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 Diabetes Pharmacology > Flashcards

B5.003 Diabetes Pharmacology Flashcards

1
Q

diabetes mellitus definition

A

symptoms of hyperglycemia due to appropriate insulin secretion or function

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

type 1 diabetes

A

autoimmune destruction of B cells

insulin dependent

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

type 2 diabetes

A

noninsulin dependent diabetes associated with obesity and metabolic syndrome
B cells desensitized to a glucose challenge
peripheral tissues resistant to insulin actions

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

type 3 diabetes

A

non pancreatic causes

drugs that impair glucose tolerance (corticosteroids, thiazide diuretics, combination oral contraceptives)

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

type 4 diabetes

A

gestational diabetes

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

major goals of treatment of diabetes

A 
treat hyperglycemia to avoid long term complications
improve all aspects of metabolism:
-fasting glucose 90-120
-2 hr post prandial glucose <150
-HbA1c <7%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

strategy of DM1 treatment

A

replacement of insulin

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

strategies of DM2 treatment

A

improve insulin sensitivity at early stages and replace insulin in later stage disease

  • change lifestyle
  • increase insulin sensitivity (liver and muscle)
  • increase insulin secretion
  • reduce glucose absorption in the gut
  • replacement insulin when compensation fails
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what stimulates insulin secretion

A

increased ATP/ADP ratio (metabolic stimuli)

  • glucose and other sugars
  • amino acids
  • fatty acids
  • parasympathetic activity
  • GLP-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

discuss the pathway of insulin release in a B cell

A

glucose transported into cell by GLUT2
metabolism of glucose into ATP
ATP closes K+ channel and depolarizes cell
depolarization opens Ca2+ channel
Ca2+ influx stimulates exocytosis of insulin vesicles

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

discuss the action of the insulin tyrosine kinase receptor

A

IR autophosphorylation leads to phosphorylation and activation of downstream signaling proteins
acts in liver, muscle, and adipose tissues 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
12
Q

how is exogenous insulin made?

A

made from recombinant human DNA to avoid immune response issues

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

how are insulin preparations classified

A

duration of action (rapid, short, intermediate, long acting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why is insulin administered subQ

A

to avoid quick rises and falls in response to digestive nutrients

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

adverse effects of insulin

A

hypoglycemia (can be severe or life threatening)

insulin allergy, lipoatrophy, weight gain and insulin edema

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

what type of insulin preparation is analogous to endogenous human insulin

A

short acting insulins

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

insulin treatment of DKA

A

IV infusion of regular insulin at a low rate
may administer glucose along with insulin to prevent hypoglycemia
add appropriate fluid and electrolytes

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

classes of DM2

A 
insulin secretagogues
insulin receptor sensitizers
inhibitors of glucose absorbance
incretins/mimics
inhibitors of glucose reuptake in the kidney
others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

mechanism of action of sulfonylureas

A

activate residual B cells to release insulin by binding to and activating SUR1 ( a subunit of the K+/ATP channel)
replace 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
20
Q

effect of sulfonylureas

A

may decrease hepatic clearance of insulin

decrease serum glucagon by simulating somatostatin release

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

first gen sulfonylureas

A

tolbutamide
tolazamide
chlorpropamide

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

second gen sulfonylureas

A

binds to SUR1 with higher affinity, lower dose required
glyburide
glipizide
glimepiride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

sulfonylureas pharmacokinetics

A

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

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

adverse effects of sulfonylureas

A

infrequent

hypoglycemia and weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
contraindications for sulfonylureas
DM1 pregnancy lactation significant hepatic or renal insufficiency
26
what class of drugs are meglitinides
insulin secretagogues (along w sulfonylureas)
27
mechanism of action of meglitinides
similar to sulfonylureas | binds to SUR1 at a different site to activate the K+/ATP channel
28
specific meglitinides drugs
repaglinide nateglinide rapid onset of action
29
adverse effects of meglitinides
hypoglycemia
30
contraindications for meglitinides
hepatic insufficiency | cleared by liver
31
what class of drugs does metformin fall under?
insulin sensitizers | biguanides
32
what is the euglycemic effect
helps maintain normal blood glucose levels without producing hypoglycemia
33
mechanism of action of metformin
reduced hepatic gluconeogenesis (main therapeutic effect) increases peripheral glucose uptake activates AMP-activated protein kinase (AMPK) inhibits mTOR-C1
34
pharmacological actions of metformin
inhibits gluconeogenesis does not promote weight gain or hypoglycemia can reduce plasma TGs by 15-20%
35
clinical uses of metformin
1st line therapy for DM2 oral dosage 500 mg- 2.55 g take with or after food also useful in treating polycystic ovary syndrome and non-alcoholic fatty liver disease (NAFLD)
36
metabolism and excretion of metformin
orally effective half life 1.5 - 3 h not bound to plasma protein, not metabolized, excreted by the kidney as parent compound
37
lactic acidosis in the context of metformin toxicity
rare but life threatening blocking gluconeogenesis, may impair metabolism of lactic acid more common in patients with renal insufficiency dose related complication
38
acute adverse effects of metformin
mostly GI related (20% of patients) | reduced B12 absorption
39
what class of drugs due thiazolidinediones (TZDs) fall into
insulin sensitizers
40
mechanism of action of TZDs
PPARy agonists with PPARa agonist activity in adipose tissue, PPARy activators promote transport of serum lipids to adipose tissue may also activate PPARy in other tissues to promote insulin sensitivity -decrease hepatic gluconeogenesis -enhance uptake of glucose by skeletal muscle cells
41
specific TZD drugs
rosiglitazone | pioglitazone
42
rosiglitazone affinity
10x more PPARy affinity than pioglitazone
43
pioglitazone affinity
balances between PPARy and PPARa
44
effect of TZD drugs
reduce glucose and TG levels | metabolized in liver
45
adverse effects of TZDs
weight gain hepatic toxicity by some congestive heart failure exacerbation losing popularity due to these effects
46
inhibitors of intestinal glucose absorption
a-glucosidase inhibitors | acarbose and miglitol
47
mechanism of action of a-glucosidase inhibitors
competitive and reversible inhibitors of pancreatic a-amylase and intestinal a-glucosidase enzymes - increased time required to absorb complex carbs - reduces postprandial glucose peak
48
effect of a-glucosidase inhibitors
monotherapy reduces fasting glucose by 20-30 and postprandial by 40-50 reduces HbA1c by 0.7-0.9% often used in combo with other agents no risk for hypoglycemia
49
adverse effects of a-glucosidase inhibitors
flatulence, bloating, and diarrhea | not recommended for those with inflammatory bowel conditions
50
what are the incretins
GLP-1 and GIP
51
secretion of GLP-1
enteroendocrine cells (L cells) in the ileum encoded by proglucagon gene and derived from the natural proglucagon protein release stimulated by nutrients entering the gut
52
physiologic effects of GLP-1
pancreas: stimulate insulin and decrease glucagon secretion stomach: delay gastric emptying hypothalamus: decrease appetite
53
what are the GLP-1 analogues
exenatide liraglutide albiglutide duraglutide
54
mechanism of action of GLP-1 analogues
increases insulin secretion suppresses glucagon secretion slows gastric emptying central appetite suppression
55
adverse effects of GLP-1 analogues
nausea, vomiting, diarrhea | low risk of hypoglycemia
56
differences between GLP-1 analogues
duration of action, longer w newer drugs exenatide- 30 min - 2 h liraglutide and albiglutide- once daily dosing duraglutide- once weekly dosing
57
other class of incretin drugs
inhibitors of DDP-4
58
function of DDP-4
degrades endogenous incretins as well as other structurally similar peptides
59
mechanism of action of DDP-4 inhibitors
increase level of endogenous incretins
60
specific DDP-4 inhibitors
sitagliptin saxagliptin linagliptin alogliptin
61
contraindication for DPP-4 inhibitors
don't use in combo with GLP-1 analogs (less susceptible to DDP-4 degradation)
62
what are inhibitors of glucose reuptake in the kidney
SGLT2 inhibitors
63
what is the function of SGLTs
glucose is freely filtered by renal glomeruli and reabsorbed in the proximal tubules by sodium glucose transporters (SGLTs) SGLT2 accounts for 90% of glucose reabsoprtion
64
effect of inhibition of SGLT2
causes glycosuria and lowers glucose levels in patients with hyperglycemia
65
contraindications of SGLT2 inhibitors
efficacy reduced in chronic kidney disease
66
major side effects of SGLT2 inhibitors
increased incidence of genital infections and UTIs affecting 8-9% of patients osmotic diuresis can cause intravascular volume contraction and hypotension weight loss
67
specific SGLT2 inhibitors
canagliflozin dapagliflozin empagliflozin
68
what is pramlintide
amylin analog
69
mechanism of action of pramlintide
mimics high dose pharmacologic effects of amylin pancreas: increases insulin and decreases glucagon secretion stomach: delays gastric emptying hypothalamus: decreases appetite similar to GLP-1 or GIP
70
pharmacokinetics of pramlintide
preprandial use as adjunct to insulin improves postprandial glucose control in DM1 and DM2 renal metabolism and excretion
71
adverse effects of pramlintide
hypoglycemia and GI symptoms
72
what is covlesevalam
bile acid sequestrant, cholesterol lowering drug
73
mechanism of action of covlesevalam
not fully understood interrupts enterohepatic circulation -decreases farnesoid X receptor (FXR) activation -may impair glucose absorption
74
what does FXR do
has multiple effects on cholesterol, glucose, and bile acid metabolism bile acids are natural ligands
75
adverse effects of covlesevalam
can exacerbate hypertriglyceridemia common in DM2
76
what is bromocriptine
dopamine agonist
77
mechanism of action of bromocriptine
unknown
78
adverse effects of bromocriptine
nausea, fatigue, dizziness, vomiting, headache
79
principles of combination therapy
combine different mechanisms of action target different proteins advantage of using lower doses fewer adverse effects
80
combination therapy in treating DM2
begin with monotherapy with metformin, GLP-1 mimic, SGLT2 inhibitor, or DDP-4 inhibitor add additional agents as needed to attain target HbA1c finally, add insulin therapy to other agents

GIR Test 1 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions