«confirm» on methodical meeting of endocrinology department a chief of endocrinology department, prof. Vlasenko M. V. “ 31 ” august 2012 y methodological recommendations icon

«confirm» on methodical meeting of endocrinology department a chief of endocrinology department, prof. Vlasenko M. V. “ 31 ” august 2012 y methodological recommendations




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MINISTRY OF HEALTH PROTECTION OF UKRAINE

Vynnitsa national medical university named after M.I.Pyrogov





«CONFIRM»

on methodical meeting of endocrinology department

A chief of endocrinology department, prof. Vlasenko M.V.


_________________

“_31_”_august___ 2012 y



METHODOLOGICAL RECOMMENDATIONS

for independent work of students

by preparation for practical classes



Scientific discipline

Internal medicine

Мodule № 1

^ Basis of Internal medicine

substantial module №1

Diagnostic, treatment and prophylactic basis of main endocrinology diseases”


Topic

Topic №3: Diabetic angyopathy. Classification. Rethynopathy. Nephropathy. Diabetic foot. Diagnostics. Treatment. dispensary supervision and medico-social expertise of the patient with diabetes mellitus.

Course

4

Faculty

Medical № 1



Vynnitsa – 2012


^ METHODOLOGICAL RECOMMENDATIONS

for the students of 4-th course of medical faculty for preparation to the practical classes from endocrinology


1.Тopic №3: Diabetic angyopathy. Classification. Rethynopathy. Nephropathy. Diabetic foot. Diagnostics. Treatment. dispensary supervision and medico-social expertise of the patient with diabetes mellitus.


^ 2. Relevance of topic: The course of Diabetes Mellitus is characterized by severe complica­tions which may cause disability and even death, such as blindness, renal insuffciency, myocardial infarction, insult, gangrene. This patient can not work and early died. The risk of long-term clinical complications vary markedly in individuals but generally increase with increasing duration of DM. Hyperglycemia causes the initial metabolic alterations in the kidney, peripheral nervous and retina in diabetics, but evidence suggests that once these structural alterations reach a given stage, factors other than hyperglycemia determine the subsequent cause/ The signs and symptoms of late complications of DM mimic those of pathologically similar or indistinguishable disease in the same organ or system in nondiabetics. The manifestations may be present at diagnosis in those with type II DM, but not in those with type I DM.

Atherosclerotic coronary artery disease (manifested by angina pectoris and / or myocardial infarction)and peripheral atherosclerotic vascular disease (manifested by intermittent claudication and gangrene) are more common in diabetics than in nondiabetics and occur at an earlier age.


^ 3. Aim of lesson:

- to know the prevalence of chronic complications of diabetes.

- to realize the main etiological and pathogenetic factors in development of chronic complications of diabetes.

- to learn classifcation of diabetic angiopathy.

- to learn classifcation of diabetic neuropathy.

- to know defnition of diabetic foot, its classifcation.

- to learn the main approaches to the diagnosis of angiopathies and neu­ropathies.

- to learn general aspects of treatment in case of micro- and macroangi-opathies.

- to emphasize the importance of learning chronic complications of Diabe­tes Mellitus, their course and treatment to help patients keep good health conditions.

- to learn the main principles of diabetic compilations prophylaxis.


4. References

4.1. Main literature

  1. Endocrinology. Textbook/Study Guide for the Practical Classes. Ed. By Petro M. Bodnar: - Vinnytsya: Nova Knyha Publishers, 2008.-496 p.

  2. Basіc & Clіnіcal Endocrіnology. Seventh edіtіon. Edіted by Francіs S. Greenspan, Davіd G. Gardner. – Mc Grew – Hіll Companіes, USA, 2004. – 976p.

  3. Harrison‘s Endocrinology. Edited J.Larry Jameson. Mc Grew – Hill, USA,2006. – 563p.

  4. Endocrinology. 6th edition by Mac Hadley, Jon E. Levine Benjamin Cummings.2006. – 608p.

  5. Oxford Handbook of Endocrinology and Diabetes. Edited by Helen E. Turner, John A. H. Wass. Oxford, University press,2006. – 1005p.

4.2. Additional literature

  1. Endocrinology (A Logical Approach for Clinicians (Second Edition)). William Jubiz.-New York: WC Graw-Hill Book, 1985. - P. 232-236.

  2. Іnternatіonal Textbook of Dіabetes Mellіtus (Ed by R.A. Defronzo, E. Ferrannіnі, H. Keen, P. Zіmmet. John Wіley & Sons, Ltd. England, 2004. – Vol. 1 – 1100p., Vol. 2 – 1913p.

  3. Joslіn’s Dіabetes Mellіtus. Selected Chapters from the 14-th ed. Edіted by C. Ronald Kahn, et al. Lіppіncott Wіllіams & Wіlkіns, USA, 2006. – 328p. Manual of Endocrinology and Metabolism (Second Edition)/ Norman Lavin. – Little, Brown and Company.- Boston-New York-Toronto-London, 1994. - P. 519-527, 561-574.

  4. The diabetic foot. 2nd edition. Edited by A.Veves, J.M.Giurini, F.W. LoGerfo (ebs), Humana Press, Totowa, New Jersey,2006. – 224p.


Basic Level.

- vascularization and inner­vation of pancreas. Struc­ture of retina, kidneys, ar­terial and venous vessels and nerves of the limbs

- pathogenesis of diabetic an­giopathy and neuropathy.

- clinical symptoms of chronic diabetic compli­cations.

- clinical course, treatment and prophylaxis of chronic diabetic com­plications.


^ Students’ Independent Study Program.


You should prepare for the practical class using the existing text books and lectures. Special attention should be paid to the following:

- Classifcation of diabetic angiopathy.

- Etiology and pathogenesis of diabetic micro- and macroangiopathies.

- Laboratory investigations and instrumental techniques for the diagnosis of diabetic angiopathy

- Methods of treatment of diabetic angiopathies.

- Diagnosis of diabetic retinopathy.

- Diagnosis of diabetic nephropathy.

- Diagnosis of diabetic low extremitas angiopathy.

- Classification of neuropathy.

- Diagnosis of diabetic polyneuropathy.

- Diagnosis of diabetic encephalopathy.

- Diagnosis of diabetic visceral (autonomic) neuropathy.

- Syndrome of diabetic foot, its defnition, classifcation, clinical picture, diagnosis and treatment.


Short content of the theme.

Classification of chronic (long-term) complications of DM.

  1. Diabetic angiopathy:

  1. Microangiopathy:

  1. nephropathy;

  2. retinopathy;

  3. angiopathy of lower extremitas.

  1. Macroangiopathy:

  1. ischemic heart disease;

  2. stroke or transitory ischemic atack

  3. angiopathy of lower extremities.

  1. Diabetic neuropathy:

  1. central (encephalopathy);

  2. peripheral;

  3. visceral (dysfunction of inner organs).


The long-term degenerative changes in the blood, vessels, the heart, the kidneys, the nervous system, and the eyes as responsible for the most of the morbidity and mortality of DM. There is a causal relationship and the level of the metabolic control.


^ Diabetic retinopathy.

Background retinopathy (the initial retinal changes seen on the ophthalmoloscopic examination) does not significantly alter vision, but it can lead to processes that cause blindness (e.g., macular edema or proliferative retinopathy with retinal detachment or hemorrhage.

Evidence of retinopathy, rarely present at diagnosis in type I DM, is present in up to 20 % of type II DM patients at diagnosis. About 85 % of all diabetics eventually develop some degree of retinopathy.

Diabetic retinopathy is classified according to the changes seen at background during ophthalmoscopic examination with pupils dilated.

  1. Background (nonproliferative) retinopathy (it is usually the earliest sigh and consists of retinal microaneurysms, hard and soft exudates, punctum haemorrages).

  2. Maculopathy or preproliferative retinopathy (it is characterized by macular edema and/or big retinal hemorrhages).

  3. Proliferative retinopathy (the hallmark of this complication is neovascularization, i.e., growth of new vessels in areas of hypoperfusion. Adhesion of the vessels to the vitreous leads to retinal detachment, vitreous hemorrhage and others. The prognosis is extremely poor. 5 years after recognition of this complication 50 % of the patients are blind).

The mechanisms involved in the development of retinopathy are not clearly known. Genetic predisposition, growth hormone, hypoxia, and metabolitic abnormalities particularly of lipids, have been implicated.


^ Diabetic nephropathy.

It is usually asymptomatic until end stage renal disease develops, but it can course the nephrotic syndrome prior to the development of uremia. Nephropathy develops in 30 to 50 % of type I DM patients and in small percentage of type II DM patients. Arteriolar hyalinosis, a deposition of hyaline material in the lumen of the afferent and efferent glomerular arterioles, is an almost pathognomic histologic lesion of DM.

Classification of diabetic nephropathy by Mogensen.

  1. Hyperfunction of kidneys. (It is characterized by:

  • increased renal blood circulation;

  • increased glomerular filtration rate (GFR) (> 140 ml/min);

  • hypertrophy of kidneys;

  • normoalbuminuria (<30 mg/day).)

  1. Stage of initial changes of kidney structure. (It is characterized by:

  • mesangial changes due to accumulation of immunoglobulins (IgG, IgM), complement and other nonimmunologic proteins (lipoproteins, fibrin);

  • high GFR;

  • normoalbuminuria.)

  1. Initial nephropathy or microalbuminuria stage (It is characterized by:

  • microalbuminuria (30 to 300 mg/day);

  • high or normal GFR;

  • periods of blood hypertension.)

  1. Nephropathy or proteinuria stage. (It is characterized by:

  • persistent proteinurea (>500 mg/day);

  • normal or decreased GFR;

  • persistent blood hypertension.)

  1. Chronic renal failure or uremia.. (It is characterized by:

  • decreased GFR;

  • blood hypertension;

  • increased serum creatinine;

  • signs of intoxication.



Defnition of stages of diabetic kidney disease






Normoalbu-minuria

Microalbuminuria

Clinical nephropathy

Urinary albumin concen­tration

< 20 mg/l

20 – 300 mg/l

> 300 mg/l

24 – h collection

< 30 mg/24h

30 – 299 mg/24h

≥ 300 mg/24h

Albumin/ creatinine ratio

Men

Women

< 2,5 mg/mmol < 3 mg/mmol

2,5 – 20 mg/mmol 3 – 30 mg/mol

>20 mg/mmol > 30 mg/mmol

Key features

– Urinary albumin excretion rate nor­mal.

– Blood pressure may be raised (type 2 diabetes)

– Urinary albumin excretion rate raised. – Blood pressure in­creased.

– Cardiovascular risk increased.

– Urinary albumin excretion rate raised. – Blood pressure in­creased.

– Cardiovascular risk increased. – Other complica­tions of diabetes likely.

Main aim

Primary preven­tion.

Prevent progression

Prevent decline in renal function.

Glycemic control

Intervention threshold: HbAlc > 8 % Ideal < 7 %

Intervention thresh­old:

HbAlc >8 % Ideal < 7 %




Antihyperten-sive therapy

– Intervention

threshold: 140/190

mm/Hg

– Ideal: 130/180

mm/Hg

Intervention thresh­old: 140/190 mm/Hg – Ideal: 130/180 mm/Hg




Lifestyle modifcation

– Angiotensin converting enzyme inhibitor frst line. – Carbohydrate restriction. – Smoking cessa­tion.

– Modest salt in­take

– Angiotensin con­verting enzyme inhibitor or angioten-sin type 2 receptor blocker frst line. – Carbohydrate re­striction.

– Smoking cessation. – Modest salt intake

– Angiotensin con­verting enzyme inhibitor or angioten-sin type 2 receptor blocker frst line. – Carbohydrate re­striction.

– Smoking cessation. – Modest salt intake – Protein restriction. – Low-fat diet.


^ Diabetic angiopathy of lower extremities.

Atherosclerosis of large vessels (macroangiopathy) leads to intermittent claudication, cold extremities and other symptoms which can be also find while arteriols and capillaries are affected (microangiopathy).

Classification of diabetic angiopathy of lower extremities:

1 stage – nonclinic stage (you can not find any complaints and symptoms at objective research, but changes could be find only during instrumental examination only immediately after physical loading (arteries spasm in duplex scan and dooplerography of lower extremities)

2 stage – functional stage. It is characterized by complaints, which appear only after physical loading – walking on distance of 800 m or 1 km and disappear at the rest (acute pain in the shins muscles named intermittent claudication, feet are cold and pale). But pulsation on aa. dorsalis pedis at aa. tibialis posterior is satisfactory or decrase a little. On doplerography we see the 1 stage of legs ischemia – arterial stenosis less than 19%.

3 stage – organic stage. It is characterized by trophic changes of the lower extremities: atrophy of shins and feet muscles, the skin is dry, pale or reddening, trophic macule on the skin of shins and feet. Hairs on the leg are reduced or absent. Hyperceratosis of nail and plantes. Pulsation on aa. dorsalis pedis and aa. tibialis posterior is reduce or absent. But wound, gangrene of the fingers and feet are absent in organic stage.

On doplerography we see the ^ 2a stage of legs ischemia – arterial stenosis on 19-26% and intermittent claudication after walking on distance of 500-800 m, 2b stage of legs ischemia – arterial stenosis on 26-60% and intermittent claudication after walking on distance of 300-500 m, 3 stage of legs ischemia – arterial stenosis on 60-78% and intermittent claudication after walking on distance less than 300 m.

4 stage – gangrenous stage. It is characterized by wound, gangrene of the fingers and feet, acute ischemic pain in the feet at the rest and this disorders need amputation of lower extremities. On doplerography we see the 4 stage of legs ischemia – arterial stenosis more than 78%.


Ischemic heart disease.

  1. Cardiovascular changes tend to occur earlier in patients with DM when compared with individuals of the same age.

  2. Frequency of myocardial infarction (MI) and mortality is higher in diabetics than that in nondiabetis og the same age.

  3. The prognosis is even worse if ketoacidosis, or other complications of DM are present.

  4. Diabetic patients have more complications of MI (arrhythmias, cardiogenic shock and others) than nondiabetic ones.

  5. Often can observe atypical forms (without pain).

  6. Male : female = 1 : 1 (nondiabetics = 10 : 1).


Diabetic neuropathy.

It is an old clinical observation that the symptoms of neuropathic dysfunction improve with better control of DM, lending support to the idea that hyperglycemia plays an important role. Accumulation of sorbitol and fructose in the diabetic nerves leads to damage of the Schwann cells and segmental demyelination.


Classification of diabetic neuropathy.

  1. Encephalopathy (central neyropathy) is characterized by decreased memory, headache, unadequate actions and others.

  2. Peripheral polyneuropathy (radiculoneuropathy). There are three types of radiculoneuropathy:

  • distal polyradiculoneuropathy (It is characterized by symmetrical sensory loss, pain at night and during the rest, hyporeflexia, decreased responce touch, burning of heels and soles. The skin becomes atrophic, dry and cold, hair loss may be prominent. The decreased response to touch and pain predisposes to burns and ulcers of the legs and toes.);

  • truncal polyradiculoneuropathy (It is an asymmetric, and characterized by pain (which is worse at night), paresthesia and hyperesthesia; muscular weakness involves the muscles of the anterior thigh; reflexes are decreased; weight loss is common.);

  • truncal monoradiculoneuropathy (It is usually involves thorasic nerves and the findings are limited to the sensory abnormalities in a radicular distribution.).

  1. Visceral dysfunction:

  1. gastrointestinal tract:

  • esophageal neuropathy (It is characterized by segmental distribution with low or absent resting pressure in the low or absent resting pressure in the lower esophageal sphincter and by absence of peristalsis in the body of the esophagus.);

  • diabetic gastroparesis (It leads to the irregular food absorption and is characterized by nausea, vomiting, early satiety, bloating and abdomen pain.);

  • involvement of the bowel (It is characterized by diarrhea (mostly at night time, postural diarrhea), constipation, malabsorption and fecal incontinence;

  1. urinary tract:

  • neurogenic vesical dysfunction (It is characterized by insidious onset and progression of bladder paralysis with urinary retention.);

  1. sexual disorders:

  • retrograde ejaculation (which is caused by dysfunction of the pelvic autonomic nervous system);

  • impotence, and sometimes decreased libido;

  1. cardiovascular system:

  • orthostatic hypotension (It is characterized by dizziness, vertigo, faintness, and syncope upon assumption of the upright posture and is caused by failure of peripheral arteriolar constriction.);

  • tachicardia (but it does not occur in response to hypotension because of sympathetic involvement).


^ Neuropathic arthropathy (Charcot’s joints)

is characterized by painless swelling of the feet without edema or signs of infection. The foot becomes shorter and wider, eversion, external rotation, and flattening of the longitudinal arch. This arthropathy is associated with sensory involvelvement, particularly impairment of afferent pain proprioceptive impulses.


Diabetic foot.

Appearance of diabetic foot is caused by a combination of vascular insufficiency, neuropathy, and infection.

Diabetic foot is divided on:

  • ischemic;

  • neuropathy;

  • mixed.




Ischemic

Neuropatic

Temperature of the skin

decreased

normal

Color of the skin

pallor or cyanotic

normal or pink

Pulsation on peripheral vessels

decreased or absent

normal

Odema

absent

can be

Sensibility

partly decreased or normal

decreased or absent

Ulcers

peripheral (distant)

under the pressure

Gangrene

Dry

moist


Tests and Assignments for Self-assessment.

Multiple Choice.

Choose the correct answer/statement:

  1. How many stages of diabetic nephropathy do you know?

  1. 1.

  2. 2.

  3. 3.

  4. 4.

  5. 5.

  1. What stage of diabetic retinopathy will have a patient with the presence off hemorrhages on the background (during ophthalmoscopic examination)?

  1. I.

  2. II.

  3. III.

3. Patient Н., 32 years, suffers from diabetes 2 type, average dur­ing 12 years. 5 years ago he has noticed edemas on the face in the morning which were decreased by the evening. Objective: the face is pastose, arterial pressure - 160/100 mmHg, Ps - 92 /min. The general analysis of urine: den­sities - 1002, protein - 1,6 g/l, leucocytes - 10-15 in sight, erythrocytes -1-2 fresh in sight, hyaline cylinders - single. The glomerular fltration - 42 ml/min. What is the diagnosis:

  1. Diabetic nephropathy

  2. Diabetes insipidus

  3. Chronic pyelonephritis

  4. Chronic glomerulonephritis

  5. Idiopathic hypertension

4. The patient of 53 years has diabetes type 1. He is treated in the hospital. Some days ago hypoglycemic status was observed. From that time the decompensation of diabetes, ketonuria are present, disturbing pain behind the breast bone which strengthen at the slight exercise stress. The aggravation of symptoms is connected with:

  1. Acute myocardial infarction

  2. Consequence of transient hypoglycemia

  3. Overdosage of insulin

  4. Diabetic neuropathy

  5. Inadequate physical loadings

5. The woman of 59 years, suffers from diabetes for 20 years. She was treated by oral antidiabetic drugs, last year she was treated with insulin. Her diabetes is decompensated, she does not follow diet. Now abdominal pains, meteorism, diarrhea of 5-7 times during a day are present, the skin is dry, hyperpigmented, tongue is red, geographical. The abdomen is painful at the palpation, the inferior edge of liver is on 4 cm below a costal arch. The diagnosis is:

  1. Diabetic gastroenteropathy

  2. Hepatitis

  3. Colitis

  4. Cholecystitis

  5. Pancreatitis


Answer: 1 – D. 2 – B. 3 – A. 4 – A. 5 – A.


Real-life situations to be solved:


Patient Н., 30 years, has DM for 10 years and takes insulin in dose 46 OD per day, in two injections. In anamnesis frequent hypoglycemic commas, decreasing of visual acuity, pain in the lower extremities. At the background of the eyes During ophthalmoscopic examination was found: microaneurisms, hemorrhages, distension of retinal veins. On the rheovasogram of the lower extremities is lowering of pulse amplitude. Fast serum glucose level is 13,2 mmol/l. What is your diagnosis?

Answer: Type I DM, hard (severe) degree, stage of the subcompensation. Diabetic preproliferative retinopathy (maculopathy) II stage. Diabetic angiopathy of lower extremities (functional stage) II stage.


Patient B., 42 years, has the type I of DM for 15 years. Complaints on persistent hypertension (during the last year), appearing of the edema on the legs and face. In the urine test: proteinurea is 0,99 gm/l, glucosurea is 20 gm/lt. Creatinine, urea within the pale of norm. Fast serum glucose level is 11,2 mmol/l. What is your diagnosis?

Answer: Type I DM, hard (severe) degree, stage of the subcompensation. Diabetic nephropathy, III (nephrotic) stage.


Students Practical Activities.

Work 1 : Students’ group is divided into 2 sub-groups, that work near the patients’ bed: ask the patients on organs and systems, take anamnesis of the disease , anamnesis of life, make objective exam. With the teacher’s presence. In the class-room they discuss the patients, learn data of laboratory and instrumental exam. of these patients.

1.To group the symptoms into the syndromes.

2.To find out the leading syndrome and make differential diagnosis.

3.To formulate the diagnosis.

4.To make a plan of treatment.


Methodological recommendation prepared assistant, c.m.s. Chernobrova O.I.

It is discussed and confirm on endocrinology department meeting

" 31 " august 2012 y. Protocol № 1.

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