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competency 10/11 > endo: DM > Flashcards

endo: DM Flashcards

1
Q

t1dm

A
  • absolute insulin deficiency: autoimmune destruction of pancreatic B cells (immune mediated, or positive antibodies)
  • chromosome 6
  • usually <40yo
  • normal to wasted
  • typically presents with DKA
  • responds to insulin
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2
Q

stages of t1dm

A

stage 1: autoimmunity (positive antibodies), normoglycemia, presymptomatic
stage 2: autoimmunity (positive antibodies), dysglycemia, presymptomatic
stage 3: autoimmunity (positive antibodies), new onset hyperglycemia, symptomatic

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3
Q

t2dm

A
  • progressive loss of adequate B-cell insulin secretion on the background of insulin resistance
  • unknown genetic basis
  • usually >40yo
  • usually obese
  • a/w HTN, HLD
  • typically presents with HONK
  • responds to oral hypoglycemia drugs, may eventually need insulin
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4
Q

insulin resistance

A

in the presence of insulin, glucose utilisation is impaired and hepatic glucose output incerased

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5
Q

criteria for diagnosis of T2DM: FPG>=

A

7 (no caloric intake for at least 8hrs)

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6
Q

criteria for diagnosis of T2DM: 2hr plasma glucose >=

A

11.1 (using a glucose load containing the equivalent of 75g anhydrous glucose dissolved in water)

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7
Q

criteria for diagnosis of T2DM: random plasma glucose >=

A

11.1 (w classic symptoms of hyperglycemia or hyperglycemic crisis)

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8
Q

criteria for diagnosis of T2DM: pre-diabetic

A

FPG 6.1-6.9
-> do an OGTT
-> if =< 7.8: impaired fasting glucose
-> if 7.9-11: impaired glucose tolerance
-> if>=11.1: dm

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9
Q

WHY IS A1C NOT USED FOR DIAGNOSIS IN SINGAPORE?

A

lack of evidence in Asians and high rate of thalassemia in Asia

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10
Q

how many abnormal test results from the same sample, in order to establish diagnosis of t2dm?

A

2!

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11
Q

DM treatment goal: HbA1c

A

=< 7% (7-8.5% for vulnerable patients)

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12
Q

DM treatment goal: FPG

A

5-7

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13
Q

DM treatment goal: PPG

A

<10

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14
Q

more stringent HbA1c targets for

A
  • short disease duration
  • long life expectancy
  • no significant cvd
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15
Q

less stringent HbA1c targets for

A
  • hx of severe hypoglycemia
  • limited to life expectancy
  • advanced complications
  • extensive comorbid conditions
  • those in whom target is difficult to attain despite intensive SMBG, repeated counselings and effective pharmacotherapy
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16
Q

monitoring parameters in T2DM

A
  • Hb1Ac: every 3 months, or 6 months if stable
  • Lipid panel: every 3-6months if not controlled, annually if controlled (metabolic syndrome/cv - macrovascular)
  • BP: every visit {metabolic syndrome/cv - macrovascular)
  • eye exam: every 6 months if unstable, annually if stable (retinopathy - microvascular)
  • albuminuria/renal function: every 6 months or annually depending on presence of protein/albumin in urine (nephropathy - microvascular)
  • foot exam: every day by patient, annually by podiatrist (neuropathy - microvascular)
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17
Q

metabolic syndrome

A

abdominal obesity: >90cm (M), >80cm (W)
- TG >1.7 or on meds
- HDL<1.0 (M) or <1.3 (F)
- BP>130/85 or on meds
- FPG >5.6
^ abdominal obesity + any 2/4 of the factors

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18
Q

which oral hyppoglycemia meds can be used in T1DM?

A

metformin, does not involve B-cells:
- primary: decr hepatic glucose production
- secondary: incr peripheral/muscle glucose uptake and utilisation (ie, insulin sensitivity)

a-glucosidase inhibitors (PPG)

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19
Q

biguanides MOA

A

metformin
- primary: decr hepatic glucose production
- secondary: incr peripheral/muscle glucose uptake and utilisation (ie, insulin sensitivity)

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20
Q

which oral hyperglycemic agent is used off-label for PCOS?

A

metformin

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21
Q

Metformin adr

A

Common: GI, anorexia, metallic taste (usually transient, take w food to alleviate)
Long-term use my decr vit B12, consider periodic measurement especially in those with anemia or peripheral neuropathy
Rare but not fatal: lactic acidosis

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22
Q

Max dose for metformin immediate release

A

2.55g/d

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23
Q

Max dose for metformin extended release

A

2g/d

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24
Q

Lactic acidosis

A

S/sx: nausea, shallow/laboured breathing, mental confusion
- glucose gets broken down into pyruvate for ATP
-> pyruvate gets broken down to lactate when there is a lack of oxygen (anaerobic respiration)
-> lactic acidosis results from incr production or decr clearance of lactate: metformin, hypoxia state

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25
Q

Metformin c/i

A

Severe renal impairment, hypoxia states or at risk for hypoxemia (HF, sepsis, liver impairment, alcoholism, >80y)

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26
Q

Which oral hyperglycemic agent to avoid in acute HF?

A

Metformin, incr risk for hypoxeia and hypoperfusion

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27
Q

Metformin DDI

A
  • alcohol: incr risk of lactic acidosis
  • iodinated contrast material/radiologic procedure: temporarily hold metformin > 48hrs after contrast administration, restart when renal function returns to normal post procedure (incr risk of AKI,, will cause accumulation of metformin)
  • cationic drugs eg. Digoxin: may incr metformin conc by competing for renal tubular transport
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28
Q

Sulfonylurea MOA

A

Primary: stimulate insulin secretion by blocking K+ channels of the B-cells
Secondary: decr hepatic glucose output and incr insulin sensitivity

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29
Q

First gen SU

A

Tolbutamide, others are rarely used due to incr likelihood for adverse effects

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30
Q

second gen SU

A

glipizide, gliclazide glibenclamide

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31
Q

third gen SU

A

glimepiride

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32
Q

which SU to use in renal impairment?

A

tolbutamide, glipizide

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33
Q

which SU to avoid use if CrCl<50ml/min

A

glibenclamide

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34
Q

tolbutamide dosing

A

1-2g/day in divided doses (max 3g/d)

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35
Q

glipizide dosing

A

5mg BD (max 40mg/d)

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36
Q

glibenclamide dosing

A

2.5mg OD-BD (max 10mg BD)

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37
Q

gliclazide dosing

A

80mg OD, dose >120mg should be taken in BD (max 320mg/day)

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38
Q

glimepiride dosing

A

1-4mg OD *max 8mg/d)

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39
Q

SU adr

A

weight gain, hypoglycemia, blood dyscrasias

40
Q

SU c/i

A

hypersensitivity to any SUs

41
Q

SU ddi

A
  • BB, may mask sx of hypoglycemia
  • disulfiram-like reactions (1st gen»>2nd/3rd gen)
  • CYP2C9 inhibitors eg. amiodarone, 5-FU, fluoxetine - may incr glimepiride, glipizide
42
Q

meglitinides MOA

A

stimulate insulin secretion by binding to a different site within the SU receptor of B-cells

43
Q

meglitinides adr

A

weight gain, hypoglycemia, elevated LFTs (rare)

44
Q

meglitinides c/i

A

severe hepatic disease

45
Q

in which group of patients must you use SU/megllitinides with caution?

A

patients with irregular meal schedules
- targets PPG (secretes insulin when needed)
- if pt skips meal, should skip SU dose too

46
Q

TZDs

A

pioglitazone: max 45mg OD
rosiglitazone: max 8mg OD, single dose or in 2 divided doses

47
Q

TZD moa

A

peroxisome proliferator activated receptor agonists, promote glucose uptake into target cells (skeletal muscle, adipose)
- decr insulin resistance, incr insulin sensitivity
- no effects on insulin secretion
(takes up to 1 month to work)

48
Q

TZD black box warning

A

incr risk of CHF
- c/i in NYHA 3/4
- after initiation or dose incr, observe pt for s/sx of HF
- if cfm HF, appropriate mgmt of HF should be initiated: discontinuation or dose reduction should be considered

49
Q

TZD c/i

A

NYHA 3/4, active liver disease

50
Q

adr of TZD

A

hepatotoxicity
- edema
- fracture, incr risk - more likely in women
- weight gain
- bladder cancer (pioglitazone)
- elevated LDL (rosiglitazone)

51
Q

TZDs place in therapy: appears to be beneficial in pts with ____

A

fatty liver disease; NASFLD, NASH

52
Q

a-glucosidase inhibitors moa

A

delay glucose absorption and decr PPG by competitively inhibiting brush burder a-glucosidase enzyme required for breakdown of complex carb - acts locally

53
Q

are a-glucosidase inhibitors ok to use in pregnancy?

A

yes, cat b

54
Q

a-glucosidase inhibitors c/i

A
  • breast feeding
  • gi disease: obstruction, IBD
55
Q

a-glucosidase inhibitors ddi

A

intestinal adosrbents and digestive enzyme preparations may decr effects of a-glucosidase inhibitors

56
Q

a-glucosidase inhibitors adr

A
  • GI: flatulence, abdominal pain, diarrhea
  • elevated LFT
57
Q

incretins MOA

A

naturally occuring hormones released from GIT
GLP-1 receptor agonists, acts like endogenous GLP-1 and binds to the receptors on the B-cells
- decr gastric emptying
- incr insulin secretion
- decr glucagon synthesis
- reduce appetite

58
Q

oral GLP-1 agonist

A

semaglutide

59
Q

GLP-1 agonist, black box warning

A

thyroid C-cell tumours in animals, human relevance unknown
- counsel pt regarding risk of medullary thyroid carcinoma and the symptoms of thyroid cancers
- avoid in pt w thyroid cancers or prior hx of cancer

60
Q

GLP-1 agonist adr

A

lots of GI side effects: n/v/diarrhea, acute pancreatitis

61
Q

moa of DPP4-inhibitors

A

incr conc of endogenous incretins

62
Q

which DPP4i does not require renal dose adj?

A

linagliptin

63
Q

sitagliptin dose

A

100mg OD

64
Q

linagliptin dose

A

5mg OD

65
Q

renal dose adj for sitagliptin

A

CrCl 30-49: 505mg OD
ESRD or severe renal impairment: 25mg OD

66
Q

sitagliptin adr

A

acute pancreatitis, HA, n/v, abdominal pain, skin reaction, angioedema

67
Q

linagliptin adr

A

nasopharyngitisn

68
Q

DPP4i warnings

A

severe joint pain, can be disabling

69
Q

SGLT2i moa

A

leads to incr renal glucose excretion, hence decr blood glucose

70
Q

canagliflozin dose

A

100mg OD, taken before first meal of the day, can incr to 300mg OD if eGFR>60
- do not use if eGFR<30

71
Q

empagliflozin dosing

A

10mg OD, taken in the morning with or without food, may incr to 25mg OD
- do not use if eGFR<45

72
Q

dapagliflozin dosing

A

5mg OD, may incr to 10mg OD
- do not use if eGFR<45

73
Q

SGLT2i adr

A
  • hypotension, hypoglycemia, renal impairment, incr LDL, urinary urgency
  • genital mycotic infection/UTI
  • incr risk of DKA, esp euglycemic DKA
  • fournier’s gangrene (v bad UTI)
  • canagliflozin specific: amputations, hyperK, fractures
74
Q

SGLT2i c/i

A

ESRD or dialysis

75
Q

antidiabetic agents for gestational DM

A

metformin, SU, DPP4i, insulin

76
Q

insulin moa

A

regulation of:
- carbs: facilitate glucose uptake in muscle and adipose tissue, inhibit hepatic glucose output
- fats: enhance fat storage and inhibit mobilisation of fat or energy in adipose tissue
- protein: increase protein synthesis and inhibit proteolysis in muscle tissue

77
Q

SQ insulin

A

stays in fatty area, forms deposit tissue, slowly release into bloodstream

78
Q

how long can you keep an unopened insulin stored in refrigerator?

A

good till expiration date

79
Q

how long can you keep an unopened insulin NOT stored in refrigerator?

A

28 days

80
Q

how long can you keep an opened insulin?

A

good for 28 days regardless of refrigeration

81
Q

considerations about oral therapies when injectables are started: metformin

A

continue

82
Q

considerations about oral therapies when injectables are started: TZDs

A

discontinue when initiating insulin, or reduce dose

83
Q

considerations about oral therapies when injectables are started: SUs

A

discontinue or reduce dose of SU by 50% when basal insulin is initiated (at risk of hypoglycemia), discontinue if mealtime insulin initiated or premix regimen
- effectiveness will eventually wear off and might have to completely rely on insulin

84
Q

considerations about oral therapies when injectables are started: SGLT2i

A

continue

85
Q

considerations about oral therapies when injectables are started: DPP4i

A

discontinue DPP4i if GLP-1 agonists initiated, but both can be continued if insulin therapy initiated

86
Q

how do you convert most insulin dosing?

A

1:1

87
Q

how much do you reduce dose of insulin if patient is at high risk of hypoglycemia?

A

10-20%, but generally depends on clinical judgement

88
Q

exceptions for 1:1 insulin dosing conversion?

A
  • switching from twice daily NPH to once daily glargine/detemir: decr dose by 20%
  • switching from glargine U-300 to other alternative basal insulin analog: decr by 20%
89
Q

s/sx of hypoglycemia

A

blurry vision, sweating, tremor, rapid HR, hunger, confusion, anxiety, shaking, dizziness, headache, weakness and fatigue, irritability

90
Q

adr of insulin

A

hypoglycemia, nocturnal (morning headache, weakness and fatigue, profuse sweating, nightmares)

91
Q

15g of fast acting carbs

A
  • 1/2 cup of fruit juice
  • 2 tablespoon of raisin
  • 3 cubes or 1 tablespoon of sugar
  • 5-6 hard candies
  • 1/2 cup of regular soft drinks
  • 1 tablespoon of honey
92
Q

adr of insulin

A

hypoglycemia, weight gain, lipodystrophy, local allergic reaction, systemic allergic reaction, rare insulin resistance (immune phenomenon)

93
Q

lipoatrophy

A

concavity or pititng of adipose tissue due to immune response, due to pork and beef insulin

94
Q

lipohypertrophy

A

bulging of adipose tissue due to not rotating inj sites

95
Q

when will insulin be considered before GLP-1 agonists?

A
  • ongoing catabolism (weight loss)
  • s/sx of hyperglycemia (diabetic emergencies)
  • A1C>10%
  • BG>16.7mmol/L
96
Q
A

competency 10/11 (31 decks)

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