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BRS missed out > Endochrinology > Flashcards

Endochrinology Flashcards

1
Q

What other function besides anti diuresis does ADH have?

A

V1 receptor - vasoconstriction
Stimulates ACTH in anterior pituitary

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2
Q

Describe the osmotic and non osmotic regulators of ADH

A

Osmotic - the organum vasculosum & subfornical organ around the third ventricle is highly vascularised and responds to systemic circulation (no BBB). The nerves project to the suppraoptic neurons allowing release of ADH during high osmolality.

Non osmotic- atrial stretch receptors in the right atria inhibits the secretion of ADH via baga; afferents to hypothalamus, when there is less stretch e.g during heamorrhage, the inhibition of ADH is reduced so more ADH secreted

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3
Q

What are the causes of Nephrogenic diabetes insipidus?

A

Drugs - Lithium
Mutation - V2 receptor, AQP2

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4
Q

What clinical investiations would you run following polyuria, nocturia , polydyspia once you’ve confirmed it isn’t diabetes mellitus?

A

Blood osmolarity- Hyper osmolar
Urine osmolarity - Hypo osmolar
Hypernatraemia
Glucose levels

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5
Q

How do you distinguish between psychogenic polydypsia and diabetes insipidus?

A

Water deprivation test - and you measure urine volume ,urine and blood osmolarity, you also have to weigh regularly if they lose > 3% of their weight then need to stop test but semi- confirms DI

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6
Q

Differentiate DI and PP in terms of plasma osmolarity

A

DI Hyperosmolar
PP hypo osmolar

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7
Q

How do you treat DI

A

CDI- demsopressin- intranasally or tablet
NDI- hard to tret, thiazide diuretics or

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8
Q

Signs of SIADH

A

Reduced urine output

High urine osmolality

Low plasma osmolality

Dilutional hyponatraemia

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9
Q

Causes of SIADH

A

CNS

Head injury, stroke, tumour,

Pulmonary disease

Pneumonia, bronchiectasis

Malignancy

Lung cancer (small cell)

Drug-related

Carbamazepine, Serotonin Reuptake Inhibitors (SSSRIs)

Idiopathic

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10
Q

What are the functional names for tumours of anteior pituitary cells?

A

Lactotrophs - Prolactinoma
Somatotrophs - Acromegaly
Corticotrophs - Cushings
Thyrotophs- TSHoma
Gonadotrophs - Gonadotrophinoma

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11
Q

What is the imaging modality for pituitary tumours and how are they decribed?

A

Size

-Microadenoma <1cm (10mm)
-Macroadenoma >1cm (10mm)

Sellar or suprasellar

Compressing optic chiasm or not

Invading cavernous sinus or not

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12
Q

What does benign and malignant pituitary tumours relate to?

A

Pituitary carcinoma very rare (<0.5% of pituitary tumours)
Mitotic index measured using Ki67 index – benign is <3%
Pituitary adenomas can have benign histology but display malignant behaviour

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13
Q

Causes of elevated prolactin levels

A

Physiological
-Pregnancy/breastfeeding
-Stress: exercise, seizure, venepuncture
-Nipple/chest wall stimulation

Pathological
-Primary hypothyroidism
-Polycystic ovarian syndrome
-Chronic renal failure

Iatrogenic
-Antipsychotics
-Selective serotonin re-uptake inhibitors
-Anti-emetics
-High dose oestrogen
-Opiates

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14
Q

What receptor do dopamine agonist like cabergoline work on?

A

D2 receptors

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15
Q

What are the symptoms of acromegaly?

A

Sweatiness
Headache
Coarsening of facial features
Macroglossia
Prominent nose
Large jaw - prognathism
Increased hand and feet size
Snoring & obstructive sleep apnoea
Hypertension
Impaired glucose tolerance/diabetes mellitus

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16
Q

How do we diagnose acromegaly?

A
  • Elevated serum IGF-1 helps
  • Failed suppression (paradoxical rise) of GH following oral glucose load- oral glucose tolerance test- we don’t know why
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17
Q

How do we treat acromegaly?

A

Trans-sphenoidal pituitary surgery
-Aim to normalise serum GH and IGF-1

Radiotherapy

If nto surgery or to reduce tumour size:
Somatostatin analogues eg octreotide – ‘endocrine cyanide’

Dopamine agonists eg cabergoline (GH secreting pituitary tumours frequently express D2 receptors)

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18
Q

Causes of Cushing’s syndrome

A

ACTH independent

  • Taking steroids by mouth (common)
  • Adrenal adenoma or carcinoma

ACTH dependent

  • Cushing’s disease (corticotroph adenoma)
  • Ectopic ACTH (lung cancer)
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19
Q

Diagnosis of Cushing’s syndrome

A
  • Elevation of 24h urine free cortisol- increased cortisol secretion
  • Elevation of late night cortisol- salivary or blood test- loss of diurnal rhythm
  • Failure to suppress cortisol after oral dexamethasone (exogenous glucocorticoid)- increased cortisol secretion

If high, measure ACTH, then if high, MRI

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20
Q

What do non functioning adenomas often present with?

A

Bitemporal hemianopia

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21
Q

What is it called in grave’s disease where the antibodies go behind the eye and push it out

A

exophthalmos

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22
Q

What is Toxic nodular goitre (Plummer’s disease)

A

Benign adenoma that is overactive at making thyroxine
- One cell has grown a lot on one side of the thyroid so that side is large
- This makes a lot of thyroxine which suppresses TSH and lack of TSH means the normal side of the gland atrophies and gets smaller

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23
Q

What are the effects of thyroxine on the sympathetic nervous system?

A
  • Sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline
  • Thus there is apparent sympathetic activation
  • Causes tachycardia, palpitations, tremor in hands, lid lag
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24
Q

What is a thyroid storm?

A
  • Medical emergency- 50% mortality untreated
  • Blood results confirm hyperthyroidism
  • Need aggressive treatment
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25
Q

Criteria for thyroid storm

A
  • Hyperpyrexia >41°C
  • Accelerated tachycardia/arrhythmia
  • Cardiac failure
  • Delirium/frank psychosis
  • Hepatocellular dysfunction; jaundice
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26
Q

What classes of drugs are used in the treatment of hyperthyroidism?

A

The thionamides (thiourylenes; anti-thyroid drugs)

	- propylthiouracil (PTU)

	- carbimazole (CBZ)

Potassium Iodide
Radioiodine
β-blockers

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27
Q

What is the function of thionamides and how does it work?

A

Daily treatment of hyperthyroid conditions - aim to stop after 18 months

Inhibition of thyroid peroxidase

Biochemical effect hours, cliical effect weeks so may use propanolol to reduce beta sympathetic activity related symptoms

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28
Q

What are the four steps of T4 synthesis

A

Uptake of iodide active transport
Iodination
Coupling reaction: Storage in colloid
Endocytosis and secretion

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29
Q

Side effects of thionamide

A

Agranulocytosis (neutropenia)
Rashes

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30
Q

What is the function of iodide treatment in hyperthyroidism and how does it work?

A

1a. preparation of hyperthyroid patients for surgery
1b. severe thyrotoxic crisis (thyroid storm)
hyperthyroid symptoms
reduce within 1-2 days
vascularity and size of gland reduce within 10-14 days

  1. Inhibits thyroid peroxidase, inhibits iodination of thyroglobulin using WOLFF–CHAIKOFF effect
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31
Q

Problems with surgery for hyperthyroidism

A

Risk of voice change (recurrent laryngeal nerve)

Risk of also losing parathyroid glands

Scar

Anaesthetic

32
Q

Radioiodine in hyperthyroidism

A

Swallow a capsule containing about 370 MBq (10 mCi) of the isotope I (131)

Contraindicated in pregnancy
Need to avoid children and pregnant mums for a few days

For scans only (not treatment), 99-Tc pertechnetate is an option.

33
Q

Symptoms of Viral (de Quervain’s) thyroiditis

A
  • Pyrexia (fever)
  • Malaise
  • Painful dysphagia
  • Hyperthyroidism
  • Thyroid inflammation
  • Tender + palpable thyroid
  • Thyroid gland visibly enlarged on one side
34
Q

What is the biochemistry of primary hyperparathyroidism?

A
  • High calcium
  • High PTH (not suppressed by hypercalcaemia negative feedback)
  • Low phosphate- increased renal phosphate excretion (inhibition of sodium-phosphate transporter in kidney)
35
Q

What are the causes of secondary hyperparathyroidism?

A
  • Most common cause is vitamin D deficiency due to diet, reduced sunlight
  • Less common, due to renal failure- can’t make calcitriol in renal failure
36
Q

What is the treatment for secondary hyperparathyroidism in people with and without kidney failure?

A

Without renal failure:
25 hydroxy vitamin D- inactive vit D
They convert it to 1,25 dihydroxy vitamin D via 1alpha hydroxylase
Can give ergocalciferol (25 hydroxy vitamin D2) or cholecalciferol (25 hydroxy vitamin D3)
Can get at chemists/supermarket

With renal failure:
There’s inadequate 1alpha hydroxylation, so can’t activate 25 hydroxy vitamin D
We give them alfacalcidol- 1alpha hydroxycholecalciferol- this is active vitamin D
Reserved for renal failure patients so needs to be prescribed

37
Q

What happens in tertiary hyperparathyroidism?

A

When you have chronic renal failure you can’t make calcitriol so you have chronic vit D deficiency
Parathyroid glands start secreting more PTH to make up for drop in calcitriol so calcium doesn’t become low
One or more of these glands enlarge (hyperplasia) to the point where they can’t be switched off
Autonomous PTH secretion happens causing hypercalcaemia

38
Q

What happens in hypercalcaemia due to malignancy? (2)

A
  • There is high calcium
  • There is low or suppressed PTH
39
Q

Hormonal control of serum calcium

A

Increase -
Vitamin D
Parathyroid hormone (PTH) (secreted by parathyroid glands)

Decrease -
Calcitonin (secreted by thyroid parafollicular cells)
Can reduce calcium acutely, but no negative effect if parafollicular cells are removed eg thyroidectomy

40
Q

What is a good indicator of body vitamin D status

A

Serum 25-OH vitamin D

41
Q

How does calcitrol regulate its own synthesis?

A

by decreasing transcription of 1 alpha hydroxylase

42
Q

Effect of calcitrol

A

Kidney :Increase Ca2+ and PO43- reabsorption

Gut: ↑ PO43- absorption
↑Ca2+ absorption

Bone: Increase osteoclast activity

43
Q

Actions of PTH

A

↑ Ca2+ reabsorption
↑ PO43- excretion
↑ 1-a-hydroxylase activity
↑ 1,25 (OH)2D3 synthesis
Ca++ resorption from bone

44
Q

Regulation of serum phosphate by FGF23

A

Phosphate is reabsorbed via sodium phosphate cotransporter channels in PCT

PTH inhibits renal phosphate reabsorption by inhibiting these transporters

FGF23 (from bone) inhibits phosphate reabsorption in the kidneys by inhibiting these transporters

inhibits synthesis of calcitriol, causing less phosphate absorption from the gut

45
Q

Hypocalcaemia symptoms & signs

A

CATs go numb

Chvosteks’ sign – facial paresthesia
Trousseau’s sign – carpopedal spasm

46
Q

Causes of hypocalcaemia

A

Low PTH levels = hypoparathyroidism
Surgical – neck surgery
Auto-immune
Magnesium deficiency
Congenital (agenesis, rare)
Low vitamin D levels
Deficiency – poor diet/malabsorption, lack of UV light, impaired production (renal failure)

47
Q

Hypercalcaemia signs and symptoms

A

Stones, abdominal moans and psychic groans

48
Q

Causes of hypercalcaemia

A

Primary hyperparathyroidism
Malignancy
Vitamin D excess (rare)

49
Q

What tests do we do following suspicion of Addisons?

A

(Addisons) - Morning 9am cortisol (low) and ACTH (high)
- Short synacthen test:
1.cortisol blood test
2. synacthen IM
3. measure cortisol response
if little response then we know its Addison’s

50
Q

What is the aldosterone treatment for Addisons, what’s the issue with the standard treatment and how have we fixed it?

A
  • Aldosterone replacement- problem is its half life is too short for safe once daily administration
  • We solve this by sticking a fluorine on aldosterone to make fludrocortisone
  • Fludrocortisone binds to both MR (mineralocorticoid) and GR (glucocorticoid) receptors
  • Its half life is 3.5h and effects are seen for 18h
51
Q

What are the consequences of adrenocortical failure? (6)

A
  • Fall in bp
  • Loss of salt in urine
  • Increased plasma potassium
  • Fall in glucose due to glucocorticoid deficiency
  • High ACTH resulting in increased pigmentation
  • Eventual death due to severe hypotension
52
Q

Describe Congenital adrenal hyperplasia (CAH) - 3 + 1 disease

A

Most commonly caused by - 21-hydroxylase deficiency - Can be complete or partial deficiency

Complete 21- hydroxylase deficiency:
Aldosterone + Cortisol deficiency
Sex steroids + testosterone in excess (girls may therefore present with ambiguos genitalia)
Presents as a neonate - salt losing Addisonian crisis

Partial 21 hydroxylase deficiency:
Aldosterone + Cortisol scarse
Sex steroids + testosterone in excess
Presents at any age
Girls - hirtulism and virilisation
Boys - precocious puberty

11 hydroxylase deficiency:
There’s a build up of 11 deoxycorticosterone - behaves like aldosterone could cause hypertension / hypokalaemia

Cortisol and aldosterone deficiency
Excess 11 deoxycorticosterone, sex steroids and testosterone

17 hydroxylase deficiency -
Cortisol and Sex steroid deficiency
Excess 11 deoxycorticosterone, aldosterone

53
Q

What two types of drugs can be given for cushings and when would they be used and what are we concerned about?

A

Metyrapone -inhibition of 11b-hydroxylase
Control of Cushing’s syndrome prior to surgery.
Control of Cushing’s symptoms after radiotherapy (which is usually slow to take effect)
Hypertension on long-term administration
Hirsutism

Ketoconazole - blocks 17a hydroxylase
treatment and control of symptoms prior to surgery
Liver damage - possibly fatal - monitor liver function weekly, clinically and biochemically

54
Q

Describe Conns; pathophysiology, diagnosis and management

A
  • Benign adrenal cortical tumour (zona glomerulosa)
  • Aldosterone in excess (aldosterone controls bp, Na and lowers K remember)
  • Hypertension and hypokalaemia

Diagnosis: renin - angiotensin pathway should be suppressed

MR antagonist

55
Q

Describe phaeochromocytoma, clinical features and management

A

tumours of the adrenal medulla which secrete catecholamines (adrenaline and noradrenaline)

  • Hypertension in young people- severe hypertension can cause myocardial infarction or stroke
  • Episodic severe hypertension (after abdominal palpitation)
  • High adrenaline can cause ventricular fibrillation & death- it’s a medical emergency

Management:
- Eventually need surgery, but patient needs careful prep as anaesthetic can precipitate a hypertensive crisis
- Alpha blockade is the first therapeutic step to block adrenaline effects for surgery
- Patients may need intravenous fluid as alpha blockade commences (because blockade causes blood pressure crash so we need the fluid)
- Beta blockade added to prevent tachycardia

56
Q

What are the two types of infertility?

A

Primary - Have never had a live birth
Secondary - has had a live birth > 12 months ago

57
Q

What are the three categories of infertility causes in men?

A

Pre testicular
Testicular
Post testicular

58
Q

What are pre testicular causes in men?

A

Congenital & Acquired Endocrinopathies

 Klinefelters 47XXY

 HPG, Testosterone, PRL issues
59
Q

What are testicular causes in men?

A

Congenital
Cryptorchidism
Infections - STDs
IMmunological - anti sperm AB
Vascular
Trauma/ Surgery
Toxins

60
Q

What are post testicular causes in men?

A

Congenital ( Absence of vas deferens)
Obstructive Azoospermia
Erectile dysfunction
Iatrogenic - vasectomy

61
Q

Describe Cryptorchidism

A

Undescended testis (90% in inguinal canal)

62
Q

What are some categories of infertility causes in women?

A

Pelvic causes
Tubal causes
Ovarian causes
Uterine causes
Cervical causes
Unexplained

63
Q

Endometriosis:
Description -
Symptoms -
Management-

A
  1. Presence of functioning endometrial tissue outside of the uterus
  2. Menstrual pain
    Menstrual irregularities
    Deep dyspareunia
    Infertility
  3. Oestrogen
64
Q

Fibroids:
Descriptions -
Symptoms -
Management -

A

Benign tumours of the myometrium

Usually asymptomatic - may present with deep dyspareunia, menstrual irregularities, increased menstrual pain, infertility

65
Q

Kallmann Syndrome:
Description
Symptoms

A

Failure of migration of GnRH neurons with olfactory fibres

Anosmia
Failure of puberty
INferitlity

66
Q

Klinefelters syndrome:
Symptoms

A

Tall stature
Decreased facial hair
Breast development
Female - type pubic hair pattern
Small penis and testes
Infertility
Mildly impaired IQ
Narrow shoulders
Reduced chest hair
Wide hips
Low bone density

67
Q

Male infertility diagnostic overview

A

Key history: Duration, previous children, pubertal milestones, associated symptoms, meidcations/ drugs

Key examination: BMI, sexual characteristics, testicular volume, anosmia

Key investigations: Semen analysis, Blood tests, Imaging

68
Q

Male infertility key investigations

A

Semen analysis -
Volume
Sperm concentration ( Azospermia, Oligospermia)
Total motility

Blood test- LH, FSH, PRL, morning fasting testosterone, karyotyping

Imaging - Scrotal US/ Doppler

MRI pituitary if indicated

69
Q

Male infertility management

A

Treat treatable causes - hyperPRL

General lifestyle - Optimise BMI, SMoking cessation, Alcohol reduction/ cessation

Specific treatment -
Gonadotrophin treatment for fertility
Testosterone - if no fertility required
Surgery - microtesticular sperm extraction

70
Q

Premature ovarian insufficiency
Description/ Diagnosis

Causes

A

Conception may still happen, diagnosis high FSH > 25iU/ L ( x 2 at least 4 weeks apart)

Autoimmune, Genetic, Cancer therapy

71
Q

Polycystic Ovarian syndrome:
Diagnosis -

A

Rotterdam PCOS Diagnostic criteria 2/3

  1. Oligo or Anovulation
  2. Clinical (Acne, Hirsutism, Alopecia) + Biochemical Hyperandrogenism
  3. PCO using ultrasound
72
Q

PCOS treatment

A

Metformin- Irregular menses/ amenorrhoea & increased insulin resistance

IVF - infertility

Oral contraceptive - Ireegular menses/ amenorrhea

Anti- androgens (Spironolactone) - Hirsutism

Creams, waxing - hirsutism

Progesterone courses - Endometrial cancer risk

73
Q

Turners Syndrome
Description
SYmptoms

A

One X chromosome

Short stature, low hairline, shield chest, wide- spaced nipples, short 4th metacarpal, small fingernails, brown nevi, characteristic faces, webbed neck, coarction of aorta, poor breast development, elbow deformity, underdeveloped reproductive tract, amenorrhea

74
Q

Female infertility diagnosis overview

A

Key history: Duration, Previous Children, Pubertal Milestones, Menstrual History, Medications/ Drugs

Key examination: BMI, Sexual characteristics, Hyperandrogenism signs, Anosmia

Key investigations: Blood test, pregnancy test, Imaging

75
Q

Female inferitility key investigations

A

Blood test - LH, FSH, PRL, Oestrodial, Androgens, Mid - Luteal Prog, Karyotyping

Pregnancy test

Imaging - US (transvaginal)
Hysterosalpingogram
MRI pituitary if indicated

76
Q
A

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