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MEH > Lecture 18 > Flashcards

Lecture 18 Flashcards

1
Q

Where do you find the adrenal glands?

A

On top of the kidneys

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2
Q

What is the structure of the adrenal glands and where are they derived from?

A

Fibrous capsule around entire gland
Cortex (mesoderm origin-envelopes medulla)
-zona glomerulosa (produces mineralocorticoids)
-zona fasiculata (produces glucocorticoids)
-zona reticularis (produces glucocorticoids and some androgens)
Medulla (from neural crest cells)
-chromaffin cells (secrete mostly adrenaline, but also noradrenaline)

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3
Q

What are chromaffin cells?

A

Post ganglionic neuronal cells with no axon

  • usually sympathetic
  • secrete NA/A into bloodstream
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4
Q

Give an example of a mineralocorticoid:

A

Aldosterone

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5
Q

Give some examples of glucocorticoids:

A
  • cortisol (main)
  • corticosterone
  • cortisone
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6
Q

Give some examples of androgens:

A

Sex hormones
-dehydroepiandrosterone
-androstenedione
These are converted to testosterone/oestrogen in peripheral tissues

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7
Q

What is the main function of corticosteroids?

A

Steroid hormones bind to intracellular receptors as they are lipid soluble and affect gene transcription

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8
Q

What are the steroid hormones derived from and where are they synthesised?

A

Derived from cholesterol

Synthesised in adrenal glands and gonads

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9
Q

Why is the enzyme 21-hydroxylase clinically important?

A

Deficiency in this causes congenital adrenal hyperplasia

  • decreased cortisol and aldosterone= health problems
  • increased androgens= early puberty and genital changes
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10
Q

Method of action of corticosteroids:

A

-readily diffuse across plasma membrane
-bind to glucocorticoid receptors
-binding causes dissociation of chaperone proteins
-receptor ligand complex translocates to nucleus
(dimerisation with other receptors can occur)
-receptors bind to glucocorticoid response elements (GRE’s) or transcription factors

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11
Q

Give an example of a chaperone protein:

A

Heat shock protein 90

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12
Q

How is aldosterone transported in blood?

A

Bound to serum albumin (sometimes to transcortin)

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13
Q

What is the role of aldosterone?

A

Regulation of gene transcription

Regulation of plasma Na+/K+/arterial blood pressure
-acts on collecting duct of nephron to promote expression of Na+/K+ pump
-promoting reabsorption of Na+ and excretion of K+
=influencing water retention, blood volume and therefore BP
(reabsorbing more Na+ causes more water to be reabsorbed)

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14
Q

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

A

Angiotensin 2 acts on the adrenal cortex to produce aldosterone when A2 receptors are activated

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15
Q

What are the types of hyperaldosteronism?

A

Primary: defect in adrenal cortex

  • bilateral idiopathic adrenal hyperplasia (most common)
  • aldosterone secreting adenoma (Conn’s syndrome)

Secondary: over activity of RAAS

  • renin producing tumour
  • renal artery stenosis: reduced blood supply stimulates production of renin
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16
Q

How do you distinguish between primary/secondary hyperaldosteronism?

A

Primary: low renin levels (high aldosterone:renin ratio)
Secondary: high renin levels (low aldosterone:renin ratio)

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17
Q

What are the signs and treatment for hyperaldosteronism?

A

Signs

  • high BP
  • left ventricular hypertrophy
  • stroke
  • hypokalaemia
  • hypernatraemia (high calcium)

Treatment:

  • aldosterone producing adenomas are removed by surgery
  • drug called spironolactone used (mineralcorticoid receptor agonist)
18
Q

When is cortisol released?

A

In response to ACTH, released by zona fasiculata

-negative feedback (increased cortisol) to hypoathalmus inhibits CRH/ACTH release

19
Q

How is cortisol transported?

A

Bound to carrier protein in plasma called transcortin

20
Q

What is the action of cortisol?

A

-increased proteolysis in muscle
-increased lipolysis in fat
(catabolic effects)
-increased gluconeogenesis in liver
-anti-inflammatory effects (useful for allergic reactions as inhibits macrophage activity/mast cell degranulation)
-depression of immune response (given to transplant patients)

21
Q

Effect of glucocorticoids (cortisol) on metabolism:

A

Net effects

  • increased glucose production
  • breakdown of protein
  • redistribution of fat (to abdomen, supraclavicular fat pads:buffalo hump, dorso-cervical fat pads: moon face)
  • reduced sensitivity to insulin in muscles as cortisol inhibits GLUT4 translocation
  • increased glycogen stores in liver
22
Q

What is Cushing’s syndrome and its causes?

A

Excessive exposure to cortisol

  • prescribed glucocorticoids
  • benign pituitary adenoma secreting ACTH (Cushing’s disease)
  • excess cortisol produced by adrenal tumour (Adrenal Cushing’s)
  • non pituitary-adrenal tumours producing ACTH (small cell lung cancer)
23
Q

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

A
  • plethoric moon shaped face
  • buffalo hump
  • abdominal obesity
  • purple striae (weakened strength of skin due to proteolysis)
  • acute weight gain
  • hyperglycaemia
  • hypertension
24
Q

Give some examples of steroid drugs and what they are used to treat:

A 
Prednisolone
Dexamethasone
-asthma 
-IBS
-RA
(inflammatory diseases)
-used to supress immune reaction in transplant patients
25
Q

What are the side effects of steroid drugs?

A

Same as those of higher cortisol levels

26
Q

Important point about steroid dosage:

A

Dosage should be reduced gradually not stopped suddenly

27
Q

What is Addison’s disease?

A

Chronic adrenal deficiency

  • due to autoimmune response (attacking adrenal cortex)
  • affects women more
  • can be due to fungal infection/adrenal cancer/adrenal haemorrhage
28
Q

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

A
  • postural hypotension
  • lethargy
  • weight loss (due to reduced food intake due to alpha MSH)
  • anorexia
  • increased skin pigmentation
  • hypoglycaemia
29
Q

Why do you get hyperpigmentation in Addison’s disease?

A
  • decreased cortisol
  • negative feedback on anterior pituitary
  • more POMC required to produce more ACTH and alpha-MSH
  • alpha-MSH controls melanin synthesis
  • ACTH can also activate melanocortin receptors on melanocytes
30
Q

What is Addisonian crisis?

A

Life threatening emergency

  • nausea
  • vomiting
  • pyrexia
  • hypotension
  • vascular collapse
31
Q

What is the treatment for Addisonian crisis?

A
  • fluid replacement

- cortisol

32
Q

What is Addison’s crisis precipitated by?

A
  • severe stress
  • salt deprivation
  • infection
  • trauma
  • cold exposure
  • over-exertion
  • abrupt steroid withdrawal
33
Q

What are androgens and what are they regulated by?

A

Regulated partially by ACTH/CRH
-in men DHEA (dehydroepiandrosterone) is converted to testosterone in testes
-in women adrenal androgens promote libido and are converted to oestrogen by other tissues (after menopause this is the only source of oestrogens)
Promote axillary and pubic hair growth

34
Q

What enzymes do the chromaffin cells that produce NA instead of adrenaline lack?

A

N-methyl transferase which converts NA to adrenaline

chromaffin cells release 20% NA and 80% adrenaline

35
Q

What are the hormonal actions of adrenaline?

A

Fight/flight

  • increase HR and contractility via B1
  • bronchodilation via B2
  • vasoconstriction via A1
  • vasodilation via B2
  • increased renin secretion via B1/B2
  • glycolysis via A1/B2
  • glycogenolysis via A1/B2
  • lipolysis via B2
  • glucagon secretion via A2
  • insulin secretion via A2/B2
  • glycogenolysis/gluconeogenesis via A1/B2
36
Q

Give some examples of adrenergic receptors:

A

B1/B2
A1/A2
G-coupled

37
Q

What is phaeochromocytoma?

A

Chromaffin cell tumour

  • tumour stains dark with chromium salts
  • mainly NA
38
Q

What are the symptoms of phaeochromocytoma?

A
  • severe hypertension (life-threatening)
  • headaches
  • palpitations
  • anxiety
  • weight loss
  • elevated blood glucose
  • diaphoresis (excessive sweating)
39
Q

What are NA/adrenaline derived from?

A

Tyrosine

40
Q

What are the differences between hormones from cortex/medulla?

A 
Cortex: (cortisol/aldosterone/androgens)
-endocrine 
-lipid soluble
-nuclear receptors
-slow response
-death if none of these are present
Medulla: (adrenaline/NA)
-neurocrine 
-water soluble
-GPCR's
-fast response
-no ill effects from lack of these

MEH (22 decks)

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