Aula 6 - Respiratory Disease Flashcards
1
Q
Question:
What are the differences between the cricoid cartilage and the tracheal cartilages?
A
Both the cricoid cartilage and the tracheal cartilages are cartilages that surround the trachea, which is the beginning of the tracheobronchial tree.
However, while the tracheal cartilages are C-shaped (incomplete) rings, the cricoid cartilage is the only complete ring of cartilage around the trachea.
2
Q
Complete the sentence:
The tracheobronchial tree begins at the ________ and bifurcates at the ________ into the left and right ________, which continue to divide into smaller ________.
A
trachea, carina, bronchi, bronchioles
3
Q
Complete the sentence:
The lungs are divided in ________, which are separated by ________.
A
lobes, fissures
4
Q
Question:
What is the pleura?
A
The pleura are two flattened closed sacs made of serous membranes filled with pleural fluid, each one surrounding each lung.
5
Q
Complete the sentence:
Intrapleural pressure is usually ________ (positive/negative).
A
negative
6
Q
Question:
What does a negative intrapleural pressure mean?
A
It means that the intrapleural pressure is lower than the atmospheric pressure.
7
Q
Question:
What is a pneomothorax?
A
A pneumothorax is when air gets inside the chest cavity and creates pressure against the lungs, causing it them to collapse partially or fully.
8
Q
Question:
Why does difficulty breathing caused by an open pneumothorax worsen the condition?
A
If a patient has difficulty breathing, they will probably try to breathe in deeply and that will actually lead to more air entering the lungs and the chest cavity, aggravating the collapse.
9
Q
Question:
What is the main function of the respiratory system?
A
To guarantee the introduction of oxygen (O2) into the blood and the removal of carbon dioxide (CO2).
10
Q
Question:
What are the four main acessory functions of the respiratory system?
A
- Olfaction of volatile molecules (and distinguishing pleansant and unpleasant smells)
- Speech production
- Acid-base balance
- Synthesis of vasoactive substances
11
Q
Question:
What is the role of carbon anhydrase in acid base balance?
A
It’s an enzyme that helps convert carbon dioxide into bicarbonate and protons, helping to regulate pH.
12
Q
Question:
Why does hyperventilation increase the pH?
A
Hyperventilation increases the pH of the blood because breathing too fast removes too much carbon dioxide (CO₂), decreasing the CO₂ partial pressure. Since CO₂ reacts with water in the blood to form carbonic acid (H₂CO₃), less CO₂ means less acid. This makes the blood less acidic (more alkaline), increasing the pH.
13
Q
Question:
Why does hypoventilation decrease the pH?
A
Hypoventilation decreases the pH of the blood because breathing too slowly (e.g., in case of difficulty breathing) causes CO₂ to build up in the body. More CO₂ reacts with water in the blood to form carbonic acid (H₂CO₃), which releases hydrogen ions (H⁺). This makes the blood more acidic, lowering the pH.
14
Q
Question:
What is the name of excessive CO₂ in the body?
A
Hypercapnea
15
Q
Question:
What is the role of the respiratory system in the synthesis of Angiotensin II?
A
The Angiotensin converting enzyme (ACE) is produced by vascular endothelial cells throughout the body, but especially in the lungs. And ACE is responsible for converting Angiotensin I in Angiotensin II, a vasoconstrictor hormone.
16
Q
Complete the sentence:
In inspiration, the atmospheric pressure is ________ (lower/higher) than the intrapulmonary pressure, allowing for air inflow. Therefore, inspiration requires a ________ (positive/negative) pressure.
A
higher
17
Q
Complete the sentence:
In expiration, the atmospheric pressure is ________ (lower/higher) than the intrapulmonary pressure, allowing for air outflow. Therefore, expiration requires a ________ (positive/negative) pressure.
A
lower, negative
18
Q
Complete the sentence:
Inspiration involves the ____________ (contraction/relaxation) of the inspiratory muscles, contrarly to expiration.
A
contraction
19
Q
Question:
What is the the lung surfactant, where is it produced and what’s its role?
A
Lung surfactant is a thin film of lipids and proteins that lines the lungs’ alveoli, produced by the pneumocytes type II (a type of alveolar cells). The lung surfactant prevents the collapse of smaller alveoli.
20
Q
Question:
What is alveolar ectasia? What are the cause and complications?
A
Alveolar ectasia is a condition where the air sacs in the lungs are abnormally dilated (enlarged). This condition can result from structural weakness in the alveolar walls, often due to chronic lung diseases or aging-related loss of elasticity. Enlarged alveoli may reduce the surface area available for oxygen and carbon dioxide exchange, leading to lower oxygen levels in the blood (hypoxemia) and less efficient gas exchange (since the air prefers to go to larger alveoli, even though they are less efficient for gas exchange).
21
Q
Question:
What is the ideal ventilation/perfusion (V/Q) ratio?
A
The ideal ventilation/perfusion ratio is V/Q = 1, since ideally ventilation would be equivalent to perfusion.
22
Q
Question:
In what lung region is there an evident ventilation/perfusion ratio (V/Q) mismatch (i.e., very different from 1)?
A
In the apex of the lung, since there is limited perfusion compared with ventilation.
23
Q
Question:
What are the 2 main receptors and the 2 main reflexes involved in the regulation of breathing?
A
Receptors:
* Peripheral receptors (pO₂ and pCO₂)
* Central receptors (pCO₂ and pH)
Reflexes:
* Chemoreflex
* Hering-Breuer reflex
24
Q
Question:
What is the Hering-Breuer reflex?
A
It’s a reflex triggered to prevent the over-inflation of the lung. Pulmonary stretch receptors present on the wall of bronchi and bronchioles of the airways respond to excessive stretching of the lung during large inspirations.
25
# **Question:**
What activates the chemoreflex?
The chemoreflex is activated by hypoxia (low pO₂) or hypercapnea (high pCO₂).
26
# **Question:**
What happens when the chemoreflex is activated?
The activation of the chemoreflex induces:
* Tachypnea
* Tachycardia
* Vasoconstriction
27
# **Question:**
What are two ways of mechanical breathing/ventilation?
**Positive Pressure Ventilation** is when air is pushed into the lungs using external force, for example: **Tracheal Intubation** and **Tracheostomy**.
**Negative Pressure Ventilation** is when air is pulled into the lungs by creating a vacuum around the chest, simulating normal breathing and mimicking natural diaphragm movement. For example, the **Iron Lung** (used for polio patients in the past) is a chamber around the chest reduces pressure, expanding the lungs and drawing in air.
28
# **Question:**
Give examples of diagnostic tests and exams for the respiratory system.
* Lung Function tests (e.g., spirometry)
* Exercise stress test (e.g., treadmill)
* Arterial gasimetry
* Pulse oximetry
* Chest X-ray
* Bronchoscopy
* Microbial cultures
29
# **Question:**
Distinguish type 1 and type 2 respiratory failure.
Respiratory failure type 1 is also called hypoxemic respiratory failure and is characterized by hypoxia, i.e., a decrease in pO₂ in peripheral blood.
Respiratory failure type 2 is also called hypercapnic respiratory failure and is characterized by hypercapnea, i.e., an increase in pCO₂ in peripheral blood.
30
# **Question:**
How can a type 2 respiratory failure (hypercapnic respiratory failure) present without acidemia?
A type 2 respiratory failure corresponds to hypercapnea (increased pCO₂). More CO₂ reacts with water in the blood to form carbonic acid (H₂CO₃), which releases hydrogen ions (H⁺). Therefore, there is more acid production, which lowers the pH, possibly resulting in acidemia. **However, this acidemia might be compensated by the kidney, which might be retaining bicarbonate (HCO₃⁻) to maintain pH homeostasis.**
31
# **Question:**
What are the 3 main causes of respiratory failure?
* **Ventilation dysfunction:** caused by obstruction of the respiratory tract, muscle weakness or paralysis or trauma to the thoracic wall.
* **Ventilation/Perfusion Ratio mismatch:** caused by chronic obstructive lung disease (COPD), restrictive lung disease, lung infections pr vascular lung disease.
* **Hematosis dysfunction:** caused by pulmonary edema.
32
# **Question:**
What are the two types of lung disease?
Obstructive and Restrictive
33
# **Question:**
What are the 4 main types of Obstructive Lung Disease?
* Asthma
* Chronic Bronchitis
* Emphysema
* Chronic Obstructive Lung Disease (COPD)
34
# **Question:**
What is obstructive lung disease?
It's the partial or irreversible obstruction of the lower airways.
35
# **Question:**
Asthma is a type of ________ (reversible/irreversible) of obstructive lung disease.
reversible
36
# **Question:**
What is Asthma?
It's a disease of airway inflammation and airflow obstruction.
37
# **Question:**
What are the main symptoms of Asthma?
* Wheezing
* Chest tightness
* Dyspnea
* Cough
* Bronchial hyperresponsiveness
38
# **Question:**
Distinguish intrinsic and extrinsic Asthma.
Extrinsic asthma usually presents at a younger age and is less severe, since it is linked with **hypersensitivity reactions and atopy** (tendency to produce an exaggerated immunoglobulin E immune response), normally triggered by **allergerns**.
Intrinsic asthma normally appears later in life and is associated with a greater severity, mainly due to the lack of an obvious cause, since it presents an apparent **lack of atopy** and **non-allergic triggers**.
39
# **Question:**
Are tachypnea and tachycardia always present in asthma?
No, they are usually absent in mild disease but present in acute exacerbations.
40
# **Question:**
What is the first physiological event in asthma that leads to hypoxemia and respiratory acidosis?
Airway obstruction.
41
# **Questão:**
How does airway obstruction affect the ventilation/perfusion (V/Q) ratio?
It decreases the V/Q ratio, leading to inadequate ventilation in certain lung areas.
42
# **Question:**
What happens to oxygen (O₂) and carbon dioxide (CO₂) levels in severe asthma?
O₂ decreases (hypoxemia) and CO₂ increases (hypercapnia), leading to respiratory acidosis.
43
# **Question:**
How does the body respond to hypoxemia and hypercapnia in severe asthma?
By activating the chemoreflex, which induces tachypnea, tachycardia and vasoconstriction.
44
# **Question:**
What are the effects of the chemoreflex in asthma?
Increased respiratory rate (tachypnea) and increased heart rate (tachycardia).
45
# **Question:**
What are the two main categories of allergens that trigger extrinsic asthma?
* **Low-molecular weight chemicals** (e.g., drugs, isocyanate, anhydrides, chromate)
* **Complex organic molecules** (e.g., animal danders, dust mites, enzymes, wood dusts)
46
# **Question:**
What types of drugs can trigger asthma symptoms?
Beta blockers and NSAIDs.
47
# **Question:**
Name two physiologic and pharmacologic mediators of smooth muscle that can trigger asthma.
Histamine and ATP.
48
# **Question:**
What are some physicochemical agents that can trigger asthma?
* Exercise, hyperventilation with cold, dry air
* Air pollutants
* Viral infections (e.g., Influenza A)
49
# **Question:**
What are the two phases of an asthma response to a trigger?
* **Early response:** occurs within **10-15 minutes**
* **Late response:** occurs within **4-8 hours**
50
# **Question:**
What are the main causes of cough in asthma?
* Airway narrowing
* Mucus hypersecretion
* Neural hyperresponsiveness
51
# **Question:**
What is the primary cause of wheezing in asthma?
Caliber reduction leading to turbulent airflow.
52
# **Question:**
Does wheezing correlate well with the severity of airway narrowing?
No.
53
# **Question:**
What are the three main causes of dyspnea and chest tightness in asthma?
* **Decreased lung compliance** → increased muscular effort
* **Airway obstruction** → thoracic distension, hypoxia, hypercapnia
* **Hypoxia and hypercapnia** → increased respiratory rate and depth
54
# **Question:**
How does airway obstruction contribute to dyspnea?
It leads to thoracic distension, hypoxia, and hypercapnia, increasing respiratory effort.
55
# **Question:**
What causes increased inspiratory effort in asthma?
* Increased airway resistance
* Decreased O₂ levels (hypoxemia)
* Increased CO₂ levels (hypercapnia)
56
# **Question:**
How does increased inspiratory effort affect venous return in pulsus paradoxus?
Increased inspiratory effort → Increased venous return to the right heart → Increased right ventricular filling.
57
# **Question:**
What is pulsus paradoxus in asthma?
A decrease in blood pressure during inspiration due to increased airway resistance and altered cardiac dynamics.
58
# **Question:**
What happens to the interventricular septum during pulsus paradoxus?
The interventricular septum deviates to the left due to increased right ventricular filling.
59
# **Question:**
How does pulsus paradoxus affect the left ventricle?
* Decreased left ventricular filling
* Decreased left ventricular ejection
60
# **Question:**
Why does increased airway resistance contribute to pulsus paradoxus?
Increased airway resistance forces the patient to generate a stronger inspiratory effort, altering intrathoracic pressure and cardiac filling dynamics.
61
# **Question:**
How does increased right ventricular filling affect the left heart during pulsus paradoxus?
The right ventricle expands more than usual, making the interventricular septum shift to the left, which reduces left ventricular filling. Consequently, cardiac output and arterial pulse decrease during inspiration.
62
# **Question:**
Why is pulsus paradoxus clinically significant in asthma?
It is a sign of severe airway obstruction and can indicate impending respiratory failure, requiring urgent intervention.
63
# **Question:**
What is chronic bronchitis?
Chronic bronchitis is a chronic airway inflammation with subsequent obstruction. It's a type of chronic obstructive pulmonary disease (COPD).
64
# **Question:**
What is Chronic obstructive pulmonary disease (COPD)?
Chronic obstructive pulmonary disease (COPD) is a type of progressive lung disease characterized by progressive airflow limitation and tissue destruction in the airways and/or lung.
65
# **Question:**
What are the top three causes for COPD?
* Cigarette smoking
* Genetic susceptibility
* Alpha-1 protease inhibitor deficiency
66
# **Question:**
What is the leading cause of COPD?
Cigarette smoking
67
# **Question:**
Is age a risk factor of COPD?
Yes, COPD typically begins in the adult age.
68
# **Complete the sentence:**
One of the clinical manifestations of chronic bronchitis is ________ (pink puffer/blue bloater).
blue bloater
69
# **Complete the sentence:**
One of the clinical manifestations of pulmonary emphysema is ________ (pink puffer/blue bloater).
pink puffer
70
# **Question:**
What are the characteristics of a productive cough in chronic bronchitis?
* Thick sputum (contains free DNA from lysed cells)
* Purulent sputum (suggests bacterial infection)
* Hemoptysis (due to damaged mucosa)
* Less effective in clearing sputum
* Duration of at least 3 months in 2 consecutive years
71
# **Question:**
What happens to the mucosa, the mucus-secreting glands and the bronchial wall in chronic bronchitis?
* Inflamed and edematous mucosa
* Hypertrophy and hyperplasia of mucus-secreting glands
* Fibrosis and thickening of the bronchial wall
72
# **Question:**
What causes wheezing in chronic bronchitis?
Persistent airway narrowing due to inflammation and mucus obstruction.
73
# **Question:**
What causes crackles in chronic bronchitis?
Increased mucus production leading to airflow obstruction and turbulence in the airways.
74
# **Question:**
What is the Blue Bloater phenotype in chronic bronchitis?
* Cyanosis (blue) due to chronic hypoxia
* Obesity and fluid retention (bloater) due to right heart failure (cor pulmonale)
75
# **Question:**
Why does chronic bronchitis lead to hypoxia and hypercapnia?
Mucus plugging and airway obstruction cause ventilation-perfusion (V/Q) mismatch. This reduces oxygen exchange, leading to hypoxia (low O₂) and hypercapnia (high CO₂).
76
# **Question:**
How does fibrosis contribute to airway obstruction in chronic bronchitis?
Fibrosis thickens the bronchial walls, making the airways less flexible and more resistant to airflow.
77
# **Question:**
Why does tachycardia occur in acute hypoxic exacerbations of chronic bronchitis?
Increased airway obstruction decreases the V/Q ratio, inducing hypoxia (↓O₂) and hypercapnia (↑CO₂) and, thus, resulting in respiratory acidosis. This activates the chemoreflex, which triggers tachycardia (increased heart rate), tachypnea and vasoconstriction (increased pulmonary resistance).
78
# **Question:**
How does chronic hypoxia lead to right heart failure in chronic bronchitis?
Hypoxia (↓O₂) and hypercapnia (↑CO₂) trigger pulmonary vasoconstriction, due to activation of the chemoreflex. Consequently, an increased pulmonary resistance (increased resistance in the pulmonary circulation that enters the right side of the heart) puts strain on the right ventricle, leading to right heart failure (cor pulmonale).
79
# **Question:**
What are the clinical signs of right heart failure in chronic bronchitis?
* Jugular venous distension (due to increased central venous pressure)
* Peripheral edema (fluid retention in lower limbs)
* Hepatomegaly (congestion of the liver due to right heart failure)
80
# **Question:**
How does chronic hypoxia cause polycythemia in chronic bronchitis?
Low oxygen levels (↓O₂) stimulate erythropoietin secretion from the kidneys, which promotes erythropoiesis (red blood cell production). An increased number of red blood cells results in an increased hematocrit (polycythemia), which improves oxygen-carrying capacity.
81
# **Complete the sentence:**
Chronic bronchitis, Pulmonary emphysema and Asthma are all types of ________.
Chronic obstructive lung disease (COPD)
82
# **Question:**
What is Pulmonary Emphysema?
Emphysema is a progressive chronic lung condition in which the alveolar septal walls are destroyed, leading to permanently dilated and inflated alveoli.
83
# **Question:**
What are the major contributive factors to emphysema?
* Genetic defects (e.g., α1-antitrypsin deficiency)
* Smoking (induces oxidative stress and protease activity)
* Bacterial colonization (chronic inflammation damages alveoli)
84
# **Questions:**
What are the three key pathophysiological changes in emphysema?
1. **Destruction of alveoli walls** → Progressive ventilatory dysfunction
2. **Increased air trapping** → ↑ Residual volume
3. **Lung hyperinflation** → Reduced elastic recoil
85
# **Question:**
Does emphysema lead to compensatory anatomical changes?
Yes.
* Rectilinization of the ribcage → Increased PA (anteroposterior) diameter ("barrel chest")
* Flattening of the diaphragm due to hyperinflation
86
# **Question:**
What are the clinical signs of emphysema?
* **Dyspnea** (due to impaired gas exchange)
* **Tachycardia** (during acute hypoxic exacerbations)
* **Right heart failure** (if hypoxia is chronic)
87
# **Question:**
Why are emphysema patients called "pink puffers"?
* Mild hypoxemia with preserved oxygenation → Pink skin
* Increased respiratory effort ("puffing") to compensate for alveolar damage
88
# **Question:**
How does emphysema affect ventilation/perfusion ratio (V/Q)?
Emphysema increases the ventilation/perfusion ratio (V/Q) due to the destruction of alveolar walls and the loss of capillaries.
89
# **Question:**
Why does emphysema lead to a compensatory increase in minute ventilation?
The destruction of alveolar walls in emphysema reduces gas exchange efficiency, prompting a compensatory increase in minute ventilation to maintain normal O₂ and CO₂ levels.
90
# **Question:**
What is the consequence of a high ventilation/perfusion (V/Q) ratio in emphysema?
A high V/Q ratio in emphysema can lead to poor matching of ventilation and perfusion, which makes gas exchange less efficient.
91
# **Question:**
How does the compensatory increase in minute ventilation help in emphysema?
The increase in minute ventilation helps maintain normal oxygen (O₂) and carbon dioxide (CO₂) levels despite reduced efficiency in gas exchange.
92
# **Question:**
What are restrictive lung diseases?
Group of diseases characterized by a **widespread lung fibrosis**, leading to decreased lung compliance and to a **decreased total lung capacity**.
93
# **Question:**
What are the main causes of pulmonary fibrosis?
* Granulomatous (e.g. Sarcoidosis)
* Pneumoconiosis
* Inherited
* Idiopathic pulmonary fibrosis
* Collagen-vascular and pulmonary renal syndromes
* Other (dystrophies, skeletal and neurological disorders)
94
# **Question:**
What is idiopathic pulmonary fibrosis?
Infiltration of inflammatory cells and fluid in the lung parenchyma leading to scarring and fibrosis, without a known causative agent.
95
# **Question:**
What is the first step in the progression of Idiopathic Pulmonary Fibrosis?
The first step is tissue injury, where the lung tissue is damaged, initiating the inflammatory and fibrotic process.
96
# **Question:**
How does increased capillary permeability contribute to Idiopathic Pulmonary Fibrosis?
Increased capillary permeability allows fluid and proteins to leak into the alveolar space, promoting inflammation and further tissue damage.
97
# **Question:**
What is the role of epithelial injury in the development of Idiopathic Pulmonary Fibrosis?
Epithelial injury disrupts the integrity of the alveolar lining, triggering inflammation and fibroblast activation, which contribute to fibrosis.
98
# **Question:**
How do leucocytes contribute to Idiopathic Pulmonary Fibrosis?
Leucocyte influx and proliferation occur in response to tissue injury, amplifying the inflammatory response and promoting the release of cytokines that stimulate fibrosis.
99
# **Question:**
What happens after leucocyte influx in the progression of Idiopathic Pulmonary Fibrosis?
After leucocyte influx, further tissue injury occurs, followed by tissue remodelling and fibrosis, leading to scarring of the lung tissue and impaired lung function.
100
# **Question:**
What are the five main steps involved in Idiopathic Pulmonary Fibrosis?
1. Tissue injury
2. Increased capillary permeability
3. Epithelial injury
4. Leucocyte influx and proliferation
5. Further tissue injury, remodelling and fibrosis
101
What are common symptoms of Idiopathic Pulmonary Fibrosis (IPF)?
Common symptoms include:
* chronic cough
* dyspnea (shortness of breath)
* tachypnea (rapid breathing)
* inspiratory crackles
* digital clubbing
102
# **Question:**
How does idiopathic pulmonary fibrosis lead to tachypnea?
Fibrosis causes a thickening of the capillary-alveolar barrier, leading to impaired gas exchange and hypoxia (low oxygen levels), which triggers tachypnea (increased respiratory rate) as the body attempts to compensate for reduced oxygen.
103
# **Question:**
How does idiopathic pulmonary fibrosis lead to dyspnea (shortness of breath)?
Fibrosis stiffens the lung tissue, reducing its ability to expand and contract properly, which decreases lung compliance (the ability of the lungs to stretch and expand during breathing). Decreased lung compliance makes the lungs stiffer, requiring greater effort to expand with each breath, leading to an increased work of breathing and causing dyspnea (difficulty breathing).
104
# **Question:**
What causes inspiratory crackles in Idiopathic Pulmonary Fibrosis patients?
Inspiratory crackles occur due to the opening of collapsed alveoli during inspiration, which is a hallmark sign of Idiopathic Pulmonary Fibrosis.
105
# **Question:**
What causes dyspnea and tachypnea in Idiopathic Pulmonary Fibrosis?
Dyspnea and tachypnea in IPF are caused by fibrosis, which thickens the capillary-alveolar barrier, leading to hypoxia (low oxygen levels) and increased respiratory effort.
106
# **Question:**
How does decreased lung compliance affect patients with Idiopathic Pulmonary Fibrosis?
Decreased lung compliance results in stiffer lungs, requiring increased respiratory effort, which causes dyspnea (shortness of breath).
107
# **Question:**
Why does digital clubbing occur in Idiopathic Pulmonary Fibrosis?
Digital clubbing, a widening of the fingertips, occurs in IPF due to chronic hypoxia, which leads to changes in the blood vessels and soft tissues of the fingers and toes.
108
# **Question:**
How does the body compensate for the hypoxia caused by fibrosis in Idiopathic Pulmonary Fibrosis?
In response to hypoxia, the body increases the respiratory rate (tachypnea) in an attempt to deliver more oxygen to the tissues.
109
# **Question:**
What is Pneumoconiosis?
Pneumoconiosis is a group of interstitial lung diseases caused by prolonged occupational or environmental exposure to inhalation of dust particles, leading to lung damage and interstitial fibrosis. It affects miners, builders, and other workers who breathe in certain kinds of dust on the job.
110
# **Question:**
How does pneumoconiosis develop over time?
It develops through long-term inhalation of dust particles, which causes inflammation of the lung parenchyma (lung tissue) and gradual destruction of connective tissue.
111
# **Quesion:**
What is the typical onset of pneumoconiosis symptoms?
The disease typically has an **insidious onset**, with dyspnea (shortness of breath) being the first symptom to appear.
112
# **Question:**
What happens to the lung tissue in pneumoconiosis?
In pneumoconiosis, continuous exposure to dust particles leads to inflammation and progressive damage to lung tissue, resulting in fibrosis and scarring.
113
# **Question:**
What are common examples of pneumoconiosis?
Common examples include **asbestosis**, caused by asbestos exposure, and **silicosis**, caused by inhaling silica dust.
114
# **Question:**
What are pulmonary vascular diseases (or vascular lung diseases)?
Pulmonary vascular disease is a term for a group of conditions that affect the blood vessels in the lungs.
115
# **Question:**
What is the main type of pulmonary vascular disease?
Acute pulmonary embolism
116
# **Question:**
What are the possible causes of acute pulmonary embolism?
It can be caused by:
* Thrombi (thromboembolism)
* Gas (e.g., surgery, central venous catheters)
* Tumor cells (e.g., renal carcinoma with inferior vena cava invasion)
* Oil (e.g., lymphangiography)
* Fat (e.g., trauma)
* Liquid (e.g., amniotic fluid)
* Parasite eggs (e.g., schistosomiasis)
117
# **Question:**
What is the main consequence of large thrombi or multiple small thrombi in acute pulmonary embolism?
Large or multiple small thrombi can lead to **vascular occlusion**, which prevents blood flow to the lungs.
118
# **Question:**
Where do thrombi that cause pulmonary embolism usually originate?
Thrombi commonly originate from:
* Popliteal veins
* Femoral veins
* Iliac veins
* Upper limbs (e.g., from catheters)
* Right heart chambers (e.g., from pacemaker wires)
119
# **Question:**
What are the two main risk factors for pulmonary embolism?
* **Increased venous stasis:** immobilization, heart failure, pregnancy, obesity, blood hyperviscosity, vascular lesions, advanced age
* **Increased coagulability:** tissue trauma (surgery, trauma, myocardial infarction), malignancy, nephrotic syndrome, oral contraception, genetic disorders
120
# **Question:**
What are the hemodynamic changes in pulmonary embolism?
Hemodynamic changes in pulmonary embolism include:
* Increased pulmonary vascular resistance
* Increased pressure in the pulmonary trunk
* Increased strain on the right ventricle
121
# **Question:**
How does the ventilation/perfusion (V/Q) ratio change in pulmonary embolism?
Changes in the V/Q ratio include:
* Increased V/Q mismatch
* Decreased CO₂ excretion and accumulation
* Compensatory hyperventilation
* Hypoventilation leading to type II pneumocyte dysfunction
* Loss of surfactant causing edema, alveolar collapse, and atelectasis
* In perfused alveoli, decreased V/Q ratio
* Hypoxemia
122
# **Question:**
What is the clinical presentation of a small pulmonary embolism?
Small emboli typically present with pleuritic pain, cough, and dyspnea.
123
# **Question:**
What is the clinical presentation of a large pulmonary embolism?
Large emboli present with pleuritic pain, tachypnea, dyspnea, hemoptysis, fever, and hypoxia.
124
# **Question:**
What is the clinical presentation of a massive pulmonary embolism?
Massive emboli present with pleuritic pain, hypotension, and loss of consciousness.
125
# **Question:**
How does hypoventilation affect type II pneumocytes in the lungs?
Hypoventilation occurs in areas of the lung that are not receiving sufficient perfusion (blood flow) due to the embolism. The lack of adequate ventilation leads to type II pneumocyte dysfunction. Type II pneumocytes are responsible for producing surfactant, which prevents alveolar collapse by reducing surface tension in the lungs. Dysfunction leads to impaired surfactant production.
126
# **Question:**
What is the role of surfactant in the lungs?
Surfactant reduces surface tension in the alveoli, helping to keep them open and preventing alveolar collapse during exhalation. It is essential for maintaining normal lung function.
127
# **Question:**
What happens when there is a loss of surfactant in pulmonary embolism?
Loss of surfactant results in increased surface tension, leading to alveolar collapse, reduced gas exchange, and the development of pulmonary edema.
128
# **Question:**
What is alveolar collapse, and how does it occur in pulmonary embolism?
Alveolar collapse occurs when the small air sacs (alveoli) in the lungs deflate due to the lack of surfactant, causing impaired gas exchange and contributing to atelectasis (lung tissue collapse).
129
# **Question:**
What is atelectasis and how is it related to pulmonary embolism?
Atelectasis is the partial or complete collapse of lung tissue. In pulmonary embolism, it occurs due to the loss of surfactant and alveolar collapse, leading to decreased ventilation in the affected areas.
130
# **Complete the sentence:**
In acute pulmonary embolism, the ventilation/perfusion ratio is ________ (increased/decreased).
increased
| (due to reduced perfusion)
131
# **Question:**
Why is the V/Q ratio increased in acute pulmonary embolism?
In Pulmonary Embolism, a blockage in the pulmonary arteries (due to thrombi, fat, gas, etc.) leads to reduced blood flow (perfusion) to certain areas of the lungs, while ventilation (airflow) to those areas remains unchanged or even increases as a compensatory mechanism.
132
# **Question:**
Why is there a compensatory hyperventilation in pulmonary embolism?
As perfusion to parts of the lungs is impaired (due to embolism), less blood can pick up CO₂ from the tissues. This leads to a **reduced ability to excrete CO₂**, resulting in its accumulation in the bloodstream, a condition known as **hypercapnia**.
In response to the accumulation of CO₂ (and the decreased oxygen levels from impaired gas exchange), the body compensates by hyperventilating (rapid, deep breathing). This is an attempt to expel excess CO₂ and increase oxygen intake.
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# **Question:**
Why is there a decreased V/Q ratio in perfused alveoli in pulmonary embolism?
In areas where perfusion (blood flow) is still intact but ventilation is impaired (due to alveolar collapse or hypoventilation), the V/Q ratio decreases. This is because blood flow is still going to these areas, but the lack of airflow (due to collapsed or poorly ventilated alveoli) means that these areas are less efficient at oxygenating the blood.
