IAS10 Flashcards
purpose of micronutrients
Form prosthetic groups of enzymes or serve as their cofactors
Hormones
Cell growth, proliferation and differentiation
coenzyme
organic compound that binds with an enzyme to catalyse a reaction
vitamin vs mineral
vitamin: essential non-caloric INORGANIC
mineral: essential non-caloric ORGANIC
broad classification of vitamins
lipid soluble: ADEK
water soluble: C, B6;
energy releasing: B1,2,3,5,7
haematopoietic: B9,12
broad deficiency & excess cause of micronutrient
inadequate intake (malnutrition), increased demand (pregnancy, lactation, growth spurt), poor absorption from GI tract (old age), inefficient utilisation, inc. excretion loss
excess caused by excess supplement intake
fat v water soluble vitamin
fat: absorbed into lymph alongside fat w/ help of bile salts -> into blood, transport by carrier proteins & receptors
water: absorbed directly into blood, B12 requires transport proteins
fat: surplus stored in liver/fat tissues, hypo- rare, hyper- common, intake required in wks
water: not stored, excess excreted, hypo- common, hyper- rare, intake required in day
vitamin A types & function
4A: beta-carotene antioxidant
retinal for vision in dim light (produces rhodopsin) (aura),
retinoic acid for proper differentiation & maintenance of epithelial cells & growth promotion (activation); growth, differentiation & proliferation; embryonic dev & organogenesis
isoretinoin treat severe acne
vitamin A in sight (OPTIONAL)
vitamin A in corneal epithelium & retina
produces rhodopsin -> conformational change when exposed to light -> elicit nerve impulse, recognized by brain as light
vitamin A in cell differentiation (OPTIONAL)
retinoic acid (nuclear hormone) binds to transcription factor -> activates transcription of some genes -> cellular differentiation
hypovitaminosis A
night blindness
keratomalacia (defective epithelialization & corneal formation, cornea soften & opaque) -> permanent blindness
growth impediment, poor wound healing
birth defect, abnormal bone formation
hypervitaminosis A
liver toxicity, bone reduction
excess isoretinoin teratogenic i.e. disrupt fetal dev. & cause abnormal preg -> birth defect e.g. cleft palate, abnormal heart
vitamin D generation & conversion into active form
7-dehydrocholesterol -> (sunlight) cholecalciferol / D3
(note: 15 min sunlight give adequate intake)
ergocalciferol / D2 & D3 obtained in diet
D3 -> 25-(OH)-D3 in liver, -> 1,25-(OH)2-D3 in kidney i.e. active form, calcitriol
vitamin D function
Ca uptake: increases plasma Ca levels by increasing Ca absorption from GI tract / renal reabsorption, mobilization from bone -> restore plasma Ca levels
hypovitaminosis D
hypo- due to above reasons & poor functioning of the liver & kidneys, hypoparathyroidism, lack of sun exposure
rickets in children, osteomalacia in adults
hypervitaminosis D
hypercalcemia, Ca deposition in organs esp. joints, arteries & kidney -> hypercalciuria, kidney stones
vitamin E & deficiency
tocopherol for antioxidant (protect cells from ROS effect)
hypo: mostly in premature infants, adult cause due to defective lipid absorption / transport (CF, abetalipoproteinemia)
Haemolytic anaemia (no antioxidant -> RBC susceptible to rupture by ROS –> haemolysis) among others: retinopathy, neurological & neuromuscular dysfunction
ROS
reactive oxygen species: unstable & reactive -> damage biomolecules & cells
vitamin K function & property
4C: clotting factor, crushed by warfarin, cofactor of gamma carboxylation, cannot find in newborn infant
diet K (phylloquinone) -> active K (hydroquinone)
glutamate residue -> (by gamma carboxylase) active clotting factor & active K -> K epoxide; -> diet K
warfarin (anticoagulant) inhibit conversion of diet K into active K
newborn infant have sterile gut -> no K -> normalize when food absorption starts
hypovitaminosis & hypervitaminosis K
hypo- occurs in disruption of lipid absorption, anticoagulant taken, in premature infants
susceptible to bleeding & bruising, Anaemic, weak, heavy menstruation, nose, gums & GI bleeding
hyper- DNE except in prolonged intake of synth. K (menadione), liver toxicity & haemolytic anaemia
vitamin B functions
TRNPPBFC The Really Nice Parrots Prefer Big Fruits Carefully
Essential for normal metabolism
Coenzymes in many reactions in carbohydrate, fat & protein metabolism
Vitamin B1 & deficiency
thiamine: carb metabolism, coenzyme of pyruvate DH & OGDH in TCAC
hypo: reduced ATP production -> impaired cellular function –> beriberi / wernicke-korsakoff syndrome in chronic alcoholics
Vitamin B2 & deficiency
riboflavin: forms FMN & FAD (coenzyme for succinate DH (TCAC); acyl CoA DH; retinal dehydrogenase; complex I (ETC)
FAD & FMN coenzyme for vitamin-activating enzyme
hypo: skin lesions
VItamin B3 & deficiency
niacin: forms part of NAD+ (e- carrier from TCAC to ETC)
hypo: pellagra in skin, GI tract & NS -> diarrhoea, dementia, dermatitis, death (4D)
Vitamin B5 (can skip)
pantothenic acid: acetyl-CoA component
Vitamin B6 & deficiency (can skip)
pyroxidine: coenzyme for AA metabolism
hypo: neurological symptoms & anaemia
Vitamin B7 & deficiency (can skip)
biotin: coenzyme for fat, glycogen, AA synthesis
created by intestinal flora
hypo (by eating raw eggs): depression, dermatitis, muscle pain
Vitamin B9 & deficiency
folic acid: one-carbon metabolism in biosynthesis of serine, purines & TMP; haematopoiesis
hypo: megaloblastic anaemia (less synthesis of purines & ATP): cells unable to make DNA -> no division -> large cells in bone marrow w/ fragile membrane -> lyse -> low RBC count; neural tube defects (spina bifida & anencephaly in 1st trimester: rapid cell growth in neural tube deveopment)
one carbon metabolism
Tetrahydrofolate (reduced folate) receives one-carbon fragments from donors (e.g. serine, glycine, histidine) i.e. THF acts as coenzyme
-> transfer to intermediates in the synthesis of serine, purines and TMP
Vitamin B12 & deficiency
cobalamin: conversion of N5-methyl-THF to THF, methylmalonyl-CoA -> succinyl-CoA, homocysteine -> methionine (3 Rx)
also in nucleic acid synthesis, haematopoiesis, recycling of folates
(effects of B12 prominent in rapidly dividing cells, require N5-methyl-THF for nucleic acid synthesis)
hypo-: megaloblastic anaemia
vitamin C & deficiency
ascorbic acid: antioxidant -> prevent dev. of chronic disease, reducing agent for Fe2+; collagen formation
hypo: scurvy, hyper-: kidney stones
dietary supplementation of vitamins
Health benefit in supplementation:
- B9 during pregnancy
- D for people living in areas of low sunlight
but there are harmful effects or uncertain / controversial outcomes
-> Fruits and vegetables are best source of vitamins
macro & micro minerals
macro: >100mg/d: Na, Cl, K, Ca, Mg, P
micro: <100 mg/d: Fe, Zn, Cu
Na+, K+, Cl- functions
- Major electrolytes maintaining osmotic pressure in body, body fluid conc. & acid-base balance
- Nerve & muscle excitability
disorders of Na+, K+, Cl-
deficiency due to above, vomiting and diarrhea
hyponatremia: dilute body fluid -> cerebral edema
hypernatremia: conc. body fluid due to water loss -> dehydration
hypo-/hyperkalaemia: arrythmia
hypo-/hyperchloremia: acid-base disturbance
Ca2+, PO43-, Mg2+ storage & functions
Stored in the matrix of bone and teeth (reservoir): bone degradation mobilises ions to perform other body functions
- Ca2+ & Mg2+: nerve impulse propagation, muscle contraction, maintain electric potential of nerve & muscle membrane
- Mg2+: Important cofactor for all ATP-using enzymes (ATP readily forms a mandatory complex with Mg2+)
- Ca2+: Blood clotting, hormonal signalling
- PO43-: Component of NA & ATP; phosphorylation
Ca2+, PO43-, Mg2+ disorders
hypocalcemia: osteoporosis, arrythmia
hypercalcemia: kidney stones
hyperphosphatemia: calcification of soft tissues
hypomagnesemia: impaired metabolism (reduced ATP production & utilization), arrythmia
regulation of blood levels of Ca2+ & Mg2+ due to
- Calcitriol (D)
- Parathyroid hormone (PTH) – produced by parathyroid gland
- Calcitonin – produced by thyroid
Fe2+ functions
component of heme: in Hb and myoglobin (O2 binding) & redox enzymes incl. ETC proteins (e.g. IV) for energy metabolism
non-heme form: complexed to sulphur in proteins, found in complex 1 of ETC
Fe2+ regulation
hepcidin, degrades ferroportin (Fe-transporting protein channel), levels affect Fe2+ absorption: high [Fe] = ↑Hepcidin = ↓Ferroportin = ↓Iron absorption
Fe2+ disorders
deficiency (depletion occur through bleeding e.g. menstruation): iron deficiency anaemia, common in menstruating and pregnant women)
excess: poisoning i.e. haemochromatosis
- Inherited from increased Fe consumption
- Fe accumulates in heart, liver and pancreas and can cause liver cirrhosis, HCC, diabetes, heart failure
Zn2+ function & storage
- Contained in approximately 100 enzymes associated with carb and energy metabolism, protein synthesis and degradation, and nucleic acid synthesis
- Not stored in body
- requirements inc. in patients with major catabolic illness and increased GI losses
Zn2+ deficiency
common, occurs in patients w/ major burns or in dialysis or in IV feeding
Affects growth, skin integrity, wound healing
Cu2+ function
– Scavenges superoxide and other reactive oxygen species i.e. antioxidant
– found in ETC complex IV
Cu2+ deficiency & excess
deficiency (rare but premature infants have low Cu stocks): anaemia / ATP production impaired (no complex iv) -> heart pathology
Excess -> liver cirrhosis
