Rohani, 30, 2 past pregnancies in the past, currently 3rd pregnancy
Occupation=work in paddy field, strenous, under hot sun.
Cone biopsy in the past because of cervical carcinoma in situ. Increased frequency, T=38C
Urinalysis=positive for blood and UTI.
Membrane intact, 2cm dilated. 30th week of pregnancy.
Ddx=Pre-term labour, UTI?
Diagnosis=Pre-term labour.
Causes of preterm labour?
=multiple pregnancies, infection, drugs, stress, low SES(malnutrition etc), cone biopsy.
Definition, Causes, Epid :Kaarthik
Signs and Symptoms : Pik Yin
Normal physiology of labour : Huey Ting, Jun Beng
Causes of pre-term labour :Fuad
Management of pre-term labour, pre-term neonatal care(APGAR Score, normal scores for heart rate, Oxygen saturation, RR, Pa02) : Kee Hao, Mona
Prognosis of baby delivered 30/40
complications of baby(10 weeks early:respiratory, cranial haemorrhage, T regulation and mother
Breastfeeding complications, Respiratory Distress Syndrome : Prish, Shakir, Ewe Jin
Psychosocial and cultural issues
involving mother and preterm baby, family support : Rui Wan
Thursday, October 14, 2010
Thursday, October 7, 2010
PCL 10 - Waterworks
Symptoms:
Nocturia
Urgency
Dribbling
Diff Dx:
Benign Prostatic Hyperplasia (most likely la ha.)
Prostate Cancer
Bladder Cancer
Learning Issues:
Definition for BPH, Prevalence, Incidence, Types (How common are these symptoms in the population) -Mona
Signs and Symptoms (IPSS - Internation prostate symptom score) - Prish
Anatomy of the Prostate, Pathophysio (What is BPH compared to prostate cancer?) - Fuad, Huey Ting
Causes - Ewe jin
Diagnosis and investigation (What are you likely to find through DRE?; Diagnostic accruacy of DRE ; Characteristics that indicate BPH or malignancy; What happens if the test is positive, negative, or inconclusive? ; investigation for BPH and prostate cancer; reliability of available tests; PSA; Biopsy complications) - Alex, Karthik, Jun Beng
Management (consider risk and benefits.) - Pik Yin
Prognosis and complications - Shakir
Psychosocial and cultural issues (Why was Marzuki embarrassed to admit his problem?) - Kee Hao
Nocturia
Urgency
Dribbling
Diff Dx:
Benign Prostatic Hyperplasia (most likely la ha.)
Prostate Cancer
Bladder Cancer
Learning Issues:
Definition for BPH, Prevalence, Incidence, Types (How common are these symptoms in the population) -Mona
Signs and Symptoms (IPSS - Internation prostate symptom score) - Prish
Anatomy of the Prostate, Pathophysio (What is BPH compared to prostate cancer?) - Fuad, Huey Ting
Causes - Ewe jin
Diagnosis and investigation (What are you likely to find through DRE?; Diagnostic accruacy of DRE ; Characteristics that indicate BPH or malignancy; What happens if the test is positive, negative, or inconclusive? ; investigation for BPH and prostate cancer; reliability of available tests; PSA; Biopsy complications) - Alex, Karthik, Jun Beng
Management (consider risk and benefits.) - Pik Yin
Prognosis and complications - Shakir
Psychosocial and cultural issues (Why was Marzuki embarrassed to admit his problem?) - Kee Hao
Thursday, September 30, 2010
Waterworks
Been trying to have baby for 2 years but fail.
Night manager at tesco and primary school teacher, not stress
examination done before, breast examination, uterus, sperm, no ED or premature ejaculation ( 15ml of testicles-normal size and texture )
37 years old (W)
40 years old (H)
sex 2-3 times a week
Takes folic acid (W)
BMI 23
uterus ovaries not enlarges
pap smear not done for 3 years
smoke 15-20 ciggs/day, half a bottle of wine/day (W) (H)
Diet - good, healthy (W) (H)
Renal system - ok (H)
Menstrual hx - not heavy, regular, not painful, menarche 14 yrs old, frequency? features? STD?
Married in past for 10 years and failed to get children and ex-wife have 2 children (H)
on OCP sometime ago but stop 2 years ago, also had pregnancy 10 years ago with former husband but termination at 10 weeks (suction)(W)
catholic (W) think being punished for her past.
Differentials: Infertility
Tasks:
Definition for infertility(primarysecondary,)fecundability, Prevalance, Incidence - Shaq
Normal ovarian cycle and what happens when pregnancy occurs - Kaarthik
Key factors on history and examination - Alex
Causes for male and female - Jun Beng & Huey Ting
Diagnosis and investigation for male and female - Fuad & Mona
Management and cost where applicable - Kee Hao
Prognosis and complications - Piggy
Psychosocial and cultural issues - Prish & Ewe Jin
Night manager at tesco and primary school teacher, not stress
examination done before, breast examination, uterus, sperm, no ED or premature ejaculation ( 15ml of testicles-normal size and texture )
37 years old (W)
40 years old (H)
sex 2-3 times a week
Takes folic acid (W)
BMI 23
uterus ovaries not enlarges
pap smear not done for 3 years
smoke 15-20 ciggs/day, half a bottle of wine/day (W) (H)
Diet - good, healthy (W) (H)
Renal system - ok (H)
Menstrual hx - not heavy, regular, not painful, menarche 14 yrs old, frequency? features? STD?
Married in past for 10 years and failed to get children and ex-wife have 2 children (H)
on OCP sometime ago but stop 2 years ago, also had pregnancy 10 years ago with former husband but termination at 10 weeks (suction)(W)
catholic (W) think being punished for her past.
Differentials: Infertility
Tasks:
Definition for infertility(primarysecondary,)fecundability, Prevalance, Incidence - Shaq
Normal ovarian cycle and what happens when pregnancy occurs - Kaarthik
Key factors on history and examination - Alex
Causes for male and female - Jun Beng & Huey Ting
Diagnosis and investigation for male and female - Fuad & Mona
Management and cost where applicable - Kee Hao
Prognosis and complications - Piggy
Psychosocial and cultural issues - Prish & Ewe Jin
Thursday, September 23, 2010
PCL 8: IT'S A BOY....NOT!!!
DDx:
1. Congenital Adrenal Hyperplasia (CAH)
Learning issues
1. definitions, incidence, prevalence (Why might there have been some doubt at the assignation of Kamal sex at the time of birth?) - Prish
2.signs and symptoms (Why might Kamal be losing salt?, What other things might go wrong other than losing sodium?) -Huey Ting
3. pathophysiology (If Kamal has been exposed to excess androgen in fetal life and has a deficiency in the production of mineralocorticoids, how could have these come about?, Why is a genitalia ambiguous? What causes this?, What do you think Kamal's internal reproductive organs may have been like?, Why both of glucocorticoid and mineralocorticoid are necessary?) -Alex, Kee Hao
5. commonest causes and provoking factors - Karthik
7. investigations, genetics (Can prenatal diagnosis be achieved?) - Shakir
8. treatment, management and prevention -Mona
9. Psychosocial randoms (What are the parental issues? What sources of information they could identify with?Comment on the quality of those sources of information, What are the arguments for and against raising Kamal as a girl?, What do you think of the decision to raise the baby as a girl or boy?)- JB
What were the specific instructions that Lisa and Omar receive regarding the medications for Nabila(Kamal as a girl) when she became sick and what was the rational behind that advice?, Doctor-patient interaction regarding this condition,
If the parents present to Dr. Yasmin with a large quantity of information, how should the doctor respond and how should the parents act upon it?,- FUAD
How would you as a doctor to help the parents make this difficult decision? What sort of question would you put to them and how would you help work through it? Would or should you give advice or recommendation?, - TJ KOH
What sort of impact might be raised on Nabila on her mental health and social functioning? What ethical issues can you identify regarding Nabila's decision to have a surgery? - py
-Ewe Jin, Fuad, Pik Yin, JB
www.rch.org/cah_book
1. Congenital Adrenal Hyperplasia (CAH)
Learning issues
1. definitions, incidence, prevalence (Why might there have been some doubt at the assignation of Kamal sex at the time of birth?) - Prish
2.signs and symptoms (Why might Kamal be losing salt?, What other things might go wrong other than losing sodium?) -Huey Ting
3. pathophysiology (If Kamal has been exposed to excess androgen in fetal life and has a deficiency in the production of mineralocorticoids, how could have these come about?, Why is a genitalia ambiguous? What causes this?, What do you think Kamal's internal reproductive organs may have been like?, Why both of glucocorticoid and mineralocorticoid are necessary?) -Alex, Kee Hao
5. commonest causes and provoking factors - Karthik
7. investigations, genetics (Can prenatal diagnosis be achieved?) - Shakir
8. treatment, management and prevention -Mona
9. Psychosocial randoms (What are the parental issues? What sources of information they could identify with?Comment on the quality of those sources of information, What are the arguments for and against raising Kamal as a girl?, What do you think of the decision to raise the baby as a girl or boy?)- JB
What were the specific instructions that Lisa and Omar receive regarding the medications for Nabila(Kamal as a girl) when she became sick and what was the rational behind that advice?, Doctor-patient interaction regarding this condition,
If the parents present to Dr. Yasmin with a large quantity of information, how should the doctor respond and how should the parents act upon it?,- FUAD
How would you as a doctor to help the parents make this difficult decision? What sort of question would you put to them and how would you help work through it? Would or should you give advice or recommendation?, - TJ KOH
What sort of impact might be raised on Nabila on her mental health and social functioning? What ethical issues can you identify regarding Nabila's decision to have a surgery? - py
-Ewe Jin, Fuad, Pik Yin, JB
www.rch.org/cah_book
Thursday, August 26, 2010
The Wedding
Differentials:
1. Hyperthyroidism
2. HIV
3. Infections: Parasitic ( no fever, acute onset)
Learning Issues:
1. definitions, incidence, prevalence (fuad)
2.signs and symptoms(shakir)
3. pathophysiology(pik yin)
4. what is thyroid and its function(jun beng)
5. commonest causes and provoking factors(huey ting)
6. what distinguishes grave's and other forms of hyperthyroidism(ewe jin)
7. investigations and why (alex, prish)
8. management , esp grave's disease (mona, kaarthik)
9. psychological stress affects immune function such as grave's (keehao)
Websites:
www.mja.com.au/public/issues/180_04_160204/top10414_fm.html
www.betterhealth.vic.gov.au/bhcv2/bhcpdf.nsf/ByPDF/Thyroid_disorders_hyperthyroidism/$File/Thyroid_disorders_hyperthyroidism.pdf#search='hyperthyroidism'
www.acadmed.org.my/cpg/thyroid_consensus2000
3.
1. Hyperthyroidism
2. HIV
3. Infections: Parasitic ( no fever, acute onset)
Learning Issues:
1. definitions, incidence, prevalence (fuad)
2.signs and symptoms(shakir)
3. pathophysiology(pik yin)
4. what is thyroid and its function(jun beng)
5. commonest causes and provoking factors(huey ting)
6. what distinguishes grave's and other forms of hyperthyroidism(ewe jin)
7. investigations and why (alex, prish)
8. management , esp grave's disease (mona, kaarthik)
9. psychological stress affects immune function such as grave's (keehao)
Websites:
www.mja.com.au/public/issues/180_04_160204/top10414_fm.html
www.betterhealth.vic.gov.au/bhcv2/bhcpdf.nsf/ByPDF/Thyroid_disorders_hyperthyroidism/$File/Thyroid_disorders_hyperthyroidism.pdf#search='hyperthyroidism'
www.acadmed.org.my/cpg/thyroid_consensus2000
3.
Thursday, August 19, 2010
Cushing Syndrome Week 6
Siti 43
Have hypertension
Depressed
Growing moustache (Hirsutism)
Took steroids, immunosuppresants?
Round plethoric face
oily skin with acne
abdominal obesity with striae
new bruises
infected tear in the skin
Hirsutism
Differential
Cushing syndrome
PCOS
Hypothyroidism
Metabolic syndrome
Learning issues for CUSHING SYNDROME
Definition, Prevalance Incidence, Differential diagnosis - Alex
Pathophysiology - 4 different thyroid hormones testosterone oestrogen glucocorticoids. names, site of production and site of release, main target organs and means of transport and feedback loop. Rship between blood pressure and cushing syndrome - Pik Yin and Kee Hao and Fuad
Causes and Risk Factors - Mona
Sign and Symptoms : explain S&S why facial hair oily skin how bruising happens, striae, potential for easy tear, reasons of weight gain - Jun Beng
Examination and Investigation - 24 hour urinary free cortisol - Kaarthik
Treatment and Management - (lifestyle, medical, firstline, CAM, surgical), ACTH and adrenal, dexamethasone, microsurgical and why headache after surgery, why HRT necessary after surgery and complications of surgery - Shakir and Huey Ting
Complications, Prognosis - Ewe Jin
Psychosocial, How does it affect? - Prish
Have hypertension
Depressed
Growing moustache (Hirsutism)
Took steroids, immunosuppresants?
Round plethoric face
oily skin with acne
abdominal obesity with striae
new bruises
infected tear in the skin
Hirsutism
Differential
Cushing syndrome
PCOS
Hypothyroidism
Metabolic syndrome
Learning issues for CUSHING SYNDROME
Definition, Prevalance Incidence, Differential diagnosis - Alex
Pathophysiology - 4 different thyroid hormones testosterone oestrogen glucocorticoids. names, site of production and site of release, main target organs and means of transport and feedback loop. Rship between blood pressure and cushing syndrome - Pik Yin and Kee Hao and Fuad
Causes and Risk Factors - Mona
Sign and Symptoms : explain S&S why facial hair oily skin how bruising happens, striae, potential for easy tear, reasons of weight gain - Jun Beng
Examination and Investigation - 24 hour urinary free cortisol - Kaarthik
Treatment and Management - (lifestyle, medical, firstline, CAM, surgical), ACTH and adrenal, dexamethasone, microsurgical and why headache after surgery, why HRT necessary after surgery and complications of surgery - Shakir and Huey Ting
Complications, Prognosis - Ewe Jin
Psychosocial, How does it affect? - Prish
Friday, August 13, 2010
Anatomy Pract Abdomen V
Q 1, 2, 3 - Prish, Ewe jin, Jun Beng
Q 4, 5 - Alex, Mona, Fuad
Q 6, 7, 8 - Kaarthik, Pikky, HT
Q 4, 5 - Alex, Mona, Fuad
Q 6, 7, 8 - Kaarthik, Pikky, HT
Thursday, August 12, 2010
PCL Week 5
Pek Har's Reflux
Pek Har, 50, presented with chest pain (burning sensation)
Past 2-3 months, usually after big meals, lying down, and being anxious.
Duration of pain: couple of hours.
Medication to alleviate: Quik-eze and Gaviscon
Similar episode 30 years ago while pregnant
Medications: CCBs and NSAIDs
Smoking: 20/d Alcohol: 1-2 glasses of wine every night
BP: 135/80 Pulse rate: 80 BMI: 32
DDx:
GERD
Dyspepsia
Fun fact:
20% of adults experience heartburn once a week
Learning issues for GERD
Definition, Stats, Differences between GERD and Dyspepsia. (What is reflux? Stats.) - Huey Ting
Pathophysiology - Jun Beng
Causes and Risk Factors - Shakir
S&S (Typical, Atypical, Alert), What is PEG feed? (www.gesa.org.au/consumer/publications/peg/PEG.pdf) - Pik Yin
Examination and Investigation - When and how investigate. Advantages and disadvantages of endoscopy. Is the finding of hiatal hernia significant? Alternatives for endoscopy for GERD. Should you look for H. pylori? Is H. pylori the culprit? - Fuad, Ewe Jin
Treatment and Management - Management of GERD (lifestyle, medical, firstline, CAM, surgical) - Alexandra Kang, Kaarthikeshen
Complications, Prognosis (Barrett's oesophagus, dysphagia and causes for dysphagia) - Mona
Articles + oesophageal cancer, types of oesophageal cancer including risks - Prisheila, Lai Kee Hao
Pek Har, 50, presented with chest pain (burning sensation)
Past 2-3 months, usually after big meals, lying down, and being anxious.
Duration of pain: couple of hours.
Medication to alleviate: Quik-eze and Gaviscon
Similar episode 30 years ago while pregnant
Medications: CCBs and NSAIDs
Smoking: 20/d Alcohol: 1-2 glasses of wine every night
BP: 135/80 Pulse rate: 80 BMI: 32
DDx:
GERD
Dyspepsia
Fun fact:
20% of adults experience heartburn once a week
Learning issues for GERD
Definition, Stats, Differences between GERD and Dyspepsia. (What is reflux? Stats.) - Huey Ting
Pathophysiology - Jun Beng
Causes and Risk Factors - Shakir
S&S (Typical, Atypical, Alert), What is PEG feed? (www.gesa.org.au/consumer/publications/peg/PEG.pdf) - Pik Yin
Examination and Investigation - When and how investigate. Advantages and disadvantages of endoscopy. Is the finding of hiatal hernia significant? Alternatives for endoscopy for GERD. Should you look for H. pylori? Is H. pylori the culprit? - Fuad, Ewe Jin
Treatment and Management - Management of GERD (lifestyle, medical, firstline, CAM, surgical) - Alexandra Kang, Kaarthikeshen
Complications, Prognosis (Barrett's oesophagus, dysphagia and causes for dysphagia) - Mona
Articles + oesophageal cancer, types of oesophageal cancer including risks - Prisheila, Lai Kee Hao
Thursday, August 5, 2010
A Lot Of Fuss
DD
1.Crohns Disease
2. Irritable Bowel Syndrome-ulcerative colitis,
3.Celiac Disease
4.Gastric Cancer
5.Malabsorption
6.
Symptoms
abdoinal; pain, flatuence. anemia, bloating, fatigue
Learning Issues for Coeliac Disease
1.Crohns Disease
2. Irritable Bowel Syndrome-ulcerative colitis,
3.Celiac Disease
4.Gastric Cancer
5.Malabsorption
6.
Symptoms
abdoinal; pain, flatuence. anemia, bloating, fatigue
Learning Issues for Coeliac Disease
- Definition, Incidence and Prevalence, DD-why are ppl with celiac disease misdiagnosed with IBS -Pik Yin
- Causes(diet-gluten &gluten free diet,other causes of anemia, risk factors,prevention-Kee hao
- Signs and symptoms (nutritional deficiency among ppl with coeliac disease)-u jin
- Histology(funct of villi and microvilli), pathophysiology- jb, prisheila
- complication and prognosis,reason for bone deficiency test-mona
- investigations-blood test,antibody test.-alex
- treatments and management-other treatments besides gluten free diet-shakir
- phychososcial-impact of gluten free diet on personal lifestyle, challenges if a child is diagnosed with celiac disease,naturopath and dieticianm, role of dietician in management of celiac disease-huey ting, fuad
- health promotion-hw to increase the rates of diagnosis in the community, list of gluten free diets available in the market-kaarthik
Wednesday, August 4, 2010
Anatomy Practical
Q 1 and 2 - Prish, Jun Beng, Mona
Q 3 and 4 and 5 - Fuad, Alex , Pik yin
Q 6 and 7 and 8 - Ewe Jin, Kh, HT
Whoever not coming for practical speak now or forever hold your Peace!!
Q 3 and 4 and 5 - Fuad, Alex , Pik yin
Q 6 and 7 and 8 - Ewe Jin, Kh, HT
Whoever not coming for practical speak now or forever hold your Peace!!
Thursday, July 29, 2010
male, mid aged teacher,
passing small bowl motions, with fresh bloody crap
receding hair line and over weight
father had cancer at 60
little bro had it too
constipation
large solid mass upon rectal exam
occasional drinker
had colonoscopy 10 yrs ago
going for CAT scan and colonosocypy
wat wud u like to know????? biopsy, blood tests,
DD:
-colon cancer
-rectal cancer
-colorectal cancer
-internal hemorrhoids
-inflammation of rectum
-tchulangaishlonghe
-def. (incidence, prevalence),differential diagnosis, minor ---kee hai---
-pathophysio, pathology ---mona---
-risk factors, causes, signs and symptoms (how does the bleeding occur?) ---fuad---
-investigations,cancer markers ---shakir, prish---
-treatment, other treatment, and management, follow up, palliative care, what aspects of care might a palliative care team deal with? ---ujin, waiting---
-prevention, advice of dr to pts to reduce risks ---jun beng---
-complications, prognosis (staging of cancer, dukes criteria, TNM) ---alex--
-What factors influence outcome of surgery ---piggy---
-psychosocial, implications on family, can they influence incidence of cancer? religion? is it protective or causative? what sorta pain will he feel in the end of his life? ---tick---
passing small bowl motions, with fresh bloody crap
receding hair line and over weight
father had cancer at 60
little bro had it too
constipation
large solid mass upon rectal exam
occasional drinker
had colonoscopy 10 yrs ago
going for CAT scan and colonosocypy
wat wud u like to know????? biopsy, blood tests,
DD:
-colon cancer
-rectal cancer
-colorectal cancer
-internal hemorrhoids
-inflammation of rectum
-tchulangaishlonghe
-def. (incidence, prevalence),differential diagnosis, minor ---kee hai---
-pathophysio, pathology ---mona---
-risk factors, causes, signs and symptoms (how does the bleeding occur?) ---fuad---
-investigations,cancer markers ---shakir, prish---
-treatment, other treatment, and management, follow up, palliative care, what aspects of care might a palliative care team deal with? ---ujin, waiting---
-prevention, advice of dr to pts to reduce risks ---jun beng---
-complications, prognosis (staging of cancer, dukes criteria, TNM) ---alex--
-What factors influence outcome of surgery ---piggy---
-psychosocial, implications on family, can they influence incidence of cancer? religion? is it protective or causative? what sorta pain will he feel in the end of his life? ---tick---
Thursday, July 22, 2010
DD
Gastritis
Dyspepsia
Gastric ulcer
Duodenal ulcer
cron's disease
Acute cholecystitis
Lactose intolerance
Cholangitis
Choledocholithiasis - gallstone in the CVD' accumilates near papillae
Cholecystitis - stone in cystic duct from gallbladder
Learning issues
1. Definition, prevalence, incidence, Anatomy (biliary tree, site of obstruction)- (JB)
2. pathophysiology (cholesterol and bile pigment gallstone eg calcium binerubinate) ( Shakir)
3. Signs and symptoms - which disease causes which symptoms (all three!!) (Pik Yin)
4. causes and risk factors (Mona)
5. examination and investigations (blood test, liver function test, imaging techniques) and types of gallstones (Prish and HT)
6. treatment- pain relief, antibiotics, hydration and surgery. cholecystectomy (lapro and open)- ERCP, Spinchterotomy and stone collection, choledocholithomy
, bile duct clearance (Alex, kaarthik and KH)
7. complications (gallstone induced pancreatitis, surgical problems regarding choledocholithomy and mortality and morbidity) and prognosis (Fuad And EJ)
Gastritis
Dyspepsia
Gastric ulcer
Duodenal ulcer
cron's disease
Acute cholecystitis
Lactose intolerance
Cholangitis
Choledocholithiasis - gallstone in the CVD' accumilates near papillae
Cholecystitis - stone in cystic duct from gallbladder
Learning issues
1. Definition, prevalence, incidence, Anatomy (biliary tree, site of obstruction)- (JB)
2. pathophysiology (cholesterol and bile pigment gallstone eg calcium binerubinate) ( Shakir)
3. Signs and symptoms - which disease causes which symptoms (all three!!) (Pik Yin)
4. causes and risk factors (Mona)
5. examination and investigations (blood test, liver function test, imaging techniques) and types of gallstones (Prish and HT)
6. treatment- pain relief, antibiotics, hydration and surgery. cholecystectomy (lapro and open)- ERCP, Spinchterotomy and stone collection, choledocholithomy
, bile duct clearance (Alex, kaarthik and KH)
7. complications (gallstone induced pancreatitis, surgical problems regarding choledocholithomy and mortality and morbidity) and prognosis (Fuad And EJ)
Sunday, July 18, 2010
Learning Issues
1. Read the 2003 clinical practice guidelines www.acadmed.org.my/cpg/CPG-Obesity.pdf
www.nhmrc.gov.au/publications/pdf/n33.pdf (Ewe jin, Kaarthik)
2. visit www.ifnotdieting.com, read the 3 articles printed under Australian Family Physicians under Tips for long term weight management (Fuad)
3. using the internet or other sources, find out what each of the diet involves and what are the proposed mechanisms by which it is aimed to produce weight loss.
what is the scientific support for the diets being effective and what are the possible risks and disadvantages in following these diets (Atkins-Prisheila, Ornish and Pritikin-Mona, Sears-Kee Hao, The Zone-Huey Ting and The South Beach Diet-Alex, weight watchers-Pik Yin)
4. Search the internet beginning with the key words "unilever + atkins diet" to find example to explore the questions as to what potential impact a popular diet such as the Atkins diet mught have on:-
(a) the low fat diet industry
(b) the food industry in general. (Shakir)
The Atkins diet is apparently inconsistent with main stream healthy diet recommendations. What impact do these have on mainstream public health nutrition campaigns and how should these issues be addressed. (Jun Beng)
1. Read the 2003 clinical practice guidelines www.acadmed.org.my/cpg/CPG-Obesity.pdf
www.nhmrc.gov.au/publications/pdf/n33.pdf (Ewe jin, Kaarthik)
2. visit www.ifnotdieting.com, read the 3 articles printed under Australian Family Physicians under Tips for long term weight management (Fuad)
3. using the internet or other sources, find out what each of the diet involves and what are the proposed mechanisms by which it is aimed to produce weight loss.
what is the scientific support for the diets being effective and what are the possible risks and disadvantages in following these diets (Atkins-Prisheila, Ornish and Pritikin-Mona, Sears-Kee Hao, The Zone-Huey Ting and The South Beach Diet-Alex, weight watchers-Pik Yin)
4. Search the internet beginning with the key words "unilever + atkins diet" to find example to explore the questions as to what potential impact a popular diet such as the Atkins diet mught have on:-
(a) the low fat diet industry
(b) the food industry in general. (Shakir)
The Atkins diet is apparently inconsistent with main stream healthy diet recommendations. What impact do these have on mainstream public health nutrition campaigns and how should these issues be addressed. (Jun Beng)
Thursday, May 27, 2010
Week 13...tonight's gonna be a good night!!!
1. Definition, incidence, prevalence, what is thrombo-embolism and DVT?( Kaarthik) screw you Fuad!!!
2. Causes, risk factors (DVT)(Shakir)
3. Pathophysiology, Virchow's triad (Jun Beng, Kee Hao)
4. What underlying medical conditions can cause thrombosis and how they are managed? (Fuad)
5. Sign,symptoms, summary of clinical findings and why it occurs?( HT)
6. Investigations. What investigations are required and what they show? ( EJ, Mona)
7. Treatment and management of Anne's DVT. ( Pikky)
8. Complication and prognosis of DVT considering Anne's situation? Would there be any restrictions to Anne's lifestyle after diagnosis of DVT.? What is her prognosis and what are the possible complications and prevention of DVT? ( 1 page)( Alex, Prish)
2. Causes, risk factors (DVT)(Shakir)
3. Pathophysiology, Virchow's triad (Jun Beng, Kee Hao)
4. What underlying medical conditions can cause thrombosis and how they are managed? (Fuad)
5. Sign,symptoms, summary of clinical findings and why it occurs?( HT)
6. Investigations. What investigations are required and what they show? ( EJ, Mona)
7. Treatment and management of Anne's DVT. ( Pikky)
8. Complication and prognosis of DVT considering Anne's situation? Would there be any restrictions to Anne's lifestyle after diagnosis of DVT.? What is her prognosis and what are the possible complications and prevention of DVT? ( 1 page)( Alex, Prish)
Thursday, May 20, 2010
PCL 12
www.donateblood.com.au
www.who.int
Learning Objectives & Tasks
- Definition & Prevalence MONA
- Pathophysiology & causes PIK YIN & PRISHIELA
- Risk factors & Internet as a source of information- pros and cons EWE JIN
- Signs & symptoms
- Examination & Investigation ALEX & JUN BENG
- interpretation of FBC and Blood Film
- Role and procedures of bone marrow biopsy
- Treatment & Management- SHAKIR & HUEY TING & KEE HAO
(oral iron- slow or poorly tolerated, IM injections- painful, risk of skin staining, blood transfusions-issues on blood transfusions Jehovah Witnesses, hospitalization, severe reactions, quick and long lasting, cost, blood borne disease risk- HIV, how much iron you get from blood)
- Complications & Prognosis FUAD
- Normal red blood cell development KARTHIK
- Definition of Poikilocytosis, Anisocytosis, Spherocytes, hypochromia
Suggested areas
- Review of oxygen transport
- How oxygen is converted in muscles
- What does a baby haemoglobin remains oxygenated in the uterus
- Review the role of vitamin B12 & folic acid in blood formation (absorption, storage and transport)
- Would you transfuse Lily? Justify your decisions in physiological terms.
- How much blood is donated in Red Cross
- What are the beliefs of jehovah witness on blood transfusion?
- What are the patients rights & what are YOUR duties as a doctor in relation to previous questions.
- What are the religious beliefs that impact the patients choice on blood transfusion? like animal products eg. bovine for hindus and pigs for muslims
- what is vegan?
How is FBC taken?
www.who.int
Learning Objectives & Tasks
- Definition & Prevalence MONA
- Pathophysiology & causes PIK YIN & PRISHIELA
- Risk factors & Internet as a source of information- pros and cons EWE JIN
- Signs & symptoms
- Examination & Investigation ALEX & JUN BENG
- interpretation of FBC and Blood Film
- Role and procedures of bone marrow biopsy
- Treatment & Management- SHAKIR & HUEY TING & KEE HAO
(oral iron- slow or poorly tolerated, IM injections- painful, risk of skin staining, blood transfusions-issues on blood transfusions Jehovah Witnesses, hospitalization, severe reactions, quick and long lasting, cost, blood borne disease risk- HIV, how much iron you get from blood)
- Complications & Prognosis FUAD
- Normal red blood cell development KARTHIK
- Definition of Poikilocytosis, Anisocytosis, Spherocytes, hypochromia
Suggested areas
- Review of oxygen transport
- How oxygen is converted in muscles
- What does a baby haemoglobin remains oxygenated in the uterus
- Review the role of vitamin B12 & folic acid in blood formation (absorption, storage and transport)
- Would you transfuse Lily? Justify your decisions in physiological terms.
- How much blood is donated in Red Cross
- What are the beliefs of jehovah witness on blood transfusion?
- What are the patients rights & what are YOUR duties as a doctor in relation to previous questions.
- What are the religious beliefs that impact the patients choice on blood transfusion? like animal products eg. bovine for hindus and pigs for muslims
- what is vegan?
How is FBC taken?
Thursday, April 29, 2010
Wk 9 Complications - Nephrotic Syndrome
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)
- 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 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
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