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PHYSL 214 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is endocrinology?

A

study of hormones, their receptors, intracellular signalling pathways, and diseases/conditions associated w/ them

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2
Q

what’s the difference btwn an endocrine vs exocrine gland?

A

endocrine: does not have a duct system (thyroid)
exocrine: has a duct system (salivary)

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3
Q

what is an ex of a gland that is endocrine and exocrine?

A

pancreas

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4
Q

what is a hormone?

A

compound that are secreted into bodily fluids, particularly the blood stream, by a specific group of cells and regulate activity of other cells (greek: “setting in motion”)

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5
Q

what are the 3 kinds of hormones based on structure?

A

proteins, lipids, monomamines

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6
Q

what are 3 kinds of protein hormones?

A

small peptides, polypeptides, glycoproteins

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7
Q

what is a characteristic of protein hormones?

A

are water-soluble (plasma)

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8
Q

what are 2 kinds of lipid hormones?

A

steroids (from cholesterol), eicosanoids (from arachidonic acid)

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9
Q

what is a characteristic of lipid hormones?

A

water-insoluble (lipid-soluble)

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10
Q

what are 2 categories of monoamine hormones?

A

catecholamines and thyroid hormones (both from tyrosine)

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11
Q

what steroid hormones can cholesterol be converted into? (6)

A

cholesterol->pregnenolone->progesterone or testosterone, progesterone->aldosterone or cortisol or testosterone, testosterone->estrogen

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12
Q

what’s the difference btwn endocrine, neuronendocrine, paracrine and autocrine signalling?

A

endocrine: cell-cell through blood
neuroendo: neuron-cell in blood
para: cell-cell through ECF
auto: cell-self through ECF

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13
Q

what are 2 kinds of hormone receptors and their ligands?

A

cell-surface: proteins and catecholamines (lipid-insoluble, water-soluble)
intracellular: steroid and thyroid (lipid-soluble-pass through memb)

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14
Q

what are 2 kinds of cell surface receptors?

A

GPCRs and catalytic receptors (tyrosine kinases)

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15
Q

what are 3 locations for intracellular receptors?

A

in cytoplasm, in nucleus, bound to DNA

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16
Q

what is similar btwn all intracellular receptors?

A

all end up in nucleus and act as transcription factors

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17
Q

what are 4 factors that affect hormone activity?

A

synthesis/secretion, binding to plasma proteins, metabolism, #/location of receptors

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18
Q

where are most protein hormones secreted from?

A

hypothalamus, pituitary, pancreas, parathyroid, GI

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19
Q

where are catecholamines (monoamines) secreted from?

A

adrenal medulla

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20
Q

what are 7 similarities btwn protein and catecholamine hormones?

A

water-soluble, from aa (catecholamines from tyrosine), in granules/exocytosed, don’t need solubilization in blood, cell-surface receptors, change intracellular pathways, effects within mins/hours

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21
Q

what are 7 similarities btwn steroids and thyroid hormones?

A

lipid-soluble, from cholesterol (thyroid Hs from tyrosine), not stored/diffusion, bound to plasma proteins, intracellular receptors, regulate genes, effects in days/weeks

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22
Q

where are most steroid hormones released from? (3)

A

adrenal cortex, ovaries, testes

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23
Q

where are thyroid hormones released from?

A

thyroid gland

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24
Q

What supplies the anterior and posterior pituitary with neurons?

A

Hypothalamus

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25
Q

What joins the hypothalamus and the anterior and posterior pituitary?

A

Pituitary stalk

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26
Q

What is the region right above the pituitary stalk?

A

Median eminence

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27
Q

What is the anterior pituitary a.k.a.?

A

Adenohypophysis

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28
Q

The posterior pituitary a.k.a.?

A

Neurohypophysis

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29
Q

What is the posterior vs anterior pituitary a growth of?

A

Posterior: down growth of brain
Anterior: up growth of mouth region

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30
Q

How are NTs supplied to the anterior pituitary? (4)

A

hypothalamic neurons synapse onto the primary plexus (supplied by an artery directly in the hypothalamus), portal blood vessels bring hypothalamic NTs to second plexus in anterior pituitary where veins carry ant. pit. NTs

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31
Q

what is the NT system btwn the hypothalamus and ant. and post. pit.?

A

neuroendocrine

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32
Q

how are NTs supplied to the post. pit.? (3)

A

neurons in supraoptic and paraventricular nuclei (SON, PVN) travel from hypothalamus to post. pit., hypothalamic NTs transfer into post pit. plexus (supplied by an artery directly in post. pit.), veins export NTs

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33
Q

compare the hypothalamus innervation of the ant vs post pit.

A

ant: neurons in hypo terminate at median eminence in primary plexus, portal blood vessels bring hypo NTs to ant pit. where veins export ant pit. NTs
post: SON and PVN supply neurons from hypo that terminate in post pit., veins export hypothalamic NTs (are stored in post pit.)

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34
Q

what are 6 ant pit hormones?

A

follicle-stimulating hormone, luteinizing hormone, adrenocorticotropic hormone, thyroid-stimulating hormone, prolactin, growth hormone

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35
Q

what does FSH stand for?

A

follicle-stimulating hormone

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36
Q

what does LH stand for?

A

luteinizing hormone

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37
Q

what does ACTH stand for?

A

adrenocorticotropic hormone

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38
Q

what does TSH stand for?

A

thyroid-stimulating hormone

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39
Q

what does PRL stand for?

A

prolactin

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40
Q

what does GH stand for?

A

growth hormone

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41
Q

what is the mnemonic to remember ant pit hormones?

A

FLAT P(I)G

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42
Q

what are all ant pit hormones?

A

proteins

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43
Q

t/f: ant pit hormones come from diff cell types

A

true, EXCEPT for FSH and LH which come from same cells

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44
Q

what is the main target of FSH and LH?

A

Ovaries and testes

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45
Q

What is the main target of adrenocorticotropic hormone?

A

Adrenal cortex

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46
Q

What is the main target of thyroid-stimulating hormone?

A

Thyroid gland

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47
Q

What is the main target of prolactin?

A

Mammary glands

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48
Q

What is the main target of growth hormone?

A

Most tissues (bone)

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49
Q

What is the hypothalamus-pituitary-target gland axis?

A

higher brain centers control hypothalamus which releases hypothalamic hormones that stim/inh ant pit to release ant. pit hormones that mediate target gland, target gland hormones can work in +/- feedback mech to adjust hypo or ant pit.

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50
Q

what is the mnemonic to remember hypothalamus hormones?

A

The Drunk Girl Got Some Courage

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51
Q

what are the 6 hypothalamic hormones?

A

thyrotropin-releasing hormone, prolactin inhibiting hormone (dopamine), growth hormone-releasing hormone, gonadotropin-releasing hormone, growth hormone inhibiting hormone (somatostatin), corticotropin releasing hormone

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52
Q

what does GnRH stand for?

A

gonadotropin-releasing hormone

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53
Q

What does CRH stand for?

A

Corticotropin-releasing hormone

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54
Q

What does TRH stand for?

A

Thyrotropin-releasing hormone

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55
Q

What does PIH (DA) stand for?

A

Prolactin inhibiting hormone/dopamine

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56
Q

What does GHRH stand for?

A

Growth hormone-releasing hormone

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57
Q

What does SS/GHIH stand for?

A

somatostatin/growth hormone inhibiting hormone

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58
Q

what are all hypothalamic hormones? exception?

A

peptides, except PIH/DA (monoamine)

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59
Q

what is the most abundant ant pit hormone?

A

growth hormone

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60
Q

t/f: growth hormone shows species specificity

A

true

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61
Q

what are 2 features of GH secretion?

A

pulsatile (in bursts) and circadian rhythm (cyclical pattern)

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62
Q

what are 2 targets of GH?

A

bone (for growth) and metabolism

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63
Q

what kind of receptors does GH act on?

A

cell-surface (protein kinase)

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64
Q

what are the epiphysis, epiphyseal plate, and diaphysis of a bone?

A

epiphysis: end of bone
epiphyseal plate: cartilage that separates epiphysis and diaphysis
diaphysis: shaft of bone

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65
Q

what is the epiphyseal plate being open vs closed mean?

A

open: responsive to GH
closed: bone can’t grow (puberty)

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66
Q

what cells and processes cause bone growth?

A

progenitor cells/fibroblasts differentiate into cartilage cells/chondrocytes which proliferate into more cartilage cells, ossification of cartilage cells makes bone

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67
Q

what does GH only causing growth in vivo but not in vitro suggest?

A

it causes the release of another hormone (IGF) that causes growth (can be direct too)

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68
Q

what are the effects of GH on fats? (2)

A

incr lipolysis, incr free fa (for E)

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69
Q

how does GH effect carbohydrates?

A

decr glucose uptake by cells so incr [glucose] in blood (hyperglycemia) - “diabetogenic”

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70
Q

what are the effects of GH on proteins? (3)

A

incr aa uptake into cells, incr protein synthesis, incr cell size (hypertrophy)

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71
Q

what 2 hormones incr GH secretion?

A

GHRH, ghrelin

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72
Q

what 3 hormones decr GH secretion?

A

GHIH/somatostatin, GH and IGF (- feedback)

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73
Q

what 2 metabolic signals incr GH secretion?

A

hypoglycemia (GH incr blood glucose), incr aa/arginine (GH incr aa cellular uptake)

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74
Q

what 2 metabolic signals decr GH secretion?

A

hyperglycemia and incr fa (- feedback)

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75
Q

what 2 other factors incr GH secretion?

A

deep sleep, “stress” (exercise)

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76
Q

what other factor decr GH secretion?

A

ageing

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77
Q

what 2 abnormalities can too much GH cause?

A

gigantism (bone lengthening), acromegaly (bone thickening, enlargement of extremities)

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78
Q

what 2 abnormalities can too little GH cause?

A

dwarfism (decr GHRH, GH, IGF or receptors), metabolic effects

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79
Q

what are the 2 post pit hormones?

A

antidiuretic hormone/vasopressin, oxytocin

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80
Q

what does ADH stand for?

A

antidiuretic hormone

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81
Q

what does OXY stand for?

A

oxytocin

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82
Q

where are post pit hormones from?

A

SON and PVN in hypothalamus (neurons extends from hypo and terminal ends in post pit where NTs are stored)

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83
Q

what is the source of ADH vs OXY?

A

ADH: SON
OXY: PVN

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84
Q

what are the 2 main targets of ADH?

A

kidneys (antidiuretic), blood vessels

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85
Q

what are the 2 main targets of OXY?

A

uterus, mammary glands

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86
Q

what kinds of hormones are ADH and OXY?

A

peptides

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87
Q

what is the mechanism of action of ADH in the kidney? (3)

A

ADH in blood acts on ADH receptors (V2) on basal side on principle cells (in collecting duct), incr cAMP which transports vesicles w/ inactive aquaporins (AQ2) onto apical memb, incr renal H20 reabsorption from filtrate

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88
Q

what 2 factors affect ADH secretion?

A

incr osmotic P/osmolarity (dehydration), decr ECF/blood V (hemorrhage)

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89
Q

what receptors detect incr osmotic P for ADH secretion?

A

osmoreceptors in hypothalamus

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90
Q

what receptors detect decr ECF/blood V for ADH secretion?

A

baroreceptors in cardiovasc. system

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91
Q

what do incr osmotic P and decr ECF/blood V both do to incr ADH secretion?

A

cause release of ADH from neurons in post pit which acts on kidneys for antidiuresis

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92
Q

what are 3 effects of ADH on kidneys?

A

incr renal H2O reabsorption, decr osmotic P of ECF, incr ECF/blood V

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93
Q

what abnormality does too much ADH cause?

A

syndrome of inappropriate ADH secretion (SIADH) - incr BV

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94
Q

what 2 abnormalities does too little ADH cause? diff?

A

central or neurogenic diabetes insipidus (decr ADH, incr dilute urine), nephrogenic diabetes insipidus (abnormal ADH receptors in kidneys, incr dilute urine)

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95
Q

what 2 factors affect and are the effects of oxytocin?

A

affect: cervical stretch during parturition and suckling causes +FB (incr OXY) effects: uterine contractions during parturition (incr cervical stretch), and lactation (milk ejection reflex)

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96
Q

what are the 3 zones of the adrenal cortex? (outside to in)

A

zona glomerulosa, zona fasciculata, zona reticularis

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97
Q

what are all hormones of the adrenal cortex?

A

corticosteroids (cortex-steroids)

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98
Q

what is the hormone family, ex, and function of the zona glomerulosa?

A

mineralocorticoids, aldosterone, salt

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99
Q

what is the hormone family, ex, and function of the zona fasciculata?

A

glucocorticoids, cortisol, sugar

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100
Q

what is the hormone family, ex, and function of the zona reticularis?

A

androgens, DHEA and androstenedione, sex

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101
Q

what is a trick to remember the functions of the zona glomerulosa, fasciculata, and reticularis? (out to in)

A

functions get sweeter (salt, sugar, sex)

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102
Q

how are corticosteroids made? (4)

A

cholesterol -> pregnenolone -> progesterone -> cortisol, aldosterone, adrenal androgens (DHEA, androstenedione) - pregnenolone can make products

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103
Q

what kind of steroid is cortisol?

A

glucocorticoid

104
Q

what kind of steroid is aldosterone?

A

mineralocorticoid

105
Q

what kind of steroids are DHEA and androstenedione?

A

adrenal androgens

106
Q

what are 4 major actions of aldosterone?

A

in kidney: incr Na and H2O (2nd) reabsorption (to blood), incr K and H secretion (loss in urine)

107
Q

what does aldosterone do in the principal vs intercalated cells of the collecting duct? (5)

A

incr gene transcription of 5 proteins:
principal cells: apical Na channels (Na reabsorption), apical K channels (K secretion), apical NHE (Na reabsorption, H secretion), basolateral Na/K ATPase (Na reabsorption, H secretion)
intercalated cells: apical H pump (H secretion)

108
Q

how does aldosterone cause incr H2O reabsorption?

A

H2O follows Na back into bloodstream by osmosis

109
Q

what 4 factors affect and are the effects of aldosterone?

A

affect: decr ECF V, BP, [Na], incr [K] in ECF
effects: incr ECF V, BP, [Na], decr [K] in ECF

110
Q

what is the RAAS mechanism regulated to return ECF, BP, and Na levels back to normal? (6)

A

decr ECF V, BP, or [Na] causes kidneys to release renin (enzyme from juxtaglomerular cells), converts angiotensinogen (substrate in plasma) to AT1 (inactive peptide), ACE (lung enzyme) converts AT1 to AT2 (active peptide), AT2 causes vasoconstriction and adrenal cortex to release aldosterone, incr Na and H2O reabsorption, incr ECF V, BP and [Na]

111
Q

what is the homeostatic mechanism regulated by aldosterone to return K levels back to normal? (3)

A

incr K in ECF acts on adrenal cortex to incr aldosterone, K secretion incr, and K in ECF decr (diff from ECF V/BP/Na which act on kidney)

112
Q

What are effects of cortisol on metabolism in muscles (2), adipose (2), liver (2), vasculature (1), CNS (1)?

A

Muscles: incr protein breakdown, decr glucose uptake
Adipose tissue: incr fat breakdown, decr glucose uptake
Liver: incr glucose formation (gluconeogenesis), incr glycogen formation
Vascular: incr blood glucose (hyperglycemia)
CNS: incr glucose uptake

113
Q

What are 5 effects of cortisol on immune system?

A

Decr lymph node size, decr lymphocyte #, decr humoral/cellular immunity, decr production of inflammatory substances (anti-inflammatory), incr infections

114
Q

What 5 other systems (and their effects/1 ea) are impacted by cortisol?

A 
GIT: incr acid secretion
CVS: incr CO
Bones: decr growth
Kidneys: incr GFR
CNS: depression/irritability
115
Q

What is the general difference btwn stress hormones released from the adrenal medulla vs cortex?

A

Cortex: hormones for chronic stress
Medulla: hormones for acute stress

116
Q

What is the hypothalamus-pituitary axis for cortisol? (Including initiator: 8)

A

Stress +> hypo +> CRH (corticosteroid releasing hormone) +> ant pit +> ACTH (adrenocorticotropic releasing hormone) +> adrenal cortex +> cortisol -> hypo/ant pit (neg feedback)

117
Q

What is the 5 step process for catecholamine synth?

A

Tyrosine -> Dihydroxyphenylalanine (DOPA) -> dopamine -> NA/NE -> A/E

118
Q

Where does catecholamine synthesis occur?

A

Chromaffin cells of adrenal medulla

119
Q

What hormones are primarily made in catecholamine synth (and %)?

A

NA/NE: 20%

A/E: 80%

120
Q

What disorder results from too much aldosterone (4 effects)?

A

Conn’s syndrome: incr ECF V, incr BP, hypokalemia, metabolic alkalosis

121
Q

What disorder results from too little aldosterone (3 effects)?

A

Addison’s disease: hypotension (decr BP), metabolic acidosis, hyperkalemia

122
Q

What disorder results from too much cortisol (4 effects)?

A

Cushing’s disease/syndrome: incr blood glucose, muscle wasting (incr protein breakdown), “moon face”/“buffalo hump” (incr fat in ventral area, decr in extremeties), decr resistance to infection (decr inflammatory response)

123
Q

What disorder results from too little cortisol (1 effect)?

A

Addison’s disease (same as too little aldosterone): decr blood glucose

124
Q

What results from too much (1) vs too little (2) adrenal androgens?

A

Too much: masculinization of females (vs males proportionally)
Too little: decr sexual hair growth, decr female libido

125
Q

What 3 systems do catecholamines affect (majorly)?

A

Cardiovascular system, smooth muscle, metabolism

126
Q

What are 5 effects of catecholamines (NA/A) on the cardiovascular system?

A

Incr HR, contractility, CO, and BP, also blood redistribution (skin, gut, etc. -> heart, brain, skeletal muscle)

127
Q

What are 3 effects of catecholamines (NA/A) on smooth muscle?

A

Dilation of pupils, bronchodilation, decr GIT motility

128
Q

What are 3 effects of catecholamines (NA/A) on macromolecule metabolism?

A

Incr glycogenolysis (glycogen breakdown in liver and skeletal muscle), incr lipolysis (fa for E), incr gluconeogenesis (glucose synth)

129
Q

How is catecholamine secretion controlled? (3)

A

Splanchnic nerve (symp pregang) stimulates adrenal medulla by releasing ACh, chromaffin cells (~postgang) release NA/A, catecholamines move into blood vessels for export (act as hormones - are also NTs)

130
Q

What is the external structure of the thyroid gland?

A

Butterfly shape around trachea (lobes wrap around to back)

131
Q

What is the internal structure of the thyroid gland?

A

Epithelial/follicular cells form globules filled with colloid, parafollicular/c cells are btwn follicular cells

132
Q

What do parafollicular/c cells secrete?

A

Calcitonin

133
Q

What is the diff btwn active vs resting thyroid follicles?

A

Active: decr colloid due to incr thyroid hormone secretion
Resting: incr colloid due to thyroid hormone build up (flattens epi cells)

134
Q

What is the process of thyroid hormone synthesis -> storage? (6)

A

I- (iodide) uptake from blood (active transport by I-/Na pump) into follicular cells, pendrin exports I- into colloid, thyroglobulin (tyrosine-containing glycoprotein) synthesis (in cell), iodination of Tyr (MIT or DIT) on thyroglobulin by thyroid peroxidase (in colloid), coupling of iodotyrosines (T3 or T4), storage in colloid

135
Q

What controls PTH secretion?

A

blood Ca levels (inverse relationship, low Ca = high PTH, high Ca = low PTH)

136
Q

T/f: the hypo-pit axis controls PTH secretion

A

False, controlled by blood Ca levels

137
Q

What detects Ca levels to control PTH secretion?

A

Chief cells in parathyroid gland have “Ca sensors” that are GPCRS (Gi and Gq)

138
Q

What are 2 sources of vitamin D?

A

Sunlight (UV-B) and from diet (fish, eggs)

139
Q

What form of vitamin D does sunlight provide?

A

7-dehydrocholesterol

140
Q

What is the process of active vitamin d synthesis?

A

Cholecalciferol (vit D) is converted to 25-OH cholecalciferol in the liver, and converted to 1.25(OH)2-cholecalciferol by 1a-hydroxylase in the kidneys

141
Q

What is 1.25(OH)2-cholecalciferol aka?

A

Calcitriol or active vitamin D

142
Q

What major form of vitamin d is stored?

A

25-OH cholecalciferol

143
Q

How does PTH incr active vit D3? Process?

A

incr 1a-hydroxylase; incr conversion of 25-OH cholecalciferol to active vit D (in kidneys)

144
Q

Where in the GIT is Ca absorbed?

A

Duodenum of sm intes

145
Q

What is the process of Ca absorption in an enterocyte (duodenal cell)? (5)

A

Ca in lumen (from diet) passes through apical Ca channels, binds to calbindin, transverses to basolateral side of cell, dissociates, Ca exits through basal Ca ATPases

146
Q

What incr Ca absorption in the gut?

A

Vitamin D (incr transcription of proteins for entire process-Ca channels, calbindin, etc.)

147
Q

What is the structure of PTH, active vit D3, and calcitonin?

A

PTH: peptide
Vit D3: steroid-like
Calcitonin: peptide

148
Q

What is PTH, active vit D3, and calcitonin secreted from?

A

PTH: parathyroid gland (chief cells)
Vit D3: kidney (prox tubule cells)
Calcitonin: thyroid gland (parafollicular/c-cells)

149
Q

How does PTH, active vit D3, and calcitonin effect blood Ca?

A

PTH: incr blood Ca
Vit D3: incr blood Ca
Calcitonin: decr blood Ca

150
Q

How does PTH, active vit D3, and calcitonin effect blood phosphate?

A

PTH: decr blood phosphate
Vit D3: incr blood phosphate
Calcitonin: decr blood phosphate

151
Q

How does PTH (3), active vit D3 (3), and calcitonin (1) effect Ca and phosphate levels?

A

PTH: incr bone resorption, incr Ca and decr P reabsorption in kidneys, indirectly incr Ca and P absorption in GIT by incr vit D3/1a-hyroxylase
Vit D3: incr Ca and P absorption in GIT, incr bone resorption (w/ PTH), incr reabsorption of Ca and P in kidneys
Calcitonin: decr bone resorption

152
Q

What incr secretion of PTH, active vit D3, and calcitonin?

A

PTH: decr blood Ca
Vit D3: PTH
Calcitonin: incr blood Ca

153
Q

What is MIT vs DIT?

A

MIT: mono-iodotyrosine (1 I2 + Tyr)
DIT: di-iodotyrosine (2 I2 + Tyr)

154
Q

What is T3 vs T4?

A

T3: tri-iodothryonin (MIT + DIT)
T4: tetra-iodothryonine or thyroxine (2 DIT)

155
Q

Is more T3 or T4 stored in the colloid?

A

T4

156
Q

What is the process of thyroid hormone release -> binding?

A

Endocytosis of colloid into follicular cell, breakdown and recycling of I- and Tyr by lysosomal enzymes, secretion of T3 and T4 into blood, transport in bound form (plasma proteins), T4 converted to T3 in tissues, hormone binding to nuclear receptor

157
Q

Is more T3 or T4 secreted into blood from thyroid gland?

A

T4

158
Q

Is majority of T3 and T4 transported in bound or free form?

A

Bound (free T3 = 0.4% and free T4 = 0.03%)

159
Q

What makes T3 the major thyroid hormone not T4 if more T4 is stored and secreted?

A

T4 acts as a prohormone (most converted to T3 in tissues)

160
Q

Does T3 or T4 bind more strongly to receptor in nucleus?

A

T3

161
Q

What is the half life of T3 vs T4?

A

T3: 1 day
T4: 7 days (relatively long)

162
Q

What are 3 general physiological actions of thyroid hormones?

A

Act on most tissues to change transcription/translation, incr “metabolism” (sum of all chem rxns), necessary for growth and development

163
Q

What are 6 specific actions of thyroid hormones on metabolism?

A

incr BMR (incr O2 consumption and heat production), incr carb absorption/utilization, incr protein (muscle) breakdown, incr fat breakdown, incr cholesterol metabolism (excretion in bile), decr blood cholesterol levels (catabolism > anabolism, both incr)

164
Q

What are 4 specific actions of thyroid hormones on growth/development?

A

Act as “tissue growth factors”, incr protein synthesis (small amounts), incr GH/IGF production, proper CNS maturation in fetus/newborn

165
Q

How can thyroid hormone cause incr protein breakdown but also protein synthesis?

A

Dose-dependent (small amounts incr synthesis)

166
Q

What are 4 other specific actions of thyroid hormones?

A

Incr HR/F, potentiation of symp system (B-adrenergic Rs), proper function and fertility of reproductive system, incr bone turnover

167
Q

What is the hypothalamus-pit axis for thyroid hormones? (7)

A

(Cold?) +> hypo +> TRH (thyrotropin-releasing hormone) +> ant pit +> TSH (thyroid stimulating hormone) +> thyroid gland +> thyroid hormones (T3 and T4) -> hypo and anti pit (TRH and TSH)

168
Q

What disease is caused by over activity of the thyroid gland? Cause? 3 symptoms?

A

Grave’s disease; autoimmune rxn (Ab) stimulates thyroid gland receptors; incr BMR, exophthalmos (protrusion of eyeballs), goitre

169
Q

What is goitre?

A

Enlargements of thyroid gland

170
Q

What disease is caused by under activity of the thyroid gland (hypothyroidism)? 2 causes? 3 symptoms?

A

Hashimoto’s disease; autoimmune rxn destroys thyroid gland/blocks hormone release or iodine deficiency (TH synthesis); myxedema (skin puffiness), goitre, cretinism in children (abnormal brain development)

171
Q

What is total body Ca (1kg) stored in body? Maj?

A

Bone (1kg) > other tissues (11g)

172
Q

Where is Ca (11g) in tissues stored? Maj?

A

ICF (10g) > ECF (1g)

173
Q

What form is Ca stored in ECF (1g)? Maj?

A

Free Ca (500mg) = bound Ca (500mg)

174
Q

What form is Ca stored in ICF (10g)? Maj?

A

Free Ca (0.1mg) < bound Ca (10g)

175
Q

Is there more free Ca in ICF or ECF?

A

ECF (500mg vs 0.1mg in ICF)

176
Q

Where is Ca obtained from?

A

Diet

177
Q

What are the processes of Ca in blood plasma -> bones vs bones -> blood plasma?

A

Ca in plasma -> bone: ossification/mineralization

Ca in bone -> plasma: resorption/demineralization

178
Q

What organs control Ca filtration/excretion?

A

Kidneys

179
Q

What are 4 reasons Ca is important?

A

Structural role (bones, teeth, etc.), blood coagulation, intracellular messenger, regulates neuromuscular excitability

180
Q

What are 3 reasons phosphate (P) is important?

A

Structural role (w/ Ca), “metabolism” (phosphorylation: ATP, nucleus acids, etc.), buffer

181
Q

What 3 hormones regulate Ca and P levels? Source?

A

PTH (parathyroid hormone) from parathyroid gland, vitamin D from kidneys, calcitonin from thyroid gland (parafollicular/c cells)

182
Q

What are 3 targets for PTH, vit D, and calcitonin?

A

Bone (Ca and P storage), GI tract (Ca and P absorption/secretion), kidneys (Ca and P retention/excretion)

183
Q

What comprises the calcified matrix of bone?

A

Protein framework (Osteoid) and Ca and phosphate salts

184
Q

What protein mainly comprises osteoid?

A

Collagen

185
Q

What salt mainly comprises salts embedded in osteoid?

A

Hydroxyapatite

186
Q

What are 3 bone cells and diff functions?

A

Osteoblasts: bone building
Osteoclasts: bone destroying
Osteocytes: respond to stress?

187
Q

What is the most common bone cell?

A

Osteocytes

188
Q

Where are the parathyroid glands located? Usual #?

A

Embedded in back lobes of thyroid gland; 4

189
Q

What are the effects of PTH on Ca and phosphate levels in plasma?

A

Incr Ca and decr P

190
Q

What cells in the parathyroid gland release PTH?

A

Chief cells

191
Q

What is the process of osteocytic osteolysis? 3 steps?

A

Breakdown of bone by osteocytes; osteocytes (centre of bone) take up Ca via Ca channels, Ca transported from osteocytes to osteoblasts (surface), osteoblasts export Ca via Ca pumps (to ECF)

192
Q

What is the process of osteoclastic resorption? General process?

A

Resorption of bone by osteoclasts; osteoclasts form a ruffled border (closed spaces) and secrete proteolytic enzymes and H+ (acidic) to break down collagen and Ca/P resp.

193
Q

How is bone repaired following osteoclastic resorption? (4)

A

Osteoblasts (on surface of bone) fill hole made by osteoclasts, secrete osteoid (mainly collagen), osteoblasts trapped in colloid become osteocytes (in centre of bone), Ca and P deposited on surface

194
Q

How does PTH incr Ca and decr phosphate in blood plasma? (Bone, GIT, kidneys)

A

Bone: incr bone resorption (Ca and P to blood)
GIT: incr absorption (Ca and P to blood)
Kidneys: incr Ca retention and P excretion

195
Q

What causes NET phosphate decr w/ PTH if it is absorbed from bone and GIT?

A

PTH incr P excretion in kidneys (not Ca, therefore accumulates in blood plasma)

196
Q

How do Ca sensors in parathyroid chief cells alter PTH secretion? (3)

A

Incr Ca binding to Ca sensors, decr cAMP (Gi) and incr IP3/intracellular Ca (Gq), PTH decr

197
Q

What disorders occur w/ too much vs too little PTH?

A

Too much: “bones, stones, and groans” (incr resorption, Ca -> kidney stones, pain)
Too little: tetany (muscle spasms)

198
Q

What disorders occur with too little active vitamin D3?

A

Rickets in children and osteomalacia in adults

199
Q

What’s the difference btwn rickets in children and osteomalacia in adults?

A

Rickets: decr vit D causes decr Ca absorption, causes decr mineralization on growth plate/cartilage of bone, remains closed and decr growth/bone softening
Osteomalacia: decr vit D causes decr Ca absorption, causes decr mineralization on osteoid of bone, causes bone softening

200
Q

What disorders occur with decr calcitonin?

A

None discovered yet (physiological significance still uncertain)

201
Q

What is a possible explanation for inverse relationship btwn Ca and excitability? (Decr PTH causing tetany)

A

Low PTH = low EC Ca which favours opening of Na channels = incr excitability

202
Q

What are 2 cell types in the pancreas? Secretions?

A

Exocrine: acinar cells secrete pancreatic juice/enzymes (has ducts-duct cells)
Endocrine: islets of langerhans secrete pancreatic hormones into nearby blood vessels

203
Q

What are islets of langerhans? 2 cell types?

A

Clusters of cells in endocrine pancreas; alpha and beta (maj.) cells

204
Q

What are the 5 hormones of the pancreas?

A

Glucagon, insulin, somatostatin, pancreatic polypeptide, vasoactive intestinal polypeptide

205
Q

What cells secrete glucagon vs insulin?

A

Glucagon: alpha cells of islets of langerhans
Insulin: beta cells of islets of langerhans

206
Q

What % of islet cells are alpha (secretes glucagon) vs beta (secretes insulin)?

A

Alpha: 15-20%
Beta: 65-90%

207
Q

What are 5 highlights in the discovery of pancreatic hormones (insulin)?

A

1889: Minkowski and con Mering removed dog pancreas which caused diabetes mellitus (sweet urine)
1921: Frederick Banting, Charles Best, James Collin and John Macleod found pancreatic extract (crude insulin) treated diabetes in dogs
1922: insulin use in humans
1923: Banting and Macleod awarded Nobel prize for insulin discovery
1922/23: Kimball and Merlin discovered glucagon in pancreatic extract

208
Q

What are overall actions of glucagon vs insulin?

A

Insulin: incr glucose absorption, decr breakdown of storage
Glucagon: decr glucose absorption, incr breakdown of storage

209
Q

What is a way to remember functions of insulin vs glucagon?

A

Insulin: “feasting” (absorb glucose from blood)
Glucagon: “fasting” (release glucose from storage)

210
Q

what is the effect of insulin in the liver? (2 glycogen, 5 glucose, 2 protein)

A

glycogen: incr glycogenesis, decr glycogenolysis
glucose: incr glycolysis, decr gluconeogenesis, incr fat synthesis (FA, TriG), decr fat breakdown, decr ketogenesis,
proteins: incr synthesis, decr breakdown

211
Q

what is the effect of insulin in muscle? (1 glucose, 2 glycogen, 3 protein)

A

glucose: incr glucose uptake
glycogen: incr glycogenesis, decr glycogenolysis
protein: incr aa uptake, incr protein synthesis, decr protein breakdown

212
Q

what is the effect of insulin on adipose tissue? (2 glucose, 3 FA)

A

glucose: incr glucose uptake, incr glycolysis
FA: incr FA uptake, incr fat (TriG) synthesis, decr fat breakdown

213
Q

what is the structure of the insulin receptor? 4 subunits?

A

tyrosine kinase; 2 a extracellular, 2 B transmembrane subunits

214
Q

how/what does the insulin receptor exhibit its intracellular effects on?

A

tyrosine kinase activity phosphorylates insulin receptor substrates (IRS)

215
Q

what are 3 effects of insulin receptor substrates (IRS)?

A

affects: transport systems, enzyme activity, gene expression

216
Q

what are 2 mechanisms for glucose transport?

A

2ndary active transport (uphill, Na-dependent) and facilitated transport (downhill, Na-independent)

217
Q

what 2 major proteins enable 2ndary active transport of glucose?

A

SGLT 1 and 2

218
Q

what 2 major proteins enable facilitated transport of glucose?

A

GLUT 1 and 2

219
Q

what glucose transporter is insulin-dependent?

A

GLUT 4 (facilitated transport)

220
Q

what is the process of glucose uptake w/ vs wo/ insulin in muscle/adipose tissue?

A

wo/ insulin: vesicle w/ GLUT4 don’t merge w/ pmemb

w/ insulin: GLUT4 vesicles translocate to pmemb (via IRS)

221
Q

which tissues exhibit insulin dependant vs independent glucose transport?

A

insulin-dependent: muscle and adipose

insulin-independent: liver

222
Q

where is the main site of action of glucagon?

A

liver

223
Q

where does glucose come from in ST, LT and longer LT?

A

ST: bloodstream after a meal
LT: liver glycogen stores (glycogenolysis)
longer LT: glucose made from aa (non-carb gluconeogensis)

224
Q

what are the actions of glycogen? (7)

A

decr glycogenesis, incr glycogenolysis, decr glycolysis, incr gluconeogenesis, decr lipogenesis, incr lipolysis, incr ketogenesis

225
Q

how does insulin vs glucagon affect blood sugar levels?

A

insulin: hypoglycemia
glucagon: hyperglycemia

226
Q

what does amylin do? (pancreatic H)

A

may decr food intake, decr rate of gastric emptying, and decr glucagon secretion (secreted w/ insulin)

227
Q

what does somatostatin do? (pancreatic H)

A

may inhibit insulin and glucagon secretion from pancreas (paracrine)

228
Q

what does pancreatic polypeptide do?

A

may decr pancratic enzyme secretion and inhibit gallbladder contraction

229
Q

what does vasoactive intestinal polypeptide do? (pancreatic H)

A

may decr pancreatic water secretion, diarrhea in excess

230
Q

how does glucose cause insulin secretion in the pancreas? (7)

A

glucose enters B islet cells via GLUT 2 (insulin-dep), incr intracellular ATP, closes ATP-sensitive K channels, intracell K incr (cant exit through channel), depol, Ca channels open, Ca causes release of storage vesicles w/ insulin

231
Q

what effect does incr glucose have on insulin and glucagon secretion?

A

insulin: incr
glucagon: decr

232
Q

what effect does incr aa have on insulin and glucagon secretion?

A

insulin: incr
glucagon: incr

233
Q

what effect does incr GIT Hs (CCK, secretin, etc) have on insulin and glucagon secretion?

A

insuline: incr
glucagon: depends on incretin

234
Q

what effect does incr SS have on insulin and glucagon secretion?

A

insulin: decr
glucagon: decr

235
Q

what effect does incr insulin have on insulin and glucagon secretion?

A

insulin: none
glucagon: decr

236
Q

what effect does incr glucagon have on insulin and glucagon secretion?

A

insulin: incr
glucagon: none

237
Q

what effect does incr parasympathetic activity (ACh) have on insulin and glucagon secretion?

A

insulin: incr
glucagon: none

238
Q

what effect does incr sympathetic activity (NA) have on insulin and glucagon secretion?

A

insulin: depends on receptor
glucagon: incr

239
Q

how do insulin and glucagon restore blood glucose levels after a meal?

A

incr blood glucose, incr insulin, decr blood glucose (incr storage), and decr glucagon, decr blood glucose (decr breakdown)

240
Q

why is glucagon incr by aa?

A

protein-rich meal causes no initial change in blood glucose, aa cause incr insulin (to store aa) which decr glucose, so glucagon must be released to raise glucose back to normal

241
Q

what are 2 potential causes for incr insulin (too much)?

A

insulin-secreting tumour, insulin overdose

242
Q

what are 3 consequences of having too much insulin?

A

decr blood glucose (hypoglycemia), ANS and endocrine responses (incr symp activity, incr “counter Hs”), hunger/confusion/drowsiness

243
Q

what is type 1 diabetes mellitus?

A

type 1: autoimmune disease, B islet cells destroyed, insulin deficiency, younger ppl (5-10% cases)

244
Q

what is type 2 diabetes mellitus?

A

type 2: insulin resistance, initial incr insulin secretion, decr insulin effects, adults but incr in younger ppl (obesity, 90-95% cases)

245
Q

what is the most common issue with diabetes mellitus?

A

hyperglycemia

246
Q

where/how is glucose uptake affected w/ diabetes mellitus?

A

decr uptake into insulin-dependent tissues (muscle, adipose), incr uptake into insulin independent tissues (liver)

247
Q

metabolism of what macromolecules is affected w/ diabetes mellitus?

A

carbs, proteins, and fats

248
Q

what are 5 current/future treatments for type 1 diabetes mellitus?

A

insulin administration, pancreatic transplant, islet cell transplant (Edmonton protocol), gene therapy, incr islet cell growth

249
Q

what are 3 current/future treatments for type 2 diabetes mellitus?

A

dietary control and exercise, drugs to incr insulin secretion/response to insulin, insulin administration

250
Q

how does decr insulin cause polyphagia?

A

decr glucose uptake, decr intracell glucose, hunger, polyphagia

251
Q

how does decr insulin cause polydipsia?

A

incr glucose release, incr blood glucose, glucosuria, osmotic diuresis, dehydration, thirst, polydipsia

252
Q

how does decr insulin cause decr BP/kidney failure?

A

incr glucose release, incr blood glucose, glucosuria, osmotic diuresis, dehydration, decr blood volume, decr BP and kidney failure

253
Q

how does decr insulin affect aa/proteins?

A

decr aa uptake and incr protein breakdown, incr blood aa, incr gluconeogenesis in liver (incr blood glucose)

254
Q

how does decr insulin cause metabolic acidosis?

A

decr fa uptake and incr fat breakdown, incr blood fa, excess acetyl-CoA, incr ketone bodies (acids), metabolic acidosis (incr respiration)

255
Q

how does decr insulin cause tissue wasting?

A

incr fat and protein breakdown

256
Q

what is ketogenesis?

A

production of ketone bodies in the metabolism of fats

PHYSL 214 (6 decks)

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