GMC Domains

• THE DOCTOR AS A SCHOLAR
  • TD 8: APPLICATION OF BIOMEDICAL SCIENTIFIC PRINCIPLES, METHOD AND KNOWLEDGE
    • Medical knowledge: ANATOMY (TD 8.1)
    • Medical knowledge: PHYSIOLOGY (TD 8.2)
    • Medical knowledge: BIOCHEMISTRY (inc. Metabolism) (TD 8.3)
    • Medical knowledge: CELL BIOLOGY (TD 8.4)
    • Medical knowledge: MOLECULAR BIOLOGY and GENETICS (TD 8.5, 8.6)
    • Medical knowledge: PATHOLOGY (TD 8.7)
    • Medical knowledge: CANCER
    • Medical knowledge: IMMUNOLOGY and INFLAMMATION (TD 8.8)
    • Medical knowledge: MICROBIOLOGY and INFECTION (TD 8.9)
    • Medical knowledge: PHARMACOLOGY (TD 8.10)
    • Medical knowledge: NUTRITION (TD 8.11)
    • Medical knowledge: CLINICAL FEATURES of DISEASE (TD 8 b)
  • TD 9: APPLICATION OF PSYCHOLOGICAL PRINCIPLES, METHOD AND KNOWLEDGE
    • Medical knowledge: PSYCHOLOGY (TD 9 a-g)
  • TD 10: APPLICATION OF SOCIAL SCIENCE PRINCIPLES, METHOD AND KNOWLEDGE
    • Medical knowledge: SOCIOLOGY (TD 10 a-e)
  • TD 11. PRINCIPLES, METHODS AND KNOWLEDGE OF POPULATION HEALTH
    • Medical knowledge: PUBLIC HEALTH and GLOBAL HEALTH (TD 11 a-j)
  • TD 12; APPLICATION OF SCIENTIFIC METHOD AND APPROACHES TO MEDICAL RESEARCH
    • Medical knowledge: EPIDEMIOLOGY
    • Medical Knowledge: SCIENTIFIC METHOD & RESEARCH
• THE DOCTOR AS A PRACTITIONER
  • TD 13: CARRY OUT A CONSULTATION WITH A PATIENT
    • Clinical skills: HISTORY (TD 13 a-b)
    • Clinical skills: PHYSICAL EXAMINATION (TD 13 c)
    • Clinical skills: MENTAL STATE EXAMINATION (TD 13 d)
  • TD 14: DIAGNOSE AND MANAGE CLINICAL PRESENTATIONS
    • Clinical skills: INTERPRETING FINDINGS AND INITIAL ASSESSMENT (TD 14 a-b)
    • Clinical skills: PLANNING AND INTERPRETING INVESTIGATIONS (TD 14 c-d)
    • Clinical skills: MAKING A DIAGNOSIS and CLINICAL JUDGEMENT (TD 14 e-f)
    • Clinical skills: FORMULATING A TREATMENT PLAN (TD 14 g)
    • Clinical skills: SURGERY and ANAESTHETICS (TD 14 g)
    • Clinical skills: SUPPORTING PATIENTS and IDENTIFYING ABUSE and NEGLECT (TD 14 h-i)
    • Clinical Skills: CARE OF PATIENTS AND RELATIVES AT END OF LIFE (TD 14 j)
  • TD 15: COMMUNICATE EFFECTIVELY WITH PATIENTS AND COLLEAGUES
    • Clinical skills: INTERACTION WITH PATIENTS (TD 15 a-b)
    • Clinical skills: MANAGING INFORMATION (TD 15 c)
  • TD 16: PROVIDE IMMEDIATE CARE IN MEDICAL EMERGENCIES
    • Emergency Management of Patients (TD 16 b-e)
  • TD 17: PRESCRIBE DRUGS SAFELY, EFFECTIVELY AND ECONOMICALLY
    • Clinical skills: PRESCRIBING DRUGS SAFELY AND EFFECTIVELY (TD 17 a-h)
  • TD 18: CARRY OUT PRACTICAL PROCEDURES SAFELY AND EFFECTIVELY
    • Clinical skills: DIAGNOSTIC PROCEDURES (TD 18 a)
    • Clinical skills: THERAPEUTIC PROCEDURES (TD 18 b)
  • TD 19: USE INFORMATION EFFECTIVELY IN A MEDICAL CONTEXT
    • Clinical skills: EVIDENCE BASED MEDICINE
• THE DOCTOR AS A PROFESSIONAL
  • TD 20: BEHAVE ACCORDING TO ETHICAL AND LEGAL PRINCIPLES
    • Professional issues: ETHICS and LAW (TD 20 a-g)
  • TD 21: REFLECT, LEARN AND TEACH OTHERS
    • Professional Issues: PERSONAL LIMITS OF CARE (TD 21e)
    • Professional issues: LEARNING (TD 21 a-d)
    • Professional issues: TEACHING AND MENTORING (TD 21 f)
  • TD 22: LEARN AND WORK EFFECTIVELY WITHIN A MULT-PROFESSIONAL TEAM
    • Professional issues: WORKING IN TEAMS (TD 22 a-c)
  • TD 23: PROTECT PATIENTS AND IMPROVE CARE
    • Professional issues: DUTIES OF A DOCTOR (TD 23 a-b)
    • Professional issues: MEDICAL FRAMEWORK IN THE UK (TD 23 c)
    • Professional issues: RISK MANAGEMENT and PATIENT SAFETY (TD 23 d)
    • Professional issues: GOVERNANCE, QUALITY MATTERS and AUDIT (TD 23 e)
    • Professional issues: PERSONAL ATTITUDES and SELF CARE (TD 23 f-j)

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TD 8: APPLICATION OF BIOMEDICAL SCIENTIFIC PRINCIPLES, METHOD AND KNOWLEDGE: Medical knowledge: BIOCHEMISTRY (inc. Metabolism) (TD 8.3)

Introduction

Biochemistry: The study of the chemical substances and vital processes occurring in living organisms

Index

• General Outcomes for Biochemistry
• Metabolism

• General Outcomes for Biochemistry
  • Biochemistry - General
    1. Describe the properties of nitric oxide and its mechanism of synthesis in vascular endothelium (GEP/CO2)
    2. 1. To describe the extracellular architecture 
    3. Describe the properties of nitric oxide and its mechanism of synthesis in vascular endothelium
    4. Be able to define and describe with examples, the volume of distribution, clearance and elimination half life (GEP/BB)
    5. To define and explain drug absorption (GEP/BB)
    6. 2. To appecriate the key components that make up most of the ECM including 
    7. 2. To appecriate the key components that make up most of the ECM including 
    8. 1. collagen
    9. 1. collagen
    10. Understand the problem of the source of nitric oxide in exercising muscle
    11. 2. proteoglycans
    12. 2. proteoglycans
    13. 3. To appreciate the mechanism that allow cells to adhere and move through the extracellular matrix
    14. 3. To appreciate the mechanism that allow cells to adhere and move through the extracellular matrix
    15. 4. To describe how loss of cell ahesion can lead to diseases
    16. 4. To describe how loss of cell ahesion can lead to diseases
  • Amino Acids
    1. List three metabolic fates of dietary amino acids.
    2. Be able to cite a common clinical example of acid base becoming unbalanced. (FM1)
    3. Define the terms: essential amino acid, non-essential amino acid, carbon skeleton, glucogenic amino acid, ketogenic amino acid.
  • Acid-Base Balance
    1. Define 'pH' and state the normal range for arterial pH and the range compatible with life. Comment on the differences between normal arterial and mixed venous pH values.
    2. Have an understanding of acid base balance and the causes of acidosis and alkalosis.
    3. Perform simple calculations to illustrate the use of the Henderson-Haselbalch equation and the pH equation.
    4. Be able to define the term buffer system and explain how it resists changes in pH (FM1)
    5. Understand the basic physiological principles behind acid base balance.
    6. Be able to state the normal pH and hydrogen concentration of human blood plasma and the ranges compatible with life. (FM1)
    7. Review the operation of the acid-base balance using respiratory acidosis as an example.
    8. Understand the relationship between respiratory and metabolic control of acidaemia
    9. List causes of a normal and high anion gap.
    10. State the four major forms of acid-base disturbance and explain how systems such as the Flenley nomogram can be used to analyse acid-base status.
    11. Use the Flenley nomogram and 'rule of thumb' methods to work out the acid-base status for a series of patient scenarios.
    12. Describe common causes of lactic acidosis.
    13. Use the Flenley nomongram to explain the processes of disturbance, buffering and compensation.
    14. Outline the role of hydrogen carbonate, phosphate and ammonium ions in the renal excretion of acid, noting the relationship between tubular pCO2, hydrogen carbonate reabsorption and proton excretion
    15. Name the FOUR simple classes of acid-base disturbance, stating the primary disturbance and the form of compensation for each class. Comment on the time scale for renal as compared with respiratory compensation and give ONE clinical cause for each class.
  • Fatty Acids
    1. Describe the control of fatty acid synthesis via regulation of acetyl-CoA carboxylase.
    2. Understand the purpose of triglyceride mobilisation (lipolysis).
    3. State the products of lipolysis and contrast the metabolic fates of the glycerol and fatty acid moieties in triglyceride.
    4. Understand how the activity of hormone-sensitive (triglyceride) lipase is regulated.
    5. Outline the overall pathway of fatty acid activation and transport into the mitochondrial matrix via the carnitine shuttle.
    6. Be aware of the regulatory importance of malonyl-CoA for regulation of mitochondrial long-chain fatty acid oxidation at the level of carnitine palmitoyl transferase I.
    7. Outline the general features of the beta-oxidation spiral and understand the role of beta-oxidation in ATP production.
    8. State the site and mechanism of ketone body production (ketogenesis).
    9. Specify the fate of ketone bodies in tissues such as the muscle and brain.
    10. Describe the effects of excessive ketone body production.
  • Fluid Balance
  • Nitrogen Balance
    1. Draw a diagram indicating the main components of N intake and excretion in a normal person, and explain the information which can be obtained by N balance studies.
    2. Explain obligatory Nitrogen loss
  • Sodium Balance
  • Urea Cycle
    1. Draw the molecular structure of urea, state the average daily output of urea in man, and describe the reactions of the Urea cycle (names only).
  • Blood Gases
  • Biochemistry - Renal System
    1. Outline renal handling of important electrolytes
    2. By means of labelled diagrams, show the changes in volume and osmolality of tubular fluid along the length of the nephron, in the presence or absence of anti-diuretic hormone (ADH)
    3. Be aware of the various types of renal tubular acidosis and their biochemical basis
• Metabolism
  • Metabolism - General
    1. Discuss by means of a relevant example the ways in which the integration of carbohydrate, protein and fat metabolism are deranged in human disease.
    2. Discuss the links between metabolism and nutrition
    3. Define inherited metabolic disorders and list common inherited metabolic disorders. (GEP/DGM)
    4. Explain why an understanding of Metabolism is important in terms of normal human physiology and disease states. Explain the links between digestion, catabolic and anabolic pathways. (GEP/DGM)
    5. Draw the general molecular structure of an amino acid.
    6. Outline the metabolic impact of Von Gierke's disease. (GEP/DGM)
    7. Discuss with examples the integration of metabolism in different human organs and different cell compartments. (GEP/DGM)
    8. Explain the significance of linkage between the important metabolic pathways, and their apparent complexity
    9. Outline the biochemical basis and consequences of galactosaemia. (GEP/DGM)
    10. Discuss with examples the significance of the regulation of metabolism in humans. (GEP/DGM)
    11. Describe with examples, the coordination of metabolism between the organs and between subcellular compartments
    12. Outline the biochemical basis and consequences of McArdle's disease (GEP/DGM)
    13. Discuss the mechanisms for and the importance of the control of metabolism
    14. Describe the consequences of a deficiency of liver fructokinase or fructose 1-phosphate aldolase. (GEP/DGM)
    15. Outline the inherited metabolic disorders of amino acid metabolism (GEP/DGM)
    16. Describe the consequences of phenylketonuria. (GEP/DGM)
    17. List the genetic causes of dyslipidaemia. (GEP/DGM)
    18. Describe the consequences of familial hypercholesterolaemia. (GEP/DGM)
  • Energy from Metabolism
    1. Outline the characteristics of muscle slow twitch (type 1) and fast twitch (type 2) fibres.
    2. Define basal metabolic rate and total energy expenditure and indicate how they can be (a) measured (b) estimated.
    3. Calculate the energy requirements in health. Define resting metabolic rate and the thermogenic effect of food and   physical activity. Note that disease may increase resting metabolism but often reduces activity. (GEP/DGM)
    4. Define basal (resting) metabolic rate (BMR)
    5. Describe how, after digestion, the simple molecules of food are largely broken down to a final common aerobic pathway of energy metabolism in which an acetate group is oxidised in order to power ATP production (Krebs cycle and oxidative phosphorylation)
    6. Compare the metabolic pathways employed during sprinting, middle-distance running and marathons.
    7. Note that a thermodynamically favourable reaction is driven by a favourable one and that ATP to ADP or ADP to AMP are the common drivers. (GEP/DGM)
    8. Describe the regulatory role of AMP-activated protein kinase (AMPK) in exercise.
    9. Distinguish between the two peripheral types of muscle fibre indicating how white fibres favour anaerobic metabolism and red fibres aerobic, endurance related exercise.
    10. ATP is regenerated by the oxidation of (removal of electrons from) food. Oxygen is the final electron acceptor but this is indirect via a number of mitochondrial molecules or   electron carriers based on water soluble vitamins. This reforming of (GEP/DGM)
    11. Describe how AMP affects glucose handling by skeletal muscle.
    12. Discuss the relative energy expenditure during some common daily forms of exercise.
    13. Understand the mechanism whereby AMPK lowers malonyl-CoA concentrations and allows increased fat oxidation.
    14. 1st stage of food oxidation: Large molecules protein, fats,  polysaccharides/starch  broken down to small  molecules - no ATP formed (GEP/DGM)
    15. Explain why the oxidation of pyruvate is a key step in human metabolism.
    16. 2nd stage of food oxidation: Numerous small molecules degraded to a few  central  molecules particularly Acetyl CoA with some generation  of ATP (GEP/DGM)
    17. Outline the metabolic adaptations occurring during fatigue.
    18. Describe the metabolic organisation and role of the Krebs cycle.
    19. 3rd stage of food oxidation: Citric acid cycle produces electrons from acetyl CoA and oxidative phosphorylation passes the electrons via the electron acceptors to oxygen to form much more ATP. (GEP/DGM)
    20. Explain how co-enzymes link oxidative metabolism and ATP synthesis.
    21. Acetyl CoA is another (of several) carrier of a group (acetyl) with a thermodynamically favourable high transfer potential. CoA is based on the B vitamin, pantothenate. Most water soluble vitamins are components of coenzymes. (GEP/DGM)
    22. Most biosynthetic processes require the reduction of precursors (donation of electrons to the precursor).  The electron donor is usually NADPH, another form of a B vitamin. (GEP/DGM)
  • Fat Metabolism
    1. Discuss briefly the significance of lipid as a source of metabolic energy in the human body.
    2. List the major metabolic actions of insulin on glucose and lipid metabolism in the postprandial state
    3. Compare and contrast the biosynthesis and the breakdown of triacylglycerols (triglycerides).
    4. Learn basic biochemistry about lipids, particularly chylomicrons, cholesterol, VLDL, HDL (CR3)
    5. Discuss briefly the hormonal control of triacylglycerol in metabolism.
    6. Differentiate between types of lipids in relation to protection from and contribution to cardiovascular disease
    7. Describe how fatty acids are delivered from adipose tissue to the mitochondria of cells in other organs.
    8. Describe how fatty acids are degraded by b-oxidation in mitochondria.
    9. Describe in outline how cholesterol is synthesised and metabolised.
  • Iron Metabolism
    1. Outline the nutritional and metabolic aspects of iron (including dietary iron, iron absorption, body iron distribution and transport) (CR3)
    2. Outline the nutritional and metabolic aspects of iron (including dietary iron, iron absorption, body iron distribution and transport) and the concept of iron overload.
  • Glucose and Glycogen Metabolism
    1. Outline the role of liver glycogen as a source of blood glucose during a normal feeding cycle. (GEP/DGM)
    2. Define gluconeogenesis and state the tissues in which gluconeogenesis occurs.
    3. Summarise the effects of inadequate insulin secretion or action upon carbohydrate and fat metabolism, including the aetiology of diabetic ketoacidosis
    4. Outline the mechanisms of glucose uptake into cells
    5. List the major metabolic actions of insulin on glucose and lipid metabolism in the postprandial state
    6. Describe the actions of glucagon on glucose and lipid metabolism in the post absorptive and fasting states
    7. Outline the advantages of glycogen as a storage molecule.
    8. State the circumstances under which gluconeogenesis will occur.
    9. Outline the potential metabolic fates of glucose 6-phosphate
    10. Distinguish between the facilative glucose transporters (GLUT's) with respect to tissue distribution and kinetic characteristics
    11. Describe the structure of glycogen. (GEP/DGM)
    12. Describe how fatty acid oxidation facilitates gluconeogenesis.
    13. Understand the significance of the regulatory and kinetic characteristics of glucokinase and hexokinase with respect to their tissue locations and physiological roles.
    14. List the major precursors used for gluconeogenesis, and identify their tissues of origin.
    15. Phosphofructokinase is the major control point of glycolysis. Specify how it responds to cellular messages.
    16. Outline the circumstances under which glycogen synthesis and degradation will occur. (GEP/DGM)
    17. Outline the overall pathway of glycogen synthesis and degradation.
    18. Note enzymes in the gluconeogenic pathway that by-pass irreversible steps in glycolysis (glucose 6-phosphatase, fructose 1,6-bisphosphatase, phosphoenolpyruvate (PEP) carboxykinase, pyruvate carboxylase).
    19. Understand that the key enzymes glycogen synthase and glycogen phosphorylase are controlled both by reversible phosphorylation.and by metabolite effectors
    20. Understand that glycolysis can produce ATP by substrate level phosphorylation.
    21. Outline the hormonal regulation of gluconeogenesis.
    22. Understand the different roles of glycogen storage in muscle and liver. Be aware of the differences in the fate of the glucose 1-phosphate that results from glycogenolysis in muscle and liver.
    23. Lactose (milk sugar) is an important source of galactose. Understand how galactose is metabolized and the cause and consequences of galactosaemia.
    24. Understand the different roles of glycogen storage in muscle and liver.
  • Nitrogen Metabolism
    1. Understand that the body balances nitrogen intake and output and define the term nitrogen balance. (MET1)
    2. Understand why some amino acids are essential in the diet. (MET1)
    3. Outline the potential uses of amino acids, including their role as signalling molecules. (MET1)
    4. Understand the difference between glucogenic and ketogenic amino acids.
    5. Appreciate the general metabolism of the carbon skeletons and amino groups from amino acids and how this interfaces with carbohydrate and lipid metabolism.
    6. Understand the function of alanine and glutamine in interorgan carbon and nitrogen flow.
    7. Understand that surplus amino acids contribute nitrogen to urea for excretion. (MET1)
    8. Outline how amino groups are funnelled into the urea cycle. Understand why urea is a better excretion product than ammonia.

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