Mechanisms Cellular Adaption (Mon 23rd)

Question 1

Pathology

Answer 1

Study of the effect and causes of disease so treatments can be identified.

Question 2

Disease

Answer 2

Any abnormality in the structure or function of the body.

Question 3

Morbidity

Answer 3

Being in a diseased state, that may cause death later on.

Question 4

Hyperlasia

Answer 4

Increase in no.of cells. Due to increased functional demand, e.g. thyroid disease

Question 5

Aetiology

Answer 5

Aetiology: the cause of disease, can be identified through post mortem, genetic studies, using Koch’s postulates (testing whether a micro-organism causes a specific disease, and epidemiology (study of disease in populations).

Question 6

Pathogenesis

Answer 6

The way the cause of the disease (the aetiological agent, like a virus) causes disease manifestation, e.g. releasing toxins causing structural damage.

Question 7

Hypertrophy/ Atrophy

Answer 7

Increased / decreased size of cells or tissue (not no.)

Question 8

How does the body respond to injury?

Answer 8

Either the cells adapt or they die. If adapted, and further injury can still die

Question 9

Illness

Answer 9

The whole being sick experience, mental and social factors included.

Question 10

Cell Cycle

Answer 10

G1 protein synthesis
S DNA synthesis.
G2 assembly of mitotic apparatus
M mitosis, when the two sets of chromosomes are pulled apart and the cell divides.
G0 resting phase of the cell cycle: the cell is not cycling, but can be stimulated to re-enter the cycle by, for example, growth factors which interact with receptors on the cell surface.

Question 11

Differentation

Answer 11

Differentiation begins in life at the stage of the 8 cell embryo. Loss of differentiation is a feature of cancer.

Question 12

Define necrosis, apoptosis, pyknosis, free radical damage and hypoxic changes including ischemia and infarction

Answer 12

Necrosis: Death of cells due to injury. Not controlled or organised. The apoptosis process is a natural part of the cell’s life cycle, and the body is ready to carry the dead cell materials away. In necrosis, however, the body isn’t prepared to remove the dead cells, and as a result, causes an inflammatory response. Loss of cell membrane integrity, no ATP required.

Apoptosis: Organised and controlled cell death at the end of the cell’s life. No inflammatory response. Loss of cytochrome c activating pro- apoptotic proteins.

Pyknosis: The irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is followed by karyorrhexis, or fragmentation of the nucleus. Pyknosis is from Greek pyknono meaning “to thicken up, to close or to condense.”

Free Radical Damage: Atoms or molecules that are highly reactive with other cellular structures because they contain unpaired electrons. Free radicals can cause damage to parts of cells such as proteins, DNA, and cell membranes by stealing their electrons through a process called oxidation.

Hypoxic Changes: A condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level.

Ischaemia: Reduced blood flow- can cause hypoxia.

Infarction: Obstruction of blood flow, no blood flow at all causing tissue death.

Question 13

Describe the mechanisms by which cells become injured, e.g. free radicals, chemicals, viruses, hypoxia, autoimmunity and irradiation

Answer 13

Mechanism Free Radical Damage: React with bio-molecules in cells, including DNA. The resulting damage to DNA, which is also called oxidative damage to DNA, is implicated in mutagenesis, carcinogenesis, and ageing.

Chemicals Mechanism of Injury: Loads of ways, like poison. Inflammation, radiation and chemicals can cause generation of reactive oxygen species. ROS oxidise fatty acids to form lipid peroxidases, which disrupt organelles. Oxidise proteins, abnormal folding, loss function. DNA oxidation causes mutations.

Viruses Mech of Injury: release toxins

Hypoxia: If a cell does not have sufficient oxygen, it cannot make enough ATP to survive. Since many normal processes in a cell require energy, the housekeeping functions of the cell break down: the cell membrane loses its ability to keep certain ions in or out, proteins are not made, DNA and RNA cannot be made, etc. Eventually, the cells either die and disintegrate or commit a form of suicide called apoptosis.

Autoimmunity: Is the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune response is termed an “autoimmune disease”.

Irradiation: Being exposed to radiation causes free radical formation, damages DNA, if DNA fails to repair, cell division is inhibited leading to cell death, or if there is abberant repair, teratogenesis (malformations in embryo) carcinogenosis (tumours).

Question 14

List the types of necrosis

Answer 14

There are six types of necrosis:
Necrosis can be due to reduced blood supply (ischaemia) or casous (due to death of masses of macrophages in TB, looks like cheese)

Coagulative necrosis: 
Liquefactive necrosis: 
Caseous necrosis.
Fat necrosis.
Fibroid necrosis.
Gangrenous necrosis.

Question 15

Morphological (form, shape, structure) changes used to identify cell death

Answer 15

Nucleus condenses, apoptic bodies form and get phagocytosed into fragments,.

Question 16

Describe changes occurring in cell adaptation and sub lethal injury, e.g. fat accumulation and cytoskeletal damage

Answer 16

During cell injury that is not lethal, water is accumulated in cells (hydropic changes). Fat also accumulates (vacuolation). Injury affects membrane, nucleus and mitochondria.

Membrane. I: Toxins, complement fixation, perforin mediated injury, chemical and physical damage.

Nuclear. I: Genetic disease, irradiation, chemicals (mediated by free radicals), results in loss of nuclear function (neoplasia). Non-lethal damage (mutation) of genes controlling cell division, apoptosis and DNA repair leads to unregulated proliferation (tumour).

Mitochondrial. I: Reduced blood flow, reduced oxidative phosphorylation, leads to reduced sodium potassium pump removing sodium. Leads to influx of sodium, calcium and water. Efflux of potassium. Causing swelling, loss of mirovilli and blebs/bulges.
Reduced OP means anaerobic. R has to happen, which causes lactic acid buildup, lowers pH, causing nuclear chromatin to clump up.
Rough ER swells, so ribosomes drop off, no protein synthesis.

Cytoskeleton damage:

Question 17

Difference between apoptosis and necrosis?

Answer 17

In apoptosis, there is no inflammatory response, ATP is required, enzymes destroy DNA and cytoskeleton and the cell membrane remains intact.

In necrosis, it is an inflammatory response, so lose membrane integrity. Lysosomal enzymes degrade the cell.