Published April 22, 2013 by niniebulabula3161743

Abnormal cell growth can be a precursor for tumors either benign or malignant. The type of tumors have slightly different traits which helps distinguish them. Presence of the tumor can exhibit general symptoms of disease. The immune system can also fight normal tissue cells, which are mistakened as pathogens.


Normal cell growth is vital for optimum function of the cell, tissue or organ. The normal growth can avoid processes such as atrophy ( decrease in size), hyperplasia and hypertrophy (increase in size), metaplasia( replacement of one cell type with another), neoplasia ( growth of tumor) and anaplasia( no differentiating) of the cell. These processes are a result of cellular adaptation of growth to preserve the cells fuction. In my first blog I mentioned cell injury.If the injury is non-fatal it can lead to adaptation of the cell by conforming into one of the processes. The processes can either be physiological or pathological.


figure 1.1 A diagram indicating the

events during pathological and physiological

hypertrophy of the heart.


figure 1.2 . An image showing muscular autrophy


figure 1.3 . Endometrium hyperplasia due to overgrowth of endometrium


figure 1.4. transitional- squamous metaplasia


There was a time when I thought the word ” TUMOR” only referred to cancerous cell growth. Not knowing that a tumor can either be benign or malignant. In my understanding a tumor is the abnormal overgrowth of cells .A malignant tumor can become metastatic resulting in a lethal effect to the bodies physiology. Where as a benign tumor cannot and usually has a good prognosis. ” Tumors are classified according to the tissue of origin, epithelial, connective tissue, haemopoietic, neural and a miscellaneous  group and then into benign and malignant within these groups”. 1. JJ Rippey (1994). This is the extent of resemblance they depict of the tissue they originated from, which can be well or poor differentiation. The differentiation is often a sign of how serious the outcome of the tumor can be.


figure 2.1 growth of malignant and benign tumors


I recall feeling a lump in my breasts for the first time in my early years of high school, my first thought was its ” cancer”, only to find out it was a breast fibroadenoma. Had it been a malignant tumor the lump would have had a different feel. ‘ malignant tumors grow by local invasion and infiltration with destruction of surrounding tissue.” JJ Rippey (1994). A malignant tumor has a hard irregular shape which is not easily eradicated. ” Tumors often lose differentiation features over time as they become more malignant.”  2.BF Burns. The differentiation often aids diagnosis and coming up with the appropriate therapy considering the extent and nature of the growth.


figure 3.1 a video about malignant and benign tumors


” Local spread takes place by invasion and infiltration between tissues.” JJ Rippey (1994).  The cancer cells form an “army” removing/destroying original tissue and taking over the site by means of rapid proliferation. During invasion they leave the tumor site and continuously spread into neighboring tissue. Malignant tumors are best removed in their early stages due to to this phenomenon of metastasis, I often see the use of different therapies such as chemotherapy or surgical procedures in removing these tumors on TV.  I now know why it is so vital to try and eradicate these tumors, considering their nature an the damage they can cause.

spread of malignant tumor

figure 4.1 the spread of a malignant tissue


Cancer is responsible for many deaths, which is can be caused by many factors. ” cancer is a complex group of diseases with many possible causes, including genetic factors and lifestyle factors.” 3. American cancer society. Age can also determine the chances of being diagnosed with cancer, which could be a build up of everyday damage to our cells and genes. Genetics and the enviroment are also contributing  factors, such as long- term sun exposure, smoking  or even viruses.


figure 5.1 . video showing formation of cancer

causes of cancer

figure 5.2. a few causes of cancer


” Benign tumors can cause pressure and obstruction, functional activity, local anatomical complications and malignant complications. Malignant tumors can cause pressure and obstruction, destruction of tissue, ulceration, hemorrhage and secondary infection and pain.” JJ Rippey (1994).  The effects caused by tumors are not different to signs and symptoms which manifest in other diseases. Some can appear to be non-fatal, which could cause misdiagnosis.


“An autoimmune disorder is a condition which occurs when the immune system mistakenly destroys healthy body tissue” 4. D Dugdale (2011). Psoriasis is an autoimmune disease which I am familiar with. The T-cells mistakenly identify the skin cells as foreign cells, resulting in the cells being attacked, the skin cells are harmed and damaged.


figure 6.1 Body parts that can be affected by autoimmune diseases


In the process of this group of diseases, the immune system problems affect collagen. ” Some of these diseases have similarities, including arthritis and inflammation of arteries in the tissues that connects  joints and other tissues.”6. M.E Makover (2011).systemic sclerosis

figure 7.1 systemic sclerosis due to excessive collagen deposition


Cellular adaptation after injury can result in change in cells morphology, this is the cells way of fighting for survival. Tumors take on abnormal accumulation and over growth of cells and sometimes on abnormal structure. This reflects the possibilities of the tumor being malignant or benign. The immune system is there to fight off foreign substances in our bodies such as cancers. But in some cases the immune system can not differentiate whether a cell is normal or foreign, this is how autoimmune diseases come about.


1. JJ Rippey , General Pathology, 1994, Witswatersrand, pg 210, 215, 225, 289, 290.

2. Dr Bruce. F Burns, Anatomical Pathology, Neoplasia, Ottawa Hospital.

http://www.google.co.za/url?q=http://www.med.uottawa.ca/patho/assets_secure/documents/graduate/neoplasia.ppt  . 21 April 2103.

3. American society, What is cancer. http://www.google.co.za/url?q=http://www.cancer.org/cancer/cancercauses/&sa=U&ei=7X91UaqHE8LgOt7jgJgO&ved=0CB8QFjAA&sig2=pmoC5mxJ5G5irAXrxfsVdA&usg=AFQjCNFCuOs2Y-Hv_yEldQHqZuUhhCvwgg . 22 April 2013.

4. D.C Dugdale, Autoimmune disorders, 2011, University of Washington.http://www.nlm.nih.gov/medlineplus/ency/article/000816.htm. 22 April 2013.

5. M.E Mkover, Collagen Vascular Disease, 2011, New York University Medical centre. http://www.nlm.nih.gov/medlineplus/ency/article/001223.htm. 22 April 2013

Normal and abnormal fluid distribution and function

Published April 15, 2013 by niniebulabula3161743

Normal functioning of cells and tissues is not only dependant on circulation of nutrients but also on normal fluid balance. In this blog i will be giving my insight on normal and abnormal fluid distribution and function, based on what i have learn’t during my lectures and from a couple of other sources. The different processes that I will be referring to are FLUID AND ELECRTROLYTE BALANCE, OEDEMA, HYPERAERMIA AND CONGESTION, HAEMORRHAGE, SHOCK, THROMBOSIS AND EMBOLISM, ISCHAEMIA AND INFARCTION.
This module outlined the basics of fluid ditribution, such as the distribution of body water. I am now well aware that 2/3 of water are in the cells and 1/3 is in the extracellular compartment.(1.JJ RIPPEY 1994). If the balance of the fluid in the body is disrupted, different mechanisms are triggered such as thirst or urine loss (these are just simple examples, there are many more other mechanisms). Electrolyte imbalance is also to be considered in such a case, because it is most likely to be associated with the fluid imbalance. A simple example I can think of is during an episode of my intense exercise routines. I exercise 5 days a week, which 2 of those days I do vigorous exercise which consist mainly of cardiovascular exercise. I noticed that during these workout sessions i sweat more and my sweat is highly salty, my thirst becomes excessive, my breathing accelerates and my body heats up. This is my body’s response to loss of water and sodium(electrolyte) through sweating caused by heat generation in the body, this causes increased thirst signaling that I should replace the lost water by water intake. One would think sodium loss is not a big deal, i certainly did not think so before studying this module. A source stated that “low sodium levels can cause muscle cramping, dehydration and hyponatremia (dangerously low sodium levels in the blood.)”.(2.R.Morris, Are you a salty runner). After reading this statement it occured to me i had suffered the first two signs during exercise, i now know that it is due to low sodium levels.
The link below is for viewing a video about fluid and electrolyte balance in the body.

Oedema is increased fluid in the interstitial tissue spaces or it is a fluid accumulation in the body cavities in excessive amount.(3.M Bezabeh 2004). Before studying this module the only knowledge I had about oedema is that its caused by fluid retension in the tissues, and it is manifested in kwashiorkor. Oedema can be generalised or localised.( JJ RIPPEY 1994). Example of localised oedema is pulmonary oedema : ” this usually occurs in left ventricular failure, it may occur in adult respiratory distress syndrome, the lung increases 2.3 times its normal weight”.(M Bezabeh 2004). An example of generalised oedema also known as anasarca is: “reduction of albumin due to excessive loss or reduced synthesis caused by liver cirrhosis, mulnutrition and protein-losing enteropathy.”( M Bezabeh 2004). For generalised oedema in the case of liver cirrhosis i deduce that this can be caused by by the effect of long term alcoholism. liver cirrhosis being the death of liver cells is bound to cause impaired liver functioning. Ascites is the edema in the peritoneal space.( JJ RIPPEY 2004). This phenomenon occurs in the liver during liver cirrhosis leading to abnormal functioning. There are many more types of localised and generalsied oedema besides the examples I have mentioned above.
figure 2. pitting oedema an example of localised oedema.


figure 3. oedema in face and eyelids due to renal oedema, an example og generalised oedema

This module was new knowledge for me, i did not know anything about hperaemia or congestion prior to studying this module. Both of them are a local increase in blood volume in particular tissue. Like oedema which is accumulation of fluid in particular tissue. So this is the common ground between these two modules, which made me understand this module easily.


figure 4. this figure shows the normal flow of blood, hyperaemia and congestion.

Hperaemia – increased blood flow due to ateriole and artery dilation

Congestion – reduced venous drainage causing increased deoxygenated hemoglobin in blood.( JJ RIPPEY 1994)

During exercise hyperaemia is also manifested. “During exercise, skeletal muscle contractions induce an increase in blood flow (hyperaemia), proportional to the metabolic demand of tissue”. (4. P. Branney 2010). In case of congestion cardiac failure became apparent to me, with the congestion of the veins, the heart loses its ability to pump enough blood to the body’s tissue, therefore the tissues do not receive enough oxygen to function properly.


This is the escape of blood from blood vessels, implying that there has been a damage to the vessel.( JJ RIPPEY 1994)

The most simple example of a hemorrhage would be a cut which leads to bleeding. The blood vessel has been damged, blood moves out externally. This is due to physical trauma. Another cause could be inadequate blood clotting due to too few or decreased platelet functioning or low amount of clotting factors in the blood.

subconjunctival hemorrhage

figure 5. A subconjuctival hemorrhage. blood vessel of the eye has been damaged causing bleeding into conjuctiva.


Before study of this module, i only associated the word  ‘Shock’ with horror or a disturbed emotional state. ” the term SHOCK can be regarded as a clinical description of a patient who is pale,  has clammy skin, a rapid thready pulse, low blood pressure and rapid respiration”. (JJ Rippey1994) I realised that my knowledge of the word ‘shock’ was not so far off the clinical term because when some one is ‘shocked’ they do show some of the clinical signs such as a cold sweat and rapid pulse. There are different types of shock


Table 1. this table shows the different types of shock and how they effect the blood.

The first example of shock that came into mind after going through my notes is suicide attempt by wrist cutting or cutting as self mutilation. During these episodes the individual cuts themselves blood is lost, and if it is continuous bleeding it results in a state of cardiac arrythmia which would lead to hypovolaemic shock. In some cases this leads to death.


Thrombosis is defined as the formation of a solid or semisolid mass from the
constituents of the blood within the vascular system during life. ( M . Bezabeh 2004). I now know that thrombosis is due to haemostasis ( process that causes bleeding to stop). In a nut shell thrombosis is the clotting of blood in response to hemorrhage as a way of restoring homeostasis. the pathogenesis of thrombosis is endothelial injury, stasis or turbulence of blood flow and  blood coagulability. A typical example of thrombosis that I have come to know is Deep vein thrombosis (DVT). During this process blood clots in a vein of the leg, blood is not able to move through the vein as normal because of the block caused by the clot. the blood pressure in the vein increases causing swelling and pain. This swelling caused by blood can be referred to as edema. the video below shows how the process of thrombosis occurs in DVT. How deep vein thrombosis (DVT) forms

Thrombosis can lead to the fate of embolism. Embolus is a travelling thrombus, it travels from one part of the vascular system to another.” An arterial ebolism may be caused by one or more clots, which get stuck in the artery and block blood flow”.(5. DC .Dugdale 2012) In my first blog I discussed cell injury, ischaemia being one of the causes of injury which leads to necrosis( cell death). Since embolism causes a block in blood flow necrosis is due to take place. Hence embolism can lead to infarction.


As I have mentioned in blog 1 that infarction is due to necrosis, causing tissue to die . This is all due to reduced blood flow ( Ischaemia). ” Nearly 99% of all infarcts result from thrombotic or embolitic events” ( M. Bezabeh 2004). i found this fact very interesting, this showed how much of a big role thrombosis and embolism played in disease development. This shows how important normal blood flow through the body is. A healthy lifestyle will save you from all these damaging processes. The video below depicts the process of myocardial infarction due to thrombosis, and the risk factors that can lead to these processes.



The common ground between these modules is that they they fall under hemodynamic disorders. They involve blood movement in the circulation. In a case of each of these processes the body tries to alter the disorder by trying to achieve homeostasis. The body will produce signs and symptoms and different disease states in particular tissue as a way of maintaining balance. This helps to identify when an internal disorder takes place. For example: during edema, the abnormal accumulation of ECF in ICF tissue, the body alerts you of the disruption by producing swelling of the affected tissue.  With hyperaemia the body can manifest erythema, or in a case of congestive heart failure, shortness of breath, leg swelling and exercise intolerance can occur. In a case of hemorrhage seeing blood externally is not normal besides menstruation. Shock comes with its symptoms which i mentioned earlier on which are abnormal manifestations of the body. Thrombosis and embolism too are shown as disruptions during episodes of stasis blood in different tissues, resulting in edema. And infarctions due to ischaemia will show in the weakening of tissue as the tissue cells die and lose function.


1. JJ Rippey, General pathology, 1994, Witswatersrand, pg 65, 75, 83, 89, 93.

2.R Morris,2013,Are you a salty sweater, http://www.runningplanet.com/training/salty-sweater.html.  21 March 2013.

3. M Bezabeh, General pathology, 2004, Jimma University, pg 61, 64, 72, 78.

4. P Branney, 2010, What causes exercise hyperaemia?, http://www.livestrong.com/article/333853-what-causes-exercise-hyperemia/  . 21 March 2013

5.DC Dugdale, 2012, Arterial ebolism, http://www.nlm.nih.gov/medlineplus/ency/article/001102.htm . 21 March 2013.

The process of inflammation, healing & repair and infection

Published April 15, 2013 by niniebulabula3161743

Inflammation plays a protective role in our bodily tissue, it can last from a few minutes to a few years. With inflammation comes different processes such healing and sometimes infection. This blog is my understanding of these processes after going through a couple of articles, textbooks and journals.


There are two types of  inflammation, acute inflammation and chronic inflammation.  ” Acute and chronic inflammation are crudely based on duration of the lesion and histological appearances”1. M Bezabeh (2004) . The causative agent and amount of damage caused are the sources of the classification of inflammation. ” Classification can be based upon the nature of the inflammatory exudate, the duration of the inflammation and the site of  inflammation.”2. Rippey (1994) . The inflammatory exudate replaces damaged area with the exudate components to steer away bacteria that might cause infection. The duration of the inflammation is dependent on type of inflammation, acute inflammation takes less time as compared to chronic inflammation, which can take years.

Acute and Chronic Inflammation – YouTube

The video above gives an overall view of acute and chronic inflammation.

Acute inflammation

I remember how i smashed my finger with a door, not only once but on several occasions. OUCH!!! The pain was excruciating and  unbearable. With the pain ( Dolor) came a sudden rush of heat ( Calor), which I quickly tried to ease by running cold water on the finger. I can’t say that helped, instead the pain became even worse. This was followed by redness, swelling ( Tumor) and loss of function. With the knowledge I have now gained about acute inflammation, the signs that i mentioned are clinical signs of inflammation. According to M. Bezabeh redness is due to dilation of small blood vessels in damaged tissue. Heat is due to increased blood flow (hyperemia) due to regional vascular dilation. Swelling is due to accumulation of fluid in the extra-vascular space, which in turn is due to increased vascular permeability. Pain partly results from stretching and destruction of tissue due to inflammatory oedema, chemicals of inflammation – bradykinins, prostaglandins and serotonin ( induce pain ). Loss of function is due to inhibition of inflammed area by pain and severe swelling.


figure 1. This image shows am inflammed finger, swelling and redness are visible

Chronic inflammation

A moderate measure of inflammation is beneficial in demolishing infectious bacteria and healing after an injury. If the measure of inflammation is increased and the response doesn’t cease, chronic inflammation occurs. ” It acts like a slow- burning fire, continuing to stimulate pro-inflammatory immune cells when they may not be needed”. 3.M. Pick (2011). My mother was diagnosed with rheumatoid arthritis a couple of years ago, attacking mainly the joints of the hands, wrist and knees. ” The inflammatory process primarily affects the linning of the joints, or affect other organs. Rheumatoid arthritis is believed to result of a faulty immune response” 4. This can cause permanent joint destruction and deformity. Chronic infammation is an example of  imbalance in homeostasis. The increased inflammatory response exceeds threshold causing the body to manifest signs and symptoms which is its  a way of restoring balance. This results in the designated type of chronic inflammation, which may be ‘non-specific’ or ‘granulomatous’.

mechanism of acute and chronic inflammation im asthma

figure 2. this image shows the mechanisms of acute and chronic inflammation in asthma.

 Healing and repair

You get a cut, hemorrhage takes place and ceases eventually, it is then followed by the signs and symptoms of inflammation ( as mentioned above ). As time passes you notice the cut begginning to dry up, getting scabby and brown in colour. This occurs during the process of healing, it is one example in many other types of healing. The scabby layer protects the wound, while the damaged skin is healing and forming new beneath it. The healing process may involve resolution, regeneration and organisation.  ” resolution – restore normal structure and function of tissue. regeneration – loss of normal architecture. organisation – replacement of lost tissue with granulation tissue.” Rippey (1994).

Tissue damage = inflammation – removal of dead tissue & injurious agent = replacement by fibrous tissue ( scarring) or specialised tissue ( regeneration) = HEALING

Above is a summary of the process of healing. The healing process is determined by 3 cell types, Labile cells, Stable cells and Permanent cells.


figure 3. This image shows the process of wound healing.

Infection and some infectious diseases

My basic understanding of an infection is that, its the contamination or entry of pathogenic  micro organisms in body tissue. These micro organisms multiply in the tissue causing a state of disease. Infection can spread in many ways, an example can be direct spread during coughing, the micro organism can escape and infect an0ther person.

infectious diseases

Above is a video about the history of infection, causes and control.


Inflammation, healing and infection are inter-linked. The ultimate goal of inflammation is repairing tissue and eliminating the causative agent, which in turn achieves homeostasis. Inflammation can also result due to the presence of infectious microbes. Healing repairs the damage in tissue, assembling and forming new tissue for protection against pathogens.


1. M Bezabeh, General pathology, 2004, Jimma University, pg 34,35

2. JJ Rippey, General Pathology, 1994, Witwatersrand University, pg 142, 155

3 .M Pick, what is chronic inflammation, 2011,http://www.womentowomen.com/inflammation/whatischronicinflammation.aspx. 8 April 2013

4. http://www.cdc.gov/arthritis/basics/rheumatoid.htm#. 8 April 2013

The study of amyloids, calcification, pigmentation and jaundice.

Published March 4, 2013 by niniebulabula3161743

The most basic definition of an amyloid is that its an “abnormal protein”. Amyloid are insoluble fibrous protein aggregates with similar structural traits but are chemically different.
“Amyloids are unlike other fibrous proteins, they do not have a structural, supportive or motility role. Their formation can accompany diseases characterized by a specific protein or peptide that aggregates.” Rambaran ,N 2008, ‘Abnormal protein assembly’, Prion, vol.2(3), Jul-Sep, 112-117. In my understanding of the amyloid process , the proteins are not insoluble from the beginning. The proteins begin as normal soluble proteins which “misfold” into insoluble fibrils made up of the beta-pleated sheets. These insoluble fibrils gather and collocate in tissue initializing the production of amyloidosis. In amyloidosis the the protein fibrils interfere with the normal structure and functioning of the tissue, which results in a state of disease. Amyloidosis is associated with a couple of diseases such as Alzheimer’s, diabetes type2, spongiform encephalopathies. The amyloid fibrils are deposited extracellularly in the the tissue producing a pathogenic effect.
Amyloidosis is classified into amyloid light chain( AL) and associated amyloidosis ( AA). The cause of AL is unknown but it is linked to defective and abnormal antibodies. In AA the deposited protein is serum amyloid A (SAA). The plasma concentration of SAA is highest during inflammation. So AA is associated more with inflammatory diseases.
“Diagnosis of amyloidosis is based upon clinical examination of sample tissue. The examination should depict evidence of characteristic amyloid deposits”. Congo red is the most useful stain in diagnosis of amyloidosis. When combined with polarized light the Congo red stain makes the amyloid deposits appear green.
Calcification is calcium deposits accumulating in soft tissue causing it to get hard. Since the calcium deposition does not occur at a normal site such as bones and teeth, the result of the deposition is bound to be abnormal. A question I ask myself is “ What causes the calcium deposition in the wrong site?”. And another question is “is there a link between a hyper-parathyroid hormone and calcification?”
Firstly according to Harvard Medical School, abnormal calcification does not result from normal consumption of calcium in our diets. Even though high levels of calcium in our blood can lead to abnormal calcification. “The primary cause of hypercalcemia in adults is hyperthyroidism”. Martini, Nath, 2009, Anatomy and physiology, 8th edition,p1022 . This statement makes me consider it to be a possibility for a hyper parathyroid hormone to be linked to calcification .“ calcification can be due to infection, kidney or metabolic disorders, problems with blood vessels or simply ageing” McAdams, M 2011, Calcium deposits and calcification, livestrong.
Calcification can be classified into metastatic and dystrophic calcification. “Dystrophic occurs in damaged tissues either dead or degenerative” . With knowledge of the previous modules, I believe that dystrophic calcification is associated with cell injury. This is a digestive process, whereby macrophages digest necrotic tissue. During this process calcium salts accumulate. “ metastatic calcification may occur in normal tissue whenever there is hypercalcemia” . This statement also contributes to my conclusion that hyperthyroidism is linked to calcification. Metastatic calcification tends to occur where acidic areas excreted ( HCL acid in stomach, uric acid in kidneys, carbonic acid in lungs). This is because calcium precipitates upon alkalization of pH.
Pigmentation means colouring. Skin is given its pigment by skin cells producing melanin( the colour pigment). The darker the hair and skin the individual has, the higher the melanin production. Melanin is not the only pigment associated with the body. There are a couple of other endogenous pigments, like melanin these pigments are produced inside the body. The exogenous pigments are produced externally.
Endogenous pigments such as hemosiderin, hematin, bilirubin and hematoidin are associated with hemoglobin breakdown. Red blood cells are continuously undergoing a hemolysis process, degradation of the red blood cells causes the breakdown of hemoglobin in to globin, iron and heme. The bilirubin arises from the heme, and is eventually excreted in bile and urine. Bilirubin is responsible for the yellow colouring of bruises, and also gives urine its yellow colour. A question that I ponder upon is “ what is bilirubin’s role in the body, and is it needed?”. Wikipedia states that “ bilirubin demonstrates potent antioxidant activity.” This leads to the hypothesis that bilirubin’s main physiological role is as a cellular antioxidant. I would consider this as beneficial, since antioxidants are there to protect our bodies from reactive oxygen species. This could be applicable to adequate levels of bilirubin since high levels can be toxic leading to jaundice. Hematoidin I would consider to have the same action as bilirubin, but in a different area such as tissue instead of bile.
Jaundice results from toxic levels of bilirubin in peripheral tissue, giving the tissue a yellow colour. Hence jaundice is not a diagnosis but a sign of abnormality in the body.
Jaundice can occur in many different diseases. Too much bilirubin being produced and excreted into the blood leads to these diseases. Jaundice can be reflected in the skin pigmentation and eyes.
Common ground between these four processes
A common trait between amyloidosis and calcification is the abnormal accumulation at a foreign site. This leads to defects in function a structure of particular organs or tissue. Pigmentation and jaundice share much more common ground, in the sense that the result of jaundice is caused by a pigment which is bilirubin.
Importance of understanding these processesAmyloidosis,_Node,_Congo_Red



In a clinical situation, a patient may consult me showing particular signs and symptoms associated with any of these processes. With the knowledge of these processes I will have to identify the symptoms and which diseases they are related to. This could lead to diagnosis of a particular disease. For example: a patients exhibits yellow coloured skin, stool check depicts light coloured feaces, urine is dark and brown (this is an abnormal colour). By considering these signs and symptoms of jaundice I would then have a way forward to finding the cause of the jaundice.
1.Rambaran ,N 2008, ‘Abnormal protein assembly’, Prion, vol.2(3), Jul-Sep, 112-117
2.”. Martini, Nath, 2009, Anatomy and physiology, 8th edition,p1022
4.” McAdams, M 2011, Calcium deposits and calcification, livestrong.


Published February 18, 2013 by niniebulabula3161743

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.


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.

• International Journal of Cell Biology
• Volume 2010 (2010), Article ID 214074
• Martini
• Jj rippey