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endocrine Flashcards

1
Q

autocrine cell

A

prods substance that binds to specific receptor on own cell surface/receptors inside cell

local mediator

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2
Q

paracrine cell

A

prods substance that binds specific receptor on nearby target cell, e.g. NMJ

local mediator

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3
Q

endocrine cell

A

prods substance transported in blood, bind to specific receptors on distant target cells

sys to circulate hormones

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4
Q

endocrine glands

A

collection glands that secr hormones directly into circulatory sys to carry to distant target

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5
Q

cell types in islet of langerhans

A
  1. alpha secr glucagon
  2. beta secr insulin
  3. delta secr somatostatin
  4. F secr pancreatic polypeptide
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6
Q

production of insulin

A

beta cells synth pro-hormone proinsulin -> active insulin by removal water soluble polypep

half life 5-8mins

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7
Q

what does insulin bind to

A

specific tyrosine kinase mem receptor

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8
Q

how do beta cells cause prod insulin

A
  1. glucose enters via GLUT2
  2. raised intracellular gluc = incr ATP
  3. ATP sensitive potassium channs blocked
  4. K+ accumulates in cyt => depol cell mem
  5. causes V-gated Ca2+ channs open
  6. Ca2+ in => exocytosis vesicles cont insulin

neg feedback mech

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9
Q

further control of insulin

A
  • GI hormones GIP + GLP-1 = anticipatory release to prevent surge in gluc absorp after meal
  • parasymp activity incr secr during + after meal
  • symp activity inhibit secr
  • incr plasma aas after meal incr secr
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10
Q

where is gluc uptake independent of insulin

A
  • brain (GLUT3 transporters)
  • mammary gland, GI tract + kidney = 2AT coupled to Na+ transport
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11
Q

overview how insulin cause effects

A
  1. binds tyrosine kinase receptor
  2. receptor phosphorylates insulin-receptor substrates
  3. 2nd messenger pathways alter prot synth + existing prots
  4. => cell metab + mem transport changed
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12
Q

insulin in the liver

A

GLUT2 receptors can work either way
1. fasted = hepatocytes make gluc + transport out -> blood
2. fed = gluc -> hepatocyte + insulin stims hexokinase gluc -> gluc-6-p for low intracellular conc gluc

GLUT2 always present in cell mems

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13
Q

clinical signs insulin deficiency

A
  • hyperglycaemia
  • weight loss bc decr prot synth + incr prot breakdown
  • PU/PD
  • ketoacidosis bc lots B-ox bc needing E from fat metab => krebs = oxaloacetate -> liver for gluconeogenesis = ketone bods => lots
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14
Q

glucose in CNS

A

metab almost 100% reliant on gluc = steady transport in + can’t incr/decr rate

gluc level in CSF direct proportional to blood sugar
* excess incr osmolarity CSF => water out neurons
* too little = neurons starve

cells not sensitive to insulin

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15
Q

functions of insulin

A
  • incr glucose oxidation
  • incr glycogenesis
  • incr lipogenesis
  • incr prot synth
  • inhibit enzs in catabolic processes
  • inc cellular uptake of gluc + aas

==> incr stores glycogen, fat + prot

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16
Q

glucagon

A
  • alpha cells secr + store as active
  • water soluble polypeptide
  • binds specific G-prot coupled mem receptor

half life 4-6 mins

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17
Q

what stims release glucagon

A
  • decr blood gluc
  • incr plasma aas after meal = avoid prot induced hyperinsulinemia (=> hypoglycaemia)
  • parasymp activity
  • symp activity
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18
Q

effects of glucagon

A
  • incr gluconeogenesis
  • incr glycogenolysis
  • incr ketogenesis

catabolic

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19
Q

somatostatin effects

A
  • decr secr growth hormone
  • paracrine inhibition of insulin + glucagon release
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20
Q

diabetes mellitus clinical signs

A
  • hyperglycaemia
  • PD + PU
  • ketoacidosis

can get a combo of type I + II

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21
Q

type I vs type II diabetes mellitus

A

1 = due inadequate insulin secr (more common dogs)
2 = due abnormal target cell responsiveness (more common cats)

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22
Q

why does diabetes cause PU/PD

A

incr gluc in blood => freely filtered into nephron + renal threshold for reabsorp exceeded => glucosuria => incr urine

AND ECF vol decr + plasma osmolarity incr => thirst centre in hypothal stimmed

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23
Q

why does diabetes cause ketoacidosis

A

‘fasted state’ => adipose tiss broken down => FAs in blood => liver uses beta-ox to break down but not all acetyl CoA can enter citric acid cycle => excess forms ketone bods, e.g. acetone => large amounts cause illness

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24
Q

topographical anatomy pituitary gland

A
  • extends down from brain via thin stalk
  • cradled + protected by sphenoid bone
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25
Q

anterior pituitary

A

made up endocrine cells derived from oral ectoderm of Rathke’s pouch = upgrowth epithel of pharynx towards base brain = endocrine gland

anterior wraps round posterior
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26
Q

posterior pituitary

A

extension of hypothal (neural ectoderm) into anterior pit
* cell bods in hypothal
* axons = stalk of post pit
* nerve endings in post lobe

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27
Q

anatomy pituitary

A

2 fused glands

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28
Q

function post pit

A

release hormones synthed hypothal cell bods (oxytocin + ADH) -> caps

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29
Q

cap sys pit gland

A

== hypothalamic-hypophyseal cap portal sys in series
1. neurones synth tropic hormones -> cap sys 1
2. portal vessels carry neurohormones -> ant pit to act on endocrine cells
3. endocrine cells release peptide hormones -> cap sys 2 -> bod

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30
Q

tropic vs trophic hormones

A

tropic = causes release of another hormone
trophic = regs growth + development target organ

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31
Q

anterior pituitary hormones + their effect/target organ

A

all trophic hormones, all but prolactin tropic hormones

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32
Q

what kind of feedback do tropic hormones allow

A

short loop as ant pit hormones feedback to hypothal + long end-organ loop that can feedback to hypothal or ant pit

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33
Q

intermediate lobe of pituitary

A
  • same embryological origin as ant lobe
  • secr melanocyte=stimming hormones == MSH
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34
Q

label

A
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35
Q

thyroid location

A

2 lobes either side trachea just below larynx

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36
Q

hormone path to stim thyroid gland

A

neurones secr thyrotropin releasing hormone (TRH) -> portal vessels -> endocrine cells secr thyrotropin/thyroid stimulating hormone (TSH) -> thyroid gland

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37
Q

thyroid gland structure

A

spherical grps epithelial follicular cells around non-cellular filling

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38
Q

synth thyroid hormone

A

follicular cells:
1. trap iodide via NaI symporter, ox it to iodine + transport -> colloid
2. synth + transport thyroglobulin, tyrosine, enzs -> colloid
3. T3 + T4 synthed in colloid + bound thyroglobulin
4. droplets colloid reenter follicular cells by pinocytosis + bind lysosomes
5. Ts cleaved from thyroglob - lipophilic = diff into blood
6. Ts prot bound in blood

T(no.) indicates no. iodines it has

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39
Q

what are T3 + T4 bound to in blood

A
  • 70-80% to thyroxine binding globulin (TBG)
  • 20-30% to albumin
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40
Q

what are thyroid hormones

A

T3 = triiodothyronine
T4 = thyroxine

T4 = main hormonal product, T3 more biologically active so T4->T3 in peripheral tiss

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41
Q

metab of tyroid hormones

A

free T4 -> T3/reverseT3 (inactive, from deiodination)

free T3 in peripheral tiss (mostly from metab T4) - partic liver, musc, kidney

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42
Q

storage thyroid hormones

A
  1. colloid = store 2-3mo, bound to thyroglobulin
  2. prot bound in blood = store few days

as free mols bind target receptors more mols dissociate from TBG

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43
Q

reg thyroid hormones

A

secr TRH from hypothal driven by CNS
* long-loop + short-loop feedback but dominant reg pathway = TSH (incr thyroid horms in blood inhibit it)
* no TSH = thyroid follicular cells inactive

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44
Q

effect prolonged incr TSH conc

A

follicular hyperplasia + hypertrophy

goitre = enlarged thyroid gland

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45
Q

role thyroid hormones

A
  • incr metab rate all tiss (except gonad, brain, spleen)
  • => incr O2 consumpt + thermogenesis (so more thyroid horms after prolonged cold)
  • required normal growth + development - incr prot synth + cell division
  • required normal CNS development
  • promote target responsiveness to symp NS
  • promote axonal conductivity
  • required normal gonadal function

all cells but CNS + testes have intracellular receptors for thyroid horm

46
Q

iodine deficiency

A

sheep are prone if on sheep deficient pasture
* cabbage reduces iodine uptake

47
Q

hormone classes

A
  1. water soluble bind receptors on cell surface - insulin, glucagon
  2. lipid soluble mostly bind receptors in cyt/nucleus
48
Q

water soluble hormones

A
  • freely soluble in plasma
  • bind cell surface receptors
  • activate 2nd messenger sys w/in cell = amplify signal
  • rapid action
  • short half-life
  • metabed by liver + excreted in kidney
49
Q

lipid soluble horms

A
  • mostly bind cytosolic/nuclear receptors
  • prot bound in plasma (store) + free portion physiologically active
  • require carrier prot for transport in blood
  • less immediate action
  • longer 1/2-life

affected disturbances plasma prot conc

50
Q

advantages carrier prots for horms

A
  1. hormone reservoir - active interacts w receptor, used, new particles detach from transport prot
  2. hormone buffer - prevent spikes in active hormone conc, e.g. during synth = more stable long-term conc
  3. reduce hormone loss - prot bound horms no filtered out at kidneys but free lost in urine
51
Q

disads carrier prots for horms

A
  • affected by disruptions blood levels carrier prot - decr = incr free horm conc
  • competition from substances like drugs - esp less specific, e.g. albumin
52
Q

reg growth hormone (GH) secr

A

by 2 hypothalamic neurohorms:
1. GHRH
2. GHIH = somatostatin

direct effects + stims liver prod insulin growth factor-1
* mediates growth-stimming effects of growth horm (neg feedb on GH secr cells in pit + stims GHIH in hypothal)

from ant pit

53
Q

GH vs IGF-1

A
  1. prot (191aas) vs peptide (70aas)
  2. 50 vs 95% prot bound
  3. both tyrosine kinase receptor
  4. GH sim struct prolactin vis IGF sim proinsulin

GH-synthing cells = most abundant cells in ant pit

54
Q

what incr GH secr

A
  • CNS input
  • strenuous physical activity
  • starvation
  • stress
  • decr plasma gluc + FFAs
  • incr plasma aas
  • ghrelin from parietal cells + hypothal
  • thyroid horm, androgens + oestrogens
55
Q

functions GH

A
  • stim growth body mass + elongation bones - essential growth until sk complete)
  • bone, cart, soft tiss growth
  • lactation
  • anabolic: stim prot synth, lipolysis, inhibit tiss uptake + use gluc
56
Q

what is required for normal growth

A
  • GH
  • thyroid hormones
  • insulin
  • sex horms at puberty
  • adequate diet, absence chronic stressors, disease
57
Q

result of excessive GH prod

A

before growth plate closure = gigantism
after growth plate closure = acromegaly = grow too fast

58
Q

how is Ca in bone found

A

hydroxyapatite = complex of calcium phosphate

59
Q

calcium homeostasis where

A

reg Ca2+ + phosphate linked conc free Ca in plasma
* tight reg w/in 2% of limits at 2.5mM/l (50% free, 10% assoc anions, 40% prot bound)

60
Q

how does Ca homeostasis occur

A
  • intestinal absorp
  • renal excr
  • release + uptake from bone
61
Q

vit Ds where proded

A

D2 proded by plants
D3 proded by action UV light

v lil biological activity until hydroxylated

62
Q

hydroxylation vit D

A
  1. 1st in liver -> stored adipose tiss
  2. 2nd in kidney -> active form calcitrol

active form inhibits enzs hydroxylase enzs to reg

63
Q

role calcitrol

A

transported bound globulin -> bind intracellular receptors incr conc Ca in plasma by:
* incr Ca2+ + PO43- uptake from SI
* incr renal reabsorp Ca
* incr mobilisation Ca from bone

lipid soluble

64
Q

parathyroid glands

A

2 pairs glands (cr + cd) at poles 2 lobes thyroid
* chief cells make parathyroid horm (PTH)

65
Q

release PTH

A

cells in gland detect v small decr free Ca => release PTH incr Ca conc in plasma:
1. incr absorp Ca from GI tract (indirect via calcitrol)
2. incr mobilisation Ca from bone
3. decr urinary excr Ca

neg feedback loop

66
Q

PTH related prot (PTHrP)

A

same struct as N terminal end PTH = activates same receptors w same function
* more diverse actions, e.g. cell proliferation
* proded some cancers = no neg feedback = overprod = hypercalcaemia

proded most tisses

67
Q

calcitonin

A

made C-cells (parafollicular cells) of thyroid gland

68
Q

label

A

thyroid follicle

69
Q

role calcitonin

A

secr in response incr free Ca2+ to decr by affecting transport mechs in bone
* targets osteoclasts = bone remodelling less active = flux Ca/P bone -> plasma decr

not essential in terrestrial vertebrates

70
Q

oter effects calcitonin

A
  • incr urinary loss
  • decr gut absorp Ca
71
Q

how is phophate in bod

A

85% in bone as hydroxyapatite
ICF + ECF as:
* inorganic phosphates (H2PO4-) + (HPO42-)
* organic phosphates: phospholipids, nucleotides, ATP…

72
Q

phosphate homeostasis

A

normally kept w/in normal limits in Ca2+ metab
* absorbed in intestines, filtered, reabsorb, secr in urine
* calcitrol incr absorp from GI tract

depends on urinary excr as opposed absorp from SI for Ca2+

73
Q

what does PTH do to phosphate

A
  • decr serum phosphate
  • incr urinary excr phosphate
  • incr calcitrol secr
74
Q

result of chronic kidney disease

A

hyperphosphataemia stims PTH prod + inhibits activation vit D

75
Q

late preg/partur + Ca homeostasis

A
  • mammary cells extract large amount Ca2+ from ECF
  • mineralisation foetal skeleton late preg

homeostatic mechs have supply incr demand Ca

76
Q

laying hens + Ca homeostasis

A
  • 2wks b4 lay oestrog + progest stim extra bone dep BM cavities
  • incr oestrog = incr Ca-binding plasma prots
  • shell synth starts = PTH incr…
77
Q

adrenal gland

A

== suprarenal gland
* paired beneath peritoneum
* cranio-medial to each kidney

78
Q

zones adrenal gland

A
  1. medulla = symp neuroendocrine cells ((nor)adrenaline)
  2. zona reticularis secr androgens
  3. zona fasciculata secr glucocorticoids - cortisol
  4. zona glomerulosa secr mineralocorticoids - aldosterone
79
Q

derivation steroid horms

= adrenocortical horms

A
  1. all from cholesterol -> prenenalone
  2. -> glucocorticoids/mineralocorticoids/androgens

proded on demand, not stored locally

1 = rate-limiting step

80
Q

glucocorticoids

A
  • affect CHO (gluc), lipid + prot metab + help animals resist effects of stress
  • bound CBG + albumin in blood
  • inactivated liver

1/2 life longer than aldosterone bc more tightly prot bound

81
Q

what do mineralocorticoids do

A

homeostasis of Na+ + K+ in blood (affects blood vol/press)
* bound corticosteroid-binding globulin (CBG) + albumin in blood
* inactivated in liver

1/2 life 20mins

82
Q

what does aldosterone do

A
  • cause rapid incr Na+ reabsorp + K+ secr in principal cells DCT + CD
  • incr Na+ reabsorp salivary glands + LI

==> reabsorp water = incr vol ECF + incr art press

83
Q

methods reg aldosterone

A
  1. plasma K+ depolarises cell mem proding cells = prod
  2. RAAS renin in response decr bp
  3. ACTH required secr but minor role reg
  4. decr Na+ in ECF moderately stims secr
84
Q

glucocorticoids release

A
  • receptors in all nucleated cells
  • released response high sustained levels stress (infection, trauma, psychological)

essential for life

85
Q

variation in secr glucocorticoids

A

circadian variation strong in humans + in domestics but less pronounced

86
Q

what do glucocorticoids do relation gluc

A

reg gluc metab:
* promote gluconeogenesis in liver
* decr gluc uptake by tiss other than brain
== incr blood sugar levels = assist bod cope w stress

87
Q

Cushing’s syndrome

A

hyperadrenocorticism = too much glucocorticoids + mineralocorticoids = hyperglycaemia, muscle wastage, hair loss, PU/PD due interference w ADH

88
Q

Addisons disease

A

hypoadrenocorticism = not enough glucocorticoids/mineralocorticoids = keep too much K+, lose too much Na+ =
* cardiac arrhythmias (K+) inc bradycardia
* hypovolaemia (bc hyponatraemia)

==> hypovolaemic shock (can’t incr HR) = circulatory collapse

89
Q

what do glucocorticoids do related fat + prot

A
  • incr lipolysis
  • incr breakdown sk musc prots = substrate for gluconeogenesis

==> for ox FAs + aas for E use = preserve gluc

90
Q

other roles glucocorticoids

A
  1. permissive action on other horms, e.g. catecholamines cause vasoconstr
  2. IS to maintain low-level inflammation - high conc cortisol (e.g. at partur) = immunosuppression (stop inflamm, allergic reactions)
  3. Ca balance via effects GI tract, bone, kidney
  4. prot catabolism inhibits DNA synth so growth
91
Q

reg glucocorticoids

A

neg feedback as cortisol inhibits ant pit + hypothal + ACTH (stims cortisol) inhibits hypothal

92
Q

acth

adrenocorticotropic hormone

A
  • required for cholesterol -> pregnenolone (= for all hormones proded adrenal cortex)
  • regs androgen + glucocorticoid prod
93
Q

reg glucocorticoids vs mineralocorticoids

A

mineralocorticoids = also renin, Na+ conc (external factors)

94
Q

catecholamine secr

A

normally low, not essential for low, incr by stress + hypoglycaemia

95
Q

catecholamines

A

adrenaline, noradrenaline, dopamine
* proded adrenal medulla
* derived aa tyrosine
* water soluble

96
Q

reg catecholamine release

A

controlled preganglionic symp nerve fibres

97
Q

functions catecholamines

A
  • incr CO (incr HR, contractility, bp)
  • redistribute blood -> sk musc
  • incr plasma [gluc] (glycogenolysis, gluconeogenesis)
  • incr breakdown triglycerides -> FAs

urinary excr adrenaline good measure activity adrenal medulla

98
Q

horms that influence blood gluc

w origin + effect

A
  1. insulin, pancreatic beta, decr
  2. GLP-1, intestinal L, decr
  3. somatostatin, pancreatic delta, decr
  4. glucagon, pancreatic alpha, incr
  5. adrenaline, adrenal medulla, incr
  6. cortisol, adrenal cortex, incr
  7. growth hormone, ant pit, incr
  8. thyroxine, thyroid gland, incr
99
Q

prolactin vs GH

A

v similar struct w similar receptor (tyrosine kinase)
* water soluble

100
Q

what does prolactin do

A
  • stims growth + diff mammary tiss
  • stims milk prod after partur
  • important in maternal behaviour
  • luteotrophic in bitch
  • incr prior to onset brooding in birds
101
Q

reg prolactin

A

horms from hypothal:
* TRH stims
* dopamine inhibits

  • oestradiol stims secr via direct effect on proding cells in ant pit (causes hyperplasia + hypertrophy)
  • suckling reduces dopamine secr = incr prolactin secr
102
Q

pineal gland

A
  • centre of brain bet 2 hemispheres behind thalamus outside BBB
  • tryptophan -> serotonin -> melatonin (secrs m)

in mammals

103
Q

what affects melatonin secr

A

light exposure to eyes (photoperiods)

104
Q

circadian rhythms

body clock

A

primary clock in suprachiasmic nuclei in hypothal w inputs from cells at back retina
* melatonin causes drowsiness + lowers body temp

105
Q

leptin is

A
  • peptide horm in grp adipokines
  • stored in adipose tiss + secr incr in parallel w body fat stores so plasma level indicated level triglyc stored adipocytes
106
Q

leptin does

A

regs E intake + expenditure inc appetite + hunger, metab + behaviour
* binds receptor in hypothal to inhibit food intake

insufficient food = decr leptin = incr appetite

107
Q

clinical signs milk fever

A
  • sk musc weakness, tremors, recumbency
  • head tucked into flank
  • hypothermia
  • bloat
  • constipation
  • urine retention
  • dystocia = uterine inertia
  • dilated pupils

older = slower to mobilise Ca stores = more common

108
Q

CKD in relation Ca + P

A

less P excr = retained = hyperphosphataemia => hyperparathyroidism
1. directly
2. P binds ionised Ca = hypocalcaemia => release PTH
3. P decr calcitriol prod + calc decr PTH release normally

109
Q

label

A

pituitary gland

110
Q

label

A

thyroid + parathyroid glands
* CT capsule around each
* trabeculae to divide each into lobules

pink thyroid colloid
111
Q

label

A

pancreas

112
Q

label

A

mammary gland

NSF (22 decks)

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