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🄼💊MSY2 Pharm (Endocrine/Repro/Thyroid) > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Describe DMT2 diet (4)

A

DEC Refined sugar

DEF Saturated Fat

INC Complex Carbs (low glycemic index)

INC Fiber

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2
Q

Weight loss goal for T2DM

A

DEC Weight by 5%

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3
Q

Name the insulin sensitizers (2)

A
  1. [Metformin Biguanide]
  2. Thiazolidinediones (Pioglitazone/Rosiglitazone)
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4
Q

Name the Thiazolidinediones (2)

A
  • Pioglitazone
  • Rosigliazone
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5
Q

What are the 2 classes of [insulin secretogogues]

A

Sulfonylurea

Meglitinides

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6
Q

Sulfonylurea Drugs (5)

A
  1. Chlorpropamide
  2. Tolbutamide
  3. Glimepiride
  4. Glyburide
  5. Glipizide
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7
Q

Meglitinide Drugs (2)

A
  1. Repaglinide
  2. Nateglinide
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8
Q

Which Type2DM drugs are [Incretin Mimetic GLP1 Homologs] (2)

A
  1. Exenatide
  2. Liraglutide
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9
Q

Which Type2DM drugs are [DPP4 inhibitors]

A
  1. Sitagliptin
  2. Saxagliptin
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10
Q

Which Type2DM drugs inhibit Carb digestion

A

Alpha-Glucosidase inhibitors

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11
Q

[Alpha Glucosidase inhibitor] Drugs (2)

A

Acarbose

Miglitol

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12
Q

Amylin Homolog

A

Pramlintide

Amylin is ABSENT in Type2DM

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13
Q

[SGLT2 inhibitors] Drugs (2)

A

Canagliflozin

Dapagliflozin

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14
Q

Bile Acid Binding resin

A

Colesevelam

Preventing Bile acid reabsorption –> INC Bile Acid Synthesis. Bile Acids bind to [Intestinal TGR5 –> GLP1 secretion]

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15
Q

How are [Incretin Mimetic GLP1 Homologs] administered and whats the dosage

A

Parenteral

SubQ QD vs. BID

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16
Q

How is [Pramlintide Amylin Homolog] administered

A

Parenteral

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17
Q

Metformin Indication

A

First line Type2DM tx after [Diet & Exercise] have been ruled out

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18
Q

Metformin Effect (4)

A
  1. DEC Hepatic Gluconeogenesis
  2. INC Insulin Sensitivity –> INC Glucose utilization
  3. DEC Weight (SE)
  4. Lowers fasting Glucose
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19
Q

How much does Metformin lower [HbA1C %]?

A

1.5 %

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20
Q

Advantages of Metformin (4)

A
  1. DEC Weight
  2. No hypOglycemia
  3. Improves Lipids
  4. DEC MI
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21
Q

Metformin MOA

A

Inhibitis Mitochondria complex 1 –> [INC AMPK] –> [DEC Adenylate Cyclase]

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22
Q

Metformin SE (3)

A
  1. Lactic Acidosis
  2. GI (NV & Anorexia)
  3. DEC B12 absorption–>Megaloblastic Anemia
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23
Q

Which pts are most at risk for [Metformin induced Lactic Acidosis] (5)

A
  • Renal Failure
  • Liver Failure (i.e. EtOH abuse)
  • CHF / MI
  • hypoxia (COPD)
  • Illness (viral vs. septicemia)
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24
Q

Sx of Lactic Acidosis (3)

A
  1. Deep but Rapid breating
  2. Vomiting / Abd Pain
  3. [Leg/Arm Muscle Weakness]
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25
Q

Metformin Contraindications (6)

A
  1. Renal Failure
  2. MI
  3. CHF
  4. Pregnancy
  5. Age >80
  6. Liver Failure
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26
Q

What’s the only Type2DM tx for Pregnant pts

A

Insulin only

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27
Q

Clearance of Metformin

A

Renal only

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28
Q

Thiazolidinediones MOA

A

[PPARgamma Agonist] (expressed in Fat, Muscle, Liver, Heart & MACS)–> transcription factor activation

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29
Q

Thiazolidinediones Effect (3)

A
  1. INC Insulin sensitivity
  2. DEC Fasting glucose
  3. DEC Insulin resistance
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30
Q

How long does it take for Thiazolidinediones to reach MAX Effect

A

6-14 Weeks

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31
Q

Thiazolidinediones SE (4)

A
  1. ​CHF-BLACK BOX WARNING
  2. Wt Gain (SubQ usage)–> [insulin sensitive adipose]
  3. [Peripheral Edema from Fluid Retention]
  4. Bone Fractures in Women
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32
Q

Thiazolidinedione Contraindications (3)

A
  1. CHF
  2. CVD
  3. Liver Dz
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33
Q

Compare onset of Sulfonylureas and Meglitinides

A

Sulfonylurea: Slower onset

Meglitinide: rapid onset (15-30 min)

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34
Q

Compare half-life of Sulfonylureas and Meglitinides

A

Sulfonylurea: Long

Meglitinide: short (60-90 min.)

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35
Q

Compare [Duration of Action] between Sulfonylureas and Meglitinides

A

Sulfonylurea: Long (14-16 Hrs)

Meglitinide: short (2-4 Hrs)

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36
Q

Sulfonylurea Effect (2)

A
  1. INC Insulin Secretion
  2. DEC Fasting Glucose
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37
Q

Meglitinides Effect (2)

A
  1. DEC Postprandial Glucose
  2. INC Insulin Secretion
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38
Q

Name the First Generation Sulfonylurea (2)

A
  1. Chlorpropamide
  2. Tolbutamide
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39
Q

Name the SECOND Generation Sulfonylurea (3)

A
  1. Glimepiride
  2. Glyburide
  3. Glipizide
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40
Q

Repaglinide [Drug Class]

A

Meglitinide

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41
Q

Nateglinide [Drug Class]

A

Meglitinide

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42
Q

Sulfonylureas MOA

A

Inhibits B-cell [K+ Sur1 channel] –> Insulin Secretion

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43
Q

Sulfonylurea SE (2)

A
  1. hypOglycemia
  2. Wt Gain
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44
Q

Clearance of Sulfonylureas

A

Liver only

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45
Q

Excretion of Sulfonylureas

A

Kidney

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46
Q

Which Sulfonylurea maybe safer for pts with renal insufficiency & elderly?

A

Glipizide (it has no active metabolites)

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47
Q

Which Sulfonylurea are not safe for pts with renal insufficiency & elderly (2)?

A

Glyburide & Glimepiride

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48
Q

Sulfonylurea Contraindications (4)

A
  1. Renal Failure
  2. Liver Failure
  3. Elderly
  4. Co-admin with Highly Protein bound drugs
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49
Q

Meglitinide MOA

A

Inhibits B-cell [K+ Sur1 channel] –> Insulin Secretion

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50
Q

Why does Meglitinide have a lower risk of hypOglycemia than Sulfonylureas?

A

Meglitinide is GLUCOSE DEPENDENT

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51
Q

Which Meglitinide drug acts to [DEC Postprandial AND Fasting Glucose]

A

Repaglinide

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52
Q

Elimination of Repaglinide

A

90% Fecal & 10% Renal

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53
Q

Metabolism of Repaglinide

A

Liver

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54
Q

Repaglinide Indication

A

Alternative to Sulfonylurea when pt has Renal Dz

55
Q

Metabolism of Nateglinide

56
Q

Meglitinides SE (2)

A
  1. hypOglycemia
  2. Wt Gain

MUCH LESS THAN SULFONYLUREA

57
Q

Meglitinide Contraindication

58
Q

Describe [Incretin Effect] and how it is in Type2DM pts

A

GI Tract produces hormones that act on beta cells and potentiates glucose-induced insulin production –> Plasma Insulin response to Oral Glucose is greater than IV Glucose.

Incretin Effect is DEC in Type2DM

59
Q

[GLP1 homolog] Structure

A

Short-lived hormone (<2 min) from [small intestine L-cells]

60
Q

[Incretin Mimetic GLP1 Homolog] Effect (8)

A
  1. Glucose-dependent Insulin Secretion
  2. DEC Pancreatic Glucagon
  3. DEC Liver Gluconeogenesis
  4. DEC Gastric Emptying
  5. DEC Fasting Glucose
  6. DEC Postprandial Glucose
  7. DEC Wt
  8. INC Satiety
61
Q

When is [Incretin Mimetic GLP1 Homologs] used?

A

Alternative to starting insulin in Type2DM pts who are refractory to all other meds

62
Q

[Duration of Action] for Exenatide

63
Q

[Duration of Action] for liraglutide

64
Q

[Incretin Mimetic GLP1 Homologs] SE

65
Q

[Duration of Action] for [DPP4 inhibitors]

A

24 hours (take daily)

66
Q

[DPP4 inhibitors] Effect (2)

A
  1. DEC Fasting Glucose
  2. DEC Postprandial Glucose
67
Q

How are the [DPP4 inhibitors] prescribed

A

Monotherapy vs. [Adjunct with Meformin or Thiazolidinedione] for Type2DM

68
Q

[DPP4 inhibitors] MOA

A

Inhibits DPP4 (DPP4 Causes GLP1 homolog degradation)

69
Q

[DPP4] SE

70
Q

[Alpha Glucosidease inhibitors] MOA

A

Delays Glucose absorption by inhibiting Carb conversion –> Monosaccharide in [small intestine brush border]

71
Q

[Alpha Glucosidase inhibitor] SE

A

Significant GI Side Effects from Unabsorbed Carbs

72
Q

[Alpha Glucosidase inhibitors] Contraindication (3)

A
  1. Ulcerative Colitis
  2. IBD
  3. Intestinal Dz
73
Q

[SGLT2 inhibitors] MOA

A

Inhibits [PCT Sodium Glucose Transporter 2] –> INC Glucose Urine Excretion

74
Q

[SGLT2 inhibitors] MOA

A

Inhibits [PCT Sodium Glucose Transporter 2] –> INC Glucose Urine Excretion

75
Q

How much does [SGLT2 inhibitor] lower [HbA1C %]?

A

0.5 - 0.9 %

76
Q

[SGLT2 inhibitor] SE (3)

A
  1. Candidiasis UTI (from INC urine glucose)
  2. Dehydration (osmotic diuresis)
  3. Hyperkalemia (especially if with [K+ sparing diuretics vs. Renal impairment])
77
Q

[SGLT2 inhibitor] Contraindication

A

Renal Impairement

78
Q

Bromocriptine MOA

A

[D2 Dopamine agonist] that INC Dopamine defecits in Type2DM (given within 2 hours of awakening)

79
Q

Bromocriptine Effect on Type2DM (3)

A
  1. INC insulin sensitivity
  2. DEC Hepatic Gluconeogenesis
  3. DEC Lipolysis
80
Q

How much does Bromocriptine lower [HbA1C %]?

81
Q

How is Colesevelam prescribed & MOA

A

Adjunct Type2DM tx that indirectly INC GLP1 expression

82
Q

Colesevelam MOA

A

[Bile Acid Binding Resin] that prevents Bile acid reabsorption –> INC Bile Acid Synthesis.

These INC Bile Acids bind to [Intestinal TGR5 –> GLP1 secretion]

83
Q

How much does Colesevelam lower [HbA1C %]?

84
Q

How much does Sulfonylureas lower [HbA1C %]?

85
Q

Insulin Indication (3)

A
  1. Any Pt with [HbA1C %] > 10%
  2. Late onset Type1 DM (Wt. Loss + Polyuria + PolyDispsia)
  3. Second line for Type2DM > 8.5 HbA1C% (will require more insulin since Type2 are insulin resistant)
86
Q

How is [Pramlintide Amylin] used

A

Used as an ADJUNCT for [Refractory DM 1 vs.2] when using insulin

87
Q

[Pramlintide Amylin] Effect (5)

A
  1. DEC Hepatic Gluconeogenesis
  2. DEC postprandial Glucagon production
  3. DEC Gastric emptying–> DEC rate of Glucose absorption
  4. INC Satiety
  5. Wt Loss
88
Q

How does [Pramlintide Amylin] affect [Insulin Dosage]

A

Effects are ADDITIVE when given with insulin and [Pramlintide Amylin] DEC amount of short/rapid insulin needed by 50%

It’s injected along with Insulin

89
Q

[Pramlintide Amylin] SE (2)

A
  1. ​Severe hypOglycemia (since it’s given with insulin)
  2. Constitutional (NV/HA)
90
Q

Classic Regimen for Entire DM Progression

A

Initial Impaired Glucose intolerance= Diet & Exercise

0-5 years = Diet + Metformin

>5 years = Combination therapy + Insulin

91
Q

Which Type2DM tx is given when [HbA1C > 7%]

A

[Metformin Biguanide]

92
Q

Which [Type2DM Combination therapy] is useful in overweight pts

A

Metformin + Exenatide

93
Q

Which [Type2DM Combination therapy] is useful if [HbA1C > 8.5%]

A

Metformin + Insulin

94
Q

Tx for Type1DM

A

Insulin only

95
Q

How does Insulin work metabolically

A

Anabolic effect

96
Q

What are the 4 treatment goals for any DM

A
  • HbA1C < 7%
  • BP < 140/90
  • Fasting Glucose= 90-130
  • Tolerance Test < 180
97
Q

List the [rapid acting] insulin

A

Glulisine (Girls)

Aspart (And)

Lispro (Lads)

98
Q

[Rapid acting insulin] formulation

A

Amino acid substituted insulin variant that are monomeric –> Fast absorption

99
Q

[Rapid acting insulin] onset time

100
Q

[Rapid acting insulin] Peak time

101
Q

[Rapid acting insulin] Duration

102
Q

[Rapid acting insulin] Usage (2)

A

[Injection right before meal] vs. [Acute hyperglycemia]

103
Q

[Regular insulin] formulation

A

Forms Hexamers that dissociate into monomers prior to absorption. Zinc added for stability

104
Q

[Regular insulin] onset time

105
Q

[Regular insulin] Peak time

106
Q

[Regular insulin] Duration

107
Q

[Regular insulin] Usage (2)

A

[Injection (30-45 min) before meal] vs. [Acute hyperglycemia]

Requires Injection

108
Q

[NPH Isophane Insulin] formulation

A

Since it’s conjugated with protamine, this delays absorption until proteolytically cleaved by endogenous tissue protease

109
Q

[NPH Isophane Insulin] onset time

A

1.5-2 HOURS

110
Q

[NPH Isophane Insulin] Peak time

A

6-10 HOURS

111
Q

[NPH Isophane Insulin] Duration

A

16-24 HOURS

112
Q

[NPH Isophane Insulin] Usage (2)

A

Basal insulin and Overnight Coverage

113
Q

List the [intermediate acting] insulin

A

[NPH Isophane]

114
Q

[LONG acting Insulin] formulation for GlarGine

A

Amino Acid substituted variant that forms large precipitant at body pH –> slow absorption

115
Q

[LONG acting Insulin] onset time

116
Q

[LONG acting Insulin] Peak time

A

DOESN’T PEAK

117
Q

[LONG acting Insulin] Duration

A

6-24 HOURS for Detmir

20-24 HOURS for GlarGine

“Don’t Go <–last word”

118
Q

[LONG acting Insulin] Usage (2)

A

Basal insulin and Overnight Coverage

119
Q

List the [LONG acting insulin]

A

Detmir

GlarGine

120
Q

[LONG acting Insulin] formulation for Detmir

A

Debbie was a Fatty Ass

Contains [Fatty acid side chain] that associates with tissue bound albumin –> slows absorption

121
Q

Routes Of Insulin Administration (5)

A

Inhaled

or

SubQ in:

Upper Arm

Abd

Butt

Thigh

122
Q

What’s the problem with persistent injection of insulin into 1 body site?

A

lipodystrophy = inappropriate lipid storage

123
Q

Regimen for Conventional Insulin therapy

A

BID injection of Mix:

(NPH isophane 50-75%)

+

(Regular or rapid insulin 25-50%)]

124
Q

When, during the day, are Insulin pts most at risk for hypOglycemia

A

During the NPH peak (late afternoon and night)

125
Q

When, during the day, are Insulin pts most at risk for Hyperglycemia and what is this called

A

Dawn Phenomenon = INC blood glucose in morning from cortisol release –> Hyperglycemia

126
Q

Regimen for intensive insulin therapy (2)

A

[QD/BID injection of Basal Insulin (NPH isophane or GlarGine)]

+

[Rapid Insulin right before meals]

127
Q

Dose of a pre-meal [Fast acting insulin] bolus is determined by what 3 things?

A
  1. Blood glucose
  2. Meal Size & Composition
  3. Anticipated Physical Activity
128
Q

Lab value for hypOglycemia

A

<60 mg/dL –> potentially fatal

129
Q

Mild hypOglycemia Sx (4)

A
  • Tremor
  • Palpitations
  • Sweating
  • Hunger
130
Q

Moderate hypOglycemia Sx (4)

A
  1. HA
  2. Mood changes
  3. Drowsiness
  4. Requiring assistance to get up
131
Q

Tx for Moderate hypOglycemia

A

Oral Simple Carb

132
Q

SEVERE hypOglycemia Sx (2)

A
  1. UNRESPONSIVE VS. UNCONSCIOUS
  2. CONVULSIONS

LEADS TO DEATH

133
Q

TX FOR SEVERE hypOglycemia (2)

A

IV glucose vs. Glucagon Pen

🄼💊MSY2 Pharm (Endocrine/Repro/Thyroid) (6 decks)

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