Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Metabolism, Endocrinology, Haematology > Endocrinology Session 5 > Flashcards

Endocrinology Session 5 Flashcards

1
Q

What are the components of the adrenal gland?*

A
  • Capsule
  • Cortex
  • Medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 zones of the adrenal cortex and what do they produce?*

A
  • Zona glomerulosa (mineralocorticoids; aldosterone)
  • Zona fasciculata (glucocorticoids; cortisol)
  • Zona reticularis (glucocorticoids and androgens)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do the chromaffin cells of the medulla produce?

A
  • Adrenaline 80%
  • Noradrenaline 20%
    (Cell bodies that secrete catecholamines into the bloodstream)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the adrenal glands?

A

Multifunctional endocrine glands that have a combined weight of 6-8g

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the properties of steroid hormones?

A
  • Synthesised from cholesterol

- Lipid soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do steroid hormones work?

A

Bind to receptor of the nuclear receptor family (as cross the plasma membrane readily) and modulate gene transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the types of steroid hormones?

A

Glucocorticoids, mineralocorticoids, androgens, oestrogens, progestins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do corticosteroids act?*

A
  • Diffuse across plasma membrane
  • Bind to glucocorticoid receptors
  • Binding = dissociation of chaperone proteins
  • Receptor-ligand complex translocates to nucleus
  • Dimerises with other receptors
  • Receptors bind to glucocorticoid response elements on DNA or other transcription factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is aldosterone carried?

A

Serum albumin (main) and transcortin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the connective tissue capsule contain?

A

Capsular plexus - many blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the function of aldosterone?

A

Regulating Na+, K+ and arterial BP

- Upregulation of epithelial sodium channels in collecting duct for more reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the main action of aldosterone?

A

Distal tubules and collecting ducts - promotes the expression of the Na/K pump that promotes Na+ reabsorption

Na+ is osmotically active, so water will follow and more water will be reabsorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the renin-angiotensin-aldosterone system?*

A
  • Renin cleaves angiotensinogen into angiotensin I
  • Angiotensin I cleaved by ACE in lung endothelial cells to Angiotensin II
  • Angiotensin II acts on arteries to cause vasoconstriction
  • Angiotensin II acts on the adrenal cortex/zona glomerulosa to release aldosterone, which increases Na+ and water reabsorption in kidney
  • Angiotensin II acts on posterior pituitary to release ADH which adds more aquaporin channels in kidney and promotes reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does the RAAS cause?

A

Increased blood pressure and blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes the kidney to release renin in the first place?

A

Hypotension and hypovolaemia - decrease in renal perfusion which activates baroreceptors due to increased sympathetic tone = more renin released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is hyperaldosteronism?

A

Overproduction of aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of primary hyperaldosteronism?

A

Defects in the adrenal cortex:

  • Bilateral idiopathic adrenal hyperplasia (common)
  • Conn’s syndrome (aldosterone-secreting adenoma)
  • Low renin levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the causes of secondary hyperaldosteronism?

A

Overactivity of RAAS:

  • Renin producing tumour
  • Renal artery stenosis
  • High renin levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the signs of hyperaldosteronism?

A
  • High blood pressure
  • Left ventricular hypertrophy
  • Stroke
  • Hypernatraemia
  • Hypokalaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the treatments for hyperaldosteronism?

A
  • Adenomas - surgery

- Spironolactone - mineralocorticoid receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the features of cortisol?

A
  • Synthesised in response to ACTH

- Negative feedback to hypothalamus inhibits CRH and ACTH release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is cortisol carried?

A

Transcortin (carrier protein)

23
Q

What are the catabolic effects of cortisol?

A
  • Increased protein breakdown in muscle
  • Increased lipolysis
  • Increased gluconeogenesis in liver
24
Q

What are the other effects of cortisol?

A
  • Anti-inflammatory (meds for allergic reactions)
  • Depression of immune response

Regulates gene transcription.

25
Q

What is the hypothalamic-pituitary-adrenal axis?*

A

Production of cortisol in response to ACTH which is released from the anterior pituitary gland in response to CRH release from the hypothalamus (regulated by negative feedback)

26
Q

When is CRF secreted?

A

In response to physical, chemical and emotional stressors (eg. temperature, hypoglycaemia)

27
Q

Why should time always be taken into account when measuring cortisol levels?

A

Blood cortisol levels vary throughout the day (peak in morning, fall at night)

28
Q

What is the effect of cortisol on MUSCLE?*

A

Inhibition of insulin-induced GLUT4 in muscle

  • Prevents glucose uptake
  • Less glucose utilisation so more protein degradation
29
Q

What is the effect of chronic high levels of cortisol on FAT?

A

Redistribution of fat in abdomen, supraclavicular fat pads and face (less glucose utilisation so more lipolysis)

30
Q

How do glucocorticoids affect the LIVER?*

A
  • Increased glycogen storage and gluconeogenesis

- More insulin due to more insulin, so more liver glycogen stores

31
Q

What are the net effects of glucocorticoids?

A
  • Increased glucose production
  • Breakdown of protein
  • Fat redistribution
32
Q

What is Cushing’s syndrome caused by?

A

Chronic, excessive exposure to cortisol

33
Q

What are the external causes of Cushing’s syndrome?

A

Prescribed glucocorticoids (common)

34
Q

What are the endogenous causes of Cushing’s syndrome?

A
  • Benign, pituitary ACTH secreting adenoma (C. Disease)
  • Excess cortisol produced by adrenal tumour
  • Non-pituitary adrenal tumour producing ACTH (eg. small cell lung cancer)
35
Q

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

A
  • Moon-shaped face
  • Buffalo hump
  • Abdominal obesity
  • Purple striae (increased proteolysis due to weaker integrity of the skin)
  • Acute weight gain
  • Hyperglycaemia
  • Hypertension
36
Q

What are the examples of steroid drugs?

A

Prednisolone, dexamethasone

37
Q

What are the properties of steroid drugs?

A
  • Have anti-inflammatory and immunomodulatory effects
  • Used to treat disorders, eg. asthma, IBD, RA
  • Immunosuppression after organ transplants
  • Same side effects as higher levels of cortisol
38
Q

Why should steroids be reduced gradually and not stopped abruptly?

A

The body will stop making some of its own steroids = sharp fall in blood glucose and BP

39
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency

40
Q

What can cause Addison’s disease?

A
  • Complication of TB
  • Destructive atrophy from autoimmune response
  • More common in women
  • Rare: cancers, trauma, infections
41
Q

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

A
  • Postural hypotension
  • Lethargy
  • Weight loss
  • Anorexia (related to an increase in beta-endorphins?)
  • Increased skin pigmentation
  • Hypoglycaemia
42
Q

What causes hyperpigmentation in Addison’s disease?*

A
  • Decreased cortisol causes more CRH and ACTH production (neg. feedback)
  • More POMC needed to synthesise ACTH
  • Increased ACTH, so increased POMC
  • POMC can also produce more MSH
  • Alpha-MSH stimulates melanocytes in the skin to produce more melanin - more pigment

ACTH ITSELF CAN ALSO ACTIVATE MELANOCORTIN RECEPTORS

43
Q

What is Addisonian crisis?

A

Acute medical emergency whereby the adrenal glands stop working and there is not enough cortisol in body

44
Q

What can precipitate Addisonian crisis?

A
  • Severe stress
  • Infection
  • Trauma
  • Cold exposure
  • Overexertion
  • Abrupt steroid withdrawal
45
Q

What are the symptoms of Addisonian crisis?

A
  • Nausea and emesis
  • Hypotension
  • Pyrexia
  • Vascular collapse
46
Q

What is the treatment for Addisonian crisis?

A
  • Fluid replacement

- Cortisol

47
Q

What androgens are secreted from the zona reticularis and what do they do?

A
  • DHEA and androstenedione
    Male: DHEA converted to testosterone in testes
    Female: promote libido, converted to oestrogens by other tissues (only oestrogen source post-menopause)

PROMOTE AXILLARY AND PUBIC HAIR GROWTH

48
Q

What is the adrenal medulla?*

A

Modified sympathetic ganglion of ANS - chromaffin cells have no axons

49
Q

What conversions happen in the adrenal medulla?

A
  • Tyrosine - (tyrosine hydroxylase) > Levodopa
  • Levodopa - (DOPA decarboxylase) > Dopamine
  • Dopamine - (Dopamine B-hydroxylase > NAd
  • NAd - (N-methyl transferase) > Ad
50
Q

Why can’t some chromaffin cells make adrenaline?

A

Lack N-methyl transferase

51
Q

What are the actions of adrenaline (fight or flight)?**

A
  • Increase in HR and contractility
  • Bronchodilation (B2)
  • Vasoconstriction (a1) and vasodilation (B2)
  • Renin secretion in kidney
  • Glycolysis and glycogenolysis (muscle, + gluconeogenesis in liver)
  • More glucagon secretion
  • Lipolysis
52
Q

What is a phaeochromocytoma?*

A

Tumour of the chromaffin cells = rare, catecholamine-secreting tumour that secretes noradrenaline and can cause lifethreatening hypertension

53
Q

What are the symptoms of a phaeochromocytoma?*

A
  • SEVERE HYPERTENSION
  • Headaches
  • Palpitation
  • Excessive sweating/diaphoresis
  • Anxiety
  • Weight loss
  • Hyperglycaemia

Metabolism, Endocrinology, Haematology (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions