Empfohlen
Weitere ähnliche Inhalte
Was ist angesagt?
Was ist angesagt? (20)
Andere mochten auch
Andere mochten auch (20)
Ăhnlich wie Acute Complications of Diabetes Mellitus
Ăhnlich wie Acute Complications of Diabetes Mellitus (20)
Mehr von Reshma Ann Mathew
Mehr von Reshma Ann Mathew (8)
KĂźrzlich hochgeladen
KĂźrzlich hochgeladen (20)
Acute Complications of Diabetes Mellitus
- 1. Acute Complications of Diabetes -Reshma Ann Mathew
- 2. DIABETES It is a GROUP of metabolic disease characterised by chronic hyperglycemia with DISTURBANCE in the carbohydrate, fat & protein metabolism resulting from DEFECTS in insulin secretion, insulin action or both .
- 3. Pancreas beta cells Insulin actions Glucose entry and utilization (oxidation, storage) Glucose entry and oxidation TG synthesis Normal glucose and fat metabolism
- 4. Pancreas beta cells Insulin actions Glucose entry and utilization (oxidation, storage) Glucose entry and oxidation TG synthesis Metabolic consequences of insulin deficiency/resistance
- 5. Clinical Features of DM due to insulin lack Polyphagia (decr. leptin?) Starvation in the midst of plenty Hyperosmolar hyperglycemic syndrome (HHS) Lactic acidosis Lactic acidosis Muscle protein breakdown Acetoacetate,0H-butyrate, acetone
- 7. ⢠Insulin level increases when? a) Glucose administered by mouth (food intake) b) Glucose given by IV (glucose infusion) c) No difference
- 9. ď CLASSIFICATION 1) Type 1 2) Type 2 3) Other specific types 4) Gestational diabetes
- 10. DIABETIC KETOACIDOSIS ⢠It is a MEDICAL emergency ⢠PRINCIPALLY seen in type 1 diabetes ⢠Mortality- ⢠CHILDREN & ADOLESCENTS- cerebral edema ⢠ADULTS- hypokalemia, acute respiratory distress syndrome & co-morbid conditions
- 11. ď PATHOPHYSIOLOGY Insulin Counterregulatory hormones Glucagon, Epinephrine, Cortisol, Growth hormone NORMAL
- 13. Insulin Deficiency Glucose uptake Proteolysis Lipolysis Amino Acids Glycerol Free Fatty Acids Gluconeogenesis Glycogenolysis Hyperglycemia Hepatic Ketogenesis Metabolic Acidosis Osmotic diuresis Dehydration & electrolyte loss Excess counterregulatory hormones Forces H+ ions into cells & displaces K+ Ketosis
- 14. ⢠The cardinal biochemical features are- 1) Hyperketonemia (> 3mmol/L) & Ketonuria (> 2+ on standard urine sticks) 2) Hyperglycaemia (blood glucose > 200mg/dL) 3) Metabolic acidosis (venous bicarbonate <15mmol/L and/or venous pH<7.3)
- 15. Insulin Deficiency Glucose uptake Proteolysis Lipolysis Amino Acids Glycerol Free Fatty Acids Gluconeogenesis Glycogenolysis Hyperglycemia Ketogenesis Acidosis Osmotic diuresis Polyuria, Polydipsia Fruity breath (acetone smell) Kussmaul breathing (acidotic) Mental status changes Dehydration (Dry tongue, Tachycardia, Hypotension) Abdominal pain Electrolyte imbalance Clinical manifestations
- 17. ď MANAGEMENT ďąInvestigations- oVENOUS BLOOD- for urea, electrolytes, glucose & bicarbonates oARTERIAL BLOOD GAS- to assess severity of acidosis oURINE- for ketones oECG oINFECTION SCREEN ďąTreatment- 1) SHORT ACTING SOLUBLE insulin 2) Fluid replacement- 0.9% saline (NaCl) 3) Potassium replacement 4) Sodium bicarbonate- in SEVERELYACIDOTIC patients 5) Antibiotics- if INFECTION is present
- 18. ď COMPLICATIONS 1) Cerebral edema- due to RAPID REDUCTION of blood glucose, USE of hypotonic fluids and/or bicarbonates 2) ARDS (Acute Respiratory Distress Syndrome) 3) Thromboembolism 4) DIC(Disseminated Intravascular Coagulation) 5) Acute Circulatory Failure
- 19. Hyperglycaemic Hyperosmolar State ďąHSS occurs due to- â˘Relative INSULIN DEFICIENCY â˘Inadequate FLUID INTAKE
- 20. ď PATHOPHYSIOLOGY Insulin deficiency SEVERE HYPERGLYCEMIA GLUCOSURIA WEIGHT LOSS OSMOTIC DIURESIS POLYURIA POLYDIPSIA LIPOLYSIS Without KETOSIS SEVERE OSMOTIC DEHYDRATION
- 21. ⢠It is characterised by 1) SEVERE hyperglycaemia (>600mg/dL) 2) Hyperosmolality (serum osmolality >320 mOsm/kg) 3) Dehydration (in the ABSENCE of significant hyperketonemia or acidosis)
- 22. ď CLINICAL MANIFESTATIONS ⢠Polyuria, weight loss, and diminished oral intake ⢠Profound dehydration ⢠Hypotension, tachycardia and altered mental status ⢠Mental confusion, lethargy or coma
- 23. ď MANAGEMENT ⢠Normalise osmolality- 0.45% saline ⢠Replace fluid and electrolyte losses ⢠Normalise blood glucose
- 24. HYPOGLYCEMIA ⢠Hypoglycemia (<63mg/dL) in DIABETES occurs due to insulin overdose or hyperinsulinemia ⢠Whippleâs triad- a) Symptoms consistent with HYPOGLYCEMIA b) Low plasma glucose conc. (measured with a precise method) c) Relief of symptoms after plasma glucose level is RAISED
- 25. Causes of Hypoglycemia in patients taking insulin ďMissed, delayed or inadequate meal ďUnexpected or unusual exercise ďAlcohol ďErrors in oral anti-diabetics or insulin dose/schedule/administration ďPoorly designed insulin regimen ďLipoatrophy at injection sites ďFactitous (deliberately induced) ďBreasting feeding by DIABETIC mother
- 26. NORMAL When blood glucose level FALLS Endogenous insulin release is SUPRESSED Release of glucagon is INCREASED Autonomic nervous system is ACTIVATED Release of catecholamine; stress hormones are INCREASED in blood REDUCTION of whole blood glucose uptake & INCREASES hepatic glucose production Thus, maintaining glucose supply to brain
- 27. TYPE 1 DIABETES CANNOT regulate insulin once it is injected subcutaneously Hypoglycemia
- 29. ď MANAGEMENT MILD (self treated) ⢠Oral fast acting carbohydrate (10-15g) is taken as glucose drink or tablets or confectionery ⢠Followed with a snack containing complex carbohydrate SEVERE ⢠If patient is SEMI-CONSCIOUS OR UNCONSCIOUS- oIV 75mL 20% dextrose (0.2g/kg in children) OR IM glucagon (0.5mg in children) ⢠If patient is CONSCIOUS and able to SWALLOW- oGive oral refined glucose as drink or sweets (25mg)
- 30. Dawn phenomenon & Somogyi effect ⢠DAWN PHENOMENON occurs when endogenous insulin secretion decreases ⢠SOMOGYI EFFECT is seen in cases of excessive amounts of exogenous insulin
- 31. SOMOGYI EFFECT TOO MUCH INSULIN HYPOGLYCEMIA GLUCAGON IS RELEASED LIPOLYSIS GLUCONEOGENESIS GLYCOGENOLYSIS REBOUND HYPERGLYCEMIA + KETOSIS
- 32. DAWN PHENOMENON Bodyâs response to hormones released in early morning hours Counter-regulatory hormones are released Glucose level increases In DM, there is decrease in insulin levels So HIGH GLUCOSE levels in morning
- 34. DKA vs. HHS HHSDKA More in elderlyMore in childrenAge More in type IIMore in type IDM type > 600> 250Glucose + or -+++++Ketonuria/emia >7.3<7.3pH >15<15HCO3 HyperosmolarityVariableS osmolarity Sensitive to small doseVariableSensitivity to insulin
- 35. DKA vs. HYPOGLYCEMIA HypoglycemiaDKA Insulin overdose or hyperinsulinemia Insulin deficiency or increased counter-reg hormones Etiology AcuteGradualOnset -S of Brain glucopenia - S of sympathetic overactivity S of hyperglycemia S of dehydration S of acidosis Symptoms and signs hypoglycemiahyperglycemiaRBS NoYesKetonuria NoYesKetonemia Rapidly recover if earlyNo effectIV glucose
Hinweis der Redaktion
- Balanitis â candadiasis;
- Following food intake, a number of other factors {amino acids(food contains fats, proteins, carbohydrates), hormones(glucagon like peptide 1 & gastrointestinal peptide)} released from the gut following food intake can increase the insulin release-known as incretin effect
- Incretin effect pic These are effective in incretin based therapies
- Mortality is high in developing countries and among non-hospitalised patients Co-morbid conditions- acute MI, sepsis or pneumonia
- Insulin deficiency is RELATIVE or ABSOLUTE
- 1) Electrolyte loss mostly Na & K-causes hyperaldosteronism 3) Elevated catecholamines & other stress hormones cause lipolysis -when hepatic ketogenesis exceeds in the body, acidic ketones accumulate in blood(metabolic acidosis)
- Insulin deficiency is Relative