Diabetes & eating disorders

Question 1

Discuss the flow of glucagon and insulin post-prandially in T2DM.

Answer 1

Glucagon stays high during meals, as it is not inhibited by the insulin release as in healthy subjects
Insulin release is delayed and reduced.

Question 2

What are the anabolic actions of insulin in glucose metabolism?

Answer 2

o Glucose transport into muscle and adipose tissues (GLUT4)
o Glycolysis –> energy
o Glycogenesis

Question 3

What are the anabolic actions of insulin in lipid metabolism?

Answer 3

o	Lipogenesis (TG in adipose tissues and synthesis of FFAs in liver)
o	Lipoprotein lipase activity (LPL; adipose tissue)

Question 4

What are the anabolic actions of insulin in protein and electrolyte metabolism?

Answer 4

o Transport of amino acids
o Protein synthesis
o Potassium enters into the cell

Question 5

What are the actions of insulin in glucose metabolism that decrease catabolism?

Answer 5

o Decreased gluconeogenesis (liver)

o Decreased glycogenesis (liver and muscle)

Question 6

What are the actions of insulin in lipid metabolism that decrease catabolism?

Answer 6

Decreased...
o	Lipolysis
o	LPL (muscle)
o	Ketogenesis
o	Fatty acid oxidation (liver)

Question 7

What are the actions of insulin in protein metabolism that decrease catabolism?

Answer 7

Decreased Protein catabolism

Question 8

Explain how glucose stimulates insulin release in healthy people.

Answer 8

Glucose enters the beta cells with GLUT2 –> To glucose-6-phosphate by glucokinase –> glycolysis to pyruvate –> TCA cycle –> ATP –> K channels shut –> Ca 2+ channels open –> insulin storage granules go to membrane –> insulin release

Insulin secreted as pro-insulin (Insulin + P-peptide)

Question 9

Discuss the 2 phases of insulin secretion and how it relates to diabetes

Answer 9

First phase insulin
• The initial burst of insulin, 5-10 minutes after Beta cells are exposed to a rapid increase in BG (5-10 min after meal)
• “uncontrolled” flux of release
• Important to decrease glucagon, decrease hepatic gluconeogenesis, decrease lipolysis and prepare target cells for the action of insulin

Second phase insulin
• Lasts longer than phase 1
• After the acute response (first phase), insulin secretion rises more gradually and is directly related to the degree and duration of the stimulus
–> Diabetic patients do not have the first phase = problem
The second phase is better preserved in type 2 diabetes (= lasts longer)

Question 10

What are 2 incretins and where are they produced?

Answer 10

• GLP-1 is secreted from proglucagon in the enteroendocrine L-cells (ileum and colon)
• GIP is derived from proGIP in the K-cells of the jejunum
  Both are released in the presence of nutrient ingestion

Question 11

Diabetes is the cause of __% of strokes

Answer 11

30%

Question 12

Diabetes is the cause of __% of heart attacks

Answer 12

40%

Question 13

Diabetes is the cause of __% of kidney failure requiring dialysis

Answer 13

50%

Question 14

Diabetes is the cause of __% of non-traumatic leg and foot amputations

Answer 14

70%

Question 15

Diabetes is the cause of __% of blindness

Answer 15

Leading cause

Question 16

What is LADA?

Answer 16

Latent autoimmune diabetes of adults;
Type of type 1 diabetes diagnosed in adulthood, often with a slower course of onset than type 1 diabetes diagnosed in juveniles (islet failure, not insulin resistance)

Question 17

What is MODY?

Answer 17

Maturity onset diabetes of the young” (MODY) refers to any of several hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production

Question 18

Explain the onset of T1DM in a person.

Answer 18

1. Genetic predisposition (100% of B cells present and functional)
2. Silent insulin/B cell destruction (% B cells goes down. This process can take years) – Autoimmune
3. 30% of B cell function = alterations in glucose tolerance
4. 15% of B cells – diagnostic –> clinical diabetes

Question 19

Who has the highest chance of developing T1DM:
Offspring of affected mother?
Offspring of affected father?

Answer 19

Offspring of affected mother: 1 in 50

Offspring of affected father: 1 in 14

Question 20

Incidence of type 1 diabetes increases with time, while type 2 has stabilized. Why?

Answer 20

• Genetics? HLA, DR3, DR4
• Infection? Coxsackie virus
• Alimentation (Cow’s milk?)
  Seasonal variations in T1DM: vitamin D?

Question 21

What proportion of people with T1DM get diagnosed during adulthood?

Answer 21

42% (almost half) of people with type 1 diabetes were diagnosed between age 31 and 60. People often assume they have type 2 diabetes.

Question 22

What proportion of B-cell loss is needed for pre-diabetes? For diabetes diagnosis?

Answer 22

Loss of 50% of B cell mass/function = pre-diabetes

Loss of 80% of B cell mass/function = type 2 diabetes diagnosis

Question 23

Name 6 possibilities for insulin resistance in non-diabetic people

Answer 23

• Children in puberty
• People with type 2 diabetes
• Late term pregnant women
• People ill with an infection
• People on steroids
• People experiencing high stress levels

Question 24

What are the 4 values for diabetes diagnosis and when are they used for diagnosis?

Answer 24

FPG >= 7.0 mmol/L (need 2 measurements if asymptomatic)
o Fasting = no intake for at least 8h

A1C >= 6.5% (in adults)
o Not for suspected T1DM

2hPG in a 75g OGTT >= 11.1 mmol/L

Random PG >= 11.1 mmol/L

Question 25

What are the 3 values for pre-diabetes diagnosis?

Answer 25

Postprandial glycemia (or post load) ≥ 7.8 mmol/L = IGT FPG ≥ 5.6 mmol/L = IFG A1C 6.0-6.5% = Prediabetes

Question 26

What is the recommended macronutrient distribution in diabetes? Fiber? Trans fat? SFA?

Answer 26

CHO 45-60% Protein 15-20% (or 1.0-1.5 g/kg BW) Fats 20-35% Fiber: Increased to 30-50g/d; > 1/3 (10-20g/d) from viscous soluble fiber (e.g oats, barley, psyllium, konjac mannan, pulses, F&V) Avoid trans fats; reduce SFA to < 9% of kcals; replace with PUFAs from mixed n-3/n-6 sources (e.g. nuts, canola oil, soybean oil, flaxseed), MUFAs from plant sources (e.g. extra virgin olive oil, high oleic oils, avocados), whole grains, or low GI CHO

Question 27

What can a weight loss of 5-10% accomplish in people with diabetes and BMI≥25?

Answer 27

Nutritionally balanced, calorie reduced diet should be followed to achieve and maintain a lower, healthier BW Weight loss of 5-10% of initial BW = improved insulin sensitivity, glycemic control, BP control, lipid levels

Question 28

What should people with diabetes replace SFA with?

Answer 28

Polyunsaturated fatty acids (PUFAs) from mixed n-3/n-6 sources (e.g. nuts, canola oil, soybean oil, flaxseed) Monounsaturated fatty acids (MUFAs) from plant sources (e.g. extra virgin olive oil, high oleic oils, avocados), Whole grains, or Low-GI carbohydrates

Question 29

What is the first step for management of hyperglycemia after diagnosis of T2DM? What if not at target? What is the time goal for attainment of A1C?

Answer 29

1. Initiate intensive healthy behaviour interventions or E restriction and increased PA to achieve and maintain healthy BW (+ Provide counselling on a diet best suited to the individual based on the values, preferences, and treatment goals) 2. If not at target: Add pharmacotherapy Timely adjustments to healthy behaviour interventions and/or pharmacotherapy should be made to attain A1C within 2-3 months for healthy behaviour interventions alone or 3-6 months for any combination with pharmacotherapy

Question 30

Name advantages of the mediterranean diet

Answer 30

Decreased A1C Decreased CVD Decreased retinopathy, BP, CP Increased HDL

Question 31

Name advantages and disadvantages of a low-GI diet

Answer 31

Advantages: Decreased A1C Decreased CVD Decreased LDL, CRP, hypoglycemia, diabetes medication Disadvantage: None

Question 32

Name advantages and disadvantages of a high-fiber diet

Answer 32

Advantages: Decreased A1C (viscous fiber) Decreased CVD Decreased LDL, non-HDL-C, ApoB Disadvantage: GI side effects

Question 33

Name advantages and disadvantages of a vegetarian diet

Answer 33

``` Advantages: Decreased A1C Decreased CHD Decreased weight Decreased LDL ``` Disadvantage: Low B12

Question 34

Name advantages and disadvantages of the DASH diet

Answer 34

Advantages: Decreased A1C Decreased CHD Decreased weight, BP, LDL, CRP Disadvantage: None

Question 35

Name advantages and disadvantages of the Portfolio diet

Answer 35

Advantages: Decreased CVD Decreased LDL, CRP, BP Disadvantage: None

Question 36

Name advantages and disadvantages a diet high in dietary pulses/legumes

Answer 36

Advantages: Decreased A1C Decreased CVD Decreased weight, LDL, BP Disadvantage: GI side effects

Question 37

Name advantages and disadvantages of a diet high in nuts

Answer 37

Advantages: Decreased A1C Decreased CVD Decreased LDL, TG, FPG Disadvantage: Nut allergies

Question 38

Name advantages and disadvantages of a diet high in F&V

Answer 38

Advantages: Decreased A1C Decreased CVD Decreased BP No disadvantages

Question 39

How many CHO servings should be provided for meals in DB? For snacks?

Answer 39

Typically, choose 3-5 CHO servings per meal; and 1-2 servings for snacks

Question 40

What should we substract from the total CHO content of a food for CHO counting?

Answer 40

* Adjust for dietary fiber intake | * Foods that contain polyols (sugar alcohols (substract half of them))

Question 41

What are polyols? Give examples? | What are the side effects of polyols?

Answer 41

Sugar alcohols o Erythritol, glycerol (glycerin/glycerine), isomalt, lactitol, maltitol, mannitol, sorbitol, xylitol o If intake > 10g/d = side effects: bloating, diarrhea…

Question 42

Nutrition therapy can reduce A1C by how much?

Answer 42

1-2%

Question 43

LCS use is associated with what?

Answer 43

Higher BMI | Higher T2DM incidence

Question 44

What are the 4 proposed mechanism for the link between LCS and T2DM?

Answer 44

* Sweet taste receptor mediated changes in gut hormones * Impaired predictive relationship between sweet taste and calories/weight gain * Altered nutrient absorption via changing the gut microbiota * Changes in taste preferences and dietary patterns

Question 45

Name 4 benefits of LCS

Answer 45

* More variety in food  enables people that are carb sugar or calorie conscious to take in a wider range of foods that they would either not be allowed to eat or could only eat in such tiny amounts that they were not satisfying * Does not raise BG * Does not contain calories * Can help avoid dental caries, while still enhancing flavor

Question 46

Name 6 health concerns/disadvantages of LCS.

Answer 46

* Associated with cancer? Cell damage? * Can cause bloating * Can be associated to hypertriglyceridemia and GI symptoms * Can be associated with increased incidence of T2DM * Can be associated with increase in weight and obesity * Provides no nutritional value

Question 47

In which patients should snacks be planned?

Answer 47

- Time between supper and bed is > 3 hours - The lean/young are more likely to require snacks (6 small meals, eat every 3h) - If client has a gap of 5 hours (on insulin) or 6 hours or more (without insulin) between their meals, then a snack should be planned - Patients who regularly have low BG at a certain time of day will need a snack at that time - If client is starting a new exercise program, exercising for a longer period than usual, or has a fairly low BG reading prior to starting an intensive exercise - Whenever a delay to the next meal is possible (stuck in traffic driving, waiting at airport for a flight…)

Question 48

What are health risk behaviours? Give 4 examples

Answer 48

unhealthy behaviours you can change 1. Lack of exercise or physical inactivity 2. Poor nutrition 3. Tobacco use 4. Excessive drinking

Question 49

Define health behaviour. Give 3 examples

Answer 49

Any activity undertaken for the purpose of preventing or detecting disease or for improving health and well-being “Behavior patterns, actions and habits that relate to health maintenance, to health restoration and to health improvement” Examples • Medical service usage (physician visits, vaccination, screening) • Compliance with medical regimens (e.g. medication regimens, assistive devices) • Self-directed health behaviors (e.g. diet, exercise, smoking, sleep, alcohol consumption)

Question 50

What is self-management?

Answer 50

“involves the person with the chronic disease engaging in activities that promote and protect health, monitoring and managing the symptoms and signs of illness, managing the impact of illness on functioning, emotions and interpersonal relationships and adhering to treatment regimens”

Question 51

What factors influence adhering to healthier eating patterns in persons living with chronic diseases? (Individual/internal factors)

Answer 51

o Knowledge, health literacy o Culture & language capabilities o Financial resources o Co-morbidities (if they have many chronic conditions and they need to do many different things = overwhelming) o Perceived risk (how serious people think their condition actually is – affected by attitude of HC provider) o Belief regarding benefits (e.g. if they think insulin is actually going to make a difference on their BG control) o Self-efficacy o Attitudes/perceived social norms (everyone has weight to lose… why should I be losing some?) o Poor social support o Mental health/psychological adjustment (stress)

Question 52

Is knowledge a predictor of health behaviour change?

Answer 52

No. Relationship between knowledge and health outcomes is inconsistent Knowledge is needed for behaviour change, but it alone does not necessarily lead to risk-reducing behaviour

Question 53

Why do people with diabetes have emotional distress?

Answer 53

o Most often in the areas of not having enough money to buy supplies and medications (25%) o Feeling deprived of food (32%) o Concerned with future complications of the disease (38%)

Question 54

Why is treatment of depression useful in people with chronic diseases?

Answer 54

Treatment of depression contributes improved health behaviours (e.g. healthy eating) and health outcomes (e.g. compliance with medication, functional ability) Studies: people with chronic conditions - When we treat their depression, we see benefits in terms of QOL, better control of disease…)

Question 55

What is the single question to ask for screening for depression?

Answer 55

Are you depressed most of the time?

Question 56

Name 3 external factors influencing health behaviour change/self-management

Answer 56

* Access to services and information * Provider attitude, beliefs, knowledge, skills, level of integration in HC system * Overall social norms (e.g. cannabis)

Question 57

Define self-efficacy

Answer 57

Definition: One’s confidence in being able to successfully perform an action to produce the desired outcomes (i.e. healthy eating --> improved health)

Question 58

According to Bandura, what are the 3 cognitive mediating processes that determine behaviour? Explain them.

Answer 58

Self-efficacy expectancy: Beliefs/expectations about capacity to perform the behaviours to achieve an outcome; situation & behaviour specific Outcome expectancy: Estimate of probability a change will lead to a desired outcome or result Outcome value: The value we place on the outcome

Question 59

Degree of self-efficacy for a given health behaviour is complex and involves 3 interrelated domains. What are they?

Answer 59

1. Having tacit task knowledge and related skills 2. Having a sense of confidence in one’s ability to mobilize motivation and cognitive resources needed to perform the specific task even when faced with barriers 3. Having confidence in one’s ability to successfully execute a behaviour in a given context

Question 60

What are the 4 main strategies to boost self-efficacy?

Answer 60

1. Performance accomplishment 2. Vicarious experience/modeline 3. Reinterpreting symptoms 4. Persuasion

Question 61

How can we increase a patient's performance accomplishment?

Answer 61

Break task into small tasks; set realistic goals, provide feedback so they can improve their skills

Question 62

How can we increase a patient's vicarious experience/modeling?

Answer 62

Access to DVDs with patients with similar problems, discuss how they overcame barriers Many credible national websites have those videos in them to increase self-efficacy

Question 63

How can we increase a patient's reinterpretation of symptoms?

Answer 63

Educate regarding beliefs about health behaviours and specific symptoms; evidence-based options to reduce stress Teach patients to distinguish between types of pain

Question 64

How can we do verbal persuasion in a patient?

Answer 64

Start by giving verbal support and encouragement for small steps in behavior change; last resort emphasize the consequences of not changing the behaviour

Question 65

Can stress management increase self-efficacy?

Answer 65

Yes

Question 66

Name 2 alternatives to HbA1C measurements and how often they should be measured

Answer 66

Glycosylated serum albumin (GSA) or glycosylated total serum proteins (GSP) Measured q 3-4 weeks (reflects BG over shorter periods)

Question 67

What is the preprandial BG goal to maintain A1C ≤ 7.0%?

Answer 67

5-10 mmol/L | 5-8 mmol/L if unable to maintain A1C ≤ 7.0%

Question 68

What is the 2h post BG goal to maintain A1C ≤ 7.0%?

Answer 68

4-7 mmol/L | 4-5.5 mmol/L if unable to maintain A1C ≤ 7.0%

Question 69

Name things that can decrease A1C

Answer 69

```  Use of EPO, Fe or B12  Reticulocytosis ( high immature RBCs)  Chronic liver disease  ASA, Vitamin C/E  Hemoglobinopathies  Increased erythrocyte pH  Hemoglobinopathies  CRF  Splenomegaly  Rheumatoid Arthritis  HAART meds, Ribavirin  Dapsone • Hypertriglyceridemia ```

Question 70

How does erythrocyte pH affect A1C?

Answer 70

Increased erythrocyte pH --> increased A1C | Decreased erythrocyte pH --> Decreased A1C

Question 71

Describe the glycemic targets for children and adolescents < 18

Answer 71

``` < 18 years old: Goal is A1C ≤ 7.5 % FPG goal: 4.0 – 8.0 mmol/L (vs. adults 4.0 – 7.0) 2hPG: 5.0 – 10.0 (vs. adults 5.0 – 10.0) ``` • Consider preprandial targets of 6.0 – 10.0 mmol/L as well as higher A1C targets in children and adolescents who have had severe or excessive hypoglycemia or have hypoglycemia unawareness

Question 72

What are the initial choices of therapy in patients have... 1. A1C < 1.5% over target? 2. ≥ 1.5% over target? 3. Symptomatic hyperglycemia and/or metabolic decompensation? 4. For all of those if not at target within 3-6 months?

Answer 72

1. Healthy behaviour interventions and start metformin if not at target in 3 months OR start metformin with healthy behaviour interventions 2. Start metformin with healthy behaviour interventions AND Consider second concurrent agent 3. Initiate insulin +/- metformin 4. Add pharmacotherapy based on presence of clinical CVD

Question 73

What are the 3 best OHA for CVD?

Answer 73

Empagliflozin (SGLT2i) Liraglutide (GLP1 RA) Canagliflozin (SGLT2i)

Question 74

What are the 3 best categories of OHA for patients with with high risk of hypoglycemia?

Answer 74

DPP-4 i GLP1 RA SGLT2 i

Question 75

Name 3 risks of metformin/biguanides

Answer 75

o GI side effects (nausea, cramping) o Lactic acidosis: rarely occurs if contraindications are taken into account o B12 deficiency (long-term)

Question 76

Name 2 benefits of insulin secretagogues

Answer 76

o 0.7-0.8% reduction in A1C | o Decreases microvascular risks

Question 77

Name 4 risks of insulin secretagogues

Answer 77

o All associated with risks of hypoglycemia --> Caution for:  Kidney disease  Liver problems  Elderly o Weight gain (especially glyburide) o Bad for heart o Drug loses its effect on someone more rapidly than metformin

Question 78

Name 4 benefits of alpha-glucosidase inhibitors

Answer 78

``` o 0.6% reduction in A1C (Reduction of postprandial glycemia) o Negligible risk of hypo o Weight neutral o In persons with IGT (pre-diabetes) …  49% reduction in CV events  Prevention of T2DM ```

Question 79

Name 4 risks of alpha-glucosidase inhibitors

Answer 79

``` o GI side effects o TID dosing o Not recommended as initial therapy in people with A1C ≥ 8.5% o Contraindications  DKA  IBD (d/t effect on GI) ```

Question 80

Name 3 benefits of TZDs

Answer 80

``` o 0.8% reduction in A1C Longer duration of glycemic control with monotherapy vs. metformin or glyburide o Negligible risk of hypo o Cardiovascular effects  Increase in HDL  Decrease in TGs  Decrease in CVD events ```

Question 81

Name 7 risks of TZDs

Answer 81

``` o Weight gain o Cardiovascular effects (CV controversy)  May induce edema and/or CHF  May increase MI  Increase in LDL o 6-12 weeks for full glycemic effect o Macular edema (rare) o Rare risk of bladder cancer (pioglitazone) o Risk of fractures o Contraindications  Serious liver dysfunction  Known clinical heart failure or evidence of left ventricular dysfunction ```

Question 82

Name 5 benefits of DPP4i

Answer 82

``` o 0.7% reduction in A1C  Reduction in postprandial glycemia  Combo with metformin o Negligible risk as monotherapy o Weight neutral o Neutral CV studies (no effect) o Well-tolerated ```

Question 83

Name 3 risks of DPP4i

Answer 83

o Rare cases of pancreatitis o Long-term safety o Cardiac insufficiency in Saxagliptin

Question 84

Physiological level of GLP-1: DPP4i or GLP1 RA?

Answer 84

DPP4i | GLP-1 receptor agonists = pharmacological levels of GLP-1

Question 85

Name 5 effects of GLP-1 RA that do not apply to DPP-4i

Answer 85

- Decrease gastric emptying - Increase satiety - Decrease energy intake - Increase nausea - Decreases weight (same as DPP4i: Increased insulin secretion, decreased glucagon secretion)

Question 86

Name 6 benefits of GLP1-RA

Answer 86

o 1.0% reduction in A1C --> Reduction in postprandial glycemia o Negligible risk of hypo o Significant weight loss o Decreases BP, weight, A1C o Lira: Decreases CV events, mortality, kidney protection o Potential for improved B cell mass/function

Question 87

Name 8 risks of GLP1-RA

Answer 87

``` o GI side effects (nausea) o Rare cases of pancreatitis o Parafollicular cell hyperplasia o Contraindications: Personal/family Hx of medullary thyroid cancer or MEN2 o Problem with long-term safety o Injectable --> requires refrigeration of the pen prior to first use as well as handwashing and visual inspection of the medication for cloudiness or particulate matter before use o Gallstone disease o $$$$ ```

Question 88

Name 5 benefits of SGLT2 i

Answer 88

``` o 0.7-1.0% decrease in A1C o Negligible risk for hypos o Weight loss (-3kg) o Cardiovascular benefits: Decreases A1C, BP and weight Decreases CV events (Empa), decrease mortality, decreased cardiac insufficiency o Increase kidney protection ```

Question 89

Name 5 risks of SGLT2 i

Answer 89

``` o Mycotic genital infections o Hypovolemia  BP, eGFR (both glucose and Na are excreted when SGLT2 is blocked) o Increases LDL o Euglycemic ketoacidosis o Problem with long-term safety ```

Question 90

When should SGLT2i be stopped prior to a major surgical procedure?

Answer 90

Given that the half-life of SGLT2 inhibitors ranges from 11-13h and the SGLT2 inhibitor effect can persist for at least a few days after d/c, these agents should be d/c ≈ 3 days before major surgical procedures

Question 91

Which 2 OHAs decrease BP?

Answer 91

SGLT2 i | GLP1 RA

Question 92

Name 4 rapid-acting insulins. When should they be taken compared to meals?

Answer 92

Glulisine (Apidra): 0-15 min before Lispro (Humalog): 0-15 min before Aspart (Novorapid): 0-10 min before Faster-acting insulin aspart (Fiasp): 0-2 min before

Question 93

When should short acting insulins be injected?

Answer 93

Around 30 min before meals

Question 94

Name 5 long-acting insulins

Answer 94

``` Detemir (Levemir) Glargine U100 (Lantus) Glargine U300 (Toujeo) Glargine biosimilar (Basaglar) Degludec (Tresiba) ```

Question 95

Name 6 neurogenic symptoms of hypoglycemia

Answer 95

``` Trembling Palpitations Sweating Anxiety Hunger Nausea ```

Question 96

Name 7 neuroglycopenic symptoms of hypoglycemia

Answer 96

``` Difficulty concentrating Confusion Weakness Drowsiness Vision changes Difficulty speaking Dizziness ```

Question 97

Differentiate mild from moderate from severe hypoglycemia

Answer 97

Mild: Autonomic (neurogenic) symptoms present Individual is able to self-treat Moderate Autonomic and neuroglycopenic symptoms Individual is able to self-treat Severe Requires the assistance of another person Uncounsciousness may occur; but may just require help from someone else (d/t +++ confusion) Plasma glucose is typically < 2.8 mmol/L

Question 98

Name risk factors for severe hypoglycemia in people treated with sulfonylureas or insulin

Answer 98

* Prior episode of severe hypoglycemia * Current low A1C (<6.0%) * Hypoglycemia unawareness * Long duration of insulin therapy * Autonomic neuropathy * CKD * Low economic status, food insecurity * Low health literacy * Preschool-age children unable to detect and/or treat hypos on their own * Adolescence * Pregnancy * Elderly * Cognitive impairment

Question 99

What are the 5 steps to address hypoglycemia?

Answer 99

1. Recognize autonomic or neuroglycopenic symptoms 2. Confirm if possible (BG < 4.0 mmol/L) 3. Treat with “fast sugar” 15g to relieve symptoms 4. Retest 15 minutes later to ensure BG > 4 mmol/L and retreat 5. Eat usual snack or meal due at that time of the day or a snack with 15 g CHO + protein Severe hypoglycemia: Give 1 mg glucagon subcutaneously or intramuscularly and call 911

Question 100

Who is at risk for DKA?

Answer 100

* Children < 2 years old; they have 3x higher risk of developing DKA compared to those greater than 2 years * Ethnic minorities have greater risk than non-Hispanic white youth * Lower socioeconomic status * Lack of private health insurance * Lower parental education * Lower BMI * Preceding infection * Adolescent girls (body image issues)

Question 101

What can cause false positives in urine ketones? False negatives?

Answer 101

False positives: Several sulfhydryl drugs (e.g. captopril) False-negatives: Test strips exposed to air for extended periods of time or highly acidic specimens, such as after large intakes of ascorbic acid

Question 102

When should diabetics test for ketones?

Answer 102

Acute illness accompanied with elevated BG Stress Consistently elevated BG levels (> 14 mmol/L) Symptoms of ketoacidosis (e.g. nausea, vomiting, abdominal pain) Pregnancy

Question 103

Name 6 precipitating factors of DKA

Answer 103

``` • Insulin omission (most common cause) • New diagnosis of diabetes • Infection/sepsis • Myocardial infarction o Small rise in troponin may occur without overt ischemia o ECG changes may reflect hyperkalemia • Thyrotoxicosis (XS thyroid hormones) • Drugs ```

Question 104

How much of a decrease in A1C is necessary to decrease the risk of complications in T2DM?

Answer 104

1%

Question 105

How does diabetes lead to retinopathy?

Answer 105

Loss of pericytes - Role in vessel stability and regulate control of endothelial proliferation and angiogenesis Changes in the Retinal vasculature - Thickening of basement membrane - Hyperpermeability - Microaneurysm formation - Microvascular occlusion and ultimately neovascularization

Question 106

When do we initiate screening for retinopathy?

Answer 106

When to initiate screening  T1DM: 5 years after diagnosis in all individuals >= 15 years  T2DM: Children, adolescents and adults at diagnosis If retinopathy is not present  T1DM: rescreen annually  T2DM: Rescreen every 1-2 years  Review glycemic, BP and lipid control, and adjust therapy to reach targets as per guidelines  Screen for other diabetes complications

Question 107

Which 3 factors accelerate neuropathy?

Answer 107

Smoking Lack of PA Alcohol (> 4 drinks/d)

Question 108

What are the different types of neuropathy?

Answer 108

Diffuse Peripheral: Legs, feet, arms, hands Diffuse Autonomic/Visceral: Heart, digestive, sexual organs, urinary tract, sweat glands Focal Eyes, face, mouth, hearing, pelvis, lower back, thigh, abdomen

Question 109

What is the earliest clinical evidence of nephropathy?

Answer 109

Persistent microalbuminuria

Question 110

What is the mechanism of hyperlipidemia in type 1 diabetes? In type 2?

Answer 110

Type 1 - HyperTG due to defective removal of chylomicrons and VLDL resulting from impaired LPL activity (insulin dependent) - HDL and LDL-C may be normal Type 2 - Hypertriglyceridemia due to elevated de novo synthesis from glucose - Low HDL-C (due to obesity) - LDL-C may be normal

Question 111

Who should receive statins?

Answer 111

 Clinical CVD or  Age ≥ 40 years or  Microvascular complications or  Diabetes > 15 years duration and age > 30 years  Warrants therapy based on the 2016 Canadian Cardiovascular Society Guidelines for the Dx and Tx of Dyslipidemia

Question 112

Name 2 possible explanations for why Co-Morbid depression worsens clinical outcomes in T2DM

Answer 112

* Lower levels of physical fitness | * Reduces adherence to medications

Question 113

How is A1C a predictor of mental health outcomes?

Answer 113

A1C is a predictor of mental health outcomes. Each 1% elevation in A1C increases the risk of MCI and dementia

Question 114

Which diabetic medications are the best to prevent NASH?

Answer 114

All OHA are good for NASH

Question 115

Name 2 medications approved for the treatment of obesity in T2DM

Answer 115

GI lipase inhibitor  Side effects: Loose stools, GI upset, rare liver failure  Oral medication that decreases fat absorption, may require vitamin supplementation  $$$ GLP-1 receptor agonist  Side effects: Nausea, GI upset, rare gallstones and pancreatitis  Subcutaneous injectable, increases satiety  $$$$

Question 116

Name 3 embryopathic medications

Answer 116

o ACEi / ARB | o Statin therapy

Question 117

Who must not fast for ramadan?

Answer 117

* Poorly controlled T1DM (Defined as pre-Ramadan A1C > 9%) * Severe hypoglycemia within 3 months, recurrent hypoglycemia and/or hypoglycemia unawareness * DKA within 3 months * Hyperglycemic hyperosmolar coma within 3 months * Acute illness * Advanced macrovascular complications, renal disease (on dialysis, stage IV or V CKD), cognitive dysfunction, or uncontrolled epilepsy * Pregnancy in diabetes or GDM – treated with insulin

Question 118

Who should theoretically not fast during ramadan?

Answer 118

* T2DM with sustained poor glycemic control * Well-controlled T2DM on MDI or mixed insulin * Pregnant T2DM or GDM controlled by diet only * CKD stage 3 or stable macrovascular complications * Performing intense physical labour * Well-controlled T1DM

Question 119

Who can fast during ramadan?

Answer 119

* Well-controlled diabetes * Treated with lifestyle alone, or with: metformin, acarbose, incretin therapies, second generation sulfonylureas, SGLT2 inhibitors, TZDs or basal insulin in otherwise healthy individuals

Question 120

On average, how much time does it take before initiating insulin in T2DM? Is it soon enough?

Answer 120

Insulin in uncontrolled T2DM is initiated earlier than before but not soon enough (9 years)

Question 121

Name 4 disadvantages of intensive therapy

Answer 121

- More injections - CHO counting should be part of the deal - Frequent monitoring (4x/d) is necessary - Weight gain due to less glycosuria, extra insulin for extra food, over treating of hypos

Question 122

Name 4 benefits of intensive therapy

Answer 122

50-76% reduction in microvascular complications associated with T1DM 42% risk reduction in any CV event 25% decrease in microvascular complications in T2DM Better QOL, overall better glycemic control

Question 123

Name 4 reasons why most people with diabetes do not achieve A1C target

Answer 123

- Limited time for clinic staff to interact and follow up with patients is a practice challenge (Often “no shows” or “DNA”) - The need to administer a complicated regimen of multiple insulin doses titrated to carbohydrate intake and activity, and frequent SMBG testing, can lead to dose omissions and incomplete adherence. - Lack of social support - Coincident common psychiatric conditions such as depression can affect adherence - Myths regarding insulin therapy leading to UNDERUTILIZATION of insulin in Type 2 patients: - Inadequate understanding of the consequences of poor control

Question 124

What to do in cases of hypoglycemia unawareness?

Answer 124

Remind symptoms to patients Have patients “regain symptoms” --> allow them to go higher (in terms of BG) for some time and then they will start re-feeling the symptoms again Ask them at what number they react/feel low

Question 125

Which measure of BG is an independent predictor of MIin T2DM?

Answer 125

PPG

Question 126

Which, of FPG or PPG, has more impact on A1C levels?

Answer 126

FPG has a higher impact on A1C. But as it gets closer to target, 2hPG has more impact

Question 127

Why does breakfast usually have a higher glycemic excursion?

Answer 127

- epinephrine, cortisol, GH, glucagon = higher peak in BG even with same CHO intake (Dawn Phenomenon) - Breakfast also usually very CHO-rich and low in protein

Question 128

Name 7 factors that affect PPG

Answer 128

* Pre-meal BG status and timing of injection * GI of the food * Large volume rich in fat, protein and/or fiber * Time of day (e.g. breakfast = higher peak) * Stress, illness, PA, hormones * Gastroparesis (need to adjust insulin doses) * Is there adequate basal? if meal is skipped, does BG stay at target?

Question 129

Compared to the meal, when should we inject rapid-acting insulin? Why?

Answer 129

Administration of rapid-acting insulin analogs 15 minutes before mealtimes result in lower postprandial glucose excursions and more time spent in the 3.5-10.0 mmol/L range, without increased risk of hypoglycemia - The postprandial glucose peak has a mean peak time of 75 minutes - Rapid-acting insulin analogs display a maximum effect at around 100 minutes after subcutaneous injection The insulin peak action is better synchronized with the glycemic excursion after a meal, thereby potentially minimizing the height of the postprandial glucose excursions

Question 130

Name 5 signs/symptoms of night time hypos?

Answer 130

``` “Wicked” morning headaches “Foggy head” Waking up with messed up blankets +++ sweating Nightmares and vivid dreams ```

Question 131

Why does one episode of hypoglycemia increase the risk of another?

Answer 131

Having one reaction increases the risk of having another in 24h Low BG = high release of stress hormones = symptoms Second reaction will be harder to recognize due to depleted stress hormones

Question 132

What is lipohypertrophy? what can it cause?

Answer 132

Medical term that refers to a lump under the skin caused by an accumulation of extra fat and scar tissue at the site of many subcutaneous injections of insulin. It may be unsightly, mildly painful, and may change the timing or completeness of insulin action. “No pain” during injections may be a sign.

Question 133

What is TDD? What is it composed of? How is it calculated?

Answer 133

Total Daily Dose (TDD) Includes both basal and bolus insulin (50-50%) To start, 0.5-0.7U/kg is most commonly used o 0.5 U/kg = healthy BW o 0.7 U/kg = overweight o 1.0 U/kg = obese with A1C > 9% New onset of T1: 0.3 U/kg Young adults (age 18-21) “still growing” causing insulin resistance… higher doses required (0.7-1.0 U/kg)

Question 134

What is ICR? How is it calculated?

Answer 134

How many grams of CHO does 1U of insulin cover? (A) If TDD > 40 units total: 500/TDD = 1U: _ g CHO (B) If TDD < 40 units total: 450/TDD = 1U: _ g CHO Compare with weight-recommended formula: (5.7 x weight (kg))/TDD = 1U: _ g CHO

Question 135

What is ISF? When is it used? How is it calculated?

Answer 135

The drop in BG in mmol/L that each U of insulin will provide Useful for correcting glucose once a target is set = better control How to estimate ISF? 100/TDD = ISF

Question 136

What is the BEAM method? What is it used for?

Answer 136

Used to know if basal is adequate Check overnight first using BEAM (Bedtime/AM glucose) – should be no more than 2 mmol/L difference If go to bed within target and wake up within target --> don’t change basal If > 3-4 mmol/L change between bedtime and AM  significant

Question 137

What should be the max elevation 2h post meal? What should be done if it is higher?

Answer 137

Aim for no more than 3 mmol/L elevation | If higher, adjust bolus

Question 138

Define self-management education (SME)

Answer 138

A systematic intervention that involves active patient participation in self-monitoring and/or decision-making

Question 139

What are the 3 criteria for anorexia nervosa

Answer 139

* Restriction of energy intake relative to requirements leading to a significantly low body weight in the context of age, sex, developmental trajectory and physical health * Intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain even though at a significant low weight * Disturbances in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or lack of recognition of the seriousness of the current low body weight

Question 140

What are the 2 types of anorexia nervosa?

Answer 140

Restrictive type | Binge eating/purging type

Question 141

Name attributes of a person with anorexia nervosa

Answer 141

- excessive dieting & food preoccupation - Excessive concern about weight, shape or health - excessive perfectionism - cognitive rigidity - self-denial (does not worry) - Social withdrawal - extreme focus on job or school work - anxiety

Question 142

What are the categories of severity of anorexia nervosa?

Answer 142

``` Specific Severity is based on BMI o BMI > 17: Mild o BMI 16-16.99: Moderate o BMI 15-15.99: Severe o BMI < 15: Extreme ```

Question 143

How do we categorize a case that is like anorexia but the patient has a higher BMI?

Answer 143

OSFED (atypical AN)

Question 144

What are the 3 criteria for bulimia nervosa?

Answer 144

Recurrent episodes of binge eating characterized by both of the following:  Eating in a discrete amount of time (within a 2h period) large amounts of food  Sense of lack of control over eating during an episode Recurrent inappropriate compensatory behavior to prevent weight gain: Fasting, strict deprivation, self-induced vomiting, compulsive exercise, use of laxatives, diuretics, medication Self-evaluation is unduly influenced by body shape and weight Occurs at least once a week for 3 months on average

Question 145

Name attributes of a person with bulimia nervosa

Answer 145

- Obsessive thoughts focused on restricting and bulimia - excessive concerns about weight loss and shape - Body weight fluctuations (dehydration, water retention, binge more, binge less, alcohol) – can gain weight - Inability to accurately identify and express feelings - Chaotic relationships and interactions - Impulsivity (common trait; vs AN = compulsive trait, more rigidity) - Anxiety - Labile mood

Question 146

What are the categories of severity of bulimia nervosa?

Answer 146

``` Specific severity based on the average number of compensatory behavior episodes per week o Mild: 1-3 o Moderate: 4-7 o Severe: 8-13 o Extreme: 14+ ```

Question 147

How is binge eating disorder (BED) defined?

Answer 147

Recurrent episodes of binge eating. An episode of binge eating is characterized by the following: - Eating in a discrete amount of time (within a 2h period) large amounts of food - Sense of lack of control over eating during an episode Three or more of the following - Eating much more rapidly - Until feeling uncomfortably full - Not feeling physically hungry - Eating alone - Feeling disgusted by oneself, depressed, or very guilty afterwards Not associated with the recurrent use of inappropriate compensatory behavior (ex. purging) – although they can restrict, but do not use compensatory behaviour (or will do so very occasionally) On average, at least once a week for 3 months

Question 148

How is the severity of BED categorized?

Answer 148

``` Specific severity based on average number of binge eating episodes per week (same as bulimia) o Mild: 1-3 o Moderate: 4-7 o Severe: 8-13 o Extreme: 14+ ```

Question 149

Is BED associated with weight gain or weight loss?

Answer 149

* Long-term weight gain – more at risk of diabetes, HTN… --> those people will even gain weight during treatment, and then lose weight. * No short-term weight loss when reaching abstinence

Question 150

Name 5 examples of OSFED (other specified feeding or eating disorder)

Answer 150

- Atypical anorexia nervosa: Weight within or above the “average” range for age and height - Bulimia nervosa of low frequency and/or limited duration - BED of low frequency and/or limited duration - Purging disorder: Persistent purging without binge eating - Night eating syndrome: Excessive consumption of food following and evening meal or after waking from sleep in the night, which causes extreme psychological distress and interferes with daily functioning

Question 151

What are the 4 criteria in the definition of avoidant restrictive food intake disorder (ARFID)

Answer 151

1. An eating or feeding disturbance (e.g. apparent lack of interest in eating or food, avoidance based on sensory characteristics of food; concern about aversive consequences of eating) as manifested by persistent failure to meet appropriate nutritional and/or energy needs associated with one or more of the following: - Significant weight loss (or failure to achieve expected weight gain or faltering growth in children) - Significant nutritional deficiency - Dependence on enteral feeding or nutritional supplements - Marked interference with psychosocial functioning 2. The disturbance is not better explained by lack of available food or by an associated culturally sanctioned practice 3. The eating disturbance does not occur exclusively during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which one’s body weight or shape is experienced (or body image issue) 4. The eating disturbance is not attributable to a concurrent medical condition or not better explained by another mental disorder. When the eating disturbance occurs in the context of another condition or disorder, the severity of the eating disturbance exceeds that routinely associated with the condition or disorder and warrants additional clinical attention (Afraid of the consequences of eating e.g. choking, vomiting, digestive problems, intoxication)

Question 152

Are people with ARFID concerned with their weight?

Answer 152

Often want to gain weight, are concerned about their low weight. (unlike AN)

Question 153

In which part if the population is ARFID usually seen? What attributes are common in these people?

Answer 153

- Broad range of eating disturbances more commonly seen in childhood - not characterized by concern about body weight or size - May develop from food refusal to maladaptive coping strategies (distracted or forced feeding) - Anxiety is common in ARFID - Unresolved in 3-10% of ARFID children

Question 154

What are unspecified feeding and eating disorders

Answer 154

When details of a patient’s eating disorder are not determined. May happen as a first diagnosis

Question 155

What is the prevalence of AN in men and women? Bulimia? BED?

Answer 155

Anorexia Nervosa o 1% in women o 0.5% in men Bulimia o 1.5-2% in women o 0.5% in men Binge-eating disorders o 1.6-3.5% in women o 0.8-2.0% in men

Question 156

What proportion of patients with AN eventually normalize weight? What are predictors of positive outcomes? of negative outcome?

Answer 156

2/3 of patients normalize weight, but the rest are chronic cases Patients with illness onset before 17 years old achieve a better outcome than adult onset. Higher rate of full recovery and lower mortality rate in adolescents than adults Prepubertal onset confers a more difficult course

Question 157

Compare the mortality rate among AN vs among other disorders

Answer 157

Mortality rate among anorexia nervosa is the highest among psychiatric disorders

Question 158

What is the average time to complete remission in AN?

Answer 158

5-6 years

Question 159

What are risk factors for ED?

Answer 159

Genetic predisposition o Identified genes for AN ``` Family history o Eating disorders o Obesity o Anxiety o Depression ``` ``` Neuro-cognitive vulnerabilities o Anxiety o Obsessionality o Perfectionism o Negative affect ``` ``` Developmental and environmental factors o Adverse pre/peri/neonatal events o Prematurity o Early childhood eating problems o Personality traits o Puberty o Body dissatisfaction – may have body image issues since they were children o Perceived pressure for thinness o Perceived pressure to perform (e.g. some sports) o Strict dieting o Interest in health and nutrition o Excessive exercise o Low self-esteem o Substance abuse o Sexual abuse and other traumas ```

Question 160

What are the common comorbidities with EDs?

Answer 160

 Mood disorder  Anxiety disorder  Obsessive compulsive traits/disorder  Post-traumatic stress disorder  Personality disorder (impulsiveness, emotion dysregulation)  Substance misuse or dependence  Attention deficit hyperactivity disorder

Question 161

What are common dietary patterns in BN? In AN?

Answer 161

BN: - Restrictive eating, removal of meals, CHO phobia, fasting (intermittent fasting), objective binge eating, forbidden foods usually found in binge content AN: Gradual decrease in food intake, Removal of high energy food, Gradual decrease of portion sizes, Distortion of size of portion, overestimate portion size, Limited to bulky nutrient-poor foods (High vegetables, etc.), Rigid schedule of eating, Limited food choices/amount of calories, Food avoidance related to digestive symptoms (think they have gluten intolerance), Vegetarianism and veganism, Fluid avoidance of excessive fluid intake

Question 162

What causes binge eating? How can we help?

Answer 162

Need to explain to patients that food deprivation and restrictive eating leads to binge eating and compensatory behaviours. Need to break the cycle by giving up food deprivation. The focus needs to be on the restriction rather than on the bulimia (compensatory behaviour). Same for anorexia and bulimia. Work on being less restrictive.

Question 163

Is vomiting effective in weight loss/control?

Answer 163

No. Short term weight loss due to dehydration. (people with BN are more dehydrated than AN) Digestive resistance Vomiting --> recurrent binge eating --> long term weight gain

Question 164

Name 3 laxatives. Which electrolytes are lost with laxatives? What does laxative use clinically lead to?

Answer 164

Stimulant type (Bisacodyl, Senna, Cascara) – more powerful type Dehydration and electrolyte loss (K and bicarbonate) Dehydration stimulates the renin-angiotensin-aldosterone system – more sodium and water absorption = water retention --> weight gain, distress Hyperaldosteronism and edema

Question 165

What are clinical signs of AN: Skin?

Answer 165

- Acrocyanosis (blue finger/toes) (d/t vasoconstriction and decreases blood flow – cold hands) - Hair loss - Dry skin - Lanugo-like body hair (very fine) - Stomatitis - Increased acne

Question 166

What are clinical signs of BN: Skin?

Answer 166

- Russell's sign (scar over dorsal surface of hand) - Nose bleeds (epistaxis) - Subconjunctival hemorrhage

Question 167

What are clinical signs of AN: CV system?

Answer 167

``` Hypotension, bradycardia Heart palpitations, chest pain Arrhythmia Loss of cardiac muscle mass Mitral valve prolapses (rare) Prolongation of QTC interval Pericardial effusions ```

Question 168

What are clinical signs of BN: CV system?

Answer 168

Dizziness Heart palpitations Chest pain Arrhythmia

Question 169

What are clinical signs of AN: endocrine?

Answer 169

``` Feeling cold Frequent bladder emptying (ADH is low) Fatigue Amenorrhea in women Impotency in men Sleep disturbances (common) Hypoglycemia (usually asymptomatic but could be symptomatic in the first 2 weeks of refeeding) Hyperactivity (related to low leptin levels; called malnutrition-induced hyperactivity) ```

Question 170

What are clinical signs of BN: endocrine?

Answer 170

Irregular menses Feeling cold Fatigue Sleep disturbances

Question 171

What are clinical signs of AN: Muscle/bone mass/dental system?

Answer 171

Muscle loss Muscle cramps/weakness Rhabdomyolysis (breakdown of damaged skeletal muscles d/t intense exercising) Osteopenia Osteoporosis (especially when no menses -->Need enough calcium and VD intake) Stress fracture Usually normal electrolytes

Question 172

What are clinical signs of BN: Muscle/bone mass/dental system?

Answer 172

Muscle cramp/weakness (electrolyte imbalances) Perimyolysis (dental erosion) Do not encourage brushing teeth after purging. Rather, rinse mouth with baking soda to protect enamel Enlargement of parotid glands (hyperstimulation of the glands) Often happens when you stop vomiting Dental caries (losing enamel of teeth d/t frequent vomiting)

Question 173

What are clinical signs of AN: digestive system?

Answer 173

Early satiety (will feel full easily at the beginning of the refeeding process) Epigastric discomfort Delayed gastric emptying, gastroparesis Constipation/diarrhea Bloating, abdominal pain SMA syndrome (superior mesenteric artery syndrome – when the duodenum is compressed between two arteries. Refeeding helps with this)

Question 174

What are clinical signs of BN: digestive system?

Answer 174

``` Swollen salivary glands Epigastric discomfort Esophagitis, hematemesis (vomiting; Mallory Weiss syndrome = blood in vomiting) Gastric reflux Constipation/diarrhea Hemorrhoids, rectal bleeding (laxatives) Rectal prolapsus Loss of normal colon function ```

Question 175

What are clinical signs of AN and BN: kidney function?

Answer 175

Water retention | Reduced kidney function (reversible with refeeding and water repletion)

Question 176

What are clinical signs of AN and BN: brain?

Answer 176

Brain atrophy changes Neurocognitive functioning impairment “When you gain weight, you gain brain”

Question 177

What are clinical signs of AN and BN: cognitive changes?

Answer 177

Loss of concentration Loss of memory Difficulty to take decision

Question 178

What are clinical signs of AN: psychological changes?

Answer 178

``` Intense food preoccupation Obsessive compulsive behaviour Irritability Loss of interest (loved ones, things you like...) Social isolation ```

Question 179

What are clinical signs of BN: psychological changes?

Answer 179

``` Intense food preoccupation Mood changes Irritability Loss of interest Social isolation ```

Question 180

Lab findings in EDs: Does BUN go up or down? Why?

Answer 180

Up (dehydration)

Question 181

Lab findings in EDs: Does complement 3 go up or down? Why?

Answer 181

Down (malnutrition)

Question 182

Lab findings in EDs: Do WBCs go up or down? Why?

Answer 182

Leukopenia/thrombocytopenia (WBCs and platelets go down)

Question 183

Lab findings in EDs: Does Hgb go up or down? Why?

Answer 183

Down (anemia)

Question 184

Lab findings in EDs: Does glucose go up or down? Why?

Answer 184

Down (malnutrition) --> non-symptomatic hypoglycemia; | Up (insulin omission among diabetics)

Question 185

Lab findings in EDs: Does sodium go up or down? Why?

Answer 185

Down (water loading or laxatives)

Question 186

Lab findings in EDs: Does potassium go up or down? Why?

Answer 186

Down (vomiting, laxatives, diuretics, refeeding) Potassium usually drops because of loss in vomitus but can drop because of lack of renal absorption due to magnesium deficiency

Question 187

Lab findings in EDs: Does Mg go up or down? Why?

Answer 187

Down (poor nutrition or RS)

Question 188

Lab findings in EDs: Does phosphorus go up or down? Why?

Answer 188

Down (RS)

Question 189

Lab findings in EDs: Does chloride go up or down? Why?

Answer 189

Down (vomiting); | Up (laxatives)

Question 190

Lab findings in EDs: Does bicarb go up or down? why?

Answer 190

Up (vomiting - metabolic alkalosis) Down (laxatives) Even if K is normal, seeing a high bicarbonate is a good indication that the patient may be vomiting

Question 191

Lab findings in EDs: Does creat go up or down? why?

Answer 191

Up (dehydration, renal dysfunction) Serum creatinine may be normal in the face of renal failure. This is because the serum creatinine is proportional to body muscle which is low

Question 192

Lab findings in EDs: Does CPK (creatine phosphokinase) go up or down? why?

Answer 192

Up (muscle breakdown); | Down (reduced muscle mass) – may also happen with high PA

Question 193

Lab findings in EDs: Does Amylase go up or down? why?

Answer 193

Up (salivary origin – vomiting) – although not followed on a regular basis

Question 194

Lab findings in EDs: Do liver enzymes (ALT, AST, total bilirubin) go up or down? why?

Answer 194

Up (liver dysfunction)

Question 195

What are the best psychosocial interventions for: - Adolescent AN - Adult AN - BN and BED

Answer 195

- Adolescent AN: Family-based treatment - Adult AN: No specific approach with clear superiority - BN and BED: Cognitive behavioural therapy, Dialectical behavioural therapy, Interpersonal therapy, acceptance and commitment therapy

Question 196

What is Cognitive behavioural therapy?

Answer 196

Working on beliefs that maintain the maladaptive behavior, how self-esteem is related to body image and weight. Also working on emotion regulation related to maladaptive eating behaviors o Psychoeducation is a component of CBT o Includes cognitive restructuring – bring facts and work on questioning beliefs o Definition: short-term, goal-oriented psychotherapy treatment that takes a hands-on, practical approach to problem-solving. Its goal is to change patterns of thinking or behavior that are behind people's difficulties, and so change the way they feel.

Question 197

What is dialectical behavioural therapy?

Answer 197

o About working on emotion regulation and developing strategies to cope with emotions (e.g. mindful eating) o Mindfulness is used is psychotherapy and can also be useful for behavior intervention o Provides clients with new skills to manage painful emotions and decrease conflict in relationships

Question 198

What is interpersonal therapy?

Answer 198

About developing interpersonal skills among patients

Question 199

What is acceptance and judgement therapy?

Answer 199

o Developing adequate behaviour despite disordered thoughts o Focusing on maintaining the adequate behaviour o Acceptance and commitment therapy invite people to open up to unpleasant feelings, and learn not to overreact to them, and not avoid situations where they are invoked

Question 200

What are useful medications for AN? BN? BED?

Answer 200

- No medication to specifically treat AN - Fluoxetine (Prozac: Selective Serotonin Reuptake Inhibitors) has been shown effective in BN - Lisdexamfetamine (Vyvanse) and topiramate (Topamax) for moderate to severe BED (they have an effect on appetite) Use of psychoactive medications are useful for comorbidities (e.g. depression, mood disorders) in bulimia and AN

Question 201

What is the prognosis in terms of weight for people with AN?

Answer 201

AN and BN participants followed over 10 years or over 22 years Modest increase in BMI from year 2 to year 5 Plateau from year 5 to 10 At 22 years… - 14% were underweight - 69% were normal weight - 17% were overweight - 4% obese Still lower chances of becoming overweight or obese vs. the general population

Question 202

What is the prognosis in terms of fat mass and distribution for people with AN?

Answer 202

After gaining back some weight, people with EDs also have a normal % fat mass after recovery. BUT the fat distribution has been shown to be different! - AN adolescent females lose more central body fat while adult females lose more peripheral fat - Partial weight gain in adolescent females lead to greater fat mass deposition in the trunk region than other regions (extremities) - After short term partial or complete weight restoration, adults show a central adiposity phenotype with respect to health age-matched controls - Central fat distribution is associated with increased insulin resistance, but does not adversely affect ED psychopathology or cause distress in female adults - Abnormal central fat distribution seems to normalize after long-term maintenance of complete weight restoration

Question 203

Name 7 hospitalization admission criteria for patients with EDs

Answer 203

* Severe or rapid weight loss * Severe binge eating and purging * Medical complications: Unstable vital signs, cardiac abnormalities, electrolyte imbalances * Lack of response to outpatient treatment * Severe psychiatric co-morbidity (e.g. suicidal) * For laxative withdrawal * To clarify a diagnosis

Question 204

Name 7 hospitalization admission criteria for patients with EDs

Answer 204

* Severe or rapid weight loss * Severe binge eating and purging * Medical complications: Unstable vital signs, cardiac abnormalities, electrolyte imbalances * Lack of response to outpatient treatment * Severe psychiatric comorbidity (e.g. suicidal) * For laxative withdrawal * To clarify a diagnosis

Question 205

What is the weight gain goal on the day program? In hospitalization?

Answer 205

Day program/day hospital: 500g per week if BMI < 20 | Hospitalization: 1 kg/week

Question 206

Are F&V allowed during hospitalization?

Answer 206

Reduce the use of raw fruits and vegetables to prevent discomfort or pain o Patients may not be able to digest them or develop some intolerances

Question 207

What are warning signs of ED among T1DM patients?

Answer 207

* High A1C * Frequent episodes of DKA * Frequent hospitalizations * Poor glycemic monitoring * Negative attitudes towards diabetes * Excessive preoccupation toward weight and body shape * Low intake of CHO * Excessive exercise * Weight fluctuations * Amenorrhea or irregular menses * Resistance to correct hypoglycemia * Missing appointments at the diabetes clinic * Poor interest and withdrawal.

Question 208

How much time does an insulin pump last on the skin?

Answer 208

3 days

Question 209

Pumps calculate precise accurate doses based on...

Answer 209

ICR, ISF, IOB, targets

Question 210

Who is a pump candidate?

Answer 210

* One who has small insulin needs (minimum is 0.025 U vs.0.5 U for pens) * Hypoglycemia unawareness or nocturnal hypo * Dawn phenomenon * Planning conception and/or pregnancy * Shift work * Frequent travel * Regular PA, athletes * Often hospitalized * Not reaching BG target, elevated A1C * Gastroparesis (slowed digestion) * Desire better control, less injections * Now T2DM

Question 211

Why can DKA happen with a pump?

Answer 211

 Infusion set/site issue (redness/blood at site or in tubing, site in longer than 3 days, air in tubing or tubing not connected correctly to reservoir, leak in tubing or at the site, cannula dislodge/kink, lipohypertrophy)  Insulin pump issue (forgot last bolus, empty cartridge, basal rate not well-programmed, fault with pump)  Personal factors (miscounted CHO, sickness, stress, pre-menstrual, pain, new medication, exercise, gastroparesis, battery dead)  Insulin issues (expired, cloudy, insulin at RT > 28 days, exposed to extreme temperatures)

Question 212

What to do if your BG is between 4-16 but blood ketones are > 0.6? When your BG is > 16 with < 0.6 ketones? When BG > 16 and ketones between 0.7-1.4? When BG is > 16 and blood ketones between 1.5-3.0?

Answer 212

BG is between 4-16 but ketones are > 0.6 --> take 10% of TDD When your BG is > 16 with < 0.6 ketones --> Take 10% of TDD When BG > 16 and ketones between 0.7-1.4 -->Take 15% of TDD When BG is > 16 and blood ketones between 1.5-3.0 --> take 20% of TDD

Question 213

How is pump TDD calculated from MDI TDD?

Answer 213

1. Calculate current TDD x 0.75 (reduced dose) 2. Then, calculate weight dose: kg x 0.5 (or lb x 0.23) = Weight dose 3. (Reduced dose x weight dose) / 2 = Pump TDD to start

Question 214

How is basal dose determined from pump TDD? What about basal dose?

Answer 214

50% for each

Question 215

How is basal rate determined?

Answer 215

Basal dose / 24 hours

Question 216

How do we test basal rate? Which circumstances are needed?

Answer 216

``` Needs to be done in circumstances when… • BG is between 5.6 and 8.3 (5-10) • Last carb or correction bolus was 4 hours ago • Last meal was low in fat • No hypoglycemia in the last 5 hours • BG/hr (except night BR) ``` Steps: 1. Skip meal (can have water, no caffeine) 2. Monitor BG If BG decreases by ≥ 1.7 (2.0) mmol/L over 4-5 hours: BR is too high 3. Do 3 basal test periods on different days a. Overnight (From bedtime, monitor 2AM, monitor when waking up) b. Breakfast to afternoon (skip breakfast) – monitor q 1-2h c. Afternoon to bedtime (skip lunch) – monitor q 1-2h If basal requires change at a certain moment of the day, decrease or increase 2-3h before the BG was wrong --> will adjust the right moment of the day. Always start with 10% change

Question 217

Name 4 signs that basal rate is too high

Answer 217

- BG is low AC (before) breakfast without bolus during the night - BG goes low if a meal is skipped or if > 5h between meals - BG often low AC meals - Frequent hypos and BR > 55% of TDD

Question 218

Name 4 signs that basal rate is too low

Answer 218

- BG breakfast > Hs BG - BG rises between middle of the night and breakfast (dawn phenomenon) - BG rises when a meal is skipped - Frequent highs and BR total < 45% of TDD

Question 219

How much time does insulin remain in the body in adults?

Answer 219

4-5 hours

Question 220

What is the target BG range for daytime in normal people? Hypo unawareness? Pregnancy?

Answer 220

Daytime: 5.0-6.0 mmol/L Hypoglycemia-unawareness: 6.0-8.0 Pregnancy 4.4-5.0 (tighter)

Question 221

How much time do continuous glucose monitors last on the skin?

Answer 221

between 6 (medtronic) and 14 days (flash freestyle libre)

Question 222

What is the max increase in BG after a meal not to increase bolus?

Answer 222

3 mmol/L

Question 223

What are some questions to ask the patient in cases of hypoglycemia?

Answer 223

- When is the patient exercising? - Alcohol? - How much insulin ingested? Over-correcting? - Enough CHO at meals? - Any changes in life, weight, schedule? - How are you correcting for lows? - Do you feel the lows?

Question 224

What are possible causes of hypers?

Answer 224

``` o Not enough insulin, too much eating o Stress o Illness, medication o Issues with infusion set/insulin o Lifestyle/activities ```

Question 225

WHat is the order of things to correct/look for in patients with pumps?

Answer 225

1. Hypos 2. Basal rates BEAM = < 2.0 mmol difference? Skip meal w/o IOB: BG stable? 3. ICR and ISF

Question 226

How to test ISF? Which circumstances are needed?

Answer 226

* Your BG > 11 mmol/L * It has been at least 3h since you last ate * It has been at least 4h since your last bolus Steps: 1. Administer your correction dose 2. Do not eat for 4 hours unless your BG goes low 3. Test blood sugar every hour for 4h - - If BG ends up 2 mmol/L above your target range after 4h = ISF is too high - - If BG ends up 2 mmol/L below your target range after 4h = ISF is too low Repeat the test on a different day until a correction factor consistently brings your BG within a 2 mmol/L of your target by 5h without going low

Question 227

When can larger correction boluses be given?

Answer 227

extremely high BG, DKA, infection, pre-menstrual periods, or the use of prednisone

Question 228

When can smaller correction boluses be given?

Answer 228

Weight loss, increased activity Be careful in bedtime corrections: consider the use of a larger factor (less insulin) to lessen the risks of night lows If your correction factors vary significantly throughout the day, your basal rates likely need to be changed

Question 229

In which conditions should one test his ICR?

Answer 229

Test your ratio when: • No hypo symptoms in the last 4h • BG between 5-9 mmol/L before a meal • You have not eaten in the last 3h or given yourself a bolus in the last 4h • You are eating a low-fat meal that you can reasonably predict the CHO content for (e.g. frozen meal)

Question 230

What are the steps in testing an ICR?

Answer 230

Steps 1. Eat enough CHO to challenge your ratio (g of CHO should be ≈ ½ your weight in lbs) 2. Test your BG, enter the grams of carbs into your pump and take the carb bolus no more than 20 minutes before eating 3. Test your BG 2hPP and 4hPP - Good ICR if BG rises 2-3 mmol/L 2hPP and is within 1.7 mmol/L your pre-meal BG 4hPP - If your BG rises by more than 2-3 mmol/L 2hPP, use a smaller I:C ratio to give more insulin - If your BG rises by less than 2 mmol/L 2hPP, use a larger I:C ratio to give less insulin

Question 231

What is considered as a good SD for glucose control?

Answer 231

2

Question 232

Name 4 main reasons to override (correct) a pump

Answer 232

1. High CHO intake 2. Low insulin 3. Lack of exercise 4. Stress/sickness/illness

Question 233

What are some risks of hypoglycemia?

Answer 233

* Car accidents * Falling/injuries * Unconsciousness * Hypo unawareness * CVD (both with hyper and hypos!) * Memory loss * Weight gain * Hyperglycemia

Question 234

What is advance bolusing? What are the 2 types of advance bolusing? Explain them. What are they used for?

Answer 234

Mimics both phase 1 and phase 2 of pancreatic insulin release in non-diabetic individuals --> Use when we see a trend of hypos after a meal followed by hypers. 2 types: 1. Dual wave/Combo - A percentage of insulin delivered immediately and the remainder over an extended period of time. - Usually for high fat, high protein meals - May start with 50% up front and 50% over 2h, for example.; test BG every hour after to see how it works, and adjust % up front and duration as needed 2. Square wave/extended - Delivers insulin equally over a set period of time decided by the user - Usually for high fiber meals with low GI - Gastroparesis - Buffet (continuous eating) May also use advance bolusing for very high insulin needs (too much at once may be uncomfortable) If BG doesn’t drop after the meal and doesn’t rise before the next meal, it worked!

Question 235

When should one use temporary basal rates (TBR)?

Answer 235

- Alcohol (70% BR x 4-6h) - Aerobic exercise (Decrease BR 60-90 min before PA, during and extender afterwards) * If exercise is within 60-90 min of a bolus, decrease the bolus - Sickness (Increase BR for 24h; e.g. fever = increase by 25% for 24h) - Food

Question 236

What are the PA recommendations for diabetic people? Compare them to the non-diabetic people's recommendations.

Answer 236

Exercise recommendations are the same vs. non-diabetic people - Adults: 150 minutes/week of moderate- to vigorous- PA (brisk walking or greater) with no more than 2 days off in a row + strength training 2-3x/week - Youth: 60 minutes/day of moderate- to vigorous- PA (420 minutes per week), including vigorous-intensity activities 3+ days/week and strength building activities (for muscles and bone) 3+ days/week

Question 237

What are the benefits of PA in diabetes?

Answer 237

``` Weight management, increased LBM Reduced CV risk factors - Lower BP - Lower unfavorable and higher favorable lipids Improved insulin sensitivity Psychological benefits - Improved sense of well-being - Improved self-esteem ```

Question 238

What are challenges of exercise in diabetes?

Answer 238

- Injury - Impact on overall glycemic management varies (A1C) (exercise improves A1C but effect may be mitigated by attempts to avoid hypos) - Hypos - first reported barrier to PA (immediate or delayed (6-15h after)) - Hyperglycemia (anaerobic exercise) - Retinopathies - Neuropathies (may not feel injuries)

Question 239

Why is someone with diabetes more likely to get an hypoglycemia later in the day after PA?

Answer 239

Increase in absorption of insulin from subcutaneous area Increase in rate of glucose transport into muscles Diminished hepatic glucose production (elevated I:G ratio in portal vein) --> Hypoglycemia --> Blunting of counter-regulatory hormones responses in patients with T1DM = increased risk of hypo later (night time) 1. High glucose requirement during and right after exercise 2. Also, higher glucose requirements 7-11h later (late hypoglycemia risk) a. High requirement of glucose d/t increased insulin sensitivity for glycogen restoration (GLUT4 stays on the cell membranes for hours after exercise b. Impaired counter-regulation c. Relative excessive circulating insulin d. Absence of CHO intake

Question 240

What are 3 solutions to decrease the risk of nocturnal hypos with PA?

Answer 240

Bedtime snack Decrease insulin (Pump – TBR decrease from e.g. midnight to 3AM; MDI: Decrease bolus of last meal) Exercise in the morning

Question 241

What are the 4 likely causes of hypo episodes in PA?

Answer 241

1. Too much insulin 2. Not enough CHO 3. Type of exercise (aerobic) 4. Duration of exercise

Question 242

Why does PA often cause hypoglycemia in diabetic individuals?

Answer 242

Muscle contraction sends glut4 to the side of the cells – do not need insulin to make glucose enter + exogenous insulin also brings GLUT4 to the side After exercise: GLUT4 stays on cells for hours to replenish muscle glycogen

Question 243

Does training increase insulin sensitivity?

Answer 243

Yes, a more fit person is more sensitive. May adapt amounts with time as person gets more fit

Question 244

Why does anaerobic exercise cause hyperglycemia?

Answer 244

Epinephrine and norepinephrine are released: o Increase liver glycogen breakdown --> increase plasma glucose o Decrease muscle glucose uptake BG remains high for ≈ 2 hours

Question 245

Why is sprinting used?

Answer 245

Hypoglycemia prevention using short duration sprinting - Intermittent high intensity exercise (several high intensity exercise bouts lasting 4-5 seconds) to maintain BG while reducing CHO intake - Used to counter the rapid fall in glycemia due to moderate-intensity exercise in individuals with T1DM o Decreases the risk of post-exercise hypoglycemia o Efficacy of sprinting is likely to decrease in over-insulinized individuals - NOTE: Repeated circuits of high intensity exercise, especially when mixed with aerobic exercise, could result in significant reductions in BG

Question 246

What are the warm up recommendations for T1DM?

Answer 246

o If hyperglycemic (≥ 14 mmol/L) and ketotic (≥ 1.5 mmol/L plasma ketones) because of insulin deficiency, don’t exercise until hyperglycemia and ketones are restored with insulin o If mildly hyperglycemic (8-14 mmol/L), do a 10-15 minutes mild aerobic warm-up

Question 247

What are the cool-down recommendations for T1DM?

Answer 247

o Always cool down for ≈ 20 minutes – aerobic, easy intensity o Consider conservative insulin correction if remain hyperglycemic (≥ 12.2 mmol/L)

Question 248

What 2 characteristics of PA have an impact on BG? What should be done in those cases?

Answer 248

Intensity and duration --> mild aerobic exercise: decrease last bolus by 25%, 50% if 60 min --> Moderate aerobic exercise: decrease last bolus by 50% if 30 min, 75% if 60 min. etc Intense aerobic or anaerobic: no reduction

Question 249

If we want to disconnect the pump during exercise, when should we do it?

Answer 249

1h-1.5h before

Question 250

How should basal dose be reduced before PA in MDI? pump?

Answer 250

MDI: do not reduce except if 2x/d or if PA lasts whole day CSII: Basal insulin dose reduction of 60-80% (= 20-40% of dose given) may be useful for exercise over 45 to 60 minutes Dose could be reduced up to 90 minutes before exercise

Question 251

How should basal dose be reduced after PA in MDI? pump?

Answer 251

MDI: Reduce night time dose by 20% Encourage increased CHO consumption to prevent nocturnal hypoglycemia Test BG during the night CSII: Reduce insulin dose by 20% to 3AM Encourage increased CHO consumption Test BG during the night *Consider reducing the bolus insulin dose during the post-exercise meal by 50%

Question 252

Name recommendations for patients to avoid nocturnal hypos after PA

Answer 252

 Set alarms to check BG during the night  Advise household members on signs of severe hypoglycemia, and on appropriate use of glucose gels or glucagon  Avoid alcohol following exercise (the risk of hypos is however minimal if a moderate intake of alcohol is combined with CHO intake)  CGM should be used with the benefits of: o Alarms in cases of hypoglycemia o No alerts if no hypo is detected (don’t have to wake up)

Question 253

What is the optimal BG to undergo PA? What to do if it is below? Above?

Answer 253

Optimal: 7-15 mmol/L --> aerobic, anaerobic, and interval high intensity exercise can be started < 5 mmol/L --> Ingest 10-20g CHO; delay exercise until BG > 5 mmol/L 5-6.9 mmol/L --> ingest 10g CHO; anaerobic and interval high intensity exercise can be started > 15 mmol/L --> Check blood ketones and perform low intensity exercise, or give small corrective dose of insulin Low intensity exercise may be okay if blood ketones are <1.4 mmol/L. consider small corrective dose of insulin. No exercise if >1.5 mmol/L

Question 254

What to do if we want to initiate insulin added to OHA?

Answer 254

1- Start with 10 un/day (= 1 injection at bedtime) 2- Add 1 un per day until target is reached (except Degludec: 2 units every 3-4 days or 4 units per week)

Question 255

What is the prevalence of GDM in Canada? Why is it increasing?

Answer 255

In Canada, between 3-20% | why? Women are having children older + increased rate of obesity worldwide

Question 256

Name GDM risk factors

Answer 256

• Age 35+ • Being in a high-risk group (African, Arab, Asian, Hispanic, Indigenous, South-Asian) • Using corticosteroid medication (betamethasone for pre-term babies to speed up lung development and maturation) o Lungs usually last organ to develop in utero o Some women use corticosteroids for IBD --> GD --> increased risk of pre-term deliveries and still births • Obesity (BMI ≥ 30) • Prediabetes • GDM in a previous pregnancy • Given birth to a baby that weighed more than 4 kg • Parent, brother or sister with T2DM • PCOS or acanthosis nigricans (darkened patches of skin)

Question 257

How does interpregnancy weight affect GDM risk?

Answer 257

- If BMI increases in the interpregnancy period in women with normal BMI or BMI > 27 = higher risk of GD in their second pregnancy - If BMI decreases in the interpregnancy period in women with overweight or obesity = lower risk of developing GD in their second pregnancy

Question 258

What are maternal complications of GDM?

Answer 258

* Pre-eclampsia * Polyhydramnios * HTN * Preterm labour * C-section/difficult delivery due to large baby * Still birth before 40 weeks of gestation

Question 259

What are neonatal complications of GDM?

Answer 259

* Macrosomia weight > 4 kg * LGA > 90th percentile (by US) * Shoulder dystocia/birth injury (dislocation of shoulder) * Early rupture of membranes due to increased amniotic fluid * Neonatal hypoglycemia * Respiratory distress * Hyperbilirubinemia * NICU admission

Question 260

Name maternal postpartum possible outcomes of GDM

Answer 260

* Future diabetes * Future GDM * Metabolic syndrome

Question 261

Name possible risks in the offspring of women with GDM

Answer 261

* ?? Childhood obesity | * ?? T2DM in early childhood

Question 262

Describe IR in a normal pregnancy

Answer 262

 Healthy pregnancy can be associated with insulin resistance which increase with maternal adiposity and cortisol production from the placenta  The development of IR in the second half of the pregnancy serves as a physiological adaptation of the mother to ensure adequate CHO supply to the rapidly growing fetus  Maternal IR leads to more use of fats than CHO for energy by mother and spares CHO for fetus  Changes in glucose and lipid metabolism occur progressively during pregnancy to ensure a continuous supply of nutrients to the growing fetus despite intermittent maternal food intake At the third trimester, insulin sensitivity may gradually decline to 50% of the normal expected value This increase in insulin resistance is mediated by a number of factors including increase in the level of estrogen, progesterone, human placental lactogen (hPL)

Question 263

What is hPL? What are its functions?

Answer 263

Human placental lactogen (hPL), also called human chorionic somatomammotropin (HCS), is a polypeptide placental hormone. hPL is present only during pregnancy, with maternal serum levels rising in relation to the growth of the fetus and placenta. Metabolic: • ↓ maternal insulin sensitivity, leading to an increase in maternal blood glucose levels. • ↓ maternal glucose utilization, which helps ensure adequate fetal nutrition (the mother responds by increasing beta cells --> more insulin). Chronic hypoglycemia leads to a rise in hPL. • ↑ lipolysis with the release of free fatty acids. With fasting and release of hPL, FFAs become available for the mother as fuel, so that relatively more glucose can be utilized by the fetus. Also, ketones formed from free fatty acids can cross the placenta and be used by the fetus. These functions help support fetal nutrition even in the case of maternal malnutrition.

Question 264

Can insulin cross the placenta? Ketones?

Answer 264

Yes to both. Insulin from the mother is passed on to the baby, but the baby will also start making its own insulin.. Ketones can be used by the fetus for energy

Question 265

What is the main functional unit of the placenta?

Answer 265

chorionic villi

Question 266

What happens to the placenta in women with GDM? When does it happen?

Answer 266

• Placentas from GDM mother are frequently larger, and the villi are hypervascularized resulting in a larger feto-placental endothelial surface --> Placenta has its own metabolic processes This happens within the 2nd and 3rd trimesters. During those trimesters, the baby also makes +++ insulin due to hyperglycemia (Glucose from mother enters by GLUT)

Question 267

Why is the 2nd half of pregnancy considered a diabetogenic state?

Answer 267

because the elevated gestational hormones and increased maternal weight place a demand on the body for extra insulin. Maternal metabolism usually compensates for this altered state by secreting extra insulin. Women with GDM, however, decompensate from a euglycemic state to a hyperglycemic state.

Question 268

Why is GDM associated with maternal dyslipidemia?

Answer 268

Gestational diabetes is associated with maternal dyslipidemia d/t increased insulin resistance • High TG, low HDL, high LDL • Excess supply of lipids to placenta --> greater transplacental transport --> lipid storage and/or lipotoxicity • Increased fetal body fat mass --> macrosomia

Question 269

What are the effects of GDM on the placenta?

Answer 269

1. XS insulin stimulates fetal aerobic glucose metabolism --> increases the oxygen demand of the fetus 2. Higher oxygen affinity of A1C, thickening of the placental basement membrane, and reduced utero-placental or fetoplacental blood flow --> inadequate oxygen supply and reduced oxygen delivery to the intervillous space 3. Both of these cause fetal hypoxemia (abnormally low O2 in the blood) 4. --> Placental angiogenesis --> hypercapillarization --> placentomegaly (Type 1 > GDM)

Question 270

What are the effects of the placenta on GDM?

Answer 270

The placenta synthesizes a variety of cytokines (low-grade inflammation) developing during the third trimester of pregnancy --> overproduction of placental leptin and TNF-alpha in T1DM and GDM Overexpression of placenta TNF-alpha --> increased fetal adiposity TNF-alpha, leptin and resistin --> increased pregnancy-induced insulin resistance by adding a placental component to the insulin resistance already developing in the mother Placental leptin expression in patients with GDM is increased. Conversely, leptin itself increases production of TNF-α and interleukin 6 (IL-6) by monocytes and stimulates the production of CC-chemokine ligands. Therefore, a vicious circle develops aggravating the inflammatory situation. Chronic insulin administration increases leptin secretion by adipocytes. Consequently, hyperinsulinemia in GDM might further stimulate leptin production. Resisten is secreted by the adipocytes and is associated with increasing insulin resistance; inflammatory-type protein

Question 271

Explain the effect of maternal hypoglycemia on the fetus

Answer 271

High BG affects the placenta by affecting blood flow and oxygen delivery --> fetus lacks oxygen; lungs have not matured --> can lead to things such as respiratory distress syndrome in the fetus, pre-term labour, XS water, LGA, increased lipogenesis Sustained hyperglycemia and hyperinsulinemia may cause fetal acidemia and hypoxia and a remarkably reduced tolerance to lack of oxygen. RDS: caused by compromised lung maturation, could lead to death of newborn. At 32 wks lungs have developed therefore increasing risk of RDS in preterm delivery and in premies.

Question 272

What 2 measures are indicators of macrosomia?

Answer 272

Fetal abdominal circumference (AC) > 70th percentile | Estimated fetal weight (EFW) > 50 to 60th percentile

Question 273

When does screening for GDM occur in pregnant women?

Answer 273

24-28 weeks | BUT if high risk of GDM based on multiple clinical factors, screening should be offered at any stage in the pregnancy

Question 274

Explain the preferred approach for GDM diagnosis (include the cutoff values)

Answer 274

50g OGTT, 1h later... - < 7.8 mmol/L --> Normal - 7.8-11.0 mmol/L --> do 75g OGTT - ≥ 11.1 mmol/L ---> GDM ``` 75 OGTT - FPG ≥ 5.3 mmol/L - 1hPG ≥ 10.6 mmol/L - 2hPG ≥ 9.0 mmol/L If 1 value is met or exceeded --> GDM ```

Question 275

Describe the main nutrition intervention for women with GDM

Answer 275

- Women should aim for 3 moderate-sized meals and 2 or more snacks (of which one should be at bedtime) - Small frequent meals will help women minimize nausea and ketone formation * GD: Pancreas cannot produce a very large amount of insulin – CHO must be spread out! **Breakfast: 15-20g CHO, preferably no fruit or milk, as BG is particularly high in the morning and some women may be sensitive to both fructose and lactose Certain low-lactose dairy products may be tolerated such as Greek yogurt Support consumption of Greek yogurt during pregnancy, especially if woman has meat aversion **Lunch and dessert: 30-45g CHO, vegetables should make up the majority of the plate - Each meal should contain CHO, PRO and FAT --> will lower GI load

Question 276

Which 2 foods should be avoided in GDM (esp. at breakfast)?

Answer 276

Avoid milk and fruits at breakfast (except avocados) Tropical fruits are sweeter compared to other fruits. Greek yogurt is encouraged

Question 277

What is the macronutrient distribution for women with GDM?

Answer 277

carbs: 40-45%, protein 20-25%, fats: 30-35%

Question 278

What should snacks be composed of in GDM? When should night time snacks be considered?

Answer 278

• Snacks will help women feel full in between meals (avoiding low BG levels) and prevent them from overeating at their next meal (avoiding spikes in BG levels) • Should consist of 15-30g CHO • Snacks should consist of a source of CHO + a source of protein Hs snacks are not necessary for everybody – but if patient shows up with ketones > 2 in urine = recommend snack at night

Question 279

Name 5 important nutrients in pregnancy and why.

Answer 279

• EFAs: involved in brain development of the baby *vegetable oils, 2 low-mercury fish servings a week, and supplements (fish oil or algae-based docosahexaenoic acid). • Iron: d/t increased blood volume in 3rd trimester • Folic acid: prevents NTDs • Vitamin D: bone formation of baby • Calcium: bone formation of baby

Question 280

What nutrient do common prenatal MVs lack?

Answer 280

do not contain enough Mg, Ca and VA (do not meet needs) Especially calcium: Evaluate calcium intake in diet and see if the patient would benefit from another calcium supplement Same for vitamin A, do not worry too much about magnesium (vegetables)

Question 281

How much energy do pregnant women with GDM need?

Answer 281

1. Use ROT like non-pregnant adult women a. BMI < 20: 35 kcal/kg b. BMI 20-25: 30 kcal/kg c. BMI > 25: 25 kcal/kg 2. If BMI > 30, use adjusted BW: a. Adjusted BW: Actual pregavid BW – IBW using max BMI x 0.25 + IBW 3. Then add the estimated requirement for pregnant women per trimester

Question 282

Why are hypocaloric diets not recommended in GDM?

Answer 282

Hypocaloric diets have been used for the obese woman with GDM. Risk of high levels of ketones and risk of sacrificing maternal nutritional status are higher in women who consume hypocaloric diets. Women placed on this diet should have the benefit of team management. Monitor ketones closely

Question 283

What are the cutoffs for each trimester? How much extra energy is needed during those trimesters?

Answer 283

 First trimester (0-13 weeks): No extra  2nd trimester (14-26 weeks): Add 340 kcal  3rd trimester (27 to 40 weeks): add 452 kcal  Breastfeeding post-partum: add 452 kcal

Question 284

What are the DRIs for CHO, protein and fiber in pregnant women with and without GDM?

Answer 284

* Minimum 175 g CHO * Minimum of 71g protein (1.1 g/kg/d) * Minimum of 28 g fiber

Question 285

What are the weight gain recommendations during pregnancy?

Answer 285

Underweight: - Total <28-40 - 1 lb/week during the 2nd and 3rd trimester Normal weight - Total 25-35 - 1 lb/week during the 2nd and 3rd trimester Overweight - Total 15-25 - 0.6 lb/week during the 2nd and 3rd trimester Obese - Total 11-20 - 0.5 lb/week during the 2nd and 3rd trimester

Question 286

How often should BG be monitored in women with GDM?

Answer 286

QID - AC and PC breakfast - 1hPC lunch - 1h PC supper

Question 287

Which antihyperglycemic agents should be used in pregnancy?

Answer 287

Insulin (sometimes metformin)

Question 288

What are the target BG levels in GDM?

Answer 288

* Fasting < 5.3 mmol/L (JGH between 4.2-5.2 mmol/L) * 1h after a meal < 7.8 mmol/L (JGH between 5.5-7.7) * 2h after a meal < 6.7 mmol/L

Question 289

What is the effect of PA on GDM?

Answer 289

Regular exercise and a healthy diet helps: • Improve glycemic control • Facilitate weight control • Improve insulin sensitivity The risk of GDM is inversely proportional to the degree of physical activity in the year prior to pregnancy Exercise before and during early pregnancy is associated with 51% and 48% reductions in GDM risk, respectively. Exercise started before and continued throughout pregnancy may lead to GDM risk reductions of 69%.

Question 290

What is the PA goal for women with GDM?

Answer 290

Goal: 30 minutes or more per day, can be both aerobic and non-weight-bearing exercises (yoga, stretching…) Lifestyle therapy for GDM results in lower birth weight and a lower incidence of large-for-gestational-age births and pre-eclampsia  In total, it is recommended that most pregnant women do 150 minutes/week (approximately 3-5 sessions of 30-45 minutes each)  It is important for those who were not active prior to being pregnant to start very gradually  Examples of some activities (should be done at light-moderate intensity) o Swimming, walking, cycling, jogging

Question 291

What are the benefits of breastfeeding in women with GDM?

Answer 291

Breastfeeding for a minimum of 4 months to prevent hypoglycemia in newborn, obesity in childhood, and diabetes for both mother in child  Baby is feeding on demand: small frequent meals. Breast milk is not as sweet as formula (lower GI). Insulin is produced by the baby in utero  baby still has a lot during labour and after birth. With breast milk, we want to try to normalize the baby’s insulin production Breast feeding not only helps the mother lose the weight gained during pregnancy, it also reduces blood pressure and helps control blood glucose (sugar) levels and thus prevent type 2 diabetes

Question 292

When should women with GDM be screened for T2DM?

Answer 292

* Within 6 weeks to 6 months of giving birth * Before planning another pregnancy * Every 3 years (or more depending on risk factors)