IC12-14 DM Flashcards
pre-DM screening
recommended individuals, types of test
asymptomatic individuals aged ≥40 &/or with risk factors for diabetes:
- Fasting plasma glucose (FPG)
- HbA1c
pre-DM screening
test results
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
pre-DM management
- lifestyle modification
- metformin
pre-DM management
1. lifestyle modification
- Healthy diet
- Increased physical activity (every week):
at least 150 minutes of moderate intensity exercise (such as brisk walking, leisure cycling)
pre-DM
2. metformin
when to start, recommended individuals
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.
T1DM
background
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
T1DM staging
- Normoglycemia + Presymptomatic
- Dysglycemia + Presymptomatic
- New onset hyperglycemia + Symptomatic
T2DM background
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
T2DM effects
glucose utilisation is impaired (inability to utilise glucose pumps) & hepatic glucose output increased
T1DM characteristics
Primary cause, Insulin production (check C-peptide level), Age of onset, Onset of clinical presentation, Physical appearance, Proneness to ketosis (DKA)
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
T2DM characteristics
Primary cause, Insulin production (check C-peptide level), Age of onset, Onset of clinical presentation, Physical appearance, Proneness to ketosis (DKA)
Insulin resistance
Impaired insulin secretion
(-) Ab
Normal/ abnormal
Often > 40 years
But increasing prevalence in obese children & younger adults
gradual
Often overweight
uncommon
signs & symptom of hyperglycemia
causes
too much food, too little insulin/ diabetes medication, illness, stress
signs & symptom of hyperglycemia
onset
gradual, may progress to diabetic coma
signs & symptom of hyperglycemia
3Ps: polydipsia (extreme thirst), polyuria (increased urination), polyphagia (increased hunger)
Dry skin (due to dehydration), blurred vision, drowsiness, decreased healing
signs & symptoms of hypoglycemia
cause
too little food, too much insulin/ diabetes medication, extra activity
signs & symptoms of hypoglycemia
onset
sudden, might progress to insulin shock
signs & symptoms of hypoglycemia
activation of SNS
- Shaking, fast heartbeat, sweating, dizziness, anxious
- Hunger, impaired vision, weakness & fatigue, headache, irritable
- Nocturnal → nightmare, restless sleep, profuse sweating, morning headache
diagnostics for DM
- Fasting plasma glucose (FPG)
* No calorie intake for ≥ 8 hrs - Random or casual plasma glucose
* Glucose level at any time of the day, regardless of meals - Postprandial plasma glucose (PPG)
* Glucose level measured after meal; usually after 2 hours - 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]
Basal & postprandial contributions to hyperglycemia by HbA1c range
High HbA1c → largely contributed by basal hyperglycemia
Important to start on insulin → targets basal hyperglycemia
diagnosis process for DM
- Determine HbA1c values
- 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] - If HbA1c >7.0%, patient is confirmed to have T2DM
criteria for no DM
- HbA1c < 6.0%
- HbA1c 6.1-6.9%, but FPG < 6.0mmol/L or 2hOGTT < 7.8 mmol/L
criteria for pre-DM
HbA1c 6.1-6.9%, and FPG 6.1 - 6.9 mmol/L or 2hOGTT 7.8-11.0 mmol/L
criteria for DM
- HbA1c 6.1-6.9%, but FPG >7.0mmol/L or 2hOGTT >11.0 mmol/L
- HbA1c > 7.0%
complications of DM
- macrovascular
- microvascular
will lower overall life expectancy by 5-10 years
complications of DM
macrovascular
Increases CVD by 2-4x
* Stroke, MI, clogging of peripheral arteries (in hands & legs)
* Might require stent in heart/ extremities to allow blood flow
complications of DM
microvascular
- Retinopathy, blindness
New & small BV swell → BV will start to burst & release blood into eyeball, causing blindness - Nephropathy, kidney failure
Glucose causes larger pores in kidney tubules, thus causing leakage of albumin (albuminuria) - Neuropathy (60-70%), amputation
Increased sugar levels impedes recovery of wound
screening for DM complications
- HbA1c
- BP
- lipid panel
- eye exam
- albuminuria/ renal function
- Foot exam
screening for DM complications
Eye exam
when to start - T1DM & T2DM
Adults with T1DM: within 5 years after onset of DM
People with T2DM: at time of diabetes diagnosis
screening for DM complications
Eye exam
frequency
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
screening for DM complications
Eye exam
women with DM
- 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
screening for DM complications
foot exam
frequency
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
screening for DM complications
foot exam
what to look out for
Inspection of skin, assessment of foot deformities, neurological assessment, vascular assessment
screening for DM complications
foot exam
advice
Encourage smokers to quit smoking → will reduce risks of lower extremity amputations
Educate on good foot care & appropriate footwear
screening for DM complications
renal function/ albuminuria
when to start - T1DM & T2DM
Beginning 5 years after T1DM diagnosis
at time of diagnosis for T2DM
screening for DM complications
renal function/ albuminuria
frequency
every 6 months/ annually; depends on presence of protein/ albumin in urine
screening for DM complications
renal function/ albuminuria
tests
- Serum Cr &/or eGFR
Cr → estimates how quickly kidneys filter blood (GFR)
Low filtration = poor kidney function
AND - Urine albumin/ creatinine ratio (uACR)
Ratio measures how much albumin in urine sample relative to how much creatinine there are
OR - Protein-creatinine ratio (uPCR)
Normal: <30 ug/mg; microalbuminuria: 30-299 ug/mg; macroalbuminuria: >300 ug/mg
diabetic emergencies
DKA
T1DM vs T2DM
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
diabetic emergencies
DKA
labs
increased: sugar, acid & ketones
diabetic emergencies
DKA
BG level, mental status
BG >14 mmol/L
Alert
diabetic emergencies
DKA
result of ketone formation
Found in blood & urine
Fruity breath odour
Acidosis
diabetic emergencies
HHS
background (ketones?)
No ketones formed
* Due to residual insulin
* No acidosis
diabetic emergencies
HHS
BG, mental status
BG >33 mmol/L; patient usually in state of dehydration
in stupor
Dawn phenomenon & Somogyi effect
High BG levels at dawn, but bedtime BG is normal
Dawn phenomenon cause
Release of cortisol in the morning
⇒ BG levels rises sharply
Somogyi effect cause
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
Somogyi effect management
To reduce night dose of glucose lowering agent/ basal insulin
treatment goals
non-DM –> HbA1c, FBG & PPG
HbA1c <5.7% , FBG <5.6 & PPG <7.8
treatment goals
DM –> HbA1c, FBG & PPG
HbA1c <7% , FBG 4-7 & PPG <10
difference in HbA1c goals
normal vs strict vs less strict
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
Metformin indications
Monotherapy with diet & exercise
in combination with other antidiabetic agents and/or insulin in patients with T2DM
Metformin MOA
Primary: ↓ hepatic glucose production (endogenous production of glucose)
Secondary: ↑ peripheral/muscle glucose uptake & utilisation
Metformin PD
time for onset & max effect
Onset: within days
max effects take up to 2 weeks
Metformin formulations
dosing for each type
- 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 - 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
Metformin ADR
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)
Metformin c/i
- severe renal impairment
- hypoxic states (or disease that can cause it)
Metformin DDI
- Alcohol: ↑ risk for lactic acidosis
- Iodinated contrast material (used in radiologic procedure)
Will cause worsening of kidney function → undesirable as metformin is cleared renally - Inhibitors/inducers of organic cationic transporters (OCT)
OCT 2 inhibitors (e.g. cimetidine, dolutegravir, ranolazine) may ↑ metformin by ↓ renal elimination; accumulation of metformin
TZD indication
Alternative monotherapy for patients who cannot take metformin
in combination with other antidiabetic agents → more common
MOA
TZD MOA
(PPARgamma) agonist to promote glucose uptake into target cells (skeletal muscle/adipose tissue)
↓insulin resistance; ↑ increase insulin sensitivity
TZD time for max effect
Takes up to a month for maximal effect
TZD elimination
liver
* avoid if have liver impairment
TZD dosing
Start with 15 mg or 30 mg OD
for an inadequate response, ↑ dose by 15 mg, up to max of 45 mg OD
TZD DDI
When co-administered by CYP3A4 & CYP2C8 inhibitors/ inducers
TZD AE
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
TZD c/i
- active liver disease
- HF
- active/ have hx of bladder cancer
TZD benefits
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
Sulfonylureas indication
When hyperglycemia cannot be managed by diet & exercise alone
may be used concomitantly with other glucose lowering agents and/or insulin
Sulfonylureas MOA
Primary: stimulate insulin secretion by blocking K+ channel of ß- cells
Secondary: ↓ hepatic glucose output & ↑ insulin sensitivity
Sulfonylureas when to administer
Generally take 15-30 mins before food
Because drug requires time for absorption & to work on ß- cells → secretion of insulin before food intake
Sulfonylureas AE
Hypoglycemia (especially in elderly) → if eat too little
Weight gain (~2-5 kg)
Sulfonylureas DDI
ß-blockers may mask s/sx of hypoglycemia
ie: will slow down HR
Disulfiram-like rxn with alcohol (1st gen»_space; 2nd/3rd gen)
Can suggest skipping SU dose if patient plans to drink alot
Flushing, tremors
CYP2C9 inhibitors
DDP4i effects
Inhibits DPP4 enzyme & increases concentration of endogenous incretins
Essentially prolonging the effects of active GLP1
DDP4i
effects of incretin
- Decreases gastric emptying → slows down food from exiting stomach
- Increases glucose-dependent insulin biosynthesis & secretion
- Decreases glucagon (reduced gluconeogenesis → lesser glucose being produced endogenously)
- Decrease food intake
DDP4i indication
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
DDP4i formulations & doses
- Sitagliptin
100 mg OD
eGFR ≥30 to <45 mL/min/1.73 m2: 50mg OD
eGFR < 30 mL/min/1.73 m2: 25mg OD - 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 - Linagliptin: 25 mg OD
DDP4i AE
severe joint pain
Bullous pemphigoid, skin rash
Headache
SGLT2i MOA
Reduces reabsorption of glucose @ PCT
Leads to ↑renal glucose excretion ⇒ ↓ blood glucose
SGLT2i formulations & dose
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
SGLT2i ADR
Hypotension
Hypoglycemia
UTI
DKA
genital mycotic fungal infection
SGLT2i Considerations for renal function
for glycemic control only vs cardiorenal protective (initiation & stop)
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
SGLT2i Benefits towards 3 conditions
ASCVD, HF, CKD
ASCVD: canagliflozin & empagliflozin
HF: empagliflozin & Dapagliflozin
* Shortens hospitalisation & delays HF from occurring
CKD: Dapagliflozin
α-Glucosidase Inhibitors
indication
used as adjunct therapy (those who refuse insulin)
T1Dm patients requiring additional PPG control
α-Glucosidase Inhibitors MOA
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)
α-Glucosidase Inhibitors onset & time for administration
Onset is rapid with each meal → take with meals
* best if take with largest meal/ meal with most carbs
α-Glucosidase Inhibitors dosing
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)
α-Glucosidase Inhibitors AE
GI: flatulence, abdominal pain, diarrhoea
most common cause of drug discontinuation
↑ LFT (specific for acarbose; ↑risk at dose >100 mg TD
α-Glucosidase Inhibitors c/i
GI diseases → obstruction, IBD
Liver cirrhosis
insulin indications
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
insulin target organs
pancreas
adipose tissue
muscle
liver
insulin effects
on carbohydrates, proteins & fats
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
insulin PD
onset & different ROA
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
insulin PK
ADME
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
insulin
factors affecting absorption
T, JI, L
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
insulin AE
- hypoglycemia
- weight gain
- allergic reaction
- lipodystrophy
- immune reaction
insulin AE
managing hypoglycemia
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)
insulin AE
weight gain
More than patients on SU
Benefits of glycemic control > weight gain
* To remind patient about diet, exercise & losing weight
insulin allergic reactions
Local: redness, swelling, itching at injection site
More common with beef/ pork insulin
Systemic → rare
types of insulin
onset, peak, duration of action
- 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) - 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) - Intermediate acting: NPH (insulatard)
1-2 hours; 6-12 hours; 10-16 hours OR 2 injections for 24 hours coverage - 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
insulin - ultrarapid acting
additional excipients
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
insulin - ultralong acting
duration of action
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
insulin conversion from IV to SC
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)
insulin premix - suitable
Regular + NPH
Rapid-acting + NPH
pre-mixed insulin
onset, peak, duration of action
(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
pre-mixed insulin advantages
Mealtime & basal coverage possible
Benefits patients with difficulty measuring & mixing insulin (from vial)
Retains individual PD profiles
Less injections
Have multiple peaks
pre-mixed insulin disadvantages
Challenging to titrate & adjust dose
* Must adjust both basal & prandial coverage together; less flexible titration
Oral therapies & insulin
continue? stop?
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
GLP-1 receptor agonists
administration & dosing
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
GLP-1 receptor agonists
AE
Common: Nausea & vomiting
* To start with low dose → titrate up
Others: headache, acute pancreatitis, acute cholecystitis,
SC injections: injection site reactions
GLP-1 receptor agonists
c/i
patients with hx or active thyroid cancers
oral semaglutide measures to increase absorption
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
requirements for oral semaglutide absorption (in GIT)
alkaline environment
oral semaglutide formulation
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
oral semaglutide place in therapy
benefits, glucose-lowering effects
ASCVD benefits, weight loss (due to N/V effects), no hypoglycemic effects
Recommended over insulin as first-line injectable if greater glucose lowering needed
oral semaglutide c/i
hx of pancreatitis or with family hx of thyroid cancer
dose conversion for insulin
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
comorbidities to manage in DM
- Blood pressure
- Lipid levels
- ASCVD
- CKD
comorbidities to manage in DM
BP
target BP, drug choice, purpose
Target BP: < 130/80 mmHg
Preferred first line agents: ACEi/ ARB
Reduces CVD mortality & slows CKD progression
comorbidities to manage in DM
lipid levels
primary & secondary prevention + goals; drug choice
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
comorbidities to manage in DM
ASCVD
drug choice, primary & secondary prevention
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
comorbidities to manage in DM
CKD
drug choices
- ACEi/ ARB
- SGLT2i
- Fineronone
comorbidities to manage in DM
CKD: ACEi/ ARB
indication, purpose, dose
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
comorbidities to manage in DM
CKD: SGLT2i
benefits, indication, purpose, concurrent drug
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
comorbidities to manage in DM
CKD: Fineronone
MOA, indication, benefits, SE
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
glucose monitoring (types)
- Blood glucose monitoring (BGM)
- Intermittently scanned CGM (isCGM)
- Real time CGM (rtCGM)
