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Endocrinology > Physiology 3 > Flashcards

Physiology 3 Flashcards

1
Q

Zona Glomerulosa

A

Adrenal Cortex
-make mineralcorticoids (aldosterone)
15%

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2
Q

Zona Fasciculata

A

Adrenal Cortex
75%
Glucocorticoids (Cortisol)
some androgens, estrogen

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3
Q

Zona Reticularis

A 
Adrenal Cortex
10%
Androgens
Estrogens
some cortisol
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4
Q

Adrenal Medulla

A

Catecholamines
Epi/Norepi
(Adrenaline and noradrenaline)

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5
Q

Function of Mineralocorticoids

A

(aldosterone)

-increase Na adsorption and K secretion to maintain body fluid volume

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6
Q

Function of Glucocorticoids

A

(cortisol)

  • provede sustained energy source (glucose, FAs, AAs)
  • enhance gluconeogenesis in liver
  • increase fatty acids as an alternative energy source
  • raise blood glucose
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7
Q

Catecholamines

A

(epinephrine & norepinephrin)
-rapid response to stress: fuel availability (glucose, fatty acids) to increase CV function and performance (heart, lung, muscle)

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8
Q

Adrenal Sex Hormones

A

-growth developmental control in men and women

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9
Q

The transport of adrenocortical hormones in blood

A
  • steroid hormone-binding serum proteins
    1) globulins
    2) albumin
    3) cortisol
    4) aldosterone
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10
Q

Globulins

A
  • high-affinity reversible binding:
    • corticosteroid-binding globulin (CBP, transcortin)
    • aldosterone-binding globulin
    • sex-steroid-binding protein (SSB)
    • progesterone-binding globulin (PBG)
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11
Q

Albumin

A

-low affinity reversible binding

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12
Q

Cortisol

A

~90% bound to transcortin (majority) and albumin (less)

  • 10% is in plasma is free
  • t1/2 60-90 min
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13
Q

Aldosterone

A

~60% is bound to transcortin, aldosterone-binding globulin and albumin

  • 40% is free
  • t1/2 is 20min
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14
Q

Purposes of hormone protein-binding?

A

1) suppresses biological activity of steroid hormones (inactive pool)
2) protect hormone from structural alterations
3) to extend the life-time of hormones in the plasma
4) provide active hormone to target tissue rapidly when needed

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15
Q

Cholesterol

A

-source for synthesis of all steroid hormones

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16
Q

LDL

A

-main provider of cholesterol
~80% cholesterol for steroid synthesis
~20% cholesterol is synthesized in adrenal gland

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17
Q

Transport of Cholesterol to Adrenal Cells

A
  • LDL binding to LDL receptors on plasma membranes of adrenal cortical cells
  • LDL transported into cell by endocytosis in clathrin-coated pits
  • formation of endosomes (early and late) and lysosomes (cholesterol is released from receptors)
  • LDL receptors are recycled to plasma membranes
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18
Q

Cholesterol Storage

A

-esterified and stored in cytoplasmic vesicles until it is needed for synthesis of corticosteroid hormones

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19
Q

Adrenal Corticosteroid Synthesis

A

-mitochondrial rate limiting step: cholesterol to pregnenolone
Enzyme is CYP11A1 (P450) (cholesterol desmolase)

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20
Q

Neuroendocrine control of steroidogenesis

A
  • ACTH (hypothalamus-pituitary axis)
  • stimulates the activity of CYP11A1
  • increases cholesterol uptake (by upregulating LDL receptors)
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21
Q

Mineralocortiocoids

A

-Aldosterone (most potent) ~90% of all activity
-Deoxycorticosterone (DOC, aldosterone precursor)
1/30 aldosterone potency
-9alpha-Fluorocortisol: synthetic potent aldosterone analogue, slightly more than aldosterone

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22
Q

Key Enzymes in Mineralocorticoid Biosynthesis

A

-CYP11A1 (cholesterol desmolatse) upregulated by ACTH
-Aldosterone Synthase (upreg by ACTH)
corticosterone to aldosterone (final step of synthesis)

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23
Q

Organs that have Mineralocorticoid Receptors

A

target organs for aldosterone

  • kidney
  • brain
  • lungs
  • heart
  • vascular tissues
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24
Q

Specific ligand of MR - Aldosterone

A
  • high receptor affinity

- low blood level

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25
Q

Non-specific activation of MRs by glucocorticoids

A 
Cortisol
-high receptor affinity
-high blood level
-active ligand 
Cortisone
-low receptor affinity
-inactive ligand
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26
Q

Mineralocorticoid Effects of Gene Expression

A

UP REGULATION

1) aldosterone binds MRs in cytoplasm
2) hormone-receptor complex translocated to nucleus
3) binding to promoter area of specific genes
4) upregulating of gene expression (Na+/K+ ATPase, Na+, K+ transporters)
- NON-GENOMIC effects - cAMP, IP3, Ca2+ dep regulation, protein phosphorylation mediated cell signaling pathways (SGK-1, ERK1/2, JNK)

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27
Q

Corticosterone

A

-aldosterone precursor

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28
Q

Cortisol

A

-hydrocortisone; mineralocorticoid activity

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29
Q

Cortisone

A

-slight mineralocorticoid activity

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30
Q

Enzymatic inactivation of cortisol

A

(adrenal cortex, liver)
-11 beta hydroxysteroid dehydrogenase (11betaHSD) converts cortisol to cortisone

casuse increase selectivity of MRs to aldosterone

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31
Q

Aldosterone-Regulated Genes

A

1) Na,K ATPase -transport Na out and K in
2) Epitheilial sodium channel (ENaC)
3) Serum and GLucocorticoid - regulated Kinase 1
4) Renal Outer Medullary K channel (ROMK) an ATP-dependent K channel that transports K out of cells

Sgk1 activated Na/K ATPase, ENaC, and ROMK to maintain:
low intracellular Na
high intracellular K

32
Q

Renal Effects of Mineralocorticoids

A
  • Na+ reabsorption to increase total body Na
  • K+ secretion to decrease plasma K
  • H+ secretion - metabolic alkalosis
  • HCO3- production - metabolic alkalosis
  • H2O reabsorption for volume expansion
33
Q

Cortisol

A

Glucocorticoids
-(hydrocortisone) most potent
~95% of total glucocorticoid activity

34
Q

Corticosterone

A

-cortisol precursor, modest potency

~4% of total glucocorticoid activity

35
Q

Synthetic Glucocorticoids

A
  • more potent than natural
  • Dexamethasone (30X cortisol)
  • Methylprednisone (5X)
  • Prednisone (4X)
36
Q

Key Enzymes in Cortisol Biosynthesis

A
  1. CYP11A1 (MX) cholesterol desmolase inhibited by: Ketoconazole
  2. 17alpha-hydroxylase
  3. 3beta-hydroxylase
  4. 21betahydroxylase
  5. 11beta-hydrolylase (mx) inhibited by metyrapone; etomidate
37
Q

Genomic Effects of Glucocorticoids

A
  1. Glucocorticoids are cell-permeable
  2. Binding to glucocortiocid receptors in cytoplasm
  3. The hormone-receptor complex translocates into the nucleus
  4. Binding to promoter regions of target genes (5-25% of genome)
  5. Stimulation or repression of gene expression (transactivation)
  6. Suppression of genes via transcriptional factors (NFkappaB) (transrepression)
38
Q

Glucocorticoids on Liver

A
  • promotes gluconeogenesis from amino acids
  • upregulate key enzymes
  • mobilization of amino acids from muscle into blood
  • enhanced glycogen formation to store glucose in liver
39
Q

Glucocorticoids on Pancreas

A
  • increase insulin production

- increase plasma insulin

40
Q

Glucocorticoids on Other organs

A

-insulin resistance increases (insulin-sensitive glucose uptake is not enhances)

41
Q

Glucocorticoids on glucose uptake and utilization by most cells

A

decrease

-via inhibiting insulin sensitive glucose transporters and enzymes involved in glucose catabolism

42
Q

Glucocorticoids on Blood

A

glucose level increase (up to 50%)

-protection against hypoglycemia

43
Q

Glucocorticoids on Brain

A

-enhanced glucose supply increase (insulin-independent)

44
Q

Glucocorticoids & Protein Metabolism

A

-various organs (except liver)
Stimulate protein catabolism
-increase protein degradation to amino acids
-amino acids in blood increase
-amino acid transport to tissues decrease
-decrease protein synthesis (muscle, lymphoid tissue) decrease
-body weight decrease
-muscle weakening
-immune functions suppressed, deccreased involution of thymus

45
Q

Glucocorticoids and Liver

A
  • increased protein synthesis (upregulation of key enzymes)

- increase gluconeogenesis (convert amino acids to glucose)

46
Q

Overall purpose

A

-mobilize protein from the peripheral tissues to provide glucose supply to the brain and other tissues

47
Q

Glucocorticoids on Adipose Tissue

A
  • promote lipolysis
  • enhance mobilization & oxidation of fatty acids as an alternative energy source at time of starvation
  • fat degradation to fatty acids in the cells
  • fatty acids in blood increase
  • oxidation of fatty acids in cells increase
48
Q

Glucocorticoids with Food

A
  • increase food uptake
  • redistribution of body fat
  • paradoxical fat deposits in the body
49
Q

Cushing’s Syndrome

A
  • high doses of Glucocorticoids
  • fat in chest, head, fat lump between shoulders, purple stretch marks on skin, rounded face
  • HTN, diabetes, bone loss
50
Q

Effects of Cortisol on Immunity and Inflammation

A

main targets are macrophages and T-lymphs

  • dec. production of inflammatory cytokines
  • function on inflammatory cells dec
  • apoptosis increase
  • atrophy of lymphoid tissue
51
Q

Suppression of inflammation?

A
  • Initial stages of inflammation (lysosomal disruption)
  • prevents edema (decreased permeability of blood capillaries)
  • decreases leukocyte migration to the inflamed area
  • suppresses immune system (T lymphocytes)
  • attenuates fever (IL-1 release)
  • prevents immunological rejection of transplanted organs and tissues
52
Q

Glucocorticoids in Skin

A

-collagen syntheses dec.

53
Q

Glucocorticoids in Intestine

A

-Ca2+ absorption dec.

54
Q

Glucocorticoids in Kidney

A

-Ca2+ reabsorption dec.

55
Q

Glucocorticoids in blood

A

Ca2+ level dec.

-blood clotting reduced, resulting in bruising

56
Q

Glucocorticoids in bones

A
  • Ca2+ mobilization inc. leads to bone demineralization (osteoporosis)
  • growth suppression
57
Q

Glucocorticoids in blood vessels

A

-vasoconstrictioin, promotes hypertension

58
Q

Glucocorticoids in GI

A

-stimulate GI function, gastric acid and enzyme production

59
Q

Glucocorticoids in Nervous System

A
  • suppress hypothalamic-pituitary-adrenal axis

- increase appetite, influence sleep and mood

60
Q

Adrenal Sex Hormones

A

-androgen precursors and androgens
(dehydroepiandrosterone DHEA, androstenedione, testosterone) - moderately active male sex hormones
Function: developmental regulation of reproductive organs

61
Q

Adrenal Sex Hormones: Adult males

A

-weak effects

62
Q

Adrenal Sex Hormones: Adult females

A
  • the major androgens
  • excess leads to suppression of gonadal function and masculinization - adrenogenital syndrome
  • Progesterone and estorgen
  • important during post-menopausal period
63
Q

Epinephrine

A 
Adrenal Medulla (80%)
-adrenaline
-secreted to blood
-amino acids derivatives (catecholamines)
from Tyrosine
64
Q

Norepinephrine

A

Adrenal Medulla (20%)

  • noradrenaline
  • amino acids derivatives (catecholamines)
65
Q

Hormones of Adrenal Medulla Target

A
  • heart
  • lungs
  • muscles
  • vessels
66
Q

Functions of Adrenal Medulla Hormones

A
  • inc. heart rate, breathing, BP, glucose release from liver, blood glucose level, metabolic rate, vasodilation of blood vessels, blood flow to skeletal muscle, fat metabolism, free fatty acids
  • dec. digestive processes, urine production

Neural Control (sympathetic nervous system)

67
Q

Hypothalamic-pituitary-adrenal-axis

A

-regulates stress response, energy usage, immune response, digestion

68
Q

CRH

-Hypothalamus - Pituitary

A

-corticotropin-releasing hormone (CRH) stimulates the pituitary gland to secrete Adrenocorticotropic Hormones (ACTH)

69
Q

Pituitary - Adrenal

A

ACTH stimulates adrenal cortex (production of glucocorticoids, mineralocorticoids, sex hormones)
-ACTH also stimulates adrenal medulla to produce adrenalin

70
Q

Feedback Regulation of Hypothalmic-Pituitary-Adrenal axis

A

-cortisol, via glucocorticoid receptors (GluRs), initiates a neg. feedback reg by inhibiting the hippocampus, hypothalamus, and pituitary gland
-negative feedback loop
suppression of inhibitory input of hippocamous
suppression of CRH release by hypothalamus
suppression of ACTH production by pituitary gland

71
Q

Long Term Treatment with Dexamethasone

A
  • cortisol production dec

- functional atrophy of the hypothalamic-pituitary-adrenal axis

72
Q

Stress

A
  • non-specific response of body to any demand

- stress causes: starvation, infection, trauma, debilitating disease, psychological stress, anxiety, depression

73
Q

Moderate Stress

A

-activates hypothalamic - pituitary - adrenal axis while maintaining negative feedback

74
Q

Acute Stress

A
  • Heart rate inc
  • Breathing rate inc
  • Blood glucose inc
  • Glucose utilization inc
  • Energy productioin inc
75
Q

Effects of Sustained Severe Stress on Hypothalamic-Pituitary-Adrenal Axis

A

-excessive activation and dysregulation of hypothalamic-pituitary-adrenal axis (overriding negative feedback)
-continuous stimulation of adrenal steroid hormones
-enlargement of adrenal glands, adrenocortical hyperfunction
Major Health Problems:
-Heart disease, immunosuppression, digestive problems, sleep disorders, anxiety, depression

Endocrinology (15 decks)

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