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Biochemistry Exam #3 > Diabetes Mellitus Type 1 and 2 > Flashcards

Diabetes Mellitus Type 1 and 2 Flashcards

1
Q

What is the only way by which all disorders of Diabetes Mellitus are related?

A

Hyperglycemia

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2
Q

What are the two types of primary DM? Describe the onset age and metabolic defects that categorize each (hint: Type 2 DM has two).

A

Type 1 DM: juvenile-onset
- Autoimmune destruction of pancreatic beta-cells leading to lack of insulin production

Type 2 DM: adult-onset
- Insulin resistance AND pancreatic beta-cell dysfunction; non-autoimmune etiology

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3
Q

What are the three onset symptoms of Type 1 DM? Describe why each symptom occurs.

A
  • Polyuria: too much glucose for the kidneys to reabsorb so glucose is excreted in the urine
  • Polydipsia: renal water loss triggers thirst receptors in brain
  • Polyphagia: catabolism of proteins and fats leads to negative energy balance and increased appetite
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4
Q

What are the three antibodies detected in blood serum of Type 1 DM patients?

A
  • Anti-islet cell antibodies
  • Insulin antibodies
  • GAD65 antibodies
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5
Q

In uncontrolled Type 1 DM, what are the three metabolic changes present?

A
  • Hyperglycemia
  • Hypertriacylglyceridemia
  • Ketosis
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6
Q

What is the typical I/G ratio of a Type 1 DM patient?

A

Low I/G ratio because lack insulin - in fasting state

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7
Q

Describe Hyperglycemia in uncontrolled Type 1 DM patients - increased production versus decreased clearance?

A

Increased production:

  • Liver glycogenolysis (early on)
  • Gluconeogenesis, specifically use of muscle protein (results in muscle loss)

Decreased clearance:

  • GLUT4 receptors in muscle and adipose are insulin-dependent so without insulin, they are immobile and glucose is not taken up by the muscle
  • Glycogen in muscle
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8
Q

Describe Hypertriacylglyceridemia in uncontrolled Type 1 DM patients - increased production versus decreased clearance?

A

Increased production:

  • Excessive lipolysis due to increased HSL activity (activated by low I/G ratio)
  • Fatty Acyl CoA repackaged into VLDLs from liver

Decreased clearance:
- LPL activity is inhibited because there is no insulin for LPL synthesis

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9
Q

Describe Ketosis in uncontrolled Type 1 DM patients - why does this occur and what can it lead to acutely?

A

Excessive lipolysis causes highly active beta-oxidation > produces large amounts of Acetyl CoA which is the starting substrate of ketogenesis > high production of ketone bodies
- Can lead to DKA when combined with dehydration (from hyperglycemia)

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10
Q

What are the two acute complications of Type 1 DM?

A
  • Diabetic Ketoacidosis (DKA)

- Hypoglycemic shock

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11
Q

What are the three triggers often seen with DKA?

A
  • Low insulin
  • Illness
  • Stress (triggers Epi release causing increased HSL activity)
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12
Q

What are the six signs/symptoms of DKA?

A
  • Urinary ketones
  • Fruity odor to breath
  • Rapid breathing
  • Shock
  • Coma
  • Death
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13
Q

What are the two recommended treatments for DKA and how does each work?

A
  • IV insulin: promote glucose uptake/inhibit lipolysis

- IV fluids: relieve dehydration

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14
Q

What do the blood results of a DKA patient look like? (hint: 3 important results)

A
  • Elevated glucose levels
  • Elevated ketone bodies
  • Decreased blood pH
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15
Q

In DKA patients, why is blood pH decreased?

A

In DKA, there are elevated ketone bodies and 2/3 of ketone bodies are acidic

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16
Q

What are the four triggers of hypoglycemic shock and following what event do they typically occur?

A

AFTER AN INSULIN INJECTION…

  • Skipping a meal
  • Eating at wrong time
  • Strenuous exercise
  • Medication
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17
Q

Why does it matter that the hypoglycemic shock triggers occur post-insulin injection?

A

After the insulin injection, the Type 1 DM patient will be in fed state but without a meal (carbs), the fed state pathways will not be able to run

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18
Q

How does a patient with hypoglycemic shock typically present symptomatically?

A

Shaky, nervous, tired, sweaty/chilled, hungry, confused irritable, impatient

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19
Q

What are the three recommended treatments for hypoglycemic shock and how does each work?

A
  • Eat something with high glycemic index
  • Glucagon injection (to lower I/G ratio)
  • Arrange IV glucose
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20
Q

Is Type 1 or Type 2 DM more influenced by genetics?

A

Type 2 DM

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21
Q

In uncontrolled Type 2 DM, what are the two metabolic changes present?

A
  • Hyperglycemia

- Hypertriacylglyceridemia

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22
Q

What are the three Phases in the time development of Type 2 DM?

A
  1. Insulin resistance and hyperinsulinemia (high insulin)
  2. Pancreatic beta-cell dysfunction
  3. Further progression of pancreatic beta-cell dysfunction
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23
Q

What is the most common cause of insulin resistance? What are the two tissue types most affected by insulin resistance?

A

Obesity

  • Muscle tissue
  • Adipose tissue
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24
Q

Describe Hyperglycemia in uncontrolled Type 2 DM patients - increased production versus decreased clearance?

A

Same as Type 2 DM

Increased production:

  • Liver glycogenolysis (early on)
  • Gluconeogenesis, specifically use of muscle protein (results in muscle loss)

Decreased clearance:
- GLUT4 receptors in muscle and adipose are insulin-dependent so with low insulin, they are immobile and glucose is not taken up by the muscle

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25
Q

Describe Hypertriacylglyceridemia in uncontrolled Type 2 DM patients - increased production versus decreased clearance?

A

Increased production:

  • Very high lipolysis due to increased HSL activity (activated by low I/G ratio)
  • Fatty Acyl CoA repackaged into VLDLs from liver (less severe than Type 1 DM)

Decreased clearance:
- LPL activity is inhibited because there is less insulin for LPL synthesis

26
Q

What is the acute complication of Type 2 DM?

A

Hyperosmolar Syndrome

27
Q

What are the three triggers often seen with Hyperosmolar Syndrome?

A
  • Stress
  • Alcohol consumption
  • Infection/illness
28
Q

What are the ten signs/symptoms of Hyperosmolar Syndrome?

A
  • Fruity odor on breath
  • Polydipsia
  • Polyuria
  • Dehydration
  • Fatigue
  • Confusion
  • Rapid breathing
  • Blurred vision
  • Vomiting
  • Weakness
29
Q

What do the blood results of a Hyperosmolar Syndrome patient look like? (hint: 3 important results)

A
  • Very elevated glucose level
  • Normal ketone bodies
  • Normal blood pH
30
Q

What are the two recommended treatments for Hyperosmolar Syndrome?

A
  • IV insulin: promote glucose uptake/inhibit lipolysis

- IV fluids: relieve dehydration

31
Q

Why can’t Type 2 DM patients experience DKA, but Type 1 DM patients can?

A

Type 2 DM patients have some insulin being produced (10-25%) so there is high beta-oxidation, gluconeogenesis and ketogenesis, but it is not as excessive as it is with Type 1 DM (no insulin to inhibit HSL)

32
Q

What is the recommended treatment for Type 1 DM?

A

INSULIN ALWAYS NEEDED

33
Q

What is the first recommended treatment for Type 2 DM? If that does not work, what is the alternative treatment?

A

Lifestyle and diet changes

- Then oral hypoglycemic drugs

34
Q

What is AMPK and how is it regulated?

A

AMPK serves as an energy monitor; when it is active, ATP-producing pathways are activated and ATP-consuming pathways are inhibited

  • Activated: low ATP/high AMP
  • Inhibited: high ATP/low AMP
35
Q

What are the three ATP-producing processes activated by AMPK?

A
  • Glycolysis
  • Beta-oxidation
  • Glucose uptake
36
Q

What are the four ATP-consuming processes inhibited by AMPK?

A
  • Glycogenesis
  • FA synthesis
  • Protein synthesis
  • Cholesterol synthesis
37
Q

How does AMPK treat Type 2 DM patients?

A

AMPK function increases GLUT4 activity to help lower hyperglycemia (insulin-independent way)

38
Q

How does Metformin work to treat Type 2 DM patients?

A

Metformin is thought to inhibit AMP deaminase, which breaks down AMP
- This inhibition leads to higher AMP levels and activation of AMPK

39
Q

What are the six function of GLP-1 that lower blood glucose?

A
  • Inhibits break down of beta-cells
  • Promotes beta-cell growth
  • Increases insulin secretion
  • Decreases glucagon secretion
  • Inhibits appetite
  • Delays gastric emptying
40
Q

What are the six function of GLP-1 that lower blood glucose?

A
  • Inhibits break down of beta-cells
  • Promotes beta-cell growth
  • Increases insulin secretion
  • Decreases glucagon secretion
  • Inhibits appetite
  • Delays gastric emptying
41
Q

What are the two incretin-based approaches to manage Type 2 DM?

A
  • Incretin mimetics

- DPP-4 inhibitors

42
Q

How do incretin mimetics work (5 things)? What is an example of an incretin mimetic?

A
  • Minimize beta-cell exhaustion
  • Increase insulin release after meals
  • Decrease glucagon levels
  • Decrease in appetite
  • Reduced post-meal hyperglycemia

Example: Byetta

43
Q

How do DPP-4 inhibitors work?

A

Inhibit DPP-4 (cleaves GLP-1), which increases the half-life of GLP-1

44
Q

What is the OGTT and what does it entail?

A

Oral Glucose Tolerance Test entails 3-day carb diet then 8 hours of fasting, then oral glucose administered and blood drawn 2 hours later

45
Q

Why is a 3-day carb diet necessary for the OGTT?

A

High carb diet = high insulin, which means that glycolytic enzymes will be in adequate amounts

46
Q

What are the advantages (1) and disadvantages (1) of OGTT?

A
  • Advantages: easy for patient

- Disadvantages: only used to diagnose gestational diabetes

47
Q

What is the cut-off level for DM diagnosis for the OPTT test?

A

200 mg/dL or above

48
Q

What is the FPG test and what does it entail?

A

Fasting Plasma Glucose entails 8 hours of fasting then blood draw

49
Q

What are the advantages (1) and disadvantages (2) of FPG?

A
  • Advantages: easy for patient
  • Disadvantages: can be affected by outside factors (other medications, smoking); less reliable because only measures acute levels
50
Q

What is the cut-off level for DM diagnosis for the FPG test?

A

126 mg/dL or above

51
Q

What is the HbA1c test and what does it entail?

A

HbA1c entails a single blood draw to check glycated form of HbA

52
Q

What are the advantages (3) of HbA1c?

A
  • Easy for patient (no fasting required)
  • Sample stability
  • Measures blood glucose for previous 6-8 weeks (can evaluate patient compliance)
53
Q

Which primary DM is antibodies used to diagnose and why?

A

Antibodies test for Type 1 DM because insulin antibodies are only present with Type 1 DM

54
Q

Which primary DM is C-peptide levels used to diagnose and why?

A

C-peptide levels test for Type 2 DM because there is a 1:1 ratio of insulin:C-peptide, so if C-peptides are elevated, insulin will be elevated too - C-peptide also has a longer half-life than insulin so it is a better reflection of insulin resistance than insulin itself

55
Q

What are the three major chronic complications of DM?

A
  • Vascular damage
  • Musculoskeletal damage
  • Eye, kidney, nerve damage
56
Q

What are AGEs?

A

AGEs (advanced glycation-end products): glucose binds to any protein, changing its structure and function

57
Q

How do AGEs affect vascular damage? What do they increase risk for (4)?

A

AGEs damage vascular endothelium results in increased risk for:

  • Inflammation
  • CVD
  • HTN
  • Atherosclerosis
58
Q

How do AGEs affect musculoskeletal damage? What do they increase risk for (2)?

A

AGEs damage collagen resulting in increased risk for:

  • Reduced joint flexibility/mobility
  • Immune system function, increasing risk for infection and amputation
59
Q

How do AGEs affect eye, kidney, and nerve damage? What do they increase risk for (3)?

A

AGEs affect small blood vessels resulting in increased risk for:

  • Retinopathy
  • Nephropathy
  • Neuropathy
60
Q

What is the polyol pathway, and how does it work in the presence of increased glucose?

A

Normally, aldose reductase has lower affinity for glucose but with hyperglycemia, there is extra glucose available for aldose reductase to produce sorbitol

61
Q

What is sorbitol and what are the three undesired consequences of its production?

A

Sorbitol is produced by aldose reductase during hyperglycemia, resulting in:

  • High sorbitol = low NADPH = low GSH, inducing oxidative stress
  • Sorbitol accumulates in lens cells, increasing osmotic pressure and leading to cataracts and tissue swelling
  • Sorbitol > Fructose produces NADH, NADH is the unpreferred version so this impairs several metabolic reactions

Biochemistry Exam #3 (8 decks)

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