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CABS3: endocrine > Thyroid, Parathyroid A&P Pathophysiology (incomplete) > Flashcards

Thyroid, Parathyroid A&P Pathophysiology (incomplete) Flashcards

1
Q

what increased iodide uptake

A

thyroid stimulating hormone

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2
Q

what helps to inhibit the production of TSH in a negative feedback loop

A

somatostatin

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3
Q

what is the middle portion of the thyroid gland that connects the two lobes called

A

isthmus

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4
Q

what is the blood supply to the thyroid gland

A

superior thyroid artery - off external carotid
also from inferior thyroid after (off of the thyrocervical trunk from the suprascauplar artery)

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5
Q

what innervates the thyroid gland

A

recurrent laryngeal nerve - branch off the vagus nerve (CN X)

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6
Q

how much hormone does the thyroid store

A

2-3 months worth

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7
Q

what is the thyroid gland made up of

A

follicular cells surrounded by colloid
follicular cells are sites for binding of TSH and trigger release of stored TH
can also be neurally controlled by acetylcholine and catecholamines

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8
Q

what is the active form of TH

A

triodothyronin (T3)

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9
Q

what is made within the follicular cell

A

thyroglobulin - large protein that contains significant amount of tyrosine amino acids - stored in colloid

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10
Q

what is able to oxyidize the iodide into active form of iodine

A

thyroid peroxidase

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11
Q

what is the advantaged of T4

A

longer half life

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12
Q

where is iodide aborbed

A

in the GI tract

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13
Q

what is thyroid hormone bound to within the blood stream

A

thyroxine binding globulin
small amount bound to albumin

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14
Q

is thyroid hormone water soluble or lipid soluble

A

lipid soluble

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15
Q

what are the actions of thyroid homrone

A

changing ion channel regulation
increase protein catabolism
increase number and size of mitochondria
stimulate glucose metabolism which will increase the basal metabolic rate and encourage glucose uptake, glycoysis
increases thermogenesis

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16
Q

what is primary hyperthyroidism

A

elevated thyroid hormone (T3 and T4), low thyroid stimulating hormone (does not need to stimulate the thyroid for the elevated production)

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17
Q

what is seen on labs with secondary hyperthyroidism

A

elevated TH, elevated TSH (excess being production/secreted in the pituitary)

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18
Q

what is thyrotoxicosis

A

symptomatic elevation in circulating thyroid hormone (hyperthyroidism)
Major primary cause of this is Graves disease

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19
Q

what is the secondary cause of thyrotoxicosis

A

(not as common) active TSH pituitary adenoma

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20
Q

What is an autoimmune disorder that causes 50-80% of hyperthyroidism

A

Graves disease

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21
Q

what are the ophthalmologic manifestations of graves disease

A

lid lag (both upper and lower)
exophthalmos: inflammation, edema, too much content in the orbit

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22
Q

what is the dermatologic manifestations of Graves disease

A

pretibial myxedema - aka graves dermopathy

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23
Q

what causes pretibial myxedema

A

thryoid stimulating immunoglobulins causing increased stimulation of T lymphocytes
increased hyaluronic acid production
swelling/induration/erythema to anterior lower extremities

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24
Q

when do nodular thyroid diseases occur

A

during stressor - typically will normalize after stressor

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25
Q

what is the presentation of hyperthyroid

A

heat intolerance
sweating
weight loss
diarrhea
weakness
psychiatric disorders
fatigue but inability to sleep
excitable

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26
Q

what is the most common disorder of the thyroid

A

hypothyroidism

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27
Q

what is primary disease state of hypothyroidism

A

low thyroid hormone (T3 and T4), high thyroid stimulating hormone (trying to up regulate to TH)

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28
Q

what is secondary disease state of hypothyroidism

A

low TH, low TSH ( the low TSH is causing the low TH) - associated with trauma, lesions, CVA

29
Q

what is the most common type of hypothyroidism worldwide

A

deficiency

30
Q

what is Hashimoto disease

A

an autoimmune thyroiditis - hypothyroidism

31
Q

what does the central cause of hypothyroidism lead to

A

decreases TRH and/or TSH

32
Q

what is Sheehan syndrome

A

necrotic pituitary from postpartum syndrome

33
Q

what is the presentation of hypothyroidism

A

cold intolerance, fatigue, low body temp
weight gain, decreased appetite, bradycardia, constipation, fatigue, dry skin, thin nails
may lead to goiter

34
Q

what is central hypothyroidism

A

damage to hypothalamus leading to decrease TRH or damage to the anterior pituitary leading to decreased TSH

35
Q

what are labs indicative of hypothyroidism

A

low TSH
low T3
low T4

36
Q

what is an autoimmune thyroiditis with autoantibodies attaching follicular cells

A

hashimotos thyroiditis

37
Q

if someone has primary hypothyroidism what are their labs going to show

A

High TSH
Low T3 and T4

38
Q

what can Graves disease develop into

A

Hashimotos

39
Q

what is Hashitoxicosis

A

as cells undergo apoptosis it can cause transient hyperthyroidism (so many hormones released all at once)

40
Q

what is myxedema

A

prolonged significant hypothyroidism - typically near zero TH

41
Q

what is myxedema coma

A

rare and often fatal condition associated with untreated, longstanding hypothyroidism in which the body has not been able to compensate - no true coma

42
Q

what is the presentation of myxedema coma

A

AMS
HTN
dry, cool skin - hypothermia
constipation, distension - illeus, impaction, myxedema megacolon
hypoventilation
arrhythmias, heart block
facial changes
nonpitting edema
acquired von willebrand syndrome

43
Q

what is cretinism

A

occurs with profoundly low thyroid hormone during development, infancy or early childhood

44
Q

what is cretinism associated with

A

agenesis or under developed
mom will supply some in utero

45
Q

how do you treat cretinism

A

iodine and T4 - will lead to normal growth

46
Q

what is an abnormal cellular growth of the thyroid

A

goiter

47
Q

what can thyroid goiters be associated with

A

inability to trap iodide
not enough peroxidase so that iodine can not be oxidized into iodine
lack of or defective thyroid peroxidase (unable to go through final steps of TH formation)

48
Q

what does the parathyroid release

A

parathyroid hormone which regulates calcium concentration

49
Q

what cells are the primary creator of the parathyroid hormone

A

chief cells

50
Q

is PTH water or lipid soluble

A

lipid soluble?

51
Q

what triggers the release of PTH

A

hypocalcemia

52
Q

what does PTH first trigger

A

inhibition of osteoblasts

53
Q

what does PTH work with

A

vitamin D to allow for absorption in GI tract

54
Q

what activates vitamin D

A

kidney and liver

55
Q

when can the parathyroid gland enlarge in live

A

during pregnancy and breast feeding

56
Q

what are the action of PTH in the kidney

A

bind to cell within distal collecting duct
– increase in calcium channels to cause respiration of Ca2+ from urine, will cause increased phosphate excretion

57
Q

what are the actions of PTH in the intestine

A

induces the conversion of Vitamin D to active vitamin D - allows for absorption in GI tract

58
Q

what type of hormone is vitamin D

A

steroid hormone

59
Q

what secreted calcitonin

A

thyroid has C cells - to lower calcium levels in blood

60
Q

what is the purpose of calcitonin

A

decrease circulating Ca2+

61
Q

what is the most common cause of hyperparathyroidism

A

solitary parathyroid adenoma

62
Q

what is secondary hyperparathyroidism

A

elevated PTH but b/c of low Ca2+
- typically associated with CKD or vitamin D deficiency

63
Q

what is seen with hyperparathyroidism

A

elevated PTH
hypercalcemia
hypophosphatemia (causes increased renal excretion)
elevated phosphate in urine
elevated calcium in urine

64
Q

what are the signs of hyperparathyroidism

A

elevated calcium: fatigue, nephrolithiasis, polydipsia, polyuria, N/V/D, abd discomfort, arrhythmia, osteoporosis, neurologic symptoms

65
Q

what is seen with significant hypercalcemia

A

stones, bones, groans, moans and psychiatric overtones
-kidney stones, bone break down, constipation, pancreatitis, fatigue, psychiatric disturbances

66
Q

what is the most common cause of Hypothyroidism

A

damage to the parathyroid*
-accidental removal with thyroidectomy
-neck radiation
-purposefully removed

67
Q

what can you see with hypocalcemia

A

muscular tetani
Chvostek sign
Trousseau sign
AMS
prolonged QT

68
Q

what is Chvostek sign

A

tap facial nerve anterior to the ear - causes facial twitch

69
Q

what is Trousseau sign

A

BP cuff will cause carpal spasm - wrist flexion, MCP flexion, interphalangeal joint extension

CABS3: endocrine (5 decks)

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