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Physio II (mine) > Endocrine: Thyroid/Adrenal Systems > Flashcards

Endocrine: Thyroid/Adrenal Systems Flashcards

1
Q

HPA

A

Hypothalmus Pituitary Axis

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2
Q

Types of hormones

3

A
  1. Steroid: receptor in cytoplasm
  2. Thyroid: receptor in nucleaus
  3. Peptide: receptor on cell membrane
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3
Q

The 4 F’s

A
  1. Feeding
  2. Fighting
  3. Flight
  4. F-ing

Stress>HPA>Endocrine system> Altered behavior

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4
Q

Median Eminence

What hormones

A
  • CRH: corticotropin-releasing hormone (releasing)
  • TRH: thyrotropin-releasing hormone (releasing)
  • SS: somatostatin (Inhibiting)
  • DA: dopamine (Inhibiting)
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5
Q

Anterior Pituary makes what?

A

ACTH: Adrenocorticotropic hormone
TSH: Thyroid-stimulating hormone

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6
Q

Anterior Pituitary

Structures, pathway, hormones

A
  1. Neurons: Parvicellular (hypothalamus)
  2. Median eminence: DA, SS, CRH, TRH
  3. Ant Pituitary: ACTH, TSH
  4. Systemic circulation
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7
Q

Posterior Pituitary makes what?

A
  1. OT: Oxytocin
  2. AVP: Arginine Vasopressin (same as ADH)
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8
Q

Posterior Pituitary

Structures, pathway, hormones

A
  1. Neurons: Magnocellular (hypothalmus)
  2. Magno Produces: OT, AVP
  3. Stored: in synaptes of Post Pit
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9
Q

Neurohormones

Releasing Hormones

A
  • Hypothalmic Secretions
  • Target Ant Pit
  • TRH, CRH
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10
Q

Tropic Hormones

A
  • Ant pit secretions
  • Target endocrine glands
  • TSH, ACTH
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11
Q

Trophic?

A

Induce growth of the target endocrine gland
i.e. TSH during a goiter

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12
Q

Non-tropic Hormones

A
  • Endocrine gland secretions
  • Targets cells not glands
  • i.e. Cortisol, Epi, NO, T3, T4
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13
Q

Primary verse Secondary

A

Primary: Dysfuntion of gland itself
Secondary: Dysfuntion elsewhere in the pathway

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14
Q

Stimulation and Supression Tests

A
  1. Stim: determines gland ability to respond to control mechanism
  2. Supress: Determine if negative feedback is working
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15
Q

what is the thyroid glands secretory functional unit?

A

follicle

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16
Q

what does the thyroid follicle include?

A

cuboidal cells (follicular cells)
colloid (lumen)
c-cells (parafollicular cells)

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17
Q

cuboidal cells function

A

TG synthesis
(I2) iodine

TG: Thyroglubulin

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18
Q

colloid cell function

A

TG storage
T4/T3 storage

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19
Q

c cells function

Parafollicular or Parathyroid cells

A

calcitonin

lowers calcium in plasma

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20
Q

Hyptothamus-Pituitary-Thyroid Axis Regulation

HPTA / Stimulation and Inhibition

A
  1. Stimulation
    * TRH: Thyrotropin Releasing Hormone
    * TSH: Tyroid Stimulating Hormone
    * TBG: Thyroid Binding Globulin (T3/T4/ bind to this)
    * TSI: Thyroid Stimulating Immunoglobulin (Attaches to TSH receptor)
  2. Inhibits
    * T4/T3 (Inhibits Ant Pit and Hypothamlus)
    * Decrease TBG lvls (liver disease)
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21
Q

TSH

A

Thyroid Stimulating Hormone

Precursor: TRH

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22
Q

TSI

A

Thyroid-stimulating immunoglobulin

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23
Q

TBG

A

Thyroid binding globulin

Binds to T3/T4

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24
Q

what are the 8 steps to synthesis of t3/t4

TNOOCEHD

A

1 TG synthesis and transport to lumen
2 Na/I cotransport into membrane
3 oxidation of I by peroxidase
4 organification of I into MIT and DIT on tyrosine on TG by peroxidase
5 coupling of MIT and DIT into t3/t4 by peroxidase
6 endocytosis of TG
7 hydrolysis and entering circ of t3/t4 by proteases
8 deiodination of MIT and DIT, recycle I and tyrosine

Tyrosine precurser for TG sythesis / TG = Thyroglobulin

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25
Q

T3 Coupling

A

MIT+DIT

DIT+MIT doesn’t do anything

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26
Q

T4 coupling

A

DIT+DIT

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27
Q

what are the 4 B’s of normal T3 function?

A

basal metabolic rate
beta adrenergic effects
brain maturation
bone turnover– bone growth

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28
Q

what is hashimotos thyroiditis?

levels of T4, TSH, TRH, Goiter?

A

chronic lymphocytic thyroiditis
(primary HYPOthyroidism)
T4- decrease
TSH- increase
TRH- increase
Goiter? possible

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29
Q

what is pituitary hypothyroidism?

levels of T4, TSH, TRH, Goiter?

A

secondary hypothyroidism
T4- decrease
TSH- decrease
TRH- increase
Goiter? no

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30
Q

what is graves disease? BUG EYES

levels of T4, TSH, TRH, Goiter?

A

TSI autoimmune primary HYPERthyroidism
T4- increase
TSH- decrease
TRH- decrease
Goiter? possible

31
Q

does the thyroid make more t4 or t3?

A

t4 90%

t3/rt3 10% (made mostly by other tissues deiodinizing)

32
Q

in the circulation are t3/t4 free or bound?

A

bound 70% to TBG

bound 29% to albumin

33
Q

does birth control increase or decrease TBG?

A

increase

34
Q

does liver failure increase or decrease TBG?

A

decrease

35
Q

to have a goiter what do you need?

A

activation of TSH receptor, by TSH or TSI

36
Q

does t3 or t4 have greater affinity for the THR?

THR: Thyroid Hormone Replacement

A

t3

37
Q

when would you have an increased likelihood of fracture? hypo or hyper thyroidism?

A

BOTH

38
Q

what is a good starting point to test thyroid function?

A

TSH

39
Q

Is Iodine deficiency hypo or hyper? TSH?

A

hypo, TSH increase

40
Q

is HPA depression hypo or hyper? TSH?

A

hypo, TSH decrease

41
Q

is pituitary adenoma hypo or hyper? TSH?

A

hyper, TSH increase

42
Q

what are the clinical manifestations of thyroid storm?

DAFT-NV

A

diarrhea
arrhythmias
fever
tachycardia
nausea
vomit

43
Q

what pts are most likely to have thyroid storm?

A

graves disease
thyroid tumor
high dose thyroid meds
subclinical hyperthyroidism

Subclinical: no clinical symptoms of disease yet, but still has disease

44
Q

what are the treatments for thyroid storm?

A

PTU (inhibit t4/t3)
potassium iodide (wolff-chaikoff effect, too much iodine)
beta blocker (also slow t4-t3 conversion)

45
Q

once thyroid hormones are transported to tissue cells what happens?

A

bind to hormone receptors that bind DNA and alter gene transcription

46
Q

what are the two functional glands of the adrenal cortex?

A

cortex (3 layers that surround the medulla)

medulla (functions as modified sympathetic ganglion)

47
Q

what are the 3 layers of the cortex

G-F-R

A

glomerulosa
fasciculata
reticularis

48
Q

Primary Regulator: ANGII/⬆K+

A

Cortex: Zona Glomerulosa
Hormone: Aldosterone

Mineralcorticoid (salts)

49
Q

Primary Regulatory: ACTH

A

Cortex: Zona fasciculata
Hormone: Cortisol

Glucocortisol (regulate sugar)

50
Q

Primary Regulatory: ACTH

A

Cortex: Zona reticularis
Hormone: Androgens

DHEA and androstenedione (sex hormones)

51
Q

Primary Regulator: ACTH/Cortisol
Pre-ganglionic SNS (Ach)

Crommafins

A

Medulla
Hormone: Epi

from stress

52
Q

Synthesis of NE and EPI in chromaffin cells

Adrenal medulla / 10 steps

A
  1. Tyrosine
  2. TH (Tyrosine Hydroxylase)
  3. L-DOPA
  4. AADC
  5. DA: Dopamine
  6. DBH: Dopamine B-hydroxylase
  7. NE (20%)
  8. PNMT (80%)
  9. EPI
  10. Pre-gang sympathtetic Ach releases EPI/NE

T-T-L-A-D-D-N-P-E-P (bolded answers enchance rxn)

53
Q

17alpha-OH deficient, ACTH? BP? aldosterone? androgen?

A

ACTH- increase
BP- increase
Aldosterone- increase
androgen- decrease

54
Q

21beta-OH deficient, ACTH? BP? aldosterone? androgen?

A

ACTH- increase
BP- decrease
Aldosterone- decrease
androgen- increase

55
Q

11beta-OH deficient, ACTH? BP? aldosterone? androgen?

A

ACTH- increase
BP- increase
Aldosterone- increase
androgen- increase

56
Q

what in cortisol production causes skin pigment changes?

A

MSH

Melanocyte-stimulating hormone

57
Q

how much of cortisol is protein bound?

A

CBG 92% (less available)

albumin 8%(bioavailable)

58
Q

when is cortisol highest in the day

A

morning

59
Q

what are the critical effects of cortisol? BIG FIB

A

BIG
increase in BP
increase in Insulin resistance
increase in Glucose
FIB
decrease in Fibroblasts (stretch marks)
decrease in Inflammation and immunity
decrease in Bone formation
BONUS:
impaired learning/mem

60
Q

what things make cortisol anti inflammitory

CHILL-PW

A

A
stabilizes lysosomal membranes
decrease capillary permi
decrease WBC migration
decrease lymphocyte prolif
decrease in interleukin, histamine, prostaglandin

61
Q

if you are fasting and have acute stress what are the results?

A

liberation of all forms of energy: increase EPI/NE
liver- glycogen to glucose
sm- protein breakdown, glycogen to glucose
adipose- fat breakdown

62
Q

if you are overfed and chronically stressed

A

muscle wasting/ IR/ weight gain: decrease EPI/NE
CNS- increase appetite
liver- increase glycogen synthesis
sm- protein breakdown, decrease glucose uptake
adipose- decrease fat breakdown, TG synthesis, decrease glucose uptake

63
Q

what is cushings syndrome usually caused by

A

ACTH secreting tumor
adrenocortical hyperplasia
excess cortisol

64
Q

what does cushings disease look like?

HUMID-BSB

A

unusual obesity
striae
bone loss
muscle wasting
buffalo hump
diabetes
HTN
Infection Risk

HUMID-BSB

65
Q

what can increase aldosterone?

A

mostly RAAS = ANGII
increases serum K+
increases ACTH

66
Q

what does aldosterone do to Na and K?

A

increases Na reabsorption

increases K secretion

67
Q

what is the half life of aldosterone?

A

20min

68
Q

how do corticoid receptors fx?

A

hormone binds to receptor in cytosol and sends regulatory proteins that allow the hormone-receptor complex to bind to DNA and alter transcription

69
Q

does aldosterone bind MR or GR?

A

MR

70
Q

does cortisol bind MR or GR?

A

MR and GR

71
Q

what is addisons disease caused by?

A

autoimmune attack on adrenal cortex

decreased cortisol and aldosterone

72
Q

what are the symptoms of addisons disease?

HIHH-HID

A

hypoglycemia
increased lymphocytes
hypoNa
Hypotension
hyperK
increase ACTH (increase MSH, why JFK had tan)
decrease vascular response to adrenergics

73
Q

short term stress response

A

adrenal medulla releases EPI
increase BP, HR, blood sugar, metabolic rate
changes in blood flow to vital organs
dilate bronichioles

74
Q

long term stress response

A

Adrenal cortex release Aldosterone and Cortisol
Increase in Na and water retention
Increase in blood volme = HTN
Protiens and fat brokedown or converted to glucose
Increased blood sugar
Supression of immune system

Physio II (mine) (6 decks)

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