Pathology - adrenal gland Flashcards

1
Q

causes of cushings

A

exogenous corticosteroids
primary adrenal adenoma, hyperplasia or carcinoma
ACTh secreting pituitary adenoma
paraneoplastic ACTH secretion

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2
Q

what is the result of exogenous corticosteroids

A

decreased ACTH

bilateral adrenal atrophy

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3
Q

what is the results of primary adrenal denoma, hyperplasia or carcinoma

A

decreased ACTH
atrophy of uninvolved adrenal gland
can also present with pseudohyperahldosteronism

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4
Q

result of ACTH secreting pit adenoma and ectopic ATCH production

A

increase ACTH

bilateral adrenal hyperplasia

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5
Q

what is responsible for the most endogenous cases fo cushign syndrome

A

cushign disease - ACTH secreting pit adenoma

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6
Q
hypertension
weight gain
moon faces
buffalo humo
skin thinning and striae
osteoporosis
hyperglycemia
amenorrhea
immunosuppression
A

cushing synrome

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7
Q

what are the screening tests for cushing syndrome

A

24 hour urine cortisol - should be increased in all causes
midnight salivary cortisol - should be increased in all causes
low dose dexamethasone - no suprression

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8
Q

after you have screend for cushing then what do you do?

A

measure serum ACTH
decreased - adrenal tumor
increased - further testing

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9
Q

how do you distinguish between pit adenoma and ectopic ACTH in cushing syndrome

A

high does dexamethasone
will suppress pit ACTH levels
will not suppress ectopic ACTH levels

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10
Q

describe results of CRH stimulation test

A

CRH stimulation test for pit adenoma: increased ACTH and cortisol
CRH stimulat test for ectopic: no increase in ACTh or cortisol

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11
Q

define adrenal insufficiency

A

inability of adrenal gland to secrete enough glucocorticoids/mineralocorticoids for bodys needs

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12
Q
weakness
fatigue
orthostatic hypotension
muscle aches
weight loss
gi disturbances
sugar and or salt craving
A

adrenal insufficiency

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13
Q

how do you diagnose adrenal insufficiency

A

measure serum electrolyes
morning/random serum corticol and ACTh
response to ACTH setimulation test

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14
Q

what is metyrapone

A

blocks last step of cortisol production ie 11deoxycortisol to cortisol
normal response - less cortisol - less engative feedback - increased ACTH
adrenal insufficiency - no effect on ACTh

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15
Q

what causes primary adrenal insufficiency

A

loss of gland function

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16
Q
hypotension
hyponatremic colume contraction
hyperkalemia
metabolic acidosis
skin and mucosal hyperpigmentation
A

primary adrenal insufficiency

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17
Q

why sxs in primary adrenal insufficiency

A

hypotension - lsos fo Na - low aldosterone
hyperkalemia, acidosis - low aldosterone
skin and muosal hyperpigmentation - high ACTH - MSH levels increase

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18
Q

what causes acute primary adrenal insufficiency

A

shock, hemorrhage, acute acrenal curisis

  • abrupt withdrawal of corticosteorids MOST COMMON
  • waterhouse friedrichson
  • anticoagulants
19
Q

what causes chronic primary adrenal insufficiency

A

addisons dz - adrenal atrophy or desertion by disease

TB, autoimmune, mets

20
Q

what can cause destruction of adrenal gland

A

TB, autoimmune diseases, mets, N Neisseria septicemia/DIC

21
Q

nuchal rigidity
petechial rash
young child
endotoxic shock

A

waterhouse friendrichsen syndrome

22
Q

what is waterhouse friedrichson syndrome

A

acute primary adrenal insufficiency due to afrenal hemorrhage associated with septicemia usual N meningitis , DIC and endotoxic shock

23
Q

what causes secondary adrenal insufficiency

A

decreased pituitary ACTH production

24
Q

symptom to differentiate primary form secondary adrenal insufficiency

A

primary - hyperpigmentation

secondary - noppers

25
Q

what causes tertiary adrenal insufficiency

A

chronic exogenous steroid use precipitated by abrupt withdrwal
aldosterone sytnehsis is unaffected

26
Q

labs in adrenal insufficiency please

A
increased ACTH
hyponatremia
hyperkalemia
hypoglycemia
eosphinphilia, lymphocytosis, neutropenia
decreased cortisol
dereased HCO3
27
Q

neuroblastoma maligi or beining

A

maligi

28
Q

abdominal distension
firm, irregular mass that can cross midline
< 4 years old

A

neuroblastoma

29
Q

what cell gives rise to neuroblastma

A

neural crest cells

30
Q

where can neuroblastoma occur

A

anywhere along the sympathetic chain

31
Q

histo characteristics of neuroblastma

A

homer write rosettes: nueroblasts surrounding a central space
small round bule/purple nuclei in cells

32
Q

what is the paraneoplastic syndrome of neuroblastoma

A

opsoclonus myoclonus syndrome

33
Q

what is increased in urine in neuroblastoma

A

HMA (DA) and VMA (NE)

34
Q

staining of neuroblastoma

A

bombesin and neuron specific enolase positive

35
Q

hypertension risk in neuroblastoma

A

less likely

but look for child with ab mass and hypertension for diagnosis

36
Q

genetics of neutoblastoma

A

overexpression of n-myc oncogene

37
Q

most common adrenal medulla tumor in adults

A

pheochromocytoma

38
Q

cell of origin of pheochromocytoma

A

chromaffin cells <– neural crest cells

39
Q

rule of tens

A
10% maligi
10% bilateral
10% children
10% extra-adrenal
10% calcify
40
Q

what do pheochromocytomas secrete

A

Da, Ne, epi from most tumours

41
Q

what diseases are associated with pheochromocytomas

A

NF-1
von hippel landau
Men IIa
Men IIb

42
Q

what will you find in urine and plasma in pheochromocytoma

A

increased catecholamines and metanephrines in urine and plasma

43
Q

how to treat pheochromocytoma

A

irreversible alpha antagonsits - phenoxybenzamine and then beta blockrs - need alpha blocaked before beta or can have a hypertensive crisis

44
Q

describe the episodic hyperadrenergi symptoms

A
FIVE PS
pain - headache
pressure - increasd bp
perspiration - excessive diuresis
palpitations - tachycardia
pallor
and anxiety. 
orthostatic hypotension
ileus