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Physiology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

endocrinology

A

study of biosynthesis, storage, chemistry, + physiological function of hormones secreted from endocrine glands or other tissues

study of hormones, their receptors, the intracellular signaling pathways invoked and the disease + conditions associated

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2
Q

endocrine gland

A

lacks duct system
secretions are released into blood
ex. thyroid gland

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3
Q

exocrine gland

A

has a duct system
secretions released into duct
ex. salivary gland

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4
Q

endocrine + exocrine glands

A

ex. pancreas
has both

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5
Q

types of cell communication

A

endocrine = release hormones into blood → target
neuroendocrine = hormone released by neuron
paracrine = effect on proximal cells
autocrine = self-stimulating

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6
Q

endocrine signaling

A

hormone secretion by endocrine gland into blood
travels over long distance
slow in response
multiple target cells (less specificity)

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7
Q

nervous system signaling (ex. paracrine)

A

NTs released by diffusion from secretory cell
acts locally (short distance)
fast in action
more target specific

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8
Q

path for every hormone

A
  1. synthesis
  2. cell secretion
  3. storage/release + transport
  4. detection by receptors
  5. signal transduction + amplification of response
  6. changes in cellular response of target cell
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9
Q

classification of hormones

A

based on structure:
→ site of receptor + mechanism of action
- solubility → water or lipid soluble

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10
Q

proteins

A

water soluble
- small peptides ex. TRH, oxytocin, ADH
- polypeptides ex. insulin, glucagon, GH
- glycoproteins (CHO added) ex. FSH, LH, TSH

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11
Q

lipids

A

lipid soluble
- steroids (from cholesterol) ex. cortisol, aldosterone, sex hormones
- eicosanoids (from arachidonic acid) ex. prostaglandings, leukotrienes

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12
Q

monoamines

A

made from tyrosine
- catecholamines = water soluble ex. DA, NE, E
- thyroid hormones = lipid soluble ex. T3, T4

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13
Q

protein hormone synthesis

A
  1. synthesis: preprohormone → prohormone
  2. packaging: prohormone → hormone
  3. storage
  4. secretion: hormone + any “pro” fragments

stored after synthesis + secreted when needed

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14
Q

steroid hormone synthesis

A

cholesterol → pregnenolone → testosterone → estrogen
pregnenolone → progesterone → testosterone → estrogen
progesterone → aldosterone + cortisol

not stored, synthesized as needed

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15
Q

water soluble hormones

A

peptide hormones + catecholamines
active after synthesis/secretion = quick acting
metabolism = inactivation

bind to cell surface receptors

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16
Q

lipid soluble hormones

A

steroids + thyroid hormones
move through body bound to plasma proteins (inactive)

synthesis + metabolism control activity

bind to intracellular receptors

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17
Q

target cell receptors

A

selectively recognize + bind specific hormones
binding of hormone = formation of hormone receptor complex → changes in target cell responses

cellular localization: cell surface or intracellular

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18
Q

cell surface receptors

A

found in plasma membrane
fast metabolism
classified according to activation mechanism
- GPCR
- catalytic receptors

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19
Q

GPCR

A

ex. adrenaline, glucagon

hormone = 1st messenger → carried by blood to receptor on cell surface
binding = form complex → activation of G proteins + membrane-bound enzyme
→ 2nd messenger → protein kinase → protein phosphorylation → response

amplification of signal: one hormone causes large response

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20
Q

GPCR ex. vasopressin

A

G-protein cascade
membrane bound enzyme = Adenyl Cyclase
2nd messenger = cAMP
protein kinase = PKA

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21
Q

GPCR ex. **

A

G-protein cascade
membrane bound enzyme = phospholipase C
2nd messenger = DAG
protein kinase = PKC

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22
Q

GPCR ex. **2

A

G-protein cascade
membrane bound enzyme = ***
2nd messenger = Ca2+
intermediate = Ca2+/calmodulin complex
protein kinase = Ca2+/calmodulin dependent kinase

Ca2+ signaling via one of 2 ways:
- enters cell through Ca2+ channels during cell activation
- mobilized from storage by IP3 (activated by phospholipase C)

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23
Q

amplification of signal

A
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24
Q

catalytic receptors

A

ex. insulin, GH

hormone binds to transmembrane receptor = activation of tyrosine kinase
→ protein phosphorylation → response of target cell

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25
Q

catalytic receptors ex. insulin

A

receptor has TK domain in cytosol
autophosphorylation of tyrosine → phosphorylation of proteins

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26
Q

catalytic receptors ex. GH

A

binding of hormone to receptor = recruitment of activated TK
translocation of TK to receptor → phosphorylation of proteins

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27
Q

protein phosphorylation

A

important in cell signaling
protein kinase = either activation or inactivation of protein to turn on/turn off

protein phosphatase = hydrolysis (reverse phosphorylation) to either activate or inactivate protein

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28
Q

intracellular receptors

A

hormone binds receptor = ends up in nucleus + acts as transcription factors (bound to DNA)
alter gene transcription → synthesis of new proteins = response of target cell
slow metabolism

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29
Q

intracellular receptors in cytoplasm

A

ex. steroid hormone receptors in adrenal cortex

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30
Q

intracellular receptors in nucleus

A

ex. sex steroid receptors

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31
Q

intracellular receptors bound to DNA

A

ex. thyroid hormone receptors

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32
Q

up regulation

A

increase in number of receptors for a hormone
low amounts of hormone = use all to maximize response

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33
Q

down regulation

A

decrease in number of receptors for a hormone
prevent continuous activation

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34
Q

permissive action

A

hormone A must be present for full action of hormone B to occur (small effect in absence of A)
A may upregulate receptors for B on target cell

ex. thyroid hormone permits maximum effect of epinephrine

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35
Q

tropic (trophic) hormone

A

hormone that controls the secretion of another hormone
- hormone A signals release of hormone B from target cell
- hormone X signals increase secretion of hormone Y + stimulates growth of target cell Y

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36
Q

negative feedback control

A

dampen response

ex. PTH secretion + blood Ca2+
low Ca2+ triggers PTH release from endocrine cell → PTH targets bone/GI to ↑ Ca2+
→ negative feedback = ↓ PTH release
homeostasis = dampen significant changes in blood Ca2+

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37
Q

positive feedback control

A

amplify response

ex. small contraction/stretch in uterus initiates posterior pituitary secretion of oxytocin → signals uterine muscles to ↑ contraction + cervical stretch
= ↑ stimulation of posterior pituitary to ↑ oxytocin
amplify uterine contraction

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38
Q

hyposecretion

A

secretion of too little hormone

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39
Q

hypersecretion

A

secretion of too much hormone

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40
Q

hypo-responsiveness

A

reduced responsiveness of target cells due to:
- abnormal receptors ex. Laron dwarfism
- defective cell signaling
- defective enzyme function

ex. diabetes incepitus

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41
Q

hyper-responsiveness

A

increased responsiveness of target cells

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42
Q

pituitary gland

A

in midbrain
inferior to hypothalamus
contained in bony space

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43
Q

anatomy of hypothalamus + pituitary

A

hypothalamus → median eminence → pituitary stalk → posterior pituitary (anterior pituitary)

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44
Q

anterior pituitary

A

adnenohypophysis
frontal lobe of gland
neurosecretory neurons in hypot synthesize + release protein hormones into primary plexus (capillary bed fed by arterial blood) → hypothalamic-hypophyseal portal system (single blood vessel) → secondary plexus in ant. pituitary
hormone released → signals to endocrine cell = release hormone back into venous blood

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45
Q

posterior pituitary

A

neurohypophysis
posterior lobe of gland
neurosecretory neurons in hypothalamus extend through hypothalamic-posterior pituitary stalk to posterior pituitary = release of hormone into blood

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46
Q

hormones

A

ADH (39)
oxytocin (39)
GH (ant. pit.)
PTH

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47
Q

FSH

A

follicle stimulating hormone
released by anterior pituitary
targets ovaries and testes
stimulated by GnRH

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48
Q

LH

A

luteinizing hormone
released by anterior pituitary
targets ovaries and testes
stimulated by GnRH

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49
Q

ACTH

A

adrenocorticotropic hormone
released by anterior pituitary
targets adrenal cortex
stimulated by CRH

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50
Q

TSH

A

thyroid stimulating hormone
released by anterior pituitary
targets thyroid gland
stimulated by TRH

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51
Q

PRL

A

prolactin
released by anterior pituitary
targets mammary gland
inhibited by PIH

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52
Q

GH

A

growth hormone
released by anterior pituitary
targets most tissues
stimulated by GHRH + inhibited by SS

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53
Q

GnRH

A

gonadotropin releasing hormone
released by hypothalamus
targets anterior pituitary
↑ LH + FSH secretion

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54
Q

CRH

A

corticotropin releasing hormone
released by hypothalamus
targets anterior pituitary
↑ ACTH secretion

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55
Q

TRH

A

thyrotropin releasing hormone
released by hypothalamus
targets anterior pituitary
↑ TSH secretion

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56
Q

GHRH

A

growth hormone releasing hormone
released by hypothalamus
targets anterior pituitary
↑ GH secretion

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57
Q

GHIH

A

growth hormone inhibiting hormone (somatostatin)
released by hypothalamus
targets anterior pituitary
↓ GH secretion

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58
Q

PIH

A

prolactin inhibiting hormone (dopamine)
released by hypothalamus
targets anterior pituitary
↓ PRL secretion

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59
Q

hormones released by hypothalamus

A

peptide hormones
(exception: Dopamine)

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60
Q

hypothalamus-pituitary-target gland axis

A

input → hypothalamus = release of neurohormones → anterior pituitary = release of hormones → target gland = release of hormones
→ feedback systems

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61
Q

long-loop feedback system

A

negative
most body mechanisms
hormones released from target gland travel to anterior pituitary or hypothalamus + inhibit hormone release or the responsiveness of secretory cells

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62
Q

short loop feedback system

A

negative
anterior pituitary hormones signal target gland but do not cause other hormone release → also travel to hypothalamus to inhibit neurohormone release
ex. prolactin

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63
Q

posterior pituitary hormones

A

oxytocin + ADH
produced in the cell bodies of hypothalamus: paraventricular + supraoptic nucleus
carried by axons to posterior pituitary → released

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64
Q

growth hormone

A

most abundant anterior pituitary hormone
protein hormone
acts on cell surface receptors and is associated with protein kinase activity
secreted throughout life but slows with age
promotes growth mainly after birth
not secreted linearly (pulsatile)
follows circadian rhythm

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65
Q

GH effect on tissue growth

A

in vitro = no growth → doesn’t cause tissue growth alone, works with other hormones
reproductive organs ↑ growth at puberty
brain growth occurs most between 0-8yo
total body height → two growth spurts ~after birth + 14 yo

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66
Q

bone growth

A

especially in long bones
growth in length = proliferation of cartilage cells at epiphyseal growth plates
fibroblasts differentiate into chondrocytes → proliferation in response to GH = cells build up layers (growth)
ossification as minerals are added → strength = bone

stops once growth plates seal

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66
Q

fibroblasts

A

progenitor cells (stem cells)
differentiate into chondrocytes

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66
Q

GH effect on metabolism

A

↑ aa uptake into cells → ↑ protein synthesis = ↑ growth of most tissues (cell hypertrophy + hyperplasia)
↑ lipolysis = ↑ free fatty acids (energy source)
↓ glucose uptake from blood into muscles (anti-insulin effects) = hyperglycemia
↑ gluconeogenesis by liver

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66
Q

chondrocytes

A

cartilage cells
proliferate during growth
deposition of minerals = ossification

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67
Q

hyperplasia

A

↑ cell division = ↑ number of cells in tissue

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68
Q

hormonal control of GH secretion

A

↑ by GHRH
↓ by somatostatin, GH (autocrine), IGF-1 (released from liver)

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69
Q

metabolic control of GH secretion

A

↑ by hypoglycemia, ↑ aas in blood
↓ by hyperglycemia, ↑ fatty acids

70
Q

other controls of GH secretion

A

↑ by deep sleep, acute stress (ex. exercise)
↓ by prolonged malnutrition, chronic stress

71
Q

gigantism

A

too much GH
onset in children
increased linear growth

72
Q

acromegaly

A

too much GH
onset in adults
thickening of bone, large hands + feet + joints, coarse features
metabolic effects → hyperglycemia

73
Q

dwarfism

A

too little GH
onset in children
caused by ↓ GHRH release from hypot or ↓ GH synthesis + secretion from pituitary
= no linear growth; metabolism effects → suppression of GH effect on blood glucose levels, lipolysis

74
Q

Laron dwarfism

A

mutation of GH receptor
levels are normal but cells don’t respond to hormone

75
Q

ADH

A

antidiuretic hormone (vasopressin)
major source: supraoptic nucleus in hypot.
released in posterior pituitary
targets kidneys, blood vessels
stimulated by ↑ osmolarity in ECF or ↓ ECF/bp (hemorrhage)

76
Q

↑ ADH release

A

changes detected by osmoreceptors in hypot or baroreceptors in hypot.
↑ production in hypot → ↑ release by post. pituitary
carried to kidney duct cells = ↑ water reabsorption + urine concentration
= ↓ ECF osmolarity or ↑ ECF vol/bp

77
Q

SIADH

A

syndrome of inappropriate ADH secretion
too much ADH = ↑ water retention + blood vol

78
Q

central diabetes insipidus

A

too little ADH due to problem in hypot.
large vol of dilute urine

79
Q

nephroenic diabetes insipidus

A

too little ADH due to abnormal ADH receptors in collecting duct cells
do not respond to hormone signaling
large vol of dilute urine

80
Q

oxytocin

A

major source: paraventricular nucleus in hypot.
released in posterior pituitary
targets uterus, mammary glands
stimulated by cervical stretch + suckling

81
Q

adrenal glands

A

sits on top of kidneys
cortex (outside) + medulla (inside)
3 zones in cortex = each release different hormones

82
Q

zona glomerulosa

A

releases mineralocorticoids = aldosterone
regulation of salt

83
Q

zona fasciculata

A

releases glucocorticoids = cortisol
regulation of sugar

84
Q

zona reticularis

A

releases androgens = DHEA and androstenedione
regulation of sex

85
Q

adrenal androgens

A

sex hormones
less potent than testosterone
have no role in adult males
role in adult females, fetal development, puberty onset

86
Q

synthesis of corticosteroids

A

cholesterol → progesterone → aldosterone + cortisol + adrenal androgens

87
Q

aldosterone

A

↑ Na+ and water (second) reabsorption by kidneys
= increased retention by body
↑ K+ and H+ secretion by kidneys
= loss in urine

88
Q

control of aldosterone secretion

A

↓ ECF blood vol/ ↓ bp / ↓ Na+
= kidney releases renin → cleaves angiotensinogen (from liver) into ATI = converted to ATII by ACE
ATII is carried to adrenal cortex = secretion of aldosterone
↑ K+ in ECF also signals cortex to ↑ aldosterone release

↑ K+ secretion = ↓ K+ in ECF → negative feedback to ↓ aldosterone release from cortex

= not under control of anterior pituitary tropic hormone

89
Q

cortisol

A

affects metabolism of glucose
↑ secretion during stress conditions → maintain + protect body
permissive action on E and NE → exert control on vasc tone
= helps maintain blood pressure

90
Q

actions of cortisol

A
  1. vascular tone
  2. metabolism
  3. immune system

also effects during fetal + neonatal life
= development of CNS, GIT, adrenal gland, and surfactant in lungs

91
Q

metabolic effects of cortisol

A

↑ blood glucose = ↑ availability for CNS
↓ glucose uptake in liver = prevent use by peripheral tissues
↑ gluconeogenesis in liver
↑ conversion of glucose → glycogen = storage
↑ protein + fat breakdown

92
Q

immune system effects of cortisol

A

normal = suppression to prevent over activation → auto immune disease

too much = over-suppression
↓ lymphocytes, lymph node size
↓ humoral + cellular immunity
↓ production of inflammatory substances (ex. leukotrienes + prostaglandins)
↓ capillary permeability + prevention of neutrophil diapedesis to site of infection + edema
↓ proteolytic content release from lysosomes
= ↑ susceptibility to infection

93
Q

pharmacological use of cortisol

A

suppress organ rejection after transplant

94
Q

control of cortisol secretion

A

stress factors
diurnal rhythm affects hypot. release of CRH → stimulates ant. pituitary to release ACTH → stimulates adrenal cortex release of cortisol (fasciculata)

negative feedback on pituitary + hypot.

95
Q

Conn’s syndrome

A

too much aldosterone

hypernatremia (Na+ retention) → water retention = ↑ ECF vol = hypertension
hypokalemia (K+ secretion) → metabolic alkalosis

96
Q

Addison’s disease

A

too little aldosterone + cortisol
hypotension, metabolic acidosis, hyperkalemia
↓ blood glucose, ↑ skin pigmentation (↑ melanin)

97
Q

Cushing’s disease

A

too much cortisol
endogenous cause: overproduction bc of pituitary tumor, adrenal tumor, other cause
exogenous cause: too much glucocorticoid-containing medicine

↑ blood glucose, muscle wasting, ↓ resistance to infection
“moon face” = fluid accumulation causes round + puffy face
“buffalo hump” = fat deposition at back of neck

98
Q

virilization

A

too much androgens
masculinization in females

99
Q

too little androgens

A

↓ hair growth, ↓ sexual response in females

100
Q

adrenal medulla

A

release catecholamines
E (80%) + NE

secretion regulated by sympathetic innervation of medulla - splanchnic nerve (preG) releases ACh onto chromaffin cells (postG) = release E + NE into blood

101
Q

synthesis of catecholamines

A

tyrosine → DOPA → dopamine → NE → E

102
Q

action of catecholamines

A

sympathetic response: short term stress
CV = ↑ hr, ↑ force of contraction, ↑ cardiac output, ↑ bp
smooth muscle = pupil dilation, bronchodilation, ↓ GI motility
metabolism = ↑ glycogenolysis, ↑ lipolysis, ↑ gluconeogenesis

103
Q

thyroid gland

A

in front of trachea, butterfly shaped
follicular cells (thyrocytes) make up follicles → contain colloid
parafollicular cells sit in between follicles

104
Q

follicle

A

resting (no stimulation) = thin, flat cells; filled with colloid
active = TSH trophic action → cells swell + secrete thyroid hormones

105
Q

thyroid hormones

A

T3 and T4 (secreted from follicles)
synthesized from tyrosine and iodine
transported in blood mainly bound to TBP (small amount = free)
T3 is more potent (biologically active)

calcitonin (secreted from parafollicular cells)

106
Q

thyroid hormone synthesis

A
  1. thyroglobulin in synthesized in follicle cell + secreted to colloid = backbone for attachment of tyrosine rings
  2. iodide is contransported with Na+ from blood into cell → diffuses across cell; moved into lumen by pendrin (transporter)
  3. I- is oxidized + attached to tyrosine rings (1 I- = MIT; 2 I- = DIT)
  4. iodotyronsines are coupled = T3 + T4 attached to TG backbone
  5. when body needs T3/T4, molecule is endocytosed
  6. lysosomal enzymes release T3 + T4 from TG backbone
  7. hormones = lipid soluble → released into ISF → blood
107
Q

TPO

A

thyroperoxidase = enzyme
under control of TSH
acts in oxidation of I- and coupling of MIT/DIT to DITs

108
Q

T3 + T4

A

T3 = MIT + DIT
T4 = DIT + DIT

MIT = 1 I-
DIT = 2 I-

109
Q

thyroid hormone secretion

A

neural inputs = ↑ TRH secretion from hypothalamus→ ↑ TSH secretion from ant. pituitary → ↑ thyroid hormone secretion from thyroid gland → target cells
= T4 (prohormone) converted to T3 in peripheral cells and liver
T3 binds to nuclear receptors

negative feedback of thyroid hormone on pituitary + hypothalamus

110
Q

thyroid hormone actions

A

act on most tissues = changes in transcription + translation processes to synthesize new proteins
increase metabolism
required from growth and development

111
Q

catabolic effect of T3

A

↑ breakdown of protein (muscles) + fat
↑ cholesterol metabolism
↓ serum cholesterol

112
Q

anabolic effect of T3

A

↑ basal metabolic rate (=↑ O2 consumption + ↑ heat production)
↑ CHO absorption + utilization

113
Q

TH actions: growth + development

A

act as tissue growth factors
small amounts stimulate protein synthesis
↑ GH/IGF-1 production
needed for CNS maturation during fetal stage

114
Q

maternal hypothyroidism

A

poor fetal CNS development + mental developmental disability

115
Q

permissive actions of TH

A

CV = targets beta-adrenergic receptors → ↑ hr and contractility, ↑ bp
SNS = targets beta-2 adrenergic receptors → potentiation
reproductive system = needed for normal function + fertility

116
Q

Grave’s disease

A

autoimmune disorder
overactivity of thyroid gland

TSH receptor antibodies stimulate thyroid hormone production (even in absence of TSH = continual tropic effect)
trophic effect in eyes + thyroid = ↑ cell growth
↑ BMR, weight loss, exophthalmos, goitre

117
Q

Hashimoto’s thyroiditis

A

autoimmune disorder
underactivity of thyroid gland
TPO antibodies destroy gland to block TPO action = no hormone synthesis
myxedema (weight gain, lethargy), cretinism (↓ growth in children)

118
Q

symptoms of hypothyroidism

A

lethargy, weight gain, cold intolerance
constipation, nausea/low appetite, menorrhagia, edema
shortness of breath, dry skin, brittle hair + nails
myxedema madness

119
Q

goitre formation

A

hyperthyroidsim: high T3 + T4 levels, low TSH levels
- antibody stimulation of gland causes topic + trophic effect (negative feedback = inhibition of TSH levels)

hypothyroidism (non-autoimmune cause): high TSH + TRH, low T3 + T4 levels
- low iodine in diet = unable to synthesize T3/T4 even with ↑ TSH = ↑ thyroglobulin → gland enlarges (no negative feedback)

120
Q

best test for thyroid function

A

TSH measurement
changes in TSH occur before measurable changes in T3/T4
= reflection of true state of free T3/T4

121
Q

iodine deficiency

A

from diet = most common cause of hypothyroidism, goitre, developmental/intellectual disability, preventable brain damage
North America consumes iodized salt = prevent deficiency
only need 150 ug per day

122
Q

parathyroid gland

A

4 glands, embedded on posterior thyroid gland
chief cells secrete PTH

123
Q

PTH

A

parathormone
peptide hormone
involved in calcium balance → [Ca2+] = more in ECF than ICF

↑ plasma [Ca2+] and ↓ plasma [phosphate]

124
Q

calcium in body

A

99% stored in bone
1% = free Ca2+ + bound calcium
- 0.1% in ECF
- 0.9% in ICF

125
Q

calcium

A

structural role - bone + teeth
blood coagulation
intracellular messenger
regulation of excitability

126
Q

phosphate

A

structural role
metabolism (ATP, nucleic acids)
buffer (maintaining pH balance)

127
Q

calcium balance

A

PTH = from parathyroid gland; targets bone
active vit D = from kidneys; targets GI tract
calcitonin = from thyroid gland; targets kidneys

128
Q

bone

A

organic = collagen type 1
inorganic = calcium phosphate + hydroxyapatite
bone cells = oblasts, oclasts, ocytes

129
Q

bone cells

A

osteoblasts: bone makers
osteoclasts: bone breakers
osteocytes: bone maintainers

130
Q

resorption

A

breakdown of bone
by oclasts
bone remodelling process

131
Q

hormonal regulation of Ca2+ balance

A

↓ plasma Ca2+ = ↑ PTH secretion from parathyroid glands
→ kidneys = ↑ Ca2+ reabsorption + ↑ active vitD formation
→ bone = ↑ resorption
restore plasma Ca2+ levels

132
Q

control of PTH secretion

A

influenced by small changes in plasma [Ca2+]
low Ca2+ stimulates parathyroid endocrine cell to release PTH → target cell (bone; GI) = response to ↑ Ca2+ in blood
ideal Ca2+ level = neg feedback to parathyroid cells

133
Q

synthesis of active vitamin D3

A

dietary vit D2/D3 or sunlight (converts 7-dehydrocholesterol found in skin to vit D3) = ↑ plasma vit D
25-hydroxylase in the liver = hydroxylation of vit D to 25-OH D → travels through blood to kidneys
1-hydroxylase in kidneys = hydroxylation of 25-OH D to 1,25-(OH)2D
stimulates GI tract to ↑ absorption of Ca2+ + phosphate into blood

134
Q

1-hydroxylase

A

enzyme in kidneys
hydroxylation of 25-OH D to synthesize potent form of vitD
activity stimulated by PTH

135
Q

VitD regulation of Ca2+ absorption

A

protein upregulation through transcriptional changes (enters cell + binds to receptor → translocation to nucleus)
- ECaC: epithelial calcium channel
- calbindin protein
- basolateral calcium pump

136
Q

Ca2+ absorption

A

Ca2+ enters cell in duodenum through ECaC
binds to calbindin to diffuse across cell
crosses basolateral membrane by PMCA1 (Ca2+ ATPase pump)

137
Q

rickets

A

deficiency of active Vit D
in children: deficiency in mineralization of bone matric = bones remain soft
- soft spot is slow to close; curved bones; large joints; bowed legs

138
Q

osteomalacia

A

active vitD deficiency in adults
(similar to rickets)

139
Q

hormones favouring bone formation

A

insulin
growth hormone
insulin-like growth factor-1
estrogen
testosterone
calcitonin

140
Q

hormones favouring bone resorption

A

PTH
cortisol
thyroid hormones = T3 + T4

141
Q

tetany

A

low plasma calcium increases nerve + muscle excitability via opening of Na+ channels
causes carpopedal spasm (sustained muscle contraction in wrist)

142
Q

pancreas

A

islet of Langerhans = cluster of cells
alpha cells (15-20%) = glucagon
beta cells (55-90%) = insulin
delta cells (3-10%) = somatostatin

endocrine secretions
also pancreatic polypeptide and vasoactive intestinal polypeptide

143
Q

insulin

A

feasting hormone
increases uptake + storage of fuels (glucose, triglycerides, amino acids)
anabolic

144
Q

glucagon

A

fasting hormone
increases mobilization of fuels when needed
catabolic

145
Q

target for insulin action

A

skeletal/cardiac muscle
adipocytes
hepatocytes

146
Q

insulin actions in liver

A

↑ glycogenesis + ↓ glycogenolysis
↑ glycolysis + ↓ gluconeogenesis
↑ fat synthesis + ↓ fat breakdown
↓ ketogenesis
↑ protein synthesis + ↓ protein breakdown

147
Q

insulin actions in muscle

A

↑ glucose uptake; ↑ glycogenesis
↓ glycogenolysis
↑ amino acid uptake
↑ protein synthesis + ↓ protein breakdown

148
Q

insulin actions in adipose tissue

A

↑ glucose uptake
↑ glycolysis
↑ fatty acid uptake
↑ fat synthesis
↓ fat breakdown

149
Q

activation of insulin receptor

A
150
Q

glucose transport

A

insulin-sensitive GLUT-4 facilitated transport (independent of Na+)
insulin causes translocation of vesicles + insertion of transporters into membrane = glucose uptake

151
Q

short-term glucose source

A

CHO = readily available in blood immediately after a meal

152
Q

long term glucose source

A

glycogen (stored glucose) = broken down by glycogenolysis in liver
12-24 h after meal
post-absorptive phase

153
Q

fasting: long term glucose source

A

gluconeogenesis = new synthesis of glucose from non CHO sources like aas and fatty acids
post-24 h

154
Q

feasting: insulin effect on glucose

A

glucose is stored as glycogen in liver + muscle

155
Q

feasting: insulin effect on fat

A

fatty acid synthesis in liver by acetyl-coA
triglyceride synthesis in adipose tissue

156
Q

feasting: insulin effect on proteins

A

protein synthesis in liver and muscles
use amino acids

157
Q

insulin deficiency

A

relative or absolute
associated with catabolic state = glucagon predominates
energy substrates are released from storage into blood
impaired glucose uptake into fat + muscle (90% of GLUT4 transporters are held intracellularly in vesicles)

  • ↑ gluconeogensis
  • muscle breakdown
  • fat breakdown
158
Q

fasting: glucagon effect on glucose

A

glycogen breakdown in muscle + liver

159
Q

fasting: glucagon effect on fat

A

liver: glycerol → glucose; free fatty acids → ketone
adipose: lipolysis
muscle: fatty acids used for energy

160
Q

fasting: glucagon effect on protein

A

liver: gluconeogenesis from aas
muscle: protein catabolism

161
Q

blood glucose levels

A

net effect of hormone actions
insulin = decreased
glucagon = increased

162
Q

control of insulin secretion

A

beta cells are stimulated to ↑ insulin secretion by:
- ↑ plasma glucose
- ↑ plasma amino acids
- incretins
- ↑ parasympathetic activity

inhibited by sympathetic activity = ↑ plasma epinephrine

163
Q

hypersecretion of insulin

A

causes: pancreatic tumor, overdose
consequences: hypoglycemia → autonomic + hormonal response changes in brain
= ↑ sympathetic activity → palpitations, sweating
↑ production of counter regulatory hormones
tired, confusion, drowsy
convulsions, coma

164
Q

hyposecretion of insulin

A

deficiency
- hyperglycemia
- diabetes mellitus
- ketoacidosis

165
Q

type I diabetes

A

autoimmune disease
early onset
beta cells are destroyed
absolute insulin deficiency
~5-10% of cases in N.A.

166
Q

type II diabetes

A

increased resistance to insulin
associated with obesity
relative insulin deficiency
more common in adults
~90% of cases in N.A.

167
Q

insulin deficiency

A

leads to catabolic state
- hyperglycemia, wasting, acidosis, ketogenesis
= diabetic ketoacidosis

168
Q

ketoacidosis

A

glucagon stimulates break down of stores in liver = production of ketones
severe metabolic decompensation leads to hyperosmolarity, dehydration, and death

169
Q

polyuria

A

cardinal symptom of diabetes mellitus
↑ urine vol
↑ frequency of urination

170
Q

glucosuria

A

cardinal symptom of diabetes mellitus
glucose in urine

171
Q

polyphagia

A

cardinal symptom of diabetes mellitus
increased hunger

172
Q

polydipsia

A

cardinal symptom of diabetes mellitus
increased thirst

173
Q

chronic complications of diabetes mellitus

A

myocardial infarctions
hemorrhages
long term high levels of glucose leads to blindness, renal failure, atherosclerosis, changes in sensation, poor wound healing

174
Q

type I treatments

A

administration of insulin
islet cell transplant
gene therapy

175
Q

type II treatments

A

dietary control + exercise
drugs which ↑ insulin secretion + response to insulin
insulin administration

Physiology (12 decks)

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