Insulin therapy for T1D + T2D Flashcards
Rapid acting insulin analog
- name
- method
- onset of action
- duration
Humalog
Novolog
Glulisine
subcutaneous injxn
onset: 5-15 min,
last 3-5 hrs
When should you use rapid acting insulin analogs?
inject subQ just before a meal to prevent postprandial hyperglycemia
(no adv over IV infusion of recombinant hu insulin)
Short acting human insulin
- name
- method
- onset of action
- duration
Regular insulin
(humulin R, Novolin R)
SubQ or IV
Onset: 30-60 min (IV has immediate effect)
Lasts: 6-8 hours
When should you use short acting hu insulin?
use 30 min prior to meals,
IV: DKA, hyperosmolar/hyperglycemic state, perioperatively
- has immediate effect
Long acting insulin analogs
- name
- method
- onset of action
- duration
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)
When should you give long acting insulin?
once a day to provide basal coverage
*note: acid pH, cannot be mixed with other insulins
Intermediate acting insulins
- name
- method
- onset of action
- duration
NPH, Humulin N, Novolin N.
*cloudy
SubQ
Onset: 1-3 Hrs
Duration: 12-16 hoursd
When should you give intermediate acting insulins?
NPH used to treat mid day hyperglycemia associated with lunch, and to act as a basal insulin
- twice daily injxns
Bolus insulin made up of?
Prandial and correctional insulin doses
- pts on this are on the “basal bolus therapy”
Basal insulins you can use
glargine
Detemir
NPH
(without this, pts with T1D can get DKA, and T2D can get severe hyperglycemia)
Prandial insulins you can use
humalog
novolog
apidra
*same same for correctional
Correctional doses of insulin you can use
Humalog
novolog
apidra
*same for prandial insulins
Ratio of number of grams of carbs that 1 unit of insulin is anticipated to cover
C:I
15:1 or 20:1
(insulin R indiv are 10:1)
How many KCal/g is in carbs and fat
Carbs: 4KCal/g
Fat: 9KCal/g
(average expenditure is 30KCal/kg/day)
dawn phenomenon
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)
LDL = ?
TC - HDL - (TG/5)
TG/5 is estimate of VLDL
early morning hyperglycemia can be due to?
Clinical pearls
- inadequate basal insulin dosing
- bedtime hyperglycemia
- waning effect of basal insulin
- somogyi effect
Somogyi effect
nocturnal hypoglycemia causing a surge of CRH –>
morning hyperglycemia
*dawn phenom: surge of GH
preferred method for achieving control of inpatient hyperglycemia
insulin therapy
- discontinue oral agents at time of hospital admission
INsulin secretagogues
- action
sulfonureas
- enhance endogenous insulin by increasing b cell secretion by closing ATP sensitive K channels in membrane . . . yadi yada
side effects of sulfonureas
hypoglycemia
weight gain
Metformin
- action
acts at liver to potentiate effects of insulin on glucose production
(helps insulin)
- does not stimulate insuling secretion (sulfonureas)
Side effects of metformin
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
Contraindications to metformin use
- CHF
- IV iodinated contrast media
- Renal impairment
- met acidosis
Thiazolidinediones (TZDs)
true insulin sensitizers that enhance insulin action at level of skeletal m and adipose tissue
- binding of TZD to PPAR-y receptor
side effects of Thiazolidinediones (TZDs)
fluid retention/edema
hemodilution
exacerbation of HF
contraindications for TZDs
- active liver disease
- severe CHF
- Sig CV risk
Side effects of incretin enhancers
hypoglycemia
weight gain
persistent postprandial hyperglycemia
(their main effect is enhance insulin secretion and suppress glucagon secretion)
GIP-1 receptors are expressed in ____ and GLP-1 receptors are expressed in _____. Both are inactivated by ___.
GIP
- pancreatic iiiiiiiislet
GLP
- brain and heart
BOth are inactivated supah fast by DPP-4
GIP is produced in ______ GLP-1 is produced in _____ cells
Both are incretins:
GIP-1
intestinal K cells in duodenum
GLP-1
- intestinal L cells in distal ileum and colon
*GLP-1 controls:
made by L cells, act on receptors in brain and heart
- effects: controls blood glucose, and CNS satiety
GIP controls:
Made by K cells , act on rcptrs in pancreatic iiislets
- secreted after nutrient ingestion
- not effective in T2D due to insulin resistance
When should you not use GLP-1
pts with active pancreatitis, hx of pancreatitis, pancreatic carcinoma
DPP-4 inhibitors
“gliptins”
inhibit endogenous DPP-4 activity for 24 hrs
- leads to 2-3 higher circulation of active endogenous GLP-1 and GIP
Adverse effects of DPP-4
nasopharyngitis
headache
Drugs that induce weight loss
GLP-1 receptor agonist
Amylin analog (pramlintide)
SGLT-2
Drugs that induce weight gain
sulfonylureas
weight neutral insulin drugs
metformin
DPP-4
Amylin action
- inhibits gastric emptying + glucagon secretion acutely,
- reduces short term food intake
SGLT-2 inhibitors
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
DCCT
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
