Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
71 Cards in this Set
- Front
- Back
Normal blood glucose fasting levels?
|
3.3-3.5mmol/l
|
|
how does active insulin reach the blood?
What kind of hormone is insulin? What does that mean? |
portal vein
Anabolic - build things up/ storage |
|
Does insulin stimulate glucose synthesis? What then (2)?
Where else does the latter conversion happen? |
No - glycogen or fatty acids.
Glucose -> fatty acids in the liver. |
|
What system does glucagon activate to increase blood glucose?
|
cAMP 2nd messenger system.
|
|
What happens to blood glucose several hours after a meal? What is the response?
|
Decreases below fasting levels, so initiate glucagon.
|
|
What is the shared characteristic of diabetes mellitus?
|
hyperglycemia.
|
|
What is the leading cause of blindness, lower leg amps, and renal failure?
|
T2D
|
|
In order to run an oral glucose tolerance test, what are the two pre-test requirements?
When is the test completed ? |
3 days of:
1) normal PA 2) at least 150g CHO daily After an overnight fast . |
|
After a OGTT, what range of fasting glucose = impaired fasting glucose & impaired glucose tolerance?
How about after a meal. |
impaired fasting glucose (prediabetes) = 5.5-7
post meal = 7.8-11 impaired glucose tolerance =more than 7 post meal = greater than 11. |
|
T1D etiology
|
cell mediated autoimmune destruction of B cells in the pancreas.
|
|
What is LADA?
What is the clinical indicator? |
latent autoimmune diabetes of adults.
T2D initial diagnosis but really T1D. Islet failure not insulin resistance found via raised antibodies against islets of Langerhans. |
|
What is often the first sign of T1D?
|
ketoacidosis.
|
|
What is T1D pathophysiology?
Why does this lead to dehydration? Why does T1D lead to ketone production? |
absolute insulin deficiency due to beta cell destruction - body can't use glucose for energy.
hyperglycemia = glycosuria = increased urination Increased demand on lipolysis. |
|
What is the most common cause of premature death with diabetic individuals? Example?
|
cardiovascular disease - atherosclerosis.
|
|
How does diabetes cause vascular disease?
|
make more pron to endothelial damage.
|
|
What is the single leading cause of chronic kidney disease?
|
nephropathy - changes in glomerular blood vessels = decreased filtering ability.
|
|
What is retinopathy? When can it be caused?
|
eye damage linked to hyperglycemic damage to its blood vessels - diabetes.
|
|
What are the diabetic effects on the nervous system (3)?
|
1) impaired sensation in hands or feets (diabetic ulcers).
2) gastroparesis - delayed gastric emptying - results from damaged vagus nerve. 3) carpel tunnel |
|
What is the ratio you must consider with insulin therapy?
|
insulin: glucose.
|
|
How is insulin types classified (3)?
What kind insulin is involved with subcutaneous infusion? What kind with intensive insulin therapy? What is intensive therapy? |
expected onset, peak time, and duration of action.
rapid or short acting intermediate or short acting - multiple injections |
|
What are the three targets of T1D nutritional goals?
What is a common technique? how is this based? How are fats and vitamins/ minerals prescribed? |
1) blood glucose
2) lipoproteins 3) BP CHO counting - 15g CHO = 1 CHO choice. Based on entire population. |
|
What is hemoglobin A1C?
High blood glucose = ? What can you measure? |
measures amount of glucose bound to hemoglobin.
high blood glucose = more glycated hb average blood glucose for 2-3 months |
|
How many times should you self monitor glucose per day?
|
3 times.
|
|
Where and how often is continuous glucose monitoring?
|
under the skin - every 5 mins.
|
|
When is hypoglycemia a risk with exercise (2)?
Can you go hyperglycemic with exercise too? |
exercise greater than 1 hr and within 24hr window of strenuous activity
Yes |
|
What is the effect of alcohol on blood glucose?
|
alcohol can inhibit liver ability to release glucose - therefore hypoglycemia.
|
|
Is T2D genetic?
How is alcohol related to T2D etiology? |
YES - clearly inherited.
U-shaped association - moderate consumption = low risk. |
|
What population is at the greatest risk of Canada diabetes?
|
Aboriginals.
|
|
How does the pancreas respond to T2D initially?
Eventually?? |
Increases more insulin release
inability to produce insulin. |
|
What was found to better reduce risk of T2D, diet or exercise?
|
exercise you nutrition betches.
|
|
How does fat play into T2D?
What type of fat increases insulin sensitivity? |
insulin resistance INDEPENDENT of obesity
unsaturated. |
|
What evidence exists and does not exist for fat and T2D risk?
What is a major finding? Specific fat type and women risk of t2D? |
NO long-term RCT
Yes epidemiological studies. saturated fat intake independently predicted insulin resistance. Trans-fats |
|
What has intervention studies with fat and diabetes?
potential mechanism? |
SFA free diet improved insulin sensitivity.
fat quality affects membrane FA composition which alters insulin receptor binding/ affinity |
|
What is glycemic index?
What food is it compared to? Why is this important? |
ability to raise blood glucose levels.
white bread. GI associated to increased t2d risk |
|
What does medical therapy for T2D encompass?
|
PA, nutrition, and medication.
|
|
What are four functions of T2D drugs?
|
1) decreases insulin resistance
2) stimulate insulin secretion in glucose presence. 3) decreases hepatic glucose production and increases insulin uptake in muscle (metformin) 4) delays intestinal absorption of glucose |
|
Weight loss and blood glucose
|
moderate weight loss improves glycemic control and reduces CVD risk
|
|
Are low CHO diets recommended for T2D?
why (2)? |
No
Increased protein may be a risk factor for nephropathy Increased fat = bad . |
|
What screening technique used for gestational diabetes?
|
OGTT
|
|
What is etiology for gestational diabetes?
Result. Fetus result |
metabolic alterations to meet maternal and fetal demands - can lead to islet cell dysfunction
result = insulin secretion cannot meet increased insulin needs. fetus = fetus exposed to hyperglycemia and they produce too much insulin - fetal hyperinsulinemia. |
|
What is plan a and b for gestational diabetes?
|
a = nutrition therapy
b = insulin therapy |
|
what is the increased protein requirement in 2nd and 3rd trimester?
|
1.1g/kg.
|
|
Is hypertension symptomatic?
|
no
|
|
pre vs. stage 1 vs. stage 2 hypertension SP&DBP
|
pre = 120-139/ 80-89
stage 1 = 140-159/ 90-99 stage 2 = greater than 160/ greater than 100 |
|
2 types of hypertension
|
primary = idiopathic
secondary = occurs as a result of another problem |
|
vasopressin and hypertension
|
works like angiotensin II
hypertensive people have more vasopressin from hypothalamus. |
|
What is the maximal BP for medical reduction goal?
|
140/80
|
|
What is the dose-response daily alcohol drink with hypertension risk?
|
above 2 per day for men and 1 for women.
|
|
What is the DASH diet?
How are K+, Ca++, Mg+ +related to BP? |
dietary approaches to stop hypertension.
reduce sodium K+, Ca++, Mg+ +reduce BP |
|
What does salt sensitivity mean?
|
individuals respond differently to changing salt in diet and blood pressure responses.
|
|
how are lipids transported in the blood?
|
lipoproteins
|
|
what is dyslpidemia?
|
high ldl and low hdl
|
|
what is the role of HDLs?
|
reverse lipid transport - tissue to liver.
|
|
What is the single strongest indicator of CVD risk and involved in athersclerotic process?
|
LDL
|
|
What process of LDL initiates plaque build up?
|
oxidation
|
|
What are the two phases in atherosclerosis pathophysiology?
|
1) fatty streaks - LDL reacts with ROS and oxidized LDL call upon monocytes. Monocytes plus macrophages = foam cells.
2) fibrous plaque - smooth muscle migrates into fatty streak and secretes fibrous proteins - narrow arteries. |
|
What do statins do?
|
lower blood cholesterol
|
|
What is the belief of nutritional therapy for atherosclerosis?
|
interferes with plaque formation by inhibiting inflammatory response that causes the changes within the blood vessels.
|
|
Should you reduce total dietary fat with atherosclerosis?
|
NO. You should switch to reducing SFA and trans
|
|
SFA maximal of total kcal?
|
7%
|
|
How are trans fats formed?
|
hydrogenation of unsaturated fats.
|
|
what do monounsat fat - omega 3 FA (linolenic acid) and polyunsat fat do to cholesterols?
|
LDL nothing to HDL.
|
|
What predicts serum cholesterol?
|
fat predicts serum cholesterol.
|
|
Coconut oil SFA case
|
SFA = lauric acid - raises HDL.
|
|
How does fibre affect cholesterols (2) ?
|
fibre reduces LDL and serum cholesterol
|
|
How does fibre reduce risk of CVD?
|
slows gastric emptying and maintains satiety.
|
|
Can plant sterol slower LDL
|
YES F*&( this course
|
|
What is the nutrition therapy for immediately after a myocardial infarction?
|
progression from liquids to solids.
|
|
What is the main etiology of heart failure?
|
impaired left ventricular myocardial function
|
|
how does the heart respond to hypertrophy left ventricle with heart failure? how does this play into the disease?
How is the left ventricle re-modeled? How does this affect contractility? |
increases SNA and RAS and increases symptoms.
dilated - decreases contractility. |
|
What is essential in medical therapy for heart failure?
Therefore, what is a nutritional therapy technique (2) ? |
control of BP
reduce sodium and fluid (reduce blood volume = reduce blood pressure). |