Forwarded from H J
Energy Input
Apoptosis is energy-dependent, meaning it requires input from a cell for cell death to occur, leading to the term "cell suicide." Necrosis does not require any energy input from a cell, as external factors or localized infections are what trigger necrosis.
Caspases
For the apoptotic pathways that cause cell suicide, the primary molecular signals are inactive proenzymes called caspases. Necrosis sometimes makes uses of caspases, but to a much lesser degree, and often the process makes no use of them, as a cell itself is destroyed in an uncontrolled fashion during necrotic events. For example, necrosis is the process behind dying, or necrotic, tissue that surrounds, say, a venomous spider bite.
Research has identified as many as 13 caspases, broadly categorized as initiators, effectors, or executioners (the ones that directly trigger cell death), and inflammatory. Despite what it may sound like, inflammatory caspases actually inhibit inflammation. As necrosis lacks the inflammatory caspase input, inflammation is always present in necrotic cell death.
Apoptosis is energy-dependent, meaning it requires input from a cell for cell death to occur, leading to the term "cell suicide." Necrosis does not require any energy input from a cell, as external factors or localized infections are what trigger necrosis.
Caspases
For the apoptotic pathways that cause cell suicide, the primary molecular signals are inactive proenzymes called caspases. Necrosis sometimes makes uses of caspases, but to a much lesser degree, and often the process makes no use of them, as a cell itself is destroyed in an uncontrolled fashion during necrotic events. For example, necrosis is the process behind dying, or necrotic, tissue that surrounds, say, a venomous spider bite.
Research has identified as many as 13 caspases, broadly categorized as initiators, effectors, or executioners (the ones that directly trigger cell death), and inflammatory. Despite what it may sound like, inflammatory caspases actually inhibit inflammation. As necrosis lacks the inflammatory caspase input, inflammation is always present in necrotic cell death.
Forwarded from H J
Apoptotic and Necrotic Symptoms
Because apoptosis is a normal part of an organism's cellular balance, there are no noticeable symptoms related to the process. In contrast, necrosis is an uncontrolled change in an organism's cell balance, so it is always harmful, resulting in noticeable, negative symptoms.
Necrosis is accompanied in its early stages by inflammation, as components (including cell structures, cytoplasm, and DNA/RNA) of the ruptured or damaged cells are released. To an organism, this unregulated flow of proteins, chemicals, and genetic material triggers emergency responses, such as inflammation to protect surrounding tissues, as well as an increase in white blood cells, macrophages, and T cell production to fight off infection. These reactions are often accompanied by a metabolic boost and fever, which can lead to fatigue and an overall weakened immune system.
If left untreated, necrotic tissues will lose vascularity, meaning they will lose blood flow, and thus start dying. When this happens, the necrosis is called gangrene, a condition where tissue ultimately dies and must be removed to stop necrosis from expanding.
Because apoptosis is a normal part of an organism's cellular balance, there are no noticeable symptoms related to the process. In contrast, necrosis is an uncontrolled change in an organism's cell balance, so it is always harmful, resulting in noticeable, negative symptoms.
Necrosis is accompanied in its early stages by inflammation, as components (including cell structures, cytoplasm, and DNA/RNA) of the ruptured or damaged cells are released. To an organism, this unregulated flow of proteins, chemicals, and genetic material triggers emergency responses, such as inflammation to protect surrounding tissues, as well as an increase in white blood cells, macrophages, and T cell production to fight off infection. These reactions are often accompanied by a metabolic boost and fever, which can lead to fatigue and an overall weakened immune system.
If left untreated, necrotic tissues will lose vascularity, meaning they will lose blood flow, and thus start dying. When this happens, the necrosis is called gangrene, a condition where tissue ultimately dies and must be removed to stop necrosis from expanding.
Forwarded from H J
When Apoptosis is Unhealthy
Apoptosis becomes abnormal only when the cellular processes that keep the body in balance either cause too many cell deaths or cause too few. Many autoimmune diseases, such as muscular dystrophy and Alzheimer's, are believed to be related to excessive apoptosis, causing muscle or nerve cells to die before their time. Cells that grow without control, meaning apoptosis is not happening often enough, usually lead to tumors, which themselves can become cancerous.
General Causes of Apoptosis and Necrosis
There are three mechanisms that cause cell death:
Self-generated signals in a cell, which may arise from age, infection, irregular mitosis (cell division), or other causes. This mechanism is known as the intrinsic or mitochondrial pathway, whereas the following two types of cell death are extrinsic pathways.
The triggering of death activators, receptors on a cell's surface that respond to external signals such as hormones or other chemical messengers.
External triggering by reactive oxygen species, such as free radicals, which are dangerous to the body.
In general, apoptosis is part of life, the continuation of the cellular cycle initiated by mitosis. However, apoptosis can be triggered by a variety of harmful stimuli, such as heat, radiation, lack of oxygen (hypoxia), drugs and trauma, among others. In these cases, apoptosis rids the body of damaged cells or cells that can no longer perform normally and helps heal damaged areas. Higher degrees of damage from the same stimuli can lead to necrosis. For example, a mild burn can cause a small blister that heals in a week, but a third-degree burn will cause necrosis in the affected area.
Apoptosis can also be caused by hormonal and chemical changes in the body, a process most often seen in embryonic development. Both the immune and nervous systems develop with a large over-production of cells that are reduced before birth through selective processes carried out by apoptosis. For example, fetuses develop hands and feet without individual digits; once a chemical messenger is released, the webbed tissue between the fingers and toes dies off, separating each digit. A similar process occurs with sexual differentiation, as hormones guide fetal development to suppress or eliminate certain tissues and structures in favor of developing others. On the other hand, if necrosis is present during fetal development, some form of medical intervention is often required, and deformation or miscarriage may occur.
Types of Necrosis and Their Causes
In necrosis, a cell's death is usually caused by a sudden and uncontrolled rupture based on two mechanisms:
Interference with the cell's energy supply (blood, plasma, oxygen, etc.).
Direct damage to the cell membrane.
Necrosis is categorized in five ways, depending on the cause:
Bacterial or fungal infections may cause liquefactive necrosis. This is necrosis that includes the liquefied mass of dead tissue known as "pus."
The necrosis that arises from denatured proteins that impede proper circulation is called coagulative necrosis. This type is seen most often in the heart after an infarction, as well as in kidneys and adrenal glands.
Fungal and mycobacterial infections, such as tuberculosis, can cause gaseous necrosis. This combination of liquefactive and coagulative necrosis is caused by dead cells that are not completely digested by microphages; they leave a granular residue that impedes circulation.
Necrosis that occurs only in fatty tissue is called fat necrosis. The most common form of this necrosis is associated with pancreatitis, severe inflammation of the pancreas.
Deposits of antigens and antibodies combined with fibrin can adhere to and eventually block arteries and destroy their structure. This is called fibrinoid necrosis.
Treatment
Apoptosis and necrosis are treated in very different ways, primarily based on the fact that one process is often normal and the other is patently abnormal.
Although much of the apoptosis process is identified, the mechanisms and activation cascade is not yet fully understood. Rese
Apoptosis becomes abnormal only when the cellular processes that keep the body in balance either cause too many cell deaths or cause too few. Many autoimmune diseases, such as muscular dystrophy and Alzheimer's, are believed to be related to excessive apoptosis, causing muscle or nerve cells to die before their time. Cells that grow without control, meaning apoptosis is not happening often enough, usually lead to tumors, which themselves can become cancerous.
General Causes of Apoptosis and Necrosis
There are three mechanisms that cause cell death:
Self-generated signals in a cell, which may arise from age, infection, irregular mitosis (cell division), or other causes. This mechanism is known as the intrinsic or mitochondrial pathway, whereas the following two types of cell death are extrinsic pathways.
The triggering of death activators, receptors on a cell's surface that respond to external signals such as hormones or other chemical messengers.
External triggering by reactive oxygen species, such as free radicals, which are dangerous to the body.
In general, apoptosis is part of life, the continuation of the cellular cycle initiated by mitosis. However, apoptosis can be triggered by a variety of harmful stimuli, such as heat, radiation, lack of oxygen (hypoxia), drugs and trauma, among others. In these cases, apoptosis rids the body of damaged cells or cells that can no longer perform normally and helps heal damaged areas. Higher degrees of damage from the same stimuli can lead to necrosis. For example, a mild burn can cause a small blister that heals in a week, but a third-degree burn will cause necrosis in the affected area.
Apoptosis can also be caused by hormonal and chemical changes in the body, a process most often seen in embryonic development. Both the immune and nervous systems develop with a large over-production of cells that are reduced before birth through selective processes carried out by apoptosis. For example, fetuses develop hands and feet without individual digits; once a chemical messenger is released, the webbed tissue between the fingers and toes dies off, separating each digit. A similar process occurs with sexual differentiation, as hormones guide fetal development to suppress or eliminate certain tissues and structures in favor of developing others. On the other hand, if necrosis is present during fetal development, some form of medical intervention is often required, and deformation or miscarriage may occur.
Types of Necrosis and Their Causes
In necrosis, a cell's death is usually caused by a sudden and uncontrolled rupture based on two mechanisms:
Interference with the cell's energy supply (blood, plasma, oxygen, etc.).
Direct damage to the cell membrane.
Necrosis is categorized in five ways, depending on the cause:
Bacterial or fungal infections may cause liquefactive necrosis. This is necrosis that includes the liquefied mass of dead tissue known as "pus."
The necrosis that arises from denatured proteins that impede proper circulation is called coagulative necrosis. This type is seen most often in the heart after an infarction, as well as in kidneys and adrenal glands.
Fungal and mycobacterial infections, such as tuberculosis, can cause gaseous necrosis. This combination of liquefactive and coagulative necrosis is caused by dead cells that are not completely digested by microphages; they leave a granular residue that impedes circulation.
Necrosis that occurs only in fatty tissue is called fat necrosis. The most common form of this necrosis is associated with pancreatitis, severe inflammation of the pancreas.
Deposits of antigens and antibodies combined with fibrin can adhere to and eventually block arteries and destroy their structure. This is called fibrinoid necrosis.
Treatment
Apoptosis and necrosis are treated in very different ways, primarily based on the fact that one process is often normal and the other is patently abnormal.
Although much of the apoptosis process is identified, the mechanisms and activation cascade is not yet fully understood. Rese
Forwarded from H J
arch into the pathways is widespread and expanding as the clinical findings have direct applications to autoimmune diseases, such as Parkinson's, Huntington's, amyotrophic lateral sclerosis, and HIV/AIDS, as well as nearly all types of cancer. Because apoptosis is a process of health and disease, the more it is understood, the better the chances are of developing more effective and better-targeted treatments. In all cases, untreated necrosis is dangerous and can lead to death.
In the case of autoimmune diseases, where apoptosis is causing too many cell deaths, treatment consists of inhibiting the caspase triggers or reducing the external triggers that may be precipitating the increased cell suicides. For cancer, the opposite is needed, so treatment to induce apoptosis in the tumor cells, making the cells more vulnerable to drugs and radiation, is a key part of most therapies. A promising new treatment involves the generic compound dichloroacetic acid (DCA), which has been shown to be highly-effective in "reigniting" apoptosis in certain cancerous tumors.
The common treatments for necrosis are:
Antibiotics/NSAIDs: these fight the infectious and inflammatory nature of necrosis and are often the first line of defense against its damage. In extreme cases, immunosuppressing drugs may be prescribed to reduce the inflammatory response.
Debridement: removal of the dead tissue, from simple cleaning of the area to surgery, including amputation. Fly larvae (maggots) are also used quite effectively in some forms of debridement.
Antioxidants: may be used to treat internal necrotic tissues, most often related to ischemia, the end result of heart tissue losing vascularity after an infarction (heart attack).
Occurrence
With over 50 billion cells naturally dying in an adult human body each day, apoptosis is very common and typically benign, if not entirely beneficial. Necrosis is relatively rare by comparison, and the degree of cellular death depends greatly on whether effective treatments, such as antibiotics and anti-inflammatory drugs, are applied.
In the case of autoimmune diseases, where apoptosis is causing too many cell deaths, treatment consists of inhibiting the caspase triggers or reducing the external triggers that may be precipitating the increased cell suicides. For cancer, the opposite is needed, so treatment to induce apoptosis in the tumor cells, making the cells more vulnerable to drugs and radiation, is a key part of most therapies. A promising new treatment involves the generic compound dichloroacetic acid (DCA), which has been shown to be highly-effective in "reigniting" apoptosis in certain cancerous tumors.
The common treatments for necrosis are:
Antibiotics/NSAIDs: these fight the infectious and inflammatory nature of necrosis and are often the first line of defense against its damage. In extreme cases, immunosuppressing drugs may be prescribed to reduce the inflammatory response.
Debridement: removal of the dead tissue, from simple cleaning of the area to surgery, including amputation. Fly larvae (maggots) are also used quite effectively in some forms of debridement.
Antioxidants: may be used to treat internal necrotic tissues, most often related to ischemia, the end result of heart tissue losing vascularity after an infarction (heart attack).
Occurrence
With over 50 billion cells naturally dying in an adult human body each day, apoptosis is very common and typically benign, if not entirely beneficial. Necrosis is relatively rare by comparison, and the degree of cellular death depends greatly on whether effective treatments, such as antibiotics and anti-inflammatory drugs, are applied.
.#للاسفادة 🔬💉
. إعادة نشر
.
.
ﻣﺼﻄﻠﺤﺎﺕ ﻃﺒﻴﺔ ﻟﻔﻨﻲ ﻣﺨﺘﺒﺮﺍﺕ
ﻣﻌﻤﻞ ﺃﻭ ﻓﻨﻰ ﻣﺨﺘﺒﺮ ﺃﻭ ﺗﻘﻨﻰ ﻣﺨﺘﺒﺮ
Laboratory Technician
ﻣﻌﻤﻞ Laboratory
ﺗﺤﻠﻴﻞ Analysis
ﺍﻟﻤﺠﻬﺮ ﺃﻭ ﺍﻟﻤﻴﻜﺮﻭﺳﻜﻮﺏ Microscope
ﺍﻟﺤﻀﺎﻧﺔ Incubator
ﺍﻟﺤﻤﺎﻡ ﺍﻟﻤﺎﺋﻰ ( ﻟﻠﺘﺴﺨﻴﻦ ﺍﻟﻐﻴﺮ ﻣﺒﺎﺷﺮ ﺑﺎﻟﻤﺎﺀ ) Water bath
ﺟﻬﺎﺯ ﺍﻟﺘﻌﻘﻴﻢ ﺗﺤﺖ ﺿﻐﻂ ﺍﻟﺒﺨﺎﺭ Autoclave
ﺟﻬﺎﺯ ﺍﻟﻄﺮﺩ ﺍﻟﻤﺮﻛﺰﻯ Centrifuge
ﺟﻬﺎﺯ ﻗﻴﺎﺱ ﺍﻷﻟﻮﺍﻥ Colorometar
ﺍﻟﻤﺎﺻﺔ ( ﻣﻨﻬﺎ ﺯﺟﺎﺝ / ﺃﻭﺗﻮﻣﺎﺗﻚ ﺛﺎﺑﺖ ﻭﻣﺘﻐﻴﺮ ) Pipette
ﺻﻔﺮ ﺗﻌﺪﻳﻞ ﺍﻟﺠﻬﺎﺯ ( ﻗﺒﻞ ﺍﻟﻘﺮﺍﺀﺓ ) Zero adjustment
ﺍﻟﻘﻴﺎﺱ Measurement
ﻣﺤﻠﻮﻝ ﺍﻟﻤﺴﺢ ( ﺗﺼﻔﻴﺮ ﺍﻟﺠﻬﺎﺯ ) Reagent blank
ﻃﻮﻝ ﺍﻟﻤﻮﺟﺔ ( ﺗﺮﺩﺩ ﺍﻟﻘﺮﺍﺀﺓ ﻋﻠﻰ ﺍﻟﺠﻬﺎﺯ Wavelength
ﻛﻴﻮﻓﻴﺖ (ﻟﻠﻘﺮﺍﺀﺓ ﻋﻠﻰ ﺟﻬﺎﺯﻗﻴﺎﺱ ﺍﻷﻟﻮﺍﻥ ) Cuvet
ﻣﺤﺎﻟﻴﻞ( كواشف) Reagent
ﻣﺤﻠﻮﻝ ﻗﻴﺎﺳﻰ Standard R.
ﺍﻟﻌﻴﻨﺎﺕ Samples
ﺍﻟﻤﺼﻞ Serum
ﺍﻟﺒﻼﺯﻣﺎ plasma
ﻣﺮﺍﻗﺒﺔ ﺍﻟﺠﻮﺩﺓ Quality control
ﺍﻹﺳﺘﻘﺮﺍﺭ ﺃﻭ ﺍﻟﺜﺒﺎﺕ stability
ﻛﺎﺷﻒ ﻟﻮﻧِﻰ color reagent
ﻣﺪﻯ ﺍﻟﻘﻴﻢ ﺍﻟﻤﺘﻮﻗﻌﺔ (ﺍﻟﻄﺒﻴﻌﻴﺔ )Range expected values
ﺟﻠﻮﻛﻮﺯ (ﺳﻜﺮﺍﻟﺪﻡ ) Glucose
ﻣﻨﺤﻨﻰ ﺍﻟﺴﻜﺮ ﻓﻰ ﺍﻟﺪﻡ Blood Sugar Curve
ﺗﺤﻠﻴﻞ ﺍﻟﺴﻜﺮ ﺍﻟﻌﺸﻮائي Random Blood Glucose
ﻧﺴﺒﺔ ﺍﻟﺴﻜﺮ ﺻﺎﺋﻢ Fasting Blood Sugar
ﺍﻟﻌﺘﺒﺔ ﺍﻟﻜﻠﻮﻳﺔ ﻟﻠﺠﻠﻮﻛﻮﺯ Renal threshold
ﺗﺤﻠﻴﻞ ﺍﻟﺴﻜﺮ ﺑﻌﺪ ﺳﺎﻋﺘﻴﻦ ﻣﻦ ﺍﻷﻛﻞPost Prandial Blood Glucose
ﺗﺤﻠﻴﻞ ﻣﻨﺤﻨﻰ ﺗﺤﻤﻞ ﺍﻟﺴﻜﺮ Glucose Tolerance Test ( GTT )
ﺍﻟﻬﻴﻤﻮﺟﻠﻮﺑﻴﻦ ﺍﻟﺴﻜﺮي Glycosylated Haemoglobin - HbA 1
ﺍﻟﺒﺮﻭﺗﻴﻨﺎﺕ ﺍﻟﺴﻜﺮﻳﺔ Glycosylated Protein
ﻏﻴﺒﻮﺑﺔ ﺍﻧﺨﻔﺎﺽ ﺍﻟﺴﻜﺮ Hypoglycaemic Coma
ﻏﻴﺒﻮﺑﺔ ﺍﺭﺗﻔﺎﻉ ﺍﻟﺴﻜﺮ Hyperglycaemic Coma
ﺇﺧﺘﺒﺎﺭﺍﺕ ﻭﻇﺎﺋﻒ ﺍﻟﻜﻠﻰ Kidney Function Tests
ﻛﺮﻳﺎﺗﻴﻨﻴﻦ Creatinine
ﺍﺳﺘﺨﻼﺹ ﺍﻟﻜﻠﺮﻳﺎﺗﻴﻨﻴﻦ Creatinine Clearance
ﺣﻤﺾ ﺑﻮﻟﻴﻚ Uric Acid
ﺑﻮﻟﻴﻨﺎ ( ﻳﻮﺭﻳﺎ ) Urea
ﺍﻟﻜﻮﻟﻴﺴﺘﻴﺮﻭﻝ ﺍﻟﻜﻠﻰ Total cholesterol
ﺍﻟﺠﻠﻴﺴﺮﻳﺪﺍﺕ ﺍﻟﻜﻠﻴﺔ Triglycerides
ﻛﻮﻟﻴﺴﺘﻴﺮﻭﻝ ﻋﻠﻰ ﺍﻟﻜﺜﺎﻓﺔ HDL cholesterol
ﻛﻮﻟﻴﺴﺘﻴﺮﻭﻝ ﻣﻨﺨﻔﺾ ﺍﻟﻜﺜﺎﻓﺔ LDL cholesterol
ﺍﻟﻘﺪﺭﺓ ﺍﻟﺘﺼﻨﻴﻌﻴﺔ Synthetic Functions
ﺍﻟﺴﺎﺋﻞ ﺍﻟﻤﻨﻮﻯ Semial Fluid
ﺍﻟﻠﺰﻭﺟﺔ Viscosity
ﺗﺤﻠﻴﻞ ﺑﻮﻝ URINE Analysis
ﺍﻟﻔﺤﺺ ﺍﻟﻤﻴﻜﺮﻭﺳﻜﻮﺑﻰ Microscopi examination
ﺃﻣﻼﺡ ﻣﺸﻜﻠﺔ Crystals
ﺃﻣﻼﺡ ﻏﻴﺮ ﻣﺸﻜﻠﺔ Amorphou
ﺃﺳﻄﻮﺍﻧﺎﺕ Casts
ﺧﻼﻳﺎ ﺻﺪﻳﺪ pus cells
ﻛﺮﺍﺕ ﺩﻡ ﺣﻤﺮﺍﺀ R.B.cs
ﺧﻼﻳﺎ ﺑﺸﺮﻳﺔ Epithellal cells
ﺃﺳﻄﻮﺍﻧﺎﺕ ﺷﻔﺎﻓﺔ Hyaline Casts
ﺃﺳﻄﻮﺍﻧﺎﺕ ﻣﺤﺒﺒﺔ Granuler Casts
ﻃﻔﻴﻠﻴﺎﺕ Parasites
ﺍﻟﺪﻳﺪﺍﻥ Worms
ﺍﻟﺒﻴﺾ Ova
ﺍﻟﻴﺮﻗﺎﺕ Larvae
ﺍﻟﻐﺬﺍﺀ ﺍﻟﻐﻴﺮ ﻣﻬﻀﻮﻡ Undigested food
ﺑﻠﻬﺎﺭﺳﻴﺎ ﺑﻮﻟﻴﺔ Schistosoma hematobium
ﺑﻠﻬﺎﺭﺳﻴﺎ ﻣﻌﻮﻳﺔ Schistosoma mansony
ﺃﻣﻼﺡ ﺻﻔﺮﺍﺀ Bile salts
ﺻﺒﻐﺎﺕ ﺻﻔﺮﺍﺀ Bile Pigments
ﺍﻟﻤﻈﻬﺮ Aspect
ﺍﻟﺮﻭﺍﺳﺐ Deposit
ﺍﻟﻜﺜﺎﻓﺔ ﺍﻟﻨﻮﻋﻴﺔ Specific Gravity
الفحص الكهربائي ﻟﻠﺒﺮﻭﺗﻴﻨﺎﺕ ﻓﻰ ﺍﻟﺪﻡ Electrophoresis
. إعادة نشر
.
.
ﻣﺼﻄﻠﺤﺎﺕ ﻃﺒﻴﺔ ﻟﻔﻨﻲ ﻣﺨﺘﺒﺮﺍﺕ
ﻣﻌﻤﻞ ﺃﻭ ﻓﻨﻰ ﻣﺨﺘﺒﺮ ﺃﻭ ﺗﻘﻨﻰ ﻣﺨﺘﺒﺮ
Laboratory Technician
ﻣﻌﻤﻞ Laboratory
ﺗﺤﻠﻴﻞ Analysis
ﺍﻟﻤﺠﻬﺮ ﺃﻭ ﺍﻟﻤﻴﻜﺮﻭﺳﻜﻮﺏ Microscope
ﺍﻟﺤﻀﺎﻧﺔ Incubator
ﺍﻟﺤﻤﺎﻡ ﺍﻟﻤﺎﺋﻰ ( ﻟﻠﺘﺴﺨﻴﻦ ﺍﻟﻐﻴﺮ ﻣﺒﺎﺷﺮ ﺑﺎﻟﻤﺎﺀ ) Water bath
ﺟﻬﺎﺯ ﺍﻟﺘﻌﻘﻴﻢ ﺗﺤﺖ ﺿﻐﻂ ﺍﻟﺒﺨﺎﺭ Autoclave
ﺟﻬﺎﺯ ﺍﻟﻄﺮﺩ ﺍﻟﻤﺮﻛﺰﻯ Centrifuge
ﺟﻬﺎﺯ ﻗﻴﺎﺱ ﺍﻷﻟﻮﺍﻥ Colorometar
ﺍﻟﻤﺎﺻﺔ ( ﻣﻨﻬﺎ ﺯﺟﺎﺝ / ﺃﻭﺗﻮﻣﺎﺗﻚ ﺛﺎﺑﺖ ﻭﻣﺘﻐﻴﺮ ) Pipette
ﺻﻔﺮ ﺗﻌﺪﻳﻞ ﺍﻟﺠﻬﺎﺯ ( ﻗﺒﻞ ﺍﻟﻘﺮﺍﺀﺓ ) Zero adjustment
ﺍﻟﻘﻴﺎﺱ Measurement
ﻣﺤﻠﻮﻝ ﺍﻟﻤﺴﺢ ( ﺗﺼﻔﻴﺮ ﺍﻟﺠﻬﺎﺯ ) Reagent blank
ﻃﻮﻝ ﺍﻟﻤﻮﺟﺔ ( ﺗﺮﺩﺩ ﺍﻟﻘﺮﺍﺀﺓ ﻋﻠﻰ ﺍﻟﺠﻬﺎﺯ Wavelength
ﻛﻴﻮﻓﻴﺖ (ﻟﻠﻘﺮﺍﺀﺓ ﻋﻠﻰ ﺟﻬﺎﺯﻗﻴﺎﺱ ﺍﻷﻟﻮﺍﻥ ) Cuvet
ﻣﺤﺎﻟﻴﻞ( كواشف) Reagent
ﻣﺤﻠﻮﻝ ﻗﻴﺎﺳﻰ Standard R.
ﺍﻟﻌﻴﻨﺎﺕ Samples
ﺍﻟﻤﺼﻞ Serum
ﺍﻟﺒﻼﺯﻣﺎ plasma
ﻣﺮﺍﻗﺒﺔ ﺍﻟﺠﻮﺩﺓ Quality control
ﺍﻹﺳﺘﻘﺮﺍﺭ ﺃﻭ ﺍﻟﺜﺒﺎﺕ stability
ﻛﺎﺷﻒ ﻟﻮﻧِﻰ color reagent
ﻣﺪﻯ ﺍﻟﻘﻴﻢ ﺍﻟﻤﺘﻮﻗﻌﺔ (ﺍﻟﻄﺒﻴﻌﻴﺔ )Range expected values
ﺟﻠﻮﻛﻮﺯ (ﺳﻜﺮﺍﻟﺪﻡ ) Glucose
ﻣﻨﺤﻨﻰ ﺍﻟﺴﻜﺮ ﻓﻰ ﺍﻟﺪﻡ Blood Sugar Curve
ﺗﺤﻠﻴﻞ ﺍﻟﺴﻜﺮ ﺍﻟﻌﺸﻮائي Random Blood Glucose
ﻧﺴﺒﺔ ﺍﻟﺴﻜﺮ ﺻﺎﺋﻢ Fasting Blood Sugar
ﺍﻟﻌﺘﺒﺔ ﺍﻟﻜﻠﻮﻳﺔ ﻟﻠﺠﻠﻮﻛﻮﺯ Renal threshold
ﺗﺤﻠﻴﻞ ﺍﻟﺴﻜﺮ ﺑﻌﺪ ﺳﺎﻋﺘﻴﻦ ﻣﻦ ﺍﻷﻛﻞPost Prandial Blood Glucose
ﺗﺤﻠﻴﻞ ﻣﻨﺤﻨﻰ ﺗﺤﻤﻞ ﺍﻟﺴﻜﺮ Glucose Tolerance Test ( GTT )
ﺍﻟﻬﻴﻤﻮﺟﻠﻮﺑﻴﻦ ﺍﻟﺴﻜﺮي Glycosylated Haemoglobin - HbA 1
ﺍﻟﺒﺮﻭﺗﻴﻨﺎﺕ ﺍﻟﺴﻜﺮﻳﺔ Glycosylated Protein
ﻏﻴﺒﻮﺑﺔ ﺍﻧﺨﻔﺎﺽ ﺍﻟﺴﻜﺮ Hypoglycaemic Coma
ﻏﻴﺒﻮﺑﺔ ﺍﺭﺗﻔﺎﻉ ﺍﻟﺴﻜﺮ Hyperglycaemic Coma
ﺇﺧﺘﺒﺎﺭﺍﺕ ﻭﻇﺎﺋﻒ ﺍﻟﻜﻠﻰ Kidney Function Tests
ﻛﺮﻳﺎﺗﻴﻨﻴﻦ Creatinine
ﺍﺳﺘﺨﻼﺹ ﺍﻟﻜﻠﺮﻳﺎﺗﻴﻨﻴﻦ Creatinine Clearance
ﺣﻤﺾ ﺑﻮﻟﻴﻚ Uric Acid
ﺑﻮﻟﻴﻨﺎ ( ﻳﻮﺭﻳﺎ ) Urea
ﺍﻟﻜﻮﻟﻴﺴﺘﻴﺮﻭﻝ ﺍﻟﻜﻠﻰ Total cholesterol
ﺍﻟﺠﻠﻴﺴﺮﻳﺪﺍﺕ ﺍﻟﻜﻠﻴﺔ Triglycerides
ﻛﻮﻟﻴﺴﺘﻴﺮﻭﻝ ﻋﻠﻰ ﺍﻟﻜﺜﺎﻓﺔ HDL cholesterol
ﻛﻮﻟﻴﺴﺘﻴﺮﻭﻝ ﻣﻨﺨﻔﺾ ﺍﻟﻜﺜﺎﻓﺔ LDL cholesterol
ﺍﻟﻘﺪﺭﺓ ﺍﻟﺘﺼﻨﻴﻌﻴﺔ Synthetic Functions
ﺍﻟﺴﺎﺋﻞ ﺍﻟﻤﻨﻮﻯ Semial Fluid
ﺍﻟﻠﺰﻭﺟﺔ Viscosity
ﺗﺤﻠﻴﻞ ﺑﻮﻝ URINE Analysis
ﺍﻟﻔﺤﺺ ﺍﻟﻤﻴﻜﺮﻭﺳﻜﻮﺑﻰ Microscopi examination
ﺃﻣﻼﺡ ﻣﺸﻜﻠﺔ Crystals
ﺃﻣﻼﺡ ﻏﻴﺮ ﻣﺸﻜﻠﺔ Amorphou
ﺃﺳﻄﻮﺍﻧﺎﺕ Casts
ﺧﻼﻳﺎ ﺻﺪﻳﺪ pus cells
ﻛﺮﺍﺕ ﺩﻡ ﺣﻤﺮﺍﺀ R.B.cs
ﺧﻼﻳﺎ ﺑﺸﺮﻳﺔ Epithellal cells
ﺃﺳﻄﻮﺍﻧﺎﺕ ﺷﻔﺎﻓﺔ Hyaline Casts
ﺃﺳﻄﻮﺍﻧﺎﺕ ﻣﺤﺒﺒﺔ Granuler Casts
ﻃﻔﻴﻠﻴﺎﺕ Parasites
ﺍﻟﺪﻳﺪﺍﻥ Worms
ﺍﻟﺒﻴﺾ Ova
ﺍﻟﻴﺮﻗﺎﺕ Larvae
ﺍﻟﻐﺬﺍﺀ ﺍﻟﻐﻴﺮ ﻣﻬﻀﻮﻡ Undigested food
ﺑﻠﻬﺎﺭﺳﻴﺎ ﺑﻮﻟﻴﺔ Schistosoma hematobium
ﺑﻠﻬﺎﺭﺳﻴﺎ ﻣﻌﻮﻳﺔ Schistosoma mansony
ﺃﻣﻼﺡ ﺻﻔﺮﺍﺀ Bile salts
ﺻﺒﻐﺎﺕ ﺻﻔﺮﺍﺀ Bile Pigments
ﺍﻟﻤﻈﻬﺮ Aspect
ﺍﻟﺮﻭﺍﺳﺐ Deposit
ﺍﻟﻜﺜﺎﻓﺔ ﺍﻟﻨﻮﻋﻴﺔ Specific Gravity
الفحص الكهربائي ﻟﻠﺒﺮﻭﺗﻴﻨﺎﺕ ﻓﻰ ﺍﻟﺪﻡ Electrophoresis
كل مايهم الطب والصيدله والتحليلات والتمريض
[] Pathology 😣 👇👇👇👇👇 #Neoplasia_ :- اول كم منشور صعب جدا بس فهمك لباقي يعتمد على فهمك لاول منشورات ▬▬▬▬▬▬▬▬▬▬▬▬ #INTRODUCTION_ :- 👈 يعرف أي شي قبل ما نفصل فيه. #Neoplasia_translate :- Neo = New يعني جديد. Plasia = Growth or tissue.…
طريقة الشرح شوية مو واضحة، يعني اي كلام اذا مزدوج عربي و انكلش شوية يصير لبس و خربطة بفهمه.
نريد نسوي فهرسه لعيادات الأطباء في بغداد والمحافظات اي عياده تندلها اكتب
#اسم_الطبيب
#واختصاصه
#عنوانه
#وقت_دوامة
ودزه هنا 👇
@haeedr55
حتة ننشرة ونفيد الناس
شاركوا
#اسم_الطبيب
#واختصاصه
#عنوانه
#وقت_دوامة
ودزه هنا 👇
@haeedr55
حتة ننشرة ونفيد الناس
شاركوا
كل مايهم الطب والصيدله والتحليلات والتمريض pinned «نريد نسوي فهرسه لعيادات الأطباء في بغداد والمحافظات اي عياده تندلها اكتب #اسم_الطبيب #واختصاصه #عنوانه #وقت_دوامة ودزه هنا 👇 @haeedr55 حتة ننشرة ونفيد الناس شاركوا»
مِےـصِےـطٌےـفُےـى:
دكتور جاسم محمد اخصائي مفاصل المكان بساحة بيروت دوام مساءا
دكتور جاسم محمد اخصائي مفاصل المكان بساحة بيروت دوام مساءا
مِےـصِےـطٌےـفُےـى:
دكتور حسان اخصائي اطفال بغداد الجديدة يداوم صبح وعصر
دكتور حسان اخصائي اطفال بغداد الجديدة يداوم صبح وعصر
دكتور فلاح السوداني اخصائي مفاصل بساحة بيروت.
دكتور مزعل غياض بغداد الجديدة قرب الحذاء الذهبي اخصائي شرايين و أوردة.
دكتور فارس بالكرادة اخصائي عيون.
عمار فؤاد بالكرادة اخصائي عيون.
دكتورة سعاد باقر مدينة الصدر قرب مرطبات ارز لبنان طبيبة نسائية.
دكتور مزعل غياض بغداد الجديدة قرب الحذاء الذهبي اخصائي شرايين و أوردة.
دكتور فارس بالكرادة اخصائي عيون.
عمار فؤاد بالكرادة اخصائي عيون.
دكتورة سعاد باقر مدينة الصدر قرب مرطبات ارز لبنان طبيبة نسائية.
Hsalwan Ali:
سلام عليكم
د.زيد فوزي اختصاص جراحة كسور ومفاصل
د.عبدالوهاب عباس اختصاص باطنية قلبية صدرية
حي القاهرة شارع حسينية آل الرسول
سلام عليكم
د.زيد فوزي اختصاص جراحة كسور ومفاصل
د.عبدالوهاب عباس اختصاص باطنية قلبية صدرية
حي القاهرة شارع حسينية آل الرسول
هاي محافظات..
دكتور سامر الحمداني اخصائي مفاصل بصرة.
دكتور ضياء غازي اذن وحنجرة كوت.
دكتور كريم طعمة جلدية كوت.
دكتور جمال بايش القريشي اخصائي باطنية كوت.
دكتور حكمت الزركاني اخصائي صدرية كوت.
دكتورة سندس عبد عبد الحسين طب اسنان و جراحة فكين كوت.
دكتور حسين طب عيون بالكوت.
دكتور اياد طب عيون بالكوت.
دكتور سامر الحمداني اخصائي مفاصل بصرة.
دكتور ضياء غازي اذن وحنجرة كوت.
دكتور كريم طعمة جلدية كوت.
دكتور جمال بايش القريشي اخصائي باطنية كوت.
دكتور حكمت الزركاني اخصائي صدرية كوت.
دكتورة سندس عبد عبد الحسين طب اسنان و جراحة فكين كوت.
دكتور حسين طب عيون بالكوت.
دكتور اياد طب عيون بالكوت.
دكتور موسى عمران الغزالي اخصائي مفاصل بالديوانية شارع الاطباء.