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From Flashcardlet > PHYSIOL A > Flashcards

PHYSIOL A Flashcards

0
Q

what are the targets of homeostatic control?

A
  • conc. of O2 & CO2, nutrients, salts & electrolytes, waste products
  • temp
  • volume and pressure of extracellular fluid
  • pH of internal environment
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1
Q

define homeostasis:

A

regulation of internal environment so as to maintiain appropriate life sustaining conditions to cells and tissues of the body

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2
Q

what is the concept of positive feedback?

A

amplifies initial change by amplifying signal indefinitely - ended by a separate mechanism

allows large response to develop from small initial signal

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3
Q

describe blood clotting as a positive feedback mechanism:

A
  • tear in vessel wall
  • stimulates platelet aggregation
  • platelets release chemicals to attract other platelets
  • newly attracted platelets further release chemicals to attract other platelets
  • clot formation complete other inhibitory processes prevent further aggregation
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4
Q

simply describe Ferguson reflex:

A

fetus’ head stretches isthmus - stimulates stretch receptor neurons

  • signals to brain relayed to pituitary stimulates release of oxytocin from posterior pituitary …oxytocin stimulates contraction
  • fetus’ head pushes against isthmus more => more oxytocin produced and released
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5
Q

what is the homeostatic control of blood pressure?

A
  1. haemorrhage reduced BP
  2. stretch of baroreceptors decreases
  3. info sent afferent path to brain
  4. info through efferent to heart and vessels
  5. response = heart beats faster and blood vessels constrict to raise blood press to normal level (“homeostatic” level)
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6
Q

effects of excessively low blood glucose(Hypoglycaemia)?

<4mmol/L

A
  • CNS dysfunction
  • dysfunction/damage to retina, germinal epithelium and RBCs

cells almost exclusively glucose for energy

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7
Q

what do endocrine cells release?

A

hormones

which can be either paracrine or autocrine

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8
Q

what do nerve cells release in terms of homeostasis regulation?

A

neurotransmitters - physical connections through synapses

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9
Q

what do chemical signals act on?

A

receptors at target site, on membrane or within cell

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10
Q

in terms of thermoregulation what happens when the environmental temperature is higher than body temperature?

A
  • vasodilatation, moving blood away from skin surface
  • sweating
  • hair follicles relax, air flow next to skin increases heat loss by convention
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11
Q

in terms of thermoregulation what happens when body temp is higher than environmental temperature?

A
  • reduced sweating
  • piloerection(hairs erect due to pilorum muscles) goose bumps!
  • constriction of skin arterioles
  • shivering(muscles)
  • metabolic changes(brown fat mitochondrion)
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12
Q

describe the blood glucose feedback loop in steps:

A
  1. eating increases blood glucose
  2. this change in blood glucose is detected by beta cells in pancreas
  3. causes insulin release into blood stream
  4. insulin acts on target tissues(liver/muscles)
  5. response of target tissues will result in removal of glucose from circulation - due to the increased uptake by liver & muscle
  6. blood glucose levels decrease, restoring homeostasis
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13
Q

when blood glucose rises, cells increase their uptake but what do they do with the glucose?

A
  • used for metabolic energy
  • fat synthesis (storage)
  • glycogen synthesis (storage)
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14
Q

in periods of fasting describe the feedback mechanism that brings blood glucose back to homeostatic levels:

A
  1. low blood glucose is recognised by beta cells in pancreas
  2. pancreas is stimulated to secrete glucagon
  3. increase of circulating glucagon(but cannot be used yet)
  4. glycogen broken down in liver
  5. released into blood stream for use
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15
Q

what goes wrong in type 1 diabetes?

A

beta cells fail to detect blood glucose, therefore failure to release insulin into blood stream to stimulate uptake of increased blood glucose

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16
Q

what goes wrong in type 2 diabetes?

A

tissue cells are desensitised to insulin,

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17
Q

what are 5 important roles of calcium in homeostasis?

A
  1. neurotransmitter and hormone release mechanism
  2. muscle contraction
  3. hardening of teeth and skeleton
  4. blood clotting
  5. cell devision and excitability
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18
Q

describe blood calcium regulation:

A
  1. decrease in plasma calcium concentration
  2. decrease detected by CHEMOreceptors in PARATHYROID gland
  3. this stimulates release of ParaThyroid Hormone(PTH) release into blood stream
  4. PTH acts on target tissues (bone, kidney, gut)
  5. response= increase REsorption FROM bone, BY kidney, TO gut(where it is absorbed)
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19
Q

some potential consequences of diabetes mellitus?

A
  • CVD

- retinopathy/neuropathy (think glucose only energy supply)

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20
Q

in terms of feedback mechanisms what is the cause of rickets?

A

rickets is a disease surround calcium levels in the blood
When one has rickets, low blood causes PTH hormone release and increased resorbtion of Calcium from bone BUT vitamin D3 is needed for this, its not there so, calcium isn’t resorbed meaning it cannot be absorbed in gut

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21
Q

what are the communication types in the endocrine system?

A
  • gap junctions(cell to cell)
  • contact-dependent signals(interaction between membrane molecules)
  • local communication(paracrine/autocrine)
  • long-distance communication(through blood=endocrine)
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22
Q

what are the major endocrine glands(top to bottom)?

A
  • pituitary gland
  • thyroid gland
  • parathyroid gland
  • adrenal glands(on tops of kidneys
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23
Q

roles of endocrine system?

A

4 x regulation of metabolism
H2O and electrolytes
growth and development
responding to stress
3 x controlling wake-sleep patterns
temperature
repoduction

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24
Q

describe endocrine glands:

A

ductless

release into surrounding FLUID

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25
Q

describe exocrine glands:

A

ducts

substances travel along ducts to SURFACE

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26
Q

what 3 things can stimulate hormone release?

A
  • hormonal
  • neural
  • humoral
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27
Q

describe the action of hormonal stimulation of hormone release?

A

hypothalamus stimulates anterior pituitary which in turn stimulates thyroid gland, adrenal cortex, gonads which release hormones

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28
Q

describe the action of neural stimulation of hormone release?

A

this is stimulation from nerve fibres

CNS(spinal cord) acts through SNS fibres on the adrenal medulla which secretes CATECHOLAMINES through blood capillaries

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29
Q

describe the action of humoral stimulation of hormone release?

A

stimulation by detection of levels of substances in blood eg. ions
eg. low Ca2+ in capillaries stimulates release of PTH from parathyroid gland

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30
Q

define “up-regulation”:

A

target cells form more receptors in response to the hormone

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31
Q

define “down-regulation”:

A

target cells lose receptors in response to hormone

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32
Q

define permissiveness:

A

when a hormone must be present to permit another hormones effect

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33
Q

define synergism:

A

combination of hormones produces an effect greater than the sum of their separate effects

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34
Q

define antagonism:

A

a hormone reduces the effectiveness of another hormone

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35
Q

what is a hormones half life?

A

the length of time taken for the hormone concentration to drop by half

can range from seconds to days

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36
Q

percentage of endo/exocrine glands in the pancreas?

A

98% exocrine

2% endocrine

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37
Q

where does the release of insulin and glucagon occur?

A

at the islands of langaham

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38
Q

what are the 2 types of endocrine dysfunction?

A

hyper + hypo secretion

primary = abnormality within the gland
secondary = gland is normal, but too little/much stimulation
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39
Q

what are the 3 main hormone types?

A
  1. peptide: derived from chains of AA
  2. amines: derived from AAs tyrosine and tryptophan
  3. steriods: derived from cholesterol
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40
Q

what is the most common type of hormone?

A

peptide!

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41
Q

steps in synthesis and release of peptide hormones?

A
  1. synthesised at preprohormone in the RER
  2. can be modified to prohormone in the golgi apparatus
  3. released into extracellular space via secretory vesicles
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42
Q

how do pepide hormones influence a cell?

A

peptide hormones cannot diffuse across cell membranes, so second messenger cascade systems are needed
- cascade leads to signal amplification, rapid effects ..HOW?
receptor-ligand complex activates an amplifier enzyme resulting in a single signal molecule turning into many second messenger molecules

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43
Q

name the Amine hormones and from which AAs they are derived from:

A

Catecholamines FROM tyrosine
Thyroid hormones FROM tyrosine

Melatonin FROM tryptophan

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44
Q

what is the difference between catecholamines and thyroid hormones?

A 
C = tyrosine derivative       TH = iodinated tyrosine derivative
C = hydrophilic                   TH = hydrophobic
C = cell surface recept       TH = intracellular receptors 
C = activates 2nd messen TH = activates genes
C = few secs half life          TH = few days for half life
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45
Q

what are steroid hormones derived from?

A

cholesterol (lipophilic)

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46
Q

how are steroids transported?

A

needs to be bound to carrier proteins

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47
Q

where are receptors for steroid hormones?

A

in the cytoplasm or nucleus

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48
Q

how do steroid hormones effect singular cells?

A

effects target cell by activating target genes for protein synthesis

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49
Q

why do membrane receptors usually elicit a faster response than intracellular receptors?

A

because receptors in cytoplasm and nucleus often cause transcription which is a slower process

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50
Q

what tissues make up the 2 sections of the pituitary gland?

A 
anterior = glandular epithelial tissue 
posterior = nervous tissue
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51
Q

how are neurohormones made?

A

via neurohypophysis
made and packaged in cell body of neurons in hypothalamus that transport neurohormones in vesicles directly to posterior pituitary where they are stored in hypothalamic neuron terminals

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52
Q

what does the posterior pituitary do? which 2 hormones does it release?

A

it does NOT synthesise hormones, but stores the hormones formed in hypothalamic neurons
secretes hormones directly into the blood
Releases: AntiDiuretic Hormone, Oxytocin

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53
Q

what stimulates release of AntiDiuretic Hormone from posterior pituitary?

ADH produced by neurosecretory cells in supraoptic and paraventricular nucleus

A
  1. increase in osmolarity
  2. decrease in blood pressure
  3. increase stressors(adrenergic)
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54
Q

what converts cholesterol into steroid hormone?

A

enzymes in mitochondria and endoplasmic reticulum of tissues

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55
Q

what is ADH effect on blood and renal vessel?

A

increase of vasoconstriction

- works to retain fluid

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56
Q

what is ADH effect on CNS?

A

increase in thirst

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57
Q

what is ADH effect on kidney?

A

increases H2O reabsorption

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58
Q

what is ADH effect on the anterior pituitary gland?

A

increases secretion of AdrenoCorticoTrophic Hormone (ACTH)
which LEADS to
-> increase aldosterone secretion and the
-> increase conservation of Na+ and H2O

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59
Q

what stimulates contraction of uterine smooth muscle during childbirth:

A
  • decreased levels of progesterone(at end of pregnancy)
  • cervical stretch receptors

this is a positive feedback system

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60
Q

how do hypophysiotrophic hormones get to the ANTERIOR pituitary?

A

synthesised in neurons in hypothal

uptake into special blood capillaries that go direct to anterior pituitary via Hypothalamic-Hypophyseal portal system

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61
Q

what are the 2 types of hypophysiotrophic hormones?

A
  1. releasing hormones (stimulates release of…)

2. inhibiting hormones (suppresses release of…)

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62
Q

what are the endocrine cells of the anterior pituitary controlled by?

A

hypophysiotrophic hormones

endocrine cells secrete anterior pituitary hormones into systemic blood
**NOTE endocrine cells = anterior pituitary hormones
hypothalamic-hypophyseal portal system = hypophysiotrophic hormones

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63
Q

what type of hormones are hypophysiotrophic hormones?

A

peptide neurohormones

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64
Q

what do stressors trigger in the endocrine system?

A

both internal and external stressors trigger the release of cortisol via 2 hormonal intermediates: CRH(from brain to anterior pituitary), ACTH(anterior pituitary to adrenal cortex)
these hormonal intermediates are self regulated via negative feedback

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65
Q

state steps of stress release of hormones:

A 
BRAIN
1. CRH
ANTERIOR PITUITARY
2. ACTH
ADRENAL CORTEX 
3. cortisol
TARGET CELL ...=> response!
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66
Q

what are the 5 hormones of the anterior pituitary?

A
  1. TSH Thyroid Stimulating Hormone
  2. ACTH
  3. Prolactin
  4. LH & FSH
  5. Growth Hormone
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67
Q

what does Thyroid Stimulating Hormone TSH do?

A

it has a positive influence on thyroid gland stimulating release of T3 and T4
-> Metabolic Rate

68
Q

what does ACTH do?

A

influences Adrenal Cortex
stimulates release of Cortisol
-> Metabolic rate, stress response

69
Q

what does Prolactin do?

A

influences mammary glands

stimulates breast growth and milk secretion

70
Q

what does LH and FSH do?

A

both influence the Gonads(MALE = testes FEMALE = ovaries)
LH: sex hormone secretion
FSH: gamete production

71
Q

what sex hormones are produced in males and females?

A 
females = oestrogen & progesterone 
males = testosterone
72
Q

what are gamete?

A

person creating stuff
female = ova
male = sperm

73
Q

what does Growth Hormone do?

A 
influences liver(+) 
stimulates release of somatomedins -> bone & soft tissue = growth

also influences other tissues(both + and -)

74
Q

what factors influence growth:

A
  • nutrition
  • genetics
  • free from stress and disease
  • growth influencing hormone
75
Q

what does the growth hormone act via?

A

somatomedins

- these are produced in the liver and at the target sites of bone and muscle

76
Q

what is growth hormone regulated by?

A

antagonistic GHRH and GHIH (somatostatin)

77
Q

what is the overall effect of growth hormone?

A
  • uses up fat stores

- promotes protein synthesis

78
Q

are is the different between somatotropin, somatostatin, somatomedins:

A 
somatotropin = growth hormone
somatostatin = growth hormone inhibiting hormone
somatomedins = insulin-like growth factors (IGF)
79
Q

what are IGFs?

A

Insulin like Growth Factors = peptide hormone
produced in the liver
encourage cell division
2 types: IGF-1 - effects most cells, inhibits apoptosis
IGF-2 - growth promotion during gestation

80
Q

describe the release pattern of growth hormone

A

it is release in bursts due to the firing pattern of neurons

-> during sleep growth hormone fires more

81
Q

what increases amplitude of bursts to growth hormone, thus increasing release rate?

A
  • exercise
  • stress
  • hypoglycemia
  • fasting (IGF-1 is low)
  • circadian rhythm …anything that requires use of fat stores basically
82
Q

what effects does the growth hormone have on growth?

A
  • hyperplasia (increase NUMBER of cells)
  • hypertrophy (increase SIZE of cells)
  • increase protein synthesis
  • increase bone growth
83
Q

what effect does growth hormone have on metabolism?

A
  • increase fat breakdown
  • increase glucose output from liver
  • decrease insulin sensitivity in muscle => decrease glucose uptake by muscle => instead muscles use free fatty acids resulting in increased blood glucose
84
Q

what happens with the hypersecretion of growth hormone? give an example of the cause:

A

eg. tumour of the anterior pituitary

85
Q

functions of vasopressin:

A
  • produced in hypothalamus
  • increases kidney reabsorption of water
  • potent arteriolar vasoconstrictor
  • released when osmolarity of the plasma increases
86
Q

what hormone is released from hypothalamus:

A

CRH

87
Q

what hormone is primarily regulated by the anterior pituitary?

A

cortisol

88
Q

what does the anterior pituitary primarily secrete?

A

trophic hormones

89
Q

how does growth hormone exert its effects on bone?

A

via somatomedin release

90
Q

excessive growth hormone secretion in adults leads to?

A

acromegaly

- disproportionate growth resulting in thickened bones and coarse features

91
Q

what does LH stimulate?

A

formation of the corpus luteum

92
Q

T OR F
noradrenaline is released from sympathetic nerve terminals, whereas adrenaline is the most abundant secretory product of adrenal medulla

A

true

93
Q

what are Catecholamines important for?

A

maintenance of blood pressure

94
Q

what will a student experiencing psychological and emotional stress secrete?

A

CRH (from hypothal)
ACTH
cortisol
and may experience greater risk of infection due to immune system suppression

95
Q

what does increased levels of ACTH lead to?

A

increased plasma cortisol

96
Q

primary function of ACTH is to?

A

stimulate cortisol secretion from adrenal cortex

97
Q

describe layers of adrenal gland from outer most to inner most:

A 
connective tissue capsule 
glomerulosa 
fasciculata
reticularis
medulla
98
Q 
different levels of the adrenal glands produce different things:
Glomerulosa:
Fasciculata:
Reticularis:
Medulla:
A 
Glomerulosa = mineralocorticoids
Fasciculata = glucocorticoids
Reticularis = glucocorticoids and androgens
Medulla = catecholamines
99
Q

how does movement of thyroid hormone from follicular cells into the circulation occur?

A

through exocytosis

100
Q

where does T3 come from?

- use percentages

A 
10% = secreted directly from thyroid 
90% = obtained from conversion of T4 in tissues(deiodinase enzyme)
101
Q

what is a goiter?

A

an enlarged thyroid hormone

may occur with hyper or hypothyroidism

102
Q

what is associated with hypothyroidism?

A
  • poor resistance to cold
  • dry coarse hair
  • weight gain
  • slow speech, poor memory
103
Q

what disease is associated with bulging eyes?

A

Grave’s disease

104
Q

basic cause of Conn’s disease?

A

inappropriately high aldosterone

105
Q

basic cause of Cushing’s disease?

A

Hyeradrenalism…Excess cortisol

106
Q

what are 3 hormonal factors that influence Ca2+ metabolism?

A

parathyroid hormone (PTH)
calcitonin
vit D

107
Q

what secretes the hormone causing bone resorption?

A

parathyroid

108
Q

what secretes the hormone causing calcium deposition?

A

thyroid

109
Q

what is the most important hormone in control of calcium metabolism?

A

PTH

110
Q

how does vit D increase Ca2+ absorption?

A
  1. increasing expression of Ca channels on apical membrane
  2. increasing expression of calbindin which ferries Ca across cell
  3. increasing expression of Ca-ATPase pumps on the basolateral membrane
111
Q

what happens when plasma calcium is low?

A
  • positive stimulus on parathyroid glands
  • increase PTH
  • increase plasma Ca2+
112
Q

what happens when plasma calcium is high?

A
  • positive stimulus on thyroid C cells
  • increase in calcitonin
  • decrease in plasma Ca2+
113
Q

when you think parathyroid hormone…

A

CALCIUM regulation

PTH

114
Q

what can hypothyroidism be due to?

A

iodine deficiency

115
Q

what can hyperthyroidism be due to?

A

Grave’s disease

116
Q

what hormones do Gonadotropins refer to?

A

LH
FSH
produced by GONADOTROPHS in the anterior pituitary

117
Q

what do gonadotrophs do in males?

A

FSH stimulates sperm production in testes

LH stimulates testosterone secretion by leydig cells

118
Q

what stimulates gonadotrophic hormone release from anterior pituitary?

A

GnRH

119
Q

what do gonadotrophic hormones do in females?

A

FSH promotes follicular growth, stimulates follicular growth

LH surge stimulates ovulation(when the egg thing bursts out of shell thing) and maintains development of corpus luteum and estrogen + progesterone secretion

120
Q

function of chondrocytes?

A

divide in bone to add to LENGTH and produce cartilage

121
Q

function of osteoblasts?

A

lay down bone on top of cartilage

122
Q

briefly describe menstruation phases:

A
  1. early to mid-follicular(low estrogen, negative effect on GnRH)
  2. late follicular and ovulation(high estrogen, increases LH release, FSH suppressed by inhibin)
  3. early to mid-luteal(Decrease in FSH & LH: high estrogen/progesterone/inhibin = corpus luteum)
  4. late luteal(Increase FSH(stimulating new follicules) & LH(corpus luteum dies => decrease in estrogen and progesterone)
123
Q

function of prolactin?

A

produced by lactotrophs
release determined by hypothalamic hormones (PIH)
stimulates lactation

124
Q

what causes release of hormones from adrenal cortex?

A

sympathetic stimulation
- acetylcoline
“fight” or “flight” response

125
Q

main form, major function and region released of catecholamines:

A

adrenaline
resist stress - fight or flight
medulla

126
Q

main form, major function and region released of androgens:

A

DHEA - DiHydroEpiAndosterone
‘masculizing’ hormone convert to testosterone in the testes
zona reticularis

127
Q

main form, major function and region released of Glucocorticoids:

A

cortisol
helps resist stress, role in metabolism of macro
zona fasciculata

128
Q

main form, major function and region released of mineralo-corticoids:

A

aldosterone
electrolyte balence and blood pressure
zona glomerulosa

129
Q

what does zona reticularis release?

A

sex hormones

130
Q

what does medulla secrete?

A

catecholamines - adrenaline

131
Q

what does zona fasciculata secrete?

A

glucocorticoids - cortisol

132
Q

what does zona glomerulosa secrete?

A

aldosterone -

133
Q

PNS -> nicotinic receptors -> muscarinic receptors

A

SNS -> nicotinic -> beta and alpha

134
Q

what is acute stress response?

A
  • stimulation of SNS

- activation of release of catecholamine

135
Q

long term stress response?

A
  • cortisol release from zona fasciculata
136
Q

describe how cortisol release is governed?

A

secretion of cortisol governed by ACTH which is itself governed by CRH(from hypothalamus)

137
Q

stress feedback circuit?

A
  1. stress picked up by brain
  2. CRH
  3. ACTH
  4. Cortisol - released from adrenal cortex(zona fasciculata)
  5. effects
138
Q

primary role of cortisol?

A
  • increase blood glucose at expense of fats and protein
  • stimulates liver gluconeogenesis(new glucose made from protein)
  • inhibits glucose uptake EXCEPT brain
  • inhibits bone formation
  • anti-inflammatory and immunosuppressive
139
Q

how does a cell respond to steroid hormone?

A

steroid hormone enters cell and binds to hormone-receptor complex, which moves to nucleus and binds to complementary hormone-response element in DNA
=> initiating gene transcription => synthesis of new proteins

140
Q

what is the only sex hormone produced in adrenal gland?

A

DHEA

DeHydroEpiAndrosterone

141
Q

what does ACTH act primarily on?

A

zona fasciculata and reticularis to simulate release of cortisol and androgens

142
Q

describe effects of hypersecretion of cortisol:

A

Cushing’s syndrome
adrenal cortext is over stimulated meaning more cortisol secretion leading to increased circulating glucose(by inhibiting uptake) so body has store it somewhere, redirected to the face
does not inhibit it in the brain

143
Q

describe the absorptive state:

A 
absorptive state is when you are feed and nutrients are high
insulin is released to:
- increase glucose oxidation 
- increase glycogen synthesis
- increase protein and fat synthesis
144
Q

describe the postabsorptive state:

A

fasted state where nutrients are required to come out storage
glucagon works to:
- increase glycogenolysis(glycogen -> glucose)
- increase gluconeogenesis(proteins -> glucose)
- increase ketogenesis
- increase protein breakdown

145
Q

where is insulin release?

A

beta cells in pancreas

reduces blood sugar levels

146
Q

what do alpha cells in pancreas release?

A

glucagon

works to increase blood glucose, with primary target cells being in the liver

147
Q

what do delta cells in the pancreas secrete?

A

somatostatin

which decreases gastric secretion and inhibits digestion of nutrients

148
Q

what cells are sensitive to glucose in blood?

A

beta cells of islets of langerhaus in pancreas

149
Q

describe how glucose stimulates insulin secretion:

A
  • enters cell through GLUT-2 transporter
  • increase in ATP/ADP ratio closes K+ channels(ball on string)
  • causing depolarisation, Ca2+ channels respond
  • Ca2+ enters causing exocytotic insulin vesicles to be released
    (insulin is made in endoplasmic reticulum pre-proinsulin -> proinsulin)
150
Q

what are the glucose transporters?

A

GLUT-1,2,3 and 4

only 4 is regulated by insulin

151
Q

insulin promotes glucose entry into cells…how?

A
  1. insulin binds to receptor
  2. signal transduction cascade
  3. exocytosis of vesicles with GLUT-4 receptors
  4. glucose enters cell
152
Q

in the fed state what is metabolism under the influence of?

A

insulin

153
Q

in the fasted state what is metabolism under the influence of?

A

glucagon

154
Q

where is glycogen stored?

A

in hepatocytes in the liver, which stain pink

155
Q

type 1 diabetes?

A

destruction of beta cells so no insulin secreted

156
Q

type 2 diabetes?

A

gradual development of insulin resistance

157
Q

thyroid hormone functions?

A
  • acts on almost every cell in the body
  • increases basal metabolic rate
  • rapid protein synthesis
  • enhances effect of growth hormone
  • regulates body temp
158
Q

what cells secrete in thyroid gland?

A

c cells = calcitonin

follicular cells = thyroid hormone TH

159
Q

where is TH stored?

A

within colloid, in the middle of follicular cells(extracellular)

160
Q

what are the types of TH?

A 
T3 = 3 iodine
T4 = 4 iodine
161
Q

describe the steps involved in creation of thyroid hormone:

A
  1. Rough ER: synthesises Thyroglobulin -> exocytosed to lumen
  2. iodine pumped into cell via I-, Na+ symporter
  3. iodine is oxidised by ThyroPerOxidase(TPO) on the luminal membr..
  4. iodine “meets up with” thyroglobulin and is attached to tyrosine = DIT & MIT
  5. iodinated tyroines couple to form T3 and T4
  6. thyroglobulin is exocytosed and combined with a lysosome
  7. enzymes of lysosomes cleave T3 and T4 from thyroglobulin and exit cell moving to peripheral tissues
162
Q

how does the body obtain iodine?

A

it must be obtained by the diet
it is reduced from I to I- and absorbed by the small intestine
it is then transported through the blood stream and enters thyroid cells via the I-/Na+ symporter
iodine is then oxidised and attached to tyrosine and coupled to form T3 & T4 thyroid horome

163
Q

what is the carrier protein of T3 and T4 in blood? and how do they enter target cell?

A

Thyrosine binding globulin

enter target cell via diffusion

164
Q

describe the regulation of thyroid hormone release circuit:

A

Hypothalamus: TRH (Thyrotropin-Releasing Hormone) travels to anterior pituitary
-> triggers release of Thyroid-Stimulating Hormone
-> stimulates Thyroid gland to release T4 and T3
NEGATIVE feedback maintains steady supply of thyroid hormones

165
Q

how/where is thyroid hormone stored?

A

stored in thyroglobin form

can have enough stored to supply for months

166
Q

HOW does TSH stimulate thyroid gland to release T3 & 4?

A

TSH binds to TSH receptors -> cAMP which stimulates transcription

effects:
- iodine uptake
- iodination and coupling
- thyroglobulin production
- increase T3 & 4 production

167
Q

what is hypothyroidism due to?

A

iodine deficiency

which leads to no thyroid hormone to create negative feedback loop

From Flashcardlet (34 decks)

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