Brainscape's Knowledge GenomeTM

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


See full index

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

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

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

what are drugs that can cause T3DM

A

Corticosteroids
Thiazide diuretics
Combination oral contraceptives

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

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

treatment strategy for T1DM

A

replacement of insulin

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

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

what stimulates insulin secretion

A 
increase in ATP/ADP ratio
glucose and other sugars
AAs
FAs
PARA
GLP-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what stimulates insulin synthesis

A

nutrients

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

insulin acts through stimulation of what

A

tyrosine kinase receptor

IR autophosphorylation leads to phosphorylation and activation of downstream signaling proteins

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

where does insulin act

A

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

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

who gets exogenous insulin

A

T1DM patients

final drug of choice for T2DM, postpancreatectomy and gestational diabetes

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

adverse effects of exogenous insulin

A 
hypoglycemia
insulin allergy
lipoatrophy
weight gain
insulin edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do insulin regiments tailor to

A

activity and diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

rapid acting insulins

A

Lispro
Aspart
Glulisine
given with a meal

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

short acting insulins

A

like normal endogenous
regular Novolin
regular Humulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

intermediate acting insulins

A

NPH humulin

NPH novolin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

long acting insulins

A

detemir, levemir

glargine, lantus

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

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

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

mechanism of action of sulfonylureas

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

first generation sulfos

A

tolbutamide, tolazamide, chlorpropamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

whats the diff between 1st gen and 2nd gen sulfonylureas

A

second gen binds to SUR1 with higher affinity so lower dose is required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

2nd gen sulfos

A

glyburide, glipizide, glimepiride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

pharmacokinetics of sulfonylureas

A

orally available, bound to plasma albumin; metabolized by the liver; metabolites excreted in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

AEs of sulfonylureas

A

hypoglycemia, weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what patient would get first gen solfonylureas

A

pts with kidney issues or elderly at high risk of hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

contraindications of sulfonylureas

A

T1DM
pregnancy
lactation
significant hepatic or renal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

MOA of meglitinides

A

similar to sulfonylureas by binding SUR1 but at a different site to activate K/ATP channel

32
Q

what are the meglitinides

A

Repaglinide (Prandin)

Nateglinide (Starlix) - more rapid onset

33
Q

pharmacokinetics

A

cleared by liver, so not suitable for patients wiht hepatic insufficiency

34
Q

major AE of meglitinides

A

hypoglycemia

35
Q

what are biguanides

A

metformin

36
Q

what is the euglycemic effect and what drug produces it

A

helps maintain normal blood glucose levels, typically without producing hypoglycemia

37
Q

MOA of metformin

A

reduces hepatic gluconeogenesis
increases peripheral glucose uptake
activates AMPK
inhibits mTOR-C1

38
Q

pharma actions of metformin

A

inhibits gluconeogensis in liver
does not promote weight gain or hypoglycemia
can reduce plasma TGs by 15-20%

39
Q

clinical uses of metformin

A

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
Q

metabolism and excretion of metformin

A

orally effective, T1/2: 1.5 - 3 hrs

not bound to plasma protein; not metabolized; excreted by kidney as parent compound

41
Q

metformin toxicity

A

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
Q

what do thiazolidinediones (TZDs) do

A

PPAR gamma agonists with PPAR alpha agonist activity

43
Q

what is the MOA of TZDs

A

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
Q

what are the TZDs

A

Rosiglitazone 10x affinity

Pioglitazone

45
Q

whats troglitazone

A

a TZD that was pulled bc of liver toxicity

46
Q

TZDs effective at reducing what

A

glucose and TG levels

47
Q

where are TZDs metabolized

A

liver

48
Q

what are AEs of TZDs

A

weight gain
hepatic toxicity
CHF

49
Q

MOA of alpha glucosidase inhibitors

A

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
Q

what are the glucosidase inhibitors

A

acarbose and miglitol

often used in combination with other hypoglycemic agents

51
Q

AEs of glucosidase inhibitors

A

NO risk for hypoglycemia

flatulence, bloating, diarrhea

52
Q

incretins

A

GLP-1 and GIP

53
Q

what does GLP-1 do

A 
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
Q

what is GIP

A

another hormonal signal that has similar effects to GLP-1

55
Q

AEs of GLP-1 analogues

A

nausea, vomiting, diarrhea

LOW risk of hypoglycemia

56
Q

what are the GLP-1 analogues

A

exenatide
liraglutide
albigutide
duraglutide

57
Q

what do DDP-4 inhibitors do

A

normally DDP-4 degrades endogenous incretids, so inhibitors block that from happening

58
Q

what are the DDP-4 inhibitors

A

Sitagliptin
Saxagliptin
Linagliptin
Alogliptin

59
Q

what are DDP-4i not used in combination with

A

GLP-1 analogs, because they are less susceptible to DPP-4 degradation inherently and it would be redundant

60
Q

what do SGLT2 inhibitors do

A

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
Q

AEs of SGLT2 inhibitors

A 
glycosuria
genital infections 
UTIs
hypotension
weight loss
62
Q

what are the SGLT2 inhibitors

A

canagliflozin
dapagliflozin
empagliflozin

63
Q

what is pramlintide

A

amylin analog

mimics high dose pharmacologic effects of amylin

64
Q

MOA of pramlintide

A

pancreas - increases insulin secretion and decreases glucagon secretion
delays gastric emptying
decreases appetite

65
Q

how is pramlintide given

A

preprandial use as an adjunct to insulin in T1 and T2 DM

66
Q

pharmacokinetics of pramlintide

A

renal metabolism and excretion

67
Q

AEs of pramlintide

A

hypoglycemia

GI symptoms

68
Q

colesevalam

A

bile acid sequestrant, cholseterol lowering drug

MOA not fully understood

69
Q

MOA of colesevalam

A

interrupts enterohepatic circulation

decreases farnesoid X receptor nuclear receptor activation

70
Q

AE of colesevalam

A

can exacerbate hypertriglyceridemia common in T2D

71
Q

what does bromocriptine do

A

dopamine agonist

72
Q

AEs of bromocriptine

A 
nausea
fatigue
dizziness
vomiting
headache
73
Q

principles of combination therapy

A

combine different mechanisms
target different proteins
advantage of using lower doses
fewer AEs

74
Q

combo therapy in treating T2DM

A

begin with monotherapy Metformin

GLP-1 mimic, SGLT-2 inhibitors, or DDP-4 inhibitor

75
Q

what are second choice agents for T2DM

A

sulfonylureas and TZDs

GIR Test 1 (15 decks)

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