11. A 6-yr-old boy has an actual weight of 15 kg & height of 105 cm. Compute for the wt-for-ht%. Actual Wt = 15 kg Actual Ht = 105 cm IBW based on actual age (6 yr) = 20 kg IBW based on plotted Ht = 17 kg Wt-for-Ht% = 15/ 17 = 0.88 Wt-for-age% = 15/ 20 = 0.75 Ht-for-age% = 105 / 110 = 0.95
43. Rickets A teenage male w/ rickets. Note bow legs & compromised height. Distal femur, proximal tibia and fibula in rickets. Note widening epiphysis, resorption of provisional zone of calcification, flaring metaphysis & bone deformity.
44.
45. Osteomalacia A young male w/ osteomalacia. Note a pseudofracture in the medial edge of the upper femoral shaft (arrow). Xray showing a pseudofracture (red arrow) from an adult who has x-linked hypophosphatemic rickets. This sign is seen only in osteomalacia, but not in many of the cases. AP pelvis in a patient w/ osteomalacia. The film shows diffuse osteopenia, & a Looser zone (arrow) in the superior ramus of the right obturator ring.
93. Be master of your habits, Or they will master you. Thank You!
Notas del editor
PEM describes certain signs & symptoms in infants & young children which result from a deficiency of calories &/or proteins in their diets.
*Wasting : acute, current, short-duration undernutrition, where weight-for-age & weight-for-height are low but height-for-age is normal *Stunting : past, chronic undernutrition, where weight-for-age and height-for-age are low but weight-for-height is normal *Wasting and stunting : acute and chronic or current long-duration undernutrition, where weight-for-age, height-for-age and weight-for-height are all low. This classification makes a distinction between current and past influences on nutritional status. It helps the examiner assess the likelihood that supplementary feeding will markedly improve the nutritional status of the child, and it gives the clinician some clue as to the history of the malnutrition in the patient. It also has advantages for nutritional surveys and surveillance. In general, stunting is more prevalent than wasting worldwide.
*Another factor that is attributed to the development of kwashiorkor is aflatoxin poisoning. Aflatoxins are produced by certain molds, and are ingested in connection with moldy foods. They can damage the liver DNA and subsequently interfere with the production of serum albumin.
*Thus, it affects many physiologic processes, including reproduction, growth, embryonic and fetal development, and bone development, in addition to respiratory, gastrointestinal, hematopoietic, and immune functions.
*The risk of symptomatic vitamin E deficiency increased by the use of formulas that has a high content of PUFAs high content of PUFAs in RBCs + Fe (increases the production of oxygen radicals) oxidative stress ** Loss of deep tendon reflexes usually initial finding Subsequent include limb ataxia (intention tremor, dysdiadochokinesia), truncal ataxia (wide-based, unsteady gait), dysarthria, ophthalmoplegia (limited upward gaze), nystagmus, decreased proprioception (positive Romberg test), decreased vibratory sensation, and dysarthria Pigmentary retinopathy may progress to blindness Cognition and behavior may also be affected Myopathy and cardiac arrhythmias less common
Thiamine, Riboflavin, Niacin, Pyridoxine are cofactors to enzymes in energy metabolism, hence, deficiencies show up in quickly growing tissues such as epithelium as well as nerve cells that use lots of energy .
A block in DNA synthesis due to folate deficiency slows down the maturation of red blood cells, causing production of abnormally large "macrocytic" red blood cells with fragile membranes. The rapid hemolysis of these macrocytes leads to a hemolytic anemia. A macrocytic anemia associated with megaloblastic changes in the bone marrow is fairly characteristic of folate deficiency.
*The megaloblastic anemia associated with the B12 deficiency is thought to be due to the effect of B12 on folate metabolism. High levels of supplemental folate can overcome the megaloblastic anemia but not the neurological problems. **The neurological disorders seen in B12 deficiency are due to progressive demyelination of nervous tissue. It has been proposed that the methylmalonyl- CoA which accumulates in B12 deficiency interferes with myelin sheath formation.
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