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USMLE STEP 1 - OLD > Endocrine - Anatomy/physiology > Flashcards

Endocrine - Anatomy/physiology Flashcards

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1
Q

Endocrine

What are 2 parts of fetal adrenal gland?

A

Inner active fetal zone and outer dormant/inactive adult zone

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2
Q

Endocrine

What are 2 parts of adult adrenal gland?

A

Inner adrenal medulla and outer adrenal cortex

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3
Q

Endocrine

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

A

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

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4
Q

Endocrine

Mechanism by which fetus produces androgens in utero?

A

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

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5
Q

Endocrine

What are 3 parts of adrenal cortex?

A

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

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6
Q

Endocrine

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

A

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

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7
Q

Endocrine

Embryologic origin:Adrenal cortex?Adrenal medulla?

A

Cortex - MesodermMedulla - Neuroectoderm (neural crest cells)

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8
Q

Endocrine

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

A

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

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9
Q

Endocrine

Adrenal tumors:MCC in adults?MCC in children?

A

Adults - PheochromocytomaChildren - Neuroblastoma

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10
Q

Endocrine

Venous drainage:Left adrenal gland?Right adrenal gland?

A

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

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11
Q

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?

A

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.

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12
Q

Endocrine

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

A

Heart, lungs, liver, and skeletal muscle

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13
Q

Endocrine

Precursor of all steroid hormones synthesized in adrenal cortex?

A

Cholesterol

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14
Q

Endocrine

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

A

Cholesterol –> pregnenoloneReaction catalyzed by cholesterol desmolase

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15
Q

Endocrine

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

A

ACTH

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16
Q

Endocrine

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

A

Ketoconazole

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17
Q

Endocrine

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

A

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

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18
Q

Endocrine

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

A

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

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19
Q

Endocrine

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

A

11-deoxycorticosterone –> corticosterone via 11β-hydroxylase

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20
Q

Endocrine

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

A

Corticosterone –> aldosterone via aldosterone synthase

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21
Q

Endocrine

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

A

Angiotensin II

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22
Q

Endocrine

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

A

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

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23
Q

Endocrine

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

A

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

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24
Q

Endocrine

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

A

DHEA –> androstenedione via 3β-hydroxysteroid dehydrogenase

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25
Q

Endocrine

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

A

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

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26
Q

Endocrine

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

A

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

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27
Q

Endocrine

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

A

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

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28
Q

Endocrine

Relationship b/w anterior pituitary and hypothalamus?

A

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

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29
Q

Endocrine

Relationship b/w posterior pituitary and hypothalamus?

A

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.

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30
Q

Endocrine

Anterior pituitary:Another name?Embryologic origin?Hormones?

A

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

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31
Q

Endocrine

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

A

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

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32
Q

Endocrine

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

A

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

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33
Q

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?

A

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

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34
Q

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?

A

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

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35
Q

Endocrine

Chromophobes?

A

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

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36
Q

Endocrine

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

A

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

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37
Q

Endocrine

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

A

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

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38
Q

Endocrine

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

A

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.

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39
Q

Endocrine

Mechanism by which posterior pituitary hormones are released into bloodstream?

A

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

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40
Q

Endocrine

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

A

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

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41
Q

Endocrine

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

A

GHRH stimulates GH

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42
Q

Endocrine

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

A

GnRH stimulates FSH, LH

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43
Q

Endocrine

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

A

TRH stimulates TSH and prolactin

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44
Q

Endocrine

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

A

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

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45
Q

Endocrine

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

A

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.

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46
Q

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?

A

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

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47
Q

Endocrine

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

A

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

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48
Q

Endocrine

What are 2 functions of TSH on thyroid gland?

A

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

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49
Q

Endocrine

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

A

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

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50
Q

Endocrine

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

A

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

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51
Q

Endocrine

Negative feedback mechanism for TSH secretion?

A

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.

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52
Q

Endocrine

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

A

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

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53
Q

Endocrine

Thyroid stimulating immunoglobulins (TSI)?

A

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

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54
Q

Endocrine

Mechanism by which thyroid hormones act in target cells?

A

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

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55
Q

Endocrine

Thyroglobulin (TG)? Synthesized from what precursor?

A

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.

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56
Q

Endocrine

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

A

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

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57
Q

Endocrine

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

A

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

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58
Q

Endocrine

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

A

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

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59
Q

Endocrine

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

A

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

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60
Q

Endocrine

Mechanism by which T3 and rT3 are synthesized?

A

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

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61
Q

Endocrine

Mechanism by which thyroid hormones are cleared by body?

A

Glucuronidation in liver

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62
Q

Endocrine

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

A

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

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63
Q

Endocrine

Wolff-Chaikoff effect?

A

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

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64
Q

Endocrine

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

A

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

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65
Q

Endocrine

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

A

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

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66
Q

Endocrine

Drug that inhibits both thyroid peroxidase and 5’-deiodinase?

A

Propylthiouracil (PTU)

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67
Q

Endocrine

Drug that inhibits only thyroid peroxidase?

A

Methimazole

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68
Q

Endocrine

Why does thyroid gland synthesize predominantly T4?

A

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

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69
Q

Endocrine

Colloid?

A

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

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70
Q

Endocrine

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

A

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

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71
Q

Endocrine

Mechanism by which MIT and DIT are recycled?

A

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

72
Q

Endocrine

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

A

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.

73
Q

Endocrine

Thyroid levels in liver failure?

A

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

74
Q

Endocrine

Thyroid levels in pregnancy and OCP use?

A

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)

75
Q

Endocrine

Functions of thyroid hormone?

A

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

76
Q

Endocrine

Mechanism by which thyroid hormone increases basal metabolic rate?

A

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

77
Q

Endocrine

Mechanism by which thyroid hormone increases metabolism?

A

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

78
Q

Endocrine

Mechanism by which thyroid hormone increases cardiac output?

A

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

79
Q

Endocrine

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

A

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

80
Q

Endocrine

Hypothyroidism in perinatal period?

A

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

81
Q

Endocrine

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

A

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

82
Q

Endocrine

Steroid hormone synthesis:Location of cholesterol –> pregnenolone reaction?

A

Mitochondria

83
Q

Endocrine

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

A

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

84
Q

Endocrine

Hypothalamic nuclei important in glucocorticoid (cortisol) secretory regulation?

A

Suprachiasmatic nuclei b/c controls circadian rhythm

85
Q

Endocrine

Pro-opiomelanocortin (POMC)?

A

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

86
Q

Endocrine

Negative feedback mechanism in glucocorticoid (cortisol) secretion?

A

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

87
Q

Endocrine

Mechanism by which cortisol acts in target cells?

A

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.

88
Q

Endocrine

Cortisol:Effect on blood pressure?Mechanism?

A

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

89
Q

Endocrine

“Cortisol is permissive for catecholamines” –> Explain

A

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

90
Q

Endocrine

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

A

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

91
Q

Endocrine

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

A

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.

92
Q

Endocrine

Cortisol:Effect on gluconeogenesis?Mechanism?

A

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

93
Q

Endocrine

Cortisol:Effect on fibroblasts?Clinical correlate?

A

Cortisol inhibits fibroblasts –> Abdominal striae in Cushing disease

94
Q

Endocrine

Cortisol:Effect on bone?Mechanism?

A

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

95
Q

Endocrine

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

A

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

96
Q

Endocrine

Stimulation of aldosterone synthesis (x2)?

A

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

97
Q

Endocrine

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

A

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

98
Q

Endocrine

Aldosterone:Compensatory mechanism in response to hyperkalemia?

A

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

99
Q

Endocrine

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

A

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

100
Q

Endocrine

What are somatomedins and when are they produced?

A

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

101
Q

Endocrine

GH secretion:Feedback mechanisms (x4)?

A

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

102
Q

Endocrine

Only direct function of GH?

A

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

103
Q

Endocrine

Somatomedins:Function?Act on what 3 tissue types?

A

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

104
Q

Endocrine

Somatomedins:Chondrocytes?Muscle?Most other organs?

A

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

105
Q

Endocrine

GH deficiency before puberty:Clinical presentation?Treatment?

A

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

106
Q

Endocrine

GH excess before puberty:Clinical presentation?Treatment?

A

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

107
Q

Endocrine

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

A

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)

108
Q

Endocrine

Negative feedback mechanism in prolactin secretion?

A

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

109
Q

Endocrine

What are 3 functions of prolactin?

A

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

110
Q

Endocrine

What are 2 milk products in breast milk?

A

Casein, lactalbumin

111
Q

Endocrine

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

A

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

112
Q

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?

A

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

113
Q

Endocrine

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

A

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

114
Q

Endocrine

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

A

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

115
Q

Endocrine

Mechanism by which serum Ca2+ levels control PTH secretion?

A

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

116
Q

Endocrine

What are 2 causes of hypomagnesemia?

A

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

117
Q

Endocrine

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

A

Increase Ca2+, decrease phosphate

118
Q

Endocrine

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

A

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

119
Q

Endocrine

Cutaneous source of vitamin D?

A

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

120
Q

Endocrine

Cholecalciferol (vitD3) processing?

A

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

121
Q

Endocrine

25-OH-cholecalciferol processing (x2)?

A

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

122
Q

Endocrine

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

A

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

123
Q

Endocrine

Vitamin D deficiency:In adults –> ?In children –> ?4 causes of deficiency?

A

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

124
Q

Endocrine

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

A

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

125
Q

Endocrine

What are 3 functions of vitamin D?

A

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

126
Q

Endocrine

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

A

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

127
Q

Endocrine

Vitamin D increases bone resorption: Mechanism?

A

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

128
Q

Endocrine

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

A

1) Increases bone resorption –> Brings both Ca2+ and phosphate from bone mineral into serumAlone, 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

129
Q

Endocrine

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

A

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

130
Q

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?

A

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

131
Q

Endocrine

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

A

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

132
Q

Endocrine

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

A

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

133
Q

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?

A

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

134
Q

Endocrine

What are 3 forms of Ca2+ in serum?

A

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

135
Q

Endocrine

Increased pH –> Affect on Ca2+ levels in serum?

A

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

136
Q

Endocrine

Negative feedback mechanism for PTH secretion?

A

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

137
Q

Endocrine

Calcitonin:Site of synthesis?Function?

A

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

138
Q

Endocrine

Calcitonin:Trigger of secretion?

A

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

139
Q

Endocrine

Mechanism by which calcitonin opposes PTH action to “tone” Ca2+ levels?

A

Calcitonin inhibits osteoclast bone resorption

140
Q

Endocrine

PTH –> Increases bone resorption by acting on [?]Calcitonin –> Decreases bone resorption by acting on [?]

A

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

141
Q

Endocrine

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

A

Located peripherallySecrete glucagon

142
Q

Endocrine

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

A

Located centrallySecrete insulinINSulin cells –> INSide islet

143
Q

Endocrine

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

A

Intermixed throughout isletSecrete somatostatin

144
Q

Endocrine

Proinsulin: Site of processing?Mechanism of processing?

A

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

145
Q

Endocrine

Structure of insulin?

A

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

146
Q

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?

A
  • 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
147
Q

Endocrine

Mechanism by which α- and β-cells communicate?

A

Gap junctions

148
Q

Endocrine

Insulin receptor structure?

A

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

149
Q

Endocrine

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

A

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

150
Q

Endocrine

1st phosphorylation event triggered by activation of insulin receptor?

A

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

151
Q

Endocrine

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

A

Metabolic pathway Mitogenic pathway

152
Q

Endocrine

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

A

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

153
Q

Endocrine

Mitogenic pathway of insulin signaling:Signaling mechanism?Function?

A

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

154
Q

Endocrine

Mechanism by which glucagon mediates insulin resistance?

A

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

155
Q

Endocrine

Mechanism by which TNFα mediates insulin resistance?

A

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 pathwaySame as glucagon

156
Q

Endocrine

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

A

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

157
Q

Endocrine

Effect of insulin on fats?

A

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

158
Q

Endocrine

Effect of insulin on proteins?

A

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

159
Q

Endocrine

Effect of insulin on K+ levels?

A

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

160
Q

Endocrine

Effect of insulin on Na+ levels?

A

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

161
Q

Endocrine

Glucose - Cross placenta?Insulin - Cross placenta?

A

Glucose crosses placenta Insulin does NOT cross placenta

162
Q

Endocrine

Stimulators of insulin secretion (x3)?

A

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

163
Q

Endocrine

Inhibitors of insulin secretion (x4)?

A

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

164
Q

Endocrine

Mechanism by which GH stimulates insulin secretion?

A

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

165
Q

Endocrine

Only insulin-dependent glucose transporter?

A

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

166
Q

Endocrine

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

A

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

167
Q

Endocrine

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

A

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

168
Q

Endocrine

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

A

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

169
Q

Endocrine

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

A

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

170
Q

Endocrine

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

A

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

171
Q

Endocrine

Stimulator of glucagon secretion (x1)?

A

Hypoglycemia

172
Q

Endocrine

Inhibitors of glucagon secretion (x3)?

A

HyperglycemiaSomatostatinInsulin

173
Q

Endocrine

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

A

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

174
Q

Endocrine

Effect on lipids:Insulin?Glucagon?

A

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

175
Q

Endocrine

Effect on ketoacids:Insulin?Glucagon?

A

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

176
Q

Endocrine

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

A

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

USMLE STEP 1 - OLD (12 decks)

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