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phase 2a mine > endocrine > Flashcards

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
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2
Q

appetite regulation centers in brain are where

(2)

A

hypothalamus

  • hunger centre = lateral hypothalamus
  • satiety centre = ventromedial hypothalamus
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3
Q

hunger =

def

A

need of eating

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4
Q

appetite def =

A

desire to eat

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5
Q

anorexia def=

A

lack of appetite

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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
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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
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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
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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
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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
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11
Q

stretch receptors in stomach activated –>

A

satiety

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12
Q

oral receptors –>

A
  • meter food intake
  • suppress feeding
  • alter food pleasentness
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13
Q

POMC = proopiomelanocortin receptors

  • signal what
  • absence / defieicnecy –
A
  • signal satiety

- obesity and hyperphagia and ginger

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14
Q

hyperphagia =

A

excessive appetite

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15
Q

t3/t4

  • which more abundant
  • which quicker relaese any why
A
  • t4

- t3 (t4 inactive, needs to be converted to t3)

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16
Q

hypogonadism effects

A
  • infertility
  • lack of development of secondary sex characteristics eg body hair
  • ammennhorhea
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17
Q

is pituitary in or out of blood brain barrier

A

out

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18
Q

blood supply to pituitary

A

portal venous circulation from hypothalamus (so brings releasing factors from there too, in the blood)

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19
Q

which part of the adrenal glands does the pituitary affect

A

adrenal cortex

anterior pit –> acth

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20
Q

which two factors released from the hypothalamus affect GH secretion from the anterior pituitary

A

somatostatin - inhibits

GHRH - stimulates

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21
Q
  • growth hormone stimulates what

- how does this product contribute to neg feedback

A
  • IGF-1 from liver

- only to hypothalamus, not pituitary

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22
Q
  • where is dopamine secreted from

- effect

A
  • hypothalamus
  • inhibits prolactin release form ant pit lactotrophs
  • inhibits GH release
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23
Q

tumour causing bitemporal hemianopia?

A

of the pituitary

presses on optic chiasm from below

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24
Q

hypo/hyperpituitarism

A

hypo- pressure on pit from tumour

hyper- functioning tumour of the pit- excess hormones

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25
Q

hirsutism=

A

excessive body hair where not normal

eg facial hair for girls

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26
Q

galactorrhea=

A

milk production from nipples

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27
Q

goitre=

A

thyroid enlargement

caused by over/under production of thyroid homrones

28
Q

cushings syndrome vs disease

A

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
Q

cortisol function (7)

A
  • increased carb and protein catabolism (breakdown)
  • increased deposition of fat and glycogen
  • Na retention
  • increased renal k+ loss
  • diminished host response to infection
30
Q

where is cortisol released from

A

zona fasciculata in adrenal cortex

31
Q

crh

  • =?
  • from where
  • and when (in day)
A

corticotroponin releasing hormone

hypothalamus

highest morning (7-9am)
lowest night (midnight)
32
Q

Prognathism

in what

A
  • think like movement like going from overbite to underbite

- acromegaly

33
Q

arthralgia

A

join ache/pain

34
Q

acroparaesthesia

A

tingling/numbness of exremeties

acromegaly

35
Q

Ft4

eg in a test of pituitary

A 
free T4 (thyroxine)
testing pituitary-thyroid axis
36
Q

stereotactic radiotherapy

A

more accurate.

single fraction rather than small fractions daily – so less damage to surrounding tissues

37
Q

goitre

1) =?
2) types
3) graves=
4) causes (meh)

A

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
Q

name some conditions that may increase ur risk of graves

A 
Vitiligo (pale white patches on skin) 
Addison’s disease 
Pernicious anaemia
Myasthenia gravis
Type 1 DM
39
Q

thyrotoxicosis=

A

hyperthyroidism

40
Q

pyrexia=

A

fever

also = febrile

41
Q

arthralgia

A

joint pain

42
Q 
adh = ?
made where?
released where?
released when?
causes what? where?
A

=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
Q

renal calculi=

A

kidney stones

44
Q

what is needed for PTH secretion

A

magnesium

45
Q

what is the key axis for circadian rhythms?

A

hypothalamo-pituitary -adrenal axis (HPA axis)

46
Q

what does zona fassiculata produce?

A

glucocorticoids eg cortisol

47
Q

what controls cortisol release?

A

hypothalamus –> CRH (corticotropin releasing hormone)
ant pit –> ACTH (adrenocorticotropic hormone)
adrenal –> cortisol - which negatively feeds back to hypothalamus and ant pit

48
Q

cortisol- is it stored or synthesised and released on demand

A

no stores, only synthesised in response to ACTH

as it is a fat-soluble hormone

49
Q

cortisol levels time of day

A

low when asleep, high when awake

peak in morning

50
Q

how are circadian rhythms kept

A

‘clock’ inside each cell

set by light

51
Q

where is the ‘central clock’ in the body

A

in the eye

SCN = suprachiasmatic nuclei

other clocks = peripheral clocks

52
Q

official name for anterior and posterior pituitary

A 
ant= adenohypophysis
post = neurohypophysis
53
Q

what endocrine issue is common and should be looked out for in pregnancy

A

hypothyroidism

gestational thyrotoxicosis (hyperthyroidism) is more rare

can be dangerous for both baby and mum

54
Q

orchidometer measures

A

testicular volume in mL

55
Q

thelarche

  • length
  • induced by
A

breast development

  • first visible sign of puberty
  • 3 years
  • oestrogen, also involves prolactin, insulin and glucocorticods
56
Q

uterus/ovaries puberty development

A

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
Q

vaginal puberty developement

A

not routinely looked at

mucosa colour (red) dulls and darkens

mucosa thickens

pH: neutral –> acidic

length increases

discharge commences before puberty

58
Q

what causes pubic and axillary hair development in puberty

A

adrenal androgens and ovarian androgens

59
Q

vulva puberty development

  • caused by
  • changes
A

oestrogen affects

labia majora and minora increase in size and thickness
clit enlargens

60
Q

adrenarche

  • what happens
  • age
  • effects
A

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
Q

HPG axis

A

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
Q

precocious puberty

  • types- and features of each
  • how to distinguish them
A

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
Q

treatment for precocious puberty

A

GnRH super agonist

stimulates in a way that suppresses pulsatility, meaning feedback system is disrupted, causing down-regulation of androgen production

64
Q

precocious puberty effects

A

grow quickly but stop and then are short

high sexuality behaviour, esp girl- higher risk of sexual abuse

65
Q

delayed puberty

  • defined
  • more m or f
  • effects
A

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
Q

constitutional delay

A
  • extreme of normal variation
  • common, esp boys
  • puberty

phase 2a mine (38 decks)

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