2. What is substrate level phosphorylation? 

3. How does oxidation of metabolites of glycolysis drive ATP formation? 
4. How does ATP drive metabolic reactions of glycolysis forward? 

5. How does anaerobic and aerobic glycosylation differ with respect to replenishing NAD+? 

2. How are i) pyruvate ii) amino acids and iii) lactate used to produce glucose during gluconeogenesis? 

3. What is meant by reciprocal regulation of gluconeogenesis? 

- Infection makes you sick and can be spread.
What is meant by active TB?
- Bacteria is walled off within the body, you have no symptoms and cannot spread the disease, 
Outline the epidemiology of TB in respect to: 1. distribution (numbers affected, who, when where) 2. determinates (why, how) and the treatment and prevention. 
What type of TB does Miriam have. How do we know this?
Active TB 

2. a) What are the 2 anatomical / functional portions of the respiratory tract? (not clinical: upper and lower respiratory tracts) 

b) Which components of the respiratory tract fall into which portion? 

3. Follow the “Day in the life of an oxygen molecule” to outline route of air (in lecture) 

2. What are the cell types found in the intra-alveolar septum and what is the function of each cell type? 

b. How do the general structures link to the function? 

2. a. What is the function of the respiratory portions of the respiratory tract? 

b. How do the general structures link to the function? 

2. a. How do the left and right lungs differ? (Fissures, lobes, size etc.) 

b. Why are the left and right lungs different sizes? 
3. Where do they lie? a. What ribs levels are they found between?
b. What is below them?
c. What is between them? 
4. What covers them? 
5. Can you draw a labelled diagram of the hilum of the lungs? 6. What is difference between the root and the hilum of the lungs? 

2. Where is the pleural fluid? 

3. What secretes the pleural fluid? 

4. a) What are the regions or potential spaces that the lungs can expand into during inhalation called? 

b) Where are they deepest? 

2. How are oxygen and carbon dioxide movements affected by changes in partial pressure gradients in pulmonary gas exchange and tissue gas exchange? 

3. What is ventilation-perfusion matching? 

4. What are the factors that influence the rate of gas transfer across the alveolar membrane? 

5. What are the ways in which oxygen is transported in blood and explain how it is loaded and unloaded 

6. What are the ways in which carbon dioxide is transported in blood, and outline what happens in the reversible reaction that converts carbon dioxide and water to carbonic acid. 

7. Outline the oxygen-haemoglobin saturation curve. (details covered in Biochemistry) 

8. What are the factors that affect the haemoglobin saturation? How do these factors affect saturation and what is their effect on the Oxygen-Haemoglobin Saturation curve? 

9. What is the relationship between CO2, blood pH and ventilation? 

10. Explain the effect of hyperventilation and hypoventilation on blood pH 

11. Explain the respiratory reflex initiated in response to an increase in pCO2 

12. Explain the respiratory reflex initiated in response to a decrease in pCO2 

13. What are some of the physical factors that influence respiratory rate? 

2. How does a dendritic cell promote CD4 T cells to launch an antigen specific response? What are the roles of MHCII, TCR, CD28, B7-1? 

3. How do cytokines from APC influence CD4 T cell function? 

4. How do cytokines from CD4 T cells influence innate immune cell function? 

5. What cytokines are likely tohelp control a TB infection? Students could look up IFNg, TNF, IL-12. 

In forced inspiration:

In expiration, the opposite of inspiration occurs. The thoracic cavity volume decreases, causes decreased lung volume and hence increased intra-alveolar pressure. The increased pressure rises above atmospheric pressure and the air flows out of the lungs along the pressure gradient. There are two types of expiration: passive and active. 

In passive expiration:

In active expiration:

This is the most basic control. Pacemaker cells in medulla oblongata generate cycles of contractions in diaphragm. The rhythmicity centres establish pace of respiration by adjusting pacemaker cells and coordinating other respiratory muscles. Each centre is divided into two groups: the ventral respiratory group (VRG) and dorsal respiratory group (DRG).

-          Dorsal respiratory group 

It is located primarily in the medulla. The group receives input from peripheral chemoreceptor, baroreceptors and receptors in the lungs.

It controls basis rhythm of respiration (even in absence of sensory or regulatory stimuli) and inspiratory muscles, contains an inspiratory centre, functions in quiet and forced breathing and sets the basic drive if ventilation.

-          Ventral respiratory group 

Located in ventral medulla. It contains both respiratory and expiratory neurons, functions during forced breathing, inactive during normal quiet breathing and activates accessory muscles involved in inspiration and expiration.

-          Pre-botzinger complex

Located in the medulla. It is poorly understood but is essential to all forms of breathing and generates respiratory rhythm. Neurons project to DRG and modulates rate at which DRG neurons rhythmically fire.

These are paired nuclei in pons that adjust the output of the respiratory rhythmicity centre

-          Apneustic centre 

Neurons project to DRG and increase duration of inspiratory signals: Increases duration of diaphragmatic contraction, more complete lung filling and decreased breathing rate.

-          Pneumotaxic centre 

Neurons project to DRG and inhibit inspiration which limits size of tidal volume (amount of air inspired or expired during normal quiet ventilation) therefore increasing rate of respiration

Located in the hypothalamus, limbic system and cerebral cortex. It can alter activity of the pneumotaxic centres (normal breathing can occur with higher input). 

 

 

 

 

 

 

 

Importance of gluconeogenesis:

A precursor is a compound that is transformed into another. Precursors of gluconeogenesis are compounds that can be transformed into substrates or intermediates of the gluconeogenic pathway. An intermediate is a compound that occurs in the pathway between the starting materials and the end-products of the pathway. Glucogenic compounds produce:

Precursors for gluconeogenesis:

Glucogenic amino acids:

Lactate is a precursor for gluconeogenesis. It is used in the Cori cycle, which is the combination of anaerobic glycolysis in muscle transporting lactate to the liver for use in gluconeogenesis and transporting the glucose back for anaerobic glycolysis, using the blood as a transport medium.

Process of gluconeogenesis:

Gluconeogenesis occurs in the mitochondria and in the cytosol. The three irreversible steps (of glycolysis) are bypassed in gluconeogenesis, but the other 7 reversible steps use the same enzyme for both pathways. Gluconeogenesis requires the use of ATP to bypass the irreversible steps of glycolysis. Pyruvate is converted to oxaloacetate, which is converted to phosphoenolpyruvate. This conversion uses 4 ATP (2x ATP + 2x GTP). The PEP follows glycolysis in reverse. The step of conversion of 3-phosphoglycerate to 1,3-bisphosphoglycerate (I.e. formation of a high energy compound) uses up 2ATP. From there it is essentially the reverse of glycolysis.

Oxygen is carried in the blood by haemoglobin (98%) and small amount is dissolved in plasma (2%)

-          Haemoglobin- irons in the molecule bind oxygen. One molecule binds 4 O₂ atoms. The oxygen-haemoglobin combination is called Oxyhaemoglobin (HbO₂) and reduced haemoglobin/deoxyhaemoglobin (HHb) is haemoglobin that released O₂.  The protein binds and releases oxygen by two reactions: loading and unloading.

-          Loading- Oxygen from alveoli binds to Hb in the capillaries which converts deoxyhaemoglobin to oxyhaemoglobin. Oxygen rich blood then moves to the left side of the heart and is pumped to systemic circulation. Reaction is favoured when there is a higher blood PO₂.

-          Unloading- Hb in system circulation releases oxygen to cells and oxygen-poor blood returns to the right side of the heart to the lungs. Favoured when PCO₂ is low.

CO₂ is transported by dissolving in plasma (7-10%), as bicarbonate ions (70%) and bound to Hb (20%) binds to polypeptide chain forming carbaminohaemoglobin.

-          CO₂ diffuses into red blood cells and combine with H₂0 to form H₂CO₃ (carbonic acid) which dissociates into H+ (buffered by Hb) and HCO₃- which is more soluble than CO₂

 

 

-          Systemic capillary- HCO₃- dissolves into blood plasma (chloride moves in) while H+ bind to Hb.

-          Pulmonary capillary- Carbonic acid is re-formed and converted into water and CO₂ that can then diffuse into alveoli.

 

-          Carbonic acid-bicarbonate buffer system resist shifts in blood pH. HCO₃- acts as the alkaline reserve part of the system. If [H+] increases the excess is removed by combining with bicarbonate ion to form carbonic acid. If [H+] decreases carbonic acid dissociates releasing H+ and lowering pH.

-          The rate and depth of breathing alters blood carbonic acid levels (causes blood pH change). Hyper and hypo ventilation can quickly alter changes in pH.

-          Hyperventilation- increase in rate and depth of breathing, CO₂ is exhaled and PCO₂ decreases meaning that less carbonic acid is formed and fewer H+ ions are formed resulting in a rise in pH (more basic). More oxygen may be dissolved.

-          Hypoventilation- decrease in the rate and/ depth of breathing, increase in PCO₂ (less is exhaled). More carbonic acid and hydrogen ions are formed resulting in the blood being more acidic. Oxygen level drops- hypoxemia.

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