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PR3152 Study Deck - Pharmacotherapeutics > Understanding Diabetes and First Line for T2DM > Flashcards

Understanding Diabetes and First Line for T2DM Flashcards

1
Q

Describe the pathophysiology behind Type 1 Diabetes

A

Absolute deficiency of pancreatic B-cell function

Pancreas unable to produce insulin due to immune mediated destruction and positive antibodies

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2
Q

What are the different stages of T1DM?

A

Stage 1: Autoimmunity (Positive antibodies), Normoglycemia and presymptomatic

Stage 2: Autoimmunity (positive antibodies), Dysglycemia and presymptomatic

Stage 3: Autoimmunity, new onset of hyperglycemia and symptomatic

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3
Q

What are the types pf positive antibodies present? HINT: List all 5

A

Insulin
Islet cell autoantibodies
Autoantibodies to GAD
Tyrosine phosphatases IA-2 and IA-2b
Zinc transporter 8

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4
Q

Describe the pathogenesis of Type 2 DM.

A

Progressive loss of adequate B-cells insulin secretion on the background of insulin resistance

In presence of insulin, glucose utilization is impaired and hepatic glucose output increased.

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5
Q

Name the differences between T1DM and T2DM.

A

Primary causes
- T1: autoimmune mediated pancreatic beta cell destruction; positive antibodies
- T2: insulin resistance, impaired insulin secretion and negative antibodies

Insulin production
- T1: Absent
- T2: Normal/ Abnormal

Age
- T1: Usually < 30
- T2: > 40y; increased in obese children and young adults

Onset of clinical presentations
- T1: Abrupt
- T2: Gradual

Physical appearance
- T1: Thin
- T2: Overweight

Proneness to ketosis
- T1: Frequent
- T2: Uncommon

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6
Q

What are the signs and symptoms of hyperglycemia?

A

Dry skin
Extreme thirst
Frequent urination
Drowsiness
Decreased healing
Hunger

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7
Q

What are the signs and symptoms of hypoglycemia?

A

Shaking
Fast heartbeat
Dizziness
Sweating
Impaired vision
Weakness / fatigue
Headache
Anxious
Irritable
Hunger

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8
Q

What are some monitoring parameters used to measure DM?

A

Fasting plasma glucose

Random plasma glucose

Postprandial plasma glucose

Hba1C

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9
Q

Define the following monitoring parameters. (FPG, PPG, Hba1c)

A

FPG: No calorie intake for more than 8 hours

PPG: Glucose level measured after meal, usually after 2h
- Use standardized 75g oral glucose tolerance test

Hba1c: average amount of glucose in blood over past 3 months

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10
Q

What is the relationship between Hba1c, FPG and PPG?

A

Hba1c = 3 months average of (FPG + PPG)

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11
Q

Why is Hba1c not often used to diagnose DM? Which is a better parameter? (ref slide 17)

A

Hba1c provide a range of basal and postprandial contributions.

Better indicator would be basal hyperglycemia since it contributes a larger proportion at high Hba1C

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12
Q

What is the purpose of glucometers?

A

Monitor hypo/hyperglycemia
Adjust medications, diet and exercise

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13
Q

What is the frequency of use of glucometers in T1DM? When should glucose monitoring be done?
What other populations also following the T1DM regime?

A

More than 4 times daily

To do glucose reading:
- Before meals
- At bedtime
- At 3AM

Pregnant, insulin pump users

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14
Q

How often should those with T2DM on multiple injections of insulin check their glucometer reading?

A

More than or equal 3 times daily

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15
Q

When is the ideal time for patients to check their glucose reading?

A

Before breakfast

2h after largest meal

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16
Q

Patient comes in with HbA1c < 6.0%, what is the clinical susceptibility of diabetes? What should you advice a patient and when should the next test be done?

A

No diabetes

To maintain a healthy lifestyle and weight. Repeat test in 3 years

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17
Q

Patient comes in with HbA1c < 6.1-6.9%, what should you do?

A

Proceed to FPG or PPG

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18
Q

What is the criteria to diagnose no diabetes?

A

Hba1C < 6.0%

FPG < 6.0 mmol/L

PPG < 7.8 mmol/ L

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19
Q

When should pre diabetes be suspected?

A

FPG 6.1-6.9 mmol/L

PPG 7.8 - 11.0 mmol/L

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20
Q

When should diabetes be suspected ?

A

FPG > 7.0mmol/L

PPG > 11.1 mmol/L

Hba1C > 7%

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21
Q

Patient comes in with HbA1c > 7.0%, what does this mean?

A

No further test needed

Patient likely have diabetes

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22
Q

Is Hba1C needed to diagnose those with diabetes?

A

No

2 abnormal readings of FPG and PPG are generally recommended

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23
Q

What are the potential complications associated with diabetes? Categorize them according to microvascular and macrovascular complications.

A

Microvascular:
Retinopathy, blindness, Nephropathy, kidney failure, Neuropathy, Amputation

Macrovascular: CVD

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24
Q

How are macrovascular and microvascular outcomes related to the lowering of Hba1c?

A

Decrease in Hba1c can help lower risk of microvascular complications

Relationship not clear between degree of glucose control and risk of macrovascular CV events

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25
Q

What is the general target goal of Hba1c, FPG and PPG?

A

Hba1c < 7.0%
FPG: 5.0 - 7.0
PPG: < 10

26
Q

When should more stringent Hba1c goals (3) be set? Define the more stringent Hba1c goal.

A

Hba1c: 6.0-6.5%

Shorter disease duration
Longer life expectancy as patient is young
No significant CVD

27
Q

When should less stringent Hba1c goals (5) be set? Define the less stringent goals.

A

Hba1c: 7.5-8.0%

History of severe hyperglycemia
Limited life expectancy
Advanced complications
Extensive comorbidities
Target difficult to attain despite intensive SMBG, repeated lifestyle changes and effective counselling

28
Q

How frequent should the following parameters be monitored for stable DM patients?
HbA1C
Lipid
BP
Eye Exam
Renal function test
Foot Exam

A

Hba1c: Every 6 months
Lipid panel: 1 year
BP: Every visit
Eye exam: 1 year
Renal function test: every 6 months/ annually
Foot exam: annually by podiatrist

29
Q

Which are the parameters to be monitored more frequently and how frequent should they be monitored?

A

Hba1c: every 3 months
Lipid panel: 6 months
Eye exam: 6 months

30
Q

What are the nonpharmacological advice to give patients with diabetes?

A

Quit smoking

Weight reduction by 7% of initial body weight

Exercise about 150min/ week and spread into at least 3 days a week

Balanced diet

Restrict alcohol and simple carbs

31
Q

How can T2DM be prevented or delayed?

A

Lifestyle intervention through weight loss and physical activity

Initiating metformin for those BMI > 35, aged < 60 years and women with prior gestational diabetes mellitus

32
Q

What is the indication for use of metformin?

A

Monotherapy with diet and exercise

Combination therapy with other antidiabetic agents and/or insulin

33
Q

What is the mechanism of action of metformin?

A

Decreases hepatic glucose production

Increase peripheral glucose uptake and utilization and hence, increases insulin sensitivity

34
Q

How is Metformin excreted?

A

Renally

35
Q

What are some adverse drug events associated with the use of Metformin?

A

Diarrhea
Anorexia
Metallic tase
Decrease serum B12 concentration hence to check hemolytic anemia
Lactic acidosis

36
Q

How does lactic acidosis occur?

A

Lactic acidosis occurs when
1. Glucose broken down in pyruvate
2. Pyruvate breaks down to lactate and H+ in the presence of no oxygen which can be caused by metformin

37
Q

What are some contraindicated group of patients where Metformin use should be reconsidered to prevent lactic acidosis?

A

Heart failure
Sepsis
Liver impairment
Alcoholism
More than 80 years old

38
Q

What are some drug drug interactions of Metformin and how do they affect its efficacy?

A

Alcohol: increase patient risk of lactic acidosis

Iodinated / contrast media

Cationic drugs such as cimetidine and digoxin: Increase metformin by competing for renal tubular transport

39
Q

How is dose adjustment done for patients with renal insufficiency?

A

eGFR
> 60: no dose adjustment

45 - 60: continue but monitor renal function every 3-6 months

30-45: use lower dose and monitor every 3 months; do not initiate metformin for those not started

< 30: stop

40
Q

What are the benefits of using Metformin?

A

Decrease A1c level by 1.5%
Negligible weight fain and hypoglycemia
Low incidence of side effect
Helps prevent T2DM

41
Q

What are the types of sulfonylureas? HINT: Generations

A

First Gen: Tolbutamide

Second Gen: Glipizide, Gliclazide, Glibenclamide

Third Gen: Glimepride

42
Q

What is the preferred drug for those renally impaired?

A

Glipizide

43
Q

Describe the mode of action for sulfonylureas

A

Stimulates insulin secretion by blocking K+ channel of B cells

Decreases hepatic glucose output and increase insulin sensitivity

44
Q

What is a strict criteria for sulfonylureas to work?

A

Functional beta cells

45
Q

What are the adverse effects of sulfonylureas?

A

Hypoglycemia (NOTE: Prevalent in elderly)
Weight gain
Blood dyscracia

46
Q

What are the drug-drug interactions of sulfonylureas?

A

Alcohol

Beta blockers: Mask effect of hypoglycemia

CYP2C19 inhibitors (e.g. Amiodarone, 5-FU; Fluoxetine): increase conc of sulfonylureas

47
Q

What advice should be given for those on sulfonylureas?

A

Take 15-30 minutes before meal to allow drug to work post-meal (CAUTION those with irregular meals)

48
Q

Name the drugs that are TZD

A

Pioglitazone
Rosaglitazone

49
Q

What is the mode of action of TZDs?

A

Perioxidase proliferator activates receptors by acting as agonist

Promoting glucose uptake into target cells

Decrease insulin resistance and increase insulin sensitivity

50
Q

How are TZDs eliminated?

A

Liver
Benefit patients with NAFLD or NASH

51
Q

What are the adverse drug events related to TZD?

A

Hepatotoxicity
Edema
Fractures: Increased risk in women
Weight gain

Pioglitazone: bladder cancer
Rosaglitazone: increase LDL

52
Q

How is ALT used to guide the initiation / continuation of TZD?

A

> 3 ULN OR symptoms of hepatic dysfunction: discontinue/ do not initiate

> 1.5 ULN: continue and repeat LFT until normal

53
Q

What are the contraindications of TZD?

A

Acute Liver Disease

HF Class III and IV

54
Q

What are the indications to use alpha glucosidase inhibitors?

A

Act as adjunct therapy with other agents when hyperglycemia cannot be managed by diet alone

55
Q

What is the mode of action of alpha glucosidase inhibitors?

A
  1. Competitively inhibit brush border alpha glucosidases enzymes
  2. Delaying glucose absorption
56
Q

Name the alpha glucosidase inhibitor

A

Acarbose

57
Q

What are the adverse effects of acarbose?

A

GI: Flatulence, abdominal pain and diarrhea

Increases LFT at high doses

58
Q

Who are contraindicated from the use of acarbose?

A

Breastfeeding
GI diseases such as obstructive IBD

59
Q

Name the DDI associated with acarbose

A

Intestinal adsorbants e.g. charcoal
Digestive enzymes preparations

60
Q

What advice should you give patients who intend to take alpha-glucosidase inhibitors?

A

Take with large meal

PR3152 Study Deck - Pharmacotherapeutics (10 decks)

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