Author Archives: Alila Medical Media

Presbyopia

Below is a narrated animation of the Near Vision of the Eye. Click here to license this video and other similar images/videos on Alila Medical Media website.

Presbyopia is a very common age-associated condition in which the eye loses the ability to adjust to near vision.

For information on eye anatomy other common defects click here.

How near vision is achieved?

When the eye is focused on a faraway object, light rays coming from the object are almost parallel and have no difficulty to converge on the retina (Fig. 1, upper panel).

When looking at a nearby object, light rays coming from the object are too divergent to come into focus on the retina without any help. In order to see nearby objects clearly, the eye has to make the following adjustments:

– Convergence of the two eyes – this is to make sure the object is focused on the same area of both retinas of the two eyes. Failure of doing so (e.g. when eye muscles are weak) would result in double vision.

– Constriction of pupil – this is to reduce spherical aberration. Spherical aberration occurs when light rays strike on the edge of a lens and produce blurriness. Constricted pupil allows light rays to enter the lens only at the center where they are best refracted.

– Accommodation of the lens – ciliary muscles contracted to make the lens thicker, more convex. This increases the optical power of the lens, it now can converge the light rays on the retina (Fig. 1, lower panel).

Fig. 1: The near response of the eye. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Presbyopia and correction

With age, the lens loses its flexibility and becomes stiff. It can no longer change its shape to accommodate near vision. This results in prebyopia – inability to see nearby objects.

Prebyopia is corrected with convex lenses that converge the light rays slightly before they enter the eye (Fig. 2). However, as this is needed only for looking at close-range objects, bifocal lenses are usually recommended.

Fig. 2: Presbyopia and correction lenses. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Presbyopia is not to be confused with hyperopia, a condition in which the eyeball is too short.

> See all Ophthalmology topics

How the eye works

Anatomy of the eye

Below is a narrated animation of eye anatomy and common defects. Click here to license this video (and other related videos) on Alila Medical Media website.

The eyeball is roughly a sphere of about one inch in diameter. The main components of the eye include:

– The cornea – the transparent front part of the eye. The cornea refracts light and accounts for about two-thirds of the eye’s total focusing power.

– The iris – the pigmented part of the eye that makes up the eye color. The iris regulates the amount of light that enters the eye by adjusting the size of the pupil – an opening in the center of the iris.

– The crystalline lens – a clear biconvex structure located behind the pupil and helps to focus light further. The lens is capable of changing its shape to accommodate near vision.

Fig. 1 : Anatomy of human eye. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Light refracted by the cornea and the lens creates an image of the visual object on the retina. The retina is a light-sensitive tissue lining the inner surface of the eye. Within the retina, optical information is converted into neural action potentials which are then transmitted to the visual cortex of the brain through the optic nerve.

– The fovea (fovea centralis) is the (small) central area of the retina where the sharpest central vision is achievable.

Common eye defects

In the normal eye, light rays converge right on the retina. This results in sharp vision.

Fig. 2 : Light focusing in normal vision (upper panel), hyperopia (middle panel) and myopia (lower panel). Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

In myopia, or nearsightedness, a condition in which the eyeball is too long, light rays converge before they reach the retina. The focal plane is located in front of the retina resulting in blurry vision. This happens when the person is looking at faraway objects. Myopia is corrected with concave lenses which diverge the light rays slightly before they enter the eye (Fig. 2).

In hyperopia, or farsightedness, a condition in which the eyeball is too short, light rays have not yet converged when they reach the retina. The focal plane is located behind the retina resulting in blurry vision. This happens when the person is looking at nearby objects. Hyperopia is corrected with convex lenses which converge the light rays slightly before they enter the eye (Fig.2).

> See all Ophthalmology topics

Cell cycle

Most cells divide periodically to give rise to two daughter cells. A cell cycle covers a period of time from one cell division to the next.

Phases of cell cycle

– First gap phase – G1 phase – cell grows in size and prepares for DNA replication. G1 checkpoint (see below) makes sure everything is ready for DNA replication. This is also the period where the cells carry out their normal metabolic roles for the body.

– Synthesis phase – S phase – DNA replication occurs, the cell makes a second, identical set of DNA molecules. It now has two sets, ready to distribute to the two daughter cells.

– Second gap phase – G2 phase – preparation for cell division, cell synthesizes proteins/enzymes that are necessary for mitosis. G2 checkpoint (see below) makes sure the cell is ready for division.

– Proper cell division – M phase – mitosis phase where the mother cell is split into two daughter cells by the process of mitosis. Mitosis has four phases on its own : prophase, metaphase, anaphase and telophase (commonly with cytokinesis).

Fig. 1 : A typical cell cycle with four phases. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

The G1, G2 and S phases are together called interphase – the time in between M phases. The length of cell cycle varies greatly from one cell type to another with the length of G1 phase being most variable.

G0 (G zero) phase

In an adult multicellular organism, it’s very common for cells to stop dividing permanently or temporary for a certain period of time. Such cells are said to be in G0 phase (resting phase), or to be quiescent. They usually enter G0 phase from G1 phase (Fig. 2). Fully differentiated skeletal muscle cells and neurons are post-mitotic and stay in G0 for the rest of their life. Some other cells can be stimulated to get back to G1 when needed (e.g. liver cells). Finally, there are cells that never enter G0 and continue dividing for life (e.g. epithelial cells).

Fig. 2 : A cell cycle diagram showing exit to G0. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Cell cycle checkpoints

Checkpoints are control mechanisms to ensure that cell division proceeds with highest accuracy. Before going into the next phase, the cell has to check if everything is ready, scan for DNA damage and activate repair if needed. If the cell is not ready, cell cycle will be arrested. This is to ensure that damaged or incomplete DNA molecules are not passed onto daughter cells.

There are three main checkpoints in the cell cycle:

– G1 checkpoint ( also called restriction point in animal cell, or start point in yeast) is located at the end of G1 phase, before the entrance to S phase. This is the point when the cell needs to make a decision to divide or not depending on the environmental factors. The cell may proceed to cell division (to S phase), delay division waiting for more signals (stay in G1), or enter resting phase (to G0 phase).

– G2 checkpoint is located at the end of G2 phase, before commitment to M phase. Here the cell needs to check if everything is ready for mitosis. Most importantly, it has to check for any DNA damages that may have occurred during DNA synthesis (S phase). If damages are detected, cell cycle will be arrested at this point.

– Metaphase checkpoint (spindle checkpoint) is located in metaphase, before the onset of anaphase. This is to make sure that ALL the chromosomes are properly aligned at the metaphase plate before the sister chromatids can be pulled apart in anaphase. If a chromosome is “late” to come to its position, the metaphase will be arrested waiting for it. This is how the cell ensures that the two daughter cells will have exactly the same set of chromosomes. Failure of this would result in a daughter cell with an extra chromosome and the other missing a chromosome, a situation that is deleterious for both.

Molecular regulators of cell cycle

Cyclins and cyclin-dependent kinases (CDKs) form cyclin-CDK complexes that determine the progression of cell cycle through different phases. Cyclins are regulatory subunits of the complexes and are expressed only at specific stages of cell cycle. CDKs are catalytic subunits of the complexes and are activated by binding to cyclins. Upon binding to a cyclin, CDK acquires ability to phosphorylate target proteins. CDKs are constitutively expressed. Combination of different CDKs to different cyclins determine substrate specificity of the complexes.

Inhibitors of cell cycle or tumor suppressors – a class of molecules that prevent the progression of the cell cycle. Many of these arrest the cell cycle in G1 phase by binding to and inactivating cyclin-CDK complexes.

Regulation of cell cycle and cancer

The number of cells in a tissue is determined by the balance between cell division and cell death. The proportion of cells actively dividing versus those in resting (G0) phase plays an important role and must be strictly controlled. Disregulation of cell cycle would result in uncontrollable cell division and formation of abnormal growths called tumors. Tumors that can spread to other organs are cancers. Cancerous cells are characterized by an inability to stop diving and to enter resting phase.

Coronary Angioplasty

Coronary angioplasty is a non-surgical procedure used to widen coronary arteries with cholesterol plaques. It can also be performed as an emergency treatment for heart attack (myocardial infarction).

The first part of the procedure is to localize the site of blockage (Fig. 1). This part is called cardiac catheterization and can be performed without subsequent angioplasty, i.e. just for diagnostic purposes.

Below is a narrated animation about myocardial infarction, cardiac catheterization and coronary angioplasty. Click here to license this video and/or other cardiovascular related videos on Alila Medical Media website.

A catheter (guiding catheter) is inserted through the femoral artery at the groin, or less commonly, through the radial artery in the arm (Fig. 1 and 2) and threaded all the way to the aorta. The tip of the catheter is placed at the beginning of the coronary artery to be investigated (it does not go inside the artery). A radio-opaque dye is injected through the catheter into the coronary artery. This enables real-time visualization of the artery using X-ray imaging. A narrowed part of an artery would appear as a bottle neck on an x-ray image (Fig.1).

Click here to see an animation of cardiac catheterization on Alila Medical Media website where the video is also available for licensing.

Fig. 1: Cardiac catheterization procedure for diagnosis of blocked site. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

After the location of stenosis (narrowed artery) is identified, angioplasty can begin. A thin guidewire with radio-opaque tip is inserted inside the guiding catheter and threaded past it into the location of plaque. Reminder : the guiding catheter stops at the start of coronary artery, but the guidewire would go further into it and to the location of blockage. An angioplasty catheter (a catheter with deflated balloon) is then inserted in such a way that the guidewire now is inside of it. The balloon is pushed to the location of blockage where it would be inflated and thus crushing the plaque (see Fig. 2 and 3). At the end of procedure, the balloon is again deflated and removed together with all catheters and guidewire.

Click here to see an animation of balloon angioplasty on Alila Medical Media website where the video is also available for licensing.

Fig. 2: Coronary angioplasty procedure. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Fig. 3: Balloon angioplasty procedure. The guidewire is the thin line that goes past the plaque. The guiding catheter is (of course) NOT on this picture as it stays outside of the coronary artery. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

In some cases, a stent is inserted together with the balloon (Fig. 4), inflated and left on place of the plaque to keep the artery open permanently. The stent can be bare-metal (the original version) or drug-eluting (newer versions). Bare-metal stents simply provide a mechanical support. Drug-eluting stents are coated with various drugs that are released over time and act to prevent tissue growth at the site and/or modulate inflammatory response. The benefit of using stents is still debatable.

Fig. 4: Stent angioplasty procedure. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Click here to see an animation of stent angioplasty on Alila Medical Media website where the video is also available for licensing.

> See all Circulatory topics

Heart attack

Myocardial infarction, commonly referred to as heart attack, is the sudden death of part of the heart muscle (the myocardium) due to loss of blood flow (ischemia). This occurs when one of the coronary arteries – the arteries that supply blood to the heart – is blocked.

Fig. 1: Coronary arteries supply blood to the heart. They branch out from the first part of the aorta. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

The blockage is commonly due to atherosclerosis – cholesterol plaques/fat deposits on the wall of blood vessels. As the plaque builds up, the vessel becomes narrow restricting blood flow. Under stress, the plaque may rupture. This triggers formation of blood clot on top of the plaque leading to complete blockage of blood flow. When this happens in a coronary artery, the downstream patch of the myocardium dies from lack of oxygen (Fig. 2). Weaken heart muscle may disrupt electrical activity of the heart and cause fibrillation with subsequent cardiac arrest.

Fig. 2: Anatomy of a heart attack due to atherosclerotic plaque. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Click here to see an animation of heart attack on Alila Medical Media website where the video is also available for licensing.

Signs and symptoms

The most common symptom is described as a heavy pressure and squeezing pain inside the chest which often radiates to the shoulder and left arm. Other symptoms include shortness of breath, sweating, weakness, nausea and vomiting.

In a number of cases, especially in elderly and people with diabetes, no chest pain or other symptoms are reported. These are called silent myocardial infarction. In such a case, myocardial infarction is diagnosed later with electrocardiograms (ECG), blood enzyme tests or an autopsy.

Risk factors and Causes

Heart attack is caused by build-up of atherosclerotic plaques. Risk factors include smoking, alcohol consumption, obesity, sedentary lifestyle, stress. Incidence increases with age, also, men are more at risk than women.

Onset of acute myocardial infarction is commonly associated with physical and/or psychological exertion. When the body is under physical or emotional stress, blood flow is increased. This leads to stretching of the wall of blood vessels and potentially rupture of plaques.

Treatments

Immediate treatments for suspected heart attack include blood thinners such as aspirin. Blood thinners are drugs that prevent further blood clotting. If this doesn’t help, another class of drugs called thrombolytic may be used. Thrombolytic drugs act to dissolve blood clots. This process is called thrombolysis.

Severe cases will require interventional therapy such as angioplasty where the blocked blood vessel is forced to open wider with a balloon and possibly a stent.

People with multiple sites of blockage may require heart bypass surgery. In this surgical procedure, a piece of healthy artery or vein taken from elsewhere in the body is used as a graft to “bypass” the blocked part of coronary artery.

> See all Circulatory topics

Circulatory system

The circulatory system (Fig. 1) includes the heart, blood vessels (arteries and veins) and the blood. There are two circuits of blood circulation: the pulmonary and the systemic.

– The pulmonary circuit carries the oxygen-poor blood from the heart to the lungs for gas exchange and returns oxygen-rich blood to the heart.

– The systemic circuit carries oxygen-rich blood from the heart to the rest of the body and returns oxygen-poor blood to the heart.

Fig. 1: The circulatory system, the heart and main arteries (red) and veins (blue) are illustrated. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

How the heart works

Below is a narrated animation of blood flow through the heart. Click here to license this video and/or other cardiovascular related videos on Alila Medical Media website.

The heart has two sides: right and left; each side has two chambers : an atrium and a ventricle (Fig. 2). The right side of the heart is in charge of the pulmonary circuit, it receives oxygen-poor blood from the body and pumps it into the lungs for gas exchange. The left side of the heart is in charge of the systemic circuit, it receives oxygen-rich blood from the lungs and pumps it through the aorta to the rest of the body.

The heart has four valves : two atrioventricular valves (AV valves) and two semilunar valves. Their function is to ensure that the blood flows only in one direction throughout the heart, i.e. they prevent blood backflow.

– The right AV valve, also called tricuspid valve, is located between the right atrium and right ventricle.

– The left AV valve, also called mitral valve, is located between the left atrium and left ventricle.

– The semilunar pulmonary valve is located at the base of the pulmonary trunk – the large artery that takes blood to the lungs.

– The semilunar aortic valve is located at the base of the aorta – the large artery that takes oxygen-rich blood to the rest of the body.

Fig. 2: The pathway of blood flow through the heart. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

If you have watched the video, there is no need to read all the text below!

Oxygen-poor blood from your body returns to the right atrium of the heart. Blood from upper body returns through superior vena cava, blood from lower body returns through inferior vena cava. As the right atrium is filled with blood, it contracts, the tricuspid valve opens and blood is pumped into the right ventricle of your heart. When the right ventricle is full, the tricuspid valve closes to prevent blood from flowing back into the atrium. The right ventricle contracts, pulmonary valve opens and blood is pumped into the pulmonary artery and to your lungs. Pulmonary valve closes to prevent blood from flowing back into the ventricle.

Oxygen-rich blood from the lungs returns to the left atrium of the heart. As the left atrium is filled with blood, it contracts, the mitral valve opens and blood is pumped into the left ventricle of your heart. This occurs at the same time as the right atrium pumps blood into the right ventricle on the other side of the heart. As the left ventricle is full, the mitral valve closes, the aortic valve opens, the left ventricle contracts and oxygen-rich blood is pumped into the aorta to reach all parts of your body. This happens at the same time as the right ventricle pumps blood into the pulmonary artery on the other side of the heart. The aortic valve quickly closes to prevent blood from flowing back to the heart. Meanwhile, the atria have filled with blood and the cycle repeats itself.

> See all Circulatory topics

Bone remodeling

Bone remodeling (bone metabolism) is the process of removal of old bone tissue and formation of a new one.

Functions of bone remodeling

– Renewal of bone tissue to prevent accumulation of old bone with multiple micro-damages.

– Repair of small injuries : In response to small fractures, the damaged tissue is removed and new bone matrix is formed to replace it.

– Adjustment of bone architecture to meet changing mechanical needs: new bone matrix is deposited where needed, old bone tissue is removed elsewhere.

– Role in maintenance of calcium homeostasis of blood plasma.

Bone remodeling process

Bone remodeling involves the removal of bone tissue by osteoclasts followed by the formation of new bone matrix deposited and mineralized by osteoblasts (Fig. 1).

Fig. 1: Bone remodeling cycle: resorption, reversal and formation. See text for details. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Bone resorption : removal of old bone tissue by osteoclasts. Osteoclasts are bone-dissolving cells. They derive from hematopoietic stem cells and are product of fusion of several cell precursors. Because of this, osteoclasts are unusually large and multinuclear. Osteoclast resembles an octopus crawling on the bone surface due to the presence of a ruffled border – multiple infoldings of plasma membrane – served to increase its surface area. They also have a foamy appearance as they contain lots of lysosomes.

Reversal: Mononuclear cells (monocytes, macrophages) clean up the debris on bone surface.

New bone formation : Recruitment of pre-osteoblasts to the surface, these mature to become osteoblasts. Osteoblasts are bone – forming cells. They synthesize the organic matter of bone matrix (osteoid). Osteoid mineralized and becomes new bone.

Osteocytes are former osteoblasts that have been trapped in the bone matrix they deposited. They can no longer synthesize bone matrix and instead serve as mechanical sensors. When they detect a strain in a bone, they communicate with the osteoblasts on the bone surface. These latter would deposit bone matrix where needed in response.

Bone modeling versus Bone remodeling

Bone modeling is the process in which bones change their overall shape to adapt to physiological and mechanical changes. In bone modeling, the two sub-processes of bone resorption and bone formation are less coordinated, i.e. bone resorption may happen without subsequent new bone formation and vice versa: new bone formation may happen without old bone being removed. Bone modeling is more frequent in growing children while bone remodeling is more frequent in adults.

Disorders of bone metabolism

Bone resorption and formation must be in balance to maintain healthy bone metabolism. When bone resorption overtakes new bone formation, bone loss – osteoporosis – may result (Fig. 2). Osteoporosis (or porous bone) is very common in older adults, especially in post-menopause women. This condition usually affects all the bones in the body.

Fig. 2: Bone loss in osteoporosis (right panel) compared to normal bone tissue (left). Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Another disorder of bone remodeling is Paget’s disease of bone (osteitis deformans). This condition is characterized by larger and denser but weaker bones. Paget’s disease typically is localized to just a few bones. The pelvis, lower spine and long bones of the legs are the most commonly affected.

> See all Orthopedic topics

How blood glucose is regulated?

Blood glucose levels are regulated by the cells of the pancreatic islets (islets of Langerhans). When glucose level is high (e.g. after a meal), beta cells of the islet release insulin into the bloodstream. Insulin stimulates target cells (e.g. muscle cells) to use glucose as energy source. Insulin also induces liver cells to store glucose in the form of glycogen (this process is called glycogenesis). When glucose levels fall (e.g. in the morning before breakfast), another hormone called glucagon is released by alpha cells of the pancreatic islets. Glucagon acts on liver cells to convert glycogen back to glucose and release it into the bloodstream (this process is called glycogenolysis).

How glucose induces insulin release in beta cells?

Shortly after a meal, level of glucose in the blood is up. High glucose level stimulates beta cells to secrete insulin into the bloodstream (Fig. 1 and 2).

Fig. 1: Anatomy of a pancreatic islet (islet of Langerhans): beta cells = blue, alpha cells = red; and an enlarged beta cell (lower panel). Glucose enters beta cell and stimulates exocytosis of vesicles containing insulin. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Glucose enters beta cell through glucose transporter 2 – GLUT2. Increased intake of glucose => increased production of ATP => ATP/ADP ratio is up => ATP-sensitive potassium channel closed => depolarization of cell membrane => voltage-gated calcium channel opens => increased calcium inside the cell => insulin granule exocytosis.

Fig. 2: Chain of events that lead to secretion of insulin from beta cells. See text for details. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

How insulin induces glucose uptake in target cells?

Insulin and glucose travel in bloodstream to reach target organs (e.g. muscles, liver,..). In target organs, insulin induces cells to take up glucose. Insulin binds to insulin receptor on target cell => phosphorylation of cytoplasmic domain of receptor => a cascade of signaling events brings the GLUT4 (glucose transporter 4) to the membrane of the cell => glucose enters target cell through GLUT4.

Fig. 3: Insulin signaling in target cell. See text fior details. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Glucagon

Glucagon is secreted into the bloodstream in response to hypoglycemia – low blood sugar. Glucagon has the opposite effect of insulin, its action increases blood glucose level. Glucagon secretion from alpha cells is suppressed by high level of glucose. Low concentration of glucose => increase level of glucagon. Glucagon stimulates breakdown of glucogen stored in liver cells (hepatocytes) and release of glucose into the blood.

> See all Endocrinology topics

Diabetes type 1 and type 2

What is Diabetes?

Diabetes mellitus includes a group of conditions characterized by a high level of blood glucose, commonly referred to as blood sugar. Too much sugar in the blood can cause serious, sometimes life-threatening health problems.

There are two types of chronic (lasts for life) diabetic conditions : type 1 diabetes and type 2 diabetes. Pregnant women may acquire a transient form of the disease called gestational diabetes which usually resolves after the birth of baby. Prediabetes is when your blood sugar is at the borderline : higher than normal, but lower than in diabetics. Prediabetes may or may not progress to diabetes.

Insulin and Metabolism of Glucose

In order to understand diabetes we should first understand glucose metabolism and role of insulin. Carbohydrate (carb) in food breaks down to glucose which is carried by the bloodstream to various organs of the body where it is either consumed as an energy source (e.g. in muscles), or is stored for later use (in the liver). Insulin is a hormone produced by beta cells of the pancreas and is necessary for glucose intake by the target cells. In other words, when insulin is deficient, muscle or liver cells won’t be able to use or store glucose and as a result, glucose will accumulate in the blood (Fig. 1).

How blood glucose is regulated ? A feedback loop is in place to ensure that glucose level in the blood is never too high or too low, i.e. in normal range. Shortly after a meal, level of glucose in the blood is up. High glucose level stimulates beta cells to secrete insulin into the bloodstream. Insulin and glucose travel in bloodstream to reach target organs (e.g. muscles, liver,..). In target organs, insulin induces cells to take up glucose for use as energy or store for later use. As glucose is consumed by target organs, its concentration in the blood goes down and no more insulin is secreted from beta cells, insulin level goes down, glucose is no longer taken into cells, this prevents glucose level from going down further. When blood sugar level is too low (e.g. before meal time), previously stored glucose in the liver is released back into the bloodstream thanks to the action of another pancreatic hormone called glucagon. In short, insulin lowers blood sugar level while glucagon increases it. Regulation and ratio of these two hormones are vital for maintaining blood glucose levels within normal range.

Type 1 and type 2 Diabetes

Type 1 diabetes = insulin dependent : The pancreas does not produce enough insulin due to lack of beta cells. Not enough beta cells in the pancreas => not enough insulin => organs can not use or store glucose => glucose accumulates in the bloodstream. Type 1 is characterized by early (juvenile) onset, symptoms commonly start suddenly and before the age of 20. Type 1 diabetes is normally managed with insulin injection.

Fig. 1: Type 1 diabetes. The pancreas produces less insulin, liver and muscle cells absorb less glucose, glucose stays in the blood, blood sugar level increased. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Type 2 diabetes = insulin resistant : Insulin is produced normally by the pancreas, but for some reasons, the cells of target organs (e.g. muscles, liver,..) do not response to insulin and therefore can not use or store glucose, glucose accumulates in the blood (Fig. 2). Type 2 is characterized by adult onset, symptoms usually appear gradually and start after the age of 30. Type 2 diabetes accounts for about 80-90% of all diabetics. Management focuses on weight loss and includes a low-carb diet.

Fig. 2: Type 2 diabetes. The pancreas produces the same amount of insulin but organs are unresponsive, glucose can not be used and stays in the blood, blood sugar level increased. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

> Causes and Symptoms

Diabetes causes and symptoms

Overview of Diabetes type 1 and type 2 < PREVIOUS

Causes

Causes are very different for each case as diabetes is a group of diseases that share the same outcome : high blood sugar. As the process of blood sugar control is complex and involves many steps, anything that goes wrong at any step would result in the disease (Fig. 1).

Fig. 1: Type 1 and 2 diabetes. In healthy people (upper panel), pancreas produces enough insulin, insulin binds to receptor on target cell and induces glucose intake. In type 1 diabetes (middle panel) insulin production is reduced, less or no insulin binds to receptor, glucose stays outside target cell (in the blood). In type 2 diabetes (lower panel) pancreas produces enough insulin but something goes wrong either with the receptor binding or insulin signaling in the target cell, glucose stays outside the cell (in the blood). Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Causes of type 1 diabetes: In type 1 diabetics, beta cells of the pancreas are destroyed by the immune system by mistake – autoimmune disease (Fig.2). The reason why this happens is unclear, but genetic factors are believed to play a major role.

Fig. 2: Anatomy of a pancreatic islet showing beta cells selectively destroyed in type 1 diabetes. Click on image to see a larger version on Alila Medical Media website where the image is also available for licensing.

Causes of type 2 diabetes: These are more diverse as there are many steps that could possibly go wrong. In some cases, beta cells are dysfunctional and produce a modified version of insulin that can no longer bind to its receptor. In other cases, the problem lies within insulin receptor or in the downstream signaling in target cells. The common hallmark is the normal level of insulin in the blood. Here again, genetic factors predispose susceptibility to the disease, but it’s believed that lifestyle plays a very important role. Typically, obesity, inactive lifestyle, and unhealthy diet are associated with higher risk of type 2 diabetes.

Causes of gestational diabetes: hormonal changes during pregnancy, notably the presence of placental hormone lactogen, may interfere with insulin receptor on target cells and make them less responsive to insulin. This occurs in about 5 to 10% of all pregnancies, more commonly during the third trimester, and if left untreated, may progress to type 2 diabetes.

Symptoms

Type 1 symptoms tend to come sudden, quickly, type 2 symptoms may develop over a long period of time. The earliest signs of diabetes are excessive thirst, frequent urination, then come excessive hunger, fatigue, weight loss, high blood pressure, blurred vision, frequent infections (especially in the skin, genitals, bladder). Long term untreated diabetes may lead to other complications including vascular diseases (heart attack, stroke), nerve damage (most commonly loss of feeling in the feet), kidney damage, diabetic coma,…