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Endocrine Path "Bites" Flashcards

1
Q

What disease is associated with each #

A
  1. 2’ or 3’ HypoT
  2. RARE–> recheck labs
  3. 1’ HypoT
  4. subclinical HyperT
  5. subclinical HypoT
  6. 1’ HyperT
  7. RARE– recheck
  8. 2’ or 3’ HyperT
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2
Q

Whether its Hyper or hypo thyroidism, where are the problems located for 1’, 2’, or 3’ diseases/dysfxn?

A

1’= thyroid

2’= pituitary [ant.]

3’ = hypothalamus

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3
Q

Explain Lid lag & Thyroid storm

What disorder are these 2 findings indicative of?

A

lid lag: ask pt to look down or follow a finger with their eyes–> lids stay raised/open longer = bug-eyed appearance

Thyroid storm: can be really bad, sudden release of a bunch of Thyroid H–> affects heart particularly–>arr’s–>potentially fatal

***associated w/ HyperT!

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4
Q

Describe myxedema & myxedema coma?

What DO are these associated with?

Who is most likely to show these Sx’s?

A

myxedema: tissue is full of myxoid substance–> accumulate in tissue and make it bigger [can happen anywhere, legs, throat, etc]

  • often huge swollen bags under eyes

myxedema coma: deteriorating mental status

MC: elderly women in the cold [weather]

***associated with HypoT

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5
Q

What is congenital HypoT?

A

MCC: iodine deficient or genetics

***most often in 3rd world countries where there is no access to salt/iodinized water

Sx’s: short! mental deficits! other hypoT Sx’s

AKA “Cretinism”

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6
Q

What is thyroiditis in general?

who is it most often seen in?

What would we see in a thyroid scan?

A

Inflammation of the thyroid gland

  • there are 4 types
  • F > M
  • can be euT, hypoT, or hyperT
  • radioactive iodine: decreased uptake
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7
Q

What is Hashimoto’s Thyroiditis?sh

What would lab tests show?

A

Autoimmune destrxn of thyroid

Think “Mrs. Potatohead” = HASHbrowns, F, & myxedema

  • common!!!
  • painless, big thyroid
  • F>>M
  • eventual hypoT

LABS: ^^TSH, decreased T4

**anti-peroxidase antibodies

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8
Q

What cells could you see in Hashimoto troiditis biopsy?

A

Hurthle cells

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9
Q

What cell type(s) cause Hashimoto’s?

A

Tcells:

  • dont recognize own thyroid Ag’s
  • attack thyroid
  • stimulate B cells–>

B cells (unwitting accomplices)

  • anti-TSH-R antibody
  • anti-Thyroglobulin antibody
  • anti-peroxidase antibody
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10
Q

What is DeQuervain Thyroiditis?

-what cell types are involved

A

Think “Rex”= looks big & scary, but really harmless

  • big, sore thyroid
  • recent URI [viral]
    • Ag causes initial ^^in CD8 Tcells
    • damage follicles–>leak colloid
    • foreign body giant cell rxn ensues
  • early, HyperT
  • self-limiting
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11
Q

What would we see on a DeQuervain thyroid biopsy?

A

Lymphoid infiltrate

Degenerating

Giant multinucleated cells

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12
Q

What is Silent thyroiditis?

what are some proposed causes of this?

A

Think “Bullseye horse”: silent, doesnt cause problems

  • post-partum or middle age
  • painless, slightly enlarged thyroid
  • mild hyperT early on

***will also lymphoid infiltrate in this type

causes:

  • inherited [HLA?]
  • autoI [autoAB’s?]
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13
Q

What is Reidel Thyroiditis?

A

FIbrosing thyroiditis

Think “Woody”: he’s a “rider”, and woody= fibrosis

  • RARE
  • Rock-hard neck mass [fibrosis]
  • HypoT
  • tracheal compression
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14
Q

What is the Graves Disease triad?

A
  1. HyperT
  2. Opthalmopathy
  3. dermopathy
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15
Q

What is Graves Disease?

A

Type of hyperT

  • common
  • F>>M
  • triad
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16
Q

What would you see on a Graves thyroid biopsy?

what would an iodine scan show?

A

biopsy: papillae & scalloped colloid
iodine: diffuse ^^uptake

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17
Q

What antibodies are associated with graves disease?

A

ANTI-TSH-R ACTIVATING antibodies affect:

  • follicular cell proliferation–>
    • thyroid gets big
  • thyroid H release–>
    • Sx’s of hyperT
  • retroorbital tissues–>
    • opthalmolpathy
  • pretibial fibroblasts–>
    • dermopathy
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18
Q

What are tx’s for graves?

A

decrease sx’s:

  • B-blocker
  • surgery if needed

Decrease TH synthesis:

  • drugs
  • 1 time ablation w/ 131Iodine
  • surgery
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19
Q

What are the 2 broad causes of a goiter?

A
  1. inflammatory [thyroiditis]
  2. defective T4 synthesis = no I, enzyme defect, unknown [non-inflam]
  • decreased T4–> ^^TSH–>big thyroid
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20
Q

What can cause a multinodular goiter?

A

simple goiter–> trauma [hyperplasia & involution]–>multinodular

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21
Q

When is it more likely to be a thyroid cancer vs. benign?

A

^^cancer risk:

  • male
  • solitary nodule
  • cold nodule [doesnt take up Iodine]
  • Hx of radiation
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22
Q

Are thyroid adenomas benign or malignant?

what will lab tests show usually?

genetics?

Tx?

A

Thyroid adenomas= BENIGN & common!!!

  • pts usually euT, some HyperT
  • solitary, encapsulated nodule

LABS: norm TSH & T4, most are cold

genetics: may have Gp mutation or GOF mutation

_Tx: _ TAKE IT OUT!

  • even if benign, need to see whole capsule to tell if its carcinoma [look similar]
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23
Q

What is the MC type of thyroid carcinoma?

A

papillary [80%]!! aka LIL’ ORPHAN ANNIE TUMOR

  • F>M, 30s-50s [younger women]
  • local LN mets are common
  • visceral mets = RARe
  • excellent Px [>95% 10 yr survival]
    • usually well behaved, seldom kills ppl
    • stix around for yrs w/o getting bigger
    • nuclei resemble Annie’s eyes
    • psammoma bodies = greek for sand, Annies dog=Sandy
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24
Q

What kind of cells/abnormal morphologies will you see on a papillary carcinoma biopsy of the thyroid?

A

orphan annie nuclei [picture]

psammoma body

psuedoinclusions

nuclear grooves

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25
What is this a picture of?
psammoma body of thyroid [papillary carcinoma]
26
Tell me about Follicular Thyroid Carcinoma
* F\>M, 40s-50s\ * mets [if present] to lung & bone * 95% 10 year survival in young pts w/ small, minimally invasive tumor * **Px worsens with ^age, tumor size, & invasiveness** **\*\*biopsy: vascular invasion**
27
What is medullary Thyroid carcinoma
* uncommon malignancy of C cells [parafollicular] * F\>M, 50s-60s * sporadic [MC] or familial * 90% 10 y survival if confined to thyroid * 20% 10 y survival if distant mets present
28
What is Anaplastic Thyroid carcinoma
* rare * F\>M, 50s-60s * bulky, fast growing, invasive neck mass * usually metastatic @ Dx * very bad Px [\<10% 5y survival]
29
What are the major causes of HyperCa+?
MD PIMPS ME ## Footnote M: malignancy M: milk-alkali syndrom D: diuretics E: endocrine [thyrotoxicosis] P: parathyroid I: idiopathic M: megadose of vitD P: paget disease S: sarcoidosis
30
MCC of Sx'c hyperCa+? MCC of aSx'c hyperCa+?
Sx'c: malignancy Asx'c: hyperPT
31
What are the 1', 2', 3' & psuedo causes of hyperPT?
1'= PT problem [adenoma] 2' = chronic hypoCa+ [renal failure] 3' = autonomous PT's --\>hyper-fxnl for some reason PsuedoHPT = PTH-related protein [lung cancer]
32
What are signs/sx's of 1' HyperPT?
often ASx'c but... STONE: K stones, and others BONE: pain, brown tumors, worse [osteoP?] GROAN: GI problems MOAN: mental changes
33
Lab findings in 1' HyperPT?
^^Ca+ ^^PTH decreased phosphate
34
What is MCC of 1' HyperPT? what genetics may be involved?
MCC = PT Adenoma genetics: PRAD1 overexpression * MEN1 loss or mutation
35
MCC of 2' HyperPT?
**renal failure**--\> chronic hypoCa * can't excrete phosphate--\> ^^PO4 * excess PO4 --\> binds Ca+ * Ca+ decreases = hypoCa+ * hypoCa+ --\> stims PT's
36
What are signs and Sx's of hypoPT?
* •Neuromuscular irritability * •Perioral numbness * •Muscle weakness, cramps, tetany * •Chvostek’s sign * •Trousseau’s sign * •Heart arrhythmias * •Dental abnormalities [enamel hypoplasia]
37
What are the main causes of hypoPT?
* iatrogenic * hereditary * DiGeorge syn * Agenesis [X-linked] of PT's * Idiopathic atrophy
38
What are the major fxns of cortisol?
cortisol is BBIIG: ## Footnote maintains BP breaks down Bone suppresses Inflammation suppresses Immune system stimulates Gneo
39
What are the the 4 forms of cushing syndrome?
1' = adrenal tumor secreting cortisol 2' = pituitary tumor secreting excess ACTH--\> ^^cortisol 3'= paraneoplastic/ectopic--\> small cell carcinoma of the lung secretes ACTH Iatrogenic: taking steroids --\> ^^cortisol in drugs * but leads to adrenal atrophy
40
What is the MCC of Cushing Syndrome?
Iatrogenic Cushings! [steroid use] * atrophy of adrenal cortex * labs: ^^cortisol & decreased ACTH
41
What would you see in pituitary cushings? - labs - adrenal glands - what would happen with a high dose DEX test
* hyperplastic adrenal cortices * labs: ^^cortisol * ^^ACTH * Hi DEX: suppresses cortisol!!!
42
What would you see in adrenal cushings? - causes? - morph of adrenal - labs? - dex test?
Causes: adenoma, hyperplasia, carcinoma * cortex: hypoplastic or hyperplastic * labs: ^^cortisol, decreased ACTH DEX: no suppression!!!
43
What would you see in paraneoplastic cushings? -cause labs? adrenal cortices? DEX?
causes: small cell lung carcinoma secretes ACTH - adrenal hyperplastic cortices LABS: ^^cortisol & ^^"fake"ACTH DEX: no suppression
44
What findings would yuo see in hyperaldosteronism?
^^aldosterone: duh ^^BP hyperNa+ hypoK+
45
1' hyperaldosteronism causes? Sx's?
* ­ ^^aldosterone --\> decreased renin [thru (-) feedback] * Cortical adenoma (Conn syndrome) * Cortical hyperplasia _SX's:_ * HTN [hyperNa] * weakness/fatigue/psychosis [hypoK] ​LABS: ^^aldo--\>decreased renin hyperNa, hypoK, metabolic alk
46
2' hyperaldosteronism -sx's common cause/assoc
* ­ ^^renin--\> ^^aldosterone * Congestive heart failure * decreased renal blood flow * Renin-producing tumors ## Footnote \*\*same sx's & findings as 1' but with **^^renin **too
47
What should we associate with sudden virilization?
adrenocortical tumor * rare * abd mass * necrotic, "ugly" tumor * Bad Px
48
What is the MCC of congenital adrenal hyperplasia [CAH] - what adrenal cortex H's will be elevated & decreased? - what are 3 types of this deficiency?
21-hydroxylase deficiency * decreased cortisol * decreased aldosterone [HoTN, hypoNa] * ^^sex steroids [virilization] Types: [depends on mutation, XX virilization] 1. salt-wasting [no mineralocorticoids aka aldosterone] 2. simple virilizing [some mineraloCs] 3. late-onset virilizing [some mineraloC, some cortisol]
49
What are causes of 1' chronic adrenal insufficiency? MCC? Sx's?
too little cortisol & mineraloC's MCC: autoI--\> Addison Disease _Sx's:_ weakness, fatigue, GI complaints * hypoTN * skin hyperpigmented
50
What do we Tx Addison's Disease with?
Tx Sx's [in crisis]: w/ IV NA+, dextrose, hydrocortisone Daily after crisis: **cortisol & prednisone** [carries crisis kit: hydrocortisone]
51
Primary Acute Adrenal Insufficiency causes?
adrenals suddenly aren't releasing their stuff _causes:_ * addisonian crisis * rapid steroid w/drawal * massive adrenal hemorrhage * WF syndrome
52
What is Waterhouse-Friderichsen Syn?
*leads to 1' Acute Adrenal Insufficiency* * Bacterial infection (N. meningitidis) * Hypotension, shock * DIC * Massive, bilateral adrenal hemorrhage * Rapidly progressive
53
WI 2' adrenal insufficiency? causes? findings?
Decreased ACTH--\> decreased adrenal products _causes:_ * pit or hypothalamic insufficiency * tumor, infxn, radiation, infarxn _findings_: * Sx's of decreased cortisol & sex steroids * mineraloCs are normal [renin axis is intact] * no hyperpigmentation
54
Pheochromocytoma...WI it? 10%.... what is found in the urine?
RARE neoplasm of catecholamine-producing cells * causes HTN * Urine: catecholamines, VMA & metanephrines **10%...** * extra-adrenal tumor "paraganglioma" * bilateral * familial * malignant * dont present w/ HTN
55
What are the Sx's of pheochromocytoma? 6 P's!!!
* Pressure [^^BP] * Pain [HA] * Perspiration * Palpitations [tachyC] * Pallor * Paroxysms
56
When I say Zellballen, you say...?
pheochromocytoma zellballen= configuration of cells in tumor
57
Where is neuroblastoma derived from? what gives a better Px?
relatively common childhood tumor **of neural crest cells** ^^Px: * kids\<18 months * lower stage tumors * lower grade tumors * hyperdiploid tumors * fewer copies of **N-myc**
58
What cell types will be in adrenal neuroblastoma biopsy?
homer-wright rosettes
59
What characteristics give MEN syndrome WORSE Px?
younger multiple organs multifocal aggressive
60
Who is sexy? Brad Pitt or John Cleecy?
John Cleecy!!!
61
Where would you find tumors in MEN 1 vs MEN2?
_MEN1_: Every other endocrine organ can have tumors * NOT much in Thyroid _MEN2:_ medullary carcinoma of the thyroid * NOT much in other endocrine organs
62
What are the 3 P's of MEN1? & other!
_PT hyperplasia:_ MC manifestation, hyperCa+ _Pancreatic endocrine tumors:_ gastrinoma {ZE syn}, Insulinoma [hypoGly], usually metastatic at Dx, BAD news _**PITT**uitary adenoma:_ prolactinoma usually _Other_ duo gastrinoma, carcinoid, thyroid/adrenal adenomas, lipomas \*\*\*brad Pitt is men1
63
What are the genetics associated w/ MEN1?
**MEN1 gene mutation** [a tumor suppressor gene that encodes menin] \*\*brad Pitt = men1: run of the mill & turns you off
64
MEN 2A syndrome? what tumors? what guy?
* medullary thyroid carcinoma * all pts get this? aggressive, multifocal, **C-cell hyperplasia **[precursor to getting the cancer] * see chunky stuff on Bx= calcitonin secreted 4m Ccells * pheochromocytoma * 50% of pts, bilateral, extra-adrenal * benign or malignant * PT hyperplasia * 10-20% or pts, hyperCa
65
What are the genetics of MEN2A?
RET gene mutation **protooncogene** encodes tyrosine kinase R mutation turns you on!!! like john cleecy
66
Where do you see tumors in MEN2B? what genetics are involved
MEN2B tumors: * medullary thyroid carcinoma [c-cells remember] * pheochromocytoma * **neuromas** [lesions of N sheath cells in your skin] * **Marfanoid** habitus [look like marfans but dont have it] * NO PT hyperplasia Gentetics: RET gene John cleecy = bRETon gene, one of a kind and always turned on

Endo/Repro Block1 (11 decks)

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