Endocrinology Flashcards
(123 cards)
1
Q
Describe the blood supply of the thyroid
A
- Superior thyroid artery (from external carotid)
- Inferior thyroid artery (from thyrocervical trunk)
2
Q
What structures lie laterally to the thyroid gland?
A
Recurrent laryngeal nerves
3
Q
Describe the tissue composition of the thyroid gland
A
Follicular cells producing thyroglobulin, surrounding a colloid which contains iodinated thyroglobulin
4
Q
What are C Cells of the thyroid and what do they produce?
A
Neuroendocrine cells which produce Calcitonin
5
Q
Name two molecules that thyroid hormones are bound to in the blood
A
- Thyroxine Binding Globulin
- Albumin
6
Q
Describe three actions of thyroid hormones
A
- Increase Basal Metabolic Rate
- Increase Heart Rate
- Children’s growth
7
Q
Name two non thyroid causes that can affect Thyroid Function Tests
A
- Pregnancy
- Medication (Lithium, Amioderone)
- amioderone can cause thyrtoxicosis
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
9
Q
What is Secondary Hypothyroidism? What would the TFTs show?
A
Cause is a TSH deficiency (Pituitary problem) Low T4 Low TSH
10
Q
Describe the TFTs of Hyperthyroidism
A
High T3/T4 Very low TSH
11
Q
What would the TFTs of high T3/T4 and high TSH show?
A
TSH secreting adenoma
thyroid hormone resistance
assay interference
12
Q
State 4 causes of Hyperthyroidism
A
Graves (autoimmune) Nodular Thyroid Disease Thyroiditis Ectopic Thyroid Tissue
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
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
15
Q
Describe the pathophysiology of Thyroiditis
A
Inflammation from viral infection/childbirth/medication causes release of Thyroxine
16
Q
Using the mnemonic SWEATING, describe the features of Hyperthyroidism
A
Sweating Weight Loss Emotional Appetite Increased Tachycardia Intolerance to heat Nervousness Goitre
17
Q
What happens to children with Hyperthyroidism?
A
Accelerated growth and behavioural disturbances
18
Q
why is lid lag seen in any cause of of hyperthyroidsism?
A
due to increased sympathetic tone of the upper eyelid
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
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
21
Q
What do the TFTs normal T3/T4 and low TSH demonstrate?
A
Subclinical Hyperthyroidism
22
Q
Name two markers used to diagnose Hyperthyroidism
A
- Thyroid Peroxidase Antibodies
- TSH Receptor Stimulating Ab
23
Q
Describe how iodine uptake assesses thyroid functionality
A
Increased uniform uptake - Graves Non Uniform Increased uptake - Nodular disease Absent Uptake - Thyroiditis
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
25
Hyperthyroidism medication can take 4-6 weeks to work, what cover could you give in the mean time for symptomatic relief?
Beta Blockers
26
How is Radioactive Iodine used to treat Hyperthyroidism and what are it's disadvantages?
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
27
Describe two complications of a thyroidectomy
Recurrent Laryngeal Nerve Damage Hypoparathyroidism
28
Give 3 complications of Hyperthyroidism
Heart Failure AF Osteoporosis
29
State 5 causes of Primary Hypothyroidism
Autoimmune Pregnancy Iodine Deficiency Genetic (Familial Thyroid Dyshormonogenesis) Drugs (Amioderone, Lithium)
30
Using the mnemonic 'MOMS SO TIRED', describe the presentation of Hypothyroidism
Memory Loss, Obesity, Menorrhagia, Slowness, Skin and Hair Dryness, Onset Gradual, Tiredness, Intolerance to Cold, Raised BP, Energy levels fall, Depression
31
Name a marker for Hypothyroidism
Thyroid Peroxidase Antibodies
32
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
33
Give a complication of Hypothyroidism
Myxoedema Coma
34
Name two molecules that Cortisol is bound to in the blood
Cortisol Binding Globulin Albumin
35
Describe the relationship between Cortisol Binding Globulin and Oestrogen and its implications
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
36
When are cortisol levels at it's highest and lowest?
Highest at 8am Lowest at midnight
37
Give 4 causes of Addisons/Primary Adrenal Insufficiency
Genetic Abnormalities in steroid synthesis TB Metastases Waterhouse Friderichson Syndrome
38
The symptoms of Addisons are very non specific, describe them
Fatigue Anorexia Nausea Dizziness
39
Describe a sign of Addisons disease and the pathophysiology behind it
Increased Pigmentation Increased stimulation of ACTH which also activates MSH
40
What electrolyte abnormalities will be present in Addisons?
Hyperkalaemia Hyponatraemia
41
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.
42
What is secondary adrenal insuffiency?
Decreased ACTH production from Pituitary Commonly due to long term steroids, or pituitary problems
43
How will Primary and Secondary Adrenal Insufficiency presentations differ?
Secondary will not have any increased pigmentation or reduced mineralocorticoids
44
Describe the management of Addisons
Glucocorticoid Replacement (Hydrocortisone) Mineralocorticoid Replacement (Fludrocortisone) Doses doubled in times of illness Steroid card and Medic Alert Bracelet
45
Give 3 causes of an Addisonian Crisis
Infection Trauma Surgery
46
Addisonian Crisis presents like shock, describe the 2 emergency management steps
100mg IV Hydrocortisone STAT IV Fluid Bolus
47
What is a Phaeochromocytoma?
Catecholamine producing tumours arising from collections of chromaffin cells
48
What is a Paraganglioma?
Extra adrenal version of Phaeochromocytomas, often occuring at aortic bifurcation
49
What is the 10% rule of Phaeochromocytoma?
10% Malignant 10% Extra-Adrenal 10% Bilateral 10% Familial
50
What is the triad presentation of Phaeochromocytoma?
Episodic Headaches Sweating Tachycardia
51
Name three possible investigations of Phaeochromocytoma
24hr Urinary Metanephrines Abdo CT/MRI MIBG Scan (radioactive imaging)
52
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.
53
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)
54
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)
55
Give 2 causes of Secondary Hyperaldosteronism
Diuretics Renal Artery Stenosis
56
What is Bartter's Syndrome?
Sodium and Chloride channel leak in the Loop of Henle causing salt wasting, then RAAS becomes activated
57
What are the symptoms of Hyperaldosteronism?
May be asymptomatic or have signs of hypokalaemia (weakness, cramps)
58
How would you manage Hyperaldosteronism?
Conns - Surgical removal and Spironolactone Hyperplasia - Spironolactone GRA - Dexamethasone
59
Describe the embryological origins of the anterior and posterior pituitary
Anterior - ectodermal in origin, upgrowth of pharyngeal roof (Rathke's Pouch) Posterior - neurectodermal in origin, extension of inferior forebrain
60
Describe the superior and lateral relations of the pituitary gland
Superior - Optic Chiasm Lateral - Cavernous Sinus (III,IV,Va,Vb,VI)
61
State the 5 axis of the Pituitary Gland
Growth Adrenal Gonadal Thyroid Prolactin
62
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
63
Describe the Adrenal axis of the PG
CRH from Hypothalamus stimulates ACTH to be released from anterior pituitary which subsequently causes Cortisol release
64
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
65
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
66
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
67
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
68
State the four different assessments of the PG
Clinical Biochemical Dynamic Imaging
69
Describe the timings of PG hormone level testing
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
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
71
One of the dynamic tests for the PG is the Insulin Tolerance test, describe it
Used to test Pituitary reserves Administering Insulin induces frank hypoglycaemia causing physiological stress and subsequent ACTH and GH release
72
What imaging technique is used for the PG? If a tumour is found, how is it classified?
MRI with Contrast Microadenoma\<1cm Macroadenoma\>1cm
73
Give 4 causes of Hyperprolactinaemia
Prolactinoma Pregnancy Compression of pituitary stalk Dopamine Antagonists (Haloperidol, Metaclopramide)
74
Give 3 symptoms for Women and Men respectively of Hyperprolactinaemia
W - Amenorrhoea, Low Libido, Galactorrhoea M - ED, Decreased facial hair, Galactorrhoea
75
How is Hyperprolactinaemia managed medically? What is the risk?
Dopamine Agonists such as Cabergoline (weekly) or Bromocriptine (daily) If a tumour, reducing the size may cause a CSF leak and subsequent meningitis
76
Give 3 serum investigations that might be relevant in Hyperprolactinaemia
Basal Prolactin Pregnancy Test TFTs
77
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
78
Give 4 features of Acromegaly
Increased size of hands/feet Coarsening of facial features Soft tissue swelling (carpal tunnel/snoring) Headache (HTN)
79
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.
80
What surgical approach would you take to surgically remove a tumour causing Acromegaly?
Transphenoidal
81
Give two pharmacological options to treat Acromegaly
Octreotide - Somatostatin Anologues Pegvisomant - GH Antagonists
82
What are NFPAs?
Non Functioning Pituitary Adenomas May present with Headache/Hypopitutarism/Visual Field Loss
83
What are the 3 levels of Hypopituiarism? Give two causes of each.
Hypothalamus - Infection, Tumour Stalk - Surgery, Carotid Artery Aneurysm Pituitary - Radiation, Ischaemia
84
State the order that hormones are affected in Hypopituitarism
GH, FSH/LH, TSH, ACTH, PRL
85
Hypopituitarism in adulthood presents quite non specifically, but in childhood how will it present?
Short Stature
86
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
87
Name two tumours that could cause Cushing's Disease
SCC of the Lung Carcinoid Tumours
88
Name two causes of Cushing's Syndrome
Excess steroid use Adrenal Adenoma
89
Give 3 symptoms and 3 signs of Cushing's
Symptoms - Weight gain, weakness, irritability Signs - Moon face, Buffalo hump, Abdominal Striae
90
State one static and one dynamic test for Cushings
Static - 24hr Urinary Free Cortisol Dynamic - Dexamethasone Supression Test
91
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)
92
Give 3 possible managements of Cushings
Stop steroid medication if possible (GRADUALLY TAPER) Removal of tumours Metyrapone - inhibits cortisol production
93
What might Hypocalcaemia be an artefact of?
Hypoalbuminaemia
94
Give 2 causes of Hypocalcaemia with high phosphate
CKD Hyperparathyroidism
95
Give 2 causes of Hypocalcaemia with low phosphate
Osteomalacia Acute Pancreatitis
96
Using the mnemonic SPASMODIC, describe the features of Hypocalcaemia
Spasms Perioral Paraesthesia Anxious Seizures Muscle tone increased (smooth) Orientation impaired Dermatitis Impetigo Herpetiformes Chvostek's Sign
97
What is Trosseau's Sign?
A sign of Hypocalcaemia Shows Carpopedal Spasm when you inflate cuff above systolic for 3 minutes
98
What is Chvostek's Sign?
A sign of Hypocalcaemia Twitching of facial muscles in response to tapping over facial nerve distribution
99
How do you treat mild and severe Hypocalcaemia respectively?
Mild - Calcium PO every 6 hours Severe - 10ml 10% Calcium Gluconate over 30 mins
100
Give five causes of Hypercalcaemia
Malignancy Hyperparathyroidism Sarcoidosis Thyrotoxicosis Lithium
101
Give four symptoms of Hypercalcaemia
Bone pain Renal Stones Depression Constipaton
102
If the cause of Hypercalcaemia was malignancy what would the blood tests show?
Low Albumin Low Chloride Low Potassium High Phosphate Alkalosis
103
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
104
Describe 3 actions of the parathyroid gland
Increase Osteoclast activity Increase Calcium reabsorption from the kidney Increase Calcitriol production
105
What is Primary Hyperparathyroidism?
Overactivity causes HIGH calcium 80% Solitary Adenoma 20% Gland Hyperplasia Associated with MEN syndrome
106
What is Secondary Hyperparathyroidism?
Low Calcium and appropriately raised PTH Causes - CKD, Low Vit D
107
What is Tertiary Hyperparathyroidism?
Occurs after prolonged Secondary Hyperparathyroidism, the gland becomes autonomous Inappropriate raised PTH and raised Ca2+
108
Name 3 tumours that can produce PTHrP
SCC of lung Breast carcinomas RCC
109
Give 2 causes of Primary Hypoparathyroidism
Autoimmune Congenital (DiGeorge)
110
Give 2 causes of Secondary Hypoparathyroidism
Surgery Hypomagnesaemia (Magnesium required for PTH secretion)
111
What is Pseudohypoparathyroisism? How will it present?
Target cells fail to respond to PTH Round face Short Stature Short Metacarpals
112
Hirsutism is male pattern hair growth in women, give 3 causes
PCOS Cushings Familial
113
Give 3 pharmacological options for Hirsutism
COCP Metformin Spironolactone
114
Describe the pathophysiology of PCOS
LH increases relative to FSH causing increased testosterone relative to oestrogen Link with hyperinsulinaemia
115
Describe 5 features of the classical presentation of PCOS
Oligomenorrhoea Sub/Infertility Hirsutism Obesity Acanthosis Nigracans (demonstrates insulin resistance)
116
What is the diagnostic criteria of PCOS called? What does it include?
Rotterdam Criteria Polycystic Ovaries (12 or more follicles) Oligo/Anovulation Clinical/Biochemical signs of Hyperandrogenism
117
Women with PCOS are often given the IUS, why?
Counteracts the endometrial hyperplasia caused by oligo-ovulation
118
Give 4 pharmacological managements for PCOS
Co-Cyprindriol - Hirsutism and Acne COCP - Metformin Orlistat (Lipase Inhibitor)
119
What is a Plethora?
Describes the facial appearance in Cushing
120
How do you treat ectopic ACTH production?
Metyrapone
121
What is Bartters Syndrome
Congenital salt wasting from LoH causing RAAS activation
122
What is Nelson’s Syndrome?
occurs when an adrenocorticotrophic hormone (ACTH) secreting tumour develops following therapeutic total bilateral adrenalectomy for Cushing's disease.
123
What Cortisol level in a Dexamethasone Supression test would exclude Cushing?
\<50 nmol /l
