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thyroid & parathyroid patho Flashcards

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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
Gross morphology of thyroid gland in graves disease
- symmetrical diffuse enlargement - soft, reddish meaty cut suface
26
What are some thyroid neoplasms that are of non-follicular cell origin?
Medullary carcinoma Lymphoma
27
BENIGN thyroid neoplasms of follicular cell origin:
Follicular adenoma Oncocytic adenoma
28
LOW grade MALIGNANT thyroid neoplasms of follicular cell origin:
Papillary thyroid carcinoma Follicular carcinoma
29
HIGH grade MALIGNANT thyroid neoplasms of follicular cell origin:
Poorly differentiated thyroid carcinoma Differentiated high grade thyroid carcinoma
30
UNDIFFERENTIATED MALIGNANT thyroid neoplasms of follicular cell origin:
Anaplastic thyroid carcinoma
31
Morphology of adenoma
- rounded, encapsulated - well demarcated - no capsular/vascular invasion
32
Key features of follicular adenoma
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
What is follicular carcinoma?
Follicular adenoma + capsular and/or vascular INVASION = follicular carcinoma
34
What are the variants of papillary thyroid carcinoma?
1. classic PTC 2. follicular variant PTC
35
4 Key nuclear features of Papillary Thyroid Carcinoma
1. finely dispersed chromatin - ground glass nuclei 2. nuclear grooves (coffee beans) 3. pseudoinclusions 4. oval nuclei
36
Features of classic PTC
4 key features of PTC + well formed papillae with fibrovascular cores
37
Features of follicular variant PTC
4 key features of PTC + follicular architecture (no papillae)
38
What is a possible differential diagnosis of follicular variant PTC?
follicular carcinoma (will not exhibit the 4 key features of PTC)
39
Features of anaplastic carcinoma
1. cells highly pleomorphic (variation in sizes) - giant tumour cells - spindle cells - small anaplastic cells 2. pale chromatin 3. prominent nucleoli
40
Features of medullary carcinoma
Cells - epithelioid or spindled - salt and pepper chromatin
41
Calcium metabolism mainly occurs at ____
bones (25 mol)
42
What are the hormones involved in calcium regulation?
parathyroid hormone vitamin D calcitonin adrenal hormones thyroid hormones osteoclast activating factor prostaglandins
43
PTH secretion is controlled by
1. Ionised calcium concentration 2. 1,25 dihydroxyvitamin D 3. Magnesium as a co-factor
44
Actions of PTH
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
causes of hypercalcaemia
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
lab investigations: Increase plasma calcium, decrease plasma phosphate
primary hyperparathyroidism malignancy (HHM)
47
lab investigations: Increase plasma calcium, increase plasma phosphate
malignancy hypervitaminosis D
48
lab investigations: decrease plasma calcium, increase plasma phosphate
hypoparathyroidism renal failure (untreated)
49
lab investigations: decrease plasma calcium, decrease plasma phosphate
vitamin D deficiency
50
hyperparathyroidism vs malignancy
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
causes of hypocalcaemia
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
adrenal cortex secretes:
aldosterone, cortisol, sex hormones
53
adrenal medulla secretes:
epinephrine, norepinephrine
54
what condition will lead to Cushing's disease?
benign adenoma of anterior pituitary -> ant pit produces more ACTH -> produces more cortisol
55
possible causes of Cushing's syndrome
- 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
in overnight dexamethasone test, failure to suppress is
suggestive of Cushing's syndrome
57
what are the causes of primary hyperaldosteronism?
- adrenal aldosterone producing adenoma - idiopathic hyperaldosteronism with bilateral adrenal hyperplasia
58
consequences of primary hyperaldosteronism
- increase Na+ retention - increase water retention => increase BP - increase ECF => decrease plasma renin - decrease K+ -> hypokalemia - decrease H+ => metabolic alkalosis
59
phaechromocytoma is the tumour of the
adrenal medulla -> leads to overproduction of catecholamines
60
symptoms and signs of pheochromocytoma
hypertension sweating tachycardia and palpitations headache
61
diagnostic tests used to detect catecholamine-secreting tumours
serum: - free unconjugated catecholamines - metanephrines (24h) urine: - free unconjugated catecholamines - metanephrines (24h) - VMA (24h)
62
primary causes of chronic adrenal insufficiency (ENTIRE adrenal gland becomes non-functioning)
1. idiopathic adrenal atrophy 2. granulomatous diseases - tuberculosis - histoplasmosis - sarcoidosis 3. neoplastic infiltration 4. haemochromatosis 5. amyloidosis 6. post bilateral adrenalectomy
63
secondary causes of chronic adrenal insufficiency (ENTIRE adrenal gland becomes non-functioning)
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
what are the 2 tests used for Addison's disease (insufficient cortisol/aldosterone)?
Long and Short Synacthen Tests
65
What is the purpose of short synacthen test?
an increase in cortisol to >550 nmol/L would rule out Addison's disease
66
What is the Wolff-Chaikoff effect?
- an autoregulatory phenomenon - excess iodine is transported to thyroid gland - inhibit thyroid peroxidase enzyme - cause decrease synthesis of thyroid hormones
67
Is liothyronine or levothyroxine better for chronic replacement treatment?
levothyroxine, because the half life of liothyronine is short and high cost
68
Long term use of high dose L-T4 will cause:
increase bone resorption and decrease bone mineral density
69
Who are the special considerations of L-t4 replacement?
1. Pregnant patients 2. Elderly patients 3. Patients with Ischemic heart disease 4. Patients with subclinical hypothyroidism
70
causes of hyperthyroidism
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
causes of hyperthyroidism
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
what is the half-life of PTU and carbimazole?
PTU: 75 mins carbimazole: 4-6h
72
Contraindication of using iodide for hyperthyroidism treatment
Pregnancy: avoid use in pregnant/breastfeeding women to avoid causing fetal goitre

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