Immune system – Immunity how it works and how to improve it

The purpose of your immune system is to protect your body from unknown and risky attackers. Such intruders are bacilli (bacteria, viruses, and fungi), parasites, malignant cells, transplanted organs, and tissues. The immune system destroys everything dangerous to your body.

To protect your body from these attackers, your body must be able to distinguish what is known to your body from what is foreign to your body.

All bodies that are foreign to the body should cause a certain immune reaction in your body.  These bodies are called antigens.  A normal immune system response involves identifying a potentially dangerous antigen—also the organization and initiation of the defense against him and the attack on him. If the immune system makes a mistake and recalculates what is known and what is foreign, some parts of the organism can be attacked. This condition is called an autoimmune disorder ( rheumatoid arthritis, thyroiditis, systemic lupus erythematosus).

Diseases of your immune system occur when your body produces immune reactions against itself (an autoimmune disorder), your body cannot produce adequate immune reactions against microbial attacks (immunodeficiency disorder), unnecessary immune reactions to harmless antigens that damage normal tissue (allergic reaction)

Your body has a defense schedule in the following circles:

Physical barriers

This round belongs to the first phase of defense and protection from attackers. Examples of physical barriers are the cornea’s skin, the lining membranes of the respiratory, digestive, and urinary tracts.

As long as this type of protection is not damaged, many attackers cannot infiltrate the body. If the protection is damaged, such as the skin in the form of burns or cuts, there is an increased risk of infection. Also, these protective membranes have the ability to release enzymes such as sweat, various forms of secretions, tears that have the ability to remove microorganisms.

Leukocytes

leukocytes immune system

This is an advanced circle of defense found in the blood and tissue, moving with the help of circulation and looking for microbes that have managed to infiltrate the body and other segments that attack the body.

Initiation of immunity:  No encounter with microbes or other forms of attack is required in this fragment. The immune system in this segment reacts to the attacker instantly. It triggers numerous white blood cells such as phagocytes (macrophages, monocytes, neutrophils, dendritic cells) which destroy the attackers by swallowing.

Some types of white blood cells emit substances associated with swelling or allergenic reactions like histamine.

Acquired immunity: In this case, lymphocytes (B cells and T cells) observe and attack intruders in a special way, acquiring special tactics for certain attackers. After a certain time, they attack and attack certain foreign bodies more efficiently.

Acquired immunity takes some time to mature after meeting a new attacker because lymphocytes need time to adjust their attack to its weak points.

Lymphatic organs

These organs extend throughout the body. These include bone marrow (it produces various white blood cells such as neutrophils, eosinophils, basophils, B cell, and T cell monocytes) and lymph glands.

Lymphatic system

Your lymphatic system is the energy part of the immune system. It is a network of lymph nodes and lymph vessels. This system transmits lymph throughout the body. This fluid contains oxygen, proteins, and other nutrients that nourish the tissue. Lymph also transmits microbes, malignant cells, and lifeless or damaged cells. All substances transferred to the lymph pass through at least one lymph node, where foreign substances are filtered and destroyed before the fluid returns to the bloodstream.

These are the secondary lymphatic organs:

-Lymph nodes

-Tonsils

-Payer’s plate in the appendix

-Spleen

Operation immune system

Your immune system is a set of processes in your body that allows it to find and exterminate microbes and tumor cells from the body. It acts as a protection mechanism against organisms that cause your body problems. With the help of the immune system’s proper functioning, your body will be healthy and protected from external and internal enemies.

The immune system protects the body, but it also attacks the parts of the body that are unusable and disrupt the harmony of the body’s functioning. All changes in the body caused by a disease’s action, malignant and benign tumor cells and various other internal enemies affect the body’s proper functioning and the immune system’s efficiency. Lack of protein and the impact of the lack of many other ingredients can affect the immune system’s ability to cleanse the body of malignant cells.

Therapies for immune system

Modern therapies are focused on the following:

Achieving goals in the body that the immune system was not able to achieve

Work in cooperation with the immune system to get rid of the factors that hinder the immune system’s functioning and development.

The main focus is on improving or stimulating the immune system’s appropriate functions. If it works properly in cancer patients, the reality is that the immune system would not work. Cancer cells appeared, and they would not have cancer. 

When your immune system functions properly, it recognizes and destroys these cells daily. If the body does not have enough defensive responses and does not produce enough cells that destroy cancer cells, more cancer cells are produced than destroyed, resulting in a source of malignancy in the body. 

Once started, the process allows these cells to multiply countless times.

Vitamin C and immune system

vitamin c

Countless studies have highlighted the data on impoverished values of vitamin C in the blood of people suffering from any form of cancer. Vitamin C deficiency damages the functions of the defense system and cellular immunity. This creates disorders of neutrophiliclic movement and, on the other hand, interferes with the creation of inflammatory processes.  Extremely high doses of vitamin C tend to increase cellular and humoral immunity.

Vitamin C helps the immune system and its functionality by intensifying T cells’ productiof or T lymphocytes of the type of white blood cells that play a central role in cellular immunity. They also slow down the development of microbes in your body.

Enzymes and organism

Enzymes are helpers in your body’s chemical reactions, and they are essential in maintaining many vital functions in the body. A prolonged lack of certain enzymes worsens the condition of the immune system, encourages the development of the disease, and in some cases leads to the development of malignancy.

About 22 types of different enzymes are produced in the body in large quantities of pancreatic enzymes whose production decreases as the body ages. The three elemental digestive enzymes are amylase, lipase, and protease, which break down carbohydrates, fats, and proteins. Cellulose and lactose are also used to break down fibers. These enzymes are used in the stomach in the pre-digestion phase, and also, when digestion occurs, these enzymes are completely broken down and destroyed.

In the absence of some enzymes, the immune system has a problem recognizing malignant cells and destroying them. In the absence of enzymes, microbes and malignant cells become covered with a fibrin membrane, which reduces the immune system’s ability to recognize and destroy them. This rubber cover can be fifteen times thicker than a normal cell membrane. It prevents the efficiency of the immune system. It reduces the semipermeability of the cell membrane by reducing the ability to deliver nutrients to the cancerous cell, increasing cell acidity, and reducing the ability to transport oxygen to the cell. In this case, metabolic enzymes are necessary. Most of these enzymes are proteases that have proteolytic properties (accelerate protein disintegration). Inappropriate amounts, they assimilate the protective fibrin membrane and detect malignant cells and microorganisms in the immune system.

Since the pancreas produces most of these enzymes, supplementing this organ with metabolic enzymes successfully maintains malignancy in the body at the optimum. People with cancer use the metabolic enzyme pancreas to treat malignancies.

Proteolytic pancreatic enzymes have intense anti-malignant action. These enzymes help destroy malignant cells when they are present in appropriate amounts. They burn the protective proteins of malignant cells, which, combined with the reactions of the immune system, leads to the death of malignant cells.

Mushrooms with medical properties

medicinal shiitake mushrooms

Building a strong immune system is one of the most important things you can do to maintain your health and body in optimal conditions. There is nothing more important to an individual than the information that the immune system is a miracle of life that protects the body from destructive bacteria, viruses, and other invaders. The strength of your immune system depends only on you.

There is a whole group of mushrooms known as medicinal mushrooms, which are often consumed in the form of tea, tincture, distillate in capsules, or powder. These are powerful boosters of the immune system, and many consider natural remedies. Medicinal fungi have many similarities with the human structure if we look at their chemical and genetic composition. Many scientists claim that herbal mushrooms are closer to humans in structure than any other plant.

Science carefully observes all the medicinal mushrooms’ values in the treatment of dangerous medical conditions, including autoimmune diseases and treating malignancy. Mushrooms are valued as natural foods with fewer calories but rich in natural proteins, vitamins, minerals, chitin, iron, zinc, fiber, and essential amino acids. They have a very pronounced use in Chinese traditional medicine.

Operation medical mushroom

Their effects are very well known, with the help of which various health problems are corrected, the organism’s vitality is increased, and adaptive capacities are increased. Many studies have concluded that you should use mushrooms as a probiotic. In the domain of the organism’s biological health, medicinal mushrooms have been identified as one of the most powerful promoters of immunity and as fighters against many diseases.  These amazing facts are very often ignored, while mushrooms can also be used as excellent culinary specialties or food supplements, and thus the body receives various health benefits, which are:

-Immune system control

-Increase the necessary vitamins and nutrients in the body

-Fight against malignant diseases

Throughout the last century, many studies have been conducted on mushrooms as an effective means of treating cancer. Mainstream research has been conducted in Japan and other Asian countries. However, in the past few years, American researchers have also begun to consider the use of medicinal mushrooms as an integral part of therapy to treat people suffering from various forms of cancer.

Some of the more important mushrooms for cancer treatment are Maitake, Ganoderma, and many others. All these mushrooms are very available worldwide, and you can find them in natural pharmacies and health food stores.

Maitake The King of Mushrooms

This fungus is very effective in various forms in preventing and inhibiting development in cases of liver cancer and breast cancer. This fungus has a pronounced anti-microbial effect and improves the characteristics of the immune system that affect the prevention of viral infections. One of America’s leading cancer research centers, Memorial Sloan Kettering Cancer Center from New York, conducts clinical trials with this fungus.

Maitake is a suitable mushroom for human consumption and is used in traditional Asian medicine remedy for diabetes and hypertension. Its distillate is available and used to improve the immune system and adjunct to therapies for HIV and cancer.

One of its most famous energy components is the polysaccharide beta-glucan 1.6. Maitake distillates show low blood sugar as a result of taking them. Maitake fungus marrow colonies’ formations in bones and reduce doxorubicin’s harmfulness, reducing and limiting metastases.

When studying postmenopause, which was accompanied by breast malignancy, oral intake of maitake distillate showed an immunomodulatory effused on its effect on the immune system.

Medicinal herbs in the treatment of diseases of the immune system

medicinal herbs for the immune system

Despite the progress of science and technology, we have faced an increasing number of infectious diseases in recent years. The issue of immunity – the ability to defend our body from disease, is becoming increasingly important because the immune system monitors our body and prevents the development of unhealthy cells in the body.

A healthy life is a prerequisite for healthy immunity, and it consists of: a healthy diet, enough sleep, physical activity, hygiene, appropriate living and working conditions, as well as avoiding stressful situations.

Various herbal preparations are used to raise immunity: green tea, nettle, dandelion, lemon balm, pomegranate, birch, and other herbs, usually in combination with honey, lemon, or propolis.

Recipe for raising immunity

Add three tablespoons of olive oil to the frying pan. Add two teaspoons of garlic to the oil and fry it for 1 minute. Add 5 tablespoons of honey and 50 ml of strong green tea, half a coffee teaspoon of red pepper and ¼ a teaspoon of natural res, and one tablespoon of apple cider vinegar to the fried onion. Heat the resulting mixture to boiling and cook for 5 minutes. Cool the resulting syrup and store it in a glass jar.
Drink 1 teaspoon a day, preferably in the morning.

Tincture to improve blood count

Mix 1 tablespoon of finely chopped young walnut leaves, rosemary, ragweed, sea buckthorn fruit, burdock root, and lynx root. Pour the resulting mixture of herbs with 1 liter of homemade brandy and pour into a glass container – bottle. Close the bottle and keep it in a warm place for 30 days (preferably in the sun). Shake the bottle several times a day. After 30 days, strain the bottle’s contents and drink 1 glass of brandy before breakfast, lunch, and dinner. This tincture is mostly used to improve the blood picture of the elderly.

Strengthening immunity (for children and adults)

Mix 100g of raisins, almonds, pine nuts, dried apricots, plums, and walnuts. Add the rind of two lemons and chop everything together (by chopping or grinding). Deliver everything to a glass jar. Add to the resulting mixture as much honey as the previous mixture’s volume. Mix everything.
Take as a dessert: children 1-2 teaspoons a day, and adults 3 times a day 1 tbsp.

Summary

The research has identified many factors that affect the functioning of the immune system and its strength, but the complete picture of the immune system is not fully explained. For science, all its factors remain hidden under a veil of secrecy. One thing is for sure, without a functional immune system, we cannot have a functional and healthy organism. As a result, we become extremely susceptible to external influences and diseases.

In the previous text, I explained the basic elements of the impact on the immune system, hoping that you will successfully fight by improving its action with some diseases that are the biggest scourge of today.

 

Angiogenesis – Prevention of tumor angiogenesis naturally

Cancer is a frightening disease that represents abnormal tissue growth, otherwise known as a tumor.  Tumors need nutrients and an oxygen supply for their growth and progress. For these purposes, tumors need an influx of large amounts of blood, which can provide them with a sufficient influx of oxygen and nutrients. Therefore, as cancer progresses, it builds its own blood vessel structure that provides it with everything it needs to survive and grow. This process is known as angiogenesis.

Normal tissues that build blood vessels secrete specific polypeptides. Tumors can also form these VEGF and APN polypeptides. The secretion of these peptides results in the disorganized formation of blood vessels, which provide tumor oxygen and nutrients.

Angiogenesis therapy:

Newer methods of treating cancerous diseases use drugs that prevent new blood vessels. These drugs have very low toxicity because their purpose is to affect blood circulation and blood vessel formation but not the tumor itself. When blood vessels’ formation stops, the tumor does not get enough oxygen and nutrients, and thus its cells begin to die.

Judah Folkman was the first doctor to use the possibilities of some drugs against angiogenesis to treat cancer. After his successful attempts, a complete line of drugs was formed, which affects the reduction of the tumor’s supply of new blood supplies.

A new generation of drugs is used to reduce the angiogenesis factor of monoclonal antibodies such as bevacizumab. Such drugs can increase the life expectancy of people with cancer.

Such therapies work best if combined with chemotherapy or radiotherapy. This fact is supported by research. It has been proven that agents that stop angiogenesis are of key importance, but that combined with the above-mentioned therapies, they achieve even greater success.

How do tumors metastasize?

First of all, tumor cells begin to grow.  After that, these cells, which are rapidly developing and growing, are supplied with oxygen and nutrients by angiogenesis.  This occurs when cancer cells release factors such as VEGF and APN. Then, these cells occupy the tissue that surrounds them. Some of these cells go beyond the tumor’s shape and are released into the bloodstream or lymphatic system. From there, these cells move to other organs where they bind to the tissue and multiply again, causing angiogenesis and forming new blood vessels. In this way, tumors can spread to distant parts of the body.

When VEGF and APN are increased, angiogenesis and tumor development are increased.

Therapy against angiogenesis may depend on the location of the tumor and its environment:

Tumor angiogenesis
Tumor angiogenesis

Angiogenesis factors such as VEGF are secreted not only from the tumor but also from the surrounding tissue. Tumor.  So the microenvironment of the tumor can also affect the tumor’s development. Due to this fact, any drug used should target both the tumor and the surrounding tissue’s angiogenic factors. In that sense, natural remedies work very well because, in small doses, they affect various points of the angiogenesis pathway. In this way, they can be effective against a variety of tumors.

Use of plants against angiogenesis:

The first anti-angiogenic plant used for this purpose was fumagillin, which is actually an antibiotic produced by a single fungus. Some of the plants used today to inhibit angiogenesis include Aloe barbadensis, Chemillia Sinensis, ginger, garlic, aloe vera, licorice, resveratrol, etc. Some of these plants specifically target VEGF, and these are Angelica Sinensis, Viscum album, Taxus brevifolia, and others.  These herbs are given continuously in low doses, so that side effects are minimized.

More about these plants:

Viscum album or Iscador . This plant acts on VEGF and causes the death of tumor cells.

Sweet wormwood or artemisia annua. This plant’s derivative, artemisinin, is used as an anti-malarial agent. This plant also reduces the formation of new blood vessels as it inhibits the formation of internal capillaries called the endothelium.

Resveratrol is obtained from red grapes. This compound reduces the production of VEGF. It also affects other pathways and reduces the production of MMP-2, which is another factor that affects tumor growth.

Silybum marianum: These flavonoids act on many factors involved in tumor growth. This plant is effective against ovarian cancer.

Quercetin: This flavonoid is present in several fruits, including apples and citrus fruits. This compound affects several pathways, including VEGF, COX-2, Lipoxygenas-5, and some enzymes. These pathways are involved in angiogenesis, and inhibiting them limits tumor growth.

Camellia is found in green tea, so green tea is considered very good for health, especially as an anti-tumor agent. This compound has been studied in rodents and humans, and so far, research has shown promising results.

Anti-copper agents:

blood vessel tumor development

Copper is needed for the various steps of forming new blood vessels. Plants that act as agents on copper can reduce tumor angiogenesis. These are Caryophylli flos and Cinnamomi cortex.

Products obtained from animals:

The formation of cartilage in the body does not allow new blood vessels. Shark cartilage derivatives are being studied to stop angiogenesis. One of the compounds and shark cartilage AE-941 inhibits angiogenesis and reduces tumor formation. Research on this compound is ongoing.

Anti-angiogenesis factors are beneficial for tumor suppression. Using natural products for that purpose is something that medicine should pay more attention to. The best thing is that these drugs are relatively safe and can be given together with chemotherapy to improve the effects of cancer treatment.

Blood group determination of inheritance and Rh factor

Human blood is divided into blood groups based on the absence or presence of certain antigens on the surface of red blood cells. Before the blood transfusion, blood group tests are performed, and during the examination of pregnant women to determine the Rh factor. Blood grouping is done to determine if there is any likelihood that two people are blood-related.

One of the most important antigens in the blood is blood group antigens (ABOs) and Rh-antigen. That is why tests related to these blood groups are most often performed, although there are other ways to determine blood groups. Both types of testing are determined on a blood sample taken from a vein.

The antigens he mentioned include proteins, glycoproteins, carbohydrates, and glycolipids. Still, it all depends on the blood group system, and some of the antigens are present on the surfaces of other cells.

Determination of blood groups A, B, AB or 0

blood group donation

Human blood is divided into four blood groups:

• If antigen A is located on the surface of blood cells, it is blood group A. Plasma, i.e. the liquid part of the blood, contains blood group B antibodies

• If antigen B is on the surface of red blood cells, it is blood group B. Then the plasma contains antibodies against blood group A.

• If neither of these two antigens is present on the surface, it is a blood group because, in the plasma, there are antibodies against blood group A and also antibodies against blood group B.

• There is a possibility of being on the surface red blood cells find antigen A and antigen B, which would mean that there are no antibodies in the plasma, and such persons have blood group AB.

Blood received through a transfusion must have the same antigens and red cells as the person receiving it. In short, the blood of the donor and recipient must be compatible. If incompatible blood is received, the antibodies will recognize the received blood as foreign and destroy the red blood cells.
Such a transfusion reaction occurs immediately after receiving a blood transfusion and can have serious consequences for the recipient’s health and can even lead to death.

Blood group 0 negative in the shadow does not have any antigen, so we call it universal, which means that it is compatible with all blood groups. Blood group AB positive is called the universal recipient, which means that people with this blood group can receive any blood group blood.

Antigens that are not so important and are located on the surface of red blood cells can cause problems, and before removal, their compatibility with those in the recipient’s blood is checked.

We note that transfusion reactions are rare today, precisely because of blood groups’ determination.

Determination of Rh factor

rh factor

Rh-factor testing determines its presence or absence in the blood.

• If there is Rh-factor in the blood – it will be Rh-positive
• If Rh-factor is not in the blood – it will be Rh-negative
• Blood containing Rh and A antigen is then A-positive
• Blood that contains Rh-factor and B antigen – then it is a B-negative blood group

The division of blood concerning the Rh factor is significant for pregnant women. The problem that can arise is that a woman has Rh-negative blood and carries a child with Rh-positive blood, which we call Rh-incompatibility. During childbirth or pregnancy, the baby’s Rh-positive blood and the Rh-negative blood of the mother may mix, after which the mother begins to produce antibodies. This production of antibodies is called Rh-sensitization, leading to the destruction of a child’s red blood cells.

Rh-sensitization does not affect the health of the child carried by the mother when sensitization occurs. But if a woman in her second pregnancy again carries a child who has Rh-positive blood, there could be problems of varying intensities, from mild to very dangerous.

This condition is called hemolytic disease of the newborn, and if treatment is not carried out and the mother is sensitized, in rare cases, the child may die.

Testing for this Rh-factor is done during the first examination of the uterus. If a woman has Rh-negative blood, she is given a vaccine, Rh-immunoglobulin, which prevents sensitization.

Note that after discovering the vaccine, the problems caused by Rh-sensitization are minimal and almost rare.

Blood group inheritance

inheritance-of-blood-groups

We ourselves know that blood type determination is also done to determine paternity, in case the mother, father, or both parents’ identity is not completely certain.

In determining paternity, the blood groups of persons who could be the father of the child are compared with the mother and the child’s blood groups, and the birth father is determined by excluding persons for whom it is impossible to be fathers.

A child inherits genes A, B, or 0 from each parent. Geb B and gene A are dominant, while gene 0 is recessive
Determination of human blood group is done in the case of:

• Operations

• Blood transfusions

• Before the person donates blood

• Before a person donates an organ for a transplant

• At the first examination of the pregnant woman

• In case of blood relationship

Determination of blood group is done by taking a blood sample from a vein in a widespread and painless way. It is important to note that the contrast agent used in the X-ray procedure before determining the blood group may affect the blood group examination accuracy.

Also, taking medications like methyldopa, levodopa, and the like. It may show a false-positive result. Also, carcinoma or leukemia can cause a change in blood type. In addition to this improper handling of blood samples, the samples’ results may prove inaccurate.

Blood group 0

This blood type responds perfectly to stress, is an outstanding leader, very determined and experienced, stable, and lives well. It is good that with this blood group, breast cancer has a lower mortality rate than others, while bladder cancer has the highest risk of tumor progression. It poses the greatest danger of melanoma and is prone to gastritis, ulcers, and various allergies.

Signs of toxicity of this blood group:

• Inflammation

Menstrual problems

• Cramps

• Inflammation of the joints

• Fatigue

• Exhaustion

• Mental hyperactivity

Tips for this blood type:

• Chew food slowly

• Reduce cigarettes if you are a smoker

• More physical activity

• Talk to people

• Practice the technique of overcoming anger

Exercises for this blood type:

• Gymnastics

• Aerobics

• Riding a bike

• Weightlifting

Blood type 0 diet

Proper nutrition helps our health greatly. You will find tips on what is very good for you to consume in the following sentences. It is important to avoid caffeine and alcohol, especially when you are under stress because of the very high adrenaline in you.

Poultry and meat:

– Good foods: veal liver, game, heart, lamb, beef
– Neutral foods: chicken, turkey, chicken
– Avoid: pork, bacon, and ham

Seafood and fish:

– Good foods: pike, leaf, cod
– Neutral foods: salmon, oysters, sardines, grouper, and mussels
– Avoid: squid, sea snail, octopus

Eggs and dairy products:

– Good foods: Dairy products make you fat and stimulate the production of gastrin
– Neutral food: butter, cheese, feta cheese, eggs
– Avoid: parmesan, kefir, sour cream, ice cream, smoothies, yogurt

Vegetables:

– Good ingredients: onion, beet, artichoke, spinach, ginger, paprika, chard
– Neutral foods: mushrooms, garlic, celery, olives, beets
– Avoid: pickles, capers, olives, potatoes

Fruit:

– Good foods: pineapple, figs, mango, plums, cherries
– Neutral foods: melon, strawberry, grapes, cranberries
– Avoid: blackberries, avocados, oranges, coconut

Drink:

– Good foods: green tea, mineral water
– Neutral foods: red wine
– Avoid: white wine, carbonated drinks, coffee, black tea

Blood group A

It has been determined that this is the oldest blood group. The first carriers are farmers and farmers. For this blood type, the connection between body and mind is vital.

Here we classify analytical types of people with a good sense of detail. They love to be brought to perfection and are very sensitive. They react more strongly to stress due to the increased adrenaline concentration in the body. People are susceptible to the needs of others.

People with this blood type suffer a lot from cancer, for which they have the lowest cure rate. There is also a risk of developing gynecological tumors and thyroid cancer.

Signs of toxicity of this blood group:

• Low sugar

• Flatulence

• Psoriasis, acne

Depression

• Cholesterol

Tips for this blood type:

• Eat more protein at the beginning of the day

• Do not skip meals

• Determine the work rhythm

• Sleep at least 8 hours

• Have your heart checked regularly

Exercises for this blood type:

• Aromatherapy

• Deep breathing

• Tai Chi

• Yoga

Blood group A diet

Proper nutrition greatly helps our health, in the following text you will find tips on what is good to consume, what is neutral and what should be avoided.

Meat and poultry

– Animal proteins are not recommended and should be avoided
– Avoid foods: beef, veal, game
– Neutral foods: turkey and chicken

Fish and seafood

– Good foods: sardines, cod, mackerel, trout
– Avoid foods: anchovies, oysters, eels, shrimp
– Neutral foods: grouper, dentex, tuna

Dairy Products:

– Use these products in as small quantities as possible
– Avoid foods: parmesan, emmentaler cheese, edam cheese, butter
– Neutral foods: feta cheese, goat’s milk, chicken eggs, kefir, yogurt

Vegetables:

– Good foods: chard, broccoli, garlic, celery, artichokes
– Neutral foods: mushrooms, cauliflower, cabbage, chicory, zucchini, radishes
– Avoid foods: capers, tomatoes, eggplant, peppers

Fruit:

– Good foods: pineapple, figs, lemon, cranberry, grapefruit
– Neutral foods: peaches, melons, strawberries, apples, watermelons
– Avoid foods: coconut, oranges, tangerines and mangoes

Drinks:

– Good drinks: red wine, coffee and green tea
– Neutral foods: white wine
– Avoid foods: sweet carbonated drinks, spirits, beer, mineral water

Blood donation

Blood is very important in treating people who need it. Today there is a big problem of getting blood so it is very humane to give blood if you are able to do it. Giving blood takes about half an hour with all the procedure that needs to be done, which we will explain below.

In the half hour you spend you can save someone’s life. Alcohol should not be consumed before (the day before) when donating blood.

When donating blood, you will first fill out a questionnaire with some questions that are important and you are expected to answer them honestly. The questionnaire exists to protect the health of the person who will receive your blood but also to ask you about some of the questions in the questionnaire.

Blood donation is a humane act

Your hemoglobin, a blood dye-containing iron, is checked before donating blood. Iron deficiency indicates possible anemia. So you get a small sting in your fingertip, and you will make test hemoglobin on site.

Also, your doctor will measure your blood pressure, obeys the heart and lungs work, which means a kind of small systematic examination.

450 milliliters of blood are taken when donating blood. Needles and bags that are sterile and used only once are used. Taking the said amount of blood does not pose a health hazard to a healthy person. Just taking blood takes about 10 minutes. It is important to alert your doctor to any changes you notice or if you start to feel unwell.

After donating, your blood is tested for hepatitis B and C, HIV (AIDS), and syphilis. You can transmit these diseases through the blood. If any of the tests are positive, your doctor will contact you.

After donating blood, you must sit still for about 10 minutes, keeping the injection site pressed to prevent bruising and subsequent bleeding from the injection site.

After donating blood, you also receive a Thanksgiving meal, and it is recommended that you take at least the offered drink to make up for the lost volume.

So, be humane and donate blood. That way, you can save someone’s life!

Heart transplantation

A heart transplant is a transplant of a complete human heart. Heart failure (or congestive heart failure) is a condition in which the heart cannot pump enough blood to meet other bodily organs’ needs. People with heart failure should not strain because they are short of breath and tired. They can also have life-threatening irregular heart rhythms.

Last year, more than 41,000 Americans died of congestive heart failure, and as many as 4.8 million of them live with it.

Scientists have made progress in identifying diseases that cause heart failure. Medications for the treatment of congestive heart failure are also being worked on.

Still, when the heart is so damaged that it is impossible to repair, current treatment methods are sometimes unable to alleviate symptoms and prolong life. When all hope of improvement is lost, a more drastic approach should be considered – such as a heart transplant.

In heart transplantation, the diseased heart is removed and replaced with a healthy human heart. In special cases, the diseased heart does not have to be removed, but the surgeon can place a healthy heart next to the diseased one (so-called ‘transplant’ heart transplant) to act as a supplementary pump.

Medical science has made great strides over the past 20 years. Once a science sensation and a science fiction dream, heart transplantation have become a reality today. For those who do not respond to other heart disease treatment types, a heart transplant can be a miracle that will save their lives.

Problems in the first years

The first human heart transplant was performed by Dr. Christian Barnard 3. December 1967 in a celebrated operation in Capetown, South Africa.

In the first years, heart transplants were usually not successful because the patient’s body often ‘rejected’ the new heart. This happened because of the human body’s immune system, made up of white blood cells and other cells that recognize ‘foreign’ material and react to it.

Take the example of a person who cuts a finger. If bacteria enter the incision, white blood cells move toward the incision to destroy them before the infection begins. This is a normal defensive response.

A similar response occurs toward a newly donated heart after a transplant. It is exposed to attacks. At the time of the first proceedings, heart transplantation medical science could not interpret how the body’s immune system ‘sees’ the transplanted heart as foreign. Today, survival rates after heart transplants have gradually improved thanks to an understanding of how the immune system works. 

Today’s heart transplant results

heart transplant pulse

Today heart transplantation is performed in more than 2,300 Americans each year at over 150 heart transplant centers. Over two out of five of these patients are expected to survive for a year, and over seven out of ten will be alive three years after surgery.

  • Heart transplants are performed each year in more than 2,300 Americans.
  • The one-year survival rate is 89%
  • The three-year survival rate is 84%

Patients with the longest survival live more than 20 years after transplantation.

Quality of life also improves dramatically after a heart transplant. Many activities – walking, dancing and even running – can return to normal. Rather, heart transplant recipients competed in a marathon, and one person became a professional athlete (in the Grand Futsal League).

Transplant recipients must take lifelong medications (known as immunosuppressive or anti-rejection drugs) to prevent organ transplant rejection and deal with these drugs’ side effects.

The transplanted heart is ‘denervated’ for at least a year after surgery. This means that it is not connected to the rest of the body via the nervous system. The network of fine nerves broken during the old heart’s removal cannot be reconnected surgically. The denervated heart normally works, which does not cause any recipient problems. However, it can cause a faster pulse after transplantation. A normal resting heart regularly beats 60 to 80 times per minute, while a transplanted heart can beat 130 times per minute.

Indications for heart transplantation

Heart transplantation is performed when congestive heart failure or heart injury cannot be treated by any other medical or surgical method. Heart transplantation is reserved for people at high risk of dying from heart disease within one to two years.

Most patients who undergo a transplant have either of two problems. The first is irreversible heart injury due to the arteries’ calcification (coronary heart disease) and multiple heart attacks. Another problem is heart muscle disease (cardiomyopathy). In this condition, the heart cannot contract normally due to damage to the heart muscle cells.

Sometimes heart transplants are performed in people with other forms of heart disease, and these include the following: 1) heart valve abnormalities that cause damage to the heart muscle; 2) abnormalities of the heart muscle or other structures present at birth (congenital heart defects); or 3) rare conditions such as heart tumors.

Until recently, anti-rejection drugs’ side effects prevented heart transplants in very young or older people. That, however, has changed. Now transplantation can be performed in people of all ages, from newborns to those in their seventies.

The chances of successful heart transplantation, in the long run, depend in part on the extent of damage or disease to other organs that cannot be cured. (This may include a fatal stroke, chronic lung, liver, or kidney disease.) In people with these conditions, transplantation would be of little or no benefit. If the pulmonary arteries’ blood pressure rises too much and cannot be lowered, it can prevent a heart transplant. This is because a normal, gifted heart may be unable to cope with the flow of blood through diseased blood vessels. A ‘transplant’ heart transplant can be applied in such a case.

Other medical issues are also considered when deciding whether a person is a good candidate for a heart transplant. These include a proven active infection, diabetes, or blood clots in the lungs.

As recipients must withstand the emotional burden of transplantation and its consequences, a support network among family members and friends plays an important role. The recipient must also be able to deal with potentially serious drug side effects and the need for lifelong treatment and medical care.

Selection and recruitment of providers

It is estimated that 16,000 people in the United States would benefit from a heart transplant each year. However, only about 2,300 surgeries are performed each year because too few hearts are donated.

All in all, it is a matter of public awareness and legislation. Some families of potential donors refuse to give consent to donate organs to their loved ones because they think they will have to pay the cost of organ harvesting. That is not correct!

Hospitals today are required to develop policies and procedures to explain to families organ donation. Legal provisions for this ‘requested application’ have been adopted in 42 states and in the District of Columbia (DC). Likewise, hospitals with Medicare and Medicaid programs must have written provisions in place to identify potential organ donors and report them to the procurement authority (OPO). Since January 1988. all hospitals must have elaborate policies and procedures in place to identify potential donors. Sometimes the hospital is unable to identify a good donor despite the hospital requirements. If the donation is not requested from the family of a potential donor, and the family would like to give someone else a chance at life, they should consult a doctor or nurse.

When a hospital or OPO as a member of the Unified Organ Donation Network ( United Network for Organ Sharing / UNOS / ) identifies the donor, the person in charge of identifying the donor should do two things: determine whether the donated organ is suitable for transplantation and coordinate the distribution of the organ. However, all this depends on the family of the potential donor. If the family does not allow the use of organs, the organs will not be removed.

Most donors donate multiple organs. For example, the heart, liver, kidneys, pancreas, and lungs can be obtained from the same donor.

Donated hearts are given to patients based on the donor’s blood type and body weight, and the blood type, body weight, disease severity, and geographic location of the potential recipient. All this data is stored in the UNOS computer. Preference is given to seriously ill recipients at the nearest transplant center.

A suitable donor is a young to middle-aged person for whom brain death has been reported based on standard criteria whose heart is still working well. All donors are tested for the presence of hepatitis B and C viruses and human immunodeficiency virus (which causes AIDS). Any evidence of these infections means that the person in question is not eligible as an organ donor.

When the transplant team at the recipient’s hospital receives notification of a suitable heart, they travel quickly to the donor’s hospital. There the heart is taken out and placed in a special cold solution to keep it alive (though not beating). The heart can be disconnected from the donor’s bloodstream in about four hours without losing its ability to function normally. Time, then, is crucial. When the heart is removed, the team returns to their hospital and performs surgery.

The process of donating the heart

  • The potential donor signs the organ donor card.
  • After brain death, contact with the donor’s relatives is made.
  • The closest relative gives consent.
  • The acceptability of the heart, lungs, liver, kidneys, cornea, bone, and skin for possible transplantation is determined.
  • Recipients are identified and prioritized via a local program or UNOS computer.
  • The recipient is notified and admitted to the hospital.
  • Surgical teams from the transplant centers arrive at the donor’s hospital at a pre-arranged time.
  • Surgical removal of the donor’s organs begins.
  • The recipient is brought to the operating room, where the removal of the diseased heart is coordinated with the donor organ’s arrival.

Complications

 Heart transplantation is a treatment method for those people whose life expectancy is minimal and in whom there are no other options. It is not a ‘cure’ because a new heart requires lifelong care. Complications can occur after transplantation. Despite the complications, in most people, the quality of life after transplantation is excellent. Those who worked before a heart transplant usually return to work after a short recovery period.

The most common early complications after heart transplantation are organ rejection and infections. Strict precautions are needed to prevent them from occurring.

All adult patients undergo a heart biopsy procedure, taking small heart tissue pieces. The procedure is performed under local anesthesia, after which a long instrument is inserted through a vein. The pieces of tissue are then examined under a microscope. Identifying the white blood cells that cause the immune response is the only available method to diagnose rejection.

In most cases, doctors may detect rejection before the patient begins to feel unwell or some active sign appears that the heart is not working normally. Rejection is treated by increasing the dose of the immunosuppressive agent. Six to eight months after a heart transplant, the body’s effort to reject the donor’s heart decreases. A certain form of ‘submitting’ a new heart develops. Although anti-rejection drugs should be taken continuously and for life, their dose may be reduced after this high-risk early period. This, in turn, will help eliminate the side effects of these drugs.

Two-thirds of deaths in the first year after transplantation occurs in the first three months. The vast majority of them are caused by early rejection or infection.

Drug side effects

Side effects of anti-rejection medications are common. Corticosteroids, especially prednisone, cause many side effects when given high doses early after transplant surgery. Patients may gain weight, retain fluid, or have an unusual distribution of body fat. (Weight increases more in the abdomen and hips than in the arms and legs.) There may be a strangely rounded shape of the face (moon face), weakening of the skin and hair, diabetes (which often needs to be treated), Gallstones, bone weakness, stunted growth (in children), joint damage, and infections. Often these problems are sought to be reduced by interrupting or lowering the steroid dose.

Azathioprine (Imuran) is another drug given to many organ recipients. It can cause abnormalities in kidney or liver function, and lower white blood cell counts. This, in turn, facilitates the development of infection in the recipient concerned.

Cyclosporine is an immunosuppressive agent. He is partly responsible for the dramatic improvement in survival rates in recent years. Cyclosporine causes an increase in blood pressure (hypertension), which needs to be treated in most cases. Abnormalities of renal and hepatic function may also occur, and these side effects may be alleviated by lowering the dose of the drug. Cyclosporine interacts with many other medicines that the person may be taking, so it should be closely monitored for successful use.

Immunosuppressive therapy

Heart transplant patients receiving immunosuppressive therapy have a higher incidence of cancer than the general population.

Infection is also a major problem after transplantation in all people taking anti-rejection drugs. The reason for this is simple. The same white blood cells that attack the transplanted heart are responsible for removing foreign particles (such as bacteria) from the bloodstream. Thus, measures taken to protect against rejection may increase infection risk. This is especially true in the event of rejection when it is necessary to increase the dose of anti-rejection drugs.

After the first year, the main threat to survival comes from blockages in the arteries of the transplanted heart. Clogged heart vessels generally do not cause chest pain because the heart is not connected to the nervous system. Most centers perform cardiac catheterization and angiogram (examination of the heart and blood vessels using dye) at a certain time after transplantation.

This form of vascular disease develops in about 25 percent of heart transplant patients within three years of transplantation. If this blockage continues, abnormalities in the work of the heart muscle or irregular heartbeat can occur so that another transplant may be considered. Intensive medical research is being conducted to determine the causes of this serious complication and find ways to prevent them.

Heart transplantation in the future

Heart transplantation has seen a dramatic improvement over the last 20 years. It has benefited, extended, and enabled many people to live a more active life. With new scientific advances, long-term survival is becoming increasingly likely.

Medical science has made great strides in diagnosing rejection and developing immunosuppressive drugs. Several new anti-rejection drugs are in the early stages of development. Several new rejection prevention options with fewer side effects are expected to be available soon.

New techniques are also being developed to diagnose rejection without a heart biopsy. Researchers are focusing on blockages in the blood vessels that form in the new heart. They work tirelessly to identify the causes of this serious complication and learn how to treat and prevent it most effectively.

Even if these problems are addressed, the current lack of donated organs prevents a new heart transplant from anyone who needs it. Other methods will be needed. Artificial heart pumps or mechanical support systems could be permanently installed instead of a new heart in some people. Likewise, a better understanding of the immune system may allow physicians to transplant organs of other types (xenotransplant) instead of selectively using human organs. These technologies will be more widely available within the next 20 years.

PROSPECTS FOR THE FUTURE

  • New anti-rejection drugs
  • A better understanding of vascular disease
  • Greater availability of donated organs
  • Other heart replacement options

The research will also focus on identifying people with early heart disease. Better medical treatment may prevent the disease from reaching a point when a heart transplant is needed.

There is still a reason for optimism in cases where this does not happen. As medical scientists become more aware of immune responses, donated organs will be applied with increasing success. In turn, that will result in increasing improvements in heart transplantation.

Learn all about anemia

Anemia  (hr.  anemia;  ICD-10:  D50-D64) is strictly defined as a decrease in red blood cell mass (erythrocytes, RBC from red blood cell) and is the most common blood disorder.  Erythrocytes’ role is to deliver oxygen from the lungs in tissues and carbon dioxide from tissues into the lungs. This is achieved using hemoglobin (Hb), a tetrameric protein composed of heme and depth. Anemia, therefore, impairs the body’s ability to exchange these gases, reducing the number of erythrocytes that can carry oxygen and carbon dioxide.

Anemia, like fever, is only a symptom, a consequence (or clinical condition) that requires investigation of a further causal etiology.

Erythrocyte measurement methods

erythrocyte examination

Erythrocyte mass measurement methods are time-consuming, expensive, and often require transfusion of radioisotope-labeled erythrocytes. Therefore, in practice, anemia is often detected and quantified by measuring the number of erythrocytes, hemoglobin concentration, and hematocrit. However, these values should be interpreted with caution, as concentrations are affected by plasma volume changes. For example, dehydration raises these values, and increased plasma volume in pregnancy can decrease values without actually affecting erythrocyte mass.

Etiology

Basically, all causes of anemia can be grouped into three basic groups: due to anemia blood loss (hemorrhage  ), anemia due to increased destruction of erythrocytes  ), and anemia due to decreased erythrocyte production (ineffective hematopoiesis  ). These cases include several etiologies (genetic, nutritional, physical,  chronic, and malignant diseases, infectious diseases  ) that require specific and appropriate therapy.

Another clinically useful approach to anemia classifications is a change in red blood cell morphology, which often indicates a specific cause. Morphological features that indicate etiology include erythrocyte size (normocytes, microcytes, or macrocytes); the amount of hemoglobin reflected in cell color (normochromic or hypochromic); and cell shape. In general, microcytic hypochromic anemias are caused by hemoglobin synthesis disorders (most commonly iron deficiency). In contrast, macrocytic anemias most commonly originate from abnormalities that impair erythroid precursors’ maturation in the bone marrow. Normochromic normocytic anemias have different etiologies: in some of these anemias, specific erythrocyte-shaped abnormalities observed on the peripheral blood smear provide an important etiological signpost.

In emergency services, by far, the most common cause of anemia is acute bleeding.

Drug-induced anemia

Medicines or other chemicals often cause aplastic and hypoplastic group disorders. Certain types of these causative agents are dose-related, and others are idiosyncratic. Any man exposed to a sufficient dose of inorganic arsenic, benzene, radiation, or conventional chemotherapeutic agents develops bone marrow suppression with pancytopenia. In contrast, only occasionally does a reaction occur among idiosyncratic agents that result in the suppression of one or more cell lines (1 in 100 to 1 in a million). Thus chloramphenicol can cause pancytopenia, while granulocytopenia is more commonly seen with sulfonamides or antithyroid drugs.

Epidemiology

Prevention of anemia

The prevalence of anemia in population studies of healthy people (excluding pregnant women) depends on the hemoglobin concentration selected as the lower limit of normal. The World Health Organization (WHO) selects 12.5 g / dL for adult and adult women. So it is estimated that approximately  4% of men and 8% of women have values lower than this. A significantly higher prevalence is observed in the patient population.  In less developed countries, the prevalence of anemia 2-5 is higher than in developed countries, which is probably influenced by geographical diseases (sickle cell anemia, thalassemia, malaria, chronic infections), and nutritional factors iron deficiency and, to a lesser extent folic acid deficiency. Populations with little red meat in the diet have a higher incidence of anemia due to iron deficiency because iron from heme is better absorbed than inorganic iron present in vegetables.

Age and a half

Overall, anemia is twice as common in women as in men. The difference is significantly greater during the fertile years due to pregnancy and menses. Approximately 65% of all iron in the body is incorporated into circulating hemoglobin. One gram of hemoglobin contains 3.46 mg of iron (1 mL of blood with a hemoglobin concentration of 15 g / dL; therefore contains 0.5 mg of iron). Every healthy pregnancy takes the mother approximately 500 mg of iron.

While a man must absorb about 1mg of iron to maintain balance, premenopausal women must absorb an average of 2mg of iron per day. Further, since women eat less food than men, they must have twice as effective iron absorption to avoid deficiency.

Women have a significantly lower incidence of X-linked anemias, such as G-6-PD deficiency and sex-linked sideroblastic anemias, than men. Additionally, in younger age groups, men have a higher incidence of acute anemia due to traumatic causes.

Previously, severe, genetically acquired anemias (e.g., sickle cell anemia, thalassemia, Fanconi syndrome) were more common in children because they did not survive adulthood. However, with advances in medical care and advances in transfusion and chelation, along with fetal hemoglobin modifiers, life expectancy in people with these diseases has been significantly prolonged.

Acute anemia has a bimodal frequency distribution, affecting mainly younger adults and people in their late fifties. Causes among young adults include trauma, menstrual and ectopic bleeding, and acute hemolysis problems.

In people between the ages of 50 and 65, acute anemia is usually the result of acute blood loss with a chronic anemic condition. This is the case with uterine and gastrointestinal bleeding.

Anemia and ethnic groups

blacks anemia

The prevalence of neoplasms increases with each decade of life. It can cause anemia through bleeding, invasion of the bone marrow by a tumor (where the bone marrow is replaced by a tumor, or for example, granuloma -[podtiip] myelophthisical anemia[/podtip] ), or the development of anemia associated with chronic disorders. The use of aspirin, nonsteroidal antirheumatic drugs, and warfarin also increases with age and can create gastrointestinal bleeding.

As mentioned earlier, certain ethnic groups have an increased prevalence of genetic factors associated with certain types of anemia. Diseases such as hemoglobinopathies, thalassemia, and G-6-PD deficiency have different mortality in different populations due to differences in the genetic abnormalities that create the disorder. For example, G-6-PD deficiency and thalassemia have lower morbidity in African Americans than in the Mediterranean due to genetic differences. Conversely, sickle cell disease has higher morbidity and mortality in African Americans than in Saudis.

Ethnicity is also a factor in nutritional anemias and anemias associated with untreated chronic diseases. Socioeconomic benefits that positively affect diet and access to health care lead to a reduction in the prevalence of these types of anemias. Thus, iron deficiency anemia is more prevalent in developing countries (which have less meat in their diet) than in developed countries. Similarly, chronic disease anemia is common in populations with a high incidence of chronic infectious diseases (e.g., malaria, tuberculosis, AIDS). This is partially exacerbated by these populations’ socioeconomic status and their limited access to adequate health care.

Pathophysiology

Physiological responses to anemia vary with acuteness and type of stroke.

The gradual onset of the disease may allow the activation of compensatory mechanisms. Except for anemia due to chronic renal failure, in which the cells produce erythropoietin, a decrease in tissue oxygenation that accompanies anemia usually triggers increased erythropoietin production. Erythropoietin stimulates compensatory hyperplasia of erythroid precursors in the bone marrow, and in severe anemia, the appearance of extramedullary hematopoiesis in secondary hematopoietic organs (spleen, liver, and lymph nodes).

In well-nourished individuals who become anemic due to acute bleeding or hemolysis, the compensatory response may also increase red blood cell regeneration five to eight-fold. The main feature of increased erythrocyte production in the bone marrow is reticulocytosis, i.e., the characteristic appearance of an increased number of newly formed cells (reticulocytes) in the peripheral blood. In contrast, disorders with decreased erythrocyte production (regenerative anemia) are characterized by reticulocytopenia.

Anemia due to acute blood loss

In anemia due to acute blood loss, a decrease in oxygen transfer capacity occurs along with a decrease in intravascular volume, with resultant hypoxia and hypovolemia. Hypovolemia leads to hypotension, which is detected by baroreceptors in the carotid bulb, aortic arch, heart, and lungs. These receptors transmit impulses to the vagus’s afferent fibers and glossopharyngeal nerves in the medulla oblongata, cerebral cortex, and pituitary gland.

Development 1

In the medulla oblongata, sympathetic tone increases as a reflex response, while parasympathetic activity decreases. Increased sympathetic tone leads to the release of norepinephrine from the sympathetic nerve endings and adrenaline release and noradrenaline from the adrenal medulla. Sympathetic association with hypothalamic nuclei increases the secretion of antidiuretic hormone (ADH) from the pituitary gland. ADH increases the reabsorption of water from the distal collecting tubules of the kidney. The response is reduced renal perfusion, juxtaglomerular cells in afferent arterioles releasing renin into the renal circulation, leading to elevated angiotensin I, which angiotensin-converting enzyme (ACE) converts to angiotensin II.

Development 2

Angiotensin II has a potent pressor effect on arteriolar smooth muscle. Angiotensin II also stimulates the adrenal cortex’s glomerular zone to produce aldosterone. Aldosterone increases the reabsorption of sodium from the kidney’s proximal tubules, thus increasing the intravascular volume. The sympathetic nervous system’s primary effect is to maintain tissue perfusion by increasing systemic vascular resistance. Increased venous tone increases preload and final diastolic volume, increasing stroke volume. Therefore, stroke volume, heart rate, and systemic vascular resistance are maximized by the sympathetic nervous system. Improving oxygen delivery is made possible by increased blood flow.

Hypovolemic hypoxia

In hypovolemic hypoxia conditions, increased venous flow due to increased sympathetic tone is likely to dominate the vasodilatory effects of hypoxia. Counterregulatory hormones (e.g., glucagon, adrenaline, cortisol) are likely to move intracellular water into the intravascular space, possibly due to the resulting hyperglycemia. This contribution to intravascular volume has not yet been fully elucidated.

Patient prognosis

The prognosis usually depends on the underlying cause of the anemia. However, the severity of the anemia, its etiology, and the rate at which it develops may play an important role in the prognosis. Similarly, the patient’s age and the existence of other comorbid conditions affect the outcome of the disease.

Liver cirrhosis

Approximately 30% of patients with cirrhosis of the liver die from bleeding. The prognosis for traumatic aortic rupture is also poor, where approximately 80% of patients die before reaching the hospital, and most patients who do not receive adequate care die within 2 weeks. Non-traumatic aneurysm rupture also has a poor prognosis and is essentially fatal if left untreated. In patients with sickle cell anemia, homozygotes (Hgb SS) have the worst prognosis because they are more likely to have crises. In contrast, heterozygotes (Hgb AS) have crises only in extreme conditions.

Thalassemia

In thalassemia, homozygotes (Cooley’s anemia or thalassemia major) have a worse prognosis than patients with any other thalassemia. The chances of survival are worse for patients with idiosyncratic aplasia caused by chloramphenicol and viral hepatitis and better when paroxysmal nocturnal hemoglobinuria or antisepticizes are probable causes. The prognosis for idiopathic aplasia lies between these two extremes, where the mortality rate for untreated cases is approximately 60-70% within two years of diagnosis.

Hyperplastic bone marrow

Among patients with hyperplastic bone marrow and decreased erythrocyte production, one group has an excellent prognosis, and the other does not respond to therapy and has a relatively poor prognosis. The first group includes patients with relative bone marrow failure disorders due to nutritional deficiency where appropriate treatment with vitamin B12, folic acid, or iron leads to the correction of anemia once the appropriate etiology is established. The second group includes patients with idiopathic hyperplasia who may partially respond to pyridoxine therapy but more often do not respond. These patients have annular sideroblasts in the bone marrow, suggesting inappropriate use of iron in mitochondria for heme synthesis.

Other cases of anemia

As for other conditions, such as ectopic pregnancy, the prognosis with prompt care is excellent, with a mortality rate of only 1-2%. In patients with hemophilia, about 15% of them eventually develop factor VIII inhibitors and may die from bleeding complications. Patients with idiopathic platelet purpura usually respond to immunosuppression or splenectomy and have an excellent prognosis. Approximately 80-90% of patients with TTP who receive plasmapheresis fully recover. Hemolytic-uremic syndrome carries significant morbidity and mortality if left untreated. Up to 40% of patients may die, and almost 80% develop renal failure.

Pernicious anemia

Chronic illness/anemia resulting from insufficient absorption of vitamin B 12. 

 

It occurs in adults due to gastric atrophy (you cannot absorb vitamin B12). Parietal cells in the stomach that produce an intrinsic factor required to absorb vitamin B12 and their destruction lead to a deficiency of this essential vitamin.

The name pernicious anemia has remained since this type of anemia was fatal, which is no longer the case, but the name has been retained for historical reasons. 

To lack vitamin B12 it can lead to several diseases and conditions. Still, pernicious anemia is understood only due to atrophic gastritis and loss of parietal cell function.

Dr. Addison was the first to describe this disease, and until 1920, people died from it a year to 3 years after diagnosis. Three physicians in their thirties treated this anemia so that patients consumed raw liver juice in large quantities. That is why they deservedly won the Nobel Prize in 1934, curing a hitherto incurable disease !!

We are very grateful for the progress and the fact that we do not have to drink raw liver, but we elegantly solve the lack of this vitamin with tablets or injections!

Vitamin B12 and anemia

Vitamin B12 cannot be created/synthesized in the human or animal body, so we must ingest it through food. It is essential for the brain and nervous system; it participates in every cell’s metabolism in the body.

We get the most vitamin B12 from meat (especially liver), fish, shellfish, and dairy products.

The genetic variant of pernicious anemia is an autoimmune disease with a definite genetic predisposition. Antibodies (anti parietal) occur in 90% of people with pernicious anemia, while they are present in only 5% of people in the general population.

Classical pernicious anemia occurs due to the lack of intrinsic factors synthesized in the stomach’s parietal cells. There is no absorption of vitamin B12, the result: megaloblastic anemia.

Any disease or malabsorption condition can lead to vitamin B12 deficiency and macrocytic/megaloblastic anemia accompanied (though not always) by neurological outbursts.

Causes of vitamin B12 deficiency

  • Insufficient consumption (strict vegetarian diet: vegans)
  • Atrophy or severe disorder of the gastric mucosa
  • Deficiency or impaired function of intrinsic factor
  • Pancreatic enzyme deficiency
  • Inflammation of the small intestine, ileitis, celiac disease, intestinal amyloidosis, intestinal resection, Crohn’s disease
  • Infection with the parasite Diphyllobothrium latum: this parasite interferes with the absorption of vitamin B12

Frequency:

It most often occurs in the northern European population: English, Scandinavians, Irish, Scots, aged 40 to 70.

Symptoms:

  • Weight loss, subfebrile fever
  • Anemia: paradoxically anemia is well tolerated, even when hemoglobin is extremely low (40-50), MCV (mean corpuscular volume) is high: angle over 100
  • About 50% of patients have a very smooth tongue, without papillae (glossitis)
  • Changes in character and personality
  • Thyroid dysfunction
  • Diarrhea
  • Paresthesias: tingling in the arms/legs
  • The most severe: neurological outbursts: balance problems, unsteady gait, muscle weakness. In the elderly, people with symptoms of dementia must exclude vitamin B12 deficiency as memory problems, hallucinations. Irritability may occur.

Diagnosis:

Laboratory tests: complete blood count, peripheral blood smear, levels of vitamin B12, folate, methylmalonic acid, and homocysteine in the blood

 Schilling test: the patient’s ability to absorb vitamin B12 is checked.

The presence of antibodies to intrinsic factors in the blood.

Therapy:

As you have probably guessed so far, the therapy is: to replace vitamin B12. The synthesized vitamin B12 is called cyanocobalamin. It does not exist in nature but is synthesized and administered to patients orally, transdermally, intranasally, or by injection (intramuscularly, subcutaneously).
Today, some tablets contain high doses of vitamin B12: 500-1000 mcg, so there is quite enough vitamin to keep the cells in the body functioning well.

If in doubt, it is certainly advisable to give replacement therapy in the form of an injection! 

Famous people with this disease:

Alexander Graham Bell
Annie Oakley: 1925. died from the effects of pernicious anemia in 65 g of life

Avitaminosis hypovitaminosis for all vitamins

Avitaminosis is any disease caused by chronic or long-term vitamin deficiency or a disease caused by a defect in metabolic conversion, such as that of tryptophan to niacin.

Fat-soluble vitamins

Fat-soluble vitamins are K, A, D, and E. Precisely because they are fat-soluble, they can accumulate in the body, and avitaminosis occurs when fat absorption is impaired. Their lack is noticed only after a few months since they are stored. Diseases of the pancreas, liver, bile, and bile ducts and prolonged and fatty diarrhea can cause a deficiency of these vitamins.

Vitamin A avitaminosis

avitaminosis vitamin a

Vitamin A (retinol, carotene) is important for maintaining normal differentiation of epithelium, skeletal muscle, and cell membrane components. It is essential for photosensitive retinal epithelium. Because vitamin A deficiency  (ICD-10:  E50) causes xerophthalmia and night blindness. In nature, vitamin A appears as retinol  (a more important form in which it is stored, transmitted, and actively involved in the function of sight) or as beta-carotene (provitamin A in yellow and leafy vegetables).

In the absence of vitamin A, the epithelium irregularly keratinizes and shows signs of the cylindrical epithelium’s squamous metaplasia. We see such changes in the trachea, bronchi, renal droplets, uterus, pancreatic ducts, and salivary gland ducts. You cannot regenerate rhodopsin so that vision disorders will occur. In short, in vitamin A deficiency, we have:

  • eye changes –  night blindness due to retinol deficiency,  xerophthalmia  (dry eyes), increased frequency of infections,  Bitot spots, softening of the cornea with consequent susceptibility to infections (keratomalacia).
  • skin changes – follicular hyperkeratosis due to impaired keratinization of the epithelium in hair follicles,
  • respiratory epithelial metaplasia with favoring infections and bronchopneumonias
  • pyelonephritis.

Vitamin D deficiency

vitamin d foods

Vitamin D’s function is to maintain normal plasma calcium and phosphorus levels. Calcium deficiency disrupts neural excitation and muscle relaxation, leading to hypocalcemic tetany. You should remember the sign of hypocalcemia –  Chvostek’s sign (tapping on the facial muscle causes facial muscle spasms) and Trousseau’s sign (arm muscle spasms when a cuff like a pressure gauge is put on).

Vitamin D deficiency in children causes rickets, and in adults, osteomalacia. The underlying disorder in both diseases is reduced mineralization of the newly formed bone matrix. In children, growth is not yet complete, so the pineal glands are open, there is insufficient mineralization of the newly formed bone and cartilaginous matrix in the growth zone. Epiphyseal cartilage overgrows without adequate calcification and normal cartilage cell maturation. The growth zone is wide and irregular. The cartilaginous cells are large, irregularly distributed, only in rows. The thickened ossification border is macroscopically observed as a spherical spindle thickening called a rickets crown.

Due to the abundance of osteoids, the bone is soft, flexible, and suitable for distortion and deformation. The softened occipital bone that dies when touched is called the craniotabes. The head takes on a square shape due to many osteoids created in frontal and parietal protuberances (square head –  square head ). And the spine is softened, causing kyphoscoliosis. The sternum protrudes or dents (pectus carinatum or pectus excavatum). The bones of the limbs are thick and stocky and shorter. The softer bones in the legs bend and form deformed O or X-shaped legs. In women, the pelvis becomes narrowed due to the sacrum’s impression and the suppression of the acetabulum ( pelvis angusta ) or flat ( pelvis plan ).

Vitamin K

Vitamin K comes in two forms: K 1  in plants and K 2, synthesized by the bacterial intestinal flora. Vitamin K serves as a cofactor in glutamic acid’s carboxylation to gamma-carboxyglutamic acid (in the liver). It is necessary for the functioning of the three clotting factors (VII, IX, and X) and proteins C and S. The natural deficiency of vitamin K occurs in newborns because they have sterile intestines. The most important complication is hemorrhagic diathesis (bleeding tendency), with the most dangerous manifestation being intracranial hemorrhage. Therefore, vitamin K is given to newborns prophylactically to avoid vitamin K avitaminosis.

Water-soluble vitamins

Vitamin B 1 (thiamine)

Vitamin B avitaminosis 1 (thiamine) is known as beriberi. It most commonly occurs in alcoholics. Thiamine deficiency is manifested by changes in peripheral nerves, the brain, and the heart. Peripheral nonspecific neuropathy or dry beriberi is asymmetrical neuropathy that first appears on the legs, followed by weakened reflexes, atrophy, and muscle weakness. It is characterized by myelin degeneration and axon fragmentation. Changes in the cardiovascular system or wet beriberi are characterized by peripheral vasodilation leading to AV shunts and consequent dilatation of the heart.

The heart is dilated, thinned walls, heavier and reduced stroke volume, leading to peripheral edema. As mentioned earlier, alcoholics develop Wernicke-Korsakoff syndrome due to thiamine deficiency, two syndromes,  Wernicke’s encephalopathy and  Korsakoff’s psychosis, which often occurs together for the same cause. Encephalopathy is characterized by ophthalmoplegia (weakening of extraocular muscles), ataxia (incoordination of voluntary movements), and confusion.

Korsakoff’s syndrome is also called an amnesia-confabulatory syndrome due to retrograde amnesia, inability to remember new information, and confabulation.

Vitamin B 2 (riboflavin)

Vitamin B 2  (riboflavin) coenzyme is in various oxidation and reduction reactions. Today, its deficiency is a rarity. The morphological changes it causes are changes in the scalp, lips, tongue, cornea, and erythroid lineage. Ketosis is a characteristic change. Some fissures radiate and sometimes become secondarily infected in the corner of the lips. Glossitis is also present.

Vitamin B 3 (niacin)

vitamin b3 niacin

Niacin avitaminosis causes a disease called pellagra. It is most commonly found in alcoholics and chronic patients and in people whose diet is poor in tryptophan and rich in leucine (leucine inhibits the conversion of tryptophan to niacin). Pellagra is clinically manifested by dermatitis, diarrhea, and dementia. Long-term untreated pellagra is fatal.

Vitamin B 6 (pyridoxine)

Vitamin B 6  (pyridoxine) is a cofactor in a number of enzymes involved in the metabolism of lipids and amino acids, and its deficiency is rare

Vitamin B 12 and folic acid

Vitamin B 12  or cyanocobalamin occurs in two active forms – coenzyme B 12  and methylcobalamin. It is essential to synthesize methionine, nucleic acids, and folic acid metabolism. It is found exclusively in food of animal origin. Plants cannot produce it (that is why people who eliminate animal origin products from their diet sometimes cannot compensate for B 12, and they should be suspected of B after 12  deficiency). For the absorption of vitamin B. 12, gastric cells’ intrinsic factor is necessary.

Vitamin B 9  or folic acid (pteroylmonoglutamic acid) is an oxidized folate form. It has a similar role as cobalamin.

Both vitamins are absorbed in the small intestine. Avitaminosis of both vitamins causes megaloblastic anemia. Since DNA synthesis is disrupted, changes are first observed in the fastest-dividing hematopoietic cells. Glossitis is present. The mucosa of the digestive tract is atrophied. The bone marrow is hyperplastic and, as in the blood, megalocytes and megakaryoblasts predominate.

Anemia leads to tissue hypoxia, so there will be a fatty change in the parenchymal organs. The posterior and lateral columns of the spinal cord are demyelinated. A diet low in folic acid in the first trimester of pregnancy increases the risk of neural tube rupture.

Vitamin C

vitamin c from fruits

Vitamin C ( ascorbic acid ) has the property of reversible oxidation and reduction, on which its action is based. In the body, there is a balance of reduced (L-ascorbic acid) and oxidized (L-dehydroascorbic acid) form:
L-ascorbic acid ↔ dehydro-L-ascorbic acid + 2H +  + 2e .

Vitamin C as a cofactor of proline hydroxylase

This system is associated with other reducing and oxidizing agents. Vitamin C acts in the synthesis of collagen as a coenzyme hydroxylase that hydroxylates the amino acid residues (prolyl and lysyl) of procollagen, a condition for the stabilization of collagen. It also participates in the synthesis of norepinephrine from 3,4-dihydroxy phenyl-ethylamine, carnitine from butyrobetaine 5-hydroxy-tryptophan from tryptamine. The absorption of iron from the intestine is better with ascorbic acid because it reduces the ferric form of iron to the ferrous form. Before the ferritin release, iron is converted to ferric form with ascorbic acid. Ascorbic acid protects tetrahydrofolate from the action of oxidizing substances.
In addition to collagen synthesis, vitamin C is important in synthesizing intercellular substances such as ostemucine, chondromucine, and dentin.

Humans, monkeys, and guinea pigs cannot synthesize ascorbic acid due to a mutation in the gene for the enzyme L-gluconolactone oxidase, which catalyzes the transition L-gluconogamalactone to L-ascorbic acid. The daily requirement for vitamin C in quiet conditions is 60 mg, but this need increases two to three times in stress, infection, after surgery, in pregnancy, breastfeeding, and hyperthyroidism. The reserve is small, so it wears out quickly. The kidneys excrete it as oxalate or sulfate.

Vitamin C avitaminosis is rare and causes scurvy, a disease characterized by bone disorders, bleeding, and inability to heal wounds. The cause of this is the formation of abnormal collagen, where the bleeding that accompanies scurvy is the result of a defect in collagen as an integral part of the capillary wall and venules. Therefore, we often see spotting (ecchymoses and purpura) on the mucous membranes.

Often bleeding gums, teeth can fall out due to alveolar bone resorption. Poor connection between the periosteum and bone can lead to subperiosteal bleeding. Due to insufficient production of the osteoid matrix and excessive cartilage growth, wide pineal glands are formed. Anemia is common due to frequent bleeding and reduced release of iron from ferritin reduced absorption of iron from the intestine, and reduced amount of effective folate due to the irreversible oxidation of N 10 formyl-tetrahydrofolate into ineffective metabolites.

Susceptibility to infections is a logical outcome.

Stroke, how to prevent it

A stroke occurs when a blood vessel in the brain ruptures or becomes clogged. The affected part of the brain does not get the necessary blood, and within a few minutes, it begins to die.

If you have a stroke, you may die, remain paralyzed, or have difficulty speaking or understanding speech. And you can damage your eyesight. You may also lose emotional control or fall into it depression. Each stroke causes unique effects.

If you notice warning signs of a stroke, don’t wait. Call the emergency number or anyone to immediately take you to the nearest hospital. Every second count!

What can I do to prevent a stroke?

Stroke is the leading cause of disability and the third most common cause of death in the United States. It is a fatal disease, and it is essential to minimize that risk.

Aging, male, then African-American, Hispanic or Asian, diabetes, a history of stroke, or a family history of stroke increase stroke risk. These are factors you can’t influence.

But you can influence the following factors: high blood pressure, heart disease, minor strokes (transient ischemic attacks, TIA), smoking, and high red blood cell counts. High blood pressure is particularly pronounced among African-Americans. In blacks, high blood pressure occurs earlier than in whites and usually takes a more severe form. Blacks also have almost double the rate of fatal stroke.

Regardless of your race, it’s important to check your blood pressure – and treat it if it’s high.

What is high blood pressure?

brain pressure

When your blood pressure is checked, your doctor measures two values. The first number (systolic pressure) indicates your arteries’ pressure during heart House. The second number (diastolic pressure) indicates the pressure as the heart rests between beats.

Normal blood pressure is in a certain range; numbers do not specify it. However, it should be less than 140/90 in adults. If your blood pressure rises above this limit and stays at that value, you have high blood pressure.

“If I had at least gone to the doctor to check my blood pressure, he would have prescribed me a drug to regulate high blood pressure … Maybe then I wouldn’t have had a stroke.”

What causes high blood pressure?

In 90 to 95 percent of cases, the cause is unknown. In fact, you can have it for years without even knowing it. That is why it is an insidious cause – it simply arises quietly, without warning. There is some other underlying problem in the remaining cases, such as a kidney disorder, an adrenal tumor, or a congenital heart defect.

Why is high blood pressure harmful?

It is dangerous because you may already damage your body’s organs by the time you find out you have it. Compared to people who regulate their high blood pressure, you are seven times more likely to have a stroke; the probability of congestive heart disease is six times higher. The probability of coronary heart disease (which leads to a heart attack) is three times higher.

“Basically, high blood pressure is harmful because it puts extra strain on your heart and damages your arteries. And that’s by no means healthy.”

Tips on how to live with it?

There is only one sure way to find out if you have high blood pressure: go check it out! If you have normal blood pressure, you should check it every two years. If your blood pressure is close to the upper limit of normal or high blood pressure in your family history, you are at increased risk of developing high blood pressure. Your doctor will tell you how often you need to measure it.

Measuring blood pressure is quick and painless.

You can do this in a doctor’s office, hospital clinic, school, nurse’s room, in the clinic of your company, or public on the occasion of health actions if the appropriate equipment is available. You can also contact the Red Cross or a hospital.

What else can I do to reduce the risk of stroke?

  • If you smoke, quit now!
  • Smoking significantly increases the risk of stroke.
  • Recognize and treat diabetes.
  • If you have diabetes, never stop taking your medication without first talking to your doctor.
  • Don’t drink too much alcohol.
  • More than one drink a day can raise blood pressure.
  • Engage in physical activity.

Physical activity helps reduce the risk of heart disease, a risk factor for stroke.

Try to do moderate to heavy activities for 30 minutes at least 3-4 times a week.

Eat healthily.

Eat foods that are low in fat, cholesterol, and sodium.

You go for regular medical checkups.

Instead of a conclusion

Reduce the risk of disability or death from stroke:  CHECK YOUR BLOOD PRESSURE TODAY!

“High blood pressure and this stroke didn’t just sneak up on me like that. It found my whole family unprepared. Now they’re taking care of me.”

If your doctor tells you that you have high blood pressure (hypertension), it is important to know the following:

  • You can’t ignore high blood pressure; he will not disappear.
  • He can be treated.
  • Treating high blood pressure can prevent heart attack, stroke, or kidney failure.

Enzymes – structure and general characteristics

ENZYMES – structure and general characteristics

Enzymes are carriers of many metabolic reactions in the body. Metabolic reactions in the human body would not be possible without enzymes’ presence. Substrates are compounds that are chemically modified by the action of enzymes. The first enzyme isolated in the crystalline state was urease (Summer).

Enzymes contain an active center that is part of their chain and is specially folded. By denaturing the enzyme, they lose their function, although the amino acid sequence remains the same. Many enzymes consist of a protein part and a non-protein (prosthetic) part. Apoenzymes bind such a group reversibly, and the prosthetic group is called a coenzyme.

Enzymes are stereospecific. They react with only one stereoisomer of the substrate.

The properties of enzymes can be divided into 4 rules:

  1. They reversibly bind the substrate.
  2. They do not change the direction of the chemical reaction but accelerate it in both directions.
  3. Chemically unchanged (physically altered) come out of the reaction.
  4. Enzymatic catalysis can be regulated.

Activation energy

 

Steps in reactions with enzymes:

The coupling of enzyme and substrate to enzyme-substrate (ES) is an exergonic reaction.

Enzyme-product (EP) formation, wherein P is bound to the active site.
 
Product release

Peter’s law of action applies to every step. Reactions in the body are mostly androgens, and in the presence of enzymes, they are accelerated by a factor of 〖10〗 ^ 8- 〖10〗 ^ 10.

The intermediate reactions by which the overall process occurs are not in balance because one product is always consumed. The second reaction must be exergonic for G = 0 to be valid in total.

Enzyme structure

Enzymes are mainly globular proteins, molecular Peter from 1000 – 10000. They can combine into multi-enzyme complexes, which become important sites of regulation. The multiple folded part of the chain creates a skeleton to stabilize the active center. At this point, the substrate binds with the release of energy.

The center is located in a groove where side chains of amino acids and sometimes covalently bound substrates can react with the substrate. This structure is not rigid but dynamic and achieves reversible conformational changes. In the binding reaction, the participants’ spatial arrangement is also important, and an induced conformational change of the substrate and enzymes occurs.

Enzymes are mostly isolated in crystalline form, and their structure is determined by X-ray diffraction.

The active site generates multiple portions of the polypeptide chain. The substrate enters the groove, exposed to reactive groups of polypeptide side chains. It can be bound by ionic bond, metal (magnesium ion), hydrophobic, or hydrogen. There is also a conformational change on the substrate and enzyme called induced adaptation.

During the binding reaction, the substrate is removed from the aqueous environment and enters a new one, where a different equilibrium constant, the so-called internal equilibrium constant. The substrate is acted upon by various functional groups in the groove, acting as acceptors or proton donors. Steric and electronic deformation of the substrate occurs.

These above-mentioned processes create a transitional state where the product is also released in addition to the release of energy.

Ping-Pong mechanism

The Ping-Pong mechanism is based on the fact that multiple substrates bind in a certain order. In this process, functional groups transition from one substrate to another. The second substrate binds to the active site only after dissociation of the first. An example of this mechanism is aminotransferases for an amino group transfer, whereby a Schiff base is formed.

In the activation center, some side chains are destined to interact:

Histidine

Histidine contains an imidazolyl residue, which can receive electrons and pass into the imidazolium ion, forming a ring with two equivalent nitrogen atoms (pKa = 6 – 7). Histidine can be a proton acceptor or donor in a neutral environment, and it is an effective catalyst in acid-base reactions.

Carboxylate ion glutamine and aspartic acid can be proton acceptors.

Arginine

Arginine has a strongly basic guanidino group that can bind negatively charged groups and thus participate in substrate binding.

Lysine

Lysine can contribute to substrate binding, and the reactive –NH2 group can form Schiff bases with carbonyl compounds.

Cysteine

Cysteine contains -SH group, which is weakly acidic and is an effective nucleophile. This group reacts with iodoacetamide and N-ethylmaleinimide, and the -SH group is blocked, i.e., enzyme poisoning occurs. Heavy metal ions (Hg, Cu…) and mercury organic compounds also lead to enzyme poisoning. The SH group plays an important role in forming covalent intermediates, such as, e.g., thioesters, which are energy-rich compounds.

Serine

Serine contains an –OH group that can participate in covalent catalysis. In a serine protease, the hydroxyl group binds to the rest of the peptide chain. This group can also form hydrogen bonds and thus participate in binding the substrate.

Tyrosine

Tyrosine contains a phenolic group which may be a nucleophile in dissociated form, while in the protonated state, it is a participant in hydrophobic interactions with aromatic substrates.

The affinity labeling method synthesizes a substrate that binds to the active site. By cleaving the enzyme with a protease and examining the resulting peptides, it can be determined which amino acids from the active site are involved in substrate binding and other reactions.

Groups that can be reversibly protonated are also found on enzyme proteins’ surfaces. Their degree of dissociation depends on the pH, and therefore the conformation of the protein and its catalytic action change depending on the pH.

The amount of pH at which the catalytic action is best is called pH-optimum.
As the temperature increases, so does the enzyme activity until denaturation begins.

In enzymatic catalysis, due to the catalytic center’s specificity, only one reaction is always catalyzed. Due to the size, conformation, and distribution of the charge, there is a specificity towards the substrate, which can be expressed differently. Specificity to stereoisomers is particularly pronounced and applies to both chiral and non-chiral substrates.

Sometimes several substances react with a single enzyme, so we are talking about group specificity (glycosidases).

Isoenzymes

Isoenzymes catalyze the same reaction but differ in structure, which can be genetically determined. There are either really different genes or oligomers composed of different subunits. An isoenzyme is aldolase or lactate dehydrogenase, which has 5 different tetramers, and the expression of individual subunits depends on the organ. They may differ from each other in terms of specificity for a substrate or sensitivity to regulatory factors.

Multienzyme complexes

Multienzyme complexes are aggregates of several enzymes that catalyze a series of related reactions (pyruvate or oligomeric supra structures are composed in part of enzymatic proteins formed by gene fusion. Their principle of action is that the intermediate of the enzymatic reaction is transferred from one enzyme to another within the complex (supra structure).

Pneumonia infection

Pneumonia is an infection of the pulmonary alveoli or walls of the alveolar sacs. The diagnosis of pneumonia is quite obvious; however, as many organisms can cause pneumonia, determining the cause in a particular case can be very difficult.

Numerous microorganisms can cause pneumonia, but they most commonly cause its bacteria. Common causes depend on the patient’s immune status, the location where the patient developed pneumonia, the patient’s age, and the type of pneumonia the patient exhibits (e.g., typical of interstitial pneumonia). Clinical and epidemiological factors are used to determine the most likely cause of each particular pneumonia case.

pneumonia pneumonia table 1
pneumonia 2

Manifestations of pneumonia

Many patients diagnosed with pneumonia mention that they have previously had similar symptoms, flu, or upper respiratory tract infection. A patient with pneumonia will often continue to have an upper respiratory tract infection and develop respiratory symptoms that indicate a lower respiratory tract infection – cough, dyspnea, sputum production, and tachycardia. A pneumonia diagnosis is more likely if the patient also has a fever (except neonatal diagnosed with afebrile Chlamydia trachomatis pneumonia) and auscultatory findings that include abnormal breathing sounds, abnormal percussion findings, and crepitations.

Chest X-ray of a patient with Q fever. The arrow indicates the consolidation of the lower right part of the lung and the thickened pericardium.

Pneumonia can be classified depending on the rate of pneumonia development. Pneumonia with an acute onset develops within 24-48 hands is common in typical pneumonia patients. The patient’s only complaint may be an infection of the upper respiratory tract. Still, the manifestations of typical pneumonia develop rapidly – high fever, shivering, dyspnea, tachycardia, productive cough with purulent sputum, and lung consolidation as seen on X-ray.

Interstitial pneumonia (atypical pneumonia) has a subacute onset; it may take several days to a week before the patient develops signs and symptoms of pneumonia – lower-grade fever, shivering, paroxysmal cough with or without mucoid sputum production, and pulmonary infiltrates seen on chest X-ray.

Chronic pneumonia takes weeks to months to develop full symptoms. Patients usually present a history of night sweats, low-grade fever, significant weight loss, productive cough with purulent sputum, dyspnea;  Ghon hotspots can be seen on an X-ray of the lungs.

The symptoms of aspiration pneumonia are similar to other acute-onset pneumonia, except that patients experience recurrent rigor rather than cold-induced rigor. The consolidation of lung segments is seen on X-ray. About half of patients with aspiration pneumonia will have unpleasant-smelling sputum.

Some causes of pneumonia that give unique signs and symptoms:

  • Legionnaires’ disease caused by Legionella sp . may result in pneumonia with relative bradycardia, abdominal pain, vomiting, diarrhea, hematuria, mental confusion, abnormal liver, kidney test results, and increased serum creatinine phosphokinase levels.
  • Psittacosis cause by Chlamydophilae psittaci  (formerly known as Chlamydia psittaci ) may result in pneumonia with relative bradycardia, epistaxis,  Horder points, splenomegaly, or normal or low white blood cell counts. The disease is associated with people who care for parrots.
  • Q fever caused by Coxiellae burnetti can cause pneumonia with relative bradycardia, hepatomegaly, endocarditis, and abnormal liver function tests. Q fever is associated with farmers who have recently given birth to animals.
  • Erythema nodosum and hilar adenopathy can be seen in patients with pneumonia due to fungi like  Histoplasma capsulatum and  Coccidioides immitis.
  • Fungal pneumonia most commonly causes Blastomyces dermatitidis. It can also produce rough verrucous skin lesions.

Epidemiology of pneumonia

  • In the United States alone, two to three million pneumonia cases are reported annually.
  • In the U.S. alone, pneumonia patients are responsible for over 10 million doctor visits, half a million hospitalizations, and 45,000 deaths a year. Expensive influenza and pneumonia are the seventh leading cause of death in the United States.
  • A patient with pneumonia usually had a previous viral infection of the upper respiratory tract.
  • Inhalation and aspiration are the two most common ways of acquiring infectious pneumonia.
  • Pneumonia is more common in the winter months and in people over 65.
  • Elderly patients are more likely to be hospitalized and have a higher mortality rate after the onset of pneumonia.
  • Aspiration pneumonia is an endogenous infection.
  • The following conditions predispose a person to aspiration pneumonia: altered level of consciousness, alcoholism, seizures, anesthesia, central nervous system disorders, trauma, dysphagia, esophageal disorders, and nasogastric probes.

Pathogenesis of pneumonia

Bacteria are not present in the lower respiratory tract of patients with pneumonia. Organisms that enter the alveoli are eliminated through alveolar macrophages, which are considered to be the most important pathway for the elimination of organisms that manage to escape the defense mechanisms in the upper respiratory system.

  • When a microorganism enters the alveoli, IgG can be opsonized in the fluid lining the alveoli and then digested. Macrophage via the Fc receptor.
  • If no specific antibody to the organism is present, the macrophage can still phagocytose the microorganism using C-reactive protein or complement receptors or via receptors for pathogen-associated molecular patterns (PAMPs). Mannan, lipopolysaccharides, lipoteichoic acid, N-formylated methionine-containing peptides, muramyl peptides, and peptidoglycans are examples PAMPs that alveolar macrophages can use to phagocytose bacteria.
  • When a microorganism phagocytoses, macrophages destroy the microorganism, if possible, and present microbial antigens on the surface for B and T lymphocytes.
  • When activated, B and T lymphocytes can produce more antibodies and activate macrophages. Macrophages simultaneously release factors that help carry polymorphonuclear leukocytes out of the bloodstream and initiate an inflammatory response. Polymorphonuclear cells, antibodies, and complement components are useful in destroying microorganisms.

Bacterial survival in areoles

Many bacteria that cause pneumonia can initially survive in the alveoli due to the following self-defense mechanisms:

  • Capsules (e.g., Streptococcus pneumoniae, Haemophilus influenzae ) prevents phagocytosis by alveolar macrophages.
  • Viruses and  Chlamydia invade the host cell before alveolar macrophages can phagocytose them.
  • Mycobacterium tuberculosis can survive in alveolar macrophages even after macrophages phagocytose them.

If organisms survive in the alveoli, microbial growth can cause tissue injury, stimulating the host to amplify the inflammatory response. Tissue injury can also occur due to exotoxins produced by bacteria, cell lysis caused by viruses, or the death of alveolar macrophages and the release of their lysosomal contents into the alveoli due to the growth of microorganisms in phagocytes.

Vascular permeability increases and polymorphonuclear cells arrive in the area with many serum components, trying to retain and eliminate microorganisms. While microorganisms damage the alveoli, other alveolar macrophages are recruited into the area of inflammation. Lung-associated lymphoid tissue (mediastinal lymph nodes) becomes enlarged after B and T lymphocytes’ activation. Chest X-ray may show enlargement of mediastinal lymph nodes in patients with pneumonia.

Typical or lobar pneumonia

Accumulation of microorganisms, immune system cells, and serum components can cause alveolar filling. This inflammatory response is called opacity or consolidation on chest X-ray and is commonly seen in patients with pneumonia caused by S.pneumoniae. This type of pneumonia is called typical or lobar pneumonia. The inflammatory response to infection produces factors that allow microorganisms to leave the lungs and cause systemic effects such as fever. Examples of microbial factors that may have systemic effects include gram-negative bacterial endotoxin that causes fever and septic shock and gram-positive bacterial cell wall components that can lead to fever and septic shock.

Organisms like Mycoplasma pneumoniae and influenza virus do not initially cause the accumulation of large amounts of fluid in the alveoli. However, after infection with these organisms, inflammation in the interstitial spaces (alveolar walls) occurs, resulting in interstitial or atypical pneumonia. Thoracic X-ray in patients with this type of pneumonia shows fine granular diffuse infiltrates.

Other organisms like Staphylococcus aureus, gram-negative rod-shaped bacteria, and anaerobic bacteria from abscesses or microabscesses. In these infections, the immune system can isolate itself from organisms and create localized abscesses or microabscesses that usually show a well-localized circular lesion with necrotic translucent centers on chest X-ray.

Diagnosing pneumonia

Patients with pneumonia may present with chest discomfort, cough (productive or unproductive paroxysmal cough), rigore (patients with typical pneumonia), or feeling cold (patients with interstitial pneumonia), dyspnea, and fever. Physical examination may reveal increased respiratory rate and mucus on percussion over the affected regions of the lungs.

rtg snimak dijagnozaChest X-rays show new consolidations or infiltrations and help diagnose pneumonia. When the alveolar sacs are filled with inflammatory cells and fluid, chest X-rays show consolidated well-defined density areas – unilateral (inhalation or aspiration pneumonia), bilateral (hematogenous spread to the lungs), localized, or uniform. When a chest X-ray shows inflammation and thickening of the alveolar septa surrounding the alveoli, rather than filling the alveolar sacs with inflammatory material, a diagnosis of interstitial pneumonia is more likely.

Some organisms form abscesses in the lungs (e.g., S.aureus, Enterobacteriaceae, Pseudomonas aeruginosa, and anaerobic organisms); in such cases, a chest X-ray is useful for detecting abscesses. If present, certain radiological samples may have diagnostic value, e.g.:

A sign of a convex fissure as seen in Klebsiella pneumoniae infection (but also in other infections such as S. pneumoniae, P.aeruginosa, S.aureus, Legionella, and sometimes bronchoalveolar carcinoma.

  • Infection Klebsiella pneumoniae causes consolidation of the upper lobes, resulting in a “bulging fissure sign,” i.e., by dilating the affected part of the lung.
  • S.aureus  lung infections can cause multiple bilateral nodular infiltrates with central cavitation. In children, chest X-rays may show thin cavities (pneumatocele), bronchopleural fistulas, and empyema.
  • P.aeruginosa  infections can result in microabscesses that can merge into large abscesses.
  • Infections with gram-negative rods (e.g., Klebsiella, Proteus, E.coli ) often cause lung necrosis.
  • Consolidation of individual lung segments may indicate aspiration pneumonia.

Pathogen identification

To identify the specific pathogen that causes pneumonia, clinical and epidemiological data must be considered to limit the number of possible causes of pneumonia.

Gram staining of sputum in a patient with pneumonia due to Streptococcus pneumoniae. Gram-positive diplococci are seen in the sputum, and many polymorphonuclear leukocytes are present.

Gram staining of sputum of a patient with suspected pneumonia can help identify the cause of pneumonia. Some pathogens are poorly Gram-stained or not stained at all; other colors can be ordered: Dieterle silver color ( Legionella sp .), acid-fast Mycobacteria ), Gomori methenamine silver staining (fungi and Pneumocystis ).

Laboratory tests at diagnosis

Additional laboratory tests that can help establish a definitive diagnosis:

  • Sputum culture,
  • culture of blood samples for bacteria, fungi, or viruses,
  • serology for the detection of antibodies against pathogens (e.g., cold agglutination for M.pneumoniae; detection of antibodies to the capsule S.pneumoniae ),
  • antigenic tests to detect certain antigens produced by pathogens (e.g., polysaccharides for S.pneumoniae  and H.influenzae ),
  • skin tests to detect delayed hypersensitivity to certain pathogens (e.g., Mantoux test for M.tuberculosis, B.dermatitis, H.capsulatum, C.immitis).
  • PCR (polymerase chain reaction) for sputum samples and rapid determination of pathogens,
  • Urinalysis for  Legionella  antigens.

Treatment and prevention of pneumonia

Since bacteria cause most pneumonia cases, treatment usually involves antibiotic therapy. The tables list empirical treatments for patients with pneumonia. In about half of the patients, the etiological agent can be determined, and if it is known, more precise therapy can be started.

Two vaccines can be given to adults to help prevent pneumonia. The S.pneumoniae vaccine contains 23 types of capsular antigens and is used in people over 65 years of age. The influenza vaccine can be given annually to all people over the age of 50 to help prevent viral pneumonia or secondary bacterial pneumonia that can occur after an influenza virus infection. Chemoprophylaxis to prevent influenza infections is useful in preventing secondary bacterial pneumonia.

Conjugated heptavalent S.pneumoniae  The vaccine is important in preventing these infections in younger children. The conjugated H.influenzae type b (Hib) vaccine prevents H.influenzae infections in childhood. Premature neutropenic infants can prevent respiratory syncytial virus infections or infants with different predispositions to infection by periodic injections of immune globulin for respiratory syncytial virus or humanized murine monoclonal antibody (palivizumab). Annual immunization of children with influenza vaccine prevents infections in vaccinated children and appears to prevent the virus’s spread by close contact.

Menstrual cycle

The reproductive system of women, unlike the male system, shows regular cyclical changes that can be considered periodic preparations for fertilization and pregnancy. In humans and other primates, the cycle is called the menstrual cycle. Its most obvious feature is vaginal bleeding that occurs with peeling of the uterus’ lining (menstruation). The cycle’s length is notoriously variable, but the average figure is 28 days from the beginning of one menstrual cycle to the beginning of another. In practice, the days of the cycle are marked with a number, where the countdown begins on the first day of menstruation.

Ovarian cycle

Follicular phase

ovulation

At birth, there are many primordial follicles under the ovarian capsule in women. Each contains an immature ovum. At the beginning of each cycle, several of these follicles enlarge, and a cavity is created around this (creation of an antrum). This cavity is filled with follicular fluid. In humans, usually, one of these ovarian follicles begins to grow rapidly, and around the sixth day, it becomes the dominant follicle, while the others undergo regression and become atretic follicles. The atretic process involves apoptosis.

It is not clear the mechanism by which one of the follicles is selected to become the dominant follicle in this follicular phase of the menstrual cycle, but this appears to be related to the follicle’s ability to secrete estrogen, needed for final maturation. Many follicles develop simultaneously when women are given highly purified human pituitary gonadotropins by injection.

The primary source of circulating estrogen in ovarian granulosa cells; Theca cells of the inner layer of the follicle are necessary for estrogen production as they secrete androgens that are aromatized into estrogens in granulosa cells.

Ovulation

At about 14. on the day of the cycle, the follicle ruptures, and the egg is released into the abdominal cavity – this is called the ovulation process. The ovum is “collected” by the fallopian tubes’ hairy ends. It is transmitted to the uterus and, unless fertilization occurs, further out through the vagina.

Luteal phase

At the time of ovulation, the ruptured follicle quickly fills with blood, forming something sometimes called the corpus hemorrhagic. Minor bleeding from the follicles into the abdominal cavity can irritate the lower abdomen’s peritoneum and dull pain. Granulosa and theca follicle cells multiply rapidly, and clotted blood is rapidly replaced by yellowish, lipid-rich luteal cells, forming the corpus luteum. This begins the menstrual cycle’s luteal cycle, during which luteal cells secrete estrogen and progesterone. The growth of the corpus luteum depends on developing an adequate blood supply. There is evidence that vascular endothelial growth factor (VEGF) is likely essential for this process.

If pregnancy occurs, the corpus luteum remains preserved, and there is usually no menstruation until after delivery. If pregnancy does not occur, the corpus luteum begins to degenerate about four days before the next menstruation (day 24 of the cycle) and is eventually replaced by scar tissue, forming the corpus Albicans.

New eggs are not formed after birth. During fetal development, the ovaries contain about 7 million primordial follicles. Yet many involute before birth, and others are lost after birth. There are about 2 million eggs at the time of birth, but 50% are atretic. A million normal ones then go through the first part of the meiotic division and enter stagnant prophase in which those who survive to remain in the prophase until adulthood. Atresia continues during development, and the number of eggs in both ovaries at puberty decreases to less than 300,000. Only one of these eggs per cycle (about 500 during normal reproductive life) normally reaches maturity – the rest decays.

Just before ovulation, the first meiotic division is completed. One of the daughter cells, the secondary oocyte, takes up the most cytoplasm, while the other, the first polar body, fragments and disappears. The secondary oocyte immediately begins a second meiotic division, but this division stops in metaphase and is completed only if the egg is fertilized. At that time, the second polar body is discarded, and the fertilized egg begins to form a new individual.

Uterine cycle

At the end of menstruation, all layers, except the endometrium’s deep layers, are peeled off. The new endometrium then grows again under estrogen’s influence from developing ovarian follicles. The endometrium thickens rapidly from 5. to 14—days of the menstrual cycle. As the thickness increases, the uterine glands elongate but have no secretion. These uterine endometrium changes are called the proliferative phase, or sometimes the preovulatory or follicular phase of the cycle. After ovulation, the endometrium becomes more vascularized and somewhat edematous under the influence of estrogen and progesterone from the corpus luteum. The glands become more convoluted and begin to secrete clear fluid. Consequently, this phase of the cycle is called the secretory or luteal phase. Late in the luteal phase, the endometrium, an anterior pituitary gland, produces prolactin, but its role is unknown.

The endometrium is supplied with blood by two arteries. The superficial two-thirds of the endometrium that exfoliates during menstruation (stratum functional) is perfused by long, convoluted spiral arteries. Short and straight basilar arteries perfuse the deeper layer that is not exfoliated (stratum basale).

When the corpus luteum involutes, hormones’ flow to the endometrium stops. The endometrium thins, which contributes to further twisting of the spiral arteries. Foci of necrosis appear on the endometrium. Also, degeneration and spasm of the spiral arteries’ walls occur, leading to punctate hemorrhages that produce menstrual blood.

Locally released prostaglandins probably create vasospasm. Large amounts of prostaglandins are present in the secretory endometrium and menstrual blood, and infusions of prostaglandin PGF2-alpha create endometrial necrosis and bleeding.

From the perspective of endometrial function, the menstrual cycle’s proliferative phase represents the renewal of the epithelium from the previous menstruation. The secretory phase represents the uterus’s preparation for implantation and fertilization of the ovum. The length of the secretory phase is constant (about 14 days), and the variations seen with the length of the menstrual cycle are mainly the result of the variation in the length of the proliferative phase. If fertilization does not occur during the secretory phase, the endometrium peels off, and a new cycle begins.

Normal menstruation

menstrual cycle menstruation

Menstrual blood is mostly arterial – only 25% of blood is of venous origin. It contains tissue debris, prostaglandins, and relatively large fibrinolysin from endometrial tissue. Fibrinolysin lyses clots, so menstrual blood does not contain clots unless the amount of blood is excessive.

The usual duration of menstruation is 3 to 5 days, but it can be 1 day to 8 days, which is not considered abnormal. The amount of blood lost can vary from a few drops to 80 mL; the average amount lost is 30 mL. Loss of more than 80 mL is abnormal. The amount of blood lost can be influenced by various factors, including endometrial thickness, medications, and diseases that affect the blood clotting system.

Cyclic changes of the cervix of the uterus and vagina

Although the cervix continues directly to the uterus’ body, the cervical mucosa does not undergo cyclic desquamation but only through changes in cervical mucus. Estrogen makes mucus less viscous and more alkaline – changes that help sperm survive and transport. Progesterone, on the other hand, makes mucus more viscous and cellular. Mucus is the least viscous at the time of ovulation.

Under estrogen’s influence, the vaginal epithelium becomes cornified, and you can identify the cornified cells in the vaginal smear. Under the influence of progesterone, viscous mucus is secreted, and the epithelium proliferates and is infiltrated by leukocytes.

Cyclic breast changes

Although lactation does not normally occur until the end of pregnancy, cyclical changes occur in the breasts during the menstrual cycle. Estrogens cause duct proliferation, while progesterone causes the growth of lobules and alveoli. The swelling of the chest and the pain that many women feel ten days before menstruation are probably the results of ductal distension, hyperemia, and edema of the interstitial breast tissue. All of these changes regress, along with symptoms, during menstruation.

Changes during sexual intercourse

During sexual arousal in women, fluid is secreted into the vaginal walls, probably due to the release of VIP (gastrointestinal polypeptide) from the nerves of the vagina. The vestibular glands also secrete a lubricating fluid. The upper part of the vagina is sensitive to stretching, while tactile stimulation of the labia minora and clitoris helps with sexual arousal. These stimuli are amplified by tactile stimulants from the breast and, as in men, by visual, auditory, and olfactory stimuli that can all together lead to a crescendo known as orgasm. During orgasm, autonomically mediated rhythmic contractions of the vaginal walls occur. Impulses also travel to the pudendal nerves and create rhythmic contractions of the bulbocavernosus and ischiocavernosus muscles. Vaginal contractions can help transport sperm but are not essential for this, as egg fertilization is not dependent on orgasm.

Ovulation indicators

Knowing when ovulation occurs during the menstrual cycle is essential for increasing fertility or, conversely, family planning. A simple and fairly safe indicator of ovulation time is a change – usually an increase – in basal body temperature. The increase in body temperature begins one to two days after ovulation. Women interested in getting the correct body temperature should use a digital thermometer and measure the temperature (oral and rectal) in the morning before getting out of bed. The cause of the change in body temperature at the time of ovulation is probably an increase in progesterone secretion, as progesterone is thermogenic.

A sudden increase in LH secretion triggers ovulation, and ovulation normally occurs about 9 hours after LH concentration peak. The egg lives for approximately 72 hours after being excreted from the follicle but can be fertilized in a much shorter period of time. In a study examining the association of isolated intercourse with pregnancy, 36% of women were pregnant after intercourse on the day of ovulation. Still, with intercourse on the days after ovulation, the percentage was zero.

Isolated sexual intercourse on the first and second days before ovulation also led to pregnancy in about 36% of women. Several pregnancies resulted from sexual intercourse 3., 4. or Day 5 before ovulation, although this percentage was much lower, for example, 8% 5th day before ovulation. Therefore, some sperm can survive in the female genital tract and fertilize the egg up to 120 hours before ovulation, but the most fertile period is apparently 48 hours before ovulation. However, for those interested in contraception methods by counting “fertile days,” it should be noted that there are rare cases of pregnancy due to sexual intercourse for each day of the cycle.