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LUNG + RENAL STEP 2 > Lung 1 > Flashcards

Lung 1 Flashcards

1
Q

invasive aspergilosis - special biomarkers

A

positive cell wall biomarkers: galactomannan, beta D glucam.

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2
Q

an example of increased and decreased tactile fermitus

A

increased: consolidation
decreased: pleural effusion

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3
Q

ACE - when is the cough

A

within 1 week of initiation of increasing of dosage

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4
Q

approach to patient with suspected PE

A

stabilize patient with O2 and IV fluids –> evaluate for absolut contraindications to anticoagulation:

  1. yes: obstain diagnostic test for PE: (+) –> consider IVC filter, (-) –> no further
  2. no –> Wells criteria –>
    - likely: consider anticoagulation esp if patient has no contraindications, moderate to severe distress –> diagnostic test
    - unlikely –> diagnostic test
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5
Q

infl + pneumonoccoccal vaccination in COPD –> mortality

A

not decrease

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6
Q

goodpasture disease - systemic symptoms

A

uncommon

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7
Q

Invasive aspergiolsis - risk factors

A

immune

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8
Q

invasive aspergillosis - findings

A
  1. triad of fever, chest pain, hemoptysis
  2. pulm nodules with halo
  3. positive cultures
  4. positive cell wall biomarkers (galactomannan, betal D glucam
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9
Q

invasive aspergillosis -management

A

voriconazole +/- caspofungin

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10
Q

chronic pulmonary aspergilosis - risk factors

A

lung disease/damage (cavitary TB)

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11
Q

chronic pulm aspergilosis - findings

A
  1. more than 3 months: weight loss, hemoptysis, fatique
  2. cavitary lesion +/- funfus ball
  3. positive aspergillus IgG seology)
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12
Q

Chronic pulm aspergilosis - management

A

resect aspergilloma (if possible)

  1. azole (vorizonazole)
  2. embolization (if severe hemoptysis)
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13
Q

tumors of the mediastinum - location

A

anterior: thymoma, thyroid, teratoma, lymphoma
middle: bronchogenic cysts
posterior: neurogenic, esoph leiomyomas

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14
Q

hospitalized vs ventilator acquired pneumonia - definition

A

hosptial: 48 or more hours after admission
ventilator: 48 or more hours after intubation

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15
Q

Acute exacerbation of COPD - management

A
  1. O2 (target 88-92)
  2. inhaled bronchodilators
  3. systemic glucocrticoids (β2 or anticholinerg)
  4. antibiotics if at least 2 of dyspnea, more frequent cough, change in colore or volume of sputum)
  5. oselramivir if evidence of flu
  6. noninvasive (+) pressure ventilation
  7. intubation
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16
Q

acute exacerbation of COPD - steroids - route of administration

A

IV

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17
Q

pulm nodule sorrounded by ground glass

A

invasive aspergilosis (halo sign)

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18
Q

causes of obstructive pattern (and their DLCO)

A

asthma: normal/increaed
emphysema: decreasd
chronic bronchitis: normal

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19
Q

causes of increased DLCO

A
  1. asthma
  2. morbit obesity
  3. polycythemia
  4. pulm hemorrhage
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20
Q

increased PCWP is an indicator of

A

LA pressure

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21
Q

lung problems - PCWP?

A

not affected

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22
Q

asbesotis exposure - when develop disease

A

after 20 years of initial exposure

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23
Q

aspiration syndromes - types and mechanism

A

pneumonia: parenchyma infection, anaerobes microves
pnemonitis: parenchyma infl, aspiration of gastric acid

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24
Q

aspiration syndrome - types and clinical features

A
  1. pnemonia: daus after aspiration, fever, cough, sputum. CXR infiltrates, can progress to abscess
  2. pneumonitis: hours after event, from asymptomatic to resp distress, CXR infiltrates (1 or both lower lobes)
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25
Q

aspiration syndrome - types and management

A

pneumonia: clindamycin or b lactam + lactamase inh
pneumonitis: supportive (no antibiotics)

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26
Q

negative pressure pulm edema

A

when a patient has upper airway obstruction that results in large negative intrathoracic pressure (due to inspiration against obstruction)

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27
Q

the 3 MCC of clubbing

A
  1. Lung ca
  2. Cystic fibrosis
  3. R –> L cardiac shunts
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28
Q

Clubbing in COPD

A

copd does not cause

if there is, search for ca

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29
Q

management of PE if more than 4 wells

A

first antigoagulant, and after diagnostic tests

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30
Q

classic ECG in PE

A

prominent S in lead I, Q in lead III, and inverted T in head III (S1Q3T3)

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31
Q

management after Wells criteria

A
  1. PE likley –> CT pulm angiography –> if (-) is excluded, if (+) is confirmed
  2. PE unlikely –> D dimers –>: if more more than 500 –> CT pulm angiography, if less excluded
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32
Q

Modified Wells criteria

A
  • 3 points: Clinical signs of DVT, alternate diagnosis is less likley
  • 1.5 points: previous PE or DVT, herat rate more than 100, Recent surgery or immobilazation
  • 1 point: hemoptyisis, cancer
    MORE THAN 4 –> LIKELY
    4 OR LESS –> UNLIKELY
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33
Q

fat embolism - time after event

A

12-78h

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34
Q

pulm contusion - symptoms can be worsen by

A

fluid overvolume

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35
Q

COPD indications for O2 at home

A
  1. resting PaO2 55 or lower
  2. SaO2: 88 or less
  3. Those with RHF or HCT higher than 55 should be started if Pao2 lower than 60 or Sao2 lower than 90
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36
Q

the 3 MCC of chronic cough are

A
  1. upper airway cough syndrome (postnasal drip_
  2. asthma
  3. GERD
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37
Q

POSTNASAL SYNDROME

A

caused by rhinosinus conditions including allergic, perennial nonallergic and vasomotor rhinitis –> mechanical stimulation of cough reflex
treatment: chlorpheniramine

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38
Q

COPD exacerbation - when to give antibiotics

A

if 2/3 of:

  1. increaed dyspnea
  2. increased cough (more frequent o sever
  3. sputum production (change in color or volume)
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39
Q

anaphylaxis - IV vs IM epinephrine?

A

IM –> if no response –> IV

NO IMMEDIATELY IV DUE TO SE (arrhythmia)

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40
Q

the most effective way to differentiate asthma from COPD

A

spirometry before and after administration of a bronchodilator (usually albuterol)

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41
Q

COPD - factors that decrease mortality

A
  1. smoking cessation
  2. Long term supplemental 02 decreases mortality if:
    - SpO2 under 88%
    - SpO2 under 89% + RHF or erythrocytosis (HCT more than 55)
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42
Q

solitary pulm nodule - definition

A

round opacity up to 2 cm in diameter within and surrounded by pulm parenchyma
by convention: no pleural effusion, adenopathym atelectasis

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43
Q

solitary pulm nodule - DDX

A
  1. 1ry lung Ca
  2. Metastatic ca
  3. Benigh infect granulomas (TB, histopl, other fungus)
  4. Benign neolasm (lipomas, hamartomas, fibroma)
  5. vascular (AV malformation)
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44
Q

Solitary pulm nodule on routine chest X-ray - management

A

previous chest x-ray:
- stable over 2-3 years –> no further testing
- No previous imaging or possible nodule growth –>
CT:
1. Benign features –> serial CT scans
2. High suspicious for malignancy –> surgery
3. indeterminate or suspicious for malignancy –> biopsy or PET

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45
Q

high risk vs low risk for solitary pulm nodule

A

low: smaller than 0.8 cm, younger than 40, never skomed or smoking cessation more than 15 years, smooth margins
high: larger than 2 cm, older than 60, current smoker or cessation less than 5 years before, corona radiata or spiculated margins

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46
Q

Causes of recurrent pneumonia

A
  1. involving same region: local airway obstruction, aspiration –> CT
  2. involving different regions of lung: immunoddef, sinopulm disease, noninfectious (Vasculitis, etc)
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47
Q

antitryps def - smoking

A

COPD 10 years earlier compare to nonsmoking

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48
Q

empiric treatment of CAP

A
  1. outpatient:macrolide or doxycycline (healthy)
    resp quinolone or beta lactam + macrolide (comorbitities)
  2. inpatients: quinolone (IV) or betal lactam + macrolide
  3. ICU: beta lactam + macrolide or quinolne + beta lactam
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49
Q

resp quinolones

A

levo-, moxifloxacin

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50
Q

CURB-65

A 
Confusion
Urea more than 20
Respiration more than 30
Blood pressure lessthan 90/60
Age 65 or more
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51
Q

CURB-65 interpretation

A

0: low mortality –> outpatient
1-2 intermediate –> likley inpatient
3-4 urgent inpatient –> possibly ICU if socre more than 4

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52
Q

initial drug in stable PE in patient with RF

A 
unfractionated heparin (if severe: GFR lower than 30)
(the others are contraindicated)
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53
Q

SIADH - treatment

A

Fluid restrition (best initial) +/- salt tablets
hypertonic (3%)saline for severe
- DEMECLOCYCLINE ONLY IF THE OTHERS FAIL

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54
Q

PE - Aa gradient

A

increased

55
Q

anemia - Aa gradient

A

low

56
Q

dead space ventilation?

A

air in non-perfused areas

57
Q

subacute vs chronic cough

A

subacute: 3-8 wks
chronic: more than 8 wks

58
Q

evaluation of subacute or chronic cough

A

evaluate and treat as indicated (stop ACEi, H1 for upper airway cough, OFT for asthma, PPI for GERD) –> if no improvement –> Cest X-ray
- parenchymal disease, purulent sputum, immune, no specific etiology –> chest x-ray

59
Q

atelectasi - PCO2

A

low

60
Q

upper airway obstruction - graph

A

decrease the airflow rate during insipration and expiration –> flattening both the top and bottom of the flow - volume loop

61
Q

FRC in ankylosing spond

A

normal or increased due to fixation of a rib in the inspiratory position

62
Q

pulsus paradoxus - seen in

A
  1. cardiac teponade 2. asthma 3. obstructive sleep apnea

4. pericarditis 5. croup

63
Q

asthma - histology

A
  1. smooth muscle hypertrophy
  2. Curschmann spirals: shed epithelium forms whorled mucus plugs
  3. Charcot - Leyden crystals: eosinophilic, hexagonal, double-pointed, needle-like crystal from breakdown of eosinophils in sputum
64
Q

asthma drugs

A
  1. β2 agonists (albuterol, salmeterol, formoterol)
  2. corticosteroids (fluticasone, budesonide)
  3. Muscarinic antagonists (ipratropium)
  4. Antileukotrienes (montelukast, zafirlukast, zileuton)
  5. omalizumab
  6. Methylxanthines (theophylline)
  7. Metacholine
65
Q

role of corticosteroids (fluticosine, budesonide) in asthma therpay
asthma - albuterol used in

A
  • 1st line therapy for chronic asthma

- during acute exacerbation

66
Q

asthma - ipratropium vs tiotropium according to action

A

tiotropium is long acting

67
Q

montelukast, zafirukast mechanism of action

A

block leukotriene receptor (CysLT1)

68
Q

Zileuton mechanism of action / SE

A

5-lipoxygenase pathway inhibitor. Block conversion of arachnoid acid to leukotrienes
- hepatotoxic

69
Q

adenosine receptor antagonists

A
  1. theophylline

2. caffeine

70
Q

theophylline adverse effects

A
  1. cardiotoxicity
  2. neurotoxicity
    narrow therapeutic index
71
Q

think asthma as a diagnosis when

A
  1. Recurrent episodes of wheezing
  2. Cough at night
  3. Coughing or wheezing after exercise
  4. Cough, wheezing, chest tightness after exposure to allergens or pollutants
  5. Colds “go down to the chest” or take longer than 10 days
72
Q

inspiratory reserve volume (IRV)

A

air that can still be breathed in after normal inspiration (3.3L)

73
Q

Expiratory reserve volume (ERV)

A

air that can be breathed out after normal expiration (1L)

74
Q

Inspiratory capacity (IC)

A

inspiratory reserve volume (IRV) + tidal volume (TV)

3.8L

75
Q

Vital capacity (VC)

A

Maximum volume of gas that can be expired after a maximal inspiration (4.8L)
inspiratory reserve volume (IRV) + tidal volume (TV) + Expiratory reserve volume (ERV)

76
Q

Functional residual capacity (FRC)

A 
Volume of gas in lungs after normal expiration (2.2L)
Residual volume (RV) + Expiratory reserve volume (ERV)
77
Q

minute ventilation (Ve)

A

total volume of gas that entering lungs per minute

Ve = tidal volume x respiratory rate

78
Q

Alveolar ventilation (Va)

A

volume of gas per unit time that REACHES ALVEOLI

Va = (tidal volume - physiological dead space) x respiratory rate

79
Q

situations that alter FEV1/FVC

A

decreased: obstructive lung disease
increased: restrictive lung disease

80
Q

IRV is used during

A

exercise

81
Q

Causes of increased Vital capacity

A

acromegaly

82
Q

physiologic dead space equation

A

tidal volume (Vt) x (arterial PCO2- expired PCO2)/ arterial PCO2

83
Q

physiologic dead space definition

A

anatomic dead space of conducting airways plus alveolar dead space
Volume of inspired air that does not take part in gas exchange

84
Q

alveolar dead space distribution

A

apex of healthy lung is largest contributor of dead space

85
Q

Physiologic dead space (per breath) normal

A

150 ml/breath

86
Q

pathologic dead space

A

when part of the respiratory zone becomes unable to perform gas exchange (ventilated but not perfused)

87
Q

Lung cancer - complication

A

mnemonic: SPHERE + dysphagia + phrenic nerve paresis - heart or pericardial invasion +pleural invasion
1. Superior vena cava syndrome 2. Pancoast tumor
3. Horner syndrome 4. Endocrine (paraneoplastic)
5. Recurrent laryngeal nerve compression (hoarseness)
6. Effusions (pleural or pericardial)

88
Q

Lung cancer - risk factors

A
  1. smoking 2. secondhand smoking 3. radon 4. asbestos 5. family history 6. Asbestosis 7. Silicosis
  2. Coal
89
Q

primary lung cancer - types (small or non small?) / location

A
  1. small cell (oat cell) carcinoma - central
  2. adenocarcinoma (non-small) - peripheral
  3. Squamous cell carcinoma (non-small) - central
  4. Large cell carcinoma (non-small) - peripheral
  5. Bronchial carcinoid tumor (non-small) - central or peripheral
90
Q

lung small cell (oat cell) carcinoma may cause/produce

A
  1. Cushing syndrome (ACTH) 2. SIADH
  2. antibodies against presynapitc Ca2+ channels (Lambert-Eaton myasthenic syndrome)
  3. or neurons (paraneoplastic myelitis/encephalitis, sabacute cerebellar degeneration)
91
Q

lung small cell (oat cell) carcinoma - gene amplification

A

MYC

92
Q

lung small cell (oat cell) carcinoma - histology

A
  1. neoplasm of neuroendocrine Kulchitsky cells (small dark blue cells)
  2. chromogranin A positive
  3. undifferentiated (very aggressive)
  4. Neuron specific enolase positive
93
Q

lung squamous cell carcinoma - may cause/produce / CXR

A
  1. cavitation
  2. hypercalcemia (produce PTHrP)
    - CXR: Hillar mass arising from bronchus
94
Q

bronchial carcinoid tumor - histology

A

nests of neuroendocrine cells

chromogranin A positive

95
Q

chromogranin A positive lung tumors

A
  1. bronchial carcinoid tumor

2. lung small cell (oat cell) carcinoma

96
Q

bronchial carcinoid tumor - presentation/symptoms

A
  1. symptoms due to mass effect

2. carcinoid syndrome (flashing, diarrhea, wheezing)

97
Q

lung Large cell carcinoma - treatment / it can secrete …

A
  1. less responsive to chemotherapy
  2. remove surgically
    - β-hCG
98
Q

MC primary lung cancer

MC lung cancer in non smokers

A

adenocarcinoma

99
Q

lung adenocarcinoma activating mutations / paraneoplastic

A
  1. KRAS 2. EGFR 3. ALK

- hypertrophic osteorarthropathy (clubbing)

100
Q

adenocarcinoma in siitu

A

bronchioarveolar subtype (hazy infiltrates similar pneumonia)

101
Q

bronchioarveolar subtype - smoking

Bronchial carcinoid tumor - smoking

A

both no relationship

102
Q

mesothelioma - risk factors

A

asbestosis

smoking is not a risk factor

103
Q

mesothelioma - histology / RF

A
  • psammoma bodies
  • calretinin and cytokeratin (+) in almost all mesotheliomas, ((-) in most carcinomas)
  • RF: ASBESTOSIS (not smoking)
104
Q

pancoast tumor (superior sulcus tumor) may cause

A

Compression of locoregional structures:

  1. Horner syndrome
  2. Superior vena cava syndrome
  3. hoarseness
  4. sensorimotor deficits
105
Q

superior vena cava syndrome - medical emergency because

A

it can raise intracranial pressure (if obstruction is severe)
–> headaches, dizziness, increased risk of aneurysm/rupture of intracranial arteries

106
Q

Lung Ca - MC symptom

Lung Ca - single most common area of metastasis

A
  • cough (75%)

- brain

107
Q

lobar pneumonia - typical organisms

A
  1. S pneumonia
  2. Legionella
  3. Klebsiella
108
Q

Bronchopneumonia - typical organisms

A
  1. S. pneumonia
  2. S. aureus
  3. H. influenza
  4. Klebsiella
109
Q

interstitial (atypical) pneumonia - typical organisms

A
  1. Viruses (influenza, CMV, RSV, adenovirus)
  2. Mycoplasma
  3. Legionella
  4. Chlamydia
110
Q

organism that causes BOTH Lobar and Bronchopneumonia

A

Klebsiella

S. pneumonia

111
Q

bronchopneumonia - distribution

A

patchy distribution involving >= 1 lobe

112
Q

walking pneumonia

A

interstitial (atypical) pneumonia –> generally follows a more indolent course

113
Q

interstitial atypical pneumonia - typical presentation

A

relatively mild URI symptoms

114
Q

lung abscess - organisms

A
  1. anaerobes (bacteroids, peptostreptococcus, fusobacterium)
  2. S aureus
  3. Klebsiella
115
Q

S. aureus - pneumonia type?

A

Bronchopneumonia (or lung abscess)

116
Q

H. infl - pneumonia type?

A

bronchopneumonia

117
Q

Lung abscess 2ry to aspiration is most often found in …. (location)

A

right lung:
upright –> basal segment of right lowr lobe
supine –> posterior segment of right upper lobe or superior segment of right lower lobe

118
Q

structure perforating diaphragm (an where)

A

T8: IVC
T10: esophagus vagus
T12: aorta, thoracic duct, azygos vein

119
Q

Screening test for fetal lung maturity

A
  1. lecithin/sphingomyelin ration in amniotic fluid –>
    - if more than 2 –> healthy
    - if less than 1.5 –> predictive of NRDAS
  2. foam stability test
  3. surfactant/albumin ratio
120
Q

Pulmonary surfactant synthesis by time

A

begins around week 26 of gestation, but mature levels are not achieved until around week 35

121
Q

neonatal respiratory distress syndrome - persistently low O2 tension - risk of

A
  1. PDA
  2. metabolic acidosis
  3. necrotizing enterocolitis
122
Q

neonatal respiratory distress syndrome - therapeutic supplemental of O2 can result in

A
  1. retinopathy of prematurity
  2. Intraventricular haemorrhage (brain)
  3. Bronchopulmonary dysplasia
123
Q

hemoglobin (hb) - properties

A
  1. positive cooperativity

2. negative allostery

124
Q

hemoglobin (hb) - positive cooperativity

A

tetrameric Hb molecule can bind 4 02 molecules and has higher affinity for each subsequent O2 molecule bound

125
Q

methemoglobin vs normal hemoglobin - iron status

A

normal: resuced state Fe2+ (FERROUS)
methemoglobin: oxidized state Fe3+ (FERRIC)

126
Q

methemoglobin properties

A
  • it does not bind 02 as readily

- it has increased affinity for cyanide

127
Q

methoglobinemia may present with

A
  1. cyanosis 2. chocolate-colored blood
128
Q

methoglobinemia can can be treated with

A
  1. methylene blue

2. vitamin C

129
Q

how to treat cyanide poisoning (and the mechanism)

A

nitrites followed by thiosulfate

nitrites: hemoglobin –> methoglobin which bind cyanide
thiosulfate: to bind cyanide, forming thiocyanate , which is renally excreted

130
Q

substance that cause poisoning by oxidizing F2+ to F3+ (found in)

A
  1. nitrites (from dieaary intake or polluted/high altitude water)
  2. benzocaine
131
Q

methylene blue is used to

A

treat methoglobinemia

132
Q

how to improve oxygenation in incubation

A

increase PEEP of FiO2

if FiO2 already higher than 60, prefer PEEP

133
Q

goals for oxygenation in ARDS

A
  • 88-95

- 55-80

LUNG + RENAL STEP 2 (5 decks)

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