12. Micronutrients Flashcards
What are micronutrients?
What are their many roles?
List and describe brief properties of the
a) fat-soluble vitamins
b) water-soluble vitamins
Vitamins (organic) + trace elements (inorganic)
Cofactors, coenzymes, antioxidant, genetic control, structure ===> HEALTH! Maintain homeostasis in adults, more important in children (energy, growth etc. - bone density established 10-20yrs)
a) A K E D - can be stored, ocasionally toxic in excess
b) B, C, Biotin, Folate - normally not stored, often coenzymes, excess excreted in urine
Give a source of the following vitamins:
A K E D B1 B2 B3 B6 Biotin Folate
What are trace elements?
What are the key trace elements?
A (coloured fruit/veg), K (dark greens), E (oils), D (oily fish, dairy), B1 (wholegrain), B2 (bread/cereal), B3 (milk), B6 (banana), Biotin (yeast), Folate (fruit and veg)
Dietary minerals that are necessary, in minute quantities, for normal organism function
Ca, Phosphorous, Fe, Selenium, Zn, Cu
What might you see if you have a deficiency in the following:
Ca Phosphorus Fe Selenium Zn Cu
Distinguish between kwashiorkor and marasmus.
Ca (osteoporosis, muscle spasms, parasthesia), Phosphorous (bone pain, proximal muscle weakness, rickets, short kids, neurological manifestations), Fe (anaemia), Selenium (cardiomyopathy), Zn (growth retardation, slopecia, dermatitis, diarrhoea, congenital malformations), Cu (growth retardation)
Kwashiorkor: neonates, protein-wasting malnutrition, micronutrient and anti-oxidant deficiencies. Marasmus: older, severe malnutrition, muscle wasting/protein loss
What are these 3 deficiencies?
R: angular stomatitis - Fe deficiency
Middle: rickets - vit D deficiency in mother’s blood
L: keratomalacia - vit A deficiency
What deficiencies will fat malabsorption, alcoholism and liver disease produce when there is a viatmin D deficiency?
Describe vitamin D metabolism
Rickets and osteomalacia.
Vit D enters body from sun/diet -> liver (calcidiol)-> kidney.
PTH from parathyroid gland acts on
a) kidney (calcitriol) -> small intestine = increases Ca2+ absorption, and calcitriol also releases Ca2+ and phosphorous from bone
b) bone -> releases Ca2+ and phosphorus
= INCREASED SERUM CA2+
What can cause vitamin D deficiency?
What are some additional actions of vitamin D.
What is the target serum level of vit D? And current daily intake guidelines for people?
Lack of sunlight (non-caucasions need more exposure time. UK = insufficient UVB between Oct-March. Suncreens block 99% dermal vitamin D synthesis.)
Lifestyle factors: obesity, smoking, alcohol, exercise
Disease factors: reduced skin synthesis, drug-related, increased excretion, decreased bioavailability, impaired hydroxylation
Extraskeletal vit D receptors (neurons, immune cells, cardiomyocytes, vasuclar endothelial cells), vit D deficiency implicated in cancers, autoimmune disease, CDV
>75nmol/l (rickets = <25). About 400IU/day
What are the signs/symptoms of osteomalacia?
How does this compare to rickets?
Reduced bone strength, increase in bone fracture, bone pain bending of bones, muscle weakness, waddling gait
In children prior to epiphyseal fusion, growth retardation, expansion of growth plate (pic)
What can vit B1 (thiamine) deficiency lead to?
What is vitamin B1 involved with, and where is it absorbed?
What are the signs/symptoms?
Wernicke’s encephalopathy and Korsakoff’s psychosis
Carbohydrate and BCAA (branched chain AA) metabolism. Need it to produce pyruvic acid for Krebs cycle. If no thiamine, build up pyruvic acid = destroys neurons irreversibly. Absorbed in jejunum.
Anorexia and weight loss, cognitive impairment, muscle weakness. Most commonly seen in malignancy and alcoholism.
What is beri beri?
What are some sigs/symptoms of Wernicke’s encephalopathy?
What is Wernicke-Korsakoff syndrome?
Associated with thiamine deficiency, collection of symptoms. Wet BB: affects heart, neurological, and circulatory system; Dry BB: wasting and partial paralysis (symmetric peripheral neuropathy)
Horizontal nystagmus, opthalmoplegia (eyes go diff ways), cerebellar ataxia (ataxic gait). This triad present in 10% of cases. Assume intoxicated pt has thiamine deficiency and Wernicke’s so need to treat presumed deficiency or else won’t recover when unintoxicated.
Mental impairment (additional loss of memoray and confabulatory psychosis)
What can vitamin B3 (niacin) deficiency result in?
What is vit B3 used for in the body?
What may cause deficiency?
Pellagra
Central to redox reactions (precursor of NAD and NADP), excess excreted in urine
Vegetarianism, alcoholism, Hartnup’s disease (kids = congenital defects of intestinal and kidney absoprtion of tryptophan), Carcinoid syndrom, Isoniazid use (TB - so need B3 replacement)
Describe the signs and symptoms of
a) Early pellagra
b) Late pellagra
What are the adverse effects of niacin (usually if unable to excrete excess niacin)?
a) appetite loss, weakness, irritability, abdominal pain, vomiting, bright red glossitis (tongue)
b) 4 D’s: DEMENTIA, DIARRHOEA, DERMATITIS, DEATH Casal’s necklace (pic), vaginitis, oesophagitis, depression, seizures
Flushing at theraputic doses, glucose intolerance, macular oedema and cysts, fulminant hepatitis
What can B12 (cobalamin) deficiency cause?
Why can the B12 pathway be affected by lots of things?
How can B12 be administered?
How is it absorbed?
Anaemia, GI and neurological disturbance
It’s a complex pathway involving the stomach, bowel and IF etc. so if have gastrectomy, Crohn’s or pernicious anaemia etc. = problem!
Many forms - orally or injections.
Dissociated from proteins in stomach -> complexes with IF in small intestine -> absorbed via specifc receptors in terminal ileum (50% absorbed, 50% excreted in urine/bile)
How might someone become B12 deficient?
What related symptoms might you see in a B12 deficient person:
a) haematological
b) GI
c) neurological (often reversible)
Vegans, terminal ileum disorders, inadequate IF production, defective release of cobalamin from food, transcobalamin II deficiency (rare), congenital enzyme defects (rare)
a) megaloblastic anaemia, neutropaenia and thrombocytopenia
b) beefy red glossitis, malabsorption and diarrhoea, anorexia
c) sensory disturbance, gait abnormalities, memory loss and disorientation
What can iron deficiency cause?
What is iron used for in the body, and where is it absorbed?
Describe the 2 disease states and how they are treated.
Anaemia (microcytic), lethargy and constitutional disturbance. 1% are associated with renal cancer, so screen pts with urinalysis. Seen in bariatric pts.
O2 transport in Hb, myoglobin function. Absorbed in upper small bowel, transported by transferrin, stored in liver and bone marrow as ferritin.
- Fe deficiency (common): microcytic anaemia, lethargy and fatigue (adults), cognitive impairement (kids). Treat - iron tablets
- Fe excess: haemochromatosis: lethargy and fatigue, abdominal and joint pain, skin bronzing, diabetes, cirrhosis, cardiomyopathy. Treat - bloodletting
What is refeeding syndrome?
How is it managed?
Downregulation of membrane pumping: leakage of intracellular cations and phoshpate, Na+ and H2O leak into cells. Associated with respiratory failure, coma and death.
(Starved -> become catabolic = upregulation of certain proteins and downregulation of others. Refeeding - switch from cat to anabolism takes 48-72hrs, if too quick get massive influxes and efluxes of electrolytes, levels plummet b/c driven into cells -> death).
Agressive electrolyte replacement (IV), nutritional supplementation (sip drinks, NG feeding, parental vitamins), treat underlying medical problems, early dietician review, maybe cardiac monitoring
