N- Eating disorders, diabetes, cancer Flashcards

1
Q

Methods to measure body shape…

A

 BMI
 Skin fold thickness
 Waist to hip ratio
 Dual energy x-ray absorptiometry (DXA)

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2
Q

The eating disorders (3)

A
  • Anorexia nervosa (av duration 8yr but…)
  • Bulimia nervosa – in the 1970s (av duration 5 yr but..)
  • Binge eating disorder (BED)
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3
Q

Scoff Test

A
  • Sick make yourself because feel full
  • Control worry over loss of in relation to food
  • One stone lost in 3m
  • Fat see yourself as fat when others don’t
  • Food dominates life
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4
Q

Why might someone develop an eating disorder?

A
  • Peer/ family pressure
  • Media eg very thin models in fashion magazines
  • Stress
  • Genetic component- esp in Anorexia
  • Sports, hobbies such as gymnastics and ballet
  • Social media
  • Role of Serotonin
  • Leptin & ghrelin function
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5
Q

Prevalence of anorexia in UK

A
  • 1: 150 15 year old girls

* 1:1000 15 year old boys

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6
Q

What is Anorexia Nervosa?

A
  • Fear of gaining weight so eat little
  • 15% below wt. for ht./age
  • BMI < 17.5
  • Body Image dysfunction
  • Denial of low weight
  • If reproductive years –amenorrhoeic for @ least 3m
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7
Q

Medical consequences of AN?

A
  • Starvation and dehydration; circulatory problems, kidney/heart fail
  • Long term - stunting of growth, osteoporosis possibly fertility problems
  • 5% DIE or commit suicide
  • Dehydrated- kidney failure
  • Cardiac (all the muscles are wasting)- heart failure… death
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8
Q

General treatment for AN/BN

A
  • Cognitive therapy in improving mental health (but W/L)
  • Individual / group/ psychotherapy
  • Life skills; nutritional advice
  • Drugs (BN – SSRIs eg fluoxetine)
  • In – patient care may be necessary
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9
Q

Specific tx for AN

A
  • Early intervention best
  • Aim to attain viable weight
  • Alter feelings about body image/food
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10
Q

Prognosis AN

A
  • 50% recover after treatment
  • 30% retain partial symptoms

Approximately:

  • 20% become chronic
  • 5% die –
  • starvation, heart failure or suicide
  • AN has one of highest rates of suicide of all psychiatric illnesses
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11
Q

Dental considerations for AN?

A
  • Halitosis: pear drops (ketosis)
  • Dry mouth- TCAs
  • Drug doses
  • Reduced immune response: periodontal disease, angular chelitis (malnutrition)
  • Medical emergencies: vasovagal syncope (faint), cardiac arrest
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12
Q

What is Orthorexia Nervosa?

A
  • Obsession with eating pure or clean foods
  • Feelings of extreme guilt if something unhealth is eaten
  • Judging others
  • Management: therapies to tackle underlying mental health disorder (CBT, counselling)
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13
Q

Clinical features of Orthorexia nervosa?

A
  • Fatigue
  • Poor immune response
  • Malnutrition; angular cheilitis, recurrent aphthous ulceration
  • Deficiencies e.g. B12
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14
Q

What is Bulimia Nervosa (BN)?

A
  • May be of any weight
  • Eating pattern
  • Binge eating (recurrent) of high calorie food, followed by secret purging.
  • Food hidden in secret places
  • Use of laxatives & diuretics to control weight fluctuations
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15
Q

Prevalence of BN

A
  • Female : Male = 20:1
  • Mainly young people
  • Up to 20% females binge @ some time
  • Anorexia- 0.25% population
  • Bulimia – approx 1%
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16
Q

Medical consequence of BN

A
  • GI -cramps, constipation , diarrhoea
  • Electrolyte imbalance
  • Damage oesophageal sphincter, muscles
  • Lower bowel damage
  • Throat ulcers
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17
Q

Oral presentation of BN, may have:

A
  • Dental erosion (gastric acid PH 2.9)
  • Dry mouth ( ↓ salivary flow)
  • Inflamed palate
  • Dry, chapped lips
  • Parotid enlargement
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18
Q

Dental features: erosion from bulimia

A
  • Vomit pH is roughly 3.8
  • Palatal surfaces of incisors
  • Perimylolysis (molars)
  • Caries

• Treat teeth as needed when BN under control

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19
Q

Dental erosion- diagnostic criteria for BN

A
  • Palatally on upper incisors (often extensive)
  • Palatal aspects upper posterior teeth “cupping”
  • Occlusal & buccal surfaces U & L posterior teeth (variable)
  • “Squeaky clean “ teeth but could have gingivitis
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20
Q

Management of OW/OB- Long term plans & goals to be approached incrementally

A
•	Control of diet 
•	Behaviour management
•	Regular Exercise                 
•	Drug treatment                    
•	Surgery
ON-GOING MONITORING &amp; REINFORCEMENT
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21
Q

Effect of increasing levels OW/OB on dental care

A
  • More diabetic patients, (periodontal problems, care with appointment times)
  • Cardio – vascular disease (anti coagulants, high BP
  • Arthritis (mobility problems)
  • More chronic periodontal disease to treat 1
  • Increased caries? Decreased stimulated salivary flow rate 2
  • Bariatric equipment may be needed
  • Increased GA & sedation risk
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22
Q

Uses of blood glucose

A
  • Muscle storage for later use (glycogen)
  • Energy source for muscle and other tissues
  • Storage as fat (triglycerides)
  • Excretion in urine with high blood sugar, 160mg/dL
  • Energy for CNS and brain (60-70%)
  • Liver storage for later use (glycogen)
23
Q

What is Diabetes Mellitus?

A
  • Metabolic disorder of carbohydrate metabolism
  • Characteristic: Hyperglycaemia ( blood glucose)
  • High morbidity & mortality
24
Q

Blood Glucose levels fasting:

Normal and diabetic?

A

Normal Fasting conditions: 3 to 5 mmol/l

Diabetic Fasting conditions: 4-7 mmol/l

25
Q

Blood Glucose levels after a meal?=

Normal and diabetic?

A

Normal: less than 10 mmol/l 90 min post food

Diabetes: >20 mmol/l

26
Q

Symptoms of diabetes?

A
  • Blurry vision
  • Increased thirst and need to urinate
  • Feeling tired/ill
  • Recurring skin, gum, bladder infections
  • Dry itchy skins
  • Unexpected weight loss
  • Slow healing cuts and bruises
  • Loss of feeling in feet
27
Q

Types of diabetes…

A

1- Type 1 (insulin dependent)
2- Type 2
3- Gestational diabetes
4- Impaired glucose tolerance (IGT) and impaired fasting glycaemia (IFG)

28
Q

What is Type I diabetes?

A
  • Chronic (generally) childhood disease
  • Affects 18-20 per 100 000 children in UK
  • Genetic susceptibility shown
  • Linked to viral infection (e.g. congenital rubella syndrome)
  • Lack of insulin production
  • Thought to be autoimmune mediated disorder
  • Affects islets of Langerhans
  • Beta cells are killed by antibodies
  • Therefore, lack of insulin production
  • Most cases <40
29
Q

Type 2 Diabetes

Non-insulin dependent or adult-onset diabetes

A

Can be caused by hyperglycaemia

  • Obesity
  • Multiple genetic susceptibilities…
  • Primary beta-cell defect
  • Damaged/inadequate insulin secretion
30
Q

Main symptoms of type 2 diabetes

A
  1. Polyuria (frequent urination due to osmotic diuresis)
  2. Polydisia (Increased thirst & increased fluid intake due to polyuria)
  3. Polyphagia (Increased appetite)

Other symptoms:
Dry mouth, itchiniess, increased incidence of thrush, cramps, skin infections

31
Q

What is Gestational Diabetes?

A
  • 2-5 % of all pregnancies
  • Onset in late 2nd trimester (20-28 weeks)
  • Predisposing factors

age (>35 although can occur in younger mums)
ethnic group
Obesity

32
Q

Symptoms of Gestational diabetes?

A

 excessive thirst
 frequent urination
 increased appetite
No obvious external symptoms

33
Q

Causes of gestational diabetes?

A

Hormonal changes  cells less responsive to insulin
Increase resistance to insulin
… Increased blood glucose

34
Q

Long term effect of gestational diabetes

A
  • Larger babies

* Mum at risk of Type 2 diabetes

35
Q

How are diabetes & pre-diabetes diagnosed?

A
  • Glucose testing

- Fructosamine test

36
Q

Describe the 3 glucose tests for diabetes

A

• Fasting plasma glucose (FPG)
– Measures blood glucose when the person has not eaten for at least 8h (detect diabetes & pre-diabetes)

• Oral glucose tolerance test (OGTT)
– Measures glucose after an individual has fasted for at least 8h and 2h after consuming a glucose containing drink (detect diabetes & pre-diabetes)

• Random plasma glucose test
– Casual plasma glucose test; i.e. measures glucose irrespective of whether the person has eaten or not (diagnoses diabetic only)

37
Q

How to monitor/ maintain control of diabetes test…

Using red cells and glycated haemoglobin A1c

A

Red cells have a span of 8-12 weeks!

Hb1Ac in red cells gives an indication of the average glucose levels for 8-12 weeks.

Normal= 3.5-5.5%
Diabetes= 6.5%
38
Q

What is the Fructosamine test?

A

• Fructosamine is formed from serum proteins such as albumin
– (reaction between fructose & amine)

• Used in cases of:
– blood loss
– haemolytic anaemia
– sickle cell anaemia

  • Gives an average results for the last 2-3 weeks
  • Tends to be basis of over-the-counter tests
39
Q

What else could cause hyperglycaemia?

A

 Steroids
 Antipsychotics
 Diuretics
 Antihypertensive

40
Q

What else could cause Hypoglycaemia

A

 Alcohol
 Hormone deficiencies
 Prolonged starvation

41
Q

Management of diabetes- aim: to lower blood glucose levels

A

• Type 1
– Insulin (Essential)
– Exercise
– Diet (low in fat, cholesterol & simple sugar)

•	Type 2
–	Weight reduction
–	Diet
–	Exercise
–	If above not successful then,
•	Oral hypoglycaemic medications &amp; then insulin
42
Q

Managing diabetes…

A

• Sugar
– Avoid adding sugar to food
– Avoid foods sweetened with sugar or honey
• Cholesterol & fat
– Increase carbohydrates before sustained exercise
– Limit intake of saturated and hydrogenated fats and cholesterol
• Monitor blood glucose regularly
• Regular meal times
• Important to follow-up care

43
Q

Treatments- Oral hypoglycaemic agents

A

Biguanides (Metformin)- Type 2 diabetes & Type 1 with insulin therapy

Sulphonylureas

44
Q

What do Biguanides do?

A
  • Inhibits glucose production by the liver (gluconeogenesis)
  • Useful in patients who are obese

Unwanted effects:
• GI disturbance
• Lactic acidosis (contraindicated for those with renal, severe pulmonary or cardiac conditions)

45
Q

What do Sulphonylureas do?

A

Increase amount of insulin made in pancreas (requires functional islets of Langerhans)
Long lasting effect
• Problem: hypoglycaemia in elderly patients or those with kidney problems

Unwanted effects:
•	Appetite stimulants (weight gain)
•	Hypoglycaemia 
•	GI upsets (3% of patients)
•	Potentially teratogenic (do not use in pregnancy or planning one)
46
Q

• Some drugs AUGMENT hypoglycaemic effects of sulfonylureas e.g.

A
  • NSAIDs
  • Alcohol
  • Antibacterial (Sulphonamides, trimethoprim, chloramphenicol)
  • Antifungal (Miconazole, fluconazole)
47
Q

• Some drugs DECREASE the actions of sulfonylureas e.g

A
  • Diuretics

* Corticosteroids

48
Q

Dental diseases due to diabetes.. gum disease is very common

A

 Red & swollen gums
 Increased bleeding while brushing
 Increased plaque

Results in periodontitis & gingivitis
Gum disease followed by tooth decay
Inflamed & sore tissues, ulcers

49
Q

Dental hygiene, diabetes & heart problems:

A

Bacteria can enter blood stream - endocarditis

Cholesterol build up in blood stream – atherosclerosis

50
Q

How to dental care with diabetics

A
  • Diet control
  • Morning app
  • Medication taken?
  • Tx breaks…
  • Regular visits
  • Antibiotic requirements
51
Q

Collecting the evidence linking diet and cancer: Human studies

A
  • Ecological studies
  • Case-control studies
  • Prospective cohort studies
  • Randomised controlled trials
52
Q

Investigating mechanisms

A
  • In vitro
  • Exfoliated cells
  • Cells in culture
  • Animal models
  • Human studies
53
Q

Mechanisms for the role of diet in carcinogenesis

A

Diet may influence the chance of developing cancer by:
– Increasing exposure to chemical carcinogens (Chinese style salted fish)
– Facilitating the action of viruses (HPV)
– Influencing effects of hormones (adiposity and oestrogen, fibre and steroids)
– Minimising oxidant and other damage to DNA
– Influencing DNA repair genes