endocrine Flashcards
1
Q
leptin
- secreted from?
- acts on?
- effect
- higher after meal or after fasting
A
- white fat
- leptin receptor in hypothalamus
- inhibits hunger/appettite
- after meal
2
Q
appetite regulation centers in brain are where
(2)
A
hypothalamus
- hunger centre = lateral hypothalamus
- satiety centre = ventromedial hypothalamus
3
Q
hunger =
def
A
need of eating
4
Q
appetite def =
A
desire to eat
5
Q
anorexia def=
A
lack of appetite
6
Q
CCK
- produced by
- acts on
- effect
- higher after meal or after fasting?
A
- eneteroendocrine cells in duodenum
- gall bladder, sphincter of oddi stomach, liver and hypothalamus, and vagus
- inhibits hunger, delaying gastric emptying and causing gall bladder contraction and sphincter of oddi relaxation and insulin release
- after meal
7
Q
ghrelin
- produced by
- acts on
- effect
- higher after meal or after fasting?
A
- stomach mainly
- vagus, hypothalamus,
- stimulates hunger /increases appetite. stimulates GH release, inhibits vagus stimulation
- after fasting
8
Q
NPY
- stands for
- release stimulated by
- released alongside
- effect
- higher after meal or after fasting?
A
- neuropeptide Y
- exercise and fasting
- agouti related peptide
- increases appetite
- after fasting
9
Q
agouti related peptide
- produced by
- released alongside
- effect
- higher after meal or after fasting?
A
- hypothalamus in NPY- containing bodies
- NPY
- increase appetite, long term.
decrease metabolism
decrease energy expenditure - after fasting
10
Q
peptide YY (PYY)
- produced where
- acts where
- effect
- higher after meal or after fasting?
A
- ileum/colon mainly (also higher up)
- on NPY receptors
- stops hunger
- after meal
11
Q
stretch receptors in stomach activated –>
A
satiety
12
Q
oral receptors –>
A
- meter food intake
- suppress feeding
- alter food pleasentness
13
Q
POMC = proopiomelanocortin receptors
- signal what
- absence / defieicnecy –
A
- signal satiety
- obesity and hyperphagia and ginger
14
Q
hyperphagia =
A
excessive appetite
15
Q
t3/t4
- which more abundant
- which quicker relaese any why
A
- t4
- t3 (t4 inactive, needs to be converted to t3)
16
Q
hypogonadism effects
A
- infertility
- lack of development of secondary sex characteristics eg body hair
- ammennhorhea
17
Q
is pituitary in or out of blood brain barrier
A
out
18
Q
blood supply to pituitary
A
portal venous circulation from hypothalamus (so brings releasing factors from there too, in the blood)
19
Q
which part of the adrenal glands does the pituitary affect
A
adrenal cortex
anterior pit –> acth
20
Q
which two factors released from the hypothalamus affect GH secretion from the anterior pituitary
A
somatostatin - inhibits
GHRH - stimulates
21
Q
- growth hormone stimulates what
- how does this product contribute to neg feedback
A
- IGF-1 from liver
- only to hypothalamus, not pituitary
22
Q
- where is dopamine secreted from
- effect
A
- hypothalamus
- inhibits prolactin release form ant pit lactotrophs
- inhibits GH release
23
Q
tumour causing bitemporal hemianopia?
A
of the pituitary
presses on optic chiasm from below
24
Q
hypo/hyperpituitarism
A
hypo- pressure on pit from tumour
hyper- functioning tumour of the pit- excess hormones
25
hirsutism=
excessive body hair where not normal
| eg facial hair for girls
26
galactorrhea=
milk production from nipples
27
goitre=
thyroid enlargement
| caused by over/under production of thyroid homrones
28
cushings syndrome vs disease
cushings syndrome = too much cortisol (general), regardless of cause
cushing's disease = too much cortisol as a result of pituitary tumour causing excess ACTH release
29
cortisol function (7)
- increased carb and protein catabolism (breakdown)
- increased deposition of fat and glycogen
- Na retention
- increased renal k+ loss
- diminished host response to infection
30
where is cortisol released from
zona fasciculata in adrenal cortex
31
crh
- =?
- from where
- and when (in day)
corticotroponin releasing hormone
hypothalamus
```
highest morning (7-9am)
lowest night (midnight)
```
32
Prognathism
=
in what
- think like movement like going from overbite to underbite
| - acromegaly
33
arthralgia
join ache/pain
34
acroparaesthesia
tingling/numbness of exremeties
| acromegaly
35
Ft4
| eg in a test of pituitary
```
free T4 (thyroxine)
testing pituitary-thyroid axis
```
36
stereotactic radiotherapy
more accurate.
| single fraction rather than small fractions daily -- so less damage to surrounding tissues
37
goitre
1) =?
2) types
3) graves=
4) causes (meh)
1- swelling of thyroid gland, due to high levels of TSH
2- diffuse goitre = whole thyroid gland swells so feels smooth
nodular goitre = nodules in thyroid so feels bumpy
3) graves --> diffuse goitre
4)over/underactive thyroid
- hypo -- low t3/4 so lots of TSH (feedback)
- hyper -- lots of TSH so high t3/4
thyroid cancer
thyroiditis
hormonal changes etcc.
38
name some conditions that may increase ur risk of graves
```
Vitiligo (pale white patches on skin)
Addison’s disease
Pernicious anaemia
Myasthenia gravis
Type 1 DM
```
39
thyrotoxicosis=
hyperthyroidism
40
pyrexia=
fever
| also = febrile
41
arthralgia
joint pain
42
```
adh = ?
made where?
released where?
released when?
causes what? where?
```
=anti-diuretic hormone/ vasopressin
made: paraventricular nucleus of the hypothalamus
released: posterior pituitary. when low water, high osmolality (baroreceptors, osmoreceptors)
causes: binds to g protein receptors:
- V1a : in vessels --> vasoconstriction
- V1b: in pituitary --> ACTH release (--> glucocorticoid hormone from adrenal --> glucose increase)
- V2: in collecting duct--> causes aquaporin 2 channels to move to apical membrane so more water reabsorbed from lumen. then water moves into blood through aquaporin 3/4 channels from collecting duct wall to vessels
43
renal calculi=
kidney stones
44
what is needed for PTH secretion
magnesium
45
what is the key axis for circadian rhythms?
hypothalamo-pituitary -adrenal axis (HPA axis)
46
what does zona fassiculata produce?
glucocorticoids eg cortisol
47
what controls cortisol release?
hypothalamus --> CRH (corticotropin releasing hormone)
ant pit --> ACTH (adrenocorticotropic hormone)
adrenal --> cortisol - which negatively feeds back to hypothalamus and ant pit
48
cortisol- is it stored or synthesised and released on demand
no stores, only synthesised in response to ACTH
as it is a fat-soluble hormone
49
cortisol levels time of day
low when asleep, high when awake
| peak in morning
50
how are circadian rhythms kept
'clock' inside each cell
| set by light
51
where is the 'central clock' in the body
in the eye
SCN = suprachiasmatic nuclei
other clocks = peripheral clocks
52
official name for anterior and posterior pituitary
```
ant= adenohypophysis
post = neurohypophysis
```
53
what endocrine issue is common and should be looked out for in pregnancy
hypothyroidism
gestational thyrotoxicosis (hyperthyroidism) is more rare
can be dangerous for both baby and mum
54
orchidometer measures
testicular volume in mL
55
thelarche
- length
- induced by
breast development
- first visible sign of puberty
- 3 years
- oestrogen, also involves prolactin, insulin and glucocorticods
56
uterus/ovaries puberty development
corpus (body): cervix goes from 1:2 to 2:1
uterus shape from tubular to pear
ovary volume increases
endometrium thickens
uterus length and volume increases
57
vaginal puberty developement
not routinely looked at
mucosa colour (red) dulls and darkens
mucosa thickens
pH: neutral --> acidic
length increases
discharge commences before puberty
58
what causes pubic and axillary hair development in puberty
adrenal androgens and ovarian androgens
59
vulva puberty development
- caused by
- changes
oestrogen affects
labia majora and minora increase in size and thickness
clit enlargens
60
adrenarche
- what happens
- age
- effects
maturation of adrenal gland
- secrete more adrenal androgens : DHEA
- normally 2/3 yrs (earlier and more pronounced if overweight). peaks 10-14 yrs, acne
- bone, axillary hair, oily skin, body odour
61
HPG axis
hypothalamo pituitary gonadal axis
hypoth--> GNRH
ant pit --> LH, FSH
gonads--> oes, test (neg feed back on hypo and pit and also affect the periphery)
62
precocious puberty
- types- and features of each
- how to distinguish them
early puberty
onset of secondary sexual charachteristics before 8 (f) /9 (m)
1. 'true'- HPG axis activated, GnRH dependant. females mainly. may be idiopathic (girls mainly idiopathic) or brain tumour (look for if boy) or infection, or psychosocial
2. 'psuedo'- HPG axis not activated. tumours (anywhere) produce hCG (similar to LH) causing hormone excess. or cysts
```
differentiated by GnRH (LHRH) test
- inject GnRH
- measure change in LH and FSH levels.
- 'true' = increased LH and FSH
'pseudo'= low increase/ suppression (HPG axis not activated)
```
63
treatment for precocious puberty
GnRH super agonist
stimulates in a way that suppresses pulsatility, meaning feedback system is disrupted, causing down-regulation of androgen production
64
precocious puberty effects
grow quickly but stop and then are short
high sexuality behaviour, esp girl- higher risk of sexual abuse
65
delayed puberty
- defined
- more m or f
- effects
abscence of secondary sexual charachteristics by 14 (F) 16 (m)
- m>f
```
f
- lack of thelarche by 13
- lack of pubic hair by 14
- lack on menarche by 15
- 5+ yrs between thlarche and menarche
m
- lack of testes growth by 14
- lack of pubic hair by 15
- 5+ yrs between first signs and genital enlargement
```
- reduced peak bone mass and osteoporosis
- defects in reproduction
- psychological problems
66
constitutional delay
- extreme of normal variation
- common, esp boys
- puberty
