NITROGENOUS COMPOUNDS • The daily requirement of prot ein for adults is 0.5-1g/kg body weight. The minimum requirements of protein are about 20g first class protein per day. • The protein allowance for children is relativ ely higher because of the protein needs of growth. The d aily requirements for inf ants and children are 2-3g/kg and 2g/kg body weight respectively.
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Non-Protein Nitrogenous Constituents of Blood - Urea, Uric Acid Etc
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• There are special clinical effects of protein deficiencywhich are important not only from a diagnostic pointof view but also for an understanding of the associatedmedical and surgical problems.
• A moderate inadequacy of protein in the diet leads tofatigue and irritability before the symptoms associatedwith protein deficiency develop. In children, proteindeficiency retards growth.
• Some of the manifestations associated with prolongedperiods of protein deficiency are as follows:
• Liver damage and greater susceptibility of theliver to intoxication by drugs. In growing children,chronic protein and vitamin deficiency mayproduce chronic hepatitis similar to cirrhosis
• Protein deficient persons are susceptible to liverdamage disease because diets deficient inproteins are also deficient in lipotrophic factorswhich protect the integrity of the liver cells.
• The lipotrophic factors are substances which arresponsible for normal hepatic metabolism oflipids eg. Choline and mithionine
• In Africa, such a condition constitutes the principalfeature of the nutritional disease known askwashiorkor. This condition occurs in children who livesolely on carbohydrate after weaninig
• It is characterized by oedema, as well as skin and hairdilutions. In marasmus, a condition which occurs as aresult of protein and carbohydrate deficiency, there isless oedema or skin and hair change than in
kwashiorkor• A biochemical assessment of protein malnutrition may
• This is usually observed during growth andpregnancy. It may also result from the action ofexcess protein anabolic hormones which may begive n as treatment eg. Testosterone
administration fro the treatment of carcinoma ofthe breast.
• In people whose diet contains adequatequantities of energy and the various classes of
food substances, high dietary proteins lead to apositive nitrogen balance and increased levels oftissue protein.
NITROGEN PROTEIN BALANCE• Deficient protein intake
a negative nitrogen balance ensues within 48 hours after thedietary protein intake has fallen far below the acceptableminimum i.e. 0.5g/Kg body weight. This condition may alsoresult when protein intake is qualitatively inadequate or whentotal energy intake is low.
Diminished protein digestion
this condition ensues in the event of pancreatic dysfunctionowing to the impaired secretion of proteolytic enzymes
(trypsin, chymotrypsin, carboxypeptidase, etc) thisimpairment also results during kwashiorkor
• Pregnancy: owing to the tendency ofincreased glomerular filtration rate anddiversion of nitrogen to the foetus as well as
water retention during late pregnancy, lowplasma urea levels are encountered.
• Acute hepatic necrosis may lead to lowplasma urea levels owing to the inability ofthe liver to further metabolize amino acidsand hence impaired urea synthesis.
• Steps b, c and 2 are causes of secondaryhyperuricaemia. Increased synthesis(i.e. step a)due to impaired feed back control, is probably themost important mechanism causing primaryhyperuricaemia.
• EFFECTS OF HYPERURICAEMIA: GOUT
• The solubility of urate in plasma is limited; its
precipitation in tissues is influenced by pH andtrauma. At physiological pH, plasma urate occursas the monosodium salt.
• Crystallization of this salt from supersaturatedbody fluids particularly in joints results in theclassical pictures of gout or gouty arthritis whichwas first described by Hippocrates in 469 BC.
• The acute joint manifestation of gout results fromthe fact that the urate crystals in joint cavities arephagocytosed by leucocytes; the lysosomal
membranes of which are destroyed by thecrystals causing the release of lactic acid andtherefor a full in the local pH.
• There may be precipitation of urate in thekidney leading ultimately to kidney failure ifthere is an obstruction ot outflow of urine.
• In the absence of other diseases, gout is acondition of the male, with only 3-7% of theprimary cases occurring in women. It oftenappears in the fourth decade of life. Shortly
before and during an acute attack, the plasmaurate rises to about 0.9mmol/l.
• The biochemical lesions in most cases of gout arenot well characterized. Some patients have apartial deficiency of HGPRT leading to reducedsynthesis of guanine monophosphate and inosine
monophosphate by the salvage route.• There is concomitant increase in the
concentration of PRPP and thus and elevation ofthe de novo synthesis of purine nucleotides. In
some other cases, the enzymes responsible forthe synthesis of PRPP are very high; hence thehigh levels of PRPP which is observed.
• Children with this condition have grossly distortedbehavior. Though capable of warm affection, theyusually lapse into excessive aggression, directed atthemselves as well as others
• Glucose-6-phosphate deficiency (von Gierke’s Disease)which leads to increased channeling of glucose-6-phosphate into the pentose phosphate pathway whichultimately enchances urate production and glycolysis,
thus increasing lactic acid production, which reducesrenal urate excretion.
• The normal level of plasma creatine is 15-60mmol/L and forplasma creatinine for both male and female is 60-120mmol/L. for females only, it is 40-110mmol/L and formales, it is 60-130mmol/L. plasma creatinineconcentration is used as a diagnostic tool in the assessment
of renal function.• Creatinuria
• This condition is found in patients with muscle disease.When active breakdown of muscle ensues, the conversionof creatine to creatinine is impaired thus leading to
increased plasma creatine concentration. Thus ultimalyleads to high levels of creatine in the urine.
• The normal amino acids excretion in the urine ofadults(healthy) is 4-20mmol/24 hours. The factorswhich could lead to in creased amounts of amino acids
in the urine may be catalogued into two as follwos:
• primary amino acidurias are a group of inborn errorsof metabolism characterized by and enzyme defecteither in the pathway by which a specific amino acid si
metabolized, eg. Phenylketonuria; or in the specificrenal tubular transport system by which the amino acidis reabsorbed eg. cystinuria
• Secondary amino aciduria is due to disease of an organsuch as the liver, (which is an active site of amino acidmetabolism), to generalized renal tubular dysfunctionor to protein-energy malnutrition.
• Amino aciduria may also be ‘overflow’ or ‘renal’
• ‘overflow’ amino aciduria which may be either primaryeg. Phenylketonuria; or secondary eg. Fulminanthepatic failure, is due to increase in the plasma level of
one or more amino acids to such an extent that anexcess passes into the urine.