Chapter 8 Growth and Nutrition PDF

CHAPTER 8 Growth and Nutrition 123 Examination and Findings M1—Tanner 1 (preadolescent). Only the nipple is raised above the level of the breast, as in the child. M2—Tanner 2. Budding stage; bud-shaped elevation of the areola; areola increased in diameter and surrounding area slightly elevated. M3—T...

CHAPTER 8 Growth and Nutrition 123 Examination and Findings M1—Tanner 1 (preadolescent). Only the nipple is raised above the level of the breast, as in the child. M2—Tanner 2. Budding stage; bud-shaped elevation of the areola; areola increased in diameter and surrounding area slightly elevated. M3—Tanner 3. Breast and areola enlarged. No contour separation. M4—Tanner 4. Increasing fat deposits. The areola forms a secondary elevation above that of the breast. This secondary mound occurs in approximately half of all girls and in some cases persists in adulthood. M5—Tanner 5 (adult stage). The areola is (usually) part of general breast contour and is strongly pigmented. Nipple projects. FIG. 8.10 Five stages of breast development in females. (From Van Wieringen et al., 1971.) Delayed onset of puberty and secondary sexual characteristic development (at an age later than the average) may be a normal variant in both males and females or may be a deliberate consequence of the use of puberty blockers in transgender and gender-­diverse youth. It is usually accompanied by a lag of stature growth. A parent or sibling often may have had a similar adolescent growth pattern. Once pubertal changes begin, the sequence of development is the same as for other adolescents, but it may occur over a different time span. Ultimate height may still be the same. Further evaluation is needed if no evidence of pubertal development is seen in a male by 14 years of age or a female by 13 years of age (Kaplowitz et al., 2016). Early development of sexual hair without signs of sexual maturation may be an indication of premature pubarche. In these children, pubescence usually occurs at the expected time, as with healthy children. Think About It How Do Puberty Blockers Work? Puberty blockers -­ Gonadotropin-­releasing hormone (GnRH analogs) are a synthetic form of the human body’s GnRH hormone. When taken regularly, GnRH analogs work by suppressing the secretion of LH and FSH which ultimately suppress the body’s release of sex hormones, including testosterone and estrogen, during puberty. Blocking the release of these hormones delays changes in both the primary and secondary sex characteristics that can affect gender expression. In those identified as male at birth, GnRH analogs decrease the growth of facial and body hair, prevent voice deepening, and limit the growth of genitalia. In those identified as female at birth, GnRH analogs stop breast development, widening of the hips, and delay or stop menstruation. Puberty blockers do not stop acne, body odor, or axillary and pubic hair development, as these changes are not controlled only by estrogen or testosterone. The use of GnRH analogs does not cause permanent changes in an adolescent’s body. Instead, it pauses puberty, providing time to solidify gender identity, treat gender dysphoria, and promote mental well-­being. If an adolescent stops taking GnRH analogs, puberty will resume. Examination and Findings 124 CHAPTER 8 Growth and Nutrition P1—Tanner 1 (preadolescent). No growth of pubic hair. P2—Tanner 2. Initial, scarcely pigmented straight hair, especially along medial border of the labia. P3—Tanner 3. Sparse, dark, visibly pigmented, curly pubic hair on labia. P4—Tanner 4. Hair coarse and curly, abundant but less than adult. P5—Tanner 5. Lateral spreading; type and triangle spread of adult hair to medial surface of thighs. P6—Tanner 6. Further extension laterally, upward, or dispersed (occurs in only 10% of women). FIG. 8.11 Six stages of pubic hair development in females. (From Van Wieringen et al., 1971.) Pregnant Patients Calculate the weight gain during pregnancy from the patient’s prepregnancy weight. To provide guidance in weight gain during pregnancy, first determine the prepregnancy BMI. Then, monitor the patient’s weight throughout pregnancy using the BMI weight gain curve guidelines on the prenatal weight gain chart (Fig. 8.14). Guidelines for recommended weight gain during pregnancy are based on the patient’s prepregnancy BMI to improve reproductive outcomes. Patients with a prepregnancy BMI of 19.8 to 26.0 should gain 11.5 to 16 kg (25 to 35 lb) over the entire pregnancy. Underweight patients (BMI 29) should gain no more than 5 to 9.1 kg (11 to 20 lb) (Institute of Medicine and National Research Council, 2009). Adjust the recommended weight gain for patients with a twin or triplet pregnancy. Obese patients are at increased risk of complications during pregnancy such as gestational hypertension, preeclampsia, gestational diabetes, cesarean delivery, and fail- ure to initiate breastfeeding (Reinold et al., 2011). Pregnant adolescents younger than 16 years, or less than 2 years after menarche, may still be in their growth spurt. They may require higher weight gains during pregnancy to achieve an optimal infant birth weight (Fernandez et al., 2008). Note any variation from the expected weight gain. First trimester gain is variable, from 1.4 to 2.7 kg (3 to 6 lb). In the second and third trimesters, weekly weight gain should be approximately 0.23 to 0.45 kg (0.5 to 1 lb) per week. Patients who gain too little weight during pregnancy are at risk for having a low-­birth-­weight infant. Those who gain too much weight are at risk for having a high-­ birth-­weight infant, which may lead to a difficult delivery (Reinold et al., 2011). Older Adults Measurement procedures for the older adult are the same as those used for other adults. Calculate the BMI. Identify any problems with underweight that could be associated with a health condition or food insecurity. Of older adults in the United States in 2017–18, 42.4% of men and 43.3% of women were obese (Hales et al., 2020). Growth and Nutrition G1—Tanner 1. Testes, scrotum, and penis are the same size and shape as in the young child. G2—Tanner 2. Enlargement of scrotum and testes. The skin of the scrotum becomes redder, thinner, and wrinkled. Penis no larger or scarcely so. G3—Tanner 3. Enlargement of the penis, especially in length; further enlargement of testes; descent of scrotum. G4—Tanner 4. Continued enlargement of the penis and sculpturing of the glans; increased pigmentation of scrotum. This stage is sometimes best described as “not quite adult.” 125 G5—Tanner 5 (adult stage). Scrotum ample, penis reaching nearly to bottom of scrotum. FIG. 8.12 Five stages of penis and testes/scrotum development in males. (From Van Wieringen et al., 1971.) ABNORMALITIES GROWTH Acromegaly A rare disease of excessive growth and distorted proportions caused by hypersecretion of growth hormone and insulin-­like growth factor after closure of the epiphyses PATHOPHYSIOLOGY A benign pituitary adenoma or other rare tumor is the most common cause; familial syndromes (e.g., multiple endocrine neoplasia type 1 and McCune-­ Albright syndrome). Growth hormone excess leads to slow skeletal growth and soft tissue enlargement. Most common in middle-­aged adults. PATIENT DATA Subjective Data Slow progressive changes in facial feature exaggeration Increased shoe size, ring size No change in height Oily and sweaty skin Excessive snoring, sleep apnea Decreased exercise tolerance Pain in joints and hands See Fig. 8.15 Objective Data Face and skull—frontal skull bossing, cranial ridges, mandibular overgrowth, maxillary widening, teeth separation, malocclusion, overbite Skin thickening on the face (tongue, lips, and nose), hands, and feet leading to enlargement Joint enlargement, swelling, pain; vertebral enlargement, kyphoscoliosis Cardiac ventricular enlargement bilaterally with decreased exercise tolerance Abnormalities CHAPTER 8