1. Paulʼs Weight Loss and Kemalʼs Obesity
Scenario Introduction
1. What is Crohn’s Disease?1
2. What is a fistula?2
3. What is the equation for BMI?3
4. What is the minimum length of small bowel required to prevent malabsorbtion?4
5. Why would troponin level be elevated in a patient with malabsorbtion?5
Energy Balance and Control of Body Weight
1. What is the average weight of a newborn baby in the UK?6
2. What percentage of a newborn baby’s weight is fat?7
3. What % fat is normal for an adult female and adult male?8
4. Why would you use mid-arm circumference to measure body composition rather
than mid-leg?9
5. Out of the following which has the highest energy content in terms of kcal/g and
which has the least in pure form: carbohydrate, fat, alcohol, protein?10
1Inflammation of the entire GI wall from lumen to serosa usually in the terminal ileum. Inflammation can
cause fistula/ulcer allowing gut contents to escape into another fused area of the gut e.g. colon, leading to
malabsorbtion
2 Abnormal communication between two epithelial surfaces (e.g. between small and large intestine)
3 Weight (kg) / height (m) 2
4 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 malabsorbtion
6 3.4kg
7 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 patients
10 Fat has the most at 9.2kcal/g, then alcohol at 7kcal/g, carbohydrate has the least at 4kcal/g

2. 6. What percentage of metabolised energy is lost as heat?11
7. How is basal metabolic rate calculated?12
8. Which trimester of pregnancy brings the greatest increase in energy requirement?
13
9. What is satiety?14
10.What peptides are secreted when the stomach is empty to induce feeling of
hunger?15
11. Which group of drugs have been used to treat obesity in the past but found to
be lethal?16
12.Give 2 examples of other drugs used to treat severe obesity?17
Macronutrients
1. How much fat is in the average UK dies (g/day) and what percentage of energy
comes from this?18
2. What are the biological uses of fat in the body?19
3. What is the difference between linoleic acid and linolenic acid?20
11 50% of all metabolised energy (ATP) is lost as heat
12 kj/hour/kg body weight. Accounts for the energy used to cover basic breathing, digestion, maintenance of
ionic 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 decreased
activity.
14 The hypothalamus initiating the sensation of fullness. Signalled by leptin, which is proportional to the size
of adipose tissue stores. (the fatter you are the more leptin you have)
15 Ghelin and neuropeptide
16 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 with
low fat diet.
18 88g/day, 40% of energy
19 Phospholipid bilayer, precursor of eicosanoids, thromboxanes and prostaglandins.
20 Linoleic acid is omega 6 and linolenic acid is omega 3

3. 4. What defines omega fatty acids as essential (omega-6) or non-essential
(omega-3)?21
5. What is the daily requirement in saturated fats (g/day) for an average adult?22
6. What is the difference between cis and trans fat?23
7. What proportion of energy in the diet do carbohydrates provide in the least
developed countries vs the UK?24
8. What kind of monosaccharide can be used in a diabetic diet to alleviate the
symptoms of diabetes?25
9. What are the two most common types of disaccharide?26
10.What are the characteristics of polysaccharides?27
11.What are the main uses of protein in the body?28
12.What is Kwashiorkor?29
13.What is Marasmus?30
Vitamins
21 Omega-x refers to the number of carbon units the double bond is from the opposite end of the chain to the
methyl group. Omega 6 and omega 3 are configured differently based on this.
22 2-5g
23 Refers to cis or trans configuration in the carbon chain, cis are kinked and therefore allow greater fluidity in
the membrane whereas trans are straight and make less permeable membranes.
24 90% of energy in LEDCs, 30% in the UK
25 Sorbitol - a monosaccharide that does not increase blood glucose
26 sucrose and lactose
27 Starch, crystalline, insoluble.
28 10-15% of total energy, synthesis of catecholamines, thyroid hormones, neurotransmitters, glutathione
29 Protein deficiency manifest as to decreased oncotic gradient exerted by the blood (because of low blood
protein) giving rise to edema particularly in the abdomen.
30 General deficiency of both energy and protein, causes muscle wasting and 60% expected body weight for
age and gender. Manifests in first year of life.

4. 1. Which vitamins are water soluble and which are fat soluble, what does this mean
for consumption of these vitamins?31
2. What are the signs of thiamin deficiency?32
3. Damage to the eyes, in particular gel like appearance is a sign of which vitamin
deficiency?33
4. Rickets is deficiency of which vitamin?34
5. What are the main uses of B group vitamins?35
6. Which foods are sources of thiamine (B1) and which are anti-thiamines?36
7. Why does alcohol cause Korsakoff’s Psychosis?37
8. What is the function of riboflavin (B2) and what are its main sources, what
happens with B2 deficiency?38
9. What is the function of niacin (B3) and what are its main sources, what happens
with B3 deficiency?39
10.What are the main functions of pyrioxidine (B6) and what are its main sources,
what happens with B6 deficiency?40
31 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 peripheral
neuropathy. Korsakoffʼs Psychosis - main sign of Thiamine deficiency in alcoholics. Infantile Beri-Beri
(cardiovascular symptoms), Acute cardiac Beri-Beri (includes enlarged heart, liver damage, engorged neck
veins). Wernickeʼs Encapalopathy.
33 Vitamin A
34 D
35 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 the
intestine, inhibits the enzyme Thiamine Phosphatase which converts thiamine into its active form. A cirrhotic
liver 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 for
converting glucose into glycogen. Present in numerous foods, widely available.

5. 11. What is pernicious anaemia?41
12. What are the dietary sources of vitamin B12 and what is it used for?42
13.What are the dietary sources of folate (B6) and what is it used for?43
14.What happens to MeTHF levels in the case of B12 deficiency and why?44
15.Why is inhibition of folate (B6) sometimes used in treating cancer?45
16.Why should you not give B12 to people who are B6 deficient?46
17.What are the causes of B12 deficiency?47
18.What are the causes of B6 deficiency?48
19.What are the functions and sources of biotin (B7)?49
20.Which metabolite is produced in excessive quantities in vitamin C mega-dosing?50
21.Why could a low fat diet over a long period cause deficiency of vitamins A, D and
K?51
41 Refers to anemia caused by loss of gastric parietal cells which are responsible for the secretion of intrinsic
factor, 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 to
glycoproteins secreted from gastric cells and requires intrinsic factor. Function is as a carrier of methyl
groups in metabolism and branched amino acid metabolism
43 Sources are green veg, liver and whole grains. Function is to transfer reactions in purine and pyridine
synthesis (DNA/RNA synthesis) and amino acid metabolism.
44 Rise excessively because B12 is required to convert MeTHF back into tetrafolate. MeTHF is a derivative of
tetrafolate from vitamin B6.
45 Because B6 gives rise to a number of interconvertible factors which produce purines, pyridimines and
amino 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 to
tetrahydrofolate 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: prosthetic
group for carboxylation in metabolic reactions (e.g. oxaloacetate/pyruvate, acetyl-coa/malolyl coa)
50 Oxaloacetate
51 Because these are fat soluble

6. 22.What is vitamin C used for in collagen formation?52
23.What are retinol and carotene?53
24.Which demographic group are most likely to be vitamin D deficient?54
25.What is the function of vitamin D?55
26.What are the functions and sources of vitamin K, and who is most likely to be
deficient?56
27.What is the reccomended daily allowance of vitamin C for a typical adult?57
Lipid Transport in the Blood
1. Why is fat synthesised only when glucose is in large excess in the blood?58
2. Describe the reaction activated by insulin for producing Manolyl-CoA in the fed
state?59
3. What is inhibited by Manolyl-CoA?60
4. What is the hexose monophosphate shunt?61
52 Hydroxylation of lysine and proline in collagen formation and stabilization. Maintains Fe2+ in ferrous state
so 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 placenta
easily
55 Acts like a steroid hormone by binding receptors which interact with DNA. Ensures calcium absorbtion
from 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 increases
clotting time. Babies are sometimes deficient because vitamin K content of human milk is low and cannot
cross the placenta easily.
5740mg/day, because vitamin C is a water soluble vitamin and therefore not stored, regular intake is needed
58 Glucose is preferentially converted to glycogen in the fed state, however the liver can only store a finite
amount of glycogen, so excess is converted to fats and an unlimited amount can be stored in adipose tissue
59 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-oxidation
61 Pathway for producing NADPH and glucose. Particularly active in liver and mammary glands (lipid
synthesis), NADPH is used in fatty acid synthesis.

7. 5. What are the constituent parts of a triglyceride (fat storage molecule)?62
6. What is the purpose of apoproteins in lipid transport?63
7. What are the main differences in function between lipid carrying molecules:
chylomicrons, HDLs, LDLs andVLDLs?64
8. What does density refer to when describing the above molecules?65
9. How is TAG transported across capillary membranes after being transported by
chylomicrons from small intestine, which enzyme does this require?66
10.Which hormone activates the enzyme in (9)?67
11.Which transport molecule takes fat from the liver to the tissues to be broken
down?68
12.Which enzyme picks up cholesterol from tissues when activated by ApoAI on
HDLs?69
13.What reaction and enzyme activity is inhibited when cholesterol enters a cell?70
14.Which drugs inhibit this reaction too?71
62 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 tissue
regardless of insulin
64 Chylomicrons are the least dense, largest and contain the most TAG, HDLs carry cholesterol from the
peripheral tissues to the liver where it can be broken down, LDLs carry cholesterol from source areas to the
tissues, VLDLs are the 2nd most dense and carry endogenous TAG
65 Higher density is increased concentration of fat in the molecule, the lowest being chylomicrons. The lower
density, the lower concentration of TAG.
66 TAG has to be broken down by lipoprotein lipase in the capillary and then reassembled once it has
crossed into the tissue as free fatty acid
67 Insulin
68 VLDLs
69 Actyl transferase
70 Activity of cholesterol synthesizing enzymes, inhibits production of cholesterol. The reaction is Acetyl-CoA
converted to cholesterol in the presence of HMG-CoA reductase.
71 Statins

8. 15.Which receptors remove LDL cholesterol from circulation and are absent in the
case of familial hypercholesterolaemia?72
16.How would the following affect the levels of chylomicrons, LDL orVLDL in
blood?
(i) Defective LDL receptors,
(ii)Lipoprotein lipase deficiency,
(iii) Deficiency of C-II
(iv) Deficiency of apoproteins involved in remnant uptake73
Minerals
1. What are the two minerals that are essential to form oxygen carrying proteins,
name the main O2 carrying protein?74
2. What levels of Iron, Copper and Zinc would you find in a typical 70kg adult?75
3. What is the significance of minerals in the body to the toxic ions superoxide and
peroxide as well as Xanthine oxidase?76
4. Name two enzymes which contain a haem group?77
5. How much more Iron do women need than men?78
6. Where are the two largest reserves of Iron in the body?79
7. What dangerous effect can Fe2+ have in the presence of the enzyme superoxide
dismutase?80
72 B-100 receptors
73 (i) Defective LDL receptors = high LDLs as not taken up by liver (ii)Lipoprotein lipase deficiency = high
chylomicrons and VLDLs as needed to break these down (iii) Deficiency of C-II = high chylomicrons and
VLDL (iv) Deficiency of apoproteins involved in remnant uptake = high chylomicron and VLDL remnant
(because many remnants present in blood)
74 Fe2+ and Cu2+, Cytochrome Oxidase
75 2-3g of Iron and Zinc, 140mg of Copper
76 These ions are products of O2 reduction and combine with metallic enzymes to become compounds
without the toxic effects. Xanthine Oxidase is an O2 radical inactivated by Iron.
77 catalase and peroxidase
78 2/3 times more than men
79 Haemoglobin (67%), and storage mainly in the liver (27%)
80 Produces hydroxyl radicals

9. 8. What pathology leading to death by infection could be caused by Zinc deficiency?
81
9. List the main functions of Iron other than oxygen carriage?82
10.How saturated is ferritin (soluble form of storage iron) in the body under normal
conditions?83
11.How many Fe3+ ions can a single ferritin bind?84
12.What could high levels of ferritin in the plasma or mucosa indicate?85
13.What is haemosiderin?86
14.Transferrin is the most important Iron store in the body (although not the
largest) because of its very high rate of turnover, how many Fe3+ ions can a single
transferrin bind at any one time?87
15.What change in physical environment can affect the affinity of transferrin for Iron
molecules?88
16.How is Iron from transferrin taken up into cells and ultimately into ferritin in the
cells?89
17.What are the signs and symptoms of type 1 genetic haemochromatosis (where
the body absorbs an extra 3-4mg of iron a day from the diet?90
81 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 synthesis
83 2/3 saturated
84 Up to 4300 in the Fe3+ state (which they keep for transport and storage), converted to Fe2+ for functional
uses such as O2 transport
85 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 and
liver. 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 Iron
overload.
89 Receptor mediated endocytosis into cell after which receptor-transferrin complexes migrate into cell in
clathrin coated pits. Intra vesicular pH rises to 5.5 and clathrin coat is lost, Fe2+ released and transferrin
return to cell surface.
90 Liver failure, diabetes mellitus, cardiac failure and pigmentation of the skin (due to production of increased
melanin). Cell destruction can result in iron-catalysed lipid peroxidation reactions (membranes).

10. 18.How would you test for type 1 haemochromatosis?91
19.What is the treatment of type 1 haemochromatosis?92
20.What is the main non-genetic cause of haemochromatosis?93
21.In genetic haemochromatosis, mutations of which proteins give rise to types (i) 1
(ii) 2a (iii) 2b (iv) 3 (v) 4 ?94
22.What is chelation therapy and what is the most common chelator?95
23.What is the name of the new orally active chelator?96
24.What is the main function of copper in the body?97
25.Which disease is the inability to absorb copper from the intestine?98
26.What is Wilson’s disease and how is it treated?99
The Fed and Fasting State
1. What is the difference between covalent and allosteric modification of an enzyme?
100
91 If measured transferrin saturation is greater than 50% in men or 55% in women then measure serum
ferritin (level of stored iron). Normal levels are less than 300micrograms in men or 200 in women. Can do
genetic 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 of
cell)
95 Treatment of haemchromatosis with drugs able to bind iron. Deferoxamine is the most widely used
chelator but has to be given IV over an extended time period so is highly limiting to patients.
96 Deferiprone
97 Copper producing enzymes
98 Menkeʼs disease
99 Impaired biliary secretion of Cu (where most Cu is lost) so buildup of Cu in liver and liver damage, brain
damage 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. 2. What substances/hormones affect the release and activity of insulin?101
3. Where are insulin and glucagon produced?102
4. What does somatostatin do?103
5. Why are there only low affinity glucose transporters in the islet cells when high
affinity would be more efficient?104
6. What is the mechanism of response to glucose and amino acids within the islet
cell?105
7. How does the insulin secreted in vesicles have to be changed structurally before it
is active?106
8. And what is the clinical use of this?107
9. Describe the chemical pathway for fatty acid synthesis from excess glucose?108
10.How does insulin stimulate uptake of glucose by muscles and adipose tissue?109
11.How does this mechanism also inhibit hormone sensitive lipase and so inhibit the
breakdown of glycerol and fatty acids?110
101 Adrenaline inhibits, growth hormone stimulates, cortisol (stress hormone) inhibits to release more
glucose, presence of amino acids and glucose in blood increases, GI tract secretion of secretin hormone
stimulates. 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 pancreas
103 Produced by delta cells in the Islets of Langerhans, it inhibits both insulin and glucagon to stop levels
getting too high
104 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 opens
Ca+ 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 the
insulin 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 from
vesicles 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 PKA
which inactivates hormone sensitive lipase.

12. 12.Hormone sensitive lipase inside the cell is inactivated by insulin, but lipoprotein
lipase is activated when outside the cell, why is this?111
13.What are the two main intermediary factors involved in insulin affecting
transcription factor?112
14.Which liver processes are activated by glucagon?113
15.What is the precursor for formation of ketone bodies?114
16.Which enzyme activates glycolysis?115
17.Which transport molecules take fat to adipose tissue once converted from
excess glucose in the liver?116
18.How is glycogen synthase activated?117
19.What is the function of Acetyl-CoA carboxylase?118
20.Which areas of the body are said to be ‘insulin independent’ and can therefore
use glucose at high and low concentrations?119
21.Which product of metabolism can be converted into pyruvate?120
22.Why is it mainly protein that is metabolised in fasting and not fat?121
111 Allows fatty acid esterification, breaks down into small units so can cross the membrane to be stored.
112 Ras and MAPK
113 Glycogenolysis (breakdown of glycogen), gluconeogenesis (production of glucose from stored protein),
uptake of amino acids by the liver for gluconeogenesis
114 Fatty acid oxidation in the fasting state
115 Glucokinase, Phosphofructokinase and pyruvate kinase
116 VLDLs, responsible for transporting fat from liver to adipose tissue
117 Activated by dephosphorylation (using phosphatase enzyme), inactivated by phosphorylation (adding
phosphate) with kinase enzyme.
118 Irreversible production of malolyl-CoA from acetyl-CoA (from glycolysis) in fatty acid synthesis
119 Brain (fatty acids cannot cross blood brain barrier so relies on glucose) and erythrocyte (no mitochondria)
120 Lactate
121 Although fat can be broken down into ketone bodies, the pyruvate dehydrogenase (converting pyruvate
into acetyl CoA) enzyme is irreversible, so fat cannot be converted back into glucose whereas amino acids
can by glyconeogenesis.

13. 23.What are the key differences between diabetes type 1 and type 2?122
24.What mechanism to prevent excessive protein breakdown in fasting metabolism
is not present in diabetes?123
25.What are the complications of diabetes?124
Eating Disorders
1. What % of people with anorexia die from it?125
2. How is anorexia defined and what are the main symptoms?126
3. How does bulimia nervosa differ from this?127
4. What biological factor may increase the chance of having an eating disorder?128
5. What kind of childhood environmental factors may lead to development of an
eating disorder?129
6. What is the difference between Obsessive Compulsive Personality Disorder
(OCPD) and Obsessive Compulsive Disorder?130
122 Type 1 is childhood onset, can lead to hyperglycaemia and ketoacidosis, results from autoimmune
destruction of pancreatic B cells so said to be insulin dependent. Type 2 is adult onset, caused by insulin
resistance, associated with lifestyle factors such as obesity although is milder than type 1 and does not lead
to ketoacidosis.
123 Insulin release stimulated by high level of ketone bodies. Leads to uncontrolled production of KB in type
1.
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 of
menstrual period). Emaciation, bradycardia and hypotension, anaemia and leucopenia (decrease in white
cells) leading to poor immunity
127 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 sufferers
are aware that these are irrational and unwanted thoughts.

14. 7. What is ‘multi-impulsive bulimia’?131
8. Bulimia suffers tend to maintain a normal or above average weight, so what are
the physical symptoms?132
9. What BMI range is obese?133
10.What is Russell’s sign?134
131 Alcohol and drug misuse, sexual disinhibition and poor impulse control coexist with food binges and self
harm.
132 Amenorrhoea in 50% of cases, hypokalemia (related to vomiting), which may cause dysrhythmias or renal
damage. Oesophageal tearing and poor dental health.
133 30 and over
134 Callouses on the knuckles from making repeated contact with teeth from self induced vomiting in bulimia