COPD Flashcards
Distinguish between the two main types of chemoreceptor that control ventilation.
central chemoreceptors - medulla, detect changes in pH and the partial pressure of CO2.
peripheral chemoreceptors - aortic arch and carotid arteries, sensitive to changes in the partial pressure of O2 in arterial blood, as well as changes in pH.
Describe the effects of PaCO2, PaO2 and pH on chemoreceptors and ventilation.
Increased partial pressure of CO2 causes CO2 to diffuse out the blood vessels, forming H+ ions and leads to hyperventilation. Hyperventilation decreases the partial pressure of CO2 in the blood and cerebrospinal fluid and leads to hypoventilation.
Decreased arterial O2 leads to hyperventilation, which is when arterial pO2 falls below 13.3kPa.
Explain the relationship between the chemical control of ventilation and acid-base balance in the body.
- respiratory acidosis: hypoventilation, increased excretion of hydrogen ions, increased carbonate reabsorption.
- respiratory alkalosis: hyperventilation, increased hydrogen ion reabsorption, increased carbonate excretion.
- metabolic acidosis: decreased ability of the kidneys to excrete H+ and to reabsorb HCO3-, ventilation increased to decrease carbon dioxide partial pressure.
- metabolic alkalosis: increase in pH and carbonate in the kidneys, ventilation is decreased to increase the partial pressure of carbon dioxide.
State that neural regulation is faster than chemical regulation
Neural regulation is faster than chemical regulation as it is dependent on fast acting impulses to and from the central nervous system. Chemical control responds to changes in the partial pressure of CO2 and O2.
Explain the origin of the respiratory rhythm and differentiate between the medulla respiratory centres, the pons respiratory centres, and vagal control
- medulla: dorsal respiratory group (DRG) and the ventral respiratory group (VRG).
- DRG: innervates the diaphragm and the external intercostal muscles. DRG neurons switch on for two seconds and then switch off for three seconds, causing a rhythmic pattern.
- VRG - innervates the abdominal muscle and the internal intercostal muscles. Activity is enhanced during forced expiration.
- pons: pneumotaxic centre transmits signals to the DRG, limits inspiration and ‘fine tunes’ breathing by sending inhibitory impulses to the DRG, limits the period of inspiration to two seconds and prevents over inflation of the lungs.
- apneustic center: responsible for prolonged inspiratory gasps (apneusis), prolongs DRG stimulation.
- vagus nerve: sends afferent information from the lungs to the DRG, prevents over inflation of the lungs by switching off inspiration.
Explain the influence of higher brain centres on breathing
cerebral cortex: stimulates the motor neurones of the inspiratory muscles, bypasses the medullary centres when consciously controlling breathing, such as when holding the breath.
hypothalamus: associated with strong emotions, pain and changes in temperature that can alter respiration rate and rhythm. Apnoea (the suspension of breathing) can be induced by anger, pain, or a decrease in temperature. Tachypnoea (rapid breathing) can be induced by excitation, or an increase in temperature.
Describe examples of reflexes which modulate breathing
- stretch receptors: located in the smooth muscle of the trachea and the bronchi, sensitive to lung expansion.
- juxtapulmonary receptors: alveolar wall between the epithelium and the endothelium, close to the pulmonary cavities, stimulated by congestion, oedema, and histamines, activation results in apnoea or rapid shallow breathing, bronchoconstriction and mucus secretion.
- irritant receptors: located between epithelial cells and are sensitive to irritant gases, smoke and dust, activation results in shallow rapid breathing, cough, bronchoconstriction, mucus secretion, and augmented breaths.
- receptors in the bronchioles: promotes airway constriction. Stimulation of receptors in the trachea and bronchi promotes coughing. Stimulation of receptors in the nasal cavity leads to sneezing.
Describe the range of situations in which an acute inflammatory reaction can occur
The purpose of the acute inflammatory reaction is to destroy or neutralise the damaging agent, to liquefy and remove dead tissue, and to prepare the damaged area for healing.
List the main steps in the acute inflammatory response
This response happens by the production of an acute inflammatory exudate derived from blood components from capillaries adjacent to the damaged areas. This exudate comprises fluid, fibrin, neutrophils and a few macrophages and lymphocytes.
The exudate fluid dilutes any toxins and carries nutrients, mediators and antibodies. The function of fibrin is speculative. Neutrophils are actively phagocytic of living tissue and necrotic debris.
Describe the composition of an acute inflammatory exudate and some of its clinical effects
The blood vessels near the damaged tissue become dilated, blood flow increases initially, then slows down. The axial flow pattern of blood is lost.
Substances released by the dead tissue act on blood vessels, and water, salts and proteins (including fibrinogen) leak out into the damaged area, causing swelling. Neutrophils then stick to endothelial cells and migrate through the capillary into the damaged area.
Serous exudate is fluid rich and cell poor. Purulent exudate is filled with polymorphs and fibrinous exudate is full of fibrin. Fibrino-purulent exudate has a mixture of fibrin and polymorph components.
Define the term chronic inflammation and list three circumstances under which it arises
Chronic inflammation occurs when a damaging stimulus persists and complete healing cannot occur. Damage, organisation and repair occur at the same time. The population profile changes and the tissue is infiltrated by macrophages and immune cells. This type of inflammation always heals by scarring.
Causes of chronic inflammation can be that the damaging stimulus is not amenable to eradication or neutralisation, the bacteria pesticides because they’re distanced from neutrophils, or the bacteria persists because they are resistant to neutrophil phagocytosis.
Describe the pathological features of chronic inflammation and its outcome
Macrophages are the main effector cells and are activated by gamma interferon. They have a phagocytose role and a secretary role. They are mediators of inflammation, oxygen metabolites, protease and hydroplanes. They secrete cytokines and growth factors.
Describe the features of granulomatous inflammation and give examples of diseases associated with this pattern of response
granulomatous inflammation is a special type of inflammation in which macrophages are involved early as part of the immune response. Macrophages aggregate around the damaging agent with lymphocytes and fibroblasts, forming a granuloma. The macrophages can fuse together to form giant cells
Granulomatous inflammation can be caused by low pathogenicity organisms which excite a type IV immune response, organic or inorganic foreign material and some fungi.
Evaluate the effects of a simulated ventilatory deficit on lung function parameters.
- In a restrictive ventilatory deficit, TLC, FRC, and RV will all decrease. A pattern of reduced FEV1 and FVC but preserved FEV1/FVC ratio is indicative of a restrictive respiratory deficit.
- In an obstructive ventilatory deficit, TLC remains unchanged, FRC and RV will increase. A decrease in FEV1 and FEV1/FVC is consistent with a diagnosis of airflow obstruction.
Counsel a patient on how to use a peak flow meter.
the teeth and tongue should obstruct the mouthpiece.
