Diabetes Flashcards

1
Q

What is Diabetes Mellitus

A

a group of metabolic diseases - inability to produce sufficient amounts of insulin or to use it properly, or both

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2
Q

What is the result of diabetes mellitus

A

hyperglycemia

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3
Q

What is hyperglycemia

A

high blood glucose - BG levels poorly managed, diabetic ketoacidosis, hyperosmolar nonketotic syndrome

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4
Q

What is hypoglycemia?

A

low blood glucose - too much insulin, too little carb, missed meals, excessive or poorly planned exercise

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5
Q

What is hypersmmolar syndrome

A

your body tries to rid itself of of the excess blood sugar by passing it into your urine

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6
Q

What are the key factors in the development of the complication

A

impaired glucose clearance from the circulation and an increase in the production of glucose by hepatocytes and portal adipocytes

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7
Q

What are microvascular diseases

A

retinopathy, nephropathy

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8
Q

What are macrovascular diseases?

A

cardiovascular, cerebrovascular

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9
Q

What are neuropathies

A

Autonomic and peripheral - when nerve endings are exposed to high blood glucose over time, those nerve endings lose function

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10
Q

What is ketoacidosis

A

muscle cells are not able to get enough glucose in because of insulin resistance, switch to fatty acid metabolism which produces ketone bodies

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11
Q

Diabetes afflicts ______ people in the US. Approximately ______ are undiagnosed and ____ with pre diabetes.

A

~34 million; 25%; ~88 million

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12
Q

What are some reasons for the epidemic?

A

increasing overweight and obesity, increasing sedentary lifestyle, aging of population

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13
Q

What are some risk factors for diabetes

A

age >/= 45 years, BMI >/= 25 kg/m^2 or central adiposity (defined by waist circumference), habitual physical inactivity, having a first degree relative with DM, african american latino native american asian american or pacific islander race/ethnicity

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14
Q

What are the categories of diabetes

A

Type 1: beta cell destruction leading to insulin deficiency
Type 2: ranges from insulin resistance to insulin deficiency
Gestational

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15
Q

what is type 1 diabetes

A

A. immune mediate (autoimmune disease) - T lymphocytes attack beta-cells labeled with antigens
B. Idiopathic

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16
Q

What is type 2 diabetes

A

could include insulin secretion defect, insulin resistance, or both; strong genetic influence

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17
Q

What is gestational diabetes

A

glucose intolerance on with pregnancy; fetal hormonal secretions may impact insulin-receptor binding in the mother; increase mother BG -> increase Fetal BG -> increase fetal fat deposits

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18
Q

What is glucose tolerance

A

assessment of physiological response to a normal glucose load

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19
Q

what does glucose tolerance consist of

A

Normal response by the pancreas
- secretion of insulin
- stop secreting glucagon
Normal response of muscle and adipose tissue to insulin
- insulin stimulated glucose uptake

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20
Q

describe the molecular pathway responsible for insulin function

A

Insulin activates insulin receptor (IR)
IR associates with IRS proteins
IRS proteins activate PI3 kinase
PI3 kinase activates AKT
AKT facilitates:
- glycogen synthesis
- glucose intake
- protein synthesis
- cell growth, proliferation
AKT prevents:
- gluconeogenesis

21
Q

What is fasting plasma glucose

A

measures glucose levels in a person who has been fasting for at least 8 hours

22
Q

What is fasting plasma glucose

A

measures glucose levels in a person who has been fasting for at least 8 hours

23
Q

What is the 75 g oral glucose tolerance test

A

requires fasting before drinking a glucose solution. Following a 2 hour waiting period, blood is drawn

24
Q

What is the hemoglobin A1C test

A

does not require fasting, and measures the blood level of glycosylated hemoglobin over the past 2 to 3 months

25
Q

What is insulin resistance

A

normal amounts of insulin are inadequate to produce normal insulin response in adipose, muscle, and liver tissue; contributes to elevated BG levels

26
Q

Results of lack of insulin response in muscle and liver

A

reduced glucose uptake in skeletal muscle
inability to inhibit glycogenolysis and GNG in liver

27
Q

What is the primary cause of Type 2 Diabetes?

  1. inactivity
  2. hypercaloric diet
  3. genetic predisposition
  4. inflammation
  5. smoking
  6. air pollution
A
  1. inflammation
28
Q

What are adipocytes

A

major cells in fat tissues:
- storage of lipids, carbohydrates
- secretion of inflammatory mediators

29
Q

What are hepatocytes

A

(70-80% of the liver mass):
- protein synthesis and storage
- carbohydrate metabolism
- synthesis of cholesterol, bile salts, and phospholipids
- detoxification, modification and excretion of exogenous and endogenous substances
- secretion of inflammatory mediators

30
Q

What is another reason for insulin resistance other than inflammation?

A

hyperglycemia and hyperlipidemia - causes stress to ER and mitochondria, induces Reactive Oxygen Species (ROS) –> ER stress and ROS further activates MAP kinases such as JNK (inhibits insulin signaling

31
Q

What can cause endothelial dysfunction?

A

high serum glucose levels induce reactive oxygen species

32
Q

Inflammatory complications of diabetes: Kidney Failure

A

caused by excessive expression of inflammatory mediators and exposure to ROS. Will damage the endothelium

33
Q

Inflammatory complications of diabetes: eye complications

A

retinopathy (loss of blood supply)

34
Q

Inflammatory complications of diabetes: diabetic wound

A

reduced ability in wound repair because reduced levels and activities of progenitor cells and blood supply

35
Q

What are signs and symptom’s of diabetes

A

polydipsia (excessive thirst)
polyuria (frequent urination)
polyphagia (increase appetite)
infections and cuts that are slow to heal
blurry vision
fatigue

36
Q

_____% of those with T2DM do not know it

A

25%

37
Q

What does a physical exam focus on?

A

potential diabetes complications:
- elevated resting HR
- loss of sensation
- loss of reflexes (esp. lower extremities)
- foot sores or ulcers with poor healing
- excessive bruising
- retinal vascular abnormalities

38
Q

Cardiovascular exercise testing is indicated for those with one or more of _______

A
  • age > 40 yr diabetics with or without CVD risk factors
  • age >30 yr diabetics and
    type 1 or type 2 diabetes for >10 yr, hypertension, dyslipidemia, retinopathy, nephropathy
39
Q

What should be tested 1-2 times a year in diabetic adults >45 yrs?

A

HbA1C testing, dilated eye exam, foot exam, blood pressure, blood lipid assessment, renal functioning testing

40
Q

What is medical nutrition therapy

A

may ultimately focus on large weight loss from a complete meal replacement diet or bariatric surgery

41
Q

Oral glucose lowering medication types

A

sulfonylureas (first and second gen)
Biguanides (metformin)
Dipeptidylpeptidase-4 inhibitors
Alpha-glucosidase inhibitors
Insulin

42
Q

What is sulfonylureas (first and second gen)

A

increases insulin production by the beta cells in the pancreas

43
Q

What is Biguanides (metformin)

A

decreases hepatic production of glucose

44
Q

What is Dipeptidylpeptidase-4 inhibitors

A

prolong and enhance the activity of the insulin by limiting its breakdown

45
Q

What is Alpha-glucosidase inhibitors

A

reduce the rate of digestion of carbs in the proximal small intestine, primarily lowering postprandial glucose concentrations as they inhibit intestinal alpha-glucosidase enzymes

46
Q

What is insulin

A

the last line of treatment and is reserved for those patients who fail to respond adequately to a combo of orals and injectable antidiabetic agents

47
Q

Why do we give T2DM patients insulin if they still produce it?

A

insulin has many pathways of action to cause glucose uptake into cell

48
Q

Which diabetic medication could be contraindicated for exercise?

  1. insulin
  2. sulfonylurea
  3. biguanides
  4. glucosidase inhibitors
A
  1. insulin
    exercise and insulin together can significantly decrease blood glucose causing diabetic coma. Have to wait 1 hour after insulin injection before exercise
49
Q

How does exercise increase glucose uptake for diabetics?

A

exercise induces an increase in glut4 transporter translocation from separate storage sites
glucose uptake is increased in active muscle fibers, but not in inactive muscle