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Block X; Week 2-M > Adrenal Path-Usera > Flashcards

Adrenal Path-Usera Flashcards

1
Q

What are the 3 parts of the adrenal cortex? What does each secrete?

A

Capsule (GFR)
Zona Glomerulosa-mineralcorticoids, aldosterone
Zona Fasciculata-glucocorticoids-cortisol
Zona Reticularis-sex hormones

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2
Q

What is the adrenal medulla derived from? What does it secrete?

A

neural crest cells

catecholamines, like NE, Epi

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3
Q

Describe how tyrosine becomes catecholamines?

A

Tyrosine–>DOPA–>dopamine->NE–>Epi

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4
Q

What are 3 forms of adrenocortical insufficiency?

A

Acute adrenocortical insufficiency
Chronic adrenocortical insufficiency (Addison’s disease)
Adrenogenital syndrome (congenital adrenal hyperplasia)

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5
Q

What can cause acute adrenocortical insufficiency?

A

Abrupt withdrawal of corticosteroids
Adrenal Hemorrhage–
1.Anticoagulation therapy
2.Waterhouse-Friderichsen syndrome

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6
Q

What is waterhouse friderichsen syndrome?

A

bilateral adrenal hemorrhage
associated with neisseria meningitidis sepsis
endotoxic shock with DIC
**can cause acute adrenocortical insufficiency

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7
Q

80% of chronic adrenocortical insufficiency cases are ______.

A

autoimmune

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8
Q

Other causes of chronic adrenocortical insufficiency?

A

INfectious–TB, histoplasmosis
metastatic cancer (from lung or renal cell carcinoma)
AIDS
adrenogenital syndrome

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9
Q

What are the clinical findings in chronic adrenal insufficiency?

A

weakness
hypotension
hyperpigmentation (from too much POMC released w/ ACTH)

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10
Q

What are the lab findings for chronic adrenal insufficiency?

A 
Hyponatremia-no aldosterone
Hyperkalemia
Metabolic acidosis (normal anion gap)
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11
Q

Other findings in chronic adrenal insufficiency?

A 
Fasting hypoglycemia
Lymphocytosis, 
eosinophilia, 
neutropenia
Increased acth
No response to acth stimulation test
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12
Q

Why do you see hypoglycemia and eosinophilia in chronic adrenal insufficiency?

A

cortisol released from adrenal cortex is gluconeogenic & sequesters eosinophils in lymph nodes.
W/o this–>hypoglycemia & lots of eosinophils in the blood stream.

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13
Q

Once again, why is there hyponatremia, hyperkalemia, and metabolic acidosis with chronic adrenal insufficiency?

A

Aldosterone causes you too keep Na+, get rid of K+ and get rid of some H+.
W/o it: hyponatremia, hyperkalemia, metabolic acidosis

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14
Q

What is the metyrapone test?

A

Inhibits 11ß-hydroxylase and prevents cortisol synthesis
Should result in acth secretion and ↑steroid precursors
↑Acth and no increase in 11-deoxycortisol indicates adrenal insufficiency

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15
Q

What causes adrenogenital syndrome/congenital adrenal hyperplasia?

A

aut rec disorders of enzymes

21-hydroxylase deficiency
11-hydroxylase deficiency
17-hydroxylase deficiency

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16
Q

Which ones of the enzyme deficiencies is the most common cause of adrenogenital syndrome? 90-95% of cases?

A

21-hydroxylase deficiency

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17
Q

Which enzyme deficiency causes hypogonadism w/ adrenogenital syndrome?

A

17-hydroxylase deficiency

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18
Q

What happens in adrenogenital syndrome?

A

Causes ↑acth, and accumulation of precursors proximal to enzyme block
Increased 17-ketosteroids
testosterone

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19
Q

What is the presentation of 21-hydroxylase and 11-hydroxylase deficiency?

A

Precocious puberty in males, and females

Rapid growth as children, but short stature as adults

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20
Q

What is the presentation of 17-hydroxylase deficiency?

A

Decrease in Glucocorticoids and androgens
“salt retainers” -b/c still have aldosterone
Females: delayed menarche and 2˚ sexual characteristics
Males: “pseudohermaphroditism”

21
Q

What are some examples of adrenocortical hyper function?

A

Cushing Syndrome

Hyperaldosteronism (Conn’s Syndrome)

22
Q

What are some things that can cause Cushing Syndrome?

A

Cushing Disease–ACTH secreting pituitary adenoma
prolonged corticosteroid use
hyperfunctional adrenal adenoma
ectopic ACTH production

23
Q

What is involved in Cushing’s syndrome?

A 
moon facies
buffalo hump
easy bruising
abdominal weight gain
striae (weakened collagen, rupture bv)
hirsutism (increased androgens)
diastolic HTN (increased mineral corticoids)
weakness
24
Q

Why the weight gain in Cushing’s syndrome?

A

Hyperinsulinism 2˚ to hyperglycemia

25
Q

Why the muscle weakness in Cushing’s?

A

muscle breakdown b/c of gluconeogenesis

26
Q

What are the lab findings in Cushing’s Syndrome?

A

increase in urine free cholesterol
dexamethasone suppression test
hyperglycemia
hypokalemic metabolic alkalosis (too much aldosterone)

27
Q

What happens in the dexamethasone suppression test for Cushing’s disease?

A

–in Cushing disease, only high doses can suppress cortisol in cases of ACTH-secreting pituitary adenoma

28
Q

What is Conn’s Syndrome?

A

Big yellow benign tumor

ALDOSTERONE SECRETING ADRENAL ADENOMA–in adrenal cortex, zona glomerulosa

29
Q

What are the clinical findings in Conn’s Syndrome?

A

diastolic HTN

muscle weakness

30
Q

What are the lab findings in Conn’s syndrome?

A

Too much aldosterone

HYPERNATREMIA, HYPOKALEMIA, ALKALOSIS
↓PLASMA RENIN

31
Q

What are 2 types of adrenal medullary hyper function?

A

pheochromocytoma

neuroblastoma

32
Q

What is a pheochromocytoma?

A

catecholamine secreting tumor in medulla

secretes Norepi & epi

33
Q

What is the Rule of 10s for pheochromocytoma?

A

Rule of 10’s
10% bilateral
10% malignant
10% extramedullary (paraganglioma)

34
Q

What does a paraganglioma produce? Where is it located? What is present in adrenal medulla pheochromocytoma but not in paraganglioma?

A

paraganglioma–only produces Norepi
located next to sympathetic ganglia in posterior space of thoracic & abdominal cavities
NO phenylethamin-n-methyltransferase

35
Q

Which genetic things are associated with a pheochromocytoma?

A

nf-1
men iia and iib
Von hippel lindau syndrome

36
Q

Pheochromocytoma means increased sympathetic tone. What are the clinical findings?

A 
*Paroxysmal and/or sustained systolic hypertension with palpitations
Headache
*sweating
*Anxiety
Chest pain
Orthostatic intolerance
constipation
37
Q

Why are palpitations, sweating, and anxiety important symptoms of pheochromocytoma?

A

b/c these are symptoms that differentiate pheochromocytoma from essential hypertension.

38
Q

What are the lab findings of pheochromocytoma?

A

Plasma free metanephrines – best confirmatory test
*24-hour urine metanephrines – best sensitivity
24-hour urine vma
No suppression with clonidine
Hyperglycemia
Neutrophilia

39
Q

What is involved in the surgery for pheochromocytoma?

A

can’t touch it easily b/c it can secrete a lot of catecholamines
need to have an alpha inhibitor (like clonidine), & a beta blocker

40
Q

What are metanephrines?

A

by-product of catecholamine synthesis

see increase w/ paraganglioma, adrenal medulla pheochromocytoma

41
Q

What is a neuroblastoma?

A

Malignant neoplasm of post-ganglionic sympathetic neurons

Common in children, <5 yrs old

42
Q

After doing cytologic studies…what makes for a better prognosis for neuroblastoma?

A

Good: <1 yr old, hyper diploid

hyper diploid means more activity, better response to chemotherapy

43
Q

After doing cytologic studies…what makes for a worse prognosis for neuroblastoma?

A

N-myc amplification, 20-30% of cases, marker of aggressive behavior

Bad: >1 yr old, 1p deletion

44
Q

What % of neuroblastoma cases are metastatic when they are first detected?

A

70% metastatic

45
Q

When you have to do cytologic studies on a neuroblastoma what fluid must you NOT put it in?

A

formalin

46
Q

What is the prognosis of neuroblastoma cases?

A

overall survival 40%

47
Q

What is the outside evidence of neuroblastoma?

A

large palpable abdominal mass

48
Q

What is the lab finding for neuroblastoma?

A

increased urine VMA & HVA

49
Q

What does neuroblastoma look like on histo?

A

small round blue cell tumor

Homer-wright rosette

Block X; Week 2-M (7 decks)

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