Endocrine

Question 1

image of adrenal glands what are the parts for the adrenal galnds

Answer 1

• cortex
• medulla
• capsule

Question 2

what are the zones to the adrenal glands

Answer 2

• zona glomerlulosa (aldosterone)
• zona fasiculalta (cortisol)
• zona reticularis (androgens)
• right at the bottom are chromatic cells wc produced adrenaline (80%) and noradrenaline (20%)

Question 3

adrenaline synthesis and degradation

Answer 3

• Acetyl coA + choline = ACh and Co A (uses choline acetyltransferase) CAT)
• acetylcholine + acetate and choline (uses acetylcholinesterase) (AchE)

Question 4

hormones of the adrenal glands (label and then branches )

Answer 4

• corticosteroids
• zona glomerulosa (mineralocorticoids)
• zona fasiculata (glucosteriods )
• zona reticularis (androgens )

Question 5

androgens

Answer 5

• can be converted to testosterone and oestrogen in distal organs (testes and ovaries)

Question 6

what are corticosteroids received from?

Answer 6

• synthesised from cholesterol in adrenal glands and gonads
• lipid soluble hormones
• bind to receptors of the nuclear receptor family to modulate gene transcription

Question 7

congenital adrenal hyperplasia

Answer 7

-21 hydroxyls enzyme c more androgen production that normal c indistinguishable sex organs between males and females

Question 8

aldosterone

Answer 8

• 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

Question 9

aldosterone

Answer 9

• 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

Question 10

RAAS

Answer 10

• 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

Question 11

hyperaldosteronnism

Answer 11

• primary : defect in Cortec

- secondary ; due to overactive RAAS

Question 12

primary hyperaldosteronism

Answer 12

• bilateral idopathic adrenal hyperplasia (most common c)
• aldosterone secreting adrenal ademona (Conn’s syndrome)
• low renin levels

Question 13

signs of primary hyper.

Answer 13

• high bp
• LVH
• stroke
• hypernatraemia
• hypokalaemia

Question 14

distinguish between primary and seodnary

Answer 14

• renin (high in secondary) b its RAAS system c

- renin (low in the primary)

Question 15

treatment

Answer 15

• depends on type
• surgery
• spironalactone ( mineralcorticoid receptor antagonist)

Question 16

cortisol

Answer 16

• 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

Question 17

functions of cortisol

Answer 17

• 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

Question 18

what do immunosuppressant contain

Answer 18

• corticosteroids b they reduce the immune response

Question 19

glucocosteroid effects on metabolism

Answer 19

• 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

Question 20

how are the fat pads made

Answer 20

• precursors are being used to make glucose and lipolysis

Question 21

Cushing’s syndrome

Answer 21

-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)

Question 22

what happens with corticosteroids

Answer 22

• have to wean them off slowly cant take them off the drugs compeletely

Question 23

Cushing’s disease

Answer 23

• adenoma that c secretion of ACTHso ^ cortisol

Question 24

where are the adrenal glands in anatomical vocab

Answer 24

• upper lobes of the kidneys and lie against the diaphragm in the retroperitoneal space

Question 25

how does adrenal cortex get its b supply

Answer 25

capsular plexus

Question 26

what rhythm does cortisol secretion follow

Answer 26

- circadian | - peaks at 7am and decreased by 7pm so b measures of cortisol should be through the day

Question 27

whats the mechanism of cortisol production

Answer 27

- 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

Question 28

how is cortisol transported in the blood

Answer 28

- 90% on transcortin (aka cortiocosteroidbinding globin CBG) | - 10% serum albumin

Question 29

what is the mechanism of action of cortisol

Answer 29

- 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

Question 30

whats released by the adrenal medulla? what type of cells are they

Answer 30

- chromaffin cells wc are modified sympathetic ganglion | - synthesis catecholamines ; ADRENALINE AND NORADRENALINE

Question 31

effects of adrenaline and noradrenaline

Answer 31

- CVS :^ cardiac output and bsuppy to muscle - CNS: ^ mental alterness - ^carb metabolism(glucogenolysis) - lipid metabolism^(lpolysisin adipose tissue)

Question 32

clinical consequence of over-secretion of adnrealine

Answer 32

- dtumour PHAEOCHROMOCYTOMA | - associated with hyper tension, anxiety, palpitations , pallor, sweating and glucose intolerance

Question 33

bushings syndrome

Answer 33

- 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

Question 34

signs and symptomsof cushings syndrome

Answer 34

- plethoric moon-shaped face - buffalo bump - abdominal obesity - purple straie (dweakedened integrity fo skin) - acute weight gain - hyperglycaemia - hypertension

Question 35

steroid drugs

Answer 35

- prednisolone and dexamethasone - anti-inflammatory and immunoregulatory effects - used in transplant, asthma,RA, IBS - weign off it not suddenly

Question 36

adrenal diseases

Answer 36

- cushings syndrome | - addisons disease

Question 37

addison's disease

Answer 37

- insufficent adrenal gland (chronic) because of autoimmune response c atrophy - SS ;postural hypotension,lethargy, weight loss, anorexia, increased skin pigmentation, hypoglycaemia

Question 38

why do people with Addison's get hyperpigmentation

Answer 38

- 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

Question 39

addisonian crisis

Answer 39

- 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

Question 40

androgens

Answer 40

- 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

Question 41

pheochromocytoma

Answer 41

- chromaffin cell tumour - may precipitate life theatheing hypertension - characteristics; severe hypertension, diaphoresis, palpitations, anxiety, weight loss, elevated bgl

Question 42

why do women get gestational pregnancy

Answer 42

- 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