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Physio post midterm > Endocrine Fun Facts > Flashcards

Endocrine Fun Facts Flashcards

1
Q

Graves Disease

A
  1. Thyroid Enlargement
  2. Exophthalmos
  3. increased antibody TSH-R-Ab (stim)) causes opthalmopathy and pretibial myxedema. Due due GAG deposits in the bones and eyes
  4. Decreased TRH,TSH
  5. TSH-R-Ab comes along and stimulates the thyroid gland and this causes increase production of thyroid hormones.
  6. Tx –> beta blocker or iodine blocker
  7. If left untreated = thyroid storm
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2
Q

cAMP second messenger systems?

A
  1. Glucagon
  2. ACTH
  3. ADH (V2)
  4. LH/FSH
  5. TSH
  6. Epi/norepi (beta receptor)
  7. Somatostain
  8. GHRH
  9. dopamine
  10. CRH
  11. HCG
  12. PTH
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3
Q

Receptor Associated Tyrosine kinase messenger systems?

A

GH
Prolactin
GNRH

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4
Q

Tyrosine Kinase messenger systems?

A

Insulin

IGF-1

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5
Q

Intracellular messenger systems?

A 
Steroid Hormones (all cortical hormones aldosterone, cortisol, epi/ne) 
Iodothyronines 
Ca in blood
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6
Q

IP3/DAG messenger systems?

A 
ADH (V1) and PTH 
GNRH
Oxytocin 
TRH
Histamin (H1)
Angiotension II 
Gastrin
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7
Q

Which hormone is responsible for preventing milk production during pregnancy?

A

High levels of estrogen and progesterone

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8
Q

How would you inhibit thyroid hormone synthesis?

A

Ingest excess Potassium Iodide (wolff-Chaikoff Effect: Transient inhibition of T4/T3 release by inhibition of I pump)

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9
Q

what hormones are high during pregnancy?

A

Estrogen

Corticosteroid binding globulin (CBG/transcortin)

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10
Q

PTH secreting hormone?

A

Primary hyperparathyroidism
excess PTH causes increased calcium (serum and urine) and phosphaturia and PUD
(stones, bones and abdominal groans)
Secondary hyperparathyroidism
diet deficient in Vit D
normal Ca in serum and decreased urine Ca
decreased serum phosphate levels and increased urine PO4 levels

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11
Q

Addisons Disease

A

Primary Adrenocortical Disease
Autoimmune destruction of all zones of the adrenal cortex
loss of all hormones
increased secretion of ACTH and hyperpigmentation of skin secondary to alpha MSH molecule secretion

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12
Q

Male without testosterone receptors, what happens?

A

Less negative feedback so LH increases (less testosterone production)

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13
Q

What is androgen binding protein important for?

A

keeping the testosterone level in the seminiferous tubule high

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14
Q

In the second trimester progesterone is made mainly by what?

A

placenta (corpus lutem for the first trimester)

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15
Q

what anterior pituitary hormone will be elevated in lactating women compared to non pregnant women?

A

lactating woman will have higher prolactin

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16
Q

What will increase prolactin?

A

Dopamine receptor antagonist

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17
Q

Proliferative phase. when does it happen and what hormone is responsible ?

A

Estrogen

days 5-14 (preovulation, preparation of endometrium for implantation)

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18
Q

What is the difference between primary and secondary hyperaldosteronism?

A

Primary –> adrenal tumor that is secreting aldosterone

Secondary –> Increase renin levels

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19
Q

Give some features of growth hormone

A
  1. large hormone with a long half life
  2. secreted by somatotrophs in the AP
  3. Skeletal and Soft tissue growth
  4. Increase production with exercise, hypoglycemia and stress
  5. GH binds to receptor and acts on tyrosine kinase
  6. Somatostatin(GHIH) inhibits the secretion of GH
  7. Occurs in periodic bursts with max peak at night
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20
Q

Gives the actions of GH in the liver, adipose tissue and muscle

A

Liver: Increases glucose synthesis –> Increases BG
increases IGF synthesis –> increases IGF
Increase synthesis of IGF binding protein –> Increase IGF-BP
Adipose Tissue: Increases lipid breakdown –> Increases FFA and glycerol
Decreases Glucose Uptake –> Increases BG
Muscle: Increases AA uptake and therefore Increase Protein Synthesis
Decrease Glucose uptake–> increases BG

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21
Q

Thyroid Hormone T4 (thyroxine) and T3 (tri-iodothyronine)

A
  1. T3 –> 9% but much more potent and physiological active form
  2. T4 –> 90% but much less potent (unbound form is active)
    3 .Both released from follicular cells of the thyroid gland
  3. T3 provides a negative feedback mechanism on the hypothalamus
  4. TRH–>AP–>Thyroid gland –> thyroid hormone
22
Q

Thyroid hormone synthesis

A

Made from iodination of tyrosine molecules grouped together in thyroglobulin
70% of T3 and T4 are bound to thyroxine binding globular (TBG)
Pregnancy and estrogen levels increase TBG

23
Q

If there is a pump failure or some issue with the iodine pump then what happens?

A

If no I- or I0 then T4 and T3 can not be synthesized and this leads to increased TSH levels.

24
Q

What enzyme converts T4 to T3?

A

5’- deiodinase

25
Q

Actions of Thyroid Hormone?

A

Increase Oxygen consumption and heat production of most cells
increase basal metabolic rate
increases intracellular mitochondria, resp enzyme, Na/K pump and other enzymes (which leads to increase O2 and metabolic rates)
increases glucose absorption from the GIT
increases use of glucose fat and protein for energy use.
glycogenesis and gluconeogenesis
decreased body weight

26
Q

PTH

A

Produced from chief cells
short half lives
most important regulator for Ca
Decreased ionized Ca in blood –> parathyroid gland –> increased PTH
converts 25-hydroxycholecalciferol in the liver to 1,25 Oh cholecalciferol in the renal cortex
inhibits phosphate reabsorption in the proximal tubule
increases calcium reabsorption in the DCT

27
Q

Action of PTH on bone

A

Osteoclast development and action (increases bone reabsorption)

28
Q

Insulin secretion post meal (post prandial state) ?

A

After eating a meal insulin secretion is increased. As a result, there is an increased rate of glucose uptake by both the liver and the muscle. Insulin also inhibits hormone sensitive lipase, which decreases hydrolysis of triglycerides in fat cells.

29
Q

ATP blocks what from leaving the cell?

A

K efflux therefore this leads to insulin synthesis

30
Q

Cortisol (Zona fasciculta)

A

Main glucocorticoid in the body
highest levels at 8am and lowest at 12pm
ACTH –> Receptor–> increased cAMP –> increased PKA—> phosphorylation of proteins
Function–> adaptive response to stress and fasting
only negative feedback system onto the AP in the zona fasciculta and zona reticularis
metabolized in the liver and excreted in the urine
crosses the blood brain barrier
increases insulin secretion and increase glucose and increase AA breakdown as well as protein breakdown

31
Q

Prolactin

A

negative feedback system
big peptide so long half life
main functions is breast development and milk production
NOT EJECTION
inhibits ovulation in lactating females and suppresses GnRH synthesis and release and decreases sex drive
Hypothalamus (PIF) —>Anterior Pituitary (prolactin) –> decreased prolactin
really high levels of estrogen (like during pregnancy) or TRH stimulate prolactin release)

32
Q

what is an example of a dopamine agonist?

A

bromocriptine

33
Q

During menopause which hormone is the highest?

A

increase in FSH and LH (FSH is more though)

34
Q

Initiation of Partuition?

A

estrogen to progesterone ratio?

35
Q

hCG acts on LH receptors to maintain what?

A

maintain progesterone levels and keep corpus luteum active

36
Q

Fetal Hormone Production

A

idk

37
Q

ABP maintains what?

A

testoterone levels in the semineferous tubules

38
Q

lady comes into the ER with a broken leg, she has low Ca with brittle bones and high PTH

A

secondary hyperparathyroidism

39
Q

what does effect does an increased T3/T4 have on TSH?

A

Lowers TSH due to neg feedback system

40
Q

what affect does increased secretion of cortisol from the adrenal cortex have on ACTH?

A

Lowers ACTH again due to the neg feedback system

41
Q

patient takes GH levels at 6am after fasting 10 hour, take GH levels 1 hour before eating which hormone will be the lowest?

A

insulin

42
Q

what hormones are elevated to inhibit lactation?

A

progesterone and estrogen

43
Q

what hormone is elevated and needed for milk ejection?

A

oxytocin

44
Q

what is high in a sample with 21 alpha hydroxylase deficiency?

A

ACTH high because your not making aldosterone or cortisol

45
Q

somatostatin binds to anterior hypothalamus, what is the mechanism?

A

GI –> reducing cAMP

46
Q

increase number of binding globulins what do you increase?

A

increase half life

47
Q

patient comes into the ER that is hypoglycemic, hypovolemic and hypoglycemic. what is deficient?

A

low cortisol

48
Q

what happens if the liver stops secreting IGF?

A

decrease in somatostatin

49
Q

beta cell, glucose binds what is the mechanism?

A

increase in ATP inhibits K channel

opens Ca channel

50
Q

what does cortisol upregulate in the adrenal medulla?

A

PNMT

51
Q

which value is higher in umbilical artery/vein?

A

PCO2 higher in artery

Physio post midterm (4 decks)

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