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IMS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Describe 7 of the most common endocrine organs

A 
Hypothalamus/pituitary (in head) 
Thyroid (in neck) 
Parathyroid (behind thyroid) 
Pancreas (in abdomen) 
Adrenal (on top of kidneys) 
Ovaries / testes
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2
Q

what are the two types of pituitary glands and what are the basic differences

A

divided into two lobes
anterior - produces various hormones and controlled by the hypothalamus
posterior - stores various hormones produced by the hypothalamus

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3
Q

which hormones are released from the anterior pituitary and what are they stimulated by for release

A

GH growth hormone - due to GHRH
ACTH adrenocorticotrophic hormone - due to CRH
FSH follicle stimulating hormone- due to GnRH
LH luteinising hormone- due to GnRH
TSH thyroid stimulating hormone- due to TRH
PRL prolactin - no direct stimulation but under inhibitory effect of hypothalamus

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4
Q 
what are the effects of these hormones
GH 
ACTH
LH / FSH 
TSH 
PRL
A

growth hormone - skeletal growth, important in children - excess in adults causes acromegaly
adrenocorticotrophin hormone - stimulates adrenals to produce steroids
LH/FSH - stimulate ovaries / etsticales to produce sex hormones (pulsatile)
TSH - stimulates thyroid to produce thyroid hormones
Prolactin - stimulates breast milk production

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5
Q

what are the posterior pituitary hormones and what do they do

A

ADH - stimulates water reabsorption baby kidneys

Oxytocin - helps uterine contractions during labour

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6
Q

what is made in the intermediate zone

A

melanocyte stimulating hormone

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7
Q

what does cortisol switch off

A

switch off release of ACTH and CRH

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8
Q

what does GH release switch off

A

GH and GHRH

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9
Q

what does thyroid hormones release switch off

A

TSH and TRH

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10
Q

what do sex hormones switch off

A

FSH/LH and GnRH

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11
Q

what is the anatomy of the thyroid made up of

A

midline isthmus
right lobe
left lobe

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12
Q

what cells make up the thyroid gland

A

cells are arranged in follicles and produce thyroid hormones
also have C cells which produce calcitonin for calcium metabolism

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13
Q

what are the effects of released thyroid hormones

A

interact with receptors in various organs regulating gene expression and aspects of organ function, interact with heart - too much of these hormones leads to tachycardia

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14
Q

what is the specific mechanism of hormone release from the thyroid gland

A

T4 (80% - inactive form) is converted to T3 (20% - active hormone) in different organs by deiodinase enzyme
TSH stimulates release of T3 and T4
both T3 and T4 have negative feedback on hypothalamus and pituitary glands

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15
Q

how is calcium metabolism controlled

A

mainly controlled y 4 parathyroid hormones - also controlled by the kidney (produces secretion and VIT D which helps with absorption of Ca)
the gut which absorbs calcium
bone stores calcium
thyroid gland produces calcitonin which reduces amount of Ca in which over stimulation can lead to osteoporosis (brittle bone)

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16
Q

what is the adrenal gland made up of

A

90% adrenal cortex

10% adrenal medulla

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17
Q

what is released by the adrenal cortex and what is it stimulated by

A 
stimulated by the pituitary gland 
produces: 
corticosteroids (cortisol) 
androgens (male hormone) 
mineralcorticocoids (aldosterone - important in the RAS system to control blood pressure)
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18
Q

what is the adrenal medulla stimulated by and what does it release

A

stimulated by sympathetic preganglionic neurons

releases catecholamines such as A, NA, dopamine - which are related to blood pressure

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19
Q

where are the ovaries situated and what do they contain

A

either side of the uterus and contain follicles which has the oocyte depending on the stage of maturation

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20
Q

describe the life cycle of FSH and LH release from the ovary

A

first half of cycle - more FSH secretion from pituitary which means more oestrogen from ovary
second half - more LH secretion form pituitary which means more progesterone

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21
Q

what does inhibin do

A

negative feedback pituitary gland for FSH and LH

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22
Q

what effect will high levels of oestrogen do to hormones

A

negative feedback on FSH but positive feedback on LH

it can also either stimulate or inhibit GnRH release from hypothalamus

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23
Q

which cells in the testis produce testosterone

A

leydig cells

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24
Q

what do seminiferous tubules do

A

they are the site of germination, maturation and transport of sperm cells within the testes

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25
Q

if testosterone is too high what happens

A

inhibits hypothalamus via negative feedback which in combination with inhibin inhibit FSH and LH from the pituitary

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26
Q

what is the difference between primary and secondary over/under secretion

A

primary - problem with gland itself
when there is a problem with the influencer of the gland such as a problem with the pituitary gland telling another gland to produce too many or too little hormone

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27
Q

what is special about a tumour in a gland

A

it can be present without causing effect on the hormone it produces or its mechanism

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28
Q

what is a static test with thyroid as an example

A

tests for problems with thyroid, sex glands and prolactin secretion. Can immediately test for primary thyroid problems and can test for T£/4 and TSH levels

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29
Q

how would primary vs secondary differ in the thyroid gland

A

primary hyperthyroidism then T3 and or T4 is elevated with suppressed TSH
if secondary hyperthyroidism then T3/T4 is elevated with elevated TSH

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30
Q

what is a stimulation test give examples

A

for suspected hormonal under secretion where the static test is not enough
take blood, give hormone, test again, if individual fails to respond to hormone then gland failure
test for adrenal insufficiency by giving ACTH (synacthen test)
insulin stress test - increases insulin via injection and causes blood sugar levels to decrees making stressful situation on body - hopefully hormonal secretion occurs to try and increase blood sugar such as glucagon

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31
Q

what is a suppression test and give examples

A

for hormonal over secretion - hormone given should suppress natural production of hormone ie negative feedback
if still present then gland is ver producing - used to test for steroid production and glusgcoe for GH secretion (would switch off in normal situations)

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32
Q

what is over secretion and under secretion usually caused by

A

over - tumour in the gland

under - gland destruction due to inflammation or autoimmune conditions, infection etc

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33
Q

high hormone but low stimulating hormone =
low hormone and high stimulating hormone =
high hormone and high stimulating hormone =
low hormone and low stimulating hormone =

A

primary hyper
primary hypo
secondary hyper
secondary hypo

34
Q

what is a prolactinoma

A

relatively common - pituitary tumour of prolactin releasing cells

35
Q

what is the clinical presentation of prolactinoma

A

galactorrhea (breast milk production) amenorrhoea (irregular or no periods) in women and sexual dysfunction in men - headaches and visual field problems

36
Q

what are the different in symptoms between a large and a small prolactinoma

A

small - usually just amenorrhea

large - people can’t see peripheral visual field and tumour on pituitary may compress optic nerve

37
Q

how would you test and treat for prolactinoma

A

use static test to test for over secretion or high levels of prolactin or pituitary MRI
given drugs to reduce secretion - don’t usually operate

38
Q

what could cause high prolactin other than a tumour

A 
drugs 
stress 
pregnancy 
sex 
nipple stimulation 
non-functioning pituitary tumour
39
Q

what are the differences in excess GH in the child vs in the adult

A

child - gigantism, enlarged hands and feet and excessive growth
adult - acromegaly, effects sex, skeletal muscle, large hands and feet, disproportioned jaw

40
Q

what are the effects of excess GH

A

can effect visual field of view as push on optic nerves but can also not
can cause hypertension, diabetes increase cancer risk

41
Q

how would you test for excess GH

A

suppression test - glucose given and GH measurements at different times (normally high glucose surpasses GH) - imaging done after to confirm tumour

42
Q

what is the treatment of over secretion fo GH

A

surgical removal of tumour - radiotherapy and drugs

if high GH but asymptomatic then no need to remove tumour

43
Q

what is cushing syndrome and what is it caused by

A

excess levels of cortisol or excessive ACTH production

can be from a pituitary tumour for ACTH or adrenal tumour for cortisol

44
Q

what is the clinical presentation of cushing syndrome

A

growth arrest in children - runs moon like face - acne - excessive body hair - fat around the middle and thin extremities - thin skin, easy bruising

45
Q

what physiologically can be the symptoms of cushing syndrome

A

hypetension
diabetes
high risk of infections
poor wound healing

46
Q

how do you test for cushing syndrome

A

suppression test

use dexamethasone suppression test - confirms failure to suppress cortisol production

47
Q

what are the two types of cushing syndrome

A

adrenal cushing - ACTH suppressed

pituitary cushing - high ACTH

48
Q

what is the treatment for cushing

A

surgery
radiotherapy
drugs
can be caused by cancer so treat that first to see symptoms effected

49
Q

what are the different types of over secretion of thyroid hormone

A 
primary / secondary hyperthyroidism 
both more common in women 
secondary due to pituitary TSh secretion 
graves disease 
thyroiditis 
drug induced (amiodarone or lithium)
50
Q

what is graves disease

A

makes up 80% of hyperthyroidism cases
autoimmune disorder - antibodies mimic TSH which stimulates thyroid all the time - gland is large and smooth and can be caused by viral infections which triggers genetic condition

51
Q

what percentage of hyperthyroid ism if causes by toxic of multiple nodules

A

15%

52
Q

what is thyroiditis

A

1%

overstimulation of thyroid hormone due to viral infection leading to inflammation of the thyroid gland

53
Q

what drug induces hyperthyroidism

A

amiodarone
used to treat cardiac arrhythmias - huge amount of iodine messes up thyroid
lithium - used in psychiatric disorders

54
Q

what is the clinical presentation of hyperthyroidism

A 
hyperactivity 
irritability
insomnia 
heat intolerance 
increased sweating
arrhythmias 
atrial fibrillation 
weight loss despite over eating 
menstrual problems
55
Q

how would you examine for hyperthyroidism

A 
hand tremor 
increased sweating 
fast pulse 
large goitre (swelling of neck)
hard to swallow 
protrusion of eye balls - caused but fat inflammation behind eyes increasing water - unable to fully close eyes and can't look up
56
Q

how would you test and treat for hyperthyroidism

A

thyroid blood test
raised thyroid and suppressed TSH - static test
anti thyroid drugs - radioactive iodine or surgery if cancerous

57
Q

what happens to children with under secretion of GH

A

in children causes growth failure which is always treated

in adults you don’t always treat can be asymptomatic or causes depression / tiredness

58
Q

what is the test and treatment for under secretion of growth hormone

A

stimulation test needed
glucagon stimulates GH production if no production then deficiency
if no result then do insulin stress test forcing GH secretion
treatment via growth hormone replacements but is expensive

59
Q

what are the causes of under secretion of cortisol

A

maybe due to adrenal failure or pituitary failure

patients using steroid for long time could cause negative feedback on pituitary to switch off ACTH

60
Q

what is the clinical presentation of under active cortisol

A 
failure to grow in children 
severe tiredness 
dizziness due to low blood pressure 
abdominal pain 
vomiting and diarrhoea
61
Q

how do you test and treat under secretion of cortisol

A

stimulation test - synacthen test - give ACTH if primary adrenal failure suspected - give GST or IST if secondary suspected
treatment is replacing missing hormone via tablets - are cheap
failure to diagnose could cause death

62
Q

what causes thyroid hormone under secretion and who is commonly affected

A

older ladies
primary is thyroid failure and inability to produce hormone - usually autoimmune or drug induced
secondary is failure to produce TSH usually part of pituitary failure

63
Q

what are the symptoms of thyroid under secretion

A

weakness and dry skin, decreased sweating, impaired memory, weight gain and hair loss

64
Q

how do you diagnose and treat thyroid under secretion

A

static test
treatment is thyroid hormone replacement (cheap)
T4 is given over T3 as half life is too short so would give symptoms of hyperthyroidism

65
Q

what causes primary and secondary under secretion in sex hormones of males and females

A

primary in males - testicular failure - in females = ovarian failure
secondary in both is pituitary failure

66
Q

what are the clinical signs of sex hormone under secretion in males

A

erectile dysfunction, reduced libido

67
Q

what are the clinical signs in women for under secretion of sex hormones

A

amenorrhea
(but this is very common and could be due to many other things such as problems associated with uterine/ovarian/pituitary/hypothalamic

68
Q

how is low sex hormone production tested and treated

A

static test - males testosterone
females - osetsorgen
both - LSH or FH
hormone replacement therapy of pituitary hormone replacement
testosterone can be give as a cream but may rub off onto partner so usually given as injection as not good orally

69
Q

what causes pituitary failure and how would you diagnose this condition

A

may be due to large tumour, infarction ie limited blood supply to the gland
usually a combination of multiple hormones so both static and stimulation test required
confirm first with endocrine test eg basal = thyroid/prolactin/sex hormone or dynamic = glucagon/insulin then do MRI imaging

70
Q

what controls increased parathyroid secretion

A

calcium and vit D

71
Q

what are the causes of over stimulation of increased parathyroid

A

primary hyperparathyroidism, cancer, drugs, high calcium suppresses parathyroid - if doesn’t suppress then problem with gland

72
Q

what are the signs of over stimulation of parathyroid

A 
present as hypercalcemia - high Ca in blood 
thirst 
passing too much urine 
constipation 
abdominal pain
73
Q

what do steroid hormones and Vit D derive from

A

cholesterol

74
Q

what do thyroid hormones and catecholamines derive from

A

amino acids (thyroxine)

75
Q

how to steroid hormones and thyroid hormones alter cell activity

A

act via intracellular receptors within the nucleus to alter gene transcription

76
Q

describe how steroid hormones travel from the blood to take action inside the cell

A

hydrophobic and lipophilic, travel in blood attached to carrier proteins, dissociate from carrier protein and pass through plasma membrane, where bind to intracellular receptor proteins in cytosol (or nucleus) and go into nucleus, hormone-receptor complex acts as transcription factor (turns on/off genes), mRNA is transcribed, leaves the nucleus (translated into specific protein) which carries out function in target cell, roles include carbohydrate regulation, mineral balance, reproductive functions

77
Q

describe the physiological production of thyroid hormones

A

Thyroid hormones, derived from tyrosine, majority in inactive form T3 produced in the peripheral tissues though deiodination of T4, cells concentrate iodine for thyroid hormone synthesis, iodine attached to tyrosine residues on protein named thyroglobulin, synthesised by cross-linking iodotyrosine molecules in thyroglobulin and cutting thyroxine out

78
Q

describe how thyroid hormones bind and effect cells

A

Thyroid hormone receptors are two separate genes with slightly different actions to one another, recognition sequence the thyroid hormone recognition element (TRE) in front of various genes of energy metabolism and heart function switched on by thyroid hormones, thyroid hormone receptor with bound thyroid hormone binds to TRE in DNA, binding of hormone determines whether proteins that activate or switch off transcription bind to the complex, can be very complicated as can pair with other transcription factors

79
Q

how do nuclear hormone receptors bind to DNA inside the cell

A

Sequences upstream of minimal promoter region which affect transcription are binding sites for nuclear hormone receptors, may increase or decrease transcription, regions are small sequences of 6-10 nucleotides to which factors bind, often two copies with spacer in between, sometimes direct repeats sometimes palindromes

80
Q

how to nuclear hormone receptors take action to DNA inside the nucleus

A

Activation is ligand-activated transcription factors, sequence specific DNA binding proteins that regulate co-activator RNA polymerase recruitment to induce transcription at target gene promoters, activated by hormones via direct binding, receptor usually inactive due to inhibitory protein, when ligand binds produces conformational change, inhibitory protein dissociates, hormone-receptor complex binds to DNA and activates transcription, receptors have similar protein structure with very similar DNA binding domain and hormone binding domain making them specific

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