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PHPY 305 > Diabetes Management > Flashcards

Diabetes Management Flashcards

1
Q

Diabetes Mellitus

A

Glucose Homeostasis: insulin promotes uptake of glucose by cells
- reduces blood glucose
Glucagon promotes conversion of glycogen stores to glucose
- increases blood glucose

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2
Q

Stimulation of insulin release

A
  1. Glucose enters cell through GLUT transporter
  2. Glucose metabolized, increases ATP
  3. ATP inhibits Katp channel
  4. This leads to calcium entry through calcium channels
  5. Calcium entry leads to exocytosis of insulin
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3
Q

Diabetes Mellitus key feature

A

Sustained elevations in blood glucose

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4
Q

High blood glucose leads to these complications (5)

A 
Circulatory disorder 
Neuropathy
Nephropathy 
Retinopathy 
Cardiovascular disease
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5
Q

The two types of diabetes and how they are different

A

Type 1: insulin deficiency (reduced secretion)

Type 2: Insulin resistance and (then) reduced secretion

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6
Q

Type 1 characteristics

A

Low insulin

  • due to destruction of pancreatic beta cells
  • likely autoimmune
  • also genetic component
  • typically earlier onset but not always
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7
Q

Type 2 characteristics

A

Often associated with/or worsened by obesity
Typically later onset but that is changing
About 90% of DM cases are type 2

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8
Q

Treatment overview for type 1 and 2 diabetes

A

Type 1: manage with insulin
Type 2: lifestyle changes - diet, exercise, etc.
Manage initially with oral hypoglycaemic
May need to add insulin later as beta cells fail

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9
Q

Monitoring of glucose (acute)

A
  • self-monitoring of blood glucose (glucometer)
  • target fasting blood glucose (4-7 mmol/L)
  • Post-prandial (2 hours): 5-10 mmol/L
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10
Q

Monitoring of glucose (chronic)

A

Hemoglobin A1c

  • glycated hemoglobin
  • Glucose attached to Hb in blood
  • Considered a more stable measure of Glycemic control over time
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11
Q

Insulin

A
  • a 51 amino acid protein

- consists of two peptide chains (A & B) joined by 2 disulphide bridges

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12
Q

Actions of Insulin

A

Promotes entry of glucose into the cells

  1. Insulin binds to tyrosine kinase receptor
  2. Prompts a cascade of intracellular signalling events (protein synthesis and glycogen synthesis)
  3. Prompts translocation of GLUT-4 transporters to cell membrane
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13
Q

Actions of insulin in the liver

A
  • decreases glucose synthesis (Gbuconeogensis)

- increases conversion of glucose to glycogen (storage)

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14
Q

Actions of insulin in muscle

A
  • Increase in glucose to glycogen

- increase in protein synthesis.

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15
Q

Actions of Insulin in Fat

A
  • Increases in Lipogenesis

- decrease in Lipolysis

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16
Q

Insulins route of administration

A

Injected: Subcutaneous

  • intravenous in emergencies
  • absorption depends on site of injection: more rapid in abdomen, slower in thigh or buttocks and exercise, heat tend to increase absorption
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17
Q

Rapid acting insulins

A

Regular insulin: onset is 1/2 hour, peak around 2 hours, duration 8 hours
Aspart insulin: onset is 1/4 hour, peak in 1-1.5 hours, duration 4 hours

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18
Q

Intermediate/long acting insulins

A

NPH: onset 1-2 hours, peak 6-12, duration 18
- Neutral Protamine Hagedorn
Glargine insulin: onset 3-4 hours, duration 20-24 hours

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19
Q

SIde effects of Insulin

A

Hypoglycemia: symptoms include sweating, tachycardia, confusion
- can progress to coma/death
Treatment: SUGAR

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20
Q

Other side effects of Insulin

A

Weight gain
Immune reactions
Lipodystrophy
- atrophy of subcutaneous fat at injection site

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21
Q

Insulin secretagogues two classes

A

Sulfonylureas

Meglitinides

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22
Q

Sulfonylureas example

A

Glyburide

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23
Q

Sulfonylureas mechanism

A
  • act on pancreatic beta cells

- bind to the sulfonylurea receptor-1 (SUR-1) and stimulate insulin release while inhibiting Katp channel

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24
Q

Risk of Sulfonylureas

A

Stimulates insulin regardless of blood glucose levels

Risk of hypoglycemia

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25
Q

Side effects of Sulfonylureas

A 
Weight gain
Rash (hypersensitivity to sulpha)
Gastrointestinal 
Concern over cardiovascular effects:
- receptors in the cardiovascular system
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26
Q

Meglitinide example

A

Repaglinide

27
Q

Repaglinide mechanism

A

Bind to a different sire of SUR-1 and stimulate insulin release
More rapid onset and shorter duration of action
- may lower risk of hypoglycemia
- more flexibility with regards to food intake
- need to be taken more often

28
Q

Biguanides example

29
Q

Biguanides mechanism

A

Increases activity of AMP-dependent protein kinase (AMPK)

  • AMPK is normally activated when cellular energy stores reduced
  • may have protective (anti-oxidant) effects on endothelial cells
30
Q

Key effects of AMPK:

A

Enhanced glucose uptake/cell sensitivity to insulin
Reduced Glycogenolysis
Reduced Gluconeogenesis

31
Q

Biguanides pharmacokinetics

A

Eliminated by kidneys

Avoid using in patients with impaired renal function

32
Q

Biguanides Side effects

A

Gastrointestinal: Nausea, diarrhea
Rare - Lactic acidosis
Avoid using in patients with decompensated heart failure

33
Q

First line drug for Type 2 Diabetes?

A

Biguanides: good efficacy

  • not associated with weight gain
  • does not stimulate insulin release (hypoglycemia unlikely)
  • Good safety profile
34
Q

Incretins mediate

A

Mediate communication between gut and brain

- potential target for weight loss drugs

35
Q

Examples of Incretins

A

Glucagon-like Peptide-1 (GLP-1)

Glucose dependent insulinotropic peptide (GIP)

36
Q

The two variations of Incretins

A

GLP-1 agonists

DPP-4 inhibitors

37
Q

GLP-1 agonist example

A

Liraglutide

38
Q

DPP-4 inhibitors example

A

Sitagliptin

39
Q

Incretins mechanism of action

A
  1. Increase insulin secretion
  2. Inhibit glucagon secretion
  3. Delay gastric emptying
  4. Reduce appetite
40
Q

Administration of GLP-1 agonists

A

All administered by subcutaneous injection

41
Q

Administration of DDP-4 inhibitors

A

All administered Orally

42
Q

Difference in GLP-1 agonists and DPP-4 inhibitors

A
  • GLP-1 agonists have more pronounced effects on the GI tract than DDP-4 inhibitors
  • May reduce gastric emptying enough to interfere with drugs needing rapid absorption
43
Q

Side effects of Incretins

A

Hypoglycemia: less common than with insulin or the insulin secretagogues, Incretins response to bodies need for insulin
Rare AE: Pancreatic disease, pancreatitis, cancer

44
Q

GLP-1 agonist side effects

A

Gastrointestinal: Nausea, vomiting, diarrhea (or constipation), gall stones

  • incretins effect communication between gut and brain
  • GLP-1 agonists have a greater effect on the GI tract than DPP-4 Inhibitors: more GI side effects but more weight loss, liraglutide approved as a weight loss drug
  • increases heart rate, arrhythmia, possible link to thyroid cancer
45
Q

DPP-4 inhibitors (dipeptidyl peptidase 4) side effects

A
  • Gastrointestinal: less common than GLP-1 agonists
  • Increased risk of infection: typically upper respiratory or urinary tract
  • DPP-4 plays role in the immune system (lymphocytes)
46
Q

Thiazolidinediones example

A

Pioglitazone

47
Q

TZD facts

A
  • Peroxisome proliferator-activated receptor-gamma (PPAR-y) agonists
  • PPAR-y receptors regulate genes related to glucose and lipid metabolism
  • because they work on gene expression, TXD effects tend to be delayed
48
Q

TZD actions

A
  • insulin sensitizer: increases uptake of glucose
  • Enhances uptake of free fatty acids into adipose tissue
  • less FFA available to enter other tissues
  • higher adipose tissue levels tend to reduce sensitivity to insulin
49
Q

TZD actions on blood glucose

A

Reduce hepatic production of glucose

- reduced gluconeogenesis

50
Q

TZD actions on lipids

A

Reduce triglycerides, increase HDL

51
Q

Thiazolidinediones problems

A

Consistent safety issues have limited their use

Hepatotoxicity, myocardial infarction, bladder cancer

52
Q

TZD side effects

A

Cardiovascular: heart failure
Edema
Weight gain: reduces leptin levels
Fractures (women)

53
Q

Alpha-glucosidase inhibitors

A
  • Glucosidases break down carbohydrates to glucose

- AGIs inhibit breakdown of carbs, preventing absorption

54
Q

AGI example

55
Q

Side effects of AGI

A

Gastrointestinal: bloating, diarrhea, pain. Bacteria feed on undigested carbs, release gas
Low risk of hypoglycemia: if it does occur, need to use glucose because sucrose won’t be absorbed

56
Q

SGLT2 inhibitors mechanism

A
  • inhibit renal mechanism for reabsorbing glucose
  • in non-diabetic individuals, all filtered glucose is reabsorbed
  • 90% of glucose reabsorption occurs at the proximal tubule
57
Q

SGLT2 inhibitor example

A

Empagliflozin

58
Q

Empagliflozin mechanism

A

Acts at the proximal tubule

Inhibits sodium-glucose Co-transporter 2 (SGLT)

59
Q

Inhibition of SGLT2 results in

A
  • reduction in glucose reabsorption: osmotic diuresis, reduces blood glucose
  • induces weight loss
    May reduce blood pressure via osmotic diuresis
60
Q

SGLT2 inhibitors adverse effects

A
  • Increased glucose in the nephron increases risk of infections: urinary tract infections, genital infections
  • Dizziness, hypotension
  • Nausea
  • Hyperkalemia
  • Rare cases of diabetic ketoacidosis
61
Q

Type 2 diabetes combinations

A

Metformin + anything
Benefits: adding drugs that cause weight gain lead to a neutral effect
Common examples: Metformin + insulin and Metformin + Sulfonylurea
These combinations also decrease the risk of Hypoglycemia

62
Q

Other Drug combinations

A

Metformin + SGLT2 inhibitor + DPP-4 inhibitor

- addition of drugs with neutral effect on weight or weight loss can enhance the weight loss

63
Q

Future direction of Insulin administration

A
  • inhaled insulin, powdered form through mouth
    Problems: cost, first device failed to catch on, concerns over bronchospasm
  • Patches: use micro needle technology, patches contain insulin or beta cells which then secrete insulin
  • Stem cells: Islet cell transplants

PHPY 305 (14 decks)

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