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diabetes exam > diabetes exam > Flashcards

diabetes exam Flashcards

1
Q

3 causes of hyperglycemia

A

lack of insulin

  1. decreased glucose dependent uptake in cells where glucose uptake is insulin-dependent
  2. decreased glycogen synthesis
  3. increased conversion of amino acids to glucose
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2
Q

cause of hyperlipidemia

A

increased fatty acid mobilization from fat cells

increased fatty acid oxidation (KETOACIDOSIS)

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3
Q

cause of ketoacidosis

A

increased fatty acid oxidation

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4
Q

complications of diabetes

A

cardiovascular - micro and macro angiopathies
neuropathy - increased BG levels lead to increased utilization of the polyol pathway and increased cytosolic water in neural cells
nephropathy - renal vascular changes and changes in the glomerular basement membrane
ocular - cataracts, retinal microaneurysms and hemorrhage
increased susceptibility to infections

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5
Q

role of alpha subunits

A

regulate the insulin receptor
repress the catalytic activity of the beta subunit
repression is relieved by insulin binding

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6
Q

insulin effects on liver

A 
inhibits glycogenolysis
inhibits ketogenesis
inhibits gluconeogenesis
stimulates glycogen synthesis
stimulates triglyceride synthesis
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7
Q

insulin effects on skeletal muscle

A

stimulates glucose transport

stimulates AA transport

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8
Q

insulin effects of adipose tissue

A

stimulates TG storage

stimulates glucose transport

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9
Q

fasting glucose disposal

A

75% non-insulin dependent: liver, GI, brain
25% insulin-dependent: skeletal muscle
glucagon secreted to prevent hypoglycemia

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10
Q

fed glucose disposal

A

85% insulin-dependent: skeletal muscle
5% insulin-dependent: adipose tissue
glucagon secretion is inhibited
insulin inhibits release of FFA from adipose tissue

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11
Q

GLUT 1

A

Km 1-2 mM - will pull glucose constantly
constitutive
widely expressed

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12
Q

GLUT 2

A

Km 15-20 mM - requires higher concentrations of glucose to transport
constitutive
B-cells, liver

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13
Q

GLUT 3

A

Km

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14
Q

GLUT 4

A

Km 5 mM - because high enough glucose to require insulin
insulin-induced
skeletal muscle, adipose tissue

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15
Q

alpha cells produce…

A

glucagon: stimulates glycogen breakdown; increases BG

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16
Q

delta cells produce…

A

somatostatin: general inhibitor of secretion of alpha and beta cells

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17
Q

beta cells produce…

A

insulin: stimulates uptake and utilization of glucose
amylin: cosecreted with insulin; slows gastric emptying, decreases food intake; inhibits glucagon secretion

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18
Q

proinsulin

A

cleaved into A and B chains and C (connecting) peptide

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19
Q

ultra rapid/very short action insulin

A

lispro (humalog), aspart (novolog), glulisine (aprida)

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20
Q

rapid/short action insulin

A

regluar

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21
Q

intermediate insulin

A

NPH

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22
Q

long acting insulin

A

glargine (lantus), detemir (levemir) (binds serum albumin extensively)

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23
Q

____ leads to covalent modification of proteins

A

hyperglycemia
loss of normal protein function, acceleration of aging process, theorized to account for may long-term complications of diabetes

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24
Q

adverse reactions to insluin

A

hypoglycemia
lipodystrophy - lump of fat at over used injection site
lipoatrophy - concavities in SC tissue
insulin resistance - immune response to insulin

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25
Q

signs of hypoglycemia

A

weakness, sweating, hunger, tachycardia, increased irritability, tremor, blurred vision, seizures, coma, increased sympathetic output

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26
Q

overview of treatment of T1DM and T2DM

A

T1 - diet + exercise + insulin

T2 - diet + exercise; diet + exercise + oral agents; diet + exercise + insulin

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27
Q

T2DM most commonly develops in pts who are

A

obese and over 35

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28
Q

insulin receptor binding stimulates

A

PDK1: activate protein kinase C to increase amount og glucose transporters to membrane = more glucose uptake
PKB: more glucose transporters; upregulate glycolysis to use glucose
MAPK: cause proliferatin and cell growth to store fatty acids with glycerol

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29
Q

drugs that increase BG

A

catecholamines, GCs, OCs, thyroid hormones, somatotropin

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30
Q

drugs that increase risk of hypoglycemia

A

ethanol, somatostatin, beta-blockers

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31
Q

sulfonylurea structure

A

SO2-NH-CO-NH

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32
Q

sulfonylurea mechanism

A

high glucose activates GLUT2 to transport more glucose in = increased ATP = close K+ channel and open Ca+ channel = Ca influx = exocytosis of insulin
low glucose leads to higher ADP:ATP causing K+ channels to remains open and cell remains repolarized
sulfonylureas mimic high ATP:ADP to lead to closed K+ channels and increased insulin released

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33
Q

sulfonylurea SE

A

hypoglycemia (lasting depolarization of B cells and persistent insulin secretion), GI, weight gain, secondary failure of B cells leading to need of insulin

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34
Q

GLP-1

A

released in response to a meal to cause “incretin effect”: glucose-mediated insulin released and B-cell proliferation.

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35
Q

GLP-1 MOA

A

stimulates insulin secretion, suppression of glucagon secretion, slows gastic emptying, but only in glucose-dependent manner

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36
Q

GLP-1 SE

A

N/V, pancreatitis, risk of thyroid tumors (liraglutide), abiglutide is DPP-IV resistant (longer half-life)

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37
Q

DPP-IV

A

degrades GLP-1; inhibitors are orally active

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38
Q

DPP-IV inhibitors

A

sitagliptin, saxagliptin, linagliptin, alogliptin; enhance GLP-1 action

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39
Q

DPP-IV inhibitors AE

A

N/V, constipation, HA, severe skin rxn, reduced white blood cell count, risk of cancer
low risk of hypoglycemia, may facilitate weight loss (feeling full)

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40
Q

amylin analog

A

pramlintide; slows gastric emptying, decreases food intake, inhibits glucagon secretion; can be used in T1 and T2; used in conjunction with insulin

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41
Q

alpha-glucosidase inhibitors

A

decrease absorption of carbohydrates from intestine via inhibition of gut glucosidases; acarbose and miglitol AE: GI, diarrhea, nausea, flatulence

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42
Q

SGLT2 MOA

A

increase amount of glucose excreted by blocking transporter that reabsorbs glucose back into blood

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43
Q

canagliflozin AE

A

increased risk of UTI, increased urine flow/volume depletion, increased risk of hypoglycemia, CI in renal failure

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44
Q

dapagliflozin AE

A

increase risk of hypoglycemia especially in use w SU and insulin

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45
Q

Empagliflozin AE

A

increased risk of UTI, increased urine flow/volume depletion, increased risk of hypoglycemia, CI in renal failure

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46
Q

insulin resistance

A

decreased responsiveness to insulin - less glucose uptake
caused by obesity (abdominal cavity) or inactivity
occurs in skeletal muscle (less uptake), adipose tissue (less uptake, less lipolysis to mobilize FA) and liver (less inhibition of gluconeogensis and glycogenolysis)

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47
Q

insulin resistance mechanism

A

excess nutrients activate mTOR pathway to phosphorylate serine residue on insulin receptor substrate (IRS) = inhibition of PI3 kinase = no GLUT 4 brought to membrane
cytokines can induce serine phyosphorylation as well

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48
Q

metformin advantages

A

rarely causes hypoglycemia or weight gain

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49
Q

metformin works by…

A

increasing sensitivity to insulin in the liver, fat, and muscle cells by decreasing hepatic gluconeogensis and increasing glucose uptake and glycolysis in muscle and fat cells

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50
Q

metformin mechanism in liver

A

stimulates organic cation transporter (OCT1) to suppress formation of ATP and increase concentration of AMP

  • activation of AMPK that blocks lipid and cholesterol synthesis
  • [blocks glucagon action of increasing cAMP and PKA = prevents gluconeogenesis
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51
Q

metformin mechanism in skeletal muscle

A

activation of AMPK stimulates translocation of GLUT4 to membrane to increase glucose uptake

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52
Q

thiazolidinediones (TZDs)

A

decrease insulin resistance or improve target cell response to insulin
activators of PPARgamma (transcription factor)

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53
Q

main target of TZDs

A

adipocytes: enhance differentiation, enhance FFA uptake into SC fat, reduce serum FFA, shift lipids into fat cells from non-fat cells
- live to enhance glucose uptake, reduce gluconeogenesis
- skeletal muscle: enhance glucose uptake

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54
Q

Rosiglitazone

A

restricted due to cardiovascular toxicity, CI in CHF

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55
Q

Pioglitazone

A

some hepatotoxity, does not cause hypoglycemia, CI in CHF

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56
Q

factors regulated by activation of PPARgamma

A

resistin, adiponectin, TNFa, leptin, angiotensinogen, plaminogen activator inhibitor 1

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57
Q

resistin

A

elevated in T2DM, TZDs decrease level

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58
Q

adiponectin

A

decreased in T2DM; generally reduces BG and insulin resistance; TZDs increase level

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59
Q

TNFa

A

increased in T2DM; stimulates lipolysis and insulin resistance; TZDs decrease levels

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60
Q

leptin

A

increased in T2DM and obesity, signal satiety

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61
Q

angiotensinogen

A

elevated in obesity; excess leads to HTN

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62
Q

plaminogen activator inhibitor 1

A

elevated in obesity; increase of blood clots with obesity

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63
Q

glucose uptake by brain is

A

insulin independent

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64
Q

glucose uptake by tissues other than brain is

A

insulin dependent

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65
Q

s/sx of diabetes

A

polyuria, polydipsia, polyphagia, weight loss, fatigue, UTI, URI, ketoacidosis (T1), blurred vision

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66
Q

drugs that decrease insulin secretion

A

phenytoin - inhibit insulin secretion, more profound in patients with pre-existing hyperglycemia
B-blockers - decrease insulin release in response to hyperglycemia
CCB - decrease insulin release in response to hyperglycemia and can increase proteinuria

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67
Q

drugs that increase hepatic glucose output

A

GC, sympathomimetics

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68
Q

beta blockers in diabetics

A

CAN USE THEM
issue: may blunt s/sx of hypoglycemia, less likely w cardio selective agents, caution w use in brittle diabetics (esp w ultra short acting agents), always consider indication

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69
Q

drugs that increase insulin resistance

A

thiazide diuretics - not an issue until > 50 mg/day
niacin - w higher doses
GC

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70
Q

drugs that are toxic to beta cells

A

pentamidine - prevents insulin secretion

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71
Q

diagnostic criteria

A 
2 positive:
FBG >126
AIC > 6.5%
random glucose > 200 with sx of DM
2 hr PPG > 200 during an OGTT (75gm glucose)
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72
Q

“normal” values

A

FBG 100-126

A1C

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73
Q

microvascular complications

A
  • Cataracts, retinopathy (yearly eye exams)
  • Nephropathy = decrease GFR
  • Neuropathy: peripheral, gastroparesis (slow transit), urinary retention, postural hypotension, impotence
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74
Q

macrovascular complications

A

-Coronary Heart Disease – leading cause of death in T2DM
+BP Goal 7.5%
-Stroke: keep BP under control
-Peripheral vascular disease: leading cause of non-traumatic amputations; causing leg pain, cold feet, and absent pulses
-Periodontal disease: requires dentist visits every 6 months
-Antiplatelets: consider aspirin for primary prevention in patients with high CVD risk

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75
Q

SMBG goals

A

ADA:
FBG 80-130mg/dL
PPG (2 hours after eating)

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76
Q

A1C goals

A

ADA

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77
Q

statin use in pts

A

ADA:
no risk = none
CVD risk = mod-high
overt CVD = high

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78
Q

statin use in pts 40-75

A 
ADA:
no risk = mod
CVD risk = high
overt CVD = high
ACC/AHA:
mod
high for pts w 10y ASCVD > 7.5%
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79
Q

statin use in pts >75

A

ADA:
no risk = mod
CVD risk = mod-high
Overt CVD = high

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80
Q

every 1% drop in A1C results in

A

18% reduction in risk of CVD events

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81
Q

A1C

A

short duration of DM, no CVD, long life expectancy

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82
Q

4 “m” components of therapy

A

meals movement monitoring medications

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83
Q

goal carb intake

A

women 45 gm/meal

men 60 gm/meal

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84
Q

medical nutrition therapy components

A

moderate caloric restriction, modest weight loss, monitor carb intake, limit sugar-sweetened beverages, sat fat

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85
Q

insulin used as IV

A

regular

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86
Q

insulin that can’t be used IV

A

NPH (suspension)

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87
Q

insulin that precipitates at physiologic pH

A

glargine (Lantus and Toujeo)

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88
Q

insulin that binds albumin

A

detemir

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89
Q

insulin uses

A

T1DM and T2DM
-fasting glucose >280-300
-ketoacidosis
-gestational diabetes
-when deemed appropriate by clinician and patient
hyperkalemia (even w no DM)
T2DM in combination with various oral agents

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90
Q

ultra short acting insulin examples

A

aspart, lispro, glulisine

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91
Q

ultra short insulin onset

A

15-30 min
skip meal = skip dose
inject when food is in front of you

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92
Q

ultra short peak

A

1-2 hours

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93
Q

ultra short duration

A

3-4(5) hours

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94
Q

ultra short compatibly mixed w

A

NPH (and degludec?)

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95
Q

short acting insulin examples

A

regular (U-100 and U-500)

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96
Q

short acting onset

A

30-60 min

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97
Q

short acting peak

A

2-3 hours

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98
Q

short acting duration

A

4-6 hours

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99
Q

short acting compatibly mixed w

A

NPH

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100
Q

intermediate insulin examples

A

NPH

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101
Q

intermediate onset

A

2-4 hours

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102
Q

intermediate peak

A

4-8 hours

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103
Q

intermediate duration

A

8-12 hours

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104
Q

intermediate compatibly mixed w

A

rapid or short acting

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105
Q

long acting insulin examples

A

glargine and detemir

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106
Q

long acting onset

A 
4-5 hours (glargine)
2 hours (detemir)
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107
Q

long acting peak

A

none

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108
Q

long acting duration

A

22-24 hours (glargine)

14-24 hours (detemir)

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109
Q

long acting compatibly mixed w

A

none

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110
Q

ultra long acting examples

A

degludec

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111
Q

ultra long acting onset

A

1-2 hours

112
Q

ultra long peak

A

none

113
Q

ultra long duration

A

over 24 hours

114
Q

rate of absorption of insulin from different routes

A

IV > IM > SQ

115
Q

rate of absorption of insulin from different sites

A

stomach > buttocks and thighs

116
Q

lower dose absorbed more ___

A

rapidly

117
Q

renal failure effect on insulin

A

renal failure decreases insulin clearance and therefore increases insulin action

118
Q

stress effect on insulin

A

stress increases insulin clearance and increases BG

119
Q

insulin vials stable at ___ for ___

A

insulin vials stable at room temperature for 28 days
exception : levemir stable for 42 days
insulin pens are variable (7-56 days)

120
Q

opened insulin vials should be discarded ___

A

after 28 days

121
Q

pre-filled syringes are stable for ___

A

28 days with refrigeration as long as not mixed; 10-28 days at room temperature

122
Q

mixed insulin stability

A

regular/NPH: 7 days in fridge
aspart, glulisine or lispro with NPH: give immediately
glargine and detemir with other insulin: NEVER

123
Q

hypoglycemia s/sx

A

tremors, tachycardia, diaphoresis, confusion, slurred speech, drowsiness, weakness, agitation, blurred vision

124
Q

hypoglycemia tx

A
  • 15-30 gm carbohydrate (start w 15 gm unless BS 1 hr away) ex: granola bar, 1/2 PBJ, apple and cheese, crackers
  • glucagon for severe patients, 1 mg SQ, IM or IV
125
Q

examples of 15 gm carbs

A

4 oz OJ, 6 oz cola, 5-6 livesavers, 2 tsp sugar, 1 tbsp honey, glucose tabs (4-5 gm/tab) or gel

126
Q

complications of insulin Tx

A

hypoglycemia, weight gain, lipohypertrophy, lipoatrophy, allergic rxn

127
Q

rapid acting insulin advatages

A

decrease PPG, fewer overall occurances of hypoglycemia, flexibility, can give after meal based on what was eaten, stimulates physiologic insulin secretion relative to meals

128
Q

rapid acting insulin disadvantages

A

risk without meal, need to combine with longer acting, give immediately after mixing

129
Q

long acting insulin advantages

A

24+ hours coverage without peaking, helpful for nocturnal hyperglycemia

130
Q

long acting insulin disadvantages

A

cannot be mixed, cost

131
Q

changing therapy: NPH to glargine/detemir/degludec

A

keep dose the same

132
Q

changing therapy: lantus to tuojeo

A

same dose, but may need increased dose

133
Q

changing therapy: BID NPH to glargine/detemir/degludec

A

decrease dose by 20%

134
Q

insulin dose in T1DM

A

start with 0.1-0.4 units/kg/day

end with 0.5-0.6 units/kg/day (ACTUAL BW)

135
Q

ideal testing in T1DM

A

before meals and at bedtime (QID)

occasionally at 3 am to adjust doses

136
Q

basal bolus is usually __:__

A

50:50

can be 50-70:30-50

137
Q

basal bolus dosing w NPH and short-acting

A

2/3 AM and 1/3 PM
2/3 of each dose NPH and 1/3 short acting
less flexibility w dose adjustments

138
Q

NPH in basal bolus can be given

A

PM or HS

139
Q

T2DM starting insulin

A

usually long-acting or intermediate is started in combination with oral agents

  • usually betime
  • some orals (often SU and TZDs) may be discontinued, esp w basal/bolus initiate
140
Q

T2DM insulin starting dose

A

0.15-0.2 U/kg/day
10-15 U
FBS/18
kg/10

141
Q

T2DM dose adjustments

A

adjust every 3-4 days

  • adjust by 1-2U for every 20 mg/dL of FBS over 100 mg/dL or by 2-4 U for every 50 mg/dL of FBS over 150 mg/dL
  • increase by 1-2U/day until FBS 80-130 mg/dL
142
Q

bolus in T2DM

A

0.1 U/kg/meal or 1-2 units of insulin for every 15 gm CHO in the meal

143
Q

when AIC > 10%, 70% of the problem involves ___

A

FBS

144
Q

when A1c

A

PPG

145
Q

adjust insulin every - days

A

3-7 days until goals are met

146
Q

CF at bedtime

A

only give 50% of dose

147
Q

empiric starting poins

A

T1DM: increase insulin by ~2 units decreases BG by ~50 mg/dL
T2DM: increase insulin by ~4 units decreases BG by ~50 mg/dK

148
Q

U500 used

A

when pts exceed 300 units of total insulin daily

149
Q

T1DM carbohydrate ratio

A

1 unit:15 gm CHO (start)

150
Q

T2DM carb ratio

A

1 unit:10-15 gm CHO (adult)

1 unit:20-30 CHO (kids)

151
Q

rule of 500

A

500/total insulin = g CHO/unit of bolus insulin

may have more than one CHO ratio each day depending on CHO intake at meal

152
Q

rule of 1800

A

(1500 for regular)
1800/total daily insulin dose = mg/dL BG will drop per unit of insulin
used to add a dose of prandial when BG is elevated before a meal

153
Q

illness and DM

A
  • continue insulin even if food intake is decreased (stress increases insulin requirements)
  • maintain fluid intake (12, 8 oz glasses/day)
  • test BG q4h
  • test urine for ketones w each urination
154
Q

ideal non-insulin treatment would…

A

preserve B cell fxn, prevent weight gain, prevent hypoglycemia

155
Q

oral agents

A

metformin, SU, DPP-4 inhibitors, TZDs, meglitinides, alpha glucosidase inhibtors, SGLT2 inhibitors, bile acid sequestrats

156
Q

injectable non-insulin agents

A

GLP-1 agonists, pramlintide

157
Q

metformin MOA

A

DRUG OF CHOICE FOR T2DM

  • improves insulin sensitivity
  • increase tissue uptake and utilization of glucose by muscle
  • decreases hepatic production of glucose
158
Q

metformin clinical applications

A
  • adjunct to diet in T2 uncontrolled
  • in combination with insulin and other non-insulin agents in T2DM
  • ADA recommendations: use for all T2DM if tolerated and not CI
  • reduces risk of mortality and CV death
  • first-line agent
159
Q

metformin efficacy

A
  • A1C decrease 1.5-2% (up to 3%)

- FBG decrease 60-80 mg/dL

160
Q

metformin pharmacokinetics

A

excreted unchanged in the urine

161
Q

metformin advantages

A
  • less risk of hypoglycemia (no insulin release)
  • decrease TG and LDL 8-15%
  • no weight gain or even loss (2-3 kg)
  • cheap
  • CV protection
  • decrease macrovascular complication and risk of total mortality
  • decrease risk of stroke and all-cause mortality (compared to insulin and SU)
  • decrease diabetes-related death and MI (vs conventional treatment)
162
Q

metformin disadvantages

A

may cause lactic acidosis, GI effects (N/V, diarrhea, flatulence)
-take w largest meal and titrate

163
Q

metformin cautions and CI

A

renal dysfunction, HF (esp class III and IV), alcoholics, increased risk of lactic acidosis

164
Q

metformin and renal dysfunction

A

caution in males w SCr > 1.5 mg/dL
caution in females with SCr > 1.4 mg/dL
caution in patients w CrCl

165
Q

metformin and HF

A 
CONTRAINDICATED in class III and IV
class I and II are low risk
166
Q

metformin and alcoholics

A

watch excessive intake and avoid use with heavy intake

overall increased risk of LA in these pts

167
Q

patient at risk for LA

A

post MI, COPD, hepatic failure, shock, surgery/procedure (hold metformin 2-3 days)

168
Q

metformin dosing

A
  • start: 500 mg po BID or 850 mg PO QD with meals
  • titrate weekly and increase 250-500 mg
  • maximum clinical dose: 2 gm/day
  • max package insert dose: 2.550 gm/day
169
Q

metformin dosing in renal insufficiency

A
  • GFR > 60; no renal CI, monitor SCr annually
  • GFR 60-45; continue use, monitor SCr q3-6mo
  • GFR 30-45; reduce dose by 50%, monitor SCr q3mo
  • GFR
170
Q

SU MOA

A

stimulate insulin release from B cells

may increase binding between insulin and receptors or increase number of receptors

171
Q

SU clinical applications

A

adjunct to diet and exercise in T2DM
used in combination with insulin and non-insulin agents
HAVE TO HAVE ABILITY TO PRODUCE INSULIN

172
Q

SU efficacy

A

A1C decrease 1.5-2%

FBG decrease 60-70 mg/dL

173
Q

first generation SU

A

acetohexamide, chlorpropamide, tolazamide, tolbutamide

174
Q

second generation SU

A

glyburide (diabeta, micronase, glynase)
glipizide (glucotrol)
glimepiride (amaryl)

175
Q

PK of 2nd gen SU

A

glyburide and glipizide more effective when take 30 minutes AC
metabolized by liver
some excreted in urine

176
Q

SU AE

A

hypoglycemia (renal/hepatic insufficency pts, elderly or malnourished pts, concurrent hypoglycemic drugs)
weight gain and GI upset
hematologic: leucopenia, thrombocytopenia, aplastic anemia
allergic rxns/photosensitivity

177
Q

SU drug interactions

A
  • increased hypoglycemic effect: warfarin, azole antifungals, gemfibrozil, clofibrate, sulfonamides, MAOIs, trycyclic antidepressants, alcohol, cimetidine, aspirin and concominant agents for DM
  • decreased hypoglycemic effect: beta-blockers, CCBs, choletyramine, GC, phenytoin, OC, rifampin, thiazides, niacin
178
Q

general SU dosing

A

start low
increase dose every 1-2 weeks until at max
exceeding max increases SE but does not decrease BG
current max now being questioned

179
Q

use SU cautiously in these pts due to increased risk of hypoglycemia

A

elderly or pts w renal/hepatic disease, irregular dietary intake, alcoholics, pts taking concimitant hypoglycemic agents

180
Q

best SU candidates

A

no T1DM, short duration of DM, FBS

181
Q

SU treatment failure

A

25% primary - poor blood sugar control after a trial of 6-12 weeks on medications and diet
50-75% secondary - failure of medication after initial control, common for these medications to fail after 6-12 months, place in therapy is declining

182
Q

short acting insulin secretagogues or meglitinides

A

repaglinide (Prandin) and Nateglinide (Starlix)

183
Q

meglitinides MOA

A

non-sulfonylurea moiety of glyburide

stimulates release of insulin from pancreatic beta cells

184
Q

meglitinides clinical applications

A
  • adjunct to diet and exercise to patients with uncontrolled T2DM
  • in combination with metformin to lower BS in pts who are uncontrolled w diet, exercise and either agent alone
  • rapid onset and short duration of action, so given with meals to enhance PPG utilization
  • can be used in pts w renal insufficiency
  • alternative in patients experienceing hypoglycemia with low-dose SU
  • no added benefit in combination w SUs
185
Q

meglitinides efficacy

A

AIC decrease 0.8-1%
FBG decrease 40 mg/dL
decrease PPG

186
Q

meglitinides PK

A
  • rapidly absorbed and short t1/2 of 1-1.5 hours
  • metabolized by liver into inactive metabolites
  • mostly eliminated in the feces
  • watch dosing w hepatic insufficiency
187
Q

meglitinides AE

A
  • hypoglycemia (elderly and patients with hepatic/renal dysfunction; less risk than SU)
  • weight gain (~2-3 kg)
188
Q

meglitinides drug interactions

A
  • CYP450 3A4 metabolism, potential for interactions
  • gemfibrozil increased half-life thereby increasing risk of hypoglycemia
  • some noted interaction w anticonvulsants
189
Q

meglitinides dosing

A

-if A1c 8%:
start 1-2 mg repaglinide or 120 mg nateglinide with each meal
-max: repaglinide: 16 mg/day but clinical 6 mg; nateglinide: 120 mg/day
-take 15-30 min AC
-adjust weekly
-skip meal = skip dose
-add meal = add dose

190
Q

DPP4 inhibitors

A

sitagliptin (Januvia)
Saxagliptin (Onglyza)
Linagliptin (Tradjenta)
Alogliptin (Nesina)

191
Q

DPP4 Inhibitors MOA

A
  • increases activity of endogenous incretin hormones (GLP-1 and GIP)
  • incretin hormones? gut hormones that enhance insulin secretion in response to food
192
Q

GLP-1

A
  • released from cells in ileum and colon after eating and is normally degraded quickly by DPP-4
  • studies show reductions of GLP-1 after meals in T2DM
  • stimulates insulin response from beta cells in a glucose dependent manner (prevents hypoglycemia; inhibits glucagon secretion by alpha cells, inhibits gastric emptying, reduces food intake and body weight)
  • GLP-1 is degraded by DPP4 enzyme
193
Q

DPP4 inhibitors clinical application

A
  • monotherapy and add on therapy with metformin or TZDs in T2DM; can be used in combo w SU
  • reduced A1C by itself and in combo w metformin or pioglitazone, helped patients reach A1C goals, effective as a therapy add on to metformin and SU
194
Q

DPP4 inhibitors efficacy

A

A1C decrease 0.7-1%
FBS decrease 20 mg/dL
PPG decrease 20-40 mg/dL
weight neutral

195
Q

DPP4 inhibtors PK

A
  • excreted unchanged in the urine

- adjust dose for renal function (exception: linagliptin)

196
Q

DPP4 inhibtors AE

A
  • nasopharyngitis
  • URIs
  • HA
  • joint pain (sx usually resolve within one month of drug discontinuation)
  • acute pancreatits - counsel s/sx
197
Q

DPP4 inhibitors drug interactions

A
  • small increase in digoxin conc w sitagliptin
  • saxagliptin and ketoconazole/itraconazole, PIs, clarithromycin, telithromycin, and rifampin which decreases saxagliptin AUC by 76%
198
Q

sitagliptin dosing

A

100 mg QD for CrCl >50 mL/min
50 mg QD for CrCl 30-50 mL/min
25 mg QD for CrCl

199
Q

saxagliptin dosing

A
  1. 5-5 mg QD

2. 5 mg QD for CrCl

200
Q

Linagliptin dosing

A

5 mg QD

201
Q

alogliptin dosing

A

25 mg QD

  1. 5 mg QD CrCl 30-60
  2. 25 CrCl
202
Q

SGLT2 inhibitors

A

Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)

203
Q

SGLT2 inhibitors MOA

A
  • SGLT2 is major transporter of renal glucose to assist in glucose reabsorption
  • inhibiton of SGLT2 leads to renal glucose excretion
204
Q

SGLT2 inhibtors clinical application

A

adjunct to diet and exercise in patients w targeted CrCl

benefits to empagliflozin: significantly lower rates of CV death, HF hospitilizations and death overall

205
Q

SGLT2 inhibitors efficacy

A

A1C decrease 0.6 - 1%

weight decrease

206
Q

SGLT2 inhibitors PK

A

glucuronidation by UGT1A9 and UGT2B4 to inactive metabolites
CYP3A4 metabolism is minimal
excreted mostly in feces but 1/3 in urine

207
Q

SGLT2 inhibitors AE

A
  • UTI, female genital fungal infections, increased urination
  • less common: hypoglycemia, hypotension, hyperkalemia, increased cholesterol
  • FDA warning for DKA (possibly triggered by illness, decrease food or water intake, and decrease insulin dose)
  • bone fractures
208
Q

SGLT2 drug interactions

A

canagliflozin increases digoxin levels

rifampin, phenytoin, phenobarbital and ritonavir can decrease canagliflozin (they induce UGT)

209
Q

canagliflozin dosing

A

Contraindicated if CrCl

210
Q

TZDs

A

pioglitazone (actos)

rosiglitazone (Avandia)

211
Q

TZDs MOA

A
  • Bind to peroxisome proliferator activator receptor-γ (PPAR-γ) on fat cells and vascular cells
  • Improves cellular response to insulin w/o increasing pancreatic insulin secretion
  • Decreases insulin resistance
  • Decreases hepatic glucose production
  • results in reduction in exogenous insulin dosage when used in combination
212
Q

TZDs benefits

A
  • Pioglitazone can ↓ TG by 10-20%
  • LDL remains unchanged on pioglitazone
  • -Some rosiglitazone studies have shown ↑ in LDL
  • Both meds convert small atherogenic LDL particles to large fluffy ones
  • Both medications ↑ HDL by 3-9 mg/dL
  • Endothelial function has improved and blood pressure may decrease slightly
213
Q

TZD clinical application

A
  • As an adjunct to diet and exercise

- In combination with a sulfonylurea, metformin, DPP-4, or insulin

214
Q

TZD efficacy

A

A1C decrease 0.5-1.5%

FBG decrease 60-70 mg/dL

215
Q

TZD PK

A
  • 99% protein bound

- Metabolized hepatically

216
Q

TZD AE

A
  • hepatatoxicity (check baseline LFTs, dont start in pts w baseline LFTs > 2.5x normal, check LFTs periodically, d/c if LFTs > 3x normal, monitor NV, abdominal pain, fatigue, anorexia, dark urine)
  • resumption of ovulation
  • exacerbation of HF (caution in NYHA class III and IV, increased edema, > 10 lb weight gain in some pts)
  • macular edema
  • inc fracture risk
  • inc CV and MI ?
217
Q

TZD dosing

A

pioglitazone: initial 15-30 mg daily; max 30-45 mg daily
rosiglitazone: initial 4 mg daily; max 8 mg daily
titrate every 12 weeks

218
Q

alpha-glucosidase inhibitors

A

Acarbose (Precose)

Miglitol (Glyset)

219
Q

alpha-glucosidase inhibitors MOA

A
  • Competitive reversible inhibition of intestinal alpha-glucosidase (enzyme that breaks down polysaccharides to glucose)
  • Delays glucose absorption and lowers postprandial hyperglycemia
  • Does not enhance insulin secretion
  • Less chance for hypoglycemia
  • No effect on weight or lipids
220
Q

alpha-glucosidase inhibitors clinical application

A
  • As an adjunct to diet and exercise in type 2 diabetes

- In combination with other agents

221
Q

alpha-glucosidase inhibitors efficacy

A

A1C decrease 0.3 - 1%
FBG minimal effect
PPG decreased 40-50 mg/dL

222
Q

alpha-glucosidase inhibitors

AE

A

GI (flatulence, diarrhea, abdominal pain/cramping - MUST TITRATE), rashes, increased LFTs

223
Q

alpha-glucosidase inhibitors CI

A

DKA, IBD, colonic ulceration, intestinal obstuction, hypersensitivity

224
Q

alpha-glucosidase inhibitors drug interactions

A

acarbose and miglitol can decrease digoxin levels

miglotil can decrease propranolol, ranitidine, glyburide and metformin

225
Q

managing hypoglycemia that occurs w alpha-glucosidase inhibitors

A

use dextrose, complex sugars in juices/sodas will NOT be broken down, glucose tabs and gel are good

226
Q

alpha-glucosidase inhibitors dosing

A

25 mg QD w first-bite of main meal for 7-14 days, 25 mg BID week 3-4, 25 mg TID weeks 5-12, 50 MG TID (max if 50 kg)

227
Q

Colesevelam

A
  • Bile acid sequestrant
  • Mechanism to lower blood glucose is not fully known
  • 0.4% A1C reduction
  • May also lower LDL and is considered weight neutral
  • 3.75 mg per day, and this may be split into two doses
228
Q

Bromocriptine

A
  • Dopamine agonist
  • Mechanism to lower blood glucose is not fully known
  • 0.1-0.4% A1C reduction
  • 0.8-1.6 mg PO daily, up to 4.8 mg daily
229
Q

Glucovance

A

glyburide/metformin

230
Q

Metaglip

A

glipizide/metformin

231
Q

Actoplus Met

A

pioglitazone/metformin

232
Q

Duetact

A

pioglitazone/glimepiride

233
Q

Janumet

A

sitagliptin/metformin

234
Q

Jentadueto

A

linagliptin/metformin

235
Q

Kazano

A

alogliptin/metformin

236
Q

Juvisync

A

sitagliptin/simvastatin

237
Q

Kombiglyze

A

saxagliptin/metformin

238
Q

Glyxambi

A

empagliflozin/linagliptin

239
Q

Invokamet

A

canagliflozin/metformin

240
Q

Xigduo XR

A

dapagliflozin/metformin

241
Q

Avandamet

A

rosiglitazone/metformin

242
Q

Avandaryl

A

rosiglitazone/glimepiride

243
Q

Oseni

A

pioglitazone/alogliptin

244
Q

future agents

A
  • IL-1 beta cell receptor antagonists
  • Oral insulin
  • Islet cell transplantation
  • Artificial pancreas
245
Q

Pramlintide

A

Pramlintide (Symlin®)

non-insulin injectable

246
Q

Pramlintide MOA

A
  • Synthetic analog of human amylin, a naturally occurring hormone
  • made in Β cells and co-stored and co-secreted with insulin
  • Inhibits glucagon secretion
  • Delays gastric emptying -Satiety agent
247
Q

pramlintide clinical application

A

-In type 1 patients, A1C decreased by 0.67% after 13 weeks (QID pramlintide plus insulin vs. insulin alone)
-In type 2 patients, A1C decreased by 0.62% in 120mcg group after
52 weeks (all patients continued usual insulin regimen)
-Also being studied for weight loss (3.5kg loss in one trial with 240 mcg TID)

248
Q

pramlintide efficacy

A

A1C: ↓ 0.4-0.7%
Weight: ↓ 1.5 kg

249
Q

pramlintide AE

A
  • Risk of severe hypoglycemia with concomitant insulin administration
  • Nausea, vomiting, and anorexia, but these decrease over time
250
Q

pramlintide dosing

A
  • Type 1 patients: 15 mcg and titrate upward by 15 mcg up to 30-60 mcg, Give prior to major meals, ↓ dose of rapid-acting and short-acting insulins by 50%
  • Type 2 patients: 60 mcg and titrate up to 120 mcg, titrate dose after nausea resolves, Give prior to major meals, ↓ dose of rapid-acting and short-acting insulins by 50%
  • Inject SQ in abdomen and thigh
  • Rotate sites of injection
  • Never mix with insulin, but store like insulin
251
Q

pramlintide place in therapy

A
  • Approved for use in type 1 and type 2 patients who are already on insulin but not achieving adequate control
  • High cost: Three more syringes daily, AWP $100-$400/month, More frequent glucose monitoring
  • May be a small niche of patients
252
Q

exenatide, liraglutide or albiglutide

A

Exenatide (Byetta®, Bydureon®), Liraglutide (Victoza®), or Albiglutide (Tanzeum®)

253
Q

Exenatide, Liraglutide, or Albiglutide MOA

A
  • Glucagon-Like Peptide 1 (GLP-1) agonists/analogs from salivary gland of the lizard Heloderma suspectum (exenatide) and through recombinant DNA technology (liraglutide)
  • GLP-1 potentiates glucose-dependent insulin secretion by stimulating Β-cell growth and differentiation and insulin gene expression
  • Has been shown to inhibit Β-cell death
  • Exenatide and liraglutide are resistant to dipeptidyl peptidase IV, the enzyme that rapidly inactivates natural GLP-1
  • Increases in both first and second-phase insulin secretion after meals occur
254
Q

Exenatide, Liraglutide, or Albiglutide clinical applications

A
  • When compared to SU in type 2 patients, 10 mcg exenatide group showed decreased A1C of 0.86% vs. an increase of 0.12% in placebo group
  • When compared to metformin in type 2 patients, 10 mcg exenatide group had decreased A1C of 0.8% vs. an increase of 0.1% in placebo group
  • LEAD trials: Liraglutide Effect and Action in Diabetes (5 trials): Liraglutide (0.6-1.8 mg daily) compared to and used in combination with metformin, sulfonylureas, and TZDs, A1C ↓ up to 1.6% for liraglutide and weight ↓ up to 3.2 kg in liraglutide groups, Nausea was also the most frequent adverse effect (5-29% of patients)
  • When compared to exenatide (10 mcg BID) in type 2 patients on maximal doses of metformin, sulfonylurea, or both, liraglutide (1.8 mg daily) decreased the A1C by 1.12% vs. 0.79% in the exenatide group (p
255
Q

Exenatide, Liraglutide, or Albiglutide efficacy

A
  • A1C: ↓ ~0.8-1% Byetta®; ↓ 1.6% Bydureon®; ↓ 0.8-1.5% liraglutide; ↓ 0.8-1.% albiglutide
  • Weight: ↓ 1.5-3 kg
256
Q

Exenatide, Liraglutide, or Albiglutide AE

A
  • Nausea
  • Hypoglycemia
  • Pancreatitis—some fatalities
  • Black box warning for liraglutide (also with Bydureon®) - thyroid c-call tumors
257
Q

Exenatide dosing

A
  • 5 mcg BID within 60 minutes prior to morning and evening meals
  • Do not administer after a meal
  • Can increase the dose to 10 mcg BID after one month
  • May be administered in thigh, abdomen, or arm
  • Available in pre-filled pens with 60 doses
258
Q

Liraglutide dosing

A
  • 0.6 mg SQ daily for one week, then increase to 1.2 mg daily
  • May titrate dose to 1.8 mg daily if needed for BS control
  • May be given at any time of the day, independent of meals
  • May be administered in thigh, abdomen, or arm
  • Available in pre-filled pens with 18 mg per pen
259
Q

Albiglutide dosing

A

30 mg once a week; may increase to 50 mg weekly

  • May be given at any time of the day, independent of meals
  • May be administered in thigh, abdomen, or arm
  • Available in single dose pens
260
Q

T2DM treatment principles

A
  • Treat aggressively to reach goals
  • Consider the following when selecting pharmacotherapy: Duration of disease, Blood glucose level to be targeted, Degree of A1C lowering needed, ADRs and the patient tolerability, Patient preference for route of administration
  • Start lifestyle modifications (↓ A1C by ~1-2%) and start metformin 500 mg BID with titration to 1,000 mg BID (↓ A1C ~2%)
  • If goals not achieved after 3 months, use combination therapy
  • If goals not yet achieved after 3-4 months, go to triple therapy
  • Do not delay insulin if that is what is truly needed
  • Go to basal-bolus insulin for tight control
  • For patients with postprandial hyperglycemia, target with DPP-4 inhibitors, GLP-1 analogs, amylin analog, or alpha glucosidase inhibitors
261
Q

glimeperide dosing

A

start 1-2 mg daily, go to 1-8 mg

262
Q

glipizide dosing

A

start 2.5-5 mg daily
30 min AC, go to 2.5-40 mg
XL start 2.5-5 mg daily, go to 2.5-20 mg

263
Q

glyburide dosing

A

start 1.25-5 mg daily, go to 1.25-20 mg

264
Q

aspirin use in DM pts

A

-ADA recommends to consider aspirin (75-162 mg/day) for primary CVD prevention in patients with ↑ CV risk (10 year > 10%) or for men > 50 or women > 60 with one major risk factor (FH CVD, HTN, smoking, HLD)
-ADA also recommends to not use aspirin for primary prevention for those at low
CVD risk or for men

265
Q

all diabetics w HTN should be on either an ___ or ___

A

ACEI or ARB

266
Q

all diuretics can ___ glucose

A

increase

267
Q

ACC/AHA recommendations for lipid goals in DM pts

A

40-75 mod - high statin if 10y ASCVD rick > 7.5%

268
Q

high intensity statins

A

Atorvastatin 40-80 mg Rosuvastatin 20 mg

269
Q

moderate intensity statins

A

Atorvastatin 10-20 mg Rosuvastatin 5-10 mg Simvastatin 20-40 mg Pravastatin 40-80 mg Lovastatin 40 mg Fluvastatin 40-80 mg Pitavastatin 2-4 mg

270
Q

DKA diagnostics

A
  • Blood Glucose: >250mg/dL

- pH: Mild: 7.25-7.3; Moderate 7.00 to 600mg/dL, no acidosis, Bicarb >18mEq/L

271
Q

DKA treatment

A

fluid replacement, insulin, electrolyte management

272
Q

fluid replacement in DKA

A
  • Fluid Replacement: 0.9% NaCl 15-20 mL/kg/hr or 1-1.5 L during first hour
  • Na is low (
273
Q

insulin in DKA

A
  • Continuous IV infusion of regular insulin

- Do not start insulin if hypokalemia (

274
Q

electrolyte management in DKA

A
  • Potassium Goal: Maintain 4-5mEq/L

- Bicarb: If venous pH

275
Q

DKA resolution

A

-DKA: Blood glucose 1.5mEq/L, Venous pH >7.3, Anion gap

diabetes exam (1 decks)

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