By P. Armon. University of Baltimore.
The polyol pathway of sorbitol production and the HMP shunt pathway are linked by which of the following? The pathways for oxidation of fatty acids bupron sr 150mg with mastercard mood disorder nos icd 10, Krebs first formulated its reactions glucose buy bupron sr 150mg without a prescription mood disorder hcc, amino acids, acetate, and ketone bodies all generate acetyl CoA, into a cycle. It is also called the “citric acid which is the substrate for the TCA cycle. As the activated 2-carbon acetyl cycle” because citrate was one of the first group is oxidized to two molecules of CO2, energy is conserved as NADH, compounds known to participate. The most common name for this pathway, the tricar- FAD(2H), and GTP (Fig. NADH and FAD(2H) subsequently donate boxylic acid or TCA cycle, denotes the electrons to O2 via the electron transport chain, with the generation of ATP involvement of the tricarboxylates citrate from oxidative phosphorylation. Thus, the TCA cycle is central to energy gen- and isocitrate. Within the TCA cycle, the oxidative decarboxylation of -ketoglutarate is cat- The major pathways of fuel oxida- alyzed by the multisubunit -ketoglutarate dehydrogenase complex, which con- tion generate acetyl CoA, which is tains the coenzymes thiamine-pyrophosphate, lipoate, and FAD. In plex, the pyruvate dehydrogenase complex (PDC), catalyzes the oxidation of the first step of the TCA cycle, the acetyl por- pyruvate to acetyl CoA, thereby providing a link between the pathways of glycoly- tion of acetyl CoA combines with the 4- sis and the TCA cycle (see Fig. In the next two oxidative transferred to NAD and FAD and also the carbon in the two CO2 molecules that decarboxylation reactions, electrons are are produced. Oxaloacetate is used and regenerated in each turn of the cycle (see transferred to NAD to form NADH, and 2 Fig. However, when cells use intermediates of the TCA cycle for molecules of electron-depleted CO2 are released. Subsequently, a high- energy phosphate bond in GTP is generated from Glucose Fatty acids substrate level phosphorylation. In the Pyruvate remaining portion of the TCA cycle, succi- Ketone bodies nate is oxidized to oxaloacetate with the generation of one FAD(2H) and one NADH. CO2 The net reaction of the TCA cycle, which is the sum of the equations for individual Acetate Acetyl CoA Amino acids steps, shows that the two carbons of the CoASH acetyl group have been oxidized to two mol- OxaloacetateOxaloacetate + (4c)(4c) ecules of CO2, with conservation of energy NADH + H Citrate (6c)Citrate (6c) as three molecules of NADH, one of Malate (4c)Malate (4c) Isocitrate (6c)Isocitrate (6c) FAD(2H), and one of GTP. Fumarate (4c)Fumarate (4c) Tricarboxylic acid NADH + H+ FAD (2H) (TCA) cycle Succinate (4c)Succinate (4c) CO 2 αα-Ketoglutarate (5c)-Ketoglutarate (5c) GTP Succinyl-Succinyl- NADH + H+ GDP CoACoA (4c) CO2 Net reaction Acetyl CoA + 3NAD+ + FAD 2CO + CoASH + 3NADH + 3H+ 2 + GDP + P + 2Hi 2O + FAD (2H) + GTP Fig. The TCA cycle occurs in the mitochondrion, where its flux is tightly coordi- nated with the rate of the electron transport chain and oxidative phosphorylation through feedback regulation that reflects the demand for ATP. The rate of the TCA cycle is increased when ATP utilization in the cell is increased through the response of several enzymes to ADP levels, the NADH/ NAD ratio, the rate of FAD(2H) oxidation or the Ca2 concentration. For example, isocitrate dehydro- genase is allosterically activated by ADP. There are two general consequences to impaired functioning of the TCA cycle: (1) an inability to generate ATP from fuel oxidation, and (2) an accumulation of TCA cycle precursors. For example, inhibition of pyruvate oxidation in the TCA cycle results in its reduction to lactate, which can cause a lactic acidosis. The most common situation leading to an impaired function of the TCA cycle is a rela- tive lack of oxygen to accept electrons in the electron transport chain. THE WAITING ROOM Otto Shape, a 26-year-old medical student, has faithfully followed his diet and aerobic exercise program of daily tennis and jogging (see Chapter 19). He has lost a total of 33 lb and is just 23 lb from his college weight of 154 lb. His exercise capacity has markedly improved; he can run for a longer time at a Vitamins and minerals faster pace before noting shortness of breath or palpitations of his heart. Even his required for the TCA cycle test scores in his medical school classes have improved. In Riboflavin (FAD) addition to a low body weight, decreased muscle mass, glycogen, and fat Pantothenate (CoA) stores, she has iron-deficiency anemia (see Chapter 16). She has started to Thiamine gain weight, and is trying a daily exercise program.
For vitamin cheap 150 mg bupron sr overnight delivery depression symptoms negative thinking; it can be synthesized in the body from GTP quality 150 mg bupron sr mood disorder screening test. However, as is the case with the most part, the condition appears to be other cofactors, the body contains limited amounts. Therefore, dihydrobiopterin benign, and dietary restriction of protein must be reconverted to tetrahydrobiopterin for the reaction to continue to produce returns plasma tyrosine levels to normal. The biochemical defect is most likely a low level, tyrosine. Because this Phenylalanine enzyme requires ascorbate, ascorbate sup- plementation also aids in reducing circulat- ing tyrosine levels. Other types of tyrosinemia are related to Tyrosine specific enzyme defects (see Fig. Tyrosinemia II is caused by a genetic defi- Tryptophan ciency of tyrosine aminotransferase (TAT) and may lead to lesions of the eye and skin as well Homogentisic acid as neurologic problems. Patients are treated Formate with a low-tyrosine, low-phenylalanine diet. Tyrosinemia I (also called tyrosinosis) is Fumarate TCA caused by a genetic deficiency of fumary- Alanine Threonine lacetoacetate hydrolase. The acute form is Glucose associated with liver failure, a cabbagelike Pyruvate odor, and death within the first year of life. Glucose Acetyl CoA Acetoacetate Nicotinamide moiety of Lysine Leucine NAD, NADP Isoleucine Succinyl CoA In addition to methionine, threo- Glucose nine, isoleucine, and valine (see Fig. Some of these amino acids (tryptophan, phenylalanine, the -end of odd-chain fatty acids, and tyrosine) also contain carbons that can form glucose. Leucine and lysine are strictly keto- form succinyl CoA by this route (see Chapter genic; they do not form glucose. These infants exhibit CO2 normal phenylalanine hydroxylase (PAH) OH activity but have a deficiency in dihy- dropteridine reductase (DHPR), an enzyme C – CH2 COO required for the regeneration of tetrahydro- C biopterin (BH4), a cofactor of PAH (see Fig. Less frequently, DHPR activity is nor- mal but a defect in the biosynthesis of BH4 Alcaptonuria homogentisate oxidase exists. In either case, dietary therapy cor- rects the hyperphenylalaninemia. However, BH4 is also a cofactor for two other hydroxy- lations required in the synthesis of neuro- Tyrosinemia I fumarylacetoacetate hydrolase transmitters in the brain: the hydroxylation of tryptophan to 5-hydroxytryptophan and O of tyrosine to L-dopa (see Chapter 48). It has –OO COO– CH C CH OO– 3 2 been suggested that the resulting deficit in Fumarate Acetoacetate central nervous system neurotransmitter activity is, at least in part, responsible for the Fig. The carboxyl carbon forms CO2, and neurologic manifestations and eventual the other carbons form fumarate or acetoacetate as indicated. Deficiencies of enzymes (gray death of these patients. Tryptophan tryptophan are insufficient, the Tryptophan is oxidized to produce alanine (from the non-ring carbons), formate, and condition known as pellagra acetyl CoA. Tryptophan is, therefore, both glucogenic and ketogenic (Fig. The symptoms of pellagra are der- matitis, diarrhea, dementia, and, finally, NAD and NADP can be produced from the ring structure of tryptophan. In addition, abnormal metabolism of fore, tryptophan “spares” the dietary requirement for niacin. The higher the dietary tryptophan occurs in a vitamin B6 deficiency. Threonine, Isoleucine, Leucine, and Lysine vitamin B6. Consequently, these intermedi- ates enter a minor pathway for tryptophan As discussed previously, the major route of threonine degradation in humans is by metabolism that produces xanthurenic acid, threonine dehydratase (see section III. In a minor pathway, threonine degra- which is excreted in the urine.
The need for a supported head- rest in this group is variable bupron sr 150mg on-line depression great, and has to be assessed on an individual basis generic bupron sr 150mg mood disorder hallucinations. A lap tray should always be ordered for use when children are sitting in the chair and engaged in upper extremity activities. The lap tray is also an im- portant assist for postural control to prevent forward slouching. Especially for young children, the work surface to do upper extremity activities is al- Figure 6. The lap tray is very important most never at the right height unless a lap tray is routinely used. This lap tray and should not be forgotten as part of the allows children to have the ideal level and most functional work area for fine wheelchair. It is an important aspect of po- motor skills activity development (Figure 6. Usually, these trays are at- sitioning to prevent the child from leaning tached to adjustable armrests so they can be raised or lowered to the correct forward. It is a work and feeding area for the child, and if the tray is made of clear mate- height for the individual child. Adolescent Needs There is a group of adolescents with fair upper extremity function who can propel themselves in the community. However, it is much more common for adolescents who require a wheelchair for all community ambulation to have so little upper extremity function that self-propelling a wheelchair is not pos- sible. If these individuals are otherwise appropriate, a power mobility system is preferred. At this age, it is very important to have flip-up or swing-away footrests as the caretakers now depend much more on standing transfers. Usually, the seating system must continue to have a similar construction, as described earlier. Again, some of these adolescents can use crutches for short household ambulation, and in these cases, the wheelchair should be fitted with crutch holders. Children Who Are Dependent in All Transfers Childhood Needs Children who are fully dependent for all their transfer needs usually require sig- nificant supportive seating by age 12 months, and the first special seating and mobility system is typically obtained between the ages of 12 and 24 months. Usually, this first chair is a tilt-in-space stroller base with solid footrests. The seating system requires full chest laterals, anterior trunk support, and a head- rest to assist with head control. A lap tray should be included because the system is often used as a feeding and seating system, and is a play area for these children’s play stimulations and fine motor skills development. By the second or third wheelchair, usually obtained around 5 or 6 years of age, a standard wheelchair base is ordered. A completely supported seating system is still required. Often, a tilt-in-space base is helpful to allow children to tilt back and rest. These children are seldom candidates for power mobility con- sideration until late childhood or early adolescence. Exceptions to this are chil- dren with athetosis who often have excellent cognitive function and demon- strate sufficient hand function. Occasionally, children with these indications may be considered for power mobility as young as 4 or 5 years of age. Usually, at age 10 to 12 years, a final evaluation can be made to assess the possibility of these adolescents using power mobility. This age is also when skeletal deformities are most common and problematic to deal with from a seating perspective. As children are getting heavier and having some increasing deformities, the possibility of skin breakdown also becomes most predominant.
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