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Physio Test 4 > Endocrine Day 4- Thyroid and Pancreas > Flashcards

Endocrine Day 4- Thyroid and Pancreas Flashcards

1
Q

Hormones involved in thyroid HPA axis

A
  • TRH- released from anterior hypothalamic area
  • TSH released from thyrotrophs in anterior pituitary
  • TH released from thyroid
    • T4- 10x more secreted then T3
    • T3- less secreted, more potent
  • SOmatostatin can inhibit thyrotrophs as well
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2
Q

TSH is similar in structure to which hormones?

A
  • LH
  • FSH
  • HCG

All have same alpha subunit

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3
Q

What is the functional unit of the thyroid gland? How does it appear with activation of TSH and unstimulated?

A

Follicle

  • Without activation of TSH, T3/t4 thyroglobulin matrix is stored inside colloid
  • With activation of TSH, invaginations appear on colloid membrane to reabsorb T3/T4
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4
Q

What is the biosynthesis of T3/T4?

A
  • Tyrosine (AA) converts to monoidotyrosine or diiodotyrosin in the presence of iodinase
  • Monoido and di iodo can combine to make T3
  • 2 diiodotyrosine can combine to make T4
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5
Q

What causes T3/T4 to be synthesized inside thyroid cell?

A
  • Binding of TSH causes activation of Na-I transport (secondary active transport) (Na/K ATPase dependent)
    • this brings iodide into cell
  • Organification of Iodide via peroxidases inside cell
  • “Coupling” of MIT and DIT to itself makes T3/T4
  • Attaches to thyroglobulin backbone (all stored together in colloid)
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6
Q

What occurs to cause secretion of T3/T4?

A
  • With continued TSH production, apical membrane of thyroid cell develops invaginations to pinch off colloid and bring it into cell
  • Inside cell, lysosomes have proteolytic and hydrolytic enzymes
    • liberates MIT, DIT, T3, T4 from thyroglobulin
  • T3/T4 aromatase ring allows it to freely leave plasma membrane into blood
  • MIT, DIT stays inside thyroid cell to be reused
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7
Q

TSH acts to increase ___ inside cell

A

cAMP

  • important to remember because cAMP can be stimulated by other things and this will also increase thyroid hormone production
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8
Q

What are 2 major end effects of TSH on the cell?

A
  • Stimulates thyroid gland hormone production
  • increases thyroid cell size and cellular proliferation by increase cAMP levels
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9
Q

When T4 binds to cell, it is converted to ____ by _____.

A

T3; 5’-deiodinase

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10
Q

What actions does T3 have once inside target cell? (at normal physiologic levels)

A
  • Stimulates Na-K ATPase
  • Increases mitochondria and respiratory enzymes
  • increases other enzymes, proteins such as growth hormone
  • proteins for growth and maturation

At normal physiologic levels, TH is anabolic

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11
Q

What whole body effects does high level of TH have on body?

A

At high physiologic levels, TH is catabolic

  • increased O2 consumption causes
    • increased CO
    • Increased ventilation
  • Increased upatke of substrates
    • increase food uptake
    • increased mobilization of endogenous carbs, protein, fat
  • Increased metabolic rate
    • increase CO2, heat
    • increase urea
    • decrease muscle mass
    • decrease adipose tissue
    • increase thermogenesis
    • increase sweating
    • increase insensible loss
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12
Q

What whole body effects does TH have on metabolic rate?

A
  • Increase CO2, increase urea,
  • increase muscle mass
  • decrease adipose tissue
    *
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13
Q

How is TSH production affected in cold environment?

A

Stimulated

Increase in TH then maintains body temperature

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14
Q

What is TSH production in warm environment?

A
  • Inhibit TRH-TSH-TH levels
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15
Q

What are TSH levels like in hypothyroidism?

A

Very high due to lack of negative feedback from TH

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16
Q

What are TSH levels like in hyperthyroidism?

A

Very low due to increased negative feedback from thyroid hormone

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17
Q

What are TSH levels like in hypopituitarism?

A
  • Very low d/t inability to make TSH
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18
Q

What happens when you inject TRH into patient with hypothyroidism?

A

HUGE increase in TSH

  • With loss of TH, TRH receptors are upregulated on thyrotrophs
  • so, when TRH injected, get exaggerated release of TSH
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19
Q

What happens when you inject TRH into hyperthyroid patient?

A

No change in TSH production

  • With increase TH production, get downregulation of receptors, so no response from injected TRH
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20
Q

What is grave’s disease?

A
  • Autoimmune diseaes caused by production of autoantibody called thyroid stimulating immunoglobulin
    • antibody binds to TSH receptor, elevates cAMP and stimulates excess TH production
  • Symptoms
    • exophthalmus
    • rasies BMR
    • accerlerates organ activity
    • increases beta adrenergic receptors on CV tissue
      • more sensitive to catecholamines
    • hyperphagia
    • increase body temp
    • smooth, velvety skin
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21
Q

What is goiter?

A
  • Increased proliferation of thyroid cells d/t excessive TSH secretion from lack of TH
  • Occurs with iodine deficiency, no iodine to make TH
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22
Q

What is cretinism? (congenital hypothyroidism)

A
  • Arises from perinatal deficiency of thyroid hormone
  • lack of TH results in slowing of mentation d/t failure of
    • dendritic branching of neurons
    • reduction in synapses
    • reduced myeline formation
  • Avoided by admin of TH to newborn if TH found to be low
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23
Q

What is Myxedema?

A
  • Adult hypothyroidism
  • lacks TH, results in accumulation of mucopolysaccharides
    • causes osmotic effect and edematous appearance
  • leads to incrase fat accumulation and impair wound healing
  • slow metabolism, constipation, cold intolerance and dry skin
24
Q

Why is KI given before thyroid surgery?

A
  • decreases proliferation of TH
  • May cause less of a problem at surgery if pt is pretrated with KI
25
Q

What is thyroid storm?

A
  • d/t increased TH, increased beta adrenergic receptors, when hyperthyroid patient goes into surgery, they can release a lot of catecholamines
  • with extra beta adrenergic receptors, this can result in VF, MI
  • To prevent thyroid storm, can give KI preop or treat HR during sx with propranolol
26
Q

What is the Wolf-Chaikoff effect?

A

decrease in TH caused by excess iodine admin with KI

27
Q

What do beta cells in pancreas secrete?

A

insulin

28
Q

What do alpha cells in pancreas secrete?

A

Glucagon

29
Q

What do delta cells in pancreas secrete?

A

Somatostatin

30
Q

All hormones inside pancreas exhibit ____ response

A

paracrine

31
Q

What does increase insulin cause?

A
  • Decrease in glucagon
  • stores substrate
32
Q

What does increase glucagon cause?

A
  • increases insulin
  • increases substrate in blood
33
Q

Somatostatin is the ____

A

seesaw

  • has ability to inhibit both glucagon, insulin to a balance
34
Q

In order to make sure SS doesn’t get out of control, it has its own ____ action

A

autocrine

35
Q

Glucagon also _____ somatostatin

A

stimulates

36
Q

What kind of molecule is insulin?

A
  • Human Proinsulin molecule manufactured by beta cell
  • Has A, B, chain and C peptide
  • not active until c peptide cleaved then mature insulin is created and can be secreted from beta cells
    • pro-insulin and intermediate processing molecuels have little biologic activity
  • 51 AA molecule secreted into blood from beta cells has 100% activity at insulin receptor
  • C peptide made in equimolar quantities as inuslin
    • no biologic effect on own
    • can be used to evaluate endogenous insulin production
37
Q

What effect does insulin have on cell?

A
  • Insulin stimulates processes that result in uptake or influx of certain solutes
    • especially glucose, FFA, K, PO4
  • causes series of autophosphorylation of enzymes
  • Stimulates
    • glycogen synthase (glucose–> glycogen)
    • pyruvate dehydrogenase
    • protein synthesis
  • Inhibits
    • lipolysis (wants to store FFA as fats, so will inhibit breakdown of fats)
    • protein degradation (Because you want to store protein)
    • gluconeogenesis (because you want to store glucose)
38
Q

How is glucose moved into cell upon binding of insulin?

A
  • Binding of insulin stimulates translocation of glucose transporter molecules stored inside cell
  • glucose transporters inserted on plasma membrane
    • FD brings glucose into cell
  • THese are called GLUT transproters. different GLUT transporters found on different membrane
39
Q

What happens to glucose transporters once insulin removed?

A

Glucose transporters removed from plasma membrane and stored in cell.

40
Q

What happens to insulin/glucagon levels with exogenous fuels? What are the outcomes?

A
  • Exogenous fuels such as flucose, FFA, stimualte insulin secretion by beta cell signaling
  • also inhibits glucagon secretion
    • when insulin high, directly inhibits glucagon by alpha cells
  • Causes
    • increase in glycogenesis
    • increase lipogenesis
    • increase protein biosynthesis
41
Q

What happens to insulin and glucagon when no exogenous fuels present? What does this cause?

A
  • Increase in glucagon (alpha), decrease in insulin
    • further increase in glucagon because there is no insulin to inhibit it
  • Causes
    • increase in glucogenolysis
    • increase lipolysis
    • increase ketogenesis
    • increase gluconeogenesis
  • Creates endogenous fuel production
42
Q

What’s the difference in insulin/glucagon/glucose levels in carb vs protein meal?

A
  • Carb meal
    • glucose increase in blood stream as it’s processed through GI tract
    • glucose causes robust increase in insulin level
    • driving force to decrease glucagon rapidly, is insulin
    • SO overall, spike in insulin, rapid decrease glucagon, quick plateau in glucose caused by slope down (by action of insulin) (chart on right)
  • Protein meal (left chart)
    • Nitrogenous compounds increase after protein intake
    • AA can stimulate beta cell release of insulin, but it is not as robust as glucose
    • Insulin doesn’t restrain glucagon, so glucagon levels are going up
      • insulin then rises, causing AA to be taken up by target tissue
    • Eventually raise glucose levels, but more steps in process
43
Q

What do cellular processes looking like in resting state?

A
  • Glucagon and insulin are in balance
  • Insulin stimulates uptake of substrates by liver, muscle fat
    • insulin is not needed for uptake of glucose into brain
  • As insulin is placing glucose into cell, need to replace glucose in blood stream SO
    • glucagon acts on liver to liberate glucose from glycogen stores
44
Q

What happens in cells in fight or flight response (in relation to insulin/glucagon)

A
  • stres activates sympathetic inputs to pancreas
  • In fight or flight response, increase glucagon causes release of glycogen stores from the liver (glycogenolysis)
    • push more substrates into bloodstream for use
  • Inhibit insulin
    • working muscle does not require insulin for glucose uptake
      • physical movement of myosin/actin moves glucose transporters to cell of membrane of muscle cells
45
Q

What is effect on glucagon and insulin during famine?

A
  • If no substrate consumed, absence of substrate leads to inhibiton of insulin
  • Inhibiton of insulin removes restraint on glucagon
  • Glucagon stimulated
    • ​increase release of glycogen from liver
      • stores run out in 4-6 hours
    • then increase alternate substrate called ketones made from FFA from fat stores
    • brain and fat cells can use ketones as energy source
  • metabolic acidosis from excess ketone produciton, however, can lead to failure of CNS
46
Q

What is the anticipatory rise of insulin?

A
  • Rise in insulin due to presence of food and food substrate in GI tract, even before substrate arrives in circulation
  • incrase PSNSN to pancreas d/t feeding and stimulation also increases insulin secretion
  • promotes quick arrival of substrate into blood stream
47
Q

What is type I diabetes?

A
  • Complete absence of insulin d/t destruction of beta cells
    • usually occurs because of virus
      • virus has coating like beta cells, immune system makes response to clear virus, and also kills beta cells in process
  • Glucagon goes WAY up, nothing to provide negative feedback
  • Increase in glycogenolysis, gluconeogenesis, increasing glucose into circulation
    • BUT can’t take up glucose into muscle cells in absence of insulin
  • Glucose builds up in circulation, can be released by kidneys in urine
  • eventually, renal cells will become damaged by excess glucose
48
Q

What is type 2 diabetes?

A

insulin resistance by high levels of insulin downregulating receptors from desensitization

49
Q

What 3 things does insufficient insulin cause?

A
  • Increase lipolysis
  • decrase glucose utilization
  • increase protein catabolism
50
Q

What does decrease in glucose utilization cause?

A
  • decrease lipogenesis
  • decrease protein anabolism
51
Q

What are ketons formed from?

A

FFA from increased lipolysis, causing ketonemia, and eventually ketonuria

52
Q

What does hyperglycemia cause in the body?

A
  • Glucosuria
  • osmotic diuresis
  • loss of H2O, Na, K, Cl, PO4
  • Hypovolemia
  • decrease CO
  • Hypotension
  • Decrease renal blood flow
  • decrease renal function
    • this further worsens metabolic acidosis because body can’t excrete excess H ions d/t poor kidney function
53
Q

What does increase in protein catabolism and decrease in protein anabolism cause?

A
  • Increase in AA
    • increase in BUN
  • Increase in kalemia
  • increase in phosphatemia
54
Q

What is eventual end result in untreated DKA?

A

Neuronal dehydration causing death

55
Q

Do you see ketosis in Type II diabetics?

A

Not typically

  • Enough insulin to restrain glucagon output from pancreas
  • doesn’t drive pathway of ketogenesis
  • usually suffer form neuronal dehydraiton
56
Q

What happens to cells with ongoing hyperglycemia?

A
  • Glycosylation of cells
  • creates HbA1c- glycosylation of HGB
    • impairs ability to release O2 to tissue, causing tissue to be anoxic
  • glycosylation of neurons causes neuropathies
  • impairs flexibility of RBC
    • can’t fit thourhg capillaries and contribute to perfusion

Physio Test 4 (11 decks)

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