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PR3152 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Why need to have ideal blood glucose level?

A

For brain and cellular function (energy)

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2
Q

Hormones secreted by alpha and beta cells of islets of Langerhans (in the pancreas) respectively? Exocrine or endocrine function?

A

Glucagon; Insulin

Endocrine

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3
Q

effects of insulin (5)

A
  • Lower blood glucose
  • Lower blood fatty acids
  • Lower blood amino acids
  • Increase protein synthesis
  • Increase fuel storage
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4
Q

which GLUTs are freely permeable to glucose at all times?

A

GLUT1 and GLUT3

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5
Q

How does adaption to metabolic demands increase glucose uptake into cells?

A

during exercise: insulin bind to insulin receptors on muscle cells and GLUTs like GLUT4 can increase presence on cell membrane to transport more glucose into the cell –> meet energy demand of muscle

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6
Q

Insulin is a (catabolic/anabolic) hormone that
1. (increase/decrease) glucose uptake into muscle cells
2. (increase/decrease) glycogenesis (storage of glucose as glycogen in liver cells)
3. (increase/decrease) gluconeogenesis

A

anabolic; increase; increase; decrease

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7
Q

hallmark signs and symptoms of hyperglycemia

A

3Ps
polyuria
polydipsia
polyphagia

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8
Q

Insulin sensitisers

A

metformin
thiazolidinediones (TZDs)

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9
Q

MOA of metformin

A

reduce gluconeogenesis in liver
increase glucose uptake into tissues

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10
Q

What can be started for pre-diabetic patients who does not respond to lifestyle intervention?

A

start metformin to prevent and delay onset of T2DM especially when BMI >= 23, younger than 60 and have history of gestational DM

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11
Q

Metformin HbA1c reduction

A

1.5 - 2.0%

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12
Q

Renal dose adjustment for metformin

A

eGFR 30 - 45 ml/min/1.73m2 –> half dose
eGFR < 30 –> discontinue

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13
Q

What constitutes hypoxic state or at risk for hypoxemia?

A

HF, sepsis, respiratory failure, liver impairment, alcoholism, >=80yo

ADHF due to increase risk for hypoxemia and hypoperfusion

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14
Q

For patient on metformin and require a radiologic procedure, what should be done?

A

withhold metformin for at least 48h (risk of AKI with procedure)
restart when renal function stable

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15
Q

Metformin is a substrate of organic cationic transporters (OCT) in proximal tubules. What drugs can possibly interact with metformin?

A

OCT Inhibitors: cimetidine, dolutegravir, ranolazine

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16
Q

HbA1c reduction in thiazolidinediones (TZD)

A

0.5 - 1.4%

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17
Q

Indication for TZD

A

alternative monotherapy for patients who cannot take metformin or in combination with other antidiabetic agents

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18
Q

contraindications to TZD

A
  • active liver disease
  • symptomatic or history of HF (NYHA class iii or iv)
  • active or history of bladder cancer
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19
Q

First gen sulfonylurea

A

tolbutamide

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20
Q

Second gen sulfonylurea

A

glipizide, gliclazide, glibenclamide

(glibenclamide: risk of prolonged hypoglycemia and highly protein bound – more affected by hypoalbuminemia; used less)

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21
Q

Why is sulfonylureas only indicated for T2DM?

A

Sulfonylureas require residual beta cell function since it stimulates insulin secretion in beta cells

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22
Q

Sulfonylurea target

A

beta cell ATP-sensitive potassium channel

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23
Q

Why should SUs be given 15-30mins before meals? In what group of patients should be cautioned when using SUs?

A

MUST eat after taking SU (works by increasing insulin secretion. if dont eat, patient will be hypoglycemic)
cannot miss or delay any meal
caution in patients with irregular meal schedules (hypoglycemia risk)

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24
Q

Sulfonylurea HbA1c reduction

A

1.5%

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25
Q

How does hypoalbuminemia affect the PK of SU?

A

SUs have extensive plasma protein binding mainly to albumin (>99%)
Hypoalbuminemia will lead to increased [free drug] and have greater clearance of drug

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26
Q

Agents that cause weight gain?

A

Sulfonylurea, TZD, insulin

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27
Q

DPP-4i HbA1c reduction

A

0.5 - 0.8%

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28
Q

MOA of DPP-4i

A

binds and inhibits DPP4 enzyme > prevents degradation of incretin > stimulate pancreas to release MORE insulin

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29
Q

Renal adjustment for sitagliptin

A

eGFR 30 - 45 > half dose to 50mg OD
eGFR <30 > half dose further to 25mg OD

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30
Q

Common autoimmune skin reaction caused by gliptins (DPP-4i) in elderly

A

bullous pemphigoid

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31
Q

Adverse effects of gliptins (DPP-4i)

A
  • GI disturbances
  • Flu like symptoms (headache, running nose, sore throat)
  • Acute pancreatitis
  • Skin reactions (bullous pemphigoid)
  • Use with caution in patients with history of pancreatitis (since action is on pancreatic cells)
  • Severe joint pain that can be disabling (arthralgia, rare AE)
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32
Q

Adverse effects of sulfonylureas

A
  • Hypoglycemia (more risk in elderly, bring sweets around)
  • Weight gain (not very suitable for obese patients (2-5kg, dose-dependent))
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33
Q

Action of active GLP-1

A
  1. Lower gastric emptying (acting on stomach)
  2. Increase glucose-dependent insulin biosynthesis and secretion
  3. Lower glucagon
  4. Improved beta cell function
  5. Decrease food intake (acting on brain – higher satiety and eat less)
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34
Q

GLP-1 RA HbA1c reduction

A

1-2%

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35
Q

GLP-1 RA with CKD benefit

A

SC semaglutide

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36
Q

GLP-1 RA with ASCVD benefit

A

liraglutide, dulaglutide, SC semaglutide

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37
Q

Adverse effects of GLP-1 RA

A
  • N/V (better when body adjusts to treatment)
  • Diarrhea/constipation
  • Headache/tiredness
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38
Q

Can GLP-1 RA be used in pregnant mothers?

A

No

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39
Q

PO semaglutide is co-formulated with absorption enhancer SNAC. What does it do?

A

Cause temporary and reversible local increase in pH which protects against proteolytic degradation

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40
Q

When should PO semaglutide be taken?

A

at least 30min-1h before other medications/food/drinks

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41
Q

MOA of SGLT2i

A

Inhibit sodium-glucose co-transporter-2 (SGLT2) > less reabsorption of filtered glucose > lower renal threshold for glucose > increase urinary glucose excretion

42
Q

Which big 3 benefit does SGLT2i have?

A

ASCVD, HF, CKD (all 3)

43
Q

SGLT2i HbA1c reduction

A

0.8 - 1.0%

44
Q

Why is SGLT2i not indicated for T1DM?

A

Risk of DKA, further exacerbated in T1DM

45
Q

eGFR cut offs for dapagliflozin and empagliflozin initiation for cardiorenal benefit

A

Dapa: eGFR < 25
Empa: eGFR < 20

46
Q

Discontinue SGLT2i when for cardiorenal benefit?

A

Start of dialysis

47
Q

Discontinue SGLT2i when for glycemic control?

A

eGFR persistently < 45

48
Q

Adverse effects of SGLT2i

A
  • UTI (glucosuria)
  • Increase urination
  • Hypotension, hypoglycemia, increase LDL
  • Renal impairment – initially within 2 weeks, but long term is supposed renoprotective
  • Female genital mycotic (fungal) infection (glucosuria)
  • Fournier’s gangrene
  • Euglycemia DKA
  • N/D/V
49
Q

When is alpha-glucosidase inhibitor most effective?

A

When taken with large carbohydrate meal

50
Q

Top reason for discontinuation of alpha-glucosidase inhibitor?

A

Flatulence

51
Q

alpha-glucosidase inhibitor HbA1c reduction

A

0.5 - 0.8%

52
Q

Tirzepatide (dual GLP-1/GIP RA) HbA1c reduction

A

2 - 2.4%

53
Q

Antidiabetic agents with weight loss benefits

A

Metformin, GLP-1 RA, SGLT2i

54
Q

Diabetes screening recommended for:

A

Individuals >=40 and/or risk factors for diabetes

55
Q

To diagnose pre-diabetes, what are the test ranges for
HbA1c
FPG
2hOGTT

A

HbA1c: 6.1 - 6.9%
FPG: 6.1 - 6.9 mmol/L
2hOGTT: 7.8 - 11.0 mmol/L

56
Q

If a patient presents with HbA1c of 6.4%, what FPG & 2hOGTT level should he have to diagnose diabetes?

A

FPG => 7.0 mmol/L
2hOGTT => 11.1 mmol/L

57
Q

Mr Tan sees the doctor for annual health screening. His HbA1c is 6.8%. He took a further test (2hOGTT) and his 2hOGTT results was 10.8 mmol/L.

What is his diagnosis?

A

Pre-diabetes

58
Q

Frequency of diabetic foot screening, kidney panel, retinal funal photography

A

At least once a year. More frequent for higher risk

59
Q

Jane has T2DM and she wants to get pregnant in the next few months. What should she do with regards to her screening for retinopathy?

A

Do eye exam before getting pregnant or during first trimester and closely following during and after pregnancy up to 1 year

60
Q

Frequency of HbA1c screening

A

Every 3 months; every 6 months if stable

61
Q

Frequency of lipid panel

A

every 3-6months if uncontrolled.
Annually if controlled

62
Q

Frequency of BP screening

A

Every visit

63
Q

Insulin HbA1c reduction

A

up to 2.5%

64
Q

Route of elimination of insulin?

A

Exogenous insulin: mainly by kidneys
Endogenous insulin: mainly by liver

65
Q

Common gauge sizes

A

31 and 32

66
Q

Stability of unopened insulin and opened insulin

A

Unopened insulin: good until expiration if refrigerated, if not refrigerated: 4 weeks

Opened insulin: 4 weeks regardless of refrigeration

67
Q

Rapid acting insulin

A

Aspart, lispro, glulisine

68
Q

Short acting insulin

A

Regular insulin (Actrapid)

69
Q

Intermediate acting insulin

A

NPH (BD dosing)

70
Q

Long acting insulin

A

glargine, detemir

71
Q

Ultra long acting insulin

A

Degludec, U-300 glargine

72
Q

Stable mixes of insulin

A

NPH + regular
NPH + rapid acting (aspart, lispro, glulisine)
rapid acting + rapid acting insulin with protamine (becomes intermediate acting)

73
Q

What oral therapeutics to stop/continue when injectable therapy is started?

A

Stop dose: TZD (or reduce; risk of hypogly), SU (or reduce when basal started; stop when premix or prandial insulin start), DPP-4i (when GLP-1 RA initiated)

Continue: Metformin, SGLT2i

74
Q

How to convert when switching from BD NPH to OD glargine/detemir

A

Decrease by 20%

75
Q

Conversion from U-300 glargine to other basal insulin

A

decrease by 20%

76
Q

Basal initiation of insulin

A

Bedtime NPH 10u
OR
0.1-0.2units/kg/day basal insulin

77
Q

How to titrate basal insulin to hit FPG goal?

A

o Increase insulin 2u every 3 days until FPG goal
o May increase 4u every 3 days if FPG constantly >10mmol/L
o Decrease by 10-20% if no clear reason for hypoglycemia
o Target range 5.0-7.0mmol/L

78
Q

How to intensify therapy after hitting basal dose > 0.5units/kg OR FPG already at goal?

A

Add prandial coverage (1 dose with largest meal - 4u or 10% of basal whichever is lower)
if A1c < 8% then decrease basal dose by 4u or 10%

IF on bedtime NPH: consider splitting dose into 2 dose (2/3 AM and 1/3 PM)

79
Q

How does DKA happen?

A

Result from absolute/relative insulin deficiency

Insulin inhibits lipolysis but insulin deficiency = stimulate lipolysis > increase circulating levels of free fatty acids > increase oxidation to ketone bodies in liver (strong acids) > DKA

80
Q

How does HHS happen? (hyperglycemic hyperosmolar state)

A

Stress: Stimulates insulin counter-regulatory hormones (glucagon, catecholamines, glucocorticoids, growth hormone) when v sick > hyperglycemia
Also increases gluconeogenesis, lower peripheral insulin sensitivity and lead to hyperglycemia

81
Q

How to check if patient’s high FPG is due to Somogyi effect?

A

Check BG levels at 2-3am to confirm.

Cut down on antidiabetic meds especially @ night
(BG levels drop sharply at night then feedback mechanism kicks in to bump up BG levels)

82
Q

If patient has history of ASCVD, HF, CKD, what agents should he be put on to reduce cardiorenal risk?

A

ASCVD: SGLT2i or GLP-1 RA
HF: SGLT2i
CKD: SGLT2i > GLP-1 RA

83
Q

When to consider insulin instead of GLP-1 RA?

A
  • Ongoing catabolism (weight loss, muscle wasting, appearing cachexic)
  • Symptoms of hyperglycemia (3Ps)
  • A1c > 10%
  • BG > 16.7mmol/L
    (no area for weight loss and need for glucose lowering)
84
Q

Recommended blood pressure? and the benefits (2)?

A

130/80mmHg
1. reduce CVD mortality
2. slow CKD progression

85
Q

First line agents for diabetic patients with hypertension

A

ACEi/ARBs because it’s renoprotective!

86
Q

Secondary prevention for lipids for diabetic patients with ASCVD

A

High intensity statin therapy

Atorvastatin 40mg (avoiding 80mg bc risk of rhabdomyolysis)
OR
Rosuvastatin 20-40mg

87
Q

LDL cholesterol goals for secondary prevention of ASCVD (lipid management)

A

LDL reduction of 50% from baseline or LDL goal 1.4mmol/L, whichever is lower

88
Q

Primary prevention for lipids for ______y/o and agents indicated

A

40-75y/o

Moderate intensity statin therapy:
atorvastatin 10-20mg
rosuvastatin 5-10mg
simvastatin 20-40mg
etc

High intensity if additional ASCVD factors

89
Q

Target LDL for primary prevention of ASCVD (Lipid management)

A

LDL reduction of 50% from baseline or LDL goal 1.8mmol/L, whichever is lower

90
Q

ASCVD risk factors

A

LDL >2.6, high BP, smoking, CKD, albuminuria, family hx of premature ASCVD

91
Q

Secondary prevention of diabetic patients with ASCVD (Antiplatelet therapy)

A

Aspirin
Clopidogrel if allergic to aspirin

92
Q

Primary prevention of ASCVD in what group of patients?

A

Patients >50 years and with at least 1 additional major risk factors (after discussion with patient)

93
Q

ACEi/ARB recommended for what kidney condition?

A

Micro- and macroalbuminuria

94
Q

Primary prevention for CKD:

A

Blood glucose control
Blood pressure control

95
Q

Target glucose variability in ambulatory glucose profile

A

lower than or equal to 36%

96
Q

Target proportion of time in range (3.9-10mmol/L)

A

70% to achieve A1c of 7.0%

97
Q

What else can be added on to optimise lipids after statin therapy is insufficient to hit LDL goal?

A

Ezetimibe or PCSK9i (repatha, alirocumab, inclisiran)

98
Q

Benefits of ACEi/ARBs, SGLT2i and finerenone in terms of cardiorenal risk?

A

Reduce kidney disease progression and reduce CV events

99
Q

GM is a 59 year old female here for follow up evaluation of her diabetes. She also has a history of hypertension and dyslipidemia, currently controlled. She states her diet and exercise habits are healthy. Her labs and vitals are within normal limits except:

A1c 8.6% (goal <7.5%)
Weight 89 kg (BMI 34 kg/m2)
Current medications: metformin 1g BD, canagliflozin 300 mg OM, lisinopril 10 mg OM, atorvastatin 20 mg OM

Which treatment options would likely have the greatest therapeutic benefits for this patient?

A

Initiating GLP-1 RA
* weight loss benefits (GM is overweight with BMI > 30)
* uncontrolled A1c
* insulin cause weight gain > not preferred

100
Q

A patient with type 2 diabetes has adopted several lifestyle changes. He has lost 7 kg in the past 3 months. All lab work, vital signs, and physical examination findings are normal except for mild nonproliferative retinopathy and chronic kidney disease (eGFR consistently between 35 and 50 mL/min/1.73 m2 for the past year) with albuminuria. The patient’s A1C today is 6.2%. The patient’s current treatment regimen includes metformin 500 mg BD with meals, lisinopril 40 mg daily, rosuvastatin 20 mg daily.
Which of the following medication changes should be recommended today?

Start dapagliflozin
Discontinue metformin
Discontinue lisinopril
Increase metformin

A

Start dapagliflozin > cardiorenal benefits
* keep metformin since eGFR > 30 and A1c is okay
* keep lisinopril because ACEi have cardiorenal benefits

PR3152 (2 decks)

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