What is Lupus - Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disorder that may affect many organ systems within the body. In particular it is associated with a distinctive rash and joint pain, however the most potentially serious problems are due to effects on the brain and kidneys.

Who gets Lupus - Systemic Lupus Erythematosus?

SLE occurs worldwide, but racial differences are seen. It is estimated to affect 1 in every 250 African-American women. There is a female predominance (9:1), and peak age of onset is between 20-40 years. The disease affects 0.1-0.2% of the general population. The disease affects 0.1-0.2% of the population, and is much more common in Africans.

Predisposing Factors

Cause unknown but probably multi-factorial. Factors thought to be involved:

* Genetic: 70% concordance between identical twins and increased incidence of HLA-B8 and HLA-DR3.
* Immunological: antinuclear antibodies are present which are thought to result from polyclonal activation of B cells by an antigenic stimulus (possibly viral). May be associated with impaired T cell regulation and deficiencies in complement.
* Drugs: hydralazine, isoniazid, anticonvulsants and procainamide may cause a mild lupus like syndrome which often resolves with withdrawal of the drug.
* Infection: viral infections may be responsible.
* Hormonal factors: high incidence in women suggest female hormones may modify the immune system.
* Sunlight is an exacerbating factor for the cutaneous (affecting the skin) manifestations in most cases.

Progression

SLE usually occurs in episodes, with flares and remissions that may last for long periods of time. In some patients, it may persist as a chronic illness. Generally speaking, if serious complications have not developed by the first few years, they are unlikely to do so.

Probable Outcomes

With current treatments, prognosis is good. Survival rates have increased from 50% at five years during the 1950s, to approximately 90% at 10 years presently.

How Will Lupus - Systemic Lupus Erythematosus Affect Me?

Features typical of SLE include:

* fever
* joint pains
* fatigue
* rash that worsens with sun exposure
* mouth ulcers
* hair loss
* urticaria (hives)

There may have been previous problems with pregnancy (multiple miscarriages), or a family history of autoimmune disease such as rheumatoid arthritis.

Other features may include:

* raised blood pressure.
* mouth ulcers.
* dry eyes
* hair loss.
* joint tenderness or swelling.
* signs of fluid in the lungs.
* signs of inflammation of the fibrous sac surrounding the heart (pericarditis).
* protein in the urine.
* scaly red rash in a ‘butterfly’ distribution over the face and other sun exposed areas.

How is Lupus - Systemic Lupus Erythematosus Diagnosed?

A combination of clinical and physical findings, plus appropriate tests are needed to make a diagnosis of SLE.

Tests may include:

* Blood tests
* Immunological tests
* Urine testing (protein in the urine suggests kidney involvement)
* Biopsy (taking a sample of the skin or kidney to look for abnormalities)
* MRI scan to look for involvement of the brain.

How is Lupus - Systemic Lupus Erythematosus treated?

Treatment depends on symptoms and severity of the disease.

* NSAIDs - useful for mild disease with arthralgia
* Hydroxychloroquine - mild disease when symptoms cannot be controlled with NSAIDS or for cutaneous disease.
* Corticosteroids - mainstay of treatment. Particularly for moderate to severe disease. Aim is to control disease activity before gradually reducing the dose.
* Immunosuppressives (azathioprine, cyclophosphamide) - usually in combination with corticosteroids for severe disease (e.g. renal or cerebral disease).
* Topical steroids - for discoid lupus. Should also avoid excessive sunlight (suncream and clothing).

Lupus - Systemic Lupus Erythematosus References

1. Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison’s Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001
2. Cotran, Kumar, Collins 6th edition. Robbins Pathologic Basis of Disease. WB Saunders Company. 1999.
3. Hurst JW (Editor-in-chief). Medicine for the practicing physician. 4th edition Appleton and Lange 1996.
4. Kumar P, Clark M. CLINICAL MEDICINE. WB Saunders 2002 Pg 427-430.
5. Longmore M, Wilkinson I, Torok E. OXFORD HANDBOOK OF CLINICAL MEDICINE. Oxford Universtiy Press. 2001

Symptoms of This Disease:

* Inflammation
* Joint pain (Arthralgia)
* Raynaud’s Phenomenon Raynaud’s disease

Drugs/Products Used in the Treatment of This Disease:

* Methotrexate Injection and Tablets (DBL)
(Methotrexate)

* Azahexal
(Azathioprine)

* Endoxan
(Cyclophosphamide)

* Plaquenil
(Hydroxychloroquine)

* Solone
(Prednisolone 5mg, 25mg)

What is Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a disease in which the joints in the body become inflamed. RA is the most common form of inflammatory arthritis. It is different to osteoarthritis. You may have heard of people referring to their rheumatism. This is a non-medical word that people use to describe a range of joint problems some of which may be RA.

In RA, the body’s own immune system gets confused and attacks the joints and sometimes other tissues. The immune cells that normally fight infections turn on the body’s own tissues. This self attack (autoimmune) causes inflammation in the joints. People notice this as painful, swollen, red joints.

Usually it affects the joints of the hand and feet and then the larger joints. It usually affects both sides of the body.

There are many good treatments for RA now. Most people are able to continue working.

Who gets Rheumatoid Arthritis?

RA affects 0.5-3% of the population depending on where people come from. It may start at any time from early childhood (rare) to old age. However it usually starts between 30-50 years of age.

Before menopause women are affected 3 times more often than males. Following menopause the frequency in both sexes is similar. A family history of RA is common.

People who have a family member with RA are slightly more likely to get RA. However their risk is still very small.

Predisposing Factors

Doctors don’t know the exact reason. They know that it is a mixture of a person’s genes and things that they are exposed to can cause it, such as smoking. However, even identical twins don’t always both get it. One study showed less than one in six identical twins both get it if one already has it. It is thought that a chain of events occur that leads the immune system to be confused.

Probable Outcomes

How Will Rheumatoid Arthritis Affect Me?

RA affects the whole body but mostly affects the joints. It causes pain and swelling in the joints which makes people stiff especially in the morning. The joint problems make it hard to do things day to day like turning on a tap. If the inflammation is left untreated, it can cause damage to the joints, causing them not to work properly.

The chemicals from the inflammation in the joints spill in the bloodstream. This makes people with RA more tired - a bit like as if they had the flu.

Everyone with RA is slightly different and it means different things to different people. Some people have more pain than stiffness, some have tiredness as their main problem, some experience dry eyes. Listen to the case histories to hear how it has affected other people. Most people get their RA under control but still sometimes it can get active.

How is Rheumatoid Arthritis Diagnosed?

There is no one test to say a person has RA. It is diagnosed on a mixture of their story, what is found on examination by the doctor and a range of blood tests and x-rays.

How is Rheumatoid Arthritis treated?

Unfortunately there is no cure for RA and it only rarely goes away. So people with RA are treated with medications to suppress the inflammation and allow them to do normal things.

People with RA are usually looked after by several medical personnel. This might include a rheumatologist, a GP, a physiotherapist and occupational therapist. The medications used to treat RA fall into two main groups. The first group aims to put the fire out by suppressing the inflammation in the joints. The first group is given the long name: disease modifying anti-rheumatic drugs (DMARDs). You might see your medications called DMARDs. Commonly used DMARDs are methotrexate, sulfasalazine, leflunomide, prednisone and hydroxychloroquine.

The second group helps with pain. It includes medications like paracetamol and anti-inflammatories like Brufen, Celebrex. The name anti-inflammatories is a bit confusing. These medications can help with the inflammation from things like a sprained ankle but do not treat the inflammation in RA.

The aims of treatment are to suppress joint inflammation to prevent day to day pain and stiffness hence to prevent long term joint damage. Unfortunately the medications that treat RA work well but most take several weeks to months to have there full effects. So don’t worry if it doesn’t work straight away. Also, like all medications these drugs can have some side effects. Most patients need to have regular blood tests whilst they are on medication for their RA. This is also the reason that people are started on lower doses on some medications like methotrexate and then have them increased.

This information is only meant as a starting point. Use it to help you understand RA. Ask you medical team for further information.

(Kindly contributed by Dr Malcolm Turner, Rheumatology Research fellow at the Diamantina Institute for Cancer, Immunology and Metabolic Medicine, Princess Alexandra Hospital, Brisbane, Queensland and Editorial Advisory Board member of the Virtual Rheumatology Centre.)

Rheumatoid Arthritis References

1. Amos M. ‘ABC of Rheumatology: Rheumatoid Arthritis-II: Treatment,’ BMJ 1995; 310: 652-654.
2. Apley G. Concise system of orthopaedics and fractures. 2nd ed. Arnold, 2001.
3. Buckley C. ‘Treatment of rheumatoid arthritis,’ BMJ 1997; 315: 236-238.
4. Collier, Longmore, Scally. Oxford handbook of clinical specialties, 6th ed. 2003, Oxford University Press.
5. Hakim A, Clunie G. Oxford Handbook of Rheumatology, Oxford University Press, London, 2002.
6. Kumar and Clark. Clinical Medicine 5th ed. WB Saunders, 2002.
7. O’Dell J, ‘Therapeutic Strategies for Rheumatoid Arthritis,’ NEJM 2004, 350: 25; 2591-2602.
8. Sadovsky R. Preventing Progression of Rheumatoid Arthritis. Am F Phys 2000. (online) http://www.aafp.org/afp/20000315/tips/12.html
9. Smith R, Smolen J. ‘Rheumatoid Arthritis,’ eMedicine. Web MD, 2006. Accessed (online) from http://www.emedicine.com/med/topic2024.htm (2/4/06).

(Kindly reviewed by Dr John Quintner MB BS MRCP FFPMANZCA, Consultant Physician in Rheumatology and Pain Medicine, Western Australia.)

Symptoms of This Disease:

* Joint pain (Arthralgia)
* Raynaud’s Phenomenon Raynaud’s disease

Treatments Used in This Disease:

* Corticosteroids for pain relief
* NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)
* Aminosalicylates
* Individual Therapy

Drugs/Products Used in the Treatment of This Disease:

* Methotrexate Injection and Tablets (DBL)
(Methotrexate)

* Brufen
(Ibuprofen)

* Celebrex
(Celecoxib)

* Enbrel
(Etanercept)

* Humira
(Adalimumab)

* Imuran
(Azathioprine)

* Mabthera
(Rituximab)

* Mobic
(Meloxicam)

* Remicade
(Infliximab)

* Salazopyrin, Salazopyrin EN-tabs
(Sulfasalazine)

* Voltaren Rapid 12.5/ 25/ 50
(Diclofenac potassium)

What is Rotavirus Infection

Viral gastroenteritis is an inflammation of the stomach and intestines caused by a viral infection. Rotavirus is the most common virus that causes viral gastroenteritis. It mainly affects the small intestines.

Who gets Rotavirus Infection?

Rotavirus infection is the most common cause of childhood viral gastroenteritis in both developed and developing countries. A significant proportion of illness and death in young children is linked to gastroenteritis, and rotavirus causes about 111 million episodes each year. About 25 million clinic visits are because of rotavirus, which is the reason for approximately 2 million hospital admissions and 352,000-592,000 deaths every year. The majority of rotavirus deaths are in developing countries, where about 82% of rotavirus infections result in death.

In Australia, rotavirus gastroenteritis is the causes almost 50% of paediatric admissions. In numerical terms, this is about 10,000 children in one year. Death because of rotavirus is rare in Australia, even though dehydration still causes death. Indigenous children are at a higher risk and have longer hospital stays. Winter and spring are the seasons with high infection rates.

Predisposing Factors

Rotavirus infection is spread predominantly by exposure to faeces or respiratory secretions.

Predisposing factors include:

* Poor hygiene, including inadequate handwashing.
* Outbreaks occurring in nurseries and primary schools.

Progression

Infection without any symptoms are common, and bottle-fed babies are more likely to show symptoms than breastfed babies. Adults who become infected with the virus usually have mild or no symptoms.

Probable Outcomes

Most infections will resolve spontaneously. Children may become severely ill from dehydration caused by diarrhoea. Occasionally a malabsorption syndrome with lactose intolerance can follow the infection, though this usually resolves spontaneously.

How Will Rotavirus Infection Affect Me?

An affected child may have acute vomiting, fever and diarrhoea. These are common symptoms of gastroenteritis. If there is dehydration, other symptoms of dehydration like low urine output (nappy is not as wet as usual), dry skin with poor elasticity, and other signs will be present. A child who has these symptoms, is not drinking well and has abdominal pain needs medical attention.

Clinical Examination

The physician will look for signs of dehydration like:

* Dry skin with poor elasticity
* Heart palpitations
* Reduced blood circulation
* Low urine output
* Sunken eyes
* Decreased blood pressure

How is Rotavirus Infection Diagnosed?

* Blood test results may reveal dehydration.
* Arterial Blood Gases may yield abnormal results in patients with severe dehydration.

How is Rotavirus Infection treated?

Treatment should be directed at replacing the fluid loss with adequate oral rehydration solution:

* A baby who is currently breastfeeding should continue being fed even when rehydration solution is used to replace lost fluid.
* Do not use undiluted cordial or carbonated drinks to replace fluids.
* If the child is severely ill then the physician will admit the child and give intravenous fluid.
* There are now vaccines available against rotavirus. In Australia, there are two kinds of vaccines. You can consult with your physician regarding the rotavirus vaccines.

Rotavirus Infection References

1. Elliott E. Management of acute gastroenteritis in children. Current Therapeutics. 2001; 42(10): 55-9.
2. Ramig RF. Pathogenesis of intestinal and systemic rotavirus infection. J Virol. 2004; 78(19): 10213-20.
3. Kirkwood CD, Cannan D, Bogdanovic-Sakran N, Bishop RF, Barnes GL. Australian Rotavirus Surveillance Program: Annual report, 2006-07. Communicable Diseases Intelligence Quarterly Report. 2007; 31(4): 375-6.
4. Schultz R. Rotavirus gastroenteritis in the Northern Territory, 1995–2004. Medical Journal of Australia. 2006; 185(7): 354-6.
5. Indumathy AD, Stanley B, Shobhna D, Bellamy RA, Berriman JA. Rotavirus spike structure and polypeptide composition. J Virol. 1991; 65(8): 4334-40.
6. Nelson R. Two vaccines show efficacy against rotavirus. Lancet Infectious Diseases. 2006; 6(2): 77.

What is Hypothyroidism

Hypothyroidism causes underactivity of the thyroid gland. It may be primary from disease of the thyroid gland or secondary to hypothalamic-pituitary axis.

Who gets Hypothyroidism?

* Spontaneous hypothyroidism is infrequent with a prevalence of 1-2% and occurs more commonly in women (8-10 times).
* Atrophic (autoimmune) hypothyroidism: six times more common in females.
* Incidence increases with age.
* Hashimoto’s thyroiditis: more common in females and in late middle age.

Predisposing Factors

* Autoimmune disease (Hashimoto’s thyroiditis): Autoimmune disorders occur when your immune system produces antibodies that attack your own tissues, as is the case in Hashimoto’s thyroiditis. Sometimes this process occurs within the thyroid gland. It is still unclear as to why the body produces antibodies against its own tissues. A genetic flaw is a valid suggestion, but one that is yet to be proven
* Treatment with radioactive iodine: The most common treatment for people who produce too much thyroid hormone (hyperthyroidism) is radioactive iodine. Sadly on many occasions this form of treatment can have the effect of curing a person of their over active thyroid and leave them with an under active one.
* Radiation therapy: Radiation used to treat cancers of the head and neck can affect your thyroid gland and may lead to hypothyroidism.
* Thyroid surgery: Removing all or a large portion of your thyroid can diminish or halt it capability to produce hormones. Thyroid hormone treatment would then have to be taken for life.
* Medications: A number of medications can contribute to hypothyroidism. One of the most common is lithium, which is used to treat certain psychiatric disorders.

On rare occasions the following may lead to hypothyroidism:

* Congenital disease: Approximately one in 3,000 babies in the United States is born with a defective thyroid gland or no thyroid gland at all.
* Iodine deficiency: The trace mineral iodine ? found primarily in seafood, seaweed, plants grown in iodine-rich soil and iodized salt ? is essential for the production of thyroid hormones.
* Pregnancy: Some women develop hypothyroidism during or after pregnancy (postpartum hypothyroidism), often because they produce antibodies to their own thyroid gland. Left untreated, hypothyroidism increases the risk of miscarriage, premature delivery and preeclampsia- a condition that causes a significant rise in a woman’s blood pressure during the last three months of pregnancy. It can also seriously affect the developing fetus.
* Pituitary disorders: About 1 percent of cases of hypothyroidism are caused by the failure of the pituitary gland to produce enough TSH - usually due to a benign tumor of the pituitary gland.

Probable Outcomes

In most patients older than 3 years, the signs and symptoms of hypothyroidism are reversed with thyroid hormone treatment.

How is Hypothyroidism Diagnosed?

* Full blood count: anaemia
* Liver function tests: increased serum aspartate transferase levels
* Urea and electrolytes: due to an increase in ADH and impaired free water clearance
* Creatine Kinase: increased levels associated with myopathy.
* Lipids: hypercholesterolaemia.

How is Hypothyroidism treated?

Replacement therapy with thyroxine: required for life. Assess clinically and by thyroid function tests after six weeks on a steady dose. Dose should be lower if co-existant ischaemic heart disease.

Hypothyroidism References

1. Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison’s Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001
2. Cotran, Kumar, Collins 6th edition. Robbins Pathologic Basis of Disease. WB Saunders Company. 1999.
3. Hurst JW (Editor-in-chief). Medicine for the practicing physician. 4th edition Appleton and Lange 1996.
4. Kumar P, Clark M. CLINICAL MEDICINE. WB Saunders 2002 Pg 427-430.
5. Longmore M, Wilkinson I, Torok E. OXFORD HANDBOOK OF CLINICAL MEDICINE. Oxford Universtiy Press. 2001

Symptoms of This Disease:

* Muscle cramps
* Memory Loss

Drugs/Products Used in the Treatment of This Disease:

* Tertroxin
(Liothyronine sodium)

What is Angina Pectoris and Unstable Angina

Angina Pectoris and unstable Angina is a condition of the coronary arteries - the arteries that supply blood to the heart muscle. When the heart is not receiving sufficient blood supply because of the narrowing of the coronary arteries - this causes pain referred to as “angina”. The narrowing of the arteries is usually due to a process called “atherosclerosis” or “atheroma”, where the walls of the arteries become coated with a fatty plaque over time.

Who gets Angina Pectoris and Unstable Angina?

About 2% of the overall population suffer from angina pectoris as a result of coronary artery disease. The condition is much more common in older patients with the risk factors mentioned below.

Predisposing Factors

There are many risk factors for coronary artery disease:

1. Hypercholesterolaemia (elevated levels of cholesterol in the blood) plays a central role in the development of the plaques.
2. Increased age and being of the male sex.
3. Family history of coronary artery disease.
4. Smoking: The risk is directly related to number of cigarettes smoked.
5. Diabetes mellitus: Abnormal blood sugar levels promote vascular damage and the development of plaques.
6. Hypertension: High blood pressure promotes artery damage which may initiate or exacerbate atherosclerosis causing plaque rupture. It should be noted that hypertension also worsens myocardial ischaemia (heart attack) through the adaptive changes it causes in the left ventricle. In hypertension the heart has to work harder to pump blood and as a consequence the left ventricle becomes hypertrophied (increased muscle bulk). This bulkier muscle then has higher blood requirements. This is theoretically independent of vessel narrowing.

Other, less important risk factors (soft factors) include:

* Stress/anxious personality.
* Obesity.
* Alcohol consumption. It should be noted that a variant form of angina pectoris exists called Prinzmetal Angina which usually occurs at rest. This is not due to atherosclerosis but rather to spasmodic contraction of the coronary arteries. Prinzmetal angina is rare.

Progression

Early in the disease process angina pectoris (chest pain) is experienced when the demand for blood is increased, as in exercise. Angina may progress to become unstable angina. This is when the chest pain becomes more frequent, or begins to occur at rest. However a definitive diagnosis of MI cannot be made because no ECG or enzymatic patterns are seen. Left untreated, over 10% of cases will progress to frank MI (heart attack), consequently when it is discovered it is treated aggressively.

Probable Outcomes

Angina spontaneously remits in 1/3 of patients. It is associated with a mortality rate of up to 4% per year depending on the number of vessels affected. Unstable angina has a higher mortality of 15% within one year if untreated.

How Will Angina Pectoris and Unstable Angina Affect Me?

Angina can limit the amount of work one is able to perform and can result in hospitalisation.if untreated it can result in a heart attack and death.

Clinical Examination

the physical examination will involve the doctor taking the blood pressure,feeling the pulse and listening to the heart.

How is Angina Pectoris and Unstable Angina Diagnosed?

ECG (electrocardiogram): Resting ECG generally shows nothing in between attacks. During an attack, slight changes may be seen such as ST segment flatting or depression. Exercise ECG may be very useful in confirming a clinical diagnosis of angina by reproducing the symptoms.

How is Angina Pectoris and Unstable Angina treated?

1. General Treatment: this involves addressing the risk factors and counselling the patient to: cease cigarette smoking; lose excess weight; achieve good diabetes control.

2. Medical Treatment: includes preventative therapy, symptomatic therapy, and interventions.

Preventative therapy:

* Aspirin: reduces the risk of adverse events (myocardial infarction) by reducing the coagulability of the blood.
* Statins (eg. simvastatin): these drugs decrease the amount of cholesterol in the blood and increase the percentage of good fats (HDL- high density lipoproteins).

Symptomatic Relief:

* Vasodilators (Nitrates, Beta Blockers and Calcium channel blockers) all help to prevent attacks of angina. The nitrates ( eg. GTN-glyceryl trinitrate) are particularly effective at relieving the pain of an attack.
* Heparin - in the case of unstable angina: use either in intravenous form or as low molecular weight heparin (subcutaneous).
* Analgesia: In the case of unstable angina morphine and metoclopramide may be given.
* Newer drugs such as the Potassium channel agonist Nicorandel and the Nitric Oxide modulator Perhexiline are being used in cases of angina which are not sufficiently controlled with more traditional regimes.
* The use of Spinal Cord Stimulation is currently being investigated for treatment of chest pain in patients with Angina.

Interventions:

* Coronary angioplasty: Percutaneous transluminal coronary angioplasty (PTCA) is a technique whereby a catheter is introduced into the coronary arteries by way of the femoral artery. When an area of stenosis (narrowing) is detected on angiography, it can then be stretched open by the introduction of a “balloon” which is inflated by the cardiologist. Once this has been achieved, a decision on whether to place a stent is made. A stent is a metallic mesh tube which then holds the stretched portion of the artery open, preventing re-stenosis. In general, patients with single discrete stenoses are good candidates for PTCA. In stable angina which is well controlled by medication, angioplasty may confer better symptomatic control but is of uncertain prognostic benefit.

Coronary Artery Bypass Grafting (CABG): This is a surgical procedure where a donor blood vessel from another site in the body is used to bypass area of stenosis. CABG confers significant symptomatic and prognostic benefits in patients with severe triple vessel disease (areas of stenosis in all three coronary arteries). Wherever possible the LIMA (left internal mammary artery) is used to supply blood to the coronary circulation downstream from the stenosis. Grafts using the saphenous vein (from the leg) are still frequently used. Newer minimally invasive techniques using laparoscopic (keyhole) technology are currently being developed.

Angina Pectoris and Unstable Angina References

1.
Kumar P, Clark M. CLINICAL MEDICINE. WB Saunders 2002.
2.
Longmore M, Wilkinson I, Torok E. OXFORD HANDBOOK OF CLINICAL MEDICINE. Oxford Universtiy Press. 2001.
3.
Topol, Eric J.TEXTBOOK OF CARDIOVASCULAR MEDICINE (3rd Edition).Lippincott Williams & Wilkins, 2007
4.
Grundy S.M., Primary prevention of coronary heart disease: integrating risk assessment with intervention. Circulation (1999) 100 : pp 988-998.
5.
Grundy S.M., Coronary calcium as a risk factor: role in global risk assessment. J Am Coll Cardiol (2001) 37 : pp 1512-1515.
6.
Fuster V., Pearson T.A., Co-Chairs , 27th Bethesda conference: matching the intensity of risk factor management with the hazard for coronary disease events. J Am Coll Cardiol (1996) 27 : pp 957-1047.
7.
Kelemen MD,Angina pectoris:evaluation in the office. Med Clin North Am(2006) 90(3) pp 391-416
8.
National Cholesterol Education Program (NCEP) Expert Panel on High Blood Cholesterol. Detection, evaluation, and treatment of high blood cholesterol in adults: adult treatment panel III [third report]. Washington, DC: National Heart, Lung and Blood Institute; 2001. Bethesda (MD), NIH Publication #01-3670. Available at: http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htm. Accessed January 7, 2008.
9.
Boden W.E., High-density lipoprotein cholesterol as an independent risk factor in cardiovascular disease: assessing the data from Framingham to the Veterans Affairs high-density lipoprotein intervention trial. Am J Cardiol (2000) 86 : pp 19-22.
10.
Beller G., Relative merits of cardiovascular diagnostic techniques. E. D.P. P. Heart disease: a textbook of cardiovascular medicine 6th edition. 2001Philadelphia: WB Saunders, : pp 422-441
11.
Abrams J., Chronic stable angina. N Engl J Med (2005) 352 : pp 2524-2533.
12.
Hoffman S.N., et al. A meta-analysis of randomized controlled trials comparing coronary artery bypass graft with percutaneous transluminal coronary angioplasty: one- to eight-year outcomes. J Am Coll Cardiol (2003) 41 : pp 1293-1304.
13.
Hannan E.L., et al. Long-term outcomes of coronary-artery bypass grafting versus stent implantation. N Engl J Med (2005) 352 : pp 2174-2183.
14.
Al Suwaidi J., et al. Impact of coronary artery stents on mortality and nonfatal myocardial infarction: meta-analysis of randomized trials comparing a strategy of routine stenting with that of balloon angioplasty. Am Heart J (2004) 147 : pp 815-822

Symptoms of This Disease:

* Chest Pain

Treatments Used in This Disease:

* LDL (Low Density Lipoprotein) Cholesterol Lowering
* Introduction to Neurostimulation

Drugs/Products Used in the Treatment of This Disease:

* Adalat 10, Adalat 20
(Nifedipine)

* Adalat Oros
(Nifedipine)

* Anginine
(Glycerol trinitrate)

* Atenolol (Terry White Chemists)
(Atenolol)

* Barbloc
(Pindolol)

* Corbeton
(Oxprenolol hydrochloride)

* Deralin
(Propranolol hydrochloride)

* Diltiazem (Terry White Chemists)
(Diltiazem hydrochloride)

* Glyceryl Trinitrate for Injection (DBL)
(Glyceryl trinitrate)

* Heparin Injection BP (DBL)
(Heparin sodium)

* Ikorel
(Nicorandil)

* Isosorbide Mononitrate-BC
(Isosorbide mononitrate)

* Metoprolol-BC
(Metoprolol tartrate)

* Nifedipine-BC
(Nifedipine)

* NitroDur
(Glyceryl trinitrate)

What is Peptic Ulcer Disease

Peptic Ulcer Disease occurs mainly in the stomach or proximal duedenum.

Rarely, however, peptic ulcers can also occur in the oesophagus, jejunum (in Zollinger Ellison syndrome) or sometimes in a Meckel’s diverticulum.

A: Stomach
B: Duodenum
C: Oesophagus
Peptic Ulcer Disease (PUD)

Who gets Peptic Ulcer Disease?

Peptic ulcers are common, occurring in some 10-15% of the population at any one time, with duodenal ulcers being four times more common than gastric ulcers. PUD is more common in men (four times) and more common in elderly people. Ulcer rates are declining for young men and increasing for older individuals - since non-steroidal anti-inflammatory drugs (NSAIDS) are becoming a more prevalent cause with the other major cause, Helcobacter pylori infection being readily treated.

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Diseases

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Peptic Ulcer Disease (PUD)

* What is Peptic Ulcer Disease?
* Who gets Peptic Ulcer Disease?
* Predisposing Factors
* Progression
* Probable Outcomes
* How is Peptic Ulcer Disease Diagnosed?
* How is Peptic Ulcer Disease treated?
* Peptic Ulcer Disease References
* Drugs/Products Associated with Peptic Ulcer Disease

What is Peptic Ulcer Disease

3D Animation on
Gastric UlcersThis animation brought to you by Blausen Medical Communications.
Contact Andrew Walbank.
Peptic Ulcer Disease occurs mainly in the stomach or proximal duedenum.

Rarely, however, peptic ulcers can also occur in the oesophagus, jejunum (in Zollinger Ellison syndrome) or sometimes in a Meckel’s diverticulum.

A: Stomach
B: Duodenum
C: Oesophagus
Peptic Ulcer Disease (PUD)

Who gets Peptic Ulcer Disease?

Peptic ulcers are common, occurring in some 10-15% of the population at any one time, with duodenal ulcers being four times more common than gastric ulcers. PUD is more common in men (four times) and more common in elderly people. Ulcer rates are declining for young men and increasing for older individuals - since non-steroidal anti-inflammatory drugs (NSAIDS) are becoming a more prevalent cause with the other major cause, Helcobacter pylori infection being readily treated.

Predisposing Factors

The two main causes of PUD are H. pylori infection and prolonged NSAID use. Peptic ulceration is also associated with smoking (impairs mucosal healing), excess alcohol hyperparathyroidism/ hypercalcaemia, Zollinger Ellison syndrome, excessive corticosteroid use, and stress.

Progression

Patients may present with the clinical features listed. Peptic ulcers are chronic and recurrent lesions. Untreated, peptic ulcers can take around 15 years to heal but they heal quickly with present day therapies. Treating the cause or removing the exacerbating factor should be curative and patients can resume normal activity. The most important complications are perforation of the ulcer, obstruction due to excessive growth of fibrous tissue with stricture formation, and haemorrhage. These acute complications can be serious and require immediate emergency surgery.

Probable Outcomes

With removal of the causative factor when appropriate (e.g. NSAID use) and the use of appropriate treatment - H.Pylori eradication therapy, Proton Pump Inhibitors, most peptic ulcers heal within a few weeks. The complications of PUD can be associated with significant morbidity, and acute presentations with haemorrhage and perforation can be associated with significant mortality (up to 25%), however, with the early introduction of appropriate treatment these are now much less common. PUD is not considered to be associated with a risk of cancer, although cancers can ulcerate and be mistaken for peptic ulcers.

How is Peptic Ulcer Disease Diagnosed?

The only labaratory finding may be of iron-deficiency anaemia.

How is Peptic Ulcer Disease treated?

The mainstay of treatment is eradicating H.Pylori when present and treating the cause - e.g. stopping of NSAID use if excessive.

Ulcers associated with H.pylori:

Eradicating H.pylori is associated with healing rates of over 90% and prevents re-occurrence unless reinfection occurs. The usual treatment is “triple therapy” - with a proton pump inhibitor, and two antibiotics against H. Pylori.

Ulcers not associated with H.pylori:

Usually associated with excessive use of NSAIDS. Therefore, stop NSAID or other causative agents, if possible and give acid suppressing drugs (H2 blocker or PP inhibitor). This will heal 80%-90% of ulcers over two months. Antacids and antireflux methods (decrease weight, stop smoking, decrease alcohol, raise bed head, small regular meals, avoid hot drinks and eating less than 3 hours before bed) may also be used to compliment the above medical management. Complications (haemorrhage, perforation, gastric outlet obstruction) are managed in hospital with appropriate resuscitation, and definitive management which usually requires surgery and/or endoscopy.

Peptic Ulcer Disease References

1. Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison’s Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001
2. Cotran, Kumar, Collins 6th edition. Robbins Pathologic Basis of Disease. WB Saunders Company. 1999.
3. Haslet C, Chiliers ER, Boon NA, Colledge NR. Principles and Practice of Medicine. Churchill Livingstone 2002.
4. Hurst JW (Editor-in-chief). Medicine for the practicing physician. 4th edition Appleton and Lange 1996.
5. Kumar P, Clark M. CLINICAL MEDICINE. WB Saunders 2002
6. Longmore M, Wilkinson I, Torok E. OXFORD HANDBOOK OF CLINICAL MEDICINE. Oxford University Press. 2001
7. McLatchie G and LEaper DJ (editors). Oxford Handbook of Clinical Surgery 2nd Edition. Oxford University Press 2002.
8. MEDLINE Plus
9. Raftery AT Churchill’s pocketbook of Surgery. Churchill Livingsone 2001.
10. Tjandra, JJ, Clunie GJ, Thomas, RJS,; Textbook of Surgery, 2nd Ed, Blackwell Science, Asia. 2001.

Symptoms of This Disease:

* Pain
* Flatulence (gas)
* Abdominal Pain
* Rectal bleeding

Drugs/Products Used in the Treatment of This Disease:

* Pariet
(Rabeprazole sodium)

* Somac (Injection)
(Pantoprazole)

* Somac (Oral)
(Pantoprazole)

* Alu Tab
(Aluminium hydroxide)

* Amfamox
(Famotidine)

* Carafate
(Sucralfate)

* Cytotec
(Misoprostol)

* GenRx Cimetidine
(Cimetidine)

* GenRx Ranitidine
(Ranitidine hydrochloride)

* Klacid Hp 7
(Multiple actives)

* Losec Hp 7
(Amoxycillin trihydrate; Clarithromycin; Omeprazole magnesium)

* Nexium
(Esomeprazole magnesium trihydrate)

* Probitor
(Omeprazole)

* Pylorid-KA Compliance Pack
(Hyperacidity, reflux and ulcers)

* Tazac
(Nizatidine)

* Titralac
(Calcium carbonate)

* Zoton
(Lansoprazole)

What is Atrial Septal Defect - ASD

Atrial septal defect (ASD) is a congenital heart defect. In fetal circulation there is normally an opening between the two atria (the upper chambers of the heart) to allow blood to bypass the lungs. This opening usually closes about the time the baby is born. If the opening is persistent it is called an ASD, and thus blood continues to bypass the lungs. This is called a shunt.

Atrial Septal Defect - ASD (Paediatric Cardiology)

Who gets Atrial Septal Defect - ASD?

About 1 in 2000 live births.

Predisposing Factors

The aetiology of congenital heart defects is not understood but several factors are known to be associated:

1) Maternal drug abuse, alcohol abuse and radiation exposure.

2) Maternal infection, particularly rubella.

3) Genetic abnormalities.

4) Chromosomal abnormalities (septal defects are associated with Trisomy 21- Down’s syndrome).

Progression

ASDs may occur in isolation or may be associated with other malformations:

* Spontaneous closure of ASDs is rare after the first 2 years of life.
* ASDs allow shunting of blood from one side of the circulation to the other. There are no great pressure differentials across the two atria and shunting is usually from left to right due to the greater compliance of the right heart chambers. Flow rates across the defect are usually not high2.
* Increased flow to the pulmonary circulation eventually leads to pulmonary hypertension, usually by the 4th decade. Atrial arrhythmias, particularly AF are common due to the physical distention of the atria5.
* In severe cases the shunt can eventually reverse so that blood bypasses the lungs - this is termed Eisenmenger’s syndrome and is a poor prognostic factor2.

Probable Outcomes

Most commonly symptoms dont develop until the twenties when evidence of pulmonary vascular disease becomes apparent. With increasing age, risk of developing cardiac rhythm disturbances increases. By the age of 40 most patients are severely symptomatic.

Cardiac failure is the most common cause of death. Others include emboli and infections.

How is Atrial Septal Defect - ASD Diagnosed?

Chest x-ray: Prominent pulmonary vasculature may be seen. Right ventricular hypertrophy may be seen.
ECG: May show some right bundle branch block and right axis deviation.

How is Atrial Septal Defect - ASD treated?

Large ASDs (where pulmonary blood flow is greater than 150% normal) should be repaired surgically as early as possible, preferably before 10 years. The outlook is good if pulmonary hypertension (high blood pressure in the lungs) has not developed.

Otherwise, medical management of heart failure and other complications such as arrhythmias should be instigated.

Atrial Septal Defect - ASD References

[1] Anderson et al. Paediatric Cardiology. Churchill Livingstone 1987.
[2] Behrman, Kliegman, Jenson. Nelson Textbook of Paediatrics 17th Ed. Saunders 2004.
[3] Hurst’s The Heart 8th Edition, McGRAW-HILL 1994.
[4] Kumar and Clark Clinical Medicine 4th Edition, W.B SAUNDERS 1998.
[5] Rudolph et al. Rudolphs’s Paediatrics (21st edition). McGraw-Hill 2003.

What is Ventricular Septal Defect

Ventricular Septal Defect (VSD) is a disease of the heart, namely the septum (or division) between the two ventricles (or main chambers of the heart).

Ventricular Septal Defect (VSD)

Who gets Ventricular Septal Defect?

3-4 per 1000 live births. VSD is the most common congenital cardiac malformation.

Predisposing Factors

The aetiology (origins) of congenital heart defects is not understood but several factors are known to be associated with this condition:

1) Maternal drug abuse, alcohol abuse and radiation exposure.
2) Maternal infection during pregnancy, particularly rubella.
3) Genetic abnormalities.
4) Chromosomal abnormalities (septal defects common with Trisomy 21- Down’s syndrome).

Progression

VSDs may occur in isolation or may be associated with other malformations. Small VSDs usually close spontaneously.

Moderate to large VSDs often become smaller but remain patent and allow shunting of blood from one side of the circulation to the other. Because the left (systemic) blood pressure is higher than the right (pulmonary), the shunt is left to right and increased blood is circulated through the lungs.

Eventually, the increased flow rates through the pulmonary circulation lead to obliteration of the lung tissue and pulmonary hypertension. When the pulmonary circulatory pressure is equal to or greater than the systemic, the shunt reverses and becomes right to left. This is called “Eisenmenger’s syndrome.” When this occurs, less blood flows through the pulmonary circulation and the patient may become cyanosed (skin and mucous membranes turn blue) as a result of poor blood oxygenation.
Ventricular septal defects are rarely “acquired,” as in myocardial infarction involving the ventricular septum.

Probable Outcomes

Approximately 24% of small defects close spontaneously by 18 months. Up to 75% are closed by the age of 10. Large septal defects threaten life early on through congestive failure. The risk of death is 11%. If large defects are not corrected before pulmonary hypertension develops the outlook is poor. Patients with the Eisenmenger’s syndrome have an average life expectancy of 33 years. Fortunately surgical techniques may provide a better outcome.

How is Ventricular Septal Defect Diagnosed?

Chest x-ray: small VSDs may show nothing. Moderate may show cardiomegaly and enlarged pulmonary arteries due to increased pulmonary vascular flow rates.
ECG: features of right ventricular enlargement may be seen.

How is Ventricular Septal Defect treated?

For small defects medical treatment may be tried (eg. treating heart failure) if the defect is expected to improve spontaneously. Frequent measurement
of pulmonary pressure should be performed to monitor this condition.

Moderate to large defects should be corrected surgically.

Ventricular Septal Defect References

[1] Anderson et al. Paediatric Cardiology. Churchill Livingstone 1987.
[2] Behrman, Kliegman, Jenson. Nelson Textbook of Paediatrics 17th Ed. Saunders 2004.
[3] Hurst’s The Heart 8th Edition, McGraw-Hill 1994.
[4] Kumar and Clark, Clinical Medicine 4th Edition, W.B SAUNDERS 1998.
[5] Rudolph et al. Rudolphs’s Paediatrics (21st edition). McGraw-Hill 2003.

What is Anal Cancer

The main type of anal cancer is Squamous Cell Carcinoma of the Anus.

The anus is a canal that connects the lower part of the large intestine (rectum) to the outside of the body. It allows the faeces to pass from the large intestine during a bowel movement. Faeces are formed in the longest part of the large intestine (colon), stored in the rectum, and pass through the anus. Squamous cell carcinoma of the anus forms from the lining of the anal canal. They are the most common type of anal cancer.

Who gets Anal Cancer?

Anal cancer is fairly rare. In young people anal cancer is more common in men. The average age for anal cancer sufferers is 60 years of age.

Predisposing Factors

Many people believe anal cancer is caused by the Human Papilloma Virus. Predisposing factors include:
# Smoking.
# HIV
# Lowered immunity.
# Increased sexual activity.
# Fistulas (abnormal openings).

Progression

Anal cancer spreads by local invasion initially, and then via the lymphatics - with inguinal, pelvic, para-aortic and iliac nodes being the most common sites of early anal cancer spread.

Probable Outcomes

Anal cancer prognosis depends upon the size of the anal tumour, where the anal tumour is and whether it has spread to the lymph nodes.

How is Anal Cancer Diagnosed?

Signs of anal cancer are checked through routine blood tests for anaemia and infection.

How is Anal Cancer treated?

Anal cancer treatment depends upon the stage of the anal cancer and the level of local and extended involvement. Anal surgery is generally conducted, either local resection or an abdominoperineal resection.

Radiotherapy and chemotherapy are employed if the cancer is in any of the later stages.

Chemotherapy for anal cancer typically involves:

* Mitomycin C 10 mg/m2 IV day 1 only
* 5-Fluorouracil 800 mg/m2/day continuous infusion days 1-4 and 43-46

* Radiotherapy for anal cancer typically involves: Initial phase 4 week 36 Gy
* A 2 week break
* Second phase 1/2 to 2 weeks (varies) 14.4-18 Gy
(Some radiation oncologists do not have the break. In week 5, 5FU is infused)

Regimens Used in the Treatment of This Disease:

* Capecitabine + Oxaliplatin
* Mitomycin
* Topotecan

Drugs/Products Used in the Treatment of This Disease:

* Fluorouracil Injection BP
(Fluorouracil)

* Mitomycin C Kyowa
(Mitomycin)

What is Adrenal Gland Cancer

Adenocarcinoma is a malignant (one that can spread throughout the body) cancer of the adrenal glands. The adrenal glands are paired organs that sit on top of the kidneys in the back of the upper abdomen. The adrenal cortex (the outer layer of the adrenals) is part of the endorcrine system. It secretes hormones to deal with stress (glucocorticoids), hormones to deal with water, salt and blood pressure control (aldosterone) and also some sex hormones. Some cancers of the adrenal gland also produce these hormones, which in excessive amounts cause a distinctive set of symptoms.

Who gets Adrenal Gland Cancer?

Adrenal gland cancer (Adrenocorticol carcinomas) is rare (1 in 2,000,000 of all cancers). They occur at any age including childhood, however the median age is 44 years.

Predisposing Factors

The cause of adrenal gland cancer unknown.

Progression

Adrenal gland cancer (Adrenocorticol carcinomas) tend to metastasise or spread early on. This occurs through the blood and lymph. Distant growth often occurs within the lungs and other internal organs. Metastases within bones is rare.

Probable Outcomes

Adrenal gland cancer prognosis depends upon the size of the tumour and how successful surgery is in removing it. Many drenal gland cancer tumours have spread beyond the adrenals by the time they are diagnosed.

How is Adrenal Gland Cancer Diagnosed?

Blood and urine testing for hormone levels is used in the detection of adrenal gland cancer

How is Adrenal Gland Cancer treated?

Adrenal gland cancer treatment is based on a combination of surgery, chemotherapy and radiotherapy depending on the stage and spread of tumour. Adrenal gland cancer surgery will remove adrenals and any surrounding lymph nodes or tissues that are affected by the cancer (an Adrenalectomy). Chemotherapy uses the drug Mitotane to target the adrenal gland specifically. Radiotherapy is used to combat aggressive tumours.

Drugs/Products Used in the Treatment of This Disease:

* Mitotane
(Mitotane)