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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
- ZONA FACSCIULATA Glucocorticloids - cortisol - sugar control
- ZONA GLOMERULOSA Mineralocorticoids - aldosterone - salt and water

Mineralocorticoids are blocked by spironolactone and eplenerone

Exogenous glucocorticoids - dexamethasone, betamethasone

Exogenous mineralocorticloids -
fludrocortisone

ZONA RETICULARIS - androgens. primarily DHEA
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 is amenorrhoeic. If. no breast development by 15 if have periods

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, which inhibits protein kinase A
- Hormones that inhibit - progesterone, inhibin, relaxin

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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/BMD
Deficiency G6PD
Daemophilia
Dont see colour

DMD
G6PD deficiency
Haemophilia
Red-green colour blindness

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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

25
What is the role of ALDOSTERONE? Where is it released from? What stimulates it? What does it cause?
Na/water regulation Released from the zona glomerulosa of the adrenal cortex. Stimulated by: - K+ being high - Angiotensin 2 - 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 - Vasoconstriction
26
What is the blood flow per minute through the uterine artery at term vs non pregnancy
Term = 750ml/minute. At term counts as 12% of full maternal circulation Non pregnancy = 45ml/minute
27
What are the inhibitors of prolactin?
THERE ARE TWO OF THEM Somatostatin Dopamine
28
What is DHEA? Where is it produced in the fetus?
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
What is the main endogenous mineralocorticloid
Aldosterone Progesterone is another example
30
In broad terms, what do mineralocorticoids do? What do glucocorticoids do?
BOTH STEROIDS HORMONES Mineralo - salt and water balance Gluco - glucose balance
31
What are the types of haemoglobin and what are they made from? What are the thalassaemias caused by in terms of genetic defect?
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
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
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
Summary of Addisons: What is it? Main symptoms? Main tests?
Primary adrenal insufficiency Cortisol and adrenal insufficiency Clinical features: hypotension, hyponatraemia, hyperkalaemia Testing: cortisol/ short synacthen
34
Summary of Cushings: What is it? Main symptoms? Main tests?
Increase in cortisol Symptoms: hypertension, weight gain, moon face, diabetes, buffalo neck lump Test: dexamethasone suppression test, 24h cortisol
35
Summary of Conn's: What is it? Main symptoms? Main tests?
Primary hyperaldosteroneism Symptoms: hypokalaemia, hypernatraemia, weight loss, tanned skin, hypertension Test: Renin:aldosterone, salt suppression or fludrocortisone suppression
36
What is the role of aromatase? Where is aromatase produced?
Causes conversion of androgens produced by the theca cells into oestrogen (happens in the granulosa cells) Aromatase is produced in the granulosa cells
37
What is the major oestrogen of pregnancy and where is it produced
Estriol. Produced by the placenta
38
What are the types of oestrogen and what are their functions?
E1 - Estrone (produced in adipose tissue) E2 - Estradiol (predominant in reproductive years) E3 - Estriol (predominant during pregnancy - produced by the placenta)
39
What is the definition of primary ovarian insuffficiency
Menopause before the age of 40
40
How do you diagnose perimenopause/menopause?
>45 by perimenopausal symptoms or no periods for 12 months <45 can use FSH
41
Give examples of prolactin antagonists? What receptors do they act on?
Bromocriptine Cabergoline They act on D2 receptors They are dopamine AGONISTS. They are therefore prolactin antagonists.
42
Most common cause of acromegaly
Pituitary adenoma
43
What is Conn's syndrome? Bloods? Causes?
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
Define endocrine/autocrine/exocrine/paracrine
Endo - secrete hormone into circultion to act elsewhere Auto - acts within a cell Exo - secrete into ducts Paracrine - near by cells
45
What is the definition of puberty in girls
Stage 2 breast development
46
In relation to ovulation when does the LH surge occur
24-36h prior to ovulation
47
What is the classification system for puberty? what is the first sign in girls?
Tanner classification Breast development is first sign in girls
48
What are the test results for: - Primary hyperparathyroidism - Secondary hyperparathyroidism - Tertiary hyperparathyroidism
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
What happens to T3/T4 levels in pregnancy
FREE T3/4 - drop Total T3/4 - increase
50
Cause of hypothyroidism WITH antibodies
Hashimotos De Quervains - not autoimmune. Get hyperT then hypoT. Wont have abs
51
Commonest cause of hypothyroidism worldwide? In UK?
Worldwide - iodine deficiency UK - hashimotos
52
Phaeochromocytoma How much HTN is caused by this? How much is familial?
0.1% 20% familial
53
What is the drug of choice to promote lactation? What inhibits it?
Promote - domperidone Inhibit - cabergoline, bromocriptine
54
What is the cause of the hyperpigmentation in hypoadrenalism
The high ACTH. Therefore in secondary adrenal insufficiency the skin is not discoloured
55
What causes angiotensinogen to turn into angiotensin 1
renin

MRCOG part 1 (30 decks)

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