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.
4 types of adipsia:
Type A
Type A (essential hypernatremia syndrome) involves an increase of the level in which solvent molecules can pass through cell membranes (osmotic threshold) for vasopressin release and the activation of the feeling of thirst. This is the most characterized sub-type of adipsia, however there is no known cause for Type A adipsia. There is debate over whether osmoreceptor resetting could lead to the increase in threshold. Other studies have shown that it is the loss of osmoreceptors, not resetting, that cause the change in threshold. Patients with Type A adipsia can be at risk of seizures if they rapidly re-hydrate or quickly add a significant amount of sodium into their bodies. If not treated, Type A adipsia could result in both a decrease in the size of the brain and bleeding in the brain.
Type B
Type B adipsia occurs when vasopressin responses are at decreased levels in the presence of osmotic stimuli. Although minimal, there is still some secretion of AVP. This type may be due to some elimination of osmoreceptors.
Type C
Dopamine pathways in the brain. The production of dopamine is concentrated in the Ventral Tegmental Area and the Substantia Nigra.
Type C adipsia (type C osmoreceptor dysfunction) involves complete elimination of osmoreceptors, and as a result have no vasopressin release when there normally would be. Type C is generally the adipsia type found in patients with adipsic diabetes insipidus.
Type D
Type D is the least commonly diagnosed and researched type of adipsia. The AVP release in this subtype occurs with normally functioning levels of osmoregulation.
Osmoreceptors – ADH release
Eating Disorders
- This term was traditionally used for low food intake
- However the definition has changed
EDs are a range of psychologic disorders that lead to abnormal relationship with food.
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.
Obesity
Not just in high income countries, worldwide obesity has nearly tripled since 1995
1) Predicted that by 2030-51% of population will be obese
2) Already 72 million in 2009
Obesity is Associated with Comorbidities
