<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hematuria and explain in detail? [/INST] Hematuria or haematuria is defined as the presence of blood or red blood cells in the urine. “Gross hematuria” occurs when urine appears red, brown, or tea-colored due to the presence of blood. Hematuria may also be subtle and only detectable with a microscope or laboratory test. Blood that enters and mixes with the urine can come from any location within the urinary system, including the kidney, ureter, urinary bladder, urethra, and in men, the prostate. Common causes of hematuria include urinary tract infection (UTI), kidney stones, viral illness, trauma, bladder cancer, and exercise. These causes are grouped into glomerular and non-glomerular causes, depending on the involvement of the glomerulus of the kidney. But not all red urine is hematuria. Other substances such as certain medications and foods (e.g. blackberries, beets, food dyes) can cause urine to appear red. Menstruation in women may also cause the appearance of hematuria and may result in a positive urine dipstick test for hematuria. A urine dipstick test may also give an incorrect positive result for hematuria if there are other substances in the urine such as myoglobin, a protein excreted into urine during rhabdomyolysis. A positive urine dipstick test should be confirmed with microscopy, where hematuria is defined by three of more red blood cells per high power field. When hematuria is detected, a thorough history and physical examination with appropriate further evaluation (e.g. laboratory testing) can help determine the underlying cause.

Differential diagnosis
Hematuria can be classified according to visibility, anatomical origin, and timing of blood during urination.In terms of the visibility, hematuria can be visible to the naked eye (termed "gross hematuria") and may appear red or brown (sometimes referred to as tea-colored), or it can be microscopic (i.e. not visible to the eye but detected with a microscope or laboratory test). Microscopic hematuria is present when there are three or more red blood cells per high power field.
In terms of the anatomical origin, blood or red blood cells can enter and mix with urine at multiple anatomical sites within the urinary system, including the kidney, ureter, urinary bladder, and urethra, and in men, the prostate. Additionally, menstruation in women may cause the appearance of hematuria and may result in a positive urine dipstick test for hematuria. The causes corresponding to these anatomic locations can be divided into glomerular and non-glomerular causes, referring to the involvement of the glomerulus of the kidney. Non-glomerular causes can be further subdivided into upper urinary tract and lower urinary tract causes.
In terms of the timing during urination, hematuria can be initial, terminal or total, meaning blood can appear in the urine at the onset, midstream, or later. If it appears soon after the onset of urination, a distal site is suggested.  A longer delay suggests a more proximal lesion. In other words, shorter times suggest distal sites while longer times suggest proximal sites. Hematuria that occurs throughout urination suggests that bleeding is occurring above the level of the bladder. This is very significant in regards to developing a differential diagnosis and eventually for the purposes of creating a treatment plan for the patient.Many causes may present as either visible hematuria or microscopic hematuria, and so the differential diagnosis is frequently organized based upon glomerular and non-glomerular causes.

Glomerular hematuria
Glomerular causes include:

IgA nephropathy
Thin glomerular basement membrane disease
Hereditary nephritis (Alports disease)
Hemolytic uremic syndrome
Postinfectious glomerulonephritisCertain infectious agents like Group B Strep(strep pyogenes) can cause a person to get a very specific manifestation known as post-streptococcal glomerulonephritis. This manifestation results in a person having the symptom of cola-colored urine.
Membranoproliferative glomerulonephritis
Lupus nephritis
Henoch-Shonlein purpura
Nephritic syndrome
Nephrotic syndrome
Polycystic kidney disease
Idiopathic hematuria

Non-glomerular hematuria
Visible blood clots in the urine indicate a non-glomerular cause. Non-glomerular causes include:

Urinary tract infections, such as pyelonephritis, cystitis, prostatitis, and urethritis
Kidney stones
Cancers, such as renal cell carcinoma and bladder cancer (particularly transitional cell carcinoma), and in men, prostate cancer
Urinary tract strictures
Benign prostatic hyperplasia
Renal papillary necrosis
Trauma or damage to the lining of the urinary tract
Intense exercise
Increased tendency to bleed due to acquired or genetic conditions (e.g. sickle cell disease or vitamin K deficiency bleeding) or certain medications (e.g. blood thinners)

Mimickers of hematuria
Pigmenturia
Not all red or brown urine is caused by hematuria. Other substances such as certain medications and certain foods can cause urine to appear red.Medications that may cause urine to appear red include:

Phenazopyridine
Nitrofurantoin
Doxorubicin
RifampicinFoods that may cause urine to appear red include:

Blackberries
Food dyes.
Beets
Rhubarb
Fava beans

False positive urine dipstick
A urine dipstick may be falsely positive for hematuria due to other substances in the urine. While the urine dipstick test is able to recognize heme in red blood cells, it also identifies free hemoglobin and myoglobin. Free hemoglobin may be found in the urine resulting from hemolysis, and myoglobin may be found in the urine resulting from rhabdomyolysis. Thus, a positive dipstick test does not necessarily indicate hematuria; rather, microscopy of the urine showing three of more red blood cells per high power field confirms hematuria.

Menstruation
In women, menstruation may cause the appearance of hematuria and may result in a urine dipstick test positive for hematuria. Menstruation can be ruled out as a cause of hematuria by inquiring about menstruation history and ensuring the urine specimen is collected without menstrual blood.

Evaluation
The evaluation of hematuria is dependent upon the visibility of the blood in the urine (i.e. visible/gross vs microscopic hematuria). Visible hematuria must be investigated, as it may be due to a pathological cause. In those with visible hematuria, urological cancer (most frequently bladder or kidney cancer) is discovered in 20-25%. Hematuria alone without accompanying symptoms should be raise suspicion of malignancy of the urinary tract until proven otherwise. The initial evaluation of patients presenting with signs and symptoms that are consistent of hematuria include assessment of hemodynamic status, underlying cause of hematuria, and ensuring urinary drainage. These steps include assessment of the patients heart rate, blood pressure, a physician exam taken by a healthcare professional, and blood work to ensure the patients hemodynamic status is adequate. It is important to obtain a detailed history from the patient (i.e. recreational, occupational, and medication exposures) as this information can be helpful in suggesting a cause of hematuria. The physical exam can also be helpful in identifying a cause of the hematuria as certain signs found on the physical exam can suggest specific causes of the hematuria. In the event the initial evaluation of hematuria does not reveal an underlying cause  then evaluation by a physician who specializes in Urology may proceed. This medical evaluation may consist of, but is not limited too, a history and physical exam taken by healthcare personnel, laboratory studies (i.e. blood work), cystoscopy, and specialized imaging procedures (i.e. CT or MRI).

Visible hematuria
The first step in evaluation of red or brown colored urine is to confirm true hematuria with urinalysis and urine microscopy, where hematuria is defined by three of more red blood cells per high power field. Although a urine dipstick test may be used, it can give false positive or false negative results. In gathering information, it is important to inquire about recent trauma, urologic procedures, menses, and culture-documented urinary tract infection. If any of these are present, it is appropriate to repeat a urinalysis with urine microscopy in 1 to 2 weeks or after treatment of the infection. If the results of the urinalysis and urine microscopy reveal a glomerular origin of hematuria (indicated by proteinuria or red blood cell casts), consultation of a nephrologist should be made. If the results of the urinalysis indicate a non-glomerular origin, a microbiological culture of the urine should be performed, if it has not been done already. If the culture is positive, treatment of the infection should follow and urinalysis and urine microscopy should be repeated once complete. If the culture is negative or if hematuria persists after treatment, CT urogram and cystoscopy should be performed. Of note, hemodynamic stability should be monitored and a complete blood count should be ordered to assess for anemia.In summary, those with visible hematuria confirmed by urinalysis and urine microscopy and with no recent trauma, urologic procedures, menses, or urinary tract infection should undergo cystoscopy and CT urogram.

Microscopic hematuria
After detecting and confirming hematuria with urinalysis and urine microscopy, the first step in evaluation of microscopic hematuria is to rule out benign causes. Benign causes include urinary tract infection, viral illness, kidney stone, recent intense exercise, menses, recent trauma, or recent urological procedure. After benign causes have resolved or been treated, a repeat urinalysis and urine microscopy is warranted to ensure cessation of hematuria. If hematuria persists (even if there is a suspected cause), the next step is to stratify the risk of the person for urothelial cancer into low, intermediate, or high risk to determine next steps. To be in the low risk category, one must satisfy all of the following criteria: Has never smoked tobacco or smoked less than 10 pack-years; is a female less than 50 years old or a male less than 40 years old; has 3-10 red blood cells per high power field; has not had microscopic hematuria before; and has no other risk factors for urothelial cancer. To be in the intermediate risk category, one must satisfy any of the following criteria: Has smoked 10-30 pack-years; is a female 50–59 years old or a male aged 40–59 years old; has 11-25 red blood cells per high power field; or was previously a low-risk patient with persistent microscopic hematuria and has 3-25 red blood cells per high power field. To be in the high risk category, one must satisfy any of the following criteria: Has smoked more than 30 pack-years; is older than 60 years of age; or has above 25 red blood cells per high power field on any urinalysis. For the low risk category, the next step is to either repeat a urinalysis with urine microscopy in 6 months or perform a cystoscopy and renal ultrasound. For the intermediate risk category, the next step is to perform a cystoscopy and renal ultrasound. For the high risk category, the next step is to perform a cystoscopy and CT urogram. If an underlying cause for hematuria is discovered, it should be managed appropriately. However, if no underlying cause is discovered, the hematuria should be re-evaluated with urinalysis and urine microscopy within 12 months. Additionally, for all risk categories, if a nephrologic origin is suspected, consultation of a nephrologist should be made.

Pathophysiology
The pathophysiology of hematuria can often be explained by damage to the structures of the urinary system, including the kidney, ureter, urinary bladder, and urethra, and in men, the prostate. Common mechanisms include structural disruption to the glomerular basement membrane and mechanical or chemical erosion of the mucosal surfaces of the genitourinary tract.

Management
Medical Emergency: Acute clot retention
Acute clot retention is one of three emergencies that can occur with hematuria. The other two are anemia and shock. Blood clots can prevent urine outflow through either ureter or the bladder. This is known as acute urinary retention.
Blood clots that remain in the bladder are digested by urinary urokinase producing fibrin fragments. These fibrin fragments are natural anticoagulants and promote ongoing bleeding from the urinary tract. Removing all blood clots prevents the formation of this natural anticoagulant. This in turns facilitates the cessation of bleeding from the urinary tract.The acute management of obstructing clots is the placement of a large (22-24 French) urethral Foley catheter. Clots are evacuated with a Toomey syringe and saline irrigation. If this does not control the bleeding, management should escalate to continuous bladder irrigation (CBI) via a three-port urethral catheter. If both a large urethral Foley catheter and CBI fail, an urgent cystoscopy in the operating room will be necessary. Lastly, a transfusion and/or a correction of a coexisting coagulopathy may be necessary.

Medical Emergency: Urosepsis
Urosepsis is defined as sepsis caused by a urogenital tract infection and comprises about 25% of all sepsis cases. Urosepsis is the result of a systemic inflammatory response to infection and can be identified by numerous signs and symptoms (e.g. fever, hypothermia, tachycardia, and leukocytosis). Signs and symptoms that indicate a urogential tract infection is the source of the sepsis may include, but are not limited to, flank pain, costovertebral angle tenderness, pain with micturition, urinary retention, and scrotal pain. In terms of the visibility, hematuria can be visible to the naked eye (termed "gross hematuria") and may appear red or brown (sometimes referred to as tea-colored), or it can be microscopic (i.e. not visible to the eye but detected of urosepsis. In addition to imaging tests, patients may be treated with antibiotics to relieve the infection and intravenous fluids to maintain cardiovascular and renal perfusion </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Nosebleed and explain in detail? [/INST] A nosebleed, also known as epistaxis, is bleeding from the nose. Blood can flow down into the stomach, and cause nausea and vomiting. In more severe cases, blood may come out of both nostrils. Rarely, bleeding may be so significant that low blood pressure occurs. Blood may also come up the nasolacrimal duct and out from the eye.Risk factors include trauma, including putting the finger in the nose, blood thinners, high blood pressure, alcoholism, seasonal allergies, dry weather, and inhaled corticosteroids. There are two types: anterior, which is more common; and posterior, which is less common but more serious. Anterior nosebleeds generally occur from Kiesselbachs plexus while posterior bleeds generally occur from the sphenopalatine artery. The diagnosis is by direct observation.Prevention may include the use of petroleum jelly in the nose. Initially, treatment is generally the application of pressure for at least five minutes over the lower half of the nose. If this is not sufficient, nasal packing may be used. Tranexamic acid may also be helpful. If bleeding episodes continue, endoscopy is recommended.About 60% of people have a nosebleed at some point in their life. About 10% of nosebleeds are serious. Nosebleeds are rarely fatal, accounting for only 4 of the 2.4 million deaths in the U.S. in 1999. Nosebleeds most commonly affect those younger than 10 and older than 50.

Cause
Nosebleeds can occur due to a variety of reasons. Some of the most common causes include trauma from nose picking, blunt trauma (such as a motor vehicle accident), or insertion of a foreign object (more likely in children). Relative humidity (including centrally heated buildings), respiratory tract infections, chronic sinusitis, rhinitis or environmental irritants can cause inflammation and thinning of the tissue in the nose, leading to a greater likelihood of bleeding from the nose.Most causes of nose bleeding are self-limiting and do not require medical attention. However, if nosebleeds are recurrent or do not respond to home therapies, an underlying cause may need to be investigated. Some rarer causes are listed below:Coagulopathy

Thrombocytopenia (thrombotic thrombocytopenic purpura, idiopathic thrombocytopenic purpura)
Von Willebrands disease
Hemophilia
Leukemia
HIV
Chronic liver disease—cirrhosis causes deficiency of factor II, VII, IX,& XDietary

Sulfur dioxide (sulphur dioxide) E220 (as a food preservative used particularly in wines, dried fruits, etc. )
Sulphites as food preservatives
Salicylates naturally occurring in some fruits and vegetablesInflammatory

Granulomatosis with polyangiitis
Systemic lupus erythematosusMedications/Drugs

Anticoagulation (warfarin, heparin, aspirin, etc.)
Insufflated drugs (particularly cocaine)
Nasal sprays (particularly prolonged or improper use of nasal steroids)Neoplastic

Squamous cell carcinoma
Adenoid cystic carcinoma
Melanoma
Nasopharyngeal carcinoma
Nasopharyngeal angiofibroma
Nosebleeds can be a sign of cancer in the sinus area, which is rare, or tumors starting at the base of the brain, such as meningioma. Due to the sensitive location, nosebleeds caused by tumors are typically associated with other symptoms, such as hearing or vision problems.Traumatic

Anatomical deformities (e.g. septal spurs)
Blunt trauma (usually a sharp blow to the face such as a punch, sometimes accompanying a nasal fracture)
Foreign bodies (such as fingers during nose-picking)
Digital trauma
Middle ear barotrauma (such as from descent in aircraft or ascent in scuba diving)
Nasal bone fracture
Septal fracture/perforation
Surgery (e.g. septoplasty and functional endoscopic sinus surgery)
Nasal bleeds may be due to fracture of facial bones namely maxilla and zygoma.Vascular

Hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu disease)
Angioma
Aneurysm of the carotid artery

Pathophysiology
The nasal mucosa contains a rich blood supply that can be easily ruptured and cause bleeding. Rupture may be spontaneous or initiated by trauma. Nosebleeds are reported in up to 60% of the population with peak incidences in those under the age of ten and over the age of 50 and appear to occur in males more than females. An increase in blood pressure (e.g. due to general hypertension) tends to increase the duration of spontaneous epistaxis. Anticoagulant medication and disorders of blood clotting can promote and prolong bleeding. Spontaneous epistaxis is more common in the elderly as the nasal mucosa (lining) becomes dry and thin and blood pressure tends to be higher. The elderly are also more prone to prolonged nosebleeds as their blood vessels are less able to constrict and control the bleeding.
The vast majority of nosebleeds occur in the front anterior (front) part of the nose from the nasal septum. This area is richly endowed with blood vessels (Kiesselbachs plexus). This region is also known as Littles area. Bleeding farther back in the nose is known as a posterior bleed and is usually due to bleeding from Woodruffs plexus, a venous plexus situated in the posterior part of inferior meatus. Posterior bleeds are often prolonged and difficult to control. They can be associated with bleeding from both nostrils and with a greater flow of blood into the mouth. Sometimes blood flowing from other sources of bleeding passes through the nasal cavity and exits the nostrils. It is thus blood coming from the nose but is not a true nosebleed, that is, not truly originating from the nasal cavity. Such bleeding is called "pseudoepistaxis" (pseudo + epistaxis). Examples include blood coughed up through the airway and ending up in the nasal cavity, then dripping out.

Prevention
People with uncomplicated nosebleeds can use conservative methods to prevent future nosebleeds such as sleeping in a humidified environment or applying petroleum jelly to the nasal nares.

Treatment
Most anterior nosebleeds can be stopped by applying direct pressure, which helps by promoting blood clots. Those who have a nosebleed should first attempt to blow out any blood clots and then apply pressure for at least five minutes and up to 20 minutes. Pressure should be firm and tilting the head forward helps decrease the chance of nausea and airway obstruction as seen in the picture on the right. When attempting to stop a nosebleed at home, the head should not be tilted back. Swallowing excess blood can irritate the stomach and cause vomiting. Vasoconstrictive medications such as oxymetazoline (Afrin) or phenylephrine are widely available over the counter for treatment of allergic rhinitis and may also be used to control benign cases of epistaxis. Those with nosebleeds that last longer than 20 minutes (in the setting of direct pressure as seen in the image to the right) should seek medical attention.

Nasal packing
If pressure and chemical cauterization cannot stop bleeding, nasal packing is the mainstay of treatment. There are several forms of nasal packing that can be contrasted by anterior nasal packing and posterior nasal packing. Traditionally, nasal packing was accomplished by packing gauze into the nose, thereby placing pressure on the vessels in the nose and stopping the bleeding. Traditional gauze packing has been replaced with products such as Merocel and the Rapid Rhino. The Merocel nasal tampon is similar to gauze packing except it is a synthetic foam polymer (made of polyvinyl alcohol and expands in the nose after application of water) that provides a less hospitable medium for bacteria. The Rapid Rhino stops nosebleeds using a balloon catheter, made of carboxymethylcellulose, which has a cuff that is inflated by air to stop bleeding through extra pressure in the nasal cavity. Systematic review articles have demonstrated that the efficacy in stopping nosebleeds is similar between the Rapid Rhino and Merocel packs; however, the Rapid Rhino has been shown to have greater ease of insertion and reduced discomfort. People who receive nasal packing need to return to a medical professional in 24–72 hours in order to have packing removed. There are also several dissolvable packing materials that stop bleeding through use of thrombotic agents that promote blood clots, such as surgicel. The thrombogenic foams and gels do not require removal and dissolve after a few days. Posterior nasal packing can be achieved by using a Foley catheter, blowing up the balloon when it is in the back of the throat, and applying traction. Complications of nasal packing include abscesses, septal hematomas, sinusitis, and pressure necrosis. In rare cases toxic shock syndrome can occur with prolonged nasal packing. As a result, many forms of nasal packing involve use of topical antistaphylococcal antibiotic ointment.

Tranexamic acid
Tranexamic acid helps promote blood clotting. For nosebleeds it can be applied to the site of bleeding, taken by mouth, or injected into a vein.

Cauterization
This method involves applying a chemical such as silver nitrate to the nasal mucosa, which burns and seals off the bleeding. Eventually the nasal tissue to which the chemical is applied will undergo necrosis. This form of treatment is best for mild bleeds, especially in children, that are clearly visible. A topical anesthetic (such as lidocaine) is usually applied prior to cauterization. Silver nitrate can cause blackening of the skin due to silver sulfide deposit, though this will fade with time.

Surgery
Ongoing bleeding despite good nasal packing is a surgical emergency and can be treated by endoscopic evaluation of the nasal cavity under general anesthesia to identify an elusive bleeding point or to directly ligate (tie off) the blood vessels supplying the nose. These blood vessels include the sphenopalatine, anterior and posterior ethmoidal arteries </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is 2 and explain in detail? [/INST] 2 (two) is a number, numeral and digit. It is the natural number following 1 and preceding 3. It is the smallest and only even prime number. Because it forms the basis of a duality, it has religious and spiritual significance in many cultures.

Evolution
Arabic digit
The digit used in the modern Western world to represent the number 2 traces its roots back to the Indic Brahmic script, where "2" was written as two horizontal lines. The modern Chinese and Japanese languages (and Korean Hanja) still use this method. The Gupta script rotated the two lines 45 degrees, making them diagonal. The top line was sometimes also shortened and had its bottom end curve towards the center of the bottom line. In the Nagari script, the top line was written more like a curve connecting to the bottom line. In the Arabic Ghubar writing, the bottom line was completely vertical, and the digit looked like a dotless closing question mark. Restoring the bottom line to its original horizontal position, but keeping the top line as a curve that connects to the bottom line leads to our modern digit.In fonts with text figures, digit 2 usually is of x-height, for example, .

Etymology of two
The word two is derived from the Old English words twā (feminine), tū (neuter), and twēġen (masculine, which survives today in the form twain).The pronunciation /tuː/, like that of who is due to the labialization of the vowel by the w (combare from womb), which then disappeared before the related sound. The successive stages of pronunciation for the Old English twā would thus be /twɑː/, /twɔː/, /twoː/, /twuː/, and finally /tuː/.

In mathematics
Two is the smallest prime number, and the only even prime number, and for this reason it is sometimes called "the oddest prime". As the smallest prime number, it is also the smallest non-zero pronic number, and the only pronic prime. The next prime is three, which makes two and three the only two consecutive prime numbers. Two is the first prime number that does not have a proper twin prime with a difference two, while three is the first such prime number to have a twin prime. In consequence, the first pair of twin primes, three and five, encase four in-between, which is the square of two, or

          2

            2

    {\displaystyle 2^{2}}
  . Two is the first Sophie Germain prime, the first factorial prime, the first Lucas prime, and the first Ramanujan prime. It is also a Motzkin number,  a Bell number, an all-Harshad number, a meandric number, a semi-meandric number, an open meandric number, and the third (or fourth) Fibonacci number.An integer is called even if it is divisible by 2. For integers written in a numeral system based on an even number such as decimal, divisibility by 2 is easily tested by merely looking at the last digit. If it is even, then the whole number is even. In particular, when written in the decimal system, all multiples of 2 will end in 0, 2, 4, 6, or 8.Two is the base of the binary system, the numeral system with the fewest tokens that allows denoting a natural number n substantially more concisely (with log2 n  tokens) than a direct representation by the corresponding count of a single token (with n tokens). This binary number system is used extensively in computing.
For any number x:

x + x = 2 · x addition to multiplication
x · x = x2 multiplication to exponentiation
xx = x↑↑2 exponentiation to tetrationExtending this sequence of operations by introducing the notion of hyperoperations, here denoted by "hyper(a,b,c)" with a and c being the first and second operand, and b being the level in the above sketched sequence of operations, the following holds in general:

hyper(x,n,x) = hyper(x,(n + 1),2).Two has therefore the unique property that 2 + 2 = 2 · 2 = 22 = 2↑↑2 = 2↑↑↑2 = ..., disregarding the level of the hyperoperation, here denoted by Knuths up-arrow notation. The number of up-arrows refers to the level of the hyperoperation.
Two is the only number x such that the sum of the reciprocals of the natural powers of x equals itself. In symbols,

          ∑

            k
            =
            0

            ∞

            1

              2

                k

        =
        1
        +

            1
            2

        +

            1
            4

        +

            1
            8

        +

            1
            16

        +
        ⋯
        =
        2.

    {\displaystyle \sum _{k=0}^{\infty }{\frac {1}{2^{k}}}=1+{\frac {1}{2}}+{\frac {1}{4}}+{\frac {1}{8}}+{\frac {1}{16}}+\cdots =2.}
  This comes from the fact that:

          ∑

            k
            =
            0

            ∞

            1

              n

                k

        =
        1
        +

            1

              n
              −
              1

            for all

        n
        ∈

          R

        >
        1.

    {\displaystyle \sum _{k=0}^{\infty }{\frac {1}{n^{k}}}=1+{\frac {1}{n-1}}\quad {\mbox{for all}}\quad n\in \mathbb {R} >1.}
  A Cantor space is a topological space

          2

              N

    {\displaystyle 2^{\mathbb {N} }}
   homeomorphic to the Cantor set. The countably infinite product topology of the simplest discrete two-point space, {0, 1}, is the traditional elementary example.
The sum of the reciprocals of all non-zero triangular numbers converges to

        2

    {\displaystyle 2}
  .Powers of two are central to the concept of Mersenne primes, and important to computer science. Two is the first Mersenne prime exponent.
Taking the square root of a number is such a common mathematical operation, that the spot on the root sign where the index would normally be written for cubic and other roots, may simply be left blank for square roots, as it is tacitly understood.
The square root of 2 was the first known irrational number.
The smallest field has two elements.
In a set-theoretical construction of the natural numbers, 2 is identified with the set {{∅},∅}. This latter set is important in category theory: it is a subobject classifier in the category of sets.
Two consecutive twos (as in "22" for "two twos"), or equivalently "2-2", is the only fixed point of John Conways look-and-say function </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Dislocation of jaw and explain in detail? [/INST] Dislocations occur when two bones that originally met at the joint detach. Dislocations should not be confused with Subluxation. Subluxation is when the joint is still partially attached to the bone.When a person has a dislocated jaw it is difficult to open and close the mouth. Dislocation can occur following a series of events if the jaw locks while open or unable to close. If the jaw is dislocated, it may cause an extreme headache or inability to concentrate. When the muscles alignment is out of sync, a pain will occur due to unwanted rotation of the jaw.If the pain remains constant, it may require surgery to realign the jaw. Depending on the severity of the jaws dislocation, pain relief such as paracetamol may assist to alleviate the initial chronic pain. If the pain relief is taken for an extended period of time, it may negatively affect the person while talking, eating, drinking, etc.

Symptoms
The symptoms can be numerous depending on the severity of the dislocation injury and how long the person is inflicted with the injury. Symptoms of a dislocated jaw include a bite that feels “off” or abnormal, hard time talking or moving jaw, not able to close mouth completely, drooling due to not being able to shut mouth completely, teeth feel they are out of alignment, and a pain that becomes unbearableThe immediate symptom can be a loud crunch noise occurring right up against the eardrum.  This is instantly followed by excruciating pain, particularly in the side where the dislocation occurred.Short-term symptoms can range from mild to chronic headaches, muscle tension or pain in the face, jaw and neck.Long-term symptoms can result in sleep deprivation, tiredness/lethargy, frustration, bursts of anger or short fuse, difficulty performing everyday tasks, depression, social issues relating to difficulty talking, hearing sensitivity (particularly to high pitched sounds), tinnitus and pain when seated associated with posture while at a computer and reading books from general pressure on the jaw and facial muscles when tilting head down or up. And possible causing subsequent facial asymmetry.In contrast, symptoms of a fractured jaw include bleeding coming from the mouth, unable to open the mouth wide without pain, bruising and swelling of the face, difficulty eating due to the constant pain, loss of feeling in the face (more specifically the lower lip) and lacks full range of motion of the jaw.

Anatomy
The joint involved with jaw dislocation is the temporomandibular joint (TMJ). This joint is located where the mandibular condyles and the temporal bone meet. Membranes that surround the bones help during the hinging and gliding of jaw movement. For the mouth to close it requires the following muscles: the masseter, temporalis, and medial pterygoid muscle. For the jaw to open it requires the lateral pterygoid muscle.

Pathophysiology
There are four different positions of jaw dislocation: posterior, anterior, superior and lateral. The most common position is anterior, while the other types are rare. Anterior dislocation shifts the lower jaw forward if the mouth excessively opens. This type of dislocation may happen bilaterally or unilaterally after yawning. The muscles that are affected during anterior jaw dislocation are the masseter and temporalis which pull up on the mandible and the lateral pterygoid which relaxes the mandibular condyle. The condyle can get locked in front of the articular eminence. Posterior dislocation is possible for people who get injured by being punched in the chin. This dislocation will push the jaw back affecting the alignment of the mandibular condyle and mastoid. The external auditory canal may be fractured. Superior dislocations occur after being punched below the mandibular ramus as the mouth remains half-open. Since great force occurs in a punch, the angle of the jaw will be forced upward moving towards the condylar head. This can result in a fracture of the glenoid fossa and displacement of the condyle into the middle cranial fossa, potentially injuring the facial and vestibulocochlear nerves and the temporal lobe. Lateral dislocations move the mandibular condyle away from the skull and are likely to happen together with jaw fractures.Posterior, superior and lateral dislocations are uncommon injuries and usually result from high-energy trauma to the chin. By contrast, anterior dislocations are more often the result of low-energy trauma (e.g. tooth extraction) or secondary to a medical condition that affects the stability of the joint (e.g. seizures, ligamentous laxity, degeneration of joint capsule).

Diagnosis
As with other joint dislocations, clinical history and examination are crucial for diagnosis of a jaw dislocation. Commonly, plain and panoramic X-ray radiographies are used to determine the relative position of the mandibular condyle. If a complex or unusual injury is suspected, three-dimensional computed tomography is most reliable in diagnosing dislocation and possibly associated fractures or soft tissue injuries.In case of dislocations resulting from high-energy trauma, attention must also be paid to possible other injuries, particularly blunt or indirect trauma to the skull and cervical spine. Acutely life-threatening conditions need to be ruled out or treated in first line. For superior jaw dislocation in particular, serious intracranial complications such as epidural hematoma are possible and must be recognized and managed to prevent disability or even death. Therefore, neurological status has to be examined in patients with complex dislocations involving temporal bone fractures. Hearing deficits on the injured side may indicate damage to structures of the ear.

Treatment
Most temporomandibular disorders (TMDs) are self-limiting and do not get worse. Simple treatment, involving self-care practices, rehabilitation aimed at eliminating muscle spasms, and restoring correct coordination, is all that is required. Nonsteroidal anti-inflammatory analgesics (NSAIDs) should be used on a short-term, regular basis and not on an as needed basis </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Viral disease and explain in detail? [/INST] A viral disease (or viral infection) occurs when an organisms body is invaded by pathogenic viruses, and infectious virus particles (virions) attach to and enter susceptible cells.

Structural Characteristics
Basic structural characteristics, such as genome type, virion shape and replication site, generally share the same features among virus species within the same family.
Double-stranded DNA families: three are non-enveloped (Adenoviridae, Papillomaviridae and Polyomaviridae) and two are enveloped (Herpesviridae and Poxviridae). All of the non-enveloped families have icosahedral capsids.
Partly double-stranded DNA viruses: Hepadnaviridae. These viruses are enveloped.
One family of single-stranded DNA viruses infects humans: Parvoviridae </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Alcoholic cardiomyopathy and explain in detail? [/INST] Alcoholic cardiomyopathy is a disease in which the chronic long-term abuse of alcohol (i.e., ethanol) leads to heart failure </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Cardiac tamponade and explain in detail? [/INST] Cardiac tamponade, also known as pericardial tamponade (), is the buildup of fluid in the pericardium (the sac around the heart), resulting in compression of the heart. Onset may be rapid or gradual. Symptoms typically include those of obstructive shock including shortness of breath, weakness, lightheadedness, and cough. Other symptoms may relate to the underlying cause.Common causes of cardiac tamponade include cancer, kidney failure, chest trauma, myocardial infarction, and pericarditis. Other causes include connective tissues diseases, hypothyroidism, aortic rupture, autoimmune disease, and complications of cardiac surgery. In Africa, tuberculosis is a relatively common cause.Diagnosis may be suspected based on low blood pressure, jugular venous distension, or quiet heart sounds (together known as Becks triad). A pericardial rub may be present in cases due to inflammation. The diagnosis may be further supported by specific electrocardiogram (ECG) changes, chest X-ray, or an ultrasound of the heart. If fluid increases slowly the pericardial sac can expand to contain more than 2 liters; however, if the increase is rapid, as little as 200 mL can result in tamponade.Tamponade is a medical emergency. When it results in symptoms, drainage is necessary. This can be done by pericardiocentesis, surgery to create a pericardial window, or a pericardiectomy. Drainage may also be necessary to rule out infection or cancer. Other treatments may include the use of dobutamine or in those with low blood volume, intravenous fluids. Those with few symptoms and no worrisome features can often be closely followed. The frequency of tamponade is unclear. One estimate from the United States places it at 2 per 10,000 per year.

Signs and symptoms
Onset may be rapid (acute) or more gradual (subacute). Signs of cardiac tamponade typically include those of cardiogenic shock including shortness of breath, weakness, lightheadedness, cough and those of Becks triad e.g. jugular vein distention, quiet heart sounds and hypotension. Other symptoms may relate to the underlying cause.Other general signs of shock (such as fast heart rate, shortness of breath and decreasing level of consciousness) may also occur. However, some of these signs may not be present in certain cases. A fast heart rate, although expected, may be absent in people with uremia and hypothyroidism.According to Reddy, cardiac tamponade and its progression can be described in 3 different phases. In phase I, the required filling pressure increases due to the high stiffness of the ventricles. This is because of the accumulation of pericardial fluid in the pericardial cavity. During phase II, the pericardial pressure exceeds the ventricular filling pressure caused by the further accumulation of pericardial fluid. This results in a decrease in cardiac input and output. A further decrease of cardiac input and output is typical in phase III of the progression of cardiac tamponade. This is caused by the equilibration of left ventricular filling and pericardial pressure, leading to “severe deterioration of end-organ perfusion.” Some of the symptoms, as a consequence, include abdominal pain due to liver engorgement.

Causes
Cardiac tamponade is caused by a large or uncontrolled pericardial effusion, i.e. the buildup of fluid inside the pericardium. This commonly occurs as a result of chest trauma (both blunt and penetrating), but can also be caused by myocardial infarction, myocardial rupture, cancer (most often Hodgkin lymphoma), uremia, pericarditis, or cardiac surgery, and rarely occurs during retrograde aortic dissection, or while the person is taking anticoagulant therapy. The effusion can occur rapidly (as in the case of trauma or myocardial rupture), or over a more gradual period of time (as in cancer). The fluid involved is often blood, but pus is also found in some circumstances.

Surgery
One of the most common settings for cardiac tamponade is in the first 7 days after heart surgery.  After heart surgery, chest tubes are placed to drain blood.  These chest tubes, however, are prone to clot formation.  When a chest tube becomes occluded or clogged, the blood that should be drained can accumulate around the heart, leading to tamponade.

Pathophysiology
The pericardium, the double-walled sac surrounding the heart, consists of a fibrous pericardium layer on the outside and a double-layered serous pericardium on the inside. Between the two layers of the serous pericardium is the pericardial space, which is filled with lubricating serous fluid that prevents friction as the heart contracts. The outer layer of the heart is made of fibrous tissue which does not easily stretch, so once excess fluid begins to enter the pericardial space, pressure starts to increase. Consequently, the heart becomes compressed due to its inability to fully relax.If fluid continues to accumulate, each successive diastolic period leads to less blood entering the ventricles. Eventually, increasing pressure on the heart forces the septum to bend in towards the left ventricle, leading to a decrease in stroke volume. This causes the development of obstructive shock, which if left untreated may lead to cardiac arrest (often presenting as pulseless electrical activity). The decrease in stroke volume can also ultimately lead to a decrease in cardiac output, which could be signaled by tachycardia and hypotension.

Diagnosis
The three classic signs, known as Becks triad, are low blood pressure, jugular-venous distension, and muffled heart sounds. Other signs may include pulsus paradoxus (a drop of at least 10 mmHg in arterial blood pressure with inspiration), and ST segment changes on the electrocardiogram, which may also show low voltage QRS complexes.

Medical imaging
Tamponade can often be diagnosed radiographically. Echocardiography, which is the diagnostic test of choice, often demonstrates an enlarged pericardium or collapsed ventricles. A large cardiac tamponade will show as an enlarged globular-shaped heart on chest x-ray. During inspiration, the negative pressure in the thoracic cavity will cause increased pressure into the right ventricle.  This increased pressure in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. At the same time, right ventricle volume is markedly diminished and sometimes it can collapse.

Differential diagnosis
Initial diagnosis of cardiac tamponade can be challenging, as there is a broad differential diagnosis. The differential includes possible diagnoses based on symptoms, time course, mechanism of injury, patient history. Rapid onset cardiac tamponade may also appear similar to pleural effusions, shock, pulmonary embolism, and tension pneumothorax.If symptoms appeared more gradually, the differential diagnosis includes acute heart failure.In a person with trauma presenting with pulseless electrical activity in the absence of hypovolemia and tension pneumothorax, the most likely diagnosis is cardiac tamponade.In addition to the diagnostic complications afforded by the wide-ranging differential diagnosis for chest pain, diagnosis can be additionally complicated by the fact that people will often be weak or faint at presentation. For instance, a fast rate of breathing and difficulty breathing on exertion that progresses to air hunger at rest can be a key diagnostic symptom, but it may not be possible to obtain such information from people who are unconscious or who have convulsions at presentation.

Treatment
Pre-hospital care
Initial treatment given will usually be supportive in nature, for example administration of oxygen, and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. Some teams have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury.Prompt diagnosis and treatment is the key to survival with tamponade.  Some pre-hospital providers will have facilities to provide pericardiocentesis, which can be life-saving.  If the person has already suffered a cardiac arrest, pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action.

Hospital management
Initial management in hospital is by pericardiocentesis </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Lactose intolerance and explain in detail? [/INST] Lactose intolerance is a common condition caused by a decreased ability to digest lactose, a sugar found in dairy products. Those affected vary in the amount of lactose they can tolerate before symptoms develop. Symptoms may include abdominal pain, bloating, diarrhea, flatulence, and nausea. These symptoms typically start thirty minutes to two hours after eating or drinking milk-based food. Their severity typically depends on the amount a person eats or drinks. Lactose intolerance does not cause damage to the gastrointestinal tract.Lactose intolerance is due to the lack of the enzyme lactase in the small intestines to break lactose down into glucose and galactose. There are four types: primary, secondary, developmental, and congenital. Primary lactose intolerance occurs as the amount of lactase declines as people age. Secondary lactose intolerance is due to injury to the small intestine. Such injury could be the result of infection, celiac disease, inflammatory bowel disease, or other diseases. Developmental lactose intolerance may occur in premature babies and usually improves over a short period of time. Congenital lactose intolerance is an extremely rare genetic disorder in which little or no lactase is made from birth. The onset of primary lactose intolerance, the most common type, is typically in late childhood or early adulthood, but prevalence increases with age.Diagnosis may be confirmed if symptoms resolve following eliminating lactose from the diet. Other supporting tests include a hydrogen breath test and a stool acidity test. Other conditions that may produce similar symptoms include irritable bowel syndrome, celiac disease, and inflammatory bowel disease. Lactose intolerance is different from a milk allergy. Management is typically by decreasing the amount of lactose in the diet, taking lactase supplements, or treating the underlying disease. People are able to drink at least one cup of milk without developing symptoms, with greater amounts tolerated if drunk with a meal or throughout the day.Worldwide, around 65% of adults are affected by lactose malabsorption. Other mammals usually lose the ability to digest lactose after weaning and this was the ancestral state of all humans before the recent evolution of lactase persistence, which extends lactose tolerance into adulthood. Lactase persistence evolved in several populations independently, probably as an adaptation to the domestication of dairy animals around 10,000 years ago. Today the prevalence of lactose tolerance varies widely between regions and ethnic groups. The ability to digest lactose is most common in people of European descent, and to a lesser extent in parts of the Middle East and Africa. Traditional food cultures reflect local variations in tolerance and historically many societies have adapted to low levels of tolerance by making dairy products that contain less lactose than fresh milk. The medicalization of lactose intolerance as a disorder has been attributed to biases in research history, since most early studies were conducted amongst populations which are normally tolerant, as well as the cultural and economic importance of milk in countries such as the United States.

Terminology
Lactose intolerance primarily refers to a syndrome with one or more symptoms upon the consumption of food substances containing lactose sugar. Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms.
Hypolactasia is the term specifically for the small intestine producing little or no lactase enzyme.  If a person with hypolactasia consumes lactose sugar, it results in lactose malabsorption.  The digestive system is unable to process the lactose sugar, and the unprocessed sugars in the gut produce the symptoms of lactose intolerance.
Lactose intolerance is not an allergy, because it is not an immune response, but rather a sensitivity to dairy caused by a deficiency of lactase enzyme. Milk allergy, occurring in about 2% of the population, is a separate condition, with distinct symptoms that occur when the presence of milk proteins trigger an immune reaction.

Signs and symptoms
The principal manifestation of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi, and vomiting (particularly in adolescents). These appear one-half to two hours after consumption. The severity of these signs and symptoms typically increases with the amount of lactose consumed; most lactose-intolerant people can tolerate a certain level of lactose in their diets without ill effects.Because lactose intolerance is not an allergy, it does not produce allergy symptoms (such as itching, hives, or anaphylaxis).

Causes
Lactose intolerance is a consequence of lactase deficiency, which may be genetic (primary hypolactasia and primary congenital alactasia) or environmentally induced (secondary or acquired hypolactasia). In either case, symptoms are caused by insufficient levels of lactase in the lining of the duodenum. Lactose, a disaccharide molecule found in milk and dairy products, cannot be directly absorbed through the wall of the small intestine into the bloodstream, so, in the absence of lactase, passes intact into the colon. Bacteria in the colon can metabolise lactose, and the resulting fermentation produces copious amounts of gas (a mixture of hydrogen, carbon dioxide, and methane) that causes the various abdominal symptoms. The unabsorbed sugars and fermentation products also raise the osmotic pressure of the colon, causing an increased flow of water into the bowels (diarrhea).Lactose intolerance in infants (congenital lactase deficiency) is caused by mutations in the LCT gene. The LCT gene provides the instructions for making lactase. Mutations are believed to interfere with the function of lactase, causing affected infants to have a severely impaired ability to digest lactose in breast milk or formula. Lactose intolerance in adulthood is a result of gradually decreasing activity (expression) of the LCT gene after infancy, which occurs in most humans. The specific DNA sequence in the MCM6 gene helps control whether the LCT gene is turned on or off. At least several thousand years ago, some humans developed a mutation in the MCM6 gene that keeps the LCT gene turned on even after breast feeding is stopped. Populations that are lactose intolerant lack this mutation.  The LCT and MCM6 genes are both located on the long arm (q) of chromosome 2 in region 21. The locus can be expressed as 2q21. The lactase deficiency also could be linked to certain heritages and varies widely. A 2016 study of over 60,000 participants from 89 countries found regional prevalence of lactose malabsorption was "64% (54–74) in Asia (except Middle East), 47% (33–61) in eastern Europe, Russia, and former Soviet Republics, 38% (CI 18–57) in Latin America, 70% (57–83) in the Middle East, 66% (45–88) in northern Africa, 42% (13–71) in northern America, 45% (19–71) in Oceania, 63% (54–72) in sub-Saharan Africa, and 28% (19–37) in northern, southern and western Europe." According to Johns Hopkins Medicine, lactose intolerance is more common in Asian Americans, African Americans, Mexican Americans, and Native Americans. Analysis of the DNA of 94 ancient skeletons in Europe and Russia concluded that the mutation for lactose tolerance appeared about 4,300 years ago and spread throughout the European population.Some human populations have developed lactase persistence, in which lactase production continues into adulthood probably as a response to the benefits of being able to digest milk from farm animals. Some have argued that this links intolerance to natural selection favoring lactase-persistent individuals, but it is also consistent with a physiological response to decrease lactase production when it is not needed in cultures in which dairy products are not an available food source. Although populations in Europe, India, Arabia, and Africa were first thought to have high rates of lactase persistence because of a single mutation, lactase persistence has been traced to a number of mutations that occurred independently. Different alleles for lactase persistence have developed at least three times in East African populations, with persistence extending from 26% in Tanzania to 88% in the Beja pastoralist population in Sudan.The accumulation of epigenetic factors, primarily DNA methylation, in the extended LCT region, including the gene enhancer located in the MCM6 gene near C/T-13910 SNP, may also contribute to the onset of lactose intolerance in adults. Age-dependent expression of LCT in mice intestinal epithelium has been DNA methylation in the gene enhancer.Lactose intolerance is classified according to its causes as:

Primary hypolactasia
Primary hypolactasia, or primary lactase deficiency, is genetic, only affects adults, and is caused by the absence of a lactase persistence allele. In individuals without the lactase persistence allele, less lactase is produced by the body over time, leading to hypolactasia in adulthood. The frequency of lactase persistence, which allows lactose tolerance, varies enormously worldwide, with the highest prevalence in Northwestern Europe, declines across southern Europe and the Middle East and is low in Asia and most of Africa, although it is common in pastoralist populations from Africa.

Secondary hypolactasia
Secondary hypolactasia or secondary lactase deficiency, also called acquired hypolactasia or acquired lactase deficiency, is caused by an injury to the small intestine. This form of lactose intolerance can occur in both infants and lactase persistent adults and is generally reversible. It may be caused by acute gastroenteritis, coeliac disease, Crohns disease, ulcerative colitis, chemotherapy, intestinal parasites (such as giardia), or other environmental causes.

Primary congenital alactasia
Primary congenital alactasia, also called congenital lactase deficiency, is an extremely rare, autosomal recessive enzyme defect that prevents lactase expression from birth. People with congenital lactase deficiency cannot digest lactose from birth, so cannot digest breast milk. This genetic defect is characterized by a complete lack of lactase (alactasia). About 40 cases have been reported worldwide, mainly limited to Finland. Before the 20th century, babies born with congenital lactase deficiency often did not survive, but death rates decreased with soybean-derived infant formulas and manufactured lactose-free dairy products.

Diagnosis
In order to assess lactose intolerance, intestinal function is challenged by ingesting more dairy products than can be readily digested.  Clinical symptoms typically appear within 30 minutes, but may take up to two hours, depending on other foods and activities.  Substantial variability in response (symptoms of nausea, cramping, bloating, diarrhea, and flatulence) is to be expected, as the extent and severity of lactose intolerance varies among individuals.The next step is to determine whether it is due to primary lactase deficiency or an underlying disease that causes secondary lactase deficiency. Physicians should investigate the presence of undiagnosed coeliac disease, Crohn disease, or other enteropathies when secondary lactase deficiency is suspected and infectious gastroenteritis has been ruled out.Lactose intolerance is distinct from milk allergy, an immune response to cows milk proteins. They may be distinguished in diagnosis by giving lactose-free milk, producing no symptoms in the case of lactose intolerance, but the same reaction as to normal milk in the presence of a milk allergy. A person can have both conditions. If positive confirmation is necessary, four tests are available.

Hydrogen breath test
In a hydrogen breath test, the most accurate lactose intolerance test, after an overnight fast, 25 grams of lactose (in a solution with water) are swallowed. If the lactose cannot be digested, enteric bacteria metabolize it and produce hydrogen, which, along with methane, if produced, can be detected on the patients breath by a clinical gas chromatograph or compact solid-state detector. The test takes about 2.5 hours to complete. If the hydrogen levels in the patients breath are high, they may have lactose intolerance. This test is not usually done on babies and very young children, because it can cause severe diarrhea.

Lactose tolerance test
In conjunction, measuring blood glucose level every 10 to 15 minutes after ingestion will show a "flat curve" in individuals with lactose malabsorption, while the lactase persistent will have a significant "top", with a typical elevation of 50% to 100%, within one to two hours. However, due to the need for frequent blood sampling, this approach has been largely replaced by breath testing.After an overnight fast, blood is drawn and then 50 grams of lactose (in aqueous solution) are swallowed. Blood is then drawn again at the 30-minute, 1-hour, 2-hour, and 3-hour marks.  If the lactose cannot be digested, blood glucose levels will rise by less than 20 mg/dl.

Stool acidity test
This test can be used to diagnose lactose intolerance in infants, for whom other forms of testing are risky or impractical. The infant is given lactose to drink. If the individual is tolerant, the lactose is digested and absorbed in the small intestine; otherwise, it is not digested and absorbed, and it reaches the colon. The bacteria in the colon, mixed with the lactose, cause acidity in stools. Stools passed after the ingestion of the lactose are tested for level of acidity. If the stools are acidic, the infant is intolerant to lactose.
Stool pH in lactose intolerance is less than 5.5.

Intestinal biopsy
An intestinal biopsy must confirm lactase deficiency following discovery of elevated hydrogen in the hydrogen breath test.  Modern techniques have enabled a bedside test, identifying presence of lactase enzyme on upper gastrointestinal endoscopy instruments.  However, for research applications such as mRNA measurements, a specialist laboratory is required.

Stool sugar chromatography
Chromatography can be used to separate and identify undigested sugars present in faeces. Although lactose may be detected in the faeces of people with lactose intolerance, this test is not considered reliable enough to conclusively diagnose or exclude lactose intolerance.

Genetic diagnostic
Genetic tests may be useful in assessing whether a person has primary lactose intolerance. Lactase activity persistence in adults is associated with two polymorphisms: C/T 13910 and G/A 22018 located in the MCM6 gene. These polymorphisms may be detected by molecular biology techniques at the DNA extracted from blood or saliva samples; genetic kits specific for this diagnosis are available. The procedure consists of extracting and amplifying DNA from the sample, following with a hybridation protocol in a strip. Colored bands are obtained as result, and depending on the different combinations, it would be possible to determine whether the patient is lactose intolerant. This test allows a noninvasive definitive diagnostic.

Frequency
Lactose intolerance is most common in people of East Asian descent, with 70 to 100 percent of people affected in these communities. Lactose intolerance is also more common in people of West African, Arab, and Jewish descent, while only about 5 percent of people of European descent are lactose intolerant.

Management
When lactose intolerance is due to secondary lactase deficiency, treatment of the underlying disease may allow lactase activity to return to normal levels. In people with celiac disease, lactose intolerance normally reverts or improves several months after starting a gluten-free diet, but temporary dietary restriction of lactose may be needed.People with primary lactase deficiency cannot modify their bodys ability to produce lactase. In societies where lactose intolerance is the norm, it is not considered a condition that requires treatment. However, where dairy is a larger component of the normal diet, a number of efforts may be useful. There are four general principles in dealing with lactose intolerance: avoidance of dietary lactose, substitution to maintain nutrient intake, regulation of calcium intake, and use of enzyme substitute. Regular consumption of dairy food by lactase deficient individuals may also reduce symptoms of intolerance by promoting colonic bacteria adaptation.

Dietary avoidance
The primary way of managing the symptoms of lactose intolerance is to limit the intake of lactose to a level that can be tolerated. Lactase deficient individuals vary in the amount of lactose they can tolerate, and some report that their tolerance varies over time, depending on health status and pregnancy. However, as a rule of thumb, people with primary lactase deficiency and no small intestine injury are usually able to consume at least 12 grams of lactose per sitting without symptoms, or with only mild symptoms, with greater amounts tolerated if consumed with a meal or throughout the day.
Lactose is found primarily in dairy products, which vary in the amount of lactose they contain:

Milk – unprocessed cows milk is about 4.7% lactose; goats milk 4.7%; sheeps milk 4.7%; buffalo milk 4.86%; and yak milk 4.93%.
Sour cream and buttermilk – if made in the traditional way, this may be tolerable, but most modern brands add milk solids.
Butter – the process of making butter largely removes lactose, but it is still present in small quantities; clarified butter contains a negligible amount of lactose.
Yogurt – lactobacilli used in the production of yogurt metabolize lactose to varying degrees, depending on the type of yogurt. Some bacteria found in yogurt also produce their own lactase, which facilitates digestion in the intestines of lactose intolerant individuals.
Cheese – fermentation also reduces the lactose content of cheeses and aging reduces it further; traditionally made hard cheeses might contain just 10% of the lactose found in an equivalent volume of milk. However, manufactured cheeses may be produced using processes that do not have the same lactose-reducing properties.There is no standardized method for measuring the lactose content of food. The stated dairy content of a product also varies according to manufacturing processes and labelling practices, and commercial terminology varies between languages and regions. As a result, absolute figures for the amount of lactose consumed (by weight) may not be very reliable. Kosher products labeled pareve or fleishig are free of milk. However, if a "D" (for "dairy") is present next to the circled "K", "U", or other hechsher, the food product likely contains milk solids, although it may also simply indicate the product was produced on equipment shared with other products containing milk derivatives.
Lactose is also a commercial food additive used for its texture, flavor, and adhesive qualities. It is found in additives labelled as casein, caseinate, whey, lactoserum, milk solids, modified milk ingredients, etc. As such lactose is found in foods such as processed meats (sausages/hot dogs, sliced meats, pâtés), gravy stock powder, margarines, sliced breads, breakfast cereals, potato chips, processed foods, medications, prepared meals, meal replacements (powders and bars), protein supplements (powders and bars), and even beers in the milk stout style. Some barbecue sauces and liquid cheeses used in fast-food restaurants may also contain lactose. Lactose is often used as the primary filler (main ingredient) in most prescription and non-prescription solid pill form medications, though product labeling seldom mentions the presence of lactose or milk, and neither do product monograms provided to pharmacists, and most pharmacists are unaware of the very wide scale yet common use of lactose in such medications until they contact the supplier or manufacturer for verification.

Milk substitutes
Plant-based milks and derivatives such as soy milk, rice milk, almond milk, coconut milk, hazelnut milk, oat milk, hemp milk, macadamia nut milk, and peanut milk are inherently lactose-free.  Low-lactose and lactose-free versions of foods are often available to replace dairy-based foods for those with lactose intolerance.

Lactase supplements
When lactose avoidance is not possible, or on occasions when a person chooses to consume such items, then enzymatic lactase supplements may be used.Lactase enzymes similar to those produced in the small intestines of humans are produced industrially by fungi of the genus Aspergillus. The enzyme, β-galactosidase, is available in tablet form in a variety of doses, in many countries without a prescription. It functions well only in high-acid environments, such as that found in the human gut due to the addition of gastric juices from the stomach. Unfortunately, too much acid can denature it, so it should not be taken on an empty stomach. Also, the enzyme is ineffective if it does not reach the small intestine by the time the problematic food does. Lactose-sensitive individuals can experiment with both timing and dosage to fit their particular needs.
While essentially the same process as normal intestinal lactose digestion, direct treatment of milk employs a different variety of industrially produced lactase. This enzyme, produced by yeast from the genus Kluyveromyces, takes much longer to act, must be thoroughly mixed throughout the product, and is destroyed by even mildly acidic environments. Its main use is in producing the lactose-free or lactose-reduced dairy products sold in supermarkets.

Rehabituation to dairy products
Regular consumption of dairy foods containing lactose can promote a colonic bacteria adaptation, enhancing a favorable microbiome, which allows people with primary lactase deficiency to diminish their intolerance and to consume more dairy foods. The way to induce tolerance is based on progressive exposure, consuming smaller amounts frequently, distributed throughout the day. Lactose intolerance can also be managed by ingesting live yogurt cultures containing lactobacilli that are able to digest the lactose in other dairy products.

Epidemiology
Worldwide, about 65% of people experience some form of lactose intolerance as they age past infancy, but there are significant differences between populations and regions. As few as 5% of northern Europeans are lactose intolerant, while as many as 90% of adults in parts of Asia are lactose intolerant.Some populations, from an evolutionary perspective, have a better genetic makeup for tolerating lactose than others. In northern European countries, early adoption of dairy farming conferred a selective evolutionary advantage to individuals that could better tolerate lactose. This led to higher frequencies of lactose tolerance in these countries. For example, almost 100% of Irish people are predicted to be lactose tolerant. Conversely, regions of the south, such as Africa, did not adopt dairy farming as early and tolerance from milk consumption did not develop the same way as in northern Europe. Lactose intolerance is common among people of Jewish descent, as well as from West Africa, the Arab countries, Greece, and Italy. Different populations will present certain gene constructs depending on the evolutionary and cultural pre-settings of the geographical region.

History
Greater lactose tolerance has come about in two ways. Some populations have developed genetic changes to allow the digestion of lactose: lactase persistence. Other populations developed cooking methods like milk fermentation.Lactase persistence in humans evolved relatively recently (in the last 10,000 years) among some populations. Around 8,000 years ago in modern-day Turkey, humans became reliant on newly-domesticated animals that could be milked; such as cows, sheep, and goats. This resulted in higher frequency of lactase persistence. Lactase persistence became high in regions such as Europe, Scandinavia, the Middle East and Northwestern India. However, most people worldwide remain lactase non-persistent. Populations that raised animals not used for milk tend to have 90–100 percent of a lactose intolerant rate.  For this reason, lactase persistence is of some interest to the fields of anthropology, human genetics, and archaeology, which typically use the genetically derived persistence/non-persistence terminology.The rise of dairy and producing dairy related products from cow milk alone, varies across different regions of the world, aside from genetic predisposition. The process of turning milk into cheese dates back earlier than 5200 BC.DNA analysis in February 2012 revealed that Ötzi was lactose intolerant, supporting the theory that lactose intolerance was still common at that time, despite the increasing spread of agriculture and dairying.Genetic analysis shows lactase persistence has developed several times in different places independently in an example of convergent evolution.

History of research
It is not until relatively recently that medicine recognised the worldwide prevalence of lactose intolerance and its genetic causes. Its symptoms were described as early as Hippocrates (460–370 BC), but until the 1960s, the prevailing assumption was that tolerance was the norm. Intolerance was explained as the result of a milk allergy, intestinal pathogens, or as being psychosomatic – it being recognised that some cultures did not practice dairying, and people from those cultures often reacted badly to consuming milk. Two reasons have been given for this misconception </s>