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endo y3s1 > IC12-14 DM > Flashcards

IC12-14 DM Flashcards

1
Q

pre-DM screening

recommended individuals, types of test

A

asymptomatic individuals aged ≥40 &/or with risk factors for diabetes:

  • Fasting plasma glucose (FPG)
  • HbA1c
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2
Q

pre-DM screening
test results

A

Asymptomatic individuals with result suggestive of DM based on FPG & HbA1c → to repeat test the next day

when 2 different tests are available & results > diagnostic thresholds ⇒ confirmed diagnosis of DM

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3
Q

pre-DM management

A
  1. lifestyle modification
  2. metformin
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4
Q

pre-DM management
1. lifestyle modification

A
  • Healthy diet
  • Increased physical activity (every week):
    at least 150 minutes of moderate intensity exercise (such as brisk walking, leisure cycling)
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5
Q

pre-DM
2. metformin

when to start, recommended individuals

A

glycaemic status does not improve despite lifestyle intervention
Unable to adopt lifestyle intervention

especially if persons have BMI of ≥ 23 kg/m2, are younger than 60 years of age, or are women with a history of gestational diabetes.

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6
Q

T1DM
background

A

Due to insufficient insulin secretion (+ resistance to action of insulin)

Absolute deficiency of pancreatic β-cell function
* Immune mediated destruction → autoimmune
* Positive antibodies → developed during childhood

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7
Q

T1DM staging

A
  1. Normoglycemia + Presymptomatic
  2. Dysglycemia + Presymptomatic
  3. New onset hyperglycemia + Symptomatic
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8
Q

T2DM background

A

Resistance of action of insulin → results in decreased function of pancreas ⇒ may lead to insufficient insulin secretion

Body is able to produce insulin but body does not accept it (resistant)
Progressive loss of adequate β-cell insulin secretion on the background of insulin resistance

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9
Q

T2DM effects

A

glucose utilisation is impaired (inability to utilise glucose pumps) & hepatic glucose output increased

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10
Q

T1DM characteristics

Primary cause, Insulin production (check C-peptide level), Age of onset, Onset of clinical presentation, Physical appearance, Proneness to ketosis (DKA)

A

Autoimmune-mediated pancreatic β-cell destruction
(+) Ab

Absent; no insulin is produced

Usually < 30 years

Abrupt

No insulin at all

Often thin

Due to loss of sugar in urine

Frequent
Increase in blood sugar & lack of insulin ⇒ body prone to producing ketones

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11
Q

T2DM characteristics

Primary cause, Insulin production (check C-peptide level), Age of onset, Onset of clinical presentation, Physical appearance, Proneness to ketosis (DKA)

A

Insulin resistance
Impaired insulin secretion
(-) Ab

Normal/ abnormal

Often > 40 years
But increasing prevalence in obese children & younger adults

gradual

Often overweight

uncommon

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12
Q

signs & symptom of hyperglycemia
causes

A

too much food, too little insulin/ diabetes medication, illness, stress

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13
Q

signs & symptom of hyperglycemia
onset

A

gradual, may progress to diabetic coma

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14
Q

signs & symptom of hyperglycemia

A

3Ps: polydipsia (extreme thirst), polyuria (increased urination), polyphagia (increased hunger)

Dry skin (due to dehydration), blurred vision, drowsiness, decreased healing

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15
Q

signs & symptoms of hypoglycemia
cause

A

too little food, too much insulin/ diabetes medication, extra activity

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16
Q

signs & symptoms of hypoglycemia
onset

A

sudden, might progress to insulin shock

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17
Q

signs & symptoms of hypoglycemia

A

activation of SNS

  • Shaking, fast heartbeat, sweating, dizziness, anxious
  • Hunger, impaired vision, weakness & fatigue, headache, irritable
  • Nocturnal → nightmare, restless sleep, profuse sweating, morning headache
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18
Q

diagnostics for DM

A
  1. Fasting plasma glucose (FPG)
    * No calorie intake for ≥ 8 hrs
  2. Random or casual plasma glucose
    * Glucose level at any time of the day, regardless of meals
  3. Postprandial plasma glucose (PPG)
    * Glucose level measured after meal; usually after 2 hours
  4. Haemoglobin A1c (HbA1c or A1C)
    * Average amount of glucose in a person’s blood over the past 3 months [3 month average of FPG + PPG]
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19
Q

Basal & postprandial contributions to hyperglycemia by HbA1c range

A

High HbA1c → largely contributed by basal hyperglycemia
Important to start on insulin → targets basal hyperglycemia

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20
Q

diagnosis process for DM

A
  1. Determine HbA1c values
  2. If HbA1c 6.1-6.9%, conduct further testing with FPG or 2hOGTT
    Requires 2 abnormal results [1 from HbA1c, 1 from FPG/ 2hOGTT to determine T2DM diagnosis]
  3. If HbA1c >7.0%, patient is confirmed to have T2DM
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21
Q

criteria for no DM

A
  1. HbA1c < 6.0%
  2. HbA1c 6.1-6.9%, but FPG < 6.0mmol/L or 2hOGTT < 7.8 mmol/L
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22
Q

criteria for pre-DM

A

HbA1c 6.1-6.9%, and FPG 6.1 - 6.9 mmol/L or 2hOGTT 7.8-11.0 mmol/L

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23
Q

criteria for DM

A
  1. HbA1c 6.1-6.9%, but FPG >7.0mmol/L or 2hOGTT >11.0 mmol/L
  2. HbA1c > 7.0%
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24
Q

complications of DM

A
  1. macrovascular
  2. microvascular

will lower overall life expectancy by 5-10 years

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25
Q

complications of DM
macrovascular

A

Increases CVD by 2-4x
* Stroke, MI, clogging of peripheral arteries (in hands & legs)
* Might require stent in heart/ extremities to allow blood flow

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26
Q

complications of DM
microvascular

A
  1. Retinopathy, blindness
    New & small BV swell → BV will start to burst & release blood into eyeball, causing blindness
  2. Nephropathy, kidney failure
    Glucose causes larger pores in kidney tubules, thus causing leakage of albumin (albuminuria)
  3. Neuropathy (60-70%), amputation
    Increased sugar levels impedes recovery of wound
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27
Q

screening for DM complications

A
  1. HbA1c
  2. BP
  3. lipid panel
  4. eye exam
  5. albuminuria/ renal function
  6. Foot exam
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28
Q

screening for DM complications
Eye exam

when to start - T1DM & T2DM

A

Adults with T1DM: within 5 years after onset of DM
People with T2DM: at time of diabetes diagnosis

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29
Q

screening for DM complications
Eye exam

frequency

A

If no evidence of retinopathy for 1/more annual eye exams + glycemia well controlled
Screening every 1-2 years

Any level of diabetic retinopathy present
Subsequent examinations to be repeated at least annually

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30
Q

screening for DM complications
Eye exam

women with DM

A
  • before becoming pregnant/ during first trimester of pregnancy
  • To be closely followed during pregnancy & up to 1 year after giving birth
  • Pregnancy may cause DR to develop/ worsen
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31
Q

screening for DM complications
foot exam

frequency

A

At least 1x a year by podiatrist, but by patient should be everyday
Check more frequently for those at higher risk of diabetic foot ulcers

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32
Q

screening for DM complications
foot exam

what to look out for

A

Inspection of skin, assessment of foot deformities, neurological assessment, vascular assessment

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33
Q

screening for DM complications
foot exam

advice

A

Encourage smokers to quit smoking → will reduce risks of lower extremity amputations
Educate on good foot care & appropriate footwear

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34
Q

screening for DM complications
renal function/ albuminuria

when to start - T1DM & T2DM

A

Beginning 5 years after T1DM diagnosis

at time of diagnosis for T2DM

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35
Q

screening for DM complications
renal function/ albuminuria

frequency

A

every 6 months/ annually; depends on presence of protein/ albumin in urine

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36
Q

screening for DM complications
renal function/ albuminuria

tests

A
  1. Serum Cr &/or eGFR
    Cr → estimates how quickly kidneys filter blood (GFR)
    Low filtration = poor kidney function
    AND
  2. Urine albumin/ creatinine ratio (uACR)
    Ratio measures how much albumin in urine sample relative to how much creatinine there are
    OR
  3. Protein-creatinine ratio (uPCR)
    Normal: <30 ug/mg; microalbuminuria: 30-299 ug/mg; macroalbuminuria: >300 ug/mg
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37
Q

diabetic emergencies
DKA

T1DM vs T2DM

A

More common in T1DM
absolute/ relative insulin deficiency → cells cannot take up glucose
* Leads to lipolysis + metabolism of free fatty acid
Formation of beta-hydroxybutyrate (ketones), acetoacetic acid & acetone in the liver
* Stress → stimulates insulin counter-regulatory hormones (ie glucagon)
Excess glucagon: ↑ gluconeogenesis and ↓ peripheral ketone utilisation

T2DM
Have residual insulin production ⇒ protected against excessive lipolysis & ketone production

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38
Q

diabetic emergencies
DKA

labs

A

increased: sugar, acid & ketones

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39
Q

diabetic emergencies
DKA

BG level, mental status

A

BG >14 mmol/L

Alert

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40
Q

diabetic emergencies
DKA

result of ketone formation

A

Found in blood & urine
Fruity breath odour
Acidosis

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41
Q

diabetic emergencies
HHS

background (ketones?)

A

No ketones formed
* Due to residual insulin
* No acidosis

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42
Q

diabetic emergencies
HHS

BG, mental status

A

BG >33 mmol/L; patient usually in state of dehydration

in stupor

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43
Q

Dawn phenomenon & Somogyi effect

A

High BG levels at dawn, but bedtime BG is normal

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44
Q

Dawn phenomenon cause

A

Release of cortisol in the morning
⇒ BG levels rises sharply

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45
Q

Somogyi effect cause

A

BG levels drop sharply at night (due to missing bedtime snack/ too much insulin)
Hypoglycemic status sensed by body

Body responds by releasing glucagon
BG level rises; rebound hyperglycemia

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46
Q

Somogyi effect management

A

To reduce night dose of glucose lowering agent/ basal insulin

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47
Q

treatment goals

non-DM –> HbA1c, FBG & PPG

A

HbA1c <5.7% , FBG <5.6 & PPG <7.8

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48
Q

treatment goals

DM –> HbA1c, FBG & PPG

A

HbA1c <7% , FBG 4-7 & PPG <10

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49
Q

difference in HbA1c goals

normal vs strict vs less strict

A

General goal: <7.0%
Normal adults

More stringent: 6.0-6.5%
Short disease duration, long life expectancy, no significant cardiovascular diseases
Usually younger patients

Less stringent: 7.5-8.0%
History of severe hypoglycemia, Limited 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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50
Q

Metformin indications

A

Monotherapy with diet & exercise

in combination with other antidiabetic agents and/or insulin in patients with T2DM

51
Q

Metformin MOA

A

Primary: ↓ hepatic glucose production (endogenous production of glucose)
Secondary: ↑ peripheral/muscle glucose uptake & utilisation

52
Q

Metformin PD
time for onset & max effect

A

Onset: within days
max effects take up to 2 weeks

53
Q

Metformin formulations

dosing for each type

A
  1. IR
    * Start with 500-850 mg OD
    * ↑ by 500 – 850 mg OD every 1-2 weeks in divided doses (OD to TDS)
    * Max dose: 2500 – 2550 mg per day
  2. ER
    * Start with 500 mg OD.
    * ↑ by 500 mg weekly
    * Max dose: 2000 mg OD.
    * May divide dose to 1000 mg BD if glycemic control not achieved with OD dosing
    if dose > 2000 mg needed, switch to regular release
54
Q

Metformin ADR

A

GI disturbances (diarrhoea, N/V), loss of appetite, metallic taste
usually transient
take with food & increase dose gradually to minimise GI disturbances
Important to start at lowest possible dose (usually give 500mg in hospitals regardless)

Long-term use may ↓serum B12 concentrations
consider periodic measurement especially in those with anaemia or peripheral neuropathy
To check if patient experiences numbness in legs & hands

Rare but fatal:** lactic acidosis** (3/100,000 patients/year)

55
Q

Metformin c/i

A
  1. severe renal impairment
  2. hypoxic states (or disease that can cause it)
56
Q

Metformin DDI

A
  1. Alcohol: ↑ risk for lactic acidosis
  2. Iodinated contrast material (used in radiologic procedure)
    Will cause worsening of kidney function → undesirable as metformin is cleared renally
  3. Inhibitors/inducers of organic cationic transporters (OCT)
    OCT 2 inhibitors (e.g. cimetidine, dolutegravir, ranolazine) may ↑ metformin by ↓ renal elimination; accumulation of metformin
57
Q

TZD indication

A

Alternative monotherapy for patients who cannot take metformin

in combination with other antidiabetic agents → more common
MOA

58
Q

TZD MOA

A

(PPARgamma) agonist to promote glucose uptake into target cells (skeletal muscle/adipose tissue)

↓insulin resistance; ↑ increase insulin sensitivity

59
Q

TZD time for max effect

A

Takes up to a month for maximal effect

60
Q

TZD elimination

A

liver
* avoid if have liver impairment

61
Q

TZD dosing

A

Start with 15 mg or 30 mg OD
for an inadequate response, ↑ dose by 15 mg, up to max of 45 mg OD

62
Q

TZD DDI

A

When co-administered by CYP3A4 & CYP2C8 inhibitors/ inducers

63
Q

TZD AE

A

Hepatotoxicity
Monitor LFT before initiation & periodically thereafter
Do not initiate therapy/discontinue if ALT >3x ULN or liver failure patients
If ALT > 1.5x ULN during therapy, repeat LFTs then weekly until normal
Discontinue if s/sx of hepatic dysfunction regardless of ALT level
Jaundice & urine colour

Fluid retention (caution use in NYHA Class I or II Heart Failure)
Monitor s/sx of heart failure after initiation/dose adjustment
Fracture (increased risk; more likely in women) → non-spinal/ vertebra
Weight gain (dose related); linked to fluid retention
Risk of bladder cancer
Increased risk of hypoglycemia with insulin therapy

64
Q

TZD c/i

A
  1. active liver disease
  2. HF
  3. active/ have hx of bladder cancer
65
Q

TZD benefits

A

Appears beneficial in patients with Fatty Liver Disease → LFTs are still normal
Nonalcoholic fatty liver disease (NAFLD)
Nonalcoholic steatohepatitis (NASH)

CV Effects
Potential reduction in risk of stroke

66
Q

Sulfonylureas indication

A

When hyperglycemia cannot be managed by diet & exercise alone

may be used concomitantly with other glucose lowering agents and/or insulin

67
Q

Sulfonylureas MOA

A

Primary: stimulate insulin secretion by blocking K+ channel of ß- cells
Secondary: ↓ hepatic glucose output & ↑ insulin sensitivity

68
Q

Sulfonylureas when to administer

A

Generally take 15-30 mins before food
Because drug requires time for absorption & to work on ß- cells → secretion of insulin before food intake

69
Q

Sulfonylureas AE

A

Hypoglycemia (especially in elderly) → if eat too little
Weight gain (~2-5 kg)

70
Q

Sulfonylureas DDI

A

ß-blockers may mask s/sx of hypoglycemia
ie: will slow down HR

Disulfiram-like rxn with alcohol (1st gen&raquo_space; 2nd/3rd gen)
Can suggest skipping SU dose if patient plans to drink alot
Flushing, tremors

CYP2C9 inhibitors

71
Q

DDP4i effects

A

Inhibits DPP4 enzyme & increases concentration of endogenous incretins
Essentially prolonging the effects of active GLP1

72
Q

DDP4i
effects of incretin

A
  1. Decreases gastric emptying → slows down food from exiting stomach
  2. Increases glucose-dependent insulin biosynthesis & secretion
  3. Decreases glucagon (reduced gluconeogenesis → lesser glucose being produced endogenously)
  4. Decrease food intake
73
Q

DDP4i indication

A

Second or third-line agents in T2DM treatment
Usually used as dual/ triple combination therapy
Good for patients with kidney failure/ on dialysis who refuse insulin
Ideal for mildly raised HbA1c

74
Q

DDP4i formulations & doses

A
  1. Sitagliptin
    100 mg OD
    eGFR ≥30 to <45 mL/min/1.73 m2: 50mg OD
    eGFR < 30 mL/min/1.73 m2: 25mg OD
  2. Vadagliptin
    50mg BD if with metformin or TZD
    50 mg OD if with SU
    CrCL ≥50mL/min: 50mg BD
    CrCL <50 mL/min: 50mg daily
  3. Linagliptin: 25 mg OD
75
Q

DDP4i AE

A

severe joint pain
Bullous pemphigoid, skin rash
Headache

76
Q

SGLT2i MOA

A

Reduces reabsorption of glucose @ PCT
Leads to ↑renal glucose excretion ⇒ ↓ blood glucose

77
Q

SGLT2i formulations & dose

A

Canagliflozin
100 mg OD, taken before the first meal of the day
increase to 300 mg OD if eGFR >60 ml/min & need further BG control
do not initiate if eGFR<30 ml/min

Empagliflozn
10 mg OD, taken in the morning with or w/o food
May increase to 25 mg OD
do not initiate if eGFR <45 ml/min

Dapagliflozin
5 mg OD, taken in the morning with or w/o food
may increase to 10 mg OD if further BG control is needed
do not initiate if eGFR<60 ml/min

78
Q

SGLT2i ADR

A

Hypotension
Hypoglycemia
UTI
DKA
genital mycotic fungal infection

79
Q

SGLT2i Considerations for renal function

for glycemic control only vs cardiorenal protective (initiation & stop)

A

Glycemic control
* do not initiate if eGFR <45
* stop if persistently eGFR <45

Cardiorenal protective
* do not initiate if eGFR <25 for Dapagliflozin or eGFR <20 for Empagliflozin
* stop when start on dialysis

80
Q

SGLT2i Benefits towards 3 conditions

ASCVD, HF, CKD

A

ASCVD: canagliflozin & empagliflozin
HF: empagliflozin & Dapagliflozin
* Shortens hospitalisation & delays HF from occurring
CKD: Dapagliflozin

81
Q

α-Glucosidase Inhibitors
indication

A

used as adjunct therapy (those who refuse insulin)

T1Dm patients requiring additional PPG control

82
Q

α-Glucosidase Inhibitors MOA

A

Binds to receptors lining GIT
Delay glucose absorption & ↓PPG by competitively inhibit brush border α-glucosidases enzyme required for breakdown of complex carbohydrates to simple sugars (that can be absorbed by GIT)

83
Q

α-Glucosidase Inhibitors onset & time for administration

A

Onset is rapid with each meal → take with meals
* best if take with largest meal/ meal with most carbs

84
Q

α-Glucosidase Inhibitors dosing

A

Administration: weight based
Start with 25 mg BD - TDS with each meal
Lower dose due to bloating → might affect compliance
↑ by 25 mg/day every 2-4 wks to max dose of 150 mg/day (≤ 60 kg) or 300 mg/day (> 60 kg)

85
Q

α-Glucosidase Inhibitors AE

A

GI: flatulence, abdominal pain, diarrhoea
most common cause of drug discontinuation
↑ LFT (specific for acarbose; ↑risk at dose >100 mg TD

86
Q

α-Glucosidase Inhibitors c/i

A

GI diseases → obstruction, IBD
Liver cirrhosis

87
Q

insulin indications

A

T1DM ⇒ required

T2DM ⇒ for symptomatic patients; once have improvements, can switch back to oral agents

Pregnant patients with DM
* Possible to take metformin, but insulin = safer & easier to titrate + can be used during mealtimes

88
Q

insulin target organs

A

pancreas
adipose tissue
muscle
liver

89
Q

insulin effects

on carbohydrates, proteins & fats

A

Glucose: facilitating uptake of glucose in muscle and adipose tissue & by inhibiting hepatic glucose output (glycogenolysis and gluconeogenesis)

Fat: enhancing fat storage (lipogenesis) & inhibiting the mobilisation of fat for energy in adipose tissue (lipolysis and free fatty acid oxidation)

Protein: increasing protein synthesis & inhibiting proteolysis in muscle tissue

90
Q

insulin PD

onset & different ROA

A

varying respose

More rapid & shorter for IV>IM>SC
* IV For DKA/ HHS patients; severe/ toxic condition due to pancreas inability to work OR preparing for surgery
* SC: More common & less painful
* IM & SC ⇒ requires time for absorption into bloodstream

91
Q

insulin PK

ADME

A

Absorption
Activity after SC administration from the injection site = rate limiting step (SC depot formation)
Insulin moving from fat cells into bloodstream → generally fast
Onset of action depends on absorption
Distribution

Enters bloodstream directly after SC administration
Targets 4 key organs to exert effect

Metabolism/ excretion
Exogenous insulin → mainly via kidneys
Renal failure may lead to accumulation ⇒ requires dosing down
Endogenous insulin → mainly via liver

92
Q

insulin
factors affecting absorption

T, JI, L

A

Temperature
Heat = (↑)
Cold = (↓)
Jet injectors= (↑); administration via pressure
Lipodystrophy
1. Lipoatrophy (↑): concavity/ pitting of adipose tissue due to immune response towards pork & beef insulin
Rarer → due to switch to synthetic human insulin
2. Lipohypertrophy (↓): bulging of adipose tissue due to not rotating injection sites

93
Q

insulin AE

A
  1. hypoglycemia
  2. weight gain
  3. allergic reaction
  4. lipodystrophy
  5. immune reaction
94
Q

insulin AE
managing hypoglycemia

A

Management: 15-15-15 rule
15g of fast acting carbohydrates
Wait for 15 mins → for sugar to enter body
Check BG levels; BG, if still < 4.0 mmol/L then another 15g of fast acting carbohydrates

Fast acting carbohydrates
At home: fruit juice (½ cup), sugar (1 tbsp)

95
Q

insulin AE
weight gain

A

More than patients on SU

Benefits of glycemic control > weight gain
* To remind patient about diet, exercise & losing weight

96
Q

insulin allergic reactions

A

Local: redness, swelling, itching at injection site
More common with beef/ pork insulin
Systemic → rare

97
Q

types of insulin

onset, peak, duration of action

A
  1. Rapid acting: Aspart (Novorapid), Lispro (Humalog), Glulisine (Apidra)
    5-15 mins; 1-2 hours; 3-5 hours OR 1 injection per meal
    (5 mins before meal)
  2. Fast acting: Regular (Actrapid)
    30-60 mins; 2-4 hours; 6-8 hours OR 1 injection per meal
    (30 mins before meal; requires time for absorption)
  3. Intermediate acting: NPH (insulatard)
    1-2 hours; 6-12 hours; 10-16 hours OR 2 injections for 24 hours coverage
  4. Long acting: Detemir & Lantus
    D –> 0.8-2 hours onset; 12 hours for 0.2 units/ kg (2 injections better coverage) OR 20-24 hours for 0.4 units/ kg
    L –> 1.5 hours
    peakless; ~24 hours OR 1 injection for 24 hours coverage
98
Q

insulin - ultrarapid acting

additional excipients

A

Aspart (Fiasp)
Vit B3: increase speed of initial absorption
L-arginine: stabilises formulation

Lispro-aabc (Lyumjev)
Tresporstinil: enhances absorption via vasodilation
Citrate: enhances vascular permeability

99
Q

insulin - ultralong acting

duration of action

A

Degludec
Peakless; duration of action = 42 hours

Glargine [U-300]
More concentrated insulin (300 per meal)
Amount injected lesser but can obtain larger dose
Peakless; duration of action = 36 hours

100
Q

insulin conversion from IV to SC

A

To give glargine 2 hours before stopping IV insulin
At 10am → highest peak reached at 2pm; covers basal insulin
Followed by giving Aspart to cover bolus insulin (mealtime)

101
Q

insulin premix - suitable

A

Regular + NPH
Rapid-acting + NPH

102
Q

pre-mixed insulin

onset, peak, duration of action

A

(NovoMix® 30)
10-20 mins; 1-4 hours; 18-24 hours

(Humalog® Mix 75/25)
15-30 mins; 1-6.5 hours; 14-24 hours

(Humalog® Mix 50/50)
15-30 mins; 0.8-4.8 hours; 14-24 hours

(Mixtard® 70/30)
30 mins; 2-12 hours; 18-24 hours

103
Q

pre-mixed insulin advantages

A

Mealtime & basal coverage possible
Benefits patients with difficulty measuring & mixing insulin (from vial)
Retains individual PD profiles
Less injections
Have multiple peaks

104
Q

pre-mixed insulin disadvantages

A

Challenging to titrate & adjust dose
* Must adjust both basal & prandial coverage together; less flexible titration

105
Q

Oral therapies & insulin

continue? stop?

A

Metformin & SGLT2i⇒ continue
TZDs
Discontinuing when initiating insulin OR reduce dose
Sulfonylureas
discontinue/ reduce dose by 50% when basal insulin initiated
If patient is at risk of hypoglycemia
Discontinue when mealtime insulin initiated/ on premix regimen
Effectiveness on SU will wear off ⇒ requires completely relying on insulin
DDP-4i: discontinue if GLP-1 agonists initiated

106
Q

GLP-1 receptor agonists
administration & dosing

A

Liraglutide (Victoza®)
* SC injection once DAILY regardless of meals
* Initiate at 0.6mg → titrate to 1.2mg after 1 wk
Can increase to 1.8mg

Dulaglutide (Trulicity®)
* SC injection once WEEKLY regardless of meals
* 0.75mg → titrate to 1.5mg after 4 wks
Can increase to 3mg & 4.5mg

Semaglutide (Ozempic®)
* SC injection once WEEKLY regardless of meals
* Initiate at 0.25mg → titrate to 0.5mg after 4 wks
Can increase to 1mg

Semaglutide (Rybelsus®)
* PO once daily 30 mins before first meal of the day
* Initiate at 3mg → titrate to 7mg after 30 days
Can increase to 14mg

107
Q

GLP-1 receptor agonists
AE

A

Common: Nausea & vomiting
* To start with low dose → titrate up
Others: headache, acute pancreatitis, acute cholecystitis,
SC injections: injection site reactions

108
Q

GLP-1 receptor agonists
c/i

A

patients with hx or active thyroid cancers

109
Q

oral semaglutide measures to increase absorption

A

Dose in morning on empty stomach
At least ½ hour before other meds/ food/ drink
Take with <120 mL of water
Can take with PPIs (ie omeprazole) ⇒ reduces stomach acidity

110
Q

requirements for oral semaglutide absorption (in GIT)

A

alkaline environment

111
Q

oral semaglutide formulation

A

Co-formulated with absorption enhancer SNAC
* Protects semaglutide passing through GIT
* Causes temporary & local reversible increase in pH (alkaline environment required to release drug) ⇒ enhances bioavailability

~1% of semaglutide absorbed; remaining is degraded by GIT

112
Q

oral semaglutide place in therapy

benefits, glucose-lowering effects

A

ASCVD benefits, weight loss (due to N/V effects), no hypoglycemic effects

Recommended over insulin as first-line injectable if greater glucose lowering needed

113
Q

oral semaglutide c/i

A

hx of pancreatitis or with family hx of thyroid cancer

114
Q

dose conversion for insulin

A

Switching from NPH 2x daily → glargine/ detemir 1x daily
To decrease dose by 20%; combination of BD dose = too large to give at once
Example: 20 units NPH 2x daily [daily 40 units] → 32 units glargine/ detemir 1x daily [can titrate up if needed]

Switching from U-300 glargine to other alternative basal insulin analog (intermediate/ long acting insulin)
To decrease dose by 20%; U-300 have increased concentration
Example: 40 units U-300 glargine → 32 units U-100 glargine/ detemir

115
Q

comorbidities to manage in DM

A
  1. Blood pressure
  2. Lipid levels
  3. ASCVD
  4. CKD
116
Q

comorbidities to manage in DM
BP

target BP, drug choice, purpose

A

Target BP: < 130/80 mmHg

Preferred first line agents: ACEi/ ARB

Reduces CVD mortality & slows CKD progression

117
Q

comorbidities to manage in DM
lipid levels

primary & secondary prevention + goals; drug choice

A

Secondary prevention
* Have hx of ASCVD (stroke, MI)
* Target LDL reduction of 50% from baseline & goal of <1.4 mmol/L
Agents
* High intensity statin therapy ⇒ atorva 40-80 mg
* Add ezetimibe/ PSCK9 inhibitor if goal not achieved

Primary prevention
* Individuals aged 40-75 years, but NO hx of ASCVD
* Target LDL reduction of 50% from baseline & goal of <1.8 mmol/L
Agent: moderate intensity statin therapy ⇒ atorva 10-20 mg

118
Q

comorbidities to manage in DM
ASCVD

drug choice, primary & secondary prevention

A

General: give aspirin

Secondary prevention→ patients with diabetes & hx of ASCVD
Use clopidogrel 75mg OD for those with allergy
Primary prevention → patients with diabetes & increased risk of ASCVD (no hx)
* To discuss risks & benefits of bleeding
* Patients > 70 years old ⇒ generally do not start aspirin
* Patients 50-70 years old + ASCVD RF ⇒ start aspirin
* NOT recommended for those with low risk of ASCVD

119
Q

comorbidities to manage in DM
CKD

drug choices

A
  1. ACEi/ ARB
  2. SGLT2i
  3. Fineronone
120
Q

comorbidities to manage in DM
CKD: ACEi/ ARB

indication, purpose, dose

A

Recommended for those with micro- OR macroalbuminuria
NOT recommended for primary prevention of patients with normal BP

To reduce kidney disease progression

Titrated to maximum tolerated dose based on BP, kidney fx

121
Q

comorbidities to manage in DM
CKD: SGLT2i

benefits, indication, purpose, concurrent drug

A

Cardiorenal protective
For those with T2DM + DKD + eGFR > 20 mL/min/1.73 m2
To reduce kidney disease progression & CVS events
To use concurrently with ACEi/ ARB

122
Q

comorbidities to manage in DM
CKD: Fineronone

MOA, indication, benefits, SE

A

Non-steroidal MRA → blocks aldosterone effect
Kidney tubules cannot reabsorb Na & h2o ⇒ lower BP

Recommended for those with micro- OR macroalbuminuria + eGFR > 25 mL/min/1.73 m2; patient should also already be on ACEi/ ARB
Indication for patients with CKD associated with T2DM

Benefits: lesser risks of gynecomastia compared to spironolactone
Side effects: hyperkalemia, hypotension

123
Q

glucose monitoring (types)

A
  1. Blood glucose monitoring (BGM)
  2. Intermittently scanned CGM (isCGM)
  3. Real time CGM (rtCGM)

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