Flashcards in Gastroenterology - Nutritional disorders Deck (48):
How is body weight normally maintained?
Bodyweight is maintained at a "set point" by a balance between intake and total energy expenditure (the sum of the resting or basal metabolic rate, physical activity, and the thermic effect of food). Weight gain is almost always due solely to an increase in energy intake which exceeds the total energy expenditure. Occasionally, weight gain is due to a decrease in energy expenditure, e.g. hypothyroidism, or due to fluid retention, e.g. heart failure or ascites.
Weight loss associated with cancer and chronic diseases is due to a reduction in energy intake secondary to a loss of appetite (anorexia).
Which patients are at risk of vitamin deficiency?
Vitamin deficiency is rare in the Western world except in specific groups e.g. alcohol dependent and patients with small bowel disease, who may have multiple vitamin deficiencies, and patients with liver and biliary tract disease who are susceptible to deficiencies of the fat soluble vitamins (A, D, E and K).
Dietary deficiency of vitamin B6 (pyridoxine) is also extremely rare, but drugs (e.g. isoniazid and penicillamine) that interact with pyridoxal phosphate, may cause B6 deficiency and a polyneuropathy.
How should a patients nutritional status be checked?
Patients should be screened for nutritional status on admission to hospital:
- Patients should answer simple questions about recent weight loss, their usual weight, and whether they have been eating less than usual
- their weight and height should be recorded and body mass index calculated, BMI 20-25 for men and 19-24 for women
Which patients require nutritional support?
Nutritional support should be given to:
- all severely malnourished patients on admission to hospital: severe malnutrition is indicated by a BMI less than 15
- moderately malnourished patients (BMI 15-19) who, because of physical illness, are not expected to eat for 3-5 days
- normally nourished patients not expected to eat for 7-10 days
What is enteral nutrition?
Food can be given by:
- fine bore nasogastric tube for short term enteral nutrition
- Percutaneous endoscopic gastrostomy (PEG): this is useful for patients who need feeding longer than 2 weeks
- Percutaneous jejunostomy where a tube is inserted directly into the jejunum either endoscopically or at laparotomy
Enteral nutrition is cheaper, more physiological and has less side effects than parenteral nutrition. It is given provided the GIT is functioning normally. A polymeric diet with whole protein, carbohydrate and fat is usually used; sometimes an elemental diet composed of amino acids, glucose and fatty acids is used for patients with CD.
What is total parenteral nutrition (TPN)?
Parenteral nutrition may be given via a feeding catheter placed in a peripheral vein or a silicone catheter placed in the subclavian vein. Central catheters must only be placed by experienced clinicians under strict aseptic conditions in a sterile environment. The risk of introducing infection is reduced if these catheters are only used for feeding purposes, and not the administration of drugs or blood. Peripheral feeding lines usually only last for about 5 days and are reserved for when feeding is necessary for a short period. Central lines may last for months to years. It is used for patients who are at risk of severe malnutrition or who have a non functioning GIT.
What complications are associated with TPN?
Catheter related: sepsis, thrombosis, embolism and pneumothorax
Metabolic, e.g. hyperglycaemia, hypercalcaemia
What monitoring do patients receiving nutritional support require?
Patients receiving nutritional support should be weighed twice weekly: they require regular clinical examination to check for evidence of fluid overload or depletion. Patients receiving nutritional support in hospital initially require daily measurements of urea and electrolytes and blood glucose. More fre- quent measurement of blood glucose with BM sticks is indicated in patients beginning TPN. Liver biochemistry, calcium and phosphate are measured twice weekly. Serum magnesium, zinc and nitrogen balance are measured weekly.
What is nitrogen balance and why is it important to check in patients receiving nutritional support?
It is necessary to give 40-50g of protein per 24 hours to maintain nitrogen balance, which represents the balance between protein breakdown and synthesis. The aim of any regime is to achieve a positive nitrogen balance, which can usually be obtained by giving 3-5g of nitrogen in excess of output. The amount of protein required to maintain nitrogen balance in a particular individual can be calculated from the amount of urinary nitrogen loss, using the formula:
Nitrogen loss = (Urinary urea x 0.028) + 2
Urinary nitrogen x 6.25 = grams of protein required
Most patients require about 12g of nitrogen per 24 hours.
What is refeeding syndrome?
Refeeding syndrome occurs in the first few days from either oral, enteral or parenteral feeding. It involves a shift from the use of fat as an energy source during starvation to the use of carbohydrate as an energy source during refeeding. With the introduction of artificial nutrition and carbohydrate by any source, insulin release is augmented and there is rapid intracellular passage of phosphate, magnesium and potassium resulting in hypophosphataemia, hypo- magnesaemia , and hypokalaemia. Phosphate is an integral part of cellular machinery. Deficiency results in widespread organ dysfunction (muscle weakness, rhabdomyolysis, cardiac failure, immune suppression, haemolytic anaemia, thrombocytopenia, coma, hallucinations, fits). Thiamine deficiency can be precipitated.
Which patients are at risk of refeeding syndrome?
Patients at risk of refeeding are underweight (e.g. anorexia nervosa, alcohol dependent syndrome) or those with recent rapid weight loss (5% within preceding month), including patients after treat- ment for morbid obesity. These at-risk patients should receive high-dose vitamin B and C vitamins, e.g. Pabrinex® 1 pair twice daily, for 5–7 days beginning before feeding, and begin feeding at 25–50% of estimated calorie requirements, increasing by 100 calories per day. Serum phosphate, mag- nesium, calcium, potassium, urea and creatinine, bodyweight and evidence of fluid overload should be checked daily for the first week, and electrolyte de deficiencies corrected as necessary.
What is the definition of obesity?
This is an excess of body fat contributing to comorbidity. A BMI of 30 or greater is the standard used to define obesity. Overweight is defined as a BMI of 25-30 and is associated with a mildly increased risk of complications that have been identified in obese patients.
What is the important epidemiology of obesity?
Prevalence of obesity increases with age until the 6th decade of life after which, it declines due to weight loss.
Obesity is an independent risk factor for ischaemic heart disease. Risk factors for increased morbidity/ mortality are associated with the type of fat distribution:
- excess central fat (i.e. waist and flanks) is more important than other areas
- excess visceral fat in the abdominal cavity has greater significance than excess sub cutaneous fat
What is the pathogenesis of obesity?
Energy balance dysfunction (EBD) is the problem in obesity. Energy balance involves complex neuronal circuitry in the hypothalamic centres, such arcuate nucleus and paraventricular nuclei. These centres receive input from the stomach (ghrelin) and adipose tissue (leptin) that impact on these circuits to control food input.
- ghrelin is a hormone secreted by the stomach; it increases food intake (stimulates orexigenic centres and inhibits anorexigenic centres) and decreases energy expenditure
- leptin is a hormone secreted by adipose tissue; it decreases food intake and increases energy expenditure
EBD involves a decrease in or dysfunction of leptin so ghrelin activity is unopposed.
Other than EBD, what other factors contribute to the pathogenesis of obesity?
Genetic factors account for 5-10% of obesity - e.g. metabolic syndrome
Acquired causes - e.g. chronic caloric intake, hypothalamic lesions
Insulin normally increases TG in adipose tissue but in type 2 DM hyperinsulinaemia (due to decreased sensitivity) leads to increased TG stores in adipose tissue.
What cancers are obese patients at increased risk of?
Increased incidence of oestrogen related cancers (e.g. endometrial, breast) because of increased aromatase stores in adipose and conversion of androgens to oestrogens.
What cardiovascular complications are associated with obesity?
Hypertension - hyperinsulinaemia increases sodium retention, leading to increased plasma volume; LVH and stroke complicate hypertension
Hypertriglyceridaemia - hypertriglyceridaemia decreases serum high density lipoproteins, increasing risk of CAD
T2DM - increased adipose downregulates insulin receptor synthesis; hyperinsulinaemia increases adipose tissue stores; weight reduction upregulates insulin receptor synthesis
(fatty liver, obstructive sleep apnoea and cholelithiasis are other complications)
How should I counsel an obese patient about weight reduction?
Weight reduction can be achieved with a reduction in calorie intake and an increase in physical activity, although in practice this is difficult to achieve. The most common diets allow a daily energy intake of 4200 kJ (1000 kcal) which in a middle-aged woman would result in a daily energy de cit (expenditure vs intake) of about 4200 kJ. A week of dieting would result in a total energy de cit of 25–29 MJ (6000–7000 kcal) and weight loss of about 1 kg. A 10% loss of body weight (i.e. 10 kg in a 100 kg person) is associated with a fall in blood pressure and a reduced risk of diabetes and overall mortality.
What medial and surgical treatments are available for obesity?
Orlistat is an inhibitor of pancreatic lipase and hence fat digestion that is sometimes used in severely obese patients.
Surgical treatment is used in some patients with morbid obesity (BMI >40 kg/m2) or patients with a BMI >35 kg/m2 and obesity-related complica- tions, after conventional medical treatment has failed. The techniques used are restrictive, such as gastric banding (which restricts the ability to eat) or intestinal bypass (which reduces the ability to absorb nutrients - Roux-en-Y gastric bypass).
How are fat soluble vitamins normally reabsorbed?
Reabsorption of fat soluble vitamins is associated with micelle formation for reabsorption of fats. Malabsorption of fat leads to fat soluble vitamin deficiencies. Vitamin toxicity is more common in fat soluble vitamins than water soluble ones, the latter excess being lost in urine.
The fat soluble vitamins are A, D, E and K
What are the causes of vitamin A deficiency?
Diet lacking sufficient yellow and green vegetables
Fat malabsorption (e.g. coeliac disease, etc)
What causes vitamin A toxicity?
Consuming livers of polar bears, whales and sharks
Megadoses of vitamin A
Treatment of acne with isotretinoin
What are the clinical findings of vitamin A deficiency?
1) Impaired NIGHT VISION is an early finding. Blindness may occur due to squamous metaplasia of the corneal epithelium, which is normally nonkeratinizing squamous epithelium (produces keratomalacia). Conjunctival epithelium (normally pseudostratified columnar epithelium with goblet cells) also undergoes squamous metaplasia, producing localized keratin debris (called Bitot spot) or more extensive areas of keratinization (called xerophthalmia). Vitamin A deficiency is a major cause of blindness worldwide
2) Follicular hyperkeratosis may occur from loss of sebaceous gland function related to plugging of the ducts by excess keratin
3) Vitamin A deficiency is a major cause of worldwide growth retardation in children. Other findings in vitamin A deficiency include pneumonia (squamous metaplasia of the ciliated columnar epithelium of the bronchi) and renal calculi.
What are the clinical findings of vitamin A toxicity?
Signs of hypervitaminosis A include papilledema with blurred vision; seizures (due to an increase in intracranial pressure); hepatitis; bone pain (due to periosteal proliferation); and bone resorption and fractures (retinoic acid stimulates osteoclast production and activation).
What are the causes of vitamin D deficiency?
1) Renal failure is the most common cause of vitamin D deficiency due to a decrease in 1 alpha hydroxylation
2) Inadequate exposure to sunlight leads to inadequate photoconversion to vitamin D3
3) Fat malabsorption --> decreased micelle formation --> vitamin D/ fat malabsorption
4) Chronic liver disease --> decreased synthesis of 25 -(OH) - D in the cytP450 system
5) Induction of liver enzymes leads to increased metabolism of 25-(OH)-D into an inactive metabolite
6) Infants with exclusive breast feeing without vitamin D supplementation
What are the causes of vitamin D toxicity?
Megadoses of vitamin D
Increased synthesis of vitamin D in granulomas in sarcoidosis
What are the clinical features of vitamin D deficiency in adults?
Signs of vitamin D deficiency in both adults and children include pathologic fractures, due to an excess of unmineralized osteoid; tibial bowing, due to soft bones; continuous muscle contraction (tetany), due to low serum ionized calcium levels.
What are the clinical features of vitamin D deficiency seen in children?
Signs of vitamin D deficiency (rickets) exclusively seen in children include craniotabes (soft skull bones with delayed suture and fontanel closing); rachitic rosary (defective mineralization and overgrowth of unmineralized epiphyseal cartilage in the costochondral junctions); frontal bone thickening and bossing of the forehead; short stature (often 3rd percentile); pectus carinatum (“pigeon breast,” anterior protrusion of the sternum). Adults who develop vitamin D deficiency do not have craniotabes or rachitic rosaries, because the bone or cartilage in these areas has already been mineralized. Bone remodeling is defective, because newly formed osteoid is excessive and left unmineralized, causing the bone to be soft, hence the term osteomalacia (soft bone).
What are the symptoms of vitamin D toxicity?
Signs of hypervitaminosis D include hypercalcemia with metastatic calcification of soft tissue, renal calculi, and bone pain.
What are the main causes of vitamin E deficiency?
1) Fat malabsorption in children with cystic fibrosis
- chronic pancreatitis is universal in cystic fibrosis, therefore pancreatic lipase is deficient and unable to hydrolyse dietary fat into monoglycerides and fatty acids
2) Abetalipoproteinanaemia - due to chylomicrons accumulating in villi and preventing micelle resorption into the small intestine
What are the clinical features of vitamin E deficiency?
Hemolytic anemia may result from free radical damage to the lipid in the RBC membrane.
Peripheral neuropathy and degeneration of the posterior column (poor joint sensation) and spinocerebellar tracts (ataxia) may result from free radical damage.
In the neonate, vitamin E deficiency presents with hemolytic anemia, peripheral edema, and thrombocytosis.
What are the clinical features of vitamin E toxicity?
Excessive intake of vitamin E has a synergistic effect with warfarin anticoagulation. It causes over- anticoagulation manifested by bleeding and a markedly prolonged prothrombin time and calculated INR. Giving vitamin K reverses the over-anticoagulation.
What is the main function of vitamin K?
Majority of vitamin K is synthesised by colonic bacteria.
Liver enzyme epoxide reductase activates vitamin K.
Coumarin derivatives (e.g. warfarin) inhibit epoxide reductase.
Vitamin K gamma carboxylates vitamin K dependent clotting factors (X, IX, VII and II, plus protein C and S). Gamma carboxylation allows these factors to bind calcium in fibrin clot formation.
What are the main causes of vitamin K deficiency?
1) Broad spectrum antibiotics - MCC vitamin K deficiency
- antibiotics destroy bacteria in the colon that synthesise vitamin K
- lack bacterial colonisation bowel until 5-6 days old
- newborns must receive an IM injection of vitamin K
3) Warfarin/ coumarin derivatives/ cirrhosis
- BOTH of these decrease epoxide reductase activation of vitamin K
- cirrhosis decreases synthesis of vitamin K dependent clotting factors
4) Fat malabsorption
Why do patients need to be placed on both warfarin and heparin when starting anticoagulation with warfarin?
Warfarin is an anticoagulant that inhibits epoxide reductase, which prevents any further γ-carboxylation of the vitamin K–dependent coagulation factors. However, full anticoagulation does not immediately occur, because previously γ-carboxylated factors are still present. Prothrombin has the longest half-life; therefore full anticoagulation requires at least 3 to 4 days before all functional prothrombin has disappeared. This explains why patients are initially placed on both heparin and warfarin, because heparin provides immediate anticoagulation in the patient by enhancing ATIII activity.
What are the clinical signs of vitamin K deficiency?
Newborns with vitamin K deficiency develop hemorrhagic disease of the newborn (CNS bleeding, ecchymoses) due to deficiency of the vitamin K dependent coagulation factors (II, VII, IX, and X). Adults with vitamin K deficiency develop gastrointestinal bleeding and ecchymoses (bleeding) in the skin. The prothrombin time and partial thromboplastin time are both prolonged.
What are the clinical features of vitamin K toxicity?
If a pregnant woman is taking excessive amounts of vitamin K, the newborn child may develop a haemolytic anaemia, jaundice, and kernicterus.
What causes thiamine deficiency?
Chronic alcoholism MCC
Diet of unenriched rice
What are the clinical features of thiamine deficiency?
Dry beriberi: peripheral neuropathy (demyelination)
Wernicke syndrome: ataxia, confusion, nystagmus, ophthalmoplegia; hemorrhages present in the mamillary bodies
Korsakoff syndrome: antegrade and retrograde amnesia; demyelination in the limbic system
Wet beriberi: dilated cardiomyopathy with biventricular heart failure and dependent pitting edema; cardiac muscle lacks ATP; intravenous thiamine reverses cardiomyopathy in some cases
What are the features of riboflavin (vitamin B2) deficiency?
Corneal neovascularization, glossitis (magenta tongue), cheilosis (cracked lips), angular stomatitis (fissuring at the angles of the mouth)
What are the causes of niacin deficiency?
1) Corne based diets - deficient in niacin and tryptophan
2) Deficiency of tryptophan - used to synthesise niacin/ serotonin
- corne based diet
- Hartnup disease (in borne error of metabolism with inability to reabsorb tryptophan from the small bowel or kidneys)
- carcinoid syndrome
What are the clinical features of niacin (vitamin B3) deficiency?
Pellagra: diarrhea, dermatitis (hyperpigmentation in sun-exposed areas; see Fig. 8-9A), dementia (3 Ds of pellagra)
What are the causes of pyridoxine (vitamin B6) deficiency?
Pyridoxine is needed for haem synthesis, transamination and neurotransmitters.
Deficiency is caused by:
- isoniazid (drug inactivates vitamin)
- goat milk
- chronic alcoholism
What are the clinical findings of pyridoxine deficiency?
Sideroblastic anemia (microcytic anemia with ringed sideroblasts, convulsions, peripheral neuropathy
What are the clinical features of cobalamin deficiency (vitamin B12)?
Megaloblastic anemia with hypersegmented neutrophils , pancytopenia, neurologic disease (posterior column and lateral corticospinal tract demyelination, peripheral neuropathy, dementia), glossitis.
Vitamin B12 deficiency in infants exclusively seen in breast-fed infants of vitamin B12–deficient mothers
What are the features of folic acid deficiency?
Megaloblastic anemia with hypersegmented neutrophils, pancytopenia, and glossitis; neurologic abnormalities not present/
Open neural tube defects: several gene defects affecting enzymes and proteins involved in transport and metabolism of folic acid implicated in pathogenesis of open neural tube defects.
What are the functions of ascorbic acid (vitamin C)?
1) Collagen synthesis
2) Antioxidant activity
3) Reduces nonhaem iron to haem iron which is now suitable for reabsorption in the duodenum
4) Cofactor for conversion of dopamine to noradrenaline in catecholamine synthesis