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MRCOG part 1 > endocrine > Flashcards

endocrine Flashcards

1
Q

Describe the layers of the adrenal glands and what each layer produces?
Endogenous?
Exogenous?
Blockers?

A

Adrenal cortex - steroids hormones
- Glucocorticloids - cortisol - sugar control
- Mineralocorticoids - aldosterone - salt and water

Mineralocorticoids are blocked by spironolactone and eplenerone

Exogenous glucocorticoids - dexamethasone, betamethasone

Exogenous mineralocorticloids -
fludrocortisone

Adrenal medulla
- Adrenaline, noradrenaline

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2
Q

How do you define delayed puberty in girls?

How about in boys?

What is precocious puberty?

A

No breast development by age 13

No testicular development or <4ml by age 14

Precocious puberty - development of secondary sexual characteristics before age 8

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3
Q

What are the causes of raised prolactin?

A

Physical:
- Pituitary tumour

Drugs:
- Antipsychotics
- SSRIs
- opiates
- Ranitidine - H2 blockers

Endocrine:
- Hypothyroidism
- Lactation
- Pregnancy
- Acromegaly

Medical conditions:
- Liver failure
- Renal disease
- PCOS

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4
Q

Describe the cells present in the ovaries and their various functions

A

Theca cells
- Produce androgens but cant convert to oestradiol
- LH stimulates production of androgens
- LH also stimulates contraction of the smooth muscle layer of the theca externa which causes the mature oocyte to pop.

Granulosa cells
- FSH signals granulosal cells to produce aromatase which in turn converts the androgens to oestradiol.
- Produce progesteron

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5
Q

Where is glucagon produced?
What does it cause?What are the stimulants of glucagon?
What are the inhibitors of glucagon?

A

Alpha cells of pancreas

Increases blood glucose
Increases glycogenosysis
Increase gluconeogenesis

Stimulants
- Hypoglycaemia
- Adrenaline
- Acteylcholine
- Arginine/alanine
- Cholecystokinin - producted in small intesting and triggers release of enzymes to digest fat and protein

Inhibits:
- Insulin
- Raised urea
- Somatostatin
- keto-acids

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6
Q

What happens in pregnancy with:
- TSH
- T3/T4

A

Decreased TSH (remember the limits of normal go down in pregnancy)

Increase total T3/T4 but gradually go down a bit from 1-3 trimester.
Free T3/T4 is decreased

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7
Q

What is the typical finding on an FBC with addisons disease?

A

eiosinophilia - dont know why

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8
Q

Addisons disease.

What is it?
Causes?
Symptoms/signs?
Blood test results?
Treatment?

A

Primary adrenal insufficiency

Causes:
- Autoimmune adrenalitis (most common)
- Secondary - low ACTH from pituitary
- Tertiary - low CRH from hypothalamus

Symptoms:
- Fatigue
- Darkening of the skin
- Weight loss
- Hypotension
- Myalgia/arthralgia

Bloods:
- High K
- Low Na
- eiosinophilia
- Metabolic adicosis
- Hypoglyaemia

Treatment
- Hydrocortisone
- Fludrocortisone if BP low

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9
Q

Which hormones are structurally similar to TSH

What other group is similar?

A

FSH, HCG, LH
HAT - think HCG, androgen stimulating, TSH

Prolactin, GH, human placental lactogen

PHaG - prolactin, hpl, GH

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10
Q

What are the levels for:
- Osteopenia
- Ostoporosis
- Severe osteoporosis

A

Osteopnia -1 to -2.5
Osteoporosis <-2.5
Severe osteoporosis <-2.5 with fragility fracture

Fragility fracture: NOF, foosh, spine, proximal humerus

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11
Q

How does oxytocin stimulate the contraction of the uterus?

What inhibits contractions?

A

Activates phospholipase C –> producs IP3 –> Calcium release.

Ultimately needs to release intracellular calcium. Triggers this with activating phospholipase C to produce IP3 which then causes release of the calcium

Inhibitors of contractions:
- cAMP
- Protein kinase A

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12
Q

What is the common precursor molecule for creation of androgens

A

cholesterol

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13
Q

What conditions lead to an increase in SHBG?

What is the function of SHBG

A

In general, conditions causing weight loss lead to an increased SHBG e.g.
- liver cirrhosis
- hyperthyroidism
- anorexia

In contrast, weight gain –> lower SHBG
- PCOS
- Hypothyroidism
- Cushings
- Anabolic steroids use

SHBG
- Binds 70% of testosterone
- Other 20-30% bound to albumin
- Approx 1% unbound

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14
Q

What is the first line investigation for addisons?

A

U&E
AM cortisol

After this there is a place for the short synacthen test

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15
Q

Which are the X linked dominant conditions

A

3 Rs

Rickets, Retts, Rgile X

Fragile X
Rett syndrome
Vit D resistant rickets

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16
Q

What are the X linked recessive conditions

A

Ds:

DMD
Dalport syndrome
Deficiency G6PD
Daemophilia

DMD
Alport syndrome
G6PD deficiency
Haemophilia

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17
Q

What are the inheritence patterns of the PKDs

A

ADULT PKD - AD
Infantile PKD - recessive

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18
Q

Which conditions are associated with phaeochromocytoma

What is phaeochromocytoma?

What are the symptoms?

A

NOT MEN 1

MEN 2
Von hippel lindau
Neurofibromatosis 1
Paraganglioma syndromes 1,3,4

Neuroendocrine tumour of the medulla of the adrenal glands. Produces high levels of catecholamines

Symptoms:
- Sweating
- Headaches
- Palpitations

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19
Q

MEN 1 vs MEN 2

A

MEN 1 - PPP
- Pituitary
- Parathyroid hyperplasia
- Pancreas

MEN 2 - PMP
- Parathyroid hyperplasia
- Medullary thyroid carcinoma
- Pheochromocytoma

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20
Q

What do the islets in the pancreas secrete

A

Alpha cells - glucagon
Beta cells - Insulin
Delta cells - somatostatin
Gamma cells - Pancreatic polypeptide

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21
Q

Where does somatostatin come from?

What is it’s function?

A

Comes from the delta cells of the pancreas.

Function = THE MAIN INHIBITOR. Primarily prevents growth

Inhibits: pancreas/gastric/pituitary hormone release
- Both glucagon and insulin
- Growth hormone
- Prolactin
- TSH

We think it plays a role in preventing unnecessarily fast cell division

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22
Q

Which hormones are responsible for:

Ductal morphogenesis
Alveolar morphogenesis

A

Ductal - oestrogen and GH
DOM is resonsible for the ductal morphogenesis
- Ductal
- Oestrogen
- Morphogenesis

Alveolar - HPL, prolactin, progesterone
PAM is responsible for the alveolar morphogenesis
- Progesterone
- Alveolar
- Morphogenesis

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23
Q

What are the causes of cushing’s syndrome/disease

A

DISEASE - endogenous - pituitary adenoma.

SYNDROME - exogenous - steroids

24
Q

How much testosterone is bound to SHBG

A

70%

25
Q

What is the role of ALDOSTERONE?

Where is it released from?

What stimulates it?

What does it cause?

A

Na/water regulation

Released from the zona glomerulosa of the adrenal cortex.

Stimulated by:
- K+ being high
- Renin from the kidneys via RAAS
- ACTH and steroid hormones (minor)

It causes:
- Na resorption and therefore water resorption from the collecting duct in the kidneys
- Upregulates eNACs - epithelial sodium resorption - distal part of the nephron

26
Q

What is the blood flow per minute through the uterine artery at term vs non pregnancy

A

Term = 750ml/minute. At term counts as 12% of full maternal circulation

Non pregnancy = 45ml/minute

27
Q

What are the inhibitors of prolactin?

A

THERE ARE TWO OF THEM

Somatostatin
Dopamine

28
Q

What is DHEA?
Where is it produced in the fetus?

A

Dihydroeipandosterone (DHEA) is a steroid hormone.

It is made from cholesterol (via pregnenarone). It is produced in the adrenals in the fetus which stimulates the placenta to produce oestrogen - keeps the pregnancy going.

The production of DHEA stops at birth and starts again around 6-8 before puberty

29
Q

What is the main endogenous mineralocorticloid

A

Aldosterone

Progesterone is another example

30
Q

In broad terms, what do mineralocorticoids do?

What do glucocorticoids do?

A

BOTH STEROIDS HORMONES

Mineralo - salt and water balance

Gluco - glucose balance

31
Q

What are the types of haemoglobin and what are they made from?

What are the thalassaemias caused by in terms of genetic defect?

A

Adult Hb - 2x alpha, 2x beta (97% of HB)

HBa2 - 2x alpha, 2x delta (1-3% of HB)

HBF - 2x alpha, 2x gamma

Chromosome 16 codes for the alpha Hb - therefore alpha thalassaemia is a defect in chromosome 16

Chromosome 11 codes for the beta and delta hb - therefore beta/delta thalassaemia is a defect in chromosome 11

32
Q

Give a summary of the homones that are released from the following areas:

Hypothalamus

Pituitary

Thyroid

Parathyroid

Pancreas

Adrenals

Ovary

Bowel

Placenta

Uterus

Adipose

Kidney

Liver

A

Hypothalamus
- TRH
- GRH
- CRH
- GHRH
- Oxytocin
- ADH/vasopressin
- Somatostatin

Pituitary
- ANTERIOR - prolactin, FSH, LH, TSH, GH, ACTH
- POSTERIOR - released but not synthesised - ADH, oxytocin

Thyroid
- T3/T4 (epithelial cells)
- Calcitonin (parafollicular cells)

Parathyroid
- Parathyroid hormone

Pancreas
- Insulin
- Glucagon
- Somatostatin

Adrenals (GETS SWEETER NEAR THE CENTRE)

  • Zona glomerulosa CORTEX - mineralocorticoids - aldosterone
  • Zona fasicularis CORTEX - glucocorticoids - cortisol
  • Zona reticulata CORTEX - androgens
  • Chromaffin cells MEDULLA - adrenaline
  • Chromaffin cells MEDULLA - dopamine
  • Chromaffin cells MEDULLA - noradrenaline

Ovary
- AMH (granulosa cells)
- Androgens (theca cells)
- Oestrogen
- Progesterone

GIT
- Stomach - Gastrin (g cells), Somatostatin (D cells)z, Histamine (StomachECL cells)
- Duodenum - Secretin (S cells), Cholecystokinin (I cells)

Placenta
- Human placental lactogen
- Progresterone
- HCG

Uterus
- Prolactin (decidual cells)
- Relaxin (decidual cells)

Adipose
- Leptin
- Estrone
- Small amount of progesterone

Kidney
- Renin
- EPO
- Thrombopoetin

Liver
- Insulin like growth factor
- Angiotensinogen, angiotensin
- Thrombopoetin

33
Q

Summary of Addisons:

What is it?
Main symptoms?
Main tests?

A

Primary adrenal insufficiency

Cortisol and adrenal insufficiency

Clinical features: hypotension, hyponatraemia, hyperkalaemia

Testing: cortisol/ short synacthen

34
Q

Summary of Cushings:

What is it?
Main symptoms?
Main tests?

A

Increase in cortisol

Symptoms: hypertension, weight gain, moon face, diabetes, buffalo neck lump

Test: dexamethasone suppression test, 24h cortisol

35
Q

Summary of Conn’s:

What is it?
Main symptoms?
Main tests?

A

Primary hyperaldosteroneism

Symptoms: hypokalaemia, hypernatraemia, weight loss, tanned skin, hypertension

Test: Renin:aldosterone, salt suppression or fludrocortisone suppression

36
Q

What is the role of aromatase?

Where is aromatase produced?

A

Causes conversion of androgens produced by the theca cells into oestrogen (happens in the granulosa cells)

Aromatase is produced in the granulosa cells

37
Q

What is the major oestrogen of pregnancy and where is it produced

A

Estriol. Produced by the placenta

38
Q

What are the types of oestrogen and what are their functions?

A

E1 - Estrone (produced in adipose tissue)
E2 - Estradiol (predominant in reproductive years)
E3 - Estriol (predominant during pregnancy - produced by the placenta)

39
Q

What is the definition of primary ovarian insuffficiency

A

Menopause before the age of 40

40
Q

How do you diagnose perimenopause/menopause?

A

> 45 by perimenopausal symptoms or no periods for 12 months

<45 can use FSH

41
Q

Give examples of prolactin antagonists?

What receptors do they act on?

A

Bromocriptine
Cabergoline

They act on D2 receptors

They are dopamine AGONISTS.

They are therefore prolactin antagonists.

42
Q

Most common cause of acromegaly

A

Pituitary adenoma

43
Q

What is Conn’s syndrome?

Bloods?

Causes?

A

Primary hyperaldosteroneism

HYPERTENSION - water retention

Tests:
- Aldosterone:renin ratio is useful first test
- Diagnosis - saline suppression test/fludrocortisone suppression test

Bloods:
- Hypernatraemia
- Alklaemia
- Sometimes low K but often normal

Causes:
- Adrenal hyperplasia (60%)
- Adrenal adenoma (technically Conns)

44
Q

Define endocrine/autocrine/exocrine

A

Endo - secrete hormone into circultion to act elsewhere

Auto - acts within a cell

Exo - secrete into ducts

45
Q

What is the definition of puberty in girls

A

being capable of reproduction

46
Q

In relation to ovulation when does the LH surge occur

A

24-36h prior to ovulation

47
Q

What is the classification system for puberty?

what is the first sign in girls?

A

Tanner classification

Breast development is first sign in girls

48
Q

What are the test results for:
- Primary hyperparathyroidism
- Secondary hyperparathyroidism
- Tertiary hyperparathyroidism

A

Primary - high PTH, high Ca
Secondary - high PTH, low Ca (usually due to renal failure)
Tertiary - High PTH, high Ca (usually after prolonged period of secondary, there will be a history of renal failure)

49
Q

What happens to T3/T4 levels in pregnancy

A

FREE T3/4 - drop
Total T3/4 - increase

50
Q

Cause of hypothyroidism WITH antibodies

A

Hashimotos

De Quervains - not autoimmune. Get hyperT then hypoT. Wont have abs

51
Q

Commonest cause of hypothyroidism worldwide?

In UK?

A

Worldwide - iodine deficiency

UK - hashimotos

52
Q

Phaeochromocytoma

How much HTN is caused by this?

How much is familial?

A

0.1%

20% familial

53
Q

What is the drug of choice to promote lactation?

What inhibits it?

A

Promote - domperidone

Inhibit - cabergoline, bromocriptine

54
Q

What is the cause of the hyperpigmentation in hypoadrenalism

A

The high ACTH. Therefore in secondary adrenal insufficiency the skin is not discoloured

55
Q

What causes angiotensinogen to turn into angiotensin 1

A

renin

MRCOG part 1 (20 decks)

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