Tuesday, 20 June 2017

Endogenous Pathway of Lipoprotein Metabolism (June 2017)

In an integrated curriculum, which our Medical School deploys, temporal distribution of related topics can be an issue which may seriously affect students' learning. This problem can go unnoticed by both lecturers and students. It is a worry when scheduling related topics far apart. They would be close together in a conventional curriculum.

Let me give you an example of what I mean.

  1. The topic Exogenous Pathway of Lipoprotein Metabolism was covered in two ways - guided self-learning (GSL5) and a class lecture. However, these two inputs were spaced far apart on the time-table.
  2. The GSL5 module was made available to students at the e-learning portal on 19 Sept 2016
  3. The lecture Lipoprotein Metabolism was delivered in the lecture hall on 1 March 2017
  4. Time difference between GSL5 and the lipoprotein lecture was 4.5 months
  5. A semester exam was conducted on 19 June 2017 (7.5 months after GSL5 and 2.5 months after lecture

PHASE I MD 2016/2017
Prepared by
Updated on
22 August 2016
Medical Doctor (MD) Programme Phase I
Academic Session 2016/2017
Cell & Tissue Course (GMT 101)
Week 2
GSL 5: Structure and Function of Carbohydrates, Lipids, Amino Acids
and Nucleic Acids (Biomolecules) ... uploaded at e-learning portal
19 Sept 2016
Phase I
Year 1 Sem 2
Academic Session 2016/2017
CVS Course (GMT 107)
Week 3
Lipoprotein Metabolism
1 March 2017

Even though the lecture on Lipoprotein Metabolism was given late in first year (Sem 2), in the CVS Course (GMT 107), it should not be an excuse for students who are unable to connect with or recall earlier topics (Learning Issues, LI, or Learning Objects, LO).

Students may not be able to recall or connect that the same topic and essay questions have appeared earlier - in the self-learning module or guided self-learning (GSL), in their first week of Medical School (Sem 1, Cell & Tissue Course (GMT 101).

This shows that students often do not revise, re-study or check back on what they have learned very early in their medical course. There is a gap and topics early in their medical studies may have been forgotten altogether. However, they only need to revise, re-study or check back. They may not be able to connect past topics if they did not re-check, revise or re-study the topics that they have learned many months before to exam.

There are 3 possible essay questions concerning the topic Lipoprotein Metabolism. Any of these 3 essay questions can pop up on any exam - Term and Professional. Therefore, students should be aware that there are these 3 options. They should be prepared, rather than not be aware and be unprepared or go blank during exam.

For June 2017 exam, though a large number of students passed (77/124 or 62%), I am quite disappointed that quite a large number of students (47/124 or 38%) still failed a repeat essay question on lipoprotein metabolism, which have been made available to students in their first week of Medical School since 2014 (and earlier). What a shame!

The essay question below was taken directly from the GSL, that was made available online at the e-learning portal on 19 Sept 2016, to all incoming first-year medical students. Students either saw it but overlooked it, or took it seriously, studied and attempted to answer it! There is no excuse for failing this essay question.

Describe the endogenous pathway of lipoprotein metabolism. (10 marks)

Proposed Model Answer

(i) Diagram
Is a diagram required?
No and it is not necessary.
A diagram is not required since it is not specifically asked.
However, you can draw a labelled diagram or flowchart if it helps and guides you to answer the question.
Refer to any diagram on "endogenous pathway of lipoprotein metabolism" in any textbook or Google it.

(ii) Text

Any 10 Statements pertaining to the following, or other statements relevant to the topic.
Max. 10 Marks
Endogenous pathway happens all the time.
It involves VLDL-LDL metabolism or “LDL cascade” and LDL receptor-mediated uptake in liver.
Synthesis of VLDL:

The liver synthesizes VLDL. Hepatocytes release nascent VLDL into the Space of Disse àVLDL enter sinusoids à VLDL enter systemic circulation.
VLDL have several fates:

a)      VLDL transport triglycerides from liver to peripheral tissues for utilization.
b)      When VLDL reach vascular/capillary beds, they undergo hydrolysis (lipolysis) by LPL where their triglycerides contents are hydrolysed to free fatty acids (FFAs) and glycerol.
c)      VLDL remnants are taken up by liver via LDL (B,E) receptors.
d)     The VLDL are reduced in size (but increased density) and are converted into VLDL remnants and IDL, as a result of lipoprotein lipase (LPL) activity, hydrolysis or delipidation, which requires apolipoprotein C-II as cofactor.

Unesterified FFAs have several fates:

a)      During lipolysis, some FFA can be carried by plasma albumin and dispersed in plasma for delivery to other cells. Not much of this happens.
b)      Normally, FFA can enter underlying adipocytes by simple diffusion. Inside the adipocytes, the FFA are re-esterified to form triglycerides (TG) once more. Adipocytes store TG until required (as an energy source during fasting or starvation). A majority of FFA are stored in adipocytes following lipolysis.
c)      In times of starvation, when blood glucose is low and glycogen reserves are low, triglycerides stored in adipose tissues are hydrolysed by hormone sensitive lipase (HSL) and the FFAs are released from adipose tissue. FFAs then attach to circulating albumin and are brought to liver for beta-oxidation, for continued energy supply.

IDL have several fates:

a)      IDL can be converted into LDL by LPL in blood (intravascular).
b)      IDL can be taken up by hepatic receptors.
c)      IDL can be converted into LDL by hepatic lipase (HTGL) in liver.

LDL have several fates:

a)      Normally, LDL are taken up by hepatic LDL (B,E) receptors. The contents of LDL are broken down into FC, CE, PL, TG/ DG/ MG/ FFA and amino acids. These are kept within the hepatocytes or recycled for use by other cells. Hepatic contents of FC and CE are regulated by acyl cholesterol acyltransferase (ACAT). Few things can happen if cholesterol is low, specifically in the cell or in the blood. If there is low cellular FC, stored cholesterol (as cholesteryl ester, CE) is broken down to free cholesterol (FC) by ACAT. If there is low plasma FC, the liver cell makes more FC via increased HMG-CoA reductase activity. The 2 enzymes, ACAT and HMG-CoA reductase, are sensitive to cellular and blood cholesterol levels, and combined, they regulate cholesterol levels in cells and blood.
b)      LDL can also deliver its contents directly to cells, eg adrenal glands, for synthesis of steroid hormones.
c)      Under abnormal levels of LDL in the blood (eg hyperlipidaemia), LDL can be taken up by the scavenger receptors present on extrahepatic tissues (EHT).
d)     LDL apoB-100 will be oxidized due to the prolonged presence of LDL in blood. Also, the LDL particle is now smaller and apoB-100 is unstable at this stage. ApoB-100 becomes easily oxidised. Oxidised apoB-100 has higher affinity for macrophages. Thus, oxidised LDL will be taken up by macrophages in EHT.
e)      Macrophages contain scavenger receptors on their surface. Macrophages are present on blood vessel walls. Oxidised LDL will attach to the receptors and be internalised by macrophages.
f)       The oxidised LDL are hydrolysed into component cholesterol, fatty acids, glycerol and amino acids, which are stored within the macrophages.
g)      This uptake of oxidised LDL is unregulated (ie, uncontrolled). The macrophages take up as much LDL as they can until they stop functioning and die - becoming foam cells.


Students' English proficiency
  1. Some can write well
  2. A few cannot write correct English sentences and seemed to struggle
  3. Not knowing how to properly use some words in sentences makes it difficult to comprehend what students are writing or trying to convey. Use of certain words seem difficult for students: constituent, composition, comprise, compose; retained, remained, degrade, bind, combine, uptake, consumed, utilised, undergo, etc
  4. Understanding of reciprocal relationships - lipoprotein density increases as size decreases
  5. Practice will make essay writing perfect, but there is lack of written assignments in first-year Medical School.
  6. There may be greater underlying problems such as learning the relevant science subjects in Bahasa Malaysia in primary and secondary schools. Subjects such as Biology, Chemistry, Physics, may have been taught in Bahasa. They should be taught in English if students have to master English at university level, and especially in a medical course.
  7. Students have tried their best to answer in English.
Students' answering difficulties
  1. No schema or outline to use to answer the question
  2. Careless writing 
  3. Haphazard writing 
  4. Don't know how & where to begin
  5. No proper writing style
  6. Page improperly utilised
  7. Considerable amount of scribbling at edges
  8. Diagrams in pencil and not ink 
  9. Thinking and writing at full speed 
  10. No knowledge to even write anything
  11. Blank or stuck
  12. Unexpected essay question
  13. No time to check answers
Students' handwriting
  • Handwriting was terrible for a majority of the scripts.
  • Most handwriting were tiny and had to be read close-up.
  • 1 script was intelligible (hard to read and comprehend)
Students' creativity
  • Abbreviations for VLDL, IDL and LDL were various and incorrect
  • Swapped functions of VLDL and HDL
  • New abbreviations were created! ILDL, LDLL, LPLL, CDL, etc. 
  • New terminologies were created! Empty HDL
  • Mixed up abbreviations! ADH instead of ADP.
Diagrams drawn by students
  • Interesting diagrams, but some were incomplete
  • There were 11 little diagrams of sorts. Some were weird.
  • There were 2 big flowcharts that filled the entire page and were easy to follow.
  • There was a tiny pathway that looked like the Intrinsic Pathway for Clotting Factors; could be a Physics answer or something, but not E = mc2.

23 students scored 0 marks (18.5%)

Breakdown of problems faced by students who scored 0 marks:
  • 8 students handed in empty answer scripts (completely no answer; nothing written).
  • 7 students answered wrongly on Chylomicron Metabolism* 
  •    *Chylomicron Metabolism is Exogenous pathway of lipoprotein metabolism.
  • 5 students answered on Lipid Digestion (2) / Micelles and Chylomicron / Lipid Digestion and Chylomicron / Stomach Functions and Chylomicron
  • 1 student answered on Cholesterol Synthesis
  • 1 student answered on Ketogenesis
  • 1 student drew a pathway that looked like the Intrinsic Pathway for Clotting Factors, without any text.

FOCUS of this essay question

Since this essay question is specifically about VLDL-IDL-LDL metabolism or endogenous pathway, any answer on chylomicron metabolism or exogenous pathway will be incorrect. Since HDL metabolism is not asked, there is no need to touch on HDL metabolism, except its associated role in the endogenous pathway.

Other answers such as stomach contents and functions, lipid digestion (formation of micelles, enzymic digesiton of lipids), lipid absorption, formation of chylomicron in enterocytes, passage of chylomicron from lacteals via lymphatics to liver are all irrelevant.

Other processes in the liver such as cholesterol synthesis and ketogenesis are irrelevant as this question is specific and focused on the metabolism of lipoproteins containing apo B-100.

FALSE Statements
  1. This VLDL is major transported [transporter?] of phospholipid [F]. VLDL then could send the phospholipid to cell for cell integrity or to the cell that uses it for the production of energy [F].[VLDL is the major transporter of endogenous triglycerides ... from adipose tissues. Phospholipid is not used to generate energy.]
  2. Endogenous pathway of lipoprotein metabolism is for metabolism of chylomicrons [F].

The essay question specifically asked about endogenous pathway (VLDL-IDL-LDL metabolism), which occurs all the time in the body, whether we are fasting or not. There is no need to write about other topics. There is no need to write about carbohydrate metabolism (polysaccharide digestion, glucose and rbc metabolism). There is no need to write about GIT (stomach contents and functions). There is no need to write about lipid digestion and absorption. Stay focussed on the topic.

(a) Glucose & rbc metabolism
  1. Glucose is converted into pyruvate which will form the cholesterol.
  2. When rbc is damaged, or aged, lipoprotein will metabolised to be store into the body as a source of heat, membrane fluidity.
(b) Lipid digestion and absorption 
  1. So lipoprotein metabolism functions to break down lipid and protein to their respective basic units for better absorption.
  2. Lipid is broken down to its simplest form which are fatty acids and 3 glycerols with the help of ADH for energy.
  3. Lipid will enter lacteals (specialised lymph in the villi) to be utilised by the body again (as chylomicra).
(c) Carbohydrate digestion 
  1. From complex polysaccharide, it is broken down into disaccharide by removal of water. Then disscharide is broken down to amino acids which is the simplest form of protein.
Student Answers on

[F] = False statement
[?] = examiner's query

(a) Students' understanding of the different lipoprotein pathways
  1. There are 2 pathway(s) involved in lipoprotein mechanism which are through endogenous pathway and exogenous pathway
  2. Endogenous pathway is about VLDL
  3. Endogenous pathway of lipoprotein is when it is synthesis from cholesterol inside the liver.
  4. Endogenous Pathway is occur within circulation. Endogenous Pathway of lipoprotein metabolism consist of VLDL-LDL metabolism, LDL metabolism and LDL-mediated receptor (uptake).
(b) Ambiguous statements written by students
  1. Lipoprotein metabolism occur in liver. It is combination of lipid and protein.[Abstract writing!]
  2. Cholesterol is transported from the GIT to the liver in both estercifed [esterified] and free form in the liver. [Meaning?]
  3. Cholesterol under go oxidation estirification and compannded with protiens Apo proteins to form lipoproteins which are sent to the bloodstream as VLDL. [Meaning?]
(c) Lipoprotein structure
  1. Lipid basic structure and triglyceride and fatty acids
  2. For proteins, its amino acids
  3. Cholesterol combines with apolipoprotein
  4. Cholesterol, apolipoprotein, phospholipid and triglyceride will form VLDL and also empty HDL
  5. Lipoprotein is constituent of both lipid and protein.
  6. Triglyceride has about 60% in VLDL [This is better written as VLDL contains approximately 60% triglycerides.]
  7. VLDL has Apo B-100 molecule [This is better written as Each VLDL has an apo B-100 molecule.]
  8. IDL is high in cholesterol
(d) Classes of lipoproteins
  1. There are 2 lipoprotein(s) that (are) present in (the) body which are high density lipoprotein (HDL) and low density lipoprotein (LDL). [F] [There are 4 major classes of lipoproteins.]
  2. The last one is HDL
(e) Function of lipoproteins
  1. LDL is described as bad cholesterol
  2. LDL is major transporter of cholesterol. It send the cholesterol (to) the cell of adipose and liver to be stored.
  3. HDL is described as good cholesterol
  4. The function of HDL is to transport excess cholesterol to the liver to be metabolised. The HDL is the could be recycle for the next  use.
(f) Lipoprotein conversions
  1. In lipoprotein metabolism, chylomicron is converted into very low density lipoprotein (VLDL) [F]. VLDL in then convert into intermediate low density lipoprotein (ILDL) [F]. ILDL will form low density lipoprotein (LDL) which then converted into high density lipoprotein (HDL) [F].
  2. Chylomicron will bind to Apo E and C to become high density lipoprotein [F]. Then it become  intermediate density lipoprotein, low density lipoprotein and very low density lipoprotein [F]. 
  3. After the VLDL will converted into IDL or LDL
  4. Triglyceride in VLDL is further dehydrolysed leads to conversion of VLDL to IDL.
  5. Very low density lipoprotein (VLDL) is degraded by IDL [F]. [VLDL is degraded by LPL to IDL.] Then, forming Low density lipoprotein (LDL) and exocytosed [endocytosed?] either via (scavenger) receptor-mediated or via hepatic (receptors). Then, LDL is taken up to the hepatocytes [taken up by hepatocytes?]. LDL converted to free cholesterol in liver.
(g) Lipoprotein movements
  1. Lipid (from circulation) will flow into the liver to (be) metabolised.
  2. VLDL will transport cholesterol from tissue to liver for excretion and HDL will transport cholesterol from liver to tissue [F]. [What does VLDL transport?]
  3. When it enters the blood circulation, VLDL attaches to Apo C and Apo E
  4. Upon entering the circulation, Apo CII activates lipoprotein lipase (LPL). Lipoprotein lipase hydrolyses triglyceride into free fatty acid and glycerol
  5. IDL is taken up by the hepatic cells. This is because hepatic cell recognise Apo E on IDL. Apo C and Apo E is retained from IDL [retained with IDL?]. IDL is hydrolysed [to what?]
(h) Products of lipoprotein hydrolysis by LPL
  1. Free fatty acid is used for energy, milk lactating
  2. Glycerol is needed in glucogenesis and gluconeogenesis
(i) Lipoprotein uptake
  1. Macrophages engulfing lipoprotein becomes foam cell
(j) Depth of students' understanding of the topic asked
  1. LDL is low density lipoprotein which collects cholesterol from liver to body
  2. HDL is good cholesterol which collects cholesterol from body to the liver
  3. Liver will produce VLDL with attachment of Apolipoprotein B-100 which is produced by hepatocyte
  4. VLDL will combine with Apo E and Apo CII
  5. CII will activate lipoprotein lipase to breakdown triglyceride into fatty acid and glycerol
  6. Fatty acid can be used in synthesis of lipid, energy storage, production of milk fat in mammary gland
  7. The breakdown of triglyceride reduce the VLDL into IDL (VLDL remnant)
  8. IDL will transport into the hepatocyte by binding of Apo E on the surface of liver (LDL receptor)
  9. IDL will also degrade into LDL with the help of HTL (hepato ... lipase) [HTL or HTGL is hepatic triglyceride lipase.]
  10. LDL is more dense and reduce in size [Meaning?] [LDL is smaller and denser than IDL.]
  11. It contain more cholesteryl ester
  12. LDL can enter the liver by binding of Apo B-100 at the LDL receptor. [Meaning?] [Where is apo B-100 located?] [LDL apo B-100 binds to LDL receptors present on hepatocytes. OR LDL binds to LDL receptors via its apo B-100.]

CORRECT answers attempted by students (10 marks)
Text only. Associated diagrams are not included here.

Example 1
  1. VLDL (very low density lipoprotein) is synthesized in the liver and consist of triglycerides and Apo B-100. [F] [VLDL contains 4 lipid classes and apo B-100.]
  2. Then, VLDL is goes out of the liver into blood circulation.
  3. Inside the circulation, it receives two apolipoprotein from HDL which is apo C and apo E.
  4. Then, VLDL is hydrolysed by lipoprotein lipase which hydrolyse the triglycerides in(to) fatty acids and monoglycerides.
  5. This make VLDL size and density decrease [F].[VLDL size is reduced, but its density increases after lipolysis by LPL.]
  6. Before transported back into liver, apo C return back to HDL and VLDL remnants diffuse into liver by lipoprotein receptor and by endocytosis. [Diffuse into liver or taken up by liver?]
  7. The VLDL remnants become IDL but IDL does not remain for a long time before it converted into LDL (low density lipoprotein). [IDL exists transiently in blood.]

Example 2
  1. VLDL (very light density lipoprotein) is form(ed) endogenously in liver. 
  2. It consist(s) of free amino acid, cholesterol, cholesteryl ester, phospholipid, triacylglycerol and apo B-100. [VLDL cannot contain free amino acids! Apo B-100 is a large protein!]
  3. It is released into circulation.
  4. It then take up apo C and apo E from HDL (High density lipoprotein).
  5. Apo C will activate Lipoprotein lipase in cappilary epithelium to break down triacylglycerol in VLDL into fatty acid and glycerol. [It should be capillary endothelium.]
  6. Now VLDL decrease in volume increase in density and now convert to IDL (intermediate density lipoprotein).
  7. IDL bind to lipoprotein receptor at hepatocyte  via apo E through endocytosis. [IDL are internalized by endocytosis.]
  8. In the hepatocyte, triacylglycerol in IDL (undergo) further break down by hepatic lipase.
  9. Now the compound is increase in density and rich in cholesterol.
  10. It is now LDL (low density lipoprotein).
  11. It will (be) released by the hepatocyte.
  12. After that LDL (is) either absorb(ed) by the liver or posthepatic tissues to (be) further metabolize(d).

Example 3
  1. In the lipoprotein metabolism, it consist the exogenous pathway, endogenous pathway and the reverse metabolism pathway. [F] [There is no such thing as reverse metabolism pathway! There is reverse cholesterol transport.]
  2. During the endogenous pathway it is started in the liver.
  3. From the very low density lipoprotein (VLDL) which is present inside our body will produce in the liver, 
  4. It is function to bring the cholesterol to the tissue cell for storage.
  5. When it enter the circulation it will undergo lypolysis and converted into the Intermediate density lipoprotein (IDL). 
  6. This IDL is appear in the blood just for a while. [Transient]
  7. Next the IDL will undergo the lipolysis and then being the low density lipoprotein (LDL).
  8. This LDL will deposit into our tissue.
  9. Plus the LDL is very anthrogenic [atherogenic], thus LDL will lead into the formation of the atherosclerotic plaque and lead to other disease.
  10. This plaque prone to forming more at the abdominal aorta than the thoracic aorta.
  11. This LDL that deposit inside the tissue will be taken up back into the liver via the high density lipoprotein (HDL) during the reverse lipoprotein pathway. [Reverse cholesterol transport]
  12. The LDL serve as the bad cholesterol inside our body.
  13. {Diagram}

WRONG answers attempted by students (0 marks)

Example 1
  1. Chylomicrons are found in intestinal mucosa from dietary lipid. 
  2. During the endogenous pathway, high density lipoprotein (HDL) serves as reservoir for apo-C and apo E. [F] [Chylomicron metabolism is exogenous pathway.]
  3. The apo-C and apo-E will bind to chylomicrons.
  4. As chylomicrons enters the blood circulatory system, lipoprotein lipase (LPL) will hydrolyse the triglycerides into free fatty acid and glycerol.
  5. As the triglycerides are broken down, the size of chylomicrons decreases, becomes smaller but its density increases.
  6. The Apo-I in chylomicrons will restore back to high density lipoprotein before reaching liver  while the apo-E will stay with the chylomicrons. [Which apolipoproteins go where?]
  7. The remnants of chylomicrons reach liver, and will be metabolized as source of energy, heat energy. [F] [What do chylomicron remnants contain?]

Example 2
  1. Endogenous pathway of lipoprotein metabolism begins with the absorption of chylomicrons. [F]
  2. The chylomicron binds with Apo B-II. [F] [There is no such thing as Apo B-II.]
  3. The chylomicron then travels through the lymphatic system while being metabolised by lipoprotein lipase .
  4. After a few stages of digestion, the chylomicron enters the liver.

WRONG answers mixed with correct answers

Example 1 (2 marks)
  1. Endogenous pathway.
  2. The lipoprotein is transported as VLDL. [1 mark]
  3. Then, it changes into LDL. [1 mark]
  4. The LDL form chylomicron. [F]
  5. Chylomicron is absorb(ed) by lacteal. [irrelevant]
  6. Then it moves into blood. [irrelevant]

Example 2 (4 marks)
  1. When dietary lipids and cholesterol enter intestine, they (are) converted to tryglyceride, monoglyceride  and fatty acids by intestinal lipase. [The correct spelling is triglyceride.]
  2. They are absorbed into intestinal cells which (are) then converted into tryglyceride by golgi apparatus [Golgi apparatus].
  3. Tryglyceride, cholesterol will be bind forming chylomicrons (CM). 
  4. Chylomicrons are too big to enter blood vessels so it will enter lacteals which then enter blood vessels.
  5. CM are utilised by lipase that (are) present in blood vessels forming smaller lipids to be transported to muscle cells for energy and to liver for storage,
  6. CM are then transported to liver.
  7. Cholesterol will bind to Apo B to form very low density lipoprotein (VLDL). [1 mark]
  8. VLDL will be transported in blood vessels where it  (is) utilised by tissues converting it to Intermediate density lipoprotein (IDL). [1 mark]
  9. IDL (is) transported to liver forming Low density lipoprotein (LDL). [1 mark]
  10. LDL is then again circulated in blood to be utilised by tissues for energy. [1 mark]


Sunday, 2 April 2017

Diabetic Coma

The Malaysian cuisine is delicious and is easily available just about everywhere one walks. Malaysians generally eat well, are well-fed and eat three main meals a day. There is so much food and many food choices today as compared to the 1950s and 1960s. The cuisines today are varied and exquisite, from spicy to bland, from slow-cook to fast food, from pounded to blended, from sauteed to deep fry. The culinary magic is among Malaysia's strong points that supports its tourism industry and hospitality industry. People are eating all the time and everywhere. All these are possible because Malaysia is a hot pot of many ethnicity from the globe. There may not be Vikings and Inuits in Malaysia, but there are Malays, Chinese, Indians, Mongols, Thais, Filipinos, Indonesians, Nepalese, Uyghurs, Japanese, Koreans, etc in Malaysia. They have contributed much to Malaysia's unique international cuisine. Malaysians are mostly obese. Diabetes is common in Malaysia.

Diabetes is Malaysia's biggest health problem, apart from overweight and obesity. Malaysians are not scared of diabetes. They just dislike it and let it take its course. They toy around trying to find a traditional cure for their diabetes. No amount of doctors' advice will ever change them (hard core). They trust and prefer the methods of their ancestors when dealing with diabetes. They do not like Western medicine and do not heed the dangers of diabetes. They will come to hospital at the last minute, but still, they will not comply with medical advice. Nothing will change them. Thus, we see a number of diabetic complications.

Up in the male surgical ward, there were men with amputated limbs. There was a man whose rotten leg stump was placed in a bamboo; it was stinking badly. Over in the ladies ward at another hospital, there was a woman who had undergone wound debridement; she was moaning in pain and wanted to go home, but she died in hospital. In a few homes, family members with severe neuropathy were playing with their own poop and had to be chained. There are many horror stories of Malaysian diabetics.

There is a group of diabetic patients who have made the hospital their second home. They suffer from pre-diabetic coma. Diabetes is reversible, and so is diabetic coma. Diabetic coma is a medical emergency and patients need to be brought to hospital immediately. Semi-conscious patients are brought to hospital Accident & Emergency (A&E) Department by their caregivers, family members, relatives or friends.

Often, the national identity card (MyKad) and hospital registration card (HUSM RN) are the two documents used to identify local patients. If the patient is registered at the hospital where he/she is currently being admitted, doctors have access to the patient's file, medical history and medical status of the last hospital visit to the Diabetes Clinic. Weight and blood pressure (BP) readings should be in the patient's folder. Obesity and hypertension can be made out.

Unconscious or comatose patients can't speak for themselves; doctors will need to work on their medical status and underlying causes. For diabetics, there are four possible causes of coma or unconsciousness:

(1) Hypoglycaemia causes altered consciousness - inability to focus, giddiness, dizziness, etc. This could be due to inappropriate injection of insulin (insulin overdose).
(2) Hyperglycaemia - dangerously high glucose levels in blood. This could be due to skipping insulin doses or skipping insulin altogether, and preferring to try traditional herbal medicine instead (which usually don't work in diabetes).
(3) Dehydration - not consuming sufficient fluids or loss of fluids - vomiting, diarrhoea, drugs, medications, herbal prep etc.
(4) Alcohol consumption worsens pre-existing dehydration in diabetics.

There will be biochemical and pathological changes in the body in diabetic coma:

(1) Acid-base imbalance: Metabolic acidosis; diabetic ketoacidosis (DKA)
(2) Fluid imbalances: Hypovolaemia; edema
(3) Electrolyte imbalances: Hyperkalaemia
(4) Kidney problems: Anuria/oliguria; ketonuria; kidneys cannot filter blood properly
(5) Respiratory system: Acetone breath
(6) Blood: Ketonemia; hyperglycaemia;
(7) Blood lipids: Lipaemia; hypercholesterolaemia; hypertriglyceridaemia; increased fatty acids
(8) Liver: Fatty liver (30%-40% of liver is fatty)

There are Standard Operating Procedures (SOP) for Diabetic Coma under Intensive Care Medicine. Treatment of diabetic coma will depend on the status of the patient:

(1) Hyperglycaemia: infuse insulin
(2) Hypoglycaemia: infuse glucagon
(3) Acidosis: infuse alkali
(4) Hypovolaemia: infuse saline
(5) Lipaemia: apheresis
(6) Fatigue:
(7) Pain:
(8) Fever/infection(s):
(9) Neurology:
(10) Heart:
(11) Blood: dialysis

There will be medical and ethical issues to deal with once the patient pulls through after dialysis, before he/she exits the Intensive Care Unit (ICU) to the open ward. Some patients die soon after dialysis due to cardiogenic shock. This is often stated as "badan reject dialisis" among family members present outside the ICU.

Families can expect patients to pull through by two weeks hospitalisation at ICU and the open ward. Patients are able to sit up in bed and eat hospital food. But families often prefer to supply home food to newly recovered patients (as a gesture of caring). Salty food and certain fruits will set off the biochemical imbalances again. Care has to be accorded to observe that families comply with doctors' strict orders for proper patient care and rapid recovery while still in hospital. But families tend to think that they know better than doctors and choose to disobey.

External links:

Friday, 31 March 2017

ESWL for kidney stones

Kidney stones
Kidney stones are known as renal stones or renal calculi (single renal calculus). There are many causes of renal stones - dietary, hereditary (genetic), idiopathic (unknown).

Passing stones in urine
Tiny kidney stones can exit via urine. However, kidney stones are actively growing crystals in the kidneys and these can grow to be quite big if not removed. When these big kidneys stones (like staghorns) try to exit the kidneys into the ureters, they will get lodged, bruise and tear the ureters, causing pain and blood in urine.

Bladder stones
Bladder stones form in the urinary bladder. The bladder is a big elastic pouch - ie, it expands with urine, bladder stone or both. Bladder stones can become as big as a softball or hockey ball.

Blood in urine
The presence of blood in urine is known as hematuria. Passing stones in urine can cause hematuria. Bloody urine is worrying as it can mean an active infection or kidney stones.


Kidney stones and bladder stones occur commonly in Malaysian families. We have long hot weather and people tend not to drink sufficient water. They prefer to ignore the dangers of dehydration and possible kidney stone formation.

Malaysia is famous for its thick sweet milk tea (teh tarik or chai), which is consumed in the morning, afternoon and evening. It is taken with roti canai or plain dry biscuits (biskut Marie or biskut Cap Ping Pong). Teh tarik and roti canai are Indian cuisine, which Malaysians have adopted and blended into Malaysian cuisine.

Scenario 1: There was a big elderly man who liked thick sweet milk tea so much that he must consume it daily. He had a bladder stone for a long time before he decided to have it removed. When the bladder stone was removed, it was a big chalk-white ball - as big as a softball (bigger than a hockey ball). He kept the bladder stone as a souvenir! His unusual souvenir became an attraction for the village elderly.

Scenario 2: A young working girl liked thick sweet milk tea and often consumed it daily. She had little kidney stones which exited in her urine. However, one day, an usually large elongated kidney stone tried to exit her body, but got stuck half-way out at the orifice. She was in so much pain. She was rushed to the hospital in an ambulance, where the stone was pulled out without anaesthesia! She screamed! Hospitalisation was necessary to monitor her condition and she was discharged after two days. She switched jobs and became a successful entrepreneur. However, she has short stature and features of a kidney stone sufferer.

Scenario 3: A father of seven worked as a field supervisor for his college students. He refused to drink water when he was doing field work as there were no proper public toilets. He would only drink water at home. After working 30+ years, he developed kidney stones and suffered excruciating pain, which was relief with traditional ointment. He lived in a hot house and sweated profusely. No amount of water seemed to be able to replace his water loss. He refused intravenous saline and glucose infusions. He could not open his dry eyes and therefore could not see his food nor his children around him. He eventually died of severe dehydration - just skin and bones.


Stones can form often when we don't drink sufficient water or eat certain food. There are many causes of kidney-related problems (also known as renal problems).

Kidney stone and pain
Kidney stones are also known as renal calculi (single calculus). They can form in the kidney and if they break off, the broken pieces can travel down the ureters (urine tubes) and lodge there. Whether the stones are lodged in the kidneys or the ureter, they will give rise to pain, sometimes very severe pain. Kidney stones cause excruciating pain known as renal colic.

Patients with renal stones suffer excruciating pain, which makes them unable to enjoy daily activities and sports. Life can be dreary for kidney sufferers. Some choose to ignore little pain or experience no pain.

Renal pain will cause patients to go to hospital to seek treatment and relief. Some will go to hospital only when nothing else seems to work at home. Some will call up friends to find help. Some will wait for someone to come by and visit them at home while stuck in bed. Patients are at a loss as to what they can do for themselves.

All of a sudden, relatives and close ones find themselves in charge of a patient with kidney problems, and often times, a kidney stone sufferer with the stone not yet removed. They don't know what to do either. All they can do is watch someone in pain till help comes along.

Chemistry of kidney stones
Kidney stones are chemical precipitates. As precipitates they can therefore be dissolved chemically. Some stones are easily dissolved. However, some stones maybe harder to dissolve.

Lemon peels contain huge amounts of oxalates. The oxalates turn into crystals within our body and interrupt calcium absorption to a large extent. The unabsorbed calcium solidifies within the kidneys and gallbladder in the form of stones (calcium oxalate stones).


Kidney stones are detected by x-ray, IVP, ultrasound, and CT scan.

AXR = abdominal x-ray (x-ray of the abdomen)
KUB = kidney, ureter, bladder
IVP = intravenous pyelogram
CT = computed tomography
Renal profile

Abdominal x-ray
Kidney stones are opaque and can be seen on x-ray of the abdomen (known as AXR). X-ray of the kidney, ureter, bladder is known as KUB. 

A dye or contrast media is used to detect structures of the KUB. It detects problems of the urinary tract due to kidney stones etc.

Kidney ultrasound
Kidney stones can be detected by ultrasound of the abdomen - KUB. The patient must drink sufficient water an hour prior to the procedure and have his/her bladder full for this procedure. The patient then lies on the stomach and the KUB region is scanned.

Abdominal CT
CT of the abdomen and pelvis helps to detect cause of pain due to kidney and bladder stones.

Renal profile
This looks for abnormality of serum calcium and serum phosphate as well as altered kidney function.

The Urine Dipstick Test looks for possible infection of the renal system.
Urine FEME looks for microscopic evidences such as casts (epithelial cells), crystals, yeasts, red blood cells, white blood cells, pus and other (if any).


1. Cystone
2. Tamsulosin
3. ESWL = Extracorporeal Shockwave Lithotripsy

An Ayurvedic herbal prep which can help to dissolve kidney stones rapidly is Cystone. It is sold at local pharmacies. There are wonder stories about using Cystone for getting rid of kidney stones from patients who suffered years from kidney stones. Patients pass out sandy urine for a few days and the kidney stone is gone for good. https://medicinenewbie.blogspot.my/search?q=cystone

Tamsulosin is used to assist kidney stones exit in urine in difficult cases. It is also used in men with enlarged prostate gland as in prostate cancer, where urination is problematic.

Larger kidney stones must be removed in the renal clinic or surgery. Large kidney stones can be removed by blasting the kidney stones as in the procedure extracorporeal shockwave lithotripsy (ESWL). ESWL is a mechanical means to break up kidney stones. This procedure is an outpatient procedure and the patient goes home after the procedure, unless there are other complications and need for extended stay. Patients may need some form of anaesthesia. The patient lies on a waterbed and laser light is passed through the kidney stone to break it up. The fine broken stone pieces will pass out in the urine. If a piece of kidney stone is too big and trapped in the ureter, it will need to be pushed back up into the kidney for further ESWL, until it is sufficiently small and safe to pass through the ureter and out into urine.


Will kidney stones recur? It depends. If the diet is unchanged and patients continue to consume little water (remains dehydrated), then kidney stones may return. Adding more fruits and vegetables to the diet will help patients to stave off kidney stones .... hopefully for good.

Patient education
For patients who have hypertension, have kidney problems (eg kidney stones), and live in hot climate, some dietary modifications are necessary and consuming plenty of fluids will help. Personal education and willingness to make changes are of prime importance in patients with kidney problems. No amount of advice will help them unless patients themselves choose to change - ie, consume sufficient water daily, reduce salty food consumption, eat more fruits and vegetables daily, and stay out of the sun.


Conditions at home
Most patients cannot afford the luxury of this life and do not have air-conditioning at home. They live in extremely hot houses without shirts on (for men) and just wrapped in sarongs (kemban for women). Sometimes old houses suffer from severe heat due to the nature of roofs that are installed. Previously people used attap roof for kampung houses. Nowadays people use Addex roof for kampung houses. Attap is cooler but has lost favour among villagers. Addex is preferred today, but it is not as good as attap. As such patients have no means to make their living quarters cool and conducive for safe living.

Designing homes
Thus, house design is of great importance in hot countries of the Equator, like Malaysia. Not all house designs and building materials are suitable for hot weather. Some form of natural ventilation and affordable means of cooling houses are needed. Architects and engineers have thus to come up with better house designs so that kidney problems can be reduced among poor people living in the Equator.

Global warming
Malaysia is hot (31C) at midday and cooler (24C) at night.  Reducing exposure to the sun and heat maybe helpful for those with kidney problems. Drinking plain water before leaving home/office should help. Refusing to drink sufficient fluid in order to avoid having to go to toilet is a big reason why many refuse to drink sufficient fluid daily. Thus, these people fall victim to kidney problems, including kidney stones. As global warming heightens and the kidney stone belt widens, we can expect to see more patients with kidney problems.

External links:

Monday, 20 March 2017

Immune Health

What constitutes innate immunity?

What determines immunity?

Can immunity be developed?

Can immunity be improved? How?

Can immunity be transferred?

Can immunity be acquired?

What is not immunity?

How can immunity be compromised? What can be done?

Is there just one immunity for everything that can harm us, or are there many different immunity profiles for different things that can harm us?

Can immunity be modulated? How

How does immunity work? Can it be turned on and off? Does it sleep?

What things govern immunity?

Does immunity matter?

Do we all have immunity?

Is immunity permanent?

Why do the young and elderly get sick easily?

Is poor immunity detrimental to one's health?

Should immunity always be high even when nothing bad is around?

External links:

Tuesday, 14 March 2017

Technical report

A. Hits

The # of hits for this website on 14 March 2017 is 445,458. This is good for a website that has been in existence for 7 years.

B. "404" Error Code

I also received a message from Google Analytics that there are errors in this website, which returned Increase in "404" on searches or search links. This means that the link-to pages, images or objects have been removed, omitted or deleted.

                   Increase in “404” pages on http://medicinenewbie.blogspot.com/

I have downloaded from Google Analytics, a list of this website searches that returned "404" and I will try and remedy that.

C. I have not added AMP (Accelerated Mobile Pages) to this website. Will work on this.

D. I have redirected this website to https to make it more secure.

E. Feedback

For those who wrote comments, thank you for your kind effort.

For those who liked this website as the images loaded very fast, I also want to thank you for even noticing it. I have picked and used a template that loads images very fast. These templates come free and anyone can use them. I have only tried one sample of these fast templates for this website. They don't look nice as they are meant for speed - ie, fast loading.

However, the images also loaded doubly fast as I have converted the original high resolution images to web images for even faster loading. To do this, I have used Zoner Photo Studio version 15. However, Zoner has updated their software to version 18, which also has the photo optimization for web images, but has removed other useful features such as annotation etc, which I particularly liked. As many useful features have been removed from recent versions, I am unable to annotate images/photos after version 15.

The photos/images that I have used in this website are mostly my own. The rest are from various Internet pages and I have indicated their sources in the caption, or somewhere on the respective pages.

If there are topics that you would like to see at this website, you can email to me and I will see what I can do. This website is meant for general reading and knowledge, with some relevance to medicine and health. It does not provide medical advice and patients must depend on their doctors' advice.

This website is meant for those who want to search for new things, review old things, and maybe also look into health issues about the future of things. I write on topics which people tend to overlook, but I think are important to our health. Medical students may find the pages useful. Parents may get some ideas about what we teach at the university in this digital era.

I cannot advocate the use of traditional medicine (herbs, herbals and herbal medicine) on this website, but I provide information about them here for general knowledge. There is more information from the Ministry of Health Malaysia web pages and individual websites. I taught about them long ago, but just for ethical consideration in our Ethics & Behavioural Science Block.

14 March 2017

Monday, 13 March 2017

Academic Scholarship

It is nice and feels great to be in academia. However, academia demands a high level of time, energy, dedication and passion. There is one thing that kills academia, and that is cheating.

In academic indulgence, scholarship, research, writing and publication, there is a lot of room for cheating. There are many ways in which university lecturers have used to cheat their way to the top. I have seen too many times and thus this warrants a write-up first-hand.

When lecturers first get research students at their door, the student is almost always in a self-pity state. It is derogatory to get a begging student, doesn't matter whether it is a male or female. I have often accepted them, but I find that these beggar students are not worth my hard work of toil looking and supervising them.

A sad and begging student is a falsehood of everything that academia needs. I should turned away all research students who come into this category. They may succeed in obtaining their postgraduate degree, but they are undeserving and often ungrateful souls. I don't ever want them back with me or working with me.


Here are some instances I can cite and you can judge how former students and lecturers cheat. Cheating is big time at university.

Scenario 1

A beggar student with a low CGPA comes to your door - begging to be your postgraduate student. He gets accepted for begging hard. He turns out to be aligned to other researchers with even bigger grants. So he is just registered under you, but actually works for somebody else on the faculty.

Scenario 2

A beggar student with a reasonably good CGPA comes to your door, begging to be your postgraduate student. She gets accepted for begging hard. She turns out to be inclined to make better friends with your head of department. After graduation, she continues her research with your head of department, while you are oblivious to their research. Somehow, technology shows their publication, which you found by surprise. Of course your name is not on any of their research while the research involves learning off your back.

Scenario 3

This is like from rags to riches. An average student barely makes through the grades and graduates. She become a research assistant. Then she found herself a lecturer job by befriending a head department whom she met earlier during her struggling days. She gets promoted and landed a job as a research director. Good job but a sick attitude. How in the world can one appreciate an almost dropout student to easily become a research director?

Scenario 4

A medical lecturer tired to overpower her subordinate and tries to take away his research to call it her own. He defends himself and refuses to give it all up for her. He transfers. She has another plan - to take up his residual research and make it big and as if her own. Since she is head, it is big time for her. She is acknowledged, but for what? People must be blind not to see how a medical lecturer with just an average pass in MMed can be a director of a specialised field of research that someone else did before her.

Scenario 5

This one is what I call a killing. You have a medical lecturer as your head of department. She only has an MRCP but no PhD. You have a PhD and lots of other skills that all tertiary academics should have. Of course and in due time, the head of department will make a sure kill - kill you in your sleep, kill you till you cannot claim your academic freedom, kill you and make sure you don't get your academic promotions.

Scenario 6

This one is an old man who refuses to quit. Yes, the retirement age has been increased to 60, so many lecturers stay on till bald and forgetful. However, they are meaner. They have a hand in every university affair and decision that you can't even have a breathing space. Sometimes you just wish that old man will wither and just die, so lecturers can live, wish and work well in the university.

There is so much madness in academia. It feels great to survive torture, but it feels even greater to win battles against such cheaters and nerds.