Paulʼs Weight Loss and Kemalʼs ObesityScenario Introduction1. What is Crohn’s Disease?12. What is a fistula?23. What is the...
6. What percentage of metabolised energy is lost as heat?117. How is basal metabolic rate calculated?128. Which trimester ...
4. What defines omega fatty acids as essential (omega-6) or non-essential(omega-3)?215. What is the daily requirement in sa...
1. Which vitamins are water soluble and which are fat soluble, what does this meanfor consumption of these vitamins?312. W...
11. What is pernicious anaemia?4112. What are the dietary sources of vitamin B12 and what is it used for?4213.What are the...
22.What is vitamin C used for in collagen formation?5223.What are retinol and carotene?5324.Which demographic group are mo...
5. What are the constituent parts of a triglyceride (fat storage molecule)?626. What is the purpose of apoproteins in lipi...
15.Which receptors remove LDL cholesterol from circulation and are absent in thecase of familial hypercholesterolaemia?721...
8. What pathology leading to death by infection could be caused by Zinc deficiency?819. List the main functions of Iron oth...
18.How would you test for type 1 haemochromatosis?9119.What is the treatment of type 1 haemochromatosis?9220.What is the m...
2. What substances/hormones affect the release and activity of insulin?1013. Where are insulin and glucagon produced?1024....
12.Hormone sensitive lipase inside the cell is inactivated by insulin, but lipoproteinlipase is activated when outside the...
23.What are the key differences between diabetes type 1 and type 2?12224.What mechanism to prevent excessive protein break...
7. What is ‘multi-impulsive bulimia’?1318. Bulimia suffers tend to maintain a normal or above average weight, so what aret...
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Paul's weight loss and kemal's obesity

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Paul's weight loss and kemal's obesity

  1. 1. Paulʼs Weight Loss and Kemalʼs ObesityScenario Introduction1. What is Crohn’s Disease?12. What is a fistula?23. What is the equation for BMI?34. What is the minimum length of small bowel required to prevent malabsorbtion?45. Why would troponin level be elevated in a patient with malabsorbtion?5Energy Balance and Control of Body Weight1. What is the average weight of a newborn baby in the UK?62. What percentage of a newborn baby’s weight is fat?73. What % fat is normal for an adult female and adult male?84. Why would you use mid-arm circumference to measure body composition ratherthan mid-leg?95. Out of the following which has the highest energy content in terms of kcal/g andwhich has the least in pure form: carbohydrate, fat, alcohol, protein?101Inflammation of the entire GI wall from lumen to serosa usually in the terminal ileum. Inflammation cancause fistula/ulcer allowing gut contents to escape into another fused area of the gut e.g. colon, leading tomalabsorbtion2 Abnormal communication between two epithelial surfaces (e.g. between small and large intestine)3 Weight (kg) / height (m) 24 Normally 6m long, can function on as little as 120m if particular regions (such as terminal ileum) are intact.Bile salts are not reabsorbed if terminal ileum is lost.5 Troponin level may be elevated because of heart damage due to vitamin D malabsorbtion6 3.4kg7 14%8 28% in adult female, 14% in adult male (does not change from newborn)9 Because legs are a common site of edema in sick patients10 Fat has the most at 9.2kcal/g, then alcohol at 7kcal/g, carbohydrate has the least at 4kcal/g
  2. 2. 6. What percentage of metabolised energy is lost as heat?117. How is basal metabolic rate calculated?128. Which trimester of pregnancy brings the greatest increase in energy requirement?139. What is satiety?1410.What peptides are secreted when the stomach is empty to induce feeling ofhunger?1511. Which group of drugs have been used to treat obesity in the past but found tobe lethal?1612.Give 2 examples of other drugs used to treat severe obesity?17Macronutrients1. How much fat is in the average UK dies (g/day) and what percentage of energycomes from this?182. What are the biological uses of fat in the body?193. What is the difference between linoleic acid and linolenic acid?2011 50% of all metabolised energy (ATP) is lost as heat12 kj/hour/kg body weight. Accounts for the energy used to cover basic breathing, digestion, maintenance ofionic equilibria across membranes (driven by Na+/K+ ATPase).13 3rd trimester because foetus is undergoing greatest rate of growth and is at greatest size at this stage.Although the net extra requirement is relatively little because this is mostly compensated for by decreasedactivity.14 The hypothalamus initiating the sensation of fullness. Signalled by leptin, which is proportional to the sizeof adipose tissue stores. (the fatter you are the more leptin you have)15 Ghelin and neuropeptide16 Uncouplers - which uncouple oxidative phosphorylation from the electron transport chain.17 Sibutramine, which increases seratonin levels and induces feelings of happiness, decreasing appetite.Orlistat, which decreases fat absorbtion in the small intestine, but can result in steatthorea if not taken withlow fat diet.18 88g/day, 40% of energy19 Phospholipid bilayer, precursor of eicosanoids, thromboxanes and prostaglandins.20 Linoleic acid is omega 6 and linolenic acid is omega 3
  3. 3. 4. What defines omega fatty acids as essential (omega-6) or non-essential(omega-3)?215. What is the daily requirement in saturated fats (g/day) for an average adult?226. What is the difference between cis and trans fat?237. What proportion of energy in the diet do carbohydrates provide in the leastdeveloped countries vs the UK?248. What kind of monosaccharide can be used in a diabetic diet to alleviate thesymptoms of diabetes?259. What are the two most common types of disaccharide?2610.What are the characteristics of polysaccharides?2711.What are the main uses of protein in the body?2812.What is Kwashiorkor?2913.What is Marasmus?30Vitamins21 Omega-x refers to the number of carbon units the double bond is from the opposite end of the chain to themethyl group. Omega 6 and omega 3 are configured differently based on this.22 2-5g23 Refers to cis or trans configuration in the carbon chain, cis are kinked and therefore allow greater fluidity inthe membrane whereas trans are straight and make less permeable membranes.24 90% of energy in LEDCs, 30% in the UK25 Sorbitol - a monosaccharide that does not increase blood glucose26 sucrose and lactose27 Starch, crystalline, insoluble.28 10-15% of total energy, synthesis of catecholamines, thyroid hormones, neurotransmitters, glutathione29 Protein deficiency manifest as to decreased oncotic gradient exerted by the blood (because of low bloodprotein) giving rise to edema particularly in the abdomen.30 General deficiency of both energy and protein, causes muscle wasting and 60% expected body weight forage and gender. Manifests in first year of life.
  4. 4. 1. Which vitamins are water soluble and which are fat soluble, what does this meanfor consumption of these vitamins?312. What are the signs of thiamin deficiency?323. Damage to the eyes, in particular gel like appearance is a sign of which vitamindeficiency?334. Rickets is deficiency of which vitamin?345. What are the main uses of B group vitamins?356. Which foods are sources of thiamine (B1) and which are anti-thiamines?367. Why does alcohol cause Korsakoff’s Psychosis?378. What is the function of riboflavin (B2) and what are its main sources, whathappens with B2 deficiency?389. What is the function of niacin (B3) and what are its main sources, what happenswith B3 deficiency?3910.What are the main functions of pyrioxidine (B6) and what are its main sources,what happens with B6 deficiency?4031 Water soluble vitamins are B group and C and are not stored by the body so must be regularly consumed.Vitamins A, D and K are fat soluble and can be stored in the body so do not need to be consumed often.32 Wet Beri Beri - swelling in face, edema. Dry Beri Beri - skinny bandy legs, symmetrical peripheralneuropathy. Korsakoffʼs Psychosis - main sign of Thiamine deficiency in alcoholics. Infantile Beri-Beri(cardiovascular symptoms), Acute cardiac Beri-Beri (includes enlarged heart, liver damage, engorged neckveins). Wernickeʼs Encapalopathy.33 Vitamin A34 D35 All B group enzymes act as co-enzymes in metabolic pathways.36 Raw fish, Anti thiamine = coffee, tea.37 A result of B1 deficiency because alcohol inhibits the active transport absorbtion of thiamine from theintestine, inhibits the enzyme Thiamine Phosphatase which converts thiamine into its active form. A cirrhoticliver is also less effective at storage of fat soluble vitamins (including Thiamine)38 Associated with proteins found in milk and dairy products. Function is as FAD in FMN redox reactions.39 Main sources are cereals and high protein diets, function is as NAD and NADP in redox reactions.Deficiency is photosensitive dermatitis.40 Essential for metabolism and haemopoesis, deficiency drug induced (TB drug). Active form essential forconverting glucose into glycogen. Present in numerous foods, widely available.
  5. 5. 11. What is pernicious anaemia?4112. What are the dietary sources of vitamin B12 and what is it used for?4213.What are the dietary sources of folate (B6) and what is it used for?4314.What happens to MeTHF levels in the case of B12 deficiency and why?4415.Why is inhibition of folate (B6) sometimes used in treating cancer?4516.Why should you not give B12 to people who are B6 deficient?4617.What are the causes of B12 deficiency?4718.What are the causes of B6 deficiency?4819.What are the functions and sources of biotin (B7)?4920.Which metabolite is produced in excessive quantities in vitamin C mega-dosing?5021.Why could a low fat diet over a long period cause deficiency of vitamins A, D andK?5141 Refers to anemia caused by loss of gastric parietal cells which are responsible for the secretion of intrinsicfactor, a protein essential for absorbtion of vitamin B12 in the ileum.42 Only found in animal tissues, so vegans will only get B12 from supplements. Uptake is by binding toglycoproteins secreted from gastric cells and requires intrinsic factor. Function is as a carrier of methylgroups in metabolism and branched amino acid metabolism43 Sources are green veg, liver and whole grains. Function is to transfer reactions in purine and pyridinesynthesis (DNA/RNA synthesis) and amino acid metabolism.44 Rise excessively because B12 is required to convert MeTHF back into tetrafolate. MeTHF is a derivative oftetrafolate from vitamin B6.45 Because B6 gives rise to a number of interconvertible factors which produce purines, pyridimines andamino acids required for rapid cell division and growth (such as growth of a cancer).46 Because B6 causes buildup of factors which lead to MeTHF which can only be converted back totetrahydrofolate by B12. So causes toxic excess when production accelerated in absence of B12.47 Absent or defective intrinsic factor, gastric atrophy, coeliac disease or gastrectomy limiting absorbtion.48 Alcohol, malabsorbtion (see previous answer), can be drug induced (e.g. barbiturates and anti-convulsants)49 Sources: Gut flora, peanuts, chocolate and egg yolk (but egg whites are anti-B7), Function: prostheticgroup for carboxylation in metabolic reactions (e.g. oxaloacetate/pyruvate, acetyl-coa/malolyl coa)50 Oxaloacetate51 Because these are fat soluble
  6. 6. 22.What is vitamin C used for in collagen formation?5223.What are retinol and carotene?5324.Which demographic group are most likely to be vitamin D deficient?5425.What is the function of vitamin D?5526.What are the functions and sources of vitamin K, and who is most likely to bedeficient?5627.What is the reccomended daily allowance of vitamin C for a typical adult?57Lipid Transport in the Blood1. Why is fat synthesised only when glucose is in large excess in the blood?582. Describe the reaction activated by insulin for producing Manolyl-CoA in the fedstate?593. What is inhibited by Manolyl-CoA?604. What is the hexose monophosphate shunt?6152 Hydroxylation of lysine and proline in collagen formation and stabilization. Maintains Fe2+ in ferrous stateso it can be used.53 Animal and plant forms of vitamin A. Deficiency of which leads to problems with the eye (gel like cornea),night blindness, toxicity in high doses can lead to birth defects, hair loss, hepatic dysfunction etc.54 Low birth weight in premature babies, human milk does not contain vitamin E and cannot cross placentaeasily55 Acts like a steroid hormone by binding receptors which interact with DNA. Ensures calcium absorbtionfrom the gut (hence rickets affects bones). Toxicity manifest as hypercalcemia and calcification of organs.56 Sources: green veg, milk, cereals, eggs and gut flora. Used as coagulation factor, low vitamin K increasesclotting time. Babies are sometimes deficient because vitamin K content of human milk is low and cannotcross the placenta easily.5740mg/day, because vitamin C is a water soluble vitamin and therefore not stored, regular intake is needed58 Glucose is preferentially converted to glycogen in the fed state, however the liver can only store a finiteamount of glycogen, so excess is converted to fats and an unlimited amount can be stored in adipose tissue59 Acetyl-CoA (2C) + (HCO3- in first step), (CO2 used and given off in successive steps, +3C - 1C = +2C) --->(catalyzed by Acetyl-CoA carboxylase + ATP-->ADP)--->Manolyl-CoA (3C)60 The carnitine shuttle, the mechanism carrying lipids across the cell membrane in B-oxidation61 Pathway for producing NADPH and glucose. Particularly active in liver and mammary glands (lipidsynthesis), NADPH is used in fatty acid synthesis.
  7. 7. 5. What are the constituent parts of a triglyceride (fat storage molecule)?626. What is the purpose of apoproteins in lipid transport?637. What are the main differences in function between lipid carrying molecules:chylomicrons, HDLs, LDLs andVLDLs?648. What does density refer to when describing the above molecules?659. How is TAG transported across capillary membranes after being transported bychylomicrons from small intestine, which enzyme does this require?6610.Which hormone activates the enzyme in (9)?6711.Which transport molecule takes fat from the liver to the tissues to be brokendown?6812.Which enzyme picks up cholesterol from tissues when activated by ApoAI onHDLs?6913.What reaction and enzyme activity is inhibited when cholesterol enters a cell?7014.Which drugs inhibit this reaction too?7162 3 fatty acids and a glycerol molecule.63 Make lipid soluble in water so can be transported, ApoCII also causes TAG to deposit in adipose tissueregardless of insulin64 Chylomicrons are the least dense, largest and contain the most TAG, HDLs carry cholesterol from theperipheral tissues to the liver where it can be broken down, LDLs carry cholesterol from source areas to thetissues, VLDLs are the 2nd most dense and carry endogenous TAG65 Higher density is increased concentration of fat in the molecule, the lowest being chylomicrons. The lowerdensity, the lower concentration of TAG.66 TAG has to be broken down by lipoprotein lipase in the capillary and then reassembled once it hascrossed into the tissue as free fatty acid67 Insulin68 VLDLs69 Actyl transferase70 Activity of cholesterol synthesizing enzymes, inhibits production of cholesterol. The reaction is Acetyl-CoAconverted to cholesterol in the presence of HMG-CoA reductase.71 Statins
  8. 8. 15.Which receptors remove LDL cholesterol from circulation and are absent in thecase of familial hypercholesterolaemia?7216.How would the following affect the levels of chylomicrons, LDL orVLDL inblood?(i) Defective LDL receptors,(ii)Lipoprotein lipase deficiency,(iii) Deficiency of C-II(iv) Deficiency of apoproteins involved in remnant uptake73Minerals1. What are the two minerals that are essential to form oxygen carrying proteins,name the main O2 carrying protein?742. What levels of Iron, Copper and Zinc would you find in a typical 70kg adult?753. What is the significance of minerals in the body to the toxic ions superoxide andperoxide as well as Xanthine oxidase?764. Name two enzymes which contain a haem group?775. How much more Iron do women need than men?786. Where are the two largest reserves of Iron in the body?797. What dangerous effect can Fe2+ have in the presence of the enzyme superoxidedismutase?8072 B-100 receptors73 (i) Defective LDL receptors = high LDLs as not taken up by liver (ii)Lipoprotein lipase deficiency = highchylomicrons and VLDLs as needed to break these down (iii) Deficiency of C-II = high chylomicrons andVLDL (iv) Deficiency of apoproteins involved in remnant uptake = high chylomicron and VLDL remnant(because many remnants present in blood)74 Fe2+ and Cu2+, Cytochrome Oxidase75 2-3g of Iron and Zinc, 140mg of Copper76 These ions are products of O2 reduction and combine with metallic enzymes to become compoundswithout the toxic effects. Xanthine Oxidase is an O2 radical inactivated by Iron.77 catalase and peroxidase78 2/3 times more than men79 Haemoglobin (67%), and storage mainly in the liver (27%)80 Produces hydroxyl radicals
  9. 9. 8. What pathology leading to death by infection could be caused by Zinc deficiency?819. List the main functions of Iron other than oxygen carriage?8210.How saturated is ferritin (soluble form of storage iron) in the body under normalconditions?8311.How many Fe3+ ions can a single ferritin bind?8412.What could high levels of ferritin in the plasma or mucosa indicate?8513.What is haemosiderin?8614.Transferrin is the most important Iron store in the body (although not thelargest) because of its very high rate of turnover, how many Fe3+ ions can a singletransferrin bind at any one time?8715.What change in physical environment can affect the affinity of transferrin for Ironmolecules?8816.How is Iron from transferrin taken up into cells and ultimately into ferritin in thecells?8917.What are the signs and symptoms of type 1 genetic haemochromatosis (wherethe body absorbs an extra 3-4mg of iron a day from the diet?9081 Severe skin lesions (acrodermatitis enteropathica)82 Oxidative energy production, mitochondrial respiration (succinate dehydrogenase in the Krebʼs cycle),Inactivation of harmful O2 radicals and ribonucleotide reductase in DNA synthesis83 2/3 saturated84 Up to 4300 in the Fe3+ state (which they keep for transport and storage), converted to Fe2+ for functionaluses such as O2 transport85 Iron overload (normally ferritin levels in the mucosa are very low)86 A water insoluble Iron storage protein derived from ferritin, found mainly in the spleen, bone marrow andliver. Deposited in most cells in conditions of iron overload.87 Only 25-40% (compared to ferritin 66%)88 Affinity increased at high pH, decreased in more acidic conditions. Transferrin levels increased in Ironoverload.89 Receptor mediated endocytosis into cell after which receptor-transferrin complexes migrate into cell inclathrin coated pits. Intra vesicular pH rises to 5.5 and clathrin coat is lost, Fe2+ released and transferrinreturn to cell surface.90 Liver failure, diabetes mellitus, cardiac failure and pigmentation of the skin (due to production of increasedmelanin). Cell destruction can result in iron-catalysed lipid peroxidation reactions (membranes).
  10. 10. 18.How would you test for type 1 haemochromatosis?9119.What is the treatment of type 1 haemochromatosis?9220.What is the main non-genetic cause of haemochromatosis?9321.In genetic haemochromatosis, mutations of which proteins give rise to types (i) 1(ii) 2a (iii) 2b (iv) 3 (v) 4 ?9422.What is chelation therapy and what is the most common chelator?9523.What is the name of the new orally active chelator?9624.What is the main function of copper in the body?9725.Which disease is the inability to absorb copper from the intestine?9826.What is Wilson’s disease and how is it treated?99The Fed and Fasting State1. What is the difference between covalent and allosteric modification of an enzyme?10091 If measured transferrin saturation is greater than 50% in men or 55% in women then measure serumferritin (level of stored iron). Normal levels are less than 300micrograms in men or 200 in women. Can dogenetic test for mutations in HFE gene or liver biopsy.92 Bleeding/phlebotomy (a typical 500ml of blood contains 250mg of iron)93 Long term blood transfusions particularly in B thalassemia.94 1 = HFE protein, 2 = Hemojevulin, 3 = Transferrin receptor 2, 4= ferroportin (IReg1) (exports Fe2+ out ofcell)95 Treatment of haemchromatosis with drugs able to bind iron. Deferoxamine is the most widely usedchelator but has to be given IV over an extended time period so is highly limiting to patients.96 Deferiprone97 Copper producing enzymes98 Menkeʼs disease99 Impaired biliary secretion of Cu (where most Cu is lost) so buildup of Cu in liver and liver damage, braindamage from buildup in brain. Treated using copper chelation therapy.100 Covalent is where something is physically added to the enzyme (e.g. phosphate to activate/deactivate),allosteric is where something temporarily binds to the enzyme, changing the shape of its active site.
  11. 11. 2. What substances/hormones affect the release and activity of insulin?1013. Where are insulin and glucagon produced?1024. What does somatostatin do?1035. Why are there only low affinity glucose transporters in the islet cells when highaffinity would be more efficient?1046. What is the mechanism of response to glucose and amino acids within the isletcell?1057. How does the insulin secreted in vesicles have to be changed structurally before itis active?1068. And what is the clinical use of this?1079. Describe the chemical pathway for fatty acid synthesis from excess glucose?10810.How does insulin stimulate uptake of glucose by muscles and adipose tissue?10911.How does this mechanism also inhibit hormone sensitive lipase and so inhibit thebreakdown of glycerol and fatty acids?110101 Adrenaline inhibits, growth hormone stimulates, cortisol (stress hormone) inhibits to release moreglucose, presence of amino acids and glucose in blood increases, GI tract secretion of secretin hormonestimulates. Release of glucagon stimulates release of insulin (control mechanism)102 Insulin in beta cells, glucagon in alpha cells, both in the islets of Langerhans in the pancreas103 Produced by delta cells in the Islets of Langerhans, it inhibits both insulin and glucagon to stop levelsgetting too high104 Because they only need to respond to high glucose levels and not normal glucose levels.105 Glucose and amino acids give rise to increased ATP, which closes K+ channels on the cell wall and opensCa+ channels, increased intracellular Ca2+ stimulates release of insulin vesicles.106 Secreted as pro-insulin, C-peptide must be cleaved by proteolysis to become active insulin.107 Levels of C-peptide can be measured to determine the levels of endogenous insulin release (because theinsulin itself gets used up).108 Glucose --> Pyruvate --> Acetyl-CoA --> Fatty acid (in the presence of pyruvate dehydrogenase)109 Binds to receptor which activates Active Akt/PKB which up-regulates GLUT-4 by releasing them fromvesicles and translocating to the cell wall so more glucose can be taken up.110 Active AKt/PKB up-regulated phosphodiesterase which uses cAMP in cell. Lack of cAMP inhibits PKAwhich inactivates hormone sensitive lipase.
  12. 12. 12.Hormone sensitive lipase inside the cell is inactivated by insulin, but lipoproteinlipase is activated when outside the cell, why is this?11113.What are the two main intermediary factors involved in insulin affectingtranscription factor?11214.Which liver processes are activated by glucagon?11315.What is the precursor for formation of ketone bodies?11416.Which enzyme activates glycolysis?11517.Which transport molecules take fat to adipose tissue once converted fromexcess glucose in the liver?11618.How is glycogen synthase activated?11719.What is the function of Acetyl-CoA carboxylase?11820.Which areas of the body are said to be ‘insulin independent’ and can thereforeuse glucose at high and low concentrations?11921.Which product of metabolism can be converted into pyruvate?12022.Why is it mainly protein that is metabolised in fasting and not fat?121111 Allows fatty acid esterification, breaks down into small units so can cross the membrane to be stored.112 Ras and MAPK113 Glycogenolysis (breakdown of glycogen), gluconeogenesis (production of glucose from stored protein),uptake of amino acids by the liver for gluconeogenesis114 Fatty acid oxidation in the fasting state115 Glucokinase, Phosphofructokinase and pyruvate kinase116 VLDLs, responsible for transporting fat from liver to adipose tissue117 Activated by dephosphorylation (using phosphatase enzyme), inactivated by phosphorylation (addingphosphate) with kinase enzyme.118 Irreversible production of malolyl-CoA from acetyl-CoA (from glycolysis) in fatty acid synthesis119 Brain (fatty acids cannot cross blood brain barrier so relies on glucose) and erythrocyte (no mitochondria)120 Lactate121 Although fat can be broken down into ketone bodies, the pyruvate dehydrogenase (converting pyruvateinto acetyl CoA) enzyme is irreversible, so fat cannot be converted back into glucose whereas amino acidscan by glyconeogenesis.
  13. 13. 23.What are the key differences between diabetes type 1 and type 2?12224.What mechanism to prevent excessive protein breakdown in fasting metabolismis not present in diabetes?12325.What are the complications of diabetes?124Eating Disorders1. What % of people with anorexia die from it?1252. How is anorexia defined and what are the main symptoms?1263. How does bulimia nervosa differ from this?1274. What biological factor may increase the chance of having an eating disorder?1285. What kind of childhood environmental factors may lead to development of aneating disorder?1296. What is the difference between Obsessive Compulsive Personality Disorder(OCPD) and Obsessive Compulsive Disorder?130122 Type 1 is childhood onset, can lead to hyperglycaemia and ketoacidosis, results from autoimmunedestruction of pancreatic B cells so said to be insulin dependent. Type 2 is adult onset, caused by insulinresistance, associated with lifestyle factors such as obesity although is milder than type 1 and does not leadto ketoacidosis.123 Insulin release stimulated by high level of ketone bodies. Leads to uncontrolled production of KB in type1.124 Microangiopathy (thickening of basement membrane in blood vessels), Retinopathy (blindness),Nephropathy (renal failure), Neuropathy (postural hypotension, impotence and foot ulcers)125 5-7%126 Morbid fear of fatness and body image, a BMI of less than 17.5 (underweight), amenorrhoea (lack ofmenstrual period). Emaciation, bradycardia and hypotension, anaemia and leucopenia (decrease in whitecells) leading to poor immunity127 Includes craving for food and uncontrolled binge eating followed by purging/vomiting or laxative abuse.Characterised by fluctuating weight (normal or excessive)128 Altered brain serotonin (5-HT) function contributes to disregulation of appetite and mood.129 Sexual, physical or emotional abuse, being ridiculed about size or weight, troubled family relationships,overprotective or over-controlling environment.130 In OCPD sufferers believe fully in their obsessive preoccupation with rules and order, in OCD sufferersare aware that these are irrational and unwanted thoughts.
  14. 14. 7. What is ‘multi-impulsive bulimia’?1318. Bulimia suffers tend to maintain a normal or above average weight, so what arethe physical symptoms?1329. What BMI range is obese?13310.What is Russell’s sign?134131 Alcohol and drug misuse, sexual disinhibition and poor impulse control coexist with food binges and selfharm.132 Amenorrhoea in 50% of cases, hypokalemia (related to vomiting), which may cause dysrhythmias or renaldamage. Oesophageal tearing and poor dental health.133 30 and over134 Callouses on the knuckles from making repeated contact with teeth from self induced vomiting in bulimia

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