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GIR Test 1 > B5.003 - Drugs for Diabetes > Flashcards

B5.003 - Drugs for Diabetes Flashcards

1
Q

what is diabetes mellitus

A

symptoms of hyperglycemia due to inappropriate insulin secretion or function

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2
Q

types 1-4 of DM

A

1 - autoimmune destruction of beta cells, insulin dependent
2 - noninsulin dependent, associated with diabetes and metabolic syndrome
3 - non pancreatic causes, drugs that impair glucose tolerance
4 - gestational diabetes

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3
Q

what are drugs that can cause T3DM

A

Corticosteroids
Thiazide diuretics
Combination oral contraceptives

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4
Q

major goals of treatment of diabetes

A

treat hyperglycemia and improve all aspects of metabolism
fasting glucose 90-120
2 hr post prandial <150
HgA1c <7%

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5
Q

treatment strategy for T1DM

A

replacement of insulin

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6
Q

treatment strategy for T2DM

A

improve insulin sensitivity at early stages and replace insulin in later stages
change lifestyle
reduce glucose absorption
increase insulin secretion

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7
Q

what stimulates insulin secretion

A 
increase in ATP/ADP ratio
glucose and other sugars
AAs
FAs
PARA
GLP-1
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8
Q

what stimulates insulin synthesis

A

nutrients

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9
Q

insulin acts through stimulation of what

A

tyrosine kinase receptor

IR autophosphorylation leads to phosphorylation and activation of downstream signaling proteins

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10
Q

where does insulin act

A

Liver
muscle
adipose tissue
to decrease blood glucose levels and shift from energy use to storage

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11
Q

who gets exogenous insulin

A

T1DM patients

final drug of choice for T2DM, postpancreatectomy and gestational diabetes

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12
Q

how is insulin given and why

A

subcutaneous because it slows the rate of absorption, good if you dont want a huge increase of insulin

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13
Q

adverse effects of exogenous insulin

A 
hypoglycemia
insulin allergy
lipoatrophy
weight gain
insulin edema
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14
Q

what do insulin regiments tailor to

A

activity and diet

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15
Q

rapid acting insulins

A

Lispro
Aspart
Glulisine
given with a meal

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16
Q

short acting insulins

A

like normal endogenous
regular Novolin
regular Humulin

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17
Q

intermediate acting insulins

A

NPH humulin

NPH novolin

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18
Q

long acting insulins

A

detemir, levemir

glargine, lantus

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19
Q

algorithm for adding or intensifying insulin

A

start with long acting insulin
insulin titration every 2-3 days to reach glycemic goal
if glycemic goal not met add prandial insulin or GLP-1 RA or SGLT-2i or DPP-4i

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20
Q

how is insulin used to treat DKA

A

IV infusion of regular insulin at low rate (.1 unit/kg body wt/hr)
may need to administer glucose with it to prevent hypoglycemia
add appropriate fluid and electrolytes

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21
Q

drug types to treat T2DM

A 
insulin secretagogues
insulin receptor sensitizers
inhibitors of glucose absorbance
incretins/mimics
inhibitors of glucose reuptake in kidney
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22
Q

mechanism of action of sulfonylureas

A

activate residual beta cells to release insulin by binding to and activation SUR1

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23
Q

what is SUR1

A

sulfonylurea receptor 1, a subunit of K/ATP channel. Sulfos replace the Mg2+/ADP on SUR1 that activate the channel, similar to the fed state

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24
Q

first generation sulfos

A

tolbutamide, tolazamide, chlorpropamide

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25
whats the diff between 1st gen and 2nd gen sulfonylureas
second gen binds to SUR1 with higher affinity so lower dose is required
26
2nd gen sulfos
glyburide, glipizide, glimepiride
27
pharmacokinetics of sulfonylureas
orally available, bound to plasma albumin; metabolized by the liver; metabolites excreted in urine
28
AEs of sulfonylureas
hypoglycemia, weight gain
29
what patient would get first gen solfonylureas
pts with kidney issues or elderly at high risk of hypoglycemia
30
contraindications of sulfonylureas
T1DM pregnancy lactation significant hepatic or renal insufficiency
31
MOA of meglitinides
similar to sulfonylureas by binding SUR1 but at a different site to activate K/ATP channel
32
what are the meglitinides
Repaglinide (Prandin) | Nateglinide (Starlix) - more rapid onset
33
pharmacokinetics
cleared by liver, so not suitable for patients wiht hepatic insufficiency
34
major AE of meglitinides
hypoglycemia
35
what are biguanides
metformin
36
what is the euglycemic effect and what drug produces it
helps maintain normal blood glucose levels, typically without producing hypoglycemia
37
MOA of metformin
reduces hepatic gluconeogenesis increases peripheral glucose uptake activates AMPK inhibits mTOR-C1
38
pharma actions of metformin
inhibits gluconeogensis in liver does not promote weight gain or hypoglycemia can reduce plasma TGs by 15-20%
39
clinical uses of metformin
1st line therapy for T2DM oral dosage 500mg-2.55g / day taken with or after food also useful in treating polycystic ovary syndrome and NAFLD
40
metabolism and excretion of metformin
orally effective, T1/2: 1.5 - 3 hrs | not bound to plasma protein; not metabolized; excreted by kidney as parent compound
41
metformin toxicity
lactic acidosis, by blocking gluconeogenesis may impair hepatic metabolism of lactic acid more common in pts with renal insufficiency dose related complication GI related reduced Vitamin B12 absorption
42
what do thiazolidinediones (TZDs) do
PPAR gamma agonists with PPAR alpha agonist activity
43
what is the MOA of TZDs
in adipose tissue, PPAR gamma activators promote the transport of serum lipids to adipose tissue may also activate PPAR gamma in other tissues to promote insulin sensitivity
44
what are the TZDs
Rosiglitazone 10x affinity | Pioglitazone
45
whats troglitazone
a TZD that was pulled bc of liver toxicity
46
TZDs effective at reducing what
glucose and TG levels
47
where are TZDs metabolized
liver
48
what are AEs of TZDs
weight gain hepatic toxicity CHF
49
MOA of alpha glucosidase inhibitors
competitive and reversible inhibitors of pancreatic alpha amylase and intestinal alpha glucosidase enzymes this leads to increased time required to absorb complex carbs and reduces post prandial glucose peak
50
what are the glucosidase inhibitors
acarbose and miglitol | often used in combination with other hypoglycemic agents
51
AEs of glucosidase inhibitors
NO risk for hypoglycemia | flatulence, bloating, diarrhea
52
incretins
GLP-1 and GIP
53
what does GLP-1 do
``` stimulates secretion of insulin enteroendocrine cells (L cells) in the ileum, hormonal signal that increases insulin secretion but decreases glucagon secretion in pancreas, delays gastric emptying and decreases appetite in hypothalamus ```
54
what is GIP
another hormonal signal that has similar effects to GLP-1
55
AEs of GLP-1 analogues
nausea, vomiting, diarrhea | LOW risk of hypoglycemia
56
what are the GLP-1 analogues
exenatide liraglutide albigutide duraglutide
57
what do DDP-4 inhibitors do
normally DDP-4 degrades endogenous incretids, so inhibitors block that from happening
58
what are the DDP-4 inhibitors
Sitagliptin Saxagliptin Linagliptin Alogliptin
59
what are DDP-4i not used in combination with
GLP-1 analogs, because they are less susceptible to DPP-4 degradation inherently and it would be redundant
60
what do SGLT2 inhibitors do
block SGLT2 SGLT2 are located in the proximal tubules and allow glucose reabsorption after its been freely filtered by glomeruli SGLT2 accounts for 90% of glucose reabsorption
61
AEs of SGLT2 inhibitors
``` glycosuria genital infections UTIs hypotension weight loss ```
62
what are the SGLT2 inhibitors
canagliflozin dapagliflozin empagliflozin
63
what is pramlintide
amylin analog | mimics high dose pharmacologic effects of amylin
64
MOA of pramlintide
pancreas - increases insulin secretion and decreases glucagon secretion delays gastric emptying decreases appetite
65
how is pramlintide given
preprandial use as an adjunct to insulin in T1 and T2 DM
66
pharmacokinetics of pramlintide
renal metabolism and excretion
67
AEs of pramlintide
hypoglycemia | GI symptoms
68
colesevalam
bile acid sequestrant, cholseterol lowering drug | MOA not fully understood
69
MOA of colesevalam
interrupts enterohepatic circulation | decreases farnesoid X receptor nuclear receptor activation
70
AE of colesevalam
can exacerbate hypertriglyceridemia common in T2D
71
what does bromocriptine do
dopamine agonist
72
AEs of bromocriptine
``` nausea fatigue dizziness vomiting headache ```
73
principles of combination therapy
combine different mechanisms target different proteins advantage of using lower doses fewer AEs
74
combo therapy in treating T2DM
begin with monotherapy Metformin | GLP-1 mimic, SGLT-2 inhibitors, or DDP-4 inhibitor
75
what are second choice agents for T2DM
sulfonylureas and TZDs

GIR Test 1 (15 decks)

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