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NME > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Which cells in the pancreas secrete insulin?

A

Beta cells in the pancreas secrete insulin.

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2
Q

Which cells in the pancreas secrete glucagon?

A

Alpha cells in the pancreas secrete glucagon.

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3
Q

What is the target range for blood glucose levels?

A

The target range for blood glucose levels is between 4-7 mmol/L, although ranges may vary.

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4
Q

Where does glucose homeostasis predominantly occur?

A

Glucose homeostasis predominantly occurs in the liver.

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5
Q

How is glucose stored and released in the liver?

A

Glucose is stored as glycogen in the liver and released into the circulation between meals.

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6
Q

What does insulin do in glucose homeostasis?

A

Insulin suppresses gluconeogenesis (production of glucose) and facilitates the uptake of glucose

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7
Q

What does glucagon do in glucose homeostasis?

A

Glucagon has the opposite effect of insulin. It promotes gluconeogenesis and raises blood glucose levels.

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8
Q

What is the relative insulin-to-glucagon ratio in the fed state?

A

In the fed state, the insulin-to-glucagon ratio is high (high insulin:glucagon)

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9
Q

What is the relative insulin-to-glucagon ratio in the fasting state?

A

In the fasting state, the insulin-to-glucagon ratio is low (low insulin:glucagon).

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10
Q

How is hypoglycaemia defined?

A

Hypoglycaemia is defined as blood glucose levels below 3.5mmol/L.

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11
Q

What are the symptoms of hypoglycaemia?

A

Symptoms of hypoglycaemia include sweating, tremor, nervousness, palpitations, and hunger due to the release of counter-regulatory hormones such as adrenaline and glucagon.

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12
Q

What are the neuroglycopenic symptoms associated with hypoglycaemia?

A

Neuroglycopenic symptoms of hypoglycaemia include confusion, drowsiness, slurred speech, poor coordination, irritability (anger), and seizures. These symptoms occur due to the lack of glucose supply to the brain.

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13
Q

Who is prone to hypoglycaemic unawareness?

A

Insulin-dependent diabetics are prone to hypoglycaemic unawareness.

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14
Q

What are some causes of hypoglycaemia?

A

Causes of hypoglycaemia include insulinoma (an insulin-producing tumor in the pancreas), hypoadrenalism (reduction of glucocorticoids), alcohol consumption, severe liver failure, and the use of insulin or sulphonylureas.

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15
Q

What are the management options for hypoglycaemia?

A

The management options for hypoglycaemia include eating or drinking sugar, using Hypostop (a glucose gel), administering intravenous dextrose 20% (75mL), and administering intramuscular glucagon 1mg if intravenous access is not available.

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16
Q

What is diabetes mellitus (DM)?

A

Diabetes mellitus is a condition characterized by the dysregulation of insulin and glucagon, resulting in problems controlling blood sugar levels.

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17
Q

How do insulin and glucagon influence glucose transport into cells?

A

Insulin increases glucose absorption into cells and out of plasma, while glucagon raises blood glucose levels by promoting glycogen breakdown in the liver and upregulating gluconeogenesis.

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18
Q

What happens when there is too little glucose in cells?

A

Insufficient glucose in cells leads to a reduction in carbohydrate metabolism and decreased ATP production.

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19
Q

What percentage of diabetics have Type 1 DM, and what is the cause?

A

Approximately 10% of diabetics have Type 1 DM. It is caused by a type 4 hypersensitivity response, where T-cells attack the beta cells of the pancreas, leading to insufficient insulin production.

20
Q

What are the symptoms of Type 1 DM?

A

The lack of insulin in Type 1 DM causes glycosuria (glucose in the urine) and polyuria (increased urine production). It also leads to polydipsia (excessive thirst), weight loss due to catabolic mechanisms, and polyphagia (increased hunger). These symptoms typically develop over a 4-6 week period.

21
Q

Are autoantibodies and specific HLA genes associated with Type 1 DM?

A

Yes, autoantibodies can be detected in individuals with Type 1 DM. Additionally, specific HLA genes, such as HLA DR3 and DR4 on Chromosome 6, have been identified in some Type 1 diabetics. HLA genes code for cell surface membranes involved in the immune system.

22
Q

What are the ketone bodies generated during lipolysis in Diabetic Ketoacidosis (DKA)?

A

The ketone bodies generated during lipolysis in DKA are acetone, acetoacetate, and β-hydroxybutyrate.

23
Q

What is the consequence of the accumulation of ketone bodies in DKA?

A

The accumulation of ketone bodies results in metabolic acidosis, known as ketoacidosis, due to their acidic nature.

24
Q

How does the body respond to metabolic acidosis in DKA?

A

The body responds to metabolic acidosis in DKA through Kussmaul’s breathing, which is deep breathing aimed at removing CO2 from the blood to reduce acidity.

25
Q

How does acidosis and low insulin levels in DKA lead to hyperkalemia?

A

Acidosis and low insulin levels in DKA lead to hyperkalemia by altering both the H+/K+ and Na+/K+ cell membrane transport pumps. The resulting imbalance drives H+ into cells, which in turn drives K+ out of the cell.

26
Q

What can hyperkalemia in DKA potentially cause?

A

Hyperkalemia in DKA can lead to fatal cardiac arrhythmias, posing a serious threat to the patient’s health.

27
Q

What are the common symptoms of Diabetic Ketoacidosis (DKA)?

A

DKA presents acutely with symptoms such as nausea, vomiting, fruity sweet breath (acetone odor), and confusion (due to cerebral edema caused by fluid shifts).

28
Q

What is the primary treatment for DKA?

A

The primary treatment for DKA is insulin administration.

29
Q

What is the role of IV fluids in DKA treatment?

A

IV fluids are used in DKA treatment to restore hydration and correct electrolyte imbalances.

30
Q

Why is the replacement of potassium (K+) important in DKA treatment?

A

Potassium replacement is crucial in DKA treatment because acidosis and insulin deficiency can lead to hyperkalemia initially, followed by intracellular potassium shifting, leading to hypokalemia.

31
Q

What percentage of diabetes mellitus cases does Type 2 diabetes mellitus (T2DM) account for?

A

T2DM accounts for approximately 90% of diabetes mellitus cases.

32
Q

What is the primary cause of insulin resistance in T2DM?

A

Insulin resistance in T2DM occurs at the cellular level. The exact mechanisms of insulin resistance are not fully understood, but it is believed to involve the action of inflammatory response proteins that inhibit insulin receptor substrate (IRS) action.

33
Q

How does insulin resistance affect AKT activity?

A

Insulin resistance and IRS inhibition lead to reduced AKT activity. AKT inhibition disrupts the ability to transport glucose effectively within cells.

34
Q

What are the contributing factors to the development of T2DM?

A

T2DM is associated with obesity, hypertension, and lack of exercise. Genetic factors are also believed to play a role.

35
Q

How does T2DM progress over time?

A

In T2DM, higher than normal insulin levels are initially produced by the pancreas in an attempt to normalize glucose levels. This leads to pancreatic β-cell hyperplasia. However, over time, the build-up of amylin in the beta cells causes damage, resulting in a decrease in insulin production. This leads to the development of hyperglycemia.

36
Q

What are the symptoms that develop over months in hyperglycemia secondary to Type 2 DM?

A

Polyuria (excessive urination), polydipsia (excessive thirst), and polyphagia (increased hunger) develop over months in hyperglycemia secondary to Type 2 DM.

37
Q

What occurs in hyperglycemia secondary to Type 2 DM instead of diabetic ketoacidosis (DKA)?

A

In cases where insulin is still produced by pancreatic β-cells, diabetic ketoacidosis (DKA) does not occur. Instead, Hyperosmolar Hyperglycemic State (HHS) can occur, characterized by extreme hyperosmolality and dehydration due to high blood glucose levels.

38
Q

How is diabetes diagnosed?

A

Diabetes can be diagnosed through various methods including a random blood sugar test, a raised fasting glucose test (after fasting for 8 hours), an oral glucose tolerance test (2 hours after a glucose load), and measuring HbA1c levels.

39
Q

What does HbA1c measure in the diagnosis of diabetes?

A

HbA1c (glycosylated hemoglobin) is measured to provide a time-averaged snapshot of blood glucose levels over the lifespan of red blood cells (approximately 120 days). It reflects the average blood glucose levels over a prolonged period.

40
Q

What is an oral glucose tolerance test used for in diabetes diagnosis?

A

An oral glucose tolerance test is conducted by measuring blood glucose levels 2 hours after consuming a glucose load. It helps evaluate the body’s ability to regulate blood sugar levels.

41
Q

What are the primary methods of glucose control in Type 1 DM and Type 2 DM?

A

In Type 1 DM, insulin is the primary method of glucose control. In Type 2 DM, it can involve monotherapy (using a single drug) or combination therapy (using multiple drugs).

42
Q

What are the key monitoring methods for long-term glucose control?

A

Monitoring methods for long-term glucose control include measuring HbA1c levels and daily blood sugar measurements.

43
Q

What lifestyle factors are important in long-term diabetes management?

A

Lifestyle factors such as diet and exercise play a crucial role in long-term diabetes management.

44
Q

What are some commonly used types of insulin in different regimes?

A

Commonly used insulin types include rapid-acting insulin (e.g., Novorapid), short-acting insulin (e.g., Actrapid), long-acting insulin (e.g., Insulatard), and mixed insulin (a combination of short-acting or analogue insulin with long-acting insulin, e.g., Humulin M3).

45
Q

How are slow-acting and fast-acting insulins achieved at the molecular level?

A

Slow-acting insulin is achieved by increasing the time it takes for the insulin hexameric complex (inactive form) to dissociate into active monomers. This is achieved through mutation and/or modification. Fast-acting insulin, on the other hand, is achieved by mutations or the attachment of hydrocarbons that generate aggregates which slowly dissociate into monomers.

46
Q

What is the mechanism of action of metformin in the treatment of Type 2 DM?

A

Metformin, a biguanide, decreases glucose production in the liver and increases insulin sensitivity in tissues.

NME (49 decks)

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