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1 STEP Endocrinology (patho/UW) > UW momentai > Flashcards

UW momentai Flashcards

1
Q

Glucocorticoids (eg, prednisone) in thyroid hormone conversion?

A

Glucocorticoids (eg, prednisone) decrease peripheral conversion of T4 to T3, but it is their anti-inflammatory effects that improve Graves ophthalmopathy.

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2
Q

what improves inflammation in graves?

A

Glucocorticoids (eg, prednisone) decrease peripheral conversion of T4 to T3, but it is their anti-inflammatory effects that improve Graves ophthalmopathy. Glucocorticoids decrease the severity of inflammation and reduce the excess extraocular volume. They also can prevent worsening of ophthalmopathy induced by radioactive iodine treatment.

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3
Q

Graves - what thyroid?

A

diffuse goiter - constant stimulation of TSH leads to thyroid hyperplasia and hyperthrophy
Pathoma

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4
Q

Graves - what histology? UW

A

thyroid folicular epithelium - tall and crowded with hyperactive reabsorbtion -> causing scalloping around the edges of the colloid.

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5
Q

Graves - TG serum levels? UW

A

High serum levels due to increased thyroid metabolic activity

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6
Q

what produces thyroglobulin? UW

A

thyroid folicular cells

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7
Q

levels of thyroglobulin in normal function? UW

A

small amount is released

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8
Q

levels of thyroglobulin in thyrotoxicosis due to exogenous factors? UW

A

low levels (untedectable) - noninflammatory SUPRESSION OF THYROID ACTIVITY

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9
Q

thyrotoxicosis due to exogenous factors. UW.
Why atrophy of folicules?

A

Excess T4 supplementation supresses TSH, which decreases iodine organification and coloid formation -> resulting in DIFFUSE ATROPHY OF THYROID FOLLICLES.

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10
Q

thyrotoxicosis due to exogenous factors. UW. How looks thyroid and colloid? ats is situacijos

A

Diffuse atrophy of the thyroid follicles with decreased colloid.

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11
Q

Hashimoto histopathology? UW/pathoma

A

chronic inflammation -> mononuclear infiltrate (lymphocytes and plasma cells) with germinal centers AND HURTLE CELLS

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12
Q

chronic inflammation -> mononuclear infiltrate (lymphocytes and plasma cells) with germinal centers AND HURTLE CELLS?

A

Hashimoto thyroiditis

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13
Q

Thyroglobulin in hashimoto? UW

A

elevated thyroglobulin due to inflammatory disruption of thryoid follicules.

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14
Q

elevated thyroglobulin due to inflammatory disruption of thryoid follicules?

A

Hashimoto

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15
Q

De Quervain thyroiditis histo? UW/pathoma

A

disruption of follicles and a mixed cellular infiltrate with occasional multinucleated giant cells.
GRANULOMATOUS THYROIDITIS

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16
Q

Thyroglobulin in de quervain? UW

A

elevated due to destructive thyroiditis

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17
Q

normal TSH range?

A

0,5 - 5 mcU/ml
kai vartojant vaistus <0,01 - doze per didele

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18
Q

UW. endogenous hyperthyroidism or exogenous sources -> increased Beta adrenergic receptors -> hyperadrenergic state -> cardiovascular complications

A

.

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19
Q

UW. What is the most common cardio complication in thyrotoxycosis?

A

atrial fibrillation - most common supraventricular arrhythmia

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20
Q

UW. Why might be angina in thyrotoxicosis?

A

incr. contractility -> incr. O2 demand -> precipitate angina in patients with underlying coronary disease

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21
Q

UW. Why might be high-CO HF in thyrotoxicosis?

A

Incr. EF -> CO while decrease SVR

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22
Q

thyrotoxicosis. peripheral vessels? UW

A

dilation (decr. SVR)

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23
Q

thyrotoxicosis. effect of incr. Rate? UW

A

tahycardia/palpitations
AF

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24
Q

thyrotoxicosis. 3 effects on contractility?

A

incr. EF and CO
incr. Myocardial O2 demand and and angina
incr. pulmonary artery pressure

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25
thyrotoxicosis. other 4 effects on cardio? SBP, DBP, PP UW
decr. diastolic pressure incr. systolicr pressure incr. pulse pressure High output heart failure
26
Beta blocker other effect in thyroid hormone synthesis? UW
Beta blocker other effect – decr. peripheral conversion of T4 -> T3 via inhib. 5-deiodinase
27
Iodide uptake is upregulated by? UW
Iodide uptake is upregulated by TSH.
28
Iodide uptake is upregulated by TSH. Perchlorate and pertechnetate are competitive inhibitors of the sodium-iodide symporter. UW
.
29
UW. What are Hurtle cells?
Hürthle cells (large cells with granular, eosinophilic cytoplasm) representing follicular epithelial cells that have undergone metaplastic change in response to inflammation.
30
UW table. Subacute 3 clinical features?
onset following viral infection painful enlargement transient hyperthyroid symptoms
31
UW table. Hashimoto 3 clinical features?
autoimmune etiology painless enlargement predominant hypothyroidism features
32
UW table. Subacute 2 diagnostic?
incr. ESR and CRB decr. Iodine uptake
33
UW table. Hashimoto 2 diagnostic?
positive TPO antibody (but nonspecific) variable radioiodine uptake
34
UW table. Subacute histopatho?
granulomatous inflammatory infiltrate with macrophages and GIANT CELLS
35
UW table. Hashimoto histopatho?
Chronic inflammation (lymphocytes and plasma cells) with germinal centers and hurthle cells.
36
UW. Why in subacute might be hyperthyroid phase?
due to release of stored thyroid hormone Supressed TSH, high T4
37
UW. Why decreased iodine uptake in subacute?
low TSH -> suppressed synthesis of new thyroid hormone
38
UW. 3 Phases in postpartum thyroiditis?
Hyper; hypo; recovery
39
UW. postpartum thyroiditis. When and how long hyper?
1-3 months
40
UW. postpartum thyroiditis. When and how long hypo?
4-8 months
41
UW. postpartum thyroiditis. When and how long recovery?
nera tiksliai nurodyta, bet pati trukme iki 12 men, tai cia gausis iki 4 men.
42
UW. postpartum thyroiditis. what happens in hyper?
RELEASE OF PREFORMED THYROID HORMONES
43
UW. postpartum thyroiditis. what happens in hypo?
DEPLETION OF THYROID HORMONES
44
UW. postpartum thyroiditis. what happens in recovery??
RETURN TO EUTHYROID state
45
UW. postpartum thyroiditis. when occurs/duration?
within 12 months post partum
46
UW. postpartum thyroiditis. what disorder/etiology?
autoimmune
47
kaip ir hashimoto (autoimmune) taip ir postpartum (autoimmune) turi same charakteristikas. Kokias?
positive TPO antibodies (nonspecific marker for autoimmune thyroid diseases) Elevated serum thyroglobulin - due to destruction of follicles and release of colloid in the hyperthyroid state Low radioiodine uptate - due to decreased organification of iodine and synthesis of new thyroid hormone Diffuse swelling and decr. blood flow on UG
48
UW table. In what diseases incr. TH synthesis?
Graves and toxic nodules
49
UW table. In what diseases release of preformed TH?
Silent (sporadic) thyroiditis Postpartum thyroiditis Subacute thyroiditis
50
in both new synthesis/release of preformed are increased TH (thyroxine and triiodothyroinine), and decr. TSH
.
51
UW table. TG is more increased in what?
In release of preformed TH (if synthesis also increased, but less)
52
UW table. radioiodine uptake increased where?
in synthesis; in release of preformed no
53
UW table. in whar incr. blood flow on UG?
in synthesis. in preformed not increased.
54
postpartum. what lab in hyperthyroid phase?
incr. T4 and T3, decr. TSH
55
postpartum. what lab in hypothyroid phase?
decr. T4 and T3, incr. TSH
56
postpartum. Histopatho?
Lymphocytic infiltrates +/- germinal centers NESUMAISYTI SU HASHIMOTO
57
Postpartum thyroiditis is associated with high titers of antithyroid peroxidase and antithyroglobulin autoantibodies, which activate complement in thyroid follicles and stimulate NK cells. !!!!!!!
.
58
where is problem in primary hypothyroidism?
in thyroid gland
59
what do thyroid in response to TSH from pituitary?
release T4 and T3
60
what is the most sensitive marker for primary hypothyroidism?
Serum TSH Small changes in thyroid hormone levels leads to large changes in TSH levels. TSH is more sensitive than T4 and T3 levels for primary hypothyroidism
61
Where is the problem in secondary hypothyroidism?
hypothalamic-pituitary dysfunction
62
primary vs secondary(central) hypothyroidism?
primary - low T4 and T3, but high TSH secondary - low T4, low TSH
63
secondary(central) hypothyroidism causes?
mass lesion (eg pituitary adenoma) Pituitary surgery, trauma, radiation Infiltrative disorders (sarcoidosis, hemochromatosis) Pituitary infarction (eg Sheenan)
64
secondary(central) hypothyroidism symptoms?
Hypothyroidism symtoms Mass-effect symtoms
65
Secondary (central) HYPER thyroidism is a rare disorder, usually caused by?
TSH-secreting pituitary adenoma. Both TSH and serum T4 levels are elevated.

1 STEP Endocrinology (patho/UW) (12 decks)

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