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4 - Med > Endocrinology Physiology > Flashcards

Endocrinology Physiology Flashcards

1
Q

What are the major endocrine organs ? (7)

A
  • Pituitary
  • thyroid
  • parathyroid
  • pancreas
  • adrenal
  • ovaries
  • testes
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2
Q

name the hormone produced from all of these organs
- heart
- liver
- kidney
- GI tract
- blood vessels

A
  • heart (ANP)
  • Liver (IGF-1)
  • Kidney (erythropoietin)
  • GI tract (Gastrin, incretin)
  • blood vessels: NO, endothelin
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3
Q

what are the two broad categories of hormones ?

A
  • water soluble
  • lipid soluble
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4
Q

describe water soluble hormones ? are they bound to proteins ? where do they bind to receptors ?
give examples

A

unbound to proteins so bind to surface receptors (can just dissolve in water so don’t need something to help with transport)
- peptides
(stored in vesicles and then released, shorter half life + faster clearance)

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5
Q

describe lipid soluble hormones ? are they bound to proteins ? where do they bind to receptors ?
give examples

A

bound to proteins so diffuse into cells + bind to receptors
- steroid hormones, thyroid hormones

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6
Q

what is leptin ? where is it released from ? where does it act on ?

A

eat => increased fat stores => leptin release => bind to receptors in hypothalamus => increase satiety

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7
Q

how do you know when to stop eating after a meal ? what makes you feel full ?

A

stretching of stomach by X nerve and release of CCK => brain tells you to stop eating (induces satiety)

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8
Q

what effects does CCK have ?

A

(induces satiety)
- delays gastric emptying
- gall bladder contraction and bile excretion
- insulin release

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9
Q

what is grehlin and what does it cause ?

A

elicits starvation signal
- grehlin => increase appetite + increase GH release
(vid vagal nerve)

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10
Q

Name the 6 hormones produced by the anterior pituitary ? (6)

A
  • FSH
  • LH
  • ACTH
  • TSH
  • GH
  • Prolactin
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11
Q

name the 2 hormones produced by the posterior pituitary ?

A
  • oxytocin
  • ADH
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12
Q

explain whether AP or PP stores and release hormones. ya know

A
  • AP: produces and releases hormones
  • PP: releases hormones produces by hypothalamus (so PP hormone secretion depends on stimulating or inhibiting hormones form hypothalamus)
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13
Q

describe the vasculature of the AP ?

A

has no arterial blood supply
- receives blood through portal venous circulation form hypothalamus

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14
Q

what is thyroid hormone basic function ?

A

BMR, growth

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15
Q

what is parathyroid basic function ?

A

calcium regulation

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16
Q

what is cortisol basic function ?

A
  • stress response
  • ## glucose regulation
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17
Q

what is aldosterone basic function ?

A
  • BP
  • sodium regulation
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18
Q

what is ANP basic function ?

A

sodium regulation

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19
Q

what is vit D basic function ?

A

calcium regulation

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20
Q

what does TRH stimulate release of from pituitary ? what does this hormone then cause ?

A

TSH release from pituitary
- controls how much energy your body uses (metabolic rate)

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21
Q

what does CRH stimulate release of from pituitary ? what does this hormone then cause ?

A

ACTH release from pituitary
- regulates glucocorticoid synthesis
- acutely stimulates cortisol release

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22
Q

what does GHRH stimulate release of from pituitary ? what does this hormone then cause ?

A

GH release from pituitary
- linear growth (children)
- acquisition of bone mass
- stimulates protein synthesis, lipolysis, glucose metabolism
(muscle + bone)

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23
Q

what does GnRH stimulate release of from pituitary ? what does this hormone then cause ?

A

LH + FSH release from pituitary
- LH: causes estradiol secretion from theca cells (female) and testosterone from leading cells (male)
- FSH: causes inhibit secretion from sertolli cells (male) and granuloma cells (female)

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24
Q

what does dopamine stimulate release of from pituitary ? what does this hormone then cause ?

A

prolactin release from pituitary
- positive feedback
- milk production => increased prolactin

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25
Q

what are the 2 parts to the adrenal gland ?

A
  • adrenal cortex
  • adrenal medulla
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26
Q

what is made in the adrenal cortex ?

A

corticosteroids

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27
Q

what is made in the adrenal medulla ? from what cells

A

catecholamines (mainly form chromatin cells)

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28
Q

what are the different sections to the adrenal cortex ?

A
  • zona glomerulosa
  • zona fascicolata
  • zona reticularis
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29
Q

what does zona glomerulosa produce ? what is the action of this ?

A

affects GLOMerulus
- mineralocorticoids (aldosterone)
(SALT)

30
Q

what does zona fasciculata produce ? (type of hormone and example) what is the action of this ?

A

act Fast (stress, cortisol)
- glucocorticoids (cortisol)
(SUGAR, STRESS)

31
Q

what does zona reticularis produce ? (type of hormone and example) what is the action of this ?

A

androgen precursor to be converted to oestrogen + testosterone in gonads
- androgens (DHEA)
(SEX)

32
Q

what does GH act on ? stimulate secretion of what ?

A

acts on liver to secrete IGF-1 which acts on bone + other (growth)

33
Q

in a fasting state, where does glucose come from ? by what process ?

A

all glucose comes from liver (little bit form kidney) by glycogenolysis

34
Q

after feeding, describe the glucose and insulin levels ?

A

high glucose => high insulin => replenish glycogen stores in liver and muscles

35
Q

describe the actions of insulin (4)

A
  • decrease glycogenolysis
  • decrease gluconeogensis
  • increase glucose uptake into glucose dependant cells
  • decrease lipolysis
  • oppose glucagon
36
Q

what is the action of glucagon ?

A
  • increase hepatic glucose output
  • increase peripheral release of gluconeogneic precursors
37
Q

where does gluconeogenesis take place ? how do the precursors get here ?

A

in the liver
- precursors transported to the liver to make glucose (FFA from lipids provide energy to drive this process)

38
Q

what are insulins counter regulatory hormones ?

A
  • Glucagon
  • Ad
  • cortisol
  • GH
39
Q

what do Alpha, beta and gamma cells of islets of langerhan produce ?

A

alpha: glucagon
beta: insulin
gamma: somatostatin

40
Q

how does high glucose lead to insulin release ? on a cellular level

A

glucose enters beta cells (facilitated diffusion through GLUT 2 glucose transporter) => Ca2+ flood in => insulin release

41
Q

does the action of insulin at a cellular level

A

insulin travels to muscle + fat cells => binds to insulin receptor => intracellular signalling cascade => GLUT-4 vesicles travel to + incorporate themselves within membrane => glucose enters cell through GLUT 4 transporter

42
Q

how is Ad response level affected in diabetes ? what does this then mean ?

A

Ad defence level is reset at a lower blood glucose level = BAD (glucose level needs to be even lower to elicit response)
- brain doesn’t work properly so doesn’t recognise that glucose levels too low

43
Q

describe the arterial supply of the thyroid gland ? why is this important ?

A
  • superior thyroid artery (branch of external carotid)
  • inferior thyroid artery (branch of thyocervical trunk)
    (has rich arterial supply because needs iodine)
44
Q

describe the venous drainage of the thyroid gland ?

A

superior, middle and inferior thyroid veins => internal jugular

45
Q

what are the 2 different forms of thyroid hormone ?

A

T3, T4
- the thyroid produces mainly T4 and then peripheral conversion to T3 (at target tissue)
- T3 then stimulates cellular oxy consumption and energy generation

46
Q

patients with which other conditions should get screening for thyroid disease ? (7)

A
  • AF
  • hyperlipidaemia
  • DM
  • patients on amiodarone
  • patients with down/turners/addisons
47
Q

in what 3 forms is calcium present in the body ?

A
  • ionised (most useful to cell/metabolically active)
  • protein bound (not metabolically active)
  • complexed
48
Q

what is calcium regulation controlled by ? how does small change in calcium affect this ?

A

small changes in serum Ca2+ (ionised) => big PTH change
- small range because Ca2+ essential for functioning of nerves and muscles (heart)

49
Q

how does low calcium affect PTH ? what affects does this then have ?

A

low Ca2+ => high PTH =>
- Bone: increase bone resorption
- kidneys: increase Ca reabsorption, decrease phosphate reabsorption (when one up the other down)
- Gut: increase active Vit D formation => increase Ca absorption from GI tract

50
Q

how does PTH affect vit D regulation ?

A

increase PTH => increase conversion of Vit D to active form in liver => increase Ca2+ + Pi intestinal absorption

51
Q

what is calcitonin ? secreted from where ? in response to what ?

A

hormone secreted by C cells in thyroid when Ca is high to lower it

52
Q

how could low serum albumin affect Ca measurement ?

A

low serum albumin => low serum calcium but no necessarily low Ca2+ so need to correct

53
Q

what electrolyte is needed to excrete PTH ? how could this present

A

if patient presents with low CA and low PTH then could have low Mg because Mg is needed to excrete PTH

54
Q

vit D deficiency: describe the PTH, Ca2+, Phosphate levels ?

A
  • PTH: high
  • Ca: low
  • Phosphate: low
    (appropriate PTH response)
55
Q

hypoparathyroidism: describe the PTH, Ca2+, Phosphate levels ?

A
  • PTH: low
  • Ca: low
  • High: high
    (inappropriate PTH response)
56
Q

pseudohypoparathyroidism: describe the PTH, Ca2+, Phosphate levels ?

A
  • PTH: high
  • Ca: low
  • Phosphate: high
    (appropriate - parathyroid doing what its meant to)
    (pseudo…: resistance to PTH - target organs don’t respond)
57
Q

malignancy: describe the PTH, Ca2+, Phosphate levels ?

A
  • PTH: low
  • Ca: high
  • Phosphate: varies depending on cancer
    (appropriate PTH)
58
Q

primary hyperparathyroidism: describe the PTH, Ca2+, Phosphate levels ?

A
  • PTH: high
  • Ca: high
  • Phosphate: low
    (inappropriate PTH)
59
Q

where is phosphate absorbed ?

A

absorbed in small intestine: passive at high conc, active at low conc (Na dependant)

60
Q

what is involved in phosphate regulation ? main regulator ?

A
  • PTH
  • active Vit D
  • FGF-23 (main regulator)
61
Q

what is FGF-23 ? produced where ? in response to what ?

A

produced by osteocytes in response to high phosphate (to lower it)

62
Q

what are the actions of FGF-23 ? (3)

A
  • decreases expression of Na transporter in renal tubule (=> increase renal excretion)
  • reduce vit D synthesis
  • reduce gut absorption
63
Q

major extracellular cation ?
anion?
intracellular cation ?

A

major extracellular cation: Na
anion: Cl
intracellular cation: K

64
Q

describe how changes in plasma osmolality leads to ADH changes ? and what this causes ?

A

reduces plasma osmolality => increased cellular hydration => decrease thirst (so reduces water uptake) + reduces Ash (vasopressin) secretion => increase ruine water excretion by kidneys => reduces total body water

65
Q

where is ADH synthesised ? acts on what ?

A

synthesised in hypothalamus + acts on collecting duct
- concentrates urine: stops 180L daily filtrate being excreted

66
Q

how to DPP-4 inhibitors work ? what are they also known as ? give example of one

A

gliptins (sitagliptin)
- reduce peripheral breakdown of incretins (GLP-1: hormone released by small intestine in response to an oral glucose load)

67
Q

when are gliptins used ? useful in which patients

A

used when triple combo of drugs has failed
- useful in patients who are obese

68
Q

how does metformin work ?

A

increases peripheral insulin sensitivity and reduces hepatic gluconeogenesis

69
Q

how do sulfonylureas work ? name one

A

gliclazide
- augment pancreatic insulin secretion

70
Q

gliclazide SE ?

A

(sulphonylurea)
- weight gain (=> increase insulin => increase fat storage)

71
Q

how do SGLT2 inhibitors work ? name one

A

dapagliflozin
- lower blood sugar levels by preventing kidneys from reabsorbing glucose

72
Q

Dapagliflozin SE ? (2)

A

(SGLT2 inhibitor)
- SE: euglycaemic ketoacidosis
- increased UTI risk

4 - Med (11 decks)

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