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MNT Prep > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

DSME

A

Diabetes self management education

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2
Q

DSMT

A

Diabetes self-management training

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3
Q

How is pancreas impacted?

A

Insulin secretion is decreased

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4
Q

How are kidneys impacted?

A

Less glucose reabsorption

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5
Q

How is muscle impacted?

A

Decreased glucose uptake

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6
Q

Islet Alpha cells impacted?

A

Increased glucagon secretion

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7
Q

How much of the population has DM?

A

9.3%

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8
Q

It is the ____leading cause of death in US but causes it indirectly.

A

7th

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9
Q

GDM found in what % of pregnancies?

What percentage more likely for mom to
Have DM later?

A

2-10%, now 17-20%

35-60% chance of getting DM in 10-20 years

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10
Q

How many people with DM worldwide?

A

1/12 people (western pacific a lot)

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11
Q

How often and what comes out to keep us informed on DM?

A

Every January the Diabetes Care (ALWAYS) comes out.

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12
Q

3 useable names for type 1 DM?

A

T1DM, DM1, immune mediated

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13
Q

2 names for type 2 DM?

A

T2DM or DM2

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14
Q

Characteristics of type 1?

A 
Autoimmune (B cells attacked)
5-10% of all cases 
Genetic related 
Rapid onset
Death from ketoacidosis
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15
Q

Characteristics of T2DM?

A 
90-95% of cases
Pancreas doesn't make enough or useable insulin
Genetic related 
80% are obese 
Death from HHNS
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16
Q

HHNS

A

Hyperglycemic hyperosmolar non-ketoic syndrome

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17
Q

Why is T2DM associated with obesity?

A

Lipoprotein lipase is stimulated by insulin so more fat can be stored in adipose.

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18
Q

What does insulin so

Cellular level?

A 
Glycogen synthesis 
Fatty acid synthesis 
Fatty acid esterification 
Lowers K in blood and raises K in cells 
Increase HCl secretion
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19
Q

High insulin levels= what are HCl and K levels?

A

Low blood K
High cellular K
More HCl in the stomach

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20
Q

Anti catabolic role of insulin

A

Stops proteolysis, lipolysis, gluconeogenesis, glycogenolysis

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21
Q

What is DKA?

A

Diabetic ketoacidosis from T1DM
Caused by inadequate insulin
Energy is made from fat
Leads to metabolic acidosis

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22
Q

What is HHNS?

A

Hyperglycemic hyperosmolar non-ketotic syndrome
BG at 600-2000 mg/dL
Treat with hydration and insulin

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23
Q

Hypoglycemia

A

BG less than 50 mg/dL

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24
Q

How to treat hypoglycemia?

A

If BG under 70, eat 15g CHO and test blood every 15 minutes until where you want

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25
Q

3 macrovascular complications?

A

CVD (low LDL and high TG)
Stroke
HTN

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26
Q

Non-insulin dependent tissues

A

Kidneys
Eyes
Nerves
RBC

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27
Q

What is a marker of long-term exposure to high BG on RBC?

A

Glycosylated Hb or A1C?

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28
Q

Microvascular problems?

A

Retinopthy from blood vessel damage (need DM/HTN control)
Nephropathy from glomerulus damage in 20-40% of DM cases
Neuropathy from less nerve function. In 60-70% DM cases. Autonomic and cardiac nerves impacted

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29
Q

Gastroparesis

A

Less nerves in stomach empties less often and lower glucose level to blood

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30
Q

What is a normal A1C reading?

A

5 A1C due to normal EAG levels

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31
Q

CGMS

A

Continuous Glucose Monitoring Systems

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32
Q

What is the DCCT study?

A

Diabetes control and complications trial

  • 1993 10-year study
  • intensive versus conventional care
  • intensive was better with pre-meal carb counting, specific insulin injections
  • increased glucose control means better A1C
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33
Q

What is the DPP?

A

Diabetes Prevention Program

- study showed pre diabetes can change to DM and counselor/exercise/diet can make a preventative difference

34
Q

What was the look AHEAD study?

A

Action for health in diabetes

Intensive lifestyle intervention used by DPP looked at 8-year weight loss of subjects

35
Q

Pathway of T1DM?

A

No glc in cell–> break fat and proteins for energy–> ketones

No glc–> feel hungry/weight loss–> polyphagia

Fruity breath, DKA, ketonemia, ketonuria

36
Q

Pathway of T2DM?

A

Some glc enters–> polyphagia(still feel hungry)–> weight gain–> HHNS

37
Q

Hyperglycemia pathway

A

High BG–> glucouria–> glc pulls water into blood–>polyuria–> dehydration–> polydipsia

38
Q

Pre diabetes BG level?

A

100-126ml/dL

A1C- 5.7-6.4%

39
Q

Diabetes BG level?

A

FBG over 126

A1C over 6.5%

40
Q

How long of BG level does A1C represent?

A

3-4 months because that is how long RBC lives

41
Q

Anacthosis nigricans

A

Black leathery dark skin on some peoples fold and joints (Indians, African Americans. )

42
Q

What was the ADAG study?

A

A1C derived average glucose study

Came up with mathematical relationship between EAG and A1C

Finger stick and regular monitoring

43
Q

Urine glucose (can’t be used as Dx)

A

Glucose will “only” be in urine once BG is over 250mg/dL

That is the renal threshold

44
Q

Urine ketones (not a Dx)

A

Only looked at for T1DM when BG consistently over 300mg/dL

45
Q

What does serum Na show?

A

Glucose in blood pulls H2O out of the cells into blood
Serum Na goes down (1.6 mEq for every 100mg/dL glc above normal)

Low serum Na could be a DM sign (osmotic diuresis)

High blood volume with low blood values and high BP

46
Q

Diabetes definition

A

Group of metabolic diseases with hyperglycemia from no insulin secretion, action or both.

Chronic disease managed by self or continuing care.

47
Q

What’s complications are you trying to avoid when using nutrition therapy to treat diabetes?

A

Normalize blood pressure, normalize blood lipid levels, and control blood glucose

48
Q

What are four major goals of nutrition therapy as treatment for diabetes?

A

Eating nutrient dense foods, individualizing diet by preferences and culture, only limit foods if backed up by research, and promote foods not nutrients.

49
Q

What are the goal levels for people with diabetes? ( A1C, LDL, TG, HDL, blood pressure)

A 
A1C- less than 7% 
LDL- less than 100
TG- less than 150
HDL- over 40 (me ) or 50 ( women)
BP- 140/90 mmHg
50
Q

What are the energy balance goals for overweight individuals with diabetes?

A

Meet physical activity guidelines, lose 7 to 8.5% bodyweight, and meet with registered dietitian frequently.

51
Q

What is the glycemic index?

A

Shows the effect on blood glucose that a food containing 50 g of carbohydrate has on the body. The number is compared to a glucose or white bread standard. Jenkins, Toronto.

52
Q

What are three major downfalls of the glycemic index?

A

It really depends on the rightness and cooking of food.
Blood glucose levels can differ from day today in the same person and differ between people.
The previous meal composition can change blood glucose reading.

53
Q

How do glycemic load and indexed differ?

A

Glycemic load depends on the actual portion size of a food, so carrots actually have a low glycemic load. The glycemic index deals with large amounts of food to contain 50 g of carbohydrate, so carrots are very high.

54
Q

What effect do protein rich carbohydrates have on the glucose and insulin?

A

They decrease blood glucose spike and increase insulin response. This would not be recommended for someone struggling with hypoglycemia.

55
Q

What effect does alcohol have on blood glucose?

A

Alcohol stops gluconeogenesis so it causes delayed hypoglycemia. Someone may need to use more insulin as a hyperglycemic medication while drinking.

56
Q

What is the major difference between exchange list and carb counting?

A

In the exchange list milk is 12 g carbohydrate and carb counting milk is 15 g carbohydrate.

57
Q

Why do type two diabetic’s sometimes use insulin?

A

Being allergic to oral agent, having hyperglycemia even after large amounts of oral agents, or having high hyperglycemia in the beginning.

58
Q

What are four different types of insulin?

A

Rapid, short, intermediate, and long. This describes the pattern and activity rate.

59
Q

Why do insulin doses differ?

A

Bodies respond differently and habituate overtime.

60
Q

What are the two regimens of insulin?

A

Continuous subcutaneous insulin infusion, which is a pump. Or multiple does insulin, which is more than three injections per day.

61
Q

CSII

MDI

A

Continuous subcutaneous insulin infusion

Multiple dose insulin

62
Q

What are the three delivery methods of insulin?

A

Pump, syringe, and pens.

63
Q

What are the three stages of the action of insulin?

A

Onset- when it begins to work

Peak- when it’s at its greatest effect. Max work ability.

Duration- how long it stays in the system.

64
Q

What are the two phases of insulin acting in your body?

A

First phase: the big release of insulin, stops liver from making glucose, stops glucose bike after eating, starts after two minutes of eating.

Second phase: works until normal blood glucose is reached.

65
Q

Define basal.

A

It is the background insulin that is working to normalize blood glucose between meals. Pancreas is away spitting out a little bit.

66
Q

What is bolus?

A

It is the insulin that is secreted to match the amount of food you’re eating. It is covering the cost of food. It represents the first and second phase.

67
Q

Define basal/Bolus.

A

It is used with healthcare professionals to describe an insulin pump or more than four injections per day. It is a form of intensive therapy.

68
Q

Are three new forms of insulin on the market?

A

Earlobe monitor Glucotrack
Rapid acting human insulin powder(Afrezza)
Smart insulin patch which is an artificial pancreas.

69
Q

Blood glucose “GOALS” for T1DM?

A

80-130mg/dL before a meal
Less than 180 mg/dL 2 hours after meal
A1C less than 7%

70
Q

What is target glucose when managing T1DM?

A

A specific number within the ADA recommended glucose goal.

71
Q

What is the current gold standard for insulin protocols?

A

MDI

Lantus for background and Humalog for Bolus (30-90 min)

72
Q

What is the T1DM insulin dose for normal wt?

A

.5-1.0 unit/kg/day

(Half for basal and half for Bolus, so divided between meals)

T2dm? .5 to 1.2 units/kg/day

73
Q

Define and other name for rebound hyperglycemia?

A

Somogyi Effect

Too much insulin at night so hypoglycemia in middle of the night causes glucagon to raise BG a lot by morning.

74
Q

Define dawn phenomenon

A

High morning BG because too much CHO at night or too little insulin to cover nightly meal. BG steadily increased during the night, no hypoglycemic drop.

75
Q

4 examples of insulin resistant people. More or less SSi?

A

T2DM, corticosteroid use, infection, illness (severe)

Need more insulin

76
Q

2 examples of insulin sensitive people. More or less SSi?

A

Less SSi needed

T1DM and kidney failure

77
Q

Are the 2 core defects of type two diabetes?

A

beta cell dysfunction and insulin resistance

78
Q

5 steps to T2DM tx?

A

Lifestyle changes
Add med: metformin
Add med: insulin or OHA if A1C is over 9%
Add med: basal or intense insulin or OHA
Insulin: intensified (BG over 300-350 or A1C 10-12%)

79
Q

What is the goal of MNT and OHA?

A

Slow the progression of disease!

80
Q

3 main ways DM meds work?

A

Induce insulin secretion from pancreas
Slow the movement of food through GI tract (stomach)
Increase insulin sensitivity to move glc from blood to tissues/cells

81
Q 
Primary site of action for...
Sulfonylureas 
DPP-4 inhibitors
Biguanides 
TZDs
SGLT-2 inhibitors
A

Pancreas- more insulin secretion
Stomach- slow food digestion/move
Liver- decrease liver glc output
TZDs- increase insulin sensitivity in liver, adipose and muscle
Kidney- block Na/glc transport system. Increase glc urine output.

82
Q

Two types of TZD that are now only used as last resort?

A

Actos and avandia

Cause increased CVD And CHF risk. Bladder cancer?

MNT Prep (27 decks)

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