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Junior - endo II > 11a - DM Part 1 > Flashcards

11a - DM Part 1 Flashcards

1
Q

How many people in US have DM?

A
  1. 1 million

1. 25million w DM1

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2
Q

How much does DM cost?

A

$1 out of every $5 spent on health care

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3
Q

What type of syndrome is DM?

A

A syndrome of disordered metabolism and inappropriate hyperglycemia

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4
Q

DM age at onset?

A

DM1: <30, peaks at 12-14

DM2: <40 (traditionally)

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5
Q

DM pancreatic function

A

DM1: none

DM2: insulin present in low, normal, or high amounts
Its a sensitivity issue

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6
Q

DM pathogenesis

A

DM1: autoimmune beta cell destruction

DM2:

  • defect in insulin secretion,
  • tissue resistance to insulin,
  • increased hepatic glucose output
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7
Q

DM fam hx?

A

DM1: none

DM2: strong

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8
Q

DM obesity?

A

DM1: uncommon (unless using insulin wrong)

DM2: common (60-90%)

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9
Q

DM ketoacidosis hx

A

DM1: common

DM2: rare

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10
Q

Dm clinical presentation

A

DM1: moderate to sever 3p’s

DM2: mild polyuria, fatigue, often diagnosed incidentally

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11
Q

DM insulin required?

A

DM1: yes

DM2: no/yes/merica!

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12
Q

DM fasting C peptide

A

DM1: very low

DM2: normal to high

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13
Q

What is DM1?

A

“DM of childhood”

Autoimmune destruction of beta cells of pancreas islets of lagerhans

A catabolic disorder

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14
Q

What is DM2?

A

Insulin resistance + beta cell loss and dysfunction

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15
Q

What is the greatest risk factor for DM2?

A

Obesity

Especially visceral obesity

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16
Q

What is MODY?

A

Maturity onset diabetes of the young

Doesnt fit type 1 or 2

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17
Q

Characteristics of MODY

A 
Non-insulin dependent DM
Age <25
Non obese
Impaired glucose-induced secretion of insulin
Autosomal dominant inheritance
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18
Q

What are the secondary causes of MODY?

A

Insensitivity to insulin from tumors, drugs, liver disease

Reduced insulin secretion from pheo, pancreatitis, or drugs

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19
Q

Other names for metabolic syndrome?

A

Syndrome X

Dysmetabolic syndrome

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20
Q

Metabolic syndrome and the heart?

A

Metabolic syndrome is an independent risk factor for cardiovascular disease

Increased risk of coronary artery disease and stroke

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21
Q

Clinical abnormalities associated with metabolic syndrome

A 
Insulin resistance
Dyslipidemia
HTN
Hypercoagulability
Proinflammatory state
Hyperuricemia
Hyperinsulinemia
Abdominal obesity
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22
Q

Dyslipidemia in metabolic syndrome?

A

H: TG
L: HDL
H: LDL

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23
Q

Why does metabolic syndrome cause hypercoagulability?

A

Elevated plasminogen activator inhibitor-1
Hyperfibrinogenemia
Increased PLT aggregation

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24
Q

Metabolic proinflammatory state indications?

A

Elevated CRP

Endothelial dysfunction

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25
Q

Define abdominal obesity in reference to metabolic syndrome?

A

Males: waist > 40”

Females: waist > 35”

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26
Q

How is metabolic syndrome diagnosed?

A 
Must have 3 of 5
Obesity: 40,35
Insulin resistance
Hyperlipidemia (TG >150)
Hypercholesterolemia (HDL <40)
Hypertension (>130/85)
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27
Q

SS of DM1?

A

Polyuria
Polydipsia
Polyphagia

Blurred vision
Wt loss
Lpostural HOTN
Paresthesias
Ketoacidosis
LOC
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28
Q

What causes the polyuria in DM1?

A

Osmotic diuresis from hyperglycemia

Leads to glucose, free water and electrolytes into the urine

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29
Q

What is often the 1st sign of DM2?

A

Candidiasis

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30
Q

S/S of DM2?

A

Asymptomatic (often)
Skin infections
Obesity
Acanthosis nigricans

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31
Q

What are rare symptoms of DM2?

A

Hyperglycemic hyperosmolar coma

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32
Q

What types of skin infections are common with DM2?

A

Candidiasis
Generalized pruitis
Vaginitis

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33
Q

What labs are good for DM?

A

UA

  • glucose
  • ketonuria

Blood

  • glucose
  • oral glucose tolerance test
  • HbA1C
  • Fructosamine
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34
Q

What is nondiabetic glycosuria?

A

Benign condition often seen during pregnancy and other times, where glucose spills into urine while blood glucose is normal

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35
Q

What level of ketonuria leads to hostpitalization?

A

> 3.0mmol/L

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36
Q

What is the lifespan for glycohemoglobins?

A

They live for the 120d lifespan of RBCs

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37
Q

What does HbA1C show?

A

Glycemia of previous 8-12 weeks.

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38
Q

What is used to screen for DM, what is not?

A

HbA1C can be a screening tool

UA cannot

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39
Q

What will cause false high/low HbA1C?

A

High: low red cell turnover

  • iron deficiency
  • b12 deficiency
  • folate deficiency
  • kidney/liver failure

Low: rapid red cell turnover

  • hemolysis
  • recent transfusion
  • anemia
  • heavy bleeding
  • kidney/liver failure
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40
Q

What should serum glucose levels be?

A

Fasting >126 mg/dL: diabetes
Fasting 100-125 mg/dL: impaired

Random: >200mg/dL w symptoms: diabetes

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41
Q

What is pre-diabetes?

A

A gray zone between normal and diabetic

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42
Q

What if pt has normal HbA1C levels but abnormal fasting glucose?

A

It may be pre-diabetes

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43
Q

What do pre-diabetics need to do?

A

Make some changes

Decreasing body wt 5-10%, diet, exercise, and drugs can prevent/delay DM2

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44
Q

How is the oral glucose tolerance test performed?

A

Pt eats 150-200g carbs/day x 3 days
NPO after midnight

75g glucose in H2O
Blood is collected at 0 and 120 min post ingestion

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45
Q

What are the normal, impaired and diabetic ranges for oral glucose tolerance test?

A

Normal: <100 fasted and <140 at 2 hr

Impaired 140-199 at 2 hr

Diabetes >126 fasting and or >200 at 2 hr

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46
Q

HbA1C levels, normal, impaired, DM

A

Normal: <5.7
Impaired: 5.7-6.4
Diabetes: >6.5

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47
Q

Of the diabetic complications what is most sensitive to raises in HbA1C?

A

Retinopathy followed closely by neuropathy

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48
Q

What does an HbA1C of 5 represent in glucose?

A

97

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49
Q

What does an HbA1C of 7 equate to in glucose

A

154

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50
Q

Why do we look at fructosamine?

A

It is similar to HbA1C but the 1/2 life is shorter than hemoglobin so we can see changes in glucose after 1-2 weeks

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51
Q

What is serum fructosamine/

A

Formed by non enzymatic glycosylation of serum proteins

Predominantly albumin

52
Q

What labs will help diferentiate between DM1 and DM2?

A

Insulin
C-peptide
Autoantibodies

53
Q

What are c-peptides?

A

Fragment of proinsulin

They are markers for insulin secretion

54
Q

Is c-peptide a reliable test for DM1 and DM2?

A

Not really it cant always distinguish between them

55
Q

What autoantbodies are seen with DM1?

A

Islet-cell (IA2)
Anti-glutamic acid decarboxylase (antiGAD65)
Anti-insulin

56
Q

How are DM labs confirmed?

A

Any abnormal labs must be confirmed on a different day to make a diagnosis

57
Q

What are the symptoms seen with glucose >200mg/dL?

A

Thirsty
Dry
Tired

58
Q

What are the symptoms seen with glucose <60mg/dL?

A

Shaky
Sweaty
Weak

59
Q

What is the margin of error for finger sticks <60mg/dL?

A

Up to 20% different than lab testing

60
Q

Are urine tests reliable for DM monitoring?

A

Not at all

61
Q

Does tight monitoring affect 5 yr mortality?

A

No change in 5 yr mortality

There is a slight increase in CV event risk

62
Q

What diet is recommended for DM by the ADA?

A

45-65% carbs
25-35% fats
10-35% protein

63
Q

What are some other dietary recommendations for DM patients?

A

High soluble fiber content
High insoluble fiber
High insoluble fiber
Low Glycemic index foods

64
Q

Why are DM pts advised to eat fiber?

A

Soluble fiber

  1. The favorable effect on lipids
  2. Slows glucose absorption

Insoluble fiber
1. Helps you poo

65
Q

What is the glycemic index?

A

Carbohydrate foods are rated based on their speed of transformation into glucose.

Lower glycemic foods are 55 or less
-fruits, veggies, whole grains, legumes
Higher glycemic foods are >70
-potato, white bread, rice

66
Q

What are the alcohol recommendations for ETHO?

A

Moderation (LOL)

Men 2 drinks/day
Women 1 drink/day

67
Q

What does ETOH do to DM pts?

A

Causes hypoglycemia

68
Q

What effect does wt loss have on DM?

A

5-10% loss of weight decreases insulin resistance

69
Q

What medications do DM pts need to be on?

A

Glycemic control drugs
ASA
Lipid lowering
BP lowering (ace/arb preferred)

70
Q

What are the available types of glycemic control agents?

A

Oral

Insulin

71
Q

Broad strokes; how do the oral agents work?

A
  • Stimulate insulin secretion
  • Stimulate liver, muscle, adipose to lower glucose
  • Affect absorption of glucose
72
Q

What classes of oral glycemic control agents are available?

A 
Binguinides
GLP-1 RA
SGLT-2i
DPP-4i
TZD
AGI
SU/GLN
73
Q

What is the go to oral agent?

A

Biguinides - metforman

1st line for new DM-2

74
Q

How do biguanides work?

A

Suppress hepatic gluconeogenesis and increase hepatic insulin sensitivity

75
Q

What are the advantages to metformin (glucophage)

A

It improves lipids
NO hypoglycemia risk
Cheap
Weight neutral

76
Q

What are the disadvantages of metformin?

A

GI effects

Lactic acidosis risk (renal insufficiency pts)

77
Q

Contraindications for metformin?

A

CKD
Alcoholics
CHF

78
Q

What are SGLT2?

A

Selective sodium dependent glucose Co Transporter - 2 Inhibitors

Empagliflozin (jardiance)
Canagliflozin (invokana)

79
Q

How do SGLT2s work?

A

Reduce reabsorption of filtered glucose and lowers the renal threshold for glucose resulting in increased urinary glucose excretion

80
Q

What SGLT2 is FDA approved for reducing CV risk?

A

Empagliflozin (jardiance)

81
Q

Advantages for SGLT2s?

A

Potential CV benefit “class effect”

82
Q

Disadvantages of SGLT2?

A 
Wt loss
Increased urination
BP reduction (slight)
Genital fungal infections 
UTI
83
Q

CI for SGLT2?

A

Renal dysfunction

84
Q

What are GLP1 drugs?

A

Glucagon-like peptide 1 receptor agonist

Exanatide (byetta)
Liraglutide (victoza)

85
Q

How are GLP1 drugs prescribed?

A

Add on therapy only w metformin or sulfonylurea

86
Q

Advantages of GLP1s?

A

Wt loss

Address post prandial glucose

87
Q

What are the disadvantages for GLP1s?

A

Injection
GI effects
Pancreatitis
Medullary thyroid cancer(?)

88
Q

CI for GLP1s?

A

MEN2
Medullary thyroid cancer
Gastroparesis

89
Q

What are DPP4 inhibitors?

A

Dipeptidyl peptidase-4

Sitagliptin (januvia)
Saxagliptin (onglyza)

90
Q

What do DPP4 inhibitors do?

A

Stabilize insulin secretion

Decrease glucagon release

91
Q

Advantages of DPP4?

A

Wt neutral
Non-injection
Low hypoglycemia risk

92
Q

Disadvantages of DPP4Is?

A

Serious reactions
Pancreatitis
URI symptoms

93
Q

CI for DPP4Is?

A

Renal impairment (adjust dose)

94
Q

What are TZDs?

A

Thiazoladinediones

Rosiglitazone (avandia)
Pioglitazone (actos)

95
Q

What do TZDs do?

A

Sensitizes peripheral tissue to insulin

96
Q

Advantages to TZDs?

A

Improved lipids

Slows DM progression

97
Q

Disadvantages to TZDs?

A

Increased risk of angina/MI
Edema (3-4% of pax)
Anemia
Wt gain

98
Q

What are AGIs?

A

A-glucosidase inhibitors

Acarbose (precose)
Miglitol (glyset)

99
Q

How to AGIs work?

A

Affect glucose absorption by delaying carb absorption (what a concept)

100
Q

Advantages of AGIs?

A

Wt neutral

Addresses post-prandial glucose

101
Q

Disadvantages of AGIs?

A

Gi effects

102
Q

Contraindications for AGIs?

A

Chronic intestinal disorders
Cirrhosis
Renal impairment

103
Q

How do secretagogues work?

A

They stimulate insulin release from pancreatic B cells

104
Q

Examples of secretagouges?

A

Sulfonylureas
1st gen: tolbutamide (orinase)
2nd gen: glipizide (glucotrol)

Meglitinide analogs
- repaglinide (prandin)

D-phenylalanine derivitive
- nateglinide (starlix)

105
Q

Advantages of secretagouges?

A

Longevity

Cheap

106
Q

Disadvantages of secretagogues?

A

Hypoglycemia

Wt gain

107
Q

CI for secretagogues?

A

Sever liver or renal disease

108
Q

Normal glucose indices?

A

Average FPG or preprandial: <100

Average 2hr postprandial: <140

Average bedtime glucose: <120

HbA1C: <6%

109
Q

Goal (for DM) glucose indices?

A

Average FPG or preprandial: 90-130

Average 2hr postprandial: <150

Average bedtime glucose: 110-150

HbA1C: <7%

110
Q

What glucose indices require action?

A

Average FPG or preprandial: <80 or >140

Average 2hr postprandial: >180

Average bedtime glucose: <110 or >160

HbA1C: >/= 7%

111
Q

How to use oral agents if HbA1C is <9?

A 
Titrate agent over 3 months
Reinforce med, diet and exercise
Recheck HbA1C and after 6 months
Still not good? Add agent (triple therapy)
Recheck at 9 mo, still bad- insulin
112
Q

What if HbA1C is >9 with symptoms?

A

Start with insulin + metformin

113
Q

HbA1C therapy levels?

A

A1C <7.5: monotherapy

A1C >7.5: dual therapy, triple therapy

A1C >9: insulin + metformin

114
Q

What type of insulin do we use? Why?

A

Highly purified human insulin

It has fewer reactions than Pig insulin

115
Q

Formulations of insulin?

A

Rapid acting
Intermediate acting
Long acting

116
Q

Rapid acting insulin ultra short acting?

A

Humalog (lispro)
Novolog (aspart)
Apidra (glulisine)

117
Q

Rapid acting insulin short acting?

A

Humulin R (regular)

Not oft used

118
Q

Intermediate acting insulin?

A 
Humulin N (NPH)
Lente

Onset 2-4 hrs, peak at 9

119
Q

Long acting insulin?

A

glargine (Lantus)
Detemir (levemir)

Bedtime dose

120
Q

What is the preferred DKA insulin tx?

A

Humulin R (regular)

121
Q

How to add insulin to oral glucose agents?

A

Continue oral agents at same dose
Add single bedtime insulin dose

If still not fixed:
Add daytime

Adjust doses weekly

122
Q

What oral agent is not administered with insulin?

A

Sulfonylureas

123
Q

What is pre-breakfast hyperglycemia?

A

Dawn phenomenon
Somogyi effect

Both are high morning levels

Check glucose at 0200-0300

124
Q

What is the dawn phenomenon?

A

Elevated glucose at 0200-0300
Leads to nocturnal GH secretion
Morning hyperglycemia

Tx is increase bedtime insulin

125
Q

What is the somogy phenomenon?

A

Low glucose at 0200-0300 glucose
Stimulates epinephrine -> high glucose levels by 0700
Increases the glucose release from the liver)

Tx: reduce bedtime insulin

126
Q

How common is the dawn phenomenon?

A

As many as 75% of DM1 pts experience this

127
Q

How many apples grow on a tree?

A

All of them

Junior - endo II (7 decks)

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