Endocrine - Anatomy/physiology

Question 1

Endocrine

What are 2 parts of fetal adrenal gland?

Answer 1

Inner active fetal zone and outer dormant/inactive adult zone

Question 2

Endocrine

What are 2 parts of adult adrenal gland?

Answer 2

Inner adrenal medulla and outer adrenal cortex

Question 3

Endocrine

Part of adrenal gland immature when baby born? When functional?

Answer 3

Zona reticularis of adrenal cortex is immature at birth and not fully developed until 3 years after birth.

Question 4

Endocrine

Mechanism by which fetus produces androgens in utero?

Answer 4

Fetus requires PLACENTAL 3β-hydroxysteroid dehydrogenase enzyme to convert pregnenolone to progesterone for synthesis of androgens

Question 5

Endocrine

What are 3 parts of adrenal cortex?

Answer 5

Zona glomerulosa, zona fasciculata, zona reticularis (“GFR”)

Question 6

Endocrine

Zona glomerulosa secretes?Zona fasciculata secretes?Zona reticularis secretes?

Answer 6

Glomerulosa –> Mineralocorticoids (aldosterone)Fasciculata –> Glucocorticoids (cortisol)Reticularis –> Androgens (androstenedione)

Question 7

Endocrine

Embryologic origin:Adrenal cortex?Adrenal medulla?

Answer 7

Cortex - MesodermMedulla - Neuroectoderm (neural crest cells)

Question 8

Endocrine

Adrenal medulla is composed of what cell type? Secretory product?

Answer 8

Chromaffin cells - Secrete catecholamines (epinephrine, NE)Chromaffin cells are modified postganglionic sympathetic neurons that receive sympathetic input (neuroendocrine cells).

Question 9

Endocrine

Adrenal tumors:MCC in adults?MCC in children?

Answer 9

Adults - PheochromocytomaChildren - Neuroblastoma

Question 10

Endocrine

Venous drainage:Left adrenal gland?Right adrenal gland?

Answer 10

Left adrenal gland –> Left adrenal vein –> Left renal vein –> IVCRight adrenal gland –> Right adrenal vein –> IVCNote - Same as left/right gonadal (e.g., testicular) veins

Question 11

Endocrine

Sympathetic preganglionic neurons release [?], which activates [?] receptors on postganglionic neurons.These postganglionic neurons release [?] to activate [?] receptors on target tissues.What are 2 exceptions to this principle?

Answer 11

Sympathetic preganglionic neurons release ACh, which activates AChR receptors on postganglionic neurons.These postganglionic neurons release NE to activate ADRENERGIC receptors on target tissues.Exceptions:1) Postganglionic neurons that innervate sweat glands release ACh, not NE.2) Chromaffin cells of adrenal medulla - Innervated by preganglionic sympathetic nerons that release ACh and bind AChRs on chromaffin cell surface. However, these cells are MODIFIED postganglionic neurons. They release catecholamines (80% epi, 20% NE) directly into blood stream to activate adrenergic receptors in target tissues.

Question 12

Endocrine

Adrenal medulla releases catecholamines (epi, NE) that bind adrenergic receptors in what 4 locations in body to mediate acute stress response?

Answer 12

Heart, lungs, liver, and skeletal muscle

Question 13

Endocrine

Precursor of all steroid hormones synthesized in adrenal cortex?

Answer 13

Cholesterol

Question 14

Endocrine

What is 1st reaction in synthesis of all steroid hormones in adrenal cortex? Reaction catalyzed by what enzyme?

Answer 14

Cholesterol –> pregnenoloneReaction catalyzed by cholesterol desmolase

Question 15

Endocrine

What hormone stimulates cholesterol desmolase activity, thereby increasing production of adrenal cortex steroid hormones?

Answer 15

ACTH

Question 16

Endocrine

What drug inhibits cholesterol desmolase activity, thereby decreasing production of adrenal cortex steroid hormones?

Answer 16

Ketoconazole

Question 17

Endocrine

What are 2 fates of pregnenolone? What enzymes catalyze these reactions?

Answer 17

Mineralocorticoid pathway:Pregnenolone –> progesterone via 3β-hydroxysteroid dehydrogenaseGlucocorticoid pathway:Pregnenolone –> 17-hydroxypregnenolone via 17α-hydroxylase

Question 18

Endocrine

What are 2 fates of progesterone? What enzymes catalyze these reactions?

Answer 18

Mineralocorticoid pathway:Progesterone –> 11-deoxycorticosterone via 21β-hydroxylase*This reaction traps cholesterol metabolism in pathway that generates mineralocorticoidsGlucocorticoid pathway:Progesterone –> 17-hydroxyprogesterone via 17α-hydroxylase

Question 19

Endocrine

What is 1 fate of 11-deoxycorticosterone? What enzyme catalyzes this reaction?

Answer 19

11-deoxycorticosterone –> corticosterone via 11β-hydroxylase

Question 20

Endocrine

What is 1 fate of corticosterone? What enzyme catalyzes this reaction?

Answer 20

Corticosterone –> aldosterone via aldosterone synthase

Question 21

Endocrine

What hormone stimulates aldosterone synthase activity, thereby increasing production of aldosterone?

Answer 21

Angiotensin II

Question 22

Endocrine

What are 2 fates of 17-hydroxypregnenolone? What enzymes catalyze these reactions?

Answer 22

Glucocorticoid pathway:17-hydroxypregnenolone –> 17-hydroxyprogesterone via 3β-hydroxysteroid dehydrogenaseAndrogen pathway:17-hydroxypregnenolone –> dehydroepiandrosterone (DHEA) via 17,20-lyase

Question 23

Endocrine

What are 2 fates of 17-hydroxyprogesterone? What enzymes catalyze these reactions?

Answer 23

Glucocorticoid pathway: 17-hydroxyprogesterone –> 11-deoxycortisol via 21β-hydroxylase*This reaction traps cholesterol metabolism in pathway that generates glucocorticoidsAndrogen pathway:17-hydroxyprogesterone –> androstenedione via 17,20-lyase

Question 24

Endocrine

What is 1 fate of DHEA? What enzyme catalyzes this reaction?

Answer 24

DHEA –> androstenedione via 3β-hydroxysteroid dehydrogenase

Question 25

# Endocrine What are 2 fates of androstenedione? What enzymes catalyze these reactions?

Answer 25

Androstenedione --> estrone via aromatase; estrone --> estradiolAndrostenedione --> testosterone

Question 26

# Endocrine What are 2 fates of testosterone? What enzymes catalyze these reactions?

Answer 26

Testosterone --> estradiol via aromataseTestosterone --> dihydrotestosterone (DHT) via 5α-reductase

Question 27

# Endocrine Pituitary gland, also called [?], rests in [?], a depression in [?] bone.Pituitary gland is divided into what 2 parts?

Answer 27

Pituitary gland = hypophysisRests in sella turcica, a depression in sphenoid boneAnterior (adenohypophysis) and posterior (neurohypophysis) pituitary glands

Question 28

# Endocrine Relationship b/w anterior pituitary and hypothalamus?

Answer 28

Anterior pituitary is linked to hypothalamus via hypothalamic-hypophyseal portal systemBlood directly draining hypothalamus, which contains high concentrations of hypothalamic hormones, is delivered to anterior pituitary

Question 29

# Endocrine Relationship b/w posterior pituitary and hypothalamus?

Answer 29

Posterior pituitary hormones are synthesized in hypothalamusNerve cell bodies that synthesis posterior pituitary hormones are located in hypothalamus. Hormones are packaged in secretory granules and transported down axons to posterior pituitary for release into circulation.Posterior pituitary is collection of UNMYELINATED axons whose cell bodies originate in hypothalamus.

Question 30

# Endocrine Anterior pituitary:Another name?Embryologic origin?Hormones?

Answer 30

Anterior pituitary --> adenohypophysisOrigin --> UPGROWTH of oral ectoderm (Rathke's pouch)Hormones --> FLAT PiGFSH, LH, ATCH, TSH, prolactin, GH

Question 31

# Endocrine Anterior pituitary includes 5 cell types. What hormone(s) does each cell type produce?GonadotrophsCorticotrophsThyrotrophsLactotrophsSomatotrophs

Answer 31

Gonadotrophs --> FSH, LHCorticotrophs --> ACTHThyrotrophs --> TSHLactotrophs --> ProlactinSomatotrophs --> GH = somatotropin

Question 32

# Endocrine Anterior pituitary includes 3 categories of hormones. What hormone(s) is/are included in each?Glycoprotein hormonesCorticolipotropinsSomatomammotropins

Answer 32

Glycoprotein hormones --> FSH, LH, TSHCorticolipotropins --> ACTHSomatomammotropins --> GH, prolactin

Question 33

# Endocrine Chromophils are anterior pituitary cells that contain granules that react with acidophilic/basophilic stains.Acidophilic cells contain granules composed of what hormones? These cells stain what color?

Answer 33

PiG hormones --> GH, prolactinAcidophils = red/pink staining

Question 34

# Endocrine Chromophils are anterior pituitary cells that contain granules that react with acidophilic/basophilic stains.Basophilic cells contain granules composed of what hormones? These cells stain what color?Basophils also stain positive for what marker?

Answer 34

FLAT hormones --> FSH, LH, ACTH, TSHBasophils = blue/purple stainingPAS+ "B-FLAT"

Question 35

# Endocrine Chromophobes?

Answer 35

Anterior pituitary cells that lack granules and do not react with acidophilic/basophilic stains.Chromophobes include stromal cells and DEGRANULATED chromophils

Question 36

# Endocrine Posterior pituitary:Another name?Embryologic origin?Hormones?Composition?

Answer 36

Posterior pituitary --> neurohypophysisOrigin --> DOWNGROWTH of neuroectodermHormones --> ADH (vasopressin) and oxytocinComposition --> unmyelinated axons that extend from cell bodies in hypothalamus

Question 37

# Endocrine ADH pro-hormones:Synthesized in neuron cell bodies in which hypothalamic nuclei?Pro-hormones contain what 2 products?Pro-hormone --> Hormone?

Answer 37

Neuron cell bodies in hypothalamic SUPRAOPTIC NUCLEI synthesize ADH pro-hormones that contain ADH and NEUROPHYSIN II.ADH pro-hormones are packaged into secretory vesicles and transported to nerve terminals in PARS NERVOSA part of posterior pituitary.ADH pro-hormones are processed in secretory granules during transport --> Cleavage into ADH and neurophysin II.ADH has 2 names --> Antidiuretic hormone and vasopression --> NEUROPHYSIN II

Question 38

# Endocrine Oxytocin pro-hormones:Synthesized in neuron cell bodies in which hypothalamic nuclei?Pro-hormones contain what 2 products?Pro-hormone --> Hormone?

Answer 38

Neuron cell bodies in hypothalamic PARAVENTRICULAR NUCLEI synthesize oxytocin pro-hormones that contain OXYTOCIN and NEUROPHYSIN I.Oxytocin pro-hormones are packaged into secretory vesicles and transported to nerve terminals in PARS NERVOSA part of posterior pituitary.Oxytocin pro-hormones are processed in secretory granules during transport --> Cleavage into oxytocin and neurophysin I.

Question 39

# Endocrine Mechanism by which posterior pituitary hormones are released into bloodstream?

Answer 39

Action potential depolarizes nerve terminal causing neurosecretory vesicles to fuse w/ plasma membrane --> Releases ADH or oxytocin into perivascular space of highly fenestrated capillaries --> Entrance to systemic circulation

Question 40

# Endocrine Hypothalamus hormone:Corticotropin releasing hormone (CRH)Regulatory mechanism:Stimulate/inhibit?Anterior pituitary hormone(s):?

Answer 40

CRH stimulates ACTH, MSH, and β-endorphinMSH = Melanocyte stimulating hormone

Question 41

# Endocrine Hypothalamus hormone:Growth hormone releasing hormone (GHRH)Regulatory mechanism:Stimulate/inhibit?Anterior pituitary hormone(s):?

Answer 41

GHRH stimulates GH

Question 42

# Endocrine Hypothalamus hormone:Gonadotropin releasing hormone (GnRH)Regulatory mechanism:Stimulate/inhibit?Anterior pituitary hormone(s):?

Answer 42

GnRH stimulates FSH, LH

Question 43

# Endocrine Hypothalamus hormone:Thyroid releasing hormone (TRH)Regulatory mechanism:Stimulate/inhibit?Anterior pituitary hormone(s):?

Answer 43

TRH stimulates TSH and prolactin

Question 44

# Endocrine Hypothalamus hormone:Dopamine - Another name?Regulatory mechanism:Stimulate/inhibit?Anterior pituitary hormone(s):?

Answer 44

Dopamine inhibits prolactin Dopamine --> prolactin inhibiting factor (PIF)

Question 45

# Endocrine Hypothalamus hormone:Somatostatin - Another name?Regulatory mechanism:Stimulate/inhibit?Anterior pituitary hormone(s):?

Answer 45

Somatostatin inhibits GH and TSHSomatostatin --> somatotropin release inhibiting factor (SRIF)GH --> somatotropin Recall that thyroid hormones ("TSH") act synergistically with GH for bone development as way to remember somatostatin inhibits both GH and TSH.

Question 46

# Endocrine What are 3 glycoprotein hormones synthesized by pituitary gland?Glycoprotein hormones contain what 2 subunits?Which subunit is identical in all glycoprotein hormones? Which determines hormone specificity?

Answer 46

Glycoprotein hormones --> FSH, LH, TSHGlycoprotein hormones contain α- and β-subunits. --> α-subunits are identical in all glycoprotein hormones--> β-subunits determine hormone specificity

Question 47

# Endocrine What non-pituitary glycoprotein hormone shares homology with FSH, LH, and TSH?

Answer 47

hCG has identical α-subunit as glycoprotein hormones synthesized in pituitary gland

Question 48

# Endocrine What are 2 functions of TSH on thyroid gland?

Answer 48

TSH acts on follicular cells of thyroid gland to:1) Regulate growth of gland (hypertrophy/hyperplasia)2) Secrete thyroid hormones

Question 49

# Endocrine TSH binds TSH-receptors on follicular cells of thyroid and signals through what mechanism?

Answer 49

TSH activates Gs protein --> activates adenylyl cyclase --> produces cAMP 2nd messenger

Question 50

# Endocrine What are 3 thyroid hormones?Which thyroid hormone is most active?Thyroid gland produces predominantly which thyroid hormone?

Answer 50

T3, T4 (thyroxine), rT3 (inactive!)T3 is 4x more active than T4. rT3 is inactive.Thyroid gland produces predominantly T4.

Question 51

# Endocrine Negative feedback mechanism for TSH secretion?

Answer 51

Free T3 downregulates TRH receptors on thyrotrophs in anterior pituitary, thereby decreasing their sensitivity to TRH secreted by hypothalamusFree T3 induces INTERNALIZATION OF TRH RECEPTORS.

Question 52

# Endocrine Thyroid gland produces predominantly T4, yet free T3 provides negative feedback for TSH secretion - Explanation?

Answer 52

Anterior pituitary expresses 5-deiodinase enzyme that converts free T4 to free T3

Question 53

# Endocrine Thyroid stimulating immunoglobulins (TSI)?

Answer 53

Thyroid stimulating immunoglobulins, like TSH, bind and stimulate TSH receptors on thyroid gland --> Antibodies to TSH receptorGraves disease!

Question 54

# Endocrine Mechanism by which thyroid hormones act in target cells?

Answer 54

Thyroid hormones diffuse across membrane of target cells and bind to steroid receptors in NUCLEUS

Question 55

# Endocrine Thyroglobulin (TG)? Synthesized from what precursor?

Answer 55

Thyroglobulin is a glycoprotein synthesized by thyroid follicular epithelial cells. Serves as precursor for thyroid hormones.Synthesized from TYROSINE and packaged into secretory vesicles. Extruded across apical membrane into follicular lumen.

Question 56

# Endocrine Transporter located on basolateral aspect of follicular epithelial cells in thyroid gland? Function?

Answer 56

Na+/I- cotransporter that pumps both Na+ and I- into follicular epithelial cells --> Iodide trappingI- needed for thyroid hormone synthesisPolarity of thyroid follicular epithelial cell:Basolateral membrane faces blood, apical membrane faces follicular lumen

Question 57

# Endocrine What are 3 inhibitors of Na+/I- cotransporter on basolateral membrane of thyroid follicular epithelial cells?

Answer 57

Perchlorate, pertechnetate, and thiocyanateBlock iodide uptake and interfere with thyroid hormone synthesis

Question 58

# Endocrine Once transported into thyroid follicular epithelial cells, what is fate of I-?

Answer 58

I- is oxidized to I2 by thyroid peroxidase and subsequently transported across apical membrane into follicular lumen

Question 59

# Endocrine Once transported into follicular lumen, what is fate of I2?

Answer 59

I2 is enzymatically added to tyrosine residues on thyroglobulin (TG) by thyroid peroxidase to form monoiodotyrosine (MIT) and diiodotyrosine (DIT)"Organification of I2"

Question 60

# Endocrine Mechanism by which T3 and rT3 are synthesized?

Answer 60

Thyroid gland predominantly synthesizes T4T4 is converted to either T3 (4x more active than T4) or rT3 (inactive) in peripheral tissues by 5'-deiodinase enzyme

Question 61

# Endocrine Mechanism by which thyroid hormones are cleared by body?

Answer 61

Glucuronidation in liver

Question 62

# Endocrine How will pharmacologic treatment with exogenous T3 affect levels of following? Why?TRHTSHT3T4rT3

Answer 62

TRH --> T3 negatively feeds back on hypothalamus to decrease TRH synthesisTSH --> T3 negatively feeds back on hypothalamus to downregulate TSH synthesis and to cause internalization of TRH receptors (decreasing responsiveness to TRH)T3 --> Exogenous T3 will increase overall T3 levelsT4 --> T3 negative feedback on TRH/TSH will decrease thyroid gland secretion of thyroid hormones (predominantly T4), thereby causing decreased T4 levelsrT3 --> Decreased T4 levels means less T4 available to be converted to rT3 by 5'-deiodinase causing decreased rT3 levels

Question 63

# Endocrine Wolff-Chaikoff effect?

Answer 63

High I- levels temporarily inhibit thyroid peroxidase action of organification of I2 to MIT/DIT --> Temporarily inhibits synthesis of thyroid hormones

Question 64

# Endocrine S/p organification (addition of I2 to tyrosine residues on TG), how are thyroid hormones synthesized in follicular lumen?

Answer 64

Coupling reactions catalyzed by thyroid peroxidase:MIT + DIT --> T3DIT + DIT --> T4

Question 65

# Endocrine Thyroid peroxidase:Function in thyroid follicular epithelial cell?Function in follicular lumen?

Answer 65

Follicular epithelial cell --> Convert I- to I2 Follicular lumen --> Organification of I2 (addition to TG), coupling reactions

Question 66

# Endocrine Drug that inhibits both thyroid peroxidase and 5'-deiodinase?

Answer 66

Propylthiouracil (PTU)

Question 67

# Endocrine Drug that inhibits only thyroid peroxidase?

Answer 67

Methimazole

Question 68

# Endocrine Why does thyroid gland synthesize predominantly T4?

Answer 68

DIT + DIT coupling reaction that produces T4 proceeds at 10x greater rate than MIT + DIT coupling reaction that produces T3

Question 69

# Endocrine Colloid?

Answer 69

Colloid --> Thyroglobulin (TG) with bound T3, T4, MIT, and DIT stored in thyroid follicles

Question 70

# Endocrine Cellular mechanism by which thyroid hormones are released from gland in response to TSH stimulation?

Answer 70

TSH induces endocytosis of colloid (TG + T3/T4/MIT/DIT) from follicle lumen into follicular epithelial cellTG is then transported to basal membrane via microtubular transportTG fuses with lysosomal membrane and lysosomal proteases hydrolyze peptide bonds to release T3, T4, MIT, and DIT from TGT3 and T4 are transported across basal membrane into systemic circulation (bloodstream)MIT, DIT, and TG (tyrosine residues) are recycled

Question 71

# Endocrine Mechanism by which MIT and DIT are recycled?

Answer 71

MIT and DIT deiodinized by deiodinase enzyme to salvage I- and tyrosine residues

Question 72

# Endocrine Thyroid hormones:Carrier protein in blood?Physiologically active form?

Answer 72

Thyroxine-binding globulin (TBG) binds thyroid hormones in bloodstreamPhysiologically active form --> FREE T3 and T4Only SMALL amounts are actually unbound. TBG provides a large reservoir of circulating thyroid hormones that may be released and added to the pool of unbound, physiologically active form when needed.

Question 73

# Endocrine Thyroid levels in liver failure?

Answer 73

Liver failure --> Decreased synthesis of TBGDecreased levels of TBG --> Transient increase in unbound/free thyroid hormones (physiologically active) --> Free T3 provides negative feedback on anterior pituitary and inhibits thyroid hormone synthesis --> Decreased thyroid hormone levels

Question 74

# Endocrine Thyroid levels in pregnancy and OCP use?

Answer 74

High estrogen levels --> Inhibit hepatic breakdown of TBG --> Increased TBG levels --> Transient decrease in unbound/free thyroid hormones (more TBG available to bind free thyroid hormone)Decreased free T3 levels lowers negative feedback --> Activates thyroid hormone synthesisTotal T3 and T4 levels increase, but levels of unbound T3 and T4 remain same (b/c TBG levels increase)

Question 75

# Endocrine Functions of thyroid hormone?

Answer 75

4 B's --> Basal metabolic rate, B1 adrenergic receptor upregulation on heart, bone growth, and brain maturation

Question 76

# Endocrine Mechanism by which thyroid hormone increases basal metabolic rate?

Answer 76

Thyroid hormone increases activity of Na/K ATPase --> Increases O2 consumption --> Heat production --> Increases BMR, RR, and body temperature

Question 77

# Endocrine Mechanism by which thyroid hormone increases metabolism?

Answer 77

Thyroid hormone increases glucose absorption from GI tract and potentiates effects of other hormones (e.g., glucagon, GH) on gluconeogenesis, lipolysis, and proteolysisThyroid hormone induces synthesis of key metabolic enzymes

Question 78

# Endocrine Mechanism by which thyroid hormone increases cardiac output?

Answer 78

Thyroid hormone upregulates cardiac b1-adrenergic receptors that mediate effects of sympathetic nervous system to increase HR and contractility

Question 79

# Endocrine Mechanism by which thyroid hormone contributes to growth to adult stature?

Answer 79

Thyroid hormone works synergistically with GH to promote bone formation and to promote ossification and fusion of bone plates and bone maturation

Question 80

# Endocrine Hypothyroidism in perinatal period?

Answer 80

Decreased thyroid hormone levels --> Irreversible mental retardation (cretinism)Thyroid hormone essential for CNS maturation

Question 81

# Endocrine Cortisol:Synthesized by?Synthesized in response to?Carried in blood by (2 names)?

Answer 81

Synthesized by zona fasciculata of outer adrenal cortexSynthesized in response to ACTH stimulation of outer adrenal cortex (stimulates cholesterol desmolase)Cortisol carried in blood by corticosteroid binding protein (CBP) also called transcortin

Question 82

# Endocrine Steroid hormone synthesis:Location of cholesterol --> pregnenolone reaction?

Answer 82

Mitochondria

Question 83

# Endocrine Glucocorticoid (cortisol) secretion:Unique feature of secretion?Cortisol secretion highest?Cortisol secretion lowest?

Answer 83

Cortisol secretion oscillates with 24h periodicity (circadian rhythm)Cortisol secretion is highest just before waking --> 8AMCortisol secretion is lowest just before sleeping --> 12AM

Question 84

# Endocrine Hypothalamic nuclei important in glucocorticoid (cortisol) secretory regulation?

Answer 84

Suprachiasmatic nuclei b/c controls circadian rhythm

Question 85

# Endocrine Pro-opiomelanocortin (POMC)?

Answer 85

CRH stimulates anterior pituitary to synthesize POMC --> Precursor for ACTH and MSHAddison disease --> Increased ACTH levels AND increased MSH levels --> Increased pigmentation of buccal mucosa

Question 86

# Endocrine Negative feedback mechanism in glucocorticoid (cortisol) secretion?

Answer 86

Cortisol inhibits CRH release from hypothalamus and ACTH release from anterior pituitary

Question 87

# Endocrine Mechanism by which cortisol acts in target cells?

Answer 87

Cortisol diffuses across membrane of target cells and binds to steroid receptors in CYTOPLASM. Binding induces dissociation of cytoplasmic receptors from chaperone (heat shock protein). Cortisol-receptor complex translocates to nucleus.

Question 88

# Endocrine Cortisol:Effect on blood pressure?Mechanism?

Answer 88

Cortisol increases BP by upregulating a1-receptors on arterioles, increasing arteriole sensitivity to effects of NE (vasoconstrictor)

Question 89

# Endocrine "Cortisol is permissive for catecholamines" --> Explain

Answer 89

Cortisol has NO effect on vascular reactivity (vasoconstriction or vasodilation) itself, but augments/potentiates effects of catecholamines (NE) on arterioles 2/2 upregulation of a1 receptors

Question 90

# Endocrine Cortisol: Effect on prostaglandins/leukotrienes?Effect on IL-2 and T cells?Effect on histamine and serotonin?Effect on neutrophils?Effect on eosinophils?

Answer 90

Cortisol upregulates synthesis of lipocortin (cortisol binding protein) --> Lipocortin is an inhibitor of phospholipase A2, an enzyme that liberates arachadonic acid from phospholipid membranes --> Arachadonic acids are precursors for prostaglandin and leukotriene synthesis (inflammatory mediators)Cortisol inhibits production of IL-2 and thereby inhibits proliferation of T cellsCortisol inhibits release of histamine and serotonin from mast cells and plateletsCortisol inhibits leukocyte adhesion --> Demargination of neutrophils --> Increased neutrophils in bloodCortisol reduces number of eosinophils in blood

Question 91

# Endocrine Before starting treatment w/ corticosteroids always test for what infection 1st?

Answer 91

Latent TB infection b/c corticosteroids inhibit IL-2 which is necessary for maintenance of granulomas.Decreased IL-2 may lead to decomposition of granulomas and release of latent TB infection --> Reactivation of TB.

Question 92

# Endocrine Cortisol:Effect on gluconeogenesis?Mechanism?

Answer 92

Cortisol stimulates gluconeogenesis by:1) Increasing protein catabolism (proteolysis) in muscle and decreasing protein synthesis to provide more amino acids to liver for gluconeogenesis2) Decreasing glucose utilization and insulin sensitivity of adipose tissue --> Diabetogenic3) Increasing lipolysis to provide more glycerol to liver for gluconeogenesis

Question 93

# Endocrine Cortisol:Effect on fibroblasts?Clinical correlate?

Answer 93

Cortisol inhibits fibroblasts --> Abdominal striae in Cushing disease

Question 94

# Endocrine Cortisol:Effect on bone?Mechanism?

Answer 94

Cortisol decreases bone formation and increases bone resorption by decreasing activity of osteoblasts

Question 95

# Endocrine Unique feature of mineralocorticoid synthesis in zona glomerulosa of adrenal cortex?

Answer 95

Mineralocorticoid (aldosterone) synthesis regulated by renin-angiotensin-aldosteron system (ATII) and by K+ levelsZona fasciculata and reticularis regulated by ACTH ACTH receptor deficiency --> Aldosterone synthesis NORMAL

Question 96

# Endocrine Stimulation of aldosterone synthesis (x2)?

Answer 96

1) Decrease in mean arterial pressure (MAP) --> Decrease in renal perfusion pressure --> Renin production --> Renin catalyzes conversion of angiotensinogen to angiotensin I --> ACE in lungs catalyzes ATI to ATII --> ATII stimulates aldosterone synthase in zona glomerulosa to increase synthesis of aldosterone2) Hyperkalemia --> Increased K+ depolarizes cells in zona glomerulosa --> Opens voltage-gated Ca2+ channels --> Increased Ca2+ stimulates synthesis of aldosterone

Question 97

# Endocrine Aldosterone:Compensatory mechanism in response to decreased renal perfusion pressure?

Answer 97

Aldosterone acts on principal cells in late distal tubule and collecting duct to increase renal Na+ reabsorption --> H2O follows --> Restores volume

Question 98

# Endocrine Aldosterone:Compensatory mechanism in response to hyperkalemia?

Answer 98

Aldosterone acts on principal cells in late distal tubule and collecting duct to increase renal K+ wasting --> Decreases serum K+ levels to normal

Question 99

# Endocrine Growth hormone (GH) secretion:Unique feature of secretion?2 stimulators of secretion?3 inhibitors of secretion?

Answer 99

GH secretion is pulsatile with secretory bursts every 2 hoursGH secretion increased by --> Exercise and sleepGH secretion decreased by --> Hyperglycemia (high glucose), somatostatin, and somatomedins

Question 100

# Endocrine What are somatomedins and when are they produced?

Answer 100

Somatomedins --> Insulin-like growth factors (IGFs)IGFs are produced when GH acts on target tissues

Question 101

# Endocrine GH secretion:Feedback mechanisms (x4)?

Answer 101

1) GHRH released by hypothalamus feeds back on hypothalamus itself and inhibits further GHRH secretion2) GH released by anterior pituitary feeds back on hypothalamus and stimulates secretion of somatostatin --> Somatostatin = somatotropin release inhibiting factor (SRIF) --> Somatostatin inhibits GH (somatotropin) synthesis in anterior pituitary3) Somatomedins (IGFs) produced in target tissues feed back on anterior pituitary and inhibit GH secretion4) Somatomedins (IGFs) produced in target tissues feed back on hypothalamus and stimulates secretion of somatostatin --> GH inhibition

Question 102

# Endocrine Only direct function of GH?

Answer 102

GH increases blood glucose levels by decreases glucose uptake and utilization (insulin resistance) --> Diabetogenic Cortisol --> Also diabetogenic

Question 103

# Endocrine Somatomedins:Function?Act on what 3 tissue types?

Answer 103

Somatomedins increase protein synthesis --> Chondrocytes, muscle, most other organs

Question 104

# Endocrine Somatomedins:Chondrocytes?Muscle?Most other organs?

Answer 104

Chondrocytes --> Increased protein synthesis --> Increased linear growth --> PUBERTAL GROWTH SPURTMuscle --> Increased protein synthesis --> Increased lean body massMost other organs --> Increased protein synthesis --> Increased organ size

Question 105

# Endocrine GH deficiency before puberty:Clinical presentation?Treatment?

Answer 105

Failure to grow, short stature, mild obesity, delayed pubertyFailure to grow and short stature --> Decreased protein synthesis in chondrocytesMild obesity --> Decreased protein synthesis in muscleTx --> GH replacement therapy

Question 106

# Endocrine GH excess before puberty:Clinical presentation?Treatment?

Answer 106

Gigantism --> Increased linear growth --> Epiphyseal plates have yet to fuse pre-pubertyTx --> Somatostatin analog (octreotide)

Question 107

# Endocrine GH excess after puberty (adult):Clinical presentation?Treatment?

Answer 107

Acromegaly --> Increased organ size, increased hand/foot size, enlargement of tongue, coarsening of facial featuresEpiphyseal plates have already fused --> Increased protein synthesis in organs only (not chondrocytes)Insulin resistance, glucose intoleranceTx --> Somatostatin analog (octreotide)

Question 108

# Endocrine Negative feedback mechanism in prolactin secretion?

Answer 108

Prolactin feeds back on hypothalamus to stimulate dopamine (prolactin inhibiting factor) secretion, which inhibits prolactin secretion

Question 109

# Endocrine What are 3 functions of prolactin?

Answer 109

Stimulation of milk production (lactogenesis) in breastPotentiates breast development with estrogenInhibits ovulation/spermatogenesis by inhibiting synthesis/secretion of GnRH in hypothalamus --> Amenorrhea in women, decreased libido in men

Question 110

# Endocrine What are 2 milk products in breast milk?

Answer 110

Casein, lactalbumin

Question 111

# Endocrine Suckling stimulates sensory nerves that carry suckling signal from breast to [?] to promote what 3 effects?

Answer 111

Suckling signal inputs to ARCUATE NUCLEUS of hypothalamus to inhibit dopamine, thereby promoting prolactin releaseSuckling --> Prolactin and oxytocin release

Question 112

# Endocrine Prolactin:Causes of deficiency (x1)?Causes of excess (x2)?Manifestations of deficiency?Manifestations of excess?Drug(s) that stimulate(s) prolactin release?Drug(s) that inhibit(s) prolactin release?

Answer 112

Deficiency --> Destruction of anterior pituitary--> Failure to lactate --> Dopamine antagonists (estrogens/OCPs, antipsychotics) stimulate prolactin secretionExcess --> Hypothalamic destruction (loss of tonic inhibitory control by dopamine) or prolactin-secreting tumor (prolactinoma)--> Galactorrhea, amenorrhea in females or decreased libido in males, impaired ovulation/spermatogenesis (prolactin inhibits GnRH)--> Dopamine agonists (bromocriptine) inhibit prolactin secretion --> Treat prolactinoma

Question 113

# Endocrine Parathyroid hormone (PTH):Site of synthesis?Function?

Answer 113

PTH synthesized in chief cells of parathyroid glandsFunctions to regulate serum Ca2+ levels

Question 114

# Endocrine Parathyroid hormone (PTH):2 triggers that stimulate PTH?2 triggers that inhibit PTH?

Answer 114

Decreases in serum Ca2+ and MILD decreases in serum Mg2+ stimulate PTH secretionIncreases in serum Ca2+ and SEVERE decreases in serum Mg2+ inhibit PTH secretion

Question 115

# Endocrine Mechanism by which serum Ca2+ levels control PTH secretion?

Answer 115

Increased serum Ca2+ --> Ca2+ binds Ca2+-sensing receptors on chief cell membrane --> Inhibits PTH secretionDecreased serum Ca2+ --> Less Ca2+ available to bind Ca2+-sensing receptors on chief cell membrane --> Triggers PTH secretion

Question 116

# Endocrine What are 2 causes of hypomagnesemia?

Answer 116

Decreased absorption or intake of Mg2+ --> Chronic diarrhea, alcoholism Increased renal loss of Mg2+--> Diuretics (loop, thiazide)--> Drugs (aminoglycosides)

Question 117

# Endocrine PTH functions to increase [?] and decrease [?] serum levels

Answer 117

Increase Ca2+, decrease phosphate

Question 118

# Endocrine Vitamin D:Cutaneous precursor?Vitamin D2 = ?Vitamin D3 = ?

Answer 118

Cutaneous precursor --> 7-dehydrocholesterolVitamin D2 --> Ergocalciferol (dietary plant sources)Vitamin D3 --> Cholecalciferol (dietary animal sources)

Question 119

# Endocrine Cutaneous source of vitamin D?

Answer 119

On exposure to ultraviolet light, cutaneous precursor of vitamin D (7-dehydrocholesterol) undergoes photochemical cleavage to form vitamin D3 (cholecalciferol)

Question 120

# Endocrine Cholecalciferol (vitD3) processing?

Answer 120

Liver --> Cholecalciferol undergoes 25-hydroxylation to form 25-hydroxycholecalciferol 25-OH-cholecalciferol

Question 121

# Endocrine 25-OH-cholecalciferol processing (x2)?

Answer 121

25-OH-cholecalciferol --> 1,25-(OH)2-cholecalciferol via 1α-hydroxylase in kidney25-OH-cholecalciferol --> 24,25-(OH)2-cholecalciferol via 24α-hydroxylase in kidney1,25-(OH)2-cholecalciferol --> Calcitrol --> ACTIVE vitamin D24,25-(OH)2-cholecalciferol --> INACTIVE vitamin D

Question 122

# Endocrine What 3 factors increase production of active vitamin D (calcitrol)? Mechanism?

Answer 122

Decreased Ca2+, decreased phosphate, increased PTH--> Increase activity of renal 1α-hydroxylase and decrease activity of 24α-hydroxylase

Question 123

# Endocrine Vitamin D deficiency:In adults --> ?In children --> ?4 causes of deficiency?

Answer 123

Adults --> OsteomalaciaChildren --> Rickets Deficiency:--> Malabsorption--> Poor diet--> Decreased sunlight (decreased photochemical cleavage of 7-dehydrocholesterol to cholecalciferol)--> Chronic renal failure --> Impaired 1α-hydroxylase activity responsible for calcitrol production

Question 124

# Endocrine Mechanism by which vitamin D (calcitrol) acts in target tissues?

Answer 124

Vitamin D diffuses across membrane of target cells and binds to steroid receptors in NUCLEUS

Question 125

# Endocrine What are 3 functions of vitamin D?

Answer 125

1) Increase Ca2+ reabsorption in duodenum2) Increase phosphate reabsorption in jejunum and ileum3) Increases bone resorption --> Provides Ca2+ and phosphate from "old" bone to mineralize "new" bone

Question 126

# Endocrine Vitamin D increases Ca2+ reabsorption in gut: Site?Mechanism?

Answer 126

Increased Ca2+ reabsorption in duodenum Vitamin D increases production of vitamin D-depending Ca2+-binding protein --> CALBINDIN D

Question 127

# Endocrine Vitamin D increases bone resorption: Mechanism?

Answer 127

Vitamin D stimulates monocytic stem cells to become osteoclasts --> Bone-resorbing cells

Question 128

# Endocrine PTH functions to increase serum Ca2+ and decrease serum phosphate levels by coordinating what 4 independent actions?

Answer 128

1) Increases bone resorption --> Brings both Ca2+ and phosphate from bone mineral into serum*Alone, this effect would not increase serum ionized (free) Ca2+ b/c increased phosphate complexes with increased Ca2+*2) Inhibits renal phosphate reabsorption --> Increases phosphate excretion (phosphaturic effect) --> Decreases serum phosphate levels3) Increases renal Ca2+ reabsorption --> Increases serum Ca2+ levels4) Increases intestinal Ca2+ reabsorption INDIRECTLY by stimulating 1α-hydroxylase activity in kidney and increasing production of active vitamin D

Question 129

# Endocrine PTH increases Ca2+ reabsorption in [?] of kidneyPTH decreases phosphate reabsorption in [?] of kidney

Answer 129

Increased Ca2+ reabsorption --> Distal convoluted tubuleDecreased phosphate reabsorption --> Proximal convoluted tubule (phosphate --> proximal)

Question 130

# Endocrine PTH --> Increased bone resorption:PTH acts on PTH-receptors on what cell type?Receptor binding triggers what 2 processes?2 downstream effects of these processes?

Answer 130

PTH acts on PTH-receptors on osteoblast precursors (bone-forming cells)--> Increases synthesis/secretion of macrophage colony-stimulating factor (M-CSF)--> Increases expression on cell surface of "receptor activator for nuclear factor kB ligand" --> RANK-L--> M-CSF and RANK-L bind receptors on osteoclast precursors (bone-resorbing cells) to stimulate production of mature osteoclasts --> RANK-L binds receptors on mature osteoclasts to increase their bone-resorbing activity

Question 131

# Endocrine Laboratory finding that correlates with PTH actions on proximal convoluted tubule (decreased phosphate reabsorption) and distal convoluted tubule (increased Ca2+ reabsorption)?

Answer 131

Increased urinary cAMP b/c PTH signals through cAMP 2nd messenger

Question 132

# Endocrine Laboratory finding that correlates with PTH (and vitamin D) action on bone to increase matrix reabsorption?

Answer 132

Increased urinary hydroxyproline, which correlates with resorption of bone organic matrix

Question 133

# Endocrine PTH leads to ___ (increased/decreased) reabsorption of Ca2+ and ___ (increased/decreased) reabsorption of phosphate where?Vitamin D to ___ (increased/decreased) reabsorption of Ca2+ and ___ (increased/decreased) reabsorption of phosphate where?

Answer 133

PTH --> Increased reabsorption of Ca2+ and decreased reabsorption of phosphate in kidneysVitamin D --> Increased Ca2+ AND phosphate reabsorption in gut

Question 134

# Endocrine What are 3 forms of Ca2+ in serum?

Answer 134

Ionized/free Ca2+ (45%)Ca2+ bound to albumin (40%)Ca2+ bound to anions, e.g., phosphate (15%)

Question 135

# Endocrine Increased pH --> Affect on Ca2+ levels in serum?

Answer 135

Increased pH --> Increased affinity of negatively-charged albumin for Ca2+ --> Decreased free/ionized Ca2+ levels"Hypocalcemia" --> Cramps, pain, paresthesias, carpopedal spasm

Question 136

# Endocrine Negative feedback mechanism for PTH secretion?

Answer 136

Increased serum Ca2+ and vitamin D (calcitrol) levels feed back on chief cells of parathyroid glands and decrease PTH release

Question 137

# Endocrine Calcitonin:Site of synthesis?Function?

Answer 137

Calcitonin synthesized in parafollicular C cells of thyroid glandFunctions to counter actions mediated by PTH and thereby regulate "tone" or level of Ca2+--> Does NOT appear to function in normal Ca2+ homeostasis

Question 138

# Endocrine Calcitonin:Trigger of secretion?

Answer 138

Increased serum Ca2+ stimulates calcitonin release Calcitonin "tones" down Ca2+ levels by opposing actions of PTH

Question 139

# Endocrine Mechanism by which calcitonin opposes PTH action to "tone" Ca2+ levels?

Answer 139

Calcitonin inhibits osteoclast bone resorption

Question 140

# Endocrine PTH --> Increases bone resorption by acting on [?]Calcitonin --> Decreases bone resorption by acting on [?]

Answer 140

PTH --> Acts on OSTEOBLASTS--> Indirectly activates osteoclast activityCalcitonin --> Acts on OSTEOCLASTS--> Directly inhibits osteoclast activity

Question 141

# Endocrine Pancreatic islets, α cells:Location in islet?Secretory product?

Answer 141

Located peripherallySecrete glucagon

Question 142

# Endocrine Pancreatic islets, β cells:Location in islet?Secretory product?

Answer 142

Located centrallySecrete insulinINSulin cells --> INSide islet

Question 143

# Endocrine Pancreatic islets, δ cells:Location in islet?Secretory product?

Answer 143

Intermixed throughout isletSecrete somatostatin

Question 144

# Endocrine Proinsulin: Site of processing?Mechanism of processing?

Answer 144

Proinsulin is deposited in rER and transported within membrane-enclosed organelles to sacs of Golgi apparatus Within Golgi, convertases cleave proinsulin --> insulin + C peptide

Question 145

# Endocrine Structure of insulin?

Answer 145

Insulin --> 2 peptide chains (A and B chains) linked by 2 disulfide linkages

Question 146

# Endocrine Insulin secretion:- Glucose uptake into β cell via what transporter?- Fate of glucose in β cell?- 1st channel to close s/p glucose uptake?- Trigger for this channel to close?- Mechanism by which β cell membrane depolarizes?- Depolarization opens what channel?- Final trigger for insulin release?

Answer 146

- Glucose into β cell via GLUT2 transporter- Glucose undergoes glycolysis, which raises intracellular ATP - K(ATP) channels - Increased ATP closes ATP-dependent K+ channels (K+ accumulates inside cell)- Decreased K+ conductance depolarizes β cell membrane (potential is less negative)- Depolarization opens voltage-gated Ca2+ channels - Ca2+ influx triggers Ca2+-dependent Ca2+ release --> Significantly elevated Ca2+ levels trigger exocytosis of insulin granules --> Release of insulin + C peptide

Question 147

# Endocrine Mechanism by which α- and β-cells communicate?

Answer 147

Gap junctions

Question 148

# Endocrine Insulin receptor structure?

Answer 148

α2β2 heterotetrameric complex2 insulin-binding α subunits2 catalytically-active β subunits --> Intracellular tyrosine kinase activity

Question 149

# Endocrine Binding of insulin to α-subunits of insulin receptor triggers?

Answer 149

Binding of insulin to extracellular α-subunits of insulin receptor triggers tyrosine kinase activity of intracellular β-subunits1 β-subunit phosphorylates other (autophosphorylation) --> Initiates signal cascade

Question 150

# Endocrine 1st phosphorylation event triggered by activation of insulin receptor?

Answer 150

Phosphorylation of insulin receptor substrates (IRS-1, IRS-2)

Question 151

# Endocrine IRS-1 and IRS-2 phosphorylation triggers what 2 signaling pathways?

Answer 151

Metabolic pathway Mitogenic pathway

Question 152

# Endocrine Metabolic pathway of insulin signaling:Signaling mechanism?Functions (x2)?

Answer 152

Metabolic signaling --> PI3K/Akt/mTOR1) Drives GLUT-4 containing vesicles to cell membrane in adipocytes and muscle cells 2) Increases glycogen synthesis, lipid synthesis, and protein sysnthesis

Question 153

# Endocrine Mitogenic pathway of insulin signaling:Signaling mechanism?Function?

Answer 153

Mitogenic signaling -->RAS, Raf kinase, MAPKCell growth and DNA synthesis

Question 154

# Endocrine Mechanism by which glucagon mediates insulin resistance?

Answer 154

Glucagon --> Activates serine kinases that phosphorylate insulin receptor substrates (IRS-1, IRS-2) such that they're not available to be phosphorylated by insulin receptor --> Inhibits insulin signaling pathway

Question 155

# Endocrine Mechanism by which TNFα mediates insulin resistance?

Answer 155

TNFα --> Activates serine kinases that phosphorylate insulin receptor substrates (IRS-1, IRS-2) such that they're not available to be phosphorylated by insulin receptor --> Inhibits insulin signaling pathway*Same as glucagon*

Question 156

# Endocrine Mechanisms by which insulin decreases blood glucose levels (x3)?

Answer 156

1) Upregulates expression of GLUT4 receptor on adipocytes and muscle cells --> Increases glucose uptake into these cells2) Promotes formation of glycogen from glucose and inhibits glycogenolysis (breakdown of glycogen) in muscle and liver cells 3) Decreases gluconeogenesis --> Increases production of fructose-2,6-bisphosphate thereby increasing phosphofructokinase (PFK) activity --> Substrate is shunted toward glucose breakdown and away from glucose formation

Question 157

# Endocrine Effect of insulin on fats?

Answer 157

Insulin decreases fatty acid levels in blood --> Stimulates fat deposition in adipose tissue and inhibits lipolysis

Question 158

# Endocrine Effect of insulin on proteins?

Answer 158

Insulin decreases amino acid levels in blood --> Stimulates amino acid uptake into cells --> Increases protein synthesisSimultaneously, insulin inhibits protein degradation*Insulin is anabolic

Question 159

# Endocrine Effect of insulin on K+ levels?

Answer 159

Insulin promotes K+ uptake into cells --> Decreases K+ levels in blood --> Hypokalemia

Question 160

# Endocrine Effect of insulin on Na+ levels?

Answer 160

Insulin increases Na+ reabsorption in kidneys --> Increases Na+ levels in blood --> Hypernatremia

Question 161

# Endocrine Glucose - Cross placenta?Insulin - Cross placenta?

Answer 161

Glucose crosses placenta Insulin does NOT cross placenta

Question 162

# Endocrine Stimulators of insulin secretion (x3)?

Answer 162

1) Hyperglycemia 2) Growth hormone (GH)3) β2-agonists (Gs protein --> Epinephrine)

Question 163

# Endocrine Inhibitors of insulin secretion (x4)?

Answer 163

1) Hypoglycemia 2) Somatostatin3) α2-agonists (Gi protein --> Norepinephrine)4) Glucagon

Question 164

# Endocrine Mechanism by which GH stimulates insulin secretion?

Answer 164

GH decreases glucose uptake into cells and increases insulin resistance --> Stimulates increased insulin secretionGH does NOT stimulate insulin directly

Question 165

# Endocrine Only insulin-dependent glucose transporter?

Answer 165

GLUT4GLUT1, GLUT2, GLUT3, GLUT5 --> Insulin-INDEPENDENT transporters

Question 166

# Endocrine GLUT1:Present on what cell type(s)?Distinctive feature(s)/function(s)?

Answer 166

CNS, RBCsGLUT1 mediates basal glucose uptake b/c it has a very high affinity for glucose (low Km) --> Can therefore transport glucose into cells at relatively low concentrations, such as those found in fasting statesEnsures adequate transport of glucose into CNS and RBCs--> RBCs lack mitochondria --> Rely on glucose for all energy

Question 167

# Endocrine GLUT2:Present on what cell type(s)?Distinctive feature(s)/function(s)?

Answer 167

Hepatocytes and pancreatic β cells GLUT2 regulates insulin release --> low affinity for glucose (high Km) Low affinity for glucose reduces hepatic uptake of glucose during fastingBi-directional transporter --> Assists in export of glucose from hepatocytes when needed

Question 168

# Endocrine GLUT3:Present on what cell type(s)?Distinctive feature(s)/function(s)?

Answer 168

Neurons, placentaGLUT3 has a very high affinity for glucose (low Km) --> Responsible for glucose uptake into neurons even in fasting states GLUT3 mediates placental transport of glucose --> High affinity for glucose permits glucose uptake by placenta to provide developing embryo/fetus with glucose

Question 169

# Endocrine GLUT4:Present on what cell type(s)?Distinctive feature(s)/function(s)?

Answer 169

Adipocytes, muscle cellsGLUT4 --> Insulin-dependent transporter --> Sequestered within intracellular vesicles until insulin stimulation induces its expression on cell surface

Question 170

# Endocrine GLUT5:Present on what cell type(s)?Distinctive feature(s)/function(s)?

Answer 170

GI tract, spermatocytesGLUT5 responsible for fructose uptake from GI tract--> Fructose important in spermatocyte function

Question 171

# Endocrine Stimulator of glucagon secretion (x1)?

Answer 171

Hypoglycemia

Question 172

# Endocrine Inhibitors of glucagon secretion (x3)?

Answer 172

HyperglycemiaSomatostatinInsulin

Question 173

# Endocrine Mechanisms by which glucagon decreases blood glucose levels (x2)?

Answer 173

1) Increases glycogenolysis (glycogen breakdown into glucose) in muscle and liver cells 2) Increases gluconeogenesis (production of glucose in liver)--> Decreases production of fructose-2,6-bisphosphate thereby decreasing phosphofructokinase (PFK) activity --> Substrate is shunted toward glucose formation and away from glucose breakdown

Question 174

# Endocrine Effect on lipids:Insulin?Glucagon?

Answer 174

Insulin --> Decreases blood fatty acid levels b/c stimulates fat deposition in adipose tissue and inhibits lipolysis (fat breakdown)Glucagon --> Increases fatty acid levels b/c stimulates lipolysis (fat breakdown) in adipose tissue

Question 175

# Endocrine Effect on ketoacids:Insulin?Glucagon?

Answer 175

Insulin --> Inhibits ketoacid formation in liver b/c insulin decreases fatty acid production --> Less acetyl CoA substrate available for ketoacid formationGlucagon --> Increases ketoacid formation in liver b/c glucagon increases fatty acid production--> More acetyl CoA substrate available for ketoacid formation--> Glucagon senses hypoglycemia and responds to increase glucose levels in blood to provide tissues with substrate for energy production--> Glucagon stimulates ketoacid production to be used as energy as well

Question 176

# Endocrine Ketoacids:Synthesized from what precursor?What are 2 ketoacids?

Answer 176

Ketoacids via acetyl CoA precursor2 ketoacids --> Acetoacetate and β-hydroxybutyrate