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LUNG + RENAL STEP 2 > Lung 2 > Flashcards

Lung 2 Flashcards

1
Q

Acute bronchitis - etiology

A

preceding resp ilness (90% viral)

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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)

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3
Q

acute bronchitis - diagnosis + treatment

A
  1. clinical diagnosis, CXR only when pneumonia suspected

2. symptomatic treatment (eg. NSAID, bronchodilators)

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4
Q

Bronchiectasis - sign and symptoms

A
  1. cough with daily mucupurulent sputum production
  2. rhinosinusitis, dyspnea, hemoptysis
  3. crackles, wheezing
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5
Q

bronchiectasis - etiology

A
  1. airway obstraction (eg. ca)
  2. rheumatic disease (eg. RA, Sjogren), toxic inhalation)
  3. immunodef (eg. hypogammaglobulinemia)
  4. Congenital (eg. CF, α-1-antitrypsin def)
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6
Q

test to confirm bronchiectasias

A

high resolution CT

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7
Q

bronchiectasis - evaluation

A
  1. high resolution CR (needed for initial diagnosis)
  2. immunoglobulin quantification
  3. CF testing, sputum culture (bacteria, fungi, mycobacteria
  4. PFT
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8
Q

bronchiectasia is associated with (like predisposition)

A
  1. bronchial obstruction
  2. poor ciliary motility (SMOKING, kartegener syndrome)
  3. cystic fibrosis
  4. allergic bronchopulmonary aspergillosis
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9
Q

the main cause of hypercapnia in COPD

A

increased dead space ventilaiton

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10
Q

pneumonia mediated hypoventilation - mechanism

A

R to L intralpulmonary shunting and extreme ventilation /perfusion mismatched
- High O2 inspiration does not correct it

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11
Q

causes of hypoxemia (and example)

A
  1. hypoventilation: CNS depression, neuromuscular weakness
  2. dead-space ventilation (V/Q=infinity): PE
  3. diffusion limitation: emphysema, interstitial lung disease
  4. intrapulmonary shunt (V/Q=0): pneumonia, pulm edema, atelectasis
  5. intracradiac shunt (R-L): Fallot, Eisenmenger
  6. Reduced PiO2: high altitude
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12
Q

causes of hypoxemia - A-a gradient, corects with O2

A
  1. hypoventilation: normal, yes
  2. dead-space ventilation (V/Q=infinity), increased , yes
  3. diffusion limitation: increased, yes
  4. intrapulmonary shunt (V/Q=0): increased, no
  5. intracradiac shunt (R-L): increased, no
  6. Reduced PiO2: normal, yes
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13
Q

PFT in asthma

A

normal to increased TLC
normal FEV1/FVC
normal to increased DLCO

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14
Q

PFT in COPD

A

increased TLC
low FEV1/FVC
low DLCO (normal in the beginning)

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15
Q

PFT in interstitial lung disease

A

Low TLC
NORMAL FEV/FVC (or increased)
low DLCO

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16
Q

PFT in pulm arterial hypertension

A

normal TLC
normal FEV1/FVC
low DLCO

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17
Q

Restrictive chest wall disease

A

low TLC
normal FEV1/FVC
normal DLCO

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18
Q

DLCO in pulm arterial hypertention

A

low

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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
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20
Q

hypersensitivity pneumonitis - management

A

avoidance of responsible antigen

maybe steroids in acute

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21
Q

sputum and blood culutres in outpatient pneumonia

A

not required

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22
Q

lung compliance of ARDS

A

low

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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

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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

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25
Q

systemic epinephrine in severe astham exacerbation

A

only in severe when inhaled therapy cannot be given

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26
Q

mild to moderate asthma asthma exacerbation - management

A

inhaled β2 agonists –> if no improvement –> systemic steroids

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27
Q

Wegerer - diagnosis

A

ANCA: PR3, MPO
biopsy: skin (leukocytoclastic vasculitis), kidney (pauci-immune GN) lung (granulomatous vsculitis)

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28
Q

Wegener - management

A

corticosteroids + immunomodulators (MTX, cyclophosphamide)

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29
Q

it can increased the chance of FP ANCA

A

HIV

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30
Q

ACEi cause chronic non-productive cough - mechanism

A

increaesd circulating levels of kinins, substance P, PGE, TXE
(MORE COMMON IN CHINESE)

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31
Q

diagnosis from PFT

A
  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
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32
Q

ARDS - how to improve oxygenation

A

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

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33
Q

increasing of PEEP in ARDS - purpose

A

reopen of alveoli –> reduce shunting

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34
Q

MC SE of inhaled corticosteroid therapy

A

oropharyngeal thrush (oral candidiasis)

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35
Q

ARDS definition

A

clinical syndrome characterized by

  1. acute onset respiratory failure,
  2. bilateral lung opacities
  3. decreased Pa02/Fi02 ratio
  4. no HF
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36
Q

bornchodilator respone in asthma

A

improvement of FEV1 more than 12%

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37
Q

asthma severity for patients not on controller medication (steps)

A 
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
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38
Q

asthma treatment

A

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

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39
Q

position dependent hypoxemia - mechanism

A

positional changes that make the consolidation more gravity dependen worsen ventilation/perfusion mismatch –> increase iintrapulmonary shunting –> worsened hpoxemia

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40
Q

Aspirin exacerbated resp disease - mechanism

A

non-IgE mediated raction that results from aspirin induced prostagl/leukotriene misbalance

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41
Q

Aspirin exacerbated resp disease - manifestation

A

mc in history of asthma or chronic rhinsinusitisis with nasal polyposis
- bronchospasm + nasal congestion following aspirin ingestion

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42
Q

aspirin-exacerbated resp disease - treatment

A

avoidance of NSAID, desensitisation if NSAID are required, use of leukotriene receptor antagonists (eg. montelukast)

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43
Q

illegal that can cause hemoptysis

A

inhaler cocaine

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44
Q

radiation fibrosis

A

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

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45
Q

ARDS - always low TV - why

A

decrease the likelihood of overdistending alveoli

(improves mortality) –> causes barotrauma

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46
Q

ARDS under ventilator - hypercapnia

A

setting the ventilator parameters to provide low TV and low RR decreases minute ventilation –> hypercapnia and acidosis

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47
Q

ARDS - saturation target

A

greater than 88%

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48
Q

allergic rhinitis - clinical features

A
  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)
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49
Q

nonallergic rhinitis - clinical manifestation

A
  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
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50
Q

allergic rhinitis - treatment

A

intranasal glucocorticoids

antihistamines

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51
Q

nonallergic rhinitis - treatment

A

mild: intranasal antihistamine or glucocorticoids

moderate to severe: combination therapy

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52
Q

nasal cytology in nonallergic rhinitits

A

eosinophils

not required

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53
Q

clinical signs of pulm hypertension

A
  1. Left parasternal lift, RV heave
  2. Loud P2, right dsided S3
  3. pansystolic mmurmur of TR
  4. JVD, periperal edema, hepatsplenomegaly
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54
Q

systemic sclerosis on the lung

A
  • hyperplasia of the intimal SMCs layer –> incr pulm resistance –> pulm hypertension
  • interstitial fibrosis
55
Q

there are 2 types of abnormal ventilation during sleeping

A
  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
Q

sleep apnea - PaO2 levels

A

normal during the day

noctural hypoxia

57
Q

sleep apnea - complications (how)

A

noctural hypoxia –>

  1. systemic/pulmonary hypertension
  2. arrhythmias (atrial fibrillation/flutter)
  3. sudden death
58
Q

sleep apnea - types

A
  1. obstructive sleep apnea
  2. central sleep apnea
  3. Obesity hypoventilation syndrome
59
Q

obstructive sleep apnea - caused by

A
  1. excess parapharyngeal tissue in adults

2. adenotonsillar hypertrophy in children

60
Q

strongest RF for obstructive sleep apnea

A

obesity

61
Q

obstructive sleep apnea - treatment

A
  1. weight loss
  2. CPAP (continuous positive airway pressure)
  3. surgery
    also avoidance of sedatives, avoid alcohol, acoid supine posture during sleep
62
Q

central sleep apnea - due to

A
  1. CNS injury
  2. CNS toxicity
  3. opioids
  4. Heart failure
63
Q

Obesity hypoventilatin syndrome - diagnostic criteria

A
  1. BMI more than 30
  2. awake daytime hypercapnia (more than 45)
  3. no alternate cause of hypoventilation
64
Q

Obesity hypoventilation syndrome - pathophysiology

A

BMI >=30Kg/m2 –> hypoventilation (decreased RR) –> decreased PaO2 and increased PaCO2 during sleep –> increased PaCO2 DURING WAKING HOURS (retention)

65
Q

Obesity hypoventilation syndrome - blood gases abnormalities

A
  1. increased PaCO2 during sleep
  2. decreased PaO2 during sleep
  3. Increased PaCO2 during waking hours (retention)
66
Q

CHF - where is the fluid

A

61% bilateral
27% only R
12% only left

67
Q

obesity hypoventilation syndrome - workup

A

ABG on room air (normal Aa gradient, hypercapia))

  1. no intrinsic pulm disease on chest x-ray
  2. restrictive PFT
  3. Normal TSH
  4. polysomonography
68
Q

obesity hypobentilation synrome - treatment

A
  1. nocturnal positive pressure ventilation as 1st line
  2. wight loss
  3. avoidance of sedative medication
  4. resp stimulants (acetazolamide) as last choice
69
Q

Beta 2 agonists - SE

A
  1. hypokalemia –> muscle weakness, arrhythnia, EKG abnormalities
  2. tremor
  3. palpitations
  4. headache
70
Q

asthma related with GERD - management

A

omeprazole

71
Q

sarcoidosis effect on the musculoskeletal system

A

acute polyarthritis

chronic arthritis

72
Q

Lofgren syndrome

A
  1. erythema nodosum
  2. hilar adenopathy
  3. migratory polyarthralgia
  4. fever
73
Q

ankylosing spondylitis effect in lungs

A

limited chest expansion + spinal mobility–> restrictive lung disease

74
Q

COPD - seizures after 02 supplementation

A

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
Q

pulm contusion - symptoms can be worsen by

A

fluid overvolume

76
Q

resp arkalosis in incubated patient - next step

A

if appropriate TV –> decrease RR

77
Q

intemediate vs low risk solitary pulm nodule

A

interm is 8 mm or bigger

78
Q

pneumothorax - hypotension and tachycardia due to

A

compression of structures in the mediastinum –> impaired RV filling

79
Q

ideal location of endotracheal tube / if displaced to bronchus, which bronchus MC

A

2-6 cm above carina

- right (so left atelectasis)

80
Q

intubated patients - atelectasis due to misplacement vs pneumothorax

A

pneumothorax causes hemodynamically instability

81
Q

parapneumonic effusions - uncomplicated vs complicated regarding etiology

A

uncompl: sterile exudate in pleural space
complicaetd: bacterial invasion of pleural space –> continue to have symptoms despite antibiotics

82
Q

parapneumonic effusions - uncomplicated vs complicated regarding pleural fluid analysis

A

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
Q

parapneumonic effusions - complc vs uncomplicated regarding gram stain + culture

A

uncompl: negative
complic: FN due tto low bacter count

84
Q

parapneumonic effusions - uncomplc vs complic regarding treatment

A

uncomplicated: antibiotics
complic: antibiotics + drainage

85
Q

increased risk of pneumonia complicated with pleural effusion

A

immunodeficiency

86
Q

acute exacerbation of COPD is characterized by a change in at least 1 of the following

A
  1. cough severity or frequency
  2. volume or character of sputum production
  3. levels of dyspena
87
Q

Light criteria

A

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
Q

exercise induced bronchoconstriction - management

A

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
Q

normal pleural fluid ph / trandudate fluid ph / edudate

A
  • 7.6
  • 7.4-7.55
  • exudate: 7.3-7.45 (may be lower)
90
Q

pneumoconioses - types

A
  1. asbestosis
  2. Berylliosis
  3. Coal workers’ pneumoconiosis
  4. silicosis
91
Q

pneumoconioses (except berylliosi) - increased risk for

A
  1. cor pulmonale
  2. Caplan syndrome
  3. cancer
92
Q

Caplan syndrome

A

rheumatoid arthritis and pneumoconiases (coal, asbestosis, silicosis) with intrapulmonary nodules

93
Q

Asbestosis is associated with (exposure)

A
  1. shipbuilding
  2. roofing
  3. plumbing
94
Q

pathognomonic lesions of asbestosis (gross)

A

Ivory white, calcified supreadiaphragmatic and pleural plaques

95
Q

areas of asbestos plaques

A
  1. supreadiaphragmatic

2. pleural plaques

96
Q

carcinomas associated with asbestosis

A
  1. bronchogenic carcinoma (More common

2. mesothelioma

97
Q

berylliosis associated with (exposure)

A

berryllium in

  1. aerospace
  2. manufacturing industries
98
Q

lung Asbestosis - histology

A

ferruginous (asbestos) bodies: golden-brown fusiform rods resembling dumbbells, found in alveolar septum (visulized using PAS stain), often obtain by branchoalveolar lavage)

99
Q

ferruginous bodies are found in

A

alveolar septum

100
Q

berylliosis affects (area) / histology / treatment

A
  • upper lobes
  • noncaseating granoulomas in lung, hilar lymph nodes and systemic organs
  • occasionally responsive to steroids
101
Q

Coal workers’ pneumoconiosis is also known s / area

A

black lung disease

- upper lobes

102
Q

Coal workers’ pneumoconiosis - pathophysiology

A

prolonged coal dust exposure –> macrophages laden with carbon –> inflammation and fibrosis

103
Q

Anthracosis is caused by

A

mild exposure to carbon (collection of macrophages laden with carbon)

104
Q

Anthracosis - symptoms/found in

A

asymptomatic condition found in many urban dwellers exposed to sooty air

105
Q

Anthracosis - occupation

A

found in many urban dwellers exposed to sooty air

106
Q

Silicosis is associated with ….(occupation)

A
  1. foundries (factory that produces metal castings)
  2. sandblasting
  3. Mines
107
Q

Silicosis - pathophysiology

A

Macrophages respond to silica and release fibrogenic factors, leading to fibrosis. it is thought that silica may disrupt phagolysosomes and impair macrophages

108
Q

silicosis - increased risk for

A
  1. TB

2. bronchogenic carcinoma

109
Q

silicosis - CXR

A

Eggshell calcification of hilar lymph nodes

110
Q

pneumoconiases that affect upper lobes

A
  1. coal workers’ pneumoconiosis
  2. Silicosi
  3. Berylliosis
111
Q

pneumoconiases that affect lower lobes

A

asbestosis

112
Q

which are the classicfication group of pulmonary hypertension

A
  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
Q

multifactorial pulmonary hypertensions - causes

A
  1. hematologic disorders
  2. systemic disorders
  3. metabolic disorders
114
Q

pulmonary arterial hypertension (PAH) - causes

A
  1. idiopathic
  2. drugs
  3. connective tissue disease
  4. HIV infection
  5. portal hypertension
  6. congenital heart disease
  7. schistosomiasis
115
Q

pulmonary arterial hypertension (PAH) - idiopathic - pathophysiology

A

often due to inactivation mitation in BMPR2 gene –>

inhibits vascular SMCs proliferation

116
Q

primary spontaneous pneumothorax is due to

A

rupture of apical blebs or cysts in tall, thin, young males

117
Q

secondary spontaneous pneumothorax is due to

A
  1. diseased lung (bullae in emphysema, infections)

2. mechanical ventilation with use of high pressures (barotrauma)

118
Q

thrombi pulmonary emboli - histology

A

lines of Zahn: interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death

119
Q

1st generation H1 blockers - drugs

A
  1. diphenhydramine
  2. dimenhydrinate
  3. chlorpheniramine
120
Q

2nd generation H1 blockers - drugs

A
  • ADINE + cetirizine
    1. loratadine
    2. fexofenadine
    3. desloratadine
    4. cetirizine
121
Q

1st generation H1 blockers vs 2nd - used for

A

1st: 1. allergy 2. motion 3. sleep aid
2nd: allergy

122
Q

1st generation H1 blockers - toxicity

A
  1. sedation
  2. antimuscarinic
  3. anti-a-adrenergic
123
Q

2nd generation H1 blockers - toxicity

A

sedation (much less than 1st generation)

124
Q

pulmonary hypertension drugs - categories and drugs

A
  1. endothelin receptor antagonists –> BOSENTAN
  2. PDE-5 inhibitors –> SILDENAFIL
  3. Prostacyclin analogs –> EPOPROSTENOL, ILOPROST
125
Q

bosentan toxicity

A

hepatotoxicity

126
Q

pulmonary hypertensrion - prostacyclin analogs side effects

A
  1. flushing

2. jaw pain

127
Q

chronic bronchitis - pathology

A

hyperplasia of mucus-secreting glands –> Reid index >50%

128
Q

chronic bronchitis - definition

A

productive cough for >3 months PER YEAR (not necessarily consecutive) for >2 years

129
Q

causes of poor ciliary motility

A
  1. smoking

2. kartegener syndrome

130
Q

emphysema types - associations and area

A
  1. centriacinar: associated with smoking –> upper lobes

2. Panacinar: associated with α1 - antitrypsin –> lower lobes

131
Q

emphysema - diffusion capacity of CO test (and mechanism)

A

decreased diffusing capacity for CO resulting from destruction of alveolar walls

132
Q

blue bloaters vs pink puffer

A

blue: chronic bronchitis
pink: emphysema

133
Q

Restricted lung disease - drug toxicity

A
  1. bleomycin 2. busulfan

3. amiodarone 4. methotrexate

134
Q

PEAK airway pressure

A

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

LUNG + RENAL STEP 2 (5 decks)

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