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taz- year 3 med > endocrine > Flashcards

endocrine 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 (hashimotos)
Pregnancy 
Iodine Deficiency 
Genetic (Familial Thyroid Dyshormonogenesis) 
Drugs (Amioderone, Lithium)
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28
Q

Name a marker for Hypothyroidism

A

Thyroid Peroxidase Antibodies

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29
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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30
Q

Give a complication of Hypothyroidism

A

Myxoedema Coma

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31
Q

Give one drug which can cause hyperthyroidism other than levothyroxine

A

Amiodarone

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32
Q

A patient with graves has a thyroidectomy, why may they still develop thyroid eye disease

A

Autoantibodies still present, thyroid eye disease is due to autoantibodies rather than thyroid hormone

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33
Q

How is thyroid eye disease treated? (vaguely)

A

Steroids

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34
Q

When should a patient on carbimazole stop taking their medication and why

A

If they get an infection, because it can cause bone marrow surpression and decrease WBCC

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35
Q

why does the thyroid gland move when swallowing

A

as it is encased in the pre tracheal fascia

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36
Q

what is a cause of raised calcitonin

A

Calcitonin levels are elevated in medullary thyroid cancer which is a rare thyroid cancer (genetic link)

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37
Q

what are some signs and symptoms of hypothyroidism

A 
weight gain
lethargy 
cold imbalance 
HEART FAILURE 
constipation 
dry 
cold 
ect
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38
Q

what are some signs and symptoms of hyperthyroidism

A 
weight loss 
restlessness 
heat intolerance 
PALPITATIONS- arrhythmias 
sweating 
anxiety 
diarrhoea
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39
Q

Name two molecules that Cortisol is bound to in the blood

A

Cortisol Binding Globulin

Albumin

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40
Q

When are cortisol levels at it’s highest and lowest

A

Highest at 8am

Lowest at midnight

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41
Q

Give 4 causes of Addisons/Primary Adrenal Insufficiency

A

Genetic Abnormalities in steroid synthesis
TB
Metastases
Waterhouse Friderichson Syndrome

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42
Q

The symptoms of Addisons are very non specific, describe them

A

Fatigue
Anorexia
Nausea
Dizziness

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43
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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44
Q

What electrolyte abnormalities will be present in Addisons?

A

Hyperkalaemia

Hyponatraemia

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45
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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46
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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47
Q

How will Primary and Secondary Adrenal Insufficiency presentations differ?

A

Secondary will not have any increased pigmentation or reduced mineralocorticoids

48
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
49
Q

Give 3 causes of an Addisonian Crisis

A

Infection
Trauma
Surgery

50
Q

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

A

100mg IV Hydrocortisone STAT

IV Fluid Bolus

51
Q

What is a Phaeochromocytoma?

A

Catecholamine producing tumours arising from collections of chromaffin cells

52
Q

What is a Paraganglioma?

A

Extra adrenal version of Phaeochromocytomas, often occuring at aortic bifurcation

53
Q

What is the triad presentation of Phaeochromocytoma

A

Episodic Headaches
Sweating
Tachycardia

54
Q

Name three possible investigations of Phaeochromocytoma

A 
24hr Urinary Metanephrines
Abdo CT/MRI 
MIBG Scan (radioactive imaging)
55
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.

56
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)

57
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)

58
Q

Give 2 causes of Secondary Hyperaldosteronism

A

Diuretics

Renal Artery Stenosis

59
Q

What is Bartter’s Syndrome?

A

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

60
Q

What are the symptoms of Hyperaldosteronism?

A

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

61
Q

How would you manage Hyperaldosteronism?

A

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

62
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

63
Q

Name two tumours that could cause Cushing’s Disease

A

SCC of the Lung

Carcinoid Tumours

64
Q

Name two causes of Cushing’s Syndrome

A

Excess steroid use

Adrenal Adenoma

65
Q

Give 3 symptoms and 3 signs of Cushing’s

A

Symptoms - Weight gain, weakness, irritability

Signs - Moon face, Buffalo hump, Abdominal Striae

66
Q

State one static and one dynamic test for Cushings

A

Static - 24hr Urinary Free Cortisol

Dynamic - Dexamethasone Supression Test

67
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)

68
Q

Give 3 possible managements of Cushings

A

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

69
Q

Describe the clinical features of cushings syndrome

A
  • plethoric
  • moon face
  • thinning of skin
  • easy bruising
  • buffalo hump
  • central obesity
  • abdo striae
  • HTN and DM
70
Q

How could you initially screen someone you suspect has cushings? (4 options)

A
  • 24 hr urinary cortisol x3
  • ACTH (only at specialist centres)
  • Midnight cortisol (should be lowest, difficult inpractice)
  • Low dose dexamethasone surpression test (best screening test)
71
Q

What is the low dose dexamethasone surpression test good for?

A
  • give 0.5mg dexamethasone qds for 48 hrs
  • cortisol should go down to <30, if >30 (doesnt surpress) then true cushings
  • psuedocushings can be causes by alcohol or depression
72
Q

What could cause cushings?

A
  • ACTH secreting pituitary tumour
  • Ectopic ACTH (small cell carcinoma)
  • adrenal tumour
  • steroids
73
Q

How can you differentiate between ectopic ACTH and pituitary cushings?

A
  • Pituitary cushings will surpress on high dose dexamethasone surpression test- ectopic ACTH will now
  • MRI pituitary fossa may show a lesion
74
Q

State the 5 axis of the Pituitary Gland

A 
Growth
Adrenal 
Gonadal 
Thyroid 
Prolactin
75
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

76
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

77
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

78
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

79
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

80
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

81
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

82
Q

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

A

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

83
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

84
Q

Give 4 causes of Hyperprolactinaemia

A

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

85
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

86
Q

Give 4 features of Acromegaly

A

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

87
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.

88
Q

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

A

Transphenoidal

89
Q

Give two pharmacological options to treat Acromegaly

A

Octreotide - Somatostatin Anologues

Pegvisomant - GH Antagonists

90
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

91
Q

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

A

Short Stature

92
Q

how can you differentiate between prolactinomas and non functioning adenoma causing hyperprolactinaemia?

A

prolactinomas will cause prolactin to be >5000

93
Q

How are prolactinomas and nonfunctioning adenomas causing hyperprolactinaemia managed?

A

prolactinomas= dopamine agonist (inhibits prolactin release)

non functioning adenoma= cut it out

94
Q

Describe Na+ and osmolality changes to blood and urine in SIADH?

A

High Na+ conc in urine (as retaining water) and high urine osmolality (>100)
Low Na+ conc in blood (<135 mmol/l) with low serum osmolality (<280)

95
Q

Other than SIADH, what else could cause hyponatuaemia with high urine Na+?

A

Adrenal insufficiency- less mineralcoritcoid production= less reuptake of Na+ in collecting duct

96
Q

What might Hypocalcaemia be an artefact of?

A

Hypoalbuminaemia

97
Q

Give 2 causes of Hypocalcaemia with high phosphate

A

CKD

Hyperparathyroidism

98
Q

Give 2 causes of Hypocalcaemia with low phosphate

A

Osteomalacia

Acute Pancreatitis

99
Q

describe the features of Hypocalcaemia- SPASMODIC

A 
Spasms 
Perioral Paraesthesia 
Anxious 
Seizures 
Muscle tone increased (smooth) 
Orientation impaired 
Dermatitis 
Impetigo Herpetiformes 
Chvostek's Sign
100
Q

What is Trosseau’s Sign?

A

A sign of Hypocalcaemia

Shows Carpopedal Spasm when you inflate cuff above systolic for 3 minutes

101
Q

What is Chvostek’s Sign?

A

A sign of Hypocalcaemia

Twitching of facial muscles in response to tapping over facial nerve distribution

102
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

103
Q

Give five causes of Hypercalcaemia

A 
Malignancy
Hyperparathyroidism 
Sarcoidosis 
Thyrotoxicosis 
Lithium
104
Q

Give four symptoms of Hypercalcaemia

A

Bone pain
Renal Stones
Depression
Constipaton

105
Q

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

A 
Low Albumin
Low Chloride 
Low Potassium 
High Phosphate 
Alkalosis
106
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

107
Q

Describe 3 actions of the parathyroid gland

A

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

108
Q

What is Primary Hyperparathyroidism?

A

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

109
Q

What is Secondary Hyperparathyroidism?

A

Low Calcium and appropriately raised PTH

Causes - CKD, Low Vit D

110
Q

What is Tertiary Hyperparathyroidism

A

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

111
Q

Give 2 causes of Primary Hypoparathyroidism

A

Autoimmune

Congenital (DiGeorge)

112
Q

Give 2 causes of Secondary Hypoparathyroidism

A

Surgery

Hypomagnesaemia (Magnesium required for PTH secretion)

113
Q

what are some causes of SIADH (use SIADH as the pneumonic)

A
  • Surgery
  • Intracranial: infections, SAH, stroke, porphyria
  • Alveolar: SCLC (+ pancreas, prostate ca), empyema, infections (TB, Legionella, Mycoplasma, aspergillosis)
  • Drugs: carbamazepine, sulfonylureas, SSRIs/TCAs, vincristine, cyclophosphamide
  • Hormonal: Hypothyroidism, decreased Cortisol
114
Q

how would you manage SIADH

A
  • Fluid restriction
  • If Na <120 à 3% Hypertonic Saline (no faster than 1mmol/hr or à Central pontine myelinolysis)
  • Demeclocycline (Øcell response to ADH à nephrogenic DI) or furosemide
  • Vaptans (ADH-R antagonists)
115
Q

what 2 hormones may small cell lung cancer lead to

A

SIADH leads to low sodium

ACTH release leads to bushings

116
Q

what hormone may a squamous cell lung cancer release

A

PTH leading to increased calcium

taz- year 3 med (10 decks)

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