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Endocrinology- endocrine pathology, clinical investigation and presentations Flashcards

1
Q

Endocrine

A

Glands which secrete hormones or other products directly into the blood.

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2
Q

Main endocrine glands

A
  • Hypothalamus/Pituitary- brain
  • Thyroid- brain to neck
  • Parathyroid- behind thyroid
  • Pancreas- abdomen
  • Adrenal- on top of kidneys
  • Ovaries/testicles
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3
Q

The pituitary gland

A

• Controls most glands in body

Hormones of pituitary gland- pituitary gland functionally divided into two lobes

Anterior pituitary-produces various hormones
Posterior pituitary- stores various hormones

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4
Q

Anterior pituitary produces?

A

– Growth hormone (GH)
• For skeletal growth
– Adrenocorticotrophic hormone (ACTH)
• Stimulates the adrenals to produce steroids
– Gonadotrophins (FSH and LH)
• Stimulate the testicles or ovaries to produce sex hormones
– Thyroid stimulating hormone or thyrotrophin (TSH)
• Stimulates the thyroid to produce thyroid hormones
– Prolactin (PRL)
• Stimulates breast milk production

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5
Q

Posterior pituitary- stores what hormones produced in hypothalamus (doesn’t produce them)?

A

– Antidiuretic hormone (ADH)
• Stimulates water reabsorption by kidneys
– Oxytocin
• Helps uterine contractions during labour

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6
Q

How is pituitary controlled?

A

The anterior pituitary gland is under the control of the hypothalamus:

  • Corticotrophin releasing hormone (CRH): stimulates ACTH secretion
  • Growth hormone releasing hormone (GHRH): stimulates GH secretion
  • Thyrotropin releasing hormone (TRH): stimulates TSH secretion
  • Gonadotrophin releasing hormone (GnRH): stimulates FSH and LH secretion
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7
Q

What hormone is under the inhibitory effect of the hypothalamus?

A

Prolactin

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8
Q

How pituitary hormones switched off?

A
  • Cortisol switches off ACTH and CRH
  • Growth hormone switches off GH and GHRH
  • Thyroid hormones switch off TSH and TRH
  • Sex hormones switch off FSH/LH and GnRH
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9
Q

Glands not controlled by pituitary

A 
•	Adrenal medulla- medulla not controlled by pituitary, (adrenal cortex is controlled by the pituitary)
–	Produce adrenaline and noradrenaline
•	Parathyroid
–	Controls calcium levels
•	Pancreas -Controls sugar levels
•	Gut hormones
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10
Q

Thyroid gland composed of what?
Structure?
What cells do they contain?

A
  • Midline isthmus (just below the cricoid cartilage)
  • Right lobe
  • Left lobe
  • Thyroid cells arranged in follicles and produce thyroid hormones
  • The thyroid also contains C cells, which produce calcitonin (calcium metabolism)- not under control of pituitary gland- not only parathyroid glands control calcium so do the C cells
  • Thyroid hormones interact with their receptors in various organs, thereby regulating gene expression and aspects of organ function
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11
Q

How is calcium metabolism controlled?

A

Calcium metabolism

• Controlled by 4 parathyroid glands sitting behind the thyroid

Other organs involved in calcium metabolism

  • Kidneys- Calcium excretion and production of active vitamin D
  • Gut-Absorption of calcium
  • Bone- Storage of calcium
  • Thyroid- C cells produce calcitonin
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12
Q

Adrenal glands and structure

A
  • Medulla inside
  • Cortex outside

Composed of:

– Adrenal cortex, 90% of the gland and produces:
• Corticosteroids (cortisol)
• Androgens (male hormones)
• Mineralocorticoid (aldosterone)
– Adrenal medulla, 10% of the gland and produces:
• Catecholamines (adrenaline, noradrenaline and dopamine)

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13
Q

Are catecholamine and mineralocorticoid secretion controlled by pituitary?

A
  • Catecholamine secretion not controlled by pituitary (related to blood pressure)
  • Mineralocorticoid secretion not controlled by pituitary (related to renin-angiotensin system, which controls blood pressure)
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14
Q

Testes- structure

A

In adults, testes found in scrotum, except in a minority with testicular maldescent (improper or incomplete descent of a testis into the scrotum).

Composed of:
• Interstitial or Leydig cells-produce testosterone
• Seminiferous tubules-made up of germ cells producing sperms
• Sertoli cells -help in sperm production and produce inhibin

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15
Q

Clinical abnormalities of various glands- Hormonal over-secretion- primary and secondary

A

Hormonal over-secretion:
• Primary = problem with original gland e.g. thyroid
• Secondary= problem pituitary - e.g. too much TSH secreted by pituitary causing over T3/T4

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16
Q

Clinical abnormalities of various glands- Hormonal under-secretion- primary and secondary

A
  • Primary = problem with original gland

* Secondary = problem pituitary

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17
Q

Clinical abnormalities of various glands-Tumour/nodules

A

Tumour/nodules in the gland without affecting hormone secretion- normal hormone secretion-

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18
Q

Basic testing for hormonal abnormalities

A

Static tests: these can diagnose abnormalities of thyroid and sex glands.

Stimulation tests: for suspected hormonal under-secretion (gland failure) where static test NOT ENOUGH (i.e. results are equivocal)- as range so big so can’t decide if test is abnormal.

Suppression tests for some hormonal over-secretion.

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19
Q

Disease of endocrine glands

A

• Over-secretion (usually benign tumours)
• Under-secretion: gland destruction due to
– Inflammation (including autoimmune conditions)
– Infarction
– Other
• Tumours/nodules with normal hormone production

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20
Q

Prolactin over secretion causes, clinical presentation and diagnosis

A

• Due to pituitary tumour secreting prolactin (prolactinoma)
• Clinical presentation
– Galactorrhoea (breast milk production)
– Amenorrhoea (an abnormal absence of menstruation) in women and sexual dysfunction in men
– Headaches and visual field problems in large tumours. Large tumour leads to optic nerve compressed.

Diagnosis of prolactinoma- static test enough and pituitary MRI

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21
Q

Mildly raised prolactin causes and treatment

A

May be due to
• Sexual intercourse
• Nipple stimulation
• Stress
• Large number of drugs (including antipsychotics and antidepressants)
• Non-functioning pituitary tumour (compressing the hypothalamus

Treatment of prolactinomas- only over-secreting pituitary tumours that can be treated medically as they very rarely require surgical intervention

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22
Q

Growth hormone over secretion

A

• In childhood or adolescent growth hormone excess results in:
– Excessive growth spurt and increased size of feet and hands
– If left untreated growth hormone excess leads to gigantism, most serious consequence of disease
• In adults, growth hormone excess affects:
– Skin, soft tissue and skeleton
– Acromegalic (abnormal growth) face
– Wide and large hands/feet
– Increased sweating

This disease is called acromegaly.

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23
Q

Growth hormone excess- what test needed?

A
  • For diagnosis of growth hormone excess static not enough
  • Suppression tests necessary
  • Glucose given, followed by GH measurements at different time points (in healthy individuals, glucose suppresses GH production so not in those with over-secretion)
  • Imaging is necessary to confirm the presence of pituitary tumour -treatment- surgical removal, radiotherapy and medical therapy also needed as surgery not always remove whole tumour
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24
Q

Cushing’s syndrome

A

• Rare affecting around 1-2/100 000
• May be due to:
– Pituitary secreting ACTH tumour (Cushing’s disease)
– Adrenal tumours secreting cortisol
– Cancers producing ACTH (such as lung cancers)

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25
Q

Clinical presentation of Cushing’s syndrome

A 
•	Growth arrest in children (stop growing)
•	Typical facial appearance 
–	Round (moon-like) face
–	Acne
–	Hirsutism (increase in hair production)
•	Fat redistribution
–	Truncal obesity
–	Thin extremities
•	Skin abnormalities
–	Thin skin and easy bruising
–	Striae (groove) on abdomen
•	Complications
–	Hypertension
–	Diabetes mellitus
–	High risk of infections
–	Poor wound healing
26
Q

Test for Cushings

A
  • Static tests not enough and suppression tests are required to diagnose cortisols
  • Dexamethasone suppression test used to confirm failure to suppress endogenous cortisol production- take a steroid a measure cortisol levels- Cushing’s cortisol is detectable, no Cushing’s undetectable
  • How do you differentiate between adrenal and pituitary Cushing’s?- ACTH detectable- cancer producing tumour/problem with pituitary- if problem with adrenal ACTH undetectable
27
Q

Treatment of Cushing’s syndrome

A 
•	Pituitary and adrenal:
–	Surgery
–	Radiotherapy and/or medical treatment may also be required in pituitary disease
•	Cancer related
–	Treat original cancer
28
Q

Thyroid hormone overproduction

A

Primary defect in thyroid gland itself primary hyper/hypothyroidism.
Defect in pituitary gland it is secondary hyperthyroidism.

May be due to: 
–	Primary hyperthyroidism
•	Very common
–	Secondary hyperthyroidism (pituitary TSH secretion)
•	Rare
29
Q

What is hyperthyroidism due to? What are the causes?

A
  • Due to autoimmune disease
  • Prevalence around 2% in the female population
  • 10 times more common in women

Causes of hyperthyroidism

•	Graves’ disease 
–	Autoimmune condition 
•	Toxic nodule or toxic MNG 
•	Thyroiditis
•	Drug induced (amiodarone)
•	Rarities
30
Q

What are the clinical presentations of hyperthyroidism?

A
  • Hyperactivity, irritability, insomnia
  • Heat intolerance and increased sweating
  • Palpitations
  • Weight loss despite overeating
  • Menstrual problems
31
Q

Signs of thyrotoxicosis

A

– Hand tremor
– Increased sweating
– Fast pulse

32
Q

• Inspection of the thyroid

-Enlarged= Goitre

A
  • Smooth: Graves’ disease
  • Nodular: toxic nodule(s)
  • Tender: thyroid inflammation
33
Q

Extrathyroidal signs

A

Thyroid eye disease

34
Q

Investigations of extrathryoidal signs

A

• Thyroid blood test:
– Raised thyroid hormone
– Suppressed TSH
• So a static test is enough

35
Q

Treatment for thyroid eye disease

A

• Anti-thyroid drugs (rarely suppresses white blood cell production)
• Radioactive iodine
– Destroys the thyroid gland
• Surgery

36
Q

Growth hormone under secretion/deficiency

A 
•	Children
–	Failure of growth
•	Adults
–	Nothing
–	Tiredness
–	Depression
37
Q

Growth hormone under secretion/deficiency- tests

A

Stimulation test

  • Glucagon stimulation test
  • Insulin stress test (lowers blood glucose, stressing the body and forcing growth hormone secretion- (if doesn’t go up, have growth hormone deficiency)
38
Q

Treatment for hormonal under secretion

A

Treatment- Growth hormone replacement
– Injections
– Expensive

39
Q

Steroid under-secretion due to what?

A

May be due to:
– Adrenal failure
– Pituitary failure

40
Q

Steroid under-secretion clinical presentation

A

– Failure to grow in children
– Severe tiredness in adults
– Dizziness due to low blood pressure
– Abdominal pain, vomiting and diarrhoea

41
Q

Steroid under-secretion test

A

• Stimulation test:
– Synacthen test (giving ACTH) if primary adrenal failure is suspected
• GST or IST if secondary adrenal insufficiency is suspected

42
Q

Steroid under-secretion treatment

A

Replace the missing hormone
• Tablets
• Cheap

In case this diagnosis is suspected, cortisol should be given even before results of investigations are available.

43
Q

Hypothyroidism

A

• Very common condition particularly in older ladies
• Primary hypothyroidism: thyroid failure and inability to produce thyroid hormones
– Usually autoimmune in nature
– Can be drug induced
• Secondary hypothyroidism: failure to produce TSH (rare).
– Usually part of complete pituitary failure

44
Q

Diagnosis and treatment of hypothyroidism

A

• Diagnosis
– Easy: static test of thyroid function
• Treatment
– Thyroid hormone replacement (tablets, cheap)

45
Q

Sex hormone deficiency

A 
•	Primary
–	Males: testicular failure
–	Females: ovarian failure
•	Secondary
–	Pituitary failure
46
Q

Sex hormone deficiency- presentation

A 
•	Males
–	Erectile dysfunction
–	Reduced libido
•	Females
–	Menstrual abnormalities (amenorrhoea)
47
Q

Amenorrhoea

A

Amenorrhoea- where period stops

•	Very common presentation where period stops
•	Can be due to:
–	Uterine problems
–	Ovarian problems
–	Pituitary problems
–	Hypothalamic problem
48
Q

Diagnosis and treatment for sec hormone deficency

A

• Diagnosis
– Static tests are enough:
• Testosterone (males), oestradiol (females), thyroid, prolactin
• FSH/LH levels
• Treatment
– Hormone replacement therapy (testosterone for males; oestradiol/progesterone for females)
– Pituitary hormone replacement

49
Q

Pituitary failure due to what?

A

Pituitary failure may be due to:
• Large tumour
• Infarction
• Other

50
Q

Pituitary independent endocrine abnormalities

A

Increased parathyroid hormone production may be due to:
– Primary hyperparathyroidism- high PTH- nothing to do with pituitary gland
– Cancers- increase ACTH- Cushing’s syndrome
– Drugs
– Other

51
Q

Pituitary independent endocrine abnormalities- clinical presentation

A

Hypercalcaemia causes:
• Thirst and passing too much urine (osmotic symptoms)
• Constipation
• Abdominal pain

52
Q

Classes of hormones that act inside the cell

A

Steroid Hormones

Derived from cholesterol

Thyroid Hormones

Derived from tyrosine within the protein thyroglobulin

53
Q

How do steroid hormones get to the nucleus?

A

Steroid hormones cross the cell-membrane

Some meet receptor in the cytosol and go into the nucleus.

Some go straight into nucleus where receptor waiting for them.

Bind to intracellular receptor in nucleus or in the cytosol.
If the free receptor was in the cytosol the hormone receptor complex moves to the nucleus.

54
Q

Nuclear hormone receptors

A

Amino terminus- have a transcription regulation domain that interact with other proteins that regulate transcription

Next they have a DNA binding domain with ‘zinc fingers’ that bond to the DNA helix.

Loops bind to the DNA and zinc atoms/fingers. These assist steroid hormone receptors which co-ordinate with the zinc and bind into place.

Nuclear hormone receptors have a hormone binding domain at the carboxyl terminus which makes them specific.

Domain in middle is dimerization domain.
These type of receptors don’t work by themselves they go round in pairs and the dimerization domain in the middle results in two of the binding proteins, two of the nuclear factors joining together and forming dimeric structure.

55
Q

How do dimerisation domains bind?

A

Have domain binds transcription factors at one end, zinc finger domain, dimerisation domain and recognition domain.

Two hormone binding factors acting in opposite directions.

56
Q

Breast cancer- how oestrogen receptors effect

A
  • There are two closely related versions of the oestrogen receptor, termed ERα and ERβ
  • Healthy breast tissue normally expresses more ERβ than ERα
  • Some types of breast cancer strongly express ERα
  • Oestrogen promotes the rapid division of ERα- positive breast cancer cells

• ER-positive breast cancers (ER+) can be detected by staining sections of tumour biopsies with antibodies against the oestrogen receptor. (ERα positive cells are stained brown).

57
Q

How can breast cancer be inhibited?

A

• The growth and spread of these cancers can be inhibited by administering anti-oestrogen drugs such as tamoxifen

58
Q

How is thyroxine formed?

A

Tyrosine molecules on the protein thyroglobulin are iodinated. The iodotyrosine molecules in thyroglobulin are cross-linked. The thyroxine molecule is then cut out of the thyroglobulin.

59
Q

Thyroid receptor hormones how are they different to nuclear hormone receptors?

A
  • There are two separate genes for thyroid hormone receptors
  • The two receptors have slightly different actions to one another
  • This recognition sequence, the TRE (thyroid hormone response element) is in front of various genes of energy metabolism and heart function that are switched on by thyroid hormones
  • In addition, thyroid hormone is a key regulator of development in some species.
60
Q

Are thyroid receptors always bound to the DNA?

A

The difference is the thyroid receptors are always bound to the DNA, when pick up hormone change in receptor, results in transcription of mRNA and protein being made. Steroid hormone receptors pick up the steroid and then bind to the DNA.

61
Q

How are thyroid hormone receptors bound to the DNA?

A

In the nucleus, thyroid hormone receptors (TR) are bound to thyroid hormone response elements (TRE) in the DNA. In the absence of hormone, the hormone receptors bind repressor molecules that switch off transcription.

In the presence of hormone, the co-repressor leaves, a coactivator binds to the receptor and transcription starts.

The binding of T3 causes the release of proteins that switch off (repress) transcription and the binding of proteins that activate transcription.

62
Q

What is the dominant negative effect?

A

V-erbA binds to the TRE but can’t activate transcription and inhibits the efficient binding of TR.

IMS (13 decks)

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