Endocrine Adrenal Glands II Flashcards by Karin Golob

What is the blood supply of the adrenal glands?

Aorta –> phrenic and renal arteries:

renal arteries –> inferior adrenal arteries –> adrenal glands

phrenic –> suprarenal arteries –> adrenal glands

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What is the embryological origin of the adrenal glands?

Medulla - neural crest ectoderm

Cortex - intermediate mesoderm

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What are the zones of the adrenal cortex?

Capsule

Zona Glomerulosa - “Salt”
Aldosterone

Zonal Fasiculata - “Sugar”
Glucocorticoids

Zona Reticularis - “Sex”
DHEA/androgens

Medulla

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What does the medulla make and why is the blood flow critical for this?

Medulla makes epinephrine, which requires large amounts of cortisol

–> blood flow in the adrenal allows cortisol from the cortex to be brought to the medulla

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What is the role of the zona fasiculata?

Synthesize glucocorticoids (esp. cortisone)

Regulates glucose synthesis, storage, usage

(look “foamy” histologically due to many lipid droplets)

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What is cortisol?

glucocorticoid that mobilizes glucose and free fatty acids

Made in adrenal cortex

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What is aldosterone?

Mineralcorticoid that stimulates Na reabsorption in the kidney

Made in Adrenal cortex

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What is Dehydroepiandosterone Sulfate?

DHEA = Androgen
of weak action

Made in adrenal cortex

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What is the hypothalmic puitary adrenal axis?

Hypothalmus releases CRH, activating ACTH release from pituitary to activate the adrenal gland into producing cortisol (which inhibits ACTH release), etc.

–> This axis is driven by:
Circadian Rhythms
Stress (which can override negative feedback)

–> Epi and VP increase anterior pituitary sensitivity to CRH

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What are the 4 dominant mechanisms of secretory control of ACTH?

1. Negative feedback regulation
Cortisol inhibits ACTH release

2. Episodic (pulsitile) secretion

3. Diurnal rhythm

4. Stress
Epi and VP increase sensitivity of ant. pit. to CRH

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How is cortisol degraded?

Make it water soluble so it is released through the urine

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What does cortisol do?

Anabolic (on liver) and catabolic (other organs) actions

–> allows fasting for days to weeks

–> shifts the peripheral body over to ketone bodies and AAs and turns gluconeogensis on in the liver to make glucose for the brain

–> Down regulates insulin receptors on the peripheral organs so they don’t use glucose

**That’s why Cushing’s leads to significant weight gain and insulin resistance (diabetes)

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What are the effects of cortisol on the Immune System in high dose?

Immunosuppression

Stabilizes lysosomal membranes
Decreases capillary permeability
Dpresses white cell proliferation and phagocytosis
Inhibits local accumulation of white cells
Reduces proliferation of fibroblasts
Prevents degranulation of mast cells
Inhibits cytokine production/signaling

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What are effects of cortisol on the cardiovascular system?

Central nervous system?

Fetus?

Cardiovascular = increases vascular tone

CNS = euphoria

Fetus = surfactant
Fetal adrenal gland starts working ~2weeks prior to partruition

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What are causes of cortisol excess?

Primary Cushing’s - adrenal

Secondary Cushing’s - pituitary

Tertiary Cushing’s - hypothalamus

Ectopic ACTH - often small cell carcinoma of the lung

Iatrogenic - pharmaceutical

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What is the difference of Cushing’s Disease and Cushing’s Syndrome?

Disease has set point for negative feedback operating, but is set too high for good health

All other forms of Cushing’s syndrome lack any form of set point regulation

(Cushing’s disease is a subset of Cushing’s syndrome)

What causes the striae of Cushing’s syndrome?

Increased deposition of fat and breakdown of collagen

They are purple due to vasculature being more visible

What are symtpoms of Cushing’s syndrome?

Diabetes

Moon faces

Increased girth

purple striae

Skin bronzing

Acne

Osteoporosis

Etc.

How do you diagnose the cause of Cushing’s syndrome?

What causes the skin bronzing of Cushing’s syndrome?

High levels of ACTH

ACTH acts like melanin, but is usually in too low of levels because it’s very weak

What is hypocortisolism? What are the types?

A state of cortisol deficiency

Primary hypocortisolism: Addison’s diseaes
Hypocortisolism due to adrenal destruction

Secondary hypocortisolism: Sheehan’s disease
Failure of pituitiary gland to produce ACTH

Tertiary hypocortisolism:
Failure of the hypothalamus to produce CRH

How is aldosterone regulated?

Renin-Angiotensin-Aldosterone System
Serum potassium primarily
ACTH to a lesser degree

What is the action of aldosterone?

Acts on the kidney to actively absorb Na and increase K and H secretion

–> not effective when tubular Na is reduced (i.e. dietary Na restriction)

How does salt ingestion affect the RAAS?

Intake of Na load –> increase blood Na (hypernatremia) –> Decreased secretion of Aldosterone (via renin-angiotensin) –> decreased reabsorption of Na and increased reabsorption of K –> uptake of K into cells to maintain normal blood levels –> Restoration of blood Na as Na load passes –> aldosterone secretion restored to normal rate –> Na reabsorption increases to normal rate –> K excretion increases to pass the extra taken up into cells

What are the functional components of the JG apparatus?

- Baroreceptor (releases renin at low volume, low pressure) - Chemosensor (releases renin at low osmolarity - low Na⁺, K⁺) - Neuroendocrine transducer

What are two major forms of aldosterone excess?

**Primary:** Adrenal Tumor Autonomous secretion Renin suppressed **Secondary:** Acites (fluid leakage into thoracic/abdominal cavity) Adrenal driven to increase aldosterone due to H2O loss Renin is activated Profound edema

What are results of hyper aldosteronism?

* *Hypernatremia (due to increased Na reabsorption)** - -\> increased plasma volume - -\> HTN - -\> Suppresed RAAS * *Hypokalemia (due to increased K excretion)** - -\> Weakness and paralysis - -\> Metabolic alkalosis (increased H+ secretion) - -\> Polyuria

How does Primary Hyperaldosteronism affect: Effective arterial blood volume Total body fluid volume Renin-angiotensin Clinical Expression Secondary?

How does renal artery stenosis affect RAAS?

They have a severely increased RAAS output due to restriction of blood flow to JGA --\> leads to life threatening HTN

What is congenital adrenal hyperplasia?

Commonly: 21-Hydroxylase deficiency Hyperplasia of adrenal gland --\> increased DHEA production Can cause virilization in females, precocious puberty in males Aldosterone and Cortisol are not produced due to enzyme deficiency --\> life threatening levels of Angiotensin II cause vasoconstriction and high BP

What are chromaffin cells?

Cells in the medulla of the adrenal gland that synthesize, store, secrete catecholamines: NE and Epi - Conversion of NE to Epi depends on Phenylethanolamine-N-methyltransferase enzyme

What do the catecholamines produced by the adrenal medulla affect the body?

1. Cardiovascular system - increased cardiac output 2. Metabolic function - fuel mobilization 3. Arousal - heightened awareness

What is the biochemical process of catecholamine production?

Tyrosine --\> Dopa Enzyme: tyrosine hydroxylase Dopa --\> Dopamine Enzyme: Aromatic L-amino Acid Decarboxylase Dopamine --\> NE Enzyme: Dopamine hydroxylase NE --\> Epi Enzyme: PNMT

What are clinical features of pheochromocytoma?

**Hypertension** due to extreme amounts of catecholamines **Symptoms during or following paroxysms:** Headache Sweating Forceful heartbeat w/ or w/o tachy Anxiety or fear of impending death Tremor Fatigue/exhaustion Abdominal or chest pain visual disturbances **Symptoms between paroxysm:** Increased sweating cold hands and feet weight loss constipation

What are paroxysms of pheochromocytoma and how do you stop them?

They are extreme explosion of catecholamines into the circulatory system caused by movement of the adrenal gland and tumor --\> stopped by catecholamines: Reuptake into the tumor Taken up into target cell Metabolized (catecholamine-N-methyl transferase)

What are causes of death in patients with unsuspected pheochromocytomas?

MI Cerebrovascular accident Arrhythmias Irreversible shock Renal failure Dissection aortic aneurysm