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DEMS Unit 02-01 > Insulin therapy for T1D + T2D > Flashcards

Insulin therapy for T1D + T2D Flashcards

1
Q

Rapid acting insulin analog

  • name
  • method
  • onset of action
  • duration
A

Humalog
Novolog
Glulisine

subcutaneous injxn

onset: 5-15 min,
last 3-5 hrs

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2
Q

When should you use rapid acting insulin analogs?

A

inject subQ just before a meal to prevent postprandial hyperglycemia

(no adv over IV infusion of recombinant hu insulin)

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3
Q

Short acting human insulin

  • name
  • method
  • onset of action
  • duration
A

Regular insulin
(humulin R, Novolin R)

SubQ or IV

Onset: 30-60 min (IV has immediate effect)
Lasts: 6-8 hours

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4
Q

When should you use short acting hu insulin?

A

use 30 min prior to meals,

IV: DKA, hyperosmolar/hyperglycemic state, perioperatively
- has immediate effect

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5
Q

Long acting insulin analogs

  • name
  • method
  • onset of action
  • duration
A

Glargine
Detemir

Sub Q
Onset: 1.5 hours
Duration: 24 hours

(note: it is injected into the pH neutral SubQ even though it is acidic, bc that is what gives it the slow release)

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6
Q

When should you give long acting insulin?

A

once a day to provide basal coverage

*note: acid pH, cannot be mixed with other insulins

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7
Q

Intermediate acting insulins

  • name
  • method
  • onset of action
  • duration
A

NPH, Humulin N, Novolin N.

*cloudy

SubQ

Onset: 1-3 Hrs
Duration: 12-16 hoursd

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8
Q

When should you give intermediate acting insulins?

A

NPH used to treat mid day hyperglycemia associated with lunch, and to act as a basal insulin

  • twice daily injxns
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9
Q

Bolus insulin made up of?

A

Prandial and correctional insulin doses

- pts on this are on the “basal bolus therapy”

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10
Q

Basal insulins you can use

A

glargine
Detemir
NPH

(without this, pts with T1D can get DKA, and T2D can get severe hyperglycemia)

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11
Q

Prandial insulins you can use

A

humalog
novolog
apidra

*same same for correctional

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12
Q

Correctional doses of insulin you can use

A

Humalog
novolog
apidra

*same for prandial insulins

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13
Q

Ratio of number of grams of carbs that 1 unit of insulin is anticipated to cover

A

C:I
15:1 or 20:1

(insulin R indiv are 10:1)

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14
Q

How many KCal/g is in carbs and fat

A

Carbs: 4KCal/g
Fat: 9KCal/g

(average expenditure is 30KCal/kg/day)

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15
Q

dawn phenomenon

A

hyperglycemia in response to surge in growth hormon/cortisol (CRH)

  • give them a bit more insulin (0.9 units/hr instead of 0.6 in between 4am-8am)
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16
Q

LDL = ?

A

TC - HDL - (TG/5)

TG/5 is estimate of VLDL

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17
Q

early morning hyperglycemia can be due to?

A

Clinical pearls

  1. inadequate basal insulin dosing
  2. bedtime hyperglycemia
  3. waning effect of basal insulin
  4. somogyi effect
18
Q

Somogyi effect

A

nocturnal hypoglycemia causing a surge of CRH –>
morning hyperglycemia

*dawn phenom: surge of GH

19
Q

preferred method for achieving control of inpatient hyperglycemia

A

insulin therapy

- discontinue oral agents at time of hospital admission

20
Q

INsulin secretagogues

- action

A

sulfonureas

  • enhance endogenous insulin by increasing b cell secretion by closing ATP sensitive K channels in membrane . . . yadi yada
21
Q

side effects of sulfonureas

A

hypoglycemia

weight gain

22
Q

Metformin

- action

A

acts at liver to potentiate effects of insulin on glucose production
(helps insulin)

  • does not stimulate insuling secretion (sulfonureas)
23
Q

Side effects of metformin

A

GI:
n/v
bloating
diarrhea

-lactic acidosis if they are at higher risk

on plus side, thanx to that, NO weight gain! NO hypoglycemia when used as monotherapy

24
Q

Contraindications to metformin use

A
  • CHF
  • IV iodinated contrast media
  • Renal impairment
  • met acidosis
25
Q

Thiazolidinediones (TZDs)

A

true insulin sensitizers that enhance insulin action at level of skeletal m and adipose tissue

  • binding of TZD to PPAR-y receptor
26
Q

side effects of Thiazolidinediones (TZDs)

A

fluid retention/edema
hemodilution
exacerbation of HF

27
Q

contraindications for TZDs

A
  • active liver disease
  • severe CHF
  • Sig CV risk
28
Q

Side effects of incretin enhancers

A

hypoglycemia
weight gain
persistent postprandial hyperglycemia

(their main effect is enhance insulin secretion and suppress glucagon secretion)

29
Q

GIP-1 receptors are expressed in ____ and GLP-1 receptors are expressed in _____. Both are inactivated by ___.

A

GIP
- pancreatic iiiiiiiislet

GLP
- brain and heart

BOth are inactivated supah fast by DPP-4

30
Q

GIP is produced in ______ GLP-1 is produced in _____ cells

A

Both are incretins:

GIP-1
intestinal K cells in duodenum

GLP-1
- intestinal L cells in distal ileum and colon

31
Q

*GLP-1 controls:

A

made by L cells, act on receptors in brain and heart

  • effects: controls blood glucose, and CNS satiety
32
Q

GIP controls:

A

Made by K cells , act on rcptrs in pancreatic iiislets

  • secreted after nutrient ingestion
  • not effective in T2D due to insulin resistance
33
Q

When should you not use GLP-1

A

pts with active pancreatitis, hx of pancreatitis, pancreatic carcinoma

34
Q

DPP-4 inhibitors

A

“gliptins”
inhibit endogenous DPP-4 activity for 24 hrs
- leads to 2-3 higher circulation of active endogenous GLP-1 and GIP

35
Q

Adverse effects of DPP-4

A

nasopharyngitis

headache

36
Q

Drugs that induce weight loss

A

GLP-1 receptor agonist
Amylin analog (pramlintide)
SGLT-2

37
Q

Drugs that induce weight gain

A

sulfonylureas

38
Q

weight neutral insulin drugs

A

metformin

DPP-4

39
Q

Amylin action

A
  • inhibits gastric emptying + glucagon secretion acutely,

- reduces short term food intake

40
Q

SGLT-2 inhibitors

A

SGLT-2 is responsible for reabsorption of glucose in prox renal tubule
- normally reabsorbs 99% of 180g of glucose.

Stop that shit, stop reabsorbing and start excreting it, and reduce circulating glucose levels

41
Q

DCCT

A

first large RCT that showed that intensive blood glucose control lead to reduced risk of development/progression of microvascular complications in T1D
- follow up: legacy effect

DEMS Unit 02-01 (10 decks)

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