The normal cell
Cell injury
Cell death and necrosis-gangrene
The cells are the basic unit of life, they are the smallest units that perform physiological functions. Each cell maintains homeostasis at the cellular level. Defects in or on the the cell can result in disruption of homeostasis. This can lead to a state of disease.
In a case of cell injury, which can be inflicted by various agents, the cell has to undergo physiological changes in order for it to adapt to the new conditions and for homeostasis to be restored. During cell injury the biochemical mechanisms that take place are loss of energy, mitochondrial damage, loss of calcium homeostasis, defects in plasma membrane permeability and generation of free radicals. In cases of fatal injury the cell can undergo cell death. During cell injury caused by an aetiological agent the cell first attempts to adapt by either wasting, decreasing in size, increasing in size or change in morphology. All of these adaptations will somehow help in the protection of the cell, preventing cell death. If the injury is non-fatal, the injury can be reversible and only the structure and morphology of cell change. If the injury is irreversible, the cell dies resulting in necrosis.
Cell response to stress can differ, which can range from survival pathways to cell death, resulting in elimination of damaged cells. Necrosis is the accidental cell death due to cell injury, and it is the cells response to stress. During necrosis the cell losses control of ionic balance, uptake of water, swelling and cellular lysis. Morphologically , necrosis appears as a gain in cell volume. Organelles swell and the plasma membrane ruptures resulting in loss of intracellular contents. If the stress stimuli does not go beyond a certain threshold, the cell can cope, giving a protective cellular response, ensuring the cells survival. Failure to maintain this protective cellular response results in cell death. Stress exerted on the cell may be too strong, allowing little time for recovery. And the cell may not have the ability to handle high levels of stress, causing a disease. There are different types of necrosis which are:
• Coagulative necrosis – due to ischaemia causing infarction.
-Tissue appears firm, with retained cellular outlines
– eg: splenic infarction, renal infarction, myocardial infarction and adrenal infarction.
• Colliquative necrosis – occurs when there is a rapid enzymatic dissolution of tissue and complete destruction of cells.
– Dead tissue is semi-solid
– Eg: Cerebral infarction, lung abscess, liver abscess
• Caseous necrosis – commonly associated with TB
– Dead cells have no appearance and no cellular outlines.
The other types of necrosis are : fat necrosis, supparative necrosis, gummatous necrosis, fat necrosis and fibrinoid necrosis.
Gangrene – is a form of necrosis occurring after an infection or injury or in people suffering with a chronic illness affecting blood circulation. It can only occur in living tissue.
There are different types of gangrene- dry gangrene, wet gangrene and gas gangrene.
Dry gangrene – there is no infection of saprophytic organisms. And there is no edema or gas.
Wet gangrene – this is true gangrene. The affected tissue has fluid(edema)
Gas gangrene – caused by clostridial organisms, producing a large variety of enzymes and toxins which destroy the tissue.
HOW THESE MODULES HAVE CHANGED MY CONCEPT OF DISEASE
These modules have contributed a lot to my knowledge of the disease process, how it begins and develops with time. I now have detailed knowledge of the normal cell and the consequences of injury to a cell. In a summary : due to an injury of the cell, which is often biochemical, the cell changes and adapts to its new environment. Depending on the level of the cell injury, the cell can either survive or die resulting in necrosis. Necrosis leads to infarction of different organs which leads to a state of disease.
REFERENCES
• http://www.vetmed.vt.edu/education/Curriculum/VM8304/vet%20pathology/CASES/CHRONINF/PAGE3-4.htm
• International Journal of Cell Biology
• Volume 2010 (2010), Article ID 214074
• Martini
• Jj rippey
clinicalscienceblogbabongile 
Although well written, and a good summary of the text book, there are a few areas of concern.
Firstly, your lay out of text does not make for easy reading. You need to define paragraphs better with spacing, and also the bullets are too compressed. Adequate use of paragraphs is important.
Then, although you re-publish facts from the text book, you have not really addressed your insight into the ‘reflection’ aspect of the blogs. How do you relate to the work. Furthermore, the blog brief called for a discussion of the role of the cell in the broader sense of health and disease, which was not addressed.
Referencing is very poor. You need to write more details on books used. You must also show in the text what has been referenced and where, including the prescribed text book.
No audio-visual use either?
Overall, this appears to be a last minute and late writing, basically from the text book directly. There is much room for deeper consideration of the knowledge and how it builds on what you already know and how it raises further questions.