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18 Cards in this Set

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Cause of red dry scaly (squamous) dermatitis with easily bleeding lesions, which can be treated by rubbing the skin with sunflower oil
Linolenic Acid in diet
6,9,12-octadecatrienoic acid.
A young child presents with a LONGSTANDING COAGULOPATHY by promyelocyte (PML) differentiation failure
PML gene fuses with the RAR gene (Retinoic Acid Receptor) on chromosome 17 to initiate PML differentiation
Cofactor for XANTHINE OXIDASE
Molybdenum
for Uric Acid formation
Cofactor for:
SUPEROXIDE DISMUTASE
GLYCOSYL TRANFERASE
Manganese
for mucopolysaccharides formation
Cofactor for:
GLUTATHIONE PEROXIDASE
Selenium
serve as an antioxidant role in the cytoplasm to minimize oxidative injury
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
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
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
Excess of which Vit can cause ALOPECIA (baldness), HEADACHE, yellow-like skin (no bilirubin), Arthralgia, sore thoart, fatigue
Vitamin A
Which of vitamins involve aa metabolism
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
Dark urine is apparent upon standing
- 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
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
ADH Effects on CNS
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
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]
AVPR1B: V1b receptor
- phosphatidylinositol/calcium
- pituitary gland, brain
- Adrenocorticotropic hormone secretion in response to stress[4];
- Social interpretation to olfactory cues[5]
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
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
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