Pharmacology & Exercise for Diabetes Flashcards

1
Q

insulin therapy in Type 1 diabetes - 2 options

A

basal-bolus injection therapy or continuous subcutaneous insulin infusion

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2
Q

basal-bolus injection therapy

A

this is considered intensive therapy - bc requires at least 3-5 injections and is the co=losest to our bodies physiological response
bolus insulin at meal times and basal injection once or twice daily
- covers insulin requires fro meal

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3
Q

continuous subcutaneous insulin infusion

A

insulin pump therapy via catheter into subcutaneous tissue

- covers insulin need throughout the day and into the night- this is also considered intensive therapy

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4
Q

what is conventional therapy?

A

more commonly used in elderly and less educated patients and it is limited to 2 injections a day

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5
Q

why is basal insulin important?

A

bc our normal physiological response is never at zero - insulin has a base level - need to maintain this in therapy

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6
Q

why is bolus insulin important?

A

to cover the glucose bumps after meals

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7
Q

human basal injection

A

requires one injection/day in the morning
- it reaches basal insulin levels higher than required and has a slow release which will peak around lunch time, then reaches normal physiological peaks later in the day

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8
Q

analogue basal insulin

A

this is better formulated than the human basal insulin bc it maintains basal levels closer to normal physiological levels and avoids a peak in the middle of the day

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9
Q

human bolus

A

3 injections per day

- inject right before meal, and peak will be slightly delayed

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10
Q

analogue bolus

A

3 injection per day

- better pairing with blood glucose compared to human bolus

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11
Q

conventional therapy

A

not recommended or preferred treatment

- premixed insulin ( mis of long and short actin insulin with different ratios)

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12
Q

human vs analogue premixed insulin

A

human will partially cover break, lunch and dinner

analogue will cover quite well breakfast and dinner but skip lunch almost entirely ( risks of hypo and hyper)

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13
Q

types of bolus insulin

A

rapid acting (Lispo/humalog) and short acting (regular/ humulin)

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14
Q

types of basal insulin

A

intermediate acting ( NPH?humulin) long acting (Glargine/Lantus)

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15
Q

premixed

A

30 % reg / 70% NPH

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16
Q

considerations for conventional insulin therapy

A

strict meal plan, consistent meals day to day, PA may lead to hypoglycemia

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17
Q

intensive therapy considerations

A
more flexible with mea timing
- MUST learn carb counting
- dose may be adjusted for exercise
-alwasys preferred over conventional 
-
18
Q

why is intensive therapy better?

A

DCCT study showed that intensive sharply declined A1C, whereas conventional remained high (8.5%)

also reduced the risk of non-fatal MI, stoke and health from CVD (60% decrease- this is HUGE)

19
Q

Metformin (glucophage) mechanism

A

first line medication for diabetes

  • has 2 actions:
    1. in liver- decrease gluconeogeneis
    2. increase insulin sensitivity
20
Q

other benefits of metformin

A

known safety, no hypoglycaemia, weight management, few side effects

21
Q

what are side effects

A

mostly just GI , B12 and folate must be monitored annually!

22
Q

contraindications for metaformin

A

renal insufficiency, liver or heart failure

23
Q

Alpha-glucosidase inhibitors mechanism

A

in the intestine to delay intestine glucose absorption (must be taken with meals)

24
Q

insulin secretagogues

A

will stimulate the secretion of insulin - short acting 4-7 hours or long lasting - once daily

25
Q

side effects in insulin secretagogues

A

hypoglycemia

26
Q

Incretins mimetics

A
  • not pills, injectables
  • stimulates insulin release and reduces glucagon secretion
  • delays gastric emptying
27
Q

mechanism of incretin mimetics (DPP-4 inhibitors)

A

normally when GLP-1 is released into circulation it gets degraded by DPP-4 enzyme through neg feedback. DPP-4 inhibitors block this and extend the life of GLP-1

28
Q

mechanism of GLP-1 agonist (incretins memitics)

A

will enhance the action of GLP-1 on the receptor

  • GLP-1 acts on the hypothalamus (regular satiety)
  • stimulates insulin release, inhibit glucagon, slow gastric emptying and increase satiety = better weight control
29
Q

Thia-zo-lidined-iones

A

increase insulin sensitivity in peripheral tissues and liver

30
Q

SGLT2 inhibitors mechanims

A

block glucose transport on the proximal renal tubule so glucose cannot be reabsorbed back into the blood- gets excited - glycosuria = lower mood glucose and lower weight

31
Q

side effects of SGLT2 inhibitors

A

dehydration ( lots of water loss and sodium loss) this is how SGLT2 also help control HPT
- risk of UTI, genital infections, hypotension, more risk of keto acidosis

32
Q

some more advantages of SLGT2 inhibitors

A

raise HDL, lower BP and rare hypoglycemia

33
Q

what are symptoms of hyperglycemia

A

polydipsia and polyuria and/or metabolic decompensation

34
Q

what is the goal of treatment

A

normalize A1C levels

35
Q

can insulin increase BW, why?

A

yes bc since we are injecting insulin into subcataneous tissue we need to inject greater levels than what is actually required endogenously–> this may lead to weight gain and risk of hypoglycemia

36
Q

TZD lead to weight gain?

A

yes bc increase insulin sensitivity, intake glucose, lipid and proteins

37
Q

why is it important to consider wight gain or loss in medications?

A

need to inform patient and need to monitor dietary patterns as further weight gain may be harmful

38
Q

insulin secretagogues should avoid?

A

alcohol 9 bc mask the symptoms of hypoglycaemia)

39
Q

pharmacotherapy for HPT in patients with diabetes considerations

A
  1. check potassium and creatinine at baseline within 1 to 2 weeks of initiation
  2. combination of agents that block RAAS should not be used
  3. more than 3 drugs may be needed to reach target values for patients with diabetes
40
Q

which diabetic patients should receive statins?

A
  • CVD
  • ages greater than 40
  • DM for more than 15 yrs