Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine / Chemical Pathology > Histo: Endocrine disease > Flashcards

Histo: Endocrine disease Flashcards

1
Q

What types of cell are the anterior and posterior pituitary made up of?

A

Anterior = epithelial cells (derived from developing oral cavity)

Posterior = nerve cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the blood supply to the anterior pituitary?

A

Pituitary portal system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do the nerves that make up the posterior pituitary originate?

A

Paraventricular nucleus
Supraoptic nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 symptoms catergories of pituitary disease?

A
  • Hyperpituitarism symptoms - due to excess hormone secretion
  • Hypopituitarism symptoms - due to deficiency of hormone secretion
  • Mass effect symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the most common cause of hyperpituitarism?

A

Functional adenoma

  • Orignally classified by morphology of predominant cell type (e.g. acidophil, basophil, chromophobe)
  • Now classified by hormone produced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the most common type of pituitary adenoma?

A

Prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a microadenoma?

A

A pituitary adenoma with a diameter < 1 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Outline the clinical features of prolactinoma.

A
  • Amenorrhoea
  • Galactorrhoea
  • Loss of libido
  • Infertility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the clinical manifestations of growth hormone adenomas?

A
  • Gigantism (prepubertal children)
  • Acromegaly (adults)
  • Diabetes
  • Muscle weakness
  • Hypertension
  • Heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What disease is caused by corticotroph cell adenomas?

A

Cushing’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List some causes of hypopituitarism.

A
  • Non-secretory pituitary adenoma
  • Ischaemic necrosis
  • Iatrogenic (surgery, radiotherapy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the most common cause of ischaemic necrosis of the pituitary gland?

A

Sheehan’s syndrome - the pituitary enlarges during pregnancy and is more susceptible to ischaemia. A post-partum haemorrhage may induce ischaemia.

Other causes: DIC, sickle cell anaemia, shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List some clinical features of hypopituitarism.

A
  • Growth failure in children (pituitary dwarfism)
  • Gonadotrophin deficiency - amenorrhoea and infertility (women); impotence and loss of libido (men)
  • Hypothyroidism and hypoadrenalism
  • Prolactin deficiency - failure of post-partum lactation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which hormones are produced by the posterior pituitary?

A

ADH and oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which conditions involve ADH?

A

Diabetes insipidus

SIADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List some consequences of the local mass effect of pituitary tumours.

A
  • Bitemporal hemianopia (optic chiasm)
  • Headaches (raised ICP)
  • Obstructive hydrocephalus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the histological appearance of the thyroid gland.

A
  • Arranged into follicles with a small amount of stromal tissue between them
  • They are lined by epithelial cells and have a large amount of colloid in the middle
  • Parafollicular cells are found between the follicles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the physiological response of the thyroid gland to TSH.

A
  • Stimulating of TSH receptors leads to pinocytosis of the colloid by the thyroid follicular cells and promotes the conversion of thyroglobulin into T3 and T4
  • Release of thyroid hormones into the circulation results in a rise in basal metabolic rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which hormone do parafollicular cells produce?

A

Calcitonin - this promotes the absorption of calcium by the skeletal system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a non-toxic goitre?

A

Enlargement of the thyroid gland without overproduction of thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the most common cause of non-toxic goitre?

A

Iodine deficiency - leads to impaired thyroid hormone synthesis

Other causes involves hereditary enzyme defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

List some primary and secondary causes of thyrotoxicosis.

A

Primary

  • Graves’ disease
  • Toxic multinodular goitre/adenoma
  • Thyroiditis

Secondary

  • TSH-secreting pituitary adenoma (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List some causes of thyrotoxicosis that are not associated with the thyroid gland.

A
  • Struma ovarii - ovarian teratoma with ectopic thyroid hormone production
  • Factitious thyrotoxicosis - exogenous thyroid hormone intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the most common cause of endogenous hyperthyroidism?

A

Grave’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which antibodies are often seen in Graves’ disease?

A
  • TSH receptor
  • Thyroglobulin (TG)
  • Thyroid peroxidase (TPO)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the effect of TSH receptor-stimulating antibodies.

A

They stimulate thyroid hormone release and increase proliferation of the thyroid epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the triad of Grave’s?

A
  • Hyperthyroidism
  • Infiltrative ophthalmopathy - exopthalmos (40%)
  • Infiltrative dermopathy - pretibial myoedema (minority)

Also associated with other autoimmune diseases e.g. SLE, T1DM, pernicious anaemia, Addison’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

List some primary and secondary causes of hypothyroidism.

A

Primary

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

Secondary

  • Pituitary or hypothalamic failure (uncommon)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the presentation of Hashimoto’s thyroiditis.

A
  • Painless enlargement of the thyroid gland
  • Symptoms of hypothyroidism.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the histology of Hashimoto’s thyroiditis.

A
  • There are lots of lymphoid cells with germinal centres
  • The epithelial cells become large with lots of eosinophilic cytoplasm (Hurthle cells)
31
Q

Types of thyroid neoplasms:

A
  • Adenoma - benign tumours of follicular epithelium
  • Carcinoma - uncommon (accounts for < 1% of solitary thyroid nodules)
32
Q

List some features of a thyroid lump that would be suggestive of neoplasia.

A
  • Solitary rather than multiple
  • Solid rather than cystic
  • Younger patients
  • Male more than female
  • Less likely to take up radioiodine (cold nodules)
33
Q

How thyroid neoplasms diagnosed?

A
  • Fine needle aspiration cytology
  • Histology
34
Q

List some features of adenomas of the thyroid gland.

A
  • Usually solitary
  • Well circumscribed
  • Well-formed capsule
  • Small proportion will be functional
35
Q

List the four types of thyroid cancer in order of decreasing prevalence.

A
  • Papillary (80%)
  • Follicular (15%)
  • Medullary (5%)
  • Anaplastic (< 5%)
36
Q

What are some risk factors for thyroid cancer?

A
  • Genetic factors (e.g. MEN)
  • Ionisation radiation (mainly papillary)
37
Q

What is the histological features of papillary thyroid cancer?

A

Nuclear features

  • Optically clear nuclei (Orphan Annie Eye)
  • Intranuclear inclusions

There may also be psammoma bodies (round calcifications)

38
Q

What are some clinical features of papillary thyroid cancer?

A
  • Non-functional
  • Presents with painless neck lump
  • Can metastasize
  • 90% 10 year survival
39
Q

Where does papillary thyroid cancer tend to metastasise to?

A

Cervical lymph nodes

40
Q

Where does follicular thyroid cancer tend to metastasise?

A

Lungs, bone and liver (via the bloodstream)

41
Q

Which cells are medullary thyroid cancers derived from?

A

Parafollicular C cells

NOTE: 80% are sporadic (50-60 yrs), 20% are familial (MEN - younger patients)

42
Q

What tends to happen to the calcitonin produced by tumour cells in medullary thyroid cancer?

A
  • It is broken down and deposited as amyloid within the thyroid
43
Q

What is the most aggressive thyroid cancer?

A

Anaplastic

  • Occurs in elderly
  • Metastases common
  • Usually death in < 1 year
44
Q

What are the parathyroid glands derived from?

A

Developing pharyngeal pouches

45
Q

What controls PTH secretion?

A

Serum calcium concentration (sensed by CaSR)

46
Q

List the actions of PTH.

A
  • Activates osteoclasts
  • Increased renal absorption of calcium
  • Increases activation of vitamin D
  • Increases urinary phosphate exretion
  • Increases intestinal calcium absorption
47
Q

What is hyperparathyroidism usually caused by?

A
  • 80% solitay adenoma
  • 20% due to hyperplasia of all four glands (sporadic or part of MEN1)
  • < 1% carcinoma
48
Q

Describe the histological appearance of a parathyroid adenoma.

A

Very cellular tissue with no fat (whereas the normal parathyroid gland is quite fatty)

49
Q

What bone change is seen in hyperparathyroidism?

A

Osteitis fibrosa cystica - caused by bone resorption with thinning of the cortex

50
Q

What are the effects of primary hyperparathyroidism?

A
  • Bone - increased resorption (OFC)
  • Kidneys - stones and obstructive nephropathy
  • GI - constipation, pancreatitis, gallstones
  • CNS - depression, lethary, seizures
  • Muscular weakness
  • Polyuria and polydipsia

“Painful bones, renal stones, abdominal groans, psychic moans”

51
Q

What is the most common cause of secondary hyperparathyroidism?

A

Renal failure

  • Parathyroid can be enlarged
  • Leads bone disease as with primary disease

Can be caused by any condition with chronic calcium depression

52
Q

List some causes of hypoparathyroidism.

A
  • Surgical ablation
  • Congenital absence
  • Autoimmune
53
Q

List some clinical features of hypoparathyroidism.

A
  • Neuromuscular irritability - paresthesia, muscle spasm, tetany
  • Cardiac arrhythmias
  • Seizures
  • Cataracts

CATs go numb

54
Q

Which cell types constitute the cortex and medulla of the adrenal gland?

A

Cortex = epithelial

Medulla = neural

55
Q

What are the layers of the adrenal cortex and which hormones do they produce?

A
  • Glomerulosa - aldosterone
  • Fasciculata - glucocorticoids
  • Reticularis - sex steroids
56
Q

Which conditions causes adrenal hyperfunction?

A
  • Cushing’s syndrome - excess glucocorticoids
  • Hyperaldosteronism (Conn’s)
  • Virilising syndrome - excess androgens
57
Q

What is the most common cause of Cushing’s syndrome?

A

Iatrogenic - administration of exogenous corticosteroids (leads to adrenal atrophy)

58
Q

What happens to the adrenal glands in Cushing’s disease?

A

Undergo nodular hyperplasia of the cortex

59
Q

List 4 endogenous causes of Cushing’s syndrome.

A
  • Cushing’s disease - ACTH producing pituitary adenoma (> 50%)
  • Adrenal adenoma/carcinoma
  • Adrenal hyperplasia
  • Ecotopic ACTH production - small cell lung cancer
60
Q

What are the clinical features of Cushing’s syndrome?

A
  • Hypertension
  • Weight gain
  • Truncal obesity
  • Moon face
  • Buffalo hump
  • Cutaneous striae
61
Q

What are the causes of hyperaldosteronism?

A
  • 35% adenoma (Conn’s syndrome)
  • 60% bilateral adrenal hyperplasia
62
Q

List the two main clinical features of hyperaldosteronism.

A
  • Hypertension
  • Hypokalaemia
63
Q

What causes virilising syndromes?

A
  • Neoplasms (more commonly carcinoma than adenoma)
  • Congenital adrenal hyperplasia
64
Q

Describe the pathophysiology of congenital adrenal hyperplasia.

A
  • Autosomal recessive
  • Hereditary defect in an enzyme involved in cortisol synthesis leads to cortisol deficiency
  • This leads to increased ACTH release from the pituitary gland
  • ACTH stimulates adrenal hyperplasia and androgen synthesis
65
Q

What is the most common cause of CAH?

A

21-hydroxylase deficiency

66
Q

List three causes of acute primary adrenal failure.

A
  • Sudden withdrawal of corticosteroid treatment
  • Haemorrhage (neonates)
  • DIC associated with sepsis (Waterhouse-Friderichson syndrome)
67
Q

List some causes of chronic primary adrenal failure. (UK)

A
  • Autoimmune (90%)
  • TB
  • HIV
  • Metastatic tumour (lung and breast)
  • Amyloid, fungal infection, haemochromatosis, sarcoid (very rare)
68
Q

What are some secondary causes of adrenal insufficiency?

A
  • Non-functional pituitary adenoma
  • Pituitary/hypothalamic lesions including infarction
69
Q

What are the two types of adrenocortical neoplasm?

A
  • Adenomas - mostly functional, may be associated with Cushing’s syndrome or Conn’s syndrome
  • Carcinomas - rare, more commonly associated with virilisng syndromes than adenomas
70
Q

What are the two types of tumours of the adrenal medulla?

A
  • Phaeochromocytoma
  • Neuroblastoma
71
Q

What is the rule of 10s regarding phaeochromocytomas?

A
  • 10% associated with a familial syndrome (MEN)
  • 10% bilateral
  • 10% malignant
  • 10% oustide the adrenal gland (paraganglioma)

Secrete catecholamine and causes a surgically correctable form of hypertension

72
Q

Define multiple endocrine neoplasia and its inheritance.

A

A group of autosomal dominant conditions resulting in proliferative lesions (hyperplasia, adenoma, carcinoma) of multiple endocrine organs

73
Q

Outline the characteristics of tumours in MEN.

A
  • Tend to occur at a younger age
  • Tend to arise in multiple endocrine organs or may be multifocal within one organ
  • Often preceded by hyperplasia
  • Usually more aggressive than sporadic tumours
74
Q

What are the different types of MEN and the tumours associated with them?

A

Endocrine / Chemical Pathology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions