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A&P > Chapter 16 > Flashcards

Chapter 16 Flashcards

1
Q

What is the endocrine system?

A

The body’s second great regulatory system.
Integrated system of small organs that involve release of extracellular signaling molecules known as hormones

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2
Q

What does the endocrine system do?

A

Regulates cellular activities by means of chemical messengers called hormones.
Hormones act at sites independent of secretion.
Short and long-term regulatory functions.

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3
Q

How does the endocrine system differ from the nervous system control?

A

Neurons directly innervate a tissue.
Stimulation is direct and immediate.

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4
Q

What are the major endocrine organs are?

A
  1. Hypothalamus
  2. Pituitary gland (anterior and posterior)
  3. Thyroid and Parathyroid
  4. Pancreas
  5. Adrenal glands
  6. Gonads
  7. Other tissues and organs: adipose cells, pockets of cells in the walls of the small intestine, stomach, kidneys, and heart
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5
Q

What are hormones?

A

Chemical messenger secreted by cells into the extracellular fluids that affect other parts of the body

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6
Q

Classifications of hormones?

A
  1. Amino acid-based: 1 or more amino acids (amines, peptides, protein)
  2. Steroids: derived from cholesterol (gonadal, adrenocortical)
  3. Eicosanoids: biologically active lipids with local hormone-like activity
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7
Q

What are autocrines?

A

Chemicals that exert effects on the same cells that secrete them

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8
Q

What are paracrines?

A

Locally acting chemicals that affect cells other than those that secrete them

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9
Q

Are autocrines and paracrines considered hormones?

A

No because hormones are long-distance chemical signals

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10
Q

How do hormones exert a biological effect on a tissue?

A

Receptors !
1. Membrane bound
2. Intracellular

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11
Q

What is target cell specificity?

A

How the same hormones affect some tissues/organs differently than others

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12
Q

How do we regulate hormone activity?

A
  1. Hormone concentration: rate of release; rate of inactivation/removal; 1/2 life
  2. Receptor concentration: cells can increase or decrease the number of receptors expressed
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13
Q

How are hormones removed from the blood?

A

Degrading enzymes: the kidneys and liver enzyme systems

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14
Q

What are the three types of hormone interaction?

A
  1. Permissiveness: one hormone cannot exert its effects without another hormone being present.
  2. Synergism: more than one hormone produces the same effects on a target cell
  3. Antagonism: one of more hormones opposes the action of another hormone
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15
Q

What is humoral stimulation?

A

Pertaining to elements in the blood or other body fluids.
Capillary blood contains low concentration of Ca2+, which stimulates secretion of parathyroid hormone (PTH) by parathyroid glands

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16
Q

What is neural stimulation?

A

Regulated by direct nervous system input.
Preganglionic sympathetic fibers stimulate adrenal medulla cells to secrete catecholamines (epinephrine and NE)

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17
Q

What is hormonal stimulation?

A

Regulated by hormones.
The hypothalamus secretes hormones that stimulate the anterior pituitary gland to secrete hormones that stimulate other endocrine glands to secrete hormones

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18
Q

What is neurohypophysis?

A

Posterior lobe (neural tissue) and the infundibulum.
Receives, stores, and secretes hormones from the hypothalamus.

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19
Q

Explain the pathway that oxytocin and ADH travel from the hypothalamus to the posterior pituitary gland.

A
  1. Hypothalamic neurons synthesize oxytocin and ADH.
  2. Oxytocin and ADH are transported along the hypothalamic-hypophyseal tract to the posterior pituitary.
  3. Oxytocin and ADH are stored in axon terminals in the posterior pituitary.
  4. Oxytocin and ADH are released into the blood when hypothalamic neurons fire.
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20
Q

What is adenohypophysis?

A

Anterior lobe, made up of glandular tissue.

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21
Q

Pathology of Growth Hormone?

A

Class of hormone: protein.
Regulation of secretion: negative feedback control; hormonal stimulation.
Receptor: membrane bound.
Stimulated by: secretion of GHRH by hypothalamus. Produced by somatotropic cells of the anterior lobe.
Inhibited by: secretion of GHIH by hypothalamus.
Target: liver, muscle, bone, cartilage; somatic growth.
Effects:
- Direct effects: anti-insulin actions (stimulate secretion of energy substrates) and secretion of IGFs
- Indirect effects: stimulates bone growth (caused by secretion of IGFs)

22
Q

Hypersecretion of GH

A

Childhood: pituitary gigantism (before growth plates seal).
Adults: acromegaly

23
Q

Hyposecretion of GH

A

Infant: hypoglycemia.
Childhood: pituitary dwarfism.
Adult: loss of lean tissue mass

24
Q

Pathology of thyroid hormones

A

Class of hormone: amine and lipid soluble.
Regulation of secretion: negative feedback control; hormonal stimulation.
Receptor: intracellular.
Stimulated by:
- secretion of TRH (thyrotropin releasing hormone) by hypothalamus.
- secretion of TSH (thyroid stimulating hormone) by anterior pituitary.
Inhibited by:
Targets: virtually every cell in the body. Permissive
Effects:
- glucose oxidation
- increasing metabolic rate
- heat production
- maintains BP
- regenerates tissues
- develops skeletal and nervous systems
- maturation of reproduction

25
Q

Hypersecretion of TH

A

Grave’s Disease:
- autoimmune disorder where antibodies secreted by immune system directly stimulate the thyroid gland (destroys negative feedback regulation)
- overactivity of thyroid gland
- inflammation of tissues around eyes
- increases metabolic rate, sweating, rapid and irregular heart beat, nervousness, weight loss, and protruding eyeballs
- goiters

26
Q

Hyposecretion of TH

A

Goiters.
Cretenism:
- children: can be due to iodine deficiency in mother’s diet during pregnancy; causes low metabolic rate, growth retardation, developmental delay, other abnormal features.
Myxedema:
- adults: can be due to iodine deficiency; can result in low metabolic rate and skin and tissue disorder

27
Q

Pathology of prolactin

A

Class of hormone: peptide.
Regulation of secretion: hormonal regulation (PRL levels rise and fall in rhythm with estrogen blood levels.
Receptor: membrane bound.
Stimulated by:
- decreased PIH release by hypothalamus
- release enhanced by estrogens, birth control pills, breast-feeding, and dopamine-blocking drugs.
Inhibited by: secretion of PIH by hypothalamus.
Target: Mammary glands
Effects: colostrum and milk production.

28
Q

Hypersecretion of prolactin

A

Females: inappropriate milk production and cessation of menses.
Males: impotence and breast enlargement.

29
Q

Hyposecretion of prolactin

A

poor milk production.

30
Q

Pathology of Antidiuretic hormone (ADH)

A

Class of hormone: peptide.
Regulation of secretion: humoral regulation.
Receptor: membrane bound.
Stimulated by:
- high osmolality.
- impulses from hypothalamic neurons in response to increased blood solute concentration or decreased blood volume
- pain and some drugs
- low blood pressure
Inhibited by: adequate hydration; alcohol.
Target: kidneys (nephrons).
Effects:
- helps avoid dehydration
- prevents urine formation
- promotes thirst development
- opens aquaporins within collecting ducts of nephrons to reabsorb water

31
Q

Hypersecretion of ADH

A

Hyponatremia.
Elevated urine osmolality.
Excessive urine sodium excretion.
Decreased serum osmolality.

32
Q

Hyposecretion of ADH

A

Diabetes insipidus:
- increased urine output.
- increased fluid intake.
- increased thirst.
- unable to stimulate aquaporin formation
- dilute urine
- nocturia
- enuresis (bedwetting)

33
Q

Pathology of oxytocin

A

Class of hormone: peptide.
Regulation of secretion: hormonal; positive feedback control.
Receptor: membrane bound.
Stimulated by:
- impulses from hypothalamic neurons in response to stretching of the uterine cervix or suckling of infant
- the more oxytocin, the more uterine contractions
Inhibited by:
- lack of appropriate neural stimuli
- secretion stops when uterus cannot contract anymore
Target: uterus and mammary glands
Effects:
- uterine contraction
- milk ejection (letdown reflex)
- orgasms in females and fidelity in males

34
Q

Calcitonin

A

Class of hormone: peptide.
Regulation of secretion: humoral; negative feedback control.
Receptor: membrane bound.
Stimulated by: increase in blood calcium levels.
Inhibited by: decrease in blood calcium levels.
Target: skeleton.
Effect:
- lowers blood calcium
- inhibits secretion of PTH and osteoclast activity
- promotes osteoblast activity

35
Q

Pathology of Parathyroid hormone

A

Class of hormone: peptide.
Regulation of secretion: humoral; negative feedback control.
Receptor: membrane bound.
Stimulated by: decrease in blood calcium levels.
Inhibited by: increase in blood calcium levels.
Target:
- stimulates events in 3 places: bones, intestines, and kidney
Effect: raises blood calcium levels

36
Q

Pathology of Aldosterone

A

Class of hormone: steroid (mineralcorticoid).
Regulation of secretion: negative feedback control (unless chronic stress).
Receptor: intracellular.
Stimulated by:
- increased blood potassium concentration.
- decrease in blood volume/pressure.
- secretion of angiotensinogen from kidneys –> secretion of renin from liver –> secretion of angiotensin I –> binds to ACE in the lining of the lungs –> angiotensin II –> stimulates secretion of aldosterone.
Inhibited by:
- increased blood pressure/volume.
- ANP: antagonist to RAAS system
Target: kidneys (sodium potassium pump in walls of nephrons).
Effect:
- promote electrolyte balance (conserves water).
- regulate gene expression
- secretion of potassium and reabsorption of sodium

37
Q

Hypersecretion of aldosterone

A

Aldosteronism:
- adrenal cortex tumor
- overactivity of cells in zona glomerulosa
- causes hypervolemia, hypertension, edema, loss of potassium
- no effect on glucose concentration

38
Q

Hyposecretion of aldosterone

A

Addison’s Disease:
- commonly due to lack of secretion of ACTH.
- hyposecretion of adrenal cortex
- don’t retain as much sodium and don’t excrete as much potassium (not as much water as a consequence)
- severe dehydration
- hypotension
- low blood glucose

39
Q

Pathology of cortisol

A

Class of hormone: steroid.
Regulation of secretion: negative feedback control (circadian) unless experiencing stress.
Receptor: intracellular.
Stimulated by:
- HPA axis: CRH released by hypothalamus –> CRH stimulates secretion of ACTH from anterior pituitary.
- circadian pattern.
- chronic stress.
Inhibited by: excess cortisol inhibits hypothalamus from secreting CRH
Target: body cells
Effects:
- raises blood glucose
- regulates wakefulness
- coincides with changes in body temperature

40
Q

Hypersecretion of cortisol

A

Cushing’s syndrome:
- excess glucocorticoid
Cushing’s disease:
- excess ACTH (increases cortisol)
- effects of elevated cortisol: hyperglycemia, skeletal muscle atrophy, loss of bone mass, edema, buffalo hump, poor wound healing

41
Q

Hypersecretion of cortisol

A

Addison’s Disease:
- deficiency of ACTH

42
Q

Pathology of gonadocorticoids

A

Class of hormone: steroid.
Regulation of secretion: na.
Receptors: intracellular.
Stimulated by: ATCH secretion (androgen secretion by adrenal gland is low).
Inhibited by: na.
Target: reproductive organs.
Effects:
- female libido.
- development of pubic and axillary hair in females.
- source of estrogen after menopause.

43
Q

Hypersecretion of gonadotropins

A

Males: early puberty; male sex characteristics and sex drive.
Females: masculinization

44
Q

Catecholamines (epinephrine and NE)

A

Class of hormone: amine.
Receptor: adrenergic receptor (includes beta 1-3 and alpha 1-2).
Stimulated by:
- short-term stress response.
- secretion of ACh from sympathetic preganglionic fiber
Target: sympathetic target organs.
Effects: activates flight or fight, heart beats faster, raises blood pressure

45
Q

Pathology of Insulin

A

Class of hormone: amino acid based.
Regulation of secretion: negative feedback; humorally regulated.
Receptor: membrane bound.
Stimulated by: high glucose.
Inhibited by: low blood glucose.
Target: tissue cells.
Effects:
- stimulates glucose uptake
- lowers blood glucose
- parasympathetic nervous system activation

46
Q

Hyposecretion of insulin

A

Diabetes mellitus:
Type 1: insulin dependent (do not produce enough insulin)
Type 2: non-insulin dependent/adult onset (most common; body has ability to produce insulin but receptors do not stimulate uptake of glucose )
- if untreated, beta islet cells die
Gestational diabetes: women pregnant

47
Q

Pathology of Glucagon

A

Class of hormone: amino acid based.
Regulation of secretion: negative feedback; humorally regulated.
Receptor: membrane bound.
Stimulated by: low blood glucose
Inhibited by: high blood glucose
Target: liver
Effects:
- stimulates glycogen breakdown
- raises blood glucose
- sympathetic nervous system activation

48
Q

Hyposecretion of glucagon

A

Hypoglycemia

49
Q

Pathology of Atrial Natriuretic Peptide

A

Class of hormone: peptide.
Regulation of secretion: negative feedback.
Receptor: membrane bound.
Stimulated by: increased blood pressure and/or blood volume.
Inhibited by: decreased blood volume/pressure.
Target: inhibits zona glomerulosa of adrenal cortex from stimulating kidney tubules.
Effects:
- inhibits secretion of aldosterone, reabsorption of water and sodium, potassium excretion.
- lowers blood pressure/volume

50
Q

Hypersecretion of ANP

A

Less water uptake

51
Q

Hyposecretion of ANP

A

increased levels of ADH, aldosterone, angiotensin II, and blood pressure

52
Q
A

A&P (8 decks)

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