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MEH Sem 1 > Lecture 12- Adrenal Disorders > Flashcards

Lecture 12- Adrenal Disorders Flashcards

1
Q

What are the 3 diff. zones of the adrenal glands and one example of the hormones it secretes?

A

(Go Find Racks, Makes Good Sex)

  • Zona Glomerulosa: Mineralocorticoids (aldosterone)
  • Zona Fasiculata: Glucocorticoids (cortisol)
  • Zona Reticularis: Androgen (Sex hormones)
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2
Q

What is the adrenal gland seperated into?

A
  • Cortex (all the zonas)

- Medulla (chromaffin cells that secrete adrenaline + noradrenaline)

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3
Q

What type of hormone is cortisol?

A
  • Lipid sol, synthesised from cholesterol
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4
Q

How does corticosteroids affect target tissues?

A
  1. Readily diffuse across plasma membrane
  2. Bind to glucocorticoid receptor
  3. Causes dissociation of chaperone proteins
  4. Receptor ligand complex translocates to nuclues
  5. Bind with transcription factors / glucocorticoid response elements (GREs)
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5
Q

What type of hormone is aldosterone?

A
  • Lipid sol.

- Mineralcorticoid, zona glomerulosa

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6
Q

How is aldo. transported?

A
  • Mainly serum albumin

- Transcortin

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7
Q

What is the function of aldo.?

A
  • Increases expression of Na/K+ pump
  • Increases H2O + Na+ resabsorption & K+ secretion
  • Increases BP + blood vol
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8
Q

When is renin released from the kidney? And what is it’s function?

A
  • Released during hypotension or hypovolaemia (low blood vol)

Angiotensinogen (liver) –> angiotensin l –> angiotensin ll –> aldosterone/ADH

  • Angiotensinogen cleaved by renin
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9
Q

What does angiotensinll (active form) cause?

A
  • Vasoconstriction (increase BP)
  • Secretion of aldosterone (increases expression of Na+/K+ pump, increase reabsorption of H2O and Na)
  • ADH from PP (translocation of aquaporins, reabsorption)
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10
Q

What is the function of ACE inhibitors?

A
  • Antihypertensive drugs

- Prevent ACE converting angiotensin l to ll

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11
Q

What is the diff. btw primary & secondary hyperaldosteronism?

A
  • Primary:
    (i) Defect in adrenal cortex
    (ii) Bilateral idiopathic adrenal hyperplasia
    (iii) Adrenal adenoma (Conn’s syndrome)
  • Secondary:
    (i) Overactivity of RAAS
    (ii) Renin producing tumour (rare)
    (iii) Renal artery stenosis (no blood supply to kidney)
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12
Q

How do diff. btw 1 and 2 hyperaldosteronism?

A

1 (defect in adrenal cortex) has low renin, 2 (due to hyperactivity of RAAS) has high renin

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13
Q

Signs of hyperaldosteronism

A
  • High BP
  • Left ventricular hypertrophy
  • Stroke
  • Hypernatraemia (Na)
  • Hypokalaemia (K)
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14
Q

Treatment of hyperaldosteronism

A
  • Depends on type
  • Surgically remove aldosterone secreting adenoma
  • Spironolactone (mineralcorticoid receptor antagonist)
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15
Q

Function of cortisol

A
  • Increase proteolysis, lipolysis and gluconeogensis
  • Response to stress
  • Anti-inflammatory effects
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16
Q

Desc the hypothalamic-pituitary-adrenal axis

A

CRH, Corticotropic Releasing Hormone (Hypothalamus) –> ACTH, Adrenocorticotropic Hormone (AP) –> Cortisol (Adrenal) –> Tissues

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17
Q

What is the effect of cortisol on metabolism?

A
  • Increases gluconeogenesis, lipolysis and proteolysis
  • Causes redistribution of fat
  • Causes lipogenesis
  • Inhibits insulin-induced GLUT 4 translocation in muscle (prevent glucose uptake glucose sparing effect)
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18
Q

What is Cushing’s syndrome? And what are its causes?

A
  • Excessive cortisol
  • Caused by exo factors (prescribed meds) or endo
  • Endo:
    (i) Pituitary adenoma secrete ACTH (Cushing’s disease)
    (ii) Adrenal tumour secrete excess cortisol (adrenal cushing’s)
    (iii) Non pituitary-adrenal tumours producing ACTH (small cell lung cancer) *very rare
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19
Q

Signs and symptoms of Cushing’s syndrome

A
  • Plethoric (red) moon-shaped face
  • Buffalo hump
  • Abdominal obesity
  • Purple striae
  • Thin extremities
  • Hyperglycaemia
  • Hypertension
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20
Q

Give some examples of steroid drugs and their functions?

A
  • Prednisolone, Dexamethasone
  • Anti-inflammatory & immunomodulatory effects
  • Treat:
    (i) Asthma
    (ii) Rheumatoid arthritis
    (iii) Inflammatory bowel disease
21
Q

Why should steroid drugs be reduced gradually & not stopped suddenly?

A
  • Stopped sudd will induce Addisonian Crisis
22
Q

What is Addison’s disease?

A
  • Chronic adrenal insufficiency

- Used to be TB complication, now is autoimmune response

23
Q

Signs & symptoms of Addison’s disease.

A
  • Hypotension
  • Increased skin pigmentation
  • Lethargy
  • Weight loss
  • Anorexia
24
Q

Explain why does hyperpigmentation occur in Addison’s disease?

A
  • Decreased cortisol stimulates cleaving of POMC to form ACTH & aMSH
  • Activates melanocytes to form more melanin (hyperpigmentation)
25
Q

What is Addisonian Crisis?

A
  • Life threatening med. emergency due to adrenal insufficiency
26
Q

What are the symptoms & treatment of Addisonian Crisis?

A
  • S: Nausea, vomitting, pyrexia, vascular collapse, hypotension
  • T: Fluid replacement, Steroid hormone therapy
27
Q

What is Addisonian Crisis caused by?

A
  • Severe stress
  • Salt depravation
  • Infection
  • Abrupt steroid drug withdrawal
28
Q

Function of androgen

A
  • Promote secondary sexual characteristics in male n female

- Converted to testosterone & oestrogen

29
Q

Tests to diagnose Cushing Syndrome?

A
  1. Measure free cortisol: 24 hr urine sample
  2. Dexamethasone suppression test: low dose of D given, should decrease cortisol if normal
  3. Check plasma ACTH levels: Low (adrenal carcinoma/adenoma), High: Cushing disease/ectopic production
  4. Imaging
30
Q

Treatment of Cushing

A
  • Exo: gradually decrease drug
  • Pituitary adenoma: surgical exicision
  • Adrenal carcinoma/ectopic ACTH: adrenal steroid inhibitors
31
Q

What enzyme catalyses conversion of noradrenaline to adrenaline?

A

Methyl Transferase

32
Q

Which diagnostic test would typically be used to confirm Addison’s disease?

A

Short Synacthen test:

  • Synacthen is a synthetic ACTH analogue used to test adrenal function. The administration of Synacthen intramuscularly, would increase plasma cortisol by >200 nmol/L in a normal patient.
  • As steroid deficiency needs long-term (often lifelong) treatment, a Synacthen test is typically used to make a definitive diagnosis of Addison’s.
33
Q

A 26 year old woman is diagnosed with iatrogenic Addison’s disease.
What could have caused this disease in this patient?

A
  • Adrenalectomy (removal of 1 or 2 adrenal glands)

- Iatrogenic= caused by med. treatment

34
Q

Investigations show a patient has an elevated ACTH and a high cortisol, neither of which are suppressed by high dose dexamethasone.
What condition is this patient most likely suffering from and why?

A
  • Ectopic ACTH syndrome
  • Production of ACTH by the cancer cells cannot be supressed by a high dose dexamethasone test so ACTH and cortisol remain high.
  • Very rare
35
Q

At what time of the day should cortisol levels be measured for a patient that is suspected of Cushing’s Syndrome?

A
  • Midnight. Cortisol is at its lowest

N.B Addison’s 9am, cortisol highest

36
Q

Why for a patient with Cushing’s giving them low dose dexamethasone at 12am X lower ACTH/cortisol levels?

A
  • Both ACTH and cortisol would be high in a midnight blood sample (you would expect cortisol to be at its lowest at midnight due to diurnal rythmn).
  • A low dose dexamethasone supression test would not be sufficient to decrease ACTH or cortisol in Cushing’s disease but a higher dose would be enough to supress ACTH from the pituitary adenoma so you would see both cortisol and ACTH suppressed in the high dose test with Cushing’s disease.
37
Q

What is phaeochromocytoma?

A
  • A rare tumour of chromaffin cells in the adrenal medulla that results in increased secretion of adrenaline and noradrenaline
38
Q

Symptoms of pheochromocytoma

A
  • headaches, palpitations, diaphoresis, anxiety and weight loss
39
Q

What is the best method of diagnosis of phaeochromocytoma?

A

measurement of urine metanephrine

40
Q

What is the percentage of saline for rehydration?

A
  • 0.9%
41
Q

What is symptoms of Addison’s disease?

A
  • Fatigue
  • Weakness
  • Anorexia
  • Weight loss
  • Dizziness
  • Skin pigmentation
42
Q

What is signs of Addison’s disease?

A
  • Underweight
  • Vitiligo
  • Hypotension
  • Skin pigmentation
43
Q

What are some causes of primary adrenal failure?

A
  • Auto-immune disease
  • Infection (TB, AIDS)
  • Malignancy
  • Genetic
  • Iatrogenic (drugs, adrenalectomy)
44
Q

What are clinical features and treatment of Addisonian Crisis?

A
  • Collapse
  • Hypotension
  • Dehydration
  • Pigmentation
  • Coma
  • Treatment: Rapid rehydration with fluids, intravenous hydrocortisone, correction of hypoglycaemia
45
Q

What is maintanence treatment of Addison’s disease?

A
  • Lifelong treatment of glucocorticoid (hydrocortisone, prednisolone) and mineralocorticoid (fludrocortisone)
  • Education to prevent crises
    (Steroid card and bracelet, double dose glucocorticoid in times of illness)
46
Q

What and when does ACTH deficiency cause/occur?

A
  • Occurs in hypopituitarism
  • No pigmentation = ACTH X increase
  • No hyperkalaemia
  • Hyponatraemia = cortisol ⬆️
47
Q

What is primary aldosteronism associated with and what confirms it?

A
  • Hypertension and hypokalemia

- Confirmed with high aldosterone and suppressed renin

48
Q

What does Congenital Adrenal Hyperplasia (CAH) result in and what is it caused by?

A
  • Caused by block in adrenal cortex pathway: presentation depends on enzyme defect
  • Cause adrenal defect and ambiguous genitalia
  • Autosomal recessive
  • Results in: Low cortisol and aldosterone
49
Q

How is congenital adrenal hyperplasia treated and presented in clinic?

A
  • Presentation:
    (i) Hypotension
    (ii) Hyponatraemia
    (iii) Hyperkalaemia
    (iv) Hypoglycaemia
  • Treatment:
    (i) Treat adrenal crisis
    (ii) Long term GC and MC
    (iii) Corrective surgery

MEH Sem 1 (18 decks)

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