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Y3 IWB > PATHOLOGY- Endocrine disorders > Flashcards

PATHOLOGY- Endocrine disorders Flashcards

1
Q

Define cell-signalling

A

Cells communicating in the body to co-ordinate/integrate functions

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2
Q

How are signalling molecules, produced by one cell type, detected by another

A

Via receptors

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3
Q

Where are the receptors used to detect signalling molecules found

A

Cell surface
Inter-cellular

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4
Q

What are the 2 purposes of the receptors

A

Alter gene expression
Alter cell behaviour/function

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5
Q

What 3 mechanisms can signalling occur via

A

Autocrine
Paracrine
Endocrine

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6
Q

What is autocrine signalling

A

Signalling molecule acts on the same cell

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7
Q

What is paracrine signalling

A

Signalling molecule secreted into interstitial fluid, acting on nearby cells

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8
Q

What is endocrine signalling

A

Signalling molecule secreted into blood stream, acting on distant cells throughout the body

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9
Q

How are body-wide metabolic processes maintained

A

Via regulatory molecules

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10
Q

What are endocrine glands

A

Hormone-secreting specialised tissues

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11
Q

What is the endocrine system

A

System of hormone-secreting specialised tissues

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12
Q

How do hormones travel to target cells distant to site of production

A

Usually via blood

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13
Q

Explain the general process of the hypothalamic-pituatry axis

A
  1. Hypothalamus produces releasing hormones which act on the pituitary gland
  2. Pituitary gland produces trophic hormones which are released in to the blood stream and can act on specific target glands
  3. Endocrine glands receives signal from the trophic hormones. It then produces its end product OR acts directly on the cell themselves e.g growth hormone
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14
Q

Most hormones are produced by what

A

Hypothalamus

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15
Q

What is the pituitary known as

A

Conductor of endocrine orchestra

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16
Q

What is the pituitary
Where is it
How much does it weigh
What is its role

A

Small organ
Base of the brain
0.5-1g
Essential control over endocrine system

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17
Q

What are the 2 distinct parts of the pituitary

A

Anterior pituitary (adenohypophysis, 75-80%)
Posterior pituitary (neurohypophysis)

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18
Q

What is the anterior pituitary (adenohypophysis)

A
  • Stimulated by hypothalamic ‘releasing hormones’
  • Releasing hormones pass via “portal” circulation to anterior pituitary
  • Secretes six trophic hormones into systemic bloodstream
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19
Q

What is the Posterior pituitary (neurohypophysis)

A

Neural structures directly from hypothalamus which release 2 trophic hormones, ADH and oxytocin

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20
Q

What is the difference between the anterior and posterior pituitary

A

In posterior, the signal comes through modified neurons
In anterior, the signal is mediated through the blood stream

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21
Q

What 2 ways is the endocrine system regulated

A

Hormones (produced in specific circumstances)
Negative feedback

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22
Q

What is negative feedback

A

Produced hormones ‘feedback’ onto pituitary / hypothalamus to regulate secreting / trophic hormone production, therefore precisely control hormone production

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23
Q

List pituitary dysfunctions

A

Hyperpituitarism
Hypopituitarism
Local mass effects

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24
Q

What is hyperpituitarism caused by

A

Excess production of trophic hormones

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25
Q

List examples of where you can see hyperpituitarism

A

Hyperplasias
Adenomas,
Carcinomas
Secretion of pituitary-like hormones from non-pituitary tumours
Hypothalamus disorders

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26
Q

What is hypopituitarism caused by

A

Deficient production of trophic hormones

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27
Q

List examples of where hypopituitarism Is present

A

Ischaemia
Surgery
Radiation
Inflammatory disorders
Mass effect of non-functional pituitary tumours
Post-partum ischaemic necrosis (Sheehan syndrome)

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28
Q

Examples of how local mass effects can case pituitary dysfunction

A
  • Optic nerve (chiasm) - visual field defects
  • Raised intra-cranial pressure (^ICP)
  • Pituitary apoplexy = haemorrhage causing sudden enlargement = emergency!
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29
Q

What is the most common cause of hyperpituitarism

A

Pituitary adenomas (most commonly anterior lobe tumours)

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30
Q

What are pituitary adenomas classified by

A

Cell type
Hormones produced (if functional)

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31
Q

Whe do non-functional tumours tend to present and what size are they

A

Present later and are usually larger

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32
Q

Why do non functional tumours present later and are usually larger

A

Functional tumours will be producing abnormal amounts of their trophic hormones so they will be causing some biochemical abnormality, this will give some clinical manifestation when the tumour is much smaller but still producing these chemicals. Whereas nonfunctional tumours have to produce their symptoms by effects of their size

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33
Q

Who do pituitary adenomas usually present in

A

Most commonly adults, 35-60 years

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34
Q

What do the signs/symptoms of pituitary adenomas depend on

A

Hormones produced and/ or mass effect

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35
Q

What is the most common pituitary adenoma

A

Lactotroph pituitary adenoma (30%)

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36
Q

What are lactotroph pituitary adenomas

A

Prolactin producing tumours

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37
Q

What are lactotroph pituitary adenomas also known as

A

Prolactinomas

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38
Q

What symptoms does Lactotroph pituitary adenoma cause

A

Amenorrhea, galactorrhoea, loss of libido, infertility

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39
Q

Is lactotroph pituitary adenoma more easily diagnosed in men or women

A

Women

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40
Q

What is the second most common pituitary adenoma

A

Somatotroph pituitary adenoma

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41
Q

What are Somatotroph pituitary adenoma

A

Growth-hormone producing tumours

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42
Q

what symptoms do somatotroph pituitary adenomas cause

A

Gigantism in children
Acromegaly in adults

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43
Q

What is corticotroph pituitary tumours

A

Adrenocorticotrophic hormone (ACTH) producing tumours

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44
Q

What do corticotroph pituitary adenomas cause

A

Adrenal hypersecretion of cortisol
Hypercortisolism (Cushings syndrome)

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45
Q

What is the thyroid
Where is is located
What level is it on the vertebra

A

Bi-lobed organ with isthmus
Below, anterior to larynx, close to the trachea
Level of 5th to 7th vertebra

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46
Q

How does the thyroid work
What does this process need to work

A
  1. Hypothalamus send a signal via TRH through to the anterior pituitary which acts on the thyrotrophic cells which produces thyrotropin/TSH
  2. TSH passes into bloodstream and interacts with receptors on thyroid follicular cells/FCs
  3. This signals thyroid follicular cells to produce the thyroid hormones T3/T4

Iodine

  1. Thyroid hormones stored by TG in colloid
  2. When needed and released in to the blood stream by follicular cells, T4 is converted in to T3 (T3 much more active)
  3. Thyroid hormones binds nuclear thyroid receptor in variety of tissues
  4. This increases carbohydrate/lipid catabolism
  5. Also increases protein synthesis which in turn increases basal metabolic rate (BMR)
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47
Q

What is TRH

A

Thyrotropin releasing hormone

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48
Q

What is thyrotropin also known as

A

Thyroid stimulating hormone

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49
Q

Where are thyroid hormones such as T3/T4 stored

A

Stored by thyroid glands in colloid

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50
Q

How are thyroid hormones released from the glands in to the blood stream

A

Colloid is broken down

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51
Q

List the CLINICAL implications of thyroid disorders and what they are caused by

A
  • Hyperfunction (hyperthyroidism)
  • Graves disease, toxic nodules, toxic adenoma
  • Hypofunction (hypothyroidism)
  • Hashimotos, endemic goitre, iatrogenic (surgery/drugs)
  • Structural change (entire gland)
  • Graves disease, diffuse / nodular goitre
  • Structural change (nodules)
  • Dominant nodule in MNG, tumours
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52
Q

List the aetiology of thyroid disorders and what they’re caused by

A

Autoimmune
* Graves, Hashimotos

  • latrogenic
  • Surgery, radiation, drugs
  • Metabolic
  • Endemic goitre, diffuse / nodular goitre
  • Neoplastic
  • Tumours (adenoma, carcinomas)
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53
Q

Similar aetiologies can cause different what

A

Clinical features

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54
Q

What are the clinical features of hypothyroidism

A

Weight gain
Muscle weakness
Constipation

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55
Q

What are the clinical features of hyperthyroidism

A

Weight loss
Tachycardia
Anxiety

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56
Q

What diseases cause hypothyroidism

A

Hashimotos thyroiditis
Endemic goitre (I dericiency)
Iatrogenic

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57
Q

What diseases cause hyperthyroidism

A

Graves disease
Toxic nodules / tumours

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58
Q

What does goitre mean

A

Enlarged thyroid

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59
Q

What are the effects of euthyroid

A

Diffuse / nodular hyperplasia (goltre)
Tumours

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60
Q

What is euthyroid

A

Thyroid levels are normal but structural changes caused

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61
Q

What is Graves’ disease also known as

A

Diffuse hyperplasia

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62
Q

What is the most common cause of hyperthyroidism

A

Graves’ disease

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63
Q

What is graves diseases
What does it cause

A

Autoimmune disorder

Autoantibodies against multiple proteins especially TSH receptor in the thyroid. This activates TSH receptor on thyroid stimulating T3/T4 production. This causes T3/T4 levels to be high with low TSH levels (negative feedback on HPA)

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64
Q

Whta is the most common autoantibody inn Graves’ disease

A

Thyroid-stimulating immunoglobulin (TS|)

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65
Q

What are the clinical manifestations of Graves’ disease

A

Symmetrically diffusely enlarged thyroid
Follicles hyperplasticity causing papillary projections
Pale colloid

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66
Q

What are the clinical features of Graves’ disease

A
  • Hyperthyroidism (as above)
  • Enlargement of thyroid
  • Infiltrative ophthalmopathy (characteristic for Graves)
    • Activated T cells cytokines -> fibroblast proliferation, secretion of ECM
    • Infiltration of retro-orbital space - protrusion of eyeball (exophthalmos)
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67
Q

How do you diagnose Graves’ disease

A

High T3/T4, low TSH, autoantibodies

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68
Q

How do you treat Graves’ disease

A
  • Radioactive iodine
  • Drugs
  • Surgery
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69
Q

What is the most common cause of hypothyroidism

A

Chronic lymphocytic thyroiditis / Hashimotos

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70
Q

What is Chronic lymphocytic thyroiditis / Hashimotos

What does it cause

A

Autoimmune disorder

Autoantibodies against thyroglobulin / thyroid peroxidase (diagnostic)

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71
Q

What are the effects of Chronic lymphocytic thyroiditis / Hashimotos

A

Glands usually enlarged
Lymphocytic infiltration with germinal centre formation
Destruction of thyroid follicular epithelial cells
“Hurthle cell change” - reactive metaplasia due to chronic injury

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72
Q

What are the clinical features of Chronic lymphocytic thyroiditis / Hashimotos

A
  • Hypothyroidism
  • † risk of lymphoma / papillary carcinoma
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73
Q

How do you diagnose Chronic lymphocytic thyroiditis / Hashimotos

A

Low T3/T4, high TSH, TPO autoantibodies

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74
Q

What is the treatment for Chronic lymphocytic thyroiditis / Hashimotos

A
  • T3/Т4 supplement
  • Some have surgery if atypical features
75
Q

What is diffuse and modular hyperplasia/goitre

A

Result of long term proliferative stimuli e.g. iodine deficiency, genetics, idiopathic

76
Q

What causes thyroid hyperplasia

A

High TSH due to low T3/74

77
Q

Initially what happens in diffuse and modular hyperplasia

What happens later

What is the theory that causes these changes

A

Initially diffuse enlargement (goitre)
Enlargement of thyroid leading to variable degrees of nodularity (multinodular goitre)
Variable responses in thyroid follicular epithelial cells

78
Q

Why are most patients initially euthyroid

A

Result of hyperplasia

79
Q

What can large dominant nodules be mistaken for clinically

A

Thyroid carcinoma

80
Q

What can happen to nodules in nodular hyperplasia

A

May become active/hyper secretory

81
Q

What may develop with large nodules

How is this treated

A

Tracheal compression or dysphasia

Surgery

82
Q

Who do the majority of thyroid tumours affect

83
Q

The majority of thyroid tumours are what type

A

Papillary carcinoma

84
Q

Give an example of a brining thyroid tumour

A

follicular adenoma

85
Q

Give 4 examples of malignant thyroid tumours

A
  • Papillary carcinoma (85%)
  • Follicular carcinoma (5-10%)
  • Medullary carcinoma (<5%) - rare = don’t worry!
  • Anaplastic carcinoma (<5%) - rare = don’t worry!
86
Q

What is a follicular adenoma
How do they usually present
Who do they mostly affect
Are they functional/nonfunctional

A

Benign tumour if follicular epithelial cells
Usually solitary
Women
Non-functional with a small proportion being functional/toxic

87
Q

List the pathological features of a follicular adenoma

A

Solitary lesion
Small thyroid follicles (microfollicles)
Surrounded by thick capsule

88
Q

How do you know whether a follicular adenoma is benign

A

Only if there is no invasion of capsule or blood vessels
Hence can only call FA if lesion completely examined

89
Q

What are the clinical features of follicular adenomas

A
  • Solitary painless nodule
  • Incidental on examination or radiology
  • Toxic nodules (rarely) produce thyroid hormones
  • Defined by radioactive iodine uptake
90
Q

What is the treatment for follicular adenomas

A
  • Excision (needed to exclude carcinoma)
  • Carcinoma looks similar but defined by invasion through capsule / BVs
91
Q

What is the most common form of thyroid cancer

A

Papillary thyroid carcinoma

92
Q

What is the ratio of females to males that have papillary thyroid carcinoma

93
Q

What age are people affected by papillary thyroid carcinoma

A

Wide age range
Mean 43 years

94
Q

what is the prognosis for papillary thyroid carcinoma

A

Generally good prognosis (5 year survival 85-95%)

95
Q

What is the underlying cause of papillary thyroid carcinoma

A

Radiation exposure
Mutations of RAS or BRAF

96
Q

What does papillary thyroid carcinoma look like

A
  • Ill defined, infiltrative
  • Some circumscribed / encapsulated
  • May be cystic
  • Characteristic nuclear features - diagnostic
97
Q

To make a diagnosis of papillary thyroid carcinoma what do you need

A

Nuclear features
- tightly packed cells
- very open clear nuclei
- wrinkled and irregular membranes
- pseudo inclusions

98
Q

What different patterns may be seen in papillary thyroid carcinoma

A
  • “Papillary” structures = “classical” variant
  • Lots of small follicles = follicular variant
99
Q

What are the clinical features of papillary thyroid carcinoma

A
  • Painless mass
  • Incidental on examination or radiology
  • May present with LN mets
  • Hoarse voice / dysphagia if RLN involved
100
Q

What is the treatment of papillary thyroid carcinoma

A
  • Excision
  • Radio-iodine (e.g. large tumour, mets, invasion outside thyroid)
101
Q

What is follicular thyroid carcinoma

A

Malignant tumour of thyroid epithelial cells showing NO PTC NUCLEAR FEATURES

102
Q

which is more common papillary or follicular thyroid carcinoma

A

Papillary thyroid carcinoma

103
Q

who does follicular thyroid carincoma affect

104
Q

What age does follicular thyroid carcinoma affect people

A

Older onset (40-60yrs)
V rare in children

105
Q

what are the risk factors for follicular thyroid carcinoma

A

Radiation
Iodine deficiency

106
Q

what does the prognosis of follicular thyroid carcinoma depend on

A

Presence/extent of vascular invasion

107
Q

What is the effect if there is and isn’t vascular invasion in follicular thyroid carcinoma

A

No vi= excellent prognosis
Vi= prone to metastases

108
Q

What causes follicular thyroid carcinoma

A

RAS gene mutations

109
Q

What is the difference between a follicular adenoma and follicular thyroid carcinoma

A

Follicular adenoma
- micro follicular lesion
- has capsule
- no invasion beyond capsule or blood vessel invasion

Follicular thyroid carcinoma
- microfollicular lesion
- capsular invasion and or vascular invasion => malignant

110
Q

What are the clinical features of follicular thyroid carcinoma

A
  • Painless mass
  • Incidental on examination or radiology
  • Hoarse voice / dysphagia if RLN involved
  • LN mets very rare (contrast PTC)
  • Can present with distant mets (bone #, lung nodule)
111
Q

What is the treatment for follicular thyroid carcinoma

A

Excision
Radio-iodine (e.g. large tumour, mets, invasion outside thyroid)

112
Q

How many parathyroid glands are there and where are they

A

Four
One on upper / lower poles of each thyroid lobe (usually)

113
Q

What are parathyroid glands made up of

A

Mixture of chief cells, oxyphil cells and fat (fat increases with age)

114
Q

How is parathyroid gland function controlled

A

Function controlled by free calcium in blood (not via pituitary)

115
Q

What happens when there is a decrease in calcium

A
  1. Sensed by parathyroid
  2. Increases PTH levels
  3. Decreases osteoblast activity and increases osteoclast activity
  4. This increases calcium levels
116
Q

What else do the parathyroid glands act on

117
Q

What do most parathyroid abnormalities result in

A

Hyperparathyroidism (increase in PTH)

118
Q

What are the 3 forms of Hyperparathyroidism

A
  1. Primary Hyperparathyroidism
  2. Secondary Hyperparathyroidism
  3. Tertiary Hyperparathyroidism
119
Q

What is primary Hyperparathyroidism

A

autonomous overproduction of PTH, usually resulting from an adenoma or hyperplasia of parathyroid tissue

120
Q

What is secondary Hyperparathyroidism

A

compensatory hypersecretion of PTH in response to prolonged hypocalcemia, most commonly from chronic renal failure, malabsorption, vitamin D deficiency

121
Q

What is tertiary Hyperparathyroidism

A

persistent hypersecretion of PTH, even after the cause of prolonged hypocalcemia is corrected (e.g., after renal transplant)

122
Q

What is one of the most common endocrine disorders

A

Primary Hyperparathyroidism

123
Q

what is primary Hyperparathyroidism a cause of

A

Hypercalcaemia

124
Q

What are the causes of primary Hyperparathyroidism

A
  • Parathyroid adenoma (85-95%) - by far most common cause
  • Primary hyperplasia (5-10%)
  • Parathyroid carcinoma (rare ~1%)
125
Q

Who does primary Hyperparathyroidism affect

A

Usually adults
Females 4:1

126
Q

How is primary Hyperparathyroidism usually found

A

Incidentally by high calcium levels

127
Q

What is the most common cause of primary hyperthyroidism

A

Parathyroid adenoma

128
Q

What is the cause of parathyroid adenomas

A

Most sporadic, unknown cause
Molecular defects and mutations
Familial syndromes

129
Q

What does parathyroid adenoma look like histopathalogically

A
  • Usually solitary solid nodule of cells
  • Commonly chief cells but can see oxyphil cells
  • Well circumscribed, thin capsule, adjacent B/G parathyroid
  • Remaining glands small / supressed
130
Q

What are the clinical features of Hyperparathyroidism

A
  • Most diagnosed incidentally by ^Ca on blood tests -> most asymptomatic
  • Clinical manifestations of incPTH/ inc Ca -> “painful bones, renal stones, abdominal groans, and psychic moans”
  • Classical symptoms rarely seen
131
Q

What is the treatment for parathyroid adenomas

A

Extraction

132
Q

What is parathyroid carcinoma

A

malignant tumour derived from parathyroid cells

133
Q

What % of primary Hyperparathyroidism is caused by parathyroid carcinoma

134
Q

What are the symptoms of parathyroid carcinoma

A

Symptoms as per hypercalcamia

135
Q

What are the features of parathyroid carcinoma

A
  • Fibrous bands
  • Vascular invasion
  • Invasion of background tissue
136
Q

How do you treat parathyroid carcinoma

137
Q

Where are the adrenal glands in the body

A

Just above both kidneys

138
Q

What are the adrenal glands also known as

A

Suprarenal glands

139
Q

what are the 2 regions of the adrenal glands

A

Outer cortex
Inner medulla

140
Q

What does the cortex in adrenal glands produce

A
  • Glucocorticoids (mainly cortisol)
  • Mineralocoricoids (mainly aldosterone)
  • Sex steroids (mainly ostrogens / androgens)
141
Q

What does the medulla in adrenal glands produce

A

Catecholamines (mainly adrenaline/NA)

142
Q

Most adrenal defects are…

143
Q

What is hypercortisolism also known as

A

Cushing’s syndrome

144
Q

what is hypercortisolism

A

Syndrome (collection of signs and symptoms) due to increased levels of glucocorticoids which result in metabolic / abnormalities

145
Q

What is the most common cause of hypercortisolism

A

Exogenous steroids administration

146
Q

What is endogenous cushings

A

Cushings as a result of abnormalities in the endocrine system

147
Q

What are the 3 types of endogenous cushings and what are their effects

A
  • Pituitary Cushings = Pituitary adenoma (70%) + †ACTH - †cortisol (Cushing’s disease)
  • Adrenal Cushings = Cortisol via adrenal adenoma / carcinoma, hyperplasia etc. -> dec in ACTH
  • Paraneoplastic Cushings = †ACTH by tumours e.g. small cell lung cancer
148
Q

What are the clinical features of Cushing’s syndrome due to

A

Glucocorticoid excess

149
Q

What are the symptoms fo Cushing’s syndrome

A

Weight gain
Mental changes

150
Q

How would you manage cushings if it was a pituitary cause

A

Surgery
Radiotherapy

151
Q

How would you manage cushings if it was caused by other tumours

152
Q

what is the prognosis is cushings is left untreated and why

A

Poor prognosis due to hypertension

153
Q

What is hypocortisolism known as

A

Addisons disease

154
Q

what is hypocortisolism

A

Loss of entire adrenal cortex - inability to produce cortisol & aldosterone

155
Q

What is affected by hypocortisolism

A

Blood pressure
Blood sugar regulation
Water/sodium balance

156
Q

When is cortisol normally produced

A

During times of stress

157
Q

How common is Addison’s disease and who does it affect more

A

Rare
Females

158
Q

What is the vast majority of Addison’s caused by

A

Autoimmune disease

159
Q

What are less common causes of addisons

160
Q

What is the classic triad seen in Addison’s disease

A

Triad of hyperpigmentation, postural hypotension and hyponatraemia.

161
Q

How is Addisons disease treated

A

Long term steroid replacement

162
Q

If Addisons is left undiagnosed what can happen

A

Can be fatal

163
Q

Why is hyperpigmentation seen in Addisons disease

A

Decreased cortisol levels causes increases in CRH/ACTH
ACTH stimulates melanocytes to produce melanin causing hyperpigmentation

164
Q

What occurs in 80-90% of cases with Addisons

A

postural hypotension

165
Q

How is Addisons treated

A

Replacement steroids

166
Q

Why may you need additional steroids during procedures in cases with Addisons

A

dental treatment -> hypotensive -> “Addisonian crisis” (medical emergency)

167
Q

What is hyperaldosteronism

A

Excessive production of aldosterone which can result in hypertension

168
Q

what are they 2 types of Hyperaldosteronism

A

primary and secondary

169
Q

what is primary Hyperaldosteronism caused by

A

bilateral hyperplasia or solitary tumour “Conn’s syndrome”

170
Q

What is secondary Hyperaldosteronism caused by

A

due to RAS activation e.g. renal vascular disease (e.g. stenosis)

171
Q

In Hyperaldosteronism, what is the effect of increased aldosterone levels

A

Na retention, K loss, H20 retention -> |[K] & hypertension

172
Q

What does the management of Hyperaldosteronism depend on

A

depends on cause e.g. surgery for aldosterone secreting tumour

173
Q

What are hyperplasias

174
Q

What is phaeochromocytoma

A

Rare tumour of catecholamine cells of adrenal medulla

175
Q

Why is phaeochromocytoma clinically significant

A

As its a treatable cause of hypertension

176
Q

What is hypertension a result of

A

Increased secretion of adrenaline/noradrenaline

177
Q

What is the rule of 10 in regards to phaeochromocytoma

A
  • 10% extra-adrenal
  • 10% bilateral
  • 10% malignant
178
Q

What pattern does Phaeochromocytoma have

A

Nested ’zenballen’ pattern

179
Q

How is Phaeochromocytoma treated

A

surgical excision

180
Q

What are multiple endocrine neoplasia syndromes

A
  • Inherited autosomal dominant diseases
  • Proliferative / neoplastic diseases affecting multiple endocrine glands
181
Q

What are the 3 forms of multiple endocrine neoplasia syndromes

A

MEN-1
MEN-2

182
Q

What is MEN-1
What do pts with this present with

A

Mutation of MEN1 tumour suppressor gene
- Parathyroid hyperplasia / adenomas
- Pancreatic tumours (gastrin / insulin producing)
- Pituitary adenomas (most commonly prolactin)

183
Q

What is MEN-2
What do pts with this present with

A

Gain of function of RET oncogene
- 2A = Medullary carcinoma, phaeochromocytoma, parathyroid hyperplasia
- 2B = As above but no parathyroid lesions, extra-endocrine lesions seen

Y3 IWB (31 decks)

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