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MEH > Endocrine > Flashcards

Endocrine Flashcards

1
Q

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

A
  • cortex
  • medulla
  • capsule
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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%)
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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)
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4
Q

hormones of the adrenal glands (label and then branches )

A
  • corticosteroids
  • zona glomerulosa (mineralocorticoids)
  • zona fasiculata (glucosteriods )
  • zona reticularis (androgens )
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5
Q

androgens

A
  • can be converted to testosterone and oestrogen in distal organs (testes and ovaries)
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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
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7
Q

congenital adrenal hyperplasia

A

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

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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
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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
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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
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11
Q

hyperaldosteronnism

A
  • primary : defect in Cortec

- secondary ; due to overactive RAAS

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12
Q

primary hyperaldosteronism

A
  • bilateral idopathic adrenal hyperplasia (most common c)
  • aldosterone secreting adrenal ademona (Conn’s syndrome)
  • low renin levels
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13
Q

signs of primary hyper.

A
  • high bp
  • LVH
  • stroke
  • hypernatraemia
  • hypokalaemia
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14
Q

distinguish between primary and seodnary

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

- renin (low in the primary)

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15
Q

treatment

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

how does adrenal cortex get its b supply

A

capsular plexus

26
Q

what rhythm does cortisol secretion follow

A
  • circadian

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

27
Q

whats the mechanism of cortisol production

A
  • 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
Q

how is cortisol transported in the blood

A
  • 90% on transcortin (aka cortiocosteroidbinding globin CBG)

- 10% serum albumin

29
Q

what is the mechanism of action of cortisol

A
  • 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
Q

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

A
  • chromaffin cells wc are modified sympathetic ganglion

- synthesis catecholamines ; ADRENALINE AND NORADRENALINE

31
Q

effects of adrenaline and noradrenaline

A
  • CVS :^ cardiac output and bsuppy to muscle
  • CNS: ^ mental alterness
  • ^carb metabolism(glucogenolysis)
  • lipid metabolism^(lpolysisin adipose tissue)
32
Q

clinical consequence of over-secretion of adnrealine

A
  • dtumour PHAEOCHROMOCYTOMA

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

33
Q

bushings syndrome

A
  • 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
Q

signs and symptomsof cushings syndrome

A
  • plethoric moon-shaped face
  • buffalo bump
  • abdominal obesity
  • purple straie (dweakedened integrity fo skin)
  • acute weight gain
  • hyperglycaemia
  • hypertension
35
Q

steroid drugs

A
  • prednisolone and dexamethasone
  • anti-inflammatory and immunoregulatory effects
  • used in transplant, asthma,RA, IBS
  • weign off it not suddenly
36
Q

adrenal diseases

A
  • cushings syndrome

- addisons disease

37
Q

addison’s disease

A
  • insufficent adrenal gland (chronic) because of autoimmune response c atrophy
  • SS ;postural hypotension,lethargy, weight loss, anorexia, increased skin pigmentation, hypoglycaemia
38
Q

why do people with Addison’s get hyperpigmentation

A
  • 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
Q

addisonian crisis

A
  • 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
Q

androgens

A
  • 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
Q

pheochromocytoma

A
  • chromaffin cell tumour
  • may precipitate life theatheing hypertension
  • characteristics; severe hypertension, diaphoresis, palpitations, anxiety, weight loss, elevated bgl
42
Q

why do women get gestational pregnancy

A
  • 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

MEH (24 decks)

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