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Respiratory 1 > Pathology 3 > Flashcards

Pathology 3 Flashcards

1
Q

REstrictive lung disease:

A

-expansion of lung is problem

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2
Q

Things in lung that cause restriction:

A
  • edema,
  • cells in interstitium
  • inflammation
  • tumor
  • granuloma
  • fibrosis
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3
Q

chronic diffuse interstitial disease defined:

A
  • heterogeneous group of disorders characteried by inflammation and firosis of the pulm conncetive tissue
  • principally the most peripheral and delicate interstitium in the alveolar walls
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4
Q

Hallmark of chronic diffuse interstitial disease?

A

-REDUCED COMPLIANCE (stiff lungs) –> dyspnea –> hypoxia

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5
Q

Interstitial lung diseases

A

1) capacity:
- dec total lung capacity
- FEV1 normal or dec proportionately
- FEV1:FVC ratio not reduced
2) presentation
- dyspnea
- hypoxia
- end-inspiratory crackles
- eventual cyanosis
3) x-rays
- diffuse bilateral infiltrative lesion by nodules, irregular lines, or ground glass shadows
4) clinical course
- may lead to pulm HTN or cor pulmonale == HONEY COMB LUNG AT ENDSTAGE

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6
Q

Endstage interstitial lung disease:

A

-HONEY COMB(a lot of fibrosis)

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7
Q

Types of interstitial lung disease:

A

1) acute:
- acute lung injury (ALI) or ARDS
2) Chronic
- environmental 25%
- sarcoidosis
- idiopathic pulm fibrosis
- collagen vascular

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8
Q

Acute lung injury (aka non-cardiogenic pulmonary edema)

A

-abrupt onset of significant hypoxemia and pulmonary infiltrates in absence of cardiac failure

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9
Q

Acute respiratory distress syndrome ARDS-

A

severe acute lung injury with greater hypoxemia

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10
Q

Histologic manifestion of ALI and ARDS=

A

diffuse alveolar damage

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11
Q

ARDS cuased by:

A

diffuse alveolar capillary damage (DAD)
= rapid onset of life-threatening respiratory insufficiency - refractory to oxygen therapy
-may lead to multi-system organ failure
-usually severe pulm edema = most common cause of non-cardiogenic pulm edema

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12
Q

How does damage to capillary and alveolar membranes in ALI and ARDS happen?

A

1) direct injury from outside
- infectious agent (pneumonia)**
- aspiration**
- oxygen tox
2) indirect injury -systemic from inside
- shock (trauma, burns, surgery..)**
- sepsis**
- inhaled toxins
- transfusion related (TRALI)

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13
Q

Three main causes of ARDS/ALI?

A

sepsis
infection
shock

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14
Q

ALI/ARDS characteristics:

A

-bilateral pulmonary infiltrates on chest x-ray
-PaO2(arterial)/Fi(environmental)O2 normally 375-400
in ALI ratio < 300
in ARDS raio <200

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15
Q

ARDS pathogenesis:

A
  • uncontrolled activation of acute inflammatory system
  • imbalance between proinflam and antiinflam mediation
  • sequestration and activation of neutrophils
  • diffuse damage to alveolar capillary walls
  • inc vascular permeability and alveolar thickening
  • loss of diffusion capacity
  • widespread surfactant abnormalities bc of Pneumocte 1 and 2 damage
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16
Q

ARDS pathway in neonates:

A

occurs with deficiency in pulmonary surfactant

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17
Q

Symptoms of ARDS:

A

1) first dispnea and tachypnea

2) cyanosis and hypoxemia

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18
Q

What helps ARDS patients?

A

inhalation of nitric oxide - decreases PA pressure and arterial resistance
-ventilation perfusion mismathc-hypoxemia

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19
Q

Mortality of ALI/ARDS?

A

40%!! pretty high!

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20
Q

ARDS

A

1) morphology:
- lung heavy, firm red and stiff
2) micro:
- congestion
- interstitial and alveolar edema
- fibrin deposition
* -alveolar hyaline membranes**
- proliferation of T2pneuomocytes
- phagocytosis of membranes
3) organization: of exudate can follow= interstitial fibrosis —> honey comb lung down he line

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21
Q

three phases of ARD

A

1) acute exudative (0-7 day)
2) proliferative phase (1-3 weeks)
3) fibrotic/healing phase (3-4 weeks)

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22
Q

What is TRALI

A
  • trasfusion related ALI
  • within 6 hours of transfusion
  • due to anti HLA or anti HNA antibodies
  • no pre-existing acute lung injury before transfusion
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23
Q

Major categories or interstital lung disease:

A

1) fibrosiing
2) granulomatous
3) eosinophilic
4) smoking related

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24
Q

Diffuse interstitial disease

A

MORE LONG TERM

  • initially alveolitis in interstitium of alveoli (accumulation of inflammatory and immune effector cells within alveolar walls and spaces)
  • heterogenous stimuli
  • Leukocytes accumulate in the alveoli=distort normal alveolar structures; release damaging mediators; parenchyma injurred and fibrosis stimulated; MACROPHAGE PLAYS CENTRAL ROLE IN FIBROSIS
  • final stage= end stage fibrotic lung (HONEYCOMB LUNG)***
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25
Q

honeycomb lung think:

A
  • cor pulmonale
  • R sided HF
  • pulm htn
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26
Q

Idiopathic pulmonary fibrosis (IPF)

A
  • unkn etiology
  • characterized by diffuse interstitial fibrosis
  • also called cryptogenic fibrosing alveolitis
  • histology=”usual interstitial pneumonia (UIP)” but NOT specific for IPF
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27
Q

Idiopathic pulmonary fibrosis (IPF) - clinical course:

A
  • 2/3s of patients >60 yrs and M>F
  • insidious onset of SOB (6 mo)
  • nonproductive dry cough and inc dyspnea
  • advanced cases=hypoxemia, cyanosis, clubbing
  • severe pulmonary HTN, cor pulmonale, death
  • mean survival 3 year
  • only definitive tx = lung transplant
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28
Q

How to diagnose IPF=

A

diagnosis of exclusion

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29
Q

IPF IMPORTANT TO FIND?

A

ONLY ONE THAT DOES NOT RESPOND TO STEROIDS!!! ALL THE OTHERS DO

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30
Q

IPF - pathogenesis:

A
  • IPF caused by repeated cycles of epihelial activation/injury by some unidentified agent = chronic inflammation–> fibrosis
  • -> something regarding telomerase shortening and apoptosis leading to epithelial activation and injury
  • inflammation and induction of TH2 T-cells with eosin, mast cells, IL4, IL5, IL13 in lesion
  • abn wound healing = fibroblastic foci (crazy fibro prolif)
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31
Q

Early microscopic findings of IPF:

Overtime…

-Late?

A
  • alveolitis
  • fibroblastic foci
  • overtime get early and late lesions at the same time ** (temporal heterogeneity)
  • dense fibrosis –> collapse of alveolar walls, formation of cystic spaces lined by hyperplastic type II pneumocytes (HONEYCOMB LUNG!)
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32
Q

Hallmark of UIP=

A

patchy interstital fibrosis varying in intensity and age

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33
Q

UIP (IPF) TX?

A

-NEED TRANSPLANT

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34
Q 
DIP
COP (BOOP)
NSIP
PAP
HSP

TX?

A

-RESPONDS TO STEROIDS

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35
Q

Causes of honeycomb lung:

A
  • IPF
  • interstitial pneumonia
  • diffuse alveolar damage DAD
  • inorganic dust exposure
  • interstital granulomatous diseases
  • eosinophilic granuloma
  • GE Reflux/aspiration
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36
Q

Rheumatoid arthritis pulmonary involvement:

A
  • chronic pleuritis
  • difuse interstitial pneumonitis and fibrosis
  • intrapulmonary rheum nodues
  • pulm htn
37
Q

Scleroderma pulmonary involvement:

A
  • NSIP is classic
  • diffuse interstitial fibrosis-main cause of death

UNIFORM AND DENSE FIBROSIS

38
Q

SLE pulmonary involvement:

A
  • pathy, transient, parenchymal infiltrates

- occasionally severe pneumonitis

39
Q

Pneumoconioses defined:

A

-non-neoplastic lung reaction to inhalation of any aerosol, includin mineral dusts, organic and inorganic particles, fumes, or vapors (AIR POLLUTION!)

Most common:

  • coal dust
  • silica
  • asbestos
40
Q

small particles and pneumoconioses:

A

-smaller and so can get into pulm fluids and reach toxic levels = ALI

41
Q

Larger particles and pneumoconioses:

A

-resist dissolution and persist = fibrosis

42
Q

physiochemical reactivity and pneumoconioses

A
  • direct tissue damage by release of free rads and other chemical groups
  • OR triggers macros
43
Q

Most dangerous size and why w/ pneumoconioses?

A
  • 1-5micrometers
  • reach terminal small airways and alveoli
  • lodge in bifurcation of distal airways
44
Q

Key factor of pneumoconioses:

A

-How much of this stuff is inhaled and how likely is this inhaled dust to stimulate fibrosis

45
Q

Wide spectrum of pneumoconiosis in Coal miners:

A

1) asymptomatic anthracosis - no cellular reaction, msot innocuous
2) simple coat workers pneumoconiosis (CWP) - macule, nodule with collagen fibrils; minimal lung dysfunction
3) complicated CWP-progressive massive fibrosis
- compromised lung function

NO RISK FOR LUNG CANCER OR TB

46
Q

What is progressive massive fibrosis (PMF)

A
  • severe confluent, fibrosing reaction which may complicate any pneumoconiosis
  • scarring in areas of dust accumulation
47
Q

Simple CWP morphology:

A
  • 1-2mm coal macules;nodules
  • located primary adjacent to respiratory bronchioles
  • can lead to dilation of adjacent alveoli (centrilobular emphysema)
48
Q

Complicated CWP (PmF) morphology

A
  • large, black scars, multiple, bilateral and peripheral
  • appearance similar to rheumatoid nodule
  • progressive leads to PMF, pulm htn ,cor pulmonale
49
Q

Caplan syndrome:

A
  • coexistence of rheumatoid arthritis with a pneumoconiosis

- development of distinctive nodular pulmonary lesions

50
Q

Silicosis- pathogenesis:

A
  • breath it in - quartz (most dangerous crystalline)
  • quartz phagocytosed by macrophages ==> release of IL1 TNF, free radicals, fibrogenic cytokines
  • macrophage dies and releases silica particle = amplified process
  • fibroblast proliferation occurs = collagen deposition = leads to PMF

INC SUSCEPTIBILITY TO TB AND SILICA IS CARCINOGENIC!!!!

51
Q

Silicosis morphology:

A
  • concentrically arranged collagenous nodules, begin as small lesions in upper lungs = large more diffuse with disease progression
  • nodules coalesce into larger collagenous scar == leads to PMF
  • may be calcified (eggshell)

-MICRO= hyalinized WHORLS of collagen, scant inflammation

52
Q

serpentines vs amphiboles (asbestos components)

A
  • serpentines more solubleand easier to get rid of - flexible and curled
  • amphiboles = more of the problems with this guy - brittle and straight
53
Q

Amphibole exposure correlates with:

A

-MEsothelioma!

54
Q

Asbestos bodies are

A

asbestos in lungs lined by iron

  • stain with prussia nblue
  • DUMBBELL
55
Q

ASbestos morphology

A
  • begins as fibrosis around respi bronchioles –> involved alveolar sacs and alveoli
  • -> HONEYCOMB LUNG
  • typically LOWER lobes and subpleurals pace
56
Q

Consequences of asbestosis:

A
  • 5x inc risk for lung cancer
  • if smoking too = 55x inc in risk of lung cancer

-1000x increase in mesotheliomas– takes 20-40years to develop

57
Q

Clinical course of asbestosis:

A
  • dyspnea on exertion and later at rest
  • cough with sputum productin
  • can lead to CHF< cor pulmonale, honeycomb and death
58
Q

Asbestos on the lungs;;;;

A

pleural plaque

  • lung cancer
  • scaring
  • mesothelioma..
59
Q

Bleomycin pulmonary disease complication:

A

-pneumonitis and fibrosis

60
Q

Methotrexate pulmonary disease complication:

A

-hypersensitivity pneumonitis

61
Q

Amiodarone pulmonary disease complication:

A

pneumonitis and fibrosis

62
Q

nitrofurantoin pulmonary disease complication:

A

-hypersensitivity pneumonitis

63
Q

aspirin pulmonary disease complication:

A

bronchospasm

64
Q

beta antagonists pulmonary disease complication:

A

bronchospasm

65
Q

complication of radiation therapy

-radiation induced lung disease

A
  • acute - 1-6 months and therapy = fever, dyspnea, pleural effusion, infiltrates
  • GIVE STEROIDS

-chronic - failure to resolve –> fibrosis - diffuse alveolar damage ; severe atypia

66
Q

Sarcoidosis defined:

A

systeic disease of unkn cause
-noncaseating granulomas in many tissues and organs

-DIAGNOSIS OF EXCLUSION

67
Q

sarcoidosis clinical:

A
  • variable presentation depending on organs involved and disease activity
  • most frequent targets=lung or hilar LN, skin, eye
  • inc prevalence in non-smokers
  • african american females
68
Q

sarcoidosis - clinical presentation:

A
  • sometimes completely asympt
  • often = insidious onset pulmonary symptoms, fever, NS, WL
  • if acute onset=fever, erythema nodosum, polyarthritis, inc IgG calcium, ACE
69
Q

sarcoidosis diagnosis:

A

-DIAGNOSIS OF EXCLUSION

70
Q

sarcoidosis - etiology:

A

-disordered immune reg in genetically predisposed people exposed to certain environmental antigens

71
Q

sarcoidosis - immunologic factors (etiology)

A
  • interstitial and intra alveolar accumulation of CD4 Th1
  • inc levels of TH1 cytokines (IL2 & IFN gamma) = more t-cells and macro activation
  • inc cytokines (IL8 and TNF) = brings more T-cels and monocytes

CELLULAR MEDIATED (DAMAGE)=FORMS GRANULOMAS!!

72
Q

Sarcoidosis HLAs

A

HLA-A1 and HLA-B8

-familial!!

73
Q

Sarcoisosis tissue shows:

A

-CLASSIC WELL-FORMED NONCASEATING GRANULOMAS (CD4 TH1 cells surround)

  • some obstruction due to granulomas
  • eventual diffuse interstitial fibrosis –> honey comb lung

-patterns develop along lymphatics!

74
Q

Most frequently involved organ - sarcoidosis?

A

lungs durps

75
Q

Sarcoidosis of eyes and salivary glads called:

A

mikulicz syndrome

76
Q

potato nodes seen in

A

sarcoid

77
Q

sarcoid - oddities in the granulomas:

A
  • schaumann bodies: little lamellated calcified structure, usually in giant cells (also common in berylliosis)
  • asteroid bodies: star shaped eosinophilic bodies made of compressed intermediate filaments; also commonly in foreign body giant cells
78
Q

sarcoidosis - progression and outcome

A

-not bad - 70% treated well

10-15% die

79
Q

hypersensitivity pneumonitis

A
  • occupational disease resulting from inc susceptibility to inhaled antigens such as moldy hay
  • immune mediated (TYPE 3-deposition of antibody-antigen complex and 4-cell mediated delayed type), predominantly interstitial disorder caused by intense often prolonged exposure to inhaled organic dusts or antigens
  • RESTRICTIVE DISEASE PRESENTATION
  • INVOLVES PRIMARILY ALVEOLI (allergic alveolitis)
80
Q

Hypersensitivity pneumonitis - inhalation of what:

A 
-organic dusts with antigens made up of:
spores of thermophilic bac
true fungi
animal proteins
bacterial products
81
Q

Hypersensitivity pneumonitis - presentation:

A

1) acute: large exposure to antigen =
- severe dyspnea
- cough,
- high fever and chills 4-6 hrs
- resolves in several days

2) chronic: prolonged exposure to small amounts ofa ntigen=
- insidious onset of dyspnea
- cough
- fatigue
- resp failure due to chronic interstitial disease

82
Q

Hypersensitivity pneumonitis - hypersensitivtiy type 3 and 4 when?

A

3- is EARLY

4- is LATER (granulomatous)

83
Q

Hypersensitivity pneumonitis - -types/most common:

A

**-farmers lung: spores of thermophilic actinomyces in hay

  • pigeon breeders lung - proteins from bird feathers, serum, or poop
  • humidifier or air-conditioner lung: thermophilic bacteria
84
Q

Hypersensitivity pneumonitis - morphology

A

1) acute = neutrophils in interstitium

2) chronic=mononuclear interstitial infiltrate (lymphs, plasma cells, and macrophages)

85
Q

silo fillers disease (NO/NO2) - what happens:

A

-breathe the gas = pulmonary edema in minutes –> develop into widespread bronchiolitis obliterans with scar tissue

86
Q

smoking-related interstitial diseases:

A

-desquamative interstitial pneumonia (DIP)

87
Q

-desquamative interstitial pneumonia (DIP)

A
  • SMOKING RELATED INTERSTITIAL DISEASE
  • more males than females
  • insidious onset of dyspnea and dry cough
  • no desquamation
  • numerous intra-alveolar macrophages (smokers macrophages) = HARD TO BREATHE
  • with emphysema usually
  • proliferation of T2 pneumocytes

RESPONDS AWESOME TO STEROIDS 100% survival

88
Q

pulmonary alveolar proteinosis (PAP)

A
  • bilateral patchy pulmonary opacification on X-ray
  • homogeneous, granular precipitate within alveoli
  • focal to confluent consolidation of large areas of lung
  • ACCUMULATION OF ACELLULAR SURFACTANT - in intraal veolar and bronchiolar spaces (PAS+)
  • MINIMAL inflammatory response- normal alveolar walls

DOES NOT CAUSE FIBROSIS AND INTERSTITIAL THICKENING!!! !!!!!!!

89
Q

Pulmonary alveolar proteinosis - clinical shit:

A
  • insidious onset cough
  • Chunks of white gelatinous-appearing sputum jello
  • fever

-some recover others not

  • NO progression to fibrosis
  • whole lung lavage therapy

Respiratory 1 (9 decks)

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