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hours
ate-acting)
Glargine
13 to
(Lantus) 1.5-2 Once
No peak 18
(long-acting hr daily
hours
)
4.In patients with type 2 diabetes in whom oral agents
have failed, the starting dose of N insulin is 0.15 U/kg
at bedtime (when oral agents are continued) or a total
multidose regimen of 0.3 to 0.7 U/kg per day (when all
oral agents are discontinued). The total insulin dose
required in obese patients with type 2 diabetes aver-
ages 1.2 U/kg per day.
5.Lispro insulin is superior to regular insulin in
controlling postprandial glucose spikes when given in
addition to a background insulin. Other advantages of
lispro insulin are that it can be injected anytime from 15
minutes before to shortly after the meal, and it carries
less risk of hypoglycemia and weight gain.
6.Glargine insulin is a human insulin that is slowly
released, resulting in a relatively constant concentration
over 24 hours with no pronounced peak. When patients
are switched to glargine from twice-daily N insulin, it is
suggested that 10% to 20% less glargine be given than
the previous daily total dose of N insulin. Patients
require regular, lispro, or aspart insulin boluses with
each meal. Because of its consistency and prolonged
action, glargine is a superior background insulin. Other
peakless long-acting analogues (eg, Determir) will be
available soon.
B.Multiple-dose strategies
1.Near-normoglycemia usually requires two to four
daily injections or use of the insulin pump.
2.The most physiologic ratio of mealtime insulin to
background insulin is 50:50. However, some active
adolescents do best on a 60:40 ratio, whereas more
sedentary adults might need a 40:60 ratio.
Conventional and intensive insulin regimes
Regi- Bed-
men 8 time
No. of Morn- Noo Din-
AM/No dos
injec- ing n ner
on/6 e
tions dose dose dose
PM/10P
M
Two injections
40% N+R/0/ 20% 20%
meal- N+R/0 R or - R or -
time or LP LP
60% N+LP/0/
40% 20%
back- N+LP/0 - -
N N
ground
Three injections
40% 20% 20%
N+LP/0/
meal- LP or - LP or -
LP/N or
time R R
60%
N+R/0/ 40%
back- - -20%
R/N N N
ground
Three injections
50% U+R/R/ 15% 15% 20%
meal- U+R/0 R or R or R or -
time or LP LP LP
50% U+LP/L
20%
back- P/U+LP - 30% -
U
ground /0
References: See page 255.
Hypothyroidism
Hypothyroidism is second only to diabetes mellitus as the
most common endocrine disorder, and its prevalence may be
as high as 18 cases per 1,000 persons in the general
population. The disorder becomes increasingly common with
advancing age, affecting about 2 to 3 percent of older women.
I.Etiology
A.Primary hypothyroidism
1.The most common cause of hypothyroidism is
Hashimoto's (chronic lymphocytic) thyroiditis. Most
patients who have Hashimoto's thyroiditis have symmet-
rical thyroid enlargement, although many older patients
with the disease have atrophy of the gland. Anti-thyroid
peroxidase (TPO) antibodies are present in almost all
patients. Some patients have blocking antibodies to the
thyroid-stimulating hormone (TSH) receptor.
2.Hypothyroidism also occurs after treatment of
hyperthyroidism by either surgical removal or radioiodine
ablation. Less common causes of hypothyroidism
include congenital dyshormonogenesis, external
radiotherapy, infiltrative diseases, such as amyloidosis,
and peripheral resistance to thyroid hormone action.
B.Secondary and central hypothyroidism. Pituitary and
hypothalamic dysfunction can lead to hypothyroidism.
Pituitary adenomas, craniopharyngiomas, pinealomas,
sarcoidosis, histiocytosis X, metastatic disease, primary
central nervous system (CNS) neoplasms (eg, menin-
gioma), and head trauma all may cause hypothyroidism.
C.Transient hypothyroidism. Subacute thyroiditis is
frequently associated with a hyperthyroid phase of 4 to 12
weeks' duration; a 2- to 16-week hypothyroid phase follows,
before recovery of thyroid function. Subacute
granulomatous (de Quervain's) thyroiditis and subacute
lymphocytic (painless) thyroiditis are viral and autoimmune
disorders, respectively; the latter condition may occur post
partum.
II.Diagnosis
A.Symptoms and signs of hypothyroidism include fatigue,
weight gain, muscle weakness and cramps, fluid retention,
constipation, and neuropathy (eg, carpal tunnel syndrome).
Severe hypothyroidism may be associated with
carotenemia, loss of the lateral aspect of the eyebrows,
sleep apnea, hypoventilation, bradycardia, pericardial
effusion, anemia, hyponatremia, hyperprolactinemia,
hypercholesterolemia, hypothermia, and coma.
B.In patients with primary hypothyroidism, the thy-
roid-stimulating hormone (TSH) level is elevated, and free
thyroid hormone levels are depressed. In contrast, patients
with secondary hypothyroidism have a low or undetectable
TSH level.
C.TSH results have to be interpreted in light of the patient's
clinical condition. A low TSH level should not be misinter-
preted as hyperthyroidism in the patient with clinical
manifestations of hypothyroidism. When symptoms are
nonspecific, a follow-up assessment of the free thyroxine
(T4) level can help distinguish between primary and
secondary hypothyroidism.
Laboratory Values in Hypothyroidism
Free Free
T4 T3
TSH level level level Likely diagnosis
High Low Low Primary
hypothyroidism
High (>10 :U Nor- Nor- Subclinical
per mL) mal mal hypothyroidism with
high risk for future
development of overt
hypothyroidism
High (6 to 10 Nor- Nor- Subclinical
:U per mL) mal mal hypothyroidism with
low risk for future de-
velopment of overt
hypothyroidism
High High Low Congenital absence
of T4-T3nconverting
enzyme; amiodarone
(Cordarone) effect on
T4-T3 conversion
High High High Peripheral thyroid
hormone resistance
Low Low Low Pituitary thyroid defi-
ciency or recent with-
drawal of thyroxine
after excessive re-
placement therapy
Causes of Hypothyroidism
Primary hypothyroidism (95% of cases)
Idiopathic hypothyroidism
Hashimoto's thyroiditis Irradiation of the thyroid subsequent to
Graves' disease
Surgical removal of the thyroid
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