Vitamins Flashcards
1
Q
Hypervitaminosis A
A
- acute toxicity
- raised ICP
- Sx: headache, nausea, projectile vomiting
- Dry & pruritic skin (itchy skin)
- enlarged liver
- pregnancy: spontaneous abortions & congenital malformations in fetus
2
Q
Deficiency of Vit. A
A
- Causes:
- fat free diets (fad diets)
- malabsorption of fats can also lead to deficiency
- Sx:
- night blindness
- Xerophthalmia:
- dryness of conjunctive & cornea
- Bitot’s spots
- Keratomalacia: corneal erosion
- increased risk of pulm infections: loss of muco-ciliary epithelium
- immune deficiency
- skin metaplasia with hyperkeratinisation
- increased predisposition to formation of renal & urinary stones
3
Q
Clinical uses of Vit. A
A
- Routine injection of Vit. A given with measles vaccine and also in clinical cases of measles as it helps to reduce the severeity of the disease
- Role on leukemia rx: trans form given along with chemotherapy in Acute Promyelocytic Leukemia
- Rx of acne & psoriasis: topical application
4
Q
Sources & Fx of Vit. A
A
Sources
- animal derived: liver, kidney, egg yolks, fish, milk, butter
- plant derived: yellow vegetables (carrots, squash) & green leafy veg.
- Kerotene: Pro-vit
Fx
- Vision: component of rhodopsin (visual pigment). Visual cycle requires isomerization b/w cis & trans retinal
- Retinol: transport & storage form
- Retinal: component of visual pigment
- Retinoic Acid: active in epithelial differentiation & growth
- Maintenance of specialized epithelia, especially mucous secreting cells
- Growth
- Repro
- Immunity: stimulation of immune system to generate immunity against infection
5
Q
Absorption & Transport of Vit. A
A
- Diet contains retinol esters
- Hydrolysis by intestinal mucosa releasing retinol & free fatty acids
- Re-esterification & secretion in chylomicrons which are taken up by the liver where it is stored
- Plasma retinol binding protein in the liver transports to extra hepatic tissues
- Tissues contain cell retinol binding protein that carries retinoic acid to the nucleus
6
Q
Retinoids MOA
A
- retinol enters the target cell & is oxidised to retinoic acid in the cytosol
- from the cytosol, the retinoic acid moves into the nucleus with the help of cell retinoid binding proteins
- retinoic acid binds to intranuclear receptor forming an activated receptor complex
- retinoic acid-receptor complex binds to chromatin activating gene transcription
7
Q
Biochemical Events in vision
A
- retinol transported to the retina & enters the retinal pigment cells
- esterified to form a retinyl ester - storage form
- ester can be hydrolysed to form 11-cis retinol - oxidised to 11-cis retinal
- 11-cis retinal enters the rod cell where it combines with opsin to form rhodopsin (visual pigment)
- absorption of a photon of light catalyses the isomerization of 11-cis-retinal to all-trans-retinal triggering a cascade of events, leading to the generation of an electrical signal to the optic nerve which is interpreed as vision
8
Q
Metabolism of Vit. D
A
- Ergocalciferol (D2): found in plants
- Cholecalciferol (D3): found in animal tissues
- precursor of cholecalciferol synthesis in skin is 7-dehydrocholesterol (intermediate in cholesterol synthesis) in presence of sunlight.
- 1,25 Dihydroxycholecalciferol (calcitriol) is most active form:
- 25-hydroxycholecalciferol 1-hydroxylase aka alpha1-hydroxylase: converts 25-hydroxycholecalciferol -> 1, 25 dihydroxycholecalciferol
- Low plasma Ca2+ & PTH stimulate 25-hydroxycholecalciferol 1-hydroxylase
9
Q
Vit. D. Fx
A
Actions
- essential fx of Vit. D is maintenance of normal plasma Ca2+ & phosphorous levels.
- on the intestine: stimulates intestinal absorption of Ca2+ & PO43- by increased synthesis of specific Ca2+ binding proteins. PO4+ absorption is increased through the action of PTH
- Bone: stimulates the mobilisation of Ca2+ on PO43- from bone in presence of PTH
- Kidneys: Vit. D stimulates parathyroid dependent reabsorption of Ca2+ from the distal renal tubules & inhibits Ca2+ excretion by stimulating parathyroid dependent Ca2+ reabsorption.
10
Q
Vit. D sources & deficiency
A
Sources
endogenous production in presence of UV radiation in sunlight - decreased by melanin and high solar protection factor sunblocks
fortified cereals & dairy products
fish oil
egg yolks
Causes
- nutritional deficiency: decreased intake/fat malabsorption
- inadequate exposure to sunlight
- Rickets
- Osteomalacia
11
Q
Vit. E structure & Fx
A
Sructure
- 8 naturally occuring tocopherols
- alpha-tocopherol is most active
Fx
- most important role is anti-oxidant
- prevents peroxidation of lipids in conjuction with Selenium
- scavenges free radical generated
12
Q
Vit. E deficiency
A
Dietary deficiency of Vit. E is very rare since it’s abundant in foods. Occurs in association with:
- malabsorption of fat: cholestasis, pancreatic enzyme deficiency, CF
- relatively more common in premature infants with an immature GI tract
- Abetalipoproteinemia
- rare autosomal recessive syndrome of impaired Vit. E metabolism
Sx:
- Hemolytic anemia: oxidative injury by superoxide radicals generated during oxygenation of Hb
- reduced DTR (Areflexia) & gait problems due to axonal degeneration
13
Q
Vit. K metabolism & Fx
A
- in humans, it is synthesized by the intestinal bacterial flora
- exists in 2 naturally occuring forms
- Phylloquinone (plants): dietary source
- Menaquinone (bacteria): intestine
- Vit. K is active in its Reduced form
- Epoxide Reductase (liver): converts inactive Vit. K -> Active epoxide
Fx
- principal role of Vit. K is in post-translation mod by various clotting factors including:
- Prothrombin
- VII
- IX
- X
- Protein C & S
- Vit. K serves as cofactor for liver microsomal gamma carboxylase
- Vit. K dependent carboxylation of glutamate residues leads of formation of mature clotthing factors (gamma-carboxy-glutamyl (Gla) residues & is capable of subsequent activation
- gamma-carboxylation allows Ca2+ binding b/c of 2 adjacent -ve charged carboxylate groups
- clotting factor Ca2+ complex can then bind to phospholipids on the platelet membrane
14
Q
Vit. K sources & Fx
A
Sources
- most Vit. K recycled by liver which converts the oxidised form to the reduced form
- endogenous intestinal bacterial flora readily synthesise the vit and so the daily dietary requirement is low
- foods rich in Vit. K include cabbage, cauliflower, spinach, egg yolk & liver
Deficiency
Neonates:
- newborns have sterile intestines as bacterial flora have not developed & therefore cannot synthesise Vit. K
- Hemorrhagic disease of the newborn
- bleeding at various sites in the body including skin, umbilicus & viscera
- Intracranial bleeding: most serious complication
- do not confuse w/ Rh incompatibility
- Rx: im injection of Vit. K for all newborns
Adults
- Vit. K deficiency seen in cases of:
- fat malabsorption
- prolonged use of broad spectrum antibiotics
- diffuse liver disease which interferes with storage of Vit. K
- Vit. K toxicity manifests as:
- hemolytic anemia & jaundice
- hematuria
- melena (blood in stools)
- ecchymoses (brusiing)
- bleeding from gums
- Warfarin:
- Vit. K receptor antagonist
- MOA: blocks the activity of liver epoxide reductase & prevent regeneration of reduced Vit. K
- Rx for Pt with thrombo-embolic disease.
15
Q
Vit. C fx
A
- required for Iron absorption; reduces Iron to the ferrous state in stomach
- very important anti-oxidant; direct scavenger of free radicals; regenerates anti-oxidant form of Vit. E
