Case Studies

Question 1

Normal vaginal pH

Answer 1

3.8 - 4.2

Question 2

Why is the larger number of ROS more serious with respect to mitochondria ?

Answer 2

They lack catalase.

Question 3

What does catalase do?

Answer 3

Catalase is used for the decomposition of hydrogen peroxide to water and oxygen.

Question 4

How many moles of ATP produced in the Kreb’s cycle?

Answer 4

32 ATP - 38 ATP

Question 5

In patients with chronic alcohol abuse, mitochondrial dysfunction can occur why?

Answer 5

Because of the severe oxidative stress ethanol induces as well as contributing to the depletion of key antioxidants which are critical for alveolar macrophage (AM) function (phagocytosis)

Question 6

Liver patho from etoh:

Answer 6

• Alcohol is transformed into acetaldehyde, which is toxic in large amounts.
• It stimulates lipid peroxidation and oxidative stress, which disrupt cytoskeleton and membrane function.
• It contributes to malnutrition by hindering protein export from the liver and modifying the metabolism of vitamins and minerals.
• Acetaldehyde also compromises mitochondrial function, which decreases the oxidation of fatty acids and contributes to steatosis (fatty liver).
• Cellular damage stimulates an inflammatory response and the activation of Kupffer cells (liver macrophages), which leads to the development of fibrotic tissue.
• Fibrosis alters the physical structure of the liver, causing the obstruction of biliary channels and shunted blood flow.
• Hepatocytes can no longer regenerate, contributing to necrosis.
• These changes result in portal hypertension, altered metabolic processes and toxin buildup.

Question 7

Lunch patho r/t smoking

Answer 7

Tobacco smoke and air pollution are irritants, which trigger an inflammatory response in lung tissue.

Cytokines are released, which inhibit antiproteases, increase protease activity, create oxidative stress and cause the apoptosis of structural lung cells.

These factors are responsible for the breakdown of elastin within the septa and result in alveolar destruction, the loss of elastic recoil and impaired airflow.

Cellular apoptosis and early cellular senescence (the cessation of cellular division) reduce the number of alveolar cells and the surface area for gas exchange.

The loss of alveolar cells creates bullae (spaces within the lung parenchyma) and blebs (spaces adjacent to the pleura), which inhibit gas exchange and contribute to V/Q mismatching and hypoxemia.

The loss of elastic recoil reduces the amount of air that can be passively expired, effectively trapping air in the lungs.

This causes chest hyperexpansion and puts the respiratory muscles at a mechanical disadvantage.

Breathing becomes more work, which can lead to hypoventilation and hypercapnia in late stages of the disease.

Question 8

When do ROS become a problem in the mitochondria?

Answer 8

Reactive Oxygen Species aka oxidative stress contributes to mitochondrial dysfunction when large numbers overwhelm the balance of endogenous antioxidants.

Question 9

What does chronic exposure to ROS do?

Answer 9

Chronic exposure decrease DNA repair and result in mutations. Three effects of theses reactive species important to cell injury are:

• peroxidation of lipids,
• alterations of proteins causing fragmentation of polypeptide chains, and
• alterations of DNA.

Question 10

Brief patho of ROS in cells

Answer 10

The lipid-radical interactions produce peroxides which cause chain reactions in return causing cellular, membrane and organelle destruction.

Excessive production of hydrogen peroxide and eventually hydroxl radicals in mitochondria will damage lipids, proteins, and mitochondrial DNA which then causes cells to die.