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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
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?
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 ↑
26
What are the Sx of Hyperglycemia (HCH2O)?
* 3 P's * polyuria and polyphagia → polyuria * eating and peeing a lot in response to ↑ [glucose] * nocturia * lethargy * blurred vision * weight loss * ↓ wound healing
27
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?
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
28
1. How does comsuming CH2O affect plasma [glucose]? 2. What are the nml hormonal actions of insulin?
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*
29
1. What is the ADA treatment goal and target? 2. What is the more stringent target? 3. What is the less stringent target?
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
30
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?
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
31
What are the names of the available GLP-1 agonists?
* -glutide and -atide * exenatide (Byetta), LA form (Bydureon) * lixisenatide (Adlyxin) * liraglutide (Victoza) * dulaglutide (Trulicity) * albiglutide (Tanzeum) * semaglutide (Ozempic) * oral form (Rybelsus)
32
1. What are the diet lifestyle modifications for DM? 2. What are the exercise lifestyle modifications for DM?
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
33
What are the contraindications for GLP-1 agonists?
* DM 1 * severe GI dz * CrCl \< 30 ml/min \*\*Ø contraindication but avoid if any Hx of thyroid tumors\*\*
34
1. What are the ADRs for sulfoynlureas? 2. What are some clinical pearls when using SFUs?
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
35
What are the DPP-4 ADRs?
* HA * nasopharyngitis * works in pancreas so can → pancreatitis * urticaria and/or facial edema * joint pain
36
What are some clinical pearls r/t amylinomimetics?
* 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
37
1. What are the meglitinide ADRs? 2. What are some clinical pearls r/t meglitinides?
1. HoCH2O and weight ↑ 2. _Pearls_: * take before meals * insulin secretion ↑ w/ meal ingestion * if meal skipped, skip Rx
38
What is the pharm definition of Diabetes mellitus and what two conditions is it the leading cause of?
* 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
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
1. ↑ cardioprotection and fxn 2. ↓ glucose production 3. ↓ gastric emptying 4. ↑ insulin and ↓ glucagon secretion 5. ↑ neuroprotection ↓ appetite 6. ↑ glucose uptake and storage
40
1. What benefit has GLP-1 agonists been proven to have? 2. What is the overall efficacy of GLP-1 agonists?
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
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
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
What are some wellness prevention key points for DM?
* 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
What are the risk factors for the **pathology** of DM or metabolic syndrome?
* Hx of CVD * HTN * lipid disorders * prediabetes
44
What is the classification of type 2 DM?
* progressive insulin secretory defect with a background of insulin resistance * accounts for almost 90% of DM cases * more common in women vs men
45
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?
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
What criteria predicts ↑ efficacy for sulfonylureas?
* 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
What is the MoA for DPP-4 inhibitors?
* inhibits DPP-4 activity * ↑ insulin secretion * ↓ glucagon secretion
48
What are some clinical pearls associated with metformin use?
* 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
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?
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
What are the ADRs for SGLT-2 inhibitors?
* ↑ occurance of UTI (lower tract) * pyelonephritis if Ø treated, so aggressive ABX thpy * ↑ occurance of genital fungal infxn (men and women)
51
What are the 3 main characteristics that differentiate types of insulin?
* 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
What is the MoA of the GLP-1 receptor agonists?
* ↑ insulin secretion * ↓ glucagon secretion * slows absorption of food from GI tract * ↑ satiety
53
1. What is α-glucosidase? 2. What are the advantages of the α-glucosidase inhibitors?
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
1. What are the contraindications to TZD use? 2. What are some clinical pearls r/t TZDs?
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
What is LADA and what is its classification?
* 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
What are the insulin dosing and adjustment goals for DM 2 insulin therapies
* A1c \< 7% * Fasting plasma glucose: 70-130 mg/dL * 2 hr PP glucose \< 180 mg/dL
57
What are some clinical pearls r/t GLP-1 agonists?
* 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
1. What are the long acting insulins that are currently used? * What are their onset, peak, durations?
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
What are some precautions/warnings r/t SGLT-2 inhibitors?
* 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
What are the two types of non-insulin injectable medications?
* incretin mimetics → GLP-1 agonists * DM 2 only * amylinomimetics * both types
61
1. What class/group of Rx are pioglitazone (Actos) and rosiglitazone (Avandia)? 2. What is the MoA of these Rx?
1. thiazolidinediones (TZD) are insulin sensitizers 2. _MoA_: * ↑ periph insulin sensitivity * ↓ hepatic glucose prod
62
1. What are the ADRs for α-glucosidase inhibitors? 2. What are some clinical pearls?
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
What are the names of the 2nd generation sulfonylureas (SFU)? *\*\*Don't need to know 1st gen\*\**
* glyburide (Micronase, Glynase, Diabeta) * glipizide (glucotrol, glucotrol XL) * glimepiride (Amaryl)
64
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?
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
What are the advantages of meglitinides vs SFUs?
* ↓ risk of HoCH2O * can skip the dose if meal is missed * less weight gain * no dosage adjust w/ renal insuff
66
What is the classification for gestational DM (GDM)?
* 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
Who should not be on α-glucosidase inhibitors?
* any disorder that weakens the bowel structure (i.e. IBD) * bowel digestive abnormalities → ↑ pressure → colonic rupture * cirrhosis * CrCl \< 25 ml/min
68
1. What is the MoA of the sulfonylureas 2. When would there be no point in using SFU?
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
What are the three medically relevant HoCH2O levels and what do they mean?
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
What is the classification of DM 1?
* type 1 is an immune mediated or idiopathic β-cell destruction * → absolute insulin deficiency * only accounts for about 5% of DM cases
71
1. What is HgbA1c 2. How is it clinically relevant to DM 2 Dx?
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
What is the treatment for Level 1 HoCH2O?
* 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
1. What is amylin? 2. What is an incretin?
1. hormone in your body that delays gastric emptying 2. anything that binds to GLP-1 receptor, sits on it, and stimulates it
74
What are some potential causes of HoCH2O
* ↓ caloric intake, delayed or skipped meals * too much insulin or other DM meds * ↑ exercise
75
1. What is newest FDA approved glucagon rescue Rx? * Basic usage and steps?
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
1. What is the overall efficacy of sulfonylureas? 2. How are SFUs used?
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
What are some advantages of Metformin?
* no weight gain (weight neutral) * minimal HoCH2O risk in combo * almost 0% risk in monotherapy * low cost
78
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?
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
What are the risk factors for DM 2?
* 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
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?
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
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
1. 30-50 mg/dL 2. 5 units; 5-20%
82
What are the indications for amylinomimetics?
* adjunct therapy for post-prandial glucose control * Ø mono * in DM 1 and DM 2 patients who use mealtime insulin w/ poor control
83
1. What is the MoA and DoA of meglitinides? 2. How is this different from other drugs of this class?
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
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?
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
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?
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
What are some ADRs for metformin?
* GI upset * metallic taste * lactic acidosis (BBox warning)
87
What are the ADRs for GLP-1 agonists?
* 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
What is DPP-4 and what do DPP-4 inhibitors do?
* Fighting body's attempt to raise BGL * DPP-4 inhibition → ↑ GLP-1 → ↓ BLG * → ↑ insulin secretion and → ↓ glucagon secretion
89
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?
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
Why do we no longer use combo insulins as our means of glucose control?
* better insulins available * difficulty to predict meals later in the day * huge HoCH2O * crappy glucose control
91
What are the DPP-4 inhibitor agents?
* silagliptin (Januvia) * saxagliptin (Onglyza) * linagliptin (Tradjenta) * Alogliptin (Nesina)
92
What are the ADA goals to achieve more efficient insulin control regiments and result in overall ↓ A1c?
* 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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