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Histopathology > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

How can you separate endocrine pathologies?

A
  • Over/under production of hormones

- Mass lesions

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2
Q

Describe the pituitary gland

A

It has an anterior and posterior aspect

Anterior:

  • Epithelial cells
  • Blood supply by pituitary portal system

Posterior:
- Nervous cells

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3
Q

How is the anterior pituitary controlled? Name the hormones involved and their actions.

A

It is mainly controlled by the hypothalamus:

  • Thyrotrophin releasing hormone STIMULTES Thyroid stimulating hormone
  • Dopamine INHIBITS prolactin
  • Corticotrophin releasing hormone STIMULATES ACTH
  • Growth hormone releasing hormone STIMULATES growth hormones
  • Gonadotrophin releasing hormone STIMULATES gonadotrophin
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4
Q

What are the causes of hyperpituitarism?

A

Usually, a result of a functional tumour

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5
Q

What are the different types of functional adenomas of the pituitary, and the epidemiology surrounding them.

A
  • Prolactin cell (20-30%)
  • ACTH (10-15%)
  • Gonadotrophin (10-15%)
  • Growth hormone (5%)
  • TSH (1%)

Up to 20% of all pituitary adenomas are non functioning (cause hypopituitarism)

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6
Q

What are the clinical affects of the different functional adenomas of the pituitary?

A

Prolactin cell:

  • Amenorrhoea
  • Galactorrhoea
  • Reduced libido
  • Infertility

Growth hormone:

  • Gigantism (if children) or Acromegaly (if adults)
  • Diabetes mellitus, HTN and congestive cardiac failure

Corticotrophin:
- Cushing’s syndrome

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7
Q

What are the causes of hypopituitarism?

A
  • Non functioning pituitary adenomas
  • Ischaemic necrosis (Sheehan’s syndrome, DIC, Sickle cell)
  • Ablation or radiation
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8
Q

What are the symptoms of hypopituitarism?

A
  • Growth failure
  • Amenorrhoea, infertility, reduced libido, impotence
  • Hypothyroid, hypoadrenal
  • No lactation (if breastfeeding)
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9
Q

What syndromes are associated with over/under regulation of the posterior pituitary?

A

Posterior pituitary produces:

  • ADH
  • Oxytocin

ADH is important:

  • DI if under production
  • SIADH if over production (brain trauma)
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10
Q

What local affects can a mass lesion have at the pituitary?

A

Optic chiasm compression:
- Bitemporal hemianopia

Signs of raised ICP:
- Papilloedema, headaches

Obstructive hydrocephalus:
- Brain stem compression

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11
Q

What is the thyroid gland’s main role? How is it controlled? What other roles does the thyroid have?

A

It produces thyroxine.

TSH from the pituitary stimulates the thyroid to take up iodine and it uses iodine to transform thyroglobulin to T3 and T4.

The thyroid also has parafollicular cells which produce calcitonin, which stimulate calcium reabsorption by bone.

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12
Q

What is goitre? What are the types?

A

This is an enlarged thyroid; it can be:

  • Non-toxic
  • Toxic
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13
Q

What are the causes of non-toxic goitre?

A
  • Iodine deficiency
  • Ingestion of substances which interfere with hormone syntheses (brassicas)
  • Hereditary illnesses
  • Female puberty
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14
Q

What is thyrotoxicosis? What are the causes of this?

A

It is a hyperthyroid state, causing a hypermetabolic state.

Primary causes:

  • Grave’s disease
  • Multinodular goitre
  • Adenomas
  • Thyroiditis

Secondary causes:
- TSH secreting pituitary adenoma

Non-thyroid:

  • Ovarian teratoma (ectopic TSH)
  • Factitious thyrotoxicosis
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15
Q

What is grave’s disease? What are the classical features? What is the epidemiology surrounding it? What are its associations?

A

It is an autoimmune disease mainly powered by antibodies to the TSH receptor on the thyroid, causing a hyperthyroid state.

It classically has a triad of thyrotoxicosis, exophthalmos (40%) and pretibial myxoedema.

It presents in younger adults, more commonly in females.

It is associated with other autoimmune conditions:

  • SLE
  • Pernicious anaemia
  • T1DM
  • Addison’s
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16
Q

Give causes of hypothyroidism

A

Primary:

  • Post-ablative therapy
  • Autoimmune (Hashimoto’s)
  • Iodine deficiency
  • Congenital

Secondary:
- Pituitary/hypothalamic insufficiency

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17
Q

What is hashimoto’s thyroiditis? What are the classical features? What is the epidemiology surrounding it?

A

This is an autoimmune condition which causes a hypothyroid state.

It classically presents with a painless enlargement of the thyroid, and symptoms of hypothyroid disease. On histology, there are lymphoid cells, with germinal centres.

It is common in those aged 45-65, with a much higher risk in females.

18
Q

What features of nodules may make it more suspicious of neoplasm?

A
  • Solitary
  • Solid
  • Younger patient
  • Male patient
  • Cold (does not function)
19
Q

How can you differentiate the neoplasms of the thyroid? What features may assist in this?

A

Neoplasms of the thyroid can be divided into:

  • Adenomas
  • Carcinomas

Adenomas are well circumscribed lesions, within a fibrous capsule. There will be no invasion into the thyroid.

20
Q

What types of thyroid carcinoma are there? How common are they? What is the pathogenesis involved?

A

There are 4 types:

  • Papillary (75-85%)
  • Follicular (10-20%)
  • Medullary (5%)
  • Anaplastic (<5%)

They are usually as a result of radiation, or MEN (2A and 2B)

21
Q

Describe the epidemiology, cytology and features of the four thyroid cancers.

A

Papillary:

  • Any age
  • Optically clear nuclei, psammoma bodies
  • Non-functional
  • 10 year survival is 90%

Follicular:

  • Middle ages
  • Follicular morphology
  • Well demarcated
  • Metastasises to bone, lung and liver

Medullary:

  • Parafollicular cells
  • 80% are sporadic, 20% are MEN2 associated (younger patients)
  • Calcitonin is deposited as amyloid (Congo red stain)

Anaplastic:

  • Elderly patients
  • Very aggressive, death within a year
  • Commonly metastasises
22
Q

What are the parathyroid glands. How are they controlled?

A

They are found in the poles of the thyroid gland. They are controlled by calcium levels, responding to low levels by secreting parathyroid hormone.

23
Q

What are the effects of parathyroid hormone?

A

Increase calcium concentration by:

  • Increase osteoclast activity
  • Increased renal calcium reabsorption
  • Increased vitamin D activation
  • Increased renal phosphate excretion
  • Increased GI calcium absorption
24
Q

What are the main causes of hyperparathyroidism?

A
  • Solitary adenoma (80-90%)
  • Hyperplasia (10-20%) [sporadic or MEN 1 and 2A
  • Carcinoma (<1%)
25
Q

What are the symptoms of primary hyperparathyroidism?

A

All as a result of high calcium:

  • Thinning bone cortex and fractures
  • Renal stones
  • GI disturbances
  • CNS and psychiatric disturbances
  • Polyuria and polydipsia

‘Bones, stones, groans and moans’

26
Q

What is the cause of secondary hyperparathyroidism?

A

A chronic low calcium

- Chronic renal failure

27
Q

What are the main causes of hypoparathyroidism?

A
  • Surgical ablation
  • Congenital
  • Autoimmune disorders
28
Q

What are the symptoms of hypoparathyroidism?

A
  • Neuromuscular irritability (spasms, tetany)
  • Cardiac arrhythmias
  • Fits
  • Cataracts
29
Q

Describe the adrenal glands

A

Triangular glands that sit on the top of the kidney.

They have a medulla [secrete noradrenaline and adrenaline] and a cortex. The cortex is split into 3 parts:

  • Zona glomerulosa (most superficial) [secrete aldosterone]
  • Zona fasciculata [secrete glucocorticoids]
  • Zona reticulata (most deep) [secretes glucocorticoids and androgens]
30
Q

Describe what can happen in hyperadrenalism

A
  • Cushing’s syndrome (excess glucocorticoids)
  • Hyperaldosteronism
  • Virilising syndromes (excess androgens)
31
Q

What are the features of Cushing’s syndrome?

A
  • Hypertension and weight gain
  • Truncal obesity
  • Moon face and buffalo humps
  • Cutaneous striae
32
Q

What are the causes of Cushing’s syndrome

A
  • Long-term steroid prescriptions
  • ACTH adenoma
  • Hyperplasia of adrenal cortex
  • Adrenal solitary neoplasm
  • Ectopic ACTH (SCC lung tumour)
33
Q

What are the causes of hyperaldosteronism? What are the main features?

A

Primary:

  • 35% by adenoma (Conn’s syndrome)
  • 60% by hyperplasia

The main features are hypertension and hypokalaemia

34
Q

What are the main causes of high androgen levels?

A
  • Neoplasms (usually carcinomas)

- Congenital adrenal hyperplasia

35
Q

Describe congenital adrenal hyperplasia

A
  • Autosomal recessive inheritance
  • Defects in cortisol biosynthesis
  • High ACTH and high androgens
  • Affects childhood
36
Q

What are the causes of adrenal insufficiency?

A

Primary:

Acute:

  • Steroid cessation
  • haemorrhage (neonates)
  • Sepsis with DIC (Waterhouse-Friderichson Syndrome)

Chronic (Addison’s disease):

  • 75-90% autoimmune
  • TB/HIV
  • Tumour metastasis (lung, breast)
  • Amyloid/fungus/haemochromatosis/sarcoid

Secondary:
- Low ACTH (pituitary adenomas or infarction)

37
Q

What are the adrenal neoplasms?

A

Adenomas:

  • Benign
  • Cushing’s disease or Conn’s syndrome

Carcinomas:

  • Rare
  • Large
  • Cause virilising syndromes (androgens)
38
Q

What are the neoplasms of the adrenal medulla?

A
  • Phaeochromocytoma

- Neuroblastoma (childhood)

39
Q

Describe a phaeochromocytoma? What are the features?

A

It results in a very high catecholamines (noradrenaline and adrenaline) in the circulation. The main feature is surgically-correctable hypertension.

The main features follow the rule of 10s:

  • 10% are genetic (MEN 2A and 2B; von Hippel-Lindau; Sturge Weber)
  • 10% are bilateral
  • 10% are malignant
  • 10% are outside the adrenal gland (paragangliomas)
40
Q

What is multiple endocrine neoplasia? Describe their tumours. What are the types, and what organs do they affect/what do these types cause?

A

A genetic condition causing multiple neoplasia in endocrine organs.

Tumours:

  • Appear at younger ages
  • Arise in >1 organ
  • Multifocal within an organ
  • Preceded with hyperplasia
  • More aggressive than sporadic tumours

They types are 1, 2A and 2B:
1 (3Ps): Pituitary, Pancreas and Parathyroid
2A (2Ps, 1M): Parathyroid, Phaeochromocytoma, Medullary thyroid cancer
2B (1P; 2Ms): Phaeochromocytoma; Medullary thyroid cancer; Mucocutaneous neuromas (and marfanoid)

Histopathology (21 decks)

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