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BECOM II Exam 4 > Endocrine > Flashcards

Endocrine Flashcards

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1
Q

neurosecretory cells

A

above the pituitary

secrete hormones that control the anterior pituitary

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2
Q

hypothalamic/hypophyseal portal circulation

A

hypothalamic hormones released to special capillaries that feed the anterior pituitary inferiorly

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3
Q

anterior pituitary

A

derived from epithelial lining from mouth

3/4 of adult pituitary size

doubles during pregnancy –> pituitary infarctions

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4
Q

thyrotrophs

A

stimulated by TRH

secrete thyrotropin (TSH)

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5
Q

gonadotrophs

A

stimulated by GnRH

secrete gonadotropins (LH, FSH)

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6
Q

corticotrophs

A

stimulated by CRH

secrete ACTH

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7
Q

somatotrophs

A

stimulated by GHRH; inhibited by somatostatin

secrete GH

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8
Q

what are hormones released from the hypothalamus?

A

releasing hormones - can be stimulating or inhibitory

small peptides with pulsatile secretion & short half-lives

travel to the anterior pituitary for regulation

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9
Q

what are hormones released from the anterior pituitary?

A

tropic hormones

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10
Q

pulsatile secretion

A

critical for hypothalamic releasing hormone function

constant stimulation can shut down the response (ex. constant secretion of GnRH can shut down release of LH & FSH

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11
Q

circadian rhythm

A

regulation of hypothalamic releasing hormones

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12
Q

Corticotropin releasing hormone (CRH)

A

stimulates ACTH release

production of glucocorticoids by and androgens by adrenal cortex

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13
Q

Thyrotropin releasing hormone (TRH)

A

stimulates TSH release and prolactin (PRL)

production of thyroid hormones (T3,T4)

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14
Q

Growth hormone releasing hormone (GHRH)

A

stimulates GH release

postnatal body growth

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15
Q

Luteinizing hormone releasing hormone (LHRH) aka GnRH

A

stimulates FSH and LH release

ovulation, progesterone & estrogen production, testosterone production

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16
Q

Somatostatin, somatotropin release inhibiting factor (SRIF)

A

inhibits GH (&GHRH) and TSH release

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17
Q

Prolactin (PRL)

A

milk production by mammary glands

inhibited by dopamine; stimulated by TRH

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18
Q

Dopamine

A

inhibits prolactin secretion

can have leaking milk from breasts with antagonists

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19
Q

lactotrophs

A

stimulated by TRH; inhibited by dopamine

release prolactin (PRL)

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20
Q

What hormone is released in direct response to hypothalamic TRH?

A

prolactin

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21
Q

role of ACTH

A

increases synthesis of glucocorticoids and androgens in adrenal cortex

proliferation, maintenance of adrenal cortex

cAMP as 2nd messenger

synthesized from POMC (alpha-MSH & CLIP) in corticotrophs

released in response to stress

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22
Q

What is a negative feedback of ACTH and CRH release?

A

cortisol

excessive glucocorticoids over time - shut down ACTH and CRH –> adrenal cortex will atrophy

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23
Q

What happens if you have too much ACTH?

A

hyperpigmentation - stimulating melanocyte synthesis from alpha-MSH in the POMC

Addison’s disease

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24
Q

What is the enzyme used to cleave POMC?

A

pro hormone convertase I –> cleaves to ACTH and beta-lipoprotein

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25
Q

role of ADH (AVP) in ACTH release

A

stimulates production of ACTH by thirst response stress

increases BP indirectly by the production of cortisol

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26
Q

role of CRH

A

comes from the paraventricular nucleus in the hypothalamus - stimulate release of ACTH in anterior pituitary

binds to receptors on corticotrophs –> increase cAMP –> activate PKA –> POMC production/cleavage

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27
Q

role of glucocorticoids

A

negative feedback on ACTH and CRH

excessive ACTH w/o cortisol

dexamethasone suppression of ACTH

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28
Q

congenital adrenal hyperplasia

A

elevated ACTH due to lack of glucocorticoid synthesis –> adrenal hypertrophy and hyperplasia

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29
Q

what is the response to stress?

A

increased CRH secretion - stress signals override
-released during starvation

chronic stress - increases threshold for negative feedback…brain does not respond to cortisol & keeps making ACTH

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30
Q

TSH aka thyrotropin

A

share the same alpha chain with LH & FSH

regulates T3, T4 production and proliferation of thyroid follicular cells

stimulated by TRH; inhibited by thyroid hormones & somatostatin

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31
Q

what leads to an enlarged thyroid (goiter)?

A

no production of thyroid hormone to produce the negative feedback –> release too much TSH

prevented by iodine supplements

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32
Q

growth hormone (GH) aka somatotropin

A

most abundant in anterior pituitary

stimulated by GHRH; inhibited by somatostatin

filtered & eradicated quickly - short half life

JAK/STAT signaling

pulsatility higher at night & in adolescence

also acts on IGF (somatomiden)

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33
Q

somatostatin

A

inhibits GH and GHRH

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34
Q

What stimulates the release of GH?

A
  • GHRH
  • starvation, low glucose
  • gherlin
  • exercise & stress
  • thyroid hormones
  • high levels of amino acids

increases glucose levels, shuts down insulin, releases energy

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35
Q

what are the direct actions of growth hormones?

A

breaks fats (lipolysis) & glycogen –> liberates energy
oxidation of FA
ketogenic
prevents sugar uptake
inhibits insulin - diabetes
increase thyroid secretion
does not break proteins - increases synthesis & transport

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36
Q

Anabolic actions of growth hormone

A

mediated through IGF-1 (somatomedin)

increases muscle mass (protein synthesis), growth, & bone density

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37
Q

somatomedin C

A

longer half life than GH - more accurate measurement when testing to see if someone is deficient
-last longer in blood

bone and cartilage growth when stimulated by GH

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38
Q

Gigantism

A

overproduction of GH before the epiphyseal plates close

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39
Q

Acromegaly

A

overproduction of GH after the epiphyseal plates have closed –> thicker bones

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40
Q

Laron syndrome

A

GH deficiency

  • pituitary dwarfism
  • IGF deficiency
  • GH receptor mutation

will have low sugar, obesity, low muscle mass, high LDL and cholesterol, premature aging

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41
Q

role of Prolactin

A

made in lactotrophs

  • JAK/STAT signaling
  • stimulated by TRH; inhibited by dopamine
  • increase breast development & milk production
  • decrease release of LH and FSH - suppress pulses
  • absence or excess can cause infertility or cancer (breast or prostate)
  • suppress kisspeptin
  • regulation of steroid genesis
  • immune - associated w/ autoimmune diseases
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42
Q

Kisspeptin

A

peptide in hypothalamus that produces GnRH

inhibited by prolactin

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43
Q

treatment for excess prolactin secretion?

A

dopamine agonist - natural inhibitor of prolactin

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44
Q

posterior pituitary

A
  • neuroendocrine system
  • does not produce hormones
  • stores & releases oxytocin & ADH
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45
Q

oxytocin role

A

uterine contraction, milk ejection

  • levels and receptors increased during pregnancy
  • stop postpartum hemorrhage
  • linked to limbic system (emotions)
  • similar structure to ADH - water retention, [] urine, decrease urine output, increase Na+ loss
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46
Q

ADH (vasopressin) role

A

conserve water, concentrate urine

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47
Q

where are the neuron bodies located?

A

paraventricular and supraoptic nucleus in hypothalamus - secrete oxytocin & ADH - stored in posterior pituitary

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48
Q

mechanism of oxytocin

A

activates G coupled receptor –> activate PI3K

PKC and PLC increase intracellular contraction causing contraction

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49
Q

other functions of oxytocin

A
  • limbic system - maternal and social bonding
  • methylation in receptor - autism
  • role in cardiomyocytes & neural development
  • anti-depressants
  • inhibit fear
  • decreases cortisol levels
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50
Q

release of oxytocin

A
  • sucking on nipple
  • site & sound of infant
  • downward movement of fetus through birth canal
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51
Q

ADH role

A
  • water, salt, urea retention –> prevent dehydration
  • constriction of blood vessels
  • increase ACTH secretion
  • increase urine osmolarity
  • upregulate AQPA2 through cAMP/PKA signaling
  • increase Na+/K+ pump, NKCC, ROMK, NCC, ENaC, UTA-1,3
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52
Q

release of ADH

A
  • increased plasma osmolality
  • drop in blood volume
  • angiotensin II
  • thirst reflex
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53
Q

diabetes insipidus

A
  • lack of functioning ADH receptors or AQP2
  • chronic lithium ingestion
  • amyloid degeneration, polycystic kidney disease

effects: thirsty, dilute urine, hyperosmolarity blood, excess urine, hypokalemia

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54
Q

central vs. nephrogenic diabetes insipidus

A

central - no production of ADH; giving ADH helps the functioning

nephrogenic - receptors are hindered; giving more ADH does not help

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55
Q

SIADH

A

excess ADH secretion –> hyponatremia, [] urine

  • ectopic expression of ADH from tumor
  • not much change in volume due to ANP effects
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56
Q

why do you not give salt to SIADH patients?

A

will demyelinate neurons & destroy CNS

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57
Q

Another name for Anterior Pituitary

A

adenohypophysis

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58
Q

another name for Posterior Pituitary

A

neurohypophysis

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59
Q

anterior pituitary parts

A
  1. pars tuberalis - wraps around infundibulum
  2. pars intermedia - divides anterior/posterior; adjacent to pars nervosa
  3. pars distalis - largest; anterior lobe
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60
Q

posterior pituitary parts

A
  1. pars nervosa - largest

2. pars infundibulum - connecting stalk to hypothalamus

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61
Q

hormones released from posterior pituitary

A

oxytocin, ADH

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62
Q

hormones released from anterior pituitary

A

LH, FSH, ACTH, TSH

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63
Q

Hypophyseal (rathke) pouch

A

formed from oral ectoderm

forms the anterior pituitary

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64
Q

Neurohyphyseal pouch/bud

A

formed from neuroectoderm

forms the posterior pituitary

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65
Q

Hypothalamic-Hypophyseal Tract

A
  • communication b/w hypothalamus & posterior pituitary (nerves)
  • supraoptic nuclei –> synthesize ADH
  • paraventricular nuclei –> synthesize oxytocin
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66
Q

Hypothalamic-Hypophyseal Portal System

A
  • communication b/w hypothalamus & anterior pituitary (blood vessels)
  • superior hypophyseal arteries –> hypophyseal portal veins
  • 2 plexuses
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67
Q

what does the superior hypophyseal artery supply?

A

infundibulum & median eminence

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68
Q

what does the inferior hypophyseal artery supply?

A

posterior hypothalamus

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69
Q

Pars Distalis

A
  1. chromophils –> acidophils (acidic), basophils (basic)

2. chromophobes - no stain; little cytoplasm

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70
Q

acidophils - pars distalis

A
  1. somatotrophs (most) - secrete GH (somatostatin)
  2. mammotrophs (lactotrophs) - secrete PRL

polypeptide hormones

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71
Q

basophils - pars distalis

A
  1. gonadotrophs - secrete FSH, LH, & ICSH (in males)
  2. thyrotrophs - secrete TSH
  3. corticotrophs - secrete ACTH & LPH

glycoprotein hormones

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72
Q

Pars Tuberalis

A

mostly gonadotrophs (FSH, LH)

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73
Q

Pars Intermedius

A 
mostly corticotrophs (ACTH) & chromophores
cleave POTC (MSH)
colloid filled cysts (remnants of rathke)
infiltration of basophils into pars nervosa
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74
Q

Pars nervosa

A

no synthesis of hormones
PVN & SON –> neurosecretory bodies (NB)
Pituicytes - supporting glial cells for neurons

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75
Q

Pituitary Adenomas

A
  • growth in pituitary - overproduction of certain cell types (acidophils or basophils)
  • release hormone in high amounts
  • hormone producing (PRL, ACTH, GH)
  • nonfunctioning - can compress on hypothalamus & optic chiasm
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76
Q

Thyroid

A
  • produces T3,T4, & calcitonin
  • hormone stored outside of cells (lumen of follicle) & can be held for a long time
  • follicular (thyroytes) & parafollicular (C cells)
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77
Q

Follicular Cells aka thyrocytes

A
  • squamous or columnar - depending on activity
  • produce thyroglobulin stored in colloid lumen
  • rich in RER for protein synthesis
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78
Q

Parafollicular (C) cells

A
  • larger, lighter staining
  • produce calcitonin
  • upregulated Golgi apparatus for calcitonin synthesis
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79
Q

Parathyroid gland

A
  • PTH release - Ca++ regulation
  • supplied by inferior thyroid arteries
  1. Principle cells - secrete PTH; replaced w/ adipocytes during aging
  2. Oxyphil cells - nonfunctional; less PTH synthesis; more cytoplasm staining
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80
Q

Adrenal Glands

A
  • supplied by superior, middle, inferior suprarenal arteries
  • drained by suprarenal vein
  • cortex and medulla
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81
Q

Adrenal Cortex

A

no granules - secrete steroids (lipid soluble) instead of proteins - large amount of smooth ER

3 zones: zona glomerulosa, fasciculata, reticularis

82
Q

zona glomerulosa

A

secrete mineralocorticoids - ex. aldosterone

-ion regulation

83
Q

zona fasciculata

A

secrete glucocorticoids - ex. cortisol

-glucose metabolism, immune response

84
Q

zona reticularis

A

secrete androgens - ex. DHEA

-precursor for testosterone

85
Q

Addison’s disease

A

autoimmune - adrenal cortical insufficiency

-degeneration of adrenal cortex –> loss of hormone synthesis

86
Q

Adrenal Medulla

A

Chromaffin cells (arise from neural crest) –> produces Epi and NE (catecholamines)

NE = more e- dense; chromagranin proteins
Epi = less e- dense
87
Q

Pineal Gland aka epiphysis cerebri

A
  • regulates daily rhythms
  • pinealocytes - produce melatonin
  • corpus arenaceum “Brain Sand”
88
Q

beginning molecule for steroidogenesis

A

cholesterol

  • cleaved by cholesterol esterase
  • transported across mitochondria membrane by StAR
  • no StAR –> no steroidogensis
89
Q

What enzyme is used for the 1st step of side chain cleavage of cholesterol?

A

CYP11A1

-cleaves to pregnenolone

90
Q

the precursor for aldosterone

A

corticosterone

91
Q

the limiting step in aldosterone synthesis

A

aldosterone synthase (CYP11B2)

  • need ACTH, but also 2nd stimulus (K+, SNS, or angII)
  • won’t have hyperaldosteronemia w/ excess ACTH
92
Q

17-alpha hydroxylase enzyme (CYP17A1)

A
  • convertes pregnenolone and progesterone
  • not found in zona glomerulosa
  • mutation –> entire kidney would be glomerulosa and produce only aldosterone
  • needed to make cortisol & DHEA
93
Q

17, 20-lyase enzyme (CYP17A1)

A

converts from 21 C to 19 C androgens (DHEA & androstenedione)

94
Q

role of DHEA

A
  • main androgen produced by adrenal cortex
  • water soluble, sulfated –> weak steroid/androgen
  • organ must have sulfatase to use it or be able to convert to stronger Androstenedione
95
Q

mutation in 3beta-hydroxysteroid dehydrogenase (HSD3B2)

A

adrenals will only make androgens (DHEA)

96
Q

enzyme 11beta-hydroxylase (CYP11B2)

A

deoxycorticosterone –> corticosterone

deoxycycortisol –> cortisol

97
Q

how are androgens removed from the body?

A

secreted as ketones in the urine

-measure ketone [] in urine to estimate DHEA levels in blood

98
Q

CYP17 - 17alpha-hydroxylase mutation

A

low cortisol & DHEA

-no negative feedback of cortisol –> high ACTH –> hyper pigmentation

99
Q

CYP21A2 - 21 hydroxylase mutation

A
  • low deoxycortisol and cortisol
  • don’t need much aldosterone (won’t have hypoaldosteronemia)
  • high ACTH and DHEA
100
Q

CYP11B1 - 11beta-hydroxylase mutation

A
  • high deoxycortisol

- low cortisol –> continued stimulation from ACTH

101
Q

enzyme HSD11B2

A

converts active cortisol to inactive cortisone

  • cortisol - same actions as aldosterone & same affinity to MR
  • HSD1 = gives you active form
  • HSD2 = gives you inactive form
102
Q

deficiency in HSD11B2

A

renal tubules cannot convert to inactive cortisone –> apparent hyperaldosteronemia but aldosterone levels are normal

103
Q

aldosterone role

A

-carried by albumin & CBG (lower affinity & can be displaced by excessive cortisol) –> high aldosterone in blood (Na+ retention, HTN, K+/H+ secretion)

104
Q

aldosterone actions on nephron

A
  • increase Na+ reabsorption & K+ secretion
  • increase H+ secretion & bicarb reabsorption (metabolic alkalosis)
  • HTN, hypokalemia, metabolic alkalosis**
105
Q

aldosterone escape

A

not always hypernatremia w/ high aldosterone

  1. prevent long term Na+ retention by ANP
    - released from atrial stretching –> filter more water & inhibit Na+ reabsorption
  2. pressure natriuresis in HTN
106
Q

primary hyperaldosteronemia

A

tumor in glomerulosa

  • high aldosterone release
  • normal levels of renin
107
Q

secondary hyperaldosteronemia

A

excess activation of RAAS

-high renin and aldosterone

108
Q

glucocorticoids - cortisol

A
  • binds to CBG (higher affinity than aldosterone)
  • increase CBC & total blood cortisol w/ pregnancy
  • released more in morning (circadian)
  • synthesis by ACTH
  • metabolism - breaks fat & proteins, liberates glucose, insulin resistance
109
Q

result of long term treatment w/ glucocorticoids

A

negative feedback of cortisol on ACTH –> reticularis and fasciculata atrophy

110
Q

glucocorticoids in metabolism

A
  • glycogenolysis, gluconeogenesis
  • insulin resistance
  • lipolysis
  • ketogenesis (energy for CNS)
  • increase receptors for NE, Epi, and glucagon
  • increase adipocytes in long term excess (buffalo hump)
  • deficiency –> hypoglycemia
111
Q

cortisol vs. GH

A
  • both ketogenic, lead to diabetics, same action on lipids/carbs
  • cortisol –> breaks proteins
  • GH –> builds proteins
112
Q

glucocorticoids - non metabolic actions

A
  • SNS - increase alpha adrenergic receptors (HTN)
  • inhibit keratinocytes & collagen –> stretch marks, striae
  • promote osteoclasts –> osteoporosis
  • Na+ retention (HTN) –> releasing aldosterone from CBG
  • lung maturation, fetal development
  • activation of lactation by PRL
  • anti-inflammation –> block leukotrienes/prostaglandins and suppress inflammatory mediators
113
Q

Cushing’s disease

A

excess glucocorticoids

  • muscle wasting
  • striae
  • obesity (buffalo hump) - high fats/sugars
  • poor wound healing, susceptible to infection
  • osteoporosis
  • HTN
  • mood disturbances
114
Q

glucocorticoid deficiency

A

long term exogenous treatment –> shrinkage of adrenal cortex due to low ACTH
low levels of cortisol –> excess ACTH –> hyperpigment
-stress intolerance
-hypoglycemia
-low BP

115
Q

DHEA

A

androgen

  • converted to androstenedione then to estriol in placenta (estriol then converted to estrogen)
  • pubic/axillary hair, maintains sex drive
116
Q

adrenogenital syndrome - excessive DHEA

A

-deep voice, excess hair, more muscles, smaller breasts, ambiguous genitalia, precocious pseudo puberty

117
Q

Addison’s disease

A

primary adrenocortical insufficiency

  • autoimmune
  • aldosterone deficiency (hyperkalemia, hyponatremia etc.)
  • cortisol deficiency (hypoglycemia, low BP)
  • DHEA deficiency (lack of hair)
  • excess ACTH –> hyper pigmentation
118
Q

Adrenal Medulla

A

chromaffin cells - 20% NE, 80% Epi

  • modified post-ganglionic fibers that give catecholamines to blood
  • excess –> phaeochromocytoma
119
Q

thyroid gland

A
  • thyroid follicle (functional unit)
  • Thyroglobulin in colloid
  • SNS –> vasodilation –> increase T4 in blood
  • parafollicular cells (secrete calcitonin)
120
Q

T4 (thyroxin)

A
  • inactive, most abundant
  • transported in blood
  • converted to T3 in tissues
121
Q

T3

A
  • active, found in tissues

- not in blood

122
Q

rT3 (reverse T3)

A

antagonist to T3

  • prevents conversion from T4 to T3
  • produced by D3
123
Q

Thyroglobulin (Tg) synthesis

A

make Tg from ER and Golgi

  • contains a lot of tyrosines & some iodine
  • used as biomarker for thyroid cancer (found in blood when normally aren’t)
124
Q

1st step in thyroid hormone synthesis

A

make Tg & exocytose into colloid

125
Q

2nd step in thyroid hormone synthesis

A

bring Na+ and iodine in through NIS symporter

126
Q

role of thyroperoxidase (TPO)

A
  • removes charge from iodine
  • couples iodine with Tg (organification of I-)
  • upregulated by TSH & hCG during pregnancy
  • inhibitors useful for hyperthyroidism
127
Q

T1 (MIT), T2 (DIT)

A

not permeable, cannot escape, recycles

  • nonfunctional
  • failure to recycle (deficiency in iodotyrosine deiodinase) –> lost in urine –> iodine deficiency
128
Q

T3, T4

A

lipophilic, secreted out of cell

  • functional
  • T3 - has negative feedback on TRH, TSH
129
Q

role of penderin

A

move iodine into colloid with the exchange of Cl- to be acted on by TPO
-deficiency –> hypothyroidism

130
Q

TSH effect

A
  • upregulate all processes (NIS, TPO, endocytosis)
  • cause follicular cell to phagocytose the Tg in the colloid with the bound iodine
  • produces T3,T4,rT3
  • production & proliferation of follicular cells
131
Q

NIS

A

Na+/I- symporter

-can also transport bromide, thiocyanate, and perchlorate after ingestion of radioactive iodine

132
Q

what can also be transported via NIS for imaging?

A

Technetium

133
Q

increased demand of Iodine (ex. high TSH)

A
  • won’t make as much T4 (Tg/I- not in follicle as long)
  • more T3 active is produced instead
  • faster turnaround
134
Q

thyroxine binding globulin (TBG) aka Tg

A
  • carries T3, T4 (T4 higher affinity, longer half-life in blood)
  • aspirin & other drugs compete for TBG (too much T4 in blood leading to hyperthyroidism)
135
Q

hCG in pregnancy

A
  • mimics TSH on follicular cells
  • increase TBG and T3, T4 levels
  • amount bound and free is normal (increasing both)
  • elevated total thyroid level
136
Q

deionization of thyroid hormones in tissues

A

Selenodeionidases enzyme (selenium core)

  • deficiency (high T4, low T3)
  • D1 (all tissue) –> activates T4 to T3
  • D2 (CNS) –> activates T4 to T3
  • D4 –> inactivates both T4, T3
137
Q

iodine deficiency

A

-won’t make enough T3 (no negative feedback on TRH or TSH) –> excess TSH –> goiter of thyroid

138
Q

TSHR

A

G protein coupled

-increase cAMP and PLC in follicular cells

139
Q

role of sympathetic activation on thyroid

A

increase blood flow –> increase TSH to follicular cells –> more T3,T4 release

140
Q

Thyroid hormone receptor (TR) signaling

A
  1. nuclear receptor activation
    - higher affinity for T3 than T4
  2. has non-classical activation of membrane receptor as well (immediate actions)
141
Q

T3 effects

A
  1. brain development and growth
    - stimulate somatotrophs to release GH & IGF-1 for bone & muscle production
  2. increase BMR (thermogenesis)
    - increase oxidative respiration and UCP-1 to increase heat
  3. Metabolic
    - high glucose absorption, liberate glucose, breaks fat (lowers cholesterol), increase protein synthesis & degradation
  4. cardiovascular
    - increase adrenergic receptors/Beta1 (increase HR) -water hammer pulse
    - increase CO, alpha myosin heavy chain, SR Ca++ ATPase
  5. glucocorticoid inactivation –> high ACTH
142
Q

hyperthyroidism/thyrotoxicosis

A
  • excess TSRH, TSH, T4 to T3 conversion (D1)
  • thyroid tumor
  • immunoglobulins (graves disease)
  • high hCG during pregnant
143
Q

how anti-TSHR (immunoglobulins) leads to goiter

A

stimulates production of T3,T4 –> no negative feedback –> excess TSH –> goiter

144
Q

hyperthyroidism effects

A
  • heat intolerance, weight loss, hyperreflexia, palpitations, water hammer pulse
  • goiter in graves
145
Q

hypothyroidism effects

A
  • cold sensitivity, weight gain, slow reflexes, bradycardia
  • selenium deficiency (can’t convert T4 to T3, high TSH w/o negative feedback, goiter)
  • wolf chaikoff - NIS overload with iodine
146
Q

3 hormones that regulate plasma Ca2+

A
  • PTH
  • Vitamin D
  • Calcitonin
147
Q

the precursor for Vitamin D

A

cholecalciferol (D3)

  • inactive
  • made from cholesterol in skin & UV light
148
Q

self-limiting step in activation of Vitamin D

A

25-hydroxycholecalciferol

  • conversion in liver; inactive
  • negative feedback in excess
  • adding more Vit. D3 won’t make more
149
Q

activated form of Vitamin D

A

1,25-dihydroxycholecalciferol

  • conversion in kidney; active
  • PTH dependent (activated by low Ca2+)
150
Q

24, 25-dihydroxycholecalciferol

A
  • formed during high Ca2+, low PTH

- antagonist to stop making Ca2++

151
Q

vitamin D actions

A
  • activates nuclear retinoid X receptor
  • increase calbindin in intestines (increase Ca2+ absorption)
  • increase Ca2+ ATPase, NCX1, TRPV5,6 & phosphatase
  • low doses –> bone calcification
  • high doses –> bone resorption
  • anti-depressant
  • metabolites can inhibit lung cancer progression
  • increase muscle strength, activate T cells, anti-oxidants
152
Q

function of calbindin

A

shuttles absorbed Ca2+ into basolateral side from luminal side

153
Q

response to PTH

A

keep Ca2+, dump the phosphate

154
Q

PTH

A

lung peptide; main regulator for Ca2+ - increase plasma levels during hypocalcemia

  • also activates vitamin D
  • activated during low Ca2+ levels, inhibited during high levels
155
Q

effect of damaged or removed parathyroid

A

hypocalcemia - Ca2+ supplements the rest of life

156
Q

PTH-related peptide

A

secreted by cancer cells –> more Ca2+ and bone reabsorption –> hypercalcemia

157
Q

rapid effects (1st response) to PTH

A

osteolytic membrane (fluid b/w osteocytes & matrix)

  • contains already dissolved Ca2+
  • increase Ca++ pumps
  • fast (immediate) release of Ca2+ to blood
158
Q

slow/long term (2nd response) to PTH

A

activation of osteoclasts

  • no receptors on osteoclasts, so activate osteoblasts 1st
  • osteoblasts –> secrete RANKL and M-CSF that bind to preosteoclasts –> differentiate and proliferate osteoclasts
  • suppress OPG (OPG prevents RANKL binding)
159
Q

role of osteoclasts

A

destroy bone and release Ca2+

160
Q

other PTH effects

A
  • increase Ca2+ and Mg2+ reabsorption - high levels in blood
  • increase Na+ & phosphate loss - high levels in urine
  • increase 1,25-dihydroxycholecalciferol (increase intestinal Ca2+ and phosphate absorption)
161
Q

regulation of PTH

A
  • low Ca2+ levels –> increase PTH
  • high Ca2+ or vitamin D levels –> decrease PTH
  • high Ca2+ –> stimulate Ca2+ sensitive receptors (CaSR) –> shut down PTH due to activation of IP3 and DAG
162
Q

Calcitonin

A
  • produced by C cells of thyroid
  • released in response to high Ca2+
  • lowers blood Ca2+ by inhibiting activation of osteoclasts
163
Q

PTH hyper secretion (hyperparathyroidism)

A
  • hypercalcemia, hyperphosphaturia, renal stones (Ca2+ in urine after Tm is reached), bone decalcification
  • increase osteoblasts activity
  • low reflexes, arrhythmia
164
Q

PTH hypo secretion (hypoparathyroidism)

A
  • hypocalcemia and hyperphosphatemia

- hyperreflexes and tetany

165
Q

Vitamin D deficiency

A

children - rickets

adults - osteomalacia (soft bones)

166
Q

causes of osteoporosis

A
  • estrogen deficiency
  • malnutrition
  • lack of exercise
  • lack of Vit. C (builds framework of bones)
  • Cushing’s (excessive ACTH and cortisol) -cortisol stimulates osteoclasts
167
Q

pancreatic beta cells

A

secrete amylin and insulin

168
Q

pancreatic alpha cells

A

secrete glucagon

169
Q

pancreatic delta cells

A

secrete somatostatin

170
Q

pancreatic F cells

A

secrete pancreatic polypeptide (PP)

171
Q

pancreatic epsilon cells

A

secrete gherlin (suppresses insulin & slows down emptying of stomach)

172
Q

pancreatic amylin role

A
  • controls appetite - weight loss
  • satiety
  • increase emptying time of stomach - fuller longer
  • inhibit glucagon secretion
173
Q

pancreatic somatostatin

A
  • inhibits secretion of insulin, glucagon, PP
  • more inhibition of beta cells rather than alpha cells
  • stimulated by glucose, AA ingestion
  • reduces GI motility
174
Q

pancreatic peptide (PP)

A
  • reduce gastric secretion and emptying time

- marker for pancreatic cancer

175
Q

what is the precursor for insulin?

A

preproinsulin

176
Q

what enzyme converts proinsulin to insulin?

A

pro hormone convertase (PC1/3) - cleaves 2 AAs out of C peptide

  • get A, B, or C peptide fragment
  • separate C peptide from insulin
177
Q

role of C peptide

A
  • indicator for insulin secretion (high levels = insulin resistance)
  • protect against neuropathy, renal, and vascular damage
  • biomarker in gastric cancer
178
Q

regulation of insulin secretion

A

-hyperglycemia –> increase insulin –> glucose internalized in beta cells by GLUT2 and used to make ATP

179
Q

mechanism of insulin secretion

A

excess ATP close K+ leak channel –> partial depolarization to activate voltage gated Ca2+ channels–> release of insulin from storage

180
Q

what can block K+ leak channels allowing insulin release?

A
  • hyperkalemia or sulfonylurea

- amino acids through ATP production

181
Q

how does ACh lead to insulin release?

A

PLC activation –> IP3 and DAG –> increase intracellular Ca2+ –> insulin release
-store sugar with PNS

182
Q

what inhibits insulin release?

A

stimulation of alpha adrenergic receptors (SNS)

-liberate sugar with SNS

183
Q

incretin effects

A
  • secreted from intestines
  • primes beta cells for incoming hyperglycemia - release insulin after ingestion of sugar
  • increase insulin sensitivity and release (treat type II diabetics)
184
Q

3 main incretins

A

GLP-1, GIP, CCK

-GLP-1 stimulated by metformin and inhibits glucagon

185
Q

function of dipeptidyl peptidase IV inhibitors

A

increase GLP-1 and improve glucose tolerance

186
Q

what factors stimulate insulin sensitivity?

A

adiponectin and visfatin –> fat cells that take up more sugar
metformin –> prevent liver for doing gluconeogenesis
-get rid of sugar in blood

187
Q

what factors inhibit insulin sensitivity?

A
  • glucocorticoids
  • catecholamines
  • GH
  • resistin and RBP4
  • keep sugar in the blood longer
188
Q

insulin receptor (IR) signaling

A
  • insulin activates tyrosine –> activate IRS and many others
  • also activation of Ras –> activate MAPK –> cell proliferation and anti-apoptotic
189
Q

ways of inhibiting IR signaling

A
  1. PTP (tyrosine phosphatase) - dephosphorylation of tyrosine kinase terminates signal –> insulin resistance
  2. serine-threonine phosphorylation of IR –> decreases ability to autophosphorylate terminating signal –> type II diabetics
190
Q

insulin functions

A
  • promote glycogen synthesis and glycolysis
  • inhibit lipolysis & promote lipogenesis
  • promote FA synthase and lipoprotein lipase
  • inhibit hormone sensitive lipase
  • reduce ketone bodies
  • promote protein synthesis and inhibit degradation
191
Q

3 ketogenic hormones

A
  • GH
  • cortisol
  • glucagon
192
Q

other insulin functions

A
  • satiety
  • increase GLUT 4 expression and localization in fat and muscles
  • glucagon suppression
  • insulin resistance associated with deficient GLUT4 recruitment
193
Q

what else induces GLUT 4 expression?

A

exercise

194
Q

moderate exercise

A

glucose uptake and production are equal

195
Q

intense exercise

A

can have hyperglycemia

-more breakdown of glycogen and catecholamines inhibit glucose uptake –> need to liberate energy

196
Q

chronic stress

A
  • can lead to diabetes
  • no recruitment of GLUT4, but have glycogenolysis and gluconeogensis
  • increase cortisol and insulin resistance
197
Q

what stimulates glucagon release?

A
  • hypoglycemia
  • increased AAs
  • catecholamines
198
Q

what inhibits glucagon release?

A
  • fatty acids
  • somatostatin
  • insulin
199
Q

why do you increase glucagon when you increase insulin?

A
  • don’t want to get into hypoglycemia if you eat a protein rich only meal
  • balance each other out
  • insulin will tone down glucagon when it needs to hide sugar
200
Q

glucagon function

A
  • increase glycogenolysis and gluconeogensis
  • increase AA transport to liver and urea formation
  • increase lipolysis and ketogenesis

BECOM II Exam 4 (10 decks)

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