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physiology endocrine Flashcards

1
Q

Name the endogenous catecholamines? Where are they produced?

A

Adrenal medulla - adrenaline, noradrenaline and dopamine
Intrinsic adrenergic cardiac cells - adrenaline
SNS cells - dopamine

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2
Q

What are the physiological effects of adrenaline and noradrenaline?

A

act on 2 receptor types = alpha and beta
(adrenaline: beta > alpha, noradrenaline: alpha > beta)

cvs effects: vasoconstriction and dilation, increased heart rate and strength

  • alpha 1 = constriction of blood vessels (esp NA)
  • alpha 2 = central vasodilation, peripheral vasoconstriction (esp adrenaline)
  • beta 1 = positive cardiac inotropy and chronotropy (both)
  • beta 2 = dilation of skeletal muscle and liver blood vessels (esp adrenaline)
  • beta 3 = lipolysis and detrusor relaxation (esp adrenaline)

metabolic effects: increased metabolic rate, mobilises free fatty acids, glycogenolysis, increased lactic acid

  • alpha receptors = decreased insulin secretion
  • beta receptors = increased insulin secretion
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3
Q

What hormones are secreted by the adrenal medulla ?

A

adrenaline
noradrenaline
dopamine

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4
Q

What are the major effects of adrenaline, NA and dopamine?

A
  1. Alpha and beta effects

2. increase HR and force of contraction, vasoconstriction, hypertension, alertness, metabolic rate and glycogenolysis

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5
Q

How do the effects of adrenaline and NA differ on the cardiovascular system?

A

BP - NA>A
HR - NA>A
CO - NA>A
TPR - NA>A

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6
Q

How do the effects of adrenaline differ with serum concentration?

A

low concentration - mostly only beta effects

high concentration - alpha and beta effects, vasoconstriction predominates

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7
Q

what is the physiological role of aldosterone?

A
  1. Increased Na reabsorption from urine
    - acts on principal cells of the collecting duct
    leading to increased amounts of na exchanged for k and h+ in renal tubules producing a K diuresis and a fall in urine pH
    (increase na retention = water retention)
  • serum: high Na+, low K+, alkalosis
  • urine: H+ loss in urine, causing increased urine acidity
  1. Increased na reabsorption from sweat, saliva and colon

= Expanded ECF volume and shutting of the stimulus to increased renin secretion.

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8
Q

What causes increased aldosterone secretion?

A

stimulators:

-primary = 
ACTH from pituitary
angiotensin II
stress/anxiety
low pressure/volume state, 
standing, 
hyperkalaemia 
haemorrhage
surgery
physical trauma, 
increase K intake
decrease na intake
  • secondary = CCF, cirrhosis, nephrosis
  • drugs
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9
Q

How does aldosterone exert its effects on the kidney?

A

-mineralocorticoid that acts on principle cells of the collecting duct

  1. genomic effect
    it is a cytoplasmic receptor complex that -binds to receptor, moves to nucleus, alters transcription of mRNA:
    2 effects
  2. rapidly causes increased insertion of epithelial Na+ channels called ENaC
  3. slowly increases synthesis of ENaC
  4. non genomic effect -Na+ is exchanged for K+ and H+ in renal tubules, causing increased serum Na+, K+ diuresis and fall in urine pH. Action takes about 10-30 mins to develop
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10
Q

Describe the actions of aldosterone?

A
  1. Increased Na reabsorption from urine
    - acts on principal cells of the collecting duct
    leading to increased amounts of na exchanged for k and h+ in renal tubules producing a K diuresis and a fall in urine pH
    (increase na retention = water retention)
  • serum: high Na+, low K+, alkalosis
  • urine: H+ loss in urine, causing increased urine acidity
  1. Increased na reabsorption from sweat, saliva and colon
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11
Q

Describe the feedback regulation of aldosterone secretion?

A
  1. fall in ECF/blood vol - leads to reflex renal nerve discharge and decrease in renal artery pressure - leads to increased renin secretion
  2. renin converts angiotensinogen to angiotensin I (converted to angiotensin II by ACE)
  3. angiotensin II causes adrenal gland to secrete aldosterone= na and water rentention - ECF expands
  4. as ECF volume increases, there is a decrease in stimulus that initiated renin secretion
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12
Q

How is aldosterone secretion regulated?

A
  1. ACTH from pituitary
  2. renin from kidney via angiotensin II
  3. direct stimulatory effect of K on adrenal cortex - plasma k
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13
Q

What are the physiological effects of glucocorticoids?

A

cvs: increased arterial contractile sensitivity to NA, causing increased vascular resistance

bronchodilator

metabolic: increased protein catabolism, increased glycogenesis and gluconeogenesis, increases gylcogenolysis, anti-insulin on peripheral tissues, reduced GH = increase plasma glucose
immune: decreased amount of circulating eosinophils, basophils, lymphocytes
haem: increased neutrophils/ plts/ RBCs

CNS: EEG slower, personality changes - irratible

inhibitis ACTH secretion - - negative feedback loop

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14
Q

How is glucocorticoid secretion regulated?

A
  • CRH secreted from hypothalamus stimulated by nociceptive pathways, emotions and circadium rhythm
  • CRH causes ACTH release from anterior pituitary (ACTH secreted in bursts, mostly early morning, stress)
  • ACTH causes cortisol release from the adrenal cortex
  • cortisol provides a negative feedback loop on CRH (hypothalamus) and ACTH (anterior pituitary) - to decrease ACTH secretion
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15
Q

what is the vascular effect of abruptly stopping long term glucocorticoids?

A
  • vascular smooth muscle becomes unresponsive to noradrenaline and adrenaline -capillaries dilate and have increased vascular permeability
  • failure to respond to noradrenaline impairs vascular compensation for hypovolaemia and promotes vascualr collapse
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16
Q

What is the benefit of elevated glucocorticoid levels in stress?

A

increased vascular activity to catecholamines

necessary for catecholamines to mobilise FFA for emergency energy source

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17
Q

How are glucocorticoids metabolised?

A

conjugated to glucuronic acid in the liver

inactivation is depressed by liver disease

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18
Q

where is body calcium stored?

A

99% in the bone
1% in the plasma ( 2 forms: bound to protein or free)

important 2nd messenger and is required coagulation, nerve function and muscle contraction

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19
Q

How is plasma calcium level regulated?

A

-by the action of 3 hormones:
PTH, calcitriol and calcitonin

1) PTH = increases plasma ca level

directly

  1. bones - stimulates bone osteoclasts to increase bone resorption and mobilise ca = > increased plasma ca
  2. kidneys -
    - increases ca resorption in distal tubules,
    - increases calcitriol production,
    - increases phosphate excretion

indirectly
intestines - increases production of vit D - increases calcium absorption in GIT

(increases phosphate - stimulates PTH production by lowering serum ca and inhibits form of calcitriol)

2) calcitriol (1.25 dihydroxycholecalciferol): increases plasma calcium level
- bones = increases activity of osteoblasts necessary for normal ca of bony matrix
- kidneys = increases calcium reabsorption
- intestines = increases calcium and phosphate absorption via induction calbindin D proteins

3) calcitonin: decreases plasma calcium level (calcitonin from thyroid parafollicular cells)
- bones = inhibits osteoclasts and thus inhibits bone resorption and decreases calcium and phosphate levels
- kidneys = increases calcium excretion in urine

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20
Q

What are the secondary hormones involved in calcium metabolism?

A
  1. GH - increases gut absorption, and urine excretion
  2. glucocorticoids - increases bone resorption - decreases plasma ca by inhibiting osteoclast formation and activity
  3. oestrogens - inhibits osteoclasts - inhibits the stimulatory effects of cytokines on osteoclasts

increase ca2+ complication of cancer - bone erosion (local osteolytic hypercalcinaemia) and elevated PTHrP

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21
Q

How does bone resorption occur?

A
  • osteoclasts are of the monocyte family develop from stromal cells involved in bone resorption, influenced by RANKL
  • they become attached to bone via integrins in the sealing zone of the membrane
  • contain a (hydrogen dependent) proton pump that acidifies the area, which dissolves hydroxyapatite and causes depression in bone. Acid proteases breakdown collagen. Products move across osteoclast into interstitial fluid
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22
Q

Describe the regulation of PTH?

A

PTH is secreted by chief cells of parathyroid glands

inhibitors -

  • calcium by negative feedback via a membrane Ca receptor and g protein
  • calcitrol acts decrease preproPTH mRNA

stimulators -
high plasma phosphate - increases PTH by decreasing ca and 1,25DHCC (neg feedback)

magnesium required for PTH secretion

23
Q

What factors influence the level of free calcium in plasma?

A
  1. protein binding - depends on plasma protein level and pH
2. total body calcium - 
depends on intake
uptake - under influence of vit D
storage in bone  - readily exchangable
renal excretion - under influence of vit D
PTH
calcitonin
24
Q

Describe the action of parathyroid hormone?

A

PTH = increases plasma ca level

directly

  1. bones - stimulates bone osteoclasts to increase bone resorption and mobilise ca = > increased plasma ca
  2. kidneys -
    - increases ca resorption in distal tubules,
    - increases calcitriol production,
    - increases phosphate excretion

indirectly
intestines - increases production of vit D - increases calcium absorption in GIT

(increases phosphate - stimulates PTH production by lowering serum ca and inhibits form of calcitriol)

25
Q

Describe the action of calcitriol ?

A

calcitriol (1.25 dihydroxycholecalciferol): increases plasma calcium level

  • bones = increases activity of osteoblasts necessary for normal ca of bony matrix
  • kidneys = increases calcium reabsorption
  • intestines = increases calcium and phosphate absorption via induction calbindin D proteins
26
Q

Describe the action of calcitonin?

A

calcitonin: decreases plasma calcium level (calcitonin from thyroid parafollicular cells)
- bones = inhibits osteoclasts and thus inhibits bone resorption and decreases calcium and phosphate levels
- kidneys = increases calcium excretion in urine

27
Q

How does high ca affect the mechanism ca metabolism?

A

decreases calcitriol

decreases PTH

28
Q

How is the synthesis of Vit D regulated ?

A

Not closely regulated
1,25 dihydroxycholecalciferol (calcitriol) is formed in the kidney by action of the enzyme 1-alpha hydroxylase
sunlight on skin makes cholecalciferol, liver converts to 25 hydroxycholecalciferol, kidney converts to calcitriol

inhibitors -
high phosphate and calcium
vit D inhibits the enzyme involved in synthesis

stimulators -
low phosphate and calcium

29
Q

what factors determine plasma glucose level?

A

overall balance between glucose entering and leaving the bloodstream

  1. dietary intake - absorption from intestine
  2. cellular uptake - rate of entry into cells ( muscle, adipose tissue, liver, red blood cells, fat, other organs)
  3. hepatic production versus storage - gluconeogenesis in liver
  4. renal filtration (freely filtered but reabsorbed up to Tmax)
  5. hormonal effects
30
Q

Explain how blood glucose is maintained during fasting?

A

fasting - liver glycogen is broken down to glucose, released into bloodstream

prolonged fasting - glycogen is depleted, increased gluconeogenesis from glycerol and amino acids in the liver

31
Q

what factors stimulate glucagon release?

A 
hypoglycaemia
amino acids - oral / IV
CCK
gastrin
cortisol
exercise
starvation
infection
stress
beta stimulators
ACH
theophylline
protein meal
32
Q

what are the physiological effects of glucagon?

A
  1. glycogenolytic - in liver ( not muscle)
    activates adenyl cyclase - increases cAMP - breakdown of glycogen - increases glucose
  2. glucogenic - formation of glucose
  3. lipolytic - activates hormone sensitive lipase - breakdown of triglycerides to glycerol and 3 fatty acids
  4. ketogenic
  5. positive inotropic effect on the heart in large doses]6. stimulates insulin secretion and GH secretion and pancreatic somatostatin secretion
33
Q

what inhibits glucagon secretion?

A 
glucose
somatostatin 
secretin
FFA
insulin
alpha stimulators
GABA
ketones
phenytoin
34
Q

what happens to glucose homeostasis in the absence of insulin (physiological effects of insulin deficiency)?

A
  • plasma hyperglycaemia due to:
    1. decreased peripheral uptake of glucose into muscle and fat (direct effect)
    2. reduced uptake of glucose by the liver ( indirect effect)
    3. increased glucose output by the liver and lack of glycogen synthesis
    (GIT, renal, brain and red cells, glucose uptake unaffected)
intracellular glucose deficiency, 
protein/ fat catabolism, 
secondary osmotic diuresis with dehydration, 
ketosis - 2nd acidosis
breakdown of AA for energy
increase FFA breakdown triglycerides
coma
raised cholesterol
35
Q

how does exercise affect glucose levels?

A
  • increased entry of glucose into skeletal muscle cells due to increased in GLUT4 transporters into muscle cell membranes
    persist for several hours
    regular exercise can prolonged increase in insulin sensitivity
36
Q

Describe the biosynthesis of insulin?

A

insulin is a polypeptide made in beta cells of pancreas, formed of 2 chains of amino acids linked by disulphide bond
initially made as a preproinsulin in the rER, then signal peptide is cleaved in the golgi, making proinsulin
c-peptide is then cleaved, making insulin (both insulin and c-peptide are released)

37
Q

Describe the structure of the insulin receptor?

A

tyrosine kinase receptor
tetramer made up of 2 alpha and 2 beta glycoprotein subunits linked by a disulphide bonds
alpha is extracellular and binds insulin
beta is itransmembrane
intracellular parts have tyrosine kinase activity

38
Q

what metabolic effect does insulin have on the liver?

A 
decreased gluconeogenesis
decreased ketogenesis
increased glycolysis
increased glycogen synthesis
increased lipid synthesis
increased protein synthesis
39
Q

what are the principle actions of insulin?

A

based on tissue: storage of carbdohydrates, protein , fat = varies with tissues

  • skeletal muscle = increased glucose uptake, increased glycogen synthesis, increased protein synthesis
  • adipose tissue = increased glucose uptake, increased lipogenesis, decreased lipolysis
  • liver = decreased gluconeogenesis, increased glycogen synthesis, increased lipogenesis

general = cell growth

based on time:

  • rapid (seconds) = increased transport of glucose, amino acids and K+ into insulin sensitive cells
  • intermediate (minutes) = stimulation of protein synthesis + inhibits protein degradation, activation of glycolytic enzymes and glycogen synthase, inhibits phosphorylase and gluconeogenic enzymes
  • delayed (hours) = lipogenesis - increases mRNA for lipogenic
40
Q

what happens when insulin binds to its receptor?

A

insulin receptor (tetramer - 2 a + 2 b glycoslated subunits)

  • insulin binds to the extracellular alpha subunit of the insulin receptor (tyrosine kinase receptor) on insulin sensitive cells
  • insulin activity triggers tyrosine kinase acitivity
  • this causes autophosphorylation of beta subunit on tyrosine residues, causing phosphorylation and dephosphorylation of cytoplasmic proteins - that are effectors and 2nd mediators (insulin receptor substrate IRS-1, and phosphoinositol 3 kinase PI3K)

once bound insulin receptors then aggregate in patches and are taken up by endocytosis and enter a lysosome then either broken down/recycled

41
Q

what happens to insulin secretion when a person is injected with 50mls of 50% dextrose?

A

insulin secretion would go up:

glucose enters B cells via GLUT-2
glucose is metabolised via glucokinase to pyruvate leading to ATP formation
K+ channels blocked (decrease in efflux) and Ca2+ enters cells- increase in Ca2+
this then causes - exocytosis of insulin

42
Q

describe insulin secretion

A

insulin is dumped from beta cells of islets of langherans within 3-5 mins followed by a plateau at 2-3 hours by activation of enzyme system

glucose is metabolised via glucokinase to pyruvate leading to ATP formation
K+ channels blocked (decrease in efflux) and Ca2+ enters cells- increase in Ca2+
this then causes - exocytosis of insulin

43
Q

what is the main hormonal factor that stimulates the release of cortisol from adrenal cortex?

A

ACTH

44
Q

what factors determine the rate of ACTH secretion?

A

increased by

  • stress (pain/emotion)
  • drive of the circadian rhythm with burst and mostly in the morning through the hypothalamus via release CRH

inhibited by circulating cortisol - glucocorticoids and afferent from baroecptors

45
Q

what happens to ACTH levels after prolonged treatment with high doses of glucocorticoids is stopped suddenly?

A

low glucorticoid levels with inability to increase

  • prolonged exogenous glucocorticoid therapy inhibits ACTH secretion and the adrenal cortex may be unresponsive and atrophic
  • ACTH levels slowly increase over weeks (may take one month for pituitary to secrete normal levels of ACTH) - pituitary unable to secrete normal levels ACTH presumed to be 2nd to diminished ACTH synthesis

-can be avoided by slowly decreasing the dose over a long time

46
Q

How can ACTH high levels be avoided after prolonged treatment when high doses of glucocorticoids are stopped suddenly?

A

can be avoided by slowly decreasing the dose over time

47
Q

what hormones are secreted by the anterior pituitary?

A 
GH
prolactin
ACTH
TSH
FSH
LH
48
Q

What are the clinical effects of anterior pituitary insufficiency?

A
  1. -adrenal cortex atrophy: glucocorticoid levels fall, mineralocorticoid levels are maintained
  2. -hypothyroidism: due to loss of TSH stimulating thyroxine production
  3. -growth inhibition: from loss of GH
  4. -gonadal atrophy: sexual cycles cease, loss of some secondary sexual characteristics
  5. -tendency to hypoglycaemia: due to increased insulin sensitivity
49
Q

what hormones are produced by the posterior pituitary?

A

vasopressin

oxytocin

50
Q

what are the physiologic effects of vasopressin?

A
  • stimulates aquaporin 2 fusion in the membrane of the collecting duct, leading to increased water reabsorption in excess of solute - reducing body fluid osmolality
  • stimulates thirst, glycogenolysis, vasoconstriction and ACTH secretion
51
Q

How are thyroid hormones regulated ?

A
  • TRH secreted by the hypothalamus and acts on the anterior pituitary to release TSH
  • TSH acts on the thyroid gland by increasing expression of the NIS symporter (2 Na+ with I-)
  • T3 and T4 both released into the blood, most of which is bound to proteins but some in free form (T4 and small amount of T3)
  • free T3 and T4 provide negative feedback on the hypothalamus and anterior pituitary

-inhibitors of thyroid secretion:
free T3/T4, stress, warmth (esp infants), dopamine, somatostatin

-stimulators of thyroid secretion: TSH, cold

52
Q

What are the physiological effects of thyroid hormones?

A

exerts its effects by entering cells - binds to intracellular thyroid receptor on nucleus - hormone receptor complex binds to DNA - alters gene expression - 2 genesites
alpha - chr 17, beta chr 3

  1. -heart = positive chronotropic and inotropic, increased number and affinity of beta adrenergic receptors, increases alpha myosin heavy chain
  2. -adipose tissue = breakdown of fats - stimulates lipolysis
  3. -muscle tissue = breakdown of protein - catabolic
  4. -bone = promotes normal bone growth (cretin) and developmental (skeletal)
  5. -nervous system = promotes normal brain development, increases reflexes, increases CNS activity, devlopmental
  6. -gut = increased rate of carbohydrate absorption, raises blood glucose - metabolic
  7. -lipoprotein = lowers circulating cholesterol- formation of LDL receptors

8.-calorigenic = increases oxygen consumption of almost all metabolically active tissues and increases metabolic rate
(except testes, uterus, LN’s, spleen, anterior pituitary, brain)

    • general - increases activity of Na+/K+ ATPase
53
Q

Describe the steps in the synthesis of thyroid hormones?

A

1) dietary iodide (I-) absorbed by intestine and enters blood
2) iodide crosses into thyroid cells via the NIS symporter with 2 Na+ (secondary active transport)
3) iodide transported into colloid by pendrin (Cl-/I- exchanger)
4) iodide (I-) converted to iodine (I) by thyroid peroxidase
5) thyroid cells secrete thyroglobulin and iodine into colloid
6) in the colloid, iodine incorporates into thyroglobulin by thyroid peroxidase, forming iodotyrosines - MIT and DIT, which combine to form T3 and T4. some reverse T3 (inactive) is also made.
7) endocytosis and lysis from colloid into thyroid cell and then release into blood = releases free hormone

All steps controlled by TSH
T3 is also made peripherally by deiodination of T4

54
Q

what are the physiological effects of T4?

A

binds to intracellular thyroid receptor on the nucleus
complex binds to DNA - alters gene expression
2 gene sites - alpha chr 17, beta chr 3
T3 more rapid and potent
effects - as —-

  1. -heart = positive chronotropic and inotropic, increased number and affinity of beta adrenergic receptors, increases alpha myosin heavy chain
  2. -adipose tissue = breakdown of fats - stimulates lipolysis
  3. -muscle tissue = breakdown of protein - catabolic
  4. -bone = promotes normal bone growth (cretin) and developmental (skeletal)
  5. -nervous system = promotes normal brain development, increases reflexes, increases CNS activity, devlopmental
  6. -gut = increased rate of carbohydrate absorption, raises blood glucose - metabolic
  7. -lipoprotein = lowers circulating cholesterol- formation of LDL receptors

8.-calorigenic = increases oxygen consumption of almost all metabolically active tissues and increases metabolic rate
(except testes, uterus, LN’s, spleen, anterior pituitary, brain)

    • general - increases activity of Na+/K+ ATPase

viva physiology endocrine (2 decks)

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