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

L14~15 – Pathology of Endocrine Disorders Flashcards

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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?

Study These Flashcards
A

central obesity, hirsutism, hypertension, diabetes, osteoporosis

  • Cortical adenoma
  • Secondary to pituitary hypersecretion of ACTH
  • Iatrogenic by ACTH or steroid admin.
25
Which layer of the adrenal gland is affected in Conn's syndrome? Effect?
Cortical adenoma in Zona glomerulosa: mineralocorticoids Autonomous secretion of excess aldosterone>> primary hyperaldosteronism:  Renal retention of Na+  Loss of K+ >> Electrolyte disturbance
26
Histological appearance of cortical adenoma in adrenal cortex?
Very typical endocrine histology  Arranged in packets in a vascularized background  Central regular nuclei  Pale to clear, granular cytoplasm
27
Clinical presentation of pheochromocytoma? Give one fatal complication?
hypertension, tachycardia, palpitations, headache, sweating, tremor, sense of apprehension Malignant hypertension + vasoconstriction>> myocardial infarct
28
Explain why pheochromocytoma is called a "10% tumour"?
 10% extra-adrenal (along aorta)  10% sporadic tumors are bilateral  10% biologically malignant (defined by presence of metastasis)  10% not associated with hypertension
29
What is the key Dx test for pheochromocytoma?
Increased urine catecholamines, vanillylmandelic acid
30
Gross morphology of pheochromocytoma?
◦ Pale gray or brown, ◦ Hemorrhage, necrosis, cystic change
31
Histological feature of Pheochromocytoma?
◦ Zellballen, trabecular or solid pattern ◦ POLYGONAL or spindle cells + RICHLY VASCULARIZED BACKGROUND ◦ Finely basophilic or amphophilic GRANULAR cytoplasm "Dirty Blue"
32
Mechanism of aldosterone?
glomerular perfusion (e.g. low BP) >> stimulates renin-angiotensin system >> secrete aldosterone (retains Na+, water) >> brings BP back to normal
33
List 2 neoplasms from adrenal cortex, 2 from medulla?
Cortex: Adenoma and carcinoma Medulla: Pheochromocytoma and Neuroblastoma
34
Adrenal adenoma affect children more, whereas adrenal carcinoma affect adults more. T or F?
False  In adults: adenomas, carcinomas  In children: carcinoma predominates
35
Etiology, gross and histological appearance of adrenal medulla neuroblastoma?
infants, children (most before the age of 3) Grossly: soft, lobulated Histologically: small blue round cell tumor, undifferentiated
36
How to ddx lymphoma at adrenal gland vs neuroblastoma?
need immunophenotyping to distinguish
37
Normal histology of thyroid gland?
 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
Causes of thyroid hyperplasia?
1) Iodine deficiency** 2) GOITROGEN 3) Hereditary defect in enzyme synthesis >> Compensatory increase in TSH, growth of follicular cells and increase T3,T4
39
2 stages of thyroid hyperplasia?
1. Hyperplastic stage (enlarged follicles filled with colloid) 2. Colloid involution
40
Clinical presentation of multinodular goiter?
1) EUTHYROID / subclinical hyperthyroidism 2) Toxic or non-toxic 3) Compression on trachea, larynx 4) ASYMMETRICAL LOBES on neck
41
Histological appearance of multinodular goitre?
VARIABLE- SIZED FOLLICLES with FIBROSIS HEMORRHAGE into colloid cystic change, calcification Glassy appearance
42
Outline 1 benign and 4 malignant thyroid neoplasms?
Follicular adenoma (benign) ``` Malignant: ◦ Papillary carcinoma***common*** ◦ Follicular carcinoma ◦ Anaplastic carcinoma ◦ Medullary carcinoma (parafollicular cell origin) ```
43
Follicular adenoma leads to hyperthyroidism. T or F?
Most are non-functional = no hyperthyroidism
44
Histological appearance of thyroid follicular adenoma?
- ENCAPSULATED nodule, well-circumcised mass - Follicles + MICROFOLLICLES with colloid - Mild cytological atypia - No capsular or vascular invasion** - No papillary carcinoma features
45
Risk factor, peak age of incidence, prognostic factors of Papillary adenoma of thyroid?
 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
CLinical symptoms of papillary carcinoma of thyroid?
 ASYMPTOMATIC thyroid nodules (appear as multifocal tumors)  Lymphatic spread to CERVICAL LYMPH NODES  Late: hoarseness, dysphagia, cough, dyspnea
47
Histological features of thyroid papillary carcinoma?
 PSEUDONUCLEAR INCLUSIONS (pink globule in nucleus)  NUCLEAR GROOVES  PAPILLARY STRUCTURE  PSAMOMMA bodies (= calcified bodies)  Overlapping ground-glass nuclei  Multinucleated giant cells
48
2 differences between the behavior of follicular carcinoma and papillary carcinoma of thyroid?
papillary carinoma = lymphatic spread, no capsule or vascular invasion Follicular carcinoma = hematogenous metastasis (to bone, liver, lungs), invasion into capsule
49
Histological features of follicular carcinoma?
(Same as Follicular Adenoma:) ◦ Encapsulated ◦ Colloid-containing follicles and microfollicles ◦ Cytological atypia Ddx from Follicular adenoma: ◦ CAPSULAR/ VASCULAR INVASION
50
Age of onset, preceding condition, prognosis of anaplastic/ undifferentiated carcinoma of thyroid?
Mean age: 65 years (elderly) Preceding / concurrent well-differentiated thyroid carcinoma (e.g. papillary, follicular carcinoma) Bad prognosis: mortality rate approaches 100%
51
Histological appearacne of anaplastic carcinoma of thyroid?
markedly pleormorphic cells / spindle cells / squamoid cells
52
Histology of medullary carcinoma of thyroid?
No follicles, no colloid, no carcinoma features Loss of architecture
53
Cell of origin and 2 types of medullary carcinoma?
parafollicular (C) cells 70% = sporadic 30% = multiple endocrine neoplasia (MEN) syndrome
54
Define MEN syndrome?
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
Define the defective gene in MEN1 and neoplasia caused?
MEN 1 (Wermer Syndrome) MEN1 encoding MENIN  Pituitary tumor (frequently prolactinoma)  Parathyroid hyperplasia / adenoma  Pancreas endocrine tumour: islet cell tumours
56
Define the defective gene in MEN2A and 2B and compare the neoplasms caused?
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
Treatment and dx for MEN syndromes?
surgical intervention diagnose with molecular technologies (genetic test + genetic counselling)
58
General treatment of endocrine carcinoma?
- Surgical removal - Radiation ablation - Hormone replacement - Monitoring for recurrence

MBBS II ERS (37 decks)

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