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CBE > Week 5.1 > Flashcards

Week 5.1 Flashcards

1
Q

Where is mineralocorticoid produced & secreted?

A

Zona glomerulosa (cortex of adrenal gland)

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2
Q

Where is glucocorticoid produced…

A

Zona fasciculata (cortex)

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3
Q

Where is adrenal androgen produced…

A

Zona reticularis (cortex)

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4
Q

Where are catecholamines produced?

A

Medulla of Adrenal gland

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5
Q

What is the main GC:

A

cortisol / and some corticosterone

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6
Q

What is the main MC:

A

aldosterone

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7
Q

Pathway of aldosterone signalling

A

Renin -> Angiotensin (I/II) -> Aldosterone

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8
Q

The pathway of aldosterone synthesis (enzyme)

A

Cholesterol –> DOC –> Aldosterone
Enzyme: aldosterone synthase

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9
Q

Cortisol + corticosterone synthesis

A

Cortisol comes from cholesterol too
enzyme: 11-betaOH (hydroxylase)
Corticosterone comes from DOC (precursor of aldosterone)

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10
Q

is half life of aldosterone high or low?

A

low (minutes)

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11
Q

affinity of MR and GR

A

MR is higher than GR

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12
Q

is MR affected by cortisol?

A

yes

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13
Q

How is the high cortisol regulated in signalling to receptors

A

11beta-HSD2 in tissues, it blocks cortisol, so only MC will signal to MR

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14
Q

Drugs that inhibits mineralocorticoids action

A

Epi: no side effect
Spiro: side effect -> inhibits androgen receptors too

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15
Q

Drug – MC agonists

A

Fludro: substitutes for aldosterone.
Treat addison’s disease, low aldosterone.

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16
Q

aldosterone and Na+ reabsorption pathway

A
  1. Apical surface: aldosterone – MR – will let nucleus stimulate more ENaC (sodium inlet)
  2. Na+ is reabsorbed to circulation through Na/K pump, K+ comes in
  3. K+ will be pumped out through ROMK
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17
Q

Sodium reabsorption and aldosterone (side effects)

A

Hypertension:
Aldosterone will lead to reabsorption of sodium intra-cell becomes more negative.
Cl- is also pumped out -> increase in osmolarity due to ion accumulation.
releases ADH this will increase ECF and leads to hypertension.

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18
Q

Excessive aldosterone biochemical effect

A

Increased Na+ and Cl- pumped out.
Increased H+ and K+ cellular uptake.

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19
Q

Excessive aldosterone effect (symptom–)

A
  1. Hypertension
    2.Hypokalaemia - muscle cramps
    3.alkalosis.
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20
Q

Aldosterone deficiency leads to .. (biochem and symptom)

A

Due to decreased Na+ reabsorption and Cl- pumped into circulation:
1. Low BP
2. Decreased cellular uptake of K+ and H+.

21
Q

How does renal artery stenosis affect aldosterone level

A
  1. High Renin and Aldosterone
  2. Blocked artery to kidney
  3. kidney senses low BP
  4. thinks it is low blood volume
  5. Kidney stimulates renin production -> aldosterone (secondary)
22
Q

Adrenal overfunction and aldosterone

A

Primary
1. Adrenal gland produces a lot of aldosterone
2. Renin is turned off
3. High aldosterone/Renin ratio

23
Q

Pseudo-hyperaldosteronism

A

It’s actually not high aldosterone
1. Genetic mutation that leads to increased BP and decreased circulating K+.
2. Low aldosterone and renin

24
Q

Adrenal insufficiency disease

A

Addison’s

25
Q

Adrenal insufficiency and aldosterone

A

The adrenal gland will lead to decreased aldosterone production.
High renin (small -ve feedback)

26
Q

Pseudo-hypoaldosteronism

A

Apparent high K+ and low BP
Renin and aldosterone high.

27
Q

Addison’s Disease (hormone change)

A

Adrenal disease:
Low MC - aldosterone and GC - cortisol
1. high Renin (low aldo)
2. high CRH and ACTH - hypothalamus & anterior pituitary.

28
Q

Pathway of GC (cortisol) signalling

A

Hypothalamus -> Anterior Pituitary -> Adrenal cortex

29
Q

Hypothalamus hormone to anterior pit.

A

CRH (corticotropin releasing hormone)

30
Q

Anterior pituitary hormones

A

ACTH to adrenal gland
- Other hormones: LH, FSH, TSH, GH, prolactin, ADH.

31
Q

Hypothalamus dysfunction and cortisol pathway (causes - consequences)

A

Destructive hypothalamic disease:
CRH low
& downstream hormones low

32
Q

What could lead to anterior pituitary dysfunction

A

Large non-functional pituitary tumour:
The adenoma will not produce active hormones itself.

33
Q

non-functional pituitary adenoma and cortisol pathway

A

Low ACTH & other pituitary released hormones
-> low downstream hormones

34
Q

What is an apparent symptom of Addison’s disease

A

Adrenal gland dysfunction:
-> increased ACTH (along with CRH)
ACTH will lead to hyper-pigmentation

35
Q

What will excessive ACTH cause???

A

melanocyte-stimulating hormone receptor (release melanin)
hyper-pigmentation.

36
Q

Causes of Addison’s disease

A

Autoimmune, Metastasis, tuberculosis.
-> damage to the adrenal cortex

37
Q

low Cortisol effects

A

vascular tone- Low blood pressure
Low glucose
Loss of Appetite

38
Q

Pituitary ACTH deficiency

A

low cortisol and normal aldosterone (unaffected)

39
Q

Short Synacthen Test

A

Synacthen is an ACTH-like drug
It should stimulate adrenal cortex to release cortisol
If abnormal -> adrenal cortex atrophy (dysfunction)

Inaccurate within 6 months of hypot/pit. damage. Adrenal gland needs 4-6 weeks to completely fail cortisol production.

40
Q

What is Cushing’s syndrome

A

Excessive cortisol production

41
Q

Cushing’s syndrome leads to –

A

Increased circulating glucose.
Increased protein catabolism.
- skin thinning
- easy bruising
High levels of cortisol: increased bone resorption and decreased bone formation: Osteoporosis

42
Q

Causes of Cushing’s syndrome (3)

A
  1. Pituitary tumour -> excessive ACTH
  2. Ectopic ACTH.
    Leads to increased cortisol, more -ve feedback to hypothalamus and anterior pituitary.
  3. Adrenal tumour -> increased cortisol.
43
Q

Diagnosis of cause of Cushing’s syndrome

A

Urine ACTH test:
1. low ACTH -> adrenal tumour
2. high ACTH -> pituitary/ectopic ACTH tumour

44
Q

Ectopic ACTH vs Pituitary ACTH tumour

A

Pituitary ACTH tumour :
Can be suppressed by Dexamethasone suppression and CRH.

Ectopic ACTH is often more intense:
-Can have wait loss (weight gain is often the case for Cushing’s)
-ACTH is usually unaffected by dexamethasone suppression and CRH test.

45
Q

CRH test

A

For pituitary ACTH tumour -> a dose of CRH can increase the ACTH.
For Ectopic ACTH tumour-> CRH cannot affect the ectopic tumour.

46
Q

dexamethasone suppression

A

Dexamethasone -> synthetic glucocorticoid that aims to negative feedback to ACTH production.
- Can suppress in pituitary ACTH tumours.
- Cannot in ectopic ACTH tumours.

47
Q

Adrenal insufficiency symptoms

A

low cortisol–low glucose
low BP - vascular collapse
low aldosterone–low Na+, high K+
very fatigue
weight loss

48
Q

Conn’s tumour and bilateral adrenal hyperplasia

A

Excessive aldosterone.
Imaging might distinguish the two. Adrenal vein sampling where Conn’s tumour have more aldosterone on one side.

CBE (16 decks)

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