Brainscape's Knowledge GenomeTM

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


See full index

MS2 Respiratory > 9/14- Injury, Obstructive Lung Diseases, Infections, and Transplantation > Flashcards

9/14- Injury, Obstructive Lung Diseases, Infections, and Transplantation Flashcards

1
Q

What is atelectasis?

A

Collapse

  • Incomplete expansion (neonatal) or collapse of previously inflated lung (acquired; primarily adults)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the three forms of acquired atelectasis (broadly)?

A
  • Resorption (obstructive)
  • Compressive
  • Contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is resorption atelectasis? What can cause it?

A

Aka obstructive atelectasis

  • Airway obstruction, air resorption
  • Lung volume diminished and mediastinum shifts toward collapsed lung
  • May be caused by mucus plugs, foreign body, tumors…
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is compressive atelectasis? What can cause it?

A
  • Pleural cavity filled with air, fluid, blood, etc.
  • Mediastinum shifts away* from collapsed lung
  • Pleural effusion, pneumothorax, subdiaphragmatic abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is contraction atelectasis?

A

Fibrosis or tumor involving pleura or lung prevents expansion, e.g. mesothelioma (involving lung “surface”)

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

What is seen here?

A

Left: normal

Right: atelectatic lung- compressed; can see how improper drainage might predispose to infection

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

What is pulmonary edema?

What are the 2 etiologies (broadly)?

A

Fluid in lungs; heavy, wet lungs (like saturated sponges)

2 etiologies:

1. Hemodynamic

2. Microvascular injury

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

What are hemodynamic causes of pulmonary edema?

A

Increased hydrostatic pressure

  • Left-sided failure
  • Volume overload
  • Pulmonary vein obstruction

Decreased oncotic pressure

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

What are the microvascular injury causes of pulmonary edema?

A

(Alveolar/capillary junction)

Increase in capillary permeability

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

What is seen here?

A

Pulmonary edema

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

What is DAD?

Onset?

Symptoms?

Histologically?

Outcome?

A

Diffuse Alveolar Damage (Acute Respiratory Distress Syndrome)

  • Aka shock lung, Da Nang Lung, Hamman-Rich syndrome
  • Acute onset (24-48 hrs)
  • Sx: dyspnea, tachypnea, hypoxia, respiratory failure
  • Ground glass changes with consolidation on HRCT (hazy appearance on HRCT)
  • 30% mortality (most due to sepsis, multi-organ failure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the etiologies of DAD/ARDS? (covered quickly)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pathogenesis of DAD?

A
  • Damage centers on capillary/alveolar junction
  • Loss of integrity of microvascular endothelium and alveolar epithelium
  • Inflammatory cascade initiates events*
  • Leakage of fluid & inflammatory cells
  • Sloughing of epithelial cells

*Imbalance of pro-inflammatory vs anti-inflammatory mediators

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

What are the 2 phases of DAD? Time frame?

Other processes?

A
  1. Exudative (acute) phase (under 1 wk)
  2. Proliferative (organizing) phase (after 1st wk)
    - Can distinguish by macroscopic view of the lungs

Histologically:

  • Edema peaks ~ day 1
  • Hyaline membranes peak ~ day 3-4
  • Interstitial inflammation/fibrosis characterizes proliferative stage; days 11+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is seen here?

A

Left: exudative phase of DAD

  • Red appearance

Right: proliferative phase of DAD

  • Edema/fluid is gone
  • Left with granulation tissue/fibrosis of lung repairing damage in alveolar spaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the microscopic findings in the exudative phase?

A

(First week following onset injury)

Vascular congestion, interstitial/alveolar edema, intra-alveolar hemorrhage

Hyaline membranes (hist. hallmark)** key**

  • Begin day 2; peak 4-5 days after injury
  • Precipitated plasma proteins, cytoplasmic/nuclear debris from sloughed epithelial cells

Microvascular thrombi and mild chronic interstitial inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is seen here?

A

Exudative phase of DAD

(This pt died of aspiration; central feature there = vegetable matter)

  • Hemorrhage
  • Inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is seen here?

A

Acute form of DAD (exudative phase)?

  • Pink material against alveolar walls = hyaline membranes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is seen here?

A

Hyaline membranes (pink) are hallmark of acute/exudative phase of DAD

  • Mixed inflammatory infiltrate: lymphocytes and neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is seen here?

A

Again, acute form of DAD

  • Plasma proteins and nuclear/cytoplasmic debris
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the microscopic findings of the organizing (proliferative) phase of DAD?

A

(End of first week)

- Type 2 pneumocyte hyperplasia (alveolar repair cells)

- Organization of exudate with proliferation of myofibroblasts and fibroblasts (intra-alveolar granulation tissue)

  • Alveolar septal thickening (loose granulation tissue)
  • Resolution of organization (macrophages remove cell debris; granulation tissue matures into dense fibrous tissue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is seen here?

A

Alveolar septal tissue expanded due to proliferating, organizing tissue

Right: granulation tissue in alveolar space

  • Over time, incorporated into adjacent septal tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is seen here?

A

Type 2 pneumocyte lining alveoli (A) and within granulation tissue (B)

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

What is seen here?

A

Fibrosis (in proliferative phase of DAD)

  • May cause extensive narrowing of the lung and loss of lung function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are key pulmonary function value differences that distinguish obstructive vs. restrictive pulmonary disease?

A
  • Obstructive: decreased flow rate (FEV1)
  • Restrictive: decreased TLC (ex ILDs)
26
Q

What are common obstructive pulmonary diseases?

Key characteristics/pulmonary function findings?

A
  • Asthma
  • Chronic bronchitis
  • Bronchiectasis
  • Emphysema

Typically involves:

  • Increased resistance to air flow due to obstruction (asthma) or loss of elastic recoil (emphysema)
  • Decreased FEV1 (max amt of air exhaled in 1s)
27
Q

What is asthma? What is seen microscopically?

A

Chronic inflammatory disorder of airways; bronchconstriction due to bronchospasm and inflammation

  • Hyperinflated lungs (CXR)
  • Globet cell metaplasia; submucosal gland hypertrophy
  • Mucus plugs (Curschmann spirals)- mucus casts of the involved bronchioles
  • Thickened basement membrane and muscle wall hypertrophy (in response to constant bronchoconstriction)
28
Q

What population is commonly afflicted by chronic bronchitis?

A

Long time smokers

29
Q

What is chronic bronchitis?

What is seen microscopically?

A

Persistent cough with sputum production for at least 3 mo in at least 2 consecutive yrs

  • Chronic irritation leads to submucosal gland hypertrophy/hyperplasia; increase Reid index
  • Mucus plugs obstructs airways
  • Goblet cell metaplasia; chronic inflammation
30
Q

What is bronchiectasis?

Commonly seen in what population?

A
  • Destruction of muscle/elastic tissue with inflammation and fibrosis due to repeated bouts of infection and obstruction
  • Permanent dilation of bronchi/bronchioles (lower lobe disease)
  • Commonly seen with cystic fibrosis
31
Q

What is emphysema?

What are the two most common types?

A

Permanent enlargement airspaces, distal to the terminal bronchiole

Types:

  • Centriacinar (centrilobular): only central acinus involved
  • Panacinar (panlobular): entire pulmonary acinus involved in permanent enlargement of airspaces
32
Q

Which form of emphysema do smokers typically get?

A

Centriacinar (centrilobular)

33
Q

Which form of emphysema is most common?

A

Centriacinar (centrilobular)- 95% of cases

34
Q

Characteristics of centriacinar (centrilobular) emphysema?

A
  • Upper lobe dominant
  • Both emphysematous and normal airspaces present in lobule
35
Q

Characteristics of panacinar (panlobular) emphysema?

A
  • Alpha-1-antitrypsin deficiency
  • Lower lobe dominant
  • No normal airspaces in lobule
36
Q

What are the defense mechanisms of the lung?

A
  • Cough reflex
  • Mucociliary escalator
  • Alveolar macrophage
  • Host resistance

(We inhale ~10,000 microorganisms/day)

37
Q

What is the mucociliary escalator?

A

Movement of mucus containing foreign material by beating of cilia in tracheobronchial tree

38
Q

What is seen here?

A
  • Ciliated endobronchial cells
  • Some macrophages
  • Pigment seen is carbon pigment; present in ambient air
39
Q

What is the definition of pneumonia?

A

Any infection of lung parenchyma?

40
Q

What are the subtypes of pneumonia?

A
  • Community acquired
  • Nosocomial
  • Aspiration
  • Immunocompromised host
41
Q

What are the infectious agents associated with community acquired pneumonia?

A

Variety of bacteria and viruses

42
Q

What are the infectious agents associated with nosocomial pneumonia?

A
  • Gram (-) rods (Pseudomonas)
  • Staph aureus
43
Q

What are the infectious agents associated with aspiration pneumonia?

A

Variety of aerobes/anaerobes from oral flora

44
Q

What are the infectious agents associated with immunocompromised host pneumonia?

A
  • CMV
  • Aspergillosis
  • Pneumocystis
45
Q

What are the anatomic patterns of pneumonia?

A

- Bronchopneumonia

- Lobar pneumonia

May overlap; etiology most important, clinically

46
Q

What is seen here?

A

Bronchopneumonia

  • Inflammation begins with airway
47
Q

What is seen here?

A

Lobar pneumonia

  • Inflammation begins with alveolar tissue
  • Inflammatory process extending into adjacent alveolar tissue
48
Q

What are the 4 histological patterns of lobar peumonia?

A
  1. Congestion/edema
  2. Red hepatization
  3. Gray hepatization
  4. Resolution
49
Q

What is seen in the congestion/edema histologic pattern of lobar pneumonia?

A
  • Vascular congestion
  • Intra-alveolar fluid
50
Q

What is seen in the red hepatization histologic pattern of lobar pneumonia?

A
  • Massive exudate of RBCs, WBCs, fibrin
  • Airless, firm consistency (like liver)
51
Q

What is seen in the gray hepatization histologic pattern of lobar pneumonia?

A
  • Breakdown of RBCs, persistence of fibrin and neutrophils
  • Airless, firm consistency (like liver)
52
Q

What is seen in the resolution histologic pattern of lobar pneumonia?

A
  • Granulation tissue: exudate becomes organized; removed by macrophages
  • Reformation of lung architecture
53
Q

What are some complications of pneumonia?

A
  • Abscess
  • Empyema
  • Septicemia resulting in multiorgan abscesses (ex, pt with osteomyelitis)
54
Q

What are the most common indications for lung transplantation?

A
  • Idiopathic pulmonary fibrosis
  • Cystic fibrosis
  • Primary pulmonary hypertension
55
Q

What are complications of lung transplantations?

A
  • Postoperative (Rare)
  • Infections (immunosuppressed to prevent organ rejection)
  • Rejection (acute and chronic)
56
Q

Recall: more extensive list of infectious agents of an immunocompromised host (age, chemo, transplant)?

A
  • Aspergillus: Y-shaped branching of septated hyphae
  • Cryptococcus
  • Hisotplasma
  • Penumocystis
  • Herpes
  • CMV
  • Bacterial pneumonias as well
57
Q

Acute rejection

  • Timeline
  • Grading
A

Weeks to months after surgery

  • Graded by International Working Formulation
58
Q

What is seen here?

A

Different grades of acute rejection

A1- Minimal; Small perivascular lymphocyte infiltrates

A2- Mild; Large perivascular lymphocyte infiltrates

A3- Moderate; Perivascular infiltrates into interstitium

A4- Severe; Neutrophils with fibrin and hemorrhage

Switch from lymphocytes -> neutrophils as grade gets more severe

59
Q

Chronic rejection

  • Timeline
  • Characteristics
A

3-5 yrs after surgery

  • Significant problem in ~ 50% of transplants
  • Bronchiolitis obliterans (histologic hallmark**)- luminal fibrosis +/- inflammation
60
Q

Summary slide of obstructive lung diseases

A

MS2 Respiratory (26 decks)

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