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competency 10/11 > endo: DM > Flashcards

endo: DM Flashcards

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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
Metformin c/i
Severe renal impairment, hypoxia states or at risk for hypoxemia (HF, sepsis, liver impairment, alcoholism, >80y)
26
Which oral hyperglycemic agent to avoid in acute HF?
Metformin, incr risk for hypoxeia and hypoperfusion
27
Metformin DDI
- 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
28
Sulfonylurea MOA
Primary: stimulate insulin secretion by blocking K+ channels of the B-cells Secondary: decr hepatic glucose output and incr insulin sensitivity
29
First gen SU
Tolbutamide, others are rarely used due to incr likelihood for adverse effects
30
second gen SU
glipizide, gliclazide glibenclamide
31
third gen SU
glimepiride
32
which SU to use in renal impairment?
tolbutamide, glipizide
33
which SU to avoid use if CrCl<50ml/min
glibenclamide
34
tolbutamide dosing
1-2g/day in divided doses (max 3g/d)
35
glipizide dosing
5mg BD (max 40mg/d)
36
glibenclamide dosing
2.5mg OD-BD (max 10mg BD)
37
gliclazide dosing
80mg OD, dose >120mg should be taken in BD (max 320mg/day)
38
glimepiride dosing
1-4mg OD *max 8mg/d)
39
SU adr
weight gain, hypoglycemia, blood dyscrasias
40
SU c/i
hypersensitivity to any SUs
41
SU ddi
- 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
meglitinides MOA
stimulate insulin secretion by binding to a different site within the SU receptor of B-cells
43
meglitinides adr
weight gain, hypoglycemia, elevated LFTs (rare)
44
meglitinides c/i
severe hepatic disease
45
in which group of patients must you use SU/megllitinides with caution?
patients with irregular meal schedules - targets PPG (secretes insulin when needed) - if pt skips meal, should skip SU dose too
46
TZDs
pioglitazone: max 45mg OD rosiglitazone: max 8mg OD, single dose or in 2 divided doses
47
TZD moa
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
TZD black box warning
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
TZD c/i
NYHA 3/4, active liver disease
50
adr of TZD
hepatotoxicity - edema - fracture, incr risk - more likely in women - weight gain - bladder cancer (pioglitazone) - elevated LDL (rosiglitazone)
51
TZDs place in therapy: appears to be beneficial in pts with ____
fatty liver disease; NASFLD, NASH
52
a-glucosidase inhibitors moa
delay glucose absorption and decr PPG by competitively inhibiting brush burder a-glucosidase enzyme required for breakdown of complex carb - acts locally
53
are a-glucosidase inhibitors ok to use in pregnancy?
yes, cat b
54
a-glucosidase inhibitors c/i
- breast feeding - gi disease: obstruction, IBD
55
a-glucosidase inhibitors ddi
intestinal adosrbents and digestive enzyme preparations may decr effects of a-glucosidase inhibitors
56
a-glucosidase inhibitors adr
- GI: flatulence, abdominal pain, diarrhea - elevated LFT
57
incretins MOA
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
oral GLP-1 agonist
semaglutide
59
GLP-1 agonist, black box warning
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
GLP-1 agonist adr
lots of GI side effects: n/v/diarrhea, acute pancreatitis
61
moa of DPP4-inhibitors
incr conc of endogenous incretins
62
which DPP4i does not require renal dose adj?
linagliptin
63
sitagliptin dose
100mg OD
64
linagliptin dose
5mg OD
65
renal dose adj for sitagliptin
CrCl 30-49: 505mg OD ESRD or severe renal impairment: 25mg OD
66
sitagliptin adr
acute pancreatitis, HA, n/v, abdominal pain, skin reaction, angioedema
67
linagliptin adr
nasopharyngitisn
68
DPP4i warnings
severe joint pain, can be disabling
69
SGLT2i moa
leads to incr renal glucose excretion, hence decr blood glucose
70
canagliflozin dose
100mg OD, taken before first meal of the day, can incr to 300mg OD if eGFR>60 - do not use if eGFR<30
71
empagliflozin dosing
10mg OD, taken in the morning with or without food, may incr to 25mg OD - do not use if eGFR<45
72
dapagliflozin dosing
5mg OD, may incr to 10mg OD - do not use if eGFR<45
73
SGLT2i adr
- 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
SGLT2i c/i
ESRD or dialysis
75
antidiabetic agents for gestational DM
metformin, SU, DPP4i, insulin
76
insulin moa
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
SQ insulin
stays in fatty area, forms deposit tissue, slowly release into bloodstream
78
how long can you keep an unopened insulin stored in refrigerator?
good till expiration date
79
how long can you keep an unopened insulin NOT stored in refrigerator?
28 days
80
how long can you keep an opened insulin?
good for 28 days regardless of refrigeration
81
considerations about oral therapies when injectables are started: metformin
continue
82
considerations about oral therapies when injectables are started: TZDs
discontinue when initiating insulin, or reduce dose
83
considerations about oral therapies when injectables are started: SUs
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
considerations about oral therapies when injectables are started: SGLT2i
continue
85
considerations about oral therapies when injectables are started: DPP4i
discontinue DPP4i if GLP-1 agonists initiated, but both can be continued if insulin therapy initiated
86
how do you convert most insulin dosing?
1:1
87
how much do you reduce dose of insulin if patient is at high risk of hypoglycemia?
10-20%, but generally depends on clinical judgement
88
exceptions for 1:1 insulin dosing conversion?
- 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
s/sx of hypoglycemia
blurry vision, sweating, tremor, rapid HR, hunger, confusion, anxiety, shaking, dizziness, headache, weakness and fatigue, irritability
90
adr of insulin
hypoglycemia, nocturnal (morning headache, weakness and fatigue, profuse sweating, nightmares)
91
15g of fast acting carbs
- 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
adr of insulin
hypoglycemia, weight gain, lipodystrophy, local allergic reaction, systemic allergic reaction, rare insulin resistance (immune phenomenon)
93
lipoatrophy
concavity or pititng of adipose tissue due to immune response, due to pork and beef insulin
94
lipohypertrophy
bulging of adipose tissue due to not rotating inj sites
95
when will insulin be considered before GLP-1 agonists?
- ongoing catabolism (weight loss) - s/sx of hyperglycemia (diabetic emergencies) - A1C>10% - BG>16.7mmol/L
96

competency 10/11 (31 decks)

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