Endocrine Flashcards
(42 cards)
1
Q
image of adrenal glands what are the parts for the adrenal galnds
A
- cortex
- medulla
- capsule
2
Q
what are the zones to the adrenal glands
A
- zona glomerlulosa (aldosterone)
- zona fasiculalta (cortisol)
- zona reticularis (androgens)
- right at the bottom are chromatic cells wc produced adrenaline (80%) and noradrenaline (20%)
3
Q
adrenaline synthesis and degradation
A
- Acetyl coA + choline = ACh and Co A (uses choline acetyltransferase) CAT)
- acetylcholine + acetate and choline (uses acetylcholinesterase) (AchE)
4
Q
hormones of the adrenal glands (label and then branches )
A
- corticosteroids
- zona glomerulosa (mineralocorticoids)
- zona fasiculata (glucosteriods )
- zona reticularis (androgens )
5
Q
androgens
A
- can be converted to testosterone and oestrogen in distal organs (testes and ovaries)
6
Q
what are corticosteroids received from?
A
- synthesised from cholesterol in adrenal glands and gonads
- lipid soluble hormones
- bind to receptors of the nuclear receptor family to modulate gene transcription
7
Q
congenital adrenal hyperplasia
A
-21 hydroxyls enzyme c more androgen production that normal c indistinguishable sex organs between males and females
8
Q
aldosterone
A
- made by zona glomerulosa
- lipophilic (Steroid) so carrier proteins is albumin when in blood
- plays central role in regulating plasma k+,Ma+ and arterial blood pressure
9
Q
aldosterone
A
- made by zona glomerulosa
- lipophilic (Steroid) so carrier proteins is albumin when in blood
- plays central role in regulating plasma k+,Ma+ and arterial blood pressure
- plays a role in the distal tubule of the nephron and c upregulartion of the NA/K pump expression c reabsorption of NA+ and excretion of K+ c water reabsoption , blood volume ,a nd so blood pressure
- it also upregulates expression of epithelial sodium channels ENaCs in the collecting duct promoting NA+ absorption
- important in RAAS
10
Q
RAAS
A
- lower renal perfusion to the kidney so they sense it and produce renin
- baroreceptors send signals to the kidneys wc c increases
- A released by liver
- renin released by kidney cleaves angiotensiongen to get antigens 1
- at the lungs A2 formed fromAC1 via ACE
11
Q
hyperaldosteronnism
A
- primary : defect in Cortec
- secondary ; due to overactive RAAS
12
Q
primary hyperaldosteronism
A
- bilateral idopathic adrenal hyperplasia (most common c)
- aldosterone secreting adrenal ademona (Conn’s syndrome)
- low renin levels
13
Q
signs of primary hyper.
A
- high bp
- LVH
- stroke
- hypernatraemia
- hypokalaemia
14
Q
distinguish between primary and seodnary
A
- renin (high in secondary) b its RAAS system c
- renin (low in the primary)
15
Q
treatment
A
- depends on type
- surgery
- spironalactone ( mineralcorticoid receptor antagonist)
16
Q
cortisol
A
- most abundant corticosteroid
- made by zona fasiculata in réponse to ACTH
- negative feedback to hypothalamus inhibits CRH and ACTH release
- steroid hormone (made of cholesterol ), carrier protein is transcortin
17
Q
functions of cortisol
A
- increased lipolysis (at super high levels of cortisol you get redistributio of fat)\
- increases gluconegensis in liver (^hepatic gluconeogeneisis and glycogenolysis)
- increase resistance to stress (^glucose, and ^bp make vessels more sensitive to vasoconstrictors )
- reduced immune responses
- anti-inflammatory ( c mast cell degranulation wc is useful in allergic reactions, and c inhibiton of macrophages activity)
- inhibits insulin-induced GLUT translocation in the muscles wc prevents glucose uptake
- decreases amino acid uptake, v proteinsytnehsis and ^ preolysis but not in liver
18
Q
what do immunosuppressant contain
A
- corticosteroids b they reduce the immune response
19
Q
glucocosteroid effects on metabolism
A
- increased glucose production
- breakdown of proteins
- redistribution (moon face - fat in face / buffalo fat - dorsocervical fat
- desensitises muscle’s sensitivity to inslun via insulin-induced GLUT4 translocation
20
Q
how are the fat pads made
A
- precursors are being used to make glucose and lipolysis
21
Q
Cushing’s syndrome
A
-can be caused by endogenous (pit. adenoma = this is CUSHING’S DISEASE/ excess cortisol made by adrenal tumour = ADRENAL CUSHING’S/ non- pit adrenal tumours producing ACTG = small cell lung cancer) and external causes ( taking too much corticosteroids)
22
Q
what happens with corticosteroids
A
- have to wean them off slowly cant take them off the drugs compeletely
23
Q
Cushing’s disease
A
- adenoma that c secretion of ACTHso ^ cortisol
24
Q
where are the adrenal glands in anatomical vocab
A
- upper lobes of the kidneys and lie against the diaphragm in the retroperitoneal space
25
how does adrenal cortex get its b supply
capsular plexus
26
what rhythm does cortisol secretion follow
- circadian
| - peaks at 7am and decreased by 7pm so b measures of cortisol should be through the day
27
whats the mechanism of cortisol production
- ACTH released into b stream from AP
- it acts on G protein coupled receptors (corticotropin receptors)
- it uses cAMP as secondary messenger to synthesis steroid hormones like cortisol
28
how is cortisol transported in the blood
- 90% on transcortin (aka cortiocosteroidbinding globin CBG)
| - 10% serum albumin
29
what is the mechanism of action of cortisol
- it passes the membrane b its lipid based
- binds to cytoplasmic receptors
- then enters the nucleas as cortisol-receptor complex and interacts with specific region of DNA
- affects rate of transcription of specific genes
30
whats released by the adrenal medulla? what type of cells are they
- chromaffin cells wc are modified sympathetic ganglion
| - synthesis catecholamines ; ADRENALINE AND NORADRENALINE
31
effects of adrenaline and noradrenaline
- CVS :^ cardiac output and bsuppy to muscle
- CNS: ^ mental alterness
- ^carb metabolism(glucogenolysis)
- lipid metabolism^(lpolysisin adipose tissue)
32
clinical consequence of over-secretion of adnrealine
- dtumour PHAEOCHROMOCYTOMA
| - associated with hyper tension, anxiety, palpitations , pallor, sweating and glucose intolerance
33
bushings syndrome
- chronic excess exposure to cortisol
- external causes = PRESCRIBED GLUCOCORTIOCOIDS
- endogenous c = bening pitutumout secreting ACTH (CUSHINGS DISEASE) / excess crotisol being made by adrenal tumour (ADRENAL CUSHINGS) / non pituitary -adrenal tumour prodding the ACTH = SMALL CELL LUNG CANCER
34
signs and symptomsof cushings syndrome
- plethoric moon-shaped face
- buffalo bump
- abdominal obesity
- purple straie (dweakedened integrity fo skin)
- acute weight gain
- hyperglycaemia
- hypertension
35
steroid drugs
- prednisolone and dexamethasone
- anti-inflammatory and immunoregulatory effects
- used in transplant, asthma,RA, IBS
- weign off it not suddenly
36
adrenal diseases
- cushings syndrome
| - addisons disease
37
addison's disease
- insufficent adrenal gland (chronic) because of autoimmune response c atrophy
- SS ;postural hypotension,lethargy, weight loss, anorexia, increased skin pigmentation, hypoglycaemia
38
why do people with Addison's get hyperpigmentation
- decreased cortisol
- negative feed back on AP reduced
- more POMC required to synthesis ACTH
- as a result of increased POMC more MSH synthesised c hyperpigmentaitons
- aslo ACTHcanbind to melanin recpetorsand c cause hyperpigmentation
39
addisonian crisis
- life threatening emergency d chronic adrenal insufficiency
- precipitated by severe stress, salt depravation m infection m cold exposure, ver excretion , abrupt steroid drug withdrawal
- sy: nausea, vommiting, pyrexia, hypotension , vascular collapse
- treatment = fluid replacement + cortisiol
40
androgens
- synthesised by zona reticulais
- in men DHEAconverted to testerstrone in testes (esp after puberty)
- in women converted to oestrogen and only source of oestrogen in postmenapoase
- also promote libido
- promote axillary and pubic hair growth in both sexes
41
pheochromocytoma
- chromaffin cell tumour
- may precipitate life theatheing hypertension
- characteristics; severe hypertension, diaphoresis, palpitations, anxiety, weight loss, elevated bgl
42
why do women get gestational pregnancy
- endocrine pancreases is unable to respond to metabolic demands of pregnancy and pancreas fails to release increased amount of insulin required. as a consequence there is a loss of control of metabolism , b glucose increases and diabetes results
