ENDO-DM Type1 Flashcards
What is the gold standard for diabetes diagnosis?
HgbA1c for assessing glucose control over previous 6-8 weeks.
glycated hemoglobin A1c. - RBC independent of insulin
glucose molecule bonds with a protein or fat molecule without the help of an enzyme.
Why HgbA1ct test is for 3 months?
RBC 120 days.
Blood RBC exposed to sugar molecules
HbA1c formed, not altered until RBC death
What is the new diagnostic test?
Timed test
How would you describe Pathophysiology of Type 1 Diabetes to a Patient?
1] an autoimmune destruction of the beta cells- insulin deficiency. slowly or rapidly.
2] associated with Hashimoto’s thyroiditis and Celiac disease
What AUTOABS markers for type I are seen?
islet cell autoantibodies
glutamic acid decarboxylase 65 (GAD 65).
Who gets Type 1 Diabetes?
5-15%
MC metabolic disease of childhood.
children age 4 years and older.
Peak age 11-13 years.
adulthood -less aggressive with hyperglycemia without DKA)
Pt c/o the following:
polyuria, polydipsia and polyphagia,
What other findings?
1] weight loss, fatigue, nausea, muscle cramping blurred vision.
2] MC diabetic ketoacidosis or on the verge. Missed in kid until too late
How do HCP Diagnosis type I?
This population
symptoms + random BG >200mg/dl is diagnostic.
What insulin is used for meals?
1] Rapid-acting: lispro, aspart, glulisine,
“Theres a LAG in DX of DM 1”
2] Short-acting: Regular
What insulin is used for basal?
1]Intermediate-acting: NPH, Lente,
“Basal Night Light.”
2] Long-acting: Ultralente, glargine, detemir
“UGD- u got LONG diabetes”
What are pre-mixed insulin?
1] NPH/Regular Based 70/30, 50/50,
2] Lispro/NPL Based 75/25, 50/50,
3] Aspart/NPL Based 70/30
What are the new insulins?
1] degludec (Tresiba) ultra longacting insulin half life of 24 hours U100 or U200,
2] Glargine U 300 (Toujeo),
3] Humalog U200
What are the adjunct therapy to insulin for type I
Pramlintide (Symlin)
analogue Amylin.
affects post prandial glucose values by:
slowing gastric emptying-appetite suppression.
inhibiting glucagon
less post meal hyperglycemia
potential for weight loss.
Describe Amylin
secreted from the beta cells with insulin
MOA-hypoglycemia, nausea, headache and dizziness.
What is the honeymoon period for new DX patients with DM1”?
patients continue to make insulin and so their needs are less than they will eventually be.
How to initiate insulin in Type 1 DM
1] 0.3-0.5 x KG= total daily dose (TDD)
2] ½ (TDD) as basal insulin so 8u long acting insulin,
3] other ½ is the rapid acting/ #meals OR
come up with ratios, For meals 2-3u rapid acting AC
How much rapid acting insulin is needed/gm of carbohydrate ?
Rule of 500
Divide 500 by TDD = 1 unit per #
How to calculate the correction use Rule of 1800
Divide 1800 by TDD,
1u drops blood sugar
What is the insulin dosage correction?
1] BG: <210 -> 2u (for food),
2] BG: 211-320 -> 3u,
3] 321-430 -> 4u,
4] >431 -> 5u
What is the goal for all patients with type I DM
intensive insulin therapy (IIT)- long acting and rapid acting insulin (basal/bolus therapy)
continuous subcutaneous insulin infusion (CSII) an insulin pump.
what is the standard insulin sensitivity
0.5-0.8 x BW kg = TDD
Not newly diagnosed, learning new techniques of intensive insulin therapy
Your PT who has DM 2 needs to initiate insulin. What are the steps and WHy
covers hepatic glucose production in a fasting state
meal insulin to cover food ingested.
basal 0.3-0.5u/kg
replacement 0.6-1.0u/kg
Are premeal insulin based on CHO? how?
YES
I:CHO ratio
Also given a correction amount if the premeal BG is elevated -1u:50>150
What are pumps used for?
only rapid acting insulin.
continuous infusion rate (basal rate) is programmed to cover daily hepatic glucose production
insulin boluses are given for meals and to correct for an elevated glucose
programmable calculators- enter in their current BG and CHO, the pump will calculate the bolus needed.
What are the off-label medications use for type I
1] GLP-1 agonists,
2] SGLT2 Inhibitors,
3] Metformin
Pt feels hot, irritable, thirsty, drowsy, lots of urination early morning hours (2-8am). What is this effect?
insulin resistance-BG rise due to hepatic glucose production, nocturnal growth hormone release that
The Dawn Phenomenon
Pt c/o blurred vision, confusion, and dizziness upon waking? Why? What are steps to prevent?
BG drops too low at night due to excess dinner time or bedtime insulin w/ release of counter regulatory hormones such as glucagon and epinephrine.
liver converts glycogen to glucose= high BG following a hypoglycemic episode.
The Somogyi Effect
Pt should dec. Insulin amount post meal
Goal for long term success of type I
self monitor blood glucose (SMBG)
diet that is individualized for each patient.
A dietician
psychosocial stressors.
What considerations are suggestive of Type I DM
1] elevated FBG and a C-peptide level <0.6ng/mL,
2] high positive titer of GAD 65 or islet ABS
PT 6yo M in ED c/o n/v, ABD pain. Parents say he has been the following: polyuria, polydipsia, Weakness, malaise and headache.
P/E- Kussmal- Deep, rapid RR-
Work up Hyperkalcemia- 5.3 LOW Na 134 CO2 6 BUN- 15 SCr 0.3 LOW GLU- 543 Describe the acute complications of hyperglycemia in type I DM ]
Diabetic Ketoacidosis (DKA)
that causes respiratory alkalosis in an attempt to correct the metabolic acidosis, ketonemia
Usually occurs in Type 1 diabetics due to profound insulin deficiency. hormone release which causes hydrolysis of TGs, releasing free fatty acids (FFA) and glycerol (lipolysis).
glycerol l/t increased hepatic glucose production, which worsens hyperglycemia.
Excessive amounts of ketone bodies are formed in the liver from FFA
How do we treatment of DKA?
1] Hospitalization
2] Correct fluid and electrolyte disturbances.
3] Provide insulin SLOWLY D/T effects of Na/K+ pumps t
4] Watch for complications of treatment- HYPORKalemia
Describe the use of Continuous Glucose Monitors
standard of care for Type 1 DM: transcutaneous sensors that transmit a continuous glucose reading to a receiver Q 5 minutes,
calculate predicted blood glucose
expensive
Describe long term management for type I
1] ACE I or ARB prevent or delay proteinuria.
2] Aspirin therapy for all patients >40 y/o.,
3] Statin therapy if history of MI or LDL >100. CV risk
When should ACE I, ARBs, and Statins be avoided in?
DO NOT USE IN WOMEN OF CHILD BEARING AGE,
risk of fetal renal damage