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MBBS II ERS > L14~15 – Pathology of Endocrine Disorders > Flashcards

L14~15 – Pathology of Endocrine Disorders Flashcards

1
Q

List the eosinophilic cells in the pituitary gland + their secretion?

A

1) Somatotrophs =Growth hormone (GH)

2) Lactotrophs = Prolactin

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2
Q

List the basophilic cells in pituitary and their secretion?

A

1) Corticotrophs =Adrenocorticotropic hormone (ACTH)
2) Thyrotrophs = Thyroid-stimulating hormone (TSH)
2) Gonadotrophs = Follicle-stimulating hormone (FSH) and luteinizing hormone (LH)

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3
Q

How to define pituitary adenoma based on size?

A

macroadenoma (>1cm) vs. microadenoma (<1cm)

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4
Q

Which cell types are most commonly affected in Pituitary adenoma?

A

Lactotrophs
Somatotrophs
Corticotrophs

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5
Q

Describe the histological organization of pituitary adenoma?

A
  • POLYGONAL cells with round nucleus, arranged in sheets / cords
  • GRANULAR cytoplasm with rich vasculature
  • rare mitotic figures, little pleomorphism
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6
Q

Name the immunostain used for pituitary adenoma?

A

Synaptophysin = endocrine marker

Can use antibody for prolactin, growth hormone etc.

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7
Q

List some causes of hypopituitarism?

A

 Tumor / mass lesion (compresses on pituitary fossa)

 Surgery / radiation

 Trauma

 Ischemic necrosis, Sheehan syndrome (associated with pregnancy)

Infection/inflammation

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8
Q

Cell types in the endocrine component of pancreas?

A

◦ Islets of Langerhans

> > β, α, δ (somatostatin), and PP (pancreatic polypeptide)cells

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9
Q

Disease caused by hypofunctional pancreas?

A

Diabetes mellitus

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10
Q

How does DM affect glucose, protein and lipid metabolism?

A

Increase lipolysis
Decreased protein synthesis, increase proteolysis
Overproduction of glucose, failure of glycogenesis

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11
Q

3 histological features of pancreatic cells in DM?

A

◦ Low number, smaller islets**

◦ Leukocytic infiltrates** in the islets (insulitis): T lymphocytes and eosinophils

◦ Amyloid deposition** within islets, around capillaries and between cells (type 2 diabetes )

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12
Q

Name 4 hyperfunctional pancreatic disease and list one complication each?

A

islet cell tumors:

Insulinoma > hypoglycaemia

Gastrinoma > Severe peptic ulcer (Zollinger-Ellison Syndrome)

Glucagonoma > Secondary diabetes

VIP-oma >Watery diarrhea

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13
Q

Histological appearance of islet cell tumours of pancreas?

A

 Arranged in ribbons, anastomosing trabeculae

 Richly vascularized background (capillaries)

 Monotonous: round nuclei, fine chromatin, granular eosinophilic cytoplasm

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14
Q

Define the 3 layers and respective secretions in the adrenal cortex?

A

Superficial to deep:

◦ Zona glomerulosa (mineralocorticoids)

◦ Zona fasciculata (glucocorticoids)

◦ Zona reticularis (sex steroids)

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15
Q

Compare the embryonic origin between adrenal medulla and cortex?

A

Cortex = mesoderm

Medulla = neural crest&raquo_space; part of sympathetic nervous system

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16
Q

Cell types and function of adrenal medulla?

A

chromaffin cells and sympathetic nerve endings

synthesize and secrete catecholamines, mainly epinephrine, some NE

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17
Q

Difference between primary and secondary adrenal gland hypofunction?

A

Primary (etiology resides in adrenal gland itself) vs.

secondary (etiology resides higher up in the axis, e.g. hypothalamus, pituitary)

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18
Q

List 2 adrenal gland hypofunctional diseases?

A

Waterhouse-Friderichsen Syndrome = acute primary insufficiency

Addison Disease = primary chronic adrenocortical insufficiency

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19
Q

Pathogenesis of Waterhouse-Friderichsen Syndrome?

A

Acute primary insufficiency:

Overwhelming / fulminant bacterial infection

> > hypotension, shock, DIC

> > massive adrenal hemorrhage, necrosis

> > adrenocortical insufficiency

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20
Q

List causes of Addison disease/ primary chronic adrenocortical insufficiency?

A

◦ Autoimmune adrenalitis**

◦ Tuberculosis & infections

◦ Amyloidosis

◦ Metastatic cancers

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21
Q

How does AMyloidosis lead to Addison disease?

A

abnormal systemic/nonspecific extracellular matrix deposition (e.g. renal, adrenal)

> > replaces normal tissue, removes normal function of adrenal gland

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22
Q

List 4 hyperfunctional adrenal gland diseases?

A

◦ Hyperplasia
◦ Cortical adenomas
◦ Pheochromocytoma

Secondary aldosteronism

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23
Q

Which layer of the adrenal cortex is affected in Cushing’s syndrome?

A

Zona fasciculata: glucocorticoids

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24
Q

Clinical presentation and causes (3) of Cushing’s syndrome?

A

central obesity, hirsutism, hypertension, diabetes, osteoporosis

  • Cortical adenoma
  • Secondary to pituitary hypersecretion of ACTH
  • Iatrogenic by ACTH or steroid admin.
25
Q

Which layer of the adrenal gland is affected in Conn’s syndrome? Effect?

A

Cortical adenoma in Zona glomerulosa: mineralocorticoids

Autonomous secretion of excess aldosterone» primary hyperaldosteronism:

 Renal retention of Na+  Loss of K+
» Electrolyte disturbance

26
Q

Histological appearance of cortical adenoma in adrenal cortex?

A

Very typical endocrine histology

 Arranged in packets in a vascularized background
 Central regular nuclei
 Pale to clear, granular cytoplasm

27
Q

Clinical presentation of pheochromocytoma? Give one fatal complication?

A

hypertension, tachycardia, palpitations, headache, sweating, tremor, sense of apprehension

Malignant hypertension + vasoconstriction» myocardial infarct

28
Q

Explain why pheochromocytoma is called a “10% tumour”?

A

 10% extra-adrenal (along aorta)

 10% sporadic tumors are bilateral

 10% biologically malignant (defined by presence of metastasis)

 10% not associated with hypertension

29
Q

What is the key Dx test for pheochromocytoma?

A

Increased urine catecholamines, vanillylmandelic acid

30
Q

Gross morphology of pheochromocytoma?

A

◦ Pale gray or brown,

◦ Hemorrhage, necrosis, cystic change

31
Q

Histological feature of Pheochromocytoma?

A

◦ Zellballen, trabecular or solid pattern

◦ POLYGONAL or spindle cells + RICHLY VASCULARIZED BACKGROUND

◦ Finely basophilic or amphophilic GRANULAR cytoplasm “Dirty Blue”

32
Q

Mechanism of aldosterone?

A

glomerular perfusion (e.g. low BP)

> > stimulates renin-angiotensin system

> > secrete aldosterone (retains Na+, water)

> > brings BP back to normal

33
Q

List 2 neoplasms from adrenal cortex, 2 from medulla?

A

Cortex: Adenoma and carcinoma

Medulla: Pheochromocytoma and Neuroblastoma

34
Q

Adrenal adenoma affect children more, whereas adrenal carcinoma affect adults more. T or F?

A

False

 In adults: adenomas, carcinomas

 In children: carcinoma predominates

35
Q

Etiology, gross and histological appearance of adrenal medulla neuroblastoma?

A

infants, children (most before the age of 3)

Grossly: soft, lobulated

Histologically: small blue round cell tumor, undifferentiated

36
Q

How to ddx lymphoma at adrenal gland vs neuroblastoma?

A

need immunophenotyping to distinguish

37
Q

Normal histology of thyroid gland?

A

 Lobules divided by thin fibrous septa

 Each lobule consists of 20-40 follicles lined by cuboidal to low columnar epithelium: follicular and parafollicular cells

38
Q

Causes of thyroid hyperplasia?

A

1) Iodine deficiency**
2) GOITROGEN
3) Hereditary defect in enzyme synthesis

> > Compensatory increase in TSH, growth of follicular cells and increase T3,T4

39
Q

2 stages of thyroid hyperplasia?

A
  1. Hyperplastic stage (enlarged follicles filled with colloid)
  2. Colloid involution
40
Q

Clinical presentation of multinodular goiter?

A

1) EUTHYROID / subclinical hyperthyroidism
2) Toxic or non-toxic
3) Compression on trachea, larynx
4) ASYMMETRICAL LOBES on neck

41
Q

Histological appearance of multinodular goitre?

A

VARIABLE- SIZED FOLLICLES with FIBROSIS

HEMORRHAGE into colloid

cystic change, calcification

Glassy appearance

42
Q

Outline 1 benign and 4 malignant thyroid neoplasms?

A

Follicular adenoma (benign)

Malignant:
◦ Papillary carcinoma***common*** 
◦ Follicular carcinoma 
◦ Anaplastic carcinoma 
◦ Medullary carcinoma (parafollicular cell origin)
43
Q

Follicular adenoma leads to hyperthyroidism. T or F?

A

Most are non-functional = no hyperthyroidism

44
Q

Histological appearance of thyroid follicular adenoma?

A
  • ENCAPSULATED nodule, well-circumcised mass
  • Follicles + MICROFOLLICLES with colloid
  • Mild cytological atypia
  • No capsular or vascular invasion**
  • No papillary carcinoma features
45
Q

Risk factor, peak age of incidence, prognostic factors of Papillary adenoma of thyroid?

A

 Age of presentation: 25-50 years

 Risk factor: ionizing radiation exposure

Excellent prognosis:
 10-year survival rate >95%
 Prognostic factors: age, stage/metastasis, extrathyroidal extension

46
Q

CLinical symptoms of papillary carcinoma of thyroid?

A

 ASYMPTOMATIC thyroid nodules (appear as multifocal tumors)

 Lymphatic spread to CERVICAL LYMPH NODES

 Late: hoarseness, dysphagia, cough, dyspnea

47
Q

Histological features of thyroid papillary carcinoma?

A

 PSEUDONUCLEAR INCLUSIONS (pink globule in nucleus)
 NUCLEAR GROOVES
 PAPILLARY STRUCTURE
 PSAMOMMA bodies (= calcified bodies)

 Overlapping ground-glass nuclei
 Multinucleated giant cells

48
Q

2 differences between the behavior of follicular carcinoma and papillary carcinoma of thyroid?

A

papillary carinoma = lymphatic spread, no capsule or vascular invasion

Follicular carcinoma = hematogenous metastasis (to bone, liver, lungs), invasion into capsule

49
Q

Histological features of follicular carcinoma?

A

(Same as Follicular Adenoma:)
◦ Encapsulated
◦ Colloid-containing follicles and microfollicles
◦ Cytological atypia

Ddx from Follicular adenoma:
◦ CAPSULAR/ VASCULAR INVASION

50
Q

Age of onset, preceding condition, prognosis of anaplastic/ undifferentiated carcinoma of thyroid?

A

Mean age: 65 years (elderly)

Preceding / concurrent well-differentiated thyroid carcinoma (e.g. papillary, follicular carcinoma)

Bad prognosis: mortality rate approaches 100%

51
Q

Histological appearacne of anaplastic carcinoma of thyroid?

A

markedly pleormorphic cells / spindle cells / squamoid cells

52
Q

Histology of medullary carcinoma of thyroid?

A

No follicles, no colloid, no carcinoma features

Loss of architecture

53
Q

Cell of origin and 2 types of medullary carcinoma?

A

parafollicular (C) cells

70% = sporadic

30% = multiple endocrine neoplasia (MEN) syndrome

54
Q

Define MEN syndrome?

A

Multiple Endocrine Neoplasia(MEN) syndromes

group of genetically inherited diseases

> > proliferative lesions (hyperplasia, adenomas, and carcinomas) of multiple endocrine organs

MULTIFOCAL, MULTIPLE ORGANS, AGGRESSIVE

55
Q

Define the defective gene in MEN1 and neoplasia caused?

A

MEN 1 (Wermer Syndrome)

MEN1 encoding MENIN

 Pituitary tumor (frequently prolactinoma)
 Parathyroid hyperplasia / adenoma
 Pancreas endocrine tumour: islet cell tumours

56
Q

Define the defective gene in MEN2A and 2B and compare the neoplasms caused?

A

Defective gene: RET

Both MEN2A and 2B:

  • Medullary thyroid carcinoma
  • Pheochromocytoma

MEN2A:
- Parathyroid hyperplasia

MEN2B:
- Neuromas/ ganglioneuromas of skin, oral musosa, GIT, Resp. tract, eyes

57
Q

Treatment and dx for MEN syndromes?

A

surgical intervention

diagnose with molecular technologies (genetic test + genetic counselling)

58
Q

General treatment of endocrine carcinoma?

A
  • Surgical removal
  • Radiation ablation
  • Hormone replacement
  • Monitoring for recurrence

MBBS II ERS (37 decks)

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