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Block 10 Week 2 > Endocrine Pathology Adrenals-Usera > Flashcards

Endocrine Pathology Adrenals-Usera Flashcards

1
Q

What are the three layers to the adrena cortex from outside in?

A

Zona glomerulosa
Zona Fasciculata
Zona Reticularis
Medulla

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2
Q

What does the Zona Glomerulosa do?

A

secretes mineralcorticoids-> aldosterone

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3
Q

What does the Zona Fasciculata do?

A

secretes glucocorticoids-> cortisol

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4
Q

What does the zona reticularis do?

A

secretes sex hormones

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5
Q

What is the adrenal medulla derived from and wht does it produce?

A

derived from neural crest cells

catecholamie production

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6
Q

How do you make epinephrine?

A

Tyrosine-> Dihydroxphenylalanine (DOPA)-> Dopamine-> Norepinephrine-> epinephrine

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7
Q

Corticol hormones are derived from (blank)

A

cholesterol

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8
Q

What are the three ways you can get adrenocotical hypofunction?

A
  • acute adrenocortical insufficiency
  • chronic adrenocortical insufficiency (addison’s disease)
  • adrenogenital syndrome (congenital adrenal hyperplasia)
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9
Q

What is the most common way to get acute adrenocortical insufficiency?

A

-abrupt withdrawal of corticosteroids

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10
Q

What are the three ways you can get acute adrenocortical insufficiency?

A
  • abrupt withdrawal of corticosteroids
  • anticoagulation therapy (causes hemorrhage)
  • Waterhouse-Friderichesen Syndrome (causes hemmorhage)
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11
Q

How will acute adrenocortical insufficiency due to abrupt withdrawal of corticosteroids present?

A

weakness and hypotension (shock)

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12
Q

How does Waterhouse-Friderichsen syndrome present?
How do you die form this?
What causes this?

A
  • bilateral hemorrhagic necrosis of the adrenal glands
  • lack of cortisol exacerbates hypotension that leads to death
  • Neisseria meningitidis infection that caues DIC in young children
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13
Q 
What is this:
Bilateral adrenal hemorrhage
A/W Neisseria meningitidis septicemia
Endotoxic shock with DIC
Adrenal Insufficiency
A

Waterhouse-Friderichsen Syndrome

acute adrenocortical insufficiency

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14
Q

(blank) percent of chronic adrenocrotical insufficiency is due to an autoimmune problem

A

80%

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15
Q

(blank) is the most common cause of chronic adrenocortical insuffiency in the developing world

A

TB

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16
Q

What are the causes of chronic adrenocortical insufficiency?

A
  • Autoimmune (80%)
  • Infectious
  • Adrenogenital Syndrome
  • Metastases (Lung cancer and RCC)
  • AIDS
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17
Q

What are the infectious causes of chronic adrenocortical insufficiency?

A
  • TB

- Histoplasmosis

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18
Q

What are the types of cancer that metastasize into the adrenal glands and cause chronic adrenocortical insuffiency?

A
  • Lung cancer

- RCC

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19
Q

What are the clinical findings of chronic adrenal insufficiency?

A

-weakness
-hypotension
-hyperpigmentation
(increase ACTH stimulates melanocytes)
-vomiting
-diarrhea

I.e think lack of aldosterone and increase of ACTH.

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20
Q

What are the lab findings of chronic adrenal insufficiency?

A
  • hyponatremia
  • hypovolemia
  • hyperkalemia
  • metabolic acidosis
  • fasting hypoglycemia
  • lymphocytosis
  • Eosinophilia
  • Neutropenia
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21
Q

Why would chornic adrenal insuffiency cause eosinophilia and hypoglycemia?

A

Cortisol is gluconeogenic and sequesters eosinophils in lymph nodes so when you lose cortisol you will have lymphocytosis and hypoglycemia :)

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22
Q

How can you diagnosis chronic adrenal insufficiency?

A
  • Give a ACTH stimulation test-> if adrenal insufficient, shoud result in no increase of cortisol or aldosterone
  • Give metyrapone test-> if adrenal insufficient should result in increase of ACTH and no increase in 11-deoxycortisol
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23
Q

What are adrenogenital syndromes (congenital adrenal hyperplasia?

A

Autosomal recessive disorders of adrenal biosynthetic enzymes

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24
Q

What is the most common cause of adrenogenital syndrome?

A

21-hydroxylase deficiency (90-95% of cases)

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25
Q

What happens in 21 hydroxylase deficiency?

A

aldosterone and cotisol are decreased and androgens are increased.

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26
Q

What is the classic form of 21 hydroxylase deficiency?

A

Presents in neonates as hyponatremia, hyperkalemia, and hypovolemia w/ life-threatening hypotension (due to salt-wasting)
Females have clitoral enlargement (genital ambiguity)

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27
Q

What is the nonclassic form of 21 hydroxylase deficiency?

A

-nonclassic form presents later in life with androgen excess leading to precocious puberty (males) or hirsutism w/ menstrual irregularities (females)

28
Q

What happens in 11 hydroxylase deficiency?

A

Biochemically similiar to 21 hydroxylase deficiency i.e no cortisol and no aldosterone BUT has some weak mineralcorticode production (Deoxycortisone)

29
Q

What will 11 hydroxyase deficiency lead to?

A

HTN w/ sodium retention w/ mild hypokalemia (due to DIC)

-low renin and aldosterone

30
Q

What happens in 17 hydroxylase deficiency?

A

decreased cortisol and androgens! But slight increase in mineralcorticoids (DOC)

31
Q

What will 17 hydroxylase lead to?

A
  • HTN
  • mild hypokalemia
  • renin and aldosterone are low
  • decrease in glucocorticoids
  • decreased androgens
  • salt retainers
32
Q

Since 17-hyrdroxylase causes low androgens, what does this cause?

A

Females: delayed menarche (primary amenorrhea) delyed secondary sexual characteristis (lack of pubic hair)
Males: pseudohermaphroditism

33
Q

How do you screen for adrenogenital syndrome (congenital adrenal hyperplasia)?

A

-serum 17 hydroxyprogesterone production

34
Q

If you have 21 or 11 hydroxylase deficiency how will your serum 17 hydroxyprogesterone levels look?

35
Q

If you have 17 hydroxylase deficiency how will your serum 17 hydroxyprogesterone levels look?

36
Q

If you ambiguous genitalia what is indicated?

A

chromosomal analysis

37
Q

Which deficiencies cause this:
precocious puberty in males, and females
Rapid growth as children, but short stature as adults

A

21-hydroxylase deficiency

11-hydroxylase deficiency

38
Q

What will all adrenogenital syndromes cause?

A

increased ACTH and accumulation of precursors proximal to enzyme block

  • increased 17-ketosteroids
  • testosterone
39
Q

What is the workup for ambiguous genitalia?

A
  • Clitoris hypertrophy
  • Poor development of labial structure
  • No palpable gonad
40
Q

What are the causes of cushing syndrome?

A

excess cortisol

  • prolonged corticosteroid use
  • Cushing disease
  • hyperfunctional adrenal adenoma
  • ectopic ACTH production
41
Q

What is cushings disease?

A

excess ACTH causing increase cortisol due to an ACTH adenoma

42
Q

What causes hyperaldosteronism?

A

Conn’s syndrome and hyperfunctional adrenal adenomas

43
Q

What are the clinical findings of cushing’s syndrome and what causes them?

A
  1. muscle weakness w/ thin extremities
  2. moon facies, buffalo hump, truncal obestiy
  3. Abdominal striae
  4. HTN often with hypokaemia and metabolic acidosis
  5. Osteoporosis
  6. Immune suppresion
  7. hirstuitism-increased androgens
44
Q

Why does cushings syndrome cause muscle weakness?

A

cortisol break down muscle to prdoduce AAs for gluconeogenesis

45
Q

Why does Cushings syndrome cause moon facies, buffalo hump, and truncal obesity?

A

due to high insulin (caused by increased gluucose) causes increase storage of fat centrally

46
Q

Why does cushings syndrome cause Abdominal striae?

A

due to impaired collagen synthesis resulting in thinning of the skin

47
Q

Hypercortisolism (Cushings syndrome)

A
  • high cortisol increase sensitivity of peripheral vessels to catecholamines,
  • at very high levels, cortisol cross-reacts w/ mineralcorticoid receptors (aldosterone is not increased)
48
Q

What is THE test for cushing’s disease?
What are the other tests?
What are the lab findings of cushings disease?

A

increased free cortisol
-dexamethosone suppression test
(low dose cannot suppress cortisol, High dose can suppress in CUSHINGS DISEASE, but not ino ther types)

Lab findings

  • HYperglycemia
  • Hypokalemic metabolic alkalosis (increased aldosterone, retaining more sodium and getting rid of more potassium)
49
Q

Low dose dexamethasone suppresses cortisol in (blank) individuals but faits to suppress cortisol in all causes of (blank)

A

normal

Cushings syndrome

50
Q

What can plasma ACTH distinguish?
What should you do if it is independent?
Dependent?

A

b/w ACTH dependent causes and ACT indepenent causes of cushing syndrome.

  • Independent- CT to look for adrenal lesion
  • Dependent- High dose dexamethasone test
51
Q

What will a high dose dexamethasone test suppress?

A

ACTH production by a pituitary adenoma (serum cortisol is lowered) but does not suppress ectopic ACTH production (serum cortisol remains high)
i.e tells you if you have a pituitary adenoma (cushings disease)

52
Q

What is Conn’s syndrome?

A

an aldosterone secreting adrenal adenoma

53
Q

What are the clinical findings of hyperaldosteronism?

A
  • diastolic HTN

- muscle weakness

54
Q

What are the lab findings of hyperaldosteronism?

A
  • hypernatremia, hypokalemia, alkalosis

- decreased plasma renin

55
Q

What causes adrenal medullary hyperfunction?

A

pheochromocytoma

neuroblastom

56
Q

What is a tumor of chromoaffin cells that secretes catecholamines from the medulla (epo and norepi)?

A

Pheochromocytoma

57
Q

What is the rule of 10’s?

A

Describes pheochromocytoma
10% bilateral
10% malignant
10% extramedullary (paraganglioma – only produce norepi. No phenylethamin-n-methyltransferase)

58
Q

What is pheochromocytoma associated with?

A

NF-1
MEN IIA and IIB
Von Hippel Lindau Syndrome

59
Q

What are the clinical findings of pheochromocytoma?

A
  • paroxysmal and/pr sustained systolic HTN w/ palpitations
  • headache
  • sweating
  • anxiety
  • chest pain
  • orthostatic intolerance
  • constipation
60
Q

How do you diagnose pheochromocytoma?

What are the lab findings of pheochromocytoma?

A
  • plasma free metanephrines (BEST CONFIRMATORY TEST)
  • 24-hour urine metanephrines (best sensitivity)
  • 24-hour urine vma (vanillymendalic acid)
  • No suppression with clonidine
  • Hyperglycemia
  • Neutrophilia
61
Q

How do you treat pheochromocytoma?

What are we worried about with the tx and how do we fix it?

A

Surgically
Catecholamines can leak into bloodstream upon manipulation of the tumor so must use pre-op stabilization with alpha inhibitor and b-blocker to prevent hypertensive crisis

62
Q

What is this:
Malignant neoplasma of post-ganglionic sympathetic neurons
Who is it common in?

A

Neuroblastoma

Children <5 years old

63
Q

What is amplified in neuroblastoma and is a marker of aggressive behavior?

A

N-MYC (20-30% of cases)

64
Q

Neuroblastomas are (Blank) percent metastatic at diagnosis

65
Q

What is the prognosis of neuroblastoma?

A

Good 1 yr old, 1p deletion

66
Q

What will neuroblastoma look like histologically?

A

small round blue cell tumor with humor wright rosettes

67
Q

What will the lab findings be for neuroblastoma?
What will the physical findings be?
What is the prognosis?

A

Increased urine VMA and HVA (vanillylmandelic, acidhomovanillic acid)
Large, palapable abdominal mass
Overall survival =40% depends on prognostic factors

Block 10 Week 2 (7 decks)

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