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---

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)

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)

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)

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?

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)

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.