Chapter 11-Endocrine System Flashcards

(40 cards)

1
Q

Priming Effect (upregulation) vs Desensitization (downregulation)

A

upregulation occurs when a hormone induces more of its own receptors in target cells
downregulation occurs after prolonged exposure to high levels of hormone, subsequent exposure produces decreased response due to decreased number of receptors on target tissue (insulin)

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2
Q

How do peptide hormones enter the target cell?

A

peptide hormones cannot enter target cells and must combine with membrane receptors that initiate signal transduction processes

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3
Q

How do hydrophobic steroids pass through?

A

most hydrophobic steroids are bound to plasma protein carriers. only unbound hormones can diffuse into the target cell. some steroids can slide through but once they are in the cytoplasm, they will bind to a specific receptor and sneak through that nuclear pore and trigger a transcription and then translation event which elicits a response.

  • some steroids, but not many, have a membrane receptor.
  • peptide based hormones, amino based hormones and steroids that specifically bind to a cell surface receptor are going to generate a much faster response (epinephrine is an example)
  • steroids that enter cytoplasm and trigger action of peptide is a slower response
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4
Q

Adipose tissue cells

A

Leptin, several others produced here. major function of appetite, metabolic rate, reproduction

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5
Q

Adrenal cortex

A

cortisol- responds to stress, immune system
androgens- sex drive in women
aldosterone- sodium and potassium excretion by kidneys

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6
Q

Adrenal medulla

A

epinephrine- response to stress

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7
Q

GI Tract

A

Gastrin- GI tract motility and acid secretion
Ghrelin- appetite
Secretin- exocrine and endocrine secretions from pancreas
CCK- secretion of bile from gallbladder
Glucose-dependent insulinotropic peptide (GIP)- insulin secretion
Motulin- GI tract motility

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8
Q

Gonads, ovaries in females:

A

estrogen-reproductive system, secondary sex characteristics
progesterone-endometrium and pregnancy
Inhibin- follicle-stimulating hormone (FSH) secretion
Relaxin- relaxation of cervix and pubis ligaments

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9
Q

testis in males:

A

Androgen (testosterone and dihydrotesterone)-reproductive system, secondary sex characteristics sex drive
Inhibin- FSH secretion

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10
Q

Anterior pituitary

A

GH, TSH, Adrenocorticotropic hormone, prolactin, FSH, LH

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11
Q

Posterior pituitary

A

-oxytocin, vasopressin (ADH)

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12
Q

Placenta

A

Human chorionic gonadotropin (hCG)
estrogens- sex gonads
progesterone-sex gonads, ovaries
human placental lactogen-breast development

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13
Q

pre- or pro- in front of a hormone

A

Many protein hormones undergo modifications during packaging and after they have been secreted, e.g.,
pre-pro-insulin -> pro-insulin -> insulin
-anytime you see pre- or pro-means that it’s an inactive hormone that can readily be activated

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14
Q

What are the steroid hormones that are derived from cholesterol?

A

cortisol, aldosterone, testosterone, and estradiol

  • cholesterol is a non-hormone lipid molecule found in all membranes. Synthesis and secretion are simultaneous for steroids
  • cholesterol=four ringed steroid molecule
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15
Q

thyroid hormone’s permissive role with epinephrine

A

thyroid hormones have a “permissive role” in the fat-mobilization response to epinephrine

  • thyroid hormone: small amounts of fatty acids released
  • epinephrine: small amounts of fatty acids released
  • epinephrine and thyroid hormone
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16
Q

What do increased glucose levels stimulate?

A
  • increased glucose levels in the pancreas directly stimulate the secretion of insulin.
  • vast majority of hormones work at negative feedback
    1) increase in plasma glucose concentration
    2) increase in insulin secretion from insulin-secreting cells
    3) increase in plasma insulin concentration
    4) insulin’s target cells- increase actions of insulin (transport of glucose from plasma to intracellular space)
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17
Q

Interactions between endocrine and nervous systems

A
  • interactions emphasize the coordinated communications functions
  • oxytocin would be triggered in a positive feedback mechanism, oxytocin increase=increased uterine contraction, positive because oxytocin increase, uterine contraction levels increase, everything is increasing
  • adrenal gland secretes epinephrine to further increase the metabolism or the activity of whatever tissue it’s responding to
18
Q

What is the ruler of the pituitary?

A

hypothalamus is the ruler of the pituitary, hypothalamus sends hormones to pituitary and pituitary will do the same around, but only if hypothalamus allows that to happen

19
Q

Describe a typical 3-hormone sequence of hormone control:

A

1) Stimulus
2) hypothalamus increases secretion of hormone 1
3) increase in hormone 1 (in hypothalamo-pituitary portal vessels)
4) anterior pituitary increases secretion of hormone 2
5) increase in hormone 2 in plasma
6) third endocrine gland-increase in hormone 3 secretion
7) increase in hormone 3 in plasma
8) target cells of hormone 3, respond to hormone 3
~having separate parts allows fine tune response, this allows for specificity, allows for groups of systems to be activated, prevents atrophy (shrivel or shrink)
~hypertrophy-getting bigger~

20
Q

Six of the well-characterized hormones

A
  • they are secreted by the anterior pituitary gland and their targets are represented
  • FSH and LH- coming from anterior pit. triggers gonads to secrete specific hormones (FSH produces eggs or sperm) (LH produces estrogen or testosterone)
  • GH found in the liver and other cells, many organs and tissues (protein synthesis, carbohydrate and lipid metabolism)
  • TSH from thyroid: secretes thyroxine and triiodothyronine
  • prolactin: breasts, breast development and milk production
  • ACTH from adrenal cortex, secretes cortisol
21
Q

hypothalamic-pituitary portal system

A

hypothalamic “releasing” hormones are delivered to the anterior pituitary gland via the hypothalamic-pituitary portal system
-upon arrival, the releasing hormones bind to the receptors on the pituitary cells to evoke secretion of the pituitary hormones

22
Q

Relationships between hypothalamic, pituitary, and third gland hormones

A
  • hypothalamus (GnRH)-> pituitary (FSH and LH)-> Gonads (female-ovum, male-sperm), Hormones (female-estradiol, progesterone, male-testosterone)
  • hypothalamus (GHRH, SS (somatostatin)->anterior pituitary (GH)-> liver and other cells secrete IGF-1, many organs and tissues (protein synthesis, carbohydrate and lipid metabolism)
  • hypothalamus (TRH)->anterior pituitary (TSH) ->thyroid (secretes thyroxine, triiodothyronine)
  • hypothalamus (dopamine)->anterior pituitary (prolactin)->breasts(breast development and production of milk, in male may facilitate reproductive function)
  • hypothalamus (CRH)->anterior pituitary (ACTH)->adrenal cortex (cortisol)
23
Q

different regions of the adrenal gland produce different hormones

A
cortex region (top three zones) produce aldosterone, cortisol and androgens, 
medulla: epinephrine & norepinephrine
24
Q

How does adrenal steroid hormone exert a negative-feedback relationship to the hypothalamic and pituitary hormones that influence cortisol synthesis

A
  • done to prevent runaway secretion of cortisol during a stressful interval
    1) neural inputs
    2) hypothalamus increases secretion of CRH
    3) increases CRH in hypothalamic-pituitary portal vessels
    4) anterior pituitary increases secretion of ACTH
    5) adrenal cortex increases cortisol secretion
    6) increases cortisol secretion
    7) target cells for cortisol respond to increased cortisol
  • two points where negative feedback will work: hypothalamus and anterior pituitary*
25
Effects of increased plasma cortisol concentration during stress
1) Effects on organic metabolism a. stimulation of protein catabolism in bone, lymph, muscle, and elsewhere b. stimulation of liver uptake of amino acids and their conversion to glucose (gluconeogenesis) c. maintenance of plasma glucose levels d. stimulation of triglyceride catabolism in adipose tissue, with release of glycerol and fatty acids into the blood 2) Enhanced vascular reactivity (increased ability to maintain vasoconstriction in response to norepinephrine and other stimuli) 3) unidentified protective effects against the damaging influences of stress 4) Inhibition of inflammation and specific immune responses 5) Inhibition of nonessential functions (e.g., reproduction and growth)
26
Actions of sympathetic nervous system, including epinephrine secreted by adrenal medulla, during stress
1) increased hepatic and muscle glycogenolysis (provides a quick source of glucose) 2) increased breakdown of adipose tissue triglyceride (provides a supply of glycerol for gluconeogenesis and of fatty acids for oxidation) 3) decreased fatigue of skeletal muscles 4) increased cardiac function (e.g., increased heart rate) 5) diversion of blood from viscera to skeletal muscle by means of vasoconstriction in the former beds and vasodilation in the latter 6) increased lung ventilation by stimulating brain breathing centers and dilating airways
27
secondary hypersecretion due to hypothalamic problem
- if hypothalamus is broken, then the CRH will be oversecreted, ACTH will increase, cortisol from adrenal cortex will increase (negative feedback fails)-> symptoms of excess - CRH levels are high, ACTH levels are high, cortisol levels are high
28
secondary hypersecretion due to pituitary problem
- apparently negative feedback is responding to increased cortisol. hypothalamus is not broken, but anterior pituitary is broken and is hypersecreting even without a message - CRH levels low, increase in ACTH, increase in cortisol-> symptoms of excess
29
Location of the thyroid gland
-thyroid gland straddles the esophagus, just below the larynx, in the neck
30
How does thyroid hormone exert a negative-feedback relationship to the hypothalamic and pituitary hormones that influence thyroid hormone synthesis?
1) once there are neural inputs, TRH is increased from the hypothalamus, this increases plasma TRH in hypothalamic-pituitary portal vessels. 2) increase in TSH from the anterior pituitary, this increases plasma TSH 3) increase of T3 and T4 from the thyroid gland, increases plasma thyroid hormone 4) target cells for thyroid hormone: T4 is converted to T3, target cells respond to increased T3
31
Hypothyroidism due to low iodine
1) decrease in iodine in the diet leads to decrease in T3 and T4 2) hypothalamus increases TRH 3) anterior pituitary increases TSH 4) thyroid gland enlarges as a result 5) without any iodine, T3 and T4 remain low, results in no negative feedback
32
hyperthyroidism due to Grave's disease
1) decrease of TRH from hypothalamus 2) there's no stimulus so there's a decrease in TSH from anterior pituitary 3) thyroid stimulating immunoglobulins cause the thyroid gland to become enlarged, and T3 and T4 increase, resulting in a strong negative feedback loop
33
Long bone growth
-long bone growth occurs at the epiphyseal growth plate; at puberty many of these plates undergo "epiphyseal closure" as a result of the action of steroid hormones from the maturing gonads
34
Major hormones influencing growth
1) Growth hormone: major stimulus of postnatal growth; induces precursor cells to differentiate and secrete insulin-like growth factor 1 (IGF-1)-> stimulates liver to produce IGF-1, stimulates protein synthesis 2) Insulin-stimulates fetal growth, stimulates postnatal growth by stimulating secretion of IGF-1, protein synthesis 3) thyroid hormones: permissive for growth hormone's secretion and actions, permissive for the development of the central nervous system 4) testosterone: stimulates growth at puberty, in large part by stimulating the secretion of growth hormone, causes eventual epiphyseal closure, stimulates protien synthesis in male 5) estrogen: stimulates secretion of growth hormone at puberty, causes eventual epiphyseal closure 6) cortisol: inhibits growth, stimulates protein catabolism
35
Cells in the bone
- osteoblasts: build bone - osteocytes have long processes that connect with each other and to osteoblasts via tight junctions - osteobclasts catalyze bone degradation, when stimulated by the parathyroid hormone (PTH)
36
Summary of major hormonal influences on bone mass
-hormones that favor bone formation and increased bone mass: insulin, growth hormone, insulin-like growth factor (IGF-1), estrogen, testosterone, calcitonin -hormones that favor increased bone resorption and decreased bone mass: parathyroid hormone (chronic elevations), cortisol, thyroid hormones (T3, T4)
37
When is parathyroid hormone (PTH) secreted?
- direct response to an abnormal decrease in the concentration of calcium ions
38
How does parathyroid's actions help to restore calcium levels?
-increased calcium reabsorption in the kidneys, increased calcium-liberating activating activities of osteoclasts, and increased formation of vitamin D, which increases uptake of dietary calcium in the gastrointestinal tract.
39
Parathyroid hormone's response to low plasma calcium
-low plasma calcium causes increased plasma hormone secretion from the parathyroid glands -causes increase in plasma parathyroid hormone Results: increased bone resorption, increased calcium reabsorption -increased calcium reabsorption causes decrease in urinary excretion of calcium and increased bone resorption together causes restoration of plasma calcium towards normal
40
About Calcitonin
Cells of origin: C cells of thyroid gland (parafollicular cells) Chemical nature: 32-amino acid peptide biosynthesis: typical peptide transport in the circulation: dissolved in plasma Half-life: