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Clin Med II Liza Exam 2 Pulm > Interstitial Lung Dz/fibrosis > Flashcards

Interstitial Lung Dz/fibrosis Flashcards

0
Q

3 ways in which lung is affected in ILD

A

1 parenchyma (tissue) is damaged

  1. Walls of alveoli become inflamed (bronchioles or capillaries may be involved)
  2. Scarring (FIBROSIS) begins in the interstitium (tissue bwt alveoli) and LUNGS BECOME STIFF
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1
Q

Is ILD malignant or infectious

A

no

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2
Q

Which other dzs is ILD associated with

A

sarcoidosis
exposure to asbestos, coal dust, aluminum
drugs: macrobid, minocycline, amiodarone (JG), STATINS

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3
Q

2 main sx of ILD

and PE findings

A 
NONPRODUCTIVE dry cough and SOB
Wheezing and CP UNCOMMON
PE:
crackles (lower lung bases)
COR PULMONALE (late)
Cyanosis (late)
Digital Clubbing (late)
ERYTHEMA NODUSUM in sarcoidosis
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4
Q

Abnormal CXR shows which 3 characteristic findings

A

GROUND GLASS APPEARANCE (Brds!) early: Hazy opacity (ass with inflam)
RETICULAR (netlike) MOST COMMON, nodular or mixed pattern
HONEYCOMBING (small cyst spaces) is POOR PROGNOSIS

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5
Q

What do you expect to see on PFT?

A

RESTRICTIVE = interstitial:
decreased TLC
decreased FEV1 and FVC but both changes so ratio is NORMAL (or increased)

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6
Q

TLC

Spirometry

A

total amt of air in lung after full inspiration
normal is 80%
Spirometry:
FEV1 - forced expiratory volume (FEV) in 1 second )80% normal)
FVC - forced vital capacity - amnt forcefully exhaled after max inhale: all air you can exhale
ratio - normal 70-80%

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7
Q

what do you expect in restrictive PFT

A

TLC decreased
FVC decreased because can’t breath in
ratio normal

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8
Q

what do you expect in obstructive PFT

A 
TLC increased (bc can't breath out?)
FVC normal

Ratio is DECREASED

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9
Q

DLCO in ILD is

A

decreased (maybe the only finding in early stage)
Diffusing capacity = ability of gas to cross from air to interstitium to blood
Measure body’s ability to absorb CO from signle inhalation
Diffusing capacity of Lung for CO.

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10
Q

ABG

A

normal resting but severe exercise or sleep induced hypoxemia (may need serial excercise testing with ABGs)
or repiratory alkalosis (Low Pco2 because hyperventilating and losing CO2, so losing Hs)

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11
Q

GOld standard to Dx ILD

A 
Lung biopsy
to make definite Dx or to stage
indicated 
1) r/o CA or inf
2) to provide spec dx when:
-atypical or progressive sx
-  <50 yo
-fever, wgt loss, hemoptysis to r/o?
-sx wtih normal or atyp CXR
-need to confirm dx before staring serious therapy
- unexplained extrapulm manifest (erythema NODOsus)
- unexpl. pulm HTN, or cardiomegaly
-rapid clin deterioration
-sudden change in CXR
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12
Q

Types of lung biopsy

A

fiberoptic BRONCHOSCOPY with transbronchial lung biopsy:
less invasive but less tissu
often initial proceedure of CHOICE, esp if sarcoidosis, infec suspected
- Thoracoscopy
- open lung biopsy

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13
Q

Complications of ILD

A
  • pulm HTN - Cor Pulmonale (R ventricular hypertrophy) - R hrt failure:
    jvd, hepatomegaly, pedal edema (peripheral= R sided HF)
  • pneumothorax (collapsed lung)
  • high CA risk
    -progr resp insufficiency
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14
Q

Cardiac blood flow to L V is from

A

LUNGS:
from lungs to LV - to Aorta - to tissues to RA/RV - to pulm arteries (r and l) - to lungs
If blood backs up in LV - back up to lung and get pulm edema
If blood backs up in RV - back up to tissues and get periph edema

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15
Q

ILD overview

A

Inflammations -> fibrosis (scarred lung tissues)
Sx: DOE, dry cough
CXR: bilat opacities, reticular most common
PFT: can’t expand: restrictive - decreased TLC but ratio normal
DLCO low
Hypoxemia, Resp Alkalosis (low Pco2)

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16
Q

ILD classes

A 
Known cause:
occupational and envir exposures:
inorganic dust (asbestos, silica, hard metals)
organic dust (bacreria, animal proteins0
gases, fumes

Drugs and poisons

  • chemo med
  • ABx: macrobid (rare)
  • radiation CA tx

Infections

17
Q

IDL classes

A 
Dur to known dz:
Sarcordosis
CT or autoimm dz:
- scleroderma 
-SLE, RA
-Polymyositis/Derma....
-Syst Vasculitis

ILD due to unknown/idiopathic cause:
Idio Interstitial pneumonias (PNA)
Idio Pulm Fibrosis (IPF)

18
Q

PneumoCONIOSIS

A

any dz of resp tract due to inhalation of dust particles:

ASBESTOSIS, SILICOSIS

19
Q

ASBESTOSIS

A

M>F
occupation hx: construction, plumbers, welders, janitor, shipyard, auto mechanics
linked to cancer and mal mesothelioma: smoking greatly increasis risk

20
Q

Mesothelioma

A

Ca ass’d with ASBESTOS exposure:
may be short term 1-2 yrs
CA in mesothelium (protective lingin that covers most organs)
MOST COMMON IN PLEURA (lining of lungs and chest)
can occur in peritonium or pericardium
NOT CAUSED BY SMOKING
poor prognosis and rare

21
Q

PE of Asbestosis

A

No spec sx
insidious sudden onset - SOB, reduced exc tolerance
usu DRY cough
insp crackler
DIGITAL CLUBBING (40%) - no severity correlation

22
Q

Asbestosis dx studies

A

CXR - opacities in LOWER lungs, thickened pleura and plaques
(HX, PE, SX AND CXR -> suggest Dx)

Open lung biopsy - definite dx but not indicated
histology will show fibrosis and asbestos through microscope

23
Q

ASbestosis PFTs

A

Restrictive: can’t inhale :
decreased TLC
decrease FEV1
normal ratio

24
Q

Asbestosis mngt

A

SMOKING CESSATION
consult pulm - long term O2
no drugs
vaccinate : influenza, pneumovax

25
Q

Al Asbestos is

A

50 yo, male, smoker, pipefitter with PLEURAL PLAQUES and irreversible lung damage

26
Q

Silicosis

A

type of pneumoconiosis
FibroNodular lung dz
inhalation of alpha quartz (granite, slate, sandstone) or silicon dioxide
mining, construction, granite cutting, pottery making

27
Q

Silicosis

A 
no race or age
M>f
smoking increases riks
Acute or subacute
Chronic: simple or complicated
28
Q

Chronic SIMPLE slicicosis

A

10-12 yr exposure
may be asx
NON PROGRESSIVE ONCE EXPOSURE ELIMINATED
HILARE node calcificaiton (eggshell pattern)
small round opacities (silicotic nodules) on CXR

29
Q

Chronic COMPLICATED silicosis

A 
>20 yr exp
progresses even after stop exp
PE
Tachypnea, prolonged expiration (like in chronic bronchitis, COPD)
rhonci, wheezing, rales
no clubbing (uncommon)
cyanosis in advanced
COR pulmonale - advanced, increased pulm HTN bc can't get blood into restrictive fibrous tissue
30
Q

what are on CXR for chronic complicated silicosis

A

CXR : enlarging opacities even after exposure is eliminated, can cavitate (R/O TB0

PFT: restrictive: cant inhale: decreased TLC, normal ratio

31
Q

Sam silicosis is

A

male, miner, indeterminate age, SMOKER with cxr eggshel calcification

32
Q

Sarcoidosis

A

unknow etiology
NonCaseating GRANULOMAS (vs TB) - predom in lungs - can affect:
hrt, liver, spleen, joints, skin bones
- can have spont resolution of sx
AA> whites
20-40 yo
Sx: varied, asx to multisystem dz;
45% have systemic fever, anorexia, arthralgias
DOE, cough, chest pain
arthritis, cranial nerve palsies, visual dist, ERYTHEMA NODUSUM

33
Q

erythema nodosum is part of

A

sarcoidosis

34
Q

NonCaseating Granulomas are part of

A

sarcoidosis

35
Q

CXR stages 4 is

PFTs

A

pulm fibrosis

restrictive in late: can’t inhale = decreased TLC, but ratio normal

36
Q

most common pattern of LAD in sarcoidosis

A

bilat symm hilar adn R paratracheal mediastinal adenopathy

37
Q

sarcoidosis labs

A

HyperCa (increased Vit D activity)
high ESR (inflamm dz)
ghigh serium protein (excess immunoglobulins)
HIGH SERUM ACE in 60%

most cases must biopsy to Dx
fiberoptic bronchoscoty with transbronchial biopsy

38
Q

what is the most common lab finding in sarcoidosis

A

HIGH SERUM ACE IN 60%

39
Q

SALLY Sarcoidosis

A

AA female, 30ish, non-smoker wtih HILAR ADEnopathy, she’s an ACE

Clin Med II Liza Exam 2 Pulm (1 decks)

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