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MRCOG Part one > Endocrinology: Adrenal & Thyroid gland and pancreas > Flashcards

Endocrinology: Adrenal & Thyroid gland and pancreas Flashcards

1
Q

What are the 3 zones of the adrenal cortex?

A
  • Zona glomerulosa
  • Zona Fasiculata
  • Zona Reticularis
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2
Q

What hormones are produced from the adrenal cortex and from which area?

A
  • Mineralcorticoid (Aldosterone) Zona Glomerulosa
  • Glucocorticoids (Cortisol) - Zona fasciculata
  • Adroden precursor (DHEA) Zona reticularis
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3
Q

All hormones produced in the adrenal cortex are made from what compenent?

A

Cholesterol

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4
Q

Where are all adrenocortical steroids broken down

A

The liver -> Excreted in urine of as bile

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5
Q

Explain the hypothalamo-pituitary-axis and the control of cortisol section

A
  • CRH released from hypothalamus
  • Causes release of ACTH from Ant Pituitary gland
  • Acts on Adrenal cortisol to stimulated productions of cortisol (also androgens)
  • Follows cicadium rhythm
  • Negative feedback of cortisol
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6
Q

What are the effects of cortisol

A

Gluconeogensis - increase glucose

Catabolic effect - decreases protein stores

Anti-inflammatory effects

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7
Q

Explain the release of aldosterone secretion

A

1) Key detector of changes of perfusion/electrolyes is the juxtaglomerular appartatus within the glomerulus. The juxaglomerular cells on the afferent ariteriole, produce renin.

Renin converts Angiotensin (liver) -> angiotensin 1

ACE (lungs) converts angiotensin 1 -> angiotensin 2

Angiotensin 2 -> Increaseses aldosterone production, vasoconstriction and increases thirst.

2) High K causes release of aldosterone

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8
Q

What are the effects of aldosterone on the kidney?

A

Reabsorbtion of Na and K excretion.

Water follows Na passively, increases volume of fluid

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9
Q

What is produced in the adrenal medulla? Name the cells that produce this hormone

A

Epinephrine & Norepinephrine

Chromafin cells

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10
Q

What are catecholamines (epineprhine, thryoid, melatonin) made from

A

Tyrosine

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11
Q

How is the output of catecholamines from the adrenal medulla controlled?

What is the half life of carecholamines?

A

Posterior hypothalamus stimulates the release of acetylcholine form the preganglionic nerve terminals, these depolarise the chromaffin cells.

Very short - 1-2 minutes

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12
Q

Catecholeamines act on 2 broad caterogories of G protein couple receptors what are these?

A

Alpha-adrenergic -> diverts blood to skeletal muslce from bowel/liver/spleen

Beta adrenergic -> increase HR, stroke volume, BP, mobilisation of gluose, lioplysis

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13
Q

What is the difference between cushing disease and cushing syndrome?

A

Cushing disease: Excess glucorticoid from ACTH secreting pitutiary tumour

Cushing syndrome: Ectopic ACTH e.g. lung tumor - may not have classic symptoms

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14
Q

What are the clinical features of cushings syndrome

A
  • Moon face
  • Weight gain with central obesity
  • HTN
  • Mental change
  • Hirsuitism
  • Striae
  • ACEne
  • Osteoporosis
  • +/- other hypopituarism - hypothyroid, hypogondism, low GH
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15
Q

What screening tests for cushings can you consider?

A

Measure cortisol (24hrs, midnight level)

Low dose dexamethasone test combined with CRH test

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16
Q

Management of cushings

A

Surgical (pituitary tumour, adrenalectomy)

Medical:

  • Prevent hypokalaemia, K sparing diuretic, K supplement
  • Cushing syndrome - somatostatin analogues, adrenal steroid inhibitor
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17
Q

What is Conns syndrome?

A

Primary hypoeraldosteronism

  • Excess aldosterone, rentetion of Na and excretion of K, high BP
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18
Q

What are the causes of Conn Syndrome?

A

Adrenal adenoma

Adrenal gland hyperplasia

Adrenal carcinoma

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19
Q

Who should you suspect Conns Syndrome in?

A

Unproked hypokalaemia

Persistant hypokalaemia despite K sparing diuretics

Refactory HTN

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20
Q

What is the classic biochemical finding of conns syndrome

A

Low K

Metabolic alkalosis

Test plama aldosterone/plasma renin ratio (not on antihypertensives)

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21
Q

What are the treatment options for Conns Syndrome

A

If from a adrenal tumour -> surgical removal

If bilateral renal hyperplasia -> Medications (Spironolactone but has estogen SE; impotence and gynacomastia or Eplerenone; anti-aldosterone)

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22
Q

What is a phaeochromocytoma & where does it arise?

A

Rare catecholamine secreting tumour of the sympathetic nervous system

90% adrenal

10% sympathetic chain

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23
Q

Excessive catecholmine can lead to what life threatening situations?

A

Life threatening HTN

Cardiac arrythmia

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24
Q

Investigation for phaeochromocytoma

A
  • Plasma metanephrine
  • 24 hour urine catecholamine
  • Radioisotope imaging
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25
Q

Managment of phaeochromocytoma

A
  • Surgical removal
  • Pre-op Alpha adrenergic and b andrenergic blockade - to help prevent catecholmine storm with GA or operaitive handling
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26
Q

What are the causes of hypoadrenlism?

A
  1. Addisions (Primary) due to abrupt cessation of exogenic steroids (>99%)
  2. Addisons (Primary) due to autoimmunity/infection/haemorrhage/drugs (ketoconazole)
  3. Seconday - pituitary diease
  4. Tertiary - Hypothalamic disease
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27
Q

What are the symptoms of addisions disease?

A
  • Weakness
  • Weight loss
  • Pigmentation
  • Anorexia
  • Nausea
  • Abdo pain
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28
Q

What are classic biochemical features of hypoadrenalism?

A

Low Na

High K

High Ca

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29
Q

How do you test for hypoadrenalism

A

ACTH suppression test

Give synthetic ACTH & measure cortisol + ACTH

Primary: High ACTH, low cortisol

Secondary: Low ACTH, low (but slightly increased) cortistol

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30
Q

Acute management of adrenal crisis

A

A-E approach

IV access with fluid repalcemnt NaCl

Measure +/- replace glucose

100mg hydrocortisone , further 100-200mg over 24 hours

Long term

  • 2-3 daily doses hydrocortisone
  • Fludrocortisone
  • No mineralcorticoid replacment needed
  • Some replace DHEA in females
  • sick day rules for hydrocortisone
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31
Q

What is congenital adrenal hyperplasia?

A

Autosome reccessive disoders, enzyme deficient involved in the productions of cortisol or aldosterone. Examples 21-hydroxylase.

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32
Q

What is the clinical presentation of congenital adrenal hyperplasia?

A

Depends on severity and sex of the child.

  • Severe: Salt-wasting at weeks 1-4 (hypotension, low Na, highK, shock)
  • Severe famale: Ambigious genitalia at birth
  • Mild females: Precocious pubic hair, clitoromegaly, accelerated growth (simple virilising adrenal hyperplasia)
  • Milder female: oligomenrrorhia, hirsiutism +/- infertility
  • No breast/mensus +/- HTN
  • Men have normal genitialia
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33
Q

How to screen for congenital adrenal hyperplasia on bloods

A
  • Electrolytes
  • blood sugar
  • cortisol
  • aldosterone
  • 17 hydroxyprogesterone (precursor to 21 hydroxylase)
34
Q

What hormones does the Thyroid Gland produce which cells?

A
  • Follicular cells - T4 & T3
  • C Cells - calcintonin
35
Q

What suppresses TSH as part of the negative feedback loop?

A
  • Free T3 & T4
  • Somatostatin
  • Glucocorticoids
  • Chronic illness
36
Q

What percentage of T3 & T4 are bound.

How does peripheral tissue regulate these levels?

A

T3 1% unbound

T4 0.1%

Peripheral tissues change T3 synthesis, whilst T4 can be converted to T3 by deiodination

37
Q

How does thyroid hormeones bind to cells & generally what effect does this have

A

Nuclear transcription factors, receptors in nucleas and regulated gene expression. Increases metabolic rate.

38
Q

What is the most common cause of hyperthyoid in a young vs and old person

A

Young: Graves

Old: Toxic multinodular goitre

39
Q

What features are only seen in Graves disease as supposed to other causes of hyperthyroidism?

A

Opthalmopathy

Dermopathy

Diffusely enlarged smooth goitre

40
Q

In subclinical hyperthyroidism - what would you see on bloods

A

Normal free T4&T3

Suppressed TSH

41
Q

Described the presentation of radioactive iodone in: Graves, thyroiditis/iodine ingestions, multinodular goitre

A

Graves: diifusely distributed within entire gland

Thyroiditis/Iodine: poor uptake

Multinodular: multifocal areas of varying activity

42
Q

What treatment of hyperthyroidism is often used in pregnancy & why?

A

Thicarbamides - propylthiouracil over carbimazole as crosses placenta and breast milk in smaller amounts

Radioactive iodine is contraindicated in children, pregnancy & breast feeding. Must wait alteast 4 month after radioactive iodine before becoming pregnant.

43
Q

Antithyroid peroxidases seen in hashimotos disease (form of primary hypothyroidism) is associated with what early pregnancy outcomes?

A

Infertility

miscarriage

44
Q

Most common cause of hypothyroidism in developing countries

A

Iodine insufficiency

45
Q

How do you treat hypothyroidism, how does this treatment work?

After starting Tx when should you recheck TFT

A

Levothyroxine - Free T4, can be converted to T3 in peripheral tissues

Treat hypothyroid and subclinical with +ve antithyroid microsome antibodies

Recheck in 6 weeks

46
Q

Should you routinely test a critically ill person for thyroid function?

A

No - when crtically, T4 not exchanges to T3 in peripheral levels

Normal/Low TSH, Low T4, Very Low T3

47
Q

In pregnancy maternal thyriod is modulated by what 3 factors?

A
  • Increasing bHCG (similar to TSH), simulates the thyroid gland -> 1st trimester T4 normal or slightly high, TSH is low. Worse in Hyperemesis or Molar (higher bHCG)
  • Increased in excretion of uriary iodine (increased filtration rate) -> thyroid increases in size
  • Increased T4 binding globulin in 1st trimester - increased binding T4 - increased total T3&T4 but normal free T3 & T4
48
Q

Whats likely to happen to thyroid replacement requirements during pregnancy?

A

Increase

Those already on levothyroxine are liekly going to need 50% increased, needs to be closely monitored.

Those starting Tx need treatment immediately to preven fetal exposure to hypothyroid environement

49
Q

For women with no previous Hx hypothyroidism, what should happen to thyroid treatment postpartum?

A

Stop Tx and recheck function 5-6 weeks later

50
Q

When does the fetus start to develop its own TSH and T4

What are the long term effects of fetal hypothyroidism if left untreated?

A

Week 10

Profound mental and developmental restriction

51
Q
  1. What are the effects of hyperthyroidisim on mensus and fertility.
  2. Effects on mother during pregnancy
  3. Effects on the fetus
A
  1. Irregular mensus but no effect on fertility
  2. Premature labour, PET, heart failure
  3. Neonatal mortality, low birth weight
52
Q

How does pregnancy effect hyperthyroidism?

A

Little effect, pregnancy does not make hyperthyroidism harder to control

53
Q

What is the risk of fetal thyrotoxicosis if mother has Hx Graves. How does it present?

A

Thyroid stimulating antibodies can cross the placenta, even if mother has been previously treated or is in remission.

Presents in utero with persistant fetal tachycardia, growth failure, increased fetal movements - always consider if any hx of hyperthyroid in mother

54
Q

During pregnancy how should we adapt how we interpret free T4 vs Total T4

A

Normal ranges for T4

Multiply total free t4 reference range by 1.5 in 2nd and 3rd trimester

55
Q

Mother with pre-exsisitng hypothyroidism, when should the T4 dose be increased by?

A

By weeks 4-6 of pregnancy. Up to 30% increase

56
Q

When starting levothyroxine in pregnancy, what is the maximum TSH to be maintained in 1st trismester and 2nd/3rd trimester

A

1st Trimester: <2.5

2nd/3rd: <3

57
Q

When is fine needle aspiratin requireuired on a solitary thryoid nodule?

A
  • >1cm
  • Enlarging
  • Cervical lymph nodes palpable
58
Q

What is postpartum thyroiditis? When and how does it typically present?

A

5-10% within 1 st year post partum

  1. Transient Thyrotoxicosis between 2-6monts
  2. Hypothyroidism between 3-12months

High risk for developing permnant hypothyroidism

59
Q

What is the risk of developing PP thyroditis if those with antithyroid antibodies?

Risk of reoccuring in furture pregnancy?

A

90%

25%

60
Q

Do you need to treat gestational thyrotoxicosis

A

No - related to elevated bHCG seen in 1st trimester. Will imporve by 20 weeks

More common in multiple pregnancy, molar, famililal gestational thyrotoxicosis

61
Q

What are the effects of insulin on the liver/adiopse tissue and muscle

A
  • Liver glygogen synthesis
  • Adipose - rapid uptake of glucose to be converted to fatty acids
  • Muscle - rapid uptake of glucose & amino acids

Insulin causes weight gain

62
Q

What hormones are produced by the endocrine tissue of the pancreas?

A

Insulin

Glucagon

Somatostatin

Gastrin

Vasoactive intestinal peptide (VIP)

Pancreatic polypeptide

63
Q

When is glucogen released, whats its effects?

A

Low blood glucose/high amino acids/exercise

Opposite effects of insulin mobilising fuels: break down of glycogen, gluconeogensis, release of free fatty acids from adipose cells.

64
Q

What are the 2 main forms of somatostatin and where are they produced?

A

Somatostatin 14 (predominant) produced in nervous system

Somatostatin 28 in inestines

65
Q

Somatostatin 28 is more potent at inhibiting ??

Somatostatin 14 is more ptent at inhibiting?

A

28: inhibit growth hormone secretion
14: inhibit glucagon release

66
Q

What are the levels of prediabetes and diabetes for fasting plasma glucose?

A

> 7.0 diabetes

6.0-7.0 pre-diabetes

67
Q

OGTT prediabetes and diabetes levels?

A

>11.1 after 2 hours

7.8-11.2 after 2 hours

68
Q

HbA1c for Dx of DM

Changes in pregnancy?

A

6.5% >48mmol/mol

HbA1c should not be used in pregnancy to diagnose DM

69
Q

What is metabolic syndrome?

A

T2DM

HTN

Dyslipidaemia (high LDL, low HDL)

70
Q

What are the effects of metformin?

Who is it contraindicated in?

A

Impairs release of hepatic glucose

Contrindicated: Poor renal function after radioactive iodine

71
Q

Explain the peak level and long effects of the following insulins

Rapid acting

Regular/short acting

Intermediate acting

Long acting

A

Rapid: Few minutes, couple of hours

Regular/short: 30 mins, 3-6 hours

Intermediate: 2-4 hours, 18 hours

Long: 6-10 hours, 24 hours

72
Q

Main 2 regiemes for type 1

A

1/2 daily dose as either 1 long acting injection or 2 x intermediate

Remainder short acting before meals

73
Q

What is the normal starting dose of insulin based on weight for T1DM, whats it often icnreased to?

A

Starting 0.2-0.4 U/Kg

0.6-0.7 U/kg daily

74
Q

In a normal pregnancy, why happens to

  1. fasting plasma glucose
  2. fasting levels of insulin
  3. meternal hepatic production of glucose
  4. insulin sensitivity
  5. Insulin levels
A
  1. fasting plasma glucose is lower (uptake from placenta/fetus)
  2. fastiing insulin is increased
  3. maternal hepatic glucose is increased because..
  4. there is decreased insulin sensitivity
  5. progressively increases with gestation
75
Q

In a normal pregnancy (non obese, non diabetic)

  1. How much fat gain is expected
  2. Changes to triglyceride concentraion
  3. Changes to levels of Total cholesterol
  4. Chanes in LDL and HDL by mid gestation
A
  1. 3.5kg
  2. 2-4 x
  3. Increases 25-50%
  4. LDL 50%, HDL 30%
76
Q

What happens to the fetal islet cells in the pacreas in maternal DM

A

Hypertrophy, increasing insulin secretion

77
Q

What % of DM in pregnancy is GDM?

What % pregnacies are effect by GDM?

A

90%

1-4%

78
Q

Risk factors for GDM

A
  • High mat age
  • Ethnicity
  • obesity
  • gestational weight gain
  • suspected macrosomia/previous macrosomia
  • polyhydramnios
  • glycosuria
  • previous GDM
  • Hx DM
  • prv stillbirth, neonatal death, congital abnormallity
79
Q

When is testing of GDM normally perfored. For those with previous GDM

Cut of for OGTT

A

24-28 weeks, additional testing 16-18 weeks for those previosuly with GDM/

>11.1

80
Q

Fetal morbity related to DM during pregnancy

A
  • Higher rates of miscarriage, poor control rates of 44%
  • Major birth defect 4-8% increases risk -risk CV and neurological anomilies
  • Macrosomia 15-45%, unique pattern of overgrowth in central deposition and intrascapular area - realted birth injuries
  • Polycythaemia 5-10%
  • Severe hypoglycaemia 5 x increased
  • growth restriction (T1DM with vasculopathies)
  • Increased lifetime risk of imparied glucose tolerace, 20% by aged 10-16 years
81
Q

What link is there between obesity and subfertility

A

Obestity - hyperinsulinaemia and hyperandrogaemic state leading to oligo/amennorhoea, risk of anovulatory fertility.

Weight loss is essential

82
Q

Women who are obese are more likely to suffer from:

A
  • VTE
  • GDM
  • PIH/PET
  • Proteinuia >20 weeks
  • stillbirth/intrauterine death
  • Preterm labour, miscarriage, fetal chormosomal abnormality, macrosomia
  • dysfunctional labour
  • CS perioperative morbidity
  • PPH

MRCOG Part one (28 decks)

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