Diabetes Flashcards
Weight is ____ proportional to insulin resistance
Directly
What type of fat promotes insulin resistance
Visceral fat
Excess macronutrients causes ____ fatty acids
increased
What general methods are done/prescribed for weight management (DBW)
- +/- 500 kcal
- DBW x PA (Krause)
- BMI method
Formula to get ideal weight using BMI
sqrt of BMI x height (m) = weight (kg)
Hormone responsible for lowering blood glucose
insulin
Hormone responsible for increasing blood glucose
Glucagon
Difference between type 1 and type 2 DM
Type 1: no insulin at all
Type 2: low production of insulin/insulin resistance
3 Ps of DM
- Polyuria
- Polydipsia
- Polyphagia
Excessive urination
Polyuria
Excessive thirst
Polydipsia
Excessive hunger
Polyphagia
Why is excessive hunger a sign of diabetes
The brain signals the need for higher glucose uptake since cells cannot take in glucose due to insulin insensitivity
Etymology of diabetes mellitus
Diabetes = excessive passage of urine
Mellitus = sweet taste or honey-like
Diabetes Mellitus = excessive passage of urine with a sweet taste
What 2 process are responsible for glucose formation
- glycogenolysis
- gluconeogenesis
What are other effects of high blood sugar
- muscle wasting
- dehydration
- increase ketones
What happens if there is a high deposition of sugar in blood vessels
Damage lining of blood vessels causing inflammation
What condition is associated with blockage in blood vessels from high blood sugar
Atherosclerosis
Functions of insulin (7)
- Facilitates transport of glucose through insulin receptors in cell membrane
- Enhance conversion of glucose or glycogen and its storage in liver
- Stimulate lipogenesis
- Inhibit lipolysis and protein breakdown
- Promote amino acid uptake by Skeletal muscle and increase protein synthesis
- Influence glucose oxidation (glycolysis pathway - enzyme glucokinase)
What cells are insulin sensitive
- adipose
- muscle
- monocytes
True or False: Insulin receptors increase with weight gain and physical activity
False: weight loss
Screening tests for DM (5)
- urine test
- random blood sugar
- fasting plasma glucose test
- oral glucose tolerance test
- glycosylated hemoglobin (A1C) level
What test is done by measuring glucose & ketones by dipping indicator paper strips or reagent strips in urine
Urine test
Percentage in urine test that indicates diabetes
0-0.25%
What test is done where blood is drawn but fasting is not necessary
Random blood sugar
What result from random blood sugar indicate DM
Greater than or equal to 200 mg/dl
What test is done after an overnight fast for at least 8 hrs
Fasting plasma glucose test
What test is done after an overnight fast for at least 8 hrs
Fasting plasma glucose test
Normal levels for fasting plasma glucose test
70-100 mg/dl
Safe levels for fasting plasma glucose test
90-100 mg/dl
What result of FBG may indicate DM
Greater than or equal to 126 mg/dl
Test that evaluate a person’s ability to tolerate a glucose load after fasting
Oral glucose tolerance test
Common protocol for OGTT
- ingestion of 75 g glucose load
- measurement of plasma glucose after 2 hrs interval
Results of OGTT that indicates diabetes
200 mg/dl or 11 mmol/L
Results of OGTT that indicates diabetes
200 mg/dl or 11 mmol/L
Upper normal limit for OGTT
140 mg/dl (7.8 mmol/L)
What is the interpretation if OGTT results is between 140 and 200
Impaired glucose tolerance
Provides average blood glucose levels over the past 2-3 months
HbA1C
How does glycosylation of rbc occur
Glucose molecules attach themselves to the hemoglobin
Ideal percentage of glycosylated hemoglobin
Less than 7%
4 stages of DM
- Prediabetes
- Subclinical diabetes
- Latent diabetes
- Over diabetes
Meaning of IGT
impaired glucose tolerance: takes time for bg to be normal
Period from conception until development of IGT
Prediabetes
FBS and OGTT are normal
subclinical diabetes
abnormal OGTT, no symptoms
latent diabetes
Abnormal OGTT w/ symptoms as polydipsia, polyphagia, fasting hyperglycemia, glycosuria
Over diabetes
Precursor of diabetic coma
ketoacidosis
What medicine used for diabetes is used for weight loss
metformin
Cause of gallstones
High cholesterol deposits
pre-diabetic stage
impaired glucose homeostasis
How is impaired glucose homeostasis detected
- impaired fasting glucose level (above normal but lower than diabetic values)
- detected primarily through OGTT
Risk factors of impaired glucose homeostasis
- familial disposition
- race
- obesity
- age (>45 years old)
- birth to large babies (greater than or equal to 9 lbs)
- women who developed GDM
Any degree of glucose intolerance during pregnancy
Gestational DM
How many percent are normoglycemic after delivery
90%
Risks factors of GDM
- Occurence of GDM in previous pregnancy
- Delivery of previous macrosomic infant
- family history
- maternal obesity (> 120% of DBW)
Pathophysiology of GDM
- Placental & ovarian hormones decreases insulin sensitivity
- lack of pancreatic reserves
Screening OGTT results for OGTT
- fasting: ≥ 95 mg/dl
- 1 hr: ≥ 180 mg/dl
- 2 hr: ≥ 155 mg/dl
- 3 hr: 140 mg/dl
Nutritional goals of IGT and GDM
- to provide adequate energy
- to prevent weight gain
- to achieve and maintain normoglycemia
- to prevent ketone body formation
Is a normal blood sugar should be the goal
Not necessarily but blood sugar should not fluctuate
Dietary & non-dietary strategies
- individualization of meal plans
- monitoring of plasma glucose, appetite, and weight
- insulin therapy (if medically advised)
- CHO: maximum of 50% of total kcal
- CHO properly spaced throughout the day
- be physically active
Specifc goal for nutrition therapy of DM
- achieve physiologic blood glucose levels
- attain and maintain desirable body weight
- maintain desirable plasma lipid levels
- reduce likelihood of specific diabetic complications
- retard development of atherosclerosis
General goal for nutrition therapy of DM
- Consume health-promoting selection of nutrients
- maintain energy needs in timely manner
- address special requirements (e.g pregnancy)
- Tailor for therapeutic needs (e.g., renal disease)
Characteristics of T1DM
Person does not secrete enough insulin to control blood glucose level
Other terms for T1DM
- Insulin-dependent DM
- Juvenile diabetes
- Juvenile-onset diabetes
- ketosis-prone diabetes
2 types of T1DM
- idiopathic T1DM
- Immune-mediated DM
Forms of the disease that have no known etiology (mostly Asian and African origin)
Idiopathic T1DM
Results from autoimmune destruction of beta cells of pancreas
Immune-mediated DM
Etiology of T1DM
- Increase human leukocyte Antigen (HLA)-B8 and HLA-B15
- Formation of islet cell antibodies
- Attack of beta cells in the pancreas
- Hyperglycemia
- T1DM
MNT goals for T1DM
- maintain blood glucose levels within a desirable range to prevent or reduce risk of complications
- supply adequate calories for weight maintenance
Nutrient Recommendations for DM
- CHO = 50-60%; complex type; low GI vs High GI
- CHON = 20%
- Fats = max 30% (1/3 SFA + 2/3 PUFA; Cholesterol < 300 mg/day; if LDL is high, 7% kcal from SFA & 200 mg/day cholesterol)
- Increase dietary fiber
Dietary Strategies for DM
- timing of meals
- CHO counting
What is needed to do for timing of meals as dietary strategy
- eat regular meals that are evenly spaced
- 3 meals + 3 snacks
What is needed to do for CHO counting as dietary strategy
- counting the grams of CHO provided by foods
- Counting CHO portions, expressed in terms of servings
Goal of Insulin Therapy
To mimic natural insulin secretion to meet metabolic needs
Differences of forms of insulin
- onset activity
- timing of peak activity
- duration of effects
What is needed to be considered for Insulin Therapy
A diabetic’s diet must be planned so that there is a distribution of CHO and kcal to coincide with the type of insulin used
Characteristics of Rapid Acting Insulin
Preparations: Lispro Apart
Onset of Action: 15 min
Peak Activity: 30 min- 2 hr
Duration of Action: 3-5 hr
Characteristics of Short Acting Insulin
Preparations: Regular
Onset of Action: 30 min
Peak Activity: 2 - 4 hr
Duration of Action: 5-8 hr
Characteristics of Intermediate Acting Insulin
Preparations: Lente NPH
Onset of Action: 1-3 hr
Peak Activity: 5 - 10 hr
Duration of Action: 18-24 hr
Characteristics of Long Acting Insulin
Preparations: Ultralente
Onset of Action: 4-6 hr
Peak Activity: 8 - 12 hr
Duration of Action: >30 hr
Characteristics of Insulin Mixtures
Preparations: NPH/regular (70:30); NPH/regular (50:50)
Onset of Action: Variable; depends on formulation
Peak Activity: Variable; depends on formulation
Duration of Action: Variable; depends on formulation
descending order of Glucose infusion rate of different types of insulin
Insulin lispro aspart, glulisine > Regular > NPH > Insulin detemir > Insulin glargine
___% of total daily insulin replace insulin overnight
40-50%
50-60% Total daily insulin does for carbohydrate coverage (food) and high blood sugar correction
Bolus insulin replacement
Insulin to CHO ration
9g CHO : 1 unit of insulin
Formula for calculating CHO coverage insulin dose
CHO insulin does = total g of CHO in meal/ g of CHO disposed by 1 unit of insulin
Blood sugar correction
- 1 unit will drop blood sugar 50 pts
- high blood sugar correction factor: 50
- Pre-meal blood sugar target: 120 mg/dl
- Actual blood sugar before lunch is 220 mg/dl
220 - 120 mg/dl = 100 mg/dl
Correction dose = difference between actual and target blood glucose (100mg/dl)/correction factor (50) = 2 units of rapid acting insulin
Formula for Total Meal Insulin Dose
Total Meal Insulin Dose = CHO insulin dose + High blood sugar correction dose
Time between peak activity two types of insulin
Point of intersection
Ratio of CHO to insulin unit (point of intersection)
1 unit : 10-15 g CHO
2 primary defects of T2DM
- insulin resistance (diminished tissue sensitivity to insulin)
- impaired beta cell function (delayed or inadequate insulin release)
Other names for T2DM
- non-insulin dependent diabetes mellitus
- adult-onset diabetes mellitus
Risks to T2DM
- heredity
- poor diet
- aging
- obesity
- lack of physical activity
Etiology of T2DM
- overeating
- increased blood glucose level
- increased production of insulin
- hyperinsulinemia
- chronic demand for insulin exhausts B-cells
- insulin production falters
Should you give insulin if GDM is present
If severe enough, insulin may be given since some oral medications are contraindicated or the mother is undergoing insulin therapy even before pregnancy
Etiology of T2DM from Obesity
- obesity
- enlarged fat cells
- increased abdominal fat
- insulin resistance: set amount of insulin produces a subnormal effect
MNT goals and strategies for T2DM
- Achieve and maintain DBW
- Energy restricted diet
- diet should allow weight reduction of 1-2 lbs/week
Exercise goals and strategies
- glycemic control and weight loss
- lowers blood glucose and fattu acid levels; raises HDL levels
- Aerobics & strength training; mild or moderate exercise is prescribed at first
Mode of action of medications that end with -ide
stimulate insulin secretion by pancreas
Possible side effects of medicine for insulin secretion
- hypoglycemia
- weight gain
- GI side effects
- cramps
- allergic skin reactions
Mode of action of metformin
Inhibits liver glucose production
Possible side effects of metformin
- anorexia
- metallic taste
- GI side effects
- cramps
Mode of action of medicine that ends with -zone
increase insulin sensitivity
Possible side effects of medicine that ends with -zone
- fluid retention
- edema
- weight gain
- anemia
Mode of action of medicine like acarbose and miglitol
delays glucose absorption
Possible side effects of medicine
GI side effects
Cause of diabetic ketoacidosis
severe lack of insulin
Characteristics of diabetic ketoacidosis
- ketosis: acetone breath
- acidosis: hyperventilation
- hyperglycemia: polyuria
Blood glucose level of diabetic ketoacidosis
> 250 mg/dl
Blood pH of diabetic ketoacidosis
<7.3
Other symptoms of diabetic ketoacidosis
weakness, nausea, vomiting, and affected mental state
T or F: Diabetic ketoacidosis is more common in T1DM
True
Events leading to DKA
- increase ketones
- acidic plasma
- destruction of enzymes
- coma
- death
Events leading to hyperglycemia
- Hyperglycemia
- Polyuria
- Dehydrated cells
- shock
- coma
- death
Condition of sever hyperglycemia that usually develops in the absence of significant ketosis
hyperosmolar hyperglycemic state
T or F: hyperosmolar hyperglycemic state is more common in T2DM
True
Blood glucose level of hyperosmolar hyperglycemic state
> 600 mg/dl
Low blood glucose
hypoglycemia
T or F: Hypoglycemia is a result of appropriate management of diabetes
False: inappropriate
Symptoms of hypoglycemia
Hunger, sweating, shakiness, heart palpitations, slurred speech and mental confusion
Prolonged hypoglycemia may cause ___
brain damage
Which type of diabetes is hypoglycemia is commonly observed
T1DM
Disorders that affect the large blood vessels
Macrovascular diseases
Caused by accumulation of advanced glycation end product (AGEs) that accelerates atherosclerosis
macrovascular disease
example of AGEs (advanced glycation end products)
glucose/glucose fragments + CHON
Disorders that affect arterioles and capillaries
microvascular diseases
3 microvascular diseases
- diabetic retinopathy
- diabetic nephropathy
- diabetic neuropathy
Early background lesions in capillaries of the eye
retinopathy
Lesions in capillaries of the eyes result from
- microaneurysms, minute sacs formed on the capillary membrane at points of membrane weakness caused by insufficient numbers of endothelial cells
- hard exudates from capillary leakage
T or F: Diabetics are vulnerable to nerve damage and diminish transmission of nerve impulses that affect muscle function & sensory perception
true
what types of sugar do schwann cells convert glucose using enzymes aldose reductase and sorbitol dehydrogenase into?
sorbitol and fructose
T or F: sorbitol & glucose diffuse poorly across cell membranes and are osmotically active
True
earliest clinical sign of microalnuinuria
nephropathy
Basement membrane of glomerulus thickens and diffuse tissue involvement follows
nephropathy
