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Year 3 Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Describe the blood supply of the thyroid

A
  • Superior thyroid artery (from external carotid)
  • Inferior thyroid artery (from thyrocervical trunk)
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2
Q

What structures lie laterally to the thyroid gland?

A

Recurrent laryngeal nerves

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3
Q

Describe the tissue composition of the thyroid gland

A

Follicular cells producing thyroglobulin, surrounding a colloid which contains iodinated thyroglobulin

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4
Q

What are C Cells of the thyroid and what do they produce?

A

Neuroendocrine cells which produce Calcitonin

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5
Q

Name two molecules that thyroid hormones are bound to in the blood

A
  • Thyroxine Binding Globulin
  • Albumin
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6
Q

Describe three actions of thyroid hormones

A
  • Increase Basal Metabolic Rate
  • Increase Heart Rate
  • Children’s growth
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7
Q

Name two non thyroid causes that can affect Thyroid Function Tests

A
  • Pregnancy
  • Medication (Lithium, Amioderone)
    • amioderone can cause thyrtoxicosis
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8
Q

What is Primary Hypothyroidism? What would the Thyroid Function Tests show?

A

Cause is the Thyroid itself (commonly autoimmune)

Low T4 & T3

High TSH

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9
Q

What is Secondary Hypothyroidism? What would the TFTs show?

A

Cause is a TSH deficiency (Pituitary problem) Low T4 Low TSH

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10
Q

Describe the TFTs of Hyperthyroidism

A

High T3/T4 Very low TSH

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11
Q

What would the TFTs of high T3/T4 and high TSH show?

A

TSH secreting adenoma

thyroid hormone resistance

assay interference

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12
Q

State 4 causes of Hyperthyroidism

A

Graves (autoimmune) Nodular Thyroid Disease Thyroiditis Ectopic Thyroid Tissue

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13
Q

Describe the pathophysiology of Graves disease

A

Thyroid stimulating immunoglobulin mimic TSH to increase T3/T4 Relapsing course triggered by stress/infection/child birth

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14
Q

Describe the pathophyiology of Nodular Thyroid Disease

A

T3/T4 release can be from a singular nodule (Toxic Adenoma) or multiple nodules Associated with iodine deficiency

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15
Q

Describe the pathophysiology of Thyroiditis

A

Inflammation from viral infection/childbirth/medication causes release of Thyroxine

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16
Q

Using the mnemonic SWEATING, describe the features of Hyperthyroidism

A

Sweating Weight Loss Emotional Appetite Increased Tachycardia Intolerance to heat Nervousness Goitre

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17
Q

What happens to children with Hyperthyroidism?

A

Accelerated growth and behavioural disturbances

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18
Q

why is lid lag seen in any cause of of hyperthyroidsism?

A

due to increased sympathetic tone of the upper eyelid

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19
Q

what signs are specific to Graves disease?

A

lid retraction

proptosis

thyroid eye disease

skin changes - dermopathy, characterised by pre-tibial myxoedema

nail changes - thyroid acropachy

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20
Q

what causes the skin and nail changes in graves disease?

A

cross-reactivity with TSH receptors in the back of the orbit and skin

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21
Q

What do the TFTs normal T3/T4 and low TSH demonstrate?

A

Subclinical Hyperthyroidism

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22
Q

Name two markers used to diagnose Hyperthyroidism

A
  • Thyroid Peroxidase Antibodies
  • TSH Receptor Stimulating Ab
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23
Q

Describe how iodine uptake assesses thyroid functionality

A

Increased uniform uptake - Graves Non Uniform Increased uptake - Nodular disease Absent Uptake - Thyroiditis

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24
Q

State two pharmacological managements of Hyperthyroidism, their actions and their side effects

A

Carbimazole and Propylthyrouracil Reduces T3 and T4 synthesis

SE: agranulocyotisis = Bone Marrow Supression (fever/sore throat is serious) and Rash

urgent FBC to exclude pancytopaenia

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25
Q

Hyperthyroidism medication can take 4-6 weeks to work, what cover could you give in the mean time for symptomatic relief?

A

Beta Blockers

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26
Q

How is Radioactive Iodine used to treat Hyperthyroidism and what are it’s disadvantages?

A

Radioactive iodine is taken up by cells of the thyroid which are then killed as a result Disadvantages: Requires lifelong Levothyroxine, contraindicated in pregnancy, have to avoid pregnant women and children for a few weeks

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27
Q

Describe two complications of a thyroidectomy

A

Recurrent Laryngeal Nerve Damage Hypoparathyroidism

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28
Q

Give 3 complications of Hyperthyroidism

A

Heart Failure AF Osteoporosis

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29
Q

State 5 causes of Primary Hypothyroidism

A

Autoimmune Pregnancy Iodine Deficiency Genetic (Familial Thyroid Dyshormonogenesis) Drugs (Amioderone, Lithium)

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30
Q

Using the mnemonic ‘MOMS SO TIRED’, describe the presentation of Hypothyroidism

A

Memory Loss, Obesity, Menorrhagia, Slowness, Skin and Hair Dryness, Onset Gradual, Tiredness, Intolerance to Cold, Raised BP, Energy levels fall, Depression

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31
Q

Name a marker for Hypothyroidism

A

Thyroid Peroxidase Antibodies

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32
Q

To treat Hypothyroidism , you would use Thyroxine replacement. What range of units is Thyroxine given in, and what marker is used to monitor?

A

50-100 micrograms per day If primary hypothyroidism then TSH is used to monitor If secondary hypothyroidism then T4 is used to monitor

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33
Q

Give a complication of Hypothyroidism

A

Myxoedema Coma

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34
Q

Name two molecules that Cortisol is bound to in the blood

A

Cortisol Binding Globulin Albumin

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35
Q

Describe the relationship between Cortisol Binding Globulin and Oestrogen and its implications

A

CBG production is stimulated by Oestrogen When measuring Plasma Cortisol, it combines free cortisol and bound (with the bound level being the CBG level) therefore these levels are not reliable if the patient is on HRT

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36
Q

When are cortisol levels at it’s highest and lowest?

A

Highest at 8am Lowest at midnight

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37
Q

Give 4 causes of Addisons/Primary Adrenal Insufficiency

A

Genetic Abnormalities in steroid synthesis TB Metastases Waterhouse Friderichson Syndrome

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38
Q

The symptoms of Addisons are very non specific, describe them

A

Fatigue Anorexia Nausea Dizziness

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39
Q

Describe a sign of Addisons disease and the pathophysiology behind it

A

Increased Pigmentation Increased stimulation of ACTH which also activates MSH

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40
Q

What electrolyte abnormalities will be present in Addisons?

A

Hyperkalaemia Hyponatraemia

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41
Q

What dynamic test can be used in suspected Addisons?

A

Administer IV ACTH (Synacthen) and see if cortisol increases. It shouldn’t if the patient has Addisons.

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42
Q

What is secondary adrenal insuffiency?

A

Decreased ACTH production from Pituitary Commonly due to long term steroids, or pituitary problems

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43
Q

How will Primary and Secondary Adrenal Insufficiency presentations differ?

A

Secondary will not have any increased pigmentation or reduced mineralocorticoids

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44
Q

Describe the management of Addisons

A

Glucocorticoid Replacement (Hydrocortisone) Mineralocorticoid Replacement (Fludrocortisone) Doses doubled in times of illness Steroid card and Medic Alert Bracelet

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45
Q

Give 3 causes of an Addisonian Crisis

A

Infection Trauma Surgery

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46
Q

Addisonian Crisis presents like shock, describe the 2 emergency management steps

A

100mg IV Hydrocortisone STAT IV Fluid Bolus

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47
Q

What is a Phaeochromocytoma?

A

Catecholamine producing tumours arising from collections of chromaffin cells

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48
Q

What is a Paraganglioma?

A

Extra adrenal version of Phaeochromocytomas, often occuring at aortic bifurcation

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49
Q

What is the 10% rule of Phaeochromocytoma?

A

10% Malignant 10% Extra-Adrenal 10% Bilateral 10% Familial

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50
Q

What is the triad presentation of Phaeochromocytoma?

A

Episodic Headaches Sweating Tachycardia

51
Q

Name three possible investigations of Phaeochromocytoma

A

24hr Urinary Metanephrines Abdo CT/MRI MIBG Scan (radioactive imaging)

52
Q

Phaeochromocytomas are generally managed with surgical excision, what medical management is used? Explain the order in which they’re given.

A

Alpha blockade with Doxazosin first Beta Blockers given second AB given first to prevent unopposed alpha adrenergic activity and hypertension. BB then given to prevent reflex tachycardia.

53
Q

What is Hyperaldosteronism and when should you suspect it?

A

Excess production of aldosterone independent of RAAS resulting in excess sodium and water retention Suspected if Hypertensive and Hypokalaemic(not on diuretics)

54
Q

Give 3 causes of Primary Hyperaldosteronism

A

Conns (Aldosterone producing adenoma) Bilateral Adrenocortical Hyperplasia Glucocorticoid Remediable Aldosteronism (ACTH regulatory element fuses to aldosterone synthase gene, bringing it under control of ACTH)

55
Q

Give 2 causes of Secondary Hyperaldosteronism

A

Diuretics Renal Artery Stenosis

56
Q

What is Bartter’s Syndrome?

A

Sodium and Chloride channel leak in the Loop of Henle causing salt wasting, then RAAS becomes activated

57
Q

What are the symptoms of Hyperaldosteronism?

A

May be asymptomatic or have signs of hypokalaemia (weakness, cramps)

58
Q

How would you manage Hyperaldosteronism?

A

Conns - Surgical removal and Spironolactone Hyperplasia - Spironolactone GRA - Dexamethasone

59
Q

Describe the embryological origins of the anterior and posterior pituitary

A

Anterior - ectodermal in origin, upgrowth of pharyngeal roof (Rathke’s Pouch) Posterior - neurectodermal in origin, extension of inferior forebrain

60
Q

Describe the superior and lateral relations of the pituitary gland

A

Superior - Optic Chiasm Lateral - Cavernous Sinus (III,IV,Va,Vb,VI)

61
Q

State the 5 axis of the Pituitary Gland

A

Growth Adrenal Gonadal Thyroid Prolactin

62
Q

Describe the Growth axis of the PG. What increases and decreases its release?

A

GH released in a pulsatile manner from anterior pituitary and acts on Growth Factor and IGF Receptors GH released increased by GHRH GH release decreased by Somatostatin

63
Q

Describe the Adrenal axis of the PG

A

CRH from Hypothalamus stimulates ACTH to be released from anterior pituitary which subsequently causes Cortisol release

64
Q

Describe the Gonadal axis of the PG in Women

A

GnRH from the Hypothalamus causes LH and FSH release FSH - Ovarian Follicle Development, targetting granulosa cells LH - Targets Theca cells to produce androgens and oestrogen precursors

65
Q

Describe the Gonadal axis of the PG in Men

A

GnRH from the Hypothalamus causes LH and FSH release FSH - Targets Sertoli cells to increase sperm production LH - Targets Leydig cells to produce Testosterone

66
Q

Describe the Thyroid Axis of the PG

A

TRH is released from the Hypothalamus which then causes TSH to be released from the Anterior Pituitary TRH also mildly stimulates Prolactin

67
Q

Describe the Prolactin Axis of the PG

A

TRH causes mild release of Prolactin from Anterior Pituitary Dopamine inhibits release of Prolactin from Anterior Pituitary Prolactin goes on to cause lactation Prolactin inhibits FSH and LH

68
Q

State the four different assessments of the PG

A

Clinical Biochemical Dynamic Imaging

69
Q

Describe the timings of PG hormone level testing

A

Prolactin and TSH can be checked at any hour Cortisol checked at 9am LH and FSH checked within first 5 days of Menstruation in Women, or fasted at 9am in Men

70
Q

One of the dynamic tests for the PG is the Synacthen test, describe it

A

Tests for Primary Adrenal Failure Administering synthetic ACTH doesn’t correspond to a rise in Cortisol

71
Q

One of the dynamic tests for the PG is the Insulin Tolerance test, describe it

A

Used to test Pituitary reserves Administering Insulin induces frank hypoglycaemia causing physiological stress and subsequent ACTH and GH release

72
Q

What imaging technique is used for the PG? If a tumour is found, how is it classified?

A

MRI with Contrast Microadenoma<1cm Macroadenoma>1cm

73
Q

Give 4 causes of Hyperprolactinaemia

A

Prolactinoma Pregnancy Compression of pituitary stalk Dopamine Antagonists (Haloperidol, Metaclopramide)

74
Q

Give 3 symptoms for Women and Men respectively of Hyperprolactinaemia

A

W - Amenorrhoea, Low Libido, Galactorrhoea M - ED, Decreased facial hair, Galactorrhoea

75
Q

How is Hyperprolactinaemia managed medically? What is the risk?

A

Dopamine Agonists such as Cabergoline (weekly) or Bromocriptine (daily) If a tumour, reducing the size may cause a CSF leak and subsequent meningitis

76
Q

Give 3 serum investigations that might be relevant in Hyperprolactinaemia

A

Basal Prolactin Pregnancy Test TFTs

77
Q

Acromegaly is normally caused by a GH secreting tumour, what happens if it is left untreated?

A

Disfiguring Increased Bowel Cancer Risk Risk of premature death from CVD

78
Q

Give 4 features of Acromegaly

A

Increased size of hands/feet Coarsening of facial features Soft tissue swelling (carpal tunnel/snoring) Headache (HTN)

79
Q

As GH is pulsatile, it is not a reliable investigation in Acromegaly. What dynamic test could you use instead and why?

A

Glucose causes insulin release, and insulin and GH are antagonistic. Physiologically OGTT should supress GH release, however in Acromegaly GH remains high.

80
Q

What surgical approach would you take to surgically remove a tumour causing Acromegaly?

A

Transphenoidal

81
Q

Give two pharmacological options to treat Acromegaly

A

Octreotide - Somatostatin Anologues Pegvisomant - GH Antagonists

82
Q

What are NFPAs?

A

Non Functioning Pituitary Adenomas May present with Headache/Hypopitutarism/Visual Field Loss

83
Q

What are the 3 levels of Hypopituiarism? Give two causes of each.

A

Hypothalamus - Infection, Tumour Stalk - Surgery, Carotid Artery Aneurysm Pituitary - Radiation, Ischaemia

84
Q

State the order that hormones are affected in Hypopituitarism

A

GH, FSH/LH, TSH, ACTH, PRL

85
Q

Hypopituitarism in adulthood presents quite non specifically, but in childhood how will it present?

A

Short Stature

86
Q

Describe the difference between Cushing’s Disease and Cushing’s Syndrome

A

Syndrome - collection of symptoms caused by excess cortisol Disease - when the excess cortisol is caused by an ACTH secreting adenoma

87
Q

Name two tumours that could cause Cushing’s Disease

A

SCC of the Lung Carcinoid Tumours

88
Q

Name two causes of Cushing’s Syndrome

A

Excess steroid use Adrenal Adenoma

89
Q

Give 3 symptoms and 3 signs of Cushing’s

A

Symptoms - Weight gain, weakness, irritability Signs - Moon face, Buffalo hump, Abdominal Striae

90
Q

State one static and one dynamic test for Cushings

A

Static - 24hr Urinary Free Cortisol Dynamic - Dexamethasone Supression Test

91
Q

How does the Dexamethasone Supression Test work?

A

Dexamethasone is given at 10pm at night, and cortisol levels are measured at 9am the next morning High Cortisol at a low dose, and Low Cortisol at a high dose indicates Cushings High Cortisol at a high dose suggests ectopic production (adenoma unresponsive to negative feedback)

92
Q

Give 3 possible managements of Cushings

A

Stop steroid medication if possible (GRADUALLY TAPER) Removal of tumours Metyrapone - inhibits cortisol production

93
Q

What might Hypocalcaemia be an artefact of?

A

Hypoalbuminaemia

94
Q

Give 2 causes of Hypocalcaemia with high phosphate

A

CKD Hyperparathyroidism

95
Q

Give 2 causes of Hypocalcaemia with low phosphate

A

Osteomalacia Acute Pancreatitis

96
Q

Using the mnemonic SPASMODIC, describe the features of Hypocalcaemia

A

Spasms Perioral Paraesthesia Anxious Seizures Muscle tone increased (smooth) Orientation impaired Dermatitis Impetigo Herpetiformes Chvostek’s Sign

97
Q

What is Trosseau’s Sign?

A

A sign of Hypocalcaemia Shows Carpopedal Spasm when you inflate cuff above systolic for 3 minutes

98
Q

What is Chvostek’s Sign?

A

A sign of Hypocalcaemia Twitching of facial muscles in response to tapping over facial nerve distribution

99
Q

How do you treat mild and severe Hypocalcaemia respectively?

A

Mild - Calcium PO every 6 hours Severe - 10ml 10% Calcium Gluconate over 30 mins

100
Q

Give five causes of Hypercalcaemia

A

Malignancy Hyperparathyroidism Sarcoidosis Thyrotoxicosis Lithium

101
Q

Give four symptoms of Hypercalcaemia

A

Bone pain Renal Stones Depression Constipaton

102
Q

If the cause of Hypercalcaemia was malignancy what would the blood tests show?

A

Low Albumin Low Chloride Low Potassium High Phosphate Alkalosis

103
Q

Describe a three step management plan of Hypercalcaemia

A

1) Correct Dehydration (IV 0.9% Saline) 2) Bisphosphonates (Inhibit Osteoclast activity) 3) Chemo if malignancy, Steroids if Sarcoidosis

104
Q

Describe 3 actions of the parathyroid gland

A

Increase Osteoclast activity Increase Calcium reabsorption from the kidney Increase Calcitriol production

105
Q

What is Primary Hyperparathyroidism?

A

Overactivity causes HIGH calcium 80% Solitary Adenoma 20% Gland Hyperplasia Associated with MEN syndrome

106
Q

What is Secondary Hyperparathyroidism?

A

Low Calcium and appropriately raised PTH Causes - CKD, Low Vit D

107
Q

What is Tertiary Hyperparathyroidism?

A

Occurs after prolonged Secondary Hyperparathyroidism, the gland becomes autonomous Inappropriate raised PTH and raised Ca2+

108
Q

Name 3 tumours that can produce PTHrP

A

SCC of lung Breast carcinomas RCC

109
Q

Give 2 causes of Primary Hypoparathyroidism

A

Autoimmune Congenital (DiGeorge)

110
Q

Give 2 causes of Secondary Hypoparathyroidism

A

Surgery Hypomagnesaemia (Magnesium required for PTH secretion)

111
Q

What is Pseudohypoparathyroisism? How will it present?

A

Target cells fail to respond to PTH Round face Short Stature Short Metacarpals

112
Q

Hirsutism is male pattern hair growth in women, give 3 causes

A

PCOS Cushings Familial

113
Q

Give 3 pharmacological options for Hirsutism

A

COCP Metformin Spironolactone

114
Q

Describe the pathophysiology of PCOS

A

LH increases relative to FSH causing increased testosterone relative to oestrogen Link with hyperinsulinaemia

115
Q

Describe 5 features of the classical presentation of PCOS

A

Oligomenorrhoea Sub/Infertility Hirsutism Obesity Acanthosis Nigracans (demonstrates insulin resistance)

116
Q

What is the diagnostic criteria of PCOS called? What does it include?

A

Rotterdam Criteria Polycystic Ovaries (12 or more follicles) Oligo/Anovulation Clinical/Biochemical signs of Hyperandrogenism

117
Q

Women with PCOS are often given the IUS, why?

A

Counteracts the endometrial hyperplasia caused by oligo-ovulation

118
Q

Give 4 pharmacological managements for PCOS

A

Co-Cyprindriol - Hirsutism and Acne COCP - Metformin Orlistat (Lipase Inhibitor)

119
Q

What is a Plethora?

A

Describes the facial appearance in Cushing

120
Q

How do you treat ectopic ACTH production?

A

Metyrapone

121
Q

What is Bartters Syndrome

A

Congenital salt wasting from LoH causing RAAS activation

122
Q

What is Nelson’s Syndrome?

A

occurs when an adrenocorticotrophic hormone (ACTH) secreting tumour develops following therapeutic total bilateral adrenalectomy for Cushing’s disease.

123
Q

What Cortisol level in a Dexamethasone Supression test would exclude Cushing?

A

<50 nmol /l

Year 3 Medicine (15 decks)

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