Autoimmune Disorder Case Study

download Autoimmune Disorder Case Study

of 38

Transcript of Autoimmune Disorder Case Study

  • 7/28/2019 Autoimmune Disorder Case Study

    1/38

    Autoimmune disorder case study

    This case relates to autoimmune disorders; therefore, purposefully look into the medication

    use and vocabulary as they relate to autoimmune patients.

    Vocabulary: Before attempting to work the case study, define each of the vocabulary words.

    Although the words may have several subheadings, it will give you a place to begin your

    inquiry. When reviewing the vocabulary words, you might want to ask several questions:

    who, what, where, when, why and how. This should give you a much broader

    understanding of each word. Try not to give the shortest or simplest answer. Instead, use

    the following example for palliative care: Instead of answering, "Palliative care is special

    care focused on the pain experienced during a chronic or terminal illness," ask: Why would

    a person with an autoimmune disorder need this type of palliative care? Where is this type

    of care most likely to be given? When is this type of care needed? Who is eligible for this

    type of care? How is this different from hospice care? How is it similar to hospice care?

    What types of medications are used in palliative care?

    While defining the remainder of the vocabulary words, ask the following questions:

    1.Autoimmune diseases: What is an autoimmune disease? Who is at risk for an autoimmunedisease?

    Autoimmune diseases arise from an inappropriate immune response of the body againstsubstances and tissues normally present in the body (autoimmunity). This may be

    restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue

    in different places (e.g. Goodpasture's disease which may affect the basement membrane

    in both the lung and the kidney). The treatment of autoimmune diseases is typically with

    immunosuppressionmedication that decreases the immune response. A large number ofautoimmune diseases are recognized

    If you have any of the following risk factors, your chance of developing an autoimmune

    disorder is elevated:

    Gender: female. It's clear that women are at higher risk of developingautoimmune disorders, since they tend to strike women about 75 percent of the

    time. It's not entirely clear why women are more susceptible to autoimmunity,

    but some researchers speculate that women's enhanced immune systems may

    make them more vulnerable to autoimmune disorders. Hormones may also be afactor.

    Age: young to middle-aged. Most autoimmune disorders affect younger andmiddle-aged people. But each disease is different, and disorders such as

    rheumatoid arthritisare more common as people age.

    http://www.everydayhealth.com/arthritis/rheumatoid-arthritis/index.aspxhttp://www.everydayhealth.com/arthritis/rheumatoid-arthritis/index.aspxhttp://www.everydayhealth.com/arthritis/rheumatoid-arthritis/index.aspx
  • 7/28/2019 Autoimmune Disorder Case Study

    2/38

    Ethnicity: African American, American Indian, or Latino. People who are inthese ethnic groups are more likely than Caucasians to develop autoimmune

    disorders.

    Family history of autoimmune disorders. Studies have shown that the tendencyto develop autoimmune disorders can be inherited. If you have family members

    who have autoimmune disorders, your chances of getting the same disorder or

    one that is closely related are higher.

    Exposure to environmental agents. There is some evidence that exposure tocertain things in your environment may increase your risk of developing

    autoimmune disorders. For example, research shows that exposure to some

    medications (for example, procainamide or hydrolyzine) and certain medals

    (for example, mercury, gold, or silver) may be associated with the development

    of autoimmune disorders. But the scientific evidence relating environmental

    exposure to the development of autoimmune disorders is not conclusive, and

    researchers are still working to find out how environmental exposure may play

    a role.

    Previous infection. There is mounting evidence that genetically susceptiblepeople who have had certain bacterial and viral infections may be at risk for

    some types of autoimmune disorders. But it is still unclear exactly how these

    infections may increase the risk of autoimmune disorders, so researchers are

    looking into various proposed mechanisms

    2.Bowel incontinence: What are the causes of bowel incontinence? What are the medicationsused to treat bowel incontinence? Who is at risk for bowel incontinence? Is it considered

    a symptom of a disease or medication induced? Which autoimmune diseases cause bowel

    incontinence?

    Bowel incontinence is the loss of bowel control, leading to an involuntary passage of

    stool. This can range from occasionally leaking a small amount of stool and passing gas,to completely losing control of bowel movements.

    Causes include

    Constipation

    Damage to muscles or nerves of the anus and rectum Diarrhea Pelvic support problems

    Treatments include changes in diet, medicines, bowel training, or surgery.

    MedicationsDepending on the cause of fecal incontinence, the options include:

  • 7/28/2019 Autoimmune Disorder Case Study

    3/38

    Anti-diarrheal drugs Laxatives, if chronic constipation is causing your incontinence Medications to decrease the spontaneous motion of your bowel

    It is more common in women and older adults, but it is not a normal part of aging

    Bowel incontinence is a sign or symptom of a condition or disease; it is not a condition or

    disease in itself.

    Scleroderma can cause constipation, diarrhea, malabsorption, diminished peristalsis, and

    bowel incontinence because it can cause diminished peristalsis

    3. Dysphagia: What is dysphagia? What commonly causes dysphasia? Is itmedication/disease induced? Who is at risk for dysphasia? What are the medication treatments

    for dysphasia? Is this something that a person with certain types of autoimmune disorders mightdevelop?

    Dysphagia is the medical term for the symptom of difficulty in swallowing

    Normally, the muscles in your throat and esophagus squeeze, or contract, to move food

    and liquids from your mouth to your stomach without problems. Sometimes,

    though, food and liquids have trouble getting to your stomach. There are two typesof problems that can make it hard for food and liquids to travel down your

    esophagus:

    The muscles and nerves that help move food through the throat and esophagus arenot working right. This can happen if you have:

    Had a stroke or a brain or spinal cord injury.Certain problems with your nervous system, such as post-polio syndrome,multiple sclerosis, muscular dystrophy, or Parkinson's disease.An immune system problem that causes swelling (or inflammation) and weakness,such as polymyositis or dermatomyositis.

    Esophageal spasm. This means that the muscles of the esophagus suddenlysqueeze. Sometimes this can prevent food from reaching the stomach.

    Scleroderma. In this condition, tissues of the esophagus become hard and narrow.Scleroderma can also make the lower esophageal muscle weak, which may causefood and stomach acid to come back up into your throat and mouth.

    Something is blocking your throat or esophagus. This may happen if you have: Gastroesophageal reflux disease (GERD). When stomach acid backs up regularly

    into your esophagus, it can cause ulcers in the esophagus, which can then cause

    scars to form. These scars can make your esophagus narrower.

    Esophagitis. This is inflammation of the esophagus. This can be caused bydifferent problems, such as GERD or having an infection or getting a pill stuck in

    the esophagus. It can also be caused by an allergic reaction to food or things in the

    air.

    Diverticula. These are small sacs in the walls of the esophagus or the throat.

  • 7/28/2019 Autoimmune Disorder Case Study

    4/38

    Esophageal tumors. These growths in the esophagus may be cancerous or notcancerous.

    Masses outside the esophagus, such as lymph nodes, tumors, orbone spurs on thevertebrae that press on your esophagus.

    A dry mouth can make dysphagia worse. This is because you may not have enough saliva

    to help move food out of your mouth and through your esophagus. A dry mouth can becaused by medicines or another health problem.

    The following are risk factors for difficulty swallowing:

    Aging. Due to natural aging and normal wear and tear on the esophagus, and agreater risk of certain conditions, such as stroke or Parkinson's disease, older adults are at

    higher risk of swallowing difficulties.

    Certain health conditions. People with certain neurological or nervous systemdisorders are more likely to experience difficulty swallowing.

    Diabetes History ofPoliomyelitis Previous treatment for head and neck cancer Progressive neurological disorder or muscle disorder Heartburn-Overview Concussion

    Symptoms of GERD, such as heartburn, if present, are treated with medications designed to

    reduce acid levels in the stomach. These can include:

    antacids; H2 blockers such as nizatidine (Axid),famotidine (Pepcid), cimetidine (Tagamet),orranitidine (Zantac); and

    proton pump inhibitor drugs, such asesomeprazole (Nexium),lansoprazole(Prevacid), omeprazole (Prilosec, Zegerid, Kapodex), pantoprazole

    (Protonix), orrabeprazole (Aciphex).

    Patients with achalasia or other motility disorders of the esophagus can be treated

    with medications that help to relax the lower esophageal sphincter. These include

    the nitrate class of drugs, for example, isosorbide dinitrate(Isordil) and calcium-

    channel blockers, for example, nifedipine (Procardia) and verapamil(Calan). These

    drugs, however, are not very effective, and surgical intervention often is necessary.

    A more recently developed treatment for some types of dysphagia associated with

    esophageal muscle problems caused by spasm is the endoscopic injection ofbotulinum toxin (Botox), for example, into the lower esophageal sphincter toweaken the sphincter in achalasia. Treatment with botulinum toxin is safe, but the

    effects on the sphincter often last only for months, and additional injections are

    necessary.

    Corticosteroids are the treatment for dysphagia caused by eosinophilic esophagitis.

    http://www.thirdage.com/hc/c/heartburn-overviewhttp://www.thirdage.com/hc/c/heartburn-overviewhttp://www.thirdage.com/hc/c/concussionhttp://www.thirdage.com/hc/c/concussionhttp://www.thirdage.com/hc/c/concussionhttp://www.thirdage.com/hc/c/heartburn-overview
  • 7/28/2019 Autoimmune Disorder Case Study

    5/38

    Although dysfunction of the oesophagus is common in autoimmune and inflammatory

    rheumatic diseases, it is usually asymptomatic. Nevertheless, significant swallowing

    difficulties can occur and occasionally dysphagia is severe.

    Although dysfunction of the oesophagus is common in autoimmune and inflammatory

    rheumatic diseases, it is usually asymptomatic. Nevertheless, significant swallowingdifficulties can occur and occasionally dysphagia is severe. Scleroderma is anautoimmune disease can cause the weakening of tissues in the esophagus

    4. Hepatic encephalopathy: What is the pathophysiology of hepatic encephalopathy? Whodevelops hepatic encephalopathy? What is the medication treatment? What body system

    is affected? Is it an autoimmune disorder?

    Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure,particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and motor

    impairments. In these patients, the number of functional liver cells is reduced, and some

    blood is diverted around the liver before toxins are removed. As a result, toxins such asammonia and manganese can accumulate in the blood and enter the brain, where they can

    damage nerve cells and supporting cells called astrocytes

    Sedatives such as benzodiazepines (often used to suppress alcohol withdrawal oranxiety

    disorder), narcotics (used as painkillers or drugs of abuse) and sedativeantipsychotics,

    alcohol intoxication. Lactulose may be given to prevent intestinal bacteria from creating

    ammonia, and as a laxative to remove blood from the intestines. Neomycin may also beused to reduce ammonia production by intestinal bacteria. Rifaximin, a new antibiotic, is

    also effective in hepatic encephalopathy

    5.

    Hyperglycemia: What is the pathophysiology of hyperglycemia? What commonly causehyperglycemia? Why might certain medications induce hyperglycemia? How are people

    with autoimmune diseases affected?

    Hyperglycemia is the technical term for high blood glucose (sugar). High blood glucosehappens when the body has too little insulin or when the body can't use insulin properly.

    A number of things can cause hyperglycemia:

    If you have type 1, you may not have given yourself enough insulin. If you have type 2, your body may have enough insulin, but it is not as effective asit should be.

    You ate more than planned or exercised less than planned. You have stress from an illness, such as a cold or flu. You have other stress, such as family conflicts or school or dating problems. You may have experienced the dawn phenomenon (a surge of hormones that thebody produces daily around 4:00 a.m. to 5:00 a.m.).

    The drugs for treating hyperglycemia fall into several categories:

    http://en.wikipedia.org/wiki/Sedativehttp://en.wikipedia.org/wiki/Benzodiazepinehttp://en.wikipedia.org/wiki/Alcohol_withdrawal_syndromehttp://en.wikipedia.org/wiki/Narcotichttp://en.wikipedia.org/wiki/Analgesiahttp://en.wikipedia.org/wiki/Analgesiahttp://en.wikipedia.org/wiki/Narcotichttp://en.wikipedia.org/wiki/Alcohol_withdrawal_syndromehttp://en.wikipedia.org/wiki/Benzodiazepinehttp://en.wikipedia.org/wiki/Sedative
  • 7/28/2019 Autoimmune Disorder Case Study

    6/38

    (1)Drugs that primarily stimulate insulin secretion by binding to the

    sulfonylurea receptor. Sulfonylureas remain the most widely prescribed drugs

    for treating hyperglycemia. The meglitinide analog repaglinide and the D-phenylalanine derivative nateglinide also bind the sulfonylurea receptor and

    stimulate insulin secretion.

    (2)Drugs that alter insulin action: Metformin works in the liver.Thethiazolidinediones appear to have their main effect on skeletal muscle andadipose tissue.

    (3)Drugs that principally affect absorption of glucose: The -glucosidase

    inhibitors acarbose and miglitol are such currently available drugs .

    (4)Drugs that mimic incretin effect or prolong incretin action: Exenatide and

    DPP 1V inhibitors fall into this category.

    (5)Other: Pramlintide lowers glucose by suppressing glucagon and slowing

    gastric emptying.

    Historically, the agents implicated have included -blockers, thiazide diuretics,

    corticosteroids, niacin, pentamidine, and others.Of recent interest are the increasingnumbers of reported cases of new-onset diabetes mellitus (DM) in patients receivingtreatment with protease inhibitors (PIs) or atypical antipsychotic agents.

    Studies have shown patients with diabetes mellitus have higher risks of autoimmunediseases including thyroid diseases such as but not limited to Hashitomotos,

    rheumatoid arthritis, Crohns disease, and Sjogrens syndrome. Since diagnosis with

    diabetes mellitus is just a milestone of a path of repetitive postprandialhyperglycemia where the mass of the insulin-producing beta cells is reduced to 40-

    60% of the original hyperglycemia is likely the cause of autoimmune diseases.

    Several studies reveal acute hyperglycemia is capable of disrupting the immune

    system including suppressing phagocytosis, promoting inflammation, developingantibody against the glycated immunoglobulin and so on. Thus, hyperglycemia can

    weaken and change the immune system.

    6. Hyperlipidemia: What is the pathophysiology of hyperlipidemia? Who is at risk forhyperlipidemia? What commonly causes hyperlipidemia? Is it medication/disease induced?

    Is there a medication treatment for this?

    Hyperlipidemia is an excess of fatty substances called lipids, largely cholesterol and

    triglycerides, in the blood. It is also called hyperlipoproteinemia because these fatty

    substances travel in the blood attached to proteins. This is the only way that these fattysubstances can remain dissolved while in circulation.

    Hyperlipidemia, in general, can be divided into two subcategories:

    hypercholesterolemia, in which there is a high level ofcholesterol hypertriglyceridemia, in which there is a high level of triglycerides, the mostcommon form offat

    http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P2/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P2/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P4/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P4/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P4/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P4/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P4/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P5/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P5/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P5/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P6/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P6/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P6/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P6/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P6/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P6/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P5/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P4/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P4/http://www.health.am/db/more/drugs-for-treating-hyperglycemia/P2/
  • 7/28/2019 Autoimmune Disorder Case Study

    7/38

    Being overweight or obese, not getting enough exercise, and a diet high in saturated fatand cholesterol and low in fruits, vegetables and fiber can play a role in the development

    of hyperlipidemia. Beyond diet, however, there are other factors that can lead to thiscondition.

    Hyperlipidemia is caused when your diet contains too much cholesterol and fat (e.g.,

    meat, cheese, cream, eggs, shellfish, etc.), when the body produces too much cholesterol

    and fat, or both.

    Fats do not dissolve in water. In order for them to be carried in the blood (which is mostlywater) they combine with another substance called a protein to create a lipoprotein. There

    are three kinds of lipoproteins in the body:

    Low-density lipoprotein (or LDL) High-density lipoprotein (or HDL)

    Triglycerides

    Too much LDL, or bad cholesterol, can build up in the arteries (the blood vessels thatcarry blood throughout the body) and, over time, cause heart disease or stroke. On the

    other hand, having too much HDL, or good cholesterol, protects the heart by helping to

    remove the build up of LDL from the arteries. Low levels of HDL and high triglyceridescan also increase fat build up in the arteries and cause heart disease, especially in people

    who are obese or have diabetes

    Hyperlipidemia can run in families as a genetic disorder:

    Familial hypercholesterolemiaLDL levels are high Familial hypertriglyceridemiaTriglyceride levels are high Familial combined hyperlipidemia Levels of cholesterol,triglycerides, or both are high and HDL is low

    It can also be related to a hormonal disease such as diabetes mellitus, hypothyroidism andCushings syndrome; or to the use of certain medication such as birth control pills,

    hormone therapy, some diuretics (i.e., water pills), or beta-blockers to treat cardiovascular

    diseases.

    Common secondary causes of hypercholesterolemia (specifically, high LDL cholesterol)

    include hypothyroidism (that is, low thyroid hormone levels), pregnancy, and kidney

    failure.

    Common secondary causes of hypertriglyceridemia include diabetes, excess alcoholintake, obesity, and certain prescription medications (such as glucocorticoids and estrogen).

    Hyperlipidemia, along with diabetes, hypertension (high blood pressure), positive familyhistory, and smoking are all major risk factors for coronary heart disease.

    http://www.healthcentral.com/ency/408/000353.htmlhttp://www.healthcentral.com/ency/408/003445.htmlhttp://www.healthcentral.com/encyclopedia/408/571.htmlhttp://www.healthcentral.com/ency/408/001214.htmlhttp://www.healthcentral.com/obesity/obesity-basics-4547-1.htmlhttp://www.healthcentral.com/encyclopedia/408/150.htmlhttp://www.healthcentral.com/high-blood-pressure/introduction-3614-108.htmlhttp://www.healthcentral.com/high-blood-pressure/introduction-11061-108.htmlhttp://www.healthcentral.com/high-blood-pressure/introduction-11061-108.htmlhttp://www.healthcentral.com/high-blood-pressure/introduction-3614-108.htmlhttp://www.healthcentral.com/encyclopedia/408/150.htmlhttp://www.healthcentral.com/obesity/obesity-basics-4547-1.htmlhttp://www.healthcentral.com/ency/408/001214.htmlhttp://www.healthcentral.com/encyclopedia/408/571.htmlhttp://www.healthcentral.com/ency/408/003445.htmlhttp://www.healthcentral.com/ency/408/000353.html
  • 7/28/2019 Autoimmune Disorder Case Study

    8/38

    Hyperlipidemia is treated with changes in diet, weight loss and exercise. If necessary,

    your doctor will also prescribe medication. The type and dose of the medication will

    depend on your specific blood fat levels (rather than total cholesterol) and if you haveheart disease, diabetes, or other risk factors for heart disease.

    The most commonly used and effective drugs for treating high LDL cholesterol are called

    statins. The include lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor),fluvastatin (Lescol), atorvastatin (Lipitor), rosuvastatin (Crestor), and pitivastatin

    (Livalo).

    Other cholesterol-lowering medicines include:

    Bile acid-sequestering resins Ezetimibe Fibrates (such as gemfibrozil and fenofibrate) Nicotinic acid

    7. Inflammation: (include stages and major blood components): What is the pathophysiologyfor inflammation? What commonly causes inflammation? What lab test is ordered toassess for inflammation? Is it medication/disease induced? Who is at risk for

    inflammation? What are the medication treatments for inflammation?

    Inflammation is the body's attempt at self-protection; the aim being to remove

    harmful stimuli, including damaged cells, irritants, or pathogens - and begin the

    healing process

    The initial inflammation phase consists of 3 subphases: acute, subacute, and chronic (orproliferative).

    The acute phase typically lasts 13 days and is characterized by the 5 classic

    clinical signs: heat, redness, swelling, pain, and loss of function.The subacute phase may last from 34 days to about 1 mo and corresponds to a

    cleaning phase required before the repair phase.

    If the subacute phase is not resolved within about 1 mo, then inflammation is said

    to become chronic and can last for several months. Tissue can degenerate and, in thelocomotor system, chronic inflammation may lead to tearing and rupture. Alternatively,

    after the subacute inflammatory phase, tissue can repair and be strengthened during the

    remodeling phase.

    Inflammation may have many different causes. These are the most common:

    Pathogens (germs) like bacteria, viruses or fungi External injuries like scrapes or foreign objects (for example a thorn in yourfinger)

    Effects of chemicals or radiation Diseases or conditions that cause inflammation often have a name ending in -itis. For example:

    http://www.nlm.nih.gov/medlineplus/ency/article/002409.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002409.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002409.htm
  • 7/28/2019 Autoimmune Disorder Case Study

    9/38

    Cystitis, an inflammation of the bladder Bronchitis, an inflammation of the bronchi Otitis media, a middle ear infection Dermatitis, a disease where the skin is inflamed

    The acronym CRP stands forC-reactive protein, a non-specific marker (a

    substance that may indicate disease) that is measured by blood tests. It is produced bythe liver and increases during episodes of acute systemic inflammation. A number of

    studies have suggested that CRP levels might be an indication of an individual's risk for

    heart disease and that, overall, inflammation plays an important role in the development

    of cardiovascular disease. However, in evaluating cardiac risk, physicians look at a verynarrow range of CRP levels (from zero to 3.0 and above). This requires a special test

    called high sensitivity CRP (hs-CRP), which may be able to reveal inflammation going

    on at the micro-vascular level. If this test shows that your CRP is less than 1.0 mg perliter of blood, your risk of heart disease is considered low; if it is between 1.0 and 3.0,

    your risk is average; if it is above 3.0, your risk is high.

    Many steroids, to be specific glucocorticoids, reduce inflammation or swelling by

    binding to glucocorticoid receptors. These drugs are often referred to as corticosteroids.

    Non-steroidal anti-inflammatory drugsNon-steroidal anti-inflammatory drugs (NSAIDs), alleviate pain by counteracting the

    cyclooxygenase (COX) enzyme. On its own, COX enzyme synthesizesprostaglandins,

    creating inflammation. In whole, the NSAIDs prevent the prostaglandins from everbeing synthesized, reducing or eliminating the pain.

    Some common examples of NSAIDs are: aspirin, ibuprofen, and naproxen. The newer

    specific COX-inhibitors - although, it is presumed, sharing a similar mode of action -

    are not classified together with the traditional NSAIDs.

    On the other hand, there are analgesics that are commonly associated with anti-

    inflammatory drugs but that have no anti-inflammatory effects. An example

    isparacetamol, called acetaminophen in the U.S. and sold under the brand name of

    Tylenol. As opposed to NSAIDs, which reduce pain and inflammation by inhibiting

    COX enzymes, paracetamol has recently been shown to block the reuptake of

    endocannabinoids, which only reduces pain, likely explaining why it has minimal effect

    on inflammation.

    Long-term use of NSAIDs can cause gastric erosions, which can become stomach

    ulcers and in extreme cases can cause severe haemorrhage, resulting in death. The risk

    of death as a result of use of NSAIDs is 1 in 12,000 for adults aged 1645. The risk

    increases almost twentyfold for those over 75. Other dangers of NSAIDs are

    exacerbating asthma and causing kidney damage. Apart from aspirin, prescription and

    over-the-counter NSAIDs also increase the risk ofmyocardial infarction and stroke.

    http://en.wikipedia.org/wiki/Steroidhttp://en.wikipedia.org/wiki/Glucocorticoidhttp://en.wikipedia.org/wiki/Receptor_(biochemistry)http://en.wikipedia.org/wiki/Corticosteroidhttp://en.wikipedia.org/wiki/Cyclooxygenasehttp://en.wikipedia.org/wiki/Prostaglandinshttp://en.wikipedia.org/wiki/Aspirinhttp://en.wikipedia.org/wiki/Ibuprofenhttp://en.wikipedia.org/wiki/Naproxenhttp://en.wikipedia.org/wiki/Analgesichttp://en.wikipedia.org/wiki/Paracetamolhttp://en.wikipedia.org/wiki/Acetaminophenhttp://en.wikipedia.org/wiki/Tylenolhttp://en.wikipedia.org/wiki/Endocannabinoidshttp://en.wikipedia.org/wiki/Stomach_ulcershttp://en.wikipedia.org/wiki/Stomach_ulcershttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Stomach_ulcershttp://en.wikipedia.org/wiki/Stomach_ulcershttp://en.wikipedia.org/wiki/Endocannabinoidshttp://en.wikipedia.org/wiki/Tylenolhttp://en.wikipedia.org/wiki/Acetaminophenhttp://en.wikipedia.org/wiki/Paracetamolhttp://en.wikipedia.org/wiki/Analgesichttp://en.wikipedia.org/wiki/Naproxenhttp://en.wikipedia.org/wiki/Ibuprofenhttp://en.wikipedia.org/wiki/Aspirinhttp://en.wikipedia.org/wiki/Prostaglandinshttp://en.wikipedia.org/wiki/Cyclooxygenasehttp://en.wikipedia.org/wiki/Corticosteroidhttp://en.wikipedia.org/wiki/Receptor_(biochemistry)http://en.wikipedia.org/wiki/Glucocorticoidhttp://en.wikipedia.org/wiki/Steroid
  • 7/28/2019 Autoimmune Disorder Case Study

    10/38

    8. Inflammatory cardiomyopathy: What is the pathophysiology of inflammatorycardiomyopathy? Who develops this disorder? What is the medication treatment? What bodysystem is affected? How would this be classified as an autoimmune disorder?

    Myocarditis orinflammatory cardiomyopathyis inflammation of heart muscle(myocardium).

    Myocarditis is most often due to infectionby common viruses, such asparvovirus B19,

    less commonly nonviral pathogens such asBorrelia burgdorferi(Lyme disease) or

    Trypanosoma cruzi, or as a hypersensitivity response to drugs.[1]

    The definition of myocarditis varies, but the central feature is an infection of the heart,

    with an inflammatory infiltrate, and damage to the heart muscle,withoutthe blockage of

    coronary arteries that define a heart attack(myocardial infarction) or other common

    noninfectious causes

    Myocarditis is often an autoimmune reaction. Streptococcal M proteinandcoxsackievirus B have regions (epitopes) that are immunologically similar to

    cardiac myosin. During and after the viral infection, the immune system may attack

    cardiac myosin.[1]

    Viruses commonly associated with myocarditis include coxsackievirus B, which can

    cause symptoms similar to a mild case of flu; the viruses that cause the common cold

    (adenovirus); and parvovirus B19, which causes a rash called fifth disease.

    Gastrointestinal infections (echoviruses), mononucleosis (Epstein-Barr virus) and

    German measles (rubella) also are causes of myocarditis. Myocarditis is also common

    in people with HIV, the virus that causes AIDS.

    Bacteria. Numerous bacteria may cause myocarditis, including staphylococcus,streptococcus, the bacteria that causes diphtheria and the tick-borne bacterium

    responsible for Lyme disease.

    Parasites. Among these are such parasites as Trypanosoma cruzi and toxoplasma,including some that are transmitted by insects and can cause a condition called Chagas'

    disease. This disease is more prevalent in Central and South America than in the

    United States, but it can occur in travelers and in immigrants from that part of the

    world.

    Fungi. Some yeast infections (such as candida), molds (such as aspergillus) andother fungi (such as histoplasma, often found in bird droppings) can sometimes cause

    myocarditis

    n many cases myocarditis improves, either on its own or with treatment, leading to a

    complete recovery. Myocarditis treatment focuses on treating the underlying cause.

    In mild cases, your doctor may tell you to rest and may prescribe medications to help

    your body fight off the infection causing myocarditis while your heart recovers. If

    http://en.wikipedia.org/wiki/Cardiomyopathyhttp://en.wikipedia.org/wiki/Cardiomyopathyhttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Myocardiumhttp://en.wikipedia.org/wiki/Infectionhttp://en.wikipedia.org/wiki/Virushttp://en.wikipedia.org/wiki/Parvovirus_B19http://en.wikipedia.org/wiki/Borrelia_burgdorferihttp://en.wikipedia.org/wiki/Borrelia_burgdorferihttp://en.wikipedia.org/wiki/Borrelia_burgdorferihttp://en.wikipedia.org/wiki/Trypanosoma_cruzihttp://en.wikipedia.org/wiki/Trypanosoma_cruzihttp://en.wikipedia.org/wiki/Myocarditis#cite_note-Cooper-1http://en.wikipedia.org/wiki/Myocarditis#cite_note-Cooper-1http://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/M_protein_(Streptococcus)http://en.wikipedia.org/wiki/Coxsackievirushttp://en.wikipedia.org/wiki/Epitopehttp://en.wikipedia.org/wiki/Myosinhttp://en.wikipedia.org/wiki/Myocarditis#cite_note-Cooper-1http://en.wikipedia.org/wiki/Myocarditis#cite_note-Cooper-1http://en.wikipedia.org/wiki/Myocarditis#cite_note-Cooper-1http://en.wikipedia.org/wiki/Myosinhttp://en.wikipedia.org/wiki/Epitopehttp://en.wikipedia.org/wiki/Coxsackievirushttp://en.wikipedia.org/wiki/M_protein_(Streptococcus)http://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Myocarditis#cite_note-Cooper-1http://en.wikipedia.org/wiki/Trypanosoma_cruzihttp://en.wikipedia.org/wiki/Borrelia_burgdorferihttp://en.wikipedia.org/wiki/Parvovirus_B19http://en.wikipedia.org/wiki/Virushttp://en.wikipedia.org/wiki/Infectionhttp://en.wikipedia.org/wiki/Myocardiumhttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Cardiomyopathy
  • 7/28/2019 Autoimmune Disorder Case Study

    11/38

    bacteria are causing the infection, your doctor will prescribe antibiotics. Although

    antiviral medications are available, they haven't proven effective in the treatment of

    most cases of myocarditis.

    Certain rare types of viral myocarditis, such as giant cell and eosinophilic

    myocarditis, respond to corticosteroids or other medications to suppress the

    immune system response. In some cases caused by chronic illnesses, such as

    lupus, the treatment is directed at the underlying disease.

    Drugs to help your heart

    If myocarditis is causing heart failure or rapid or irregular heartbeats as a

    symptom, your doctor may hospitalize you. You may receive drugs to regulate

    your heartbeat. If your heart is weak, your doctor may prescribe medications to

    reduce your heart's workload or help you eliminate excess fluid. These

    medications may include:

    Angiotensin-converting enzyme (ACE) inhibitors, such as enalapril(Vasotec), captopril (Capoten), lisinopril (Zestril, Prinivil) and ramipril (Altace),

    which relax the blood vessels in your heart and help blood flow more easily

    Angiotensin II receptor blockers (ARBs), such as losartan (Cozaar) andvalsartan (Diovan), which relax the blood vessels in your heart and help blood

    flow more easily

    Beta blockers, such as metoprolol (Toprol-XL) and carvedilol (Coreg),which work in multiple ways to treat heart failure and help control irregular or fastheart rhythms

    Diuretics, such as furosemide (Lasix), which relieve sodium and fluidretention

    Treating severe cases

    In some severe cases of myocarditis, aggressive treatment may be necessary, such

    as:

    Intravenous (IV) medications. IV delivery of medications may improve theheart-pumping function more quickly.

    A temporary artificial heart (ventricular assist device). These devices,which can be implanted or worn outside the body, take over part of the heart's job

    of moving blood in and out.

  • 7/28/2019 Autoimmune Disorder Case Study

    12/38

    A pump in the aorta (intra-aortic balloon pump). In this procedure, aballoon is surgically inserted into the aorta. As the balloon inflates and deflates, it

    helps to increase blood flow and decrease the workload on the heart.

    Increasing the oxygen content of the blood (extracorporeal membraneoxygenation, or ECMO). With severe heart failure, doctors sometimes recommendthe use of this device to provide oxygen to the body. When blood is removed from

    the body, it passes through a special membrane in the ECMO machine that

    removes carbon dioxide and adds oxygen to the blood. The newly oxygenated

    blood is then returned to the body. The ECMO machine takes over the work of the

    heart. This treatment is used to allow the heart to recover or while waiting for

    other treatments, such as heart transplant.

    In the most severe cases, doctors may consider urgent heart transplantation

    9. Kyphosis: What is the pathophysiology of kyphosis? Who is at risk for kyphosis? Where iskyphosis seen? Is there a medication treatment for kyphosis?

    Kyphosis is a forward rounding of your upper back. Some rounding is normal, but theterm "kyphosis" usually refers to an exaggerated roundingsometimes called round

    back or hunchback. While kyphosis can occur at any age, it's most common in older

    women where the deformity is known as a dowager's hump.

    Kyphosis occurs when the vertebrae in the upper back become more wedge-

    shaped. This deformity can be caused by a variety of problems, including:

    Osteoporosis. This bone-thinning disorder can result in crushed vertebrae(compression fractures). Osteoporosis is most common in elderly women and

    in people who have taken high doses of corticosteroids for long periods of

    time.

    Disk degeneration. Soft circular disks act as cushions between spinalvertebrae. With age, these disks dry out and shrink, which often worsens

    kyphosis.

    Cancer and cancer treatments. Cancer in the spine can weaken vertebrae andmake them more prone to compression fractures, as can cancer treatmentssuch as chemotherapy and radiation.

    Scheuermann's disease. The kyphosis associated with Scheuermann's disease,a hereditary disorder, typically begins during the growth spurt that occurs

    before puberty. Boys are affected more often than are girls.

  • 7/28/2019 Autoimmune Disorder Case Study

    13/38

    Birth defects. In rare cases, a baby's spinal column doesn't develop properly inthe womb, which can result in kyphosis.

    An exaggerated curve in the upper spine also can be caused by slouching. Called

    postural kyphosis, this problem doesn't involve any deformities in the spine. It's

    most common in teenagers, particularly girls.

    Certain groups of people are at higher risk of kyphosis:

    Adolescent girls with poor posture are at greater risk of postural kyphosis. Boys between the ages of 10 and 15 are at greater risk of Scheuermann'skyphosis.

    Older adults with osteoporosis are at greater risk of spinal fractures thatcan contribute to kyphosis.

    People who have connective tissue disorders, such as Marfan syndrome,also are at greater risk.

    Therapy

    Some types of kyphosis can be helped by:

    Exercises. Stretching exercises can improve spinal flexibility. Exercisesthat strengthen the abdominal muscles may help improve posture.

    Bracing. Children who have Scheuermann's disease may be able to stopthe progression of kyphosis by wearing a body brace while their bones are stillgrowing.

    10 Multiple sclerosis: What is the pathophysiology of multiple sclerosis (MS)? Who developsMS? What is the medication treatment? What body system is affected? Is it an autoimmune

    disorder?

    Multiple sclerosis (MS) is a potentially debilitating disease in which your body's immunesystem eats away at the protective sheath (myelin) that covers your nerves. Damage to

    myelin causes interference in the communication between your brain, spinal cord and

    other areas of your body. This condition may result in deterioration of the nerves

    themselves, a process that's not reversible

    Several factors may increase your risk of developing multiple sclerosis,

    including:

  • 7/28/2019 Autoimmune Disorder Case Study

    14/38

    Age. Multiple sclerosis can occur at any age, but most commonly affectspeople who are ages 20 to 40.

    Gender. Women are about twice as likely as men to develop multiplesclerosis.

    Family history. If one of your parents or siblings has multiple sclerosis,you have a 1 to 3 percent chance of developing the diseaseas compared with

    the risk in the general population, which is just a tenth of 1 percent.

    However, the experiences of identical twins show that heredity can't be the only

    factor involved. If multiple sclerosis was determined solely by genetics, identical

    twins would have identical risks. However, an identical twin has only about a 30

    percent chance of developing multiple sclerosis if his or her twin already has the

    disease.

    Certain infections. A variety of viruses, such as Epstein-Barr virus andothers, appear to be associated with multiple sclerosis. Researchers study how

    some infections may be linked to the development of multiple sclerosis.

    Ethnicity. White people, particularly those whose families originated innorthern Europe, are at highest risk of developing multiple sclerosis. People of

    Asian, African or Native American descent have the lowest risk.

    Geographic regions. Multiple sclerosis is far more common in areas suchas Europe, southern Canada, northern United States, New Zealand and

    southeastern Australia. Researchers study why multiple sclerosis appears to morecommon in certain geographic regions.

    If a child moves from a high-risk area to a low-risk area, or vice versa, he or she

    tends to acquire the risk level associated with his or her new home area. But if the

    move occurs after puberty, the young adult usually retains the risk level

    associated with his or her first home.

    Other autoimmune diseases. You may be slightly more likely to developmultiple sclerosis if you have thyroid disease, type 1 diabetes or inflammatory

    bowel disease

    Multiple sclerosis (MS) has no cure. Treatment usually focuses on strategies to

    treat MS attacks, manage symptoms and reduce the progress of the disease. Some

    people have such mild symptoms that no treatment is necessary.

    Strategies to treat attacks

  • 7/28/2019 Autoimmune Disorder Case Study

    15/38

    Corticosteroids. Corticosteroids are mainly used to reduce theinflammation that spikes during a relapse. Examples include oral prednisone and

    intravenous methylprednisolone (Solu-Medrol). Side effects may include mood

    swings, seizures, weight gain and an increased risk of infections.

    Plasma exchange (plasmapheresis). This procedure removes some bloodfrom your body and mechanically separates your blood cells from your plasma,

    the liquid part of your blood. Doctors then mix your blood cells with a

    replacement solution and return the blood to your body.

    11.Myasthenia gravis: What is the pathophysiology of myasthenia gravis? Who developmyasthenia gravis? What is the medication treatment? What body system is affected? Is it an

    autoimmune disorder?

    Myasthenia gravis is a neuromuscular disorder. Neuromuscular disorders involve

    the muscles and the nerves that control them.

    Myasthenia gravis is a type ofautoimmune disorders. An autoimmune disorder

    occurs when the immune system mistakenly attacks healthy tissue. In people with

    myasthemia gravis, the body produces antibodies that block the muscle cells from

    receiving messages (neurotransmitters) from the nerve cell.

    The exact cause of myasthenia gravis is unknown. In some cases, it may be

    associated with tumors of the thymus (an organ of the immune system).

    Myasthenia gravis can affect people at any age. It is most common in young

    women and older men.

    Myasthenia gravis causes weakness of the voluntary (skeletal) muscles. Voluntary

    muscles are those that are under your control. In other words, you think aboutmoving your arm, and it moves. The muscle weakness of myasthenia gravis

    worsens with activity and improves with rest.

    The muscle weakness can lead to a variety of symptoms, including:

    Breathing difficultybecause of weakness of the chest wall muscles Chewing or swallowing difficulty, causing frequent gagging, choking, ordrooling

    Difficulty climbing stairs, lifting objects, or rising from a seated position Difficulty talking Drooping head Facial paralysis or weakness of the facial muscles Fatigue Hoarseness or changing voice Double vision Difficulty maintaining steady gaze Eyelid drooping

    http://www.nlm.nih.gov/medlineplus/ency/article/000816.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002223.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003075.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000733.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000047.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003048.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003048.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003028.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003088.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003088.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003054.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003054.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003029.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003029.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003035.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003035.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003035.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003029.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003054.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003088.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003028.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003048.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000047.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000733.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003075.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002223.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000816.htm
  • 7/28/2019 Autoimmune Disorder Case Study

    16/38

    There is no known cure for myasthenia gravis. However, treatment may allow you

    to have prolonged periods without any symptoms (remission).

    Lifestyle changes often help you continue your daily activities. The following

    may be recommended:

    Scheduling rest periods An eye patch if double vision is bothersome Avoiding stress and heat exposure, which can make symptoms worseMedications that may be prescribed include:

    Neostigmine or pyridostigmine to improve the communication between thenerves and the muscles

    Prednisone and other medications (such as azathioprine, cyclosporine, ormycophenolate mofetil) if to suppress the immune system response, if you have

    severe symptoms and other medicines have not worked well

    12.Myopathy: polymyositis (PM): What commonly causes myopathy? Is it medication/diseaseinduced? Who is at risk for myopathy? What are the medication treatments for myopathy?

    Polymyositis is a persistent inflammatory muscle disease that causes weakness of

    the skeletal muscles, which control movement. Medically, polymyositis is

    classified as a chronic inflammatory myopathyone of only three such diseases.

    Polymyositis can occur at any age, but it mostly affects adults in their 30s, 40s or

    50s. It's more common in blacks than in whites, and women are affected more

    often than men are. Polymyositis signs and symptoms usually develop gradually,

    over weeks or months.

    Remissionsperiods during which symptoms spontaneously disappearare

    rare in polymyositis. However, treatment can improve your muscle strength and

    function.

    The exact cause of polymyositis is unknown, but the disease shares many

    characteristics with autoimmune disorders, in which your immune system attacks

    normal body components. Normally, your immune system works to protect your

    healthy cells from attacks by foreign substances, such as bacteria and viruses. Ifyou have polymyositis, an unknown cause may act as a trigger for your immune

    system to begin producing autoimmune antibodies (autoantibodies) that attackyour body's own tissues. Many people with polymyositis show a detectable level

    of autoantibodies in their blood.

    For most people, the first step in treatment for polymyositis is to take a

    corticosteroid medication. Usually for polymyositis, the chosen medication isprednisone.

  • 7/28/2019 Autoimmune Disorder Case Study

    17/38

    Corticosteroids are medications that suppress your immune system, limiting the

    production of antibodies and reducing muscle inflammation, as well as improving

    muscle strength and function.

    13.Occupational therapy: What is occupational therapy (OT)? Who benefits from OT?How would OT benefit someone with an autoimmune disease? How is it different from

    physical therapy?

    Occupational therapy (also abbreviated as OT) is the use of treatments to

    develop, recover, or maintain the daily living and work skills of patients with a

    physical, mental or developmental condition. Occupational therapy is a client-

    centered practice that places a premium on the progress towards the clients goals.Occupational therapy interventions focus on adapting the environment, modifying

    the task, teaching the skill, and educating the client/family in order to increase

    participation in and performance of daily activities, particularly those that are

    meaningful to the client.

    14.Osteoporosis: What is the pathophysiology for osteoporosis? Who is at risk forosteoporosis? When is osteoporosis most commonly seen? Is it medication/disease

    induced? What are the medication treatments for osteoporosis? What is the difference

    between osteoporosis and osteoarthritis? What are the medications used tor osteoporosis?Osteoporosis causes bones to become weak and brittleso brittle that a fall or

    even mild stresses like bending over or coughing can cause a fracture.

    Osteoporosis affects men and women of all races. But white and Asian women

    especially those who are past menopauseare at highest risk. Medications,

    dietary supplements and weight-bearing exercise can help strengthen your bones.

    Most people reach their peak bone mass by their early 20s. As people age, bonemass is lost faster than it's created.

    How likely you are to develop osteoporosis depends partly on how much bone

    mass you attained in your youth. The higher your peak bone mass, the more bone

    you have "in the bank" and the less likely you are to develop osteoporosis as you

    age.

    Unchangeable risks

    Some risk factors for osteoporosis are out of your control, including: Your sex. Women are much more likely to develop osteoporosis than aremen.

    Age. The older you get, the greater your risk of osteoporosis. Race. You're at greatest risk of osteoporosis if you're white or of Asiandescent.

  • 7/28/2019 Autoimmune Disorder Case Study

    18/38

    Family history. Having a parent or sibling with osteoporosis puts you atgreater risk, especially if you also have a family history of fractures.

    Frame size. Men and women who have small body frames tend to have ahigher risk because they may have less bone mass to draw from as they age.

    Hormone levels

    Osteoporosis is more common in people who have too much or too little of certain

    hormones in their bodies. Examples include:

    Sex hormones. The reduction of estrogen levels at menopause is one of thestrongest risk factors for developing osteoporosis. Women may also experience a

    drop in estrogen during certain cancer treatments. Men experience a gradual

    reduction in testosterone levels as they age. And some treatments for prostate

    cancer reduce testosterone levels in men. Lowered sex hormone levels tend to

    weaken bone.

    Thyroid problems. Too much thyroid hormone can cause bone loss. Thiscan occur if your thyroid is overactive or if you take too much thyroid hormone

    medication to treat an underactive thyroid.

    Other glands. Osteoporosis has also been associated with overactiveparathyroid and adrenal glands.

    Dietary factors

    Osteoporosis is more likely to occur in people who have:

    Low calcium intake. A lifelong lack of calcium plays a major role in thedevelopment of osteoporosis. Low calcium intake contributes to diminished bone

    density, early bone loss and an increased risk of fractures.

    Eating disorders. People who have anorexia are at higher risk ofosteoporosis. Low food intake can reduce the amount of calcium ingested. In

    women, anorexia can stop menstruation, which also weakens bone.

    Weight-loss surgery. A reduction in the size of your stomach or a bypass ofpart of the intestine limits the amount of surface area available to absorb nutrients,

    including calcium.

    Steroids and other medications

    Long-term use of corticosteroid medications, such as prednisone and cortisone,

    interferes with the bone-rebuilding process. Osteoporosis has also been associated

    with medications used to combat or prevent:

    Seizures

  • 7/28/2019 Autoimmune Disorder Case Study

    19/38

    Depression Gastric reflux Cancer Transplant rejectionLifestyle choices

    Some bad habits can increase your risk of osteoporosis. Examples include:

    Sedentary lifestyle. People who spend a lot of time sitting have a higherrisk of osteoporosis than do their more-active counterparts. Any weight-bearing

    exercise is beneficial for your bones, but walking, running, jumping, dancing and

    weightlifting seem particularly helpful for creating healthy bones.

    Excessive alcohol consumption. Regular consumption of more than twoalcoholic drinks a day increases your risk of osteoporosis, possibly becausealcohol can interfere with the body's ability to absorb calcium.

    Tobacco use. The exact role tobacco plays in osteoporosis isn't clearlyunderstood, but researchers do know that tobacco use contributes to weak bones.

    TREATMENT:

    BisphosphonatesFor both men and women, the most widely prescribed osteoporosis medications

    are bisphosphonates. Examples include:

    Alendronate (Fosamax) Risedronate (Actonel, Atelvia) Ibandronate (Boniva) Zoledronic acid (Reclast, Zometa)Side effects include nausea, abdominal pain, difficulty swallowing, and the risk of

    an inflamed esophagus or esophageal ulcers. Injected forms of bisphosphonates

    don't cause stomach upset. And it may be easier to schedule a quarterly or yearly

    injection than to remember to take a weekly or monthly pill.

    Long-term bisphosphonate therapy has been linked to a rare problem in which theupper thighbone cracks, but doesn't usually break completely. Bisphosphonates

    also have the potential to affect the jawbone. Osteonecrosis of the jaw is a rare

    condition occurring after a tooth extraction in which a section of jawbone dies and

    deteriorates.

  • 7/28/2019 Autoimmune Disorder Case Study

    20/38

    Hormone-related therapy

    Estrogen, especially when started soon after menopause, can help maintain bone

    density. However, estrogen therapy can increase a woman's risk of blood clots,

    endometrial cancer, breast cancer and possibly heart disease.

    Raloxifene (Evista) mimics estrogen's beneficial effects on bone density in

    postmenopausal women, without some of the risks associated with estrogen.

    Taking this drug may also reduce the risk of some types of breast cancer. Hot

    flashes are a common side effect. Raloxifene also may increase your risk of blood

    clots.

    In men, osteoporosis may be linked with a gradual age-related decline in

    testosterone levels. Testosterone replacement therapy can help increase bone

    density.

    Less common osteoporosis medications

    If you can't tolerate the more common treatments for osteoporosisor if they

    don't work well enoughyour doctor might suggest trying:

    Teriparatide (Forteo). This powerful drug uses parathyroid hormone tostimulate new bone growth. It's given by injection under the skin. Long-term

    effects are still being studied, so therapy is recommended for two years or less.

    Denosumab (Prolia, Xgeva). Compared to bisphosphonates, denosumabproduces similar or better results while targeting a different step in the bone

    remodeling process. Denosumab is delivered via a shot under the skin every six

    months. The most common side effects are back and muscle pain.

    Calcitonin, salmon (Fortical, Miacalcin). A substance produced by thethyroid gland, calcitonin reduces bone resorption and may slow bone loss. It's

    usually administered as a nasal spray and may cause nasal irritation in some

    people. It is the least effective of the available therapies.

    Osteoarthritis is a painful, degenerative joint disease that often involves the hips,

    knees, neck, lower back, or the small joints of the hands.

    Osteoarthritis usually develops in joints that are injured by repeated overuse in the

    performance of a particular job or a favorite sport or from carrying around excessbody weight. Eventually this injury or repeated impact thins or wears away the

    cartilage that cushions the ends of the bones in the joint so that the bones rub

    together, causing a grating sensation. Joint flexibility is reduced, bony spurs

    develop, and the joint swells. Usually, the first symptom a person has withosteoarthritis is pain that worsens following exercise or immobility.

    http://arthritis.about.com/od/oa/http://arthritis.about.com/od/oa/
  • 7/28/2019 Autoimmune Disorder Case Study

    21/38

    15.Palliative Care: Refer to above questions.palliative medicine is appropriate for patients in all disease stages, including thoseundergoing treatment for curable illnesses and those living with chronic diseases, as well

    as patients who are nearing the end of life. Palliative medicine utilizes a multidisciplinary

    approach to patient care, relying on input from physicians, pharmacists, nurses, chaplains,social workers, psychologists, and other allied health professionals in formulating a planof care to relieve suffering in all areas of a patient's life. This multidisciplinary approach

    allows the palliative care team to address physical, emotional, spiritual, and social

    concerns that arise with advanced illness.

    Pallitive care refers to Nonpharmacologic interventions:

    Exercise Other lifestyle interventions, such as smoking cessation; reduction or eliminationof alcohol and caffeine

    2.Measures to prevent falls3.Individualized pharmacologic interventions:

    Calcium and vitamin D supplementation Bisphosphonates: alendronate, etidronate, ibandronate, pamidronate, risedronate,zoledronic acid

    Calcitonin nasal spray Raloxifene (selective estrogen receptor modulator) Teriparatide (parathyroid hormone)

    4.Treatment of symptoms related to skeletal deformity Treatment of acute and chronic pain (analgesics, calcitonin, ice packs, exercise) Kypho-orthosis with weights Vertebroplasty and kyphoplasty as palliative treatment of patients with severepersistent pain

    5.Measures to improve function and prevent serious complications, particularly measures toprevent falls or reduce the frequency of falling

    6.Periodic assessment, monitoring, and documentation of patient's progress7.Monitoring for side effects of osteoporosis treatments

    16.Panniculitis: What is the pathophysiology of panniculitis? Who usually developspanniculitis? What is the treatment? What body system is affected? Why might a person with

    an autoimmune disorder develop panniculitis?

    Panniculitis is a group of diseases whose hallmark is inflammation of

    subcutaneous adipose tissue (the fatty layer under the skin - panniculus adiposus).

    Symptoms include tender skin nodules, and systemic signs such as weight lossand fatigue.

    Restated, an inflammatory disorder primarily localized in the subcutaneous fat is

    termed a "panniculitis," a group of disorders that may be challenging both for the

    clinician and the dermatopathologist

    http://en.wikipedia.org/wiki/Clinical_pharmacyhttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Subcutaneoushttp://en.wikipedia.org/wiki/Adiposehttp://en.wikipedia.org/wiki/Panniculus_adiposushttp://en.wikipedia.org/wiki/Nodule_(dermatology)http://en.wikipedia.org/wiki/Weight_losshttp://en.wikipedia.org/wiki/Fatigue_(physical)http://en.wikipedia.org/wiki/Fatigue_(physical)http://en.wikipedia.org/wiki/Weight_losshttp://en.wikipedia.org/wiki/Nodule_(dermatology)http://en.wikipedia.org/wiki/Panniculus_adiposushttp://en.wikipedia.org/wiki/Adiposehttp://en.wikipedia.org/wiki/Subcutaneoushttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Clinical_pharmacy
  • 7/28/2019 Autoimmune Disorder Case Study

    22/38

    The Case:

    You are interviewing a 62-year-old female. She is 5'4" tall. Over a period of2-3 weeks,she noticed that she would have difficulty lifting her granddaughter into the air to play. She

    thought that maybe the child was just growing bigger. Today, she noticed that she could not place

    dishes on the top shelf in her kitchen~ she stated that her arms "would not move." She noticedthat when she walked up a flight of stairs yesterday for exercise, her hips and thighs did not seemto want to work very well either. Her son has brought her to the clinic.

    Recent History:

    The patient states that she has always been mostly healthy. She has a new grandchild and

    has had no recent cold or virus that she can remember. The only new medication that she

    remembers is Tagamet (cimetidine). She is worried that she may have multiple sclerosis. Her sonhad placed all her present medications in a bag, which she brought with her.

    Home Medications:

    Aspirin (Ecotrin) 325 mg orally daily

    Cimetidine (Tagamet) 300 mg 4 times a day orally

    Diltiazem hydrochloride (Cardizem) 120 mg daily orally

    Ferrous sulfate 1 tab daily orally

    Levothyroxine sodium (Synthroid) 112 mcg daily orally

    Sulfamethoxazole and trimethoprim (abbreviated TMP-SMZ; trade name: Bactrim) 1 tab

    every 12 hours for 7 days (2 tabs remaining)

    Tolterodine tartrate (Detrol) 2 mg twice a day orally

    What do we know about the above medications? Do we know the recommended dose of,

    the recommended route for, and the best time of day to give these medications? Do we know what

    lab results we need regarding each medication? Do we know the approved use of eachmedication? Do we know the most common diseases treated by the listed medications? Are any

    off-label uses approved for each drug?

    Classification, indication, side effects, adverse runs, and nursing implications

    I Aspirina.) Basics (Mechanism of Action/Pharmacokinetics) Mechanism of Action Blocks pain impulses in the central nervous system Reduces inflammation by inhibition of prostaglandin synthesis Antipyretic action results from vasodilation of peripheral vessels Decreases platelet aggregation Pharmacokinetics

  • 7/28/2019 Autoimmune Disorder Case Study

    23/38

    Enteric metabolized by liver Inactive metabolites excreted by kidneys Half life is 15-30 minutes when taken PO Peak 1-2 hours and duration is 4-6 hours well-absorbedb.) Recommended dose/route/and time of day to administer:

    In Adults typically administered orally, but can be administered rectally. Usualdose is 75-325mg, though can be dosed up to 800mg qid in appropriate clinical scenarios

    Typically administered with food or milk to decrease potential for gastritis orother gastrointestinal symptoms

    Given in scheduled doses or prn depending on use of medicationc.) Relevant labs: Though no particular lab is indicated, given the propensity forincreased risk of bleeding, it may be useful to know platelet count.

    d.) Approved use: Mild to moderate pain or fever Rheumatoid Arthritis, Osteoarthritis Thromboembolic disorders

    TIAs, CVAs Rheumatic Fever Post-MI, Post-CABG, Angina, Acute MI, Prophylaxis of MIe.) Associated with which illnesses: Pain/Fever Arthritis Thromboembolic disorders TIAs, CVAs Myocardial infarction, CABG Pericarditis Colorectal cancer Kawasaki Diseasef.) Off-label uses: Prevention of Cataracts Prevention of pregnancy loss in women with clotting disorders Bone pain Claudication Kawasaki Disease Colorectal cancer prophylaxis Pre-eclampsia prophylaxis Pericarditis

    II. Cimetidine/Tagamet

    a. Basics (Mechanism of Action/Pharmacokinetics) Mechanism of Action Inhibits Histamine at H2 receptor in gastric parietal cells and subsequentlyinhibits gastric acid secretion

    Pharmacokinetics Half-life of 1.5-2hours; 30-40% metabolized by liver

  • 7/28/2019 Autoimmune Disorder Case Study

    24/38

    Excreted in urine Onset of action 30 minutes, peak is 45-90 minutes, duration is 4-5 hours well-absorbeda. Recommended dose/route/and time of day to administer Typically administered orally 300mg qid with meals IV can be given over 1-2 minutes every 6hoursb. Relevant labs:c. Approved use: Treatment of Duodenal and Gastric Ulcers; Peptic Ulcer Disease Gastro-esophageal reflux disease management Zollinger-Ellison syndrome Prevention of upper GI bleeding & in management of GI bleeding Management of heart-burn, acid indigestiond. Associated with which illnesses: GERD Peptic Ulcer Disease GI Bleeding Prophylaxis of ulcers//gastritise. Off-label uses: Prevention of aspiration pneumonitis Stress ulcers Angioedema Molluscum contagiosum NSAIDS induced ulcer prophylaxis Verruca Vulgaris

    III. Diltiazem hydrochloride/ Cardizema. Basics (Mechanism of Action/Pharmacokinetics) Mechanism of Action

    Inhibits calcium ion influx across cell membrane during cardiacdepolarization

    Produces relaxation of coronary vascular smooth muscle Dilates coronary arteries Slows the SA/AV node conduction times Dilates peripheral arteries

    Pharmacokinetics Half-life is 3.5-9 hours Metabolized by liver and excreted in urine Onset 6-30 minutes; peak 2-3 hours; (immediate release) 10-14 hours (extended release)

    b. Recommended dose/route/and time of day to administerTypically administered orally 30mg qid increasing gradually to 180-360 mg/day

    For Children 7 mo or older IV 0.25mg/kg go ing up to 0.11mg/kg

  • 7/28/2019 Autoimmune Disorder Case Study

    25/38

    c. Relevant labs:d. Approved use:

    Angina pectoris due to coronary artery spasmHypertension

    atrial fibrillation

    Paroxysmal supraventricular tachycardiae. Associated with which illnessesHypertension

    f. Off-label uses:Unstable anginaProteinuria

    Cardiomyopathy

    Diabetic neuropathy

    IV Ferrous sulfate

    a. Basics (Mechanism of Action/Pharmacokinetics) Mechanism of Action Replace iron stores needed for RBC development as well as energy and Oxygen transportand use. Contains 20% iron

    Pharmakokinetics Excreted in feces, urine, skin, breast milk; Enters blood stream bound to transferrin crosses placenta

    b. Recommended dose/route/and time of day to administer

    For adults 0.75-1.5g/day bid-qid, child (6-12 yrs) 3mg/kg/dayc. Relevant labs:

    d. Approved use: Used in cases of Iron defeciency Anemia, prophylaxis for iron defeciency in pregnancy nutritional supplement

    e. Associated with which illnesses

    Iron defeciencyf. Off-label uses: N/ag. Side Effects

    GI: Nausea, constipation, epigastric pai, black and red tarry stooks, comitting,diarrhea

    INTEG: Temorary discoloration of tooth enamel and eyeV Levothyroxine sodium (Synthroid) 112 mcg daily orally

    a. Basics (Mechanism of Action/Pharmacokinetics) Mechanism of Action Increases metabolic rate, controls protein synthesis, increases cardiac output,

    renal blood flow, Oxygen consumption, body temperature, blood volume,development at cellular level via action of Thyroid hormone receptors

  • 7/28/2019 Autoimmune Disorder Case Study

    26/38

    b. Recommended dose/route/and time of day to administer

    Hypothyroidism, Adults

  • 7/28/2019 Autoimmune Disorder Case Study

    27/38

    UTI, Ottis media Acute and chronic prostaitis Shigellosis Pneumocystis jiroveci

    chronic bronchitis traveller diarrheae. Associated with which illnesses:

    f. Off-label uses:g. Side Effects

    CNS: Headache, insomnia, halluciantions, depression, vertigo, fatigue, anxiety CV: Allergic myocardiatis GI: Nausea, vomitting, abd pain GU: Renal failure INTEG: Rash, dermatitis, urticaria, Stevens- Johnson syndrome

    VII. Tolterodine tartrate (Detrol) 2 mg twice a day orallya. Basics (Mechanism of Action/Pharmacokinetics)

    Mechanism: Relaxes smooth muscles in urinary tract by inhibitung acetlycholine at postganglionicsites

    Pharmakokinetics Rapidly absorbe highly protein bound extensively metabolized by CP2D6 excreted in urine and feces

    b. Recommended dose/route/and time of day to administer

    Adult and geriatric PO, 2mg bid, may decrease to 1 mg Administer as whole along with liquids. Do not crush, chew or beak

    c. Relevant labs:

    d. Approved use:

    Overactive baldder Urinary incontinence

    e. Associated with which illnesses:

    f. Off-label uses:

    g. Side Effects CNS: Anxiety, Parestheisa, fatigue, dizziness, headache CV: Chest pain, hypertension, QT prolognation EENT: Vision abnormalities, xeropthalmia GI: Nausea, vomitting, anorexia, abd. Pain INTEG: Rash, pruitis RESP: Bronchitis, cough

  • 7/28/2019 Autoimmune Disorder Case Study

    28/38

    Why should you query her on the Bactrim, and would you consider it a routine home

    medication? Explain your answer.

    The main reason to question the patient on Bactrim is because she had indicated that shewas allergic to sulfa drugs and Bactrim is one of them. Even though, Bactrim is not an over the

    counter medicine it not impossible to obtain it without prescription. The patient will have to be

    asked about this.

    Patient's Allergies:

    The patient states that she is allergic to sulfa.

    Why should this allergy be further investigated?

    The presence of Bactrim amongst her medications is the reason it has to be investigated

    Do you know the signs and symptoms of an adverse reaction to sulfa?Common side effects are:

    urinary tract disorders haemopoietic disorders porphyria hypersensitivity reactions StevensJohnson syndrome toxic epidermal necrolysis

    Body Systems

    Be prepared to defend your answers:

    Can we place each medication under the body system that it commonly affects?

    Neurological

    Cardiovascular: Diltiazem hydrochloride (Cardizem); Asprin

    Hematological: Ferrous sulfate; Asprin;

    Pulmonary

    Gastrointestinal: Cimetidine (Tagamet)

    Nutrition: Ferrous sulfate

    Genitourinary/renal: Detrol

    Musculoskeletal

    Endocrine: Levothyroxine sodium (Synthroid)

    Integumentary

  • 7/28/2019 Autoimmune Disorder Case Study

    29/38

    Immune: Sulfamethoxazole and trimethoprim

    Pain/comfort: Asprin

  • 7/28/2019 Autoimmune Disorder Case Study

    30/38

    Nursing Process:

    What nursing assessments will need to be performed regarding each of the patient's medications?

    What is a priority nursing diagnosis regarding each medication? What planning andimplementation is needed to be done for each medication? How do you evaluate each

    medication's effectiveness?

    Aspirin

    Assessment History: Allergy to salicylates or NSAIDs; allergy to tartrazine; hemophilia,bleeding ulcers, hemorrhagic states, blood coagulation defects, hypoprothrombinemia,vitamin K deficiency; impaired hepatic function; impaired renal function; chickenpox,

    influenza; children with fever accompanied by dehydration; surgery scheduled within 1

    wk; pregnancy; lactation

    Physical: Skin color, lesions; T; eighth cranial nerve function, orientation,reflexes, affect; P, BP, perfusion; R, adventitious sounds; liver evaluation, bowel sounds;

    CBC, clotting times, urinalysis, stool guaiac, LFTs, renal function tests

    Interventions

    BLACK BOX WARNING: Do not use in children and teenagers to treatchickenpox or flu symptoms without review for Reyes syndrome, a rare but fataldisorder.

    Give drug with food or after meals if GI upset occurs. Give drug with full glass of water to reduce risk of tablet or capsule lodging in theesophagus.

    Do not crush, and ensure that patient does not chew SR preparations. Do not use aspirin that has a strong vinegar-like odor. WARNING: Institute emergency procedures if overdose occurs: Gastric lavage,induction of emesis, activated charcoal, supportive therapy.

    Teaching points

    Take extra precautions to keep this drug out of the reach of children; this drug canbe very dangerous for children. Use the drug only as suggested; avoid overdose. Avoid the use of other over-the-counter drugs while taking this drug. Many of these drugs contain aspirin, and serious

    overdose can occur.

    Take the drug with food or after meals if GI upset occurs. Do not cut, crush, or chew sustained-release products. Over-the-counter aspirins are equivalent. Price does not reflect effectiveness. You may experience these side effects: Nausea, GI upset, heartburn (take drugwith food); easy bruising, gum bleeding (related to aspirin's effects on blood clotting). Report ringing in the ears; dizziness, confusion; abdominal pain; rapid or difficultbreathing; nausea, vomiting, bloody stools.

    Cimetidine

    Assessment History: Allergy to cimetidine, impaired renal or hepatic function, lactation

  • 7/28/2019 Autoimmune Disorder Case Study

    31/38

    Physical: Skin lesions; orientation, affect; pulse, baseline ECG (continuous withIV use); liver evaluation, abdominal examination, normal output; CBC, LFTs, renal

    function tests

    Interventions

    Give drug with meals and at bedtime. Decrease doses in renal and hepatic impairment. Administer IM dose undiluted deep into large muscle group. Arrange for regular follow-up, including blood tests to evaluate effects.

    Teaching points

    Take drug with meals and at bedtime; therapy may continue for 46 weeks orlonger.

    Take antacids as prescribed and at recommended times. Inform your health care provider about your cigarette smoking habits. Cigarettesmoking decreases the drug's effectiveness. Have regular medical follow-up care to evaluate your response to drug. Tell your health care providers about all medications, over-the-counter drugs, orherbs you take; this drug may interact with many of these. Report sore throat, fever, unusual bruising or bleeding, tarry stools, confusion,hallucinations, dizziness, muscle or joint pain.

    Diltiazem hydrochloride

    Assessment

    History: Allergy to diltiazem, impaired hepatic or renal function, sick sinussyndrome, heart block, lactation, pregnancy

    Physical: Skin lesions, color, edema; P, BP, baseline ECG, peripheral perfusion,auscultation; R, adventitious sounds; liver evaluation, normal output; LFTs, renal function

    tests, urinalysis

    Interventions

    Monitor patient carefully (BP, cardiac rhythm, and output) while drug is beingtitrated to therapeutic dose; dosage may be increased more rapidly in hospitalized patients

    under close supervision.

    Monitor BP carefully if patient is on concurrent doses of nitrates. Monitor cardiac rhythm regularly during stabilization of dosage and periodicallyduring long-term therapy.

    Ensure patient swallows ER preparations whole; do not cut, crush, or chew.Teaching points

    Swallow extended-release and long-acting preparations whole; do not cut, crush,or chew; do not drink grapefruit juice while using this drug.

    You may experience these side effects: Nausea, vomiting (eat frequent smallmeals); headache (regulate light, noise, and temperature; medicate if severe). Report irregular heart beat, shortness of breath, swelling of the hands or feet,pronounced dizziness, constipation.

  • 7/28/2019 Autoimmune Disorder Case Study

    32/38

    Ferrous sulfate

    Assessment & Drug Effects

    Lab tests: Monitor Hgb and reticulocyte values during therapy. Investigate theabsence of satisfactory response after 3 wk of drug treatment.

    Continue iron therapy for 23 mo after the hemoglobin level has returned tonormal (roughly twice the period required to normalize hemoglobin concentration). Monitor bowel movements as constipation is a common adverse effect.

    Patient & Family Education

    Note: Ascorbic acid increases absorption of iron. Consuming citrus fruit or tomatojuice with iron preparation (except the elixir) may increase its absorption.

    Be aware that milk, eggs, or caffeine beverages when taken with the ironpreparation may inhibit absorption.

    Be aware that iron preparations cause dark green or black stools. Report constipation or diarrhea to physician; symptoms may be relieved byadjustments in dosage or diet or by change to another iron preparation.

    Do not breast feed while taking this drug without consulting physician.Levothyroxine sodium

    Assessment

    History: Allergy to active or extraneous constituents of drug, thyrotoxicosis, acuteMI uncomplicated by hypothyroidism, Addison's disease, lactation

    Physical: Skin lesions, color, T, texture; T; muscle tone, orientation, reflexes; P,auscultation, baseline ECG, BP; R, adventitious sounds; thyroid function tests

    Interventions

    BLACK BOX WARNING: Do not use for weight loss; large doses may causeserious adverse effects.

    Monitor response carefully at start of therapy, and adjust dosage. Full therapeuticeffect may not be seen for several days. Ensure that patient swallows tablet with a full glass of water. Do not change brands of T4 products, due to possible bioequivalence problems. Do not add IV doses to other IV fluids. Use caution in patients with CV disease. Administer oral drug as a single daily dose before breakfast with a full glass ofwater.

    Arrange for regular, periodic blood tests of thyroid function. For children and other patients who cannot swallow tablets, crush and suspend ina small amount of water or formula, or sprinkle over soft food. Administer immediately.

    WARNING: Most CV and CNS adverse effects indicate that the dose is too high.Stop drug for several days and reinstitute at a lower dose.

    Teaching points

    Take as a single dose before breakfast with a full glass of water.

  • 7/28/2019 Autoimmune Disorder Case Study

    33/38

    This drug replaces an important hormone and will need to be taken for life. Do notdiscontinue without consulting your health care provider; serious problems can occur.

    Wear a medical ID tag to alert emergency medical personnel that you are usingthis drug.

    Arrange to have periodic blood tests and medical evaluations. Keep yourscheduled appointments. Report headache, chest pain, palpitations, fever, weight loss, sleeplessness,nervousness, irritability, unusual sweating, intolerance to heat, diarrhea.

    TMP-SMZ

    Assessment & Drug Effects

    Be aware that IV Septra contains sodium metabisulfite, which produces allergic-type reactions in susceptible patients: Hives, itching, wheezing, anaphylaxis.

    Susceptibility (low in general population) is seen most frequently in asthmatics or atopic

    nonasthmatic persons.

    Lab tests: Baseline and followup urinalysis; CBC with differential, platelet count,BUN and creatinine clearance with prolonged therapy.

    Monitor coagulation tests and prothrombin times in patient also receivingwarfarin. Change in warfarin dosage may be indicated.

    Monitor I&O volume and pattern. Report significant changes to forestall renalcalculi formation. Also report failure of treatment (i.e., continued UTI symptoms).

    Older adult patients are at risk for severe adverse reactions, especially if liver orkidney function is compromised or if certain other drugs are given. Most frequently

    observed: Thrombocytopenia (with concurrent thiazide diuretics); severe decrease in

    platelets (with or without purpura); bone marrow suppression; severe skin reactions. Be alert for overdose symptoms (no extensive experience has been reported):Nausea, vomiting, anorexia, headache, dizziness, mental depression, confusion, and bone

    marrow depression.

    Patient & Family Education

    Report immediately to physician if rash appears. Other reportable symptoms aresore throat, fever, purpura, jaundice; all are early signs of serious reactions.

    Monitor for and report fixed eruptions to physician. This drug can cause fixederuptions at the same sites each time the drug is administered. Every contact with drug

    may not result in eruptions; therefore, patient may overlook the relationship. Drink 2.53 liters (1 liter is approximately equal to 1 quart) daily, unlessotherwise directed.

    Do not breast feed while taking this drug.Tolterodine tartrate

    Assessment

  • 7/28/2019 Autoimmune Disorder Case Study

    34/38

    History: Presence of urinary retention; uncontrolled narrow-angle glaucoma; allergy to

    the drug or any of its components; renal or hepatic impairment; pregnancy, lactation

    Physical: Bowel sounds, normal output; normal urinary output, prostate palpation; IOP,

    vision; liver function tests; renal function tests; skin color, lesions, texture; weight

    Interventions

    Provide small, frequent meals if GI upset is severe.

    Provide frequent mouth hygiene or skin care if dry mouth or skin occur.

    Arrange for safety precautions if blurred vision occurs.

    Monitor bowel function and arrange for bowel program if constipation occurs.

    Teaching points

    Take drug exactly as prescribed.

    You may experience these side effects: Constipation (ensure adequate fluid intake, proper

    diet, consult your nurse or physician if this becomes a problem); dry mouth (sucksugarless lozenges, practice frequent mouth care; this effect sometimes lessens over

    time); blurred vision (it may help to know that these are drug effects that will go away

    when you discontinue the drug; avoid tasks that require acute vision); difficulty in

    urination (it may help to empty the bladder immediately before taking each dose of drug).

    Report rash, flushing, eye pain, difficulty breathing, tremors, loss of coordination, irregular

    heartbeat, palpitations, headache, abdominal distention.

    Do you need to be considered with geriatric considerations with this patient?

    As outlined by the U.S. Preventive Services Task Force, assessment categories

    unique to elderly patients include sensory perception and injury prevention.

    Geriatric patients are at higher risk of falling for a number of reasons, including

    postural hypotension, balance or gait impairment, polypharmacy (more than three

    prescription medications) and use of sedative-hypnotic medications.

    Interventional areas that are common to other age groups but have special

    implications for older patients include immunizations, diet and exercise, and

    sexuality. Cognitive ability and mental health issues should also be evaluated

    within the context of the individual patient's social situationnot by screening all

    patients but by being alert to the occurrence of any change in mental function.Using an organized approach to the varied aspects of geriatric health, primary care

    physicians can improve the care that they provide for their older patients

    While our patient at 62 is 3 years short of being Geriatric the following tests

    would be recommended

    http://web.squ.edu.om/med-lib/med_cd/e_cds/Nursing%20Drug%20Guide/mg/tolterodine_tartrate_tp.htmhttp://web.squ.edu.om/med-lib/med_cd/e_cds/Nursing%20Drug%20Guide/mg/tolterodine_tartrate_tp.htmhttp://web.squ.edu.om/med-lib/med_cd/e_cds/Nursing%20Drug%20Guide/mg/tolterodine_tartrate_tp.htm
  • 7/28/2019 Autoimmune Disorder Case Study

    35/38

    Get her thyroid hormones checked to make sure that her dose of synthroid is providing

    adequate thyroid hormone for her metabolic function. As metabolism slows with age, it is

    possible that the dosage may need to be lowered to prevent some of the side effects that

    accompany a too-high dose of Synthroid.

    Get vitals checks since blood pressure tends to increase with age as the arteries harden,including ECG, to make sure that this calcium channel blocker is keeping her pressure in an

    acceptable range and she has not developed any arrhythmias.

    Be cognizant of her aspirin dosage as kidney function declines with age and aspirin is a

    nephrotoxic drug when taken in high doses.

    Get her ALT and AST liver enzymes checked because Cimetidine can be hepatotoxic.

    Physical Assessment Findings:

    Neurological Assessment:

    Alert and oriented; no acute distress; speech clear; grips weak bilaterally, gait uneven.

    Cardiovascular and Hematological Assessment:

    BNP negative; K+ 3.9; SI S2; monitor reveals sinus rhythm of 90.

    Pulmonary Assessment:

    Lungs clear to auscultation; respirations even, unlabored.

    Gastrointestinal and Nutr iti on Assessment:

    Hyperactive bowel sounds; no dentures, has own teeth.

    Genitour inar y/Renal Assessment:

    Voided for urine specimen/strong odor.

    Musculoskeletal Assessment:

    Weakness to muscles of the hips and thighs, upper arms. Weakness in shrugging shoulder.Gait uneven. No difficulty swallowing. No recent weight loss. Noted tenderness to hands and hipand thigh areas. Unable to raise from lying position without assistance.

    Endocrine Assessment:

    No exophthalmos; no hirsutism; no slow-healing wounds; no goiter.

  • 7/28/2019 Autoimmune Disorder Case Study

    36/38

    I ntegumentar y Assessment:

    Bruising to upper extremities. IV site to right antecubital 0.9% NS. Purplish rash on faceand neck.

    Immune Assessment:

    No palpable lymph nodes.

    Pain /Comfort Assessment:

    Muscle tenderness and joint pain.

    Physician Orders:

    Labs: ANA, ESR; MRI, EMG; T3 and T4.

    Stop TMP-SMZ.

    Urine culture and sensitivity (C & S).

    Calcium citrate (Citracal) 2 tabs daily with breakfast.

    Prednisone 2 mg every 6 hours will be given depending on results of the tests.

  • 7/28/2019 Autoimmune Disorder Case Study

    37/38

    What do you think the physician suspects?

    Based on the Labs ordered

    ANA: Antinuclear antibody, an unusual antibody directed against structures within thenucleus of the cell. ANAs are found in patients whose immune system is predisposed to cause

    inflammation against their own body tissues. Antibodies that are directed against one's own

    tissues are referred to as autoantibodies. The propensity for the immune system to work againstits own body is referred to as autoimmunity. ANAs indicate the possible presence ofautoimmunity

    ESR: Abbreviation for erythrocyte sedimentation rate, a blood test that detects andmonitors inflammation in the body. It measures the rate at which red blood cells (RBCs) in

    a test tube separate from blood serum over time, becoming sediment in the bottom of the

    test tube. The sedimentation rate increases with more inflammation. Also commonly called

    the sed rate EMGs can be used to detect abnormal electrical activity of muscle that can occur inmany diseases and conditions, including muscular dystrophy, inflammation of muscles,

    pinched nerves, peripheral nerve damage (damage to nerves in the arms and legs),

    amyotrophic lateral sclerosis(ALS), myasthenia gravis, disc herniation, and others Thyroid function tests (TFTs) is a collective term for blood tests used to check thefunction of the thyroid.TFTs may be requested if a patient is thought to suffer from

    hyperthyroidism (overactive thyroid) orhypothyroidism (underactive thyroid), or to monitor the

    effectiveness of either thyroid-suppression or hormone replacement therapy. It is also requestedroutinely in conditions linked to thyroid disease, such as atrial fibrillation and anxiety disorder. A

    TFT panel typically includes thyroid hormones such as thyroid-stimulating hormone (TSH,

    thyrotropin) and thyroxine (T4), andtriiodothyronine (T3)

    What is the classification of each medication? (Calcium citrate and Prednisone)

    Calcium citrate is a dietary calcium supplement

    Prednisone is an immunosuppressant

    Why is each usually prescribed?

    Calcium citrate is a calcium su