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physio > Q2: Thyroid > Flashcards

Q2: Thyroid Flashcards

1
Q

what are follicular and C cells

A

two cell types of the thyroid gland
follicular: main thyroid secretory cells. form a single layer of hollow spheres = functional unit = follicle. lumen = storage site for thyroid hormone. filled with COLLOID - thyroglobulin is a glycoprotein and the main constituent of colloid…

c cells; secrete calcitonin (no relation to thyroid hormone

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2
Q

what is thyroid hormone made of, whats it synthesized from/where does synth occur? what are the two types released and how they differ from eachother

A

tyrosine and iodne => thyroid hormone (T3 and T4 collectively)

  • synthesized and stored on thyroglobulin (TH remains attached to thyroglobulin after synthesis)
  • incredients = tyrosine + iodone. tyrosine is made in the body and iodine must come from the diet!!!

T3 and T4 are made

T3 = tox more potent than t4
-liver and kidney can convert t4 to t3. 80% of t3 is from t4
t3 is major biologically active thyroid hormone

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3
Q

whats the major biologicaly active thyroid hormone

A

T3!!!!!!! its 10x more potent than t4 and liver and kidney can convert t4 to t3. 80% of t3 is made from t4..

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4
Q

what % of thyroid hormone thats released is t3 vs t4

A

90% is t4, 10 % is t3 but t4 gets converted in liver and kidney

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5
Q

what is thyrotropin

A

thyroid stimulating hormone IS thyrotropin

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6
Q

what do thyrotropin releasing hormone and thyroid stimulating hormone do

A

TRH increases thyrotropin synthesis in the anterior pituitary (TSH= thyrotropin). it induces the release of thyrotropin. TRH is regulated by the level of thyroid hormone itself

Thyroid stimulating hormone (TSH, thyrotropin) increases TH synthesis and secretion frm the thyroid gland. increases size of thyroid cells. TSH is regulated by TH itself.

basal levels fluctuate by the diurnal rhythm (day/night cycle)

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7
Q

how does thyroid hormone negatively inhibit the hypothalamic pituitary thyroid axis

A

it negatively inhibts hypothalamus (TRH) and anterior pituitary (TSH)

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8
Q

how does thyroid hormone bind to targets

A

lacks a discrete target organ (virtualy all cells respond) but it crosses plasma membrane and binds nuclear receptor!!!
-thyroid hormone nuclear receptor complex binds thyroid response element on DNA this initiates transcription!

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9
Q

what is the non genomic functions of TH

A
  • reduction in pituitary deiodinase

- increase glucose and amino acid transport into cells

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10
Q

how long does the response (maximum) take from TH ation

A

long duration and long half life!! hours to days!!

the response continues even after plasma levels return to normal

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11
Q

what are the effects of thyroid hormone on :metabolic rate?

A

increases overall basal metabolic rate

-increase O2 consumption and energy expenditure (under resting conditions) increase body temperature (heat production)

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12
Q

what is the sympathomimetic effect

A

thyroid hormone has actions similar to sympathetic nervous system. thyroid hormone increases target cell responsiveness to catecholamines!!

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13
Q

how does the thyroid hormone impact the cardiovascular system?

A

increases heart rate, force of contraction. and increases cardiac output.

  • increases transcription of myosin heavy chain and calcium atpase (SERCA)
  • increases erythropoietin and BPG (2,3 biphosphoglycerate ) – which allows o2 to be released more easily (lowers affinity of hb to o2)
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14
Q

what impact does thyroid hoemone have on growth?

A

stimulates GH secretion and increases IGF1 expression

  • thyroid hormone deficiency= stunted growth. reversed with thyroid replacement therapy !
  • excess thyroid hormone doesnt produce excessive growth tho
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15
Q

what effect does thyroid hormone have on nervous system

A

crucial role in developing nervous system. in adults- essential for normal cns

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16
Q
  1. when there is primary cause of hypothyroidism- failure of the thyroid gland, what is the result of thyroid hormone/tsh and is there goiter?
  2. when there is secondary cause of hypothyroidism- hypothalamic or anterior pituitary failure-result of thyroid hormone/tsh , goiter?
A
  1. reduced t4 and t3, increased tsh, GOITER YES

2. hypothalamic; reduced TRH = reduced TSH and less t3/ t4 NO GOITER

17
Q
  1. when the cause of hypothyroidism is a lack of iodine, whats the plasma t3/t4 and is there goiter
  2. when the cause of hypERthyroidism is due to abnormal presence of thyroid stimulating immunoglobulin (TSI) whats the result on thyroid hormone, tsh ? goiter? also what disease
A
  1. reduced t3/t4, increased TSH- YES GOITER
  2. This is graves disease. the immunoglobulin stimulates thyroid to produce a high amount of TH. The TH will inhibit anterior pituitary from producing TSH. reduced TRH may also occur. So TRH/TSH are low, but TH is high and theres goiter (buildUp)
18
Q
  1. if hyperthyroidism is caused by abnormally large amounts of TH due to dysfunction of hypothalamus or anterior pituitary, what will occur with thyroid hormone, and is there goiter
  2. if hyperthyroidism is from thyroid tumor, whats th/tsh/goiter?
A
  1. increased T3 and T4, increased TRH and/or TSH. Goiter is present because theres a large enough amount of increased thyroid hormone
  2. increased t3,t4 , decreased tsh, no goiter
19
Q

what type of hormones does the adrenal cortex produce (overarching, and the 3 ) - what do each of the 3 types do

which is mineralocorticoid, glucocorticoid and which is mostly DHEA?

A

adrenocortical hormones :

  • mineralocorticoids (aldosterone) ; influence mineral -electrolyte- balance, specifically Na and K balance
  • glucocorticoids (cortisol) ; glucose, protein and lipid metabolism and adaptation to stress
  • sex hormones; similar to produced in gonad , most abundant = dehydroepiandrosterone (DHEA)
20
Q

describe the pathway that stimulates adrenocortical hormones to be released (and feedback inhibition)

A

hypothalamus releases corticotropin-releasing hormone to stimulate the release of ACTH (adrenocorticotropic hormone) from the anterior pituitary. this stimulates adrenal cortex to release adrenocortical hormones

– adrenocortical hormones from adrenal corex negatively inhibit anterior pituitary AND hypothalamus

21
Q

how do adrenocortical hormones transport in circulation 1. cortisol
2. sex hormones

A

they are all LIPOPHILIC
1. CORTISOL :
10% travel free
-75% bind to corticosteroid binding globulin, and 15% bind to albumin

  1. sex hormones : free!! bound to albumin or sex hormone binding globulin
22
Q

how do adrenocortical steroid hormones act on target cells (genomic and non genomic?)

A

steroid hormones that bind receptors within cytoplasm of their target cell.

  • receptor hormone complex enters the nucleus
  • genomic activity ; binds w/ complementary hormone response element on DNA. initiates gene transcription of the downstream target gene.

NONGENOMIC activity : activates a signal transduction pathway independent of binding to the dna

23
Q

what is the site of aldosterone action? what occurs if theres a lack of aldosterone?
-what stimulates its secretion?

A
  • site of action = distal and collecting tubules of the kidney!! promotes Na retention and K elimination during urine formation. Na retention leads to water retention and the ECF volume expands
  • lack of aldosterone = death from circulatory shock! fall in plasma volume.

stimulation of aldosterone secretion:

  1. reduction of Na retention leads to a fall in blood pressure. renin angiotensin aldosterone system (RAAS) initiation
  2. rise in plasma K concentration ; leads to direct stimulation of the adrenal cortex.
24
Q

describe how the angiotensin/renin aldosterone system works reminder

A

a decrease in Nacl / decrease in ECF volume or arterial blood pressure

  • -> stimulates renin secretion from the kidneys
  • > renin combines with angiotensinogen from the LIVER to make angiotensin 1
  • > the lungs release angiotensin converting enzyme which converts angiotensin 1 to angiotensin 2. this stimulates the adrenal cortex and triggers thirst, vasopressin release, and arteriolar vasoconstriction.
  • -> adrenal cortex triggered by angiotensin II releases aldosterone which triggers the kidney to increase na reabsorption and Cl passively follows.
  • -> all of these outcomes lead to increased BP
25
Q

describe how the angiotensin/renin aldosterone system works reminder

A

a decrease in Nacl / decrease in ECF volume or arterial blood pressure

  • -> stimulates renin secretion from the kidneys
  • > renin combines with angiotensinogen from the LIVER to make angiotensin 1
  • > the lungs release angiotensin converting enzyme which converts angiotensin 1 to angiotensin 2. this stimulates the adrenal cortex and triggers thirst, vasopressin release, and arteriolar vasoconstriction.
  • -> adrenal cortex triggered by angiotensin II releases aldosterone which triggers the kidney to increase na reabsorption and Cl passively follows.
  • -> all of these outcomes lead to increased BP
26
Q

what is conn’s syndrome?

A

primary hyperaldosteronism; hypersecreting adrenal tumor made up of aldosterone secreting cells

27
Q

what is secondary hyperaldosteronism

A

reduction in arterial blood flow to the kidneys but systemic circulation remains normal ?
-this causes kidneys to secrete renin. excessively activating RAAS ..?

28
Q

what are the symtpoms of hyperaldosterone?

A

(can be primary-conns, or secondary)

  • hypernatremia; excessive Na retention
  • hypokalemia; K+ depletion
  • High blood pressure usually
29
Q

what effect does cortisol have on blood glucose, amino acids and fatty acids

A

increases them all!!!!!!!
-stimulates gluconeogenesis; replenishes hepatic glycogen stores, maintains normal blood glucose levels between meals.

increases amino acids; stimulates protein degradation and increases amino acid in blood. amino acids used for gluconeogenesis or repair of damaged tissue or cell structures

-fatty acids used as alternative fuel- saves glucose for brain

30
Q

describe how cortisol is regulated

A

(stress/diurnal rhythym) stimulate the hypothalamus to release CRH (corticotropin releasing hormone) which stimulates the anterior pituitary to secrete ACTH, which stimulates adrenal cortex to release cortisol
-cortisol has a negative inhibition impact on anterior pituitary AND nypothalamus.

so it inhibits both crh and acth

31
Q

how does stress impact cortisol release

A

stress stimulates cortisol secretion. it can override the stabilizing control of cortisol levels.
-increased cortisol concentration, mediated by CNS through CRH-ACTH cortisol system.. levels are proportional to the stress

32
Q

how do the following change with stress: epinephrine, CRH/ACTH cortisol, glucagon, insulin, renin angiotensin aldosterone/vasopressin

A

epinephrine: increase

CRH acth cortisol: increase

glucagon: increase
insulin: decrease

renin angiotensin aldosterone/vasopressin: increase

(slide23 thyroid)

33
Q

what are the causes/symptoms of cushings

A

causes:

  • excessive CRH, ACTH or both
  • overstimulation of the adrenal cortex.
  • excessive amounts of ACTH; ACTH secreting tumors located in places other than the pituitary
  • normal ACTH ; adrenal tumors that uncontrollably secrete cortisol

symptoms: relate to exaggerated effects of glucocorticoid

34
Q

what are the types of adrenocorticol insufficiency

A

must be BOTH glands!!!
– primary (addisons) all layers of the adrenal cortex are undersecreting - autoimmune destruction of cortex is most common cause.
-both aldosterone and cortisol are deficient
CAUSE: primarily autoimmune destruction of cortex. (both aldosterone AND cortisol are deficient!)

secondary adrenocortical insufficiency- insufficient ACTH from the anterior pituitary

35
Q

what are the symptoms of adrenocortical insufficiency?

A

hyperkalemia (K retention)- reduced K loss in urine- disturbs cardiac rhythm!!
-hyponatremia (na depletion) excessive LOSS of Na. reduce ECF volume, lowers BP, hypotension!

physio (7 decks)

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