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Physiology > Lecture 13: Adrenal gland > Flashcards

Lecture 13: Adrenal gland Flashcards

1
Q

Where are the adrenal glands located in relation to kidneys

A

Dorsal-medial to kidneys

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2
Q

What is blood supply and venous drainage of adrenal gland

A

Suprarenal arteries and veins

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3
Q

What is the direction of adrenal gland perfusion

A

Blood moves through sinusoidal system through cortex first then medulla

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4
Q

What hormone does zona glomerulosa secrete and what is the target

A

Hormone= mineralocorticoids (ex: aldosterone)

Target: kidney

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5
Q

What hormones does the zona reticularis secrete and what is the target

A

Hormone= androgens (DHEA)

Target= male and female sex organs

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6
Q

What hormones does the zona fasciculata secrete and what is the target

A

Hormone= glucocorticoids (cortisol)

Target: liver (glucogenesis)

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7
Q

What hormones does the adrenal medulla produce and what is the target

A

Hormones= catecholamines (NE and E)

Target: liver, muscles, heart

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8
Q

All cells in cortex have lipid droplets, mitochondria and smooth ER why?

A

Lipid droplets- source of cholesterol
Mitochondria: first step in steroid synthesis from cholesterol —> pregnenolone

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9
Q

What regulates cholesterol—> pregnenolone

A

HPA Axis: ACTH

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10
Q

What regulates pregnenolone—> Mineralocorticoids

A

RAAS and ACTH

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11
Q

What regulates pregnenolone—> glucocorticoids and androgens

A

HPA: ACTH

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12
Q

What regulates the adrenal medulla: SNS or PNS

A

Autonomic control of the SNS

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13
Q

What enzyme differentiates adrenal corticosteroids from progesterone

A

C-21

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14
Q

What enzyme differentiates cortisol from aldosterone

A

C-17

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15
Q

Zona glomerulus synthesizes aldosterone and lacks which enzyme that is necessary for cortisol and androgen synthesis

A

17-alpha hydroxylase

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16
Q

Due to absence of 17-alpha hydroxylase in zona glomerulus, pregnenolone can only be converted to progesterone by ___

A

3B-HSD

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17
Q

What 3 mechanisms result in aldosterone synthesis

A
  1. RAAS (decrease BP or ECF)
  2. Plasma K+ (increase K+, increase aldosterone, increase K+ excretion from kidney)
  3. ACTH via HPA axis- weak effect
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18
Q

What receptor does aldosterone bind

A

Mineralocorticoid receptor

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19
Q

Aldosterone binds MR and activates what gene targets

A

Apical ENaC (increase Na+ reabsorption in CD)
Basolateral Na+/K+ ATPase

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20
Q

Which solutes are absorbed and secreted during aldosterone activation

A

Na+ reabsorbed, K+ secreted, H+ excreted

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21
Q

How does aldosterone affect BP

A

Increase BP by increasing Na+ and H20 reabsorption

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22
Q

What is Conn’s Syndrome: Primary hyperaldosteronism usually caused by

A

Aldosterone secreting tumor

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23
Q

What are the physiological effects of Conn’s syndrome: primary hyperaldosteronism

A

Hypernatremia, fluid retention, hypertension, hypokalemia, metabolic alkalosis, low renin

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24
Q

What are some common symptoms of Conn’s syndrome: primary hyperaldosteronism

A

PU/PD, hypertension, fatigue, headache, visual disturbances, neuropathy

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25
What are some symptoms of feline primary hyperaldosteronism
Hypertension, vision loss, muscle weakness, plantigrade posture
26
Zona fasciculata synthesizes cortisol, what enzyme is needed to cortisol synthesis
17-alpha hydroxylase
27
If 17-alpha hydroxylase is blocked can life be sustained?
Yes, corticosterone is a glucocorticoid produced in aldosterone synthesis and can be used a a replacement
28
What hormone requires binding proteins in order to be transported
Steroids
29
Are bound or free hormones available to signal
Free hormones
30
Where are receptors for glucocorticoid and mineralocorticoids located
Cytoplasm- steroid hormones are non-polar and lipophilic therefore they can readily diffuse across cell membrane
31
What receptors are ligand inducible transcription factors that activate transcription of specific genes
MR’s and GR’s
32
MR’s and GR’s have a shared homology in their ligand binding and DNA binding domains, what is the problem?
Plasma cortisol is 100-1000x higher than aldosterone, therefore cortisol binds MR with high affinity
33
How is selectivity of aldosterone for MR’s achieved
Tissues targeted by aldosterone contain enzyme 11B-hydroxysteroid dehydrogenase II (11B-HSD2) which converts cortisol to cortisone- inactive form so can’t bind MR’s
34
A decrease in 11B-HSD2 would lead to …..
Decreased conversion of cortisol to cortisone and increased aldosterone like effects—> including Na+ retention
35
Zona reticularis is responsible for synthesizing androgens, what enzymes are needed
17, 20 lyslase promotes converted to DHEA and androstenedione
36
Zona reticularis lacks which enzyme that permits synthesis of aldosterone
21B- hydroxylase
37
What plasma binding protein does aldosterone bind to
Albumin
38
What plasma binding protein does cortisol bind to
Transcortin
39
What plasma binding protein does DHEA bind to
Albumin
40
What are the primary hormones released by the adrenal medulla
NE and E
41
What are chromaffin cells
Cells in the medulla- modified neuronal tissue that release NE and E into the blood
42
Where does catecholamine synthesis occur
Chromaffin cells
43
What is the order of catecholamine synthesis to NE
1. L tyrosine—> tyrosine hydroxylase 2. L-DOPA—> L-aromatic amino acid decarboxylase 3. Dopamine—-> dopamine B hydroxylase 4. L-noradrenaline (NE)
44
What is the order of catecholamine synthesis to Epi
1. L tyrosine—> tyrosine hydroxylase 2. L-DOPA—> L-aromatic amino acid decarboxylase 3. Dopamine—-> dopamine B hydroxylase 4. L-noradrenaline (NE)—> PNMT (cortisol) 5. L-adrenaline (epi)
45
What converts NE to E
PNMT
46
What hormone activates synthesis of PNMT
Cortisol
47
What are the effects of catecholamines
Regulate homeostasis of cardiac and vascular tone, fight or flight response
48
How does catecholamine secretion impact the vascular system
Increase cardiac contractility, increased heart rate, increased BP, increased arteriolar vasoconstriction
49
How does catecholamine impact the mobilization of fuel in times of shock
Increased glucogenolysis, inhibition of glycogen synthesis, increased gluconeogenesis, inhibited insulin secretion, increased glucagon secretion, increased lipolysis
50
What is the goal of catecholamines in mobilizing fuel in times of shock
Promote glucose production for use by the brain
51
How does epinephrine impact alpha 1 receptors
Causes arterial smooth muscle contraction
52
How does epinephrine impact alpha-2 receptors
Inhibit- synaptic nerve endings and smooth muscle contraction
53
How do catecholamines impact B1 receptors
Affects heart activity- increased HR
54
How does epinephrine impact B2 receptors
Inhibits- smooth muscle relaxation and metabolism
55
What enzyme degrades NE
Monoamine oxidase (neuronal cytoplasm)
56
What enzyme degrades Epi
Catechol-0-methyltransferase (interstitial fluid of synapse, heart, liver kidney)
57
What is the byproduct of MAO and COMT
Vanillylmandelic acid
58
Vanillylmandelic acid serves as a measure of ___ activity
SNS
59
What is a pheochromocytoma
Catecholamine secreting tumor
60
What are some symptoms of pheochromocytomas
Hypertension, rapid pulse, chest pain, excessive sweating, headache, hyperglycemia, fatigue
61
What are some common presentations of cushings
Central obesity, collagen fiber weakness, urinary free cortisol, glucose increase, suppressed immunity, hypercortisolism, hypertension, hyperglycemia, hypercholesterolemia, latrogenic, neoplasms, glucose intolerance, growth retardation, PU/PD, alopecia, muscle weakness
62
What are 2 possible causes of Cushing’s
Endogenous- overproduction of cortisol Exogenous- taking medicines containing glucocorticoids, such as hydrocortisone
63
What are some common endogenous causes of cushings
Pituitary tumors (70%) Adrenal tumors (15%) Other (15%)
64
In dogs cortisol interferes with ___ binding resulting in incomplete central DI
ADH binding
65
What are some canine specific serum abnormalities that co-occur with Cushing’s
Elevated SAP, elevated ALT, hypercholesterolemia, hyperglycemia, decreased BUN
66
Why is cholesterol and glucose elevated in serum of patients with Cushing’s?
Elevated glucose result of increased cortisol which main function is to increase gluconeogenesis in liver Elevated cholesterol: ACTH transfer cholesterol to mitochondria in steroid synthesis
67
How is a urine cortisol: creatinine ration useful in diagnosing cushings
Elevated distinguishes between healthy and dogs with hyperadrenocorticism *prone to false +
68
How does an ACTH stim test help diagnose cushings
Measure cortisol response- useful for confirming iatrogenic hyperadrenocorticism
69
What receptor does Dexamethasone have high affinity for
Glu receptors
70
What does a low dose dexamethasone test determine
Presence of Cushing’s (DOES NOT DETERMINE WHICH TYPE)
71
How does a low does dexamethasone suppression test work and what could potential results indicate
Give low dose dex, then measure cortisol at 4-8hrs Reduction or no change in cortisol: adequate HPA axis Elevated cortisol: allows for diagnosis of cushings
72
How can you distinguish between cushing’s disease and cushing’s syndrome
High dose dexamethasone suppression
73
How does a high dose dexamethasone suppression test work (testing ACTH)
Works on principle that autonomous ACTH hypersecretion by pituitary can be suppressed by supraphysiological concentrations of steroid Reduced/no ACTH: supports diagnosis of pituitary origin unchanged ACTH: adrenal or ectopic tumor
74
How does a high dose dexamethasone suppression test work (testing CORT)
Reduced CORT: supports pituitary origin
75
Why does dexamethasone suppression not suppress cortisol concentrations as a result of adrenal tumors and which form of Cushing’s involves adrenal gland
Adrenal tumors have maximally suppressed ACTH production via normal feedback mechanism. Cushing’s syndrome- primary adrenal hyperplasia. Producing high levels cortisol without influence from ACTH which is why high dose dex test doesn’t decrease levels in Cushing’s syndrome
76
How does the reduction in ACTH or CORT following HDDS test indicate pituitary origin
dex can provide negative feedback onto pituitary and reduce ACTH and CORT is cushing's disease which is from overactive pitutiary. Cushing's syndrome is a result of primary adrenal hyperplasia releasing high levels of CORT independent of ACTH stimualtion, so adrenal origion won't respond

Physiology (10 decks)

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