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Pathology > Endocrine disease > Flashcards

Endocrine disease Flashcards

1
Q

list the major endocrine glands in the human body

A
  • pineal
  • pituitary
  • thyroid
  • pancreas
  • adrenal
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2
Q

what hormone does the pineal gland secrete

A

melatonin

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3
Q

what does melatonin (secreted by the pineal gland) regulate

A

circadian rhythm or sleep wake cycles

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4
Q

what are the chances of getting a pineal tumour

A

extremely rare
<1:200,000

but can be serious if do get the tumour

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5
Q

what % of pineal tumours comprises of inter cranial tumours

A

<1%

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6
Q

what age do pineal tumours develop

A

adults 35-60 years of age peak

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7
Q

list the presentations of pineal tumours

A
  • headaches - hydrocephalus (due to enlarged ventricles which pushes)
  • nausea
  • blurred vision
  • upward gaze palsy (parano syndrome)
  • gait
  • insomnia/sleep disturbances
  • hearing loss
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8
Q

where is the pituitary gland situated

A

sits above the thalamus & hypothalamus

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9
Q

what cells are located anterior to the pituitary gland

A
  • TRH = thyrotropin releasing hormone
  • TSH = thyroid stimulating hormones
  • PIF = prolactin inhibitory factor or dopamine
  • PRL = prolactin
  • CRH = corticotropin releasing hormone
  • ACTH = adrenocorticotropic hormone (cortitropin)
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10
Q

what cells are located posterior to the pituitary gland

A
  • GHRH = growth hormone releasing hormone (somatotrophin)
  • GIH - growth hormone inhibitory factor (somatostatin)
  • GnRH = gonadotropin
  • FSH = follicle stimulating hormone
  • LH = luteinizing hormone
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11
Q

how many % of intracranial neoplasms do pituitary tumours account for

A

10-15% (1 in 10)

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12
Q

what action of hormones occurs during pituitary tumours

A

presence of hormones, hyper secretion of hormones

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13
Q

what does destruction of pituitary i.e. ischemia (taking blood away from pituitary gland), iatrogenic cause to hormone secretion

A

absence or diminution of hormone secretion

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14
Q

what do pituitary tumours cause to adjacent structures

A

direction and extent of local expansion and invasion of adjacent structures i.e. non functioning adenoma

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15
Q

list the types of common adult pituitary tumours

A
  • prolactinomas
  • growth hormone secreting adenoma
  • non secreting adenomas
  • corticotroph adenoma (ACTH)
  • TSH, FSH, LH are all rare (sex hormones)
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16
Q

what do ~15% of pituitary adenomas secrete

A

> hormone with prolactin + growth hormone the most common combination

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17
Q

what % of tumours do prolactinomas account for

A

30%

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18
Q

what do prolactinomas (pituitary tumours) do

A

DDX - dopamine inhibition (hypothalamus neurons) 2 degrees trauma

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19
Q

what do prolactinomas (pituitary tumours) usually cause in women

A
  • amenorrhea - periods stop

- galactorrhea - ‘witch’s’ milk

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20
Q

what do prolactinomas (pituitary tumours) usually cause in men

A
  • testicular atrophy - dry up
  • gynecomastia = man boobs
  • diminished body hair
  • impotence
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21
Q

what are the signs and symptoms of growth hormone secreting tumours in a pituitary tumour

A

acromegaly
patients report gradual enlargement and coarsening of facial features, hand and feet. Tumour may be large at time of diagnosis as signs and symptoms are slow

Gh stimulates IGF-1
if child gets gigantism
if adult gets acromegaly

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22
Q

what syndrome is associated with corticotrophin secreting adenomas (ACTH) as a result of pituitary tumours and what are the symptoms

A

cushing syndrome

Females : Males = 4:1
so more common in males

  • truncal obesity
  • abdominal stress
  • moon faces
  • thin skin
  • high blood pressure
  • glucose intolerance
  • fatigue
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23
Q

who does the FSH, LH & TSH type of pituitary hormone occur mostly in

A

middle aged men and women

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24
Q

what symptoms does FSH, LH & TSH type of pituitary hormone cause

A
  • visual field loss
  • headache
  • diplopia
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25
Q

what does FSH, LH & TSH type of pituitary hormone cause in men

A

decreased libido/energy

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26
Q

which pituitary hormone is are <1%

A

TSH

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27
Q

what does a pituitary tumour rarely cause

A

hyperthryroidism

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28
Q

what are the appearance of non secreting adenomas, tumours without endocrine symptoms at time of diagnosis

A

large but usually asymptomatic except headaches

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29
Q

what symptom do patients with non secreting adenomas (tumours without endocrine symptoms) have

A

severe frontal headaches, about 50% of patients

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30
Q

what is extremely rare in the non secreting adenomas of pituitary tumours

A

papilloedema

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31
Q

what visual field defect do patients with non secreting adenomas pituitary tumours have

A

monocular or binocular hemianopia superior affected first them inferior is typical

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32
Q

which part of the brain is constricted in non secretin adenoma pituitary tumour

A

ventricles

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33
Q

what does T3 turn into for a thyroid receptor hormone

A

T4

34
Q

what do T3 + TRH affect

A

gene expression

35
Q

what does genes ON increase

A

lipid and carbohydrate catabolism + increase protein synthesis

36
Q

what is hyperthyroidism

A

hyper function of thyroid gland

37
Q

list the aetiologies of hyperthyroidism

A
  • hyperplasia (graves) ~ 85% - autoimmune
  • hyperfunctional - diffuse/multinodular
  • adenoma of thyroid - tumour
  • TSH secreting adenoma of pituitary - rare
38
Q

graves disease = thyroid associated…

A

ophthalmopathy

39
Q

how much % of hyperthyroidism is associated with graves disease

A

100%

40
Q

how much % of ophthalmopathy is associated with graves disease

A

50%

41
Q

how much % of infiltrative dermopathy is associated with graves disease

A

<5%

42
Q

what do hyperthyroid patients have symptoms of

A
  • weight loss despite good appetite
  • head or cold intolerance
  • tachycardia
43
Q

what is the prevalence of graves disease in the UK

A

2%

44
Q

what is the female:male ratio of graves disease

A

10:1

45
Q

what is the age range of graves disease

A

20-40 years

46
Q

what does graves disease have a familial tendency with

A

positive family history in 30% of cases

47
Q

what type of disease is graves disease

A

autoimmune

48
Q

what is graves disease caused by

A

break down of self tolerance

49
Q

in graves disease, what do the autoantibodies bind to or in the region of, and what does that result in

A

autoantibodies bind to or in region of TSH receptors, results in increase of T4 + T3 which = decrease of TRH from anterior pituitary - virtually undetectable

50
Q

what is increased during graves disease

A
  • sympatho adrenergic activity
    &
  • metabolic rate
51
Q

what is suppressed during graves disease

A

TSH = excess T/T

52
Q

list the symptoms/outcomes of graves disease

A
  • exophthalmus/proptosis
  • warm pulsating goitre
  • tachycardia
  • fine tremor
  • pretibial myxoedema (rash on ankles)
53
Q

how many % of patients does exophthalmus/proptosis occur in

A

60%

54
Q

which tool measures the elevation of the eye

A

exophthalmometer

55
Q

what readings from an exophthalmometer indicates exophthalmus

A

> 21mm or a difference between eyes of >2mm

56
Q

what is the cause of exophthalmus

A

swollen extra ocular muscles = painful

EOMs push onto ONH

57
Q

why do the EOMs increase in size

A
  • infiltratiion of T-cells to retro-bulbar space
  • inflammation/oedema
  • accumulation of ECM matrix components i.e. GAGS hyaluronic acid and chondroitin sulphate
  • increase number of adipocytes
  • preadipocyte fibroblasts express TSH receptor and are thus targets for autoantibodies
58
Q

why are the EOMs effected

A
  • EOMs are highly innervated compared with skeletal muscles
  • EOMs have unusually high vascular supply (more prone to antibodies arriving there) compared to skeletal muscles
  • embryological differences with neuroectodermal origin compared with mesodermal origin for skeletal muscles
59
Q

list the how abnormality of eye motility is effected from graves disease

A
  • elevation usually first to be effected (IR restricts up gaze)
  • then abduction (may have esodeviation due to tethered MR)
  • usually associated with diplopia
  • oblique muscles usually not involved
60
Q

what would you refer a px with exophthalmus for

A

CT scan to exclude tumour

61
Q

what will a CT scan for exophthalmus show

A

enlargement of EOMs

62
Q

what does fluorescin staining show of a px with exophthalmus

A
  • stressed cells

- dry eye as can’t close eyes properly

63
Q

what are the treatment considerations for graves disease

A
  • hyperthyroidism treatment does not correlate well with improvement in graves ophthalmapothy
  • can’t get graves ophthalmapothy with no thyroid gland
  • both hyperthyroidism an graves ophthalmopathy have an underlying autoimmune aetiology that affects the thyroid, eyes and skin
  • so unless the underlying autoimmune disorder is addressed there is no reason for the eyes, skin and thyroid to recover by merely rating one tissue
64
Q

what is hyperthyroidism - goitres due to

A
  • lack of iodine in diet
  • impaired synthesis of thyroid hormone (T3, T4)
  • no negative feedback on TSH
  • get a rise in TSH in serum
  • TSH causes hypertrophy and hyperplasia of thyroid follicular cells
65
Q

what causes hashimoto’s thyroiditis

A

hypothyroidism - no T4 secretion and iodinisation

66
Q

what destroys the thyroid in hashimoto’s thyroiditis

A

autoimmune T cells destroy thyroid

67
Q

what is the female:male ratio of hashimoto’s thyroiditis

A

10:1

68
Q

what is the most common age range of hashimoto’s thyroiditis

A

45-65 years

69
Q

how many patients of hashimoto’s thyroiditis have ocular signs e.g. dry eyes

A

only 2%

70
Q

which tablets are required to be taken for life to manage hashimoto’s thyroiditis

A

levothyroxine (precursor to thyroxine) sodium tablets for life

71
Q

what happens during the cause of hypothyroidism - hashimoto’s

A
  1. CD8 + cytotoxin T cells destroy thyrocytes
  2. CD4+ T-helper cells secretes interferons (cytokines) that activate macrophages that damage thyrocytes
  3. autoantibodies to thyroid cells that trigger natural killer cell mediated cytotoxicity
72
Q

what does a normal thyroid gland show in a microscopic diagram

A

follicles

73
Q

what are the symptoms of hypothyroidism - hashimoto’s

A
  • fatigue, constipation, dry skin and weight gain
  • cold intolerance
  • slowed movement and loss of energy
  • decreased sweating
  • peripheral neuropathy
74
Q

what is the cause of type 1 diabetes

A

B-cell destruction in islets of langerhans = no insulin production - no glucose uptake into cells

75
Q

what is the cause of type 2 diabetes

A

insulin resistance and B-cell dysfunction

76
Q

what does insulin provide for adipose tissue

A
  • increase in glucose uptake
  • increase in lipogenesis
  • decrease in lipolysis
77
Q

what does insulin provide for striated muscles

A
  • increased glucose uptake
  • increased glycogen synthesis
  • increased protein synthesis
78
Q

what does insulin provide for the liver

A
  • decreased gluconeogenesis
  • increased glycogen synthesis
  • increased lipogenesis
79
Q

what destructs the B cells in type 1 diabetes (destruction of islets of langerhan)

A

T-cell

80
Q

what results in insulin resistance in type 2 diabetes

A
  • adipocytes release adipokines = cytokines from adipose tissue + fatty acids + inflammatory cytokines that result in insulin resistance
  • B cells hypertrophy then atrophy (b cell failure = decreased)
81
Q

what can type 2 diabetes cause

A
  • microangiopathy cerebral vascular infarcts hemorrhage
  • retinopathy
  • cataracts
  • glaucoma
  • hypertension
  • myocardial infarction
  • atherosclerosis
  • islet cell loss:
    insulitis type 1
    amyloid type 2
  • nephrosclerosis, glomerulosclerosis, pyelonephritis
  • peripheral neuropathy
  • autonomic neuropathy
  • peripheral vascular atherosclerosis
  • gangrene (due to reduced blood supply)
  • infections

Pathology (20 decks)

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