Professional Documents
Culture Documents
(Adrenals na dapat ang start ng trans namin pero isinama ko ulit ung o Low level of 1,25 OH2D3
Calcium Homeostasis kasi may ilang slides na hindi naisama sa part na o Normal serum magnesium
un) o Low serum PTH
o X-ray of the bones: increased density limited to the
CALCIUM HOMEOSTASIS metaphyses
PTH & Vit.D are the principal regulators of calcium homeostasis o X-ray and CT of the skull: calcifications in the basal ganglia
o ECG: prolonged QT interval
Calcitonin & PTH-related peptide (PTHrP) – important primarily in
o EEG: widespread slow activity
the fetus
Management
In the parathyroid gland, pre-pro-PTH & a proparathyroid hormone o Emergency treatment for neonatal tetany: 5-10 ml of 10%
are synthesized--- pre-pro-PTH converted to pro-PTH- solution of calcium gluconate IV at a rate of 0.5-1 mL/min
converted to PTH (rapidly cleaved in the liver & kidney into smaller while HR is monitored
fragments)
PTH has C-terminal, mid-region & N-terminal fragments
o 1,25-dihydroxycholecalciferol (calcitriol) should be given –
o N-terminal – assay most useful for detecting acute secretory initial dose 0.25 ug/day & MD 0.01-0.1 ug/kg/day; given in 2
equal divided doses
changes
o Management
o C-terminus & mid-region – inert & represent 80% of plasma
o Supplemental calcium gluconate or glubionate to provide 800
immunoreactive PTH
o C-terminal assay – detects hyperparathyroidism mg of elemental calcium daily
o Reduce high phosphorus content in diet such as milk, eggs &
When serum Ca falls, secretion of PTH increases.
cheese
PTH stimulates 1-a-hydroxylase in the kidney--enhances o Frequent monitoring of serum calcium levels
production of 1,25-OH2D3-- induces synthesis of a Ca-binding
protein (calbindin-D) in the intestinal mucosa with Ca absorption HYPERPARATHYROIDISM
PTH mobilizes Ca by directly enhancing bone resorption Excessive production of PTH due to primary defect of the
Hypocalcemia induces increased PTH secretion; hypercalcemia parathyroid glands such as adenoma or hyperplasia; may also be
depresses PTH secretion. due to vitamin D excess
Calcitonin – 32-AA polypeptide; secreted in parafollicular cells (C Increased PTH production is compensatory aimed at correcting
cells) of the TG hypocalcemic states of diverse origins
o In the fetus, high levels augment bone metabolism & skeletal Childhood occurrence is rare; usually due to a single benign
growth stimulated by the normally high fetal Ca levels. adenoma manifested after 10 yrs of age
o Main biologic effect: inhibition of bone resorption by decreasing Some occur as part of multiple endocrine neoplasia (MEN)
the number & activity of bone-resorbing osteoclasts. syndrome (AD) characterized by hyperplasia or neoplasia of the
endocrine pancreas, the anterior pituitary & parathyroid glands
HYPOPARATHYROIDISM Clinical Manifestations
Hypocalcemia is common from 12-72 hrs of life esp.in premature o Muscular weakness, anorexia, nausea, vomiting, constipation,
infants, in infants with asphyxia at birth & in infants of diabetic polydipsia, polyuria, loss of weight, fever
mothers o Progressively diminished renal function in chronic cases
Clinical Manifestations o Osseous changes may produce pain in the back or extremities,
o Muscular pain and cramps – early gait disturbances, fractures
o Numbness, stiffness, tingling of the hands & feet o Abdominal pain
o (+)Chvostek or Trosseau sign or laryngeal & carpopedal spasm o Parathyroid crisis: serum calcium >15 mg/dL, progressive
o Convulsions with loss of consciousness oliguria, azotemia, stupor, coma
o Chronic: late teeth eruption, irregular enamel formation, soft o Infants: failure to thrive, poor feeding, hypotonia
teeth o Chronic cases: mental retardation, convulsions, blindness
o Dry & scaly skin Laboratory Tests
o Horizontal lines in nails of the fingers & toes o Serum calcium should always be measured at the same time
o Mucocutaneous candidiasis as PTH.
o Cataracts o Primary case: increased serum Ca; increased serum PTH;
o Permanent mental & physical deterioration occur if initiation of increased serum chloride; decreased serum phosphorus in
treatment is delayed. 50% of cases
Serum Calcium o Serum & ionized calcium elevated
o About 50% of calcium is ionized o Serum phosphorus is low <3 mg/dL
o 40-45% is bound to albumin o Serum magnesium is low
o 5-10% is bound to other anions (sulfate, PO4, lactate, citrate) o Low specific gravity of urine
o Only ionized fraction is physiologically active & can be rapidly o Serum nonprotein nitrogen & uric acid inc.
measured o Elevated serum PTH
o Blood pH should always be performed with ionized Ca o Most consistent X-ray finding is resorption of subperiosteal
(increased in acidosis; decreased in alkalosis) bone best seen along the margins of the phalanges of the
Laboratory Findings hands
o Serum calcium <5-7 mg/dL o Skull X-ray: gross trabeculation or a granular appearance due
o Serum phosphorus >7-12 mg/dL to focal rarefaction
o Serum ionized calcium (45% of the total) is low o Abdominal X-ray: renal calculi or nephrocalcinosis
o Serum alkaline phosphatase is normal or low Management
Marias 1 of 7
PEDIATRICS 2
Pediatric Endocrinology Part 2
o Surgical exploration is indicated in all instances. Renin-Angiotensin-Aldosterone System
o All glands should be carefully inspected. Major regulators of aldosterone secretion are the R-A system
o Removal of the adenoma & potassium
o Total parathyroidectomy for infants with severe hypercalcemia
o Good prognosis if recognized early & there is appropriate Renin produced by the JG apparatus reacts with renin
surgical treatment substrate --angiotensin I--angiotensin-converting
enzyme cleaves-- angiotensin II---angiotensin III (potent
stimulators of aldosterone secretion)
Both angiotensin & K act by IC signal transduction
ADRENAL GLANDS mechanisms to stimulate conversion of cholesterol to
Adrenal gland: 2 endocrine systems: medullary gland & pregnenolone.
cortical system
Adrenal cortex: Adrenal Steroids
1. Zona glomerulosa – aldosterone (15%) Glucocorticoids:
2. Zona fasciculata – cortisol & androgens o Regulate RNA & protein synthesis
3. Zona reticularis – androgens (10%) o Catabolic effect in muscles, skin, connective, adipose &
lymphoid tissues: increased degradation of protein
o Anabolic in the liver: increase protein & glycogen
content, enhances gluconeogenesis
o Effects of insulin & androgens are antagonistic to those
of glucocorticoids
Mineralocorticoids
o Aldosterone maintains electrolyte balance-blood
volume & BP stabilization
o Controls Na & H20 reabsorption in the distal tubules
Androgens
o inc. retention of N, K, P, S04
o Promote growth & have androgenic effects
o DHEAS levels begin to rise before the other hormonal
changes of puberty occur
ADRENAL MEDULLA
Catecholamines: dopamine, norepinephrine, epinephrine
Synthesis occur in the brain, sympathetic nerve endings & in
chromaffin cells
Metabolites are excreted in the urine: VMA, metanephrine,
normetanephrine
Both epi- & norepinephrine raise the mean arterial BP,
increase PVR-inc.systolic & diastolic BP
Epinephrine increases the PR-dec.PVR
Hypothalamic-Pituitary-Adrenal Axis
Pulses of ACTH & cortisol occur every 30-120 minutes, are ACTH INSUFFICIENCY
highest at about the time of waking, are low in late afternoon Addison’s disease
& evening, and reach their lowest point an hour or two after Deficient production of cortisol or aldosterone due to
sleep begins. congenital or acquired lesions of the hypothalamus, pituitary
In the hypothalamus (paraventricular nucleus): CRH is gland or adrenal cortex
synthesized which is the most important stimulator of ACTH Etiology: congenital hypo- or aplasia of the pituitary
secretion. (abnormalities of skull & brain, craniopharyngioma), adrenal
AVP augments CRH action--neural stimuli from the brain hypoplasia congenita, inborn defects of steroidogenesis,
cause the release of CRH & AVP-- pulsatile release in the autoimmune destruction of the glands, CNS demyelination,
hypophyseal-portal circulation--pulsatile release of ACTH etc.
Laboratory Tests
Role of ACTH o Low serum Na & Cl, increased K
Acute effects of ACTH: o Inc. urinary excretion of Na & Cl
o Stimulates cholesterol release o Nonprotein nitrogen plasma level is high, hypoglycemia
o Transport of cholesterol into mitochondria o Most definitive test: measurement of plasma or serum
o Binds cholesterol to P450 cytochrome level of cortisol before & after administration of ACTH
o Releases newly synthesized pregnenolone Clinical Manifestations
Long-term effects of ACTH stimulation: o S/Sx begin shortly after birth (adrenal hypoplasia,
o increase the uptake of LDL cholesterol steroidogenesis defects): failure to thrive, vomiting,
o Formation of the steroidogenic enzymes lethargy, anorexia, dehydration
Marias 2 of 7
PEDIATRICS 2
Pediatric Endocrinology Part 2
o Older children: gradual, muscular weakness, lassitude, o Flurohydrocortisone (0.05-0.3 mg daily) & NaCl 1-3 gms
anorexia, weight loss, general wasting, hypotension, given to normalize plasma renin activity
intense craving for salt o Hydrocortisone continued indefinitely in all patients with
o Increased skin pigmentation on face & hands, most classic forms of CAH
intense around the genitals, umbilicus, axilla, nipples, Management
joints o Adequate indices of control: monitor serum 17-OHP,
o Failure of suntan to disappear may be the first clue androstenedione, testosterone, renin preferably
Management measured at 8-9 am prior to taking the morning
o D5 0.9 NSS IV – to correct hypoglycemia & the Na loss medication
o Hydrocortisone succinate IV (25 mg for infants & 75 mg o Surgical correction of enlarged clitoris at 6-12 months
for children) every 6 hrs for the 1st 24 hrs old
o After 48 hrs, may discontinue fluids & shift to oral o Outcome: short stature, disordered puberty, menstrual
cortisol in 5-20 mg every 8 hrs irregularity, infertility
o Further reduction until maintenance levels & a stable
clinical situation are achieved. CUSHING SYNDROME
o May add Florinef ( flurohydrocortisone) 0.05-0.3 mg Characteristic pattern of obesity with associated
daily hypertension which is the result of abnormally high blood
levels of cortisol resulting from hyperfunction of the adrenal
C0NGENITAL ADRENAL HYPERPLASIA cortex; ACTH –dependent or independent
Etiology: functioning adrenocortical tumor (infants); pituitary
AR disorders of adrenal steroidogenesis leading to a adenomas; hyperplasia of adrenals
deficiency of cortisol-- inc. secretion of corticotropin-- Clinical Manifestations
adrenocortical hyperplasia & overproduction of intermediary o More severe in infants
metabolites o Rounded face, prominent cheeks, moon facies, buffalo
Deficiency of 21-hydroxylase accounts for 90% of affected hump, generalized obesity, abnormal masculinization,
patients impaired growth, hypertension, inc. susceptibility to
Clinical Manifestations infection
1. NON-SALT-LOSING CAH o Older children: purplish striae on hips, abdomen &
o Normal at birth but signs of sexual & somatic precocity thighs, delayed puberty, emotional lability, weakness,
appear within the 1st 6 months of life headache, renal stones
o Well developed muscles & BA > CA Laboratory Findings
o Stunted adult stature o Serum cortisol levels are normally elevated at 8 am &
o Small testes and enlarged penis decrease to <50% by 8pm--- diurnal rhythm is lost
o Usually normal mental development o Urinary excretion of free cortisol & 17-
o Females: pseudohermaphroditism; enlarged clitoris, hydroxycorticosteroids are increased
labial fusion; internal genital organs are those of a Management
normal female o Unilateral adenalectomy for benign cortical adenomas
o Masculinization progresses after birth o Bilateral tumors: subtotal adenalectomy
o Tall for age with advanced ossification
o Trans-sphenoidal pituitary microsurgery for children
2. SALT-LOSING CAH o Adequate preoperative & postoperative replacement
o Severity of virilization is generally greater in this type
therapy
o Symptoms begin shortly after birth: failure to regain o Substantial catch-up growth; abnormal bone density
birthweight, progressive weight loss, dehydration,
prominent vomiting, anorexia
PHEOCHROMOCYTOMA
o Females: virilization of external genitals
Catecholamine-secreting tumor arising from the chromaffin
o Males: genitals appear normal
cells
Laboratory Findings
o Salt-losing type: low serum Na & Cl; inc. K; low serum Most common site of origin is the adrenal medulla
cortisol Tumors may develop anywhere along the abdominal
o Inc.plasma renin; serum aldosterone sympathetic chain, likely to be located near the aorta at the
level of the IMA or at its bifurcation.
o 21-hydroxylase deficiency: increased serum 17-OHP
Periadrenal area, urinary bladder, ureteral walls, thoracic
o Pelvic ultrasound to visualize presence of uterus in
cavity, cervical region
female pseudohermaphrodites
Occur in children 6-14 yrs old
o Urinary 17-ketosteroid excretion & plasma levels of
Tumors found more often on the right side, about 1-10 cm in
DHEAS elevated with CAH & cortical tumors but very
diameter
high values favor the diagnosis of neoplasm
Bilateral in >20% affected children
o Management
Inherited as AD trait
o Glucocorticoids inhibit excessive production of
May be associated with other syndromes such as
androgens & prevents progressive virilization
neurofibromatosis, part of MEN syndromes, tuberous
o Hydrocortisone 10-20 mg/m2/day orally in 2-3 divided
sclerosis, Sturge-Weber syndrome, ataxia-telangiectasia
doses
o Monitor growth & hormonal levels
Biosynthesis & Metabolism
Marias 3 of 7
PEDIATRICS 2
Pediatric Endocrinology Part 2
Phenylalanine Tyrosine in the ovary; supporting cells --- Sertoli cells in testes or
granulosa cells in ovaries
Dopamine Dihydroxyphenylalanine In the absence of a testis-determining factor (SRY or sex-
determining region on the Y chromosome), the gonad
Norepinephrine Epinephrine develops into an ovary.
46,XX – needed for the development of normal ovaries
3-Methoxy-dopamine Normetanephrine Development of the testis requires a Y chromosome (short
Metanephrine arm of the Y is critical for sex determination)
Homovanillic acid 3-Methoxy-4-hydroxy Function of the Testes
mandelic acid (VMA)
During the 1st trimester of pregnancy – levels of placental
chorionic gonadotropin peak (8-12 wks) & stimulate the fetal
Clinical Manifestations
Leydig cells to secrete testosterone; critical period for normal
o S/Sy result from excessive secretion of epinephrine &
virilization of the XY fetus
norepinephrine
o May be symptom-free in between attacks of Shortly after birth, transient increase of gonadotropins (LH)
hypertension occurs- sharp inc. in serum testosterone which peak at 1-3
o Headache, palpitations, abdominal pain, dizziness, months old-- 6 mos.old levels dec. to low prepubertal
pallor, vomiting, sweating, convulsions levels that persist until the beginning of puberty
o Severe: precordial pain radiate into the arms, pulmonary Within specific target cells, 6-8% of testosterone is converted
edema, cardio- & hepatomegaly by 5-reductase to dihydrotestosterone & 0.3% is acted on by
o Good appetite but does not gain weight due to aromatase to produce estradiol
hypermetabolism Half of circulating testosterone is bound to sex-hormone-
o Polyuria, polydipsia, growth failure, papilledema, binding globulin (SHBG) & half to albumin; only 2%
hemorrhages, exudates & arterial constriction on circulates in the free form
ophthalmoscopy Mullerian-inhibiting substance (MIS) – earliest secreted
Laboratory Findings product of the Sertoli cells of the fetal testis; causes
o Urine contains protein & few casts involution of the embryologic precursors of the cervix, uterus
o Gross hematuria suggests that the tumor is in the & fallopian tubes during sexual differentiation; secreted in
bladder wall males by Sertoli cells both during fetal & postnatal life’ in
o Dx: demonstration of elevated blood or urinary levels of females, it is secreted by granulosa cells only postnatally
catecholamines & their metabolites Inhibin – glycoprotein secreted by the Sertoli cells of the
o Predominant catecholamine in children is testes & granulosa & theca cells of the ovary; inhibits FSH
norepinephrine derived from the adrenal gland & secretion
adrenergic nerve endings Activin – stimulates pituitary FSH secretion
o Total urinary catecholamine excretion >300 ug/day
Follistatin – protein produced by gonads that inhibits FSH
o Urinary excretion of vanillylmandelic acid (major secretion
metabolite of epi-, norepi- & metanephrine) is increased
o Vanilla-containing foods & fruits can produce falsely Function of the Ovaries
elevated levels of VMA
Oocytes are present from the 4th mo of gestation; need
o Ultrasound, CT scan, MRI: tumors
granulosa cells to form primordial follicles
o I-metaiodobenzylguanidine taken up by chromaffin
tissue is useful for localizing small tumors Most important estrogens produced by the ovary are:
Management estradiol-17 (E2) & estrone (E1); estriol is a metabolic
o Surgical removal of tumors product of these two & all three may be found in the urine of
mature females
o Preoperative a- & B-adrenergic blockers
Estrogens also arise from androgens in the adrenal glands &
o Thorough transabdominal exploration of all the usual
in the testis.
sites
o Accurate indicators of malignancy – presence of Ovary also synthesizes progesterone, a progestational
metastatic disease or local invasiveness that precluded steroid; the adrenal cortex & testis synthesize progesterone
complete resection or both as a precursor for other adrenal & testicular hormones.
o Pediatric malignant tumors – rare Estrogens, like androgens, inhibit secretion of LH & FSH.
o Prolonged follow-up is indicated because functioning In females, estrogens also provoke the surge of LH secretion
tumors at other sites may become manifested many that occurs in midmenstruation.
years after the initial operation
Conversion of Androgens to Estrogens
DEVELOPMENT OF GONADS
The undifferentiated, bipotential fetal gonad arises from a Androstenedione Testosterone
thickening of the urogenital ridge
P450 Aromatase
6 wks of gestation – gonad contains germ cells & stromal
cells -- Leydig cells in testes; theca, interstitial or hilar cells
Estrone (E1) 17B-Estradiol (E2)
Marias 4 of 7
PEDIATRICS 2
Pediatric Endocrinology Part 2
Marias 5 of 7
PEDIATRICS 2
Pediatric Endocrinology Part 2
Insulin
Insulin is synthesized in the RER of the B cells of the
pancreas- transported to the Golgi apparatus ---
packaged in membrane-bound granules-- move to the
cell wall & their membranes fuse expelling the insulin to the
exterior-- insulin crosses the basal lamina of the B cell &
the fenestrated epithelium of the capillary to reach the
bloodstream
With progressive deficiency--excessive glucose production
Effects of Insulin
& impairment of its utilization--hyperglycemia w/
• Adipose tissue
o Increase glucose entry glucosuria---resultant osmotic diuresis produces polyuria,
urinary losses of electrolytes, dehydration, polydipsia-
o Increase FA synthesis
hypersecretion of epinephrine, glucagon, cortisol & GH
o Increase glycerol phosphate synthesis
which amplifies & perpetuates metabolic derangements &
o Increase triglyceride deposition
accelerates metabolic decompensation
o Activation of lipoprotein lipase
o Increase K uptake Combination of insulin deficiency & inc. counterregulatory
hormones is responsible for accelerated lipolysis & impaired
o Inhibition of hormone-sensitive lipase
lipid synthesis- inc.plasma total lipids, cholesterol, TG,
• Muscle FFA ketone body formation w/c exceeds the capacity for
o Increase glucose entry peripheral utilization & renal excretion--metabolic acidosis
o Increase glycogen synthesis & rapid deep breathing
o Increase amino acid uptake Clinical Manifestations
o Classic: polyuria, polydipsia, polyphagia, weight loss
o Increase protein synthesis in ribosomes
(often in a less than a month)
o Decrease protein catabolism
o Clue to polyuria: onset of enuresis in a previously toilet-
o Decrease release of gluconeogenic amino acids
trained child
o Increase ketone uptake
o Pyogenic skin infections & monilial vaginitis in
o Increase K uptake
adolescent females
• Liver o Lethargy & weakness
o Decrease ketogenesis
Diagnosis
o Increase protein synthesis
o Dependent on the demonstration of hyperglycemia in
o Increase lipid synthesis
association with glucosuria with or w/o ketonuria
o Decrease glucose output due to decrease o Postprandial determinations of blood glucose or
gluconeogenesis & increase glycogen synthesis screening oral glucose tolerance tests yield low
• General detection rates in children
o Increase cell growth
Diagnostic Criteria
o Symptoms of diabetes plus a random plasma glucose
TYPE I DM >200 mg/dL or fasting plasma glucose >126 mg/dL or a
Girls=boys; peaks at 5-7 yrs old & puberty 2-hr plasma glucose during the OGTT >200 mg/dL
Basic cause of the initial clinical findings is the sharply o Polyuria, polydipsia, & unexplained weight loss with
diminished insulin secretion glucosuria & ketonuria
Mechanisms that lead to failure of pancreatic B-cell function
point to the likelihood of autoimmune destruction of DIABETIC KETOACIDOSIS
pancreatic islets in predisposed individuals Glucose >300 mg/dL, ketonemia, acidosis (pH <7.3 & HCO3
Associated with increased frequency of HLA-B8, -DR3, <15 mEq/L), glucosuria, ketonuria
-BW15, -DR4 Precipitating factors like trauma, infections, vomiting,
About 80-90% of newly diagnosed patients have islet –cell psychologic disturbances
antibodies (ICAs) directed at cell surface.
Some evidence of abnormal T-cell function with an alteration NONKETOTIC HYPEROSMOLAR COMA
in the ratio of suppressor to killer T cells at the onset Blood glucose >600 mg/dL, absence of or only slight ketosis,
nonketotic acidosis, severe dehydration, depressed
Tissue damage of pancreatic B cells is mediated by T
sensorium or coma, various neurologic signs
lymphocytes-- produce cytokines-- induce destruction of Serum osmolarity is >350 mOsm/kg
islet cells
Pre-existing neurologic damage
Effects of Insulin Deficiency Management
Marias 6 of 7
PEDIATRICS 2
Pediatric Endocrinology Part 2
o 3 phases: ketoacidosis, postacidotic or transition period The more consistently lower the level, the better the
for establishment of metabolic control, continuing phase metabolic control, the more likely it is that microvascular
of guidance of the diabetic child complications will be less severe, delayed in appearance or
o Ketoacidosis: expansion of intravascular volume, avoided.
correction of deficits in fluid, electrolyte & acid-base Use: monitor diabetic patients’ compliance with therapeutic
status; initiation of insulin therapy regimen & long-term blood glucose level control
o Blood pH & electrolytes; ECG; blood culture; monitoring In known diabetics: 7% indicates good diabetic control; 10%
I&O indicates fair diabetic control; 13-20% indicates poor diabetic
o Initial hydrating fluid is isotonic saline (hypotonic relative control
to the patient’s serum osmolality)
o Rate of fluid replacement is adjusted to provide 50-60% Somogyi Phenomenon
of the calculated deficit within the 1st 12 hrs; the Hypoglycemic episodes manifest as late nocturnal or early
remainder is given during the next 24 hrs AM sweating, night terrors & headaches alternating rapidly
o Administration of glucose (5% solution in 0.2 N saline) is within 4-5 hrs with ketosis, hyperglycemia, ketonuria &
initiated when blood glucose approaches 300 mg/dL to glucosuria suggest the possibility of Somogyi phenomenon.
limit the decline of serum osmolality & reduce cerebral Due to an outpouring of counterregulatory hormones in
edema response to insulin-induced hypoglycemia.
o Give potassium added after the initial 20 ml/kg if UO is
adequate. Dawn Phenomenon
o Bicarbonate only if pH <7.2 given slowly Elevations of blood glucose occur between 5-9 am without
o Anticipate cerebral edema – limit rate of fluid to 4 preceding hypoglycemia
L/m2/day or less Normal event; reflects the waning effects of insulin probably
o Insulin 0.1 U/kg of regular insulin followed by constant due to increased clearance of insulin & nocturnal surges of
infusion of 0.1 U/kg/hr GH that antagonize insulin’s metabolic effects
o When acidosis has been corrected, the continuous
Brittle Diabetes
infusion may be discontinued & insulin given
subcutaneously at 0.2-0.4 U/kg every 6-8 hrs while Implies that control of blood glucose fluctuates widely &
maintaining the glucose infusion until the child can fully rapidly despite frequent adjustment of insulin doses
tolerate food. Somogyi & dawn phenomena are the most common cause
o Monitor blood glucose before & 2 hrs after each meal & of “brittleness”.
the insulin dose adjusted to maintain the blood glucose To distinguish: measure blood glucose at 3,4,7 am. If blood
in the range of 80-180 mg/dL. glucose >80 mg/dL in the 1st 2 samples & markedly higher in
Nutritional Management the last ---dawn (tx: inc. evening dose of intermediate insulin
o CHO 55%, fat 30%, CHON 15% 10-15%)
o 70% of CHO content should be derived from complex If the 3 or 4 am blood glucose level is 60 mg/dL or less
CHO & intake of sucrose & highly refined sugars should followed by rebound hyperglycemia at 7 am- Somogyi (tx:
be limited. reduction of the evening intermediate-acting insulin of 10-
o Polyunsaturated:saturated fat ratio 1.2:1 15% or a delay in its injection until about 9 pm is indicated)
o Total daily caloric intake divided to provide 20% at
breakfast, 20% at lunch, 30% at dinner with 10% for
each of the midmorning, midafternoon & evening FILLER! FILLER!FILLER! FILLER!FILLER! FILLER! FILLER!
snacks.
Monitoring
o Reliable index of long-term glycemic control – measure Here’s a poem by E. E. Cummings (cited in one of
Cameron Diaz’s films)… Para kay: Rej at Jen, Aiza at
glycosylated Hgb
Patrick…patience is a virtue... To real-life lovers: Dhess &
o Glycohemoglobin (HbA1c) represents the fraction of Pats, Sheng & Myron, Roche & Fluffy, Khaye & Pau…
Hgb to which glucose has been nonenzymatically more power to you guys! To my inspiration & bestfriend,
attached in the bloodstream ‘til we meet again… Para sa mga in-lurv jan!
o The higher the blood glucose & the longer the RBC’s
exposure to it, the higher will be the fraction of HbA1c--
reflects the average blood glucose concentration of
the preceding 2-3 months i carry your heart with me (i carry it in
my heart) i am never without it
Glycohemoglobin
(anywhere
Glucose combines with Hgb continuously & nearly
irreversibly during the life span of RBC (120 days) i go you go, my dear; and whatever is
Glycated Hgb is proportional to the mean plasma glucose done
level during the previous 6-12 weeks by only me is your doing, my darling)
Glycated Hgb predicts risk of progression of diabetic
complications
HbA1c measurements obtained 3-4x/yr to get a profile of i fear no fate (for you are my fate, my
long-term glycemic control sweet) i want
Marias 7 of 7
PEDIATRICS 2
Pediatric Endocrinology Part 2
“It’s not what you say that matters, it’s how you say it”
The End
Marias 8 of 7