STATE ESTABLISHMENT DNEPROPETROVSK MEDICAL ACADEMY

OF MINISTRY OF HEALTH UKRAINE

onfirmed;
at methodical meeting
of hospital pediatrics 1 department
hief of department
professor _____________V. A. Kondratyev
______ _________________ 2013 y.

METODOLOGICAL INSTRUCTIONS
FOR STUDENTS SELF-WORK TO PREPARE FOR PRACTICAL STUD
Educational discipline
module
Substantial module
Theme of the lesson
Course
Faculty

pediatrics
3
11
DIABETES MELLITUS AT CHILDREN
5
medical

Dnepropetrovsk, 2013.

1.Urgency of the theme: Insulin-dependent diabetes mellitus (DM) is one of the most
widespread diseases of endocrine system at children and adolescents. In Ukraine there is more
than 5 thousand children having diabetes. Thus it is annually registered from 500 to 1000 cases of
again revealed sick children which forms 5-10 per 100 thousand children's population of Ukraine.
DM is chronic disease, basis of which is quickly progressing absolute or relative insulin
insufficiency and hyperglycemia, which causes severe metabolic disorders, up to development of
comas.
High morbidity, severity of the course of the disease, fast progressing development of
complications, disability and high death rate of persons of young and mature age, having DM in
the childhood, define an urgency of a problem of type I diabetes.
Timely diagnostics and the organisation of contemporary adequate treatment of type I diabetes at
children allow not only to improve quality of a life of person, having incurable disease, but also
considerably increase the life time.

2. Specific goals:
A.Student should know:
1. Definition of "diabetes mellitus ".
2. Classification of DM at children.
3. Contemporary considerations on the aetiology and pathogenesis of diabetes:
Value of genetic factors .
Value of infectious diseases.
Immunity disorder.
Value of pancreatic diseases.
Value of mental and physical factors.
4. Clinical symptoms of different variants of diabetes course at children.
5. An insulin-dependent diabetes at children.
6. A latent diabetes at children.
7. A manifested diabetes at children.
8. Criteria of compensation of diabetes at children.
9. Contemporary requirements to insulin-therapy of diabetes.
10. Complications of insulin-therapy, prevention and treatment.
11. Principles of dietotherapy of diabetes mellitus at children.
12. Principles of urgent help at different kinds of comas in children.
13. Principles of dispensary measures of children having DM.
B.Student should be able:
1. To develop the scheme of diagnostic search at DM.
2. To take the history of the patient with DM.
3. To examine the patient.
4. To evaluate the laboratory data. To choose from analyses the data which testify the DM.
5. To reveal clinical criteria of diagnosis of different forms of DM.
6. To formulate the developed clinical diagnosis according to classification.
7. To make the differential diagnosis of diabetes with other childhood diseases.
8. Make a differential diagnosis of DMs comas with comas of other origin.
9. To appoint treatment taking into account the disease form.
10. To carry out disease prophylaxis.

3. Tasks for students self-work to prepare for practical studies.

3.1. The list of basic terms, parameters, descriptions, which students
must master preparing for lessons.
Term
1. Preprandial glycemia
2. Postprandial glycemia

15. Analogues of insulin of long action (Lantus,

Levemir). (are not allowed in treatment of
children till 6 years).
16. h of arterial blood.

Definition
Fasting blood glucose level. N - 3, 3-5,5 Mmol/l
Blood glucose level after food intake. N - 4, 47,0 Mmol/l
Urine glucose level. N - 0.
Ability of carbohydrates uptake; it is defined by
means of glucose tolerance test.
Defines quality of control of the disorder of
carbohydrate metabolism. N - 6%.
Fasting glycemia 7, 0-9,0, Mmol/l postprandial 11, 1-14,0 Mmol/l, at night no less < 3,6
Mmol/l, 1<7,6%.
Fasting glycemia 4, 0-7,0 Mmol/l, postprandial 5, 0-11,0 Mmol/l, at night- no less < 3,6 or >9,0
Mmol/l, 1 7, 6-9,0 %.
Fasting glycemia >9,0 Mmol/l, postprandial>14,0 Mmol/l, at night -< 3,0 or >11,0 Mmol/l,
1 >9,0 %.
Quantity of the product which contains 12 g of
light carbohydrates.
Beginning of action: 30 (10-20) minutes, action
peak: 1-3 hour, the maximum duration of action:
6-8 (3-5) h.
Beginning of action: 1-2 hour, action peak: 4-12
hour, the maximum duration of action: 18-24
hour.
Beginning of action: 0, 5-1,0 h., action peak: 5-9
h., the maximum duration of action: 18-24 h..
Beginning of action: 0,5-1,0 h., action peak: 5-9
h., the maximum duration of action: 18-24 h.
Beginning of action: 10-20 min., action peak: 13h., 4-12 hour., the maximum duration of action:
18-24 hour.
Beginning of action: 1, 0-2,0 h., without peak,
the maximum duration of action: 11-24 hour
(Lantus), 16-24 hour (Levemir).
7,34

17. Urine ketones

Negative

18. Serum ketones

0, 6-1,7 Mmol/l

19. Plasmas osmolation

300 msm/l

3. Glycosuria
4. Tolerance to carbohydrates
5.Glycosylated haemoglobin (1, 1)
6. DM compensation (optimal glycemic control)
7. DM subcompensation (suboptimal glycemic
control)
8. DM decompensation (glycemic control of
high risk)
9. Bread unit
10. Insulin of short action (Actrapid NM,
Humulin Regular, Insuman Rapid) and its
analoges ( Novorapid, Epaidra, Humalog)
11. Insulin of long action
(Protafan NM , Humulin NPH, Insuman Bazal)
12. Preliminary mixed 30/70 (Mikstard 30/70,
Humulin 3)
13.Preliminary mixed 50/50
14 Preliminary mixed analog of insulin.
(Novomix 30)

3.2. Theoretical questions for lessons:

1. DM definition.
2. DM classification at children.
3. Etiopathogenetic theories of DM at children.
4. Clinical symptoms of DM in children.
5. Criteria of the diagnosis.
6. Contemporary principles of DM therapy at children.
7. Principles of DM dietotherapy at children.
8. Requirements to insulin therapy of DM at children.
9. Complications of insulin therapy, prevention and treatment.
10. DM comas.
11. Principles of the urgent help at various kinds of comas at children.
12. Principles of dispensary methods of children having DM.

3.3. Practical skills (tasks) mastering during practical lesson:

1. To collect complaints, case history and personal (life) history
2. To inspect the child consistently
3. To reveal early symptoms of diabetes
4. To reveal thr signs of the complications of diabetes
5. To evaluate the condition of the child and available clinical symptoms.
6. To evaluate the results of the additional methods of investigation
7. To make the clinical diagnosis according to classification.
8. To make the treatment plan.
9. To make recommendations of dispensary supervision.

4. Maintenance of the subject:

MKB-10 code:
R73.0 - Reduced glucose tolerance to glucose
10 Diabetes mellitus type I
10.9 - Diabetes mellitus type I, without complications
11 - Diabetes mellitus type II
11.9 - Diabetes mellitus type II, without complications
1. Definition (WHO, 1999):
Diabetes mellitus is the group of metabolic diseases which are characterized by a hyperglycemia
which is a consequence of defects of secretion of insulin, effects of insulin or both of these
factors.
2. Classification of diabetes mellitus (WHO, 1999):
Diabetes mellitus type I (-cells destruction, which causes absolute insulin insufficiency):
. Autoimmune
. Idiopathic

Diabetes mellitus type II (with prevailing resistance to insulin and relative insulin insufficiency or
with mainly secretory defect and thr resistance to insulin or without it).
Gestational diabetes mellitus
Other specific types:
. Genetic defects of the -cells function:
. Genetic defects at the insulin action:
. Diseases of the eczocrine part of the pancreas:
D. Endocrinopathies:
E. Diabetes mellitus, induced by drugs and chemical agents
F. Infections:
G. Unusual forms of immunogenic diabetes:
H. Other genetic syndromes, associated with diabetes:
Classification according to the degree of severity
Light form. Absent cetoacydosis, comas in anamnesis, there are no micro and macrovascular
complications of DM, there can be a diabetic retinopathy of the 1 degree or nephropathy of thr 12 degrees, achievement of ideal (optimum) glycemic control of DM is reached by the diet,
physical activities, phytotherapy.
Moderate severety:
In the anamnesis cetoacydosis; diabetic retinopathy of the 1 degree
(nonproliferative), diabetic nephropathy of the 3 degree (stage of microalbuminuria), diabetic
arthropathy, hayropathy of the first stage, diabetic foot angyopathy of the 2-3 st., diabetic distal
polyneuropathy, for the achievement of ideal (optimum) glycemic control insulin or the tableted
sugar-lowering medications or their combinations are used.
Severe form. Labile course of disease (frequent ketoacydosis, ketoacydotic comas), diabetic
retinopathy of the 2 st. (preproliferative) or 3 st. (proliferative), nephropathy of the 4 st.
(proteinuria stage) or 5 st. with chronic kidney disease, autonomic diabetic neuropathy of
different organs, somatic polyneuropathy with the expressed pain syndrome, diabetic
encephalopathy, diabetic cataracta, including the decreased vision, diabetic macroangiopathy,
diabetic osteoarthropathy, , hayropathy of the 2-3 st., delay of physical and sexual development
(Mauriac and Nobekur's syndrome), patients need permanent injections of insulin.
Classification by the degree of glycemic control:
- ideal;
- optimal;
- suboptical;
- high risk for life.
3. Etiopathogenetic theories of diabetes at children's age.
Risk factors: hereditary predisposition, exogenous factors (viral infections, effects of chemicals,
toxins, obesity, increased fat, simple carbohydrates consumption,). Pathogenetically DM - an
autoimmune disease. Stages of pathogenesis
- Genetic predisposition
- Initiation of autoimmune processes by different agents
- Stage of active autoimmune processes (chronic autoimmune insulit)
- Progressive decrease in secretion of insulin
- Death of 80-90% of pancreatic -cells pancreas, process manifestation
- Full destruction of pancreatic -cells
- Hyperglycemia, deficiency of glucose in the cell, activation of glycogenolysis, then gluconeogenesis, accumulation of ketone bodies, acids with the development of diabetic
ketoacydosis.

4. Clinical manifestations of diabetes at children.

"Early" symptoms: astenisation, poliuriya, nicturiya, polidipsiya, dryness of the mucous
membranes, skin, poliphagia or decrease in appetite, loss of weight. Further symptoms quickly
progress up to the development of ketoacydosis and coma.
DM complications:
10.2 (11.2) - diabetic nephropathy
10.3 (11.3) - diabetic retinopathy
10.4 (11.4) - diabetic neuropathy
10.5 (11.5) - diabetic angyopathy
10.6 (11.6) - other specified complications
10.7 (11.7) - multiple complications
10.8 (11.8) - not specified complications
Skin manifestations- tendency to dermatitis, furunculosis, an itching dermatosis, vulvovaginitis at
girls. GI disorders - diabetic enteropaty, a hepatopaty (fatty hepatosis). Urinary system disorders diabetic nephropathy, tendency to inflammatory diseases (pyelonephritis). Ocular symptoms diabetic retinopathy, cataract, atrophy of optic nerves. Neuropathy disorder of thr nervous
system (first of all peripheral). Macroangiopathy - disorders of microcirculatory vessels - are
found in 1/3 children at manifestation of the disease. At children with chronic deficiency of
insulin (in case of inadequate regimen of insulin administration, violations of the diet,
accompanying diseases) can be seen Mauriac's syndrome (hepatosis, growth, sexual and
intellectual development delay, obesity bu "Cushing" type) or Nobekur's syndrome (hepatosis,
growth, sexual and intellectual development delay, decreased weight)
5. Criteria of the diagnosis
Normal range of glucose in the capillary blood is 3, 3-5,mmol/l.
In case of fasting <6,1 mmol/l the standard oral test for tolerance to glucose is carried out. When
receiving twice fasting glycemia level in capillary blood >6,1 mmol/l or in the venous blood >7,0
mmol/l, or selectively >11.1 mmol/l the diagnosis of DM is established, and the test isn't carried
out. In the presence of classical clinical symptoms and glycemia >11.1 mmol/l the diagnosis of
DM is also established.
6. Contemporary principles of therapy of diabetes at children.
- Treatment is carried out for life.
- Dietotherapy:
- The dosed physical activity
- Insulin therapy.
- Symptomatic therapy, prevention of complications
7. The principles of the diet therapy at children having diabetes.
- various food, adapted to the age, corresponding to physical activity and the regimen of insulin
injection;
- advantage - to porridges, bread, vegetables and fruit;
- to limit salt and sugar;
- consumption of fats isn't forbidden to small children, but it isn't desirable for the older
children and adolescents;
- if the child has DM since infancy breast feeding is recommended to be prolonged at least to
the age of six-months;
- optimum frequency rate of food intake: 3 main and 3 additional (easy) meals;
- daily caloric content of food for the child is calculated by formula: 1000 kcal + 100 kcal for
every year of life. From this quantity: carbohydrates of 50-55%, fats - 30%, proteins - 1520%.

after calculation of quantity of calories which fall on carbohydrates, define quantity of the
grain units (GU) for the possibility of carrying out mutual substitution of products (10-12 g of
carbohydrates of food are accepted for 1 GU) that allows to replace products by equivalent
amount of carbohydrates;
8. Requirements to the insulin administration at children.
For the treatment of children and adolescents only human genetically engineered insulin or insulin
analogs are recommended for usage.
There are used medications of ultrashort, short action, medium, long action and a mix of insulin
medications of different duration action in the different ratio.
Daily requirement for insulin:
Diabetes debut - 0, 5-0,6 U/kg
Remission period - < 0,5 U/kg
Long-lasting diabetes - 0, 7-0,8 U/kg
Glycemic control with high risk (ketoacydosis)- 1, 0-1,5 U/kg
Prepubertal period - 0, 6-1,0 U/kg
Puberal period - 1, 0-2,0 U/kg
9. Complications of insulin therapy, their prevention and treatment.
Lipodistrofy: Changes of skin and subcutaneous tissues in the form of atrophy or hypertrophy
in the places of insulin injection.
Treatment:
1 . Change of places of insulin injection.
2 . Physiotherapeutic treatment: laser therapy to the lipodistorfic regions; ultrasonic therapy on
lipodistorfic regions - independently or alternating to laser therapy; hyperbaric oxygenation.
Somodzhi's syndrome is the chronic overdose of insulin, after hypoglycemic hyperglycemia.
Develops at patients with poor control over DM. Clinical manifestations: increased appetite,
growth acceleration, obesity (frequently by Cushing type), hepatomegaly, tendency to the
ketoacydosis, to the hypoglycemic events (mainly at night and early in the morning)
Hypoglycemia is the condition caused by absolute or relative insulin excess.
Light (1 degree): it is diagnosed by the patient and treated by sugar intake
Moderate (the 2nd degree): the patient can't eliminate the hypoglycemia by himself, treatment is
by sugar intake with the help of assistance
Severe (3rd degree): the patient in stupor, unconscious or in a coma, needs parenteral therapy
(glucagon or intravenous administration of glucose)
Asymptomatic, "biochemical hypoglycemia".
Rendering the urgent help
Light (1 degree) and moderate hypoglycemia (the 2nd degree):
- 10-20 g of "fast" carbohydrates
- 1-2 slices of bread
Severe hypoglycemia (the 3rd degree):
- In the prehospital setting:
children younger than 5 years: 0,5 mg of glucagon intramuscularly or subcutaneously
children older than 5 years: 1,0 mg of a glucagon intramuscularly or subcutaneously
If there is no effect within 10-20 min. - to check glycemia
- In the hospital setting intravenously by bolus:
20% solution of glucose (dextrose) 1 ml/kg (or 2 ml/kg of 10% solution) in 3 minutes,
then - 10% solution of glucose of 2-4 ml/kg, to check glycemia level, if there the patient is
still unconsciousness - to administer 10-20% glucose solution to achieve glycemia level
within 7-11 mmol/l, to check glycemia level each 30-60 min.

10. Diabetic comas.

Diabetic ketoacidosis (DKA). - 10.1,
Coma - 10.0
DKA st. - symptoms, characteristic for diabetes with poor glycemic control: thirst, poliuriya, loss
of weight, dryness of skin and mucous membranes, weakness, headache, drowsiness, acetone
smell in the air, decreased appetite, faintness. Dehydration degree no more than 5%.
DKA st. and DKA st.: nausea, vomiting, abdominal pain, brown cowering on the tongue ,
disordered consiousness, considerable dehydration (loss to 10-12% of body weigh), tachycardia,
arterial hypotonia, decreased muscular tone, tendon reflexes, the tone of the eyeballs,
hypothermia, oliguria which turns to anuria, loss of consciousness, Kussmaul breathing, a
pungent smell of acetone in the exhaled air. Degree of dehydration degree is more than 5%.
Abdominal syndrome is frequently observed at DKA which is manifested by acute abdominal
pain, faintness, frequent vomiting by coffee thick, leycocytosis. It is caused by irritant action of
the ketone bodies on the mucous membrane of the gastrointestinal tract, with the development of
hemorrhagic gastritis, numerous small hemorrhages in the peritoneum, electrolytic disturbances
in the peritoneum, intestinal paresis, dehydration.
Treatment.
Should be carry out at the resuscitation and intensive care unit
Main directions:
Rehydration
Elimination of insulin deficiency
Restoration of normal out of - and intracellular composition of electrolytes
Restoration of glucose (glycogen) reserve in the organism
Acid-base balance (ABB) restoration
Diagnostics and treatment of pathological conditions which caused comas
Treatment and prevention
- Disseminated intravascular coagulation syndrome (DICC)
- Infectious complications
- Iatrogenic hypoglycemia
- Intoxications
- Brain edema
Hemostasis correction
Carrying out therapeutic measures directed towards restoration and support of the functions of the
internal organs (heart, kidneys, lungs, etc.).
Children who have dehydration less, than 5% (DKA st.), without its clinical manifestations,
subcutaneous insulin injections and a orale rehydration should be administered.
Monitoring of patient with ketoacydosis
Capillary blood glucose - each hour (for the control - in the venous blood each 2-4 h. ) .
Blood electrolytes, urinalysis, pCO2, blood p, hemoglobin, ESR, leukocytes, hematocrit,
coagulogramme, , ECG - each 2-3 hours
Pulse, heart rate, breathing rate - each hour
Neurologic assessment - each hour
Assessment of the reaction of pupils on the light, the state of the fundus of the aye - each hour
Hyperosmolar nonketoacidotic coma (HOK).
Definition a coma which arises in patients with diabetes, caused by insufficiency of insulin and
considerable loss of liquid. It is characterized severe exicosis, absence of acidosis and early
emergence of neurologic symptoms.
Diagnostic criteria of HOK.
1 . Clinical

Arises slowly, than DKA. Thirst, poliuriya, decreased weight, signs of severe dehydration (the
expressed dryness of skin and mucous membranes, tachycardia, decreased tone of the eyeballs,
progressing weakness, brown covering of the tongue, decreased muscular tone, tendon reflexes,
oliguriya that turns to anury, temperature normal or increased, neurologic symptoms: feeling of
twitching in the muscles of extremities, aphasia, spasms, paresis, pathological symptoms,
nistagmus, hallucinations, delirium, absence of the smell of acetone in exhaled air, absence of
Kussmaul breathing (only in case of lactatacydosis), disordered consciousness - stupor or coma.
2. The paraclinical: blood glucose >33 mmol/l, arterial blood >7,3, ketonuriya absent or low,
anion difference <12 mecv/l, osmolarity >320 mOsml, additional criteria: blood bicarbonate>15
mecv/l, serum ketones low.
Treatment should be carry out at the resuscitation and intensive care unit.
Regidratation. At osmolarity >320 mOsml treatment should begin with 0.45% of NaCl solution
intravenously, at osmolarity osmolarity <320 mOsml - treatment should begin with 0.9% NaCl
solution. Infusional therapy is carried out gradually for 48 hours. It should be stopped with
restoration of consciousness, absence of vomiting, possibility of independent reception of liquid.
Insulin ttherapy. Insulin (only short action) is adnministered by small doses, continuously
intravenously. First hour: intravenously - 0,15 U/kg. Then - each hour intravenously 0,1 U/kg/h
mixed with 0,9% of NaCl (on each 100 ml of 0,9% of NaCl add 10 U insulin). If there is no
positive dynamics for the first 2-3 hours - the dose of insulin doubles. When glycemia decreases
to 13-14 mmol/l the dose of insulin should be cut twice (approximately 2-3 U per hour).

Materials for self-checking:

A. Situational clinical tasks
Case 1
A 2 -year-old girl is brought to the emergency department because of intermittent
vomiting for 1 month. She has been eating well but has lost 1.5 kg in 2 weeks. The parents also
report more wet diapers than usual.
On examination, the girl is well-developed, well-nourished, and in no distress. Her
temperature is 99F (37.2C), heart rate is 150 beats/min, and respiratory rate is 20 breaths/min.
Her height is at the 75th percentile and weight is above the 95th percentile. Except for dry oral
mucous membranes, findings on a complete physical examination are normal.
The reading on the initial chemical stick for blood glucose was reported as "high." The true
blood glucose was 776 mg/dL (42.5 mmol/L). The urinalysis showed +3 glucose and +3 ketones.
The venous blood gas revealed: pH, 7.2; PCO2, 40 torr; PO2, 54 torr; and bicarbonate, 15 mEq/L
(15 mmol/L).
Questions
1. What is the definitive diagnosis?
2. What is the complication?
3. How to treat this disorder?
4. How to prevent acute and long-term complications?
Case 2
8 year old girl has diabetes type I within 11 months. At this time she has the increase in the
weight of 5 kg, grew by 5 sm. Objectively: growth - 125 sm, weight - 31 kg. Skin is clean,

subcutaneous tissue is excessively developed, distributed evenly. Other physical investigation is

unremarkable, the liver isn't increased.
Receives before a breakfast 6 U of Protafan and 4 U of Actrapid, before dinner 4 U of Actrapid, before dinner - 4 U of Actrapid, in 22.00 - 6 U of Protafan. Keeps to a diet on
1800 kcal per day, 5 times a day, sugar value of food - 270 g. After the second dinner notes the
feeling of hunger, superficial sleep, night sweating, wakens hardly, weakness before breakfast,
headache.
Fasting blood sugar - 15,2 mmol/l, before lunch - 7 mmol/l, before dinner - 5 mmol/l. Glucosuria:
from 8 a.m. till 2 p.m. - 500 ml - 1%, 2- 8 p.m. 300ml - 0,5%, 8 p.m. - 8 a.m. - 500 ml - sugar
negative.
Questions
1. Make the clinical diagnosis
2 . List the criteria of compensation of diabetes type I.
3. Whether diabetes at this child is compensated?
4. Whether the dosage of insulin is adequate? Whether insulin is correctly distributed
within a day?
6 . Principles of treatment.
Case 3.
5 year old boy was born the 2nd pregnancy proceeding with a nephropathy, 2nd urgent
with weight 4000 g, height 52 cm. From the anamnesis it is known that the child suffers from
acute respiratory diseases. After the stress within the last 1,5 months there is observed weakness.
The child lost weight, increased thirsty urination. After the flu the condition of the child
deteriorated: the symptoms of nausea, repeated vomiting, abdominal pain, a fruit smell from the
mouth, drowsiness developed. The boy is hospitalised in intensive care unit in severe condition,
unconscious. Breathing is noisy Kussmaul type). Skin and tendon reflexes are diminished. Dry
skin, turgor of tissues and tone of eyeballs are reduced, features are pointed, expressed hyperemia
of skin at cheeks and jugal arches. Pulse is 140 beats per minute, BP is 75/40 mm hg. The tongue
is white-covered. Acetone smell in the exhaled air. The abdomen is tense at a palpation. Urination
is increased. Complete blood count: Hb - 135 g/l, Er. - 4, lxl012/l, Leyc. - 8,5109/l; bands - 4%,
segments - 50%; eosinophils - 1%, lemphocytes - 35%, monocytes - 10%, ESR - 10 mm/hour.
Urinalysis: color yellow, transparency - poorly muddy; specific weight 1035, reaction - sour;
protein - absent, sugar - 10%, acetone - +++. Biochemical analysis of blood: glucose - 28,0
mmol/l, sodium - 132,0 mmol/l, potassium - 5,0 mmol/l, general protein - 70,0 g/l, cholesterol
-5,0 mmol/l.. Acid-base: - 7,1; 02 - 92 mm hg; 2 - 33,9 mm hg.
Questions
1. What is your presumable diagnosis?
2 . What cased this condition? What are the pathogenetic mechanisms of the development
of this condition?
3 . Evaluate laboratory data.
4 . How infusion therapy at children with this pathology should be carried out?
5 . What complications can be seen in the course of infusion therapy?
B. Tests
Question 1. Type 1 diabetes mellitus is most often associated with:
A. Mumps infection
B. Coxsackievirus infection
C. Antibodies to glutamic acid dehydrogenase
D. Cow's milk

10

E. Mitochondrial DNA deletions

Answer C. Explanation: Anti-GAD antibodies, also known as anti-islet antibodies, are present in
at least 90% of children with insulin-dependent diabetes.
Question 2. Hyperglycemia during diabetic ketoacidosis may be associated with:
A. Hypocalcemia
B. Hypernatremia
C. Hyponatremia
D.Hypomagnesemia
E. Hypocholesterolemia
Answer C. Explanation: Hyponatremia may be due to measurement artifacts of serum glucose
levels. Failure of the serum sodium level to rise during therapy places the patient at risk for
cerebral edema, as the serum osmolarity drops below that in the brain, resulting in shift of fluid to
the CNS.
Question 3. Hyperkalemia in severe diabetic ketoacidosis is due to:
A. Renal failure
B. Hemolysis
C. Hyperglycemia
D. Artifact
E. Acidosis
Answer E. Explanation: Transcellular shifts of hydrogen into the cell with potassium leaving the
cell during acidosis produce transient hyperkalemia, which is usually reversed with improvement
in metabolism by insulin and improved tissue perfusion from isotonic fluids. Hypokalemia may
develop during therapy with insulin; placing potassium salts in the intravenous solution given to
the patient may reduce this risk.
Question 4. Manifestations of hyperkalemia include all of the following except:
1. Paresthesias
2. Weakness
3. Paralysis
4. Wide QRS complex
5. Tetany
Answer E. Explanation: A-D are noted in hyperkalemia. The first ECG change is peak T waves.
Lengthening of the P-R interval and QRS complex occurs later.
Question 5. A 15-year-old adolescent female has a 1-month history of urinary frequency without
dysuria and recent onset of an itchy rash beneath both breasts. She has been gaining weight over
the past year and regularly complains of fatigue. She is afebrile with a weight greater than the
99th percentile and has an erythematous, macular rash beneath both breasts characterized by
satellite lesions. Urinalysis is significant for 2+ glucosuria, but no pyuria. Which of the following
is the most likely diagnosis?
A. Diabetes mellitus
B. Fanconi syndrome
C. Human immunodeficiency virus
D. Occult malignancy

11

E. Severe combined immunodeficiency (SCID)

Answer A. The obese adolescent in this case has findings of diabetes mellitus. Her cutaneous
candidiasis is likely an indication of secondary immunosuppression related to hyperglycemia. In
diabetes, hyperglycemia promotes neutrophil dysfunction, and circulatory insufficiency
contributes to ineffective neutrophil chemotaxis during infection. HIV infection is possible and
antibody testing might be reasonable, but this scenario is most consistent with hyperglycemia.
Question 6. A 14-year-old adolescent female from another state was followed for 7 years for a
history of insulin-dependent diabetes mellitus. At your clinic her hemoglobin A1C is 14.9%. This
laboratory test indicates which of the following?
A. Her glucose control is poor.
B. She does not have insulin-dependent diabetes.
C. She has entered the honeymoon phase of her diabetes.
D. She has an underlying infection.
E. She is demonstrating the Somogyi phenomenon.
Answer A. The patient likely has poor diabetes control. The hemoglobin A1C, commonly used to
follow glucose control, measures the average glucose levels over the previous 2 or 3 months. The
hemoglobin A1C goal for most diabetics is 6% to 9%. Levels greater than 12% suggest poor
control, and levels 9% to 12% represent fair control. In the Somogyi phenomenon, a patient has
nocturnal hypoglycemic episodes manifested as night terrors, headaches, or early morning
sweating and then
presents a few hours later with hyperglycemia, ketonuria, and glucosuria. Counter-regulatory
hormones, in response to the hypoglycemia, cause the hyperglycemia.
Question 7. Six months after being diagnosed with what appears to be insulindependent diabetes,
the 5-year-old in the case presentation has a significant decrease in his insulin requirement. Which
of the following is the most likely explanation?
A. His diagnosis of insulin-dependent diabetes was incorrect.
B. He had a chronic infection that is now under control.
C. He has followed his diabetes diet so well that he requires less insulin.
D. He is demonstrating the Somogyi phenomenon.
E. He has entered the honeymoon phase of his diabetes.
Answer E. Up to 75% of newly diagnosed diabetics have a progressive decrease in the daily
insulin requirement in the months after their diabetes diagnosis; a few patients temporarily require
no insulin. This honeymoon period usually lasts a few months, and then an insulin requirement
returns. Patients are told that the honeymoon period is not a cure and that they should expect a
return to insulin requirement.
Question 8. A 16-year-old obese adolescent female has enuresis, frequent urination, a white
vaginal discharge, and a dark rash around her neck. Her serum glucose level is 250 mg/dL, and
her urinalysis is positive for 2+ glucose but is otherwise negative. Which of the following is the
most likely diagnosis?
A. Chemical vaginitis
B. Chlamydia cervicitis
C. Psoriasis
D. Type II diabetes
E. Urinary tract infection (UTI)

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Answer D. The description is of an obese adolescent female with candida vaginitis (the vaginal
discharge) and acanthosis nigricans (the nuchal dark rash) consistent with type II diabetes. This
condition is far more common in overweight children, especially those with a family history of
the condition.
Question 9. An adolescent with type I diabetes has a dramatically elevated glycosylated
hemoglobin (hemoglobin A1C ) level, indicating poor control of his diabetes over at least the
preceding
A. 8 h
B. 1 week
C 1 month
D. 2 months
E. 6 months
The answer is D. Glucose is nonenzymatically attached to hemoglobin to form glycosylated
hemoglobin. The major component of this reaction proceeds very slowly and is irreversible until
the hemoglobin is destroyed. The concentration of glycosylated hemoglobin thus reflects glucose
concentration over the half-life of the red cell, or about 2 to 3 months. The adolescent in the
question may have had poor control of his diabetes for longer than 2 to 3 months, but a
glycosylated hemoglobin is unable to determine this.
Question 10. A14-year-old with type 1 diabetes is admitted with diabetic ketoacidosis. Initial
laboratory values are as follows: glucose 563 mg/dL, sodium 136 meq/L, potassium 4.3 meq/L,
chloride 107 meq/L, CO2 9 meq/L, BUN 18 mg/dL, creatinine 0.6 mg/dL, and calcium
9.7 mg/dL. She receives a 10 cc/kg bolus of normal saline followed by IV fluids consisting
of 1/2 normal saline, as well as IV insulin. Eight hours into therapy, she develops muscle
weakness. In addition, her electrocardiogram shows flat T waves as well as U waves. What is the
most likely cause of her symptoms?
A. cerebral edema
B. hyponatremia
C. hypoglycemia
D. hypokalemia
E. hypocalcemia
Answer D. Deficiency of insulin resulting in diabetic ketoacidosis (DKA) can be associated with
several metabolic derangements. Insulin acts to drive potassium intracellularly and deficiency
of insulin decreases this movement of potassium from the extracellular space to the intracellular
space. In addition, as acidosis develops secondary to excessive ketone production, potassium is
further shifted extracellularly in exchange for a hydrogen ion which moves in the opposite
direction. With hyperglycemia, osmotic diuresis ensues and extracellular potassium is lost in the
urine. Therefore, patients with DKA are depleted of potassium even if serum levels are normal or
elevated. Patients are at risk for developing hypokalemia as treatment is initiated. Both insulin
administration and correction of acidosis shift potassium back to the intracellular compartment,
therefore dropping serum levels. Symptoms and signs of hypokalemia include muscle weakness
that may progress to paralysis, cardiac dysrhythmias, as well as flat or absent T waves and the
presence of a U wave on ECG. Potassium levels should be monitored closely and potassium
replacement started as long as hyperkalemia is not present and the patient has voided.
Cerebral edema is the most common cause of morbidity related to DKA and most often
occurs after treatment is initiated. It is not associated with weakness or ECG changes.

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Hyponatremia can also complicate therapy for DKA. Hyponatremia is not associated with the
patients symptoms or ECG changes. It should be noted that for every 100 mg/dL increase in
serum glucose, the serum sodium will decrease by roughly 1.6 meq/L. Therefore, the
patients original sodium would correct to nearly 142 meq/dL if the hyperglycemia is
considered. Hypocalcemia is associated with neuromuscular excitability and prolonged
QT interval. Hypoglycemia is another possible complication of DKA and blood sugars
must be monitored closely.
Question 11. A 3-year-old child has been diagnosed with type I diabetes mellitus, hyperosmolar
coma. The laboratory confirmed the diagnosis. Which laboratory findings are characteristic for
such condition?
A High hyperglycemia without ketonemia
B Hyperglycemia and ketonemia
C Hyperglycemia and glucosuria
D Hyperglycemia and ketonuria
E Hyperglycemia and high indicators of acid-base balance
Question 12 . A 6-year-old child has thirst, polyuria, increased appetite throughout two months.
He has lost 3 kg. Within a week night enuresis has occured. During investigation hyperglycemia
14 mmol/l is diagnoses. The diabetes, type I is established. What is the most probable
pathogenesis of this disorder?
A Autoimmune
B Viral
C Bacterial
D Neurogenous
E Viral-bacterial
Question 13. 9-year-old boy has diabetes for the first year. Takes insulin (Humulin R, NPH) 0,4
U/kg/24 hr. Insulin is injected subcutaneously into the shoulder using syringe-handle. What
should be done to prevent lypodistrophy?
A To change the place of insulin injection
B To limit fat in the diet
C To reduce insulin dose
D To pass change insulin medication periodically
E To prescribe antioxidants
Question 14. 10-year-old girl has addressed to the doctor with complaints to thirst, frequent
urination, loosing weight. The patient feels herself being ill for about a month. Objectively: the
pathology of internal organs isn't revealed. What laboratory investigation should be done first?
A Fasting blood glucose
B Urine sugar from 24 hr urine collection
C Urine acetone
D Glucose tolerance test
E Glykimic profile
Question 15 . 10-year-old boy has diabetes. During inspection the smell of acetone from the
mouth is noted. Blood sugar - 20,5 mmol/l, urine sugar - 20 g/l, acetone in urine - (+++). How
could the presense of acetone in exhaled air and urine be explained?
A Incresed breakdown of cetogenous amino acids and lipids.
B Disorders of water-electrolite balance.
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C Disorders of acid-base balance.

D Disorders of glucose phosphorilisation.
E Decreased glycolisis
Question 16. 9-year-old boy after acute respiratory infection has polydipsia, polyuria, weakness,
malaise. At inspection: unconsciousness, dry skin, soft eyeballs, Kussmaull breathing, the smell
of acetone from the mouth, heart sounds are hardly heard, abdoman is soft, painless. Blood sugar
- 19 mmol/l. Name, what acute condition has arisen?
A Ketoacydotic coma
B Hyperosmolaric a coma
C Cerebral coma
D Hepatic coma
E Acute renal insufficiency
Question 17. 15-year-old boy, which has type 1 biatetes since 2 years, complains of face edema,
puffiness of the extremities. Laboratory investigation: hyperlipidemia, disproteimenia
(hypoalbuminemia, hypergammaglobulinemia), proteinuria about 3g/24 hour. Serum urea and
creatinine are within normal limits. What pathological condition causes the resulted changes?
A Diabetic nephropathy
B Chronic pyelonephritis
C Chronic glomerulonephritis
D Chronic renal insufficiency
E Acute renal insufficiency
Question 18. 12-year-old boy is suffering from diabetes for 4 years. After excessive physical
activity has suddenly fainted. He looks sleeping, breathing is normal, the skin and mucous
membranes are moist and pale. Heart sounds are rhythmic, murmurs absent. Blood presure115/75 mm hg, in the urine analysis ketones are absent. Blood electrolits: sodium-135 mmol/l,
potassium - 4 mmol/l. What complication has developed at the child?
A Hypoglycemic coma
B Ketoacidotic coma
C Adrenal insufficiency
D Hyperosmolaric coma
E Heart failure

Literature
1. Nelson Textbook of Pediatrics. - 18th ed. / Ed. by R. Kliegman et al.-Philadelphia: Saunders
Co, 2007.- 3146 p.
2. Pediatry. Guidance Aid / . .. ; .. , .. . : ,
2007 . 158 .
3. Paediatrics at a glance / Ed. by L.Miall et al. - Blackwell Science Ltd. 2003.
4. Pediatric Clinical Advisor: instant diagnosis and treatment / [edited by] Paul D. Chan et al.
2nd ed. Elsevier. - 2007
5. Practical pediatrics. - 5th ed. / Ed. by M.J.Robinson, D.M.Roberton Elsevier. 2003.
6. Rapid paediatrics / Ed. by Helen Brough ... [et al.]. - Blackwell Publishing Ltd. 2004.
7. Rudolph`s pediatrics. - 21th ed. / Ed. by A.M. Rudolph et al. - McGraw-Hill. 2003.

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8. Clinical Pediatric Endocrinology - 5th ed. / Edited by Charles G.D. Brook et al. - Blackwell
Publishing Ltd 2005.
9. Handbook of Clinical Pediatric Endocrinology - 1st ed. / Edited by Charles G.D. Brook,
Rosalind S. Brown. - Blackwell Publishing Ltd. 2008.
Performed by senior lecturer Badogina L.P., assistant Tkachenko N.P.

Approved _________________20____y.
hief of the department, professor

Protocol _____
V. A. Kondratyev

Reconsidered
Approved _________________20____.
hief of the department, professor

Protocol _____
V. A. Kondratyev

Reconsidered
Approved _________________20____.
hief of the department, professor

Protocol _____
V. A. Kondratyev

Reconsidered
Approved _________________20____.
hief of the department, professor

Protocol _____
V. A. Kondratyev

Reconsidered
Approved _________________20____.
hief of the department, professor

Protocol _____
V. A. Kondratyev

Reconsidered
Approved _________________20____.
hief of the department, professor

Protocol _____
V. A. Kondratyev

Reconsidered
Approved _________________20____.
hief of the department, professor

Protocol _____
V. A. Kondratyev

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