Gastroenterology (Nutrition) Flashcards
Fat-soluble vitamins
- Vitamin A
- Vitamin
may accumulate in the body, such as in the liver:
Water-soluble vitamins
more readily excreted from the body, therefore toxicity is generally less likely:
* Vitamins B1, B3, and B6
* Vitamin C
Vitamin A deficiency can lead to:
also known as retinol
- Xerophthalmia – describes a spectrum of pathologies affecting the conjunctiva, cornea, and retina, including night blindness and corneal scarring
vitamin A caution
- High doses of vitamin A may be teratogenic:
- This is because retinol converts to retinoic acid, which can lead to congenital defects if levels are too high or low
- Foods with liver have high vitamin A levels and should be avoided during pregnancy
vitamin B1 (thiamine) deficiency occurs due to
- Alcohol excess:
- Due to alcohol inhibiting the uptake of thiamine
- Malnutrition
B1 (thiamine) deficiency can lead to
- Wernickes
- Korsakoff sydrome
- Beriberi
wet vs dry Beriberi
Wet beriberi – describes dilated cardiomyopathy:
- Tachycardia
- Elevated jugular venous pressure
- Paroxysmal nocturnal dyspnoea
- Shortness of breath on exertion
- Peripheral oedema
Dry beriberi – describes peripheral neuropathy:
- Numbness and tingling
- Confusion
- Hyporeflexia
deficiency in vitamin B3 (iacin)
A deficiency of B3 can lead to pellagra which is characterised by:
- Dermatitis
- Dementia
- Diarrhoea
- Hair loss
- Photosensitivity
- Glossitis
- Weakness
vitamin B6 (pyridoxine) deficiency
peripheral neuropathy
- Isoniazid – used in tuberculosis
- Penicillamine – used in Wilson’s disease
*
vitamin C deficiency
Reduced vitamin C can lead to scurvy, which occurs secondary to impaired wound healing and collagen synthesis. Features include:
- Easy bruising and ecchymosis
- Poor wound healing
- Gingivitis bleeding gums
- Weakness
- Malaise
- Anorexia
- Depression
- Synovitis
- Cautions
Scurvy is exceedingly rare in the UK. Patients with these features may have an underlying haematological malignancy, therefore, investigations should not be delayed by a trial of vitamin C treatment.
Vitamin C deficiency occurs in
- People whose exposure to sunlight is limited (e.g. those that are housebound, confined indoors, or cover their skin)
- People with dark skin as their skin is less efficient at synthesising vitamin D
- Pregnant and breastfeeding women
- Children under 4 years of age
- Intestinal malabsorption
- Chronic liver disease
vitamin D deficiency
- rickets
- osteomalacia
vitamin K
important for clotthing factors II, VII, IX AND X
- found in green vegetable and olive oil
vitamin K deficiency
Deficiency
Since vitamin K is fat-soluble, patients with fat malabsorption (such as biliary obstruction or hepatic disease) are at an increased risk of deficiency.
- Coumarin anticoagulants (such as warfarin) exert their effects by interfering with vitamin K metabolism).
- Vitamin K deficiency can lead to:
- Excessive bleeding
- Haemorrhagic disease of the newborn
RF for malnutrition in elderly
Living alone, particularly without care input
Institutionalisation
Hospitalisation
People with mental health problems
Diseases affecting appetite, eating, swallowing, or gastrointestinal function
RF for malnutrition in young
Young age
Children with co-existing illnesses
Neglect
Poverty
People are considered to be malnourished if any of the following apply:
- A BMI of less than 18.5 kg/m2
- Unintentional weight loss >10% in the last 3-6 months
- BMI of less than 20 kg/m2 and unintentional weight loss >5% in the last 3-6 months
People are considered to be at an increased risk of malnutrition if any of the following apply:
- They have eaten little or nothing for >5 days and/or are likely to eat little or nothing for the next 5 days or longer
- Have poor absorptive capacity and/or high nutrient losses and/or increased nutritional needs due to causes such as catabolism
screening tool for malnutrition
MUST
pathophysiology of Reefeeding syndrome
Pathophysiology
In starvation, insulin secretion is decreased due to reduced carbohydrate intake and fat and proteins are catabolised to release energy. This leads to an intracellular loss of electrolytes, particularly phosphate, magnesium, and potassium.
When feeding restarts, the shift from fat and protein to carbohydrate metabolism increases insulin secretion, which stimulates cellular uptake of phosphate and other electrolytes, leading to severe hypophosphataemia, hypokalaemia, and hypomagnesaemia. Phosphate is essential for the formation of ATP and other phosphorylation reactions, leading to cellular dysfunction.
Patients are deemed at high risk of refeeding syndrome if:
1 or more of the following are present:
- BMI less <16 kg/m2
- Unintentional weight loss greater than 15% within the last 3 to 6 months
- Little or no nutritional intake for more than 10 days
- Low levels of potassium, phosphate or magnesium before feeding
Or 2 or more of the following apply:
- BMI less than 18.5 kg/m2
- Unintentional weight loss greater than 10% within the last 3 to 6 months
- Little or no nutritional intake for more than 5 days
- A history of alcohol abuse or drugs including insulin, chemotherapy, antacids or diuretics
presentation of refeeding syndrome
- Hypophosphataemia
- Hypokalaemia
- Hypomagnesaemia
- Features of Wernicke-Korsakoff encephalopathy (due to thiamine deficiency)
- Hyperglycaemia – due to abnormal glucose metabolism and reduced insulin secretion
- Cardiac arrhythmia – due to electrolyte imbalances
- Fluid imbalances
- Pulmonary oedema
- Heart failure
prevention of refeeding syndrome
- Initiate feeding at no more than 50% of energy in patients who have eaten little or nothing for more than 5 days, then increase if no refeeding problems are detected on clinical or biochemical testing
- Electrolyte levels are checked once daily for 1 week then at least 3 times in the following week
refeeding is a biochemical triad of
- Hypophosphataemia
- Hypokalaemia
- Hypomagnesaemia
