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ACEM Part 1 > Physiology - Endocrine > Flashcards

Physiology - Endocrine Flashcards

1
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
  • free T3 and T4 provide negative feedback on the hypothalamus and anterior pituitary
  • inhibitors of thyroid secretion: free T3/T4, stress, warmth, dopamine, somatostatin
  • stimulators of thyroid secretion: TSH, cold
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2
Q

Thyroid hormone effects

A
  • heart = positive chronotropic and inotropic, increased number and affinity of beta receptors
  • adipose tissue = breakdown of fats
  • muscle tissue = breakdown of protein
  • bone = promotes normal bone growth
  • nervous system = promotes normal brain development, increases reflexes, increases CNS activity
  • gut = increased rate of carbohydrate absorption, raises blood glucose
  • lipoprotein = lowers circulating cholesterol
  • calorigenic = increases oxygen consumption of almost all metabolically active tissues
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3
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 peroxidase
5) thyroid cells secrete thyroglobulin into colloid
6) in the colloid, iodine incorporates into thyroglobulin, forming MIT and DIT, which combine to form T3 and T4
7) endocytosis from colloid into thyroid cell and then release into blood

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4
Q

What is the mechanism of action of T3/T4

A
  • T3 is more active, but more of T4 is made
  • thyroid hormone exerts its effects by entering cells and binding to the intracellular thyroid receptor
  • hormone-receptor complex binds to DNA and alters gene expression
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5
Q

What factors determine plasma glucose level

A
  • overall balance between glucose entering and leaving the bloodstream
    1) dietary intake
    2) cellular uptake
    3) hepatic production versus storage
    4) renal filtration (freely filtered but reabsorbed up to Tmax)
    5) hormonal effects
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6
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
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7
Q

What are the physiological effects of glucagon

A

acts on G proteins, increases blood glucose levels

  • breaks down glycogen in the liver (not muscle)
  • gluconeogenesis
  • breaks down triglycerides to glycerol and 3 fatty acids
  • ketogenic
  • positive inotropic effect on the heart
  • stimulates insulin and GH secretion
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8
Q

What stimulates/inhibits glucagon release?

A

stimulators:
hypoglycaemia, amino acids, CCK, gastrin, cortisol, exercise, infection, stress, beta stimulators, ACH

inhibitors:
glucose, somatostatin, secretin, FFA, insulin, alpha stimulators, GABA, ketones

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9
Q

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

A

-plasma hyperglycaemia due to:
decreased peripheral uptake of glucose into muscle and fat
reduced uptake of glucose by the liver
increased glucose output by the liver and lack of glycogen synthesis

-intracellular glucose deficiency, protein/fat catabolism, secondary osmotic diuresis, dehydration, ketosis

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10
Q

How does exercise affect glucose levels

A

increased entry of glucose into skeletal muscle due to increase in GLUT 4 transporters in muscle cell membranes

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11
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 disulfide bond

initially made as 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)

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12
Q

What metabolic effects does insulin have on the liver

A

decreased gluconeogenesis
increased glycogen synthesis
increased lipid synthesis
increased protein synthesis

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13
Q

What are the principle actions of insulin

A

based on tissue:

  • 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

based on time:

  • rapid (seconds) = increased transport of glucose, amino acids and K+ into insulin sensitive cells
  • intermediate (minutes) = stimulation of protein synthesis, activation of glycolytic enzymes and glycogen synthase
  • delayed (hours) = lipogenesis
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14
Q

Describe the structure of the insulin receptor

A

tyrosine kinase receptor

tetramer made up of 2 alpha and 2 beta glycoprotein subunits bound by disulfide bonds

alpha is extracellular and binds insulin

beta is transmembrane

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15
Q

What happens when insulin binds to its receptor

A
  • insulin binds to the extracellular alpha subunit of the insulin receptor (tyrosine kinase receptor)
  • this causes autophosphorylation on tyrosine residues, causing phosphorylation on cytoplasmic proteins
  • insulin receptors then aggregate in patches and are taken up by endocytosis and enter a lysosome
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16
Q

What happens to insulin secretion when a person is injected with 50ml of 50% dextrose

A
  • glucose enters B cells via GLUT-2
  • glucose is metabolised to pyruvate leading to ATP formation
  • K+ channels blocked and Ca+2 enters cells
  • exocytosis of insulin
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17
Q

Name the endogenous catecholamines and where are they produced

A

adrenal medulla

adrenaline
noradrenaline
dopamine

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18
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
-alpha 2 = central vasodilation, peripheral vasoconstriction
-beta 1 = positive cardiac inotropy and chronotropy
-beta 2 = dilation of skeletal muscle and liver blood vessels

metabolic effects:
increased metabolic rate, mobilises free fatty acids, glycogenolysis
-alpha receptors = decreased insulin secretion
-beta receptors = increased insulin secretion

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19
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
20
Q

What is the physiological role of aldosterone

A

Increased reabsorption of Na+ from kidney (leading to water retention)
decreased reabsorption of K+
-serum: high Na+, low K+, alkalosis
-urine: H+ loss in urine, causing increased urine acidity

21
Q

What causes increased secretion of aldosterone

A
  • primary = ACTH, angiotensin II, stress, low pressure/volume state, standing, hyperkalaemia
  • secondary = CCF, cirrhosis, nephrosis
22
Q

How does aldosterone exert its effects on the kidney

A

-mineralocorticoid that acts on principle cells of the collecting duct
-binds to receptor, moves to nucleus, alters transcription of mRNA
rapidly causes increased insertion of epithelial Na+ channels called ENaC
slowly increases synthesis of ENaC
-Na+ is exchanged for K+ and H+ in renal tubules, causing increased serum Na+, K+ diuresis and fall in urine pH

23
Q

Describe the feedback regulation of aldosterone secretion

A

1) fall in ECF/blood volume 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
4) as ECF volume increases, there is a decrease in stimulus that initiated renin secretion

24
Q

How is aldosterone secretion regulated

A

ACTH from pituitary
renin from kidney
direct stimulatory effect of K+ on adrenal cortex

25
Q

What are the physiological effects of glucocorticoids

A

cvs: increased arterial contractile sensitivity to NA, causing increased vascular resistance
metabolic: increased protein catabolism, increased glycogenesis and gluconeogenesis, anti-insulin, reduced GH
immune: decreased amount of circulating eosinophils, basophils, lymphocytes

26
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 and ACTH
27
Q

What factors determine the rate of ACTH secretion

A
  • increased by stress, drive of circadian rhythm with bursts and mostly in early morning
  • inhibited by circulating cortisol
28
Q

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

A
  • prolonged exogenous glucocorticoid therapy inhibits ACTH secretion and the adrenal cortex may be unresponsive
  • ACTH levels slowly increase over weeks (may take one month for pituitary to secrete normal levels of ACTH)
  • can be avoided by slowly decreasing the dose over a long time
29
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
30
Q

What is the benefit of elevated glucocorticoid levels in stress

A

increased vascular activity to catecholamines

31
Q

How are glucocorticoids metabolised

A

conjugated to glucuronic acid in the liver

32
Q

Where is body calcium stored

A

99% in bone, 1% in plasma (2 forms: bound to protein and free)

33
Q

How is plasma calcium level regulated

A

By the action of 3 hormones: PTH, calcitriol and calcitonin

1) PTH: increases plasma calcium level
- bones = stimulates bone osteoclasts to increase bone resorption and mobilise Ca+2
- kidneys = increases calcium resorption in distal tubules, increases calcitriol production, increases PO4 excretion
- intestines = increases production of vitamin D3

2) calcitriol: increases plasma calcium level
- bones = increases activity of osteoblasts
- kidneys = increases calcium reabsorption
- intestines = increases calcium absorption

3) calcitonin: decreases plasma calcium level
- bones = inhibits osteoclasts and thus inhibits bone resorption and decreases calcium levels
- kidneys = increases calcium excretion in urine

34
Q

How does bone resorption occur

A
  • osteoclasts are of the monocyte family involved in bone resorption, influenced by RANKL
  • they become attached to bone via integrins
  • contain a proton pump that acidifies the area, which dissolves hydroxyapatite and causes depression in bone
35
Q

Describe the regulation of PTH

A
  • PTH is secreted by chief cells of parathyroid glands
    inhibitors: calcium by negative feedback and calcitriol
    stimulators: high plasma phosphate
36
Q

What factors influence the level of free calcium in plasma

A
  • protein binding: depends on plasma protein level and pH
  • total body calcium: depends on uptake, storage in bone and excretion
37
Q

What are some secondary hormones involved in calcium metabolism

A
  • GH: increases gut absorption
  • glucocorticoids: increases bone resorption
  • estrogens: inhibit osteoclasts
38
Q

How is the synthesis of vitamin d regulated

A
  • 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 PO4 and Ca+2
stimulators: low PO4 and Ca+2

39
Q

What hormones are secreted by the anterior and posterior pituitary

A

anterior: GH, prolactin, ACTH, TSH, FSH, LH
posterior: vasopressin and oxytocin

40
Q

What are the clinical effects of anterior pituitary insufficiency

A
  • adrenal cortex atrophy: glucocorticoid levels fall, mineralocorticoid levels are maintained
  • hypothyroidism: due to loss of TSH stimulating thyroxine production
  • growth inhibition: from loss of GH
  • gonadal atrophy: sexual cycles cease, loss of some secondary sexual characteristics
  • tendency to hypoglycaemia: due to increased insulin sensitivity
41
Q

What are the effects of vasopressin

A
  • stimulates aquaporin 2 fusion in the membrane of the collecting duct, leading to increased water reabsorption
  • stimulates thirst, glycogenolysis, vasoconstriction and ACTH secretion
42
Q

Describe the two functions of the thyroid gland.

A

(1) Secretion of thyroid hormones, which play a role in metabolism
(2) Secretion of calcitonin, which plays a role in calcium regulation

43
Q

Name some other inhibitors of TSH secretion?

A
  • Stress +++
  • Warmth → cold stimulates TSH secretion
  • Dopamine
  • Somatostatin
  • Glucocorticoids
44
Q

Which enzyme causes de-iodination of T4 to T3 in the periphery?

A

T3 can also be produced peripherally by de-iodination of T4 by D1 thyroid deiodinase

45
Q

Describe how thyroid hormones are transported.

A
  • Majority of T3 and T4 are protein bound (~ 99.98%)
  • Most of the circulating T4 is bound to TBG (greatest affinity)
  • T3 is less bound and therefore more active than T4
  • The plasma proteins that bind thyroid hormones (in order of capacity) are:
    • Albumin
    • Transthyretin
    • Thyroxine-binding globulin (TBG)
  • Half life T3 < T4
46
Q

Describe how thyroid hormones are metabolised.

A
  • T3 and T4 are de-iodinated in the liver, kidneys and bile ducts
  • Can provide additional T3 in the bloodstream
  • Broken down by deiodinases

ACEM Part 1 (38 decks)

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