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PR3152 > IC2 > Flashcards

IC2 Flashcards

1
Q

endocrine vs nervous system

A

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

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2
Q

types of hormone receptors

A

1) cell membrane receptor
- water soluble, hydrophilic hormones
- protein, catecholamine

2) intracellular receptor
- lipid soluble, hydrophobic hormones
- steroid hormone, thyroid hormone

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3
Q

mechanism of hormone action

A

1) endocrine gland release hormone -> bind to receptor
2) signal amplification
3) hormones alter:
- func/structure of protein
- enzyme activation
- transcription

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4
Q

components of thyroid sysnthesis

A

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

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5
Q

T3 vs T4

A

T3: tyrosine + 3 iodide
T4: tyrosine + 4 iodide

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6
Q

process of thyroid synthesis

A

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

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7
Q

thyroid hormone metabolism & excretion

A

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

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8
Q

negative feedback for thyroid hormone: HPT axis - components

A

1) hypothalamus: TRH
2) anterior pituitary: TSH
3) thyroid: t3/t4

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9
Q

negative feedback for thyroid hormone: HPT axis - process

A

TRH activate anterior pituitary -> secrete TSH -> activate thyroid -> produce T3/T4

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10
Q

physiological effect of thyroid hormone - control rate of metabolism

A

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

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11
Q

physiological effect of thyroid hormone - sympathomimetic effect

A
  • increase proliferation of catecholamine to target cell receptor -> increase target-cell responsiveness
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12
Q

physiological effect of thyroid hormone - CVS effect

A

increase heart responsiveness to catecholamine -> increase HR & force of contraction -> increase CO

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13
Q

physiological effect of thyroid hormone - normal bone growth & maturation

A
  • 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
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14
Q

hypothyroidism - symptoms

A

lethargy, cold intolerance, constipation, dry skin, hair loss, weight gain

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15
Q

hyperthyroidism - symptoms (THYROIDISM)

A

Tremor
Heart rate up
Yawning
Restless
Oligomenorrhea & amenorrhea
Intolerance to heat
diarrhoea
irritability
sweating
muscle wasting & weight loss

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16
Q

Graves disease

A
  • 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
17
Q

Goiter

A
  • enlarged thyroid glands
  • common in poor countries w little iodine/seafood
  • caused by excess TSH/TSI activation
18
Q

causes of HYPOthyroidism

A

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

19
Q

causes of HYPERthyroidism

A

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

20
Q

how does glucose control insulin release

A

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

21
Q

action of insulin

A

1) increase cell glucose uptake
2) storage of metabolites
- glycogenesis
- lipogenesis
- proteogenesis
3) Decreased gluconeogenesis

22
Q

action of glucagon

A

1) release energy-rich molecules from stores & increase blood glucose levels
- glycogenolysis
- lipolysis
- proteolysis

23
Q

type 1 vs type 2 diabetes

A

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

24
Q

type 1 diabetes early symptoms

A

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

25
Q

type 1 diabetes other symptoms

A

1) insufficient glucose = need another source of energy = decreased TG synthesis & lipolysis
- fat metabolism release ketones = acid-base imbalance & increased ventilation to release more CO2

2) decreased cellular amino acid uptake + increased protein degradation
- increased gluconeogenesis -> worsen hyperglycemia
- muscle wasting = weight loss

26
Q

type 1 diabetes chronic symptoms

A
  • microvascular: retinopathy, nerve damage, kidney failure
  • macrovascular: stroke, heart attack, reduced blood circulation
27
Q

effect of epinephrine

A
  • increase HR
  • dilate bronchioles
  • dilate arteries
  • glycogen -> glucose
28
Q

effect of norepinephrine

A
  • constrict vessel of digestive system & skin
  • increase blood flow to heart, muscle, brain
  • glycogenolysis (glycogen -> glucose)

PR3152 (6 decks)

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