16. Drugs and hormones Flashcards
(38 cards)
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
2
Q
Define ‘neurotransmitters’
A
a chemical substance synthesised by neurone and secreted directly onto adjacent neurones or tissues
- where it exerts its action
3
Q
Difference between endocrine and nervous system
A
- endocrine has hormones
- neuro has neurotransmitters
4
Q
How is the endocrine system organised?
A
- endocrine glands/cells
- target cells
5
Q
Define ‘endocrine glands/cells’
A
secrete hormones into blood stream
6
Q
Define ‘target cells’
A
- cells with receptors for a given hormone
- that can alter activities in response to the hormone
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
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
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
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
11
Q
What is GRH?
A
gonadotrophin releasing H
12
Q
What is FSH?
A
follicle stimulating H
13
Q
What is LH?
A
lutenising H
14
Q
Disorders of Cortisol
A
- Cushing’s syndrome - hypersecretion of it
15
Q
Causes of Cushing’s syndrome
A
- adrenal or pituitary tumour (Cushing’s disease)
- side effect of chronic glucocorticoid therapy
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
What can stop the Katp channels in beta cells?
- sulphonylureas like glibenclamide
- block the channels so cause depolarisation
- increase insulin secretion independently of glucose levels
- need partiallu functioning beta cells
26
How is sulhonylureas's effect on diabetes useful?
- treatment for diabetes
- increases insulin secretion
27
What does estrogen do?
- sensitises LH releasing cells in pituitary
- proliferation of endometrium
- inhibits FSH so regulates cycle
28
What does progesterone do?
- 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
After ovulation what are the 2 options?
- fertilization
- no fertilization
30
What happens if no fertilization takes place after ovulation?
- 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
If a fertilized ovum is implanted, what happens?
- 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
Oral contraceptives target what?
the negative feedback system clamping secretion of GRH, FH and LH
33
2 main types of oral contraceptives
- combined oestrogen and progesterone (combined pill)
- progesterone alone (pill/minipill)
34
How does the combined pill work?
- 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
How is combined pill taken?
- for 21 days
- then 7 day pill free period
- causes withdrawal bleeding - flase period
36
How does the progesterone pill?
- mainly effective due to effect on cervical mucous
- doesn't block ovulation
37
Is the progesterone pill reliable?
yes but less so than the combined
38
How is progesterone pill taken?
daily
- can cause irregular periods but no break for false period
