Sunday 29 April 2007

Urinary catheter

-Catheters come in a large variety of sizes, materials (latex, silicone,Teflon) and
types (Foley catheter, straight catheter, coude tipcatheter).
-It is recommended to use the smallest size of catheter,if possible. Some people may
require larger catheters to control leakage of urine around the catheter or if the
urine is thick and bloody or contains large amounts of sediment.
(Be aware that larger catheters are more likely to cause damage to the urethra)
-Some people have developed allergies or sensitivity to latex after long-term latex
catheter use. These people should use the silicone or Teflon catheters.

HOW TO CARE FOR YOUR CATHETER

Most experts advise against routine changing (replacing) of the catheters. If the catheter is clogged, painful, or infected it may require immediate replacement. Routine care of the indwelling catheter MUST include daily cleansing of the urethral area (where the catheter exits the body) and the catheter itself with soap and water. The area should also be thoroughly cleansed after all bowel movements to prevent infection. Experts no longer recommend using antimicrobial ointments around the catheter as they have not been shown to actually reduce infections.

HOW TO INSERT A CATHETER (MEN)

1. Assemble all equipment
2. Wash your hands.
3. Apply the sterile gloves.
4. Lubricate the catheter.
5. Hold the penis on the sides, perpendicular to the body. Stretch the penis away from the body.
6. Begin to gently insert and advance the catheter.
7. You will meet resistance when you reach the level of the external sphincter.
Try to relax by deep breathing, and continue to advance the catheter.
8. Once the urine flow starts, continue to advance the catheter to the level of the "Y" connector. Hold the catheter in place while you inflate the balloon.

Caution : Some men have developed urethral injuries due to the balloon being inflated in the urethra. Care must be taken to ensure the catheter is in the bladder. You may try to irrigate the catheter with a few ounces of sterile water. If the solution does not easily return, you may not have the catheter far enough in the bladder.

9. Secure the catheter, and attach the drainage bag.

HOW TO REMOVE A CATHETER

Indwelling catheters may be removed in 2 ways. One method is to attach a
small syringe to the inflation port on the side of the catheter. Draw out
all the fluid until you are unable to withdraw any more fluid. Slowly
pull the catheter out until it is completely removed.

Some health care providers instruct their patient's to cut the inflation
port tubing before it reaches the main tubing of the catheter. After all
the water has drained out, slowly pull out the catheter until it is
completely removed. Be careful not to cut the catheter anywhere else.
If you cannot remove the catheter with only slight pulling, notify your
health care provider immediately.

Notify your health care provider if you are unable to urinate within 8
hours after catheter removal, or if your abdomen becomes distended and
painful.

Saturday 28 April 2007

Learning Objectives for PCL Week 8 (A Big Night Out)

1. Understand that the kidney is a key regulatory organ, integrated into a whole body system
2. Describe the structure and function of the kidneys
3. Understand the mechanisms of glomerular filtration
4. Understand some of the potential consequences of kidney failure
5. Appreciate the importance of the renal tubules in the fine regulation of sodium and water balance
6. Understand the importance of road trauma as a cause of death and appreciate some of the strategies to minimise it

(Posted by: Vivian)

Friday 27 April 2007

signs and symptoms of acute renal failure

Signs and symptoms of acute renal failure(ARF)

Clinically there may be no symptoms or signs of ARF but oliguria is common( urine output < 400ml/24h). ARF can be detected with rising plasma urea and creatinine.

In normal person
Urea 1.8g/dl conc, 21g/day output,2.5-6.7mmol/l in serum
Creatinine 150mg/dl, 1.8g/day output, 70-50 micromol/l in serum



Patients with acute renal failure, tx underlying cause

Pre renal uraemia ( uraemia: raised serum urea concentration): impaired perfusion of the kidneys with blood

Signs and symptoms
Anorexia
Nausea
Pruritus
Clouding
Drowsiness
Fits
epistaxes

kumar and clarke
oxford clinical medicine

signs and symptoms of chronic renal failure

Signs and symptoms of chronic renal failure

Early stages of CRF are often asymptomatic.
Symptoms are common when the serum urea concentrations exceed 40mmol/l but many patients develop uraemic symptoms at lower levels of serum urea.

Symptoms include:
malaise, loss of energy
loss of appetite
insomnia
nocturia and polyuria due to impaired concentrating ability
itching
nausea, vomiting and diarrhoea
paraesthesiae due to polyneuropathy
Bone pain due to metabolic bone disease
Paraesthesiae and tetany due to hypocalaemia
Symptoms due to salt and water retention- peripeheral or pulmonary oedema
Symptoms due to anaemia
Amenorrhoea in women, erectile dysfunction in men

In more advanced uraemia ( serum urea >50-60 mmol/l), symptoms are more severe, and CNS symptoms are common
mental slowing, clouding of consciousness,seizures
myoclonic twitching


anaemia: pallor, lethargy, breathlessness on exertion
platelet abnormality: epitaxis, bruising
skin: pigmentation, pruritus( itching)
GI tract: anorexia, nausea, vomiting, diarrhoea
Endocrine/ gonads: amenorrhoea, erectile dysfunction, infertility
CNS: coma, confusion, fits
CVS: uraemic pericarditis, hypertension, peripheral vascular disease, heart failure causing oedema
Renal: nocturia, polyuria, salt and water retention causing oedema
Renal osteodystrophy: osteomalacia, muscle weakness, bone path, hyperparathyroidism, osteosclerosis

Kidney function tests

'Kidney function test' is a collective term for a variety of individual tests and procedures that can be done to evaluate how well the kidneys are functioning.

Blood tests

There are also several blood tests that can aid in evaluating kidney function. These include:

Blood urea nitrogen test (BUN).
Urea is a by-product of protein metabolism. This waste product is formed in the liver, then filtered from the blood and excreted in the urine by the kidneys. The BUN test measures the amount of nitrogen contained in the urea. High BUN levels can indicate kidney dysfunction, but because blood urea nitrogen is also affected by protein intake and liver function, the test is usually done in conjunction with a blood creatinine, a more specific indicator of kidney function.

Creatinine test.
This test measures blood levels of creatinine, a by-product of muscle energy metabolism that, like urea, is filtered from the blood by the kidneys and excreted into the urine. Production of creatinine depends on an individual's muscle mass, which usually fluctuates very little. With normal kidney function, then, the amount of creatinine in the blood remains relatively constant and normal. For this reason, and because creatinine is affected very little by liver function, an elevated blood creatinine is a more sensitive indication of impaired kidney function than the BUN.

Other blood tests. Measurement of the blood levels of other elements regulated in part by the kidneys can also be useful in evaluating kidney function. These include sodium, potassium, chloride, bicarbonate, calcium, magnesium, phosphorus, protein, uric acid, and glucose.



Urine Tests

There are a variety of urine tests that assess kidney function. A simple, inexpensive screening test, called a routine urinalysis, is often the first test administered if kidney problems are suspected. A small, randomly collected urine sample is examined physically for things like color, odor, appearance, and concentration (specific gravity); chemically for substances such a protein, glucose, and pH (acidity/ alkalinity); and microscopically for the presence of cellular elements (red blood cells, white blood cells, and epithelial cells), bacteria, crystals, and casts (structures formed by the deposit of protein, cells, and other substances in the kidneys' tubules). If results indicate a possibility of disease or impaired kidney function, one or more of the following additional tests is usually performed to more specifically diagnose the cause and the level of decline in kidney function.

Creatinine clearance test.
This test evaluates how efficiently the kidneys clear a substance called creatinine from the blood. Creatinine, a waste product of muscle energy metabolism, is produced at a constant rate that is proportional to the muscle mass of the individual. Because the body does not recycle it, all of the creatinine filtered by the kidneys in a given amount of time is excreted in the urine, making creatinine clearance a very specific measurement of kidney function.The test is performed on a timed urine specimen--a cumulative sample collected over a two to twenty-four hour period. Determination of the blood creatinine level is also required to calculate the urine clearance.

Urea clearance test.
Urea is a waste product that is created by protein metabolism and excreted in the urine. The urea clearance test requires a blood sample to measure the amount of urea in the bloodstream and two urine specimens, collected one hour apart, to determine the amount of urea that is filtered, or cleared, by the kidneys into the urine.

Urine osmolality test.
Urine osmolality is a measurement of the number of dissolved particles in urine. It is a more precise measurement than specific gravity for evaluating the ability of the kidneys to concentrate or dilute the urine. Kidneys that are functioning normally will excrete more water into the urine as fluid intake is increased, diluting the urine. If fluid intake is decreased, the kidneys excrete less water and the urine becomes more concentrated. The test may be done on a urine sample collected first thing in the morning, on multiple timed samples, or on a cumulative sample collected over a twenty-four hour period. The patient will typically be prescribed a high-protein diet for several days before the test and asked to drink no fluids the night before the test.

Urine protein test.
Healthy kidneys filter all proteins from the bloodstream and then reabsorb them, allowing no protein, or only slight amounts of protein, into the urine. The persistent presence of significant amounts of protein in the urine, then, is an important indicator of kidney disease. A positive screening test for protein (included in a routine urinalysis) on a random urine sample is usually followed-up with a test on a 24-hour urine sample that more precisely measures the quantity of protein.



Abnormal results

Low clearance values for creatinine and urea indicate diminished ability of the kidneys to filter these waste products from the blood and excrete them in the urine. As clearance levels decrease, blood levels of creatinine and urea nitrogen increase. Since it can be affected by other factors, an elevated BUN, by itself, is suggestive, but not diagnostic, for kidney dysfunction. An abnormally elevated blood creatinine, a more specific and sensitive indicator of kidney disease than the BUN, is diagnostic of impaired kidney function.

Inability of the kidneys to concentrate the urine in response to restricted fluid intake, or to dilute the urine in response to increased fluid intake during osmolality testing may indicate decreased kidney function. Because the kidneys normally excrete almost no protein in the urine, its persistent presence, in amounts that exceed the normal 24-hour urine value, usually indicates some type of kidney disease as well.





Imaging tests (X-rays etc.)
A number of different kinds of test can be used to show the kidneys. These are some common examples.




Ultrasound is the most commonly used technique. It uses sound waves, not X-rays, and seems to be completely safe, even in pregnancy. The pictures look better during the examination than when 'stills' are shown.




CT - Computed tomography, the 'CAT scan', is widely used to show organs and structures.

MRI - Magnetic resonance imaging is another type of cross-sectional imaging like CT. It is sometimes useful for showing particular regions well, and it can sometimes be used to show blood vessels as an alternative to arteriography




IVU (or IVP) - intravenous urography (or pyelography). In this test an injection of a substance that is eliminated through the kidneys is given. This shows up on X-rays, and it can be followed travelling from the kidney, down the ureters into the bladder. It is useful for showing the ureters and for suspected kidney stones.





Arteriography (angiography) This is a way of showing the blood supply to the kidneys. It usually requires injection of contrast material into the artery that you are trying to see.



sources:

http://findarticles.com/p/articles/mi_g2601/is_0007/ai_2601000790
http://kidney.niddk.nih.gov/kudiseases/pubs/kidneytests/index.htm
http://renux.dmed.ed.ac.uk/edren/EdRenINFObits/NormalKidney.html


prepared by Chris Sim

chronic renal failure signs and symptoms

Signs and symptoms of chronic renal failure

Early stages of CRF are often asymptomatic.
Symptoms are common when the serum urea concentrations exceed 40mmol/l but many patients develop uraemic symptoms at lower levels of serum urea.

Symptoms include:
malaise, loss of energy
loss of appetite
insomnia
nocturia and polyuria due to impaired concentrating ability
itching
nausea, vomiting and diarrhoea
paraesthesiae due to polyneuropathy
Bone pain due to metabolic bone disease
Paraesthesiae and tetany due to hypocalaemia
Symptoms due to salt and water retention- peripeheral or pulmonary oedema
Symptoms due to anaemia
Amenorrhoea in women, erectile dysfunction in men

In more advanced uraemia ( serum urea >50-60 mmol/l), symptoms are more severe, and CNS symptoms are common
mental slowing, clouding of consciousness,seizures
myoclonic twitching


anaemia: pallor, lethargy, breathlessness on exertion
platelet abnormality: epitaxis, bruising
skin: pigmentation, pruritus( itching)
GI tract: anorexia, nausea, vomiting, diarrhoea
Endocrine/ gonads: amenorrhoea, erectile dysfunction, infertility
CNS: coma, confusion, fits
CVS: uraemic pericarditis, hypertension, peripheral vascular disease, heart failure causing oedema
Renal: nocturia, polyuria, salt and water retention causing oedema
Renal osteodystrophy: osteomalacia, muscle weakness, bone path, hyperparathyroidism, osteosclerosis

Thursday 26 April 2007

Spleen

Spleen
– an ovoid, purplish, pulpy mass about the size of one’s fist
– located in the left upper quadrant
– protected by the 9th – 11th ribs
– functions:
1. prenatal: haematopoietic organ
2. site of lymphocyte proliferation, immune surveillance and response
3. identifying, removing and destroying expended red blood cells and broken-down platelets
4. recycling iron and globin
5. serves as a blood reservoir, storing RBCs and platelets
– most vulnerable organ: a sudden marked increase in intra-abdominal pressure (eg. impalement on the steering wheel of a car) can cause the thin capsule and overlying peritoneum of the spleen to burst, rupturing the spleen, leading to intraperitoneal haemorrhage.
– NOT NECESSARY TO SUSTAIN LIFE

Splenectomy
Definition:
surgical removal of a diseased or damaged spleen

When do you need splenectomy?
1. Emergency – trauma to the spleen with uncontrolled bleeding
– spontaneous rupture (extremely rare)
2. Elective – idiopathic thrombocytopenia purpura
– congenital or acquired haemolytic anaemia
– thrombosis of the splenic blood vessels
– portal hypertension and hypersplenism
– hereditary spherocytosis
– lymphoma (enlarged spleen)

2 methods:
1. Open surgery – an abdominal incision of almost 12 inches is made, cutting through muscle
and tissue. Spleen is located and removed. Hospitalization following the
surgery may be up to a week, with a 3-4 week recuperation period.
2. Laparoscopic surgery – 3-4 small incisions are made, one for insertion of the laparoscope and
the others for specially designed surgical instruments. Patients are
usually hospitalized for 1-2 days, have less postoperative pain, and a
shorter recovery time.

Effects and prognosis of splenectomy:
1. no serious effects because most of its functions are assumed by other reticuloendothelial organs (eg. the liver and bone marrow)
2. greater susceptibility to infections (bacteria) – reduced by giving special vaccinations at least 2 weeks prior to the elective surgery (pneumococcal pneumonia, meningococcal A and C). Booster vaccinations may be needed. Children usually take daily doses of penicillin until they are 16 years old. If surgery is an emergency, vaccines are given after the operation.
3. complete recovery is anticipated in the absence of other severe injuries and medical conditions, usually 4-6 weeks
4. patients should seek medical attention even for minor illnesses such as sinus infections or sore throats, because antibiotics may be required

Sources:
http://www.nlm.nih.gov/medlineplus/ency/article/002944.htm
http://www.theuniversityhospital.com/cdtv/html/videosurgeryprocedures/spleen.htm

(Posted by: Vivian)

alcohol effect on kidney function

Gross and Microscopic changes
• Alcohol alters the form and structure of the kidney
• The basement membrane of glomerulus become abnormally thickened and was characterized by cell proliferation
• Further changes included enlarged and altered cells in kidney tubules
• These effects alter the ability of the kidneys to function normally.

Rate of blood flow
• The rate of blood flow through the kidneys is an important determinant of the amount of filtration of the blood and absorption of substances from the blood that can take place.
• Various effects of alcohol have been reported including both increased and reduced blood flow.
• These effects seem to be related to whether or not the person also had liver disease and in animal models which species of animal was used.


Effect on electrolytes balance
• Alcohol’s on electrolyte balance has major implications for the satisfactory functioning of the cells of the body
• As a prime example, the cells of the brain and particularly neurons are highly dependent upon proper amounts of sodium, potassium, chloride, and calcium being available.
• Disruption in the proper flow and availability of these electrolytes alters the ability of the neurons to function which leads to modifications in behavior and the ability of the brain to regulate other bodily processes.

Effect of Ethyl Alcohol on Electrolytes

Problem
Major Cause(s)
Low sodium level (hyponatremia Massive intake of solute-free fluid (beer
Low potassium level (hypokalemia) Dietary deficiency, gastric losses, leaky membranes, shifts from extracellular to intracellular
Low phosphorus level (hypophosphatemia) Dietary deficiency, malabsorption, increased cellular uptake
Low magnesium level (hypomagnesemia) Dietary deficiency, malabsorption, phosphorus deficiency




Fluid
• Alcohol can produce urine output within 20 minutes of consumption
• It inhibit the secretion of Anti-Diuretic Hormone(ADH) which promotes the concentration of urine by inducing the kidney to conserve water
• Under this condition, the urine become diluted and electrolytes concentration in blood simultaneously arised
• Ages makes a difference in how rapidly the body escape from alcohol’s ADH suppressive effect
• People with older age than 50 escape quicker from the ADH suppressive effect than their younger counterparts. It is thought that sensitivity to increase electrolytes concentration is enhanced with age





Acid-Base Balance
• Proper acid-base balance (i.e. hydrogen ion concentration) is crucial to the proper functioning of most of the body’s metabolic reactions.
• The kidneys play an important role in regulating this acidity, thus the rate at which metabolic processes proceed.
• Examples of alcohol-related acid-base disturbances include low levels of phosphate, which may result from hyperventilation during withdrawal from alcohol and cases of alkalosis which may be a result of severe vomiting after binge drinking.
• The latter sickness leads to losses of fluid, salt, and stomach acid.
• A potential serious condition known as alcoholic ketoacidosis is another disorder associate with abnormally high blood acidity
• This is characterized by the accumulation of ketone bodies, which is produced in the liver as a reserve fuel for brain and muscle tissues
• Typically, this happen to chronic alcohol abuser following a severe binge in which they consume alcoholic beverages and nothing else over the several days

Blood pressure
• Chronic alcohol consumption can lead to accumulation of both fluid and solutes, thereby increasing of the volume of overall body fluid
• This can contribute to high blood pressure
• Clinical studies of hypertensive patients show that reducing alcohol intake lower the blood pressure
• The mechanism responsible for this effect is not well established. However, study has showed that alcohol’s influence on blood pressure may be attributable, at least in part, to its effect on the production of hormones that act on the kidneys to regulate fluid balance or that act on blood vessels to constrict them.

Contributed by Lawrence Oh

Pathophysiology of renal failure (Powerpoint Slides for Download)


Copyright Reserved. For personal use only.

Pathophysiology of Kidney Failure

by JI KEON LOOI
Acute Kidney Failure
http://www.mayoclinic.com/health/kidney-failure/DS00280
Acute kidney failure is the sudden loss of your kidneys' ability to perform their main function — eliminate excess fluid and waste material from your blood. When your kidneys lose their filtering ability, dangerous levels of fluid and waste accumulate in your body.
Acute kidney failure is most common in people who are already hospitalized, particularly people who need intensive care. Acute kidney failure tends to occur after complicated surgery, after a severe injury or when blood flow to your kidneys is disrupted.
Loss of kidney function may also develop gradually over time, with few signs or symptoms in the early stages. In this case, it's referred to as chronic kidney failure. High blood pressure and diabetes are the most common causes of chronic kidney failure.
Acute kidney failure can be serious and generally requires intensive treatment. Unlike the chronic form, however, acute kidney failure is reversible and if you're otherwise in good health you should recover normal kidney function within a few weeks. If acute kidney failure occurs in the context of severe chronic illness — a heart attack, stroke, overwhelming infection or multiorgan failure — the outcome is often worse.
Prerenal
Prerenal problems are among the most common causes of acute kidney failure. Examples of problems that may leave your kidneys with an insufficient blood supply to function properly include:
§ Extremely low blood pressure. Severe bleeding, infection in the bloodstream (sepsis), dehydration or shock can all lead to a drastic drop in blood pressure that prevents an adequate amount of blood from reaching your kidneys. These conditions tend to occur after a traumatic injury or as a risk of major surgery.
§ Poor heart function. If your heart isn't functioning at full capacity, such as during a heart attack or with congestive heart failure, the result can be reduced blood flow to your kidneys.
§ Low blood volume. Severe dehydration — which can be brought on by prolonged vomiting or diarrhea, heatstroke or major burns — results in excessive loss of fluid, diminishing the volume of blood in your body and the amount available to your kidneys.
RenalConditions that may affect the structure and function of the kidney itself, potentially leading to acute kidney failure, include:
§ Disorders that reduce blood supply in your kidneys. Any number of disorders can lead to decreased blood supply in your kidneys, which can lead to organ damage and acute kidney failure. One example is atheroembolic kidney disease.
Atheroembolic kidney disease can occur when masses of cholesterol and cellular debris (plaques) accumulate in arteries and harden in a process called atherosclerosis. If a plaque is injured or disturbed — cardiac catheterization, a procedure used to conduct diagnostic tests and treatments on the heart, is a common cause — pieces of it may break off into your bloodstream and move throughout your body. These moving pieces are called emboli. When these emboli move to your kidneys, the cholesterol emboli accumulate in small blood vessels (arterioles). Within the arterioles, these emboli can produce severe inflammation, leading to decreased blood supply and acute kidney failure.

Other causes of reduced blood supply include a blood disorder called idiopathic thrombocytopenic purpura, development of blood clots in kidney vessels, a reaction to a blood transfusion, or a sudden onset of severe high blood pressure (malignant hypertension).
§ Hemolytic uremic syndrome. This condition, which is associated with certain strains of Escherichia coli (E. coli) bacteria, is a leading cause of acute kidney failure in infants and young children. The bacterium causes inflammation of the intestine. It also produces a toxin that causes damage and swelling in the lining of blood vessels, especially the small blood vessels (glomerular capillaries) in the kidneys. As red blood cells travel through the damaged blood vessels, they're often broken apart (hemolysis). This complex condition may result in acute kidney failure.
§ Inflammation in the kidneys. Acute kidney failure may result from sudden inflammation of the spaces between the glomeruli and the tubules (acute interstitial nephritis) and inflammation of the glomeruli (acute glomerulonephritis). Acute interstitial nephritis is usually associated with an allergic reaction to a drug. Examples include certain antibiotics — especially streptomycin or gentamicin — and common pain medications, such as aspirin and ibuprofen (Advil, Motrin, others). Antibiotics pose a greater risk of acute kidney failure for people who already have liver or kidney disease or who use diuretics or other drugs that affect your kidneys.
Acute glomerulonephritis may be associated with immune diseases, such as lupus or IgA nephropathy (Berger's disease). It may also follow an infection in another part of your body, such as strep throat, infection of a heart valve (endocarditis), typhoid fever, syphilis and malaria. Viruses that cause AIDS, mononucleosis, mumps, measles or hepatitis also may trigger glomerulonephritis.
§ Toxic injury. Because the main purpose of your kidneys is to filter toxins from your body, your kidneys are particularly vulnerable to toxic injury. Exposure to toxic substances — such as excessive amounts of alcohol, cocaine, heavy metals, solvents and fuels — can induce acute kidney failure. Certain drugs also have the potential to injure the tubules in your kidneys, including chemotherapy drugs and contrast dyes used in medical tests, such as arteriography. Contrast dyes are a common cause of acute renal failure, especially in people with diabetic kidney disease or multiple myeloma, a type of cancer.
PostrenalPostrenal causes of acute kidney failure are generally related to obstruction of the flow of urine out of your kidneys on the way out of your body. This may occur at the level of the tubes that lead from your kidneys to your bladder (ureters), or at the bladder level (urethral obstruction).
§ Ureter obstruction. Kidney stones in both ureters (or in a single ureter if only one kidney is functioning) or tumors pushing in on the ureters can cause obstruction at this level.
§ Bladder obstruction. In the bladder, the most common cause of obstruction in men is an enlarged prostate, which causes obstruction at the bladder outlet. Other obstructive bladder causes, in both men and women, include a bladder stone, blood clot, tumor or a nerve disorder that prevents the bladder from contracting properly
Chronic Renal Failure
slowly progressive loss of renal function over a period of months or years and defined as an abnormally low glomerular filtration rate, which is usually determined indirectly by the creatinine level in blood serum.
§ Diabetes. Diabetes mellitus is a leading cause of chronic kidney failure in the United States. Chronic kidney failure is related to both type 1 and type 2 diabetes.
§ High blood pressure (hypertension). Untreated or inadequately treated high blood pressure is another common cause of chronic kidney failure in the United States. The added force of elevated blood pressure exerted on the glomeruli can cause damage and scarring. When this happens, the nephrons containing the damaged glomeruli eventually lose their ability to filter waste from your blood.
§ Obstructive nephropathy. This occurs when urine outflow is blocked over time by an enlarged prostate, kidney stones or tumors, or by vesicoureteral reflux, a condition that results from urine backing up into your kidneys from your bladder. The backflow pressure in your kidneys reduces their function.
§ Kidney diseases. These include clusters of cysts in the kidneys (polycystic kidney disease), kidney infection (pyelonephritis) and inflammation of the glomeruli (glomerulonephritis), a condition that causes your kidneys to leak protein into your urine and damages nephrons.
§ Kidney (renal) artery stenosis. This is a narrowing or blockage of the kidney artery before it enters your kidney. In older adults, blockages often result when fatty deposits accumulate under the lining of the artery walls (atherosclerosis). Kidney artery stenosis can also affect young women in the form of a condition known as fibromuscular dysplasia, which causes the walls of the arteries to become thicker. Both conditions are often associated with high blood pressure.
§ Toxins. Ongoing exposure to fuels and solvents, such as carbon tetrachloride, and lead — in lead-based paint, lead pipes, soldering materials, jewelry and even alcohol distilled in old car radiators — can lead to chronic kidney failure.

http://www.mayoclinic.com/health/kidney-failure/DS00682/DSECTION=1
http://en.wikipedia.org/wiki/Chronic_renal_failure

Complications, Management & Prognosis

End stage renal failure/ stage 5 kidney disease/ established renal failure
  • When kidney function is so bad that pt is likely to die within weeks or months unless special treatment such as dialysis or transplantation is given

Complications:
Pericarditis, cardiac tamponade
Congestive heart failure
Hypertension
Platelet dysfunction
Gastrointestinal loss of blood; duodenal or peptic ulcers
Hemorrhage
Anemia
Hepatitis B, hepatitis C, liver failure
Decreased functioning of white blood cells and immune system
Infection
Peripheral neuropathy
Seizures
Encephalopathy, nervous system damage, dementia
Weakening of the bones, fractures, joint disorders
Permanent skin pigmentation changes
Skin dryness, itching/scratching with resultant skin infection
Changes in glucose metabolism
Changes in electrolyte levels
Decreased libido, impotence
Miscarriage, menstrual irregularities, infertility http://www.nlm.nih.gov/medlineplus/ency/article/000500.htm#Complications

Treatment:

  • Your treatment before end stage
    Usually kidney failure develops slowly, and at first you may not have noticed anything. Gradually most people begin to feel tired, lose their appetite and may start to itch. Some get swollen ankles or develop high blood pressure. You may have to get up several times during the night to go to the toilet. Initially, you will be treated CONSERVATIVELY. The aim is to keep you feeling well, and to delay or even prevent the need for dialysis.
    This form of treatment uses drugs and diet. You may find that you are prescribed a number of different drugs particularly those which are aimed at controlling blood pressure like ACE inhibitors. Your diet plays a very important part in looking after your kidneys and helping you feel well. You will receive advice from a dietitian - this may involve reducing the amount of protein (small amounts of meat, fish, eggs, poultry, cheese and milk) and salt in your diet, and sometimes other advice too.

http://renux.dmed.ed.ac.uk/EdREN/EdRenINFObits/CRFLong.html#anchor31913728

http://renux.dmed.ed.ac.uk/EdREN/EdRenINFObits/Dialysis_ESRFLong.html

  • End-stage treatment

1. Peritoneal dialysis (CAPD, APD)

Treatment that can usually be carried by you in your own home or at work.

a) CAPD - which stands for Continuous Ambulatory Peritoneal Dialysis - happens throughout the day, at home or at work, while the person goes about his or her daily life. Between 1.5 and 3 litres of fluid is run in four times a day, exchanging for the fluid from the previous exchange. This takes about 30-40 minutes.


b) APD - Automated Peritoneal Dialysis - in which the dialysate solution is changed by a machine, at night, while you are asleep. The machine will exchange 8-12 litres over 8-10 hours and then leave 1-2 litres to dwell during the day.

What is the Peritoneal Dialysis Fluid?

Peritoneal dialysis fluid is a sugar (glucose) solution containing other salts. Bags come in 3 strengths (1.36%, 2.27% and 3.86% or light, medium and heavy) - the "heavier" the bag (ie.3.86%), more water will be removed from the body.
  • If you have a lot of fluid in the body, you would use heavy bags to remove fluid. If you are dehydrated, you would use some light bags so that the dialysis does not remove fluid.
  • The sugar solution can be a problem for diabetic patients and changes in therapy may be needed. New solutions are being developed - Protein or starch.
  • How good is peritoneal dialysis?

    Peritoneal dialysis can provide good, efficient dialysis but needs to be monitored carefully. It needs to be performed daily with breaks only because of unusual circumstances.
  • The nurses and doctors will measure how effectively the dialysis is being performed and change the volume and strength of the fluids.
  • If good dialysis cannot be achieved it is important to think about a change - from CAPD to APD or to haemodialysis.
  • What are the problems with peritoneal dialysis?

    • There can be problems with fluid leaks in the groin or around the catheter when dialysis starts. These problems can be managed easily.
    • Infections are the major risk - either in the exit site or most importantly in the tummy itself, peritonitis. This shows as tummy pain, a fever and a cloudy fluid bag. It is important to ring the kidney unit immediately if a cloudy bag develops. Peritonitis is treated with antibiotics added to the bags and may need admission to hospital for a few days. Rarely, the infection may be so bad that the catheter has to be removed.
    • In the long term, there can be a thickening of the peritoneal membrane so that it does not work efficiently. The dialysis fluid may need to be changed or switched to haemodialysis.

    http://www.kidneypatientguide.org.uk/site/pd.php

    2. Haemodialysis = a form of dialysis in which the blood is cleaned outside the body by a machine which passes the blood across a filter.

    • Usually at a dialysis centre.
    • Home haemodialysis also available - need comprehensive training in order to become confident and self-reliant. Some alterations to your home’s plumbing and electricity supply may also be needed.

    How does it work?

    • This form of dialysis removes waste products from the blood by passing it out of the body, through a filtering system (dialyser) and returning it, cleaned, to the body.
    • While in the filtering system, the blood flows through tubes made of a membrane that allows the waste products (which are much smaller than blood cells) to pass out through it.
    • The waste products pass through the membrane into a dialysis solution (dialysate), then out of the machine. The "clean" blood is carried on through and returned safely to the body.
    • This happens over and over again throughout the dialysis session. Each time the "clean" blood is returned to the body, it picks up more waste products from the cells it circulates through, and brings these newly-collected toxins back to the dialyser to be removed.
    • Fresh dialysate is passed through continuously, to make the rate of the cleaning process as fast as possible.
    • As well as cleaning the blood, the dialysis machine also removes excess water. This part of the process is called ultrafiltration which can be done separately without dialysis.
    • It takes about 4 hours (perhaps more) to complete a good session of haemodialysis, which needs to be done 3 times a week.


    http://www.kidneypatientguide.org.uk/site/HD.php

    3. Kidney transplant


    Kidney transplants have revolutionised life for many people with kidney failure. Dialysis only keeps you OK - a successful transplant restores your health. The best treatment by far if it is suitable for you.


    Medical staff will discuss transplantation with you. For the majority of patients transplantation is the ultimate goal, but for some, particularly those with other medical conditions, long-term dialysis may be the best option.


    If transplantation is an option for you, you will undergo a series of blood tests and X-rays. After this, you will be referred to a transplant surgeon for further assessment. At this stage you will be given more information about the actual procedure.


    Most patients receive a kidney from someone who has died in hospital, usually on a life support machine. However the best transplants come from living people - who must be a close relative, or in certain cases, a partner or close friend. Live donor transplants can be carefully planned, instead of coming as a surprise at any time, and the kidney is proved in advance to be very healthy.


    The transplanted kidney is placed in one or other groin beneath the skin and muscle. As with most operations, you may feel a bit groggy for a couple of days.


    All being well, you will soon be up and about and home within a couple of weeks.


    The number of kidneys required greatly exceeds the number available, and you may have to wait a long time (sometimes years) before a kidney suited to your blood group and tissue type is found. Some patients, however, are lucky and get a kidney transplant within a few months. The type or place of treatment is irrelevant - the time you wait depends entirely on availability and suitability of the organ available. It is not a queue - it is to some extent a matter of luck.


    To prevent your body rejecting the new kidney, you will have to take some special immunosuppressive drugs for kidney diseases.These are tailored to each individual's requirements, but you will need to take at least one anti-rejection drug every day for as long as you have the transplant. Go to http://renux.dmed.ed.ac.uk/EdREN/EdRenINFObits/ISdrugs.html for more information on immunosuppressive drugs in renal disease.


    There is no need for a special renal diet following a transplant. You will, however, be advised about a healthy diet containing not too much sugar or salt, plenty of fruit, vegetables and fibre, but with less fat, particularly animal fat. You will be encouraged to maintain a healthy weight for your height.

    http://renux.dmed.ed.ac.uk/EdREN/EdRenINFObits/TransplantShort.html

    4. No dialysis


    The best option for some people may be not to have dialysis

    - reasons will be discussed in presentation, or look up the link below:


    http://renux.dmed.ed.ac.uk/EdREN/EdRenINFObits/NoRRTshort.html

    by your keynote speaker:-p

    Shantz

    Anatomy and Physiology of the Kidneys and Nephron

    Anatomy of the Kidneys:

    - Lie against the posterior wall of the abdomen at level T12 to L3.
    - Right kidney lower than left due to the liver.
    - Convex lateral surface and concave medial surface with hilum, where it receives the renal nerves, blood vessels, lymphatic vessels and urter.
    - Protected by 3 layers; from superficial to deep- the fibrous renal fascia, the adipose capsule and the renal capsule
    - Renal parenchyma (glandular tissue that forms the urine) appears C-shaped in frontal section and encircles a medial space, the renal sinus (occupied by blood and lymphatic vessels, nerves and urine-collecting structures)
    - Parenchyma divided into outer cortex and inner medulla.
    - Extension of cortex into the medulla called renal columns; divides the medulla into renal pyramids
    - Each pyramid conical with a broad base facing the cortex and the blunt tip, called the papilla facing the sinus
    - Each papilla is nestled in a minor calyx, which drains the urine and 2-3 minor calices converge to form a major calyx.
    - 2-3 major calices then converge to form the renal pelvis which continues inferiorly as the ureter.

    Functions of the kidney

    - Filter blood plasma, separate metabolic wastes from the useful chemicals and eliminate the waste while returning the rest to the bloodstream
    - Regulate blood volume and pressure by eliminating or conserving water as necessary
    - Regulate osmolarity of body fluids by controlling the relative amounts of water and solutes eliminated
    - Secrete enzyme rennin, which activates the hormonal mechanisms that control blood pressure and electrolyte balance
    - Secrete hormone erythropoietin, which controls the RBC count and oxygen carrying capacity of the blood
    - Function with the lungs to regulate PCO2 and acid-base balance of the body fluids
    - Contribute to calcium homeostasis through their role in synthesizing clacitriol (active form of Vitamin D)
    - Detoxify free radicals and drugs with the use of peroxisomes
    - Carry out gluconeogenesis in times of starvation by deaminating amino acids

    Anatomy of the nephron

    - Functional unit of the kidney
    - Each kidney contains 1.2 million nephrons
    - Each nephron consists of 2 principal parts: the renal corpuscle (where blood plasma is filtered) and the long renal tube (that processes the glomerular filtrate into urine).
    - Renal corpuscle consists of the glomerulus (ball of capillaries) enclosed in a two-layered glomerular capsule or Bowman’s capsule
    - Renal tubule consists of the Proximal Convoluted Tubule, the Nephron Loop or the Loop of Henle, the Distal Convoluted Tube


    NB: blue box: reabsorption/ pink box: secretion

    Basic Physiology of the Different parts of the Nephron

    Renal corpuscle

    Glomerular filtration occurs here. It is a process in which water and solutes in the blood plasma pass from the capillaries of the glomerulus into the capsular space of the nephron to form the glomerular filtrate

    Proximal Convoluted Tubule (PCT)

    The PCT reabsorbs about 65% of the glomerular fluid back into the peritubular capillaries, while it also removes some substances from the blood and secretes them into the tubule for disposal in the urine.

    Nephron Loop

    The primary function of the nephron loop is to generate a salinity gradient that enables the collecting duct to concentrate the urine and conserve water.

    Distal Convoluted Tubule (DCT)

    Fluid reabsorption that is subjected to hormonal control (particularly by aldosterone, Atrial Natriuretic Peptide, Antidiuretic Hormone and parathyroid hormone) takes place here.

    NB - Some terms to take note of:
    Glomerular filtrate: Fluid in the glomerular capsular space
    Tubular fluid: Fluid from the PCT to the DCT; different from the Glomerular filtrate due to substances removed or added by the tubule cells
    Urine: fluid will be called urine once it enters the collecting ducts


    Source: Saladin, Anatomy & Physiology 3rd Ed, Chap23

    Contributed by: John Lee

    Tuesday 24 April 2007

    PCL 8 A Big Night Out - tasks for this week

    1. Component of blood, blood transfusion, units of blood & IV (Madhura)
    2. Anatomy & Physiology of the kidney (gross) and nephron (detail) (John & Lawrence)

    Kidney Failure
    3. Causes/Pathophysiology - why kidneys stop working? effect of dramatic drop in renal perfussion during hypotension on the kidneys? (Ji Keon)
    4. Signs & Symptoms - indication of kidney ceases function? normal urine output? decreased urine output? (Christine)
    5. Investigations - ultrasound, kidney function tests and the significance of the results (Chris)
    6. Management, Prognosis and Complications of end stage renal failure (Shanthini)
    7. Urethral catheter - why? how? (Sri)

    8. Spleen - physiology, effects of removal, management & follow up (Vivian)
    9. Blood alcohol content effect on kidney function (Lawrence)

    Announcement

    The anatomy blog has been officially set up. Thus, all matters regarding anatomy sessions should now be directed and addressed at the new blog. This blog will be reserved specially for our PCL only.

    Thanks.

    Deep Facial Regions - Anatomy Tasks

    This is just a reminder for the tasks that we are going to do on thursday, after the 2pm lecture.

    1. Describe the temporomandibular joint. (Ji Keon)
    2. Describe the muscles of mastication. (Shanthini)
    3. Describe the maxillary artery and it's major branches. (Vivian)
    4. Describe the maxillary and mandibular nerves. (Lawrence)
    5. Describe the boundaries and contents of the temporal (John), infratemporal (Sree), and deep styloid regions (Madhura).
    6. Group and list the foramina of these regions (temporal, infratemporal and deep styloid) ; describe contents. (Chris)
    7. Demonstrate the surface anatomy of the regions and indicate clinical situations when this knowledge may be useful. (Christine)

    John

    Monday 23 April 2007

    CF - psychosocial issues

    again not my area, but just my food for thought on the part D cliff hanger...

    Issue in Pt D: Georgia (15y/o) has stopped her treatments and exercises.

    Effect of CF on a adolescents:
    • Adolescents will find it difficult to maintain a good social life due to their physical conditions and the fact that they are being controlled by their parents. Parents with children who have CF tend to be overprotective about their child doing certain things.
      These parents may fell that their chronically ill child is more susceptible to the dangers of the world.
    • keeping up with school work can be difficult when you have to stay in the hospital for months at a time.
    • If your friends have don't know you have Cystic Fibrosis, they will annoy you with questions about everything. They may wonder about your cough or all the pills you take.

    this is a quote from the video i watched:

    “Growing up has a lot of ups and downs when you have CF. The hardest thing for CF people (and me) I think, is that they want to be a normal person. No vitamins, aerosols, enzymes, Iv's, hospitalizations -- wouldn't that be great. It's hard for a lot of CF kids and even adults to remember that you have to do all those things to stay healthy. No matter what disease or problem you have, you still are a normal person. Another hard thing for me was not growing up as fast as everyone else. I'm not sure if that effects every CF person. But, for me, it sucked. In 8th grade, I only weighed 87 pounds. To me, I felt like a shrimp-- not just in 8th grade, up till about 10th grade. I didn't mature as fast as everyone else either. I hated that. I think I didn't have a lot of self confidence in myself at the time or maybe it wouldn't have mattered.
    I always felt nervous taking my pills around other people. Even know when I go out to eat, I wonder what people think (It does not bother me as much now). I know it shouldn't matter, but I think every CF person wonders about it once in a while.”

    Shantz

    CF - clinical features

    This wasn't really my area but I decided to post it up since I mentioned a couple of points during my presentation and just to expand a bit on what Vivian has done since Dr. Laksmi asked me to connect the pathophisiology with the signs and symptoms and complications...

    So as mentioned earlier, the concentration of sodium and chloride within the ECF and ICF is disrupted because of the failure of opening of the chloride channel in response to elevated cAMP in epithelial cells (CFTR is a chloride channel). Consequences of this:
    • In the sweat glands the chloride ions can not be reabsorbed from the sweat before it is expelled onto the skins surface, this also inhibits the reabsorbing of sodium ions. This results in significant loss of these ions, altering the overall balance within the body and which can cause abnormal heart rhythms.
    • In the pancreas the inability to move chloride ions out of the cell and into the ducts also prevents the movement of water in the same fashion as the water normally followed the chloride ions via osmosis. These results in digestive enzymes not being carried out into the intestines through the water, the enzymes instead digest the pancreas triggering inflammation and mucus build up (90% of CF patients have pancreatic damage)
    • The mutant CFTR also triggers mucous build-up in the lungs, causing the most noticeable symptoms of Cystic Fibrosis. The mucus can partially block parts of the lungs and most importantly is an excellent growing medium for bacteria, leading to chronic respiratory infections that inevitably result in lung damage.
    • nutritional effects - malnutrition due to malabsorption and maldigestion
    • delayed puberty and skeletal maturity
    • males are always almost infertile owing to failure of development of the vas deferens and epididymis. Females are able to conceive but often develop secondary amenorrhoea as the disease progresses

    ~shantz~

    Pathophysiology of CF

    CF (Also known as mucoviscidosis or 65 roses)


    • autosomal recessive inherited disorder (recap: both parents must be carriers; 25% chance for child to have the disease; 50% chance of being a carrier)

    • single gene disorder

    • gene mutation along long arm of chromosome 7 (7q21.3 to 7q22.1)

    • There are at least 500 different genetic mutations associated with the disease, approximately 70% of the mutations are found to be deletion at position 508 (delta F508) in the amino acid sequence on chromosome 7, making it the most common CF mutation

    • the gene codes for a membrane protein in epithelial cells which regulates chloride transport- cystic fibrosis transmembrane regulator (CFTR). Mutation results in defective CFTR

    • In 20-30% of cases the secondary and tertiary structure of the protein is altered making the protein non-functional and leading to the chloride channels failing to open in the epithelial cells. The other 70-80% of cases involve the cells quality control processes destroying all the CFTR produced as it is ‘defective’, preventing the ion channels from even forming. Both result in an inability of the cell to control the concentration of ions in the intra and Extracellular fluid.
    • So in summary (see diagram below):

    xoxo~Shantz

    source: Kumar and Clark and www.childsdoc.org

    Sunday 22 April 2007

    Tasks For Monday's PCL (Hot Summer's Night)

    1. Function of kidney
    2. Nephron (know how to draw)
    3. Kidney function
    - increase
    - decrease
    4. Urine output
    - normal
    - disease
    5. Acute Renal Failure (ARF)
    - alcohol - kidney function and urine output

    (Posted by: Vivian)

    Saturday 21 April 2007

    Addendum: Management of Cystic Fibrosis

    Prepared by: Ji Keon LOOI
    This is the very informative summary that I promised to upload.




    Below is the discussion on the antibiotics prescribed to Georgia. Only relevant information is included to avoid overloading our meddies with an avalanche of information which might inevitably cause the burnout rate to increase.

    Cannot be Emphasised More (Must know-lah)

    Pseudomonas aeruginosa is the major culprit in causing complications in patients with cystic fibrosis.

    Nice-to-know
    Tobramycin

    Ticarcillin
    • Ticarcillin is a carboxypenicillin. It is almost invariably sold and used in combination with clavulanate as Timentin®.

    • Because it is a penicillin, it also falls within the larger class of beta-lactam antibiotics. Its main clinical use is as an injectable antibiotic for the treatment of gram negative bacteria, in particular, Pseudomonas aeruginosa.

    • Ticarcillin's antibiotic properties arise from its ability to prevent cross-linking of peptidoglycan during cell wall synthesis when the bacteria tries to divide, causing death.

    Ciprofloxacin

    The information for the above drugs is all derived from http://en.wikipedia.org.

    Friday 20 April 2007

    Learning Objectives for PCL 7

    Here's a recap on the objectives for this week:

    1) Describe the causes and symptoms of cystic fibrosis
    2) Understand the process of diagnosing cystic fibrosis
    3) Understand the need for multidisciplinary teams in managing this type of chronic illness
    4) Review the principles of breaking bad news
    5) Understand the difficulties, including family pressures, when managing adolescent patients

    Hope this helps. =)

    Diagnosing and managing cystic fibrosis in the developing world

    This is the link to the summary of the article that talks about the existence of cystic fibrosis in the developing world.

    Paediatric Respiratory Reviews, Volume 7, Supplement 1, 2006, Pages S147-S150

    Diagnosing and managing cystic fibrosis in the developing world
    Sushil K. Kabra, a, , M. Kabraa, S. Shastria and R. Lodhaa aDepartment of Pediatrics, New Delhi 110029, India

    The full article is, unfortunately, inaccessible to us. Hope that the summary will be useful.

    John

    Epidemiology of Cystic Fibrosis

    Cystic Fibrosis -the most common autosomal recessive disease for individuals of European
    descent
    -1 in 2500 newborns are affected with the disease, consequently 1 in 25
    individuals are carriers.
    • life expectancy -1959 (6 months)
    • life expectancy -2006 (38.6 yr)
      -based on data compiled by Cystic Fibrosis Foundation - survival depends largely on the access to health care.
    • 1989- the discovery of CF gene
    • 1990- scientists successfully made copies of the normal gene, and added them to the CF cells in the laboratory dishes, which corrected the defective cells.
    • 1993- the first experimental gene therapy treatment was given to a patient (modified common cold virus was used as carriers or delivery vehicle-carrying the genes to CF cells in the airway)
    • the first drug therapy , 1993 =Pulmozyme (mucus-thinning drug) f(x)= improved respiratory infections and lung function.
    • 1995, ibuprofen was found to reduce lung inflammation in children with CF, under controlled condition and in high doses.
    • in late 1997, tobramycin solution for inhalation=reformulated version of antibiotics which was found to improve lung function and reduce no of hospital stays.
    • other treatment strategies to correct the protein product of the gene are currently being tested in clinical trials.
    • what makes these drugs unique is that the researchers appear to be treating the causes of CF not just the symptoms.
    • in Malaysia, approximately 16 patients were diagnosed with CF from 1997 to 2003.
    references: Cystic Fibrosis Foundation and National Peadiatric Institute

    Respiratory Disorders similar to Cystic Fibrosis

    Bronchiectasis

    Bronchiectasis is defined as a permanent dilation of bronchi and bronchioles caused by the destruction of the muscle and elastic supporting tissue resulting from or associated with chronic necrotizing infections. It is not a primary disease but one that is secondary to persisting infection or obstruction caused by a variety of conditions, including cystic fibrosis. These include:

    1. Bronchial obstruction: common causes include tumours and foreign bodies
    2. Congenital or hereditary conditions:
    - Cystic Fibrosis: obstruction and infection caused by secretion of abnormally muscid mucus
    - Immunodeficiency states (e.g. hypogammaglobulinemia - lack of 1 or more specific antibodies): increased susceptibilty to repeated bacterial infection
    3. Childhood pertussis or measles, TB and pneumonia may predispose to bronchiectasis.

    Two processes are critical and interwined in the pathogenesis of bronchiectasis: 1. obstruction and 2. chronic persistent infection. Either of these may come first. Normal clearance mechanisms are hampered by obstruction, so secondary infection soon follows. If the obstruction is chronic, the infection persists and causes damage to the bronchial walls, distending the airways permanently; conversely, chronic infection results in obstructive secretions and inflammation throughout the bronchial walls, distending the airway and leading to irreversible dilation.

    Clinical Features : -severe, persistent cough
    - expectoration of mucopurulent, sometimes fetid (foul smelling), sputum

    - sputum may contain flecks of blood
    - clubbing may develop
    - in widespread bronchiectasis, significant obstructive ventilatory defects occur leading to hypoxemia, hypercapnia, pulmonary hypertension and eventual heart failure (rarely).

    Clinical features of common Obstructive Respiratory Diseases

    Some of the clinical features of bronchiectasis are similar to other obstructive respiratory diseases, namely asthma, chronic bronchitis and emphysema, and may confuse the physician. Taking a thorough history from the patient (smoker? exposed to air irritants? dyspnea relieved by bronchodilators?) as well as having a good knowledge of the defining features of the common obstructive respiratory diseases will aid in clearing up this confusion and lead to a correct diagnosis.

    Now, let us go through the clinical features of common obstructive respiratory diseases.

    Asthma:
    - severe dyspnea and wheezing during asthmatic attacks
    - attacks last from 1 to several hours and subside either spontaneously or with bronchodilators and corticosteroids (obstruction is reversible)
    - intervals between attacks are generally free from respiratory defects but there may be persistent, subtle respiratory defects detected by the spirometer.

    Classic Emphysema (without chronic bronchitis):
    - dyspnea, begins insidiously but is slowly progressive
    - hyperventilation
    - commonly known as 'pink puffers'
    - barrel-chested


    Classic Chronic Bronchitis (without emphysema):
    - persistent, productive cough for at least 3 consecutive months in at least 2 consecutive years
    - production of sputum may persist indefinitely without ventilatory dysfunction
    - in severe cases, there may be significant outflow obstruction leading to hypercapnia, hypoxemia and cyanosis

    COPD (chronic bronchitis with emphysema):
    - features fall somewhere between those found in classic emphysema and classic chronic bronchitis
    - gradual development of pulmonary hypertension which may lead to right heart failure, respiratory acidosis, hypoxia, cyanosis and peripheral oedema
    - commonly known as 'blue bloaters'

    Source: Robins, chapter 13 Basic Pathology, 7th ed

    Contributed by John Lee

    Thursday 19 April 2007

    CAM options for Cystic Fibrosis

    By: Chris

    Sources:
    http://jpepsy.oxfordjournals.org/cgi/content/abstract/24/2/175 Oxford Journals
    http://www.umm.edu/altmed/articles/cystic-fibrosis-000045.htm University of Maryland Medical Center

    Nutrition and Supplements
    Following these nutritional tips may help reduce symptoms:
    • Eliminate potential food allergens and foods that increase mucous production, including dairy (milk, cheese, sour cream, and ice cream), wheat (gluten), soy, corn, potatoes, cabbage, bananas, sugar, preservatives, food additives and excessive salt and meats. Your health care provider may want to test for food sensitivities.
    • Eat more foods that decrease mucous production, including garlic, onions, watercress, horseradish, mustard, parsley, celery, rose hips tea, pickles, lemon, and anti-inflammatory oils (nuts, seeds, cold-water fish).
    • Eat more foods containing digestive enzymes, such as papaya and pineapple.
    • Avoid refined foods such as white breads, pastas, and sugar.
    • Eat fewer red meats and more lean meats, cold-water fish, tofu (soy, if no allergy) or beans for protein.
    • Use healthy cooking oils, such as olive oil or vegetable oil.
    • Reduce or eliminate trans-fatty acids, found in commercially baked goods such as cookies, crackers, cakes, French fries, onion rings, donuts, processed foods, and margarine.
    • Avoid coffee and other stimulants, alcohol, and tobacco.
    • Drink 6 - 8 glasses of filtered water daily.
    • Exercise moderately, for 30 minutes daily, 5 days a week.

    You may address nutritional deficiencies with the following supplements:
    • Omega-3 fatty acids, such as fish oil, 1 - 2 capsules or 1 tablespoonful of oil twice daily, to help decrease inflammation and improve immunity. Cold-water fish, such as salmon or halibut, are good food sources.
    • A multivitamin daily, containing the antioxidant vitamins A, C, D, E, the B-vitamins and trace minerals, such as magnesium, calcium, zinc, and selenium.
    • Digestive enzymes, 1 - 2 tablets three times daily with meals.
    • Coenzyme Q10, 100-200 mg at bedtime, for antioxidant and immune activity.
    • N-acetyl cysteine (NAC), 200 mg daily, for antioxidant effects. Alternative health care practitioners may use higher dosages. Check with your health care provider.
    • Probiotic supplement (containing Lactobacillus acidophilus) , 5 - 10 billion CFUs (colony forming units) a day, for maintenance of gastrointestinal and immune health. You should refrigerate your acidophilus products.
    • Grapefruit seed extract ( Citrus paradisi ), 100 mg capsule or 5 - 10 drops (in favorite beverage) three times daily, for antibacterial or antifungal activity, gastrointestinal health, and immunity.
    • Methylsulfonylmethane (MSM), 3,000 mg twice a day, to help decrease inflammation.
    • Whey protein, 10 - 20 grams daily mixed in favorite beverage, for support of immunity and weight gain, when needed.


    Herbs
    Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, you should work with your health care provider to get your problem diagnosed before starting any treatment. You may use herbs as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, you should make teas with 1 tsp. herb per cup of hot water. Steep covered 5 - 10 minutes for leaf or flowers, and 10 - 20 minutes for roots. Drink 2 - 4 cups per day. You may use tinctures alone or in combination as noted.
    • Ginkgo ( Ginkgo biloba ) standardized extract, 40 - 80 mg three times daily, for inflammation and as an antioxidant.
    • Green tea ( Camellia sinensis ) standardized extract, 250 - 500 mg daily, for antioxidant and immune effects. You may also prepare teas from the leaf of this herb.
    • Cat's claw ( Uncaria tomentosa ) standardized extract, 20 mg three times a day, for inflammation, immune and antibacterial or antifungal activity.
    • Milk thistle ( Silybum marianum ) seed standardized extract, 80 - 160 mg two to three times daily, for detoxification support.
    • Bromelain ( Ananus comosus ) standardized extract, 40 mg three times daily, for pain and inflammation.
    • Ground Ivy ( Hedera helix ) standardized extract, 50 mg three times daily, to decrease mucous production and to loosen phlegm.


    Homeopathy
    Although very few studies have examined the effectiveness of specific homeopathic therapies, professional homeopaths may consider the following treatments to alleviate respiratory symptoms (such as those experienced from cystic fibrosis) based on their knowledge and experience. Before prescribing a remedy, homeopaths take into account a person's constitutional type -- your physical, emotional, and psychological makeup. An experienced homeopath assesses all of these factors when determining the most appropriate treatment for each individual.
    The following treatments should be used under the guidance of a licensed, certified homeopath in addition to standard medical care provided by a medical doctor:
    • Antimonium tartaricum -- for wet, rattling cough (although the cough is usually too weak to bring up mucus material from the lungs) that is accompanied by extreme fatigue and difficulty breathing. Symptoms usually worsen when the person is lying down.
    • Carbo vegetabilis -- for shortness of breath with anxiety, chills, and bluish skin discoloration.


    Acupuncture
    Acupuncture may alleviate symptoms of cystic fibrosis. Acupuncture may help enhance immune function, normalize digestion, and strengthen respiratory function.


    Massage
    Therapeutic massage can help drain mucus from the lungs. Parents may reduce anxiety levels by massaging their children with cystic fibrosis and their children may benefit from receiving massage by having less anxiety and improved mood, which in turn may facilitate breathing.

    Investigation of Cystic Fibrosis

    Chest X ray of Cystic Fibrosis
    Sweat Test
    • For the past forty plus years, sweat testing has been the most effective, and therefore the most popular, test for detecting cystic fibrosis.
    How sweat test is performed
    • The sweat test is performed by using an electrode filled with pilocarpine
    • A current is run through the electrodes delivering the pilocarpine under the skin.
    • The electrodes are removed and the arm is left to rest for about a one-half hour with the filter paper.
    • The filter paper will soak up any sweat released from the person's skin. Once the one-half hour is up, the filter paper is placed into a flask and rinsed to release the sweat from the filter.
    • A digital chloridometer is used to measure the concentration of chloride ions in the fluid. If more than 60 mmol/liter is detected, cystic fibrosis is diagnosed.
    note:The sweat test may not work well in newborns because they do not produce enough sweat. In that case, another type of test, such as the immunoreactive trypsinogen test (IRT), may be used. In the IRT test, blood drawn 2 to 3 days after birth is analyzed for a specific protein called trypsinogen. Positive IRT tests must be confirmed by sweat and other tests.
    Heel Prick Test
    • is a common procedure for taking a blood sample from the heel of newborn infants.
    • Infants with cystic fibrosis 1 to 2 weeks of age show increased levels of immunoreactive trypsin in the plasma in the neonatal heel-prick test.
    • The test is positive if immunoreactive trypsin is greater than 80 mcg/litre. It is currently the best screening test for cystic fibrosis but cannot be done after the first few weeks of life since the immunoreactive trypsin falls as pancreatic insufficiency develops.
    Genetic Testing
    • The diagnosis of cystic fibrosis can also be confirmed by genetic testing in a person who exhibits one or more typical symptoms or has a history of cystic fibrosis in a sibling.
    • Finding two abnormal cystic fibrosis genes (mutations) confirms the diagnosis. However, because genetic testing can confirm only a small percentage of the more than 1000 different kinds of cystic fibrosis mutations, failure to detect two mutations does not exclude a diagnosis of cystic fibrosis.
    • The disease can be diagnosed prenatally by performing genetic testing on the fetus using chorionic villus sampling or amniocentesis
    Pulmonary Function Test
    • may show that breathing is compromised and are good indicators of how well the lungs are functioning.
    • reduced VC(Vital Capacity) suggest reduce of lung volume (restrictive lung disease),which is present in many patient with CF with advanced lung disease in whom lung parenchyma is destroyed due to chronic lung infection.Strictly speaking, restrictive lung disease may only be diagnosed is TLC(total lung capacity) is reduced
    • reduced FEV1 suggest narrowing of airway (obstructive lung disease) which is invariably present in patient with CF
    Chest X-ray & CT Scan
    • chest x-rays and computed tomography may be helpful to document lung infection and the extent of lung damage.
    • reduced VC(vital capacity) suggest reduction of lung volume (restrictive lung disease),which is present in many patient with CF with advanced lung disease in whom lung parenchyma has been destroyed due to chronic lung infection.Strictly speaking, restrictive lung disease may only be diagnosed if TLC(Total Lung Capacity) is reduced.
    • reduced FEV1 also suggest narrowing of airway (obstructive lung disease) which is almost invariably present in patient with CF
    Characteristic of CF in Chest X-Ray
    • Atelectasis

      • Discoid, segmental, lobar with RUL predominance

    • Mucoid impaction

      • Nodular and fingerlike densities along bronchovascular bundle

    • Cylindrical or cystic bronchiectasis

      • Peribronchial cuffing

    • Hilar adenopathy

    • Pulmonary arterial hypertension and cor pulmonale

    • Recurrent pneumonias, particularly Staph, Pseudomonas and P. cepacia

    • Clubbing and hypertrophic osteoarthropathy can occur

    • Recurrent pneumothorax is common

    Contributed by Lawrence Oh

    Sources:
    http://pediatrics.about.com/cs/conditions/l/bl_cf.htm
    http://www.merck.com/mmhe/sec04/ch053/ch053a.html