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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 — 0,033-0,078 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 ?-cell hyperplasia can maintain normoglycemia, but eventually ?-cell secretory dysfunction sets in, leading to impaired glucose tolerance and eventually frank diabetes. Rare instances of primary ?-cell failure can directly lead to type 2 diabetes without a state of insulin resistance.



4. Basic level.

The name of the previous disciplines


The receiving of the skills

  1. histology

  2. biochemistry

  3. physiology

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?

  1. 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.

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