Diabetes Flashcards

1
Q

basal rate

A

insulin that is constantly released at a steady rate throughout the day

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2
Q

bolus rate

A

increase in insulin secretion after food is ingested and glucose levels spike

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3
Q

normal glucose range

A

4-6 mmol/L

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4
Q

type 1 diabetes

A
  • autoimmune destruction of beta cells
  • antibodies present for months to years before clinical symptoms
  • insufficient production of insulin
  • Eventually, insulin will be required to sustain life
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5
Q

type 2 diabetes

A

pancreas
- defective beta cell secretion of insulin
- insulin resistance stimulates increased insulin secretion
- eventual exhaustion of beta cells in many people
- increased glucagon secretion

liver
- excess glucose production
- inappropriate regulation of glucose production

Adipose Tissue
- decrease in adiponectin and increase in leptin
- results in altered glucose and fat metabolism

Muscle
- defective insulin receptors
- insulin resistance
- decreased uptake of glucose by cells resulting in hyperglycemia

  • Obesity (abdominal/visceral) is a major risk factor
  • Screening begin at 40, every 3 years after
  • Pancreas continues to produce some endogenous (self made) insulin.
  • Insulin produced is insufficient or is poorly utilized by tissues.

4 causes
1) Cells become resistant to insulin (insulin resistance)
2) Decrease in the ability of the pancreas to produce insulin
3) Inappropriate glucose production by liver
4) Alteration in the production of hormones and cytokines by adipose tissue (adipocytokines)

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6
Q

gestational diabetes

A
  • Develops during pregnancy
  • Usually detected at 24–28 weeks of gestation
  • Normally glucose levels go back to normal at 6 weeks postpartum
  • Increased risk of progression to type II diabetes postpartum (sometimes 5-10 years later)
  • Treated with insulin, sometimes lifestyle changes (diet) and frequent testing are enough
  • Poorly controlled gestational diabetes increases risk for birth trauma (large baby), hypoglycemia, hyperbilirubinemia (jaundice), and respiratory distress syndrome
  • Nutritional counseling is considered to be the first-line therapy. Physical activity should be encouraged as tolerated. - - If nutritional counseling alone does not achieve target fasting, or postprandial blood glucose levels, or both, insulin therapy is usually indicated.
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7
Q

prediabetes

A
  • impaired glucose tolerance, impaired fasting glucose, or an a1c between 6.0-6.4%
  • at increased risk of developing type II diabetes and its complications
  • Signs & symptoms
    -Polydipsia, polyuria, weight gain/loss, fatigue, blurred vision
  • A1C: 6.0-6.4
  • FPG: 6.1-6.9
  • 2hPG in a 75g OGTT: 7.8-11.0
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8
Q

secondary diabetes

A
  • Treatment of a medical condition that causes abnormal blood glucose level
  • Conditions that may cause secondary DM include schizophrenia, cystic fibrosis, Cushing’s syndrome, hyperthyroidism, immunosuppressive therapy, and the use of parenteral nutrition
  • Commonly used medications that can induce secondary DM in some people include corticosteroids (prednisone), phenytoin (Dilantin), and atypical antipsychotics (e.g., clozapine [Clozaril])
  • Usually resolves when underlying condition treated
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9
Q

diagnosing diabetes

A

A1C: greater than or equal to 6.5%
FBG: higher than 7 mmol/L
2hPG in a 75g OGTT: greater than or equal to 11.1

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10
Q

A1C test

A
  • The test works by showing the amount of glucose that has been attached to hemoglobin molecules, which are attached to the red blood cell (RBC) for the life of the cell (∼120 days).
  • indicates the overall glucose control for the previous 90 to 120 days.
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11
Q

A1C targets

A
  • less than or equal to 6.5% –> adults with type 2 diabetes to reduce the risk of CKD and retinopathy if at low risk of hypoglycaemia
  • less than or equal to 7.0% –> most adults with type 1 or type 2 diabetes
  • 7.1-8.5% –> functionally dependent, recurrent severe hypoglycaemia and unawareness, limited life expectancy, frail elderly/dementia
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12
Q

ABCDE of reducing diabetes complications

A
  • A: A1C target
  • B: Blood pressure (<130/80)
  • C: Cholesterol (LDL-C <2.0 mmol/L)
  • D: Drugs for CVD risk
  • E: Exercise and healthy
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13
Q

kinds of insulin

A
  • basal
  • bolus
  • premixed
  • regular
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14
Q

basal insulin

A
  • Long lasting
  • Is generally given once a day at the same time
  • Often given at night (so it doesn’t get confused with bolus insulin)
  • Offers a relatively stable degree of glucose lowering throughout the day
  • Titrated based on fasting glucose values
  • Ex: Insulin glargine
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15
Q

bolus (rapid acting) insulin

A
  • Given at mealtimes
  • Onset: 10-15min (so should be given 10-15min before meals)
  • Offers a rapid reduction in glucose at mealtimes when glucose levels would be expected to rise
  • Carb counting is an important skill
  • Ex: Apidra
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16
Q

premixed insulin

A
  • simple regime such as twice a day
  • Increased risk of lows (big spikes and then drops off)
  • Increased risk of poorer glucose control during parts of the day when the medication troughs
17
Q

regular insulin

A
  • Regular insulin (Humulin R®, Novolin ge Toronto®)
  • Often given in hospitals
  • Typically at mealtimes
  • Routes of administration: intravenous (IV) bolus, IV infusion, intramuscular, subcutaneous
  • Onset (subcutaneous route): 30 minutes
  • Peak (subcutaneous route): 2 to 3 hours
  • Duration (subcutaneous route): 6.5 hours
18
Q

oral antihyperglycemics

A
  • metformin (biguanide)
  • insulin secretagogues (meglitinides)
  • insulin secretagogues (sulfonylureas)
  • DPP-4 inhibitors
  • GLP-1 receptor agonists
  • SGLT2 inhibitors
  • Alpha glucosidase inhibitor
  • thiazolidinediones (glitazones)
19
Q

metformin (biguanide)

A
  • first line
  • MOA: Improves insulin sensitivity, decreases glucose production by liver and GI glucose reabsorption
  • does not promote weight gain
  • side effects: GI upset, nausea, lactic acidosis
  • monitor B12 every 2-3 years
  • avoid in hepatic impairment, renal impairment (eGFR <30), alcoholism, cardiopulmonary disease
  • CT scan with contrast dye
20
Q

Insulin Secretagogues (meglitinides)

A
  • MOA: stimulates insulin release from the pancreatic beta cells
  • Example: repaglinide (gluconorm)
  • side effects: weight gain, hypoglycaemia,headache
  • do not use with plavix, DKA, severe hepatic impairment
  • must be taken with food
  • low doses with renal impairment
21
Q

Insulin Secretagogues (sulfonylureas)

A
  • MOA: Stimulates insulin release from the pancreatic beta cells, Increases insulin sensitivity; reduces glucose distribution from liver
  • Example: Diamicron MR (gliclazide)
  • side effects: weight gain, hypoglycaemia
  • contraindications: sulfa allergy, use immediate release formulation with bariatric surgery, severe hepatic impairment, do not use with eGFR <45
  • inexpensive, older drug, drug plans may require the use of this drug before others are covered
22
Q

DPP-4 inhibitors

A
  • MOA: inhibits the DPP4 enzyme, resulting in prolonged incretin levels (delays breakdown of incretin hormones). These regulate glucose balance. These medications are glucose dependent (i.e., they respond to the presence of elevated glucose and result in insulin release only when needed)
  • Example: Januvia
  • Side effects: generally well tolerated (rare cases of pancreatitis and joint pain)
23
Q

GLP-1 Receptor Agonists

A
  • MOA: acting on the same receptor as incretin; increases
    insulin secretion, decreases glucagon secretion, and slows gastric emptying (making you feel fuller, longer)
  • Example: Ozempic (once weekly injectable)
  • Side effects: GI upset, pancreatitis
  • Contraindications: personal or family hx of thyroid cancer or pancreatitis
  • can help with weight loss and CVD risk
24
Q

SGLT2 inhibitors

A
  • MOA: sodium-glucose cotransporter 2 gets inhibited, blocks the reabsorption of glucose by the kidney, increasing glucose excretion, and lowering blood glucose levels
  • Example: jardiance (empagliflozin)
  • Side effects: UTI risk, candidiasis, increased thirst, dehydration, hypotension, DKA
  • contraindications: DKA, sick day protocol, lower limb infection, regulate dose with decreased eGFR
  • helps with CVD, weight loss, and blood pressure benefits
25
Q

Alpha Glucosidase Inhibitor (aka starch blockers)

A
  • MOA: slows down the absorption of carbohydrate in the small intestine. inhibits pancreatic alpha amylase and alpha glucosidases, resulting in delayed breakdown of carbs and absorption of glucose. It also has a dose-depending reduction in insulin and glucose peaks. It can inhibit metabolism of sucrose to glucose/fructose
  • Example: acarbose
  • side effects: GI effects in 74%
  • considerations: TID dosing, not commonly used
  • contraindications: cirrhosis, eGFR <45
26
Q

thiazolidinediones (glitazones)

A
  • MOA: ↑ Glucose uptake in muscle and fat; inhibit hepatic glucose production. Increases insulin sensitivity in peripheral tissues and the liver by activation of certain receptors, which increases glucose uptake in muscles and fat
  • Example: Actos (pioglitazone)
  • side effects: edema, hypoglycaemia, significant weight gain
  • contraindications: heart failure, severe hepatic impairment, history of bladder cancer, hematuria, pregnancy
  • not commonly used
27
Q

Treatment of painful peripheral neuropathy can include:

A

anticonvulsants (Lyrica, gabapentin, etc)
antidepressants (amitriptyline, duloxetine, venlafaxine)
topical nitrite spray
topical capsaicin 0.75% cream
narcotics, non-narcotics

28
Q

erectile dysfunction

A
  • A PDE5 inhibitor is first line with men with diabetes and ED (if no contraindications)
  • Contraindication: nitrate use within 24hr; consider cytochrome p450 drug interactions
  • Possible side effects: dizziness, vision changes, priapism (erection longer than 4 hours), headaches, dyspepsia