Hyperglycemia is a condition that requires emergency treatment. Typically, patients with diabetes get hyperglycemia or high blood sugar. Lack of sufficient insulin in type 1 diabetes patients can lead to high blood sugar. Type 2 diabetes patients get it when their body’s insulin is ineffective.

There can be several causes of high blood sugar, including:
Skipping or forgetting to take insulin
Consuming more carbohydrates
Stress
Illness
Exercising less than normal
The dawn phenomenon (early morning surge in hormones)

If you suspect hyperglycemia, it is essential to seek treatment immediately since it can lead to life-threatening conditions. Early hyperglycemia symptoms are blood sugar higher than 180 mg/dL, increased thirst, frequent urination, headache, and fatigue. If not treated immediately, it can lead to nerve, blood vessel, and organ damage.

There are not too many differences present between hyperglycemia vs hypoglycemia. While hyperglycemia is high blood sugar (greater than 180 mg/dL), hypoglycemia is low blood sugar (less than 70 mg/dL). If not treated immediately, both of them can have severe consequences and may even lead to death.

How is #hyperglycemia treatment done? Can hyperglycemia cause ketoacidosis and HHNS, which are severe life-threatening conditions? We answer all your doubts in the video!

Like and share the video with your friends to let them know the dangers of high blood sugar! Subscribe to our channel for more such useful health information.

Chapters:
0:00 Intro
0:29 High Blood Sugar Causes
1:02 High Blood Sugar Symptoms
1:30 High Blood Sugar Complications
2:28 High Blood Sugar Treatment
2:50 Hyperglycemia vs Hypoglycemia

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Hyperglycemia is the term given to when your blood sugar levels are higher than 10 mmol/L. Blood sugar levels levels exceeding 7 mmol/L can damage internal organs, however, symptoms may not develop until blood glucose levels exceed 15 mmol/L so it’s worth knowing about the symptoms of hyperglycemia and how to recognise the symptoms.

Read more about hyperglycemia at: http://www.diabetes.co.uk/Diabetes-and-Hyperglycaemia.html
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A pricked finger means the immune system is hard at work. An important part of the innate immune system, the skin – has been breached, and bacteria are entering the body. The first immune cells they encounter are mast cells and dendritic cells. These cells can distinguish self from non-self thanks to the recognition of pathogen-associated molecular patterns, or PAMPs, which are molecules associated with pathogens. This recognition is not specific to any invader, but rather identifies a general attribute common to pathogens. This recognition is thanks to their pattern recognition receptors, or PRRs. The PAMPs they recognize can include bacterial lipopolysaccharides. Now that microbial components have been recognized, the body springs into action, and the inflammatory response is initiated.
The mast cells stay on the battlefield, releasing histamine and heparin. Histamine causes vasodilation of nearby blood vessels and heparin is an anticoagulant. The result is increased blood flow to the infected area, which allows more white blood cells to get there. The mast cells also release cytokines, which are cell signalling proteins that affect the behaviour of nearby cells. In this case, the cytokines are used to call macrophages and neutrophils to the area.
Neutrophils are the most abundant white blood cells. They release cytokines as well, amplifying the inflammatory response. They attack pathogens in three ways – phagocytosis (engulfing pathogens – and they can ingest up to 20 each), degranulation (release of soluble antimicrobials), and the release of neutrophil extracellular traps, or NETs. NETs are primarily composed of the neutrophils’ DNA and bind pathogens. This binding occurs thanks to positive charged proteins on the bacteria’s surface interacting with negatively charged chromatin fibers.
Dendritic cells engulf antigens – foreign substances that elicit an immune response – and break them up into smaller pieces called epitopes. Dendritic cells in the epithelial tissue move out of t he infected area and into the lymph nodes.
The innate immune system has non-specific means of intruder identification and resistance. However, when the dendritic cells enter the lymph nodes, they link the innate immune system to the adaptive immune system. The adaptive immune system consists of T cells and B cells, and brings in anti-pathogenic weaponry specific to the attacker.
T-cells are produced in the thymus, differentiating into four types: helper T-cells, cytotoxic T-cells, regulatory T-cells, or Tregs, and memory T-cells.
T-cells are specific to one antigen. After leaving the thymus, they circulate the body until an APC presents an antigen that matches their T-cell receptor, or TCR. Following this initial activation, the T-cell’s CD4 or CD8 molecule also binds the MHC of the APC, stabilizing the connection. Helper T-cells and cytotoxic T-cells also need secondary signals, as well as cytokines to become fully activated. Following these signals, the T-cell begins to divide rapidly and moves to the site of inflammation to fight the pathogen. At the infection site, mast cells, neutrophils, and epithelial cells can produce cytokines to induce further activation and proliferation of the T-cells.
Immature B-cells can be activated either by attaching to a free-floating antigen or thanks to helper T-cells or dendritic cells that present an epitope matching their B-cell receptors, or BCRs. BCRs consist of a membrane bound antibody, which is a large, Y-shaped protein that bind antigens, CD79A and CD79B. The B-cell receptor and antigen undergo cell-mediated endocytosis.
Recognition of an antigen stimulates B-cells to proliferate, and the activated B-cells undergo clonal expansion. As they proliferate, these many clones undergo somatic hypermutation. AID introduces point mutations into the clones. For some clones, this results in an increased affinity to the antigen, while for others, this means a decreased affinity. The antigen is proteolytically broken down and an epitope is then displayed on the B-cell’s surface, attached to an MHC class II protein. Before the B-cell can do anything, a helper T cell with a complementary TCR, and CD4+ glycoprotein must bind the antigen. The T helper cell then releases cytokines that let the B-cell take the next step. This is a safety mechanism to prevent accidental activation of the B-cells. The B-cells that have decreased affinity then undergo apoptosis, while the B-cells with increased affinity differentiate, becoming either a plasma cell, or a memory B-cell. The plasma cells produce antibodies matching their BCRs into the blood and lymph. Meanwhile, the memory B cells store antibodies in case of future reinfection.
When antibodies bind antigens, they label them for destruction by cells such as macrophages and neutrophils. B-cells mediate your humoral immune response, so called because it involves substances in your body fluids.
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Factors which may delay wound healing
Local and systemic factors may influence the rate of wound healing. Local factors describe the conditions in the immediate wound environment while systemic factors refer to ‘whole body’ influences on the local wounded area.
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Jaundice: Clinical essentials – Dr. Kiran Peddi MRCP(UK), FRCP(London), CCT(Gastro)

What is jaundice?
Jaundice is a condition in which the skin, sclera (whites of the eyes) and mucous membranes turn yellow. This yellow color is caused by a high level of bilirubin, a yellow-orange bile pigment. Bile is fluid secreted by the liver. Bilirubin is formed from the breakdown of red blood cells.

SYMPTOMS AND CAUSES
What causes jaundice?
Jaundice can be caused by a problem in any of the three phases in bilirubin production.

Before the production of bilirubin, you may have what’s called unconjugated jaundice due to increased levels of bilirubin caused by:

Reabsorption of a large hematoma (a collection of clotted or partially clotted blood under the skin).
Hemolytic anemias (blood cells are destroyed and removed from the bloodstream before their normal lifespan is over).
During production of bilirubin, jaundice can be caused by:

Viruses, including Hepatitis A, chronic Hepatitis B and C, and Epstein-Barr virus infection (infectious mononucleosis).
Alcohol.
Autoimmune disorders.
Rare genetic metabolic defects.
Medicines, including acetaminophen toxicity, penicillins, oral contraceptives, chlorpromazine (Thorazine®) and estrogenic or anabolic steroids.
After bilirubin is produced, jaundice may be caused by obstruction (blockage) of the bile ducts from:

Gallstones.
Inflammation (swelling) of the gallbladder.
Gallbladder cancer.
Pancreatic tumor.
What are the symptoms of jaundice?
Sometimes, the person may not have symptoms of jaundice, and the condition may be found accidentally. The severity of symptoms depends on the underlying causes and how quickly or slowly the disease develops.

If you have a short-term case of jaundice (usually caused by infection), you may have the following symptoms and signs:

Fever.
Chills.
Abdominal pain.
Flu-like symptoms.
Change in skin color.
Dark-colored urine and/or clay-colored stool.
If jaundice isn’t caused by an infection, you may have symptoms such as weight loss or itchy skin (pruritus). If the jaundice is caused by pancreatic or biliary tract cancers, the most common symptom is abdominal pain. Sometimes, you may have jaundice occurring with liver disease if you have:

Chronic hepatitis or inflammation of the liver.
Pyoderma gangrenosum (a type of skin disease).
Acute hepatitis A, B or C.
Polyarthralgias (inflammation of the joints).

DIAGNOSIS AND TESTS
—————————————-
How is jaundice diagnosed?
Doctors diagnose jaundice by checking for signs of liver disease such as:

Bruising of the skin.
Spider angiomas (abnormal collection of blood vessels near the surface of the skin).
Palmar erythema (red coloration of the palms and fingertips).
Urinalysis (urine testing) that’s positive for bilirubin shows that the patient has conjugated jaundice. The findings of urinalysis should be confirmed by serum testing. The serum testing will include a complete blood count (CBC) and bilirubin levels.

Your doctor will also do an exam to determine the size and tenderness of your liver. He or she may use imaging (ultrasonography and computer tomographic (CT) scanning) and liver biopsy (taking a sample of the liver) to further confirm diagnosis.

MANAGEMENT AND TREATMENT
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How is jaundice treated?
Jaundice usually doesn’t require treatment in adults (it’s a more severe problem in infants). The causes and complications of jaundice can be treated. For instance, if itching is bothersome, it may be eased by cholestyramine (Questran®).

What are some of the complications/side effects of the treatments of jaundice?
Constipation.
Bloating.
Stomach pain.
Gas.
Upset stomach.
Vomiting.
Diarrhea.

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Jaundice Causes,Sign, Symptoms,Treatment and Risk Factor
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At the Ohio State’s Comprehensive Wound Center we know there are many factors that affect wound healing. These factors include diabetes/high blood sugar, vascular disease/poor circulation/blood flow; pressure and immobility; infection, nutrition, smoking .

For more information about our services, or to schedule an appointment, please call 614-293-4811 or visit us at http://wexnermedical.osu.edu/go/wound

Wound care or wound healing. This video is on how to heal wounds faster, wound healing foods, vitamins, after surgery.

This video is about general advice on foods and lifestyle factors that help promote wound healing. I’ve received a lot of messages to make a video on how to make wounds heal faster after surgery. I hope my tips help! Please remember if you’re worried about your wound or just want to be sure it’s ok. It’s always best to speak to your nurse, doctor or pharmacist so they can assess and advise appropriately.

WOUND HEALING FACTORS:
Eat well, heal well: Wound healing and nutrition guide: https://www.esht.nhs.uk/wp-content/uploads/2018/02/0679.pdf
– The above nutrition guide also gives information for diabetic patients and requirement of good blood sugar levels.

HYDRATION: Dehydrated skin is less elasticated, more fragile and susceptible to breakdown. Dehydration also reduces the efficiency of blood circulation which will impair the supply of oxygen and nutrients the wound desperately needs for the healing process.

Aim for 6-8 glasses of water per day unless recommended otherwise by your healthcare professional.

PROTEIN: Deficiency can impair the rebuilding and remodelling stage of wound healing. It’s also been reported that protein deficiency can cause impairment of collagen production which reduces the wound strength and increases the risk of infection.

Protein rich foods include meat, poultry, eggs, beans and tofu – Link further above in the description to a helpful guide that explains what to eat for each tip, how much to eat and various other information for a healthy diet.

ENERGY: The main source of energy for your body and for wound healing and carbohydrate and fats. Collagen production takes the most energy. Calorie needs for healing increase with increasing size and complexity of the wound – Now if its needed your doctors will involve dieticians to help you with this.

The reason why you need the energy and carbohydrate availability is because if you don’t your body will convert those helpful proteins we mentioned earlier into energy. Fats also have a key role in structure, function of cell membranes and again preventing the body from using proteins for energy.

VITAMINS & MINERALS: Eating a varied and balanced diet should get you all of these. Supplementation is sometimes required which is usually initiated by dieticians for chronic wound healing and malnutrition.

The most important vitamins for wound healing include Vitamin A, B and the main one Vitamin C as it helps with collagen production, cross-linking as well as the formation of new blood vessels.

Vitamin C is found is a wide variety of fruits and vegetables. Such as oranges, orange juice, strawberries, broccoli. Food sources for all vitamins: https://www.nhs.uk/conditions/vitamins-and-minerals/iron/

MINERALS: Zinc, copper and iron are the main ones involved in wound healing. Again eating a varied and balanced diet should get you all of these. Food sources for all minerals: https://www.nhs.uk/conditions/vitamins-and-minerals/iron/

SMOKING: If you do smoke please try to stop and quit. Smoking delays wound healing because various reasons it reduces oxygen supply to the wound, it raises blood sugar levels and its been shown to increase pain at the wound site.

WHEN TO SEEK MEDICAL ADVICE:
If a wound becomes infected, it may:

• Become more painful.
• Look red or swollen.
• Weep or leak some blood-like liquid, pus or blood.
• Have an unpleasant smell.

If you develop a high temperature, notice any of the signs mentioned above, or have any concerns about your wound, then contact your nurse or doctor.

This is general wound advice for more information always speak to your nurse or doctor.

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DISCLAIMER:
This video is for information only and should not be used for the diagnosis or treatment of medical conditions. Abraham The Pharmacist has used all reasonable care in compiling the information but make no warranty as to its accuracy. Always consult a doctor or other healthcare professional for diagnosis and treatment of medical conditions.
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Marko Šestan and colleagues show that the hormone insulin can boost the antiviral immune system. Upon viral infection, the immune system therefore induces insulin resistance in order to increase insulin production by the pancreas, which stimulates the antiviral immune response. In lean people this is not a problem, because the pancreas easily compensates for temporary insulin resistance. But in obese people, who usually already have insulin resistance, infection may overload the ability of the pancreas to compensate, resulting in diabetes mellitus type 2.
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Developed and produced for http://www.MDPracticeGuide.com, a CME resource for physicians and healthcare providers.

Animation Description: Under normal circumstances, bacterial infection results in the release of chemokines that attract circulating neutrophils to the endothelium. This process is known as chemotaxis.

A variety of molecules are expressed on the endothelial cell surface that allow the neutrophil to be captured, then roll along the endothelium, then adhere.

Following adherence, the neutrophil migrates into the subendothelial tissue to reach the site of infection.

The neutrophil engulfs the bacteria and eliminates them via breakdown within the phagosomes — a process known as phagocytosis.

In states of hyperglycemia, chemotaxis is reduced. Adherence is also adversely affected.
Phagocytosis is also impaired by hyperglycemia.

Hyperglycemia also adversely affects the macrophage system. Under normal circumstances, circulating monocytes are attracted to sites of infection, roll, adhere, and then migrate into the subendothelial space. The monocyte then transforms into a macrophage.

which is then activated by cytokines released by the bacteria. The activated macrophage then engulfs the bacteria.

However, hyperglycemia results in decreased activation of macrophages, thereby arresting the process of macrophage phagocytosis of bacteria.

In addition to affecting neutrophil and macrophage function, hyperglycemia also affects the complement cascade. Under situations of normal glycemia, bacteria can activate the complement cascade.

Activation of the complement cascade results in the formation of transmembrane protein channels known as membrane attack complex (MAC) in bacterial membrane.

Membrane attack complexes make the bacterial membrane porous and the rapid influx of fluid results in the bacterial cell death.

Hyperglycemia inhibits the proper activation of the complement cascade, thereby reducing another pathway of the immune system.
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Catching infections while you are pregnant can be somewhat alarming as your baby can be exposed to risks and vulnerabilities. In this video, Dr Anita Gupta, Gynecologist, Fortis La Femme​ talks about ‘Infections that can affect Pregnancy and How to avoid them?’.

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Children whose mothers were hospitalized with an infection during pregnancy may be at increased risk for autism, depression and suicide later in life, according to a new study by researchers at the University of Washington School of Medicine in Seattle, Washington, and the Sahlgrenska Academy in Gothenburg, Sweden.

The findings, published March 6 in JAMA Psychiatry, suggest that any infection in the mother during pregnancy—even those of microbes that do not invade the fetal brain—may increase a child’s risk of developing autism and depression.

For more information on this story: https://bit.ly/2VHth3B

For more stories from the UW Medicine Newsroom, please visit: https://newsroom.uw.edu/.
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