Endocrine System pdf - D. Razzaq

Endocrine system

2019

…

prof. razzaq alrubaee…thiqar college of medicine

….L1

Hypothalamus &pituitary gland disorder & short stature

Thyroid &parathyroid  gland disorders
Adrenal gland disorder
Type 1  diabetes  DKA .complication

Hormones of hypothalamus and pituitary

The pituitary  gland receive signals from hypothalamus & respond  by sending pituitary hormones  to
target glands which produce hormones  that provide negative feedback  at level of hypothalamus
and pituitary

Hormones

Location

s\I(stimulate
.inhibit)

Function

ACTH

Ant. pituitary

Production of glucocorticoid
MC.miniralocorticoid.androgen

ADH

Post. Pituitary

Water reabsorption from renal
tubules

CRH. corticotropin
releasing hor.

Hypothalamus

Secretion of ACTH

FSH (female)

Ant. Pituitary

Secretion of estrogen from
ovary

FSH (male)

Ant. Pit

Production of sperm from
testes

GnRH

Hypothalamus

Secretion of LH &FSH

LH(female )

Ant. Pit

Ovulation and development of
corpus luteum

LH(male )

Ant. Pit

Production and secretion of
testosterone

Oxytocin

Post. Pit

Contraction of uterus at birth
&release of milk from breast

TSH

Ant. Pit

Secretion of T3.T4

PRL prolactin

Post. Pit

Promotion of milk synthesis

Somatostatin

Hypothalamus

Secretion of GH&TSH

TRH( thyrotropin
releasing
hormone)

Hypothalamus

Secretion of TSH & prolactin

Growth hormone deficiency &insensitivity (hypopituitarism )
Hypopituitarism :  denotes underproduction of GH growth hormone alone or in combination  with
deficiency of other pituitary hormones .

Congenital hypopituitarism :
Clinical features :
The child usually normal size and weight at birth .may have neonatal emergencies like apnea
.seizures .jaundice, cyanosis or Sever hypoglycemia with or without seizures prolonged neonatal
jaundice is common .nystagmus may suggest   septooptic dysplasia  . micropenis in boys   can be clue
for  GH def.

Physical exam: head  is round & face is short & broad ,prominent frontal bones  eyes somewhat are
bulging  .mandible and chin are underdeveloped ,delayed teeth eruption  and often crowded , short
neck  and small  larynx ,  high pitch voice  which  remain high after puberty

Evaluation of suspected growth hor. Def.

Growth related history &physical exam

  Growth failure
  Short stature
  GHD affect 1in 3500 child

Image & other evaluation

  Clinical diagnosis
  Bone age ( delayed )
  MRI,CT evaluate hypothamic

pituitary region

Lab . finding

 Measures GH with stimulation ,

IGF-1 test

Rationale for treatment

 Replacement with GHTshould be

started as soon as GHD is diagnosis

Diagnosis

: determined by low or absent level of GH in response to stimulation with insulin ,

arginine clonidine ,or glucagon to establish low level of GH <10 ng\ml and also necessary to
evaluate others pituitary hormones deficiency like ACTH, TSH cortisol ,gonadotropin .

Treatment

: recombinant hGH available since 1982 usually given in a dose 0.18-0.3 mg/kg/wk

during childhood  and higher dose needed during puberty.  Therapy should continued until near
final height  is achieved   and treatment discontinued if he or she tall enough or growth rate <I inch
/year and bone age >14 yr in girls &>16 years in boys
Indication of GH therapy :

1.  GHD                                      6-Prader willi  syndrome
2.  Turner syndrome               7-SHOX  gene abnormality  (short stature homebox )
3.  Chronic renal failure          8-noonan syndrome
4.  Idiopathic short stature
5.  Small for gestational age

Adverse effect of GH therapy .include pseudotumor cerbri ,gynecomastia ,slipped capital femoral
epiphysis & worsening scoliosis
Growth hormone insensitivity (LARON syndrome ): autosomal recessive disease.
Is a condition that occur when the body unable to utilize GH , and characterized by short stature
,hypoglycemia ,near normal at birth ,delayed puberty & short limbs (arms &legs) with obesity
.other signs include small genitals ,thin fragile hair those people have low risk of cancer and type II
diabetes .

Diagnosis :

S&S , GH usually high and reduced level of IGF1 & genetic study to show abnormality in GH gene
Treatment : no current cure for Laron syndrome  & only available treatment is subcutaneously
injection of IGF1
Prognosis :generally  good d not affect  life span .

Constitutional Growth delay

: one of the variant of normal growth . length & weight normal at

birth , growth is normal for the first 4-12 months , height sustained at low percentile during
childhood ., the pubertal growth spurt  delayed  and eventual  normal stature , normal bone age  .
GH response to provocative test tend to be  lower than in children with a more  typical   timing of
puberty . the prognosis of  those children to achieve  normal adult height is guarded

Familial short stature

: diagnosis made when child is growing at normal rate and one or both

parents are short all lab. Tests are normal

HYPERPITUITARISM ( TALL STATURE )

Either primary or secondary
Table showed differential diagnosis of tall stature & overgrowth syndromes
FETAL OVERGROWTH :

  Maternal DM
  cerebral  gigantisim (Sotos syndrome)
  Beckwith Wiedemann

Postnatal overgrowth leading to childhood tall stature

Nonendocrine causes

 Familial (constitutional tall stature )
 Exogenous obesity

  Cerebral gigantism  sotos syndrome
  Marfan synd.
  Bekwith wiedmann synd.
  Klinfelter syndrome
  Homocystinuria

ii.

Endocrine cause

  Excess GH secretion
  Precocious puberty
  Hyperthyroidism
  Mc Cune –Albright syndrome

Postnatal overgrowth leading to adult tall stature

  Familial
  Marfan
  Klinfelter
  Excess GH
  XXY
  ACTH or cortisol deficiency

THYROID GLAND DISORDER : L2

Etiological classification of congenital hypothyroidism:
Primary hypothyroidism :

  Defect of fetal thyroid development (dysgenesis )
  Defect in thyroid hormones synthesis
  Defect in thyroid hormones transport
  Resistance  tom thyroid hormones
  Maternal antibodies
  Iodine deficiency
  Maternal medication (iodides .amiodarone . methimazole  ,radioiodide )

Central hypo pituitary hypothyroidism

   TSH  deficiency
  Isolated TRH deficiency
  Multiple congenital pituitary hormones deficiencies

Clinical features of congenital hypothyroidism :

Most cases of congenital hypothyroidism are asymptomatic because partial trans placental
passage of maternal T4.

Normal weight & length at birth

Slight enlargement of head because
myxedema

Wide anterior &posterior fontanel

Prolonged physiological jaundice (early sign)

Feeding difficulties& choking &delayed
teeth eruption

Cry little &sleep much poor appetite

Constipation not respond to treatment with
umbilical hernia

Genital edema ,slow pulse ,cardiac murmur
with macrocytic anemia

Broad hands &short fingers

Dry scaly skin &little perspiration

Laboratory finding:

Heal prick between 2-5 days of age ( filter paper )
Serum level of T4 & free T4 usually low …..T3 may be normal & usually not helpful in diagnosis. ECG
show slow voltage ,echo may show pericardial effusion .

Radiological :

retarded osseous maturation at birth in 60 % of cases .
Distal femoral &proximal tibial epiphyses normally present at birth are often absent
Deformity( beaking )of the 12

thoracic or 1

or 2

lumber vertebra is common , skull show wide

sutures ,enlarge and round sella turcica

Treatment :

Levothyroxine (L-T4)given orally at morning
Recommended initial starting dose is 10-20 µg/kg/day [ serum T4 &freeT4 ,TSH ]should be checked
every 1-2 mo.in 1

6 mo. Of life .then every 2-4 mo. From 6mo. -3 yrs. Of age .

Prognosis :
Early diagnosis and adequate treatment from 1

wk.of life result in normal linear growth

&development . variable degree of brain damage may contribute to [delay diagnosis, inadequate
treatment &poor compliance in first 2-3 years of life )

HYPERTHYROIDISM

Excessive secretion of thyroid hormones it is caused by Graves disease
Clinical features of hyperthyroidism :
Symptoms :

  Hyperactivity .irritability ,altered mood, insomnia poor concentration
  Heat intolerance
  Fatigue ,weakness ,palpitation
  Dyspnea weight loss ,thirst &polyuria  with loose stool

Signs :

  Sinus tachycardia
  Fine tremor , hyperreflexia moist  &worm skin
  Palmer erythema ,
  Hair loss or thinning
  Chorea
  Osteoporosis ,hypokalemic periodic paralysis
  Psychosis

LAB. Finding :
High T3,T4 free T4  and low TSH  and  T3 usually elevated more than T4
Treatment :
Medical treatment is recommended rather than radioiodine or surgery
Propylthiouracil(PTU) &methimazole[Tapazole ]( potent 10 time than PTU)
Initial dose of Methimazole :0.25mg-1mg /kg /24hr once or twice  daily

Developmental delay ,hoarse voice &they
don’t learn to talk

Physical &intellectual impairment increase
with age with delayed sexual maturation

Clinical response appear after 3-6 wks and adequate control evident in3-4 months
Beta blocker like propranolol in dose 0.5-2 mg/kg/day orally useful in toxic patients

Disorder of parathyroid gland:

Parathyroid hormones : PTH also called parathemone secreted by parathyroid gland which is
important in bone remodeling .PTH secreted in response to low blood

serum calcium

level

.calcitonin : also called thyrocacitonin it is hormone produced primarily by Para follicular cell in
thyroid gland and act to reduce level of calcium and opposing the effect

of PTH

hormone .

HYPORARATHYROIDISM :

Etiology:

A: congenital

  Transient neonatal
  Familial isolated hypopara .(AR,AD.Xlinked )
  Di George syndrome & sanjad –sakati syndrome (short stature, retardation .dysmorphism )
  Barakat syndrome (sensorineural hearing loss with renal dysplasia )

B :acquired (autoimmune ,infiltrative ,maternal hyperparathyroidism ,hypomagnesemia)

Clinical features:

  Vary from asymptomatic  to sever form of hypocalcemia
  Muscular pain &cramps are early signs
  Numbness stiffness &tingling of hands and feet
  Chevostek or trousseau sign  or carpopedal spasm may be only signs
  Convulsion with or without loss of consciousness (mistaken as

epilepsy )

  Headache & vomiting because raised ICP
  Delayed teeth eruption &dry scaly skin
  Mucocutaneous candidiasis
  Cataract .addison diseasepernicius anemia ,alopecia .

Lab. Finding

serum calcium is low

5-7mg/dl

phosphorus level is elevated

(7-12mg/dl)

Ionized Ca which reflect 45% of
the total

Low

Alkaline phosphatase

normal or low

D3 level

Low

Magnesium

Normal

PTH

Low

Treatment :

Emergency treatment of neonatal tetany consist of injection of 5-10 ml or 1-3 mg/kg of 10%solution
calcium gluconate (elemental 9.3 mg/ml )
D3 also should be given (initial dose .25µg/24 hr .with maintenance   dose 0.01-0.1 µg/kg/24hr
Supplemental calcium in form of calcium gluconate   provide 800 mg elemental calcium  daily
PSUODOHYPOPARATHYROIDSM( PHP) :{Albright  hereditary osteodystrophy )
Parathyroid hormone  here are  normal and serum level of PTH are elevated even when patient is
hypocalcemic(peripheral resistance to PTH rather than deficiency ) .we have type 1A (common )
&type 1B less common & type 2.(tissue  specific resistant to PTH)

Hypocalcemia ,high PTH, hyperphosphotemia

Type 1A : account for majority of cases

  Tetany is often presenting sign
  Short stocky build &round face
  Brachydactyly  with dimpling dorsum of  the hand
  2

metacarpal bone involve result in index finger longer than

middle

 Short and wide phalanges .bowing ,exostoses &thickening of

calvaria

 Moderate degree of cognitive impairment
 Calcification of basal Anglia with lenticular cataract

Psudospodohypoparathyroidism(PPHP) :
Inherited disorder ,it is similar to pseudohypoparathyroidism (PHP) in presentation
serum level of calcium and phosphorus usually normal  with PTH hormone slightly elevated & no
resistant to PTH
summary

Condition

Appearance

PTH

Calcium Phosphates

Hypoparathyroidism

Normal

Low

High

Pseudohypoparathyroidism type
1A

Skeletal
defect

High

Low

High

Pseudohypoparathyroidism type
1B

Normal

High

Low

High

Pseudohypoparathyroidism type 2 Normal

High

Low

High

Pseudopseudohypoparathyroidism Skeletal

defect

Normal Normal Normal

DISORDER OF ADRENAL LAND

,,,,,,,,,,,,,,,,,,,,,,

Adrenal gland consist of cortex & medulla
1-Cortex {outer layer zona glomerularis(aldosterone secretion )
,middle  layed :zona fasiculata           (glucocorticoid &cortizole )
inner layer :zona reticularis              (androgen secretion )
2- medulla (epinephrine &epinephrine )

CONGENITAL ADRENAL HYPERPLASIA (adrenal insufficiency ):
Adrenal steroidogenesis
Cholesterol
          Cholesterol desmolase
  Pregninolone                                                  17 OH pregninolone               dehydroepiandrosterone
        3 beta hydroxylsteroid dehydrogenasae                                                  DHEA

Progesterone
                                                                              deoxycortisole                         Androsterone
        21 hydroxylase


                                                                            11 beta hydroxylase             17 OH steroid deh ydrogenase
Deoxycorticosterone

Cortisole testesterone

Corticosterone

18 oxydase

Aldosterone

A several of autosomal recessive disorder result from mutation  of  gene  for enzymes mediating
biochemical  steps of production of mineralocorticoids ,glucocorticoids & sex hormones  from
cholesterol by adrenal gland
Most  common types : 21 hydroxylase deficiency ,11β hydroxylase def..3βhydroxysteroid
dehydrogenase def.

Symptoms:

depend on the form of CAH and sex of patient

Mineralocorticoid deficiency :

 Vomiting due to salt loss(dehydration

&death

Excess androgen :

 Average size penis

 Ambiguous genitalia in females
 Early pubic hair & rapid growth in

childhood

  Precocious puberty
  Excessive facial hair virilization
  Infertility due to anovulation
   Clitoromegaly
  Undervirilization in XY male which can

result in apparently female external
genitals

Investigation : treatment

 Hypoglycemia ,hyperkalemia.

hyponatremia (due to
hypoaldosteronism )

  Low cortisole level
  High ACTH
  High 17 α hydroxyprogesterone in

blood

 High 17 ketosteroid in urine
 Most definite (measure serum cortisol

pre & after ACTH administration

 Immediate & vigorous fluid

&electrolytes replacement

 supply enough glucocorticoid to

reduce hyperplasia &
overproduction of androgen or
mineralocorticoid

 Replace enough mineralocorticoid
 Provide testesterone or estrogen

at puberty if deficient

 Optimize growth &bone

maturation



Hydrocortisone

Na succinate

10-15

m \m²\24hr TID



fludrocortisone

(synthetic

mineralocorticoid

) orally in dose

0.05-0.2

mg/day

Addison dsiaese :

(acquired adrenal insufficiency ):

Occur as a part of autoimmune polyendocrinopathy  syndrome type-2(APS-2): which consist of
Addison dis.autoimmune  thyroiditis , or type 1 DM .
Type 1 polyendocrinopathy : consist of : mucocutaneous candidiasis & various autoimmune
endocrinopathies like hypoparathyroidism ,Adrenal insufficiency .

Clinical features:

Symptoms :

 fatigue ,anorexia ,weight

loss,myalgia &joint pain

 nausea ,vomiting

Glucocorticoid deficiency

Both glucocorticoid
&mineralocorticoid

Signs :

 Low blood pressure
 Skin or mucosal hyperpigmentation

 Both mineralo&glucocorticoid lack
 Excess of proopiomelanocortin –

derived peptide

Lab .finding :

  Hyponatremia
  Hypoglycemia &ketosis
  Hyperkalemia
  Low cortisol level
  Eosinophilia &lymphocytosis
  High ACTH level
  High plasma renin activity

Treatment :
Correction of electrolyte abnormality with hypoglycemia
Steroid replacement. Hydrocortisone orally in daily dividing dose  of 10-15 m/m²/day

Cushing syndrome:

excess of cortisol or other glucocorticoid due to either adrenal tumors or central pituitary
involvement and or exogenous steroid usage (details in internal medicine lectures ).

Physiology of puberty

Between early childhood and 8-9 yr of age (prepubertal stage )the
hypothalamic –pituitary –gonadal axis is dormant as reflected  by undetected
level of LH & sex hormones testosterone in boys  and Estradiol in girls .1-3 yr
before onset of puberty low serum level of LH demonstrate  during sleep in
pulsatile fashion  . the pulsatile secretion of gonadotropins is responsible for
enlargement  and maturation of the  gonads and the secretion of  the sex
hormones  . in mid puberty the level of LH become evident  even during day
time  and occur  at about 90-120 minutes intervals

It is clear that GnRH is the primary if not the only , hormone responsible for
the onset and progression of puberty

The effect of gonadal steroid (testosterone and estradiol )on bone growth and
osseous maturation are critical , both aromatase deficiency and estrogen
receptor defect result in delayed epiphyseal closure and tall stature in affected
boys, that is mean

estrogen

rather than androgen are responsible for process

of bone maturation and epiphyseal fusion and cessation of growth

Estrogen also mediate the increased production of growth hormone which
also responsible with sex hormone for pubertal growth spurt.

The onset of puberty vary and more correlated with osseous than with
chronological maturation age

In female, breast bud(thelarche ) is first sign of puberty (10-11yrs) followed
by pubic hair (6-12 months later ), the interval to menarche usually 2-2.5 yrs.
peak height velocity usually start early 12 yr of age in girls &always precedes
menarche (12.75yr)

In male growth of testes(>2.5 cm)  and thinning of scrotum is the first sign of
puberty followed by pigmentation of scrotum and enlargement of penis .pubic
hair then appeared  . axillary hair appear in mid puberty in male unlike  female
growth acceleration appears after puberty . in male  growth spurt  usually  2
yrs   later than in females .and growth may continue beyond 18 yrs .of age

Precocious puberty :

Definition :

onset of breast development before age of 8 yrs. In girls & onset of

testicular development before age of 9 years in boys .

Etiology :

Central (gonadotropin dependent true precocity )

  Idiopathic
  Brain lesions
  Hypothalamic hamertoma
  Brain tumors
  Prolonged untreated hypothyroidism

Combined peripheral &central

 Treated CAH congenital adrenal hyperplasia

 Familial male precocity

Peripheral (gonadotropin independent precocious
puberty)

 Girls

o  Isosexual (feminizing )
o  Ovarian tumors
o  Teratoma
o  Exogenous androgens
o  Mc Cune –Albright syndrome
o  Heterosexual (masculinizing)
o  CAH
o  Exogenous androgen
o  Adrenal &ovarian tumors

 Boys

o   Isosexual ( Masculinizing)
o  CAH
o  Leydig cell tumor
o  hCG secreting tumors
o  teratoma
o  exogenous androgen
o  heterosexual (feminizing )
o  exogenous androgen

Clinical features :



hair underarm &genitalia

for boys on face

  acne
  adult   body odor
  sexual development ( breast & testes )
  emotional changes



mood swings

Diagnosis:

o Hormonal levels(sex hormones



Low

estradiol level or undetected in girls

 High testosterone (detectable in boys
 Detectable level of LH in girls & boys

o bone age (advance) osseous maturation
o ultrasound for adrenal &uterus size



MRI or CT scan role out tumors

Treatment :

GnRH .analogs are effective in arresting pubertal progression in patient with
central precocity like decapeptyle (zoladex ) monthly IM injection .
Meroxyproesterone acetate some time used to :suppress puberty and arrest
menses
Peripheral precocity :

   Testolactone which inhibit conversion of testosterone to estrogen
  Ketoconazole  inhibit steroid biosynthesis 200mg tds
  Cyproterone acetate  Potent progestin & antiandrogen,  inhibit

androgens at the receptor level / supress gonadal & adrenal
steroidogenesis : antigonadotrophic 100 mg/m2 2 divided doses

Diabetes mellitus in children (type 1 DM ):

Definition :Common chronic metabolic disease characterized by
hyperglycemia as a cardinal biochemical features .
Etiologic classification of Diabetes :

1-Type 1 DM (beta cell destruction )

 Immune mediate
 Idiopathic

2-type 2DM (insulin resistance &deficiency )

 Typical
 Atypical )

3-enetic defect of beta cell

 Mody (maturity onset diabetes of young )
 Wolfram syndrome (DDMOD diabetes mellitus

,diabetes insipidusoptic atrophy &deafness)

 Mitochondrial DNA mutation

 Thiamine responsiveness megaloplastic anemia

with diabetes

4-drug or chemical induced

  L-asparginase
  Anti rejection .cyclosporine …..
  Phenytoin
  Diazoxide
  Beta blockers

 α interferone

5- disease of exocrine pancreas

  Cystic fibrosis
  Trauma  to pancreas
  Pancreatitis

6-infection (CMV ,Rubella .HUS)
7-genetic syndromes

  Prader willi syndrome
  Downs syndrome
  Turner syndrome
  Klinefelter syndrome

8-Gestational diabetes
9-Neonatal diabetes

 Transient
 Permanent

Type 1 diabetes mellitus :

Insulin dependent or juvenile diabetes characterized by low or absent level of
endogenously produced insulin & by dependence on exogenous insulin ;

insulin act on movement of glucose into cells to subdue hepatic glucose
production & halt movement of fatty acid from periphery to liver

the natural history include 4 stages :

1. Preclinical Beta cell autoimmunity with progressive defect of insulin

production

2.  Clinical diabetes
3.  Transient  remission ,homeymoon period
4.   Established diabetes

Its  account about 10 % of  cases of diabetes  affecting >10 million people in
the  world  ,over all incidence  of type 1 DM varies from 0.7/100 000 /year
[2hin Pakistan  to 40/100 000/year In  Finland.   Girls and boys are equally
effected ,no apparent correlation with socioeconomic  status .

Age incidence ,2 peak group 5-7 yrs  and time of puberty .there   familial
clustering inT1DM with  prevalence in sibling   approaching 6% but in general
population is 0.4%in US .
HLA system mostly associated with DR3/4-DQ2/8
Natural history of  diabetes involve some or all of  the  following  stages :

1.  Initiation of autoimmunity
2.  Preclinical of autoimmunity with progressive loss of beta cell function
3.  Onset of clinical disease
4.  Transient remission
5.  Established disease
6.  Development of complications

Influence of high insulin vs low insulin on some metabolic processes in liver, muscle &adipose tissues :

High plasma
insulin(postprandial state )

Low plasma insulin (fast
state )

Liver

Glucose uptake
Glycogen synthesis
.lipogenesis
Absence of ketognesis

Glucose production
Glycogenolysis
Gluconeogenesis

Muscles

Glucose uptake
Glucose oxidation

Glycogen synthesis
Protein synthesis

Absence of glucose
uptake
Fatty acid &ketone
oxidation

Glycogenlysis
Proteolysis

Adipose tissues

Glucose uptake
Lipid synthesis

Absence of glucose
uptake
Lipolysis & fatty acid
release

Diagnosis :

Impaired glucose tolerance

Diabetes mellitus

Fasting  glucose 100-125mg/dl


Or
2hrs plasma glucose during OGTT more
or equal  140mg/dl but <200mg/dl

Symptoms of diabetes +random
plasma glucose more or equal to
200mg/dl
Or
Fasting (at least 8 hr )plasma
glucose more or equal to 126mg/dl

or
2hrs plasma glucose during OGTT
more or equal to 200mg/dl
Or HA1c >or equal to 6.5%

DM should suspected in any child with polyuria & dehydration ,poor weight
gain ,hyperglycemia ,glucosuria & ketonuria
Random serum sugar >200mg/dl with typical symptoms with or without
ketonuria is diagnostic .

Initial management of type1 DM

Most newly cases of DM are alert and able to eat and drink and can manage
with subcutaneous insulin alone . iv fluid required if the child vomiting or
dehydrated . intensive educational programme is needed for the parents and
child to cover

  Basic understanding of pathophysiology ofDM
  Insulin injection technique &sites
  Diet , regular meal & snacks ,reduced refined CHO .healthy diet no >than

30% fat intake

  match food intake  with insulin  &exercise
  blood glucose monitoring
  recognition and treatment of hypoglycemia
  the psychological impact of lifelong condition  with serious short & long

term complications

INSULIN THERAPY

Most insulin used in Iraq for children is humen with concentration
100U/ml with different types includes

 human insulin analogues . rapid acting like lispro &aspart within few

minutes

 short acting soluble insulin onset 30-60 min. peak 2-4 hrs. duration up

to 8 hrs. given 15-30 min.before meal

 intermediate acting insulin onset 1-2 hrs . peak 4-12 hrs( insulin with

protamine )

 mixed short & intermediate 30/70 mixtard
 very long acting insulin analogues e.g glargine (lantus)

teenager preferable to use bolus & basal (basal .lantus at night and short
acting before each meal )

factors affecting blood glucose :

Increase blood glucose

Decrease blood glucose

  omission of insulin
  refined food
  illness
  menstruation
  growth hormone
  corticosteroids
  sex hormones  at puberty
  stress of an operation

  insulin
  exercise
  anxiety (marked )
  some drugs

DIET : healthy diet recommended with high complex CHO &relatively low fat
content ,diet should be high in fiber

Diabetic ketoacidosis DKA :

End result of metabolic abnormalities result from sever deficiency of insulin or
insulin ineffectiveness. It is occur in 20-40 % of children with newly diagnosed
diabetes & DKA consider when serum sugar >300 mg .acidosis .+S/S of DM
with ketosis .

classification of DKA

Normal

Mild

Moderate

Sever

Co2)meq/l
venus

20-30

16-20

10-15

<10

pH venous

7.35-7.45

7.25-7.35

7.15-7.25

<7.15

Clinical

No changes

Only fatigue Kussmaul

,oriented but
sleepy

Kussmaul or
depress
respiration
,sleepy to
coma

Treatment protocol of DKA

Time

Therapy

Comment

hr.

10-20ml/kg IV bolus
0.9%NaClor LR
Insulin drip at 0.05-
0.1unit/lg/hr

Volume expansion ,NPO monitor
I/O,use flow sheet prepare manitol
1g/kg at bed side if cerebral edema
developed

hr. until DKA

resolution

0.45% Nacl plus
continue insulin drip

85ml/kg +maintenance -bolus

IV rate =
23 hr

20meq/l KPhos &20
meq/l K Ac….5%glucose
if blood >250mg/dl

If K <3meq give 0.5-1 meq as oral
solution or increase iv K to
80meq/l

Maintenance =100ml/kg for 1

kg+50ml/kg for 2

10 kg +25 ml/kg for

remaining kg
Initial bolus fluid consider part of total
fluid allowed & subtracted before
calculating iv rate

Sample calculating for
30 kg child
1

hr 300 ml iv bolus

0.9% NaCl or LR

& subsequent hrs= (85ml × 30)+1750ml -300ml = 175 ml

23 hr hr

I/O input output, NPO nothing by mouth ,KAc potasium acetate ,kphos=potasium
phosphate ….LR lactated Ringer..NaCl sodium chlodide

Long term management of DM

Aim of long term management :

1.  normal growth & development
2.  normal home & school life as possible
3.  good diabetic  control through  knowledge & technique
4.  encourage  children to be self- reliant
5.  avoidance of hypoglycemia

assessment of child with diabetes (summary )

Assessment of diabetic control :

  any episode of hypoglycemia
  school absence
  interference with normal life
  HbA1C result
  Insulin regimen ---appropriate
  Diet –healthy  diet

General overview :

  Normal growth and pubertal development , ovoid obesity
  Blood pressure checking
  Renal for microalbuminuria
  Eye ---cataract
  Feet –care
  Screening for celiac and thyroid disease

Knowledge &psychological aspects