Disorders of Appetite lecture Flashcards
LO:
- Water homeostasis: Summarise the behavioural and hormonal control of hydration
- Appetite regulation: Outline the hypothalmic circuits controlling body weight and relate these to the aetiology, complications and management of obesity and malnutrition
Session plan:
Eating disorder and obesity numbers are both growing throughout the world.
Disorders of Appetite
With disorders of appetite, we talk about problems with fluid or food intake, and this can be more or less than normal.
- Water intake – thirst
- Food intake – appetite
Intake can be less or more than normal
Pathology of Thirst Regulation
Can be too much-polydipsia, which can be further divided into primary and secondary and secondary is more common
Again adipsia can be provided into primary and secondary
Secondary Polydipsia
(Secondary-in medicine, usually means the result of another condition)
- More common
- Medical issues that disrupt any step in osmoregulation or alter ADH can cause secondary polydipsia
Regulation of Osmolality - ADH
- Antidiuretic hormone (ADH) or vasopressin
- Acts on the kidneys to regulate the volume & osmolality of urine
- Collecting duct - Aquaporin 2 channel
- When plasma ADH is low a large volume of urine is excreted (water diuresis)
- When plasma ADH is high a small volume of urine is excreted (anti diuresis).
Causes of Secondary Polydipsia
- Chronic medical conditions-diabetes probably the most common
- Medications-lead to dehydration, tend to induce urination and so patients pass lots of urine and so are thirsty and drink more. Laxative-fast course means water absorption is incomplete. Anticholinergic antidepressants make your thirsty without making you dehydrated.
- Dehydration
Diabetes Insipidus vs Mellitus & Polydipsia
Diabetes Insipidus-cranial DI-treat with desmopressin, this is synthetic/long acting form of ADH.
Diabetes Mellitus-high blood sugar levels are filtered in kidney and this draws more water forming high volume of urine. Higher urine output=dehydration and polydipsia
Treatment-control blood sugar to stop patients passing sugar in urine
What is the most likley underlying pathology of Mr Smith’s problems?
=Diabetes Mellitus is most likely diagnosis
Mr Smith-frequent urination-common sign of untreated urination, unexplained weight loss, non-healing wound (not with prostate cancer or hyperplasia), sexual problems etc.
Diabetes symptoms
Other medical conditions leading to polydipsia
- Acute kidney failure-kidney dysfunction, kidneys acutely stop working, usually after specific insult to the normal kidneys eg hypoperfusion for various reasons, which then leads to decreased blood supply, toxins eg if people drink antifreeze or taking too many NSAIDs, systemic infections, cancer, urinary obstructions, trauma to the kidneys or the vessels and heatstroke are all failures leading to AKF
- Conn’s syndrome-The hypokalemia (low potassium level) can cause symptoms like fatigue, numbness, increased urination, increased thirst, muscle cramps, and muscle weakness.
- Primary aldosteronism-over production of aldosterone
Treated by medication and lifestyle changes, primarily to control blood pressure, and in some cases people having to undergo surgery.
- Addison’s disease
- Hypoadrenocorticism-aka adrenalcorticoinsufficiency, can’t concentrate urine, despite normal kidney function, so lose lots of water in urine, so increased thirst.
Primary Polydipsia-causes:
Causes:
- Most common=Mental illness - psychogenic polydipsia (or acquired)
- Schizophrenia-approx 20% of patients with chronic schizophrenia, have polydipsia
- Mood disorders - depression and anxiety (even without medication)
- Anorexia
- Drug use
•Brain injuries-trauma to brain in areas involved in ADH secretion etc.
•Organic brain damage-eg Alzheimer’s disease or Central Pontine Myelinolysis
(Central pontine myelinolysis (CPM) is a neurological disorder that most frequently occurs after too rapid medical correction of sodium deficiency (hyponatremia). The rapid rise in sodium concentration is accompanied by the movement of small molecules and pulls water from brain cells.)
=due to diuretics
-She had heart problem, used to be able to walk, but now she gets shortness of breath. This is indication of fairly severe heart failure and she is treated with diurteics (furosemide)
This has lead to water accumulation from heart failure
Confusion is a red herring as she is just old so not Alzheimers
Why Polydipsia is a Problem?
- Kidney and bone damage-can upset the electrolyte balance, blood gets diluted and leads to hyponatremia and swelling of cells. In long term hyponatremia presents with kidney and bone damage but acutely they get:
- Headache
- Nausea
- Cramps
- Slow reflexes
- Slurred speech
- Low energy
- Confusion
- Seizures
Adipsia aka hypodipsia
(inappropriately decreased sense of thirst)
=Decreased or absent feeling of thirst
Rare disorder with little research. There are 4 types
A=most common, we would call this Essential hyponatremia, which involves increased osmotic threshold, increase in the level in which solvent molecules can pass through cell membranes (osmotic threshold) for vasopressin release and the activation of the feeling of thirst
B=occurs when ADH responses are decreased, even if there is an osmotic stimuli, probs due to the elimination of osmoreceptors
C=when the osmoreceptors are completely elimated
D=ADH release occurs with normally functioning levels of osmoregulation.
Osmoreceptors – ADH release
Eating Disorders
Mental disorder defined by abnormal eating habits, includes:
- Binge eating disorder-people eat large amount in very short amount of time
- Anorexia nervosa-eat very little due to fear of gaining weight
- Bulimia nervosa-people eat a lot but try to get rid of it eg vomiting or laxatives
- Pica-people who eat non food items, often hair or dirt or soil that have no nutritional value
- Rumination syndrome-people regurgitate food
- Avoidant/restrictive food intake disorder-selective food intake, not driven by fear of gaining weight but they fail to get nutrients they need to be healthy.
- Global eating disorder prevalence ↑ed from 3.4% to 7.8% between 2000 and 2018.
- 70 million people live with eating disorder
Pathophysiology of Anorexia
Signs
•Low BMI, continuous weight loss, amenorrhea, halitosis-bad breath, mood swings, dry hair, skin & hair thinning (due to lack of nutrients)
Causes
•Genetic, environmental, psychological, sociological
Mechanism
•Serotonin
Shown by studies eg. increase cerebrospinal fluid conc of serotonin in anorexia and metabolites of serotonin observed in blood and urine observed with changes in behaviour
=child neglect-scurvy (parents didn’t let her go to dentist)
Wouldn’t come to GP if anorexic or bullimic, also she said she wanted to eat more. Malabsorption would usually present with diarrhoea and this isnt mentioned here so most likley scurvy.
1) Predicted that by 2030-51% of population will be obese
2) Already 72 million in 2009
Obesity is Associated with Comorbidities
Why is Obesity Increasing?
Since 1980 prevelance of obesity has doubled
It is not lack of exercise
•Physical activity started to decline prior to obesity epidemic
= due to cheap, calorie-rich/nutrient poor beverages, sweets and fast food
Screening of Obesity
- Height, weight and abdominal girth
- Medical history:
- Dietary and physical activity patterns, psychosocial factors, weight-gaining medications, familial traits
Assess multiple risks for obesity
- BMI = kg/m2 (BMI alone is not enough to describe obesity, need abdominal girth as well)
- BMI of ≥30 or ≥25 + comorbidity or risk factor
On right can see 2 types of obesity, central or abdominal obesity is strongly linked to cardiovascular disease and alzheimers and diabetes.
Treatment of Obesity
- Life-style modification
- Diet?-more effective than exercise
- Exercise?
- Diet + Exercise?
Best=both together are most effective in acheiving weight loss
Surgical Treatment of Obesity
- People with a > BMI 40 or 35 + comorbidities
- Various procedures
- Most common Roux-en-Y gastric bypass & sleeve gastrectomy
- WL 5 yrs after BS: 30% - 35%
- Remission of comorbidities
- Diabetes (80%)
- OSA (80%-85%)-Sleep apnoea
Usually minimally invasive so key hole surgery, could be malabsorptive so stop food being absorbed, or restrictive which stops food being put in. Can get mixed too.
Physiological Background of Bariatric Surgery
GLP1 and GLP2 (Glucagon like peptide):
- Stimulate insulin release
- Inhibit glucagon release
Ghrelin:
- Hunger hormone
- NPY activation – initiate appetite
PYY:
- Satiety
- anorexogenic
Hormonal Changes after Bariatric Surgery
- Gastric bypass-some people have a reactive hypoglycaemia post prandially due to elevated GLP 1 and 2 levels (10 to 20 x normal), and they also found elevated PYY. Increase GLP 1 and 2 leads to improved beta cell function, hypoglycaemia (ie lower blood sugar), improved insulin sensitivity and weight loss.
Session review
Environment has an important role in eating disorders.
