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Pathology > Endocrine (Pathology) > Flashcards

Endocrine (Pathology) Flashcards

1
Q

Embryology of the parathyroid?

A

superior (4th pharyngeal pouch)

inferior (3rd pharyngeal pouch)

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2
Q

Location of the parathyroid?

A

poles of the thyroid

weight= 30-40 mg/gland (adults)

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3
Q

Most abundant cells in the parathyroid?

A

chief cells –> PTH

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4
Q

Most important stimulus for PTH secretion?

A

Hypocalcemia (–ionized Ca) –> ++PTH

  1. bone (osteoclasts - Ca ++ mobilization)
  2. renal (++ca resorb, PO excretion), 1,25 Vit D3 synthesis (++intestinal Ca absorb)
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5
Q

Age changes in PT?

A

it turns into fat by the age of 35

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6
Q

Hyperparathyroidism causes?

A

primary (MCC adenoma)

secondary (MCC Renal fail)

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7
Q

Features of Primary hyperparathyroidism

A
  1. adenoma (5g, solitary, capsulated, peripheral normal tissue (-fat, +cells)
  2. hyperplasia (1g, 4 glands, -fat, +cells, chief cell hyperplasia)
  3. carcinoma (10g, local invasion, metastasis)
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8
Q

Most important criteria for diagnosis endocrine malignancy?

A

invasion and metastasis

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9
Q

MC manifestation of primary hyperparathyroidism?

A

asymptomatic 90%

++ Serum Ionized Ca

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10
Q

Primary hyperparathyroidism?

A 
(MCC adenoma), 
>50s, F, 
cyclin D1, 
\++PTH-nephrolithiasis
\++Ca
blood(+Ca, +PTH, -PO4)
TX: surgery
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11
Q

10% pts with symptoms?

A

Adenoma:

  1. osteitis fibrosa cystica = brown tumors) (small bones)
  2. nephrolithiasis/nephrocalcinosis (renal)
  3. gallstone, acute pancreatitis, peptic ulcers
  4. seizures
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12
Q

Secondary hyperparathyroidism?

A 
(MCC Renal fail) 
old
hyperplasia
blood(+PO4 --> -- Ca or normal[established renal failure]) --> ++PTH
Tx: treat RF
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13
Q

MCC hypoparathyroidism?

A

surgery (thyroidectomy)

never preserve the parathyroid when removing the thyroid

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14
Q

Clinical features of hypoPT?

A 
Tetany (Trousseau sign, Chovstek's sign)
CNS (seizures, basal ganglia calcification)
EYE: cataracts
CVS: long QT, heart stop in diastole
DENTAL: enamel lost
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15
Q

HypoPT: Surgery

A
  1. – PTH
  2. – Ca
  3. ++ PO4
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16
Q

Pseudo-Pseudo HypoPT

A

Paternal Imprinting GNAS1 protein

All are normal

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17
Q

Pseudo HypoPT

A

End organ resistance
Albright (maternal imprinting)
hypogonadism

++ PTH
– Ca
++ PO4
(like RF)

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18
Q

Adrenal normal anatomy?

A

cortex (G F75% R)
Medulla
Weight: 4g/gland

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19
Q

Adrenal gland changes with stress?

A

acute: – wt (loss of lipid)
chronic: ++wt (hypertrophy, hyperplasia)

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20
Q

Adrenal Medulla cells?

A

chromaffin cells ==> catecholamines (epinephrine)

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21
Q

Stressful states (ER)

A

infection
trauma
surgery
sudden withdrawal of steroid admin

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22
Q

Hyperfunction (hyperAdre)

A
  1. Cushing’s syndrome (++ Cortisol)
  2. HyperAldosterone (++Aldos)
  3. Adrenogenital syndrome (++Androgenic steroid)
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23
Q

Hypofunction (hypoAdre)

Acute

A

“Waterhouse-Friderichsen”
massive bilateral hemorrhage of adrenal glands
- pts with menigococcemia (death)

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24
Q

Hypofunction (hypoAdre)

chronic

A
  1. adrenal defect - Addison’s dis
  2. pituitary defect
  3. hypothalamus defect
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25
Q

Exogenous cause of hypercortisol?

A

MCC - corticosteroid therapy excess

bilateral cortical atrophy

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26
Q

Endogenous cause of hypercortisol?

A
  1. ACTH secreting pituitary micro adenoma
  2. Primary adrenal (adenoma, hyperplasia, carcinoma)
  3. Ectopic ACTH secretions (Small CC Lung)
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27
Q

ACTH secreting pituitary micro adenoma

A 
Cushing's disease
25, F
POMC (skin pigmnt.)
nodular cortical bilateral hyperplasia
\++ACTH 
\++Cortisol
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28
Q

1* Adrenal causes?

A

ACTH indpt. Cushing’s syndrome
Adrenal syndrome
Female
Carcinoma (MC Children)

wt of gland: 300 (Carinoma)

++Cortisol
– ACTH
Atrophy of uninvolved gland

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29
Q

Ectopic ACTH secretions = Paraneoplastic syndrome

A 
Males, 50
smokers
bilateral hyperplasia
\++ACTH
\++Cortisol

Crooke hyaline change (Keratin intermediate)

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30
Q

Clinical course for Cushing’s syndrome?

A

Early: HTN, ++weight, (trunk), moon face, buffalo hump, type 2 atrophy, –muscle mass
Metabolism: ++gluconeogenesis -> 2 DM
Bone: loss of collagen -> resorb -> osteoporosis
Skin: bruise, fragile (striae)
Other: –imune, altered mental status, hirsutism

31
Q

Lab values for Cushing’s syndrome?

A
  1. 24 hr urine free cortisol levels

2. dexamethasone suppression test (PT)

32
Q

What is hyperaldosteronism?

A

++ adosterone

surgical treatable cause of HTN

33
Q

Causes of hyperaldosteronism?

A
  1. primary (adenoma = Conn’s syndrome)

2. secondary (–renal blood flow –>RAS, HTN, DM, Pregnancy)

34
Q

Pregnancy in relation with ++Aldos?

A

estrogen –> ++Renin

35
Q

Genetic markers for primary (Conn’s)?

A 
CYP11B2 (hyperplasia)
Chrimeric gene (fusion of CYP11B2 + CYP11B1)
36
Q

Lab values for primary v.s secondary HyperALD?

A

both ++Aldos

  1. low renin
  2. high renin
37
Q

Etiology for adrenogenital syndrome?

A
  1. part of Cushing’s dis (++ACTH)
  2. primary adrenocortical neaoplasm (MC: carcinoma)
  3. congenital adrenal hyperplasia (enz deficiency)
38
Q

MCC enzyme def in adrenogenital syndrome?

A

21-hydroxylase

39
Q

Genetic marker for adrenogenital syndrome?

A

CYP21A

40
Q

Clinical types of adrenogenital syndrome?

A
  1. Classic
  2. Simple
  3. Non-Classic
41
Q

Classic type syndrome
def?
clinical?

A

def: –glucocorticoid, ++androgen
clinic: salt wasting, acidosis, –BP, CVS collapse –> death
F- phalloid organ
M- normal at birth, salt wasting 1 wk later

42
Q

Simple type syndrome
def?
clinical?

A 
no salt wasting
adrenal hyperplasia
def: -- glucocorticoid, ++ACTH (adrenal hyperplasia)
F- ambiguous genitalia
M- enlarged genitalia
43
Q

Non-Classic type syndrome

clinical?

A

MC

Asymptomatic (hirsutism)

44
Q

Adrenogenital syndrome treatment?

A

glucocorticoids –> –ACTH, –Androgen activity

45
Q

MCC adrenocortical insufficiency?

A

secondary (withdrawal from corticosteroids)

46
Q

Adrenocortical inssuficiency types?

A

Primary (acute, chronic)

Secondary

47
Q

Clinical features of Adrenocortical insufficiency?

A

until 90% of cortical damage
early - weakness, fatigue, anemia, vomit, wt. loss, diarrhea
ACTH-pigmentation (not in secondary)

48
Q

– glucocorticoids?

A 
hypoglycemia
intractable vomiting
abdominal pain
--BP
coma
death
49
Q

Diagnose adrenocortical insufficiency? Exogeneous ACTH?

A

Give exogeneous ACTH

  1. no ++ in cortisol (primary)
  2. ++ cortisol (secondary)
50
Q

Causes of Primary Adrenocortical insufficiency (acute)

A 
Sudden steroid withdrawal
Hemorrhage 
New born –hypoxia, prolonged delivery)
DIC
Bacteremia (Waterhouse- Frideiricsen’s)

Life threatening (coma –> death)

51
Q

Causes of Primary Adrenocortical insufficiency (chronic)

A

Autoimmune (MCC- 70% pts) – Addison’s
Infections- TB, Fungus
Adrenal metastasis
Genetic (AHC)

granuloma (infection)

52
Q

Waterhouse-Friderichsen syndrome

A

MC = children with meningococcemia
Adrenal hemorrhage = uncertain
Histology =hemorrhage starts within medulla later into cortex

53
Q

Adrenocortical Neoplasms

A

Functional / nonfunctional
Adenomas/ carcinoma
How to know functional or not = lab tests only (not by biopsy)

54
Q

Adrenocortical adenoma

A

silent
incidental
small 2.5cm
yellow on cut section (lipid)

55
Q

Adrenocortical carcinoma

A

Functional
Large >20cm
Death in 2 yrs

56
Q

Normal Adrenal Medulla

A
  1. Specialized neural crest (neuroendocrine) cells
  2. Chromaffin cells= brown-black color after exposure to potassium dichromate

Paraganglion system= extra-adrenal Neuroendocrine cells

Synthesize/secrete catecholamines (mainly -Epinephrine or adrenaline)

57
Q

Adrenal Medulla Neoplasms

A
  1. Pheochromocytomas (chromaffin cells)

2. Neuronal (neuroblastoma, ganglioneuromas)

58
Q

Pheochromocytoma

A

Synthesize and release catecholamines (more norepinephrine unlike normal gland)

59
Q

Pheochromocytoma

“rule of 10s”

A 
10% - association with familial syndromes 
10% - extra-adrenal
10% - bilateral
10% - biologically malignant
10% - arise in childhood
60
Q

Average weight of pheochromocytoma?

A

100g

61
Q

Light microscopy of pheochromocytoma?

A

Zellballon pattern = Cells in small nests or alveoli surrounded by a rich vascular network, “salt and pepper” chromatin

62
Q

Electron microscopy of pheochromocytoma?

A

membrane-bound

electron dense granules

63
Q

Immunoreactivity of pheochromocytoma

A
  1. neuronal markers (chromogranin and synaptophysin, NSE) in the chief cells
  2. Sustentacular cells = S-100 protein (marker for schwann cells)
64
Q

Criteria for determining malignancy of pheochromocytoma?

A
  1. No single histologic feature = can predict clinical behavior
  2. Definitive diagnosis of malignancy = metastases
65
Q

Clinical course of pheochromocytoma?

A
  1. dominant deature (HTN)

2. catecholamine cardiomyopathy

66
Q

Laboratory diagnosis (pheochromocytoma)

A
  1. ↑ urinary free catecholamines

2. metabolites = metanephrines, (VMA)

67
Q

Multiple Endocrine Neoplasia Syndromes?

A

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

68
Q

Distinct features of MEN?

A 
more aggressive and recur 
multiple endocrine organs
multifocal
asymptomatic stage of endocrine hyperplasia 
younger age
69
Q

Treatment for MEN 2?

A

prophylactic thyroidectomy

70
Q 
MEN- TYPE 1
MC organ involved?
MC cause of morbidity and mortality?
MC site of gastrinoma?
Other associated lesions?
A

MC organ involved = Primary hyperparathyroidism
MC cause of morbidity/mortality =tumors of the pancreas
MC site of gastrinoma = duodenum
Other associated lesions = carcinoid tumors, thyroid and adrenocortical adenomas, and Lipoma

71
Q

Familial Medullary thyroid cancer

A

In 20% of familial pts. (older age)

72
Q

MEN-1

A

Wermer’s
Pituitary
Parathyroid
Pancreas

Gene: MEN1-TSG (ch11)

73
Q

MEN-2A

A 
Sipple's
Parathyroid
Adrenal (pheochromocytoma)
Thyroid (C-cell hyperplasia, ***Medulalry carcinoma)***
RET gene (gain of function)
74
Q

MEN-2B

A 
no parathyroid
Adrenal (pheochromocytoma)
Thyroid (C-cell hyperplasia, Medulalry carcinoma)
Mucocutaneous ganglioneuromas
**Marfanoid**

RET (ch10)

Pathology (5 decks)

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