Thyroid-denning Flashcards
(132 cards)
1
Q
Thyroid
Development
A
Eva GI nation of the developing pharyngeal mucosa
Bilobed organ with isthmus
Found in neck, inf to thyroid cartilage, same level as cricoid cartilage
2
Q
Normal thyroid
Micro
Colloid
A
Reservoir of materials for thyroid hormone production
Lesser extent, reservoir of hormones themselves
Rich in thyroglobulin
3
Q
Normal thyroid
Micro
Follicular epithelial cells
A
Convert thyroglobulin into T4 and T3
4
Q
Thyroglobulin is converted to T4 and T3 by
A
Follicular epithelial cells
5
Q
T4 and T3
Effect on metabolism
A
Inc BMR
6
Q
Normal thyroid
Micro
Parafollicular cells (C cells)
Secrete
A
Calcitonin
7
Q
Normal thyroid
Micro
Calcitonin effect
A
Causes absorption of Ca by the skeletal system
Inhibits resorption of bone by osteoclasts
8
Q
Hyperthyroidism
Define
A
Inc in free T4 and/or Free T3
Hyperfunction of thyroid (graves disease)
9
Q
Thyrotoxicosis
A
Excessive leakage of thyroid hormone
Thyroiditises
10
Q
Hyperthyroidism results in
A
Hypermetabolic state
11
Q
Hyperthyroidism
Causes (MC)
A
Graves’ disease
Ingestion of xs thyroid hormone (for Rx of hypothyroidism)
Hyperfunction multinodular goiter
Hyperfunction adenoma of the thyroid
Certain thyroiditises
12
Q
Hyperthyroidism
Less common causes
A
TSH producing pituitary adenoma
Stroma Ovarii (thyroid tissue in the ovary)
13
Q
Hyperthyroidism
S&Sx
A
Due to inc thyroid hormones
Inc BMR
GI: hypermotility, malabsorption, diarrhea
Sympathetic sx
14
Q
Hyperthyroidism
Sympathetic sx
A
Due to overactive sympathetic nervous system
Nervousness, tremor, tachycardia, palpatations, hyperreflexia and irritability
Possible CHF
Wide gazing stare and lid lag (levator palpebrae superioris)
Heat intolerance
15
Q
Hyperthyroidism
Thyroid storm
A
Medical emergency
Abrupt onset of severe and life threatening thyrotoxicosis with exaggeration of usual symptoms of hyperthyroidism
16
Q
Thyroid storm
Clinical presentation
A
CV-marked tachycardia (140bpm)
Thermoregulatory dysfunction-(104-106)
GI-N/v, diarrhea
17
Q
Thyroid storm
Common cause
A
Graves’ disease
Can also be seen following surgery on thyroid (release of xs hormone)
May cause death
18
Q
Hyperthyroidism
Screen
A
Measure fT4 and TSH
19
Q
Hyperthyroidism
Findings on screen
A
Inc fT4
Dec TSH (primary—thyroid)
Sometimes due to T3 (then measure T3)
20
Q
Hyperthyroidism
Rx
A
Beta blockers for adrenergic tone
Thionamides to BLOCK new hormone synthesis
Agents to PREVENT CONVERSION of T4 to T3
Radioiodine to ABLATE thyroid function
21
Q
Hypothyroidism
Most cases are
A
Primary (thyroid)
Surgery
Hashimoto’s thyroiditis
Primary idiopathic
22
Q
Hypothyroidism
Myxedema
A
Applied to older child or adult
Generalized apathy and mental sluggishness (mimics depression)
23
Q
Hypothyroidism
Myxedema
Sx
A
Listlessness; COLD INTOLERANT
Mucopolysaccharide-rich edema (skin and subcutaneous tissue)
Constipation
Pericardial effusions; obesity
24
Q
Hypothyroidism
Labs
A
TSH is most sensitive
Inc in primary (thyroid)
Dec in secondary (pituitary)
T4 dec in both
25
Graves' disease
Pt
20-40
Females
60% concordance
26
MC cause of endogenous hyperthyroidism
Graves' disease
27
Graves' disease
Genetics
HLA-DR3 and -B8
28
Graves' disease
S&Sx
Triad:
Thyrotoxicosis (100%) (hyperthyroidism)
Exopthalmus (40%)
PRETIBIAL myxedema (LOCALIZED, infiltration dermopathy)
Thyroid enlargement (diffuse), bruit over thyroid
29
Exopthalmus
Marked infiltration of the retro-orbital space by mononuclear cells
Inflammatory edema and swelling of extraocular mm
Accumulation of ECM components
Inc number of adipocytes
30
Graves' disease
Pathogenesis
Breakdown in self tolerance to thyroid auto ags, most important is the TSH receptor
31
Graves' disease
Autoantibodies
TSI (Binds TSH receptor) stimulates TH production
TGI (binds TSH receptor) stimulates growth
TBII--TSH binding inhibitor immunoglobulin
-prevents binding of TSH:: may stimulate or inhibit
32
Graves' disease
Morphology
Thyroid
Diffuse hypertrophy and hyperplasia
Follicular cellls: tall, columnar, and crowded
May have papillae WITHOUT FIBROVASCULAR CORE (papillary cancer has fibrovascular cores)
Colloid: shows scalloping
33
Graves' disease
Organ manifestations
Heart: hypertrophied and ischemia
Opthalmopathy: mucopolysaccharides and lymphocytes (autoimmune not direct effect)
Dermopathy: pretibial myxedma: mucopolysaccharides and lymphocytes, orange-peel texture
34
Graves' disease
Labs
Radioiodine scan: diffuse uptake
Inc fT4 and T3
Dec TSH
35
Graves' disease
Rx
Beta blockers
Thionamides (propylthiouracil)
Radioiodine ablation
Surgery
36
Goiter
Simple enlargement of the thyroid
37
MC thyroid disease
Gaiters
38
Goiters
Due to
Impaired synthesis of TH
Iodine deficiency
39
Goiters
Endemic
MC in mountainous areas
Endemic=10% of population
40
Goiters
Sporadic
Many causes
Environmental and genetic
41
Goiters
S&Sx
Enlargement may cause
Cosmetic problems
Or
Airway obstruction, dysphasia, compression of large vessels in the neck and thorax (mass effect)
42
Goiters
S&Sx
Related syndrome
Plummer's syndrome
43
Goiters
Plummer's syndrome
Hyperfunctioning nodule forms in long standing goiter, results in hyperthyroidism
No opthalmopathy or dermopathy
44
Goiters
Effects
Overall most euthyroid
Hypothyroid less common
May mask or mimic neoplasms
45
Goiters
Pathogenesis
Dec thyroid hormones cause inc TSH
Result: thyroid enlargement (eventually get autonomous groups of cells forming)
46
Goiters
Common cause
Iodine deficiency
47
Goiters
Morphology
Due to hypertrophy and hyperplasia (caused by inc TSH)
T3, T4 wnl; TSH wnl or slightly high
48
Nodular or multi nodular goiters arise from
Stimulation and involution
49
Goiters
Stimulation and involution causes
Nodular or multi nodular goiter
50
Thyroiditis (inflammation)
Types
Nonspecific lymphocytic thyroiditis
Hashimoto's thyroiditis
Subacute (granulomatous) thyroiditis :: de quervain's
51
Thyroiditis (inflammation)
Other types
Acute bacterial
Mycobacterium tuberculosis or Fungi
Riedel's thyroiditis
52
Nonspecific lymphocytic thyroiditis
Common presentation
Incidental
Euthyroid
Middle aged females
Possibly autoimmune:: HLA-DR5
53
Nonspecific lymphocytic thyroiditis
Morphology
Mild symmetric enlargement
Multifocal small lymphocytes
if germinal centers are present, think hashimotots
54
Thyroiditis
With germinal centers present
Hashimotos
55
Nonspecific lymphocytic thyroiditis
Labs
Thyrotoxicosis (due to injury of thyroid follicles)
Inc T4 and T3
Dec TSH
Radioiodine scan: dec uptake
(Graves' has inc uptake)
56
Hashimoto's thyroiditis
Presentation
Autoimmune: HLA-DR5
Female 45-65
Transient hyperthyroidism:: Hashitoxicosis
57
Hashimoto's thyroiditis
With atrophy
Gene ass
HLA-DR3
58
Hashimoto's thyroiditis
S&Sx
Painless enlargement
Symmetric and diffuse
May be localized (suspicion of neoplasm)
59
Hashimoto's thyroiditis
Pathogenesis
Similar abs as graves
But anti-TSH receptor Ab blocks action of TSH
Result: hypothyroidism
Primarily a T-cell defect
60
Hashimoto's thyroiditis
Morphology
Diffuse, symmetric enlargement
Mononuclear infiltrate WITH GERMINAL CENTERS
Mall thyroid follicles
61
Hashimoto's thyroiditis
Labs
Hashitoxicosis
Inc T4 and T3; dec TSH
Radioiodine scan: dec uptake (graves-see inc uptake)
62
Hashimoto's thyroiditis
Labs
Hypothyroid (MC)
Dec T4 and T3
Inc TSH
63
Hashimoto's thyroiditis
Ass risk
Inc risk of developing B-cell lymphomas
Predisposition to papillary carcinoma
64
De Quervains thyroiditis
Common presentation
Females 30-50
Due to viral infection
65
De Quervains thyroiditis
S&Sx
PAIN in neck (esp. when swallowing)
Fever
Malaise
Variable enlargement of thyroid
Transient hyperthyroidism (6-8wks)
66
De Quervains thyroiditis
Morphology
PMN infiltrate
Scattered lymphocytes and plasma cells
Macrophages
Disrupted follicles with extruded colloid
Result::: Granulomatous Rxn
67
De Quervains thyroiditis
Labs
Inc leukocytes
Inc sedimentation rate
Inc T4 and T3 (disrupted follicles)
Dec TSH
Radioactive iodine uptake DEC
Low TSH
Self limited
68
Riedel's thyroiditis
Presentation
Rare
"Woody Hard" Fibrosis
69
Thyroid Neoplasms
Benign 10:1
Carcinomas 10%
70
Thyroid neoplasms
Clinical clues
Solitary nodules
"Hot" nodules more likely benign
Younger pts>neoplasm
Males>neoplasm
Radiation>incidence of malignancy
71
Thyroid Adenomas
Characteristics
Derived from follicular epithelium
Solitary
72
Thyroid Adenomas
S&Sx
Painless mass
Inference with swallowing
Minority hyperfunction
Most are "COLD"---up to 10% of "cold" nodules are malignant (rare in hot)
Hot=hyperfunctioning
73
Thyroid Adenomas
Pathogenesis
Somatic mutations- chronic stimulation of cAMP pathway
Result: autonomously functioning MONOCLONAL thyroid adenoma
Mutations of Gs-alpha mimic exaggerated TSH stimulation
74
Thyroid Adenomas
Mutation
Mutations of Gs-alpha mimic exaggerated TSH stimulation
75
Thyroid Adenomas
Morphology
Solitary, spherical, encapsulated
Various histologic types
Usually NO papillary changes (unlike encapsulated papillary CA)
Well defined, intact Capsule
76
Thyroid Adenomas
Dx
Careful histologic examination
Malignant transformation does not occur except in exceptional circumstances
77
Carcinoma of the Thyroid
Presentation
Female
Childhood and late adult
78
MC Carcinoma of the Thyroid
Papillary CA
79
Carcinoma of the Thyroid
Pathogenesis
Ionizing radiation
PTC Oncogene
RET (tyrosine kinase) proto-oncogene
80
Carcinoma of the Thyroid
Types
Papillary
Follicular
Medullary
Anaplastic
81
Papillary CA
MC
82
Papillary CA
S&Sx
Mass in neck
Thyroid
Or
Cervical LN--isolated involved cervical LN doesn't change prognosis
83
Papillary CA
Morphology
Solitary or multifocal
Nuclear features-ground glass or orphan Annie nuclei
Have papillae with dense fibrovascular core
Psammoma bodies
Mets by lymphatics
84
Papillary CA
Prognosis
10 yr survival 85%
85
Follicular CA
2nd MC
86
Follicular CA
Presentation
Middle age
Predisposed: iodine deficient areas, nodular goiter
87
Follicular CA
S&Sx
Solitary "cold" nodule
88
Follicular CA
Morphology
DIFFERENTIATED FROM ADENOMA
Microscopic invasion of the capsule and vasculature
Mets via vasculature
89
Follicular CA
Tx
Surger
Better differentiated: suppression by thyroid hormones (suppresses TSH)
90
Medullary CA
Characteristics
Neuroendocrine tumor
Derived from parafollicular cells (C Cells)
Secrete calcitonin
91
Medullary CA
Sporadic
80%
5th-6th decade
92
Medullary CA
Mutation
MEN IIa and IIb
Germ line mutations of RET protooncogene
Younger pts
93
Medullary CA
S&Sx
Sporadic
Mass in neck
Dysphagia or hoarseness
May secrete VIP causing Diarrhea
94
Medullary CA
MEN
Screen for calcitonin level and mutations of RET
95
Medullary CA
Morphology
Multiple common in familial type
Polygonal to spindle shaped cells--nests trabeculae, or follicles
AMYLOID deposits of calcitonin
See ass c-cell hyperplasia in familial not sporadic
96
See ass C-cell hyperplasia
Familial NOT sporadic Medullary CA
97
Medullary CA
Prognosis
Sporadic and MEN IIb: aggressive
MET via blood
Familial that are NOT MEN: less aggressive
98
Anaplastic CA
Characteristics
Most aggressive
Elderly
Areas of endemic goiter
99
Anaplastic CA
Morphology
Bulky
Grows rapidly beyond thyroid (into neck structures)
Giant cells or squamoid cells or sarcomatous cells
Small cell (distinguish from lymphoma)
100
Anaplastic CA
Prognosis
Grow with wild abandon
Met to distant sites
Death in <1yr
101
Parathyroids
Derived
From descending pharyngeal pouches
102
Parathyroids
Controlled by
Free (ionized) ca
Dec ionized ca causes inc PTH
Inc ionized ca causes dec PTH
103
PTH
Function
Activates osteoclasts: ca released from bone (resorption)
Kidney: reabsorption of ca, inc cAMP in urine, conversion of 25OH-Vit D to 1,25 diOH-VitD, inc urinary PO4
GI: get in ca absorption with 1,25diOH VitD
Net: inc ionized ca
104
Primary hyper-PTH
Causes
MC autonomous ADENOMA
Hyperplasia 2nd
Carcinoma
105
Primary hyper-PTH
Presentation
Adults: females
Sporadic or MEN
Cause bone resorption and renal disease (stones and nephrocalcinosis)--inc ionized ca
106
Primary hyper-PTH
S&Sx
MC: inc ionized ca: can be picked up in asymptomatic pt::: mets to bone MC cause of clinically significant hyper ca
Painful BONES, renal STONES, abdominal GROANS (ulcers) and psychic MOANS
107
Primary hyper-PTH
Pathogenesis
Sporadic (95%)
Inherited: MEN I
Genetic alteration: parathyroid Adenoma 1 (PRAD 1)
108
Primary hyper-PTH
Parathyroid Adenoma 1 (PRAD 1)
Encodes cyclin D1
Inversion of Chromosome 11
Overexpression of cyclin D1
109
Primary hyper-PTH
Pathogenesis
MEN I
Homozygous loss of putative suppressor gene on chromosome 11q13
110
Primary hyper-PTH
Morphology
Adenoma: circumscribed lesion with loss of fat. RIM OF COMPRESSED NORMAL PARATHYROID
Hyperplasia: see diffuse enlargement of 2 or more glands: sporadic or MEN I or IIa
111
Primary hyper-PTH
Morphology
CA
Dx by invasion or metastasis
112
Primary hyper-PTH
Morphology
Other organs
Bone--osteitis fibrosa cystica: thinned bone with hemorrhage and cyst formation
Kidney--stones (nephrolithiasis); nephrocalcinosis
113
Primary hyper-PTH
Rx
Surgery req to remove adenoma
May have to go into MEDIASTINUM
114
Secondary hyperparathyroidism
Due to
Excessive secretion of PTH caused by hypocalcemia
Results in parathyroid hyperplasia
115
Secondary hyperparathyroidism
Common pt
Pts with CHRONIC DEPRESSION of serum calcium leading to overactivity of parathyroid gland
Ass with inc po4. Directly depresses serum Ca
116
Secondary hyperparathyroidism
MC cause
Renal failure
117
Secondary hyperparathyroidism
Other causes
Inadequate diet of ca
Steatorrhea (fat binds ca)
Vit d deficiency
118
Secondary hyperparathyroidism
S&Sx
Parathyroid glands are hyperplastic
Bone abnormalities and other changes less severe than primary
Calciphalaxis
119
Secondary hyperparathyroidism
Calciphalaxis
Seen in chronic renal failure
Due to inc phosphate (PPT. Ca in blood vessels:: may cause ischemia to skin and other organs)
120
Tertiary hyperparathyroidism
Due to
Occurs when tx for secondary hyper-PTH either quits working, does not respond or pt not treated
Due to hyperplasia
See hypercalcemia
121
Tertiary hyperparathyroidism
Relation to secondary...
Secondary hyper-PTH becomes autonomous and excessive
Can no longer reverse condition
122
Tertiary hyperparathyroidism
Rx
May need parathyroidectomy
123
Hypoparathyroidism
Less common that hyper-PTH
124
Hypoparathyroidism
Causes
Surgery (MC)
Congenital absence (Di George syndrome)
Primary (idiopathic)
125
Hypoparathyroidism
Primary (idiopathic)
60% have auto-abs directed against ca-sensing receptor:: may prevent release of PTH
126
Hypoparathyroidism
Causes
Familial hypoparathyroidism
Presents in childhood with the onset of CANDIDIASIS
Then hypoparathyroidism
In adolescence adrenal insufficiency develops
127
Hypoparathyroidism
S&Sx
Tetany due to hypocalcemis
Neuromuscular irritability, tingling to spasm to laryngospasm to seizures
Chvostek sign: tap along facial nerve, induce contractions of mm of eye, mouth or nose
Trousseau sign- inflate BP cuff, induce carpal spasm, goes always when deflate the cuff
128
Pseudohypo-PTH
Hypocalcemia, inc phosphate
Generally inc PTH (can be normal)
Insensitivity to action of PTH
Get end-organ RESISTANCE to normal or elevated PTH
129
Pseudohypo-PTH
Defects
Pseudohypoparathroidism Type 1
Diminished cAMP respons to PTH due to
Deficiency of Gs-Alpha protein
Or
Abnormalities of hormone receptor complex
130
Pseudohypo-PTH
Pseudohypoparathyroidism Type 1
Clinical
Round facies, short stature, short metacarpal and metatarsal bones (Albright hereditary osteodystrophy)
131
Pseudohypo-PTH
Defects
Pseudohypoparathyroidism Type 2
Normal PTH-induced cAMP
Blunted response to second messenger
Do not have developmental defects
132
Pseudohypo-PTH
Results in
Hypocalcemia results
Causes secondary parathyroid hyperfunction: inc PTH
