Pulmonology 4

zwinthrop's version from 2015-04-13 13:38

Control of Breathing

Question Answer
Explain how rhythmic breathing is stimulated in the brainstem.Answer: The respiratory control centers in the pons can adjust the basal rate of ventilation that established by the cooperation between the dorsal respiratory group (DRG) and ventral respiratory group (VRG). The DRG contains inspiratory autorhythmic neurons that stimulate the diaphragm and external intercostal muscles for approximately 2 seconds the cause inspirations followed by passive 3-second inspiration period. The DRG contain neurons involved in altering the patterns for ventilation in response to the physiological needs of the body for O2 and CO2 exchange and for the blood acid-base balance. These neurons are responsive to sensory information from chemo- and mechano-receptors. The VRG contains both inspiratory and expiratory neurons and is only active at times of increased ventilation. The neurons on the DRG influence the VRG to increase inspiration and stimulate forced expiration (contraction of the abdominal muscles, internal intercostals, ect.). The pontine respiratory group contains the pneumotaxic and apneustic center located in the upper pons. The pneumotaxic center has an inhibitory relationship on the dorsal respiratory group to “switch off” inhalation and coordinate the speed of respiration and passive expiration. The apneustic center has an excitatory relationship with the DRG neurons to prevent the DRG from “switching off.”
What are the 4 components of the breathing control system?(1) chemoreceptors for O2 or CO2; (2) mechanoreceptors in the lungs and joints; (3) control centers for breathing in the brain stem (medulla and pons); (4) respiratory muscles, whose activity is directed by the brain stem centers. Voluntary control can also be exerted by commands from the cerebral cortex (e.g., breath-holding or voluntary hyperventilation), which can temporarily override the brain stem.
Explain the inspiratory center. What are the afferent and efferent pathways?The inspiratory center is located in the dorsal respiratory group (DRG) of neurons and controls the basic rhythm for breathing by setting the frequency of inspiration. This group of neurons receives sensory (afferent) input from peripheral chemoreceptors via the glossopharyngeal (CN IX) and vagus (CN X) nerves and from mechanoreceptors in the lung via the vagus nerve. The inspiratory center sends its motor output (efferent) to the diaphragm via the phrenic nerve. The pattern of activity in the phrenic nerve includes a period of quiescence, followed by a burst of action potentials that increase in fre- quency for a few seconds, and then a return to quiescence.
Explain the expiratory center.The expiratory center is located in the ventral respiratory neurons and is responsible primarily for expiration. Because expiration is normally a passive process, these neurons are inactive during quiet breathing. However, during exercise when expiration becomes active, this center is activated.
What is the pneumotaxic center and what does it doThe pneumotaxic center turns off inspiration, limit- ing the burst of action potentials in the phrenic nerve. In effect, the pneumotaxic center, located in the upper pons, limits the size of the tidal volume, and secondarily, it regulates the respiratory rate. A normal breathing rhythm persists in the absence of this center.
Explain the control the cerebral cortex has over breathing.Commands from the cerebral cortex can temporarily override the automatic brain stem centers. For example, a person can voluntarily hyperventilate (i.e., increase breathing frequency and volume). The consequence of hyperventilation is a decrease in PaCO2, which causes arterial pH to increase. Hyperventilation is self-limiting, however, because the decrease in PaCO2 will produce un- consciousness and the person will revert to a normal breathing pattern.
What are central chemoreceptors?Located in the brain stem, they are the most important for the minute-to-minute control of breathing. These chemoreceptors are located on the ventral surface of the medulla, near the point of exit of the glossopharyngeal (CN IX) and vagus (CN X) nerves and only a short distance from the DRG in the medulla. Communicate directly with the inspiratory center. The brain stem chemoreceptors are exquisitely sensitive to changes in the pH of cerebrospinal fluid (CSF). The goal of central chemoreceptors is to keep arterial PCO2 within the normal range, if possible. Thus, increases in arterial PCO2 produce increases in PCO2 in the brain and the CSF, which decreases the pH of the CSF. A decrease in CSF pH is detected by central chemoreceptors for H+, which instruct the DRG to increase the breathing rate. When the breathing rate increases, more CO2 will be expired and the arterial PCO2 will decrease toward normal.
What are peripheral chemoreceptors?There are peripheral chemoreceptors for O2, CO2, and H+ in the carotid bodies located at the bifurcation of the common carotid arteries and in the aortic bodies above and below the aortic arch. Information about arterial PO2, PCO2, and pH is relayed to the DRG via CN IX and CN X, which orchestrates an appropriate change in breathing rate.
What are Lung stretch receptors.They are mechanoreceptors present in the smooth muscle of the airways. When stimulated by distention of the lungs and airways, mechanoreceptors initiate a reflex decrease in breathing rate called the Hering-Breuer reflex. The reflex decreases breathing rate by prolonging expiratory time.
What are joint and muscle receptors?Mechanoreceptors located in the joints and muscles detect the movement of limbs and instruct the inspiratory center to increase the breathing rate. Information from the joints and muscles is important in the early (anticipatory) ventilatory response to exercise.
What are Irritant receptorsIrritant receptors for noxious chemicals and particles are located between epithelial cells lining the airways. Information from these receptors travels to the medulla via CN X and causes a reflex constriction of bronchial smooth muscle and an increase in breathing rate.
What are J receptors?Juxtacapillary (J) receptors are located in the alveolar walls and, therefore, are near the capillaries. Engorgement of pulmonary capillaries with blood and increases in interstitial fluid volume may activate these receptors and produce an increase in the breathing rate. For example, in left-sided heart failure, blood “backs up” in the pulmonary circulation and J receptors mediate a change in breathing pattern, including rapid shallow breathing and dyspnea (difficulty in breathing).


Question Answer
Give examples of the physical/anatomic defenses of the respiratory tract.Branching of airways, cough (sneeze), mucociliary transport, sol layer, gel layer.
List 4 best-described antimicrobial peptides in the respiratory tract and the mechanism of each.Lysozyme-Produced by respiratory epithelial cells, serous glandular cells, and macrophages→ Lyses bacteria in proximal airways, most active against gram (+) organisms.
Lactoferrin-Produced by serous cells and neutrophils → active in airway fluid→ ations–Agglutinates and kills bacteria–Increases neutrophil adherence–Primes neutrophil superoxide production–Blocks iron from bacterial metabolism.
Defensins- α and β→ α produced by lung neutrophils; β produced by respiratory epithelial cells, Increases cell wall permeability → release of contents→ also destroys the cell membrane potential, Gram (+) and Gram (-) activity, Also present in skin, GI, and reproductive tracts.
Collectins- Surfactant Proteins A and D (SP-A, SP-D)→ Main actions:–Bind to and aggregate microbes–Facilitate interaction with other immune cells–Regulate pulmonary macrophage activity.
List 4 major phagocytic & inflammatory cells of the respiratory tract innate immune system, and describe the role and mechanism and action of each.Pulmonary alveolar macrophages- Mononuclear phagocytic cells – large, mobile→ defend against materials NOT deposited in upper airways. Adhere to alveolar epithelium→ Main actions:–Kill microorganisms (lysosomes in cytoplasm)–Recruit other inflammatory cells (via chemokines). Process huge amounts of inhaled substances without eliciting immune responses outside itself. Contains the infection (or foreign material), but at expense of surrounding tissue.
Polymorphonuclear leukocytes (PMNs)-Defend against established bacterial infections. Normal state – few in small airways and alveoli. Infection – products of complement activation and activated macrophages recruit PMNs to alveolar spaces. Main action→ Phagocytose and kill bacteria. PMN granules contain antimicrobial substances (defensins, lysozyme, lactoferrin); also by products of oxidative metabolism.
Dendritic cells-Airway epithelium, alveolar walls, peribronchial connective tissue. Main actions: –Phagocytose and process antigen, Antigen presentation to T lymphocytes. Initiates adaptive immune response. Sample the airway microenvironment, migrate to lymph nodes, and Ag –presentation occurs there.
Natural Killer (NK) cells (CD16/56)-Defense against viruses and detection of neoplasm. Main action: Identify and kill virus-infected and neoplastic cells
What would happen if you could not cough?Clinical context→ Muscular dystrophy, quadriplegia--> Tracheostomy, vocal cord paralysis.Clinical consequences- Increased respiratory infections, upper and lower.
What would happen if impaired mucociliary transport?Clinical context–Genetic – primary ciliary dyskinesia (PCD); PCD – aka immotile cilia, Kartagener’s syndrome - chronic sinusitis, bronchiectasis,situs inversus. Normal ciliary movement thought to be necessary for correct rotation of the heart and positioning of intraabdominal organs during embryonic development. –Environmental – viral infection*, smoking, general anesthesia, ventilator. Viral infections cause temporary damage to tracheobronchial mucosa – affects ciliary movement – imp mechanism for bacterial superinfection after viral infection. Vent also is a conduit for bacteria into the trachea (colonized or contaminated ET tube or tubing). Clinical consequences. –50% with PCD can have situs inversus (Kartagener’s syndrome). –Recurrent otitis media, chronic sinusitis, chronic bronchitis, bronchiectasis
What would happen with Defense Failure of Phagocytic & Inflammatory cells?Clinical context–Macrophage deficiency – viral infections, smoking, hypoxia, starvation, alcoholism→ Impaired killing–Macrophage deficiency – chronic systemic steroids→ Impaired migration and function–Neutrophil deficiency – leukemia, chemotherapy, congenital → Decreased numbers Neutropenia: incr infxn risk at <1000/mm3 of blood, esp <500/mm3 of blood. Systemic steroids also affects lymphocytes and other aspects of the immune system. Clinical consequences–Macrophage deficiency→ Bacterial bronchitis, pneumonia–Neutropenia→ Bacterial infections, Aspergillus–NK cell deficiency→ Viral infections – especially varicella, other herpesviruses, CMV. Fungal infections more commonly thought if in cellular immune deficiency, but Aspergillus imp resp tract pathogen in n-penia. NK deficiency rare, relatively newly described – quantitative and functional defects. Most cases died in childhood/adolescence
Describe the categories of lung infections that are associated with cellular and humoral immunodeficiencies.Humoral Deficiency–Recurrent bacterial respiratory infections–Bronchiectasis, “normal” bacteria, just more frequent and/or severe. Cellular Deficiency–Infections with intracellular bacteria (mycobacteria)–Fungal, Pneumocystis infections–Viral infections (CMV). Deficiency may be “primary”, or “secondary”– systemic steroids, immunosuppressive drugs, HIV infection. Cellular – opporunistic also
Summarize the humoreal and cellular immune systems in context of the respiratory system.Humoral immune system components in respiratory tract are B cells, T cells, IgG and secretory IgA. IgA in nasopharynx and upper airway .IgG in lower airway. B and T cells are in lymphoid tissues (adenoids, tonsils). Humoral defects = bacterial respiratory infections. Cellular immune defects = intracellular bacteria, fungal, viral infections

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