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m2 CA2 > thyroid & parathyroid patho > Flashcards

thyroid & parathyroid patho Flashcards

1
Q

symptoms of hyperthyroid

A
  1. weight LOSS
  2. INCREASED appetite
  3. HEAT intolerant
  4. DIARRHOEA
  5. IRRITABLE
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2
Q

symptoms of hypothyroid

A
  1. weight GAIN
  2. POOR appetite
  3. COLD intolerant
  4. CONSTIPATION
  5. mental SLOWness
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3
Q

signs of hyperthyroid

A
  1. thin
  2. staring gaze, lid lag
  3. warm, sweaty
  4. tachycardia
  5. pretibial myxoedema (graves), proximal myopathy
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4
Q

normal weight of the thymus?

A

20-25g

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5
Q

location of the thymus?

A

lower part of the anterior neck

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6
Q

if the mass presses on the trachea, it will lead to ___ symptoms

A

difficulty breathing, stridor

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7
Q

if the mass presses on the oesophagus, it will lead to ___ symptoms

A

difficulty swallowing

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8
Q

if the mass presses on the Recurrent Laryngeal Nerve, it will lead to ___ symptoms

A

hoarseness

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9
Q

signs of hypothyroidism

A
  1. mildly obese
  2. peaches and cream skin
  3. dry, cool
  4. bradycardia
  5. proximal myopathy
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10
Q

Hashimoto’s is a ________ disease

When T4 is ____, if TSH is high, it is ___________
When T4 is ____, if TSH is low, it is ___________

A

Hashimoto’s is a hypothyroidism disease

When T4 is low, if TSH is high, it is primary hypothyroidism
When T4 is low, if TSH is low, it is secondary hypothyroidism

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11
Q

Graves is a _______ disease

When T4 is ____, if TSH is low, it is __________

A

Graves is a hyperthyroidism disease

When T4 is high, if TSH is low, it is primary hyperthyroidism

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12
Q

What are some diseases that can result in DIFFUSED goitre?

A

Graves disease
Hashimoto thyroiditis
DeQuervain thyroiditis
Simple goitre

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13
Q

What are some diseases that can result in LOCALISED nodule goitre?

A

Nodular goitre
Neoplasms

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14
Q

Pathogenesis of simple diffused goitre (non-toxic)

A

Impaired synthesis of thyroid hormones
-> compensatory increase in TSH
-> hypertrophy and hyperplasia of follicular cells
-> enlargement of thyroid gland (simple goitre)

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15
Q

Morphology of simple diffused goitre

A
  1. Hyperplastic stage
    - diffuse mild enlargement
    - micro: crowded columnar cells, pseudopapillae
  2. Colloid involution
    - abundant colloid
    - micro: flattened cuboidal epithelium
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16
Q

Pathogenesis of localised nodular goitre

A

Impaired synthesis of thyroid hormones
-> compensatory increase in TSH
-> hypertrophy and hyperplasia of follicular cells
-> enlargement of thyroid gland (simple goitre)
-> recurrent hyperplasia and involution
-> nodular enlargement

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17
Q

Features of localised nodular goitre

A
  • evolution from simple goitre
  • extreme, irregular enlargement
  • cystic change
  • commonest cause of goitre
  • mass effects (compression on trachea, RLN, oesophagus)
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18
Q

What is the most common cause of goitre?

A

Localised Nodular goitre

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19
Q

Pathogenesis of Hashimoto thyroiditis

A

Breakdown of self-tolerance to thyroid antigens
-> destruction of thyroid parenchyma
-> progressive thyroid failure
#1 cause of hypothyroidism

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20
Q

Gross morphology of thyroid gland in Hashimoto disease

A

Pale, enlarged gland
Pale yellow firm cut surface

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21
Q

Hashimoto thyroiditis can lead to higher risk of ___________

A

B cell lymphoma of thyroid eg MALT lymphoma

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22
Q

Clinical triad of Graves disease

A
  1. Hyperthyroidism
  2. Infiltrative ophthalmopathy
  3. Infiltrative dermopathy (pretibial myxoedema)
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23
Q

Pathogenesis of Graves disease

A

Thyroid stimulating immunoglobulin
-> binds to TSH receptor
-> mimics TSH
-> increased released of thyroid hormones
-> increased growth of thyroid gland
TSH-binding inhibitor immunoglobulins

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24
Q

there will be ______ radioiodine uptake (imaging test) in graves disease

A

increased
(hyperfunctioning thyroid will take up radioiodine)

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25
Q

Gross morphology of thyroid gland in graves disease

A
  • symmetrical diffuse enlargement
  • soft, reddish meaty cut suface
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26
Q

What are some thyroid neoplasms that are of non-follicular cell origin?

A

Medullary carcinoma
Lymphoma

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27
Q

BENIGN thyroid neoplasms of follicular cell origin:

A

Follicular adenoma
Oncocytic adenoma

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28
Q

LOW grade MALIGNANT thyroid neoplasms of follicular cell origin:

A

Papillary thyroid carcinoma
Follicular carcinoma

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29
Q

HIGH grade MALIGNANT thyroid neoplasms of follicular cell origin:

A

Poorly differentiated thyroid carcinoma
Differentiated high grade thyroid carcinoma

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30
Q

UNDIFFERENTIATED MALIGNANT thyroid neoplasms of follicular cell origin:

A

Anaplastic thyroid carcinoma

31
Q

Morphology of adenoma

A
  • rounded, encapsulated
  • well demarcated
  • no capsular/vascular invasion
32
Q

Key features of follicular adenoma

A
  1. Completely intact fibrous capsule with no capsular or vascular invasion
  2. Nuclei small and round
  3. No vascular or capsular invasion
  4. Microfollicular mixed with macrofollicular
33
Q

What is follicular carcinoma?

A

Follicular adenoma + capsular and/or vascular INVASION = follicular carcinoma

34
Q

What are the variants of papillary thyroid carcinoma?

A
  1. classic PTC
  2. follicular variant PTC
35
Q

4 Key nuclear features of Papillary Thyroid Carcinoma

A
  1. finely dispersed chromatin - ground glass nuclei
  2. nuclear grooves (coffee beans)
  3. pseudoinclusions
  4. oval nuclei
36
Q

Features of classic PTC

A

4 key features of PTC + well formed papillae with fibrovascular cores

37
Q

Features of follicular variant PTC

A

4 key features of PTC + follicular architecture (no papillae)

38
Q

What is a possible differential diagnosis of follicular variant PTC?

A

follicular carcinoma (will not exhibit the 4 key features of PTC)

39
Q

Features of anaplastic carcinoma

A
  1. cells highly pleomorphic (variation in sizes)
    - giant tumour cells
    - spindle cells
    - small anaplastic cells
  2. pale chromatin
  3. prominent nucleoli
40
Q

Features of medullary carcinoma

A

Cells
- epithelioid or spindled
- salt and pepper chromatin

41
Q

Calcium metabolism mainly occurs at ____

A

bones (25 mol)

42
Q

What are the hormones involved in calcium regulation?

A

parathyroid hormone
vitamin D
calcitonin
adrenal hormones
thyroid hormones
osteoclast activating factor
prostaglandins

43
Q

PTH secretion is controlled by

A
  1. Ionised calcium concentration
  2. 1,25 dihydroxyvitamin D
  3. Magnesium as a co-factor
44
Q

Actions of PTH

A

DIRECT:
Bone - stimulates bone resorption
Kidney
- increase distal nephron calcium reabsorption
- phosphate excretion

INDIRECT:
Kidney - promotes formation of vitamin D
-> vit D promotes reabsorption of calcium from the gut
-> vit D stimulates bone resorption

45
Q

causes of hypercalcaemia

A

1) hyperparathyroidism
- primary
- tertiary
*secondary hyperparathyroidism is physiological

2) malignancy
- bone metastasis -> seeds into the bone and causes bone resorption
- multiple myeloma -> secretes osteoclast activating factor and causes bone resorption
- cancer cells secrete parathyroid hormone related peptide
-> behaves similar to PTH
-> causes humoral hypercalcaemia of malignancy (HHM)

3) Vitamin D Excess
- sarcoidosis
- vit D intoxication

4) milk alkali syndrome

5) immobilisation

6) familial hypocalciuric hypercalcaemia

7) endocrine disorders
- thyrotoxicosis
- Addisons disease

8) drugs
- thiazide diuretics

46
Q

lab investigations:
Increase plasma calcium, decrease plasma phosphate

A

primary hyperparathyroidism
malignancy (HHM)

47
Q

lab investigations:
Increase plasma calcium, increase plasma phosphate

A

malignancy
hypervitaminosis D

48
Q

lab investigations:
decrease plasma calcium, increase plasma phosphate

A

hypoparathyroidism
renal failure (untreated)

49
Q

lab investigations:
decrease plasma calcium, decrease plasma phosphate

A

vitamin D deficiency

50
Q

hyperparathyroidism vs malignancy

A

hyperparathyroidism:
hypercalcaemia <3.5mmol/L
months/years
slow rate of increase of calcium
renal stones common
increase in plasma PTH

malignancy:
hypercalcaemia >3.5mmol/L
weeks/months
rapid rate of increase of calcium
renal stones uncommon
low plasma PTH

51
Q

causes of hypocalcaemia

A

1) hypothyroidism
2) vitamin D deficiency
- malabsorption
- inadequate diet
- poor exposure to sunlight
3) renal disease
- can lead to vit D deficiency because the 1-alpha hydroxylase enzyme found in the kidney
4) pseudohypoparathyroidism

52
Q

adrenal cortex secretes:

A

aldosterone, cortisol, sex hormones

53
Q

adrenal medulla secretes:

A

epinephrine, norepinephrine

54
Q

what condition will lead to Cushing’s disease?

A

benign adenoma of anterior pituitary
-> ant pit produces more ACTH -> produces more cortisol

55
Q

possible causes of Cushing’s syndrome

A
  • ectopic ACTH (benign or malignant) -> some tumour elsewhere releasing ACTH
  • adrenal adenoma or carcinoma (benign or malignant)
  • iatrogenic Cushing’s syndrome (exogenous glucocorticoids)
  • Cushing’s disease
56
Q

in overnight dexamethasone test, failure to suppress is

A

suggestive of Cushing’s syndrome

57
Q

what are the causes of primary hyperaldosteronism?

A
  • adrenal aldosterone producing adenoma
  • idiopathic hyperaldosteronism with bilateral adrenal hyperplasia
58
Q

consequences of primary hyperaldosteronism

A
  • increase Na+ retention
  • increase water retention
    => increase BP
  • increase ECF
    => decrease plasma renin
  • decrease K+
    -> hypokalemia
  • decrease H+
    => metabolic alkalosis
59
Q

phaechromocytoma is the tumour of the

A

adrenal medulla
-> leads to overproduction of catecholamines

60
Q

symptoms and signs of pheochromocytoma

A

hypertension
sweating
tachycardia and palpitations
headache

61
Q

diagnostic tests used to detect catecholamine-secreting tumours

A

serum:
- free unconjugated catecholamines
- metanephrines (24h)

urine:
- free unconjugated catecholamines
- metanephrines (24h)
- VMA (24h)

62
Q

primary causes of chronic adrenal insufficiency (ENTIRE adrenal gland becomes non-functioning)

A
  1. idiopathic adrenal atrophy
  2. granulomatous diseases
    - tuberculosis
    - histoplasmosis
    - sarcoidosis
  3. neoplastic infiltration
  4. haemochromatosis
  5. amyloidosis
  6. post bilateral adrenalectomy
63
Q

secondary causes of chronic adrenal insufficiency (ENTIRE adrenal gland becomes non-functioning)

A
  1. tumours
    - pituitary
    - craniopharyngioma
    - tumour of the 3rd ventricle
  2. pituitary infarction and haemorrhage
    - postpartum necrosis
    - haemorrhage in tumours
  3. granulomatous disease
    - sarcoidosis
  4. post hypophysectomy
  5. prolonged-exogenous steroid administration
64
Q

what are the 2 tests used for Addison’s disease (insufficient cortisol/aldosterone)?

A

Long and Short Synacthen Tests

65
Q

What is the purpose of short synacthen test?

A

an increase in cortisol to >550 nmol/L would rule out Addison’s disease

66
Q

What is the Wolff-Chaikoff effect?

A
  • an autoregulatory phenomenon
  • excess iodine is transported to thyroid gland
  • inhibit thyroid peroxidase enzyme
  • cause decrease synthesis of thyroid hormones
67
Q

Is liothyronine or levothyroxine better for chronic replacement treatment?

A

levothyroxine, because the half life of liothyronine is short and high cost

68
Q

Long term use of high dose L-T4 will cause:

A

increase bone resorption and decrease bone mineral density

69
Q

Who are the special considerations of L-t4 replacement?

A
  1. Pregnant patients
  2. Elderly patients
  3. Patients with Ischemic heart disease
  4. Patients with subclinical hypothyroidism
70
Q

causes of hyperthyroidism

A
  1. graves disease
  2. overactive thyroid gland
  3. increased consumption of iodine
  4. increased consumption of thyroid hormones
  5. inflammation of release of stored thyroid hormones
70
Q

causes of hyperthyroidism

A
  1. graves disease
  2. overactive thyroid gland
  3. increased consumption of iodine
  4. increased consumption of thyroid hormones
  5. inflammation of release of stored thyroid hormones
71
Q

what is the half-life of PTU and carbimazole?

A

PTU: 75 mins
carbimazole: 4-6h

72
Q

Contraindication of using iodide for hyperthyroidism treatment

A

Pregnancy: avoid use in pregnant/breastfeeding women to avoid causing fetal goitre

m2 CA2 (22 decks)

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