Flashcards in Endocrine disease Deck (81):
1
list the major endocrine glands in the human body
- pineal
- pituitary
- thyroid
- pancreas
- adrenal
2
what hormone does the pineal gland secrete
melatonin
3
what does melatonin (secreted by the pineal gland) regulate
circadian rhythm or sleep wake cycles
4
what are the chances of getting a pineal tumour
extremely rare
<1:200,000
but can be serious if do get the tumour
5
what % of pineal tumours comprises of inter cranial tumours
<1%
6
what age do pineal tumours develop
adults 35-60 years of age peak
7
list the presentations of pineal tumours
- headaches - hydrocephalus (due to enlarged ventricles which pushes)
- nausea
- blurred vision
- upward gaze palsy (parano syndrome)
- gait
- insomnia/sleep disturbances
- hearing loss
8
where is the pituitary gland situated
sits above the thalamus & hypothalamus
9
what cells are located anterior to the pituitary gland
- TRH = thyrotropin releasing hormone
- TSH = thyroid stimulating hormones
- PIF = prolactin inhibitory factor or dopamine
- PRL = prolactin
- CRH = corticotropin releasing hormone
- ACTH = adrenocorticotropic hormone (cortitropin)
10
what cells are located posterior to the pituitary gland
- GHRH = growth hormone releasing hormone (somatotrophin)
- GIH - growth hormone inhibitory factor (somatostatin)
- GnRH = gonadotropin
- FSH = follicle stimulating hormone
- LH = luteinizing hormone
11
how many % of intracranial neoplasms do pituitary tumours account for
10-15% (1 in 10)
12
what action of hormones occurs during pituitary tumours
presence of hormones, hyper secretion of hormones
13
what does destruction of pituitary i.e. ischemia (taking blood away from pituitary gland), iatrogenic cause to hormone secretion
absence or diminution of hormone secretion
14
what do pituitary tumours cause to adjacent structures
direction and extent of local expansion and invasion of adjacent structures i.e. non functioning adenoma
15
list the types of common adult pituitary tumours
- prolactinomas
- growth hormone secreting adenoma
- non secreting adenomas
- corticotroph adenoma (ACTH)
- TSH, FSH, LH are all rare (sex hormones)
16
what do ~15% of pituitary adenomas secrete
>hormone with prolactin + growth hormone the most common combination
17
what % of tumours do prolactinomas account for
30%
18
what do prolactinomas (pituitary tumours) do
DDX - dopamine inhibition (hypothalamus neurons) 2 degrees trauma
19
what do prolactinomas (pituitary tumours) usually cause in women
- amenorrhea - periods stop
- galactorrhea - 'witch's' milk
20
what do prolactinomas (pituitary tumours) usually cause in men
- testicular atrophy - dry up
- gynecomastia = man boobs
- diminished body hair
- impotence
21
what are the signs and symptoms of growth hormone secreting tumours in a pituitary tumour
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
22
what syndrome is associated with corticotrophin secreting adenomas (ACTH) as a result of pituitary tumours and what are the symptoms
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
23
who does the FSH, LH & TSH type of pituitary hormone occur mostly in
middle aged men and women
24
what symptoms does FSH, LH & TSH type of pituitary hormone cause
- visual field loss
- headache
- diplopia
25
what does FSH, LH & TSH type of pituitary hormone cause in men
decreased libido/energy
26
which pituitary hormone is are <1%
TSH
27
what does a pituitary tumour rarely cause
hyperthryroidism
28
what are the appearance of non secreting adenomas, tumours without endocrine symptoms at time of diagnosis
large but usually asymptomatic except headaches
29
what symptom do patients with non secreting adenomas (tumours without endocrine symptoms) have
severe frontal headaches, about 50% of patients
30
what is extremely rare in the non secreting adenomas of pituitary tumours
papilloedema
31
what visual field defect do patients with non secreting adenomas pituitary tumours have
monocular or binocular hemianopia superior affected first them inferior is typical
32
which part of the brain is constricted in non secretin adenoma pituitary tumour
ventricles
33
what does T3 turn into for a thyroid receptor hormone
T4
34
what do T3 + TRH affect
gene expression
35
what does genes ON increase
lipid and carbohydrate catabolism + increase protein synthesis
36
what is hyperthyroidism
hyper function of thyroid gland
37
list the aetiologies of hyperthyroidism
- hyperplasia (graves) ~ 85% - autoimmune
- hyperfunctional - diffuse/multinodular
- adenoma of thyroid - tumour
- TSH secreting adenoma of pituitary - rare
38
graves disease = thyroid associated...
ophthalmopathy
39
how much % of hyperthyroidism is associated with graves disease
100%
40
how much % of ophthalmopathy is associated with graves disease
50%
41
how much % of infiltrative dermopathy is associated with graves disease
<5%
42
what do hyperthyroid patients have symptoms of
- weight loss despite good appetite
- head or cold intolerance
- tachycardia
43
what is the prevalence of graves disease in the UK
2%
44
what is the female:male ratio of graves disease
10:1
45
what is the age range of graves disease
20-40 years
46
what does graves disease have a familial tendency with
positive family history in 30% of cases
47
what type of disease is graves disease
autoimmune
48
what is graves disease caused by
break down of self tolerance
49
in graves disease, what do the autoantibodies bind to or in the region of, and what does that result in
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
what is increased during graves disease
- sympatho adrenergic activity
&
- metabolic rate
51
what is suppressed during graves disease
TSH = excess T/T
52
list the symptoms/outcomes of graves disease
- exophthalmus/proptosis
- warm pulsating goitre
- tachycardia
- fine tremor
- pretibial myxoedema (rash on ankles)
53
how many % of patients does exophthalmus/proptosis occur in
60%
54
which tool measures the elevation of the eye
exophthalmometer
55
what readings from an exophthalmometer indicates exophthalmus
>21mm or a difference between eyes of >2mm
56
what is the cause of exophthalmus
swollen extra ocular muscles = painful
EOMs push onto ONH
57
why do the EOMs increase in size
- 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
why are the EOMs effected
- 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
list the how abnormality of eye motility is effected from graves disease
- 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
what would you refer a px with exophthalmus for
CT scan to exclude tumour
61
what will a CT scan for exophthalmus show
enlargement of EOMs
62
what does fluorescin staining show of a px with exophthalmus
- stressed cells
- dry eye as can't close eyes properly
63
what are the treatment considerations for graves disease
- 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
what is hyperthyroidism - goitres due to
- 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
what causes hashimoto's thyroiditis
hypothyroidism - no T4 secretion and iodinisation
66
what destroys the thyroid in hashimoto's thyroiditis
autoimmune T cells destroy thyroid
67
what is the female:male ratio of hashimoto's thyroiditis
10:1
68
what is the most common age range of hashimoto's thyroiditis
45-65 years
69
how many patients of hashimoto's thyroiditis have ocular signs e.g. dry eyes
only 2%
70
which tablets are required to be taken for life to manage hashimoto's thyroiditis
levothyroxine (precursor to thyroxine) sodium tablets for life
71
what happens during the cause of hypothyroidism - hashimoto's
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
what does a normal thyroid gland show in a microscopic diagram
follicles
73
what are the symptoms of hypothyroidism - hashimoto's
- fatigue, constipation, dry skin and weight gain
- cold intolerance
- slowed movement and loss of energy
- decreased sweating
- peripheral neuropathy
74
what is the cause of type 1 diabetes
B-cell destruction in islets of langerhans = no insulin production - no glucose uptake into cells
75
what is the cause of type 2 diabetes
insulin resistance and B-cell dysfunction
76
what does insulin provide for adipose tissue
- increase in glucose uptake
- increase in lipogenesis
- decrease in lipolysis
77
what does insulin provide for striated muscles
- increased glucose uptake
- increased glycogen synthesis
- increased protein synthesis
78
what does insulin provide for the liver
- decreased gluconeogenesis
- increased glycogen synthesis
- increased lipogenesis
79
what destructs the B cells in type 1 diabetes (destruction of islets of langerhan)
T-cell
80
what results in insulin resistance in type 2 diabetes
- 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