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MEH > Adrenal Disorders > Flashcards

Adrenal Disorders Flashcards

1
Q

adrenal gland parts and their function

A

outer = cortex (most outer layer to inner)

  • zona glomerulosa ; mineralocorticoids (aldosterone) NA+ and K+ levels
  • zona fasciculata ; glucocorticoids ( cortsiol and corticosterone metabolism of carbohydrates
    • zona reticularis ; ​androgens sex hormone
      • ​

​

inner = medulla

  • adrenaline
    • noradrenaline
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2
Q

disorders of the adrenal cortex

A

too much hormones of the adrenal corex or too little

  • adrenal insufficiency
  • congenital adrenal hyperplasia
  • hyperaldosteronism
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3
Q

disorders of the adrenal medulla

A

pheochromocytoma and paraganglioma

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4
Q

clinical presentation of adrenal hormone deficiency

A

-autoimmune infiltration of immune cells -addisons disease ; v in

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5
Q

what hormones are decreased in adrenal deficiency

A

cortisol , androgens , mineralocorticoid

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6
Q

why is androgen deficiency worse in women

A

because its the only source of androgen

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7
Q

cortisol def.

A
  • tired, lethargy , low blood sugar since its anti -insulin -treatment is tablets
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8
Q

aldosterone def.

A
  • dizziness, since lose water, too much potassium
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9
Q

androgen def.

A
  • loss of hair and axillae, and v libido
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10
Q

too much cortisol

A
  • cushings syndrome
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11
Q

too much aldosterone

A
  • high blood pressure and low potassium
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12
Q

excess ACTH

A
  • d low cortisol
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13
Q

adrenal medulla dsiease

A

palpitations,, ^/vbp, anzixety

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14
Q

assessment for adrenal cortex diseases

A
  • blood tests basal cortisol test 0900 - stimulation test ; give ACTH
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15
Q

stimulation test vs supressio test

A
  • give ACTH
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16
Q

supress

A
  • electrolytes -cortisol midnight - 24hours urine cortisol
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17
Q

how to test the adrenal medulla

A
  • 24 urine catechol - 24 urine metanephrines (break down components of ad/nad) - plasma metanephrine (more sensitive than urine) - tell patients to not have coffee, chocolate, vanilla
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18
Q

imaging of adrenal diseases

A

-CT -MRI -functional imaging -PET -MBG

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19
Q

Addisons disease

A

-primary adrenal failure -skin pigmentation., vitiligo, pig. accentuation of the nipples , freckling , darkening of hair, underweight , thyroid problems , low bp when stand up, nausea -c autoimmune isolated or polyglandular, -infection (TB< FUNGAL< AIDS -infiltration , amyloid, -malignancy lung, breast, -T = lifelong meds of gluocortisol , mineralocorticoid

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20
Q

adrenal crisis

A
  • § ; collapse, hypotension, dehydration, pigmentation, coma - treatment is rehydration and cortisol
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21
Q

long term steroids c

A
  • ACTH deficiency - so can get adrenal rises
22
Q

steroids

A

-asthma, eczema , herbal treatments

23
Q

adrenal cushings

A
  • pitu tumour - §; hirsutism , acne, greasy skin - large tumours ; androgenic shock,
24
Q

young patient, on tablets hypertension

A

hyperadosteroism

25
Q

CAH

A

-autosomal recessive, but marrying cousins you get autosomal homozygous - blooming of an enzyme -lack of cortisol and aldosterone but really high androgen so with baby girl you get them looking like boys

26
Q

phaechromocytome

A

-

27
Q

paraganglioma

A

outside the adrenal cortex -can c sudden death - management ; a and b blockage

28
Q

histology of pphaechromocytoma

A

-

29
Q

embryology of the adrenal cortex

A

during development he cortex is derived from mesoderm, whereas the medulla is derived from the neural crestcells wc migrae to the developing cortex

30
Q

how does aldosterone work

A

it controles the rate at which NA”+ are reabsorbed or excreted, and it useds the NA/K+ pump.

since sodium is osmotticaly actie it plays a role in water control and so BP

t affects the expresionof basolateral NA/K+ pump,more expressed more NA+ reabosrbed (but also theres a risk of losing too much K+ and becoming hypokalemic)

it also affects the expression of epithelial sodium channel ENaCs on the collecting duct and so more na+ reabsorption

it is also part of the RAAS system

31
Q

whats the function and structure cortisol

A

its a a member of the c12 steroid family, and since its a steroid hormone its lipophilic and synthesised from cholesterol

enters cells and bind to cytoplasmic receptros forming hormone-receptor complex then enters the nucleus and interacts with specific regionsof DNA affecting the rate fo trasncription of specific genes

it causes things like ;

  • v rate of amino acid uptake
  • v protein syntehsis
  • ^hepatic gluconeogenesis and glycogenolysis
  • ^lipolysis in adipose tissue
  • peripheral uptake of glucose

secretion is controlled by ACTH

os it lipophilic and so is transorted bond to plasma proteins, the main transporter being transcortin 90% , the rest 10% is transported on albumin

32
Q

describe whats in the adrenal medulla and how its synthesised

A

chromaffin cells convert amino acid tyrosine into dopamine, then dopamine is converted into adrenaline

funcitons of adrenaline are

^ CVS

^ mental alertness

^ glycogenolysis in liver and muscel

^lipolysis

adrenaline binds to GCPR a and beta

33
Q

excess cortisl secretion

A

cortisol fucntion is to ^liplysis/^glycogenolysis and gluconeogenesis/vproteinsynthesis/vaminoacid upatake/vglucose uptake(anti-insulin)

hypoeractivity of adreanl cortex can cause Cushing’s syndrome;

symptoms =

  • steroid diabetes = ^ proteolysis, ^glyco.. c can cause hyperglycaemia associated with polyuria and polydipsia s steroid diabetes
  • lipogenesis so deposition of fat in the abdomen, neck and face giving moon-shped face an weigth gain
  • purple striae in the lower abdomen, upper arms and thighs due to the protein lysis c easy brusing as a result of the thinning of skin and subcutaneous tissue
  • immunosupressive, anti=inflammtomry, anti-allergic reactions can cause ^ bacterial infections and acne
    • pain and collapse of ribs due to osteoporosis caused. by distrubance of calciummetabolism and loss of bone matrix
      • too much cortisol can cause aldosterone secretion so you get fluid retneion issues and hypertension
34
Q

causes of excess cortisol

A

increased acrivity of adrenal cortex due to primary cortisol producing adrenal adenoma

ACTH secretion disorders due to pituatiary adenome like in cushings disease

ectopic secretions of ACTH from small cell tumours of the lungs

35
Q

cushings disease vs syndrome and which is more common

A

disease = pituitary adenoma

syndrome = symptoms due to excess cortsiol

syndrome

36
Q

too little cortsil

A

due to decreased aactivity in the adrenal cortex - addisons disease

its due to autoimmune destructionof the adrenal cortec but you also find reduced glucocorticoids and meralcorticoids

disorder of the piut/hypo that causes v ACTH or CRF adn this affects only glucocorticoids

37
Q

addisons disease vs crisis

A

cris = autoimmune destrution that involves loss of mineralcortiocid and corisol wc presents as an actue emergency

disease = chronic debilitating disorder

38
Q

how do patients in addison’s disease / crisis present?

what makes it worse

A

disease ;

  • tired, fatugues,
  • vague abdominal pain
  • weightloss,
  • dizzinesss
  • extreme muscular weakness and dehydration
  • increased sin pigmentaion (especiallyin areas of friction, buccal mucosa, scars, palmar creass) this is due ot increased POMC(alpha MSh and gamma MSh wc stimulate melaocytes to produce more melanin
  • decreased blood pressure d sodium depletion anfluid
  • postural hypotension due to depletion
  • hypoglycaemic epsiodes on fasting due to lack of glucocorticoid

made worse by stress, trauma,severe infetion,

39
Q

how do you treat addison crisis

A

Ivfluids because tehir fluid is very low and IV cortisol to avoid death

40
Q

qhats the most common causeof cushings syndrome

A

prescribed glucocorticoids (sterid hormones) anti-infamm drugs

41
Q
A
42
Q

clinical tests for adrenocorticlal function

A
  • measure plasma cortisol adn ACTH levels
  • 24 hours urinary excretion of cortisol and break down products (17-hydroxysteroids)
  • dynamic functioning test = dexamethasone (suspresses ACTH and so cortsiol
43
Q

how do you test for addison’s disease

A

give synacthen intramuscularly and it increases the plsma cortisol by >200nmol/L

this wouldn’t happen to someone with addison’s disease

44
Q

what tests do you to differentiate betweent eh different causes of ^ b cortisol levels without imaging

A
  • cushing’s disease = dexamethasone , inhibits ACTH release and so cortsiol levels should go down to normal
  • due to adrenalcortex overfunctioning; then mineralcorticoids are also high adn so check aldosterone levels
  • if you give dexamethasone and the ACTH levels are still high then its due tot cancer secreteing tumour thats secreting ACTh
45
Q

congential adrenal hyperplasia

A
  • theres a genetic defect an enzyme in the biosytnehitic pathway to make cortisol and so ^^ACTH due to negative feedback to try and increase cortisol levels, but cortisol cant be made well and so there’s adrenal hyperplasia
  • most common genetic defect in the 21-hyroxylase enzyme means that the the biosynthesis of corticosteriuds from cholesterol doesnt occur as per usual so in return the precursor 21-hydroxypregnenolone is used in androgen synthesis (+testersone), thsi results in salt water rising (^^ NA+ in pee due to v aldosterone ) and female gential amiguity
46
Q

what are the clinical presentation of people with congential adrenal hyperplasia

A

salt water rising due ot low aldosterone

female genitalia ambiguiity

47
Q

whats conn’s disease

A

hyperaldosteronism

it can be unilateral or bilateral malfunctioning of the adrenal glands, uni = adenoma, bi= hyperaldodersternism type 1 or 2 genetic disease

48
Q

symptoms of conn’s disease

A

high blood pressure , , occasional muscle weakness and spasm, tingling sesnsation an dexcessive urination

due to the potassium levels being so low hypokalcemia

49
Q

how do you diagnose conn’s without imaging

A

decreasing renin will usually decrease aldosterone in normal people but people with conn’s syndrome the aldoserone levels dont decrease with low renin

50
Q

whats the structure of a steroid receptor homology

A

nuclear hormones (so are thyroid and VD)

cortisol can bind to mineralcorticoid and adnrogens receptors when conc is really high

51
Q

excess androgen in women

A
  • congenital adrenal hyperplasia female genitalia ambiguity
  • hirsutism (excessive hair growth)
  • testerone ^
  • deeper voice
  • menstrural issues
  • increased muscle bulk
52
Q

whats the difference between type 1 and type 2 hyperaldosteronism

A

type 1

  • due to adenoma of the adrenal cortex = conn’s syndrome
  • bilateral idiopathic adrenal hyperplasia
  • low rein:aldo

type 2

  • due to overactive RAAS system
  • d renal artery stenosis or renin producing tumour (rarely)like juxtaglomerular tumour

MEH (24 decks)

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