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Reproductive and Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What are 5 types of diabetes?

A 
Type 1 Diabetes Mellitus
Type 2 Diabetes Mellitus
Maturity Onset Diabetes of the Young
Secondary Diabetes
Gestational Diabetes
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2
Q

What causes Type 1 Diabetes Mellitus?

A

Autoimmune beta cell destruction (type 4 hypersensitivity reaction), causing insulin deficiency.

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3
Q

What causes Type 2 Diabetes Mellitus?

A

Relative insulin deficiency caused by a combination of insulin resistance and beta cell dysfunction.

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4
Q

What are the 3 main effects of Metformin (biguanide)?

A

1) Reduces absorption of glucose from the intestine
2) Reduces hepatic glucose production by gluconeogenesis and glycogenolysis
3) Increases insulin sensitivity to increase glucose uptake by muscle for glycogenesis and glycolysis

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5
Q

What are the three advantages of Metformin?

A

Reduces HbA1c by about 1%.
Weight neutral
Improves cardiovascular mortality and morbidity

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6
Q

What are the side effects of Metformin?

A

1) Nausea and vomiting
2) Lactic acidosis
3) Vitamin B12 deficiency

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7
Q

What are sulphonylureas?

A

Insulin secretagogues (e.g gliclazide) which increase insulin secretion by pancreatic beta cells. They reduce HbA1c by 1-1.5%.

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8
Q

What are the disadvantages of sulphonylureas?

A

There is a risk of hypoglycaemia, and they can cause weight gain.

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9
Q

What are thiazolidinediones/glitazones?

A

PPAR-gamma agonists, which act on a nuclear response element to increase transcription of insulin sensitising genes in hepatocytes, muscle cells, adipocytes.

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10
Q

What are the disadvantages of thiazolidinediones?

A

The side effects include: bone fractures, weight gain, oedema, congestive cardiac failure.

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11
Q

What is the Incretin Effect?

A

The increase in insulin secretion is greater in response to orally-administered glucose than to intravenously-administered glucose. This suggests the presence of glucose in the GI tract leads to the release of something (incretins) which stimulates the pancreas.
The incretin effect is diminished in people with diabetes mellitus.

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12
Q

What are the two incretin hormones?

A 
GLP-1 = released by L cells in the intestine
GIP = released by K cells in the intestine
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13
Q

What is the enzyme that breaks down incretins?

A

DPP-4

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14
Q

What is the effect of GIP?

A

Stimulates beta cells to secrete insulin.

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15
Q

What are the effects of GLP-1?

A

Stimulates beta cells to secrete insulin, inhibits glucagon secretion by alpha cells.
Inhibits appetite and reduces gastric emptying, which leads to weight loss.

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16
Q

What characteristic of the action of both GLP-1 and GIP means they carry no hypoglycaemia risk?

A

Their stimulation of beta cells and suppression of alpha cells is GLUCOSE DEPENDANT.

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17
Q

What is the advantages of GLP-1 analogues e.g exenatide?

A

Metabolised slower than GLP-1 so prolong effect. Reduce HbA1c and lead to weight loss.

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18
Q

What are the side effects of GLP-1 analogues?

A

Gastrointestinal disturbances including GORD and reduced appetite.
Possible link to pancreatitis.

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19
Q

What are the advantages of DPP-4 inhibitors (gliptins)?

A

Prolong effect of endogenous GLP-1, so reduce HbA1c.

They are weight neutral.

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20
Q

What are the side effects of DPP-4 inhibitors (gliptins)?

A

Respiratory infections
Acute pancreatitis
Gastrointestinal disturbances
Exfoliative dermatitis

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21
Q

What is the name of the genetic disease characterised by being asymptomatic except for the presence of glucose in the urine (glucosuria), so there is no hypoglycaemia or hypovolaemia, and what causes it?

A

Familial Renal Glucosuria - defect in SGLT-2 which is supposed to resorb 90% of glucose from the proximal convoluted tubule in the kidney, meaning only 10% of glucose is resorped in the Loop of Henle by SGLT-1.

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22
Q

What is the advantage of SGLT-2 inhibitors (gliflozins)?

A

Improve HbA1c, but don’t carry glycaemic risk.

Promote weight loss, and improve cardiovascular mortality and morbidity.

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23
Q

What are the side effects of SGLT-2 inhibitors (gliflozins)?

A

Increased genitourinary infections.

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24
Q

What are the indications for insulin?

A

1) Type 1 diabetes (can’t survive without insulin)
2) Type 2 diabetes that is inadequately controlled by oral antihyperglycaemic agents, or where oral antihyperglycaemic agents are contraindicated
3) Gestational diabetes
4) Type 2 diabetes in pregnancy
5) Surgery or acute illness in people with type 2 diabetes

25
Q

What are the three different species of insulin?

A

1) Human - genetically engineered using recombinant DNA technology and either yeast or E. coli
2) Beef - increased incidence of allergic problems
3) Pork - less antigenic than beef insulin, and available as purified insulin

26
Q

What is the time action profile of short-acting/soluble insulin (e.g Humulin S)?

A

Onset = 30 minutes
Peak = 1 - 3 hours
Duration of action = 8 hours

27
Q

When is short-acting insulin taken?

A

Just before a meal to control post-prandial blood glucose levels.

28
Q

What is the time action profile of intermediate-acting/isophane/NPH insulin (e.g Humulin I)?
NPH - neutral protamine hagedorn

A

Onset = 1.5 hours
Peak = 4 - 12 hours
Duration of action = 24 hours

29
Q

What is the time action profile of premixed/biphasic insulin (e.g Humalog mix 25)?

A

Onset = 30 minutes
Peak = 2 - 8 hours
Duration of action = 24 hours

30
Q

What is the Humalog mix 25 comprised of?

A

25% short-acting insulin, and 75% intermediate or long-acting insulin.

31
Q

How does the time action profile of long-acting analogues compare to NPH?

A

The peak is reduced so it is a flatter time profile than NPH, and it has a longer duration of action depending on dose.

32
Q

Since normally there needs to be a background level of insulin in the blood to cope with the background blood glucose level, what is the ideal insulin regime for diabetics?

A

BASAL long-acting insulin to deal with the background blood glucose level, and BOLUS short-acting insulin to deal with a glucose challenge.

33
Q

What are the three types of exogenous insulin profiles?

A

1) One injection of isophane before breakfast each day
2) Two injections of 30/70 mix per day - before breakfast and before evening meal
3) One intermediate-acting insulin per day plus a short-acting insulin before each meal - BASAL BOLUS regimen

34
Q

Which is the best exogenous insulin profile and why?

A

Basal-Bolus regimen, as it most closely reflects the normal physiological insulin model, and it is also most flexible (e.g the person can skip lunch without risking hypoglycaemia if they just don’t take the short-acting bolus)

35
Q

What are the two types of insulin devices which can be used for insulin delivery>

A

Durable - insulin cartilage is replaced

Disposable - no need to replace insulin cartilage

36
Q

What are the 3 advantages of insulin devices and pens?

A

1) Improved dose accuracy - dials up insulin automatically
2) More convenient, easy to use, quick and discreet, portable - preferred by patients to syringes
3) Remove barriers to self-management, so increase patient quality of life and lead to better management of the disease

37
Q

How do insulin pumps work?

A

Continuous Subcutaneous Insulin Infusion (CSII), provides basal insulin throughout the day and bolus insulin before meals.
Needles and catheters must be changed every 2 - 3 days.
Not widely used in the UK but represent an alternative for highly motivated patients.

38
Q

What are the 4 side effects of insulin?

A

1) Hypoglycaemia (insulin shock) - can result from an insulin overdose or from skipping meals on a less flexible regimen
2) Allergic reactions
3) Lipoatrophy of subcutaneous fat - so there is a need to change the injection site often
4) Injection site problems - infections, abscesses, etc.

39
Q

How much does diabetes shorten your lifespan?

A

20 years

40
Q

What is the difference between the polyuria experienced in diabetes insipidus, and the polyuria experienced in diabetes mellitus?

A

In diabetes insipidus the polyuria does not decrease with reduced fluid intake, but in diabetes mellitus it does because it is caused by osmotic diuresis.

41
Q

What are the two types of diabetes insipidus?

A

Neurogenic - caused by a deficiency in ADH secretion

Nephrogenic - caused by an insensitivity to ADH

42
Q

What is the Hygiene Hypothesis for the cause of Type 1 diabetes?

A

Type 1 diabetes is more common in the Western world because of the lack of parasitic infections.

43
Q

How much of the total NHS resources is consumed by diabetes care?

A

10%

44
Q

Production of which hormone during pregnancy is thought to cause gestational diabetes?

A

Human Placental Lactogen

45
Q

Of the adults in the UK who have diabetes, what percentage have type 1 and what percentage have type 2? What do the percentages change to when you include children?

A

UK adults: 90% type 2 diabetes, 10% type 1 diabetes

UK adults and children: 85% type 2, 15% type 1

46
Q

What are 4 similarities in the symptoms of type 1 and type 2 diabetes?

A

Polyuria
Polydipsia
Fatigue
Risk of life threatening hyperglycaemia leading to collapse, coma and death

47
Q

What are the three factors that contribute to the aetiology of type 1 diabetes?

A 
Immunological factors (cytotoxic T cells and autoantibodies that target proinsulin)
Genetic factors
Environmental factors (enterovirus infection)
48
Q

What is the life threatening condition that can develop in untreated type 1 diabetes, especially in children, and why?

A

Ketoacidosis, caused by the build up of ketone bodies from increased fatty acid breakdown. This leads to a decrease in blood pH.
Hypotension is caused by the dehydration resulting from vomiting, the vasodilation resulting from acidosis, and the polyuria caused by hyperglycaemia and osmotic diuresis.

49
Q

What is thought to cause the autoimmune reaction in type 1 diabetes?

A

1) Insufficient negative selection in the thymus, so auto reactive T cells escape
2) Deficiency in the regulatory T cells whose role is to suppress the auto reactive T cells
3) Infection by an enterovirus with virus antigens similar to beta cell antigens
4) T cells therefore attack the virus then destroy the beta cells
5) OR an infection in the pancreas damages beta cells, so beta cell antigens are released and attacked by T cells

50
Q

What are some microvascular complications of diabetes?

A 
Erectile dysfunction
Diabetic retinopathy
Cataracts
Diabetic nephropathy (renal disease)
Neuropathy
Foot problems
51
Q

What are some macrovascular complications of diabetes?

A 
Stroke
Heart disease
Hypertension
Peripheral vascular disease
Foot problems
52
Q

What is diabetic kidney disease?

A

Caused by damage to the glomerulus in the kidney, can lead to chronic kidney failure.

53
Q

What is diabetic neuropathy (nerve damage)?

A

Bilateral peripheral sensory nerve damage, giving “glove and stocking” effect.
Autonomic neuropathy

54
Q

What is autonomic neuropathy?

A

Damage to autonomic neurones due to diabetes, leading to postural hypotension, gastric pareisis (reduced gastric emptying which can lead to vomiting), erectile dysfunction, Charcot arthropathy (disintegrating joints due to poor bone resorption).

55
Q

What is diabetic foot disease?

A

Caused by damage to the peripheral nerves and blood vessels and significantly increases risk of amputation.

56
Q

What is diabetic eye disease?

A

Retinopathy and cataracts which typically occurs 10 years after onset of diabetes. It is directly linked to high blood glucose but is also exacerbated by factors like smoking and hypertension.

57
Q

What does it mean that a high HbA1c has cumulative risk?

A

The longer your HbA1c is high, the greater your risk of complications.

58
Q

When is it most critical to keep the blood glucose levels very close to normal in order to have a very low risk of complications later on?

A

The first 2 years after diagnosis.

Reproductive and Endocrine (11 decks)

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