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Part 1 MRCOG > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Hypocalcaemia symptoms

A

Paresthesia, muscle spasms, cramps, tetany, circumoral numbness, and seizures.
Prolonged QT interval on ECG

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2
Q

Where is calcitonin produced?

A

C Cells (parafollicular cells) of the thyroid

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3
Q

Major oestrogen produced by placenta & its precursor

A

Estriol (E3)

Precursor: 16-OH DHEAS (160 hydroxydehydroepiandrosterone sulfate)

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4
Q

Major oestrogen produced in premenopausal women

A

Estradiol (E2)

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5
Q

Predominant oestrogen in postmenopausal women

A

Estrange (E1)

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6
Q

Hormones structurally similar to TSH (same alpha subunit)

A

hCG, FSH, LH

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7
Q

Most common cause of hypothyroidism worldwide

A

Iodine deficiency

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8
Q

Healthy adult- response to fall in blood glucose

A

Decreased insulin, increased glucagon

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9
Q

Generalised fatigue, raised ALP, non-pregnant

A

Vitamin D deficiency

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10
Q

Rate of pheochromocytoma in pregnancy

A

1 in 54000

Neuroendocrine tumour of the medulla of the adrenal glands secreting high amounts of catecholamines

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11
Q

Where is glucagon produced?

A

Alpha islet cells of pancreas

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12
Q

Where is somatostatin produced?

A

Delta islet cells of pancreas

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13
Q

What do the gamma islet cells of the pancreas produce?

A

Pancreatic polypeptide

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14
Q

Action of glucagon

A

Increases plasma glucose level

Stimulates Glycogenolysis (breakdown glycogen to glucose)

Gluconeogenesis (formation glucose from amino acids)

Inhibits glycolysis (conversion glucose into pyruvate)

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15
Q

Glucagon stimulants/ inhibitors

A

Glucagon Stimulants
Hypoglycemia
Epinephrine
Arginine
Alanine
Acetylcholine
Cholecystokinin

Glucagon Inhibitors
Somatostatin
Insulin
Uraemia
Increased free fatty acids and keto acids into the blood

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16
Q

Causes of raised prolactin

A
  • Hypothyroidism
  • Chronic renal failure
  • Liver disease
  • Pregnancy
  • Stress
  • Lactation
  • Chest wall stimulation & surgery
  • Drugs (Opiates, H2 antagonists e.g. Ranitidine, SSRI’s e.g. Fluoxetine, Verapamil, Atenolol, some antipsychotics e.g risperidone and haloperidol, Amitriptyline, Methyldopa and Oestragen conatining compounds)
  • Hypothalamus tumours
  • Prolactinoma
  • Acromegaly
  • PCOS
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17
Q

What percentage of pregnancies are affected by hypothyroidism (including subclinical hypothyroidism)?

A

2.5%

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18
Q

Most common cause of AI hypothyroidism?

A

Hashimotos (antibodies to thyroid peroxidase- TPO)

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19
Q

Causes of high/ low SHBG?

A

Causes of Low SHBG:
- Androgens (inc anabolic steroids)
- PCOS
- Hypothyroidism
- Obesity
- Cushing’s syndrome
- Acromegaly

Causes of High SHBG:
- Oestrogens e.g. oral contraceptives
- Pregnancy
- Hyperthyroidism
- Liver cirrhosis
- Anorexia nervosa
- Drugs e.g. clomid, anticonvulsants

As a general rule conditions leading to weight gain will lead to a drop in SHBG.
NB low SHBG means more free testosterone, which can lead to hirsutism

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20
Q

Delayed puberty occurs in what percentage of children?

A

3%

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21
Q

Definition of puberty/precocious/ delayed puberty?

A

Normal puberty in girls is defined by becoming capable of sexual reproduction.

Precocious puberty is defined as the development of secondary sexual characteristics at <8 years of age.

Delayed puberty is defined by the absence of testicular development (or a testicular volume lower than 4 ml) in boys beyond 14 years old or by the absence of breast development in girls beyond 13 years old

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22
Q

What are the 3 types of ovulation disorder?

A

WHO type I hypo-gonadotropic, hypo-estrogenic (15%)
e.g. hypothalamic amenorrhoea

WHO type II normo-gonadotropic, normo-estrogenic (80%)
e.g. PCOS

WHO type III hyper-gonadotropic, hypo-estrogenic (5%) e.g. premature ovarian insufficiency

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23
Q

Most common cause of Cushing’s syndrome?

Most common cause of endogenous Cushing’s syndrome?

Test to confirm diagnosis?

A

Steroid treatment

Endogenous: pituitary adenoma (Cushing’s disease)

Dexamethasone suppression test

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24
Q

Conn’s Syndrome & causes

How is it diagnosed?

A

Results from primary hyperaldosteronism

Aldosterone increases resorption of sodium ions (& water) in exchange for potassium in the kidney. The result is increased BP (due to increased blood vol).
Hypokalaemia can be present, but may be normal.
May also get hypernatraemia and alkalosis.

Main cause: adrenal hyperplasia (65%) and adrenal adenoma (30-35%)

Secondary hyperaldosteronism is due to increased renin production in conditions like renal artery stenosis/ renin producing tumour.

Aldosterone to renin ratio (would be high)
Saline suppression test
Ambulatory salt loading test
Fludrocortisone suppression test

CT/ MRI to look for adrenal adenoma

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25
Q

What conditions are associated with increased risk of pheochromocytoma?

A

MEN type 2
Paraganglioma syndromes type 1, 3 and 4
Neurofibromatosis type 1

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26
Q

Prolactin is structurally similar to what other molecules?

A

Growth Hormone & hPL

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27
Q

What other hormones are structurally similar to FSH?

A

LH
HCG
TSH

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28
Q

Addisons disease

Causes
Signs & symptoms
Biochemical features

A

Chronic adrenal insufficiency

Addisons = primary ardrenal insufficiency.
AI adrenalitis is most common cause.

Secondary and tertiary adrenal insufficiency refer to insufficient adrenal hormone production due to a cause external to the kidney.

Secondary adrenal insufficiency is due to deficient ACTH production by the pituitary

Tertiary adrenal insufficiency is due to deficient CRH production by the hypothalamus

Signs & Symptoms
Hypotension
Hyperpigmentation (this is due to increased ATCH production)
Myalgia
Arthralgia
Weight loss
Anxiety/personality change
Coma in Addisons crisis

Biochemical features
Hypercalcemia
Hypoglycemia
Hyponatremia
Hyperkalemia
Eosinophilia and lymphocytosis
Metabolic acidosis

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29
Q

What is deficient in Addisons and what impact does this have?

A

Both glucocorticoid and mineralocorticoid hormones are deficient

Main mineralocorticoid is aldosterone (accounts for >90% mineraocorticoid activity in humans).

Aldosterone should drive the Na/K pump in the kidney and result in sodium & water retention & K+ secretion.
Should also drive H+ secretion, therefore deficiency leads to acidosis

Cortisol (hydrocortisone) is the main glucocorticoid. It stimulates gluconeogenesis. Deficiency can result in hypoglycaemia.

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30
Q

Which hormones stimulate ductal/ alveolar morphogenesis during pregnancy?

A

Ductal morphogenesis: oestrogen and GH

Alveolar morphogenesis: progesterone, prolactin and hPL (cell growth and cellular differentiation during mammary gland development)

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31
Q

Physiology of ovulation

A

LH surge causes increased cAMP, resulting in increased progesterone and PGF2 production.

PGF2 causes contraction of the theca external smooth muscle cells resulting in rupture of the mature oocyte

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31
Q

Roles of LH and FSH

A

FSH stimulates aromatase production in the granulosa cells (which coverts testosterone to 17B-estradiol)

LH stimulates androgen production (testosterone) in the theca (interna) cells

LH also stimulates contraction of the smooth muscle cells of the theca external –> increases intrafollicular pressure –> rupture of mature oocyte

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32
Q

Structure of the follicle in the ovary

A

A healthy secondary follicle contains a fully grown oocyte surrounded by the zona pellucida, 5-8 layers of granulosa cells, a basal lamina, a theca interna and externa with numerous blood vessels

33
Q

Function of theca/ granulosa cells of ovarian follicle and roles of LH/ FSH

A

Theca: androgen (androstenedione) production, theca lutein cells produce progesterone

Granulosa: convert androgen to estradiol via aromatase. Granulosa lutein cells produce progesterone (from cholesterol)

FSH stimulates aromatase production in the granulosa cells
LH stimulates androgen production in the theca (internal) cells
LH stimulates contraction of the smooth muscle cells of the theca external, this increases intrafollicular pressure which results in rupture of mature oocyte.

34
Q

What percentage of progesterone is bound to SHBG/ albumin?

A

SHBG: 70%
Albumin: 25-30%

35
Q

What stimulates aldosterone production?

A

Raised potassium directly stimulates aldosterone

Juxtaglomerular cells of kidney release renin in response to low BP, stimulating aldosterone

There are several other modulators of aldosterone including ACTH and steroid hormones

36
Q

Physiological impact of aldosterone

A
  • Upregulates Na/K pumps in the DCT and collecting ducts of the nephron resulting in Na+ reabsorption in exchange for K+ ions (water follows sodium)
  • Upregulates epithelial sodium channels (ENaCs) resulting in increase sodium reabsorption (ADH also stimulates ENaCs)
  • Also has a role in H+/ K+ ion exchange, thus regulating acid/ base balance
37
Q

Where is angiotensin II produced?

A

Angiotensin I is converted to angiotensin II by ACE in the lung

38
Q

Where is angiotensinogen produced?

A

Liver.
Converted to angiotensin I by renin (produced by afferent arterioles of the kidney from specialised cells called granular cells of the juxtaglomerular apparatus)

39
Q

What is endemic goitre caused by?

A

Iodine deficiency

40
Q

When does the LH surge occur in relation to ovulation?

A

24-36 hours before ovulation

41
Q

First line tests for investigating Addison’s?

A

9 am cortisol level and U&E

Cortisol <100nanomol/L –> admit, urgent referral to endocrine

Cortisol 100-500nmmol/ L. Refer to endocrine for synacthen test

Cortisol >500, addisons unlikely

42
Q

Role of DHEA produced by fetal adrenal glands?

A

Dehydroepiandrosterone (DHEA) is a steroid hormone synthesised from cholesterol (via pregnenolone) by the adrenal glands.

Fetus makes DHEA, which stimulates the placenta to form oestrogen, thus keeping a pregnancy going.

Production of DHEA stops at birth, then begins again around age 7 and peaks when a person is in their mid-20s

43
Q

Where are ADH (vasopressin) and oxytocin synthesised/ produced?

A

Synthesised in the supraoptic and periventricular nuclei in the hypothalamus. They are then stored and eventually produced from the posterior pituitary.

44
Q

What hormones are produced in the adrenal glands?

A

Cortisol (zona fasciculata cortex)

Androgens (zona reticularis cortex)

Aldosterone (zona glomerulosa cortex)

Epinephrine (Chromaffin cells Medulla)

Dopamine (Chromaffin cells Medulla)

Norepinephrine (Chromaffin cells Medulla)

45
Q

What hormones are produced in the thyroid?

A

T3 (Epithelial cells)

T4 (Epithelial cells)

Calcitonin (parafollicular cells)

46
Q

What hormones are produced in the hypothalamus?

A

Growth hormone releasing hormone

Gonadotrophin releasing hormone

Thyrotropin-releasing hormone

Corticotropin-releasing hormone

Oxytocin

Vasopressin (ADH)

Somatostatin

Vasopressin

47
Q

What hormones are produced in the anterior pituitary?

A

Growth Hormone
TSH
Prolactin
ACTH
FSH
LH

48
Q

What hormones are produced by the placenta?

A

Progesterone
hCG (Syncytiotrophoblast)
hPL (Syncytiotrophoblast)

49
Q

What hormones are produced by the GIT?

A

Gastrin (Stomach G cells)

Somatostatin (Stomach D cells)

Histamine (StomachECL cells)

Secretin (S cells duodenum)

Cholecystokinin (I cells duodenum)

50
Q

Hormones produced by the liver?

A

Insulin like growth factors

Thrombopoietin (regulates platelet production)

Angiotensinogen and angiotensin

51
Q

Hormones produced by the ovary?

A

Oestragens
Progesterone
Androgen (theca cells)
AntiMullerian Hormone (Granulosa cells)

52
Q

Hormones produced by the uterus? (when pregnant)

A

Prolactin (Decidual cells)
Relaxin (Decidual cells)

53
Q

Hormones produced by adipose cells?

A

Leptin
Small amounts Progesterone
Estrone

54
Q

Hormones produced by the kidney?

A

Renin (granular cells of the juxtaglomerular apparatus)

Erythropoietin (Extraglomerular mesangial cells)

Thrombopoietin (regulates platelet production)

55
Q

Typical finding in FBC for patient with Addison’s disease?

A

Eosinophilia and lymphocytosis- mechanism unclear

56
Q

Autosomal dominant conditions

A

Achondroplasia
Adult PKD
Ehlers Danlos
Familial Hypercholesterolaemia
FAP
HHT
Huntingtons
Marfans
MEN
Myotonic Dystrophy
Neurofibromatosis
Noonans
Osteogenesis Imperfecta
Retinoblastoma
Spherocytosis
Tuberous Sclerosis
Von Willebrand
Von Hippel Lendeau

57
Q

Autosomal recessive conditions

A

Albinism
Congenital Adrenal Hyperplasia
Cystic Fibrosis
Fredrichs Ataxia
Glycogen Storage Disease
Haemochromatosis
Homocystenuria
Infantile PKD
Kartagner’s Syndrome
PKU
Sickle Cell
Tay Sachs
Thalassemia
Usher Syndrome
Wilsons Disease
Wolfram’s Syndrome

58
Q

X-linked dominant conditions

A

Fragile X
Rett Syndrome
Vitamin D resistant Ricketts

59
Q

X linked recessive conditions

A

Alport Syndrome
Duchenne Muscular Dystrophy
Fabry’s
G6PD deficiency
Haemophilia
Hunters
Menke’s
Nephrogenic Diabetes Insipidus
Red/Green Colour Blindness
Wiskott Aldrich Syndrome
X-linked ichthyosis

60
Q

Primary/ Secondary/ Tertiary hyperparathyroidism

A

Primary: excessive PTH due to parathyroid adenoma, causes hypercalcaemia

Secondary: secondary to hypocalcaemia. PTH rises to try and correct calcium
Causes: chronic renal failure, Vit D deficiency

Tertiary: after long periods of excessive PTH secretion (e.g. prolonged secondary), the parathyroid gland secretes PTH autonomously even if the cause of secondary hyperparathyroidism is corrected

61
Q

What does somatostatin inhibit?

A

GH
TSH
Prolactin
Glucagon
Insulin
Gastrin
CCK
Secretin
Motilin
Vasoactive intestinal peptide
Gastric inhibitory polypeptide
Enteroglucagon

62
Q

Oxytocin causes increased myometrial contraction via what messenger pathway?

A

Activated phospholipase-C which produces IP3, which triggers intracellular calcium ion release

63
Q

Features of acromegaly

A

Elargement of the hands, feet, nose, lips and ears

Skin thickening

Generalised soft tissue swelling of internal organs including the heart.

Deepening of voice and slowing of speech

Skull enlargement with frontal bossing

Mandibular protrusion (prognathism)

Macroglossia (enlargement of the tongue)

Teeth spacing

64
Q

Structure of haemoglobin and chromosomes the genes are located

A

Adult Hb (HbA): 4 globular protein chains (2 alpha chains and 2 beta chains) = 97% of Hb in an adult

HbA2 = normal variant of Hb consisting of two alpha and two delta chains (1.5-3% total Hb)

HbF (Fetal Hb): main Hb in fetus and persists 6 months after delivery = two alpha and two gamma subunits

Alpha subunit is coded for by genes on chromosome 16.
The beta and delta globulin chains are coded for by genes on Chromosome 11.

65
Q

Most common cause of premature menopause in the UK?

A

Idiopathic

66
Q

Changes to thyroid in pregnancy

A

20% increase in thyroid size due to hyperplasia and increased vascularity

Relative state of iodine insufficiency dye to increased renal clearance and overall losses to placenta and fetus

HG and molar pregnancies can be associated with gestational transient thyrotoxicosis (biochemical hyperthyroidism due to higher HCG concentrations)

Fetal thyroxine comes wholly from mother in early pregnancy. Fetal thyroid gland becomes functional 18-20weeks

Thyroxine binding globulin (TBG)- rises 2-3x because oestrogen production increases TBG production

T4 & T3 rise due to increased TBG, but free levels are usually unchanged.

TSH suppressed in 1st trimester (same alpha subunit as HCG), but normalise after 1st trimester

PTH gland increases in size to meet increased calcium requirements for fetal growth

67
Q

What drugs can be used to stimulate lactation?

A

Domperidone (preferred)
Metoclopramide

68
Q

Pheochromocytoma accounts for how many cases of HTN?

A

0.1%

69
Q

Blood flow through uterine artery at term

A

750ml/min (12% maternal cardiac output)

70
Q

Bone mass density classifications (T scores)

A

Normal: T score >= -1
Osteopenia: T score <= -1, but >=-2.5
Osteoporosis: T score <= -2.5
Severe osteoporosis: T score <= -2.5 & fragility fracture

71
Q

Diabetes insipidus

A

Due to a deficiency in vasopressin (ADH).

Either real due to lack of production of ADH in hypothalamus/ posterior pituitary (central) or normal levels of ADH, but ADH receptors on kidney are dysfunctional (Nephrogenic)

72
Q

HCG
- half life
- Peak in pregnancy
- Source
- Clinical application

A

Half life: 24h

Peaks 8-10 weeks, then falls until 20weeks and stays stable

Produced by placental syncytiotrophoblast cells following implantation.

Stimulates production of oestrogen and progesterone within ovary

Diminishes once placenta mature enough to take over oestrogen/ progesterone production

Rescues corpus lute from involution so it can continue to produce progesterone to maintain decidua

Stimulates lending cells of male foetus to produce testosterone

Promotes relaxin secretion by corpus luteum

Immunosuppressive action, helps maintain pregnancy

73
Q

Progesterone (pregnancy)
- Source
- Clinical application

A

Produced by corpus lute in first 9 weeks, then placenta

Decreases in progesterone production promotes cervical remodels and initiates labour

Promotes decidualisation

Prevents menstruation & rejection of trophoblast

Inhibits smooth muscle contractility, prevents onset of uterine contractions

Small amount goes to foetus for conversion into glucocorticoids and mineralocorticoids by fetal adrenal glands

Prepares breast for lactation

74
Q

Oestrogen (pregnancy)
- Source
- Clinical application

A

Primarily produced by corpus lute and follicles

3-8x higher concentration n pregnancy

Placenta takes over production around 6-7 weeks

Increases uterine blood flow
Facilitates placental oxygenation and nutrition to fetus
Prepares breast for lactation
3rd trimester- increases excitability of myometrium and prostaglandin synthesis

75
Q

HPL
- Structure
- Half life
- Source
- Clinical application

A

Polypeptide of 191 AA- single chain
Half life 15mins

Source
- Produced by syncytiotrophoblast
- Increases up to 30 fold throughout pregnancy, increases up to 36 weeks (more in multiple pregnancies and big babies)

Clinical:
- Regulates maternal carbohydrate, lipid, protein metabolism and fetal growth
- Promotes growth of breast tissue
- Can decrease maternal tissue sensitivity to insulin

76
Q

Relaxin
- Structure
- Source
- Clinical application

A

Peptide hormone

Source
- Primarily produced by corpus luteum in pregnant and non-pregnant states
- Levels rise in 1st trimester
- Peaks week 14 and delivery

Clinical application:
- Increases cardiac output and arterial compliance
- Increases renal blood flow
- Relaxes pelvic ligaments, softens PS and acts on cervical ripening

77
Q

Prolactin
- Source
- Clinical application

A

Source
- Produced by anterior pituitary
- Levels rise during pregnancy x10 fold, in preparation for milk production

Clinical application
- Hypertrophy and hyperplasia of lactrotrophs under influence of oestrogen
- Aids in final stages of lung maturation for baby
- Infant sucking at breast causes secretion

78
Q

Oxytocin
- Source
- Clinical application

A

Source
- Synthesised in hypothalamus
- Secreted by posterior pituitary
- Low levels throughout pregnancy, increases in labour

Clinical application
- Acts on myometrium to increase length, strength and frequency of contraction during labour
- Promotes let down reflex, enabling breasts to produce milk

79
Q

Maternal/ fetal complications of hyper/ hypothyroidism

A

HYPO
Maternal:
- Anaemia
- PIH, PET
- Placental abruption
- PPH
- Early fetal loss
- Increased placental weight

Fetal
- Neurodevelopmental delay
- Deafness
- Preterm delivery
- Stillbirth
- Perinatal death
- Low birthweight
- Fetal distress in labour

HYPER
Maternal:
- Thyroid storm
- HF
- AF
- Anaemia
- PET, GDM
- Psychosis

Fetal
- Neonatal mortality
- Fetal thyrotoxicosis (25% mortality if untreated)
- Tachycardia
- Goitre
- IUGR
- Pre term, stillbirth
- Low birthweight
- Cognitive impairment

80
Q

Post-partum thyroiditis clinical presentation

Who is at risk?

A

AI disease, first year PP

Transient thyrotoxicosis (2- 6 months PP) followed by hypothyroidism (3-12m PP) with return of euthyroid state by 1 year

Women who express anti-TPO in first trimester have 33-50% chance of developing PPT

Most recover spontaneously after 6-8 months of treatment

81
Q

How does the anterior pituitary change in pregnancy?

A

Increases in size by 50%

Part 1 MRCOG (13 decks)

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