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Therapeutics II > Block 3: Diabetes I > Flashcards

Block 3: Diabetes I Flashcards

1
Q

What is diabetes mellitus?

A
  1. Metabolic disorders characterized by hyperglycemia
  2. Defects in fat, carb, and protein metabolism
  3. Defects in pancreatic insulin production, insulin sensitivity in the tissues or both
  4. Progressive disorder which results in chronic complications
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2
Q

What are the complications of diabetes?

A
  1. Heart disease and stroke
  2. HTN
  3. Blindness
  4. Kidney dx
  5. Neurologic dx
  6. Amputations
  7. Dental dx
  8. Poor pregnancy outcomes
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3
Q

Diabetes in the ___ leading cause of death in the US?

A

8th

Risk of death twice that of people without diabetes

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4
Q

What is the function of glucose in the body?

A

Provide fuel for the tissues of the body

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5
Q

What is the normal fasting glucose level?

A

70-99 mg/dL

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6
Q

What is the function between the pancrease?

A

Produces hormones that regulate blood glucose levels in the body

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7
Q

What is the difference betwen insulin and glucagon?

A

Insulin: b-cells, decreases glucose in bloodstream
Glucagon: a-cells, increases glucose in bloodstream

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8
Q

What is insulin important?

A

Glucose is the major energy source for the human body. Insulin is necessary to transport glucose into all tissues and organs EXCEPT the brain.

There is a finite amount of beta-cells in the pancrease

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9
Q

Describe the pharmacology of insulin?

A
  1. Anabolic and anti-catabolic hormone
  2. Major role in protein, carbohydrate and fat metabolism
  3. Lowers blood glucose levels by
    * Stimulating peripheral glucose uptake
    * Inhibits lipolysis and proteolysis
    * Enhances protein synthesis
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10
Q

What are the hormones that oppose insulin?

A
  1. Glucagon
  2. Epinephrine
  3. Growth hormone
  4. Cortisol
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11
Q

What is the post prandial state?

A

Hyperglycemia -> Insulin release from beta cells in the pancreas

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12
Q

How does insulin act during post-prandial state?

A
  1. Facilitates uptake of glucose, fatty acids, and amino acids
  2. Promotes conversion to storage forms
    * glucose -> glycogen
    * fatty acids -> triglycerides
    * amino acids -> protein
  3. Inhibtis breakdwon of glycogen in the liver
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13
Q

What occurs in the pre-prandial state?

A

Hypoglycemia ->
1. Inhibits insulin release
2. Promotes release of glucagon and other hormones from alpha cells in the pancreas
3. Causes breakdown of glycogen, protein, and triglycerides to maintain a minimum blood glucose concentration for the brain
* GLYCOGENoLYSIS: Glycogen -> glucose
* GLUCOneoGENESIS: Amino acids -> glucose
* Decrease uptake of glucose by tissues
* Triglycerides -> free fatty acids (alternate fuel source)

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14
Q

What is basal insulin?

A

Steady, low level of insulin produced all trhoughout the day

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15
Q

What is bolus insulin?

A

Higher amounts of insulin that are produced when blood glucose is high, peaks which occur after food intake

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16
Q

What are the classifications of diabtes?

A
  1. T1DM
  2. T2DM
  3. GDM
  4. Drug induces, MODY
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17
Q

What is the pathogenesis of T1DM?

A

Autoimmune desctruction of pancreatic beta-cells leading to the absolute lack of insulin and amylin secretion

No insulin released in response to hyperglycemia

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18
Q

How does the body compensate to provide fuel to cells in T1DM?

A

GLYCOGENoLYSIS (liver glycogen -> glucose)
Hepatic GLUCOneoGENESIS (amino acids -> glucose)
Lipolysis (fat -> fatty acids)

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19
Q

What are the risk factors of T1DM?

A
  1. Genetic predisposition
  2. Exposure to environmental triggers
  3. Autoimmune disorders (Hashimoto’s Thyroiditis, Graves, Addisons, celiac)
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20
Q

What are the lab presentations of T1DM?

A

Onset is rapid

  1. Less than 30
  2. Low body weight
  3. C-peptide is low or absent
  4. Autoantibodies often present
  5. 3 Ps
  6. Ketons present -> DKA
  7. Need for insulin therapy immediately or required
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21
Q

What are the clincal presentations of T1DM?

A
  1. 3 Ps
  2. Weight loss
  3. Kussmaul breathing with “acetone” breath
  4. Increased plasma osmolality (typically >300)
  5. Decreased pH (<7.3)
  6. Potassium levels may initially appear normal or elevated, but usually there is a large total-body potassium deficit
  7. Dehydration and volume depletion
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22
Q

What is the pathogenesis of T2DM?

A

Heterogenous disorder with multiple defects -> impaired insulin secretion due to beta-cell dysfunction

Insulin Resistance ->
* Impaired glucose utilization
* Increased hepatic glucose output
* Increased circulating glucose -> stimulates beta cells to produce more insulin

Relative lack of insulin with decreased secretion over time

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23
Q

What are the risk factors of T2DM?

A
  1. Age
  2. Obesity
  3. Physical inactivity
  4. Family history
  5. Race
  6. Impaired fasting glucose
  7. Impaired glucose tolerance
  8. Gestational diabetes
  9. Delivery baby weighing over 9 pounds
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24
Q

What are the lab presentations of T2DM?

A
  1. Usually overweight
  2. C-peptide usually normal or high
  3. > 40YO
  4. Autoantibodies rarely present
  5. Symptoms may or may not be present
  6. Ketones usually absent
  7. Insulin resistance often present
  8. Need for insulin therapy is usually delayed
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25
Q

What are the presentations of metabolic syndrome?

A
  1. Obesity
  2. Athersclerosis
  3. DLD
  4. HTN
  5. Increase plasminogen activator-1 (PAI-1)
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26
Q

What are the diagnostic criteria for metabolic syndrome?

A

Any 3 of the following:
* Central obesity: > 40 inches in men, > 35 inches in women
* Raised TG: >150 mg/dl
* Reduces HDL: <40 mg/dl in men, <50 mg/dl in women
* Raised BP: >130/85
* Raised fasting plasma glucose: >100 mg/dL

27
Q
A
28
Q

What is gestational diabetes?

A

Glucose intolerance first recognized during the 2nd or 3rd trimester of pregnancy

During the 1st trimester should be classified as having pre-existing pre-gestational diabetes

29
Q

What are the consequences of GDM?

A

Mother: 30-50% develop T2DM later in life
Infant:
* At birth: macrosomic birth, neonatal hypoglycemia, shoulder dystocia, obstetric emergency
* Jaundice
* Respiratory distress syndrome
* Increased risk of developing DM later in life

30
Q

What are the risk factors of GDM?

A
  1. Parent, brother, or sister with T2DM
  2. African American, Native American, Asian, Hispanic/Latino, or Pacific Islander
  3. 25 years old or older
  4. Overweight
  5. Gestational diabetes during a previous pregnancy
  6. Given birth to a baby weighing more than 9 pounds
  7. Pre-diabetes
31
Q

What is the treatment for GDM?

A

Lifestyle: Diet, physical activity
Insulin: first line
* Oral med (metformin and glyburide) should not be used first

When metformin is used to treat Polycystic Ovary Syndrome and induce ovulation, discontinue metformin by the end of the first trimester

32
Q

When should you screen for T2DM?

A
  1. Screen all adults 35 years old or older at least every 3 years
  2. Consider screening all overweight adults with one or more additional risk factors earlier and/or more often
  3. Screen patients with Pre-diabetes (A1c >5.7%, IGT, or IFG) annually
  4. Screen women with GDM or who delivered a baby > 9 lbs at least every 3 years
  5. Patients with HIV at least annually
33
Q

How should you screen diabetic the children?

A

Screening every 3 years beginning at age 10 or at puberty for overweight children with 1 or more risk factors

34
Q
A
35
Q

How do you screen for ht early abnormal glucose metabolism?

A
  1. FPG 110-125 mg/dL or A1c 5.9-6.4%
  2. Preconception planning (risk factors, consider all patients)
  3. Before 15 weeks gestation (risk factors, consider all patients)
36
Q

How do you screen for GDM at 24-28 wk gestination?

A
  1. OGTT
  2. Screen all patients who have NOT been previously identified as having met the diagnostic criteria for
    * Pre-existing prediabetes or diabetes
    * Early abnormal glucose metabolism
37
Q

How should you screen for prediabetes/diabetes after delivery?

A
  1. Resolves postpartum
  2. Test women with GDM for prediabetes or diabetes at 4-12 weeks post-partum
    * 75g OGTT
    * Treat prediabetes with intensive lifestyle modifications and metformin
  3. Screen for prediabetes and diabetes at least every 3 years for life in women with a Hx of GDM
  4. Increased risk of developing T2DM or glucose intolerance later in life
38
Q

What are the tests for screening pre-diabetes and diabetes?

A
  1. Fasting plasma glucose (FPG)
  2. Oral glucose tolearnce test (OGTT)
  3. A1c
39
Q

What are recommended diabetes screening tests for specific disease states?

A
  1. Recommended for Children with symptoms suggestive of acute onset T1DM: Fasting Plasma Glucose (FPG)
  2. Recommended for Children with Cystic Fibrosis: OGTT
  3. Preferred for Diagnosis of Post-transplantation DM: OGTT
  4. Preferred for Pregnant Adults: OGTT
40
Q

What are the tests used to diagnose diabetes?

A
  1. Fasting Plasma Glucose (FPG)
  2. Random Plasma Glucose
  3. Oral Glucose Tolerance Test (OGTT)
  4. Hemoglobin A1c (A1c)
41
Q

Based on pre-diabetes screening what are the impared lab indications?

A
  1. Impaired Glucose Tolerance (IGT): 2-hour post-load (75 gm) glucose during OGTT: 140-199 mg/ml
  2. Impaired Fasting Glucose (IFG): Fasting plasma glucose: 100-125 mg/dl
  3. High Risk for DM: A1c 5.7-6.4%
42
Q

Whare the diagnostics for diabetes?

A
  1. Fasting plasma glucose: ≥ 126 mg/dl
  2. Symptoms of diabetes + random plasma glucose: ≥ 200 mg/dl
  3. 2-hour post-load (75 gm) glucose during OGTT: ≥ 200 mg/dl
  4. Hemoglobin A1c: ≥ 6.5%
43
Q

Why is pre diabtes important?

A
  1. Increased risk of developing diabetes
  2. Diet and exercise can help prevent or delay the development of diabetes (DPP)
44
Q

How should you monitor diabetes therapy?

A
  1. Monitor glycemic control
  2. Montior long-term complications
45
Q

How do you monitor glycemic control?

A
  1. A1c
  2. Continuous glucose monitoring
  3. Time in Range (TIR) and/or Glucose Management Indicator (GMI)
  4. Finger Stick Blood Glucose Monitoring (BGM)
  5. Symptoms of hyper- and hypoglycemia
46
Q

How do you monitor long term complications?

A
  1. Retinopathy: Eye exams (annually)
  2. Nephropathy: Kidney function (annually)
  3. Neuropathy: Comprehensive foot exams (annually)
  4. Cardiovascular related disorders:
    * Blood pressure (each visit)
    * Lipids (annually)
47
Q

When should Blood Glucose Levels be tested?

A
  1. vary testing throughout the week
  2. Fasting: upon waking, before mels, at bed
  3. Postprandial
  4. Prior to exercise
  5. Symptomatic
48
Q

What are the blood glucose goals?

A
49
Q

What is an A1c?

A
  1. Rate of formation of Hgb A1c is dependent upon average glucose levels during life-span of hemoglobin (about 90 days)
  2. Reflects average blood glucose over the last 3 months
50
Q

How often should you montior an A1c?

A

At goal: test every 6 months
NOT at goal: test every 3 months

51
Q

What is estimated average glucose?

A

eAG(mg/dl)=28.7 X A1c - 46.7

“translates” A1c into a number patients can more easily understand

A1c 7% = eAG 154 mg/dl

52
Q

What are the approaches to individualizing glycemic targets?

A
  1. Hypoglycemic risk
  2. DIsease duration
  3. Life expectancy
  4. Vascular complications
  5. Cormorbidiites
  6. Patient preference
  7. Resources and suppor system
53
Q

What is the DPP?

A

Lifestyle modifications and metformin can reduce the chances a person with IGT will develop T2DM

Life style modifications&raquo_space;> metformin

54
Q

What are the non-pharms of diabetic prevention?

A
  1. Weight loss: 7%
  2. Physical activity: Increase moderate intensity physical activity to at least 150 minutes/week
55
Q

How qualifies diabetic prevention with metformin?

A

Patients age 25 to 59 with pre-diabetes:
* BMI > 35
* FBS >110
* A1c > 6%
* Women with Hx of GDM

56
Q

How do you prevent CVD in patients with prediabetes?

A
  1. Screen of risk facotrs
  2. Monitor for statin induces T2DM (stopping is not recommended)
  3. Pioglitazole (Lowers risk of stroke and MI in patients with prediabetes, insulin resistance, AND Hx of stroke)
57
Q

What is the first line treatment for diabetes?

A
  1. Diet
  2. Physical activity
  3. Pharmacological agents
  4. Comorbidity management

No Drug Can Replace a Good Well Balanced Diet

58
Q

What is the purpose for medical nutrition therapy?

A
  1. May help diabetes by imporving overall health and achive/maintaing labs
  2. Delay or prevent complications from diabetes
59
Q

What are the general healthy eating guidelines?

A
  1. Eat a variety of foods
  2. Maintain a healthy weight
  3. Choose a diet low in fat, saturated fat, and cholesterol
  4. Choose a diet high in fiber (fruits, vegetables, and whole grains)
  5. Choose a diet with moderate amounts of carbohydrates.
  6. Limit sugars and refined starches (reg. soda, white bread, etc.)
  7. Limit sodium intake
  8. Limit alcohol intake
60
Q

How can we personilze meal plan?

A
  1. Eating patterns
  2. Content of meals (macros)
  3. Portion control
61
Q

What does a serving of carbs look like?

A

12 to 15 grams of carbohydrates:
* Milk—12 gm
* Bread/starch/fruit—15 gm
* Vegetables—5 gm
* Fat/meat—0 gm

62
Q

What are the benefits of physical activity?

A
  1. Reduce CV risk factors
  2. Manages weight
  3. Improves glucose control
  4. Improves overall health
63
Q

What are the physical activity goals in different patient populations?

A

Children: 60 min/day moderate-vigorous intensity aerobic activity
Adults: 150 min/week moderate-vigorous intensity aerobic activity
Older: Additional activity to improve flexibility and balance 2-3 times per week

64
Q

Describe cut offs of overweight/obese tx?

A

Therapeutics II (30 decks)

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