Diabates Type I Flashcards

1
Q

what is HbA1c?

A
  • hemoglobin A1c (aka glycosylated hemoglobin) tells us an average BG over the life of a RBC which is 8-12 weeks
  • accurate bc the amount of glucose that combines with Hb (or glycates the hemoglobin) is directly proportional to the amount of sugar in the system at that time
  • GOLD STANDARD for assessing glucose control over previous 6-8 weeks
  • CGM download is becoming the new gold standard –> tell you percentage of time you are at blood sugar target range
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2
Q

pathophys of T1DM

A
  • autoimmune dz
  • causes destruction of beta cells
  • leads to absolute insulin deficiency
  • beta cell destruction can be slow or rapid
  • can be associated with other autoimmune disorders
  • usually slow in adults but rapid in kids
  • in children, by the time we pick it up most of their beta cells are destroyed
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3
Q

markers of autoimmune destruction

A
  • islet cell antibodies
  • insulin antibodies
  • glutamic acid decarboxylase 65 (GAD 65)
  • protein tyrosine phosphate
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4
Q

frequency and average age of onset

A
  • frequency: 5-15% of all cases –> this is the most common metabolic disease of childhood!!
  • age: diabetes usually presents in children age 4 and older; peak onset = 11-13. Can present in adulthood (presentation at this age tends to be less aggressive with hyperglycemia without DKA)
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5
Q

presentation of T1DM

A
  • usually present with polyuria, polydipsia, polyphagia
  • other sxs = weight loss, fatigue, nausea, muscle cramping, blurred vision
  • at presentation, pts typically in DKA or on the verge
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6
Q

dx of T1DM

A

-BG elevated. if they have even 3 of the sxs associated with T1DM along with BG >200mg/dl, this is DIAGNOSTIC!!

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7
Q

management of T1DM

A
  • INSULIN
  • NPH only if someone doesnt have insurance
  • Determir (levamir) is good in pregnancy (category B)
  • NEED BASAL INSULIN along with insulin for meals
  • NPH and levamir for basal insulin
  • Tresiba is the drug with the longest half life so its great for basal insulin
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8
Q

New insulins

A
  • Tresiba U100 or U200 (has ultra long half life - 24hrs)
  • Glargine U300 (Toujeo)
  • Humalog U200
  • Afrezza ultra fast acting (starts acting in 5 mins)
  • Umalog U200 = good for people taking large volumes
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9
Q

adjunct to insulin

A
  • primlintide (symlin): synthetic analogue of amylin
  • affects post prandial glucose values by slowing gastric emptying, inhibiting glucagon production in the liver and appetite suppression –> leads to less post meal hyperglycemia and potential for weight loss
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10
Q

amylin

A
  • neuroendocrine hormone cosecreted from beta cells with insulin
  • if you are missing amylin, you are also missing suppression of glucagon
  • amylin produces less post meal glucose spikes and people feel fuller faster
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11
Q

honeymoon period of DM dx

A

-pts body is still making insulin so their needs are less than they eventually will be

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12
Q

calculating total daily dose

A
  • 0.3-0.5 x weight in kg as starting total daily dose
  • if pt is 120 lbs, weight = 120/2.2 = 55kg
  • half of the TDD will be the basal insulin and half will be used for meals
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13
Q

calculating how much insulin you need per meal

A
  • rule of 500
  • divide 500 by TDD –> if we decide that TDD is 16u, then 500/16 = 31 –> this means that you need 1u insulin for every 31gm of carbohydrate
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14
Q

calculating units insulin needed for various BGs

A
BG .         Units insulin (for food)
<210 .           2u
211-320 .      3u
321-430 .      4u
>431 .            5u
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15
Q

modifiable risk factors

A

C ontrol your glucose, blood pressure and cholesterol!
E arly treatment of foot, eye, kidney, and heart problems
N o
S moking
E ducation about diabetes, nutrition and exercise

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16
Q

goal for pts with T1DM

A

-progress toward intensive insulin therapy (IIT) –> this could be long acting and rapid acting insulin (basal/bolus therapy) or continuous subcutaneous insulin infusion (CSII) with insulin pump.

17
Q

standard insulin sensitivity

A
  • 0.5-0.8 x body weight

- higher percentage because this is for people who are NOT newly diagnosed

18
Q

intensive insulin therapy

A
  • pts require basal insulin to cover hepatic glucose production hepatic glucose production in a fasting state and use meal time insulin to cover food ingested
  • pts taught to adjust premeal insulin based on carb content of meals (I:CHO ratio)
19
Q

CSII insulin pumps

A
  • pumps use ONLY rapid acting insulin
  • continuous infusion rate programmed to cover daily hepatic glucose production and insulin boluses are given for meals and to correct elevated glucose
  • have programmable calculators with I:CHO ratios, sensitivities and targets
20
Q

Off label medications

A
  • GLP1 agonists –> slow rate food moves through stomach (also tells pancreas to make insulin but type I cant make insulin so this aspect of GLP1 agonists isnt helpful)
  • SGLT2 inhibitors –> DONT USE because they can go into euglycemic DKA
  • Metformin –> you can be type 1 when you’re 12 and when you’re 40 you look like type 2
21
Q

Dawn phenomenon

A

-describes rise in BG that happens in early morning (2-8am) due to hepatic glucose production and nocturnal growth hormone release that exacerbates insulin resistance

22
Q

Somogyi effect

A

-describes BG drops too low at night due to excess dinner time or bedtime insulin and the release of counter regulatory horones such as glucagon and epinephrine –> these cause liver to convert stores of glycogen to glucose and cause period of high BG following hypoglycemic episode

23
Q

education for DM

A
  • for long term success, biggest part of management is education
  • pts need to learn how to self monitor blood glucose (SMBG) and learn appropriate diet
  • also crucial to address psychosocial stressors
24
Q

how to determine what type of diabetes it is

A
  • if unclear, elevated FBG and C-peptide level <0.6ng/mL is suggestive but not diagnostic of T1DM
  • C-peptide is formed during conversion of pro-insulin to insulin
  • high positive titer of GAD65 Abs or islet cell autoAbs is also suggestive of T1DM
  • AN EXCEPTION is the pt with T2DM who presents with very high glucose (>300), who temporarily has low insulin and/or C-peptide level but who will recover insulin production once normal glucose is restored
25
Q

diabetic ketoacidosis

A
  • usually occurs in T1DM due to profound insulin deficiency
  • causes increased counterregulatory hormone release which causes hydrolysis of TGs, releasing free fatty acids (FFA) and glycerol (lipolysis)
  • glycerol leads to increased hepatic glucose production which worsens hyperglycemia
  • excessive amounts of ketone bodies formed in the liver from FFA results in ketonemia and metabolic acidosis
26
Q

DKA sxs

A
  • polyuria, polydipsia, blurred vision, weight loss
  • weakness, lethargy, malaise, HA
  • n/v, abdominal pain
  • deep, rapid breathing that causes resp alkalosis in attempt to correct metabolic acidosis
27
Q

tx of DKA

A
  • hospitalization
  • correct fluid and electrolyte disturbances
  • provide adequate insulin to restore and maintain normal glucose metabolism and correct acidosis
  • watch for complications of tx