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Advanced Pathophysiology > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

General characteristics of hormones:

A
  • Specific rates and rhythms of secretions (diurnal, pulsatile, and cyclic)
  • Feedback systems (positive-self amplifying, negative-inhibitory)
  • Target cells with appropriate receptors
  • Liver inactivates hormones; renal excretion
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2
Q

Hormones are released:

A
  • In response to an alteration

- To maintain a regulated level (homeostatic balance)

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3
Q

Hormones are regulated by:

A 
Chemical (ie-blood sugar-insulin, Ca levels-calcitonin and PTH)
Hormonal (hormone from one endocrine gland controlling another gland.  ie-TSH to T4 release) 
Neural factors (ie- release of epi from adrenal medulla and ADH and oxytocin release stimulated by glutamate and inhibited by GABA)
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4
Q

Hormones released by Pituitary/Hypothalmus:

A

Anterior- FLATPiG
Intermediate- MSH (melanocyte stimulating hormone)
Posterior- ADH, Oxytocin (made in hypothalmus, stored in posterior pit)

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5
Q

Hormones released by the Thyroid:

A

Thyroxine, T3, T4

Calcitonin

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6
Q

What does FLATPiG consist of?

A

Anterior Pit hormones: FSH, LH, ACTH, TSH, Prolactin, and GH

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7
Q

Hormones released by the Parathyroid:

A

PTH

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8
Q

Hormones released by the Adrenal Cortex:

A 
Mineralcorticoids (ie-Aldosterone)
Glucocorticoids (ie-Cortisol)
Weak Androgens (ie-DHEA)
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9
Q

Hormones released by the Adrenal Medulla:

A

Epinephrine
Norepinephrine
Dopamine

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10
Q

Hormones released by the Pancreas:

A

Insulin
Glucagon
Somatostatin

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11
Q

Hormones released by the Ovary:

A

Progesterone

Estrogen

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12
Q

Hormones released by the Testis:

A

Testosterone

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13
Q

What is the most common type of feedback system regulating endocrine function?

A

Negative feedback

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14
Q

What is up-regulation?

A

An increase in receptor number causes an increase in hormone effect d/t ability to bind to more receptors.

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15
Q

What is down-regulation?

A

A decrease in receptor number causing a decrease in hormone effect.

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16
Q

What is the purpose of up and down-regulation?

A

Regulation of target cell sensitivity. By altering the number of receptors on target cell for a particular hormone

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17
Q

How do water soluble hormones enter target cell?

A

Water soluble hormones circulate in free/unbound forms. They cannot diffuse across the plasma membrane. Require receptor on membrane and use a second messenger.

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18
Q

How do lipid soluble hormones enter a target cell?

A

Lipid soluble hormones circulate bound to a carrier (usually a globulin). They are able to easily diffuse across the membrane and target intracellular receptors (cytosolic or nuclear) and activate RNA polymerase or DNA transcription and translation =synthesize proteins

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19
Q

Explain water soluble hormone mechanism of action.

A
  • First messenger (bind to receptor)
  • Signal transduction
  • Second messenger molecules (Ca, cAMP, or cGMP)
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20
Q

What are some examples of water soluble hormones?

A

LH, FSH, insulin, epinephrine, norepinephrine, GH, TSH

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21
Q

What are some examples of lipid soluble hormones?

A

Steroids- androgen, estrogen, progestin, glucocorticoids, mineralcorticoids, cortisol, calcitrol
T3 and T4

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22
Q

What is the hypophyseal portal system?

A

Neurons in the hypothalmus secrete releasing hormones into veins that carry the releasing hormones directly to the vessels of the anterior pituitary, thus bypassing the normal circulatory route.

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23
Q

Where are the pituitary glands located?

A

Below the hypothalmus in the sella turcica at the base of the skull.

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24
Q

What connects the hypothalmus to the posterior pituitary?

A

Pituitary stalk. Neurons within which require an action potential

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25
Q

What connects the hypothalmus to the anterior pituitary?

A

Venous connections/capillaries.

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26
Q

When is ADH(vasopressin) released by the posterior pituitary?

A

Released in response to altered serum osmolality and hypotension and causes water retention by increasing water reabsorption by the renal collecting duct.

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27
Q

When is oxytocin released by the posterior pituitary?

A

Released during sex, childbirth, and breastfeeding. Causes uterine and milk duct contractions.

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28
Q

What is the three tiered axis of the hypothalmic-qpituitary endocrine system?

A
  1. Hypothalmus (release or inhibit hormones-often in a pulsatile rhythm)
  2. Anterior Pituitary Hormones
  3. Target organ hormones
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29
Q

GH and the anterior pituitary gland?

A
  • Controlled by hypothalmic release of GHRH and growth inhibiting hormone (somatostatin). Ant pit release small pulsatile amount of GH each day.
  • Liver is the major target. Affects liver metabolism and stimulates production of insulin-like growth factor 1
  • GH affects metabolic processes. Ie- increase rate of protein synthesis and slow carb utilization
  • Hypoglycemia and increased concentration of amino acids in blood stimulates GH release
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30
Q

Prolactin and the anterior pituitary gland.

A
  • Promote breast development and lactation
  • Ability to suppress reproductive function on men and women d/t suppression of hypothalmic gonadotropin-releasing hormone
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31
Q

Gonadotropins and the anterior pituitary gland.

A
  • FSH and LH
  • Proteins that bind to specific respective receptors on target cells in the ovary or testes
  • Stimulate estrogen/progesterone in women and testosterone in men
  • Stimulated by gonadotropin-releasing hormone in a pulsatile motion and inhibited by negative feedback from sex steroids.
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32
Q

TSH and the anterior pituitary gland.

A
  • Released by thyrotropes in response to TRH.
  • Glycoprotein that bind to TSH receptors on follicle cells of the thyroid gland.
  • TSH regulates all aspects of thyroid function
  • TRH is released according to diurnal rhythm (decreased in evening)
  • Negative feedback regulates TRH and TSH by the concentration of T3
33
Q

ACTH and the anterior pituitary gland.

A
  • Produced by the corticotropes in response to hypothalmic corticotropin-releasing hormone
  • Circulation unbound with a half-life of 10minutes
  • Binds to G coupled receptors on cells in the adrenal cortex and stimulates the production of cortisol and adrenal androgens
  • Withdrawal of ACTH results in adrenal cortical atrophy
  • Overproduction of ACTH stimulates melanocyte receptors and causes darkened skin
  • CRH and ACTH are released in diurnal pattern
  • Negative feedback regulation d/t cortisol =suppress CRH and ACTH release
34
Q

Describe the negative feedback loop that occurs when there is low Ca.

A
  1. Low Ca causes PTH release from the parathyroid glands.
  2. The kidneys will reabsorb Ca and excrete Phos
  3. Calcium and Phos are released from bone
  4. The kidneys will produce more vit D to help absorb Ca from the small intestine
  5. Normal Ca levels are restored
35
Q

Describe the positive feedback loop that happens during labor.

A
  1. Baby pushes against the cervix causing stretching (stretch receptors activated)
  2. Stretching of the cervix causes nerve impulses to be sent to the brain
  3. Brain stimulates posterior pituitary to release oxytocin.
  4. Oxytocin incites uterine contractions that push baby against cervix starting the loop over again
36
Q

Describe the negative feedback loop of thyroid gland regulation.

A
  1. Hypothalmus releases TRH
  2. TRH causes the anterior pituitary to release TSH
  3. TSH causes thyroid to release T3 and T4.
  4. If too much circulating T3 and T4 signal back to anterior pituitary and hypothalmus to release less TSH
37
Q

What are 3 main mechanisms/causes of endocrine dysfunction?

A
  1. Dysfunction of a particular gland (ex-dysfunction of ovaries may causes delayed or absent puberty)
  2. Altered secretion of the stimulating hormones for that gland
  3. Altered response to the hormone itself at that target cell (ex-insulin receptors)
38
Q

What are some causes of hypofunction of the endocrine system?

A

-Pituitary- Trauma, surgery, radiation, ischemia, suppression by exogenous hormone, congenital dysgenesis.
-Endocrine Glands- Inadequate trophic hormones, genetic defects, autoimmune destruction, ischemia, non-secreting tumors
-Exogenous ectopic source-Sudden withdrawal of exogenous hormones
Peripheral target tissues- Tissue resistance, down regulation of receptor, post receptor defects.

39
Q

What are some causes of hyperfunction of the endocrine system?

A

Pituitary- Microadenoma, adenoma, adenocarcinoma
Endocrine glands- Excessive trophic hormones, secreting tumors, autoimmune stimulation
Exogenous or ectopic source- Excessive hormone administration, non-endocrine tumor production of hormones

40
Q

What is a primary endocrine d/o?

A

Defect originates in the gland

41
Q

What is a secondary endocrine d/o?

A

Alteration at level of stimulating hormone, releasing factor, or other area. Ie- hypothalmic tumor affects pituitary gland= dysfunction of pit gland

42
Q

What is a tertiary endocrine d/o?

A

Both pituitary and target organ understimulated. Dysfunction of hypothalmus.

43
Q

A patient present with high TSH and low T4. What disease are these lab values indicative of?

A

Primary hypothyroidism

44
Q

A patient presents with high TSH and high T4. What disease are these lab values indicative of?

A

Secondary hyperthyroidism

45
Q

What is panhypopituitarism?

A

Inadequate or absent production of the anterior pituitary hormones.

46
Q

What clinical manifestations would you find in a patient with panhypopituitarism?

A
  • Lack of ACTH->cortisol deficiency
  • Lack of TSH->thyroid deficiency
  • Absence of FSH and LH->loss of secondary sex characteristics
  • Absence of Prolaction->inability to produce breast milk
  • Decrease in GH->delayed growth in children, vague s/s in adults (fatigue, loss of motivation, osteoporosis, reduced lean body mass, diminished feeling of well-being)
47
Q

What can cause pituitary infarction?

A 
Shock
Sheehan syndrome
Sickle cell
Pregnancy in women with DM
Genetic abnormalities
Head trauma 
CNS infections
AVMs, SAH, tumors
48
Q

What is Sheehan Syndrome?

A

Ischemic pituitary necrosis caused by severe postpartum hemorrhage

49
Q

What does PTH do and where is it secreted?

A
  • PTH is secreted by the parathyroid glands’ parathyroid chief cells (located at the upper and lower poles of the thyroid) and regulates serum Ca and acts as an antagonist of calcitonin.
  • PTH increases Ca levels in blood by increasing resorption in gut and bone and decreasing excretion by the kidney
  • Increases osteoclast activity
50
Q

How do the parathyroid glands and PTH regulate Ca?

A
  • Sense serum Ca levels and help maintain throughout regulation of Ca absorption and resorption from gut and bone
  • Absorption of Ca from the intestines and renal tubules is dependent on vit D
  • Serum Ca levels provide feedback necessary to regulate PTH secretion
  • PTH acts on bone, intestines, and kidneys
  • NOT part of the hypo-pit axis.
  • Calcitonin produced by thyroid parafollicular cells (C cells) opposes PTH
51
Q

Describe hyperparathyroidism

A
  • Causes: Idiopathic or parathyroid adenoma
  • Increased serum Ca and bone demineralization= decreased neuromuscular excitability
  • Treatment: Remove abnormal glands and adequate hydration to prevent kidney stones
52
Q

Describe hypoparathyroidism

A
  • Causes: Idiopathic, autoimmune, secondary to surgical removal
  • Decreased serum Ca= increased excitability (cramps, spasms, tetany, Chvostek, Trousseau signs)
  • Treatement: Ca (and vit D) supplementation
53
Q

What are normal anabolic (stimulating protein synthesis, cellular growth, and proliferation) functions of GH?

A
  • Direct via GH or indirect via IGF-1
  • Increase cell size and mitosis
  • Increase development and differentiation of cells
  • Increased metabolism: protein synthesis and mobilization of fatty acids, decrease glucose utilization
  • Bone and cartilage growth
54
Q

What is Acromegaly?

A

-GH dysegulation.
-Anterior pit gland produces excess GH AFTER epiphyseal plate closure of puberty
(Large forehead, projection of jaw, and protrusion of front bone)

55
Q

What is Dwarfism?

A
  • GH dysregulation

- Insufficient GH resulting in stunted or halted growth. Puberty may be delayed indefinitely.

56
Q

What is Giantism?

A
  • GH dysregulation

- GH is produced in excess prior to epiphyseal plate closure

57
Q

What is Hashimoto Thyroiditis?

A
  • Hypothyroidism
  • Autoimmune (lymphocytic thyroiditis)
  • Enlarged thyroid gland d/t lymphocytic infiltration
  • Thyroid hormone production decreases, stimulating the release of TSH (high serum TSH levels)
  • Thyroid specific T and B cells mediate autoimmune response
  • Cytotoxic T cells are responsible for parenchymal destruction and B cells secrete inhibitory anti-TSH receptors and other antibodies (antithyroglobulin and antithyroid peroxidase Abs are useful serologic markers of disease)
58
Q

What is Grave’s Disease?

A
  • Hyperthyroidism
  • Autoimmune
  • Thyroid auto-Ab’s (TSHR-Ab) activate the TSH receptor thereby stimulating increased T3 and T4 synthesis, secretion, and thyroid growth (goiter)
  • In response to high T3 and T4 levels that are stimulated by these auto-Ab’s the pit gland stops producing TSH (TSH serum levels very low)
59
Q

Characteristic s/s of hypothyroidism:

A
  • Dry, coarse hair
  • Loss of eyebrow hair
  • Puffy face
  • Enlarged thyroid
  • Bradycardia
  • Arthritis
  • Cold intolerance
  • Depression
  • Dry skin
  • Fatigue
  • Forgetfulness
  • Heavy menses
  • Infertility
  • Muscle ache
  • Weight gain
  • Constipation
  • Brittle nails
60
Q

Characteristics s/s of hyperthyroidism:

A
  • Hair loss
  • Exopthalmus
  • Sweating
  • Enlarged thyroid
  • Tachycardia
  • Difficulty sleeping
  • Heat intolerance
  • Infertility
  • Irritability
  • Muscle weakness
  • Nervousness
  • Scant menses
  • Weight loss
  • Frequent bowel movements
  • Warm, moist palms
  • Tremor in fingers
  • Soft nails
61
Q

Which cells are responsible for synthesis of thyroid hormones?

A

Thyroid epithelial cells

62
Q

What do parafollicular or C cells do?

A

Secrete calcitionin

63
Q

What do chief cells do?

A

Secrete PTH

64
Q

What is myxedema?

A
  • Associated with prolonged thyroid deficiency

- Generalized non-pitting edema d/t accumulation of glycosaminoglycans in the interstitial space that then retain fluid

65
Q

Where are the adrenal glands located and what types of hormones do they produce?

A

One on each kidney. They produce steroids (mineralcorticoids, glucocorticoids, androgens) and catecholamines (epi, norepi and dopa)

66
Q

What do the adrenal cortex synthesize?

A

The three S’s

  • Salts (mineralcorticoids)
  • Sugars (glucocorticoids)
  • Sex hormones (androgens)
67
Q

What are the three distinct zones of the adrenal cortex and what they produce?

A
  • Zona Glomerulosa (outer; mineralcorticoid-aldosterone)
  • Zona Fasciculata (glucocorticoid-cortisol)
  • Zona reticularis (inner; adrogens-DHEA)
68
Q

What do all adrenal cortex steroid hormones need for synthesis?

A

Cholesterol

69
Q

Describe Addison’s Disease

A

(Adrenocortical d/o (insufficiency)

  • Hyposecretion of adrenocortical hormones resulting from disease of the adrenal cortex
  • Causes: idiopathic, autoimmune, Tb, trauma, or hemorrhage of the adrenals (anticoagulants), fungal disease, or neoplasia
  • S/s may not be noticed until 90% of cortical tissue is nonfunctional
  • Low aldosterone causes low Na and high K

**Addisonian crisis- May be triggered by trauma or stress. Medical emergency causes by inadequate levels of glucocorticoids and mineralcorticoids in the circulation. Diminished vascular tone, reduced CO, inadequate blood volume may lead to lethal vascular collapse. Hypotension, tachycardia, and s/s of shock

70
Q

What is Cushing’s Syndrome?

A

Cushing syndrome is the term used to describe the clinical features of hypercortisolism regardless of causes.

71
Q

What is Cushing’s Disease?

A

(Adrenocortical d/o)
Hypercortisolism d/t secondary disease of the adrenal cortex caused by hyperfunction of the ant pit ACTH-secreting cells.

72
Q

What are classic s/s of Cushing syndrome?

A
  • Mood swings, insomnia, and loss of libido
  • Fine hair
  • Moon face and ruddy complexion
  • Hirsutism
  • Truncal obesity with pendulous breast and abdomen
  • Broad purple stria (stretch marks)
  • Dorsocervical fat pad
  • Supraclavicular fat pad
  • Thinning extremities with muscle wasting and fat mobilization
  • Thinning pubic and axillary hair in women
  • Ecchymosis
  • Thin fragile, skin
  • Impaired wound healing and immune response
73
Q

Describe DI

A
  • Insufficient ADH activity

- Characterized by excessive thirst and excessive loss of water in urine

74
Q

Describe Central or Neurogenic DI

A
  • Decreased/inhibited/deficient ADH synthesis, transport, or release
  • With insufficient ADH, urine cannot be concentrated and free water is lost, causing hyperosmolality and hypernatremia
  • D/t: Pit tumors, brain tumors, infections, immunologic problems, or thrombotic problems
75
Q

Describe Nephrogenic DI

A
  • Renal tubule insensitive to ADH
  • ADH levels are normal but the tubules do not respond to hormone
  • D/t: pyelonephritis, amyloidosis, destructive uropathies, polycystic kidney disease, anesthetic drug use, lithium carbonate
76
Q

Describe Psychogenic DI

A
  • Compulsive water drinking.
  • Normal ADH, too much H2O
  • Periodic polyuria, high urine volume, and plasma osmolality of less than 285 mOsm/kg
77
Q

Describe SIADH

A
  • Excessive release of ADH from the posterior pit gland or another source (adrenal insufficiency and hypothyroidism)
  • Increase in total body fluid= hypervolemia
  • Results in dilutional hyponatremia; free water is conserved and dilutes the serum Na concentration below normal.
  • In hyponatremia there is an excess in water relative to solute= cells swell, may be profound on neurons
  • Serum osmolality low because of dilution by reabsorbed water=urine osmolality high
78
Q

Pheocromocytoma is:

A
  • A tumor of chromaffin tissue that results in the excessive production and release of catecholamines
  • Usually located in the adrenal medulla
  • HTN d/t high circulating catecholamine levels stimulating the sympathetic nervous system
  • Triad of dx= HA, tachy, diaphoresis

Advanced Pathophysiology (12 decks)

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