Chapter 31 Pedia
Chapter 31 Pedia
HYPOPITUITARISM
- diminished secretion of one or more
pituitary hormones
Consequences:
● gonadotropin deficiency (decrease LH
or FSH) - children show absence or
regression of secondary sexual
characteristics
● GH deficiency - children display stunted
somatic growth
● TSH deficiency - produces
hypothyroidism
● corticotropin deficiency - adrenal
hypofunction
ADRENAL HORMONES
Bone density
- studies for evidence of osteoporosis
Skull radiographs
- to determine enlargement of the sella
turcica may also aid in the diagnosis.
Type 2 diabetes
- insulin resistance
➔ in which the body fails to use
insulin properly combined with
relative (rather than absolute)
insulin deficiency.
Pathophysiology body fluid from the intracellular
space to the interstitial space
Insulin and then to the extracellular
- is needed to support the space and into the glomerular
metabolism of carbohydrates, filtrate to “dilute” the
fats, and proteins, hyperosmolar filtrate.
➔ primarily by facilitating - Normally, the renal tubular
the entry of these capacity to transport glucose is
substances into the adequate to reabsorb all the
cells glucose in the glomerular
- needed for the entry of glucose filtrate.
into the muscle and fat cells, - When the glucose
prevention of mobilization of concentration in the glomerular
fats from fat cells, and storage filtrate exceeds the renal
of glucose as glycogen in the threshold (180 mg/dl), glucose
cells of liver and muscle spills into the urine (glycosuria)
- not needed for the entry of along with an osmotic diversion
glucose into nerve cells or of water (polyuria), a cardinal
vascular tissue sign of diabetes.
- chemical composition and - The urinary fluid losses cause
molecular structure of insulin the excessive thirst (polydipsia)
are such that it fits into receptor observed in diabetes.
sites on the cell membrane. - This water “washout” results in
➔ it initiates a sequence a depletion of other essential
of poorly defined chemicals, especially potassium.
chemical reactions that - Protein is also wasted during
alter the cell membrane insulin deficiency.
to facilitate the entry of - Because glucose is unable to
glucose into the cell enter the cells, protein is
and stimulate broken down and converted to
enzymatic systems glucose by the liver
outside the cell that (glucogenesis); this glucose
metabolize the glucose then contributes to the
for energy production hyperglycemia.
- With a deficiency of insulin, - These mechanisms are similar
glucose is unable to enter the to those seen in starvation
cells, and its concentration in when substrate (glucose) is
the bloodstream increases. absent.
- The increased concentration of - The body is actually in a state of
glucose (hyperglycemia) starvation during insulin
produces an osmotic gradient deficiency.
that causes the movement of
- Without the use of ● Any excess is eliminated in the urine
carbohydrates for energy, fat (ketonuria) or the lungs (acetone
and protein stores are depleted breath). The ketone bodies in the blood
as the body attempts to meet (ketonemia) are strong acids that lower
its energy needs. serum pH, producing ketoacidosis.
- The hunger mechanism is
triggered, but increased food Ketones
intake (polyphagia) enhances - are organic acids that readily produce
the problem by further excessive quantities of free hydrogen
elevating blood glucose. ions, causing a fall in plasma pH.
Three groups of children who are candidates for ● Postprandial blood glucose
diabetes are determinations and the traditional
(1) children who have glycosuria, polyuria, OGTTs
and a history of weight loss or failure ➔ have yielded low detection
to gain despite a voracious appetite; rates in children and are not
(2) those with transient or persistent usually necessary for
glycosuria; and establishing a diagnosis.
(3) those who display manifestations of ● Serum insulin levels
metabolic acidosis, with or without ➔ may be normal or moderately
stupor or coma elevated at the onset of
diabetes; delayed insulin
● diabetes must be considered if there is response to glucose indicates
glycosuria, with or without ketonuria, impaired glucose tolerance.
and unexplained hyperglycemia. ● Ketoacidosis
● Glycosuria by itself is not diagnostic of ➔ must be differentiated from
diabetes. other causes of acidosis or
● Other sugars, such as galactose, coma, including
➔ can produce a positive result ◆ hypoglycemia
with certain test strips, and a ◆ uremia
mild degree of glycosuria can be ◆ gastroenteritis with
caused by other conditions, metabolic acidosis
such as: ◆ salicylate intoxication
◆ infection encephalitis
◆ trauma ◆ other intracranial
◆ emotional or lesions.
◆ physical stress DKA
◆ hyperalimentation - is a state of relative insulin insufficiency
◆ some renal or and may include the presence of
endocrine diseases ● hyperglycemia
➔ (blood glucose level
DM is diagnosed based on any of the following ≥200 mg/dl),
four abnormal glucose metabolites: ● acidosis
(1) 8-hour fasting blood glucose level of ➔ (pH <7.30 and
126 mg/dl or more, bicarbonate <15
(2) a random blood glucose value of 200 mmol/L),
mg/dl or more accompanied by classic ● glycosuria
signs of diabetes, ● ketonuria
(3) an oral glucose tolerance test (OGTT)
finding of 200 mg/dl or more in the
2-hour sample, or
glucose oxidase tapes (Keto-Diastix) ● Consequently, insulin levels in the blood
- Tests used to determine glycosuria and increase and decrease coincidentally,
ketonuria with the rise and fall in blood glucose
levels.
Therapeutic Management ● Insulin
➔ secreted directly into the portal
child is unable to produce circulation;
➔ definitive treatment: replacement of ➔ herefore the liver, which is the
insulin major site of glucose disposal,
receives the largest
❖ Medical and nutritional guidance are concentration of insulin.
primary, but management also includes ● No matter which method of insulin
continuing diabetes education, family replacement is used, this normal
guidance, and emotional support. pattern cannot be duplicated.
● Subcutaneous injection
Insulin Therapy ➔ results in absorption of the drug
● Insulin replacement into the general circulation,
➔ is the cornerstone of thus reducing the
management of type 1 DM concentrations of insulin to
● Insulin dosage which the liver is exposed.
➔ is tailored to each child based
on home blood glucose Insulin Preparations
monitoring. ● Insulin
● Goal of insulin therapy: ➔ is available in highly purified
➔ is maintaining near-normal pork preparations and in
blood glucose values while ● human insulin biosynthesized by and
avoiding too frequent episodes extracted from bacterial or yeast
of hypoglycemia. cultures.
● Insulin ● Most clinicians suggest human insulin
➔ is administered as two or more as the treatment of choice.
injections per day or as ● Insulin
continuous subcutaneous ➔ is available in rapid-,
infusion using a portable insulin intermediate-, and long-acting
pump. preparations; all are packaged
● Healthy pancreatic cells in the strength of 100 U/ml.
➔ secrete insulin at a low but ● Some insulin is available as premixed
steady basal rate with insulins, such as 70/30 and 50/50
superimposed bursts of ratios,
increased secretion that ➔ the first number indicating the
coincide with intake of percentage of
nutrients. intermediate-acting insulin and
the second number the
percentage of rapid-acting - takes 6 to 14 hours to start
insulin. working.
- It has no peak or a very small
Types of Insulin peak 10 to 16 hours after
injection.
There are four types of insulin, based on the - The insulin stays in the blood
following criteria: between 20 and 24 hours.
● How soon the insulin starts working
(onset) Some insulins come mixed together (e.g.,
● When the insulin works the hardest Novolin 70/30).
(peak time) ➔ For example, you can buy regular
● How long the insulin lasts in the body insulin and NPH insulins already mixed
(duration) in one bottle, which makes it easier to
inject two kinds of insulin at the same
However, each person responds to insulin in his time.
or her own way. That is why onset, peak time, ➔ However, you cannot adjust the amount
and duration are given as ranges. of one insulin without also changing
how much you get of the other insulin.
(1) Rapid-acting insulin
- (e.g., NovoLog) Dosage.
- reaches the blood within 15 ● Conventional management
minutes after injection. - a twice-daily insulin regimen of
- The insulin peaks 30 to 90 a combination of rapid-acting
minutes later and may last as and intermediate-acting insulin
long as 5 hours. drawn up into the same syringe
(2) Short-acting (regular) insulin and injected before breakfast
- (e.g., Novolin R) and before the evening meal.
- usually reaches the blood ● The amount of morning regular insulin
within 30 minutes after is determined by patterns in the late
injection. morning and lunchtime blood glucose
- The insulin peaks 2 to 4 hours values.
later and stays in the blood for ● The morning intermediate-acting
about 4 to 8 hours. dosage
(3) Intermediate-acting insulins - is determined by patterns in the
- (e.g., Novolin N) late afternoon and supper
- reach the blood 2 to 6 hours blood glucose values.
after injection. ● Fasting blood glucose patterns at
- The insulins peak 4 to 14 hours breakfast
later and stay in the blood for ➔ help determine the evening
about 14 to 20 hours. dose of intermediate insulin,
(4) Long-acting insulin ● and the blood glucose patterns at
- (e.g., Lantus) bedtime
➔ help determine the evening ● Some children require more frequent
dose of rapid-acting (regular) insulin administration. This includes
insulin. children with difficult-to-control
● For some children, better morning diabetes and children during the
glucose control is achieved by a later adolescent growth spurt.
(bedtime) injection of
intermediate-acting insulin. Methods of administration.
● Regular insulin ● Daily insulin
- best administered at least 30 - SQ by twice-daily injections, by
minutes before meals. multiple-dose injections, or by
- allows sufficient time for means of an insulin infusion
absorption and results in a pump
significantly greater reduction ● insulin pump
in the postprandial rise in - an electromechanical device
blood glucose designed to deliver fixed
● Intensive therapy amounts of regular or lispro
- consists of multiple injections insulin continuously (basal
throughout the day with a rate), thereby more closely
once- or twice-daily dose of imitating the release of the
long-acting (Ultralente) insulin hormone by the islet cells.
➔ to simulate the basal ● Using aseptic technique, the child or
insulin secretion and parent changes the needle and
injections of catheter every 48 to 72 hours and then
rapid-acting insulin tapes them in place.
before each meal. ● Pump therapy
● A multiple daily injection program - is expensive and requires
reduces microvascular complications of commitment from the parent
diabetes in young, healthy patients who and child.
have type 1 DM. ● It should also not be removed for more
● The precise dose of insulin needed than 1 hour at a time, which may limit
cannot be predicted. some activities.
● Usually 60% to 75% of the total daily ● Skin infections
dose is given before breakfast, and the - are common, and as with any
remainder is given before the evening other mechanical device, it is
meal. subject to malfunction.
● Furthermore, insulin requirements do ● pumps are equipped with alarms that
not remain constant but change signal problems, such as a depleted
continuously during growth and battery, an occluded needle or tubing,
development; the need varies according or a microprocessor malfunction.
to the child’s activity level and pubertal
status.
● Illness also alters insulin requirements.
Monitoring
Record Keeping
● Home records are invaluable aid to
diabetes self-management
● Child and family are encouraged to
observe for patterns of blood glucose
responses to events
● If lapses in management occur, the child
should be encouraged to note this and
not be criticized for the transgression
Self-management
● Key to close control
● As children grow and assume more
responsibility of self-management,
○ they develop confidence in
their ability to manage their
disease and confidence in
themselves
● Puberty is associated with decreased
sensitivity to insulin that normally
would be compensated for by an
increase insulin secretions