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2nd shift lecs > Diabetes Milletus > Flashcards

Diabetes Milletus Flashcards

1
Q
  • Most common endocrine disorder
A

Diabetes Mellitus

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2
Q
  • Chronic condition
A

Diabetes Mellitus

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3
Q
  • A group of metabolic disease
    characterized by inappropriate
    chronic hyperglycemia with
    disturbances of carbohydrates, fats and protein metabolism resulting from defect in insulin secretion, insulin action or both
A

Diabetes Mellitus

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4
Q
  • Infantile or
    Childhood
  • Young
  • Adult
  • Elderly
A

1965

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5
Q
  • Insulin
    dependent DM
  • Non-Insulin
    Dependent DM
  • Other Types
A

1985

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6
Q
  • type 1
  • type 2
A

1999

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7
Q
  • type 1
  • type 2
  • specific type due to other causes
  • gestational diabetes
A

2023

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8
Q
  • Destruction of pancreatic beta cell
    responsible of insulin production
  • Associated with autoimmune disease
  • Usually develops in children and
    young adult
  • Associated with a faster onset of
    symptoms, leading to dependency on
    extrinsic insulin for survival
A

type 1 DM

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9
Q
  • More common type of diabetes
  • Occurs in adults older than 40 years
  • Peaks onset between 60 and 70
    years
  • Caused by a relative insulin
    deficiency and the body’s inability to
    effectively use insulin
  • Symptoms are slower in onset and
    less marked than those of Type 1 DM
A

Type 2 DM

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10
Q
  • Hyperglycemia that is first detected during pregnancy, usually
    diagnosed during the 2nd or 3rd trimester
A

Gestational diabetes

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11
Q
  • Hyperglycemia in pregnancy is associated with adverse
    outcomes, including hypertension or pre-eclampsia, fetal
    macrosomia or fetal death
A

Gestational diabetes

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12
Q

adverse outcomes from hyperglycemia in pregnancy

A

pre-eclampsia, fetal macrosomia, fetal death

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13
Q

Diabetes is a result of a pre-existing condition

A

Specific Type due to other causes

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14
Q

Acute, symptomatic

A

Type 1 DM

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15
Q

Slow, often asymptomatic; symptoms occur when condition is already chronic

A

Type 2 DM

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16
Q

Weight loss, polyuria,
polydipsia, polyphagia

A

Type 1 DM

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17
Q

If symptomatic, similar with T1DM + obese, strong family history of T2DM, PCOS

A

Type 2 DM

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18
Q

body burns fat for energy instead of glucose

A

ketosis

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19
Q

Ketosis: Almost always present

A

Type 1 DM

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20
Q

Ketosis: Usually absent

A

Type 2 DM

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21
Q

Biomarker that indicates how much insulin your body has

A

C-peptide

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22
Q

C-peptide: Low or absent

A

Type 1 DM

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23
Q

C-peptide: Normal or elevated

A

Type 2 DM

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24
Q

Antibodies
- Positive: Islet Cell Antibodies
(ICA), ICA 512, Anti-Glutamic
Acid Decarboxylase (Anti-GAD)

A

Type 1 DM

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25
Q

Antibodies
- Negative: Islet Cell Antibodies (ICA), ICA 512, Anti-Glutamic Acid Decarboxylase
(Anti-GAD)

A

Type 2 DM

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26
Q

Insulin

A

Type 1 DM

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27
Q

Lifestyle modification, Oral anti-diabetic agents, Insulin

A

Type 2 DM

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28
Q

Associated auto-immune
diseases: yes

A

Type 1 DM

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29
Q

Associated auto-immune
diseases: No

A

Type 2 DM

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30
Q

Glucose enters the cell via theGLUT 2 transporter → glycolysis → ATP (by product) will bind to ATP sensitive K-channels →K-channel will close, preventing K efflux → depolarization due to increased K → signal Ca channel to open → entry of Ca inside cell→ stimulation of insulin production through a vesicle → bloodstream

A

main pathway

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31
Q

Glutamic acid -> Glutamic acid decarboxylase -> GABA -> insulin

A

alternative pathway

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32
Q

inhibits formation of GABA and will lead to Type 1 DM

A

Anti-GAD antibodies

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33
Q

Hormones affecting sugar
levels in the body

A
  • insulin
  • counterregulatory hormones
  • incretin hormones
  • amylin
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34
Q

Regulates CHO, CHON and
lipid metabolism by
promoting glucose uptake
into the cell

A

Insulin

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35
Q

Promotes conversion of
glucose to glycogen

A

Insulin

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36
Q

Facilitates cellular uptake of
amino acids

A

Insulin

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37
Q

Decreases the breakdown of
fatty acids into ketone bodies

A

insulin

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38
Q

Produced during low glucose
levels to increase the amount
of glucose in the body

A

Counterregulatory hormones

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39
Q

Antagonizes insulin effects

A

Counterregulatory hormones

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40
Q

Promotes conversion of
glycogen to glucose

A

Counterregulatory hormones

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41
Q

glucagon, growth hormones,
catecholamines, cortisol

A

Counterregulatory hormones

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42
Q

Released or secreted after
meal or nutrient intake to
stimulate release of insulin

A

incretin

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43
Q

Inhibits inappropriate glucone
secretion and increases beta
cell growth and reproduction

A

incretin

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44
Q

Suppresses appetite

A

incretin

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45
Q

Gastric inhibitory peptide
(GIP) and Glucagon-like
peptides (GLP)

A

incretin

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46
Q

Co-secreted with insulin

A

amylin

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47
Q

Lowers post-prandial blood
glucose level by prolonging
the gastric emptying time

A

amylin

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48
Q

Reduces post-prandial
glucagon secretion

A

amylin

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49
Q

Suppresses appetite
(2)

A

amylin

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50
Q

Human Leukocyte Antigen (HLA) DQA
and DQB appear to code for either
disease susceptibility or resistance

A

T1DM Genetics

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51
Q

Viral, chemical or dietary

A

T1DM environment

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52
Q

Assigns if person is susceptible or resistant to DM

A

DQA and DQB

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53
Q
  • Anti-insulin ,anti-beta cell antibodies
  • Antibodies to glutamic acid
    decarboxylase
A

T1DM autoimmunity

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54
Q

> 90% concordance rate in identical twins if one has _______

A

T2DM genetics

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55
Q

Improper insulin secretion

A

T2DM Beta cell dysfunction

56
Q

Post-receptor binding, a decreased number of insulin receptor or defects in insulin receptors can lead to hyperglycemia

A

T2DM peripheral site defect

57
Q

Risk factors for diabetes

A
  • overweight or obesity (+)
  • Maternal history of DM or GDM during the child’s gestation
  • Family history of T2 DM in first- or second-degree relative
  • Race/ethnicity (Native American, African American, Latino, Asian American, Pacific Islander)
  • Signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans, HTN, dyslipidemia, PCOS, or small-for-gestational-age birth weight)
58
Q
  • Glucosuria
  • Polyuria
  • Polydipsia
  • Polyphagia
  • Weight loss
A

Most common clinical manifestations

59
Q

≥ 126 mg/dL

A

Fasting Blood Glucose Level

60
Q

≥ 200mg/dL

A

Random Blood Glucose Level/ Oral Glucose Tolerance Test

61
Q

≥ 6.5%

A

Hemoglobin A1c

62
Q
  • Atherosclerosis
    >Stroke, Heart Attack, Artery Disease
  • Retinopathy
    >Cataract, Glaucoma
  • Neuropathy
    >Diabetic Foot, nerve endings
  • Nephropathy
    > liver, nephron damage
A

Complications associated with Diabetes

63
Q

acanthosis nigricans, HTN, dyslipidemia, PCOS, or small-for-gestational-age birth weight

A

Clinical conditions with Insulin resistance

64
Q
  • Prevent Complications
  • Optimize Quality of Life
A

Treatment goals

65
Q

< 7.0%

A

A1C - glycemic recommendations for many nonpregnant adults with diabetes

66
Q

80 - 130 mg/dl

A

pre prandial CPG - glycemic recommendations for many nonpregnant adults with diabetes

67
Q

<180 mg/dl

A

peak post-prandial CPG (1-2 hours after meal) - glycemic recommendations for many nonpregnant adults with diabetes

68
Q
  • Required for glycemic management in individuals with T1DM
  • May be used in combination with oral agent or amylin agonist
  • May also be initial or adjunctive agent for individual with T2DM
A

Insulin

69
Q
  • Stimulates hepatic glycogen synthesis
  • Increase protein synthesis
  • Facilitates triglyceride synthesis and storage by adipocytes
  • Inhibits lipolysis
  • Stimulates peripheral uptake of glucose
A

MOA of Insulin

70
Q
  • inject 10 -15 mins before mealtime
  • typically used in conjunction with longer-acting insulin
A

RAPID acting

71
Q

Inject at least 20-30 minutes before mealtime

A

SHORT acting

72
Q
  • commonly used twice daily
  • often combined with rapid or short acting insulin
A

INTERMEDIATE acting

73
Q
  • covers insulin needs for 24 hrs
  • if needed, often combined with rapid or short acting insulin
A

LONG acting

74
Q
  • combination of intermediate and short acting insulin
  • commonly used twice daily before mealtime
A

PRE-MIXED

75
Q

Long acting no peak

A

Lantus or Glargine

76
Q

Amylin Receptor Agonists

A

Pramlintide

77
Q

Enhance post-prandial control in individual with
T1DM and T2DM

A

Amylin Receptor Agonists indication

78
Q

Gastric motility disorder

A

Amylin Receptor Agonists contraindication

79
Q
  • Slow gastric emptying time
  • Decrease post-prandial glucagon secretion
  • Suppresses appetite
A

MOA of Amylin Receptor Agonists

80
Q

GLP-1 agonist

A

Incretin mimetics

81
Q

Incretin mimetics

A

Exenatide, Liraglutide, -glutides

82
Q

Management of T2DM

A

Indication of incretin mimetics

83
Q

Severe GI motility, pancreatitis, renal or hepatic impairment

A

Contraindication of incretin mimetics

84
Q
  • Increase glucose-dependent insulin secretion,
  • Decrease hepatic glucose output
  • Increase beta cell growth and replication
  • Slow gastric emptying time
  • Enhance satiety or feeling of fullness to suppress appetite
A

MOA of Incretin mimetics

85
Q

Dipeptidyl peptidase IV (DPP IV) inhibitors

A

Sitagliptin, Saxagliptin, Linagliptin

86
Q

Patients with T2DM with normal or impaired
hepatic and renal function

A

Indication of Dipeptidyl peptidase IV (DPP IV) inhibitors

87
Q

Pancreatitis

A

Contraindication of Dipeptidyl peptidase IV (DPP IV) inhibitors

88
Q
  • Prevents the inactivation of incretin hormones by the
    enzyme DPP IV during hyperglycemia
  • Inhibits the breakdown of GLP-1 allowing increased
    insulin secretion and decrease hepatic glucose production
A

MOA of Dipeptidyl peptidase IV (DPP IV) inhibitors

89
Q
  • Targets fasting blood glucose level
  • Binds to and inhibits the ATP-sensitive potassium channels to increase the beta cell sensitivity to glucose and stimulate the secretion of insulin
  • Protein-bound
  • Prone to drug-drug interactions
A

Sulfonylureas

90
Q
  • Typically not prescribed since 2nd gen has fewer ADR
  • Associated with thrombocytopenia, agranulocytosis, hemolytic anemia, hyponatremia, SIADH, disulfiram-like reactions
A

1st Generation Sulfonyureas

91
Q
  • Tolbutamide, Tolazamide, Chlorpropamide
A

1st Generation Sulfonyureas

92
Q

Glyburide, Glipizide, Glimepiride

A

2nd Generation Sulfonyureas

93
Q

Meglitinide

A

Repaglinide

94
Q

Phenylalanine derivatives

A

Netaglinide

95
Q

Insulin Secretagogues

A

Sulfonyureas, Meglitinide, Phenylalanine derivatives

96
Q
  • Management for T2DM
  • Targets post-prandial glucose control
A

Indication of Meglitinide and Phenylalanine derivatives

97
Q

Binds to ATP-sensitive potassium channel to stimulate secretion of insulin from pancreatic Beta cell, reduces hepatic glucose output

A

MOA of Meglitinide and Phenylalanine derivatives

98
Q

Severe renal and hepatic dysfunction
- Used in caution in elderly due to increased risk of fall

A

Contraindication of Meglitinide and Phenylalanine derivatives

99
Q

Biguanides

A

Metformin

100
Q
  • Used for the glycemic control for management of T1DMand T2DM
  • Targets fasting blood glucose
A

Biguanides

101
Q

First line medication for newly diagnosed diabetes

A

Metformin

102
Q

Renal disease, Hepatic impairment, HF

A

Contraindication of Biguanides

103
Q
  • Inhibits hepatic glucose output, thus exerting beneficial effects on fasting blood glucose level
  • Promotes glucose uptake by fat and muscles, improving insulin sensitivity
  • Minor role in decreasing intestinal absorption of glucose
A

MOA of biguanides

104
Q

Thiazolidinediones (TZDs)

A

Pioglitazone, Rosiglitazone

105
Q

Glycemic control in T2DM and primarily affects
fasting blood glucose level

A

Indication of Thiazolidinediones (TZDs)

106
Q

Hepatic dysfunction, Class III/IV HF, Anemia, Fracture risk

A

Contraindication of Thiazolidinediones (TZDs)

107
Q

Alpha-glucosidase Inhibitors

A

Acarbose, Miglitol

108
Q

Management of post-prandial blood glucose

A

Indication of Alpha-glucosidase Inhibitors

109
Q

IBD

A

Contraindication of Alpha-glucosidase Inhibitors

110
Q

with serum creatinine of > 2.0mg/dL or
creatinine clearance of < 25mL/min; hepatic impairment

A

Acarbose

111
Q

Competitive inhibition of alpha-glucosidase in the
intestinal brush border, which leads to slower
absorption of complex carbohydrates

A

MOA of Alpha-glucosidase Inhibitors

112
Q

Sodium-Glucose Cotransporter Inhibitors
-New class of oral hypoglycemic agent

A

Canagliflozin, Dapagliflozin, and Empagliflozin

113
Q

Selectively and reversibly inhibits the sodium-glucose
cotransporter which is selectively expressed in the
proximal renal tubule

A

MOA of Sodium-Glucose Cotransporter Inhibitors

114
Q

T2 DM + Atherosclerotic
Cardiovascular Disease (ASCVD)

A

Monotherapy of Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RA) or Sodium Glucose Cotransporter 2 (SGL2) Inhibitors [Canagliflozin, Dapagliflozin, Empagliflozin]

115
Q

T2 DM + Atherosclerotic
Cardiovascular Disease (ASCVD)
> If A1C above target

A

consider combination therapy or add Thiazolidinediones (TZDs) [Pioglitazone, Rosiglitazone]

116
Q

T2 DM + Heart Failure

A

Sodium-Glucose Cotransporter 2 (SGL2) Inhibitors [Canagliflozin, Dapagliflozin, Empagliflozin]

117
Q

T2 DM + Chronic Kidney Disease (CKD)

A

Sodium-Glucose Cotransporter 2 (SGL2) Inhibitors [Canagliflozin, Dapagliflozin, Empagliflozin] OR Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RA) [Exenatide,
Liraglutide]

118
Q

T2 DM + Chronic Kidney Disease (CKD)
> If A1C above target

A

consider combination therapy of SGL2I and GLP-1 RA

119
Q

Glycemic Control

A

Metformin

120
Q

If glycemic control is not achieved

A

combination therapy with other oral hypoglycemic agents

121
Q

(Efficacy for Glucose Lowering) Very high

A
  • high dose dulaglutide
  • semaglutide
  • tirzepatide
  • insulin
  • combination GLP-1RA-Insulin
122
Q

(Efficacy for Glucose Lowering) High

A
  • GLP-1 RA
  • Metformin
  • SGLT2i
  • Sulfonylureas
  • TZDs
123
Q

(Efficacy for Glucose Lowering) Intermediate

A

DPP4 Inhibitors

124
Q

(Efficacy for Weight Loss) Very high

A
  • Semaglutide
  • Tirzepatide
125
Q

(Efficacy for Weight Loss) High

A
  • Dulaglutide
  • Liraglutide
126
Q

(Efficacy for Weight Loss) Intermediate

A

GLP-1RA, SGLT2i

127
Q

(Efficacy for Weight Loss) Neutral

A
  • DPP4 inhibitors
  • Metformin
128
Q

T2 DM + Weight Control Problems

A
  • Set individualized weight management goals
  • Lifestyle modification, nutrition programs,
    physical activity, metabolic surgery
129
Q

HbA1c <9%
FBS < 250

A
  • Monotherapy
  • Option for combination
130
Q

HbA1c >= 9%
FBS >= 250

A
  • combination
  • insulin
131
Q

World diabetes day

A

Nov 14

132
Q

three things to remember in DM

A

chronic, uncontrolled, and hyperglycemia

133
Q

Insulin should not be stopped (t or f)

A

T

134
Q

Blood glucose less than 13 mmol/L (or less than 230 mg/dL)

A

Continue with current medication

135
Q

Blood glucose 13-22 mmol/L (or 230-390 mg/dL)

A

Patient should inject insulin by 2 units per injection, even if unable to eat

136
Q

Blood glucose greater than 22 mmol/L (or 390 mg/dL)

A

Patient should increase his insulin by 4 units per injection, even if unable to eat

2nd shift lecs (21 decks)

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