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
Describe two complications of a thyroidectomy
Recurrent Laryngeal Nerve Damage | Hypoparathyroidism
26
Give 3 complications of Hyperthyroidism
Heart Failure AF Osteoporosis
27
State 5 causes of Primary Hypothyroidism
``` Autoimmune (hashimotos) Pregnancy Iodine Deficiency Genetic (Familial Thyroid Dyshormonogenesis) Drugs (Amioderone, Lithium) ```
28
Name a marker for Hypothyroidism
Thyroid Peroxidase Antibodies
29
To treat Hypothyroidism , you would use Thyroxine replacement. What range of units is Thyroxine given in, and what marker is used to monitor?
50-100 micrograms per day If primary hypothyroidism then TSH is used to monitor If secondary hypothyroidism then T4 is used to monitor
30
Give a complication of Hypothyroidism
Myxoedema Coma
31
Give one drug which can cause hyperthyroidism other than levothyroxine
Amiodarone
32
A patient with graves has a thyroidectomy, why may they still develop thyroid eye disease
Autoantibodies still present, thyroid eye disease is due to autoantibodies rather than thyroid hormone
33
How is thyroid eye disease treated? (vaguely)
Steroids
34
When should a patient on carbimazole stop taking their medication and why
If they get an infection, because it can cause bone marrow surpression and decrease WBCC
35
why does the thyroid gland move when swallowing
as it is encased in the pre tracheal fascia
36
what is a cause of raised calcitonin
Calcitonin levels are elevated in medullary thyroid cancer which is a rare thyroid cancer (genetic link)
37
what are some signs and symptoms of hypothyroidism
``` weight gain lethargy cold imbalance HEART FAILURE constipation dry cold ect ```
38
what are some signs and symptoms of hyperthyroidism
``` weight loss restlessness heat intolerance PALPITATIONS- arrhythmias sweating anxiety diarrhoea ```
39
Name two molecules that Cortisol is bound to in the blood
Cortisol Binding Globulin | Albumin
40
When are cortisol levels at it's highest and lowest
Highest at 8am | Lowest at midnight
41
Give 4 causes of Addisons/Primary Adrenal Insufficiency
Genetic Abnormalities in steroid synthesis TB Metastases Waterhouse Friderichson Syndrome
42
The symptoms of Addisons are very non specific, describe them
Fatigue Anorexia Nausea Dizziness
43
Describe a sign of Addisons disease and the pathophysiology behind it
Increased Pigmentation | Increased stimulation of ACTH which also activates MSH
44
What electrolyte abnormalities will be present in Addisons?
Hyperkalaemia | Hyponatraemia
45
What dynamic test can be used in suspected Addisons?
Administer IV ACTH (Synacthen) and see if cortisol increases. It shouldn't if the patient has Addisons.
46
What is secondary adrenal insuffiency?
Decreased ACTH production from Pituitary | Commonly due to long term steroids, or pituitary problems
47
How will Primary and Secondary Adrenal Insufficiency presentations differ?
Secondary will not have any increased pigmentation or reduced mineralocorticoids
48
Describe the management of Addisons
``` Glucocorticoid Replacement (Hydrocortisone) Mineralocorticoid Replacement (Fludrocortisone) Doses doubled in times of illness Steroid card and Medic Alert Bracelet ```
49
Give 3 causes of an Addisonian Crisis
Infection Trauma Surgery
50
Addisonian Crisis presents like shock, describe the 2 emergency management steps
100mg IV Hydrocortisone STAT | IV Fluid Bolus
51
What is a Phaeochromocytoma?
Catecholamine producing tumours arising from collections of chromaffin cells
52
What is a Paraganglioma?
Extra adrenal version of Phaeochromocytomas, often occuring at aortic bifurcation
53
What is the triad presentation of Phaeochromocytoma
Episodic Headaches Sweating Tachycardia
54
Name three possible investigations of Phaeochromocytoma
``` 24hr Urinary Metanephrines Abdo CT/MRI MIBG Scan (radioactive imaging) ```
55
Phaeochromocytomas are generally managed with surgical excision, what medical management is used? Explain the order in which they're given.
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
What is Hyperaldosteronism and when should you suspect it?
Excess production of aldosterone independent of RAAS resulting in excess sodium and water retention Suspected if Hypertensive and Hypokalaemic(not on diuretics)
57
Give 3 causes of Primary Hyperaldosteronism
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
Give 2 causes of Secondary Hyperaldosteronism
Diuretics | Renal Artery Stenosis
59
What is Bartter's Syndrome?
Sodium and Chloride channel leak in the Loop of Henle causing salt wasting, then RAAS becomes activated
60
What are the symptoms of Hyperaldosteronism?
May be asymptomatic or have signs of hypokalaemia (weakness, cramps)
61
How would you manage Hyperaldosteronism?
Conns - Surgical removal and Spironolactone Hyperplasia - Spironolactone GRA - Dexamethasone
62
Describe the difference between Cushing's Disease and Cushing's Syndrome
Syndrome - collection of symptoms caused by excess cortisol | Disease - when the excess cortisol is caused by an ACTH secreting adenoma
63
Name two tumours that could cause Cushing's Disease
SCC of the Lung | Carcinoid Tumours
64
Name two causes of Cushing's Syndrome
Excess steroid use | Adrenal Adenoma
65
Give 3 symptoms and 3 signs of Cushing's
Symptoms - Weight gain, weakness, irritability | Signs - Moon face, Buffalo hump, Abdominal Striae
66
State one static and one dynamic test for Cushings
Static - 24hr Urinary Free Cortisol | Dynamic - Dexamethasone Supression Test
67
How does the Dexamethasone Supression Test work?
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
Give 3 possible managements of Cushings
Stop steroid medication if possible (GRADUALLY TAPER) Removal of tumours Metyrapone - inhibits cortisol production
69
Describe the clinical features of cushings syndrome
- plethoric - moon face - thinning of skin - easy bruising - buffalo hump - central obesity - abdo striae - HTN and DM
70
How could you initially screen someone you suspect has cushings? (4 options)
- 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
What is the low dose dexamethasone surpression test good for?
- 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
What could cause cushings?
- ACTH secreting pituitary tumour - Ectopic ACTH (small cell carcinoma) - adrenal tumour - steroids
73
How can you differentiate between ectopic ACTH and pituitary cushings?
- Pituitary cushings will surpress on high dose dexamethasone surpression test- ectopic ACTH will now - MRI pituitary fossa may show a lesion
74
State the 5 axis of the Pituitary Gland
``` Growth Adrenal Gonadal Thyroid Prolactin ```
75
Describe the Growth axis of the PG. What increases and decreases its release?
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
Describe the Adrenal axis of the PG
CRH from Hypothalamus stimulates ACTH to be released from anterior pituitary which subsequently causes Cortisol release
77
Describe the Gonadal axis of the PG in Women
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
Describe the Gonadal axis of the PG in Men
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
Describe the Thyroid Axis of the PG
TRH is released from the Hypothalamus which then causes TSH to be released from the Anterior Pituitary TRH also mildly stimulates Prolactin
80
Describe the Prolactin Axis of the PG
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
One of the dynamic tests for the PG is the Synacthen test, describe it
Tests for Primary Adrenal Failure | Administering synthetic ACTH doesn't correspond to a rise in Cortisol
82
One of the dynamic tests for the PG is the Insulin Tolerance test, describe it
One of the dynamic tests for the PG is the Insulin Tolerance test, describe it
83
What imaging technique is used for the PG? If a tumour is found, how is it classified?
MRI with Contrast Microadenoma<1cm Macroadenoma>1cm
84
Give 4 causes of Hyperprolactinaemia
Prolactinoma Pregnancy Compression of pituitary stalk Dopamine Antagonists (Haloperidol, Metaclopramide)
85
Acromegaly is normally caused by a GH secreting tumour, what happens if it is left untreated?
Disfiguring Increased Bowel Cancer Risk Risk of premature death from CVD
86
Give 4 features of Acromegaly
Increased size of hands/feet Coarsening of facial features Soft tissue swelling (carpal tunnel/snoring) Headache (HTN)
87
As GH is pulsatile, it is not a reliable investigation in Acromegaly. What dynamic test could you use instead and why?
Glucose causes insulin release, and insulin and GH are antagonistic. Physiologically OGTT should supress GH release, however in Acromegaly GH remains high.
88
What surgical approach would you take to surgically remove a tumour causing Acromegaly?
Transphenoidal
89
Give two pharmacological options to treat Acromegaly
Octreotide - Somatostatin Anologues | Pegvisomant - GH Antagonists
90
What are the 3 levels of Hypopituiarism? Give two causes of each.
Hypothalamus - Infection, Tumour Stalk - Surgery, Carotid Artery Aneurysm Pituitary - Radiation, Ischaemia
91
Hypopituitarism in adulthood presents quite non specifically, but in childhood how will it present?
Short Stature
92
how can you differentiate between prolactinomas and non functioning adenoma causing hyperprolactinaemia?
prolactinomas will cause prolactin to be >5000
93
How are prolactinomas and nonfunctioning adenomas causing hyperprolactinaemia managed?
prolactinomas= dopamine agonist (inhibits prolactin release) | non functioning adenoma= cut it out
94
Describe Na+ and osmolality changes to blood and urine in SIADH?
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
Other than SIADH, what else could cause hyponatuaemia with high urine Na+?
Adrenal insufficiency- less mineralcoritcoid production= less reuptake of Na+ in collecting duct
96
What might Hypocalcaemia be an artefact of?
Hypoalbuminaemia
97
Give 2 causes of Hypocalcaemia with high phosphate
CKD | Hyperparathyroidism
98
Give 2 causes of Hypocalcaemia with low phosphate
Osteomalacia | Acute Pancreatitis
99
describe the features of Hypocalcaemia- SPASMODIC
``` Spasms Perioral Paraesthesia Anxious Seizures Muscle tone increased (smooth) Orientation impaired Dermatitis Impetigo Herpetiformes Chvostek's Sign ```
100
What is Trosseau's Sign?
A sign of Hypocalcaemia | Shows Carpopedal Spasm when you inflate cuff above systolic for 3 minutes
101
What is Chvostek's Sign?
A sign of Hypocalcaemia | Twitching of facial muscles in response to tapping over facial nerve distribution
102
How do you treat mild and severe Hypocalcaemia respectively?
Mild - Calcium PO every 6 hours | Severe - 10ml 10% Calcium Gluconate over 30 mins
103
Give five causes of Hypercalcaemia
``` Malignancy Hyperparathyroidism Sarcoidosis Thyrotoxicosis Lithium ```
104
Give four symptoms of Hypercalcaemia
Bone pain Renal Stones Depression Constipaton
105
If the cause of Hypercalcaemia was malignancy what would the blood tests show?
``` Low Albumin Low Chloride Low Potassium High Phosphate Alkalosis ```
106
Describe a three step management plan of Hypercalcaemia
1) Correct Dehydration (IV 0.9% Saline) 2) Bisphosphonates (Inhibit Osteoclast activity) 3) Chemo if malignancy, Steroids if Sarcoidosis
107
Describe 3 actions of the parathyroid gland
Increase Osteoclast activity Increase Calcium reabsorption from the kidney Increase Calcitriol production
108
What is Primary Hyperparathyroidism?
Overactivity causes HIGH calcium 80% Solitary Adenoma 20% Gland Hyperplasia Associated with MEN syndrome
109
What is Secondary Hyperparathyroidism?
Low Calcium and appropriately raised PTH | Causes - CKD, Low Vit D
110
What is Tertiary Hyperparathyroidism
Occurs after prolonged Secondary Hyperparathyroidism, the gland becomes autonomous Inappropriate raised PTH and raised Ca2+
111
Give 2 causes of Primary Hypoparathyroidism
Autoimmune | Congenital (DiGeorge)
112
Give 2 causes of Secondary Hypoparathyroidism
Surgery | Hypomagnesaemia (Magnesium required for PTH secretion)
113
what are some causes of SIADH (use SIADH as the pneumonic)
* 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
how would you manage SIADH
* 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
what 2 hormones may small cell lung cancer lead to
SIADH leads to low sodium ACTH release leads to bushings
116
what hormone may a squamous cell lung cancer release
PTH leading to increased calcium