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N5315 Advanced Pathophysiology Pulmonary, Study notes of Pathophysiology

Cambridge Technical InstitutePathophysiology

N5315 Advanced Pathophysiology Pulmonary

Typology: Study notes

2025/2026

Available from 06/28/2026

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N5315 Advanced Pathophysiology
Pulmonary
I. Pulmonary Disease- General Comments
a. Pulmonary diseases are often classified into 2 broad categories.
i. Restrictive versus Obstructive is the first classification of pulmonary
disorders.
1. Restrictive disorders refer to the inability of the person to
breathe in adequate amounts of air. Typically, these individuals
have low lung volumes on pulmonary function tests. Lung
volumes are essentially the amount of air the lungs contain at a
given time during respirations. Disease examples include
aspiration, pulmonary fibrosis, atelectasis, bronchiectasis,
bronchiolitis, and pulmonary edema.
2. Obstructive disorders refer to the inability of the person to
completely exhale that air which is inhaled. Typically, on
PFTs these individuals will have high lung volumes because
they are retaining air in the lungs. Disease examples include
asthma & COPD.
ii. Infectious versus Non-infectious is the second classification for pulmonary
disorders.
1. Infectious examples include Pneumonia & Tuberculosis.
2. Non-infectious examples include pulmonary fibrosis, lung cancer,
and pulmonary HTN.
b. Overview of Pulmonary Disease States
i. Acute Respiratory Failure is classified into two main types.
a. Hypoxemia respiratory failure is defined as a PaO2 of </=
50mmHg.
b. Hypercapnic respiratory failure is defined as a PaCO2 >/=
50mmhg.
c. In either case, the main dysfunction is an impairment
in diffusion which results in low oxygen levels or the
accumulation of CO2.
2. Acute respiratory failure may result from direct injury to the lungs
or may simply be triggered by an injury or dysfunction to one or
more body systems or organs. It may also occur as a post-operative
complication secondary to anesthesia or narcotics.
ii. A Pneumothorax is the presence of air or gas in the pleural space. The air
in the thoracic cavity may press on the lung and cause it to collapse
completely, or it may be a small amount of air that does not cause any
difficulties. The two main types are spontaneous pneumothorax and
secondary pneumothorax.
1. A spontaneous pneumothorax occurs in young, tall thin males.
They may also occur as a result of bleb rupture in persons who
have emphysema.
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N5315 Advanced Pathophysiology

Pulmonary

I. Pulmonary Disease- General Comments a. Pulmonary diseases are often classified into 2 broad categories. i. Restrictive versus Obstructive is the first classification of pulmonary disorders.

  1. Restrictive disorders refer to the inability of the person to breathe in adequate amounts of air. Typically, these individuals have low lung volumes on pulmonary function tests. Lung volumes are essentially the amount of air the lungs contain at a given time during respirations. Disease examples include aspiration, pulmonary fibrosis, atelectasis, bronchiectasis, bronchiolitis, and pulmonary edema.
  2. Obstructive disorders refer to the inability of the person to completely exhale that air which is inhaled. Typically, on PFTs these individuals will have high lung volumes because they are retaining air in the lungs. Disease examples include asthma & COPD. ii. Infectious versus Non-infectious is the second classification for pulmonary disorders.
  3. Infectious examples include Pneumonia & Tuberculosis.
  4. Non-infectious examples include pulmonary fibrosis, lung cancer, and pulmonary HTN. b. Overview of Pulmonary Disease States i. Acute Respiratory Failure is classified into two main types. a. Hypoxemia respiratory failure is defined as a PaO2 of /= 50mmhg. c. In either case, the main dysfunction is an impairment in diffusion which results in low oxygen levels or the accumulation of CO2.
  5. Acute respiratory failure may result from direct injury to the lungs or may simply be triggered by an injury or dysfunction to one or more body systems or organs. It may also occur as a post-operative complication secondary to anesthesia or narcotics. ii. A Pneumothorax is the presence of air or gas in the pleural space. The air in the thoracic cavity may press on the lung and cause it to collapse completely, or it may be a small amount of air that does not cause any difficulties. The two main types are spontaneous pneumothorax and secondary pneumothorax.
  6. A spontaneous pneumothorax occurs in young, tall thin males. They may also occur as a result of bleb rupture in persons who have emphysema.
  1. A secondary pneumothorax is caused by trauma. A tension pneumothorax occurs when air becomes trapped in the thoracic cavity and cannot escape. The site of the injury on the pleural membrane acts as a one-way value and only lets air into the thoracic cavity. In this instance the person may experience a complete lung collapse. If this occurs the individual will have a deviated trachea, shortness of breath, and hypotension. iii. Pulmonary Edema is the accumulation of water in the pulmonary alveolar sacs. This prevents the proper exchange of gases and leads to dyspnea, chest pain, and hypoxia. Often individuals will also have orthopnea or paroxysmal nocturnal dyspnea.
  2. The most common cause is left-sided heart failure. In left-sided heart failure the backup of blood to the lungs increases capillary hydrostatic pressure which pushes fluid out into the alveolar sac. iv. Acute Respiratory Distress Syndrome is a type of respiratory failure which results from massive lung inflammation and disseminated alveolar capillary damage. This damage significantly impairs gas exchange and the patient will have significant issues with oxygenation. Pneumonia, sepsis, massive trauma, burns, aspirations, DIC and pancreatitis all increase the risk of developing ARDS.
  3. The pathologic hallmarks of ARDS include: a. Diffuse alveolar capillary damage, poor gas exchange, severe pulmonary edema & hypoxemia b. The three phases of ARDS are the inflammatory, proliferative and fibrotic phases. i. The inflammatory phase occurs within the first 72 hours. The inflammatory cascade is triggered by an insult or injury to the capillary membranes, which then increases the capillary permeability. Fluid, proteins, and blood cells then leak into the pulmonary interstitium and alveoli and impair gas exchange. ii. During the proliferative phase the pulmonary edema resolves. This phase lasts one to three weeks. Intra- alveolar exudate turns into a cellular granulation tissue and worsens the hypoxemia. iii. The fibrotic phase occurs between 14-24 days. As you may notice there is some overlap between this phase and the proliferative phase. During this phase the alveoli undergo fibrosis, and ultimately this causes a decrease in pulmonary function which may be permanent. Review the classification and manifestations in your textbook.

include bacterial, viral, or fungal organisms or it may simply be caused by aspiration.

  1. Community-Acquired Pneumonia is a pneumonia which occurs outside of the healthcare system. a. Common bacterial causes include the following organisms: i. Streptococcus Pneumoniae is the most common cause of PNA. It is seen more frequently in the elderly and debilitated patients such as those who are malnourished or have cardiopulmonary diseases. ii. Staphylococcus Aureus often arises as a complication from influenza or a viral pneumonia. This is seen mainly in the elderly, debilitated hospitalized patients and those persons with chronic lung disease. iii. Streptococcus Pyogenes occurs as a complication of a viral infection such as influenza or measles. iv. Klebsiella Pneumoniae is common in hospitalized debilitated patients, diabetics, or alcoholics. Elderly infected with this bacteria have a high mortality. v. Haemophilus Influenza is commonly seen in infants and children. It occurs commonly in those adults with COPD. b. Healthcare-Associated Pneumonia is a PNA which is diagnosed in any individual who has had contact with the healthcare system. Persons who have received infusion therapy or dialysis or have resided in a nursing home within 90 days of the diagnosis are said to have a healthcare-associated pneumonia. c. Hospital-Acquired Pneumonia is one which is diagnosed 48 hours after being admitted to the hospital. Common causes include gram-negative bacteria such as Klebsiella, Pseudomonas aeruginosa, and Escherichia Coli. These organisms are also common ones implicated in healthcare- associated pneumonia too. viii. Tuberculosis is a pulmonary infection which occurs worldwide and most commonly in disadvantaged populations. It is caused by the mycobacterium tuberculosis and is spread via air droplets containing the organism.
  2. In primary infection, macrophages engulf the mycobacterium and form a granuloma called a Ghon. This triggers the inflammatory cascade, which causes the center of the lesion to necrose and eventually calcify. This infection is usually asymptomatic and usually does not cause active disease.
  3. In secondary infection, the Ghon has activated and the infection has spread to additional sites within the lung. Individuals with secondary infection experience symptoms such as fever,

hemoptysis, pleural effusion, wasting, and weight loss. Lesions often occur in the apices of the lungs. These individuals are infectious and can spread the disease.

  1. The mycobacterium can spread to other parts of the body via the blood or lymphatic systems. ix. Lung Cancers are usually malignant. Most lung cancer lesions are metastatic lesions from a different primary cancer. Primary lung tumors are not as common. Lung cancer is the leading cause of death from cancer in both men and women. Smokers develop 90% of primary lung cancer tumors. The incidence of primary lung cancer is directly related to the length of time an individual has smoked. The most common primary lung cancer tumors are small cell and squamous cell carcinomas. Lung cancer is often diagnosed in later stages and unfortunately there are not any good screening tests which can be used to help diagnose the cancer while it is in an earlier stage. Complications include superior vena cava syndrome, hoarseness, pleural effusion, malnutrition, and weight loss. c. Pulmonary Arterial Hypertension i. Think of PAH as hypertension in the pulmonary artery. Clinically a person meets the diagnostic criteria for PAH, if they have a mean pulmonary arterial pressure of greater than 25mmHg at rest. Normal PA pressure is between 15-18mmHg. Idopathic PAH occurs mainly in women but is not very common. PAH may be secondary to a genetic defect in the gene which codes bone morphogenetic protein receptor type II (BMPR2). ii. Risk factors for the development of PAH include diet medications, amphetamines, and cocaine. PAH may also be caused by left ventricular heart failure, or left sided valvular heart disease. A defect in the left ventricular or the aortic or mitral valves will cause back up of blood into the lungs, thus causing PAH. COPD may also cause PAH and is the most common pulmonary condition to do so. Lastly a pulmonary embolus may also cause PAH. iii. Understanding the potential causes helps us a clinicians with your evaluation of these patients. When we suspect that someone has a disorder such as PAH, we have to determine what caused it. This means that we have to do a thorough work up to see if any of the known causes are responsible for the disorder. Then if an underlying disorder is identified it must be treated. iv. The pathophysiology includes an over abundance of vasoconstrictors and an insufficient amount of vasodilators. This imbalance causes a constriction of the pulmonary artery. Additionally, there are changes in the precapillary pulmonary arteries which make them resistant to vasodilation. There are increased levels of calcium which causes vasoconstriction, phosphodiesterases which increase cellular proliferation, increased serotonin levels which cause vasodilation all of which add to the pathogenesis of this disorder. The higher pressure in the pulmonary artery causes the right ventricle to work harder. It has to push against the

shock this increases the workload of the already failing left ventricle and makes it more difficult for the left ventricle to pump blood and worsens the shock state. c. Sepsis is most commonly caused by gram positive bacteria, follow by gram negative bacteria. The infective agent triggers a systemic vasodilation. The problem is not a loss of volume but rather the vascular system has expanded; thus, the available volume is insufficient to completely fill the vascular system. Gram- negative bacteria have endotoxins which are released when they are killed and this makes the septic shock worse, when it is caused by a gram negative bacteria. Antibiotics do not have any effect on endotoxins and they trigger a massive inflammatory and immune reaction. The classification of sepsis changed in early

  1. The classifications of SIRS, Sepsis, Severe Sepsis, and Septic Shock, presented in the text book no longer apply. You are not responsible for knowing these particular classifications of sepsis or the new classification of sepsis. d. Neurogenic shock results from a widespread vasodilation caused by an imbalance between the sympathetic and parasympathetic nervous systems. In normal physiology, the sympathetic nervous system opposes the effects of the parasympathetic nervous system. It increases the heart rate, decreases digestion and causes vasoconstriction. An imbalance between the two systems causes neurogenic shock. The issue with this type of shock is not with loss of volume. The volume has not changed. The tank (vasculature) has just gotten bigger and the volume is not enough to fill the tank. It may be caused by trauma to the spinal cord or dysfunction of the medulla. Severe general trauma may cause this as well. e. Anaphylactic shock results from a pathologic immune and inflammatory reaction to an antigen. In this type of shock, the individual experiences a significant allergic reaction to an antigen which results in a systemic inflammatory process and a widespread vasodilation. This occurs as a result of the release of products of inflammation, mainly histamine. This is an example of a type I hypersensitivity reaction which is IgE mediated reaction.