Monday, April 8, 2024

Erythroblastosis Fetalis

Erythroblastosis Fetalis

Introduction

The adult human body is home to trillions of red blood cells, also known as RBCs or erythrocytes. These blood cells carry oxygen, iron, and many other nutrients to the appropriate places in the body.

When a woman is pregnant, it’s possible that her baby’s blood type will be incompatible with her own. This can cause a condition known as erythroblastosis fetalis, where the mother’s white blood cells (WBCs) attack the baby’s RBCs as they would any foreign invaders.

This condition is highly preventable and the typical, severe form is now very rare in developed countries. Catching it early can ensure a successful pregnancy for mother and child. If left untreated, however, it can be life threatening for the baby.

Erythroblastosis fetalis is now known as hemolytic disease of the newborn.

Symptoms of Erythroblastosis Fetalis

Babies who experience erythroblastosis fetalis symptoms may appear swollen, pale, or jaundiced after birth. A doctor may find that the baby has a larger-than-normal liver or spleen.

Babies who experience erythroblastosis fetalis symptoms may appear swollen, pale, or jaundiced after birth. A doctor may find that the baby has a larger-than-normal liver or spleen.

Blood tests can also reveal that the baby has anemia or a low RBC count. Babies can also experience a condition known as hydrops fetalis, where fluid starts to accumulate in spaces where fluid is normally not present. This includes spaces in the:

Abdomen
Heart
Lungs

Causes

There are two main causes of erythroblastosis fetalis: Rh incompatibility and ABO incompatibility. Both causes are associated with blood type. There are four blood types:

A
B
AB
O

In addition, blood can be either Rh positive or Rh negative. For example, if you’re type A and Rh positive, you have A antigens and Rh factor antigens on the surface of your RBCs. Antigens are substances that trigger an immune response in your body. If you have AB negative blood, then you have both A and B antigens without the Rh factor antigen.

Rh incompatibility

Rh incompatibility occurs when a Rh-negative mother is impregnated by a Rh-positive father. The result can be a Rh-positive baby. In such a case, your baby’s Rh antigens will be perceived as foreign invaders, the way viruses or bacteria are perceived.

Your blood cells attack the baby’s as a protective mechanism that can end up harming the child. If you’re pregnant with your first baby, Rh incompatibility isn’t as much of a concern.

However, when the Rh-positive child is born, your body will create antibodies against the Rh factor. These antibodies will attack the blood cells if you ever become pregnant with another Rh-positive baby.

ABO incompatibility

Another type of blood type mismatch that can cause maternal antibodies against her baby’s blood cells is ABO incompatibility.

This occurs when the mother’s blood type of A, B, or O isn’t compatible with the baby’s. This condition is almost always less harmful or threatening to the baby than Rh incompatibility.

However, babies can carry rare antigens that can put them at risk for erythroblastosis fetalis. These antigens include:

Kell
Duffy
Kidd
Lutheran
Diego
Xg
P
Ee
Cc
MNSs

Diagnosed

To diagnose erythroblastosis fetalis, a doctor will order a routine blood test during your first prenatal visit. They’ll test for your blood type.

The test will also help them determine whether you have anti-Rh antibodies in your blood from a previous pregnancy.

The fetus’s blood type is rarely tested. It’s difficult to test for a fetus’s blood type and doing so can increase the risk for complications.

Frequency of testing

If initial testing shows your baby may be at risk for erythroblastosis fetalis, your blood will be continually tested for antibodies throughout your pregnancy — approximately every two to four weeks.

If your antibody levels start to rise, a doctor may recommend a test to detect fetal cerebral artery blood flow, which isn’t invasive to the baby. Erythroblastosis fetalis is suspected if the baby’s blood flow is affected.

Rh incompatibility

If you have Rh-negative blood, the father’s blood will be tested. If the father’s blood type is Rh negative, no further testing is needed. However, if the father’s blood type is Rh positive or their blood type isn’t known, your blood may be tested again between 18 to 20 weeks of pregnancy, and again at 26 to 27 weeks.

You’ll also receive treatment to prevent erythroblastosis fetalis.

ABO incompatibility

If your baby is jaundiced after birth, but Rh incompatibility isn’t a concern, the baby may be experiencing problems due to ABO incompatibility. ABO incompatibility occurs most frequently when a mother with an O blood type gives birth to a baby who has an A, B, or AB blood type.

Because O blood types may produce both A and B antibodies, the mother’s blood can attack the baby’s. However, these symptoms are generally much milder than a Rh incompatibility.

ABO incompatibility can be detected via a blood test known as a Coombs test. This test, along with a test to determine the baby’s blood type, is performed after the baby is born. It can indicate why the baby may appear jaundiced or anemic.

These tests are usually done for all babies whose mothers have type O blood.

Treatment 

If a baby experiences erythroblastosis fetalis in the womb, they may be given intrauterine blood transfusions to reduce anemia. When the baby’s lungs and heart mature enough for delivery, a doctor may recommend delivering the baby early.

After a baby is born, further blood transfusions may be necessary. Giving the baby fluids intravenously can improve low blood pressure. The baby may also need temporary breathing support from a ventilator or mechanical breathing machine.

Long-term outlook

Babies born with erythroblastosis fetalis should be monitored for at least three to four months for signs of anemia. They may require additional blood transfusions.

However, if proper prenatal care and postpartum care are delivered, erythroblastosis fetalis should be prevented and the baby shouldn’t experience long-term complications.

Prevention

A preventive treatment known as RhoGAM, or Rh immunoglobulin, can reduce a mother’s reaction to their baby’s Rh-positive blood cells. This is administered as a shot at around the 28th week of pregnancy.

The shot is administered again at least 72 hours after birth if the baby is Rh positive. This prevents adverse reactions for the mother if any of the baby’s placenta remains in the womb.

Carbon-14 Dating

Carbon-14 Dating 

Introduction

Radiocarbon dating, or carbon-14 dating, is a scientific method that can accurately determine the age of organic materials as old as approximately 60,000 years. First developed in the late 1940s at the University of Chicago by Willard Libby, the technique is based on the decay of the carbon-14 isotope. Radiocarbon dating has been used for historical studies and atmospheric science, and triggered archaeology’s “Radiocarbon Revolution.”

Carbon-14 dating

The invention of radiocarbon dating elegantly merged chemistry and physics to develop a scientific method that can accurately determine the age of organic materials as old as approximately 60,000 years.

It is based on the fact that living organisms—like trees, plants, people, and animals—absorb carbon-14 into their tissue. When they die, the carbon-14 starts to change into other atoms over time. Scientists can estimate how long the organism has been dead by counting the remaining carbon-14 atoms. The technique was developed in the late 1940s at the University of Chicago by chemistry professor Willard Libby, who would later receive the Nobel Prize for the work.

The breakthrough introduced a new scientific rigor to archaeology, allowing archaeologists to put together a history of humans across the world, but it had a significant effect in other fields, too. 

Carbon dating has helped us reveal how our bodies work, to understand the climate of the Earth and reconstruct its history, and to track the sun’s activity and the Earth’s magnetic fields. Radiocarbon dating was also instrumental in the discovery of human-caused climate change, as scientists used it to track the sources of carbon in the atmosphere over time.

Radiocarbon dating working principle


It starts with cosmic rays—subatomic particles of matter that continuously rain upon Earth from all directions. When cosmic rays reach Earth’s upper atmosphere, physical and chemical interactions form the radioactive isotope carbon-14.

Living organisms absorb this carbon-14 into their tissue. Once they die, the absorption stops, and the carbon-14 begins very slowly to change into other atoms at a predictable rate. By measuring how much carbon-14 remains, scientists can estimate how long a particular organic object has been dead.

From there, the problem becomes how to measure the carbon-14. Libby and fellow chemists at the University of Chicago and other institutions developed techniques to purify a sample so that it emits no other type of radiation except for carbon-14, and then run it through a detector sensitive enough to accurately count the pings emitted by the decay of single atoms. A newer, faster method developed in the 1970s works by using a particle accelerator to count the atoms of carbon-14.

Radiocarbon dating can be used on any object that used to be alive. That includes pieces of animals, people, and plants, but also paper that was made from reeds, leather made from animal hides, logs that were used to build houses, and so forth.

Carbon Dating Invention

Carbon dating was invented in the late 1940s by Willard Libby, a chemistry professor at the University of Chicago and former Manhattan Project scientist.

Libby built upon the work of Martin Kamen (PhD’36) and Sam Ruben, who discovered the carbon-14 isotope in 1940. Carbon-14 has a half-life of about 5,730 years. That means half the atoms in a sample will change into other atoms, a process known as “decay,” in that amount of time.

Libby proposed the idea of carbon dating in the journal Physical Review in 1946. He further developed the concept with members of his research group and published more in Science in 1947 and 1949. 

In a crucial step, Libby’s first graduate student, Ernest C. Anderson, established that organic materials contained essentially the same natural abundance of radiocarbon at all measured latitudes reaching nearly from pole to pole.

Libby worked with colleagues, including anthropologist Robert Braidwood of UChicago’s Oriental Institute (now known as the Institute for the Study of Ancient Cultures), to develop the carbon-14 method. 

Samples taken from artifacts in the museum collections were used to test the accuracy of radiocarbon dating, since archaeologists already knew their ages by tree-ring dating and other evidence. 

The many materials Libby tested while developing the method included a rope sandal found in an Oregon cave, the dung of an extinct ground sloth, linen wrappings from the Dead Sea Scrolls, and part of a funeral ship deck placed in the tomb of Sesostris III of Egypt.

News of the technique spread rapidly. By 1960, more than 30 radiocarbon labs had been established worldwide. (One of the first was led by physicist Hilde Levi, who spent several months at UChicago working with Libby on radiocarbon-related problems in 1947 and 1948).

“Libby’s method remained the only way to measure carbon-14 in samples for several decades and was long considered the most accurate means of dating carbon decay,” said David Mazziotti, a UChicago professor in chemistry. (Today, scientists also use a different way to measure carbon-14 called accelerator mass spectrometry, which can get more precise results from a far smaller amount of sample but is more expensive).

A plaque in the foyer of UChicago’s Kent Laboratory building commemorates the discovery, as a National Historic Chemical Landmark designated by the American Chemical Society. Libby’s invention earned him the 1960 Nobel Prize in chemistry “for determinations in archaeology, geology, geophysics, and other branches of science.”

UChicago science historian Emily Kern has documented how radiocarbon dating developed in an unusual Cold War context.  She described how the technique developed into a wide-ranging, global network from a technology that had roots in World War II’s Manhattan Project to build the atomic bomb. The technology, unbound by national security concerns, meant that carbon-14 laboratories could arise in Australia, Denmark, New Zealand and elsewhere.

Limitations of Carbon-14 Dating

The various dating techniques all have limitations. Each works best for different types of problems. Radiocarbon dating works on organic materials up to about 60,000 years of age.

Conventional radiocarbon dating requires samples of 10 to 100 grams (0.35 to 3.5 ounces) of an object, depending on the material in question. Newer forms of dating can use much smaller amounts, down to 20 to 50 milligrams or 0.0007 to 0.0018 ounces. In both cases, the material is destroyed during the test.

Radiocarbon samples are also easily contaminated, so to provide accurate dates, they must be clean and well-preserved. Dirt and other matter must be washed off with water, but chemical treatments and other cleaning procedures are also often needed. 

This is because there are so few atoms to count; even a little extra carbon from contamination will throw off the results significantly. A million-year-old sample contaminated by only a tiny amount of carbon could yield an invalid age of 40,000 years, for example.

Other dating methods have different strengths. Dendrochronology, also known as tree-ring dating, depends upon the preservation of certain tree species; it can extend to about 12,500 years ago for oak trees and to 8,500 years for bristlecone pine.

Potassium-argon dating can date volcanic materials ranging from less than 100,000 to more than 4 billion years old. Rubidium-strontium dating can be used to determine the ages of items ranging from a few million to a few billions of years old; it is widely used to understand how the Earth and solar system formed and to trace human migration and trade in archaeology.

Improved version

Technological and analytical advances have made radiocarbon dating faster and much more precise—and expanded its range of uses by reducing the size of the sample needed. The latest form of radiocarbon dating, called accelerator mass spectrometry, needs samples of only 20 to 50 milligrams (0.0007 to 0.0018 ounces); however, it is also more expensive.

Another newer development is Bayesian statistical modeling, which applies probability analytics to radiocarbon dates, which always involve an error margin. Bayesian modeling hones the final date range by considering factors such as which layer of sediments the samples come from or their relationship to artifacts of known age.

Discoveries that carbon-14 testing Revealed

Since its discovery, carbon-14 testing has had a major impact on our understanding of fields from archaeology to history to geology.

Dual Process Theory - Psychology

Dual Process Theory

Introduction

Dual process theory is a framework used to explain how people think. It traces its roots back to William James (an early American philosopher and psychologist). At its core is the idea that humans have two different streams or means of thinking. These dual means of thinking give rise to the name dual process theory.

“Dual process theory says that humans have two systems for thinking. System 1 is unconscious, quick, makes use of shortcuts, is a bit sloppy but is relied upon most of the time. System 2 is intentional, calculated and often more accurate, but it takes effort and is slow”.

These dual processes are sometimes referred to as “systems” and known as “system 1” and ”system 2”. System 1 is evolutionarily older, more automatic, instinctive, implicit and unconscious. System 2 is evolutionarily newer, intentional, effortful, explicit and conscious.

Dual process theory continues to evolve. It remains a popular framework in the field of cognitive psychology. It also has some applications in learning theory and in relation to how humans process and store information. More recently it has sprung up in behavioral economics as well. Danny Kahneman’s interpretations in his excellent book “Thinking, Fast and Slow”, helped bring these concepts to the mainstream.

Dual process theory also has a key role to play in understanding how we make decisions.

System 1: Our Automatic Processor

Humans constantly function. The majority of time we do so without really thinking about it. We know what our senses are telling us and we know what they mean we should do.

If we’re hungry, we should eat. And, if we’re a bit tired, we should sleep. If we see some information we dislike, we should ignore it… or perhaps not. We don’t think about walking. And we don’t calculate the trajectory of our steps. We don’t use our knowledge of physics to help us throw a ball. All of these things come naturally.

We’ve developed rules, internal processes and shortcuts in our thinking and decision making that help us survive without conscious effort. And it’s this system of automatic processing that’s known as System 1. We use it to get along in our daily lives without really needing to try too hard or think too much. We also find that the more tired we are, the more we use System 1.

This is economic in many ways. It’s fast too, allowing us to respond almost instantly in many situations. It’s also often reasonably accurate and effective. It also reserves our mental energy for draining thoughtful effort when it’s really required. It does though, rely on generalities and is prone to some sloppy errors.

System 2: Our Controlled Thinking

Sometimes we, as humans, find ourselves in situations where we either don’t have mental shortcuts that we can use, or where we need to be more than just reasonably accurate.

In these circumstances we need to focus on our thoughts. We need to consciously think our way through key factors and reach logical, calculated, informed decisions. To do this we need to slow our thinking down. We ignore our mental shortcuts, we start from the building blocks of information that we have and use logic to reach decisions and conclusions.

This way of thinking is known as System 2 thinking. It often produces better (or at least more reasoned) answers for us, but it’s effortful and it’s slow. This process is excellent in some environments and situations, but dreadful in others. If you rely on system 2 to calculate the moment when a leaping tiger will reach you and plot your escape, then you’ll never finish your calculations.

System 2: Characteristics

System 2 has lots of different characteristics. Some of the most important ones are as follow:

System 2 thinking requires focus and energy

It’s conscious,
Mostly voluntary,
Mostly detached from emotions,
Explicit,
Controlled,
High effort,
Small capacity,
Slow,
More objective (and fact / rule based),
Evolutionarily recent,
Logical and rational.

Dual Process Theory in the World of Work

Many of the challenges that individuals and leaders face in the world of work stem from the very natural tendency for individuals to predominantly use System 1 thinking as opposed to System 2 thinking.

In fact, most cases of sloppy thinking by otherwise capable individuals probably result from their use of System 1 thinking. And this is entirely natural. System 2 thinking requires a lot more effort, and a lot more focus. And this means that to use System 2, individuals normally need to be more motivated.

From a leadership perspective it’s helpful to be aware of these two different types of thinking. The more you can use system 2 thinking yourself, the better the decisions that you make will probably be. And similarly, the more you can help your team use system 2 thinking, the better their decisions will probably be.

Bipolar Disorder

Bipolar Disorder

Introduction

Bipolar disorder, formerly called manic depression, is a mental health condition that causes extreme mood swings that include emotional highs (mania or hypomania) and lows (depression).

When you become depressed, you may feel sad or hopeless and lose interest or pleasure in most activities. When your mood shifts to mania or hypomania (less extreme than mania), you may feel euphoric, full of energy or unusually irritable. These mood swings can affect sleep, energy, activity, judgment, behavior and the ability to think clearly.

Episodes of mood swings may occur rarely or multiple times a year. While most people will experience some emotional symptoms between episodes, some may not experience any.

Although bipolar disorder is a lifelong condition, you can manage your mood swings and other symptoms by following a treatment plan. In most cases, bipolar disorder is treated with medications and psychological counseling (psychotherapy).

Symptoms

There are several types of bipolar and related disorders. They may include mania or hypomania and depression. Symptoms can cause unpredictable changes in mood and behavior, resulting in significant distress and difficulty in life.

*Bipolar I disorder. You've had at least one manic episode that may be preceded or followed by hypomanic or major depressive episodes. In some cases, mania may trigger a break from reality (psychosis).

*Bipolar II disorder. You've had at least one major depressive episode and at least one hypomanic episode, but you've never had a manic episode.

*Cyclothymic disorder. You've had at least two years — or one year in children and teenagers — of many periods of hypomania symptoms and periods of depressive symptoms (though less severe than major depression).

*Other types. These include, for example, bipolar and related disorders induced by certain drugs or alcohol or due to a medical condition, such as Cushing's disease, multiple sclerosis or stroke.

Bipolar II disorder is not a milder form of bipolar I disorder, but a separate diagnosis. While the manic episodes of bipolar I disorder can be severe and dangerous, individuals with bipolar II disorder can be depressed for longer periods, which can cause significant impairment.

Although bipolar disorder can occur at any age, typically it's diagnosed in the teenage years or early 20s. Symptoms can vary from person to person, and symptoms may vary over time.

Mania and hypomania

Mania and hypomania are two distinct types of episodes, but they have the same symptoms. Mania is more severe than hypomania and causes more noticeable problems at work, school and social activities, as well as relationship difficulties. Mania may also trigger a break from reality (psychosis) and require hospitalization.

Both a manic and a hypomanic episode include three or more of these symptoms:

*Abnormally upbeat, jumpy or wired.

*Increased activity, energy or agitation.

*Exaggerated sense of well-being and self-confidence (euphoria).

*Decreased need for sleep.

*Unusual talkativeness.

*Racing thoughts.

*Distractibility.

*Poor decision-making — for example, going on buying sprees, taking sexual risks or making foolish investments.

Major depressive episode

A major depressive episode includes symptoms that are severe enough to cause noticeable difficulty in day-to-day activities, such as work, school, social activities or relationships. An episode includes five or more of these symptoms:

*Depressed mood, such as feeling sad, empty, hopeless or tearful (in children and teens, depressed mood can appear as irritability).

*Marked loss of interest or feeling no pleasure in all — or almost all — activities.

*Significant weight loss when not dieting, weight gain, or decrease or increase in appetite (in children, failure to gain weight as expected can be a sign of depression).

*Either insomnia or sleeping too much.

*Either restlessness or slowed behavior.

*Fatigue or loss of energy.

*Feelings of worthlessness or excessive or inappropriate guilt.

*Decreased ability to think or concentrate, or indecisiveness.

*Thinking about, planning or attempting suicide.

Other features of bipolar disorder

Signs and symptoms of bipolar I and bipolar II disorders may include other features, such as anxious distress, melancholy, psychosis or others. The timing of symptoms may include diagnostic labels such as mixed or rapid cycling. In addition, bipolar symptoms may occur during pregnancy or change with the seasons.

Symptoms in children and teens

Symptoms of bipolar disorder can be difficult to identify in children and teens. It's often hard to tell whether these are normal ups and downs, the results of stress or trauma, or signs of a mental health problem other than bipolar disorder.

Children and teens may have distinct major depressive or manic or hypomanic episodes, but the pattern can vary from that of adults with bipolar disorder. And moods can rapidly shift during episodes. Some children may have periods without mood symptoms between episodes.

The most prominent signs of bipolar disorder in children and teenagers may include severe mood swings that are different from their usual mood swings.

Causes

The exact cause of bipolar disorder is unknown, but several factors may be involved, such as:

*Biological differences. People with bipolar disorder appear to have physical changes in their brains. The significance of these changes is still uncertain but may eventually help pinpoint causes.

*Genetics. Bipolar disorder is more common in people who have a first-degree relative, such as a sibling or parent, with the condition. Researchers are trying to find genes that may be involved in causing bipolar disorder.

Risk factors

Factors that may increase the risk of developing bipolar disorder or act as a trigger for the first episode include:

#Having a first-degree relative, such as a parent or sibling, with bipolar disorder.

#Periods of high stress, such as the death of a loved one or other traumatic event.

#Drug or alcohol abuse.

Complications

Left untreated, bipolar disorder can result in serious problems that affect every area of your life, such as:

Problems related to drug and alcohol use.

Suicide or suicide attempts.

Legal or financial problems.

Damaged relationships.

Poor work or school performance.

Co-occurring conditions

If you have bipolar disorder, you may also have another health condition that needs to be treated along with bipolar disorder. Some conditions can worsen bipolar disorder symptoms or make treatment less successful. Examples include:

Anxiety disorders.

Eating disorders.

Attention-deficit/hyperactivity disorder (ADHD)
Alcohol or drug problems.

Physical health problems, such as heart disease, thyroid problems, headaches or obesity.

Prevention

There's no sure way to prevent bipolar disorder. However, getting treatment at the earliest sign of a mental health disorder can help prevent bipolar disorder or other mental health conditions from worsening.

If you've been diagnosed with bipolar disorder, some strategies can help prevent minor symptoms from becoming full-blown episodes of mania or depression:

#Pay attention to warning signs. Addressing symptoms early on can prevent episodes from getting worse. You may have identified a pattern to your bipolar episodes and what triggers them. Call your doctor if you feel you're falling into an episode of depression or mania. Involve family members or friends in watching for warning signs.

#Avoid drugs and alcohol. Using alcohol or recreational drugs can worsen your symptoms and make them more likely to come back.

#Take your medications exactly as directed. You may be tempted to stop treatment — but don't. Stopping your medication or reducing your dose on your own may cause withdrawal effects or your symptoms may worsen or return.

Fecal Microbiota Transplantation (FMT)

Fecal Microbiota Transplantation (FMT)

Introduction

Fecal microbiota transplantation (FMT) is a procedure that delivers healthy human donor stool to a child via colonoscopy, enema, nasogastric (NG) tube, or in capsule form (popularly called “poop pills”). It may be prescribed for debilitating gasterointestinal infections, such as Clostridium difficile (C. diff), that keep recurring despite antibiotic therapy.

C. diff is a serious infection — one that causes debilitating diarrhea and in the U.S., in 2011 alone, C. diff was responsible for 29,000 deaths in adults. Treating C. diff begins with administering antibiotics; however, recurrence is common. By the third episode of severe C. diff, it is unlikely antibiotics will cure the infection; so, your child’s doctor may consider FMT as an option.

Based on successful treatment of C. diff infections, FMT is now being looked at for a wide range of conditions. However, it’s still considered an experimental treatment, and shouldn’t be attempted without medical supervision.

Not all children are good candidates for FMT. The procedure carries some risk, particularly if your child is taking immunosuppressant medication or has had a recent bone marrow transplant.

Working principle

The GI tract has an “ecosystem” of thousands of bacteria and other organisms that help keep the body healthy. When your child is given an antibiotic, this ecosystem is disrupted, allowing the growth of disease-causing bacteria, such as C. diff.

With a fecal transplant, “good” microorganisms from the donor stool are infused into the patient. Healthy bacteria begin to grow and prevent C. diff from recurring.

Stool donors are rigorously screened and stool samples are extensively tested before being used for FMT.

Preparation

The long-term results of FMT are unknown, so you’ll need to sign an informed-consent form on behalf of your child.

To prepare for the transplant, your child should have an empty GI tract. This often means drinking only clear fluids and abstaining from eating for 24 hours before the procedure.

If your child has mild or moderate C. diff, they may also be asked to drink a liquid to encourage a bowel movement; however, children with more severe infections will not follow this same protocol.

Procedure

There are several different FMT techniques:

#Colonoscopy: A thin, hollow tube with an attached camera is placed up the colon, and a catheter-tipped syringe is used to inject donor stool through the channel.

#Enema: Although less invasive than a colonoscopy, a fecal enema often needs to be performed more than once, because the donor stool doesn’t reach the colon.

#Nasogastric (NG) tube: Using a thin, flexible feeding tube, doctors insert donor stool through a patient’s nostril, down the throat, and into the stomach.

#Oral capsules, known as “poop pills.”

Future

Recent studies show how FMT can be beneficial to children who have specific GI conditions, such as Crohn’s disease or ulcerative colitis. We are also starting to test FMT for peanut allergy, based on evidence that transferring “good” bacteria can rebalance the immune system.

FMT is a hot topic among researchers and clinicians. ClinicalTrials.gov reveals some 170 studies on FMT, with applications as diverse as type 2 diabetes, cirrhosis, and HIV. And, in a clinical trial at Boston Children’s Hospital, researchers are looking at whether giving peanut-allergic people the “good” bacteria from a non-allergic person (in the form of “poop pills”) prevents allergic reactions.

Blood– Brain Barrier (BBB)

Blood– Brain Barrier (BBB) 

Introduction

The brain is the epicentre of an eclectic array of physiological activity. It integrates information from the external environment with signals from the internal environment in order to execute specific activities.

With all the special activities that occur at the neuronal level, it is paramount that the chemical environment in which these cells operate is strictly regulated. This is the primary function of the blood-brain barrier.

This article will look at the overall structure of the blood-brain, blood-nerve, and blood-cerebrospinal fluid barriers found throughout the nervous system. Additionally, special attention will be paid to those areas within the brain that lack a blood-brain barrier and to clinically relevant points with respect to this membrane.

Definition

Blood-Brain Barrier (BBB) is a selectively permeable membrane regulates the passage of a multitude of large and small molecules into the microenvironment of the neurons. It achieves this feat by with the aid of multiple cellular transport channels scattered along the membrane. 

These include:

*amino acid transporters.

*glucose transporter 1 (GLUT1).

*nucleouside & nucleotide transporters.

*monocarboxylate transporters (MCT1 and MCT2).

*ion transporters (Na+/K+-ATPase pumps) that facilitate the transport of essential molecules into the brain.

In addition to facilitating the uptake of amino acids, the amino acid transporters may inadvertently transport undesirable heavy metals into the brain’s immediate environment. 

Consequently, at high enough concentrations, this will result in neurotoxicity. GLUT1 and the MCT transporters carry glucose, and lactate and ketones, respectively.

Blood–brain barrier structure

The brain has a large network of arterial and venous vessels taking blood to and from (respectively) brain tissue. However, most of the action occurs at the level of the capillaries. Both the luminal and abluminal (outer surface of the vessel) sides are lined by key structures that contribute to the integrity of the cells. 

Firstly, squamous epithelial cells form the endothelial wall of the capillaries; the luminal surface of these cells comes into contact with circulating blood and its constituents. The abluminal surface is in contact with a circumferentially continuous basement membrane.

The endothelial cells are anchored to each other by zonula occludens or tight junctions, as well as zonulae adherens. The former provide structural support to the endothelial wall, while the latter physically connects adjacent cells. 

Additionally, the tight junctions circumscribe the cells and provide a seal with all adjacent cells. Therefore, the endothelium functions as an impermeable barrier between the capillary lumen and brain tissue.

Studies conducted on other mammals have implicated pericytes as integral components in the formation of the blood-brain barrier. These cells encircle endothelial cells of capillaries and are able to contract in order to regulate capillary blood flow. 

Consequently, the contractility also regulates the amount of blood flowing through the capillaries, thus enhancing the blood-brain barrier. Furthermore, some theories suggest that pericytes not only promote the formation of tight junctions, but they also inhibit the production of chemicals that promote vascular permeability.

Astrocytes are highly branched cells with small bodies found both in white matter (fibrous astrocytes) as well as in grey matter (protoplasmic astrocytes). 

The podocytes of both fibrous and protoplasmic astrocytes not only encircle nerve fibres and neuronal somas (respectively), but they also surround the abluminal surface of the capillaries. At this point, the processes are referred to as perivascular endfeet.

Blood–nerve barrier

A similar architectural construct exists in the peripheral nervous system that also limits the interaction between the peripheral nerves and circulating blood. This system is informally referred to as the blood-nerve barrier.

Blood–cerebrospinal fluid barrier

There is a similar barrier system in place that acts as an interface between blood and cerebrospinal fluid. This is known as the blood-cerebrospinal fluid barrier. The main similarities between the blood-cerebrospinal fluid barrier and the blood-brain barrier are:

Endothelial cells found in the capillary beds.

Circumferential basement membrane around the abluminal surface of the capillary.

And perivascular endfeet of the astrocytes also on the abluminal surface of the capillaries.

The blood-cerebrospinal fluid barrier, however, also has fenestrated endothelial cells which allow easier passage of water, gases and lipophilic substances from the blood to the cerebrospinal fluid. 

Additionally, there are choroidal epithelial cells that are integral to the production of cerebrospinal fluid.

Choroid epithelium consists of ciliated cuboidal cells, equipped with microvilli, encompassing capillary tufts. Although the choroid epithelium is continuous with the ependymal layer (simple ciliated columnar cells) of the ventricle, it contains more tight junctions and consequently act as an effective barrier between blood and cerebrospinal fluid.

Circumventricular organs

There are regions of the brain where the blood-brain barrier is absent. This anatomical adaptation allows areas of the brain to monitor homeostatic changes within the systemic circulation. As a result, the brain is able to detect these changes and effect necessary protective physiological processes to mitigate these activities. There are seven such areas that are collectively referred to as the circumventricular organs. They can be further subdivided in secretory and sensory organs:

Secretory organs

Secretory organs, as the name suggests, are structures that release their products directly into the bloodstream or cerebrospinal fluid. The products may either be neurohormonal or other proteins. 

The secretory circumventricular organs include the neurohypophysis (posterior pituitary gland), pineal gland, subcommissural organ and median eminence.

1.Neurohypophysis – is also known as the posterior pituitary gland. It is the region of the hypophysis cerebri that originates from neuroectoderm and stores hypothalamic hormones (namely oxytocin and vasopressin). Hormones are delivered to the posterior pituitary gland by way of nerve fibres travelling from the paraventricular and supraoptic hypothalamic nuclei.

2.Pineal gland – is a pine-shaped organ situated in the posterior aspect of the third ventricle. It lies just superior to, and in the midline of, the corpora quadrigemina (superior and inferior colliculi). The gland is encapsulated and lobulated (internally). Its constituent cells – pinealocytes – produce and cyclically release melatonin with the oscillating circadian rhythm (which is regulated by the suprachiasmatic nucleus). The absence of a blood-brain barrier here allows melatonin to be secreted into the rich blood supply coming from the posterior choroidal artery (branch of the posterior communicating artery) and internal cerebral veins (tributary to the great vein of Galen).

3.Subcommissural organ – is situated near to the caudal limit of the pineal recess (in the third ventricle) at the opening of the cerebral aqueduct of Sylvius. Here, it is caudally and ventrally related to the posterior commissure. The ependymal cells here, unlike those covering the other circumventricular organs, are tall ciliated columnar cells. The capillaries at this level are not as abundant or significantly fenestrated as those in other circumventricular organs. The subcommissural organ releases SCO-spondin, which is a glycoprotein that aggregates within the third ventricle and forms Reissner’s fibres. These fibres have been implicated in maintaining the patency of the aqueduct of Sylvius and their absence results in congenital hydrocephalus.

4.Median Eminence – has an intricate communication with the hypophyseal portal system that permits communication between systemic circulation and cerebrospinal fluid by way of the large number of fenestrated capillary beds it contains. The median eminence, which is located at the floor of the hypothalamus, is anterior to the tuber cinereum (ventral extent of the third ventricle). The median eminence also contains specialized cells known as tanycytes, which assist in modifying the permeability of the membrane to allow macromolecules to enter the peripheral circulation.

Sensory organs

Sensory organs are responsible for monitoring the peripheral circulation and responding appropriately to reverse these changes or eliminate toxins. These organs include the subfornical organ, the organum vasculosum of the lamina terminalis and the area postrema.

1.Subfornical organ – is a small region at the interventricular foramen of Monro that is comprised of glial cells, neurons and a densely packed tuft of fenestrated capillaries. Like other circumventricular organs, the subfornical organ is covered by flattened ependymal cells. The subfornical organ has multiple homeostatic functions, including cardiovascular regulation, osmoregulation and energy regulation, among others. This concept is supported by its efferent projections to the lateral hypothalamus, the median preoptic area and organum vasculosum.

2.Organum vasculosum – also known as the organum vasculosum of the lamina terminalis (OVLT) or simply, the vascular organ, it is cranial to the optic chiasm and caudal to the anterior commissure. The vascular bed of this organ is highly fenestrated and the ependyma contains flattened cells with very sparsely distributed cilia. The primary role of the vascular organ is to regulate fluid balance. As such, it receives afferent fibres from the subfornical organ, several hypothalamic nuclei and the locus coeruleus. It then projects to the supraoptic and median preoptic nuclei.

3.Area postrema – is probably the most commonly known circumventricular organ. It is a paired structure that is located at the caudal extent of the floor of the fourth ventricle. This bilateral structure is an important component of what is commonly termed the vomiting center. The absence of a blood-brain barrier in this location allows the area postrema to identify chemical irritants and stimulate a vomiting response.

Gut - Brain Axis (GBA)

Gut - Brain Axis (GBA) 

Introduction

The gut-brain connection is no joke; it can link anxiety to stomach problems and vice versa. Have you ever had a "gut-wrenching" experience? Do certain situations make you "feel nauseous"? Have you ever felt "butterflies" in your stomach? We use these expressions for a reason. The gastrointestinal tract is sensitive to emotion. Anger, anxiety, sadness, elation — all of these feelings (and others) can trigger symptoms in the gut.

The brain has a direct effect on the stomach and intestines. For example, the very thought of eating can release the stomach's juices before food gets there. This connection goes both ways. 

A troubled intestine can send signals to the brain, just as a troubled brain can send signals to the gut. Therefore, a person's stomach or intestinal distress can be the cause or the product of anxiety, stress, or depression. That's because the brain and the gastrointestinal (GI) system are intimately connected.

This is especially true in cases where a person experiences gastrointestinal upset with no obvious physical cause. For such functional GI disorders, it is difficult to try to heal a distressed gut without considering the role of stress and emotion.

Gut health and anxiety

Given how closely the gut and brain interact, it becomes easier to understand why you might feel nauseated before giving a presentation, or feel intestinal pain during times of stress. 

That doesn't mean, however, that functional gastrointestinal conditions are imagined or "all in your head." Psychology combines with physical factors to cause pain and other bowel symptoms. 

Psychosocial factors influence the actual physiology of the gut, as well as symptoms. In other words, stress (or depression or other psychological factors) can affect movement and contractions of the GI tract.

In addition, many people with functional GI disorders perceive pain more acutely than other people do because their brains are more responsive to pain signals from the GI tract. Stress can make the existing pain seem even worse.

Based on these observations, you might expect that at least some patients with functional GI conditions might improve with therapy to reduce stress or treat anxiety or depression. 

Multiple studies have found that psychologically based approaches lead to greater improvement in digestive symptoms compared with only conventional medical treatment.

Gut-brain connection, anxiety and digestion  

Are your stomach or intestinal problems — such as heartburn, abdominal cramps, or loose stools — related to stress? Watch for these and other common symptoms of stress and discuss them with your doctor. 

Together you can come up with strategies to help you deal with the stressors in your life, and also ease your digestive discomforts.

Autism Spectrum

Autism Spectrum 

Introduction

Autism spectrum disorder is a condition related to brain development that impacts how a person perceives and socializes with others, causing problems in social interaction and communication. The disorder also includes limited and repetitive patterns of behavior. The term "spectrum" in autism spectrum disorder refers to the wide range of symptoms and severity.

Autism spectrum disorder includes conditions that were previously considered separate — autism, Asperger's syndrome, childhood disintegrative disorder and an unspecified form of pervasive developmental disorder. Some people still use the term "Asperger's syndrome," which is generally thought to be at the mild end of autism spectrum disorder.

Autism spectrum disorder begins in early childhood and eventually causes problems functioning in society — socially, in school and at work, for example. Often children show symptoms of autism within the first year. A small number of children appear to develop normally in the first year, and then go through a period of regression between 18 and 24 months of age when they develop autism symptoms.

While there is no cure for autism spectrum disorder, intensive, early treatment can make a big difference in the lives of many children.

Symptoms

Some children show signs of autism spectrum disorder in early infancy, such as reduced eye contact, lack of response to their name or indifference to caregivers. Other children may develop normally for the first few months or years of life, but then suddenly become withdrawn or aggressive or lose language skills they've already acquired. Signs usually are seen by age 2 years.

Each child with autism spectrum disorder is likely to have a unique pattern of behavior and level of severity — from low functioning to high functioning.

Some children with autism spectrum disorder have difficulty learning, and some have signs of lower than normal intelligence. Other children with the disorder have normal to high intelligence — they learn quickly, yet have trouble communicating and applying what they know in everyday life and adjusting to social situations.

Because of the unique mixture of symptoms in each child, severity can sometimes be difficult to determine. It's generally based on the level of impairments and how they impact the ability to function.

Below are some common signs shown by people who have autism spectrum disorder.

Social communication and interaction

A child or adult with autism spectrum disorder may have problems with social interaction and communication skills, including any of these signs:

Fails to respond to his or her name or appears not to hear you at times.

Resists cuddling and holding, and seems to prefer playing alone, retreating into his or her own world.

Has poor eye contact and lacks facial expression.

Doesn't speak or has delayed speech, or loses previous ability to say words or sentences.

Can't start a conversation or keep one going, or only starts one to make requests or label items.

Speaks with an abnormal tone or rhythm and may use a singsong voice or robot-like speech.

Repeats words or phrases verbatim, but doesn't understand how to use them.

Doesn't appear to understand simple questions or directions.

Doesn't express emotions or feelings and appears unaware of others' feelings.

Doesn't point at or bring objects to share interest.

Inappropriately approaches a social interaction by being passive, aggressive or disruptive.

Has difficulty recognizing nonverbal cues, such as interpreting other people's facial expressions, body postures or tone of voice.

Patterns of behavior

A child or adult with autism spectrum disorder may have limited, repetitive patterns of behavior, interests or activities, including any of these signs:

Performs repetitive movements, such as rocking, spinning or hand flapping.

Performs activities that could cause self-harm, such as biting or head-banging.

Develops specific routines or rituals and becomes disturbed at the slightest change.

Has problems with coordination or has odd movement patterns, such as clumsiness or walking on toes, and has odd, stiff or exaggerated body language.

Is fascinated by details of an object, such as the spinning wheels of a toy car, but doesn't understand the overall purpose or function of the object.

Is unusually sensitive to light, sound or touch, yet may be indifferent to pain or temperature.

Doesn't engage in imitative or make-believe play.

Fixates on an object or activity with abnormal intensity or focus.

Has specific food preferences, such as eating only a few foods, or refusing foods with a certain texture.

As they mature, some children with autism spectrum disorder become more engaged with others and show fewer disturbances in behavior. Some, usually those with the least severe problems, eventually may lead normal or near-normal lives. Others, however, continue to have difficulty with language or social skills, and the teen years can bring worse behavioral and emotional problems.

Medication

Babies develop at their own pace, and many don't follow exact timelines found in some parenting books. But children with autism spectrum disorder usually show some signs of delayed development before age 2 years.

If you're concerned about your child's development or you suspect that your child may have autism spectrum disorder, discuss your concerns with your doctor. The symptoms associated with the disorder can also be linked with other developmental disorders.

Signs of autism spectrum disorder often appear early in development when there are obvious delays in language skills and social interactions. Your doctor may recommend developmental tests to identify if your child has delays in cognitive, language and social skills, if your child:

Doesn't respond with a smile or happy expression by 6 months.

Doesn't mimic sounds or facial expressions by 9 months.

Doesn't babble or coo by 12 months.

Doesn't gesture — such as point or wave — by 14 months.

Doesn't say single words by 16 months.

Doesn't play "make-believe" or pretend by 18 months.

Doesn't say two-word phrases by 24 months.

Loses language skills or social skills at any age.

Causes

Autism spectrum disorder has no single known cause. Given the complexity of the disorder, and the fact that symptoms and severity vary, there are probably many causes. Both genetics and environment may play a role.

#Genetics. Several different genes appear to be involved in autism spectrum disorder. For some children, autism spectrum disorder can be associated with a genetic disorder, such as Rett syndrome or fragile X syndrome. For other children, genetic changes (mutations) may increase the risk of autism spectrum disorder. Still other genes may affect brain development or the way that brain cells communicate, or they may determine the severity of symptoms. Some genetic mutations seem to be inherited, while others occur spontaneously.

#Environmental factors. Researchers are currently exploring whether factors such as viral infections, medications or complications during pregnancy, or air pollutants play a role in triggering autism spectrum disorder.

Risk factors

The number of children diagnosed with autism spectrum disorder is rising. It's not clear whether this is due to better detection and reporting or a real increase in the number of cases, or both.

Autism spectrum disorder affects children of all races and nationalities, but certain factors increase a child's risk. These may include:

*Your child's sex. Boys are about four times more likely to develop autism spectrum disorder than girls are.

*Family history. Families who have one child with autism spectrum disorder have an increased risk of having another child with the disorder. It's also not uncommon for parents or relatives of a child with autism spectrum disorder to have minor problems with social or communication skills themselves or to engage in certain behaviors typical of the disorder.

*Other disorders. Children with certain medical conditions have a higher than normal risk of autism spectrum disorder or autism-like symptoms. Examples include fragile X syndrome, an inherited disorder that causes intellectual problems; tuberous sclerosis, a condition in which benign tumors develop in the brain; and Rett syndrome, a genetic condition occurring almost exclusively in girls, which causes slowing of head growth, intellectual disability and loss of purposeful hand use.

*Extremely preterm babies. Babies born before 26 weeks of gestation may have a greater risk of autism spectrum disorder.

*Parents' ages. There may be a connection between children born to older parents and autism spectrum disorder, but more research is necessary to establish this link.

Complications

Problems with social interactions, communication and behavior can lead to:

1.Problems in school and with successful learning.

2.Employment problems.

3.Inability to live independently.

4.Social isolation.

5.Stress within the family.

6.Victimization and being bullied.

Prevention

There's no way to prevent autism spectrum disorder, but there are treatment options. Early diagnosis and intervention is most helpful and can improve behavior, skills and language development. However, intervention is helpful at any age. Though children usually don't outgrow autism spectrum disorder symptoms, they may learn to function well.

Dementia

Dementia

Introduction 

Dementia is a term used to describe a group of symptoms affecting memory, thinking and social abilities. In people who have dementia, the symptoms interfere with their daily lives. Dementia isn't one specific disease. Several diseases can cause dementia.

Dementia generally involves memory loss. It's often one of the early symptoms of the condition. But having memory loss alone doesn't mean you have dementia. Memory loss can have different causes.

Alzheimer's disease is the most common cause of dementia in older adults, but there are other causes of dementia. Depending on the cause, some dementia symptoms might be reversible.

Symptoms

Dementia symptoms vary depending on the cause. Common symptoms include:

Cognitive changes:

Memory loss, which is usually noticed by someone else.
Problems communicating or finding words.
Trouble with visual and spatial abilities, such as getting lost while driving.
Problems with reasoning or problem-solving.
Trouble performing complex tasks.
Trouble with planning and organizing.
Poor coordination and control of movements.
Confusion and disorientation.

Psychological changes:

Personality changes.
Depression.
Anxiety.
Agitation.
Inappropriate behavior.
Being suspicious, known as paranoia.
Seeing things that aren't there, known as hallucinations.

Causes

Dementia is caused by damage to or loss of nerve cells and their connections in the brain. The symptoms depend on the area of the brain that's damaged. Dementia can affect people differently.

Dementias are often grouped by what they have in common. They may be grouped by the protein or proteins deposited in the brain or by the part of the brain that's affected. 

Also, some diseases have symptoms like those of dementia. And some medicines can cause a reaction that includes dementia symptoms. 

Not getting enough of certain vitamins or minerals also can cause dementia symptoms. When this occurs, dementia symptoms may improve with treatment.

Progressive dementias

Dementias that are progressive get worse over time. Types of dementias that worsen and aren't reversible include:

1.Alzheimer's disease. This is the most common cause of dementia.

Although not all causes of Alzheimer's disease are known, experts do know that a small percentage are related to changes in three genes. These gene changes can be passed down from parent to child. While several genes are probably involved in Alzheimer's disease, one important gene that increases risk is apolipoprotein E4 (APOE).

People with Alzheimer's disease have plaques and tangles in their brains. Plaques are clumps of a protein called beta-amyloid. Tangles are fibrous masses made up of tau protein. It's thought that these clumps damage healthy brain cells and the fibers connecting them.

2.Vascular dementia. This type of dementia is caused by damage to the vessels that supply blood to the brain. Blood vessel problems can cause stroke or affect the brain in other ways, such as by damaging the fibers in the white matter of the brain.

The most common symptoms of vascular dementia include problems with problem-solving, slowed thinking, and loss of focus and organization. These tend to be more noticeable than memory loss.

3.Lewy body dementia. Lewy bodies are balloonlike clumps of protein. They have been found in the brains of people with Lewy body dementia, Alzheimer's disease and Parkinson's disease. Lewy body dementia is one of the more common types of dementia.

Common symptoms include acting out dreams in sleep and seeing things that aren't there, known as visual hallucinations. Symptoms also include problems with focus and attention. Other signs include uncoordinated or slow movement, tremors, and stiffness, known as parkinsonism.

4.Frontotemporal dementia. This is a group of diseases characterized by the breakdown of nerve cells and their connections in the frontal and temporal lobes of the brain. These areas are associated with personality, behavior and language. Common symptoms affect behavior, personality, thinking, judgment, language and movement.

5.Mixed dementia. Autopsy studies of the brains of people age 80 and older who had dementia indicate that many had a combination of several causes. People with mixed dementia can have Alzheimer's disease, vascular dementia and Lewy body dementia. Studies are ongoing to determine how having mixed dementia affects symptoms and treatments.

Other disorders linked to dementia

1.Huntington's disease. Huntington's disease is caused by a genetic change. The disease causes certain nerve cells in the brain and spinal cord to waste away. Symptoms include a decline in thinking skills, known as cognitive skills. Symptoms usually appear around age 30 or 40.
Traumatic brain injury (TBI). This condition is most often caused by repetitive head trauma. Boxers, football players or soldiers might develop TBI.

2.Dementia symptoms depend on the part of the brain that's injured. TBI can cause depression, explosiveness, memory loss and impaired speech. TBI also may cause slow movement, tremors and stiffness. Symptoms might not appear until years after the trauma.

3.Creutzfeldt-Jakob disease. This rare brain disorder usually occurs in people without known risk factors. This condition might be due to deposits of infectious proteins called prions. Symptoms of this fatal condition usually appear after age 60.

Creutzfeldt-Jakob disease usually has no known cause but it can be passed down from a parent. It also may be caused by exposure to diseased brain or nervous system tissue, such as from a cornea transplant.

4.Parkinson's disease. Many people with Parkinson's disease eventually develop dementia symptoms. When this happens, it's known as Parkinson's disease dementia.

Dementia-like conditions that can be reversed

Some causes of dementia-like symptoms can be reversed with treatment. They include:

Infections and immune disorders. Dementia-like symptoms can result from a fever or other side effects of the body's attempt to fight off an infection. Multiple sclerosis and other conditions caused by the body's immune system attacking nerve cells also can cause dementia.

Metabolic or endocrine problems. People with thyroid problems and low blood sugar can develop dementia-like symptoms or other personality changes. This also is true for people who have too little or too much sodium or calcium, or problems absorbing vitamin B-12.

Low levels of certain nutrients. Not getting enough of certain vitamins or minerals in your diet can cause dementia symptoms. This includes not getting enough thiamin, also known as vitamin B-1, which is common in people with alcohol use disorder. It also includes not getting enough vitamin B-6, vitamin B-12, copper or vitamin E. Not drinking enough liquids, leading to dehydration, also can cause dementia symptoms.

Medicine side effects. Side effects of medicines, a reaction to a medicine or an interaction of several medicines can cause dementia-like symptoms.

Subdural bleeding. Bleeding between the surface of the brain and the covering over the brain can be common in older adults after a fall. Subdural bleeding can cause symptoms similar to those of dementia.

Brain tumors. Rarely, dementia can result from damage caused by a brain tumor.

Normal-pressure hydrocephalus. This condition is a buildup of fluid in the cavities in the brain known as ventricles. It can result in walking problems, loss of bladder control and memory loss.

Risk factors

Many factors can eventually contribute to dementia. Some factors, such as age, can't be changed. You can address other factors to reduce your risk.

Risk factors that can't be changed

1.Age. The risk of dementia rises as you age, especially after age 65. However, dementia isn't a typical part of aging. Dementia also can occur in younger people.

2.Family history. Having a family history of dementia puts you at greater risk of developing the condition. However, many people with a family history never develop symptoms, and many people without a family history do. There are tests to determine whether you have certain genetic changes that may increase your risk.

3.Down syndrome. By middle age, many people with Down syndrome develop early-onset Alzheimer's disease.

Risk factors you can change

You might be able to control the following risk factors for dementia.

1.Diet and exercise. Research has found that people at higher risk of dementia who followed a healthy lifestyle lowered their risk of cognitive decline. They ate a diet that included fish, fruits, vegetables and oils. They also exercised, had cognitive training and participated in social activities. While no specific diet is known to reduce dementia risk, research indicates that those who follow a Mediterranean style diet rich in produce, whole grains, nuts and seeds have better cognitive function.

2.Drinking too much alcohol. Drinking large amounts of alcohol has long been known to cause brain changes. Several large studies and reviews found that alcohol use disorders were linked to an increased risk of dementia, particularly early-onset dementia.

3.Cardiovascular risk factors. These include obesity, high blood pressure, high cholesterol, and the buildup of fats in the artery walls, known as atherosclerosis. Diabetes and smoking also are cardiovascular risk factors. Having diabetes can increase the risk of dementia, especially if it's poorly controlled. Smoking might increase the risk of developing dementia and blood vessel disease.

4.Depression. Although not yet well understood, late-life depression might indicate the development of dementia.
Air pollution. Studies in animals have indicated that air pollution particulates can speed degeneration of the nervous system. And human studies have found that air pollution exposure — particularly from traffic exhaust and burning wood — is associated with greater dementia risk.

5.Head trauma. People who've had a severe head trauma have a greater risk of Alzheimer's disease. Several large studies found that in people age 50 years or older who had a traumatic brain injury (TBI), the risk of dementia and Alzheimer's disease increased. The risk increases in people with more-severe and multiple TBIs. Some studies indicate that the risk may be greatest within the first six months to two years after the TBI.

6.Sleep problems. People who have sleep apnea and other sleep disturbances might be at higher risk of developing dementia.

7.Low levels of certain vitamins and nutrients. Low levels of vitamin D, vitamin B-6, vitamin B-12 and folate can increase the risk of dementia.

8.Medicines that can worsen memory. These include sleep aids that contain diphenhydramine (Benadryl) and medicines to treat urinary urgency such as oxybutynin (Ditropan XL).

Also limit sedatives and sleeping tablets. Talk to a health care professional about whether any of the medicines you take might make your memory worse.

Complications

Dementia can affect many body systems and, therefore, the ability to function. Dementia can lead to:

Poor nutrition. Many people with dementia eventually reduce or stop eating, affecting their nutrient intake. Ultimately, they may be unable to chew and swallow.

Pneumonia. Trouble swallowing increases the risk of choking. And food or liquids can enter the lungs, known as aspiration. This can block breathing and cause pneumonia.

Inability to perform self-care tasks. As dementia gets worse, people have a hard time bathing, dressing, and brushing their hair or teeth. They need help using the toilet and taking medicines as directed.

Personal safety challenges. Some day-to-day situations can present safety issues for people with dementia. These include driving, cooking, and walking and living alone.

Death. Coma and death can occur in late-stage dementia. This often happens because of an infection.

Prevention

There's no sure way to prevent dementia, but there are steps you can take that might help. More research is needed, but it might be beneficial to do the following:

*Keep your mind active. Mentally stimulating activities might delay the onset of dementia and decrease its effects. Spend time reading, solving puzzles and playing word games.

*Be physically and socially active. Physical activity and social interaction might delay the onset of dementia and reduce its symptoms. Aim for 150 minutes of exercise a week.

*Quit smoking. Some studies have shown that smoking in middle age and beyond might increase the risk of dementia and blood vessel conditions. Quitting smoking might reduce the risk and improve health.

*Get enough vitamins. Some research suggests that people with low levels of vitamin D in their blood are more likely to develop Alzheimer's disease and other forms of dementia. You can increase your vitamin D levels with certain foods, supplements and sun exposure.

*More study is needed before an increase in vitamin D intake is recommended for preventing dementia. But it's a good idea to make sure you get adequate vitamin D. Taking a daily B-complex vitamin and vitamin C also might help.

*Manage cardiovascular risk factors. Treat high blood pressure, high cholesterol and diabetes. Lose weight if you're overweight.

*High blood pressure might lead to a higher risk of some types of dementia. More research is needed to determine whether treating high blood pressure may reduce the risk of dementia.

*Treat health conditions. See your doctor for treatment of depression or anxiety.

*Maintain a healthy diet. A diet such as the Mediterranean diet might promote health and lower the risk of developing dementia. A Mediterranean diet is rich in fruits, vegetables, whole grains and omega-3 fatty acids, which are commonly found in certain fish and nuts. This type of diet also improves cardiovascular health, which also may help lower dementia risk.

*Get good-quality sleep. Practice good sleep hygiene. Talk to a health care professional if you snore loudly or have periods where you stop breathing or gasp during sleep.

*Treat hearing problems. People with hearing loss have a greater chance of developing problems with thinking, known as cognitive decline. Early treatment of hearing loss, such as use of hearing aids, might help decrease the risk.

Coagulation Cascade Pathway (Blood Clotting)

Coagulation Cascade Pathway (Blood Clotting)

Introduction

Blood flows through the blood vessels to deliver the needed oxygen and nutrients to the different cells in the body. The blood clotting process or coagulation is an important process that prevents excessive building in case the blood vessel becomes injured. It plays a crucial role in repairing blood vessels.

Otherwise known as blood clotting, coagulation plays a pivotal role in the repair of blood vessels. The heart pumps blood throughout the body with the aid of the arteries, and in turn, blood goes back to the heart through the veins. When the blood vessels become injured, it will trigger the blood clotting process. This way, the body will repair the damage to stop hemorrhage or bleeding from happening.

For instance, the damage happens in the lining of the blood vessels, the platelets will form an initial plug on the affected area. They will initiate the clotting process with the aid of certain clotting factors produced in the body.

Clotting Factors

Clotting factors are components found in plasma that are linked to the blood clotting process. These factors are named and numbered based on their discovery. Though there are a total of 13 numerals, there are only 2 clotting factors. Factor VI was discovered to be part of another factor.

The clotting factors are Factor I (fibrinogen), Factor II (prothrombin), Factor III (tissue thromboplastin or tissue factor), Factor IV (ionized calcium), Factor V (labile factor or proaccelerin), Factor VII (stable factor or proconvertin), and Factor VIII (antihemophilic factor). Additionally, the coagulation factors also include Factor IX (plasma thromboplastin component or the Christmas factor), Factor X (Stuart-Prower factor), Factor XI (plasma thromboplastin antecedent), Factor XII (Hageman factor), and Factor XIII (fibrin-stabilizing factor).

The liver uses vitamin K to produce some of the factors such as Factors II, VII, IX, and X. Normally, vitamin K can be consumed through the diet from plant and animal sources. The normal flora of the intestine also produces vitamin K.

Blood Clotting Process

Hemostasis is a way of the body to stop injured blood vessels from bleeding. One of the most important parts of hemostasis is the clotting of the blood. Subsequently, the body needs to control the mechanisms to control and limit clotting. 

These include dissolving excess clots that are not needed anymore. When there is an abnormality in any part of the system that controls bleeding, it can lead to hemorrhage or excessive clotting. These are potentially life-threatening.

Too much clotting can lead to stroke and heart attacks because blood clots can travel and clog the vessels. On the other hand, poor clotting can lead to severe blood loss even with just a slight injury to the blood vessels.

Hemostasis has three major processes namely the constriction of blood vessels, activity of the platelets, and activity of the proteins found in blood (clotting factors).

Injury

The first phase of the blood clotting process is injury or when a blood vessel becomes damaged. This can be in the form of a small tear in the blood vessel wall that may lead to bleeding.

Blood Vessel Constriction

The body will constrict the blood vessel to control blood loss. It will limit the blood flow to the affected area.

Platelet Plug

In response to the injury, the body activates platelets. At the same time, chemical signals are released from small sacs in the platelets to attract other cells to the area. They make a platelet plug by forming a clump together. A protein called the von Willebrand factor (VWF) helps the platelets to stick together.

Fibrin Clot

When a blood vessel becomes injured, the coagulation factors or clotting factors in the blood are activated. The clotting factor proteins stimulate the production of fibrin, which is a strong and strand-like substance that forms a fibrin clot. For days or weeks, this fibrin clot strengthens and then dissolves when the injured blood vessel walls close and heal.

Blood clotting is a crucial process that can help prevent blood loss due to injury. If there is an abnormality in any part of the process, it can lead to dangerous complications such as severe blood loss. Commonly, people with clotting disorders are closely monitored to prevent injuries and bleeding.

Coagulation

Coagulation is the formation of a blood clot, and is essential to haemostasis. Haemostasis is the body’s physiological response to damaged blood vessels, to slow down, minimise and eventually cease the bleeding.

The coagulation process is characterised by a cascade of events which lead to the formation of a blood clot. Proteins called clotting factors initiate reactions which activate more clotting factors.

This process occurs via two pathways which unite downstream to form the common pathway. These are:

The Extrinsic pathway: This is triggered by external trauma which causes blood to escape the circulation.

The Intrinsic pathway: This is triggered by internal damage to the vessel wall.

Extrinsic Pathway of Coagulation

The extrinsic pathway unfolds as follows:

*Damage to the blood vessel means that factor VII exits the circulation into surrounding tissues.

*Tissue factor (factor III) is released by damaged cells outside the circulation.

*Factor VII and factor III form a complex, known as the TF-VIIa complex.

*TF-VIIa then activates factor X into its active form, factor Xa.

*In conjunction with factor Va, this triggers the formation of thrombin.

Note that the extrinsic pathway is believed to be responsible for the initial generation of activated Factor X (Factor Xa), whereas the intrinsic pathway amplifies its production.

Intrinsic Pathway of Coagulation

The intrinsic pathway is the longer and more intricate pathway:

*Factor XII is activated once it comes into contact with negatively charged collagen on the damaged endothelium, triggering the cascade.

*Along with clotting factors, platelets form a cellular ‘plug’ at the site of injury. These platelets also release mediators that facilitate further clotting, including Factor VIII.

*Factor IX combines with Factor VIII to form an enzyme complex that activates factor X, which along with factor Va, stimulates the production of thrombin.

Common Pathway of Coagulation

The intrinsic and extrinsic pathways converge to give rise to the common pathway. The activated factor X causes a set of reactions resulting in the inactive enzyme prothrombin (also called factor II) being converted to its active form thrombin (factor IIa) by Prothrombinase.

The thrombin then converts soluble fibrinogen (also referred to as factor I) into insoluble fibrin strands. The fibrin strands which comprise the clot are stabilised by factor XIII.

Regulation of Clotting

To prevent excessive clotting and subsequent disease, mediators including Protein C and Protein S provide negative feedback on the clotting cascade.

Protein C is activated following contact by thrombomodulin, which is itself activated by thrombin. Along with co-factors including protein S, activated protein C degrades factor Va and factor VIIIa, thus slowing the rate of clotting.

Calcium ions play a role through their interaction with the activation of several clotting factors. Low levels of calcium are therefore inhibitory to the clotting cascade.

Antithrombin is a protease inhibitor that degrades thrombin, factor IXa, factor Xa, factor XIa and factor XIIa. It is constantly active but can be activated further by a group of common anticoagulants known as heparins.

Restoring Blood Flow – Fibrinolysis

In order for blood flow to be re-established as the blood vessel heals, the thrombus must eventually be degraded. During fibrinolysis, fibrin is dissolved leading to the consequent dissolution of the clot.

The endothelial cells of the blood vessel wall secrete tissue plasminogen activators (tPAs) which convert the precursor plasminogen into plasmin. Plasmin subsequently cleaves the fibrin within the thrombus, leading to its degradation.

tPAs are released very slowly following trauma from the endothelial cells, and therefore there is a substantial time delay until there is a sufficient concentration for fibrinolysis.

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