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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
What happens in 21 hydroxylase deficiency?
aldosterone and cotisol are decreased and androgens are increased.
26
What is the classic form of 21 hydroxylase deficiency?
Presents in neonates as hyponatremia, hyperkalemia, and hypovolemia w/ life-threatening hypotension (due to salt-wasting) Females have clitoral enlargement (genital ambiguity)
27
What is the nonclassic form of 21 hydroxylase deficiency?
-nonclassic form presents later in life with androgen excess leading to precocious puberty (males) or hirsutism w/ menstrual irregularities (females)
28
What happens in 11 hydroxylase deficiency?
Biochemically similiar to 21 hydroxylase deficiency i.e no cortisol and no aldosterone BUT has some weak mineralcorticode production (Deoxycortisone)
29
What will 11 hydroxyase deficiency lead to?
HTN w/ sodium retention w/ mild hypokalemia (due to DIC) | -low renin and aldosterone
30
What happens in 17 hydroxylase deficiency?
decreased cortisol and androgens! But slight increase in mineralcorticoids (DOC)
31
What will 17 hydroxylase lead to?
- HTN - mild hypokalemia - renin and aldosterone are low - decrease in glucocorticoids - decreased androgens - salt retainers
32
Since 17-hyrdroxylase causes low androgens, what does this cause?
Females: delayed menarche (primary amenorrhea) delyed secondary sexual characteristis (lack of pubic hair) Males: pseudohermaphroditism
33
How do you screen for adrenogenital syndrome (congenital adrenal hyperplasia)?
-serum 17 hydroxyprogesterone production
34
If you have 21 or 11 hydroxylase deficiency how will your serum 17 hydroxyprogesterone levels look?
increased
35
If you have 17 hydroxylase deficiency how will your serum 17 hydroxyprogesterone levels look?
decreased
36
If you ambiguous genitalia what is indicated?
chromosomal analysis
37
Which deficiencies cause this: precocious puberty in males, and females Rapid growth as children, but short stature as adults
21-hydroxylase deficiency | 11-hydroxylase deficiency
38
What will all adrenogenital syndromes cause?
increased ACTH and accumulation of precursors proximal to enzyme block - increased 17-ketosteroids - testosterone
39
What is the workup for ambiguous genitalia?
- Clitoris hypertrophy - Poor development of labial structure - No palpable gonad
40
What are the causes of cushing syndrome?
excess cortisol - prolonged corticosteroid use - Cushing disease - hyperfunctional adrenal adenoma - ectopic ACTH production
41
What is cushings disease?
excess ACTH causing increase cortisol due to an ACTH adenoma
42
What causes hyperaldosteronism?
Conn's syndrome and hyperfunctional adrenal adenomas
43
What are the clinical findings of cushing's syndrome and what causes them?
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
Why does cushings syndrome cause muscle weakness?
cortisol break down muscle to prdoduce AAs for gluconeogenesis
45
Why does Cushings syndrome cause moon facies, buffalo hump, and truncal obesity?
due to high insulin (caused by increased gluucose) causes increase storage of fat centrally
46
Why does cushings syndrome cause Abdominal striae?
due to impaired collagen synthesis resulting in thinning of the skin
47
Hypercortisolism (Cushings syndrome)
- high cortisol increase sensitivity of peripheral vessels to catecholamines, - at very high levels, cortisol cross-reacts w/ mineralcorticoid receptors (aldosterone is not increased)
48
What is THE test for cushing's disease? What are the other tests? What are the lab findings of cushings disease?
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
Low dose dexamethasone suppresses cortisol in (blank) individuals but faits to suppress cortisol in all causes of (blank)
normal | Cushings syndrome
50
What can plasma ACTH distinguish? What should you do if it is independent? Dependent?
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
What will a high dose dexamethasone test suppress?
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
What is Conn's syndrome?
an aldosterone secreting adrenal adenoma
53
What are the clinical findings of hyperaldosteronism?
- diastolic HTN | - muscle weakness
54
What are the lab findings of hyperaldosteronism?
- hypernatremia, hypokalemia, alkalosis | - decreased plasma renin
55
What causes adrenal medullary hyperfunction?
pheochromocytoma | neuroblastom
56
What is a tumor of chromoaffin cells that secretes catecholamines from the medulla (epo and norepi)?
Pheochromocytoma
57
What is the rule of 10's?
Describes pheochromocytoma 10% bilateral 10% malignant 10% extramedullary (paraganglioma – only produce norepi. No phenylethamin-n-methyltransferase)
58
What is pheochromocytoma associated with?
NF-1 MEN IIA and IIB Von Hippel Lindau Syndrome
59
What are the clinical findings of pheochromocytoma?
- paroxysmal and/pr sustained systolic HTN w/ palpitations - headache - sweating - anxiety - chest pain - orthostatic intolerance - constipation
60
How do you diagnose pheochromocytoma? | What are the lab findings of pheochromocytoma?
- 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
How do you treat pheochromocytoma? | What are we worried about with the tx and how do we fix it?
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
What is this: Malignant neoplasma of post-ganglionic sympathetic neurons Who is it common in?
Neuroblastoma | Children <5 years old
63
What is amplified in neuroblastoma and is a marker of aggressive behavior?
N-MYC (20-30% of cases)
64
Neuroblastomas are (Blank) percent metastatic at diagnosis
70%
65
What is the prognosis of neuroblastoma?
Good 1 yr old, 1p deletion
66
What will neuroblastoma look like histologically?
small round blue cell tumor with humor wright rosettes
67
What will the lab findings be for neuroblastoma? What will the physical findings be? What is the prognosis?
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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