Lecture 4: Calcium Homeostasis Flashcards

1
Q

What are the example hormonal regulators of fuel metabolism and their brief function and location

A

Insulin: released when blood glucose is high.

Glucagon: released from the pancreas when blood glucose is low.

Epinephrine: released from the adrenal medulla in response to need for activity.

Cortisol: released from the adrenal cortex in response to stress.

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2
Q

Diagram of glucose regulation

A

Lecture notes

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3
Q

What is the effect of insulin

A

facilitates entry of glucose into muscle, adipose and several other tissues.

stimulates the liver to store glucose in the form of glycogen.

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4
Q

What is the effect of glucagon

A

Stimulating the liver to break down glycogen to be released into the blood as glucose.

Activating gluconeogenesis, the conversion of amino acids into glucose.

Breaking down stored fat (triglycerides) into fatty acids for use as fuel by cells.

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5
Q

What are the counter regulatory hormones and what is their function

A

Cortisol: mobilizes reserves from adipose tissue, causes muscle protein breakdown and stimulates gluconeogenesis in liver.

Growth Hormone (GH) is secreted from the anterior pituitary and has an anti-insulin effect	
it inhibits the insulin-mediated cell uptake of glucose. Its overall effect is to raise blood glucose and FFA levels.	
GH secretion is stimulated by hypoglycaemia and inhibited by hyperglycaemia. 

Epinephrine: released from the adrenal medulla in response to need for activity.

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6
Q

What is a counter regulatory horomone?

A

work against the action of insulin, raising blood glucose levels in response to hypoglycemia (low blood sugar).

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7
Q

What is the types of diabetes and brief description

A

Type 1: Due to not enough insulin being made in the pancreas

Type 2: Due to insulin resistance on insulin receptors on cells, so glucose cant enter

Gestational: pregnancy

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8
Q

Compare Type 1 and Type 2 diabetes

A
Type 1:
Onset: Sudden
Age of onset: Child
Body Size: Normal
Ketoacidosis: Common
Autoantiobodies: Yes
Endogenous Insuin: Low/absent
Identical twins: 50%
Prevalance: 10%
Type 2:
Onset: Gradual
Age of onset: Adult
Body Size: Obese
Ketoacidosis: Rare
Autoantiobodies: No
Endogenous Insuin: Normal, decreased or increased
Identical twins: 90%
Prevalance: 90%
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9
Q

How is diabetes diagnosed in the lab?

A

Fasting plasma glucose ≥126 mg/dL (7.0 mmol/L) (Fasting is defined as no caloric intake for at least 8 hours)

Symptoms of DM and a casual plasma glucose ≥200 mg/dL (11.1 mmol/L) (Casual is defined as any time of day without regard to time since last meal)

Classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss

2-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) during oral glucose tolerance test (OGTT)
HbA1c ≥6.5%

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10
Q

What are the 3 main ways that the body gets sugar

A
  1. Intestinal absorption from food
  2. Gluconeogenesis from liver
  3. Glycogen breakdown
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11
Q

What is the role of insulin

A

It can inhibit the breakdown of glycogen or the process of gluconeogenesis.

It can stimulate the transport of glucose into fat and muscle cells.

It can stimulate the storage of glucose in the form of glycogen

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12
Q

Pathophysiology flow diagram for metabolic acidosis

A

If the amount of insulin available is insufficient
If cells respond poorly to the effects of insulin
If the insulin itself is defective

Then glucose will not be absorbed properly by the body cells

The net effect is persistently high levels of blood glucose, poor protein synthesis, and break down of fat storage

Metabolic acidosis

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13
Q

Why does metabolic acidosis occur in diabetics?

A

When you have diabetes and don’t get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel.
Breaking down fatty acids produces ketones bodies (Beta-hydroxybutyrate), which can make your blood acidic.

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14
Q

Why does electrolyte inbalance occur in diabetics?

A

High blood sugar causes excessive urination and spillage of sugar into the urine.
This leads to loss of body water and dehydration as well as loss of important electrolytes, including sodium and potassium.
The level of another electrolyte, bicarbonate, also falls as the body tries to compensate for excessively acidic blood.

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15
Q

Why does osmotic diuresis occur in diabetics

A

The primary cause of osmotic diuresis is an elevated blood glucose (hyperglycemia) which is sometimes the result of poorly controlled diabetes.

When there is excess glucose in the blood, and it passes through the kidneys for filtering, the excess glucose accumulates in the tubules within the kidneys- volume depletion and dehydration

Once there, it blocks the reabsorption of water, leading to an increased concentration of water in the bloodstream.
The kidneys then act to remove the excess water, causing increased urine production and increased frequency in urination.

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16
Q

How is diabetes monitored?

A

The attachment of the hexose molecule occurs continually over the entire life span of the erythrocyte and is dependent on blood glucose concentration and the duration of exposure of the erythrocyte to blood glucose.

Therefore, the HbA1c level reflects the mean glucose concentration over the previous period (approximately 8-12 weeks, depending on the individual) and provides a much better indication of long-term glycemic control than blood and urinary glucose determinations.

Diabetic patients with very high blood concentrations of glucose have from 2 to 3 times more HbA1c than normal individuals- suggesting poor control of diabetes.

17
Q

What is HbA1c

A

Hemoglobin A1c (HbA1c) is a result of the nonenzymatic attachment of a hexose molecule to the N-terminal amino acid of the hemoglobin molecule.

18
Q

pathogenesis of diabetic ketoacidosis

A

Lecture slide