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ENRP Exam 2 > Pathology of the Adrenal Glands- Hillard > Flashcards

Pathology of the Adrenal Glands- Hillard Flashcards

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1
Q

where are the adrenal glands

A

above the kidney in a superior location

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2
Q

what are the parts of the adrenal gland

A

capsule, adrenal cortex, adrenal medulla

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3
Q

what is the blood supply to and from the adrenal glands

A

arteries: suprarenal arteries
vein: adrenal vein

has a robust blood supply so it is less disturbed by interuptions to blood flow

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4
Q

what are the three parts of the adrenal cortex

A

zona glomerulosa

zona fasiculata

zona reticularis

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5
Q

the zona golmerulosa creates _

A

mineralocorticoids: aldosterone which helps to increase salt retention by the kidney

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6
Q

the zona fasciulata creates _

A

cortisol which is released during times of stress

and increases glucose in the blood

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7
Q

the zona reticularis creates

A

androgens

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8
Q

an increase in androgens will have a _ affect

A

virilizing/masculining effect

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9
Q

the adrenal medulla creates _

A

catecholamines (epinephrine and noreepinephirne)

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10
Q

cushing syndrome is caused by an excess of?

A

glucocorticoid cortisol

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11
Q

what are the symptoms of cushing disease

A

HTN- multifactorial cortisol increases vascular sensitivity and drives renin production

fat redistribution- central obesity and fat behind the neck, cheecks, and side of head (moon facies)

secondary diabetes - increased blood sugar levels and increased glucose in the urine

catbolic state breaking down bone and collagen - skin thinning and osteoporosis

mood swinfs

depressed immune system

hirtuism

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12
Q

cortisol is a potent driver of _

A

glucoenogenesis and created glucose from energy stores

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13
Q

high cortisol causes the body to be in a _ (anabolic/catabolic) state

A

catabolic

breakdown bone and collagen

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14
Q

describe the HPA of cortisol

A

increased stress will stimulate CRH release from the hypothalamus, which acts on the the anterior pituitary to release ACTH. ACTH then acts on the adrenal gland (zone fasiculata) to produce cortisol

cortisol has negative feedback on the AP and the hypothalamus

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15
Q

what are the two types of cushing syndrome

A

EXOGENOUS/ IATROGENIC- too much cortisol being absorbed

ENDOGENOUS- body is producing too much cortisol

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16
Q

what is cushing disease

A

problem in the pituitary or higher

usually a pituitary adenoma that causes hyperfunctioning: cortioctrophic adenoma that creates too much ACTH and causes excess cortisol release from the adrenal glands

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17
Q

what is ectopic cushing disease

A

ACTH is produced in an ectopic location most notably due to a paraneoplastic syndrome: small cell carcinoma of the lung

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18
Q

what is an adrenal gland cushing syndrome

A

this is when excess cortisol is being produced from the adrenal glands

most commly from adrenal adenoma, carcinoma or hyperplasia

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19
Q

does adrenal cushing disease dependent on ACTH

A

no, it would actually be suppresed by cortisol negative feedback

cushing disease and ectopic cushing disease are dependent on ACTH - all of them are endogenous

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20
Q

what is the most common cause of ACTH INDEPENDENT endogenous hypercortisolism

A

adrenal adenomas

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21
Q

how does an adrenal adenoma look?

A

well demarcated and yellow cut surface

impossible to tell grossly if it is nonfunctional or secreting cortisol or secreting aldosterone

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22
Q

how do adrenal adenomas look under the microscope?

A

they are well circumscribed tumors

tumors recapitulate cells in the adrenal cortex- can have atypica

  • atypia is not an evidence of malignancy

must look for invasion/metastasis to rule out malignancy

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23
Q

hyperplasia of the adrenal gland is most commonly seen with?

A

pituitary cushing syndrome and paraneoplastic/ectopic cushing syndrome

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24
Q

if hyperplasia of the adrenal gland is the only presenting feature then it may be a result of what genetic disease

A

mcCune albright

or carney complex (PRKAR1A, lactotrophs and somatotrophs)

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25
what is mccune albright syndrome
this is replacement of bone with firbous tissue and cafe au lait spots with precoccious puberty
26
what is carney complex
mucocutaneous pigmentation and myocmatous tumors
27
what does the adrenal gland look like when given exogenous cortisol/corticosteroids
atrophic and shrunken
28
why do the adrenal glands become atrophic and shrunken with chronic corticosteroid use?
because they no longer need to produce steroids there will be a loss of cortical layers/cells ## Footnote must taper off corticosteroids
29
paraneoplastic cushing syndrome is most often caused by?
small cell lung carcinoma ## Footnote lung is the first source to consider if there is ectopic cushing syndrome
30
how would you screen someone for cushing syndrome
start by taking a good history and physical make sure they are not taking any exogenous steriods rule out physiological reasons as to why there is increased cortisol ( pregnancy, obesity)
31
what are the screening tests for cushing syndrome
low dose dexamethasone suppresion test 24 hr urinary cortisol salivary cortisol (late night)
32
after the diagnosis of cushings syndrome is made what do we do now?
check ACTH levels to see if it is ATCH independent or dependent
33
if cushing syndrome is ACTH independt ACTH levels will be?
suppressed ## Footnote then you should do imaging of the adrenal glands
34
if ACTH is dependent in cushing syndrome meaning ACTH levels are? you then do what?
normal to high high dexamethasone suppresion test pituitary MRI inferior petrosal sinus sampling
35
in a dexmathasone suppresion test what happens
in a normal person this should suppress ACTH
36
in a pituitary adenoma is acth suppresed in a high dexamethasone test?
yes then it is cushing disease!
37
in ectopic acth tumors does a dexamethasone test suppress ACTH
no so check the lungs for paraneoplastic syndrome: small cell carcinoma of the lungs
38
what does a pituitary MRI do?
it checks for cushing disease (pituitary tumor) by looking at the pituitary
39
what is an inferior petrosal sinus sampling
measuing ACTH directly from the veins rhat drain the pituitary gland to check for tumor
40
aldosterone is normally released in response to _
renin
41
renin is released by the kidney when?
when there is low volume or low blood pressure
42
renin converts angiotensionogen to
angiotensin I
43
angiotensin I is converted to angiotensin II by?
angiotensin converting enzyme (ACE)
44
angiotension II stimulates the adrenal gland to release _
aldosterone
45
what are the actions of aldosterone
causes the kidney to absorb sodium and water and increases blood volume
46
what is hyperaldosteronism
this is chronic elevation of aldosterone
47
what are the types of hyperalldosteronism
primary- adrenal gland produces too much aldosterone and renin is low secondary- extradrenal cause of too much aldosterone and renin is high
48
explain primary hyperaldosteronism
the adrenal gland will produce too much aldosterone which will raise blood pressure and blood volume, this in turn will adequately perfuse the kidney and cause renin to decrease
49
explain secondary hyperaldosteronism
decreased blood flow to the kidney (globally or locally) can cause renin to increase and increase aldosterone
50
what is the most common cause of primary hyperaldosteronism
idiopathic hyperaldosteronism where there is hyperplasia of the zona glomerulosa
51
what is the second most common type of primary hyperaldosteronism
an aldosterone secreting ADENOMA in the zona golmerulosa aka conn syndtome
52
what is a rare cause of primary hyperaldosteronism
glucocorticoid suppresible primary hyperaldosteronism
53
what is glucocorticoid suppresible primary hyperaldosteroinsm
hybrid cells ar ein the zona glomerulosa due to a genetic abnormality and release aldosterone in reponse to ACTH so aldosterone is increased when ACTH increases
54
does the dexamethasone test suppress ACTH in glucocorticoid suppresible primary hyperaldosteronism
yes, once ACTH is suppressed then aldosterone release will decrease from teh hybrid cells
55
what are the symptoms of primary hyperaldosteronism
hypertension and hypokalemia hypokalemia can cause a metabolic alkalosis low postassium- can cause muscle cramps, neuromusclar isssues, weakness | aldosterone increases Na+ absorption and K+ excretion ## Footnote in practice hypokalemia is inconsistently seen
56
what is the screening test for primary hyperaldosteronism
aldosterone to renin ratio ratio should be high
57
if the aldosterone to renin ratio is high you should do what confirmatory test?
a saline infusion (aldosterone suppresion test) if aldosterone does not suppress you have primary hyperaldosteronism
58
adrenal adenomas in primary hyperaldosteronism can show?- on hsitology
spironlactone bodies on histology used to treat an adrenal adenoma (conns syndrome)
59
what do spironolactone bodies look like?
circular whorled eosionophilic structures in the tumor that represent endoplasmic reticulum material bound to aldosterone
60
secondary hyperaldosteronism is caused by conditions that activate? what are three things that can cause secondary hyperaldosteroinsim
activate the RAS system from decreased blood flow to the kidney or from global hypovolemia and edema renin producing tumor
61
what can lead to decreased renal artery perfusion
renal artery stenosis, renal fibromusclar dysplasia
62
what can lead to global hypovolemia and edema
heart failure and neprhotic syndrome
63
normal pregnacy can also induce an increase in renin and aldosterone how?
due to an increase in ovarian secretion oand decidual release and high estrogen levels which drive production of angiotensionogen
64
congenital adrenal hyperplasia is a group of autosomal _ disorders in wheich the enzyme invovled in the biosynthesis of _ is deficent
recessive cortisol
65
what mutation is involved in CAH and what enzyme is deficient
CYP21A2 is mutated 21-hydroylase def
66
congenital adrenal hyperplasia typically presents at _ and shows what sigsn?
birth decreased cortisol decreased aldosterone virulization
67
why does adrenal hyperplasia occur in CAH
there is decreased cortisol the hypothalamus is no longer inhibited and will create more CRH and the pituitary wont be inhibited from secreting ACTH which will act on the adrenal gland and cause hyperplasia/enarlgement
68
21 hyrdoylase converts precursor products that are originally derived from _ to aldosterone and cortisol
cholesterol
69
with a 21 hydroxylase def there is an enzymatic def in the conversion of
progesterone becoming 11-dexycorticosterone and eventually aldosterone 17-hydroy progesterone becoming 11-doexycortisol and eventually cortisol
70
because of the 21 hydroylase def in CAH what happens
17- hydroxyprogesterone is converted to androsteniodione and eventually androgens like testosterone and give virulizing effects
71
an infant with CAH will look?
clitoral enlargment labial fusion in XX penis enlargement in XY usually just effects external genitalia salt wasting
72
low aldosterone leads to
salt wasting and hyperkalemia
73
low cortisol leads to?
medullary defects, low epinephrine, hypotension and collapse
74
intraadrenal glucocorticoids are necessary for _ production
catecholamines (epineprhine and norepinephrine)
75
what test is diagnositc for CAH
elevated 17 hydroxyprogesterone (17 OHP_ heel puncture taken 2-4 days after birth
76
what are the three types of CAH
classic form with salt wasting- present in neonate simple virulizing- presents in neonates non-classic- late onset (present in adolescents/adult) ## Footnote usually the 21 def is shown on the neonatal newborn screen
77
what is acute primary adrenocorticoal insufficiency
there is a problem in the adrenal gland that causes a lack of adrenal hormone from being produced ## Footnote doesnt make mineralocorticoids or glucorticoids like it should
78
what are the causes of acute primary adrenocortical insuficiency
chronic steroid use rapid withdrawl massive adrenal hemorrhage waterhouse friederichsen syndrome
79
why does excogenous steroid use and withdrawl cause acute primary adrenocortical insufficiency
use of steroids results in atrophy of the adrenal gland, upon removal of them the adrenal gland cannot make the hormones it needs
80
how does acute adrenal hemorrhae cause adrenocortical insufficiency
due to the size and vasculatitiry of the adrenal gland at birth any time hypoxia occurs the adrenal gland will recieve more blood and cause increased pressure and hemorrage into the adrenal gland damaging it
81
what is waterhous friederichsen syndrome
bilateral adrenal hemorrhage that is a result of neisseria meningitis (infection) ## Footnote can be causse dby any bacterial organism
82
exogenous steroids can cause _ and rapid withdrawl of steroids can cause
cushing syndrome acute primary adreocortical insufficency
83
neisseria meningitdis is manifested with DIC what is this?
intravascular coagulation that causes abnormal clotting through the bodys blood vessels that can ruputre in the adrenal glands
84
key symptoms of primary adrenocaortical insufficiency
abdominal pain, nausea, vomiting, weakness, lethary, shock , and confusion ## Footnote acute adrenocortical insufficiency can also be seen in chronic adrenocortical insuffiency when there is a major stressor
85
what is chronic adrenocortical insufficiency symptoms
addisons disease chronic fatigue ! abdominal pain, N/V, postural hypotension hyperpigmentation of the skin
86
why is skin hyperpigmentation seen in addisons disease
a feedback loop increases melanin synthesis low cortisol drives increased production of POMC causing increased ACTH and increased melanocyte stimulating hormone
87
is hyper pigmentation seen in secondary adrenocortical insuficiency
no
88
what are the common causes of chronic primary adrenocortical insufficiency
autoimmune adrenalitis infections metastatic neoplasms congenital
89
what is autoimmune adrenalitis what are the mutations
the most common cause of primary chronic adrenocortical insuffciency that has a mutation in AIRE genes APS1- fungal infections, teeth abnormalities, other autoimmune diseases like hypoparathyroidism APS2- autoummune thyroiditis
90
APS-1 mutations also cause
hypoparathyroidism and fungal infections ## Footnote adrenal isuf. too
91
APS-2 mutations also cause
autoimmune thyroiditis ## Footnote adrenal insuf. too
92
what does autoimmune adrenalitis look like on histology
lymphocytic infiltrate actively attacking the adrenal glands
93
what infection can cause primary chronic adrenocortical insufficiency
tuberculosis showing caseous necrosis (cheesy) in the adrenal gland
94
congenital adrenal insufficiency can also casue chronic primary adrenocortical insufficency what are the two types
adrenoleukodystrophy and adrenal hypoplasia
95
what is adrenoleukodystrophy
the accumulationof very long chain fatty acids that cannot be brolen down and settle in the brain, nervous system, and adrenal gland it is x linked and leads to learning diabilities, sezuires, adrenal insufficiency, and skin hyperpigmentation
96
what is congential adrenal hypoplasia
a genetic cause of chronic primary adrenocortical insuffiency that is from an underdeveloped adrenal cortex
97
what is secondary adrenocortical insufficiency
adrenal insuffiency due to ACTH secretion def in the pituitary
98
what is tertiary adrenocortical insufficiency
low cortisol due to def in CRH secretion
99
what is the major difference in secondary and teritary adrenocortical insufficiency in comparision to primary insufficiency
there is no hyperpigmentation
100
adrenal carcinomas are typically _ (small/large) and poorly circumscribed there is necrosis and hemorrhage and _ confirms malignancy
large metastasis or local invasion ## Footnote poor prognosis -2 years
101
what are adrenal incidentalomas
an adrenal mass larger than 1cm that comes to attention on workup asymptomatic if they are not causing any problems just repeat imaging rule out cushing syndrome, pheochromocytoma etc. ## Footnote any alarming features shuold be worked up
102
what is an adrenal myelolipoma
this is a benign lesion that consists of mature fate and hematopoientic elements trilineage- erythrocytes, myeloid, megakarycytes grossly: yellow fat with dark hematopoetic areas
103
what is a pheochromocytoma
this is a tumor of the adrenal medulla chromaffin cells it secretes catecholamines
104
what are the sympotms of a pheochromocytoma
elevated blood pressure abrupt elevations in blood pressure with the sudden release of catecholamines increased HR, sweating, headache, diaphoresis, palpitations, anxiety
105
how do you test for pheochromocytoma?
urinary or plasma metanephrines which will be elevated in disease
106
what is the pathophysiology of a pheochrmocytoma
release of catecholamines epinephrine acts on beta 2 receptors and increases cardiac output norepineprhine works on alpha 1 receptors and increases cardiac output and constricts blood vessels causes hypertension
107
what is the rule of 10s for a pheochromocytoma
10% are extra-adrenal 10% of sporadic tumors are bilateral 10% are malignant 10% do not show hypertension 25% show familal mutations
108
gross apperance of pheochromocytoma
well circumscribed, yellow/tan
109
histology of pheochromocytoma
discrete nests of supporting sustentacular cells called zellballen endoctine atypia (doesnt mean malignancy)

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