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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
describe the hormone pathway of the thyroid gland and the end result, how if affects the body
- 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
26
what element is required in the thyrotrophin hormone process?
iodine
27
where are the T3 and T4 hormones stored?
in sacs called colloids - when hormones are needed, the colloids are broken down, releasing the hormone
28
give disorders/conditions which relate to: - hyperthyroidism - hypothyroidism - structural changes - entire gland - structural changes - nodules
hyperthyroidism - Graves Disease hypothyroidism - Hashimotos entire gland structural changes - Grave's Disease, Nodular Goitre nodular structural change - tumours, dominant nodule in MNG
29
Grave's Disease - aetiology
aetiology - autoimmune
30
describe the pathogenesis of Grave's Disease
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
31
clinical features of Grave's Disease
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
32
with Grave's Disease - how is infiltrative opthalmopathy a characteristic?
- autoimmune response - T cell cytokines activate - fibroblast proliferation - Extracellular matrix secreted behind the eyes - ECM infiltrates retro-orbital space - eyeballs protrude = exophthalmos
33
how is Grave's Disease treated?
- radioactive iodine - destroys overactive thyroid cells - drugs - surgery
34
Hashimoto's Thyroiditis - aetiology
aetiology - autoimmune
35
where are the proteins thyroglobulin and thyroid peroxidase found? state their functions.
in the thyroid follicular epithelial cells - involved in manufacturing of thyroid
36
describe the pathogenesis and clinical features of Hashimoto's Thyroiditis
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
how is Hashimoto's treated?
T3/4 supplements - some have surgery if there are atypical features
38
what is it called when thyroid hormone levels are normal but structural changes are occuring?
euthyroid
39
Nodular Goitre - definition, epidemiology and aetiology
definition - enlarged thyroid aetiology - metabolic - iron deficiency
40
describe the pathogenesis and clinical features of Nodular Goitre
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
why can nodular goitre be mistaken as cancer?
large dominant nodules can appear to look like thyroid carcinoma
42
is nodular goitre hyperthyroidism, hypothyroidism or euthyroidism?
euthyroidism - structural changes but no hormonal changes
43
what can be the problems of nodular goitre having enlarged nodules?
- over active - tracheal compression - dysphagia - difficulty swallowing
44
Thyroid Tumours - epidemiology and aetiology
epidemiology - 3,700 annual in UK - 1% of all cancers - mainly in women
45
give an example of a benign thyroid tumour and 2 examples of malignant thyroid tumours
benigns - follicular adenoma malignant - papillary carcinoma - follicular carcinoma
46
what are the follicular cells of the thyroid?
the cells that form the thyroid with colloids in the middle
47
Follicular Adenoma - describe what it is - epidemiology - functional?
- benign tumours of follicular cells - usually solitary epidemiology - 3% of population - more females = non-function - doesn't produce any thyroid hormones
48
Follicular Adenoma - pathological features.
- solitary lesion - small follicles surrounded by thick capsule - only benign if there is no invasion through capsule or blood vessel
49
how are Follicular Adenomas treated?
- excision - cutting out
50
Papillary Thyroid Carcinoma - epidemiology - aetiology - prognosis
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
Papillary Carcinoma - clinical featured
- 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
how is papillary carcinoma treated?
excision radio-iodine
53
Follicular Thyroid Carcinoma - describe what it is - epidemiology - aetiology - prognosis
- 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
how does follicular thyroid carcinoma differ from papillary?
follicular has no nuclear features
55
follicular thyroid carcinoma - clinical features
painless mass hoarse voice dyshphagia lymph nets are rare can present with distant mets
56
how are follicular thyroid carcinoma treated?
excision radio-iodine
57
where are the parathyroid glands located?
one on each upper, lower poles of each thyroid lobe = 4 in total
58
what do the parathyroid glands consist of?
chief cells oxyphil cells fat - increases with age
59
how are the parathyroid glands regulated by calcium?
- drop in calcium - detected by parathyroid - increase parathyroid hormone - decrease osteoblast activity - increase osteoclast activity - bone breakdown - calcium is released into blood
60
what is hyperparathyroidism?
excess release of parathyroid hormone
61
what are the 3 forms of hyperparathyroidism?
primary hyperparathyroidism secondary hyperparathyroidism tertiary hyperparathyroidism
62
describe primary hyperparathyroidism and how it comes about
- overproduction of parathyroid hormone why? - from parathyroid adenoma or hyperplasia of thyroid tissue
63
primary hyperparathyroidism - epidemiology, aetiology
epidemiology - more female aetiology - unknown cause - mutations in CCDN1, MEN1, CDC73 can link
64
primary hyperparathyroidism - clinical features
- 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
describe the effects of secondary hyperparathyroidism
- vitamin D deficiency - malabsorption - low level of calcium - chronic renal failure
66
describe tertiary hyperparathyroidism
persistent hypersecretion of parathyroid hormone even after calcium levels are regular why? - can be after surgery - renal transplant
67
how does parathyroid carcinoma appear?
fibrous bands vascular invasion
68
where are the adrenal glands situated?
above both kidneys = suprarenal glands
69
describe the structure of the adrenal glands
outer cortex inner medulla
70
the cortex is part of the adrenal glands, what does it produce?
- glucocorticoids - cortisol - mineralocorticoids - aldosterone - sex steroids - oestrogens and androgens
71
the medulla is part of the adrenal glands, what does it produce?
catecholamines - mainly adrenaline/noradrenaline
72
what is Cushings Syndrome?
when there are increased levels of glucocorticoids produced by the cortex of the adrenal glands, resulting in abnormalities
73
what is the most common cause for cushings disease?
exogenous steroids
74
what are the 3 types of endogenous Cushings Syndrome?
pituitary cushings adrenal cushings paraneoplastic cushings
75
describe pituitary cushings syndrome
increase levels of adrenocorticotrophic hormone, ACTH - increase levels of cortisol
76
describe adrenal cushings syndrome
increase in cortisol due to adrenal adenoma/carcinoma - ACTH decreases due to negative feedback
77
describe paraneoplastic cushings syndrome
increase in ACTH produced by non-adrenal tumours - more cortisol
78
how is cushings syndrome treated?
usually surgery - poor prognosis if untreated
79
what is Addisons Disease? - definition, epidemiology, aetiology
loss of entire adrenal cortex - cortisol and aldosterone not produced = hypocortisolism epidemiology - more female - rare disease aetiology - 90% autoimmune - other causes: TB
80
Addisons Disease - clinical features
hyperpigmentation postural hypotension hyponatraemia - lower levels of sodium in blood
81
Addisons Disease - treatment. what if it isn't treated?
replace steroids - cortisol and aldosterone fatal if not treated
82
when is cortisol usually produced? what impact does it have?
times of stress - e.g. dental surgery affects - BP - blood sugar regulation and water - sodium balance
83
with Addisons Disease, why is there hyperpigmentation
- adrenal cortex damaged - less cortisol - pituitary increases ACTH to try stimulate cortisol production - ACTH also stimulates melanocytes - melanin is produced
84
what is hyperaldosteronism?
excessive production of aldosterone - sodium retention - potassium loss - water retention - leading to hypertension
85
what are the two forms of hyperaldosteronism?
primary - due to conns syndrome - solitary tumour or bilateral hyperplasia secondary - due to RAS activation
86
what is Phaechromocytoma? what does it cause and how is it treated
a rare tumour of catecholamine cells in the adrenal medulla - causes hypertension due to increase adrenaline - treated by excision
87
what are Multiple Endocrine Neoplasia Syndromes?
a group of inherited autosomal dominant disease - proliferative neoplastic diseases affecting multiple endocrine glands
88
what are the 2 groups of Multiple Endocrine Neoplasia Syndromes? describe them.
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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