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
2
Q
What type of epithelium is in the respiratory tract?
A
Ciliated pseudostratified columnar
- may have goblet cells (mucus glands)
3
Q
Describe olfactory epithelium.
A
- non-ciliated
- pseudostratified
- NO goblet cells
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
5
Q
Describe alveoli structure.
A
- single layer of squamous pneumocytes
- cuboidal pneumocytes producing surfactant
- capillaries
- dust cells
6
Q
Name the acute upper respiratory tract infections.
A
- Infectious Rhinitis
- Sinusitis
- Pharyngitis/Tonsilitis
7
Q
Name the vascular respiratory diseases.
A
- Embolism/ Infarction
- Pulmonary hypertension
- Goodpasture syndrome
- Pulmonary edema
8
Q
Know acute respiratory distress syndrome (ARDS)
A
9
Q
Name the obstructive diseases.
A
- Emphysema
- Asthma
- Cystic fibrosis
10
Q
Name the restrictive diseases.
A
- Pneumoconiosis
- Hypersensitivity pneumonitis
- Sarcoidosis
11
Q
Name the pleural diseases.
A
- Pleural effusion
- Pneumothorax
12
Q
List the immunological specific lung defenses.
A
- Antibody mediated (B-lymphocyte-dependent)
- Antigen presentation to lymphocytes
- Cell mediated (T-lymphocyte-dependent) immunologic responses
- Non-lymphocyte cellular immune responses
13
Q
What are the clinical signs of infectious rhinitis?
A
- nasal congestion with watery discharge
- sneezing
- scratchy, dry, sore throat
14
Q
What is the most common pathogen for rhinitis?
A
- Rhinoviruses
- less common include influenza, coronaviruses, adenoviruses, enteroviruses
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
16
Q
Describe the pathogenesis of rhinitis.
A
- Infection initiates immune response
- Immune mediators cause edema
–> swelling and fluid leakage causing congestion and discharge
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)
18
Q
What is sinusitis?
A
Impairment of sinus drainage
- usually bacterial, or can be viral
19
Q
Sinusitis most commonly occurs after what other infection?
A
Rhinitis
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
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
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
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
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
25
What are the 3 types of atelectasis?
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
26
What is pulmonary embolism?
- 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
27
How does pulmonary embolism lead to pulmonary infarct?
Embolism--> damage to lungs--> pulmonary infarct
- approximately 10% of emboli end up causing pulmonary infarct
28
What are the consequences of pulmonary embolism?
- 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
29
What is the treatment for pulmonary embolism?
- Anticoagulant (ex: heparin)
- Thrombolytic (risky)
--> breaks up blood clot, but can potentially cause severe hemorrhage b/c possibly unable to seal blood vessels
30
Explain pulmonary hypertension.
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
31
Pathogenesis of pulmonary hypertension
- Chronic obstructive or interstitial lung diseases
- Heart disease
- Recurrent emboli
- Autoimmune diseases
- Obstructive sleep apnea
- Idiopathic
32
What are the symptoms of pulmonary HTN?
- 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)
33
What is the treatment for pulmonary HTN?
- 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
34
What is Goodpasture syndrome?
-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
35
Explain the pathology of Goodpasture syndrome.
- 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
What is pulmonary edema?
Leakage of fluid (plasma) into alveolar space (NOT blood)
37
What is pulmonary edema caused by?
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
Describe hemodynamic edema.
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
What is microvascular injury edema?
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
What is acute respiratory distress syndrome (ARDS)?
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
What are some causes of ARDS?
- mechanical trauma
- near drowning
- sepsis
- barbiturate overdose
- gastric aspiration
42
Describe the pathogenesis of ARDS.
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
What happens due to the loss of squamous (I) pneumocytes?
increased permeability of alveolar wall to blood and immune cells
44
What happens due to the loss of cuboidal (II) pneumocytes?
- decreased surfactant production
- alveolar collapse risk increased
45
What are the symptoms of ARDS?
Lungs
- heavy
- filled with fluid (wet)
Clinical
- lungs become stiff due to loss of surfactant
- dyspnea/tachypnea
- cyanosis/ hypoxemia
46
What is pneumonia?
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
What are the 4 types of pneumonia?
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
What causes pneumonia?
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
What are the 2 types of bacterial pneumonia?
1. Bronchopneumonia (opaque spots)
2. Lobar (x-ray- whole lobe is opaque)
50
What is the clinical course of bacteria pneumonia?
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
Describe the stages of acute pneumonia.
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
Describe viral pneumonia.
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
What is histoplasmosis?
Fungal infection with Histoplasma capsulatum
- dimorphic fungi
- T cell mediated response to contain
- geographical distribution (often assoc. with caves)
54
Describe clinical histoplasmosis.
1. acute pulmonary infection
2. chronic (granulomatous) infection
3. disseminated miliary disease--> tiny infection spots throughout the lung
55
Describe the pathology of histoplasmosis.
- 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
Which diseases are obstructive?
1. Emphysema
2. Asthma
3. Cystic fibrosis
57
What is an obstructive disease?
- partial or complete obstruction at any level
- increased resistance to air flow, so not getting as much air into the lungs
58
Describe inhalation.
- 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
Describe exhalation.
- Muscles relax and elastic fibers retract
- Decreased volume expels air
- Decreased volume--> increased pressure relative to atmosphere and air moves out of lungs
60
What is emphysema?
- 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
Describe the patterns of emphysema.
- 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
What is the pathology of emphysema?
- Enlargement of airways
- Destruction of walls
- No fibrosis
63
Describe emphysema pathogenesis.
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
What is asthma?
Complex multigenic disorder
- Increased airway responsiveness to stimuli
--> may not provoke a response in unaffected individuals
--> ex: adenosine, exercise
65
What are the characteristics of asthma?
- Episodic bronchoconstriction
- Bronchial wall inflammation
- Increased mucus production
66
Name the 4 types of asthma.
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
What is chronic inflammatory airway disease?
- Recurrent episodes
--> wheezing, breathlessness, chest tightness, cough
- Bronchoconstriction
--> widespread, but variable
- Airflow limitation
--> at least partially reversible
68
How does asthma alter airway structure with repeated attacks?
- Increased mucus production
- Increased goblet cells
- Proliferation of smooth muscle
- Increased glands
- Increased vascularization and congestion of blood vessels
69
How is asthma triggered?
- B and T lymphocytes
- IgE
- Mast cells
- Eosinophils
70
Describe the cellular response in asthma.
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
What is cystic fibrosis?
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
What is CTFR?
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
Describe the tissue specificity of chloride channels.
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
What is the problem with viscous mucus?
Plugs passageways
- in lung, obstructs air movement
- in glandular tissue, obstructs secretion
- in digestive tract, causes blockages
75
What pancreatic changes occur in cystic fibrosis patients?
- ducts plugged with thick mucus/ discharge
- damage to exocrine tissue and can no longer make/ secrete digestive enzymes
- malnutrition
76
What are the restrictive diseases?
1. Pneumoconiosis
2. Sarcoidosis
3. Hypersensitivity pneumonitis
77
What does a restrictive disease do?
- Reduced expansion of parenchyma
- Decreased total lung capacity
78
Pneumoconiosis is what kind of restrictive disorder?
Fibrosing disorder
- caused by particles
- recognized as foreign
- cannot be eliminated
79
What are some examples of fibrosing disorders?
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
What is coal miner's pneumoconiosis?
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
Describe clinical pneumoconiosis.
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
Name and describe a Granulomatous disorder.
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
Describe the pathology of allergic alveolitis.
- Patchy infiltrates in the interstitium
- Loose granulomas w/out necrosis
- Cells: lymphocytes, plasma cells, epithelioid macrophages (usually found around bronchioles)
84
What happens during acute attacks in clinical hypersensitivity alveolitis?
- Result of inhalation of antigenic dust
- Fever
- Dyspnea
- Cough
- Leukocytosis- increased WBC in blood
85
What happens during chronic exposure in clinical hypersensitivity alveolitis?
- Progressive respiratory failure
- Dyspnea
- Cyanosis
- Decrease in lung capacity and compliance (measure of lung's ability to expand)
86
What is sarcoidosis?
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
