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IAS10 Flashcards

1
Q

purpose of micronutrients

A

Form prosthetic groups of enzymes or serve as their cofactors
Hormones
Cell growth, proliferation and differentiation

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2
Q

coenzyme

A

organic compound that binds with an enzyme to catalyse a reaction

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3
Q

vitamin vs mineral

A

vitamin: essential non-caloric INORGANIC
mineral: essential non-caloric ORGANIC

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4
Q

broad classification of vitamins

A

lipid soluble: ADEK
water soluble: C, B6;
energy releasing: B1,2,3,5,7
haematopoietic: B9,12

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5
Q

broad deficiency & excess cause of micronutrient

A

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

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6
Q

fat v water soluble vitamin

A

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

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7
Q

vitamin A types & function

A

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

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8
Q

vitamin A in sight (OPTIONAL)

A

vitamin A in corneal epithelium & retina
produces rhodopsin -> conformational change when exposed to light -> elicit nerve impulse, recognized by brain as light

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9
Q

vitamin A in cell differentiation (OPTIONAL)

A

retinoic acid (nuclear hormone) binds to transcription factor -> activates transcription of some genes -> cellular differentiation

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10
Q

hypovitaminosis A

A

night blindness
keratomalacia (defective epithelialization & corneal formation, cornea soften & opaque) -> permanent blindness
growth impediment, poor wound healing
birth defect, abnormal bone formation

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11
Q

hypervitaminosis A

A

liver toxicity, bone reduction
excess isoretinoin teratogenic i.e. disrupt fetal dev. & cause abnormal preg -> birth defect e.g. cleft palate, abnormal heart

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12
Q

vitamin D generation & conversion into active form

A

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

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13
Q

vitamin D function

A

Ca uptake: increases plasma Ca levels by increasing Ca absorption from GI tract / renal reabsorption, mobilization from bone -> restore plasma Ca levels

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14
Q

hypovitaminosis D

A

hypo- due to above reasons & poor functioning of the liver & kidneys, hypoparathyroidism, lack of sun exposure
rickets in children, osteomalacia in adults

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15
Q

hypervitaminosis D

A

hypercalcemia, Ca deposition in organs esp. joints, arteries & kidney -> hypercalciuria, kidney stones

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16
Q

vitamin E & deficiency

A

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

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17
Q

ROS

A

reactive oxygen species: unstable & reactive -> damage biomolecules & cells

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18
Q

vitamin K function & property

A

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

19
Q

hypovitaminosis & hypervitaminosis K

A

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

20
Q

vitamin B functions

A

TRNPPBFC The Really Nice Parrots Prefer Big Fruits Carefully
Essential for normal metabolism
Coenzymes in many reactions in carbohydrate, fat & protein metabolism

21
Q

Vitamin B1 & deficiency

A

thiamine: carb metabolism, coenzyme of pyruvate DH & OGDH in TCAC
hypo: reduced ATP production -> impaired cellular function –> beriberi / wernicke-korsakoff syndrome in chronic alcoholics

22
Q

Vitamin B2 & deficiency

A

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

23
Q

VItamin B3 & deficiency

A

niacin: forms part of NAD+ (e- carrier from TCAC to ETC)
hypo: pellagra in skin, GI tract & NS -> diarrhoea, dementia, dermatitis, death (4D)

24
Q

Vitamin B5 (can skip)

A

pantothenic acid: acetyl-CoA component

25
Vitamin B6 & deficiency (can skip)
pyroxidine: coenzyme for AA metabolism hypo: neurological symptoms & anaemia
26
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
27
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)
28
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
29
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
30
vitamin C & deficiency
ascorbic acid: antioxidant -> prevent dev. of chronic disease, reducing agent for Fe2+; collagen formation hypo: scurvy, hyper-: kidney stones
31
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
32
macro & micro minerals
macro: >100mg/d: Na, Cl, K, Ca, Mg, P micro: <100 mg/d: Fe, Zn, Cu
33
Na+, K+, Cl- functions
- Major electrolytes maintaining osmotic pressure in body, body fluid conc. & acid-base balance - Nerve & muscle excitability
34
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
35
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
36
Ca2+, PO43-, Mg2+ disorders
hypocalcemia: osteoporosis, arrythmia hypercalcemia: kidney stones hyperphosphatemia: calcification of soft tissues hypomagnesemia: impaired metabolism (reduced ATP production & utilization), arrythmia
37
regulation of blood levels of Ca2+ & Mg2+ due to
- Calcitriol (D) - Parathyroid hormone (PTH) – produced by parathyroid gland - Calcitonin – produced by thyroid
38
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
39
Fe2+ regulation
hepcidin, degrades ferroportin (Fe-transporting protein channel), levels affect Fe2+ absorption: high [Fe] = ↑Hepcidin = ↓Ferroportin = ↓Iron absorption
40
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
41
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
42
Zn2+ deficiency
common, occurs in patients w/ major burns or in dialysis or in IV feeding Affects growth, skin integrity, wound healing
43
Cu2+ function
– Scavenges superoxide and other reactive oxygen species i.e. antioxidant – found in ETC complex IV
44
Cu2+ deficiency & excess
deficiency (rare but premature infants have low Cu stocks): anaemia / ATP production impaired (no complex iv) -> heart pathology Excess -> liver cirrhosis

IASM (15 decks)

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