Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine 2 > Robbins - Thyroid > Flashcards

Robbins - Thyroid Flashcards

1
Q

Midline, anterior mass w/ mucinous secretions, lined by epithelium w/ pleomorphic lymphocytic infiltrate

Origin? Leading to a persistent ____

A

Thyroglossal duct cyst

Thyroid tube remnant
Persistent SINUS TRACT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

TSH receptor type? Function?

A

Gs

Stimulates thyroid growth and hormone production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

2 cell types within the thyroid (w/ functions)

A

Follicular cells - produce thyroglobulin, release T4 (and T3)

Parafollicular cells (C cells) - release calcitonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Calcitonin - functions

A

Increase calcium absorption by bones, inhibits osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens to T4 once released into blood?

A

Bound by TBG and transthyretin, then deiodinated to T3 in the periphery, which binds to thyroid hormone receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Propylthiouracil (PTU) - functions (2)

Acting as a _____

A
  • Inhibits iodine oxidation –> inhibits T3/T4 production
  • Inhibits T4 deiodination (periphery)

Goitrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Iodine (large doses) - function

Acting as a _____

A

Blocks proteolysis of thyroglobulin –> inhibits T3/T4 release

Goitrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Elevated circulating levels of T3 and T4 - name?

Causes (3) - general

A

Thyrotoxicosis

  • Hyperthyroidism (primary or secondary)
  • Thyroiditis (excess release)
  • Extrathyroid souce
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Excess thyroid hormone:

  • Skin
  • BMR
A 
Skin = Warm, flushed, sweating, heat intolerance
BMR = weight loss w/ increased appetite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Excess thyroid hormone:

- Heart

A

Tachy, palpitations, cardiomegaly, A. fib, CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Excess thyroid hormone:

- CNS

A

Tremor, hyperactivity, anxiety, insomnia, emotional lability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Excess thyroid hormone:

  • Muscles
  • GI
A

Muscles = proximal mm weakness, decreased mass

GI = diarrhea, malabsorption (overactive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Excess thyroid hormone:

- Eyes

A

Wide staring gaze, lid lag (overstimulation of sup. tarsal m)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Excess thyroid hormone:

  • Bones
  • Bones microscopically
A

Bone resorption, osteoporosis, fractures

Micro = infiltration of fat and lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Excess thyroid hormone:

- Liver

A

Minor enlargement (fatty change in hepatocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Thyroid storm:

  • Symptoms
  • Causes
  • Association
A

Symptoms = fever, tachycardia, arrhythmias (deadly)

Causes = increased catecholamine release (infection, surgery, stress, stopping antithyroid meds)

Association = GRAVE’S DISEASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Older adult, unexplained weight loss, worsening of heart disease, increase thyroid hormones

A

Apathetic hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

A patient presents w/ thyrotoxicosis. TSH levels are slightly raised. How to determine if it’s secondary (pituitary) hyperthyroidism?

A

TRH stimulation test

- Normal increase in TSH = NEGATIVE = NOT 2º

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Primary hyperthyroidism is diagnosed. How to determine the etiology? Result for each? (3)

A

Radioactive iodine test

  • Diffuse uptake = GRAVES
  • Solitary nodular uptake = TOXIC ADENOMA
  • Decreased uptake = THYROIDITIS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Treatment of hyperthyroidism (5)

A
  • Beta blocker (block symptoms)
  • Thionamide (block synthesis)
  • Iodine (block release)
  • T4 deiodination inhibitor (block action)
  • Radioiodine ablation (kill thyroid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

BEST single diagnostic test for ANY thyroid problem suspicion

Why?

A

TSH level

Decreased even at the subclinical level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Infant/child in Asia/Africa, retardation, small, coarse facial features, protruding tongue, umbilical hernia

Most common cause?

A

Cretinism (developmental hypothyroidism)

Usually = dietary iodine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Older child or adult, normal hypothyroid symptoms - general term

A

Myxedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hypothyroidism symptoms

A
  • Fatigue, apathy, mentally slow (CNS)
  • Cold intolerance, cool skin, pale (low blood flow)
  • Overweight (BMR low)
  • SOB, decreased exercise tolerance (reduced C.O.)
  • Increased cholesterol, LDL, CV risk
  • Non-pitting edema (glycan, hyaluronic acid deposition)
  • Coarse facial features (glycan, hyaluronic acid deposition)
  • Enlarged tongue (glycan, hyaluronic acid deposition)
  • Deepening voice (glycan, hyaluronic acid deposition)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Diffuse PAINLESS enlargement of thyroid, major mononuclear infiltrate, germinal centers, atrophic follicles, epithelial cells w/ abundant eosinophilic, granular cytoplasm, fibrosis

What are those epithelial cells?

A

Hashimoto’s thyroiditis

Hurthle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe Hashimoto’s pathogenesis

A

Breakdown in self-tolerance to thyroid tissue, causing…

  • CD8 T-cell destruction (Fas-FasL)
  • CD4 T-cell / Macrophage destruction (cytokines)
  • Plasma cell / Antibodies / NK cell destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hashimoto’s autoantibodies

A

Anti-microsomal, Anti-peroxidase, Anti-thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hashimoto’s genetics (2)

A

CTLA4, PTPN22 - T-reg cell regulators

29
Q

May see what labs at onset of Hashimoto’s

Term for this?

A

Increased T3/T4, low TSH, low iodine uptake - increased release of hormones

Hashitoxicosis

30
Q

Hashimoto’s = increased risks?

A
  • Other autoimmune diseases (Type 1 DM, Autoimmune adrenalitis, SLE, Myasthenia gravis, Sjogren)
  • Extranodal marginal zone lymphoma
31
Q

What is DIFFERENT about subacute lymphocytic thyroiditis compared to Hashimoto’s, symptom-wise?

Common presentation of it?

A
  • HYPERthyroidism (mild)

POSTPARTUM woman, anti-thyroid-peroxidase antibodies OR family history of autoimmune disorders

32
Q

What is DIFFERENT about subacute lymphocytic thyroiditis compared to Hashimoto’s, morphology-wise?

What is the SAME?

A

No fibrosis, no Hurthle cell metaplasia

Lymphocytic infiltrate, germinal centers, follicle collapse

33
Q

What is DIFFERENT about Granulomatous Thyroiditis compared to Hashimoto’s or Subacute Lymphocytic, symptoms wise?

Presentation/history-wise?

Prognosis?

A

PAINFUL thyroid enlargement

SUMMER, acute URI viral infection previously

SELF-LIMITED (diminishing after 2-6 weeks)

34
Q

Granulomatous thyroiditis - unique morphology (EARLY)

A

Neutrophilic microabscesses in damaged follicles

35
Q

Granulomatous thyroiditis - unique morphology (LATE)

A

Multinucleate giant cells around colloid (thyroglobulin)

36
Q

Does damage in granulomatous thyroiditis happen at the same time or in waves?

A

WAVES - different morphologies w/in the same gland

37
Q

Granulomatous thyroiditis - hyper or hypothyroidism?

A

HYPERthyroidism

38
Q

Extensive fibrosis of thyroid AND surrounding structures AND maybe other organs

What is it?

A

Riedel thyroiditis

Systemic autoimmune IgG4 sclerosing disease

39
Q

Diffuse, symmetric hypertrophy of thyroid, exophthalmos, pretibial myxedema (dermopathy), bruit in neck

A

Grave’s disease

40
Q

Grave’s disease - most common antibody

Function?

A

Thyroid-stimulating immunoglobulin (TSI)

Binds TSH receptor, mimics its action, released hormones

41
Q

Grave’s disease - genetics

A

CLTA4, PTPN22, HLA-DR3

42
Q

Grave’s disease - eyes

Why?

A

Protrusion due to increased connective tissue and EOMs

Antibodies stimulate TSH receptor on fibroblasts behind the eye

43
Q

Diffuse enlargement of the thyroid, hypertrophy/hyperplasia of the follicles, papillae w/o fibrovascular cores, lymphocytic infiltrate, germinal centers

A

Grave’s disease

44
Q

Grave’s disease - increased risks?

A

Autoimmune diseases (SLE, pernicious anemia, type 1 DM, Addison’s disease)

45
Q

Goiters - fundamental cause

How does the enlargement happen?

Most common cause?

A

Impaired synthesis of thyroid hormone

Decreased T3/T4 = increased TSH = hypertrophy

Iodine deficiency

46
Q

Most (but not all) people w/ goiters have what T3/T4 level?

What about TSH level?

A

NORMAL (compensatory due to increased mass)

Elevated TSH

Symptoms = mass effect

47
Q

A patient has multinodular goiter. What can be assumed about the history of the disease?

Why does this happen?

A

STARTED AS SIMPLE GOITER, then progressed

Episodes of hyperplasia and involution happening simultaneously in different parts of the gland

48
Q

Cause of endemic goiter?

Why does prevalence vary in these places?

A

Iodine deficiency

Dietary goitrogens vary from place to place - cabbage, cauliflower, brussel sprouts, turnips, cassava

49
Q

Goiter (large) - symptoms

A

Airway obstruction, SVC syndrome

50
Q

A patient has had long-term goiter. After 10 years, she develops symptoms of hyperthyroidism. Why?

A

Plummer syndrome - autonomous “toxic” nodule forms w/in the goiter, producing thyroid hormone

51
Q

Most thyroid neoplasms are ____ (#) and ____ (prognosis)

A

Solitary, benign

52
Q

Thyroid nodule - neoplasia vs. benign (clues)

Common symptoms in all of them (if big enough)

A

Neoplasia - solitary, young, male, Hx of radiation to H/N
Benign - multiple, older, female, functional (“hot”)

Difficulty swallowing, SVC syndrome

53
Q

Solitary thyroid mass, painless, found on routine exam. Fully encapsulated, well-demarcated, uniform cell population w/ colloid, Hurthle cells occasionally

What about hormone production/radioiodine uptake?

A

Thyroid adenoma

Can be “hot” or “cold” - most are nonfunctional (“cold”)

54
Q

How to BEST distinguish cause of follicular neoplasm?

A

Capsule evaluation (adenoma = full, cancer = NOT)

55
Q

Papillary vs. follicular thyroid carcinoma – History?

A

Papillary - often radiation exposure

Follicular - often iodine deficiency (think like goiter)

56
Q

4 general types of thyroid carcinoma

MOST thyroid carcinomas are what type?

A

Papillary, follicular, anaplastic, medullary

Papillary

57
Q

Follicular carcinoma - genetics
Anaplastic carcinoma - genetics
Papillary carcinoma - genetics

Papillary carcinoma - bad prognostic indicator?

A 
Follicular = RAS/PI3K, PTEN, (2;3)(PAX8:PPARG)
Anaplastic = SAME (except not the translocation)
Papillary = RAS, RET/PTC (fusion gene), BRAF

BRAF(V600E)

58
Q

***Solitary thyroid nodule, finely-dispersed chromatin (clear/empty appearance), pseudo-inclusions or invaginations or nuclear grooves, psammoma bodies

A

Papillary thyroid carcinoma

59
Q

Ground glass or Orphan Annie nuclei

A

Papillary thyroid carcinoma (clear/empty-looking)

60
Q

Nuclear features of papillary carcinoma, follicular architecture

Higher incidence of what genetic thing?

A

Follicular variant of papillary carcinoma

RAS mutation (not BRAF or RET/PTC)

61
Q

Papillary carcinoma nuclei, eosinophilic columnar cells lining the papillae

Higher incidence of what genetic things?

A

Tall-cell variant of papillary carcinoma

BRAF mutation, RET/PTC translocation

62
Q

Younger person (even children), papillary carcinoma nuclei, extensive fibrosis throughout the gland, LN (not vascular) metastases

Higher incidence of what genetic thing?

A

Diffuse sclerosing variant of papillary carcinoma

RET/PTC translocation (not BRAF)

63
Q

Painless solitary thyroid nodule, small clusters of uniform cells w/ colloid, capsular invasion, small foci of hemorrhage

A

Follicular thyroid carcinoma

64
Q

Follicular carcinoma - metastasis

A

Vascular - bone, lungs, liver (NOT LN’s)

65
Q

Rapidly enlarging bulky neck mass, extracapsular invasion, dyspnea, dysphagia, hoarseness, cough

Prognosis?

A

Anaplastic thyroid carcinoma

Nearly 100% DEATH (no effective therapies)

66
Q

Solitary thyroid nodule, amyloid in the stroma, diarrhea, elevated CEA

Cell type? (both types)
What else will be seen on labs? (both types)

A

SPORADIC Medullary thyroid carcinoma

Parafollicular cells (C cells)
Elevated CALCITONIN
67
Q

B/L thyroid nodules, amyloid in the stroma, adrenal or parathyroid masses

A

FAMILIAL Medullary thyroid carcinoma

68
Q

Sporadic medullary thyroid carcinoma - diarrhea - why?

A

VIP paraneoplastic secretion

69
Q

Familial medullary thyroid carcinoma - genetics? Syndrome?

A

RET mutation - MEN2 syndrome

Endocrine 2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions