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Pharmacology > Exam #4- DM > Flashcards

Exam #4- DM Flashcards

1
Q

physiologic difference between diabetes type 1 and type 2

A

type 1= pancreas attacks cells that produce insulin- body CAN’T make insulin

type 2= body is resistant to insulin- body MAKES insulin, but body doesn’t respond to it

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2
Q

natural hx DM2

A

insulin resistance, insulin secretory defect that is NOT auto-immune related, and increase in glucose production by the liver

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3
Q

clinical presentation for type 1 DM

A

polyuria

polydipsia

polyphagia

weight loss

weakness

dry skin

ketoacidosis

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4
Q

clinical presentation for type 2 DM

A

possibly asymptomatic

polyuria

polydipsia

polyphagia

fatigue

weight loss

most are discovered while performing urine glucose screening

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5
Q

A1C parameters for diagnosis of DM and prediabetes

A

DM: >6.5

prediabetes: 5.7-6.4

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6
Q

fasting BG parameters for diagnosis of DM and prediabetes

A

DM: >126

prediabetes: 100-125

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7
Q

goals of DM management

A

lower A1C<7%, decrease microvascular complications and macrovascular dx

stringent goals (<6.5%) for some pts

less stringent goals (<8%) for pts. w/hx of severe hypoglycemia, limited life expectancy, or other conditions that make <7% hard

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8
Q

1st line agent for DM unless CI

A

biguanides (metformin)

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9
Q

MOA of biguanides/metformin

A

decreased hepatic glucose production

increased insulin mediated peripheral glucose uptake

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10
Q

efficacy of biguanides/metformin

A

decreases fasting plasma glucose 60-70 mg/dL

decreases A1C 1-2%

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11
Q

ADE of biguanides/metformin

A

diarrhea/abdominal discomfort

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12
Q

BBW for biguanides/metformin

A

LACTIC ACIDOSIS (rare renal failure and tissue hypoxia)

no weight gain w/possible modest weight loss

may cause small decrease in LDL cholesterol level and triglycerides

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13
Q

contraindication for biguanides/metformin

A

**pts w/impaired renal function (Cr>1.4)

HOLD 24 hrs before and 48 hours post-
IV dye load

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14
Q

MOA of sulfonylureas

A

increases endogenous INSULIN SECRETION (secretagogue) by binding to receptors on pancreatic beta cells

leads to insulin secretion

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15
Q

efficacy of sulfonlylureas

A

decreases fasting plasma glucose 60-70

decreases A1C by 1-2%

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16
Q

ADE of sulfonylureas

A

hypoglycemia risk (increased w/other agents)

weight gain

rash

HA

N/V

photosensitivity

caution in renal/hepatic impairment (avoid in CrCl<50)

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17
Q

MOA of thiazolidinediones (TZDs)

A

decreases insulin resistance by increasing muscle and fat sensitivity to insulin

also suppresses hepatic glucose production

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18
Q

efficacy of TZDs

A

decreases fasting plasma glucose 35-40

decreases A1C 0.5-1%

6-12 weeks for effect

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19
Q

ADE of TZDs

A

weight gain

edema

hypoglycemia

increased fracture risk

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20
Q

BBW for TZDs

A

**CI in HF pts (class III and IV)

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21
Q

considerations for TZDs

A

caution in hepatic impairment

may improve HDL and triglycerides

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22
Q

MOA of meglitinides

A

similar to sulfas- more rapid onset and shorter acting

stimulate insulin secretion (rapidly and short duration)

most effective in presence of glucose (has to be given with meals)

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23
Q

efficacy of meglitinides

A

decreases peak postprandal glucose

decreases plasma glucose 60-70

decreases A1C 0.5-1% (depends on glucose for activity)

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24
Q

ADE of meglitinides

A

hypoglycemia

weight gain

rare SJS

no significant effect on plasma lipid levels

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25
Q

CI of meglitinides

A

not given w/gemfibrozil

caution in hepatic dysfunction

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26
Q

MOA of alpha glucosidase inhibitors

A

work in the gut- block enzymes that digest starches in small intestine

slows glucose absorption

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27
Q

efficacy of alpha-glucosidase inhibitors

A

decreases peak postprandial glucose 40-50

decreases A1C 0.5-1%

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28
Q

ADE of alpha-glucosidase inhibitors

A

flatulence

diarrhea

abdominal discomfort

no specific effect on lipids or BP

no weight gain

hypoglycemia risk w/ secretagogue

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29
Q

CI for alpha-glucosidase inhibitors

A

in pts w/ IBD or cirrhosis

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30
Q

MOA of dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitor)

A

inhibits breakdown of glucagon-like peptide-1 (GLP-1) secreted during meals

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31
Q

SQ form of dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitor)

A

mild increase in glucose-mediated insulin release

suppresses glucagon secretion

delays gastric emptying

promotes satiety

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32
Q

efficacy of DPP-4 inhibitor

A

0.5-0.8% A1C reduction

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33
Q

ADE of DPP-4 inhibitor

A

decreases risk of hypoglycemia (except when given w/sulfa drugs)

pancreatitis

N/V

hypersensitivity- angioedema, anaphylaxis, caution in renal insufficiency

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34
Q

sitagliptin (DPP-4 inhibitor)

A

r/t SJS

caution in renal insufficiency

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35
Q

meds in the DPP-4 inhibitor class end in what?

A

gliptin

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36
Q

MOA of glucagon-like peptide-1 agonists (GLP-1 agonist)

A

analog of GLP-1: binds to GLP-1 receptors

increases glucose mediated insulin release (when you eat)

suppresses glucagon secretion

delays gastric emptying

promotes satiety

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37
Q

how are GLP-1 agonists given?

A

via SQ injection

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38
Q

efficacy of GLP-1 agonists

A

0.9-1.1 A1C reduction

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39
Q

ADE of GLP-1 agonists

A

weight loss

low risk hypoglycemia

GI s/s

pancreatitis

caution in renal dysfunction and severe gastroparesis

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40
Q

MOA of SGLT2 inhibitors

A

block renal glucose resorption

glucosuria (pee out the sugar, so it’s not in blood)

41
Q

efficacy of SGLT2 inhibitors

A

decreases fasting glucose and post-prandial glucose

0.5-1% A1C reduction

42
Q

ADE of SGLT2 inhibitors

A

**GU infections* (because you’re peeing out sugar)

weight loss

polyuria

osmotic diuresis

dehydration

CI in severe renal impairment

fracture risk (bone density loss)

dose related increase in LDL

43
Q

how are amylin analogs (pramlintide) given?

A

SQ immediately prior to meal

44
Q

MOA of amylin analogs (pramlitidine)

A

binds to amylin receptors

slows gastric emptying (like GLP1 analogs)

used in BOTH DM1 and DM2

suppresses glucagon secretion

delays gastric emptying

suppresses appetite

45
Q

efficacy of amylin analogs (pramlintide)

A

0.5-1% A1C reduction

effective post-prandial glucose reduction

46
Q

ADE of amylin analogs (pramlintide)

A

BBW in DM1 for increased risk of hypoglycemia

CI in hypoglycemic unawareness and/or frequent hypoglycemia

you need to decrease short acting insulin (prandial) dose by 50% when starting (i.e. you usually give 10 units lispro before dinner- when starting an anylin analog, you need to decrease the dose to 5 units lispro before dinner)

caution in gastroparesis

nausea, HA, cough

47
Q

MOA of bile acid sequestrants

A

bile acid binder

decreases glucose via unknown mechanisms

48
Q

efficacy of bile acid sequestrants

A

minimal

49
Q

ADE of bile acid sequestrants

A

constipation

indigestion

flatulence

hypersensitivity reactions

large pills (dysphagia is a problem)

can make hypertriglyceridemia worse

not systemically absorbed

pregnancy category B

50
Q

principles of insulin therapy in DM1

A

starting dose is based on weight

daily dosing (basal-single injections and prandial-determined by estimating carb content of meal)

higher total daily insulin needed for obese pts, sedentary lifestyle, and during puberty

51
Q

action profile of endogenous insulin

A

spikes high and drops rapidly

52
Q

action profiles of bolus insulins (lispro, aspart, glulisinine, regular)

A

spikes high and then drops off after 4-8 hours

53
Q

action profiles of basal insulins (NPH, detemir, glargine, degludec)

A

does not spike as high but lasts for 17-20 hours

degludec lasts for 42 hours

54
Q

injection pens

A

fast and easy

increased pt adherence

accurate dosing mechanisms

55
Q

insulin pumps

A

for motivated pts

expensive

continuous

only use rapid acting insulin

programmed to give basal and bolus doses

hx feature

lots of support and education

56
Q

modern meters

A

accurate

check FS intermittently

57
Q

continuous glucose monitoring

A

benefits: more complete glucose profile than traditional SMBG, tracking of meal related glycemic trends, detection of nocturnal hypoglycemia, facilitation of changes in insulin regimens, alarm for highs and lows
challenges: daily SMBG still required, not suited to many pts, limited accuracy (esp hypoglycemia), glycemia pattern results confusing and subject to interpretation

58
Q

weight gain on insulin

A

reverses catabolic effect of DM

glycosuria decreased

risk of hypoglycemia

pts increase caloric intake and avoiding exercise

risk of weight gain decreases w/more physiologic insulin admin

flexible insulin dosing to meet dietary and exercise needs

59
Q

physiologic multiple injection regimen

A

BASAL=BASELINE. controls glucose production between meals and overnight. near constant level.

BOLUS (mealtime/prandial)- limits hyperglycemia after meals. immediate rise and sharp peak at 1 hour post meal

60
Q

ideal insulin replacement

A

each component should come from a different insulin w/a specific profile or via insulin pump (w/1 insulin)

you want your insulin peaks to correspond w/meals

61
Q

typical daily insulin requirements in adults

A

total daily dosage affected by body size, adiposity (fat), physical activity, and remaining endogenous insulin

daily dosage usually 0.3-0.8 U/Kg in adults

daily dosage usually 50% basal/50% bolus insulin

62
Q

regular +NPH

A

give 2/3 dose in AM (prior to meal- 2/3 NPH and 1/3 regular)

give 1/3 in PM (prior to meal/bedtime- 1/3 NPH+1/3 regular)

advantage- inexpensive, 2-3 injections/day

disadvantage- does NOT mimic physiologic insulin secretion

63
Q

basal/bolus insulin

A

physiologic insulin therapy/”poor man’s insulin pump”

50% insulin requirement=long acting (controls fasting BG, basal insulin dose)

50% insulin requirements as rapid acting insulin (divide into 3 doses, controls post prandial plasma glucose, bolus insulin doses w/meals)

ex: total requirement= 60 U/day- lantus 30 units QHS and 10 units humalog w/meals

64
Q

basal/bolus insulin considerations

A

education: need to learn carb counting. must be a motivated/competent patient.
advantages: mimics physiologic insulin secretion, less hypoglycemia, flexible
disadvantages: cost, frequency of injections

65
Q

correction insulin “1800 rule”

A

used in addition to basal/bolus dosing

assists in controlling post prandial hyperglycemia

“1800 rule”= if pt requires 50 U/day, 1800/50=36. suggests that 1 unit of rapid acting insulin will decrease BG by 36

can be more pt specific than regular sliding scale

66
Q

glargine AM, PM, or bedtime with rapid-acting analogue w/each meal

A

glargine 18 U at bedtime

lispro 6 U before breakfast/lunch/dinner

67
Q

detemir at PM or bedtime, or in AM plus PM or bedtime with rapid-acting analogue w/each meal

A

detemir 8 U before breakfast
glulisine 6 U before breakfast/lunch/dinner

detemir 10 U at bedtime

68
Q

insulin dose adjustments

A

based on glycemic pattern over several days

generaly, change only 1 component of insulin at a time!!!

morning fasting glucose too high/low so increased/decrease total basal insulin by 10%

post-prandial glucose too high/low so adjust carb to insulin ratio

PPG too low so decrease bolus insulin

correction dose insufficient so adjust correction factor

69
Q

ADA/EASD DM 2 tx algorithm

A

monotherapy-metformin

dual therapy if you don’t get goal A1C after 3 months of monotherapy- metformin and another drug

triple therapy- metformin and another drug and another drug

70
Q

what medication should you always start with for type 2 DM?

A

metformin unless there’s a CI (i.e. women w/Cr of 1.5)

withhold metformin before and after any type of IV dye

71
Q

defect of beta cells

A

increased insulin available d/t use of secretagogues/exogenous insulin

72
Q

defect of liver

A

suppressed hepatic glucose production d/t impaired counter regulatory response

73
Q

defect of skeletal muscle

A

increased glucose uptake d/t exercise

74
Q

defect of alpha cells

A

suppressed glucagon d/t impaired counter regulatory response

75
Q

defect of brain

A

hypoglycemia unawareness

76
Q

insulin, glucagon, and glucose homeostasis

A

brain senses plasma glucose concentration and provides regulatory inputs which leads to homeostasis

77
Q

GLP1

A

glucagon like peptide 1

stimulates insulin secretion and inhibits glucagon secretion which leads to decreased post meal glucose abnormalities

78
Q

incretin effect in DM2

A

increases stimulation of insulin secretion from PO glucose

in pts w/DM2, the incretin effect is decreased which leads to increased blood sugars

79
Q

CSII in DM2 pt candidates

A

absolutely insulin deficient

take 4 or more insulin injections/day

assess BG 4x or more/day

motivated to achieve tighter glucose control

competency in carb counting, insulin correction, and adjustment formulas

ability to troubleshoot problems related to pump operation and plasma glucose levels

stable life situation

frequent contact w/HCP’s

80
Q

risk factors for hypoglycemia

A

risk factors: older pt females, AA’s, longer duration of DM, neuropathy, renal impairment, previous hypoglycemia, missing meals, increased A1C

81
Q

consequences of hypoglycemia

A

cognitive changes (confusion, irritability)

accidents

falls

recurrent hypoglycemia and hypoglycemia unawareness

refractory DM

dementia (elderly)

CV events: cardiac autonomic neuropathy, cardiac ischemia, angina, fatal arrhythmias

82
Q

symptoms of hypoglycemia

A

mild- 50-70: neurogenic- palpitations, tremor, hunger, sweating, anxiety, paresthesia

severe- <50: severe confusion, unconscious, seizure, coma, death

83
Q

higher risk of hypoglycemia with which medications?

A

metformin+SULFONYLUREAS and INSULIN (basal, basal-plus, premixed)

84
Q

tx of hypoglycemia

A

conscious: give glucose. repeat Q15 min after episodes
unconscious: glucagon injection and taken to hospital

85
Q

age considerations in making A1C goals for patients

A

older adults- decreased life expectancy, higher CVD burden, decreased GFR, at risk for adverse events from polypharmacy, more likely to be compromised from hypoglycemia

86
Q

weight considerations in making A1C goals for patients

A

majority of DM2 are overweight/obese, intensive lifestyle program, metformin, GLP-1 receptor agonists, bari surgery

87
Q

sex/race considerations in making A1C goals for patients

A

latinos= more insulin resistant

east asians= more beta cell dysfunction

gender may drive concerns (i.e. bone loss from TZDs)

88
Q

comorbid disease in DM

A

CAD- avoid TZDs!!!

HF- avoid TZDs and metformin!

renal dx- increased risk of hypoglycemia and lactic acidosis, caution w/sulfa, DPP-4- dose adjusted for renal dx, avoid exenatide GFR<30

liver dx- insulin is best option

hypoglycemia

89
Q

ADA guidelines for glycemic, BP and lipid control

A

A1C<7%

pre-prandial (fasting) 70-130

post-prandial <180

BP< 130/80

lipids:
LDL<100, <70 w/CVD
HDL>40 (men) and >50 (women)
TG<150

90
Q

eye complications of diabetes

A

microvascular

high blood glucose and high blood pressure can damage eye blood vessels, causing retinopathy, cataracts and glaucoma

91
Q

kidney complications of diabetes

A

microvascular

high blood pressure damages small blood vessels and excess blood glucose overworks the kidneys, resulting in nephropathy

92
Q

neuropathy complications of diabetes

A

microvascular

hyperglycemia damages nerves in the peripheral nervous system. this may result in pain and/or numbness.

feet wounds may go undetected, get infected and lead to gangrene.

93
Q

brain complications of diabetes

A

macrovascular

increased risk of stroke and cerebrovascular disease, including transient ischemic attack, cognitive impairment, etc.

94
Q

heart complications of diabetes

A

macrovascular

high blood pressure and insulin resistance increase risk of coronary heart disease

95
Q

extremities complications of diabetes

A

macrovascular

peripheral vascular disease results from narrowing of blood vessels which increases the risk for reduced or lack of blood flow in legs

feet wound are likely to heal slowly contributing to gangrene and other complications

96
Q

what is the foundation of DM2 programs?

A

diet, exercise, and education

97
Q

after trying metformin first, what is the next step?

A

combination therapy w/ 1-2 other oral injectable agents is reasonable

98
Q

how often should you evaluate therapy?

A

Q3 months until stable

Pharmacology (3 decks)

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