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Diabetes mellitus

Diabetes mellitus. DM – Definition, Prevalence. chronic metabolic disease caused by absolute or relative insufficiency of insulin (or their combination) in the world approximately 270 million diabetic patients raising incidence, mainly DM type 2. Classification DM. DM type 1 DM type 2

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Diabetes mellitus

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  1. Diabetes mellitus

  2. DM – Definition, Prevalence • chronic metabolic disease caused by absolute or relative insufficiency of insulin (or their combination) • in the world approximately 270 million diabetic patients • raising incidence, mainly DM type 2

  3. Classification DM • DM type 1 • DM type 2 • Gestational DM • Other specific types of DM(e.g. MODY-hereditary forms linked to mitochondrias, drug induced DM - glucocorticoids, β-blockers, thiazides)

  4. Acute Complications of DM • diabetic ketoacidosis(typical for DM type 1, but can also occur at DM type 2) • hyperosmolar coma(typical for DM type 2) • hypoglycaemic coma

  5. Chronic Complications of DM • diabetic macroangiopathy =acceleration of atherosclerosis • diabetic microangiopathy = damage of retinal and renal vessels • diabetic nephropathy • diabetic neuropathy = senzo-motoric affection

  6. Prevention of Complications • good long-term diabetes controll • complex treatment of concomitant risk factors(hypertension, dyslipidemia, obesity...)

  7. DM type 1 • most often among children • genetically determined(allele DQ8, DR3,4) • autoimune destruction of B-cells in pancreas by Tc lymphocytes • absolute insufficiency of insulin • requires whole-life treatment with insulin

  8. DM type 1 - Diagnosis • clinically:polyuria, polydypsia, loosing of weight, acetone foetor ex ore • biochemically:  fasting glycemia >7 mmol/l  oGTT - glycemia 120 min. >11mmol/l  C-peptide ↓ or 0  urine: + ketonuria, glucose

  9. DM type 1 - Treatment • nowadays exclusively only human insulins • effort to imitate diurnal secretion of insulin (basal + postprandial) • important education of parents and also children (selfmonitoring, regimen precaution)

  10. Insulins According to Origin 1. Semisynthetic – from porcine insulin by the change of AA(Insuman) 2. Prepared by recombinant DNA method (Humulin - HM) 3. Insulin analogues(exchange, change of sequence or type of AA)= better pharmacocinetic

  11. Insulins according to Length of Action A. Short acting:  fast beginning of the effect (15 - 30 min.)  acting 3 - 6 hours  water soluable  s.c. or i.v. administration (acute states require i.v. administration !!!)

  12. Insulins according to Length of Action B. Intermediate acting (NPH) :  slower beginning of the effect (1 - 3 hours)  acting 4 - 12 hours  suspensions  only s.c. administration (after i.v. administration risk of embolisation !!)

  13. Insulins according to Lenght of Action B. Insulins with prolonged action:  slow beginning of the effect (3 - 4 hours)  acting 10 - 24 hours  suspensions  only s.c. administration

  14. Insulin Analogues • Insulins lispro + aspart  beginning of the effect till 15 min., lasts shortly (cca 1 hour)  possible to administer right before meal • Insulins glargine + detemir  act 16 – 24 hours  usually enough to administer one time per day

  15. Adverse Effects of Insulin • hypoglycemia:↑ dose, insufficient food income, interaction with alcohol • lipodystrophy:at human ins. rarely • weight gain:at ↑ daily doses of insul. at DM type 2 • local allergy: rarely

  16. Insulin Regimens • the conventional regimen 1-2 s.c. injections/day  at DM type 2 after failure of treatment with PAD or + PAD • intensified regimen (basal + bolus)  standard at DM type 1  at DM type 2 after failure of PAD

  17. Intensified Regimen • the best imitation of physiologic insulin secretion • Important is patient education (selfmonitoring) • most often 4-5 s.c. injections/day • intermediate ins. only at evening or in morning – at evening (basal), short-acting ins. before main meal morning-noon-evening (bolus)

  18. Insulin Pump • continual s.c. administration of insulin • only for good cooperating patients after adequate education • the best compensation of diabetes • in case of combination with sensor to monitor glycemia, automatic adjustment of doses

  19. Aplication Forms of Insulin • injection • insulin pens • ins. pump • inhaled insulin (powder) • peroral forms = in development

  20. Indications of Insulin Therapy • DM type 1 • DM type 2  loss of PAD effectiveness  surgery, intercurrent diseases • gestational DM • states after pancreatectomia, pankreatitis

  21. Goals of DM Type 1 Therapy • prevention of chronic complications by good diabetes compensation  long-term glycemia ≤ 7 mmol/l  HbA1c (glykosyled Hb) < 7% • keeping stabilized glycemia  without frequent hypo-hyperglycemias • keeping the best possible quality of patient´s lives

  22. DM Type 2 • insulin resistance at postreceptor level = relative insulin deficiency, later also absolute • the same CV risk as patients after MI !!! • marked therefore as also „CV disease” • frequently part of metabolic syndrome

  23. DM Type 2 - Treatment • must be complex (hypertension, dyslipidemia, obesity...) • important regimen precautions  loss of weight  reduction diet  physical activity

  24. Peroral Antidiabetics 1. Stimulators of insulin secretion a. derivates of sulfonylurea b. derivates of meglitinides 2. Insulin sensitisers a. biguanines b. thiazolidindiones (glitazones) 3. Inhibitors of intestine glukosidases 4. New antidiabetics

  25. Derivates of Sulfonylurea • stimulation of endogenous insulin secretion • effect depends on the functional B-cells of pancr. • in monotherapy or in combination • binding to albumin > 90%=interactions !!! • AE - hypoglycemia (carefull, interactions with NSA, alcohol, warfarin) • risk of hypoglycemia mainly glibenclamid, less glipizid and gliklazid

  26. Derivates of Meglitinide • short-lasting stimulation of insulin secretion = influencing postprandial glycemia • taking before the main meal • metabolism in liver = possibility to give to patients with renal insufficiency • mostly in combination with metformin • AE -hypoglycemia • repaglinid, nateglinid

  27. Biguanines - Metformin • insulin sensitisers =increase sensitivity of tissues to insulin, ↓ level of TAG, anorectic and antabus effect • drug of the 1st choice in the treatment of DM type 2 • after treatment failure combination with other PAD • AE - GIT intollerance, lactic acidosis (↑ risk among alkoholitics andat chronic renal, hepatal and respiratorydiseases)

  28. Thiazolidindions (Glitazons) – Rosiglitazone, Pioglitazone • activators of nuclear receptor PPARy(transkriptional factor) = increase sensitivity of tissues to insulin, ↓ TAG, ↑ HDL • AE -↑ weight(fat redistribution),fluid retention = oedemas, heart failure, among risk patients↑ CV mortality !! • not the 1st choice, only incombination withother PAD

  29. Inhibitors of Intestine Glukosidases (Akarbose) • inhibition of disacharidases in small intestine = slowing down of composite sacharides hydrolysis • influencing only postprandial glycemia • oft AE -flattulence, diarrhoea, stomach pain • less used, only in combination

  30. New Antidiabetics • on the ground of GLP-1(glucagon-like peptide 1) = incretin, released in small intestine after stimulation with food, degraded by DPP-4 (dipeptidyl peptidáza 4)  stimulates insulin secretion from B-cells  decreases glucagon secretion  has anorectic effect • low risk of hypoglycemia • don´t lead to weight gain • in combination with metformin

  31. New Antidiabetics 1. Analogues of GLP-1 = liraglutid, exenatid  s.c. aplication 2. Inhibitors of DPP-4 (gliptins) = sitagliptine  p.o. aplication AE -nasopharyngeal + urinary infections

  32. DM Type 2 as the part of Metabolic Syndrome • metabolic sy = ↑↑↑ CV risk  insulin resistance (± DM type 2)  abdominal obesity (weist circumference)  hypertension  dyslipidemia  protrombotic state  hyperuricaemia

  33. DM Type 2 as the part of Metabolic Syndrome = need of complex therapy of all risk factors • hypertension -ACEI, Sartans, CaCB(telmisartan = PPARy agonist) • protrombotic state -aspirin, clopidogrel • dyslipidemia - statins • obesity - diet, excercise, antiobesitic drugs

  34. Obesity • key etiologic factor of metabolic sy(ins. resistance) • CV risk mainly abdominal obesity (weist circumference > 102 cm men, > 88 cm women) • without weight loss is good compensation of DM type 2 almost impossible !!!

  35. Case • 13 year old boy, last days is feeling more tired, urinates several times per day also at night, permanently feels thirst despite of drinking more than 2 l fluids per day, fainted at school, before cramp pain of stomach • Anamnesis: not seriously ill before, family history without no remarkable • Objectively at admission: skin pale, intensificated breathing, signs of dehydration, foetor ex ore after fruit, BP: 90/60, P: 95/min.

  36. Case 1. What is susspicious diagnosis? 2. What examinations would you recommend ? 3. What is pseudoperitonitis diabetica? 4. Make pharmacoterapeutic plan

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