MINISTRY OF PUBLIC HEALTH OF UKRAINE
BUKOVINIAN STATE MEDICAL UNIVERSITY
Approval on methodological meeting
of the department of pathophisiology
Protocol №
Chief of department of the pathophysiology,
professor
Yu.Ye.Rohovyy
“___” ___________ 2008 year.
Methodological Instruction
to Practical Lesson
Мodule 1 : GENERAL PATHOLOGY.
Contenting module 3. Typical disorders of metabolism.
Theme17: Pathology of the carbohydratic metabolism. Diabetis Mellitus.
Chernivtsi – 2008
1.Actuality of the theme. Diabetes mellitus is a disease resulting from
absolute or relative insulin insufficiency and accompanying by disturbance of
metabolism mainly, carbohydrate one. The main manifestation of diabetes
mellitus is hyperglycemia, sometimes reaching 25 mrnol/1, glucosuria with
glucose in urine up to 555-666 mmol/1 (100-200 g/day), polyuria (to 10-12 I of
urine per day), polyphagia and polydipsia. It is also characterized by the
increased level of lactic acid (lactocydemia) — over 0.8 mmpl/1 (N — 0,0330,078 mmol/1); lipemia — 50-100 g/1 (N — 3,5-8 g/1), sometimes ketonemia (by
determination of acetone) with the increased level of ketone bodies to 5200
mcmol/1 (N < 517 mcmol/I).
2.Length of the employment – 2 hours.
3.Aim:
To khow: the pathology of carbohydrate metabolism, main cause of
pancreas alteration: Hereditary predisposition, emotional overstrain, trauma, tumor,
inflammatory process under influence infection/ viruses, autoimmune conflict,
hypoxia, overeating.
To be able: to analyse of the pathogenesis of the Diabetis Mellitus.
To perform practical work: to analyse the pathogenesis of type 2 diabetes
mellitus. Genetic predisposition and environmental influences converge to cause
insulin resistance. Compensatory β-cell hyperplasia can maintain normoglycemia,
but eventually β-cell secretory dysfunction sets in, leading to impaired glucose
tolerance and eventually frank diabetes. Rare instances of primary β-cell failure
can directly lead to type 2 diabetes without a state of insulin resistance.
4. Basic level.
The name of the previous disciplines
1.
2.
3.
histology
biochemistry
physiology
The receiving of the skills
Scheme of normal glycogen metabolism in
the liver and skeletal muscles.
Significance of carbohydrates for the
organism.
Interconnection of carbohydrate, lipid and
protein metabolism.
Neuroendocrine regulation of carbohydrate
metabolism.
5. The advices for students.
1. Site of origin and effects of hormones.
Pancreatic islets of Langerhans. Insulin. Promotes utilization of glucose, lowers
serum glucose, 30 % glucose conversion to glycogen, depressed lipolysis and
stimulation of lipogenesis (30 % glucose conversion to fat), decreased
glyconeogenesis. Glucagon. Promotes utilization of glycogen, raises serum
glucose.
2. Describe the main cause of pancreas alterations.
1. Hereditary predisposition.
2. Emotional overstrain.
3. Trauma, tumor.
4. Inflammotory process under influence of infection/ viruses.
5. Autoimmune conflict.
6. Hypoxia.
3. Pathogenesis of diabetes mellitus.
Diabetes mellitus is either a disease with a primary beta-cell defect or failure,
termed type I diabetes mellitus, or non-insulin dependent, termed type II diabetes
mellitus with insulin resistance having inadequate insulin secretion, there are other
types of diabetes mellitus as well.
4. Note the Classification of Diabetes and Glucose Intolerance Conditions
Diabetes mellitus (DM)
Type I
Beta cell deficiency
Type II
Resistant to insulin
Impaired glucose tolerance (IGT)
Gestational diabetes mellitus (GDM)
Former Terminology
Juvenile-onset diabetes
Insulin-dependent diabetes mellitus (IDDM)
growth-onsed diabetes melltus
Adult-onset, maturity-onset diabetes (over age 40) Non-insulin-dependent
diabetes mellitus (NIDDM)
maturity-onset diabetes
Asymptomatic, chemical, subclinical, borderline, latent diabetes
Same as above
Characteristics
Few or no islet cells, acute onset at puberty, long preclinical record, insulin
dependent, ketosis prone, autoimmune and genetic-environment etiology, thin
individual.
Usually not insulin-dependent but they may use insulin, decreased islet cells, not
ketosis prone, frequently obese, strong familial pattern.
Abnormal fasting glucose levels and glucose tolerance tests, 10–15 % will
convert to type II diabetes within 10 years.
Glucose intolerance develops during pregnancy (third trimester), increased risk
of developing diabetes within years after parturition.
5. Identify the acute complication of diabetes mellitus; describe the features
of each.
Acute complications of diabetes mellitus include hypoglycemia or insulin shock,
diabetic ketoacidosis (DKA), and hyperosmolar hyperglycemic nonketotic
syndrome (HHNKS).
Acute Complications of Diabetes Mellitus
Variable
Onset
Symptoms
Skin
Mucous membranes
Respiration
Those at risk
Blood sugar/dL
Treatment
Insulin Shock Hypoglycemia
Rapid
Weak, anxious, confused
Sweating
Type I and II DM, fluctuating blood glucose levels, insufficient food intake,
excessive exercise, oral medication, excessive insulin
30 mg or less in newborns, 60 mg or less in adults
Fast-acting carbohydrate, intravenous glucose, subcutaneous glucagon
Slow
Nausea, vomiting, polyuria, polyphagia, polydipsia, headache, irritable,
comatose
Hot, flushed, dry
Dry
Hyperventilation, fruity or acetone breath odor
Type I DM, stressful situations, omission of insulin
300–750 + mg
Low-dose insulin, electrolyte and fluid replacement
HHNKS
Slowest
Similar to DKA; stuporous, focal motor seizures, dehydration
Very dry
Extremely dry
Elderly or young
Type II high carbohydrate diets, diuresis, hyperosmolar dialysis
600–4800 mg
Fluid replacement with crystalloids and colloids
6. Describe the chronic complications of diabetes mellitus.
Before the discovery of long-acting insulin, the survival time of diabetics was
short, especially for individuals with type I diabetes. Today, long-term survival is
common. As a result, the problems of neuropathy, vascular disease, and infection
have become important in clinical management of diabetic individuals.
Chronic Complications of Diabetes Mellitus
Diabetic Neuropathies
Axonal and Schwann cell degenerations, impaired motor nerve conduction, pain
and paresthesias
Microvascular Disease
Retinopathy
Nephropathy
Capillary basement membrane thickening, decreased tissue perfusion or
ischemia, hypertension
Macrovascular Disease
Coronary heart disease
Peripheral vascular disease
Proliferation of fibrous plaques, atherosclerosis because of high serum lipids,
ischemia.
Infection
Sensory impairment, atherosclerosis, ischemia, hypoxia, leukocytic impairment.
5.1. Content of the theme. Site of origin and effects of hormones.
Describe the main cause of pancreas alterations. Pathogenesis of diabetes mellitus.
Note the Classification of Diabetes and Glucose Intolerance Conditions. Identify
the acute complication of diabetes mellitus; describe the features of each. Describe
the chronic complications of diabetes mellitus.
5.2. Control questions of the theme:
1. Site of origin and effects of hormones.
2. Describe the main cause of pancreas alterations.
3. Pathogenesis of diabetes mellitus.
4. Note the Classification of Diabetes and Glucose Intolerance Conditions.
5. Identify the acute complication of diabetes mellitus; describe the features of
each.
6. Describe the chronic complications of diabetes mellitus.
5.3. Practice Examination.
Task 1. In the patient hyperglycemia, glucosuria, polyuria, polydipsia, polyphagia
are revealed. These symptoms are connected with disorder of secretion of
some hormone. Which exactly?
А. Thyroxin В. Testosterone C. Glucagon D. Insulin Е. Cortisol
Task 2. The 80 years old patient complains on increased appetite, heartburn,
excretion of increased urine quantity, change for the worse of the state
after meal. What endocrine disease is characterized these symptoms for?
А. Hypercorticism В. Thyrotoxicosis С. Cushing’s disease
D. Diabetes insipidus
Е. Diabetes mellitus
Task 3. In severe form of diabetes mellitus acidosis develops. The components of
what buffer system are changed the first of all?
А. Bicarbonate В. Phosphate С. Hemoglobin D. Oxyhemoglobin
Е. Protein
Task 4. In a 60 years old man (growth 170 сm, weight 110 kg) the level of sugar in
blood increases periodically to 6,8-7,0 mmole/l. The content of insulin is
normal. The tolerance to glucose is lowered. On the basis of what signs
can we consider the patient’s diabetes as insulin independent?
А. Decreased tolerance to carbohydrates В. Periodic hyperglycemia
С. Age of the patient D. Normal level of insulin in blood Е. Overweight
Task 5.
А. The healthy person В. The patient with latent diabetes mellitus
С. The patient with insulin dependent diabetes mellitus
D. The patient with insulin independent Е. The patient with thyrotoxicosis
Real-life situations to be solved:
Task 1
The examined has the following results of test with a sugar load (50 g of glucose
fasting in the morning) : level of sugar in blood fasting is 7,0 mmol/l, in 1 hour
after reception of glucose it equals to 8,8 mmol/l, in 2 hours after reception of
glucose –
7,2 mmol/l.
1. What do these results testify about?
2. Draw the curve of change of sugar level in blood of the healthy person
within two hours after sugar load.
3. What is the differense in test result in healthy person and the patient?
4. What practical significance has the test with glucose load, how is it
called?
Task 2
The patient was brought to the clinc in coma. Breathing is noisy, deep. In exhaled
air the smell of acetone. The content of glucose in blood is 16,1 mmol/l. There is
sugar in urine. Urine reaction on acetone is sharply positive.
1. For what disease are such disorders characterized?
2. Evaluate the level of glucose in blood.
3. How do you imagine the mechanism of appearance of glucose in urine?
4. Why does acetone appear in patient’s urine?
5. What are the causes of breathing disorders?
6. What does the smell of acetone testify about?
Task 3
After removal of pancreas in dog diabetes mellitus occured.Will it appear, if we
instead of pancreas removal:
1. Tie up its output duct?
2. Introduce alloxan?
3. Introduce parathormone ?
Literature:
1. Gozhenko A.I., Makulkin R.F., Gurcalova I.P. at al. General and clinical
pathophysiology/ Workbook for medical students and practitioners.-Odessa, 2001.
2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study
guide for medical students and practitioners.-Odessa, 2003.
3. Robbins Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay Kumar,
Tucker Collins.-Philadelphia, London, Toronto, Montreal, Sydney, Tokyo.-1999.