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Pharm > Diabetes Oral Meds > Flashcards

Diabetes Oral Meds Flashcards

1
Q

Glucagon

A

Made by 𝛼 cells
Stimulates breakdown of stored liver glycogen
Promotes hepatic gluconeogenosis and ketogenesis

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2
Q

Insulin

A

Made by β cells
Affects glucose metabolism and storage of ingested nutrients
Promotes glucose uptake by cells
Suppresses postprandial glucagon secret ion
Promotes protein and fat synthesis
Promotes use of glucose as an energy source

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3
Q

Amylin

A

Made by β cells
Suppresses post prandial glucagon secretion
Slows gastric emptying
Reduces food intake and body weight

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4
Q

GLP-1

A

Enhances glucose dependent insulin secretion
Suppresses postprandial glucagon secretion
Slows gastric emptying
Reduces food intake and body weight
Promotes Β cell health

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5
Q

Which works when BG is high, insulin or glucagon?

A

Insulin

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6
Q

______ signals muscles cells to convert glycogen back to glucose

A

Glucagon

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7
Q

_________ signals liver to release glucose from glycogen

A

Glucagon

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8
Q

_________ signals the liver to store glucose as glycogen

A

Insulin

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9
Q

__________ moves BG into muscle cells for energy or to be stored as glycogen

A

Insulin

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10
Q

___________ signals fat cells to make ketones as an alternate energy source

A

Glucagon

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11
Q

__________ signals fat cells to store excess glucose as fat

A

Insulin

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12
Q

What should happen in a normal person without diabetes?

A

Insulin should be released from the pancreas—> insulin binds to receptors—> glucose can enter the cell

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13
Q

What happens in Type 1 DM?

A

No insulin is produced by the patient—> nothing binds to the insulin receptor—> glucose stays in blood stream and does NOT enter the cell

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14
Q

What happens in Type 2 DM?

A

Insulin is secreted in an amount which may or may not be sufficient + resistance to the insulin binding to the receptor—> glucose cant get into cell

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15
Q

Most common type of DM for someone to have

A

Type 2

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16
Q

TYPE 1 DM

A

Absolute lack of insulin

Due to cellular-mediated AI destruction of pancreatic β cells

Possible triggers: Genetic, viral, environmental

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17
Q

Idiopathic Type 1 DM

A

No known etiology
no β cell AI
STRONG HEREDITARY COMPONENT

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18
Q

TYPE 2 DM

A

Relative insulin deficiency
Also have peripheral insulin resistance
NO AI DESTRUCTION

Typically overweight or obese

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19
Q

TYPE 2 DM risk factors

A

> 45
Fam hx
Obesity
Physical inactivity
Prior gestational DM
HTN
Dysplipidemia
PCOS
Ethnicity (AA, Latino, Asian American)

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20
Q

S&S of diabetes (hyperglycemia)

A

Fagtigue
Polydipsia
Polyphasic
Polyuria
Tingling, numbness in extremities
Poor healing
Blurred vision

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21
Q

3 P’s of diabetes

A

Polydipsia
Polyphasic
Polyuria

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22
Q

Criteria for diabetes dx

A

FPG > 126mg/dL (no caloric intake for at least 8 hr)

2- hg PG ≥ 200mg/dL during OGTT

A1C ≥ 6.5%

Classic sx of hyperglycemia or hyperglycemic crisis + PG ≥ 200mg/dl

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23
Q

Macrovascular chronic complications of diabetes

A

CAD
CVD
PVD (increased risk infection or amputation)

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24
Q

Microvascular complications of chornic diabetics

A

Retinopathy
Nephropathy—> leading cause of ESRD

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25
Q

Risks of Microvascular complications including retinopathy, neuropathy, and nephropathy can be controlled with _________

A

Adequate glycemic control

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26
Q

Non- Pharmacologic therapies to improve glycemic control include:

A

Weight reduction ( <3500kcal/wk)
Increased activity
Reduced alc intake
Smoking cessation

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27
Q

Classes of Pharmacotherapy for diabetes

A

Biguanides
Sulfonylureas
Meglitinides
Thiazolidinediones
𝛼 Glucosidase inhibitors
SGLT2 inhibitors
Others

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28
Q

7 class targets for treatment of T2DM

A

Increased insulin availability
Improving sensitivity to insulin
Decrease hepatic glucose ouput
Decrease glucagon
Delay delivery and absorption of CHO
Slow gastric emptying
Increase urinary glucose excretion

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29
Q

How is insulin sensitivity measured?

A

As the amount of glucose cleared from the blood in response to a fixed dose of insulin

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30
Q

What is insulin resistance

A

Failure of normal amounts of insulin to elicit the expected response

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31
Q

What factors are insulin sensitivity affected by?

A

Age
Body weight
Physical activity levels
Illness
Meds

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32
Q

What type of diabetes has a reduced response to isulin?

A

Type 2

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33
Q

Major insulin-responsive tissues

A

Skeletal muscle
Adipose tissue
Liver

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34
Q

Metformin MOA

A

Reduces hepatic glucose p roduction
Increases skeletal muscle glucose uptake (increases sensitivity)
Decreases intestinal absorption of glucose

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35
Q

First line Oral diabetes agent

A

Metformin

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36
Q

Metformin advantages

A

Rarely Causes hypoglycemia
Effective A1C reduction (1-2%)

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37
Q

Impact of Metformin on Cardiovascular system

A

May reduce CV mortality

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38
Q

Weight impact of Metformin

A

Weight neutral

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39
Q

Side effects of metformin

A

GI: diarrhea, abdominal, cramping, nausea
Lactic acid (rare)
Vit B-12 deficiency with long term use (monitor for peripheral nephropathy)

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40
Q

Metformin Precautions

A

GFR:
- contraindicated <30ml/min
- nor recommended 30-45ml/min

Increase risk lactic acidosis:
Acute CHF, dehydration, excessive alc intake, hepatic and renal impairment, sepsis

Iodinated Contrast media
- can lead to renal failure and increase risk of lactic acidosis
- withhold Metformin before procedures and for at least 48hrs after until GFR normalized

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41
Q

What can you do to alleviate abdominal sx on metformin?

A

Decrease dosage

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42
Q

Sulfonylureas MOA

A

Increases insulin release

Stimulates insulin release by binding to a specific site on the β cell Katp channel complex and inhibiting its activity—> binding inhibits efflux of K+ ions—> depolarization—> influx of Ca+ ions—> release of preformed insulin

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43
Q

Advantages of Sulfonylureas

A

Effective A1C reduction (1.5-2%)

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44
Q

What is the CV impact of first generation Sulfonylureas?

A

Tolbutamide—> associated with worse CV outcomes
Others unknown

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45
Q

What are the CV impacts of second generation Sulfonylureas?

A

Unknown/ not clearly establishes

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46
Q

Weight impact of Sulfonylureas

A

Weight gain

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47
Q

Sulfonylurea Precautions

A

Cross-allergenicity with sulfa allergy & sulfonamides

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48
Q

Side effects of Sulfonylureas

A

Hypoglycemia
Primary or secondary failure

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49
Q

What is primary failure of Sulfonylureas?

A

They never worked in the first place

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50
Q

What is secondary failure of Sulfonylureas?

A

More prevalent failure
Works then stops working

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51
Q

Causes of secondary failure of Sulfonylureas?

A

Progression of disease with pancreatic failure
Poor diatary compliance
Exogenous diabetogenic factors (obesity, illness, drugs, thiazides, corticosteroids)
Tachyphylaxis

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52
Q

First gen Sulfonylureas

A

Chlorpropamide
Tolbutamide
Tolazamide

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53
Q

Second Gen Sulfonylureas

A

Glyburide
Glipizide
Gilmepiride

54
Q

Glyburide

A

Longer DOA than Glipizide
Associated with severe, prolonged hypoglycemia

55
Q

Who should we be careful with using Glyburide in?

A

Caution in frail, elderly, or patients predisposed to hypoglycemia

56
Q

What Sulfonylurea is a better choice for elders, those with renal impairment, or those at risk for hypoglycemia?

A

Glipizide

57
Q

Why is Glipizide best for the elders, renal impaired, and those at risk for hypoglycemia?

A

Short half life
Broken down to inactive metabolites

58
Q

Indications of use for Sulfonylureas:

A

Initial therapy when contraindication to metformin

Can be used in combo with other orals in patients who fail initial therapy with metformin

59
Q

Can Sulfonylureas be added to metformin? If so, when?

A

Sulfonylureas can be added to metformin if the desired A1C is not being attained with just metformin alone

60
Q

MOA of Meglitinides

A

Close K-ATP channels on β cell membranes—> increased insulin secretion
Quick onset (15-60min) and short DOA— concentrates effect around the meal time glucose load

61
Q

What is the difference between Meglitinides and Sulfonylureas?

A

Meglitinides are fast acting so you use them around meal time and if you dont eat, you skip the dose

62
Q

Advantages of Meglitinides

A

A1C reduction .5-1.5%
Reduces postprandial glucose
1-30 min before meals
FLEXIBLE DOSING- skip meal—> skip dose

63
Q

Why would Sulfonylureas not be a good choice for diabetes treatment in patients who skip meals?

A

Increased risk of hypoglycemia

64
Q

CV impacts and weight impacts of Meglitinides

A

CV- unknown
Weight impact—> weight gain

65
Q

Side effects of Meglitinides

A

Hypoglycemia

66
Q

Meglitinides indications

A

Alone or in combo with metformin or other oral diabetes meds
NO WITH SULFONYLUREAS (SU)

Consider them over Sulfonylureas (less risk hypoglycemia and better postpranidal glucose control)

67
Q

Names of Meglitinides

A

Nateglinide
Repaglinide

68
Q

MOA of Thiazolidineodiones (TZDs)

A

Increase tissue sensitivity of insulin by activiating Peroxisome Proliferator-activated receptor γ (PPAR-γ ) nuclear receptors

Causes increased glucose uptake in muscles and adipose tissues, inhibits hepatic gluconeogenesis

Circulating insulin levels decrease—> reduction in insulin resistance

69
Q

Why did the FDA restrict prescription of Rosiglitazone prior to 2013?

A

Increased risk of acute MI and CV deaths

70
Q

Advantages of Thiazolidineodiones

A

A1C reduction of .5-1.4%
Hypoglycemia (rare)

71
Q

CV impact of thiazolidinediones

A

Pioglitizone and Rosiglitazone—> risk of HF

72
Q

TZD weight impact

A

Weight gain

73
Q

Side effects of TZDs

A

Fluid retention
Peripheral edema
Increased risk of bone fractures
Hepatotoxicity (mon LFTs)
Possible increased risk of bladder CA—> pioglitiazone

74
Q

How does Pioglitazone affect patient lipid levels?

A

Reduces triglycerides

75
Q

How does Rosiglitazone affect lipid profiles

A

Increases LDL

76
Q

Contraindications of TZDs

A

Symptomatic HF
NYHA class III or IV HF
Active or hx of bladder CA
Hx of fx or high risk of bone fx
Active liver disease

77
Q

Indications of use for TZDs

A

Patients with contraindications to metformin or Sulfonylureas—> Pioglitazone
For combo, try other agents bc side effect profile is high with TZDs

78
Q

Names of TZDs

A

Pioglitazone
Rosiglitazone

79
Q

𝛼 glucosidase inhibitor MOAs

A

Inhibit the upper GI enzymes (𝛼-glucosidase) that convert complex polysaccharide CHOs into monosaccharides

SLOWS ABSOPRTION of glucose and reduces prostprandial glucose concentrations

80
Q

What to 𝛼 glucosidase inhibitors target?

A

Target post-prandial glucose excursions and are taken with first bite of meal

81
Q

When should you take AGIs?

A

With the first bite of a meal because drug needs to be onboard to prevent absorption of CHOs

82
Q

Advantages of 𝛼 glucosidase inhibitors

A

Rarely causes hypoglycemia
Will get an A1C reduction of .3-1%

83
Q

CV impact of AGIs

A

Miglitol- unknown
Acarbase- neutral

84
Q

Weight impact of AGIs

A

Neutral

85
Q

Side effects of AGIs

A

Flatulence and diarrhea

86
Q

Contraindications of AGIs

A

Cirrhosis- increase liver enzymes
SrCr >2mg/dL
Major intestinal issues (IBD or CID)— worsened by increased gas formation such as colonic ulceration or partial intestinal obstruction

87
Q

How to treat hypoglycemia caused by miglitol or acarbose?

A

glucose tablets of glucose gels

88
Q

Why are CHOs not effective in treating Hypoglycemia caused by AGIs?

A

Will not be absorbed

89
Q

Are AGIs considered 1st line therapy? If not why?

A

No they are not

Reduced efficacy and poor tolerance

90
Q

What are the 2 𝛼 glucosidase inhibitors used?

A

Acarbose
Miglitol

91
Q

DPP-4 inhibitor MOA

A

Increases GIP (glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like-protein) , which are incretin hormones, via DPP-IV inhibition—> increased insulin secretion and decreased glucagon section—> decreased hepatic glucose production

92
Q

What hormones do DPP-IV inhibitors enahnce? Decrease?

A

Decrease: glucagon,, insulin, amylin
Enhance- GLP-1 (suppresses postprandial glucagon section and slows gastric emptying)

93
Q

Advantages of DPP-IV inhibitors

A

Rarely cause hypoglycemia
A1C reduction .5-.8%

94
Q

CV impact of DPP-IV inhibitors

A

Neutral in regard to morbidity and mortality
Increased risk of HF related admissions with alogliptin and saxagliptin

95
Q

Weight impact of DPP-IV inhibitors

A

Neutral

96
Q

Side effects of DPP-IV inhibitors

A

Angioedema
Urticaria and other immune-mediated derm effects
Acute pancreatitis
Arthralgias
Headache
Nasopharyngitis

97
Q

Who should we caution use pf DPP=IV inhibitors in?

A

HF patients (increased HF hospitalizations)

98
Q

Indications of use of DPP-IV inhibitors

A

Add on therpay for those not well controlled on metformin, TZDs, or Sulfonylureas
Monotherapy IF intolerant of or have contraindications to metformin, Sulfonylureas, or TZDs

FOR PATIENTS WITH CKD—> Linagliptin (bold)

99
Q

What hormones do DPP-IV inhibitors enahnce? Decrease?

A

Decrease: glucagon,, insulin, amylin
Enhance- GLP-1 (suppresses postprandial glucagon section and slows gastric emptying)

100
Q

Advantages of DPP-IV inhibitors

A

Rarely cause hypoglycemia
A1C reduction .5-.8%

101
Q

CV impact of DPP-IV inhibitors

A

Neutral in regard to morbidity and mortality
Increased risk of HF related admissions with alogliptin and saxagliptin

102
Q

Weight impact of DPP-IV inhibitors

A

Neutral

103
Q

Side effects of DPP-IV inhibitors

A

Angioedema
Urticaria and other immune-mediated derm effects
Acute pancreatitis
Arthralgias
Headache
Nasopharyngitis

104
Q

Who should we caution use pf DPP=IV inhibitors in?

A

HF patients (increased HF hospitalizations)

105
Q

Indications of use of DPP-IV inhibitors

A

Add on therpay for those not well controlled on metformin, TZDs, or Sulfonylureas
Monotherapy IF intolerant of or have contraindications to metformin, Sulfonylureas, or TZDs

FOR PATIENTS WITH CKD—> Linagliptin

106
Q

are the 4 DPP-IV inhibitors used in treatment of diabetes?

A

Sitagliptin
Saxaliptin
Alogliptin
Lingaliptin

107
Q

What DPP-IV inhibitor DOES NOT require renal dosing?

A

Lingalipitin

108
Q

SGLT2 inhibitor MOA

A

Inhibit SGLT2 receptors in the proximal nephron—> blocks glucose reabsorption by the kidney—> increased urinary excretion of glucose—> decreased plasma glucose

109
Q

Advantages of SGLT2 inhibitors

A

Reduce A1C by .7-1%
Rare hypoglycemia
Reduces blood pressure (bc cuases slight osmotic diuretic effect)

110
Q

Weight impact of SGLT2 inhibitors

A

Weight LOSS

111
Q

CV impacts of SGLT2 inhibitors

A

Ertugliflozin- neutral
Canagliflozin, Dapagliflozin, Empagliflozin—> improves outcomes

112
Q

Renal impact of SGLT2 inhibitors

A

Can prevent kidney endpoints by reducing the progression of kidney disease
Empagliflozin, Dapagliflozin, & Canagliflozin= improve renal outcomes

113
Q

Side effects of SGLT2 inhibitors

A

GU fungal infections
UTIs—> urosepsis
Diuresis
Volume depletion—> dehydration
Hypotension
Ketoacidosis
Necrotizing Fasciiitis of the perineum (Fournier gangrene)

114
Q

Canagliflozin specific SE

A

Increased risk of bone fractures
Increased risk of LE amputation

115
Q

Specific Side effect with Dapagliflozin

A

Increased risk bladder cancer

116
Q

What population is likely to develop Ketoacidosis with SGLT2 inhibitor use and should avoid them?

A

Diabetic patients which have fx predisposing to DKA
Pancreatic insufficiency
IVDU or alcohol use disorder

117
Q

Biggest thing to keep in mind about SLGT2 inhibitors

A

They is no long term safety data with regards to its effect of chronic glucosuria

118
Q

If you do lab work on a patient taking an SGLT2 inhibitor, what will you expect to find?

A

Glucose in urine

119
Q

Contraindications/ Precaustions of SLGT2 inhibitors

A

Older patients or those taking diuretics, ACEi, or ARBs—> can cause symptomatic HTN

Caution in conjunction with other meds that predispose people to acute renal injury (ACE, ARB, NSAIDs)

120
Q

What are the 4 SGLT2 inhibitors

A

CEED
Canagliflozin
Empagliflozin
Ertugliflozin
Dapagliflozin

121
Q

How are SGLT2 inhibitors dosed?

A

Renally (dose reductions dependent on the SGLT2 and whether or not they are being used for glycemic control)

122
Q

Indications of use for SGLT2 inhibitors

A

Not considered initial therapy for T2DM
Cardiorenal comorbidities- consider SGLT2 inhibitors for their benefit in this pop

123
Q

Bile Acid Sequestrants MOA in diabetes

A

Uncertain
Proposed:
act in GI tract to reduce glucose absorption
Reduce hepatic glucose production and increase incretin levels

124
Q

Advantages of Colesevelam (BAS)

A

A1C reduction .5%
Rarely cause hypoglycemia

125
Q

Effect of Colesevelam on lipids

A

Decreased LDL
Increase triglycerides

126
Q

Colesevelam side effects

A

Constipation

127
Q

MOA of dopamine 2 agonists in DM

A

Believed to affect circadian rhythms
May reset hypothalamic circadian activities (altered by obesity)—> reversal of insulin resistance and decreased hepatic glucose production

128
Q

A1C reduction caused by dopamine 2 agonists

A

.4-.5%

129
Q

Side effects of Dopamine 2 agonists

A

Dizziness
Syncope
Nausea
Fatigue

130
Q

What is the name of the Dopamine 2 agonist used in diabetes treatment?

A

Bromocriptine

Pharm (4 decks)

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