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year 1 flash cards > TOPIC 9 - endocrinology > Flashcards

TOPIC 9 - endocrinology Flashcards

1
Q

what are the main endocrine glands?

A
  • hypothalamus
  • pituitary
  • thyroid
  • parathyroid
  • pancreas
  • adrenals
  • ovaries/testicles
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2
Q

what does the pituitary gland control?

A

most glands in the body

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3
Q

what two lobes is the pituitary gland split into?

A

anterior pituitary

posterior pituitary

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4
Q

what does the anterior pituitary do?

A

produces various hormones

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5
Q

what does the posterior pituitary do?

A

stores various hormones produced by hypothalamus

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6
Q

what hormones does the anterior pituitary produce?

A
  • GH: Growth Hormone
  • ACTH: adrenocorticotrophic hormone
  • Gonadotrophins: FSH/LH
  • TSH: thyroid stimulating hormone/thyrotrophin
  • PRL: prolactin
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7
Q

what does GH do?

A

growth hormone, for skeletal growth

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8
Q

what does ACTH do?

A

adrenocorticotrophic hormone, stimulates adrenals to produce steroids

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9
Q

what do gonadotrophins (LH/FSH) do?

A

follicle stimulating hormone/luteinising hormone, stimulate testes/ovaries to produce sex hormones and sperm/ova

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10
Q

what does TSH do?

A

thyroid stimulating hormone, stimulates thyroid to produce thyroid hormones

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11
Q

what does prolactin do?

A

PRL, stimulates breast milk production

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12
Q

what does ADH do?

A

antidiuretic hormone, stimulates water reabsorption by the kidneys

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13
Q

what does oxytocin do?

A

helps uterine contractions during labour

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14
Q

what controls the anterior pituitary gland?

A

hypothalamus

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15
Q

what stimulates ACTH secretion?

A

corticotrophin releasing hormone (CRH)

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16
Q

what stimulates GH secretion?

A

growth hormone releasing hormone (GHRH)

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17
Q

what stimulates TSH secretion?

A

thyrotropin releasing hormone (TRH)

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18
Q

what stimulates FSH and LH secretion?

A

gonadotrophin releasing hormone (GnRH)

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19
Q

what stimulates prolactin secretion?

A

prolactin releasing hormone does not exist and prolactin is under the inhibitory effect of the hypothalamus

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20
Q

what is the effect on prolactin if we cut the connection between the hypothalamus and pituitary gland?

A

increase levels of prolactin as we no longer have the inhibitory effect of the hypothalamus

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21
Q

what switches off ACTH and CRH?

A

cortisol

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22
Q

what switches off GH and GHRH?

A

growth hormone

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23
Q

which hormone switches off TSH and TRH?

A

thyroid hormone

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24
Q

which hormone switches off FSH/LH and GnRH?

A

sex hormones

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25
Q

what process switches hormone secretion off?

A

negative feedback

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26
Q

what are the 4 glands not controlled by the pituatry?

A
  • adrenal medulla
  • parathyroid
  • pancreas
  • gut hormones
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27
Q

what hormone does adrenal medulla produce?

A

adrenaline and noradrenaline

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28
Q

what does the parathyroid control?

A

Controls calcium levels

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29
Q

what is the thyroid gland composed of

A
  • midline isthmus (just below the cricoid cartilage)
  • right lobe
  • left lobe
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30
Q

how are the thyroid cells arranged and what do they produce?

A

arranged in follicles and produce thyroid hormones

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31
Q

what other cell does the thyroid follicle contain and what does this produce?

A

C cells
produce calcitonin
(calcium metabolism only nothing to do with thyroid hormone)
•Pituitary gland does not control calcium secretion

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32
Q

how do thyroid hormones work?

A

interact with their receptors in various organs, thereby regulating gene expression and various aspects of organ function

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33
Q

what is calcium metabolism controlled by?

A

4 parathryoid glands sitting behind the thyroid

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34
Q

what other organs, other than the parathyroid are involved in calcium metabolism?

A
  • Kidneys- Calcium excretion and production of active vitamin D
  • Gut - Absorption of calcium
  • Bone- Storage of calcium
  • Thyroid
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35
Q

what are the adrenal glands composed of?

A
  • adrenal cortex

- adrenal medulla

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36
Q

what does the adrenal cortex produce

A
  • Corticosteroids (cortisol)
  • Androgens (male hormones)
  • Mineralocorticoid (aldosterone)
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37
Q

is cortisol essential for life?

A
  • yes severe deficiency can be fatal

- inject person with cortisol when suspected even before results of test=save life

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38
Q

what do the adrenal medulla produce?

A

-Catecholamines (adrenaline, noradrenaline and dopamine)

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39
Q

does pituitary control the adrenal cortex?

A

controls part of the adrenal cortex

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40
Q

is catecholamine secretion controlled by the pituitary ?

A

no - related to BP

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41
Q

is mineralocorticoid (aldosterone) controlled by the pituitary?

A

no- related to renin-angiotensin system, which controls the blood pressure
- in low BP= increase in aldosterone secretion

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42
Q

where are the ovaries situated?

A

pelvis on either side of the uterus

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43
Q

what do the ovaries contain?

A

follicles (each containing an oocyte) at different stage of maturation during reproductive life
- limited no. of oocyte

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44
Q

what hormones control the female reproductive system?

A
  • GnRH- which switches on and off
  • FSH and LH
  • Oestradiol- switches FSH off (- feedback) and LH on (+ feedback)
  • Progesterone also produced by ovaries (- feedback on LH)
  • Inhibin - only negative feedback
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45
Q

does the secretion of FSH and LH depend on the time of the cycle?

A

yes

FSH at first part cycle, LH at second part

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46
Q

where are testes found?

A

the scrotum- except in a minority with testicular maldescent

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47
Q

what are testes composed of?

A
  • intersitial/Leydig cells
  • Seminiferous tubules
  • Sertoli cells
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48
Q

what do the intersitial/Leydig cells do?

A

produce testosterone

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49
Q

what do the Seminiferous tubules do?

A

made up of germ cells producing sperms

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50
Q

what do the Sertoli cells do?

A

help in sperm production and produce inhibin

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51
Q

are FSH and LH important in male hormone production?

A

yes

  • FSH important for sperm production
  • LH important for testosterone production
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52
Q

what is a primary abnormality of a gland?

A

when the abnormality comes from the gland itself

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53
Q

what is a secondary abnormality of a gland?

A

when the abnormality is influenced by something other than the gland- eg. the pituitary

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54
Q

what are the 3 main abnormalities that affect hormones?

A
  • Hormonal over-secretion
  • Hormonal under-secretion
  • Tumour/nodules in the gland without affecting hormone secretion
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55
Q

what are the 3 main tests we do for hormonal abnormalities?

A
  • Static tests
  • Stimulation tests
  • Suppression tests
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56
Q

why would we take a static test?

A

can diagnose abnormalities of thyroid and sex glands

-single blood sample will make diagnosis

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57
Q

in one with primary hyperthyroidism (thyroid hormone overproduction) what would we test for?

A

–Thyroid hormones (T3 and T4)
–TSH
-If primary hyperthyroidism (abnormality in thyroid itself independent from pituitary) is present then T3 and/or T4 is elevated with suppressed (undetectable) TSH

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58
Q

why would we take a stimulation test?

A

for suspected hormonal under-secretion where a static test is NOT ENOUGH (i.e. results are equivocal)

  • stimulates gland to produce hormones
  • If levels don’t go up drastically= person has under secretion in gland
  • With mild cases can go undetectable
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59
Q

give an example of a specific stimulation test

A
  • giving ACTH to test for adrenal insufficiency
  • If an individual fails to respond to a stimulation test then gland failure is diagnosed
  • Other examples: glucagon stimulation and insulin stress test for pituitary failure (tests for ACTH and GH response
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60
Q

what happens in an insulin stress test?

A

put person in state hyperglycaemia
so pituitary secretes hormones to raise glucose levels
this inc. ACTH
if levels fail to rise= diabetes

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61
Q

why would we use a suppression test

A

for some hormonal over-secretion

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62
Q

give examples of 2 suppression tests

A

–Giving steroids and testing for endogenous steroid production (external steroids should switch off internal steroid production)
–Giving glucose and testing GH secretion (glucose switches off GH secretion in normal individuals)

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63
Q

if both Free T4 levels are higher and TSH levels are lower than normal- what is the diagnosis ?

A

primary hyperthyroidism

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64
Q

if Free T4 levels are lower and TSH are higher than normal - diagnosis?

A

primary hyporthyroidism

more TSH due to negative feedback- trying to increase the Free T4 levels

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65
Q

if we have too much Free T4 and TSH- diagnosis?

A

secondary hyperthyrodism

problem in pitiuatry

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66
Q

what does over secretion of endocrine glands leads to?

A

benign tumours

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67
Q

what does under secretion of endocrine glands lead to?

A

gland destruction due to:
–Inflammation (including autoimmune conditions)
–Infarction
–Other

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68
Q

what is the last disease of endocrine glands?

A

Tumours/nodules with normal hormone production

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69
Q

how do we get prolactin oversecreation?

A

pituitary tumour secreting prolactin (prolactinoma)

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70
Q

what is the clinical presentation of overactive prolactin?

A

–Galactorrhoea (breast milk production)
–Menstural problems in women
–Amenorrhoea (no period) in women and sexual dysfunction in men
–Causes irregular periods
–Headaches and visual field problems in large tumours

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71
Q

how do we diagnose prolactin?

A
  • Static test is enough- prolatictin test

* Pituitary MRI- to see if they have tumour

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72
Q

with what kind of tumours do we get defects in visual fields?

A

pituitary gland tumour

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73
Q

why do we get visual fields defects with pituitary tumours?

A

the tumour puts pressure on the optic chiasm (which receives signals from right and left side) = half of visual field is taken away

74
Q

what are the reasons for mildly raised prolactin?

A
  • Sexual intercourse
  • Nipple stimulation
  • Stress
  • Large number of drugs (including antipsychotics and antidepressants)- always advice check prolactin before the drugs and only test prolactin if we have to
  • Non-functioning pituitary tumour (compressing the hypothalamus and interfering with the inhibitory effect on prolactin secretion)
75
Q

how do we treat prolactinomas?

A

usually over-secreting pituitary tumours that can be treated medically dopamine agonists

surgical intervention
If its due to stalk compression

76
Q

GH oversecreation in childhood or adolescents leads to….

A

–Excessive growth spurt and increased size of feet and hands

–If left untreated growth hormone excess leads to gigantism

77
Q

GH oversecreation in adults leads to…..

A

–Acromegalic face
–Wide and large hands/feet
–Increased sweating (common complaint)
- visual defects in tumour compressing optical chiasm

78
Q

diagnosis of GH oversecreation

A
  • Suppression tests are necessary
  • Glucose is given followed by GH measurements at different time points (in healthy individuals, glucose suppresses GH production and hence plasma levels of the hormones fall but not in those with over-secretion)
  • Imaging is necessary to confirm the presence of pituitary tumour
79
Q

treatment of overactive GH

A
  • Surgical removal of the tumour

* Radiotherapy and medical therapy may also be needed as surgery does not always remove the whole tumour

80
Q

what are the main causes of cushing’s syndrome

A

–Pituitary secreting ACTH tumour (Cushing’s disease)
–Adrenal tumours secreting cortisol
–Cancers producing ACTH (such as lung cancers= lots of ACTH= too much coritsol)

81
Q

what is the clinical presentation of cushing’s syndrome

A 
•Growth arrest in children
•Typical facial appearance 
–	Round (moon-like) face
–	Acne
–	Hirsuitism
•Fat redistribution
–	Truncal obesity
–	Thin extremities
•Skin abnormalities
–	Thin skin and easy bruising
–	Striae on abdomen
•Complications
–	Hypertension
–	Diabetes mellitus
–	High risk of infections
–	Poor wound healing
82
Q

tests for cushing’s syndrome?

A
  • Static tests are not enough and suppression tests are required.
  • Dexamethasone suppression test is used to confirm the failure to suppress endogenous cortisol production.
83
Q

How do you differentiate between adrenal and pituitary Cushing’s?

A

meausre ACTH

84
Q

what are steroid hormones derived from?

A

cholesterol

85
Q

what are thyroid hormones derived from?

A

tyrosine residues within the protein thyroglobulin

86
Q

what property do both steriod and thyroid hormones have in common?

A

Both classes of hormone are hydrophobic- so both can diffuse across plasma membrane into cytosol

87
Q

what class of hormones are sex hormones

A

androgens and eostrogens are steroid hormones

88
Q

do androgens have an aromatic ring?

A

no

89
Q

which sex hormone has an aromatic ring?

A

oestrogen’s such as oestrdiol have aromatic ring introduced by enzyme aromatase

90
Q

how do steroid hormones effect transcription- whats the process?

A

1- steriod hormones cross the cell membrane
2- the hormone binds to an intracellular receptor present in either nucleus or cytosol
3- if free receptor was in cytosol the hormone- receptor complex moves into nucleus (whether in cytosol or nucleus we always end up in nucleus)
4- the hormone receptor complex acts as a transcription factor
5- mRNA is transcribed and protein is produced

91
Q

where are promoter elements located on genes?

A

some very close to the transcription start site

other elements- eg.yellow boxes- several kB away

92
Q

how many domains do nuclear hormone receptors have?

A

4 domains

93
Q

what is the name of the domain that specifically recognises hormone?

A

hormone binding domain at carboxyl terminus which makes them specific

94
Q

what is the name of the domain that pairs up?

A
  • dimerization domain
  • pair up so they are facing opposite directions =C terminus of one next to N terminus of another
  • the two hormone receptors bind to make dimer
95
Q

what is the name of the domain that binds to the DNA helix?

A

the DNA binding domain

-with ‘zinc fingers’ - what bind to DNA helix

96
Q

what are zinc fingers?

A
  • projections in protein sequence that insert themselves into grooves of DNA helix
  • loops of protein that contain Zn2+ atom
  • in the case of steriod hormone receptors: coordinated with 4 cysteine residues
97
Q

why are cystine residues in zinc fingers of importance?

A

cystine residues have SH groups that coordinate with zinc to hold it in position

98
Q

what domain do nuclear hormone receptors have at the amino terminus?

A

transcription regulation domain

interacts with other proteins that regulate transcription

99
Q

what is vitellogenin?

A

a protein made by egg laying insects, molluscs, fish, reptiles, birds and monotremes (egg-laying mammals)

100
Q

what is the process which vitellogenin ends up in egg yolks?

A
  • vitellogenin synthesised in liver of female fish reptiles and birds
  • released into blood stream into oocyte
  • cleaved by proteases into functional fragments
  • incorporated into egg-yolk as these smaller proteins
101
Q

what hormone regulates the production of vitellogenin?

A

oestrogens

102
Q

what animal synthesised a large amount of vitellogenin?

A

frogs and toads

103
Q

what kind of sequence is the oestrogen response element in vitellogenin?

A

a palindrome

sequence reads same forwards and backwards

104
Q

how does the oestrogen receptor bind to the palindrome of vitellogenin?

A

one pair of the dimers recognises of one the palindromes and the other dimer recognises the other strand
- as the 2 nuclear factors face opposite directions = can interact with the two elements of the palindrome which face in different directions

105
Q

where in vitellogenin is the palindrome located?

A

300bp upstream of the transcription site

lies next to other sequences that are thought to promote vitellogenin transcription

106
Q

what are the 2 closely related oestrogen receptors?

A

ERa

ERb

107
Q

do healthy tissues express more ERb or ERa?

A

ERb

108
Q

what type of oestrogen receptor is strongly expressed in some breast cancers?

A

ERa

109
Q

what hormone promotes rapid division of ERa+ in breast cancer cells?

A

oestrogen

110
Q

how can ERa+ breast cancers be detected?

A

by staining sections of tumour biopsies with antibodies against the oestrogen receptor on thin slices of tissues . (ERα positive cells are stained brown).

111
Q

how can the growth and spread of these breast cancers be inhibited?

A

administering anti-oestrogen drugs such as tamoxifen- block action of oestrogen = strop rapid dividing of cells .

112
Q

what kind of drug is tamoxifen

A

pro drug

gets converted to an active form within body

113
Q

what is the usual process of oestrogen binding to an oestrogen receptor?

A
  • once oestrogen bound to receptor = acquires changed shape

- eostrogen receptor can then bind to coactivators

114
Q

how does tamoxifen work?

A
  • tamoxifen molecule binds to oestrogen receptor
  • receptor does not acquire changed shape
  • receptor cannot bind to coactivators
  • transcription pathway unactivated = oestrogen action blocked = tumour cannot proliferate in same way
115
Q

what has X-ray crystallography determined?

A

exact shape of oestrogen receptor with hormone molecule bound and with tamoxifen bound

116
Q

what is T4 and where is it synthesied?

A

tetra-iodothyronine/thyroxine

synthesised in thyroid gland

117
Q

what other protein is made in the thyroid?

A

thryroglobin

118
Q

what is the process by which we form thyroxine molecule

A

1- aromatic ring on a couple of tyrosine molecules on protein thyroglobulin are iodinated
2- iodotyrosine molecules in thyroglobulin are cross-linked
3- One of the thyrosine aromatic rings loses its original position in the protein molecule = so we get thyroxine being made
4- thyroxine molecule is cut out of thyroglobulin.

119
Q

how do we get the active form of hormone T3(tri-iodothyronine) formed?

A

produced in the peripheral tissues through deiodination of T4- one of iodine atoms taken off T4

120
Q

how many genes are there for thyroid hormone receptors?

A

2 separate genes

121
Q

how many receptors are there for each thyroid and oestrogen

A

both have 2 receptors

two receptors have slightly different actions to one another

122
Q

what is the recognition sequence in the promoter region of the thyroid hormone?

A

TRE (thyroid hormone response element)

123
Q

where is the TRE?

A

upstream of various genes of energy metabolism and heart function that are switched on by thyroid hormones

124
Q

do thyroid hormones act similar to steroid hormones?

A

yes both bind to nuclear hormone receptors that promote transcription

  • some differences
  • eg. thyroid hormone receptor always bound to DNA wether thyroid present or not
125
Q

in the nucleus what do thyroid hormones receptors (TR)bind to

A

bound to thyroid hormone response elements (TRE) in the DNA both in the presence or absence of hormone.

126
Q

in the absence of thyroid hormone what binds to TR instead

A

the hormone receptors bind repressor molecules that switch off transcription.

127
Q

describe process of thyroid hormone binding to TR

A

1- in the presence of hormone - co-repressor leaves

2- coactivator bonds to receptor and transcription starts

128
Q

is the second nuclear receptor molecule which TR pairs with another TR or a different nuclear receptor?

A

might be another TR- homodimer
often a different nuclear receptor - heterodimer
= v complicated transcription process

129
Q

how many essential genes does the genome of a reterovirus contain?

A

3 essential genes with repeat sequences at the end

130
Q

can a reterovirus combine with host DNA?

A

yes every so often

they can still generate infectious viruses and be carried into the next cell they infect

131
Q

what is v-erbA

A
  • a highly mutated version of thyroid hormone receptor that has been found in transforming reteroviruses
  • occurred naturally
132
Q

what does v-erbA cause?

A

erythroblastosis and leukaemia in chickens

133
Q

how does transcription usually happen with T3?

A

1- T3 binds and a number of genes are transcribed
2- Proteins A,B,C are made in response
3- one or more of these proteins is a tumour supressor gene which protects against cancer development

134
Q

what happens to transcription with T3 when V-erbA binds?

A

1-V-erbA binds to TRE but cannot activate transcription and inhibits/prevents efficient binding of TR and hence blocks thyroid hormone action.
= dominant negative effect
2- proteins A,B,C not made to sufficient level = protection against development of cancer is lost

135
Q

mutations in THR in humans have been linked to which cancers?

A
  • liver
  • kidney
  • breast
  • pitutary
  • thyroid
136
Q

what is the dominant negative effect?

A

Mutation only to be in one of the (thyroid) gene to cause malfunction

137
Q

what is thyroid hormone overprodution due to?

A

–Primary hyperthyroidism: Very common

–Secondary hyperthyroidism (pituitary TSH secretion): Rare

138
Q

id thyroid overproduction more common in men or women?

A

women

139
Q

causes of hyperthyroidism

A
  • graves disease (80%)
  • toxic nodule or MBG (15%)
  • thyroiditis (1%)
  • drug induced (amiodarone) - used for cardiac arthymias
  • rarities
140
Q

what is graves disease?

A

body producing antibodies that mimic action of TSH – attach to TSH receptor= thyroid overactive = organ specific (only effects one organ)
autoimmune condition

141
Q

what is thyroiditis?

A
  • inflammation of thyroid gland= destruction of thyroid cells = increase in thyroid hormones
  • cells then go under active as thyroid cells try to recover- if too severe = under active thyroid persists
142
Q

clinical presentation of hyperthyroidism

A
  • Hyperactivity, irritability, insomnia
  • Heat intolerance(feel warm all the time) and increased sweating
  • Palpitations
  • Weight loss despite overeating
  • Menstrual problems
143
Q

examination for hyperthyroidism

A 
•Signs of thyrotoxicosis
–Hand tremor
–Increased sweating
–Fast pulse
•Inspection of the thyroid
•Enlarged (usually)
•Smooth: Graves’ disease
•Nodular: toxic nodule(s)
•Tender: thyroid inflammation
144
Q

how can you tell if a pateint has a large goitre?

A

thyroid moves up when you swallow

NB- in a massive goiture Goitre was so big compressing windpipe and effecting swallowing

145
Q

Extrathyroidal signs thyroid eye disease

A
  • inflamtion in muscles around eyes and fat tissue around eyes
    •Swelling around the eyes
    •Protrusion of the eye ball (proptosis)- eyes pushed out
    •Paralysis of eye muscles- too much inflammation = people get double vision
    •Periorbital swelling – swelling around eyes
146
Q

how to test for overactive thyroid

A

•Thyroid blood test:
–Raised thyroid hormone
–Suppressed TSH
static test is enough

147
Q

treatment for overactive thyroid

A

• Anti-thyroid drugs: disease remission in 50% of patients after treatment for 6-18 months can suppress white cell production (very rare)
•Radioactive iodine- can use in graves, TMN and TN
–Destroys the thyroid gland
• Surgery

148
Q

do anti-thyroid drugs treat all overactive thyroid diseases?

A

Only with graves disease does the drug work – in toxic nodule or toxic multiple nodule goitre the drug only controls not treat

149
Q

what symptoms does GH deficiency cause in children

A

Failure of growth

150
Q

what symptoms does GH deficiency cause in adults

A

– Nothing
– Tiredness
Depression

151
Q

how do you test for GH deficiency

A

Stimulation test
•Glucagon stimulation test
•Insulin stress test (lowers blood glucose, stressing the body and forcing growth hormone secretion)- failure of GH to rise= GH deficiency
• Insulin stress test= can be very stressful for people

152
Q

treatment for GH deficiency

A

•Growth hormone replacement
–Injections
–Expensive (choose adult patients carefully)- don’t want to give to people asympotomatic

153
Q

what is steroid under secretion due to?

A

–Adrenal failure (1’ adrenal failure )

–Pituitary failure(2’ failure)

154
Q

what is the clinical presentation of steroid undersecretion

A

–Failure to grow in children
–Severe tiredness
–Dizziness due to low blood pressure
–Abdominal pain, vomiting an diarrhoea

155
Q

tests for steroid under secretion

A

•Stimulation test:
–Synacthen test (giving ACTH) if primary adrenal failure is suspected
–GST or IST if secondary adrenal insufficiency is suspected: as both GH and ACTH go up

156
Q

treatment for steroid undersecreation

A

Replace the missing hormone
• Tablets
• Cheap
Failing to diagnose this may result in death. In case this diagnosis is suspected, cortisol should be given even before results of investigations

157
Q

what is primary hypothyroidism

A

thyroid failure and inability to produce thyroid hormones (common).
–Usually autoimmune in nature-n destruction of thyroid gland
–Can be drug induced

158
Q

what is secondary hypothyroidism

A

failure to produce TSH (rare).

–Usually part of complete pituitary failure

159
Q

Symptoms of hypothyroidism

A 
Weakness and dry skin	
Sensation of cold and decreased sweating		
Impaired memory					
Constipation
Weight gain						
Hair loss
160
Q

diagnosis of hypothyroidism

A

static test of thyroid function- low T4 and high TSH

161
Q

treatment if hypothyroidism

A

Thyroid hormone replacement (tablets, cheap)

162
Q

what is primary sex hormone deficiency

A

–Males: testicular failure

–Females: ovarian failure

163
Q

what is secondary sex hormone deficiency

A

–Pituitary failure

164
Q

what is the presentation of sex hormone deficiency in males

A

–Erectile dysfunction

–Reduced libido/sexual desire

165
Q

what is the presentation of sex hormone deficiency in females

A

–Menstrual abnormalities (amenorrhoea

166
Q

what is amenorrhoea and what can be its causes

A 
•Very common presentation
NO PERIOD
•Can be due to:
–	Uterine problems
–	Ovarian problems
–	Pituitary problems
–	Hypothalamic problem
167
Q

diagnosis of sex hormone deficiency

A

–Static tests are enough:
• Testosterone (males), oestradiol (females)
• FSH/LH

168
Q

treatment of sex hormone deficiency

A

–Hormone replacement therapy (testosterone for males; oestradiol/progesterone for females)
–Pituitary hormone replacement

169
Q

what is pituitary failure due to?

A
  • large tumour
  • infarction
  • other rare causes
170
Q

how do we test for pituitary failure

A

It usually involves multiple hormones and therefore a combination of static and stimulatory tests are required to make the diagnosis
- for suspected tumour= MRI

171
Q

what might an increase in parathyroid hormone production be due to

A

–Primary hyperparathyroidism
–Cancers
–Drugs
Other

172
Q

what are the clinical presentation of hypercalcemia

A

Hypercalcaemia causes:
•Thirst and passing too much urine (osmotic symptoms)
•Constipation
Abdominal pain

173
Q

if Ca levels are high and PTH are high what is diagnosis?

A

hyperparathryroidism

174
Q

is family history important in hyperthyroidism?

A

yes: history of autoimmune disorders- eg. diabetes type 1, excema

175
Q

what are the complications for surgery of hyperthyroidism

A
  • hoarse voice= nerve damage

- hypocalceamia = damage to parathyroid glands

176
Q

where is the hypothalamus located?

A

head

177
Q

where is the pituitary gland located?

A

head

178
Q

where is the thyroid gland loacted?

A

neck

179
Q

where is the parathyroid gland located?

A

neck (behind thyroid)

180
Q

where is the pancreas located?

A

abdomen

181
Q

where are the adrenals located?

A

abdomen

182
Q

what is the function of the pancreas?

A

control sugar levels

year 1 flash cards (23 decks)

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