To obtain a distinction in the viva, students had to pass all 3 components of the viva - Anatomy, Physiology and Biochemistry. The panel must come to a unanimous verbal decision whether you get/don't get a distinction.
Group A panel comprised Prof Musalmah Mazlan (Biochemistry, External Examiner, UiTM), Dr Nurul Aiman Mohd Yusof (?) and Dr Liza Nordin (?). Observer: Dr Amida Mohd Safuwan.
Group B panel comprised myself (Biochemistry), Dr Mohd Asnizam Asari (Anatomy), and Dr Ainul Bahiyah Abu Bakar (Physiology). Observer: Dr Nazlahshaniza Shafin.
Group C panel comprised Dr Asma' Hj Hassan (Anatomy), Assoc. Prof. KNS Sirajudeen (Biochemistry), and Dr Che Badariah Ab Aziz (Physiology). Observer: Dr Md Rizman Md Lazim.
My panel interviewed 8 students and we decided not to give any distinction to any of our students as none met our expectations.
Anatomy
- Bone specimen. The bone specimen was 2 vertebrae. The students were asked various parts of the vertebrae and what lies in the spinal canal.
- Spleen. The students were asked relations to the spleen.
Physiology
- Thyroid. The students were asked about the thyroid hormones, their syntheses and iodine deficiency.
- Goitre. The students were asked about the etiology of goitre.
Biochemistry
- Macromolecules. There are 4 terms - biomolecules, macromolecules, micromolecules, micronutrients. Biomolecules are all the molecules in our body, ie biological molecules. Macromolecules are large molecules in our body, ie proteins, lipids, carbohydrates, and nucleic acids (DNA and RNA). Amino acids are monomers for proteins. Amino acids are not macromolecules, but proteins are. Fatty acids are components of triglycerides, phospholipids and cholesteryl esters. Fatty acids are not macromolecules, but triglycerides, phospholpids, and cholesteryl esters are. Nucleotides are components of nucleic acids. Nucleotides are not macromolecules, but DNA and RNA are. Micromolecules are small molecules in our body, ie glucose, amino acids, glycogen, acetyl CoA, pyruvate, citrate, etc. Micronutrients are substances that are needed in small quantities by the body, ie vitamins, trace metals, and essential fatty acids (EFA).
- Metabolism. This time I asked about lipid metabolism (the other 2 choices are protein metabolism and carbohydrate metabolism). I asked about fat metabolism during fasting. Triglycerides are lipid storage molecules in adipose tissues found under the skin and spaces in between organs. There are 2 stages of how we obtain energy during fasting - an early stage and a latter stage. In the early stage, there is glycolysis and protein breakdown. In the latter stage, there is fat mobilisation and ketolysis as energy sources. I asked the students to start with fat mobilisation; some have problems recalling the processes for energy sources during fasting. Triglycerides are complex lipids; they need to be broken down first before the body can use it as an energy source. Triglycerides are hydrolysed by hormone sensitive lipase (HSL) in a stepwise fashion, first to diglyceride (DG), then monoglyceride (MG) and finally to glycerol (G) and free fatty acids (FFA). Fat mobilisation is the breakdown and movement of simple lipids (fatty acids and glycerol) from adipose tissue to the liver, via albumin as a carrier protein. Ketolysis is the breakdown of ketone bodies from muscle and liver, and subsequent oxidation of ketone bodies in the liver. In the long term, the body utilises FFA and ketone bodies as an energy source. Some students prioritised that brain prefers glucose as an energy source, and can't utilise ketone bodies because of the blood-brain barrier (BBB).
- Hormones. I asked how is blood glucose controlled. Most answered by 2 hormones, insulin and glucagon. I then asked what are the actions of insulin. Some accidentally said insulin raised blood glucose! Most could answer well about the mode of action of insulin. I also asked about the action of glucagon. Many could not answer about action of glucagon. I think students don't know or can't recall that glucagon is considered a counter-regulatory hormone, ie its actions are the opposite of those of insulin. I asked what are the causes of diabetes. Some answered well, but some explained the pathophysiology wrongly.
- Cancer. I asked about cancer - causes (DNA mutation, uncontrolled mitosis), treatment (surgery, radiotherapy, chemotherapy), and anti-cancer drugs (enzyme inhibitors). I asked about causes of cancer and some students mentioned DNA mutation. I probed about the nature of the DNA mutation, how the mutation occurs and the nature of DNA damage. I asked if the mutations can be corrected or repaired. Many students talked about presence of repair system that corrected the mutation. Some answered something about the cell cycle, disrupted apoptosis and uncontrolled mitosis, leading to cell proliferation. I asked the students whether they have studied and know about enzymes. Some could hardly recall the enzymes. A few students managed to answer well about the 2 types of enzyme inhibition - competitive inhibition and non competitive inhibition.
- Antioxidants. I asked about antioxidants - what they are and how they function. I asked what are antioxidants. I asked how free radicals cause damage. I probed about reactive oxygen species (ROS) and body's defenses. Some mentioned the antioxidants are glutathione system. Some answered lipid peroxidation affected lipid bilayers, biomembranes. I asked the significance of lipid peroxidation and related changes to lipid bilayer. Some mentioned lipoproteins and LDL oxidation. I asked about lipoprotein composition (PL, FC, CE, and TG). I asked about function of LDL. I asked about what happened to oxidised LDL (oxLDL). Some students mentioned LDL are easily oxidised to oxLDL, which cause plaque at the arterial endothelium, and lead to atherosclerosis (some said arteriosclerosis). I then asked what happened next after atherosclerosis. Some answered heart attack and (myocardial) infarction. Nobody mentioned stroke. Prolonged hyperlipidaemia leads to oxidation of LDL. Oxidised LDL (oxLDL) are small destructive particles as they can easily penetrate the arterial intima and cause harm. The macrophages consumed the oxLDL till they become foam cells and die, leading to changes in the arterial intima and underlying area.
Prof Faridah
