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PR3152 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What are the signs and symptoms of Hyperglycemia?

A
  1. Polydipsia (extreme thirst)
  2. Polyphagia (extreme hunger)
  3. Polyuria (frequent urination)
  4. Dry skin
  5. Blurry vision
  6. Decrease wound healing
  7. Drowsiness
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2
Q

What are the signs and symptoms of Hypoglycemia?

A
  1. Sweating
  2. Shaking
  3. Anxious
  4. Irritability
  5. Fast heartbeat
  6. Dizziness
  7. Hunger
  8. Fatigue and weakness
  9. Headache
  10. Impaired vision
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3
Q

What is the difference between T1DM and T2DM

A

Type 1 DM:
- Absolute deficiency of pancreatic B-cell function
- Positive antibodies
- Autoimmune
- C peptides absent
- Usually <30 years
- Highly prone to diabetic ketosis

Type 2 DM:
- Insulin resistance with progressive loss of adequate B-cell insulin secretion
- No antibodies
- Often overweight
- C peptides present or abnormal
- usually >40 years

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4
Q

Parameters used to measure glucose and their treatment goals for DM

A

FPG (after 8hrs of no calorie intake): 5 – 7 mmol/L
PPG (after 2hours of meal): ≤10 mmol/L
HbA1c (avg amount of glucose in the blood over past 3 months): ≤7% (7.5 – 8% in more vulnerable patient population)

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5
Q

Criteria for the diagnosis of T2DM

A
  1. HbA1c ≥7%
  2. HbA1c 6.1 – 6.9% + FPG ≥7.0mmol/L or PPG ≥11.1mmol/L
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6
Q

Criteria for the diagnosis of pre-diabetes

A

HbA1c 6.1 – 6.9% + FPG 6.1 – 6.9mmol/L or PPG 7.8-11.0mmol/L

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7
Q

When to rule out diabetes

A
  1. HbA1c ≤6%
  2. HbA1c 6.1 – 6.9% + FPG ≤6mmol/L or PPG <7.8mmol/L
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8
Q

What are the 3 microvascular complications of DM?

A
  1. Retinopathy
  2. Nephropathy
  3. Neuropathy
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9
Q

When is a less stringent hbA1c target used (7.5 – 8%)?

A
  1. Hx of hypoglycemia
  2. Limited life expectancy
  3. Advanced complications
  4. Extensive comorbid conditions
  5. Target is difficult to attain despite effective pharmacotherapy
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10
Q

Monitoring parameters in T2DM and frequency

A
  1. HbA1c: Every 3 months; 6 months if stable
  2. Lipid panel: Every 3-6 months; annually if stable
  3. BP: Every visit
  4. Eye exam: Every 6 months; annually if stable
  5. Albuminuria/ Renal panel: 6 month - yearly if stable depending on presence of albuminuria
  6. Foot exam: Daily by individual; yearly by podiatrist
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11
Q

Non-pharmacologic therapy for diabetes

A
  1. Smoking cessation
  2. Weight loss (>7% loss of initial body weight)
  3. Exercise (150mins per week spread over 3 days or more; strength training for 2 days to be included; and in older (>55yo) patients, balancing and functional training to be incorporated too
  4. Diet modification (green leafy vegetables, lean meat, low-fat dairy product
  5. Restrict alcohol consumption and simple carbohydrates (reduce TG)
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12
Q

List all the affordable therapeutics for diabetes

A
  1. Biguanide – metformin
  2. Sulfonylureas (SUs)
  3. Thiazolidinediones (TZDs) – Pioglitazone, Rosiglitazone
  4. Alpha-glucosidase inhibitors – Acarbose
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13
Q

MOA of metformin

A
  1. Decrease hepatic glucose output and production (Inhibit gluconeogenesis in liver)
  2. Increase insulin sensitivity –> increase intracellular glucose uptake into periphery or muscles
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14
Q

Side effects associated with metformin use

A
  1. Lactic acidosis (Black Box Warning; Rare)
  2. Anorexia
  3. Metallic taste
  4. GI disturbances
  5. Vitamin B12 deficiency –> lead to megaloblastic anemia
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15
Q

C/I to metformin

A
  1. Renal insufficiency
  2. Hypoxic state (eg. Heart failure, hypoperfusion, sepsis, liver impairment)
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16
Q

DDI with metformin

A
  1. Ethanol (increased risk of lactic acidosis)
  2. Iodinated contrast media (renal toxicity –> restart metformin after renal function normalize)
  3. Cationic drugs (eg. digoxin, cimetidine) –> may compete with metformin for renal excretion
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17
Q

Renal dose adjustment of metformin

A

eGFR ≥60: OK. Monitor renal function yearly.
eGFR 45-60: OK but monitor renal panel every 3-6 months
eGFR 30-45: Half-dose; do not start metformin in new patients. Monitor every 3 months.
eGFR <30: Stop metformin (c/i)

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18
Q

What other benefits does metformin have?

A
  1. Positive effect on lipid profile (TG, cholesterol, LDL)
  2. Weight loss (negligible weight gain)
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19
Q

Prevention/ delay of T2DM in pre-diabetic patients

A
  1. Lifestyle modifications (diet, exercise, weight loss, smoking cessation)
  2. metformin therapy (for obese [BMI ≥35], those age <60yo, women with prior gestational DM)
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20
Q

MOA of Glipizide

A
  1. Stimulate insulin secretion by inhibiting K+ channel in functional B-cell of the pancreas
  2. Increase insulin sensitivity
  3. Decrease hepatic output of glucose
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21
Q

Administration of glipizide

A

Take 15-30mins before food

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22
Q

Which SUs can be used in renal impairment

A

Glipizide, Tolbutamide

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23
Q

Which SUs are renally excreted?

A

Gliclazide, Glibenclamide, Glimepiride (hepatic > renal)

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24
Q

DDI of SUs

A
  1. Beta-blockers (mask hypoglycemic symptoms)
  2. Ethanol (disulfiram-like reaction; more common in 1st gen)
  3. CYP2C9 inhibitors (eg. amiodarone, 5FU, fluoxetine) –> may increase Glimepiride and glipizide concentrations)
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25
Q

What is the special requirement for SUs to work?

A

Functioning Beta-cells in pancreas

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26
Q

MOA of Pioglitazone

A
  1. Increase intracellular glucose uptake into target cells (peroxisome proliferation activated receptors agonist)
  2. Decrease insulin resistance
  3. Increase insulin sensitivity
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27
Q

ADR associated with TZDs

A
  1. Increase risk of congestive HF (NYHA group I and II)
  2. Hepatotoxicity (stop if ALT >3x ULN or signs of hepatic dysfunction)
  3. Bone fracture
  4. Edema
  5. Weight gain
  6. Bladder cancer (pioglitazone)
  7. Elevated LDL (Rosiglitazone)
28
Q

Contraindication of TZDs

A
  1. NYHA class III and IV heart failure
  2. Acute liver disease
29
Q

MOA of Acarbose

A
  1. Delay glucose absorption and decrease PPG by competitively inhibiting brush borders alpha-glucosidase enzymes required for the breakdown of complex carbohydrates
  2. Acts locally
30
Q

Most prominent ADR of acarbose

A

Flatulence
other GI ADRs include diarrhea, abdominal pain

31
Q

Contraindications of acarbose

A
  • Breastfeeding
  • GI impairment
32
Q

What class of drug is liraglutide?

A

GLP-1 agonist

33
Q

What is liraglutide MOA?

A
  1. Delay gastric emptying
  2. Increase insulin secretion (activates GLP-1 receptors –> increase adenylate cyclase –> increase cAMP -> increase PKA –> increase insulin secretion)
  3. Decrease glucagon release
  4. Reduce appetite
  5. Improve beta-cells function
34
Q

ADR of liraglutide

A
  1. Acute pancreatitis
  2. GI disturbances (N/V/D)
35
Q

What is the Black Box Warning for liraglutide?

A

Thyroid C cell tumour

36
Q

Additional benefits of GLP-1 agonist?

A
  1. Weight loss
  2. Improve ASCVD
  3. Improve CKD (minimal benefits)
37
Q

Examples of DPP-4 inhibitors?

A
  1. Sitagliptin
  2. Linagliptin
38
Q

MOA of DPP-4 inhibitors

A

Decrease enzymatic degradation of endogenous GLP-1

39
Q

Renal dose adjustment of Sitagliptin

A

Half-dose when CrCl ≥30 but <50 mL/min

40
Q

ADR associated with Sitagliptin

A
  1. Acute pancreatitis (caution with use in patients with Hx of pancreatitis)
  2. Heart attack
  3. GI disturbances
  4. Abdominal pain
  5. Skin reaction
  6. Angioedema
  7. Flu-like symptoms
41
Q

Warnings and precautions with DPP-4 inhibitors use

A
  1. Severe joint pain that can be disabling
  2. Acute pancreatitis with use of Sitagliptin
42
Q

MOA of SGLT2i

A
  1. Decrease renal reabsorption of filtered glucose
  2. Decrease renal threshold for glucose –> increase urinary glucose excretion
43
Q

Renal dose adjustments for SGLT2i agents

A

Canagliflozin: Stop if eGFR <30ml/min; but continue if albuminuria >300mg/dL
Empagliflozin and dapagliflozin: Stop if GFR <45ml/mion

44
Q

ADR of SGLT2i

A
  1. Hypotension
  2. Hypoglycemia
  3. Renal impairment
  4. Increase LDL
  5. Urinary urgency
  6. UTI
  7. Genital mycotic infection
  8. Increased risk for euglycemic diabetic ketoacidosis
45
Q

Contraindications of SGLT2i

A
  1. End stage renal failure
  2. Dialysis
46
Q

Guidelines for SGLT2i use

A

As long as eGFR ≥30ml/min, it is safe to initiate SGLT2i and keep using once initiated

47
Q

Additional benefits of SGLT2i

A
  1. Slgith weight loss
  2. HF
  3. ASCVD
  4. CKD
48
Q

MOA of insulin

A
  1. Increase intracellular uptake of glucose
  2. inhibit hepatic glucose output (inhibit gluconeogenesis and glycogenolysis)
  3. Enhance lipogenesis
  4. Inhibit lypolysis
  5. Increase protein synthesis
  6. inhibit proteolysis
49
Q

When do you need to inject the insulin needle at 45 degrees?

A
  1. Frail elderly
  2. Cachexic patients
  3. Childrens
50
Q

Factors that increases absorption of insulin

A
  1. Heat
  2. Massage
  3. Exercise
  4. jet injection
  5. Lipoatrophy (when bovine or porcine insulin is used too much)
  6. IM administration
51
Q

How does lipohypertrophy happen and what are the consequences?

A

When you never rotate the site of injection when injecting the lower abdomen
Lipohypertrophy leads to decreased absorption

52
Q

Benefits of using ultra-short acting insulin

A

Can be administered with meal or 20mins after starting a meal

53
Q

What are the modifications done to ultra-short acting insulin?

A

Insulin aspart (Fiasp): 2 excipients added (Vitamin B3 to increase speed of absorption and L-arginine to stabilize formulation

Insulin lispro aabc (Lyumjev): 2 excipients added (Treprostinil to enhance absorption via vasodilation and Citrate to increase vascular permeability)

54
Q

List the 3 rapid acting insulin

A
  1. Aspart
  2. Lispro
  3. Glulisine
55
Q

How would you counsel a patient taking rapid-acting insulin?

A

Take 15mins before each meal

56
Q

List the 2 ultra-long acting insulin

A
  1. Glargine U-300
  2. Degludec
57
Q

How would you counsel a patient taking long-acting insulin

A

Take once a day at the same time everyday

58
Q

Which insulins are compatible when mixed together?

A
  1. Regular + NPH
  2. Rapid acting + NPH
  3. Aspart + Degludec
59
Q

Which insulins are incompatible with each other?

A
  1. Glulisine + any other insulin (except NPH)
  2. Long-acting insulin (Glargine/ Detemir) + any other insulin
60
Q

What is Novomix a mix of?

A

Aspart + NPH

61
Q

What is Humalog a mix of?

A

Lispro + NPH

62
Q

What is mixtard a mix of?

A

Regular + NPH

63
Q

Insulin dose conversion from NPH to long-acting?

A

Reduce total NPH daily dose by 20% –> that will be the new dose of the long-acting

64
Q

Management of hypoglycemia associated with insulin use?

A

15-15-15 rule
- 15g of fast acting carbohydrate
- Wait 15 mins
- Check blood glucose if it is still <4 mmol/L, give another. 15g fast-acting carbohydrate

65
Q

When will insulin be considered?

A

Despite being on pharmacotherapy:
1. Ongoing catabolism (weight loss)
2. Symptoms of hyperglycemia
3. HbA1c >10%
4. FPG >16.7mmol./L

66
Q

Insulin dosing?

A
  1. Start FPG insulin first (NPH or long-acting) at a dose of <10IU at bedtime (usually 0.1 IU/kg)
  2. If HbA1c and FPG is still uncontrolled (FPG goal: 5-7mmol/L) after 3 consecutive days of monitoring via SMBG, increase basal insulin dose by 2IU every 3 days (or 4IU if FPG >10mmol/L)
  3. If HbA1c is still above goal despite FPG insulin dose already at >0.5IU/kg or FPG at goal: Add PPG coverage one dose with largest meal of the day (or if on bedtime NPH, consider splitting dose into 2 doses –> 2/3 in the morning and 1/3 in the night)
  4. Dose of PPG insulin is 4IU or 10% of the FPG insulin dose (whichever is lower); if HbA1c is ≤8%, decrease FPG insulin dose by 4IU or 10% as well
67
Q

Diabetic ketoacidosis (DKA) vs Hyperglycemic hyperosmolar state (HHS)

A

DKA:
1. Affects type 1 DM patients
2. Ketones can be found in blood and urine
3. Fruity breath and odour
4. patient is still alert
5. FPG >14mmol/L

HHS:
1. Affects type 2 DM patients (residual insulin left)
2. No ketones
3. Usually extremely dehydrated (FPG >33mmol/L
4. usually stupor

PR3152 (7 decks)

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