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18 Cards in this Set
- Front
- Back
Cause of red dry scaly (squamous) dermatitis with easily bleeding lesions, which can be treated by rubbing the skin with sunflower oil
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Linolenic Acid in diet
6,9,12-octadecatrienoic acid. |
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A young child presents with a LONGSTANDING COAGULOPATHY by promyelocyte (PML) differentiation failure
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PML gene fuses with the RAR gene (Retinoic Acid Receptor) on chromosome 17 to initiate PML differentiation
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Cofactor for XANTHINE OXIDASE
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Molybdenum
for Uric Acid formation |
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Cofactor for:
SUPEROXIDE DISMUTASE GLYCOSYL TRANFERASE |
Manganese
for mucopolysaccharides formation |
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Cofactor for:
GLUTATHIONE PEROXIDASE |
Selenium
serve as an antioxidant role in the cytoplasm to minimize oxidative injury |
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Cofactor for:
COLLAGENASE CO2 ANHYDRASE; CARBOXYPEPTIDASE; ALKALINE PHOSPHOTASE LACTASE DEHYDROGENASE DNA & RNA POLYMERASE |
Zinc
Its deficiency leads to a Scurvy-like syndrome with a concomitant decrease in smell & state |
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Cofactor is used to form
Methylmalonyl-CoA Is used in various carboxylation reactions |
Biotin = Vit B7
Conversion of: Pyruvate --> Oxaloacetate Acetyl-CoA --> Malonyl-CoA Propionyl-CoA --> MethylMalonyl-CoA |
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Vit deficiency can has lesions
1- Perioral lessions, malar rash, glossitis 2- Beefy glossitis & 3D's: Diarrhea, Dermatitis, Dementia (Pellagra's) 3- Angular cheilitis, glossitis 4- Bright red, atrophic tongue 5- Swollen gums, bruising, poor wound healing |
1- B2 Riboflavin
2- B3 Niacin (PP): anti-black-tongue factor 3- B6 Pyridoxine 4- B12 Cobalamin 5- C Ascorbic Acid |
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Excess of which Vit can cause ALOPECIA (baldness), HEADACHE, yellow-like skin (no bilirubin), Arthralgia, sore thoart, fatigue
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Vitamin A
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Which of vitamins involve aa metabolism
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1) B3: is derived from Tryptophan, NADP --> NAD
2) K : catalyzes gamma-carboxylation of glutamic acid residues 3) C : Hydroxylation of prolin & lysine in collagen synthesis |
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Dark urine is apparent upon standing
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- ALKAPTONURIA: AR by mutation in HGD gene on 3q
Excretion of homogentisic acid Homogentisate 1,2-dioxygenase deficiency In the catabolism of phenylalanine and tyrosine - PORPHYRIA Disorders involving heme biosynthesis, May be inherited (Uroporphyrinogen I synthase defection -> - Uroporphyrin but +++ Delta ALA & Porphobilinogen) or be acquired (hexachlorobenzene) Psychiatric and abdominal symptoms |
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Arginine vasopressin (AVP) = argipressin = antidiuretic hormone (ADH)
V1 receptor |
AVP allows water reabsorption by the introduction of additional water channels in cortical and inner medullary collecting ducts
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ADH Effects on CNS
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1- Implicates in memory formation
2- Involves in aggression, blood pressure regulation and temperature regulation. 3- Seems to induce the male to become aggressive towards other males |
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AVPR1A: V1a receptor
- phosphatidylinositol/calcium - In liver, kidney, peripheral vasculature, brain |
- Vasoconstriction, gluconeogenesis
- Platelet aggregation,release of factor VIII & von Willebrand factor - Social recognition[2], circadian tau[3] |
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AVPR1B: V1b receptor
- phosphatidylinositol/calcium - pituitary gland, brain |
- Adrenocorticotropic hormone secretion in response to stress[4];
- Social interpretation to olfactory cues[5] |
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AVPR2: V2 receptor
- adenylate cyclase/cAMP - apical membrane of lined collecting duct cells (especially the cortical and outer medullary of it) |
- Insertion of aquaporin-2 (AQP2) channels (water channels)which allows water to be reabsorbed down an osmotic gradient, and so the urine is more concentrated.
- Release of von Willebrand factor and surface expression of P-selectin through exocytosis of Weibel-Palade bodies from endothelial cells |
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HARTNUP disease
- Autosomal Recessive - Increased urinary excretion of tryptophan derivatives - tryptophan for nicotinic acid synthesis -> damage to nervous S. & skin. |
- Aminoaciduria which is due to a defect of Na+-neutral amino acid cotransport in renal tubulars
- Sx: Pellagralike, light-sensitive skin rash. temporary cerebellar ataxia |
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Cystinuria
- Autosomal Recessive - Increased urinary excretion of Cystine, Arginine, lysin, ornithine & nephrolithiasis |
- Defect of the amino acid exchanger for neutral & dibasic acids in renal tubulars.
- In familial protein intolerance the reabsorption of dibasic amino acids is abnormal |