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Endocrine > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

What are the 3 general classes of hormones?

A
  1. Proteins and polypeptides (pituitary gland, pancreas = insulin, glucagon; parathyroid = PTH)
  2. Steroids (Adrenal cortex = Cortisol and aldosterone; ovaries = estrogen, progresterone; testes = testosterone)
  3. Derviatives of AA Tyrosine (thyroid = thyroxine, triidothronine); adreanl medulla (epinephrine and norepinephrine)
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2
Q

What are steroid hormones synthesized from?

A

Cholesterol

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3
Q

What are amine hormones synthesized from?

A

Tyrosine

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4
Q

Name 3 second messenger systems.

A
  1. cAMP
  2. Cell membrane phospholipid - Activates Phospholipase C (PIP2 into IP3 (mobilized Ca) and DAG (activates PKC))
  3. Calcium-calmodulin = Activates protein kinases (MLCK - myosin light chain kinase)
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5
Q

What is an ELISA and how does it work?

A

Samples or standards are added to each well, followed by secondary antibody (specific to hormone and binds to it), third antibody is added that recognized and binds to the secondary antibody - this antibody is coupled to an enzyme that is converts suitable substrate to a product that is easily detected colorimetic or fluorescent
○ Used excess antibodies so that all hormone molecules are captured in antibody-hormone complexes
○ Thus the amount of hormone present in sample or standard is proportional to amount of product formed

Basic principles of the enzyme-linked immunosorbent assay (ELISA) for measuring the concentration of a hormone (H). AB1 and AB2 are antibodies that recognize the hormone at different binding sites, and AB3 is an antibody that recognizes AB2. E is an enzyme linked to AB3 that catalyzes the formation of a colored fluorescent product (P) from a substrate (S). The amount of the product is measured using optical methods and is proportional to the amount of hormone in the well if there are excess antibodies in the well.

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6
Q

How does a radioimmunoassay work?

A

Natural hormone in the assay fluid and the radioactive standard hormone compete for binding sites of the antibody
• Process of competing = quantity of each of 2 hormones (natural and radioactive) that binds is proportional to is concentration in the assay fluid
• After equilibrium reached, Antibody-hormone complex is separated and the radioactive hormone bound to it complex is measured (measuring radioactivity)
○ If large amount of radioactive hormone bound to antibody = Only small amount of natural hormone to compete
○ If only small amount of radioactive hormone bound = Large amount of natural hormone present

Compared to standard curve for the assay

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7
Q

Name 6 hormones from in the hypothalamus.

A
  1. Thyrotropin-releasing hormone (TRH) = Stimulates secretion of TSH and prolactin
  2. Corticotropin-releasing hormone (CRH) = Release of ACTH
  3. Growth Hormone Releasing Hormone (GHRH) = Release of growth hormone
  4. Growth Hormone Inhibitory Hormone (somatostatin) = Inhibits release of growth hormone
  5. Gonadotropin-Releasing Hormone (GnRH) = Release of LH and FSH
  6. Dopamin or prolactin inhibiting factor (PIF) = Inhibits release of prolactin
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8
Q

Name 6 hormones from the anterior pituitary gland.

A
  1. Growth Hormone: Stimulates protein sysnthesis and overall growth of most cells and tissue
  2. TSH: Stimulates synthesis and secretion of thyroid hormones (thyroxine, triiodothyronine)
  3. ACTH: Stimulates synthesis and secretion of adrenocortical hormones (cortisol, androgens, aldosterone)
  4. Prolactin: Promotes development of breasts adn secretion of milk
  5. FSH: Causes growth of follicles in ovaries and sperm maturation in Sertoli cells of testes
  6. LH: Stimulates testosterone synthesis from Leydig cells of testes; stimulates ovulation, formation of corpus luteum, estrogen and progresterone synthesis in ovaries
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9
Q

Name 2 hormones from the posterior pituitary.

A
  1. Antidiuretic hormone (ADH - Vasopressin) = Increases water reabsoprtion by kidneys and causes vasoconstriction and increased blood pressure
  2. Oxytocin: Stimulates milk ejection from breasts and urterine contractions
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10
Q

Name 2 hormones from the thyroid gland.

A
  1. Thyroxine (T4) and triiodothyronine (T3) = Increased rates of chemical rxn in most cells = Increasing body metabolic rate
  2. Calcitonin: Promotes deposition of Ca in bone and decreases extracellular fluid Ca ion concentration
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11
Q

Name 2 hormones from the adrenal cortex.

A
  1. Cortisol: Multiple metabolic functions - controlling metabloism of proteins, carbs, fats, anti-inflammatory effects
  2. Aldosterone: Increased renal Na reabsorption, K secretion, and H+ secretion
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12
Q

Name 2 hormones from the adrenal medulla.

A

Norepinephrine and epinephrine = Sympathetic stimulation

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13
Q

Name 2 hormones from the pancreas.

A
  1. Insulin (B cells) = Promotes glucose entry in many cells, thus controls carb metabolism
  2. Glucagon (Alpha cells) = Increased synthesis and release of glucose from the liver into body fluids
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14
Q

Name 1 hormone from the parathyroid gland.

A

PTH = Controls serum Ca concentrations by increasing Ca absorption by the gut and kidneys and release Ca from bone

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15
Q

Name 1 hormone from the testes.

A

Testosterone = Promotes development of male repro system and male secondary sex characteristics

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16
Q

Name 2 hormones from the ovaries.

A
  1. Estrogen = Promotes growth and development of female repro system, beasts, and female secondary sex characteristics
  2. Progesterone = Stimulates secrection of ““uterine milk”” by uterine endometrial glands and promotes development of secretory apparatus of breasts
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17
Q

Name 3 hormones from the kidneys.

A
  1. Renin = Catalyzes conversion of angiotensinogen to angiotensin I (enzyme)
  2. 1,25-dihydroxycholecalciferol = Increases intestinal absorption of Ca and bone mineralization
  3. Erythropoietin = Increased RBC production
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18
Q

Name 1 hormone from the heart.

A
  1. Atrial natriuretic peptide (ANP) = Increases Na excretion by kidneys, reduced blood pressure
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19
Q

Name 1 hormone from the stomach.

A
  1. Gastrin = Stimulates HCL secretion by parietal cells
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20
Q

Name 2 hormones from small intestines.

A
  1. Secretin = Stimulates pancreatic acinar cells to release bicarbonate and water
  2. Cholecystokinin (CCK) = Stimulates GB contraction and release of pancreatic enzymes
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21
Q

Name 1 hormone from adipocytes.

A
  1. Leptin = Inhibits appetite, stimulates thermogensis
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22
Q

What are the 5 cell types in the anterior pituitary gland and what to they produce?

A
  1. Somatotropes (hGH)
  2. Corticotropes (ACTH)
  3. Thyrotropes (TSH)
  4. Gonadotropes (LH and FSH)
  5. Lactotropes (Prolactin)
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23
Q

What are the 2 hormones in the posterior pituitary and where are they synthesized?

A
  1. ADH
  2. Oxytocin
    Synthesized in hypothalamus and transported to posterior pituitary by axoplasm of neurons
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24
Q

What other names for anterior and posterior pituitary gland?

A 
Anterior  = Adenohypophysis
Posterior = Neurohypophysis
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25
Q

Which system controls secretion of the pituitary hormones?

A

The Hypothalamus (either by hormonal or nervous signals)

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26
Q

How does the hypothalamus control pituitary secretions?

A
  1. Hormonal Release (from nerves in hypothalamus released in the median eminence and travel via the hypothalamic-hypophysial portal vessels to the anterior pituitary) = TRH, CRH, GHRH, GRH, prolactin inhibitory hormone
  2. Nervous signal for the posterior pituitary
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27
Q

What are the 3 major meatbolic effects of growth hormone?

A
  1. Promotes protein deposition in tissue
  2. Enhances fat utilization (ketogenic)
  3. Decreased carbohydrate utilization (diabetogenic)
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28
Q

What controls growth hormone release?

A

GHRH (hypothalamus) is sensitive to blood glucose levels = release of cAMP, increased Ca2+ = GH vesicles released from anterior pituitary gland

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29
Q

What area of the hypothalamus is related to ADH?

A

When osmoreceptors in the hypothalamus sense an increase in ECF osmolality = Secretion of ADH from the supraoptic nuclei and it travels down to posterior pituitary via neurophysins (carrier proteins) to be released into the capillaries there

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30
Q

What part of the hypothalamus is responsible for oxytocin release?

A

Paraventricular nuclei and then the posterior pituitary

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31
Q

Are the hypothalamic hormones present in systemic circulation?

A

No! Due to the hypothalamic-pituitary portal vessels

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32
Q

What is the breakdown of thyroid hormone release from the thyroid?

A

93% thyroxine (T4) and 7% triiodothyronine (T3)

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33
Q

What form of thyroid hormone do the tissues use?

A

Almost all T4 is eventually converted to T3 in the tissue

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34
Q

Which form of thyroid hormone is most potent?

A

T3 is 4x as patient as T4

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35
Q

What controls thyroid hormone secretion?

A

TSH (secreted by anterior pituitary)

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36
Q

Which cells secrete calcitonin?

A

Parafollicular cells or C (clear) cells - located in the periphery of follicle and liw in the basal lamina, no exposure to the follicle

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37
Q

What is the major component of colloid in the thyroid gland?

A

Thyroglobulin (large glycoprotein that contains thyroid hormones)

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38
Q

In what form is iodine ingested?

A

Iodine ingested as iodides

About 20% taken up by thyroid gland and the rest rapidly excreted by kidneys

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39
Q

What transporter is responsible for uptake of iodide by the thyroid gland and how is this gradient established?

A

Sodium-Iodide Symporter (NIS) - Cotransports 1 iodide with 1 Na ions across basolateral membrane (energy from Na/K ATPase in this membrane)

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40
Q

What is iodide trapping in the thyroid gland?

A

Iodide concentrations in cells via iodide pump (NIS) = 30x concentration of iodide in thyroid > blood)
This NIS pump is controlled by [TSH]

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41
Q

How is iodide pumped across apical membrane into follicle?

A

By chloride-iodide pump countertransporter = PENDRIN

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42
Q

Where is thyroglobulin made and secreted?

A

Thyroglobulin (contains about 70 tyrosine AA) - Synthesized in follicular cells and secreted into colloid

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43
Q

What combined with iodide to make the thyroid hormones in the follicle?

A

Tyrosine combine with iodine to form thyroid hormones (hormones WITHIN thyroglobulin and remain in colloid)

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44
Q

What is the two major steps once the iodine is within the follicle of the thyroid gland?

A
  1. Oxidation: Iodide to Iodine (so that it can combine with tyrosine) - catalyzes by thyroid peroxidase in the apical membrane = H2O2
  2. Organification: Binding of iodine with tyrosine residues on thyroglobulin - Catalyzed by thyroid peroxidase in the apical membrane
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45
Q

Describe the 4 major combinations of thyroid hormones.

A
  1. Thyroglobulin + iodine → MIT (monoiodotyrosine)
  2. MIT + iodine → DIT (diiodotyrosine)
  3. Coupling of DIT + DIT → T4
  4. MIT + DIT → T3, or occasionally reverse T3
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46
Q

After synthesis how many thyroid hormones are on the thyroglobulin?

A

About 30 T4 and few T3 (but enough thyroid hormone for months!)

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47
Q

How are the thyroid hormones secreted from the thyroid colloid?

A

Colloid globules pinocytosed (pseudopods from apical surface of thyroid cell) → taken into follicular cell fuse with lysosomes → proteolysis of thyroglobulin → diffusion through base of thyroid cells → release of T3, T4, RT3 into blood

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48
Q

How much MIT and DIT is released from thyroglobulin?

A

About of 75% iodinated tyrosine in thyroglobulin was still MIT and DIT; during digestion, the iodine from these molecules is cleaved by deiodinase enzyme → iodine recycles within the gland

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49
Q

What happens to T4 and T3 once it gets into the blood?

A

It is immediately bound to proteins (>99%) = (thyroxine-binding globulin&raquo_space; thyroxine-binding prealbumin, albumin)
Changes in the TBG DO NOT influence free thyroid hormone concentration

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50
Q

What is the active form of thyroid hormone that is used by the cells and how does it get converted to this?

A

T3 is the form of thyroid hormone used by cells. Therefore T4 (major form of thyroid hormone in blood) is converted to T3 by iodinase in the cells.

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51
Q

Once T3 is in the cell, how does it work?

A
  1. Binds to heterodimer of thyroid hormone receptor + retinoid X receptor that is in close proximity to DNA (in particular thyroid hormone response elements in the DNA)
  2. Results in increased transcriptions = increased function (cellular metabolism)
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52
Q

Are there nongenomic effects of thyroid hormones?

A

YES!
These occur within mins in the pituitary, heart, and adipose
Regulate ion channels and phosphorylation (cAMP, PKA) - thought to act in the plasma membrane, cytosol, mitochondria

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53
Q

What controls thyroid hormone secretion from the thyroid gland?

A
  1. TRH released from hypothalamus into the hypothalamic-pituitary portal system
  2. TSH (thyrotropin) released from anterior pituitary into systemic circulation
  3. TSH binds to TSH receptors on basolateral aspect of thyroid follicular cells (acts via cAMP - PKA - phosphorylation)
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54
Q

Name 5 actions of TSH on thyroid follicular cells, what is the most important mechanism?

A 
MOST IMPORTANT = Increased proteolysis of stored thyroglobulin
Increased NIS (iodide pump) = Increased iodide trapping
Increased iodination of tyrosine, increased coupling of thyroid hormone
Increased size of thyroid cells/gland = hypertrophy of thyroid gland (increased # thyroid cells)
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55
Q

Name the major negative feedback for thyroid hormone secretion.

A

High levels of T3 and T4 result in negative inhibition of TSH secretion from the anterior pituitary

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56
Q

What is the MOA for methimazole?

A

Prevents formation of thyroid hormone
1. Blocks perioxidase (on apical membrane) needed for iodination of tyrosine
2. Partially blocking coupling of 2 iodinated tyrosines to form T3 and T4
Results in increased TSH

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57
Q

What is Grave’s disease in humans?

A

Autoimmune dz where antibodies (thyroid stimulating Igs) form against TSH receptors in thyroid gland
Bind to and stimulate TSH receptors = Leading to hyperthyroidism

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58
Q

How does a goiter form?

A

insufficient dietary iodide (not enough iodine in soil) → thyroid gland cannot produce T4 or T3 → TSH stimulated → increased secretion of thyroglobulin into colloid → thyroid gland grows massively but lack of negative feedback on TSH since no T4/T3
o Can also be caused by abnormalities of enzyme system that forms thyroid hormones (deficient iodide trapping, deficient peroxidase, deficient DIT coupling, of deficiency of deiodinase enzymes for recycling iodine)

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59
Q

What is myxedema in hypothyroidism?

A

Increased quantities of hyaluronic acid and chrondroitin sulfate binding with proteins to form excess tissue gel in interstitial spaces

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60
Q

What is cretinism?

A

Hypothyroidism = Growth failure and mental retardation in humans
““Cretins”

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61
Q

How is the problem solved since the thyroid gland is secreting the less active form of thyroid hormone, T4?

A

Solved by target tissues which convert T4 into T3 using an iodinase

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62
Q

Does reverse T3 have any biological activity?

A

No

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63
Q

Name 3 unusual features of thyroid hormone synthesis.

A
  1. Thyroid hormone contain a large amount of iodine, which must be adequately supplied by diet
  2. Synthesis of thyroid hormone is partially intracellular and partially extracellular, with completed hormone stored in the extracellular follicular lumen until needed
  3. T4 is the major secretory product of the thyroid gland, but it is NOT the most active form of thyroid hormone
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64
Q

What does the adrenal medulla secrete?

A

Catecholamines (epi and norepi) = Extension of SNS

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65
Q

What are the three parts of the adrenal cortex?

A
  1. Zone Glomerulosa = Mineralcorticoids - Aldosterone
  2. Zona Fasciculata = Cortisol (some androgens)
  3. Zona Reticularis = Androgens (DHEA, Anrostenedione) (some cortisol)
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66
Q

What layers of the adrenal cortex undergo hypertrophy when stimulated by ACTH?

A

Zone Fasciculata and Reticularis

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67
Q

What type of compounds are the adrenocortical hormones?

A

Steroid compounds

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68
Q

What are all adrenocortical hormones synthesized from?

A

Cholesterol

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69
Q

In what parts of the cells does synthesis of adrenocortical hormones occur?

A

Mitochondria and ER

70
Q

How is cortisol transported in the blood?

A

Mainly protein bound to cortisol binding globulin (transcortin)

71
Q

How is cholesterol transported in the adrenocortical cells for synthesis of adrenocortical hormones?

A
  • LDLs attach to receptors in coated pits on adrenocortical cell membranes → endocytosis → vesicles fuse with lysosomes → release cholesterol
  • Transport of cholesterol into adrenal cells is regulated by feedback mechanisms including ACTH
72
Q

Once cholesterol is in the mirochondria what is the rate liming step in synthesis of adrenocortical hormones?

A

Cholesterol → Pregnenolone (Enzyme = Cholesterol desmolase)

73
Q

What controls the rate limiting step of adrenocortical hormone synthesis?

A

Enzyme = Cholesterol desmolase (Cholesterol → Pregnenolone) = Controlled by ACTH (fasciculata) and Angiotensin II (glomerulosa)

74
Q

What are the main factors that control aldosterone secretion?

A
  1. Increased K+ concentration = Increased aldosterone

2. Increased activity of RAAS and angiotensin II = Increased aldosterone

75
Q

Name the 3 sites of actions of aldosterone?

A
  1. Principal cells of the collecting ducts
  2. Colon
  3. Sweat and salivary glands
76
Q

What is the main role of aldosterone?

A

Renal tubular resorption of Na+ (leading to water resorption) and secretion of K+

77
Q

What are the main actions of aldosterone on principal cells of the collecting ducts?

A
  1. Aldosterone moves into the cytoplasma and binds to MR (mineralocorticoid receptor)
  2. This activated MR moves the nucleus and binds to specific DNA segments that result in an increase in mRNA
  3. Proteins are made to results in Na/K ATPase (basolateral) and Na and K channels (apical)
78
Q

What 2 main changes occur when aldosterone is in excess?

A
  1. Loss of K+ in urine = Hypokalemia

2. Secretion H+ in exchange for Na+ (intercalcated cells) = Metabolic alkalosis

79
Q

What is aldosterone escape?

A

When increased Na+ and water resorption → increased interstitial fluid volume → hypertension → pressure antriuresis/diuresis → returns to normal Na and water excretion

80
Q

How does cortisol affect carbohydrate metabolism?

A
  1. Increases gluconeogensis = AA from muscle (BAD!)
  2. Decreased glucose utilization by cells
  3. Hyperglycemia (decreased tissue insulin sensitivity)
81
Q

How does cortisol affect protein metabolism?

A
  1. Decreased cellular protein stores → Decreased in protein synthesis and increase in protein catabolism
  2. Increased liver proteins and plasma proteins → increased delivery of AA to liver
82
Q

How does cortisol affect fat metabolism?

A

Increased mobilization of FAAs from adiocytes

83
Q

How does cortisol affect anti-inflammatory?

A
  1. Lysosomal stabilization
  2. Decreased migration and phagocytosis in WBCs
  3. Decreased lymphocyte (T cell) reproduction
  4. Decreased fever = Decreased IL-1
84
Q

How does cortisol inpart its actions?

A

Mostly genomic actions
Cortisol (cytoplasmic) → Binds to cortisol receptor → Complex to nucleus → Interacts with glucocorticoid response elements on DNA → Change in transcription (mRNA) → Proteins

85
Q

What is the preprohormone that is secreted from the anterior pituitary?

A

POMC (proopiomelanocortin)

86
Q

What occurs when ACTH gets to the adrenocortical cells?

A

ACTH binds to receptor on the plasma membrane that interects with adenyl cyclase → increased cAMP → Protein kinase A → interacts with cholesterol desmolase (RATE LIMITING RATE STEP) - Converts cholesterol to pregnenolone to make the adrenocortical hormones

87
Q

What are the 3 classes or steroids hormones that the adrenal cortex secretes?

A
  1. Glucocorticoids
  2. Mineralocorticoids
  3. Androgens
88
Q

Name 2 enzymes that are shared in all zones of the adrenal cortex.

A
  1. Cholesterol Desmolase

2. 3b - Hydroxysteroid dehydrogenase

89
Q

What enzyme is unique to the zona glomeruloma?

A

Aldosterone synthase

90
Q

What is the final step in making cortisol in the zona fasciculata?

A

11-Deoxycortisol → Cortisol (Enzyme = 11,b Hydroxylase)

91
Q

Which mineralocorticoid has some glucocorticoid activity?

A

Corticosterone

92
Q

When can the zone glomerulosa not make cortisol?

A

It does not have 17 a Hydroxylase to convert to the needed intermediates! Otherwise it has all the enzymes required!

93
Q

Which area of the adrenal cortex is under the control of ACTH and RAAS?

A

Zona glomerulosa (ACTH in the first, rate limiting step only = “tonic effect only”), then the RAAS

94
Q

When is cortisol at the highest levels?

A

In the AM (diurnal) and pulsatile secretion

95
Q

The affinity of cortisol t mineralocorticoid receptors is high, how does the kidney only respond to aldosterone then?

A

The kidney has 11b - Hydroxysteroid dehydrogenase that converts cortisol to cortisone which has a lower affinity for mineralocorticoid receptors = Thus the cortisol is effectively inactivated in mineralocorticoid target tissues

96
Q

How does the kidney “see” levels of aldosterone compared to cortisol?

A

Due to 11b - Hydroxysteroid dehydrogenase that converts cortisol to cortisone which has a lower affinity for mineralocorticoid receptors

97
Q

What is the main unit of the endocrine pancreas?

A

Islets of Langerhans

98
Q

What are the 4 cells types of the islets of Langerhans and what do they each secrete?

A
  1. Beta Cells = Insulin (about 60-65%)
  2. Alpha Cells = Glucagon (about 20-25%)
  3. Delta CellS = Somatostatin (about 10%)
  4. PP Cells = Pancreatic Polypeptide and other peptides
99
Q

Which portion of the pancreas makes the digestive enzymes?

A

Pancreatic acini

100
Q

In which tissue is insulin NOT required for glucose uptake?

A

Brain (only glucose is used as an energy source)

101
Q

What is the primary controlled of insulin secretion?

A

Blood glucose that is sensed by the beta cells

102
Q

Name 4 other factors that control insulin secretion?

A
  1. Increased AA (insulin for uptake into cells)
  2. GI hormones (gastrin, secretin, CCK, gastric inhibitory hormone) = Anticipatory increase in insulin
  3. Cortisol and growth hormone (antagonizes effects on insulin on glucose uptake = increased BG) = Beta Cell Exhaustion
  4. PNS (Beta-adrenergic stimulation) - NOTE (inhibited by SNS - alpha-adrenergic)
103
Q

Which specific transporter moves glucose from blood into Beta cells by facilitated diffusion?

A

GLUT 2 = Transport of glucose into Beta Cell

104
Q

Name the 8 steps in secretion of insulin by the Beta Cells.

A
  1. Glucose transported into Beta Cell by GLUT 2 receptors (facilitated diffusion)
  2. Glucose phospharylates to glucose-6-phosphate (glucokinase)
  3. Glucose-6-phospahte oxidized to form ATP
  4. When ATP increased the ATP sensitive K+ channels close = Depolarization of cell
  5. Depolarization of cell membrane
  6. Depolarization opens voltage-sensitive Ca2+ channels
  7. Ca 2+ flows into Beta cell (down electrochemical gradient) = Increased intracellular Ca2+
  8. Increased intracellular Ca2+ causes insulin secretion (exocyotsis of insulin containing secretory granules)
105
Q

Why is oral glucose MORE effective than giving IV dextrose to rise the blood glucose level?

A

Oral glucose stimulates the secretion of glucose-dependent insulinotrophic peptide (GIP) - GI hormone that has independent stimulatory effest on insulin secretion (adding to direct effect of glucose on the Beta cells)
IV glucose does NOT cause the secretion of GIP = thus it only acts directly

106
Q

Describe the structure of the insulin receptor on target tissue.

A

Insulin receptor = Tetramer (2 a subunits and 2 b subunits) - which have tyrosine kinase acitvity

107
Q

Name the 5 steps of activation of target insulin receptors.

A
  1. Insulin binds to a subunits (extracellular) that result in a confirmational change
  2. Activates 2 b subunits (transmembrane)
  3. Results in autophosphorylation = Tyrosine kinase
  4. Phosphorylation/activation = Insulin Receptor Substrates (IRS)
  5. Increased cellular permeability to glucose (also K+, phosphate, and AA), also effects on gene transcription
108
Q

What happens to the insulin receptor once it is activate?

A

Once the insulin receptor is activated the insulin-receptor complex is internalized (endocytosis) = Insulin regulates its own down regulation of its receptor (decreased insulin sensitivity)

109
Q

What are 3 things that insulin ensures?

A

Excess nutrients

  1. Stores as glycogen in liver
  2. Fat in adipose tissue
  3. Protein in muscles
110
Q

What receptor is on target cells that insulin can increase the glucose transport?

A

GLUT 4 transporters

111
Q

What are the 3 ways that insulin decreases blood glucose?

A
  1. Increases glucose transport into target cells (muscle and adipose) by directing insertion of GLUT 4 transporters into cell membrane
  2. Insulin promotes formation of glycogen from glucose in liver (and muscle) = Inhibits glycogenolysis
  3. Insulin inhibits gluconeogenesis (synthesis of new glucose) - Increasing production of fructose 2,6-bisphosphate = Increases phosphofructokinase activity (substrates directly away from formation of glucose)
112
Q

What effect does insulin have on fat metabolism?

A

Insulin decreases blood fatty acid and ketoacid concentration
Stimulates fat deposition and inhibits lipolysis

113
Q

What effect does insulin have on amino acids?

A

Insulin decreased amino acids in blood = Anabolic effect!!

114
Q

What is the overall effect of insulin on: glucose, fatty acids, ketoacids, and amino acids?

A

Insulin will decrease all these levels in the blood (increased glucose uptake by cells, increased glycogen formation, decreased glycogenolysis, decreased gluconeogensis, increased protein synthesis, increased fat deposition, decreased lipolysis, increased K+ uptake into cells)

115
Q

What is the hormone of starvation and why?

A

Glucagon

Promotes that mobilization and utilization of metabolic fuels

116
Q

What stimulates alpha cells to secrete glucagon?

A

Decreased in blood glucose (major player)
Ingestion of proteins (esp arginine and alanine)
CKC (secreted when protein or fat ingested)
Sympathetic alpha-adrenergic receptors

117
Q

What effects does glucoagon have on: glucose, fatty acids, ketoacids?

A

It will increase all of them in the blood (increased glycogenolysis, increased gluconeogensis, increased lipolysis, increased ketoacid formation)

118
Q

How does glucagon increased blood glucose?

A
  1. Stimulates glycogenolysis and inhibits glycogen formation
  2. Increased gluconeogenesis by decreased production of fructose 2,6-bisphosphate (decreased phosphofructokinase activity) - Substrates to form glucose (AA are utilized for gluconeogensis)
119
Q

How does gucagon increased fatty acids and ketoacids?

A 
Increased lipolysis and inhibits fatty acid synthesis
So ketoacids (Beta-hydrozybutyric acid and acetoacetic acid) are made by fatty acids
120
Q

What is the primary role of pancreatic somatostatin?

A

Inhibits glucagon and insulin secretion via paracrine actions of alpha and beta cells

121
Q

When is pancreatic somatostatin secreted?

A

In response to a meal - though to modulate or limit the response of insulin and glucoagon to ingestion of food

122
Q

What does Ca2+ complex with in the blood?

A

Phosphate, citrate, bicarb, lactate

123
Q

What percentage of Ca in the blood is ionized?

A

About 50%

124
Q

How does Ca2+ affect neurons?

A

If hypoCa2+ = increased Na+ in neurons = AP easier = tetanic

If HyperCa2+ = Neuron depression

125
Q

What is the store of Ca2+ in the bone that can be rapidly absorbed to buffer the blood concentrations of Ca2+?

A

CaHPO4

126
Q

What are the 3 major steps in bone resorption?

A
  1. PTH binds to osteoblasts
  2. Osteoblasts release RANK-L (OPGL)
  3. OPGL activates preosteoclasts
  4. Osteoclasts release proleolytic enzymes and acids (lactic and citric)
127
Q

What is the substance in the bone that allows for bone salts of Ca2+ and phosphorus?

A

Hydrozyapatite

128
Q

What are the 2 main locations of Ca2+ excretion in the kidney?

A 
90% = Proximal tubule (follows Na)
10% = Distal tubule (under control of PTH)
129
Q

What vitamin is required for PTH to result in bone resorption?

A

Vitmain D

130
Q

What are the main effects of vitamin D?

A
  1. Intestinal: Increased absorption of Ca2+ (effects on brush border), little increased in Phosphorus absorption
  2. Kidney: Decreased excretion of Ca2+ and phosphorus
  3. Bone: Promotes absoprtion when PTH is present
131
Q

What is the major effect of calcitriol?

A

Increases iCa and Phosphate

  1. Intestinal: Enhance GI absorption of Ca and phosphorus
  2. Bone: Enhance osteoclastic resorption of Ca and phosphate from bone
  3. Kidney: Enhance reabsorption of Ca and phosphorus
  4. Parathyroid gland: Suppress PTH release
132
Q

What is the chemical name for calcitriol?

A

1,25-dihydrozycholecalciferol

133
Q

How is calcitriol made?

A

Cholecalciferol (Vitamin D3) from diet → 25, hydrozycholecalciferol (Calcidiol, converted in liver) → 1,25,-dihydroxycholecalciferol (calcitrol, converted in kidney) until influence of PTH

134
Q

What controls conversion of calcidiol to calcitriol in kidney?

A

Under the influence of PTH

135
Q

Which cells of the parathyroid gland secrete PTH?

A

Chief cells

136
Q

What are the major effects of PTH on Ca2+ and phosphorus?

A

Increased Ca2+ = increased bone resorption and decreased renal excretion
Decreased phosphorus = decreased renal absorption (MAJOR effect) - very little bone effect

137
Q

What is the primary function of PTH?

A

Elevate serum iCa and lower PO4

138
Q

What are the 3 major effects of PTH?

A
  1. Stimulates bone resorption of calcium and phosphate salts (promotes formation of more osteroclasts, inhibits osteoblasts, osteoblasts PUMP Ca2+ into ECF with help of Vit D)
  2. Renal resorption of iCa and PO4 excretion (1a - hydroxylase in kidney) coverts calcidiol to calcitriol = renal vitamin D activation
  3. Stimulates intestinal absorption of iCa and PO4 (Calcitriol (made via stimulation by PTH) stimulates formation of Ca binding proteins in SI epithelium to increase rate of Ca absorption
139
Q

Where is vitamin D activated?

A

Kidneys: 1a - hydroxylase converts calcidiol to calcitriol

140
Q

Which cells secrete calcitonin?

A

Parafollicular cells or C (clear) cells

141
Q

What is the overall action of calcitonin?

A

Opposes effects of PTH = Decreased iCa

142
Q

What are the major effects of calcitonin?

A

Overall decrease in iCa and decreased in PO4

  1. Bone: Inhibits osteoclasts = decreased bone resorption
  2. Kidney: Inhibits iCa resorption and PO4 resorption
  3. Intestine: Inhibits iCa absoprtion
143
Q

What hormone can increase calcitonin after a meal?

A

Increased gastrin leads to secretion of calcitonin

144
Q

What electrolyte is needed for PTH activation?

A

Magnesium

145
Q

Which hormone opposes the actions of PTH?

A

Calcitonin

146
Q

What is the biologically active form of calcium?

A

iCa (about 50% of total calcium)

147
Q

Explain that the changes that are seem with iCa with acid-base changes.

A

When acidemia = More H+ that bind to albumin, meaning that less Ca2+ can bind → Increased iCa
When alkalemia = Less H+ that bind to albumin, meaning that MORE Ca2+ can bind → Decreased iCa

148
Q

What are the 3 major organ systems that are involved with calcium homeostasis?

A
  1. Bone
  2. Kidney
  3. Intestines
149
Q

What are the 3 hormones that are involved with calcium homeostasis?

A
  1. PTH
  2. Calcitonin
  3. Vitamin D
150
Q

In general what needs to occur to ensure that Ca2+ is balanced?

A

The kidneys must excrete the same amount of Ca2+ that is absorbed from the GIT

151
Q

What is sensed by the chief cells in the parathyroid to result in PTH release?

A

Low iCa2+ levels = sensed by calcium-sensing receptors in parathyroid gland

152
Q

Which cell in the bone has receptors for PTH?

A

Osteoblasts (NOT the osteoclasts - these are stimulated indirectly)

153
Q

What mechanism occurs in the kidney that is critical for increasing iCa when PTH is present?

A

Phosphaturic action of PTH is critical because Phosphate that is resorbed from bone is excreted in the urine = otherwise this phosphate would complex with Ca2= in ECF and iCa would not change
THUS excreting phosphorus in urine ““allows”” plasma iCa to increase!!!

154
Q

What is the indirect effect of PTH?

A

PTH indirectly stimulates intestinal Ca2+ resorption via activation of Vitamin D (PTH stimulates renal 1a-hydroxylase)

155
Q

What are the effects of primary hyperparathyroidism on the following: PTH, calcitriol, bone, urine, [Ca2+], [Phosphorus]?

A

PTH: Increased!!!
Calcitriol: Increased (PTH effect on renal 1a-hydroxylase)
Bone: Increased resorption
Urine: Increased Ca2+ resorption and increased phosphaturia
[Ca2+]: Increased
[Phosphorus]: Decreased

156
Q

What is the primary effect with primary hyperparathyroidism?

A

Increased PTH

157
Q

What are the effects of secondary hyperparathyroidism on the following: PTH, calcitriol, bone, urine, [Ca2+], [Phosphorus]?

A

PTH: Increased (Secondary to hypocalcemia)
Calcitriol: Decreased!!!!
Bone: Osteinalacia (decreased calcitriol) and increased resorption (increased PTH)
Urine: Decreased phosphaturia (dt decreased GFR with CDK)
[Ca2+]: Decreased to normal (dt decreased calcitriol)
[Phosphorus]: Increased (dt decreased phosphaturia)

158
Q

What is the primary effects with secondary hyperparathyroidism?

A

Decreased calcitriol

If CKD = decreased phosphaturia

159
Q

What are the effects of hypoparathyroidism on the following: PTH, calcitriol, bone, urine, [Ca2+], [Phosphorus]?

A 
PTH:  Decreased!!!!
Calcitriol:  Decreased (decreased PTH effects on renal 1a-hydroxylase)
Bone:  Decreased resorption
Urine: Decreased phosphaturia 
[Ca2+]:  Decreased 
[Phosphorus]:  Increased
160
Q

What is the primary effects with hypoparathyroidism?

A

Decreased PTH

161
Q

What are the effects of hypercalcemia of malignacy on the following: PTH, calcitriol, bone, urine, [Ca2+], [Phosphorus]?

A 
PTHrp increased
PTH:  Decreased!!!!
Calcitriol:  Increased
Bone:  Increased resorption
Urine: Increased phosphaturia  and increased Ca2+ resorption
[Ca2+]:  Increased 
[Phosphorus]:  Decreased
162
Q

What is the major stimulus for secretion of calcitonin?

A

Increased Ca2+

163
Q

What is the overall result of calcitonin release?

A

Decreased iCa and decreased phosphate

164
Q

What is the immediate action of calcitonin?

A

Decreased bone resorption = Ca2+ deposition in bone

165
Q

In general what is the role of PTH?

A

PTH is to maintain plasma Ca2+ - actions coordinated to increased iCa2+ toward normal

166
Q

In general what is the role of Vitamin D?

A

Promote mineralization of new bone, actions are coordinated to increased BOTH Ca2+ and phosphate concentrations so that these elements can be deposited into the new bone

167
Q

What 3 factors result in increased activity of renal 1a-hydroxylase?

A
  1. Decreased [Ca2+]
  2. Increased PTH
  3. Decreased [phosphorus]
168
Q

Where is the major site/role of calcitriol?

A

Intestines!! Need to increase BOTH Ca2+ and PO4

169
Q

What is the effect of calcitriol on the intestines?

A

Increased absorption of Ca2+ and PO4

170
Q

What is the effect of calcitriol on the kidney?

A

Increased resorption of Ca2+ and PO4

171
Q

What is the effect of calcitriol on the bone?

A

Increased osteoclast activity = Increased Ca2+ and PO4
Seems weird since the major action of calcitriol is to ““make new bone””, BUT needed for new bone formation = bone remodeling

Endocrine (4 decks)

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