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Karboski's Pharmacology - UT AEMSN > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What do insulin secretagogues do?

A

Rx that act to ↑ the secretion of insulin

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2
Q
  1. What class of Rx is metformin (Glucophage)?
  2. What is the MoA
A
  1. insulin sensitizer
  2. MoA:
    • ↓ hepatic glucose production
    • ↑ GLP-1 secretion
    • ↑ glucose uptake by liver and skeletal muscle
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3
Q

What are some clinical pearls r/t DPP-4 inhibitors?

A
  • weight neutral
  • causes insulin secretion but unlikely to → HoC2O by itself
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4
Q
  1. What two agents are α-glucosidase inhibitors?
  2. What is the MoA of these agents?
  3. What is the overall efficacy?
A
  1. Agents:
    • acarbose (Precose)
    • miglitol (glyset)
  2. slows intestinal CH2O digestion and absorption
  3. very low efficacy
    • A1c ↓ by 0.3 - 1%
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5
Q

What is the general (not specific #’s) ranking of oral anti-HCH2O efficacy?

A
  • sulfonylureas and metformin best
  • TZDs then meglitinides
  • DPP-4 inhibitors
  • at the bottom are α-glucosidase inhibitors and SGLT2 inhibitors
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6
Q

What are the contraindications for Metformin use?

A
  • ↓ kidney fxn
    • eGFR < 30 ml/min
      • CrCl or MDRD
  • Before and 48 hr s/p IV contrast
  • breastfeeding
  • chronic EtOH abuse
    • potentiates lactic acid prod

**Almost all contraindications involve preventing lactic acidosis**

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7
Q

What are the steps to take when reviewing glucose logs for the purpose of insulin dosing adjustments?

Some clinical pearls?

A
  1. Check pattern (use avg) of HoCH2O
  2. Is FBGL (prebreakfast) at goal
    • tells us if long acting insulin is working
    • Somogyi vs Dawn
  3. Is premeal glucose at goal?
  4. Correct earliest values that are abnormal (not highest)

Pearls:

  • correct 1 insulin at a time
  • assess patterns and averages
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8
Q
  1. What are the advantages to using TZDs?
  2. What are the ADRs?
A
  1. Advantages:
    • low HoCH2O risk
    • positive lipid effects
      • ↑ HDL and ↓ TRG
  2. ADRs:
    • edema, weight ↑
      • CV risk r/t excess fluid
    • risk of fracture ↑
      • mostly women, hands/feet
    • may induce ovulation
    • other possible risks
      • bladder CA (family risk/Hx?)
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9
Q
  1. What is the overall efficacy of SGLT-2 inhibitors?
  2. What are the advantages of these Rx?
A
  1. slightly more effectiveness than α-glucosidase inhibitors
    1. 0.5%-1% vs 0.3%-1%
  2. Advantages:
    • ↓ CV M/M AND lower A1c at the same time
    • VERY low risk of HoCH2O
      • Ø risk as monotherapy
    • weight ↓
    • ↓ blood pressure
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10
Q
  1. What is metformin’s overall efficacy?
  2. What is it indicated for?
A
  1. ↓ A1c by 1.5 - 2%
    • overall great efficacy
  2. indications:
    • monotherapy w/ diet
    • in combo with other Rx
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11
Q

At approx what % β-cell mass remaining do we start to see DM Sx?

A

Sx start to present when approx 10-15% β-cell mass remains in the pancreas

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12
Q
  1. What are preventative measures for nephropathy, retinopathy?
  2. What are preventative measures for neuropathy and diabetic foot infections?
A
  1. glycemic control and blood pressure control
  2. glycemic control, annual foot exams, daily self-foot checks, and diabetic shoes
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13
Q

What are the diagnostic criteria for DM?

A
  • Any ONE of the following:
    • A1c ≥ 6.5%
    • FBG ≥ 126 mg/dL (Ø calorie intake > 8hrs)
      • 126 mg/dL = 7 mmol/L
    • 2 hr plasma glucose ≥ 200 during a 75g OGTT
    • Random BG ≥ 200 mg/dL AND classic Sx of HCH2O or hyperglycemic crisis
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14
Q

What are the complications of DM?

A
  • hypoglycemia (HoCH2O)
  • microvascular
    • nephro-, retino-, neuropathy
  • macrovascular
    • coronary heart dz
    • cerebrovasc dz
    • periph vasc dz
  • diabetic foot infxns
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15
Q
  1. What is the overall efficacy of meglitinides?
  2. What are the indications for their use?
A
  1. Less effective than SFUs and insulin sensitizers
    • approx 1%
  2. indications:
    • monotherapy w/ diet
    • combo therapy with metformin or TZDs
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16
Q

What is the patho of DM2/progressive insulin resistance on:

  1. The Liver
  2. The Muscles
  3. Fat
A
  1. Cont to secrete glucose w/out food intake
  2. insulin action ↓ or delayed that → slower glucose uptake of cells
  3. ↑ plasma [glucose] → ↑ fat stores
    • → insulin resistance and impaired insulin secretion
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17
Q
  1. Which organs/tissues are non-insulin-dependent and how much glucose disposal does this account for?
  2. Which organs/tissues are insulin dependent and how much glucose disposal does this account for?
A
  1. Brain, liver, and other GI tissues
    • Approx 75% of total glucose disposal
  2. Muscle tissue
    • Approx 25% of total glucose disposal
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18
Q

What are the contraindications for SGLT-2 inbihitor use?

A
  • renal impairment
    • GFR < 30-60 ml/min (depending on agent used)
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19
Q

What are the ADRs for amylinomimetics?

A
  • LOTS of GI SE
    • nausea (everyone gets it no matter)
    • vomiting, anorexia
    • dose titration limited by nausea
  • insulin-induced HoCH2O
    • Ø by itself, but w/ insulin can make it worse
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20
Q
  1. What is the name only current amylinomimetic?
  2. What is the MoA of an amylinomimetic?
  3. What is its overall efficacy?
A
  1. pramlintide (Symlin)
  2. amylin analog
    • ↓ gastric emptying that → satiety
  3. ↓ A1c about the same as GLP-1 agonists and SGLT-2 inhibitors (0.5-1% ↓)
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21
Q
  1. What is the efficacy of the TZDs?
  2. What are their indications?
  3. Why are these Rx not used as much?
A
  1. ↓ A1c by 1.5% (good to moderate)
  2. monotherapy and combination
  3. A lot more SE vs other options
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22
Q
  1. What class of drugs are meglitinides?
  2. What are the names of the drugs in this group?
A
  1. secretegouges
  2. Agents:
    • repaglinide (Prandin)
    • nateglinide (Starlix)
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23
Q
  1. What are the SGLT-2 inhibitor agents?
  2. What is the MoA of this group of Rx?
A
  1. Agents: “the -gliflozin’s”
    • canagliflozin
    • dapagliflozin
    • empagliflozin
    • ertugliflozin
  2. MoA: (↑ the peeing out of glucose)
    • inhib SGLT-2 in prox renal tubules
      • ↓ reabsorption of glucose
      • ↑ urinary glucose excretion and ↓ plasma [glucose]
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24
Q
  1. What benefit does bolus insulin provide?
  2. What forms of insulin do we use to simulate bolus insulin?
  3. Appox what % of total daily dose does bolus insulin represent?
A
  1. ↓ post-prandial glucose
  2. rapid or short-acting insulins
  3. approx 50% of TDD
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25
Q
  1. What is insulin and what does it do?
  2. Why do we give exogenous insulin?
  3. What are the two main ADRs of insulin?
A
  1. anabolic and anticatabolic hormone w/ major role in protein, CH2O, and fat metabolism
    • binds to cell to allow glucose to enter
  2. Given to ↓ HCH2O in Pt w/ DM
    • given to all DM 1, eventually to most DM 2
  3. HoCH2O and weight ↑
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26
Q

What are the Sx of Hyperglycemia (HCH2O)?

A
  • 3 P’s
    • polyuria and polyphagia → polyuria
    • eating and peeing a lot in response to ↑ [glucose]
  • nocturia
  • lethargy
  • blurred vision
  • weight loss
  • ↓ wound healing
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27
Q
  1. What are the 3 types of rapid acting insulins
    • What are their onset, peak, and duration
  2. What is the benefit of using rapid acting insulin over other types?
A
  1. lispro (Humalog), glulisine (Apidra), aspart (Novalog)
    • onset: 15-30 mins for all
    • peak: 1-2 hr for all
    • duration:
      • 3-4 hr (lispro and glulisine)
      • 3-5 hr (aspart)
  2. Better mealtime control of CH2O load
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28
Q
  1. How does comsuming CH2O affect plasma [glucose]?
  2. What are the nml hormonal actions of insulin?
A
  1. ↑ plasma [glucose]
  2. inslulin from β-cells:
    1. ↓ hepatic glucose prod
      • no need to make more glucose
    2. ↑ glucose uptake by periph tissue
      • gotta use what we just ate
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29
Q
  1. What is the ADA treatment goal and target?
  2. What is the more stringent target?
  3. What is the less stringent target?
A
  1. Glycemic control and A1c < 7%
  2. < 6.5% if
    • can w/out significant HoCH2O
  3. < 8% if
    • labile HoCH2O or unawareness
    • limited life expectancy
    • advanced DM complications
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30
Q
  1. What is the definition of HoCH2O?
  2. What are the Sx of HoCH2O?
  3. What is more important than knowing the list of Sx?
A
  1. BGL < 70 mg/dL
  2. Symptoms:
    • dizzy, shaky, fatigue, sweaty, anxious, irritable
    • HA, tachycardia, pale skin
    • confusion, seizure
  3. That ppl know their HoCH2O Sx b/c no all have the same Sx
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31
Q

What are the names of the available GLP-1 agonists?

A
  • -glutide and -atide
    • exenatide (Byetta), LA form (Bydureon)
    • lixisenatide (Adlyxin)
    • liraglutide (Victoza)
    • dulaglutide (Trulicity)
    • albiglutide (Tanzeum)
    • semaglutide (Ozempic)
      • oral form (Rybelsus)
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32
Q
  1. What are the diet lifestyle modifications for DM?
  2. What are the exercise lifestyle modifications for DM?
A
  1. Diet:
    • moderate CH2O intake
    • sat fat < 7%
    • calorie restrictions in DM 2 to ↓ weight
  2. Exercise:
    • 150 min/wk of mod aerobic
    • x2/wk of resistance training
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33
Q

What are the contraindications for GLP-1 agonists?

A
  • DM 1
  • severe GI dz
  • CrCl < 30 ml/min

**Ø contraindication but avoid if any Hx of thyroid tumors**

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34
Q
  1. What are the ADRs for sulfoynlureas?
  2. What are some clinical pearls when using SFUs?
A
  1. ADRs:
    • HoCH2O
    • weight ↑
    • less common: rash, GI upset
    • disulfiram rxn (Antabuse)
  2. Pearls:
    • take in AM before meals (SFUs are long acting)
    • longer the DM Hx = ↓ effectiveness
    • consistent meals to avoid HoCH2O
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35
Q

What are the DPP-4 ADRs?

A
  • HA
  • nasopharyngitis
  • works in pancreas so can → pancreatitis
  • urticaria and/or facial edema
  • joint pain
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36
Q

What are some clinical pearls r/t amylinomimetics?

A
  • inject right before meal
  • GI SE ↓ over time
  • avoid in Pts with:
    • slow gut (gastroparesis)
    • slow brain (HoCH2O unawareness)
  • ↓ short-acting insulin by 50% before starting
    • if you don’t cause dangerous HoCH2O
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37
Q
  1. What are the meglitinide ADRs?
  2. What are some clinical pearls r/t meglitinides?
A
  1. HoCH2O and weight ↑
  2. Pearls:
    • take before meals
    • insulin secretion ↑ w/ meal ingestion
    • if meal skipped, skip Rx
38
Q

What is the pharm definition of Diabetes mellitus and what two conditions is it the leading cause of?

A
  • A metabolic disorder characterized by hyperglycemia that is associated with abnormalities in CH2O, fat, and protein metabolism
  • Leading cause of blindness and kidney failure
39
Q

What are some of the effects of GLP-1 stimulation on:

  1. heart
  2. liver
  3. stomach
  4. pancreas
  5. brain
  6. adipose and muscle tissue
A
  1. ↑ cardioprotection and fxn
  2. ↓ glucose production
  3. ↓ gastric emptying
  4. ↑ insulin and ↓ glucagon secretion
  5. ↑ neuroprotection ↓ appetite
  6. ↑ glucose uptake and storage
40
Q
  1. What benefit has GLP-1 agonists been proven to have?
  2. What is the overall efficacy of GLP-1 agonists?
A
  1. Have been shown to ↓ cardiovascular M/M
    • Ø the case for all Rx of this class
    • oral form of semaglutide Ø proven to ↓ CV M/M
  2. mild to moderate ↓ A1c
    • same as SGLT-2 inhib (0.5-1% ↓)
41
Q

If a Pt is on maximum dose of first line interventions what drugs of choice are recommended for each of the following co-occuring conditions?

  • ASCVD
  • HF/CKD
  • HoCH2O risk
  • Need Weight ↓
  • Cost Issues
A
  1. CKD/HF or ASCVD
    • ASCVD → SGLT-2 IH or GLP-1 RA
    • CKD/HF → SGLT-2 IH
  2. HoCH2O issues
    • DPP-4, GLP-1 RA, SGLT-2 IH, TZD
  3. Need weight loss
    • GLP-1 RA or SGLT-2 IH
  4. Cost issues
    • SFU or TZD
42
Q

What are some wellness prevention key points for DM?

A
  • Ø smoking
  • daily ASA
  • regular check ups
    • dental
    • podiatry - shoes, foot care
    • opthalmology
  • immunizations up-to-date
    • annual flu (COVID ?)
    • pneumococcal x1 + x1 > 65yo
    • Hep B
43
Q

What are the risk factors for the pathology of DM or metabolic syndrome?

A
  • Hx of CVD
  • HTN
  • lipid disorders
  • prediabetes
44
Q

What is the classification of type 2 DM?

A
  • progressive insulin secretory defect with a background of insulin resistance
  • accounts for almost 90% of DM cases
  • more common in women vs men
45
Q
  1. What is the initial basal insulin dose for DM 2 Pt already on metformin or another non-insulin agent?
  2. How/when do we adjust the dose?
  3. How do we adjust for HoCH2O
  4. What do we use to determine how well they’re doing?
A
  1. start 10 U/day or 0.1 - 0.2 U/kg/day
  2. adjust 10-15% or 2-4 units once or twice/wk to → FBG target
  3. look for cause and address
    • Ø find or no real cause → ↓ by 10-20% or 4 units
  4. Intermitent BGL (finger sticks)
46
Q

What criteria predicts ↑ efficacy for sulfonylureas?

A
  • Any indication that the pancreas is still making enough insulin by itself that the added boost will help
    • diabetes duration < 5 yrs
    • Ø prev insulin thpy OR good control on < 40 U/day
    • initial FPG ≤ 200 mg/dL
47
Q

What is the MoA for DPP-4 inhibitors?

A
  • inhibits DPP-4 activity
    • ↑ insulin secretion
    • ↓ glucagon secretion
48
Q

What are some clinical pearls associated with metformin use?

A
  • Take w/ food → ↓ GI upset
  • metformin → B12 deficiency, suppl as needed
  • weekly titration to max dose
    • ↑ by 500 mg/wk
    • max dose 2000 mg/day
  • if using XR, give w/ PM meal
49
Q
  1. What naming convention differentiates intermediate acting insulins from other types?
    • What is the onset, peak and duration of this type of insulin?
  2. In what Pt population are we using intermediate acting insulins today?
A
  1. The brand names all have an “N” at the end and there is only one generic NPH
    • onset: 2-4 hr
    • peak: 4-8 hr
    • duration: 8-12 hr
  2. In patients that can’t afford long-acting insulins by using more smaller doses of NPH
50
Q

What are the ADRs for SGLT-2 inhibitors?

A
  • ↑ occurance of UTI (lower tract)
    • pyelonephritis if Ø treated, so aggressive ABX thpy
  • ↑ occurance of genital fungal infxn (men and women)
51
Q

What are the 3 main characteristics that differentiate types of insulin?

A
  • Onset
    • length of time it take to enter blood and start ↓ blood glucose
  • Peak
    • time to get to max blood glucose ↓-ing strength
  • Duration
    • how long it lowers blood glucose
52
Q

What is the MoA of the GLP-1 receptor agonists?

A
  • ↑ insulin secretion
  • ↓ glucagon secretion
  • slows absorption of food from GI tract
  • ↑ satiety
53
Q
  1. What is α-glucosidase?
  2. What are the advantages of the α-glucosidase inhibitors?
A
  1. An enzyme in your gut that breaks down complex CH2O so your intestine can absorb them as glucose
  2. Advantages:
    • focuses on PP glucose
    • weight neutral
    • no HoCH2O
    • better timing with meals (w/ 1st bite of food)
54
Q
  1. What are the contraindications to TZD use?
  2. What are some clinical pearls r/t TZDs?
A
  1. Contraindications:
    • NYHA Class 3-4 d/t vol
    • Active hepatic dz
      • ALT ≥ 2.5x ULN
    • Pregnancy/breastfeeding
  2. Pearls:
    • max glycemic lowering Ø seen until 3-4 mo
    • warn perimenopausal women about possible ovulation
    • metformin used unless they have a contraindication
55
Q

What is LADA and what is its classification?

A
  • Latent Autoimmune Diabetes in Adults (aka type 1.5)
  • autoimmune component like DM 1
  • Sx and age of onset like DM 2
  • prolly 1/4 of DM 2 may be LADA
56
Q

What are the insulin dosing and adjustment goals for DM 2 insulin therapies

A
  • A1c < 7%
  • Fasting plasma glucose: 70-130 mg/dL
  • 2 hr PP glucose < 180 mg/dL
57
Q

What are some clinical pearls r/t GLP-1 agonists?

A
  • weight ↓
  • ↑ β-cell fxn
  • exentatide must be admin w/in 60 mins prior to meal
  • liraglutide and exentatide ER may be given regardless of meals
58
Q
  1. What are the long acting insulins that are currently used?
    • What are their onset, peak, durations?
A
  1. determir (Levemir), glargine (Lantus), degludec (Tresiba)
    • onset/duration
      • determir → 2 hr / 14-24 hr
      • glargine → 4-5 hr / 22-24 hr
      • degludec → 1.5 hr / > 24 hr
    • peak: none for all
59
Q

What are some precautions/warnings r/t SGLT-2 inhibitors?

A
  • statistically significant ↑ in amputations
    • must ↑ DM foot awareness/prevention
  • Conditions r/t Δ fluid volume
    • HoTN (if suceptible)
    • dehydration
  • ↑ Scr
  • Euglycemic ketoacidosis
    • routine keto urine eval
60
Q

What are the two types of non-insulin injectable medications?

A
  • incretin mimetics → GLP-1 agonists
    • DM 2 only
  • amylinomimetics
    • both types
61
Q
  1. What class/group of Rx are pioglitazone (Actos) and rosiglitazone (Avandia)?
  2. What is the MoA of these Rx?
A
  1. thiazolidinediones (TZD) are insulin sensitizers
  2. MoA:
    • ↑ periph insulin sensitivity
    • ↓ hepatic glucose prod
62
Q
  1. What are the ADRs for α-glucosidase inhibitors?
  2. What are some clinical pearls?
A
  1. GI side effects - flatulence, diarrhea, ABD cramping
    • Ø beer
  2. Pearls:
    • give w/ 1st bite of food
    • treat HoCH2O w/ disaccharide or monosaccharide
      • small molecule or already broken down
63
Q

What are the names of the 2nd generation sulfonylureas (SFU)?

**Don’t need to know 1st gen**

A
  • glyburide (Micronase, Glynase, Diabeta)
  • glipizide (glucotrol, glucotrol XL)
  • glimepiride (Amaryl)
64
Q
  1. What benefit does basal insulin provide?
  2. What forms of insulin do we use to simulate basal insulin?
  3. About how much of daily dose does basal insulin represent?
A
  1. provides consistent insulin level to ↓ BGL through night and btw meals and it ↓ FBG levels
  2. intermediate and long-acting insulins
  3. approx 50% of TDD
65
Q

What are the advantages of meglitinides vs SFUs?

A
  • ↓ risk of HoCH2O
  • can skip the dose if meal is missed
  • less weight gain
  • no dosage adjust w/ renal insuff
66
Q

What is the classification for gestational DM (GDM)?

A
  • DM dx during pregnancy that is clearly Ø overt DM
  • occurs approx 7% of preg
  • most return to nml s/p preg
  • 30-50% will develop DM 2 or glucose intol
67
Q

Who should not be on α-glucosidase inhibitors?

A
  • any disorder that weakens the bowel structure (i.e. IBD)
    • bowel digestive abnormalities → ↑ pressure → colonic rupture
  • cirrhosis
  • CrCl < 25 ml/min
68
Q
  1. What is the MoA of the sulfonylureas
  2. When would there be no point in using SFU?
A
  1. binds to receptor on pancreas to stimulate 2nd phase insulin release
    • 2nd phase serves to normalize BGL from b/d of complex CH2O
  2. No point in using sulfonylureas in DM 1 b/c they can’t produce insulin
    • DM 2 has Ø phase 1 but has longer phase 2
69
Q

What are the three medically relevant HoCH2O levels and what do they mean?

A
  1. ≤ 70 mg/dL (3.9 mmol/L) → needs CH2O and dose adjustment
  2. < 54 mg/dL → clinically important HoCH2O
  3. Severe cognitive impairment (no threshold)
    • b/c baseline levels are important
70
Q

What is the classification of DM 1?

A
  • type 1 is an immune mediated or idiopathic β-cell destruction
  • → absolute insulin deficiency
  • only accounts for about 5% of DM cases
71
Q
  1. What is HgbA1c
  2. How is it clinically relevant to DM 2 Dx?
A
  1. Glycosylated A1c
    • glucose irreversibly bound to RBC in relation to serum [glucose] for life of RBC
  2. Tells us about avg BGL for 2-3 mo period
    • no better indicator of long-term M/M in DM 2
    • PO Rx therapy driven by A1c
72
Q

What is the treatment for Level 1 HoCH2O?

A
  • eat 15-20 grams of glucose
    • not diet…duh
  • recheck via self-monitored blood glucose (SMBG) in 15 mins
  • eat something once SMBG level is nml
    • prevents reoccurance
73
Q
  1. What is amylin?
  2. What is an incretin?
A
  1. hormone in your body that delays gastric emptying
  2. anything that binds to GLP-1 receptor, sits on it, and stimulates it
74
Q

What are some potential causes of HoCH2O

A
  • ↓ caloric intake, delayed or skipped meals
  • too much insulin or other DM meds
  • ↑ exercise
75
Q
  1. What is newest FDA approved glucagon rescue Rx?
    • Basic usage and steps?
A
  1. Glucagon Nasal Powder (Baqsimi) is a 3 mg single use nasal powder
    • keep plastic wrap on until its used
    • Instill into single nostril, Ø inhale
      • push all the way to the green line
    • call 911 after using
    • can do 2nd dose after 15 mins if Ø response
      • either IM or nasal powder
    • can use if Pt has nasal congestion or rhinorrhea
76
Q
  1. What is the overall efficacy of sulfonylureas?
  2. How are SFUs used?
A
  1. ↓ A1c about the same as metformin (1.5 - 2%)
  2. Uses:
    • monotherapy w/ diet
    • combo with:
      • metformin, acarbose, miglitol, TZDs, bedtime insulin
    • Ø used in combo w/ meglitinides (both secretagogues)
77
Q

What are some advantages of Metformin?

A
  • no weight gain (weight neutral)
  • minimal HoCH2O risk in combo
    • almost 0% risk in monotherapy
  • low cost
78
Q
  1. What is the standard treatment for Level 2 or 3 HoCH2O?
  2. What form does it come in and why?
  3. Where is it administered?
A
  1. 1 mg (1 unit) glucagon injections
  2. dry powder form b/c solution is not very stable
  3. IM injection is gluteal or thigh muscles
79
Q

What are the risk factors for DM 2?

A
  • obesity - BMI ≥ 25 mg/m2
  • had baby > 9lbs or Dx of GDM
  • physical inactivity
  • 1° relative w/ DM
  • high risk ethnicity
    • pretty much everyone except white people, not joking
80
Q
  1. What naming convention differentiates regular insulin from other types?
    • What is the onset, peak and duration?
  2. What is the issue with the onset time?
A
  1. All regular insulin brand names have an “R” after them
    • Onset: 0.5 - 1 hr
    • Peak: 2-3 hr
    • Duration: 4-6 hr
  2. There is a ↑ disconnect btw time of admin and intake of food OR hard to match insulin to CH2O load
81
Q
  1. Increasing rapid/short acting insulin by 1-2 units will lower BGL by about __________ mg/dL?
  2. Do not change any insulin by more than _________ units or _________ of TDD
A
  1. 30-50 mg/dL
  2. 5 units; 5-20%
82
Q

What are the indications for amylinomimetics?

A
  • adjunct therapy for post-prandial glucose control
    • Ø mono
  • in DM 1 and DM 2 patients who use mealtime insulin w/ poor control
83
Q
  1. What is the MoA and DoA of meglitinides?
  2. How is this different from other drugs of this class?
A
  1. stim glucose-dependent release of insulin and has a DoA of only 2-4 hrs
  2. Amount of insulin secreted depends on how much glucose present
    • Ø eating → low insulin release vs eating → large insulin release
84
Q
  1. What are the types of insulin pens available?
  2. What are some benefits to insulin pens?
  3. What are some cons to insulin pens?
A
  1. Types:
    • disposable
    • replaceable cartridges
  2. Benefits:
    • more accurate dosing
    • faster and easier
    • more discreet
    • ↑ compliance
  3. Cons:
    • Ø all insulin types available
    • can’t mix insulins
    • $$
85
Q
  1. What is the Somogyi Effect?
    • How does this affect basal insulin admin?
    • How do we r/o Somogyi Effect?
  2. What is Dawn Phenomenon?
    • How does this affect basal insulin admin?
    • What should you rule out first?
A
  1. noctunral HoCH2O → stim of counter-regulatory hormones that markedly raises FBGL in the AM before 1st meal
    • means we need to give LESS PM basal
    • r/o by checking 3AM BGL
  2. reduced insulin sensitivity btw 5AM - 8AM
    • need to give MORE basal insulin
    • need to r/o Somogyi first before giving more basal
86
Q

What are some ADRs for metformin?

A
  • GI upset
  • metallic taste
  • lactic acidosis (BBox warning)
87
Q

What are the ADRs for GLP-1 agonists?

A
  • GI: N/V/D
    • ↓ w/ time and cont use
  • HoCH2O is possible
  • acute pancreatitis
  • thyroid tumors in rats
    • liraglutide, ER form
    • so → Ø GLP-1 agonists if fam Hx of thyroid tumors
88
Q

What is DPP-4 and what do DPP-4 inhibitors do?

A
  • Fighting body’s attempt to raise BGL
  • DPP-4 inhibition → ↑ GLP-1 → ↓ BLG
    • → ↑ insulin secretion and → ↓ glucagon secretion
89
Q
  1. What is the first line intervention for Pts with A1c > target goal?
  2. What criteria must be met to move to 2nd line agents?
A
  1. first Rx of choice = metformin + lifestyle modifications
  2. If A1c > target and on max metformin + LS mods then proceed to 2nd line agents
90
Q

Why do we no longer use combo insulins as our means of glucose control?

A
  • better insulins available
  • difficulty to predict meals later in the day
    • huge HoCH2O
    • crappy glucose control
91
Q

What are the DPP-4 inhibitor agents?

A
  • silagliptin (Januvia)
  • saxagliptin (Onglyza)
  • linagliptin (Tradjenta)
  • Alogliptin (Nesina)
92
Q

What are the ADA goals to achieve more efficient insulin control regiments and result in overall ↓ A1c?

A
  • fasting plasma glucose: 80-130 mg/dL
  • 2 hr PP glucose < 180 mg/dL
  • time in range (TIR) ≥ 70%
    • used with insulin pumps

Karboski's Pharmacology - UT AEMSN (11 decks)

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