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The adrenal gland Flashcards

1
Q

What blood vessels connect to the adrenal glands?

A

Many arteries but only one vein.

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2
Q

What does the left adrenal vein drain into?

A

Left Renal vein

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3
Q

What does the right adrenal vein drain into?

A

Inferior vena cava.

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4
Q

What makes up the adrenal cortex?

A

Zona glomerulosa, zona fasciculata and zona reticularis

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5
Q

What is the middle portion of the adrenal gland called?

A

Adrenal medulla.

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6
Q

What does the zona glomerulosa produce?

A

Aldosterone.

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7
Q

What does the zona fasciculata produce?

A

Cortisol.

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8
Q

What does the zona reticularis produce?

A

Androgens.

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9
Q

What does the adrenal medulla produce?

A

Catecholamines.

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10
Q

What does the adrenal cortex produce?

A

Corticosteroids.

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11
Q

Name 3 catecholamines

A

Adrenaline, noradrenaline and dopamine.

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12
Q

What converts cholesterol to pregnenolone?

A

Side chain cleavage.

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13
Q

What converts pregnenolone to progesterone?

A

3 beta hydroxy steroid dehydrogenase.

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14
Q

Series of enzymes that convert progesterone to aldosterone?

A

21,11,18 hydroxylase.

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15
Q

Series of enzymes that convert progesterone to cortisol?

A

17,21,11 hydroxylase.

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16
Q

Where are Na+ pumps activated in response to aldosterone.

A

distal convoluted tube and cortical collecting duct in kidney

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17
Q

How does aldosterone work?

A

Binds to intracellular receptor. Gene expression results in greater Na+ reabsorption from urine into blood by activating Na+ pumps in distal convoluted tube and cortical collecting duct in the kidney. Na+ is pumped into blood and K+, H+ are pumped out of blood into urine by active transport. Increased Na+ reabsorption results in increased water reabsorption and so increased blood volume.

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18
Q

How does the renin angiotensin system work?

A

Drop in blood pressure (drop is renal perfusion pressure). juxtaglomerular cells detect drop in renal perfusion pressure and macula densa can detect drop in Na+. Release of renin from kidney (juxtaglomerular cells). Renin converts angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by ACE (lots in the lung).

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19
Q

What does angiotensin II do?

A

Vasoconstrictor. Increases synthesis of aldosterone from zona glomerulosa of adrenal cortex. Also stimulates release of AVP from anterior pituitary.

20
Q

How does angiotensin II increase aldosterone synthesis?

A

Activates enzymes in the zona glomerulosa of adrenal cortex - side chain cleavage, 3 beta hydroxysteroid dehydrogenase, 21 hydroxylase, 11 hydroxylase and 18 hydroxylase.

21
Q

Cortisol hormone effects in the body?

A

Increased peripheral protein catabolism, increased gluconeogenesis, increased lipolysis - increased blood glucose. Increased vascular permeability, increased urine output.

22
Q

What does cortisol inhibit?

A

The release of ACTH and CRH.

23
Q

How does ACTH result in release of cortisol from zona fasciculata?

A

Activation of enzymes - side chain cleavage, 3 beta hydroxysteroid dehydrogenase, 17,21,11 hydroxylase.

24
Q

How is cortisol released?

A

Pulsatile release. Diurnal rhythm

25
Q

What is addison’s disease?

A

Primary adrenal failure. Insufficient amount of aldosterone, glucocorticoids.

26
Q

Causes of addison’s disease?

A

Destruction of adrenal cortex by immune system. Can also be caused by TB of the adrenal glands.

27
Q

Markers for addison’s disease

A

High ACTH, low cortisol, high MSH, low aldosterone

28
Q

Symptoms of addison’s disease?

A

Hyperpigmentation, low blood pressure, weakness and vitiligo.

29
Q

What causes hyperpigmentation in addison’s disease?

A

High MSH results in increased production of melanin resulting in darker skin.

30
Q

What is MSH?

A

Melanocyte stimulating hormone.

31
Q

What results in low blood pressure in addison’s disease?

A

Low aldosterone.

32
Q

What results in vitiligo in addison’s disease?

A

Autoimmune destruction of melanocytes.

33
Q

Explain why a patient with addison’s disease has a tan?

A

ACTH is a peptide hormone. It is produced from a prohormone called proopiomelanocortin. When proopiomelanocortin is cleaved it produces ACTH and another hormone called MSH. High production of ACTH results in high levels of MSH. Melanocyte stimulating hormone stimulates melanocytes to produce melanin resulting in patients having a tan.

34
Q

How would you treat an addison’s crisis? Explain your management.

A

Administer saline solution by iv to patient to treat hyponatremia caused by deficiency in aldosterone. Give dextrose to treat low blood glucose caused by deficiency in glucocorticoids. Give hydrocortisone if you know its addison’s disease to treat low cortisol.

35
Q

What is secondary hypoadrenocortism and what are the biomarkers?

A

When the pituitary gland doesn’t secrete enough ACTH. Results in reduced levels of cortisol and ACTH.

36
Q

What is cushing’s syndrome?

A

Excess cortisol or other glucocorticoid production.

37
Q

What is cushing’s disease?

A

Pituitary tumour resulting in too much ACTH release.

38
Q

What are the 4 causes of cushing’s syndrome?

A

Cushing’s disease - pituitary tumour causing too much ACTH release.
Adrenal tumour - too much cortisol release.
Taking oral steroids.
Ectopic ACTH - ACTH secreting tumour outside of pituitary gland (e.g lung cancer).

39
Q

What is the principle cause of cushing syndrome symptoms?

A

Loss of protein, gain of fat.

40
Q

Cushing syndrome symptoms

A

Depression, easy bruising, red stretch marks, poor wound healing, immunosuppression.

41
Q

What are the precursor amino acids for catecholamines?

A

Tyrosine and phenylalanine.

42
Q

What is the catecholamine pathway? Explain the biochemical changes that take place.

A

Phenylalanine to tyrosine. Tyrosine to dopa (hydroxylation). Dopa to dopamine (decarboxylation - removal of carboxyl group). Dopamine to noradrenaline (hydroxylation). Noradrenaline to adrenaline (methylation).

43
Q

Where are catecholamines stored and when are they released?

A

Cytoplasmic granules and released in response to ACh from preganglionic sympathetic neurones.

44
Q

How are catecholamines degraded and what are the degradation enzymes?

A

Monoamine oxidase(deamination) or catechol - O methyl transferase(methylation).

45
Q

Catecholamine half life compared to corticosteroids?

A

Catecholamines are short lived molecules.

46
Q

Catecholamines effect in the body?

A

Tachycardia, sweating, increased blood glucose and vasoconstriction.

47
Q

What are adrenaline and noradrenaline bound to in blood?

A

Albumin.

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