Lecture 5 Flashcards

1
Q

How much of the pancreas is the islet of langerhans?

A

1%

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2
Q

How many types of cells are there in the islet of langerhans?

A

4 types

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3
Q

What kind of shape do the cells of the islet of langerhans have?

A

spherical

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4
Q

What is insulin?

A

Peptide hormone

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5
Q

From where is insulin secreted from?

A

beta cells

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6
Q

What is the inactive precursor for insulin?

A

proinsulin

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7
Q

What are stimuli for the release of insulin?

A
  1. increased blood glucose (normal: 70-110mg/dl)

2. increased blood arginine/leucine

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8
Q

What is the antagonist for insulin?

A

glucagon

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9
Q

How is arginine/leucine formed?

A

Breakdown of protein

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10
Q

What are the five redundant actions in insulin?

A
  1. increased rate of glucose transport into target cell
  2. increased rate of glucose utilization and ATP generation
  3. increased conversion to glycogen (in liver and skeletal muscle)
  4. increased amino acid absorption and protein synthesis
  5. increased tryglyceride synthesis (from adipose tissue)
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11
Q

What are the three redundant actions in glucagon?

A
  1. increased conversion to glucose
  2. increased breakdown to fats (triglycerides) to fatty acids
  3. increased protein breakdown to amino acids
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12
Q

What are the two types of diabetes mellitus?

A

Insulin Dependent Diabetes Mellitus (IDDM)/type 1

Non-insulin Dependent Diabetes Mellitus (NIDDM)/type 2

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13
Q

What are symptoms of IDDM?

A
  1. lack of insulin from beta-cells
  2. cells cannot take up glucose (body reacts as if glucose levels are low - lipids and proteins broken down and ketone bodies produced - can cause ketoacidosis leads to death)
  3. high glucose levels in urine which leads to polyuria
  4. chronic hyperglycema and dehydration
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14
Q

Why does high glucose levels lead to polyuria?

A

Glucose has a high osmotic pull so a lot of fluid is dragged into the nephrons

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15
Q

What kind of problems do chronic hyperglycema and dehydration cause?

A

fatigue, muscle wasting, neuropathy, retinopathy

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16
Q

Can IDDM be diagnosed from eye exams?

A

Yes; retinopathy can appear when the patient becomes blind

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17
Q

What demographic of individuals tend to have NIDDM?

A

Typically obese individuals over 40 years old

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18
Q

How does NIDDM develop?

A

The body desensitizes to insulin; can become non-diabetic after losing fat

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19
Q

How much of diabetes cases are NIDDM?

A

90%

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20
Q

Why would losing weight make the person non-diabetic?

A

Metformin (which lowers glucose synthesis and release at liver) works well

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21
Q

What is metformin?

A

Oral hypoglycaemic agent of the biguanide group

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22
Q

What is the half-life of metformin?

A

3 hours

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23
Q

What does metformin do?

A
  1. causes increase in glucose uptake by muscle
  2. reduces hepatic production of glucose
  3. does ot cause hypoglycaemia but prevents hyperglycaemia
24
Q

What are some unwanted effects of metformin?

A

GI disturbances

lactic acidosis

25
Q

What is the diabetes look alike?

A

diabetes insipidus

26
Q

What causes diabetes insipidus?

A

Posterior pituitary gland fails to produce adequate levels of antidiuretic hormone (ADH)

27
Q

What are symptoms of diabetes insipidus?

A

polydipsia (excessive drinking)
polyuria (excessive urination)
above are symptoms of diabetes mellitus
nothing to do with sugar or insulin

28
Q

How many women have cysts?

A

20%

29
Q

How many women with cysts have polycystic ovarian syndrome?

A

6-10%

30
Q

What is a major feature polycystic ovarian syndrome?

A

Insulin resistance accompanied by hyperinsulinemia

31
Q

What does increased insulin cause?

A

hyperandrogenism

32
Q

What is hyperandrogenism in women?

A

produces more testosterone than usual

33
Q

What can hyperandrogenism lead to?

A

Reduces fertility (due to increased hair and weight)

34
Q

How is PCOS treated?

A

cut out affected areas in ovary to recover

35
Q

How do follicle cells develop in women with PCOS?

A

In normal people: 1 develop in ovaries

In PCOS: multiple develop in ovaries

36
Q

What are the hormones of the thyroid gland?

A
  1. Iodine + tyrosine = monoiodotyrosine (T1)
  2. iodine + iodine + tyrosine = diiodotyrosine (T2)
  3. monoiodotyrosine + diiodotyrosine = triiodothyronine (T3)
  4. 2*T2 = thyroxine (T4)
37
Q

What is the metabolic rate?

A

total body energy expenditure per unit time

38
Q

What is the basal metabolic rate?

A

Metabolic rate when at mental and physical rest but not sleeping, at comfortable temperature and fasted for at least 12 hours

39
Q

What does the thyroid hormone stimulate?

A

protein synthesis
increased use of glucose and free fatty acids (ffa) for ATP production
increased lipolysis

40
Q

Which effects of thyroid hormone are similar to other endocrine hormones?

A

insulin and growth hormone - Amino acids to proteins

glucagon and growth hormone - lipids int ffa and liberate glucose from glycogen

41
Q

What are calorigenic effects?

A

TRH: Detects low body temperature
TSH: Stimulates thyroid hormone production

42
Q

Too liitle calorigenic effect leads to…

A

Cretinism, myxodema

43
Q

What is cretinism?

A

Congenital hypothyroidism

44
Q

What are symptoms of cretinism?

A

mentally immature, cannot hear or speak
bone growth retarded
sexually immature

45
Q

What is myxodema?

A

Adult hypothyroidism

46
Q

What leads to myxodema?

A

Low TSH and low T3 and T4

47
Q

What is a symptom of myxodema?

A

Low cardiac output - edema

48
Q

What is a treatment for myxodema?

A

T3 and T4 injection

49
Q

Too much calorigenic effect leads to…

A

graves disease, golter

50
Q

Does graves disease affect males or females more?

A

Female: *10

51
Q

What is graves disease?

A

Autoimmune disease

52
Q

How is graves disease an autoimmune disease?

A

Antibodies mimic TSH

53
Q

The pressure behind eyes caused by graves disease causes…

A

exophthalmos

54
Q

What can golter be associated with?

A

thyroid disorder

55
Q

What is golter usually attributed to?

A

Low dietary intake of iodine

56
Q

What are treatments for golter?

A

Injection of irregular isotopes

remove thyroid