Endocrine Flashcards

(58 cards)

1
Q

name the 4 main classes of hormones

A

modified amino acids
steroids
peptides
proteins

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2
Q

what type of hormone is adrenaline

A

amino acid

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3
Q

what type of hormone is cortisol or testosterone

A

steroids

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4
Q

what type of hormone is ACTH or ADH

A

peptides

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5
Q

what type of hormone is insulin

A

protein

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6
Q

why is the signal transduction cascade that occurs when hormone binds to receptor important

A

it typically causes an amplification of signal

this amplification is important due to the scarcity of the original signal

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7
Q

what makes the synthesis and release of steroid hormone different from that of amines, peptides and proteins?

A

steroid is synthesised and secreted upon demand
the others are presynthesised and stored in vesicles

steroid is hydrophobic, the rest are hydrophilic - steroid requires a carrier protein to travel in blood
the others are released via Ca2+ dependant exocytosis

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8
Q

steroid hormones have the shortest 1/2 life and amines have the longest. true?

A

false - amines have the shortest, steroids have the longest

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9
Q

which hormone receptor is activated by amines

A

G-protein coupled receptor

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10
Q

which hormone receptor is activated by proteins/peptides

A

receptor kinases

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11
Q

which receptors are cell surface receptors and have a hydrophilic ligand

A

GPCR

receptor kinases

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12
Q

which hormone activates class I nuclear receptors

A

steroid hormones

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13
Q

describe the movement of class I nuclear receptors in presence of activating ligand

A

in the absence of activating ligand = found in cytoplasm

when activated, they are bound to inhibitory heat shock proteins and move to nucleus

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14
Q

what hormone activates class II nuclear receptors

A

lipids

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15
Q

what hormones activate hybrid class nuclear receptors

A

thyroid hormones

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16
Q

which hormone receptors are intracellular with a lipophilic ligand

A

all the nuclear receptors

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17
Q

does the Gs protein increase or decrease cAMP production. what does this cause

A

increases production of PKA, causing MORE cellular effects

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18
Q

does the Gi protein increase or decrease cAMP production. what does this cause

A

decreases production of PKA, causing LESS cellular effects

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19
Q

what does Gq G protein convert. what does this do

A

INCREASES the conversion of PIP2 –> IP3 by phospholipase C

causes increased calcium release from ER
this causes increased cellular effects

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20
Q

how does glucose enter the B cells and what is it phosphorylated by

A

through GLUT 2

phosphorylated by glucokinase into glucose - 6 phosphate

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21
Q

what happens to the glucose-6-phosphate

A

it goes through the TCA cycle and produces 36 ATP

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22
Q

in the process of insulin secretion, what does the increased ATP levels cause

A

inhibit the ATP-sensitive K+ channel (KATP), causing depolarisation of the cell membrane

this results in opening of the voltage gated Ca2+ channels
an increase in intracellular Ca2+ levels causes fusion of secretory vessels and release of insulin

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23
Q

what are the 2 proteins that make up the KATP channel

A

KIR6- congenital mutations of this can lead to neonatal diabetes
SUR1

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24
Q

what is the gist of diabetic ketoacidosis

A

a state of absolute insulin deficiency
if you have no insulin, GLUT2 won’t open, so no glucose can get into cells –> cells are starved of glucose

you get a build up of glucose in the blood, and an increase in production of counter-regulatory hormones

they make more glucose to try and get it into the cells and ketone levels in blood increases

25
what are the counter regulatory hormones that are produced in DKA and what is their effect
glucagon, cortisol and GH they cause an increase in gluconeogenesis, glycogenolysis and lipolysis contributes to the hyperglycaemia and ketone overload in blood
26
which hormones are released by the anterior pituitary`ry
GH, TSH, ACTH, FSH
27
which hormones are released by posterior pituitary
ADH and OT - synthesised in the hypothalamus
28
what does pituitary lie immediately inferior to
the optic chiasm
29
what is the function of leptin and how is it affected in obesity
it tells your body how full you are no leptin = brain thinks you're starving if you have lots of fat stores, leptin isn't as effective and causes a flat dose response curve this means that there is little increase in response over a wide range of doses
30
what is adaptive thermogenesis
the body perceives weight loss as a threat to survival as you're eating less to lose weight, your body will lower metabolic rate, making it harder to lose the weight
31
where is the thyroid found
on the 5th cervical/1st thoracic vertebrae | in between 2nd and 4th tracheal rings
32
what gives parasympathetic innervation to the thyroid
the vagus nerve
33
what gives sympathetic innervation to the thyroid
sympathetic fibres - superior, middle and inferior ganglia of sympathetic trunk
34
what is the blood supply to the thyroid
superior and inferior thyroid arteries
35
what does the colloid contain
tyrosine containing thyroglobulin
36
what cells encapsulate the colloid
follicular cells
37
what do the parafollicular C cells secrete
calcitonin
38
what does iodine attach to when it enters the follicular cell and what does this form
attaches to tyrosine residues on thyroglobulin to form MIT and DIT
39
what is T3 made up of
1x MIT | 1x DIT
40
what is T4 made up of
2xDIT
41
where are T3 and T4 stored until they are required
the colloid thyroglobulin
42
are T3 and T4 hyrophobic or phillic
hydrophobic - they need to bind to plasma proteins to be transported
43
does metabolic rate correlate more closely with free or bound thyroxine
free T3 and T4
44
what causes an increase in total T4 but not in fT4
pregnancy, newborn state HEPA, chronic active hepatitis, biliary cirrhosis acute intermittent porphyria heroin.
45
what causes a decrease in total T4 but not in fT4
androgens loss of glucocorticoids, Cushing's syndrome active acromegaly chronic liver disease, nephrotic syndrome severe systemic illness
46
how do thyroid hormones increase responsiveness to adrenaline and noradrenaline
by increasing no of receptors | this is why you need to use B Blocker during initial therapy for hyperthyroidism
47
what effect does stress have on TRH and TSH release
inhibits their release, causing hypothyroidism
48
what enzymes are important in the activation/deactivation of thyroid hormones
deiodinase enzymes D2 activates T4 --> T3
49
what is the pituitary derived from
rathke's pouch
50
what are the 3 zones of the cortex in the adrenal gland and what does each produce
zona glomerulosa - produces aldosterone zona fasciculata -produces glucocorticoids zona reticularis - produces adrenal androgens
51
what does the medulla of the adrenal gland produce
catchecolamines (epinephrine)
52
what effect does the RAAS system have on ion levels
it causes K+ excretion | increased Na+ absorption (the water follows salt, so you get increased water reabsorption)
53
what hormone is calcium absorption in small intestine controlled by
parathyroid hormone
54
what effect does hypocalcemia have on PTH excretion
hypocalcemia causes INCREASED secretion of PTH
55
what is calcitonin and where is it produced
it opposes the action of PTH (a parathyroid hormone antagonist) it is produced in the parafollicular cells in thyroid gland
56
calcitonin is released in response to hypocalcemia? true?
no! calcitonin released in response to Hypercalcemia | it surpasses osteoclast activity
57
what is bone mostly made up of and what is this compound composed of
hydroxyapatite made up of calcium phosphate
58
what enzyme is responsible for the production of hydroxyapatite
alkaline phosphatase