Endocrine Flashcards

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
Q

what are the counter regulatory hormones that are produced in DKA and what is their effect

A

glucagon, cortisol and GH

they cause an increase in gluconeogenesis, glycogenolysis and lipolysis

contributes to the hyperglycaemia and ketone overload in blood

26
Q

which hormones are released by the anterior pituitary`ry

A

GH, TSH, ACTH, FSH

27
Q

which hormones are released by posterior pituitary

A

ADH and OT - synthesised in the hypothalamus

28
Q

what does pituitary lie immediately inferior to

A

the optic chiasm

29
Q

what is the function of leptin and how is it affected in obesity

A

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
Q

what is adaptive thermogenesis

A

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
Q

where is the thyroid found

A

on the 5th cervical/1st thoracic vertebrae

in between 2nd and 4th tracheal rings

32
Q

what gives parasympathetic innervation to the thyroid

A

the vagus nerve

33
Q

what gives sympathetic innervation to the thyroid

A

sympathetic fibres - superior, middle and inferior ganglia of sympathetic trunk

34
Q

what is the blood supply to the thyroid

A

superior and inferior thyroid arteries

35
Q

what does the colloid contain

A

tyrosine containing thyroglobulin

36
Q

what cells encapsulate the colloid

A

follicular cells

37
Q

what do the parafollicular C cells secrete

A

calcitonin

38
Q

what does iodine attach to when it enters the follicular cell and what does this form

A

attaches to tyrosine residues on thyroglobulin to form MIT and DIT

39
Q

what is T3 made up of

A

1x MIT

1x DIT

40
Q

what is T4 made up of

A

2xDIT

41
Q

where are T3 and T4 stored until they are required

A

the colloid thyroglobulin

42
Q

are T3 and T4 hyrophobic or phillic

A

hydrophobic - they need to bind to plasma proteins to be transported

43
Q

does metabolic rate correlate more closely with free or bound thyroxine

A

free T3 and T4

44
Q

what causes an increase in total T4 but not in fT4

A

pregnancy, newborn state
HEPA, chronic active hepatitis, biliary cirrhosis
acute intermittent porphyria
heroin.

45
Q

what causes a decrease in total T4 but not in fT4

A

androgens
loss of glucocorticoids, Cushing’s syndrome
active acromegaly
chronic liver disease, nephrotic syndrome
severe systemic illness

46
Q

how do thyroid hormones increase responsiveness to adrenaline and noradrenaline

A

by increasing no of receptors

this is why you need to use B Blocker during initial therapy for hyperthyroidism

47
Q

what effect does stress have on TRH and TSH release

A

inhibits their release, causing hypothyroidism

48
Q

what enzymes are important in the activation/deactivation of thyroid hormones

A

deiodinase enzymes

D2 activates T4 –> T3

49
Q

what is the pituitary derived from

A

rathke’s pouch

50
Q

what are the 3 zones of the cortex in the adrenal gland and what does each produce

A

zona glomerulosa - produces aldosterone
zona fasciculata -produces glucocorticoids
zona reticularis - produces adrenal androgens

51
Q

what does the medulla of the adrenal gland produce

A

catchecolamines (epinephrine)

52
Q

what effect does the RAAS system have on ion levels

A

it causes K+ excretion

increased Na+ absorption (the water follows salt, so you get increased water reabsorption)

53
Q

what hormone is calcium absorption in small intestine controlled by

A

parathyroid hormone

54
Q

what effect does hypocalcemia have on PTH excretion

A

hypocalcemia causes INCREASED secretion of PTH

55
Q

what is calcitonin and where is it produced

A

it opposes the action of PTH (a parathyroid hormone antagonist)

it is produced in the parafollicular cells in thyroid gland

56
Q

calcitonin is released in response to hypocalcemia? true?

A

no! calcitonin released in response to Hypercalcemia

it surpasses osteoclast activity

57
Q

what is bone mostly made up of and what is this compound composed of

A

hydroxyapatite

made up of calcium phosphate

58
Q

what enzyme is responsible for the production of hydroxyapatite

A

alkaline phosphatase