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ABBEY MSII Unit 5 > Pharm diabetes > Flashcards

Pharm diabetes Flashcards

1
Q

type 1 diabetes

A

autoimmune beta-cell destruction

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2
Q

type 2 diabetes

A

progressive insulin secretory defect

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3
Q

what are the other types of diabetes?

A

gestational, genetic defects in beta-cell function and insulin action, diseases of the exocrine pancreas, drug or chemical induced

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4
Q

what is A1C?

A

average glucose levels. greater than 6.5 = diabetes

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5
Q

what is the A1C goals in a younger, healthier person with T2D? older person with comorbidities/longer duration of T2D? T1D? regular T2D?

A

younger/healthier: 6-6.5%
older, comorbidities: 7.5-8.5%
T1D: 7-7.5%
T2D: less than 7%

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6
Q

what are the general concepts of treatment of diabetes mellitus?

A
  1. diet, weight, and physical activity optimization
  2. self-monitoring of blood glucose and ketones
  3. patient self-management education and training
  4. reduction of cardiovascular risk (smoking cessation, BP, lipid control)
  5. pharmacologic therapy
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7
Q

progression of type 2 diabetes

A

fasting glucose greater than 120
in prediabetes: beta cells are able to make more glucose to make up for insulin resistance, then the cells stop responding/die off

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8
Q

how do the islets of langerhans appear in T2D?

A

alpha cell dysfunction: secrete high levels of glucagon
fewer Beta cells: secrete insufficient levels of insulin/mass declines over time
amyloid plaques

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9
Q

incretin hormone: where produced and why? example

A

synthesized in L cells in ileum and colon in response to incoming nutrients

  • stimulate insulin secretion
  • example: glucagon-like peptide 1
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10
Q

glucagon-like hormone 1 (GLP-1) actions

A
  • incretin hormone that enhances glucose-dependent insulin secretion
  • slows gastric emptying
  • suppresses glucagon secretion
  • promotes satiety
  • receptors are in islet cells, CNS, elsewhere
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11
Q

what happens to GLP-1 release in T2D?

A

release is reduced (causing decreased insulin and increased blood sugar)

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12
Q

what are the main pathophysiological defects in T2DM?

A
  1. decreased pancreatic insulin secretion and increased glucagon secretion
  2. decreased peripheral glucose uptake
  3. increased hepatic glucose production (esp at night)
  4. decreased incretin effect causing gut carbohydrate delivery and absorption
    - combined effect of hyperglycemia
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13
Q

recommendations for therapy for type 2 diabetes

A
  • initiate metformin therapy along with lifestyle interventions (unless contraindicated)
  • if they are markedly symptomatic - consider insulin right away
  • if metformin/noninsulin monotherapy does not achieve or maintain the A1C target - add second oral agent such as GLP-1 receptor agonist
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14
Q

metformin: class, mechanism, action

A
  • class: biguanides
  • mechanism: activates AMP-kinase and inhibits mitochondrial sioform of glycerophosphate dehydrogenase
  • action: decreases hepatic glucose production
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15
Q

metform: advantages/disadvantages

A
  • advantages: no weight gain, no hypoglycemia, reduction in cardiovascular events
  • disadvantages: GI SE (start at low dose and build up), lactic acidosis, vit B12 deficiency
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16
Q

what is a contraindication of metformin?

A

reduced kidney function

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17
Q

glibenclamide/glyburide, glipizide, gliclazide, glimepiride: class, mechanism, action

A
  • class: sulfonylureas
  • mechanism: closes K ATP channels on beta-cell plasma membranes (works directly in pancreas)
  • action: increase insulin secretion
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18
Q

glibenclamide/glyburide, glipizide, gliclazide, glimepiride: advantages/disadvantages

A

-advantages: generally well tolerated
-disadvantages: relatively glucose-independent stimulation of insulin secretion: hypoglycemia
weight gain, blunt myocardial ischemia preconditioning

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19
Q

repaglinide/nateglinide: class, mechanism, action

A
  • class: meglitinides
  • mechanism: closes K ATP channels on beta-cell plasma membranes
  • action: increases insulin secretion
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20
Q

repaglinide/nateglinide: advantages/disadvantages

A
  • advantage: accentuated effects around meal ingestion (short acting)
  • disadvantage: hypoglycemia, weight gain, blunt myocardial ischemic preconditioning, dosing frequency (compliance)
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21
Q

pioglitazone: class, mechanism, action

A
  • class: thiazolidinediones
  • mechanism: activates the nuclear transcription factor PPAR-gamma
  • action: peripheral insulin sensitivity increased
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22
Q

pioglitazone: advantages/disadvantages

A
  • advantages: no hypoglycemia, HDL cholesterol increased, triglycerides decreased, possible reduction in myocardial infarcts
  • disadvantages: weight gain, edema, heart failure, bone fractures, increased bladder cancer
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23
Q

rosglitazone: class, mechanism, action

A
  • class: thiazolidinediones
  • mechanism: activates the nuclear transcription factor PPAR-gamma
  • action: peripheral insulin sensitivity increased
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24
Q

rosglitazone: advantages/disadvantages

A
  • advantages: no hypoglycemia
  • disadvantages: LDL cholesterol increased, weight gain, edema, heart failure, bone fractures, increased cardiovascular events
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25
Q

why pioglitazone over rosglitazone?

A

pioglitazone is cheaper (generics)

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26
Q

when is rosglitazone contraindicated?

A

heart disease

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27
Q

acarbose/miglitol: class, mechanism, action

A
  • class: alpha-glucosidase inhibitor
  • mechanism: inhibits intestinal alpha-glucosidase
  • action: intestinal carbohydrate digestion (and consequentyl glucose absorption) slowed
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28
Q

acarbose/miglitol: advantages/disadvantages

A
  • advantages: nonsystemic medication, post prandial glucose decreased, weight neutral, no hypoglycemia
  • disadvantages: GI side effects, dosing frequency, modest reduction in A1C
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29
Q

exenatide, liraglutide, albiglutide, dulaglutide: class, mechanism, action

A
  • class: GLP-1 receptor agonists
  • mechanism: activates GLP-1 receptors
  • action: insulin secretion increased, glucagon secretion decreased (both glucose-dependent), slows gastic emptying, increases satiety
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30
Q

exenatide, liraglutide, albiglutide, dulaglutide: advantages/disadvantages

A

advantages: weight reduction and potential for improved beta-cell mass/function
disadvantages: GI SE, cases of acute pancreatitis, hypoglycemia, caution with renal insufficiency, C-cell hyperplasia/medullary thyroid tumors in animals, injectable

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31
Q

difference between exenatide/liraglutide/albidlutide/dluaglutide

A

exenatide: twice daily or weekly
liraglutide: daily
albiglutide: weekly
dulaglutide: weekly

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32
Q

sitagliptin/alogliptin/saxagliptin/linagliptin: class, mechanism, action

A
  • class: DPP-4 inhibitors (incretin enhancers)
  • mechanism: inhibit DPP-4 activity
  • action: active GLP-1 concetration and GIP concentration, increased insulin secretion and decreased glucagon secretion
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33
Q

sitagliptin/alogliptin/saxagliptin/linagliptin: advantages/disadvantages

A

-advantages: no hypoglycemia, weight neutral
-disadvantages: occasional reports of urticaria/angioedema, URIs, headache, arthralgias
pancreatitis

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34
Q

canagliflozin/dapagliflozin/empagliflozin: class, mechanism, action

A
  • class: SGLT2 (sodium glucose cotransporter 2) inhibitor
  • mechanism: reduces glucose resorption in the kidney: alpha cell agonist
  • action: urinary glucose excretion increases and increased glucagon secretion
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35
Q

canagliflozin/dapagliflozin/empagliflozin: advantages/disadvantages

A
  • advantages: no hypoglycemia and weight loss possible
  • disadvantages: volume depletion, hyperkalemia, ketoacidosis, UTIs, hypersensitivity, increased LDL, reduced bone density (increased fracture risk)
36
Q

what is hypoglycemia most common treatment?

A

sulfonylurea drugs (glibenclamide/glyburide, glipizide, gliclazide, glimepiride) and insulin

37
Q

is hypoglycemia MC in type 1 or type 2? what are risk factors

A

type 1
risk factors: over 60, impaired renal function, poor nutrition, liver disease, increased physical activity, longer duration of diabetes

38
Q

symptoms of hypoglycemia

A

confusion, slurred speech, dizzy, weakness, shaking, nervous, sweating, palpitations, extreme hunger, headache, mood/behavior change, tingling of hands/tongue/lips, vision change, poor coordination, unresponsiveness, unconsciousness or seizures

39
Q

recommendations for hypoglycemia

A
  • glucose preferred treatment

- glucagon prescribed for all individuals at sig risk of severe hypoglycemia

40
Q

glucagon emergency kit: use and who has prescription

A

use: only if unconscious or unable to swallow (never given to self)
- turn on side - nausea vomiting call 911
- type 1 has prescription and type 2 with previous severe low blood sugar

41
Q

how is severe hypoglycemia in the hospital treated?

A

IV dextrose

42
Q

amylin

A

peptide released with insulin from beta cells in response to eating

  • deficient in T1D; variable levels in T2D
  • slows gastric emptying, suppresses postprandial glucagon secretion, may reduce appetite
43
Q

pramlintide

A

amylin analog:

  • injected before each meal
  • used in adults with insulin-requiring diabetes
  • reduces post-prandial glucose levels (inhibits glucagon production, slows gastric emptying)
  • use with short/rapidly acting insulin
44
Q

pramlintide: advantages/disadvantages

A
  • advantages: prevent amyloid fibrils in beta cell, slows gastric emptying, inhibits glucagon production, decrease appetite and promotes weight loss
  • disadvantages: GI SE (nausea), significant risk of hypoglycemia
45
Q

indications for insulin therapy in T2D

A
  • significant hyperglycemia at presentation
  • hyperglycemia on maximal doses of oral agents
  • decompensation (acute injury, stress, infection, MI, severe hyperglycemia w/ ketonemia, uncontrolled weight loss)
  • surgery
  • pregnancy
  • serious renal or hepatic disease
46
Q

what are the least expensive insulins available?

A

regular and NPH insulins

47
Q

what are the rapid acting insulin analogs? how do they work?

A

lispro, aspart, glulisine

-change amino acid to work faster

48
Q

detemir

A
  • intermediate-long acting insulin
  • duration of action is dose-dependent (lower doses = intermediate acting, higher doses = 24h)
  • delayed release from subcutaneous injection site due to self-association and binding to albumin
49
Q

which insulin should not be diluted or mixed with any other insulin preparations?

A

detemir

50
Q

glargine

A

long-acting insulin analog of rDNA origin

-basal insulin - can be given at high concentrations (U300)

51
Q

degludec

A

ultra long-acting basal insulin analog

WANT A LONG DIC (DEC)

52
Q

what is the MC insulin concentration? what dose is used for severe insulin resistence?

A

MC: U100

severe insulin resistance: U500

53
Q

what is glucagon-like hormone 1 (GLP-1) metabolized by? which drug is this a target for?

A

DPP-4

target of DPP-4 inhibitors (-gliptins)

54
Q

why is there no hypoglycemia with metformin?

A

inhibits liver break down of glucose

55
Q

explain in detail the mechanism of sulfonylureas. which drugs are the sulfonylureas?

A
  • glucose is normally taken into beta cell by GLUT2 to make ATP
  • ATP blocks the potassium channels
  • increased K in cell (because channel is blocked) causing increase in voltage
  • increased voltage opens Ca ion channels
  • increased ca in cell causes release of insulin
  • -> sulfonylureas close the potassium ATP channels themselves, causing increased insulin secretion
  • GLI- drugs (glibenclamide, glipizide, gliclazide, glimepiride)
56
Q

why do sulfonylurease (gli-) cause hypoglycemia?

A

glucose-independent stimulation of insulin secretion

57
Q

what is the difference between sulfonylureas and meglitinides?

A
  • they have the SAME mechanism!!!
  • meglitinides (-glinides) are short acting
  • good for “meals on wheels”
58
Q

explain in detail the mechanism of thiazolidinediones. what are the thiazolidinediones?

A

activates the nuclear transcription factor PPAR-gamma, which increases uptake of glucose into adipocytes
-glitazones (pioglitazone and rosiglitazone)

59
Q

acarbose and miglitol mechanism. what do these drugs cause a lot of?

A

inhibits alpha-glucosidase (the enzyme that degrades glucose) causing intestinal carbohydrate digestion to be slowed
-this causes a lot of FARTS! carbs are digested by the bacteria in gut

60
Q

what makes degludec long acting?

A

soluble MULTIhexamers must all be broken down

61
Q

what are the advantages to premixed insulins?

A
  • convenient
  • longer shelf-life
  • fewer dosing errors
62
Q

what are the disadvantages to premixed insulins?

A
  • loss of flexibility with matching to carb intake and physical activity
  • harder to treat short-term hi or low glucose levels
  • hypoglycemia risk
63
Q

insulin storage

A

refridgerated - good in room temp for 1 month

-never freeze, avoid direct sunlight

64
Q

peak action of rapid-acting subcutaneous injections (lispro, aspart, glulisine)

A

.5-3 hours
(onset 5-30 min)
(duration 3-5 hours)

65
Q

what are the intermediate acting insulins and what is their onset of action/peak action/duration of action?

A 
NPH, NPL, NPA
-onset: 1-4 hr
-peak: 4-10 hr
-duration: 14-24hr
Detemir
-onset: 3-4 hr
-peak: 4-8 hr
-duration: 6-24 hr
66
Q

what is the long action insulin and what is its onset of action/peak action/duration of action?

A

glargine

  • onset: 2-3 hr
  • peak NONE
  • duration 22-30 hr
67
Q

what is the ultra long acting insulin and what is its onset of action/peak action/duration of action?

A

degludec

  • onset: steady start after 2-3 days
  • peak: none
  • duration: 42+ hrs
68
Q

what is the best place to inject insulin?

A

abdomen because it is most stable

followed by arm, butt, thighs (increased blood flow increases absorption)

69
Q

insulin treatment of type 2 diabetes

A

begin with once daily insulin and continue oralmedications

-intensification (basal insulin + fasting acting with meals) needed with progressive decline in beta cell mass

70
Q

split-mix insulin therapy: what is it? advantages, disadvantages

A
  • 2 fast acting and bedtime intermediate
  • advantages: easy, lower cost with NPH and regular
  • disadvantages: not very physiological, greater likelihood of nocturnal hypoglycemia (bc peak of NPH at presupper), greater chance of fasting hyperglycemia
71
Q

basal/bolus insulin concept

A

basal: suppresses glucose production between meals and overnight (40-50% daily needs)
bolus: matched to carb intake, premeal glucose, anticipated activity, limiting hyperglycemia after meals

72
Q

what is the disadvantage of using long-acting analogs over intermediate NPH?

A

more expensive - even though better

73
Q

adverse reactions of insulin

A
  • hypoglycemia (inject glucagon for emergencies at home, dextrose in hospital)
  • weight gain
  • local or systemic allergic reactions
  • lipohypertrophy (avoid injecting in same spot)
  • lipatrophy (rare)
74
Q

when to use continuous glucose monitoring

A
  • repeated hypoglycemia
  • hypoglycemic unawareness
  • discrepancies between A1C and SMBG
  • pregnancy
  • unable to achieve goals
75
Q

potential problems and solutions for hypoglycemia

A

problem: basal rate or basal insulin dosing too high –> decrease basal insulin
problem: large bolus near bedtime –> reduce short acting insulin for food correction near ngiht time

76
Q

potential problems and solutions for hyprglycemia

A

problem: basal rate or basal insulin dose too low –> increase basal rate
problem: food intake in evening/night –> reduce intake or cover food with insulin

77
Q

what should peak glucose values be lower than?

A

180 mg/dl

78
Q

pre-prandial

A

period just before a snack or meal

79
Q

which drugs increase insulin secretion?

A

glipizide, repaglinide

80
Q

which drug decreases glucose production from the liver?

A

metformin

81
Q

which drug slows carbohydrate absorption?

A

acarbose

82
Q

which drug reduces glucose resorption in the kidney?

A

canagliflozin

83
Q

which drug rarely can cause lactic acidosis?

A

metformin

84
Q

which is the most rapidly acting insulin?

A

lispro

85
Q

which drug is used for meal time coverage?

A

fast acting (lispro)

86
Q

which drug is a basal insulin with no peak

A

insulin glargine

87
Q

which drug is used intravenously?

A

regular insulin

ABBEY MSII Unit 5 (8 decks)

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