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ER Week 1 > Adrenal Pathology > Flashcards

Adrenal Pathology Flashcards

1
Q

How many adrenal glands do we have?

A

two - at the upper poles of the kidneys

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2
Q

What are the two separates parts of the adrenal glands?

A

cortex (three zones) and medulla

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3
Q

What are the three zonas of the cortex?

A

zona glomerulosa
zona fasciculata
zona reticularis

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4
Q

What does the zona glomerulosa secrete? THe outside part….

A

mineralocorticoids

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5
Q

What does the zona fasciculata secrete? The middle part….

A

glucocorticoids

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6
Q

What does the zona reticularis secrete? The inside part….

A

sex hormones

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7
Q

What does the medulla secrete?

A

epinephrine and norepinephrine

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8
Q

What are the three disorders that arrise from too much adrenal hormone?

A 
Cushing syndrome (too much cortisol)
Hyperaldosteronism (too much aldosterone)
Adrenogenital syndrome (too much catecholamines?)
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9
Q

What is the mnemonic for what cortisol does?

A

cortisol is BBIIG

maintains Blood pressure
breaks down Bone
suppresses Inflammation
suppresses Immune system
stimualtes Gluconeogenesis
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10
Q

What are the symptoms of cushing syndrome?

A 
hypertension
weight gain
characteristic habitus
weakness
glucose intolerance
thin skin
osteoporosis
infeciton
mental changes
hirsutism
menstrual abnormalities
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11
Q

What lab tests do you use for diagnosis of Cushing’s syndrome?

A

24 hour urine free cortisol

loss of normal diurnal cortisol secretion

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12
Q

What two tests do you use to determine the cause of the cushing syndrome?

A

ACTH level (tells you if the issue is with the pituitary)

Dexamethasone suppression test

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13
Q

What is the most common cause of cushing syndrome?

A

Iatrogenic! Taking steroids

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14
Q

What will lab tests show in iatrogenic cushing syndrome?

A

increased cortisol (with no Dexa supression)

decreased ACTH (the prednisone does feedback inhibition on the pituitary)

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15
Q

What causes cushing DISEASE?

A

pituitary cushing syndrome - a tumor in the atnerior pituitary makes too much ACTH

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16
Q

What will happen to the adrenal cortices in pituitary cushing syndrome (cushing disease)?

A

they will become hyperplastic

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17
Q

What will lab tests show in pituitary cushing syndrome?

A 
increased cortisol (with dexa suppression)
 (note this is surprising, but pituitary adenomas can be turned off with high dose dexa)

increased ACTH

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18
Q

Is the adrenal cortex hypoplastic or hyperplastic in ADRENAL cushing syndrome?

A

can be either

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19
Q

What will lab tests show in adrenal cushing syndrome?

A

increased cortisol (with no dexa suppression)

decreased ACTH

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20
Q

What lung cancer will cause paraneoplastic cuhshing syndrome?

A

small-cell

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21
Q

Will the adrenal cortices be hypoplastic or hyperplastic in paraneoplastic cushings?

A

hyperplastic because of all the fake ACTH stimulation

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22
Q

What will lab tests show in paraneoplastic cushing syndrome

A

increased cortisol (with no Dexa suppression)

increased “fake” ACTH because the test can’t differentiate true ACTH from the cancer’s ACTH

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23
Q

Back to CRRAB…How is the release of aldosterone triggered?

A

angiotensinogen is converted to angiotensin 1 by renin

Ang 1 is converted to Ang II by ACE

Angiotensin II then triggers the release of aldosterone

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24
Q

So increased renin leads to ___ aldosterone

A

increased

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25
What does aldosterone do?
1. retain Na and water 2. pee out K so hypernatremia, increased BP and hypokalemia
26
What will hypertension do to aldosterone levels?
decresas renin, so decreased aldosterone hence, you pee out Na and H20 and retain K, leading to hyponatremia, decreased BP and hyperkalemia
27
What is the general cause of primary hyperaldosteronism? Two specific causes?
you have increased aldosterone release, leading to decreased renin via feedback caused by a cortical adenoma or cortical hyperplasia
28
What syndrome is associated with cortical adenoma?
Conn syndrome
29
What are the main symptoms of primary hyperaldosteronism?
hypertension (hypernatremia) weakness fatigue psychosis (hypokalemia)
30
What will the lab findings be in primary hyperaldosteronism?
``` elevated aldosterone low renin hypernatremia hypokalemia metabolic alkalosis (loss of H+ along with the K+) ```
31
What is the general cause of secondary hyperaldosteronism?
abnormally increased renin
32
What are three causes of the abnormally increased renin that leads to secondary hyperaldosteronism?
CHF decreased renal blood flow (like in RAS) renin-producing tumors
33
What are the symptoms of secondary hyperaldosteronism?
same as primary.... hypertension (hypernatremia) weakness, fatigue and psychosis (hypokalemia)
34
What will the lab findings be in secondary hyperaldosteronism?
``` elevated aldosterone high renin hypernatremia hypokalemia metabolic alkalosis (loss of H along with K) ```
35
What makes these lab findings different from primary hyperaldosteronism?
high renin
36
What are the two general cuases of virilization?
1. primary gonadal disorders | 2. primary adrenal disorders
37
What are the two general primary adrenal disorders?
adrenocortical neoplasms | congenital adrenal hyperplasia
38
Adrenocortical carcinoma is super rare, but how does it present?
you get sudden virilization in a girl or woman sometimes has a palpable abdominal mass
39
Does an adrenocortical carcinoma have a good or gad prognosis?
bad
40
What's wrong in congenital adrenal hyperplasia?
the patient has a deficiency in an enzyme in volved in making either/or the minerlocorticoids of the glucocorticoids, which means you 1. lose the feedback inhibition on the pituitary and 2. have all the hormone precursors being shunted into the sex steroid synthesis pathway this means they have low aldosteron, low cortisol (with all those symptoms) and high testosterone leading to virilization
41
What is the most common enzyme deficiency that leads to congenital adrenal hyperplasia?
21 hydroxylase deficiency, which is required for both cortisol and aldosterone synthesis
42
What are the three types of 21 hydroxylase CAH?
1. salt-wasting (wher eyou get no aldosterone whatsoever) 2. simple virilizing (some aldosterone) 3. laste-onset virilizing some aldosteron and some cortisol) all depends on how much active enzyme you have
43
So in congenital adrenal hyperplasia, which layer of the cortex will be big?
the zona reticularis (wince that's what makes the sex steroids(
44
What are the two general kinds of primary adrenal insufficiency?
acute or chronic
45
What is the more common name for primary chronic adrenal insufficiency?
Addison disease
46
What is Addison's disease?
typically an autoimmune destruction of the adrenal cortex such that the patient cannot make cortisol and mineralocorticoids
47
What are the main symptoms of addison's disease?
weakness, fatiuge, GI complains hypotension (no aldosterone) skin hyperpigmentation
48
Why do you get the skin hyperpigmentation in addisons?
You don't have cortisol or aldosteron feeding back to inhibit the pituitary, so the pituitary just keeps making a ton of ACTH remember that ACTH is derived from POMC. Remember that melanocyte stimulating factor is also derived from POMC, so you get lots of melanocyte stimulation leading to a bronzing effect
49
What is the management for an acute exacerbation of addison's?
IV Na+ (bc they're hyponatremic due to lack of aldosterone) hydrocortisone (since they can't make cortisol) dextrose
50
What does Addison's disease look like on histology?
you see very little cortex left and what is there will be filled with lymphocytes
51
Although Addison's can present in an acute-like manner, it's really a chronic problem. What are the two most common causes of actual primary acute adrenal insufficiency?
1. rapid steroid withdrawal (because their adrenal glands have hypertrophied) 2. Massive adrenal hemorrhage
52
What is the classic setting for massive adrenal hemorrhage and what is the syndrome called?
waterhouse-friderichsen syndrome A young child with a N. meningitidis infection presenting in DIC with hypotension and shock they just get massive bilateral adrenal hemorrhage which rapidly progresses. Often fatal
53
What is secondary adrenal insufficiency typically caused by?
pituitary or hypothalamic insufficiency related to tumor, infection, radiation or infarction
54
What are the clinical features of secondary adrenal insufficiency?
you have decreased ACTH, so you have decreased adrenal products you get the symptoms of decreased cortisol and decreased sex steroids
55
Why will mineralocorticoids be normal in secondary adrenal insufficiency?
because the renin axis is intact, so the signal for aldosteron release is still there
56
Why don't you have the hyperpigmentation in secondary adrenal insufficiency?
beause the issue is with too little ACTH. If you have no ACTH, then you're probably not making melanocyte stimulating factor either
57
There are two tumors of the adrenal medulla. What are they?
1. pheochromocytoma | 2. neuroblastoma
58
What is a pheochromocytoma a neoplasm of?
catecholamine-producing cells in the medulla
59
What are the symptoms of pheochromocytoma?
episodic in nature... ``` pressure (HTN) pain (headache) perspiration palpitations (tachycardia) pallor ```
60
What labs can you do to diagnose a pheochromocytom?
urine analysis for catecholamien break-down products like VMA and metanephrines
61
Why is a pheochromocytoma called the 10% tumor?
``` 10% are extra-adrenal (paragangliomas) 10% are bilateral 10% are familial 10% are malignant 10% of patients don't have HTN ```
62
What does a pheochromocytoma look like under histology?
littles that hang out in ball-like packets called zellballen
63
What kind of cells is a neuroblastoma derived from?
neural crest
64
Neuroblastoma presents in what stage of life?
childhood
65
True or false: prognosis for neuroblastoma is better in children over 18 months of age
false - better for children less than 18 months
66
True or false: prognosis is better for hyperdiploid tumors
true (whichi s unusual)
67
Prognosis is better if the tumor has fewer copies of what tumor promoter gene?
N-myc
68
True or false: in really young children, some neuroblastoma (even metastatic) can go away with time.
true!
69
What does neuroblastoma look like micrscopically
it's in the calss of small round blue cell tumors so it has small round blue cells arranged in homer-wright rosettes
70
WHat is in the center of a homer-wright rosette?
neuropil

ER Week 1 (11 decks)

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