Feeding & Eating Disorders in Infants: Types & Management

Types of Disorders 

• Anorexia Nervosa
  • Underweight
  • But feels overweight
• Bulimia Nervosa
  • Has compensatory behavior
• Binge eating disorder
• ARFID
  • No distorted body image.
• Pica
• Rumination
• In psychiatric disorders, eating disorder has the highest mortality. Especially in anorexia nervosa.

Categories of Feeding and Eating Disorders in DSM-5

Anorexia nervosa

Characterized by an intense fear of gaining weight or becoming fat and a distorted body image

that leads to extreme dieting.

Binge eating disorder

Characterized by recurring episodes of eating large amounts of food in a short time and a sense of lack of control over-eating during the episodes.

Bulimia nervosa

Marked by frequent binge-eating episodes followed by inappropriate behaviors to avoid

weight gain (e.g. self-induced vomiting; misuse of laxatives, diuretics and other medications; fasting; excessive exercise)

Avoidant/restrictive food intake disorder (ARFID)

Persistent failure to meet appropriate nutritional and/ or energy needs associated with significant weight loss or failure to gain weight, substantial nutritional deficiency,

dependence on enteral feeding and marked interference with psychosocial functioning.

Feeding and eating disorders not otherwise specified

Includes atypical anorexia nervosa (not yet underweight), purging disorder (no binges), subthreshold bulimia nervosa, subthreshold binge eating disorder, and night eating syndrome.

Also read: Achalasia Cardia: Diagnosis, Types, Treatment & Management

Diagnostic Criteria for Anorexia Nervosa

Diagnostic and Statistical Manual of Mental Disorders, Fifth edition (DSM-5) Criteria for Anorexia Nervosa

• Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health.
• Significantly low body weight is a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected.
• Intense fear of gaining weight or becoming fat or persistent behavior that interferes with weight gain, even though at a significantly low weight.
• Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of current low body weight

• Restricting type: No recurrent episodes of binge eating or purging behavior within the last three months; weight loss is accomplished through dieting, fasting, and/or excessive exercise.
• Binge eating/purging type: Recurrent episodes of binge eating or purging behavior within the last three months (ex. self-induced vomiting or the misuse of laxatives, diuretics, or enemas).
• In partial remission: After full criteria for anorexia nervosa were met, criterion A has not been met for some time but criterion B or C is still met.
• In full remission: After full criteria for anorexia nervosa were met, none of the criteria have been met for a sustained period of time.

Severity Classification of Anorexia Nervosa.

Bulimia Nervosa

• DSM 5 Criteria
• Eating large amounts of food in a discrete time frame
• Sense of lack of control over eating during episodes
• Recurrent inappropriate compensatory behaviors to prevent weight gain
• Self-evaluation is unduly influenced by body shape

Also read: Alcoholic Liver Disease: Symptoms, Diagnosis, Treatment & Risks

Binge Eating Disorders

• DSM 5 criteria
• Eating large amounts of food in a discrete time frame
• Sense of lack of control over eating during episodes
• 3 or more of the following:
  • Eating more rapidly than normal
  • Eating till uncomfortably full
  • Eating large quantities when not hungry
  • Eating alone due to embarrassment
  • Feeling disgusted, depressed, or guilty afterwards

Management 

• AN: Cognitive behavior therapy
• BN-fluoxetine + CBT
• BED-Lisdexamphetamine + CBT

Functions of Liver

• Biosynthetic functions
  • Acute-phase reactants are proteins whose levels increase during stress (CRP, Haptoglobin, Ferritin)
    • Albumin (Liver is the only source)
  • Normal serum albumin level is 3.5 to 4.5 gm/dL
  • The liver does not produce immunoglobulins.
  • The liver produces alpha and beta globins.
  • The liver produces clotting factors:
  • 1, 2, 5, 7, 10, 12, and 13
  • Prothrombin Time assesses 1, 2, 5, 7, and 10.
  • Vitamin K dependent: 2, 2, 5, 7, 10
  • Vitamin K requires the carboxylation of these.
  • The liver produces hormone-binding proteins:
  • Cortisol-binding globulin (CBG)
  • Thyroid hormone binding (TBG)
  • The rate of albumin production by the liver is 200 mg/kg of albumin daily—15 g of albumin/day.
• The liver is part of the reticuloendothelial system.
  • Kuffer cells, also known as stellate cells, are the principle macrophages of the liver.
• Detoxification of toxic substances, whether they are endogenously produced or exogenous toxins.
  • Phase I detoxification
    • Oxidation
    • Hydroxylation
  • Phase II detoxification (esterification): These are conjugation reactions.
    • Glucuronidation
    • Sulfation
• Nutrient metabolism
  • Carbohydrate metabolism: The liver is known as a glucose buffer system.
  • Patients with liver problems have hypoglycemia.
  • Fat storage, and if more than 5% of cells are fat-laden, we call it fatty liver.
  • Storage organ for micronutrients [trace elements as well as trace minerals and vitamins (fat-soluble and water-soluble)]
  • B12 and vitamin K are stored in the liver.
• Formation and secretion of bile
  • Bile composition: the majority is water
  • Bile salts are for fat absorption
  • Bile pigments: bilirubin, Biliverdin
  • Alkaline phosphatase
  • Cholesterol

Also read: Recurrent and Autoimmune Pancreatitis

Heme metabolism

• Source: hemoglobin
• Hemolysis is needed
• RBC's life span is 120 days
• Site of action: reticular epithelial system (Liver and other—happening in macrophage)
• Globin is broken down into constituent amino acids, and they go for protein synthesis
• Heme gets converted to biliverdin in macrophages with the help of enzyme heme oxygenase.
• Biliverdin is then converted to bilirubin. Catalyzed by Biliverdin reductase.
• The transported molecule is albumin, which is brought to the liver. Albumin plus bilirubin combination reaches the liver.
• Albumin has 2 binding sites: high and low.
• Hepatocytes are present inside the liver arranged in chains and have a canalicular surface attached to bile canaliculi.
• The endothelial-lined space is called the sinusoids.
• Albumin and bilirubin come into the sinusoid, albumin gets dissociated, and bilirubin enters hepatocytes.
• The transport molecule is an organic acid transport protein that facilitates the entry of bilirubin in hepatocytes. This is facilitated diffusion.
• When bilirubin enters hepatocytes, it must be converted to nontoxic bilirubin that is conjugated bilirubin.
• For conjugation in hepatocytes, we require an enzyme called UDP glucuronosyltransferase. It will cut the bilirubin molecules and add UDP glucuronic acid, becoming bilirubin monoglucuronate. The same enzyme, UDP glucuronosyltransferase, will convert this by adding one more UDP glucuronosyl acid and becoming bilirubin glucuronide. This is what we call conjugated bilirubin.
• Proteins involved to prevent diffusion of bilirubin out of hepatocytes: Ligandin and ProteinY.
• Mutation of UDP glucuronosyltransferase- Gilbert syndrome Criggler-Najar syndrome Type I, II.
• Rate-limiting step: conjugated bilirubin should be separated in the bile and cleared in the stool. The secretion of conjugated bilirubin in the bile canalicular is the limiting step. The protein involved here is MRP2. It will come out as part of the bill.
• In the gut, conjugated bilirubin gets acted upon by the gut microbiota, which has glucuronidase, which forms urobilinogen, which gets oxidized to stercobilinogen and excreted in feces.
• Urobilinogen, when it moves to the kidney, is changed to urobilin and then excreted in the urine.
• Conjugated bilirubin gets reabsorbed and enters enterohepatic circulation.

Also read: Menetrier's Disease: Epidemiology, Etiopathogenesis

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