Thyroid Parathyroid Pituitary Flashcards
(172 cards)
1
Q
Thyroid
A
Ok
2
Q
What thyroid hormones do
A
Increase BMR
Protein catabolism glucose utilization, growth maturation
3
Q
TSH
A
Ligand for thyroid receptor, bind active and thyroid hormones elaborated
4
Q
Colloid
A
TSH bind receptor on follicle and stimulate all step
- 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
5
Q
Primary of secondary hyperthyroidism( more common
A
Primary
6
Q
Primary hyperthyroidism
A
Diffuse hyperplasia 9graves)
Hyperfunctioing multinodular goiter
Hyperfunctioning thyroid adenoma (neoplastic
7
Q
Secondary hyperthyroidism
A
Pituitary adenoma
8
Q
How determine if primary of secondary
A
Check thyroid hormone in conjunction to TSH
9
Q
Elevated T3 T4 high and low TSH
A
High secondary
Low primary
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
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)
12
Q
Hyperthyroid general
A
Cardiac and GI
13
Q
What constitutes acute thyroid storm
A
High fever that remains elevated
Precipitating history -preg and postpartum, hemithyroidectomy, drugs
HISTORY AND FEVER**
14
Q
Pregnant
A
Thyroid storm can put you at risk
15
Q
Hemithyroidectomy
A
If hyperthyroid and take out a lobe, sometimes the remaining lobe starts hyperfunctioning to thyroid storm level
16
Q
Amiodarone
A
Can cause thyroid storm
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
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
19
Q
Grave histo
A
Row of white vacuoles-absorption droplets bubbles around edge. Of follicles and follicles are enlarged
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
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
22
Q
Pretibial myxedema
A
Hard ANS scaly rash anterior lower extremities
Matrix production probably
23
Q
Need all three for graves
A
No
24
Q
How test for graves
A
Original pathogenesis
Primary hyperthyroidism elevated thyroid hormones and elevated tsh and test for thyroid stimulating antibodies
25
TSI antibody test
Sensitive and specific for graves
26
Hypothyroidism kid cretinism
Mental retardation, growth retardation, coarse facial features, umbilical hernias
27
Why cretinism
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
28
Hypothyroidism present in adult
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
29
Thyroidisit
Hashimoto
Granulomatous
30
Hashimoto
Autoimmune most common hypothyroidism ind enveloped world
31
Why get hashimoto
Autoantibodies against thyroglobulin and thyroid peroxidase
32
Signs hashimoto
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)
33
Hashimoto exhaust histo
Lymphocytic infiltrate looks like lymph node in thyroid
Germinal centers with lymphocytic infiltrate
Atrophic follicle cells with eosinophilic change -HURTHLE CELL METAPLASIA
34
HURTHLE CELL
Eosinophilic change red glands
35
Hashimoto vs graves histo
Hashimoto-follicles shrunken and red meaning they have given up
Graves-hyperactive
36
Antibodies graves and hashimoto
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
37
Granulomatous thyroiditis
De quervain
Painful granulomata
Histiocytosis, inflammation, painful
Viral origin
Wanes in a few months though for normal granulomatous thyroiditis
38
Riddle thyroiditis
Fibrosing process extends from the thyroid into adjacent tissue
39
Fibrosis of Riehle
Start in thyroid and get hypothyroid but doesn’t stop extends to adjacent tissue
40
Surgeon with riedel
Cement
Anaplastic carcinoma or reidel-are what surgeon will think when feel how hard
41
Histology riedel
Fibrosis!!! And inflammatory infiltrate see lymphocytes and plasma cells
42
IgG4
Riedel they’re all related...fibrosis with plasma cells is riedel
Sclerosing process effects multiple systems
43
What is happening with IgG4
Differentiation of fibroblast, plasma fell and IgG4 whihc will give you the bad things
44
IgG4 related diseases
Autoimmune pancreatitis
Multifocal fibrosclerosis-sclerosing mediastinitis
Idiopathic retroperitoneal fibrosis
45
Hasimoto cause, histology, thyroid state, TPO
Autoimmune
Lymphocytes
Hypothyroidism
High titer
46
Subacute lymphocytic cause, histology, thyroid states, TPO
Autoimmune, lymphocytes, hypo or hyperthyroidism, high titer
47
Granulomatous cause histology, thyroid state, TPO
Unknown, granulomata, hypo or hyperthyroid
Low titer or absent
48
Riedel cause histology, thyroid , TPO
Unknown, fibrosis, euthyroid, variable
49
Goiter
Large thyroid can be diffuse or nodular, non toxic or toxic, benign or malignant
50
Diffuse nontoxic goiter
Not nodular
Endemic goiter->iodine defiency most commonly
51
Goitrogens of diffuse nontoxic goiter
Cassava root, brasssicaceae(broccoli, cauliflower, cabbage, radish
If good better!! Raw bad
52
Sporadic goiter
More commmon in females not sure why
53
Euthyroid diffuse goiter
Function normal a lot...so come to attention from mass effect
54
Mass effect diffuse nontoxic goiter
Dysphagia, hoarseness, stridor, SVC syndrome
55
Raise arm goiter
Venous occlusion, face problem
56
Multinodular goiter why get
Hyperplasia, regression cycle
Varied response of nodules to stimuli
Neoplastic nature of some nodules(adenomas-neoplastic)
57
Mass effect multinodular
Can be huge!!!! Neck doesn’t give much room for growth...so tuck behind sternum and into chest cavity
58
Substernal goiter
So large go behind the sternum
59
Benign substernal goiter
Yup
60
Radioisotope scanning
If nodule is hyperfunctional
61
If hyperfunctional nodule with hyperthyroid HOT
Can be treated with excision or ablation
62
Cold nodule
Don’t know what dealing with....more likely to be neoplastic/malignant though
63
Hot nodule
Benign more likely
64
Most thyroid nodules benign of not for hot and cold
Benign
65
What if cold
FNA-molecular testing can be used for diagnostic purposes
66
Presence of thyroid low TSH hot or cold
Take out
Cold-back to patients not hyperthyroid and do FNA find out what patient has
67
FNA
Tell how suspicious for malignancy
68
Thyroid nodules benign
Hyperplastic nodules and follicular adenomas
69
Malignant nodule
Papillary thyroid carcinoma, follicular hurtle cell carcinoma, anaplastic carcinoma, medullary carcinoma
70
Hyperplastic nodules
Respond to things
71
Follicular adenoma
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
Follicular
Benign neoplastic
73
Papillary thyroid carcinoma
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
Papillary and follicular stage
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
Stage II 55 or younger
Stage IVb in older 55
76
Papillary histo
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
What defines papillary thyroid carcinoma
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
Does pappilary have to be papillary
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
Follicular variant PTC
Follicular architecture, but nuclear features
80
Genetics follicular variant of PTC
RAS (similar to follicular carcinoma and adenoma)
Not ret-ptc rearrangements or BRAF
81
Tall cell variant of papillary carcinoma
Tall cells, same nuclei
Older patients and aggressive
82
Difffuse sclerosing variant
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
Follicular carcinoma
Less common than papillary
Most common in areas with goiter from iodide defiency
84
Genetics follicular adenoma
RAS-not specific
PAX8/PPARG mutations more characteristic
85
Histology follicular
Normal nuclei
INVADED vessels or capsules
86
Qualify follicular carcinoma
Invasion of capsule (mushroom)
Angioinvasion
Still a differentiated thyroid carcinoma
87
Angioinvasion from follicular carcinoma
Hematogenous metastasis
LUNGS LIVER therapy
88
Therapy
Surgery
radioactive iodine.....drink and find thyroid carcinoma and ablate it
If refractory-chemo, tyrosine kinase inhibitors (still in progress)
89
Anaplastic carcinoma
Uncommon 5%tend to occur in elderly
HIGHLY aggressive
-present with mass effect and die in a year of local invasion
90
Histology anaplastic carcinoma
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
Genetics anaplastic carcinoam
TP53
92
Follicular neoplasm non specific genetic
RAS PTEN
Don’t care
93
Follicular carcinoma genetics
PAX8-PPARG
94
Papillary carcinom
RET/PTC rearrangements->constitutive tyrosine kinase activity
BRAF gain of function mutation->MAP kinase signaling
95
C cells parafollicular secrete what
Calcitonin
96
Calcitonin stain
Can see calcitonin C cells
97
Tumor from C cell
Medullary carcinoma
98
Medullary carcinoma
Neuroendocrine carcinoma from c cell
| -small round blue cell tumours, amyloid, c cell hyperplasia
99
Amyloid
Amyloid deposition in medullary carcinoma. Pink staining on apple green birefringence on right Congo red stain
100
Congo red stain positive
Amyloid apple green medullary
101
Sporadic medullary
Middle age or older
Univocal
Aggressive (hard to treat)
102
Familial medullary thyroid carcinoma
BEST prognosis of all forms 100% 15 year survival
Younger age 40s
103
10 year survival medullary carcinom
Depend on staging
Depend on metastasis
104
Ret protooncogene
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
Parathyroid anterior or posterior thyroid
Posterior
106
Cell types of parathyroid
Chief cells-white cytoplasm secrete PTH
Oxyphil cells-secretory in nature
Adipocytes-normal constituent of parathyroid tissue
107
Lose fat parathyroid
Sad parathyroid
108
Chief cells
Central round, uniform nuclei
Light pink or white cytoplasm
Secretory granules
109
Oxyphil cells
Smaller, darker nuclei
Less active
110
PTH
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
Primary
Organ that is names
112
Cushing disease
Of the pituitary it is a primary pituitary
113
Primary hyperparathyroidism
Adenoma most, primary hyperplasia, parathyroid carcinoma
114
Adenoma
One gland
115
Hyperplasia
Multiple
116
Carcinoma
Deviate esophagus and invade
117
Primary hyperparathyroidism have elevated ___
PTH and Ca
118
What do with hyperparathyroidism with high Ca and PTH
Technetium scan to see where hypersecretion is coming from.
Single-adenoma increased uptake or carcinoma
119
Parathyroid adenoma
Benign neoplasm of the parathyroid chief or oxyphil cells
Solitary
Can be surrounded by a run of normal parathyroid tissue
120
Why other parathyroid glands shrunken in adenoma
Down regulate
121
Histology parathyroid adenoma
No fat ... with normal rim(fat)
122
MEN1
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
Parathyroid hyperplasia
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
Histology parathyroid hyperplasia
No rim of normal and all are big
SEE NO FAT IN AN IMAGE
125
Hyperplasia vs adenoma how tell
Sometimes simple
But others not
Often occur together
126
Treatment hyperparathyroidism from primary EITHER
Surgically excise
127
How know if got the parathyroid that hyperfunctions
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
Parathyroid carcinoma hyperparathyroidism
Malignant if metastasis.
See invasion of adjacent tissues, vascular invasion
Elevated PTH no down after surgery
129
Elevated PTH that doesn’t go down after surgery
Parathyroid carcinoma
130
Symptoms primary hyperparathyroidism
Painful bones, stones, abdominal groans, psychic moans
131
Painful bones
Osteoporosis/osteitis fibrosis cystica
132
Renal stones
Nephrolithiasis
133
Abdominal groans
Constipation gall stones
134
Psychic moans
Lethargy seizure
135
Heart
Calcification of valve from hypercalcemis
136
Weak and fatigue
Hyperca
137
Do we see symptoms like this
No...most cases occur slowly and more commmon to seen as having high. Incidentally then manifest symptoms
We monitor this
138
Osteitis fibrosis cystica (Von recklinghausen disease of bone)
Brown tumor
Osteoclast driven bone destruction
Small fractures
Hemorrhage and receive tissues
Can look like metastatic disease
139
Why not see osteitis fibrosis cystica
Rare for initial presentation, most hyperparathyroidism states are identified in the asymptomatic phase
140
Symptoms primary hyperparathyroidism
Asymptomatic hypercalcemia
141
Symptomatic hypercalcemia
Malignancy
142
Hypercalcemia what look at
PTH, and Ca
143
Secondary hyperparathyroidism
No difference in way parathyroid looks from primary, but pathology is different it is a response!! Not a cause
144
What causes secondary parathyroidism
Decreased ca feedback and produce hyperplasia
Renal disease!!-hypocalcemia from renal failure and get adaptive incrase in parathyroid volume across all four glands
145
Tertiary hyperparathyroidism
Prolonged hypocalcemia, parathyroid glands so accumstomed to overfuncting keep cranking out this stuff
146
Secondary and tertiary
Four enlarged hyperplastic parathyroid glands
147
Renal osteodystrophy
Secondary hyperparathyroidism
Can lead to rugger jersey sign
-give you a dissecting osteitis, see a limited osteoporotic defect in vertebral body
148
Calciphylaxis
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
What are patients with calciphylaxis dying from
Sepsis from gangrenous areas high risk for infection and sepsis
150
Secondary hyperparathyroidism
Fast and soft tissue effected mainly
151
Hypercalcemia of malignancy
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
PTHrP
Squamous carcinoma get PTHrP
153
VD related hypercalcemis
Vd from lymphoma. Increased 1,25 OH2 D3
154
Local osteopathic
Common in primary bone disease and cancer
Feast cancaer and multiple myeloma
155
Present hyperca how work up
Measure PTH
156
High PTH
Evaluate for primary hyperparthyroid state
157
PTH low
PTHrP check
158
Increase ca and not pth
Humoral hypercalcemia of malignancy
159
Low ca and high PTH
Secondary hyperparathyroidism like renal failure
160
Low ca low pth
Hypoparathyroidism
161
Hypoparathyroidism
Iatrogenic, autoimmune , congenital
162
Congenital hypoparathyroidism
Di George
163
Digeorge
Developmental defects in 3rd to 4th pharyngeal pouches
| -parathyroid glands may be absent or underdeveloped
164
CASR germline mutation
Familial hypocalcemia hypercalciuria
| -hyperactive calcium sensing receptors
165
Familial isolated hypoparathyroidism
Precursor PTH cant get all the way to functional PTH
166
CASR hypersensitive
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
CASR not working
Not sensing so retain calcium in urine and push out PHT
Hypercalcemis hypocalciuria
168
Hypoparathyroidism symptoms
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
Pseudohypoparathyroidism
Normal or elevated PTH->hypocalcemia and hyperphosphatemia
170
Why get pseudohypoparathyroidism
Resistance to PTH
G protein receptor GNAS
Can affect other hormone pathways TSH LH/FSH
171
So pseudohypoparathyroidism
Not effecting bone and renal tubules
Hypocalcemia despite high PTH
172
Radial fracture 45 year old man onset of pain in left forearm after gripping a rail yesterday
Ostoporosis, mottling of bone
PTH over 3,000 (normal 10-65)
Serum ca 13 mg (normal 8-10)
Surgery-parathyroid mass
Pathology” parathyroid carcinoma
