Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

usmle > Exam3 Pulmonary > Flashcards

Exam3 Pulmonary Flashcards

1
Q

What is the epithelium of bronchus?

A

Pseudostraified ciliated columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bronchus layer?

A

Goblet cell, smooth muscle, submucosal seromuscious glands, cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Feature of Bronchioles?

A

lack of cartilage and submucosal glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

layer of respiratory bronchiole and alveoli

A

Simple cuboidal epithelium of respiratory bronchiole,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Function of type II penumocytes?

A

release surfactant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is FEV1?

A

Forced expiratory volume in 1 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is FVC?

A

forced virtal capaity like volume of air exhaled with force following maximal inhalation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is DLCO?

A

Measurement to assess the lung’s ability to transfer gas from inspired air to the bloodstream
Carbon monoxide is used bc of its high affinity for hemoglobin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When is DLCO reduced?

A

increased thickness of diffusion barrier(fiborsis, fluids)

- loss of surface area(emphysema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is pulmonary edema?

A

Accumulation of excessive interstitial fluid in the alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is etiology of pulmonary edema?

A
  • Increased hydrostatic pressure ex CHF. mitral stenosis

- Increased capillary permeability ex alveolar wall injury as seen in ARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is clinical features of pulmonary edema?

A
  • shortness of breath
  • cough with pink frothy sputum
  • crackles on auscultation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Investigation of pulmonary edema?

A

Chest X ray: bilateral lung infiltrates
ABG: Hypoxemia
DLCO: reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Acute lung injury?

A 
- Characterized by 
Abrupt onset of dyspnea
Hypoxemia
Bilateral pulmonary edema
In the absence of cardiac failure
-manifestation of severe acute lung injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is etiopathogenesis of ARDS:

A

Direct : Pneumonia, aspiration, inhalation injury, drowning, oxygen toxicity
Indirect: Sepsis (most common cause of ARDS) , trauma with shock, acute pancreatitis, severe burn .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is pathogenesis of ARDS?

A

Endothelial cells are activated secondarily to pneumocyte injury or by circulating inflammatory factors.

  1. Neutrophils adhere to the activated endothelium and migrate into the interstitium and alveoli, where they dregranulate and release inflammatory mediators.
  2. Alveolar inflammation and injury- loss of diffusion and surfactant deficiency (type II cell damage). protein rich like fibroblast, procollagen, ) + cellular debris organizae into hylaine membrane.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is resolution of injury?

A

If the inflammatory stimulus lessens: macrophages remove intra-alveolar debris

  • release fibrogenic cytokine such as transforming growth factor B (TGF beta)
  • stimulation of fibroblast growth and collagen deposition - fibrosis of alveolar wall
  • residual type II penumocytes profliferate to replace type I pneumocytes, reconstituting the alveolar lining
  • endothelial restoration occurs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is morphology of ARDS?

A
  • Acute (day 1-7)
    : Heavy and firm lungs
  • Congestion of alveolar capillaries
    Interstitial and intra-alveolar edema/hemorrhage
  • necrosis and sloughing of alveolar epithelial cells
    Hyaline membranes
  • Organizing phase(Day 7-21)
    : Proliferation of type II cells
    Granulation tissue forms in the alveolar walls and spaces
    In most cases, granulation tissue resolves
    But in some, fibrotic thickening (scarring) of alveolar septa occurs

Fibrotic phase - beyond three weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the signs/ symptoms of ARDS?

A
  • rapid onset of dyspnea
  • Cyanosis
  • respiratory failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Investigation of ARDS

A

Chest Xray: Diffuse bilateral infiltrates
ABG: Hypoxemia (refractory to oxygen therapy)
High resolution of CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are poor prognostic indicators?

A
  • Advanced age
  • Bacteremia/ sepsis
  • progression to multisystem organ failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Difference of pulmonary edema?

A

Cardiogenic: increased hydrostatic pressure
cause: CHF, mitral stenosis
Microscopy : transudate, hemosiderin- laden macrophages(heart failure cells)
Chest X ray: Bilateral bibasilare infiltrates(dependent edema: Dependent edema is a term that doctors use to describe gravity-related swelling in the lower body.)

*Non- cardiogenic: 
Increased vascular permeability
Cause: ARDS
Microscopy: Exudate, hyaline membrane
Chest Xray: Bilateral infiltrates- uniform distribution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is hemosiderin -laden macrophages?

A

When blood leaves a ruptured blood vessel, the red blood cell dies, and the hemoglobin of the cell is released into the extracellular space. Phagocytic cells (of the mononuclear phagocyte system) called macrophages engulf (phagocytose) the hemoglobin to degrade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Difference between Obstructive vs Restrictive diseases

A
  1. Obstructive lung disease
    Site: Airway disorder
    PAtho: Increased resistance to air flow (expiration lung problem )
    Spirometry: Decreased FEV1: FVC ratio
    Examples: EMphysema, chronic bronchitis, asthma, Bronchiectasis
  2. Restrictive lung disease
    Site: Chest wall/ Parenchmal Disorder
    PAtho: Decreased expansion with reduced lung volumes : inhalation problem
    Spirometry: Normal to increased FEV1: FVC ratio
    Examples: Acute restrictive disease- ARDS
    Chronic restrictive diseases: Interstitial fibrosis
    Pneumoconiosis
    Granulomatous
    Chest wall deformities: KYphoscoliosis
    Neuromuscular disorders affecting the chest wall muscles.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is COPD:

A 
Chronic obstructive pulmonary disease
- Includes emphysema.chronic bronchitis
- both related to smoking 
- similar clinical features
similar management
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is emphysema?

A

Irreversible enlargement of airspaces distal to the terminal bronchioles (respiratory acinus) accompanied by destruction of the alveolar wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the patterns of emphysema?

A
  • Centriacinar
  • Panacinar
  • distal acinar(para-septal)
  • Irregular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is centriaciar?

A
  • respiratory bronchiole is affected and distal alveoli are spared
  • smoking related
  • upper lung zone
  • most common type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is panacinar?

A
  • REspiratory bronchiole to terminal alveoli are affected
  • Alpha-1 antitrypsin deficiency
  • lower lung zones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is para-septal(distal acinar)?

A 
- Next to atelectasis, along septa, subpleural 
rare
more common in upper lobes
may form bullae(large air space)
Can lead to pneumothorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is irregular(paracicatricial)?

A

Surrounding scar

Asymptomatic- incidental finding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is pathogenesis of emphysema?

A

-Loss of elastin leading to destruction of alveolar septa
Smoking plus air pollutant and genetic predisposition
- oxidative stress, increased apoptosis and senescence( cell age)
- inflammatory cells, release of inflammtory of mediators
- Protease-antiprotease imbalance( congenital alpha 1- antitrypsin)
leading to alveolar wall destruction

Net result: Overdistention of alveoli which can’t collapse during expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are protease and antiproteases and function of them?

A

Protease: normally derived from the leukocytes (mainly neutrophils)
Proteases like elastase destroy lung tissue

Antiproteases: Inhibit proteases, thereby play a protective role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what does protease- antiprotease imbalance lead to ?

A

destruction of the alveolar parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When protease and antiprotease imbalance occurs?

A
  1. Increase in neutrophils in the lung tissue (smoking)

2. Decreased antiprotease activity(alpha-1 antitrypsin deficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is Alpha-1 antitrypsin deficiency?

A
  • Point mutation in the Pi gene on chromosome 14
  • PIMM= normal, PiZZ- most abnormal
  • defect in the synthesis of alpha-1 antitrypsin by the liver, misdoing the protein and failing to release it into the circulation
  • it accumulates in the liver and can eventually lead too chronic liver disease
  • characterized by panacinar emphysema, seen at younger age and is more severe if patients smokes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is polymorphisms in TGF- B gene?

A
  • reduced TGF- B signaling causes inadequate repair elastin injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How is pathological features of emphysema?

A
  • Gross: Hyperinflated lungs with/without bulla formation.
    Parenchyma has moth- eaten appearance

Microscopy: Destruction of alveolar septa

  • free floating alveolar septa in air spaces
  • overdistended alveolar spaces
  • but without fibrosis of alveoli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does loss of elastin lead to expiratory dyspnea?

A
  1. loss of elastin recoil- use of accessory muscles- forced expiratory
  2. REduced radial traction on respiratory bronchioles- collapse of bronchioles during expiration (air can’t go out)- functional airway obstruction like air trapping leading to expiratory dyspnea
    `
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How does loss of septa lead to pulmonary hypertension?

A
  1. reduced surface area- reduced gas exchange- hypoxemia- pulmonary vasoconstriction - pulmonary hypertension
  2. Loss of capilaries- increased resistance in remaining capilaries- pulmonary hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the clinical features of emphysema?

A
  • expiratory dyspnea which is insidious in onset and progressive
  • barrel- chest(increased antero-posterior diameter of the chest)
  • Sitting in a forward hunched position trying to squeeze air out of the lungs
  • prolonged expiration through pursed lips
  • weight loss: due to hyperventilation and use of accessory muscles for respiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Investigation of emphysema?

A
  • Spirometry: Obstructive pattern: reduced FEV1:FVC
  • DLCO: Reduced(due to loss of surface area)
  • Chest Xray= hyperinflated lungs, flat domes of diaphragm
  • ABG: Normal until late (no cyanosis initially) later hypoxemia, hypercapnia, and respiratory acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Complications of emphysema?

A

Pulmonary hypertension &Cor pulmonale

- Absence of cyanosis+breathing through pursed lips = Pink Puffers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is Chronic bronchitis?

A

Definition: persistent cough with mucoid sputum
For at least 3 months
In the past 2 consecutive years
In the absence of any other identifiable cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the etiopathogenesis of chronic bronchitis?

A

Common among smokers and urban dwellers, inhaled irritant

  1. Submucosal gland hypertrophy- hypersecretion of mucus : distinct feature
  2. goblet cell metaplasia in bronchioles
  3. Smooth muscle hyperplasia and peribronchiolar fibrosis- small airway obstruction distally
  4. Inflammation: infiltrate of CD8 Tcell , macrophages, and neutrophils eventually fibrosis === No eosinophils in constrast to asthma
  5. Small airway obstruction due to fibrosis and mucus plugging.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the pathological features of chronic bronchitis?

A

Gross: hyperemia and edema of mucous membranes
Excessive mucinous or mucopurulent secretion

Microscopy: Thickening of the mucus gland layer
Goblet cell hyperplasia &metaplasia
chronic inflammation &fibrosis
Squamous metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Clinical features of chronic bronchitis?

A

Early disease- persistent cough productive of mucoid sputum
over time progreses to dyspnea on exertion
Cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Investigation of chronic bronchitis?

A

Spirometry: Obstructive pattern Reduced FEV1: FVC
Chest X ray: Dilated heart, prominent vessel
ABG: hypoxemia, hypercapnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Complication of chronic bronchitis?

A

Secondary Infection
Over time- pulmonary hypertension and cor pulmonale
Chronic bronchitis (pulmonary hypersion and cor pulmonale happened early)

Peripheral edema +cyanosis : blue bloaters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is bronchiectasis?

A

Bronchi and bronchioles and ectasia meaning dilation

  • destruction of smooth muscles and elastic tissue by inflammation.
  • stemming from persistent or severe infection
  • leads to permanent dilation of bronchi and bronchioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the etiology of bronchiectasis?

A
  1. Bronchial obstuction : tumor, foreign body, and impaction of mucus.
  2. Necrotizing suppurative penumonia: Virulent organisms
  3. Congenital / herediatry conditions that predispose to chronic infections:
    cystic fibrosis– mucous thickening
    immunodeficiency states
    primary cillary dyskinesia
    Kartagener syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Pathogenesis of bronchiectasis?

A

Impaired clearance of airways- accumulation of mucuous secretion- secondary infection - damaged/weakend wall- bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the pathological features of bronchiectasis?

A

Gross: usually affects the lower lobes bilaterally, particularly those air passages that are most vertical
- cut surface of lung shows markedly dilated bronchi that extend to subpleural regions, some filled with mucopurulent material

Microscopy: Squamous metaplasia of bronchial epithelium

  1. Intense acute and chronic inflammatory exudate in bronchial walls, necrotizing ulceration
  2. Fibrosis of bronchiolar walls leading to bronchiolitis obliterans / bronchiolitis meaning chronic inflammation of bronchioles and obliterans producing obstruction due to fibrosis)
  3. Lung abscess meaning pus may be present.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the clinical features of bronchiectasis?

A

severe persistent cough, fever
Expectorationn of foul smelling, sometimes bloody sputum
Dysonea and orthopnea in severe cases
Symptoms often episodic
- paroxysms of cough particularly frequent when the patient rises in the morning change in position cause collection of pus and secretion to drain into bronchi
- Obstructive respiratory insufficiency can lead to marked dyspnea and cyanosis
- clubbing of the fingers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the complication of bronchiectasis?

A
  • sepsis and brain abscess
  • pulmonary hypertension and cor pulmonale
  • systemic amlyoidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is primary ciliary dyskinesia?

A

Inheritance autosomal recessive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the pathogenesis of primary cillary dyskinesia?

A

Mutation in cilia gene- defective ciliary motor protein- defective ciliary function - imparied mucociliary clearance- accumulation of secretion - recurrent infection - bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is kartagener syndrome?

A

Subset of primary of ciliary edsyskinesia
- characterized by triad: 1. bronchiectasis
2. Dextrocardia- defective movement of the organ during embryogenesis
3. sinusitis( impaired mucocilliary clearance- recurrent sinus infection )
Males - infertility ( due to sperm dysmitlity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is bronchial asthma?

A 
Heterogenous disease charcterzied by 
chronic airway inflammation 
Variable expiratory airflow obstruction
Produces symptoms such as wheezing, shortness of breath, and chest tightness and cough
vary over time and in intensity
60
Q

What are the classification of bronchial asthma?

A
  1. atopic : evidence of allergen sensitization and immune activation
  2. Non atopic: No evidence of allergen sensitization
    Based on trigger: Drug, occupational, seasonal, exercise induced
61
Q

Difference between atopic and non atopic?

A

Atopic: Type I (Ig-E mediated) hypersensitivity reaction
Trigger:Environemntal : dust, pollen
Children
family history common
Immediate wheal (itchy&flare ): Skin test
serum IgE level increased
Atopy : allergic rhinitis or atopic eczema

Non-atopic: Not related to hyperesensitivity
Viral respiratory infection 
No particular age grouo
 less common 
Non reactive skin test
normal Ig E level
Absent atopy (genetic disposition )
62
Q

What is pathogenesis of atopic asthma?

A

Caused by Th2 mediated immune response to environmental allergen in genetically predisposed individuals.
Type I (Ig E mediated) hypersensitivity reaction
Th2 release cytokines - IL-4 for IgE
IL-5 for eosinophils
IL-13 for mucus production from bronchial submucosal galnds
IgE binds to Fc receptor on mast cells

63
Q

What happened to early phase of atopic asthma?

A

On re-exposure of allergen, immediate reaction is triggered by antigen induced cross linking of Ig E bound to Fc receptors on mast cells- degranulation of mast cells- histamine for vasodilation and increased vascular permeability, leukotrienes- increased vascular permeability, bronchoconstriction

Vagal nerve stimulation - activation of muscarinic receptor- bronchoconstriction
- bronchoconstriction, edema and increased mucus production lead to airway narrowing in immediate phase.

64
Q

Late phase of asthma?

A

Inflammatory mediator stimulate epithelial cells to produce chemokines (eotaxin) - Recuritment of Th2 cells eosinophils, other leukocytes
- amplification of inflammatory reaction.
Eosinophils release major basic protein which causes damage to epithelium

65
Q

What is Airway remodeling?

A

Repeated bouts of inflammation lead to structural change in the bronchial wall that are collectively refereed as airway remodeling.

66
Q

Features of airway remodeling?

A
  1. Thickening of airway wall
  2. Sub basement membrane fibrosis
  3. Increased vascularity
  4. Increase in the number and size of the submucosal glands.
  5. Goblet cell hyperplasia
  6. Hypertrophy and hyperplasia of the bronchial wall smooth muscle
67
Q

While acute airflow obstruction is primarily attributed to ……………………………………………….. and air way remodeling may contribute to ………………………..

A
  1. bronchoconstriction, edema and mucus plugging, chronic irreversible airway obstruction.
68
Q

Features of non atopic asthma

A
  • no evidence of sensitiation
    IgE level is normal
    Viral infection of upper respiratory tract or inhaled irritant like SO2 , No2 and O3
    Virus- induced mucosal damage lowers threshold of subepithelial vagal receptor to irritant

Inflammatory mediators are the same as atopic asthma
Treatment is similar

69
Q

What is Drug induced asthma and pathogenesis?

A

Aspirin sensistive asthma
occurs in individuals with recurrent rhinitis and nasal polyps
Inhibit COX pathway of arachidonic acid without affecting lipo-oxygenase route- bronchoconstriction mediated by leukotrienes

70
Q

What are the pathological features of asthma?

A

Gross: In patients dying of acute severe asthma
Occulusion of airways by thick mucus plugs
hyperinflation of lungs.

71
Q

Microscopy image of asthma

A

Curschmann spirals: cleared mucus plugs containing whorls of shed epithelium
2. Charcot leyden crystals = crystalloid made up of the eosinophils proteins
Features of airway remodeling.

72
Q

What are the clinical features of asthma?

A

Asthma attacks:
by severely dyspnea, wheezing , chest tightness, cough
occurs at night and early mornings, last for couple of hours and subside sponatenously or with therapy

Acute severe asthma: Acute exacerbation that doesn’t respond to inital standard therapy
Increased risk for respiratory failure
requires emergency management

73
Q

Investigation of asthma?

A

Spirometry: during attacks: obstructive picture
Sputum: Curschmann spirals, Charcot leyden crystals, eosinophils
CBC: eosinophilia
ABG: hypoxemia, hypercapnia, respiratory acidosis

74
Q

What is restrictive lung disease?

A
  1. Parenchymal(Interstitium): Interstitial lung disease
    infiltrative lung disease, diffuse parenchymal lung disease Characterized by normal FEV1:FVC, reduced DLCO, and Increased A&a gradient.
  2. Extra-parenchymal: chest wall disorders such as kyphoscoliosis , neuromuscular disease, obesity, pleural disorders, characterized by normal FEV1:FVC, normal DLCO, normal A&a gradient.
75
Q

What is interstitial lung disease?

A

Heterogeneous group of lung parenchymal disorders.

  • involving inflammation and fibrosis of the alveolar septa
  • hallmark: involvement of intersititum
76
Q

PAthogenesis And clinical features.

A

Unknown

  • Alveolitis - damage to pneumocytes and endothelial cells
  • Leads to leukocytes releasing cytokines which mediate and stimulate intersitial fibrosis which leads to decreased lung compliance (stiff)
  • dry cough
  • hypoxia- pulmonary vasoconstriction - pulmonary hypertension and corpulmonale
77
Q

Investigation of interstitial lung disease

A

Spirometry: normal or increased FEv1:FVC
DLCO: reduced
A-a gradient: increased
chest x ray= Bilateral infiltration which can be nodular reticular or ground glass
HRCThigh resolution CT: Investigation of choice

78
Q

What is idiopathic pulmonary fibrosis?

A

Clinopathologic syndrome marked by progressive intersitital pulmonary fibrosis and respiratory failure.

Synonyms: Usual interstitial pneumonia (UIP)

79
Q

Etiology of UIP

A

Arises in genetically predisposed individuals who are prone to aberrant repair of recurrent alveolar epithelial cell injuries caused by environmental exposures.

80
Q

Pathogenesis of UIP

A

Environmental factors - alveolar epithelial injury- persistent of inflammation - fibrosis

81
Q

Gross image and hisotogy of UIP

A

Gross: Cobble stone appearance of pleural surface - retraction of scars along interlobular septa
Firm, fibrotic parenchyma markedly in lower lobe and subpleural region
Honey comb cyst

Micro: Patchy intersittial fibrosis
Temporal and geographic heterogeneity
- mature fibrosis and young fibroblast foci with bluish myxoid extracellular matrix
Accentuation beneath the pleura and along interlobular septa
- Areas of spared, normal lung
Honeycomb change- cystic spaces lined by type II pneumocytes or respiratory epithelium (dense fibrosis will destroy the arachitecture of the parenchyma creating cyst)

82
Q

Clinical features of UIP

A

Insidious onset of dry cough and dyspnea on exertion which progress gradually,
Cyanosis, cor pulmonale and clubbing in late stages

83
Q

Course of the UIP

A

Progression is relentless
Poor prognosis
Lung transplantation is only option

84
Q

What is nonspecific interstitial pneumonia ?

A

Etiology: unknown.
female non-smoker
Histology: Uniform fibrosing process chicken wire
Two variant: Cellular variant (infiltrate of lymphocytes) or fibrosing variant or both.
Treatment : Better prognosis than UIP

85
Q

What is cryptogenic organizing pneumonia ?

A

Also called Bronchiolitis obliterans organizing pnumonia (BOOP)
Clinical presentation: Cough, dyspnea

86
Q

What is the feature of histology for cryptogenic organizing penumonia?

A

Polypoid plugs of loose organizing connective tissue (masson bodies) in alveoli, alveolar ducts and often bronchioles.
No interstitial fibrosis or honeycomb lung
Connective tissue is all of the same age, and the underlying lung architecture is normal.

Radio: Patchy subpleural or peribronchial areas of airspace consolidation.

87
Q

Organizing pneumonia with intra-alveolar fibrosis may be seen in

A 
Infectious pneumonia 
Inhaled chemicals and toxins
Transplantation - lung and bone marrow 
Connective tissue diseases 
Then it is not crytogenic . Prognosis depends on the underlying condition
88
Q

Collagen Vascular disease

A
  • Lupus,
  • rheumatoid arthritis
  • Systemic sclerosis
  • Dermatomyositis- polymyositis
Pathological finding: 
UIP- pattern of fibrosis
NSIP
Organizing penumonia
Bronchiolitis + /- fibrosis
Lymphoid interstitial pneumonia
Pleural involvement can occur
89
Q

What is pneumoconiosis?

A

describe the non-neoplastic lung reaction to inhalation of mineral, dusts encountered in the workplace, now also includes disease induced by chemical fumes and vapor’s

90
Q

What is pathogenesis of penumoconiosis?

A
  • Dust retention: affected by impaired muco- ciliary clearance like in smoking.
  • Particle size: 1-5 diameter particles reach terminal airways and get deposited there
  • Particle solubility and cytotoxicity : smaller size- more soluble- rapid acute lung injury- whereas larger size- less soluble - persist for years and cause fibrosing lung diseases
  • Activation of inflammasome- phagocytosis of particles by macrophages - release of IL-1
91
Q

What is ASbestos related diseases?

A

Inhalation of asbestos fibers= pro inflammatory

Serpentine (more common) and amphibole (more pathogenic) form

92
Q

What is occupational exposure to for asbestos related disease ?

A

mining, milling, insulation, construction, demolition

93
Q

How’s spectrum of asbestos disease?

A
  • Pleural effusions, recurrent
  • Parenchymal interstitial fibrosis (asbestosis)
  • Lung carcinoma (more common)
  • Mesothelioma (more specific)
  • Laryngeal, ovarian and perhaps other extrapulmonary neoplasms, including colon carcinoma
94
Q

Pathogenesis of asbestos disease?

A

Asbestos fiber deposition in lungs - asbestos body formation . Golden brown beaded rods with translucent center. Called ferruginous bodies

  • Opsonization with surfactant; adsorption of proteins and iron - iron catalyzed reactions with generation of free radicals- depletion of antioxidant defenses- oxidative stress- production of cytokines and other inflammatory mediators leading to cell injury and proliferation leading to dna damage- carcinogenesis
  • Diffuse interstitial fibrosis
95
Q

Gross image for asbestos disease?

A

Markedly thickened visceral pleura covers the lateral and diaphrgamatic surface of the lung
- Severe interstitial fibrosis diffusely affecting the lower lobe of the lung

  • pleural plaques: contain dense collagen and calcification.
    : frequently on anterior and posterolateral aspects of the parietal pleura and over the domes of the diaphragm
96
Q

Clinical features of asbestos disease?

A

-progressively worsening dyspnea
cough and sputum
Concomitant cigarrete smoking greatly increases the risk for lung carcinoma but not for mesothelioma
- Poor prognosis

97
Q

What is Silicosis?

A

By inhalation of proinflammatory crystalline silicon dioxide.

Risk factors: occupational exposure to mining, demolition, stonecutting, sandlblasting, grinding, foundry work, ceramics.

98
Q

Pathogenesis of silicosis?

A

Inhaled particles interact with macrophages and epithelial cells- activation of inflammasome leading to release of inflammatory mediators: IL-1, IL-8.
leading to fibrosis
—- Increased risk of pulmonary tuberculosis- crystalline silica inhibits the ability of pulmonary macrophages to kill phagocytosed mycobacteria.

99
Q

Morphological changes for silicosis?

A
  1. Collagenous nodule/ scar(usually in the hilar lymph nodes and upper lung field)
  2. Eggshell calcification
  3. Progressive massive fibrosis

Microscopy: Central area of whorled collagen fibers with dust laden macrophages

100
Q

CLinical course of silicosis?

A

Slow progression
Increased susceptibility to tuberculosis
Increased risk of lung cancer
Shortness of breath later stage

101
Q

What is coal worker’s penumoconiosis?

A

Lung disease caused by inhalation of coal particles and other admixed forms of dust.
Mostly carbon

102
Q

Morphological changes of coal workers

A

Anthracosis: accumulation of carbon pigment in peri lymphatic region and lymph nodes … asymptomatic
Simple CWP: /macules and nodules …. aggregates of dust laden macrophages..

Complicated CWP: Coalescence of nodules into fibrous scars.
Impaired pulmonary function

103
Q

What is sarcoidosis?

A

Characterized by noncaseating granulomatous inflammation in many tissue and organs.

Risk factors: Danish, Swedish, African Americans, Higher prevalence in nonsmokers

  • Eiology: Suggest disordered immune regulation in susceptible individuals when exposed to certain environment trigger
104
Q

Pathogenesis of Sarcoidosis?

A

Cell mediated (type IV) hypersensitivity reaction
CD4+ helper T cell driven process
- Intra alveolar and interstitial accumulation of CD4 Th1 cells - secrete Th1 specific cytokines (IFN-y, IL-2)
- Peripheral depletion
- Anergy to skin test with candida antigen / PPD
-polyclonal hypergammaglobulinemia

105
Q

Morphological features of sarcoidosis?

A

Non-necrotizing epithelioid granulomata in a lymphangitic distribution

  • Over time, collagen replaces the granuloma yielding a hyalinized scar.
  • Schaumann bodies: laminated concretion of calcium and protein
  • Asteroid bodies: Stellate inclusion in giant cells
106
Q

Clinical features of sarcoidosis?

A
  1. Asymptomatic
  2. gradual development of respiratory symptoms
  3. Constitutional symptoms
    Other organ system involved
107
Q

What is laboratory investigation of sarcoidosis?

A

May be associated with hypercalcemia(Activation of Vitamin D by epithelioid cells)
Elevated serum angiotensin converting enzyme
CD4 to CD8 T cell ratio in bronchoalveolar lavage is increased

108
Q

Chest Xray for sarcoidosis?

A

Typical bilateral hilar lymphadenopathy
Parenchymal infiltrates or fibrosis

Biopsy: Non-necrotizing granulomas

109
Q

What is hypersensitivity pnuemonias?

A

caused by intense, often prolonged exposure to inhaled organic antigen- primarily involving alveolar walls- restrictive lung disease

110
Q

Etiology of hypersensitivity pneumonias?

A

Associated to inhaled organic antigen

  1. Farmer’s lung: moldy hay, thermophilic actinomycetes bacteria
  2. Silo fillers disease: inhalation of gases from plant material (oxides of nitrogen)
  3. Byssinosis: Cotton, linen, hemp, textile factory works
111
Q

Pathogenesis of hypersensitivity penumonitis?

A

First exposure- IgG antibodies in serum
Second exposure- Antibodies combine with inhaled antigen to form immune complexes - inflammatory response in lung )interstitial
Chronic exposure- granuloma formation

112
Q

Morphological change of hypersensitivity pneumonitits?

A

Airwy centered process
chronic inflammatory infiltrate
organzing pnemonia
poorly formed non necrotizing granulomata with giant cell

113
Q

What is pulmonary alveolar proteinosis?

A

rare disease caused by defects in pulmonary macrophages function due to deficient granulocyte-macrophages colony stimulating factor signaling.

Morphology: accumulation of intra-alveolar precipitates containing surfactant proteins, causing focal to confluent consolidation of large areas of the lungs with minimal inflammatory reaction.

Radio: bilateral patchy asymmetric pulmonary opacification.

114
Q

What is acute interstitial pneumonia?

A
  • also called Hamman rich syndrome.
    very aggressive form
    occur as an acute phase of acceleration of IPF
    ( interstitial pulmonary fibrosis)
115
Q

What is pulmonary thromboembolism?

A

Blood clot travels to the lungs within a pulmonary artery or its downstream branch

  • The most common cause : Deep vein thrombosis
  • blood clot forms in the deep vein of the lower extremity
116
Q

What are the risk factors of pulmonary thromboembolism?

A
  • immobility
  • surgery
  • severe trauma
  • congestive heart failure
  • oral contraceptive pills(elevated estrogen)
  • Disseminated maligancy- trousseau syndrome
  • hypercoagulability disorders: Factor V Leiden , protein C, protein S,
117
Q

Pathogenesis of pulmonary thromboembolism?

A

Deep vein (popliteal- femoral- illiac) inferior vena cava- right atrium- right ventricle- pulmonary artery- pulmonary capilaries

118
Q

consequences of pulmonary embolism?

A

depend on

  1. The size of embolus
  2. the cardiopulmonary status of the aptient.
    - Increase in pulmonary artery pressure from blockage of flow
  3. Ischemia of the downstream pulmonary parenchyma
119
Q

Hypoxemia develops as a result of multiple mechanism:….

A
  1. Ventiliation - perfusion mismatch
  2. the decrease in cardiac output
  3. right to left shunt of blood may occur through a patient foramen ovale,
120
Q

Large embolus…..

A

as a saddle embolus

  • diminished cardiac output, cause sudden death.
  • no time for morphologic alteration in the lung
121
Q

Smaller emboli……

A

Bc of dual circulation of lung (bronchial arterial flow), the vitality of the lung parenchyma is maintained.

  • alveolar hemorrhage occur
  • With compromised cardiovascular status - infarction results.
122
Q

clinical features of pulmonary embolism?

A

60-80% asymptomatic

123
Q

Investigation of pulmonary embolism?

A
  • chest X- ray - limited utility
  • Workup for DVT: D-dimer, ultrasound doppler for lower extremities.
  • VQ scan (ventilation - perfusion scan)
  • CT angiogram- gold standard to see embolus
124
Q

What is pulmonary hypertension?

A

Pulmonary artery pressure greater than or equal to 25mm Hg at rest.

125
Q

Classification of pulmonary hypertension?

A

Group 1 Pulmonary arterial hypertension
A. Idiopathic
B. Secondary to systemic disorders
2. Left heart disease like left ventricular failure, mitral stenosis
3. Lung disease/hypoxia:COPD,ILD
4.Chronic thromboembolic pulmonary hypertension
5. Pulmonary hypertension from unclear mechanis,m

126
Q

Pathogenesis of Idiopathic lung hypertension

A
  • inactivating germ line mutation in the gene encoding bone morphogenetic protein receptor 2 BMPR2
  • defects in BMPR2 signaling leads to dysfunction of endothelium and proliferation of vascular smooth muscle cells in the pulmonary vasculature
127
Q

morphological features of pulmonary hypertension

A
  • main elastic artery= atheromas
  • medium sized muscular arteries= wall thickening
  • smaller arteries/ arterioles =thickening, medial hypertrophy, reduplication of internal and external elastic lamina
  • plexiform lesion= multiple lumina (= lumen)within a small artery at a branch point from a larger artery.
  • right ventricular hypertrophy
  • marked medial hypertrophy
  • plexiform lesion
128
Q

Clinical features of pulmonary hypertension?

A

-Primary pulmonary hypertension:
Young women ,
fatigue, syncope, dyspnea on exertion, chest pain

129
Q

What is diffuse alveolar hemorrhage syndromes?

A
  • triad of symptoms: hemoptysis, anemia, diffuse pulmonary infiltrates
130
Q

Three diseases related to diffuse alveolar hemorrhage syndromes?

A
  1. Goodpasture syndrome
  2. Wegener’s granulomatosis
  3. Idiopathic hemosiderosis
131
Q

What is goodpasture syndrome?

A
  • autoimmune disease
  • age group : teens and 20s
  • pulmonary- renal syndrome: proliferative and rapidly progressive glomerulonephritis and hemorrhagic interstitial pneumonitis
132
Q

Pathogenesis of goodpasture syndrome?

A
  • kidney and lung injury are caused by circulating autoantibodies against the non-collagenous domain of the a3 chain of Collagen IV.
  • the antibodies - cause inflammatory destruction of the basement membrane in renal glomeruli and pulmonary alveoli
  • linear deposition of Ig G along basement membrane- glomerular basemnt or alveolar septa
133
Q

Morphological change for goodpasture syndrome?

A

Gross: heavy lungs, red-brown consolidation
Micro: intra-alveolar hemorrhage
patchy necrosis of alveolar walls
- intra alveolar hemosiderin.
-septal thickening and reactive hypertrophy of type II cells in later stages.

134
Q

investigation of goodpasture syndrome?

A

Chest X ray= focal consolidation

Immunofluorescene studeis- Ig G depositon

135
Q

What is granulomatosis with polyangiitis or wegener’s granulomatosis?

A

Autoimmune disease

  • PR3- ANCA
  • Granulomas of the lung upper respiratory tract
  • vasculitis of small medium sized vessels
  • glomerulonephritis
136
Q

Clinical features of wegener’s granulomatosis:

A
  • lung and upper respiratory tract: pneumonitis with nodules and cavitary lesion and chronic sinusitis
  • mucosal ulcertation of nasopharynx
  • hematuria , proteinuria
137
Q

histopathology of wegener’s granulomatosis:

A
  • necrosis geographic meaning irregular
  • neutrophilic micro abscesses
  • granulomas
  • vasculitis necrotizing capilaries
  • necrotizing crescentic glomerulonephritis
138
Q

What is acquired atelectasis?

A

refers either to incomplete expansion of the lungs or to the collapse of previously inflated lungs

139
Q

pathogenesis of atelectasis?

A

loss of lung volume secondary to alveolar collapse - decreased oxygenation- ventilation perfusion mismatch

140
Q

Three types of atelectasis

A
  1. resorption
  2. compression
  3. contraction
141
Q

Resorption atelectasis

A

Cause

  • most caused by excessive secretion like mucus plugs or exudates within smaller bronchi
  • aspiration of foreign bodies
  • intrabronchial tumors
  • over time- air is resorbed from distal alveoli - which collapse since lung volume is diminished, the mediastium shifts toward the atelectatic lung.
142
Q

Clinical features of resorption atelectasis

A
  • ipsilateral deviation of trachea and mediastinum
  • ipsilateral diaphragmatic elevation
  • absent breath sounds and absent vocal vibratory sensation
  • collapsed lung doesn’t expand on inspiration- decreased movment
143
Q

What is compression atelectasis?

A

Cause : air , fluid , tumor

  • mechanism: air or fluid accumulation in pleural cavity- increased pressure- collapses underlying lung
    ex: tension pneumothorax and pleural effusion.

Clinical features: trachea and mediastinum shift away from the affected lung

144
Q

What is contraction atelectasis?

A

Occurs when focal or generalized pulmonary or pleural fibrosis prevents full lung expansion ‘

-

145
Q

What is the course and complication of atelectasis?

A
  • atlectasis is potentially reversible except contraction one.
  • should be treated promptly to prevent hypoxemia and superimposed infection of the collapsed lung
146
Q

When blood leaves a ruptured blood vessel , the red blood cell dies, and the hemoglobin of the cell is released into the extracellular space.
- White blood cells called macrophages engulf the hemoglobin to degrade it , producing ……… and ………….

A

hemosiderin and biliverdin.
- hemosiderin is causes the purple color of 2 day old bruises.

  • biliverdin is the pigment responsible for the greenish color of 5 day old bruises and breaks down into bilirubin , causing bruise to turn yellow in 7-10 days.

usmle (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions