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Pathophysiology > Endocrinology: Thyroid and Parathyroid > Flashcards

Endocrinology: Thyroid and Parathyroid Flashcards

1
Q

what is the second largest endocrine gland?

A

thyroid

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2
Q

location of thyroid

A

base of neck

below SCM

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3
Q

thyroid hormones derived from which AA?

A

tyrosine

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4
Q

thyroid hormone is under regulation by____? (2)

A

dietary idodine

HPA (tsh coming from AP)

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5
Q

what inhibits TSH release (4)

A 
glucocorticoids
somatostatin
dopamine 
AND 
incr plasma levels of T3 and T4
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6
Q
  1. TRH binds to_______ in the _____
  2. causing ___ in intracellular [_____]
  3. which results in ____ and release of ___ into ___
A
  1. G protein coupled rec, AP
  2. INCR, CA2+
  3. exocytosis, TSH, systemic circulation
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7
Q

t4

A

tetraiodothyronine

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8
Q

t3

A

triiodothyronine

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9
Q

is the thryoid vascular?

A

yes very vascularized

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10
Q

follicular cells

A

involved with thyroid hormonesynthesis

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11
Q

which cells are involved with thyroid hormone synthesis

A

follicular cells

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12
Q

parafollicular cells or____

-produce?

A

c cells

-produce calcitonin

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13
Q

what does calcitonin do

A

metabolizes calcium

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14
Q

main funct of thyroid gland

A

to produce and store thyroid hormone

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15
Q

what fills the follicle?

-what is contained in it?

A

colloid

contains protein–thyroglobulin (tg)

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16
Q

role of thyroglobulin

A

synthesis and storage of thryoid hormone

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17
Q

TSH stimulates productino of___

A

T4

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18
Q

explain polarity of thyroid follicular cells?

A

each side or compartment of cell has specific functions pertaining to synthesis of T hormones

  • –apical surface: faces follicular lumen–colloid storage
  • –basolateral surface: faces interstitum–exposed to bloodstream
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19
Q

where does TSH bind to?

A

receptor sites on PLASMA MEM of follicular cells

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20
Q

what happens after TSH binds to rec in follicular cell? (4 steps)

A
  1. immed release of stored thyroid hormone
  2. incr in iodide uptake and oxidation
  3. incr in thyroid hormone synthesis
  4. incr of prostaglandin synthesis and secretion
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21
Q

where are t3 and t4 produced.. stored?

A

in thyroid gland

STORED: follicles–in the sacs with thyroglobulin

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22
Q

which is more potent.. t3 or t4

A

t3

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23
Q

in blood, which is normally in higher levels t3 or t4

A

t4 45X higher

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24
Q

what does the activity of t3 depend on

A

enzyme that converts t4–t3

*found outside thyroid

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25
Q

what is the enzyme responsible for converting t4–t3

A

type 1 Deiodinase

type 2 Deiodinase

type 3 ‘’

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26
Q

type 1 Deiodeinase is found where and what is its function

A

liver kidney and thyroid

functoin: generates T3 for circulation

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27
Q

type 2 deiodinase is found where and function

A

cells of brain, pituitary and brown fat tissue

Function: converts T4–T3

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28
Q

type 3 deiodinase is found where and function

A

placenta, brain and skin

leads to generation of rT3

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29
Q

what do we need when we want to convert t4–t3?

List the carrier proteins

A

carrier proteins
*they bind and transport T4/T3

  1. Thyroxine binding globulin
  2. albumin
  3. thyroid binding prealbumin
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30
Q

release of TSH is mostly inhibited by T3 or T4

*circulation or pituitary T3?

A

T3

**pituitary/hypothalamic T3 has greater effect

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31
Q

thyroglobulin is synthesized in?

A

follicular cell

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32
Q

Tg is secreted throuhg____? and into____?

A

apical membrane into follicular lumen–storaged in Colloid

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33
Q

what diseases can ciruclating thyroglobulin levels are elevated?

A

graves

thyroiditis

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34
Q

where is thyroxine binding globulin produced

A

in liver

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35
Q

Thyroid produces 90% _____ (T4 or T3?) and 10%_____

A

90%=T4

10%=T3

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36
Q

where is Iodine stored?

A

Follicles

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37
Q

when there is active secretion, what is the morphology of the follicular cell?

A

columnar

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38
Q

hypo or hyperthyroidism if we do not get in enough iodine from diet?

A

HYPOthyroidism—bc we cannot make T3 from T4

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39
Q

Role of thyroid hormones

A
  • Neuronal and skel development
  • Heat production and oxygen consumption at rest
  • Stim bone turnover–increasing formation and reabsoprtion
  • secretes calcitonin to lower serum Ca levels
  • incr number of catecholamine receptors in heart
  • incr RBC production
  • alter metabolism of carbs, fats, and protein
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40
Q

the synthesis of thyroid hormones takes place____

A

in colloid space

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41
Q

the apical surface of the follicuar epithelium faces??

A

the colloid
NOT interstitial space
no access to bloodstream

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42
Q

main functions of thyroid hormones

A 
breathing 
energy production 
HR 
cognitive function 
mood
body wt 
muscle strength 
menstrual cycle 
body temp 
cholesterol levels 
growth and development 
intestinal flow
digestion
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43
Q

which hormone is the indicator measured in a lood test to screen for hypothyroidism?

A

TSH

44
Q

TSH LAB LEVELS:

  1. HIGH tsh indicates?
  2. LOW TSH inds?
A
  1. LOW thyroid hormones–hypothyroidism

2. HIGH thyroid hormones–hyperthyroidism

45
Q

list some factors that increase conversion of T4 to T3

A 
stress
trauma 
low cal diet 
inflamamtion
toxins 
infections 
liver/kidney issues
46
Q

which enzyme is mostly resp for conversion of T4-T3 in hyperthyroid PTs?

A

Type 1 deiodinase

47
Q

which enzyme is the main source of T3 in euthyrioid state

-imp source of_____?

A

Type 2 deiodinase

**imp source of intracellular T3

48
Q

thyroid hormone affect on cardiovasc systm?

A

+inotropic
+chronotropic
incrs CO and blood volyme
decrs systemic vasc resistance

49
Q

which is MC primary or secondary hypoT?

A

primary–95% cases

50
Q

what can occur if hypotyroidism occurs in utero?

A

cretinism or mental retardation

51
Q

pathophys behind primary hypothyroidism

-causes?

A

AUTOIMMUNE–Hashimoto
destruction of the thyroid parenchyma

can also be result from surgery or radioactive iodine tx

52
Q

define secondary hypoth

  • what is decrease

- causes

A

decrease TSH and decrease T4 T3
disorder of anterior pituitary or hypothal
lack of stimulation of the TSH receptor because of impaired TRH release

53
Q

Hyperthyroidism hgiher in M or W?

A

women

54
Q

MC cause of hyper T in adults?

A

diffuse toxic goiter or **Grave’s disease****

55
Q

define graves disease

A

AUTOIMMUNE–excess thyroid hormone bc of TSH receptor stimulation by immunoglobulin G
-results in continuous stimulation of TSH-receptor by TSH-like antibodies–results in excess T4/T3 production

56
Q

Graves disease MC in M or W?

A

WOMEN

*third to fourth decades of life

57
Q

TSH secreting pituitary adenomas

A

increased thyroid hormone release in response to elevated TSH levels from TSH-secreting adenoma on AP

  • small percent of all pituitary adenomas
  • results=increase TSH levels
58
Q

why is TSH low in primary hypert?

A

beacuse the thyroid gland is secreting T4/T3 without being told to do so… aka:

  • increase neg feedback to AP
  • ending in decrease levels of TSH and HIGH t4/t3 because issue is the thyroid gland and not AP
59
Q

Why is TSH high in secondary hyperthyroidism?

A

because the increase in T4/T3 levels is due to AP issue aka over-secreting of TSH…. the negative feedback is not working on the AP since the AP gland is the issue

60
Q

what is the hormone in determining primary and secondary hyper/hypo thyroidism?

A

TSH

61
Q

why is TSH high in primary hypothyroidism?

A

since thyroid gland is root cause of decrease levels of t3/t4…… this decreases negative feedback to AP….telling AP to release MORE tsh.. but thyroid gland is not listening

62
Q

Why is TSH low in secondary hypothyroidism?

A

now AP gland is the issue:

-AP is not secreting enough TSH— therefore the thyroid is not going to secrete enough T3/T4

63
Q

list causes for hyperthyrodism

A 
toxic nodules 
Grave's disease 
Pituitary tumor 
Amiodarone toxicity 
Struma Ovarii--ovarian tumor that secretes thyroid horm
64
Q

what is a toxic nodule

A

thyroid nodule that become independent of the pituitary and secretes excess thyroid hormone

65
Q

what is graves disease

patho *

A

autoimmune *** primary hyperthyroidism
body produces antibodies AGAINST (autoantibodies)–they bind to TSH receptors on thyroid and act like TSH–stimulating release of T3/T4

66
Q

MC cause of hyperT?

A

Grave’s disease

67
Q

where are the largest calcium storage

A

bones

68
Q

list the three hormones that regulate [ca]

A

parathyroid hormone (PTH)
calcitonin
Vit D

69
Q

Calcium:____?
Iodine:_____?

A

Ca—>parathyroid

Iodine—?thyroid

70
Q

PTH and Vit D effects on blood calcium levels

A

they increase it

71
Q

calcitonin’s effect on blood Ca levels

A

decreases it

72
Q

where is calcitonin secreted

A

follicular cells of thyroid

73
Q

when is PTH released?

A

when blood calcium levels are LOW

74
Q

is PTH secretion regulated by ant pit?

A

NO

75
Q

what regulates secretion of PTH?

A

serum [ca]

76
Q

three ways PTH increases blood [ca]?

A
  1. stimulates osteoclasts to b/d bone
  2. increase reabsorption of CA in kidneys
  3. incr conversion of inactive Vit D–>active vit D–>increases [ca] in GI tract
77
Q

what is normal CA range?

A

8.9–>10.1 mg/dL

78
Q

Other than increase [ca], what else does PTH do?

A

decreases phosphate

  • tells kidney to decr phosphate reabsoprtion
  • this prevents hyperphosphatemia beacuse PTH tells bones to breakdown–releases CA annnnnnnnd Phosphate—-
79
Q

what do bones release when they break down

A

CA

Phosphate

80
Q

PTH causes serum [ ] of:
Ca to ____
Phosphate to____

A

increase [ca]

decrease [phos]

81
Q

role is vit d in body (3)

*what is vit D’s affect on blood [ ] of ca and phos?

A
  • increases absorption of ca and phosphate from GUT
  • increases bone resorption–so Ca and phos can be released into blood
  • increases phosphate reabsorption in kidneys

INCREASES blood [ca] and [phos]

82
Q

both vit d and PTH ___ calcium

A

increase

83
Q

calcitonin is made in what cell

A

parafollicular cells of THYROID

84
Q

Ca2+ is imp for?

A

muscle contractility

85
Q

vit d is converted to active vit d where?

A

liver

86
Q

PTH and relationship to bones

A

PTH increases osteoclastic activity–tells bones to break down the Ca + phosphate (mainly CA)

87
Q

PTH and relationship to kidneys

A

tells renal tubular cells to incr reabsorbe CA and decrease reabsoprtion of phosphate—so phopshate is excreted in urine

88
Q

intestinal absoprtion of calcium increases via?

A

vit D

89
Q

agonist hormone to vit d and PTH

A

Calcitonin

90
Q

role of Vit D

A
  • increases absorption of CA and phosphate from gut

- increases bone resorption to help release CA into circulation

91
Q

role of calcitonin

A

decrs blood CA by using CA to build bone—decreasing renal reabsoprtion of calcium

92
Q

excess of PTH and or VIt D can cause?

A

hypercalcemia

93
Q

too little PTH and or vit d can cause?

A

hypocalcemia

94
Q

too much calcitonin or too little calcitonin can cause?

A

not much in terms of hypo or hypercalcemia — role in this case is more minor compared to PTH and Vit D

95
Q

bone breakdown and decreased renal excretion of CA can lead to?

A

hypercalcemia

96
Q

bone sequestration of calcium and renal failure can lead to?

A

hypocalcemia

97
Q

MC pathology for cause of hyperparathyroidism?

A

parathyroid adenoma in one gland or more

98
Q

PTH inhibits reabsorption of?

A

phosphate and HCO3

**then phosphate is excreted in urine

99
Q

intestinal absoprtion of ____ is ____ via actions of vit D

A

calcium

increasd

100
Q

how does calcitonin decease [ca]

A

uses calcium to build bone–decreasing renal absorption of calcium

101
Q

99% of CA is found?

A

in bone

102
Q

where is most of the CA? ECF or ICF?

A

ECF

103
Q

nornal CA levels?

A

8.5-10 mg/dk

104
Q

what is required for intestinal ca absoprbs?

A

vit d

105
Q

ca2+ is important for what?

A

blood clotting
bone
normal celluar and neruomuscular function

106
Q

three hormoes that regulate CA

A

vit d (calcitriol) and PTH—>stimulate ca reabsoption into body
-increases blood CA levels
-

calcitonin–> decreases CA blood levels

107
Q

PTH affect on phosphate

A

inhibits reabsoprtion

***so phosphate is usually in opp direction of PTH in PRIMARY parathyroid issues

Pathophysiology (13 decks)

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