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YR 3 - Illness and Wellbeing > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

define endocrine signalling

A

a signalling molecule is secreted into the blood stream, acting on distant cells throughout the body

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2
Q

give the 3 types of signalling

A

autocrine - signalling acts on the same molecules
paracrine - signal is released into interstitial fluid and acts on nearby cells
endocrine - signal released into bloodstream, acts on distant cells

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3
Q

describe the endocrine system and its purpose

A

endocrine glands - secrete hormones which travel via blood to target cells

  • regulates all biological processes in the body
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4
Q

describe the Hypothalamus-Pituitary Axis and how it controls the endocrine system.

A
  • hypothalamus
  • receive signal
  • produce ‘releasing hormones’
  • hormones act on pituitary gland
  • pituitary produces ‘trophic hormones’
  • bloodstream
  • act on endocrine gland
  • produces end productive or acts directly on the cells
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5
Q

where is the pituitary found? how heavy is it?

A

found at the base of the brain

-0.5-1grams

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6
Q

what are the two parts of the pituitary?

A

anterior pituitary
aka adenohypophysis

posterior pituitary

aka neurohypophysis

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7
Q

describe how the adenohypohysis and neurohypophysis works.

A

adenohyphosis
- releasing hormones arrive via bloodstream - portal circulation
- it then releases 6 different trophic hormones into systemic bloodstream

neurohypohysis
- signal arrives via neurons
- releases 2 trophic hormones
- ADH and oxytocin

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8
Q

describe the path of Thyrotropin-Releasing Hormone (TSH)

A
  • releasing hormone from the hypothalamus
  • anterior pituitary
  • stimulates release of thyroid-stimulating hormone from pituitary
  • acts on the thyroid gland
  • produces T3 and T4
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9
Q

describe the 2 ways in which the endocrine system is regulated.

A
  • by specific circumstance - e.g. diet and insulin
  • negative feedback
  • signal is sent to hypothalamus or pituitary to reduce the amount of hormone release/trophic hormone production
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10
Q

what is hyperpituitarism and how does it occur?

A

the excess production of trophic hormones

  • due to hyperplasias, adenomas, carcinomas, hypothalamus disorders, secretion of pituitary-like hormones from non-pituitary tumours
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11
Q

what is hypopituitarism and how does it occur?

A

when there is a deficient production of trophic hormones

  • due to damage of the tissue
  • ischaemia, radiation, surgery, inflam disorders, postpartum ischaemic necrosis and mass effect of non-functional pituitary tumour
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12
Q

what is Sheehan Syndrome, how does it link to the pituitary?

A

post-partum ischaemic necrosis
- women became hypovolemic
- excess blood loss

  • hypopituitarism
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13
Q

how can the dysfunction of the pituitary affect the eye, inter-cranial pressure and emergency from a tumour?

A

eye
- pituitary sits on top of optic nerve
- mass can push on the optic chiasm
= visual defects

  • mass can raise the intercranial pressure
  • sudden haemorrhage into a tumour
    = sudden enlargement
    = pituitary apoplexy
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14
Q

what is the most common cause of hyperpituitarism?

A

pituitary adenomas

  • excess production of trophic hormones
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15
Q

what is the most common pituitary tumour?

A

pituitary anterior lobe tumour

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16
Q

pituitary adenomas - epidemiology

A

epidemiology
- 35-60 years

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17
Q

how are pituitary adenomas classified?

A

by the cell type and hormones produced

if it produces functional hormones
- detected early
- deregulates chemicals in the body
- symptoms appear fast

if non-functional hormones are produced
- detected later on
- why?
- no chemical imbalances
- symptoms only appear when the size of tumour is great enough

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18
Q

give 3 types of pituitary adenomas

A

lactotroph pituitary adenoma

somatotroph pituitary adenoma

corticotroph pituitary adenoma

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19
Q

what is the most common pituitary adenoma?

A

lactotroph pituitary adenoma

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20
Q

describe lactotroph pituitary adenomas
- what are they also known as
- what hormone is produced
- what are the clinical features
- diagnostic effectivity

A

AKA prolactinomas

hormone = prolactin

clinical features
- amenorrhea - loss of menstrual cycle
- galactorrhoae - excess production of milk
- loss of libido
- infertility

  • easier to diagnose women v men
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21
Q

describe somatotroph pituitary adenomas
- what hormones are produced
- clinical features

A

hormone = excess growth hormones

clinical features
- children = gigantism
- adults = acromegaly
- oversized limbs

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22
Q

describe cortiocotroph pituitary adenomas
- the hormones
- path of the hormone

A

hormone
- adrenocorticotrophic hormone
ACTH
- hormone travels to adrenal gland
- stimulates excess secretion of cortisol

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23
Q

corticotroph pituitary adenomas lead to hypersecretion of cortisol, what major syndrome does this lead to?

A

Cushing’s syndrome

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24
Q

describe the structure of the thyroid

A
  • bi-lobed organ
  • isthmus joins the left and right side
  • anterior to larynx
  • level 5-7 of vertebrae
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25
Q

describe the hormone pathway of the thyroid gland and the end result, how if affects the body

A
  • hypothalamus release thyrotropin releasing hormone to anterior pituitary
  • act on thyrotropic cells
  • release thyrotropin (thyroid-stimulating hormone) into blood
  • thyrotropin binds to receptors on thyroid follicular cells
  • activates production of T3 and T4 hormones
  • T4 converted into T3 - more active
  • T3 travels in blood
  • binds to nuclear thyroid receptors
  • increase in carbohydrate/lipid catabolism (break down)
  • increases protein synthesis and basal metabolic rate
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26
Q

what element is required in the thyrotrophin hormone process?

A

iodine

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27
Q

where are the T3 and T4 hormones stored?

A

in sacs called colloids
- when hormones are needed, the colloids are broken down, releasing the hormone

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28
Q

give disorders/conditions which relate to:
- hyperthyroidism
- hypothyroidism
- structural changes - entire gland
- structural changes - nodules

A

hyperthyroidism
- Graves Disease

hypothyroidism
- Hashimotos

entire gland structural changes
- Grave’s Disease, Nodular Goitre

nodular structural change
- tumours, dominant nodule in MNG

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29
Q

Grave’s Disease - aetiology

A

aetiology
- autoimmune

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30
Q

describe the pathogenesis of Grave’s Disease

A

pathogenesis

  • signal required by pitutary for thyroid gland is bypassed
  • stimulates thryoid gland
  • thyroid-stimulating immunoglobulin (TSI) produced
  • activates TSH receptor to produce T3 and T4
  • autoantibodies against TSH receptor
    = low TSH levels

as a result
= negative feedback
- lots of T3/T4 production
- low TSH levels

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31
Q

clinical features of Grave’s Disease

A

clinical feature
- hyperthyroidism
- structural changes to the entire gland
- enlarged thyroid
- anxiety
- weight loss
- tachycardia
- follicles become hyper plastic = papillary projections
- pale colloids - not storing T3 and T4
- infiltrative opthalmopathy - eyeballs stick out

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32
Q

with Grave’s Disease - how is infiltrative opthalmopathy a characteristic?

A
  • autoimmune response
  • T cell cytokines activate
  • fibroblast proliferation
  • Extracellular matrix secreted behind the eyes
  • ECM infiltrates retro-orbital space
  • eyeballs protrude = exophthalmos
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33
Q

how is Grave’s Disease treated?

A
  • radioactive iodine - destroys overactive thyroid cells
  • drugs
  • surgery
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34
Q

Hashimoto’s Thyroiditis - aetiology

A

aetiology
- autoimmune

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35
Q

where are the proteins thyroglobulin and thyroid peroxidase found? state their functions.

A

in the thyroid follicular epithelial cells

  • involved in manufacturing of thyroid
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36
Q

describe the pathogenesis and clinical features of Hashimoto’s Thyroiditis

A

clinical feature
- hypothyroidism
- enlarged gland
- lymphocytic infiltration with germinal centres - cluster of B cells - destroys thyroid tissue
- hurtle cell change - metaplasia due to cell injury
- weight gain
- muscle weakness
- constipation

pathogenesis:
- autoantibodies against thyroglobulin and thyroid peroxidase
- antibodies destroy thyroid tissue
- high TSH
- low T3/4

37
Q

how is Hashimoto’s treated?

A

T3/4 supplements
- some have surgery if there are atypical features

38
Q

what is it called when thyroid hormone levels are normal but structural changes are occuring?

A

euthyroid

39
Q

Nodular Goitre - definition, epidemiology and aetiology

A

definition
- enlarged thyroid

aetiology
- metabolic
- iron deficiency

40
Q

describe the pathogenesis and clinical features of Nodular Goitre

A

clinical feature
- structural change to the entire gland
- thyroid is hyperplastic- trying to make more T3/4
- enlarged thyroid

pathogenesis
- long term proliferative stimuli of lack of iodine or genetics
- high levels of TSH
- low levels of T3/4

41
Q

why can nodular goitre be mistaken as cancer?

A

large dominant nodules can appear to look like thyroid carcinoma

42
Q

is nodular goitre hyperthyroidism, hypothyroidism or euthyroidism?

A

euthyroidism
- structural changes but no hormonal changes

43
Q

what can be the problems of nodular goitre having enlarged nodules?

A
  • over active
  • tracheal compression
  • dysphagia - difficulty swallowing
44
Q

Thyroid Tumours - epidemiology and aetiology

A

epidemiology
- 3,700 annual in UK
- 1% of all cancers
- mainly in women

45
Q

give an example of a benign thyroid tumour and 2 examples of malignant thyroid tumours

A

benigns
- follicular adenoma

malignant
- papillary carcinoma
- follicular carcinoma

46
Q

what are the follicular cells of the thyroid?

A

the cells that form the thyroid with colloids in the middle

47
Q

Follicular Adenoma
- describe what it is
- epidemiology
- functional?

A
  • benign tumours of follicular cells
  • usually solitary

epidemiology
- 3% of population
- more females

= non-function - doesn’t produce any thyroid hormones

48
Q

Follicular Adenoma - pathological features.

A
  • solitary lesion
  • small follicles surrounded by thick capsule
  • only benign if there is no invasion through capsule or blood vessel
49
Q

how are Follicular Adenomas treated?

A
  • excision - cutting out
50
Q

Papillary Thyroid Carcinoma
- epidemiology
- aetiology
- prognosis

A

epidemiology
- most common thyroid carcinoma
- mainly women
- wide age range

aetiology
- high link to radiation exposure
- rare genetic links

prognosis
- 85-95% 5 year survival - good

51
Q

Papillary Carcinoma - clinical featured

A
  • ill defined
  • infiltrative - carcinomas init
  • some can be encapsulated
  • some can be cystic
  • painless
  • can have hoarse voice and dysphagia
  • characteristic nuclear features:
  • highly packed cells
  • wrinkled, open, clear nuclei
  • irregular membranes
  • pseudo inclusions
52
Q

how is papillary carcinoma treated?

A

excision
radio-iodine

53
Q

Follicular Thyroid Carcinoma
- describe what it is
- epidemiology
- aetiology
- prognosis

A
  • malignant tumour of epithelial cells

epidemiology
- less common than papillary thyroid carcinoma
- more females
- older onset - 40-60 yrs

aetiology
- radiation
- maybe iodine deficiency
- RAS gene mutations

prognosis
- good prognosis IF there is no vascular invasion

54
Q

how does follicular thyroid carcinoma differ from papillary?

A

follicular has no nuclear features

55
Q

follicular thyroid carcinoma - clinical features

A

painless mass
hoarse voice
dyshphagia
lymph nets are rare
can present with distant mets

56
Q

how are follicular thyroid carcinoma treated?

A

excision
radio-iodine

57
Q

where are the parathyroid glands located?

A

one on each upper, lower poles of each thyroid lobe
= 4 in total

58
Q

what do the parathyroid glands consist of?

A

chief cells
oxyphil cells
fat - increases with age

59
Q

how are the parathyroid glands regulated by calcium?

A
  • drop in calcium
  • detected by parathyroid
  • increase parathyroid hormone
  • decrease osteoblast activity
  • increase osteoclast activity
  • bone breakdown
  • calcium is released into blood
60
Q

what is hyperparathyroidism?

A

excess release of parathyroid hormone

61
Q

what are the 3 forms of hyperparathyroidism?

A

primary hyperparathyroidism
secondary hyperparathyroidism
tertiary hyperparathyroidism

62
Q

describe primary hyperparathyroidism and how it comes about

A
  • overproduction of parathyroid hormone

why?
- from parathyroid adenoma or hyperplasia of thyroid tissue

63
Q

primary hyperparathyroidism - epidemiology, aetiology

A

epidemiology
- more female

aetiology
- unknown cause
- mutations in CCDN1, MEN1, CDC73 can link

64
Q

primary hyperparathyroidism - clinical features

A
  • can look like thyroid adenoma
  • solitary nodule of cells
  • mainly pale chief cells, some pink oxyphil cells
  • well defined
  • thin capsule
  • other glands = suppressed
  • more calcium levels
  • painful bones
  • renal stones
  • abdominal groans
  • moans
65
Q

describe the effects of secondary hyperparathyroidism

A
  • vitamin D deficiency
  • malabsorption
  • low level of calcium
  • chronic renal failure
66
Q

describe tertiary hyperparathyroidism

A

persistent hypersecretion of parathyroid hormone even after calcium levels are regular

why?
- can be after surgery - renal transplant

67
Q

how does parathyroid carcinoma appear?

A

fibrous bands
vascular invasion

68
Q

where are the adrenal glands situated?

A

above both kidneys = suprarenal glands

69
Q

describe the structure of the adrenal glands

A

outer cortex
inner medulla

70
Q

the cortex is part of the adrenal glands, what does it produce?

A
  • glucocorticoids - cortisol
  • mineralocorticoids - aldosterone
  • sex steroids - oestrogens and androgens
71
Q

the medulla is part of the adrenal glands, what does it produce?

A

catecholamines - mainly adrenaline/noradrenaline

72
Q

what is Cushings Syndrome?

A

when there are increased levels of glucocorticoids produced by the cortex of the adrenal glands, resulting in abnormalities

73
Q

what is the most common cause for cushings disease?

A

exogenous steroids

74
Q

what are the 3 types of endogenous Cushings Syndrome?

A

pituitary cushings
adrenal cushings
paraneoplastic cushings

75
Q

describe pituitary cushings syndrome

A

increase levels of adrenocorticotrophic hormone, ACTH
- increase levels of cortisol

76
Q

describe adrenal cushings syndrome

A

increase in cortisol due to adrenal adenoma/carcinoma

  • ACTH decreases due to negative feedback
77
Q

describe paraneoplastic cushings syndrome

A

increase in ACTH produced by non-adrenal tumours
- more cortisol

78
Q

how is cushings syndrome treated?

A

usually surgery
- poor prognosis if untreated

79
Q

what is Addisons Disease? - definition, epidemiology, aetiology

A

loss of entire adrenal cortex
- cortisol and aldosterone not produced
= hypocortisolism

epidemiology
- more female
- rare disease

aetiology
- 90% autoimmune
- other causes: TB

80
Q

Addisons Disease - clinical features

A

hyperpigmentation
postural hypotension
hyponatraemia - lower levels of sodium in blood

81
Q

Addisons Disease - treatment. what if it isn’t treated?

A

replace steroids - cortisol and aldosterone

fatal if not treated

82
Q

when is cortisol usually produced? what impact does it have?

A

times of stress - e.g. dental surgery

affects
- BP
- blood sugar regulation and water
- sodium balance

83
Q

with Addisons Disease, why is there hyperpigmentation

A
  • adrenal cortex damaged
  • less cortisol
  • pituitary increases ACTH to try stimulate cortisol production
  • ACTH also stimulates melanocytes
  • melanin is produced
84
Q

what is hyperaldosteronism?

A

excessive production of aldosterone
- sodium retention
- potassium loss
- water retention
- leading to hypertension

85
Q

what are the two forms of hyperaldosteronism?

A

primary - due to conns syndrome - solitary tumour or bilateral hyperplasia

secondary - due to RAS activation

86
Q

what is Phaechromocytoma? what does it cause and how is it treated

A

a rare tumour of catecholamine cells in the adrenal medulla
- causes hypertension due to increase adrenaline

  • treated by excision
87
Q

what are Multiple Endocrine Neoplasia Syndromes?

A

a group of inherited autosomal dominant disease
- proliferative neoplastic diseases affecting multiple endocrine glands

88
Q

what are the 2 groups of Multiple Endocrine Neoplasia Syndromes? describe them.

A

MEN-1
- mutation of MEN1 tumour suppressing gene
- patients can have:
- parathyroid hyperplasia
- parathyroid adenomas
- pancreatic tumours - produces gastrin and insulin
- pituitary adenomas

MEN-2
- when there is a gain of function of RET oncogene
- 2A - medulla carcinoma, phaechromocytoma, parathyroid hyperplasia
- 2B - same but no parathyroid lesions, extra-endocrine lesions seen

YR 3 - Illness and Wellbeing (31 decks)

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