Lung 2 Flashcards
(134 cards)
1
Q
Acute bronchitis - etiology
A
preceding resp ilness (90% viral)
2
Q
acute bronchitis - clinical presentation
A
cough for more than 5 days to 3 wks ( +/- purulent sputum, +/- blood)
2. absent systemic findings
3. Wheezing or ronchi, chet wall tenderness
NO FEVER (if present think pneumonia or flu)
3
Q
acute bronchitis - diagnosis + treatment
A
- clinical diagnosis, CXR only when pneumonia suspected
2. symptomatic treatment (eg. NSAID, bronchodilators)
4
Q
Bronchiectasis - sign and symptoms
A
- cough with daily mucupurulent sputum production
- rhinosinusitis, dyspnea, hemoptysis
- crackles, wheezing
5
Q
bronchiectasis - etiology
A
- airway obstraction (eg. ca)
- rheumatic disease (eg. RA, Sjogren), toxic inhalation)
- immunodef (eg. hypogammaglobulinemia)
- Congenital (eg. CF, α-1-antitrypsin def)
6
Q
test to confirm bronchiectasias
A
high resolution CT
7
Q
bronchiectasis - evaluation
A
- high resolution CR (needed for initial diagnosis)
- immunoglobulin quantification
- CF testing, sputum culture (bacteria, fungi, mycobacteria
- PFT
8
Q
bronchiectasia is associated with (like predisposition)
A
- bronchial obstruction
- poor ciliary motility (SMOKING, kartegener syndrome)
- cystic fibrosis
- allergic bronchopulmonary aspergillosis
9
Q
the main cause of hypercapnia in COPD
A
increased dead space ventilaiton
10
Q
pneumonia mediated hypoventilation - mechanism
A
R to L intralpulmonary shunting and extreme ventilation /perfusion mismatched
- High O2 inspiration does not correct it
11
Q
causes of hypoxemia (and example)
A
- hypoventilation: CNS depression, neuromuscular weakness
- dead-space ventilation (V/Q=infinity): PE
- diffusion limitation: emphysema, interstitial lung disease
- intrapulmonary shunt (V/Q=0): pneumonia, pulm edema, atelectasis
- intracradiac shunt (R-L): Fallot, Eisenmenger
- Reduced PiO2: high altitude
12
Q
causes of hypoxemia - A-a gradient, corects with O2
A
- hypoventilation: normal, yes
- dead-space ventilation (V/Q=infinity), increased , yes
- diffusion limitation: increased, yes
- intrapulmonary shunt (V/Q=0): increased, no
- intracradiac shunt (R-L): increased, no
- Reduced PiO2: normal, yes
13
Q
PFT in asthma
A
normal to increased TLC
normal FEV1/FVC
normal to increased DLCO
14
Q
PFT in COPD
A
increased TLC
low FEV1/FVC
low DLCO (normal in the beginning)
15
Q
PFT in interstitial lung disease
A
Low TLC
NORMAL FEV/FVC (or increased)
low DLCO
16
Q
PFT in pulm arterial hypertension
A
normal TLC
normal FEV1/FVC
low DLCO
17
Q
Restrictive chest wall disease
A
low TLC
normal FEV1/FVC
normal DLCO
18
Q
DLCO in pulm arterial hypertention
A
low
19
Q
hypersensittivity pneomonitis - - definition / manifestation
A
inflammation of the lung parenchyma caused by antigen exposure
- acute episodes present with cough, breathlessness, fever, malaise that occure within 4-6 h of antigen exposure
chronic: weight loss, clubbing, honycombing of the lung
20
Q
hypersensitivity pneumonitis - management
A
avoidance of responsible antigen
maybe steroids in acute
21
Q
sputum and blood culutres in outpatient pneumonia
A
not required
22
Q
lung compliance of ARDS
A
low
23
Q
ARDS - pulm arterial pressure
A
increased due to hypoxic vasconstriction, destruction of lung parechyma, and compression of vascular structures from positive airway pressure in mechanicall ventilated patinets
24
Q
severe asthma exacerbation - management
A
inhaled short acting β2 agonists, inhaled ipratropium , systemic corticosteroids –> elevated or even normal partial pressure of CO2 suggest failure of medical therapy and resp collapse –> entrotracheal intubation
25
systemic epinephrine in severe astham exacerbation
only in severe when inhaled therapy cannot be given
26
mild to moderate asthma asthma exacerbation - management
inhaled β2 agonists --> if no improvement --> systemic steroids
27
Wegerer - diagnosis
ANCA: PR3, MPO
biopsy: skin (leukocytoclastic vasculitis), kidney (pauci-immune GN) lung (granulomatous vsculitis)
28
Wegener - management
corticosteroids + immunomodulators (MTX, cyclophosphamide)
29
it can increased the chance of FP ANCA
HIV
30
ACEi cause chronic non-productive cough - mechanism
increaesd circulating levels of kinins, substance P, PGE, TXE
(MORE COMMON IN CHINESE)
31
diagnosis from PFT
1. low FEV1/FVC ratio --> obstructive --> DLCO?
- decreased: COPD
- normal/increased: Asthma
2. normal or high FEV1/FVC --> restrictive --> DLCO?
- normal: chest wall weakness
- decreased: interstitial lung disease
32
ARDS - how to improve oxygenation
by increaeing either FIO2 or positive end-expiratory prssure (PEEP
- if high levels of FIO2 (more than 60% are required to mainttain oxygenation, PEEP level should be increased to allow for reduction in the FIO2 as oxygenation improves (prolonged high FIO2 causes O2 toxicity)
ALWAYS KEEP LOW TV
33
increasing of PEEP in ARDS - purpose
reopen of alveoli --> reduce shunting
34
MC SE of inhaled corticosteroid therapy
oropharyngeal thrush (oral candidiasis)
35
ARDS definition
clinical syndrome characterized by
1. acute onset respiratory failure,
2. bilateral lung opacities
3. decreased Pa02/Fi02 ratio
4. no HF
36
bornchodilator respone in asthma
improvement of FEV1 more than 12%
37
asthma severity for patients not on controller medication (steps)
```
step 1 (intermittent): max 2 days a week symptoms, max 2 nighttime awakening per month
step 2 (mild persistent): more than 2 days / wk, 3-4 awaakenings per month
step 3 (moderate): daily symptoms, more than 1 awakening /wk
step 4 or 5) (severe): throughout day, 4-7 awakening / wk
```
38
asthma treatment
step 1 --> SABA
step 2 --> Low dose inhaled cortic
step 3 --> low dose inhaled cosrticost + LABA or medium inhaled costic
step 4: medium dose inh cortic + LABA
step 5: High dose inh cosrtic + LABA + omalizumab if allegy
step 6: High dose inh cortic + LABA + Oral cortic + Omalizumab if allergy
39
position dependent hypoxemia - mechanism
positional changes that make the consolidation more gravity dependen worsen ventilation/perfusion mismatch --> increase iintrapulmonary shunting --> worsened hpoxemia
40
Aspirin exacerbated resp disease - mechanism
non-IgE mediated raction that results from aspirin induced prostagl/leukotriene misbalance
41
Aspirin exacerbated resp disease - manifestation
mc in history of asthma or chronic rhinsinusitisis with nasal polyposis
- bronchospasm + nasal congestion following aspirin ingestion
42
aspirin-exacerbated resp disease - treatment
avoidance of NSAID, desensitisation if NSAID are required, use of leukotriene receptor antagonists (eg. montelukast)
43
illegal that can cause hemoptysis
inhaler cocaine
44
radiation fibrosis
MC in patients who received lung field radiation --> dyspnea, nonproductive cough, chest pain within 4-24months after therapy
x-ray: volume loss with coarse opacities
45
ARDS - always low TV - why
decrease the likelihood of overdistending alveoli
| (improves mortality) --> causes barotrauma
46
ARDS under ventilator - hypercapnia
setting the ventilator parameters to provide low TV and low RR decreases minute ventilation --> hypercapnia and acidosis
47
ARDS - saturation target
greater than 88%
48
allergic rhinitis - clinical features
1. watery rhinorrhea, sneezing, eye symptoms
2. early age of onset
3. identifiable allergen or seasonal pattern
4. pale/bluish nasal mucosa
5. associated with other allergic disorders (eczema, asthma etc)
49
nonallergic rhinitis - clinical manifestation
1. nasal congestion, rhinorrhea, sneezing, postnasal drainage (dry cough)
2. onset after 20 years old
3. parennial symptoms (may worsen with seasonal changes)
4. erythematous nasal mucosa
50
allergic rhinitis - treatment
intranasal glucocorticoids
| antihistamines
51
nonallergic rhinitis - treatment
mild: intranasal antihistamine or glucocorticoids
| moderate to severe: combination therapy
52
nasal cytology in nonallergic rhinitits
eosinophils
| not required
53
clinical signs of pulm hypertension
1. Left parasternal lift, RV heave
2. Loud P2, right dsided S3
3. pansystolic mmurmur of TR
4. JVD, periperal edema, hepatsplenomegaly
54
systemic sclerosis on the lung
- hyperplasia of the intimal SMCs layer --> incr pulm resistance --> pulm hypertension
- interstitial fibrosis
55
there are 2 types of abnormal ventilation during sleeping
1. apnea: cessation of breathing for 10 or more sec)
2. hypopnea: reduced airflow causing SaO2 to decrease by 4%
in symptomatic paitnes, experiencing 5 or more obstructive resp events (apneas or hypopneas) per hour is diagnostic of obstructive sleep apnea)
56
sleep apnea - PaO2 levels
normal during the day
| noctural hypoxia
57
sleep apnea - complications (how)
noctural hypoxia -->
1. systemic/pulmonary hypertension
2. arrhythmias (atrial fibrillation/flutter)
3. sudden death
58
sleep apnea - types
1. obstructive sleep apnea
2. central sleep apnea
3. Obesity hypoventilation syndrome
59
obstructive sleep apnea - caused by
1. excess parapharyngeal tissue in adults
| 2. adenotonsillar hypertrophy in children
60
strongest RF for obstructive sleep apnea
obesity
61
obstructive sleep apnea - treatment
1. weight loss
2. CPAP (continuous positive airway pressure)
3. surgery
also avoidance of sedatives, avoid alcohol, acoid supine posture during sleep
62
central sleep apnea - due to
1. CNS injury
2. CNS toxicity
3. opioids
4. Heart failure
63
Obesity hypoventilatin syndrome - diagnostic criteria
1. BMI more than 30
2. awake daytime hypercapnia (more than 45)
3. no alternate cause of hypoventilation
64
Obesity hypoventilation syndrome - pathophysiology
BMI >=30Kg/m2 --> hypoventilation (decreased RR) --> decreased PaO2 and increased PaCO2 during sleep --> increased PaCO2 DURING WAKING HOURS (retention)
65
Obesity hypoventilation syndrome - blood gases abnormalities
1. increased PaCO2 during sleep
2. decreased PaO2 during sleep
3. Increased PaCO2 during waking hours (retention)
66
CHF - where is the fluid
61% bilateral
27% only R
12% only left
67
obesity hypoventilation syndrome - workup
ABG on room air (normal Aa gradient, hypercapia))
2. no intrinsic pulm disease on chest x-ray
3. restrictive PFT
4. Normal TSH
5. polysomonography
68
obesity hypobentilation synrome - treatment
1. nocturnal positive pressure ventilation as 1st line
2. wight loss
3. avoidance of sedative medication
4. resp stimulants (acetazolamide) as last choice
69
Beta 2 agonists - SE
1. hypokalemia --> muscle weakness, arrhythnia, EKG abnormalities
2. tremor
3. palpitations
4. headache
70
asthma related with GERD - management
omeprazole
71
sarcoidosis effect on the musculoskeletal system
acute polyarthritis
| chronic arthritis
72
Lofgren syndrome
1. erythema nodosum
2. hilar adenopathy
3. migratory polyarthralgia
4. fever
73
ankylosing spondylitis effect in lungs
limited chest expansion + spinal mobility--> restrictive lung disease
74
COPD - seizures after 02 supplementation
increased CO2 retention due to
- loss of compensatory vasoconstriction in areas of ineffective gas exhange worsens V/Q mismatch
- increase on HbO2 reduces the uptake of CO2 from tissues
- Decreased resp drive and slowing of the resp rate causes reduced minute ventilation
- -> reflex cerebral vasodilation --> seizures
75
pulm contusion - symptoms can be worsen by
fluid overvolume
76
resp arkalosis in incubated patient - next step
if appropriate TV --> decrease RR
77
intemediate vs low risk solitary pulm nodule
interm is 8 mm or bigger
78
pneumothorax - hypotension and tachycardia due to
compression of structures in the mediastinum --> impaired RV filling
79
ideal location of endotracheal tube / if displaced to bronchus, which bronchus MC
2-6 cm above carina
| - right (so left atelectasis)
80
intubated patients - atelectasis due to misplacement vs pneumothorax
pneumothorax causes hemodynamically instability
81
parapneumonic effusions - uncomplicated vs complicated regarding etiology
uncompl: sterile exudate in pleural space
complicaetd: bacterial invasion of pleural space --> continue to have symptoms despite antibiotics
82
parapneumonic effusions - uncomplicated vs complicated regarding pleural fluid analysis
uncompl: ph 7.2 or more, glucose 60 or more, WBC 50.000 or less
complic: ph less than 7.2, glucose less than 60, WBC more than 50.000
83
parapneumonic effusions - complc vs uncomplicated regarding gram stain + culture
uncompl: negative
complic: FN due tto low bacter count
84
parapneumonic effusions - uncomplc vs complic regarding treatment
uncomplicated: antibiotics
complic: antibiotics + drainage
85
increased risk of pneumonia complicated with pleural effusion
immunodeficiency
86
acute exacerbation of COPD is characterized by a change in at least 1 of the following
1. cough severity or frequency
2. volume or character of sputum production
3. levels of dyspena
87
Light criteria
at least 1
1. Pleural protein/serum protein more than 0.5
2. pleural LDH/ serume LDH more than 0.6
3. Pleural LDH more than 2/3 of the upper limit of normal for serum LDH
88
exercise induced bronchoconstriction - management
short acting beta-adrenergic agnostis administered 10-20 mins before exercise are the 1st line treatment if only few times a week
- if daily: inhaled corticosteroids or antileukotriene
89
normal pleural fluid ph / trandudate fluid ph / edudate
- 7.6
- 7.4-7.55
- exudate: 7.3-7.45 (may be lower)
90
pneumoconioses - types
1. asbestosis
2. Berylliosis
3. Coal workers' pneumoconiosis
4. silicosis
91
pneumoconioses (except berylliosi) - increased risk for
1. cor pulmonale
2. Caplan syndrome
3. cancer
92
Caplan syndrome
rheumatoid arthritis and pneumoconiases (coal, asbestosis, silicosis) with intrapulmonary nodules
93
Asbestosis is associated with (exposure)
1. shipbuilding
2. roofing
3. plumbing
94
pathognomonic lesions of asbestosis (gross)
Ivory white, calcified supreadiaphragmatic and pleural plaques
95
areas of asbestos plaques
1. supreadiaphragmatic
| 2. pleural plaques
96
carcinomas associated with asbestosis
1. bronchogenic carcinoma (More common
| 2. mesothelioma
97
berylliosis associated with (exposure)
berryllium in
1. aerospace
2. manufacturing industries
98
lung Asbestosis - histology
ferruginous (asbestos) bodies: golden-brown fusiform rods resembling dumbbells, found in alveolar septum (visulized using PAS stain), often obtain by branchoalveolar lavage)
99
ferruginous bodies are found in
alveolar septum
100
berylliosis affects (area) / histology / treatment
- upper lobes
- noncaseating granoulomas in lung, hilar lymph nodes and systemic organs
- occasionally responsive to steroids
101
Coal workers' pneumoconiosis is also known s / area
black lung disease
| - upper lobes
102
Coal workers' pneumoconiosis - pathophysiology
prolonged coal dust exposure --> macrophages laden with carbon --> inflammation and fibrosis
103
Anthracosis is caused by
mild exposure to carbon (collection of macrophages laden with carbon)
104
Anthracosis - symptoms/found in
asymptomatic condition found in many urban dwellers exposed to sooty air
105
Anthracosis - occupation
found in many urban dwellers exposed to sooty air
106
Silicosis is associated with ....(occupation)
1. foundries (factory that produces metal castings)
2. sandblasting
3. Mines
107
Silicosis - pathophysiology
Macrophages respond to silica and release fibrogenic factors, leading to fibrosis. it is thought that silica may disrupt phagolysosomes and impair macrophages
108
silicosis - increased risk for
1. TB
| 2. bronchogenic carcinoma
109
silicosis - CXR
Eggshell calcification of hilar lymph nodes
110
pneumoconiases that affect upper lobes
1. coal workers' pneumoconiosis
2. Silicosi
3. Berylliosis
111
pneumoconiases that affect lower lobes
asbestosis
112
which are the classicfication group of pulmonary hypertension
1. pulmonary arterial hypertension (PAH)
2. PH due to left heart disease
3. PH due to lung disease or hypoxia
4. chronic thromboembolic PH
5. multifactorial PH
113
multifactorial pulmonary hypertensions - causes
1. hematologic disorders
2. systemic disorders
3. metabolic disorders
114
pulmonary arterial hypertension (PAH) - causes
1. idiopathic
2. drugs
3. connective tissue disease
4. HIV infection
5. portal hypertension
6. congenital heart disease
7. schistosomiasis
115
pulmonary arterial hypertension (PAH) - idiopathic - pathophysiology
often due to inactivation mitation in BMPR2 gene -->
| inhibits vascular SMCs proliferation
116
primary spontaneous pneumothorax is due to
rupture of apical blebs or cysts in tall, thin, young males
117
secondary spontaneous pneumothorax is due to
1. diseased lung (bullae in emphysema, infections)
| 2. mechanical ventilation with use of high pressures (barotrauma)
118
thrombi pulmonary emboli - histology
lines of Zahn: interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death
119
1st generation H1 blockers - drugs
1. diphenhydramine
2. dimenhydrinate
3. chlorpheniramine
120
2nd generation H1 blockers - drugs
- ADINE + cetirizine
1. loratadine
2. fexofenadine
3. desloratadine
4. cetirizine
121
1st generation H1 blockers vs 2nd - used for
1st: 1. allergy 2. motion 3. sleep aid
2nd: allergy
122
1st generation H1 blockers - toxicity
1. sedation
2. antimuscarinic
3. anti-a-adrenergic
123
2nd generation H1 blockers - toxicity
sedation (much less than 1st generation)
124
pulmonary hypertension drugs - categories and drugs
1. endothelin receptor antagonists --> BOSENTAN
2. PDE-5 inhibitors --> SILDENAFIL
3. Prostacyclin analogs --> EPOPROSTENOL, ILOPROST
125
bosentan toxicity
hepatotoxicity
126
pulmonary hypertensrion - prostacyclin analogs side effects
1. flushing
| 2. jaw pain
127
chronic bronchitis - pathology
hyperplasia of mucus-secreting glands --> Reid index >50%
128
chronic bronchitis - definition
productive cough for >3 months PER YEAR (not necessarily consecutive) for >2 years
129
causes of poor ciliary motility
1. smoking
| 2. kartegener syndrome
130
emphysema types - associations and area
1. centriacinar: associated with smoking --> upper lobes
| 2. Panacinar: associated with α1 - antitrypsin --> lower lobes
131
emphysema - diffusion capacity of CO test (and mechanism)
decreased diffusing capacity for CO resulting from destruction of alveolar walls
132
blue bloaters vs pink puffer
blue: chronic bronchitis
pink: emphysema
133
Restricted lung disease - drug toxicity
1. bleomycin 2. busulfan
| 3. amiodarone 4. methotrexate
134
PEAK airway pressure
the maximum pressure measured as the TV is being delivered = the sum of the resistive pressure (flow x resistance) and the platue pressure
platue pressure: the P measured during an insiratory hold maneuver, when pulm airflow and thus resistive pressure are both 0 = elastic P + PEEP
PEEP is calculated with the end expir hold maneuver
