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

Diabetes Mellitus Type 1 and 2 Flashcards

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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
Describe Hypertriacylglyceridemia in uncontrolled Type 2 DM patients - increased production versus decreased clearance?
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
What is the acute complication of Type 2 DM?
Hyperosmolar Syndrome
27
What are the three triggers often seen with Hyperosmolar Syndrome?
- Stress - Alcohol consumption - Infection/illness
28
What are the ten signs/symptoms of Hyperosmolar Syndrome?
- Fruity odor on breath - Polydipsia - Polyuria - Dehydration - Fatigue - Confusion - Rapid breathing - Blurred vision - Vomiting - Weakness
29
What do the blood results of a Hyperosmolar Syndrome patient look like? (hint: 3 important results)
- Very elevated glucose level - Normal ketone bodies - Normal blood pH
30
What are the two recommended treatments for Hyperosmolar Syndrome?
- IV insulin: promote glucose uptake/inhibit lipolysis | - IV fluids: relieve dehydration
31
Why can't Type 2 DM patients experience DKA, but Type 1 DM patients can?
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
What is the recommended treatment for Type 1 DM?
INSULIN ALWAYS NEEDED
33
What is the first recommended treatment for Type 2 DM? If that does not work, what is the alternative treatment?
Lifestyle and diet changes | - Then oral hypoglycemic drugs
34
What is AMPK and how is it regulated?
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
What are the three ATP-producing processes activated by AMPK?
- Glycolysis - Beta-oxidation - Glucose uptake
36
What are the four ATP-consuming processes inhibited by AMPK?
- Glycogenesis - FA synthesis - Protein synthesis - Cholesterol synthesis
37
How does AMPK treat Type 2 DM patients?
AMPK function increases GLUT4 activity to help lower hyperglycemia (insulin-independent way)
38
How does Metformin work to treat Type 2 DM patients?
Metformin is thought to inhibit AMP deaminase, which breaks down AMP - This inhibition leads to higher AMP levels and activation of AMPK
39
What are the six function of GLP-1 that lower blood glucose?
- Inhibits break down of beta-cells - Promotes beta-cell growth - Increases insulin secretion - Decreases glucagon secretion - Inhibits appetite - Delays gastric emptying
40
What are the six function of GLP-1 that lower blood glucose?
- Inhibits break down of beta-cells - Promotes beta-cell growth - Increases insulin secretion - Decreases glucagon secretion - Inhibits appetite - Delays gastric emptying
41
What are the two incretin-based approaches to manage Type 2 DM?
- Incretin mimetics | - DPP-4 inhibitors
42
How do incretin mimetics work (5 things)? What is an example of an incretin mimetic?
- Minimize beta-cell exhaustion - Increase insulin release after meals - Decrease glucagon levels - Decrease in appetite - Reduced post-meal hyperglycemia Example: Byetta
43
How do DPP-4 inhibitors work?
Inhibit DPP-4 (cleaves GLP-1), which increases the half-life of GLP-1
44
What is the OGTT and what does it entail?
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
Why is a 3-day carb diet necessary for the OGTT?
High carb diet = high insulin, which means that glycolytic enzymes will be in adequate amounts
46
What are the advantages (1) and disadvantages (1) of OGTT?
- Advantages: easy for patient | - Disadvantages: only used to diagnose gestational diabetes
47
What is the cut-off level for DM diagnosis for the OPTT test?
200 mg/dL or above
48
What is the FPG test and what does it entail?
Fasting Plasma Glucose entails 8 hours of fasting then blood draw
49
What are the advantages (1) and disadvantages (2) of FPG?
- Advantages: easy for patient - Disadvantages: can be affected by outside factors (other medications, smoking); less reliable because only measures acute levels
50
What is the cut-off level for DM diagnosis for the FPG test?
126 mg/dL or above
51
What is the HbA1c test and what does it entail?
HbA1c entails a single blood draw to check glycated form of HbA
52
What are the advantages (3) of HbA1c?
- Easy for patient (no fasting required) - Sample stability - Measures blood glucose for previous 6-8 weeks (can evaluate patient compliance)
53
Which primary DM is antibodies used to diagnose and why?
Antibodies test for Type 1 DM because insulin antibodies are only present with Type 1 DM
54
Which primary DM is C-peptide levels used to diagnose and why?
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
What are the three major chronic complications of DM?
- Vascular damage - Musculoskeletal damage - Eye, kidney, nerve damage
56
What are AGEs?
AGEs (advanced glycation-end products): glucose binds to any protein, changing its structure and function
57
How do AGEs affect vascular damage? What do they increase risk for (4)?
AGEs damage vascular endothelium results in increased risk for: - Inflammation - CVD - HTN - Atherosclerosis
58
How do AGEs affect musculoskeletal damage? What do they increase risk for (2)?
AGEs damage collagen resulting in increased risk for: - Reduced joint flexibility/mobility - Immune system function, increasing risk for infection and amputation
59
How do AGEs affect eye, kidney, and nerve damage? What do they increase risk for (3)?
AGEs affect small blood vessels resulting in increased risk for: - Retinopathy - Nephropathy - Neuropathy
60
What is the polyol pathway, and how does it work in the presence of increased glucose?
Normally, aldose reductase has lower affinity for glucose but with hyperglycemia, there is extra glucose available for aldose reductase to produce sorbitol
61
What is sorbitol and what are the three undesired consequences of its production?
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

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