IC2 Flashcards
(28 cards)
endocrine vs nervous system
1) endocrine
- slow acting hormone
- long term response
- more for activities that require duration rather than speed
2) nervous system
- fast acting electrochemical impulses by neurons
- short term response
types of hormone receptors
1) cell membrane receptor
- water soluble, hydrophilic hormones
- protein, catecholamine
2) intracellular receptor
- lipid soluble, hydrophobic hormones
- steroid hormone, thyroid hormone
mechanism of hormone action
1) endocrine gland release hormone -> bind to receptor
2) signal amplification
3) hormones alter:
- func/structure of protein
- enzyme activation
- transcription
components of thyroid sysnthesis
1) tyrosine
2) iodine
- obtained from diet (dietary iodine -> iodide (I-) -> absorbed by small intestine
3) thyroglobulin (Tg)
- produced by endoplasmic reticulum/golgi complex of thyroid follicular cells
T3 vs T4
T3: tyrosine + 3 iodide
T4: tyrosine + 4 iodide
process of thyroid synthesis
1) Tg + tyrosine -> tyrosine containing Tg -> exported in vesicles from follicular cells into colloid (exocytosis)
2) thyroid capture I- from blood -> transfer to follicular cell by iodide pump against concentration gradient
3) iodide oxidised by membrane bound TPO -> active iodide
4) active iodide exit into colloid through channel
5) membrane bound TPO attach iodide to tyrosine within Tg molecule
- attach 1 I = mono-iodotyrosine (MIT)
- attach 2 I = di-iodotyrosine (DIT)
6) iodine coupling via peptide bonds -> T3/T4
7) stimulate thyroid hormone secretion -> follicular cell phagocytose piece of colloid -> internalise portion of Tg-hormone complex
8) lysozyme attack engulfed vesicle -> split iodinated products from Tg
9) T3/T4 highly lipophilic so diffuse through membrane into blood -> bind to plasma protein for transport
10) iodinase remove iodide from MIT/DIT -> free iodide recycles
thyroid hormone metabolism & excretion
1) T4 broken down by deiodinase into T3 (Active) & rT3 (inactive)
2) both metabolised by conjugation w glucuronic acid in liver -> secreted into bile -> eliminated mostly in shit & lil bit in pee
negative feedback for thyroid hormone: HPT axis - components
1) hypothalamus: TRH
2) anterior pituitary: TSH
3) thyroid: t3/t4
negative feedback for thyroid hormone: HPT axis - process
TRH activate anterior pituitary -> secrete TSH -> activate thyroid -> produce T3/T4
physiological effect of thyroid hormone - control rate of metabolism
Increase basal metabolism rate (BMR) & heat production
- increase size & number of mitochondria & enzymes that regulate oxidative phosphorylation -> increase oxygen consumption & energy use under resting condition
- calorigenic effect
physiological effect of thyroid hormone - sympathomimetic effect
- increase proliferation of catecholamine to target cell receptor -> increase target-cell responsiveness
physiological effect of thyroid hormone - CVS effect
increase heart responsiveness to catecholamine -> increase HR & force of contraction -> increase CO
physiological effect of thyroid hormone - normal bone growth & maturation
- stimulate GH secretion & increase IGF-1 production by liver
- promote effect of GH & IGF-1 on synthesis of new structural protein & skeletal growth
- thyroid deficient = stunt growth but excess thyroid doesnt mean more growth
hypothyroidism - symptoms
lethargy, cold intolerance, constipation, dry skin, hair loss, weight gain
hyperthyroidism - symptoms (THYROIDISM)
Tremor
Heart rate up
Yawning
Restless
Oligomenorrhea & amenorrhea
Intolerance to heat
diarrhoea
irritability
sweating
muscle wasting & weight loss
Graves disease
- autoimmune disease cuz body wrongly produce TSI
- TSI bind to TSH receptor on thyroid cell -> mimic TSH -> secrete thyroid
- TSI not subjected to negative feedback -> uncontrolled secretion
Goiter
- enlarged thyroid glands
- common in poor countries w little iodine/seafood
- caused by excess TSH/TSI activation
causes of HYPOthyroidism
1) primary thyroid gland failure
- low T3/T4, high TSH
- goiter
2) secondary to hypothalamic/anterior pituitary gland failure
- low T3/T4, low TSH, low TRH
- no goiter
3) lack of dietary iodine
- low T3/T4, increase TSH
- goiter
causes of HYPERthyroidism
1) Graves disease
- high T3/T4
- low TSH, high TSI
- goiter
2) secondary to excess hypothalamic/anterior pituitary secretion
- high T3/T4
- high TSH, high TRH
- goiter
3) hypersecreting thyroid tumour
- high T3/T4
- low TSH
- no goiter
how does glucose control insulin release
1) glucose enter beta cell by passive diffusion through GLUT-2
2) glucose phosphorylated -> glucose-6-phosphate (X move out of cell -> high conc)
3) enter Kreb cycle -> release ATP
4) ATP activate ATP-sensitive K+ channel to close -> K+ accumulate -> cell depolarisation
5) depolarisation -> stimulate voltage-gated Ca2+ channel -> increase Ca2+ in beta cell
6) Ca2+ stimulate insulin exocytosis
action of insulin
1) increase cell glucose uptake
2) storage of metabolites
- glycogenesis
- lipogenesis
- proteogenesis
3) Decreased gluconeogenesis
action of glucagon
1) release energy-rich molecules from stores & increase blood glucose levels
- glycogenolysis
- lipolysis
- proteolysis
type 1 vs type 2 diabetes
1) type 1
- autoimmune process -> body not producing enough insulin
- beta cells destroyed
- onset during childhood
- genetic & env factors
2) Type 2
- body not responding to insulin
- body not producing enough insulin
- onset during adulthood (resistance)
- lifestyle & genetic habits
type 1 diabetes early symptoms
1) insulin deficiency = liver increase glucose output = hyperglycemia
2) kidney X filter so much glucose = excreted in urine = glucosuria
3) glucosuria = osmotic diuresis = POLYURIA
4) polyuria = dehydration
- compensate w excess thirst = POLYDISPIA
- nervous system shrink
- decreased blood volume = peripheral circulatory failure
5) decreased glucose uptake by cells = intracellular deficiency = not enough energy = increase appetite = POLYPHAGIA
