TO DO LIST
- Incidence and Prevalence and Definition - WHAT IS GFR? (SHAQ)
- Causes & Risk factors – WHAT IS RSHIP WITH DIABETES (PIGGY)
- Pathophysiology - FIND RSHIP FOR PLASMA CREATININE LEVELS & GFR (HUEY TING & EWE JIN)
- Sign and symptoms – SUMMARY OF CLINICAL FINDINGS AND WHY OCCURS (JB)
- Investigations and Examination – TEST TO MEASURE AND MONITOR RENAL FUNCTION, WHAT IS CREATININE CLEARENCE, WHAT IS EGFR AND ITS LIMITATIONS (ALEX & PRISH)
- Treatment Management – WHAT CAN BE DONE TO SLOW DOWN HOA’s KIDNEY DISEASE (FUAD & KAARTHIK)
- Complication and Prognosis – RETINOPATHY, NEUROPATHY, ARTHEROSCLEROSIS WHY OCCUR AND HOW TO PREVENT (KEE HAO & MONA)
Thursday, April 29, 2010
Thursday, April 15, 2010
Pathophysiology of COPD
The most consistent pathological finding is hypertrophy and increase in number of the mucus secreting goblet cells of the bronchial tree, evenly distributed throughout the lungs but mainly seen in the larger bronchi.
In more advanced cases, bronchi themselves are inflamed ; there will be infiltration of the walls of the bronchi and bronchiole with acute and chronic inflammatory cells and lymphoid follicles.
The epithelial layer may become ulcerated and when ulcers heal, squamous epithelium may replace the columnar cells – squamous metaplasia
Inflammation is then followed by scarring and a remodeling process that thickens the walls and leads to widespread narrowing in the small airways.
If the airway narrowing is combined with emphysema, then the resulting airflow is even more severe.
The small airways are particularly affected in the initial stage of the disease, initially without the development of any significant breathlessness.
The initial inflammation of the small airways are reversible ; there will be improvement if smoking stops early. In later stages, the inflammation continues even if smoking is stopped.
Emphysema leads to expiratory airflow limitation and air trapping. The loss of lung elastics recoil increases total lung capacity while the loss of alveoli with emphysema results in decreased gas transfer.
V/Q mismatch occurs because of damage and mucus plugging of smaller airways from chronic inflammation and partly because of the rapid closure of the smaller airways owing to loss of elastic recoil from emphysema.
This leads to a fall in PO2 and an increase in the work of respiration.
However, many patients will show low normal PCO2 values – pink puffers – seek to maintain their blood gases by increasing their respiratory effort.
Other patients who fail to maintain their respiratory effort will have a high level of CO2.
In the short term, the rise in CO2 level will stimulate the increase in respiration rate but in the long term, these patients become insensitive to CO2 and come to depend on hypoxemia to drive the ventilation.- adaptation of central chemoreceptors due to kidney compensation
These patients appear less breathless, and because they run on low PO2 level, production of RBCs and retention of fluid will be stimulated and hence, polycythaemia.
In consequence, they will become bloated, plethoric and cyanosed.
Attempts to abolish hypoxemia may make the situation much worse by decreasing respiratory drive in patients who rely on hypoxia to drive their ventilation.
In summary, 3 mechanisms are suggested for the limitation of airflow :
Loss of elasticity and alveolar attachments of air airways due to emphysema.
Inflammation and scarring – narrowing of airways
Mucus secretion which blocks the airways
Pathophysiology of asthma
Airways of asthma patients are hypersensitive type 1 hypersensitivity bronchi spasm inflammation
Parasympathetic of afferent nerve endings in the lining of the bronchus is stimulated and impulse travels to brain then efferent nerve endings releasing Ach and causing formation of inositol 1,4,5-triphosphate (IP3) in bronchial smooth muscles shortening bronchoconstriction.
Bronchial inflammation
Allergens gets ingested by antigen-presenting cells and present the allergen to immune cells TH0 and gets ignored, but in asthma, TH0 transform into TH2.
Activates humoral immune system antibodies against the inhaled allergen Inflammation wall of airway thicken, remodeling due to scaring of the airway, mucus producing cells grow larger and produce more and thicker.
The "hygiene hypothesis" postulates that an imbalance in the regulation of these TH cell types in early life leads to a long-term domination of the cells involved in allergic responses over those involved in fighting infection. The suggestion is that for a child being exposed to microbes early in life, taking fewer antibiotics, living in a large family, and growing up in the country stimulate the TH1 response and reduce the odds of developing asthma
Pathophysiology of Emphysema
Panacinar (or panlobular) emphysema: The entire respiratory acinus, from respiratory bronchiole to alveoli, is expanded. Occurs more commonly in the lower lobes, especially basal segments, and anterior margins of the lungs.[2]
Centroacinar (or centrilobular) emphysema: The respiratory bronchiole (proximal and cen-tral part of the acinus) is expanded. The distal acinus or alveoli are unchanged. Occurs more commonly in the upper lobes.[2]
Toxicants are breathed into the lungs, it is trapped in the alveoli Localized inflammation
One of the inflammatory response, leucocyte elactase cause alveolar septum to disintegrate.(Septal rupture) Deformed alveoli Reduced surface area Decrease gas exchange
Also decreased elastin, loss of support alveoli tend to collapse limiting air flow
With reduced surface area Thoracic cage expansion (barrel chest), and diaphragm contraction (flat-tening) CO2 exhalation impaired
As it continues to break down hyperventilation unable to compensate for shrinking surface area insufficient O2 vasoconstriction (hypoxic pulmonary vasoconstriction) pulmonary hypertension increased strain on right side of heart, right heart hypertrophy jugular venous distension blood start backing up (liver)
Alpha 1-antitrypsin (A1AT) breaks down elastase
Thus, increased risk in patients with alpha 1-antitrypsin deficiency for emphysema
However, more recent studies have brought into light the possibility that one of the many other numer-ous proteases, especially matrix metalloproteases might be equally or more relevant than neutrophil elastase in the development of non-hereditary emphysema.
In more advanced cases, bronchi themselves are inflamed ; there will be infiltration of the walls of the bronchi and bronchiole with acute and chronic inflammatory cells and lymphoid follicles.
The epithelial layer may become ulcerated and when ulcers heal, squamous epithelium may replace the columnar cells – squamous metaplasia
Inflammation is then followed by scarring and a remodeling process that thickens the walls and leads to widespread narrowing in the small airways.
If the airway narrowing is combined with emphysema, then the resulting airflow is even more severe.
The small airways are particularly affected in the initial stage of the disease, initially without the development of any significant breathlessness.
The initial inflammation of the small airways are reversible ; there will be improvement if smoking stops early. In later stages, the inflammation continues even if smoking is stopped.
Emphysema leads to expiratory airflow limitation and air trapping. The loss of lung elastics recoil increases total lung capacity while the loss of alveoli with emphysema results in decreased gas transfer.
V/Q mismatch occurs because of damage and mucus plugging of smaller airways from chronic inflammation and partly because of the rapid closure of the smaller airways owing to loss of elastic recoil from emphysema.
This leads to a fall in PO2 and an increase in the work of respiration.
However, many patients will show low normal PCO2 values – pink puffers – seek to maintain their blood gases by increasing their respiratory effort.
Other patients who fail to maintain their respiratory effort will have a high level of CO2.
In the short term, the rise in CO2 level will stimulate the increase in respiration rate but in the long term, these patients become insensitive to CO2 and come to depend on hypoxemia to drive the ventilation.- adaptation of central chemoreceptors due to kidney compensation
These patients appear less breathless, and because they run on low PO2 level, production of RBCs and retention of fluid will be stimulated and hence, polycythaemia.
In consequence, they will become bloated, plethoric and cyanosed.
Attempts to abolish hypoxemia may make the situation much worse by decreasing respiratory drive in patients who rely on hypoxia to drive their ventilation.
In summary, 3 mechanisms are suggested for the limitation of airflow :
Loss of elasticity and alveolar attachments of air airways due to emphysema.
Inflammation and scarring – narrowing of airways
Mucus secretion which blocks the airways
Pathophysiology of asthma
Airways of asthma patients are hypersensitive type 1 hypersensitivity bronchi spasm inflammation
Parasympathetic of afferent nerve endings in the lining of the bronchus is stimulated and impulse travels to brain then efferent nerve endings releasing Ach and causing formation of inositol 1,4,5-triphosphate (IP3) in bronchial smooth muscles shortening bronchoconstriction.
Bronchial inflammation
Allergens gets ingested by antigen-presenting cells and present the allergen to immune cells TH0 and gets ignored, but in asthma, TH0 transform into TH2.
Activates humoral immune system antibodies against the inhaled allergen Inflammation wall of airway thicken, remodeling due to scaring of the airway, mucus producing cells grow larger and produce more and thicker.
The "hygiene hypothesis" postulates that an imbalance in the regulation of these TH cell types in early life leads to a long-term domination of the cells involved in allergic responses over those involved in fighting infection. The suggestion is that for a child being exposed to microbes early in life, taking fewer antibiotics, living in a large family, and growing up in the country stimulate the TH1 response and reduce the odds of developing asthma
Pathophysiology of Emphysema
Panacinar (or panlobular) emphysema: The entire respiratory acinus, from respiratory bronchiole to alveoli, is expanded. Occurs more commonly in the lower lobes, especially basal segments, and anterior margins of the lungs.[2]
Centroacinar (or centrilobular) emphysema: The respiratory bronchiole (proximal and cen-tral part of the acinus) is expanded. The distal acinus or alveoli are unchanged. Occurs more commonly in the upper lobes.[2]
Toxicants are breathed into the lungs, it is trapped in the alveoli Localized inflammation
One of the inflammatory response, leucocyte elactase cause alveolar septum to disintegrate.(Septal rupture) Deformed alveoli Reduced surface area Decrease gas exchange
Also decreased elastin, loss of support alveoli tend to collapse limiting air flow
With reduced surface area Thoracic cage expansion (barrel chest), and diaphragm contraction (flat-tening) CO2 exhalation impaired
As it continues to break down hyperventilation unable to compensate for shrinking surface area insufficient O2 vasoconstriction (hypoxic pulmonary vasoconstriction) pulmonary hypertension increased strain on right side of heart, right heart hypertrophy jugular venous distension blood start backing up (liver)
Alpha 1-antitrypsin (A1AT) breaks down elastase
Thus, increased risk in patients with alpha 1-antitrypsin deficiency for emphysema
However, more recent studies have brought into light the possibility that one of the many other numer-ous proteases, especially matrix metalloproteases might be equally or more relevant than neutrophil elastase in the development of non-hereditary emphysema.
Job distribution
HYPONATREMIA
Definition & types fuad
Normal physiology: alex, kee hao, prish
Major sources of input and output of fluid in body, sources of sodium input and output of body
What is dextrose and why 5%? Difference btwn osmolarity, osmolality & tonicity
How fluid is distributed ECF and ICF?
What happens to osmolarity on input and output of water?
How is total input and output balanced- mechanism?
Pathophysiology & causes mona
Signs & symptoms . pikkie
Investigation/clinical examination karthik, jb
How to assess low sodium- normal blood test reading.
How to measure plasma osmolarity and tonicity
How did Sara find out?
Treatment/management shakir, ej
How to give dosage of saline/fluids.
Why is maintaining sodium level important? What happens to plasma volume?
Complications & prognosis huey ting
Definition & types fuad
Normal physiology: alex, kee hao, prish
Major sources of input and output of fluid in body, sources of sodium input and output of body
What is dextrose and why 5%? Difference btwn osmolarity, osmolality & tonicity
How fluid is distributed ECF and ICF?
What happens to osmolarity on input and output of water?
How is total input and output balanced- mechanism?
Pathophysiology & causes mona
Signs & symptoms . pikkie
Investigation/clinical examination karthik, jb
How to assess low sodium- normal blood test reading.
How to measure plasma osmolarity and tonicity
How did Sara find out?
Treatment/management shakir, ej
How to give dosage of saline/fluids.
Why is maintaining sodium level important? What happens to plasma volume?
Complications & prognosis huey ting
Wednesday, April 14, 2010
Signs & Symptoms and Causes of Chronic bronchitis
Definition- Bronchitis
Bronchitis is a term that describes inflammation of the bronchial tubes (bronchi and the smaller branches termed bronchioles) that results in excessive secretions of mucus into the tubes, leading to tissue swelling that can narrow or close off bronchial tubes. Bronchial tubes extend from the trachea and terminate at the alveoli in the lungs; the bronchial system resembles an inverted tree and is sometimes termed the "bronchial tree." A few authors include the trachea and upper airway in the definition. There are two major types of bronchitis, acute and chronic.
Definition-chronic bronchitis
Chronic bronchitis is defined as a cough that occurs every day with sputum production that lasts for at least three months, two years in a row. This definition was developed to help select uniform patients for research purposes i.e. to study medication therapies for treatment of chronic bronchitis. Many of the bronchi develop chronic inflammation with swelling and excess mucus production in chronic bronchitis; the inflammation, swelling, and mucus frequently and significantly inhibit the airflow to and from the lung alveoli by narrowing and partially obstructing the bronchi and bronchioles. Many cells that line the airway lose the function of their cilia (hair-like appendages that are capable of beating rapidly), and eventually the ciliated cells are lost. Cilia perform the function of moving particles and fluid (usually mucus) over the epithelial surface in such structures as the trachea, bronchial tubes, and nasal cavities to keep these hollow structures clear of particles and fluids. Mucus-producing cells increase due to irritation. These cells produce a viscous fluid that facilitates cleansing of the airway. If the mucus becomes thick (less fluid or viscous, it may contribute to airway blockage.
With long standing inflammation, as can be seen in chronic bronchitis, scarring inside the bronchial tree may develop. These scarred areas do not clear particles and secretions very well, and can result in a fixed, non reversible narrowing of the airway and the condition, chronic obstructive pulmonary disease (COPD). Chronic coughing develops as the body attempts to open and clear the bronchial airways of particles and mucus or as an overreaction to ongoing inflammation. Chronic bronchitis can be a progressive disease; symptoms (listed below) increase over time.
COPD also includes the entities of emphysema, chronic bronchitis, and chronic asthma. These conditions are not always separable and patients often have components of each. In the case of chronic bronchitis, the fixed airway obstruction, airway inflammation and retained secretions can result in a mismatch of blood flow and airflow in the lungs. This can impair oxygenation of the blood as well as removal of the waste product, carbon dioxide.
Although people of any age can develop chronic bronchitis, the majority of people diagnosed with the disease are 45 years of age or older.
Causes
There can be many causes of chronic bronchitis, but the main cause is cigarette smoke. Statistics from the US Centers for Disease Control and Prevention (CDC) suggest that about 49% of smokers develop chronic bronchitis and 24% develop emphysema/COPD. Some researchers suggest that about 90% of cases of chronic bronchitis are directly or indirectly caused by exposure to tobacco smoke.
Many other inhaled irritants (for example, smog, industrial pollutants, and solvents) can also result in chronic bronchitis.
Viral and bacterial infections that result in acute bronchitis may lead to chronic bronchitis if people have repeated bouts with infectious agents.
Also, underlying disease processes (for example, asthma, cystic fibrosis, immunodeficiency, congestive heart failure, familial genetic predisposition to bronchitis, and congenital or acquired dilation of the bronchioles, known as bronchiectasis) may cause chronic bronchitis to develop, but these are infrequent causes as compared to cigarette smoking.
Signs & Symptoms
Cough and sputum production are the most common symptoms; they usually last for at least three months and occur daily. The intensity of coughing and the amount and frequency of sputum production vary from patient to patient. Sputum may be clear, yellowish, greenish, or occasionally, blood-tinged. Since cigarette smoke is the most common cause for chronic bronchitis, it should not be surprising that the most common presentation is so called smoker's cough. This is characterized by a cough that tends to be worse upon arising and is often productive of discolored mucus in the early part of the day. As the day progresses, less mucus is produced.
Dyspnea (shortness of breath) gradually increases with the severity of the disease. Mucus plugs up and makes it hard for them to bresthe. Usually, people with chronic bronchitis get short of breath with activity and begin coughing; dyspnea at rest usually signals that COPD or emphysema has developed.
Wheezing (a coarse whistling sound produced when airways are partially obstructed) often occurs.
In addition, symptoms of fatigue, sore throat, muscle aches, nasal congestion, and headaches can accompany the major symptoms. Severe coughing may cause chest pain; cyanosis (bluish/grayish skin coloration) may develop in people with advanced COPD. Fever may indicate a secondary viral or bacterial lung infection. When symptoms worsen or become more frequent, this is often referred to as an exacerbation of chronic bronchitis. These exacerbations often require antibiotics, and may need steroid medication and an increase in respiratory inhaled medications.
Diagnosis
Using a combination of a person's medical history, physical exam, and diagnostic tests. A history of a daily productive (sputum production) cough that lasts at least three months, especially if has occurred two years in a row, fits the criteria for a clinical diagnosis of chronic bronchitis. The physical examination often allows caregivers to hear wheezes, a sign of airflow obstruction.
A chest X-ray is often performed to help rule out other lung problems (for example, pneumonia, bronchial obstructions). Additional tests such as a complete blood count(CBC), arterial blood gas measurements, CT scan of the chest, and pulmonary function tests are often done to characterize the structure and function of the lungs and to exclude other conditions.
Reference:
http://www.medicinenet.com/chronic_bronchitis/article.htm#what
http://familydoctor.org/online/famdocen/home/articles/280.printerview.html
http://www.nlm.nih.gov/medlineplus/bronchitis.html
Bronchitis is a term that describes inflammation of the bronchial tubes (bronchi and the smaller branches termed bronchioles) that results in excessive secretions of mucus into the tubes, leading to tissue swelling that can narrow or close off bronchial tubes. Bronchial tubes extend from the trachea and terminate at the alveoli in the lungs; the bronchial system resembles an inverted tree and is sometimes termed the "bronchial tree." A few authors include the trachea and upper airway in the definition. There are two major types of bronchitis, acute and chronic.
Definition-chronic bronchitis
Chronic bronchitis is defined as a cough that occurs every day with sputum production that lasts for at least three months, two years in a row. This definition was developed to help select uniform patients for research purposes i.e. to study medication therapies for treatment of chronic bronchitis. Many of the bronchi develop chronic inflammation with swelling and excess mucus production in chronic bronchitis; the inflammation, swelling, and mucus frequently and significantly inhibit the airflow to and from the lung alveoli by narrowing and partially obstructing the bronchi and bronchioles. Many cells that line the airway lose the function of their cilia (hair-like appendages that are capable of beating rapidly), and eventually the ciliated cells are lost. Cilia perform the function of moving particles and fluid (usually mucus) over the epithelial surface in such structures as the trachea, bronchial tubes, and nasal cavities to keep these hollow structures clear of particles and fluids. Mucus-producing cells increase due to irritation. These cells produce a viscous fluid that facilitates cleansing of the airway. If the mucus becomes thick (less fluid or viscous, it may contribute to airway blockage.
With long standing inflammation, as can be seen in chronic bronchitis, scarring inside the bronchial tree may develop. These scarred areas do not clear particles and secretions very well, and can result in a fixed, non reversible narrowing of the airway and the condition, chronic obstructive pulmonary disease (COPD). Chronic coughing develops as the body attempts to open and clear the bronchial airways of particles and mucus or as an overreaction to ongoing inflammation. Chronic bronchitis can be a progressive disease; symptoms (listed below) increase over time.
COPD also includes the entities of emphysema, chronic bronchitis, and chronic asthma. These conditions are not always separable and patients often have components of each. In the case of chronic bronchitis, the fixed airway obstruction, airway inflammation and retained secretions can result in a mismatch of blood flow and airflow in the lungs. This can impair oxygenation of the blood as well as removal of the waste product, carbon dioxide.
Although people of any age can develop chronic bronchitis, the majority of people diagnosed with the disease are 45 years of age or older.
Causes
There can be many causes of chronic bronchitis, but the main cause is cigarette smoke. Statistics from the US Centers for Disease Control and Prevention (CDC) suggest that about 49% of smokers develop chronic bronchitis and 24% develop emphysema/COPD. Some researchers suggest that about 90% of cases of chronic bronchitis are directly or indirectly caused by exposure to tobacco smoke.
Many other inhaled irritants (for example, smog, industrial pollutants, and solvents) can also result in chronic bronchitis.
Viral and bacterial infections that result in acute bronchitis may lead to chronic bronchitis if people have repeated bouts with infectious agents.
Also, underlying disease processes (for example, asthma, cystic fibrosis, immunodeficiency, congestive heart failure, familial genetic predisposition to bronchitis, and congenital or acquired dilation of the bronchioles, known as bronchiectasis) may cause chronic bronchitis to develop, but these are infrequent causes as compared to cigarette smoking.
Signs & Symptoms
Cough and sputum production are the most common symptoms; they usually last for at least three months and occur daily. The intensity of coughing and the amount and frequency of sputum production vary from patient to patient. Sputum may be clear, yellowish, greenish, or occasionally, blood-tinged. Since cigarette smoke is the most common cause for chronic bronchitis, it should not be surprising that the most common presentation is so called smoker's cough. This is characterized by a cough that tends to be worse upon arising and is often productive of discolored mucus in the early part of the day. As the day progresses, less mucus is produced.
Dyspnea (shortness of breath) gradually increases with the severity of the disease. Mucus plugs up and makes it hard for them to bresthe. Usually, people with chronic bronchitis get short of breath with activity and begin coughing; dyspnea at rest usually signals that COPD or emphysema has developed.
Wheezing (a coarse whistling sound produced when airways are partially obstructed) often occurs.
In addition, symptoms of fatigue, sore throat, muscle aches, nasal congestion, and headaches can accompany the major symptoms. Severe coughing may cause chest pain; cyanosis (bluish/grayish skin coloration) may develop in people with advanced COPD. Fever may indicate a secondary viral or bacterial lung infection. When symptoms worsen or become more frequent, this is often referred to as an exacerbation of chronic bronchitis. These exacerbations often require antibiotics, and may need steroid medication and an increase in respiratory inhaled medications.
Diagnosis
Using a combination of a person's medical history, physical exam, and diagnostic tests. A history of a daily productive (sputum production) cough that lasts at least three months, especially if has occurred two years in a row, fits the criteria for a clinical diagnosis of chronic bronchitis. The physical examination often allows caregivers to hear wheezes, a sign of airflow obstruction.
A chest X-ray is often performed to help rule out other lung problems (for example, pneumonia, bronchial obstructions). Additional tests such as a complete blood count(CBC), arterial blood gas measurements, CT scan of the chest, and pulmonary function tests are often done to characterize the structure and function of the lungs and to exclude other conditions.
Reference:
http://www.medicinenet.com/chronic_bronchitis/article.htm#what
http://familydoctor.org/online/famdocen/home/articles/280.printerview.html
http://www.nlm.nih.gov/medlineplus/bronchitis.html
Financial and social implications of asthma
The stress of living with a chronic disease reveals itself in many ways among the various family members.
Someone with asthma may be more likely to
• get involved in fights
• be less cooperative
• be stubborn
• depressed
• anxious
• Withdrawn
• Be timid
Parents of kids with asthma are more likely to suffer from
• Fatigue
• Headaches
• Insomnia
• Depression and
• Appetite loss
Siblings of kids with asthma may
• Feel guilty, thinking that somehow they have caused the illness.
• They also may be jealous or angry because of the additional attention their sibling receives
• or they may be afraid that they may get the asthma themselves
• Some may also feel embarrassed by the symptoms that their sibling displays
Financial Strain
Nebulizer - RM 15-20 each time, at clinic
Medication for the inhaler
• Nonsteroidal RM 20
• Steroidal RM 40
Drugs - for when needed RM 20
But………………….
These are not the only costs…………………
1. MEDICAL RELATED COSTS
Pharmaceutical
Medical Consultations
Hospital
Indirect Medical - Secondary illnesses
CM - such as acupuncture, homoeopathy, physiotherapy or chiropractice
Ambulance
2. INDIRECT COSTS .
Absenteeism
Lost Productivity At Work
Travel Cost and Time For Treatment
http://www.healthinsite.gov.au/expert/Asthma___Expert_View
Someone with asthma may be more likely to
• get involved in fights
• be less cooperative
• be stubborn
• depressed
• anxious
• Withdrawn
• Be timid
Parents of kids with asthma are more likely to suffer from
• Fatigue
• Headaches
• Insomnia
• Depression and
• Appetite loss
Siblings of kids with asthma may
• Feel guilty, thinking that somehow they have caused the illness.
• They also may be jealous or angry because of the additional attention their sibling receives
• or they may be afraid that they may get the asthma themselves
• Some may also feel embarrassed by the symptoms that their sibling displays
Financial Strain
Nebulizer - RM 15-20 each time, at clinic
Medication for the inhaler
• Nonsteroidal RM 20
• Steroidal RM 40
Drugs - for when needed RM 20
But………………….
These are not the only costs…………………
1. MEDICAL RELATED COSTS
Pharmaceutical
Medical Consultations
Hospital
Indirect Medical - Secondary illnesses
CM - such as acupuncture, homoeopathy, physiotherapy or chiropractice
Ambulance
2. INDIRECT COSTS .
Absenteeism
Lost Productivity At Work
Travel Cost and Time For Treatment
http://www.healthinsite.gov.au/expert/Asthma___Expert_View
Differences between patients suffering from emphysema (pink puffers) and chronic bronchitis (blue bloaters)
Clinical feature................Emphysema...............Chronic bronchitis
Dyspnoea.........................Sever........................Mild
Cough.......................After Dyspnoea starts.......Before Dyspnoea starts
Sputum.........................Scantly mucoid.................Purulent
Mucopurulent relapses...........Less frequent................More frequent
Cyanosis...........................Absent..............Present (Blue bloaters!!)
Hyperventilation...............Late and mild...............Early and severe
Dyspnoea.........................Sever........................Mild
Cough.......................After Dyspnoea starts.......Before Dyspnoea starts
Sputum.........................Scantly mucoid.................Purulent
Mucopurulent relapses...........Less frequent................More frequent
Cyanosis...........................Absent..............Present (Blue bloaters!!)
Hyperventilation...............Late and mild...............Early and severe
Smoking statistics & smoking cessation guidelines
Global statistics
•About 12x more British people have died from smoking than from WWII.
•One British survey found that nearly 99% of women did not know of the link between smoking and cervical cancer.
•Around 80,000 – 100,000 children worldwide start smoking every day – roughly half of whom live in Asia.
•In Asia, tobacco companies are among the top 10 advertisers in Cambodia, Indonesia, Malaysia, Myanmar and the Philippines.
•A survey in the UK found about half of smokers think that smoking “can’t really be all that dangerous, or the Government wouldn’t let cigarettes be advertised”.
WHO, 2002 (stats in Malaysia)
•About 50% Malaysian men smoke.
•About 30% of adolescent boys (aged 12 to 18) smoke.
•The numbers of female teens smoking rose from 4.8% to 8% from 1996 – 1999. Nearly one in five teens smokes.
•Smoking rates are highest in rural Kelantan and lowest in urban Penang and Sarawak.
•Malaysia has been dubbed the "indirect advertising capital" of the world.
•Some of the tobacco industry's most obvious efforts to target young people can be seen here.
Smoking Cessation Guidelines
http://www.ahrq.gov/clinic/tobacco/clinhlpsmksqt.htm
•About 12x more British people have died from smoking than from WWII.
•One British survey found that nearly 99% of women did not know of the link between smoking and cervical cancer.
•Around 80,000 – 100,000 children worldwide start smoking every day – roughly half of whom live in Asia.
•In Asia, tobacco companies are among the top 10 advertisers in Cambodia, Indonesia, Malaysia, Myanmar and the Philippines.
•A survey in the UK found about half of smokers think that smoking “can’t really be all that dangerous, or the Government wouldn’t let cigarettes be advertised”.
WHO, 2002 (stats in Malaysia)
•About 50% Malaysian men smoke.
•About 30% of adolescent boys (aged 12 to 18) smoke.
•The numbers of female teens smoking rose from 4.8% to 8% from 1996 – 1999. Nearly one in five teens smokes.
•Smoking rates are highest in rural Kelantan and lowest in urban Penang and Sarawak.
•Malaysia has been dubbed the "indirect advertising capital" of the world.
•Some of the tobacco industry's most obvious efforts to target young people can be seen here.
Smoking Cessation Guidelines
http://www.ahrq.gov/clinic/tobacco/clinhlpsmksqt.htm
Saturday, April 10, 2010
COPD - Financial & Social Burden, Kicking the Habit
Financial Burden
In 2008, the financial cost of COPD in Australia was $8.8 billion.
Of this:
¡ $6.8 billion was productivity lost due to lower employment, absenteeism and premature death of Australians with COPD
¡$0.9 billion was direct health system expenditure
¡- $1.2 billion including welfare payments and taxation foregone, and other indirect costs such as aids and home modifications
Additionally, the overall value of loss of wellbeing due to COPD is estimated at a further $89.4 billion
Health costs - in 2008, COPD will cost the economy an estimated $98 billion
In Europe, 2001:
¡Per patient Direct costs £819.42
¡Per patient Indirect costs £819.66
Social Burden
Depression and anxiety much higher (in COPD) than in the general community:
¡40% to 12.3% depression
¡ 36% anxiety to 9% depression
Feeling fatigued easily makes activities less enjoyable and frustrating. Sometimes even stressful. Increased stress leads to many psychological problems which increases social burden.
Kicking the Habit
Employers may introduce an incentive to smokers vs. non-smokers. Eg. Charge an extra RM150 to smokers for health insurance. Ask a loved one to help in quitting smoking. Join a support group.
Nicotine Replacement Therapy:
¡involves "replacing" cigarettes with other nicotine substitutes, such as nicotine gum, patch, nasal spray, inhaler, and lozenges.
¡Delivers “small and steady doses” of nicotine into the body to relieve some of the withdrawal symptoms without the tars and poisonous gases found in cigarettes.
Drug Therapy
¡Buproprion. Similar to varenicline, but less desirable safety profile. (eg. Causes fits)
¡In Malaysia, Pfizer markets varenicline.
Hypnosis
¡Places a suggestion in the subconscious in order to strengthen will against smoking.
Behavioural therapy
Motivational therapy
Friday, April 2, 2010
Investigations for Obstructive Sleep Apnea
Polysomnography
Basically a diagnostic sleep study. Measures sleep cycles of a person by recording information such as:
-Blood oxygen levels (Oximeter)
–Body position (Device placed on chest)
–Brain waves (EEG): Measurement of electrical signals from the brain to determine whether you are awake or asleep and what stage of sleep you are in.
–Breathing rate
–Eye movement (EOG) – to determine REM sleep. Some people have worse symptoms in REM sleep.
–Heart rate
AHI measures the number of atypical breathing incidents during 1 hour of sleep. An AHI of 5 or less is normal; 5 to 14 is mild obstructive sleep apnea; 15 to 29 is moderate obstructive sleep apnea; more than 30 is severe. RDI is AHI/hr. All oxygen desaturations <90% during sleep are considered medically significant.
Performed at a special sleep center. The test is often done during the night so that your normal sleep patterns can be studied. Electrodes will be placed on your chin, scalp, and the outer edge of your eyelids. These must remain in place while you sleep.
Signals from electrodes are recorded while you are awake (with your eyes closed) and during sleep. The time it takes you to fall asleep is measured, as well as the time it takes you to enter REM sleep.
Monitors to record your heart rate and breathing will be attached to your chest. These also must remain in place while you sleep. A specially trained health care provider will directly observe you while you sleep and note any changes in your breathing or heart rate. The number of times that you either stop breathing or almost stop breathing will be measured. In some sleep study centers, a video camera records your movements during sleep.
Multiple Sleep Latency Test: In some cases, a multiple sleep latency test is performed on the day after the overnight test to measure the speed of falling asleep. In this test, patients are given several opportunities to fall asleep during the course of a day when they normally would be awake.
At-Home Sleep Apnea Test: To diagnose sleep apnea, a portable test, which can be conducted at home can be used as an alternative to polysomnogram for diagnosing obstructive sleep apnea. The home tests are portable devices that are composed of a recording device, belts, sensors and other cables. The data gathered overnight has to be reviewed by sleep specialist and thereby diagnosis and treatment plan has to be developed.
Sleep studies can also determine whether you have a problem with your stages of sleep. Normally, NREM and REM alternate 4 to 5 times during a night's sleep. A change in this cycle may make it hard for you to sleep soundly. Non-REM sleep is in turn further divided into four different stages (1 through 4), with stages 3 and 4 often referred to as "deep sleep." Normal sleep patterns break down your time asleep as follows: stage one sleep for 5% of the time, stage two for 55% of the time, stage three and four at 20% of the time and REM sleep for 20%.
ECG
Not a gold standard exam to diagnose OSA. Research has been done to diagnose OSA using ECG, with high success rate (80 to 95% accuracy). Use of algorithms. However, in a sleep study, ECG is used to detect irregularities in heart beat or rhythm. Complications of OSA is right ventricular hypertrophy, which may eventually lead to cor pulmonale. Also may be left ventricular hypertrophy. Can be detected by ECG – right or left axis deviation.
Basically a diagnostic sleep study. Measures sleep cycles of a person by recording information such as:
-Blood oxygen levels (Oximeter)
–Body position (Device placed on chest)
–Brain waves (EEG): Measurement of electrical signals from the brain to determine whether you are awake or asleep and what stage of sleep you are in.
–Breathing rate
–Eye movement (EOG) – to determine REM sleep. Some people have worse symptoms in REM sleep.
–Heart rate
AHI measures the number of atypical breathing incidents during 1 hour of sleep. An AHI of 5 or less is normal; 5 to 14 is mild obstructive sleep apnea; 15 to 29 is moderate obstructive sleep apnea; more than 30 is severe. RDI is AHI/hr. All oxygen desaturations <90% during sleep are considered medically significant.
Performed at a special sleep center. The test is often done during the night so that your normal sleep patterns can be studied. Electrodes will be placed on your chin, scalp, and the outer edge of your eyelids. These must remain in place while you sleep.
Signals from electrodes are recorded while you are awake (with your eyes closed) and during sleep. The time it takes you to fall asleep is measured, as well as the time it takes you to enter REM sleep.
Monitors to record your heart rate and breathing will be attached to your chest. These also must remain in place while you sleep. A specially trained health care provider will directly observe you while you sleep and note any changes in your breathing or heart rate. The number of times that you either stop breathing or almost stop breathing will be measured. In some sleep study centers, a video camera records your movements during sleep.
Multiple Sleep Latency Test: In some cases, a multiple sleep latency test is performed on the day after the overnight test to measure the speed of falling asleep. In this test, patients are given several opportunities to fall asleep during the course of a day when they normally would be awake.
At-Home Sleep Apnea Test: To diagnose sleep apnea, a portable test, which can be conducted at home can be used as an alternative to polysomnogram for diagnosing obstructive sleep apnea. The home tests are portable devices that are composed of a recording device, belts, sensors and other cables. The data gathered overnight has to be reviewed by sleep specialist and thereby diagnosis and treatment plan has to be developed.
Sleep studies can also determine whether you have a problem with your stages of sleep. Normally, NREM and REM alternate 4 to 5 times during a night's sleep. A change in this cycle may make it hard for you to sleep soundly. Non-REM sleep is in turn further divided into four different stages (1 through 4), with stages 3 and 4 often referred to as "deep sleep." Normal sleep patterns break down your time asleep as follows: stage one sleep for 5% of the time, stage two for 55% of the time, stage three and four at 20% of the time and REM sleep for 20%.
ECG
Not a gold standard exam to diagnose OSA. Research has been done to diagnose OSA using ECG, with high success rate (80 to 95% accuracy). Use of algorithms. However, in a sleep study, ECG is used to detect irregularities in heart beat or rhythm. Complications of OSA is right ventricular hypertrophy, which may eventually lead to cor pulmonale. Also may be left ventricular hypertrophy. Can be detected by ECG – right or left axis deviation.
Thursday, April 1, 2010
tasks for pcl week 6
Learning issues
· Definition, types of COPD, Prevalence & incidence of COPD in Australia & msia Kaarthik
· Pathophysiology – emphysema, chronic bronchitis, respiratory physiology & pathology hueyting, kee hao
· Patterns of respiratory function (diagram – norm, severe, restrictive, obstructive), difference between patients suffering from emphysema(pink puffers) & chronic bronchitis (blue bloaters)mona
· Causes of severe symptoms & aetiology of COPD, signs & symptoms of emphysema, chronic bronchitis, clinical findings, why it occurs?shakir, jun beng
· Investigation – definitive test for COPD, test for monitoring & potential complication prisheila
· Financial & social burden in health for COPD, Smoking cessation guidelines (TAK NAK campaign), smoking statistics, how to motivate patient to quit smoking? – NOT prochaska-diclemente (eg: nicotine patch) fuad, pikyin
· Management of COPD, benefits of seeing a regular doctor, Difference between asthma & COPD – irreversible? Etc…lung function test ewejin
· Complication & prognosis of COPD, Long term prognosis for Shamila as smoker & non smokeralex
· Definition, types of COPD, Prevalence & incidence of COPD in Australia & msia Kaarthik
· Pathophysiology – emphysema, chronic bronchitis, respiratory physiology & pathology hueyting, kee hao
· Patterns of respiratory function (diagram – norm, severe, restrictive, obstructive), difference between patients suffering from emphysema(pink puffers) & chronic bronchitis (blue bloaters)mona
· Causes of severe symptoms & aetiology of COPD, signs & symptoms of emphysema, chronic bronchitis, clinical findings, why it occurs?shakir, jun beng
· Investigation – definitive test for COPD, test for monitoring & potential complication prisheila
· Financial & social burden in health for COPD, Smoking cessation guidelines (TAK NAK campaign), smoking statistics, how to motivate patient to quit smoking? – NOT prochaska-diclemente (eg: nicotine patch) fuad, pikyin
· Management of COPD, benefits of seeing a regular doctor, Difference between asthma & COPD – irreversible? Etc…lung function test ewejin
· Complication & prognosis of COPD, Long term prognosis for Shamila as smoker & non smokeralex
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