Author Archives: Alila Medical Media

Blood Types, Blood Group Systems and Transfusion Rule, with Animation

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A blood type refers to the PRESENCE or ABSENCE of a certain marker, or ANTIGEN, on the surface of a person’s red blood cells. For example, in the ABO system, presence of A or B antigen gives type A or B, presence of both antigens gives type AB, while their ABSENCE gives type O.
Blood typing is critical for blood transfusion, as there are very SPECIFIC ways in which blood types must be MATCHED between the donor and recipient for a safe transfusion. The rule is simple: patients should NOT be given antigens that their own blood does NOT have. This is because the recipient’s immune system may recognize any “NEW” antigen as “FOREIGN” and develop antibodies to target it for destruction. Depending on the scale of the triggered immune response, the reaction can be serious or fatal.
Applying the rule, a type A patient, who is NEGATIVE for B antigen, can only receive blood from type A and type O donors, whose blood does NOT contain B antigen. A type AB patient, having both antigens, can receive blood from anyone, while a type O person, being NEGATIVE for both A and B, can only receive from type O donors, but can give blood to anyone.
Another important system is the Rh system, for which, D antigen, or Rh factor, is best known. The blood type for this antigen can be either Rh-positive or Rh-negative. By the same rule, a Rh-negative patient canNOT receive blood from a Rh-positive donor, while the reverse direction is fine.
Each of the 4 types of the ABO system can be Rh-positive or negative. This gives 8 possible combinations – the 8 basic blood types everyone knows about.
But ABO and Rh are only a FRACTION of the 35 currently known blood group systems, many of which can cause serious reactions during transfusion if mismatched. Altogether there are HUNDREDS of antigens, giving rise to a gigantic number of possible blood types. A fully specified blood type should describe the COMPLETE SET of antigens that a person has. In theory, this list must be determined for both donor and recipient before a transfusion can take place. In reality, however, most people only need to care about their ABO type and Rh factor.
The ABO and Rh systems are the most important in blood transfusion for 2 reasons. First, most people can produce ROBUST antibodies against A, B and D antigens, which may NOT be the case for other antigens. In fact, anti-A and anti-B antibodies are usually developed during the first year of life. Second, the 8 basic blood types are distributed in comparable proportions that make mismatching a likely event. Most other antigens occur at such frequencies that ONLY a VERY SMALL subset of patients is potentially at risk. For example, if 99.99% of a population is positive for a certain antigen and only 0.01% is negative, only that tiny fraction of negative patients is at risk regarding that antigen. To account for possible INcompatibility OUTSIDE ABO and Rh, an ADDITIONAL test is usually made before transfusion. A blood sample from the patient is mixed with a sample of donor blood and the mixture is examined for CLUMPS. No clumping means a compatible match.

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Membrane Transport, with animation

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All animal cells are enclosed in a plasma membrane, which consists of 2 layers of phospholipids. The hydrophobic nature of the cell membrane makes it intrinsically permeable to small NON-polar and uncharged polar molecules, but NON-permeable to large polar molecules and CHARGED particles. Charged particles, such as ions, must use special channels to move through the membrane.
Transport of a molecule can be passive or active. PASSIVE transport does NOT require energy input because it moves the molecules “DOWNHILL”, for example, from HIGHER to LOWER concentration. ACTIVE transport, on the other hand, moves the molecules AGAINST their gradients and therefore requires ENERGY expenditure.
Ion channels permit PASSIVE transport of ions. These are transmembrane proteins that form PORES for ions to pass through. Most ion channels are SPECIFIC for a certain type of ion.
Ion channels can be classified by how they change their OPEN-CLOSED state in RESPONSE to different factors of the environment. Common types of ion channels include:
– LEAK channels: these channels are almost always OPEN allowing more or less steady flow of ions; examples are potassium and sodium leak channels in neurons.
– LIGAND-gated ion channels: these channels OPEN upon BINDING of a LIGAND. They are most commonly found at synapses, where neurons communicate via chemical messages, or neurotransmitters. An example is the GABA receptor, a chloride channel located on POST-synaptic neurons. It OPENS upon binding to GABA, a neurotransmitter released by the PRE-synaptic neuron, and allows chloride ions to flow into the cell.
– VOLTAGE-gated ion channels: these channels are REGULATED by membrane voltage. They OPEN at some values of the membrane potential and CLOSE at others. These are the channels that underlie ACTION POTENTIALS in neurons and cardiac muscles.
ACTIVE transport of ions is carried out by ion transporters, or ion PUMPS. These are transmembrane proteins that PUMP ions AGAINST their concentration gradient using cellular ENERGY, such as ATP. Most notable example is the sodium-potassium pump which maintains the resting potential in neurons by pumping two potassium IN and three sodium OUT of the cell.
Another type of ion transporters, known as SECONDARY transporters, do NOT use ATP directly. Instead, they move ONE ion DOWN its concentration gradient and use THAT ENERGY to POWER the transport of a SECOND ion. Symporters transport the two ions in the same direction, while antiporters pump the coupled molecule in the OPPOSITE direction.

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Aortic Valve Diseases, with animation

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The aortic valve serves to ensure ONE-WAY flow of oxygen-RICH blood from the LEFT ventricle to the aorta and to the body. It OPENS when the left ventricle contracts and pumps blood; and CLOSES when the ventricles refill, to prevent blood from flowing BACK to the left ventricle. The aortic valve consists of three leaflets, or cusps.

A defective valve is one that FAILS to either OPEN or CLOSE properly. Aortic STENOSIS happens when the aortic valve does not OPEN fully, REDUCING blood flow. Aortic REGURGITATION, on the other hand, occurs when the valve does not CLOSE tightly, causing BACKWARD flow to the ventricle.

The common outcome of both situations is that the heart does NOT pump enough blood to the body, and heart failure may result. Symptoms may develop suddenly or SLOWLY over decades, and may include: fatigue, shortness of breath, especially when exercising; chest pain or tightness; dizziness, fainting, swelling in the ankles and feet; and poor feeding and growth in children.

In attempts to compensate for the low blood output, the left ventricle grows LARGER to generate higher pressures and pump harder. This enlargement may help to relieve symptoms at first, but eventually it causes the ventricle to become weak and fail.

Risk factors for both conditions include:

– Congenital heart valve disease: some people are born with ABnormal structures that increase the risks of valve MALfunctioning. Common defects include having two leaflets, instead of three; fused leaflets, and dilation of the aortic root.

– STIFFENED valve due to calcium deposits, as a result of AGING.

– and valve DAMAGE due to infection or inflammation in conditions such as endocarditis and rheumatic fever.

Aortic valve diseases produce characteristic heart murmurs that are useful for diagnosis.

Aortic stenosis gives rise to a crescendo-decrescendo systolic murmur which starts shortly after the first heart sound. It is often preceded by an ejection click caused by the opening of the STENOTIC valve. The murmur is loudest in the aortic area and the sound radiates to the neck.

Aortic regurgitation produces a diastolic murmur which is heard along the left sternal border. It peaks at the beginning of diastole when the flow is largest, then rapidly decreases as the ventricles are filled.

Diagnosis is usually confirmed by echocardiography.

A damaged valve usually requires surgical repair or replacement. Several repair procedures are available depending on the type of defect. Valve replacement is often preferred as a long-term solution, especially for aortic stenosis, in which the valve tends to become narrow again after a repair procedure. Artificial valves can be mechanical or bio-prosthetic. Mechanical valves last longer but usually require life-long administration of anticoagulant medications to prevent formation of blood clots.

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Cholesterol Metabolism, with Animation

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Despite having a BAD reputation as a high-risk factor for cardiovascular diseases, cholesterol is an ESSENTIAL component of all animal cells. It is an INTEGRAL part of the cell membrane, providing membrane FLUIDITY and participating in a number of cellular processes. Cholesterol also serves as a PRECURSOR for production of bile, steroid hormones, and vitamin D. While the body can obtain cholesterol from food, many cells SYNTHESIZE their own ENDOGENOUS cholesterol. Cellular production of cholesterol is under NEGATIVE FEEDBACK control. LOW levels of intracellular cholesterol INDUCE its own production, while HIGH cholesterol levels INHIBIT it.
Cholesterol, together with other lipids, is transported in blood plasma within large particles known as LIPOPROTEINS. A lipoprotein is an assembly of lipids and proteins. Lipoproteins are classified based on their DENSITY. Because lipids are LIGHTER than proteins, particles that contain MORE lipids are LARGER in size but have LOWER density. Different types of lipoproteins have different sets of proteins on their surface. These proteins serve as “ADDRESS tags”, determining the DESTINATION, and hence FUNCTION, of each lipoprotein. For example, LOW-density lipoprotein, LDL, carries cholesterol FROM the liver to other tissues, while HIGH-density lipoprotein, HDL, RETURNS excess cholesterol TO the liver.
Major events in cholesterol metabolism include:
– Dietary cholesterol ABSORBED in the intestine and carried via blood circulation to the liver.
– The liver PACKAGES its cholesterol pool – a combination of endogenous and dietary – together with triglycerides, another type of lipid, into particles of VERY-LOW-density lipoprotein, VLDL.
– VLDL travels in bloodstream to other organs. During circulation, muscle and adipose tissues EXTRACT triglycerides from VLDL, turning it into LOW-density lipoprotein, LDL.
– Peripheral cells TAKE UP LDL by endocytosis, using LDL receptor. Cholesterol is used in cell membrane and other functions.
– EXCESS cholesterol is exported from the cells and delivered to HIGH-density lipoprotein, HDL, to be RETURNED to the liver in a process called REVERSE cholesterol transport.
– The liver uses cholesterol to produce BILE; bile is secreted to the intestine, where it helps break down fats. Part of this bile is EXCRETED in feces; the rest is RECYCLED back to the liver.
LDL has the highest cholesterol content and is the MAJOR carrier of cholesterol in the blood. High levels of LDL in the blood are associated with cholesterol plaque build-up and cardiovascular diseases such as heart attacks and strokes. For this reason, LDL is known as “BAD” cholesterol. On the other hand, HDL is called “GOOD” cholesterol, because it REMOVES EXCESS cholesterol from tissues and bloodstream.
Common drugs used to LOWER cholesterol include: INHIBITORS of endogenous cholesterol PRODUCTION; INHIBITORS of intestinal cholesterol ABSORPTION; and INHIBITORS of bile reuptake.

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Ventricular Septal Defect explained with animation

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Ventricular septal defect, or VSD, refers to an OPENING in the interventricular septum that separates the two ventricles of the heart.
In normal circulation, oxygen-poor blood from the body returns to the RIGHT side of the heart where it is pumped into the pulmonary artery and to the lungs. After being oxygenated, oxygen-rich blood from the lungs returns to the LEFT side of the heart to be pumped into the aorta and out to the body.
Pathology: A VSD allows abnormal blood flow between the two ventricles. The NET flow of blood, called a SHUNT, is usually from LEFT to RIGHT due to significantly HIGHER blood pressure in the LEFT side of the heart. This is because the left side has to pump blood all over the body while the right side only needs to send it to the lungs. If the defect is small, the shunt is negligible and does not result in any symptoms. A large defect, on the other hand, may OVERLOAD the right side of the heart, causing it to FAIL. Heart failure symptoms usually appear during the first few weeks of life and include: fatigue, shortness of breath, difficulty feeding and poor growth.
Without treatment, other complications may also occur. As the right ventricle continuously pumps MORE blood to the lungs, the entire pulmonary vasculature may be overloaded and pulmonary Hypertension may result. To OVERCOME the high pressure in the lungs, the right ventricle has to generate even HIGHER pressure, which eventually becomes GREATER than that of the LEFT ventricle. This REVERSES the direction of the shunt, causing oxygen-POOR blood to flow from RIGHT to LEFT and be sent to all tissues of the body. The resulting oxygen DEPRIVATION may be seen as a BLUISH skin color, known as CYANOSIS.
A VSD can happen alone or in combination with other congenital defects in conditions such as Down syndrome, or tetralogy of Fallot. The cause is unknown but likely to involve both genetic and environmental factors.
The turbulence of abnormal blood flow in VSD produces heart murmurs, which can be heard using a stethoscope. Diagnosis is confirmed by echocardiography.
VSD is the most common congenital heart defect in infants, but the defect is small in most cases. Small defects usually close on their own in early childhood and no treatment is needed. Large defects that produce symptoms usually require surgical closure in the first year of life.

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Membrane Potential, Equilibrium Potential and Resting Potential, with Animation

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Membrane potential, or membrane voltage, refers to the DIFFERENCE of electric charges across a cell membrane. Most cells have a NEGATIVE transmembrane potential. Because membrane potential is defined RELATIVE to the exterior of the cell, the negative sign means the cell has MORE negative charges on the INSIDE.

There are 2 basic rules governing the movement of ions:

– they move from HIGHER to LOWER concentration, just like any other molecules;

– being CHARGE-bearing particles, ions also move AWAY from LIKE charges, and TOWARD OPPOSITE charges.

In the case of the cell membrane, there is a THIRD factor that controls ion movement: the PERMEABILITY of the membrane to different ions. Permeability is achieved by OPENING or CLOSING passageways for specific ions, called ION CHANNELS. Permeability can change when the cell adopts a DIFFERENT physiological state.

Consider this example: 2 solutions of different concentrations of sodium chloride are separated by a membrane. If the membrane is EQUALLY permeable to BOTH sodium and chloride, both ions will diffuse from higher to lower concentration and the 2 solutions will eventually have the same concentration. Note that the electric charges remain the same on both sides and membrane potential is zero.

Now let’s assume that the membrane is permeable ONLY to the positively-charged sodium ions, letting them flow down the concentration gradient, while BLOCKING the negatively-charged chloride ions from crossing to the other side. This would result in one solution becoming INCREASINGLY positive and the other INCREASINGLY negative. Since opposite charges attract and like charges repel, positive sodium ions are now under influence of TWO forces: DIFFUSION force drives them in one direction, while ELECTROSTATIC force drives them in the OPPOSITE direction. The equilibrium is reached when these 2 forces COMPLETELY counteract, at which point the NET movement of sodium is ZERO. Note that there is NOW a DIFFERENCE of electric charge across the membrane; there is ALSO a CONCENTRATION gradient of sodium. The two gradients are driving sodium in OPPOSITE directions with the EXACT SAME force. The voltage established at this point is called the EQUILIBRIUM potential for sodium. It’s the voltage required to MAINTAIN this particular concentration gradient and can be calculated as a function thereof.

A typical RESTING neuron maintains UNequal distributions of different ions across the cell membrane. These gradients are used to calculate their equilibrium potentials.  The positive and negative signs represent the DIRECTION of membrane potential. Because sodium gradient is directed INTO the cell, its equilibrium potential must be POSITIVE to drive sodium OUT. Potassium has the REVERSE concentration gradient, hence NEGATIVE equilibrium potential. Chloride has the same INWARD concentration direction as sodium, but because it’s a negative charge, it requires a NEGATIVE environment inside the cell to push it OUT.

The resting membrane potential of a neuron is about -70mV. Notice that ONLY chloride has the equilibrium potential near this value. This means chloride is IN equilibrium in resting neurons, while sodium and potassium are NOT. This is because there is an ACTIVE transport to keep sodium and potassium OUT of equilibrium. This is carried out by the sodium-potassium PUMP which constantly brings potassium IN and pumps sodium OUT of the cell. The resulting resting potential, while costly to maintain, is essential to generation of action potentials when the cell is stimulated.

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Amenorrhea, Pathology and Causes, with Animation

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Amenorrhea is the ABSENCE of menstrual periods in a woman of reproductive age. Absence of menses is normal in pregnant, breastfeeding and menopausal women, but pathological otherwise. Amenorrhea is not a disease on its own, but rather a symptom of a variety of underlying conditions. PRIMARY amenorrhea is when a woman has NEVER had her periods, while SECONDARY amenorrhea is when a woman has STOPPED having them.

Menstruation is part of the menstrual cycle, the monthly events that occur within a woman’s body in preparation for the possibility of pregnancy. Each month, an egg is released from an ovary in a process called ovulation. At the same time, the lining of the uterus THICKENS, ready for pregnancy. If fertilization does NOT take place, the lining of the uterus is shed in menstrual bleeding and the cycle starts over. The menstrual cycle is under control of multiple hormones secreted by the hypothalamus, pituitary gland, and ovaries. Basically, the hypothalamus produces gonadotropin-releasing hormone, GnRH; the anterior pituitary secretes follicle-stimulating hormone, FSH, and luteinizing hormone, LH; while the ovaries produce estrogen and progesterone. These hormones are involved in a REGULATORY network that results in monthly cyclic changes responsible for follicular maturation and ovulation.

Amenorrhea can be caused by ANATOMICAL or ENDOCRINE problems.

Anatomical causes refer to abnormalities in the female reproductive system and include:

– absent or underdeveloped female organs in some genetic disorders, such as MRKH syndrome

– congenital defects that OBSTRUCT blood outflow

– and destruction of the uterine cavity by previous infections or surgeries.

Endocrine problems refer to structural or functional defects of the hypothalamus, pituitary gland and ovaries. A common cause in this category is the impaired function of the hypothalamus which occurs when the hypothalamic-pituitary-ovarian axis is SUPPRESSED due to an ENERGY DEFICIT. This can result from weight loss, eating disorders, excessive exercise, malabsorption syndromes, or emotional stress. The common feature is a REDUCED production of GnRH by the hypothalamus, which results in corresponding LOW levels of FSH and LH and subsequent impairment of follicular maturation and absence of ovulation.

Other endocrine causes include:

– Kallmann’s syndrome, a genetic disorder associated with congenital defects of the hypothalamus, causing GnRH deficiency.

– Sheehan’s syndrome, a condition in which excessive blood loss during childbirth or chronic hypotension during pregnancy IMPAIRS PITUITARY functions.

– Tumors, infections, trauma or autoimmune destruction of the pituitary gland.

– Polycystic ovary syndrome, an endocrine disorder in which FSH deficiency disrupts follicle maturation.

– Loss of normal ovarian function in conditions such as Turner’s syndrome

– Thyroid disorders

Treatment is by addressing the underlying cause and can range from nutrition plans, hormonal therapy to surgical interventions.

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Vascular Dementia Pathology, with Animation

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Vascular dementia (also known as Vascular Cognitive Impairment) refers to a group of conditions in which IMPAIRED blood supply to the brain causes neuronal DYSfunction, leading to loss of memory and other cognitive abilities. It is the second most common type of dementia, after Alzheimer’s – a neurodegenerative disease.
Vascular dementia may develop following a stroke, or a series of mini-strokes. A stroke can be ischemic or hemorrhagic. An ischemic stroke happens when a blood clot BLOCKS an artery, interrupting blood flow. Blood clots may form locally, on top of cholesterol plaques as these rupture; or, travel to the brain from the heart, in a condition known as atrial fibrillation, where the heart does not pump properly, blood stagnates and coagulates. Hemorrhagic stroke, on the other hand, occurs when an artery leaks or ruptures. This can result from high blood pressures, overuse of blood-thinners/anticoagulant drugs, or abnormal formations of blood vessels such as aneurysms. As a hemorrhage takes place, brain tissues located BEYOND the site of bleeding are deprived of blood supply. Bleeding also induces contraction of blood vessels, narrowing them and thus further limiting blood flow.
Dementia symptoms may appear SUDDENLY following a SINGLE LARGE stroke, or develop in a STEPWISE fashion as a result of multiple, sometimes unnoticeable, small strokes. Symptoms VARY from person to person depending on the part of the brain that is affected, and may include: problems with memory or thinking skills, confusion, mood changes, speech disorders, impaired balance and movement. The way the symptoms appear can be used to differentiate stroke-related dementia from Alzheimer’s disease, which usually develops GRADUALLY, with specific symptoms appearing in a largely typical order.
But vascular dementia may also progress silently in a CONTINUOUS manner, as a result of age-related vascular wear-and-tear, or any conditions that DAMAGE or NARROW blood vessels over time, such as high blood pressure, high cholesterol, diabetes and amyloid deposit. These factors often affect SMALLER blood vessels deep inside the white matter of the brain, causing small blockages and microbleeds that often go unnoticed to the patients. This is known as “cerebral small vessel disease” and is the most common cause of vascular dementia in older adults.
Another cause of vascular dementia is HYPOperfusion of the entire brain. This may result from heart failures, hypotension, or carotid artery occlusion.
There is no cure for vascular dementia but prevention by controlling vascular risk factors, such as high blood pressures, can be effective. Life style changes such as healthy diets, quitting smoking, and physical exercise have been proven to be beneficial. Treatment is by managing the underlying conditions.

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HIV and AIDS infection stages, HIV life cycle, Transmission, Diagnosis and Treatment, with Animation

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HIV, for human immunodeficiency virus, is a virus that attacks the immune system, weakening the body’s ability to fight infections. Progressive destruction of the immune system eventually leads to its failures, a state known as “acquired immunodeficiency syndrome”, or AIDS, when the body is INcapable of defending itself from common infections.

HIV targets a specific group of cells called CD4+ cells. CD4 is a receptor expressed on the surface of many immune cells, including T helper cells, macrophages and dendritic cells, where it is essential for cell communication and hence normal function of the immune system. HIV hijacks this receptor to gain access to the cells. Apart from CD4 receptor, another factor, called a co-receptor, is also required for HIV entry and infection. Several co-receptors have been identified in different cell types, with CXCR4 and CCR5 being the most common. CXCR4 is expressed on many T-cells, but usually not on macrophages, and is used by T-tropic strains of HIV. CCR5 is expressed on macrophages, some T-cells, and is used by M-tropic strains. Some HIV strains use CCR5 to infect initially but evolve to use CXCR4 later during disease progression. Viruses that can use both co-receptors are call dual-tropic. Some people are born with a deletion in CCR5 and are substantially RESISTANT to HIV infection.

HIV life cycle starts with attachment of a HIV envelope protein, gp120, to CD4 receptor and co-receptor, followed by fusion of HIV with host cell. The virus then injects its content, HIV RNA and several enzymes, into the cell. One of these enzymes, known as “reverse transcriptase”, is used to convert HIV RNA into DNA, an important step that would allow the virus to integrate into host cell DNA. Once in the nucleus, HIV enzyme INTEGRASE inserts the viral DNA into the host DNA. At this point the virus may adopt either LATENT or ACTIVE infection.

In active infection, HIV uses the host machinery to produce multiple copies of its RNA and proteins, which are then assembled into new virus particles, ready to infect more CD4 cells.

In latent infection, the virus remains integrated in host DNA, and may lie dormant for years, forming a latent HIV reservoir, which can REactivate and infect again at a later time.

HIV is transmitted through infected body fluids, most commonly via sexual contacts, shared contaminated needles, and mother to child during childbirth or through breastfeeding. It is not transmitted through air or casual contacts.

Diagnosis is by detection of viral protein, RNA, proviral DNA , or antibody produced against HIV.

There are three stages of HIV infection:

The ACUTE stage generally develops within a couple of weeks after a person is infected with HIV. During this time, patients may experience flu-like symptoms. HIV multiplies RAPIDLY resulting in HIGH viral load in the blood and INcreased risks of transmission.

The CHRONIC stage, also called clinical latency, is usually Asymptomatic. HIV continues to multiply but at much SLOWER speeds. Patients may not have any symptoms, but they can still spread HIV to others. Without treatment, the disease usually progresses to AIDS within 2 to 10 years.

AIDS is the final stage of HIV infection. As the immune system is failing, the body can’t fight off common diseases, and opportunistic infections take hold. AIDS is diagnosed when CD4 cell count is LOWER than 200 per microliter, or if certain opportunistic infections are present.

There is currently no cure but treatment with anti-retroviral therapy can SLOW DOWN progression to AIDS and reduce transmission risks. Anti-retroviral drugs are classified based on their ability to interfere with certain stage of HIV life cycle. Accordingly, there are: entry and fusion inhibitors, reverse transcriptase inhibitors, integrase inhibitors, and protease inhibitors. These drugs, however, can NOT reach the LATENT virus, which hides out safely in healthy T-cells but may reactivate and infect again. This is the major reason why HIV infection is not curable with current available treatments.

 

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Polycystic Ovary Syndrome, with animation

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Polycystic Ovary Syndrome: Diagnosis, Causes, Pathology, Treatment

Polycystic ovary syndrome, or PCOS, is a common HORMONAL disorder affecting about 10% of all women of reproductive age. PCOS is diagnosed when AT LEAST 2 of the following symptoms are present:

  • irregular periods due to MISSED ovulation.
  • excess male hormone (androgen) as evidenced by lab tests or physical signs, such as excess facial and body hair, severe acne, and baldness.
  • presence of numerous small fluid-filled cysts in the ovaries which can be seen as dark circles on an ultrasound image. This is the symptom that originally gave the condition its name but is NOT always present in PCOS patients.

PCOS is highly heritable, but the inheritance pattern is complex, with multiple genetic factors implicated in the susceptibility to the disease. While the exact cause of PCOS is unknown, disturbances in a number of hormones are thought to be responsible. PCOS patients usually have EXCESS luteinizing hormone, LH, together with a relatively LOW level of follicle-stimulating hormone, FSH, and increased levels of insulin.

An ovary contains hundreds of thousands of IMMATURE eggs, each of these is enclosed in a structure called a follicle. Each month, a number of these follicles develop, compete with each other; and one of them survives and gives rise to a MATURE egg that is released during ovulation. Follicle development is mediated by FSH, a pituitary hormone. In PCOS patients, FSH deficiency results in ARREST of follicular maturation: the follicles stop halfway through their development and become cysts. IMPAIRED follicular development means NO mature egg produced or released, hence the ABSENCE of ovulation.

Insulin is a hormone produced by the pancreas and is necessary for consumption of blood glucose by the body’s cells. INcreased insulin level in PCOS patients is a result of the body compensatory response to insulin RESISTANCE associated with PCOS. Excess insulin, together with high levels of luteinizing hormone, induce and maintain OVERproduction of androgen by the ovaries.

Common complications of PCOS include: infertility, miscarriage or premature birth, type 2 diabetes, obesity, cardiovascular diseases, mood disorders, and endometrial cancer.

While the choice of treatment may depend on the patient’s individual concerns, treating insulin resistance is generally recommended for all women with PCOS. Life style changes such as exercise, dieting and weight loss, and medications such as metformin, can LOWER both insulin and androgen levels, thus reducing the risks of type 2 diabetes, and improving ovulation. Patients who want to get pregnant may also be prescribed anti-estrogen medications such as clomiphene.  On the other hand, when fertility is not the goal of treatment, hormonal birth control, a combination of estrogen and progestin, is usually prescribed to regulate the menstrual cycle and reduce risks of endometrial cancer. This treatment may also help improve acne and reduce extra body hair.

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