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Phase 3b > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define hypothyroidism

A

Inadequate production of thyroid hormones by the thyroid gland

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2
Q

What is the most common cause of hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis

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3
Q

What is Hashimoto’s thyroiditis?

A

Cased by autoimmune inflammation of the thyroid gland.
Associated with anti-TPO and anti thyroglobulin antibodies
Initially it causes a goitre after which there is atrophy of the thyroid gland

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4
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

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5
Q

What are the causes of hypothyroidism?

A 
Hashimoto's thyroiditis
Iodine deficiency
Primary atrophic hypothyroidism
Post-thyroidectomy (thyroid surgery)
Subacute thyroiditis
Drug induced -> Antithyroid drugs (carbimazole), amiodarone, radio-iodine, lithium
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6
Q

What is secondary hypothyroidism?

A

When the pituitary gland fails to produce enough TSH.

Known as hypopituitism

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7
Q

Symptoms of hypothyroidism

A 
Tired
Sleepy/lethargic
Intolerant to cold
Weight gain/decreased appetite
Constipation
Menorrhagia
Reduced memory/cognition/concentration
Hoarse voice
Depression
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8
Q

Signs of hypothyroidism

A

BRADYCARDIC

Bradycardia
Reflexes relax slowly
Ataxia (cerebellar)
Dry thin skin/hair
Yawning/drowsy/coma
Cold hands
Ascites
Round puffy face/double chin/obese (myxoedema)
Defeated demeanour
Immobile +/- ileus
CHF
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9
Q

Associations of hypothyroidism

A 
Type 1 diabetes mellitus
Addison's disease
Pernicious anaemia
CF
Turner's and Down syndrome
Primary biliary cirrhosis
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10
Q

Investigations for hypothyroidism

A

Thyroid function tests (TFT’s):
Primary hypothyroidism = High TSH, Low T3/T4
Secondary hypothyroidism = Low TSH, Low T3/T4
Thyroid antibodies = anti-TPO and anti-Tg

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11
Q

Treatment for hypothyroidism

A

Oral levothyroxine (T4)

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12
Q

What is sick euthyroid?

A

Low TSH, T3 and T4 in any systemic illness

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13
Q

What is hyperthyroidism?

A

Over production of the thyroid hormones by the thyroid gland

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14
Q

What is thyrotoxicosis?

A

Abnormal and excessive quantity of thyroid hormone in the body

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15
Q

What is primary hyperthyroidism?

A

Due to thyroid pathology

The thyroid itself is behaving abnormally and producing excessive thyroid hormone

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16
Q

What is secondary hyperthyroidism?

A

Overstimulation of TSH.

Pathology is in the hypothalamus or pituitary

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17
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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18
Q

What are the causes of hyperthyroidism?

A

Grave’s disease
Toxic multinodular goitre
Toxic adenoma
De Quercain’s thyroiditis
Drugs (amiodarone and lithium - more common for hypothyroidism)
Ectopic thyroid tissue
Exogenous - iodine excess, levothyroxine excess

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19
Q

How does Grave’s disease present

A

Most common, in 75% of cases
Autoimmune condition
Abnormal TSH receptor anti bodies
Signs: Exopthalmos - protruding eyes bilaterally, Pretibial myxoedema, Grave’s eye disease - diplopia, photophobia, grittiness. Diffuse goitre (without nodules)

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20
Q

Describe toxic multinodular goitre

A

Nodules develop on thyroid gland and continuously produce excessive thyroid hormone
Seen in elderly and iodine excess
2nd most common cause
Goitre with firm nodules

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21
Q

Describe toxic adenoma

A

Single abnormal thyroid nodule releasing thyroid hormone (T3 & T4)
Treated with surgical removal of nodule

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22
Q

Describe De Quervain’s thyroiditis

A

Viral infection
Fever, neck pain, tenderness, dysphagia
Hyperthyroid phase then hypothyroid (due to negative feedback)
Raised ESR
Self-limiting - treat with NSAIDs (aspirin) and beta blockers

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23
Q

Risk factors for hyperthyroidism

A

High iodine intake

Smoking

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24
Q

Symptoms of hyperthyroidism

A 
Diarrhoea
Weight loss/increased appetite
Sweating
Heat intolerance
Tremor
Irritable
Oligomenorrhoea
Anxiety
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25
Q

Signs of hyperthyroidism

A 
Fine tremor
Tachycardia
Thin hair
Lid lag + lid retraction
Goitre
Palmar erythema
Pretibial myxoedema
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26
Q

Investigations in hyperthyroidism

A

TFT’s: TSH Low, T3/T4 High
Anti-TSHR and anti-thyroglobulin elevated in Grave’s
ESR raised
Visual acuity

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27
Q

Treatment for hyperthyroidism

A 
Carbimazole - 1st line
Propylthiouracil - 2nd line
Beta blockers - propanolol 
Radioactive iodine
Thyroidectomy
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28
Q

What is a thyrotoxic crisis

A

Severe hyperthyroidism

Occurs in Grave’s or toxic multinodular goitre

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29
Q

Signs of a thyrotoxic crisis

A 
Pyrexia
Tachycardia
Confusion
Delirium
AF
Diarrhoea
Vomiting
Abdominal pain
Heart failure
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30
Q

Precipitants to a thyrotoxic crisis

A

Infection
Recent thyroid surgery
Radioiodine

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31
Q

Treatment for a thyrotoxic crisis

A

Oxygen + fluid
Beta blockers - propanolol
Digoxin - slow the heart
Antithyroid drugs - carbimazole, Lugol’s solution - aqueous iodine

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32
Q

Define myxoedema coma

A

The ultimate hypothyroid state before death

May have had radioiodine, thyroidectomy or pituitary surgery

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33
Q

Symptoms and signs of a myxoedema coma

A

Symptoms: Hypothermia, hyporeflexia, bradycardia, coma, seizures
Signs: Goitre, cyanosis, low BP, heart failure

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34
Q

Treatment for a myxoedema coma

A 
ICU
Give T3 slowly
High flow oxygen if cyanosed
Hydrocortisone if pituitary hypothyroidism suspected
Antiobiotics (cefuroxime) if infection
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35
Q

Differential diagnosis of diffuse goitre

A

Grave’s

Hashimoto’s

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36
Q

Differential diagnosis of nodular goitre

A

Multinodular goitre
Adenoma
Carcinoma

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37
Q

Differential diagnosis of painful goitre

A

De Quervain’s

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38
Q

Define hypercalcaemia

A

High levels of calcium in the blood

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39
Q

Causes of hypercalcaemia

A 
Primary hyperparathyroidism (if high PTH)
Malignancy (if low PTH)(from bone metastases, myeloma, PTHrP -> from squamous cell lung cancer)
TB
Sarcoidosis
Vitamin D intoxication
Thyrotoxicosis
Mikk-alkali syndrome
Familial hypocalciuric hypercalcaemia
Lithium
Thiazides
Acromegaly
Dehydration
Zolinger-Ellison syndrome
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40
Q

Symptoms of hypercalcaemia

A

Groans, stones, moans

Abdominal pain
Vomiting
Constipation
Anorexia
Polyuria
Polydipsia
Dehydration
Renal stones
Depression
Dementia
Confusion
Muscle weakness
Fatigue
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41
Q

What are the ranges for normal, mild, moderate and severe hypercalcaemia?

A 
Normal = 2.25 - 2.5 mmol/L
Mild = < 2.8 mmol/L - Polyuria, polydipsia, depression, mild cognition
Moderate = < 3.5 mmol/L - Muscle weakness, fatigue, constipation, anorexia
Severe = > 3.5 mmol/L - Abdominal pain, vomiting, dehydration, short QT, coma
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42
Q

Investigations for hypercalcaemia

A

Hyperparathyroidism = High PTH

Malignancy = Low albumin, low chloride, alkalosis, high phosphate, high alkaline phosphate

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43
Q

Treatment for hyerpcalcaemia

A

Correct dehydration - IV 0.9% Saline
Bisphosphonates - Pamidronate or zoledronic acid
Calcitonin - acts similar to bisphosphonates
Steroids (e.g. prednisolone) in sarcoidosis

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44
Q

Causes of hypocalcaemia

A 
High PTH: Chronic kidney disease
Vitamin D deficiency
Hypoparathyroidism (post thyroid surgery)
Pseudohypoparathyroidism
Rhabdomyolysis
Hypomagnesaemia

Low PTH: Acute pancreatitis
Over hydration
Osteomalacia
Respiratory alkalosis

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45
Q

Symptoms of hypocalcaemia

A

SPASMODIC

Spasms (carpopedal spasm) = Trousseau's sign
Perioral paraesthesia
Anxious, irritable, irrational
Seizures
Muscle tone increased in smooth muscle
Orientation impaired and confusion
Dermatitis (e.g. atopic)
Impetigo herpetiformis
Cataracts
Cardiomyopathy (long QT on ECG)
Choreoathetosis
Chvostek's sign - tapping facial nerve causes face spasms
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46
Q

Investigations for hypocalcaemia

A

Calcium

PTH

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47
Q

Treatment for hypocalcaemia

A

Mild = oral calcium
Alfacalcidol (in CKD or still mild after calcium)

Acute onset = IV calcium gluconate when severe/medical emergency

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48
Q

Define hyperkalaemia

A

High serum potassium

It is an emergency and can lead to ventricular fibrillation and cardiac arrest

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49
Q

Causes of hyperkalaemia

A 
Acute kidney injury
Chronic kidney disease
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
Medications: ACE inhibitors, NSAIDs, ARB's, Spirolactone, cyclosporin, heparin
Burns/excretion
Haemolysis
Type 4 renal tubular acidosis
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50
Q

What are the ranges for mild, moderate and severe hyperkalaemia?

A 
Mild = 5.5 - 5.9 mmol/L
Moderate = 6.0 - 6.4 mmol/L
Severe = > 6.5 mmol/L
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51
Q

Symptoms of hyperkalaemia

A

Palpitations
Chest pain
Weakness
Fast irregular pulse

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52
Q

Investigations for hyperkalaemia

A

ECG= Tall tented T waves,
Loss of P waves
Wide QRS complex
Ventricular fibrillation

U&E’s

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53
Q

What are the ECG findings in hyperkalaemia?

A

Tall tented T waves (occurs first)
Loss of P waves
Wide QRS complex
Ventricular fibrillation

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54
Q

Management of hyperkalaemia

A

Insulin and dextrose
Calcium gluconate
Oral calcium resonium - removes K via stools

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55
Q

Causes of hypokalaemia

A 
Diuretics
Vomiting + diarrhoea
Pyloric stenosis
Conn's syndrome
Cushing's syndrome
Renal tubular acidosis
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56
Q

Give the ranges for mild, moderate and severe hypokalaemia

A 
Mild = 3.1 - 3.5 mmol/L
Moderate = 2.5 - 3.0 mmol/L
Severe = < 2.5 mmol/L
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57
Q

Symptoms of hypokalaemia

A 
Mild = asymptomatic
Moderate = Muscle weakness, muscle pain, constipation
Severe = Hypotonia, paralysis and weakness, ileus
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58
Q

Investigations for hypokalaemia

A

ECG: Long PR interval, ST depression, small or inverted T waves, prominent U waves, Long QT
U&E’s
Serum magnesium

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59
Q

ECG findings in hypokalaemia

A 
Long PR interval
ST depression
Small or inverted T waves
Prominent U waves
Long QT
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60
Q

Management for hypokalaemia

A 
Mild = Potassium supplementation - Sando-K
Severe = IV potassium
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61
Q

Define hypernatraemia

A

Usually due to water loss in excess of sodium loss

Water deficit

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62
Q

Causes of hypernatraemia

A 
Diarrhoea
Burns
Vomiting
Diabetes insipidus
Incorrect IV fluid replacement
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63
Q

Symptoms of hypernatraemia

A 
Nausea and vomiting
Confusion
Polydipsia
Polyuria
Dehydration
Convulsions
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64
Q

Investigations for hypernatraemia

A

High sodium
High urea
High albumin

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65
Q

Management for hypernatraemia

A

Water orally

IV glucose

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66
Q

Define hyponatraemia

A

May be caused by water excess or sodium depletion

High water in blood -> water moves into brain and causes cerebral oedema

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67
Q

Causes of hyponatraemia

A

Urinary sodium >20mmol/L: Hypovolaemic - Diuretics, renal failure, Addison’s disease
Euvolaemic - SIADH, Hypothyroidism, Desmopressin, ACE-i, oxytocin, Antidepressants, omeprazole

<20mmol/L: Hypovolaemic - Vomiting, diarrhoea, burns
Hypervolaemic - Heart failure, liver failure/cirrhosis, nephrotic syndrome/renal failure

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68
Q

Symptoms of hyponatraemia

A 
Mild: Anorexia
Nausea and vomiting
Malaise
Headache
Irritability
Weakness/muscle cramps

Severe: Confusion
Seizures/coma
Reduced GCS

Increased risk of falls in the elderly

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69
Q

What are the ranges for mild, moderate and severe hyponatraemia

A 
Mild = 130 - 134 mmol/L
Moderate = 120 - 129 mmol/L
Severe = < 120 mmol/L
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70
Q

Define acute hyponatraemia

A

Develops within 48 hours

Usually from excessive fluid intake

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71
Q

Define chronic hyponatraemia

A

Occurs after 48 hours

Symptoms are usually less severe than acute

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72
Q

Management of hyponatraemia

A

Mild = Fluid restriction, Diuretics

Moderate = Hypertonic 3% saline in first 3-4 hours

Severe = Bolus of hypertonic saline, Vasopresser receptor antagonists e.g. Conivaptan

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73
Q

What is a complication of hyponatraemia?

A

Central pontine myelinosis/Osmotic demyelination syndrome/locked-in syndrome

74
Q

Define Central pontine myelinosis

A

Overcorrection of severe hyponatraemia (>8mmol/L per day)
Occurs after 48-72 hours
Symptoms: Dysarthria - mutism, dysphagia, paraparesis, seizures, confusion, neurological deficit

75
Q

Define Cushing’s syndrome

A

Refers to the signs and symptoms that develop after prolonged abnormal elevation of cortisol -> prolonged exposure to glucocorticoids

76
Q

What is the different between Cushing’s syndrome and Cushing’s disease?

A

Cushing’s disease is where a pituitary adenoma (tumour) secretes excessive ATCH -> can cause Cushing’s syndrome

77
Q

Causes of Cushing’s syndrome

A

ACTH dependent (Increased ACTH):
Cushing’s disease - 80% - pituitary adenoma
Ectopic ACTH production (due to small cell lung cancer) - 20%

ACTH independent (Low ACTH due to negative feedback):
Adrenal adenoma
Adrenal nodular hyperplasia
Exogenous steroids

78
Q

Symptoms of Cushing’s syndrome

A 
Central obesity
Round moon face
Buffalo neck
Proximal limb wasting
Hypertension
Abdominal striae
Type 2 diabetes mellitus
Depression
Lethargy
Psychosis
Insomnia
Bruises
Osteoporosis - curved spine
Infection prone
Amenorrhoea/ED
79
Q

Investigations for Cushing’s syndrome

A

Overnight dexamethasone suppression test - 1st line:

1mg dexamethasone overnight, do serum cortisol at 8am. Dexamethasone acts by suppressing the release of cortisol by negative feedback on the hypothalamus and pituitary. This causes ACTH output to be reduced. No suppression in Cushing’s syndrome

48 hour dexamethasone suppression test - 2nd line:

Performed after abnormal first test. Measure cortisol at 0 and 48 hours.
In Cushing’s disease both cortisol and ACTH are suppressed.
In adrenal adenoma, ACTH is suppressed, cortisol isn’t/
In ectopic ACTH, both ACTH and cortisol are not suppressed

24 hour urinary free cortisol
FBC - raised WCC
Chest CT - small cell lung cancer
Abdominal CT - adrenal tumour
MRI brain - pituitary adenoma
80
Q

Treatment for Cushing’s syndrome

A

Cushing’s disease = trans-sphenoidal removal of pituitary adenoma
Adrenal adenoma = removal of adrenal tumour
Ectopic ACTH = removal of tumour

81
Q

Define Addison’s disease

A

Destruction of adrenal cortex and subsequent reduction in output of adrenal hormones: glucocorticoids (cortisol) and mineralocorticoids (aldosterone)

82
Q

What is primary adrenal insufficiency? (Addison’s disease)

A

Inability of adrenal glands to produce steroid

High ACTH as no negative feedback

83
Q

Causes of primary adrenal insufficiency

A

Autoimmune
TB
Congenital adrenal hyperplasia
Adrenal metastases

84
Q

Define secondary adrenal insufficiency

A

Inadequate ACTH stimulating adrenal glands resulting in low cortisol release

85
Q

Causes of secondary adrenal insufficiency

A 
Exogenous steroids (long term steroids) -> these should be tapered off slowly
Damage to pituitary gland - surgery to remove tumour/infection
86
Q

Define tertiary adrenal insufficiency

A

Inadequate CRH release by hypothalamus

87
Q

Symptoms of Addison’s disease

A 
Muscle cramps
Fatigue and weakness
Anorexia
Nausea and vomiting
Abdominal pain
Weight loss
Faints
Depression
88
Q

Signs of Addison’s disease

A

Postural hypotension
Pigmented palmar creases (and abdomen) and buccal mucosa (ACTH stimulates melanocytes to produce melanin)
Dry mucous membranes

89
Q

Investigations for Addison’s disease

A

Low sodium (hyponatraemia) - due to lower mineralocorticoid
High potassium (hyperkalaemia) - due to lower mineralocorticoid
Low cortisol
Low glucose

Short ACTH stimulation test (Synacthen):
Take cortisol level. Give 250 mg Synacthen IM, after 30 mins retake cortisol. If cortisol rises >550mmol/L -> exclude Addison’s.

ACTH high in primary
ACTH low in secondary

21-hydroxylase adrenal autoantibodies in >80%
CT/MRI adrenals - tumour
Renin and aldosterone
High urea

90
Q

Treatment for Addison’s

A

Replace steroids - Hydrocortisone (replaces cortisol)
Fludrocortisone (mineralocorticoid) - replaces aldosterone
Give steroid card
Double steroids in acute/febrile illness

91
Q

What is an Addisonian crisis

A

Acute presentation of severe Addison’s. Absence of steroid hormones (glucocorticoids and mineralocorticoids) leads to life threatening presentation.
Biggest risk factor is withdrawal of long-term steroids

Other triggers: Infection, trauma, surgery

92
Q

Symptoms of Addisonian crisis

A 
Reduced consciousness
Hypotension
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Shock
93
Q

Management of an Addisonian crisis

A

IV hydrocortisone
IV fluid bolus - rehydration
Glucose IV if hypoglycaemic

94
Q

Define Conn’s syndrome

A

Primary hyperaldosteronism
Excess production of aldosterone (mineralcorticoid) from adrenal glands.
Aldosterone acts on kidney to increase sodium reabsorption and increase potassium secretion.

95
Q

Causes of Conn’s syndrome

A

Adrenal adenoma (secreting aldosterone) - most common 80%
Bilateral adrenal hyperplasia 20%
Adrenal carcinoma
Familial hyperaldosteronism

96
Q

What is secondary hyperaldosteronism

A

Where excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high.

Occurs in: Renal artery stenosis, heart failure, renal artery obstruction, Bartter’s syndrome

97
Q

Symptoms of Conn’s syndrome

A

Oedema
Hypertension
Hypokalaemic symptoms -> weakness, cramps, paraesthesia, polyuria, polydipsia
Metabolic alkalosis

98
Q

Investigations for Conn’s syndrome

A

Renin/aldosterone ratio
High aldosterone + low renin = primary hyperaldosteronism
High aldosterone + high renin = secondary hyperaldosteronism

U&E’s - hypernatraemia & hypokalaemia
CT/MRI adrenals - for adrenal adenoma
BP - high
Blood gas analysis (alkalosis)

99
Q

Treatment for Conn’s syndrome

A

Laparoscopic adrenalectomy
Spironlactone (4 weeks) = controls BP and K

BAH = Spironolactone - blocks aldosterone
Aldosterone antagonists e.g. Eplerenone

100
Q

Define Acromegaly

A

Excessive growth hormone secretion

101
Q

Causes of acromegaly

A

Pituitary adenoma

Cancer - lung or pancreatic

102
Q

Signs and symptoms of acromegaly

A 
Headaches
Bitemporal hemianopia - pituitary tumour presses on optic chiasm
Spadelike hands
Growth of jaw and feet
Fontal bossing (prominent forehead and brow)
Large nose
Large tongue (macroglossia)
Widely spaced teeth
Increased sweating
Snoring
Arthralgia
Osteoarthritis
Dark, thick oily skin
Bilateral carpal tunnel
Hypertension
Type 2 diabetes mellitus
Amenorrhoea
Loss of libido
103
Q

Investigations for acromegaly

A

Raised serum IGF-1

Oral glucose tolerance test to confirm a raised IGF
MRI brain - pituitary tumour
Visual fields and acuity

104
Q

Treatment for acromegaly

A

First line = Trans-sphenoidal surgery
Second line = Somatostatin analogues e.g. Octreotide/lanreotide
GH antagonist e.g. Pegvisomant
Dopamine agonists e.g. bromocriptine

105
Q

What is phaeochromocytoma?

A

Excessive production of adrenaline

106
Q

Where are the chromaffin cells located?

A

Adrenal glands - adrenal medulla

107
Q

What is phaeochromocytoma a tumour of?

A

Chromaffin cells

108
Q

What is the 10% rule in phaeochromocytoma?

A

10% are malignant
10% are extra adrenal (outside the adrenal gland)
10% are bilateral

109
Q

Symptoms of phaeochromocytoma

A

Headache
Sweating
Tachycardia

Anxiety
Palpitations
Tremor
Hypertension

110
Q

Investigations for phaeochromocytoma

A

24 hour urine catecholamines
Plasma free metanephrines
Abdominal CT/MRI - for extra adrenal tumours

111
Q

Treatment for phaeochromocytoma

A

Adrenalectomy to remove tumour is definitive management

Pre-surgery alpha blocker (phenoxbenzamine) then beta blocker (propanolol)

112
Q

What is a phaeochromocytoma emergency?

A

Hypertensive crisis

113
Q

What causes a phaeochromocytoma emergency?

A 
Anesthesia
Contrast imaging
Childbirth
Stress
Opiates
114
Q

Symptoms of a phaeochromocytoma emergency

A 
Pallor
Pulsating headache
Hypertension
Feels 'about to die'
Pyrexial
115
Q

Treatment for a phaeochromocytoma emergency

A

ICU
IV alpha blocker e.g. phentolamine
Then phenoxybenzamine when BP controlled

116
Q

What is carcinoid syndrome?

A

Tumours of enterchromaffin cells

117
Q

What are the common locations for carcinoid syndrome?

A

Appendix 45%
Ileum 30%
Rectum 20%

118
Q

Symptoms of carcinoid syndrome

A

Triad: Flushing
Diarrhoea
Cardiac failure

Wheeze
Palpitations
Abdominal pain

119
Q

Investigations for carcinoid syndrome

A

24 hour urine 5H1AA
Chest x-ray/chest/pelvis MRI/CT
Plasma chromogranin A

120
Q

Treatment for carcinoid syndrome

A

Octreotide (somatostatin analogue) -> to prevent carcinoid crisis
Surgical resection - tumours are intense yellow

121
Q

What causes primary hyperparathyroidism?

A

Tumour of the parathyroid glands

122
Q

Symptoms of primary hyperparathyroidism

A 
Leads to hypercalcaemia:
Abdominal pain
Vomiting
Constipation
Dehydration
Depressed
Renal stones
Fatigue 
Weakness
Muscle pain
Osteoporosis
123
Q

Investigations for primary hyperparathyroidism

A

Increased PTH
Increased Ca
Decreased Phosphate

124
Q

Treatment for primary hyperparathyroidism

A

Mild = increase fluid intake, avoid thiazides
Excision of the adenoma
Bisphosphonates - alendronate
Cinacalcet

125
Q

What is secondary hyperparathyroidism?

A

Insufficient vitamin D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bones
Parathyroid gland reacts to low serum calcium by excreting more PTH -> number of cells in parathyroid gland increase = hyperplasia
Causes hypocalcaemia

126
Q

Investigations for secondary hyperparathyroidism

A

Increased PTH
Low Calcium
Increased Phosphate
Low vitamin D

127
Q

Treatment for secondary hyperparathyroidism

A

Correct vitamin D deficiency

128
Q

What is tertiary hyperparathyroidism?

A

Occurs after prolonged secondary hyperparathyroidism.
Leads to hyperplasia of the glands
High level of PTH causes high absorption of Calcum

129
Q

Investigations for tertiary hyperparathyroidism

A

Increased PTH
Increased calcium
Increased phosphate

130
Q

Treatment for tertiary hyperparathyroidism

A

Surgical removal of part of the parathyroid tissue

131
Q

Define primary hypoparathyroidism

A

Low PTH secretion due to gland failure

Hypocalcaemia

132
Q

Causes of primary hypoparathyroidism

A

Di George syndrome
Neck surgery
Wilson’s disease
Alcohol

133
Q

Symptoms of primary hypoparathyroidism

A

Symptoms of hypocalcaemia

‘SPASMODIC’

134
Q

Investigations for primary hypoparathyroidism

A

Low Calcium
High Phosphate
Low PTH

135
Q

Treatment for primary hypoparathyroidism

A

Calcium supplements

Calcitriol

136
Q

Causes of secondary hypoparathyroidism

A

Radiation
Surgery (thyroidectomy, parathyroidectomy)
Hypomagnesaemia

137
Q

Define pseudohypoparathyroidism

A

Failure of target cell response to PTH - end-organ resistance to PTH

138
Q

Signs of pseudohypoparathyroidism

A

Low IQ
Short 4th and 5th metacarpels
Short stature
Round face

139
Q

Investigations for pseudohypoparathyroidism

A

Low Calcium

High PTH

140
Q

Treatment for pseudohypoparathyroidism

A

Calcium

141
Q

Define hypopituitarism

A 
Decreased secretion of anterior pituitary hormones:
GH
FSH
LH
Prolactin
TSH
ACTH
142
Q

Causes of hypopituitarism

A

Hypothalamus: Kallman’s syndrome, Tumour, inflammation, TB, meningitis
Pituitary stalk: Trauma, surgery, mass lesion, meningioma, carotid artery aneurysm
Pituitary: Tumour, irradiation, inflammation, ischaemic (pituitary apoplexy, DIC, Sheehan’s syndrome), autoimmunity

143
Q

Features of hypopituitarism

A

GH lack: Central obesity, atherosclerosis, dry skin, reduced cardiac output, osteoporosis, reduced balance, reduced exercise ability, reduced wellbeing

FSH/LH lack: Oligo/amenorrhoea, reduced fertility, reduced libido, osteoporosis, ED, hypogonadism

Thyroid lack: Hypothyroidism signs - BRADYCARDIC

ACTH lack: Adrenal insufficiency signs

Prolactin lack: Absent lactation

144
Q

Investigations for hypopituitarism

A

Low LH, FSH. Testosterone, T4. Cortisol, IGF-1

Short synacthen test - assess adrenal axis
Insulin tolerance test - assess adrenal and GH axes

MRI scan - look for hypothalamic/pituitary lesion

145
Q

Treatment for hypopituitarism

A

Hormone replacement and treat underlying causes
Hydrocortisone for secondary adrenal failure
Thyroxine if hypothyroid
Somatotropin for GH

146
Q

What are the types of pituitary tumours?

A

Chromophobe - 70%
Eosinophil/Acidophil - 15%
Basophil - 15%

147
Q

Features of a chromophobe pituitary tumour

A

Many are non-secretory
Half produce prolactin, a few ACTH or GH
Local pressure effect in 30% - often visual loss

148
Q

What hormone is most commonly produced from pituitary tumours?

A

Prolactin

149
Q

Features of an eosinophil/acidophil tumour

A

Secrete GH or prolactin

150
Q

Features of a basophil tumour

A

Secrete ACTH - presents with Cushing’s

May enlarge post adrenalectomy (Nelson’s syndrome)

151
Q

Features of local pressure due to pituitary tumour

A 
Headaches - bilateral
Visual field defects (bilateral temporal hemianopia)
Palsy of cranial nerves 3, 4 and 6
Squint
Diabetes insipidus
152
Q

Investigations for pituitary tumours

A

MRI
Visual fields
Pituitary function tests: PRL, IGF-1, ACTH, Cortisol, TFT’S, FSH/LH
Glucose tolerance test if acromegaly suspected
Water deprivation if DI suspected

153
Q

Treatment for pituitary tumours

A

Start hormone replacement
Steroids given before levothyroxine to prevent adrenal crisis
Prolactinoma = bromocriptine
GH = somatostatin analogues - Octreotide
Surgery - trans-sphenoidal -> give hydrocortisone pre-op
Radiotherapy

154
Q

Define pituitary apoplexy

A

Rapid pituitary enlargement due to a bleed into tumour

Causes mass effect, CV collapse, acute hypopituitarism

155
Q

Symptoms of pituitary apoplexy

A

Acute onset headache
Meningism
Reduced GCS
Visual field defect/double vision

156
Q

Treatment for pituitary apoplexy

A

IV hydrocortisone
IV saline fluid balance
Surgery

157
Q

What is craniopharyngioma?

A 
Tumour from Rathke's pouch. Between pituitary and 3rd ventricle floor
Commonest childhood intracranial tumour
Adults present with: Amenorrhoea and DI
Investigations: CT/MRI
Treatment: Surgery
158
Q

Define prolactinaemia

A

Commonest hormonal disturbance of the pituitary
Hyperprolactinaemia is raised prolactin in the blood
Prolactin is secreted from anterior pituitary and release is inhibited by dopamine

159
Q

How does hyperprolactinaemia present in women?

A

Inhibits GNRH -> reduced FSH/LH -> menstrual dysfunction and galactorrhoea -> low oestrogen

Amenorrhoea/oligomenorrhoea
Infertility
Loss of libido
Weight gain
Hirsutism
160
Q

How does hyperprolactinaemia present in men?

A

Decreased libido and ED

Reduced facial hair

161
Q

Causes of hyperprolactinaemia

A

Excess production from the pituitary e.g. Prolactinoma
Compression of pituitary stalk - reducing dopamine levels
Dopamine antagonists - Metoclopramide, domperidone, neuroleptics
Pregnancy, breastfeeding, stress
Other drugs: Haloperidol, antipsychotics (TCA, MAOI, SRI’s)
Head injury - trauma
Craniopharyngioma
Pituitary adenomas
Hypothyroidism
Hypothalamic tumours

162
Q

What are the two types of prolactinomas?

A 
Microadenoma = <1cm 90%
Macroadenoma = >1cm 10% - Presents with headache, reduced acuity, diplopia, bitemporal hemianopia, upper temporal quadrantanopia
163
Q

Investigations for hyperprolactinaemia

A

PRL= Normal <400, Mild 400-1000, True prolactinoma >5000
TFT’s
Exclude pregnancy
MRI pituitary

164
Q

Treatment for hyperprolactinaemia

A

Dopamine agonist - 1st line
E.g. Bromocriptine/cabergoline
Trans-sphenoidal surgery - 2nd line

165
Q

Complications of hyperprolactinaemia

A

Headache
Visual loss
Both as a result of pituitary apoplexy

166
Q

Define diabetes insipidus

A

The passage of large volumes (>3L/day) of dilute urine due to impaired water resorption by the kidney

Can be due to reduced ADH secretion from the posterior pituitary (cranial DI) or impaired response of the kidney to ADH (nephrogenic DI)

167
Q

Define cranial DI

A

Reduced secretion of ADH from the posterior pituitary due to damage to the hypothalamus

168
Q

Causes of cranial DI

A 
Idiopathic
Brain tumours
Trauma
Infection - TB, meningitis, encephalitis
Sarcoidosis
Brain surgery
Congenital - Wolfram's syndrome, defects in ADH gene
169
Q

Define nephrogenic DI

A

When the collecting ducts of the kidneys do not respond to ADH

170
Q

Causes of nephrogenic DI

A 
Drugs - lithium, demeclocycline
Hypokalaemia
Hypercalcaemia
Chronic renal disease
Mutations on AVPR2 gene on X chromosome that codes for the ADH receptor
171
Q

Symptoms of DI

A

Polyuria
Polydipsia
Dehydration
Hypernatraemia -> lethargy, weakness, confusion

172
Q

Investigations for DI

A

Low urine osmolality - diluted
High serum osmolality
Water deprivation test (desmopressin stimulation test)
Urine dipstick - negative for glucose (Exclude DM)
MRI pituitary/hypothalamus

173
Q

How does the water deprivation test work?

A

Tests the ability of the kidneys to concentrate urine
Patient avoid fluids for 8 hours
Urine osmolality is measured
Desmopressin is given (synthetic ADH)
8 hours later urine osmolality is measured again

174
Q

What are the findings from the water deprivation test?

A

Cranial DI= Low urine osmolality after deprivation and high after ADH

Nephrogenic DI= Low urine osmolality after deprivation and low after ADH

Primary polydipsia = High urine osmolality after deprivation and high after ADH

175
Q

Treatment for DI

A

Cranial DI = Desmopressin -> overdose = hyponatraemia

Nephrogenic DI = treat underlying cause, NSAIDs, bendroflumethazide

176
Q

Define SIADH

A

Large amounts of ADH
Results in excessive water reabsorption in the collecting ducts -> the water dilutes the sodium in the blood causing hyponatraemia

177
Q

Where is ADH secreted from?

A

Produced in the hypothalamus and secreted by the posterior pituitary gland

178
Q

Causes of SIADH

A

Malignancy - small cell lung cancer, pancreas, prostate, lymphoma
CNS disorders - meningitis, stroke, SAH, trauma, abscess
Chest disease - TB, pneumonia, small-cell lung cancer, lung abscess
Endocrine disorders - Hypothyroidism
Drugs - SSRI’s, NSAIDs, thiazide diuretics, opiates, cyclophosphamide

179
Q

Symptoms of SIADH

A 
Confusion
Nausea and vomiting
Fatigue
Muscle aches
Seizures/coma -> from hyponatraemia
180
Q

Investigations for SIADH

A

U&E’s = Na low <135mmol/L = hyponatraemia
Urine osmolality high
Urine sodium high
Normal renin and adrenal function

181
Q

Management for SIADH

A

Stop causative medication
Correct sodium slowly to prevent central pontine myelinolysis
Fluid restriction
ADH receptor blockers ‘vaptans’ e.g. Tolvaptan
Demeclocycline

Phase 3b (18 decks)

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