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STEP 8: EndoRepro PATHOMA FA > Endocrine Associations_PATHOMA > Flashcards

Endocrine Associations_PATHOMA Flashcards

1
Q

What is the #1 cause of ENDOGENOUS CUSHING SYNDROME?

A

CUSHING DISEASE - ACTH-secreting pituitary adenoma

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2
Q

Which causes of CUSHING SYNDROME will there be bilateral adrenal hyperplasia? (BAH)

A
  1. CUSHING DISEASE - ACTH Secreting pituitary adenoma

2. PARANEOPLASTIC ACTH SECRETION (Small cell lung carcinoma, bronchial carcinoids)

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3
Q

DECREASED ACTH (Corticotropin). What are the only 2 possible causes of CUSHING SYNDROME?

A

ACTH-independent CUSHING SYNDROME: Exogenous corticosteroids + adrenal adenoma
Excess cortisol is NOT dependent on a high level of ACTH

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4
Q

INCREASED ACTH (CORTICOTROPIN). What are the only 2 possible causes of CUSHING SYNDROME?

A 
ACTH-DEPENDENT CAUSES: 
Cushing Disease (ACTH-secreting pituitary adenoma) + Ectopic paraneoplastic ACTH secretion by small cell lung carcinoma
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5
Q

Bilateral atrophy of adrenal glands. What cause of Cushing Syndrome am I?

A

EXOGENOUS CORTICOSTEROIDS - MORE COMMON

Non-functioning adenoma of anterior pituitary

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6
Q

UNILATERAL ATROPHY, UNILATERAL HYPERTROPHY of adrenal glands. What cause of Cushing Sydnrome am I?

A

Adrenal Adenoma/hyperplasia/carcinoma

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7
Q

What is the most common type of CONGENITAL ADRENAL HYPERPLASIA?

A

21-beta hydroxylase deficiency

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8
Q

Which type of CAH do you get HYPOTENSION + HYPERKALEMIA?

Which type of CAH do you get HYPERTENSION + HYPOKALEMIA?

A

HYPOTENSION + HYPERKALEMIA - 21-beta hydroxylase deficiency

HTN + HYPOKALEMIA - 11OH-ase and 17-OHase deficiency

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9
Q

Why do you get HTN with 11-OHase deficiency?

A

Bec you still get 11-DEOXYCORTISONE (weak mineralocorticoid) production -> HTN

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10
Q

What is common in all types of CAH?

A

LOW CORTISOL -> Loss of negative feedback -> HIGH ACTH -> Bilateral adrenal hyperplasia

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11
Q

Which types of CAH is there HIGH 17-OH progesterone and which type(s) has LOW 17-OH progesterone?

A

HIGH - 21-OHase, 11-OHase deficiency (shunting towards androgen pathway)
LOW - 17-OHase deficiency (shunting AWAY from androgen/GC pathway, and only towards MC pathway)

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12
Q

What is the most common cause of PRIMARY HYPERALDOSTERONISM

A

CONN SYNDROME (primary adrenal adenoma hypersecreting aldosterone)

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13
Q

What is the most common cause of SECONDARY HYPERALDOSTERONISM in females? in males?

A

FEMALES: FIBROMUSCULAR DYSPLASIA
MALES: ATHEROSCLEROSIS
Both are causes of renovascular HTN

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14
Q

How does one distinguish between PRIMARY and SECONDARY/TERTIARY ADRENAL INSUFFICIENCY in terms of clinical signs?

A

PRIMARY - YES hyperpigmentation, HYPERKALEMIA

SECONDARY/TERTIARY - NO hyperpigmentation, NO Hyperkalemia

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15
Q

What is the most common bacterial organism associated with ACUTE PRIMARY ADRENAL INSUFFICIENCY?

A

NEISSERIA MENINGITIDIS

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16
Q

What is the classic syndrome of ACUTE PRIMARY ADRENAL INSUFFICIENCY

A

WATERHOUES-FRIDERICHSEN SYNDROME

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17
Q

What is the most common cause of CHRONIC PRIMARY ADRENAL INSUFFICIENCY in the Western world?

A

Autoimmune destruction

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18
Q

What is the most common cause of CHRONIC PRIMARY ADRENAL INSUFFICIENCY in the developing world?

A

TB

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19
Q

What is the #1 cause of CUSHING SYNDROME?

A

EXOGENOUS CORTICOSTEROIDS

20
Q

What is the most common tumor of the adrenal medulla in ADULTS?

A

PHEOCHROMOCYTOMA

21
Q

What is the most common tumor of the adrenal medulla in children

A

NEUROBLASTOMA

22
Q

What are the 90%s of PHEOCHROMOCYTOMA?

A

BOAS: Benign, onesided, adrenal only, sporadic

23
Q

In 10% of the HEREDITARY PHEOCHROMOCYTOMA cases, what are the 3 common genetic mutations?

A

**RETgene mutation [proto-oncogene]- MEN2A/MEN2B
VHL
NF-1 gene [RAS oncogene regulator] - neurofibromatosis

24
Q

Name the 3 carcinomas of MEN2A and MEN2B.

A

MEN2A: Medullary carcinoma of thyroid + Pheo + Parathyroid adenoma
MEN2B: “ + “ + ganglioneuroma of oral mucosa

25
Q

VHL increases the risk of which 3 conditions?

A
  1. Renal cell carcinoma (RCC), 3pdel, CLEAR CELL VARIANT (CCC)
  2. Hemangioblastoma of the cerebellum
  3. Pheochromocytoma
26
Q

What are the 3 main clinical features to look out for in PHEOCHROMOCYTOMA? Are PHEO pts volume depleted or volume overloaded?

A

PAROXYSMAL HTN
Cutaneous Pallor
Tachycardia/Palpitations

VOLUME DEPLETED

27
Q

BROWN TUMOR. What should I think of?

A

PHEOCHROMOCYTOMA

28
Q

What is the standard Tx protocol for a PHEOCHROMOCYTOMA Tx?

A

PHENOXYBENZAMINE or -zosins (alpha blockers) -> BETA BLOCKER -> Surgical Resection
Pharmacotherapy given before surgical resection to prevent hypertensive crisis during resection where touch can create a massive surge of E/NE that can be life-threatening

29
Q

Pt comes in with TENDER THYROID. What should be on the top of your Ddx?

A

SUBACUTE GRANULOMATOUS (de QUERVAIN) Thyroiditis

30
Q

40yo pts comes in with a NON-TENDER, hard as wood thyroid with dysphagia + Respiratory compromise. What does the pt MOST likely have?

A

RIEDEL FIBROSING THYROIDITIS

31
Q

80yo pt comes in with NON-TENDER Thyroid with dysphagia + respiratory compromise. What does pt MOST likely have?

A

ANAPLASTIC CARCINOMA

32
Q

Carcinomas generally like to spread to the lymph nodes. What are the 4 carcinoma exceptions to this general principle and likes instead to spread to the BLOOD (hematogenously)?

A

RENAL CELL CARCINOMA
HEPATOCELLULAR CARCINOMA
FOLLICULAR CARCINOMA
CHORIOCARCINOMA

33
Q

Which lab findings particularly distinguish between PRIMARY and SECONDARY HYPERPARATHRYOIDISM?

A

PRIMARY - Excess PTH due to parathryoid adenoma (most common cause) - HYPERCALCEMIA, HYPOPHOSPHATEMIA

SECONDARY - Excess PTH due to chronic renal failure - HYPERPHOSPHATEMIA, binds up free Ca and thus HYPOCALCEMIA

34
Q

Which hyper or hypo parathryoidism has INCREASED ALP? (alkaline phosphatase)

A

PRIMARY/SECONDARY/TERTIARY Hyperparathyroidism - all due to INCREASED PTH -> Increased osteoblast activity -> Increased ALP secretion

35
Q

Ddx of HYPOCALCEMIA + INCREASED PTH

A

SECONDARY HYPERPARATHYROIDISM

PSEUDOHYPOPARATHYROIDISM (end organ resistance to PTH)

36
Q

PERIORAL TINGLING + TROUSSEAU SIGN + CHVOSTEK SIGN

What am I?

A

HYPOPARATHYROIDISM

Trousseau and chvostek due to muscle spasm (tetany) + perioral tingle all due to hypocalcemia

37
Q

What is the genetic defect of PSUEDOHYPOPARATHYROIDISM?

A

Genetic defect of Gs-alpha subunit (downstream mediator of PTH that results in cAMP activation) -> Develops end-organ resistance to PTH

38
Q

What is the inheritance pattern of PSEUDOHYPOPARATHYROIDISM TYPE 1A (ALBRIGHT HEREDITARY OSTEODYSTROPHY)

A

AUTOSOMAL DOMINANT - inherited from mother by imprinting

39
Q

Which PSEUDOHYPOPARATHYROIDISM is inherited from the father?

A

PSEUDOPSEUDOHYPOARATHYROIDISM

40
Q

SHORT STATURE + SHORTENED 4th/5th digits

A

PSEUDOHYPOPARATHYROIDISM (BOTH TYPE 1A + PSEUDOPSUEDO)

41
Q

What are the 2 differences between PSEUDOPSEUDOHYPOPARATHYROIDISM AND PSEUDOHYPOPARATHYROIDISM TYPE 1A?

A

PSEUDOPSEUDO: No end-organ resistance to PTH + Inheritance from father
Type 1A: YES, end-organ resistance to PTH + Inheritance from mother

42
Q

Which type of DIABETES MELLITUS has a stronger genetic predisposition?

A

TYPE II DM

43
Q

Obesity related to Type II DM is related to what aspect of the pathophysiology of NIDDM dvlm?

A

DECREASE IN INSULIN RECEPTORS

44
Q

What is the genetic predisposition factor of TYPE I DM (IDDM)?

A

HLA DR-3, HLA-DR4

45
Q

What are the 3 ways of diagnosing TYPE II DM (NIDDM)?

A

RANDOM GLC >200
FASTING GLC >126
GLC TOLERANCE TEST: GLC>200 2hrs after Glc loading

46
Q

What are the 3 areas of OSMOTIC DAMAGE-mediated by TYPE II DM (NIDDM)?

A
  1. SCHWANN CELLS - No myelin production for PNS -> Peripheral neuropathy
  2. PERICYTES OF RETINAL BV -Weakening of retinal BV wall -> Aneurysm -> Rupture = hemorrhage
  3. LENS - Cataracts

These 3 are locations where insulin is NOT required for cellular Glc uptake.
ALDOSE REDUCTASE converts Glc to SORBITOL -> Induces osmotic damage

STEP 8: EndoRepro PATHOMA FA (7 decks)

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