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3152 - nat > ic12 DM part 1 + IC11 DM Pharmacology > Flashcards

ic12 DM part 1 + IC11 DM Pharmacology Flashcards

1
Q

What is the diagnosis of Pre-diabetes?

A

When HBA1C 6.1 - 6.9%, proceed to do FPG or 2hOGTT

then FPG 6.1 - 6.9mmol/L
or
2hOGTT 7.8 - 11.0mmol/L

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2
Q

When should metformin be recommended for people with pre-DM? (2 points)

A

When glycemic status does not improve despite lifestyle intervention or unable to adopt lifestyle intervention
+
BMI>23, younger than 60, woman with gestational diabetes

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3
Q

What is the contribution of basal VS postprandial hyperglycemia as hba1c increases?

A

Low Hba1c (< 7.3%) –> Postprandial hyperglycemia contributes more
High Hba1c (> 10.2%) –> Basal hyperglycemia contributes more

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4
Q

How to diagnose no dm, pre-dm, and dm?

A

No DM
hba1c lower than 6%
if hba1c 6.1-6.9%, fbg < 6 or 2hOGT < 7.8

DM
if Hba1c 6.1-6.9%, fbg > 7 or 2hOGT > 11.1
if Hba1c >7%, confirm diabetes, no tests needed

pre-DM
if hba1c 6.1-6.9%, fbg 6.1 - 6.9 or 2hOGT 7.8 - 11

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5
Q

What are tests for kidney function in DM patients (3 points)

A

Serum creatinine and eGFR

Urine Albumin / Creatinine ratio (uACR)
Protein-Creatinine Ratio (uPCR)

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6
Q

Goals for non-DM patients (Hba1c, FBG, PPG)

A

Hba1c < 5.7%
FBG < 5.6
PPG < 7.8

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7
Q

Goals for DM patients

A

Hba1c < 7%
FBG: 5 - 7
PPG < 10

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8
Q

What are macrovascular and microvascular outcomes of DM?

A

Macrovascular: Cardiovascular disease eg. stroke, heart attack
Microvascular: Neuropathy (foot), Nephropathy (kidney), retinopathy (eyes)

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9
Q

When should we adopt a more stringent hba1c control for DM patients? (3 points)

A

More stringent (6 - 6.5%)
Short disease duration
Long life expectancy
No significant cardiovascular diseases

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10
Q

When should we adopt a less strict hba1c control for DM patients? (4 points)

A

Less stringent (7.5 - 8%)
History of severe hypoglycemia
Limited life expectancy
Advanced complications
Difficulty in achieving target despite intensive Self Monitoring Blood Glucose (SMBG), counselling, effective pharmacotherapy

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11
Q

Primary and Secondary MOA of Metformin

A

Primary: Inhibit hepatic glucose production
Secondary: Increase tissue sensitivity to insulin

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12
Q

Clinical efficacy of Metformin

What is the additional benefit of Meformin?

A

Reduce hba1c by 1.5-2%

Does not cause hyperinsulinemia or hypoglycemia

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13
Q

What is the max dose of IR Meformin per day?

Starting dose of IR Metformin

A

2550mg per day

500-850mg OD, increase frequency to 3 times a day

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14
Q

Starting dose of Metformin XR

Max dose of Metformin XR

A

500mg OD
Max dose: 2000mg OD or split up to BD

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15
Q

Side effects of Metformin

A

GI nausea, vomiting, loss of appetite, metallic taste

Long term: Vitamin B12 deficiency -> cause numbness

Rare: Lactic acidosis

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16
Q

Which special population can take metformin?

Which patient should not take Metformin XR

A

Pregnant can take

Children cannot take

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17
Q

Contraindicated populations for Metformin (2 points)

A

1) Severe renal impairment: GFR < 30ml/min

2) Patient at risk for hypoxia, lactic acidosis eg. heart failure, sepsis

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18
Q

Drug interactions with Metformin (3 points)

A

1) Alcohol
Increase risk of lactic acidosis

2) Iodinated contrast material
Cause unstable renal function
Withhold metformin for at least 48hrs
Inhibitors or Inducers of Organic

3) Cationic transporters (OCT)
Eg. Cimetidine, Dolutegravir, Ranolazine

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19
Q

MOA of TZD

Example of TZD

A

PPAR agonist, increase insulin sensitivity
increase uptake of glucose into skeletal muscle and adipose tissue

Pioglitazone

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20
Q

Starting dose and Max dose of Pioglitazone

A

Start with 15-30mg OD
Max: 45mg OD

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21
Q

When to discontinue TZD?

A

When ALT > 3x ULN

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22
Q

Adverse effects of TZD (3 points)

A

Fluid retention, Weight gain from fluid retention

Fracture

Risk of bladder cancer

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23
Q

Contraindicated populations for TZD (3 points)

A

1) Active liver disease

2) Symptomatic or history of heart failure

3) Active or history of bladder cancer

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24
Q

Efficacy of TZD in Hba1c

Other benefit?

A

0.5% - 1.4%

Beneficial for patients with Fatty liver disease (even though its hepatotoxic)

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25
Q

Similarity and Difference between Metformin and TZD

A

Similarity:
Similar MOA, both increase tissue sensitivity to insulin

Difference
Metformin is renally cleared, cannot use when CrCl <30ml/min
TZD is hepatotoxic

26
Q

What are some examples of Sulfonyureas?

MOA of SU? (Primary, Secondary)

A

Glipizide, Gliclazide MR

Primary: Stimulate secretion by blocking K+ channels of beta cells

Secondary: Decrease hepatic glucose output and Increase insulin sensitivity

27
Q

What happens to SU in beta cell, and how does it cause insulin release?

A

SU inhibit receptor protein SUR1, inhibit K+ from releasing from beta cells

Accumulation of K+ cause depolarisation, which causes voltage sensitive Ca2+ to open and allow Ca2+ to enter

Ca2+ causes release of insulin

28
Q

How are most SU eliminated?

Which SU should be used for renal impairment?

A

Renally

Glipizide

29
Q

Counselling point of SU

A

Take 15-30 mins before meal so to allow release of insulin before eating

30
Q

Adverse effects of SU (2 points)

A

1) Hypoglycemia, esp in elderly that eat little

2) Weight gain (2-5kg)

31
Q

Drug drug interactions with Glipizide (3 points)

A

1) Beta blockers: can mask symptoms of hypoglycemia

2) Alcohol: disulfiram like reaction, use 2nd or 3rd gen instead

3) CYP2C9 inhibitors

32
Q

Clinical efficacy of SU

A

Lower hba1c by 1.5%

33
Q

MOA of DPP4i

Examples of DPP4i and their doses (3 points)

A

Inhibit the breakdown of incretins eg. GLP1, which triggers insulin production, decrease glucagon secretion, slow gastric emptying and feel full

Sitagliptin 100mg OD

Vildagliptin
50mg OD with SU
50mg BD with Metformin or TZD
(how to rmb: higher dose with agents that dont increase insulin)

Linagliptin 5mg OD

34
Q

Adverse effects of DPP4i

A

Severe joint pain

Acute pancreatitis

35
Q

Clinical efficacy of DPP4i if used as monotherapy

A

0.5-0.8% reduction in hba1c

36
Q

MOA of SGLT2i

A

Inhibit transporters in proximal tubule
→ blocking reabsorption of glucose
→ increase renal glucose excretion

37
Q

Examples of SGLT2i and doses

A

Dapagliflozin 5, 10mg OD
Empagliflozin 10, 25mg OD

38
Q

Adverse effects of SGLT2i (4 points)

A

Increased urination

Urinary tract infection

Diabetic Ketoacidosis

Hypotension

39
Q

What is diabetic ketoacidosis?

Who does it frequently occur in?

A

When high sugar and low insulin, body cannot use sugar to produce insulin

Hence will convert fats to energy instead, and ketones are produced also

usually occurs in type 1 DM

40
Q

Renal considerations for SGLT2i

A

If want glycemic control, must be more strict
(dont initiate, discontinue) eGFR <45

If want big 3 cardiorenal benefit , can be more lenient
(dont initiate) eGFR < 25 for Dapa, eGFR < 20 for Empa
(discontinue) patient start dialysis

41
Q

When SGLT2i is used for glycemic control on patients with no cardio conditions, what is the cut off for initiation? (egfr < __)

A

When eGFR < 45

42
Q

When patient has comorbidities eg. HF, MI, CKD, what is the cut off for SGLT2i initiation?

A

Do not initiate if EGFR < 25 for dapa and < 20 for empa

Stop when patient starts dialysis

43
Q

Hba1c reduction of SGLT2i

A

0.8 - 1%

44
Q

Out of the SGLT2i, use which one for ASCVD, Heart failure, CKD?

A

ASCVD: Empa
HF, CKD: Dapa

45
Q

what are the big 3 outcomes for SGLT2i?

A

ASCVD, HF, CKD

46
Q

What class of drugs is Arcabose?

MOA of Arcabose

A

a-glucosidase inhibitors

Delay glucose absorption by blocking breakdown and absorption of carbs in GI

Only works for Post Prandial glucose, not Fasting glucose

47
Q

Starting dose of Acarbose

A

25mg 2-3x a day with each meal
Max dose: 150mg a day (60kg or less), 300mg a day (>60kg)

48
Q

Adverse effects of Acarbose

A

GI flatulence, abdominal pain, diarrhoea

49
Q

What is the class that acts as Incretins?

Example and dose?

A

GLP1 receptor agonist

Liraglutide
0.6mg, 1.2mg (1 week), 1.8mg

Semaglutide
(SC injection) 0.25mg, 0.5mg (1 month), 1mg
(PO) 3mg, 7mg (1 month), 14mg

Dulaglutide
0.75mg, 1.5mg (1 month), 3mg, 4,5mg

50
Q

Which GLP 1 agonist needs to be taken on empty stomach?

A

Semaglutide oral, 30 mins before eating

the other SC injections can be taken anytime

51
Q

Adverse effects of GLP-1

A

Headache
Nausea, vomiting
acute pancreatitis

52
Q

Absolute contraindication with GLP-1 agonist

A

Thyroid cancer

53
Q

MOA of GLP-1

A

Bind to GLP-1 receptor found in beta cells, Increase insulin secretion and Decrease glucagon release, decrease gastric emptying, make you feel full

54
Q

Which drug works on fasting BG the most? Why?

A

Metformin, cos it targets the hepatic glucose output

55
Q

Drugs good for weight loss

A

Metformin (ic11)
GLP-1 agonist
SGLT2i (slight weight loss)

56
Q

Drugs with risk of hypoglycemia

A

Insulin
SU

57
Q

Drugs that can cause weight gain

A

TZD (from fluid retention)
SU (2-5kg)
Insulin

58
Q

Drugs that can increase insulin sensitivity

A

Metformin (secondary)
TZD
SU (secondary)

59
Q

Drugs contraindicated with Alcohol

A

Metformin (increase risk of lactic acidosis)

SU (disulfiram like reaction, worse with Tolbutamide)

60
Q

Drugs taken with relation to food

A

15 mins before food:
Sulfonylurea

With food:
Acarbose

On empty stomach:
PO Semaglutide

61
Q

Drugs that have big 3 benefits

A

SGLT2i
GLP-1 Agonists

3152 - nat (16 decks)

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