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IASM > IAS10 > Flashcards

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 promotion; differentiation & proliferation of cell, embryonic dev & organogenesis
isoretinin 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 softening & opaque cornea) -> 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 hyporetinin 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 i.e. 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
brittle bones i.e. 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 & alpha-ketoglutarate DH in TCAC
hypo: due to beriberi & chronic alcoholism, leads to reduced ATP production -> impaired cellular function

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

A

pantothenic acid: acetyl-CoA component

25
Q

Vitamin B6 & deficiency

A

pyroxidine: coenzyme for AA metabolism
hypo: neurological symptoms & anaemia

26
Q

Vitamin B7 & deficiency

A

biotin: coenzyme for fat, glycogen, AA synthesis
created by intestinal flora
hypo (by eating raw eggs): depression, dermatitis, muscle pain

27
Q

Vitamin B9 & deficiency

A

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
Q

one carbon metabolism

A

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
Q

Vitamin B12 & deficiency

A

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
Q

vitamin C & deficiency

A

ascorbic acid: antioxidant -> prevent dev. of chronic disease, reducing agent for Fe2+
hypo: scurvy, hyper-: kidney stones

31
Q

dietary supplementation of vitamins

A

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
Q

macro & micro minerals

A

macro: >100mg/d: Na, Cl, K, Ca, Mg, P
micro: <100 mg/d: Fe, Zn, Cu

33
Q

Na+, K+, Cl- functions

A
  • Major electrolytes maintaining osmotic pressure in body, body fluid conc. & acid-base balance
  • Nerve & muscle excitability
  • note: Kidneys regulate electrolyte & body fluid levels
34
Q

disorders of Na+, K+, Cl-

A

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
Q

Ca2+, PO43-, Mg2+ storage & functions

A

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 DNA, RNA & ATP; Phosphorylation

36
Q

Ca2+, PO43-, Mg2+ disorders

A

hypocalcemia: osteoporosis, arrythmia
hypercalcemia: kidney stones
hyperphosphatemia: calcification of soft tissues
hypomagnesemia: impaired metabolism (reduced ATP production & utilization), arrythmia

37
Q

blood levels of Ca2+ & Mg2+

A

regulated by 3 hormones
- Calcitriol (D)
- Parathyroid hormone (PTH) – produced by parathyroid gland
- Calcitonin – produced by thyroid

38
Q

Fe2+ functions

A

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
Q

Fe2+ regulation

A

hepcidin, degrades ferroportin (Fe-transporting protein channel), levels affect Fe2+ absorption: high [Fe] = ↑Hepcidin = ↓Ferroportin = ↓Iron absorption

40
Q

Fe2+ disorders

A

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
Q

Zn2+ function & storage

A
  • 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
Q

Zn2+ deficiency

A

common, occurs in patients w/ major burns or in dialysis or in IV feeding
Affects growth, skin integrity, wound healing

43
Q

Cu2+ function

A

– Scavenges superoxide and other reactive oxygen species i.e. antioxidant
– found in ETC complex IV

44
Q

Cu2+ deficiency & excess

A

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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