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METABOLISM, ENDOCRINOLOGY AND HAEMATOLOGY > Adrenal glands > Flashcards

Adrenal glands Flashcards

1
Q

Where are the adrenal glands found?

A

Sits right above each kidney

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2
Q

What are the 3 parts of the adrenal glands?

A
  • Capsule
  • Cortex
  • Medulla
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3
Q

What are the 3 zones of the adrenal cortex?

hint: girls fart rainbows

A

1) Zona glomerulosa (outer)
2) Zona fasiculata (middle)
3) Zona reticularis (inner)

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4
Q

What is the broad name for the hormones of the adrenal cortex?

A

Corticosteroids

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5
Q

What are the three subdivions of corticosteroids?

A

1) Mineralocorticoids (aldosterone)
2) Glucocorticoids (cortisol, corticosterone, oestrogen)
3) Androgens (testosterone and oestrogen)

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6
Q

Describe the characteristics of steroid hormones

A
  • Lipid soluble
  • Synthesised from cholesterol in adrenal glands and gonads
  • Bind to receptors of nuclear receptor family
  • Modulate gene transcription
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7
Q

What is (most commonly) deficient in congenital adrenal hyperplasia?

A

21-hydroxylase

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8
Q

Briefly describe the mechanism of corticosteroids

A

1) Readily diffuse across plasma membrane and bind to glucocorticoid receptors
2) Binding leads to chaperone proteins dissociating
3) Receptor ligand complex translocates to nucleus
4) Receptors bind to glucocorticoid response elements or other transcription factors

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9
Q

What are chaperone proteins (give an example)?

A

Proteins that assists conformational folding and unfolding e.g. heat shock protein 90

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10
Q

Where is Aldosterone produced?

A

Zona glomerulosa of the adrenal cortex

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11
Q

What is the carrier protein for aldosterone?

A

(mainly) serum albumin and to some extent transcortin

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12
Q

What is the effect of aldosterone to the body and how does it do so?

A
  • Regulation of plasma Na+, K+ and arterial blood pressure
  • Upregulates expression of Na+-K+ ATPase increasing the concentration gradient
  • Also upregulates epithelial sodium channels (ENaCs)
  • Greater reabsorption of Na+ and water retention
  • Acts on DCT and collecting tubules of the nephron
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13
Q

What is aldosterone a central component of?

A

The renin-angiotensin-aldosterone system (RAAS)

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14
Q

What is the renin-angiotensin-aldosterone system (RAAS)?

A

A system of hormones involved in the regulation of plasma sodium concentration and arterial blood pressure

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15
Q

Describe the mechanism of RAAS

A
  • Decrease in blood pressure (renal perfusion) or in plasma Na+ concentration stimulates the kidneys to release RENIN
  • RENIN cleaves ANGIOTENSINOGEN (produced in the liver) giving ANGIOTENSIN 1
  • ANGIOTENSIN 1 is further cleaved into ANGIOTENSIN 2 by ANGIOTENSIN-CONVERTING ENZYME (ACE)
  • ANGIOTENSIN 2 increases blood pressure
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16
Q

How does angiotensin 2 increase blood pressure?

A
  • Potent vasoconstrictor
  • Stimulates adrenal cortex to release aldosterone
  • Stimulate posterior pituitary to release ADH
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17
Q

What is hyperaldosteronism?

A

Too much aldosterone produced

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18
Q

What are the signs of hyperaldosteronism?

A
  • High blood pressure
  • Left ventricular hypertrophy
  • Stroke
  • Hypokalaemia
  • Hypernatraemia
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19
Q

What is the treatment for hyperaldosteronism?

A

Treatment is dependant on which type

  • Aldosterone-producing adenomas = surgery
  • Spiranolactone (mineralocorticoid receptor antagonist)
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20
Q

What are the two types of hyperaldosteronism?

A

1) Primary = defect in adrenal cortex
- Most common cause: bilateral idiopathic adrenal hyperplasia
- Aldosterone secreting adrenal adenoma (Conn’s syndrome)
- Low renin levels

2) Secondary = over activity of the RAAS
- Renin producing tumour
- Renal artery stenosis
- High renin levels

Differentiate based on renin levels

21
Q

What type of hormone is cortisol and where is it produced?

A

Cortisol is a glucocorticoid produced from the zona fasiculata of the adrenal cortex

22
Q

How is cortisol transported in the blood stream?

A

Transcortin (90%) and serum albumin (10%)

23
Q

What stimulates the release of cortisol?

A

ACTH from the anterior pituitary (which is stimulated by CRH)
-ACTH binds to corticotropin receptors (melanocortin receptor/MC2) which is a GPCR

24
Q

What effects does cortisol have on the body?

A
  • Increased proteolysis
  • Increased lipolysis
  • Increased gluconeogenesis
  • Increased resistance to stress (increase supply of glucose, raise blood pressure by making vessels more sensitive to vasoconstrictors)
  • Anti-inflammatory effects (inhibit macrophages)
  • Depression of immune response (for organ transplant)
25
Q

What are the effects of glococorticoids on metabolism?

A
  • Increased glucose production (decrease utilisation, prevent glucose uptake by GLUT4 in muscles)
  • Breakdown of proteins
  • Redistribution of fat (abdomen, dorso-cervical fat pad)
26
Q

What is Cushing’s syndrome?

A

chronic excessive exposure to cortisol

27
Q

What are external causes of Cushing’s syndrome?

A

Prescribed glucocorticoids

28
Q

What are endogenous causes of Cushing’s syndrome?

A
  • Benign pituitary adenoma secreting ACTH (Cushing’s disease)
  • Excess cortisol from adrenal tumour (Adrenal cushing’s)
  • Non-pituitary-adrenal tumours producing ACTH e.g. small cell lung cancer
29
Q

What are the signs and symptoms of Cushing’s syndrome?

A
  • Plethoric moon-shaped face
  • Buffalo hump
  • Abdominal obesity
  • Purple striae
  • Acute weight gain
  • Hypertension
  • Hyperglycaemia
30
Q

What are steroid drugs and give examples

A

Anti-inflammatory and immunomodulatory drugs for conditions such as asthma, rheumatoid arthritis and organ transplant. Examples: prednisolone and dexamethasone

31
Q

Why should dosage of steroid drugs be reduced gradually and not stopped completely?

A

Cortisol is a steroid thus steroid drugs have similar effects to cortisol. Abrupt withdrawal is a life threatening emergency (Addisonian crisis)

32
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency

-used to be caused by TB, now is destructive atrophy from immune response

33
Q

What are the signs and symptoms of Addison’s disease?

A
  • Lethargy
  • Weight loss
  • Postural hypotension
  • Anorexia
  • Hypoglycaemia
  • Increased skin pigmentation
34
Q

Why do you get increased skin pigmentation in Addison’s disease?

A

1) Decreased cortisol
2) Negative feedback to anterior pituitary
3) More POMC required to synthesis ACTH
4) ACTH has alpha-MSH that synthesises melanin

35
Q

What is Addisonian crisis?

A

A life threatening emergency due to adrenal insufficiency

36
Q

What can trigger addisonian crisis?

A
  • Severe stress
  • Salt depravation
  • Infection
  • Trauma
  • Cold exposure
  • Over exertion
  • Abrupt steroid drug withdrawal
37
Q

What are the symptoms of addisonian crisis?

A
  • Nausea
  • Vomiting
  • Pyrexia
  • Hypotension
  • Vascular collapse
38
Q

What is the treatment for addisonian crisis?

A
  • Fluid replacement

- Cortisol

39
Q

What hormones does the zona reticularis of the adrenal cortex produce?

A

Androgens

  • Dehydroepiandosterone (DHEA)
  • Androstenedione
40
Q

What is DHEA converted to in males?

A

Testosterone in testes

41
Q

What happens to adrenal androgens in females?

A

Converted to oestrogen

-only source after menopause

42
Q

What is the adrenal medulla?

A

The central most part of the adrenal glands

-A modified sympathetic ganglion of autonomic nervous system

43
Q

What are the main cells in the adrenal medulla and what chemical messengers do they produce?

A

Chromaffin cells

  • Adrenaline (Epinepharine)
  • Nor-adrenaline (Norepinepharine)
  • Dopamine
44
Q

Describe the synthesis of adrenaline and noradrenaline in chromaffin cells

A

Tyrosine -> (Levodopa) -> Dopamine -> Noradrenaline -> Adrenaline

-20% of chromaffin cells dont have N-methyl transferase (converts noradrenaline to adrenaline)

45
Q

What are adregenic receptors?

A

G-protein coupled receptors

  • Adenylyl cyclase
  • CAMP
  • Protein Kinase A
46
Q

What is the effect of adrenaline on the body?

A

Fight or flight response

  • inc. heart rate (B1)
  • inc. heart contractility (B1)
  • bronchodilation (B2)
  • Vasoconstriction (A1)
  • Vasodilation (B2)
  • inc glycolysis and glycogenolysis (A1 B2)
  • inc. lipolysis (B2)
47
Q

What is a phaeochromocytoma?

A

A rare catecholamine-secreting tumour (mainly noradrenaline)

-dark stains with chromium salt

48
Q

What are the characteristics of phaeochromocytoma?

A
  • Severe hypertension
  • Headaches
  • Diaphoresis (excessive sweating)
  • Palpitations
  • Anxiety
  • Weight loss
  • Elevated blood glucose

METABOLISM, ENDOCRINOLOGY AND HAEMATOLOGY (19 decks)

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