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Endocrine Physiology > Adrenal Cortex > Flashcards

Adrenal Cortex Flashcards

1
Q

Main components of the axis

A

Hypothalamus, paraventricular nucleus, CRH, ADH, ACTH cells, ACTH, adrenal cortex, steroid hormones

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2
Q

CRH receptor

A

Gs linked with cAMP

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3
Q

ACTH receptor

A

Gs linked with cAMP

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4
Q

Glucocorticoid and androgen receptor

A

Nuclear

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5
Q

Negative feedback

A

Glucocorticoids can act at the POMC and the paraventricular nuclei

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6
Q

Primary regulator of steroidogenesis

A

ACTH

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7
Q

Rate limiting step of steroidogenesis

A

Cholesterol delivery into the mitochondria

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8
Q

P450scc

A

Enzyme that converts cholesterol to pregnenolone inside the inner chamber of the mitochondria

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9
Q

How cholesterol gets into the mitochondria

A

A cholesterol channel

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10
Q

StAR protein

A

Protein that gets inserted into the mitochondrial membrane when stimulated by ACTH to let cholesterol in

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11
Q

PBR

A

Resident receptor in the membrane that has to couple with StAR to let cholesterol in

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12
Q

Only steroids from adrenal cortex that aren’t regulated by ACTH

A

Mineralocorticoids

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13
Q

Biotransformation of steroids

A

Converted into less biologically active forms so they’re more water soluble

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14
Q

Conjugation of steroids

A

Form steroid sulphites and glucuronides in the liver to make them even more soluble

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15
Q

Excretion of steroids

A

Urine and bile

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16
Q

Genomic effects of steroids

A

Modification of gene expression

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17
Q

Non-genomic effects of steroids

A

Affect mRNA stability, trans member and currents, calcium levels, and phosphorylation events

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18
Q

Physiological functions of androgen

A

Maybe libido, secondary sex characteristics, dominance behaviour

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19
Q

Physiological effects of glucocorticoids

A

Change carbohydrate, protein, and lipid metabolism, anti inflammatory and immunosuppressive, increases fetal lung surfactant, CNS actions

20
Q

Glucocorticoid deficiency effect on CNS

A

Anorexia and fatigue, increased smell, taste, and hearing

21
Q

Glucocorticoid excess effect on CNS

A

Alternating euphoria and depression, impaired learning and memory

22
Q

Addison’s disease

A

Weight loss, hypoglycemia, depletion of liver and muscle glycogen, increased urea, depression, weakness

23
Q

Waterhouse-Frederichsen syndrome

A

Adrenal hemorrhage and insufficiency due to meningitidis

24
Q

Cushing’s syndrome

A

Hyperglycaemia, increased lipolysis and protein catabolism, increased androgens, increased urination

25
Q

Loss of ACTH causes

A

Glucocorticoid hyposecretion but not mineralocorticoid

26
Q

Congenital adrenal hypoplasia and primary hypoadrenocorticism causes

A

Hyposecretion of all adrenal steroids

27
Q

Physiological roles of aldosterone

A

Increases sodium and water reabsorption, decreases potassium

28
Q

3 functions of the mammalian kidney

A

Glomerular filtration (passive), tubular reabsorption, tubular secretion

29
Q

Where aldosterone affects reabsorption and secretion

A

In the distal tubule and collecting duct

30
Q

Aldosterone’s effect on DT and CD

A

Recruits Na/K ATPases in basal membrane, as well as sodium and potassium channels in apical membrane

31
Q

ADH effect on CD cells

A

Recruits aquaporins so water is recovered

32
Q

Juxtaglomerular apparatus

A

Associated with distal tubule and glomerulus

33
Q

Macula densa

A

Sensory cells in juxtaglomerular apparatus that monitor sodium in filtrate and blood pressure in kidney and stimulate release of renin from nearby cells if sodium is low

34
Q

Angiotensinogen

A

Constituent of blood protein that forms ATI

35
Q

ATII

A

Converted by ACE in lungs, causes vasoconstriction and increases blood pressure, also causes release of aldosterone

36
Q

Receptors for ADH

A

V1A, V1B, V2

37
Q

V1A

A

ADH receptor that causes vasoconstriction

38
Q

V1B

A

ADH receptor that causes ACTH secretion and acts via IP3 pathway

39
Q

V2

A

ADH receptor that decreases urine production, increases salt and water reabsorption and is cAMP dependent

40
Q

Osmoreceptors

A

Atrial receptors that signal a change in osmolality to the brain to cause ADH release

41
Q

Diabetes insipidus

A

Central lack of ADH or nephrogenic renal insensitivity to ADH

42
Q

Diabetes insipidus symptoms

A

Polyuria and polydipsia

43
Q

Diagnosis and treatment of diabetes insipidus

A

Pitressin, desmopressin

44
Q

Atrial natriuretic peptide

A

Produced by cardiomyocytes of RA, antagonizes RAAS and defends against corticoid and diet related salt retention, inhibits renin secretion and aldosterone, decreases salt appetite

45
Q

Medullary chromaffin cells

A

Where catecholamines are produced

Endocrine Physiology (7 decks)

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