Factors affecting antipathy towards health care system
-bad experiences (unfriendly medical staff, death of loved ones)
-long waiting times (in public health care system)
-expensive private health care (exclusive to wealthy citizens)
-environment of hospital not exactly 'pleasant'
-distrust of modern medicine (instead relying on traditional healers and medicine)
use acronym "BLEED"
Possible solutions?
-public awareness of medical developments and treatment
-enhance interpersonal skills among medical staff (doctors, nurses etc.)
-patient-centred collaborative approach to treatment (as opposed to paternalistic treatment)
Prepared lovingly by chris :P
Showing posts with label pcl 11. Show all posts
Showing posts with label pcl 11. Show all posts
Thursday, 17 May 2007
PathoPhysiology of Nephrotic Syndrome
Note: Below is the summary of the pathophysiology of NS. As seen, it is the outline of our presentation.
1 Pathophysiology of Nephrotic Syndrome
Madhura S Naidu (Physiology)
Ji Keon Looi (Pathology)
MED2031, Monash University Malaysia
2 A constellation of clinical findings (IMPORTANT)
Proteinuria
Hypoalbuminemia
Hyperlipidaemia
Oedema
Lipiduria
Proteinuria
Hypoalbuminemia
Hyperlipidaemia
Oedema
Lipiduria
3 Overview
Nephrotic syndrome is caused by various disorders that damage
the kidneys, particularly the basement membrane of the
glomerulus.
This immediately causes abnormal excretion of protein in the
urine.
Nephrotic syndrome is caused by various disorders that damage
the kidneys, particularly the basement membrane of the
glomerulus.
This immediately causes abnormal excretion of protein in the
urine.
4 Glomerulus under normal conditions
5 GBM (filtration membrane)
6 Pathogenesis
The concentration of heparan sulfate mucopolysaccharide in the basement membrane is lower, and large amounts of
protein cross the barrier and are excreted. Why?
High glomerular permeability leads to hyperalbuminuria and, eventually, to hypoalbuminemia.
In turn, hypoalbuminemia lowers the plasma colloid osmotic pressure, causing greater transcapillary filtration of
water and the development of edema.
The concentration of heparan sulfate mucopolysaccharide in the basement membrane is lower, and large amounts of
protein cross the barrier and are excreted. Why?
High glomerular permeability leads to hyperalbuminuria and, eventually, to hypoalbuminemia.
In turn, hypoalbuminemia lowers the plasma colloid osmotic pressure, causing greater transcapillary filtration of
water and the development of edema.
7 Revision of oedema causation
In a steady state, the flux of water across the capillary wall can be expressed by the following formula
Qw = K ([Pc - Pi] - [pp - [pi])
Qw is net flux of water
K is the capillary filtration coefficient
Pc is plasma fluid hydrostatic pressure
Pi is the interstitial fluid hydrostatic pressure
pp is the plasma oncotic pressure
pi is the interstitial fluid oncotic pressure
In a steady state, the flux of water across the capillary wall can be expressed by the following formula
Qw = K ([Pc - Pi] - [pp - [pi])
Qw is net flux of water
K is the capillary filtration coefficient
Pc is plasma fluid hydrostatic pressure
Pi is the interstitial fluid hydrostatic pressure
pp is the plasma oncotic pressure
pi is the interstitial fluid oncotic pressure
8 In Nephrotic Syndrome
9 Nephrotic Dyslipidemia
The two mechanisms contributing to dyslipidemia are:
• Increased production of lipoproteins
• Impaired catabolism of lipoproteins
~ The liver is the site of synthesis of lipids and albumin, therefore hypoalbuminemia leads to an increased
stimulus for synthesis of proteins and VLDL/LDL
Important enzymes involved in cholesterol catabolism leak out the GBM defect in
conversion/catabolism of lipoproteins
Therefore, increased VLDL/LDL & lipoprotein (a), normal or decreased HDL serum levels
10 Summary
11 Thank you
http://www.patient.co.uk/showdoc/27000748/
http://www.emedicine.com/med/topic1612.htm (By Mahendra Agraharkar)
http://www.nlm.nih.gov/medlineplus/ency/article/000490.htm
Guyton Textbook of Medical Physiology 11th edn
investigations for nephrotic syndrome
Pcl 11_investigations and blood test for the nephritic syndrome
Ix
URINE analysis : determination of urine production rate and concentrating power of the kidneys; investigation of urinary tract infections; urinary protein indicates integrity glomerular filter; exclusion of diabetes mellitus; investigation of glomerular or tubular lesions
· dipstick( haematuria and proteinuria)
o reagent strips mainly detect raised albumin levels in urine (100-200 mg/L)
o if proteinuria is confirmed on repeated testing, 24 hr urine collections should be done
· Microscropy (RBCs, casts)
o Casts: cylindrical bodies in the shape of a tubular lumen
o 3 types: hyaline, granular or cellular
o Hyaline and fine granular casts represent precipitated protein and may be seen in normal urine, especially aftyer exercise
o Course granular casts occur with pathological proteinuria in glomerular and tubular disease
o Red cells casts are always indicative of renal disease
· Culture/sensitivity
· 24hr collection
BLOOD analysis: determination of integrity of renal function; glomerular filtration rate can be calculated from urinary and plasma creatinine concentration and urinary flow.
*full blood count
*blood test: for this case, plasma albumin, LDL,VLDL, HDL and glucose levels would be relevant
*Urea and electrolytes and creatinine in plasma
*Liver function test
*Erythrocyte sedimentation rate
*C- reactive protein
*Cholesterol: increase in low density lipoprotein, very low density lipoprotein, and/or intermediate density lipoprotein but no change in high density lipoprotein, resulting in an increase of the LDL/HDL cholesterol ratio.
*Immunoglobulins
*Serum electrophoresis
*Complement ( C3 and C4)
*Autoantibodies
IMAGING: determination of kidney size and symmetry; investigation of suspected tumours, cysts; etc; detection of calculi; position and integrity of ureters
*X-rays: chest x-ray may show cardiomegaly, pulmonary oedema, plain x-ray
*Renal ultrasound
RENAL BIOPSY
Carried out under ultrasound control
Helpful in investigation of nephrotic syndrome
Albumin
· Protein made in the liver
· Most abundant protein in the blood \Mostly responsible for oncotic pressure
· Used in transport of various substances (so they can be plasma soluble)
· More studies show that early detection of kidney disease (eg. via urine tests) ® Much better outcomes
Albumin in the urine is classified by quantity:
– Microalbuminuria = 30-300mg/24hrs
– Macroalbuminuria = >300mg/24hrs
– Proteinuria = >3g/24hrs
Glomerular Filtration Rate (GFR) = Rate that plasma is filtered through the glomeruli in the kidneys. Clinically we use Creatinine Clearance as a measure of GFR.
Creatinine Clearance = amount of plasma cleared of creatinine in one minute (we use creatinine because it is not really reabsorbed and only a little secreted).
– Normal Male = 90-140mL/min
– Normal Female = 80-125mL/min
Clearance (mL/min) = (U x V)/P where U = [Creatinine] in urine
V = Rate of urine output (mL/min)
P = [Creatinine] in plasma
**Note that serum creatinine will only begin to rise when Renal Fn has decreased to ~50%. Remember the exponential graph depicting a rise in Serum [Cr] after 50% loss of function
\Normal Serum [Cr] ¹ Normal Renal Fn.
Nephrotic Syndrome
Sign and Symptoms
1. Proteinuria – because problems with the glomerulus membrane.
2. Hypoproteinemia (hypoalbuminemia) – because lost in the urine.
3. Hyperlipidemia, hypercholesterolemia – due to increased lipoprotein synthesis to try to compensate for the loss of plasma albumin to maintain the plasma oncotic pressure. Also because there’s a decrease in clearance of triglyceride-rich lipoproteins due to inhibition of lipoprotein lipase and triglyceride lipase.
4. Oedema – because decrease in plasma oncotic pressure causing an extravasation of plasma water into the interstitial space. Noticeable in the face in the morning and predominately in lower extremities later in the day.
5. Facial swelling – due to the oedema (noticeable in the morning).
6. Swollen abdomen – accumulation of fluid in the abdominal cavity (ascites).
7. Shortness of breath – fluid accumulation in the space around the lungs (pleural effusion).
8. Foamy appearance of the urine – due to presence of protein in the urine.
9. Weight gain from fluid retention.
Others:
Poor appetite
High blood pressure
Susceptible to infections
Hypertension, hematuria and azotemia (rare)
Thromboembolism
Causes and Risk Factors
1. Minimal change disease
- idiopathic, but can occur due to drug use (NSAIDs) and hematologic malignancies (Hodgkin
lymphoma)
- edema and proteinuria but renal function normal
- more common in children age 2-6
2. Membranous Nephropathy
- deposition of immune complexes on the GBM causing GBM thickening (inflammation?)
- idiopathic but can be due to infection (Hepatitis B), drugs (gold, penicillamine, NSAIDs),
autoimmune (SLE), cancer
- more common after the age 40
3. Focal Segmental Glomerulosclerosis
- scattered (segmental) mesangial sclerosis in some but not all glomeruli.
- usually idiopathic, but can be caused by heroin use, HIV infection, obesity or nephron loss
(reflux nephropathy, subtotal nephrectomy), genetic causes
*http://www.cdc.gov/genomics/hugenet/reviews/NPH2.htm*
4. Diabetes mellitus (diabetic nephropathy)
- hyperglycaemia causes glycosylation of glomerular protein which is responsible for the
vascular endothelial damage, causing the GBM to become thickened.
- positive nodular deposits (mucopolysaccharides, fibrils and collagen) appear in the
mesangial space, at the periphery of the glomerulus, pushing the capillaries
- arteriosclerosis of the afferent and efferent arterioles
- walls of the vessels become abnormally thick but weak (bleed, leak protein, slow flow of
blood)
- occurs in long-standing diabetic patients
5. Systemic lupus erythematosus
- similar to membranous nephropathy
6. Renal amyloidosis (insoluble protein fibers are deposited in tissues and organs, making them
more rigid)
7. Infection (Hepatitis B & C)
8. Drug exposure (Gold, NSAIDs, penicillamine, heroin taken intravenously)
9. Malignancy (lymphoma, leukaemia)
10. Hereditary disorders
11. Immune disorders
1. Proteinuria – because problems with the glomerulus membrane.
2. Hypoproteinemia (hypoalbuminemia) – because lost in the urine.
3. Hyperlipidemia, hypercholesterolemia – due to increased lipoprotein synthesis to try to compensate for the loss of plasma albumin to maintain the plasma oncotic pressure. Also because there’s a decrease in clearance of triglyceride-rich lipoproteins due to inhibition of lipoprotein lipase and triglyceride lipase.
4. Oedema – because decrease in plasma oncotic pressure causing an extravasation of plasma water into the interstitial space. Noticeable in the face in the morning and predominately in lower extremities later in the day.
5. Facial swelling – due to the oedema (noticeable in the morning).
6. Swollen abdomen – accumulation of fluid in the abdominal cavity (ascites).
7. Shortness of breath – fluid accumulation in the space around the lungs (pleural effusion).
8. Foamy appearance of the urine – due to presence of protein in the urine.
9. Weight gain from fluid retention.
Others:
Poor appetite
High blood pressure
Susceptible to infections
Hypertension, hematuria and azotemia (rare)
Thromboembolism
Causes and Risk Factors
1. Minimal change disease
- idiopathic, but can occur due to drug use (NSAIDs) and hematologic malignancies (Hodgkin
lymphoma)
- edema and proteinuria but renal function normal
- more common in children age 2-6
2. Membranous Nephropathy
- deposition of immune complexes on the GBM causing GBM thickening (inflammation?)
- idiopathic but can be due to infection (Hepatitis B), drugs (gold, penicillamine, NSAIDs),
autoimmune (SLE), cancer
- more common after the age 40
3. Focal Segmental Glomerulosclerosis
- scattered (segmental) mesangial sclerosis in some but not all glomeruli.
- usually idiopathic, but can be caused by heroin use, HIV infection, obesity or nephron loss
(reflux nephropathy, subtotal nephrectomy), genetic causes
*http://www.cdc.gov/genomics/hugenet/reviews/NPH2.htm*
4. Diabetes mellitus (diabetic nephropathy)
- hyperglycaemia causes glycosylation of glomerular protein which is responsible for the
vascular endothelial damage, causing the GBM to become thickened.
- positive nodular deposits (mucopolysaccharides, fibrils and collagen) appear in the
mesangial space, at the periphery of the glomerulus, pushing the capillaries
- arteriosclerosis of the afferent and efferent arterioles
- walls of the vessels become abnormally thick but weak (bleed, leak protein, slow flow of
blood)
- occurs in long-standing diabetic patients
5. Systemic lupus erythematosus
- similar to membranous nephropathy
6. Renal amyloidosis (insoluble protein fibers are deposited in tissues and organs, making them
more rigid)
7. Infection (Hepatitis B & C)
8. Drug exposure (Gold, NSAIDs, penicillamine, heroin taken intravenously)
9. Malignancy (lymphoma, leukaemia)
10. Hereditary disorders
11. Immune disorders
Urine Test & GFR (Normal Vs Pathological)
GFR (Glomerular Filtration Rate)
- amount of filtrate formed per minute by two kidneys combined
- best test to measure the level of kidney function and determine the stage of kidney disease
- doctor can calculate it from the results of patient's blood creatinine test, patient's age, race, gender and other factors
- Normal GFR varies according to age, sex, and body size; in young adults it is approximately 120-130ml/min/1.73 m2 and declines with age.
- GFR can be expressed in ml/min or ml/min/1.73 m2
- GFR in Males approx 5mls higher, females approx 5mls lower). Therefore values >90 are normal for all. Converting for average surface area (per 1.73m2) removes the sex difference.
Attention: For clearer image of the above diagram, pls click on the picture. Creatine Clearance Test
- The creatinine clearance test compares the level of creatinine in urine with the creatinine level in the blood, usually based on measurements of a 24-hour urine sample and a blood sample drawn at the end of the 24-hour period. Clearance is often measured as milliliters/minute (ml/min).
- Because creatinine is found in stable plasma concentrations, is freely filtered and not reabsorbed, and is minimally secreted by the kidneys, creatinine clearance is used to estimate the glomerular filtration rate (GFR) -- the standard by which kidney function is assessed.
- Creatinine clearance overestimates GFR in a variety of circumstances, because of tubular secretion. This is particularly important at low levels of GFR. To calculate it, pay close attention to units and remember that there are 1440 minutes in 24hr . However 24 hour urine collections are error-prone and have been shown to be less accurate for estimating GFR than deductions from plasma creatinine.
Calculations: everyone knows it's UV/P but the units get a little confusing. This formula shows SI units.
| UV: | Amount of creatinine in 24h of urine is reported by the lab in mmol/24h. x1000 to convert to micromols |
| P: | Serum creatinine is reported in micromols/l. x1000 to do calculation for mls |
| 1440: | Number of minutes in 24h |
|
| |
How 24-hours Urine test is performed?
- On day 1, urinate into the toilet when you get up in the morning.
- Afterwards, collect all urine in a special container for the next 24 hours.
- On day 2, urinate into the container when you get up in the morning.
- Cap the container. Keep it in the refrigerator or a cool place during the collection period. Label the container with your name, the date, the time of completion, and return it as instructed.
- do not exercise more than usual while collecting urine
- if any urine is spilled and not collected, 24-hours urine test needed to be restarted.
GFR from Creatinine Clearance Test Result
- Normal values of GFR are as follows (normal value ranges may vary slightly among different laboratories):
* Male: 97 to 137 ml/min.
* Female: 88 to 128 ml/min.
Note: ml/min. = milliliters per minute
http://www.kidney.org/kidneydisease/ckd/knowGFR.cfm
http://www.nlm.nih.gov/medlineplus/ency/article/003611.htm
Contributed by Lawrence Oh
Wednesday, 16 May 2007
Epidemiology of Diabetes Mellitus
'Diabetes Can Kill More People Than Bird Flu,' says International Diabetes Institute Director Prof Paul Zimmet.
(Source: Bernama News)
Seriously?! Let's have a look at the statistics then...
Prevalence of diabetes
World: 246 million worldwide in 2006; mostly type 2 (90-95%); affects 5.9% of the world’s adult population; caused >3.8million deaths worldwide; 4th leading cause of death in most developed countries
Malaysia: estimated 1.2 million / roughly 1 in 10 adult Malaysians; more than half unaware that they’ve disease (2007); 95% type 2
By ethnicity, the prevalence of known diabetes in Indians 11.5% was significantly higher than other. There are geographical variations in the observed prevalence of diabetes by states. The highest observed prevalence of known diabetes occurred in the more developed states like Selangor 7.3%, and Penang 7.3.
Incidence of diabetes
World: 7 million develop diabetes each year
Malaysia: increasing at an estimated rate of 0.2 percent per year
Prevalence of complications in diabetic patients in Malaysia
Malaysia: Number of patients admitted into government hospitals due to diabetic complications had increased 100% from 21,872 in 1995 to 41,375 in 2005.
Diabetic Nephropathy
Malaysia: Diabetic nephropathy accounted for 47% of new cases of End-Stage Renal Failure
Generally speaking, Nephropathy develops in 20-40% of diabetics
Definition: Diabetic Nephropathy is a spectrum of progressive renal lesions secondary to diabetes mellitus ranging from renal hyperfiltration to ESRD.
Rates of control of diabetes in diabetic patients in Malaysia
A recent study carried out by the Institute of Health Management showed that only 10.5% of diabetics, who underwent follow-up treatment at establishments under the Health ministry, had their condition under control.
Add-on:
Many patients with type 2 diabetes are asymptomatic, and their disease is undiagnosed for many years. Studies suggest that the typical patient with new-onset type 2 diabetes has had diabetes for at least 4-7 years before it is diagnosed. Among patients with type 2 diabetes, 25% are believed to have retinopathy; 9%, neuropathy; and 8%, nephropathy at the time of diagnosis.
NB: This data was gathered from a study done in US. The figures for the prevalence of nephropathy in type 2 diabetics differ among countries. I could not obtain figures for the Malaysian scene but it is estimated by the Malaysian Diabetes Association that 10% of all diabetics patients suffer from nephropathy.
Hope this helps.
Contributed by John Lee
Sources:
International Diabetes Federation & Unite for Diabeteshttp://www.idf.org/home/index.cfm?unode=7F22F450-B1ED-43BB-A57C-B975D16A812D
http://www.unitefordiabetes.org/press/about/
Persatuan Diabetes Malaysia (Malaysian Diabetes Association) http://www.diabetes.org.my/article.php?aid=110
Universiti Sains Malaysia
http://www.medic.usm.my/~ssu/ARTICLES/article_12.htm
Clinical Practice Guideline on Diabetic Nephropathy 2003 by Malaysian Society of Nephrology
http://www.acadmed.org.my/cpg/Diabetic_Nephropathy_CPG_final.pdf
Quote from Minister of Health Datuk Seri Dr Chua Soi Leck
http://web5.bernama.com/ssig/index.php?option=com_content&task=view&id=9258&Itemid=95
Quote from Chairman Persatuan Diabetis Malaysia, Penang Branch
http://www.lions308b2.org.my/phpBB/viewtopic.php?p=146&sid=15ad39a5daf2b319fc4f73eede77e1a5
The Star Online 010507
http://thestar.com.my/news/story.asp?file=/2007/5/1/nation/17596213&sec=nation
Diabetes Mellitus, Type 2 - A Review, Scott R Votey, MD http://www.emedicine.com/emerg/topic134.htm
Tuesday, 15 May 2007
Diabetes Mellitus Type I and II
Ultimately, all forms are due to the beta cells of the pancreas being unable to produce sufficient insulin to prevent hyperglycemia.
-Type 1 is usually due to autoimmune destruction of the pancreatic beta cells which produce insulin.
-Type 1 diabetes mellitus—formerly known as insulin-dependent diabetes (IDDM), childhood diabetes or also known as juvenile diabetes, is characterized by loss of the insulin-producing beta cells of the islets of Langerhans of the pancreas leading to a deficiency of insulin.
-The main cause of beta cell loss leading to type 1 diabetes is a T-cell mediated autoimmune attack. The principal treatment of type 1 diabetes, even from the earliest stages, is replacement of insulin. Without insulin, ketosis and diabetic ketoacidosis can develop and coma or death will result.
-Type 2 is characterized by tissue-wide insulin resistance and varies widely; it sometimes progresses to loss of beta cell function.
-Type 2 diabetes mellitus—previously known as adult-onset diabetes, maturity-onset diabetes, or non-insulin-dependent diabetes mellitus (NIDDM)—is due to a combination of defective insulin secretion and insulin resistance or reduced insulin sensitivity (defective responsiveness of tissues to insulin), which almost certainly involves the insulin receptor in cell membranes
-There are numerous theories as to the exact cause and mechanism for this resistance, but central obesity (fat concentrated around the waist in relation to abdominal organs, and not subcutaneous fat, it seems) is known to predispose individuals for insulin resistance, possibly due to its secretion of adipokines (a group of hormones) that impair glucose tolerance. Abdominal fat is especially active hormonally. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes.
Diabetes Insipidus
-Diabetes insipidus is caused by the inability of the kidneys to conserve water, which leads to frequent urination and pronounced thirst.
-DI caused by a lack of ADH is called central diabetes insipidus. When DI is caused by failure of the kidneys to respond to ADH, the condition is called nephrogenic diabetes insipidus. The major symptoms of diabetes insipidus are excessive urination and extreme thirst. The sensation of thirst stimulates patients to drink large amounts of water to compensate for water lost in the urine.
Insulin Pen
Where should I inject the insulin?
Pull back on the plunger to draw insulin into the syringe.
The usual places to inject insulin are the upper arm, the front and side of the thighs, and the abdomen (tummy area).
How do I take insulin?
Insulin is normally injected under the skin with a very small needle. It can also be taken with an insulin pen. Here are some general tips on using insulin:
Clean the injection area using cotton and alcohol. Pinch an area of skin and inject insulin.
1. Wash your hands.
2. Take the plastic cover off of the insulin bottle and wipe the top of the bottle
with a cotton swab that you have dipped in alcohol.
3. Pull back the plunger of the syringe, drawing air into the syringe equal to the
dose of insulin that you are taking (measured in units). Put the syringe needle
through the rubber top of the insulin bottle. Inject air into the bottle by
pushing the syringe plunger forward. Turn the bottle upside down.
4. Make sure that the tip of the needle is in the insulin. Pull back on the
syringe plunger to draw the correct dose of insulin into the syringe .
5. Make sure there are no air bubbles in the syringe before you take the needle
out of the insulin bottle. If there are air bubbles, hold the syringe and the
bottle straight up, tap the syringe with your finger and let the air bubbles
float to the top. Push on the plunger of the syringe to move the air bubbles
back into the insulin bottle. Then withdraw the correct insulin dose by pulling
back on the plunger.
6. Clean your skin with cotton dipped in alcohol. Grab a fold of
skin and inject the insulin at a 90-degree angle. (If you’re thin, you may need
to pinch the skin and inject the insulin at a 45-degree angle.)
Prepared by:
Sri Murniati Rosli
Reference:
MedLine Plus
http://www.nlm.nih.gov/medlineplus/ency/article/000377.htm
Ultimately, all forms are due to the beta cells of the pancreas being unable to produce sufficient insulin to prevent hyperglycemia.
-Type 1 is usually due to autoimmune destruction of the pancreatic beta cells which produce insulin.
-Type 1 diabetes mellitus—formerly known as insulin-dependent diabetes (IDDM), childhood diabetes or also known as juvenile diabetes, is characterized by loss of the insulin-producing beta cells of the islets of Langerhans of the pancreas leading to a deficiency of insulin.
-The main cause of beta cell loss leading to type 1 diabetes is a T-cell mediated autoimmune attack. The principal treatment of type 1 diabetes, even from the earliest stages, is replacement of insulin. Without insulin, ketosis and diabetic ketoacidosis can develop and coma or death will result.
-Type 2 is characterized by tissue-wide insulin resistance and varies widely; it sometimes progresses to loss of beta cell function.
-Type 2 diabetes mellitus—previously known as adult-onset diabetes, maturity-onset diabetes, or non-insulin-dependent diabetes mellitus (NIDDM)—is due to a combination of defective insulin secretion and insulin resistance or reduced insulin sensitivity (defective responsiveness of tissues to insulin), which almost certainly involves the insulin receptor in cell membranes
-There are numerous theories as to the exact cause and mechanism for this resistance, but central obesity (fat concentrated around the waist in relation to abdominal organs, and not subcutaneous fat, it seems) is known to predispose individuals for insulin resistance, possibly due to its secretion of adipokines (a group of hormones) that impair glucose tolerance. Abdominal fat is especially active hormonally. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes.
Diabetes Insipidus
-Diabetes insipidus is caused by the inability of the kidneys to conserve water, which leads to frequent urination and pronounced thirst.
-DI caused by a lack of ADH is called central diabetes insipidus. When DI is caused by failure of the kidneys to respond to ADH, the condition is called nephrogenic diabetes insipidus. The major symptoms of diabetes insipidus are excessive urination and extreme thirst. The sensation of thirst stimulates patients to drink large amounts of water to compensate for water lost in the urine.
Insulin Pen
Where should I inject the insulin?
Pull back on the plunger to draw insulin into the syringe.
The usual places to inject insulin are the upper arm, the front and side of the thighs, and the abdomen (tummy area).
How do I take insulin?
Insulin is normally injected under the skin with a very small needle. It can also be taken with an insulin pen. Here are some general tips on using insulin:
Clean the injection area using cotton and alcohol. Pinch an area of skin and inject insulin.
1. Wash your hands.
2. Take the plastic cover off of the insulin bottle and wipe the top of the bottle
with a cotton swab that you have dipped in alcohol.
3. Pull back the plunger of the syringe, drawing air into the syringe equal to the
dose of insulin that you are taking (measured in units). Put the syringe needle
through the rubber top of the insulin bottle. Inject air into the bottle by
pushing the syringe plunger forward. Turn the bottle upside down.
4. Make sure that the tip of the needle is in the insulin. Pull back on the
syringe plunger to draw the correct dose of insulin into the syringe .
5. Make sure there are no air bubbles in the syringe before you take the needle
out of the insulin bottle. If there are air bubbles, hold the syringe and the
bottle straight up, tap the syringe with your finger and let the air bubbles
float to the top. Push on the plunger of the syringe to move the air bubbles
back into the insulin bottle. Then withdraw the correct insulin dose by pulling
back on the plunger.
6. Clean your skin with cotton dipped in alcohol. Grab a fold of
skin and inject the insulin at a 90-degree angle. (If you’re thin, you may need
to pinch the skin and inject the insulin at a 45-degree angle.)
Prepared by:
Sri Murniati Rosli
Reference:
MedLine Plus
http://www.nlm.nih.gov/medlineplus/ency/article/000377.htm
Monday, 14 May 2007
tasks for week 11
overview of diabetes mellitus,insipidus and insulin pen_sri
nephrotic syndrome
pathophysiology( parts of kidney affected,what?where?how?)
overview of oedema( in relation to nephrotic syndrome + albumin levels + cholesterol levels)
acquire hospital form_ ji keon and madhura
signs and symptoms, risk factors_vivian
Investigations and blood test_christine
GFR,normal vs pathological
24hr urine test( comparison b/w normal and pathological)_lawrence
management, prognosis and complications_shantz
_________________________________________________________________________
epidemiology of diabetes mellitus and nephrotic syndrome in m'sia, aus and around the world_john
antipathy of patient towards the healthcare system
management of the antipathy_chris
_________________________________________________________________________
groupings for research on treatment of diabetic complications
1)vivian, sri and ji
2)lawrence, shantz, chris
3)the rest
hey,sri beware of THE CHAIRMAN.oh,sorry about being late today,in view of my lateness,i shall bring some food on friday to make everyone happy!!!ahahahha,ok,i betta NOT forget that.hmm.
LOTS OF LOVE AND HATE
THE CHAIRMAN
nephrotic syndrome
pathophysiology( parts of kidney affected,what?where?how?)
overview of oedema( in relation to nephrotic syndrome + albumin levels + cholesterol levels)
acquire hospital form_ ji keon and madhura
signs and symptoms, risk factors_vivian
Investigations and blood test_christine
GFR,normal vs pathological
24hr urine test( comparison b/w normal and pathological)_lawrence
management, prognosis and complications_shantz
_________________________________________________________________________
epidemiology of diabetes mellitus and nephrotic syndrome in m'sia, aus and around the world_john
antipathy of patient towards the healthcare system
management of the antipathy_chris
_________________________________________________________________________
groupings for research on treatment of diabetic complications
1)vivian, sri and ji
2)lawrence, shantz, chris
3)the rest
hey,sri beware of THE CHAIRMAN.oh,sorry about being late today,in view of my lateness,i shall bring some food on friday to make everyone happy!!!ahahahha,ok,i betta NOT forget that.hmm.
LOTS OF LOVE AND HATE
THE CHAIRMAN
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