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YEAR 3 & 5 CORE CONDITIONS > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the most common cause of hypothyroidism in the UK?

A

Hashimoto’s thyroiditis

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2
Q

Which of the autoimmune hypothyroidisms present with a goitre?

A

Hashimoto’s thyroiditis (due to lymphocytic and plasma cell infiltration)

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3
Q

What is the most common cause of hypothyroidism worldwide?

A

Iodine deficiency

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4
Q

What are the effects of hypothyroidism on the body and how do these manifest?

A

Decrease in basal metabolic rate leads to decreased oxygen and substrate consumption, which causes:

  • Apathy and slowed cognition - depression and dementia like symptoms
  • Skin dryness and alopecia
  • Increased LDLs and triglycerides
  • Cold intolerance

Decreased sympathetic activity causes:

  • Decreased sweating
  • Cold skin due to decreased blood flow
  • Constipation due to decrease GI motility
  • Bradycardia

Hyperprolactinaemia - increased prolactin production is stimulated by TRH, which supresses LH, FSH, GnRH, testosterone but stimulates breast tissue growth

Myxoedema - due to accumulation of glycosaminoglycans within the reticular layer of the dermis

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5
Q

What are the signs on examination of hypothyroidism (remember the mnemonic)?

A

BRADYCARDIC

Bradycardia
Reflexes relax slowly (Woltman sign) 
Ataxia
Dry thin hair and skin
Yawning
Cold 
Ascites + non-pitting oedema
Round puffy face
Defeated demeanour 
Ileus 
Cystic fibrosis
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6
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (synthetic T4 - which is then peripherally converted to the active T3)

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7
Q

What is the main contraindication of levothyroxine?

A

Ischaemic heart disease

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8
Q

What would TFTs of primary hypothyroidism look like?

A 
TSH = high (compensatory)
T4/T3 = low
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9
Q

What would TFTs of secondary hypothyroidism look like?

A 
TSH = normal or low if there is a lack from pituitary 
T4/T3 = low
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10
Q

What causes secondary and tertiary hypothyroidism?

A

Secondary = pituitary disorders

Tertiary = hypothalamic disorders causing a deficiency of TRH (thyrotropin-releasing hormone)

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11
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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12
Q

What is the pathophysiology of Grave’s disease?

A

Autoimmune disease causes IgG antibodies to bind to TSH receptors, causing thyroid enlargement and increased hormone production

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13
Q

Aside from Grave’s disease, what else can cause hyperthyroidism?

A

Toxic multinodular goitre
Toxic adenoma = solitary nodule producing T3 and T4
Ectopic thyroid tissue - metastatic follicular thyroid cancer

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14
Q

What are the classic symptoms of hyperthyroidism?

A 
Weight loss but increased appetite
Insomnia
Heat intolerance
Sweating
Diarrhoea
Tremor
Anxiety or psychosis 
Palpitations
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15
Q

What signs would you see/feel in the hands with hyperthyroidism?

A 
Palmar erythema
Acropachy - painful finger swelling
Sweaty palms
Fine tremor 
Fast/irregular pulse
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16
Q

What signs do you see in the eyes in Graves disease?

A

Lid lag
Lid retraction
Exophthalmos

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17
Q

What is the main drug treatment for hyperthyroidism?

A

Block and replace therapy

Give carbimazole and thyroxine simultaneously

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18
Q

Why is it better to do the block and replace therapy rather than just give carbimazole?

A

Reduces risk of iatrogenic hypothyroidism

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19
Q

What are some dangerous side effects of carbimazole?

A

Neutropenia (agranulocytosis) which can lead to neutropenic sepsis

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20
Q

What risk is there during a thyroidectomy and what would it cause?

A

Damage to laryngeal nerve

Cause a hoarse voice

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21
Q

What can be used to destroy the thyroid gland to treat hyperthyroidism?

A

Radioiodine (iodine 131) given as a drink

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22
Q

What is the risk of giving radioiodine?

A

Thyroid storm

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23
Q

How does a thyroid storm present?

A

Severe hyperthyroidism:

  • Fever
  • Agitation
  • Confusion
  • Coma
  • AF
  • Diarrhoea + vomiting
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24
Q

What are TFTs like in hyperthyroidism?

A

TSH = low (suppressed)

T4 + T3 = high

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25
Q

What drug can cause both hypo and hyperthyroidism?

A

Amiodarone

It has iodine in it

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26
Q

How can you test to see if a neck lump is a goitre?

A

Ask patient to drink some water and swallow. A goitre will move up.

Then ask the patient to stick their tongue out. A goitre will not move but a thyroglossal cyst will.

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27
Q

What is Cushing’s syndrome compared to Cushing’s disease?

A

Cushing’s syndrome is the clinical state produced by chronic glucocorticoid excess

Cushing’s disease is excessive ACTH from the pituitary - usually a pituitary adenoma

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28
Q

What is the main cause of Cushing’s syndrome?

A

Excess oral steroids

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29
Q

Aside from Cushing’s disease, what is another ACTH-dependent cause of Cushing’s syndrome?

A

Ectopic ACTH tumours e.g. small cell lung cancer

The classical symptoms of Cushing’s are absent in this one

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30
Q

What does a Cushing’s person look like?

A
  • Moon face
  • Acne
  • Buffalo hump
  • Cataracts
  • Psychosis, depression, sleep disturbance
  • Truncal obesity
  • Abdominal striae
  • Muscle/tendon wasting - recurrent Achilles tendon rupture
  • Skin thinning
  • Hirsutism
  • Gonadal dysfunction - erectile dysfunction, irregular periods
  • Hypertension
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31
Q

What condition are people with Cushing’s at risk of?

A

Diabetes

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32
Q

What is the first-line screening test (after establishing a raised plasma cortisol) for Cushing’s? What conditions can cause false positives?

A

Overnight low-dose dexamethasone suppression test

  • give 1mg dexamethasone at midnight
  • do serum cortisol at 8am
  • normally, cortisol suppresses to <50nmol/L but in Cushing’s there would be no suppression
  • False positives are seen in depression, obesity, alcohol excess, inducers of liver enzymes
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33
Q

What is an alternative screening test to the overnight dexamethasone suppression test? What conditions can cause false positives?

A

24 hour urinary free cortisol

  • 3 collections
  • also measures creatinine excretion
  • diagnosed in 2+ collections measure cortisol excretion as >3 times the lab upper limit of normal
  • false positives occur in pregnancy, anorexia, exercise, psychoses, alcohol
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34
Q

What is the normal circadian rhythm for cortisol?

A

Lowest at midnight

Highest early in the morning

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35
Q

How can you show that there is a loss of the normal circadian rhythm in Cushing’s?

A

Midnight cortisol levels

  • take bloods at midnight during sleep
  • shows increased cortisol at midnight (when it should be at lowest)
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36
Q

Apart from oral steroids, what are some other ACTH-independent causes of Cushing’s?

A
  • Adrenal adenoma

- Adrenal nodular hyperplasia

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37
Q

What test can you do to localise the cause of Cushing’s?

A

Serum ACTH

  • if it is undetectable, it is likely to be an adrenal tumour
  • if it is raised, it is an ACTH-dependent cause (Cushing’s disease or ectopic ACTH production)
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38
Q

How do you distinguish between a pituitary cause or ectopic ACTH producing cause of Cushing’s?

A

High dose dexamethasone suppression test - there is a greater than 90% reduction in urinary cortisol in pituitary adenoma

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39
Q

What drugs can be used to lower cortisol levels?

A

Metyrapone - most commonly used

Ketoconazole

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40
Q

If the source of Cushing’s is unlocateable, what surgical treatment would you do?

A

Bilateral adrenalectomy

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41
Q

What is the main complication of a bilateral adrenalectomy?

A

Nelson’s syndrome = increased skin pigmentation (ACTH reacts with melanin receptors) and ACTH-producing pituitary adenoma

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42
Q

Name an adrenolytic drug and what is it used for?

A

Mitotane

Used for adrenal adenoma/carcinoma

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43
Q

What are the two different types of pituitary adenoma and what is the most common of each?

A

Secretory pituitary adenoma - prolactinoma

Non-secretory pituitary adenoma - gonadotroph adenoma

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44
Q

How does a growth hormone-producing tumour in children or adults?

A 
Children = gigantism
Adults = acromegaly (increased sweating, headaches, hands and feet enlargement)
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45
Q

What visual defects do you get from a pituitary adenoma and why?

A

Bilateral temporal hemianopia due to compression of the optic chiasm

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46
Q

What cranial nerve palsies can occur due to a pituitary adenoma? Why? And how does it present?

A

CN III, IV, VI due to pressure on the cavernous sinus Presents as a squint causing diplopia

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47
Q

Describe a headache secondary to pituitary adenoma

A

Worse on waking
Retro-orbital
Bitemporal

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48
Q

What other condition can be caused by pituitary adenoma?

A

Diabetes insipidus (which is not related to diabetes mellitus).
Characterised by polydypsia and polyuria
It is due to reduced ADH secretion from the posterior pituitary

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49
Q

What is an MRI defining in a pituitary adenoma?

A

Whether there is intra or supra-sellar extension

Size of the pituitary gland

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50
Q

When treating hypothyroidism secondary to hypopituitarism, what must you give before levothyroxine and why?

A

Steroids because thyroxine could precipitate and Addisonian crisis (=adrenal crisis)

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51
Q

What normally causes parathyroid hormone to be secreted?

A

Low calcium levels

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52
Q

How does PTH increase calcium levels and decrease phosphate levels?

A
  1. Increases osteoclast activity, which releases calcium and phosphate from bones
  2. Increases calcium reabsorption + decreases phosphate reabsorption from kidney
  3. Increases vitamin D3 production
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53
Q

Who is primary hyperparathyroidism most common in ?

A

Post-menopausal women

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54
Q

What is the main cause of primary hyperparathyroidism?

A

Solitary adenoma of the parathyroid gland

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55
Q

What gene is primary hyperparathyroidism sometimes associated with?

A

MEN1 or MEN2 (multiple endocrine neoplasia)

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56
Q

What 4 steps should you take if someone presents with hypercalcaemia in order to find the cause?

A
  1. Look for drug causes e.g. lithium, thiazides
  2. Repeat plasma albumin-adjusted calcium levels
  3. Check renal function
  4. Measure PTH
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57
Q

What cancer is MEN2 associated with?

A

Thyroid cancer

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58
Q

How do you treat primary hyperparathyroidism?

A

Increase fluid intake

Parathyroidectomy to remove the respective gland

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59
Q

What are the calcium levels like in secondary hyperparathyroidism? Why?

A

Normal or low

The hyperparathyroidism occurs because the parathyroid glands become hyperplastic after longterm hypocalcaemia

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60
Q

What are the 2 main causes of secondary hyperparathyroidism?

A

Chronic kidney disease - most common cause

Vitamin D deficiency

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61
Q

What drug can be used to treat secondary hyperparathyroidism?

A

Cinacalcet - it increases the sensitivity of parathyroid cells to calcium, therefore decreasing PTH secretion

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62
Q

What are the calcium levels like in tertiary hyperparathyroidism and why?

A

High
Due to prolonged secondary hyperparathyroidism, the glands act autonomously so they produce excessive PTH even after hypocalcaemia is fixed

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63
Q

What drugs can cause hypoglycaemia?

A 
Insulin
Sulphonylureas
GLP-1 analogues
DPP-4 inhibitors
Beta-blockers
Alcohol
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64
Q

How can you distinguish between the presence of exogenous and endogenous insulin?

A

High insulin ANDhighC-peptide and proinsulin = Endogenous production

High insulin ANDlowC-peptide and proinsulin = Exogenous administration

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65
Q

What can be given in mild hypoglycaemia (i.e. they are still conscious)?

A

Glucogel
15-20g glucose tablets
Sweets
Fruit juice

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66
Q

What can be given in severe hypoglycaemia (i.e. they are not conscious)?

A

150ml 10% dextrose or 75ml 20% dextrose IV

1mg/kg glucagon IM if no IV access

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67
Q

In which patients would IM glucagon not be effective?

A

Acute alcohol - alcohol blocks gluconeogenesis

Patients with depleted glycogen stores:

  • Adrenal insufficiency
  • Insulinoma
  • Anorexic pts - chronic starvation
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68
Q

What is the triad of Grave’s disease?

A
  1. Diffuse goitre
    - Smooth, uniformly enlarge goitre
    - Bruit heard at superior poles of lobes due to increased vascularity
  2. Ophthalmopathy
    - Exophthalmos
    - Lid retraction
    - Diplopia
  3. Pretibial myxoedema
    - Non-pitting oedema and firm plaques on the anterior and lateral aspects of legs
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69
Q

What thyroid antibodies are specific to Grave’s disease?

A

TRAbs (TSH receptor antibodies)

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70
Q

What is the triad of Graves disease?

A
  1. Diffuse goitre
  2. Ophthalmopathy
  3. Pretibial myxoedema
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71
Q

Describe the goitre in Graves disease

A

Smooth, uniformly enlarged goitre

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72
Q

What antibodies can be tested for in Graves disease?

A

TRAbs (TSH receptor antibodies) - specific to Graves and would be raised
Anti-TPO and anti-Tg would also be raised but are non-specific

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73
Q

What imaging can be done to diagnose Graves disease?

A

Thyroid scintigraphy

  • Shows a diffuse uptake of radioactive iodine (123-I)
  • Contraindicated in pregnancy

Thyroid ultrasound with colour Doppler

  • For pregnant women
  • Shows enlarged, hypervascular thyroid
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74
Q

What medication provides symptomatic relief in hyperthyroidism?

A

Propanolol

75
Q

What are the symptoms of hypercalcaemia as seen in primary hyperparathyrodism?

A
  • CVD - hypercalcaemia leads to the calcification of arteries and myocardium
  • Renal stones
  • Polyuria and polydipsia
  • Bone, muscle and joint pain
  • Pseudogout
  • Osteitis fibrosa cystic (cyst-like brown tumours)
  • Weight loss
  • Constipation
  • Peptic ulcers (hypercalcaemia leads to high levels of gastrin which stimulates stomach acid production)
  • Pancreatitis
  • Psychological disturbances
76
Q

What is Addison’s disease?

A

Primary adrenocortical insufficiency

A condition where the adrenal cortex has been destroyed so there is a deficiency of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)

77
Q

What are the most common causes of Addison’s in the UK and worldwide?

A

UK - autoimmune

TB - worldwide

78
Q

What causes secondary adrenocortical insufficiency?

A

Sudden discontinuation of steroids of physiological stress (infection, trauma, surgery) during prolonged steroid therapy

Hypopituitarism

79
Q

How does hypopituitarism cause secondary adrenocortical insufficiency?

A

There is a decrease in ACTH release which leads to decreased endogenous cortisol production

80
Q

What causes tertiary adrenocortical insufficiency?

A

Conditions that decrease corticotropin-releasing hormone (CRH) production

  • Sudden discontinuation of steroid therapy
  • Hypothalamic dysfunction (trauma, mass, haemorrhage, anorexia)
81
Q

What three hormones are produced by the adrenal cortex?

A
  1. Androgen
  2. Cortisol
  3. Aldosterone
82
Q

How does low androgen present?

A
  • Loss of libido

* Loss of axillary and pubic hair

83
Q

How does low cortisol present?

A
  • Weight loss
  • Fatigue, lethargy
  • GI symptoms - nausea, vomiting, diarrhoea
  • Orthostatic hypotension
  • Hypoglycaemia
84
Q

How does low aldosterone present?

A
  • Hypotension

* Salt craving

85
Q

Why do you get orthostatic hypotension with low cortisol?

A

Glucocorticoids play an important role in catecholamine-induced vasoconstriction and myocardial contractility

86
Q

In Addison’s disease there is raised ACTH; how does this present and why?

A

Hyperpigmentation

Increased ACTH - leads to increased POMC production (in order to boost ACTH production), which increases melanocyte-stimulating hormone, causing hyperpigmentation of the skin

87
Q

Which of the adrenal hormones is not affected in secondary and tertiary adrenal insufficiency?

A

Aldosterone synthesis is not affected because mineralocorticoid production is controlled by RAAS, not by ACTH

88
Q

How does an adrenal crisis present?

A
  • Hypotension, shock
  • Reduced GCS
  • Fever
  • Vomiting and diarrhoea
  • Severe abdominal pain that resembles peritonitis
89
Q

What are the U+Es like in Addison’s disease?

A

Hyponatraemia, hyperkalaemia - due to aldosterone
High urea
Mildly high calcium

90
Q

What would a VBG/ABG show in Addison’s?

A

Metabolic acidosis

Hypoglycaemia - due to cortisol

91
Q

What is the best initial test for diagnosing low cortisol?

A

Morning serum cortisol levels

OR

Morning serum ACTH level (short synacthen test) - ACTH is high in primary insufficiency but low in secondary

92
Q

What is the confirmatory test for low cortisol? What does it involve?

A

ACTH stimulation test

  • Measurement of serum cortisol before and 30 minutes after administration of ACTH
  • In primary there would not be a sufficient rise in cortisol; in secondary/tertiary there would be a normal rise in cortisol
93
Q

What tests can be done to diagnose low aldosterone?

A
  • High plasma renin concentration

* Low urine aldosterone levels

94
Q

What test is diagnostic of low androgen from the adrenal glands?

A

Low DHEA-S - DHEA-S is only synthesised in the adrenal glands (note that low adrogen can be caused by hypogonadism too but would have normal DHEA-S)

95
Q

What investigations allow you to distinguish between primary, secondary and tertiary adrenal insufficiency?

A
  • Serum ACTH levels distinguish between primary and secondary/tertiary adrenal insufficiency
  • CRH stimulation test is used to distinguish between secondary and tertiary adrenal insufficiency
96
Q

What is the treatment of adrenocortical insufficiency?

A

Hydrocortisone for glucocorticoid replacement - administer in 2-3 doses daily to mimic natural diurnal rhythm

Fludrocortisone for mineralocorticoid replacement - only required in primary

97
Q

What are the rules for patients on long-term steroid therapy?

A
  • Carry a steroid card on their person
  • Have a medic-alert bracelet
  • If they have any illness they should double their regular steroid medication dose
98
Q

How is an Addisonian crisis managed?

A
  1. Fluid resuscitation
  2. IV hydrocortisone 100mg TDS
  3. IV 50% dextrose
  4. Swap back to oral steroids after 3 days
  5. Fludrocortisone if caused by adrenal problem
99
Q

Which cancers most commonly cause hypercalcaemia of malignancy?

A
  • Non-small cell lung cancer
  • Multiple myeloma
  • Breast carcinoma
  • Renal cell carcinoma
  • Head and neck cancers
100
Q

What is seen on an ECG in hypercalcaemia?

A 
Bradycardia
Short QT interval
Wide T waves
Prolonged PR interval
BBB
Arrhythmias
101
Q

What is included in a bone profile?

A 
Calcium
Phosphate
Albumin
Total protein
ALP
102
Q

What blood levels indicate hypercalcaemia of malignancy rather than primary hyperparathyroidism?

A
  • Low albumin
  • Low chloride
  • Alkalosis
  • Low potassium
  • High phosphate
  • High ALP
103
Q

What is the management of hypercalcaemia?

A
  1. IV 0.9% saline 1L every 4 hours for 24h then every 6 hours for 48-72h
  2. Zolendronic acid 4mg IV or IV pamidronate
  3. Salmon calcitonin (S/C or IM) and corticosteroids (prednisolone PO)
104
Q

What are the most common causes of hypoparathyroidism?

A

Postoperative due to injury of the parathyroid glands during thyroidectomy/parathyroidectomy

Autoimmune - second most common

105
Q

How does acute hypoparathyroidism present and what signs can be found on examination?

A

Hypocalcaemia causes hyperexcitable nerves

Tetany
Chvostek sign - tapping the facial nerve on the cheek causes contraction of facial muscles
Trousseau sign - carpal spasm on inflation of BP cuff

106
Q

How is hypoparathyroidism treated?

A

Calcium and vitamin D supplementation (AdCal)

107
Q

What are the most common and second most common types of thyroid cancer?

A
  1. Papillary carcinoma (70%)

2. Follicular (10-20%)

108
Q

What gene is medullary carcinoma of the thyroid associated with?

A

MEN2

109
Q

How can thyroid cancer present?

A
  • Firm, painless thyroid nodules
  • Hoarse voice
  • Horner syndrome
  • Dysphagia
110
Q

What type of thyroid cancer has an extremely poor prognosis?

A

Anaplastic (undifferentiated) carcinoma

111
Q

What is the management for papillary and follicular thyroid carcinomas?

A

Thyroidectomy (hemi/total depending on size)

Radioiodine given post-surgery to destroy remaining disease tissue and locate metastases

After surgery and radioiodine therapy, even if there is functioning thyroid tissue left, patients may be given levothyroxine to suppress TSH secretion, which reduces risk of stimulating remaining malignant tissue and helps monitor the presence of any further carcinoma as high levels of T3/T4 present in the blood at this stage hint at further disease presence

112
Q

What is a goitre?

A

Goitre = enlarged palpable thyroid gland, which moves on swallowing

113
Q

What can cause a multinodular goitre?

A

Toxic goitre

  • Grave’s disease
  • Toxic multinodular goitre

Hypothyroid goitre

  • Hashimoto’s
  • Congenital

Endemic - iodine deficiency

114
Q

What are the different grades of goitre on palpation of the thyroid?

A

Grade 0 - no goitre palpable or visible

Grade 1 - palpable goitre, not visible when neck is in normal position

Grade 2 - swollen neck and palpable goitre

115
Q

What is the best imaging modality of thyroid?

A

USS - can determine size, nodules, consistency, vascularity

116
Q

What is the difference between simple and multinodular goitres in terms of thyroid hormones?

A

Simple goitres are associated with normal thyroid hormone levels

Multinodular goitres secrete autonomously and can cause hyperthyroidism

117
Q

How are non-toxic goitres managed?

A
  • No treatment required if patient is asymptomatic

* Schedule follow-ups for possible thyroid function issues and obstructive symptoms

118
Q

How are large goitres managed?

A
  • Surgery to avoid obstructive complications

* Radioiodine therapy if unsuitable surgical candidate

119
Q

What is a thyroid nodule?

A

An abnormal growth within the thyroid gland

120
Q

Thyroid nodules can be benign (95%) or malignant (5%). What is the most common thyroid nodule? Give examples of other thyroid nodules

A

Follicular adenoma - most common

Thyroid adenomas

  • Follicular adenoma
  • Toxic adenoma
  • Papillary adenoma

Thyroid cysts

Hashimoto thyroiditis

121
Q

What are the first line investigations for a suspected thyroid nodule?

A

TSH levels

USS of neck

122
Q

What are the criteria for carrying out fine needle aspiration of a thyroid nodule?

A
  • Solid nodule with oval shape/irregular border/calcifications that are 1+cm in diameter
  • Nodules <1cm in patients with risk factors for malignancy
  • Large thyroid nodules (>1.5-2cm) even if they appear benign
123
Q

What is hashitoxicosis, what is it caused by and how does it present?

A

Transient hyperthyroidism due to follicular rupture of hormone-containing thyroid tissue

Irritability, heat intolerance, diarrhoea

124
Q

What is De Quervain thyroiditis also called?

A

Subacute granulomatous thyroiditis

125
Q

What is De Quervain thyroiditis usually preceded by?

A

Viral infections e.g. mumps, coxsackie, influenza, adenovirus

126
Q

Go through the triphasic response of De Quervain thyroiditis?

A
  1. Thyrotoxic phase (2-8 weeks) - caused by damage to follicular cells and release of thyroid hormones causing features of hyperthyroidism
  2. Hypothyroid phase (2-8 weeks) - caused by depletion and impaired synthesis of thyroid hormones due to damage of follicular cells
  3. Euthyroid phase: thyroid function recovers and pathological changes no longer visible on the gland
127
Q

What should you not give in the thyrotoxic phase of De Quervain thyroiditis?

A

Do not give carbimazole in thyrotoxic phase because it target the synthesis of thyroid hormones and the thyrotoxic phase is caused by damage to follicular cells and release of thyroid hormones

128
Q

What investigation assesses visual field defects?

A

Perimetry

129
Q

What is the first line treatment of prolactinomas?

A

Dopamine agonists (cabergoline 0.25-1mg weekly or twice weekly) to shrink the pituitary adenoma

130
Q

What is the second line treatment of prolactinomas?

A

Transphenoidal hypophysectomy (resection of pituitary gland) +/- adjuvant radiotherapy

131
Q

How are non-secretory pituitary microadenomas managed?

A

No treatment, just follow-up, they often cease growing on their own

132
Q

What is the order in which anterior pituitary hormones are affected in hypopituitarism?

A
  • GH - muscle and bone
  • FSH - ovary
  • LH - testes
  • Prolactin - breast
  • TSH - thyroid
  • ACTH - kidney + adrenals
133
Q

What is the most common cause of hypopituitarism?

A

Pituitary adenoma

134
Q

Why is the pituitary vulnerable to ischaemia?

A

It receives blood supply from relatively low-pressure arterial system

135
Q

What syndrome causes pituitary apoplexy?

A

Sheehan syndrome: postpartum necrosis of pituitary gland following postpartum haemorrhage

136
Q

What syndrome causes a congenital deficiency of hypothalamic hormones?

A

Kallman syndrome - GnRH deficiency

137
Q

How does GH deficiency present?

A

Weight gain
Weakness
Depression

138
Q

How does FSH/LH deficiency present in males/females?

A 
Females…
• Oligomenorrhoea or amenorrhoea
• Reduced fertility
• Reduced libido
• Osteoporosis
• Breast atrophy
• Dyspareunia 
Males…
• Erectile dysfunction
• Low libido
• Low muscle bulk
• Hypogonadism
139
Q

How do you test for GH deficiency?

A

IGF-1 (insulin-like growth factor) - decreased

140
Q

Why are GH levels an inaccurate test of GH deficiency?

A

GH is secreted in pulsatile manner

141
Q

What further test for GH deficiency can be done in a specialist centre and what does it assess?

A

Assesses the adrenal and GH axes

Insulin tolerance test

  • IV insulin to induce hypoglycaemia and increase in cortisol and GH secretion
  • It is a fasting test
  • Measure cortisol and GH levels when glucose < 2.2mmol/L
  • Normal GH >20 and cortisol >550
142
Q

How do you test for FSH/LH deficiency?

A

GnRH stimulation test

  • Decreased LH in males
  • Decreased FSH and LH in females

Serum DHEA and testosterone levels between 8am and 10am - low

Oestradiol levels - low

143
Q

What is pheochromocytoma?

A

Rare tumour of adrenal glands, which releases catecholamines (adrenaline and noradrenaline)

144
Q

What do pheochromocytoma tumours arise from?

A

Tumours arise from chromaffin cells, which are derived from the neural crest

145
Q

Where are most pheochromocytoma tumours located?

A

90% are located in the adrenal medulla - the adrenal medulla is considered a modified sympathetic ganglion, which is innervated by sympathetic preganglionic neurons

146
Q

What are the 5 Ps of pheochromocytoma?

A
  1. increase blood Pressure
  2. head Pain
  3. Perspiration
  4. Palpitations
  5. Pallor
147
Q

What is the best initial test to investigate pheochromocytoma?

A

Plasma metadrenaline and normetadrenaline test (metabolites of catecholamines) - best initial test, highly sensitive

148
Q

What is the confirmatory test for pheochromocytoma?

A

24 hour urine metadrenalines and catecholamines - confirmatory test, highly specific

149
Q

What would be found on 24 ABPM in pheochromocytoma?

A

Absence of BP drop overnight

150
Q

What is the treatment for pheochromocytoma in the acute setting?

A
  1. Phentolamine IV(short acting alpha blocker) - to initially control BP
  2. Phenoxybenzamine(longer acting alpha blocker) - to control BP before surgery can be arranged
  3. Labetolol(beta blocker) - can be used if patient has tachyarrhythmia but only AFTER alpha blockade
151
Q

What is the definitive management of pheochromocytoma?

A

Adrenalectomy - 4-6 weeks after blood pressure has been controlled

152
Q

What can occur during abdominal examination in pheochromocytoma?

A

Hypertensive crises can be triggered by palpation of the tumour on abdominal examination due to a massive release of catecholamines

153
Q

What is Conn’s disease?

A

Hyperaldosteronism

154
Q

What is the main cause of hyperaldosteronism?

A

Adrenal adenoma (80%)

155
Q

What is the effect of excess aldosterone on the kidneys?

A

Excess aldosterone acts on the distal renal tubule, resulting in retention of sodium and excretion of potassium and calcium

156
Q

How does Conn’s disease present?

A
  • Polyuria
  • Polydipsia
  • Lethargy
  • Headaches
  • Osteoporosis
  • Secondary hypertension - treatment resistant to multiple agents
157
Q

What would U+Es show in hyperaldosteronism?

A

Hypokalaemia

Hypernatraemia

158
Q

What test confirms the diagnosis of hyperaldosteronism?

A

Aldosterone/renin ratio - ratio > 800 confirms diagnosis and prompts investigation for cause

159
Q

How do you treat hyperaldosteronism?

A

Surgical resection of affected gland

Spironolactone (potassium-sparring diuretic)

160
Q

What is the diagnostic criteria for HHS?

A
  • Severe hyperglycaemia >=30mmol/L
  • Hypotension
  • Hyperosmolality - >320 mosmol/kg
161
Q

How is blood osmolality calculated?

A

Glucose + urea + 2xNa

162
Q

What is the management of HHS?

A
  1. Fluid resuscitation - 0.9% sodium chloride :
    a. 1L over 1-2 hours
    b. 1L (+KCl) over 2-4 hours
    c. 1L (+KCl) over 4-6 hours
    d. 1L (+KCl) over 6-8 hours
    e. 1L (+KCl) over 8-10 hours
  2. Insulin at0.05 units/kg/hour
    - only if ketones >1mmol/L or glucose fails to fall
  3. VTE prophylaxis - these patients are high risk due to dehydration
163
Q

What are the two different types of diabetes insipidus?

A

Central diabetes insipidus - most common

Nephrogenic diabetes insipidus - rare

164
Q

What is the pathophysiology behind diabetes insipidius?

A

Central diabetes insipidus - insufficient/absent hypothalamic synthesis or secretion of ADH from the posterior pituitary gland

Nephrogenic diabetes insipidus - defective ADH receptors in distal tubules and collecting ducts

ADH enables the integration of aquaporins in to the plasma membrane of collecting duct cells, leading to reabsorption of free water
Reduced ADH leads to dilute urine

165
Q

What are some secondary causes of central diabetes inspidius?

A

Brain tumours - craniopharyngioma, cerebral mets from lung cancer and leukaemia/lymphoma
Neurosurgery - after resection of macroadenomas
Traumatic brain injury
Pituitary ischaemia e.g. Sheehan syndrome
Inflammatory conditions e.g. sarcoidosis
Infection e.g. meningitis

166
Q

What drugs can cause nephrogenic diabetes insipidus?

A

Lithium

Tetracyclines

167
Q

How does diabetes insipidus present?

A
  • Polyuria > 3L/day
  • Nocturia
  • Polydipsia
  • Dehydration
168
Q

What test is diagnostic of diabetes insipidus?

A

The 8 Hour Water Deprivation Test - the purpose of this test is to see if the kidneys persist in producing dilute urine despite dehydration, and then to localise the cause

169
Q

What is the first line treatment for central diabetes insipidus?

A

Desmopressin - synthetic vasopressin without vasoconstrictive effects

170
Q

What is the second line treatment for central diabetes insipidus?

A

Chlorpropamide - increases ADH secretion

171
Q

What can be given to patients with lithium-induced NDI?

A

Amiloride - it blocks lithium entry through the Na+ channel

172
Q

What are normal sodium levels?

A

135-145mmol/L

173
Q

What levels indicate mild, moderate and severe hyponatraemia?

A
  • Mild – 125 – 134 mol/L
  • Moderate – 120-124 mmol/L
  • Severe – <120 mol/L
174
Q

What are the three types of hyponatraemia?

A

Hypovolaemic
Euvolaemic
Hypervolaemic

175
Q

What can cause hypovolaemic hyponatraemia?

A

• Renal causes

  • Diuretics - particularly thiazide diuretics
  • Adrenal insufficiency (Addison’s)
  • Osmotic diuresis - low glucose and urea
  • Nephropathy

• GI

  • Vomiting and diarrhoea
  • Pancreatitis
  • Bowel obstruction
  • Peritonitis
  • Burns
  • Rhabdomyolysis
  • Excessive sweating
  • Bleeding
176
Q

What type of hyponatraemia does SIADH cause?

A

Euvolaemic hyponatraemia

177
Q

What can cause SIADH?

A

CNS disturbances - infection, inflammation, trauma, psychosis
Malignancy - SCLC
Pain
Pulmonary disease - especially pneumonia
Drugs - SSRI, ecstasy, carbamazepine, opiates, MAOI

178
Q

What causes hypervolaemic hyponatraemia?

A
  • Heart failure
  • Renal failure - nephrotic syndrome
  • Liver failure
  • Hyperglycaemia
179
Q

At what sodium levels do symptoms start?

A

Na < 125 mmol/L

180
Q

What are the symptoms of hyponatraemia?

A
  • Confusion
  • Lethargy
  • Seizures
  • Coma
  • Muscle weakness
181
Q

How do you manage SIADH?

A
  1. Fluid restriction (up to 750ml/day) and treat underlying cause
  2. ADH antagonists (e.g. tolvaptan, deomeclocycline)
  3. Oral sodium and furosemide
182
Q

If a patient with hyponatraemia is having seizures, what further management is required?

A

Hypertonic 3% sodium chloride in ICU

183
Q

Why do you need to avoid rapid correction of hyponatraemia?

A

It can lead to osmotic demyelination syndrome (central pontine myelinosis) - brain was oedematous then extra Na+ influx causes water to go out of brain quickly leading to demyelination

YEAR 3 & 5 CORE CONDITIONS (30 decks)

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