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Yr3 - General Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

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1
Q

Anatomy of the thyroid gland

A

2 lobes joined by a central isthmus

Sits anteriorly to thyroid cartilage in the neck - distinguished from other neck features by its movement on swallowing

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2
Q

Vascular supply of the thyroid gland

A

Inferior and superior thyroid arteries

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3
Q

Constituents of thyroid tissue

A

Colloid - stores iodinated thyroglobulin
Follicular cells - synthesises thyroglobulin
Neuroendocrine cells (c-cells) - secrete calcitonin

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4
Q

Types of thyroid hormones

A

T4 (thyroxine) - main circulating hormone - converted peripherally to T3
T3 (triiodothyronine) - more potent and shorter acting

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5
Q

How are thyroid hormones transported?

A

Thyroxine binding blobulin (TBG)
Transthyretin
Albumin

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6
Q

Thyroid hormone receptors

A

Free hormone acts on intracellular thyroid receptors
TRα
TRβ

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7
Q

Actions of thyroid hormones

A

Increase basal metabolic rate and growth in children
Increase heart rate
Effect CNS and reproductive system

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8
Q

Interpretation of thyroid function tests

A

TRH stimulates pituitary TSH secretion

This drives T3 and T4 secretion

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9
Q

Features of primary hypothyroidism

A

Problem with thyroid gland itself - commonly autoimmune

Characterised by reduced circulating T4 and high TSH

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10
Q

Features of secondary hypothyroidism

A

Due to TSH deficiency - usually pituitary disease

Characterised by low T4 and non-elevated TSH

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11
Q

Features of hyperthyroidism

A

Characterised by increased T3/T4 with suppressed TSH

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12
Q

Things that can affect thyroid function tests

A

Acute illness
Medication - lithium and amiodarone
Pregnancy

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13
Q

Define thyrotoxicosis

A

Hyperthyroidism

Commonly affects young women

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14
Q

Causes of thyrotoxicosis

A

Autoimmune (Graves) - presence of TSH receptor stimulating antibodies
Nodular hyperthyroidism - autonomous secretion of T3/T4
Thyroiditis - inflammation of the thyroid gland causing release of thyroxine

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15
Q

Features of Graves disease

A

Hyperthyroidism
Commonly affects young women
Follows a relapsing-remitting course

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16
Q

Features of nodular hyperthyroidism

A

Typically presents at an older age

Either solitary toxic nodule or numerous nodules situated within a toxic multi-nodular goitre

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17
Q

Features of thyroiditis

A 
Follows
- viral infection
- medication - amiodarone
- childbirth
Often followed by hypothyroid phase
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18
Q

Symptoms of hyperthyroidism

A

Increased sympathetic action

  • weight loss with increased appetite
  • insomnia
  • irritability
  • anxiety
  • heat intolerance
  • palpitations
  • tremor
  • pruritus
  • increased bowel frequency and loose motions
  • menstrual disturbance and reduced fertility
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19
Q

How may hyperthyroidism present in elderly patients?

A

Reduced energy levels - apathetic thyroidtoxicosis

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20
Q

Signs of hyperthyroidism

A

Resting tachycardia - sinus rhythm or atrial fibrillation
Warm peripheries
Resting tremor
Hyperflexia
Lid lag - increased sympathetic tone of upper eyelid`

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21
Q

Clinical features of Graves disease

A

Lid retraction
Exopthalmus
Thydroid eye disease
Skin changes - pre-tibial myxoedema and thyroid acropachy

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22
Q

Investigations for hyperthyroidism

A

Elevated free T4 and T3 with undectebtable TSH
Thyroid peroxidase antibodies are unspecific markers
TSH-receptor stimulating antibodies more specific

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23
Q

Imaging for hyperthyroidism

A

Nuclear imaging - determine functionality and cause
- Graves disease - uniform uptake
- Nodular disease - increased uptake in autonomous nodules
- Thyroiditis - absent uptake
USS - nodular thyroid disease but not activity

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24
Q

Treatment for hyperthyroidism

A 
Medication
- thionamides reduce synthesis of T3+4 - carbimazole and propylthiouracil
- beta-blockers to control symptoms
Surgery
- thyroidectomy
Radioactive iodine
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25
Potential side-effects of thionamides
Agranulocyotisis - bone marrow suppression - unexplained sore-throat or fever - urgent full-blood count to exclude pancytopaenia Generalised rash - disappears after cessation
26
What does radioactive iodine therapy involve?
Single dose of 131I
27
Cons of radioactive iodine
Pregnancy May flare up eye disease in patients with pre-exisitng ophthalmopathy Causes hypothyroidism - requires lifelong thyroxine replacement Patients emit small amount of radiation after administration - avoid close contact to young children and pregnant women
28
Complications of thyroid surgery
Bleeding Infection Damage to recurrent laryngeal nerve Temporary or permanent hypocalcaemia
29
Features of thyroid surgery
Effective definitive treatment for those who can't comply with radiation restriction - mothers with young children Thyroid function should be controlled pre-op to avoid anaesthetic problems Beta-blockers used during anaesthetic if thyroid function not optimal - prevent peri-operative atrial fibrillation
30
Causes of primary hypothyroidism
``` Autoimmune disease - Hashimotos thyroiditis Pregnancy Iodine deficiency -> cretinism Drugs - amiodarone - lithium Iatrogenic - intentional treatment of hyperthyroidism - inadvertent damage from radiation to head/neck ```
31
Causes of secondary hypothyroidism
TSH deficiency - due to hypothalamic-pituitary disease Characterised by low free T4 with non-elevated TSH
32
Clinical features of hypothyroidism
``` Weight gain Cold intolerance Fatigue Constipation Bradycardia Myxoedema - thickening of skin and puffiness around eyes ```
33
Investigations for hypothyroidism
Low fT4 with elevated TSH Thyroid antibodies - auto-immune hypothyroidism Thyroid peroxidase - Hashimotos thyroiditis
34
Treatment for hypothryoidism
Thyroxine replacement - dose sufficient to improve symptoms and normalise thyroid function - 50-100ug/day - elderly pts and those with IHD started on 25ug/day
35
Issues with thyroxine replacement therapy
Persistently elevated TSH - under-replacement - poor compliance - malabsorption - coeliac disease, concurrent medication (iron, calcium or PPIs) Suppressed or undetectable TSH - over-replacement - increased risk of atrial fibrillation and osteoporosis
36
Define subclinical hypothyroidism
Normal fT4 with elevated TSH | If pts asymptomatic treatment may not be needed
37
Features of cortisol
Glucocorticoid Synthesis regulated by ACTH Highest at 08:00 and lowest at midnight Most bound to cortisol binding globulin (CBG) and albumin
38
Cortisol feedback loop
Cortisol exerts negative feedback on: - hypothalamus - reduce CRH and vasopressin - anterior pituitary - reduce ACTH
39
Features of adrenal androgens
Mainly controlled by ACTH DHEA, DHEA-S and androstenedione are converted to more potent testosterone and dihydrotestosterone in peripheral tissues Exert effects on sebaceous glands, hair follicles, prostate gland and external genitalia
40
Features of mineralcorticoids
Aldosterone | Regulated by renin-angiotensin system
41
Features of RAAS system
Renin activated in response to low circulating blood volume, hyponatreamia or hyperkalaemia Catalyses conversion of angiotensin to angiotensin I Converted to angiotensin II by ACE Stimulates aldosterone release upon binding to angiotensin receptor Aldosterone acts on renal distal convoluted tubule on its receptor to cause sodium retention and potassium loss
42
Layers of the adrenal cortex
Zona glomerulosa - mineralcorticoids - aldosterone Zona fasciculata - glucocorticoids - cortisol Zona reticularis - androgens - DHEA
43
Features of the adrenal medulla
``` Sympathetic nervous system tissue Secretes - adrenaline - noradrenaline - dopamine ```
44
What is Addisons disease
Primary adrenal insufficiency Destruction of adrenal gland or genetic defects in steriod synthesis Effects all 3 zones
45
Symptoms of Addisons disease
Non-specific and gradual onset Fatigue Weakness Anorexia Weight-loss Nausea Abdo pain Dizziness and postural hypotension - mineralocorticoid deficiency Hypoglycaemia, increased pigmentation - glucocorticoid loss Reduced libido and loss of axillary and pubic hair - androgen deficiency
46
Investigations for Addisons disease
``` Biochemical hallmarks - hyponatraemia - hyperkalaemia - raised urea - hypoglycaemia - mild anaemia Confirmatory tests - low 9am cortisol - raised ACTH concentration ```
47
Management of Addisons diseasee
Lifelong glucocorticoid and mineralcorticoid replacement therapy - hydrocortionse 1st line - double at times of illness - fludrocortisone Provide steriod emergency card, encourage to wear medical alert jewellery and emergency contacts for endocrine team
48
Causes of secondary adrenal insufficiency
ACTH deficiency | - long term steriod use - sudden cessation -> adrenal crisis
49
Define a phaeochromocytoma
Catecholamine-secreting tumour which arises from the adrenal medulla
50
Define a paraganglioma
Catecholamine-secreting tumour which arises from the extra-adrenal chromaffin tissue
51
Clinical features of phaeochromocytoma
``` Headache Sweating Pallor Palpitations Anxiety/panic attacks Hypertension ```
52
Complications of untreated phaeochromocytoma
``` Hypertensive crisis Encephalopathy Hyperglycaemia Pulmonary oedema Cardiac arrhythmias Death ```
53
Investigations for phaeochromocytoma
``` Elevated catecholamines - 24hr urinary catecholamines - plasma metanephrines Radiological localisation of the tumour - CT or MIR abdo - 123I-MIBG - PET ```
54
Management of phaeochromocytoma
Surgical excision - laparo or open Alpha+/-beta blockers at diagnosis - phenoxybenzamine or doxazosin
55
Growth pituitary axis
``` GH is secreted in pulsatile manner - peak during REM sleep Acts on liver to produce IGF-1 Role in MSK growth in children Positive control - GHRH Negative control - somatostatin ```
56
Adrenal pituitary axis
ACTH has circadian rhythm - peak in early morning and lowest at midnight ACTH stimulates cortisol release Positive control - CRH Negative control - cortisol
57
Gonadal pituitary axis
FSH leads to ovarian follicle development in women and sperm production in men LH - women - mid-cycle ovulation during LH surge and formation of corpus lutem - men - testosterone secretion from the Leydig cells of testes Positive control - GnRH Negative control - testosterone, cortisol
58
Thyroid pituitary axis
TSH drives thyroxine release via stimulation of TSH receptors in the thyroid gland Positive control - TRH Negative control - thyroxine
59
Prolactin pituitary axis
Prolactin causes lactation Direct inhibitory effect on LH and FSH Negative control - dopamine
60
Clinical assessment of pituitary gland
``` Functional pituitary tumours = clinical syndromes - acromegaly - GH - Cushings disease - ACTH - prolactinoma - PRL - TSHoma - TSH Non-functioning - hypopituitarism - compression of local structures - bitemporal hemianopia ```
61
Biochemical assessment of pituitary gland
Prolactin and TSH do not fluctate at time of day LH and FSH - women - within 1st 5 days of menstrual cycle - men - 0900 in fasting state Basal cortisol checked at 0900 IGF-1 maker of GH - low levels suggest GH deficiency, high levels suggest GH excess
62
Dynamic tests of pituitary gland
Synacthen test - assess primary adrenal failure and pituitary ACTH reserve - atrophy of adrenal cortex -> inadequate response to synacthen - not acute Insulin Tolerance Test - ACTH and GH reserve - frank hypoglycaemia achieved with symptoms - ACTH and GH will rise - not performed in pts with IHD or epilepsy due to risk of triggering coronary ischaemia and seizures
63
Pituitary gland imaging
``` MRI - injection of contrast - > 1cm = macro-adenomas - < 1cm = micro-adenomas CT if unable to have MRI PET to determine functionality ```
64
Differenentials for high prolactin levels
``` Pregnancy Medication - dopamine antagonists - anti-emetics, anti-psychotics Profound hypothyroidism PCOS ```
65
Features of a micro-prolactinoma
``` More frequently in women than men < 1cm Present with - menstrual disturbance - hypogaonadism in men - galactorrhoea - infertility ```
66
Distinguishing features of PCOS compared to prolactioma
``` Androgenic symptoms - hitsutism - acne Less elevated prolactin levels - <1000 miU/L Absence of pituitary lesion on MRI ```
67
Features of macro-prolactinomas
> 1cm More common in men Prolactin > 5000 miU/L
68
Treatment for prolactinomas
Dopamine agonists (D2) - cabergoline - 1/2 weekly - better tolerance - bromocriptine - daily
69
Side effects of D2 agonists
Nausea Postural hypotension Psychiatric disturbance
70
Complications of treatment of macro-prolactinomas
CSF leak due to rapid reduction of size of lesion - risk of meningitits Cardiac valve abnormalites in Parkinson's disease
71
Causes of high prolactin
``` Pituitary - prolactinoma - non-functioning adenoma - infiltrative disease Hypothalmic - tumours - infiltrative disease Secondary - renal failure - primary hypothyroidism - adrenal insufficiency - PCOS Analytical - macroprolactin - heterophilic antibodies Medication - antipsychotics - antiemetics - antihypertensives - oestrogen Physiological - pregnancy - breast stimulation - stress ```
72
Causes of acromegaly
GH-secreting pituitary tumour
73
Complications of untreated acromegaly
Disfiguring features Premature death from CVS disease Increased risk of bowel cancer
74
Clinical features of acromegaly
Increased size of hands and feet Facial features become coarser - frontal bossing of forehead, protrusion of chin and widely spread teeth Soft tissue swelling - enlargement of tongue and soft palate, sleep apnoea, puffiness of hands, carpal tunnel syndrome Sweating Headaches Hypertension Diabetes mellitus
75
Investigations for acromegaly
Oral glucose tolerance test and IGT-1 - failure to suppress GH after OGTT and elevated IGF-1 levels Pituitary MRI shows tumour
76
Management of GH-secreting pituitary tumours
``` Medical - somatostatin analogues improve symptoms and control GH and IGF-1 - GH receptor blockers control IGF-1 - dopamine agonists may control GH Radiotherapy - external beam - stereotactic - more targeted treatment at higher dose Surgery - treatment of choice ```
77
Monitoring of acromegaly
OGTT post-surgery to indicate if persistent disease Long term follow up to monitor GH and IGF-1 levels and exclude recurrence Periodic screening colonoscopy
78
Define non-functioning pituitary adenomas (NFPAs)
Biochemically inactive tumours
79
Clinical features of NFPAs
Visual field loss Headache Hypopituitarism
80
Indications for surgical treatment of NFPAs
Visual field defect of threat to vision | Trans-sphenoidal or trans-cranial
81
Causes of acquired hypopituitarism
Pituitary tumour Inflammatory and infiltrative disorders Traumatic brain injury Radiotherapy
82
Clinical features of hypopituitarism
``` Lethary Weight gain Sexual dysfunction Short stature in children Acute hypo-adrenal crisis - hyponatraemia - hypotension ```
83
Investigation for hypopituitarism
Exclusion of adrenal insufficiency Secondary hypothyroidism - low T4 and non-elevated TSH Secondary hypogonadism - low sex hormones with non-elevated LH and FSH GH deficiency - low IGF-1 levels MRI - empty fossa or pituitary tumour
84
Treatment for hypopituitarism
ACTH deficiency - hydrocortisone replacement TSH deficiency - thyroxine replacement Gonadotropin deficiency - men - testosterone - women - oestrogen and progesterone GH deficiency - GH as daily subcut injection
85
Features of Cushings Disease
``` Central obesity Dorso-cervical fat pad Increased roundness of face Red face - plethora Thick skin Easy bruising Proximal myopathy ```
86
Complications of Cushings Disease
Hypertension Premature osteoporosis Diabetes mellitus
87
Investigations for Cushing’s Disease
Screening - alcoholism and severe depression may cause a cushingoid look - 24hr urine free cortisol - elevated - low dose dexamethasone suppression test - failure to suppress - overnight dexamethasone suppression test - failure to suppress
88
Differentials for Cushing’s disease
``` Pituitary - pituitary MRI Adrenal - accelerated hirsutism - low ACTH Ectopic ACTH due to lung cancer or another malignancy - hypokalaemia - smoker - weight loss - whole body CT or PET scan ```
89
Management of Cushing’s disease
Adrenal tumour -> Laparoscopic adrenalectomy Ectopic ACTH -> Treatment of underlying malignancy Pituitary adenoma -> Trans-sphenoidal removal of the pituitary adenoma Medical treatment - Metyrapone - Ketoconazole - Radiotherapy
90
Symptoms of hyponatraemia
``` Early - headache - nausea - vomiting - general malaise Late - confusion - agitation - drowsiness Acute Severe - seizures - respiratory depression - coma - death ```
91
Investigations for hyponatraemia
``` Full history and examination Drug history - thiazide diuretics Hydration status Biochemical investigations - serum osmolality - urine osmolality - urine sodium - thyroid function - assessment of cortisol reserve - 09:00 cortisol or synacthen test ```
92
Treatment of hyponatraemia
Acute severe - hypertonic saline - prevent cerebral oedema Cause-specific treatment Appropriate fluid replacement - normal saline
93
Characteristics of SIADH
Low plasma Na+ Low serum osmolality High urine osmolality High urine Na+
94
Causes of SIADH
``` Malignancy - lung small cell - pancreas - prostate - thymus - lymphoma CNS disorders - meningoencephalitis - abscess - stroke - subarachnoid/subdural haemorrhage - head injury/neurosurgery - vasculitis Chest diease - TB - pneumonia Drugs - opiates - psychotropics - SSRI - cytotoxics ```
95
Treatment of SIADH
Treat cause Restrict fluid Consider salt + loop diuretics if severe Vasopressin receptor antagonists
96
Causes of hyponatremia
``` Urine osmolality < 100 mOsm/kg - primary polydipsia - inappropriate IV fluids - low solute intake Urine osmolatlity > 100 mOsm/kg - urine Na+ < 30 mmol/L - low effective arterial volume - heart failure - portal hypertension - nephrotic syndrome - hypoalbuminaemia - GI loss - urine Na+ > 30 mmol/L - normal apparent circulating volume - SIADH - NSAIDs - low effective arterial volume - primary salt wasting - vomiting - hypoadrenalism ```
97
Define Diabetes Insipidus
Cranial - vasopressin deficiency Nephrogenic - vasopressin resistance Leads to passing of large volumes of dilute urine with profound unquenchable thirst
98
Biochemical hallmarks of DI
High serum osmolality Low urine osmolality High urine volume
99
Complications of DI
Hypernatraemia Dehydration Death
100
Cranial vs nephrogenic DI
Cranial usually seen in pituitary disease Strong family history suggests genetic cause Nephrogenic - metabolic and electrolyte disturbance - renal disease - drugs affecting the kidney
101
Common causes of hypercalcaemia
Primary hyperparathyroidism - non-suppressed PTH Malignancy - suppresed PTH levels TB and sarcoidosis - suppressed PTH
102
Definition of hypercalcaemia
Serum calcium > 2.6 mmol/L
103
Malignant causes of hypercalcaemia
Squamous cell epithelial tumours - secretion of PTH-related peptide (PTH-rP)
104
Primary hyperparathyroidism causes
Single parathyroid adenoma | Parathyroid hyperplasia - genetic cause
105
Investigations of hypercalcaemia
``` High PTH - primary hyperparathyroidism Low PTH - malignancy Low phosphate - PTH causes excretion High ALP - increased bone turnover Bone density reduced - distal radius Nephrocalcinosis - renal USS ```
106
Clinical features of hypercalcaemia
``` Non-specific symptoms - tiredness - generalised aches and pains - abdo pain - constipation - kidney stones Primary hyperparathyroidism - asymptomatic Nephrogenic DI - polyuria and polydipisa ```
107
Define familial hypocalciuric hypercalcaemia (FHH)
Genetic defect in calcium sensing receptor Low urine calcium/creatinine ratio Family history of mild hypercalcaemia
108
Localisation of parathyroid adenoma
USS - 70-90% | SETAMIBI isotope scanning used alongside USS
109
Treatment of hyperparathyroidism
``` Surgery - serum calcium > 2.85 mmol/L or symptoms debilitating - young patients - parathyroidectomy Medical management - calcimimetic drugs Simple observation ```
110
Acute severe hypercalcaemia
Medical emergency Presentation - profound dehydration - renal impairment
111
Define hypocalcaemia
Serum calcium < 1.9 mmol/L
112
Causes of hypocalcaemia
``` Post-surgical hypoparathyroidism Post-thyroidectomy - usually temporary - may be permanent due to damage or removal of parathyroid glands Severe vitamin D deficiency ```
113
Vitamin D deficiency presentation
Low phosphate - elevated PTH levels | Seizures and tetany in neonates - due to hypocalcaemia
114
Features of hypomagnesaemia
Causes functional hypoparathyroidism - normal or low PTH
115
Causes of hypomagnesaemia
GI loss Alcohol Drugs - PPIs
116
Clinical features of acute severe hypocalcaemia
Laryngospasm Prolonged QT interval Seizures
117
Clinical features of hypocalcaemia
Muscle cramps Carpo-pedal spasm Peri-oral and peripheral paraesthesia Neuro-psychiatric symptoms Positive Chvosteks sign - facial spasm when cheek gently tapped Trousseasus sign - carpo-pedal spasm induced after inflation of sphygmomanometer
118
Treatment of hypocalcaemia
Calcium replacement - acute - 10ml 10% calcium gluconate IV over 30 mins - mild - 5mmol/6h PO calcium Reverse cause
119
Treatment of vitamin D deficiency
Loading dose cholecalciferol 20,000 IU per week for 7 weeks Maintenance dose of 1-2000 IU per week
120
Treatment of hypoparathyroidism
1-alfacalcidol 0.25mcg/day or calcitriol - dose titration according to clinical and biochemial response Oral calcium supplements - Sandocal and Adcal D3 Aim to keep calcium levels at lower end of normal - reduce risk of nephro-calcinosis
121
Treatment of magnesium deficicency
``` Acute - precipitating drugs stopped - IV MgSo4 24mmol/24hrs Chronic - GI loss or alcohol ingestion - specialist input ```
122
Define psuedo-hypoparathyroidism
Mutation in G protein coupled to PTH receptor | Leads to PTH resistance
123
Characteristics of pseudo-hypoparathyroidism
Characterised by - hypocalcaemia - high phosphate - high PTH - normal vitamin D
124
Clinical features of pseudo-hypoparathyroidism
Short stature Round face Short 4th and 5th metacarpals

Yr3 - General Medicine (9 decks)

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