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Pathology > Thyroid Parathyroid Pituitary > Flashcards

Thyroid Parathyroid Pituitary Flashcards

1
Q

Thyroid

A

Ok

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2
Q

What thyroid hormones do

A

Increase BMR

Protein catabolism glucose utilization, growth maturation

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3
Q

TSH

A

Ligand for thyroid receptor, bind active and thyroid hormones elaborated

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4
Q

Colloid

A

TSH bind receptor on follicle and stimulate all step

  1. Thyroglobulin synthesized and stored in clobulin
    - transport of iodide from circulation to follicular cell increase pulled into follicular cell into colloid and get MIT and DIT then pulled back into cell to become T4 and T3

Released into blood

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5
Q

Primary of secondary hyperthyroidism( more common

A

Primary

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6
Q

Primary hyperthyroidism

A

Diffuse hyperplasia 9graves)

Hyperfunctioing multinodular goiter

Hyperfunctioning thyroid adenoma (neoplastic

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7
Q

Secondary hyperthyroidism

A

Pituitary adenoma

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8
Q

How determine if primary of secondary

A

Check thyroid hormone in conjunction to TSH

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9
Q

Elevated T3 T4 high and low TSH

A

High secondary

Low primary

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10
Q

Symptoms hyperthyroidism

A

Cardiac-palpitation/tachycardia heart fluttering fast and high pulse (early and apparent and DIRE)
*cardiac arrest one of most severe complications of it
Perspiration-flushing
Nervous, excitability restlessness(b stimulation)

Exophthalmos-graves

Diarrhea, muscle wasting

Breast enlargement

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11
Q

Thyroid storm

A

Crisis sudden severe onset of thyrotoxicosis manifestations

Fever, cardiac (tachycardia, CHF), GI (diarrhea and jaundice)

Precipitation history-pregnant.postpartum, hemithyroidectomy, drugs amiodarone)

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12
Q

Hyperthyroid general

A

Cardiac and GI

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13
Q

What constitutes acute thyroid storm

A

High fever that remains elevated

Precipitating history -preg and postpartum, hemithyroidectomy, drugs

HISTORY AND FEVER**

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14
Q

Pregnant

A

Thyroid storm can put you at risk

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15
Q

Hemithyroidectomy

A

If hyperthyroid and take out a lobe, sometimes the remaining lobe starts hyperfunctioning to thyroid storm level

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16
Q

Amiodarone

A

Can cause thyroid storm

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17
Q

Treat hyperthyroid

A

Beta blockers, NSAIDS

High doses of iodine (Wolff chaikoff effect-when give large dose shuts down thyroid hormone), this amide , radioiodine ablation, surgery

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18
Q

Graves

A

Most common hyperthyroidism

Hyperthyroidism, infiltration ophthalmopathy, pretibial myxedema)

Row of white vacuoles-absorption droplets bubbles around edge. Of follicles and follicles are enlarged

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19
Q

Grave histo

A

Row of white vacuoles-absorption droplets bubbles around edge. Of follicles and follicles are enlarged

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20
Q

Reabsorption droplet

A

Duringactive secretory phase, intracytoplasmic droplets appear (representing colloid in endocytosis vesicles generated by pseudopodial extension of cytoplasm at luminal surface )

——grabbing colloid!!! Indicate hyperfunction

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21
Q

Ophthalmopathy

A

Extraocular muscles extremely thickened

Graves is autoimmune-get lymphocyte infiltratio
Fibroblasts have TSH receptor so when get Thyroid stimulating antibodies get it and get fat and smooth msucle accumulation

Matrix production

Inflammation, smooth msucle, fat, and matrix get mass behind eyes

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22
Q

Pretibial myxedema

A

Hard ANS scaly rash anterior lower extremities

Matrix production probably

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23
Q

Need all three for graves

A

No

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24
Q

How test for graves

A

Original pathogenesis

Primary hyperthyroidism elevated thyroid hormones and elevated tsh and test for thyroid stimulating antibodies

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25
Q

TSI antibody test

A

Sensitive and specific for graves

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26
Q

Hypothyroidism kid cretinism

A

Mental retardation, growth retardation, coarse facial features, umbilical hernias

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27
Q

Why cretinism

A

Endemic areas. No iodine
Depends on time of onset in mom . Can be a result of genetic alterations in normal thyroid metabolic pathways

Iodized salt reversed this wide spread

Single most correctable cause of mental retardation globally

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28
Q

Hypothyroidism present in adult

A

Sluggish slowing down BMR slowing

Lethargy

Weight gain, cold intolerance, cardiac effect (lower output), increased cholesterol), hair loss, face edema, dry skin, brittle hair and nails

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29
Q

Thyroidisit

A

Hashimoto

Granulomatous

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30
Q

Hashimoto

A

Autoimmune most common hypothyroidism ind enveloped world

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31
Q

Why get hashimoto

A

Autoantibodies against thyroglobulin and thyroid peroxidase

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32
Q

Signs hashimoto

A

Diffuse painless enlargement of thyroid (infiltrate with lymphocyte originally hyperactivity and enlargement although brief and subclinal but if severe come to attention hashitoxicosis, but then exhaust follicular cells and shrink)

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33
Q

Hashimoto exhaust histo

A

Lymphocytic infiltrate looks like lymph node in thyroid

Germinal centers with lymphocytic infiltrate

Atrophic follicle cells with eosinophilic change -HURTHLE CELL METAPLASIA

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34
Q

HURTHLE CELL

A

Eosinophilic change red glands

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35
Q

Hashimoto vs graves histo

A

Hashimoto-follicles shrunken and red meaning they have given up

Graves-hyperactive

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36
Q

Antibodies graves and hashimoto

A

TSI in both, but more graves

Thyroglobulin and thyroperoxidase was up hasimoto

Graves TSH antiglobulins up a lot but can have up with others away

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37
Q

Granulomatous thyroiditis

A

De quervain

Painful granulomata

Histiocytosis, inflammation, painful

Viral origin

Wanes in a few months though for normal granulomatous thyroiditis

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38
Q

Riddle thyroiditis

A

Fibrosing process extends from the thyroid into adjacent tissue

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39
Q

Fibrosis of Riehle

A

Start in thyroid and get hypothyroid but doesn’t stop extends to adjacent tissue

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40
Q

Surgeon with riedel

A

Cement

Anaplastic carcinoma or reidel-are what surgeon will think when feel how hard

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41
Q

Histology riedel

A

Fibrosis!!! And inflammatory infiltrate see lymphocytes and plasma cells

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42
Q

IgG4

A

Riedel they’re all related…fibrosis with plasma cells is riedel

Sclerosing process effects multiple systems

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43
Q

What is happening with IgG4

A

Differentiation of fibroblast, plasma fell and IgG4 whihc will give you the bad things

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44
Q

IgG4 related diseases

A

Autoimmune pancreatitis

Multifocal fibrosclerosis-sclerosing mediastinitis

Idiopathic retroperitoneal fibrosis

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45
Q

Hasimoto cause, histology, thyroid state, TPO

A

Autoimmune

Lymphocytes

Hypothyroidism

High titer

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46
Q

Subacute lymphocytic cause, histology, thyroid states, TPO

A

Autoimmune, lymphocytes, hypo or hyperthyroidism, high titer

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47
Q

Granulomatous cause histology, thyroid state, TPO

A

Unknown, granulomata, hypo or hyperthyroid

Low titer or absent

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48
Q

Riedel cause histology, thyroid , TPO

A

Unknown, fibrosis, euthyroid, variable

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49
Q

Goiter

A

Large thyroid can be diffuse or nodular, non toxic or toxic, benign or malignant

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50
Q

Diffuse nontoxic goiter

A

Not nodular

Endemic goiter->iodine defiency most commonly

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51
Q

Goitrogens of diffuse nontoxic goiter

A

Cassava root, brasssicaceae(broccoli, cauliflower, cabbage, radish

If good better!! Raw bad

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52
Q

Sporadic goiter

A

More commmon in females not sure why

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53
Q

Euthyroid diffuse goiter

A

Function normal a lot…so come to attention from mass effect

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54
Q

Mass effect diffuse nontoxic goiter

A

Dysphagia, hoarseness, stridor, SVC syndrome

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55
Q

Raise arm goiter

A

Venous occlusion, face problem

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56
Q

Multinodular goiter why get

A

Hyperplasia, regression cycle

Varied response of nodules to stimuli

Neoplastic nature of some nodules(adenomas-neoplastic)

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57
Q

Mass effect multinodular

A

Can be huge!!!! Neck doesn’t give much room for growth…so tuck behind sternum and into chest cavity

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58
Q

Substernal goiter

A

So large go behind the sternum

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59
Q

Benign substernal goiter

A

Yup

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60
Q

Radioisotope scanning

A

If nodule is hyperfunctional

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61
Q

If hyperfunctional nodule with hyperthyroid HOT

A

Can be treated with excision or ablation

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62
Q

Cold nodule

A

Don’t know what dealing with….more likely to be neoplastic/malignant though

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63
Q

Hot nodule

A

Benign more likely

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64
Q

Most thyroid nodules benign of not for hot and cold

A

Benign

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65
Q

What if cold

A

FNA-molecular testing can be used for diagnostic purposes

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66
Q

Presence of thyroid low TSH hot or cold

A

Take out

Cold-back to patients not hyperthyroid and do FNA find out what patient has

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67
Q

FNA

A

Tell how suspicious for malignancy

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68
Q

Thyroid nodules benign

A

Hyperplastic nodules and follicular adenomas

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69
Q

Malignant nodule

A

Papillary thyroid carcinoma, follicular hurtle cell carcinoma, anaplastic carcinoma, medullary carcinoma

70
Q

Hyperplastic nodules

A

Respond to things

71
Q

Follicular adenoma

A

Discrete colonial population of follicular cells”thyroid autonomy”

Soft and circumscribed in center have thyroid follicles with white Rhine around which is fibrous capsule(BENIGN no invade in its capsul)

Not invading and no nuclear features of papillary thyroid carcinoma

72
Q

Follicular

A

Benign neoplastic

73
Q

Papillary thyroid carcinoma

A

Majority of malignant tumors of the thyroid (85%)
Most occur between 25-50 years of age
-staging info

Typically present without symptoms
-palpable nodule, US

74
Q

Papillary and follicular stage

A

Under 55 stage I and II no matter what (II is if metastatic at distant site)

Over 55 can be I-IV, similar to tumors from other sites

Only tumor take age into consideration

75
Q

Stage II 55 or younger

A

Stage IVb in older 55

76
Q

Papillary histo

A

Papillary architecture, psammoma bodies, RET-PTC mutations, BRAF

-papillary buds of tumor forming and get papillary formations pinched off processes of tumor growing, psomma calcifications around concentric calcification

77
Q

What defines papillary thyroid carcinoma

A

Nuclear orphan Annie eye nuclei. Enlarged nuclei with clear apperance

Nuclear characteristics are the diagnostic features allowing for a diagnosis of PTC

Orphan Annie eye

78
Q

Does pappilary have to be papillary

A

Nope, but all will have nuclei with clear apperance and intranuclear inclusions
Orphan Annie eye nuclei

Nuclear characteristics are the diagnostic feature allowing for a diagnosis of PTC

79
Q

Follicular variant PTC

A

Follicular architecture, but nuclear features

80
Q

Genetics follicular variant of PTC

A

RAS (similar to follicular carcinoma and adenoma)

Not ret-ptc rearrangements or BRAF

81
Q

Tall cell variant of papillary carcinoma

A

Tall cells, same nuclei

Older patients and aggressive

82
Q

Difffuse sclerosing variant

A

Kids and young adults

Distant metastasis to lung, brain, bone and liver on presentation

But despite that, most have disease specific survival at 10 years

Very treatable !!! Why staging matters in terms of age

83
Q

Follicular carcinoma

A

Less common than papillary

Most common in areas with goiter from iodide defiency

84
Q

Genetics follicular adenoma

A

RAS-not specific

PAX8/PPARG mutations more characteristic

85
Q

Histology follicular

A

Normal nuclei

INVADED vessels or capsules

86
Q

Qualify follicular carcinoma

A

Invasion of capsule (mushroom)

Angioinvasion

Still a differentiated thyroid carcinoma

87
Q

Angioinvasion from follicular carcinoma

A

Hematogenous metastasis

LUNGS LIVER therapy

88
Q

Therapy

A

Surgery

radioactive iodine…..drink and find thyroid carcinoma and ablate it

If refractory-chemo, tyrosine kinase inhibitors (still in progress)

89
Q

Anaplastic carcinoma

A

Uncommon 5%tend to occur in elderly

HIGHLY aggressive
-present with mass effect and die in a year of local invasion

90
Q

Histology anaplastic carcinoma

A

Mass has obliterated beyond thyroid cant see thyroid gland anymore

Ugly multinucleated cells, can have high grade and papillary carcinoma they can be heterogenous in nature.

If elderly and aggressive think of this disease process first

91
Q

Genetics anaplastic carcinoam

92
Q

Follicular neoplasm non specific genetic

A

RAS PTEN

Don’t care

93
Q

Follicular carcinoma genetics

A

PAX8-PPARG

94
Q

Papillary carcinom

A

RET/PTC rearrangements->constitutive tyrosine kinase activity

BRAF gain of function mutation->MAP kinase signaling

95
Q

C cells parafollicular secrete what

A

Calcitonin

96
Q

Calcitonin stain

A

Can see calcitonin C cells

97
Q

Tumor from C cell

A

Medullary carcinoma

98
Q

Medullary carcinoma

A

Neuroendocrine carcinoma from c cell

-small round blue cell tumours, amyloid, c cell hyperplasia

99
Q

Amyloid

A

Amyloid deposition in medullary carcinoma. Pink staining on apple green birefringence on right Congo red stain

100
Q

Congo red stain positive

A

Amyloid apple green medullary

101
Q

Sporadic medullary

A

Middle age or older

Univocal

Aggressive (hard to treat)

102
Q

Familial medullary thyroid carcinoma

A

BEST prognosis of all forms 100% 15 year survival

Younger age 40s

103
Q

10 year survival medullary carcinom

A

Depend on staging

Depend on metastasis

104
Q

Ret protooncogene

A

Chromosome 10

Mutated int germline in medullary and sporadic medullary thyroid carcinoma

Lot of mutations can be responsible for MEN2A, MEN2B and familial from germline

Majority sporadic RET protooncogene oncogene

105
Q

Parathyroid anterior or posterior thyroid

106
Q

Cell types of parathyroid

A

Chief cells-white cytoplasm secrete PTH

Oxyphil cells-secretory in nature

Adipocytes-normal constituent of parathyroid tissue

107
Q

Lose fat parathyroid

A

Sad parathyroid

108
Q

Chief cells

A

Central round, uniform nuclei

Light pink or white cytoplasm

Secretory granules

109
Q

Oxyphil cells

A

Smaller, darker nuclei

Less active

110
Q

PTH

A

Resorption of calcium from bone

Kidney convert to active VD
Secrete phosphate (stop binding Ca so more functional ca there is )

Intestine increase ca absorption

111
Q

Primary

A

Organ that is names

112
Q

Cushing disease

A

Of the pituitary it is a primary pituitary

113
Q

Primary hyperparathyroidism

A

Adenoma most, primary hyperplasia, parathyroid carcinoma

114
Q

Adenoma

115
Q

Hyperplasia

116
Q

Carcinoma

A

Deviate esophagus and invade

117
Q

Primary hyperparathyroidism have elevated ___

A

PTH and Ca

118
Q

What do with hyperparathyroidism with high Ca and PTH

A

Technetium scan to see where hypersecretion is coming from.

Single-adenoma increased uptake or carcinoma

119
Q

Parathyroid adenoma

A

Benign neoplasm of the parathyroid chief or oxyphil cells

Solitary

Can be surrounded by a run of normal parathyroid tissue

120
Q

Why other parathyroid glands shrunken in adenoma

A

Down regulate

121
Q

Histology parathyroid adenoma

A

No fat … with normal rim(fat)

122
Q

MEN1

A

Tumor suppressor gene

Germline mutations are responsible for familial MEN1 and can manifest with parathyroid adenomas

But more common are sporadic parathyroid adenomas, with somatic MEN1 mutations (seen in 20-30% of sporadic)

Still associated if not germline, can get somatic mutations

123
Q

Parathyroid hyperplasia

A

Can cause primary hyperparathyroidism (not reactive state)

Get in multiple glands

MEN syndromes MEN1

Secondary hyperplasia much more common..

No normal rim of parathyroid tissue

124
Q

Histology parathyroid hyperplasia

A

No rim of normal and all are big

SEE NO FAT IN AN IMAGE

125
Q

Hyperplasia vs adenoma how tell

A

Sometimes simple

But others not
Often occur together

126
Q

Treatment hyperparathyroidism from primary EITHER

A

Surgically excise

127
Q

How know if got the parathyroid that hyperfunctions

A

In real time measure parathyroid hormone level that drops in minutes. 15 min after get out PTH should be lowered due to short half life. Common technique

128
Q

Parathyroid carcinoma hyperparathyroidism

A

Malignant if metastasis.

See invasion of adjacent tissues, vascular invasion

Elevated PTH no down after surgery

129
Q

Elevated PTH that doesn’t go down after surgery

A

Parathyroid carcinoma

130
Q

Symptoms primary hyperparathyroidism

A

Painful bones, stones, abdominal groans, psychic moans

131
Q

Painful bones

A

Osteoporosis/osteitis fibrosis cystica

132
Q

Renal stones

A

Nephrolithiasis

133
Q

Abdominal groans

A

Constipation gall stones

134
Q

Psychic moans

A

Lethargy seizure

135
Q

Heart

A

Calcification of valve from hypercalcemis

136
Q

Weak and fatigue

137
Q

Do we see symptoms like this

A

No…most cases occur slowly and more commmon to seen as having high. Incidentally then manifest symptoms

We monitor this

138
Q

Osteitis fibrosis cystica (Von recklinghausen disease of bone)

A

Brown tumor

Osteoclast driven bone destruction

Small fractures

Hemorrhage and receive tissues

Can look like metastatic disease

139
Q

Why not see osteitis fibrosis cystica

A

Rare for initial presentation, most hyperparathyroidism states are identified in the asymptomatic phase

140
Q

Symptoms primary hyperparathyroidism

A

Asymptomatic hypercalcemia

141
Q

Symptomatic hypercalcemia

A

Malignancy

142
Q

Hypercalcemia what look at

A

PTH, and Ca

143
Q

Secondary hyperparathyroidism

A

No difference in way parathyroid looks from primary, but pathology is different it is a response!! Not a cause

144
Q

What causes secondary parathyroidism

A

Decreased ca feedback and produce hyperplasia

Renal disease!!-hypocalcemia from renal failure and get adaptive incrase in parathyroid volume across all four glands

145
Q

Tertiary hyperparathyroidism

A

Prolonged hypocalcemia, parathyroid glands so accumstomed to overfuncting keep cranking out this stuff

146
Q

Secondary and tertiary

A

Four enlarged hyperplastic parathyroid glands

147
Q

Renal osteodystrophy

A

Secondary hyperparathyroidism

Can lead to rugger jersey sign
-give you a dissecting osteitis, see a limited osteoporotic defect in vertebral body

148
Q

Calciphylaxis

A

Secondary hyperparathyroidism

Can lead to extensive calcification and occlusion of blood vessels with resultant ischemia

Get ca in wall of vessels so get vascular occlusion and calcification of vessel walls. Ischemic result show up as GANGRENE!!!!!!!!

149
Q

What are patients with calciphylaxis dying from

A

Sepsis from gangrenous areas high risk for infection and sepsis

150
Q

Secondary hyperparathyroidism

A

Fast and soft tissue effected mainly

151
Q

Hypercalcemia of malignancy

A

Humoral hypercalcemia of malignancy

  • PTHrP
  • analagous
  • squamous cell carcinoma

VD related
-lymphomas

Local osteopathic hypercalcemia

  • release of ca-osteoclast bone resorption
  • breast carcinoma
  • myeloma
152
Q

PTHrP

A

Squamous carcinoma get PTHrP

153
Q

VD related hypercalcemis

A

Vd from lymphoma. Increased 1,25 OH2 D3

154
Q

Local osteopathic

A

Common in primary bone disease and cancer

Feast cancaer and multiple myeloma

155
Q

Present hyperca how work up

A

Measure PTH

156
Q

High PTH

A

Evaluate for primary hyperparthyroid state

157
Q

PTH low

A

PTHrP check

158
Q

Increase ca and not pth

A

Humoral hypercalcemia of malignancy

159
Q

Low ca and high PTH

A

Secondary hyperparathyroidism like renal failure

160
Q

Low ca low pth

A

Hypoparathyroidism

161
Q

Hypoparathyroidism

A

Iatrogenic, autoimmune , congenital

162
Q

Congenital hypoparathyroidism

163
Q

Digeorge

A

Developmental defects in 3rd to 4th pharyngeal pouches

-parathyroid glands may be absent or underdeveloped

164
Q

CASR germline mutation

A

Familial hypocalcemia hypercalciuria

-hyperactive calcium sensing receptors

165
Q

Familial isolated hypoparathyroidism

A

Precursor PTH cant get all the way to functional PTH

166
Q

CASR hypersensitive

A

Stop making PTH get hypoparathyroidism

CASR also in kidney think too much CA so it dumps ca

So hypocalcemia hypercalciuria if CASR really sensitive

167
Q

CASR not working

A

Not sensing so retain calcium in urine and push out PHT

Hypercalcemis hypocalciuria

168
Q

Hypoparathyroidism symptoms

A

Muscle cramp spasm

Trousseau EARLIEST SIGN (inflating bp cuff that occlude brachial artery and get flexion of wrist and straightening of phlangeal joints)

and chovstek(facial nerve twitch)

169
Q

Pseudohypoparathyroidism

A

Normal or elevated PTH->hypocalcemia and hyperphosphatemia

170
Q

Why get pseudohypoparathyroidism

A

Resistance to PTH

G protein receptor GNAS

Can affect other hormone pathways TSH LH/FSH

171
Q

So pseudohypoparathyroidism

A

Not effecting bone and renal tubules

Hypocalcemia despite high PTH

172
Q

Radial fracture 45 year old man onset of pain in left forearm after gripping a rail yesterday

A

Ostoporosis, mottling of bone

PTH over 3,000 (normal 10-65)

Serum ca 13 mg (normal 8-10)

Surgery-parathyroid mass
Pathology” parathyroid carcinoma

Pathology (36 decks)

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