Case 15- Puberty and SAP Flashcards
What is included in Tanner staging
Classification system that tracks the order of development of the secondary sexual characteristics in puberty:
- Male external genitalia (penis, scrotum, testicular volume)
- Female breast development
- Male and female pubic hair
Tanner staging- male external genitalia
1) Stage 1- testes less than 2.5cm
2) Stage 2- scrotum and testes enlarge and reddening of scrotal skin
3) Stage 3-continued growth of penis and testes
4) Stage 4- development of the glans, continued growth and scrotal skin darkens
5) Stage 5- adult genitalia size morphology
Testicular growth- enlargement of seminiferous tubules, epididymis and seminal vesicles and prostate increase in size
Tanner staging- female breast development
Stage 1- prepubertal, elevation of papilla only
Stage 2- areola enlarges and breast bud appears
Stage 3- breast tissue grows beyond areola but without contour separation
Stage 4- Projection of areola and papilla forms a second mound
Stage 5- adult breast contour with projection of papillar only
Tanner staging- Pubic hair development (men)
Stage 1- Villus hair only
Stage 2- Sparse hair along base of penis
Stage 3- Thicker hair, spreads to mons pubis
Stage 4- adult pattern but without spread to medial thigh
Stage 5- adult spread to medial thigh but not linea alba
Tanner staging- pubic hair (female)
Stage 1- Villus hair only
Stage 2- Sparse hair along labia
Stage 3- Hair coarse and pigmented, spreads across pubes
Stage 4- adult pattern but without spread to medial thigh
Stage 5- adult spread to medial thigh but not linea alba
Physical growth in adolescents
Growth spurt begins- 10.5 years in girls and 12.5 years in boys
Reach full adult height- 17 years in girls and 21 years in boys
Cause of growth spurt
Testosterone is converted to oestradiol causing increased release of GH from the anterior pituitary gland. GH increases anabolic hormone IGF-1 which causes somatic growth via metabolic actions i.e. an increase in trabecular bone growth. In males the larynx and vocal cords enlarge and the voice deepens in pitch.
Female timeline puberty
10.5 years- breast bud forms 11 years- pubic and axillary hair develops 11.5 years- growth spurt 13 years- menarche 13.5 years- adult pubic hair 14.5 years- adult breast
Boys puberty timeline
11.5 years- testicular enlargement
12 years- pubic and axillary hair develops
12.5 years- growth spurt
13.5 years- spermarche, nocturnal emissions begin
15 years- adult penis and testicular size
Early 20’s- adult pubic hair
GnRH and puberty
The Hypothalamus releases GnRH in a pulsatile manner, stimulating the release of FSH and LH from the anterior pituitary. FSH and LH act on the gonads to cause sex steroid hormone production and support gametogenesis. The sex steroids provide negative feedback on the hypothalamus and pituitary to keep circulating levels stable.
FSH and LH- puberty
A year before the start of puberty there is an increase in FSH and LH release. The rise in FSH stimulates an increase in oestrogen synthesis and oogenesis in females and sperm production in males. The rise in LH stimulates an increase in the production of progesterone in females and an increase in testosterone production in males.
The two hypothesis for the start of puberty
The rise in GnRH causes the onset of puberty. The two hypothesis for this are:
1) The brake release hypothesis
2) The accelerator hypothesis
Puberty- the break release hypothesis
Timed disinhibition of the inhibitory mechanisms. At the start of puberty the negative threshold of the hypothalamus to oestrogen and progesterone increases. Higher levels of oestrogen and progesterone are now needed to inhibit GnRH secretion. As the hypothalamus threshold increases (the brakes are released), the original low levels of oestrogen and progesterone cannot inhibit GnRH secretion - so FSH and LH levels rise = so higher levels of oestrogen and progesterone are secreted. Same in males but with testosterone.
Puberty- the accelerator hypothesis
Most widely accepted. The increase in permissive signals which kick start puberty. Leading up to puberty there in maturation of the CNS and activation of the Hypothalamic stimulatory centres. Upon CNS maturation, there is an induction of the pulsatile GnRH generator which leads to the increased secretion of LH and FSH. There is neuronal maturation and activation of the GnRH pulse generator. Same in males but with testosterone
Factors that affect age of menarche
- Genetics- link with maternal menarche age, genes (Kiss1)
- Metabolism and nutrition
- General health and wellbeing
- Family history of early or delayed puberty or genetic disease
- Previous growth and development
- Medical history
What weight does menarche start at
Menarche starts earlier with an increased BMI. Critical weight of 47kg must be achieved before activation of the hypothalamo-pituitary gonadal axis. A critical body weight and fat are required for the initiation of menarche.
The nutritional effects of menarche
- Leptin- adipocyte derived hormone which has permissive effect on menarche
- Insulin- modulates GnRH either directly/indirectly
Criteria for delayed puberty
- In boys- the absence of testicular development, or testicular volume less than 4ml by 14
- In girls- the absence of breast development by 13, or primary amenorrhoea with normal breast development by 15.
How common are eating disorders
Binge eating disorder is the most prevailent eating disorder and is more common in women then men. Women are more likely to have an eating disorder then men. Bullimia is more common then anorexia nervosa.
Weight and eating disorders
People with anorexia are by definition under weight, those with bulimia tend to be of normal weight and those with binge eating disorder are overweight.
The diagnostic criteria for anorexia nervosa
- Lower energy intake than needed causing significantly low body weight
- Intense fear of weight gain and/or acts to prevent weight gain
- Has body weight/shape disturbance and/or uses it to evaluate self-worth and/or doesn’t recognise seriousness (has to have one).
No longer has a BMI cut off, up to clinician. However, the lower the BMI the more likely complications are especially if they got there quickly.
Anorexia- severity (BMI)
- Mild >= 17
- Moderate 16-16.9
- Severe 15-15.9
- Extreme < 15
The visual presentation of anorexia nervosa
- Muscle wasting- loss of fat
- Skin pallor, dryness
- Lanugo hair on face/body- fine hair
- Poor circulation- blood pooling
- Thinning hair, brittle nails
- Abdominal bloating
- Oedema in extremities
The systemic presentation of anorexia nervosa
- Hypothermia
- Bradycardia, arrhythmia & heart failure- due to electrolyte disturbances
- Renal failure (acute/chronic +/- electrolyte disturbance)
- Osteopenia/ osteoporosis- weak bones
- Hypotension
- Reduced/altered sensation and/or muscle power
- Endocrine imbalance (thyroid, sex hormones)- periods stop
- Mood disturbance (++ low, ++ irritable)
- Memory/concentration problems
The psychological/behavioural presentation of anorexia nervosa
- Amotivation, anhedonia, apathy, asociality
- Irritability, mood swings, restlessness
- Depression, anxiety
- Obsessionality, rigidity, compulsions- might read cookbooks
- Food obsessions / rituals, hoarding
What maintains anorexia symptoms
A lot of the symptoms are due to starvation which maintains the disorder. Weight loss for any reason can trigger an eating disprder. Effects can be reversed once intake is normalised
The diagnostic criteria for bulimia nervosa
- Repeated binge eating episodes (at least once a week for 3 months):
Eats more food than most people would eat, in similar circumstances, in a discrete period of time (objectively large) AND Feels a lack of control over eating. - Repeated efforts to compensate for the binge to prevent weight gain: e.g. self-induced vomiting; laxative misuse; fasting; or excessive exercise.
- Uses body weight/shape to evaluate self-worth
Severity of bulimia
Frequency of compensatory behaviour per week:
- Mild = 1-3
- Moderate = 4-7
- Severe = 8-13
- Extreme = >= 14
The visual presentation of bulimia nervosa
- Lymph node & salivary/parotid gland enlargement
- Russell’s sign (incisor marks on knuckles)
- Dental enamel erosion (lingual- under side of the teeth)
- Bowel disturbance/ constipation- when laxatives are used
- Sore throat & halitosis
- Gastric reflux & involuntary regurgitation
- Gastric/oesophageal rupture
The systemic presentation of bulimia nervosa
- Dehydration
- Muscle weakness/ fatigue
- Hypotension- fluid imbalance
- Bradycardia, arrhythmia & heart failure
- Renal failure (acute/chronic +/- electrolyte disturbance)
- Endocrine imbalance (thyroid, sex hormones)
- Mood disturbance (++ low, ++ irritable)
- Memory/concentration problems- less profound then in anorexia
- Substance misuse disorders and/or self-harm
Distinguishing anorexia from bulimia
In Anorexia there is always a ‘significantly low body weight.’ Bulimia always requires the precense of frequent,objective binge-eating and compensation. Some patients with anorexia binge and compensate but this is much less frequent. Often the ‘binge-eating,’ is subjective and not objective.
Give the diagnostic criteria for binge eating disorder
- Repeated binge eating episodes (at least once a week for 3 months):
- Eats more food than most people would eat, in similar circumstances, in a discrete period of time AND
- Feels a lack of control over eating. - When binge eating, patients (at least 3 must apply)…
- Eat faster than normal
- Eat until uncomfortably full
- Eat lots without feeling physically hungry
- Eat alone because of embarrassment
- Feel disgusted with themselves, depressed, or very guilty afterwards - Feels very distressed about binge eating.
- Repeated compensatory behaviours (e.g. purging or fasting) aren’t used
Severity of binge eating
Binge frequency per week
- Mild = 1-3
- Moderate = 4-7
- Severe = 8-13
- Extreme = >= 14
The presentation of binge eating disorder
- Gastric rupture
- Clinical obesity, associated with …
- Hypertension
- Hypercholesteremia
- Cardiovascular disease
- Type II diabetes mellitus
- Increased risk of some cancers
- Non-alcoholic fatty liver disease - Mood disturbance (++ low)
- Substance misuse disorders and/or self-harm
OFSED (other specified feeding or eating disorders)
Avoidant restrictive food intake disorders. Includes PICA, rumination disorder and body dysmorphic disorder
OFSED atypical anorexia nervosa
All criteria met for anorexia nervosa except significantly low body weight
OFSED bulimia / binge eating disorder of low frequency or limited duration
All criteria met for bulimia / binge eating disorder except symptom frequency / duration
Purging disorder
Induced vomiting/ laxative abuse to influence weight and shape but no binge eating
Night eating syndrome
Recurrent eating of large amounts at night, after evening and often waking from sleep
Avoidant restrictive food intake disorder
NOT about body image, feeding/eating disturbance, shown by:
- Substantial weight loss/absence of expected weight gain
- Nutritional deficiency
- Dependence on feeding tube/dietary supplements
- Significant psychosocial interference
Body dysmorphic disorder
- Preoccupied with one/more non-existent or slight defects or flaws in physical appearance
- Repetitive/compulsive behaviours in response to the appearance concerns
- Causes distress/impairment in social, occupational, or other functioning
- Not better accounted for by an eating disorder
The muscle dysmorphia subtype of body dysmorphic disorder
Preoccupation with concerns that his/her body build is too small and insufficiently muscular
Risk factors for anorexia nervosa
- Biological- family history, female, type 1 diabetes
- Psychological- Perfectionist, behaviour inflexibility, previous anxiety disorder
- Social- peer-pressure, social media, career
Pica
An eating disorder that involves eating items that are not typically thought of as food and they do not contain significant nutritional value, such as hair, dirt and paint chips:
• Persistent over 1 month
• Is developmentally inappropriate (i.e. normal in <2year olds) and not part of cultural practice
• Risk factors: Autism + developmental disorder
Ruminition disorder
Repeated regurgitation of food for a period of at least one month. Not due to another medical disorder or eating disorder
Similaries between anorexia nervosa and bulimia nervosa- psychological
- Overvaluation of weight and shape
- Dietary restraint and restriction
- Low self-esteem, perfectionism, mood intolerance and interpersonal difficulties
- Eating and dieting is the primary source of their self worth. Why they are so keen to defend their lifestyle
Similarities between anorexia nervosa and bulimia nervosa- physical
- Hypotension, Bradycardia
- Dehydration, electrolyte disturbance
- Hormone disturbance
Restraint and restriction
Restraint- how much you are eating
Restriction- not eating certain food groups
Eating disorders and psychological comorbidities
- Major depressive disorder
- Anxiety disorder
- Personality disorders
- Substance use disorders
- Deliberate self harm
Risk factors for eating disorders
- Family- history of eating disorders/ depression/ alcohol dependence/ obesity
- Individual- female, low self esteem, premature birth, perfectionism, previous obesity, diabetes, crohns
- Possible triggers- puberty, socio-cultural pressures, family factors, comments about weight, pressure to achieve
Junior MARSIPAN
Used to assess seriousness of eating disorders in under 18’s
Treatment for anorexia
- Psych treatment only starts when a minimally safe weight is attained
- Outpatient treatment is preferable unless the patient is unstable
- Family based treatment I,e, Maudsley method is recommended for individuals living at home
- Treatment for acutely unwell patients is in hospital- refeeding with diatetic advice
- Total or partial nasogastric feeding is used when oral is unacceptable
- One medically stabilised treatment moves to a specialist ED unit for therapies (group, individual) and away from an acute setting
- Goal is to return patient to outpatient care (long process)
Why family matters in health
1) Big effect in promoting healthy living and the opposite
2) Families overacting and making the illness central to everyones life can result in worse outcomes and reduce the quality of life of the family members
3) Parents whith children with chronic disease report reduced well being and emotional swings
4) Difficult relationships and conflict can cause neuroendocrine responses i.e. hyperglycaemia
Bad effects of illness and disability to the family
1) Adjusting to psychological and emotional impacts can lead to feelings of powerlessness and mental ill health.
2) Loss of sleep directly and indirectly
3) Financial impacts due to loss income from sick person or in having to spend time caring
4) More time in hospital at appointments. Less time for leisure, socialising and well being
5) Impact on education which can affect siblings – less parental input
Carer
A carer is someone who provides unpaid care to a family member or friend who would not cope without support due to disability, illness, mental health condition of frailty.
1 in 8 adults act as unpaid carers to family or friends
Positive effects of illness and disability on the family
1) Warmer closer relationships, and the whole family coming together
2) Increases empathy and kindness in siblings and extended family
3) Increased maturity of young family members
4) Increased assertiveness, they become experts on the illness and its management
Impact of illness on relationships
1) Can be resentment in either or both directions
2) Less time or opportunity for intimacy- less sex can add strain or lead to affairs
3) Disease can alter patients beliefs, outlook and behaviour causing tension
Role of family in illness
1) Can fascilitate descisions
2) Accompany to appointments
3) Emotional support
4) Help finding resources
5) Integration into social activities
