Diabetes Flashcards

1
Q

4 ways T2 DM is diagnosed?

A
  1. 2 FBS levels > 125 mg/dL
  2. Single FBS level > 200 mg/dL + p/w Polyuria, Polyphagia, & Polydipsia
  3. Glucose tolerance testing with blood glucose > 200mg/dL
    (Blood glucose 140-199 mg/dL indicates insulin resistance)
  4. HbA1C > 6.5%
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2
Q

~ what % of T2 DM cases are controlled by weight loss alone?

A

~ 25%

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3
Q

Why are Sulfonylureas not used as 1st line Tx?

A

B/c they cause insulin release, driving glucose intracellularly & causing obesity.
Metformin used as 1st line instead.

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4
Q

Contraindications of Metformin? MOA?

A

c/i = Renal dysfunction (b/c it can accumulate & cause metabolic acidosis)

MOA = blocks gluconeogenesis

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5
Q

Contraindications of Thiazoladinediones (glitazones)?

A

CHF

because they increase fluid overload

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6
Q

Nateglinide MOA?

A

Stimulates insulin release in a manner similar to sulfonylureas (but does not contain sulfa)

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7
Q

Repaglinide MOA?

A

Stimulates insulin release in a manner similar to sulfonylureas (but does not contain sulfa)

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8
Q

Drug(s) w/ same MOA as sulfonylureas to use in a patient allergic to sulfa?

A
  • Nateglinide

- Repaglinide

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9
Q

Acarbose MOA?

A

alpha-glucosidase inhibitor — blocks glucose absorption in the bowel
(same as miglitol)
- can be used in renal insufficiency

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10
Q

Miglitol MOA?

A

alpha-glucosidase inhibitor — blocks glucose absorption in the bowel
(same as acarbose)
- can be used in renal insufficiency

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11
Q

Alpha glucosidase inhibitors (acarbose/miglitol):

- effect on HbA1C?

A
  • reduce by ~0.5
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12
Q

T2 DM drugs that can be used in renal insufficiency?

A

Alpha glucosidase inhibitors

acarbose/miglitol

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13
Q

Exenatide MOA?

A

GLP-1 agonist (incretin)

  • inc’s insulin secretion
  • dec’s glucagon secretion
  • dec’s gastric motility & aids in weight loss
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14
Q

Sitagliptin MOA?

A

DPP-4 inhibitor (incretin — which normally breaks down GLP-1)

  • inc’s insulin secretion
  • dec’s glucagon secretion
  • dec’s gastric motility & aids in weight loss
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15
Q

Saxagliptin MOA?

A

DPP-4 inhibitor (incretin — which normally breaks down GLP-1)

  • inc’s insulin secretion
  • dec’s glucagon secretion
  • dec’s gastric motility & aids in weight loss
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16
Q

Linagliptin MOA?

A

DPP-4 inhibitor (incretin — which normally breaks down GLP-1)

  • inc’s insulin secretion
  • dec’s glucagon secretion
  • dec’s gastric motility & aids in weight loss
17
Q

Exenatide side effects?

A

Pancreatitis

18
Q

Pramlinitide MOA?

A

Amylin analog (protein that is secreted normally w/ insulin)

  • Dec’s gastric emptying
  • Dec’s glucagon levels
  • Dec’s appetite
19
Q

Glargine - what is it?

A
Long-acting insulin given 1x/day 
(usually in combo w/ a short-acting insulin)
Onset = 1-2 hrs
Peak = 1-2 hours
Duration = 24 hours
20
Q

Lispro - what is it?

A

Short acting insulin
Onset = 5-15 min
Peak = 1hr
Duration = 3-4hrs

21
Q

Aspart - what is it?

A

Short acting insulin
Onset = 5-15 min
Peak = 1hr
Duration = 3-4hrs

22
Q

Glulisine - what is it?

A

Short acting insulin
Onset = 5-15 min
Peak = 1hr
Duration = 3-4hrs

23
Q

Regular insulin onset, peak, & duration?

A
Onset = 30-60 min
Peak = 2 hours
Duration = 6-8 hours
24
Q

NPH onset, peak, & duration?

A
Onset = 2-4 hours
Peak = 6-7 hours
Duration = 10-20 hours
25
Describe a person's potassium levels in diabetic ketoacidosis
Hyperkalemia in blood but decreased total body potassium b/c of urinary spillage (In Tx: Replace K+ when the K+ level comes down to a level approaching normal)
26
Tx for Diabetic Ketoacidosis | which CAN but doesn't usually p/w T2 DM
1. Large volume saline & Insulin replacement 2. Replace K+ once it comes down to a level approaching normal 3. Correct underlying cause: Noncompliance w/ meds, infection, pregnancy, or any serious illness
27
Best way to measure severity of DKA?
Serum Bicarbonate levels - if very low, there's a risk of death (high anion gap) - if high, then doesn't matter how high glucose is (lower anion gap)
28
Diabetic tests + for microalbuminuria --- how should you treat this?
Start them on an ACE-inhibitor or ARB. | These decrease the rate of nephropathy by decreasing intraglomerular hypertension & decreasing damage to the kidney.
29
How does Gastroparesis occur in diabetics & what is it?
After several years, DM decreases the ability of the gut to sense the stretch of the walls of the bowel. Stretch is the main stimulant to gastric motility. Gastroparesis = immobility of the bowels that leads to bloating, constipation, early satiety, vomiting, & abdominal discomfort
30
Gastroparesis Tx in DM?
Metoclopramide & Erythromycin | which increase gastric motility
31
What is proliferative retinopathy? Tx?
It is when neovascularization & vitreous hemorrhages are present. Tx = Laser photocoagulation, which markedly retards progression of blindness
32
How do you treat the pain in Diabetic Neuropathy?
Pregabalin, Gabapentin, or Tricyclic Antidepressants