Diabetes & eating disorders Flashcards
Discuss the flow of glucagon and insulin post-prandially in T2DM.
Glucagon stays high during meals, as it is not inhibited by the insulin release as in healthy subjects
Insulin release is delayed and reduced.
What are the anabolic actions of insulin in glucose metabolism?
o Glucose transport into muscle and adipose tissues (GLUT4)
o Glycolysis –> energy
o Glycogenesis
What are the anabolic actions of insulin in lipid metabolism?
o Lipogenesis (TG in adipose tissues and synthesis of FFAs in liver) o Lipoprotein lipase activity (LPL; adipose tissue)
What are the anabolic actions of insulin in protein and electrolyte metabolism?
o Transport of amino acids
o Protein synthesis
o Potassium enters into the cell
What are the actions of insulin in glucose metabolism that decrease catabolism?
o Decreased gluconeogenesis (liver)
o Decreased glycogenesis (liver and muscle)
What are the actions of insulin in lipid metabolism that decrease catabolism?
Decreased... o Lipolysis o LPL (muscle) o Ketogenesis o Fatty acid oxidation (liver)
What are the actions of insulin in protein metabolism that decrease catabolism?
Decreased Protein catabolism
Explain how glucose stimulates insulin release in healthy people.
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)
Discuss the 2 phases of insulin secretion and how it relates to diabetes
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)
What are 2 incretins and where are they produced?
- 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
Diabetes is the cause of __% of strokes
30%
Diabetes is the cause of __% of heart attacks
40%
Diabetes is the cause of __% of kidney failure requiring dialysis
50%
Diabetes is the cause of __% of non-traumatic leg and foot amputations
70%
Diabetes is the cause of __% of blindness
Leading cause
What is LADA?
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)
What is MODY?
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
Explain the onset of T1DM in a person.
- Genetic predisposition (100% of B cells present and functional)
- Silent insulin/B cell destruction (% B cells goes down. This process can take years) – Autoimmune
- 30% of B cell function = alterations in glucose tolerance
- 15% of B cells – diagnostic –> clinical diabetes
Who has the highest chance of developing T1DM:
Offspring of affected mother?
Offspring of affected father?
Offspring of affected mother: 1 in 50
Offspring of affected father: 1 in 14
Incidence of type 1 diabetes increases with time, while type 2 has stabilized. Why?
- Genetics? HLA, DR3, DR4
- Infection? Coxsackie virus
- Alimentation (Cow’s milk?)
Seasonal variations in T1DM: vitamin D?
What proportion of people with T1DM get diagnosed during adulthood?
42% (almost half) of people with type 1 diabetes were diagnosed between age 31 and 60. People often assume they have type 2 diabetes.
What proportion of B-cell loss is needed for pre-diabetes? For diabetes diagnosis?
Loss of 50% of B cell mass/function = pre-diabetes
Loss of 80% of B cell mass/function = type 2 diabetes diagnosis
Name 6 possibilities for insulin resistance in non-diabetic people
- 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
What are the 4 values for diabetes diagnosis and when are they used for diagnosis?
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
What are the 3 values for pre-diabetes diagnosis?
Postprandial glycemia (or post load) ≥ 7.8 mmol/L = IGT
FPG ≥ 5.6 mmol/L = IFG
A1C 6.0-6.5% = Prediabetes
What is the recommended macronutrient distribution in diabetes? Fiber? Trans fat? SFA?
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
What can a weight loss of 5-10% accomplish in people with diabetes and BMI≥25?
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
What should people with diabetes replace SFA with?
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
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?
- 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)
- 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
Name advantages of the mediterranean diet
Decreased A1C
Decreased CVD
Decreased retinopathy, BP, CP
Increased HDL
Name advantages and disadvantages of a low-GI diet
Advantages:
Decreased A1C
Decreased CVD
Decreased LDL, CRP, hypoglycemia, diabetes medication
Disadvantage: None
Name advantages and disadvantages of a high-fiber diet
Advantages:
Decreased A1C (viscous fiber)
Decreased CVD
Decreased LDL, non-HDL-C, ApoB
Disadvantage: GI side effects
Name advantages and disadvantages of a vegetarian diet
Advantages: Decreased A1C Decreased CHD Decreased weight Decreased LDL
Disadvantage: Low B12
Name advantages and disadvantages of the DASH diet
Advantages:
Decreased A1C
Decreased CHD
Decreased weight, BP, LDL, CRP
Disadvantage: None
Name advantages and disadvantages of the Portfolio diet
Advantages:
Decreased CVD
Decreased LDL, CRP, BP
Disadvantage: None
Name advantages and disadvantages a diet high in dietary pulses/legumes
Advantages:
Decreased A1C
Decreased CVD
Decreased weight, LDL, BP
Disadvantage: GI side effects
Name advantages and disadvantages of a diet high in nuts
Advantages:
Decreased A1C
Decreased CVD
Decreased LDL, TG, FPG
Disadvantage: Nut allergies
Name advantages and disadvantages of a diet high in F&V
Advantages:
Decreased A1C
Decreased CVD
Decreased BP
No disadvantages
How many CHO servings should be provided for meals in DB? For snacks?
Typically, choose 3-5 CHO servings per meal; and 1-2 servings for snacks
What should we substract from the total CHO content of a food for CHO counting?
- Adjust for dietary fiber intake
* Foods that contain polyols (sugar alcohols (substract half of them))
What are polyols? Give examples?
What are the side effects of polyols?
Sugar alcohols
o Erythritol, glycerol (glycerin/glycerine), isomalt, lactitol, maltitol, mannitol, sorbitol, xylitol
o If intake > 10g/d = side effects: bloating, diarrhea…
Nutrition therapy can reduce A1C by how much?
1-2%
LCS use is associated with what?
Higher BMI
Higher T2DM incidence
What are the 4 proposed mechanism for the link between LCS and T2DM?
- 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
Name 4 benefits of LCS
- 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
Name 6 health concerns/disadvantages of LCS.
- 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
In which patients should snacks be planned?
- 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…)
What are health risk behaviours? Give 4 examples
unhealthy behaviours you can change
- Lack of exercise or physical inactivity
- Poor nutrition
- Tobacco use
- Excessive drinking
Define health behaviour. Give 3 examples
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)
What is self-management?
“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”
What factors influence adhering to healthier eating patterns in persons living with chronic diseases? (Individual/internal factors)
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)
Is knowledge a predictor of health behaviour change?
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
Why do people with diabetes have emotional distress?
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%)
Why is treatment of depression useful in people with chronic diseases?
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…)
What is the single question to ask for screening for depression?
Are you depressed most of the time?
Name 3 external factors influencing health behaviour change/self-management
- Access to services and information
- Provider attitude, beliefs, knowledge, skills, level of integration in HC system
- Overall social norms (e.g. cannabis)
Define self-efficacy
Definition: One’s confidence in being able to successfully perform an action to produce the desired outcomes (i.e. healthy eating –> improved health)
According to Bandura, what are the 3 cognitive mediating processes that determine behaviour? Explain them.
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
Degree of self-efficacy for a given health behaviour is complex and involves 3 interrelated domains. What are they?
- Having tacit task knowledge and related skills
- 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
- Having confidence in one’s ability to successfully execute a behaviour in a given context
What are the 4 main strategies to boost self-efficacy?
- Performance accomplishment
- Vicarious experience/modeline
- Reinterpreting symptoms
- Persuasion
How can we increase a patient’s performance accomplishment?
Break task into small tasks; set realistic goals, provide feedback so they can improve their skills
How can we increase a patient’s vicarious experience/modeling?
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
How can we increase a patient’s reinterpretation of symptoms?
Educate regarding beliefs about health behaviours and specific symptoms; evidence-based options to reduce stress
Teach patients to distinguish between types of pain
How can we do verbal persuasion in a patient?
Start by giving verbal support and encouragement for small steps in behavior change; last resort emphasize the consequences of not changing the behaviour
Can stress management increase self-efficacy?
Yes
Name 2 alternatives to HbA1C measurements and how often they should be measured
Glycosylated serum albumin (GSA) or glycosylated total serum proteins (GSP)
Measured q 3-4 weeks (reflects BG over shorter periods)
What is the preprandial BG goal to maintain A1C ≤ 7.0%?
5-10 mmol/L
5-8 mmol/L if unable to maintain A1C ≤ 7.0%
What is the 2h post BG goal to maintain A1C ≤ 7.0%?
4-7 mmol/L
4-5.5 mmol/L if unable to maintain A1C ≤ 7.0%
Name things that can decrease A1C
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
How does erythrocyte pH affect A1C?
Increased erythrocyte pH –> increased A1C
Decreased erythrocyte pH –> Decreased A1C
Describe the glycemic targets for children and adolescents < 18
< 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
What are the initial choices of therapy in patients have…
- A1C < 1.5% over target?
- ≥ 1.5% over target?
- Symptomatic hyperglycemia and/or metabolic decompensation?
- For all of those if not at target within 3-6 months?
- Healthy behaviour interventions and start metformin if not at target in 3 months OR start metformin with healthy behaviour interventions
- Start metformin with healthy behaviour interventions AND Consider second concurrent agent
- Initiate insulin +/- metformin
- Add pharmacotherapy based on presence of clinical CVD
What are the 3 best OHA for CVD?
Empagliflozin (SGLT2i)
Liraglutide (GLP1 RA)
Canagliflozin (SGLT2i)
What are the 3 best categories of OHA for patients with with high risk of hypoglycemia?
DPP-4 i
GLP1 RA
SGLT2 i
Name 3 risks of metformin/biguanides
o GI side effects (nausea, cramping)
o Lactic acidosis: rarely occurs if contraindications are taken into account
o B12 deficiency (long-term)
Name 2 benefits of insulin secretagogues
o 0.7-0.8% reduction in A1C
o Decreases microvascular risks
Name 4 risks of insulin secretagogues
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
Name 4 benefits of alpha-glucosidase inhibitors
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
Name 4 risks of alpha-glucosidase inhibitors
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)
Name 3 benefits of TZDs
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
Name 7 risks of TZDs
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
Name 5 benefits of DPP4i
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
Name 3 risks of DPP4i
o Rare cases of pancreatitis
o Long-term safety
o Cardiac insufficiency in Saxagliptin
Physiological level of GLP-1: DPP4i or GLP1 RA?
DPP4i
GLP-1 receptor agonists = pharmacological levels of GLP-1
Name 5 effects of GLP-1 RA that do not apply to DPP-4i
- Decrease gastric emptying
- Increase satiety
- Decrease energy intake
- Increase nausea
- Decreases weight
(same as DPP4i: Increased insulin secretion, decreased glucagon secretion)
Name 6 benefits of GLP1-RA
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
Name 8 risks of GLP1-RA
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 \$\$\$\$
Name 5 benefits of SGLT2 i
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
Name 5 risks of SGLT2 i
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
When should SGLT2i be stopped prior to a major surgical procedure?
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
Which 2 OHAs decrease BP?
SGLT2 i
GLP1 RA
Name 4 rapid-acting insulins. When should they be taken compared to meals?
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
When should short acting insulins be injected?
Around 30 min before meals
Name 5 long-acting insulins
Detemir (Levemir) Glargine U100 (Lantus) Glargine U300 (Toujeo) Glargine biosimilar (Basaglar) Degludec (Tresiba)
Name 6 neurogenic symptoms of hypoglycemia
Trembling Palpitations Sweating Anxiety Hunger Nausea
Name 7 neuroglycopenic symptoms of hypoglycemia
Difficulty concentrating Confusion Weakness Drowsiness Vision changes Difficulty speaking Dizziness
Differentiate mild from moderate from severe hypoglycemia
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
Name risk factors for severe hypoglycemia in people treated with sulfonylureas or insulin
- 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
What are the 5 steps to address hypoglycemia?
- Recognize autonomic or neuroglycopenic symptoms
- Confirm if possible (BG < 4.0 mmol/L)
- Treat with “fast sugar” 15g to relieve symptoms
- Retest 15 minutes later to ensure BG > 4 mmol/L and retreat
- 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
Who is at risk for DKA?
- 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)
What can cause false positives in urine ketones? False negatives?
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
When should diabetics test for ketones?
Acute illness accompanied with elevated BG
Stress
Consistently elevated BG levels (> 14 mmol/L)
Symptoms of ketoacidosis (e.g. nausea, vomiting, abdominal pain)
Pregnancy
Name 6 precipitating factors of DKA
• 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
How much of a decrease in A1C is necessary to decrease the risk of complications in T2DM?
1%
How does diabetes lead to retinopathy?
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
When do we initiate screening for retinopathy?
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
Which 3 factors accelerate neuropathy?
Smoking
Lack of PA
Alcohol (> 4 drinks/d)
What are the different types of neuropathy?
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
What is the earliest clinical evidence of nephropathy?
Persistent microalbuminuria
What is the mechanism of hyperlipidemia in type 1 diabetes? In type 2?
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
Who should receive statins?
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
Name 2 possible explanations for why Co-Morbid depression worsens clinical outcomes in T2DM
- Lower levels of physical fitness
* Reduces adherence to medications
How is A1C a predictor of mental health outcomes?
A1C is a predictor of mental health outcomes. Each 1% elevation in A1C increases the risk of MCI and dementia
Which diabetic medications are the best to prevent NASH?
All OHA are good for NASH
Name 2 medications approved for the treatment of obesity in T2DM
GI lipase inhibitor
Side effects: Loose stools, GI upset, rare liver failure
Oral medication that decreases fat absorption, may require vitamin supplementation
$$$
GLP-1 receptor agonist
Side effects: Nausea, GI upset, rare gallstones and pancreatitis
Subcutaneous injectable, increases satiety
$$$$
Name 3 embryopathic medications
o ACEi / ARB
o Statin therapy
