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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 do the C Cells of the thyroid produce?

A

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 TFTs

A

Pregnancy
Medication (Lithium, Amioderone)

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8
Q

What is Primary Hypothyroidism? What would the TFTs show?

A

Cause is the Thyroid itself (commonly autoimmune)
Low T4
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

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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

There is some cross reactivity of TSH receptors in the skin and eyes. What are the resulting clinical features of this?

A

Lid Lag - high sympathetic tone of upper eyelid
Exopthalmos
Pretibial Myxoedema

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19
Q

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

A

Subclinical Hyperthyroidism

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20
Q

Name two markers used to diagnose Hyperthyroidism

A

Thyroid Peroxidase Antibodies
TSH Receptor Stimulating Ab

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21
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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22
Q

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

A

Carbimazole and Propylthyrouracil
Reduces T3 and T4 synthesis
SE: Bone Marrow Supression (fever/sore throat is serious) and Rash

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23
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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24
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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25
Q

Describe two complications of a thyroidectomy

A

Recurrent Laryngeal Nerve Damage
Hypoparathyroidism

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26
Q

Give 3 complications of Hyperthyroidism

A

Heart Failure
AF
Osteoporosis

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27
Q

State 5 causes of Primary Hypothyroidism

A

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

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28
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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29
Q

Name a marker for Hypothyroidism

A

Thyroid Peroxidase Antibodies

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30
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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31
Q

Give a complication of Hypothyroidism

A

Myxoedema Coma

Managed with IV Thyroxine and Hydrocortisone STAT

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32
Q

Name two molecules that Cortisol is bound to in the blood

A

Cortisol Binding Globulin
Albumin

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33
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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34
Q

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

A

Highest at 8am
Lowest at midnight

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35
Q

Give 4 causes of Addisons/Primary Adrenal Insufficiency

A

Genetic Abnormalities in steroid synthesis
TB
Metastases
Waterhouse Friderichson Syndrome

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36
Q

The symptoms of Addisons are very non specific, describe them

A

Fatigue
Anorexia
Nausea
Dizziness

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37
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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38
Q

What electrolyte abnormalities will be present in Addisons?

A

Hyperkalaemia
Hyponatraemia

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39
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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40
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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41
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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42
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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43
Q

Give 3 causes of an Addisonian Crisis

A

Infection
Trauma
Surgery

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44
Q

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

A

100mg IV Hydrocortisone STAT
IV Fluid Bolus

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45
Q

What is a Phaeochromocytoma?

A

Catecholamine producing tumours arising from collections of chromaffin cells

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46
Q

What is a Paraganglioma?

A

Extra adrenal version of Phaeochromocytomas, often occuring at aortic bifurcation

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47
Q

What is the 10% rule of Phaeochromocytoma?

A

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

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48
Q

What is the triad presentation of Phaeochromocytoma?

A

Episodic Headaches
Sweating
Tachycardia

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49
Q

Name three possible investigations of Phaeochromocytoma

A

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

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50
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.

51
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)

52
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)

53
Q

Give 2 causes of Secondary Hyperaldosteronism

A

Diuretics
Renal Artery Stenosis

54
Q

What is Bartter’s Syndrome?

A

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

55
Q

What are the symptoms of Hyperaldosteronism?

A

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

56
Q

How would you manage Hyperaldosteronism?

A

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

57
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

58
Q

Describe the superior and lateral relations of the pituitary gland

A

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

59
Q

State the 5 axis of the Pituitary Gland

A

Growth
Adrenal
Gonadal
Thyroid
Prolactin

60
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

61
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

62
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

63
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

64
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

65
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

66
Q

State the four different assessments of the PG

A

Clinical
Biochemical
Dynamic
Imaging

67
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

68
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

69
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

70
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

71
Q

Give 4 causes of Hyperprolactinaemia

A

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

72
Q

Give 3 symptoms for Women and Men respectively of Hyperprolactinaemia

A

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

73
Q

Hyperprolactinaemia is managed medically first line, 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

74
Q

Give 3 serum investigations that might be relevant in Hyperprolactinaemia

A

Basal Prolactin
Pregnancy Test
TFTs

75
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

76
Q

Give 4 features of Acromegaly

A

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

77
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.

78
Q

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

A

Transphenoidal

79
Q

Give two pharmacological options to treat Acromegaly

A

Octreotide - Somatostatin Anologues
Pegvisomant - GH Antagonists

80
Q

What are NFPAs?

A

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

81
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

82
Q

State the order that hormones are affected in Hypopituitarism

A

GH, FSH/LH, TSH, ACTH, PRL

83
Q

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

A

Short Stature

84
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 pituitary adenoma

85
Q

Name two tumours that could cause Cushing’s Disease

A

Pituitary Adenoma
SCC of the Lung

86
Q

Name two causes of Cushing’s Syndrome

A

Excess steroid use
Adrenal Adenoma

87
Q

Give 3 symptoms and 3 signs of Cushing’s

A

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

88
Q

State one static and one dynamic test for Cushings

A

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

89
Q

How does the High Dose Dexamethasone Supression Test work?

A

Dexamethasone is given at 10pm at night, and cortisol levels are measured at 9am the next morning

Exogenous - high cortisol, low ACTH
Pituitary Adenoma - low cortisol, low ACTH
Ectopic ACTH - high cortisol, high ACTH

90
Q

Give 3 possible managements of Cushings

A

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

91
Q

What might Hypocalcaemia be an artefact of?

A

Hypoalbuminaemia

92
Q

Give 2 causes of Hypocalcaemia with high phosphate

A

CKD
Hyperparathyroidism

93
Q

Give 2 causes of Hypocalcaemia with low phosphate

A

Osteomalacia
Acute Pancreatitis

94
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

95
Q

What is Trosseau’s Sign?

A

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

96
Q

What is Chvostek’s Sign?

A

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

97
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

98
Q

Give five causes of Hypercalcaemia

A

Malignancy
Hyperparathyroidism
Sarcoidosis
Thyrotoxicosis
Lithium

99
Q

Give four symptoms of Hypercalcaemia

A

Bone pain
Renal Stones
Depression
Constipaton

100
Q

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

A

Low Albumin
Low Chloride
Low Potassium
High Phosphate
Alkalosis

101
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

102
Q

Describe 3 actions of the parathyroid gland

A

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

103
Q

What is Primary Hyperparathyroidism?

A

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

104
Q

What is Secondary Hyperparathyroidism?

A

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

105
Q

What is Tertiary Hyperparathyroidism?

A

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

106
Q

Name 3 tumours that can produce PTHrP

A

SCC of lung
Breast carcinomas
RCC

107
Q

Give 2 causes of Primary Hypoparathyroidism

A

Autoimmune
Congenital (DiGeorge)

108
Q

Give 2 causes of Secondary Hypoparathyroidism

A

Myeloma
Sarcoidosis

109
Q

What is Pseudohypoparathyroisism? How will it present?

A

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

110
Q

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

A

PCOS
Cushings
Familial

111
Q

Give 3 pharmacological options for Hirsutism

A

COCP
Metformin
Spironolactone

112
Q

Describe the pathophysiology of PCOS

A

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

113
Q

Describe 5 features of the classical presentation of PCOS

A

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

114
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

115
Q

Women with PCOS are often given the IUS, why?

A

Counteracts the endometrial hyperplasia caused by oligo-ovulation

116
Q

Give 4 pharmacological managements for PCOS

A

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

117
Q

What is a Plethora?

A

Describes the facial appearance in Cushing

118
Q

How do you treat ectopic ACTH production?

A

Metyrapone

119
Q

What is Bartters Syndrome

A

Congenital salt wasting from LoH causing RAAS activation

120
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.

121
Q

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

A

<50 nmol /l

122
Q

What static test is first line in Acromegaly?

A

Serum IFG1

123
Q

How would you manage a myxoedema coma?

A

IV Thyroxine
IV fluids

And IV hydrocortisone as can’t distingush from addisons

124
Q

What is Pseudocushings, and how will you investigate?

A

Mimics Cushing’s, often caused by excess alcohol

Differentiated by insulin stress

Year 3 Medicine (10 decks)

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