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
Q

Describe a person’s potassium levels in diabetic ketoacidosis

A

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
Q

Tx for Diabetic Ketoacidosis

which CAN but doesn’t usually p/w T2 DM

A
  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
Q

Best way to measure severity of DKA?

A

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
Q

Diabetic tests + for microalbuminuria — how should you treat this?

A

Start them on an ACE-inhibitor or ARB.

These decrease the rate of nephropathy by decreasing intraglomerular hypertension & decreasing damage to the kidney.

29
Q

How does Gastroparesis occur in diabetics & what is it?

A

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
Q

Gastroparesis Tx in DM?

A

Metoclopramide & Erythromycin

which increase gastric motility

31
Q

What is proliferative retinopathy? Tx?

A

It is when neovascularization & vitreous hemorrhages are present.

Tx = Laser photocoagulation, which markedly retards progression of blindness

32
Q

How do you treat the pain in Diabetic Neuropathy?

A

Pregabalin, Gabapentin, or Tricyclic Antidepressants