Physiology - Aston University an der Aston University | Karteikarten & Zusammenfassungen

Lernmaterialien für Physiology - Aston University an der Aston University

Greife auf kostenlose Karteikarten, Zusammenfassungen, Übungsaufgaben und Altklausuren für deinen Physiology - Aston University Kurs an der Aston University zu.

TESTE DEIN WISSEN

Learn this

Lösung anzeigen
TESTE DEIN WISSEN

Apnea: Transient cessation of breathing

Asphyxia: O2 starvation of tissues, caused by a lack of O2 in the air, respiratory impairment, or inability of the tissues to use O2

Cyanosis: Blueness of the skin resulting from insufficiently oxygenated blood in the arteries 

Dyspnea: Difficult or labored breathing

Eupnea: Normal breathing

Hypercapnia: Excess CO2 in the arterial blood

Hyperpnea: Increased pulmonary ventilation that matches increased metabolic demands, as in exercise

Hyperventilation: Increased pulmonary ventilation in excess of metabolic requirements, resulting in decreased PCOand respiratory alkalosis

Hypocapnia: Below-normal CO2 in the arterial blood

Hypoventilation: Underventilation in relation to metabolic requirements, resulting in increased PCOand respiratory acidosis

Hypoxia: Insufficient O2 at the cellular level

Anemic hypoxia: Reduced O2-carrying capacity of the blood

Circulatory hypoxia: Too little oxygenated blood delivered to the tissues; also known as stagnant hypoxia

Histotoxic hypoxia: Inability of the cells to use available O2

Hypoxic hypoxia: Low arterial blood PO2 accompanied by inadequate Hb saturation

Respiratory arrest: Permanent cessation of breathing (unless clinically corrected)

Suffocation: O2 deprivation as a result of an inability to breathe oxygenated air. 
Lösung ausblenden
TESTE DEIN WISSEN
Tell how the magnitude of ventilation is regulated under resting conditions. 
Lösung anzeigen
TESTE DEIN WISSEN

The major mechanism controlling ventilation under resting conditions is specifically aimed at regulating the brain-ECF H1 con-centration, which in turn directly reflects changes in arterial PCO2 because CO2 that enters the brain ECF generates H1 to which the central
chemoreceptors are highly responsive. The central chemoreceptors adjust ventilation accordingly to keep the brain-ECF H1 and thus arterial PCO2 normal.

Lösung ausblenden
TESTE DEIN WISSEN

State the functions of Type I alveolar cells, Type II alveolar cells, and alveolar macrophages.

Lösung anzeigen
TESTE DEIN WISSEN

Type I alveolar cells form the walls of the alveoli,
Type II alveolar cells secrete pulmonary surfactant,
and wandering alveolar macrophages are phagocytic specialists that scavenge within the lumen of the alveoli.

Lösung ausblenden
TESTE DEIN WISSEN

Compare the muscles involved, the intra-alveolar pressure changes, and the air movement that takes place during normal quiet breathing and breathing during strenuous exercise.

Lösung anzeigen
TESTE DEIN WISSEN

During normal quiet breathing, the diaphragm and external intercostal muscles contract during inspiration, expanding the chest wall and thoracic cavity. The lungs passively follow along, with the intra-alveolar pressure dropping from 760 to 759 mm Hg as the lungs enlarge. Air moves into the lungs down its pressure gradient from the atmosphere until the intra-alveolar pressure equilibrates with the atmospheric pressure of 760 mm Hg. When these inspiratory muscles relax, the chest and lungs passively recoil to their preinspiratory size, increasing the intra-alveolar pressure to 761 mm Hg. Air moves out of the lungs down its pressure gradient to the atmosphere as a passive expiration occurs. During strenuous exercise, the diaphragm and external intercostal muscles contract more vigorously and the accessory inspiratory muscles (muscles in the neck) come into play to expand the chest and lungs even more than during quiet breathing. During this forceful inspiration, the intra-alveolar pressure drops even farther, for example to 758 mm Hg, so more air flows into the lungs before equilibration with atmospheric pressure is achieved. During active, or forced, expiration, the inspiratory muscles relax and the expiratory muscles (the abdominal muscles and the internal intercostal muscles) contract to reduce the volume of the chest even more than during passive expiration, allowing the lungs to recoil to a greater extent. As a result, the intra-alveolar pressure increases even more than during quiet breathing, for example to 762 mm Hg, so more air leaves the lungs before equilibrating with atmospheric pressure.


Lösung ausblenden
TESTE DEIN WISSEN

Define compliance and elastic recoil. 

Lösung anzeigen
TESTE DEIN WISSEN

Compliance is a measure of how much effort is required to stretch the lungs; specifically, it is a measure of the change in lung volume resulting from a given change in the transmural pressure gradient.
Elastic recoil refers to how readily the lungs rebound after having been stretched. 

Lösung ausblenden
TESTE DEIN WISSEN

Discuss the effect of hypoventilation and of hyperventilation on acid–base balance

Lösung anzeigen
TESTE DEIN WISSEN

Hypoventilation results in accumulation of CO2 because less CO2 is blown off to the atmosphere than is produced. Because CO2 generates acid, the excess H1 leads to respiratory acidosis. Hyperventilation leads to a reduction in CO2 because CO2 is blown off more rapidly than it is produced. As a result, less H1 is generated from CO2 than normal, leading to respiratory alkalosis.

Lösung ausblenden
TESTE DEIN WISSEN

State the forces that keep the alveoli open and those that promote alveolar collapse.

Lösung anzeigen
TESTE DEIN WISSEN

The forces that keep the alveoli open are the transmural pressure gradient and pulmonary surfactant (which opposes alveolar surface tension), and the forces that promote alveolar collapse are elastic recoil and alveolar surface tension.

Lösung ausblenden
TESTE DEIN WISSEN

Define partial pressure. 

Lösung anzeigen
TESTE DEIN WISSEN

Partial pressure is the individual pressure exerted independently by a particular gas within a mixture of gases.

Lösung ausblenden
TESTE DEIN WISSEN

Discuss how the alveolar air–pulmonary blood interface is ideally structured for gas exchange.

Lösung anzeigen
TESTE DEIN WISSEN

Only 0.5 µm separates the air in the alveoli from the blood in the pulmonary capillaries, and the alveolar air–blood interface presents a tremendous surface area (75 m2) for exchange. The thinness and extensive surface area of the alveolar membrane facilitate gas exchange because the rate of diffusion is inversely proportional to the thickness and directly proportional to the surface area of this interface.

Lösung ausblenden
TESTE DEIN WISSEN

List the steps of external respiration accomplished by the respiratory system and those carried out by the circulatory system.

Lösung anzeigen
TESTE DEIN WISSEN

1) ventilation or gas exchange between the atmosphere and alveoli in the lungs,
(2) exchange of O2 and CO2 between air in the alveoli and blood in the pulmonary capillaries,
(3) transport of O2 and CO2 in the blood between the lungs and the tissues, and
(4) exchange of O2 and CO2 between the blood in the systemic capillaries and the tissue cells.
The respiratory system is involved in steps 1 and 2; the circulatory system is involved in steps 2, 3, and 4.


Lösung ausblenden
TESTE DEIN WISSEN

Briefly describe how the following brain regions contribute to control of respiration: the medullary respiratory center (including the roles of the DRG and VRG), the pneumotaxic center, the apneustic center, and the pre-Bötzinger complex.

Lösung anzeigen
TESTE DEIN WISSEN

The medullary respiratory center is the primary respiratory control center. It contains the dorsal respiratory group (DRG) and ventral respiratory group (VRG).
The DRG consists mostly of inspiratory neurons that alternately fire to cause inspiration and cease firing to bring about expiration during quiet breathing.
The VRG is composed of inspiratory neurons and expiratory neurons that remain inactive during quiet breathing but are called into play by the DRG as an overdrive mechanism to cause forceful inspiration and active expiration during periods when demands for ventilation are increased.
The pneumotaxic center in the pons helps switch off the DRG inspiratory neurons, and the apneustic center in the pons prevents these inspiratory 

neurons from being switched off, in a check-and-balance system. 
The pre-Bötzinger complex generates the basic respiratory rhythm and drives the rhythmic firing of the DRG inspiratory neurons. 
Lösung ausblenden
TESTE DEIN WISSEN

Discuss the role of the peripheral chemoreceptors. 

Lösung anzeigen
TESTE DEIN WISSEN

The peripheral chemoreceptors are stimulated when the arterial POfalls to the point of being life threatening (<60 mm Hg). In turn, they stimulate the medullary inspiratory neurons as an emergency mechanism to maintain ventilation during a time when such a low arterial POdirectly depresses the respiratory center. The peripheral chemoreceptors are also responsive to changes in arterial H1 concentration and adjust ventilation accordingly to help maintain acid–base balance by altering the rate at which H1-generating CO2 is eliminated from the body. The peripheral chemoreceptors are weakly stimulated by increased arterial PCO2

Lösung ausblenden
  • 751 Karteikarten
  • 115 Studierende
  • 3 Lernmaterialien

Beispielhafte Karteikarten für deinen Physiology - Aston University Kurs an der Aston University - von Kommilitonen auf StudySmarter erstellt!

Q:

Learn this

A:

Apnea: Transient cessation of breathing

Asphyxia: O2 starvation of tissues, caused by a lack of O2 in the air, respiratory impairment, or inability of the tissues to use O2

Cyanosis: Blueness of the skin resulting from insufficiently oxygenated blood in the arteries 

Dyspnea: Difficult or labored breathing

Eupnea: Normal breathing

Hypercapnia: Excess CO2 in the arterial blood

Hyperpnea: Increased pulmonary ventilation that matches increased metabolic demands, as in exercise

Hyperventilation: Increased pulmonary ventilation in excess of metabolic requirements, resulting in decreased PCOand respiratory alkalosis

Hypocapnia: Below-normal CO2 in the arterial blood

Hypoventilation: Underventilation in relation to metabolic requirements, resulting in increased PCOand respiratory acidosis

Hypoxia: Insufficient O2 at the cellular level

Anemic hypoxia: Reduced O2-carrying capacity of the blood

Circulatory hypoxia: Too little oxygenated blood delivered to the tissues; also known as stagnant hypoxia

Histotoxic hypoxia: Inability of the cells to use available O2

Hypoxic hypoxia: Low arterial blood PO2 accompanied by inadequate Hb saturation

Respiratory arrest: Permanent cessation of breathing (unless clinically corrected)

Suffocation: O2 deprivation as a result of an inability to breathe oxygenated air. 
Q:
Tell how the magnitude of ventilation is regulated under resting conditions. 
A:

The major mechanism controlling ventilation under resting conditions is specifically aimed at regulating the brain-ECF H1 con-centration, which in turn directly reflects changes in arterial PCO2 because CO2 that enters the brain ECF generates H1 to which the central
chemoreceptors are highly responsive. The central chemoreceptors adjust ventilation accordingly to keep the brain-ECF H1 and thus arterial PCO2 normal.

Q:

State the functions of Type I alveolar cells, Type II alveolar cells, and alveolar macrophages.

A:

Type I alveolar cells form the walls of the alveoli,
Type II alveolar cells secrete pulmonary surfactant,
and wandering alveolar macrophages are phagocytic specialists that scavenge within the lumen of the alveoli.

Q:

Compare the muscles involved, the intra-alveolar pressure changes, and the air movement that takes place during normal quiet breathing and breathing during strenuous exercise.

A:

During normal quiet breathing, the diaphragm and external intercostal muscles contract during inspiration, expanding the chest wall and thoracic cavity. The lungs passively follow along, with the intra-alveolar pressure dropping from 760 to 759 mm Hg as the lungs enlarge. Air moves into the lungs down its pressure gradient from the atmosphere until the intra-alveolar pressure equilibrates with the atmospheric pressure of 760 mm Hg. When these inspiratory muscles relax, the chest and lungs passively recoil to their preinspiratory size, increasing the intra-alveolar pressure to 761 mm Hg. Air moves out of the lungs down its pressure gradient to the atmosphere as a passive expiration occurs. During strenuous exercise, the diaphragm and external intercostal muscles contract more vigorously and the accessory inspiratory muscles (muscles in the neck) come into play to expand the chest and lungs even more than during quiet breathing. During this forceful inspiration, the intra-alveolar pressure drops even farther, for example to 758 mm Hg, so more air flows into the lungs before equilibration with atmospheric pressure is achieved. During active, or forced, expiration, the inspiratory muscles relax and the expiratory muscles (the abdominal muscles and the internal intercostal muscles) contract to reduce the volume of the chest even more than during passive expiration, allowing the lungs to recoil to a greater extent. As a result, the intra-alveolar pressure increases even more than during quiet breathing, for example to 762 mm Hg, so more air leaves the lungs before equilibrating with atmospheric pressure.


Q:

Define compliance and elastic recoil. 

A:

Compliance is a measure of how much effort is required to stretch the lungs; specifically, it is a measure of the change in lung volume resulting from a given change in the transmural pressure gradient.
Elastic recoil refers to how readily the lungs rebound after having been stretched. 

Mehr Karteikarten anzeigen
Q:

Discuss the effect of hypoventilation and of hyperventilation on acid–base balance

A:

Hypoventilation results in accumulation of CO2 because less CO2 is blown off to the atmosphere than is produced. Because CO2 generates acid, the excess H1 leads to respiratory acidosis. Hyperventilation leads to a reduction in CO2 because CO2 is blown off more rapidly than it is produced. As a result, less H1 is generated from CO2 than normal, leading to respiratory alkalosis.

Q:

State the forces that keep the alveoli open and those that promote alveolar collapse.

A:

The forces that keep the alveoli open are the transmural pressure gradient and pulmonary surfactant (which opposes alveolar surface tension), and the forces that promote alveolar collapse are elastic recoil and alveolar surface tension.

Q:

Define partial pressure. 

A:

Partial pressure is the individual pressure exerted independently by a particular gas within a mixture of gases.

Q:

Discuss how the alveolar air–pulmonary blood interface is ideally structured for gas exchange.

A:

Only 0.5 µm separates the air in the alveoli from the blood in the pulmonary capillaries, and the alveolar air–blood interface presents a tremendous surface area (75 m2) for exchange. The thinness and extensive surface area of the alveolar membrane facilitate gas exchange because the rate of diffusion is inversely proportional to the thickness and directly proportional to the surface area of this interface.

Q:

List the steps of external respiration accomplished by the respiratory system and those carried out by the circulatory system.

A:

1) ventilation or gas exchange between the atmosphere and alveoli in the lungs,
(2) exchange of O2 and CO2 between air in the alveoli and blood in the pulmonary capillaries,
(3) transport of O2 and CO2 in the blood between the lungs and the tissues, and
(4) exchange of O2 and CO2 between the blood in the systemic capillaries and the tissue cells.
The respiratory system is involved in steps 1 and 2; the circulatory system is involved in steps 2, 3, and 4.


Q:

Briefly describe how the following brain regions contribute to control of respiration: the medullary respiratory center (including the roles of the DRG and VRG), the pneumotaxic center, the apneustic center, and the pre-Bötzinger complex.

A:

The medullary respiratory center is the primary respiratory control center. It contains the dorsal respiratory group (DRG) and ventral respiratory group (VRG).
The DRG consists mostly of inspiratory neurons that alternately fire to cause inspiration and cease firing to bring about expiration during quiet breathing.
The VRG is composed of inspiratory neurons and expiratory neurons that remain inactive during quiet breathing but are called into play by the DRG as an overdrive mechanism to cause forceful inspiration and active expiration during periods when demands for ventilation are increased.
The pneumotaxic center in the pons helps switch off the DRG inspiratory neurons, and the apneustic center in the pons prevents these inspiratory 

neurons from being switched off, in a check-and-balance system. 
The pre-Bötzinger complex generates the basic respiratory rhythm and drives the rhythmic firing of the DRG inspiratory neurons. 
Q:

Discuss the role of the peripheral chemoreceptors. 

A:

The peripheral chemoreceptors are stimulated when the arterial POfalls to the point of being life threatening (<60 mm Hg). In turn, they stimulate the medullary inspiratory neurons as an emergency mechanism to maintain ventilation during a time when such a low arterial POdirectly depresses the respiratory center. The peripheral chemoreceptors are also responsive to changes in arterial H1 concentration and adjust ventilation accordingly to help maintain acid–base balance by altering the rate at which H1-generating CO2 is eliminated from the body. The peripheral chemoreceptors are weakly stimulated by increased arterial PCO2

Physiology - Aston University

Erstelle und finde Lernmaterialien auf StudySmarter.

Greife kostenlos auf tausende geteilte Karteikarten, Zusammenfassungen, Altklausuren und mehr zu.

Jetzt loslegen

Das sind die beliebtesten Physiology - Aston University Kurse im gesamten StudySmarter Universum

Microbiology - Aston University

Aston University

Zum Kurs
Physiology

University of Southampton

Zum Kurs
PHYSIOLOGY

Monash University, Malaysia Campus

Zum Kurs
Physiology

University of Cape Town

Zum Kurs
Physiology

Silliman University

Zum Kurs

Die all-in-one Lernapp für Studierende

Greife auf Millionen geteilter Lernmaterialien der StudySmarter Community zu
Kostenlos anmelden Physiology - Aston University
Erstelle Karteikarten und Zusammenfassungen mit den StudySmarter Tools
Kostenlos loslegen Physiology - Aston University