Brainscape's Knowledge GenomeTM

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


See full index

MD4001 > Thyroid and Parathyroid Pathology > Flashcards

Thyroid and Parathyroid Pathology Flashcards

1
Q

Identify the most common types of presentation of thyroid pathology.

A

Goitre, and lump

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

How may goitres feel like upon palpation ? What does this tell us about its nature ?

A

Smooth, regular = hormonal drive

Acutely inflamed = viral infection

Lumpy = possibly NOT goitre but lump

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

Distinguish between toxic and non toxic in the context of thyroid pathology.

A

Toxic = excess thyroid hormones present, and clinical sequella

Non-toxic = clinically non-visible

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

Identify the main types of euthyroid goitre, and state the main causes of each type.

A
  • Diffuse: in younger people, may be physiological (part of growing up)
  • Mutlinodular: in older people, palpable in the neck, can be associated with multiple cysts and hemorrhage but NON NEOPLASIC, simple response of follicular cells abhorrently to signaling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Identify the main causes of hypothyroid goitre.

A

1) Iodine deficiency (no feedback from thyroid hormones to TSH and TRH, so raised levels of TSH cause proliferation of tissue
e.g. may be due to iodine deficiency in diet, or blocked metabolic pathway
OR
Iodine excess- iodine required for functioning of thyroid follicular cells and sythesis of mature thyroglobulins. If excess, inhibition of peroxidase enzymes and process of iodination, so iodine does not get incorporated into tyrosines
OR
Excess thiocyanate or perchlorate- Inhibit iodine trapping mechanism so no iodine taken up
-These all result in decreased thyroid hormone production, decreased levels in the blood, feedback to the hypoT-pituitary is lost, so increased levels of TRH and TSH, and high levels of TSH binds to receptor on thyroid gland and increase protein synthesis in follicular cells, resulting in hypertrophy of the thyroid. Cells can make more thyroglobulin, but cannot iodinate it.

2) Goitrogens
-Drugs: lithium
-Diet: cabbage, turnips
Lithium may interfere with signaling and feedback, so can cause goitre and hypothyroidism

Cabbage may interfere with thyroid hormone processing in thyroid causing TSH response

3) Genetic
4) Reactive (post-infectious, e.g. following mumps infection)

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

Describe possible histological findings of iodine induced goitre.

A

Cystic glands, areas with more proliferated follicles

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

Distinguish between benign and malignant masses in the thyroid region.

A
  • Benign masses are usually movable, soft, and non tender.
  • Malignancy is associated with a hard nodule, fixation to surrounding tissue, and regional lymphadenopathy (enlarged local lymph nodes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Identify the main symptoms of solitary thyroid nodules (benign or malignant)

A

• Most patients asymptomatic, but some exhibit signs and symptoms of altered levels of thyroid hormones:

  • Hyperthyroidism
  • Hypothyroidism (especially if the solitary nodule is actually nodular part of goitrous gland)

• Signs and symptoms of local nerve involvement (may be indicative or local invasiveness from malignancy) including dysphagia and hoarseness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Identify the main signs and symptoms of hypoT. What presents an obstacle for diagnosis ?

A

Indolent onset

Cold intolerance, constipation, fatigue, and weight gain (which in children, is primarily caused by the accumulation of myxedematous fluid), thickening of skin, slow speech, deep hoarse voice, lethargy, bradycardia, mental impairment.

Many populations, especially in cold, deprived areas, may demonstrate many of these symptoms without being hypOT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Identify the main signs and symptoms of hyperT.

A

Nervousness, heat intolerance, increase in skin temperature and sweating, diarrohea, loss of weight and appetite
(possible exophthalmos in Grave’s), tremor, tachycardia, high metabolic rate, muscle weakness

• Two common manifestataons are diffuse toxic goitre or toxic nodular goitre.

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

What are other differential diagnoses for what may appear to be a solitary thyroid nodule ?

A

A larger nodule which is part of a goitrous thyroid

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

Describe cytology findings of thyroid malignancy.

A

May be different sized follicles BUT may look benign even in malignancy

Fine needle aspiration can be useful if follicles look normal

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

Describe the epidemiology of solitary thyroid nodules.

A

Mainly in younger people (especially physiological, benign nodules)

Females affected more than males

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

Describe diagnosis of solitary thyroid nodules.

A

TESTS

  • Thyroid function tests - An elevated thyroid-stimulating hormone (TSH) level may indicate thyroiditis; a very low TSH level indicates an autonomous or hyperfunctioning nodule (but in many situations, asymptomatic and no change in thyroid hormones produced). Blood T3 and T4 may also be measured.
  • Antithyroid antibodies - Helpful in diagnosing chronic lymphocytic thyroiditis (Hashimoto thyroiditis)
  • Complete blood count (CBC) –Abscess (with a goitre)
  • Fine needle aspirate (can help distinguish between benign and malignancy)
  • Molecular studies (can help determine if particular mutation is present, but diff mutations exist)
IMAGING STUDIES
-Ultrasonography
•  Radionucleotide thyroid scan (123I- or 99mTcO4 -uptake) viewed by a gamma camera
-Chest radiography
-CT/MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the use of ultrasonography in the diagnosis of solitary thyroid nodules ?

A

To determine whether the nodule is cystic, solid, or mixed

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

What is the use of radioiodine scintigraphy in the diagnosis of solitary thyroid nodules ?

A

To determine whether the nodule is cold, warm, or hot.

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

What is the use of chest radiography in the diagnosis of solitary thyroid nodules ?

A

If malignancy is suspected, given the high incidence of early metastases to the lungs

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

What is the use of CT/MRI in the diagnosis of solitary thyroid nodules ?

A

To analyze the extent of disease by scanning the neck and chest

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

State the main effects of trauma on the thyroid.

A

Trauma can give rise to cystic abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why does exophthalmos occur in Grave’s associated hyperthyroidism ?

A

Because of the change in fat around the orbit, which reflects changes in the metabolism (i.e. change in thyroid hormones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the main causes of hyperT ? How does it present ?

A

Grave’s (AI, may present as diffuse toxic goitre)

Functional goitre

Toxic adenoma

Overtreatment with Thyroxine

Transient neonatal thyrotoxicosis (mother with Graves Disease)

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

Describe the immunological mechanism behind Grave’s.

A

IgG antibodies against TSH receptor on thyrocytes, leading to antibody binding, which triggers cell to produce more thyroid hormones leading to toxicity

Antibodies are called thyroid-stimulating antibody (AKA LATS/TSI)

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

Describe epidemiology of Grave’s.

A

F more than M

24
Q

What are the main causes of hypoT ?

A

-Congenital
-Autoimmune, due to:
Defective TH production either due to loss of parenchyma, or deficient TSH

25
Q

Describe epidemiology of Grave’s.

A
  • Under 40 years
  • Female:male 10:1
  • Strong family history linked to HLA DR3 and CTLA-4 (so ask patient is any family history)
26
Q

Describe cytology of Grave’s disease.

A

Colloid is not filling follicles because it is being resorbed (some follicles are empty), very busy, overstimulated cells, large number of them, resorbing colloid, iodinating thyroid hormones.

27
Q

Describe epidemiology of Hashimoto thryoiditis.

A
  • Females 30-50y

* Family history strong and other autoimmune diseases

28
Q

Describe typical presentation of Hashimoto thyroiditis.

A
  • Present as hyper- or hypo- thyroidism (initially, may be thryotoxic due to damaged follicles releasing thyroglobulin, so both thyroid hormones increases; over time, decreased number of follicles and of their function, so hypoT)
  • Upon examination and palpation:
  • Acute phase: hard (due to fibrosis following inflammation and destruction), large, tender gland
  • Chronic phase: Irregular, shrunken, hard (due to fibrosis)
29
Q

Describe the immunological mechanism underlying Hashimoto’s thryoiditis.

A
  • Autoreactive CD8 T lymphocytes (T cell mediated)
  • Autoreactive antibodies: thyroid microsomal antibodies in almost all, thyroglobulin antibodies in two thirds, minority have blocking TSH receptor antibodies (TSH-R Ab), also Thyroid peroxidase (TPO) Ab

These cause lesions in follicular cells and release of colloid- atrophy of thyroid and hypoT

30
Q

Identify causal risks for Hashimoto’s thyroiditis.

A

Increased iodine intake, viral infection (leading to altered antigen, leading to defective immune response)

31
Q

Describe cytology of Hashimoto’s.

A

Follicles are flat, very little cytoplasm, colloid present, lymphoid follicles present (because antibodies and autoreactive T lymphocytes are present)

32
Q

How is diagnosis of Hashimoto’’s made ?

A

Look for anti-thyroid antibodies (even though damage is likely due to cytotoxic T cell) + Imaging

33
Q

Identify a possible complication of Hashimoto’s.

A

Lymphoma

34
Q

What are the main thyroid neoplasms ?

A

Benign: follicular adenoma

Malignant: primary or metastatic (lymphoma)

35
Q

Identify the main primary thyroid malignancies. State the type of cell each arises from.

A 
Papillary
Follicular (follicular cells) 
Anaplasic 
Medullary (parafollicular cells)
Lymphoma
36
Q

Describe epidemiology of follicular adenoma.

A
  • 30-50y

* Female>males

37
Q

Describe appearance of follicular adenomas. How is it treated ?

A

1-3 cm at presentation
Discrete, uniform, encapsulated
Different histological subtypes

Treated it by resection

38
Q

Identify a mutation often found in follicular adenomas.

A

Ras mutation

39
Q

Which is the commonest form of primary thyroid malignancy ?

A

Papillary carcinoma

40
Q

Describe epidemiology of papillary carcinomas.

A
  • 20-50y

* Females: males 3:1

41
Q

Identify the main cause of papillary carcinomas.

A

– Radiation (e.g. Chernobyl)
– Family history
– Unknown

42
Q

Explain the genetic basis of papillary carcinomas. Which genes are defective ?

A
  • Rearrangement of RET oncogene in most

* B-RAF mutation in half – associated with increased risk of LN mets

43
Q

How do papillary carcinomas spread ? Follicular carcinomas ?

A

Papillary: Lymphatic spread
Follicular: Blood spread

44
Q

Describe epidemiology of follicular carcinomas.

A
  • Older than 40

* Female:male 3:1

45
Q

Explain the genetic basis of follicular carcinomas. Which genes are defective ?

A
  • RAS oncogene

* PAX8/PPARG rearrangements

46
Q

Describe epidemiology of anaplastic carcinomas.

A

• Female:male 4:1

47
Q

Explain the genetic basis of anaplastic carcinomas. Which genes are defective ?

A

• p53 mutation common

48
Q

Identify risk factors for anaplic carcinoma.

A

• Half have had chronic
goitre
• May have had previous thyroid neoplasia

49
Q

Describe genetic basis of medullary carcinoma.

A
  • 20% familial (in younger patients)

- RET proto-oncogene activation

50
Q

What are the main features of medullary carcinoma ?

A
  • Calcitonin producing

- Neuroendocrine tumor

51
Q

Identify the main causes of primary hyperparathyroidism.

A
  • Adenoma (mainly)
  • Hyperplasia (some familial)
  • Parathyroid carcinoma (small amount)
52
Q

Identify the main causes of secondary hyperparathyroidism.

A

• Caused by low calcium (eg in vitamin D deficiency following chronic renal failure), so increase parathyroid hormone to counter low levels of Calcium (resulting in resorption of calcium)

53
Q

Identify the main causes of tertiary hyperparathyroidism.

A

• Raised calcium in secondary (secondary hyperparathyroidism, but parathyroid causes paradoxically raised calcium, because resorb so much calcium)

54
Q

What are the effects of primary hyperparathyroidism ?

A

Calcium release, so hypercalcaemia effects:

  • Calcium resorption from bone, causing osteitis fibrosa cystica
  • Pancreatitis (due to Calcium deposition in pancreas)
  • Renal stones
55
Q

Identify and distinguish between the main types of multiple endocrine neoplasia.

A

Two major types, each characterised by a major tumor suppressor gene . Different but overlapping features, may be functional, and possible malignant potential. NOT ALL inherited, some spontaneously acquired mutations:

MEN1

  • Autosomal dominant
  • Parathryroid involvement
  • Bronchial carcinoid

MEN2

  • Autosomal dominant
  • Parathryroid involvement
  • Thyroid C cell involvement
56
Q

What is the main cause of toxic nodular goitre ?

A

Benign neoplasma/adenoma

MD4001 (74 decks)

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