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Boards Basic > Pulmonology > Flashcards

Pulmonology Flashcards

1
Q

Interpreting DLCO: decreased DLCO and reduced lung volumes

A

pulmonary fibrosis

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2
Q

Interpreting DLCO: decreased DLCO and normal LV

A

pulm vasc disease and anemia

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3
Q

Interpreting DLCO: decreased DLCO and airflow obstruction

A

COPD, bronchiectasis

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4
Q

Interpreting DLCO: increased or normal DLCO and airflow obstruction

A

asthma

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5
Q

Interpreting DLCO: increased DLCO

A

pulmonary hemmorrhage, polycythemia, or left to right shunt

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6
Q

Interpreting DLCO: normal dlco and decreased LV

A

obesity or extrapulmonary cause

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7
Q

Airway reversibility with improvement of bronchodilator signs

A

A ≥12% increase in either FEV1 or FVC and an increase ≥200 mL

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8
Q

Reversible airway disease with improvement of bronchodilator signs

A

A ≥12% increase in either FEV1 or FVC and an increase ≥200 mL from baseline

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9
Q

Restrictive airway disease ratio of FEV1 and FVC

A

Equal reductions in FEV1

and FVC

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10
Q

consider any cough that is nocturnal, seasonal, or related to a workplace
or activity as…

A

asthma

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11
Q

Bronchoprovocation testing is indicated for

A

patients with a suggestive clinical history for asthma but normal spirometry.
Bronchoprovocation testing with exercise is indicated to diagnose exercise-induced asthma in patients who have dyspnea following exercise but normal spirometry

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12
Q

does normal spirometry rule out asthma

does normal bronchoprovocation test rule out asthma

A

no

yes

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13
Q

alternative ddx for wheezing

A

HF, COPD, vocal cord dysfunction, and upper airway obstruction

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14
Q

xray in chronic eosinophilic pneumonia

A

“photographic-negative” pulmonary edema (peripheral pulmonary edema)

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15
Q

clinical findings in chronic eosinophilic pna

A

striking peripheral blood eosinophilia, fever, and weight loss in a long-term smoker

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16
Q

dx chronic eosinophilic pna

A

by bronchoscopy with biopsy or bronchoalveolar lavage showing a high eosinophil count

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17
Q

clinical findings of Allergic bronchopulmonary

aspergillosis

A

Asthma manifests with eosinophilia, markedly high serum IgE levels, and intermittent pulmonary infiltrates

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18
Q

dx of Allergic bronchopulmonary aspergillosis

A

positive skin test for Aspergillus and IgG and IgE antibodies to Aspergillus

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19
Q

xray of Allergic bronchopulmonary aspergillosis

A

radiographic opacities in the upper lobes

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20
Q

overlooked until advaced Allergic bronchopulmonary aspergillosis for

A

fixed obstruction and bronchiectasis

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21
Q

clinical findings of Eosinophilic granulomatosis

with polyangiitis

A

Upper airway and sinus disease precedes difficult-to-treat asthma

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22
Q

red flag sign of Eosinophilic granulomatosis

with polyangiitis

A

flares associated with use of

leukotriene inhibitors and glucocorticoid tapers

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23
Q

dx of Eosinophilic granulomatosis

with polyangiitis

A

Serum p-ANCA may be elevated

Hallmark diagnostic finding is eosinophilic tissue infiltrates

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24
Q

difficult to control asthma you should get what further testing

A

echo and cxr. Obtaining flow-volume loops and direct visualization of the larynx during an acute episode may be helpful in diagnosing tracheal obstruction
and vocal cord dysfunction

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25
Q

asthma is an extrapharyngeal manifestation of

A

gerd

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26
Q

symptom frequency asthma intermittent

A

<2 per week or <2 per month

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27
Q

symptom frequency asthma: mild persistent

A

Symptoms >2 per week but <1 per day or

nocturnal sx >2 per month

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28
Q

symptom frequency asthma: moderate persistent

A

Need for daily use of short-acting β-agonist ≥1 per week

nocturnal: Acute exacerbations ≥2 per week

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29
Q

symptom frequency asthma: severe persistent

A

Continual symptoms that limit physical activity nocturnal: Frequent

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30
Q

Step 1: Intermittent asthma tx

A

Select a short-acting β-agonist as needed

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31
Q

Step 2: Mild persistent ASTHMA TX

A

Add a low-dose inhaled glucocorticoid

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32
Q

Step 3: Moderate persistent asthma tx

A

Add one of the following:
1. Low to medium doses of an inhaled glucocorticoid and a LABA (preferred)
2. Medium doses of an inhaled glucocorticoid
3. Low to medium doses of an inhaled glucocorticoid and a single long-term controller medication
(leukotriene modifier or theophylline)

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33
Q

step 4: : Severe persistent asthma tx

A

Add high doses of an inhaled glucocorticoid plus a LABA or LAMA and possibly oral glucocorticoids

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34
Q

Omalizumab indications

A
  • moderate to severe asthma
  • inadequate control of symptoms with inhaled glucocorticoids
    • evidence of allergies to perennial aeroallergen
    • IgE levels between 30 and 700 kU/L
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35
Q

Anti–interleukin-5 monoclonal antibodies (mepolizumab, reslizumab) indications

A

r patients with an absolute eosinophil count >150 cells/µL and severe asthma
not controlled with standard therapy.

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36
Q

risk of theophylline and macrolide or fluoroquinolone

A

toxicity

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37
Q

risk of using laba isolated for asthma

A

increase mortality risk

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38
Q

diagnosis with patient with suspected asthma but improves immediately with intubation

A

vocal cord dx

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39
Q

COPD includes the following diseases

A

emphysema, chronic bronchitis, obliterative bronchiolitis, and asthmatic bronchitis

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40
Q

what to test in pts with COPD <45 years who have a strong family history of COPD or without identifiable COPD risk
factors

A

alpha antitrypsin dx

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41
Q

Bronchiectasis is usually associated with

A

inciting event (childhood pna, tb,

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42
Q

bronchiectasis symptoms

A

Large-volume sputum production with purulent exacerbations; hemoptysis

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43
Q

bronchiectaisis xray finding

A

tram lines diagnose with HRCT

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44
Q

adult CF characteristics

A

Obstructive pulmonary disease is most common presentation in adult patients; other symptoms may include
recurrent respiratory infections, infertility
Positive sweat chloride test result

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45
Q

Adult bronchiolitis characteristics

A

Found in current or former smokers; may be idiopathic or associated with other diseases such as RA
Poorly responsive to bronchodilators; responds to smoking cessation and glucocorticoids

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46
Q

Bronchiolitis obliterans characteristics

A

Presents with dyspnea without improvement following bronchodilators, normal or hyperinflated lungs on chest
x-ray; associated with injury to small airways; consider in patients after lung or stem cell transplantation

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47
Q

bacterial infections most common in CF pts>

A

Pseudomonas aeruginosa, Staphylococcus aureus, Haemophilus influenzae, or Burkholderia cepacia

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48
Q

• In patients with CF and acute abdominal pain consider

A

intussusception

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49
Q

supression of chronic pulm infections in cf

A

aerosolized tobramycin

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50
Q

tx for persistent secretions in cf

A

aerosolized recombinant human DNase (dornase alfa) or hypertonic saline

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51
Q

DPLD HRCT finding hilar lymphadenopathy

A

sarcoidosis

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52
Q

DPLD HRCT finding pleural effusion

A

connected tissue related disease

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53
Q

DPLD HRCT finding pleural placques

A

asbestosis

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54
Q

drugs causing dpld

A

: amiodarone, methotrexate, nitrofurantoin, chemotherapeutic

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55
Q

smoking relate dpld

A

X-ray shows ground-glass opacities and thickened interstitium

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56
Q

radiation dpld duration of onset

A

May occur 6 weeks to months after radiation therapy

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57
Q

hypersensitivity pneumonitis HRCT

A

ground-glass opacities on high resolution CT scan

58
Q

IPF xray

A

honeycombing, bibasilar infiltrates with fibrosis

59
Q

cryptogenic organizing pneumonia

A

x-ray shows focal areas of consolidation that may migrate from one
location to another

60
Q

Pulmonary alveolar

proteinosis

A

Diagnosed via bronchoalveolar lavage, which shows abundant protein in the airspaces; chest CT shows
“crazy paving” pattern

61
Q

pna/HF vs dpld Patients with dyspnea for days or weeks

A

PNA or HF

62
Q

alternatiive dx: dyspnea and pulmonary crackles but no other findings of HF

A

dpld

63
Q

characteristic findings of IPF

A

Characteristic findings

are the gradual onset of a nonproductive cough and dyspnea over approximately 3 months in older adults

64
Q

PE in IPF

A

normal temperature
• bibasilar crackles (“dry,” end-inspiratory, and “Velcro-like” in quality)
• late-phase cor pulmonale
• clubbing (25% of patients)

65
Q

IPF xray, CT scan and PFTs

A

Chest x-ray shows peripheral reticular opacities and honeycomb
changes at the lung bases. HRCT scan reveals subpleural cystic
changes and traction bronchiectasis.

66
Q

Shoud you intubate or ventilate patient’s with resp failure in IPF

A

No

67
Q

lofgren syndrome

A

fever, bilateral hilar lymphadenopathy, EN, and often ankle arthritis

68
Q

uveoparotid fever

A

featuring anterior uveitis, parotid gland enlargement, facial palsy, and fever)

69
Q

hypercalcemia in sarcoid cause

A

extrarenal production of calcitriol by granuloma cells a

70
Q

occupation with exposure to berrylium

A

light bulb or semiconductor factories)

71
Q

patients with silicosis, fever, and cough should be tested for

A

tb

72
Q

occupations at risk for asbestosis

A

construction industry, the automotive servicing industry, and the
shipbuilding and repair industry.

73
Q

the latent period for asbestosis is

A

10-15 years

74
Q

what should also be excluded when finding pleural effusion in nephronic syndrome

A

PE and renal artery thrombosis

75
Q

who should be screened for PH

A
  1. SSc
    2.liver transplantation candidates with portal hypertension
    3, first-degree relatives of patients with familial PAH
  2. patients with congenital heart disease
    with systemic-to-pulmonary shunts.
76
Q

PH cut off

A

resting mean pulmonary arterial pressure of ≥25 mm Hg

77
Q

PH 1-5

A
  1. small pulmonary arterioles resulting in high pulmonary vascular resistance (PAH)
  2. left sided CHF
  3. Respiratory illness
  4. CTEPH
  5. unknown causes
78
Q

drugs associated with PH

A

fenfluramine, amphetamines, and cocaine

79
Q

4 types of testing for PH

A
  • echocardiography as the initial study; a systolic pulmonary artery pressure >40 mm Hg is suggestive of PH
  • bubble contrast echocardiography or TEE is indicated to evaluate for intracardiac shunts (e.g., ASD)
  • right heart catheterization to confirm the diagnosis and quantify the degree of PH
  • left heart catheterization and coronary angiography exclude LV dysfunction as a cause of PH
80
Q

testing for cteph

A
  1. pulmonary arterial pressure ≥25 mm Hg in the absence of left-sided HF
  2. compatible imaging evidence of chronic thromboembolism by V/Q scanning
81
Q

most common cause of PH

A

left-sided heart disease and hypoxic respiratory disorders

82
Q

Tx for group 1 PH

A

CCB for those with vasodilator resp on rh cath

Lung or heart-lung transplantation should be considered for patients in whom drug treatment is unsuccessful.

83
Q

CTEPH tx

A

Life-long anticoagulant therapy is indicated in all patients with CTEPH. Pulmonary thromboendarterectomy is the only definitive therapy for CTEPH

84
Q

3 most common causes of hemoptsysis

A

Bronchitis, bronchogenic carcinoma, and bronchiectasis

85
Q

SOLID lung nodule: No (low-risk patient)
<6 mm
6-8 mm >8 mm

A
  1. No follow-up
  2. CT at 6-12 months, then consider CT at 18-24 months
  3. Consider CT at 3 months, PET/CT, or tissue sampling
86
Q

SOLID lung nodule: High risk
<6 mm
6-8 mm
>8 mm

A
  1. Optional CT at 12 months
  2. CT at 6-12 months, then CT at 18-24 months
  3. Consider CT at 3 months, PET/CT, or tissue sampling
87
Q

Pure Ground Glass Lung nodule
<6 mm
≥6 mm

A
  1. No follow-up

2. CT at 6-12 months to confirm persistence, then CT every 2 years until 5 years

88
Q

Subsolid lung nodule
<6 mm
≥6 mm

A
  1. No follow-up
  2. CT at 3-6 months to confirm persistence. If unchanged and solid component
    remains <6 mm, annual CT should be performed for 5 years
89
Q

common medialstinal masses

  1. anterior
  2. middle
  3. posterior
A
  1. thymus, teratoma, lymphoma and thyroid
  2. lymph nodes and cysts
  3. neurogenic (schwannomma)
90
Q

what AHI is positive on sleep study for osa

A

AHI of >5/h during a sleep study

91
Q

High-altitude periodic breathing (HAPB) pathophys and signs

A 
Hypoxia-induced hyperventilation lowers
Pco2 toward the apneic threshold,
decreasing respiratory rate, which raises
Pco2 and results in recurrent
hyperventilation

Repetitive arousals from sleep, often with
paroxysms of dyspnea

92
Q

Acute mountain sickness (AMS) pathophys and signs

A

Hypoxia and hypocarbia-induced
alterations in cerebral blood flow

Headache, fatigue, nausea, and vomiting,
in addition to disturbed sleep related to
HAPB

93
Q

High-altitude cerebral edema (HACE) pathophys and signs

A

Brain edema at altitudes typically above
10,000-13,000 feet

Confusion, irritability, ataxia, coma, and
death

94
Q

High-altitude pulmonary edema (HAPE) pathophys and signs

A

PH and pulmonary edema

Cough, dyspnea at rest, pink frothy
sputum, hemoptysis, and pulmonary
crackles

95
Q

prevention and tx of altitude illness

A

Prevention- ascend slowly
- Acetazolamide accelerates the acclimatization.

Acetazolamide, dexamethasone, and
supplemental oxygen are used to treat AMS.

Definitive treatment for HACE is immediate descent from altitude; dexamethasone,
supplemental oxygen, and hyperbaric therapy may also be used.

The HAPE treatment of choice is supplemental oxygen and rest.

96
Q

PFTs in neuromuscular disorders

A

pulmonary function tests show restriction on spirometry and lung volume measurement but normal diffusing capacity

97
Q

mild moderare severe ards cut off

A

Mild ARDS Arterial Po2/Fio2 ratio of 201-300 mm Hg, measured with PEEP ≥5 cm H2O

Moderate ARDS Arterial Po2/Fio2 ratio of 101-200 mm Hg, measured with PEEP ≥5 cm H2O

Severe ARDS Arterial Po2/Fio2 ratio of ≤100 mm Hg, measured with PEEP ≥5 cm H2o

98
Q

Diffuse alveolar

hemorrhage characteristics

A

Acute kidney injury with microscopic or gross hematuria or other evidence of vasculitis present
Associated with stem cell transplantation
Hemosiderin-laden macrophages in bronchoalveolar lavage fluid

99
Q

acute eosinophilic pneumonia

A

Cough, fever, pleuritic chest pain, and myalgia; may be precipitated by initiation of smoking
>15% eosinophils in bronchoalveolar lavage fluid

100
Q

Hypersensitivity

pneumonitis characteristics

A

slower onset than ards
mimicks ards
exposure farmers, birds, hot tubs

101
Q

Cryptogenic organizing

pneumonia

A

May be precipitated by viral syndrome
Slower onset than ARDS (>2 weeks) with progressive course; however, may present in an advanced stage,
mimicking ARDS

102
Q

when starting nppv how do you know if tx is working

A

Improvements in blood gas values and clinical condition should occur within 2 hours of starting NPPV. If not, intubation should
be considered to avoid undue delay and prevent respiratory arrest

103
Q

how to tell auto peep on ventalator

A

flow tracing on the ventilator shows continuous expiratory flow until the start of inspiratory flow

104
Q

causes and findings in auto peep

A

COPD or acute asthma, ARDS (increased flow resistance), and a high minute ventilation
(>12-15 L/min). Characteristic findings are wheezing and marked expiratory prolongation, drop in BP, and patient restlessnes

105
Q

how to improve auto peep

A
  • treat airway obstruction (e.g., bronchodilators in COPD or asthma)
  • decrease the respiratory rate or tidal volume
  • increase the inspiratory flow rate (shorten inspiratory time)
  • prolong the expiratory time
  • allow permissive hypercapnia
  • sedate and/or paralyze the patient
106
Q

how to improve respiratory

acidosis on vent

A

↓ Arterial Pco2

Increasing respiratory rate

Increasing tidal volume:

in volume control mode, directly choose the tidal volume;
in pressure control mode, increase the
inspiratory support pressure to increase
tidal volume

107
Q

Improve respiratory

alkalosis on vent

A

↑ Arterial Pco2

Decreasing respiratory rate
Decreasing tidal volume

108
Q

Improve tissue

oxygenation on vent

A

↑ O2 saturation, arterial Po2

Increasing Fio2
Increasing PEEP

109
Q

when can you extubate

A

When a patient can maintain an arterial O2 saturation >90% breathing Fio2 ≤0.5, PEEP <5 cm H2O, and pH >7.30, it is reasonable
to consider extubation
. Paired daily spontaneous awakening trials (withdrawal of sedatives) with daily spontaneous breathing
trials result in a reduction in mechanical ventilation time, ICU and hospital length of stay, and 1-year mortality rates.

110
Q

Cardiogenic shock

A

Low cardiac output, elevated PCWP, and high SVR

111
Q

Hypovolemic shock

A

Low cardiac output, low PCWP, and high SVR

112
Q

Obstructive shock

A

Low cardiac output, variable PCWP, and high SVR

113
Q

Anaphylactic shock

A

High cardiac output, normal PCWP, and low SVR

114
Q

Septic shock

A

High cardiac output (early) that can become depressed (late) and low SVR

115
Q

Malignant hyperthermia suggestive history, signs and treatment

A

Exposure to volatile anesthetic (halothane
isoflurane, succinylcholine, or
decamethonium)

Masseter muscle
rigidity; ↑ arterial Pco2

Stop the inciting drug
Dantrolene

116
Q

neuroleptic malignant syndrome suggestive history, signs and tx

A

Haloperidol, olanzapine, quetiapine, and
risperidone or withdrawal from L-dopa;
onset over days to weeks

Altered mentation,
severe rigidity, ↑ HR, ↑
BP, no clonus, ↓ reflexes

Stop the inciting drug
Dantrolene
Bromocriptine

117
Q

serotonin syndrome

A

Onset within 24 h of
initiation or increasing
dose

Agitation, rigidity,
clonus, ↑ reflexes

Stop the inciting drug
Benzodiazepines
Cyproheptadine

118
Q

what sbp should you aim for in severe preeclampsia or eclampsia, or pheochromocytoma htn crisis in first hour

A

140

119
Q

what sbp should you aim for in aortic dissection in the first hour

A

120

120
Q

dosing of epi in anaphalaxis vs anaphalactic shock

A

• IM or subcutaneous epinephrine (0.3-0.5 mg of 1:1000) is first-line treatment for classic anaphylaxis. IV epinephrine
(1:10,000) is reserved for anaphylactic shock or refractory symptoms

121
Q

how can you tell apart bradykinin angioedema from mast cell or allergic cause

A

bradykinin angioedema doesnt normally cause uticaria

122
Q

lab studies to differentiate
Hereditary angioedema

Acquired C1 inhibitor deficiency

ACE inhibitor effect Medication history

A

Low C1 inhibitor and C4 levels (fam hx)

Low C1q levels (in addition to low C4 and
C1 inhibitor levels) (lymphoma,sle, mgus)

Low C1 inhibitor and C4 levels (med hx)

123
Q

tx for mast cell mediated angioedema

A

Select epinephrine, antihistamines, and glucocorticoids for
acute episodes of mast cell–mediated (allergic) angioedema with
airway compromise or hypotension. Patients should carry an
epinephrine autoinjector

124
Q

tx for c1 deficiency angioedema

A

bradykinin mediated angioedema (hereditary or acquired angioedema); use
FFP in an emergency. For long-term management of hereditary
angioedema, select danazol and stanozolol to elevate hepatic
synthesis of C1 esterase inhibitor protein.

125
Q

along with co exposure during fires what else can patient be at risk for

A

cyanide poisoning coexposure

126
Q

what normal lab finding would exclude cyonide exposure

A

a normal ldh

127
Q

tx for cyanide tox

A

hydroxocobalamin

128
Q

Toxic tx for the following

  1. Acetaminophen
  2. Benzodiazepines
  3. β-Adrenergic blockers
  4. Calcium channel blockers
  5. Digoxin
  6. Heparin
  7. Narcotics
  8. Salicylates
  9. Tricyclic antidepressants-
A
  1. N-acetylcysteine
  2. Observation; flumazenil
  3. Glucagon, calcium chloride, pacing
  4. Atropine, calcium, glucagon, pacing
  5. Digoxin-immune fab
  6. Protamine sulfate
  7. Naloxone
  8. Urine alkalinization, hemodialysis
  9. Blood alkalinization, α-agonist
129
Q

level to diagnose sever acute carbon monoxide poisoning

A

A carboxyhemoglobin level >25% in any patient is diagnostic of severe acute carbon monoxide poisoning.

130
Q

tx for co poisoning

A

Normobaric oxygen therapy is the treatment of choice. Hyperbaric oxygen therapy is indicated for patients with severe carbon monoxide poisoning

131
Q

Sympathomimetic tox symptoms

A

Tachycardia Hypertension Diaphoresis Agitation Seizures Mydriasis

132
Q

examples of sympathomimetic

A

Cocaine Amphetamines Ephedrine Caffeine

133
Q

tx for sympathomimetic tox

A

Benzodiazepines for agitation Avoid β-blockers for hypertension
Haloperidol may worsen hyperthermia

134
Q

Cholinergic tox signs

A

“SLUDGE” Confusion Bronchorrhea Bradycardia Miosis

135
Q

cholinergic examples

A

Organophosphates (insecticides, sarin)

Carbamates Physostigmine Edrophonium Nicotine

136
Q

cholinergic tox tx

A

Organophosphates poisoning requires external decontamination
Atropine
May require ventilatory support Add pralidoxime for CNS toxicity Benzodiazepines for convulsions

137
Q

Anticholinergic tox signs

A

Hyperthermia
Dry skin and mucous membranes Agitation, delirium
Tachycardia, tachypnea Hypertension
Mydriasis

138
Q

anticholinergic examples

A

Antihistamines
Tricyclic antidepressants Antiparkinson agents Atropine
Scopolamine

139
Q

anticholinergic tx

A

Physostigmine for those with peripheral and CNS symptoms

Benzodiazepines for agitation May require ventilatory support

140
Q

Opioid tox signs

Naloxone

A

Miosis
Respiratory depression
Lethargy, confusion Hypothermia Bradycardia Hypotension

141
Q

tx for opiates

A

naloxone

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