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Endocrinology Flashcards

1
Q

Compare Nervous system and Endocrine system

A

Nervous: rapid response, short-duration response, acts via AP and Neurotransmitters, acts at specific locations, act over short distances

Endocrine: slow response, long duration response, acts via hormones into blood, acts at diffuse locations, and hormones act over long distance

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2
Q

Autocrine

A

chemical that exerts effects on same cells that secrete them

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3
Q

Paracrine

A

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

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4
Q

Water-soluble hormones

A

amino-acid except thyroid
act on plasma membrane receptors
act vis G proteins second messengers
cannot enter cell

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5
Q

Lipid-Soluble hormone

A

steroid and thyroid hormone
act on intracellular receptors that directly activate genes
can enter cell

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6
Q

Compare cAMP and PIP2-Ca signaling mechanism

A

cAMP: hormone binds to receptor-> activates G protein -> activates or inhibits adenylate cyclase -> adenylate cyclase then convert ATP to cAMP -> cAMP activates protein kinase to phosphorylate other proteins

PIP2-Ca: hormone on membrane activates G protein -> activates phospholipase C -> splits PIP2 into diacylglycerol activate protein kinase and inositol triphosphate release Ca

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7
Q

Intracellular Receptor mechanism

A

lipid-soluble hormones and thyroid hormone can diffuse into target cell bind to intracellular receptors -> enters the nucleus and binds to specific region of DNA -> helps initiate DNA transcription to produce mRNA -> mRNA then translated into specific protein

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8
Q

Stimulation of Endocrine Gland

A

Humoral stimuli: changing blood levels of ions and nutrients directly stimulate secretion of hormones

Neural stimuli: nerve fibers stimulate hormone release

Hormonal Stimuli: hormone stimulate other endocrine organs to release their hormones

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9
Q

Posterior pituitary

A

composed of neural tissue that secrete neurohormones

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10
Q

Anterior pituitary

A

consists of glandular tissue

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11
Q

ADH Regulation

A

Stim: by impulses from hypothalmic neurons in response to ncreased blood solute concentration or decreased blood vol; also timulated by pain, some drugs, low BP

inhib: adequate hydration of body and alcohol

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12
Q

ADH Target organ and effect

A

kidneys: stimulates tubule cells to reabsorb water from the forming urine back into blood

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13
Q

ADH patho

A

↑ syndrome of inappropriate ADH secretion

↓ diabetes insipidus

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14
Q

T4 composition

A

DIT plus DIT

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15
Q

T3 composition

A

DIT plus MIT

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16
Q

Where is Iodide located in the thyroid gland?

A

cytoplasm of follicular cells

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17
Q

T3 Function

A

7 Bs
brain maturation, bone growth, B adrenergic effects, basal metabolic rate, blood sugar, break down lipids, babies stimulates surfactant synthesis

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18
Q

What is T3 impact on heart?

A

increase cardiac output, HR, SV, and contractility

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19
Q

Oxytocin regulation

A

stim: impulses from hypothalamic neuros in response to stretching of the uterine cervix or sucking of infant at breast
inhib: adequate hydration of the body and by alcohol

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20
Q

Oxytocin pathway

A

neurons in paraventricular nucleus of hypothalamus

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21
Q

Oxytocin target organ and effect

A

uterus: stimulates uterine contractions, initiates labor
breast: initiates milk ejection

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22
Q

Wolff-Chaikoff effect

A

sudden exposure to excess iodine temporarily turns off thyroid peroxidase; dec T3/T4 production

reg: chemoreceptors locally of thyroid tissue

protective autoregulation

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23
Q

GH reg

A

stim: by GHRH which is triggered by low blood levels of GH, deep sleep, hypoglycemia, increases in blood levels of amino acids, low levels of fatty acids, exercise, and other types of stressors
inhib: feedback inhibition exerted by GH and IGFs, hyperglycemia, hyperlipidemia, obesity, and emotional deprivation via either increased somatostatin or decreased GHRH release

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24
Q

GH Target organ and effect

A

liver, muscle, bone, cartilage, and other issues: anabolic hormone, stimulates somatic growth, mobilizes fats, spares glucose

growth-promoting effects mediated indirectly by IGFs

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25
Q

GH patho

A

↑ gigantism in kids, acromegaly in adults

↓ dwarfism in kids, GH insufficiency in adults

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26
Q

TSH reg

A

stim: by TRH and in infants indirectly by cold temperature

inhib; by feedbakci nhibitiion exerted by thyroid hormones on ant pituitary and hypothalamus and by GHIH

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27
Q

17 aplha-hydroxylase patho

A

increase in progesterone and aldosterone

decrease in cortisol and sex hormone

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28
Q

17 aplha-hydroxylase clinical

A

a typical genitalia, undescended testes, lack of secondary sexual development, hypertension, hypokalemia,

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29
Q

21-hydroxylase patho

A

allow the sex hormones to go forward, low cortisol and aldosterone

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30
Q

21-hydroxylase clinical char

A

salt wasting, hypotension, and hyperkalemia

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31
Q

11beta-hydroxylase patho

A

stops conversion of 11-deoxycortisoterone to corticosterone and stops conversion of 11-deoxycortisoal (increases BP) to cortisol
cortisol and aldosterone decrease
increased androgens

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32
Q

11beta-hydroxylase clinical

A

hypokalemia, hypertension,

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33
Q

posterior pituitary hormones (made by hypothalmic neurons, stored in post pituitary)

A

oxytocin, antidiuretic hormone (ADH)

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34
Q

oxytocin chemical structure and cell type

A

peptide, mostly from neurons in paraventricular nucleus of hypothalamus

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35
Q

antidiuretic hormone (ADH) other names, chemical structure and cell type

A

vasopressin

peptide, mostly from neurons in supraoptic nucleaus of hypothalamus

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36
Q

growth hormone (GH) chemical structure and cell type

A

protein, somatotropic cells

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37
Q

thyroid stimulating hormone (TSH) chemical structure and cell type

A

glycoprotein, thyrotropic cells

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38
Q

TSH target organs and effects

A

thyroid gland: sitmulates thyroid gland to release thyroid hormones

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39
Q

TSH patho

A

↑ primary hyperthyroidism, secondary/tertiary hypothyroidism, graves, pituitary adenoma

↓ primary hypothyroidism; may cause myxedema, secondary/tertiary hyperthyroidism

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40
Q

adrenocorticotropic hormone (ACTH) chemical structure and cell type

A

peptide, corticotropic cells

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41
Q

ACTH regulation

A

stimulated: by CRH; stimuli that increase CRH release include fever, hypoglycemia, and other stressors

inhib; feedback inhibition exerted by glucocorticoids

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42
Q

ACTH target organs and effects

A

adrenal cortex: promotes release of glucocorticoids and androgens (mineralcorticoids to a lesser extent)

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43
Q

ACTH patho

A

↑ cushings disease

↓ rare

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44
Q

follicle-stimulating hormone (FSH) composition

A

glycoprotein, gonadotropic cells

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45
Q

FSH regulation

A

stimulated; GnRH

inhibi; by feedback inhibition exertion by inhibin, and estrogens in females and testosterone in males

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46
Q

FSH target organ and effect

A

ovaries and testes

in females, stimulates ovarian follice maturation and production of estrogens

in males, stimulates sperm production

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47
Q

FSH patho

A

↑ no important effects

↓ failure of sexual maturation

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48
Q

luteinizing hormone (LH) composition

A

glycoprotein, gonadotropic cells

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49
Q

LH regulation

A

stim; GnRH

inhib; feedback inhibition exerted by estrogens and progesterone in females and testosterone in males

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50
Q

LH target organ and effects

A

ovaries and testes;

females: triggers ovulation, stimulates ovarian production of estrogens and progesterone

males; promotes testosterone production

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51
Q

LH patho

A

same as FSH

↑ no important effects

↓ failure of sexual maturation

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52
Q

prolactin (PRL) composition

A

protein, prolactin cells

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53
Q

PRL regulation

A

stim; decreased PIH; release enhanced by estrogens, birth control pills, breastfeeding, dopamine blocking drugs

inhib; PIH (dopamine)

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54
Q

PIH target organ and effects

A

breast secretory tissue; promotes lactation

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55
Q

PRL patho

A

↑ inappropriate milk proiduction (galactorrhea); cessation of menses in females, impotence in males, low libido, gonadal dysgenesis

↓ poor milk production in nursing women, hypopituitarism, excessive dopamine, D2 agonists

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56
Q

anterior pituitary hormones

A

GH, TSH, ACTH, FSH, LH, PRL

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57
Q

where is insulin synthesized and by what cells

A

beta cells in pancreas

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58
Q

insulin chemical composition

A

2 amino acid chains connected by disulfide linkages

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59
Q

explain the processes of insulin synthesis

A

preproinsulin > proinsulin > exocytosis of insulin and C peptide equally

synthesized by beta cells in pancreas

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60
Q

describe insulin release and circulation

A

insulin is secreted into blood via secretory granules; unbound circulation in blood

half life 6 min, clearance 10-15 min

degraded by insulinase in the liver

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61
Q

why is c peptide measurement useful in type I diabetics?

A

determines how much natural insulin is being produced

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62
Q

explain the activation of target cells by insulin

A

within secs of insulin binding to membrane receptors, 80% of body cells increase glucose uptake (esp muscle and adipose, not neurons in brain)

increased glucose transport into cells > converted into energy

cell membrane more permeable to AA, K+, P+

adjustment of activity levels of enzymes intraceullatrly occur over 10-15 mins

changes rate of transcription and translation at the DNA and RNA level

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63
Q

hypothalamus hormones

A

TRH, CRH, GhRH, GhIH, GnRH, Dopamine/prolactin inhibiting factor, somatostatin, Vasopressin and oxytocin

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64
Q

what are the hormones released by thyroid?

A

thyroxine (T4)
triiodothyronine (T3)
calcitonin

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65
Q

adrenal cortex hormones

A

cortisol

aldosterone

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66
Q

adrenal medulla hormones

A

norepinephrine/epinephrine

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67
Q

pancreas hormoens

A

insulin

glucagon

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68
Q

parathyroid hormones

A

parathyroid hormone

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69
Q

testes hormones

A

testosterone

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70
Q

ovaries hormones

A

estrogen and progesterone

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71
Q

what are steroid hormones synthesized from and stored? lipid or water soluble?

A

synthesized from cholesterol, not stored

lipid soluble

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72
Q

which hormones are amine hormones

A

thyroid and adrenal medullary hormones

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73
Q

what are amine hormones derived from

A

tyrosine

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74
Q

most hormones have what composition?

A

polypeptides and proteins

polypeptides > 100AA = proteins
polypeptides <100AA = peptides

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75
Q

what cellular component are most hormones synthesized on? where are they then transferred to?

A

synthesized on rough end of ER; prohormones transferred to golgi to be packaged into secretory vesicle where they are stored until needed

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76
Q

what is the metabolic clearance rate?

A

rate of removal of hormones from blood

rate of disappearance of hormone from plasma/concentration of hormone

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77
Q

how are hormones cleared from plasma

A

metabolic destruction by tissues, binding with tissues, excretion by liver into bile, excretion by kidneys into urine

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78
Q

what hormones have receptors in or on surface of the cell membrane

A

protein, peptide, catecholamine hormones

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79
Q

what hormones have receptors in the cell cytoplasm

A

steroid hormones

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80
Q

what hormones have receptors in the cell nucleus

A

thyroid hormones

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81
Q

what types of things cause down regulation of hormone receptors

A

inactivation of receptor molecules, inactivation of intracellular protein signaling molecules, destruction of receptors by lysosomes, decreased production of receptors, temp sequestration of receptor to inside of cell

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82
Q

what is a hormone receptor complex

A

formation of complex alters funciton of receptor > activated receptor imitates hormonal effects

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83
Q

describe an ion channel linked receptor

A

all neurotransmitter substances combine with receptors in postsynaptic membrane

change in structure of a receptor (opening/closing a channel for ions)

Na, K, Ca, etc

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84
Q

describe a G protein linked hormone receptor

A

activate receptors that indirectly regulate activity of target proteins by coupling with groups of cell membrane proteins > GTP (G) binding proteins

heterotrimeric guanosine triphosphate, 7-transmembrane segments

inhibitory and stimulating G proteins

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85
Q

describe an enzyme linked hormone receptor

A

proteins that pass through membrane only once; hormone binding site EC and catelytic/enzyme bindnig site IC

ex: tyrosine kinase > leptin receptor

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86
Q

describe IC hormone receptors; activation of genes

A

adrenal and gonadal steroid hormones, thyroid hormones, vit D, and retinoid hormons bind with protein receptors within the cell (lipid soluble, pass through plasma membrane)

activated complex binds with regulatory (promotor) sequence of DNA (hormone response element) > activation/repression of transcription of genes and mRNA

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87
Q

describe the adenylyl cylcase-cAMP second messenger system

A

hormone binds receptor > coupling of receptor to G protein

adenylyl cylase (membrane bound enzyme) > converts small amount of cAMP inside cell > acitvates cAMP dependent protein kinase > phosphorylates > enzyme cascade activated

small amount of hormone = large effect

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88
Q

describe the phospholipase C second messenger system

A

enzyme catalyzes breakdown of phospholipids in cell membrane

PIP2 (second messengers)

  • inositol triphosphate (IP3) > mobilizes Ca ions from mitochondria and ER
  • diacylglycerol (DAG) > activates enzyme protein kinase C
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89
Q

describe thyroid hormones INC gene transcription

A

T3 and T4 bind to receptors in nucleus (receptors = activated transcription factors within chromosomal complex); once bound to intranuclear receptors > thyroid hormones continue to express control function for days/weeks

control function of gene promotors

activate genetic mechanisms for synthesizing many types of IC proteins

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90
Q

what is the main role of the thyroid hormones

A

control bodys metabolic rate

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91
Q

what cellular component forms thyroglobulin

A

ER and golgi apparatus

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92
Q

how/where are T4/T3 formed

A

formed from tyrosine in thyroglobulin molecule

iodine binds with thyroglobin molecule = organification > can store 2-3 months of hormones

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93
Q

what is the iodide pump? what does it do/mechanism?

A

transports iodides from blood into thyroid cells/follicles

sodium iodide symporter (iodide trapping)

basal membrane of thyroid can pump iodide into the cell

symporter co-transports 1 iodide along with 2 sodium ions

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94
Q

where does the energy for the sodium iodide symporter come from

A

NA/K ATPase pump > pumps Na out of cell giving low IC Na conc and gradient for facilitated diffusion of Na into cell

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95
Q

melatonin comes from what gland?

A

pituitary

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96
Q

function of melatonin

A

regulates circadian rhythm and reproductive hormones

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97
Q

hypersecretion of melatonin can result in what

A

in children inhibits sexual development

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98
Q

regulation of melatonin

A 
external light (-)
seratonin
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99
Q

synthesis of melatonin

A

tryptophan > 5htp > seratonin > melatonin

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100
Q

what is necessary for the synthesis of thyroid hormone

A

iodine

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101
Q

in the synthesis of thyroid hormone, iodine transport is ___

A

active

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102
Q

structural difference between T3 and T4

A 
T4 = 2 DIT residues
T3 = 1 DIT residue + 1 MIT residue
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103
Q

structural difference between T3 and T4

A 
T4 = DIT + DIT
T3 = DIT + MIT
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104
Q

explain conversion of T4 > T3

A

follicles of thyroid 5’-deiodinase converts T4 to T3 in peripheral tissue

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105
Q

what factors inhibit peripheral conversion of T4 > T3

A

glucocorticoids, beta-blockers, propylthiouracil (PTU)

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106
Q

what is reverse T3 (rT3)

A

metabolically inactive byproduct of peripheral conversion of T4 and its production

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107
Q

what increases rT3

A

GH and glucocorticoids

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108
Q

functions of thyroid peroxidase

A

oxidation, organification of iodine, coupling of monoiodotyrosine (MIT) and diiodotyrosine (DIT)

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109
Q

explain the release of T4/T3 from thyroid gland

A

cleaved by thyroglobulin molecule > free hormone release

pinocytic vesicles enter thyroid cell > lysosomes fuse with vesicles > proteases digest thyroglobulin adn release T4/T3 > diffuse through base of thyroid cell to capillaries

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110
Q

how is T4/T3 transported to tissues

A

bound to plasma proteins (synthesized in liver) > thyroxine binding globulin

released slwoly to tissue cells > bind with IC proteins and stored

slow onset and long duration of action (long latent period) - max rate after 10-12 days

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111
Q

triiodothyronine (T3) functions

A

7 B’s

-Brain maturation
-Bone growth (synergistic with GH)
-B-adrenergic effects (increases B1 reeptors in heart > increased CO, HR, SV, contractility)
-Basal metabolic rate (via increased Na+/K+- ATPase leading to increased O2 consumption, RR, and body temp)
-Blood sugar (via glycogenolysis and gluconeogensesis)
-Break down lipids (through lipolysis)
Babies > stimulates surfactant synthesis

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112
Q

effects of thyroid functions

A

increase transcription of genes
increase cellular metabolic activity
effects on growth
effects on certain body functions

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113
Q

most thyroxine –>

A

triiodothyronine

prior to acting on genes to INC genetic transcription

1 iodide removed

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114
Q

where are thyroid hormone receptors in relation to DNA?

A

attached to DNA genetic strands OR located in proximity to them

thyroid hormone receptor forms a hetereodimer with retinoid X receptor (RXR) at specific parts of DNA

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115
Q

why is most thyroxine > triiodothyronine

A

IC thyroid receptors have high affinity for T3

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116
Q

what are the cellular metabolic activities of T4/T3

A

increased number, size, and activity of mitochondria

  • total membrane surface area inc in proportion of inc metabolic rate of whole animal
  • inc ATP production

increased active transport of ions through cell membranes

  • Na+/K+ ATPase increased > inc rate of transport of Na and K ions through cell membranes > increases heat in body
  • cell membrane = leaky to Na ions
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117
Q

thyroid function on body tissues

A

normal arterial presure
muscle tremor

effects on:
plasma and liver fats
muscle function
sleep
other endocrine glands
sexual function
increased:
vitamin requirement
BMR
blood flow and CO
HR and heart strength
respiration
GI motility
carb metabolism 
fat metabolism

decreased:
body weight

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118
Q

how does thyroid stimulate carb metabolism

A

rapid glucose uptake by cells, increased glycolysis, increased insulin secretion

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119
Q

how does thyroid stimulate fat metabolism

A

lipids mobilized rapidly from fat tissue, decreasing fat stores in body

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120
Q

what is the thryoid effect on plasma and liver fats

A

increased thyroid hormone > decreased concentration of cholesterol, phospholipids, and TGs BUT increased free fatty acids

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121
Q

explain why thyroid > increased vitamin requirement

A

inc body enzymes, including vitamins. vitamin def with too much thyroid

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122
Q

how does thyroid increase blood flow and CO

A

inc tissue metabolism > inc oxygen use > vasodilation

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123
Q

what regulates thyroid secretion?

A

thyrotropin (TSH) inc thyroid secretion

TRH > stimulates TSH release > stimulates follicular cells

negative feedback control through free T3/T4

  • ant pit > dec sensitivity to TRH
  • hypothalamus > dec TRH secretion

thyroxine binding globulin (TBG) binds most T3/T4 in blood (making it inactive)

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124
Q

functions of TSH

A

increased:

proteolysis of thyroglobulin (w/in 30 mins)
activity of iodide pump
iodination of tyrosine
size and secretory activity of thyroid cells
# of thyroid cells

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125
Q

explain thyroid regulation via cyclic adenosine monophosphate
(activation of second messenger cAMP system of cell)

A

TSH binds with TSH receptors on basal membrane of thyroid cell > adenlyl cylase activated in membrane > inc cAMP formation inside cell, which acts as a 2nd messenger to activate protein kinase > phosphorylations t/o cell > immediate release in secretion of thyroid hormones and prolonged growth of thyroid gland tissue

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126
Q

chemical composition of TSH/thyrotropin

A

glycoprotein

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127
Q

chemical composition of TRH

A

tripeptide amide

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128
Q

explain TRH regulation of TSH secretion

A

TRH secreted by hypothalamus, acts on ant pit to regualte TSH secretion

binds with TRH receptors in pituitary cell membrane > activation of phospholipase 2nd messenger system inside cells > large amts of phospholipase C produced > 2nd messengers inc Ca ions > release of TSH

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129
Q

how does cold exposure affect TRH/TSH

A

cold exposure > excitation of hypothalmic centers for body temp control > inc TSH > > BMR inc 15-20%

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130
Q

explain the effect of excitement/anxiety on TSH

A

anxiety/excitement stimulate sympathetic nervous system > dec in TSH secretion

131
Q

how does prolonged fasting affect TRH

A

TRH neurons in PVN receive input from leptin responsive neurons of hypothalamus that regulate energy balance

prolonged fasting > dec leptin > indirectly inhibits TRH neurons > dec thyroid hormone secretion

132
Q

compare TSH and FT4 levels in hyper- and hypo- thyroidism

A

hyperthyroidism: low TSH, high FT4
hypothyroidism: high TSH, low FT4

133
Q

explain common clinical characteristics of hyperthyroidism

A

high excitability, sweating, heat intolerance, wt loss, diarrhea, muscle weakness, nervousness, fatigue, insomnia, tremor

134
Q

chemical comp melatonin

135
Q

TRH hypersecretion patho

A

increased TRH in 1 or 2 degree hypothyroidism may increase prolactin secretion > galactorrhea

136
Q

hyposecretion of melatonin can lead to..

137
Q

functions TRH

A

increases TSH and PRL

138
Q

functions GnRH

A

increases FSH/LH

139
Q

functions GHRH

A

increases GH

140
Q

functions CRH

A

increases ACTH/MSH/B-endorphin

dec in chronic steroid use

141
Q

function somatostatin

A

dec GH and TSH

142
Q

functions dopamine

A

dec PRL and TSH

143
Q

chemical comp GH/somatotropin

144
Q

chemical comp prolactin PRL

145
Q

chemical comp FSH

A

glycoprotein

146
Q

chemical comp LH

A

glycoprotein

147
Q

chemical comp TSH

A

glycoprotein

148
Q

chemical comp ACTH

149
Q

chemical comp oxytocin

150
Q

chemical comp insulin

151
Q

chemical comp glucagon

152
Q

chemical comp epi/norepi

153
Q

TRH originating organ

A

hypothalmic paraventricular nucleus

154
Q

somatostatin originating cells

A

delta cells of hypothalamus

155
Q

GH/somatotropin functions

A

stim linear growth and muscle mass through IGF1

increases insulin resistance

156
Q

prolactin PRL originating cell

A

lactotrophs of ant pituitary

157
Q

oxytocin originating cells/organs

A

hypothalamus; magnocellular cells of supraoptic and paraventricular nucleus

stored and secreted by post pituitary

158
Q

calcitonin originating cells

A

parafollicular C cells of thyroid

159
Q

calcitonin functions

A

dec bone resorption of Ca2+

160
Q

calcitonin regulation

A

inc serum Ca2+ > inc calcitonin

161
Q

PTH originating cells

A

chief cells of parathyroid

162
Q

PTH function/effects

A

increases:
bone resorption of Ca2+
Ki RA of Ca in DCT

Decreases: RA of Ph in PCT

163
Q

PTH patho

A

↑ primary hyperparathyroid, tertiary hyperparathyroid, PTHrP-secreting tumor

↓ hypoparathyroidism, dec serum Ca, vit D def

164
Q

PTH reg

A

inc PTH = inc Ca2+, PO4^3, Mg2+

dec PTH = dec Mg2+

165
Q

insulin function/effects

A

binds insulin receptors to induce glucose uptake into insulin deep tissues

166
Q

insuilin patho

A

↑ insulinoma

↓ type I DM, type II DM, LADA

167
Q

insulin reg

A

glucose: glc enters B cells > inc ATP > closes K channels to depolarize mmebrane > VGCa open and Ca rushes in to stimulate insulin exocytosis

168
Q

glucagon originating cell

A

pancreatic A cells

169
Q

glucagon function/effects

A

glycogenolysis
gluconeogenesis
lipolysis
ketone production

170
Q

glucagon patho

A

↑ glucagonoma

171
Q

glucagon reg

A

secreted due to hypoglycemia, inhibited by insulin, hyperglycemia, SS

172
Q

somatostatin originating cells

A

Delta cells of pancreas

173
Q

somatostatin function/effects

A

dec GH and TSH

174
Q

amide hormones

A

epi/norepi

thyroid hormones

175
Q

peptide hormones

A

insulin
parathyroid hormone
calcitonin
hypothalmic and pituitary hormones

176
Q

steroid hormones

A 
pregnelone 
cortisol
DHEA/testosterone
estrogens
progesterone
testosterone
vit D
177
Q

pineal gland cells

A 
lobular parenchyma:
pinealocytes (produce/secrete melatonin)
astrocytes
perivascular phagocytes
pineal neurons
peptidergic neuron like cells
178
Q

pineal gland location

A

between 2 brain hemoispheres near back of midbrain, between 2 sup colliculi, behind 3rd ventricle in pineal recess

179
Q

pineal gland structure

A

small reddish gray pinecone shape with pineal stalk; increases size with cold. no blood brain barrier

180
Q

pineal gland function

A

melatonin secretion
reg of pituitary (dec FSH/LH)
drug metabolism
reg bone metabolism

181
Q

central innervation for pineal gland

A

pineal stalk

182
Q

neurons from where innervate pineal gland

A

trigeminal ganglion

183
Q

ant pituitary embryologic development

A

rathkes pouch (oral ectoderm)

184
Q

ant pituitary location

A

vascularly connected to hyopthalamus via hypophyseal portal system

185
Q

ant pituitary function/control

A

all 6 hormones are peptides, all but GH activate target cells via cAMP messenger system, all but two aer tropic hormones

186
Q

post pituitary embryological

A

derived from outpocketing of oral mucosa; neuroectoderm

187
Q

post pituitary structure

A

neural tissue that secretes neurohormones

188
Q

ant pituitary structure

A

glandular tissue

189
Q

post pituitary function/control

A

stores and secrete OT and ADH from hypothalamus

190
Q

ant pituitary embryologic development

A

rathkes pouch (oral ectoderm)

191
Q

ant pituitary location

A

vascularly connected to hyopthalamus via hypophyseal portal system

192
Q

ant pituitary function/control

A

all 6 hormones are peptides, all but GH activate target cells via cAMP messenger system, all but two aer tropic hormones

193
Q

post pituitary embryological

A

derived from outpocketing of oral mucosa; neuroectoderm

194
Q

post pituitary structure

A

neural tissue that secretes neurohormones

195
Q

ant pituitary structure

A

glandular tissue

196
Q

post pituitary function/control

A

stores and secrete OT and ADH from hypothalamus

197
Q

hypothalamus location

A

in brain, connected to pituitary (hypophysis) via stalk called infundibulum

198
Q

hypothalamus organ type

A

neuroendocrine

199
Q

adrenal medulla embryologic

A

neural crest cells

200
Q

adrenal cortex embryologic

A

embryonic mesoderm

201
Q

pineal gland sympathetic innervation

A

sup cervical ganglion

202
Q

pineal gland parasymp innvervation

A

pterygopalatine and otic ganglia

203
Q

pineal gland circulatory pathway

A

blood from choroidal branches of post cerebral; profuse blood flow; NO BLOOD BRAIN BARRIER in capillaries

204
Q

thyroid innervation

A

sup laryngeal nerve

recurrent laryngeal nerve

205
Q

parathyroid embryologic

A

arise from 3rd and 4th branchial pouches

206
Q

parathyroid cells

A

chief cell: predominant epithelial cell, clear cytoplasm

oxyphil cell: eosinophilic granular cytoplasm

207
Q

IGF-1 organ

208
Q

cortisol function/effects

A

↑ appetite, BP, insulin resistance, gluconeogenesis, lipolysis, proteolysis

↓ fibroblast activity, inflammation, immune responses, bone formation, blocks IL2 production

209
Q

ghrelin function

A

stim hunger

210
Q

leptin function

A

satiety hormone

211
Q

aldosterone organ/cells

A

adrenal cortex, zona glomerulosa

212
Q

cortisol organ/cells

A

adrenal cortex, zona fasiculata

213
Q

DHEA organ/cells

A

adrenal cortex, zona reticularies

214
Q

epinephrine/norepi where its made

A

adrenal medulla, chromaffin cells

215
Q

cortisol function/effects

A

↑ appetite, BP, insulin resistance, gluconeogenesis, lipolysis, proteolysis

↓ fibroblast activity, inflammation, immune responses, bone formation, blocks IL2 production

216
Q

explain the biochem/endocrine function of 5 reductase

A

converts testosterone into DHT

217
Q

CKK organ

A

small intestine

218
Q

ANP organ

219
Q

thymopoietin organ

220
Q

explain the biochem/endocrine function of cholesterol

A

cholesterol desmolase > pregnenolone > 17ahydroxylase > 17OHpregnenolone > 17anhydroxylase > DHEA

221
Q

explain the biochem/endocrine function of 17a hydroxylase

A

converts pregnenolone into DHEA and progesterone into androstenedione

222
Q

explain the biochem/endocrine function of aromatase

A

converts androstenedione into estrone and testosterone into estradiol

223
Q

explain the biochem/endocrine function of 21 hydroxylase and 11b hydroxylase

A

convert progesterone > 11deoxycorticosteone > corticosterone (to eventually be made into aldosterone)

224
Q

regulation of calcium in the body

A

regulation via PTH > stim osteoclasts to resorb Ca from bone, increased Ca RA in DCT and inc production of vit D in kidney (decreases renal RA of phosphate)

vit D promotes RA of Ca from bone and small int

calcitonin inhibits osteoclasts, dec absorption of Ca from bone

225
Q

major regulation of PTH

A

ionized/free Ca2+ > chanegs in pH alter PTH secretion

226
Q

hyperadrenalism pathologies

A

cushing syndrome
(primary hyperaldosteronism) - conn syndrome
congenital adrenal hyperplasia

227
Q

vit D conversion

A

D2 (plants/fungi/yeast) and D3 (sun/fish/plants) > 25OHD in liver and 125 OHD in kidney

skin converts 7-DH cholesterol into D3 (cholecalciferol)

228
Q

cushing syndrome sx

A

wt gain, HTN, MOON FACE, abdominal STRIAE, truncal obesity, BUFFALO HUMP, skin changes, osteoporosis, hyperglycermia/IR, amenorrhea, immunosuppresion

229
Q

hyperaldosteronism/Conn syndrome etiology

A

aldosterone-producing adenomas, bilateral adrenal hyperplasia

230
Q

hyperaldosteronism/Conn syndrome RF

A

inc aldosterone, dec renin

secondary: inc aldosterone AND inc renin

231
Q

T3 and T4 are made from

A

coupled tyrosine molecules

232
Q

cushing syndrome etiology

A

inc cortisol

233
Q

cushing syndrome sx

A

wt gain, HTN, MOON FACE, abdominal STRIAE, truncal obesity, BUFFALO HUMP, skin changes, osteoporosis, hyperglycermia/IR, amenorrhea, immunosuppresion

234
Q

primary hyperaldosteronism/Conn syndrome etiology

A

inc aldosterone from adrenal adenoma or BL adrenal hyperplasia, dec renin

secondary: inc aldosterone and inc renin; renovascular HTN, renin tumors, edema from cirrhosis, HF, nephrotic

235
Q

primary hyperaldosteronism/Conn syndrome RF

236
Q

primary hyperaldosteronism/Conn syndrome sx

A

HTN, dec or normal K, metabolic alkalosis, no edema

237
Q

hyperparathyroidism sx

A

stones: calcium oxalate
bones: osteoporosis, osteitis fibrosa cystica, bone pain with inc alk phos
groans: stomach pain, peptic ulcers
moans: depression
thrones: polyuria

238
Q

congenital adrenal hyperplasia clinical characteristics

A

17ahydroxylase: inc mineralcorticoids and BP, dec sex hormones and K. XY ambiguous with undescended testes, XX without secondary development
21hydroxylase: dec mineralcorticoids and BP, inc sex hormones and K/renin. most common, infancy or childhood. XX viralization

11Bhydroxylase: dec aldosterone, inc 11DO corticosterone and BP, inc sex hormones, dec K and renin. XX viralization

239
Q

primary hyperparathyroidism etiology

A

most common primary endocrine disorder after DM

adenoma (80%)
diffuse hyperplasia (10-15%)
carcinoma (1-2%)

240
Q

primary hyperparathyroidism RF

241
Q

primary hyperparathyroidism complications

A

muscle atrophy

acute pancreatitis

242
Q

primary hyperparathyroidism sx

A

stones: calcium oxalate
bones: osteoporosis, osteitis fibrosa cystica, bone pain with inc alk phos
groans: stomach pain, peptic ulcers
moans: depression
thrones: polyuria

243
Q

secondary hyperparathyroidism etiology

A

caused by any condition caused by chronically diminished levels of Ca2+

most commonly from chronic renal failure/insufficiency, inadequate vit D/calcium, steatorrhea

244
Q

hyperpituitarism pathologies

A

acromegaly

gigantism

245
Q

acromegaly etiology

A

excess GH in adults, inc insulin like GF 1

typically caused by pituitary adenoma

246
Q

acromegaly complications

A

inc risk for colorectal polyps + cancer

dilated cardiomyopathy

247
Q

acromegaly sx

A

large tongue with deep furrows, deep voice, large hands/feet, frontal bossing, diaphoresis, insulin resistance, HTN

248
Q

gigantism etiology

A

excess GH in kids

pituitary adenoma
mccune albright syndrome

249
Q

gigantism complications

A

HF most common cause of death (inc size of heart)

250
Q

gigantism sx

A

rapid/excessive growth of long bones (tibia, humerus)

soft tissue/organ growth

251
Q

graves disease etiology

A

autoimmune

252
Q

graves disease RF

A

F 40-60
genetics
stress, tobacco, infxn, iodine exposure
postpartum

253
Q

graves disease sx

A

uniform soft supple goiter

254
Q

inflammatory endocrine pathologies

A

hashimoto thyroiditis

granulomatous subacute thyroiditis

255
Q

diabetes insipidus sx

A

intense thirst and polyuria with inability to concentrate urine due to lack of ADH or failure of response to circulating ADH

dec urine SG
inc serum osmolality

256
Q

endocrine vascular pathologies

A

postpartum pituitary necrosis (Sheehans)

257
Q

infectious endocrine pathologies

A

infectious thyroiditis

waterhouse-friderichsen syndrome

258
Q

diabetes insipidus etiology

A

central:
dec ADH
pituitary tumor, AI, trauma, surgery, ischemic encephalopathy, idiopathic

nephrogenic:
normal or inc ADH
hereditary, hyepr Ca, hypoK, Li, meds

259
Q

diabetes insipidus sx

A

intense thirst and polyuria with inability to concentrate urine
dec urine SG
inc serum osmolality

260
Q

hypoadrenalism pathologies

A

addison disease

primary acute insufficiency (waterhouse-friederichsen syndreome), secondary + tertiary adrenocortical insufficiency

261
Q

addison dz etiology

A

chronic adrenal insufficiency due to adrenal atrophy/destruction by disease

dec gland function > dev cortisol + dec aldosterone

262
Q

addison dz RF

A

autoimmune destruction most common in western world

TB most common in develping world

263
Q

hypoadrenalism/adrenal insufficiency complications

A

may present with shock in acute adrenal crisis

  • pain in lower back, abdomen, legs
  • fever/chills
  • severe vomiting + diarrhea
  • hypotension
  • LOC
264
Q

addison dz sx

A

skin hyperpigmentation
hyperkalemia
hypotension
metabolic acidosis

265
Q

primary acute adrenal insufficiency etiology

A

sudden onset (e.g due to massive hemorrhage)

waterhouse-friderichsen syndrome: due to adrenal hemorrhage associated with septicemia (usu neisseria meningitidis), DIC, endotoxic shock

266
Q

primary acute adrenal insufficiency sx

A

WFS: petechial rash

267
Q

secondary acute adrenocortical insufficiency etiology

A

seen with dec pituitary ACTH production

268
Q

tertiary acute adrenocortical insufficiency etiology

A

seen in pts with chornic exogenous steroid use, precipitated by abrupt withdrawl

269
Q

tertiary acute adrenocortical insufficiency RF

270
Q

secondary acute adrenocortical insufficiency etiology sx

A

NO skin hyperpigmentation

NO hyperkalemia

271
Q

hypoparathyroidism etiology

A

accidental surgical excision, AI desctruction, DiGeorge syndrome

272
Q

hypoparathyroidism sx

A

CATS go numb
tetany, hypocalcemia, hyperphosphatemia

Chvostek sign: contraction of facial muscles
Trousseau sign: carpal spasm

273
Q

hypopituitarism pathologies

A

empty sella syndrome
hypothalmic lesions
sheehan syndrome

274
Q

hypothyroidism etiology

A

nutrient deficiency (iodine or selenium)

275
Q

hypothyroidism sx

A

wt gain, cold intolerance, constipation, coarse skin, depression, poor memory, heavy menses, jaundice

inc TSH, low fT4, normal Ab

(iodine deficient goiter)

276
Q

sheehan syndrome etiology

A

ischemic infarct of pituitary after postpartum bleeding

277
Q

hasimoto thyroiditis RF

A

genetics, environmental toxins, chronic infxns, drugs, meds, smoking, diet (alcohol, goitrogens, gluten, iodine), age, pregnancy, stress, sex hormones

278
Q

hypothyroidism (iodine deficient goiter) etiology

A

nutrient deficiency (iodine or selenium)

279
Q

hypothyroidism sx

A

wt gain, cold intolerance, constipation, coarse skin, depression, poor memory, heavy menses, jaundice

inc TSH, low fT4, normal Ab

280
Q

hasimoto thyroiditis etiology

A

Th1 CD4 cells secrete cytokines that upregulate CD8 cells which cause destruction in thyroid > th2 CD4 > upregulation B cells > antibodies

OR

autoantibodies to thyroid (TPOAb, TgAb)

281
Q

hasimoto thyroiditis complications

A

most common cause of hypothyroid in western world

myxedema coma: weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, shock, death

increased CVD risk
hyperthyroidism
thyroid enlargment
primary B cell lymphoma
papillary thyroid cancer
282
Q

hasimoto thyroiditis sx

A

Weight gain, Cold intolerance, Constipation, Coarse, thin, scaly skin, Non-pitting edema, Dull, thin nails, Loss of ⅓ of eyebrow, dry brittle coarse hair, Decreased sweating, Carpal tunnel syndrome, Heavy menses

dysphagia (esophagus compressed by goiter)
uniform, nontender, locally nodular, irregular goiter
celiac disease

inc TSH, dec fT4, inc TPOAb, TgAB

hurthle cells

283
Q

granulomatous subacute thyroiditis etiology

A

(de Quervain)

self limited diseas eoften followinga flu like illness

284
Q

granulomatous subacute thyroiditis sx

A

inc ESR
jaw pain
tender thyroid

285
Q

diabetes type 1 etiology

A

autoimmune destruction of beta islet cells of pancreas > absolute insulin deficiency

islets infiltrated by t cells + inflammation and destruction ensures > islets develop fibrosis + atrophy

286
Q

DM1 RF

287
Q

DM1 sx

A 
polydipsia
polyuria
polyphagia
wt loss
blurry vision
288
Q

DM1 complications

A

diabetic ketoacidosis; rapid breathig, fruit like odor breath, disorientation, sudden coma

289
Q

DM2 etiology

A

hyperglycemia with insulin resistance and impaired insulin secretion

hyperinsulinemia > insulin ressitance > exhausted pancreas > absolute insulin deficiency

290
Q

DM2 RF

A

obesity, inflammation, aging, genetics, hyperlipidemia, HTN, metabolic syndrome

291
Q

DM2 sx

A

polydipsia, polyphagia, polyuria, wt loss

suspect in any overweight pt with genetic predisposition

292
Q

what is a thyroglossal duct cyst

A

anterior midline neck mass that moves with swallowing or protrusion of tongue (vs persistent cervical sinus leading to branchial cleft cyst in lateral neck)

293
Q

adrenal neoplasm pathologies

A

neuroblastoma

294
Q

pancreas neoplasm pathologies

A

insulinoma

295
Q

parathyroid neoplasm pathologies

296
Q

pituitary neoplasm pathologies

A 
adenoma
prolactinoma
GH adenoma
ACTH adenoma
craniopharyngioma
non-functioning tumor
297
Q

thyroid neoplasm pathologies

A 
adenoma
follicular carcinoma
papillary carcinoma
medullary carcinoma
euthyroid goiter
298
Q

other endocrine neoplasms

A

multipel endocrine neoplasia

types 1 + 2 pheochromocytoma

299
Q

insulinoma etiology

A

derived from pancreatic beta cells > secrete insulin

most common neuroendocrine tumor (2nd is gastrinoma)
10% associated with MEN1

300
Q

neuroblastoma RF

A

most common tumor of adrenal medulla in kids < 4

301
Q

neuroblastoma sx

A

abdominal distention with firm, irregular mass that can cross midline

302
Q

insulinoma complications

A

mets 5-30%

303
Q

insulinoma sx

A

hypoglycemia (whipple triad: hypoglycemia, sx of hypoG, resolution of sx after glc levels normalize)
dec blood glucose

inc insulin
inc proinsulin
inc c peptide

304
Q

parathyroid adenoma etiology

305
Q

infectious thyroiditis etiology

A

rare; bacterial, fungal, parasite

staph aureus

306
Q

waterhouse-friderichsen syndrome etiology

A

acute primary adrenal insufficiency due to adrenal hemorrhage

associated with septicemia from neisseria meningitidis, DIC, endotoxic shock

307
Q

most common cause of hypopituitarism

A

macroadenoma

308
Q

most common pituitary neoplasm

A

prolactinoma

309
Q

prolactinomas sx

A

females: galactorrhea, amenorrhea/oligomenorrhea, infertility, dec libido, low estrogen > menopausal sx, osteoporosis
males: dec libido, impotence (more common sx in men since dx is often later)

310
Q

pituitary adeoma/macroadenoma general sx

A

mass effect:
visual field defects (bitemporal hemianopsia)
inc intracranial pressure (headache, N/V)

depression, anxiety

311
Q

craniopharyngioma complications

A

pituitary tumor; causes secondary (central) hypothyroidism, dec TSH, dec fT4

312
Q

ACTH adenoma clinical characteristics

A

increased ACTH > increased cortisol + other adrenal secretions

cushings syndrome
obesity, central fat, moon face
hirsuitism excess hair
purple striae, easy bruising
superficial fungal infections
osteopenia, osteoporosis
diabetes, HTN
menstrual/mental abnormalities
313
Q

what is a nonfunctional tumor

A

one that does not have sx related to secreting excessive hormones, but may secrete other peptides

314
Q

toxic thyroid adenoma etiology

A

low iodine

315
Q

toxic thyroid adenoma sx

A

solitary palpable hot nodule

dec TSH, inc fT4/T3, inc RAIU uptake

316
Q

pheochromocytoma etiology

A

most common neoplasm of adrenal medulla (rare)

secrete excess catecholamines, often cause severe HTN

rule of 10%
extraadrenal
bilateral
malignant
arise in kids
calcify
occur with other endocrine neoplasms (MENS)
317
Q

pheochromocytoma complications

A

sever HTN

may induce stroke, MI, fatal cardiac arrhythmia

318
Q

pheochromocytoma sx

A 
palpitations
tachycardia
headache
profuse sweating
N/V
abdominal and chest pain
insomnia
319
Q

infectious thyroiditis lab values

A

inc TSH, low fT4

320
Q

pathway of synthesis of adrenal steroids: progesterone and 17oh pregnenolone

A

cholesterol > pregnenolone (ZG) >:

  1. (17ahydroxylase) > 17OH pregnenolone (ZF)
  2. progesterone (ZG) > (17ahydroxylase) > 17OH progesterone
321
Q

pathway of synthesis of adrenal steroids: aldosterone

A

progesterone (ZG) > (21hydrozylase) > 11deoxycorticosterone (ZG)> (11bhydroxylase) > corticosterone (ZG) > aldosterone (ZG)

322
Q

pathway of synthesis of adrenal steroids: cortisone

A

17 hydroxypregnenolone (ZF) > 17hydroxyprogesterone (ZF) > (21 hydroxylase) > 11 deoxycortisol (ZF) > (11bhydroxylase) > cortisol (ZF) > cortisone (ZF)

323
Q

pathway of synthesis of adrenal steroids: estradiol, testosterone, DHEA

A
  1. 17 hydroxypregnenolone (ZF) > 17hydroxyprogesterone (ZF) > androstenedione (ZR) > testosterone (ZR) + estrone (PT) > estradiol (PT)
  2. 17 hydroxypregnenolone (ZF) > DHEA (ZR):
    > DHEA-s (ZR)
    > androstenedione (ZR) > testosterone (ZR) + estrone (PT) > estradiol (PT)

NPLEX (28 decks)

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