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Confidentiality
"The  nurse  refuses  to disclose any medical information without Miriam’s consent."

Confidentiality is a legal right that a physician or other health professional will hold secret all information relating to a patient, unless the patient gives consent permitting disclosure.
We think that the nurse did the correct thing and the first step to be taken before sharing information is getting consent from the patient unless in cases that if the information is withheld it will put other people's health at risk.

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Stigma

Stigma is defined as “the identification and recognition of a bad or negative characteristic in a person or group of persons, and treating them with less respect or worth than they deserve due to this characteristic.” Stigmatization often results in prejudice, discrimination and rejection. It is often associated with shame and disgrace, and the media help promote this stigma.

Much of the TB stigma is associated with poor living conditions and 'lower class' people. TB is also associated with HIV as the disease is so prevalent in HIV+ (immunocompromised) patients. The stigmatized are often ostracized, rejected or shunned from society. The stigma of a disease can have a negative effect on the self-esteem of that person and their willingness to seek help or engage in health promoting activity.

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Oxygen transport

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.

Carbon dioxide transport

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.

Carbon dioxide, blood pH and ventilation

-          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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Control TB

Prevent TB transmission from infected patients (e.g. health workers wearing masks)

Teach coughing hygiene (coughing into your arm)

Good ventilation

Good amount of sunlight

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Gluconeogenesis

Production of glucose from non-carbohydrate sources

Different from glycogenolysis which breaks down glycogen but does not synthesis glucose from new sources.

Importance of gluconeogenesis:

Some tissues rely solely of glucose for energy

Changing metabolic state – feed-fast states of metabolism

Limited glycogen stores in the body

Maintenance of blood glucose level during fasting conditions.

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:

Glycolytic pathway intermediates

Citric acid cycle intermediates

Precursors for gluconeogenesis:

Glucogenic amino acids (muscle proteins) – alanine and other amino acids

Lactate (anaerobic glycolysis)

Glycerol (from triacylglycerols)

Pyruvate

Oxaloacetate

Glucogenic amino acids:

Amino acids that are metabolised to pyruvate (gluconeogenesis substrate)

Amino acids that are metabolised to CAC intermediates which form oxaloacetate (gluconeogenesis intermediate)

Acetyl-CoA and fatty acids are not glucogenic:

Fatty acids are metabolised to acetyl-CoA

Acetyl-CoA is not a precursor for gluconeogenesis

Acetyl-CoA cannot be metabolised to pyruvate or oxaloacetate.

Pyruvate oxidation is irreversible

There is no alternative pathway for Acetyl-CoA → pyruvate

Metabolism of acetyl-CoA in the CAC leads to production of CO2, not the net synthesis of oxaloacetate (for gluconeogenesis)

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.

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Respiratory control mechanisms

Level 1: respiratory rhythmicity centres

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.

Level 2: Apneustic and pneumotaxic centres

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

Level 3: Higher centers

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

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In quiet inspiration:

Major muscles: diaphragm and external intercostal muscles

Ribs slope downward which allows an increase in the side-to-side and front-to-back diameter during inspiration. The external intercostal muscles contract, elevating the ribs and causing the increase in volume.

When the diaphragm contracts, the dome of the muscle flattens out, increasing the volume of the thoracic cavity (in the top-to-bottom dimension).

In forced inspiration:

Diaphragm and external intercostal muscles are contracted more forcefully

Accessory inspiration muscles: sternocleidomastoid and scalenus. These muscles contract to further enlarge the thoracic cavity.

Contracting of these muscles (accessory) raises the sternum and elevates the first two ribs, increasing thoracic cavity volume.

Increased thoracic cavity volume and thus lungs expand more, causes a greater drop in intra-alveolar pressure and hence a greater inflow of air.

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:

Inspiratory muscles relax (diaphragm returns to its natural dome shaped position, elevated ribs return to normal position)

No forces are keeping the thoracic cavity and lungs expanded, they return to their normal size and the resultant decrease in volume causes increased pressure which causes outflow of air along the pressure gradient.

Expiration ceases when intra-alveolar pressure equals atmospheric pressure.

In active expiration:

Expiratory muscles contract: abdominal and internal intercostal muscles

Abdominal muscles contract, causes an upward force on the diaphragm, which increases pressure.

Internal intercostal muscles contract, pulling the ribs downward and inward, which causes a decrease in thoracic cavity volume, hence increasing intra-alveolar pressure and hence expiration.

The intrapleural pressure exceeds atmospheric pressure (which usually causes a collapsed lung) but the lungs don't collapse, due to a higher intra-alveolar pressure.

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1. What is stigma?
2. What makes people feel stigmatised?
3. Why is TB stigmatized (think about factors associated with the patient’s health, factors associated with treatment and management of TB, the terms we use to describe Tb patients)
4. How did stigma affect Miriam in this case?

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1. What are the functions of macrophages, neutrophils and dendritic cells?

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.

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1. How are pressure and volume are related? How does this relationship apply to pulmonary ventilation?

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?

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What is meant by latent TB?

- 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

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1. Are the processes (inhalation, passive exhalation & forced exhalation) active or passive? a. What is an active process vs a passive process?

2. What muscles are involved in inhalation (passive and forced) & forced exhalation?

3. What is the pressure law central to breathing?

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1. In which regions of the brainstem are the respiratory centres located?
2. What are these respiratory centers called and what are their respective functions?

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1. What are the stages of glycolysis?

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+?

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1. What are the precursors, intermediate and substrates of gluconeogenesis? Why are fatty acids not a substrate for gluconeogenesis?

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?

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1. a. What is the function of the conducting portion of the respiratory tract?

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?

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1. What are the 2 main components of the respiratory system?

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)

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1. What is the general shape of a lung, include surfaces?

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?

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1. Can you draw a cross section through the thoracic cavity and draw in and label the pleura?

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?

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1. How does type of epithelium change in structure at different sites in the respiratory system? E.g. how is the epithelium different in the inferior portions of the pharynx compared to the trachea?

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

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What is the duration of standard pulmonary TB treatment? What is meant by adherence?
Can you measure/monitor adherence? Why is adherence important?
What are the challenges related to adherence (consider the duration of treatment, the DOT system and the drug side effects)?
What were Miriam’s’ challenges once she started taking the medication? What effects would the DOT system have for Miriam?

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What is meant by surveillance?
What is meant when a disease is notifiable?
What is contact tracing and how is this done?
For surveillance of Tb what data do we collect? Where does this data come from? Is this a passive or active process?
In this case, why does the nurse need to know Miriam’s close family contacts? What will the nurse use the information for? Why are close contacts who are under 5 at high risk of contracting Tb?

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Why do we need to control TB?
What strategies and policies exist for preventing TB (consider the 4 levels of prevention and what is in place at each level), how are diagnosis, treatment, screening and infection control of TB important pillars of TB control?
How might have Miriam’s TB been diagnosed?
What other diagnostic test are there for TB?