IC11, 12, 13 Diabetes Management Flashcards
What are the differences between T1DM and T2DM?
Antibodies:
- Present
- Absent
Main cause:
- Autoimmunity, beta cells are destroyed and cannot produce insulin
- Increase cell resistance to insulin (glucose utilization is impaired & hepatic glucose output increased); decrease in insulin secretion
C-peptide (Surrogate marker for the serum insulin levels):
1. Absent
2. Normal or abnormal
Onset of presentation:
1. Abrupt
2. Gradual
Onset of diabetes:
1. <30 y/o
2. Usually >40y/o, obese children and adults
Size of patients
1. thin
2. Obese
Diabetic Ketoacidosis:
1. Common
2. Uncommon
What are the stages of T1DM and describe them.
Antibodies
Blood glucose levels
Symptoms
Stage 1:
Present
Normoglycemia
Presymptomatic
Stage 2:
Present
Dysglycemia
Presymptomatic
Stage 3:
Present
Hyperglycemia
Symptomatic
What are the symptoms of hyperglycemia and hypoglycemia?
Hyperglycemia:
- Polyphagia
- Polyuria
- Polydipsia
- Dry skin
- Blurred vision
- Drowsiness
- Reduced healing
Hypoglycemia:
- Hungry (Polyphagia)
- Tachycardia
- Shaking
- Sweating
- Impaired vision
- Dizziness
- Anxiety
- Irritable
- Headache
- Fatigue
What are the parameters used to measure blood glucose levels? What contributes to high Hba1c?
Parameters:
1. Fasting plasma glucose (FPG): need at least 8 hours of fasting
2. Oral glucose tolerance test, 2hOGTT (PPG): 2hours after meal
3. Hba1c: 3 months average of FPG and PPG
The higher the hba1c, the larger the contribution is from FPG
How to monitor BG in diff DM patients?
Monitoring:
T1DM, gestation DM, insulin pump users –> >= 4x/day (before mealtimes/snacks, at bedtime, 3am)
T2DM that frequently uses insulin –> >=3x/day
The rest –> at least 2x/day
- Once before breakfast
- Once after the largest meal
What is needed to diagnose DM?
Diagnosis of DM
Need 2 abnormal parameters, they can be from the same blood sample
E.g. FPG + OGTT, OGTT + FPG, Hba1c + OGTT/FPG, Hba1c definitive
When do you screen BG for people?
Screen for high risk of DM OR >=40y/o people
How to determine whether people are pre-diabetic, diabetic or have no diabetes?
6.0% and below:
1. No need further test, unless have symptoms or have clinical suspicion of having diabetes
No diabetes
Repeat in 3yrs
6.1-6.9%:
Do 2nd test:
FPG <= 6.0 mmol/L
OR
OGTT: < 7.8 mmol/L
No diabetes
Do 2nd test:
FPG: 6.1-6.9 mmol/L
OR
OGTT: 7.8-11 mmol/L
Pre-diabetic
Do 2nd test:
FPG >= 7.0 mmol/L
OR
OGTT >= 11.1 mmol/L
Diabetic
7.0% and above:
Definitive
Diabetic
What changes can be made for people in ramadan period?
Ramadan period (can’t eat food, drinks, medications):
- Change TDS to BD
- Decrease dose for before sunrise meds (reduce risk of hypoglycemia)
- Increase dose for sunset meds (reduce risk of hyperglycemia since they tend to binge eat at that time)
How to manage wond care for diabetic patients?
TIME for wound care
- Tissue –> debride dead tissues
- Infection –> use antibiotics if have bacterial infection
- Moisture –> clean and remove exudates
- Edge of wound –> assess for non-advancing wound edges and condition of periwound
What are the risk factors of DFI and the prevention methods?
Risk factors of DFI:
- Poor glycemic control
- Peripheral artery disease
- Peripheral neuropathy
- Visual impairment
- Smoking
Prevention:
- Self-examination of foot
- Foot examination
a. Vascular assessment of pedal pulses
b. Neurologic assessment with monofilament - Foot protection
- Nail and foot care and hygiene
- Have good glycemic control
What are the LDL goals for DM patients?
LDL goals in DM patients
Combination of low HDL, high LDL-C, and high TG –> increased risk of atherosclerosis
LDL goals:
For all DM patients, high risk for cardiovascular events
–> <2.6 mmol/L
If have target organ damage (microalbuminemia, retinopathy, neuropathy), very high risk
–> <2.1 mmol/L
What are the non-pharm and pharm ways to manage LDL/HDL/TG levels?
Non-pharmacological management:
- Saturated and trans fats –> huge increase in LDL-C
- Unsaturated fats –> marginal decrease in LDL-C
- Weight loss and exercise –> marginal decrease in LDL-C
- Weight loss and exercise –> huge increase in HDL and huge decrease in TG
- Alcohol, carbo and fructose –> huge increase in TG
Pharmacological management:
High intensity statins (decrease by 50%) –> Atorvastatin 40mg / Rosuvastatin 20mg
Doubling dose / agents –> further decrease by 6-7%
+ Ezetimibe
+ PCSK9i
What is the TG cut off point for DM patients and how to manage high TG levels?
TG goals in DM patients
When TG > 4.5mmol/L –> increased risk of acute pancreatitis –> add fenofibrate to statins
What are the heart and renal benefits of SGLT2i?
help to reduce progression of HF, remodeling and fibrosis
Conventional benefits:
1. Diuresis and reduction in BP
2. Improved glycemic control
3. Weight loss
4. Increase RBC mass and hematocrit (better HF outcomes)
Novel benefits
1. Improve myocardial energetics*
2. Improve myocardial ionic homeostasis*
3. Autophagy
4. Altered adipokine regulation
Reno-protective
o Sharp drop in GFR at during initiation of SGLT2i in the 1st few weeks
o Start to increase and have much more gradual decrease in GFR afterwards
What are the cons/counselling points for the use of SGLT2i?
- Mycotic genital infection e.g. UTI, mycotic genital infection, Fournier’s gangrene
- Due to glucosuria (esp. in the 1st few months)
- Keep area clean and dry (especially females)
- Diabetic Ketoacidosis (DKA) Common in T1DM
Also, when drop in >20% of insulin dose, women, surgical stress, trauma, alcohol abuse, lean body hiatus, intercurrent illness e.g. raging sepsis
S&S of DKA:
- Shortness of breath
- Abdominal pain
- Vomiting
Stop SGLT2i if have acute illness, and the above S&S (vomiting, diarrhea, inability to eat or drink)
Stop 2-3 days prior surgery
Avoid >20% drop in insulin dose, decrease insulin dose more gradually
- Diuresis, natriuresis
Better than loop diuretics
- Will not lead to hypokalemia or hypomagnesemia
- Reduce serum uric acid
- Hemoconcentration (increase RBC)
Risk of volume depletion, esp during acute episodes of nausea, vomiting and diarrhea
Sick day counselling:
Stop if nausea, vomiting, diarrhea until resolution
HF patients need greater liberalization of fluid restriction (when euvolemic and start on SGLT2i)
- Acute kidney injury (AKI)
Not really associated but a possibility
Fluid intake counselling
What is the algorithm for starting SGLT2i?
If T2DM + GFR > 60mL/min/1.72m32:
If hba1c < 7% / hypoglycemic:
- Consider reducing insulin dose
- Decrease SU dose
- When euvolemic / Hypervolemic:
Start SGLT2i (to avoid excessive risk of AKI)
Continue ACEi/ARBs/ ARNIs/ MRA
If euvolemic, stop loops
Sick day counselling (patients to self-manage)
SCr < 30, just monitor
Follow up in 1-3months
- Electrolytes bicarbonates, SCr
Normal: SCr increase by 30%
Abnormal: >30% increase (linked to decrease kidney function)
re-assess BP and volume status
consider reducing loops, liberalizing fluid intake or holding off SGLT2i
- Hypovolemic
Do NOT start SGLT2i until euvolemic
Decrease BP meds
Decrease loops
Liberalize fluid intake
What are the microvascular and macrovascular complications of DM? How is Hba1c linked to them?
Insulin resistance & associated risk and complications
- Microvascular
- Retinopathy (blindness), nephropathy (kidney failure), neuropathy (amputation)
- Decrease in Hba1c is proportional to improvement in microvascular complications
- Macrovascular
- Cardiovascular disease
- Decrease in Hba1c leads to improvement in macrovascular complications to a certain point
- Then further decrease in Hba1c worsens macrovascular complications
∴ Individualize Hba1c
What are the treatment goals (FBG, PPG, Hba1c etc.)?
Treatment goals (FBG, PPG, Hba1c etc.)
Hba1c goal:
General: < 7%
Stringent: 6-6.5%
- Shorter duration of diabetes
- Younger
- No significant cardiovascular diseases
Less stringent: 7.5-8%
- Severe hypoglycemia
- Older patients
- Advanced Complications
- Extensive comorbidities
- Target difficult to obtain even after intensive self-management of blood glucose (SMBG)
FBG goal: 5-7mmol/L
PPG goal: <10mmol/L
When do you monitor to assess complications of DM?
- Hba1c
3 months
6 months (stable) - Lipid panel
3-6 months
1 year (stable) - BP
Every check up - Eye check
6 months
1 year (stable) - Renal panel / albuminuria
6 months
1 year (stable) - Foot check
Self-check daily
1 year (pro)
What are the non-pharmacological ways to manage DM?
Non-pharmacologic management:
- Smoking cessation
- Weight loss by 7% of initial body weight (the greater the weight loss at the beginning, the better the prognosis)
- Exercise (150 mins per week of moderate intensity + muscle strengthening 2 days per week + balance and functional exercise for >50y/o)
- Diet e.g. reduce alcohol and simple carbohydrates (mainly reduce TG)
What are the MOA, benefits and extent of Hba1c lowering of Metformin?
MOA:
- ↓ gluconeogenesis
- ↑ Cell sensitivity to insulin
Benefits:
- Weight loss
- Improve lipids (hyperlipidemia)
- Low risk of hypoglycemia
Hba1c↓: by 1.5-2% [1st]
Does metformin affect FPG or PPG?
FBG
How is metformin used in clinical practise? What is the max dose for metformin?
Monotherapy + diet + exercise
Combi w others
Max Dose: 1g TDS (3g/day)
When do you start metformin to prevent pre-diabetes?
Pre-diabetes:
FPG 6.1-6.9 mmol/L
PPG 7.8-11mmol/L
Start metformin for pre-diabetes (look at FPG/PPG):
- BMI > 35kg/m2
- Women with prior gestational DM
- <60y/o
What are the ADRs of metformin?
- Diarrhea
- Nausea and vomiting
- Anorexia
- Metallic taste (take with food)
- ↓ Vit B12 absorption (anaemia, peripheral neuropathy)
- Lactic acidosis (mental confusion, shortness of breath, nausea, abdominal pain)
How do you renal adjust metformin?
Renal Impairment:
CrCl >=60: continue, monitor every 1yr
CrCL 45-59: continue, monitor every 3-6 months
CrCl 30-44: halve dose, monitor every 3 months OR do NOT start
CrCl <30: Stop metformin
What are the CI for metformin?
- Renal Impairment:
CrCl >=60: continue, monitor every 1yr
CrCL 45-59: continue, monitor every 3-6 months
CrCl 30-44: halve dose, monitor every 3 months OR do NOT start
CrCl <30: Stop metformin - Lactic Acidosis:
Avoid when in hypoxic state e.g. Heart failure, sepsis, alcohol abuse, hepatic impairment, >80y/o - Avoid in acute HF
What are the DDI of metformin?
DDI:
1. Alcohol –> lactic acidosis
2. Iodinated contrast medium (hold for >=48hrs after screen) –> renal impairment
3. Cationic drugs e.g. cimetidine, digoxin, dofetilide –> compete for renal tubular transport
What are the MOA, benefits and extent of Hba1c lowering of SU? How is it used in clinical practise?
MOA:
- ↑ functioning B-cell to secrete insulin by blocking K+ channel
- ↓ hepatic glucose output + ↑ insulin sensitivity
Hba1c↓: by 1.5% [1st]
Monotherapy + diet + exercise
Combi w others
