Diabetes Treatment Flashcards

1
Q

lispro, aspar, glulisine

A

rapid acting insulins

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2
Q

novolin R, humulin R

A

short acting insulins

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3
Q

NPH humulin N, NPH novolin N

A

intermediate acting insulings

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4
Q

detemir, glargine

A

long acting insulins

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5
Q

insulin secretion stimulated by increase ________ ratio

A

ATP/ADP (glucose, AA, FA, parasympathetics, GPL-1)

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6
Q

insulin acts through stimulation of _________ receptor, acts in liver/muscle/adipose to decrease blood glucose levels and shift from energy use to storage

A

tyrosine kinase

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7
Q

treatment of DKA:

  • ______ of regular insulin at low rate
  • may need to admin _____ along with insulin to prevent hypoglycemia
A

IV infusion

glucose

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8
Q
  • tolbutamide, tolazamide, chlorpropamide (1st gen)

- glyburide, glipizide, glimepride (2nd gen)

A

sulfonylureas

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9
Q
  • activate residual beta cells to release insulin, bind K/ATP channel
  • hypoglycemia and weight gain
  • control hyperglycemia in type 2DM
  • contra: type 1DM, pregnancy, hepatic or renal insufficiency
A

sulonylureas (glyburide, glipizide, glimepride, tolbutamide, tolazamide, chlorpropamide)

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10
Q
  • bind different site than sulfonylureas to activate K/ATP channel
  • hypoglycemia, conta in hepatic insufficiency
  • repaglinide, nateglinide
A

meglitinides

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11
Q
  • increase peripheral insulin sensitivity, reduce hepatic gluconeogenesis, no weight gain or hypoglycemia, reduce triglycerides
  • 1st line therapy for t2DM
  • toxicity: lactic acidosis (impair hepatic metabolism of lactic acid), GI upset, vitamin B12 deficiency
A

metformin (biguanide)

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12
Q
  • PPAR agonists, transport serum lipids to adipose tissue, promote insulin sensitivity, decrease gluconeogenesis, enhance glucose uptake in skeletal muscles
  • reduce glucose and triglycerise levels
  • adverse: weight gain, hepatix tox, CHF
A

thiazolidinediones (rosiglitazone, pioglitazone)

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13
Q
  • reversible inhibitors of pancreatic alpha-amylase and alpha glucoside (increase time required to absorb complex carbs, reduce postprandial glucose peak)
  • used in combo with other agents
  • flatulence, bloating, diarrhea
A

alpha-glucosidase inhibitors (acarbose, miglitol)

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14
Q
  • increase insulin, decrease glucoagon
  • delay gastric emptying, decrease appetite
  • release stimulated by nutrients entering gut
A

GLP-1 incretins (-tide)

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15
Q
  • increase level of endogenous incretins (inhibit degradation)
  • don’t use with GLP-1 analogs
A

DDP-4 inhibitors (-gliptin)

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16
Q
  • inhibition causes glycosuria and lowers glucose levels
  • efficacy reduced in chronic kidney disease
  • increases UTIs, osmotic diuresis causes hypotension
  • weight loss
A

SGLT2 inhibitors (-flozin)

17
Q

canagliflozin, dapagliflozin, empagliflozin

A

SGLT2 inhibitors

18
Q
  • mimics high dose effects of amylin
  • increase insulin, decrease glucagon, delay emptying, decreases appetite
  • hypoglycemia, GI symptoms
A

pramlintide

19
Q
  • bile acid sequestrant, cholesterol lowering drug

- can exacerabte hypertriglyceridemia

A

covesevalam

20
Q
  • dopamine agonist, lowers glucose levels

- nausea, fatigue, dizziness, vomiting, headache

A

bromocriptine

21
Q
  • monotherapy: begin with metformin, GLP-1, SGLT2, or DDP-4 inhibitor
  • sulfonylureas and TZDs are ______ agents
A

second choice