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PR3151 Finals > Diabetic drugs > Flashcards

Diabetic drugs Flashcards

1
Q

What are the medications that act on glucose output and uptake?

How much can they decrease HbA1c by?

A

Metformin, thiazolidinediones

Metformin: 1.5%
Thiazolidinediones: 0.5-1.4%

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2
Q

What are the dosings for metformin immediate release?

What is the max dose per day?

Which strength would you recommend to start on?

A

Immediate release: 250mg, 500mg, 850mg, 1000mg

Max dose: 2500 - 2550mg per day

Start with 500-850mg OD, ↑ by 500-850mg OD every 1-2w in divided doses

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3
Q

What are the dosings for metformin extended release?

What is the max dose per day?

Which strength would you recommend to start on?

A

Extended release: 500mg, 750mg, 1000mg

Max dose: 2000mg OD

(Not for children) Start with 500mg OD, ↑ by 500mg weekly

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4
Q

MOA of metformin? (Primary and Secondary)

A

Primary: ↓ hepatic glucose production
Secondary: ↑ insulin sensitivity → ↑ glucose uptake into tissues & utilisation

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5
Q

ADEs of metformin?

A

Usually transient. Take with food and start low dose, titrate slowly:
- GI (n/v/d)
- Loss of appetite
- Metallic taste

Others:
- Long term use → ↓ serum B12 conc (consider periodic measurement esp for pts with anaemia/ peripheral neuropathy)
- Lactic acidosis (rare)

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6
Q

What are the contraindications for metformin?

A
  • Severe renal impairment (GFR < 30ml/min)
  • Hypoxic states/ risk for hypoxemia (as risk for lactic acidosis ↑)
  • AVOID use in acute decompensated HF
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7
Q

DDIs with metformin? (3)

A
  1. EtOH (alcohol): ↑ risk for lactic acidosis
  2. Iodinated contrast material (withhold metformin at least 48h after iodinated contrast administration)
  3. Inhibitors/ inducers of organic cationic transporters (cimetidine, dolutegravir, ranolazine)
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8
Q

What are the clinical benefits of metformin?

A
  • Negligible weight gain and hypoglycemia
  • Possible ↓ in CV events for T2DM pts
  • Prevent and delay T2DM
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9
Q

What are the dosings for TZD?

What is the max dose?

Which strength would you recommend to start on?

A

15mg, 30mg

Max dose: 45mg OD

Start with 15mg or 30mg OD; if inadequate response ↑ dose by 15mg up to max dose

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10
Q

MOA of TZDs?

Does it have any effect on insulin secretion by pancreas?

A

Peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist which promotes glucose uptake into target cells.

Decreases insulin resistance and increases insulin sensitivity

NO effect on insulin secretion

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11
Q

ADEs of TZDs?

Mnemonics: HHIFWB

A
  • Hepatotoxicity*
    (LFT monitoring before initiation and periodically → DO NOT initiate/ discontinue if ALT > 3x ULN or as long as s/sx of hepatic dysfunction occurs; if ALT > 1.5x ULN repeat LFTs weekly until normal)
  • Fluid retention* (cautious use in NYHA Class I or II HF, monitor for s/sx of HF)
  • ↑ risk of fracture (more for women)
  • Weight gain
  • Risk of bladder cancer
  • ↑ risk of hypoglycemia w insulin Tx
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12
Q

DDIs of TZDs?

A

CYP3A4 or CYP2C8 inhibitors or inducers

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13
Q

Contraindications for TZDs?

A
  • Active liver disease
  • Symptomatic/ hx of HF
  • Active/ history of bladder cancer
  • Pregnancy
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14
Q

Clinical benefits of TZDs?

A
  • Beneficial to pts with fatty liver disease
  • Potential risk reduction for stroke
  • ↑ risk of HF
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15
Q

What are the medications that act on insulin secretion?

How much can they decrease HbA1c by?

A

Sulfonylureas, DPP-4i

Sulfonylureas: 1.5%
DPP-4i: 0.5-0.8%

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16
Q

Name the 1st gen, 2nd gen and 3rd gen SUs

A

1st gen- Tolbutamide
2nd gen- Glipizide, Gliclazide
3rd gen- Glimepiride

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17
Q

MOA of SUs? (Primary and Secondary)

What is one IMPORTANT thing to take note with regards to B-cells functioning?

A

Primary: stimulate insulin secretion by blocking K+ channel of B cells
Secondary: ↓ hepatic glucose output and ↑ insulin sensitivity

NEED functional B-cells to work!

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18
Q

For a renally impaired pt, what type of SUs (and gen) should we recommend. Why?

A

Recommend Tolbutamide (1st gen) or Glipizide (2nd gen).

They are cleared hepatically unlike the other SUs.

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19
Q

ADEs of SUs?

A
  • Hypoglycemia (esp elderly)
  • Weight gain (~2-5kg)
20
Q

Contraindications for SUs?

A

Hypersensitivity to SUs

21
Q

DDIs of SUs

A
  • BB may mask s/sx of hypoglycemia
  • Disulfiram-like reaction with alcohol (1st gen&raquo_space; 2nd gen → recommend Glipizide (2nd gen) to pts who drink regularly)
  • CYP2C9 inhibitors (amiodarone, 5-FU, fluoxetine) may ↑ glimepiride, glipizide
22
Q

What are the clinical effects of SUs?

A
  • NO apparent benefits other than blood glucose lowering effects
  • Use with caution in pts with irregular meals
  • Cost-effective Tx
23
Q

What are the different agents used as DPP4-i?

A

Sitagliptin- 100mg OD
Linagliptin- 5mg OD
Vildagliptin- 50mg BD with metformin/ TZS; 50mg OD with SU

24
Q

MOA of DPP-4i?

A

Inhibits DPP-4 enzyme and ↑ concentration of endogenous incretins.

MOA of endogenous incretins (eg GLP-1):
- ↓ gastric emptying
- ↑ glucose-dependent insulin synthesis and secretion
- ↓ glucagon
- Improved B-cell function
- ↓ food intake

25
Q

ADEs of DPP-4i?

A
  • Severe joint pain (rare)
  • Headache
  • Acute pancreatitis*
  • Hypersensitivity reaction
  • Bullous pemphigoid, skin rash
26
Q

Contraindications for DPP-4i?

A
  • Hypersensitivity
  • Current/ hx of pancreatitis
27
Q

DDI of DPP-4i?

A
  • Sitagliptin ↑ digoxin (minimal)
  • Linagliptin CYP3A4 inducer → ↓ Linagliptin
28
Q

What are advantages of DPP-4i compared to GLP-1 agonists?

A
  • Route of administration (GLP-1 are injectables, but recently not anymore with PO Semaglutide)
  • ↓ incidence of GI adverse effects
  • Cheaper
29
Q

What are the disadvantages of DPP-4i compared to GLP-1 agonists?

A
  • Weight neutral
  • Smaller HbA1c reduction
  • No “big 3” (ASCVD, HF, CKD) benefits
30
Q

How much can SGLT2i decrease HbA1c by?

A

0.8-1.0%

31
Q

MOA of SGLT2i?

A

Inhibits SGLT2i, ↑ renal glucose excretion → ↓ blood glucose

32
Q

ADEs of SGLT2i?

A
  • Hypotension, hypoglycemia, renal impairment, ↑ LDL, urinary urgency
  • Genital mycotic infection/ UTI
  • ↑ risk of DKA (esp euglycemic DKA)
  • Fournier’s gangrene
  • Canagliflozin (lower limb amputation, hyperkalemia, fractures)
33
Q

Contraindications of SGLT2i?

A
  • ESCKD/ dialysis
  • History of DKA
  • Recurrent, severe and difficult to treat genitourinary infections
34
Q

SGLT2i used just for glycemic control, when do we NOT initiate and discontinue?

A

DO NOT initiate when eGFR < 45

Discontinue when eGFR persistently < 45

35
Q

If SGLT2i is used also for its cardiorenal benefits, when do we NOT initiate and discontinue?

A

DO NOT initiate when eGFR < 25 (Dapa) and eGFR < 20 (Empa 10mg)

Discontinue at the start of dialysis

36
Q

What are the clinical benefits of SGLT2i?

What are the disadvantages?

A

Benefits:
- Slight weight loss benefits (urination)
- ASCVD (Cana, Empa), HF (whole class), CKD (whole class)

Disadvantages:
- Expensive

37
Q

What medication acts on glucose absorption in the GI tract?

A

α-glucosidase inhibitors

38
Q

How much can α-glucosidase inhibitors decreases HbA1c by?

A

0.5-0.8%

39
Q

When do we use α-glucosidase inhibitors?

A

Carbohydrate-rich/ heavy diets

*To control PPG

40
Q

What are the different dosings of α-glucosidase inhibitors?

A

25mg, 50mg, 100mg

41
Q

How should we administer α-glucosidase inhibitors and titrate?

A
  • Start with 25mg BD-TDS WITH LARGEST MEAL
  • ↑ by 25mg/day every 2-4 weeks to max dose of 150mg/day (60kg and below) or 300mg/day (above 60kg)
42
Q

MOA of α-glucosidase inhibitors?

A
  • Competitively inhibit brush border α-glucosidase enzymes which break down complex carbohydrates → delay glucose absorption, ↓ PPG
43
Q

ADEs of α-glucosidase inhibitors?

A
  • GI (flatulence**, abdominal pain, diarrhoea)
  • ↑ LFT (specifically acarbose – ↑ risk when dose > 100mg TDS)
44
Q

Contraindications α-glucosidase inhibitors?

A
  • GI diseases (obstruction, IBD)
  • Liver cirrhosis
  • Renal impairment (CrCl <25ml/min)
45
Q

DDIs of α-glucosidase inhibitors?

A
  • Intestinal absorbents
  • Digestive enzyme preparations

PR3151 Finals (11 decks)

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