Suprarenal Gland histology Flashcards

1
Q

What is the embryonic origin of he cortex of the adrenal gland?

A

mesodermal in origin; develops from the celomic epithelium of the posterior abdominal wall

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2
Q

What is the embryonic origin of the medulla of the adrenal gland?

A

Ectodermal in origin; develops from the neural crest cells.

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3
Q

By what week of embryonic development have the cortical elements have differentiated into a thin outer definitive cortex and a thick inner fetal cortex.

A

Week 8

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4
Q

Does the fetus produce steroids during gestation?

A

Yes.

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5
Q

HOw does the fetal adrena cortex change after birth?

A

It involutes rapidly after birth

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6
Q

By birth, what two layers of the cortex is definitive?

A

ZOna glomerulosa, and fasciulata.

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7
Q

By when does the zona reticularis fully devleop by?

A

First year of life.

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8
Q

By what week are both the cortical and medullary elements appear?

A

Between 5-6 weeks

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9
Q

Development of the adrenal medulla is in concert with the development of what other system?

A

sympathetic nervous system

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10
Q

After the adrenal medulla elements develop, what is the path of their migration to go where it is normally.

A

The medulla is derived from neural 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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11
Q

During early stage of gestation, the adrenal cortex synthesizes _ which is a precursor of the synthesis of estrogen by the placenta.

A

dehydroepiandrosterone (DHEA)

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12
Q

A lack of synthesis of progesterone, glucocorticoids, and androstenedione is attributed to lack of what enzyme?

A

3beta-hydroxysteroid dehydrogenase (3B-HSD).

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13
Q

What is the fetoplacental unit?

A

It’s the interaction between the fetal adrenal cortex and the placenta.

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14
Q

A mutation in the gene for 3B-HSD type II leads to this uncommon congenital disorder.

A

3beta-hydroxyteroid dehydrogenase II deficiency congential adrenal hyperplasia (3B-HSD CAH)

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15
Q

How do infants with milder form of 3B-HSD type II present?

A
Female = virilization 
Male = undervirilization
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16
Q

Which type of congenital adrenal hyperplasia can cause ambiguous genitalia in both sexes?

A

3B-HSD CAH type II

17
Q

Glucocorticoids, either from the mother, or synthesized from placental progesterone by the fetus are absolutely essential for what three developmental events?

A
  1. The production of surfactant by type II alvoelar cells after 8th month
  2. Development of functional hypothalamopituitary axis
  3. induction of the thymic involution
18
Q

Which adrenal cortex hormones is the zona glomerulosa NOT able to produce.

A

cortisol or sex steroids because zona glomerulosa lacks 17a-hydroxylase (CYP17).

19
Q

Which layer of the adrenal cortex makes up the majority of the cortex

A

Zona Fasiculata (75%).

20
Q

In what layer of the adrenal cortex are you llikely to find spongiocytes?

A

Zona Fasciculata

21
Q

Cortisol can be converted to cotisone in what cell types?

A

Hepatocytes

22
Q

What are the two main general function of cortisol?

A
  1. metabolic effects: stimulates gluconeogenesis to increase the concentration of glucose in blood
  2. An anti-inflammatory effect: supresses tissue responses to injury and decreases cellular and humoral immunity
23
Q

True or False, both the Zona fasiculata and reticularis contain ACTH receptors

A

True

24
Q

Which two androgens are the predominantly produced in Zona reticularis?

A

DHEA and androstenedione.

25
Q

Adrenal gland is the major source of androgens for women; what do they do in woman?

A

stimulates the growth of pubic and axillary hair during puberty

26
Q

Where are chromaffin cells found?

A

Adrenal medulla

27
Q

What cell types are regarded as the modifie sympathetic postganglionic neurons without postganglionic axons?

A

Chromaffin cells

28
Q

Why are chromaffin cells regarded as modified sympathetic post ganglion neurons without postganglion axons?

A

They are derived from neural crest cells and during embyonic development they lost their axons and dendrites.

29
Q

What innervates the adrenal medulla?

A

sympathetic preganglionic fibers that release Ach

30
Q

Explain the blood supply to the adrenal gland.

A

Superior, middle and inferior adrenal arteries enter the cortex capsule and form arterial plexus and give rise to three sets of branches: 1. subcapsular (suppies the capsule), 2. short cortical enters cortex forming straight fenestrated capillariessinusoids, percolating between the zona glomerulosa nd fasciulata and forming a capillary network int he zona reticularis
3. Long cortical aa - medullary arteries which travel without branching and supply the medulla

31
Q

What is conn’s syndrome and where is found?

A

aka. Primary aldosteronism. Its caused by a tumor in zona glomerusa and cause excessive release of aldosterone

32
Q

What is secondary hyperaldosteronism caused by?

A

increase in renin secretion

33
Q

In Cushing’s disease, what layers of the adrenal cortex does it mainly affect?

A

Zona Fasiculata

34
Q

Why is ACTH levels elevated in Addison’s disease?

A

Addisons disease is the chronic destruction of the adrenal cortex by an autoimmune process or tuberculosis, and so there is a lack of cortisol in the body. This feeds back to the hypothalamus to secreted more ACTH

35
Q

A pt appears with fatigue, malaise, muscle weakness, anorexia, postural dizziness, syncope and GI symptoms like nausea, vomiting, abd pain, diarrhea, and constipation. Pt also notes decreased libido, and amenorrhea, and changes in her skin color. Upon examaining you also notice the pt is hypotensive, has thinning of axillary and pubic hair and pt shows signs of vitiligo. What is the likely diagnosis?

A

Addison’s disease

36
Q

What causes pheochromocytoma?

A

Benign tumor of the chromaffin cells

37
Q

What is released in excess in pheochromocytoma?

A

Epi and Nor-Epi

38
Q

What are the signs and symptoms of pheochromocytoma

A

They resemble signs and symptoms of sympathetic nervous system like elevated HR, BP, palpitation, diaphoresis, axniety, HA, nausea, and pallor. It can also preciptate life-threatening hypertensionor cardiac arrhthmias.