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Physiology > Endocrine-Adrenal Gland > Flashcards

Endocrine-Adrenal Gland Flashcards

(47 cards)

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1
Q

Parts of the adrenal gland

A

Cortex (3 zones)

Medulla (part of sympathetic nervous system)

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2
Q

Ferrets

A

Get adrenal tumors normally on left gland

This is better than right gland because it is closely associated with vena cava and hard to get access to.

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3
Q

Explain venous drainage of adrenal cortex and importance

A

Bf from outside–>cortex–>medulla

Medulla receives whatever products cortex secretes like cortisol.

Cortisol enhances PMNT enzyme in medulla that allows chromaffin cells to make norpinephrine and epinephrine.
Cortisol also inhibits formation of dendrites and axons

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4
Q

Zones of adrenal cortex and their products

A

Zona glomerulose (outermost)= aldosterone

Zona fasciculata (largest)= cortisol

Zona reticularis (innermost)=makes DHEAS/adrogens

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5
Q

All cells in cortex derive from

A

Glomerulosa

So if Rx (lysodrin) kills fasciulata and reticularis, glomerulosa can regenerate those zones.

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6
Q

Chromaffin cells derived from

A

Neural crest cells

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7
Q

Major medullary hormones made

-Exception

A

80% epinephrine
20% norepinephrine
-Exception, cat makes more norepi

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8
Q

T/F majority of norepi in circulation is from adrenal medulla

A

F
30%

Rest is from postganglionic sympathetic terminals

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9
Q

What is neurotransmitter that stimulates epi/norepi release?

A

Achl

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10
Q

Precursor of norepi and epi?

A

Tyrosine

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11
Q

Enzymes that turns tyrosine to catecholamines

A

PMNT

stimulated by cortisol

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12
Q

Effects noreip and epi have

A

Increases BF to Skm
Decreases BF to smooth m
Increases blood glucose and lipolysis

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13
Q

What receptors are used for norepi and epi

A

alpha and beta receptors on target cell surface

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14
Q

Phreochromocytoma

A

Tumor of chromaffin cells that puts big burst of catecholimines out into circulation

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15
Q

Two physiologic units that controls adrenal cortex

A

Aldosterone and renin-angiotensin

Cortisol/corticosterone and hypothalamic pituitary adrenocortical (HPA) system

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16
Q

Synthesis of steroids

  • storage
  • releasal
A

Cholesterol is taken up into adrenal cells via LDLs and HDLs in blood

Cholesterol is stored in adrenal cells

When steroids need to be released, cholesterol will be moved to mitochondria and conversaion of cholesterol to pregneolone (rate limiiting sstep)

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17
Q

How is cholesterol stored inside cell

A

Ester form

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18
Q

How does cholesterol get through cell membrane of mitochondria?

A

steroid acute regulatory protein (STAR)

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19
Q

What is enzyme that is a part of rate limiting step of steroid synthesis?

Study These Flashcards
A

SIP enzyme cleaves cholesterol side chain to produce pregneolone

20
Q

Drugs that affect steroidgenesis

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A

Metyrapone (blocks 11 beta hydroxlase later in pathway)

Ketoconazone (inhibits several enzymes)

Mitotane/Lysodren (causes selective necrosis of fasciulata and reticularis

Trilostane (competitive inhibitor 3 Bhydroxysteroid DH acts early in pathway

21
Q

Drugs that affect steroidgenesis causes

Study These Flashcards
A

Decrease in cortisol

Increase in ACTH

22
Q

Steroids in circulation are bound to

Study These Flashcards
A

Binding proteins

  • corticosteroid binding globulin (CBG)
  • albumin
23
Q

What is biologically active form of steroids

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A

free fraction

24
Q

How are steroids removed from circulation?

Study These Flashcards
A

Via hepatic modification and renal excretion

25
Major fxns of aldosterone
Promotes Na+ retention to keep water and increase ECF volume Decreases K+ by secreting K+ in urine Decreases H+ by secreting H+ in urine
26
Describe pumps/channels/receptors used when aldosterone binds to nephron
Aldosterone binds to MR receptor on cell ENaC channel will allow Na+ into nephron from lumen of nephron ROMK channel will allow K+ out of nephron into lumen of nephron 3Na:2K PUMP (ATP used) will pump 3Na+ OUT of nephron into ECF and pump 2 K+ IN nephron
27
3 positive regulators for aldosterone
Ag II K+ increase ACTH increase
28
Special cells in nephron
Granular cells/juxtaglomerular cells on afferent side and secrete renin Distal tubule has specialized cells, macula densa Blood enters afferent arteriole and exits efferent arteriole
29
Give aldosterone mechanism
1-Renin is released from juxtaglomerular cells from afferent arteriole and interacts with angiotensinogen from liver to make Ag I. 2-Agiotensin converting enzyme (ACE) changes Ag I-->Ag II 3-Ag II interacts w/adrenal cortex (zona glomerulosa to make aldosterone 4-Aldosterone binds to MR receptor to initiate Na+ retention to increase ECF volume.
30
What makes up hypothalamic pituitary adrenocortical (HPA) axis
Hypothalamus: corticotropin releasing hormone (CRH) Pituitary: Adrenocorticotropin (ACTH) Adrenal: Cortisol
31
Regulation of HPA axis - type of secretion - suppression - activation
Diurnal rhythm and episodic secretion Steroids suppress Hypoglycemia, hemorrhage, trauma, mental stress, hypoxia activate
32
Give CRH cascade to make cortisol
CRH released from hypothalamus and activates PKA (GPCR) ACTH is then secreted and interacts with another PKA (GPCR) Cortisol is then released
33
POMC expression
In pituitary...made in intermediate lobe
34
Intermediate lobe vs anterior lobe processing
Processing is more complete/thorough in intermediate lobe than in anterior lobe
35
What determines how much cortisol comes out of adrenal?
1-How many cells are present -->If low ACTH, low cortisol due to shrunken cells. See with animals on steroids 2-How many cells are active -->High ACTH, high cortisol due to BIG active cells
36
Function of glucocorticoids | -Anabolic vs catabolic
Anabolic in liver -Increase gluconeogenesis, glycogen, glucose output, AA transport Catabolic in most other tissue - Proteins broken down=muscle atrophy - Fat broken down=Free FA - Glucose not being taken up=hyperglycemia, anti-insulin lke or diabetogenic
37
How glucocorticoids/cortisol puts brake to inflammation
-HPA activated by inflammatory process Phospholipas A2 inhibited (less arachidonic acid formation) Lysosomal membranes stabilized Decrease permeability of capillaries (plasma leakage) Decrease migration of WBC to inflamed site -Suppress T cell fxn
38
Immunosuppressant activity of glucocorticoids/cortisol
``` -Immunosuppressant activity decrease circulating T lymphs Increase thymus atrophy Decrease cellular-,edoate immunity No effect on AB release from B lymphocytes ```
39
Effects other than immune system related cortisol/glucocorticoids has
inhibits repro promotes bone loss Promotes collagen breakdown and thin skin Inhibits secretion and action of ADH Increases gastric acid secretion High or low level can affect mental state Involved in fetal development, especially type II alveolar cells and surfactant
40
Cortisone and cortisol | -rxns (active and inactive form?)
Cortisone is inactive form and can be converted to cortiso (active) via 11 beta hydroxysteroid DH type I -->Enzyme in liver, fat, CNS, skin Cortisol can be converted to cortisone (inactive) via 11 beta HSD1 (mineralcorticoids have this receptor) -->Enzyme in KIDNEY
41
Zona reticularis | -main products
Weak androgens - DHEA - DHEAS - Androstenedione
42
When do you see increase in DHEAS
puberty
43
Androgen precursor
DHEA
44
Alopecia X or Atypical Cushing's Disease - what - dx
When there's xs secretion of non-cortisol steroid that causes Cushing's and alopecia is observed Dx by giving exogenous ACTH and testing 12-OH progesterone, estradiol, and androstenedione. If post ACTH levels are above reference range then disease is confirmed
45
Adrenal disease in ferrets
Tumor releases sex steroids, androgens, estrogens
46
Primary hypoedrenocorticism - What - How - Signs
- Loss of entire cortex but still have medulla - Can be due to Addison's disease, autoimmune attack - There's low/no aldosterone and no cortisol - ->low Na+, high K+
47
Addison's Disease - signs - Dx
Low Na+ High K+ Test ACTH and measure cortisol...no cortisol, confirmed

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