Diabetes: week 1 Flashcards

1
Q

what happens during glycogenesis

A

glucose turning into glycogen (by insulin)

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2
Q

what kind of acid base issue does ketogenesis cause?

A

metabolic acidosis

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3
Q

which hormone stimulates glycogen breakdown into glucose

A

glucagon

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4
Q

what are the 4 hormones that increase blood glucose

A
  • epinephrine
  • cortisol
  • growth hormone
  • glucagon
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5
Q

what hormones decrease blood glucose (2)

A
  • GLP-1
  • insulin
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6
Q

what is the main difference between type 1 and type 2 DM

A
  • type one is when the pancreas fails to produce insulin due to loss of beta cells
  • type 2 is when the tissue cells become resistant to insulin (this can be due to decreased sensitivity of target cells or decreased glucose production in the liver)
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7
Q

what is the primary goal of treatment for DM

A

manage symptoms of hyperglycemia

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8
Q

what are the 5 symptoms of acute hyperglycemia

A
  • polyuria
  • poydipsia
  • weight gain
  • lethargy
  • blurred vision
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9
Q

what are the 7 major complications of chronic hyperglycemia

A
  • eye disease
  • renal failure
  • diabetic foot (ulcers)
  • stroke
  • heart damage
  • nerve disease
  • arteriosclerosis
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10
Q

how does chronic diabetes affect the eye

A

high blood glucose and high blood pressure can damage eye blood vessels, causing retinopathy, cataracts, and glaucoma

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11
Q

how does chronic hyperglycemia affect the kidneys

A

high blood pressure damages small blood vessels and excess blood glucose overworks the kidneys, causing nephropathy

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12
Q

which issue with the heart is common which high blood pressure and insulin resistance

A

coronary heart disease

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13
Q

what is coronary heart disease?

A

Coronary heart disease is the term that describes what happens when your heart’s blood supply is blocked or interrupted by a build-up of fatty substances in the coronary arteries

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14
Q

what does insulin do to amino acids and proteins

A

holds on to amino acids and increases protein synthesis

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15
Q

where does insulin act on when the body consumes amino acids and proteins

A

the muscle

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16
Q

how does insulin act on lipids

A

increases triglyceride synthesis
decreases the release of FFA and glycerol
decreases oxidation of FFA to ketoacids

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17
Q

what are the 3 major adverse effects of insulin

A
  • hypoglycemia
  • hypokalaemia
  • lipodystrophy (injection practices)
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18
Q

which type of insulin can be administered intravenously

A

Regular Insulin

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19
Q

what factors would determine which type of insulin you use? ```

A

the onset, peak and duration

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20
Q

which type(s) of insulin have short duration and are rapid acting

A
  • insulin lispro
  • insulin Aspart
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21
Q

which type(s) of insulin is short duration and short acting

A

regular insulin

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22
Q

which insulin will have intermediate duration

A

NPH

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23
Q

which type(s) of insulin will have long duration

A

insulin glargine (Lantus), and insulin detimir

24
Q

which insulin(s) have ultra long duration

A

insulin Dregludec

25
Q

what is humilin 50/50

A

combination insulin

26
Q

what are the bolus insulins

A

insulin lispro, insulin aspart, insulin glulisine and regular insulin

27
Q

what are the basal insulins

A

NPH insulin, insulin glargine and insulin detemir

28
Q

what are the 5 main categories/types of insulin’s

A
  • short duration, rapid acting
  • short duration, short acting
  • intermediate duration
  • long duration
  • ultra long duration
29
Q

what are the 2 insulin sensitisers

A
  • metformin (biguinide)
  • Rosiglitazone (TZDs)
30
Q

what are the 2 incretin agents

A
  • GLP-1 receptor agonists (Liraglutide)
  • DPP-4 inhibitors (Sitagliptin)
31
Q

what are the 2 insulin secretagogues

A
  • sulfonylureas (gliclazide)
  • meglitinides(repaglinide)
32
Q

what are the 2 glucose wasters

A
  • SGLT 2 inhibitors
  • alpha glucosidase inhibitors
33
Q

how does metformin work to lower blood glucose and improve glucose tolerance

A
  • it inhibits glucose production in the liver
  • it sensitises insulin receptors in target tissues
34
Q

can the insulin sensitizers be used to treat T1DM?

A

no, there needs to be insulin present

35
Q

which type of drug is Liaglutide

A

a GLP-1 receptor agonist

36
Q

what does GLP-1 do

A

it regulates hormones after eating to cause:
- increase in insulin
- decrease in glucagon
- slows gastric emptying
- decrease in appetite

37
Q

which anti-hyperglycemic medications are also considered non-insulin injectables

A

The incretin agents (GLP-1 receptor agents and DPP-4 inhibitors)

38
Q

what do DPP-4 inhibitors do

A
  • basically inhibits DPP-4 which allows GLP-1 to do its thing
39
Q

which drug may cause hypoglycemia if taken with DPP-4 inhibitors

A

sulfonylurea

40
Q

what type of drug is Sitagliptin

A

DPP-4 inhibitor

41
Q

what are meglitinides and what do they do

A

they stimulate the release of insulin from the pancreas (same category as gliclazide/sulfonylureas but shorter acting)

42
Q

what do alpha glucosidase inhibitors do (MOA)

A

delays the absorption of dietary carbs, reducing the spike in blood glucose after a meal

43
Q

what is alpha glucosidase and what does it do

A
  • alpha glucosidase is an enzyme located in the intestine that normally breaks down carbs for absorption (alpha glucosidase inhibitors inhibits this enzyme which slows the digestion of carbohydrates)
44
Q

how do you treat hypoglycemias in a patient who is taking alpha glucosidase inhibitors

A

don’t give sucrose, give glucose tabs (becasue sucrose needs to be broken down and the whole point of the drug is that it doesnt break down glucose)

45
Q

what is the MOA for SLGT2 inhibitors

A

they basically inhibit SGLT-2 in the kidney, reducing reabsorption of glucose
- they also increase urinary glucose excretion

46
Q

Combination insulin usually consists of which 2 types of insulin?

A

30% regular insulin and 70% NPH insulin

47
Q

what is the main benefit for sliding scale insulin

A

you can titrate to address blood sugar at that moment, prescribers will set units and rates so you just do it

48
Q

what are the three adverse effects of insulin

A

hypoglycemias
hypokalemia
lipoduistrophy

49
Q

which short duration rapid acting insulin should be given just after meals

A

insulin aspart

50
Q

what is the peak onset for insulin lispro

A

30 mins to 2.5 hours

51
Q

what is the peak of insulin aspart

A

1-3 hours

52
Q

what is the peak of NPH insulin

A

6-14 hours

53
Q

what is the peak of R insulin

A

1-5 hours

54
Q

what is the cloudy insulin

A

NPH

55
Q

out of biguanides and TZDs, which acts more on increasing insulin sensitivity (primarily)

A

TZDs are primarily going to work on insulin sensitivity, as well as inhibit glucose production in the liver

56
Q

whats the difference between glycogenesis and glucogenolysis

A

glycogenesis is glucose to glycogen, and glycogenolysis is vice versa

57
Q

whats the difference between meglitinides and sulfonurea?

A

meglitinides are shorter acting