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397 DM Mgt Flashcards

Chap 397. Diabetes Management and Treatment

1
Q

OHA with proven cardiovascular safety

A

Empagliflozin

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2
Q

OHA not given to patients with CHF FC III- IV

A

Pioglitazone

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3
Q

OHA given for patients with renal disease

A

Linagliptin

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4
Q

Anti diabetic agent with proven cardiovascular safety for DM type 1

A

Liraglutide

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5
Q

Anti diabetic agents what may be given to DM type 1

A

Amylin agonist

Alpha glucosidase

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6
Q

Anti diabetic agent that can decrease appetite

A

GLP 1 agonist: exenitide and liraglutide

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7
Q

Why is NaHCO3 is not given immediately to patients with DKA?

A

It can cause Hypokalemia, decreased cardiac output and decreased oxygenation

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8
Q

Name 2 fruits with low sucrose

A

Grapes

Avocado

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9
Q

Main component of mediterranean diet

A

Olive oil

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10
Q

US equivalent of gliclazide

A

Glibenclamide

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11
Q

Which is a main advantage of Metformin

A

Weight loss

Lowers Lipid profile

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12
Q

Target HbA1c for most individuals

A

HbA1c less than 7

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13
Q

Target HbA1c for DM Type 1

A

HbA1c less than 6.5

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14
Q

Target HbA1c for elderly, chronic illness and bedridden

A

HbA1c less than 8 or 8.5

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15
Q

Reflects glycemic status over the prior 2 weeks

A

fructosamine assay (measuring glycated albumin)

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16
Q

Reflects glycemic history over the previous 2-3 months

A

glycated hemoglobin

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17
Q

insulin- carbohydrate ratio

A

1-1.5 units/ 10 grams CHO

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18
Q

What is amylin and name an example of amylin analogue

A

Amylin is secreted by pancreatic beta cells together with insulin. A decrease in insulin also means a decrease in amylin
Example of amylin analogue is pramlintide

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19
Q

What is the side effect of pramlintide

A

slowing gastric emptying

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20
Q

Major toxicity of metformin

A

lactic acidosis

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21
Q

Analogue of GLP-1 identified in the saliva of the Gila monster

A

Exenatide

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22
Q

Reduce insulin resistance by binding to PPAR-gamma

A

Thiazolidinediones

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23
Q

Highest levels of PPAR gamma is found where?

A

Adipocytes

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24
Q

Contraindicated in CHF Class III and IV

A

Thiazolidinediones

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25
Q

Necessary for DKA to develop

A

insulin deficiency and glucagon excess

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26
Q

At what pH is HCO3 given in DKA

A

ph less than 7.0

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27
Q

How is metabolic acidosis treated in DKA

A

HCO3 50 meq in 200 Sterile water with 10 meqs KCL per hour for 2 hours until pH more than 7.0

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28
Q

Two ketones produced by DKA

A

beta hydroxybutyrate and acetoacetate

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29
Q

How can a patient have DKA when urine ketone is negative

A

Only acetoacetate and acetone are detected by urine assay; the other ketone iin DKA, beta hydroxybutyrate is detected in the serum

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30
Q

Why is IVF changed to 0.45% once CBG reaches 250 mg/dl

A

To avoid hyperchloremia

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31
Q

Underlying cause of HHS

A

relative insulin deficiency and inadequate fluid intake

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32
Q

Preferred diet for T2DM

A

Mediterranean diet rich in polyunsaturated fat

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33
Q

Sodium intake in T2DM

A

same as general population

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34
Q

True or false. Sucrose food allowed with adjustment in insulin dose

A

True.

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35
Q

Treatment goals T2DM. HbA1c

A

less than 7.0%

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36
Q

Treatment goals. Preprandial glucose

A

4.4-7.2 mmol or 80-130 mg/dl

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37
Q

Treatment goal T2DM. Postprandial glucose

A

less than 10 mmol or less than 180 mg/dl

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38
Q

Treatment goal T2DM. Blood pressure

A

Less than 140/90

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39
Q

Treatment goal T2DM. LDL

A

less than 2.6 mmol or less than 100 mg/dl

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40
Q

Treatment goal T2DM. HDL

A

more than 1 mmol or more than 40 mg/dl

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41
Q

Treatment goal T2DM. Triglycerides

A

less than 1.7 mmol or 150 mg/dl

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42
Q

True or false. To avoid exercise related hyper or hypolgycemia, individuals with Type 1 should monitor blood glucose before, during and after exercise

A

True.

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43
Q

blood glucose levels to delay exercise

A

more than 14 mmol or more than 250 mg/dl with ketones; less than 5.6 mmol or less than 100 mg/dl

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44
Q

What to do with insulin dose if planning to exercise

A

decease insulin dose before or after exercise and not to inject nonexercising area

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45
Q

relative contraindication to exercise and why?

A

untreated proliferative retinopathy and this may lead to vitreous hemorrhage or retinal detachment

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46
Q

reflects average glycemia control over the previous 2-3 months

A

HbA1c

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47
Q

standard method for assessing long term glycemic control

A

HbA1c

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48
Q

HbA1c equivalent. 6%

A

7 mmol or 126 mg/dl

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49
Q

HbA1c equivalent. 7%

A

8.6 mmol or 154 mg/dl

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50
Q

hbA1c equivalent. 8%

A

10.2 mmol or 183 mg/dl

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51
Q

hbA1c equivalent. 9%

A

11.8 mmol or 212 mg/dl

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52
Q

hbA1c equivalent. 10%

A

13.4 mmol or 240 mg/dl

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53
Q

hba1c equivalent. 11%

A

14.9 mmol or 269 mg/dl

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54
Q

hbA1c equivalent. 12%

A

16.5 mmol or 298 mg/dl

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55
Q

ADA recommendation of HbA1c

A

2x a year or every 3 months if there has been change in therapy or there is inadequate glycemic control

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56
Q

reflects glycemic status over the prior 2 weeks

A

fluctosamine assay

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57
Q

alternative indicator when HbA1c is inaccurate

A

1,5- anhydroglucitol

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58
Q

Frequency. Eye examination

A

annual or biannual

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59
Q

Frequency. Foot examination.

A

by physician: 1-2 times/year; by patient: daily

60
Q

Screening for diabetc nephropathy

A

annual

61
Q

Frequency. Lipid profile and serum creatinine

A

annual

62
Q

HbA1c goal for elderly, chronic illness and impaired activities of daily living

A

HbA1c 8.0- 8.5%

63
Q

target HbA1c for most individuals

A

less than 7%

64
Q

True or false. More stringent HbA1c target of less 6% is no beneficial

A

True.

65
Q

Short acting insulin examples

A

aspart, glulisine, lispro, regular, inhaled human insulin

66
Q

Onset. Peak. Duration. Regular insulin

A

O: 30- min 1 hr P: 2-3 hrs D: 3-6 hrs

67
Q

Onset. Peak. Duration. Lispro

A

O: 15 mins P: 30 mins- 1 hr D: 2-4 hrs

68
Q

Onset. Peak. Duration. Aspart

A

O: 15 mins P: 30 mins- 1 hr D: 2-4 hrs

69
Q

Onset. Peak. Duration. Glulisine

A

O: 15 mins P: 30 mins- 1 hr D: 2-4 hrs

70
Q

Short acting insulin with same onset, peak and duration of action

A

lispro, aspart, glulisine

71
Q

long acting insulin examples

A

degludec. Detemir, glargine, NPH

72
Q

long acting insulin with no peak.

A

degludec. Detemir, glargine

73
Q

Onset. Duration. Degludec

A

O: 1-9 hrs D: 42 hrs

74
Q

Onset. Duration. Detemir

A

O: 1-4 hrs D: 12-24 hrs

75
Q

Onset. Duration. Glargine

A

O:2-4 D: 20-24 hrs

76
Q

Onset. Duration. NPH

A

O: 2-4 P: 4-10 D: 10-16 hrs

77
Q

True or false. Aspart, lispro and glulisine is preferred over regular insulin in controlling prandial glucose

A

True.

78
Q

how is insulin glargine differ from normal insulin

A

asparagine is replaced by glycine in amino acid 21 and two arginine residues added to C terminus of B chain

79
Q

insulin the has a fatty acid side chain that reversibly binds to albumin

A

detemir

80
Q

insulin that forms multihexamers in subcutaneous tissues prolong its duration of action

A

degludec

81
Q

required prior to prescribing inhaled insulin

A

FEV1 should be measured;

82
Q

side effect of inhaled thus avoided in this subset of patients

A

inhaled insulin can cause cough and bronchospasm; avoid in patients with lung disease or who smoke

83
Q

insulin dose formula based on prepandial glucose

A

1 unit for every 2.7 mmol or 50 mg/dl over the preprandial glucose target

84
Q

T2DM agents side effects. Flatulence

A

alpha glucosidase inhibitors. Acarbose. Voglibose

85
Q

T2DM agents side effects. GI upset

A

biguianides. Metformin

86
Q

T2DM agents side effects. Edema, CHF

A

thiazolidenediones. Pioglitazone

87
Q

T2DM agents side effects. UTI, dehydration

A

SGLT2 inbibitors. Dapagliflozin, empagliflozin, canagliflozin

88
Q

T2DM agents side effects. Hypoglycemia

A

sulfonylureas. Glibenclamide, glimepiride, gliclazine

89
Q

T2DM agents. Causes weight gain

A

insulin, sulfonylureas, thiazolidinediones

90
Q

T2DM agents weight neutral

A

DPP4 inhibitors, alpha glucosidase inhibitors

91
Q

T2DM agents causes weight loss

A

Metformin, SGLT2 inhibitors, pramlintide, GLP1 agonist

92
Q

T2DM that doesn’t directly cause hypoglycemia

A

metformin, alpha glucosidase inhibitors, DPP4 inhibitors, GLP1 agonist, TZD, SGLT2 inhibitors

93
Q

class of agents that reduces hepatic glucose production and improves peripheral glucose utilization

A

biguianides. Metformin

94
Q

True or false. Metformin reduced fasting plasma glucose and insulin levels, improves lipid profile and promotes modest weight loss

A

True.

95
Q

major toxicity of metformin

A

lactic acidosis

96
Q

maximum dose of metformin

A

2000 mg daily

97
Q

EGFR when metformin dose should be reduced

A

EGFR less than 45 ml/mim

98
Q

class of agents that stimulate insulin secretion by interacting with ATP sensitive potassium channel on the beta cell

A

sulfonylureas. Glibenclamide, glimepiride, gliclazine

99
Q

True or false. Weight gain is a common side effect of sulfonylurea therapy

A

True.

100
Q

analog of GLP1 initially identified in the saliva of the Gila monster

A

exenitide

101
Q

class of agents that amplify glucose stimulated insulin secretion

A

GLP1 agonist

102
Q

class of agents that inhibit degradation of GLP1

A

DPP4 inhibitors

103
Q

class of agents that reduce postprandial hyperglycemia by delaying glucose absorption

A

alpha glucosidase inhibitors. Acarbose. Voglibose

104
Q

True or false. Alpha glucosidase inhibitors can increase levels of sulfonylureas

A

True.

105
Q

creatinine threshold for alpha glucosidase inhibitors

A

cannot be given to patients with creatinine more than 2 mg/dl or 177 mmol

106
Q

class of agent that reduce insulin resistance by bind to PPAR-gamma

A

TZD

107
Q

PPAR-gamma receptors are found highest where?

A

adipocytes

108
Q

class of agents that inhibit the sodium glucose co transporter

A

SGLT2 inbibitors. Dapagliflozin, empagliflozin, canagliflozin

109
Q

Where are SGLT2 co transporter expressed

A

proximal convoluted tubule in the kidney

110
Q

associated BP reduced with use of SGLPT2 inhibitors

A

reduced in 3-6 mm Hg SBP

111
Q

associated with Euglycemic DKA

A

SGLT2 inbibitors. Dapagliflozin, empagliflozin, canagliflozin

112
Q

what happens in euglycemia DKA

A

ongoing glucosuria masks stress induced requirements for insulin

113
Q

PE finding in DKA not observed in HHS

A

nausea, vomiting, abdominal pain, Kussmaul respirations

114
Q

underlying causes of HHS

A

relative insulin deficiency and inadequate fluid intake

115
Q

when should ketone be measures in patients with diabetest

A

when CBG is more than 13.9 mmol or more than 250 mg/dl

116
Q

what ketone is measured in blood? In urine?

A

blood: beta hydroxybutyrate; urine: acetoacetate and acetone

117
Q

prominent features of DKA

A

nausea and vomiting

118
Q

serious complication of DKA

A

cerebral edema

119
Q

pathophysiology of DKA

A

relative or absolute insulin deficiency combined with counterregulatory hormone excess (glucagon, catehcolamines, cortisol, and growth hormones)

120
Q

biochemical characteristic necessary for DKA

A

insulin deficiency and glucagon excess

121
Q

True or false. Insulin deficiency and glucagon excess shift the handling of pyruvate to glucose synthesis instead of glycolysis

A

True.

122
Q

enzyme that alters hepatic metabolism to favor ketone body formation

A

carnitine palmitoyltransferase

123
Q

characteristic of DKA

A

hyperglycemia more than 13.9 mmol or more than 250 mg/dl, ketosis and metabolic acidosis

124
Q

metabolic acidosis in DKA

A

HCO3 less than 15 meq and increased Anion gap

125
Q

True or false. In DKA, amylase is of salivary origin is not diagnostic of pancreatitis

A

True.

126
Q

Laboratory tests to get is pancreatitis suspected in a patients on DKA

A

serum lipase

127
Q

in DKA, ketone body synthesized 3x greater than the other

A

beta hydoxybutyrate

128
Q

differential diagnosis of DKA

A

starvation ketosis, alcoholic ketosis (but HCO3 more than 15 meq/L)

129
Q

fluid replacement in DKA

A

2-3 L of 0.9% saline over first 1-3 hrs (10-20 ml/kg/hr) then 0.45% at 250-500 ml/h; change to 5% glucose containing and 0.45% saline at 150-250 ml/hr when plasma glucose reaches 250 mg/dl or 13.9 mmol

130
Q

how to administer insulin in DKA

A

0.1 units/kg bolus then 0.1 unit/kg per hour; increase 2x-3x if no response by 2-4 hrs

131
Q

how replace K in DKA

A

if K is 5.0-5.2, give 10 meq/hr; if K is less than 3.5 meq/L, give 40-80 meq/h

132
Q

what to watch out when planning to give insulin infusion

A

make sure serum potassiums is not less than 3.3 meq/L

133
Q

how to adjust insulin once DKA resolve

A

infusion rate decreased to 0.02/0.1 units/kg/hr

134
Q

when to transition from insulin infusion to long acting insulin in combination with SC short acting insulin

A

when patient starts to eat

135
Q

why is insuliin infusion continued even when CBG is 250 mg/dl

A

to inhibit ketogenesis

136
Q

True or false. As ketoacidosis improves, beta hydorxybutyrate is converted to acetoacetate and it can appear to be increased on urine assay using nitroprusside reaction

A

True.

137
Q

how is metabolic acidosis treated in DKA

A

50 meq HCO3 in 200 cc sterile water to run for 2 hours until pH is more than 7.0

138
Q

when to give HCO3 in DKA

A

when ABG ph is less than 7.0

139
Q

when is do need supplement for serum phosphate

A

if less than 0.32 mmol or less than 1 mg/dl

140
Q

prototypical patient with HHS

A

elderly, T2DM, diminished oral intake, polyuria that culminates in mental confusion, lethargy or coma

141
Q

PE findings in HHS

A

tachycardia, hypotension, dehydration, altered mental status

142
Q

laboratory findings of HHS

A

hyperglycemia usually more than 5.5 mmol or 1000 mg/dl, hyperosmolality more than 350 mOsm/L and pre renal azotemia

143
Q

fluid replacement in HHS

A

1-3 L of saline over 2-3 hr; if serum sodium more than 150 meq/L to use 0.45%; free water deficit should be corrects in 1-2 days; once hemodaynamically stable, correct free water deficit with 0,.45% then D5W

144
Q

what is steroid induced hyperglycemia

A

new onset hyperglycemia during chronic treatment with supraphysiologic dose of glucocorticoid (prednisone more than 5 mg or equivalent)

145
Q

what to give with steroid induced hyerglycemia

A

if FBS is near normal, give oral agents; but if FBS is more than 11.1 mmol or more than 200 mg/dl give insulin

146
Q

Three main goal of DM management

A

Improve/eliminate symptoms
Prevent complications
Back to normal or quality of life

Endocrine (15 decks)

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