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Pharmacology > Management of Diabetes > Flashcards

Management of Diabetes Flashcards

1
Q

A group of diseases that result in too much sugar/glucose in the blood stream

A

Diabetes

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2
Q

A chronic condition in which the pancreas produces little or no insulin

A

Type I diabetes

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3
Q

Type I Diabetes:

  • Most common cause = _________; destroys pancreatic _________ cells that make insulin
  • onset is commonly ________ in life
A
  • Most common cause = AUTOIMMUNE; destroys pancreatic BETA cells that make insulin
  • onset is commonly EARILER in life
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4
Q

a chronic condition that affects the way the body processes blood sugar

A

Type 2 diabetes

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5
Q

Type 2 Diabetes:

  • body does not use ______ properly
  • Characterized by insulin ___________ (decreased ability for insulin to move glucose into cells)
  • onset is more commonly ______ in life
  • ________ common type
  • Type 2 diabetes is increasing in correlation /c increased ______ levels
A
  • body does not use INSULIN properly
  • Characterized by insulin RESISTANCE (decreased ability for insulin to move glucose into cells)
  • onset is more commonly LATER in life
  • MOST common type
  • Type 2 diabetes is increasing in correlation /c increased OBESITY levels
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6
Q

A condition in which blood sugar is high, but not high enough to be diagnosed as Type 2 diabetes

A

Prediabetes

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7
Q

Prediabetes:

  • at risk for developing type ____ diabetes, but not inevitable /c weight ________ and ______ changes
  • Fasting blood glucose = _______ mg/dl
  • A1C = ______%
A
  • at risk for developing type 2 diabetes, but not inevitable /c weight LOSS and LIFESTYLE changes
  • Fasting blood glucose = 100 - 125 mg/dl
  • A1C = 5.5 - 6.4%
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8
Q

A form of high blood sugar affecting pregnant women

A

Gestational diabetes

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9
Q

Gestational Diabetes:

  • _______ hormones can increase blood sugar
  • body is not able to make and use all the _______ it needs for pregnancy
  • increased risk for developing type ___ diabetes later in life
A
  • PLACENTAL hormones can increase blood sugar
  • body is not able to make and use all the INSULIN it needs for pregnancy
  • increased risk for developing type 2 diabetes later in life
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10
Q

What is the purpose of insulin?

A

facilitate uptake of glucose into cells to produce energy

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11
Q

Physiologic Insulin Resistance — Between Meals

  • ________ producing glucose to meet body’s energy needs
  • ________ produces insulin on continuous basis (facilitates _________ of basal glucose production)
A
  • LIVER producing glucose to meet body’s energy needs

- PANCREAS produces insulin on continuous basis (facilitates METABOLISM of basal glucose production)

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12
Q

Physiologic Insulin Resistance — With Food Intake

  • Blood glucose _______ based on carbohydrates consumed
  • Pancreas produces spike of ______
A
  • Blood glucose RISES based on carbohydrates consumed

- Pancreas produces spike of INSULIN

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13
Q

Adult Diagnosis of Diabetes Criteria

  • A1C: greater than or equal to _____%
  • FBG: greater than or equal to ______ mg/dL
  • 2 hour PG: greater than or equal to ________ mg/dl during OGTT
  • Symptoms & RPG: greater than or equal to ______ mg/dL
A
  • A1C: greater than or equal to 6.5%
  • FBG: greater than or equal to 126 mg/dL
  • 2 hour PG: greater than or equal to 200 mg/dl during OGTT
  • Symptoms & RPG: greater than or equal to 200 mg/dL
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14
Q

Diabetic Adult Goals Criteria

  • A1C < _____% for most patients (select pts < ___% or < ____%)
  • Preprandial capillary glucose: _________ mg/dL
  • Peak postprandial capillary glucose < _____ mg/dL
A
  • A1C < 7% for most patients (select pts < 6.5% or < 8%)
  • Preprandial capillary glucose: 80 - 130 mg/dL
  • Peak postprandial capillary glucose < 180 mg/dL
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15
Q

Metformin (Glucophage) — MOA

  • improves insulin _________
  • increases tissue ________ and utilization of ______ by muscle
  • Decreases hepatic production of _________
  • Used for Type _____ diabetes
A
  • improves insulin SENSITIVITY
  • increases tissue UPTAKE and utilization of GLUCOSE by muscle
  • Decreases hepatic production of GLUCOSE
  • Used for Type 2 diabetes
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16
Q

Metformin (glucophage) — Efficacy

  • A1C decreases by ________%
  • FBG decreases by ________ mg/dL (FBG&raquo_space; prandial)
A
  • A1C decreases by 1.5 - 2.0%

- FBG decreases by 60 - 80 mg/dL (FBG&raquo_space; prandial)

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17
Q

_______ is the first line treatment for diabetes per ADA and AACE

A

METFORMIN (GLUCOPHAGE) is the first line treatment for diabetes per ADA and AACE

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18
Q

Metformin (Glucophage) — Advantages

  • no ___________
  • Decreases _________ and ______
  • Shown to decreased ______ events
  • no __________ (possible ________)
A
  • no HYPOGLYCEMIA
  • Decreases TRIGLYCERIDES and LDL-C
  • Shown to decreased CVD events
  • no WEIGHT GAIN (possible WEIGHT LOSS)
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19
Q

Metformin (Glucophage) — Disadvantages

  • ____ side effects
  • ___________ risk; rare, but serious
A
  • GI side effects

- LACTIC ACID risk; rare, but serious

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20
Q

Metformin (Glucophage) — Caution and Contraindications

  • Caution: _______ dysfunction
  • Caution: patients at risk for _______________
  • Cost is ________
A
  • Caution: RENAL dysfunction
  • Caution: patients at risk for LACTIC ACIDOSIS
  • Cost is CHEAP
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21
Q

SGLT2 Inhibitors — MOA

  • “glucosuretics” - help excrete ______ out in urine
  • inhibition of SGLT2 in the proximal tubules reduces the _______ of glucose and increases ______ of glucose in urine
A
  • “glucosuretics” - help excrete GLUCOSE out in urine
  • inhibition of SGLT2 in the proximal tubules reduces the RESORPTION of glucose and increases EXCRETION of glucose in urine
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22
Q

SGLT2 Inhibitors — Efficacy

- A1C decreases by ______%

A
  • A1C decreases by 0.5 - 1%
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23
Q

SGLT2 Inhibitors — Advantages

  • low _________ risk, ________ weight, _______ blood pressure
  • Empagliflozin = decreased _________ events (indicated for ______ patients)
A
  • low HYPOGLYCEMIA risk, DECREASED weight, DECREASED blood pressure
  • Empagliflozin = decreased CARDIOVASCULAR events (indicated for CHF patients)
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24
Q

SGLT2 Inhibitors — Disadvantages

  • Efficacy is dependent on good _______ function
  • Transient increase in _______
  • increased _____
  • Volume _______/hypotension/dizziness
  • Risk of ___________ (/c canagliflozin)
  • ________ effects
A
  • Efficacy is dependent on good RENAL function
  • Transient increase in SCr
  • increased LDL
  • Volume DEPLETION/hypotension/dizziness
  • Risk of AMPUTATIONS (/c canagliflozin)
  • ADVERSE effects
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25
Q

Sulfonylureas — MOA

  • For type _____ diabetes
  • Stimulate ______ secretion from pancreatic beta-islet cells (requires functioning pancreas)
  • bind to the SUR1 subunit and block the ATP sensitive ____ channel in the beta membrane
A
  • For type 2 diabetes
  • Stimulate INSULIN secretion from pancreatic beta-islet cells (requires functioning pancreas)
  • bind to the SUR1 subunit and block the ATP sensitive K+ channel in the beta membrane
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26
Q

Sulfonylureas

- caution in what 4 groups of people?

A

(1) Elderly
(2) Renal/hepatic diseases
(3) Alcoholics
(4) pts /c concomitant hypoglycemic agents

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27
Q

Sulfonylureas — Best candidates

  • Type _____ DM
  • _______ duration of diabetes
  • ______ fasting blood glucose levels
  • When _______ is an issue
A
  • Type 2 DM
  • SHORT duration of diabetes
  • FAST fasting blood glucose levels
  • When COST is an issue
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28
Q

Sulfonylureas — Treatment Failure

  • _____% will have primary failure (d/t poor blood sugar control after initial trial of 6 - 12 weeks on medications and diet)
  • After 5 years, ______% may experience secondary failure
    - Failure after initial _______
    - Common for these medications to start to failure after ______ months (pancreatic beta-cells quit _________ insulin /c disease progression)
  • place in therapy is __________
A
  • 25% will have primary failure (d/t poor blood sugar control after initial trial of 6 - 12 weeks on medications and diet)
  • After 5 years, 50 - 75% may experience secondary failure
    - Failure after initial CONTROL
    - Common for these medications to start to failure after 6 - 12 months (pancreatic beta-cells quit PRODUCING insulin /c disease progression)
  • place in therapy is DECLINING
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29
Q

What drug class do these belong to?

  • Repaglinide (prandin)
  • Nateglinide (starlix)
A

Meglitinides

end in “glinide”

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30
Q

Meglitinides — MOA

  • oral medication, _______ acting insulin
  • __________ insulin secretion from beta-islet cells
    - insulin release is ________ dependent
    - “________ time” sulfonylurea –> if you skip a meal, skip the dose too
A
  • oral medication, SHORT acting insulin
  • STIMULATE insulin secretion from beta-islet cells
    - insulin release is GLUCOSE dependent
    - “MEAL time” sulfonylurea –> if you skip a meal, skip the dose too
31
Q

Meglitinides — Efficacy

  • A1C decreases _____%
  • affects ________ more than ___________ glucose
A
  • A1C decreases 0.4 - 2.0%

- affects PRANDIAL more than FASTING BLOOD glucose

32
Q

Meglitinides — Advantages

  • ________ absorbed and ________ half life
  • Mostly eliminated in ________ (can use in _______ impairment)
  • Given /c ________ to enhance postprandial glucose utilization
A
  • RAPIDLY absorbed and SHORT half life
  • Mostly eliminated in FECES (can use in RENAL impairment)
  • Given /c MEALS to enhance postprandial glucose utilization
33
Q

Meglitinides — Disadvantages

  • _____glycemia
  • Weight ______ (~ 3%)
A
  • HYPOGLYCEMIA

- Weight GAIN (~ 3%)

34
Q

Thiazolidinediones (TZDs) — MOA

  • activates nuclear transcription factor ________
  • _________ cellular response to insulin
  • __________ hepatic glucose production
A
  • activates nuclear transcription factor PPAR-Y
  • IMPROVES cellular response to insulin
  • DECREASES hepatic glucose production
35
Q

Thiazolidinediones (TZDs) — Efficacy

- A1C ________ 1.0-1.5%

A
  • A1C DECREASES 1.0-1.5%
36
Q

Thiazolidinediones (TZDs) — Advantages

  • No ____glycemia
  • No dose ___________ in renal impairment
  • “insulin _______”
  • _____ HDL 3-9 mg/dL
  • ________ triglycerides 10 - 20%
A
  • No HYPOGLYCEMIA
  • No dose ADJUSTMENT in renal impairment
  • “insulin SENSITIZER”
  • INCREASE HDL 3-9 mg/dL
  • DECREASE triglycerides 10 - 20%
37
Q

Thiazolidinediones (TZDs) — DISADVANTAGES

  • Weight _______
  • Increase ________ risk (i.e. wrist, forearms, ankles, or feet)
  • ______toxicity (check LFT)
  • Exacerbations of _______ failure
  • may increase myocardial _________ or ________ cancer
A
  • Weight GAIN
  • Increase FRACTURE risk (i.e. wrist, forearms, ankles, or feet)
  • HEPATOTOXICITY (check LFT)
  • Exacerbations of HEART failure
  • may increase myocardial INFARCTION or BLADDER cancer
38
Q

Alpha-Glucosidase Inhibitors — MOA

  • competitive reversible ________ of intestinal alpha-glucosidase
  • _____ intestinal carbohydrate digestion / absorption
A
  • competitive reversible INHIBITION of intestinal alpha-glucosidase
  • SLOWS intestinal carbohydrate digestion / absorption
39
Q

Alpha-Glucosidase Inhibitors — Efficacy

  • A1C _______ 0.4 - 0.9%
  • Post- prandial glucose (PPG) ________ 40 - 50 mg/dL
A
  • A1C DECREASES 0.4 - 0.9%

- Post- prandial glucose (PPG) DECREASES 40 - 50 mg/dL

40
Q

Alpha-Glucosidase Inhibitors — Advantages

  • no _____glycemia
  • __________ post-prandial glucose
  • non-_______
  • no effect on ______
A
  • no HYPOGLYCEMIA
  • DECREASES post-prandial glucose
  • non-SYSTEMIC
  • no effect on WEIGHT
41
Q

Alpha-Glucosidase Inhibitors — Disadvantages

  • _____ effects (i.e. flatulence, diarrhea, abdominal cramping)
  • rashes
  • _______ Liver function tests
  • Modest A1C _______ and _______ dosing
A
  • GI effects (i.e. flatulence, diarrhea, abdominal cramping)
  • rashes
  • INCREASED Liver function tests
  • Modest A1C EFFICACY and FREQUENT dosing
42
Q

Alpha-Glucosidase Inhibitors

- What are 3 contraindications for alpha-glucosidase inhibitors?

A

(1) Inflammatory bowel disease (IBD)
(2) Colonic ulceration
(3) intestinal obstruction

43
Q

Incretin Hormone

  • ________________ (G:P-1) & ____________________ (GIP)
  • simulates insulin response from beta-cells in ________ dependent manner (i.e. ______ gastric emptying, Reduces ________ intake and body _______, ______ glucagon secretion from alpha-cells in a glucose dependent manner)
  • Drugs targeting _______- hormones include DPP-IV inhibitors and GLP-1 receptor agonists
A
  • GLUCAGON-LIKE PEPTIDE (G:P-1) & GASTRIC INHIBITORY POLYPEPTIDE (GIP)
  • simulates insulin response from beta-cells in GLUCOSE dependent manner (i.e. SLOWS gastric emptying, Reduces FOOD intake and body WEIGHT, INHIBITS glucagon secretion from alpha-cells in a glucose dependent manner)
  • Drugs targeting INCRETIN- hormones include DPP-IV inhibitors and GLP-1 receptor agonists
44
Q

What drug class do these belong to?

  • Sitagliptin (Januvia)
  • Saxagliptin (onglyza)
  • Linagliptin (Tradjenta)
  • Alogliptin (Nesina)
A

Dipeptidyl Pepridase IV (DPP-IV) Inhibitors

45
Q

Dipeptidyl Pepridase IV (DPP-IV) Inhibitors — MOA

  • inhibits DPP-IV, the enzyme that breaks down _____ and ________ (incretin hormones)
  • Thus GLP-1 and GIP are around in the system _________
  • Dan likes to use this drug in combo /c _____________
A
  • inhibits DPP-IV, the enzyme that breaks down GLP-1 and GIP (incretin hormones)
  • Thus GLP-1 and GIP are around in the system LONGER
  • Dan likes to use this drug in combo /c METFORMIN
46
Q

Dipeptidyl Pepridase IV (DPP-IV) Inhibitors — Efficacy

  • A1C _________ 0.5 - 1.0%
  • FBG ___________ 20 mg/dL
  • PPG _____________ 20 - 40 mg/dL
A
  • A1C DECREASES 0.5 - 1.0%
  • FBG DECREASES 20 mg/dL
  • PPG DECREASES 20 - 40 mg/dL
47
Q

Dipeptidyl Pepridase IV (DPP-IV) Inhibitors — Advantages

  • No ______glycemia
  • Weight ______ (~0.5kg)
  • ______ tolerated
A
  • No HYPOGLYCEMIA
  • Weight LOSS (~0.5kg)
  • WELL tolerated
48
Q

Dipeptidyl Pepridase IV (DPP-IV) Inhibitors — Disadvantages

  • Adverse Effects: n___________, ________ respiratory infection, h__________
  • Acute _________ (caution in patients /c history)
  • Alogliptin: post-marketing reports of _______ failure
A
  • Adverse Effects: NASOPHARYNGITIS, UPPER respiratory infection, HEADACHE
  • Acute PANCREATITIS (caution in patients /c history)
  • Alogliptin: post-marketing reports of HEPATIC failure
49
Q

Bile Acid Sequestrant (ex. Colesevalam)

  • MOA = __________
  • _______ effect of A1C (~0.5%)
  • ______ & ________ are significant
  • Not a good “________”
A
  • MOA = UNKNOWN
  • MODEST effect of A1C (~0.5%)
  • GAS & BLOATING are significant
  • Not a good “ADD ON”
50
Q

Dopamine Agonist (ex. Bromocriptine)

  • MOA = _________
  • _________ effect on A1C (~0.4 - 0.6%)
  • not good as “_________”
  • Poor SE profile, includes H___________
A
  • MOA = UNKOWN
  • MODEST effect on A1C (~0.4 - 0.6%)
  • not good as “ADD ON”
  • Poor SE profile, includes HALLUCINATIONS
51
Q

Glucogon-like peptide-1 agonists (GLP-1s) & Pramintide are both _____________ injectables

A

Glucogon-like peptide-1 agonists (GLP-1s) & Pramintide are both NON-INSULIN injectables

52
Q

Insulins

  • _______ acting (meal-time/bolus) insulin
  • ______ acting insulin
  • _________ acting insulin
  • _______ acting insulin
  • ________ insulins
A
  • RAPID acting (meal-time/bolus) insulin
  • SHORT acting insulin
  • INTERMEDIATE acting insulin
  • LONG acting insulin
  • PREMIXED insulins
53
Q

Combination insulins:

- GLP-1 + _______ insulin (for type 2 diabetes)

A
  • GLP-1 + BETA insulin (for type 2 diabetes)
54
Q

What class of medications are these?

  • Exenatide (Byetta)
  • Exenatide ER (Bydureon)
  • Liraglutide (Victoza)
  • Dulaglutide (trulicity)
  • Semaglutide (Ozempic)
A

GLP - 1 REceptor Agonitsts

55
Q

GLP-1 Receptor Agonists — MOA

  • activates ________
  • ________ glucose dependent insulin secretion, ___________ inappropriate glucagon section, _______ gastric emptying, _________ food intake
  • Uses = Type _____ diabetes & ______ aides
A
  • activates GLP-1
  • INCREASES glucose dependent insulin secretion, DECREASES inappropriate glucagon section, SLOWS gastric emptying, DECREASES food intake
  • Uses = Type 2 diabetes & DIET aides
56
Q

GLP-1 Receptor Agonists — Efficacy

  • A1C ________ 0.8 - 1.5%
  • Weight ______ 1.5 - 3 kg
  • Affects PPG _______ than FBG
A
  • A1C DECREASES 0.8 - 1.5%
  • Weight DECREASES 1.5 - 3 kg
  • Affects PPG MORE than FBG
57
Q

GLP-1 Receptor Agonists — Advantages

  • Low _____glycemia risk
  • Decreases _______ and leads to weight ______
A
  • Low HYPOGLYCEMIA risk

- Decreases APPETITE and leads to weight LOSS

58
Q

GLP-1 Receptor Agonists — Disadvantages

  • ______ side effects (nausea, vomiting, diarrhea)
  • Caution in patients /c h/o acute ________
A
  • GI side effects (nausea, vomiting, diarrhea)

- Caution in patients /c h/o acute PANCREATITS

59
Q

Physiological Insulin Release
- What is the goal of insulin replacement therapy?

Basal (1x/day) and Bolus (/c food) Insulin

  • address _______ and _____ states
  • Offers best opportunity for achieving ____glycemia

Supplemental/correction insulin to lower pre-meal hyerpglycemia

  • Differs from ______ scale insulin
  • In addition to bolus or “___________” insulin to correct pre-meal hyperglycemia
A
  • Goal = mimic normal physiologic insulin secretion

Basal (1x/day) and Bolus (/c food) Insulin

  • address FASTING and FED states
  • Offers best opportunity for achieving EUGLYCEMIA

Supplemental/correction insulin to lower pre-meal hyerpglycemia

  • Differs from SLIDING scale insulin
  • In addition to bolus or “NUTRITIONAL” insulin to correct pre-meal hyperglycemia
60
Q

Insulin Profiles — Rapid Acting

  • quick _____ and _____; short ________
  • preferred for ______/_______ insulin
A
  • quick ONSET and PEAK; short DURATION

- preferred for MEALTIME/BOLUS insulin

61
Q

Insulin Profiles — Short Acting

  • Delayed _____ and ______ compared to rapid acting, Slightly _______ acting
  • Not as preferred for mealtime/bolus insulin d/t risk for insulin ________
A
  • Delayed ONSET and PEAK compared to rapid acting, Slightly LONGER acting
  • Not as preferred for mealtime/bolus insulin d/t risk for insulin STACKING
62
Q

Insulin Profiles — Intermediate Acting

  • More delayed _____ and ______, _______ duration
  • Used BID for “___________”
A
  • More delayed ONSET and PEAK, LONGER duration

- Used BID for “BASAL COVERAGE”

63
Q

Insulin Profiles — Long Acting

  • “________” and duration of ~ _____ hours
  • ______ insulin
A
  • “PEAKLESS” and duration of ~ 24 hours

- BASAL insulin

64
Q

Sliding Scale Insulin

  • not _________, but still used
  • consists of regular or rapid-acting insulin ________ any intermediate or long-acting/basal insulin
  • Not supported or recommended as ___________
A
  • not EFFECTIVE, but still used
  • consists of regular or rapid-acting insulin WITHOUT any intermediate or long-acting/basal insulin
  • Not supported or recommended as MONOTHERAPY
65
Q

Why Sliding Scale Insulin Does Not work:

(1) Corrects current _____________ — after it has already occurred (reactive approach)
(2) Does not _________ recurrence of hyperglycemic episodes (no basal or nutritional/mealtime insulin being given)
(3) Reactive approach leads to ______ variations in blood glucose levels (leaves patients at ________ risk for complications of hyper and hypoglycemia
(4) Often given without regard to: __________ intake, previously administered _________, Patient’s changing _______ needs and individual _______ condition, _______ sensitivity
(5) SSI is ________ to normal pancreatic physiology: no basal insulin — promotes ______ blood glucose rather than creating a steady state of glycemic control

A

(1) Corrects current HYPERGLYCEMIA — after it has already occurred (reactive approach)
(2) Does not PREVENT recurrence of hyperglycemic episodes (no basal or nutritional/mealtime insulin being given)
(3) Reactive approach leads to WIDE variations in blood glucose levels (leaves patients at INCREASED risk for complications of hyper and hypoglycemia
(4) Often given without regard to: CARBOHYDRATE intake, previously administered INSULIN, Patient’s changing METABOLIC needs and individual MEDICAL condition, INSULIN sensitivity
(5) SSI is CONTRARY to normal pancreatic physiology: no basal insulin — promotes LABILE blood glucose rather than creating a steady state of glycemic control

66
Q

When to Test Blood Glucose Levels?

  • If on on basal insulin –> test FBG every ________
  • If on basal insulin plus mealtime/bolus insulin –> test FBG every ________ and test prior to each _________ that insulin is being administered
A
  • If on on basal insulin –> test FBG every MORNING
  • If on basal insulin plus mealtime/bolus insulin –> test FBG every MORNING and test prior to each MEAL that insulin is being administered
67
Q

What insulin affects what numbers?

  • Basal insulin affects ____ blood glucose readings
  • mealtime / bolus insulin affects ________ blood glucose readings
    - if tested pre-prandial, adjust the insulin dose of the meal _____ (ex. pre-lunch reading is high, then increase breakfast dose)
    - if tested 2 hours post-prandial, then adjust the insulin dose of _____ meal (ex. 2 hours post-lunch reading is high, then increase the lunch dose)
A
  • Basal insulin affects FASTING blood glucose readings
  • mealtime / bolus insulin affects PRANDIAL blood glucose readings
    - if tested pre-prandial, adjust the insulin dose of the meal PRIOR (ex. pre-lunch reading is high, then increase breakfast dose)
    - if tested 2 hours post-prandial, then adjust the insulin dose of THAT meal (ex. 2 hours post-lunch reading is high, then increase the lunch dose)
68
Q

Insulin Dosing in Type-1 (insulin dependent) Diabetes

  • Pancreas is not producing insulin so you must replace it _______ (no use for oral agents here)
  • Requires _______ insulin + _______ insulin /c each meal (basal-bolus regimen)
  • _______ counting: can calculate insulin:carb ratio (500 rule: 500/total daily dose = how many carbs are covered by each unit of rapid acting insulin)
  • Once established, insulin requirements and ability to control blood glucose can move to insulin _______
A
  • Pancreas is not producing insulin so you must replace it SUBCUTANEOUSLY (no use for oral agents here)
  • Requires BASAL insulin + MEALTIME insulin /c each meal (basal-bolus regimen)
  • CARB counting: can calculate insulin:carb ratio (500 rule: 500/total daily dose = how many carbs are covered by each unit of rapid acting insulin)
  • Once established, insulin requirements and ability to control blood glucose can move to insulin PUMP
69
Q

Insulin — Adverse effects

  • ______glycemia
  • Lipo________
  • Lip_________
  • _________ reaction
  • Weight ________
A
  • HYPOGLYCEMIA
  • LIPOHYPERTROPY
  • LIPOATROPHY
  • ALLERGIC reaction
  • Weight GAIN
70
Q

Pramlintide (Symlin) — MOA

  • synthetic analog of human ________
  • Co-secreted /c insulin by pancreatic _____ cells
  • inhibits ________ secretion, delays ________ emptying, increases ___________
A
  • synthetic analog of human AMYLIN
  • Co-secreted /c insulin by pancreatic BETA cells
  • inhibits GLUCAGON secretion, delays GASTRIC emptying, increases SATIETY
71
Q

Pramlintide (Symlin) — Efficacy

  • A1C _________ 0/4 - 0/7%
  • Weight __________ 1.5 kg
A
  • A1C DECREASES 0/4 - 0/7%

- Weight DECREASES 1.5 kg

72
Q

Pramlintide (Symlin) — Advantages

- Decreases __________ and _________

A
  • Decreases APPETITE and WEIGHT
73
Q

Pramlintide (Symlin) — Disadvantages

  • Modest A1C __________
  • Risk for severe ____________ — must decrease insulin dose by _____% when initiating
  • Adverse effects: ________, ___________, and ________ (decrease over time)
A
  • Modest A1C DECREASE
  • Risk for severe HYPOGLYCEMIA — must decrease insulin dose by 50% when initiating
  • Adverse effects: NAUSEA, VOMITING, and ANOREXIA (decrease over time)

Pharmacology (10 decks)

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