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CABS endocrine > Thyroid/parathyroid > Flashcards

Thyroid/parathyroid Flashcards

1
Q

What does TSH do

A

increase production/release of thyroid hormone

increase iodide uptake and takes care of thyroid tissue

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2
Q

What helps inhibit production of TSH

A

somatostatin with the negative feedback loop

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3
Q

What joins the 2 lobes of the thyroid

A

isthmus
*pyramidal lobe projects upwards

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4
Q

What vessel supplies the thyroid

A

superior thyroid artery (off external carotid) and inferior thyroid artery

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5
Q

what innervates the thyroid

A

recurrent laryngeal nerve

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6
Q

What is the importance of the laryngeal nerve

A

voice!
*if damaged, patient will be mute

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7
Q

What type of cells make up the thyroid

A

follicular cells surrounded by colloid

*Follicular cells are what creates the thyroid hormone

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8
Q

What binds to the follicular cells

A

binding site for TSH
*triggers release of stored TH

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9
Q

What neurotransmitters can also control TSH

A

acetylcholine
catecholamines

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10
Q

Where are C cells found and what do they do

A

In the thyroid gland and secrete calcitonin to lower calcium levels in the blood

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11
Q

How does calcitonin lower calcium levels

A

inhibit osteoclastic activity and promotes osteoblastic activity

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12
Q

What is the active form of TH

A

T3

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13
Q

Where is thyroglobulin made

A

follicular cells

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14
Q

What does thyroid peroxidase do

A

oxidize the iodide into active form of iodine

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15
Q

What does T3 and T4 get packaged into before going into circulation

A

lysosomes

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16
Q

Where is iodide absorbed

A

In the GI track

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17
Q

Where is iodide secreted from

A

kidneys

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18
Q

What promotes iodide trapping

A

TSH

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19
Q

What does TH assist with

A

synthesizing enzymes, proteins, transport proteins

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20
Q

How does TSH effect carbohydrate and fat intake

A

Increase carb metabolism encouraging glucose uptake and glycolysis

stimulates fat metabolism
decreases cholesterol

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21
Q

How does TSH help decrease cholesterol

A

Increase GI motility and force cholesterol into the bile so there is increased excretion

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22
Q

How does TH effect heart

A

Increases CO, HR, Heart strength, respiration, and tissue blood flow

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23
Q

How high above normal can the metabolic rate go above normal

A

As high as 100% above normal the metabolic rate

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24
Q

What is thyrotoxicosis

A

Elevation in TH due to problem over secretion from gland, over stimulation from pituitary, ectopic production or excess exogenous intake

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25
Q

What is the major primary cause of Graves disease

A

Thyrotoxicosis

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26
Q

What is Graves disease

A

autoimmune disorder that causes 50-80% of hyperthyroidism

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27
Q

What type of hypersensitivity is graves disease considered

A

type 2

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28
Q

What ophthalmic manifestations occur with graves disease

A

Lid lag
Exophthalmus
edema etc.

29
Q

What are the dermatologic conditions of graves disease

A

Pretibial myxedema

*from thyroid stimulation immunoglobulins causing increased stimulation of T lymphocytes

30
Q

What generally causes nodular thyroid disease

A

Times during high demand or inadequate production, some cells hypertrophy to compensate

*generally after the stressor is gone, the gland will normalize

31
Q

What occurs if the enlarged thyroid does not normalize after the stressor goes away

A

It will turn into a toxic adenoma or toxic multi nodular goiter

32
Q

Since nodular thyroid disease is not autoimmune, what associate symptoms will not occur

A

Eye or skin involvement

33
Q

How will someone with hyperthyroid present

A

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

34
Q

What is the most common thyroid disorder

A

hypothyroidism

35
Q

What is secondary hypothyroidism commonly due to

A

trauma
lesions
CVA

36
Q

What is the most common type of hypothyroidism

A

iodine deficiency

37
Q

What is the most common cause of hashimotos

A

Hypothyroidism

38
Q

What is the cause of central hypothyroidism

A

tumor, hemorrhage, TBI, CVA
Sheehan syndrome

39
Q

What is central hypothyroidism

A

damage to the hypothalamus leading to a decrease in TRH or damage to the anterior pituitary to decrease TSH

40
Q

What is hashimotos thyroiditis

A

Autoimmune thyroiditis with autoantibodies attaching to follicular cells

41
Q

What do the autoantibodies in hashimotos attack

A

thyroglobulin
thyroid peroxidase
TSH receptors
(follicular cell damage)

42
Q

What is occurring within the thyroid with hashimotos

A

Infiltrates will lead to apoptosis of follicular cells = fibrosis and decrease TH production

43
Q

What is transient hyperthyroidism

A

As the apoptosis of the follicular cells occur, all the hormones are released

44
Q

What is myxedema

A

Prolonged significant hypothyroidism that leads to increased hyaluronic acid and chondroitin sulfate

45
Q

What is myxedema coma

A

Rare and often fatal condition associated with untreated, longstanding hypothyroidism in which the body cant compensate (not actual coma)

46
Q

What is cretinism

A

Occurs when there is profoundly low thyroid hormone during development, infancy, or early childhood

47
Q

What is cretinism associated with

A

genesis or underdeveloped
*typically from iodine deficiency

48
Q

what can be some causes for thyroid goiters

A

inability to trap iodide
not enough peroxidase

49
Q

What does the parathyroid gland do

A

Release PTH to regulate (increase) calcium concentration

50
Q

What cells are the primary creator of PTH

A

Chief cells

51
Q

What needs to be present for calcium to be absorbed

A

Vitamin D

52
Q

What type of receptors do chief cells have

A

g-protein calcium receptor

53
Q

What hormone is involved with vitamin D activation

A

PTH

54
Q

What type of hormone is vitamin D

A

Steroid

55
Q

What converts vitamin D to its active form

A

hydroxylation in liver or by the kidney

56
Q

What electrolyte is needed for normal cellular metabolism

A

phosphorus

57
Q

Excretion of phosphorus is controlled by what

A

PTH

58
Q

What is hypophosphatemia linked to

A

antacids

59
Q

What is hyperphosphatemia linked to

A

Kidney dysfunction

60
Q

What are causes of primary hyperparathyroidism

A

Solitary parathyroid adenoma
gland hyperplasia
MEN syndrome
Cancer

61
Q

What are some causes of secondary hyperparathyroidism

A

CKD
Vit D deficiency

62
Q

What are some causes of tertiary hyperparathyroidism

A

Around even after the underlying PTH issue is corrected

63
Q

What is the most common cause of paraneoplastic syndrome

A

SCC

64
Q

What will be seen in labs in someone with hyperparathyroidism

A

Elevated PTH
Hypercalcemia
Hypophosphatemia
elevated phosphate in urine
hypercalcinuria

65
Q

Signs of hypercalcemia

A

Fatigue
nephrotlithiasis
Arrythmia
neurologic symptoms
polydipsia/polyuria

66
Q

What is hypoparathyroidism generally associated with

A

damage to the parathyroid
Neck radiation
removal of the gland

67
Q

What are some infiltrative disorders associated with hypoparathyroidism

A

Hemochromatosis
Sarcoidosis
Wilsons disease (Copper)

68
Q

What can happen to a persons muscles with hypocalcemia

A

Tetani
*can leed to laryngospasm

CABS endocrine (5 decks)

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