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Endocrine I > Adrenal Gland Functions and Diseases Lecture (Dr. Lopez) > Flashcards

Adrenal Gland Functions and Diseases Lecture (Dr. Lopez) Flashcards

1
Q

The Adrenal Gland

A
  • TWO Adrenal Glands
  • Each located at the SUPERIOR POLES of the Two Kidneys
  • ENDOCRINE and NEUROENDOCRINE Gland
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2
Q

The Adrenal is TWO Endocrine Glands that derive from Distinct Embryological Origin

A
  • ADRENAL MEDULLA is of ECTODERMAL Origin

- ADRENAL CORTEX is of EPIDERMAL Origin

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3
Q

Adrenal Cortex Hormones (Gland)

A

1) ALDOSTERONE (Steroid)
a) PRIMARY TARGET:
- Kidney

b) MAIN EFFECT:
- Na+ and K+ Homeostasis

2) CORTISOL(Steroid)
a) PRIMARY TARGET:
- Many Tissues

b) MAIN EFFECT:
- Stress Response

3) ANDROGENS (Steroid)
a) PRIMARY TARGET:
- Many Tissues

b) MAIN EFFECT:
- Stress Response

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4
Q

Adrenal Medulla (Neuron)

A

1) EPINEPHRINE (Amino Acid Derived)
a) PRIMARY TARGET:
- Many Tissues

b) MAIN EFFECT:
- “Fight or Flight” Response

2) NOREPINEPHRINE (Amimo Acid Derived)
a) PRIMARY TARGET:
- Many Tissues

b) MAIN EFFECT:
- “Fight or Flight” Response

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5
Q

Hormone Secretion by the Adrenal Gland

A

1) Zona Glomerulusa:
- ALDOSTERONE (Mineralocorticoid)

2) Zone Fascicultata:
- CORTISOL (Glucocorticoids)
- ANDROGENS

3) Zona Reticulares:
- CORTISOL (Glucocorticoids)
- ANDROGENS

4) Adrenal Medulla:
- EPINEPHRINE and NOREPINEPHRINE (Catecholamines)

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6
Q

Pathways for the Synthesis of Steroid hormone by the Adrenal Cortex

A

KEY ENZYMES:
1) 3 Beta- Hydroxysteroid Dehydrogenase

2) 17 Alpha- Hydroxylase
3) 21 Beta- Hydroxylase
4) 11 Beta Hydroxylase
5) 17,20 Lyase

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7
Q

The Steroidogenic Acute Regulatory Protein (StAR)

A
  • StAR, is a Transport Protein that regulates CHOLESTEROL transfer within the MITOCHONDRIA, which is the RATE-LIMITING step in the Production of Steroid Hormones (DESMOLASE!!!!!)
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8
Q

Steroid Hormones

A
  • LIPOPHILIC; Easily Across Membrane
  • Cytoplasmic or Nuclear Receptors
    a) Genomic effect to ACTIVATE or REPRESS Genes for Protein Synthesis (SLOWER ACTING)
  • Cell Membrane Receptors
    a) Non-Genomic Responses
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9
Q

Adrenocorticotropic Hormone (ACTH)

A
  • ACTH stimulates Synthesis and Secretion of Adrenal Cortical Hormones:

1) Glucocorticoids (Cortisol)
2) Mineralocorticoids (Aldosterone)
3) Androgens

***** CRH (Hypo) —-> ACTH (Ant Pit)—–>

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10
Q

Adrenocorticotropic Hormone (ACTH) Cont

A
  • Produced in the ANTERIOR PITUITARY
  • Derived from POST-TRANLSAITON processing of POMC (Pro-Opiomelanocortin)
  • Is a Peptide

***Leads to MELANIN SYNTHESIS from the Alpha-MSH!!!!!!

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11
Q

HPA Axis

A
  • The Hypothalamic, Pituitary, Adrenal (HPA) Axis is under Negative FEEDBACK Control by CORTISOL!!!!!!
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12
Q

Cortisol Effects

A

1) Immune System
- Immune SUPPRESSION

2) Liver:
- Gluconeogenesis

3) Muscle:
- Protein Catabolism

4) Adipose Tissue:
- Lipolysis

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13
Q

Circadian Rhythm of Cortisol

A
  • The Secretory rates of Cortisol are HIGH Early in the Morning but LOW in the Evening
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14
Q

Exogenous Glucocorticoids have the same Negative Feedback Effect as Cortisol

A
  • Exogenous Administration may SHUT DOWN ACTH Production and Adrenal Cells that produce CORTISOL (Atrophy!)
  • Examples of Synthetic Glucocorticoids:
    a) Cortisone
    b) Prednisone
    c) Methylprednisone
    d) Dexamethasone
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15
Q

Hyper and HypoCortisolism

A 
HYPERCORTISOLISM:
1) Cushing Syndrome:
- ACTH Decrease
- CORTISOL Increase
- CRH Decrease
(Caused by ADRENAL TUMOR)

2) Cushing’s Disease:
- CORTISOL Increase
- ACTH INCREASE
- CRH Decrease
( Pituitary Tumor)

HYPOCORTISOLISM:
1) Addison's Disease 
- CRH Increase
- ACTH Increase
- CORTISOL Decrease
( Autoimmune Disease of the Adrenal Gland)

2) Secondary Adrenal Insufficiency
- CRH Decrease
- ACTH Decrease
- CORTISOL Decrease
(Glucocorticoid Drugs SUPPRESSING Hypothalamus and Pituitary)

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16
Q

HYPERCORTISOLISM

A

HYPERCORTISOLISM (Cushing’s Syndrome)
- ADRENAL Tumor that AUTONOMOUSLY Secretes Cortisol (PRIMARY: Adrenal Excess)

  • Drug Induced Hypercortisolism
  • PITUITARY Tumor that AUTONOMOUSLY Secretes ACTH (SECONDARY: Pituitary Excess)
  • **Ex: Cushing’s Disease
17
Q

HYPOCORTISOLISM

A

HYPOCORTISOLISM

  • HYPOSECRETION of all ADRENAL STEROID Hormones
  • ***Ex: ADDISON’S DISEASE (PRIMARY Adrenocortical Insufficiency)
  • Secondary Adrenocortical Insufficiecny (ACTH Deficiency)
  • **Ex: Chronic Exogenous Glucocorticoid Treatment
18
Q

Use Cosyntropin (Synthetic ACTH) Stimulation Test to Detect Adrenal Gland INSUFFICIENCY

A
  • Tests that measure the level of Hormones are used to Diagnose Pathologies
  • **Ex: COSYNTROPIN Stimualtion Test (CST)
19
Q

Regulation of Aldosterone Secretion

A

1) A DECREASE in BP —>
2) Kidney produces more RENIN —>
3) Renin converts Angiotensin into ANGIOTENSIN I —>
4) Angiotensin I converts to ANGTIOTENSIN II by ACE!!! —>
5) Angiotensin II leads to ALDOSTERONE Production —>
6) Aldosterone leads to Water/ Na+ REABSORPTION —–>
7) Water Retention leads to an INCREASE in BP

***The Primary action of Aldosterone is RENAL SODIUM REABSORPTION

20
Q

The Primary action of Aldosterone is RENAL SODIUM REABSORPTION

A

1) Aldosterone combine sixth Cytoplasmic Receptor in Distal Convoluted Tubule or Collecting Duct
2) Hormone- Receptor complex initiates Transcription in the Nucleus
3) Translation and Protein Synthesis makes new protein Channels and Pumps
4) Aldosterone- Induced Protein modulate EXISTING Channels and Pumps
5) Results in INCREASED Na+ Reabsorption and K+ Secretion

21
Q

Aldosterone Pathologies

A

1) HYPERALDOSTERONISM:
a) PRIMARY Hyperaldosteronism:
- Excessive Release of Aldosterone from the Adrenal Cortex
* * EX: CONN’S SYNDROME: Adenoma in the Adrenal Cortex

b) SECONDARY Hyperaldosteronism: Excessive RENIN Secretion by the JUXTAGLOMERULAR Cells in the Kidney

2) HYPOALDOSTERONISM:
- Destruction of the Adrenal Cortex
- Defects in Aldosterone Synthesis
- Inadequate Stimulation of Aldosterone Secretion

22
Q

Overview of Hormones produced by the Adrenal Medulla

A
  • The Adrenal Medulla produces CATECHOLAMINES: Primarily EPINEPHRINE (80%) and small amounts of NOREPINEPHRINE (20%)
  • Adrenomedullary Catecholamines are Secreted into the blood and act as Hormones
  • EPINEPHRINE
    a) Responder to STRESS such as Hypoglycemia/ Exercise

b) Influences Energy Metabolism and Cardiac Output

23
Q

Synthesis of Catecholamines

A
  • Under Control of the CRH - ACTH - Cortisol Axis
    a) ACTH Stimulates Synthesis of DOPA

b) CORTISOL increases Pheynlethanolamin - N - Methyl Transferase (PNMT) Enzyme (NOREPI —-> EPI)
- Release is triggered by CNS Control

***Norepinephrine and Epinephrine are Synthesized in DIFFERENT Cellular Compartments

24
Q

Norepinephrine and Epinephrine are Synthesized in DIFFERENT Cellular Compartments

A
  • RATE LIMITING STEP is the Hydroxylation of Tyrosine by TYROSINE HYDROXYLASE, producing DOPA
  • DOPA is converted to DA by the Cytoplasmic Enzyme, Aromatic Amino Acid Decarboxylase (AADC) and is then transported into the Secretory Vesicle (CHROMAFFIN GRANULE)
  • Within the Chromatin Granule, DA is converted to NE by Enzyme, Dopamine Beta- Hydroxylase (DBH)
25
Q

Norepinephrine and Epinephrine are Synthesized in DIFFERENT Cellular Compartments Cont.

A
  • In most Adrenomedulalry Cells, essentially all of the NE diffuses out of the Chromaffin Granule by FACILITATED TRANSPORT and is METHYLATED by the Cytoplasmic Enzyme, PHENYLETHANOLAMINE - N - METHYL TRANSFERASE (PNMT), to form Epinpehrine
  • Epinephrine is the transported back into Granule by VESICULAR MONAMINE TRANSPORTERS (VMATs)
  • Multiple molecules of Epinephrine, and to a lesser extent Norepinephrine, are stored in the Chromaffin Granule complexed with ATP, Ca2+, and protein called CHROMOGRANINS
    a) CHROMAGRANINS: Miltimolecular Complexes, thought to Decrease the Osmotic Burden of Strong Individual molecules of Epinephrine within Chromaffin Granules

b) Circulating Chromogranins can be used as a marker of Sympathetic Paraganglion-derived tumors (Paragangliomas)

26
Q

Degradation of Catecholamines

A

*** Action of Catecholamines is brief is about 10 seconds

COMT: Catecholamine- O - Methyltrasferase

MOA: Monoamine Oxidase

***Catecholamines, Metanephrines, and Vanillylmandelic Acid (VMA) can be measured to determine Total Catecholamine production

27
Q

Catecholamine Receptors

A

Epinephrine has HIGHER affinity for Beta 2 Receptors*

  • The ALPHA Receptors, BETA 3 Receptors respond better to Norepinephrine than Epinephrine
  • BETA 1 Receptors respond equally to Norepinephrine and Epinephrine
  • Epinephrine is MORE POTENT than Norepinephrine for the BETA 2 Receptors
28
Q

Pheochromocytoma

A

PHEOCHROMOCYTOMA: Tumor of the CHROMAFFIN TISSUE

a) Produces Excess CATECHOLAMINES

b) Symptoms SPORADIC
1) Hypertension (Reported that 1% of patents with Hypertension have a Pheochromocytoma)
2) Orthostatic Hypotension (Volume Depletion)
3) HEADACHES
4) SWEATING
5) Anxiety
6) PALPITATIONS
7) Chest Pain
8) Flushing

Endocrine I (13 decks)

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