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Pathophysiology > endocrine- thyroid/parathyroid > Flashcards

endocrine- thyroid/parathyroid Flashcards

1
Q

thyroid is composed of what two types of cells?

A

follicular & parafollicular (C-cells)

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2
Q

what do parafollicular cells produce?

A

calcitonin (osteoclast inhibitor)

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3
Q

thyroid hormones require ____ for synthesis, coupled to ______.

A

iodine, coupled to tyrosine.

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4
Q

what are the two forms of thyroid hormone?

A

Triiodothyronine (T3): Biologically active
Tetraiodothyronine (T4, aka thyroxine): Most secretion
Converted to T3 in periphery (5’-iodinase)

*either have 3 or 4 iodines attached to tyrosine molecule

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5
Q

what is the only gland that stores appreciable amounts of hormone?

A

thyroid gland: stores premade thyroid hormone in “colloid”

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6
Q

thyroid hormone is synergistic with the SNS : what are the 3 effects of this?

A
  1. Increase metabolic rate (cell rxn rate) & heat production (ATP production)
  2. Promote catabolism
  3. Increase HR & contractility
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7
Q

what is the “jod-basedow phenomenon”?

A

low levels of iodine - thyroid is hungry to iodine - if you give them iodine it will grab onto everything it can (iodine transport into follicular cell) and pump out all of its hormones
—> create a thyroid storm
- gland under heavy TSH stimulation

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8
Q

what can cause the “jod-basedow phenomenon”? why is this significant?

A

Treating iodine-deficient patients with heavy iodine can produce acute hyperthyroidism or even thyroid storm

takehome message: txt iodine deficiency in a slow controlled manner

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9
Q

what is the Wolff-Chaikoff effect? (kinds weeds)

A

High levels of I- inhibit coupling of I2 to TG & coupling of MIT/DIT

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10
Q

txt for hyperthyroidism (and jod-basedow phenom) ?

A
  • methimazole (inhibits TPO)
  • PTU (inhibits TPO + conversion of T4 to T3)

*TPO = thyroperozidase - catalyst for T4 and T3 production

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11
Q

what is thyroglobulin?

A

thyroglobulin - carrier proteinmolecule - most abundant thyroid binding hormone

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12
Q

what are the steps of thyroid hormone synthesis? (3)

A
  1. Thyroglobulin secreted into follicles
  2. Active transport & oxidation of iodine by Thyroid peroxidase (TPO)
  3. MIT and DIT coupled to form thyroid hormones…
    2 of the DIT (diiodotyrosin) - T4
    DIT + MIT (mono iidotyrosin) = T3
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13
Q

what is the ratio of T4 to T3 in plasma?

A

T4 > T3 secreted into plasma (9:1 ratio)

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14
Q

99% of thyroid hormones, are bound to plasma protiens… what are the three proteins thyroid hormone can be bound to? what is the most prevalent?

A

Thyroid-binding globulin (TBG)-most
Transthyretin
Albumin

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15
Q

what type of thyroid hormone is “free”?

A

Only “free” hormone is active (free to bind to target receptors)

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16
Q

how can hepatic failure and pregnancy each effect the amount of TBG (thyroid binding hormone)?

A

Hepatic failure (liver produces most plasma proteins- so failure = lower levels of thyroid binding hormones)- more free thyroid hormone

pregnancy - increase in estrogen increase level of binding protein - less free thyroid hormone

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17
Q

best way to increase thyroid binding hormone

A

give estrogen

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18
Q

how likely is Clinical hyper-/hypo-thyroidism due to binding hormones?

A

rare due to negative feedback

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19
Q

what are the hypothalamus/pituitary axis for thyroid hormone secretion?

A

Hypothalamic TRH stimulates TSH secretion
TSH stimulates thyroid growth & hormone secretion
–> T3 and T4 secretion
*negative feedback to anterior pituitary

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20
Q

What is TRAb?

A

Thyroid-stimulating antibodies

-they bind & stimulate TSH receptors (in this case, antibodies don’t destroy but actually stimulate)

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21
Q

why is measuring thyroid hormone levels easier than measuring any other hormone level?

A

secretion is constant (not pulsatile) so a “spot” level is possible

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22
Q

what is “cretinism”?

A

congenital hypothyroidism

  • screened for at birth
  • check TSH +/- T4
  • untreated can lead to mental retardation, deafness, spasticity
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23
Q

what is a “goiter”?

A

enlarged thyroid- can be from anything- hyper, hypo or normal thyroid

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24
Q

3 types of acquired hypothyroidism

A

Primary: under functioning thyroid despite normal stimulation
Secondary (central hypothyroidism): under stimulation from too little TSH (pituitary problem)
Tertiary (the other central hypothyroidism): too little TSH from too little TRH (hypothalamic abnormality)

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25
Q

which type of acquired hypothyroidism is most common? least common?

A

most: primary
least: tertiary

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26
Q

txt for all three types of acquired hypothyroidism?

A

thyroid hormone replacement (synthroid)

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27
Q

6 causes of acquired hypothyroidism?

A
  1. Lack/loss of thyroid tissue
    *2. Iodine deficiency (ultra rare in US)
    *3. Excess iodine (Wolff-Chaikoff)
    **4. Hashimoto’s (chronic autoimmune) thyroiditis (MOST COMMON)
    *5. Amiodarone - can induce wolff-chaikoff effect
    (High iodine content)
  2. Valproic acid
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28
Q

8 manifestations of hypothyroidism

A
  1. Slowing of body & mind: Mistaken for “depression”
  2. Decreased HR & contractility
  3. Increased LDL cholesterol
  4. Constipation, weight gain
  5. Coarse, brittle hair
  6. Cold intolerance
  7. Delayed “hung” DTRs (deep tendon reflexes)
  8. Myxedema
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29
Q

what is myxedema?

A 
accumulation of ground substance in connective tissues
Thick tongue
Periorbital edema
Coarse voice
(seen in hypothyroidism)
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30
Q

what is hashimoto’s thyroiditis?

A

“chronic autoimmune thyroiditis”

  • Autoimmune reaction to thyroglobulin &/or TPO ( the immune system attacks these)
  • lymphocyte infiltration of thyroid gland ( goiter common)
  • Usually euthyroid, many hypothyroid, few transiently hyperthyroid
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31
Q

what is schmidt’s syndrome? (kinda weeds)

A

a triad:
hypothyroidism
autoimmune adrenalitis - adrenal insufficeincy (addisonism)
DM type 1

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32
Q

txt of schmidt’s syndrome, what do you need to be careful to do? (kinda weeds)

A

cover with steroids THEN add synthroid
(if you don’t do this first you can kill them)
… not sure why ..

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33
Q

what is DeQuervain’s Subacute Thyroiditis?

A

viral infection of the thyroid (i.e. coxsackie)

Spotty destruction of follicular cells with release of colloid

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34
Q

presentation of DeQuervain’s Subacute thyroiditis? what can it lead to (short term and long term)?

A
  • Neck pain, fever
  • Increased ESR
  • May cause transient hyperthyroidism, may lead to hypothyroidism (longterm)
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35
Q

3 types of hyperthyroidism

A

Primary-hyper functioning thyroid despite normal stimulation
Secondary-hyper functioning thyroid due to overstimulation from excess TSH (pituitary) . Usually ectopic
Tertiary-too much TSH from too much TRH (hypothalamus)

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36
Q

what are the most and least common types of hyperthyroidism?

A

most: primary
least: tertiary

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37
Q

5 important causes of hyperthyroidism (and which are the two most common) ?

A
  1. Graves’s disease (most common)
  2. Plummer’s disease (2nd most common)
  3. Jod-Basedow (rare in US)
  4. DeQuervain’s (transient) (with initialy destruction of gland- get hypo)
  5. amiodarone
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38
Q

presentation of hyperthyroidism (5)

A
  1. increased mentation - labile, anxious
  2. hypermetabolic
  3. enhanced epinephrine effect
  4. ***Osteoporosis
  5. Lid lag/exophthalmos
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39
Q

what do the hypermetabolic effects of hyperthyroidism cause? (3)

A

Increased appetite & weight loss
Muscle atrophy
Heat intolerance

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40
Q

what does the enhanced epinephrine effect cause? (3)

A

Tremors
Bounding pulse
Atrial fibrillation

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41
Q

what is Grave’s disease ?

A

Idiopathic autoimmune production of anti-TSH receptor antibodies (TRAb)

  • TRAb stimulate TSH receptor
  • increase T4
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42
Q

what is the “classic triad” of grave’s disease?

A
  1. Goiter (diffuse toxic) (hot on throid scan)
  2. Ophthalmopathy-proptosis/exophthalmos - lid lag
  3. Pretibial myxedema-connective tissue nodules on anterior leg - tissue deposits on anterior leg
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43
Q

labs for grave’s disease

A

High T4 & low TSH

+TRAb

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44
Q

3 pharm. Txt options for Grave’s disease

A
  1. Antithyroid drugs: PTU, methimazole
  2. Propranolol (blocks some of the SNS effect- HR, tachycardia, etc)
  3. Radioactive iodine (I131) - ablation of thryoid- usually most common option. (produces Hypothyroidism)
45
Q

surgical txt for grave’s disease?

A

Near-total thyroidectomy (avoid post-op hypothyroidism)

46
Q

what is plummer’s disease?

A

“Toxic adenoma” Benign functional tumor
Hyperfunctioning tumors-mutated TSH receptor stuck in the “on” position
“Hot” nodule on thyroid scan
- rarely turn malignant

47
Q

txt for plummer’s disease?

A

surgical removal
surgical dilemma: *difficult to differentiate from malignant follicular carcinoma
- both benign and malign. tumors here can be functional- produce hormones

48
Q

what is the most common endocrine cancer overall ?

A

thyroid cancer

49
Q

4 types of thyroid cancer?

A

Papillary-most common, least deadly
Follicular-modestly aggressive
Medullary-aggressive
Anaplastic-least common, ultra aggressive

50
Q

overall, thyroid disorders more common in men or women?

A

women

51
Q

60-85% percent of thyroid cancers are what kind?

A

papillary

52
Q

while most don’t die from papillary carcinoma (thyroid cancer)- what manifestation can cause death?

A

Asphyxiation - invasion into trachea - can cause death

53
Q

where does papillary carcinoma metastasize?

A

metastasizes to cervical lymph nodes (lymphatic route of metastasis as opposed to blood)

54
Q

can you “just watch” thyroid cancers?

A

NO! all have the potential to become the ultra aggressive anaplastic kind

55
Q

what cancer is “orphan annies tumor” associated with?

A

papillary carcinoma

56
Q

what are the characteristics of “orphan annies” tumor? (5)

A
  1. Most often affects young women
  2. Stays around for years without getting bigger (comic strip around for years without her getting older)
  3. Well-behaved & doesn’t kill people
  4. Nuclei have marginated chromatin-”Orphan Annie’s eyes” (she had just whites as eyes)
  5. Psammoma bodies in cytoplasm-calcifications (Greek for sand, “Sandy” was orphan annies dog)
57
Q

prognosis of follicular carcinoma? (kinda weeds) - (% that will die if metastatic, survival, biggest risk)

A

50% will eventually die from it if metastatic
Survival commonly&raquo_space; 5 years
Iodine deficiency is greatest risk

58
Q

how does follicular carcinoma (thyroid cancer) metastisize?

A

hematogenous route of metastasis (Lungs, bone)

59
Q

what type of thyroid cancer notoriously creates the “surgical dilemma”?

A

follicular carcinoma: difficult to distinguish from follicular adenoma on frozen section
-lobectomy or total thyroidectomy? ..

60
Q

txt for follicular carcinoma

A
  • Many take up I131- (radioactive iodine) useful for detecting metastases or
  • treatment (if you dont want surgery)
61
Q

describe medullary carcinoma

A
  • cancer of C-cells (calcitonin)
    -Mutation in RET proto-oncogene on chromosome 10
    Multiple Endocrine Neoplasia type II syndrome-familial
    (more during “adrenal”)
    More often (80%) sporadic
62
Q

which thyroid cancer may you do genetic testing for? why?

A

medullary carcinoma

- Test for gene available (MEN gene) : Prophylactic thyroidectomy

63
Q

how can you tell if you got the entire tumor for medullary carcinoma surgical removal?

A

Tumors typically produce calcitonin (differentiated enough to act like normal cells) -marker for adequate surgical resection
- if calcitonin negative = you got the tumor completely

64
Q

prognosis of aplastic carcinoma (what % of thyroid cancers? arise from what?, txt?)

A

5% of thyroid cancers
Virtually all will die from it within months
Most arise from a previous papillary carcinoma
Usually offered hospice over chemotherapy

65
Q

what are the two ways we can measure T4?

A

Serum T4- total (bound + unbound) hormone

Serum free T4- unbound (active) hormone: More expensive

66
Q

which thyroid hormone do we care about measuring?

A

T3

but serum T3 and free T3 is only available at some institutions

67
Q

explain the T3RU test results (kinda weeds)

A

T3 resin uptake: inversely proportional to free sites on thyroid binding proteins

  • T3RU if high- low # free binding sites on TBG b/c they were already filled up - more bind to resin
  • if T3RU low - high # free binding sites on TBG - less bind to resin
68
Q

how does the T3RU test work? (weeds)

A
  • resin has lower affinity for T3 than natural TBG
  • dump plasma (w/ T3 bound to TBG) on resin
  • add radioactive T3: preferentially binds TBG free sites
  • leftover radioactive T3 will bind resin
  • dump mix, measure radioactive levels
69
Q

what is used to “correct for the binding abnormalities” of the T3RU test?

A

Free thyroxine index (FTI)=T4 * T3RU

70
Q

what TSH levels correlate with hypo-/hyperthyroid? (kinda weeds)

A

hypothyroid- high TSH
hyperthyroid- low TSH
*normal TSH about 0.35-5.0

71
Q

do we treat patients based on the T3/T4 levels or the symptoms?

A

TSH levels & symptoms > T3/T4 levels in guiding therapy

Treat the patient, not the numbers

72
Q

what are “hot” vs “cold” on thyroid scans?

A

Hyperfunctional tissue looks “hot” (dark)

Nonfunctional/suppressed tissue looks “cold” (white)

73
Q

thyroid scan interpretation: hot nodules most likely produce ______ while cold nodules most likely to be _____

A

Hot nodules most likely to produce hyperthyroidism

Cold nodules most likely to be malignant

74
Q

thyroid scan interpretation: diffusely hot =? diffusely cold =?

A

Diffusely hot in Graves

Diffusely cold in DeQuervain’s, factitious

75
Q

what 3 thyroid autoantibodies can we test for, what does each indicate?

A

TRAb-TSH receptor antibody (Graves’s)
TPOAb-anti-peroxidase/anti-microsomal antibody (Hashimoto’s)
TgAb-anti-thyroglobulin antibody (Hashimoto’s)

76
Q

FNA result interpretation, what do you do if result is “ nondiagnostic” ?

A

repeat with ultrasound (need another sample with better FNA- guided)

77
Q

FNA result interpretation, what do you do if result is “benign”?

A

follow clinically

78
Q

FNA result interpretation, what do you do if result is “atypia of uncertain significance”?

A

repeat FNA

79
Q

FNA result interpretation, what do you do if result is “suspicion of follicular neoplasm”?

A

lobectomy (where the “surgical dilemma” comes in.

- Benign/malignant distinction difficult

80
Q

FNA result interpretation, what do you do if result is “suspicion of malignant” or “malignant” ?

A

Suspicious for malignancy-lobectomy/thyroidectomy

Malignant-thyroidectomy

81
Q

what is the major regulator of calcium homeostasis?

A

parathyroid glands

82
Q

parathyroids contain what type of cells?

A

hormone-secreting cheif cells

83
Q

parathyroid effect on kidney

A
  1. Promotes conversion of 25-OH-D3 to active 1,25-(OH)2-D3 that increases calcium absorption from the gut
  2. Promotes reabsorption of calcium & loss of phosphate
84
Q

parathyroid effect on bone

A

Promotes resorption of calcium by osteoclasts

Promotes proliferation of osteoclasts

85
Q

parathyroid effect on gut

A

Promotes calcium absorption (INDIRECT via vitamin D activation)

86
Q

parathyroid is a rapid strong secretory response to Ca2+ < ____ mg/dL

A

Ca+2 < 10 mg/dL

87
Q

Chronic _________ impairs PTH secretion

A

hypomagnesia

88
Q

what induces feedback inhibition of PTH?

A

Normalization of Ca+2 induces feedback inhibition

89
Q

primary hyperparathyroidism is due to what? (and 3 biggest causes)

A

Primary hyperparathyroidism-due to parathyroid disease

  1. parathyroid adenoma (single gland)
  2. parathyroid hyperplasia (all glands)
  3. parathyroid carcinoma
90
Q

what is the most and least common cause of primary hyperparathyroidism?

A 
parathyroid adenoma (single gland) - MOST 85% 
parathyroid carcinoma - LEAST
91
Q

85% of people with hyperparathyroidism have what genetic abnormality?

A

MEN-I

92
Q

Incidental hypercalcemia is usual presentation of what?

A

hyperparathyroidism

93
Q

“Stones, bones, abdominal moans, & psychiatric overtones” - indicates what?

A

hyperparathyroidism

94
Q

Dx labs of hyperparathyroidism

A

High serum Ca+2, low serum P, elevated PTH

95
Q

what level defines hypercalcemia?

A

Total serum Ca+2 > 10.5 mg/dL

96
Q

two major causes of hypercalcemia?

A
  1. hyperparathyroidism

2. hypercalcemia of malignancy

97
Q

what are the general signs of hypercalcemia?

A

Polyuria, polydipsia, renal calculi
Bone demineralization, pathologic fractures
Constipation, nausea, vomiting
Fatigue, personality changes, frank psychosis
Pancreatitis

98
Q

hypercalcemic crisis causes what?

A

-hypovolemia, depressed LOC, fever, cardiac dysrhythmias/arrest

99
Q

parathyroid adenoma

A

Autonomous production of PTH

  • Other glands suppressed/atrophic
  • 10% are “ectopic” (variable location)
100
Q

4 part txt of parathyroid adenoma

A
  1. Preoperative sestamibi scan can localize
  2. surgical removal
  3. Intraoperative PTH levels determine effectiveness (if it drops near zero after you removed hot gland - tells you that you got the adenoma)
  4. post-op Ca+ supplement
101
Q

what post-operative supplement do people need after removal of parathyroid adenoma?

A

Postoperative calcium supplementation (500-100 mg /day)

102
Q

if you have a functional parathyroid adenoma, why is it hard to find the other parathyroid glands? what happens to these when you remove the cancerous one?

A

its hard to find the other parathyroid glands b/c they are atrophied. These will grow and recover when we remove the oppressive PTH - producing parathyroid.
- So the pt will not be hypoparathyroid after some time.

103
Q

parathyroid hyperplasia

A

All glands hyperplastic & autonomous
- “4 gland adenoma”
Raise suspicion for MEN I or IIa

104
Q

2nd most common cause of hyperparathyroidism?

A

parathyroid hyperplasia

105
Q

txt of parathyroid hyperplasia

A

Requires excision of majority of parathyroid tissue (take all 4)
Slithers of gland transplanted to forearm muscle to prevent hypoparathyroidism (so their calcium doesnt go very low) - if calcium still high, take a few of these implanted ones out - easier to get there than the throat)

106
Q

secondary hyperparathyroidism causes

A 
Parathyroid hyperplasia due to chronic hypocalcemia
- Renal failure (hypocalc, hyperphos.) 
- Vitamin D deficiency
 = serum Ca+ high
= bone Dz (osterodystrophy)
107
Q

txt for secondary hyperparathyroidism

A

Treated with cinacalcet or transplantation

108
Q

tertiary causes of hyperparathyroidism

A

Hyperplastic gland in renal failure becomes autonomous

- Overproduces PTH, Serum Ca+2 high

109
Q

txt of tertiary hyperparathyroidism: may regress after what? may require what?

A

May regress after renal transplantation

May require removal of adenoma

Pathophysiology (28 decks)

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