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Mechanism of Disease > Exam 2: Respiratory System Diseases > Flashcards

Exam 2: Respiratory System Diseases Flashcards

1
Q

Respiratory Diseases

Acute Upper Respiratory Tract Infections

A

Infectious Rhinitis
Sinusitis
Pharyngitis/Tonsilitis

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2
Q

Respiratory Diseases

Vascular

A

Embolism/Infarction
Pulmonary hypertension
Goodpasture Syndrome
Pulmonary Edema

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3
Q

Respiratory Diseases

Obstructive/Restrictive Diseases

A

Emphysema
Asthma
Cystic Fibrosis
Pneumoconiosis
Hypersensitivity
Penumonitis
Sarcoidosis

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4
Q

Respiratory Diseases

Pleural Disease

A

Pleural Effusion
Pneumothorax

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5
Q

Non-specific Lung Diseases

Clearance

A

Cough
Mucociliary Escalator

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6
Q

Non-specific Lung Diseases

Secretions

A

Tracheobroncial (mucus)
Alveolar (surfactant)
Cellular components

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7
Q

Non-specific Lung Diseases

Cellular Defenses

A

Nonphagocytic (epithelium)
Phagocytic (alveolar macrophages)

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8
Q

Non-specific Lung Diseases

Biochemical Defenses

A

Proteinase inhibitors
Antioxidants

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9
Q

Specific Lung Diseases: Immunological

Antibody mediated

A

B-lymphocyte-dependent
Secretory immunoglobulin (IgA)
Serum immunoglobulins

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10
Q

Specific Lung Diseases: Immunological

Antigen presentation to lymphocytes

A

Macrophages and monocytes
dendritic cells
epithelial cells

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11
Q

Specific Lung Diseases: Immunological

Cell mediated immunologic responses

A

T-lymphocyte dependent
Cytokine mediated
direct cellular cytotoxity

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12
Q

Specific Lung Diseases: Immunological

Non-lymphocyte cellular immune responses

A

Mast cell/eosinophil dependent
usually respond to secretory immunoglobulin or cytokines

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13
Q

Acute Upper Respiratory Tract Infections

Clinical symptoms of Infectious Rhinitis (The Common Cold)

A

Nasal congestion with watery discharge
sneezing
scratchy, dry, sore throat

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14
Q

Acute Upper Respiratory Tract Infections

Pathogens of Infectious Rhinitis (The Common Cold)

A

Rhinoviruses
Others are less common (influenza, cornoaviruses, adenviruses, enteroviruses)

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15
Q

Acute Upper Respiratory Tract Infections

Treatment for Infectious Rhinitis (The Common Cold)

A

Anti-viral if available
mainly support for symptoms

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16
Q

Acute Upper Respiratory Tract Infections

Pathogensis of Infectious Rhinitis (The Common Cold)

A

Infection initiates immune response
immune mediators cause edema
* swellng and fluid leakage
* congestion and discharge

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17
Q

Acute Upper Respiratory Tract Infections

Potential complications of Infectious Rhinitis (The Common Cold)

A

Bacterial infections due to swelling, fluid accumulation
Middle ear infection (otitis media)
Sinus infection (sinusitis)

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18
Q

Acute Upper Respiratory Tract Infections

Sinusitis

A

Most commonly occurs after rhinitis
usually bacterial or viral infection
impairment of sinus drainage

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19
Q

Acute Upper Respiratory Tract Infections

What causes impairment of sinus drainage during Sinusitis?

A

Mucosal edema due to inflammation
Obstruction may be complete blockage
May lead to acute sinusitis to become chronic - if not resloved

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20
Q

Acute Upper Respiratory Tract Infections

What happens if obstruction of sinus drainage is complete blockage?

A

will result in accumulation of infected mucus (suppurative exudate) -> empyema

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21
Q

Acute Upper Respiratory Tract Infections

Complications of Sinusitis

A

Infection of neighboring structures (eye, skull, brain)
Usually just discomfort
(Add Clarifier)

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22
Q

Acute Upper Respiratory Tract Infections

Pharyngitis/Tonsilitis

A

Frequent companions of upper respiratory tract viral infections
Most common with rhinoviruses, echoviruses, and adenoviruses
Bacterial infections can be secondary to viral or primary causes

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23
Q

Acute Upper Respiratory Tract Infections

Symptoms of Pharyngitis/Tonsilitis

A

Redness
Edema
Enlargment of tonsils/lymph nodes

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24
Q

Acute Upper Respiratory Tract Infections

Most serious consequences of Pharyngitis/Tonsilitis

A

Rheumatic fever
Glomerulonephritis

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25
Q

Acute Upper Respiratory Tract Infections

Most serious consequences of Pharyngitis/Tonsilitis: Rehumatic Fever

A

Acute multisystem inflammatory disease - streptococcus - myocarditis, valvular abnormalitis

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26
Q

Acute Upper Respiratory Tract Infections

Recurrent acute tonsillitis may be linked to…

A

Chronic enlargment - surgery

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27
Q

Lung Disease

Atelectasis

A

Collapse of previously inflated lung

neonatal - incomplete expansion

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28
Q

Lung Disease

Three types of Atelectasis

A

Resorption (blockage of airways)
Compression (accumulation in pleural sac)
Contraction (fibrosis restricts expansion)

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29
Q

Lung Disease

Consequences of Atelectasis

A

Lowers blood oxygen
Increases risk infection

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30
Q

Lung Disease

What types of atelectasis are reversible?

A

Resorption
Compression

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31
Q

Lung Disease of Vascular Origin

Pulmonary Embolism

A

Something blocks vessel in lung
Most frequently a clot (can be air bubble, fatty deposit, other debris)

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32
Q

Lung Disease of Vascular Origin

Consequences of Pulmonary Embolism

A

Depend on size of obstruction
signals to body control system to lower BP (decrease CO)
Lung collapse

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33
Q

Lung Disease of Vascular Origin

Pulmonary Embolism: Blockage causes

A

Ischemia downstream
Increased pressure upstream

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34
Q

Lung Disease of Vascular Origin

Approximately 10% of emboli result in…

A

Pulmonary infarct

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35
Q

Lung Disease of Vascular Origin

The larger the ____ , the ____ the vessel it will block
The larger the vessel blocked….

A

Embolus
larger
the more tissue affected

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36
Q

Lung Disease of Vascular Origin

Consequences of Pulmonary Embolism: Large Blockage

A

Large blockage will kill quickly
no pathological change in lung
increased pressure damages in heart (right side heart failure, Cor Pulmonale)

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37
Q

Lung Disease of Vascular Origin

Pulmonary Embolism: Lung may collapse due to…

A

Lack of surfactant
Reduced movement in response to pain

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38
Q

Lung Disease of Vascular Origin

Treatment of Pulmonary Embolism

A

Anticoagulant (heparin)
Thrmbolytic (risky)

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39
Q

Lung Disease of Vascular Origin

Pulmonary Hypertension

A

Heart not pumping enough out of left side so blod backs up into lungs
RA still pumping properly

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40
Q

Lung Disease of Vascular Origin

Pulmonary Hypertension: Vascular Changes

A

Medial Hypertrophy - muscular and elastic arteries in lungs
Intimal fibrosis
Plexiform lesion - advanced HTN, tuft of capillaries, dilated thin-walled arteries

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41
Q

Lung Disease of Vascular Origin

Pathogenesis of Pulmonary HTN

A

Chronic Obstructive or Interstitial Lung Diseases
Heart Disease
Reccurent Emboli
Autoimmune diseases
Obstructive sleep apnea
Idiopathic

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42
Q

Lung Disease of Vascular Origin

Pathogenesis of Pulmonary HTN: Chronic Obstructive or Interstitial Lung Diseases

A

Destroy albeolar capillaries
Increase pulmonary vascular resistance
therefore, increase pulmonary BP

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43
Q

Lung Disease of Vascular Origin

Pathogenesis of Pulmonary HTN: Heart Disease

A

Damage to left side translates back to lung arteries

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44
Q

Lung Disease of Vascular Origin

Pathogenesis of Pulmonary HTN: Autoimmune diseases

A

Most common in systemic sclerosis
Increase vascular resistance (decrease elasticity)

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45
Q

Lung Disease of Vascular Origin

____ % of pulmonary htn have genetic basis

A

80%

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46
Q

Lung Disease of Vascular Origin

Clinical Symptoms of Pulmonary HTN

A

Only detectable when advanced
Dyspnea and fatigue
Rarely, chest pain
End stage: severe respiratory distress, cyanosis

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47
Q

Lung Disease of Vascular Origin

Treatment of Pulmonary HTN

A

Secondary disease - treat primary
Autoimmune or refractory - vasodilators
Lung transplantation

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48
Q

Lung Disease of Vascular Origin

Goodpasture Syndrome

A

Pulmonary hemorrhage syndrome
Autoimmune disease
Kidney and lung injury
Inflammatory-mediated destruction of alveolar basement membranes

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49
Q

Lung Disease of Vascular Origin

Goodpasture Syndrome: Autoimmune Disease

A

Autoantibody against type IV collagen
Type IV collagen is in basement membrane (e.g. of vasculature)

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50
Q

Lung Disease of Vascular Origin

Goodpasture Syndrome when it only affects the kidneys…

A

Anti-glomerular basement membrane disease

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51
Q

Lung Disease of Vascular Origin

Goodpasture Syndrome when it affects kidneys and lung…

A

Goodpasture syndrome

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52
Q

Lung Disease of Vascular Origin

Goodpasture Syndrome: Inflammatory-mediated destruction of alveolar basement membranes

A

Epitopes recognized by antibodies are buried deep in the protein
Environmental exposure may be required to ‘expose’ epitopes
Genetic predisopsition linked to certain HLA subtypes

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53
Q

Lung Disease of Vascular Origin

Pathology of Goodpasture Syndrome: Symptoms

A

Hemoptysis; X-ray will show focal consolidations
Death is usually due to renal involvement

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54
Q

Lung Disease of Vascular Origin

Treatment of hemoptysis due to Goodpasture Syndrome

A

plasmapheresis to remove autoantibodies + immunosuppression

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55
Q

Lung Disease of Vascular Origin

Pathology of Goodpasture Syndrome: Lungs

A

Red-brown consolidation
described as heavy

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56
Q

Lung Disease of Vascular Origin

Histology of Goodpasture Syndrome

A

Intra-alveolar hemorrhage
Focal necrosis in alveolar walls
Macrophages accumulate heme

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57
Q

Lung Disease of Vascular Origin

Late stages of Goodpasture Syndrome

A

Septal fibrosis (thickened)
Type II Penumocyte hypertrophy
Blood in alveolar spaces

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58
Q

Lung Disease of Vascular Origin

Pulmonary Edema

A

Leakage of fluid into alveolar space

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59
Q

Lung Disease of Vascular Origin

Pulmonary Edema is caused by…

A

Hemodynamic disturbances
Increased capillary permeability

Combination of the two

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60
Q

Lung Disease of Vascular Origin

Pulmonary Edema: Hemodynamic Disturbances

A

Increased pressure (more common)
Decreased pressure (less common)

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61
Q

Lung Disease of Vascular Origin

Pulmonary Edema: Increased capillary permeability

A

Damage to microvasculature
Infections, gas inhalation, liquid aspiration
Drugs and chemicals
Shock, trauma, radiation, transfusion

62
Q

Lung Disease of Vascular Origin

Hemodynamic Edema

A

Most commonly the result of left-side congestive heart failure
Increases pressure in LV - increased pressure in lungs - fluid forced out of capillaries

63
Q

Lung Disease of Vascular Origin

Microvascular injury edema

A

Damage to the capillary bed
Leakage of fluids and proteins
Acute Respiratory Distress Syndrome (ARDS)

64
Q

Lung Disease of Vascular Origin

Microvascular Injury Edema: Damage to capillary bed

A

Primary to vascular endothelial cells
or to alveolar squamous pneumocytes

Both cell types impt for maintaining barrier between blood+air space

65
Q

Lung Disease of Vascular Origin

Microvascular Injury Edema: Leakage of fluids and proteins

A

Interstitial space - restrictive disease
Alveoli - pneumonia

66
Q

Lung Disease of Vascular Origin

Microvascular Injury Edema: Acute Respiratory Distress syndrome is due to…

A

Due to sudden diffuse edema

67
Q

Acute Respiratory Distress Syndrome (ARDS)

Severe Acute Lung Injury

A

Abrupt onset of hypoxemia
Bilateral pulmonary infiltrates
no cardiac failure

68
Q

Acute Respiratory Distress Syndrome (ARDS)

Acute Respiratory Distress Syndrome (ARDS)

A

Severe Acute Lung Injury
Inflammatory disease producing Diffuse Alveolar Damage (DAD)

69
Q

Acute Respiratory Distress Syndrome (ARDS)

Diffuse Alveolar Damage (DAD)

A

Increased pulmonary vascular permeability
Edema
Epithelial cell death

70
Q

Acute Respiratory Distress Syndrome (ARDS)

What are some causes of Acute Respiratory Distress Syndrome (ARDS)?

A

Mechanical trauma
near drowning
sepsis
barbituate overdose
gastric aspiration

71
Q

Acute Respiratory Distress Syndrome (ARDS)

Pathogenesis of Acute Respiratory Distress Syndrome (ARDS)

A
  1. stress activated macrophages
  2. Inflammatory mediators damage cells (endothelium, Penumocytes)
  3. Neutrophils invade and debris accumulates (hyalinization
  4. Healing starts when macrophages produce TGFB and PDGF (activate fibroblasts)
72
Q

Acute Respiratory Distress Syndrome (ARDS)

Two types of Pneumocyte damage

A

Loss of Squamous (I) - increased permeability
Loss of Cuboidal (II) - decreased surfactant, increased risk of alveolar collapse

73
Q

Acute Respiratory Distress Syndrome (ARDS)

Acute Respiratory Distress Syndrome (ARDS) Symptoms - Lungs

A

Heavy
Filled with Fluis (Wet)

74
Q

Acute Respiratory Distress Syndrome (ARDS)

Acute Respiratory Distress Syndrome (ARDS) Symptoms - Clinical

A

Lungs become stiff due to loss of surfactant
Dyspena/Tachypnea
Cyanosis/hypoxemia

harder to inflate

75
Q

Acute Respiratory Distress Syndrome (ARDS)

Treatment of Acute Respiratory Distress Syndrome (ARDS)

A

High concentrations of oxygen
mechanical ventilation
treat underlying cause (e.g. sepsis)

76
Q

Infections

Pneumonia

A

Lung infection by bacteria, viruses, mycoplasms, or fungi
responsible for 1/6 of US deaths
Characterized by lymphatic infiltrates in alveoli
Produces pulmonary edema; can also result from pulmonary edema

77
Q

Infections

Types of Pneumonia

A

Community-acquired
Hospital-acquired
Aspiration
Chronic

78
Q

Infections

Community-acquired Pneumonia

A

Typical - bacterial
Atypical - viral, mycoplasmal

79
Q

Infections

Hospital-acquired Pneumonia

A

Mechanical ventilation is a risk factor

80
Q

Infections

Aspiration Penumonia

A

Markedly debilitated patients, stroke victims
Abnormal gag/swallowing reflex

81
Q

Infections

Chronic Pneumonia

A

Localized lesion
Immunocompetent patient

82
Q

Infections

Causes of Penumonia

A

Cough reflex suppression/inhibition
* coma, anesthesia, neuromuscular disorders

Mucociliary apparatus damage
* cigarette smoke, hot gases, viral, genetic

Accumulation of secretions
* cystic fibrosis, bronchial obstruction

Decreased macrophage activity
* alcohol, tobacco, anoxia, ocygen intoxication

Edema or congestion (mucus)

83
Q

Infections

What is Aspiration Pneumonia? What causes the damage?

A

Necrotizing Pneumonia; often fatal
Chemical
Bacterial

84
Q

Infections

Aspiration Pneumonia: Chemical damage

A

Low pH of gastric acid damages cells in the airways and alveoli
Tissues necrossi and inflammation

85
Q

Infections

Aspiration Pneumonia: Bacterial Damage

A

Oral flora (more than one; more aerobes than anaerobes)
Inflammation

86
Q

Infections

Aspiration Pneumonia: Microaspiration

A

Very common (esp. in patients with GERD)
May exacerbate exisiting conditions like asthma, interstitial fibrosis, and transplant rejection

87
Q

Infections

Bacterial Pneumonia

A

same species, different patterns
depends on Tx, patient susceptibility
Bronchopneumonia
Lobar

88
Q

Infections

Bacterial Pneumonia - Bronchopenumonia

A

opaque spots
patchy consolidation
areas of acute inflammation

89
Q

Infections

Bacterial Pneumonia: Lobar

A

X-ray - whole lobe is opaque
Consolidation of lung (hepatization)
Presense of fibrin and infection fill alveoli

90
Q

Infections

Clinical Course of Pneumonia

A

Rapid onset
* fever
* chills
* cough (mucous with signs of infections)

Fibrinosuppurative pleuritis
* Lung swelling - neutrophil infiltration, fibrin aggregation
* pleuritic pain and pleural friction rub

91
Q

Infections

Stages of Acute Pneumonia

A

Stage 2: early red hepatization
* neutrophil infiltrate
* congestion of septal capillaries

Stage 3: gray hepatization
* alveolar exudate in air spaces

Stage 4: resolution
* fibromyxoid masses
* macrophages and fibroblasts

92
Q

Infections

Viral Pneumonia: SARS

A

Severe Acute Respiratory Syndrome
Coronavirus from civets in China
Transmisison through respiratory secretions
Incubation period of 2-10 days
Virus infects pneumocytes

93
Q

Infections

Initial symptoms of SARS

A

Malaise
Myalgia
Dry cough
Fever
Chills

94
Q

Infections

COVID-19

A

Virus is SARS-CoV-2
Spreads through the air in close contact
Declared pandemic in March 2020

95
Q

Infections

Complications of COVID-19

A

Pneumonia and trouble breathing
Organ failure in several organs
Heart problems
Acute respiratory distress syndrome
Blood clots
Acute kidney injury
Additional viral and bacterial infections

96
Q

Infections

Histoplasosis

A

Infection with Histoplasma capsulatum
* dimorphic fungi
* initiates T cell mediated response to contain

Geographical distribution
* Warm moist soil containing bird/bat droppings (Caves)
* OH, central S valley, Appalachia

97
Q

Infections

Histoplasmosis clinically:

A

Acute pulmonary infection
Chronic (granulomatous) infection
Disseminated miliary disease

98
Q

Infections

Pathology of Histoplasmosis

A

Macrophage aggregates filled with yeast
Will colonize nearby lymph nodes
Eventually - granulomas with giant cells - May develop fibrosis and calcifications

Gross appearance - perihilar mass lesions (can look like lymphoma)

99
Q

Obstructive and Restrictive Diseases

Inhalation

A

Intercostal muscles contract to draw ribs upwards
Diaphragm contracts and pulls down
increased volume draws air in

decrease pressure in lungs

100
Q

Obstructive and Restrictive Diseases

Exhalation

A

Muscles relax and elastic fibers retract
decreaed volume expels air

Increase pressure relative to atmospheric pressure

101
Q
A
102
Q

Obstructive and Restrictive Diseases

Obstructive and Restrictive Diseases

A

Diffuse pulmonary diseases

103
Q

Obstructive and Restrictive Diseases

Obstructive

A

partial or complete obstruction at any level
increased resistance to air flow

104
Q

Obstructive and Restrictive Diseases

Restrictive

A

Reduced expansion of parenchyma
Decreased total lung capacity

105
Q

Obstructive and Restrictive Diseases

How are Obstructive and Restrictive Diseases diagnosed?

A

Obstructive - decreased forced expiratory volume (cant expire as much)
Restrictive - decreased FRV and vital capacity

106
Q

Obstructive Diseases

Emphysema

A

with chronic bronchitis, COPD
Permanent enlargement of smaller airspaces
* destruction of walls of smaller air spaces
* no fibrosis

107
Q

Obstructive Diseases

Patterns of Emphysema

A

Disease location is the acinus
Associated with tobacco smoke inhalation
Major Symptom: Dyspnea

108
Q

Obstructive Diseases

Pathology of Emphysema

A

Enlargment of airways
Destruction of walls
No fibrosis

Less wall tissue

109
Q

Obstructive Diseases

Pathogensis of Emphysema

A

Destruction of walls
* direct damage from toxins
* inflammatory response
* proteases released from cells
* infection

110
Q

Obstructive Diseases

Emphysema Pathogenesis: Inflammatory response

A

Macrophages/epithelial cells relase leukotrienes, IL-8, TNF
Chemotaxis, inflammation, structural changes (act as growth factors)

111
Q

Obstructive Diseases

Emphysema Pathogenesis: Proteases released from cells

A

Deficiency in protease inhibitors
* genetic component to emphysema
* alpha-1 anti-trypsin inhibits release
Damage CT (including elastic fibers)

112
Q

Obstructive Diseases

Emphysema Pathogenesis: Infection

A

Not a major role, but may exacerbate inflammatory damage

113
Q

Obstructive Diseases

Asthma

A

Complex multigenic disorder
Increased airway responsiveness to stimuli
* may not provole a response in unaffected individuals (adenosine, exercise)

114
Q

Obstructive Diseases

Characteristics of Asthma

A

Episodic bronchoconstriction
Bronchial wall inflammation
Increased mucus secretion

115
Q

Obstructive Diseases

Types of Asthma

A

Atopic
* Classic hypersensitivity reaction (IgE)

Non-atopic
* Hyperirritability due to viral infection

Drug-induced
* Aspirin (and other NSAIDS) affects balance of cyclooxygenase activity

Occupational
* exposure to fumes, dust, gases, chemicals

116
Q

Obstructive Diseases

Asthma: Chronic inflammatory airway disease

A

Recurrent episodes
* wheezing, breathlessness, chest tightness, cough

Bronchoconstriction
* widespread, but variable

Airflow limitation (partially reversible)

117
Q

Obstructive Diseases

How does asthma alter airway structure?

A

Thicker mucosal layer with eosinophils inbetween goblet cells
thicker basement membrane
macrophages in lamina propria
thicker smooth muscle layer (SM proliferation)
increased glands

118
Q

Obstructive Diseases

What is involved in initiation of Asthma?

A

B and T lymphocytes
IgE
Mast cells
Eosinophils

119
Q

Obstructive Diseases

Cellular Response to Asthma: Mast Cells

A

Smooth muscle contraction
increased mucus secretion
vasodilation
* endothelial leakage
* local edema

120
Q

Obstructive Diseases

Cellular Response to Asthma: Epithelial cells

A

Cytokine production
* includes leukotrienes and prostaglandins

121
Q

Obstructive Diseases

Asthma: Damage to epithelium: What are the two eosinophil mediators?

A

Major Basic Protein (Proteoglycan 2 (PRG2))
Eosinophil Cationic Protein (ribonuclease 3)

122
Q

Obstructive Diseases

Asthma: Eosinophil Mediators: Proteoglycan 2 (PRG2)

A

Major Basic Protein
Cellular toxin (bacteria and mammalian)
Possibly by disordering cell membranes

123
Q

Obstructive Diseases

Asthma: Eosinophil Mediators: Ribonuclease 3

A

Eosinophil Cationic Protein
Binds to cell surface heparan sulfate proteoglycans (endocytosis)
Apoptosis through caspase-8
also necrosis

124
Q

Obstructive Diseases

Cystic Fibrosis

A

Mutation in chloride channel results in viscous mucus that obstructs passageways

125
Q

Obstructive Diseases

Consequences of Cystic Fibrosis

A

Chronic lung disease
* increased risk of nfections
* chronic bronchitis

pancreatic insufficiency
* steatorrhea (excess fecal fat)
* malnutrition

Hepatic cirrhosis
intestinal obstruction
male infertility

126
Q

Obstructive Diseases

Cystic fibrosis conductance regulator (CFTR)

A

Chloride channel expressed by epithelial cells
irregular folding promotes degredation
impaired secretion of chloride ion impares secretion of sodium ion and water

127
Q

Obstructive Diseases

What is the function of viscous mucus in Cystic Fibrosis?

A

Plugs Passageways
In lung, obstructrs air movement
In glandular tissue, obstructs secretion
In digestive tract, causes blockages

128
Q

Restrictive Disorders

Fibrosisng Disorders: Penumoconioses

A

Caused by particles
recognized as foreign
cannot be eliminated

129
Q

Restrictive Disorders

Examples of Penumoconioses

A

Coal workers penumoconiosis (CWP) (Black Lung)
Silicosis
Anthracosis (innocuous CWP)
Asbestosis

130
Q

Restrictive Disorders

Coal Miner’s Penumoconiosis: Complicated CWP

A

Progressive, massive fibrosis (PMF)
* more advanced disease
* compromised lung function

Black pigment associated with fibrosis

131
Q

Restrictive Disorders

Clinical Pneumoconiosis: CWP

A

Progressive Massive Fibrosis (<10% of cases)
Pulmonary dysfunction
Pulmonary hypertension
Cor pulmonale

132
Q

Restrictive Disorders

Clinical Pneumoconiosis: Silicosis

A

Increased susceptibility to TB
2X risk of lung cancer

133
Q

Restrictive Disorders

Clinical Pneumoconiosis: Asbestosis

A

Dyspnea
Increased risk of lung cancer, mesothelioma

134
Q

Restrictive Disorders

Granulomatous Disorders: Hypersensitivity pneumonia

allergic alveolitis

A

inflammation in alveoli
* decreased diffusion capacity
* decreased lung compliance
* decreased total lung volume

diverse causes, same tissue response

135
Q

Restrictive Disorders

Pathology of Allergic Alveolitis

A

Patchy infiltrates in the interstitium
Loose granulomas without necrosis
Cells: Lymphocytes, plasma cells, epitheloid macrophages

136
Q

Restrictive Disorders

Clinical Hypersensitivity Alveolitis: Acute attacks

A

Result in inhalation of antigenic dust
fever
dyspnea
cough
leukocytosis (increased WBC in blood)

137
Q

Restrictive Disorders

Clinical Hypersensitivity Alveolitis: Chronic Exposure

A

Progresisve respiratory failure
Dyspnea
Cyanosis
Decrease in lung capacity and compliance - measure of lung’s ability to expand

138
Q

Restrictive Disorders

Sarcoidosis

A

Granulomatous restrictive disease
affects other organs as well
* lungs are common
* spleen and liver
* bone marrow
* skin lesions
* eyes and muscle

unknown etiology

139
Q

Restrictive Disorders

Characteristics of Sarcoidosis

A

Non-necrotizing granulomas
Frequent giant cells
chronic - may become scar

140
Q

Restrictive Disorders

Lung Changes in Sarcoidosis

A

Granulomas are found along lymphatics
Lesions in the lung may heal, so will be fibrotic/hyalinized - interstitial fibrosis
Lymph node involvement is common

141
Q

Restrictive Disorders

Where are granulomas found in the lymphatics in Sarcoidosis?

A

Around bronchi and blood vessels
may also involve alveoli and the pleura

142
Q

Restrictive Disorders

What involvement do the Lymph Nodes have in Sarcoidosis?

A

Hilar and mediastinal
may develop calcification
tonsils are frequently affected as well

143
Q

Restrictive Disorders

What is the clinical course of Sarcoidosis?

A

Depends on location, size, number of granulomas
Lung: progressive fibrosis and cor pulmonale
Spontaneous remission/steroid therapy

144
Q

Pleural Disorders

Pleural Disorders

A

usually secondary to other lung disorders

145
Q

Pleural Disorders

Pleural Effusion

A

accumulation of pleural fluid

146
Q

Pleural Disorders

What causes fluid accumulation in Pleural Effusion?

A

Increased hydrostatic pressure (congestive heart failure)
Increased vascular permeability (pneumonia)
Decreased osmotic pressure (renal disease)
Increased intrapleural negative pressure (atelectasis)
Decreased lymphatic drainage

147
Q

Pleural Disorders

How is accumulated fluid removed in Pleural Effusion?

A

Resorbed (minimal amount)
Drained (chest tube)

148
Q

Pleural Disorders

Penumothorax

A

Air or gas in the pleural space

149
Q

Pleural Disorders

Spontaneous Pneumothorax

A

May be idiopathic (no known cause)
or: Rupture of an alveolus, abcess cavity

150
Q

Pleural Disorders

Traumatic Pneumothorax

A

Injury to the chest wall that allows air in

151
Q

Pleural Disorders

Tension Pneumothorax

A

Flap valve: allows air in (inspiration) but not out (expiration)
Accumulation of air can cuase compression of other structures, including the other lung

152
Q

Pleural Disorders

Symptoms of Pneumothorax

A

Respiratory distress due to compression, collapse, atelectasis of lung

Mechanism of Disease (11 decks)

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