Decreased oxygen content of air - normal A-a
3. V/Q mismatch
4. Shunt
5. Diffusion defects
81
How does hypoventilation lead to hypoxemia but normal A-a gradient?
1. With reduced alveolar oxygen there will also be reduced arterial oxygen (since less oxygen is available to be put into artery) - normal A-a gradient
82
What is the alveolar gas equation?
83
How does decreased oxygen content of air lead to hypoxemia but normal A-a gradient?
1. There is lower inspired O2 concentration (alveolar) so then then there is less oxygen able to get into arterial blood. The A-a gradient stays the same
84
How do you fix hypoxemia w/ normal A-a gradient?
give oxygen to increase alveolar oxygen
85
What three factors affect diffusion of oxygen from air to blood?
1. pressure difference between oxygen in air and blood
2. area of alveoli for diffusion (less air, less diffusion)
3. thickness of alveolar tissue (more thickness, less diffusion)
86
How does diffusion defects lead to hypoxemia and increased A-a gradient?
1. If diffusion is inhibited then less oxygen can get into arterial blood so there will be a greater difference between alveolar and arterial oxygen content
87
How does shunt lead to hypoxemia and increased A-a gradient?
1. At a shunt there is no ventilation but there is still perfusion. This means that V/Q = 0.
2. Blood is not being oxygenated when going from venous blood to arterial system at the “shunted location” When you average out blood at ventilated areas + blood coming from shunted areas the total blood in arterial system has low oxygen
3. inspired air (that goes to non-shunted areas) - arterial blood have larger A-a gradient
88
1. How does V/Q mismatch lead to hypoxemia and increased A-a gradient?
1. In places of the lung where there is reduced ventilation (inspired air) relative to perfusion (blood flow) there is perfusion wasted and blood is going where there is not enough O2 present
2. Since ventilation is reduced and not completely zero the blood at these alveoli still get oxygenated just not as much. When averaging the blood from areas of V/Q mismatch and non V/Q mismatch there is overall hypoxemia → increased A-a gradient
89
Out of the reasons for increased A-a gradient
* shunt
* V/Q mismatch
* diffusion defects
which can be improved with oxygen?
1. V/Q mismatch
90
How does blood flow and ventilation differ throughout the lung?
1. both blood flow and ventilation increase as you move from apex to base of lung
2. Blood flow increase a lot more by the time it gets to base of lung
91
What are the different V/Q ratios throughout the lung?
1. apex - has (high) V/Q \> 1 because at apex although both V and Q are low, Q is the lower of the two
2. Base - has (low) V/Q \< 1 because at base although both V and Q are higher than at apex, Q is higher of the two
92
What are the PAO2 and PACO2 of apex vs base of lung?
1. Highest PAO2 and lowest PACO2 at apex - because there is very low perfusion here so not much oxygen gets excreted and put into blood
2. Lowest PAO2 and highest PACO2 at base - because there is the most amount of perfusion here so oxygen uptake is larger than at apex
93
What is the A-a gradient?
the difference between alveolar and arterial oxygen
* difference increases with normal healthy aging
94
Where are the central chemoreceptors found?
ventral medulla close to the medullar respiratory center
95
Where are the peripheral chemoreceptors found?
In the aorta and carotid arteries
96
What is the role/responsibility for central chemoreceptors?
* responsible for detecting arterial PCO2 change
* These chemoreceptors are activated in response to low pH in the CSF which is caused by PCO2
* CO2 diffuses into CSF and then converts to carbonic acid which then releases H+ → more acidic/low pH
* Increases in PaCO2 cause decreased pH which causes increased ventilation, for example
97
What is the role/responsibility for peripheral chemoreceptors?
1. mediate the ventilatory response to hypoxemia, increased PaCO2, or low pH
98
What is the most important factor for controlling ventilation?
arterial PaCO2
99
What is the Hering-Breuer Reflex
* initiated by lung expansion, which excites stretch receptors in the airways.
* Stimulation of these receptors → send signals to the medulla by the vagus nerve
* This sends impulses to the off switch neurons which then inhibit integrator neurons and turns off inspiration
100
Where are J receptors found and what do they do?
1. Found in alveolar wall
2. Respond to engorgement of interstitial spaces with fluid
* Send impulses via vagus nerve and trigger rapid shallow breathing
101
Where are Bronchial C fibers found and what do they do?
1. Bronchial circulation
2. Respond to chemical composition of blood in bronchial circulation. Sensitive to inflammatory mediators in bronchial blood since they may lead to bronchonstriction.
* trigger rapid shallow breathing
102
What are the 4 ways the body adapts to altitude in terms of breathing, oxygen content, etc?
1. Hyperventilation
2. Polycythemia
3. O2 dissociation curve
4. Circulatory changes
103
How does hyperventilation help with changes oxygen saturation with altitude?
1. With altitude you have less alveolar PO2 (because of less barometric pressure in air)
2. By hyperventilating you decrease PaCO2 and thus also increase PO2 which is needed since with altitude is diminished
3. Look at ideal alveolar gas equation
104
How does polycythemia help with changes oxygen saturation with altitude?
1. increase in hematocrit causes an increase in blood O2 content (increased hemoglobin percentage)
105
How does O2 dissociation curve principles help with changes oxygen saturation with altitude?
1. With altitude there is more production of 2,3 BPG by RBC
2. increased 2,3 BPG leads to leftward shift in O2 dissociation curve → more easy to offload more oxygen to the tissue
106
How does circulatory changes help with changes oxygen saturation with altitude?
1. increased cardiac output → more oxygen for tissue
2. increased capillary formation → more O2 delivery
3. Increased oxidative enzymes → more use of oxygen
107
What is high altitude pulmonary edema? (HAPE)
it's theorized that **vessels in the lungs constrict, causing increased pressure**. This causes fluid to leak from the blood vessels to the lung tissues and eventually into the air sacs.
108
idiopathic Pulmonary Fibrosis (IPF)
1. pathogenesis
2. Type of patient most affected
3. Prognosis
1. Some irritant starts inflammation which leads to recruitment of fibroblasts which deposits a lot of collagen. Fibrous tissue is diffusely laid down in the lungs making them hard to inflate.
2. Mostly men over the age of 40
3. Poor prognosis, 3-5 years → does not respond to treatment
109
idiopathic Pulmonary Fibrosis (IPF)
1. How is this treated?
1. Inhibition of receptors for profibrotic factors
2. Lung transplant in extreme situations
3. \*\*\*DON'T USE STEROIDS FOR IPF\*\*\*
110
idiopathic Pulmonary Fibrosis (IPF)
1. what are some identifying markers seen in IPF pathology? (3)
1. Fibroblastic foci - densities around bronchioles that are paler than surrounding area (in imaging)
2. Patchy description - mix of normal lung tissue and some dense fibrosis
3. Honeycombing pattern
111
idiopathic Pulmonary Fibrosis (IPF)
1. what are some identifying markers seen in IPF radiology? (1)
1. honeycomb appearance that starts in the periphery and moves inward (arrow)
112
Nonspecific Interstitial Pneumonia (NSIP)
1. Pathophysiology
2. Typical patient
3. Prognosis
4. Types
1. Walls of alveoli become inflamed - may be idiopathic or associated with connective tissue disease
2. Mostly in female nonsmokers in their 60s
3. Better prognosis than IPF
4. Cellular vs Fibrosing
113
Nonspecific Interstitial Pneumonia (NSIP)
1. How is pathology different for cellular vs fibrosing type of NSIP?
2. What is not found in NSIP?
1. Cellular - found in younger patients. Interstitial inflammation and thickening due to inflammatory cells. This shows up more blue in pathology (top image)
2. Fibrosing - Diffuse interstitial thickening due to fibrosis → show up more pink
3. Fibroblastic foci, honeycombing, hyaline membranes, granulomas
114
Nonspecific Interstitial Pneumonia (NSIP)
1. What descriptions would be found in imaging?
1 .bilateral and symmetric opacities that are predominantly in lower lobe → spares the pleura
115
Cryptogenic Organizing Pneumonia (COP)
1. What are the symptoms of COP?
2. Pathogenesis
1. looks and behaves like an infective pneumonia and may appear with fever
2. Excessive proliferation of granulation tissue within small airways and alveolar ducts with inflammation around alveoli.
116
Cryptogenic Organizing Pneumonia (COP)
1. What are some findings in radiography imaging of COP?
1. consolidation near bronchioles but they often move if you look at serial imaging
117
Cryptogenic Organizing Pneumonia (COP)
1. What are some findings in pathology of COP?
1. Focal mass like lesion that is NOT diffuse like UIP
2. Polypoid plugs of loose connective tissue (masson bodies) within alveoli
3. Normal underlying lung architecture
118
What are the two smoking related infiltrative lung disease?
1. Desquamative interstitial pneumonia (DIP)
2. Respiratory bronchiolitis-related interstitial lung disease (RB-ILD)
119
Desquamative interstitial pneumonia (DIP)
1. Epidemiology
2. Prognosis and treatment
1. 4th-5th decade, equal in M or F
2. Excellent response to steroid therapy and smoking cessation → few progress to interstitial fibrosis
120
Desquamative interstitial pneumonia (DIP)
1. MIcroscopic features
1. Large collections of macrophages in the airspaces in a current or former smoker
121
Respiratory bronchiolitis-related interstitial lung disease (RB-ILD)
1. Epidemiology
2. Prognosis and treatment
1. 4th-5th decade with \>30 pack year history, M =F
2. improved with smoking cessation
122
Respiratory bronchiolitis-related interstitial lung disease (RB-ILD)
1. Microscopic Features
1. Chronic inflammation and peribronchiolar fibrosis
2. Pigmented intraluminal macrophages within 1st and 2nd order bronchioles
123
What are the granuloma based causes of restrictive lung disease? (2)
1. sarcoidosis
2. Hypersensitivity Pneumonitis
124
Sarcoidosis
1. Pathogenesis
2. Typical patient
1. Causes diffuse and non-caseating granulomas in lungs. Systemic inflammatory disease that affects any organ but most commonly intrathoracic LN and lungs
2. \<40 year old adults, more common in women
125
What are some physical manifestations of sarcoidosis?
1. papular Sarcodosis - can be itchy
2. Ocular sarcoidosis
126
Sarcoidosis is usually a diagnosis of exclusion but what 3 or 4 thinks will always be shown?
1. High serum ACE (angiotensin converting enzyme)
2. Hypercalcemia
3. BAL (bronchioalveolar lavange) will show increased CD4 T cells
4. Biopsy with non-necrotizing granulomas (not necessary but supports dx)
127
What are some chest X ray findings for sarcoidosis?
* Lambda sign - bilateral hilar (white) and right paratracheal (yellow) lymphadenopathy (top image)
* Reticulonodular opacities - mid and upper lung zones
128
What are some CT findings for sarcoidosis?
* Bilateral symmetrical hilar lymphadenopathy (straight solid arrow), paratracheal lymphadenopathy (solid curved arrow), subcarinal lymphadenopathy (open arrow)
129
What are some things found in pathology of Sarcoidosis?
1. Non-necrotizing granulomas (upper images) - need to rule out TB
2. Asteroid bodies in multinucleated cells
3. Schaumann body (calcium) in multinucleated cells
130
1. What is hypersensitivity pneumonitis?
2. What hypersensitivity reactions are involved?
1. Reaction to environmental antigen (dusts, microorganisms, chemicals)
2. Type III and IV (lymphocyte mediated disease)
131
hypersensitivity pneumonitis
1. What does the pathology look like/include?
1. Peribronchiolar inflammation - showing macrophages/very small granulomas
2. Lung architecture is normal unless disease progresses to fibrosing lung disease
132
1. What is UIP (usual interstitial pneumonia) pattern?
2. What disease has this pattern?
1. patchy interstitial fibrosis with alternating areas of normal lung - shows honeycombing
2. Hallmark pattern of idiopathic pulmonary fibrosis
133
Pulmonary Eosinophilia
1. What do you see in acute and chronic form?
1. Acute: You do not see peripheral eosinophils - don't see them in bronchial lavage fluid.
2. Chronic - you do see peripheral eosinophils
134
Pulmonary Eosinophilia
1. Treatment of acute vs chronic form?
2. Imaging (CXR) for both forms
1. Both respond to corticosteroids (but acute responds a lot better)
2. Acute shows diffuse infiltrates. Chronic shows focal consolidation - reverse batwing that spares the chest area
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Pulmonary Alveolar Proteinosis (PAP)
1. Pathogenesis
2. Types (+which is most common)
1. Defect in GM-CSF (macrophage dysfunction) which causes surfactant accumulation in intraalveolar and bronchiolar spaces
2. Autoimmune (most common), secondary, and hereditary
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Pulmonary Alveolar Proteinosis (PAP) - one of the rare causes of restrictive lung disease
1. What does histology look like?
1. alveolar spaces filled with fluid and within fluid are macrophages
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What is the therapeutic goals/steps to restrictive lung disease? (4)
1. Remove offending agent when known
2. suppress inflammation to reduce lung disease
3. Give steroids or immunosuppressants to stop progression
4. Lung transplant if too severe
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Coal Miners Lung
1. What does pathology of lung look like?
1. Inhalation of coal particles leads to anthracosis (black pigments seen in pathology)
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Coal Miner's Lung
1. What is Anthracosis?
1. carbon-laden macrophages in alveoli and interstitium- form nodules of black pigment
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Coal Miner's Lung
1. What is the complication that can arise from this disease?
1. progressive massive fibrosis (PMF) - occurs in 10% of cases. Large blackened scars composed of dense collagen and pigment.
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Silicosis
1. pathogenesis
2. Symptoms
1. Marcophages react to silica and cause inflammation response leading to fibroblast activation/fibrosis.
2. Usually lacks symptoms and progresses slowly which is why it is usually detected in routine CXR
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Silicosis
1. Pathology
1. Very dense silicotic nodule with irregular borders. Silica can be detected with polarized light.
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Silicosis
1. CXR findings
1. eggshell calcifications of lymph nodes and affects upper lobes normally
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Asbestosis
1. Types (which is more pathogenic)
2. Pathogenesis
3. Asbestosis is risk factor for??
1. Serpentine and Amphibole. Serpentine is more pathogenic
2. Particles are inhaled and macrophages ingest these particles → activate inflammasome → release inflammatory mediators → lead to fibrosis. Asbestos is not fully ingested by macrophages and are not broken down.
3. Tumor initiator and promoter (most commonly for bronchogenic carcinoma). Asbestos is only known risk factor for **mesothelioma**.
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Asbestosis
1. CXR findings
1. pleural plaques of asbestos
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Asbestosis
1. CT findings
1. pleural calcifications (arrows)
2. Honeycomb pattern late in disease (not in image)
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What are pathology findings of Asbestosis?
1. Asbestos bodies (dark purple circle) surrounded by a coating of iron and protein
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Beryllium (Berylliosis)
1. What three things are needed for diagnosis?
2. Pathogenesis?
1. History of exposure, positive beryllium lymphocyte proliferation test, presence of noncaseating granulomas
2. Hypersensitivity reaction that involve LNs and upper lobes of lung
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Beryllium (Berylliosis)
1. pathology
1. Preservation of lung architecture with focal mass like lesion (granuloma) - this is nonspecific so need other info to diagnose beryllium
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What are pneumoconiosis?
1. Non-neoplastic lung reaction to inhaled mineral dusts that occur due to occupational exposure
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Beta 2 agonists (SABA and LABA)
1. Mechanism of action
2. Purpose
1. Stimulates B2 adrenergic receptors which results in bronchial smooth muscle relaxation to improve airflow (activates adenylate cyclase)
2. Quick relief for acute symptoms but does not control underlying disease of asthma (inflammation)
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Beta 2 agonists
1. SABA - list a drug name (1)
2. SABA - Onset of action and how long does it last
3. LABA - list drug names (2)
4. Onset of action and how long does it last
1. Albuterol
2. Onset is 5 min and lasts 4-6 hours
3. salmeterol and formoterol
4. Salmeterol onset is 30 min
5. Formoterol onset is less than 5 minutes
6. Both last about 12 hours
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Can Salmeterol be used as a monotherapy?
1. No! It always should be used with inhaled corticosteroid because onset is 30 minutes and this can be dangerous in acute attacks
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Muscarininc antagonists (inhaled)
1. Mechanism of action
2. SAMA - list drug name
3. LAMA - list drug name
1. Blocks M receptors thereby blocking effect of aceytlcholine on M receptors in airway → airway relaxation in larger bronchioles and decreased mucus
2. Ipratropium
3. Tiotropium
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Corticosteroids
1. Mechanism of action
2. Purpose in asthma treatment?
1. Inhibits PLA2 and inhibits downstream chemical mediators like leukotrienes (which are potent bronchoconstrictors). ;;;; anti-inflammatory effects ;;;;;; decrease airway hyper-responsiveness and mucus production
2. Meant to PREVENT asthma attacks and not for relief in active attack
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Corticosteroids (**inhaled**)
1. Major side effect
2. Drug names
3. How long does it take to see full effects?
1. Oropharyngeal candidiasis
2. beclomethasone, fluticasone, budesonide
3. 2-4 weeks
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Corticosteroids (Oral or IV)
1. When are oral or IV corticosteroids used for asthma treatment?
2. Can you stop these drugs abruptly?
1. used during asthma exacerbation to gain rapid control. Given if other medications still have not given patient relief or adequate control.
2. If used less than 2 weeks then yes but if more than 2 weeks then patient needs to taper off
* long term use is bad because oral and IV steroids has detrimental side effects
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Leukotriene Receptor Antagonists
1. MOA
2. Name of drug in this category
1. Blocks leukotriene receptor site (LTD4 and LTE4) -Decreases asthma symptoms, SABA use, and asthma exacerbation
2. Montelukast - which is useful in aspirin sensitive asthma
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Omalizumab
1. MOA
2. When is this drug recruited
3. Side effects
1. IgG antibody that inhibits IgE binding to IgE receptor on mast cells and basophils so these cells don’t respond to allergens
2. Reserved for severe persistent asthma w/elevated IgE.
3. Side effects: anaphylactic reaction (rare)
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Methylxanthine
1. MOA
2. Drug name in this category
3. Side effects
1. Causes bronchodilation through inhibition of PDE (phosphodiesterase) which increases cAMP
2. Theophylline - but rarely used for asthma now
3. Cardiotoxicity-blocks adenosine receptors which increases HR and cause arrythmias. **Can't use adenosine in patients taking theophylline**
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What is considered best initial therapy for COPD treatment?
muscarinic antagonists (SAMA and LAMA)
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Roflumilast - used in COPD
1. MOA
2. What COPD conditions is this useful for
1. Phosphodiesterase-4 inhibitor, which decreases lung inflammation and can relax the airway smooth muscles
2. Used only in severe COPD (FEV \<50%) w/frequent exacerbation and despite tx w/ICS+LABA+LAMA (this is an add on drug)
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Inhaled corticosteroid → for COPD treatment
1. Not first line therapy for COPD but when is it used?
2. Purpose in these COPD scenarios?
1. Used in severe COPD (FEV1 \<50% or group C&D) with frequent exacerbation
2. ICS are meant to reduce number of exacerbations in these types of patients
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What is acute treatment of COPD episode?
1. Give oxygen
2. Give nebulized albuterol, possibly with ipratropium (this combo is called combivent)
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What is acute treatment of asthma episode?
1. give oxygen
2. Give nebulized albuterol
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For group A of COPD patients
1. Recommended first choice therapy
2. Step up from these treatment for group A?
1. SAMA as needed
2. LABA *or* LAMA
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For group B of COPD patients
1. Recommended first choice therapy
2. Step up from these treatment for group B?
1. **LAMA** or LABA
2. LAMA and LABA
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For group C of COPD patients
1. Recommended first choice therapy
2. Step up from these treatment for group C?
1. LAMA
2. LAMA and LABA
3. another step up: LABA + ICS
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For group D of COPD patients
1. Recommended first choice therapy
2. Step up from these treatment for group D?
1. LAMA+LABA or ICS+LABA
2. LAMA+LABA+ICS
3. Another step up: Roflumilast (add on)
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Chronic therapy management of Asthma (individuals 12+)
- Step 1-
1. What is treatment therapy at this step?
1. SABA as needed
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Chronic therapy management of Asthma (individuals 12+)
- Step 2-
1. What is treatment therapy at this step?
1. Low dose ICS + SABA as needed
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Chronic therapy management of Asthma (individuals 12+)
- Step 3-
1. What is treatment therapy at this step?
1. Low dose ICS+LABA or medium dose ICS
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Chronic therapy management of Asthma (individuals 12+)
- Step 4-
1. What is treatment therapy at this step?
1. Medium dose ICS + LABA
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Chronic therapy management of Asthma (individuals 12+)
- Step 5-
1. What is treatment therapy at this step?
1. High dose ICS + LABA
+consider omalizumab for patients with allergies
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Chronic therapy management of Asthma (individuals 12+)
- Step 6-
1. What is treatment therapy at this step?
1. High dose ICS+LABA+oral steroids
+consider omalizumab for patients with allergies
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What are the different classifications of asthma?
1. Intermittent (goes with step 1)
2. Persistent (mild-step 2, moderate-step 3, and severe-step 4 or 5)
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How do you determine asthma severity?
1. Rule of 2s → if patient has *more than 2 daytime symptoms a week* **OR** *more than 2 nighttime symptoms a month* → persistent asthma
2. If less than both of these then it is considered intermittent
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What would indicate a person has well controlled asthma
1. symptoms
2. night time awakenings
3. SABA use for symptoms
4. Lung function FEV1
image
* if well controlled then same regimen is used. FU in 1-6 months and if stable for ≥ 3 months then you can step down
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What would indicate a person has not well controlled asthma
1. symptoms
2. night time awakenings
3. SABA use for symptoms
4. Lung function FEV1
image
1. step up 1 step and FU in 2-6 weeks
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What would indicate a person has very poorly controlled asthma
1. symptoms
2. night time awakenings
3. SABA use for symptoms
4. Lung function FEV1
image
1. consider short course of oral corticosteroids and step up 1-2 steps w/FU in 2 weeks
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What FEV1/FVC ratio will confirm COPD diagnosis?
FEV1/FVC \< 0.7
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1. What is the GOLD criteria for COPD
1. A way of staging COPD severity based on FEV1 levels
* but now there is a better assessment to help determine severity of COPD and medications that need to be used (called the refined ABCD assessment tool)
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For the ABCD assessment tool for COPD
-What exacerbation history and mMRC (or CAT) grade is needed for
1. Group A
2. Group B
3. Group C
4. Group D
1. image
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Why is LAMA at times better than LABA for patients with COPD?
1. LABA has cardiovascular risks and the people who have COPD are typically smokers. This would give the person two risk factors for CV injury
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For what groups of COPD patients should ICS be reserved for?
Group C or D - those with frequent exacerbation
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At young ages what sex is most likely to present with asthma?
1. young boys
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What is the function of
1. IL-4
2. IL-5
3. IL-13
* IL-4 accounts for increased IgE production
* IL-5 increases eosinophil count in the area
* IL-13 degranulates mast cells and increases mucous production
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After administering pure oxygen to a patient with COPD→ what are the reasons that arterial partial pressure of CO2 would increase?
1. V/Q mismatch - You are sending blood to areas of lungs that should be “closed off”. With more O2, there is ventilation to areas of lung damage and this leads to blood moving that way -but there is no oxygen/CO2 exchange → leads to increased CO2
2. Haldane effect
3. Respiratory Drive -central chemoreceptors notice and fix abnormal PaCO2 but in COPD pts central chemoreceptors become desensitized to increased PaCO2. Peripheral chemoreceptors take over “drive for respiration” by monitoring PaO2 volumes. When given oxygen the arterial PO2 goes up body thinks there is no need to change breathing so arterial PaCO2 goes up
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Flow volume curves
1. Which one is obstructive, normal, and restrictive
image
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Aspirin - exacerbated respiratory disease
1. what causes this reaction?
1. Inhibits COX1 and COX2 leads to symptoms of nasal congestion and bronchoconstriction. This can leads to exacerbation episode.
2. More common in adults and begins 20 min - 3 hours after ingestion
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what is tx for upper airway cough syndrome?
1. intranasal steroids are usual first line
2. Upper airway cough syndrome is upper airway abnormalities causing chronic cough, usually seen with abnormal sensation in the throat
192
What is post viral cough syndrome?
How is it treated
1. Cough lasting 3-8 weeks
2. Follows an acute respiratory infection
3. Neg CXR to r/o pneumonia and no other red flags
4. Give intranasal steroids but if that doesn't work then antihistamines or trial of bronchodilator
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What is most common bacterial infection in CF patients as they get older?
P. aeruginosa
* In younger patients staph aureus is most common
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What does finger clubbing indicate? (hypertrophic osteoarthropathy)
1. typically hypoxia
2. Image
