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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
Q

thyrotoxicosis. other 4 effects on cardio? SBP, DBP, PP
UW

A

decr. diastolic pressure
incr. systolicr pressure
incr. pulse pressure
High output heart failure

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26
Q

Beta blocker other effect in thyroid hormone synthesis? UW

A

Beta blocker other effect – decr. peripheral conversion of T4 -> T3 via inhib. 5-deiodinase

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27
Q

Iodide uptake is upregulated by? UW

A

Iodide uptake is upregulated by TSH.

28
Q

Iodide uptake is upregulated by TSH. Perchlorate and pertechnetate are competitive inhibitors of the sodium-iodide symporter. UW

29
Q

UW. What are Hurtle cells?

A

Hürthle cells (large cells with granular, eosinophilic cytoplasm) representing follicular epithelial cells that have undergone metaplastic change in response to inflammation.

30
Q

UW table. Subacute 3 clinical features?

A

onset following viral infection
painful enlargement
transient hyperthyroid symptoms

31
Q

UW table. Hashimoto 3 clinical features?

A

autoimmune etiology
painless enlargement
predominant hypothyroidism features

32
Q

UW table. Subacute 2 diagnostic?

A

incr. ESR and CRB
decr. Iodine uptake

33
Q

UW table. Hashimoto 2 diagnostic?

A

positive TPO antibody (but nonspecific)
variable radioiodine uptake

34
Q

UW table. Subacute histopatho?

A

granulomatous inflammatory infiltrate with macrophages and GIANT CELLS

35
Q

UW table. Hashimoto histopatho?

A

Chronic inflammation (lymphocytes and plasma cells) with germinal centers and hurthle cells.

36
Q

UW. Why in subacute might be hyperthyroid phase?

A

due to release of stored thyroid hormone
Supressed TSH, high T4

37
Q

UW. Why decreased iodine uptake in subacute?

A

low TSH -> suppressed synthesis of new thyroid hormone

38
Q

UW. 3 Phases in postpartum thyroiditis?

A

Hyper; hypo; recovery

39
Q

UW. postpartum thyroiditis.
When and how long hyper?

A

1-3 months

40
Q

UW. postpartum thyroiditis.
When and how long hypo?

A

4-8 months

41
Q

UW. postpartum thyroiditis.
When and how long recovery?

A

nera tiksliai nurodyta, bet pati trukme iki 12 men, tai cia gausis iki 4 men.

42
Q

UW. postpartum thyroiditis. what happens in hyper?

A

RELEASE OF PREFORMED THYROID HORMONES

43
Q

UW. postpartum thyroiditis. what happens in hypo?

A

DEPLETION OF THYROID HORMONES

44
Q

UW. postpartum thyroiditis. what happens in recovery??

A

RETURN TO EUTHYROID state

45
Q

UW. postpartum thyroiditis. when occurs/duration?

A

within 12 months post partum

46
Q

UW. postpartum thyroiditis. what disorder/etiology?

A

autoimmune

47
Q

kaip ir hashimoto (autoimmune) taip ir postpartum (autoimmune) turi same charakteristikas. Kokias?

A

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
Q

UW table. In what diseases incr. TH synthesis?

A

Graves and toxic nodules

49
Q

UW table. In what diseases release of preformed TH?

A

Silent (sporadic) thyroiditis
Postpartum thyroiditis
Subacute thyroiditis

50
Q

in both new synthesis/release of preformed are increased TH (thyroxine and triiodothyroinine), and decr. TSH

51
Q

UW table. TG is more increased in what?

A

In release of preformed TH (if synthesis also increased, but less)

52
Q

UW table. radioiodine uptake increased where?

A

in synthesis; in release of preformed no

53
Q

UW table. in whar incr. blood flow on UG?

A

in synthesis. in preformed not increased.

54
Q

postpartum. what lab in hyperthyroid phase?

A

incr. T4 and T3, decr. TSH

55
Q

postpartum. what lab in hypothyroid phase?

A

decr. T4 and T3, incr. TSH

56
Q

postpartum. Histopatho?

A

Lymphocytic infiltrates +/- germinal centers
NESUMAISYTI SU HASHIMOTO

57
Q

Postpartum thyroiditis is associated with high titers of antithyroid peroxidase and antithyroglobulin autoantibodies, which activate complement in thyroid follicles and stimulate NK cells. !!!!!!!

58
Q

where is problem in primary hypothyroidism?

A

in thyroid gland

59
Q

what do thyroid in response to TSH from pituitary?

A

release T4 and T3

60
Q

what is the most sensitive marker for primary hypothyroidism?

A

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
Q

Where is the problem in secondary hypothyroidism?

A

hypothalamic-pituitary dysfunction

62
Q

primary vs secondary(central) hypothyroidism?

A

primary - low T4 and T3, but high TSH
secondary - low T4, low TSH

63
Q

secondary(central) hypothyroidism causes?

A

mass lesion (eg pituitary adenoma)
Pituitary surgery, trauma, radiation
Infiltrative disorders (sarcoidosis, hemochromatosis)
Pituitary infarction (eg Sheenan)

64
Q

secondary(central) hypothyroidism symptoms?

A

Hypothyroidism symtoms
Mass-effect symtoms

65
Q

Secondary (central) HYPER thyroidism is a rare disorder, usually caused by?

A

TSH-secreting pituitary adenoma. Both TSH and serum T4 levels are elevated.

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

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