Quiz 3: Weeks 6-8 14% Flashcards

1
Q

What is type II diabetes?

A

it’s a problem where the hormone insulin (secreted by the pancreas) does not work properly.

The pancreas is an organ sitting behind the stomach and it secretes many things for digestion and produces and secretes hormones, which are important metabolism.

Insulin is produced by the pancreas in response to high blood glucose,
for example, after you eat, glucose enters your blood, stimulates the pancreas and produces insulin.

Since there is high blood glucose, the pancreas is told to secrete more insulin
= persistent high blood glucose

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2
Q

How does insulin work normally?

A

On the liver, adipose tissue (fat), and muscles there are receptors for insulin.

High blood glucose stimulates insulin production and insulin release from the pancreas. Insulin starts different organs by binding onto their insulin receptors/insulin sensitive proteins, which decreases blood glucose levels.

This happens because the binding of insulin to the receptor/protein triggers a cascade of events within a cell = increased uptake of glucose from circulation, by producing more glucose channels/transporters on the surface of cells
= glucose moves from the blood to the cells of the organs.

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3
Q

What are the other roles of insulin?

A
  • Insulin promotes glucose storage. In the liver, insulin stimulates glycolysis and glycogenesis to store glucose as glycogen.
  • Insulin stimulates glucose to be stored as fat, which is transported to adipose tissue
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4
Q

What happens to insulin in T2DM?

A

Insulin resistance, the receptors that insulin usually binds to don’t work properly, therefore insulin doesn’t work properly on the liver, adipose tissue, and skeletal muscle.

This causes high blood glucose levels to remain for long periods of time.

Insulin resistance causes glucose to not be taken up by all the different organs
= high blood glucose

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5
Q

What are the different factors that cause insulin resistance?

A
  • genetics
  • family predisposition
  • bad eating habits
  • obesity
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6
Q

What is glucose urea?

A

Glucose travels to the kidneys to be secreted out. This results in osmotic diuresis (glucose drags water with it because it is a solute = frequent urination (polyuria))

Constant polyuria can lead to loss of water and loss of electrolytes

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7
Q

What 2 things can happen when there is a loss of water and electrolytes due to osmotic diuresis?

A
  1. Dehydration, from loss of water. Stimulates the brain to drink more water
    = polydipsia (excessive thirst)
  2. Hyperosmolar state, a medical emergency
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8
Q

What is polyphagia?

A

the feeling of hunger, an urge to eat more

If there is high blood glucose, and it doesn’t go into the tissues that need it, the organs will signal the body that it needs food

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9
Q

What happens with prolonged insulin resistance?

A

The beta cells produced by the pancreas will decrease in size because the body isn’t responding to insulin properly.

Individuals may eventually need to be on insulin injections to compensate

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10
Q

What are the 2 acute complications of T2DM?

A
  1. Diabetic ketoacidosis (DKA)
  2. Hyperosmolar hyperglycemic non-ketotic state (HHNS)
    mortality rate of 8-20%
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11
Q

What is Hyperosmolar hyperglycemic non-ketotic state (HHNS)?

A

a dangerous condition resulting from very high blood glucose levels can affect both T1DM and T2DM but is more common in T2DM

HHNA is caused by diabetes (deficiency of insulin, the body can’t adequately respond to the insulin being produced by the pancreas)

Someone with HHNS has already been diagnosed with diabetes, and they will likely have hyperglycemia (one of the defining characteristics of diabetes mellitus).

Hyperglycemia drives the events that occur in HHNS

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12
Q

Symptoms of HHNS?

A
  • fatigue
  • weight loss
  • extreme thirst
  • frequent urination
  • signs of dehydration
  • high heart rate (tachycardia)
  • low blood pressure (hypotension)
  • mucus membranes in the mouth can be dry
  • decreased skin turgor (skin sticks up when pinched)
    in severe cases,
  • confusion
  • altered mental status

Because of diabetes, glucose builds up in the blood, which results in hyperglycemia (high blood sugar). Since glucose can’t be used for energy, it can’t be taken up, this causes fatigue/decreased energy and weight loss with someone who has HNNS

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13
Q

Glucose is an osmotically active solute, what does this mean?

A

this means whenever it goes into the body, water likes to follow. Water is pulled out of the cells to keep the concentration of glucose in the blood at a relatively constant level.

As blood moves to the kidneys where it’s filtered, under normal situations, the kidneys filter out very little glucose and reabsorb almost all the glucose that’s in the blood.

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14
Q

When hyperglycemia becomes severe, what happens to the kidneys?

A

The kidneys are not able to reabsorb all the glucose and it spills out into the urine.

Glucose is still osmotically active, therefore water follows the glucose out of the blood and into the urine. The body starts to lose a lot of water and fluid very quickly, the concentration of the solutes in the blood (sodium, potassium, glucose) increases = hyperosmolarity (high concentration of osmotically active solutes)

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15
Q

What is osmotic diuresis?

A

increased urination due to the presence of certain substances in the fluid filtered by the kidneys.

it’s the reason for the intense thirst and frequent urination, severe dehydration and altered mental state in HHNS

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16
Q

What are the similarities between DKA and HNNA?

A
  • In both DKA and HHNA, the body is in a state of starvation. Even though there is plenty of energy present in the blood in the form of glucose, the body is starving for energy because it can’t utilize this energy.
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17
Q

What is ketogenesis?

A

The body’s metabolism responds as though it is starving
= ketogenesis, a process where ketones/ketone bodies/ketoacids are produced. The ketones are produced from acetyl CoA (a by-product of fat metabolism).

The production of ketones results in metabolic acidosis (a serious electrolyte disorder by an imbalance in the body’s acid-base balance)

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18
Q

What is the difference between diabetic ketoacidosis and hyperosmolar hyperglycemic non-ketotic state?

A

People with HHNS most commonly have T2B, which means they are still able to produce insulin. The pancreas is still producing insulin, it’s just the cells throughout the body can’t adequately respond to it.

The insulin that is present acts to inhibit the ketogenesis pathway. Therefore, since insulin is present in HHNS, the creation of ketone bodies is minimized = non-ketotic state.

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19
Q

How can HHNS be treated?

A

Should be treated in the intensive care unit because of how severe HHNS is.

Two major treatments:
1. administration of IV (intravenous insulin)
this helps decrease insulin deficiency and drives glucose out of the bloodstream and into the cells through the body. Decreases hyperglycemia, which decreases osmotic diuresis and fluid loss. All this also decreases the hyperosmolarity of the blood
2. aggressive rehydration with intravenous fluids (normal saline). This replenishes the fluid loss caused by osmotic diuresis. Also decreases osmolality. Rehydration helps alleviate the signs of dehydration (tachycardia, hypertension, altered mental status)

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20
Q

What is Hemoglobin A1C & an A1C Test?

A

It’s a form of hemoglobin that is chemically linked to sugar.

An A1C test is a simple blood test that measures your average blood sugar levels over the past 3 months. It’s the main test to help manage diabetes.

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21
Q

What are the A1C targets?

A

Adults with T2DM to reduce the risk of CKD and retinopathy if at low risk of hypoglycemia should be at <6.5%

Most adults with T1DM or T2DM should be at an A1C level of <7.0%

  1. 1-8% functionally dependent
  2. 1-8.5% recurrent severe hypoglycemia and/or hypoglycemia unawareness
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22
Q

What are some acute symptoms of T2DM?

A
  • unusual thirst
  • frequent urination
    when the person can’t utilize blood glucose that’s circulating in the blood from the food ingested, there’s excess glucose in the blood. The body usually converts glucose into fatty acids and then stores it.

Ppl with T2DM are insulin resistant, therefore glucose can’t be uptaken by the cells as it normally does. This causes glucose to be excreted in the urine. Glucose is an osmolar solute, which means water follows it, therefore there is a large excretion of fluids, which makes the person thirty and frequently urinate

  • weight change (gain or loss)
  • extreme fatigue or lack of energy (loss of fluid and electrolytes)
  • blurred vision (the vessels within the retina and behind the eye. When you have high glucose levels for a long period the blood thickens and the arterial walls narrow = reduced blood flow. Hyperglycemia)
  • frequent infections, cuts, bruises that are slow to heal
  • tingling and numbness in hands and feet (reduced blood flow)

Once the patient starts treatment such as meds, diet to manage their blood glucose the acute symptoms start to go away

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23
Q

What are the silent symptoms of T2DM?

A
  • elevated A1C (above 8%), high triglyceride
  • could have complications later on, or other comorbidities that put them at a higher risk for diabetes (high cholesterol, hypertension, dyslipidemia (elevated LDL)
  • started on 1-2 meds (Metformin: helps control high blood sugar) on insulin for a short period if their hyperglycemia is very bad
  • lifestyle changes
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24
Q

What happens to someone with stage 4 kidney disease and diabetes?

A

When you have stage 4 kidney disease, the cells within the kidneys are damaged. If you have stage 1 or 2 kidney disease, the functioning kidney cells still do a good job at accommodating the cells that are damaged.

Stage 4 kidney disease causes a decrease in urination because the kidney isn’t functioning properly. It’s not able to filter out the blood. This can cause retinopathy since you’re not able to excrete that excess glucose through the urine.

A specialized diet for kidney disease is needed and the diet becomes limited if someone also has diabetes. Need to control carbs very strictly. More about survival, so difficult to stay within the client’s preferences

In stage 4 kidney disease the patient may or may not be on dialysis (filtering of the blood, helps to correct disturbances in the blood mechanically)

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25
Q

What is a diabetes education center?

A

focused on medical and nutritional care for the patient. Multidisciplinary team (endocrinologists (specialize in diabetes and hormones issues), nurses, dietetics) can run group or individual sessions.

Diabetes can also be managed at the family physician level, but individuals should consider going to a diabetes education center for more comprehensive care

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26
Q

What are some common medications/hypoglycemic agents? **redo this when rewatching lecture video

A
  • Metformin (Glucophage): works at a cellular level help with the uptake of glucose
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27
Q

What’s involved in nutrition therapy?

A
  • Individualized goal setting: blood glucose levels are different for everyone, cultural foods, eating habits
  • Healthy dietary patterns: MediterraneanDASH diet, Canada’s Food Guide, the main tool we use to maintain blood glucose levels
  • Nutrient targets
  • Menu planning
  • Basic carbohydrate counting: we try to focus on healthy dietary patterns first, for someone who’s motivated
  • Glycemic index: for someone who’s motivated and can retain the info to make changes to their diets based on carbs. A more complicated topic for patients.
  • Self-monitoring of blood glucose (SMBG)
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28
Q

What is Beyond the Basics?

A
  • A tool used for meal planning for healthy eating and diabetes management. A good RD will adapt this tool to meet the needs of the patient
  • help manage blood glucose and maintain a healthy weight
  • helps choose the right food and portions
  • 1 serving - 15g or 1 carb choice
  • gives Canadian food choices, has a lot of empty boxes to fill in for patient preferences
  • if you have a patient that is Southeast Asian, include food sources for that specific person, or Mediterranean diet then choose food sources that follow the Mediterranean diet

thechildren.com/sites/default/files/cda_poster_eng.pdf

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29
Q

What are some dietary management goals?

A
  • manage blood glucose
  • manage weight
  • manage blood pressure and cholesterol to reduce the risk of any other comorbidities such as hypertension, dyslipidemia (elevated total or low-density lipoprotein LDL)
  • reduce risk of diabetes complications like stroke or heart attack. Patients with hyperglycemia, or even diabetes (uncontrolled diabetes is worse), and also have high blood pressure and cholesterol are at a higher risk for stroke and heart attack. Might be due to small vessel disease that develops as a result of these comorbidities/comorbid states.

Small vessel disease: plaque builds up in small vessels within the body or striction due to plaque and damaged vessels. Not something that can really be detected, too hard to look at the small vessels within the body

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30
Q

What are the ABCDES of Diabetes Care?

A

a reminder of the importance of tracking your blood sugar numbers along with your blood pressure and cholesterol. High blood pressure and cholesterol are well-known risk factors for heart disease and stroke. Knowing your numbers, lifestyle changes are recommended to manage diabetes and sometimes meds.

A: A1X or HbA1C. a test that measures blood glucose control over the past two to three months. The A1C target for most people is under 7%

B: Blood pressure. Nearly 2 out of 3 people with diabetes have high blood pressure. For most people with high blood pressure and diabetes, blood pressure levels should be <120/80 mm Hg. Diets can help such as the Mediterranean diet, higher potassium, lower sodium type diets

C: Cholesterol. Total cholesterol, LDL, and triglycerides should be monitored. LDL-C should be <2.0 mmol/L or >50% reduction from baseline

D: Drugs. For CVD risk reduction

E: Exercise and healthy eating

S: Stop smoking. Smoking doubles the risk of heart disease in people with diabetes

S: Screening for complications.

S: Self-management. Stress and other barriers. Teach individuals how to manage their blood glucose levels

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31
Q

What is the glycemic index?

A
  • looking at the carbs of food, macronutrient, and how it increases blood glucose levels
  • more complex for the general T2DM patients
  • there is a green light system to rank carb foods based on how much they increase blood glucose levels

Green (go): low GI (55 or less) choose most often
ex. grain bread, whole grain, steel-cut oats, quinoa, peas
Yellow (caution): medium GI (56 to 69) choose less often
ex. chapati white bread, rye bread, quick oats, brown rice
Red (stop): high GI (70+) choose least often
ex. white bread, cereals such as special K, white rice, soda crackers

It’s important to educate patients on how these foods might affect their blood glucose levels daily. Once they understand how foods affect them, they’re more inclined to make better choices

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32
Q

What are the recommendations for macronutrient distribution?

A
  • carbs: 45-60%, 4 cals per g, 225-300 cals
  • protein: 15-20%, 4 cals per g, 75-100 cals
  • fat: 20-35%, 9 cals per g, 44-78 cals
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33
Q

How to choose “healthy” fats?

A
  • avoid trans fats
  • recommendation to reduce saturated fatty acids to <9% of energy intake
  • replace with polyunsaturated fatty acids (PUFAs) such as nuts, canola oil, soybean oil, flaxseed
  • eat monounsaturated fatty acids (MUFAs) from plant sources such as extra virgin olive oil, high oleic oils, avocados
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33
Q

How to choose “healthy” fats?

A
  • avoid trans fats
  • recommendation to reduce saturated fatty acids to <9% of energy intake
  • replace with polyunsaturated fatty acids (PUFAs) such as nuts, canola oil, soybean oil, flaxseed
  • eat monounsaturated fatty acids (MUFAs) from plant sources such as extra virgin olive oil, high oleic oils, avocados
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34
Q

How to choose “healthy” carbs?

A
  • soluble dietary fibre helps with managing the health of arteries and excreting LDL cholest from circulation, helps with plaque build-up. Helps manage comorbidities
  • 30-50g of dietary fibre per day
  • 10-20g per day from viscous soluble fibre such as steel-cut oats, barley soups, eggplant
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35
Q

How to calculate Estimated Energy Requirement (EER)?

A

EER male = 622 - (9.53 x age) + PA x (15.91 x kg) + (539.6 ht (m))

Need:
Age, physical activity level, weight, height

https://www.omnicalculator.com/health/eer-estimated-energy-requirement

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36
Q

How to calculate carb choices?

A

First, you need the patient’s EER
ex. 2200 kcal/day

Step 1. Use the EER and multiply by daily percent carb intake (ex. 45-50%)

2200 x 0.5 = 1210 kcal from carbs

Step 2. Take the number from step 1 and divide it by 4.
4 = 4kcal per 1g of carbs

1210/4 = 302g carb/day

Step 3: Determine the number of carb choices

302/15 = 20 carb choices/day

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37
Q

What are some questions you can ask a T2DM patient about their eating patterns?

A
  • why are they skipping meals (if they skip), are they busy? Need quick and healthy recipes
  • times he usually eats
  • do they pack lunches from home
  • how well do they sleep
  • portion sizes
  • types of bread, rice, fish (glycemic index)
  • cooking methods for chicken and broccoli?
  • who does the most cooking at home?
  • fluids?
  • likes and dislikes
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38
Q

How to write a PES statement?

A

P: The problem: The nutrition diagnosis
E: The etiology: the cause(s) of the nutrition problem (nutrition diagnosis)
S: The signs and symptoms: the evidence that the nutrition problem (nutrition diagnosis) exists

Ex. Nutrition diagnosis term (nutrition Problem) related to (RT) the Etiology (the cause(s) of the problem or nutrition diagnosis as evidenced by (AEB) the Signs and symptoms.

Diabetes PES Statement Example:

Excessive carbohydrate intake RT limited diet compliance and diagnosis of Type 2 Diabetes, AEB reported intake of 80% calories from carbohydrates, HbA1C 8.2%, and blood sugar 240.

Inadequate blood glucose management RT family history, diet, and sedentary lifestyle as evidenced by A1C 7.5% and FGB 8.9 mmol/L

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39
Q

What is diabetic ketoacidosis?

A
  • a medical emergency
  • especially in T1DM, but can also occur in T2DM
  • there’s an increase in the acidity in the blood
  • it’s a serious complication of diabetes that occurs when your body produced high levels of blood acids called ketones
  • it develops when your body can’t produce enough insulin
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40
Q

What are the signs and symptoms of Diabetic Ketoacidosis?

A
  • nausea
  • vomiting
  • polyuria (excessive urination)
  • polydipsia (excessive thirst)
  • weight loss
  • hyperventilation (Kussmaul breathing, a type of hyperventilation that is the lung’s emergency response to acidosis) Acidosis is a condition in which there is too much acid in the body fluids
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41
Q

What are the 5 Is of triggers that cause Diabetic Ketoacidosis?

A
  1. Infection
  2. Intoxication
  3. Inappropriate withdrawal of insulin
  4. Infarction (tissue death or necrosis due to inadequate blood supply to the affected area)
  5. Intercurrent illness (a disease that intervenes during the course of another disease)
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42
Q

What happens to the pancreas in T1DM?

A
  • the pancreas normally produces insulin, in T1DM there is an autoimmune attack on the B cells (they normally produce insulin). Therefore, insulin is not being produced anymore = decrease in insulin
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43
Q

What happens when insulin is not produced in T1DM?

A
  • gluconeogenesis is not inhibited, therefore we get more production of glucose
  • increased glycogenolysis (a process where glycogen is broken down into glucose to provide immediate energy to maintain blood glucose levels during fasting)
  • decrease in glycolysis (the metabolic pathway that converts glucose into pyruvic acid)
    This all causes more glucose in the blood
    = hyperglycemia causes:
  • glucose urea (glucose is peed out)
  • polyuria (pee more than usual because glucose is an osmotic solute and draws water)
  • polydipsia (excessive thirst from losing so much fluid)
  • the decrease in insulin means that fat breaks down occur because the body is not receiving enough energy. During an infection or feeling ill, the body will break down fat because glucose (energy) is not present and is not being taken up

Fats are broken down from adipose tissue to form free fatty acids, which go to the liver and undergo ketogenesis to make more ketone bodies because the body needs some kind of energy since glucose is not present

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44
Q

What is Ketonemia?

A

occurs when there are high levels of ketone bodies in the blood
In T1DM,
the decrease in insulin means that fat breaks down occur because the body is not receiving enough energy. During an infection or feeling ill, the body will break down fat because glucose (energy) is not present and is not being taken up

Fats are broken down from adipose tissue to form free fatty acids, which go to the liver and undergo ketogenesis to make more ketone bodies because the body needs some kind of energy since glucose is not present

From high levels of ketone bodies (Ketonemia), this results in Ketonuria where ketones are being peed out

Ketones are acidic, they are acids. They reduce the pH in the blood and urine, this is the main path of DKA

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45
Q

What happens if a patient shows signs and symptoms of DKA?

A
  • need a thorough history and examination
  • need to check airways, breathing circulation: IV access is important to get blood for investigation, get base serum potassium level (K+)
  • admin IV fluids (saline)
  • admin insulin slowly (helps cells in the body take up the glucose that is in the blood)
  • monitor pH using arterial blood gas (ABG) regularly
  • full blood count, EUC for infections and electrolyte abnormalities, dehydration
  • urine analysis to check and monitor if there’s glucose, ketones, and infections
  • ECG performed to check for arrhythmias in case of potassium hyperkalemia/hypo

Monitoring K+ levels is important since insulin is being administered because insulin will cause hypokalemia (which can trigger an arrhythmia)

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46
Q

What are the main differences between T1DM and T2DM?

A

T1DM:

  • is an autoimmune condition
  • there’s damage to the beta cells in the pancreas that prevents the individual from producing insulin, which is why they have to inject it
  • prone to diabetic ketoacidosis (DKA): medical emergency, your sugars get so high your body goes into a state of acidosis. Your blood gases, pH, and electrolytes levels are not normal

T2DM:

  • ranges from insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance
  • DKA is not common because you can still make a little bit of insulin
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47
Q

What is Gestational Diabetes Mellitus (GDM)?

A
  • in pregnancy, a glucose intolerance
  • they do an oral glucose tolerance test during week 26 of pregnancy, they drink 50-75g of sugar and then test their sugars to see how their body was able to process it
  • once the woman gives birth diabetes goes away, but now she is at risk for T2DM later in life
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48
Q

What is Latent Autoimmune Diabetes in Adults (LADA)?

A
  • someone who gets diagnosed with T1DM later in life
  • can be difficult to diagnose, because of the individual’s age they might get diagnosed as a T2DM. As the disease progresses, it is realized that it is actually an autoimmune deficiency where they need insulin
  • <50 years of age (could be in their 70s)
  • BMI <25kg/m2
  • history of autoimmune disease (thyroid disorder)
  • family history of autoimmune disease
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49
Q

What is the physiology of a normal metabolism?

A
  • pancreatic beta cells regulate the storage and metabolism of glucose through the secretion of insulin
  • insulin is anabolic (muscle building), it is produced when sugars go up, the pancreas releases insulin to help the sugars come down =

biphasic pattern:
Phase 1: the insulin will release a ton of little bits of inulin when you start to eat and it notices the sugars are going up. a large burst produced in the first 3 mins after a meal
Phase 2: then there’s a smaller production of insulin over the next couple of hours

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50
Q

What are the roles of insulin in the body?

A
  • insulin allows blood sugar to enter cells of the body to be used as fuel
  • helps circulating free fatty acids to be stored as triglycerides in fat cells
  • converts glucose to glycerol, the basis of stored triglycerides in far cells
  • stimulates the storage of amino acids as protein in muscles
  • helps the liver and muscle tissue store glycogen for future use
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51
Q

What is glucose homeostasis?

A
  • it’s the balance of insulin and glucagon to maintain blood glucose
    Steps:
    1. When you eat something, your pancreas is triggered to release insulin
    2. insulin triggers the fat cells in your muscles to take up glucose/sugar, which brings sugars down
    Your liver starts to store sugar, which decreases the process of gluconeogenesis (production of carbs)
    3. these processes bring sugars down to normal levels (4-6mM)
    4. the opposite happens when you’re sleeping/fasting and not eating. When your sugars go down overnight, the pancreas releases the hormone glucagon (controls blood sugar/glucose levels)
    5. Glucagon tells the liver it needs glucose, this increases glycogenolysis (glycogen breaks down into glucose) and increases gluconeogenesis (transform non-carbs into glucose), therefore glucose increases to balance to a normal blood glucose level (4-6 mM)
How well did you know this?
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52
Q

What are the signs and symptoms of T1DM?

A
  • many individuals are diagnosed after going to the hospital for DKA
  • polyuria (pee more than normal)
  • polydipsia (excessive thirst)
  • polyphagia (excessive hunger or increased appetite)
  • fatigue, not burning energy properly because the glucose is not going where it’s supposed to, it’s sticking around in the bloodstream = not going to the muscles, not being stored in the liver
  • lean body type with notable weight loss prior to diagnosis because high blood glucose causes weight loss
53
Q

What is a clinical diagnosis of T1DM?

A
  • fasting blood glucose (FBG) >7.0 mmol/L
  • glycated hemoglobin (HbA1C/A1C) >6.5%
    Whether it is T2DM or T1DM, once someone’s A1C is over 6.5%, they are considered diabetic
    A1C test: a 3 month average of blood sugar, gives a long-term picture, gives more info
  • Random blood glucose >11.1 mmol/L
    measures the levels of glucose in the blood at any given point in the day
  • glucose tolerance tests arn’t used as much anymore, indivudal has to drink a gross drink of sugar, more conventant to run an A1C test
54
Q

What is the clinical diagnosis difference between T1DM and T2DM?

A

T1DM:

  • typically diagnosed at a younger age <25 but can occur at any age (except before 6 months)
  • usually thin, but can be overweight or obese
  • if islet autoantibodies are present, then usually confirms the person has T1DM
  • c-peptide is undetectable/low
  • DKA is common, usually how people are diagnosed because they go to the hospital since it is a medical emergency
  • insulin resistance is usually not a factor in T1DM, but if an individual puts on weight then over time insulin resistance can happen
55
Q

What are some targets for glycemic control?

A
  • A1C: 3 month average of blood sugars is <7.0%, this helps decrease the risk of microvascular and macrovascular complications
    In T1DM for children the target is 7.5% to avoid a low blood sugar = let them run a little bit higher
  • Fasting blood glucose numbers aimed to be between 4.0-7.0 mmol/L
    2 hours after a meal blood glucose target is 5.0-10.0 mmol/L

*targets can always be individualized, especially in T1DM. The risk of low sugars is dangerous. Make sure the patient is comfortable with their targets. These are the general targets set by guidelines

  • Time In Range (TIR): the amount of time the individual spends within the target range of their blood sugars. The goal is to always be at least 70% TIR
  • Coefficient of Variation: <36% tells about the variability of someone’s blood sugars, and the same with the standard deviation of 1.1 or less
56
Q

What is hypoglycemia unawareness?

A
  • when someone doesn’t experience symptoms or signs of hypoglycemia when the blood sugars fall below 3.0 mmol/L
  • can cause unconsciousness
  • can happen as people age
  • target for glycemic control is 7.1-8.5% A1C
57
Q

How is glycemic control monitored?

A
  • A1C is the gold standard recommended that individuals get their A1C checked every 3 months (for T1DM)
  • self monitoring daily is essential to have good control of sugars, important for people with T1DM don’t view it as an intervention for their disease, it to have better control and to make sure they are feeling well
  • people with T1DM have to make around 300+ extra decisions a day because they have to constantly think about their blood sugars. Therefore, there are some people who don’t check their sugars at all out of frustration and exhaustion
58
Q

What is recommended for Self-monitoring blood sugar (SMBG)?

A
  • testing sugars at least 4x a day ac meals (before meals) occasionally pc (after meals) HS (in the evening), depending on the person
  • newly diagnosed recommended testing more often to get a good picture of what their control is and make sure they don’t have low sugars if they are new to insulin therapy
  • always test before meals because that’s when they would be dosing for insulin
59
Q

List some common glucometers

A
  • One-Touch
  • Accu-Chek
  • Freestyle
  • Contour Next
  • More of a push to move away from these devices with better technology, especially for people with T1DM
60
Q

What is the difference between Continous Glucose Monitoring (CGM) and Flash Glucose Monitoring (FGM)?

A

CGM

  • no scanning involved, updates automatically every 1 to 5 mins
  • more expensive

FGM

  • scan with device or phone to check glucose levels
  • Libre

*Overall, important for an individual to check their glucose in the morning and before their first meal/snack

61
Q

What is Diabetic Ketoacidosis (DKA)?

A
  • blood sugars get too high and causes an acidosis state in the body
  • someone could go into DKA because:
    they have not taken their insulin, are sick (illness makes your sugars go up), certain medications
  • insulin deficiency, high sugars, increase in glucagon happening = urinary loss of electrolytes and potassium gets shifted out of the cells (K+ plays a big role in heart rhythm)
62
Q

How does DKA happen?

A
  • when someone has an insulin deficiency, increase in counterregulatory hormones, and increased lipolysis (a metabolic process where triacylglycerols breakdown via hydrolysis into glycerol and free fatty acids).
  • This causes a decrease in glucose uptake, and an increase in gluconeogenesis (transforms non-carb substrates into glucose), which causes an increase in hyperglycemia (too much sugar in the blood)
  • since there is an increase in lipolysis, this means there are higher amounts of free fatty acids and ketones (beta-hydroxybutyrate, acetoacetic acid, keto acids), this causes an increase in ketonemia (abnormally high concentration of ketone bodies in the blood)
  • The body tries to get rid of the high amounts of ketones, which causes ketonuria (increased ketone in the urine)
  • from the fluids lost in the urine, this causes dehydration, decrease in kidney function not enough electrolytes and acidosis in the blood (too much acid in the body fluids) = DKA
63
Q

How can you prevent DKA?

A
  • make sure the patient is well hydrated
  • testing their sugar often, SMBG 2-4 hrs
  • taking insulin as needed for good and blood sugar correction
  • testing for ketones
64
Q

What’s the difference between DKA and Hyperglycemia (HHS)?

A

DKA

  • happens more often in T1DM
  • must use insulin
  • electrolytes
  • IV fluids

HHS

  • more often in T2DM
  • may not need insulin
  • IV fluids used as well
65
Q

What is hypoglycemia?

A
  • blood sugar <4mmol/L
  • autonomic symptoms: trembling, palpitations, sweating, anxiety, hunger, nausea, tingling
  • neuroglycopenia symptoms: difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking, headache, dizziness
  • Risks:
    physical activity can increase the risk of hypoglycemia
    too much insulin
    insulin stacking: giving insulin too often
  • the more someone experiences low sugar the less sensitive they feel to the symptoms, therefore being able to eliminate someone from having a low sugar for just 3 days will help increase their sensitivity
  • before driving must be at a blood sugar of 5mmol/L “5 to drive”
66
Q

How to treat hypoglycemia?

A
  • if blood sugar is <4mmol/L, treat it by eating 15 grams of fast-acting carbs: 15g of glucose tablet, 15mL or 3 packets of table sugar dissolved in water, 5 cubes of sugar, 150mL of juice or soft drink, 6 lifesavers, 15mL of honey
    Just sugar, no protein or fats
  • after 15 mins, need to retest to make sure blood sugar is >4mmol/L
  • if <4mmol/L, then treat again with 15g of fast-acting carbs
  • if >4mmol/L, they can eat a snack with carbs and protein, unless they are going to eat a meal within a half-hour. The carbs will bring the sugars up and the protein is what keeps it stable
67
Q

What is severe hypoglycemia?

A
  • when blood sugar levels are <2.8mmol/L
  • need to treat with 20g of sugars/carbs
  • if an individual goes unconscious, must give them 1mg of glucagon subcutaneously (layer of tissue that underlies the skin/injection), intramuscularly (entering a muscle with injection), or via the nasal passage
68
Q

How to prevent hypoglycemia?

A
  • if engaging in physical activity, bring a snack or take a little less insulin the meal before they go
  • ensure there are appropriate targets
  • continue to self-monitor, such as using FGM or CGM, helps reduce the risk of hypoglycemia
  • MDI: multiple daily injections of insulin
69
Q

What is insulin therapy?

A
  • the goal is to mimic a functioning pancreas by giving insulin when the person is eating to bring their sugars down, or when their sugars are high
  • low blood sugars are always the priority if an individual is having low and high blood sugars
  • always individualized
  • 2 methods of insulin therapy:
    1. Basal-bolus insulin regimen (MDI): insulin pen with a tiny needle
    2. Insulin pump therapy (continuous subcutaneous insulin infusion)
70
Q

What is basal insulin?

A
  • long-acting insulin
  • patient administers to themselves once a day
  • can last from 16-42 hours depending on the type of insulin, but since it’s slow-releasing it’s still admin every 12-24 hours because the insulin isn’t being absorbed all at once
  • helps control sugars when sleeping and long times in between meals
71
Q

What is bolus insulin?

A
  • used to correct high sugars
  • rapid-acting insulin
  • lasts 5 hours or less
  • the insulin that a person admins when they sit down to eat a meal
  • starts working in 5-15 mins
  • peaks ar an hour and a half and out of the system 5 hours later
72
Q

What is the set dose for bolus insulin?

A
  • people with T1DM are encouraged to count carbs, but if that’s not appropriate for them then a set dose is used of rapid-acting insulin prior to a meal
  • ex. Breakfast: 3 units of Humalog (rapid-acting insulin)
    Lunch: 3 units
    Dinner: 6 units
    every day
  • this is used for newly diagnosed patients and then slowly shifted to carb counting
  • set doses are also used for people to are: cognitively impaired, elderly (due to cognition)
73
Q

To help compact mucositis, what could an RD recommend?

A

Avoiding high acidic foods

74
Q

What is a simple and inexpensive recommendation that might help a patient with xerostomia?

A

Suck sugar-free candy

75
Q

What is the medical term used to describe degenerative loss of skeletal muscle mass, quality, and strength?

A

Sarcopenia

76
Q

What is cancer?

A

cancer is a genetic disease that causes cells to divide abnormally and spread into surrounding areas

causes:
genetics
error in cell division
damaged DNA caused by environmental exposures

77
Q

What are malignant/cancerous tumours?

A
  • masses of tissue that can invade nearby tissues
  • as tumours grow, some cancer cells can break off and travel to other areas (through the blood) of the body and form new tumours = metastasis
78
Q

How is cancer diagnosed?

A
  • symptom or screening resultss may prompt a cancer investigation:
    lab tests: blood urine, tumour markers = substances produced by cancer cells or by other cells in response to cancer (blood/tissue sample)
    imaging tests: CT scan, MRI, nuclear scan, bone scan, PET scan (nuclear medicine imaging test, uses radioactive material attached to glucose that’s injected into the body through an IV, travels through the body and collects in cells that use an abundance of energy = cancer cells)
    biopsy tests: tissue obtained by needle, endoscopy, surgery
79
Q

What are the 2 types of cancer surgeries?

A
  1. open surgery
    big wound = need adequate nutrition to heal it
  2. minimally invasive surgery
80
Q

What are the two types of radiation?

A
  1. external beam
  2. internal radiation
    capsules of radiation through a catheter goes in or around the tumour to kill it
  • radiation destroys the DNA of cancer cells and unable to divide any further. Takes weeks or months to see a difference in size
81
Q

What is cancer cachexia?

A
  • multifactorial syndrome characterized by an ongoing loss of skeletal muscle mass, with or without loss of fat mass, that can not be fully reversed by conventional nutrition support
  • mechanism involved:
    anorexia
    decrease PA
    decreased secretion of host anabolic hormones
    the altered protein, lipid and carbohydrate metabolism
    systematic inflammation: hallmark of cancer cachexia, through production of acute-phase proteins
82
Q

What is starvation-related malnutrition?

A
  • chronic starvation with the absence of inflammation
  • mainly characterized by reduced energy intake, malabsorption, maldigestion when intake is normal
  • typically can be fully reversed by conventional nutrition support
83
Q

What is starvation-related malnutrition metabolism?

A
  • Day 1-2: mobilization of triglycerides from adipose tissue and gluconeogenesis by liver provide fuel. Protein from muscle is used to provide carbon sources for gluconeogenesis
  • Day 3: body begins to produce ketones - provide 1/3 of brain’s energy needs
  • Several weeks of starvation: ketones become the major fuel for the brain. Only 20 g of muscle is degraded/day (75 g prior). Once adipose tissue is depleted, the body will use muscle. The body is trying to maintain the muscle that it has at this point
  • Starvation ketoacidosis: ketones create an increased concentration of hydrogen ions. Overwhelms the body’s buffering system, leading to an acidic environment (increased ketones, bicarbonate, and pH)
84
Q

What are the main nutrition goals for oncology?

A
  • maintain/improve nutritional status
  • promote adequate hydration
  • manage symptoms
  • improve quality of life
85
Q

When is nutrition support used?

A
  • when patients are unable to meet their nutrition requirements
  • less than 50% of requirements for more than 1 week
  • 50-75% of requirements for more than 2 weeks
  • enteral nutrition is preferred if the gut works
  • parenteral nutrition is used if enteral nutrition is not feasible
86
Q

You notice that patient X is presenting with symptoms of dehydration. What is the range of fluid that you might recommend based on what was learned in the lecture?

Patien X weight = 187 lbs
Usual body weight = 200

A

2120-2968

2125-2975 ml

87
Q

In oncology patients undergoing chemotherapy, fish oil supplementation has been shown to improve

A
  • both c & d

- body weight & quality of life

88
Q

You are an RD in an oncology clinic. You would like to estimate the protein needs of patient X who has recently been diagnosed with cancer. What is the range of protein that you might recommend based on what was learned in the lecture?

Patient X = 187 lbs

A
  1. 28 - 127.2 g/kg

93. 5 - 127.5 g/kg

89
Q

In lecture, Anastasia outlined the benefits of immunonutrition supplementation for special oncology populations. What was one of the barriers for receiving and continuing on this type of intervention?

A
  • it’s too costly & not available in Canada

Both B & C

90
Q

What is immunonutrition?

A
  • liquid nutritional supplements with specific nutrients including arginine, n-3 fatty acids and nucleotides
  • recommended for upper GI cancer patients undergoing surgical resection
  • reduction in post-op infective complications
91
Q

What is oral mucositis?

A
  • an acute inflammation/ulceration of the oral or oropharyngeal mucosal membranes
  • can cause pain/discomfort, interfere with eating, swallowing and speech and may lead to infection

Caused by:

  • head and neck cancer
  • treatments: radiation therapy, chemo

Nutrition interventions:

  • daily fluid intake of 8-12 cups (2-3 litres)
  • well-balanced diet that is high in protein, Vit B and C
  • use of soft, moist, bland foods as symptoms develop (or fluids only)
  • avoid dry and coarse foods, spicy, hot, highly acidic, alcohol, tobacco
  • being unable to eat or drink fluids for more than 24 hrs = risk of dehydration
92
Q

What is xerostomia?

A
  • abnormal dryness in the mouth characterized by a marked decrease and/or thickening of saliva
  • acute or chronic in nature
  • contributing factors: treatments: radiation, chemo, graft versus host disease (transplant)
  • nutrition interventions:
  • daily fluid intake 8-12 cups (2-3 litres)
  • use of soft, moist foods
  • moisten foods with extra sauce, gravy, butter
  • alternate bites of food with sips of fluid
  • papaya may help reduce the thickness of saliva
  • suck on sugar-free candy

avoid:
- dry and coarse foods, highly acidic, coffee, tea, alcohol, tobacco

  • white patches on the inner cheeks, tongue, roof of the mouth, throat = oral candidiasis, yeast infection in the mouth
93
Q

What is dysphagia?

A
  • difficulty of discomfort in swallowing foods/fluids
  • caused by: oral, pharyngeal, esophageal cancer, treatment: radiation, chemo, surgical
  • nutrition interventions:
  • changes in food texture, consistency and temp
  • eating upright
  • eating only when alert
  • supervised eating
  • undistracted eating
  • avoid: dry and coarse foods
  • wet sounding voice during or after eating/drinking = aspirating
94
Q

What term is used to infer the spread of cancer from the primary site to nearby or distant areas through blood or lymph?

A

Metastasis

95
Q

What are diarrhea nutrition interventions?

A
  • daily fluid intake of 10-12 cups
  • increase soluble fibre foods (peeled apples, bananas, potatoes, applesauce)
  • small, frequent meals
  • reduce: insoluble fibre foods, high sugar fluids, high-fat dairy
  • avoid: sugar alcohol, deep-fried foods, spicy foods
  • blood ins tool = requires immediate medical attention
96
Q

Hot topics in oncology nutrition:

A

provide your opinion on whether the approach should or shouldn’t be recommended to oncology patients.

Ketogenic diet:

  • no clinical trials to support its use in the cancer populations
  • low palatability of the ketogenic diet may lead to inadequate intake and weight loss
  • hard to follow, especially if the patient feels nauseous

Intermittent Fasting:

  • lack of evidence of benefit
  • also not recommended due to the risk of malnutrition
  • patients may be tempted to prolong fasts
  • case series report did show a reduction in multiple chemo-induced side effects when patients fasted pre and post-chemotherapy:
    effect of fasting on normal cells = stress-resistant state
    effect of fasting on cancer cells = no change
    Therefore, during chemo, the normal cells can produce themselves and the cancer cells cannot

Low/No Sugar Diet

  • all cells (cancer cells included) need sugar as fuel for their intrinsic metabolism
  • unknown whether a tumour’s preference for glucose metabolism predicts its responsiveness to diets that alter blood glucose levels
  • avoiding or limiting sugar increase the risk of inadequate intake
  • research on the link between sugar and cancer is in its infancy

Alkaline Diet:

  • no scientific evidence to support its use in the cancer population
  • food has no impact on blood pH
97
Q

The focus of nutrition therapy in the end of life care is to?

A

ensure patient is comfortable and patients wishes are being honoured

98
Q

Which of the following would NOT result in postprandial (reactive) hypoglycemia?

A

Excessive hepatic gluconeogensis

99
Q

A friend who knows you have recently completed a nutrition course asks you about the glycemic load. You explain that the glycemic load:

A

Ranks foods by how much they raise blood glucose levels based on servings

100
Q

You receive a referral for Mr. B. Mr. B is a 61-year-old male with newly diagnosed esophageal cancer. The gastroscopy report reveals a large circumferential tumour in the esophagus. He is being considered for an esophagectomy.

The patient has difficulty swallowing and 30 lb weight loss

A
  • ask about usual body weight and current body weight, need to determine the percentage of weight loss to gage severity
  • how long has it been difficult to swallow

Nutrition goals: maintain weight, 1.1 g protein intake target

101
Q

You are an RD on an oncology ward. You see Mrs. S following surgery for removal of a tumour located in her stomach. Her blood work is completed and reveals an elevated concentration of C-reactive protein. What might this result be an indication of?

A
  • indicates inflammation in the body & patient may be experiencing cancer cachexia
    (Both A & C)
102
Q

A.S.P.E.N nutrition support recommendations for individuals living with cancer recommend that estimated energy requirements for a normometabolic patient are calculated based on:

A

25-30 kcal/kg

103
Q

What is Insulin to Carbohydrate Ratio (ICR)?

A
  • given to a patient to help teach them to carb count (goal with carb counting is to give them flexibility)
  • the amount of rapid-acting insulin needed to cover the number of carbs in a meal
  • for every x number of carbs you need 1 unit of insulin
    ex. ICR on 1:5 means 1 unit of rapid-acting insulin will cover 5 grams of carbs
  • if someone eats 25 g of carbs, the patient needs to take 5 units of rapid-acting insulin (25/5 = 5 units of insulin)
  • to determine an ICR, the patient needs to record a 3-day food record, 2-hour blood glucose with meals
    1. educate them about how to carb count: food log, blood glucose log, amount of insulin administered
    Carb counting - from food label look at how many carbs - fibre
    2. review food record, 2 hours post-meal blood glucose and amount of rapid-acting insulin at each meal. Finding the 2-hour post-meal blood glucose helps to determine if they are taking too much or too little insulin
    3. count the amount of available/net carbs consumed at meal
    4. calculate the ICR using:
    ICR = carb g/units of insulin
104
Q

What is the correction factor/insulin sensitivity factor?

A
  • an estimate of how many mmol/L 1 unity of rapid-acting insulin will decrease blood glucose by over a 2-4 hour period
  • problem: if they administered insulin too often, don’t correct more than every 4 hours because of how long the insulin stays in the system
  • calculation done to see how much insulin a patient needs to bring their sugar down by 1 point
    ex. if their correction factor is 2, it means needs 1 unit of insulin to bring their sugars down by 2 mmol/L
105
Q

What are some symptoms a patient may experience if they’re not adjusting their insulin properly?

A
  • high and low sugar
  • high sugar = thirsty, tired, peeing a lot
  • low sugars = sweaty, shaky, confused, light-headed
106
Q

Hypoglycemia is a complication of diabetes. What is one strategy to prevent hypoglycemia?

A

consume meals at regularly timed intervals

107
Q

What is the most common diagnostic characteristic of diabetes (both type 1 & 2)?

A

Hyperglycemia

108
Q

Based on Diabetes Canada targets for glycemic control, what is the hemoglobin A1C target for most adults with type 1 & 2 diabetes?

A

less than or equal to 7%

109
Q

Mr. X has type 2 diabetes. As part of your nutrition recommendations would like to estimate how many carb choices Mr. X should be prescribed. Using the following information calculate how many carb choices Mr. X can have per day.

Estimated energy requirements = 2500 kcal
Suggested daily % carb intake = 60%

A

2500 x 0.6 = 1500 kcal from carbs

1500/4 = 375 g carb/day

375/15 = 25 carb choices a day

110
Q

One carb choice is equal to how many grams of carbs?

A

15g

111
Q

Type 2 diabetes occurs most frequently in

A

Adults

112
Q

When we have too much glucose floating around in the bloodstream, this organ releases an excess of what?

A

Pancreas, insulin

113
Q

Insulin ____ blood glucose uptake by the muscles

A

facilitates

114
Q

To improve blood glucose control, a person with diabetes should remove all added sugars from their diet

A

False

115
Q

21Mk is a 30-year-old male with type 2 diabetes. Using his diet history, you determine that he should consume approximately 50% of his calories from carbs. His estimated energy requirements are 2500 kcal/day.

Medical therapy = 6 units of rapid-acting insulin

Blood glucose: within normal range pre and post-meal

How many carbs choices would you recommend for MK per day? (round up)

A

21 ?

116
Q

Which primary environmental factor aids in the development of type 2 diabetes?

A

Obesity

117
Q

JK is a 19-year-old male college student with T1DM. He stays away from home and does not follow a proper diet. His school schedule is erratic; therefore, he eats throughout the day. Currently, he takes extended long-acting analogue insulin once per day. By 8 pm his blood sugar levels start dropping to a very low value. Also, biochemical analysis shows trace amounts of ketones in his blood.

Height: 5’10” Weight: 175 pounds Hemoglobin A1C: 9%
What is the most likely cause of JK’s low blood sugar at 8 pm?

A

The timing and peak of his insulin do not match his intake

118
Q

JK is a 19-year-old male college student with T1DM. He stays away from home and does not follow a proper diet. His school schedule is erratic; therefore, he eats throughout the day. Currently, he takes extended long-acting analogue insulin once per day. By 8 pm his blood sugar levels start dropping to a very low value. Also, biochemical analysis shows trace amounts of ketones in his blood.

If JK and his doctor decide to change to multiple daily injections of insulin, what type of insulin will he be taking at each meal?

A

Bolus insulin

119
Q

Which endocrine cells of the pancreas secrete glucagon?

A

Alpha cells

120
Q

What are the three common complications associated with long-term hyperglycemia?

A

retinopathy, peripheral neuropathy, and heart disease

121
Q

Calculate the required insulin dose for carbs eaten for the following patient intake. Current units of rapid-acting insulin is 6.

Prior to assessment of breakfast meal blood sugar within normal range.

A

18.8 units

122
Q

CD has type 2 diabetes. She comes in your office for an appointment with the complaint of excessive urination and thirst. What might CD be experiencing?

A

polydipsia & polyuria

123
Q

Which of the following is not a sign or symptom of hypoglycemia?

A

Oliguria

124
Q

JK is a 19-year-old male college student with T1DM. He stays away from home and does not follow a proper diet. His school schedule is erratic; therefore, he eats throughout the day. Currently, he takes extended long-acting analogue insulin once per day. By 8 pm his blood sugar levels start dropping to a very low value. Also, biochemical analysis shows trace amounts of ketones in his blood.

If JK and his doctor decide to change to multiple daily injections, what is the most important thing that JK should learn from his dietitian?

A

carbohydrate counting

125
Q

Diabetes Canada recommends that soluble fibre be increased to 10-20g/day. Other than the positive effects of fibre on heart health, the main rationale for this recommendation is to:

A

To help reduce postprandial blood glucose spikes

126
Q

____ control is fundamental to the management of diabetes and provides the basis for monitoring and evaluation of the condition

A

Glycemic

127
Q

Individuals using conventional therapy to treat type 1 diabetes must synchronize administration of their insulin and food intake to avoid

A

Hypoglycemia

128
Q

Acute complications of hyperglycemia include all but:

A

Nephropathy?

c & d?

129
Q

What are the goals of nutrition therapy?

A
  • maintain and improve quality of life and nutritional and physiological health
  • prevent and treat acute and long term complications of diabetes, associated with comorbid conditions and concomitant disorders
  • can improve glycemic control by reducing A1C by 1.0% to 2.0%
  • nutrition therapy should align with the patient’s values, preferences, and treatment goals
130
Q

What are the risks of physical activity and blood sugar levels?

A
  • prolonged aerobic exercise (run, bike ride) can result in hypoglycemia
  • much achieve an appropriate balance of insulin and carb intake including increasing carbs before activity, decreasing ac bolus insulin or reducing basal insulin rate for insulin pump
  • brief intense exercise (hockey) can result in hyperglycemia
  • can be corrected with a small bolus of rapid-acting insulin in exercise recovery or by temp increasing the basal insulin rate for insulin pump