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Mechanisms of Disease > Week 7 Pulmonary > Flashcards

Week 7 Pulmonary Flashcards

1
Q

Describe the pathway of air into the body.

A
  • air enters through nose or mouth
  • passes through pharynx to larynx
  • through trachea to 2 bronchi
  • branches into bronchioles
  • reaches alveoli, where gas exchange occurs
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2
Q

What type of epithelium is in the respiratory tract?

A

Ciliated pseudostratified columnar
- may have goblet cells (mucus glands)

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3
Q

Describe olfactory epithelium.

A
  • non-ciliated
  • pseudostratified
  • NO goblet cells
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4
Q

Describe the epithelium in brochioles.

A
  • changes from respiratory to simple columnar
  • simple columnar changes to simple cuboidal with Clara cells
  • still ciliated
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5
Q

Describe alveoli structure.

A
  • single layer of squamous pneumocytes
  • cuboidal pneumocytes producing surfactant
  • capillaries
  • dust cells
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6
Q

Name the acute upper respiratory tract infections.

A
  1. Infectious Rhinitis
  2. Sinusitis
  3. Pharyngitis/Tonsilitis
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7
Q

Name the vascular respiratory diseases.

A
  1. Embolism/ Infarction
  2. Pulmonary hypertension
  3. Goodpasture syndrome
  4. Pulmonary edema
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8
Q

Know acute respiratory distress syndrome (ARDS)

A
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9
Q

Name the obstructive diseases.

A
  1. Emphysema
  2. Asthma
  3. Cystic fibrosis
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10
Q

Name the restrictive diseases.

A
  1. Pneumoconiosis
  2. Hypersensitivity pneumonitis
  3. Sarcoidosis
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11
Q

Name the pleural diseases.

A
  1. Pleural effusion
  2. Pneumothorax
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12
Q

List the immunological specific lung defenses.

A
  1. Antibody mediated (B-lymphocyte-dependent)
  2. Antigen presentation to lymphocytes
  3. Cell mediated (T-lymphocyte-dependent) immunologic responses
  4. Non-lymphocyte cellular immune responses
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13
Q

What are the clinical signs of infectious rhinitis?

A
  • nasal congestion with watery discharge
  • sneezing
  • scratchy, dry, sore throat
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14
Q

What is the most common pathogen for rhinitis?

A
  • Rhinoviruses
  • less common include influenza, coronaviruses, adenoviruses, enteroviruses
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15
Q

What is the treatment for rhinitis?

A
  • requires antiviral and we do not have antiviral for most of these viruses
  • therefore, support is the treatment
    –> rest, eating well, fluids
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16
Q

Describe the pathogenesis of rhinitis.

A
  • Infection initiates immune response
  • Immune mediators cause edema
    –> swelling and fluid leakage causing congestion and discharge
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17
Q

What are the potential complications during the pathogenesis of rhinitis?

A
  • bacterial infections due to swelling, fluid accumulation–> fluid has nutrients in it that colonized bacteria will take advantage of
  • middle ear infection (otitis media)
  • sinus infection (sinusitis)
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18
Q

What is sinusitis?

A

Impairment of sinus drainage
- usually bacterial, or can be viral

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19
Q

Sinusitis most commonly occurs after what other infection?

A

Rhinitis

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20
Q

Explain what happens during sinusitis.

A
  • Mucosal edema due to inflammation
  • Obstruction may be complete blockage (or partial blockage), which will result in accumulation of infected mucus (suppurative exudate)–> empyema (pockets of pus in a body cavity
  • May lead acute sinusitis to become chronic if impairment does not resolve
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21
Q

What are the complications of sinusitis?

A
  • infection of neighboring structures (eye, skull/osteomyelitis, brain/infections in ventricles of brain)
  • usually just discomfort
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22
Q

Describe pharyngitis/ tonsilitis.

A
  • Frequent companions of upper respiratory tract viral infections
  • Most common with rhinoviruses, echoviruses, adenoviruses
  • sx: redness, edema, enlargement of tonsils/ lymph nodes
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23
Q

What are the most serious consequences of pharyngitis/tonsilitis?

A
  • Rheumatic fever (acute multisystem inflammatory disease- infection with streptococcus)–> myocarditis, valvular abnormalities
  • Glomerulonephritis
  • Recurrent acute tonsillitis may be linked to chronic enlargement of tonsils
    –> impedes things like breathing and swallowing
    –> chronic enlargement= surgery to remove tonsils
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24
Q

What is atelectasis?

A
  • Collapse of previously inflated lung
    –> Neonatal–> incomplete expansion
  • lowers blood O2 (hypoxemia)
  • increases risk of infection
  • reversible
    –> except contraction type- you would have to remove fibrosis from the lungs and this is very difficult to do
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25
Q

What are the 3 types of atelectasis?

A
  1. Resorption–> blockage of airway
  2. Compression–> accumulation of fluid/air/anything else in pleural space
    - compresses lungs so they cannot expand all the way
  3. Contraction–> fibrosis restricts expansion
    - not as elastic anymore; more fibrotic
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26
Q

What is pulmonary embolism?

A
  • Something blocks vessel in lung
    –> blood clot, air bubbles, fatty deposit, other debris/ deposits or cells that get into circulation
  • Most frequently a clot
    –> 95% from large leg veins- deep vein thrombosis
  • Consequences depend on size of obstruction
  • Blockage causes:
    1. Ischemia downstream- similar to MI
    2. Increased pressure upstream- larger vessel block= more pressure increase
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27
Q

How does pulmonary embolism lead to pulmonary infarct?

A

Embolism–> damage to lungs–> pulmonary infarct
- approximately 10% of emboli end up causing pulmonary infarct

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28
Q

What are the consequences of pulmonary embolism?

A
  • Large blockage will kill quickly (virtually instantaneous death)
    –> no pathological change in lung
    –> increased pressure damages heart
    - R side heart failure (Cor Pulmonale), which can also be developed slowly with repeated emboli
  • Signals to body control system to lower BP
    –> decrease cardiac output
  • Lung may collapse due to:
    –> lack of surfactant
    –> reduced movement in response to pain
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29
Q

What is the treatment for pulmonary embolism?

A
  • Anticoagulant (ex: heparin)
  • Thrombolytic (risky)
    –> breaks up blood clot, but can potentially cause severe hemorrhage b/c possibly unable to seal blood vessels
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30
Q

Explain pulmonary hypertension.

A

Vascular changes- BP increases in lungs specifically–> may be because heart is not pumping enough blood out of L side blood is backing up in lungs
- Medial Hypertrophy–> may see more layers of smooth muscle
–> muscular and elastic arteries in lung
–> also intimal fibrosis (tunica intima)
- Plexiform Lesion
–> advanced hypertension
–> tuft of capillaries
–> dilated thin-walled arteries- b/c when capillaries are developed in the area quickly, there is no structure to handle the pressure they may be under, so you get thin-walled arteries that dilate dramatically
- more prone to rupture= patients can develop hemorrhages

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31
Q

Pathogenesis of pulmonary hypertension

A
  • Chronic obstructive or interstitial lung diseases
  • Heart disease
  • Recurrent emboli
  • Autoimmune diseases
  • Obstructive sleep apnea
  • Idiopathic
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32
Q

What are the symptoms of pulmonary HTN?

A
  • only detectable when advanced
  • dyspnea (irregular/difficulty breathing) and fatigue
  • rarely, chest pain
  • end stage: severe respiratory distress and cyanosis (blood O2 low, causing nail beds and skin around lips to look blueish)
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33
Q

What is the treatment for pulmonary HTN?

A
  • secondary disease: treat primary disease and hopefully it will resolve the HTN
  • autoimmune or refractory: vasodilators to try to reduce HTN
  • lung transplantation if damage to lungs is too severe
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34
Q

What is Goodpasture syndrome?

A

-Pulmonary hemorrhage syndrome
- Autoimmune disease (autoantibody against type IV collagen, which is in basement membrane)
- Kidney and lung injury
- Inflammatory-mediated destruction of alveolar basement membranes–> barrier for gas exchange broken down–> leakage of blood into alveolar space

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35
Q

Explain the pathology of Goodpasture syndrome.

A
  • Symptoms: hemoptysis (coughing up blood)
    –> death usually due to renal involvement
  • Treatment: plasmapheresis to remove autoantibodies and also immunosuppression
  • Lungs: red-brown consolidation
  • Histology:
    –> intra-alveolar hemorrhage
    –> focal necrosis in alveolar walls
    –> macrophages accumulate heme
  • Late stages:
    –> septal fibrosis (thickened)
    –> type II pneumocyte hypertrophy
    –> blood in alveolar spaces
36
Q

What is pulmonary edema?

A

Leakage of fluid (plasma) into alveolar space (NOT blood)

37
Q

What is pulmonary edema caused by?

A

Hemodynamic disturbances
- increased pressure (more common)
- decreased pressure (less common)
Increased capillary permeability
- damage to microvasculature
- Causes:
–> infections, gas inhalation, liquid aspiration
–> drugs and chemicals
–> shock, trauma, radiation, transfusion

38
Q

Describe hemodynamic edema.

A

Most commonly the result of left-sided congestive heart failure
- increased pressure in L ventricle–> increased pressure in lungs–> fluid forced out of capillaries

39
Q

What is microvascular injury edema?

A

Damage to the capillary bed
- primary to vascular endothelial cells
- or to alveolar squamous pneumocytes
Leakage of fluids and proteins
- leak into interstitial space–> restrictive disease
- leak into alveoli–> pneumonia
Acute respiratory distress syndrome
- due to sudden diffuse edema

40
Q

What is acute respiratory distress syndrome (ARDS)?

A

Severe acute lung injury
- abrupt onset of hypoxemia
- bilateral pulmonary infiltrates
- no cardiac failure b/c it is so quick
Inflammatory disease producing diffuse alveolar damage (DAD)
- increased pulmonary vascular permeability
- edema
- epithelial cell death (type I pneumocytes)

41
Q

What are some causes of ARDS?

A
  • mechanical trauma
  • near drowning
  • sepsis
  • barbiturate overdose
  • gastric aspiration
42
Q

Describe the pathogenesis of ARDS.

A
  1. Initiated by macrophages
  2. Inflammatory mediators damage cells
    - endothelium
    - pneumocytes
  3. Neutrophils invade and debris accumulates (hyalinization)
  4. Healing starts when macrophages produce TGFbeta and PDGF (activate fibroblasts)
    - start replacing some of the damaged cells
43
Q

What happens due to the loss of squamous (I) pneumocytes?

A

increased permeability of alveolar wall to blood and immune cells

44
Q

What happens due to the loss of cuboidal (II) pneumocytes?

A
  • decreased surfactant production
  • alveolar collapse risk increased
45
Q

What are the symptoms of ARDS?

A

Lungs
- heavy
- filled with fluid (wet)
Clinical
- lungs become stiff due to loss of surfactant
- dyspnea/tachypnea
- cyanosis/ hypoxemia

46
Q

What is pneumonia?

A

Lung infection by bacteria, viruses, mycoplasms, or fungi
- 1/6 of US deaths
- characterized by lymphatic infiltrates in alveoli
- produced pulmonary edema; can also result from pulmonary edema
–> edematous fluid can be a rich support system for bacteria

47
Q

What are the 4 types of pneumonia?

A
  1. Community-acquired
    - typical- bacteria
    - atypical- viral, mycoplasmal
  2. Hospital- acquired
    - mechanical ventilation is a risk factor
  3. Aspiration- usually assoc. with vomit
    - markedly debilitated patients, stroke victims
    - abnormal gag/ swallowing reflex
  4. Chronic
    - localized lesion, immunocompetent patient
    - in patients that are immunocompromised, it will NOT be called chronic
48
Q

What causes pneumonia?

A
  1. Cough reflex suppression/ inhibition
    - coma, anesthesia, neuromuscular disorders
  2. Mucociliary apparatus damage
    - cigarette smoke, hot gases, viral, genetic
  3. Accumulation of secretions
    - cystic fibrosis, bronchial obstruction
  4. Decreased macrophage activity
    - alcohol, tobacco, anoxia (absence of O2), O2 intoxication
  5. Edema or congestion (mucus)
49
Q

What are the 2 types of bacterial pneumonia?

A
  1. Bronchopneumonia (opaque spots)
  2. Lobar (x-ray- whole lobe is opaque)
50
Q

What is the clinical course of bacteria pneumonia?

A

Rapid onset
- fever
- chills
- cough (mucus with signs of infection)
Fibrinosuppurative pleuritis- swelling of lung due to infection
- lung swelling
–> neutrophil infiltration
–> fibrin aggregation
- pleuritic pain and pleural friction rub

51
Q

Describe the stages of acute pneumonia.

A

Stage 2: early red hepatization
- neutrophil infiltrate
Stage 3: gray hepatization
- alveolar exudate in air spaces
- more immune tissue
Stage 4: resolution
- fibromyxoid masses
- macrophages and fibroblasts trying to rebuild the tissue
- trying to wall off any remaining infection and destroy it while allowing lung tissue to recover

52
Q

Describe viral pneumonia.

A

Severe Acute Respiratory Syndrome (SARS)
- coronavirus from civets in China
- transmission was through respiratory secretions mostly
- incubation period of 2-10 days
- initial symptoms: malaise, myalgia, dry cough, fever, chills
- virus infects the pneumocytes- lower respiratory tract

53
Q

What is histoplasmosis?

A

Fungal infection with Histoplasma capsulatum
- dimorphic fungi
- T cell mediated response to contain
- geographical distribution (often assoc. with caves)

54
Q

Describe clinical histoplasmosis.

A
  1. acute pulmonary infection
  2. chronic (granulomatous) infection
  3. disseminated miliary disease–> tiny infection spots throughout the lung
55
Q

Describe the pathology of histoplasmosis.

A
  • Macrophage aggregates filled with yeast
  • Will colonize nearby lymph nodes- sometimes see inflammation of perihilar lymph nodes
  • Eventually–> granulomas with giant cells
    –> may develop fibrosis and calcifications
    Gross appearance
  • Perihilar mass lesions
    –> ends up looking like lymphoma or leukemia
56
Q

Which diseases are obstructive?

A
  1. Emphysema
  2. Asthma
  3. Cystic fibrosis
57
Q

What is an obstructive disease?

A
  • partial or complete obstruction at any level
  • increased resistance to air flow, so not getting as much air into the lungs
58
Q

Describe inhalation.

A
  • Intercostal muscles contract to draw ribs up and out
  • Diaphragm contracts and pulls down
  • Increased volume draws air in
  • Also thin layer of fluid b/t pleural layers and has the effect of drawing lungs out as well
  • Increased volume w/in lungs, which decreases pressure relative to atmospheric pressure–> which draws air into the lungs
59
Q

Describe exhalation.

A
  • Muscles relax and elastic fibers retract
  • Decreased volume expels air
  • Decreased volume–> increased pressure relative to atmosphere and air moves out of lungs
60
Q

What is emphysema?

A
  • With chronic bronchitis, COPD (chronic obstructive pulmonary disorder)
  • Permanent enlargement of smaller air spaces
    –> Destruction of walls of smaller air spaces
    –> No fibrosis
  • Centriacinar: damage to small areas; large air spaces b/c you lost the small dividers
  • Panacinar: damage overall
61
Q

Describe the patterns of emphysema.

A
  • Disease location is the acinus
  • Associated with tobacco smoke inhalation
  • Major symptom: Dyspnea (trouble breathing or irregular breathing)
  • Centriacinar: in respiratory bronchiole
  • Panacinar: in alveolar duct and aveolus
62
Q

What is the pathology of emphysema?

A
  • Enlargement of airways
  • Destruction of walls
  • No fibrosis
63
Q

Describe emphysema pathogenesis.

A

Destruction of walls
- Direct damage from toxins
- Inflammatory response
–> macrophages/epithelial cells release leukotrienes, IL-8, TNF
–> chemotaxis, inflammation, structural changes (act as growth factors)
- Proteases released from cells when damaged
–> deficiency in protease inhibitors
- genetic component to emphysema
- alpha-1 anti-trypsin inhibits elastase that breaks down elastic fibers
–> proteases damage CT (including elastic fibers)
- Infection
–> not a major role, but may exacerbate inflammatory damage

64
Q

What is asthma?

A

Complex multigenic disorder
- Increased airway responsiveness to stimuli
–> may not provoke a response in unaffected individuals
–> ex: adenosine, exercise

65
Q

What are the characteristics of asthma?

A
  • Episodic bronchoconstriction
  • Bronchial wall inflammation
  • Increased mucus production
66
Q

Name the 4 types of asthma.

A
  1. Atopic
    - classic hypersensitivity rxn (IgE)
  2. Non-atopic
    - hyperirritability due to viral infection
  3. Drug-induced
    - aspirin (and other NSAIDS) affects balance of cyclooxygenase activity
  4. Occupational
    - exposure to fumes, dusts, gases, chemicals can damage bronchi and induce asthma
67
Q

What is chronic inflammatory airway disease?

A
  • Recurrent episodes
    –> wheezing, breathlessness, chest tightness, cough
  • Bronchoconstriction
    –> widespread, but variable
  • Airflow limitation
    –> at least partially reversible
68
Q

How does asthma alter airway structure with repeated attacks?

A
  • Increased mucus production
  • Increased goblet cells
  • Proliferation of smooth muscle
  • Increased glands
  • Increased vascularization and congestion of blood vessels
69
Q

How is asthma triggered?

A
  • B and T lymphocytes
  • IgE
  • Mast cells
  • Eosinophils
70
Q

Describe the cellular response in asthma.

A

Mast cells
- smooth muscle contraction
- increased mucus secretion
- vasodilation
–> endothelial leakage
–> local edema
Epithelial cells
- cytokine production
–> includes leukotrienes and prostaglandins that affect BVs

71
Q

What is cystic fibrosis?

A

Mutation in chloride channel results in viscous mucus that obstructs passageways
- mucus very thick and does not move well because less H2O getting in the mucus
- Chronic lung disease
- Pancreatic insufficiency–> plugging of pancreatic ducts eventually destroys pancreatic tissue
–> steatorrhea
–> malnutrition
- Hepatic cirrosis
- Intestinal obstruction
- Male infertility

72
Q

What is CTFR?

A

Cystic Fibrosis Conductance Regulator
- Chloride channel expressed by epithelial cells
- Irregular folding promotes degradation
- Impaired secretion of chloride–> not enough chloride channels impairs secretion of sodium ion and water
–> ionic balance
–> osmosis

73
Q

Describe the tissue specificity of chloride channels.

A

Lumen of sweat duct
- Normal: Cl from outside is brought in and Na comes in too, reducing amount of salt in sweat
- Cystic fibrosis: cannot bring in Cl or Na and sweat will be salty
Airway
- Normal: Cl out, Na in, H2O in= normal mucus
- Cystic fibrosis: Cl cannot come out, too much Na coming in b/c excess Cl is inside–> brings in excess H2O= dehydrated mucus

74
Q

What is the problem with viscous mucus?

A

Plugs passageways
- in lung, obstructs air movement
- in glandular tissue, obstructs secretion
- in digestive tract, causes blockages

75
Q

What pancreatic changes occur in cystic fibrosis patients?

A
  • ducts plugged with thick mucus/ discharge
  • damage to exocrine tissue and can no longer make/ secrete digestive enzymes
  • malnutrition
76
Q

What are the restrictive diseases?

A
  1. Pneumoconiosis
  2. Sarcoidosis
  3. Hypersensitivity pneumonitis
77
Q

What does a restrictive disease do?

A
  • Reduced expansion of parenchyma
  • Decreased total lung capacity
78
Q

Pneumoconiosis is what kind of restrictive disorder?

A

Fibrosing disorder
- caused by particles
- recognized as foreign
- cannot be eliminated

79
Q

What are some examples of fibrosing disorders?

A
  1. Coal workers pneumoconiosis (CWP)- black lung
  2. Silicosis
  3. Anthracosis- basically early stage black lung found in urban dwellers and tobacco smokers
  4. Asbestosis
80
Q

What is coal miner’s pneumoconiosis?

A

Complicated CWP
- Progressive, massive fibrosis (PMF)
–> more advanced disease
–> compromised lung function
- Black pigment associated with fibrosis–> will restrict expansion of the lung
–> black pigment is carbon particles from the coal
- Advanced disease shown in image
–> severely compromised lung function

81
Q

Describe clinical pneumoconiosis.

A

CWP: Progressive massive fibrosis (< 10% of cases)
- pulmonary dysfunction
- pulmonary hypertension
- cor pulmonale (R side heart failure)
Silicosis
- increased susceptibility to TB
- 2X risk of lung cancer
Asbestosis
- Dyspnea
- increased risk of lung cancer, mesothelioma (tumor of the pleural membranes)
NOTE: on microscopic examination, you cannot see silicosis or asbestosis particles

82
Q

Name and describe a Granulomatous disorder.

A

Hypersensitivity pneumonia
- Aka: allergic alveolitis
- Inflammation in alveoli
–> decreased diffusion capacity
–> decreased lung compliance- lung cannot stretch as well
–> decreased total lung volume
- Diverse causes, same tissue response

83
Q

Describe the pathology of allergic alveolitis.

A
  • Patchy infiltrates in the interstitium
  • Loose granulomas w/out necrosis
  • Cells: lymphocytes, plasma cells, epithelioid macrophages (usually found around bronchioles)
84
Q

What happens during acute attacks in clinical hypersensitivity alveolitis?

A
  • Result of inhalation of antigenic dust
  • Fever
  • Dyspnea
  • Cough
  • Leukocytosis- increased WBC in blood
85
Q

What happens during chronic exposure in clinical hypersensitivity alveolitis?

A
  • Progressive respiratory failure
  • Dyspnea
  • Cyanosis
  • Decrease in lung capacity and compliance (measure of lung’s ability to expand)
86
Q

What is sarcoidosis?

A

Another granulomatous restrictive disease
- Affects other organs as well–> lungs are common, spleen and liver, bone marrow, skin lesions, eyes and muscle
- Unknown etiology (cause)
- Characteristics:
–> non-necrotizing granulomas
–> frequent giant cells
–> chronic- may become scar even if resolved

Mechanisms of Disease (10 decks)

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