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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 autoimmune disease? Autoimmune diseases arise from an inappropriate immune response of the body against substances 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 of autoimmune 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 developing autoimmune 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 a factor. Age: young to middle-aged. Most autoimmune disorders affect younger and middle-aged people. But each disease is different, and disorders such as rheumatoid arthritis are more common as people age.

Ethnicity: African American, American Indian, or Latino. People who are in these ethnic groups are more likely than Caucasians to develop autoimmune disorders. Family history of autoimmune disorders. Studies have shown that the tendency to 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 to certain 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 susceptible people 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 medications used 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. Medications Depending on the cause of fecal incontinence, the options include:

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 it medication/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 might develop? 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 types of 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 are not 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 suddenly squeeze. 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 cause food 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 by different 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.

Esophageal tumors. These growths in the esophagus may be cancerous or not cancerous. Masses outside the esophagus, such as lymph nodes, tumors, or bone spurs on the vertebrae 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 be caused 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 a greater 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 system disorders are more likely to experience difficulty swallowing.

Diabetes History of Poliomyelitis 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), or ranitidine (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 calciumchannel 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 of botulinum toxin (Botox), for example, into the lower esophageal sphincter to weaken 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.

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 swallowing difficulties can occur and occasionally dysphagia is severe. Scleroderma is an autoimmune disease can cause the weakening of tissues in the esophagus 4. Hepatic encephalopathy: What is the pathophysiology of hepatic encephalopathy? Who develops 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 as ammonia 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 be used 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 cause hyperglycemia? 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 glucose happens 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 as it 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 the body produces daily around 4:00 a.m. to 5:00 a.m.). The drugs for treating hyperglycemia fall into several categories:

(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 Dphenylalanine derivative nateglinide also bind the sulfonylurea receptor and stimulate insulin secretion. (2)Drugs that alter insulin action: Metformin works in the liver.The thiazolidinediones appear to have their main effect on skeletal muscle and adipose 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 increasing numbers of reported cases of new-onset diabetes mellitus (DM) in patients receiving treatment with protease inhibitors (PIs) or atypical antipsychotic agents. Studies have shown patients with diabetes mellitus have higher risks of autoimmune diseases 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 postprandial hyperglycemia where the mass of the insulin-producing beta cells is reduced to 4060% 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, developing antibody 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 for hyperlipidemia? 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 fatty substances can remain dissolved while in circulation. Hyperlipidemia, in general, can be divided into two subcategories:

hypercholesterolemia, in which there is a high level of cholesterol hypertriglyceridemia, in which there is a high level of triglycerides, the most common form of fat

Being overweight or obese, not getting enough exercise, and a diet high in saturated fat and 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 this condition. 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 mostly water) 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 that carry 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 triglycerides can 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 hypercholesterolemia LDL levels are high Familial hypertriglyceridemia Triglyceride 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 and Cushings 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 alcohol intake, obesity, and certain prescription medications (such as glucocorticoids and estrogen). Hyperlipidemia, along with diabetes, hypertension (high blood pressure), positive family history, and smoking are all major risk factors for coronary heart disease.

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 have heart 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 pathophysiology for inflammation? What commonly causes inflammation? What lab test is ordered to assess 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 (or proliferative). 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 the locomotor 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 your finger) Effects of chemicals or radiation

Diseases or conditions that cause inflammation often have a name ending in itis. For example:

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 for C-reactive protein, a non-specific marker (a substance that may indicate disease) that is measured by blood tests. It is produced by the 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 very narrow 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 per liter 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 drugs Non-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 ever being 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 antiinflammatory 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 of myocardial infarction and stroke.

8. Inflammatory cardiomyopathy: What is the pathophysiology of inflammatory cardiomyopathy? Who develops this disorder? What is the medication treatment? What body system is affected? How would this be classified as an autoimmune disorder? Myocarditis or inflammatory cardiomyopathy is inflammation of heart muscle (myocardium). Myocarditis is most often due to infection by common viruses, such asparvovirus B19, less commonly nonviral pathogens such as Borrelia 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,without the blockage of coronary arteries that define a heart attack (myocardial infarction) or other common noninfectious causes Myocarditis is often an autoimmune reaction. Streptococcal M protein andcoxsackievirus 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) and other 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

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) and valsartan (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 fast heart rhythms

Diuretics, such as furosemide (Lasix), which relieve sodium and fluid retention 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 the heart-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.

A pump in the aorta (intra-aortic balloon pump). In this procedure, a balloon 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 membrane oxygenation, or ECMO). With severe heart failure, doctors sometimes recommend the 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 is kyphosis seen? Is there a medication treatment for kyphosis? Kyphosis is a forward rounding of your upper back. Some rounding is normal, but the term "kyphosis" usually refers to an exaggerated rounding sometimes 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 wedgeshaped. 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 spinal vertebrae. With age, these disks dry out and shrink, which often worsens kyphosis. Cancer and cancer treatments. Cancer in the spine can weaken vertebrae and make them more prone to compression fractures, as can cancer treatments such 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.

Birth defects. In rare cases, a baby's spinal column doesn't develop properly in the 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's kyphosis. Older adults with osteoporosis are at greater risk of spinal fractures that can 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. Exercises that strengthen the abdominal muscles may help improve posture. Bracing. Children who have Scheuermann's disease may be able to stop the progression of kyphosis by wearing a body brace while their bones are still growing.

10 Multiple sclerosis: What is the pathophysiology of multiple sclerosis (MS)? Who develops MS? 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 immune system 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:

Age. Multiple sclerosis can occur at any age, but most commonly affects people who are ages 20 to 40. Gender. Women are about twice as likely as men to develop multiple sclerosis. Family history. If one of your parents or siblings has multiple sclerosis, you have a 1 to 3 percent chance of developing the disease as 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 and others, 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 in northern 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 such as Europe, southern Canada, northern United States, New Zealand and southeastern Australia. Researchers study why multiple sclerosis appears to more common 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 develop multiple 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

Corticosteroids. Corticosteroids are mainly used to reduce the inflammation 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 blood from 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 develop myasthenia 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 of autoimmune 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 about moving 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 difficulty because of weakness of the chest wall muscles Chewing or swallowing difficulty, causing frequent gagging, choking, or drooling 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

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 worse Medications that may be prescribed include: Neostigmine or pyridostigmine to improve the communication between the nerves and the muscles Prednisone and other medications (such as azathioprine, cyclosporine, or mycophenolate 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/disease induced? 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 myopathy one 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. Remissions periods during which symptoms spontaneously disappear are 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. If you have polymyositis, an unknown cause may act as a trigger for your immune system to begin producing autoimmune antibodies (autoantibodies) that attack your 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 is prednisone.

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 clientcentered 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 for osteoporosis? 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 brittle so 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 menopause are 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, bone mass 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 are men.

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 Asian descent.

Family history. Having a parent or sibling with osteoporosis puts you at greater risk, especially if you also have a family history of fractures. Frame size. Men and women who have small body frames tend to have a higher 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 the strongest 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. This can 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 overactive parathyroid 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 the development 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 of osteoporosis. 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 of part 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

Depression Gastric reflux Cancer Transplant rejection

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

Sedentary lifestyle. People who spend a lot of time sitting have a higher risk 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 two alcoholic drinks a day increases your risk of osteoporosis, possibly because alcohol can interfere with the body's ability to absorb calcium.

Tobacco use. The exact role tobacco plays in osteoporosis isn't clearly understood, but researchers do know that tobacco use contributes to weak bones. TREATMENT: Bisphosphonates For 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 the upper 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.

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 osteoporosis or if they don't work well enough your doctor might suggest trying:

Teriparatide (Forteo). This powerful drug uses parathyroid hormone to stimulate 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, denosumab produces 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 the thyroid 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 excess body 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 with osteoarthritis is pain that worsens following exercise or immobility.

15. Palliative Care: Refer to above questions. palliative medicine is appropriate for patients in all disease stages, including those undergoing 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 plan of 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 elimination of alcohol and caffeine 2. Measures to prevent falls 3. 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 severe persistent pain 5. Measures to improve function and prevent serious complications, particularly measures to prevent falls or reduce the frequency of falling 6. Periodic assessment, monitoring, and documentation of patient's progress 7. Monitoring for side effects of osteoporosis treatments

16. Panniculitis: What is the pathophysiology of panniculitis? Who usually develops panniculitis? 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 loss and 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

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 noticed that when she walked up a flight of stairs yesterday for exercise, her hips and thighs did not seem to 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 son had 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 each medication? 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 Aspirin a.)

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

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-absorbed b.) Recommended dose/route/and time of day to administer: In Adults typically administered orally, but can be administered rectally. Usual dose 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 or other gastrointestinal symptoms Given in scheduled doses or prn depending on use of medication c.) Relevant labs: Though no particular lab is indicated, given the propensity for increased 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 MI e.) Associated with which illnesses: Pain/Fever Arthritis Thromboembolic disorders TIAs, CVAs Myocardial infarction, CABG Pericarditis Colorectal cancer Kawasaki Disease f.) 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 subsequently inhibits gastric acid secretion Pharmacokinetics Half-life of 1.5-2hours; 30-40% metabolized by liver

Excreted in urine Onset of action 30 minutes, peak is 45-90 minutes, duration is 4-5 hours wellabsorbed a. 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 6hours b. 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 indigestion d. Associated with which illnesses: GERD Peptic Ulcer Disease GI Bleeding Prophylaxis of ulcers//gastritis e. Off-label uses: Prevention of aspiration pneumonitis Stress ulcers Angioedema Molluscum contagiosum NSAIDS induced ulcer prophylaxis Verruca Vulgaris III. Diltiazem hydrochloride/ Cardizem a. Basics (Mechanism of Action/Pharmacokinetics) Mechanism of Action Inhibits calcium ion influx across cell membrane during cardiac depolarization 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 administer Typically 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

c. d.

e. f.

Relevant labs: Approved use: Angina pectoris due to coronary artery spasm Hypertension atrial fibrillation Paroxysmal supraventricular tachycardia Associated with which illnesses Hypertension Off-label uses: Unstable angina Proteinuria 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 transport and 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/day c. 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 defeciency f. Off-label uses: N/a g. Side Effects GI: Nausea, constipation, epigastric pai, black and red tarry stooks, comitting, diarrhea INTEG: Temorary discoloration of tooth enamel and eye V 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

b.

Recommended dose/route/and time of day to administer Hypothyroidism, Adults <50yr orally give 1.7mcg/kg/day for 6-8 wks if over 50yrs or has heart disease Po 25-50 mcg/kg/day Myxedema coma. Adult 200-500 mcg PO Administer in am to avoid sleepyness. In case of children crush an dmix with water/ breast milk c. Relevant labs: e. Approved use: Increases metabolic rate controls protein sysnthesis increases cardia output renal blood flow Oxygen consumption body temperature f. Associated with which illnesses: Hypothyrodism Myxedema coma Thyroid hormone replacement TSH suppression Thyroid cancer g. Off-label uses: h. Side Effects CNS: Anxiety, Insomnia, tremors, headache, excitability CV: Tachycardia, palpitations, angina, dysrhythmias, hypertenison GI: Nausea, diarrhea, increase or decreae appetite OTHER: Menstural irregualrities, wight loss, heat intolorence, fever, alopecia, decreased bone mineral density VI. Sulfamethoxazole and trimethoprim (abbreviated TMP-SMZ; trade name: Bactrim) 1 tab every 12 hours for 7 days (2 tabs remaining) a. Basics (Mechanism of Action/Pharmacokinetics) Mechanism of Action: Supffamethoxazole interfers with bacterial biosynthess or protein by competitive antagonism of PABA Trimethoprim blocks synthesis of tetrahydrofolic acid The combination blocks 2 consecutive steps of bacterial sysnthesis of essential nucleic acids Pharmakokinetics Rapidly absorbed; peak of 1-4 hrs with half life of 8-13 hrs. It is excreted by urine, breast mil and corsses placenta, 68% are bound to plasma proteins, TMP achiens high leves in prostatic tissue and fluid b. Recommended dose/route/and time of day to administer Adult 160mg TMP 12hrs X10 Child Po 8mg/kg/day c. Relevant labs: d. Approved use:

e. f. g.

UTI, Ottis media Acute and chronic prostaitis Shigellosis Pneumocystis jiroveci chronic bronchitis traveller diarrhea Associated with which illnesses: Off-label uses: 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 orally a. Basics (Mechanism of Action/Pharmacokinetics) Mechanism: Relaxes smooth muscles in urinary tract by inhibitung acetlycholine at postganglionic sites 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

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 she was 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: Hematological: Pulmonary Gastrointestinal: Nutrition: Genitourinary/renal: Musculoskeletal Endocrine: Levothyroxine sodium (Synthroid) Integumentary Cimetidine (Tagamet) Ferrous sulfate Detrol Diltiazem hydrochloride (Cardizem); Asprin Ferrous sulfate; Asprin;

Immune: Pain/comfort:

Sulfamethoxazole and trimethoprim Asprin

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 and implementation 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 treat chickenpox or flu symptoms without review for Reyes syndrome, a rare but fatal disorder. 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 the esophagus. 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 can be very dangerous for children. Use the drug only as suggested; avoid overdose. Avoid the use of other over-thecounter 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 drug with food); easy bruising, gum bleeding (related to aspirin's effects on blood clotting). Report ringing in the ears; dizziness, confusion; abdominal pain; rapid or difficult breathing; nausea, vomiting, bloody stools. Cimetidine Assessment

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

Physical: Skin lesions; orientation, affect; pulse, baseline ECG (continuous with IV 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 or longer. Take antacids as prescribed and at recommended times. Inform your health care provider about your cigarette smoking habits. Cigarette smoking 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, or herbs 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 sinus syndrome, 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 being titrated 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 periodically during 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 small meals); 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.

Ferrous sulfate Assessment & Drug Effects Lab tests: Monitor Hgb and reticulocyte values during therapy. Investigate the absence of satisfactory response after 3 wk of drug treatment. Continue iron therapy for 23 mo after the hemoglobin level has returned to normal (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 tomato juice with iron preparation (except the elixir) may increase its absorption. Be aware that milk, eggs, or caffeine beverages when taken with the iron preparation may inhibit absorption. Be aware that iron preparations cause dark green or black stools. Report constipation or diarrhea to physician; symptoms may be relieved by adjustments 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, acute MI 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 cause serious adverse effects. Monitor response carefully at start of therapy, and adjust dosage. Full therapeutic effect 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 of water. Arrange for regular, periodic blood tests of thyroid function. For children and other patients who cannot swallow tablets, crush and suspend in a 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.

This drug replaces an important hormone and will need to be taken for life. Do not discontinue without consulting your health care provider; serious problems can occur. Wear a medical ID tag to alert emergency medical personnel that you are using this drug. Arrange to have periodic blood tests and medical evaluations. Keep your scheduled 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 allergictype 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 receiving warfarin. Change in warfarin dosage may be indicated. Monitor I&O volume and pattern. Report significant changes to forestall renal calculi formation. Also report failure of treatment (i.e., continued UTI symptoms). Older adult patients are at risk for severe adverse reactions, especially if liver or kidney 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 are sore throat, fever, purpura, jaundice; all are early signs of serious reactions. Monitor for and report fixed eruptions to physician. This drug can cause fixed eruptions 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, unless otherwise directed. Do not breast feed while taking this drug. Tolterodine tartrate Assessment

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 (suck sugarless 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

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 Nutrition Assessment: Hyperactive bowel sounds; no dentures, has own teeth. Genitourinary/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 hip and thigh areas. Unable to raise from lying position without assistance. Endocrine Assessment: No exophthalmos; no hirsutism; no slow-healing wounds; no goiter.

Integumentary Assessment: Bruising to upper extremities. IV site to right antecubital 0.9% NS. Purplish rash on face and 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.

What do you think the physician suspects? Based on the Labs ordered ANA: Antinuclear antibody, an unusual antibody directed against structures within the nucleus 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 against its own body is referred to as autoimmunity. ANAs indicate the possible presence of autoimmunity ESR: Abbreviation for erythrocyte sedimentation rate, a blood test that detects and monitors 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 in many 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 the function of the thyroid.TFTs may be requested if a patient is thought to suffer from hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid), or to monitor the effectiveness of either thyroid-suppression or hormone replacement therapy. It is also requested routinely 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 supplement and is used to treat a variety of conditions related to the bones such as osteoporosis. It is also used to prevent or treat low blood calcium levels in people who do not get enough calcium from their diets. Prednisone treats many different conditions such as allergic disorders, skin conditions, ulcerative colitis, arthritis, lupus, psoriasis, or breathing disorders. Why was each prescribed for this patient? Calcium citrate was probably prescribed as a precautionary measure for osteoporosis. Prednisone is an immunosuppressant, was probably prescribed because of MS as it would reduce inflammation in brain and spinal chord How is each medication administered? Calcium citrate (Citracal) is an OTC and administered orally. Prednisone is administered orally in a tablet or solution form Why would the physician stop the TMP-SMZ and order a C & S of the urine? Nursing Process:

As we had noted before the patients allergy for sulfa drugs is what must have prompted the physician to stop TMP-SMZ (Bactrin). The culture and sensitivity of the urine test was probably to check if she has a bacterial infection (UTI). If so a non-sulfa based Antibiotic would be prescribed What do we think happened to this patient and why? What do you think was the final diagnosis? Based on the health history, drug history, physical assessment and doctor's ordered labs, it seems like Bactrin is what might have cause the allergic reaction in the patieint. The ANA test indicates that an auto immune disease is suspected, the ESR and EMG test suggests that Lupus and Myasthenia Gravis may be suspected. Bruising is common for both Lupus as well as MG. Predinosone is THE MOST effective medicine for MG as well as Lupus and since this was ordered after the LABS it is possible that the patient has Mysthenia Gravis/Lupus The final clue is the purplish rash on the face and neck. This symptom is classic Lupus. However, the Lab results will ultimately help with the diagnosis The final diagnosis based on the information provided is that the patient has Lupus Erythematosus an autoimmune disease