Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Nutrition 1 Final McGill Uni > Diabetes Pharmcotherapy and the mechanism > Flashcards

Diabetes Pharmcotherapy and the mechanism Flashcards

1
Q

PA check list (4) TIMS

A
  • Try to do 150min moderate to vigorous-intensity aerobic exercise/wk
  • Include resistance exercise no less than 2 times/wk
  • Minimise uninterrupted sedentary time
  • Set a goal of PA and involve a multi-disciplinary team if available
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Exercise (5)

A

aerobic, resistant, interval, other types, use pedometers/accelerometers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ABCDEs of diabetes care (Diabetes Canada) [ compared to the ABCDEs to protect vascular system]

A

all the same except s:
S= smoking cessation
S= screening for complication
S= self-management, stress and other barriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

2 types of new insulin Tx, besides conventional

A
  1. Basal-bolus injection therapy

2. continuous subcutaneous insulin infusion (intensive therapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

the difference between basal insulin and bolus insulin

A

basal: constant during the day
bolus: fluctuate by the meal intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why analogue basal is better than human basal

A

there is no peak but more constant during the day. Moreover, the action on set is earlier.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

why analogue bolus is better than human bolus?

A

it follows the glucose level change in time and the peak is more closer to the glucose peak, which is better.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the conventional insulin therapy?

A

human and analogue premixed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the problem of premixed insulin therapy?

A

need multiple injection every day before each meal. the insulin response cannot successively follow the glucose rise. It is easier to cause hypoglycemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

in two types of premixed Therapy, which one is better? why?

A

analogue: the peak of response more follows the actual glucose peak,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Medication– Lispro: function, on set speed, peak lasting, duration, (others?)

A

Rapid-acting

  • bolus insulin
  • very fast: 10-15min
  • very short: 1-2 hrs
  • duration: 3-5hrs
  • very expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Medication– Regular: function, on set speed, peak lasting, duration, (others?)

A

Short-acting

  • bolus insulin
  • fast: 30min
  • short: 2-3hrs
  • duration: 6.5hrs
  • relatively cheap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Medication– NPH: function, on set speed, peak lasting, duration, (others?)

A

Intermediate-acting:(cloudy)

  • basal insulin
  • moderate: 1-3hrs
  • have a peak: 5-8 hrs
  • duration 10-18 hrs (2 injections/d)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Medication– Glargine: function, on set speed, peak lasting, duration, (others?)

A 
Long-acting: (cloudy)
- fast: 90 min
- NO PEAK
- very lasting: 20-24 hrs
1 injection/d
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Medication– 30/70 : function, on set speed, peak lasting, duration, (others?)

A

premixed: 30% reg + 70% NPH
- fast: 30-60min
- dual peak
- duration: 10-16 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the conventional insulin regimens?

A
  • have to inject 1-3 times/d
  • meal plan, times and CHO content are fixed
  • PA may cause hypoglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the intensive insulin regimens?

A
  • inject more than 3 times/d or continuous subcutaneous insulin infusion
  • require self-monitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the benefits of intensive therapy (3)

A
  • Basal + bolus injections of rapid type before meals: more close to the mimic physiology
  • the time and CHO content is more adjustable: must know Carb counting
  • insulin dose can adjust to exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What’s DCCT project told us?

A
  1. In long-term (21 yrs follow-up), intensive Tx always performed better than conventional Tx in terms of A1C level
  2. early intensive therapy reduced more risk of non-fatal MI, stroke or death from CVD in a long term (after 16 yrs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

3 ways of insulin intake

A

syringe, pen, pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

the advantage of continuous glucose sensor

A

can track if any

unexpected insulin burst.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

4 classes of antihyperglycemic agent （DM2 medication)

A
  1. a-glucosidase inhibitor
  2. incretin mimetics
  3. insulin secretagogoues
  4. TZDs
23
Q

mechanism of a-glucosidase inhibitor

A

delay intestinal glucose absorption

24
Q

mechanism of incretin mimetics

A

stimulate insulin and reduce glucagon secretion; delay gastric emptying

25
Q

mechanism of TZDs

A

increase insulin sensitivity in peripheral tissues and liver

26
Q

mechanism of insulin secretagonous

A

stimulate insulin secretion in short (4-7 hrs) or long (once a day) term

27
Q

which medication may cause hypoglycemia?

A

insulin secretagonous

28
Q

what is the first initial drug for DM2?

A
  • Metformin

- inhibit the gluconeogenesis in liver –> improve insulin sensitivity –> increase glucose uptake

29
Q

what is the class of the initial drug?

A

biguanide

30
Q

why it is the initial drug

A
  • known safety, no hypoglycemia, help wt control

- just a few GI side effect (less than others)

31
Q

Metformin contraindication

A

renal insufficiency, liver or heart failure

32
Q

what is the difference and similarity between DPP-4 inhibitors and GLP-1 receptor agonists

A
  • similarity:
    1. antihyperglycemic agnets
    2. the incretin mimetics: target on GLP-1 function
  • difference:
    1. DPP-4: inhibited DPP-4 enzyme activate GLP-1.
    2. GLP-1R Agonist: promotes the production of GLP-1
33
Q

Mechanism of SGLT2 inhibitor

A

block the Na-glucose transporter in the proximal renal tubule— so decrease blood glucose and lower body weight, glycouria

34
Q

advantage of SGLT2

A
  • rare hypoglycemia, lower BP, elevate HDL

- when added to metform: the best agent to improve A1C profile

35
Q

disadvantage of SGLT2

A
  • side effects: risk of urinary track infection, hypotension, more risk of diabetic ketoacidosis
  • no oral pill form, have to do injection
36
Q

what are the three antihyperglycemic agents demonstrated CV benefit?

A

empagliflozin
liraglutide
canagliflozin

37
Q

when we should start the antihyperglycemic agents demonstrated CV benefit?

A
  • after applying the first line medication Tx: metformin or insulin for Pts with symtomatic hypolycemia, the glycemic target is not achieved.
  • and the Pt have clinical CVD.
38
Q

Diagnosis of DM2: A1C>or= __should go metformin immediately

A

1.5% above target

39
Q

Diagnosis of DM2: if the glycemic target not meet after primary intervention but also no indication of clinical CVD, what’s the next step? give all conditions

A

add additional anti-hyperglycemia agents:
2 conditions
1. avoid hypoglycemia and/or weight gain with adequate glycemic efficacy
2. other concerns

40
Q

what are the medications may cause hypoglycemia

A

insulin Tx and Insulin secretagogue

41
Q

what are the medications may cause Wt gain

A

insulin, thiazolidinediones TZDs, Insulin secretagogue

42
Q

what is the most expensive medication category?

A

incretin mimetics and possible insulin

43
Q

what are the medications may help Wt loss

A

insulin
a-glucosidase inhibitor
incretin mimetics

44
Q

dietary guidance: metformin

A

reduce Vb12, folate absorption,

take with meals

45
Q

dietary guidance: TZDs

A

N/A

46
Q

dietary guidance: incretin mimetics

A

Cation of EtOH, may have GI side effect

47
Q

dietary guidance: insulin secretagogues

A

avoid EtOH

48
Q

dietary guidance: alpha-glucosidase inhibitors

A

take with the first bite of meal, limit EtOH

49
Q

What DM pts should take statin? (5)

what’s the warning to the women with child-bearing potential?

A 
1. have CVD
2 age more than 40
3. have micro-vascular complication
4. with DM > 15 yrs, and age > 30 yr
5. follow warrants therapy
- stop statin before conception; should ask for preconception counselling and reliable contraception
50
Q

pharmacotherapy for HTN in Pts w/ DM: threshold? target?

A
  • threshold: no less than 130/80 mmHg

- target: 130/80

51
Q

pharmacotherapy for HTN in Pts w/ DM: what is the key factor to determine?

A

CVD and CKD if exist

52
Q

pharmacotherapy for HTN in Pts w/ DM: what is the difference from pts w/ CVD or CKD and the one w/o?

A

the pts with CKD and CVD should not use HDP-CCB or thiazide/thiazide-like diuretics

they apply ACE inhibitor or ARB only

(w/o: can use both)

53
Q

if a pt with insulin Tx have not met the glycemic target after 3 months, what should do? why?

A

add incretin mimetics and SGLT2 inhibitor may be considered before add more dose of insulin
- minimize wt gain and prevent hypoglycemia

Clinical Nutrition 1 Final McGill Uni (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions