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DM part 1 Flashcards

1
Q

Key Players in Glucose Hemostasis
— Glucose homeostasis:
— Glucose:
— Insulin:
— Pancreatic Islet Hormones (endocrine);

A

Key Players in Glucose Hemostasis
— Glucose homeostasis: balance between hepatic glucose
production and peripheral glucose uptake and utilization
— Glucose – source of energy
— Insulin - most important regulator of glucose/metabolic
equilibrium
— Pancreatic Islet Hormones (endocrine)
◦ Maintains glucose balance
◦ 4 types of peptide-secreting cells
– Beta (B) – secrete insulin
– Alpha (A) – secrete glucagon
– Delta (D) – secrete somatostatin
– PP (also known as gamma) – secrete pancreatic polypeptide

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2
Q

Relationship between Glucose and Insulin

A

— Glucose is the main factor controlling synthesis and secretion of insulin
— Two ways insulin is released:
◦ Steady basal release of insulin
◦ Response to increased glucose
— About 1/5 of insulin stored in the pancreas of an adult is secreted daily

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3
Q

Glucose-Insulin Roller Coaster diagrammed

A
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4
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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5
Q

Diabetes Mellitus (DM)

A

— A group of complex chronic metabolic disorders characterized by high blood glucose concentrations (hyperglycemia)
◦ Insulin deficiency
◦ Often combined with insulin resistance
◦ Abnormalities in the metabolism of carbohydrates, proteins, fats and insulin.

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6
Q

Hyperglycemia can be due to:

A

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

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7
Q

Type 1 (T1DM)

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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8
Q

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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9
Q

other DM forms

A

gestational diabetes, medications - glucocorticoids

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10
Q

CLINICAL PRESENTATION of DM

A
  • Symptoms may include polydipsia, polyphagia, polyuria, nocturia, blurred vision. (More common on type 1/ occurs in varying degree in Type 2 DM).
  • Type 1 DM often associated with weight loss, ketoacidosis (dehydration)
  • Majority of Type 2 patients are asymptomatic and diagnosed by laboratory testing
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11
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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12
Q

DM increasing prevalence

A

Increasing aging population and numbers of overweight adolescents, teenagers and adults = rapid increases in prevalence

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13
Q

Lab tests for diagnosis and monitoring of diabetes (WNL, PreDM and DM)

A
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14
Q

Spectrum of normal glucose to diabetes

A
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15
Q

Systemic Complications of DM

A

Macrovascular
◦ Brain
◦ Heart
◦ Extremities (peripheral vascular disease)
—
Microvascular
◦ Eyes
◦ Kidney
◦ Nerves; Peripheral and Autonomic
◦ Periodontal disease

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16
Q

Glycemic Goals of DM tx

A
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17
Q

ndividualizing Glycemic Targets

A
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18
Q

Additional DM Goals – Risk Reduction Strategies

vascular

A

Reduce the risk of macrovascular and microvascular (and other)
complications through glycemic control and controlling co-morbid conditions to which DM contributes

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19
Q

Additional DM Goals – Risk Reduction Strategies

CV

A

Reduce cardiovascular risk factors
– Control BP
– Control lipids
– Smoking Cessations

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20
Q

Additional DM Goals – Risk Reduction Strategies

vaccines

A

Reduce the risk of vaccine-preventable diseases
– Immunizations
– Examples: Flu, Tdap/Td, Pneumococcal, Hepatitis B (others

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21
Q

Additional DM Goals – Risk Reduction Strategies

periodontal

A

Minimize periodontal complications due to diabetes mellitus,
provide safe and effective dental care and promote good oral
health

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22
Q

Non-pharmacologic therapy for DM
—

A

— Medical Nutrition Therapy
— Physical Activity

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23
Q

Medical Nutrition Therapy for DM

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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24
Q

Physical Activity for DM

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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25
Q

insulin hx

A

— History of insulin in the treatment of diabetes = interesting
◦ Insulin destroyed in GI tract
◦ Before insulin therapy Type I DM = death sentence (wasting and
dying from ketoacidosis)
◦ Breakthrough in 1920’s when insulin was isolated
– Noble Prize = Banting and Best (University of Toronto)

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26
Q

insulin soruces

A

Porcine or Bovine sources
– Bovine - discontinued in US in1978
– Porcine manufactured in US until 2005
◦ Significant variability between batches

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27
Q

insulin allergies

A

immune response to animal-based products

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28
Q

Current Insulin therapy
—form?
— bath variability?
— Modified amino acid sequences?
◦ Differences in?
◦ Categorized by?

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

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29
Q

Rapid-acting Insulin
— Rx?
— Appearance-?
— form?

A

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

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30
Q

Rapid-acting Insulin names

A

insulin lispro, aspart, and glulisine

LAG

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31
Q

insulin lispro onset/peak/duration

A
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32
Q

insulin aspart onset/peak/duration

A
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33
Q

insulin guisiline onset/peak/duration

A
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34
Q

meal timings with rapid insulins

A

given within 10-15 minutes before or up to 20 minutes after

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35
Q

rapid insulins compatability

A

NPH

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36
Q

Short-acting (Regular) Insulin
— Rx?
— Appearance?
— form?

A

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

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37
Q

short acting insulin names

A

Humulin R
Novolin R

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38
Q

onset/peak/duration Humulin R

A
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39
Q

onset/peak/duration Novolin R

A
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40
Q

short acting insulin meal timings

A

30 min before

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41
Q

compatability of short acting insulins

A

NPH

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42
Q

Inhaled Insulin - Afrezza
— rate? given with?
— route?
— Amount of insulin delivered to lungs depends on?
— Dosing conversion from?
— Contraindicated in ?
— Not recommended in?
— Risk of ?
— cost?

A

Inhaled Insulin - Afrezza
— 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!

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43
Q

Intermediate-acting (NPH)Insulin
— NPH?
— Rx?
— Appearance?
— form?

A

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

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44
Q

Intermediate-acting (NPH)Insulin names

A

Humulin N
Novolin N

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45
Q

Humulin N onset/peak/duration

A
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46
Q

Novolin N onset/peak/duration

A
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47
Q

Frequency of administration for Humulin N
and Novolin N

A

SC – usually one to two times a day

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48
Q

Humulin N/ novolin N
compatabilty

A

Can mix with aspart, glulisine, lispro, and regular insulin

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49
Q

Long-acting Insulin
— Rx?
— Appearanc?
— form?

A

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

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50
Q

Long-acting Insulin names

A

insulin glargine (100units/mL), demetir, glargine (300 units/mL)

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51
Q

onset insulin glargine

A

1.1hrs

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52
Q

onset insulin demetir

A

1.1-1.2 hrs

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53
Q

onset of 300 units/mL of glargine

A

develops over 6hrs

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54
Q

insulin glargine/demetir peak

A

mo real peak

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55
Q

insulin glargine and demetir duration

A
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56
Q

insulin glargine/demetir freq of admin

A
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57
Q

duration of 300units/mL glargine

A

over24 hrs

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58
Q

freq admin of 300units/mL glargine

A

SC once daily at the
same time each day.
May take at least 5
days to see maximum
effects

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59
Q

Long-acting Insulin compatabilites

A

Do not mix with other insulins or dilute

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60
Q

Ultra Long-acting Insulin
— Rx?
— Appearance ?
— form?

A

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

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61
Q

Ultra Long-acting Insulin name

A

insulin degludec (Tresiba)

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62
Q

insulin degludec onset, peak, and duration?

A
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63
Q

insulin degludec frequency of admin

A

SC – once daily at any time of day

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64
Q

insulin degludec compatability?

A

do not mix with other insulins

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65
Q

Summary of Duration of Action of Insulins

A
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66
Q

why would there be insulin mixtures? when are these given? are there any cons?

A

— 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 hypoglycemia

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67
Q

types of insulin pens

A
  • Reusable insulin pen– must load with insulin cartridges - sold separately
  • Disposable insulin pens - come filled with insulin and are thrown away when empty
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68
Q

advantages of insulin pens

A
69
Q

disadvantages of insulin pens

A
70
Q

Basal-bolus regimen of insulin admin

A

(4 injections total/day)
◦ Mimic physiologic insulin release

71
Q

Rapid-acting/NPH insulinmix admin

A

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

72
Q

Continuous Insulin Infusion Pumps

growing use in? mechanism? what insulin type used?

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

73
Q

Continuous Insulin Infusion Pumps mechanism

A

Programed external pump - worn continuously
◦ Delivers insulin through a cannula inserted just beneath the surface of the skin
◦ One injection site for 72 hrs

74
Q

Continuous Insulin Infusion Pumps advantages

A

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

75
Q

Continuous Insulin Infusion Pumps monitoring

A

Many pumps have Continuous Glucose Monitoring (CGM) system integrated
within the pump or they can be used separately

76
Q

Continuous Insulin Infusion Pumps Adverse Effects:
* Pump failures?
* Mechanical?
* Blockages?
* Infusion sit?
* Instability of?
* User?
* Rates?
* Importance of?
* Infections?

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
77
Q

Continuous Insulin Infusion Pumps dental implications

A

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

78
Q

Glucose Monitors and Continuous Glucose Monitoring (CGM)
— Purpose:
— Safety and efficacy?

A

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

79
Q

Blood Glucose Meters (many brands)
◦ Finger sticks?
◦ Self-monitoring of Blood Glucose (SMBG)
– Frequency of monitoring?

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

80
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

81
Q

Use of insulin in DM Type 1
◦ required?
◦ frequency?
◦ dose sizes?

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

82
Q

Use of insulin in DM type 2
◦ Other treatment options?
◦ Approximately what % benefit? all need it?
◦ Often require what doses?
◦ Often start with ?
◦ May add what if glycemic goals not met?

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

83
Q

Insulin Dosing type 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

84
Q

Insulin Dosing type 2
◦ most convenient initial insulin regimen, beginning at? depending on?
◦ Many individuals with type 2 diabetes may require?
◦ The recommended starting dose of mealtime insulin is ?
◦ After titration to goals and advancing disease, patients with Type 2 often
require?

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

85
Q

Adverse Effects of Insulin
—

A

— HYPOGLYCEMIA!
◦ Highest risk of any diabetes medication
◦ Tighter control (of glucose) = increased risk of hypoglycemia

86
Q

hypoglycemia symptoms

A

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

87
Q

how should we managed suspected hypoglycemia

A

◦ Manage patient as if hypoglycemic, until proven otherwise
◦ Check blood glucose with monitor

88
Q

Implications of hypoglycemia for Dental Practice

A

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.

89
Q

Definitions for Hypoglycemia

A

◦ Not all patients will experience hypoglycemia
– Certain antidiabetic drugs and patient risk factors increase risk
◦ Serious, clinically significant: < 54 mg/dL
◦ Glucose Alert Value: < 70 mg/dL

90
Q

tx of Hypoglycemia

rule? tx if?

A

— Rule of 15s
— Treat if < 70 mg/dl
* 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

91
Q

Management of Hypoglycemia
— Unconscious patient or unable to swallow

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.

92
Q

what is given to hypoglycemic who is unconscious or unable to swallow

A

◦ 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

93
Q

Rx affecting Glucose Production at liver

A

Biguanides
(Thiazolidinediones)
GLP1 RAs

94
Q

Rx’s affecting Glucose Absorption at intestine:

A

a-glucosidase inhibitors
Bile acid sequestrants
GLP1 RAs

95
Q

Rx’s causing Slowed Gastric Emptying:

A

Incretin & Amylin mimetics
GLP1-RAs

96
Q

Rx’s affecting insulin secretion

A

Sulfonylureas
Meglitinides
Insulin
DPP-4 inhibitors
Incretin mimetic (GLP1-RA)

97
Q

Glucagon inhibition Rx

A

Incretin mimetics
DPP-4 Inhibitors
Amylin mimetics

98
Q

Kidney dm rx

A

Sodium glucose co- transporter 2 inhibitor

99
Q

Muscle Peripheral Glucose Uptake inhibitor Rx’s

A

Thiazolidinediones
Biguanides
GLP1 RAs

100
Q

Satiety/Feeding rx’s

A

Incretin mimetics
Amylin mimetics
Dopaminergic

101
Q

Biguanides moa
—

A

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

102
Q

Metformin
— Often a drug of choice in? why? also used in?

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)

103
Q

weight gain with metformin

A

Weight neutral/ameliorates insulin-associated weight gain

104
Q

hypo risk with metformin as monotherapy

A

low risk

105
Q

metformin and GI

how can we help reduce this?

A

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

106
Q

what can become def with metformin

A

Risk of B12 deficiency (should be checked annually)
—

107
Q

metabolic ADR of metformin

A

— 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)

108
Q

Glucagon Like Peptide-1 Receptor Agonists

A

— Albiglutide, Dulaglutide, Exenatide,
Liraglutide, Lixisenatide, Semaglutide

109
Q

— Albiglutide, Dulaglutide, Exenatide,
Liraglutide, Lixisenatide, Semaglutide

A

Glucagon Like Peptide-1 Receptor Agonists

110
Q

Glucagon Like Peptide-1 Receptor Agonists
— Most options available as?
— which available sc and po?
— Dosing frequency?

A

— Most options available as injections (sc) only
— Semaglutide available sc and po
— Dosing frequency varies – BID, daily and
weekly depending on medication and formulation

111
Q

Glucagon Like Peptide-1 Receptor Agonists moa

A

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 emptying

112
Q

— Albiglutide moa

A

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 emptying

113
Q

Dulaglutide moa

A

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 emptying

114
Q

— Exenatide moa

A

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 emptying

115
Q

Liraglutide moa

A

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 emptying

116
Q

Lixisenatide moa

A

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 emptying

117
Q

— Semaglutide moa

A

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 emptying

118
Q

GLP 1- Receptor Agonists
— Benefits

A
  • weight loss
  • CV
  • renal
119
Q

GLP 1- Receptor Agonists weight

A

◦ Weight loss
◦ Higher dosages approved for weight loss
– semaglutide (Wegovy) - injection
– liraglutide (Saxenda) - injection

120
Q

GLP 1- Receptor Agonists CV

A

◦ CV benefits (except lixisenatide and immediate-release exenatide)
– Atherosclerotic Cardiovascular Disease (ASCVD)

121
Q

GLP 1- Receptor Agonists renal

preffered?

A

◦ Kidney benefits – Chronic Kidney Disease (CKD) (liraglutide, semaglutide) – but SGLT2 preferred

122
Q

GLP 1- Receptor Agonists ADE’s:
* gi?
* injection?
* panc?
* organ dx?
* * tumors?

A

nausea, diarrhea, injection site reactions, pancreatitis (rare),
gallbladder disease, risk of Thyroid-C cell tumors

123
Q

GLP 1- Receptor Agonists ADE’s risk of hypo as monetherapy

A

Hypoglycemia: low risk with monotherapy (may increase risk in
combination therapy with sulfonylureas/others that cause hypoglycemia)

124
Q

Glucose-dependent insulinotropic polypeptide (GIP) agonist + Glucagon-like, peptide-1 (GLP-1) agonist (“twincretin”)

approved for? indication?

A

Tirzepatide (Mounjaro) – FDA approved 2022 for the treatment of adults with type 2 diabetes
◦ Weight management indication

125
Q

Tirzepatide moa

A

Glucose-dependent insulinotropic polypeptide (GIP) agonist + Glucagon-like, peptide-1 (GLP-1) agonist (“twincretin”)
increases insulin secretion in response to elevated glucose, decreases glucagon secretion, slows gastric emptying

126
Q

GIP/GLP-1 Receptor Co-agonist ADE’s:
◦ GI?
◦ Pancreas?
◦ Gallbladder>?
◦ hypo?
◦ thyroid?

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

Tirzepatide

127
Q

GIP/GLP-1 Receptor Co-agonist addt info:
◦ More weight loss than?
◦ More A1c reduction than?
◦ CV/kidney?
◦ Monitor for?
◦ May delay?

A

◦ 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

128
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

129
Q

SGLT2 Inhibitors

A

Bexagliflozin, canagliflozin, dapagliflozin,
empagliflozin, ertugliflozin

130
Q

Bexagliflozin MOA

A

Blocks glucose reabsorption in the kidney, increases urinary excretion of glucose
◦ Block sodium reabsorption
— Results in increased urinary excretion of glucose

131
Q

canagliflozin moa

A

Blocks glucose reabsorption in the kidney, increases urinary excretion of glucose
◦ Block sodium reabsorption
— Results in increased urinary excretion of glucose

132
Q

dapagliflozin moa

A

Blocks glucose reabsorption in the kidney, increases urinary excretion of glucose
◦ Block sodium reabsorption
— Results in increased urinary excretion of glucose

133
Q

empagliflozin moa

A

Blocks glucose reabsorption in the kidney, increases urinary excretion of glucose
◦ Block sodium reabsorption
— Results in increased urinary excretion of glucose

134
Q

ertugliflozin moa

A

Blocks glucose reabsorption in the kidney, increases urinary excretion of glucose
◦ Block sodium reabsorption
— Results in increased urinary excretion of glucose

135
Q

SGLT2 Inhibitors (Flozins) ADEs:
◦ Genital?
◦ UT?
◦ Increased urination may lead to?
◦ electrolyte imbalance? which flozin?
◦ bone?
◦ limbs?
◦ metabolic?
◦ pancreas?
◦ Fournier’s gangrene?

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

136
Q

SGLT2 Inhibitors risk of hypo

A

Hypoglycemia:
– Low risk as monotherapy
– increased with insulin or secretagogues

137
Q

SGLT2 Inhibitors benefits

A

CV
Renal
weight loss

138
Q

SGLT2 Inhibitors CV

A

CV benefits
– Atherosclerotic Cardiovascular Disease
(ASCVD)
– Heart Failure

139
Q

SGLT2 Inhibitors renal

A

Renal benefits (Chronic Kidney Disease -
CKD)

140
Q

SGLT2 Inhibitors weight

A

weight loss

141
Q

SGLT2 Inhibitors other info:

renal dosage adjustments

A

◦ 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

142
Q

Sulfonylureas (SU)

A

— Glimepiride, glyburide and glipizide
(2 nd generation)

143
Q

Sulfonylureas (SU) moa

A

(Secretagogues)
◦ Help the pancreas release more insulin which lowers glucose
◦ Stimulate beta cells causing insulin secretion
— Lower fasting and post-prandial glucose

144
Q

Glimepiride moa

A

◦ Help the pancreas release more insulin which lowers glucose
◦ Stimulate beta cells causing insulin secretion
— Lower fasting and post-prandial glucose

145
Q

glyburide moa

A

◦ Help the pancreas release more insulin which lowers glucose
◦ Stimulate beta cells causing insulin secretion
— Lower fasting and post-prandial glucose

146
Q

glipizide moa

A

◦ Help the pancreas release more insulin which lowers glucose
◦ Stimulate beta cells causing insulin secretion
— Lower fasting and post-prandial glucose

147
Q

Meglitinides
names? similar to? difference?

A

— Nateglinide, repaglinide
— Similar to sulfonylureas but shorter acting – taken with meals
◦ hold dose if skipping meals

148
Q

Meglitinides moa

A

◦ Increase insulin release in response to food, keeping blood
glucose from rising too high after meals
— Lower post-prandial glucose

149
Q

Nateglinide moa

A

◦ Increase insulin release in response to food, keeping blood
glucose from rising too high after meals
— Lower post-prandial glucose

150
Q

repaglinide moa

A

◦ Increase insulin release in response to food, keeping blood
glucose from rising too high after meals
— Lower post-prandial glucose

151
Q

Adverse Drug Effects (ADEs)/Disadvantages of Secretagogues (SU’s and meglitinides)

hypo risk? weight? durability?

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

152
Q

Thia-zolidine-diones (TZDs)

A

— Pioglitazone and rosiglitazone

153
Q

TZD moa

A

◦ 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

154
Q

Pioglitazone moa

A

◦ 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

155
Q

rosiglitazone moa

A

◦ 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

156
Q

TZD risk of hypo as monotherapy

A

Low risk of hypoglycemia when used as monotherapy

157
Q

TZDs Adverse Effects:
◦ app?
◦CV
◦ Increased risk of?

A

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

158
Q

TZDs glycemic control over dM course

A

Glycemic control better sustained over diabetes course

159
Q

Dipeptidyl-Peptidase-4 Inhibitors (DPP-4 inhibitors,

A

Alogliptin, Linagliptin, Saxagliptin Sitagliptin

160
Q

Dipeptidyl-Peptidase-4 Inhibitors moa

A

◦ Inhibit glucagon release which results in insulin secretion, decreased gastric
emptying and decreased blood glucose level

161
Q

Linagliptin moa

A

◦ Inhibit glucagon release which results in insulin secretion, decreased gastric
emptying and decreased blood glucose level

162
Q

Alogliptin moa

A

◦ Inhibit glucagon release which results in insulin secretion, decreased gastric
emptying and decreased blood glucose level

163
Q

saxagliptin moa

A

dpp4 inhib
◦ Inhibit glucagon release which results in insulin secretion, decreased gastric emptying and decreased blood glucose level

164
Q

Sitagliptin moa

A

◦ Inhibit glucagon release which results in insulin secretion, decreased gastric
emptying and decreased blood glucose level

165
Q

dpp-4 inhib Hypoglycemia with monotherapy

A

Hypoglycemia with monotherapy – low risk

166
Q

DPP-4 inhibitors
◦ pancreas?
◦ CV? agents involved?
◦ joints

A

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

167
Q

DPP-4 inhibitors additional info :
◦ Dosage modification needed with? agents?
◦ ddi? agents?
◦ Weight?
◦ tolerated?

A

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

168
Q

Less Commonly Used Medications
—

A

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

pharm 2 (20 decks)

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