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Year 2 - Endocrinology (DP) > Physiology > Flashcards

Flashcards in Physiology Deck (209):
1

Where is the thyroid gland located?

Anterolateral to larynx and trachea

2

Where are the parathyroid glands located?

Posterior aspect of each thyroid lobe

3

What do thyroid follicles surround and what does it contain?

The colloid:
- Tyrosine-containing thyroglobulin filled sphere

4

What is the process by which T3 and T4 are made and stored?

1. Iodine taken up by follicle cells
2. Iodine attaches to tyrosine residues on thyroglobulin:
-Forms two units
> Monoiodotyrosin unit (MIT)
> Diiodotyrosine unit (DIT)
3. Coupling of MIT and DIT:
- MIT + DIT -> T3
- DIT + DIT -> T4
4. Stored in colloid thyroglobulin until required

5

What thyroid hormone is secreted in larger amounts?

T4 (90% of secreted hormone)

6

Which thyroid hormone is more potent?

T3 (~4 times more potent than T4)

7

Where is T4 converted to T3?

Liver
Kidneys

8

What thyroid hormone is the major biologically active hormone?

T3

9

Why do T3 and T4 bind to plasma proteins?

They are lipophilic

10

What plasma proteins do thyroid hormones bind to?

Thyroxine-Binding Globulin -> ~70%
Thyroxin-Binding Prealbumin -> ~20%
Albumin -> ~5%

11

What is the other name for thyroxine-binding prealbumin?

Transthyretin

12

What are the features of T3 binding? What does this allow?

Bound 10-20 times less avidly by TBG
Not bound significantly by TTR
This allows more rapid onset and offset of action

13

What does the metabolic state correlate closer to; level of free hormone of level of total plasma concentration?

Level of free hormone

14

How does Ninewells asses thyroid hormones?

Measure fT3 and fT4

15

What can cause increased levels of thyroxine-binding globulin?

Pregnancy
Newborn
Oral contraceptive (Increased oestrogen)
Tamoxifen
Hep A
Chronic Hepatitis
Billiary cirrhosis

16

What can cause decreased levels of thyroxine-binding globulin?

Androgens
Cushing's
Acromegaly
Severe systemic illness
Chronic liver disease
Nephrotic syndrome
Drugs:
- Phenytoin
- Carbamazepine

17

How do carbimazole and propylthiouracil work?

Inhibit thyroperoxidase:
- Enzyme needed to produce MIT and DIT

18

What does increased TBG cause?

Increased total T4
Normal fT4

19

What does decreased TBG cause?

Reduced total T4
Normal fT4

20

How do T3 and T4 increase the basal metabolic rate?

Increase the number and size of mitochondria
Increase oxygen use and ATP hydrolysis
Increase synthesis of respiratory chain enzymes

21

How much of thermogenesis do T3 and T4 contribute to?

~30%

22

What effects do T3 and T4 have on carbohydrate metabolism?

Increase blood glucose:
- Stimulate glyogenolysis + gluconeogenesis
Increase insulin-dependent glucose uptake

23

What effects do T3 and T4 have on lipid metabolism?

Mobilise fats from adipose
Increase fatty acid oxidation

24

What effects do T3 and T4 have on protein metabolism?

Increase protein synthesis

25

What effects do T3 and T4 have on growth?

GHRH production and secretion requires T3 and T4
Permissive actions:
- Glucocorticoid-induced GHRH release
- Allows GH and somatomedin activity

26

What effects do T3 and T4 have on the foetal and neonatal brain?

Myelinogenesis
Axonal growth

27

How do changes in T3 and T4 concentrations affect the CNS?

Hypothyroid:
- Slow intellectual functions
Hyperthyroid:
- Nervousness
- Hyperkinesis
- Emotional lability

28

What affect does T3 and T4 have on the SNS?

Increases responsiveness to adrenaline and NA:
- By increasing the number of receptors
Also increases force and rate of heart contractions

29

What happens to TRH in cold temperatures (in kids)?

TRH is released:
-> TSH released -> T3 and T4 release

30

What effect does stress have on thyroid hormone regulation?

Inhibits TRH and TSH release

31

When are thyroid hormones highest and lowest?

Highest at night
Lowest in the morning

32

What family of 3 enzymes help activate and deactivate T3 and T4?

Deiodinase enzymes

33

How do the deiodinase enzymes work?

Add/Remove an idoine atom in the outer ring of T3 and T4

34

What enzyme activates T4 to T3 in tissues?

D2

35

Where is D1 found?

Liver
Kidney

36

Where is D2 found?

Heart and skeletal muscle
CNS
Fat
Thyroid and pituitary

37

Where is D3 found?

Foetal tissue and placenta
Brain -> Except pituitary

38

Weight gain, bradycardia, fatigue, cold intolerance, myxoedema (adults) and cretinism (kids) are signs of what?

Hypothyroidism

39

How does cretinism present?

Dwarfism
Reduced mental functioning

40

Why does thyroid-stimulating Ig cause Grave's (hyperthyroidism)?

Acts like TSH:
- Unchecked by T3 and T4
- No negative feedback

41

What causes exophthalmos in Grave's?

Water-retaining carbohydrates build up behind eyes

42

What can a pituitary adenoma compress?

Optic chiasm -> Bitemporal hemianopia
CNs iii, iv and vi:
- iii -> Eye down and out
- iv -> Superior oblique paralysis -> Vertical diplopia
- vi -> Lateral rectus paralysis -> Horizontal diplopia

43

What else can a pituitary adenoma result in?

Hypoadrenalism
Hypothyroidism
Hypogonadism
DI
GH deficiency

44

What are physiological causes of raised PRL?

Breast feeding
Pregnancy
Stress
Sleep

45

What drugs can cause a raised PRL?

Dopamine antagonists (Metoclopramide)
Antipsychotics
Antidepressants (TCSa and SSRIs)
Others (Oestrogens and Cocaine)

46

What are pathological causes of a raised PRL?

Hypothyroidism
Stalk lesions:
- Iatrogenic
- RTA
Prolactinoma

47

How do women present with a raised PRL?

Early
Galactorrhoea (30-80%)
Oligo-/Amenorrhoea
Infertility

48

How do men present with a raised PRL?

Late
Impotence
Abnormal visual field
Headache
Anterior pituitary dysfunction

49

In a patient with a raise PRL, what might we see in a pituitary MRI?

Micro-/Macroprolactinoma
Pituitary stalk lesion
Optic chiasm compression

50

How is a prolactinoma treated?

Dopamine agonists:
- Bromocripton -> PO tds
- Quinagolide -> PO od
- Cabergoline -> PO twice weekly
> Least side effects (most commonly used)

51

What causes acromegaly?

GH excess

52

What soft tissue features of acromegaly are there?

Thickened skin
Large jaw
Sweaty
Large hands

53

What cardiac features are present in acromegaly?

Hypertension
CHF

54

What are some other features of acromegaly?

Vascular headaches
Snoring/Sleep apnoea
DM
Mass effects:
- Visual fields
Colonic polyps and cancer

55

How do we diagnose acromegaly?

IGF-1:
- Age and sex matched
Glucose tolerance test:
- 75g PO suppression test
- Check GH at 0, 30, 60, 90 and 120 minutes
- Normal -> GH suppressed to

56

What will the result of a glucose tolerance test be in a patient with acromegaly?

No suppression
Paradoxical rise
GH remains >1μg/L

57

Why does glucose suppress GH?

GH stimulates an increase in blood glucose levels
So if glucose is raised, negative feedback will cause GH levels to drop

58

What is the first line treatment for acromegaly?

Pituitary surgery
Followed by external radiotherapy to pituitary fossa

59

What is the second line treatment and when is it commenced?

Drug treatment:
- Cabergolin
- Octreotide (Somatostatin analogue)
- Pegvisomat
If on GTT retest, GH is still >1μg/L

60

At what GH level is a patient clinical safe from further progression of acromegaly?

GH

61

What effects do somatostatin analogues have in acromegaly?

Reduce GH in most
Shrink the tumour by 30-50%:
- 6-12 months for effect
- Recurs 6 weeks if stopped
Relieves headaches 1 hours post-op
Improve surgical outcomes

62

What are some side effects of somatostatin analogues?

Local stinging
Short term:
- Flatulence
- Diarrhoea
- Abdominal pain
Long term:
- Gastritis (

63

How does pegvisomat work?

GH antagonist:
- Binds to GH receptor competitively

64

How is pegvisomat administered?

S/C injection:
- 10-30mg/dayy

65

What effects does pegvisomat have?

No decrease in tumour size
Reduces IGF-1
May increase serum GH

66

Why is pegvisomat the last line therapy?

20mg does costs £36000/year

67

What cancers must be screened for after acromegaly has been treated?

Colon
Tubulo-villous adenoma

68

What CVS risk factors need monitored after acromegaly treatment?

BP
Lipids
Glucose

69

What regulates aldosterone?

RAAS
Plasma K+

70

What encourages the hypothalamus to increase CRH production and, hence, increase cortisol production?

Stress
Illness
Time of day (Peak at 9am)

71

When is the RAAS activated?

When blood pressure falls

72

How does angiotensin ii correct BP?

Directly by vasoconstriction
Indirectly via aldosterone:
- Increases Na+ reabsorption in kidney
- Hence water reabsorption increases

73

What are the 6 classes of steroid receptors?

Glucocorticoid
Mineralocorticoid
Progestin
Oestrogen
Androgen
Vitamin D

74

What effect does cortisol have on the CVS?

Increases cardiac output
Increases BP
Increases renal blood flow -> Increases GFR

75

What effect does cortisol have on the CNS?

Mood lability
Euphoria
Decreased libido

76

What effect does cortisol have on bone and connective tissue?

Increased rate of osteoporosis
Reduces serum calcium
Reduces collagen formation
Reduces wound healing

77

What effect does cortisol have on metabolism?

Increases blood glucose
Increases lipolysis
Increases proteolysis

78

What effect does cortisol have on the immune system?

Reduced capillary dilation
Reduced leucocyte migration
Reduced macrophage activity
Reduced cytokine production

79

What are the three main principles of using corticosteroids for clinical treatments?

Reduce inflammation -> Supraphysiological dose
Immunosuppression -> Supraphysiological dose
Replacement therapy -> Physiological dose

80

Which administration route is better for corticosteroids; IM or IV?

IM

81

What are corticosteroids used to treat (mainly)?

Allergy
Inflammatory disease:
- RA
- UC
- Crohn's
Malignancy

82

What effects does aldosterone have?

Na+/K+ balance:
- Increases Na+ reabsorption
- Increases K+/H+ secretion (and hence excretion)
Increases blood pressure:
- Water follows Na+ -> Increased water reabsorption
Regulates ECV

83

In which of these locations are mineralocorticoid receptors not found:
- Kidneys
- Heart
- Salivary glands
- Gut
- Sweat glands

Heart

84

Where does primary adrenal insufficiency arise?

Adrenal gland

85

What can cause primary adrenal insufficiency?

Addison's
CAH
Adrenal TB/Malignancy

86

What can cause secondary adrenal insufficiency?

Lack of ACTH
Exogenous steroid
Pituitary/Hypothalamic disorders

87

What causes Addison's Disease?

Autoimmune destruction of adrenal cortex

88

True or false; Addison's is the most common cause of adrenal insufficiency?

False
It is only the most common cause of primary adrenal insufficiency
Exogenous steroids are the most common cause overall

89

What is Addison's disease associated with?

T1DM
Thyroid disease (Grave's)
Pernicious anaemia

90

What are the clinical features of Addison's disease?

Weight loss
Fatigue
Hypotension -> Dizziness
GI:
- Abdominal pain
- Vomiting
- Diarrhoea
Oligo-/Amenorrhoea
Skin pigmentation:
- Skin creases
- Buccal surfaces

91

What biochemistry is seen in primary adrenal insufficiency:
- CRH
- ACTH
- Cortisol
- Aldosterone
- Renin
- Na+
- K+

CRH is high
ACTH is high
Cortisol is low
Aldosterone is low
Renin is high
Na+ is low
K+ is high

92

What is the definitive diagnosis of primary adrenal insufficiency?

Short synACTHen test:
- Measure plasma cortisol
> Before
> 30 minutes after IV/IM ACTH
Normal result:
- Baseline -> >250nmol/L
- Post-ACTH -> >550nmol/L
Cortisol will barely rise on the synacthen test

93

Should we delay treatment of adrenal insufficiency to confirm diagnosis?

NO

94

How do we treat adrenal insufficiency?

Hydrocortisone (cortisol replacement):
- IV first if unwell
- 15-30mg daily -> Divided doses
- Mimic diurinal rhythm
> 10 mg in the morning
> 5mg at lunch and at night
Fludrocortisone (aldosterone replacement):
- Monitor BP and K+

95

What causes secondary adrenal insufficiency?

Lack of CRH and ACTH (hypothalamic disease) or ACTH (pituitary disease)

96

What is the commonest cause of secondary adrenal insufficiency?

Exogenous steroids:
- High dose prednisolone
- Dexamethasone
- Inhaled corticosteroid

97

What are the clinical features of secondary adrenal insufficiency?

Similar to Addison's:
- Except no hyperpigmentation (since no ^ ACTH)
- And aldosterone production is intact

98

How is secondary adrenal insufficiency treated?

Hydrocortisone only

99

What is Cushing's syndrome?

Excess cortisol

100

What are the clinical features of Cushing's syndrome?

Easy bruising
Facial plethora
Striae
Proximal myopathy
Central obesity
Acne
Amenorrhoea
Hypertension
Osteoporosis

101

What are the ACTH-dependent causes of Cushing's syndrome?

Pituitary adenoma -> Cushing's DISEASE (68%)
Ectopic ACTH:
- Carcinoid
- Carcinoma (SCLC)
Ectopic CRH

102

What are ACTH-independent causes of Cushing's syndrome?

Adrenal adenoma (10%)
Adrenal carcinoma (8%)
Nodular hyperplasia (1%)

103

What causes primary Hypercortisolism/Primary Cushing's syndrome?

Adrenal adenoma

104

What causes secondary Cushing's syndrome?

Pituitary adenoma (Cushing's Disease)

105

How can Cushing's Syndrome be screened for?

Overnight dexamethasone suppression test
24hr urinary free cortisol
Late night salivary cortisol

106

What is the definitive diagnostic test for Cushing's Syndrome?

Low dose dexamethasone:
- 0.6mg every 6 hours for 2 days
- Repeat to confirm

107

What is the commonest cause of cortisol excess?

Prolonged high dose steroid therapy:
- Chronic suppression of ACTH production
> Adrenal atrophy

108

What is Conn's syndrome?

Primary aldosteronism due to an adrenal adenoma

109

What causes primary aldosteronism?

Autonomous production:
- Independent of Angiotensin ii and K+
Usually due to:
- Adrenal hyperplasia -> Bi-/Unilateral
- Adrenal adenoma -> Conn's syndrome
- Familial

110

True or false; Primary aldosteronism is the commonest secondary cause of hypertension?

True

111

What are the clinical features of primary aldosteronism?

Significant hypertension
Hypokalaemia
Alkalosis

112

What effects do aldosterone exert on the CVS?

Increase cardiac collagen
Synthesis of:
- Cytokines
- ROS
Na+ retention
Altered endothelial function:
- Increased pressure response
Increased SNS outflow

113

What is the net effect of all the CVS functions of aldosterone?

Increased BP
LVH
Atheroma

114

What is the commonest cause of primary aldosteronism?

Bilateral adrenal hyperplasia (60%)

115

What percentage of primary aldosteronism cases are Conn's syndrome (adrenal adenoma)?

30%

116

In what conditions are K+ channel mutations seen?

Adrenal aldosterone-producing adenomas
Hereditary hypertension

117

What is the function of the KCNJ5 channel and what happens if it is mutated?

Rectifying selective channel:
- Maintains membrane hyperpolarisation
Most mutations are gain-of-function and result in Na+ entry and depolarisation

118

What is the first step in diagnosing primary aldosteronism?

Confirm aldosterone excess:
- Measure plasma aldosterone and renin
> Calculate aldosterone-renin ratio (ARR)
If ARR is raised:
- Saline suppression test
- Give 2L of saline
> Failure to suppress aldosterone by >50%
> Primary aldosteronism

119

What is the second step in diagnosing primary aldosteronism?

Confirm subtype:
- Adrenal CT -> Demonstrates adenoma
- Adrenal vein sampling -> Confirms adenoma

120

What surgical technique can be used to treat primary aldosteronism and when is it used? What does it cure?

Unilateral laparoscopic adrenalectomy
Only if adrenal adenoma (confirmed on vein sampling)
Cures:
- Hypokalaemia
- 30-70% of hypertension

121

When is medical treatment used in primary aldosteronism and what drugs are used?

In bilateral adrenal hyperplasia
Drugs:
- Spironolacton
- Eplerenone

122

What is the commonest enzyme deficiency in CAH? What is the mode of inheritance

21-hydroxylase deficiency:
- 1 in 120,000 live births
- Autosomal recessive

123

What is classical 21-hydroxylase deficiency?

Total deficiency
Salt-wasting
Simple virilising

124

What is non-classical 21-hydroxylase deficiency?

Particl deficiency
Hyperandrogenaemia

125

How is CAH diagnosed?

Basal/Stimulated 17-OH Progesterone will be very high:
- >242nmol/L
- Normal is

126

Which of the following is not a presenting feature in males with classical CAH:
- Presentation at 2-3 weeks old
- Poor weight gain
- Clear biochemistry
- Acne

Acne

127

What is the main presenting feature in females with classical CAH?

Ambiguous genitalie

128

Which of the following is not a feature of non-classical CAH:
- Hirsutism
- Poor growth
- Acne
- Oligomenorrhoea
- Precocious puberty
- Infertility

Poor growth

129

How is CAH treated in children?

Glucocorticoids
Mineralocorticoids
Surgery
Achieve maximum growth

130

How is CAH treated in adults?

Control androgens
Restore fertility
Avoid steroid over-replacement

131

What do the following clinical signs indicate:
- Labile hypertension
- Postural hypotension
- Paroxysmal sweating
- Headaches
- Pallor
- Tachycardia

Phaeochromocytoma

132

What are some symptoms of phaeochromocytomas?

Classical triad:
- Hypertension
- Headache
- Sweating
Palpitations
SoB
Constipation
Anxiety
Weight loss
Flushing

133

What complications can phaeochromocytomas cause?

LVF
Myocardial necrosis
CVA
Shock
Paralytic ileus

134

What happens to the following in phaeochromocytomas:
- Glucose levels
- Potassium
- Haematocrit
- Calcium
- pH

Hyperglycaemia
Hypokalaemia
Increased haematocrit
Mild hypercalcaemia
Lactic acidosis

135

When should we investigate for phaeochromocytoma?

FHx
Hypertension:
- Resistant
- If younger than 50
Classical symptoms
Hypertension + Hyperglycaemia

136

How do we investigate phaeochromocytoma?

Confirm catecholamine excess:
- Two 24hr urinary catecholamines
- Plasma (At time of symptoms)

137

How can we identify the source of the catecholamine excess?

MRI:
- Abdomen
- Whole body
Meta-Iodobenzyguanidine (MIBG)
PET Scan

138

How do we treat phaeochromocytoma medically?

Full α and β blockade:
- α before β
> If β done first -> Unopposed α-stimulation
-> Malignant arrhythmia
- Phenoxybenzamine (α-blocker)
- Propanolol/Atenolol/Metoprolol
Fluid/Blood replacement

139

How do we treat phaeochromocytoma surgically?

Laparoscopic surgery:
- Total excision
- Tumour debulking

140

What syndromes are phaeochromocytomas associated with?

MEN2
Von-Hippel-Lindau Syndrome
Succinate Dehydrogenase mutations
Neurofibromatosis
Tuberose sclerosis

141

What is the mode of inheritance of MEN2?

Autosomal dominant

142

What causes MEN2?

Activating mutations in tyrosine kinase receptor:
- RET proto-oncogene

143

What is MEN2 associated with?

Medullary thyroid cancer
Parathyroid hyperplasia
Bilateral phaeochromocytomas

144

What causes Von-Hippel-Lindau Syndrome?

VHL gene mutations -> Autosomal dominant:
- HIF protein accumulation
- Cell proliferation

145

What tumours does Von-Hippel-Lindau Syndrome tend to cause?

Haemangioblastomas (CNS + retina)
Endolymph tumours
Phaeochromocytomas/Paragangliomas

146

What succinate dehydrogenase gene mutations can cause phaeochromocytomasa?

Inactivating mutations in SDH B, C + D:
- Destabilises HIF-1α

147

What do SDH-D mutations cause?

Head and neck paragangliomas
>70% penetrance

148

What do SDH-B mutations cause?

Malignant paragangliomas

149

What are catecholamines also raised in?

CHF

150

What sort of secretion do catecholamines usually have?

Episodic:
- Normal levels in plasma and urine may vary

151

What sort of tumours are less-efficient at catecholamine synthesis?

Malignant and extra adrenal:
- Dopamine > NA > Adrenaline

152

What drugs can cause hypercalcaemia?

Vitamind D
Thiazides

153

What granulomatous diseases can cause hypercalcaemia?

Sarcoidosis
TB

154

What high calcium turnover diseases can result in hypercalcaemia?

Bedridden
Thyrotoxic
Paget's

155

What are the biochemical features of primary hyperparathyroidism?

Increased serum calcium
Increased/Inappropriately normal serum PTH
Increased urine calcium excretion

156

What malignant mechanisms can result in hypercalcaemia?

Metastatic bone destruction
PTHrp from solid tumours:
- Squamous cell lung cancer
- Breast cancer
Osteoclast activating factors

157

How can we diagnose hypercalcaemia caused by malignancy?

Increased calcium and ALP
Xray/CT/MRI
Isotope bone scan

158

What is the acute treatment of hypercalcaemia?

Fluids:
- Rehydrate -> 0.9% saline 4-6L/24hrs
Consider loop diuretics once rehydrated
Bisphosphonates:
- Single does -> Reduces calcium in 2-3 days
- Max effect at one week
Occasionally steroids:
- Prednisolone -> 40-60mg/day for sarcoidosis
Salmon calcitonin

159

When is Cinacalcet used?

Tertiary hyperparathyroidism
Parathyroid cancer

160

What are indications for parathyroidectomy?

End organ damage:
- Bone disease
> Osteitis Fibrosa Cystica
> Brown tumours
> Pepper pot skull (Multiple myeloma)
- Gastric ulcers
- Renal stones
- Osteoporosis
Calcium >2.85mmol/L
Age

161

What causes primary hyperparathyroidism? What biochemistry is seen?

Primary parathyroid overactivity:
- Adenoma
Biochemistry:
- Raised PTH
- Raised calcium
- Normal renal function

162

What causes secondary hyperparathyroidism? What biochemistry is seen?

Physiological response to hypocalcaemia
Biochemistry:
- Raised PTH
- Reduced calcium

163

What causes tertiary hyperparathyroidism? What biochemistry is seen?

Autonomous parathyroid activity after secondary
Biochemistry:
- Raised PTH
- Raised calcium
- Other electrolytes skewed

164

What inheritance does Hypocalciuric Hypercalcaemia have?

Autosomal dominant

165

What mutations are present in Hypocalciuric Hypercalcaemia?

Deactivating mutations in Calcium-sensing receptor

166

How is Hypocalciuric Hypercalcaemia diagnosed?

Mild hypercalcaemia
Reduced urinary calcium
PTH may be slightly raised
Genetic screening

167

When does oogenesis begin?

In utero

168

When does oogenesis restart after suspension?

Puberty

169

When is oogenesis complete?

At fertilization

170

When does oogenesis cease?

Menopause

171

What are the primordial germ cells and what do they do?

Earliest recognisable female germinal cell
Capable of mitosis
Migrate to genital ridge by week 6 gestation

172

What is oogonia?

Completion of last pre-meiotic division -> Oocytes

173

When oocytes enter meoisis, what happens?

1st meiotic division -> Primary oocytes
2nd meiotic division -> Secondary oocytes

174

What is the polar body?

First body is one of the two products in first stage of meiosis

175

What does the presence of two polar bodies signify?

Sperm entry and completion of second meiotic division

176

What happens during the follicular phase of the menstrual cycle?

Egg matures
Ready for oculation at midcycle

177

What signifies the end of the follicular phase?

Ovulation

178

What happens during the luteal phase of the menstrual cycle?

Development of corpus luteum
Induces preparation of reproductive tract for pregnancy

179

What is the primary follicle?

Before birth, the primary oocyte is surrounded by a single layer of granulosa cells - Primary follicle

180

How many primary follicles are there at birth and what is each capable of?

~2 million
Each can produce a single ovum

181

What happens to the primary follicles until puberty?

Degenerate to scar tissue -> Atresia

182

What is the secondary follicle?

Oocyte grows (x1000) and follicle expands:
- Differentiates under hormonal influence

183

What happens to secondary follicles after puberty?

~400 are ovulated
The rest (99.98%) undergo atresia

184

What happens to follicular cells left behind after ovulation?

Undergo luteinisation:
- Become the corpus luteum

185

What does the corpus luteum secrete and what is this important for?

Progesterone:
- Prepares uterine lining for implantation

186

After ovulation, how long does the corpus luteum continue to grow?

8-9 days

187

What is the maximum length of time the corpus luteum can survive without fertilisation?

14 days

188

What does the corpus luteum do if fertilisation does occur?

Persists
Produces increasing amounts of progesterone (+oestrogen) until after pregnancy

189

Where does FSH act and what does it do?

Acts on ovaries
Stimulates follicle development
Stimulates secretion of oestradiol
Stimulates ovulation

190

Where does LH act and what does it do?

Acts on ovaries
Stimulates:
- Follicle maturation
- Ovulation
- Development of corpus luteum
- Oestrogen secretion

191

What happens during the follicular phase?

1. Hypothalamus secretes GnRH
2. Anterior pituitary secretes FSH + LH
3. Up to 15 follicles are 'rescued' and begin to mature:
- Granulosa and theca cells develop

192

What do the theca cells produce?

Androgens

193

What do the granulosa cells do?

Convert androgens to oestradiol by aromatase

194

What does oestradiol to?

Thickens endometrium
Thins cervical mucus

195

What does oestrogen do?

Suppresses FSH production:
- Selection of dominant follicle

196

What does the granulosa in the dominant follicle express?

LH receptor

197

What causes more GnRH release and when? What does this result in?

High oestrogen levels at the mid-cycle:
- Causes FSH + LH surge from anterior pituitary

198

Put the following steps of ovulation in order:
- Follicle wall weakens
- LH + FSH levels fall
- Cumulus oophorus loosens
- Ovulation -> Oocyte, Zona Pellucida and cumulus
- Inc in follicular fluid + number of granulosa
- COC picked up by oviduct

1. Inc in follicular fluid + number of granulosa
2. Cumulus oophorus loosens
3. Follicle wall weakens
4. Ovulation -> Oocyte, Zona Pellucida and cumulus
5. COC (cumulus-oocyte complex) picked up by oviduct
6. LH + FSH levels fall

199

What causes the corpus luteum to degenerate and what does it form?

At 12 days, if there is no hCG from an embryo the corpus luteum degenerates -> Corpus Albicans

200

What is the function of hCG?

Maintains the corpus luteum

201

When does the placenta take over progesterone production from the corpus luteum?

At 6 weeks gestation
(Corpus luteum -> Corpus albicans)

202

What is the function of progesterone during pregnancy?

Supports pregnancy
Suppresses ovulation

203

What role does FSH have in spermatogenesis?

Initiates spermatogenesis (with testosterone)
Causes Sertoli cells to express:
- Androgen Binding Globulin (ABG)
- Inhibin

204

What role does FSH have in spermatocytogenesis?

Leads to development of Sertoli cells:
- Act as nursing cells for spermatids

205

What role does LH have in spermatocytogenesis?

Promotes Leydig cell secretion of testosterone:
- Initiates spermatogenesis

206

When does spermatocytogenesis occur?

In males at the age of puberty (10-14 years)

207

What role does LH have in spermatogenesis?

Causes interstitial Leydig cells to secrete testosterone

208

What role does testosterone have?

Decreases release of:
- GnRH
- LH
Converted to dihydrotestosterone:
- Enlargement of male sex organs
- Secondary sexual characteristics
- Anabolism
Binds to ABG made by Sertoli cells:
- Increases its concentration in luminal fluid
> Enables spermatogenesis
> Enables sperm maturation in epididymis

209

What does inhibin do?

Decreases secretion of FSH