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CP1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Outer adrenal cortex

A

Developed from mesoderm
Secretes steroid hormones
Controlled by anterior pituitary

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2
Q

Inner adrenal medulla

A

Developed from neuroectoderm

Secretes catecholamines – Adrenaline and noradrenaline.

Under nervous control

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3
Q

What are the 3 zones of the adrenal cortex?

What do they produce?

A
  1. Zona glomerulosa
    => Secretes aldosterone.
  2. Zona fasciculata
    => Secretes cortisol (and also weak androgens)
  3. Zona reticularis
    => Secretes weak androgens (and also cortisol)
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4
Q

Cortisol production

A

Mostly produced in zona fasciculata, but also in zona reticularis

HPA axis – CRH => ACTH => stimulates production of cortisol in the adrenal cortex

There are diurnal variations in cortisol production - peak in the early morning and are low in the late evening

Negative feedback loop – cortisol acts at the hypothalamus and pituitary to suppress CRH and ACTH release

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5
Q

How does ADH affect cortisol levels?

A

AVP (ADH) acts synergistically with CRH to elevate ACTH levels – e.g. when volume levels are depleted

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6
Q

What does cortisol do?

A

Reduce protein and fat stores.

Inhibit glucose uptake by many tissues (but not the brain).

Stimulate hepatic gluconeogenesis.

Permits vasoconstrictive effect of catecholamines.

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7
Q

Weak androgen production

A

Zona reticularis (and somewhat fasciculata)

Release is regulated by ACTH (and other unknown factors), but there is no feedback on CRH/ACTH

There is age-related production of androgens, which peaks at age 21 and then gradually declines

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8
Q

What do weak androgens do?

A

Constitute about 50% of the androgen activity in women (leading to axillary/pubic hair growth and libido).

There is negligible contribution in men due to their higher levels of testosterone, which is much more potent than weak androgens

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9
Q

What is important to note about the rate of production of adrenal steroids?

A

steroids are lipophilic, they diffuse out of cells immediately upon synthesis.

So, rate of synthesis = rate of secretion.

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10
Q

Adrenaline

A

Mixed α- and β-agonist

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11
Q

Noradrenaline

A

Primarily α-agonist

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12
Q

What does stimulation of α-adrenoceptors do?

A

Primarily vasoconstriction

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13
Q

What does stimulation of β-adrenoceptors do?

A

tachycardia,
insulin resistance,
vasodilatation in arteries serving skeletal muscle

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14
Q

What is Cushing’s syndrome?

A

= an umbrella term for excessive glucocorticoid activity

Most commonly exogenous (after high-dose/long-term steroids).

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15
Q

What are primary causes of Cushing’s syndrome?

A

Adrenal carcinoma/adenoma autonomously secreting cortisol

Will be Low ACTH, High cortisol

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16
Q

What are Secondary causes of Cushing’s syndrome?

A

excessive production of ACTH

=> Pituitary tumour
=> Ectopic tumour (most commonly lung)

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17
Q

What is Cushing’s DISEASE?

A

An ACTH-producing pituitary tumour

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18
Q

Signs and Symptoms of Cushing’s Syndrome

A

Due to wide effects of cortisol, there will be varying signs and symptoms

=> Altered fat deposition
=> Excess production of adrenal androgens (if ACTH-dependent)
=> Breakdown of protein, muscle wasting, loss of collagen
=> Mental changes
=> Altered bone metabolism
=> Excess mineralocorticoid activity
=> Hyperglycaemia

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19
Q

What can glucocorticoid excess in children lead to?

A

Growth retardation

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20
Q

What mental changes are typically seen in Cushing’s syndrome?

A

Cognitive difficulties
Emotional instability
Depression
Sleep disturbances

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21
Q

What are signs of excess production of adrenal androgens ?

A

Acne
Female frontal balding
Female hirsutism
Menstrual irregularities

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22
Q

Diagnosis of Cushing’s syndrome

A

cortisol measurements

=> identify LOSS OF DIURNAL RYTHYM via a morning and evening cortisol measurement

Constantly high levels of serum cortisol would indicate Cushing’s Syndrome

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23
Q

How can you differentiate between primary and secondary Cushing’s syndrome?

A

Decreased ACTH levels would indicate a primary cause.

High ACTH levels would indicate a secondary cause.

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24
Q

Dexmethasone suppresion test

A

Dexamethasone = synthetic glucocorticoid

Giving dexamethasone should activate negative feedback loops and cause a decrease in endogenous cortisol

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25
Q

lack of suppression with low-dose dexamethasone

A

indicates hyper-/autonomous secretion of cortisol – confirms Cushing’s syndrome.

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26
Q

lack of suppression with high-dose dexamethasone

A

indicates ectopic ACTH source (not in HPA axis so no negative feedback possible)

High-dose dexamethasone should suppress cortisol release in Cushing’s disease

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27
Q

when is a CRH Stimulation Test used?

A

Used to distinguish between pituitary-dependent Cushing’s and an ectopic course of ACTH

Normally - CRH will cause an increase in both ACTH and cortisol

In pituitary-dependent Cushing’s patients, the response is exaggerated.

In ectopic ACTH syndrome, there will be no response to CRH as they do not recognise it

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28
Q

What are the long-term risks/complications of Cushing’s syndrome?

A
  • Cardiovascular disease
  • Diabetes
  • Osteoporosis
  • Obesity
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29
Q

What is Addison’s disease?

A

= Primary Adrenocortical Insufficiency

Failure of adrenal cortex leads to low aldosterone, low cortisol, low androgens

will be elevated ACTH in an attempt to raise hormone secretion due to a lack of negative feedback

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30
Q

What tends to cause Addison’s disease

A

Most commonly in UK - autoimmune
Worldwide - TB

Other cause - adrenal metastases

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31
Q

Addison’s disease - presentation

A

relatively non-specific symptoms, such as:

LACK OF MINERALOCORTICOID:
Postural hypotension
Muscle weakness, fatigue, lethargy
Hyponatraemia, hyperkalaemia

ELEVATION OF ACTH
Increased pigmentation

LOW GLUCOCORTICOIDS:
Weight loss/anorexia

ALTERED ELECTROLYTES:
Diarrhoea, nausea, vomiting

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32
Q

How does elevated levels of ACTH cause hyperpigmentation?

Where is hyper pigmentation often seen?

A

When ACTH production is increased, so is melanocyte-stimulating hormone (MSH), as they share the same POMC-precursor.

Increased MSH leads to increased melanin content in the skin.

Hyperpigmentation is most often seen in skin creases, old scars, gums and on the inside of the cheek.

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33
Q

Tests for Adrenal Failure

A

Decreased cortisol levels and increased ACTH levels indicates primary disease.

ACTH stimulation test – failure to stimulate confirms a problem with the adrenal gland.

Adrenal autoantibodies – if suspected autoimmune disease

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34
Q

Treatment of Addison’s disease

A

Treatment will be with life-long hormone replacement:

Glucocorticoid – hydrocortisone; high dose AM, lower dose PM.
Mineralocorticoid – fludrocortisone.

Higher doses of glucocorticoid are needed during periods of major stress/illness.

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35
Q

Secondary adrenal insufficiency

A

Occurs due to lack of ACTH production

Can be due to a tumour or damage to the pituitary gland/stalk. Can also be caused by exogenous glucocorticoid use.

There will be low cortisol, with around normal aldosterone levels as the RAAS remains intact.

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36
Q

Secondary adrenal suppression

A

long-term, high-dose glucocorticoid use causes suppression of ACTH production and thereby atrophy of the adrenal cortex

Causes reduction in production of endogenous cortisol

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37
Q

When should you suspect adrenal suppression in use of exogenous steroids?

A

cushingoid appearance (truncal obesity, round face, dorsocervical fat pads, striae)

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38
Q

What can happen if there is abrupt withdrawal of exogenous steroids?

A

symptoms of acute adrenal insufficiency (fatigue, N&V, anorexia, weight loss, hypotension, myalgia) due to the patient’s lack of endogenous cortisol.

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39
Q

Adrenal Crisis

A

MEDICAL EMERGENCY

acute adrenal insufficiency and becomes expressed when the patient is under stress (e.g. infection), leading to hypotension, circulatory failure and potentially death

Urgent treatment - IV fluids and hydrocortisone

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40
Q

What is Conn’s syndrome?

What causes this?

A

= primary hyperaldosteronism

An abnormally large amount of aldosterone is produced.

Most common cause is a tumour of the adrenal gland

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41
Q

What is secondary hyperaldosteronism?

A

abnormally high aldosterone levels but caused by increased RAAS activity (e.g. Renal artery stenosis or juxtaglomerular cell tumours).

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42
Q

Clinical and biochemical presentation of Conn’s Syndrome

A
  • retention of Na+ and water => hypertension
  • increased K+ elimination => hypokalaemia
  • metabolic alkalosis

Muscle weakness and cramps/spasms
Paraesthesia
Polyuria
Headaches

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43
Q

Conn’s Syndrome - investigations

A

U&Es (hypernatraemia and hypokalaemia)

Aldosterone-Renin Ratio (would be raised)

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44
Q

Conn’s Syndrome - management

A

If due to a tumour - removed with surgery.

activity of the excess aldosterone will be blocked with aldosterone receptor antagonists (e.g. spironolactone).

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45
Q

Phaeochromocytoma

A

= a rare catecholamine-producing tumour of the chromaffin cells

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46
Q

10% rule for Phaeochromocytoma

A
  • 10% malignant
  • 10% extra-adrenal
  • 10% bilateral
  • 10% familial
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47
Q

Phaeochromocytoma - clinical features

A

Classic triad of symptoms:

  1. Episodic headache,
  2. Diaphoresis (excessive sweating)
  3. Tachycardia.

Features by system:

Cardiovascular – angina, palpitations, MI, arrhythmias

CNS – tremor, Horner’s syndrome, haemorrhage

Psychiatric – anxiety, panic, confusion, psychosis, hyperactivity

GI – diarrhoea, vomiting, abdominal pain

Other:
• Hyperglycaemia (stimulation of adrenoceptors leads to glycogenolysis and gluconeogenesis)
• Sweating, flushing, heat intolerance
• Pallor

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48
Q

Phaeochromocytoma - management

A

Surgery needed to remove tumour, using alpha- and beta-blockers during surgery to avoid crisis

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49
Q

Where is the body’s calcium?

A

99% is in the bone and combined with phosphate as hydroxyapatite.

Plasma calcium is either bound to albumin or as free ions (Ca2+).

Only free Ca2+ is biologically active.

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50
Q

Plasma calcium normal range

A

2.2 - 2.6 mmol/L

Maintaining calcium at optimum range ensures normal excitability of nerve and muscle.

Calcium is also required for clotting and complement cascades.

Reference ranges are specific to laboratories and reference range can be corrected for low/high serum albumin

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51
Q

parathyroid glands

A

4 pea-sized glands

just posterior to thyroid gland

have calcium and vitamin D receptors

chief cells of the parathyroid glands are responsible for secreting parathyroid hormone (PTH)

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52
Q

When is PTH secreted?

A

when plasma calcium levels are low

also in response to low vitamin D, or high phosphate levels

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53
Q

How does PTH work to increase calcium levels?

A
  1. Directly stimulating calcium reabsorption from bone, via increased osteoclast activity.
  2. Directly increasing renal tubular calcium reabsorption.
  3. Indirectly stimulating increased GI calcium absorption.
    => Via increased vitamin D activation in the kidney

also has a secondary effect of increasing renal phosphate excretion

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54
Q

From where is calcitonin secreted?

A

secreted by the parafollicular/”C” cells of the thyroid gland in response to increased plasma calcium levels.

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55
Q

Actions of calcitonin

A

acts to decrease plasma calcium levels, by antagonism of the effects of PTH on the bone.
=> Reducing osteoclast activity
=> Decreasing renal resorption of calcium and phosphate.

BUT the importance of calcitonin is controversial

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56
Q

Actions of Vitamin D

A

acts to sustain plasma calcium and phosphate levels by increasing their absorption from the GI tract

also required for normal bone formation

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57
Q

Sources of vitamin D

A

Endogenously it is synthesised in the skin, forming D3 (cholecalciferol).
=> Action of UV light on the precursor to vitD (7-dehydrocholesterol)

Exogenously it is ingested as D3/D2
=> D3 – found in fish, liver, dairy products
=> D2 – found in plants/fungi (less potent than D3)

Vitamin D3 is hydroxylated in the liver to form 25-hydroxycholecalciferol. There is a second hydroxylation in the kidney, to produce 1,25-hydroxycholecalciferol.

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58
Q

Vitamin D deficiency can occur in those with…

A

Inadequate sunlight exposure.
Malabsorptive conditions
Liver/kidney disease

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59
Q

Symptoms of hypercalcaemia

A

Mild hypercalcaemia (<3.0 mmol/L) is usually asymptomatic.

Symptoms in hypercalcaemia (>3.0 mmol/L):

  • tiredness, dehydration, depression, confusion
  • Renal colic, polyuria
  • potentially bone pain
  • abdominal pain
  • ectopic calcification

i.e. “Bones, stones, abdominal moans, psychiatric groans”

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60
Q

Signs of hypercalcaemia

A

Corneal calcifications – subtle yellow area of sclera bilaterally at region of muscle insertion.

Renal calculi

“Brown tumour” – highly vascular lytic lesion of the bone, occurring in hyperparathyroidism.

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61
Q

What are the causes of hypercalcaemia?

A
  1. Excessive PTH secretion
  2. Malignant disease of bone
  3. Excess action of Vit D
  4. Excessive calcium intake
  5. Drugs
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62
Q

What drugs can cause hypercalcaemia?

A

Thiazide diuretics,
VitD analogues,
lithium administration,
Vitamin A

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63
Q

What can cause excessive PTH secretion?

A

Primary hyperparathyroidism

Tertiary hyperparathyroidism – occurs in renal failure.

Ectopic PTH secretion

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64
Q

What malignant diseases can cause hypercalcaemia?

A

Myeloma – cancer of plasma cells in bone marrow.

Bone metastases

Lytic lesions in bone – due to secretion of osteoclastic factors by tumours

PTH-related protein

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65
Q

Clinical features of hypocalcaemia

A

Most patients with low calcium are asymptomatic.

Abrupt changes in calcium level are more likely to produce symptoms.

CNS - irritation, confusion, cognitive changes, seizures

PNS - muscle cramps, Chvostek’s sign, tetany, paraesthesia

Cardiac - bradycardia, arrhythmias, prolonged QT interval, hypotension

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66
Q

What is Chvostek’s sign?

A

when tapping over the facial nerve causes facial muscles to twitch

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67
Q

What are the causes of hypocalcaemia?

A
  1. Hypoparathyroidism
  2. Vitamin D deficiency
  3. Increased Phosphate levels
  4. Others:
    - Drugs – calcium chelators, bisphosphonates, drugs affecting vitamin D.
    - Acute pancreatitis
    - Acute rhabdomyolysis
    - Malignancy – tumour lysis
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68
Q

What can cause hypoparathyroidism?

A

Post thyroidectomy – not enough PT gland.

Destruction of PT gland – e.g. autoimmune or tumour infiltration.

Congenital deficiency

Idiopathic hypoparathyroidism

Severe hypomagnesaemia

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69
Q

what can cause VitD deficiency?

A

Problem with absorption
Problem with conversion – CKD/liver cirrhosis
Osteomalacia/rickets
Vit D resistance

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70
Q

Clinical reasoning for hypocalcaemia

A

Rule out low albumin – make sure the reported calcium level is adjusted for albumin level

Measure Vitamin D level

Measure PTH level

Consider tissue consumption of calcium

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71
Q

When can there be increased tissue consumption of calcium?

A

precipitation of calcium into extra-skeletal tissues occurs in pancreatitis

bone formation in some malignancies

rhabdomyolysis

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72
Q

what is diabetes mellitus?

A

a group of metabolic disorders characterised and identified by the presence of hyperglycaemia in the absence of treatment

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73
Q

T1DM - pathophysiology

A

Autoimmune disease

Antibodies targeted against the insulin-secreting beta cells of the islets of Langerhans in the pancreas.

Leads to cell death and inadequate insulin secretion.

Viral infections may trigger the autoimmune process, or can be idiopathic

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74
Q

T1DM - clinical presentation

A

Presents in childhood/adolescence, with a 2-6 week history of:

  • Polyuria – high sugar content in urine leading to osmotic diuresis
  • Polydipsia – due to resulting fluid loss.
  • Weight loss – fluid depletion and fat/muscle breakdown.

Diabetic Ketoacidosis (DKA) is also a common first presentation

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75
Q

T2DM - pathophysiology

A

“Insulin resistance” – associated with aging, genetic factors, obesity, high fat diets and sedentary lifestyle.

=> Peripheral resistance – tissues become insensitive to insulin.
=> Blood insulin levels are initially normal, or even increased to compensate for insensitivity to insulin.

Eventually pancreatic beta cells decompensate and can no longer produce excess insulin, leading to hyperglycaemia.

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76
Q

T2DM - clinical presentation

A

Onset may be over many months/years.

Classic triad of symptoms (polyuria, polydipsia, weight loss) may be present, but less noticeable than T1DM.

More common presenting features:
Lack of energy
Visual blurring – glucose-induced refractive changes.
Pruritis vulvae/balantis – due to candida infection.

In older patients, it may be the complications of diabetes that are the presenting feature

77
Q

What is metabolic syndrome?

A

combination of T2DM, central obesity, HTN

78
Q

Maturity Onset Diabetes of the Young

A

Genetic defect – autosomal dominant inheritance

Defects in beta-cell function.

Usually affects those <25 years of age.

Mimics T1DM

especially consider if drug treatment does not control the hyperglycaemia.

79
Q

What are some secondary causes of diabetes?

A

Pancreatic disease – CF, chronic pancreatitis, pancreatic carcinoma, pancreatic trauma/surgery.

Endocrine disease – Cushing’s disease, acromegaly, thyrotoxicosis, phaeochromocytoma.

Drug-induced – thiazide diuretics, corticosteroids, antipsychotics, antiretrovirals.

Congenital – insulin-receptor abnormalities, myotonic dystrophy, Friedrich’s ataxia.

Gestational diabetes

Infections – congenital rubella, cytomegalovirus, mumps

80
Q

Release of insulin

A

Insulin is released by beta cells when glucose levels rise after a meal.

Insulin acts upon glucose transporters (GLUTs).
=> GLUT2 – senses glucose in beta cells.
=> GLUT4 – insulin-mediated glucose uptake in skeletal muscle and adipose tissue.

81
Q

What are the effects of insulin?

A

anabolic effects - result in glucose being converted to:

  • glycogen in muscle,
  • glycogen and triglycerides in the liver
  • triglycerides in adipose tissue.
82
Q

what occurs to blood glucose during a fasting state?

A

insulin production is down-regulated and glucose stores are released through glucagon-mediated gluconeogenesis therefore preventing a hypoglycaemic state

83
Q

What occurs in the absence of insulin?

A

glucose cannot be taken up into the cells effectively, starving the cells of their most effective substrate to make energy

this signals gluconeogenesis, glycogenolysis and lipolysis as the body can no longer make use of the glucose that is available

84
Q

Diabetic Ketoacidosis

A

= absolute insulin deficiency resulting in hyperglycaemia in the presence of acidosis and ketosis.

medical emergency.
Develops over hours to 1-2 days.

Associated with T1DM, increasingly seen in T2DM

85
Q

what are the common causes of DKA?

A

1st presentation of diabetes
stress of infection/injury
poor compliance to insulin therapy

MI can also precipitate DKA in diabetic patients.

86
Q

Pathophysiology of DKA

A

Rapid lipolysis in glucose-starved tissues.
=> will be production of ketone bodies from the conversion of free fatty acids to acetoacetate

Hepatic glucose production via glycogenolysis and gluconeogenesis
=> worsening hyperglycaemia

Hyperglycaemia causes diuresis
=> hypovolaemia and dehydration - can result in AKI and electrolyte disturbances

ABG/VBG will show metabolic acidosis due to bicarbonate consumption by acidic ketone bodies

87
Q

Where can ketones be detected?

A

In the patients breath or urine

88
Q

What electrolyte disturbances are likely to be seen in DKA?

A

hyponatraemia

hypokalaemia

89
Q

How would the body compensate for the metabolic alkalosis

A

Hyperventilation to blow off CO2 to maintain acid base balance

Initially rapid breathing will give way to Kussmaul’s breathing (deep, laboured breathing) in DKA

90
Q

what are some symptoms of DKA?

A 
polyuria, polydipsia
generalised abdominal pain
confusion, drowsiness, 
blurred vision (due to the lens being affected)
in severe cases - coma.
91
Q

Management of DKA

A

A-E Assessment (+/- urgent care review)

intravenous insulin

IV fluids with electrolyte replacement

assessment for precipitating factors and treating these

92
Q

Hyperosmolar Hyperglycaemic State (HHS)

A

severe RELATIVE INSULIN DEFICIENCY resulting in hyperglycaemia leading to diureses (leading to volume depletion, dehydration and haemoconcentration) in the absence of severe ketosis and acidosis

Mortality is 10x more likely in HHS than DKA. HHS requires the same urgent treatment

93
Q

why does ketosis not occur in HHS?

A

even a small amount of insulin is enough to prevent ketosis

94
Q

What is HHS osmolality compared normal?

A 
Normal = 280-295 mmol/kg
HHS = >320 mmol/kg
95
Q

What are the criteria for diagnosing HHS?

A

Hypovolaemia (due to osmotic diuresis)

Marked Hyperglycaemia (serum glucose >30mmol/L)

No significant ketonaemia/ketonuria (serum ketone <3mmol/L)

No significant acidosis (pH >7.3, bicarb >15mmol/L)

Osmolality >320mmol/kg

96
Q

How are the macrovascular complications of diabetes caused?

A

Hyperglycaemia => formation of advanced glycation end products (AGE) on arterial endothelial cells and activation of inflammatory pathways

this results in formation of foam cells from macrophages in the intimal layer of arteries => exacerbates the process of atheroma formation

97
Q

Microvascular complications of diabetes

A

Coronary Artery Disease
Cerebrovascular Disease
Peripheral Vascular Disease

98
Q

Microvascular complications of diabetes

A

Retinopathy
Nephropathy
Sensorimotor peripheral neuropathy
Autonomic neuropathies

99
Q

How are the microvascular complications of diabetes caused?

A

AGE-activated biochemical pathways resulting in cellular damage caused by abnormal extracellular protein matrix accumulation and reactive oxygen species production.

100
Q

What is vital to prevent complications of diabetes and why?

A

It is vital to maintain normal and stable glycaemic control in diabetic patients as well as treat hypertension

Avoid chronic hyperglycaemia, wide glycaemic fluctuations and postprandial hyperglycaemia

101
Q

Diabetic foot complications

A

an interplay between both macro and microvascular pathophysiology

results in an acute localized inflammatory condition that may lead to varying degrees and patterns of bone destruction, subluxation, dislocation, and deformity

102
Q

In which populations is HbA1c inappropriate?

A

Those <18 years old.

Those acutely unwell (glucose temporarily raised in infection/steroid use)

Pregnancy

HIV, sickle cell disease, recent blood transfusion, liver disease, CKD, iron deficiency anaemia, B12/folate deficiency anaemia

103
Q

What test results are diagnostic of diabetes in a patient WITH symptoms/signs?

A

Fasting plasma glucose values of ≥ 7.0 mmol/L

Oral Glucose tolerance test (OGTT) – 2-hour plasma glucose ≥ 11.1 mmol/L

HbA1c ≥ 48 mmol/mol

Random blood glucose ≥ 11.1 mmol/L

104
Q

What test results are diagnostic of diabetes in a patient WITHOUT symptoms/signs?

A

Repeat testing is required as soon as possible for another raised value (ideally same test)

105
Q

Impaired Fasting Glucose (IFG)

A

Fasting plasma glucose = 6.1 mmol/L to 6.9 mmol/L.

Normal 2-hour plasma glucose (<7.8)

106
Q

Impaired Glucose Tolerance (IGT)

A

2-hour plasma glucose = 7.8 mmol/L to 11.0 mmol/L.

Normal fasting plasma glucose

107
Q

“Prediabetes”

A

HbA1c is not at the diabetic level, but not normal either (i.e. 42-47 mmol/mol)

108
Q

Management of T1DM

A

Basal bolus regime of insulin – long-acting insulin alongside boluses of short-acting insulin with their meals.

Structured education on hyperglycaemic effects of different foods – adjust bolus dose accordingly.

Dose Adjustment for Normal Eating (DAFNE) = a national programme for T1DM education.

Complex carbohydrates encouraged in moderation, with low glycaemic index foods preferred).

Increased fibre intake and 5 F&V are encouraged

109
Q

Lifestyle management of T2DM

A

Focus on healthy eating and reducing CV risk.

Smoking cessation is vital.

Moderation of alcohol consumption.

Weight loss

Exercise – 20-30 minutes of physical activity per day.

110
Q

Location of pituitary gland

A

located just below the hypothalamus

sits in the sella turcica, a small bony cavity at the base of the skull

“hangs” from the hypothalamus by a stalk called the infundibulum.

111
Q

What are the two distinct lobes of the pituitary gland?

A
  1. The Posterior Pituitary/“Neurohypophysis”

2. The Anterior Pituitary/“Adenohypophysis”

112
Q

Posterior pituitary

A

The axons of hypothalamic neurons, which pass down the pituitary stalk in the hypothalamic-hypophyseal tract and terminate in the posterior pituitary.

These axon terminals store and release Oxytocin and Vasopressin (ADH)

113
Q

Oxytocin

A

A neuropeptide produced in the hypothalamus.

Stored and released by the axon terminals in the posterior pituitary.

Involved in lactation, uterine contraction (and cervical dilatation), and bonding

114
Q

Vasopressin/ADH

A

A hormone produced in the hypothalamus. It is stored and released by the axon terminals in the posterior pituitary.

Released in response to hyperosmolality of extracellular fluid.

Two primary actions:

(i) Increases water reabsorption from the collecting duct of the nephrons
(ii) Causes arteriolar constriction, acting to raise blood pressure.

115
Q

Anterior pituitary

A

The hypothalamus exerts hormonal control over the anterior pituitary via secretion of various releasing hormones into the small hypophyseal portal vein that directly supplies the adenohypophysis.

The anterior pituitary synthesises and releases:

  • Thyroid Stimulating Hormone (TSH)
  • Adrenocorticotropic Hormone (ACTH)
  • Growth Hormone (GH)
  • Follicle-stimulating Hormone (FSH)
  • Luteinising Hormone (LH)
  • Prolactin (PRL)
116
Q

Thyroid Stimulating Hormone (TSH)

A
  • Release of Thyroid stimulating hormone (TSH) is mediated by the hypothalamus, via release of Thyrotropin Releasing Hormone (TRH).
  • The TSH then stimulates the release of T3 (Triiodothyronine) and T4 (Thyroxin) from the thyroid gland.
  • The Thyroid hormones (with T3 being the more active form) primarily act to increase the basal metabolic rate. They also affect protein synthesis, neural and long-bone development, and response to catecholamines.
117
Q

Adrenocorticotropic Hormone (ACTH)

A
  • ACTH acts within the Hypothalamic-Pituitary-Adrenal axis.
  • It is released in response to stress, under the control of hypothalamic secretion of Corticotropin-Releasing Hormone (CRH).
  • The main effect of ACTH is to stimulate production and release of cortisol in the adrenal cortex.
  • ACTH is cleaved into α-melanocyte-stimulating hormone after a short period of time.
118
Q

Growth Hormone (GH)

A
  • GH is a peptide hormone that stimulates growth, cell reproduction and cell regeneration.
  • It also stimulates IGF-1 production and increases glucose and free fatty acid concentrations.
  • Its release is triggered by Growth Hormone Releasing Hormone (GHRH), which is secreted by the hypothalamus.
  • Excess Growth Hormone production in adulthood causes Acromegaly
119
Q

Follicle-stimulating Hormone (FSH)

A
  • FSH is a gonadotropic hormone, synthesised and secreted by the anterior pituitary gland.
  • Its release is triggered by Gonadotropin-Releasing Hormone (GnRH), which is secreted by the hypothalamus.
  • It performs a role in regulating development, growth, puberty, and reproductive processes.
  • FSH works with Luteinising Hormone (LH) to regulate the reproductive system.
  • In both males and females, FSH stimulates maturation of germ cells.
120
Q

How does FSH influence maturation of germ cells in males?

A

FSH sustains spermatogenesis

121
Q

How does FSH influence maturation of germ cells in females?

A

FSH initiates follicular growth, with levels declining in the late follicular phase, which selects only the most advanced follicle to proceed to ovulation.

122
Q

Luteinising Hormone (LH)

A
  • LH is a gonadotropic hormone produced and secreted by the anterior pituitary.
  • It acts together with FSH to regulate the reproductive system.
  • Its release is triggered by Gonadotropin-Releasing Hormone (GnRH), which is secreted by the hypothalamus.
  • In both males and females, LH acts upon gonadal endocrine cells to produce androgens.
123
Q

How does LH cause androgen production in males?

A

In males, LH acts upon the Leydig cells in the testis, causing them to produce testosterone.

124
Q

How does LH cause androgen production in females?

A

In females, LH supports ovarian theca cells to provide androgens. The “LH surge” at the end of the follicular phase triggers ovulation.

125
Q

Prolactin (PRL)

A
  • Prolactin is secreted from the anterior pituitary in response to a number of stimuli including eating, mating, ovulation and breastfeeding.
  • It helps to regulate metabolism and the immune system.
  • Prolactin release is inhibited by secretion of dopamine, making it the only anterior pituitary hormone whose principle control is by inhibition.
  • The main effect of Prolactin is to stimulate milk production (lactation) by the mammary glands.
126
Q

Pituitary adenoma

A

= a benign tumour of the glandular tissue.

Benign but can be life-threatening due to mass effects or secretory actions.

Account for ~10% of intracranial tumours.

Classified by size, function and histology.

127
Q

Pituitary adenoma - size

A

<10mm = microadenoma

> 10mm = macroadenoma

128
Q

Pituitary adenoma - function

A

Functioning – hypersecretion or one or more pituitary hormones.

Non-functioning.

129
Q

Pituitary adenoma - histology

A
  1. Chromophobe – secrete prolactin/non-functioning.
  2. Acidophil – secrete GH or prolactin.
  3. Basophil – secrete ACTH
130
Q

Presentation of pituitary adenoma - local effects

A 
Headache
Bitemporal Hemianopia
Occular palsies
Hypothalamic disruption
Disconnection prolactinaemia
Hydrocephalus
CSF rhinorrhoea
Pituitary apoplexy
131
Q

What is bitemporal hemianopia?

How can it be caused by a pituitary tumour?

A

Both temporal visual fields are lost

due to compression of the tumour on the optic chiasm

132
Q

Disconnection prolactinaemia

A

Compression of pituitary stalk, preventing dopamine (which inhibits prolactin release) from reaching the anterior pituitary.

Disinhibition of prolactin release => hyperprolactinaemia

133
Q

Pituitary apoplexy

A

= acute haemorrhage/infarction of pituitary gland

Sudden headache, often associated with rapidly worsening visual field defect or diplopia.

Subsequent lack of essential hormones – most notably ACTH resulting in adrenocortical insufficiency

134
Q

How can pituitary tumours cause ocular palsies?

A

Compression/infiltration of CN III, IV, VI

135
Q

How can pituitary tumours cause hydrocephalus?

A

Compression of ventricles - interruption of CSF flow.

136
Q

Presentation of pituitary adenoma - systemic effects

A

Can result from either:

  1. Hormone excess (can be wither micro- or macroadenoma)
  2. Hypopituitarism/hormone deficiency (tends to be only macroadenoma)
137
Q

Hormone excess - prolactin

A

= Hyperprolactinaemia

Galactorrhoea/Amenorrhoea/Hypogonadism

138
Q

Hormone excess - GH

A

= Acromegaly

Headache/Sweating/Change in shoe size and/or ring size

139
Q

Hormone excess - ACTH

A

= Cushing’s

Weight gain/Bruising/Myopathy/Hypertension/
Striae/Depression

140
Q

Hormone deficiency - GH

A

Lethargy

141
Q

Hormone deficiency - ACTH

A

Lethargy, Postural Hypotension, Pallor, Hair loss

142
Q

Hormone deficiency - TSH

A

Signs of hypothyroidism

e.g. Lethargy, constipation, Dry Skin, Weight Gain

143
Q

Hormone deficiency - ADH

A

Diabetes insipidus (thirst, polyuria)

144
Q

Hormone deficiency - LH/FSH

A

Lethargy, Loss of Libido, Hair loss, amenorrhoea, infertility, erectile Dysfunction

145
Q

Hypothalamic-Pituitary-Thyroid Axis and its negative feedback loops

A

TRH secreted by hypothalamus

Stimulated pituitary to produce TSH

TSH is secreted into the systemic circulation

Increased serum T3 and T4

T3 and T4 then enter cells, where they bind to nuclear receptors and promote increased metabolic and cellular activity

Levels of T3 are sensed by receptors in the pituitary and the hypothalamus.
=> If they rise above normal, TRH and TSH production is suppressed, leading to reduced T3 and T4 secretion.
=> Peripheral T3 and T4 levels fall to normal.

146
Q

Effects of TSH

A
  1. Stimulates increased thyroidal iodine uptake by the thyroid, and the synthesis and release of thyroxine (T4) and triiodothyronine (T3)
  2. stimulation of the conversion of T4 to T3 (the more active hormone) in peripheral tissues
147
Q

‘Compensated Euthyroidism’

A

If the T3 and T4 levels are low (e.g. after thyroidectomy) increased amounts of TRH and TSH are secreted, stimulating the remaining thyroid to produce more T3 and T4.

Blood levels of T3 and T4 may be restored to normal, but there will be high TSH

148
Q

What are some other regulatory factors of thyroid hormone secretion?

A

COLD
=> mainly plays a role in the newborn moving out of the womb during birth
=> cooler temperature stimulates a massive increase in TRH, which then stimulates TSH levels and thereby the release of T3 and T4.
=> The resulting increased metabolism will lead to increased body temperature to cope with the cooler environment.
=> This effect is negligible in adults unless there is chronic exposure (e.g. living in the arctic).

STRESS
=> acute stress (i.e. trauma) has an inhibitory effect on thyroid hormones.
=> directly inhibits release of TRH.
=> also stimulates the release of somatostatin from the anterior pituitary, which inhibits TSH.
=> Inhibition of release of T3/T4 prevents the conversion of stored macromolecules into heat, which is not useful in stressful situations.

149
Q

What is hypothyroidism?

A

= low levels of T3 and T4

150
Q

What occurs in primary hypothyroidism?

Will there be a goitre?

A

= associated directly with the thyroid gland – the gland is not making enough hormones, so there is minimal activation of the negative feedback loop.

This leads to elevated TRH/TSH levels.

TSH is no longer able to stimulate release of T3 and T4, so the levels of the thyroid hormones remain low.

There should be a goitre, due to the elevated levels of TSH enlarging the cells of the thyroid gland.

151
Q

Causes of primary hypothyroidism

A

90% of all hypothyroidism is primary and is due to Hashimoto’s thyroiditis, an autoimmune condition.

152
Q

Hashimoto’s Thyroiditis

A

T-cells destroy the gland, alongside B-cell secretion of inhibitory TSH-receptor antibodies.

153
Q

What occurs in secondary hypothyroidism?

Will there be a goitre?

A

Hypothyroidism secondary to hypothalamic anterior pituitary failure causing low levels of TSH.

The lack of TSH means that there is a lack of stimulation for the production of T3 and T4.

There will not be a goitre and there may even be atrophy of the thyroid gland due to the low TSH levels.

154
Q

what occurs in hypothyroidism due to lack of dietary iodine?

Will there be a goitre?

A

= most common global cause of hypothyroidism i

Lack of iodine to synthesise T3 and T4

low levels of T3 and T4 leads to minimal activation of the negative feedback loop and therefore increased TRH and TSH.

Raised TSH causes enlargement of the thyroid gland = “simple, non-toxic goitre”

155
Q

How has iodine deficiency been prevented in the UK?

A

addition of iodine to salt

156
Q

Other causes of hypothyroidism

A

Drug-induced – e.g. anti-thyroid drugs, lithium, amiodarone.

Radioactive iodine therapy, surgery

Thyroid Hormone Resistance – when the body does not recognise thyroid hormones.

157
Q

Hypothyroidism - clinical features

A

Signs and symptoms are generally related to the decrease in BMR and overall metabolic activity

Tiredness
Weight gain
Dry skin, thinning hair
Hoarse voice, slow speech
Menstrual changes – dysmenorrhoea, oligomenorrhoea, menorrhagia, infertility.
Cold intolerance
Loss of appetite
Constipation
Bradycardia
Depression, confusion, poor memory, mental “slowness”
Myxoedema in some patients – a puffy, oedematous appearance of the face and eyelids

158
Q

Features of hypothyroidism in children

A

may not show classic symptoms but can grow poorly, perform poorly at school and may not develop at puberty.

Babies are assessed for congenital hypothyroidism (born with deficiencies in thyroid hormones) by TSH and T4 levels in the heel-prick test.

159
Q

Diagnosis of hypothyroidism

A

thyroid function test to measure T3, T4 and TSH.

  • Primary hypothyroidism – low T3 and T4, high TSH
  • Secondary hypothyroidism – low T3 and T4, low TSH

Thyroid autoantibodies:

  • Thyroid peroxidase antibodies – associated with hypothyroidism
  • Thyroglobulin antibodies – associated with Hashimoto’s thyroiditis.
160
Q

Which antibodies are associated with hashimoto’s thyroiditis?

A

Thyroglobulin antibodies

161
Q

Hypothyroidism - treatment

A

Hormone replacement therapy with levothyroxine for life.

Starting dose depends on the patient – start low and titrate up to clinical effect.

Reassess every 4-6 weeks to see if TSH goes down (however TSH unreliable if secondary cause)

162
Q

What is hyperthyroidism?

A

= high levels of T3 and T4.

163
Q

What are common causes of hyperthyroidism?

A

most common cause = Graves’ Disease (~70-80%)

Also

  • Solitary toxic nodule/adenoma
  • Toxic multinodular goitre
164
Q

What occurs in Grave’s Disease?

Will there be a goitre?

A

an autoimmune condition with thyroid-STIMULATING immunoglobulins, which bind to TSH-receptors and cause release of thyroid hormones.

There will be elevated T3 and T4, and low TSH (and TRH), as T3/T4 inhibit TSH/TRH release via negative feedback loops.

There will be a goitre due to thyroid-stimulating immunoglobulins stimulating growth of thyroid cells and causing enlargement

165
Q

What are uncommon/rare causes of hyperthyroidism?

A

Secondary hyperthyroidism (excess hypothalamic/anterior pituitary secretion)

De-Quervain’s thyroiditis

HCG-stimulated thyrotoxicosis

Neonatal thyrotoxicosis (due to maternal antibodies)

Iatrogenic causes – e.g. amiodarone, exogenous iodine.

Hypersecreting thyroid tumour

HCG-producing tumour
Hyperfunctioning ovarian teratoma

166
Q

What occurs in secondary hyperthyroidism?

Will there be a goitre?

A

excess hypothalamic/anterior pituitary secretion of TRH/TSH
E.g. a TSH-secreting pituitary tumour.

too much TSH leads to the overstimulation of the thyroid gland to produce T3 and T4.

There will be a goitre due to elevated TSH levels

167
Q

De-Quervain’s thyroiditis

A

= transient hyperthyroidism associated with inflammatory process (viral infection).

Fever, malaise, pain in the neck and tachycardia.

Can cause hypothyroidism after initial over-active phase.

Acute phase treatment is with aspirin and steroids may given in severe cases.

168
Q

Hyperthyroidism - clinical features

A

generally related to the associated increase in cellular/ tissue metabolism and enhancement of beta-adrenoceptor responses

Weight loss
Sweating and heat intolerance
Diarrhoea
Tachycardia (potentially AF in older patients, so TFTs are mandatory in a patient with new AF).
Hypertension
Tremor
Anxiety, emotional, irritability, Restlessness
Goitre
Pre-tibial myxoedema
Exophthalmos in 30% of patients with Graves’ disease

169
Q

Grave’s ophthalmopathy

A
  1. Lagophthalmos – inability to close eyes properly
  2. Exophthalmos – bulging eyes
  3. Opthalmoplegia
  4. Periorbital oedema

(more common in smokers)

170
Q

How can hyperthyroidism present in children?

A

increase in height and behavioural problems

171
Q

thyroid crisis/thyroid “storm”

A

= a rare presentation of hyperthyroidism

Generally occurs in periods of stress (e.g. infection, surgery, childbirth) in people with untreated/uncontrolled hyperthyroidism.

Hyperpyrexia, severe tachycardia, profuse sweating, confusion/psychosis.

If untreated – coma and death

172
Q

Hyperthyroidism - diagnosis

A

thyroid function test to measure T3, T4 and TSH:

  • Primary – increased T3 and T4, decreased TSH.
  • Secondary – increased T3 and T4, increased TSH

If Graves’ disease is suspected, you can test for thyroid-stimulating autoantibodies

173
Q

Hyperthyroidism - goal of treatment

A

= to achieve a normal euthyroid state and symptomatic relief from increased sympathetic activity.

174
Q

Hyperthyroidism - management

A
  1. Anti-thyroid drugs
  2. Radioiodine Therapy
  3. Surgery – Thyroidectomy
175
Q

Anti-thyroid drugs

A

Most commonly carbimazole in the UK - inhibits the iodination and coupling processes via TPO

Can use propylthiouracil (PTU) instead of carbimazole – PTU also blocks the deiodination of T4 to T3

It takes several weeks for a clinical response to occur

“Dose titration” or “block and replace” method

176
Q

Why does it take several weeks for anti-thyroid drugs to have a clinical response?

A

due to high colloid stores and long half-lives of hormones

177
Q

Side effects of carbimazole

A

Rashes and pruritus are common (2-25%)

RARE complication (0.1-1.2%) – neutropenia and agranulocytosis (bone marrow suppression).

If there is sensitivity to carbimazole, use propylthiouracil

178
Q

Anti-thyroid drugs - “dose titration”

A

only anti-thyroid drugs are used;

doses are adjusted to achieve normalisation of thyroid hormone production.

This may take several months

179
Q

Anti-thyroid drugs - “block and replace”

A

anti-thyroid drugs at a very high concentration to completely block all thyroid hormone production, and then thyroxine replacement is given

quicker but normally more side effects

180
Q

What is given in combination with anti-thyroid drugs for management of hyperthyroidism?

A

Non-selective beta-blockers

given in combination with anti-thyroid drugs to reduce actions of catecholamines

provide rapid symptomatic relief of tremors, palpitations and anxiety (within 4 days), while waiting for the anti-thyroid drugs to have an effect

181
Q

Radioiodine therapy for hyperthyroidism

A

Suitable for all patients – except during pregnancy and breast feeding.

Iodine is taken up by the thyroid gland and localised radiation destroys the gland.

first-line for older patients with nodular goitres and hyperthyroidism, or when thyrotoxicosis recurs after anti-thyroid drug therapy.

Hypothyroidism may occur if too many cells are destroyed.

There is no increased risk of thyroid malignancy

182
Q

When is a thyroidectomy used?

What are the risks?

A

not frequently used:

  • Used when there is severe thyrotoxicosis associated with a large goitre or concern about tumour development
  • Used when there are obstructive symptoms (e.g. effects on swallowing).

Surgical risks – bleeding, infection, risks from general anaesthesia.

Specific risks – tracheal compression, damage to recurrent laryngeal nerve, transient hypocalcaemia.

Hypothyroidism may result if too much of the thyroid gland is removed.

183
Q

Goitre

A

Enlargement of the thyroid gland.

  • Usually painless, can be tender if acute cause.
  • Large goitres may cause dysphagia or difficulty breathing due to compression.

Can be diffuse, multi nodular, or solitary nodule.

184
Q

Diffuse goitre

A

= smooth, soft enlargement with no apparent cause;

Puberty, pregnancy
Grave’s / Hashimoto’s
Iodine deficiency
Sub-acute thyroiditis
Anti-thyroid drugs, Lithium, Iodine excess, Amiodarone
185
Q

Nodular Goitre

A

MULTINODULAR
Toxic multinodular goitre
Subacute thyroiditis

SOLITARY NODULE 
Follicular adenoma
Benign nodule
Thyroid malignancy (most important DDx)
Lymphoma 
Metastasis

INFILTRATION
TB, Sarcoid

186
Q

Examination of neck lump

A

Observation and palpation to describe:

  • Size
  • Shape
  • Consistency (hard, soft, smooth, firm)
  • Mobility (mobile or feels adhered to surrounding tissue)
  • Can the lower border be defined on palpation?
    => (If lower border cannot be defined, may indicate retro-sternal extension, which may increase likelihood goitre may affect breathing/swallowing.)
187
Q

Thyroid malignancy

A

uncommon

90% of cases present as thyroid nodules
=> The rest present as cervical lymphadenopathy or metastases (lung, bone, hepatic, cerebral).

Can be: papillary, follicular, medullary cell, anaplastic, lymphoma

188
Q

Diagnosis of thyroid malignancy

A

thyroid ultrasound and biopsy by fine needle aspiration (FNA)

189
Q

Presentation of thyroid malignancy

A

Solitary thyroid lump

Voice changes - due to recurrent laryngeal nerve being affected

Cervical lymphadenopathy (usually deep cervical or supraclavicular)

Difficulty swallowing, breathing or persistent cough (rarely)

General signs: weight loss, shortness of breath.

Symptoms of metastatic disease

CP1 (12 decks)

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