16. Drugs and hormones Flashcards

1
Q

Define ‘hormone’

A
  • a chemical substance synthesised by specific tissues and secreted into blood stream
  • where it is carried to non-adjacent sites in body and exerts its actions
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2
Q

Define ‘neurotransmitters’

A

a chemical substance synthesised by neurone and secreted directly onto adjacent neurones or tissues
- where it exerts its action

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3
Q

Difference between endocrine and nervous system

A
  • endocrine has hormones
  • neuro has neurotransmitters
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4
Q

How is the endocrine system organised?

A
  • endocrine glands/cells
  • target cells
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5
Q

Define ‘endocrine glands/cells’

A

secrete hormones into blood stream

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6
Q

Define ‘target cells’

A
  • cells with receptors for a given hormone
  • that can alter activities in response to the hormone
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7
Q

Explain the HPS axis and cortisol

A
  • stress (physical or mental)
  • detected at hypothalamic nuclei
  • releases CRH to anterior pituitary
  • releases ACTH to adrenal cortex which releases cortisol
  • negative feedback to anterior pituitary and hypothalamic nuclei
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8
Q

Effect of cortisol

A
  • increases and maintains normal blood glucose levels in blood
  • increase gluconeogenesis
  • decrease glucose uptake in to muscle and adipose tissue
  • decrease in protein synthesis (amino acid free for gluconeogenesis)
  • role in regulating brain function
  • immune response/inflammation
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9
Q

Regulation of blood glucose by insulin

A
  • high blood glucose detected by pancreas
  • releases insulin
  • to insulin receptors in liver and muscle
  • these uptake/store glucose as glycogen and inhibit fat breakdown
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10
Q

Explain the hypothalamic-pituitary-ovarian axis/tract

A
  • hypothalamus releases GRH to the pituitary gland
  • which released FSH and LH to ovaries
  • these release estrogen and progesterone
  • negative feedback with both to pituitary and hypothalamus
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11
Q

What is GRH?

A

gonadotrophin releasing H

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12
Q

What is FSH?

A

follicle stimulating H

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13
Q

What is LH?

A

lutenising H

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14
Q

Disorders of Cortisol

A
  • Cushing’s syndrome - hypersecretion of it
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15
Q

Causes of Cushing’s syndrome

A
  • adrenal or pituitary tumour (Cushing’s disease)
  • side effect of chronic glucocorticoid therapy
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16
Q

How to treat Cushing’s syndrome?

A
  • removal of tumour
  • inhibition of cortisol synthesis by metyrapone
17
Q

How does metyrapone treat Cushing’s syndrome?

A
  • 11beta-deoxycortisol with 11beta-hydroxylating enzyme becomes cortisol
  • the enzyme can be blocked by metyrapone so decreasing the amount of cortisol available for secretion
  • treats the syndrome
18
Q

At high levels, cortisol does what?

A

can inhibit inflammation and immune response

19
Q

Cushign like side effects can be due to …

A
  • long term glucocorticoid treatment
  • therapeutic agents for other reasons but here given too much cortisol
20
Q

How do beta cells in the Islets of Langerhan in the pancreas work?

A
  • detect glucose and use glycolysis to increase ATP
  • insulin in storage granules here is released
  • potassium ions diffuse out of Katp channels regulated by ATP
21
Q

Disorders of insulin

A
  • diabetes mellitus
  • can be insulin hyposecretion or insulin receptor hyposensitivity
22
Q

What is Type 1 diabetes?

A
  • insulin hyposecretion due to loss of beta-cells
23
Q

How to treat type 1 diabetes?

A
  • substitute the insulin
  • background intermediate acting (e.g isophane insulin) and short term fast acting (soluble insulin) before a meal
24
Q

What happens in type II diabetes?

A
  • metabolic demands of obesity
  • desensitization of insulin receptors
  • pancreatic insufficiency
25
Q

What can stop the Katp channels in beta cells?

A
  • sulphonylureas like glibenclamide
  • block the channels so cause depolarisation
  • increase insulin secretion independently of glucose levels
  • need partiallu functioning beta cells
26
Q

How is sulhonylureas’s effect on diabetes useful?

A
  • treatment for diabetes
  • increases insulin secretion
27
Q

What does estrogen do?

A
  • sensitises LH releasing cells in pituitary
  • proliferation of endometrium
  • inhibits FSH so regulates cycle
28
Q

What does progesterone do?

A
  • renders endometrium suitable for implanting of a fertilised ovum
  • and maintains endometrium
  • inhibits further release of GRH, FSH and LH so regulates cycle and ovulation
29
Q

After ovulation what are the 2 options?

A
  • fertilization
  • no fertilization
30
Q

What happens if no fertilization takes place after ovulation?

A
  • corpus luteum regresses, progesterone levels drop
  • endometrium can not be maintained. menstruation occurs
  • lack of progesterone also means clamp on GRH, FSH & LH is released
  • hormones are secreted again - cycle starts again with follicle development
31
Q

If a fertilized ovum is implanted, what happens?

A
  • ovum secretes human chorionic gonadotrophin
  • this stimulates corpus luteum to continue secreting progesterone
  • maintains endometrium and pregnancy
  • inhibits further secretion of GRH, FSH, LH and prevents further follicles developing
32
Q

Oral contraceptives target what?

A

the negative feedback system clamping secretion of GRH, FH and LH

33
Q

2 main types of oral contraceptives

A
  • combined oestrogen and progesterone (combined pill)
  • progesterone alone (pill/minipill)
34
Q

How does the combined pill work?

A
  • estrogen inhibits secretion ofn FSH via negative feedback, this prevents development of ovarian follicle
  • progesterone inhibits secretion of LH (negative feedback), prevents ovulation and makes cervical mucous less suitable for passage of sperm
35
Q

How is combined pill taken?

A
  • for 21 days
  • then 7 day pill free period
  • causes withdrawal bleeding - flase period
36
Q

How does the progesterone pill?

A
  • mainly effective due to effect on cervical mucous
  • doesn’t block ovulation
37
Q

Is the progesterone pill reliable?

A

yes but less so than the combined

38
Q

How is progesterone pill taken?

A

daily
- can cause irregular periods but no break for false period