Exam 2: DM Flashcards

1
Q

Def: Basal Insulin

A

Longer acting insulin that is meant to cover the body’s basal metabolic
insulin requirement (regulating hepatic glucose production); basal
insulin controls blood glucose in the fasting state

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2
Q

Def: Bolus insulin

A

Short or rapid acting insulin which is meant to reduce glycemic
excursions after meals

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3
Q

Def: Diabetic ketoacidosis

A

Serious complication related to a deficiency of insulin and increase in
insulin counter-regulatory hormones

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4
Q

Def: Dipeptidyl-peptidase 4

A

Enzyme that rapidly degrades active incretin hormones after they are
released

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5
Q

Def: Euglycemia

A

Normal concentration of glucose in the blood. Also called normoglycemia

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6
Q

Def: Fasting

A

No eating for the past 8 or more hours

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7
Q

Def: Glucose

A

Major source of energy for the body

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8
Q

Def: Glycogen

A

The stored form of glucose in the liver and skeletal muscle

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9
Q

Def: Glycogenesis

A

The synthesis of glycogen from glucose that occurs chiefly in the livery and skeletal muscle

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10
Q

Def: Glycogenolysis

A

The conversion of glycogen to glucose in the body

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11
Q

Def: Gluconeogenesis

A

The synthesis of glucose in the body from non-carbohydrates, such as proteins and fats

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12
Q

Def: Hemoglobin A1C

A

A value that represents the percent of hemoglobin in the blood that is
glycosylated. This percent reflects the glycemic control over the past 2 to 3 months

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13
Q

Def: Hyperosmolar hyperglycemic state

A

Serious condition characterized by hyperglycemia, hyperosmolarity and dehydration and the absence of ketoacidosis that may occur in type 2 diabetes

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14
Q

Def: Hypoglycemia

A

Most common acute complication of diabetes; occurs from a relative excess of insulin in the blood and is characterized by below-normal blood glucose levels

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15
Q

Def: Insulin resistance

A

the inability of peripheral target tissues to respond properly to normal circulating concentrations of insulin

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16
Q

Def: Ketosis

A

A condition characterized by the abnormal accumulation of ketones in the body tissues and fluid

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17
Q

Def: Lipolysis

A

Breakdown of fats and lipids to fatty acids (alternative fuel source)

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18
Q

Def: Macrovascular disease

A

Large blood vessels disease; most commonly affected are the coronary arteries, the large arteries in the brain, and large arteries in the periphery

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19
Q

Def: Microvascular complications

A

Small blood vessel disease caused by long term exposure to hyperglycemia; most commonly affects the eyes, kidneys, and nerves

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20
Q

Def: Nocturia

A

Excessive urination at night

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21
Q

Def: Persistent albuminuria

A

A term that reflects when the kidney is allowing an abnormal amount of protein (> 30 μg/mg) to be filtered through the glomerulous.
Marker used in addition to serum creatinine and GFR to stage chronic
kidney disease

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22
Q

Def: Polydipsia

A

Excessive thirst

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23
Q

Def: Polyphagia

A

Excessive hunger

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24
Q

Def: Polyuria

A

Excessive urination

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25
Q

Abbreviation: A1c

A

Hemoglobin A1c

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26
Q

Abbreviation: ASCVD

A

Atherosclerotic cardiovascular disease

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27
Q

Abbreviation: BG

A

Blood glucose

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28
Q

Abbreviation: BGM

A

Blood glucose monitoring

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29
Q

Abbreviation: CGM

A

Continuous glucose monitoring

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30
Q

Abbreviation: CKD

A

Chronic kidney disease

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31
Q

Abbreviation: CVOT

A

Cardiovascular outcome trial

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32
Q

Abbreviation: DKA

A

Diabetic ketoacidosis

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33
Q

Abbreviation: DPP-4

A

Dipeptidyl-peptidase 4

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34
Q

Abbreviation: FPG

A

Fasting plasma glucose

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35
Q

Abbreviation: GDM

A

Gestational diabetes mellitus

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36
Q

Abbreviation: GLP-1

A

Glucagon-like polypeptide 1

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37
Q

Abbreviation: hHF

A

Hospitalization for heart failure

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38
Q

Abbreviation: HHS

A

Hyperosmolar hyperglycemic state

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39
Q

Abbreviation: IFG

A

Impaired fasting glucose

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40
Q

Abbreviation: IGT

A

Impaired glucose tolerance

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41
Q

Abbreviation: MACE

A

Major adverse cardiovascular event

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42
Q

Abbreviation: OGTT

A

Oral glucose tolerance test

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43
Q

Abbreviation: PPG

A

Post prandial glucose

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44
Q

Abbreviation: SGLT-2

A

Sodium-glucose contransporter 2

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45
Q

Abbreviation: T1DM

A

Type 1 diabees

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46
Q

Abbreviation: T2DM

A

Type 2 diabetes

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47
Q

Abbreviation: TIR

A

Time in range

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48
Q

Abbreviation: UACR

A

Urine albumin to creatinine ratio

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49
Q

3 Hormones that control blood glucose

A
  1. Pancreatic hormones
  2. Counter-regulatory hormones
  3. Gut-derived hormones
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50
Q

Def: Pancreas

A

Glandular organ that secretes digestive enzymes and hormones

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51
Q

Pancreas: Plays a fundamental role in ___ and ____

A

Digestion and food energy utilization

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52
Q

Def: Exocrine

A

Digestion break down

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53
Q

Def: Endocrine

A

Regulates immediate utilization and storage of food energy

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54
Q

Pancreas: Endocrine function: Alpha cells

A

Secrete glucagon

Effect the breakdown of liver glycogen and increase glucose levels in the blood

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55
Q

Pancreas: Endocrine function: Beta cells

A

Secrete insulin and amylin

Increase uptake of glucose into cells and facilitate conversion of glucose to glycogen in the liver

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56
Q

Insulin is a(n) ____ hormone

A

anabolic

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57
Q

Insulin is a key regulatory hormone of ______

A

glucose disappearance

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58
Q

Insulin secretion is regulated by __ and ___ hormones

A

Glucose and incretin

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59
Q

Insulin is ___ during absorptive state and ____ during post-absorptive state

A

Increased and decreased

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60
Q

Insulin effects in liver, muscle, and adipose tissues

A

Inhibits hepatic glucose production and glucagon secretion
stimulate glycogenesis in liver
stimulates glucose uptake in muscle fat tissue

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61
Q

Amylin co-secreted with insulin in response to ___

A

nutrient stimuli

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62
Q

Amylin inhibits:

A

postprandial glucose excursions

  • suppresses digestive secretions
  • slows gastric emptying
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63
Q

Glucagon is a(n) ___ hormone

A

catabolic

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64
Q

Glucagon is a key regulatory hormone of ____

A

glucose appearance

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65
Q

T/F: Glucagon works antagonistically to insulin

A

True

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66
Q

Glucagon release is inhibited by

A

Increased glucose levels and presence of fatty acids and ketones

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67
Q

Glucagon release is stimulated by

A

decreased glucose levels and presence of amino acids

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68
Q

Def: Counter-regulatory hormones

A

Counteract the storage functions of insulin in regulating blood glucose levels during periods of fasting, exercise, stress, and other situations that either limit glucose intake or deplete glucose stores

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69
Q

4 Counter-regulatory hormones

A

Glucagon
Epinephrine
Growth hormone
Cortisol

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70
Q

4 Counter-regulatory hormones

A

Glucagon
Epinephrine
Growth hormone
Cortisol

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71
Q

Counter-regulatory Hormones: What does glucagon do?

A

Promotes gluconeogenesis and glycogenolysis, increases release of fatty acids from adipose cells

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72
Q

Counter-regulatory Hormones: What does epinephrine do?

A

Increases the use of fat for energy, promotes glycogenolysis, inhibits insulin release

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73
Q

Counter-regulatory Hormones: What does growth hormones do?

A

decreases the peripheral use of glucose

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74
Q

Counter-regulatory Hormones: What does cortisol do?

A

critical during periods of fasting and starvation, increase gluconeogenesis

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75
Q

Function of Gut: Oral ingestion of food stimulates release of ____ from _____

A

incretin hormones from the small intestine

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76
Q

Function of gut: ____ released from L cells of ileum and colon

A

GLP-1

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77
Q

Function of gut: ___ released from K cells of duodenum

A

GIP

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78
Q

2 Intestinal hormones

A

GIP and GLP-1

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79
Q

Intestinal hormones: GIP: acts at ___

A

B-cell

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80
Q

Intestinal hormones: GIP: Effects

A

Enhances glucose-dependent insulin secretion
May act as an insulin sensitizer in adipocytes
GIP has NO effect on glucagon secretion, gastric motility, or satiety

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81
Q

Intestinal hormones: GLP-1: Acts at ___

A

Alpha and B-cells

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82
Q

Intestinal hormones: GLP-1: Effects

A

Enhances glucose-dependent insulin secretion
Suppresses glucagon secretion
Slows gastric emptying
Has satiety effect on the brain

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83
Q

Def: Diabetes

A

Chronic, progressive metabolic disorder characterized by abnormalities in the ability to metabolize carbohydrate, fat, and protein, leading to a hyperglycemic state

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84
Q

Diabetes: How many with diabetes

A

37.3 million

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85
Q

Diabetes: how many with prediabetes

A

96 million

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86
Q

Diabetes: National diabetes statistics: How many Americans diagnosed every year

A

1.4 million

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87
Q

T/F: racial and ethnic minorities continue to develop diabetes at lower rates

A

False - HIGHER rates

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88
Q

T/F: New diabetes cases higher in non-Hispanic black and people of Hispanic origin

A

True

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89
Q

T/F: Less people are developing diabetes during their youth

A

False - MORE

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90
Q

Diabetes: Accepted terminology key points

A

Type 1 and Type 2 diabetes
DO NOT USE: roman numerals, “insulin dependent” “non-insulin dependent” diabetes, “adult-onset” “juvenile-onset” diabetes, diabetic

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91
Q

Diabetes etiologic classification: Type 1 diabetes

A

Autoimmune B-cell destruction, usually leading to absolute insulin deficiency

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92
Q

Diabetes etiologic classification: Type 2 diabetes

A

Progressive loss of B-cell insulin secretion frequently on the background of insulin resistance

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93
Q

Diabetes etiologic classification: Gestational diabetes (GDM)

A

Diabetes that is first diagnosed in the 2nd or 3rd trimester that is not clearly pre-existing type 1 or type 2 diabetes

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94
Q

Diabetes etiologic classification: Other causes

A

genetic defects
disease of the exocrine pancreas (cystic fibrosis, pancreatitis)
Drug-induced hyperglycemia

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95
Q

Pathophysiology of T1DM: Defect in pancreatic B-cell function&raquo_space;

A

Pancreatic B-cell fxn&raquo_space; deficiency of insulin/amylin

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96
Q

Pathophysiology of T1DM: Relative increase in ___ and its effects

A

glucagon; disequilibrium is created with insulin

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97
Q

Pathophysiology of T1DM: Increase in BG fails to ______

A

suppress production of glucagon

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98
Q

Pathophysiology of T1DM: Effects metabolism of ____

A

fat, protein, and CHOs

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99
Q

Pathophysiology of T1DM: Protein and fat breakdown occurs because of ____

A

lack of insulin – results in weight loss

100
Q

Pathophysiology of T1DM: ____ will result if no treatment

A

Ketoacidosis

101
Q

Stages of T1DM: Stage 1

A

Autoimmune
Normoglycemic
Presymptomatic

102
Q

Stages of T1DM: Stage 2

A

Autoimmune
Dysglycemic
Presymptomatic

103
Q

Stages of T1DM: Stage 3

A

Autoimmune
Hyperglycemic
Symptomatic

104
Q

Progression of T1DM: Rate of progression dependent on

A

Age at first detection of autoantibody (younger > older)
Number of autoantibodies
Autoantibody specificity
Autoantibody titers

105
Q

Metabolic defects: Muscle

A

Insulin resistance in muscle (inefficient glucose uptake)

106
Q

Metabolic defects: Liver

A

Insulin resistance in liver (increases glucose secretion)

107
Q

Metabolic defects: Pancreas

A

Pancreatic B-cell decline (reduced insulin secretion)

Increased activity of alpha-cells in the pancreas (higher blood levels of glucagon increase BG levels)

108
Q

Metabolic defects: fat cells

A

Increased free-fatty acid levels in the blood from fat cell breakdown (more insulin resistance, toxic to beta-cells)

109
Q

Metabolic defects: gut

A

Loss of incretin function from gut (deficiency/resistance)

110
Q

Metabolic defects: kidney

A

Sodium-glucose co-transporter up-regulation in the kidney (results in higher BG levels)

111
Q

Metabolic defects: brain

A

Neurotransmitter dysfunction within the brain

112
Q

Summary of pathophysiological defects in T1DM

A

Defect in pancreatic B-cell fxn

Absolute insulin deficiency

113
Q

Summary of Pathophysiological defects in T2DM

A
Insulin resistance involving muscle, liver, and adipocyte
Defects in insulin secretion
GLP-1 deficiency and resistance 
Excess glucagon secretion
Reabsorption of glucose by the kideny
Defects in signaling to the brain
114
Q

Def: Acanthosis nigricans

A

Manifestation of insulin resistance – skin thickening and pigmentation occurring on neck or armpit

115
Q

GDM: Risk factors

A

Overweight/obese
Older age (>30)
Family hx of T2DM

116
Q

GDM: pathophysiology

A

Insulin resistance

Diminished insulin secretory response (usually normal fasting glucose, PPG high)

117
Q

GDM: Risks to mother and baby

A
Macrosomia (large head, complications for vag. birth)
Shoulder dystocia (shoulder gets stuck)
Preeclampsia
C-section
Stillbirth
118
Q

DM: Clinical manifestations of hyperglycemia

A

Skin infections, genital pruritus, polydipsia, visual changes, polyuria, polyphagia, weight loss, fatigue, paresthesias

Summary: fungal microbiome growth, osmotic diuresis, poor use of food energy, tingling

119
Q

Does food INCREASE/DECREASE glucose?

A

Increase

120
Q

Does exercise INCREASE/DECREASE glucose?

A

Decrease

121
Q

Does alcohol INCREASE/DECREASE glucose?

A

Decrease

122
Q

Does stress/illness INCREASE/DECREASE glucose?

A

Increase

123
Q

Glucocorticoids, Clozapine, Olanzapine INCREASE/DECREASE glucose?

A

Increase

124
Q

T1DM: Screening: 2 most common

A

Islet cell autoantibodies (ICA)

Glutamic acid decarboxylase autoantibodies (GAD65)

125
Q

T2DM: Screening: Recommendations

A
  1. any age with overweight with 1 or more risk factors
  2. Patients with prediabetes test yearly
  3. women diagnosed with GDM test every 3 years
  4. All pts after age 35
  5. Normal results –> test minimum every 3 years
  6. people with HIV
126
Q

T2DM: Screening and Tests

A
  1. Fasting plasma glucose (FPG) - no eating at least 8 hrs
  2. Casual plasma glucose
  3. 2hr plasma glucose during oral glucose tolerance test (OGTT) – usually for pregnant women for GDM, inconvenient for pt (75g glucose dissolved in water); diagnoses more pts than A1C and FPG
  4. Hemoglobin A1C - predictive for complications with DM , reflects average glycemia over 3 months (RBC lifespan ~120 days)
127
Q

T2DM: Screening and Tests: Advantages of A1C over FPG and OGTT

A
Greater convenience (fasting not required)
Less day to day variations during stress/illness
128
Q

T2DM: Cons of A1c

A

Inaccurately reflects glycemia in conditions that alter RBC turnover

  • sickle cell disease
  • pregnancy
  • G6PD
  • ESRD
  • Recent blood loss/transfusion
  • Hemodialysis
129
Q

Diagnosis for T1DM

A

Presence of 2 or more autoimmune markers
Plasma glucose rather than A1C is used to diagnosed
C-peptide matches insulin levels –> low levels of C-peptide = T1DM

130
Q

Diagnosis: T2DM: Prediabetes

A

A1c: 5.7-6.4%
FPG: 100-125 mg/dL - impaired fasting glucose (IFP)
OGTT: 140-199 mg/dL - impaired glucose tolerance (IGT)

131
Q

Diagnosis: T2DM: Diabetes

A

A1c: ≥6.5%
FPG: ≥ 126 mg/dL
OGTT: ≥200mg/dL
Random glucose: ≥200mg/dL plus classic symptoms of hyperglycemia or hyperglycemic crisis

*requires 2 abnormal tests from same sample or 2 separate test samples for diagnosis

132
Q

DM: Goals of therapy

A

Attain optimal glycemic control
Reduce onset/progression of complications
Aggressively address CV risk factors
Improve QOL

133
Q

Glycemic goals for T1DM and T2DM

A

A1c <7%
FG 80-130
Peak PPG <180 (measured 1-2 hours after the beginning of the meal)

134
Q

Children/Adolescent gylcemic goals

A

A1c <7.5%
FG 90-130
Bedtime/overnight 90-130

135
Q

Pregnant women gylcemic goals concepts

A

Test for undiagnosed DM at first prenatal visit if at risk
Test for GDM at 24-48 weeks of gestation with 75g OGTT
Stricter glycemic goals than non-pregnant women
Majority develop T2DM later on

136
Q

Hospitalized patients gylcemic goals

A

Target glucose range 140-180 mg/dL (keep stable)

Use insulin if persistent hyperglycemia >180

137
Q

Older adults glycemic goals: Healthy

A

A1c <7-7.5
FG 80-130
Bedtime: 80-180

138
Q

Older adults glycemic goals: Complex/intermediate

A

A1c: 8%
FG: 90-150
Bedtime glucose: 100-180

139
Q

Older adults glycemic goals: Very complex/poor health

A

A1c: <8.5%
FG: 100-180
Bedtime glucose: 110-200

140
Q

Why are A1c targets >8.5% not recommended?

A

Risk from glycosuria, dehydration, hyperosmolar hyperglycemic state (HHS), poor wound healing, etc.

141
Q

A1c goals should be individualized based on

A

Duration of diabetes
Life expectance (age is just #, life expectancy tells you more)
Comorbidities
Known CVD or advanced microvascular complications
Risk of hypoglycemia
Individual patient considerations (motivation, adherence, caregiver?)

142
Q

ADA Recommendations

A

Weight loss 5-10% (7% target)
Exercise: 150min/week at least
Treat other CVD
Monitor yearly

Metformin is not better than placebo for pts >60, metformin = LTC in obese pts, metformin+ LTC decrease 50% risk in women with h/o GDM

143
Q

TLC

A

Weight loss: 7% with better food choices, less calories, more activity
Children 60min/day x3/week
Adults: at least 150min/week (no more than 2 consecutive days without exercise)

Decrease calories to increase insulin sensitivity
CHO counting (15g/serving, 3-4/meal, 1-2/snack)

25g/day fiber and whole grain

Sodium<2.3g/day

144
Q

Drug therapy: T2DM suggestions: Start with ___ and then consider addition of agents after ____

A

Metformin and after 3 months

145
Q

When to use insulin for T2DM

A

evidence of weight loss
A1c ≥10%
BG ≥300
Very symptomatic

146
Q

Biguanide: Metformin: MOA

A

Inhibit hepatic glucose production

Increase insulin sensitivity of hepatic and muscle tissues

147
Q

Biguanide: Metformin: Contraindications

A
Known hypersensitivity
Medical surgeries (restart 2 days later if good renal fxn is established
Alcohol abuse (3x LFT) 
Renal disease (risk of lactic acidosis) (eGFR <45 ok to continue but don't initiate, <30 d/c) 
Iodinated contrast media with eGFR <60, hepatic disease, alcoholism, Hf, if receiving contract intra-arterially
148
Q

Biguanide: Metformin: Adverse effects

A

GI: diarrhea, cramping, bloating (start at lower dose and titrate up to max dose or until therapeutic. Decrease dose and increase slowly)
Vit B12 deficiency (monitor 2-3 years, espp if develop neuropathic sx )
Lactic acidosis - d/c in acute medical situations

149
Q

GLP-1 RA: MOA

A

Increase glucose-dependent insulin secretion
Decrease PP glucagon secretion
Increase satiety
Decrease gastric emptying time

150
Q

GLP 1 RA: Dosing for exenatide (Byretta) and BG target

A

BID, post meal BG

151
Q

GLP 1 RA: Dosing for exenatide XR (Bdureon) and BG target

A

QWeekly, mixed BG

152
Q

GLP 1 RA: Dosing for liraglutide (Victoza) and BG target

A

QD, mixed BG

153
Q

GLP 1 RA: Dosing for dulaglutide (Trulicity) and BG target

A

QWeekly, mixed BG

154
Q

GLP 1 RA: Dosing for semaglutide (Ozempic) and BG target

A

Qweekly, mixed BG

155
Q

GLP 1 RA: Which medications recommend to inject within 3 days of missed dose?

A

Exenatide XR (Bydureon) and dulglutide (Trulicity)

156
Q

GLP 1 RA: Which medications recommend to inject within 5 days of missed dose?

A

Semaglutide (Ozempic)

157
Q

GLP 1 RA: Exenatide XR (Bydureon): Effect in ___ and dosing/titration

A

Effect in 2 weeks

No titration: 2mg SC once weekly

158
Q

GLP 1 RA: Exenatide XR (Bydureon): Caution with renal fxn

A

Use with caution if eGFR 30-50ml/min

dont use if <30ml/min

159
Q

GLP 1 RA: dulaglutide (Trulicity): Effect in ___ and dosing/titration

A

Effect in 1 week, 0.75mg sc once weekly and titrate up at 4 week intervals (1.5, 3, 4.5mg)

160
Q

GLP 1 RA: semaglutide (Ozempic): Dosing/titration

A

0.25mg SC once weekly and then titrate 0.5, 1mg at 4 week intervals

161
Q

GLP 1 RA: liraglutide (Victoza): Effect in ____ and dose/titration

A

Effect in 1 week

  1. 6mg daily for week 1
  2. 2mg daily for week 2
  3. 8mg daily thereafter
162
Q

GLP 1 RA: Order of greatest to least weight loss

A

Sema
Lira
Dula
Exena

163
Q

GLP 1 RA: Adverse effects

A

GI: N/V/D
Pancreatitis symptoms: severe abdominal pain, often radiating to the back // a/w N/V, fever

Sema: risk of DM retinopathy complications
Exenatide XR: small nodules/lumps at injection site, itchy, may be transient

164
Q

GLP 1 RA: Contraindications

A

Thyroid C-cell tumors (personal/family hx of medullary thyroid carcinoma (MTC) or multiple endocrine neoplasia syndrome type 2 (MEN 2)
Hx Pancreatitis or TG >500
Hx Gallbladder disease
Hx gastroparesis or severe GI disorder
Alcoholism (serious disease can lead to pancreatitis)

165
Q

SGLT2i: MOA

A

Inhibits SGLT2 in proximal tubule (decrease glucose reabsorption)

166
Q

SLGT2i: Caution with eGFR

A

eGFR <45 not effective (if filtering doesn’t work well, not much glucose to reabsorb)

Dapa: <45 –> AVOID for T2DM (All other indications eGFR <25 avoid starting)
Empa: <30 –> AVOID (HF patients with eGFR <20: not defined)

167
Q

SLGT2i: Adverse effects

A

Polyuria (diuretic effect) – take in AM, caution in elderly and pt using diuretics (dehydration)
Genital fungal infections (esp women)
UTI
Cana: DKA? amputations (2x risk once on black box, later removed)?

Monitor for volume depletion and hypotension

168
Q

SU/Glinide: MOA

A

Increase insulin secretion (bind to B cells)

169
Q

SU: dosing

A

Once daily or BID to minimize hypoglycemia
Take with food

Glyburide (Diabeta) - 20mg max dose (metabolized in liver to activate)
Glipizide (Glucotrol) - 40mg (or 20mg ER) [If CrCl <50 take 50% of dose]

170
Q

Glinide: Repaglinide dose

A

Start at 0.5-1mg po TID, 15min before meal
Skip med if you skip meal
Increase dose every week as needed

Max dose 16mg/day

171
Q

SU/Glinides: Generally achieve ____ efficacy at 1/2 max dose

A

80%

172
Q

SU/Glinide: Beneficial for

A
Thin body type (less insulin resistance, more likely to have secretory defect that causes hyperglycemia) 
Newly diagnosed (beta cell fxn more preserved)
Less significant hyperglycemia
173
Q

SU/Glinide: Effect in ____

A

DAYS

174
Q

SU/Glinide: Adverse Effects

A

HYPOglycemia
Weight gain
GI distress
Allergic skin rxn (but diff sulfa moiety)

Secondary failure: efficacy adequate at first and then diminishes over (beta cell decline) – failure rate 5-10%/yr

175
Q

SU/Glinide: Ramadan or fasting pt counseling

A

If A1C is higher, reduce dose to 50%

If A1C is good, omit dose

176
Q

DPP-4i: MOA

A

Inhibit DPP4 (inhibits breakdown of GLP-1 and GIP – increase effect of endogenous incretin hormones)
Facilitates glucose-dependent insulin secretion
decrease PP glucagon secretion

177
Q

DPP-4i: Don’t use with which other class of DM medications?

A

GLP-1 RA

178
Q

DPP-4i: Sitagliptin (Januvia) dosing

A

100mg PO QD

Adjust dose for renal insufficiency (no need for hepatic)

179
Q

DPP-4i: Linagliptin (Trudjenta): Dosing

A

5mg daily

No dose adj for renal and hepatic insufficiency

180
Q

DPP-4i: Good to use for

A

Frail, elderly pts that may not need significant decrease in A1C or have hypoglycemic risk, AE of other agents, or unable to use injectable

181
Q

DPP-4i: Adverse effects

A

WELL TOLERATED
Risk of pancreatitis (rare)
Saxagliptin related to hospitalizations for HF

182
Q

TZD: MOA

A

Activates PPAR-gamma (peroxisome-proliferator activated receptor)
Decrease insulin resistance (improve target cell insulin response) and increase uptake of glucose

183
Q

TZD: Effect in _____

A

2-3 weeks due to need for G-protein turnover

May take 3-4 months to see full effect

184
Q

TZD: Pioglitazone (Actos): Dosing

A

15-30mg PO daily and then titration every 3-4 weeks to max of 45mg/day

No dose adj needed for renal or hepatic insufficiency (not recommended for renal insufficiency due to fluid retention)

185
Q

TZD: Adverse effects

A
Fluid retention and edema
Weight gain
Fracture risk (decrease bone mass and increase fracture risk in women: upper arm, hand, foot but NOT spine/hip)
Macular edema (eye)
BLACKBOX: HF 
Induces ovulation -- risk of pregnancy
186
Q

TZD: Contraindications

A
NYHA class 3 or 4 HF 
Use with caution in pts with edema or class 1 or 2 HF 
Active liver disease (ALT >2.5x ULN at start of therapy and D/C LFTs >3x ULN)
187
Q

Insulin: RAA and Short acting: How many minutes before meal

A

RAA: 15 min

Short acting: 30min

188
Q

Insulin: Intermediate-acting: Duration

A

10-16hr (usually BID)

189
Q

Insulin: Long-acting: Duration

A

U-100 glargine/detemir: 24 hrs
U-300 glargine: 34hrs
degludec: 42hrs

190
Q

Which insulins are cloudy?

A

NPH, premix analogs/NPH-regular

191
Q

Insulin: Premix analogs/NPH-regular: Name all of them and dosing frequency

A
Humalog 75/25 + 50/50 - 15min before meal BID
Novolog 70/30 - 15 min before meal BID 
Ryzodeg 70/30 - QD or BID with any meal 
Humulin 70/30 - 30min before eating BID
Novolin 70/30 - 30min before eating BID
192
Q

Insulin: T1DM: Dosing

A

Starting: 0.5U/kg/day (50% basal, 50% bolus (divided into 3 meals)
OR
Carb matching: 1U=15g/CHO + additional 1U/50 over glucose goal

193
Q

Insulin: T2DM: Reasons to start/add insulin early

A
A1C >10%
Glucose ≥300
Symptoms of hyperglycemia
Ongoing catabolism (weight loss)
CI for GLP-1RA or unacceptable sx of GLP-1RA
194
Q

Insulin: T2DM: Basal dosing

A

Starting dose: 10U/day or 0.1-0.2U/kg/day for obese pts - same time every day
Increase 2-4 U (10-15%) x1-2/week until fasting target is met

195
Q

Insulin: T2DM: Basa: Overbasalization signs and what to do

A

Basal insulin dose >0.5/kg/day
High bedtime to morning (BeAM) or post to pre prandial glucose diff (>50mg/dL)
Hypoglycemia
High glycemic variability

Intensify therapy with GLP1 RA or add prandial insulin

196
Q

Insulin: T2DM: Prandial dosing

A

Starting dose: 4U (or 0.1U/kg or 10% of basal dose) – 15 min before meal (biggest meal)
Monitor PPG and increase 1-2 U 1-2x/weekly until target

D/C SU and DPP-4i, continue other oral meds

If A1C <8%, decrease basal dosing by # of prandial U
If A1C not controlled, do full basal/bolus therapy or premix

197
Q

Insulin: T2DM: Pre-mixed insulin regimen

A

Usually BID – inject 15min before meals
Increase 1-2U x1-2/weekly until target

D/C SU or DPP-4i

If A1C not controlled or hypoglycemia, change regimen

198
Q

Complications: general A1C testing

A

every 6 months if treatment is going well, 3 months if it is not

199
Q

What are some limitations to A1C

A

Doesn’t show variability or hypoglycemia

200
Q

BGM recommendations

A

4-10x/day esp for basal/bolus regiments

For GDM 4-10x/day until controlled 1-2 days

201
Q

CGM: How long can you wear and what are the goals

A

14 day wear
>70% in range
<30% above range
<5% below range

202
Q

Complications: Hypoglycemia: diagnosis

A

BG <70mg/dL
Level 1 MILD <70
Level 2 MOD <54
Level 3 SEVERE

203
Q

Complications: Hypoglycemia: Symptoms

A

Trembling, palpitations, dry mouth, sweating, hunger, anxiety, cognitive impairments, confusion, behavior change, headaches/seizures, slurred speech, weakness, loss of consciousness

  • *if occurs during sleep: nightmares, night sweats, headache
  • *BB can mask sx of hypoglycemia except sweating
204
Q

Complications: Hypoglycemia: Consequences

A

Rebound hyperglycemia (dangerous bc doctor may continue to increase therapy)
Greater risk of dementia
Prolonged QT interval – dysrhythmias, sudden death
Barrier to glycemic control/adherence bc of fears

205
Q

Complications: Hypoglycemia: Risk factors

A
Fasting, delayed/missed meals
Exercise
Drug/alcohol
Unawareness of hypoglycemia
Use of insulin or SU/glinides
Older age/frail
Cognitive impairment
206
Q

Complications: Hypoglycemia: Management

A

15g glucose - wait 15min - repeat if needed

If severe: give glucagon (IV, IM, SC, intranasal)

207
Q

What are some equivalents to 15g of glucose?

A

3-5pieces of hard candy
3-4 pieces of glucose tabs
4oz of juice/soda
1 tbsp of honey/corn syrup/jelly

208
Q

Complications: DKA: 3 Main ideas

A

Ketosis
Hyperglycemia
Metabolic acidosis

209
Q

Complications: DKA: Pathophysiology

A

No insulin > glucose from food cannot be processed > increase counter-reg H > increase glucose production > increase BG

Body need fuel > lipolysis > ketone byproduct > ketoacidosis

Glucose and ketones peed out > bring more water with it > dehydration

OVERAL: Metabolic acidosis

210
Q

Complications: DKA: Predisposing factors

A

Physical/emotional stress

Insulin deficiency

211
Q

Complications: DKA: Symptoms

A

Fatigue, headache, polyuria, polydipsia, weight loss, abdominal pain/tenderness, N/V, fruity/acetone breath, Kassmaul respirations, dry mouth, hypotension, tachycardia, mild hypothermia

212
Q

Complications: DKA: Labs

A

Glucose > 250mg/dL
Low arterial pH <7.3
Low bicarb <18mEq/L
Ketonemia and moderate ketonuria

213
Q

Complications: DKA: Complications

A

Cerebral edema (esp in children)
Respiratory distress syndrome
Thromboembolism
Rhabdomyolysis

214
Q

Complications: HHS: 3 Main ideas

A

Hyperglycemia
Hyperosmolality
Dehydration

215
Q

Complications: HHS: Pathophysiology

A

Little insulin > not enough cell energy > increase counter-reg hormones > increase glucose production > increase BG
Glucose peed out > osmotic diuresis (brings water) > dehydration and electrolyte abnormalities > hyperosmolality

216
Q

Complications: HHS: Predisposing factors

A
Pancreatitis, severe infection/illness
MI
CHO diets (tube feedings, TPN)
Dialysis 
medications antagonizing insulin
217
Q

Complications: HHS: Symptoms

A

Weakness, polyuria, polydipsia, neurological signs, dehydration, seizures, coma

218
Q

Complications: HHS: Labs

A

Glucose >600 mg/dL

Plasma osmolality >320 mOsm/kg

219
Q

Complications: HHS: Complications

A

Thromboembolism

Rhabdomyolysis

220
Q

Complications: HHS: Treatment: Add ____ when blood glucose decreases to ____

A

Dextrose when BG decreases to 250-300mg/dL

221
Q

Landmark trials for T1DM

A

DCCT

222
Q

Landmark trials for T2DM

A

UKPDS, ACCORD, ADVANCe, VADT

223
Q

T/F: intensive glycemic controls prevent macrovascular complications

A

FALSE - they prevent MICROvascular complications – Macrovascular complications come from BP/lipid/antiplatelet control

224
Q

Which landmark trial says that intensive glycemic control can increase mortality?

A

ACCORD

225
Q

What is considered ASCVD?

A
ACS
MI
Angina
Coronary revascularization
stroke
Transient ischemic attack (TIA)
Peripheral arterial disease (PAD)
226
Q

Rates of HF hospitalizations ____ with DM

A

x2

227
Q

What are some CV risk factors?

A

HLD, HTN, smoking, obesity, CKD, albuminuria, FHx of premature coronary disease (men <55 or women <65)

228
Q

Chronic complications: Prevention: BP control

A
Goal: <130/80 
Lifestyle interventions
Meds: ACEI/ARB, Thiazides, DHP-CCB 
- if UACR >30 then 1st line is ACE/ARB 
**ACEI/ARB contraindicated for pregnancy

Monitor BP every visit and at home
Monitor SCR, eGFr, and K annually

229
Q

Chronic complications: Prevention: Lipid Control

A

Get lipid profile at diabetes diagnosis and then 5 years thereafter <40yo
Primary prevention 40-75yo: moderate statin
Secondary prevention: any age: high statin

Monitor at initiation, 4-12weeks later and then annually

**statins contraindicated in pregnancy

230
Q

What are high intensity statins?

A

Atorvastatin 40-80

Rosuvastatin 20-40

231
Q

Chronic complications: Prevention: Antiplatelet control

A

Effective in reducing CV morbidity/mortality in high risk pts with previous MI/stroke (controversial for primary prevention due to bleeding risk)

Secondary prevention: low dose aspirin OR clopidogrel 75mg/day if ASA allergy

ASA in pt <21 yo contraindicated due to Reye’s syndrome

232
Q

Microvascular complications: DKD and screening

A

CKD due to DM

T1DM: annually after 5 yrs after diagnosis
T2DM: annually starting diagnosis

Albuminuria via UACR
- normal <30
- mod 30-300
- severe >300 
eGFR <60ml/min is abnormal
**use UACR and eGFR to stage CKD
233
Q

Microvascular complications: DKD: risk factors

A

HTN, poor glycemic control, HLD, smoking

234
Q

Microvascular complications: DKD: treatment

A

ACEI/ARB for HTN with albuminuria
SGLT2 regardless of glycemic control (or nonsteroidal mineralocorticoid RA finerenone)
GLP1RA suggested for CV risk reduction and slow CKD progression

235
Q

T/F: DM is leading cause of ESRD

A

True

236
Q

Microvascular complications: Diabetic retinopathy

A

Strongly related to duration of DM and level of glycemic control
Risk factors: Hyperglycemia, nephropathy, HTN, dyslipidemia

237
Q

Microvascular complications: Diabetic retinopathy: prevent

A

HTN, DM, HLD

238
Q

Microvascular complications: Diabetic retinopathy: Screening

A

Dilated and comprehensive eye exam
T1DM: annually 5 yrs after diagnosis
T2DM: annually starting at diagnosis

239
Q

Microvascular complications: Diabetic peripheral neuropathy (DPN)

A

associated with diminished perception of vibration, pain, and temperature in lower extremities (loss of feeling, touch, and position sense, paresthesias, numbness, or pain)

Cannot be reversed (prevent with glycemic control)

240
Q

Microvascular complications: Diabetic peripheral neuropathy (DPN): Screening

A

Diabetic neuropathy and sensory function (pinprick, temp, vibration, pressure)

T1DM: annually after 5 yrs of diagnosis
T2DM: annually starting at diagnosis

241
Q

Microvascular complications: Diabetic peripheral neuropathy (DPN): Treatment

A

Optimize glycemic control and foot self-care education and smoking cessation
Pregabalin and duloxetine and gabapentin (off-label)

**cannot reverse

242
Q

Which interventions are done at every visit

A

BP and smoking cessation

243
Q

Which interventions are done every 3 months

A

A1C

244
Q

Which interventions are done yearly?

A

Dilated eye exam, comprehensive foot exam, UACR, SCr, eGFR, lipid panel

245
Q

Which immunizations are recommended

A

Influenza yearly
Pneumococcal PPSV23 at diagnosis
Hep B at diagnosis (19-59 yo)