Abnormal cell growth

Figure 1.a

Figure 1.a

If I had been born a doctor, I would have never taken any sunbath in my life. Figure 1.a illustrates elders sunbathing.Sunbathing in our teen and early 20s is a very strong risk factor for getting skin cancer (basal cell carcinoma) (The Guardian 2013). Welcome to #blog 5# the focus is on cancer. I will share how engaging with modules has made my understanding of the disease clear. A section on the blog will explain how cancer such a simple concept on molecular bases, yet still individual cancers are highly complex and many difficult to treat? In progress before conclusion, I will give brief reflection on molecular similarities between the pathogenesis of cancer and auto-immunity. Hope you enjoy because this is a life threatening disease more terrifying and most are idiopathic.

I have always wanted to do positive in my life that is why I was a dedicated blood donor. I have learnt that this sets stress on my bone marrow as it results in hyperplasia and hypertrophy of my bones. One other myth that I had always carried with me was the idea that breast cancer is for woman only. I am know aware as I blog that gynaecomastia may lead to premalignant condition in males.

(Figure 1.b shows warning signs for male breast cancer). male breast cancer

They say with aging comes experience after engaging with general pathology I now know that man are risk of contracting prostate cancer as they grow-up. The latter two conditions are related with high levels of estrogen accumulation that comes with ageing in males. (Rippey 1994). It astonished me that a breast lump can be cut off completely, but within few months or years cancers cells present in the brain. The latter depends on whether the lump is benign or malignant and malignant tumors can metastasise.

Table 1 shows characteristics of Benign (B) and Malignant (M) Neoplasms.

  Clinical Histological
Presentation (B) as lump

(M) as lump, ulceration common

(B) Lump well differentiated-resembling tissue of origin

(M) lump poorly differentiated

Mode of growth (B) Grow by expiation compressing adjacent tissues. My feel round, smooth, regular, mobile.

(M)

(B) fibrous capsule can be seen, the tissue are compressed.

(M) tentacular growth(may be surrounding inflammation)

Rate of Growth (B) grow slowly-man stop growing

(M) grow rapidly and continue to grow if untreated

(B) Mitoses infrequent 1/1000 cells or less(1<per HPF)

(M) mitoses frequently 20/1000 cells (mitoses>10 per HPF).

Recurrence (B) rarely recur after removal

(M) Often recur after removal possibly because of invasive and rapid nature of growth.

 

 

Metastasis (B) never metastasise

(M) nearly metastasise in time

(M) tumour cells may be seen invading lymphatic or blood vessels
Outcome (B) usually harmless, but may exert pressure or cause local complication secrete hormone may undergo malignant change

(M) by virtue of invasion + metastasis will kill patient eventually.

 

Table 1 Shows characteristics of Benign (B) and Malignant (M) Neoplasms.

Cancer begins when a cell breaks free from the normal restraints on cell division and begins to follow its own agenda for proliferation.

(Figure 1.c)

Proliferation process

Figure 1.c – The stages of tumor development. A malignant tumor develops across time, as shown in this diagram. This tumor develops as a result of four mutations, but the number of mutations involved in other types of tumors can vary. a. The tumor begins to develop when a cell experiences a mutation that makes the cell more likely to divide than it normally would. b. The altered cell and its descendants grow and divide too often, a condition called hyperplasia. At some point, one of these cells experiences another mutation that further increases its tendency to divide. c. This cell’s descendants divide excessively and look abnormal, a condition called dysplasia. As time passes, one of the cells experiences yet another mutation. d. This cell and its descendants are very abnormal in both growth and appearance. If the tumor that has formed from these cells is still contained within its tissue of origin, it is called in situ cancer. In situ cancer may remain contained indefinitely. e. If some cells experience additional mutations that allow the tumor to invade neighboring tissues and shed cells into the blood or lymph, the tumor is said to be malignant. The escaped cells may establish new tumors (metastases) at other locations in the body

All cells produced by this un-coordinated cell from the ancestral one and its progeny also display inappropriate proliferation. A tumour, or mass of cells, formed of these abnormal cells may remain within the tissue in which it originated (a condition called in situ cancer), or it may begin to invade nearby tissues (a condition called invasive cancer). An invasive tumour is said to be malignant, and cells shed into the blood or lymph from a malignant tumour are likely to establish new tumours (metastases) throughout the body sample of what I mentioned latter paragraph. Tumours threaten an individual’s life when their growth disrupts the tissues and organs needed for survival.

One of the main problems is that cancers cells are not foreign invaders. Differentiating between cancer cells and any surrounding healthy cells has proven extremely difficult, which is why chemotherapies are fairly non-specific and presents enormous side effects. Although some patients can be successfully cured and their cancers don’t return – such as is often the case for testicular cancer and some childhood cancers – for other cancers the situation is different. The cells with cancer tend to divide at a high rate compared to normal cells one reason why it’s hard to treat them.

(Video 1 show mitoses of cancer cells  compared to normal cell in 5 days)

There is a direct relationship between infection, autoimmunity and cancer. Hepatitis B and C viruses are involved in an autoimmune condition that precedes the development of hepatocellular carcinoma. Adenovirus infection is associated with childhood leukemia. Epstein-Barr virus and human T lymphotropic virus type 1 infection is associated with abnormal lympho proliferation and Hodgkin’s lymphoma. Cytomegalovirus infection is linked to autoimmunity and testicular cancer.

While busy researching I found that gastric atrophy and pernicious anemia carries a risk for gastric carcinoma. (Kumur. Cotran and Robbins 1992)

 Clinical autoimmunity may develop when persistent infection provides a continuing high dose of antigenic stimulus, and this situation could predispose patients for the development of proliferative disorders.

In conclusion, I would say the concept of molecular cancer is a useful tool in understanding the etiology, pathogenesis, treatment and control of the disease. Cancer is however, a broad group of various diseases, all involving unregulated cell growth. (Walter and Israel 1987) I strongly belief knowing this concept and nature of cancer, can help in initiating an early detection and a strategic mechanism to alert self-exposure to carcinogens. This way, in future we should at least be worried about cancer and heredity, and factors such as tobacco use, unprotected sexual intercourse with multiply partners, radiationlack of physical activity ,obesity, and environmental pollutants can be eradicated.

References

1)    Kumur V, Cotran RS, Robbins SL. Basic Pathology. 5ed. Philalphia: WB Saunders, 1992

2)    Rippey JJ. Illustrated lecture notes –General Pathology, Johannesburg: Witwatersrand University Press, 1994.

3)    Rubin E, Farber JL. Pathology, Philadelphia: Lippincott, 1988.

4)    Walter JB, Israel MS. General Pathology. 6th ed. Edinburgh: Churchill Livingstone, 1987.

1)    The Guardian Saturday 19 January 2013, what doctors won’t do: Available from:

<http://www.guardian.co.uk/lifeandstyle/2013/jan/19/what-doctors-wont-do>

Advertisements

Inflammation a health hazard!

As a natural medicine student I learned that the body has the power to heal itself. If you’ve ever jammed your finger, scraped your knee, or sprained your ankle, you’re already familiar with inflammation. The accompanying redness (rubor), swelling (tumor), and pain (dolor) and loss function are sure signs that inflammation is taking place. Inflammation is part of your body’s response to indicate any type of physical injury. It’s one of the ways that your body protects itself, and begins its repair process.Figure 1:A young girl with fever.

figure 1: illustrates a patient suffering from fever, which is associated with a high body temperature and shivering particularly if inflammation is due to an invective cause.

Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues, figure 1.1a illustrates white blood cell types and their distribution in the blood.

Figurer 1.1a: shows LEUKOCYTES

Figurer 1.1a: shows LEUKOCYTES

Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process. Table 1: illustrates the differences in inflammation and draws attention to the duration, causative agents, major cells involved and primary mediators of inflammation,

Table 1:comparison between acute and chronic inflammation1

Table 1:comparison between acute and chronic inflammation

Perhaps I should also share my story being young and wanting to belong I joined the gym for body building. I realized that after and intense 2 hours session at the gym my body gets swollen and the muscles my biceps are in severe pain shoulder rounded with a red ring due to squats. This are the cardinal sings of inflammation acute this is physiology. But the question is if you can’t see inflammation, how do you measure it?

The answer is simple because certain chemicals in our bodies are known to increase levels of inflammation. One of these chemical makers for inflammation is a protein called C-reactive protein (CRP). CRP is often measured in conjunction with other blood tests from a clinical standpoint, a CRP level of less than 5 milligrams per litre of blood is considered normal. So If I took a test after the intense gym session I was going to present with elevated levels of CRP in my blood.

Inflammation is not always as obvious or benign as the above examples. It can silently involve every cell in our bodies and, over time, negatively affect our health and abilities. For example, allergies, joint pain, and premature aging are just a few of the common ailments linked to systemic inflammation.

To further concise this material is to bring this to your attention, if a patient presents with Asthma  is a disease with symptoms of recurrent tight chest, wheezing or cough, triggered by different stimuli (allergens, cold air, smoke ect) that respond to reliever pumps or nebulisers. The disease involves two major elements: chronic inflammation of the airways as well as episodic tightness in the chest (bronchoconstriction). Because the underlying airway inflammation causes the bronchial hyper-responsiveness, the main focus of treatment has shifted to effective and daily control of the chronic and continuous airway inflammation.

If we are to focus microscopically we find that neutrophils are a prominent component of the acute inflammatory response. The control of neutrophil efflux, mediated in part by endothelial and leukocyte adhesion receptors, is important in regulating inflammation and tissue damage. Neutrophil diapedesis occurs following leukocyte rolling on the vessel wall promoted by selectins, and firm adhesion of rolling leukocytes is mediated by members of the Be integrin family.

Acute inflammation a health Hazard!

Video 1: has a summary of inflammation as it describes the production of histamine, the mechanisms of inflammation in detail.

References

1)      Cotran RS, Kumar V, Robbins SL. Robbins’ Pathologic Basis of Disease . 4th ed. Philadelphia: WB Saunders, 1989.

2)      Rippey JJ. Illustrated lecture notes general pathology. Witwatersrand University Press: Johannesburg, 1994.

3)      Rubin E, Farber JL. Pathology. Philadelphia: Lippincott, 1988.

Pathophysiology of fluid distribution.

Blog 3 will focus on the pathophysiology of fluid distribution. The focus will be on reflection on the role that fluid plays in health and diseases and pay special attention on concepts such as “strive to survive” and the goal with this blog is to compare human pathology with human physiology as far as fluid is concern. Fluid is a ’ continuous, amorphous substance whose molecules move freely past one another and that has the tendency to assume the shape of its container; a liquid or gas’ Wikipedia.co.za.

Image

Table that illustrates fluid and electrolytes.

Electrolytes are contained within the fluid. Water makes the big part of fluid in the body and it is normally balanced by drinking thirst and intravenously and loss usually via urine, breathing is the way in which we keep our levels of pH at normal, skin and gut this is physiology. In the case low levels we have water deprivation (diabetes insipidus) or loss which may result in dehydration and which is very crucial because it may result in cell death if chronic due to flow of fluid from intracellular to extracellular by osmosis.

Image

pitting eodema of a pregnant woman at 6 months.

Image

The excessive accumulation of extracellular fluid in the intercellular tissue spaces if termed oedema. In decreased colloid osmotic pressure proteins are lost via urine in the renal disease such as the nephotic syndrome which is closely related to sodium retention and my point is to bring to your attention that if sodium is retained water is also retained leading to excess water. In heart both heart failure and renal diseases there maybe sodium retention. Hypertension to some degree is associated with heart failure for example oedema as due to adrenal hormone in the Cushing’s syndrome after administration of excess cortisone results in sodium and water retention. Oedema can be generalised or localised and it can be induced by physiology and end up pathological a good example is in pregnancy tend to suffer from gestational diabetes which induces cardiac failure and results oedema that develops in the feet and ankles. It is characterised clinically by pitting happens more especially when they had to seat for long hours during travelling.Image

Hyperaemia should not be confused with inflammation the process that result in increased blood flow with an influx of white blood cells and other chemical substances that facilitate healing, because it is merely blood flow to a body part and promotes congestion which is excessive accumulation of blood which is termed engorgement. To explain in clearer in chronic venous congestion of the lungs one of the clinical features will be intra-alveolar haemorrhage from the alveolar spaces where red cells are coughed as pink-tinged frothy sputum and I thought that this was due to the Mycobacterium t to realise that it is characterised by pulmonary congestion and hemosiderin.  If for any reason hyperaemia occurs to a bruise or any cut it will result in haemorrhage which is profuse bleeding. Haemorrhages are measure by their size and they can be internal or external, pectehiae very small, purpura up to 1cm and eccymoses are large. Internal bleeding can occur by traumatic injury such as high speed deceleration in an automobile accident, or by blood vessel rupture from high blood pressure.

Image

If the blood loss is too severe like in organ transplant this may lead to a haemorrhagic shock. Shock is describes a patient who is pale, has a cold clammy skin with thread pulse, low blood pressure and rapid respiration causing loss of fluid and electrolytes in gaseous form may result in respiratory alkalosis.

The usage of platelets and fibrin to stop blood loss by clot is termed thrombosis in physiology this mechanism counteracts haemorrhage but if it happens that clotting is too severe and the clot breaks free, the traveling clot is now known as an embolus (an abnormal mass of undissolved material which is transported from one part of the circulation to another). Thromboembolism is the combination of thrombosis and its main complication, embolism. In pathology we talk about thrombophilia which is a tendency to of occurrence of thrombosis. The most common symptoms of thrombophilia are deep vein thrombosis (DVT) and pulmonary embolism (PE), two conditions referred to together as venous thromboembolism (VTE). In cases of deep pain swelling and redness of the limb deep vein thrombosis may be a resultant cause. The clot may also break off and migrate (embolism) to the lungs. Depending on the size and the location of the embolus this may lead to sudden-onset shortness of breathchest pain, palpitations and may be complicated by collapse, shock and cardiac arrest. Disturbed blood flow may include stagnation of blood flow past the point of injury, or venous stasis which may occur in heart failureor sedentary behaviour-for example, sitting on a long airplane flight more especially for females.

Blood clot

Ischaemia is a condition of inadequate blood supply to an area of the body, this condition may be complete and result in infarct which is localised area of ischemic necrosis and much has been mentioned in the last blog about necrosis. Since oxygen is mainly bound to hemoglobin in red blood cells, insufficient blood supply causes tissue to become hypoxic, or, if no oxygen is supplied at all, anoxic. In very aerobic tissues such as heart and brain, at body temperature necrosis due to ischemia usually takes about 3–4 minutes before becoming irreversible as started by http://encyclopedia.thefreedictionary.com/ischemia.

Ischemia is a feature of heart diseasestransient ischemic attackscerebrovascular accidents, ruptured sensitive to inadequate blood supply. Ischemia in brain tissue, for example due to stroke or head injury, causes a process called the ischemic cascade.

An infarct may be as a result of blockage or by an obstruction (e.g. an arterial embolus, thrombus, ruptured by trauma (e.g. atherosclerosis or vasculatures), or vasoconstricted (e.g. cocaine vasoconstriction leading to myocardial). Infarcts can be localised meaning they attack a body part example among most is Myocardial infarction (MI), commonly known as a heart attack, is an infarction of the heart, causing some heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. Other areas include

ü  Brain (Cerebral infarction)

ü  Splenic infarction

ü  Limb infarction

ü  Bone infarction

In conclusion I would highlight that fluid Exchange is vital to normal physiology. All the processes of life occur because fluids flow: Through channels, across membranes, and within open spaces. Should the flow of fluids stagnate, all of life becomes diminished… and health is compromised. author is unknown.

Refferences

Contran RS, Kumar V, Robbins SL. Robbins’s Pathologic Basic of Disease. 4th ed. Philadelphia : WB Souders, 1989.

Rippery FF. General Pathology. Revised ed. Johannesburg : Witwatersrand University, 1994.

The abnormal deposition of material in tissues.

There were times  due to lack of knowing one focused only on AIDS not having a cure but with the help on Pathology every day there is a new disease embedded in my mind. I thought that the older the person gets the stronger and bold they become but to my surprise age is in coupled with an entire bundle of health related issues but it is a path for all human kind. I have always taken notice of the bigger picture in the sphere of diseases like AIDS and never have I thought that there are morphological diseases causing conditions that may lead to death the way ‘abnormal deposition of materials in tissues and organs’ does.

Student microscope used in viewing microorganisms with different stains.

Student microscope used in viewing microorganisms with different stains.

While growing up I thought that an albinism individual can glow at night but I was still young and still did not understand their nature only to find out that it’s not harmful to them it is bodily processes. I will in this blog reflect on how amyloid proteins, the calcification of organs, tissues and cells including the color of our stools and urine can symbols something (parthenogenesis)wrong in our bodies and further more focus on the processes that make people look the way they are skin color.

  1. Amyloid

staining of Amyloid with Congo Red

Amyloid is not only one protein it is a number of them in their abnormal state deposited extracellularly  in various organs and tissues, many times in the walls of the small blood vessels in the condition known as Amyloidosis. There are a number of stains used to identify amyloid but the most specific in general is Congo Red it gives amyloid salmon –pink colour, when viewed under polarised light and it exhibits an apple green birefringence.

major types

  • Primary amyloidosis (AL), the most common form, occurs when bone marrow produces too much of certain fragments of antibody proteins, which build up in the bloodstream and may be deposited in body tissues.
  • Familial (hereditary) amyloidosis is a genetic form passed down in families that often affects nerves and kidneys.
  • Secondary amyloidosis (AA) develops along with a chronic infectious or inflammatory disease, such as tuberculosis or rheumatoid arthritis.

Since due to our genetic makeup all patients are treated different, the main reason being that amyloids are suspended to morphological studies because to them being associated with aging suspect amyloidosis based on patients symptoms, and will perform a physical exam, including blood or urine tests but the diagnose of amyloidosis still remains as biopsy, using a needle to remove a small amount of tissue to test for amyloid. With hereditary amyloidosis, DNA tests may reveal the genetic change that caused the condition. Depending on the signs and symptoms, the tests will reveal the state of the condition. I biopsy is important and is one of the thing that every person should opt to do more especially when they get older.

2. Calcification

physiology of calcium

When a baby is born one of the most important micronutrient that the baby should get is calcium this is because calcium is deposited in bones and teeth that’s normal even for adults. When a disorder affects calcium balance leading to it being deposited in other parts of the body such as arteries, kidneys, lungs, and brain that is pathological. Calcium deposits in these parts of the body can cause problems with how these blood vessels and organs work. Calcifications can usually be seen on x-rays including it being stained specifically by Alizarin Red which stains it red. A common example is calcium depositing in arteries as part of atherosclerosis (the build-up of a waxy plaque on the inside of blood vessels)

A fetus died due to calcification

3.Jaundice and pigmentation 

young boy with albinismJaundice itself is not a disease, but rather a sign of one of many possible underlying pathological processes that occur at some point along the normal physiological pathway of the metabolism of bilirubin in blood. Pigmentation is normally perceived as the coloring of skin and the concept of pigmentation goes beyond that because when one goes to the sea and they get burned by the sun melanin get hyper and normally people will get reddish. The ability to go to the toilet and pass red stools after a diet that consisted off vegetables will not be a sign off Jaundice or a urine off a dehydrated individual will not be a very good example but how ever when an individual passes dark brown urine and feces that is a symbol of high levels of bilirubin. The unseen side off pigmentation is not obviously since accumulation off substances like dust particles I only became aware of them when I was introduced to pathology however I knew that the paleness of albinism was due to lack of melanin the hormone that causes color on the skin.

Jaundice

References 

1: http://www.livestrong.com/article/259570-what-causes-calcium-deposits-and-calcification/#ixzz2Ma9yS6or

2.^ Beckingham, IJ; Ryder, SD (2001). “Investigation of liver and biliary disease”BMJ (Clinical research ed.) 322 (7277): 33–6. doi:10.1136/bmj.322.7277.33.PMC 1119305PMID 11141153.

3. jaundiceInfoplease.com http://www.infoplease.com/encyclopedia/science/jaundice.html#ixzz2MaL85z20

4. http://www.umm.edu/altmed/articles/amyloidosis-000007.htm#ixzz2MZePljdT

Cell physiology, pathophysiology and the relationship to all human disease.

                      

early-histology of injured cell

early-histology of injured cell

A Cell is the smallest unit of our bodies and it is the most important one. The focus is the physiology, pathophysiology and the relationship to all human diseases.

There are four structures within a cell which play a vital role in the cell being diseased or healthy. The normal cell comprises of a nucleus and cytoplasm separated from the intestinal fluid by the cell membrane. The different constituents making cell protoplasm are: water, electrolytes, proteins, lipids, carbohydrates.

Flow diagram_necrosis vs apoptosis

Flow diagram_necrosis vs apoptosis

  1. Mitochondria release energy in the cell.
  2. Cell membrane is a permeable lipid-soluble substance, but is a major barrier to water soluble substances.
  3. The synthesis apparatus (Endoplasmic Reticulum) synthesise proteins, carbohydrates, lipids, lysosomes, peroxisomes, and secretory granules.
  4. Nucleus acts as a control centre of the cell and contains large amounts of DNA also contain one or more nucleoile , which do not have membranes; these contain large amounts of RNA, and are enlarged in cells actively synthesizing proteins.

There are two bottom reasons why cells die: cytoplasmic calcium accumulation and membrane damage some of the changes that accompany this cell death period can be viewed by the electron or light microscope. Cell injury occurs if there is ATP depletion then this leads to pump`s not working well, sodium and calcium accumulate inside the cell. Too much calcium in the cell is bad for this reason: It denatures proteins and thus destroys the cells structure (cytoskeleton), it poisons mitochondria by opening channels in the membrane making oxidative phosphorylation fail, resulting in pathways that make cell kills itself and it activates cellular enzymes which are harmful like phospholipases’ which breaks down membranes.

Cell injury can also be induced by free radicals molecules with a vicious single unpaired electron. If any of the organelles are not functioning proper that is a sign of damage that may induce disease, but if functioning of the organelles is not compromised then health is maintained. If the cell is at the stage of reversibility then this can be viewed: Mitochondrial densities and cellular swelling, cytoskeletal disruption (e.g., loss of microvilli, blebs).

Once you see any of the following things, a cell is considered irreversibly damaged:

1. Increased eosinophilia (pink color) in cells. Check out the image above of a myocardial infarction: the myocytes are brightly eosinophilic (remember: “red is dead!”).

2. Great big mitochondrial densities

3. Nuclear changes, such as pyknosis (a shrunken, dark nucleus), karyolysis (a fading of the nucleus), and karyorrhexis (fragmentation of the nucleus into little cookie-crumb-like pieces).

Tissue [Epithelial (surfaces), connective (structural), muscle (motion, compression), neural (coordination of functions)] injury starts with molecular or structural damage to cells. When faced with injury, cells can adapt, sustain reversible injury, or die. Cellular adaptation occurs when stressors result in a new but altered state that preserves viability of the cell:

  • Hypertrophy (when individual cells get bigger),
  • Hyperplasia (when cells increase in number),
  • Atrophy (when cells decrease in size and number),
  • Metaplasia (when one cell type is replaced by another).

There are general causes of cellular injury:

Hypoxia *ischaemia (loss of supply) *inadequate oxygenation (respiratory failure) *loss of oxygen-carrying capacity of the blood (anaemia, CO poisoning)

Physical agents *trauma *thermal insult *radiation *electric shock

Chemical agents and drugs *therapeutics *non-therapeutic agents

Infectious agents *viruses *rickettsiae *bacteria *fungi*parasites

Table that illustates the differences between two cell deaths.

Table that illustates the differences between two cell deaths.

There are two morphologic patterns of cell death they occur when a cell is unable to reverse injury or to adapt to environmental stressors: apoptosis and necrosis.

Apoptosis is characterized by chromatin condensation and fragmentation, occurs singly or in small clusters only, and results in the elimination of unwanted cells during embryogenesis and some physiologic and pathologic states also called the programmed cell death.

Necrosis is characterized by swelling, denaturation of proteins, breakdown of cellular organelles, and cell rupture the pathological cell death.

The general change concept that had changed is with the oxygen-derived free radicals which are produced in many conditions and cause damage to cell structure and function I only thought that oxygen is all the times beneficial human lives. The Loss of calcium homeostasis, with increased intracellular calcium – this activates phospholipases, proteases, ATPases and endonucleases only became aware of the functions of calcium outside bones and teeth in the module.  I was not aware that direct injury. Mercury is a good example, binding to sulfhydryl groups of cell membrane proteins, increasing permeability and inhibiting ATPase-dependent transport. I also learned that apoptosis is no bad but necrosis which I did not know till introduced to general pathology is the bad (pathologic) cell death.

References

http://www.pathologystudent.com/?p=6263

Contran RS, Kumar V, Robbins SL. Robbins’s Pathologic Basic of Disease. 4th ed. Philadelphia : WB Souders, 1989.

Rippery FF. General Pathology. Revised ed. Johannesburg : Witwatersrand University, 1994.

Biography

The first step towards getting somewhere is deciding you are not going to stay where you are. If you keep chasing yesterday, you’re going to miss tomorrow. Welcome to Masokela Tokelo’s blog. Masokela Tokelo is currently doing his third year in natural medicine. He decided to follow this career path because his grandfather used to heal people in the rural with herbs.

The general pathology will give light to the young man so that he is more informed about disease and give him a platform while referring patients to other health workers, because pathology is a language spoken in the medical field. He expects to learn more about diseases and the pathology language so as to be knowledgeable about the interventions around the health subtleties.

Masokela is also student assistance at Gorvalla residence and a house leader this endeavours are inducement because the man has a strong leadership background which he has gained over the past years in his participation around campus. He also loves writing poems, enjoys watching movies and travelling. Tokelo has recently joined the university of Western Cape fitness team that aids student whom wish to drop weight. He hopes you will enjoy the blog and will feel at home and his open for beneficial  suggestions.

 

d74958aa40b3039b67e962f385a3660f