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respiratory > UW 1 > Flashcards

UW 1 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

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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7
Q

the main cause of hypercapnia in COPD

A

increased dead space ventilaiton

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8
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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9
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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10
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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11
Q

PFT in asthma

A

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

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12
Q

PFT in COPD

A

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

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13
Q

PFT in interstitial lung disease

A

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

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14
Q

PFT in pulm arterial hypertension

A

normal TLC
normal FEV1/FVC
low DLCO

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15
Q

Restrictive chest wall disease

A

low TLC
normal FEV1/FVC
normal DLCO

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16
Q

DLCO in pulm arterial hypertention

A

low

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17
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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18
Q

hypersensitivity pneumonitis - management

A

avoidance of responsible antigen

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19
Q

sputum and blood culutres in outpatient pneumonia

A

not required

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20
Q

lung compliance of ARDS

A

low

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21
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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22
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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23
Q

systemic epinephrine in severe astham exacerbation

A

only in severe when inhaled therapy cannot be given

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24
Q

mild to moderate asthma asthma exacerbation - management

A

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

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25
Q

Wegerer - giagnosis

A

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

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26
Q

Wegener - management

A

corticosteroids + immunomodulators (MTX, cyclophosphamide)

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27
Q

it can increased the chance of FP ANCA

A

HIV

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28
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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29
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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30
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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31
Q

increasing of PEEP in ARDS - purpose

A

reopen of alveoli –> reduce shunting

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32
Q

MC SE of inhaled corticosteroid therapy

A

oropharyngeal thrush (oral candidiasis)

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33
Q

bornchodilator respone in asthma

A

improvement of FEV1 more than 12%

34
Q

asthma severity for patients not on controller medication (step 1)

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
35
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

36
Q

position dependent hypoxemia - mechanism

A

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

37
Q

Aspirin exacerbated resp disease - mechanism

A

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

38
Q

Aspirin exacerbated resp disease - manifestation

A

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

39
Q

aspirin-exacerbated resp disease - treatment

A

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

40
Q

illegal that can cause hemoptysis

A

inhaler cocaine

41
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

42
Q

ARDS - always low TV - why

A

decrease the likelihood of overdistending alveoli

(improves mortality) –> causes barotrauma

43
Q

ARDS under ventilator - hypercapnia

A

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

44
Q

ARDS - saturation target

A

greater than 88%

45
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)
46
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
47
Q

allergic rhinitis - treatment

A

intranasal glucocorticoids

antihistamines

48
Q

nonallergic rhinitis - treatment

A

mild: intranasal antihistamine or glucocorticoids

moderate to severe: combination therapy

49
Q

nasal cytology in nonallergic rhinitits

A

eosinophils

not required

50
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
51
Q

systemic sclerosis on the lung

A
  • hyperplasia of the intimal SMCs layer –> incr pulm resistance –> pulm hypertension
  • interstitial fibrosis
52
Q

strongest RF for obstructive sleep apnea

A

obesity

53
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)
54
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
55
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
56
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
57
Q

test to confirm bronchiectasias

A

high resolution CT

58
Q

Beta 2 agonists - SE

A
  1. hypokalemia –> muscle weakness, arrhythnia, EKG abnormalities
  2. tremor
  3. palpitations
  4. headache
59
Q

asthma related with GERD - management

A

omeprazole

60
Q

sarcoidosis effect on the musculoskeletal system

A

acute polyarthritis

chronic arthritis

61
Q

Lofgren syndrome

A
  1. erythema nodosum
  2. hilar adenopathy
  3. migratory polyarthralgia
  4. fever
62
Q

ankylosing spondylitis effect in lungs

A

limited chest expansion + spinal mobility–> restrictive lung disease

63
Q

sleep apnea syndrome - best initial steps

A

weight reduction, avoidance of sedatives, avoid alcohol, acoid supine posture during sleep

64
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

65
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
66
Q

pulm contusion - symptoms can be worsen by

A

fluid overvolume

67
Q

resp arkalosis in incubated patient - next step

A

if appropriate TV –> decrease RR

68
Q

intemediate vs low risk solitary pulm nodule

A

interm is 8 mm or bigger

69
Q

pneumothorax - hypertension and tachycardia due to

A

compression of structures in the mediastinum –> impaired RV filling

70
Q

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

A

2-6 cm above carina

- right (so left atelectasis)

71
Q

intubated patients - atelectasis due to misplacement vs pneumothorax

A

pneumothorax causes hemodynamically instability

72
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

73
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

74
Q

parapneumonic effusions - complc vs uncomplicated regarding gram stain + culture

A

uncompl: negative
complic: FN due tto low bacter count

75
Q

parapneumonic effusions - uncomplc vs complic regarding treatment

A

uncomplicated: antibiotics
complic: antibiotics + drainage

76
Q

increased risk of pneumonia complicated with pleural effusion

A

immunodeficiency

77
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
78
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
79
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

80
Q

normal pleural fluid ph / trandudate fluid ph / edudate

A
  • 7.6
  • 7.4-7.55
  • exudate: 7.3-7.45 (may be lower)
81
Q

CHF - where is the fluid

A

61% bilateral
27% only R
12% only left

respiratory (27 decks)

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