Sunday, November 23, 2014

The 5 Types Of Lupus Fatigue

Fatigue is the most common and disabling symptom experienced by those with autoimmune disorders. According to the Lupus Foundation, approximately 80% of those with lupus experience fatigue. I disagree, lol! I have never heard of someone with lupus that didnt experience fatigue! I have read several prominent rheumatologists say that they feel fatigue is about 100% in lupus.

Exhaustion, for us affected by Lupus is a permanent part of life. It is just as much a part of me as the fact that I have 2 feet. It will not go matter how much I beg, plead, or wish it to. I have had SLE and other AI disorders for 23 years, and I do not remember what it is like to live life without my constant passenger of fatigue. Over the years it has worsened and evolved into a more severe exhaustion. But I have also gotten much better at dealing with it and accomodating my life around it without beating myslf up so much. I grieve for my inability to be spontaneous, to go about life without carefully planning each day. And I do so long to quell my fatigue with refreshing sleep. But, there is no sense wringing my hands, as it will not change a thing to just feel sorry for myself--and it actually will make me even more tired! It is very important for us to have understanding about what our daily struggles are about. Please share this with your family and friends. It is my hope that this will help you to minimize your sources of fatigue that are controllable, and learn to recognize the cues your body is telling you to address your level of fatigue. This will serve to give us all some empowerment.

1. Daily exhaustion 
This is the inherent fatigue that I attribute to the inflammatory, autoimmune nature of Lupus and the other autoimmune disorders I have such as Rheumatoid Arthritis, Sjogren's, and Polymyositis, to nme a few. It never goes away, and can vary from day to day but is always there. Pain levels definitely increase this, as can the weather (too hot, too cold, or major weather changes that I can "feel" in my bones) Think what it feels like to function without having any sleep for 2 days. That is the blanket of exhaustion that is the basis for daily living with autoimmune illness. All of the following are added to this basic fatigue. 

2. Overdoing fatigue
 If I push myself too far and ignore the cues my body is sending me to stop and rest, my body will fight back. When I do more than I should, the result is an immobilizing fatigue. It comes on after the fact, i.e., do too much one day and feel it the next. If I push myself today, I very likely will have to cancel everything tomorrow and most likely a few days after that. An extended period of doing more than I should will almost certainly cause a flare. 

3. Crumple and collapse fatigue 
This complete exhaustion comes on suddenly, and I have to stop whatever I'm doing and sit (or lay down) as soon as possible. It can happen anywhere, at any time. This fatigue feels like I have just run 26 miles and worked out using weights muscles will literally shake from any effort. My brain loses its ability to compute anything—even simple tasks are impossible to figure out. I am unable to match socks, or even to care for my basic my body and brain are on total disconnect. I cannot complete a thought, and lists do not I will most likely either not remember to look at them, or I will not be able to understand what is on them. Others can notice this fatigue, even though I may try to hide it with incredible effort. If I do not heed the warnings from this fatigue, I will end up in a major flare. And many times I will anyways. 

4. Peanut butter fatigue  
This fatigue is present when I open my eyes in the morning and know that it is going to be a particularly bad day. This tends to happen more in the cold weather, and seems to coincide with Raynaud’s symptoms. It feels like every effort I make to move is as if the air is made of thick peanut butter. My muscles and joints hurt, and doing anything is like walking with heavy weights. That super sore and heavy feeling you get from working out too strenuously..multiplied x 10! This fatigue prevents me from exercising on days when it is present, as even a little walking will make it much worse, and actually will increase my level of exhaustion. The best thing for me to do with peanut butter fatigue is heat, rest, and gentle stretches. 

5. Flare exhaustion 
Flare-related fatigue is the mother of all unpredictable state of increased fatigue that can last for days or weeks. It can actually be all of the above types combined. There is no way to put off, or not heed this fatigue..or I will literally collapse. (Has happened) This is like someone who has had no sleep for about 3-4 days, then ran a marathon, lifted weights strenuously, and took sleeping meds..but didn't sleep! In addition, a flare brings multiple other symptoms that add to the exhaustion..pain, GI problems, like nausea, vomiting, diarrhea, abdominal pain, headache, etc. I have no choice but to rest..I will literally sleep 12-20 hours in a day during flares. Rest is vital, as is communication with my physician, as undetected infections can also disguise themselves with a flare and this fatigue. Once a flare starts, it is impossible to tell how long it will last, or how severe, and which bodily systems will be affected.   

The following issues will add to the above fatigue, so be sure that you are in touch with your physician regarding them, to minimize the effect on your level of exhaustion.
*Stress (well doh)
*Depression and Anxiety
*Thyroid problems...make sure your dr has checked these at least once a year. 3-4 times a year if you are on thyroid medications.
*Anemia (This is common with Lupus)
*Sleep Apnea
*Pulmonary fibrosis
*Low vitamin d levels
*Congestive heart failure 
*Chronic pain
*Other concurrent conditions (Diabetes, Rheumatoid Arthritis, MS, etc.)

The following medications can cause or contribute to fatigue:

*Cold and allergy meds (allegra, benadryl, dextromethorphan)
*Muscle relaxants (flexeril, zanaflex, soma, robaxin, etc)
*Narcotic pain medications (percocet, vicodin, tramadol, morphine, dilaudid, eyc.)
*Other pain medications (lyrica, neurontin)
*Blood pressure medications (lopressor, labetalol, zestril, norvasc, procardia, lasix, bumex, atenolol, etc)
*Prednisone (acts as a stimulant, preventing sleep.Talk with your Dr about dosing earlier in the day)
*Antidepressnts (paxil, zoloft, prozac, celexa, lexapro, trazodone, elevil, remeron, seroquel, abilify, effexor, cymbalta, etc)
*Anxiety Medications (valium, ativan, xanax, klonopin, buspar, vistaril, etc.)
*Migraine prevention medications (elavil, topamax, depakote, inderal, etc.)

~Jenn Schoch <3

Friday, October 3, 2014

Lupus Symptoms & Complications

Lupus Symptoms
SLE symptoms may develop slowly over months or years, or they may appear suddenly. Symptoms tend to be worse during winter months, perhaps because prolonged exposure to sunlight in the summer causes a gradual build-up of factors that trigger symptoms months later.

The most common symptom is joint pain, which occurs in about 90% of patients with SLE. Characteristics of this symptom vary widely:

It is often accompanied by swelling and redness.
It can last from hours to months.
It may be mild or severe.
It can occur in one joint, move from one to another, or flare erratically.
Pain often occurs in the morning and improves during the day, only to return later when the patient tires.
The joints most affected are fingers, wrists, elbows, knees, and ankles. (Joints in the spine and neck are not affected.)
Children may experience these symptoms as growing pains, and, in all patients, they may be the only symptoms for many years.

Fever occurs in 90% of patients with SLE and is usually caused by the inflammatory process of the disease, not by infection. It is low-grade except during an acute lupus crisis.

Three-quarters of patients with SLE have skin inflammation and skin lesions (ulcers, rashes, or other injured areas). About half of these lesions are photosensitive; that is, they are aggravated by ultraviolet (UV) radiation from sunlight, even from light coming through a window. (UV radiation may even trigger systemic flares in patients with SLE.)

A number of different skin conditions have been described in patients with SLE.

Discoid Lupus Erythematosus. About 20% of patients have discoid lesions. In such cases, the condition is often known as discoid lupus erythematosus (DLE). Patients with this condition may have the following skin abnormalities:

Discoid means coin-shaped, so these lesions are round and raised. They are also scaly. Untreated, the margins gradually extend outward as the center dries out and shrivels, causing severe scarring. If discoid lesions appear on the scalp, they can plug hair follicles and cause irreversible hair loss. Discoid lesions can also appear on the upper body.

Lupus, discoid -- view of lesions on the chest: This close-up picture of the neck clearly shows the typical rounded appearance of discoid lupus. The whitish appearance is caused by scaling. The two dark spots are biopsy sites and are not part of the disease.
A butterfly-shaped rash across the face may accompany this condition. This rash causes little scarring, although spidery, branching lines of swollen capillaries (the tiniest blood vessels) may appear.
Most patients with this condition have only a limited skin disorder. In only about 10% of cases does discoid lupus develop into full-blown SLE.

Subacute Cutaneous Lupus Erythematosus. Subacute cutaneous lupus erythematosus (SCLE) can cause skin lesions on parts of the body that are exposed to sunlight. These lesions do not cause scarring.

Vasculitis. Patients with SLE sometimes develop inflammation in the blood vessels (vasculitis) that may have the following effects on the skin:

Red welts may form across large areas of the body.
Sometimes deep red bumps may appear, particularly on the leg, where they may ulcerate.
In some people, reddish-purple lesions appear on the pads of fingers and toes or near the nails of fingers and toes.
Lesions caused by vasculitis may ulcerate or blister if they erupt on mucous membranes in the mouth, nose, or vagina and can be painful if they occur on the throat.
Vasulitis can attack blood vessels in almost any other organ, including the brain, the heart, and the gastrointestinal tract.
Other symptoms include:

Loss of appetite, nausea, and weight loss
Chest pain
Menstrual irregularities
Thought and concentration disturbances
Personality changes
Sleep disorders, such as restless legs syndrome and sleep apnea
Dryness of the eyes and mouth
Brittle hair or hair loss
Hair loss or breakage may also occur in about half of patients with SLE during severe flares or after pregnancy or severe illness. In such cases, hair grows back.

Raynaud's phenomenon is a condition in which cold or stress can cause spasms in impaired blood vessels, resulting in pain in fingers and toes. It occurs as part of the inflammatory response in blood vessels, which can narrow them and reduce circulation. In extreme cases, gangrene can result.

A number of conditions overlap with SLE:

Scleroderma: Hardening of the skin caused by overproduction of collagen
Rheumatoid arthritis: Inflammation of the lining of the joints
Sjogren syndrome: Characterized by dry eyes and dry mouth
Mixed connective tissue disorder: Similar to SLE, but milder
Myositis: Inflammation and degeneration of muscle tissues
Rosacea: Flushed face with pus-filled blisters
Seborrheic dermatitis: Sores on lips and nose
Lichen planus: Swollen rash that itches, typically on scalp, arms, legs, or in the mouth
Dermatomyositis: Bluish-red skin eruptions on face and upper body
Lyme disease: Bulls-eye rash, joint inflammation, and flu-like symptoms

Lupus Overview
Systemic lupus erythematosus (SLE) can cause systemic complications throughout the body.

Almost 85% of patients with SLE experience problems associated with abnormalities in the blood.

Anemia. About half of patients with SLE are anemic. Causes include:

Iron deficiencies resulting from excessive menstruation
Iron deficiencies from gastro-intestinal bleeding caused by some of the treatments
A specific anemia called hemolytic anemia, which destroys red blood cells
Anemia of chronic disease
Hemolytic anemia can occur with very high levels of the anticardiolipin antibody. It can be chronic or develop suddenly and be severely (acute).

Antiphospholipid Syndrome. Between 34 - 42% of patients with SLE have antiphospholipid syndrome (APS). This is a specific set of conditions related to the presence of autoantibodies called lupus anticoagulant and anticardiolipin. These autoantibodies react against fatty molecules called phospholipids, and so are called antiphospholipids. Their actions have complex effects that include causing narrowing and abnormalities of blood vessels.

Patients who have APS have a very incidence of blood clots, which most often occur in the deep veins in the legs. Blood clotting, in turn, puts patients at higher risk for stroke and pulmonary embolism (clots in the lungs).

This picture shows a red and swollen thigh and leg caused by a blood clot (thrombus) in
the deep veins in the groin (iliofemoral veins). Such a clot prevents normal return of blood from the leg to the heart.
The effects on blood vessels have also been associated with confusion, headaches, and seizures. Leg ulcers can also develop.
Patients with APS who become pregnant have a high incidence of pregnancy loss, especially in the late term.
Not all patients with APS carry both of the autoantibodies, and they can also wax and wane and so have varying effects. APS also occurs without lupus in about half of patients with the syndrome.

Thrombocytopenia. In thrombocytopenia, antibodies attack and destroy blood platelets. In such cases, blood clotting is impaired, which causes bruising and bleeding from the skin, nose, gums, or intestines. (This condition can also occur in APS, but it is not considered to be one of the standard features of the syndrome.)

Neutropenia. Neutropenia is a drop in the number of white blood cells. Patients with SLE often neutropenia, but the condition is usually harmless unless the reductions are so severe that they leave the patient vulnerable to infections.

Acute Lupus Hemophagocyte Syndrome. A rare blood complication of SLE that occurs primarily in Asians is called acute lupus hemophagocytic syndrome. It is generally of short duration and characterized by fever and a sudden drop in blood cells and platelets.

Lymphomas. Patients with SLE and other autoimmune disorders have a greater risk for developing lymph system cancers such as Hodgkin’s disease and non-Hodgkin’s lymphoma (NHL).

Heart disease is a primary cause of death in lupus patients. The immune response in SLE can cause chronic inflammation and other damaging effects that can cause significant injury to the arteries and tissues associated with the circulation and the heart. In addition, SLE treatments (particularly corticosteroids) affect cholesterol, weight, and other factors that can also affect the heart.

Patients with SLE, have a higher risk for developing the following conditions, which put them at risk for heart attack or stroke:

Atherosclerosis, or plaque buildup in the arteries
Increased stiffness in the arteries
Unhealthy cholesterol and lipid (fatty molecules) levels
High blood pressure, most likely because of kidney injury and corticosteroid treatments
Heart failure
Pericarditis, an inflammation of the tissue surrounding the heart
Myocarditis, an inflammation of the heart muscle itself (rare)
Abnormalities in the valves of the heart (rare)
Blood clots
The risk for cardiovascular disease, heart attack, and stroke is much higher than average in younger women with SLE. The risks decline as such women age.

SLE affects the lungs in about 60% of patients:

Inflammation of the membrane lining the lung (pleurisy) is the most common problem, which can cause shortness of breath and coughing.
In some cases, fluid accumulates, a condition called pleural effusion.
Inflammation of the lung tissue itself is called lupus pneumonitis. It can be caused by infections or by the SLE inflammatory process. Symptoms are the same in both cases: fever, chest pain, labored breathing, and coughing. Rarely, lupus pneumonitis becomes chronic and causes scarring in the lungs, which reduces their ability to deliver oxygen to the blood.
A very serious and rare condition called pulmonary hypertension occurs when high pressure develops as a result of damage to the blood vessels of the lungs.
The kidneys are a crucial battleground in SLE because it is here that the debris left over from the immune attacks is most likely to be deposited. Also, the immune response can also attack different parts of the kidney causing damage. About 50% of patients with SLE exhibit inflammation of the kidneys (called lupus nephritis).This condition occurs in different forms and can vary from mild to severe. Poor kidney function and kidney failure may result from this damage.

Serious complications occur eventually in about 30% of patients. If kidney injury develops, it almost always occurs within 10 years of the onset of SLE, rarely after that.

Nearly all patients with SLE report some symptoms relating to problems that occur in the central nervous system (CNS), which includes the spinal cord and the brain. CNS involvement is more likely to occur in the first year, usually during flare-ups in other organs.

Symptoms vary widely and overlap with psychiatric or neurologic disorders. They may also be caused by of some medications used for SLE. Central nervous system symptoms are usually mild, but there is little effective treatment available for them. CNS symptoms get worse as the disease progresses.

The most serious CNS disorder is inflammation of the blood vessels in the brain (vasculitis), which occurs in 10% of patients with SLE. Fever, seizures, psychosis, and even coma can occur. Other CNS side effects include:

Emotional disorders (anxiety, depression)
Mild impairment of concentration and memory
Migraine and tension headaches
Problems with the reflex systems, sensation, vision, hearing, and motor control
Infections are a common complication and a major cause of death in all stages of SLE. The immune system is indeed overactive in SLE, but it is also abnormal and reduces the ability to fight infections. Patients are not only prone to the ordinary streptococcal and staphylococcal infections, but they are also susceptible to fungal and parasitic infections (called opportunistic infections), which are common in people with weakened immune systems. They also face an increased risk for urinary tract, herpes, salmonella, and yeast infections. Corticosteroid and immunosuppressants, treatments used for SLE, also increase the risk for infections, thereby compounding the problem.

About 45% of patients with SLE suffer gastrointestinal problems, including nausea, weight loss, mild abdominal pain, and diarrhea. Severe inflammation of the intestinal tract occurs in less than 5% of patients and causes acute cramping, vomiting, diarrhea, and, rarely, intestinal perforation, which can be life-threatening. Fluid retention and swelling can cause intestinal obstruction, which is much less serious but causes the same type of severe pain. Inflammation of the pancreas can be caused by the disease and by corticosteroid therapy.

Arthritis caused by SLE almost never leads to destruction or deformity of joints. The inflammatory process can, however, damage muscles and cause weakness. Patients with SLE also commonly experience reductions in bone mass density (osteoporosis) and have a higher risk for fractures, whether or not they are taking corticosteroids (which can increase the risk for osteoporosis). Women who have SLE should have regular bone mineral density scans to monitor bone health.

Inflamed blood vessels in the eye can reduce blood supply to the retina, resulting in degeneration of nerve cells and a risk of hemorrhage in the retina. The most common symptoms are cotton-wool-like spots on the retina. In about 5% of patients sudden temporary blindness may occur.

In one study, 40% of patients with SLE quit work within 4 years of diagnosis, and many had to modify their work conditions. Significant factors that predicted job loss included high physical demands from the work itself, a more severe condition at the time of diagnosis, and lower educational levels. People with lower income jobs were at particular risk for leaving them.

Women with lupus who conceive face high-risk pregnancies that increase the risks for themselves and their babies. It is important for women to understand the potential complications and plan accordingly. The most important advice is to avoid becoming pregnant when lupus is active.

Research suggests that the following factors predict a successful pregnancy:

Disease state at time of conception. Doctors strongly recommend that women wait to conceive until their disease state has been inactive for at least 6 months.
Kidney (renal) function. Women should make sure that their kidney function is evaluated prior to conception. Poor kidney function can worsen high blood pressure and cause excess protein in the urine. These complications increase the risk for preeclampsia and miscarriage.
Lupus-related antibodies. Antiphospholipid and anticardiolipin antibodies can increase the risks for preeclampsia, miscarriage, and stillbirths. Anti-SSA and anti-SSB antibodies can increase the risk for neonatal lupus erythematosus, a condition that can cause skin rash and liver and heart damage to the newborn baby. Levels of these antibodies should be tested at the start of pregnancy. Certain medications (aspirin, heparin) and tests (fetal heart monitoring) may be needed to ensure a safe pregnancy.

Medication use during pregnancy. Women with active disease may need to take low-dose corticosteroids, but women with inactive disease should avoid these drugs. Steroids appear to pose a low risk for birth defects, but can increase a pregnant woman’s risks for gestational diabetes, high blood pressure, infection, and osteoporosis. For patients who need immunosuppressive therapy, azathioprine (Imuran) is an option. Methotrexate (Rheumatrex) and cyclophosphamide (Cytoxan) should not be taken during pregnancy.

Pregnancy Risks

Women with lupus are 20 times more likely to die during pregnancy than women without the disease. The risk for maternal death is due to the following serious conditions that can develop during pregnancy:

Miscarriages. About 25% of lupus pregnancies result in miscarriage. The risk is highest for patients with antiphospholipid antibodies, active kidney disease, or high blood pressure.
Blood clots. Women with lupus have a 6 times greater risk for developing deep vein thrombosis (blood clots) than women without the disease.

Clotting complications. Low blood platelet count and anemia are also risks. Women with lupus are 3 times more likely to need a transfusion during pregnancy than women without lupus.
Infections. Blood infections (sepsis), pneumonia, and urinary tract infections are more common in pregnant women with lupus.

Preeclampsia. Women with lupus are three times more likely than healthy women to develop preeclampsia (pregnancy-related high blood pressure), which can be potentially life threatening.
Birth Complications. Women with SLE have an increased risk of having a pre-term birth, stillbirth, or Caesarean section.
Despite these obstacles, many women with lupus have healthy pregnancies and deliver healthy babies. To increase the odds of a successful pregnancy, it is important for women to plan carefully before becoming pregnant. Be sure to find knowledgeable doctors with whom you can communicate and trust. Pregnant women with lupus should try to assemble an interdisciplinary health care team that includes a rheumatologist, high-risk obstetrician, and (for patients with kidney disease) a nephrologist.


Causes/Risk Factors for Lupus


Systemic lupus erythematosus (SLE) is a chronic, often life-long, autoimmune disease. It can be mild to severe, and affects mostly women. SLE may affect various parts of the body, but it most often manifests in the skin, joints, blood, and kidneys. SLE was first described in 1828. Its very name helps define the disease:

Systemic is used because the disease can affect organs and tissue throughout the body.
Lupus is Latin for wolf. It refers to the rash that extends across the bridge of the nose and upper cheekbones and was thought to resemble a wolf bite.
Erythematosus is from the Greek word for red and refers to the color of the rash..   
Lupus has many different symptomsn ones include:
Joint pain or swelling
Skin rashes

Systemic lupus erythematosus is a complex disorder that most likely results from a combination of processes and factors.

Environmental factors, such as viruses, exposure to chemicals, or sunlight, trigger inflammatory or immune activity. This immune activation may begin as an appropriate response to an unwanted "invader." But, because of a combination of genetic factors, an individual with lupus develops an ongoing immune response that does not shut itself off appropriately. This leads to waxing and waning flares of inflammation that can involve various organs of the body, depending on specific features of this self-perpetuating immune response in individual patients.

The exact combination of genes that predispose individuals to SLE may differ somewhat from patient to patient, but probably share certain common features which tend to impair the ability of the body to get rid of immune-triggering particles and which tend to prolong or increase the degree of immune responsiveness to these triggers.

A major characteristic of lupus is that it is an autoimmune response in which immune factors, called autoantibodies, attack the person's own cells. Some autoantibodies are normal in a well-balanced immune system, and serve various roles to help the body dispose of wastes, protect from infectious invaders, and to keep blood vessels clear. In healthy people, autoantibodies tend to be well-regulated and well "masked," or covered up, until needed. Therefore, it is probably the high activity and high detestability of autoantibodies that makes lupus unique, not the fact that they exist.

The Normal Immune System Response. The inflammatory process is a byproduct of the activity of the body's immune system, which fights infection and heals wounds and injuries:

When an injury or an infection occurs, white blood cells are mobilized to rid the body of any foreign proteins, such as a virus.
The masses of blood cells that gather at the injured or infected site produce factors to fight any infections.

In the process, the surrounding area becomes inflamed and some healthy tissue is injured. The immune system is then called upon to repair wounds by clotting any bleeding blood vessels and initiating fiber-like patches to the tissue.
Under normal conditions, the immune system has special factors that control and limit this inflammatory process.

The Infection Fighters. B cells and T cells are two important components of the immune system that play a role in the inflammation associated with lupus. Both B cells and T cells belong to a family of immune cells called lymphocytes. Lymphocytes help fight infection.

B cells and T cells are involved in the immune system's response to infection. Antigens are foreign bodies (such as bacteria and viruses) that stimulate the immune system to produce autoantibodies. When a T cell recognizes an antigen it will produce chemicals (cytokines) that cause B cells to multiply and release many immune proteins (antibodies). These antibodies circulate widely in the bloodstream, recognizing the foreign particles and triggering inflammation in order to rid the body of the invasion.

An antigen is a substance that can provoke an immune response. Typically antigens are substances not usually found in the body.
For reasons that are still not completely understood, both the T cells and B cells become overactive in lupus patients. In lupus, a complex interaction between activated immune cells and an impaired antigen-elimination process leads to a greater than normal range of what the antibodies recognize. Eventually, antibodies are made that recognize more of the body's own tissues in a stronger or more persistent manner than is healthy, and inflammatory responses are mounted in these tissues.

Autoantibodies. In the majority of patients with SLE, antinuclear antibodies (ANA) are detectable. Such autoantibodies may be present in individuals up to 7 years prior to their developing symptoms of lupus. Some subtypes of ANA are found in lupus patients and only rarely in people without lupus. These include:

Anti-ds DNA. An autoantibody called anti-double stranded DNA (anti-ds DNA) may play an important role in some lupus patients.
Anti-Sm antibodies. This antibody is found most often in lupus patients of African descent and is almost never detected in people without lupus.
Anti-Ro (SSA) and Anti-La (SSB)
Antiphospholipid antibodies

Cytokines. Most immune cells secrete or stimulate the production of powerful immune factors called cytokines. In small amounts, cytokines are indispensable for maintaining the balance of the body during immune responses, including:
Tissue repair
Blood clotting
Clearing of debris from inflamed blood vessels
Other aspects of healing.
If overproduced, however, they can cause serious damage, including dangerous levels of inflammation and cellular injury. Specific cytokines called interferons and interleukins play a critical role in SLE by regulating the secretion of autoantibodies by B cells.

Complement. Another immune factor of high interest in SLE is the complement system. This is comprised of more than 30 proteins and is important for defending and regulating the immune response. Inherited deficiencies in certain complement components (C1q, C1r, C1s, C4, and C2) have long been associated with SLE.

SLE is a complex disorder and researchers are still in the early stages of unraveling how genetic factors may alter and affect the immune system. Researchers estimate that 20 - 100 different genetic factors may make a person susceptible to SLE.

 The number of people diagnosed with lupus has more than tripled over the past four decades. This may simply indicate a greater degree of doctor training in recognizing the syndrome. GENDER About 90% of lupus patients are women, most diagnosed when they are in their childbearing ages. Hormones may be an explanation. After menopause, women are only 2.5 times as likely as men to contract SLE. Flares also become somewhat less common after menopause in women who have chronic SLE.

African-Americans are three to four times more likely to develop the disease than Caucasians and to have severe complications. Hispanics and Asians are also more susceptible to the disease.

A family history plays a strong role in SLE. A brother or sister of a patient with the disorder has 20 times the risk as someone without an immediate family member with SLE.
The disease is rare in childhood. When it does occur, it is often associated with thrombotic thrombocytopenia purpura, a condition resulting from abnormally low levels of blood platelets. SLE in children may also be caused by certain medications, including minocycline and zafirlukast.

Rheumatoid Arthritis. Studies have investigated the relationship among hormones, SLE, and rheumatoid arthritis, another autoimmune disease. Higher levels of estrogen are associated with SLE, while lower levels are associated with rheumatoid arthritis. Some research suggests that some patients, in fact, progress from one disease to the other, and that such transitions occur during major hormonal shifts, such as the onset of menopause or pregnancy. Rheumatoid arthritis is a systemic autoimmune disease that initially attacks the lining, or synovium, of the joints.

Many prescription drugs can cause lupus-like skin symptoms. These include high blood pressure (hypertension) medications, including hydrochlorothiazide, angiotensin-converting-enzyme inhibitors, and calcium-channel blockers. About 40 different drugs have been linked to lupus onset. Anyone diagnosed with cutaneous lupus erythematosus should be sure to tell their doctors all the medications (including herbs and supplements) that they are taking.

Smoking. Smoking may be a risk factor for triggering SLE and can increase the risk for skin and kidney problems in women who have the disease.

In genetically susceptible people, there are various external factors that can provoke an immune response. Possible SLE triggers include colds, fatigue, stress, chemicals, sunlight, and certain drugs.

Viruses. Patients with SLE may be more likely to have been exposed to certain viruses than the general population. These viruses include the Epstein-Barr virus (the cause of mononucleosis), cytomegalovirus, and parvovirus-B1. In particular, some research suggests a strong association between Epstein-Barr virus (EBV) and increased risk of lupus, particularly for African-Americans.

Sunlight. Ultraviolet (UV) rays found in sunlight are important SLE triggers. When they bombard the skin, they can alter the structure of DNA in cells below the surface. The immune system may perceive these altered skin cells as foreign and trigger an autoimmune response against them. UV light is categorized as UVB or UVA depending on the length of the wave. Shorter UVB wavelengths cause the most harm.

Chemicals. Clusters of SLE cases have occurred in populations with high exposure to certain chemicals. Chlorinated pesticides and crystalline silica are two suspects. A number of other chemicals are under investigation. However, it is very difficult to determine a causal role for any specific chemicals. (Silicone breast implants have been under intense scrutiny as a possible trigger of autoimmune diseases, including SLE. The weight of evidence to date, however, finds no support for this concern.) Some drugs have been associated with a temporary lupus syndrome (drug-induced lupus), which resolves when these drugs are stopped.

Hormones. Cytokines, major immune factors that are active in SLE, are directly affected by sex hormones. In general, estrogen enhances antibody production, and testosterone reduces antibody production, although their exact role in SLE may be more complicated than that since there are various ways in which each hormone might influence various immune cells. Women with SLE may have lower levels of several active male hormones (androgens), and some men who are affected by SLE may also have abnormal androgen levels. Premature menopause, and its accompanying symptoms (such as hot flashes), is common in women with SLE. Hormone replacement therapy (HRT), which is used to relieve these symptoms, increases the risk for blood clots and heart problems. It is not clear whether HRT triggers SLE flares. Women should discuss with their doctors whether HRT is an appropriate and safe choice. Guidelines recommend that women who take HRT use the lowest possible dose for the shortest possible time. Women with SLE who have active disease, antiphospholipid antibodies, or a history of blood clots or heart disease should not use HRT.

Oral Contraceptives. Female patients with lupus used to be cautioned against taking oral contraceptives (OCs) due to the possibility that estrogen could trigger lupus flare-ups. However, recent evidence indicates that OCs are safe, at least for women with inactive or stable lupus. Women who have been newly diagnosed with lupus should avoid OCs. Lupus can cause complications in its early stages. For this reason, women should wait until the disease reaches a stable state before taking OCs. In addition, women who have a history of, or who are at high risk for, blood clots (particularly women with antiphospholipid syndrome) should not use OCs. The estrogen in OCs increases the risk for blood clots.

Sources:,, hopkinslupus,

Monday, September 29, 2014

Living In The Now

Living in the Now

 Benefits of Living in The Moment:
 ✓ You become more connected with your  thoughts and feelings
 ✓ Are more connected to others
 ✓ Feel more gratitude and enjoyment of life
 ✓ If you live in the moment, it won't pass you  by
 ✓ Feel more focused, peaceful and alive
 ✓ Feel less anxious and fearful

 Like all skills, training yourself to enjoy and live in the moment takes time and practice. Begin now and see life from a fresh, new perspective. Carpe diem!

 Yes, for this moment IS your life! Living in the moment, or the now, is a conscious act that requires participation, not just observation. Every moment of your Life is a journey, rather than a destination...each step of which is a continuing discovery of yourself.

 Seizing each moment in life allows us to prolong its value and make it more meaningful. Rather than seeking quantity of time, when we live in the moment we enjoy and savor every minute.No other moment in time actually exists, so unless we live in the moment of now, we are not really living at all. We are just projecting either backwards or forwards.

 The reason our mind becomes still when we live in the moment of now is because there are no preconceptions brought forward from the past. Each moment is seen anew. So there is no guilt, no fear, no baggage filling our mind. Our mind is empty. To live in the moment, or now, means being conscious, aware and in the present with all of your senses. It means not dwelling on the past, nor being anxious or worrying about the future.

 When we concentrate our attention on the present we focus on the task at hand. We give our full attention to what we are doing and we let go of outcomes. When we train ourselves to live in each moment, we immerse ourselves in it and begin to discover its beauty and wonder. We learn focus and how to manage our energy. Professional athletes understand and employ this kind of focus very well. They know that accomplishment and success are a result of the skillful management and balancing of energy.

When we train ourselves to live in each moment, we immerse ourselves in it and begin to discover its beauty and wonder.  To make every moment count we must embrace it. Everything we do and every person we come in contact with deserves our full attention. Even when resting we should savor the moment. It gives us the opportunity to recharge, renew and gain clarity.

 Quite often we put huge expectations on ourselves and our lives. We rush to do this, hurry up with that, without actually enjoying the process. What's the rush? Where do we think we're going? If we don't stop and think about where we're at, we're probably missing the point.

Instead, when we appreciate each moment and garner the lessons from it, we live consciously, purposefully and responsibly. Likewise, when we live in the past and don't let go of painful experiences, perceived wrongs, or difficult times, we condemn ourselves to a present and future of the same. We cannot change the past. We can, however, come to terms with it, know that it's over, and move on. Living in the moment means letting go of the past and trusting in the future. When we are positive and optimistic in the present, we open the possibility of a positive and promising future. We owe it to ourselves to make every moment count - now!

Tips for Living in The Moment
Train your mind to focus on the current activity.
Engage in, and feel what you are doing.
Enjoy the process.
Learn relaxation techniques in order to be present in each moment.
Take notice of your surroundings - sights, sounds, smells, ambiance.
Listen attentively to the conversation of others, music, even silence.
Savor your food and drink.
Taste each morsel.

Enjoy the journey <3 Namaste
Jenn Schoch, MSN, FNP-BC

Tuesday, September 16, 2014



Hypertension is the medical term for elevated blood pressure. This is a higher than normal pressure within the blood vessels as blood travels through it. High blood pressure in the short term does not cause any significant damage in the body and may even go unnoticed. However, prolonged elevation of the blood pressure can lead to a host of diseases affecting primarily the cardiovascular system and having secondary effects on almost every organ and system in the  body.

Normal and High Blood Pressure
The accurate definition of hypertension is the elevation of arterial blood pressure – pressure against the arterial walls. Pressure within the arteries ensures that there is sufficient force to propel oxygen-rich blood to all the tissues in the body. It also ensures that this force is transmitted through to the veins so that the oxygen-deficient blood can return back to the heart for re-oxygenation at the lungs.
The pressure at which the blood has to be maintained without causing damage to the blood vessels or body is commonly referred to as the normal blood pressure. A systolic pressure of 120 mm Hg and diastolic pressure of 80 mm Hg is considered as a normal blood pressure in adults (120/80 mm Hg). It can be slightly higher or lower and still remain within a normal range.
If it rises significantly above this then it is defined as hypertension according to the criteria below. If the blood pressure is significantly lower than the normal value then it is defined as hypotension (low blood pressure).
With regards to the actual pressure and values, the following criteria need to be present for a diagnosis of hypertension to be established.
a systolic pressure, which is the pressure in the blood vessels during contraction of the heart, exceeding 139 mm Hg.
a diastolic pressure, which is the pressure in the blood vessels while the heart is relaxing and the ventricles filling with blood, exceeding 89 mm Hg.
Ideally, three readings showing an elevated blood pressure of 140/90 mm Hg should be recorded in order for hypertension to be diagnosed.

Types of Hypertension

Hypertension can be broadly divided into benign and malignant.
Benign hypertension includes primary (essential) hypertension and secondary hypertension.
Primary hypertension is also known as essential hypertension or idiopathic hypertension. The exact cause is unknown although the disease mechanism has been established to a large degree and a variety of hypotheses exists as to why it occurs.
Secondary hypertension is a consequence of certain diseases.
Benign hypertension, primary or secondary, can lead to a host of complications over several years or even decades.
Malignant hypertension is also known as accelerated hypertension and accounts for  a minority of hypertension cases. It is a sudden and severe form of hypertension which if left untreated can lead to death within one or two years.
Although the cause of primary hypertension is not fully understood, its close link to obesity and often improvement after weight loss may suggest one or more of the following mechanisms :
1. Cardiac output increased as blood needs to be distributed to a larger body mass.
2. Vascular resistance caused by constriction of the arteries (vasoconstriction) as a result of sympathetic activity and possibly further contributed to by hormonal influence associated with increased fat stores.
3. Salt and water retention is due to greater reabsorption from the renal tubules (kidney) and normal mechanisms for water-electrolyte balance may be disrupted in obesity.

Primary hypertension may therefore be due to a combination of one of more of the factors above. A related concept that is important to understand is the renin-angiotensin system which may lead to vasoconstriction as well as salt and water reabsorption. This system exists to help the body stabilize the blood pressure in the event of a drop in pressure. However, in patients with primary hypertension, this system appears to be overactive. The effects of the renin-angiotensin system is to cause vascular resistance and increase salt and water resistance.

Explaining High Blood Pressure
The simplest way to explain the concept of hypertension is to consider the analogy of the garden hose or hose pipe. The water needs to exit the hose at a certain pressure which will allow it to reach its destination.  The force of the water spraying out at the end is proportional to the pressure within the pipe.
The more a faucet is opened, the higher the pressure of the water and faster the speed of the spraying water. This is related to the cardiac output component of blood pressure explained above.
If the pipe is wider, the pressure is reduced and the water exits at a slower speed. If the pipe is narrower, the pressure within the pipe is greater. This aspect is related to the increased vascular resistance (vasoconstriction).
If a larger than normal volume of water is pushed through a pipe, then the pressure increases just as is the case with water retention.
Benign hypertension, primary or secondary, can lead to a host of complications over several years or eve decades.

Medications For Hypertension

There are several types of drugs to treat hypertension and the use of each is dependent on the severity, duration and type of hypertension. Other underlying diseases also have to be taken into account when prescribing the most appropriate antihypertensive drug, even if the condition is not directly contributing to the raised blood pressure. Antihypertensive drugs work by either reducing the peripheral vascular resistance, cardiac output and/or fluid volume in the body.

The four main groups of antihypertensives based on different mechanisms of action. Hypertension medication may have different names depending on the class of drugs but fall into one or more of these categories  :
Angiotensin II modulators
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin II receptor blockers
Renin inhibitors
Sympathetic (adrenergic) blockers
Centrally acting sympathetic blockers
Autonomic ganglion blockers
Sympathetic nerve terminal blockers
Adrenergic receptor blockers
Alpha blockers
Beta blockers
Thiazides and thiazide-like diuretics
Potassium-sparing diuretics
Loop diuretics
Calcium channel blockers (CCBs)
Vaso-selective blockers
Cardio-selective blockers
Potassium channel openers
Other antihypertensives

Angiotensin Converting Enzyme (ACE) Inhibitors
ACE inhibitors  inhibit formation of angiotensin II from angiotensin I. This includes drugs like captopril, enalapril, lisinopril, benazepril, quinapril, ramipril and perindopril.
ACE inhibitors reduce the constricting actions of angiotensin II on blood vessels and reduces the release of aldosterone. These two effects of reduced angiotensin II levels is primarily responsible for the blood pressure lowering action of ACE inhibitors. Bradykinin is a powerful dilator of blood vessels and it reduces peripheral vascular resistance. ACE inhibitors also inhibits break down of bradykinin and increases the levels of bradykinin. This also assists with lowering the the blood pressure.

ACE inhibitors are most useful in hypertensive patients with concomitant heart failure, diabetes mellitus, diabetic renal diseases (diabetic nephropathy), or hyperlipidemia and following a myocardial infarction (heart attack).
ACE inhibitors are not indicated in hypertensive patients with hypovolemia (low blood volume) as it can cause very low blood pressure (hypo. Use of ACE inhibitors in patients with narrowed renal arteries (renal stenosis) is not recommended as it can further damage the kidney. It is also contraindicated in pregnant women. Most common side effects of ACE inhibitors are a dry cough (due to increased levels of bradykinin) and hyperkalemia (increased levels of potassium of in blood).

Angiotensin II receptor blockers (ARBs)
Angiotensin II receptor blockers reduce blood pressure by blocking the actions of angiotensin II. This includes drugs like  losartan, valsartan, irbesartan, candesartan, telmisartan and olmesartan.
The efficacy, beneficial effects and side effect profile of angiotensin II receptor blockers are similar to that of ACE inhibitors. Unlike ACE inhibitors, the angiotensin II receptor blockers do not have any effect on bradykinin levels. This has resulted in minimal incidence of dry cough associated with angiotensin II receptor blockers.

Renin inhibitors
Renin inhibitor aliskiren decreases the conversion of angiotensin I to angiotensin II and is therefore useful in the treatment of hypertension. The side effects of rennin inhibitor are similar to that of ACE inhibitors.

Centrally Acting Sympathetic Blockers
Centrally acting sympathetic blockers reduce central sympathetic outflow and reduce norepinephrine release from adrenergic nerve endings. This includes drugs like clonidine and methyldopa.
These drugs are useful in treatment of hypertension. Clonidine is also รถuse for treating symptoms of withdrawal from abused drugs and a prominent side effect of its use is sedation. Methyldopa is safe for use in pregnant women with hypertension.

Autonomic Ganglion Blockers
Autonomic ganglion blockers block the ganglionic nicotinic receptors of acetylcholine. These includes drugs like trimethaphan which causes a fall in blood pressure. It is also associated with a wide spread action not limited to cardiovascular system. These drugs are not regularly used for treatment of hypertension.

Sympathetic Nerve Terminal Blockers
Sympathetic nerve terminal blockers reduce sympathetic flow at the sympathetic nerve terminals by interfering with storage and release of noradrenaline. This includes drugs like reserpine and guanethedine.
It is effective in reducing blood pressure but is rarely used at present because of side effects. Reserpine is associated with toxicities like severe depression with suicidal thoughts and drug–induced Parkinsonism.

Adrenergic Receptor Blockers
Alpha blockers
Alpha blockers are effective in treatment of hypertension. This includes drugs like prazosin and terazosin. Alpha blockers are considered to be third-line agents in hypertension.
Alpha blockers reduce the blood pressure by preventing the normal alpha receptor (sympathetic) mediated blood vessel constriction. Alpha blockers also relieve the difficulty in passing urine in patients with prostate enlargement. Alpha blockers are thus ideal for older men with hypertension and prostate enlargement. The most prominent drawback of alpha blockers is the postural hypotension.

Beta blockers
Beta blockers are one of the most important groups of antihypertensive drugs. The group includes drugs like propranolol, atenolol, metoprolol, pindolol, bisoprolol and carvediolol.
Beta blockers reduce blood pressure by reducing the heart rate and its force of contraction. Some of the drugs among them (like atenolol and metoprolol) are very selective in its action on heart. Drugs like propranolol are not selective for heart and have some additional constricting action on bronchi. Beta blockers are useful in treatment of hypertension, cardiac arrhythmias and in controlling symptoms of hyperthyroidism. It is also useful in long term prophylaxis against ischemic heart disease (IHD).

Carvediolol has additional alpha blocking action and is also useful in conditions like heart failure. Use of other beta blockers in heart failure can worsen it. Beta blockers are generally not recommended in patients with concomitant bronchial asthma. It can interfere with awareness and recovery from hypoglycemia (low blood sugar levels) resulting from use of anti-diabetic medicines. Hence, its use in diabetic patients has to be done very cautiously. Beta blockers can also dangerously reduce heart rate in patients with heart block and when combined with other cardiac depressant drugs (like verapamil).

Thiazides and Thiazide-like Diuretics
Thiazide diuretics (like hydrochlorothiazide) are the most important antihypertensive diuretic group. Thiazide diuretics are usually used in combination with potassium-sparing diuretics like spironolactone.
Thiazides are known to cause hypokalemia (low potassium levels), which is countered or prevented with the use of potassium-sparing diuretics. Glucose intolerance and lipid level abnormalities are other common adverse effects of thiazides. It is used in mild to moderate primary hypertension. It is also of use in patients with concomitant mild heart failure.

Potassium-sparing Diuretics
Potassium-sparing diuretics (like spironolactone, eplerenone, amiloride etc) are used along with thiazides or loop diuretics. These drugs combinations act synergistically in lowering blood pressure and in reducing or preventing hypokalemia.

Loop Diuretics
Loop diuretics are less commonly used in long term management of hypertension and includes drugs like furosemide. It may be used along with potassium-sparing diuretics in management of severe hypertension along with other antihypertensive drugs. It may be also be used in patients with concomitant heart failure.

Calcium channel blockers (CCBs)
Calcium channel blockers are important group antihypertensive drugs. Some of the calcium channel blockers block the entry of calcium into vascular smooth muscle cells. This causes vasodilation due to relaxation of the vascular smooth muscle cells. These drugs are called vaso-selective calcium channel blockers.
Some of the CCBs inhibit the calcium channels in the cardiac muscle cells. This results in depression of cardiac functions and subsequent fall in blood pressure.

These are called cardio-selective calcium channel blockers.

Vasoselective calcium channel blockers
Vaso-selective CCBs include amlodipine, felodipine, isradipine, nicardipine, nimodipine and nifedipine. These drugs primarily reduce blood pressure by dilating the blood vessels. This group of drug is used in treatment of hypertension. Hypertensive patients with concomitant peripheral vascular diseases also benefit from vaso-selective CCBs.
Postural hypotension is a common side effect for these drugs. It can also cause increase in heart rate, flushing, edema, and sometimes precipitate cardiac pain (ischemic attack). This group of CCBs can be safely combined with other cardiac suppressant drugs like beta blockers and other drugs like diuretics.

Cardio-Selective Calcium Channel Blockers
Cardio-selective CCBs include verapamil and diltiazem. These drugs reduce blood pressure by suppressing the cardiac function. Heart rate and force of contraction of the heart is therefore also reduced.
This group of drug is used in treatment of hypertension, cardiac arrhythmias and angina pectoris. Heart rate can be dangerously reduced by these drugs occasionally as a side effect. Combining with other cardiac depressants like beta blockers is contraindicated. The group is also contraindicated in heart failure patients.

Nitrates have very potent dilating action on blood vessels but are not used for regular management of hypertension. Nitrates lower blood pressure very quickly and are preferred drugs in hypertensive emergencies (acute development of very high blood pressure). It can be administered intravenously for hypertensive emergencies. Important antihypertensive nitrates include sodium nitroprusside and nitroglycerine. Use of nitrates is associated with severe headache, sweating, palpitation and postural hypotension.

Potassium channel openers
Potassium channel openers like minoxidil produce blood pressure lowering effects by dilation of the blood vessels resulting from relaxation of the vascular smooth muscles. Potassium channel openers are less commonly used as antihypertensive drugs.
Minoxidil is more commonly used for treatment of male-pattern baldness. The use of these drugs as antihypertensive drugs is associated with hirsutism (abnormal facial hair growth in women), sweating, palpitations, and postural hypotension.

Others Antihypertensives
Several other drugs are known to have antihypertensive actions. Hydralazine, diazoxide, and fenoldapam are some of these other types of hypertensives. Hydralazine is available as tablets and for intravenous use. Hydralazine tablets are now rarely used for regular treatment of hypertension. The intravenous preparation is useful in hypertensive emergencies. Diazoxide and fenoldapam are also available as intravenous preparations for use in hypertensive emergencies.

Monday, February 17, 2014

Lupus Journal/Disease Activity Tracker

Please download, print, share my Comprehensive Lupus Journal/Disease Activity Tracker--it is very helpful to fill out and bring to Dr appts..even if you have not been diagnosed yet.

Pain: How To Help Your Doctor Help You

Speaking of Pain: How to Help Your Doctor Help You

Summary of a presentation at the Living with RA Workshop

Seth A. Waldman, MD
Director, Division of Pain Management, Hospital for Special Surgery
Clinical Assistant Professor of Anesthesiology, Weill Cornell Medical College

Rheumatoid arthritis is a systemic, inflammatory, autoimmune disorder. Inflammation causes redness, warmth, and swelling of the joints. Pain comes from the inflammation of the joints and tendons. Physicians seek to combat the inflammation at each phase of the immunologic process with:

Non-steroidal anti-inflammatory drugs (NSAIDs) to control inflammation and pain in general; and
Disease-modifying anti-rheumatic drugs (DMARDs) to combat the overactive cells and their history and to alter the natural history of RA, possibly even halting the development of joint damage.
It's important that the cause of any pain be identified, if possible. People with RA can have pain from many other causes, just as anyone without RA does, and those causes need to be identified and treated, in hopes of curing or controlling the problem without long-term pain medication.

Nonetheless, people with RA still may have chronic pain, as well as acute severe pain episodes, either due to flares or to post-surgical pain. However, pain is often under-reported by patients and/or trivialized as a symptom by physicians.

This is changing, because the Federal government now has a new standard of pain care. It requires physicians to ask patients what they are feeling and what medications they are using, and to do something about the pain - in the same way they check your vital signs (temperature, pulse, and blood pressure) and do something if the signs are abnormal.

Pain Management Programs

Further, major hospitals have been developing dedicated pain management programs. For example, here at the Hospital for Special Surgery we have an acute pain service, which is part of the Anesthesia Department. It includes nurses and anesthesiologists who see you for the first few days after surgery and then transition you to milder medicine that your physician takes care of or a stronger medicine that would be managed by a chronic pain physician. We also have a pain center that manages a lot of outpatients, many of whom have rheumatoid arthritis, who arrive by referral from their rheumatologist or surgeon.

The decision to refer to a pain management specialist has to do with the patient and the comfort level of the physician caring for the patient, based on the doctor's experience with these medications and perception about how the patient is doing. Pain management specialists tend to see patients whose pain has not improved and whose doctors have tried different approaches and can't figure out why the patient has not improved on the more commonly used medications.

Descriptions of Pain

Because pain is so subjective and varies so much from one person to another, it's important for you to be as specific as possible in describing your pain to your physician. Consider the following issues.

On a scale of 1 to 10, how much pain are you having - if 10 is the worst pain you've ever had?
What is the pattern of your pain - where does it arise and where does it spreads to?
What is the duration of your pain - how long does it last - and how often does it occur?
What does your pain feel like? This is very important because the words you use to describe your pain give your doctor clues on its cause as well as what drugs might help it.

Is it a deep aching, throbbing, gnawing or dragging pain? If so, it's probably what doctors call nocioceptive - nerve endings are being injured by some ongoing disorder, such as arthritis. For example, when a joint is being destroyed, the little nerve endings in the body sense that and send a normal pain message just as if it would if you cut your hand - a normal transmission of pain. Or you may have perioperative pain as you recuperate from joint surgery. These are normal, acute types of pain Nocioceptive pain tends to respond well to routine analgesics, such as NSAIDs and opioids that act in the brain.

On the other hand, is it burning, shooting, or tingling pain? If so, it's probably neuropathic pain - caused by abnormal processes that may persist after an injury or disease; nerves that constantly transmit pain become trained, through cellular changes, to transmit pain messages in the absence of an ongoing disorder. In such chronic pain, the symptoms become "imprinted" on your nervous system, which remembers what pain feels like and continues to send those messages, for example, beyond when your surgeon thinks you should be having pain post-operatively. Neuropathic pain responds to so-called adjuvant drugs that affect the brain's perception in unexplained ways. These include antidepressants and antiseizure drugs.

What has been the psychological impact of the pain on you - the degree of suffering - which can vary from the pain person to person from the same type of pain. This can help the physician determine the meaning of the pain for you and what additional treatments (beyond medication) might be useful, such as physical therapy and exercise programs, relaxation therapy and yoga, acupuncture, psychological support for depression or anxiety disorders, which are common in people who have chronic painful illnesses. All of these approaches should be considered in a comprehensive pain management program.

What medications you are taking and in what doses and for how long - and to what extent do they help the pain?
It can be useful to keep a pain diary for a week before seeing your doctor. Note when pain occurs, where it hurts, what it felt like, what you were doing when it hit, how severe it was on a 1 to 10 scale, and what you did to try to reduce the pain and the result of what you did.

Increasing Use of Opioids for Pain Management

After surgery, for acute pain management, some people receive intravenous morphine medication or anesthetic medications that make parts of the body numb. Historically, potent narcotic drugs, such as morphine and codeine, were reserved for people who were terminally ill. Doctors were loath to prescribe them for chronic pain management because of fears of addiction and side effects. However, that attitude has changed dramatically, especially among pain specialists, as these fears have proved unwarranted. These drugs are now used very widely for people who have so-called benign pain (to distinguish it from those who have malignant tumors).

Physicians are increasingly open to prescribing very strong medications when necessary and even maintaining people on those medications after the acute period, such as immediately post-surgery, has passed. Some people can tolerate very high levels of narcotic medications, although you don't want to be on those medications long-term if you can find relief from an alternative, and most people don't need to be on narcotics long-term.

The Range of Pain Medications

Most people can find some medication that they can tolerate and that gives them very good relief. However, your need for pain medication - and the type that gives you relief - may change over time. You need to have a plan for dealing with the different types of pain you have:

the chronic background pain that may be with you frequently or all the time, and
the acute severe pain that may arise - when you don't have time to wait for an appointment with your doctor in two weeks.
Your doctor should work with you to have a "plan b" - with medications to institute - when such acute severe pain arises. Here's the range of medications from which your doctor may choose:

Acetaminophen (Tylenol)
Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen (Motrin, Advil), naproxen (Aleve); diclofenac (Voltaren), and others - with low-dose ones available over the counter and higher-dose ones available by prescription;

Adjuvant drugs, including: antidepressants such as amitriptyline (Elavil), paroxetine (Paxil) and venlaxafine (Effexor) and the SSRIs, such as fluoxitine (Prozac); anti-seizure drugs, such as gabapentin (Neurontin), carbamazepine (Tegretol), phenytoin (Dilantin) and cloazepam (Klonopin); and some anti-hypertension drugs, such as clonidine (Catapres) - although these drugs require your doctor to be comfortable with "off-label" prescribing (using an FDA-approved drug for an indication other than that for which it has been approved;

Opioid-like drugs, such as tramadol (Ultram);
Weak opioids, such as codeine;
Strong opioids, such as morphine;
Controlled-release opioids, such as Oxycontin and MS Contin;
Long-acting opioids, such as skin patches containing fentanyl (Duragesic);
Invasive analgesia, infusing drugs through a tiny catheter inserted into the spinal space.