Adrenal Gland Histology Lecture (Dr. Cole) Flashcards

1
Q

Anatomy

A
  • Suprarenal Glands, also known as Adrenal Glands
  • A pair of Triangular-Shaped Glands, each about 2 Inches long and 1 inch wide
  • SUPERIOR to the Kidneys
  • HIGHLY VASCULARIZES

A) Superior Suprarenal: Inferior Phrenic

B) Middle Suprerena;: Abdominal Aorta

C) Inferior Suprarenal: Renal Artery

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2
Q

Development of the Adrenal Glands Introduction

A
  • Two parts of the Adrenal Glands, the CORTEX and the MEDULLA develop from Two Different Origins:

1) CORTEX:
- is MESODEMAL in Origin
- Develops from the CELOMIC EPITHELIUM of the POSTERIOR ABDOMINAL WALL

2) MEDULLA:
- Is ECTODERMAL in Origin
- Develops from the NEURAL CREST Cells

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3
Q

Development of the Adrenal Glands Description

A
  • By the EIGTH Week of Fetal Development, these Cortical Elements have differentiated into a THIN OUTER DEFINITIVE Cortex and a THICK INNER FETAL Cortex
  • The FETAL Cortex actively produces FETAL STEROIDS during GESTATION, but INVOLUTES Rapidly after birth
  • ADRENOCORTICAL rests occur in up to 50% of Newborn Infants, but tend to ATROPHY and DISAPPEAR in the Early POSTPARTUM Period. They can be detected anywhere along the Path of EMBRYONIC Migration of Adrenal Cortex
  • ACCESSORY ADRENOCORTICAL NODULES (Ex: Ectopic Adrenal Gland, Accessory Cortical Tissue, Hamartoma, Asseccsory Adrenal Gland, Supernumerary Adrenal, and Adrenocortical Rest), accessory Adrenocortical Nodules are MINOR Developmental anomalies arising from Partly or Completely detached rests of the COELOMIC Epithelial Primordial form which the ADRENAL CORTEX IS DERIVED
  • Thye are most frequently located in Contact with he Capsule at ONE POLE of the Adrenal but can occur COMPLETELY SEPARATED form the Adrenal Gland in the RETROPERITONEAL FAT
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4
Q

Development of Adrenal Glands Description Cont 1

A
  • The Development of ADRENAL ZONES occurs SLOWLY after Birth in Parallel with REGRESSION of the Fetal Cortex, and is not Completed until late in the FIRST YEAR of LIFE
  • The DEFINITIVE CORTEX persists and develops into the FUNCTIONAL ADRENAL CORTEX, with Distinct ZONAE GLOMERULOSA and FASCICULATA present at BIRTH. The ZONA RETICULARIS develops during the FIRST YEAR of LIFE
  • Both CORTICAL and MEDULLARY elements appear between the FIFTH and SIXTH Weeks of FETAL GROWTH
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5
Q

Development of Adrenal Glands Description Cont 2

A
  • The Adrenal MEDULLA and Sympathetic Nervous System develop in Concert
  • The Medullary Elements, derived form NERUAL CREST, Migrate Forward to the PARA-AORTIC and PARAVERTEBRAL Regions and along the ADRENAL VEIN toward the MEDIAL aspect of the Developing ADRENAL FETAL CORTEX
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6
Q

Explain the Function of the Fetal Adrenal Cortex. What are the Three Main Developmental Events that require Glucocorticoids?

A
  • During the EARLY STAGE of Gestation, the Adrenal Cortex synthesizes DEHYDROEPIANDROSTERONE (DHEA), a precursor of the Synthesis of Estrogen by the PLACENTA
  • A lack of 3 Beta-Hydroxysteroid Dehydrogenase (3Beta- HSD) activity prevents the SYNTHESIS of PROGESTERONE, GLUCOCORTICOIDS, and ANDROSTENEDIONE
  • The interaction between the FETAL ADRENAL CORTEX and the Placenta is known as the FETOPLACENTAL UNIT
  • 3Beta-Hydroxysteroid Dehydrogeanse II DEFICIENT CONGENITAL ADRENAL HYPERPLASIA ( 3Beta- HSD- CAH) is an Uncommon form of CONGENITAL ADRENAL HYPERPLASIA (CAH)
  • Results from a Mutation in the Gene for (3Beta- HSD) TYPE II
  • There is Wide Spectrum of Clinical Presentations of 3Beta- HSD CAH, from MILD to SEVERE forms
  • MILDER forms resulting from INCOMPLETE LOSS of 3Beta- HSD Type II Function can produce VIRILIZATION of Genetically FEMALE Infants and UNDERVIRILIZATION of Genetically MALE Infants
  • This form of PRIMARY HYPOADRENALISM is the ONLY form of CAH that can cause AMBIGIOUS GENITALIA in BOTH GENETIC SEXES!!!!!!!!!!!!
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7
Q

The Main Developmental Events that Require Glucocorticoids

A
  • Glucocorticoids, either of MATERNAL Origin or Synthesized from PLACENTAL PROGESTERONE by the Fetus, are essential for THREE Main Developmental Events:
    1) The Production of SURFACTANT by TYPE II ALVEOLAR Cells after the EIGTH MONTH of Fetal Life
    2) The Development of a FUNCTIONAL HYPOTHALAMOPITUITARY AXIS
    3) The INDUCTION of THYMIC INVOLUTION
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8
Q

Organization of the Adrenal Cortex

A
  • Each Gland consists of Yellowish OUTER CORTEX (80 to 90% of the Gland) and a Reddish INNER MEDULLA (10 to 20%)
  • The Adrenal Cortex is of MESODERMAL Origin and produces STEROID HORMONES
  • The Adrenal Medulla is of NEUROECTODERMIC Origin and produces CATECHOLAMINES
  • The Adrenal Cortex consists of three Concentric Zones:
    1) OUTERMOST layer of the Cortex is the ZONA GLOMERULOSA

2) The MIDDLE Layer of the Cortex is the ZONA FASCICULATE
3) The INNERMOST layer of the Cortex is the ZONA RETICULARIS

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9
Q

Zone Glomerulosa Products

A
  • Mineralocorticoids, mainly ALDOSTERONE

- Produced in response to ANGIOTENSIN II (Also ACTH)

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10
Q

Zona Glomerulosa Description

A
  • Liws under the Capsule and represents 10 to 15% of the Cotex
  • Cells aggregate into a GLOMERULUS-like arrangement and have a Moderate amount of LIPID DROPLETS in the Cytoplasm
  • Lacks the Enzyme 17 ALPHA- HYDROXYLASE (CYP17), CANNOT produce CORTISOL or SEX STEROIDS
  • ALDOSTERONE stimulates the RETENTION of Na+ in the Kidneys, the RETENTION of Water (AS a consequence of Na+ Reabsorption), and RENAL SECRETION of K+ and H+
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11
Q

Zona Fasciculata

A
  • 75% of the CORTEX!!!!!
  • Secretes GLUCOCORTICOIDS and ANDROGENS
  • Cells contain MANY Lipid Droplets of CHOLESTEROL (Precursor in Cytoplasm)
  • Cells appear VACUOLATED (Foamy appearance)
  • **** SPONGIOCYTES!!!!!!!!!!!!!
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12
Q

Zona Fasciculata Contents

A
  • Contains CUBOID CELLS, with the structural features of Steroid-producing Cells arranged in LONGITUDINAL CORDS separated by Cortical Fenestrated Capillaries/ Sinusoids!!
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13
Q

ZF and ZR

A
  • Contain 17ALPHA- HYDROXYLASE necessary for the Production of GLUCOCORTICOIDS—- CORTISOL—- and the Enzyme 17, 20- HYDROXYLASE, required for the production of SEX HORMONES!!!!!!
  • CORTISOL is not stored in Cells and New Synthesis, stimulated by ACTH, is required for achieving a Hormonal Increase in BLOOD CIRCULATION
  • CORTISOL is converted in HEPATOCYTES to CORTISONE
  • Synthetically made CORTISONE is used as an ANTI-INFLAMMATORY and ANTI-ALLERGY Agent
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14
Q

Zona Fasciculata Effects

A

Has two major Effects:
1) A METABOLIC Effect: Stimulates GLUCONEOGENESIS to INCREASE the concentration of GLUCOSE in Blood

2) An ANTI-INFLAMMATORY Effect: SUPPRESSES tissues RESPONSES to Injury and DECREASES Cellular and Humoral Immunity

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15
Q

Zona Fasciculate and Reticularis difference

A
  • Although ZONA FASCICULATE is often associated with GLUCOCORTICOID Production- mainly CORTISOL - and the ZONA RETICULARIS with ANDROGEN Production, the Functional distinctions are NOT precise and they appear as a Functional Unit
  • BOTH LAYERS are stimulated by CORTICOTROPIN (ACTH)
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16
Q

Zona Reticularis Introduction

A
  • INNERMOST layer of the Cortex 5 to 10% of Total Volume
  • Cells arranged in IRREGULAR CORDS that form an ANASTOMOSING Network
  • Secrete GLUCOCORTICOIDS and ANDROGENS
17
Q

Zona Reticularis Products

A
  • Although cells of the Zone Fasciculate can Synthesize Androgens, the primary site of ADRENAL SEX hormone production is the ZONA RETICULARIS
  • DEHYDROEPIANDROSTERONE (DHEA) and ANDROSTENEDIONE are the Predominant Androgens produced by the Cortex of the Adrenal Gland
  • Although DHEA and Androstenedione are WEAK Androgens, they can be converted to TESTOSTERONE and even to ESTROGEN in PERIPHERAL TISSUES

***The Adrenal Gland is the MAJOR SOURCE of ANDROGENS in WOMEN; these Androgens stimulate the GRWOTH of PUBIC and AXILLARY Hair during PREGNANCY

18
Q

Adrenal Medulla: Chromaffin Cells

A
  • Composed of POLYHEDRAL CELLS arranged in CORDS or CLUMPS
  • Regarded as modified Sympathetic Postganglionic Neurons WITHOUT Postganglionic Axons
  • Derived from NERUAL CREST
  • Lost axons and Dendrites during EMBRYONIC Development and have become Secretory Cells
  • Secretory Granules of EPINEPHRINE or NOR-EPINEPHRINE
  • The Adrenal Medulla is innervated by SYMPATHETIC Preganglionic Fibers that release ACETYLCHOLINE!!!!!!
19
Q

Catecholamines

A
  • Catecholamines are secreted INOT THE BLOOD instead of being secreted into a Synapse, as in Postganglionic Terminals
  • Secreted in response to INTENSE Emotional Reactions
  • DEFESIVE Reaction to STRESS
  • INCREASE Heart Rate
  • DILATES Blood Vessels supplying Cardiac and Skeletal Muscle
  • BRONCHIOLE Dilation
  • Vasoconstriction of Blood Vessels supplying GI Tract, Kidneys, Skin….
20
Q

Blood Supply of the Adrenal Gland

A
  • Arterial Blood derives from THREE Different Sources:
    1) The Inferior Phrenic Artery, which gives rise to the SUPERIOR Adrenal Artery

2) The Aorta, from which the MIDDLE Adrenal Artery branches out
3) The Renal Artery, which gives rise to the INFERIOR Adrenal Artery

***ALL three Adrenal Arteries enter the Adrenal Gland Capsule and form an ARTERIAL PLEXUS!!!!!!!!

21
Q

Blood Supply of the Adrenal Gland Cont

A
  • Three sets of Branches emerge from the Plexus:
    1) One set supplies the CAPSULE (Subcapsular Plexus)
    2) SHORT CORTICAL Arteries: SECOND set enters the Cortex forming straight Fenestrated Capillaries/ Sinusoids, percolating between the Zona Glomerulosa and Fasciculate, and forming a Capillary Network in the Zona Reticularis before entering the Medulla
    3) LONG CORTICAL Arteries: THIRD Set generates MEDULLARY Arteries travel WITHOUT Branching and Supplying Blood ONLY to the MEDULLA
22
Q

Abnormal Secretory activity of the Adrenal Cortex and Adrenal Medulla

A
  • ZONA GLOMERULOSA: A tumor localized in the ZONA GLOMERULOSA can cause EXCESSIVE SECRETION of ALDOSTERONE
  • ** This rare condition is known as PRIMARY ALDOSTERONISM or CONN’S SYNDROME!!!!!!
  • A More Common cause of HYPERALDOSTERONISM is an INCREASE in RENIN Secretion (SECONDARY HYPERALDOSTERONISM)
23
Q

Zona Fasciculata

A
  • An INCREASE in ALDOSTERONE, CORTISOL, and ADRENAL ANDROGEN PRODUCTION— Secondary to ACTH Production—- occurs in CUSHING’S DISEASE!!!!

CUSHION’S DISEASE is caused by an ACTH-producign Tumor of the Anterior Hypophysis

  • A Functional Tumor of the Adrenal Cortex can also result in OVERPRODUCTION of CORTISOL, as well as of ALDOSTERONE and ADRENAL ANDROGENS
  • The Clinical condition is described as CUSHING’S SYNDROME (AS opposed to Cushing’s Disease)
24
Q

Addison’s Disease

A
  • A CHRONIC Destruction of the Adrenal Cortex by an AUTOIMMUNE Process or TUBERCULOSIS
  • ACTH Secretion INCREASES because of the CORTISOL Deficiency. ACTH can cause an INCREASE in SKIN PIGMENTATION, in Particular in the Skin Folds and Gums
  • The LOSS of Mineralocorticoids leads to HYPOTENSION and CIRCULATORY SHOCK
  • A Deficiency in CORTISOL causes Muscle Weakness
25
Q

Pheochromocytoma

A
  • Benign Tumor of the CHROMAFFIN CELLS
  • EPISODIC Secretion of EPINEPHRINE and NOR-EPINEPHRINE
  • Signs/ Symptoms are those of SYMPATHETIC Nervous System HYPERACTIVITY: Elevated Heart Rate, BP, Palpitations, Diaphoresis, Anxiety, Headaches, Nausea, Pallor
  • Because of EXCESSIVE CATECHOLAMINE Secretion, Pheochromocytomas may precipitate life-threatening HYPERTENSION or CARDIAC ARRHYTHMIAS
  • Up to 25% of Pheochromocytomas may be FAMILIAL!!!
26
Q

Hatfield-McCoy Feud

A
  • The most infamous FEUD in American Folklore, the LONg-Running battle between the Hatfield and Mccoys, may be partly explained by Rate, Inhertied Disease (VON HIPPEL-LANDAU) that can lead to Hair-Trigger RAGE and VIOLENT OUTBURSTS
  • No one blames the Disease for the WHOLE FEUD, but doctors say it could help explain some of the Clan’s Notorious Behavior
  • Several Genetic Experts have known about the disease Plaguing some of the McCOys for Decades, but kept it Secret
  • Roughly three-fourths of the affected McCoys have Pheochromocytomas—- Tumors of the Adrenal Gland