Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Endo > SM_187b: Diabetes Pharmacology > Flashcards

SM_187b: Diabetes Pharmacology Flashcards

(93 cards)

Start Studying
1
Q

Diabetes is a group of metabolic disorders resulting in ___

A

Diabetes is a group of metabolic disorders resulting in hyperglycemia

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

Prolonged hyperglycemia in diabetes results in ____, ____, ____, and ____

A

Prolonged hyperglycemia in diabetes results in cardiovascular disease, nephropathy, retinopathy, and neuropathy

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

____ is the key to alleviated symptoms and improving outcomes in diabetes mellitus

A

Control of blood glucose is the key to alleviated symptoms and improving outcomes in diabetes mellitus

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

Proinsulin is converted to insulin via ____

A

Proinsulin is converted to insulin via cleavage of C peptide

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

___ is the primary stimulus for insulin secretion

A

Rise in blood glucose is the primary stimulus for insulin secretion

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

Insulin receptor is a ____

A

Insulin receptor is a receptor tyrosine kinase

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

Describe the mechanism of action of the insulin receptor

A

Insulin receptor mechanism of action

  1. Insulin binds to insulin receptor
  2. Tyrosine phosphorylation of substrates activates downstream signaling
  3. Activation of PI3K-AKT pathway -> increased glycogen synthase, translocation of glucose transporters to membrane
  4. Signalging through RAS-MAPK pathway results in proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T1DM is when ___ and there is an ___

A

T1DM is when insulin is lacking and there is an absolute requirement for insulin replacement

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

T2DM is when ____ due to ____

A

T2DM is when insulin is insufficient due to inadequate secretion or target tissue resistance

(other treatments may be able to stimulate the secretion of sufficient insulin)

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

Insulin needs vary throughout the day, mainly due to ___

A

Insulin needs vary throughout the day, mainly due to blood glucose increases after meals

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

____, ____, ____, and ____ are short-acting insulins

A

Regular insulin, lispro, aspart, and glulisine are short-acting insulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lispro, aspart, and glulisine insulins have ____ onset than regular insulin because they aggregate less

A

Lispro, aspart, and glulisine insulins have faster onset than regular insulin because they aggregate less

  • Taken just before meal, activity lasts for period of meal digestion
  • Aspart and glulisine insulins are used as pumps for continuous subcutaneous insulin infusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

____, ____, and ____ are longer acting insulins

  • NPH insulin: protamine slows absorption
  • Glargine: aggregation results in slower absorption, peakless
  • Detemir: aggregates and binds to albumin, peakless
A

NPH insulin, glargine, and detemir are longer acting insulins

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

Basal / bolus insulin regimen involves ____

A

Basal / bolus insulin regimen involves glargine or detemir before breakfast or at bedtime, with preprandial injections of short acting insulin

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

Split-mixed insulin regimen involves ____

A

Split-mixed insulin regimen involves pre-breakfast and pre-supper injection of a mixture of short- and long-acting insulins

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

Insulin pump is used for ____ to provide ____ with ____

A

Insulin pump is used for continuous subcutaneous insulin infusion to provide a continuous basal rate with mealtime bolus injections based on size and nature of meals

  • Complications: abscesses, cellulitis, pump failures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe limitations to and alternatives for insulin administration methods

A

Limitations to and alternatives for insulin administration methods

  • Limitations: amount / type of food influence insulin requirement, r egional blood flow affected by exercise / temperature / smoking, and counterregulatory hormones / injury / infection / other drugs affect insulin requirement
  • Islet cell autotransplantation: infusion of own pancreatic islet cells into portal vein in liver
  • Generation of induced pluripotent stem cell derived beta cells for autologous replacement therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

____ and ____ are major side effects of insulin

A

Hypoglycemia and weight gain are major side effects of insulin

  • Risk higher in kids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment of insulin-induced hypoglycemia is ____

A

Treatment of insulin-induced hypoglycemia is glucose

  • Glucagon: acts through GPCR and cAMP, increases hepatic glucose production
  • Diazoxide (thiazide): no diuretics, interacts with beta cell K channel, decreases insulin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe mechanisms of therapeutic effects of agents for type 2 diabetes

A

Mechanisms of therapeutic effects of agents for type 2 diabetes

  • Increase insulin secretion
  • Affect glucose metabolism directly
  • Promote insulin action
  • Decrease glucose absorption
  • Increase glucose excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Sulfonylureas (glyburide) ____

A

Sulfonylureas (glyburide) increase secretion of insulin from pancreatic beta cells

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

Glyburide is a ____

A

Glyburide is a sulfonylurea

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

Sulfonylureas (glyburide) bind to ___, ____, and ____

A

Sulfonylureas (glyburide) bind to the sulfonylurea, block the KATP channel, and depolarize the beta cell

Increase secretion of insulin

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

Describe pharmacokinetics of sulfonylureas

A

Sulfonylurea pharmacokinetics

  • Rapidly absorbed after oral administration
  • Absorption can be reduced by food and hyperglycemia
  • Highly protein bound (> 90%)
  • Plasma half life of 3-5 hour but 24 hour duration of hypoglycemic action
  • Hepatic metabolism (CYP2C9)
  • Renal excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Describe types of sulfonylureas
Sulfonylureas * First generation (e.g. chlorpropamide, tolbutamide): rarely used * Second generation (e.g. glyburide): more potent and fewer drug interactions
26
\_\_\_\_ is the main adverse effect of sulfonylureas
Hypoglycemia is the main adverse effect of sulfonylureas * Weight gain, interference with alcohol metabolism, possible adverse cardiovascular effects
27
Describe drug interactions of sulfonylureas
Sulfonylurea drug interactions * Competition for plasma protein binding (especially sulfonamides) can increase [free sulfonylurea] * Hypoglycemic effect can be decreased by ethanol
28
Repaglinide is a \_\_\_
Repaglinide is a meglitinide
29
Meglitinides (repaglinide) act on ____ and have some overlap in binding sites with \_\_\_\_
Meglitinides (repaglinide) act on beta cell K channels and have some overlap in binding sites with sulfonylureas
30
Describe the pharmacokinetics of meglitinides (repaglinide)
Meglitinides (repaglinide) pharmacokinetics * Very rapid onset with oral administration * Stimulate insulin over period of meal digestion * Metabolized in liver by CYP3A4, some renal metabolism
31
Describe the mechanism of action of meglitinides (repaglinide)
Meglitinides (repaglinide) mechanism of action 1. Act on beta cell K channels 2. Increase K inside cell 3. Depolarization 4. Increase Ca flux into cell through voltage gated Ca channel 5. Insulin secretion
32
\_\_\_\_ is main toxicity of meglitinides (repaglinide)
Hypoglycemia is main toxicity of meglitinides (repaglinide)
33
\_\_\_\_ has drug interactions with meglitinides (repaglinide)
Anti-lipidemia drug gemfibrozil (Lopid) has drug interactions with meglitinides (repaglinide)
34
GLP-1 mimetics are \_\_\_\_, \_\_\_\_, and \_\_\_\_
GLP-1 mimetics are exenatide, liraglutide, and dulaglutide
35
Describe GLP-1 mimetics
GLP-1 mimetics * Incretins: GI hormones derived from proglucagon * Promote glucose-dependent insulin secretion * Effective in patients with T2DM * Can result in weight loss
36
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) function to \_\_\_\_
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) function to promote glucose-dependent insulin secretion
37
Describe mechanism of action of GLP-1 mimetics (exenatide, liraglutide, and dulaglutide)
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) mechanism of action 1. Act through GLP receptors (GPCRs) 2. Act mainly through cAMP/PKA pathway but can also stimulate other signaling pathways 3. Close K channels, increase Ca release, and increase release of insulin
38
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) are rapidly absorbed after \_\_\_
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) are rapidly absorbed after subcutaneous injection
39
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) are contraindicated in patients with \_\_\_\_
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) are contraindicated in patients with thyroid medullary carcinomas * Adverse effects: nausea, vomiting, abdominal pain, pancreatitis
40
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) have drug interactions with \_\_\_\_, \_\_\_\_, and \_\_\_\_
GLP-1 mimetics (exenatide, liraglutide, and dulaglutide) have drug interactions with antibiotics, alcohol, and oral contraceptives (exenatide)
41
Sitagliptin is a \_\_\_\_
Sitagliptin is a DPP-4 inhibitors
42
Describe the mechanism of action of DPP-4 inhibitors (sitagliptin)
DPP-4 inhibitors (sitagliptin) mechanism of action 1. Inhibit serine protease dipeptidyl peptidase-4 2. GLP-1 activated 3. Increased glucose-mediated insulin secretion and decreased glucagon
43
DPP-4 inhibitors (sitagliptin) are ____ effective and have ____ excretion
DPP-4 inhibitors (sitagliptin) are orally effective and have renal excretion
44
DPP-4 inhibitors (sitagliptin) adverse effects are \_\_\_\_, \_\_\_\_, and \_\_\_\_
DPP-4 inhibitors (sitagliptin) adverse effects are headaches, allergy, and nasopharyngitis
45
DPP-4 inhibitor saxagliptin has ___ metabolism
DPP-4 inhibitor saxagliptin has CYP3A4 metabolism
46
Biguanides (metformin) are \_\_\_
Biguanides (metformin) are oral agents that decrease glucose production
47
Metformin is a \_\_\_
Metformin is a biguanide
48
\_\_\_ is a common first line treatment for T2DM
Metformin monotherapy is a common first line treatment for T2DM
49
Biguanides (metform) activate ____ and exert \_\_\_\_
Biguanides (metform) activate AMPK and exert non-AMPK dependent actions including complex I inhibition
50
Describe mechanism of action of biguanides (metformin)
Biguanides (metformin) mechanism of action 1. Activate AMPK and exert non-AMPK dependent actions including complex I inhibition 2. Decrease haptic glucose production, suppress gluconeogenesis, increases glycogen storage in muscle
51
\_\_\_\_ is less likely to cause hypoglycemia than other agents used to treat diabetes
Metformin is less likely to cause hypoglycemia than other agents used to treat diabetes
52
Biguanides (metformin) are ___ and undergo ___ excretion
Biguanides (metformin) are not metabolized and undergo renal excretion
53
Biguanide (metformin) main adverse effect is \_\_\_\_
Biguanide (metformin) main adverse effect is decreased vitamin B12 absorption * Indigestion, cramps, and diarrhea * Lactic acidosis, promoted by comorbidities
54
\_\_\_\_ drugs compete for the proximal tubule secretory system, elevating circulating metformin
Cationic drugs compete for the proximal tubule secretory system, elevating circulating metformin
55
Thiazolidinediones (pioglitazone) are \_\_\_
Thiazolidinediones (pioglitazone) are oral agents that promote insulin action
56
Pioglitazone is a \_\_\_\_
Pioglitazone is a thiazolidinediones
57
Describe the mechanism of action of thiazolidinediones (pioglitazone)
Thiazolidinedione (pioglitazone) mechanism of action 1. Binds to and activates PPAR-gamma in complex with RXR 2. Promotes transcription of insulin-sensitive genes in liver, muscle, and adipose tissue
58
Thiazolidinediones (pioglitazone) are ____ effective and metabolized in \_\_\_\_
Thiazolidinediones (pioglitazone) are orally effective and metabolized in liver by several CYPs
59
\_\_\_\_ is the main adverse effect of thiazolidinediones (pioglitazone)
Congestive heart failure is the main adverse effect of thiazolidinediones (pioglitazone)
60
Thiazolidinediones (pioglitazone) have interactions with drug that target ____ such as \_\_\_\_
Thiazolidinediones (pioglitazone) have interactions with drug that target metabolism such as rifampin
61
Acarbose is an \_\_\_\_
Acarbose is an alpha-glucosidase inhibitor
62
Alpha-glucosidease inhibitors (acarbose) \_\_\_\_
Alpha-glucosidease inhibitors (acarbose) decrease glucose absorption
63
Describe the structure and mechanism of alpha-glucosidease inhibitors (acarbose)
Alpha-glucosidease inhibitors (acarbose) structure and mechanism * High affinity for alpha-glucosideases on the brush border of epithelial cells * Delays absorption of glucose, interfering with hydrolysis of disaccharides
64
Acarbose decreases plasma glucose increment after ____ loading
Acarbose decreases plasma glucose increment after sucrose loading
65
Alpha-glucosidease inhibitors (acarbose) have ___ absorption and ___ excretion
Alpha-glucosidease inhibitors (acarbose) have minimal absorption and renal excretion
66
Alpha-glucosidease inhibitors (acarbose) adverse effects are ____ and \_\_\_\_
Alpha-glucosidease inhibitors (acarbose) adverse effects are abdominal pain and flatulence due to bacterial metabolism of the glucose (weak effect)
67
Alpha-glucosidease inhibitors (acarbose) drug interaction is \_\_\_\_
Alpha-glucosidease inhibitors (acarbose) drug interaction is decreasing absorption (e.g. of digoxin)
68
Pramlintide is an \_\_\_\_
Pramlintide is an amylin analog
69
Amylin analogs (pramlintide) \_\_\_\_
Amylin analogs (pramlintide) decreases glucose absorption
70
Amylin analog (pramlintide) binds to ____ and mimics \_\_\_\_
Amylin analog (pramlintide) binds to amylin receptor in hindbrain and mimics physiological effects of amylin (islet amyloid peptide)
71
Describe the mechanism of action of amylin analogs (pramlintide)
Amylin analogs (pramlintide) 1. Bind to amylin receptor in hindbrain 2. Mimic physiological effects of amylin (islet amyloid peptide) 3. Slows gastric emptying / decreases post-prandial glucose concentrations, anorectic effect, inhibits glucagon release
72
Amylin analogs (pramlintide) are administered ____ prior to \_\_\_\_
Amylin analogs (pramlintide) are administered subcutaneously prior to meals (renal metabolism and excretion)
73
Amylin analogs (pramlintide) adverse effects are \_\_\_\_, \_\_\_\_, and \_\_\_\_
Amylin analogs (pramlintide) adverse effects are nausea, increasing insulin hypoglycemic risk, and contraindication in patients with disorder of GI motility
74
Amylin analogs (pramlintide) drug interactions are with \_\_\_
Amylin analogs (pramlintide) drug interactions are with other agents affecting GI motility
75
Colesevelam is a \_\_\_\_
Colesevelam is a bile binding resin
76
Bile binding residen (colesevelam) \_\_\_\_
Bile binding residen (colesevelam) decreases glucose absorption
77
Bile binding residen (colesevelam) is primarily used for treatment of \_\_\_\_
Bile binding residen (colesevelam) is primarily used for treatment of hypercholesterolemia
78
Bile binding residen (colesevelam) functions to ____ and \_\_\_\_
Bile binding residen (colesevelam) functions to lower plasma glucose in patients with T2DM and lower HbA1c
79
Bile acid binding resin (colesevelam) has ___ absorption
Bile acid binding resin (colesevelam) has minimal oral absorption
80
Bile acid binding resin (colesevelam) has adverse effects of \_\_\_, \_\_\_, \_\_\_, \_\_\_, and \_\_\_
Bile acid binding resin (colesevelam) has adverse effects of constipation, dyspepsia, abdominal pain, nausea, and increased plasma triglycerides
81
Bile acid binding resin (colesevelam) interferes with \_\_\_
Bile acid binding resin (colesevelam) interferes with absorption of many commonly used drugs and fat soluble vitamins
82
Canagliflozin is a \_\_\_\_
Canagliflozin is a SGLT2 inhibitor
83
SGLT2 inhibitors (canagliflozin) \_\_\_\_
SGLT2 inhibitors (canagliflozin) increase glucose excretion
84
Describe SGLT2
SGLT2 * Sodium/glucose co-transporter 2 (SGLT2) expressed in the proximal tubule * SGLT2 functions in reabsorption of glucose -\> returned to circulation via glucose transporters 1 and 2 * SGLT2 is low affinity, high capacity transporter * Loss of function mutations in SGLT2 cause glucosuria
85
Describe SGLT2 inhibitors (canagliflozin) pharmacokinetics
SGLT2 inhibitors (canagliflozin) pharmacokinetics * Orally effective * Peak at 1-2 hour * Metabolized and undergoes fecal and renal excretion
86
\_\_\_\_ is the main adverse effect of SGLT2 inhibitors (canagliflozin)
Increased risk of amputations is the main adverse effect of SGLT2 inhibitors (canagliflozin)
87
SGLT2 inhibitors (canagliflozin) have a drug interaction with \_\_\_\_
SGLT2 inhibitors (canagliflozin) have a drug interaction with gatifloxacin
88
Bromocriptine is a \_\_\_\_
Bromocriptine is a dopaminergic agonist
89
Describe the mechanism and action of dopaminergic agonists (bromocriptine)
Dopaminergic agonists (bromocriptine) mechanism and action * Increases dopaminergic activity in the hypothalamus * Mechanism for effects on blood glucose has not been established * Decreases postprandial glucose without increasing insulin
90
Dopaminergic agonists (bromocriptine) are \_\_\_
Dopaminergic agonists (bromocriptine) are orally effective * Nausea, vomiting, headaches, fatigue, orthostatic hypotension * Weak effect
91
Describe the treatment sequence for T2DM
Treatment sequence for T2DM 1. Metformin 2. If A1c is \> 7% after 3-4 months, a second drug is added 3. If A1c still \> 7% after another 3-4 months, 2 oral agents or insulin are added
92
Use of pioglitazone should be avoided in patients with ____ or \_\_\_\_
Use of pioglitazone should be avoided in patients with heart failure or acute diseases of the liver
93
Summarize drugs for treating diabetes
Drugs for treating diabetes

Endo (25 decks)

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