Type I diabetes - Endo Flashcards
What is Diabetes?
- Too much circulating glucose
- Insulin is not working to drive it into the cells
- Pancreas not producing; OR
- Insulin not effective; ORBoth
- Type I is a failure of the pancreas to produce insulin
- Cellular-mediated autoimmune destruction of the beta (β) cells of the pancreas
- 5% of Type 1 is idiopathic
Pathophysiology
- Rate of destruction of β-cells is rapid in children, slower in adults
- Symptoms start when 80% of islets are destroyed
- Kids present with DKA (diabetic ketoacidosis)
- Older folks have longer symptomatic prodrome and present with hyperglycemia and positive autoAbs
- Characterized by severe insulin DEFICIENCY
- Exogenous insulin is REQUIRED to control blood glucose
- Without insulin, ketosis begins in 6-8 hrs, DKA in 12-24 hrs
- Autoantibodies to insulin and other antigens are present months to years before disease
- They don’t mediate β-cell destruction
- β-cell damage is mediated by T lymphocytes
- Immunosuppression can slow damage, but no durable effect when stopped
- Early in the course, some insulin secretory capacity remains
- Insulin requirements may be lower than expected (0.3-0.4 units/kg)
- Tight control early preserves β-cell function; prevents or delays complications
- LATA (latent autoimmune diabetes in adults)
- Mild to moderate hyperglycemia early
- Responds to noninsulin therapy at first
- Progresses to insulin dependence over mo to yrs
- Have autoantibodies and require insulin earlier than T2DM
Epidemiology
- T1DM is most common diabetes in children
- Can develop at any age
- ¼ are diagnosed as adults
- 2/3 of child diabetics are T1
- 1.5 million in US
- 160,000-200,000 younger than 20
- About 20,000 diagnosed annually
- All ethnic groups
- Highest in European ancestry
- Lowest in Asians and Native Americans
Genetics
- Multiple loci in the HLA region and elsewhere implicated
- 6% of siblings or offspring develop diabetes (prevalence in gen pop 0.2-0.3%)
- Fewer than 10% of children with new dx have a parent or sib with it
- If BOTH parents have T1DM, up to 30% of offspring
- Incidence increasing dramatically worldwide
- Doubling every 20 years, all ethnic groups
- Probable environmental determinants
- No effective prevention
Diagnosis
Classic
- Polyuria, polydipsia, weight loss; Ketoacidosis
- Silent/incidental
- Post-obesity epidemic: Milder symptoms, Obesity not uncommon
- More than HALF of DKA patients have been seen in the days preceding
- Obvious signs/symptoms missed
- Canada and Scandinavia are KICKING OUR BUTTS
- Better history-taking and point of care
sxs
Polyuria
- Serum glucose >180 gm/dL exceeds renal threshold
- Spills into urine, causing osmotic diuresis
- Kid Symptoms – heavy diapers, bedwetting, drinking bathwater
Polydipsia
-Increased serum osmolality – glucose and hypovolemia
Weight Loss
- Hypovolemia and increased catabolism
- Impaired glucose utilization in skeletal muscle and increased fat and muscle breakdown
- Appetite up at first, then more thirsty than hungry, and ketosis leads to nausea and anorexia
Labs
- Random blood glucose >200 mg/dL, confirmed in lab + typical symptoms = diabetes
- Transient “stress” or steroid-induced hyperglycemia can occur with illness
- If questionable, islet autoantibodies can help
- If HbA1c normal, home glucose monitoring for several days
DKA
- Abdominal pain, nausea, and vomiting: Mimics acute abdomen
- Mild-mod dehydration
- Kussmaul respirations (Deep, rapid)
- Progressive somnolence and obtundation
-HEAVY DIAPER IN A DEHYDRATED KID
Warning – warning – warning
-It takes a few seconds to check a glucose
> 200 mg/dL is always abnormal in a child
DKA Diagnostic Criteria
-Hyperglycemia >200 mg/dL
PLUS
-Metabolic Acidosis
pH < 7.3
OR
HCO3 < 15 mEq/L
DKA Management
-First assess severity to determine Tx setting
-Neurologic status any, even subtle, disturbance
-Cerebral edema -> POOR OUTCOME
-Acid-base status
pH 7.2-7.3 and bicarb 10-15 is mild
pH 7.1-7.2 and bicarb 5-10 is moderate
pH <5 is severe
-Volume status
-Duration of symptoms
DKA Management Principles
- Correct metabolic acidosis
- Hypovolemia, potassium, phosphate, etc
- Assume 7-10% dehydration in mod-severe
Clinical signs messy
- NS or LR 10mL/kg x 1-2 initial bolus
- NS + 40K (Kphos/KCl) 1.5-2 x maint for 4-6 hrs
- 1/2NS or NS + K based on Na, K
- Plan for full restoration over 48 hrs or so … not too fast
- Monitor for cerebral edema
- Insulin replacement
Insulin Replacement
- Wait until fluid boluses are done
- Continuous infusion 0.1 unit/kg/hr: 0.05 unit/kg/hr in younger patients
- Shooting for ~100 decrease/hour
When glucose down to 250-300 range, add D5 to the IVF
- To prevent hypoglycemia
- Hyperglycemia corrects before ketoacidosis
- Continued insulin infusion helps clear ketoacidosis
-Switch to subcutaneous insulin when ketoacidosis cleared and glucose 150-200 in young kids, 100-150 in older kids
Serum Sodium
Initial concentration depends on
- Net sodium and water lossess prior to presentation
- Degree of hyperglycemia
- Degree of lipemia
DKA is a form of HYPERTONIC DEHYDRATION
- So be careful in rehydrating
- Monitor serum sodium regularly and adjust IVF as needed (q hr x 3-4, then q 2hr until stable)
Reversing hyperglycemia with fluid expansion and insulin lowers plasma osmolality
- Water moves from extracellular to intracellular
- Serum sodium goes up
If sodium is not coming up appropriately
- Patient is at risk for cerebral edema
- Consider increasing sodium in IVF
If you are doing everything right, serum sodium should gradually rise
-Corrected Na = Measured Na + [△SG/ 42]
△SG is the increment above normal in serum glucose concentration (mg/dL)
-Na should rise about 2.4 meq/L for every 100 mg/dL fall in serum glucose
Serum Potassium
- Renal and GI losses: Tends to produce hypokalemia
- Insulin deficiency impairs K entry into cells: Tends to raise serum K
- Hyperosmolality pulls K and water out of cells: Tends to raise serum K
- SO K at presentation can be high, nl, or low
- Insulin drives K into cells: Decreases serum K, Usually need to add K to IVF after 1-2 hours
Metabolic Acidosis
- Insulin and fluid repletion leads to partial correction of the acidosis
- Insulin promotes metabolism of ketoacid anions
- So bicarb is generated (ketoacids = potential bicarb)
- New ketoacid generation stops
- Improved tissue perfusion corrects lactic acidosis
- Ketoacids excreted in urine can’t make bicarb
- SO mild non-gap acidosis develops during treatment
- Don’t use bicarb unless severe problems, like cardiac arrest – increases risk for cerebral edema
