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Path > Pulmonology- through fibrotic dz > Flashcards

Pulmonology- through fibrotic dz Flashcards

1
Q

What are the two types of pneumocytes, their functions

A

Type I- epithelium

Type II- make surfactant, lung stem cells

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2
Q

What are the functions of Macrophages in the lugns

A

Digest Antigens and clear surfactant

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3
Q

What cells make surfactant?
How is it released?
What happens to extra surfactant?

A

Surfactant is made by type II pneumocytes, stored in lamellar bodies which look like onions on EM.
The tubular myelin flattens out and gets absorbed onto the surface.
Excess surfactant is either reabsorbed and recycled by the type II pneumocytes or cleared by macrophages

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4
Q

How is pulmonary vasculature different than systemic vasculature

A

Pulmonary vasculature vasoconstricts in response to decreased oxygen to shunt blood to better oxygenated BV. Systemic BV do the opposite.

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5
Q

What are the 4 congenital anomalies

A

Pulmonary hypoplasia
Bronchogenic Cyst
Tracheo-esophogeal fistula
Bronchopulmonary sequestration

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6
Q

Pulmonary Hypoplasia- Si/Sx of presentation

Etiology

A

Presentation- neonate with respiratory distress

2 etiologies - Potters sequence and Diaphragmatic hernia

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7
Q

Potters Sequence

A

Renal Agenesis or lower urinary tract blockage –> dec amniotic fluid vol –> many issues but causes BILATERAL pulmonary Hypoplasia

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8
Q

Diaphragmatic Hernia

A

If diaphragm doesnt form correctly a loop of bowel may be in the thorax and inhibit the ability of the lungs to form.
Occurs more commonly on the left because the liver is on the right.
UNILATERAL
Would see bowel on a chest xray

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9
Q

Bronchogenic Cyst

A

Cystic space lined by bronchial epithelium so it fills with muccus.
Space occupying lesion leading to respiratory insufficiency
can potentially become infected

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10
Q

Tracheo-esophogeal fistula
Most common type
Presentation
dx

A

Anomalous connection between trachea and esophagus
most commonly it is atresia of the esophagus with proximal and distal connections to the trachea
Presents during the first feeding with coughing/ spitting and predisposes the pt to lipoid pneumonia
dx w/ barium x ray

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11
Q

Bronchopulmonary sequestration

A

segment of lung that is not connected to the main bronchus.
Has a different airway connection and different vasculature connection (comes off of thoracic aorta)
This is a space occupying lesion that is fatal if hemorrhages and is predisposed to infection

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12
Q

Atelectasis- definition

A

Collapse of alveoli

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13
Q

Atelectasis- complications

A

hypoxemia due to the poor ventilation

Risk of infection

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14
Q

4 types of atelectasis

A

Resorptive
Compression
Contraction
Neonatal

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15
Q

Resoprtive Atelactasis causes

A

bronchial obstruction or tumor that isolates part of the lung leading to all of the air in those alveoli to be absorbed
Tumor or muccus

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16
Q

Compression atelectasis- casues

A

External pressure on lungs that cause the lung to collapse ie tumor, pneumothorax, pleural effusion

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17
Q

Contraction type atelactasis- scar

A

scarring of lung from

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18
Q

Neonatal atelactasis- 2 causes

A

Premature babies can have atelectasis because surfactant production doesn’t start till 28 weeks and isn’t sufficient till 34 weeks. If a baby is going to be born prematurely can give the baby gluccocorticoids to stimulate surfactant production
Maternal Diabetes- insulin inhibits surfactant production.

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19
Q

Pulmonary edema- MCC

A

Left heart failure but can also be caused by infection, toxin, drowning

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20
Q

Pulmonary edema- pathogenesis

A

hemodynamic causes ie dec hydrostatic pressure ie LHF or dec oncotic pressure
Microvaacular injury- vessels become leaky ie drugs, toxins, infections

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21
Q

Pulmonary edema progression

A

Interstitial edema- lugns become stiff and pt has SOB
Alveolar edema- fluid enters alveolar airspace causes blocked ventilation and hypoxemia. As a side note this is a good medium for pneumonia- pneumonia secondary to edema
Chronic congestion- small hemorrhages allow blood to leak into the alv leading to the eventual formation of Heart Failure cells

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22
Q

What is a Heart failure cell

A

Hemosiderin laden macrophage from digesting RBCs

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23
Q

Pulmonary edema- Gross and microscopic appearance

A

Gross- frothy fluid

Microscopic- lungs are full of fluid but there are no PMNs thats how you know its not pneumonia

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24
Q

Pulmonary Edema- Si/ Sx

A

Symptoms- paroxysmal noctural dyspnea, orthopnea, SOC on exertion
Signs- Rales/ Ronchi, evidence of HF- JVD, hepatomegaly, pedal edema

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25
Q

Pulmonary edema- appearance on CXR

A

kerley B lines and blunted costophrenic angles

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26
Q

Adult respiratory Distress Syndrome- (ARDS or DAD) MCC

A

Has a huge variety of causes- Sepsis is most common

also- shock, trauma, oxygen toxicity, drugs, gas, drowning, aspiration, trauma, pneumonia, chemo

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27
Q

ARDS- pathogenesis

A

Any of the causes can damage either the type I pneumocytes or the capillary endothelium. Damage to one quickly progresses to damage to the other

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28
Q

ARDS- first phase

A

Acute/ exudative phase has 3 charecteristics
leaky endothelium –> pulmonary edema
necrosis of type I pneumocytes –> hyaline membrane formation which serves as a barrier to gas diffusion
damage to type II pnemocytes –> atelactasis

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29
Q

ARDS- second phase

A

repair/ organization

Type II pneumocytes flatten out and become type I pneumocytes.

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30
Q

ARDS- long term sequellae

A

Pts may end up with permanent and progressive fibrosis or may end up healed

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31
Q

ARDS- presentation

A

Acute onset of SOB + hx of inciting event - LHF

Hypoxemia will be unresponsive to supplemental oxygen

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32
Q

ARDS CXR

A

bilateral opacities

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33
Q

Pulmonary embolus- Etiology

A

Form in legs or pelvis normally in the femoral vein and make their way to the lung.
Normally a thrombus but can also be air, bone marrow, or fat

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34
Q

Pulmonary embolus- risk factors

A

Virchow’s triad- statis, hypergoagulable state, endothelial damage

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35
Q

Pulmonary embolism- pathology

A

Do not form an infarction but cause hemorrhagic necrosis due to the dual blood supply

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36
Q

Pulmonary embolism- presentation

A

may be asymptomatic but can cause coughing, SOG, dyspnea, pleuritic chest pain

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37
Q

What happens if you have several asymptomatic pulmonary emboli

A

Pulmonary HTN

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38
Q

What is the main complication of a saddle embolus

A

sudden death

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39
Q

Pulmonary HTN- etiology

A

Anything that increases the vascular pulmonary resistance

40
Q

Pulmonary HTN- Causes

A

normally secondary to another cause.
Heart: Mitral stenosis, LHF, L –> R shunt
COPD can cause chronic hypoxia induced vasoconstriction
Recurrent pulmonary emboli
Idiopathic
Genetic- BMPR2 mutation
immune disease
pulmonary fibrosis
Primary is very rare can be from familial from BMPR2 mutation

41
Q

Pulmonary HTN- pathology

A

This is the only time there will be atheroslcerosis in the pulmonary pulmonary arteries. So it is pathonemonic
Onion skinning of the pulmonary arteries
Plexiform lesions of the arteriolar wall means that the HTN was severe

42
Q

What do plexiform lesions resemble

A

Glomeruli

43
Q

Pulmonary HTN- presentation

A

start as asymptomatic but later pts have fatigue, SOB, dry cough, peripheral edema

44
Q

what is a major complication of Pulmonary HTN

A

Cor Pulmonale

45
Q

Spirometry measures for obstructive vs Restrictive

A 
FEV1
FEV1: FVC
peak expiratory flow
RV
TLC
VC
46
Q

Spirometry in restrictive dz

A 
FEV1 dec or no change
FEV1: FVC inc or no change
peak expiratory flow: no change
RV variable
RLC dec
VC dec
47
Q

Spirometry in obstructive dz

A 
FEV1 dec
FEV1: FVC dec
Peak expiratory flow dec
RV inc
TLC inc
VC dec
48
Q

Restrictive lung dz- main categories

A

Chest wall disorders ie Kyphosis, phrenic nerve impairment, diaphragmatic paralysis, kyphosis, pleural dz
Interstitial dz which are split into ARDS and chronic interstitial lung dz

49
Q

3 categories of chronic interstitial lung dz

A

Fibrotic
Granulomatous
Eosinophillic

50
Q

Restrictive fibrotic lung dz

A 
Cryptogenic organizing pneumonia
Idiopathic pulmonary fibrosis
Phenoconioses
CT disorders
radiation pneumonitis
drugs
51
Q

Granulomatous lung dz

A

Sarcoidosis

Hypersensitivity pneumonitis

52
Q

Eosinophillic lung dz

A

Primary Eosinophilia

53
Q 
Characteristics of Restrictive lung dz:
Etiology
Pathogenesis
Hx
lung description
A

Disease is due to common and repeated insults
These insults trigger T cells and B cells to activate macrophages which in genetically predisposed individuals activate fibroblasts for collagen deposition for repair
Hx is very important- occupations, hobbies, travel, allergies, smoking
lungs will be stiff with dec compliance and inc elasticity

54
Q

Pneumoconiosis
description
examples

A

medium sized air particles in the air get trapped in by macrophages in the lung which cannot break them down and so they stimulate fibrosis
mostly seen in upper lungs except for asbestosis
examples- coal workers pneumoconiosis, silicosis, asbestosis, silicatosis

55
Q 
Coal Workers Pneumoconiosis
hx
etiology
pathology
versions
A

hx- coal workers or miners
coal dust is fileld with coal, organics, and silica
coal- nbd, but turns lung black
organics and silica cause damage
coal macule- build up of coal dust in the lung, its dark, and leads to centrilobular emphysema
Progressive massive fibrosis- immune response to coal can lead to scar tissue formation and is bad

56
Q 
Silicosis-
Hx
pathology
chest x ray
microscopy
A

normally occurs in sandblasters or stone grinders requiring massive amounts of long term exposure
the silica is ingested by macrophages which cant break it down –> cytokine release –> fibrogenic factor release leading to a fibrogenic response. once the silica is there there dz progresses even once exposure stops
CXR- egg shell calcification of the hilar LN
microscopic- dense ball of collagen with visible flecks of silica visible under polarized light. Will be able to see these on many specimens, not always pathologic

57
Q

Acute silicosis

A

One massive exposure leads to fibrosis

this is very rare

58
Q

Asbestosis- class of disease

A

pneumoconiosis

59
Q 
Asbestosis- 
normal population
mecahnism
causes what dz
risk factors for what dz
pathology
A

seen in- fire profing, insulation, roofing, building demolition
mechanism- long thin fibers go to the lower lobes and may penetrate –> irritation
causes- pulmonary and/ or pleural fibrosis
Risk factor for- lung cancer, more so than malignant mesothelioma
Pathology- ferrunginous bodies

60
Q

Ferrunginous bodies-
what dz
what are they

A

Asbestosis

asbestos fibers encrusted with Fe and protein

61
Q

Silcatosis- etiologic agent

A

Organic material + divalent cation

62
Q

Caplan Syndrome

A

Rheumatoid pneumoconiosis
severe immune response to pneumoconiosis + rhematoid nodules
Often seen in pts with RA and coal workers lung

63
Q

Usual interstitial penumonitis- idiopathic pulmonary fibrosis

A

repeated bouts of alveolitis triggered by an unknown agent

64
Q

UIP- describe the fibrosis

A

patchy interstitial fibrosis- heterogenous age and severity
worse in subpleural spaces and near fissures
may result in honeycombing

65
Q

UIP- pathophysiology

A

Unknown agent activates TGF beta 1 with 3 outcomes
activates fibro and myofibroblasts
inhibits calveolin in fibroblasts (normally calveolin is inhibitory)
reduces telomerase activity causing early senescence and apoptosis

66
Q

UIP- prognosis

A

poor response to anti-inflammatory tx

Poor prognosis

67
Q

Crytogenic Organizing pneumonia or bronchiolitis obliterans organizing pneumonia)

A

nodules of organizing fibrous tissue in the small airways- bronchioles, alveolar ducts and alveolia

68
Q

COP/BOOP- etiology

A

unknown

69
Q

COP/BOOP- pathology

A

homogeneous lesions

70
Q

COP/BOOP- prognosis

A

good response to steroids

71
Q

Hypersensitivity pneumonitis- types

A

farmer’s lung (moldy hay), Pidgeon breeder’s lung (pidgeon stool), Humidifier lung

72
Q

Hypersensitivity pneumonitis- mechanism

A

immune response to a known inhaled allergen

73
Q

Hypersensitivity pneumonitis- are there eosinophils or IgE Abs

A

NO EOSINOPHILS OR IGE ABS IN HYPERSENSITIVITY PNEUMONITIS

74
Q

Hypersensitivity pneumonitis- location of the lesion

A

Bronchiolar centered inflammation- granulomas and interstitial lymphoid infiltration

75
Q

Hypersensitivity pneumonitis- tx

A

avoid further exposure

76
Q

Sarcoidosis- definition

what rxn takes place

A

multisystem granulomatous dz

CD4 Th cells react to an unknown Ag

77
Q

Sarcoidosis- what organs are normally affected

A 
lungs and hilar LN
skin
eye
liver
spleen
78
Q

What immune cells are involved in sarcoidosis

A

CH4 Th

79
Q

what is the Ag is involved in sarcoidosis

A

unknown Ag

80
Q

What is typical population for Sarcoidosis

A

AA female

81
Q

symptoms of sarcoidosis

A

if they are symptomatic- cough, dyspnea, chest pain, fever, weight loss

82
Q

appearance of sarcoidosis on x ray

A

well circumcised lesion

83
Q

Pathology of sarcoidosis

A

non caseating perhilar granulomas- follow the lymphatics

ie non caseating granulomas that are next to the lymphatics

84
Q

What is associated with sarcoidosis

A

elevated ACE
elevated Vit D
inc Serum Ca

85
Q

Pulmonary Eosinophilia- definition

A

inc eosinophils in blood, sputum or lavage
pulmonary infiltrates
(results in fibrotic lung dz?)

86
Q

Pulmonary Eosinophilia- types

A

Acute- rapidly progressive
Simple- transient or treatable
Chronic

87
Q

Pulmonary Eosinophilia- associated with what dz

A 
Asthma
Aspergillus
parasites
Churg- Strauss
Collagen- Vascular
Idiopathic
88
Q

Alveolar Proteionosis

A

Autoimmune dz of inc surfactant production

89
Q

Alveolar proteonosis- pathology

A

Anti GM- CSF Ab –> dec clearance of surfactant by macrophages.

90
Q

Alveolar proteinosis- microscopy

A

accumulation of surfactant in alveolar spaces

PAS +

91
Q

Desquamative interstitial pneumonia- causes

A

related to smoking

92
Q

Desquamative interstitial pneumonia- pathology

A

accumulation of macrophages in alveolar spaces leading to mild inflammation

93
Q

Desquamative interstitial pneumonia- prognosis and tx

A

good porpoises

responds to steroids

94
Q

What causes pulmonary fibrosis

A

long standing inflammatory damage by PMNs leads to pulmonary fiborsis

95
Q

What dzs cause pulmonary fibrosis

A

Autoimmune dz- RA, scleroderma, pneumoconiosis, drugs, radiation, hypersensitivity penumonitis, sarcoidosis
Primary dz may be- usual interstitial pneumonitis

96
Q

Pulmonary fibrosis- mechanisms

A

Restrictive- lungs are stiff due to fibrosis leading to dec complacence –>
Hypoxemic b/c fibrosis is barrier to gas exchange –>
Hypertensive- b/c of inc in vascular resistance

97
Q

Pulmonary fibrosis- lung findings

A

honeycomb lung- alternating aerated and fibrotic areas

microscopic- inflammation, fibrosis, hyperplasia of pneumocytes

Path (8 decks)

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