Lecture 6: Respiratory Pathology (Pneumonia and Acute Lung Injury) Flashcards
Describe the normal alveolar structure.
Normal alveolar structure consists of:
- Type I pneumocytes: cover 95% of the alveolar surface
- Type II pneumocytes: synthesize surfactant and involves in the repair of alveolar epithelium through their ability to differentiate into type I cells
- Tissue-resident macrophages
- Capillaries (endothelial cell)
Recall the microscopic image of a normal alveolar structure
Define pneumonia.
Pneumonia are respiratory disorders involving acute inflammation of the lung structures, mainly the alveoli and bronchioles
Mention the classification of pneumonia.
- According to the causative agent:
- Infectious
- Bacterial (most common cause of pneumonia)
- Viral pneumonia
- Fungal pneumonia
- Non-infectious (usually cause Acute Lung Injury)
- Chemical pneumonia (ingestion/inhalation of irrating substance)
- Inhalation pneumonia (aspiration pneumonia)
- Infectious
Mention an example of a highly dangerous lung pathogen.
Infectious pneumonia is an ____________ infection. Explain it.
Penumonia is an opportunistic infection. It most often affects people with impaired host defences, i.e. immunocompromised individuals.
Mention the host defences in the respiratory tract.
- Muco-ciliary clearance
- Goblet cell: mucus production
- Ciliated cell: mucus transport
- Lamina Propria: layer between the epithelial and muscle layer; harbour macrophages
- Surfactant proteins:
- produced by Type II pneumocytes
- protect airways from infection
- maintain alveolar integrity - reduce surface tension
- Alveolar macrophages
_________________ influences efficiency of first-line macrophage-mediated phagocytosis.
Infectious bacterial dose
Mention examples of impaired lung defences.
- Loss/suppression of cough reflex
- can lead to aspiration of gastric contents
- patients inc oma, anaesthesia, NMD, drugs, chest pain
- Injury to mucociliary apparatus
- long-term smoking, viral infection, genetic disease (CF)
- Pulmonary congestion or oedema: due to chronic heart disease
- Low IgG &/ IgA
Differentiate between acute and chronic inflammation in the upper respiratory tract.
Describe the mechanism behind the thickening of bronchiole in chronic inflammation.
Due to the prolonged process of injury and healing, this leads to the continuous release of GFs. This GF, other than assisting in the healing process, also leads the overproliferation of smooth muscle cells - thickening the bronchiole.
This change may also be in response to increased pressure to the lung - requiring thicker muscle layers to continue function.
Describe the classification of acute inflammation in the lung.
Describe the time course of lung acute inflammation.
Describe the histopathology of early acute lung inflammation.
Describe the histopathology of a later case of acute lung inflammation.
What is the function of the pores of Kohn?
The pores allow the passage of other materials such as fluid and bacteria, which is an important mechanism of spread of infection in lobar pneumonia and spread of fibrin in the grey hepatisation phase of recovery from the same. They also equalize the pressure in adjacent alveoli and, combined with increased distribution of surfactant, thus play an important role in prevention of collapse of the lung.
What is lung hepatization?
It is a state of the lungs when gorged with effuse matter, so that they are no longer pervious to the air. Red hepatization is when there are red blood cells, neutrophils, and fibrin in the pulmonary alveolus/ alveoli; it precedes gray hepatization, where the red cells have been broken down leaving a fibrinosuppurative exudate.
Describe the complication because of acute inflammation in the lung.
Results in:
- tissue destruction and necrosis
- spread of infection and inflammation of the pleural cavity (pleurisy)
- bacteraemic dissemination (brian, heart, kidneys)
Symptoms:
- malaise, fever, chills
- chest pain secondary to pleurisy
- ARDS (Acute Respiratory Distress Syndrome)
Recall the outcomes of acute versus chronic inflammation.
Describe the histopathology of chronic inflammation in the lung.
Describe ARDS.
Mention the common causes of ARDS.
How is ARDS diagnosed?
Compare a normal alveolus and an injured alveolus in the acute phase of ALI/ARDS.
