Control of Blood Glucose and Drug Treatment of Diabetes Flashcards

1
Q

TYPE OF INSULIN:
USE:
RAPID ACTING
Humalog, Amelog* (insulin lispro)

A

Bolus dosing(meals) and insulin
pumps (administration ranges 5-15
minutes before meals –see specific
product information

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2
Q

TYPE OF INSULIN:
USE:
SHORT ACTING
Humulin R or Novolin R - Regular
insulin -

A

Bolus dosing(meals)
(administration ranges 15-30
minutes before meals –see specific
product information

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3
Q

TYPE OF INSULIN:
USE:
INTERMEDIATE-ACTING
Humulin N or Novolin N - NPH ~

A

Basal-like (administration Q day
to BID)

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4
Q

TYPE OF INSULIN:
USE:
ONG ACTING
Lantus, Basaglar* (insulin
glargine) – 100 units/mL
Toujeo (insulin glargine) – 300
unitls/mL
Levemir (insulin detemir) – dc
2024

A

Basal (administration Q day)

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5
Q

TYPE OF INSULIN:
USE:
ULTRA LONG ACTING
Tresiba (insulin degludec)

A

Basal (administration Q day,
anytime of day

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6
Q

— Glucose homeostasis:

A

balance between hepatic glucose
production and peripheral glucose uptake and utilization

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7
Q

— Glucose –

A

source of energy

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8
Q

— Insulin -

A

most important regulator of glucose/metabolic
equilibrium

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9
Q

— Pancreatic Islet Hormones (endocrine)
◦ Maintains — balance
◦ 4 types of peptide-secreting cells:

A

glucose

– Beta (B) – secrete insulin
– Alpha (A) – secrete glucagon
– Delta (D) – secrete somatostatin
– PP (also known as gamma) – secrete pancreatic polypeptide

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10
Q

Relationship between Glucose and Insulin

A

— Glucose is the main factor
controlling synthesis and
secretion of insulin

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11
Q

Two ways insulin is released:

A

◦ Steady basal release of insulin
◦ Response to increased glucose

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12
Q

About — of insulin stored in
the pancreas of an adult is
secreted daily

A

1/5

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13
Q

Glucose stimulated insulin secretion

A

— Glucose transported by glucose
transporter into beta cell
— Metabolism alters ion channel
(Ca 2+) activity leading to insulin
secretion
— Incretin hormones: glucagon-like
peptide 1 (GLP1) and glucose -
dependent insulinotropic
polypeptide (GIP) released by
cells in the small intestines after
food ingestion, stimulate insulin
secretion when the blood
glucose is above the fasting level

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14
Q

Diabetes Mellitus (DM)
— A group of complex chronic metabolic disorders
characterized by high blood glucose concentrations
(hyperglycemia)
(3)

A

◦ Insulin deficiency
◦ Often combined with insulin resistance
◦ Abnormalities in the metabolism of carbohydrates, proteins, fats
and insulin

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15
Q

Hyperglycemia due to:
(3)

A

◦ Uncontrolled hepatic glucose output
◦ Reduced uptake of glucose by skeletal muscle
◦ Reduced glycogen synthesis

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16
Q

Types of DM – Two Major Types
— Type 1 (T1DM)
(3)

A

◦ Absolute deficiency of insulin resulting from autoimmune destruction of pancreatic B
cells = insulin deficiency
◦ Commonly occurs in childhood and adolescence.
◦ Without insulin treatment patients will ultimately die of diabetic ketoacidosis

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17
Q

ypes of DM – Two Major Types
— Type 2 (T2DM)

A

◦ Hyperglycemia due to insulin resistance (proceeds overt disease) + progressive loss of
insulin secretion
◦ May have normal, increased (hyperinsulinemia) or decreased insulin levels due to
abnormal beta cell function
◦ Most commonly presents in adulthood and in obese patients
◦ Managed with diet, oral/subcutaneous (SC) antidiabetic agents and insulin SC
◦ Accounts for ~ 95% of individuals with diabetes > 30 years
◦ Alarming increases T2DM in obese children and adolescents
◦ Can be delayed or prevented with lifestyle modifications – diet, physical activity and
weight control

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18
Q
A
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19
Q

— Other forms

A

(e.g. gestational diabetes, medications - glucocorticoids)

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20
Q

CLINICAL PRESENTATION
* Symptoms may include (5)

A

polydipsia,
polyphagia, polyuria, nocturia, blurred
vision. (More common on type 1/
occurs in varying degree in Type 2
DM).

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21
Q
  • Type 1 DM often associated with
    (2)
A

weight loss, ketoacidosis (dehydration)

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22
Q
  • Majority of Type 2 patients are
    — and diagnosed by
    laboratory testing
A

asymptomatic

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23
Q

Screening for T2DM and Prediabetes in Asymptomatic
Patients

A

— The ADA’s guidelines recommend screening for prediabetes and
T2DM through an informal assessment of risk factors or with a
validated assessment tool to help physicians determine whether
a diagnostic test is appropriate for a patient.
— The guidelines provide an example of an approved assessment
tool: ADA’s Risk Test.

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24
Q

ADA’s Diabetes
Risk Test
Increasing aging
population and
numbers of

adolescents,
teenagers and
adults = rapid
increases in
prevalence

A

overweight

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25
Q

A1C =

A

Hemoglobin A1c.
Glucose binds
hemoglobin. The A1C is
a simple lab test that
shows the average
amount of glucose in a
person’s blood over the
last 3-4 months.

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26
Q

Complications —
Macrovascular
(3)
— Microvascular
(4)
— Strategic Risk
Reduction Strategies

A

◦ Brain
◦ Heart
◦ Extremities (peripheral
vascular disease)

◦ Eyes
◦ Kidney
◦ Nerves
– Peripheral
– Autonomic
◦ Periodontal disease

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27
Q

Glycemic Goals

A
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28
Q

Additional DM Goals – Risk Reduction Strategies
— Reduce the risk of (2)(and other)
complications through glycemic control and controlling co-morbid
conditions to which DM contributes

A

macrovascular and microvascular

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29
Q

Reduce cardiovascular risk factors
(3)

A

– Control BP
– Control lipids
– Smoking Cessations

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30
Q

◦ Reduce the risk of vaccine-preventable diseases
(1)

A

– Immunizations
– Examples: Flu, Tdap/Td, Pneumococcal, Hepatitis B (others)

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31
Q

— Minimize periodontal complications due to diabetes mellitus,
provide

A

safe and effective dental care and promote good oral
health

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32
Q

Non-pharmacologic therapy for DM
— Medical Nutrition Therapy
(4)

A

◦ Focus on carbohydrates for glycemic management
– Typically stay between 3-4 carbohydrate choices or 45-
60 grams of carbohydrate per meal
– Eat 3 meals or 5 smaller meals throughout day
– If numeracy skills are low, may use plate method

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33
Q

— Physical Activity
(5)

A

◦ Helps body regulate glucose and decreases insulin
resistance
◦ Lowers BP, cholesterol, stress, weight
◦ Amount
– 150 min of moderate-intensity spread over at least 3
days and no more than 2 consecutive days without
– Resistance training 2x per week

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34
Q

Insulin
— History of insulin in the treatment of diabetes = interesting
◦ Insulin destroyed in —
◦ Before insulin therapy Type I DM =
◦ Breakthrough in 1920’s when insulin was isolated
– Noble Prize = Banting and Best (University of Toronto)
◦ (2) sources
– Bovine - discontinued in US in1978
– Porcine manufactured in US until 2005
◦ Significant variability between batches
◦ Allergies – —

A

GI tract
death sentence (wasting and
dying from ketoacidosis)
Porcine or Bovine
immune response to animal-based products

35
Q

Current Insulin therapy

A

— Recombinant human insulin (made by recombinant
DNA-rDNA technology)
— Avoid batch variability and allergies from animal sources
— Modified amino acid sequences (insulin analogs)
provide rapid/short acting and long acting/basal
insulins
◦ Differences in timing to peak effect and duration
◦ Categorized by their onset or action

36
Q

Rapid-acting Insulin
— (3)

A

Rx only
— Appearance- clear/colorless
— rDNA – human insulin analogs

37
Q

Short-acting (Regular) Insulin
(3)

A

— Non-Rx – 100 units/ml (Humulin R U-500 - RX)
— Appearance- clear/colorless
— rDNA – human insulin analogs

38
Q

Inhaled Insulin - Afrezza
(8)

A

— Rapid acting insulin – given with meals
— Oral inhalation
— Amount of insulin delivered to lungs
depends on individual factors
— Dosing conversion from injected
insulin
— Contraindicated in chronic lung
disease (asthma/COPD)
— Not recommended in smokers
— Risk of bronchospasms and cough
— EXPENSIVE!

39
Q

Intermediate-acting (NPH)Insulin
(4)

A

— NPH - Neutral Protamine Hagedorn
— Non-Rx
— Appearance - cloudy
— rDNA – human isophane insulin suspension

40
Q

Long-acting Insulin
—(4)

A

Rx only
— Appearance – clear, colorless
— rDNA – human insulin analogs

41
Q

Ultra Long-acting Insulin
(3)

A

— Rx only
— Appearance – clear, colorless
— rDNA – human insulin analogs

42
Q

— NPH/Regular

A

◦ 70%/30%
◦ 50%/50%

43
Q

— Insulin aspart protamine suspension/ insulin aspart solution

A

— 70%/30%

44
Q

— Insulin degludec and insulin aspart injection

A

— Ryzodeg 70/30 ®

45
Q

— Insulin lispro protamine/insulin lispro

A

◦ 75%/25%

46
Q

— Insulin lispro protamine/insulin lispro

A

◦ 50%/50%

47
Q

— Actions of immediate/short and longer acting insulin combined
— Typically given pre-breakfast and pre-supper or pre-breakfast, lunch and supper.
— Disadvantages in dosing and individualizing therapy – more risk of —

A

hypoglycemia

48
Q
  • Reusable insulin pen–
  • Disposable insulin pens -
A

must load with insulin cartridges - sold separately

come filled with insulin and are thrown away
when empty

49
Q

Examples of Pens used in DM

A

— Apidra® SoloStar®, Humalog® KwikPen™, Humulin® Pen, Lantus® Solostar®,
Levemir® FlexPen®, NovoLog® Mix FlexPen®, NovoPen Junior®, AutoPen®

50
Q

Common Insulin Regimens
(2)

A

— Basal-bolus regimen (4 injections total/day)
◦ Mimic physiologic insulin release

51
Q

Rapid-acting/NPH
(2)

A

— 2 injections/day
◦ Rapid or regular insulin mix with NPH

52
Q

Continuous Insulin Infusion Pumps

A

— Growing use - primarily in T1DM
— Deliver exogenous insulin that more closely approximates the normal biologic
function and performance of the pancreas
◦ devices only use short- or rapid-acting acting insulin as basal insulin with
continuous delivery with bolus administration as needed
— Programed external pump - worn continuously
◦ Delivers insulin through a cannula inserted just beneath the surface of the skin
◦ One injection site for 72 hrs
— Many pumps have Continuous Glucose Monitoring (CGM) system integrated
within the pump or they can be used separately

53
Q

Continuous Insulin Infusion Pumps
— Advantages
(3)

A

◦ Improved glycemic control
◦ Decreased A1c
◦ Decreased risk of hypoglycemia

54
Q

Continuous Insulin Infusion Pumps
¾ Adverse Effects:

A
  • Pump failures – hyperglycemia or hypoglycemia
  • Mechanical failures
  • Blockages within the infusion set
  • Infusion site complications
  • Instability of the insulin stored within the pump
  • User error – usually the most common
  • Rates declining as technology improves
  • Importance of patient education
  • Infections at injection site, lipomas
  • More expensive than multiple daily injections

¾ Dental: Either Hypo- or Hyperglycemia may occur!
* If pt confused/unresponsive, always push “suspend” button immediately.
* Then check display to assess last glucose trend.

55
Q

Glucose Monitors and Continuous Glucose
Monitoring (CGM)
— Purpose:

A

to monitor blood glucose levels in patients with diabetes
— Safety and efficacy of insulin and other diabetic drugs

56
Q

— Blood Glucose Meters (many brands)

A

◦ Finger sticks – moment in time
◦ Self-monitoring of Blood Glucose (SMBG)
– Frequency of monitoring varies depending on type of diabetes and medications
– Occasional to Morning fasting, before meals, before exercise, etc.

57
Q

— Continuous Glucose Monitoring (CGM) – stand alone

A

◦ Compact medical systems that continuously monitor glucose in almost real time
– Readings generally at 5-minute intervals
– Small sensor with with a cannula is inserted into arm or abdomen – replaces every 10-14 days
(secured with adhesive)
– Reusable transmitter sends readings wirelessly, usually to phone, computer or other
monitoring device
– Alerts can be sent to notify of low or high glucose (or customized) and can share device data
with providers, parents, etc.
– Used by patients with either T1DM or T2 DM
– Insurance coverage varies with T2DM

58
Q

Use of insulin in DM
— Type 1
(3)

A

◦ Life-long insulin required along with diet management
◦ Multiple daily injections of prandial insulin and basal insulin or continuous subcutaneous insulin
infusion.
◦ Often require lower doses of insulin than Type 2 because less issue with insulin resistance

59
Q

Use of insulin in DM
— Type 2
(5)

A

◦ Other treatment options usually implemented first unless severe hyperglycemia
– Diet management
– Oral anti-diabetic agents
◦ Approximately 1/3 patients (more?) benefit from insulin
– Eventually every patient with type 2 DM requires insulin – beta cell failure
◦ Often require higher doses than Type 1 because of insulin resistance
◦ Often start with basal/long-acting insulin and continue certain oral anti-diabetic agents
◦ May add bolus to basal if glycemic goals not met

60
Q

Insulin Dosing
— Type 1
(1)

A

◦ Generally, the starting insulin dose is based on weight, with doses ranging
from 0.4 to 1.0 units/kg/day of total insulin with higher amounts required
during puberty

61
Q

Insulin dosing
— Type 2
(4)

A

◦ Basal insulin alone is the most convenient initial insulin regimen,
beginning at 10 units per day or 0.1–0.2 units/kg/day, depending on the
degree of hyperglycemia.
◦ Many individuals with type 2 diabetes may require mealtime bolus insulin
dosing in addition to basal insulin
◦ The recommended starting dose of mealtime insulin is 4 units, 0.1
units/kg, or 10% of the basal dose
◦ After titration to goals and advancing disease, patients with Type 2 often
require higher doses (unit/kg) than Type 1 because of insulin resistance

62
Q

Adverse Effects of Insulin
— HYPOGLYCEMIA!
(7)

A

◦ Highest risk of any diabetes medication
◦ Tighter control (of glucose) = é risk of hypoglycemia
◦ Symptoms: shaky/tremors, confusion, nervous, sweating, clamminess,
light headed/dizziness, fatigue, sleepiness, agitation, anxiety, hunger,
nausea tingling or numbness (especially of lips and tongue), vision
changes, headache, anger/stubbornness, sadness, tachycardia
◦ Severe hypoglycemia may result in seizures or loss of consciousness
◦ Manage patient as if hypoglycemic, until proven otherwise
◦ Check blood glucose with monitor
◦ Implications for Dental Practice: Patients skipping a meal for a dental
procedure or even a visit should not take their short/rapid acting insulin
dose. Patients who eat normally should take all of their insulin prior to a
visit.

63
Q

Definitions for Hypoglycemia

◦ Serious, clinically significant: < – mg/dL
◦ Glucose Alert Value: < – mg/dL

A

◦ Not all patients will experience hypoglycemia
– Certain antidiabetic drugs and patient risk factors increase
risk

54
70

64
Q

Management of Hypoglycemia
— Rule of 15s
— Treat if < – mg/dl

A

70

  • 15-20 gms fast acting carbs = 3-4
    glucose tablets, 4 oz juice or regular
    soda, 5 lifesavers, 3 peppermints
  • Glucose gel also available – follow
    directions on tube
  • If next meal is more than 1 hr away
    consider a small snack to prevent
    recurrence or eat meal
  • Observe patient 30-60 mins after
    recovery. Confirm normal glucose
    level before patient allowed to
    leave office
  • Consider referring patient to
    physician for follow up
65
Q

Management of Hypoglycemia
— Unconscious patient or unable to swallow
(6)

A

◦ Call 911 (have someone call or if alone call after administering 1st dose of glucagon)
◦ Stimulates gluconeogenesis - release of stored glucose ( glycogen) from the liver.
◦ 1mg glucagon intravenously or intramuscularly in buttock, arm or thigh (may give IM at almost
any body site if necessary). Repeat at 15 minutes if no response
◦ 0.5 mg for pediatrics < 44 lbs
– Patient needs glucose after injection
◦ OR, give 50ml of 50% dextrose IV
— Turn on side to prevent aspiration

66
Q

Therapy for Type 2 DM
(6)

A

— Diet Management
— Oral antidiabetic agents
◦ Possess varying amounts of hypoglycemic risk
— Insulin therapy
— Other injectable therapy (GLP1 inhibitors)
— Be able to identify the magnitude of risk for
hypoglycemic for various antidiabetic agents
— Many classes and lots endings and abbreviations for drug
classes to keep up with

67
Q

Biguanides
— Metformin (Glucophage) only available drug in class
— MOA
(4)

A

◦ Keeps the liver from releasing too much glucose
◦ ̄ Hepatic glucose production (gluconeogenesis – markedly
increased in Type 2) – PRIMARY MECHANISM
◦ Decreases insulin resistance (increases insulin sensitivity)-
glucose utilization in muscle and adipose tissues
◦ Inhibits intestinal absorption of glucose

68
Q

Metformin

A

— Often a drug of choice in Type 2 (especially in obese patients and because of lower costs)
◦ Lower cost
◦ Effective A1C lowering for oral agent
— Use in pre-diabetes (decreases risk of progression to DM)
— Weight neutral/ameliorates insulin-associated weight gain
— Low risk of hypoglycemia with monotherapy
— Notable GI adverse drug effects (ADEs) such as diarrhea/loose stools, flatulence, dyspepsia,
abdominal distension/pain, nausea/vomiting
◦ Titrating the dose up slowly can help patients tolerate and taking with food can help minimize
◦ Some patients can’t tolerate and must discontinue therapy
– XL formulation may cause less GI side effects
— Risk of B12 deficiency (should be checked annually)
— Rare risk of causing lactic acidosis
◦ watch with dehydration
◦ contraindicated in chronic kidney disease (GFR < 30 ml/min), caution with GFR between 30-45 ml/min)

69
Q

Glucagon Like Peptide-1 Receptor Agonists (GLP 1-RA, “incretin
mimetics” - Glutides)

emptying

A

— Albiglutide, Dulaglutide, Exenatide,
Liraglutide, Lixisenatide, Semaglutide
— Most options available as injections (sc)
only
— Semaglutide available sc and po
— Dosing frequency varies – BID, daily and
weekly depending on medication and
formulation
— MOA: stimulates GLP-1 receptors in the
pancreas to increases insulin secretion
in response to elevated glucose. In
addition, stimulation of GLP-1 receptors
in the GI tract and CNS decrease
glucagon secretion and slow gastric

70
Q

GLP 1- Receptor Agonists

A

— Benefits
◦ Weight loss
◦ Higher dosages approved for weight loss
– semaglutide (Wegovy) - injection
– liraglutide (Saxenda) - injection
◦ CV benefits (except lixisenatide and immediate-release exenatide)
– Atherosclerotic Cardiovascular Disease (ASCVD)
◦ Kidney benefits – Chronic Kidney Disease (CKD) (liraglutide, semaglutide) – but
SGLT2 preferred
— ADEs – nausea, diarrhea, injection site reactions, pancreatitis (rare),
gallbladder disease, risk of Thyroid-C cell tumors
— Hypoglycemia: low risk with monotherapy (may increase risk in
combination therapy with sulfonylureas/others that cause hypoglycemia)

71
Q

Glucose-dependent insulinotropic polypeptide (GIP)
agonist + Glucagon-like, peptide-1 (GLP-1) agonist
(“twincretin”)
— Tirzepatide (Mounjaro) – FDA approved 2022 for the
treatment of adults with type 2 diabetes
◦ Weight management indication
◦ MOA:

A

increases insulin secretion in response to elevated
glucose, decreases glucagon secretion, slows gastric emptying

72
Q

GIP/GLP-1 Receptor Co-agonist (“twincretin”)
— ADEs:
(5)
— Additional Information:
(5)

A

◦ GI (e.g., diarrhea, nausea,
vomiting)
◦ Pancreatitis (rare)
◦ Gallbladder disease (rare)
◦ Low risk of hypoglycemia when
used as monotherapy.
◦ Linked to medullary thyroid
cancer in rats

◦ More weight loss than GLP-1
agonists
◦ More A1c reduction than most
GLP-1 agonists.
◦ No CV or kidney outcomes data
yet!
◦ Monitor for retinopathy
progression
◦ May delay oral contraceptive
absorption

73
Q

Sodium glucose cotransporter-2 (SGLT2)
inhibitors - MOA

A

— Located in the S1 segment of the
proximal renal tubule
— SGLT2 -responsible for 90% of glucose
reabsorption
— MOA - Blocks glucose reabsorption in
the kidney, increases urinary
excretion of glucose
◦ Block sodium reabsorption
— Results in increased urinary excretion
of glucose

74
Q

SGLT2 Inhibitors (Flozins)
— Bexagliflozin, canagliflozin, dapagliflozin,
empagliflozin, ertugliflozin
— ADEs

A

◦ Genital mycotic (fungal/yeast) infections
◦ UTIs
◦ Increased urination may lead to volume
depletion, hypotension, syncope, falls, and acute
kidney injury
◦ Hyperkalemia (canagliflozin)
◦ Fractures (rare)
◦ Increased risk of amputations (rare)
◦ Ketoacidosis (rare)
◦ Acute pancreatitis (rare)
◦ Fournier’s gangrene - infection in the scrotum
(which includes the testicles), penis, or perineum
(rare)
◦ Hypoglycemia:
– Low risk as monotherapy
– with insulin or secretagogueus

75
Q

SGLT2 Inhibitors (Flozins)
— Benefits
(3)
— Other information
(3)

A

◦ CV benefits
– Atherosclerotic Cardiovascular Disease
(ASCVD)
– Heart Failure
◦ Renal benefits (Chronic Kidney Disease -
CKD)
◦ Weight loss (less than GLP1 agonists)

◦ Dosage modification needed with renal
impairment
– Do not use ertugliflozin with GFR < 60
mL/min
– Do not use other SGLT2s with GFR < 45
mL/min

76
Q

Sulfonylureas (SU)

A

— Glimepiride, glyburide and glipizide
(2 nd generation)
— MOA (Secretagogues)
◦ Help the pancreas release more insulin
which lowers glucose
◦ Stimulate beta cells causing insulin
secretion
— Lower fasting and post-prandial
glucose

77
Q

Meglitinides

A

— Nateglinide, repaglinide
— Similar to sulfonylureas but shorter acting – taken with
meals
◦ hold dose if skipping meals
— MOA (Secretagogues)
◦ Increase insulin release in response to food, keeping blood
glucose from rising too high after meals
— Lower post-prandial glucose

78
Q

Adverse Drug Effects (ADEs)/Disadvantages of
Secretagogues
— Insulin secretors/secretagogues (SU’s and meglitinides)
(4)

A

— HYPOGLYCEMIA!
— Caution using with other drugs the cause hypoglycemia
(usually discontinue with use of insulin)
— Weight gain
— “Durability” declines over time - relatively short-lived
efficacy

79
Q

Thia-zolidine-diones (glitazones, TZDs)

A

— Pioglitazone and rosiglitazone
— MOA
◦ Increase glucose uptake into muscles by enhancing the
effectiveness of endogenous insulin
◦ bind to nuclear receptor – peroxisome proliferator-activated
receptor γ(gamma) - (PPARγ) in adipose, muscle and liver
◦ Reduce glucose output
— Low risk of hypoglycemia when used as monotherapy

80
Q

TZDs Adverse Effects and Additional Information
— ADEs
(4)
— Additional information
(1)

A

◦ Edema
◦ Weight Gain
◦ Heart Failure (avoid in patients with symptomatic heart failure)
◦ Increased risk of fractures

◦ Glycemic control better sustained over diabetes course

81
Q

Dipeptidyl-Peptidase-4 Inhibitors (DPP-4 inhibitors, “gliptins”)

A

— Alogliptin, Linagliptin, Saxagliptin Sitagliptin
— MOA
◦ Inhibit glucagon release which results in insulin secretion, decreased gastric
emptying and decreased blood glucose levels
— Hypoglycemia with monotherapy – low risk

82
Q

DPP-4 inhibitors Adverse Effects and Additional Information
— ADEs
(3)
— Additional information
(4)

A

◦ May be associated with pancreatitis (rare)
◦ New or worsening heart failure (alogliptin and saxagliptin)
◦ May cause severe joint pain (rare)

◦ Dosage modification needed with renal impairment (alogliptin,
saxagliptin, sitagliptin)
◦ CYP3A4 drug interaction (linagliptin, saxagliptin)
◦ Weight neutral
◦ Generally well tolerated

83
Q

Less Commonly Used Medications
(4)

A

— Alpha-glucosidase inhibitors
— Bile acid sequestrant
— Dopaminergic agents
— Amylin analog

84
Q

Take Home Points:

A

— Diabetes mellitus (DM) is a group of chronic metabolic disorders characterized by
high blood glucose concentrations
◦ Insulin deficiency
◦ Often combined with insulin resistance
◦ Risks for microvascular and macrovascular complications
◦ Uncontrolled diabetes leads to devastating consequences
— T1DM = insulin therapy + diet management
— T2DM = diet management with oral and/or insulin/GLP1RA therapy
— The mechanisms of action of the drug therapy involved with treating DM involves
either providing/increase insulin and/or lowering glucose by various means
— Hypoglycemia is the most dangerous adverse event of some diabetic medications
◦ Knowing which ones and how to manage is important for dental practice