Lecture 4 - Pathology Flashcards

1
Q

What are the layers of the adrenal cortex?

A

Glomerulosa (outmost layer) - produces mineralocorticoids under RAAS regulation

Fasiculata and reticularis - produce and store fluocorticoids and sex steroids – controlled by ACTH regulation

Medulla - catecholamine production

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2
Q

What are the 2 different types of adrenal disorders?

A

Morphological

Functional

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3
Q

Adrenal Hyperplasia

A

bilateral disease
glands are equally enlarged on both sides

if ACTH excess – this is limited to zona fasciculata and retinularis

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4
Q

Adrenal Adenoma

A

solitary nodules, yellow
may or may not be functional disorder

incidental finding d/t imaging for something else

if its functioning and producing glucocorticoids –there will be atrophy of surrounding cortex

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5
Q

What are the NIH guidelines for incidental adrenal adenomas? (nodules)

A

if >6cm –> absolute remove

if <6cm –> monitor

if the nodule is hormonally active take it out

what people actually do is >4.5 cm remove!

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6
Q

Adrenal cortical carcinoma

A

rare
50% hormonally active

typically very big d/t retroperionteal space prevents you from feeling it grow and grow since there are no other organs to compress it and thus cause sxs

bimodal age: peds and >50y/o

poor prognosis –resistant to chemo

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7
Q

What are types of morphological adrenal disorders?

A

hyperplasia
adenoma
carcinoma

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8
Q

When are glucocorticoids highest?

A

highest on waking

lowest in early sleep

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9
Q

What are the clinical findings of Cushing’s syndrome?

A
obesity 
HTN
poor wound healing
hyperglycemia
hypokalemia
alkalosis (d/t cortisol excess) 
hirsutism 
menstrual problems (d/t androgen excess) 

moon face
buffalo hump

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10
Q

What causes cushing’s disease?

A

over production of ACTH in pituitary

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11
Q

What is the difference between cushings syndrome and disease?

A

syndrome is d/t ectopic ACTH production usually from SCC tumor in the lung

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12
Q

Adrenal Insufficiency

A

might result in mineralocorticoid deficiecny or glucocorticoid deficiency

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13
Q

Mineralocorticoid deficiency

A

dehydration
decrease in Na+
increase in K+
metabolic acidosis

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14
Q

Glucocorticoid deficiency

A

weakness
weight loss
vomiting
hypoglycemia

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15
Q

Primary Adrenal Insufficiency

A

Addison’s disease

lack cortisol and aldosteron
increase ACTH which causes abnormal pigmentation

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16
Q

What causes secondary adrenal insufficiency?

A

only lack of glucocotricoids

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17
Q

____% of the CORTEX must be destroyed to have insufficiency

A

> 90%

destruction occurs via infection or autoimmune disease

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18
Q

What are the main causes for destruction of the cortex?

A

infection in developing worlds

autoimmune disorders in Western world

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19
Q

Waterhouse - Frederichesen

A

adrenal hemorrhagic necrosis due to gram negative sepsis (often meningococcal)

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20
Q

Adrenogenital Syndrome

A

enzyme defect of the adrenal gland –abnormal hormone synthesis
inherited deficiency

usually the 21B hydroxy enzyme is missing

decrease in cortisol –> increase in ACTH –> hyperplasia

21
Q

What determines external genital development?

A

androgen —> female

if you have excess androgen you will have male-ish or ambiguous genitalia

22
Q

Which drugs stimulate the release of Epi in the adrenal medulla?

A

clonidine
ACEI
CCB

23
Q

What drugs inhibit the release of Epi in the adrenal meduall?

24
Q

Neuroblastoma

A

childhood malignant tumor of the adrenal medulla

25
Pheochromocytoma
tumor in adults from the adrenal medulla "10% tumor" - 10% being familial - 10% extraadrenal - 10% are malignant
26
What are the sxs of pehochromoctyoma?
``` HTN sweating tachycardia hyperglycemia feeling of DOOM ```
27
How are neuroblastomas dx?
Typically found as an abdominal mass
28
Basophilic vs ampiphilic vs. eosinophilic
``` pink = eosinophilic purple-ISH = ampiphilic true purple (like the nucleus) = basophilic ```
29
Can you tell if pheochromocytomia is malignant?
no 10% of them are malignant but we can't tell if they are or not only if they have metastisized
30
N-myc amplification
a detectable genetic change of the neuroblastoma that indicates poor prognosis
31
What is the most common tumor of the adrenal gland?
primary tumors are RARE | metastatic tumors are common (one of the most common metastatic locations besides LUNG)
32
Where is the pituitary located?
in sella turcica at base of skull right underneath the optic chiasm
33
Which CN might an enlarged pituitary gland effect?
CN 2,3,4 and 6
34
What happens to your pituitary gland during pregnancy?
doubles in size
35
How many hormones are produced by the anterior lobe of the pituitary?
6 hormones the posterior lobe doesnt produce anything but stores 2 types of hormones
36
How is the pituitary activated?
feedback from end organ | stimulation from hypothalamus
37
Overproduction of GH?
gigantism (children) | acromegaly (adults)
38
Underproduction of GH?
``` pituitary dwarfism (children) few sxs in adults ```
39
What are common sxs of pts with GH excess?
thick, oily skin HTN and cardiomegaly glucose intolerance (DM) degenerative joint disease
40
How can you clinically dx GH deficiency (dwarfism)?
failure of GH to respond to at least 2 stimuli
41
What chemical/hormone inhibits GH production?
glucose you can't measure GH levels so you have to test by giving the pt glucose
42
Prolactin
stimulates milk production | inhibits GnRH production
43
What causes prolactin to be released?
stress (illness) sex exercise higher in sleep
44
What are the sxs of increased prolactin?
galactorrhea (milk discharge not associated with breastfeeding/pregnancy) decrease gonadal function (menstrual irregularities)
45
What causes elevated prolactin?
prolactinoma (MC) | medications (sedative, antidepressants, blood pressure meds)
46
How do you evaluate excess prolactin?
prolactin levels upper reference limit 20-25ng/mL >200ng/mL - almost all tumors
47
Macroadenoma
pituitary adenoma >1cm
48
Mass effect
NOT DONE HERE
49
Empty Sella Syndrome
herniation of diaphragma sellae allowing CSF to enter sella and compress pituitary gland