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Foundations II- Pulmonary > Interstitial Lung Diseases > Flashcards

Interstitial Lung Diseases Flashcards

1
Q

respiratory disease stress is common in…

A

(aka hyaline membrane disease)

preterm infants

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2
Q

Cause of RDS?

A

deficiency of surfactant in immature lung –> makes gas exchange difficult

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3
Q

Infants with RDS usually present within…

A

minutes to hrs after birth, worsens over 1st 48 hrs of life

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4
Q

Signs of RDS

A

tachypnea, nasal flaring, expiratory grunting, retractions, cyanosis

decreased BS, pale, decreased peripheral pulses, low UOP, peripheral edema

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5
Q

Clinical course of RDS

A

uncomp RDS usually progressd 48-72 hrs & improves as endogenous surfactant production is increased

exogenous surfactant dramatically improves pulm func. -> sxs resolve -> shorter course

CPAP also improves clinical course

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6
Q

CXAY of pt with RDS?

A

low lung volume

classic reticulogranular ground glass appearance with air bronchograms

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7
Q

ABG in pt with RDS typically shows…

A

hypoxemia that responds to O2

as disease progresses, may see hyponatremia due to water retention

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8
Q

In RDS diagnosis is…

A

clinical, must distinguish from other causes

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9
Q

How can we prevent RDS?

A

prevent pre-term birth when possible

Antenatal steroids given to all women 23-34 wks gestation at risk of preterm delivery in the next 7 days

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10
Q

Management of RDS?

A

nasal CPAP

or Intubation + surfactant therapy + mechanical ventilation

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11
Q

How is ARDS different from RDS?

A

ARDS is acute respiratory distress syndrome in adults, is an acute, diffuse, inflammatory lung injury that leads to:

  • decreased pulmonary vascular permeability
  • increased lung weight and loss of aerated tissue-assoc. w/ high mortality rate

caused by direct or indirect injury to the lung

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12
Q

What are the 4 clinical syndromes that can be caused by Non-TB mycobacteria infections (NTM)?

A
  1. pulmonary disease (esp. in older pts with cystic fibrosis
  2. superficial lymphadenitis
  3. Disseminated disease (in severely immunocompromised)
  4. skin and soft tissue infection
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13
Q

Main cause of NTM lung infections?

A

MAC (mycobacterium avium complex)

these organisms are acquired from the environment

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14
Q

Signs/sxs of MAC pulmonary disease?

A

looks like TB but less severe and often indolent

-fatigue, malaise, weakness, cough, dyspnea, chest discomfort

lung exam often norm

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15
Q

MAC clinical presentation in those with underlying lung disease?

A

-white, middle aged or elderly men often alcoholics and/or smokers with underlying COPD

resembles TB clinically &radiographically but usu. less severe

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16
Q

MAC clinical presentation in those w/p lung disease

A

non smoking women >50 y/p who have interstitial pattern on CXR

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17
Q

How do you dx MAC pulmonary disease?

A

consistent CXR

positive sputum culture x 2

other dx have been excluded

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18
Q

What is bronchiectasis?

A

chronic condition where walls of the bronchi are thickened from inflammation and infection

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19
Q

Do you always need to tx MAC pulmonary disease?

A

NO, anti-myobacterial drugs can be dif. to tolerate

If fibrocavitary disease > TREAT

if nodular bronchiectasis > depends on presentation/status of pt

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20
Q

What abx should you give to a pt with MAC pulmonary disease?

A

depends on susceptibility

usually: Azithromycin + Rifampin + Ethambutol

for usually 15-18 months (tx until cultures -)

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21
Q

Interstitial lung disease aka…

A

pulmonary fibrosis

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22
Q

What is interstitial lung disease?

A

includes variety of chronic lung disorders

nonmalignant/noninfectious but serious

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23
Q

How is the lung affected in ILD?

A
  • lung parenchyma is damaged
  • walls of the alveoli become inflamed
  • Scarring (fibrosis) begins in the interstitium and the lung becomes stiff
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24
Q

Causes of ILD?

A

diseases (sarcoidosis, neurofibromatosis), exposures (asbestos), drugs (Macrobid), Idiopathic

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25
Q

Clinical presentation of ILD?

A

progressive dyspnea on exertion and non productive cough

usually NO wheezing of CP

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26
Q

PE in ot with ILD might reveal?

A

crackles, inspiratory squeals, cor pulmonale

advanced disease: cyanosis, digital clubbing

extrapulmonary: ass. w/ other disease ie. erythema nodusum in sarcoidosis

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27
Q

ILD CXR?

A

ground-glass appearance often early finding-hazy opacity assoc. with inflammation

reticular “netlike” most common

honeycombing –> poor prognosis

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28
Q

What other diagnostic tests can you use to dx ILD?

A

HRCT

PFTs
- will see restrictive defect: decreased TLC, decreased FEV1 and PVC but normal FEV1/FVC ratio

ABG
-may be norm or may show hypoxemia or respiratory alkalosis

Bronchoalveolar Lavage
-minor extension of bronchoscopy, allows for cellular analysis

Lung Biopsy **

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29
Q

What is a normal FEV1/FVC ratio?

A

70-80%

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30
Q

If a patient has a + bronchodilator challenge this indicates…

A

obstructive disease (like asthma)

not restrictive disease (like ILD)

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31
Q

What is meant by V/Q mismatch?

A

there will be some areas of the lungs which are better perfused than ventilated and some areas that are better ventilated than perfused

32
Q

What is diffusing capacity?

A

the ability of has to cross from air > interstitium > lung

may have reduced diffusing capacity of lung for carbon monoxide

33
Q

Indications for lung biopsy?

A

atypical or progressive sxs

Age <50 y/o

fever, weight loss, hemoptysis

ILD sxs with norm or atypical CXR

predict prognosis before initiating therapies with serious side effects, etc.

34
Q

Types of lung biopsies?

A

fiberoptic bronchoscopy with transbronchial lung biopsy- less invasive but less info

thoracoscopy

open lung biopsy

35
Q

Complications of ILD?

A

pulmonary HTN, cor pulmonale, pneumothorax, elevated CA risk, progressive respiratory insufficiency

36
Q

What are some known causes of ILD?

A

inorganic dust (asbestos), organic dust (bacteria), gases, fumes

chemo meds, abx (Macrobid), radiation tx

Infections

37
Q

What is pneumoconiosis?

A

any disease of the respiratory tract due to inhalation of dust particles
-asbests, silicosis, coal worker’s disease, berylliosis

males> females due to work hx

38
Q

What are some occupations associated with risk of asbestosis?

A

construction, auto mechanics, pipe fitters, plumbers, welders, janitors, shipyard workers

39
Q

Is mesothelioma asbestosis?

A

NO, it is associated with asbestos but isn’t asbestosis

It is a form of CA almost always associated with asbestos exposure

  • exposure can be short term
  • CA develops in mesothelium
  • not caused by smoking
  • poor prognosis (med. survical 6-12 mo after presentation)
40
Q

Asbestosis PE?

A

no specific signs/sxs

insidious onset-dyspnea, reduced exercise tolerance. usually dry cough

inspiratory crackes

41
Q

Asbestosis dx studies?

A

CXR- opacities in lower lungs, thickened pleura, pleural plaques

Definitive: open lung biopsy

PFTs - restrictive pattern

histopathology shows fibrosis and asbestos bodies

42
Q

management of asbestosis?

A

consult pulm-may need long term O2

smoking cessation, eliminate exposure

No effective therapy/drugs not effective

Vaccinate: flue, pneumovax

43
Q

Classic pt with Asbestosis?

A

“Al asbestosis”

male

~60 y/o

construction worker

smoker

*pleural plaques

44
Q

Course of asbestosis?

A

lung damage is irreversible

smoking + asbestosis= 59 x more likely to get lung CA

elevated risk for mesothelioma

45
Q

What is sarcoidosis?

A

multi-system inflammatory disease of unknown etiology

non-caseating granulomas-predominantly in the lungs

46
Q

What is a granuloma?

A

a small inflammatory nodule of macrophages-produced in response to injury/infection, boy’s attempt to “wall off” something

47
Q

besides the lungs, sarcoidosis can also affect…

A

heart, liver, spleen, joints, skin and bones

48
Q

Sarcoidosis is most common in…

A

10x greater in African Americans

20-40 y/o

females

49
Q

Sxs of sarcoidosis?

A

asymptomatic- multi-system disease

  • fever, anorexia, arthralgias, DOE, dry cough, CP
  • extrapulmonary: arthritis, CN palsies, erythema nodusum

pts can have spontaneous resolution, 1/3 develop chronic disease

50
Q

CXR stages in sarcoidosis?

A

1: hilar adenopathy
2: hilar adenopathy + diffuse infiltrates
3: only diffuse parenchymal infiltrates
4: pulmonary fibrosis

51
Q

PFTs in sarcoidosis?

A

isolated decreased in DLCO

restrictive pattern with advanced disease (decreased TLC, norm FEV/FEV1)

52
Q

What labs would you check if you are concerned for sarcoidosis?

A

calcium- hypercalcemia

ESR

serum protein - excess immunoglobulins

serum ACE- elevated in 60%

53
Q

In most causes dx of sarcoidosis requires…

A

biopsy- fiberoptic bronchoscopy with transbronchial biopsy

54
Q

Classic pt with sarcoidosis?

A

“Sally sarcoidosis”

female, African American, 30ish, non smoker

hilar adenopathy

she’s an ACE

55
Q

How do you manage sarcoidosis?

A
  • consult pulm
  • most pts resolve spontaneously- give NSAIDS for sxs
  • if severe disease –> corticosteroids (Prednisone)
  • monitor: CXRS, ACE level
56
Q

What is granulomatosis with polyangiitis?

A

aka Wegener’s granulomatosis

immune mediated systemic vasculitis

characterized by necrotizing granulomas of the upper and lower respiratory tracts

rare

57
Q

75% of pts with granulomatosis with polyangiitis have…

A

renal involvement/glomerulonephritis

sig. morbidity-> can results in ESRD

58
Q

Sxs of granulomatosis with polyangiitis

A

upper airway: most common- oral/nasal ulcers, rhinorrhea, purulent/bloody nasal DC

lower airway: dyspnea, cough, pleuritis pain, hemoptysis

59
Q

Pulmonary func. in pt with granulomatosis with polyangiitis?

A

restrictive and obstructive patterns found

DLCO

60
Q

CXR in pt with granulomatosis with polyangiitis? CT?

A

highly variable -opacities, nodules which may cavitate

blood vessels leading to nodules & cavities, irregular and stellate-shaped peripheral pulmonary aa. “vasculitis sign”

61
Q

Hilar adenopathy should prompt concern for…

A

sarcoidosis or infection (TB or fungal pna)

62
Q

Additional dx tests for granulomatosis with polyangiitis

A

Labs:

  • ESR
  • leukocytosis, thrombocytosis, normocytic anemia
  • BUN/Cr, proteinuria if renal involvement
    • ANCA (antineutrophil cytoplasmic abs)

tissue biopsy

63
Q

classic pt with Granulomatosis with Polyangiitis?

A

“Gary granulomatosis with polyangiitis”

male or female

40-50ish

upper airway sxs- in the nose

Goes to AA (+ANCA Abs)

  • vasculitis
  • renal involvement
64
Q

Management for granulomatosis with polyangiitis?

A

consult rheumatology

may tx with immunosuppressant (methotrexate or cyclophosphamide) &glucocorticoid

65
Q

Prognosis for granulomatosis with polyangiitis

A

with cyclophosphamide- 80% 8 yr survival rates

66
Q

What is idiopathic pulmonary fibrosis?

A

aka usual interstitial pna

most common of the 7 idiopathic interstitial pnas

inflammation & fibrosis of the lung and parenchyma

67
Q

Dx of idiopathic pulmonary fibrosis is made..

A

after excluding other causes of ILD

68
Q

IPF presentation?

A

insidious onset

-DOE, nonproductive cough

69
Q

IPF PE?

A

inspiratory crackles

digital clubbing

70
Q

IPF CXR?

A

bilateral diffuse reticular or reticulonodular infiltrates in periphery and bases

71
Q

Additional dx tests for IPF?

A

HRCT- reticular opacities, honeycombing indicates poor prognosis

PFTs- restrictive pattern

lung bx

72
Q

Histopathology of IPF?

A

predominantly fibrosis and scant numbers of inflammatory cells: usual interstitial pneumonitis

73
Q

Classic pt with IPF

A

Ivan IPF

male
60ish
a common man (common)
smoker

74
Q

Management of IPF?

A

consult pulm

eval for lung transplant- most common indication for lung transplant

smoking cessation

75
Q

prognosis of IPF?

A

20-40% 5 yr survival rate at time of dx

Foundations II- Pulmonary (2 decks)

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