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PR3152: Immune & Endocrine Systems > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Definition of diabetes

A

A metabolic disorder characterized by resistance to the action of insulin, insufficient insulin secretion or both

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2
Q

What is the main clinical manifestation of diabetes

A

hyperglycemia

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3
Q

Types of DM

A

Type I, Type II, Gestation, Others (Infections, drugs, monogenic diabetes syndrome, endocrinopathies, pancreatic destruction, type III)

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4
Q

What is Type I DM pathogenesis?

A

An absolute deficiency of pancreatic B-cell function:
- Immune mediated destruction
- Positive antibodies (doesnt mean +ve means have symptoms straight away).

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5
Q

What is Type II DM pathogenesis?

A
  • Progressive loss of adequate β-cell insulin secretion on the background of insulin resistance
  • Insulin resistance:
    In the presence of insulin, glucose utilization is impaired and hepatic glucose output increased.
    Simultaeneous elevations in both glucose and blood insulin levels at early stage.
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6
Q

Difference between Type I and II

A

Primary Cause:
Type I- autoimmune mediated pancreatic beta cell destruction, positive antibodies
Type II- insulin resistance, impaired insulin secretion, negative antibodies

Insulin production (C-peptide level):
Type I- absent
Type II- normal or abnormal

Age of onset:
Type I- <30y/o
Type II- >40y/o

Onset of clinical presentation:
Type I- abrupt
Type II- gradual

Physical appearance:
Type I- often thin
Type II- often overweight

Proneness to ketosis:
Type I- freq
Type II- uncommon

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6
Q

What does the presence of C-peptide mean?

A

It is a short chain a.a released as by product of formation of insulin by pancreas. If insulin is present, C-peptide will be released.

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7
Q

S&S of hyperglycemia

A

Extreme thirst (polydipsia)
Freq urination (polyuria)
Dry skin
Hunger (polyphagia)
Blurred vision
Drowsiness
Decreased healing

3Ps

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8
Q

S&S of hypoglycemia

A

Shaking
Fast heartbeat
Sweating
Dizziness
Anxious
Hunger
Impaired vision
Weakness/fatigue
Headache
Irritable

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9
Q

Common S&S of hyper and hypoglycemia

A

Hunger and impaired vision

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10
Q

What types of tests are used to measure DM

A

Fasting/Basal plasma glucose (FBG)
Random or casual plasma glucose
Postprandial plasma glucose (PPG)
Hemolobin A1c (HbA1c)

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11
Q

What to take note of for FBG test?

A

No calories intake for >=8hrs

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12
Q

When is random or casual plasma glucose taken?

A

glucose level is taken at any time of the day, regardless of meals

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13
Q

When and how is PPG taken?

A
  • Glucose level measured after meal; usually after 2 hours (Also known as 2-hour postprandial glucose -> tend to be more stable)
  • Can also be measured using a standardized 75-g oral glucose tolerance test (OGTT)
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14
Q

What does HbA1c measures?

A
  • Measures the average amount of glucose (attached to hemoglobin) in a person’s blood over the past 3 months. (3months avg of FPG + PPG)
  • Glucose stays attached to hemoglobin for the lifespan of a red blood cell (~120 days)

Notes: Depends on no. of RBC in body -> if bleeding/mensus, HbA1c is lower. If anemia, RBC dont turn over, they last for >120days so HbA1c increases.

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15
Q

How does basal and postprandial changes as HbA1c increases?

A

As HbA1c increases, basal increases and postprandial decreases.

Note: we give insulin at high HbA1c as certain insulin targets the basal/fasting hyperglycemia

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16
Q

How often should T1DM use glucometers?

A
  • Varies but generally:
  • > =4times/day
  • before meals/snacks, at bedtime, at 3am
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17
Q

How often should T2DM use glucometers?

A
  • Varies but generally:
  • > =3times/day for pts on multiple injections of insulin
  • For patients using less frequent insulin injections, noninsulin therapies, or medical nutrition therapy alone, self monitoring of blood glucose (SMBG) may be useful as a guide to the success of therapy
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17
Q

Criteria for diagnosis of T2DM:
What does HbA1c <=6.0% suggest?

A
  • Low probability of diabetes
  • No further tests needed if no smx of diabetes. Further testing with a FPG or a 2hOGTT is rec if diabetes is suspected
  • Diagnosis: no diabetes, maintain healthy lifestyle and weight. Repeat test in 3yrs
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18
Q

Criteria for diagnosis of T2DM:
What does HbA1c 6.1- 6.9% suggest?

A
  • proceed to FPG or OGTT
  • if FPG <=6.0mmol/L or 2hOGTT <7.8mmol/L: no diabetes. diagnosis same as HbA1c <=6.0%
  • If FPG 6.1-6.9mmol/L or 2hOGTT 7.8-11mmol/L: pre-diabetes
  • if FPG >=7.0mmol/L or 2hOGTT >=11.1mmol/L: diabetes
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19
Q

Criteria for diagnosis of T2DM:
What does HbA1c >=7.0% suggest?

A
  • high probability of diabetes
  • no further tests needed
  • diagnosed as diabetes straight away
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20
Q

Can FBG or OGTT be used for diagnosis if HbA1c was not done?

A

Yes, but both FPG and OGTT must be done and both give abnormal results

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21
Q

How does culture/race influence diabetes risk?

A
  • Genetics/fam Hx: asians higher risk, have less muscle and more abdominal fat which increases insulin resistance
  • Environment: stress, fast food, less exercise, poor health literacy, language barrier
  • Food: asian diet is carb heavy and tend to stir/deep fry with oil
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22
Q

What are the risks of ramadan fasting and effects on DM management?

A
  • No food: hypoglycemia, lack of exercise, binge eating for iftar
  • No water: risk of dehydration and thrombosis, risk of acute diabetes (DKA/HHS)
  • No medications: risk of hyperglycemia, risk of acute diabetes (DKA/HHS)
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23
Q

What are the general DM medication adjustments during ramadan?

A
  • TDS to BD
  • Reduce Medications With high hypoglycemia potential eg. insulin, SU
  • Evening dose potency to be higher than morning (as sunset meal is much heavier than predawn meal)
  • Be Aware That Overall, patients eat lesser during Ramadan period -> adjust accordingly
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24
Q

Risk factors for diabetic foot infections?

A

Poor glycemic control
Peripheral Artery DIsease: low supple of blood to area
Peripheral neuropathy
Visual impairment
Smoking: damages vascular tissue cause clots and reduces artery thickness -> PAD

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25
Q

What should you educate pt abt diabetic foot care?

A
  • Maximising blood glucose control/ reduce risk factors
  • Self-examination of the foot (every night, look out for any cracks, dryness, wounds. Use mirror to see bottom of feet)
  • Foot protection (cover feet with socks at all times, dont be bare footed. Nice fitting shoes + socks can be too tight, prevent blood circulation. Too loose also cause alot of abrasions -> wounds)
  • Nail & Foot Care & Hygiene
    Use moisturisers but dont moisturise btw toes -> fungal infection
    Prevent ingrown nails, dont cut too thinly, leave abit of gap, cut straight across nail and leave adges sharp to less likely for ingrown nails
    Wash feet everyday w soap. Soak in warm water 1-2minutes/day. Too long: skin gets weak.
  • Annual Foot examination (nurse/pharmacists feel pulses of foot to check for PAD or neuropathy- using filament. How strong pulse is can tell how severe PAD is).
    Vascular assessment of pedal pulses
    Neurologic exam with monofilament
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26
Q

Complications of DM?

A
  • Retinopathy (microvascular)
  • Nephropathy (microvascular)
  • Neuropathy (microvascular)
  • Decrease life expectancy
  • Increase CVD (macrovascular)
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27
Q

R/S btw macrovascular outcome and A1c?

A

CV outcomes improve as A1c decreases but eventually worsens as A1c continues to drop

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28
Q

General treatment goals for DM?

A

HbA1c: <=7%
FBG: 4-7mmol/L
PPG: <10mmol/L

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29
Q

When should HbA1c goal be more stringent?

A

❑ 6.0-6.5%
❑ Short disease duration
❑ long life expectancy (young pts)
❑ no significant cardiovascular diseases

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30
Q

When should HbA1c goal be less stringent?

A

❑ 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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31
Q

Monitoring parameters in T2DM?

A
  • HbA1c
  • Lipid panel
  • BP
  • Eye exam
  • Albuminuria/renal function
  • Foot exam
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32
Q

What are the nonpharm TLC for diabetes?

A

Quit smoking
➢ 5As: Ask, Assess, Advice, Assist, Arrange

Weight Reduction
➢ Achieve and maintain 7% loss of initial body weight -> good prognosis esp for newly diagnosed pts, helps decrease insulin resistance.

Exercise
➢ 150 min/week, spread into at least 3 days per week with no more than 2 consecutive days without exercise
Moderate intensity
➢ PLUS muscle strengthening activities at least 2 days per week
➢ If older (>55yo) – PLUS incorporating balance and functional training

Diet Modification (most challenging)
➢ Fruit, vegetables, grains, cereals, legumes
➢ Skinless poultry, fish, lean meats
➢ Low-fat dairy products
➢ Restrict alcohol and simple carbohydrates (mainly ↓ TG). Cut down on carbs

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33
Q

Types of antidiabetic drug classes

A
  • a glucosidase inhibitors
  • incretins (GLP-1 receptor agonist)
  • sulfonyurea
  • metformin
  • thiazolidinediones
  • SGLT2i
  • DPP-4i
  • meglitinides
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34
Q

What is an off-label use for metformin?

A

Polycystic ovarian syndrome (PCOS)

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35
Q

MOA of metformin

A
  • Primary: ↓ hepatic glucose production
  • Secondary: ↑ peripheral/muscle glucose uptake and utilization (i.e. ↑ insulin sensitivity)
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36
Q

How is metformin cleared?

A

renal; 90% in urine as unchanged drug -> must dose adjust.

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37
Q

SE of metformin

A
  • Common: GI (diarrhoea -> so take after food), anorexia, metallic taste (usually transient; take with food to alleviate, taste like blood)
  • Long-term use may ↓serum B12 concentrations (ADA 2017 update: consider periodic measurement especially in those with anemia or peripheral neuropathy) -> megaloblastic anemia (RBC bigger than normal)
  • Rare but fatal: lactic acidosis (3/100,000 patients/year)
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38
Q

S&S of lactic acidosis

A

nausea, shallow/labored breathing, mental confusion

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39
Q

Max dose for metformin?

A

2.55g/day

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40
Q

Is metformin safe in pregnancy?

A

Yes

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41
Q

How does lactic acidosis occur?

A
  • Glucose gets broken down into pyruvate for ATP
  • Pyruvate gets broken down to lactate when there is a lack of oxygen (anaerobic respiration)
  • Lactate acidosis results from ↑ production or ↓ clearance of lactate
    ➢Metformin
    ➢Hypoxic state (lack of oxygen in blood)
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42
Q

CI for metformin

A

➢ Severe renal impairment (Cleared by renal)

➢ Hypoxic states or at risk for hypoxemia: Heart failure, sepsis, liver impairment, alcoholism, ≥ 80 yo -> if pt is stable, can still give
Warning remains for patients with HF due to ↑ risk for hypoxemia and hypoperfusion; avoid use in acute HF

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43
Q

Drug interactions with metformin?

A

➢ EtOH: ↑ risk for lactic acidosis
➢ Iodinated contrast material/radiologic procedure
temporarily hold metformin x ≥48 hrs after contrast administration; restart when renal function returns to normal post-procedure
(Can cause contrast induced renal impairment -> metformin is renally cleared. )
➢ Cationic drugs (e.g. dofetilide, cimetidine, digoxin) may ↑ metformin by competing for renal tubular transport, less metformin is excreted.

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44
Q

How to renal adjust metformin?

A

eGFR:
30-44: lower dose (50% or half maximal dose)
<30: stop metformin

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45
Q

First line for T2DM and gestational DM

A

Metformin

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46
Q

Does metformin cause weight gain?

A

No

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47
Q

What is pre-diabetes?

A

Impaired Fasting Glucose (IFG): 6.1 - 6.9 mmol/L (fasting) OR Impaired Glucose Tolerance (IGT): 7.8 - 11.0 mmol/L (after 2h 75g OGTT).
No A1c as HbA1c is a range -> not accurate to determine if you are pre-diabetic esp in Asians.

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48
Q

How to prevent or delay Type 2 DM

A
  • Diabetes prevention programme shows that lifestyle changes is still btr than drugs.
  • Lifestyle interventions:
    ➢ Achieve and maintain 7% loss of initial body weight
    ➢ Increase moderate-intensity physical activity to at least 150mins/week
  • Metformin therapy
    ➢ Especially for those with BMI >35 kg/m2, those aged <60 years, and women with prior gestational diabetes mellitus
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49
Q

When is Sulfonylureas indicated? (SU)

A

Management of T2DM when hyperglycemia cannot be managed by diet and exercise alone; may be use concomitantly with other antidiabetic agents and/or insulin

But need functional beta cells to work

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50
Q

Examples of different generations of SU

A
  • First generation SU (rarely used due to ↑ likelihood for adverse effects except tolbutamide):
    Tolbutamide
  • Second Generation SU:
    Glipizide (blue tablet), Gliclazide, Glibenclamide (also known as Glyburide in the US)
  • Third generation SU:
    Glimepiride
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51
Q

MOA of SU

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

Notes: Need functional Beta cells to work! Hence, SU is only used in T2DM as T1DM does not have functional B cells. As T2DM progresses, B cells become less and less effective in secreting insulin so SU loses effectiveness over time.

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52
Q

How is glipizide cleared?

A

hepatic. so good for those with renal impairment

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53
Q

When should SU be taken?

A

15-30min before meals

Note: SU stimulates secretion of insulin which is what you want after eating so must be take 15-30mins before meals. If you skip a meal, dont take SU -> hypoglycemia as SU works on postprandial.

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54
Q

SE of SU

A
  • Hypoglycemia (especially in elderly)
  • Weight gain (~2-5 kg) -> as long as stimulate insulin, there will be weight gain
  • Blood dyscrasias (rare)
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55
Q

DDI for SU

A
  • ß-blockers may mask s/sx of hypoglycemia -> BB are used to treat tremors and tachy which is the same symptoms as hypoglycemia. Only sweating cannot be masked.
  • Disulfiram-like rxn with EtOH (1st gen&raquo_space; 2nd/3rd gen): tolbutamide.
  • CYP2C9 inhibitors (e.g. amiodarone- anti arrhythmic, 5-FU- cancer, fluoxetine- anti depressant) may ↑ glimepiride, glipizide
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55
Q

What to caution in pts taking SU?

A

Pts with irregular meal schedules

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55
Q

MOA of Thiazolidinediones (TZDs)

A
  • Peroxisome proliferator activated receptors agonist to promote glucose uptake into target cells (skeletal muscle/adipose):
    ↓insulin resistance; ↑ increase insulin sensitivity (effective for T2DM whr insulin is resistant so the drug kind of counteracts it)
  • No effects on insulin secretion
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56
Q

How long does it take for TZD to work?

A

Up to a month

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57
Q

How is TZD eliminated?

A

Liver

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58
Q

Which TZD is FDA approved for use in combi with insulin?

A

Pioglitazone: synergistic effect so very prone to hypoglycemia

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59
Q

BBW for TZD

A

Increases risk of congestive heart failure.

  • Contraindicated in NYHA Class III or IV HF
  • After initiation or dose increases, observe patients for signs and symptoms of HF
  • If confirmed HF signs and symptoms develop, appropriate management of HF should be initiated. Discontinuation or dose reduction should be considered.
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60
Q

SE of TZD

A
  • Hepatotoxicity:
    Do not initiate therapy if ALT >3x UNL
    Discontinue if ALT >3x UNL
    If ALT > 1.5x UNL during therapy, repeat LFTs then weekly until normal
    Discontinue if s/sx of hepatic dysfunction regardless of ALT level
  • Edema (caution in NYHA Class I or II HF)
  • Fracture (increased risk; more likely in women)
  • Weight gain (assoc w edema)
  • Bladder cancer (Pioglitazone)
  • Elevated LDL (Rosiglitazone)
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61
Q

CI for TZD

A

Active liver disease; NYHA Class III or IV HF

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62
Q

Long term use of TZD is associated with what?

A

Fractures (F > M)

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63
Q

Which antidiabetic appears to be beneficial for pts with fatty liver disease?

A

TZD

➢ Nonalcoholic fatty liver disease (NAFLD) -> usually obese pts & not due to alcohol -> usually assoc w diabetes.
➢ Nonalcoholic steatohepatitis (NASH) -> more complicated.

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64
Q

Off label use for a-glucosidase inhibitor

A

treatment in patients with T1DM who are on insulin therapy but require additional control in PPG level

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65
Q

Examples of TZD

A

Rosiglitazone, Pioglitazone

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66
Q

MOA of a-glucosidase inhibitors

A
  • Delay glucose absorption and ↓PPG by competitively inhibit brush border α-glucosidases enzyme required for breakdown of complex carbohydrates
  • Acts locally

Notes: Eg. rice is a complex carb whereby enzymes will break it down to simple sugars to be absorbed but this drug prevent you from absorbing these sugars by preventing enzymes from breaking it down so sugar stays complexed and stays in the gut.

67
Q

Onset of a-glucosidase inhibitors

A

rapid with each meal

68
Q

How is a-glucosidase inhibitors eliminated?

A

50% via feces

69
Q

Can a-glucosidase inhibitors be used in pregnancy?

A

Yes. Cat B

70
Q

Example of an a-glucosidase inhibitors and its dosing

A

Eg. Acarbose
- Dosage Forms– 25, 50, 100 mg(tablet)
- Administration (wt based!):
➢ Start with 25 mg BD-TDS with each meal; ↑ by 25 mg/day every 2-4 wks to max dose of:
150 mg/day (≤ 60 kg) or 300 mg/day (> 60 kg)

Note: ↓ PPG is dose-dependent

71
Q

SE of acarbose

A
  • GI: flatulence, abdominal pain, osmotic diarrhea- complex stay in gut, pulls water in from intestines (most common cause of drug discontinuation)
  • ↑ LFT (specific for acarbose- abit hepatotoxic; ↑risk at dose >100 mg TDS)
72
Q

CI for acarbose

A
  • Breast-feeding (not studied well altho this drug is not absorbed well)
  • GI diseases (obstruction, irritable bowel disease) -> dangerous w diarrhoea
73
Q

DDI for acarbose

A

Intestinal adsorbents and digestive enzyme preparations may ↓ effects of α-Glucosidase inhibitors eg. yakult, charcoal as they stay in gut too.

74
Q

Does acarbose control PPG or Basal glucose?

A

PPG

75
Q

Acarbose is useful for what kind of diet?

A

Carbohydrate rich diet (May consider taking with the largest meal of the day or with the meal that consists the most carbs)

76
Q

What are incretins?

A
  • Naturally occurring hormones released from the GI tract
  • Glucagon-like peptide-1 (GLP-1) is a type of incretin
  • Glucose-dependent insulinotropic polypeptide (GIP) is another incretin that is now being targeted in novel research
77
Q

Metformin dosage strengths available

A

Normal: 500mg, 850mg, 1g
XR: 500mg, 750mg, 1g

78
Q

Glipizide dosage strengths and dose

A

Available in 5 or 10mg

Dose: 5mg BD (max 40mg/day)

79
Q

Why is tolbutamide seldom used?

A

Alcohol like rxn w a little alcohol -> can get N&V and drunk easily.
Hence, glipizide is the best option among the SU

80
Q

Which GLP-1 receptor agonist is commonly used in SG?

A

Liraglutide

81
Q

Dose of liraglutide

A

Initiate at 0.6mg SC injection once daily regardless of meals. Then titrate to 1.2mg after 1 wk. Can increase to 1.8mg

82
Q

SE of GLP-1 receptor agonists

A
  • Lots of GI SE: N/V, diarrhoea
    Long acting agents has less N/V but more diarrhoea
  • Acute pancreatitis
83
Q

BBW for GLP-1 receptor agonists

A

Thyroid C-cell tumours. Avoid if pt have hx of thyroid cancer

84
Q

Does GLP-1 receptor agonist cause weight gain or weight loss?

A

Weight loss so suitable for overweight pts

85
Q

Which is the first line injectable for DM?

A

GLP-1 receptor agonists (preferred over insulin)

86
Q

What other benefits does GLP-1 receptor agonist have?

A

ASCVD: most agents have benefit
HF: no benefit
CKD: minimal benefit

87
Q

MOA of GLP-1 receptor agonist

A

Act like endogenous GLP-1 and bind to receptors on B-cells

88
Q

MOA of DPP-4 inhibitors

A

Inhibit DPP-4 enzyme, preventing break down of GLP-1 (incretins)

89
Q

Common DPP-4i used in SG

A

Sitagliptin, linagliptin

90
Q

Dose of sitagliptin

A

100mg OD

91
Q

Do you need to dose adjust sitagliptin?

A

Yes. 50mg OD if CrCL 30-49ml/min

25mg OD if sev renal impairment or ESRD

92
Q

DDI with sitagliptin

A

Increases digoxin concentration (minimal)

93
Q

SE of sitagliptin

A

Acute pancreatitis, HA, N/V, abdominal pain, skin rxn, angioedema

94
Q

Dose of linagliptin

A

5mg OD

95
Q

Do you need to dose adjust linagliptin?

A

No

96
Q

SE of linagliptin

A

> =5% nasopharyngitis

97
Q

DDI with linagliptin

A

CYP3A4 inducers will decrease linagliptin conc

98
Q

FDA Warning and Precaution for DPP-4i

A

severe joint pain

99
Q

Sitagliptin or linagliptin is more commonly used?

A

Sitagliptin as it is subsidised

100
Q

Advantage of DPP-4i over GLP-1 receptor agonist

A

Route of administration (not anymore with recently approved PO semaglutide!), lower incidence of GI adverse events

101
Q

Disadvantage of DPP-4i over GLP-1 receptor agonist

A

weight neutral (dont rly lose weight), smaller HbA1c reduction, no “big 3” benefits (ASCVD, HF,CKD)

102
Q

MOA of SGLT2i

A

SGLT2 = Sodium Glucose Cotransporter 2. They are located in the proximal tubule in the kidneys. Inhibition of SGLT2 leads to ↑ renal glucose excretion, hence ↓ blood glucose.

103
Q

Examples of SGLT2i and their strengths

A

Canagliflozin: 100, 300mg
Empagliflozin: 10, 25mg
Dapagliflozin: 5, 10mg

104
Q

Dose of SGLT2i

A

Canagliflozin: 100mg OD, taken before first meal of day. Increase to 300mg OD if eGFR>60

Empagliflozin: 10mg OD, taken in morning with or w/o food, may increase to 25mg OD

Dapagliflozin: 5mg OD, taken in morning with or w/o food, may increase to 10mg OD

105
Q

Dose adjustment for SGLT2i

A

Canagliflozin: do not initiate if eGFR<30. but if allbuminuria >300mg/d, can continue 100mg OM

Empagliflozin + Dapagliflozin: discontinue if eGFR<45

106
Q

SE of SGLT2i

A

HypoTN, hypoglycemia, renal impairment, urinary urgency (diuretic), genital mycotic infection, euglycemic DKA, fournier’s gangrene

107
Q

CI for SGLT2i

A

ESRD or dialysis

108
Q

What is KDIGO202 guidelines for SGLT2i for DM management in CKD

A

treat pts with T2DM, CKD and eGFR >=30 with an SGLT2i

109
Q

What other benefits does SGLT2i have?

A

ASCVD: only cana and empa
HF: all have benefit. dapa and empa is approved for HF
CKD: all have benefit. dapa is approved for CKD

110
Q

Which antidiabetics have the most HbA1c lowering effect?

A

Metformin, SU, meglitinides, insulin

111
Q

which antidiabetics have the least HbA1c lowering effect?

A

SGLT2i, DPP-4i, a-glucosidase inhibitors

112
Q

Which antidiabetic acts on PPG the most?

A

SU so must take before meals

113
Q

Which antidiabetic causes weight gain?

A

SU, TZD

114
Q

Which antidiabetic causes weight loss?

A

Metformin, GLP-1 agonist, SGLT2i

115
Q

What is the drug of choice in pregnant pts with DM

A

insulin

116
Q

MOA of insulin

A

Regulation of carbohydrates (CHO), fat, and amino acids:
- Glucose: facilitating uptake of glucose in muscle and adipose tissue and by inhibiting hepatic glucose output (↓glycogenolysis and ↓ gluconeogenesis)
- Fat: enhancing fat storage (↑lipogenesis) and inhibiting the mobilization of fat for energy in adipose tissue (↓ lipolysis and free fatty acid oxidation)
- Protein : increasing protein synthesis and inhibiting proteolysis in muscle tissue.

117
Q

How is insulin eliminated?

A

➢ Exogenous insulin: mainly via kidneys
➢ Endogenous insulin: mainly via liver

118
Q

How many units of insulin is in 1ml?

A

100IU

119
Q

What does high gauge size mean?

A

➢ 28, 29, 30, 31 and 32 gauges (32 is smallest gauge/thinnest as it is the diameter of the opening in the needle)
➢ Higher the gauge the finer the needle↓ pain but ↑ needle weakness & ↓ speed of injection

120
Q

Where can you inject insulin

A

Abdomen > outer upper arms > top and outer thighs > buttocks

121
Q

Why should you rotate site to inject insulin?

A

prevent lipohypertrophy

122
Q

How many units does 1 vial of insulin contain

A

1000units

123
Q

How do you store unopened and opened insulin?

A
  • Unopened insulin vials: good until expiration date only if stored in refrigerator. if not refrigerated, good for 28 days
  • Opened insulin vials: good for 28 days regardless of refrigeration
  • Other insulin containing devices (e.g. pen, refill cartridges): vary, see package insert.
  • Exception: opened detemir good for 42days.
124
Q

How to prepare insulin dose from vial?

A

Step 1: Check the insulin label for insulin type and expiration date

Step 2: Visually inspect the insulin vial for contamination or degradation
(e.g., white clumps or color change)

Step 3: For all cloudy insulins, roll the vial gently back and forth between hands

Step 4: Wipe top of vial and injection site with alcohol swabs

Step 5: Remove protective covering over the plunger and needle

Step 6: Draw up air equal to the insulin dose to be administered into the syringe

Step 7: Inject the air into the insulin vial

Step 8: With the syringe still inserted, invert the vial and withdraw the insulin dose (the “bunny ears”)

Step 9: If bubbles are present, gently tap the syringe and remove syringe from vial

125
Q

Subcutaneous injection technique

A

Step 1: Pinch the area to be injected (?depends)
Step 2: Insert the needle at a 90o angle (45o if small children
or very thin adults) to the skin in the center of the pinched area
Step 3: Release the pinch
Step 4: Press the plunger to inject
insulin
Step 5: Hold the syringe or device in
the area for 5-10 sec to
ensure full delivery of insulin
Step 6: Remove the syringe or device

126
Q

Do fatter pts need longer needles?

A

No. avg skin thickness is 2.4mm and does not differ for different BMI, race or age.
No need for >8mm needle

127
Q

When should needles be inserted in 45o angle?

A

frail elderly, cachexic adults, children

128
Q

Do you always need to pinch a skinfold?

A

No. 4mm needle dont need

129
Q

What factors alter insulin absorption?

A

Temperature:
Heat(↑)
Cold(↓)

Massage(↑)-> Dont rub area after injection

Exercise (↑)

Jet injectors (↑): via pressure rather than needle

Lipodystrophy (↓) or (↑):
- Lipoatrophy (↑): concavity or pitting of adipose tissue due to immune response due to pork and beef insulin. Rare nowadays due to phasing out of pork/beef insulin; mostly synthetic human insulin now.
- Lipohypertrophy (↓) more common: bulging of adipose tissue due to not rotating injection sties -> slows down absorption as area is thicker -> bgl still high even after injection.

Others (↓) or (↑):
Needle Size/gauge,administration technique(if IM then↑),insulin preparations, mixtures, concentration, dose, insulin stability.

130
Q

Example of rapid-acting insulin

A

Aspart (Novorapid)
Lispro (Humalog)
Glulisine (Apidra)

131
Q

Example of short-acting insulin

A

Regular (Actrapid)

132
Q

Examples of intermediate acting insulin

A

NPH (Insulatard)

133
Q

Examples of long acting insulin

A

Detemir (Levemir)
Glargine U-100 (Lantus)

134
Q

Which types of insulin target PPG?

A

Rapid and short acting as they work fast and is taken 15 and 30mins before meals respectively

135
Q

Which types of insulin target FPG?

A

Intermediate and long acting. Usually once daily at the same time

136
Q

Examples of ultra-long acting insulin

A

Degludec
Glargine U-300 (not bioequivalent to glargine U-100)

137
Q

Examples of self mixed stable insulin

A

➢ Regular + NPH
➢ Rapid-acting + NPH
➢ Rapid-acting (aspart) + degludec (only exception for LA): mix just prior to administration

138
Q

Examples of unstable mixes of insulin

A

➢ Glargine and other insulins: incompatible pH
➢ Glulisine and insulins (other than NPH): not compatible
➢ Detemir and other insulins: not recommended by manufacture

Notes: In general, LA is not compatible as formulation is formed to allow it to be LA so if you mix, it messes up formulation

139
Q

Examples of pre-mixed insulin products

A

Novomix 30: 30% aspart, 70% aspart protamine (NPH) (15min before meal)

Humalog Mix 75/25: 25% lispro, 75% lispro protamine (NPH) (15min before meal)

Mixtard 70/30: 70% NPH, 30% regular
(30min before meal)

Mixtard 50/50: 50% NPH, 50% regular
(30min before meal)

140
Q

Does premixed insulin cover both meal/snack and basal glucose?

A

Yes

141
Q

How would you adjust oral therapies when injectables are started?

A

Metformin: continue

TZD: discontinue or reduce dose

SU: discontinue or reduce dose by 50% when basal is initiated. Discontinue if mealtime insulin initiated or on a premix regimen

SGLT2i: continue

DPP4i: discontinue if GLP-1 agonist initiated

142
Q

What is the general rule of thumb for insulin dosing conversions

A

1:1 conversion

Ex: Mixtard® 30 (NPH 70%, regular insulin 30%) or Insulatard® 16 units AM and 8 units PM can be switched to NovoMix® 30 16 units AM and 8 units PM (vice versa)

143
Q

General rule of thumb to reduce insulin dose if at risk of hypoglycemia

A

10-20%

144
Q

What are the exceptions to the 1:1 dosing conversion?

A

➢Switching from twice daily NPH to once daily glargine/detemir -> decrease by 20%
Ex: 20 units NPH twice daily (40IU total) -> 32 units of glargine once daily

➢Switching from U-300 glargine (more concentrated) to other alternative basal insulin analog -> ↓ by 20%
Ex: 40 units of U-300 glargine -> 32 units of U-100 glargine/detemir

144
Q

SE of insulin

A

Hypoglycemia: BG ≤ 4.0 mmol/L (70 mg/dL):
- S/Sx (including but not limited to): blurry vision, sweating, tremor, hunger, confusion, anxiety, shaking, rapid heat beat, dizziness, headache, weakness & fatigue, irritability
- Nocturnal: nightmares, restless sleep, profuse sweating, morning headache
- Management: The 15-15-15 rule

Weight gain
- More than patients on SUs
- Type 1: weight gain of 4.6 kg more at 5 years when compared to those patients in the conventional therapy group (DCCT)
- Type 2: Weight gain was 4 kg more at 10 years when compared to patients in the conventional treatment group (UKPDS)
- Benefits of glycemic control outweigh weight gain: Always remind patients regarding diet, exercise and losing weight

Lipodystrophy
- Lipoatrophy: concavity or pitting of adipose tissue due to immune response due to pork and beef insulin
- Lipohypertrophy (more common): bulging of adipose tissue due to not rotating injection sties.

Local allergic reaction
- Redness, swelling and itching at injection site
- More common with beef or pork insulin (phasing out already)

Systemic allergic reaction: rare

Insulin resistance: rare
- Immune phenomenon

144
Q

Explain 15-15-15 rule

A
  • 15g of fast acting carbohydrates
  • Wait for 15minutes
  • Check BG, if still ≤ 4.0 mmol/L (hypogly) then another 15g of fast acting carbohydrates
145
Q

Examples of fast-acting 15g CHO

A

Fruit juices (4oz or ½ cup)
Raisins (2tbsp)
Sugar (3 cubes or 1 tbsp)
Hard candies (5-6pieces)
Regular soft drinks (4oz or ½ cup) - must not be sugar free eg. diet coke uses artificial chemicals to create sweetness
Honey (1tbsp)

146
Q

What is the preferred pharm agent for T2DM?

A

Metformin

147
Q

What pharm agent should be considered if pt have Hx of ASCVD, HF or CKD? (regardless of A1c)

A

ASCVD: GLP-1 agonist or SGLT-2
HF: SGLT-2
CKD: SGLT-2 > GLP-1 agonist

148
Q

If after adding metformin, A1c is still above goal, what should you consider?

A
  • Need to minimize hypoglycemia (eg elderly) – avoid SU, insulin (highest risk of hypogly)
  • Need to promote weight loss – GLP-1, SGLT-2
  • Financial difficulties – SUs > TZDs > DDP-4
149
Q

When should insulin be considered?

A
  • Ongoing catabolism (weight loss) -> T2DM pts shld be gaining weight so if pt start to lose weight, quite dangerous (cld be delayed T1DM instead?)
  • Symptoms of hyperglycemia
  • A1c > 10%
  • BG > 16.7 mmol/L
150
Q

Initial dose of insulin

A

10IU/day OR 0.1-0.2IU/kg a day

151
Q

Would you initiate PPG or FPG control for insulin initiation?

A

FPG as when HbA1c is high, basal predominates

152
Q

If A1c is still uncontrolled after initiation of insulin, what should you add do?

A
  • ↑ insulin 2 units every 3 days until FPG at goal
  • May ↑ insulin 4 units every 3 days if FPG consistently > 10 mmol/L
  • ↓ insulin by 10-20% if no clear reason for hypoglycemia
153
Q

What is target range for FPG?

A

5.0-7.0 mmol/L

154
Q

If A1c still above goal despite basal dose >0.5IU/kg or FPG at goal, what should you do?

A

Add prandial coverage (either rapid/regular insulin)
- 1 dose w largest meal
- 4IU or 10% basal eg. basal is 40IU then start 4IU
- If A1c <8%, to also decrease basal dose by 4IU or 10% (if not hypoglycemic)
When adding prandial, always consider premixed or selfmix insulin to ↓injectns

OR

If on bedtime NPH, consider splitting dose into two doses, ⅔ in AM, ⅓ in evening (Split NPH dose if pt dont want to add on postprandial drug)

155
Q

Why do we stop increasing basal insulin dose once >0.5IU/kg?

A

Basal insulin have ceiling effective dose. overuse can lead to weight gain, hypoglycemia and postprandial hyperglycemia

156
Q

Is Diabetic Ketoacidosis (DKA) more common in Type 1 or 2 DM?

A

Type 1 DM.

Type 2 usually have some residual insulin production so they are protected against excessive lipolysis and ketone prdtn

157
Q

How does DKA occur?

A
  • An absolute/relative insulin deficiency-> lipolysis + metabolism of free fatty acids -> formation of beta- hydroxybutyrate, acetoacetic acid, and acetone in the liver.
  • Stress -> stimulates insulin counter-regulatory hormones (glucagon, catecholamines, glucocorticoids, growth hormone). Excess glucagon ↑ gluconeogenesis and ↓ peripheral ketone utilization.
158
Q

S&S of DKA

A
  • ketones found in blood and urine
  • fruity breath odour
  • acidosis
  • usually still alert
  • BG>14mmol/L
159
Q

Is Hyperglycemia Hyperosmolar State (HHS) more common in type 1 or 2 DM?

A

Type 2 DM as there is still residual insulin, usually no ketones/acidosis

160
Q

S&S of HHS

A
  • Extremely dehydrated
  • BG can be >33mmol/L
  • Usually stupor
161
Q

What is the somogyi effect?

A

BG levels drop sharply at night (miss bedtime snack/ too much insulin, etc), body responds by releasing glucagon, BG level ↑

162
Q

What is dawn phenomenon

A

It is more common than somogyi effect. Release of cortisol (stress hormone that causes sugar to go up) in the waking hours causes BG levels to rise sharply

163
Q

What are ways to prevent and manage DM complications?

A
  • Aspirin administration (?) -CVD
  • Smoking cessation
  • Blood pressure
  • Lipid profile
  • Others:
    Metabolic Syndrome (treat each risk factor)
    Complication prevention due to low immunity: influenza, pneumococcal vaccines
164
Q

What is aspirin’s role in DM?

A

Secondary prevention of CVD in those with DM and Hx of ASCVD

OR

Primary prevention strategy in those with diabetes who are at increased CV risk, after a discussion with the patient on the benefits vs increased risk of bleeding.

165
Q

What can you give for prevention of ASCVD if pt allergic to aspirin in DM?

A

Clopidogrel 75mg/day

166
Q

When is aspirin not recommended in DM?

A

Not recommended for those at low risk of ASVCD, e.g. <50 years (young) with diabetes AND with no other major ASCVD risk factors. (not beneficial) AND pts >70y/o

Note: ASCVD risk factors include LDL cholesterol ≥ 2.6 mmol/L, high blood pressure, smoking, chronic kidney disease, albuminuria, and family history of premature ASCVD.

167
Q

What other areas of the body should DM pts take care of?

A

Skin Care
Foot Care
Eye Care
Dental and Oral Care

PR3152: Immune & Endocrine Systems (7 decks)

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