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patho II > Endocrine system I (b) > Flashcards

Endocrine system I (b) Flashcards

1
Q

Genetic association of Grave’s diseases?

A

Association with HLA-DR3 and polymorphisms in genes encoding CTLA-4 and PTPN22

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2
Q

most common casue of Hyperthyroidism?

A

Grave’s disease

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3
Q

Garve’s diseases coexists with what diseases?

A

SLE, Pernicious Anaemia (Autoimmune gastritis), DM-t1 and Addison’s disease

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4
Q

Pathogensis of Grave’s disease

A

caused by the production of IgG autoantibodies directed against the TSH receptor. These antibodies bind to and activate the receptor, causing the autonomous production of thyroid hormones

IgG: Thyroid stimulating immunoglobulin

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5
Q

Pathogenesis of Graves Opthalamopathy

A

Infiltrative Ophthalmopathy, due to:
1. T-cell activation –> lymphocytic infiltration in the retro-orbital space
2. ↑ cytokines (e.g, TNF-α, IFN-γ) –>Inflammatory oedema and swelling of extra-ocular muscles
3. Accumulation of extra-cellular matrix components
4. ↑ numbers of adipocytes

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6
Q

LAB findings of Grave’s disease + raido-iodine scan

A

1) ↑ serum free T4 and T3
2) ↓ TSH
Radio-iodine scan: increased diffuse radioactive iodine uptake

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7
Q

Macroscopic Features:
* Symmetrical, Diffuse enlargement of the thyroid gland
* Smooth and soft organ
* Intact capsule

Microscopic Findings:
* Diffuse hypertrophy and hyperplasia of the thyroid follicular epithelial cells
* Tall, columnar and crowded epithelial cells
* Small papillae, without fibrovascular cores
* Pale colloid with scalloped margins within the follicular lumen
* Lymphocytes and plasma cells, and germinal
centers

Features of?

A

Grave’s disease

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8
Q

CF of Grave’s disease

A

Triad of Manifestations
1) Thyrotoxicosis (all cases)
2) Infiltrative Ophthalmopathy –> Exophthalmos
(40% of cases)
3) Localised Infiltrative Dermopathy or Pretibial
Myxoedema (minority of cases): Scaly thickening and induration of the skin

*Exophthalamos : protruding eyes

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9
Q

cause of Diffuse & Multi-Nodular Goiter

A

Dietary iodine deficiency

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10
Q

casues of Sporadic Goiter

A
  • Intake of excessive calcium and vegetables
    of the Cruciferae family
  • Hereditary enzymatic defects –> Dyshormogenetic goiter
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11
Q

Pathogenesis of Diffuse Goiter

A

TSH-induced hypertrophy and hyperplasia of thyroid follicular cells –> Diffuse, symmetric enlargement of the gland (Diffuse Goiter)

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12
Q

Pathogenesis of Colloid Goiter

A

Increase in dietary iodine or decrease in
thyroid hormone demands –> Enlarged colloid-rich
gland (Colloid Goiter)

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13
Q

Toxic Multi-Nodular Goiter is aka?

A

Plummer Syndrome

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14
Q

CF of Plummer Syndrome (Toxic Multi-Nodular Goiter)

A

1) Airway obstruction
2) Dysphagia (difficulty swallowing)
3) Compression of large vessels in the neck and
upper thorax (Superior Vena Cava Syndrome)

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15
Q

Progression of Toxic Multi-Nodular Goiter

A

Rarely malignant (5% of cases)

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16
Q

Epi of Toxic Multi-Nodular Goiter (Plumer syndrome

A

females > 60yrs

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17
Q

cause of Toxic Multi-Nodular Goiter (PLummer Syndrome)

A

Development of autonomous nodules

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18
Q

Non-functioning Follicualr Adenomas are asociated with mutations of?

A

RAS or PIK3CA, or presence of
PAX8/PPARG fusion gene

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19
Q

Imaging findings of thyroid Follicular Adenomas

A

1) “warm” or “hot” thyroid nodule –> toxic adenoma
or
2) “Cold” nodules

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20
Q

Macroscopic Features:
* Solitary, spherical lesion
* Well-defined, intact capsule

Microscopic Findings:
* Uniform follicles, containing colloid
* Occasionally, cells with brightly eosinophilic
granular cytoplasm
* Hallmark –> Intact well-formed capsule;

features of?

A

Follicular Adenoma (aka Hürthle Cell Adenoma)

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21
Q

Macroscopic Features:
cut surface: glassy-appearing, Irregular nodules with variable amounts of brown gelatinous colloid; Areas of fibrosis, haemorrhages, calcification and cystic changes

Microscopic Findings:
* Hyperplastic epithelium (early stages)
* Flattened and cuboidal epithelium with
abundant colloid (periods of involution)

features of?

A

Multi-Nodular Goiter (Plummer syndrome)

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22
Q

Histo of Hürthle Cell Adenoma (follicular) vs. Carcinoma

A

Follicular adenoma: intact capsule
Follicular Carcinoma: invades thyroid capsule and vasculature

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23
Q

CF of Follicular Adenomas (Hurthel cell Adenoma)

A
  • Painless nodules
  • Difficulty in swallowing (larger masses)
  • Thyrotoxicosis (toxic adenomas)
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24
Q

prognosis of Follicular Adenomas

A

good prognosis
(Excellent, with no recurrence or
metastatic potential)

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25
Q

The 4 major subtypes of Thyroid Carciomas

A

1) Papillary Carcinoma (>85%)
2) Follicular Carcinoma (5-15%)
3) Anaplastic (Undifferentiated) Carcinoma (<5%)
4) Medullary Carcinoma (5%)

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26
Q

Macroscopic Features:
* Solitary or multifocal lesions
* Variable appearance: Either well-circumscribed
and encapsulated or infiltrative tumors with ill-defined margins
* Possible, areas of fibrosis, calcifications and
cystic changes
* Cut surface: Granular, sometimes with distinct
papillary foci

Microscopic Findings:
* Ground glass or “Orphan Annie eye” nuclei
* Invaginations of the cytoplasm –> Pseudo-inclusions
* Papillary architecture; papillae with dense fibrovascular cores
* Presence of “psammoma bodies”
* Foci of lymphatic invasion

features of?

(Papi and Moma adopted Orphan Annie

A

Papillary carcinoma

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27
Q

CF of Papillary Carcinoma

A

Painless, palpable mass in the neck (lymph node/thyroid)

28
Q

Prognosis of Papillary Carcinoma?

A

Good prognosis (10-year survival –> 95%)

29
Q

Microscopic Findings:
* Unifrom, small follicles

Macroscopic features:
* Invasion of the thyroid capsule and vasculature
* Possible Hemotogenous spread

features of?

A

Follicular Carcinoma

30
Q

Epi of Anaplastic/Undifferentiated carcinomas

A

Older patients > 65yrs
Quarter of patients –> Past history of a well-differentiated carcinoma (folliclar carcinoma)

31
Q

Macroscopic Features:
* Bulky mass
* Rapidly enlarging neck mass –> growth beyond thyroid capsule -> Invasion into adjacent neck structures

Microscopic Findings:
* Populations of highly anaplastic cells:
* Large, pleomorphic giant cells or
* Spindle cells with a sarcomatous appearance or
* Mixed spindle and giant cell lesions
* Foci of papillary or follicular differentiation

features of?

A

Anaplastic Carcinoma

32
Q

CF of Follicular Carcinoma

A
  • presentation as solitary cold thyroid nodules
  • Haematogenous dissemination to the lungs, bones and liver
33
Q

Prognosis of Anaplastic Carcinoma

A

poor prognosis

34
Q

*important

Medullary Carcinoma are associated with (Type of mutation)?

A

MEN 2A and 2B (RET mutations)

35
Q

pathogenesis of Medullary Carcinoma

A

Neuro-Endocrine Neoplasm
–> from Parafollicular “C cells” of the thyroid

* “C cells” –> produce Calcitonin

36
Q

Macroscopic Features:
* Solitary nodule or multiple lesions in both lobes
* Multicentricity, common in familial cases
* Areas of necrosis and haemorrhage and extrathyroidal extension (larger tumours)

Microscopic Findings:
* Sheets of Polygonal cells in the Amyloid stroma
* Multi-centric C cell hyperplasia, in familial cases

features of?

A

Medullary Carcinoma

37
Q

Immunohistochemistry of Medullary Carcinoma

A

Intracytoplasmic Calcitonin positivity

38
Q

CF of Medullary Carcinoma

A

1) Mass in the neck; possible dysphagia or
hoarseness (sporadic cases)
2) Diarrhoea, caused by the secretion of VIP

*VIP : Vasoactive intestinal Peptide

39
Q

Diagnosis of Familial cases of Medullary Carcinoma

A

elevated Calcitonin levels or RET mutations

40
Q

causes of Primary Hyperparathyroidism

A
  • Adenoma [85%-95%]
  • Primary Hyperplasia (diffuse or nodular) [5%-10%]
  • Parathyroid Carcinoma [1%]
41
Q

Genetic predispostion of Primary Hyperparathyroidism

A

MEN-1 and MEN-2A; Germ-line mutations of MEN-1 and RET, respectively

42
Q

cause of Hypercalcaemia

A

1) Hyperparthyroidism (primary, 2,3)
2) Familial Hypercalcaemia
3) Vitamine D toxicity
4) Drugs (Thiazide diuretics)
5) Hypercalcaemia malignancies (Osteolytic metastases, PTH related protein mendiated)
6) Sarcoidosis
7) Immobilisation

43
Q

genetic predispostion of Familial Hypocalciuric Hypercalcaemia

A

Inactivating mutations in the Calcium-Sensing
Receptor Gene (CSRG) (CSRG)

44
Q

Macroscopic Features:
* Well-circumscribed, soft, tan nodule
* Delicate capsule
* *Localisation: Confined to a single gland *

Microscopic Findings:
* Composed predominantly of chief cells
* Rim of compressed, non-neoplastic parathyroid
tissue, at the edges
* Cells with bizarre and pleomorphic nuclei
(endocrine atypia)
* Absence of adipose tissue

Features of?

A

Parathyroid Adenoma (caused by primary Hyperparathyroidisim)

45
Q

Microscopic Findings:
* Chief cell hyperplasia
* Diffuse or multinodular pattern
* Absence of adipose tissue within hyperplastic foci
* “Salt and pepper” like chromatin of the nuclei

Features of?

A

Parathyroid Hyperplasia (caused by Primary Hyperparathyroidism)

46
Q

Macroscopic Features:
* Gray-white, homogenous appearnace

Microscopic Findings:
* Usually uniform; Pleomorphism may be noted
* Nodular or trabecular patterns
* Dense fibrous capsule, around the tumour
* Prominent cellular Atypia

Definitive Criteria for Diagnosis:
* Invasion of surrounding tissues and metastasis

features of?

A

Parathyroid Carcinoma (caused by Primary Hyperparathyroidism)

47
Q

Lab findings of Primary Hyperparathyroidism

A

1) Increased serum ionized calcium (Hypercalcemia)
2) Hypophosphataemia
3) Increased urinary excretion of calcium and phosphate
(Hypercalciuria)

48
Q

CF of Primary Hyperparathyroidism

A
  • Painful bones
  • Renal stones
  • Abdominal groans
  • Psychic moans

* Stones, Bones, Groans, Psychiatric overtones”

49
Q

what is Osteitis Fibrosa Cystica

A

Cystic bone spaces filled w/ Brown fibrous tissue (“Brown tumour”)

50
Q

Osteitis Fibrosa Cystica is composed of?

A

“Brown tumour”:
–> osteoclasts, reactive giant cells and haemorrhagic
debris

51
Q

Osteitis Fibrosa Cystica is assciated with?

A

primary Hyperparathyroidism

52
Q

causes of Secondary Hyperparathyroidism

A

Renal failure

53
Q

patho of Secondary Hyperparathyroidism

A

Chronic renal insufficiency –> Decreased phosphate excretion –> Hyperphosphataemia (↑PO-3) –> Declined serum calcium levels (↓ Ca+2) –> Stimulation of parathyroid gland activity

54
Q

Macroscopic Features:
* Hyperplastic parathyroid glands

Microscopic Findings:
* Increased number of chief cells, in a diffuse or multinodular pattern
* Decreased number of fat cells (Adipose cells)
* Metastatic calcification in many tissues (e.g.
lungs, heart, stomach, blood vessels)

features of ?

A

Secondary Hyperparathyroidism

55
Q

Lab findings of Secondary Hyperparathyroidism

A

Near normal serum calcium levels

56
Q

CF of Secondary Hyperparathyroidism

A

1) Manifestations of Chronic renal failure
2) Metastatic calcification of blood vessels –> Ischaemic damage to skin and other organs (Calciphylaxis)

57
Q

causes of Tertiary Hyperparathyroidism

A

Secondary Hyperparathyroidism ->
increased PTH and Ca+2 (HYpercalcemia)

58
Q

casuses of Hypoparathyroidism

A
  • Surgically removed parathyroids during thyroidectomy
  • Congenital absence of parathyroid glands, in conjunction with thymic aplasia (DiGeorge Syndrome)
59
Q

CF of Hypoparathyroidism

A

1) Tetany [Chvostek’s sign and Trousseau’s sign]
2) Cardiac arrhythmias w/ and characteristic prolonged QT interval in the ECG
3) Increased intracranial pressure
4) Seizures

60
Q

Morphologic Changes in Hypoparathyroidism

A
  • Cataracts
  • Calcifications of the cerebral basal ganglia
  • Dental abnormalities
61
Q

Pseudo-Hypoparathyroidism is aka?

A

Martin-Albright Syndrome

62
Q

casuses of Martin-Albright Syndrome (Pseudo-Hypoparathyroidism)

A

Hereditary disorder, inherited through:
* X-linked dominant genes
* Autosomal dominant genes

63
Q

Lab findings of Pseudo-Hypoparathyroidism (Martin-Albright Syndrome)

A
  • low calcium levels
  • Elevated levels of phosphate and PTH
64
Q

CF of Pseudo-Hypoparathyroidism(Martin-Albright Syndrome)

A
  • Unusual sensations
  • Weakness
  • Easy fatigue
65
Q

Signs and symptoms of Pseudo-Hypoparathyroidism (Martin-Albright Syndrome

A
  • Short stature
  • Round face
  • Short neck
  • Shortened bones in the hands and feet

patho II (29 decks)

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