Respiratory

Question 1

Which parts of the upper respiratory system are characterised by C-shaped cartilagenous rings?

Answer 1

Trachea & principle bronchi (main bronchi).

Question 2

What is the name of the muscle that spans the “gap” in the C-shaped cartilaginous rings of the trachea?

Answer 2

Trachealis muscle.

Weakness in this muscle can lead to tracheal collapse, as is seen more often in certain dog breeds such as the Yorkshire Terrier.

Question 3

What types of cells are located in the epithelium of the trachea and principle bronchi?

Answer 3

Ciliated epithelial cells

Goblet cells

Basal cells

Question 4

What types of cells are located in the bronchioles? Which cells do not exist in the bronchioles?

Answer 4

Clara cells

Ciliated epithelial cells

Basal cells

There are no goblet cells in the bronchioles or further down in the respiratory tract.

Question 5

How do lobar bronchi change their calibre?

Answer 5

Even though lobar bronchi have irregular plates of cartilage around them, they change their calibre by contraction or relaxation of smooth-muscle bands arranged in a spiral.

Question 6

Since lobar bronchi don’t have C-ringed cartilage but rather irregular plates of cartilage and a spiral band of smooth muscle, how do they manage not to collapse?

Answer 6

They are encased in a vascular sheath that keeps them open.

Question 7

Do bronchioles have cartilage, vascular sheath or smooth muscle cells?

Answer 7

Bronchiole walls are lined with smooth-muscle cells. They do not have cartilage or a vascular sheath.

Question 8

What are clara cells? Where are they located and what is their purpose?

Answer 8

Clara cells are located in the bronchioles, in the conducting, terminal & respiratory bronchioles. They can be both ciliated with microvilli & non-ciliated. They secrete anti-adhesive agents that prevent adhesion to the bronchiolar walls that could cause collapse.

One major function is the synthesis and secretion of the material lining the bronchiolar lumen. This material includes glycosaminoglycans, lysozymes, and conjugation of the secretory portion of IgA antibodies. These play an important defensive role, and they also contribute to the degradation of the mucus produced by the upper airways.

Clara cells also act as a stem cell and multiply and differentiate into ciliated cells to regenerate the bronchiolar epithelium.

Question 9

What is the correct order of the tubes through which air enters the respiratory tract?

A. Principle bronchi, lobar bronchi, conducting brochioles, respiratory bronchioles, terminal bronchioles, alveoli

B. Principle bronchi, lobar bronchi, conducting brochioles, terminal bronchioles, respiratory bronchioles, alveoli

C. Principle bronchi, lobar bronchi, respiratory bronchi, terminal bronchioles, alveoli

Answer 9

B. Principle bronchi, lobar bronchi, conducting brochioles, terminal bronchioles, respiratory bronchioles, alveoli

Question 10

What type of cells make up the thin epithelium of the alveolar sacs/alveoli?

Answer 10

Type I & Type II alveolar cells, aka pneumocytes.

Question 11

Histologically, what is the difference between Type I & Type II pneumocytes (aka alveolar cells), and what in particular is important about Type II pneumocytes?

Answer 11

Type II are granular and roughly cuboidal. Type I cells do not appear granular and they are bigger than Type II.

Type II are secrete surfactant for maintaining alveolar spaces and preventing collapse. Surfactant phospholipids are stored in Type II pneumocytes in lamellar bodies, which are specialized vesicles. Release of surfactant in lamellar bodies occurs from an infant’s first breath onwards.

Type II pneumocytes can replicate in the alveoli and will replicate to replace damaged Type I pneumocytes.

Type II pneumocytes are typically found at the alveolar-septal junction. Although they comprise 60% of the alveolar lining cells, because of their shape they cover a much smaller surface area than type I cells

Question 12

What makes up the alveolar septum? Why is it important?

Answer 12

The thick alveolar septum is comprised of collagen & elastic fibres, allowing inflation & deflation of the lung.

In some diseases, there is a buildup of collagen that inhibits inflation or a loss of elastic fibres, which results in not enough recoil.

Eg., Emphysema - a breakdown of the alveolar wall, thus losing gas-exchange surface & elastic-recoil potential as elastic fibres are degraded due to macrophages secreting elastase & collagenase.

Lung Fibrosis: aka “scarring of the lung” - excess fibrous tissue builds up in lungs

Question 13

What muscles are involved in inspiration?

Answer 13

Muscles of diaphragm - contract, move diaphragm caudally to expand thorax

External intercostal muscles - expand ribcage; when they contract, they pull ribs cranially & ventrally to enlarge thoracic cavity

(Accessory) Scalene Muscles - lift first rib & expand chest cavity in some species, pulling sternum cranially

Question 14

Which muscles are engaged in expiration of air in the lungs?

Answer 14

Usually, expiration is a passive event, except in horses, which breath biphasically with passive followed by active phases

Abdominal muscles: rectus abdominis, internal & external obliques & transverse abdominis:

• Pull in/decrease thoracic cavity during exercise & activity; otherwise expiration is passive
• When these contract, pressure inside the abdomen is raised & diaphragm is pushed cranially (ie., it relaxes)
• Contract forcefully during coughing, vomiting & defecation.

Internal intercostal muscles:

• Pull ribs caudally & inward during active expiration, the OPPOSITE of external intercostal muscles, decreasing thoracic volume.
• Stiffen the intercostal spaces to prevent them from bulging outward during straining.

Question 15

What is the importance of surfactant produced by Type II pneumocytes in terms of alveoli?

Answer 15

This ability of alveoli to resist collapse (alveolar collapse = atelectasis) is due to the production of pulmonary surfactant.

The surfactant, a polar phospholipid containing DPPC (dipalmitoyl phosphatidylcholine) holds the alveoli open as the DPPC’s polar heads repel each other. Also, the mix of proteins and lipids are able to form and re-form, avoiding pooling across the alveolar surface.

Thus, surfactant:

1/ increases compliance of the lung & reduces the work of expanding it with each breath

2/ promotes stability of each alveolus

3/ keeps alveoli dry, ie., preventing oedema (fluid/plasma from blood leaking into lung tissue).

Question 16

How does Infant Respiratory Distress Syndrome illustrate the importance of surfactant in the lungs?

Answer 16

Babies, whose lungs don’t produce surfactant, suffer from:

1. atelectasis - alveolar collapse
2. stiff lungs with low compliance
3. alveoli filled with transudate

They can be treated with synthetic surfactant.

Question 17

What is the bronchial circulation?

Answer 17

Bronchial circulation refers to arterial blood that supplies the metabolic needs of tissue of the bronchial tree. Inside the lung, it anastomoses with capillaries of the pulmonary circulation.

Question 18

How does the pulmonary circulation differ from the bronchial circulation?

Answer 18

The pulmonary circulation oxygenates blood in the lungs, then returns that blood via the pulmonary veins into the left atrium, then left ventricle to be pumped out via the aorta into the systemic circulation.

The bronchial circulation starts with fully oxygenated blood directly from the aorta. The blood enters arteries of the bronchial tree, then forms anastomoses with the capillary system of the pulmonary circulation, where it gives up oxygen to the lung tissue.

It returns, partly deoxygenated, via the pulmonary vein to the left atrium. While in the pulmoary vein, it mixes with oxygenated blood.

It also returns, mixed (oxygenated & deoxygenated) via bronchial veins (different from pulmonary veins) & the azygous venous system to the RIGHT ATRIUM.

Question 19

In speaking of the bronchial circulation, what is the common capillary network & “shunt”?

Answer 19

The common capillary network refers to the capillary beds of respiratory bronchioles that are shared by arteries of both the pulmonary & bronchial systems.

The “shunt” refers to blood that enters the arterial system without going through ventilated areas of the lung. The partly deoxygenated blood, after perfusing the lung tissue, returns back to the left side of the heart via the pulmonary veins, without having to go through the alveolar system, then pumped out again through the aorta. This blood is mixed with the oxygenated blood of the pulmonary veins before it enters the heart.

Shunt is helpful, for example, if there is an obstruction in the pulmonary artery that conveys venous blood to the lungs. Some of the oxygenated blood from the bronchial circulation (oxygenated via anastomoses with pulmonary capillaries) can be returned to the left atrium.

Question 20

What is the typical PO₂ of inspired air (atmospheric air)?

Answer 20

150 mmHg

Question 21

Typically, the PCO₂ of inspired air (atmospheric air)

Answer 21

0 mmHg

Question 22

What is the PO₂ & PCO₂ of deoxygenated blood pumped through the pulmonary arteries down to the lungs and alveoli?

Answer 22

PO₂ = 40 mm Hg

PCO₂ = 45 mm Hg

Question 23

What are the PO₂ & PCO₂ of oxygenated blood returning to the heart to be pumped out of the aorta?

Answer 23

PO₂ = 100 mm Hg

PCO₂ = 40 mm Hg

Question 24

Which group of respiratory neurons in the brain’s medulla are responsible for controlling inspiration?

Answer 24

DRG - dorsal respiratory group

• cause contraction of the diaphragm, opening of the chest cavity & allowing air to come in, thorax becomes subatmospheric.
• driven by apneustic centre & causes inspiration
• DRG will continue to fire if there are no negative signals stopping it

Question 25

The DRG (dorsal respiratory group) will continue to fire, causing more inspiration, unless it receives a “stop” signal. Where does that signal come from?

Answer 25

**Pneumotaxic Centre **

aka

Pontine Respiratory Group (PRG)

Question 26

What is the role in breathing of the Apneustic Centre in the lower pons?

Answer 26

• sends signals to DRG to delay the ‘switch off’ signal of the inspiratory ramp provided by the pneumotaxic center
• effect is to ⬆breathing (ie., delays negative feedback to dial down DRG inspiration)
• controls the intensity of breathing
• inhibited by pulmonary stretch receptors. However, it gives positive impulses to the inspiratory (I) neurons.

Question 27

What is the role in breathing of the Pneumotaxic Centre aka Pontine Respiratory Group (PRG)?

Answer 27

Located in the in the rostral-dorsal-lateral pons, the PRG:

- cyclically ⬇ inspiration

• antagonises the apneustic centre
• switches off DRG “inspiratory ramp”, causing deflation of lung & letting air to move out
• alters the bursting pattern of the dorsal respiratory group.

When we find ourselves needing to breath faster, the pneumotaxic area tells the dorsal respiratory group to speed it up. And when we need to take longer breaths, the pneumotaxic area tells the dorsal respiratory group to prolong its bursts. All the information from the body that needs to feed into the control of our breathing converges in the pneumotaxic area, so that it can properly adjust our breathing.
- receives signals from chemoreceptors

Question 28

What is the role in breathing of the **Ventral Respiratory Group (VRG)? **

Answer 28

VRG kicks in during exercise and heavier breathing, mainly involved in expiration, some inspiration.

The VRG is an expiratory centre, while the DRG is an inspiratory centre.

Question 29

What are the two main groups of chemoreceptors in the body that detect oxygen & carbon-dioxide levels in the blood, thus affecting the respiratory centres to induce greater or lesser gas exchange?

Answer 29

Central chemoreceptors:

• ventral surface of medulla near exit of CN 9 & CN 10
• detect changes in CO₂ in blood in brain indirectly by detecting H⁺
• since there is no Hb in the blood in the brain to take up (buffer) H⁺, then H⁺ & bicarbonate ions will be present due to the dissociation of carbonic acid formed initially by CO₂ & H₂O
• very sensitive to changes in CO₂ that diffuses across BBB
• stimulates ventilation
• ⬇ & ⬆ breathing

Peripheral chemoreptors:

• aortic & carotid bodies (in & off the aortic arch)
• detect O₂ levels directly in arterial blood but ONLY LARGE DECREASES of O₂
• aortic bodies: contained in the walls of the aorta - induce reflex ⬆ breathing
• carotid bodies: contained in the carotid sinus, a small swelling of nerve fibres where the carotid artery branches into the internal & external carotid arteries
• not as important as central chemoreceptors

Question 30

What are the FOUR TYPES of respiratory neurons IN THE LUNGS that send signals to the brain’s respiratory centre?

Answer 30

1. Pulmonary Stretch Receptors
2. Irritant Receptors
3. J-Receptors (“juxtacapillary receptors”)
4. Bronchial C-fibres

Question 31

What are pulmonary stretch receptors & what is their role in regulating breathing?

Answer 31

Pulmonary stretch receptors are mechanoreceptors, also known as one of the “Slowly Adapting Receptors”

• When the lung expands, the receptors initiate the Hering-Breuer reflex, which **⬇ respiratory rate **(Hering-Breuer inflation reflex is triggered to prevent over-inflation of lungs)
• ⬆ firing = ⬆ production of pulmonary surfactant (to reduce risk of atelectasis)
• Intercostal muscles and diaphragm receive impulses from respiratory centre → pulmonary stretch receptors send impulses to the respiratory centre giving information about the state of the lungs → respiratory rate decreased

- signals travel via vagus nerve

Question 32

What are “Irritant receptors” & what is their role in regulation of breathing?

Answer 32

Irritant Receptors in the lungs are one of the “Rapidly Adapting Receptors”

• they sense noxious particles
• induce COUGH response to move air out of lungs faster

Question 33

What are **J-Receptors **

aka

Juxtacapillary Receptors?

What is their role in regulation of respiration?

Answer 33

• present in the alveolar interstitium
• innervated by fibers of the vagus nerve
• respond to events such as pulmonary edema, pulmonary emboli, pneumonia, congestive heart failure and barotrauma, which cause a decrease in
  oxygenation
• detect decrease in oxygen, thus lead to an increase in ventilation/respiration

- stimulation causes a reflex ⬆in breathing rate

Question 34

What are Bronchial C-fibres & what is their role in regulating respiration?

Answer 34

-non-myelinated nerve fibres with endings in the lungs that when stimulated along with myelinated irritant receptors lead to COUGH reflex

Question 35

What happens with chemoreceptors and the respiratory centre in the brain to correct hypoventilation?

Answer 35

⬆CO₂ & ⬇ in pH (lower [H+]) sensed by central chemoreceptors in brain

⬇O₂ sensed by peripheral chemoreceptors

Chemoreceptors send signal to ⬇ pneumotaxic centre “stop” signalling to DRG

⬆ DRG inspiration ramp

Chemoreceptors send signal to ⬆ apneustic centre “delay wind-down” signalling to DRG

⬆ ****DRG inspiration ramp

Question 36

What happens with chemoreceptors and the respiratory centre in the brain to correct hyperventilation?

Answer 36

⬇CO2 & ⬆ in pH (lower [H+]) sensed by central chemoreceptors in brain

send signal to ⬆ pneumotaxic centre to ⬇ DRG’s inspiration ramp

inhibits apneustic centre

DRG ⬇ inspiration

Question 37

What is the respiratory reflex during haemhorrhage?

Answer 37

⬇ Red Blood Cells

↓

⬇ O2-carrying capacity of blood

&

⬇ Blood flow in carotid and aortic bodies
↓
Anemia, Hypoxia, Acidosis
↓
⬆ chemoreceptors
↓
⬆ Respiration (medullary respiratory neurons)

&

⬆ Vasoconstrictor discharge (vasomotor centre)

Question 38

How is breathing during exercise controlled?

Answer 38

During moderate exercise, ventilation increases in proportion to metabolic production of carbon dioxide.

During strenuous exercise, ventilation increases more than needed, to compensate for carbon dioxide production. Ie., Increased glycolysis facilitates release of protons from ATP and metabolites lower pH, and thus more oxygen intake is necessary via increased breathing.

Question 39

How does an increase in carbon dioxide in the blood lead to acidosis?

Answer 39

Levels of CO₂ rise in the blood when the metabolic use of O₂ is increased beyond the capacity of the lungs to expel CO₂.

CO₂ is stored largely in the blood as bicarbonate HCO₃^- ions, by conversion first with water to carbonic acid (H₂CO₃), by the enzyme carbonic anhydrase, and then by disassociation of this acid to H⁺ and HCO₃^-.

Build-up of CO₂ therefore causes an equivalent build-up of the disassociated hydrogen ion, which, by definition, decreases the pH of the blood.

Question 40

What percentage of oxygen is transported from the lungs to the body’s tissues by haemoglobin (Hb) on red blood cells?

Answer 40

97%

• only 3% is dissolved in fluid (plasma / cytosol)

Question 41

What is the maximum amount of oxygen in mL that can combine with per gram haemoglobin in the blood?

Answer 41

About 1.34ml oxygen / g of Hb

• The average human has 15g Hb / 100ml blood, therefore 15 x 1.34 = 20.1ml O2/100ml blood.

May be expressed as “20 volumes per cent” of total oxygen in body is bound to haemoglobin.

Question 42

What is Carboxyhaemoglobin?

Answer 42

Binding of Hb with carbon monoxide.

Hb is a buffer for CO₂ & hydrogen protons