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pathology of thyroid Flashcards

1
Q

describe the biochemistry of the thyroid hormones production

A

PARA-VENTRICULAR nucleus will secrete TRH—-> TSH—–>binds to GTP TK receptor.

once in the Lumen of the thyroid you have the THYROGLOBULIN and IODIDE from the diet—-> the IODIDE is oxidazed to iodine by enzyme TPO

Iodide enters into the thyroid gland by Na/I symporter and via pendrin into the colloid (gets oxidazed)

the thyroglobulin + the idodine (2 iodine to 1 TG is (di) and 1 iodine to 1 TG is (mono) will get pacekd into the vesicle and then gets lysozomal enzyme will cleave the TG and put it back into the thyroid colloid but the T3/T4 gets released into the blood

the T3/T4 are transported into the blood by tyroxine binding globulin

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2
Q

what is the cause of goitrogenesis

A

T3 and T4 are low due to low iodine intake leads to increase TSH as compensation—> the excessive TSH causes overstimulation of the thyroid gland leading to hyperplasia

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3
Q

define this condition:
you take excessive iodine– inhibiting the biosynthesis of normal T3/T4 by blocking the thyroglobulin iodination

A

Wolff-Chaikoff effect
it is a protective effect in hyperthyroidism

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4
Q

clinical features of hyperthyrodism

A
  1. increased BMR:
    -weight lost, heat intolerance, warm flushed smooth sweaty skin ( increased blood flow and PERIPHERAL vasodilation to increase heat loss)
  2. overactive sympathetic system:
    -tremor, nervousness, emotional changes
    -eyelid lag and staring gauze- sympathetic overstimulation of sup tarsal muscle (staring gaze)
  3. GIT:
    -diarrhea with fat malabosrption- hypermotility due to sympathetic overstimulation
  4. MSK:
    -wasting, weakness, osteoporosis, increased serum calcium and alkaline phosphatase
  5. CVS- earliest and most prevalnet
    increase HR- AF
    peripheral vasodilation- due to decreased systemic vascular resistance

** there is decreased diastolic pressure and increased SYSTOLIC PRESSURE, increase pulse pressure

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5
Q

these lab findings suggest?
1. incresed serum T4 and decreased serum TSH
2. increased 123I uptake
3. hyperglycemia – high glycogenolysis
4. hypocholesterolemia–increased LDL receptor synthesis)
5. hypercalcemia

A

hyperthyroidism

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6
Q

radioiodine uptake shows normal or elevated uptake and there are focal “hot” regions” and the rest is cold

A

this is seen in TOXIC NODULES

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7
Q

radioiodine uptake shows normal or elevated uptake and there is diffuse increase uptake

A

seen in GRAVES disease

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8
Q

radioiodine uptake shows decreased uptake

A

seen in THYRODITIS and exogeneous

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9
Q

what is the most common cause of hyperthyrodism

A

GRAVES diease

HLA DR3 is the gene

CTLA-4 T-CELL receptor

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10
Q

what is the path of graves disease

A

its a autoimmune disorder against thyroid proteins and TSH receptor causes over stimulation- or blocks it

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11
Q

what are the types of autoantibodies aganist TSH receptor

A
  1. TSI: IgG antibody bings to the TSH receptor and mimics action of TSH
  2. Thyroid growth stimulating immunoglobulin– it enhances the growth of the thyroid gland
  3. TSH binding inhibitor immunoglobulin–may cause hypothyrodism
  4. antibodies to thyroglobulin, thyroid peroxidase and sodium iodide symporter
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12
Q

what is the clinical feature triad seen in hyperthyrodism

A
  1. diffusely enlarged, hyper functional thyroid
  2. infiltrative ophthalmopathy – leading to exophthalmos
  3. pretibial myxedema
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13
Q

the exophthalmos and pretibial myxedema are due to

A

it is due to fibroblast and adipocytes behind the orbit and overlying skin.
that also express TSH receptor– when they get activated the glycosaminoglycan will build up

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14
Q

what is the morphology of Hyperthyrodism

A

gross– diffusely and symmetrically enlarged. capsule intact, resembles meaty

microscopy- follicular epithelial cells are tall and columar and croweded

  • small papillae that lacks fibrovasular cords
    -colloid pale with SCALLOPED margins
    -lymphoid infiltrates ( T- cells, scattered B cells and plasma cells) are present throughout the interstitium and germinal centres may be seen
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15
Q

thyroid storm

A

this is a acute life-threatening complication of hyperthyroid presents with multisystem involvement.

  • precipitating factors: patients with secondarily increased levels of catecholamines

EVERYFEATURE OF HYPER just over over

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16
Q

goiter

A

enlargement of thyroid gland as a feedback
- diffuse and multinodular

first at a state of EUTHYROID metabolic state– the compensatory increase in TSH is enough to overcome the hormone deficiency

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17
Q

multinodular goiter- TOXIC
and adenoma- TOXIC

A

thyrotoxicosis secondary to development of autonomous nodules that function independent of TSH stimulation— eventually secretes T4/T3 on their own

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18
Q

diffuse goiter

A

diffuse symmetric enlargement of the thyroid and the follicles are lined by crowded columnar epithelium that may pile up to from projections into the lumen

  • long standing diffuse goiters become multinodular goiters over time
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19
Q

morphology of goiter

A

gross- multilobulated, asymmetrically enlarged glands

cut surface- irregular nodules containing variable amounts of brown gelatinous colloid

older lesion: fibrosis, hemorrhagic, calcification and cystic change

microscope: colloid-rich follicles lined by flattened, inactive epithelium
- areas of follicular epithelial hypertrophy and hyperplasia

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20
Q

what are the type of hypothyroidism

A
  1. cretinism
  2. myxedema
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21
Q

at what age is cretinism common

A

infancy and early childhood
* important cause of mental retardation

22
Q

what are the causes of cretinism

A
  1. iodnine deficieny
  2. maternal hypothyrodism (before the development of thyroid gland)
  3. ectopic thyroid surgical removal- accidently removed (lingual thyroid)
23
Q

what are the clinical features of cretinism

A
  1. severe mental retardation d.t impaired development of the brain
  2. skeletal abnormalities- short stature and umbilical hernia –pot belly
  3. coarse facial feature and protruding tongue, lack hair and teeth
24
Q

what age is myxedema most common in

A

older children and adults

25
what are the primary and secondary causes of myxedema
primary: 1. hashimoto thyroditis 2.iodine deficieny 3. idiopathic secondary: 1. failure of the pituitary glans lack TSH
26
what is the most sensitive test in primary hypothyrodism
TSH estimation due to the negative feedback actions
27
clinical features of hypthyrodism
1. dementia 2. cold intolerance 3. constipation 4. hypercholesterolemia--decreased sythesis of LDL receptors 5. overweight 6. DIASTOLIC HYPERTENSION- water and sodium retentation 7. brady- low cardiac output 8. cool pale skin, decreased sweat 9. PREORBIAL PUFFINESS- myxedema d.t increased hyaluronic acid in the interstitium and non pitting edema 10. proximal muscle myopathy--increased creatinine kinase 11. delayed deep tendon reflexes 12. menstrual abmormalities
28
what condition shows there lab findings: 1. decreased serum T4 and increased TSH levels 2. hypercholesterolemia
hypothyrodism
29
what is the most dangerous complications of hypothy.
There is sudden fall in the T3 and T4 levels-- Myxedema coma - there is sudden fall in temp - reduced HR - reduced BP - confusion- altered mental status - COMA
30
what are the precipitating factors of myxedema
urinary tract infections or sepsis, trauma or a side effect of medication
31
what is hashimoto thyroiditis
autoimmune causes destruction of the thyroid gland-- leading to primary hypothyroidism risk for B cell lymphoma of marginal zone age is 45-6 vs graves 20-40 eiotholgy- 1.diffuse goiter 2. antithyrgobulin and anithyroid peroxidase antibodes
32
morphology of hashimoto thyroidits
gross- diffusely enlarged palem vaguely nodular microscopy: - intense lymphoplasmacytic infiltrate with germinal centres - atrophic follicles - oncocytic changes: large cells with abundant granular eosinophilic cytoplasm in follicular epithelium as a metaplastic response to inflammation - fibrosis- fibrosing variant
33
post partum thyroidits
at the end of pregnancy there is sudden rise in immune response to thyroid-- resulting in thyroiditis it is a painless and diffuse thyromegaly -d/t to the destruction there is release of stored T4/T3 --as compensation leading to hyperthyroid,,, then later there is hypothyroid,, d.t deplection of the stores and then eventual recovery (euthyroid state) *decreased radioactive uptake **thyroid peroxidase auto-antibody is highly associated
34
what is acute suppurative thyroditis
complication of septicemia high fever redness of skin of thyroid and thyroid gland tenderness
35
subacute (de Quervain or granulomatous) thyroiditis
enlarged firm and tender thyroid gland
36
what is the pathology of thyroiditis
follows a viral infection and is associated with HLAB35
37
what is the microscopy of thyroiditis
granulomatous inflammation to extravasated colloid with lymphocytes, histiocytes, multinucleated giant cells
38
what are the features of thyroidits
self-limited resolves in 1-2 months - initial phase of hyperthyroidism followed by a hypothyroid phase the euthyroid
39
reidels thyroidits
fibrotic inflammatory process involving the thyroid gland and adjacent neck tissues NON tender goitrous enlargment associated with inflammatory fibrosclerotic conditions
40
morpholgy of reidels thyroidits
gross: tan gray, woody, avascular and no lobules apparent (hard thyroid) lost lobular archicture microscopy- extensive inflammation- consists of plasma cells (IgG-4) producing, lymphocytes, macrophages and eosinophils dense fibrous tissue- infiltrates adjacent skeletal muscle/airways mimicking malignancy
41
what the eithology of thyroid neoplasm
history of radiation of the head and neck *presents with solitary nodule
42
features of thydoid neoplams
young male, cold nodule -pain, rapid rate of growth and change in voice
43
hot nodules- increase uptake
graves and nodular goiter
44
cold nodules- decrease uptake
adenoma and carcinoma
45
follicular adenoma
benign solitary nodule vast majority are nonfunctional, few are toxic adenomas---> leading to thyrotoxicosis nonfunctional type express RAS gene
46
clinical features AND moprhology of follicular adenoma
CF: -painless nodules -larger masses: local symptoms- difficulty in swallowing -toxic adenomas can lead to hyperthyrodism most are cold nodules except the toxic ones which are hot gross- solitary well circumscribed nodule well defined intact capsule microscopy- evidence of follicular differentation - no capsular and vascular invasion
47
follicular carcinoma
frequent in areas of iodine def. solitary cold nodule hematogenous spread to lung, liver and bones morphology: gross- tan to brown solid cut surface, cystic change and hemorrhage microscopy: uniform cells forming small follicles, reminiscent of normal thyroid - follicular differentiation less apparent with higher grade tumors
48
papillary carcinoma
associated with ionizing radiation - multifocal -lymphatic spread (cervical nodes)-good progenosis painless mass in the neck
49
morpholgy of paipllary carcinoma
gross- solitary/multifocal circumscribed- encapsulated/infiltrating surrounding parenchyma -papillary excrescences with fibrovascular cord MICROSCOPY- hallmark branching papillae with fibrovascular cord covred with uniform cuboidal epithelial cells -Psammoma bodies- Concentrically calcified structures **cells- nucleus is clear with a ground glass with intranuclear inclusions and intranulear grooves
50
medullary carcionoma
secretes calcitonin MEN 2A/2B gross- multiple lesions involving both lobes areas of necrosis and hemorrhage microscopy- polygonal to spindle-shaped cells amyloid deposits- altered calcitonin in the stroma (CONGO-red stain/ IHC) presentation: mass in the neck, compression effects such as dysphagis or hoarseness, diarrhea (vasoactive intesrinal peptide secrection)
51
anaplastic carcinoma
p53 mutation firm, enlarging, bulky mass dyspnea and dysphagia arise from papillary or follicular carcinoma it has a tendency for widespread metastasis and invasion of the trachea and esophagus microscopy- undifferentiated anaplastic and pleomoprhic cells
52
genetic mutaion of 1. medullary carcinoma 2. anaplastic carcinoma 3. follicular carcinoma 4. papillary carcinoma
1. MEN-2 TK receptor activation 2. TP53 3. RAS gene 4.rearrangement of TK RET gene or point mutation BRAF

endocrine system (5 decks)

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