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MTP > Exam 5: Adrenal Corticosteroid Part 1 > Flashcards

Exam 5: Adrenal Corticosteroid Part 1 Flashcards

1
Q

What is the definition of hormone?

A
  1. Chemical regulators of cellular function
  2. Synthesized in specific cells in endocrine glands
  3. Released in circulation
  4. Acts on specific target tissues in specific target receptors
  5. Effects are of physiologic importance to the organism
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2
Q

What are examples of amino acid based hormones?

A

Insulin, GH, catecholamines

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3
Q

What are eicosanoids?

A

Locally secreted, locally acting hormones (prostaglandins)

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4
Q

What are examples of steroid derivatives of cholesterol?

A

Adrenocortical hormones (cortisol, aldosterone)
Gonadal (testosterone, estrogen)

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5
Q

What are the target cells of hormone action?

A

Receptors in plasma membranes (GPCR)
Intracellular receptors (cytoplasmic or nuclear)

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6
Q

What are the types of intracellular receptors?

A
  1. Direct nuclear gene activation or suppression)
  2. Used by steroids and thyroid hormones (lipid soluble)
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7
Q

Describe the membrane receptor mechanism for steroids?

A
  1. Hormone diffuses through plasma into cytosol
  2. Binds to intracellular or nuclear receptor to form hormone-receptor complex
  3. Hormone-receptor complex in the nucleus interacting with chromatin to affect gene transcriptional activity
  4. Transcription of mRNA
  5. Synthesis or translation of protein
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8
Q

What are the properties of steroid hormones?

A
  1. Synthesized and immediately released
  2. Derived from cholesterol
  3. Enzymes produce steroid hormones from cholesterol in the mitochondria and SER
  4. Lipid soluble and freely permeable in membranes
  5. Carried in blood by globulins
  6. Secreted by one cell and converted to the active steroid by target cell
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9
Q

What globulin carries cortisol?

A

Corticosteroid binding globulin

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10
Q

What globulin carrie estradiol and testosterone?

A

Sex steroid binding globulin

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11
Q

What are examples of a steroid that is converted to an active steroid?

A
  1. Androgens secreted by the gonads converts to estrogen in the brain
  2. 5-alpha-reductase in the prostate converts testosterone to DHT
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12
Q

What are the important roles of steroid hormones and what are the examples associated with the roles?

A
  1. Carbohydrate regulation (glucocorticoid)
  2. Mineral balance (mineralocorticoids)
  3. Reproductive functions (gonadal steroids)
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13
Q

What are the important roles of glucocorticoids?

A
  1. Inflammatory responses
  2. Stress responses
  3. Bone metabolism
  4. Cardiovascular fitness
  5. Behavior
  6. Cognition
  7. Mood
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14
Q

What is the purpose for the hypothalamus?

A
  1. Neurosecretory hormone secreting cells of the posterior pituitary via infundibular stalk
  2. Releasing and inhibitory factors that act on cells in the anterior pituitary via hypophyseal portal system
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15
Q

What is the purpose the pituitary?

A
  1. Cells that produce hormones release them into the bloodstream
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16
Q

What is the posterior pituitary?

A

Comprised of the endings of axons from cell bodies in the hypothalamus

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17
Q

What are the principal hormones of the posterior pituitary and where are they secreted?

A
  1. Vasopressin (ADH): kidneys for water reabsorption
  2. Oxytocin: Mammary glands of milk ejection and uterus for uterine contraction
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18
Q

What connects the hypothalamus to the pituitary?

A

Converging blood vessels (median eminence) in the hypophyseal portal system

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19
Q

What is secreted by the hypothalamus?

A

Releasing and inhibitory hormones

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20
Q

What are releasing hormones?

A

Released by the hypothalamus that cause the release of hormones by the anterior pituitary

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21
Q

What are inhibitory hormones?

A

Released by the hypothalamus that inhibit secretion of hormones by the anterior pituitary

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22
Q

What is ACTH (Adrenocortiotropic hormone)?

A

Stimulates cortisol secretion in the adrenal cortex

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23
Q

What is growth hormone?

A

Primary hormone responsible for regulating body growth and important for metabolism

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24
Q

What is prolactin?

A

Females: stimulates breast development and milk production
Males: Testicular function

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25
Q

What is TSH (thyroid stimulating hormone)?

A

Stimulates the secretion of thyroid hormone and growth of thyroid gland

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26
Q

What is FSH (follicle stimulating hormone)?

A

F: stimulates growth and development of ovarian follicles promoting secretion of estrogen by ovaries
M: Sperm production

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27
Q

What is LH (luteinizing hormone)?

A

F: Ovulation, formation of corpus lutes in ovary, regulation of ovarian secretion
M: Stimulates cell in testes to secrete testosterone

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28
Q

What is CRF or CRH (corticotropin releasing factor/hormone)?

A

Regulates ACTH secretion from anterior pituitary; cortisol release to blood

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29
Q

What is ACTH (adrenocorticotropin hormone)?

A

Regulates glucocorticoid (cortisol) secretion from adrenal gland

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30
Q

What are the feedback loops for cortisol secretion?

A
  1. ACTH inhibits CRH
  2. Cortisol inhibits CRH and ACTH
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31
Q

What is hyposecretion?

A

Too little hormone produced -> less than normal response

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32
Q

What is hypersecretion?

A

Excess of hormone produced -> exaggeration of normal effect

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33
Q

What is an example of primary pathology with the endocrine systems?

A

Damage to the hormone secreting gland such as tumor, death to cells, or autosomal abnormalities

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34
Q

What is an example of secondary pathology with the endocrine systems?

A

Damage to control mechanisms of glands

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35
Q

What is abnormal tissue responsiveness?

A

Receptor defect or resistance caused by mutations in receptors or second messenger pathways

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36
Q

What is a common cause of hyperpituitarism?

A

Adenoma

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37
Q

What are the outcomes of adenomas?

A
  1. Visual field changes
  2. Increased intracranial pressure
38
Q

What is the primary hormone effects of hyperpituitarism?

A
  1. Prolactin (25%)
  2. GH (15%)
    3 ACTH (15%)
39
Q

What are some conditions associated hypopituitarism?

A
  1. Ischemic injury
  2. Radiation or surgery
  3. Inflammation and autoimmune disorders
  4. Non-secreting adenomas
40
Q

What is panhypopituitarism?

A

Loss of 75% function of anterior pituitary

41
Q

What are common causes of panhypopituitarism?

A
  1. Nonsecretory pituitary adenomas
  2. Ischemic necrosis
  3. Infarction, Ablation
42
Q

What are occurs after prolonged panhypopituitarism?

A
  1. ACTH: life threatening
  2. TSH: life threatening
  3. Low GH
  4. Low MSH (Pallor)
  5. Low LH and FSH (Gonadal atrophy)
43
Q

What is the adrenal cortex?

A

Outer region of gland that produces steroid hormone based on cholesterol

44
Q

What are the 3 zones of the adrenal cortex?

A
  1. Zona glomerulosa (outer)
  2. Zona fasciculata (middle)
  3. Zona reticularis (inner)
45
Q

What secreted by the zona reticularis?

A

Gonadal steroids mostly androgens converted to testosterone and small amounts of estrogen

46
Q

What is secreted by zone glomerulosa?

A

Mineralocorticoids

47
Q

What is the purpose for Mineralocorticoids?

A

Aldosterone: Ion and water balance

48
Q

What is secreted by the zone fasciculata?

A

Glucocorticoids

49
Q

What is glucocorticoids?

A

Cortisol: Effects glucose metabolism

50
Q

What is the function of glucocorticoids?

A
  1. Helps to maintain blood glucose levels
  2. Stimulates proteolysis for gluconeogeneis
  3. Stimulate liver cells to synthesize glucose
  4. Decrease immune response
51
Q

What are glucocorticoids used for?

A

Treat allergic reactions and inflammation

52
Q

How are glucocorticoids controlled?

A
  1. Stimulated by CRH -> ACTH
  2. Stress
  3. Low plasma glucose concentrations
53
Q

What mediates glucocorticoid action?

A

Glucocorticoid receptor, an intracellular protein

54
Q

What are transcription factors?

A

Regulate the expression of Glucocorticoid-responsive elements, positively or negatively

55
Q

How is gene expression activated or repressed?

A

After glucocorticoid receptor is activated, the receptor translocates to the nucleus where they can alter gene transcription by binding to specific DNA response elements

56
Q

How can glucocorticoid receptor activation by prevented?

A

11 beta hydroxysteroid dehydrogenase converts cortisol into inactive cortisone

57
Q

What is GR knockout in mice prove?

A

GR function during gestation is essential for postnatal survival and development

58
Q

How can mobilization of amino acids counter insulin?

A

Extrahepatic tissues provide amino acid precursors for hepatic gluconeogenesis

59
Q

How does increasing blood glucose counter insulin?

A

Stimulation of gluconeogenesis in liver and glycogen breakdown

60
Q

How can adipose tissue counter insulin?

A

Lipolysis is activated and promote mobilization and oxidation of fatty acids

61
Q

How do peripheral tissues counter insulin?

A

Impart insulin resistance to cells and increases plasma glucose by other hormones

62
Q

What is the role of GC on the integumentary system?

A
  1. Regulate epithelial integrity and immune function
  2. Treating cutaneous inflammatory
63
Q

What is the role of GC on circulation?

A
  1. Maintains body fluid volume and vascular integrity
  2. Cortisol has a mild mineralocorticoid effect, not as aldosterone
  3. Sensitizes arterioles to action of NE’
  4. Decreases capillary permeability
  5. Maintains normal renal function
64
Q

What is GC effect on BP?

A

Generally increases BP

65
Q

How is cortisol-induced hypertension characterized?

A

Sodium retention and volume expansion

66
Q

How can cortisol cause hypertension?

A
  1. Increase vascular smooth muscle sensitivity
  2. Reduce NO medicated endothelial dilation
  3. Increase filtration fractions and glomerular hypertension
  4. RAAS activation
  5. Decrease prostaglandin and leukotriene synthsis
67
Q

How can GC effect bone and calcium metabolism?

A
  1. Inhibits osteoblastic cellular function
68
Q

What are osteoblasts?

A

Bone cell type that lays new bone matrix

69
Q

What is caused due to the excess of glucocorticoids in bone?

A

Osteopenia and osteoporosis

70
Q

What is primary Addison’s disease?

A
  1. Chronic
  2. Hyperpigmentation due to increased ACTH -> increased MSH -> increased melanotropic activity
71
Q

What causes secondary Addison’s disease?

A

Rapid the withdraw from exogenous steroid therapy

72
Q

What are the outcomes of secondary Addison’s disease?

A
  1. Hypothalamic lesions
  2. Hypopituitarism
  3. Pituitary adenomas
    Symptoms due to reduced CRH and/or ACTH
73
Q

How can Addisonian crisis cause adrenal insufficiency?

A
  1. Weakness and fatigue
  2. Hypotension, Decreased Na+ and increased K+
  3. Hypoglycemia
  4. GI symptoms
74
Q

How does primary Addison’s release large amounts of ACTH?

A

No cortisol to provide negative feedback in the hypothalamus

75
Q

What happens if you remove a patient from chronic corticosteroid therapy?

A

Body wil experience ACTH deficiency and secondary adrenocortical insufficiency and that may take a long time to return

Taper steroids

76
Q

What is Cushing’s syndrome?

A

Hypersecretion of ACTH and cortisol

77
Q

What causes the hypersecretion of cortisol in Cushing’s?

A

Adrenal tumor

77
Q

What causes the hypersecretion of ACTH in Cushing’s?

A

Tumor in pituitary, lungs, kidneys, or pancreas
1. Ectopic ACTH released by neoplasia

78
Q

What is caused after exogenous glucocorticoid administration?

A

Latrogenic Cushing’s syndrome

79
Q

What are the 3 factors that cause Cushing’s

A
  1. Hypothalamic-pituitary disease causing an increase in ACTH
  2. imary Adrenocortical Hyperplasia/Neoplasia causing a decrease in ACTH
  3. Ectopic ACTH by Non-Endocrine Neoplasia decreasing ACTH
80
Q

What are the effects of glucocorticoids?

A
  1. Osteoporiosis
  2. Cataracts
  3. Skin thinning and cutaneous striae
  4. Reduced protein and myopathies
  5. Connective tissue breakdown
  6. Blood changes
  7. CNS effects
81
Q

How can excess glucocorticoids effect cause blood changes?

A

Anti-inflammatory
1. Increased Neutrophils, thrombocytes, and RBC
2. Decreased lymphocytes, eosinophils, and basophils

82
Q

How can excess glucocorticoids cause CNS effects?

A
  1. Decreased mood stability
  2. Increased psychoses and excitability
83
Q

What are the symptoms of Cushing?

A
  1. Lipid tissue redistribution
  2. Fragile skin and easy bruising (cutaneous striae)
  3. Anti-inflammatory effects (masks infections)
  4. Metabolic disturbances
84
Q

What kind of lipid tissue redistribution associated with Cushing?

A
  1. Weight gain
  2. Truncal obesity
  3. Moon facies
  4. Buffulo hump
85
Q

What are the metabolic disturbances of Cushing?

A
  1. Water and salt retention (hypertension)
  2. Hyperglycemia (steroid diabetes)
  3. Loss of muscle and bone mass (muscle atrophy and osteoporosis)
86
Q

How does GC produce anti-inflammatory effects?

A
  1. Inhibits production of prostaglandins and leukotrienes by inhibiting Phospholipase A2
  2. Decreases the inflammatory reaction by decreasing permeability of capillary membranes, reducing swelling and reducing the effects of histamine and other inflammatory mediators
87
Q

In what ways can GC suppress the immune system?

A
  1. Decreases production of eosinophils and lymphocytes
  2. Inhibition of neutrophil and macrophage function
  3. Decrease T cell and antibody production
88
Q

What is the GC effect on the respiratory system?

A
  1. Inhaled corticosteroids, are the most commonly prescribed drugs for the treatment of chronic respiratory inflammatory conditions
  2. Inhibits the inflammatory response in asthma by inhibiting NF-kB and AP-1
89
Q

What is caused by inhibiting NF-kB and AP-1?

A

Suppresses the production and secretion of cytokines, chemokines, and cell adhesion molecules by the airway epithelium

MTP (15 decks)

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