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34 Cards in this Set

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List and group the fat soluble vitamins
Vitamin A (vision, epithelial tissue, growth)
Vitamin D (bone mineralisation, blood calcium regulation
Vitamin E (anti-oxidant)
Vitamin K (clotting factor synthesis)
List and group the major water soluble vitamins
Energy Metabolism - Thiamine (B1), Riboflavin (B2), Niacin (B3), Biotin, Pantothenic acid
Amino Acid Metabolism - Pyridoxine, Pyridoxal, Pyridoxamine (B6)
RBC/Neural Development - Folic acid, Cobalamin (B12)
Collagen Synthesis - Ascobic acid
Thiamin (B1):
Coenzyme Form
Requiring Reaction
Clinical Manifestation
Coenzyme Form - thiamine pyrophosphate (TPP)
Requiring Reaction
- regulates oxidative decarboxylation of pyruvate and alpha-ketoglutarate (ATP synthesis)
- co-factor for transketolase (pentose phosphate pathway)
Discuss the significance of vitamin B and C deficiencies
Vit B -
B1 (thiamine) - Beri beri, Wernicke-Korsakoff syndrome
B2 (riboflavin) - Cheilosis, Glossitis, Facial dermatitis
B3 (niacin) - Pellagra (Dermatitis, Diarrhoea, Dementia)
B12 - Megaloblastic anaemia, Neurological symptoms
Folic Acid - Megaloblastic anaemia

Vit C - Scurvy
Riboflavin (B2):
Coenzyme Form
Requiring Reaction
Clinical Manifestation
Coenzyme Form - flavin mononucleotide (FMN) & flavin dinucleotide (FAD)
Requiring Reaction - Redox reactions
Niacin (B3):
Coenzyme Form
Requiring Reaction
Clinical Manifestation
Coenzyme Form - Nicotinamide
Requiring Reaction - essential component of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). These are co-enzymes for many dehydrogenases and NADP is important for Heose Monophosphate shunt (HMP pathway) in glucose metabolism.
4 steps of Vitamin A Absorption
1. Hydrolysis by intestinal mucosa (release retinol and FFA)
2. Re-esterification and secretion in chylomicrons (storage in liver)
3. Plasma retinol binding protein in liver transports to extra hepatic tissues
4. Tissues contain cellular retinol binding protein that carries it to nucleus
Pyridoxine (B6):
Coenzyme Form
Requiring Reaction
Clinical Manifestation
Pyridoxine, pyridoxal & pyridoxamine all called pyridoxine
Coenzyme Form - Pyridoxal phosphate
Requiring Reaction - transamination, carboxylation and deamination reactions
3 Steps of Vitamin D absorption. How do problems with the liver or kidneys cause Vitamin D deficiency?
Synthesized endogenously
1. Sunlight transforms 7-dehydrocholesterol to cholecalciferol in the skin
2. This, plus dietary cholecalciferol is transformed to 25-hydroxycholecalciferol in the liver (disease stops process here)
3. 25-hydroxycholecalciferol 1-hydroxylase transforms it into 1,25 dihydroxycholecalciferol in the kidney in response to low plasma calcium. (disease stops process here)
Predict the reason for occurrence of fat soluble vitamin deficiency in patients with fat malabsorption.
If you are unable to properly digest fat from your diet, then you will not get the fat soluble vitamins diffused in them.
Describe the use of vitamin K as coenzme for gamma-carboxylation of inactive blood clotting factors in the liver.
Vitamin K dependent clotting factor precursors are: Prothrombin, VII, IX, X

A glutamyl residue in a precursor polypeptide receives O2 and CO2 for transformation to a glutamate residue, which is then capable of activation.

Up Regulation - Vitamin K
Down Regulation - Warfarin
Discuss hemorrhagic disease of the newborn. Predict the causes and effects of vitamin K deficiency
Newborn intestines have no bacteria and so cannot synthesize vitamin K. Milk provides only 20% needed.
Symptoms - bleeding at skin, umbilicus and viscera. Intracranial bleeding is most serious manifestation.
Treatment - a single intramuscular dose of vitamin K

Adult Deficiency - caused by fat malabsorption syndromes, destruction of vitamin K synthesizing bacteria (broad spectrum antibiotics) or diffuse liver disease (poor storage)
Symptoms - bleeding diathesis - susceptability to bleeding due to poor coagulation (hematomas, hematuria = blood in urine, melena = blood in feces, ecchymoses = bruising)
Discuss inhibition of gamma-carboxylation by warfarin
Blocks the activity of liver epoxide reductase, preventing regeneration of reduced vitamin K. This prevents carboxylation of Vitamin K dependent coagulation factors. They are produced, but have decreased functionality due to under-carboxylation.

Desirous in people with thrombo-embolic disease.
Discuss the toxicity of Vitamin A
(not an objective)
Toxicity - increased intracranial pressue, headaches, vomiting, papillodema and seizures which mimic brain tumors.
Symptoms - Dry skin & pruritis, dry mucous membranes, weight loss, nausea and vomitting, hepatomegaly with liver damage and fibrosis, leading to cirrhosis and portal hypertension.
Associated with very high risk of spontaneous abortions and congenital malformations!
Describe the deficiencies of dietary vitamin A and retinoids
1. Night blindness and xerophthalmia
- dryness of conjuctiva - lacrimal and mucous secreting epithelium is keritinized
- Bitot's spots - buildups of keratin debris in small opaque plaques on the sclera.
- Keratomalacia - erosion of roughened corneal surface with softening and destruction of the cornea
2. Increased risk of pulmonary infections due to loss of muco-ciliary epithelium
3. Immune deficiency - higher mortality from measles and diarrhoea.
Describe the functions of Vitamin A
(not an objective)
- Vision (retinaldehyde) - component of rhodopsin, the visual pigment of rod cells (low light vision). Visual cycle requires isomerisation of retinal.
- Growth & reproduction - ?
- Maintenance of specialized epithelial tissue (retinoic acid) - especialy differentiation of mucus secreters
- Host resistance to infection - 14 hydroxyretinol is an intermediate in metabolism that stimulates the immune system.
Discuss the formation and 4-step action of retinoic acid
Action
1. Retinol is oxidised to retinoic acid in the cytosol
2. It moves into the nucleus with the help of cellular retinoid binding proteins
3. It binds to intranuclear receptors forming and activated receptor complex
4. This complex binds to chromatin, activating the transcription of specific genes.
Describe the 7-step process of 11 -cis retinal use in vision.
1. Retinol is transported to the retina in plasma, where it enters pigment cells
2. It is esterified to a retinyl ester (trans-retinal = storage form)
3. Hydrolysed to form 11 -cis retinol or oxidised to 11 -cis retinal.
4. 11 -cis retinal enters the rod cell, combining with opsin to form rhodopsin
5. When exposed to light, rhodopsin photochemically isomerizes resulting in the bleaching of visual pigment and release of all trans retinal and opsin
6. Result is an electric signal to theoptic nerve which is interpretted as vision
7. Return to Step 4 and the regeneration of Rhodopsin.
Describe the functions of the active form of Vitamin D - 1, 25 dihydroxycholecalciferol (1, 25 dihydroxy-D) related to calcium metabolism
- It stimulates the intestinal absorption of calcium and phosphate by increasing the synthesis of calcium binding and transport proteins.

- Vitamin D and Parathyroid Hormone (PTH) collaborate to stimulat mobilisation of calcium and phosphorous from bone leading to higher blood levels.

- Kidneys Vitamin D stimulates the parathyroid dependent reabsorption of calcium from the distal renal tubules.
Describe the biochemical basis of clinical manifestation in rickets
Rickets - Net demineralisation of bone.
1. Inadequate calcification of epiphyseal cartilage during infancy
2. Formation of frontal bossing - flattening of occipital bones w/excess of osteoid production
3. Overgrowth of cartilage or osteoid tissue at costochondral junction producing rachitic rosary
4. Weakened metaphyseal areas of ribs bending inward creating protrusion of the sternum - pigeon chest deformity
5. If ambulatory, legs bow due to spine and long bone deformities
Describe the biochemical basis of clinical manifestation in osteomalacia
Osteomalacia - Weak bones, vulnerable to gross fractures in vertebral bodies and femoral necks.
Vitamin D deficiency in adults
Hypocalcemia and hypophosphatemia result in impaired mineralisation of bone matrix proteins and deranges normal bone remodelling causing osteomalacia.
Indicate the functions of some trace minerals like chromium, manganese, molybdenum and selenium
Dr. Baruah says not to worry about these.
Discuss the role of copper as a cofactor for enzymes
Cofactor for -
Cytochrome oxidase - ETC
Superoxide dismutase - removal of superoxide ions
Lysyl oxidase - collagen crosslinking
Tyrosinase - neurotransmitter synthesis
Discuss clinical manifestations and biochemical defects of defective copper metabolism in Menke's syndrome
X-linked congenital disorder where there is improper intestinal mobilisation of Cu. Involves nervous system, connective tissue and vasculature. Hair is sparse and steely and it is called Menke's kinky hair syndrome. Usually fatal in infancy.
Discuss clinical manifestations and biochemical defects of defective copper metabolism in Wilson's disease
Autosomal recessive disorder presenting around 6 yo.
1. Defective biliary secretion of Cu
2. Toxic accumulation in liver
3. Liver damage - hepatitis then cirrhosis (first symptom)
4. Excessive Cu moves to plasma
5. Secondary organs damaged
- RBCs - hemolysis
- Eye - KF rings (deposits of Cu in cornea)
- Brain - neurological damage leading to neuropsychiatric symptoms
Treatment - copper chelators - penicillamine therapy.
Discuss the labrotory findings for hereditary Hemochromatosis
Autosomal recessive disorder characterized by excessive accumlation of iron. Most of it is deposited in parenchymal organs like the liver and pancreas.
Toxic to tissues because -
1. lipid peroxidation via iron catalyses free radicals
2. DNA damage
Lab diagnosis - more common in males, presents in fourth decade of life - liver damage, diabetes (pancreatic destruction), cardiac dysfunction, actue synovitis, brownish skin pigmentation, high levels of serum iron and ferritin, iron content of unfixed liver tissue is dramatically increased.
What are the three forms of nutritional anemia. What deficiency is suffered in each?
Macrocytic - Vitamin B12, Folate
Norocytic - Protein-calorie manutrition
Microcytic - Iron, copper and pyridoxine deficiency Symptoms - weakness and pallor, fatigue, brittle nails, alopecia, pica (appetite for soil)
Compare and contrast the anticoagulant properties of Warfarin and Heparin.
X
Why can't retinoic acid be used to treat night blindness?
The active form of Vitamin A in vision is retinal. Retinoic acid is importan in the epithelium. Until it is esterized, retinol will not aid vision.
List the two steps of absorption in all fat soluble vitamins
1. Hydrolysis by intestinal mucosa (release retinol and FFA)
2. Re-esterification and secretion in chylomicrons (storage in liver)
What three pathologies is Vitamin A used as a medicine to treat?
It is used to treat dietary deficiency, acne & psoriasis (mild = retinoic acid, severe = isotretinoin), leukemia (given along with cheomotherapy for acute promyelocytic leukaemia).
What is another name for 1,25 dihydroxycholecalciferol?
Calcetriol
Discuss the biochemical basis for clinical manifestations in hereditary haemochromatosis
1. The liver releases stored iron while the intestines digest it from dietary sources.
2. Iron is converted to plasma transferrin iron.
3. This is delivered to the marrow erythroid precursors
4. Circulating erythroctyes are produced
5. RES stores are created -

If the HFE gene on the basolateral surface of intestinal crypt cells sense the systemic iron balance they stop storage. If there is a defect in this gene, absorption continues.

6. Plasma transferrin iron is recreated and stored in the liver