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Patho > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Free Fatty Acids are taken up by the liver and used for…

A

1) Energy
2) Converted to triglycerides for storage or transport
3) Made into cholesterol
4) Made into Ketones
5) Made into albumin

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2
Q

What is ketogenesis?

A

It’s the process of Acetyl-CoA being converted to Ketones in the liver cells. This process can’t be reversed. Liver cells cannot convert ketones back to acetyl-CoA.

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3
Q

Why are ketones helpful?

A

They enter the blood and are taken up by other cells like the muscle and the brain for ATP synthesis.

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4
Q

Where is insulin made?

A

Beta Cells in the pancreas.

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5
Q

What is insulin’s precursor?

A

Insulin is known as “proinsulin” (inactive form). When insulin is needed proinsulin becomes insulin (active form) and C-peptide.

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6
Q

Insulin targets three types of cells, can you name them?

A

Liver, muscles and fat cells. 50% of insulin goes directly to liver.

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7
Q

Why do we measure c-peptide when we think someone has diabetes?

A

It’s a good indicator of whether beta cells are making insulin.

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8
Q

How often is your body pumping out it’s basal dose of insulin?

A

Every 15 minutes, even when fasting

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9
Q

When is your 1st peak of insulin release when eating?

A

3-5 minutes after eating, insulin is released. This is called the “1st phase”

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10
Q

When is the 2nd peak of insulin release?

A

More gradual - over about 2-3 hours and then it’ll return to the basal release.

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11
Q

In type II diabetes, which phase is inhibited - the 1st or 2nd phase of insulin release?

A

The 1st phase - they have trouble mounting a response to rising blood sugars.

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12
Q

When does the body release insulin?

A

1) Increased level of amino acids
2) high blood sugar > 4 mol
3) Stimulation of the parasympathetic nervous system - rest and digest
4) When glucose hits the duodenum, GIP and CCK (GI hormones) trigger the release of insulin
5) Sulfonylurea drugs (anti diabetic drugs)

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13
Q

When would insulin release be inhibited?

A

When the sympathetic nervous system is stimulated - like epinephrine or norepinephrine release. This is because your body wants as much circulating glucose as possible so it stops beta cells from releasing insulin. Your body adapts to this by putting more insulin receptors on the outside of the cells so that circulating insulin can still pull glucose into the cell.

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14
Q

What stimulates insulin release?

A

When there’s high levels of glucose in the blood that’s around the beta cells of the pancreas, then

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15
Q

What are the steps of glucose stimulated insulin release?

A

1) Glucose enters the cell through Glut2 receptor
2) Glucokinase (an enzyme) phosphoralates glucose and glucose becomes glucose-6 phosphate
4) Glucose-6 phosphate can be used to make ATP
5) ATP stimulates potassium channel which brings a bunch of K+ into the cell
6) All that K+ triggers depolarization
7) Depolarization triggers calcium to enter the cell
8) Calcium helps insulin get released from storage granules and insulin gets released out of the beta cell

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16
Q

What is insulin’s main objective?

A

1) brings glucose into target cells
2) Stores glucose as glycogen
3) Prevents fat and glycogen breakdown
4) Inhibits gluconeogenesis
5) Increases protein synthesis.

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17
Q

A type II diabetic has almost no C-peptide, will diet and exercise work to manage their diabetes?

A

No, because they pretty much don’t have any beta cells so they are not making much insulin at all so they’ll likely need to get started on some medications.

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18
Q

Why does the cell need GLUT-4 (or glut 2 or glut 1) transporters?

A

They move glucose into the cell way faster than what would happen by diffusion alone.

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19
Q

What’s different between GLUT 2 and GLUT 4?

A

Glut-2 are found in the cells of the liver and beta cells. They don’t really want to bring glucose into the cell unless the plasma glucose levels are relatively high, like after a meal. Glut 4 is an insulin dependent glucose transporter - it needs to get the message from insulin before it moves the the cell membrane to let glucose to enter.

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20
Q

What is glucagon?

A

It is made in the alpha cells of the islets of Langerhans. It’s the opposite of insulin though. It produces an increase in blood glucose.

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21
Q

How does glucagon increase blood glucose?

A

1) It initiates glycogenolysis or the breakdown of liver glycogen.
2) Glucagon also stimulates gluconeogenesis by increasing the transport of amino acids into the liver and converts them into amino acids.
3) Stimulates lipolysis in adipose cells. Glycerol is delivered to liver for gluconeogenesis.

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22
Q

When glucose enters adipose cells, what does it get stored as? What is this process called?

A

Fat. Insulin stimulates the conversion of glucose to glycerol or fatty acids for trygliceride synthesis in adipose tissue. This process is called lipogenesis.

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23
Q

What happens to glucose that enters liver and muscle cells?

A

Gets stored as Glycogen. This process is called glycogenesis.

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24
Q

How does insulin assist in fat metabolism?

A

1) Insulin stimulates enzymes that are responsible for lipid uptake and triglyceride synthesis in adipose tissue.
2) Insulin also inhibits enzymes that cause lipolysis.

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25
Q

How does insulin help with protein metabolism?

A

1) stimulates amino acid uptake and protein synthesis in muscle cells
2) Inhibits protein breakdown.

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26
Q

When does glucagon get released from alpha cells?

A

1) When blood sugar is low (like between meals or during exercise)
2) After a high protein meal (because there’s not enough sugar)

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27
Q

What are the 4 types of diabetes?

A

1) Type I
2) Type II
3) Other specific types
4) Gestational diabetes

28
Q

What antibodies are responsible for destroying B cells of the pancreas leading to Type I diabetes?

A

Islet cell antibodies (ICA) , Insulin autoantibodies (IAA) and anti GAD

29
Q

What’s triggers Type I diabetes?

A

A genetic predisposition and a triggering autoimmune event causing antibodies to trigger b cells in pancreas. This stage is called “insulinitis” and it’s characterized by injury to beta cells.

30
Q

What happens in type I diabetes after the beta cells are damaged?

A

The person is not able to mount the first peak of insulin after eating and they become glucose intolerant. Later as the number of C-peptides decrease the person becomes overtly diabetic.

31
Q

Why is Type II diabetes different than type I?

A

Type II diabetes happens because cells are less responsive to insulin, due to a decrease in insulin receptors or the function of the receptors declines. For example, Glut 4 receptors might not get a signal that there’s more glucose circulating and won’t open up.

32
Q

Is there a genetic component to type II diabetes?

A

Yes. And also certain ethnicities more at risk of getting type II diabetes - african american, south asians, hispanic, asian, and canadian aboriginals.

33
Q

What lifestyle factors are associated with type II diabetics?

A

Sedentary lifestyle, obesity, and diet high in refined sugars, people with central obesity

34
Q

Why do people with visceral and central fat have an increased propensity for Type II diabetes?

A

Adipose tissue releases hormones and FFA contribute to insulin resistance.

35
Q

Why does insulin sensitivity improve with exercise?

A

Exercise improves insulin sensitivity because muscle cells become more responsive when less insulin is available. Exercise up regulates insulin receptors and then blood glucose can get out of blood circulation and be stored appropriately.

36
Q

Initially someone with type II diabetes has normal blood glucose, why is that?

A

Because the pancreas tries to compensate with Beta Cell hyperplasia. MORE BETA CELLS.

37
Q

Later on blood glucose tolerance is impaired. Why is that?

A

Beta cells start to fail. This is an early sign of type II diabetes. As more beta cells fail, the person’s blood sugar levels increase.

38
Q

Why do beta cells fail?

A

Not too sure, some theories are that the cells get exhausted, or they get desensitized to high blood glucose (glucotoxicity), or FFA inhibit the release of insulin (lipotoxicity), or amyloid proteins accumulate causing beta cell failure.

39
Q

Insulin resistance and beta cell defects can range a lot, and this is also seen in the sort of body fat distribution that type II diabetes have. Who tends to be lean?

A

People that have mild insulin resistance but severe beta cell dysfunction.

40
Q

Type II diabetics that are obsese tend to have this problem with their body

A

More of a insulin resistance and less of a beta cell defect.

41
Q

What conditions are frequently associated with insulin resistance?

A

Hypertension, impaired fasting plasma glucose, or glucose intolerance, and dyslipidemia (high LDL’s and triglycerides and low HDL’s)

42
Q

They say if you have 3 or more of these factors you could develop metabolic syndrome which makes you are risk of CAD or type II diabetes. What are the risk factors?

A

Visceral obesity, insulin resistance, high triglycerides, hypertension, and low HDL cholesterol.

43
Q

Why do pregnant ladies sometimes get gestational diabetes?

A

Hormonal changes and weight gain contribute to insulin resistance. You have a greater demand for insulin but body can’t meet the demand.

44
Q

When do women get screened for Gestational diabetes?

A

24-48 weeks with a 50 g OGTT (oral glucose challenge)

45
Q

What can happen if a mother has gestational diabetes and goes untreated?

A

Fetal malformation, high birth weight > 4 kg, neonatal hypoglycaemia (high levels of fetal insulin at birth) and premature birth. Risk of childhood obesity and type II diabetes.

46
Q

What are the risks to the mother with gestational diabetes?

A

Might need cesarean delivery, and might develop type II diabetes within 5 years following pregnancy.

47
Q

There are other causes of diabetes. One main cause of other forms of diabetes is when the pancreas is damaged. What are some examples of conditions that would damage the pancreas?

A

1) Pancreatic CA 2) Pancreatitis 3) Ischemic pancreas

4) Hemochromatosis 5) Cystic Fibrosis

48
Q

What hormonal issues might trigger diabetes?

A

Issues with cortisol like cushing syndrome, epinephrine, thyroid hormone, or glucagon.

49
Q

What’s causing people to be hyperglycemic in insulin deficiency?

A

Glucose isn’t being taken up by insulin dependent cells as well as increased gluconeogenesis (amino acids, glycerol and lactic acid making glucose) and glycogenolysis (breakdown of glycogen to make glucose)

50
Q

Why do do people that are deficient in insulin develop lipolysis?

A

Increased release of free fatty acids and glycerol from adipose tissue which gets delivered to liver

51
Q

Why do people with insulin deficiency get ketone synthesis?

A

There’s too many free fatty acids in the liver and they get converted to ketones

52
Q

Why do people with insulin deficiency/glucagon excess synthesize lipoproteins

A

Excess free fatty acids in the liver get packaged into lipoproteins for transport and they accumulate in the circulation because there’s no insulin there to store them

53
Q

How are these pt’s affected by protein breakdown?

A

Decreased amino acid uptake and decreased inhibition of protein breakdown so amino acids go to the liver for gluconeogenesis.

54
Q

Why do people pee a lot with diabetes?

A

Too much glucose in the circulation, and so can’t be reabsorbed. Glucose gets into the renal tubes acts as an osmotic diuretic and pulls more water in. K+ goes with urine and you lose electrolytes. Dehydration causes increased thirst.

55
Q

What are two reasons people with diabetes get really thirsty?

A

1) Dehydration due to polyuria
2) Hyperosmolarity of blood due to hyperglycemia so fluid shifts from the cells to the blood causing intracellular dehydration and that stimulates osmoreceptors to trigger thirst

56
Q

Why do people with diabetes experience polyphagia?

A

Increased appetite due to not enough glucose entering the cell so the insulin dependent cells are starved which stimulates appetite. Weight loss is b/c of breakdown of fat and protein for energy due to lack of glucose entry into cells causing muscle wasting.

57
Q

What’s the difference between diabetic retinopathy and recurrent episodes of blurred vision?

A

Diabetic retinopathy is a later complication due to damage to the small vessels of the ey feeding the retina. It’s irreversible. Whereas the recurrent episodes is due to hyperosmolar fluids in the eye which alters the water content of the lens and changes the lens shape. As glucose levels normalize, so will vision.

58
Q

Why do diabetic’s wounds heal slowly

A

Polyuria causes increased blood viscosity and decreased blood volume and decreased blood flow and therefore poor circulation to wound. Also peripheral vascular disease could happen due to high blood lipid levels and atherosclerosis.

59
Q

Why does a test with hemoglobin help us measure diabetes (hbga1c)

A

Hgb permanently binds glucose over the lifespan of a RBC. The glucose in the blood the more that’s bound to HbA. Normal is 4-6%. Diabetes is greater than 6.5%. Gives us an idea of how the sugars were for the last 3 months.

60
Q

Why does exercise help in Type II diabetes?

A

1) Lowers glucose levels quickly 2) Improves body’s ability to use insulin 3) Reduces insulin requirement and increases insulin sensitivity
4) Better control of diabetes 5) Reduces risk of heart disease and weight loss

61
Q

What sort of teaching could you do about diet for type II diabetic?

A

Avoid high glycemic foods and sugar intake, decrease cholesterol and saturated fat, decrease salt if hen present, increase fibre (it slows sugar absorption) and eat 3 meals a day at regular intervals.

62
Q

How do sulfonyloreas work?

A

They increase insulin secretion - target beta cells.

63
Q

How does metformin and troglitazone work?

A

Decreases hepatic glucose output and increases peripheral glucose uptake like in skeletal muscle

64
Q

How does Acarbose medication work?

A

Works on decreased glucose aborption on the gut

65
Q

What’s a side effect of acarbose?

A

Diarrhea b/c water stays with the glucose and people say they get quite gassy.

66
Q

What could make someone hypoglycaemic?

A

Too much insulin, alcohol because it interferes with glucagon absorption, exercise and stress.

67
Q

How does stress affect glucose?

A

Increased stress increases cortisol which increases glucose levels.

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