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DEMS_BTRAN > UNIT2_Diabetes & Insulin > Flashcards

UNIT2_Diabetes & Insulin Flashcards

1
Q

What are the Rapid-Acting drugs? (3)

A

“-log” drugs:

  • Humalog (Lispro)
  • Novolog (Aspart)
  • Glulisine (Apidra)
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2
Q

What class of insulin drugs has the following profile?

 Onset in 5-15 min
 Peak 1-1.5 hr
 Lasts 3-5 hrs
 Subcut injection or insulin pump

A

“-log” drugs: Rapid Acting

  • Humalog (Lispro)
  • Novolog (Aspart)
  • Glulisine (Apidra)
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3
Q

How do you use the rapid-acting “-log” insulin drugs?

A
  • Injected right before a meal to prevent post-prandial hyperglycemia.
  • used for continuous infusion pumps
  • can be mixed with NPH
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4
Q

What are the Short-Acting insulin drugs? (2)

A

“-lin R” drugs:

  • Humulin-R
  • Novolin-R
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5
Q

What class of insulin drugs has the following profile?

 Onset in 30-60 min
 Peak in 2 hrs
 Lasts 6-8 hrs
 Subcut injection, IV infusion

A

“-lin R” drugs:

  • Humulin-R
  • Novolin-R
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6
Q

Describe how you use and the details of Short-Acting insulin drugs.

A
  • Recombinant human insulin (soluble crystalline zinc –> Zn improves stability/shelf-life)
  • Inject 30 min before eating
  • Usually used in hospital setting for DKA (IV infusion of insulin)
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7
Q

What are the long-acting insulin drugs?

A

Long-Acting:

  • Glargine (Lantus)
  • Detemir (Levemir)
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8
Q

What is a special fact about the long-acting insulin drugs?

A

Cannot be mixed in same syringe with any other insulins (because of acidic pH)

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9
Q

What class of insulin drugs has the following profile?

 Onset of action 2-4 hrs
 Peak 6-7 hrs
 Lasts 10-20 hrs
 Subcut injection only (2x/day)

A

Long-Acting:

  • Glargine (Lantus)
  • Detemir (Levemir)
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10
Q

Describe how you use and the details of Bisphasic/Mixed insulin drugs.

A
  • Reduce number of injections; get basal and prandial insulin at same time
  • NPH/Regular: 70/30 or 50/50 mixes injected before breakfast and before dinner
  • Intermediate/Humalog or Novolog: admin before eating
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11
Q

What are the 2 major types of biphasic/mixed insulin drugs?

A

Biphasic/Mixed drugs:

  • NPH/Regular
  • Intermediate/Humalog -or- Novolog
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12
Q

How and when do you administer biphasic/mixed insulin?

A
  • SubQ injection

- Rapid onset right before meal, with longer lasting basal insulin

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13
Q

What are the Insulin Therapy Targets values for the following:

  • Fasting Glucose: ?
  • 2 hr post prandial: ?
  • A1C: ?
A
  • Fasting Glucose: 70-130 mg/dl
  • 2 hr post prandial <180 mg/dl
  • A1c < 7; Many different factors (i.e. age, newly diagnosed, presence of complications, etc) influence whether you will have a stringent (<6.5 HbA1c) or lenient (<8) goal.
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14
Q

Normally, the Pancreas secretes about ___ units of insulin per day.

A

30 units.

basal insulin plus insulin release in response to exogenous stimuli i.e. blood glucose > 100

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15
Q

Prandial (post-eating) insulin has two phases:

1) first phase is ____1____.
2) second phase ____2____ min after ingestion.

insulin concentrations peak at ____3____ min after ingestion

A
  1. immediate
  2. 8-10 minutes
  3. 30-45 minutes
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16
Q

Long-acting (i.e. glargine) injected once per day + rapid-insulin right before meal (calculate carbs) describes the Tx for which type of diabetes?

A

Type I Diabetes Regimen;

“Basal Bolus” Tx

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17
Q

In the Tx of T1D, what are the advantages and disadvantages of a Continuous subcutaneous insulin infusion (insulin pump): rapid-acting insulin

A
  • Advantages: eliminates multiple injections, can set different basal rates, can have partial unit, can give different bolus types.
  • Disadvantages: upfront cost, significant training, motivation, ability to troubleshoot, interruption of infusion or “bad site” can lead to DKA within hrs.
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18
Q

When do you consider using insulin for a DM2 pt.?

A
  • If have contraindications to other agents (i.e. renal or hepatic dysfunction, CHF)
  • If lifestyle plus non-insulin medications have not resulted in sufficient decrease in HbA1c (usually occurs 10 years after onset of disease)
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19
Q

When do you ALWAYS use insulin for a DM2 pt.?

A

ALWAYS use insulin if have signs of severe insulin deficiency:

  • fasting glucose >250 mg/dL
  • random glucose > 300 mg/dL
  • HbA1c > 10%
  • Hospital admission (i.e. for DKA, hyperglycemic hyperosmolar state-HHS)
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20
Q

If the patient has early morning HYPERglycemia, this is usaually due to what? (3)

A

1) inadequate basal insulin.
2) waning effect of basal insulin.
3) Somogyi effect (nocturnal HYPOglycemia causes surge of counter-regulatory hormones in the morning)

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21
Q

In a hospital, inpatient setting, you stop all oral agents and administer insulin for hyperglycemia to reach targets of random BG= ___1___ and/or premeal BG= ___2___.

A
  1. Random Blood Glucose <180 mg/dL

2. Premeal BG <140 mg/dL

22
Q

What are the barriers to insulin therapy?

A
  • fear of injections
  • hypoglycemia
  • gaining weight
  • stigma
  • inconvenience
23
Q

What is the general concept when it comes to adjusting insulin dosing?

A

eliminate the lows first and then eliminate the highs; adjust dose 10-20%

24
Q

What is the first-line drug Tx for DM2?

A

Metformin

25
Q

What diabetic drugs are the weight loss/weight neutral drugs?

A

Weight loss/weight neutral drugs:

  • Metformin
  • GLP-1 Agonist
  • DPP-IV inhibitors
  • Amylin
26
Q

What diabetic drugs are the weight gain drugs?

A

Weight gain drugs:

  • sulfonylureas
  • TZDs
  • insulin
27
Q

Insulin is most potent (biggest reduction in what lab value?); followed by Metformin and sulfonylureas

A

HbA1c

28
Q

Insulin is most potent (biggest reduction in HbA1c); followed by what drugs?

A

Metformin and sulfonylureas

29
Q

What HLAs types increase risk for T1D? Which HLA are Protective?

A
  • Risk: HLA-DR3/4
  • Protective: HLA-DR2

HLA (accounts for 50% of genetic risk, esp HLA-D which codes MHC Class II)

Genetic risk is additive!

30
Q

Describe the Insulin Gene:

A

Class I VNTR (tandem repeats) within 5’ region associated with increased risk –> less insulin expressed in thymus = decreased ability to distinguish insulin as self rather than pathogen.

31
Q

What are some environmental factors ~w/ T1D?

A
  • Viruses
  • breastfeeding
  • timing of food introduction to infants
  • hygiene hypothesis
  • accelerator hypothesis (obesity speeds up onset of disease)

!!!Vit. D may be protective!!!

32
Q

What are the ~ commodities of T1D?

A
  • Autoimmune thyroid (15-20%)
  • Celiac (5-10%)
  • Addison’s (1-1.5%)
33
Q

The etiology of T1D is not completely known: genetics predisposition and/or environmental triggers cause autoimmunity that decrease beta cell mass over time; clinical onset when have lost ____ of beta cells.

A

80-90%

34
Q

What are the clinical presentation features of T1D?

A
  • Usually in childhood (peak incidence is 10-12 yrs old, though presenting more in < 5 yrs)
  • Usually in normal weight individuals
  • Polyuria/nocturia, polydipsia
  • Weight loss
  • Blurry vision
  • Acute presentation=DKA (abdominal pain, Kussmaul, nausea/vomiting)
  • 10-20% have positive family history
35
Q

Do T1D pt. have low or high C-Peptide?

A

LOW C-Peptide ~ T1D

36
Q

Absolute lack of insulin AND increased counter-regulatory hormones is classic in what complication of diabetes?

A

DKA;

Without insulin, both glucose and ketones are overproduced but underutilized.

37
Q

Do diabetic pt. who are in DKA have HYPOnatremia?

A

Apparent (not real) hyponatremia:
• To correct: Need to add 2 mEq Na to lab value for every 100 mg/dL of excess serum glucose

  • K looks high but is low or nl (intracell K+ exchanged for extracell H+ –> so K+ looks high –> may become hypokalemic if treated with fluids).
  • HCT and Cr may be high from dehydration
38
Q

What is C-peptide labs used for?

A

Measure C-peptide to determine if low blood sugar is due to exogenous or endogenous insulin

39
Q

What are the major classes of MICROVASCULAR complications of diabetes? (4)

A
  • Retinopathy
  • Nepropathy
  • Neuropathy
  • Diabetic Foot Disease
40
Q

What are the major issues of the MACROVASCULAR complications of diabetes?

A
  • 77% of hospitalizations and 80% of mortality in DM is due to CVD
  • MI, stroke, peripheral vascular disease (2-4x greater incidence) –> leading cause of death in DM patients
  • Hyperglycemia causes endothelial cell dysfunction: decreases vasoactive peptides, secretes adhesive molecules, loses tight junctions, abnl vascular smooth muscle, decreased fibrinolysis –> increased risk of atherosclerosis and procoagulation.
  • T2DM patients often have HTN (not in T1DM unless develop renal disease)
  • Hyperinsulinemia (metabolic syndrome and insulin resistance) damages vessel wall and increases CV risk
  • DM patients should be treated as though they have cardiovascular disease (statins, BP control, ACEi/ARBs)
41
Q

What are the normal values?:

  • Fasting glucose = ?
  • 2-hr PG = ?
  • HbA1c = ?
A
  • Fasting glucose <100 mg/dl
  • 2-hr PG < 140 mg/dl
  • HbA1c <5.7
42
Q

What is required to have DM2?

A

Insulin resistance AND decreased insulin secretion are required to develop diabetes.

43
Q

In terms of the epidemiology of DM2 pts., DM2 accounts for __% of diabetes patients; __th leading cause of death in US

A

90% of all diabetes pt.

5th leading cause of death

44
Q

w.r.t. DM2:

Insulin acts via which insulin pathway to confer a metabolic signal –> this signal is disrupted in insulin resistance.

A

PI3K kinase.

(distinct from MAPK signaling which is growth/mitogenic)

• Metabolic signal disrupted –> leads to lipolysis –> release FFA –> FFA triggers hepatic production of glucose AND damage of beta cells –> hyperglycemia

45
Q

There is also Glucagon dysfunction in DM2, explain.

A

DM2 ~ glucagon dysfunction b/c alpha cells depend on beta-cell secretion to regulate:

decreased insulin –>
decreased inhibition of glucagon secretion –>
glucagon continues to stimulate liver to produce glucose –>
hyperglycemia

46
Q

Is DM2 diabetes ~w/ HLA phenotype?

A

NO!

• Associated co-morbidities: Obesity, hyperlipidemia, polycystic ovary disease, fatty liver disease

47
Q

What is the clinical presentation of DM2?

A

 Usually post-puberty; usually overweight/obese
 Usually not associated with ketoacidosis
 Polyuria/nocturia, polydipsia
 Weight loss
 Blurry vision
 >50% have positive family history

48
Q

T/F?:

In DM2, the First Phase Insulin Response (FPIR=insulin released in 1st and 3rd minute following IV glucose) is usually lost completely; the second phase is normal or exaggerated.

A

TRUE!

49
Q

In the Tx of DM2, when do pt. need insulin?

A

Usually require insulin after about 10 years of disease (or when A1c > 10%, whichever comes first).

50
Q

How/what drugs are used to Tx DM2?

A

 Diet and exercise
 Statins
 Antihypertensives
 Oral agents (Metformin first line; use 2 meds if A1c is 8-10%)

Aggressive management early on can prevent or delay complications.

51
Q

W.R.T diabetes, what are the levels of prevention?

A
  • Primary: stopping before development of autoAb (i.e. with infant diet changes—studies ongoing)
  • Secondary: prevent those with autoAb from developing clinical symptoms (i.e. with oral insulin—no clear delay in disease unless had very high Ab titers)
  • Tertiary: prevent progression of disease (i.e. with anti-CD3 antibodies, Abatacept)
52
Q

W.R.T diabetes, the prevention of those with autoAb from developing clinical symptoms (i.e. with oral insulin—no clear delay in disease unless had very high Ab titers.

Is was level of prevention?

A

Secondary

DEMS_BTRAN (8 decks)

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